CMC Vellore Handbook - EM

CMC Vellore Handbook of
EMERGENCY MEDICINE
CMC Vellore Handbook of
EMERGENCY MEDICINE
THIRD EDITION
Editor
KPP Abhilash
MBBS MD PDF (Emergency Medicine)
Professor and Head
Department of Emergency Medicine
Christian Medical College Hospital
Vellore, Tamil Nadu, India
Foreword
K Prasad Mathews
MD FRACP (Geriatrics)
Medical Superintendent, CMC
CMC Vellore Handbook of Emergency Medicine, previously called

Emergency Medicine at CMC (EMAC)
A Compendium for
Emergency Department Registrars
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CMC Vellore Handbook of Emergency Medicine / KPP Abhilash

First Edition: 2016
Third Edition: 2022
ISBN: 978-93-5465-132-8
Dedicated to
Dr Shubhanker Mitra (1981–2016) who was a fantastic colleague and friend, an

outstanding clinician and researcher. Born on January 16, 1981, he joined Christian
Medical College, Vellore, Tamil Nadu, India in the year 2000. He completed MD in
General Medicine in 2010 and joined the department of General medicine and later
Emergency department as a faculty. He lived his life with joyful exuberance, reckless
investigation, legendary neologisms, irrepressible mischief, a penchant for drama
and touching mindfulness for those around him.
Many will vouch for his diligence in the process of diagnosis, commitment to true
hands-on personal care, and willingness to teach others as he learnt. His work ethic,
devotion to his patients, and drive toward self-improvement, was exemplary and an
example to all his colleagues. As a teacher, he was instrumental in spurring many into
research fields, if not into plain pure inquisitiveness.
Over the last 5 years, he had been instrumental in resurrecting the culture of
undergraduate research. He was the force behind Cognitio: CMC’s Undergraduate
Research Conference. Our undergraduates have since gone on to be regular features
in conferences, winning awards at several conferences.
He would certainly be missed by all those who had the privilege to know and
work with him.
Contributors
Priya G MD (Anesthesiology) Sandeep David MD (Anesthesiology)

Department of Emergency Medicine Department of Emergency Medicine
Christian Medical College Christian Medical College
Vellore, Tamil Nadu, India Vellore, Tamil Nadu, India
Surendra Kumar FAEM, D Ortho Sivanandan MD Anesthesiology
Debasis Das Adhikari DCh DNB (Pediatrics) John Jesudasan FAEM
FAEM FAPEM Department of Emergency Medicine
Department of Pediatric Emergency Christian Medical College
Christian Medical College Vellore, Tamil Nadu, India
Gautham Raja FAEM MRCEM
David Vincent FAEM Department of Emergency Medicine
Department of Emergency Medicine Christian Medical College
Anne George MD O(bstetrics and Gynecology)
Ashwin Rajanesh MD (General Medicine) Department of Community Medicine
Department of Emergency Medicine Christian Medical College
Moses Kirubairaj DipNB (Family Medicine)
Vineet Subodh FAEM FAEM
TS Ravi Kumar MSc (Nursing) Jeyalinda Christopher MSc (Nursing)
Christian Medical College Christian Medical College,
Esther Paul BSc (Nursing) Sri Ranjani BSc (Nursing)
Sisha Liz Abraham MS DipNB Suma Mary Thampi MD (Anesthesiology)
(Otorhinolaryngology) FHNS Department of Anesthesia
Department of ENT Christian Medical College
Deepu David MD DM (Gastroenterology)
Roshna Rose Paul MS (Otorhinolaryngology) Department of Gastroenterology Christian
Department of ENT Medical College
Foreword
I am very happy to write the foreword for the 3rd Edition of the
Handbook of Emergency Medicine. “Emergency Medicine” is an
emerging specialty in India. Christian Medical College, Vellore,
Tamil Nadu has been at the forefront of Emergency Medicine in
India and has been conducting the course on “Early management
of Trauma” from 1998.
The Department of Emergency Medicine has grown
exponentially over the years. The volume and variety of patients managed has
increased dramatically. The number of faculty and staff has increased accordingly.
Training for all doctors in emergency medicine through standardized protocols
written in this book has greatly helped in improving the quality of patient care.
Early trauma management and the art of making a quick diagnosis are essential
for the quick recovery of the patient. This manual provides a valuable resource in
emergency medicine for doctors working in all settings.
I wish the Emergency Medical team all the very best in their efforts to educate
more doctors and paramedical workers in this important specialty.
K Prasad Mathews
MD FRACP (Geriatrics)
Medical Superintendent
CMC Medical Superintendent
Christian Medical College
Preface to the Third Edition
There has been a perceived need to have comprehensive

guidelines for all acute medical and surgical emergencies
presenting to the emergency department (ED) of Christian
Medical College (CMC), Vellore, Tamil Nadu, India. This book
is a compilation of all management guidelines and protocols
followed in our ED. Since the ED of CMC was formed 22 years
ago, there have been various changes in the structure and
concept of emergency care.
Our adult ED is one of the largest in the country with 100 beds and an annual
patient load of more than 80,000 patients. The ED registrars are exposed to a wide
spectrum of disease conditions. The COVID-19 pandemic thrust the emergency
department to the forefront and all emergency physicians rose up to the challenge
and weathered the storm. Through this book an attempt has been made to cover
the basics of all the commonly seen medical and surgical conditions in our ED
and the emergency management principles in a simplified manner. Many newer
concepts have replaced the traditional management practices. Every effort has
been taken to incorporate the latest evidence-based recommendations in the
CMC Handbook of Emergency Medicine.
I hope that this book would serve the purpose of achieving the goal of protocol-
based evaluation and evidence-based management of the common emergencies. If
this book helps to provide better patient care and stimulates interest in emergency
medicine among medical, nursing, and paramedic students, our efforts will indeed
have been worthwhile.
All comments and constructive suggestions are welcome for further editions of
the Handbook of Emergency Medicine.
Wishing all the readers the very best!
KPP Abhilash
MBBS MD PDF (Emergency Medicine)
Professor and Head
Emergency Department
Christian Medical College
Acknowledgments
• I acknowledge all the contributions who helped to prepare the 1st, 2nd, and 3rd
editions of this handbook of emergency medicine. The final product is the result
of intensive work put in by these contributors.
• Mr Senthil, Ms Bagyalakshmi, and Mr Sathish Kumar for their assistance in
putting it all together.
• Dr Latif Rajesh Johnson for the photoshoot of the cover picture.
• The “emergency department” registrars, consultants, nurses and paramedics for
all their suggestions and comments.
• The patients in the emergency department who teach us something new every
day.
• To my parents, Dr KPA Chandrasekhar and Mrs KLT Priyadarshini, brother, sister-
in-law, my niece, and friends for their everlasting support.
• We especially appreciate the constant support and encouragement of
Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director),
Mr MS Mani (Group President), Jaypee Brothers Medical Publishers (P) Ltd,
New Delhi, India in publishing this handbook and also their associates
particularly Dr Richa Saxena (Associate Director-Professional Publishing),
and Ms Prerna Bajaj (Development Editor) who have been prompt, efficient,
and most helpful.
Advice to the Readers
• Treat the patient’s symptoms. Do not treat the monitors or laboratory

investigations.
• Do not start your workup by looking at outside investigations. Your diagnosis
will be totally biased.
• History is the most vital component needed to make a diagnosis. A wrong
history will always lead you to the wrong diagnosis.
• Never ignore abnormal vital signs. They are more accurate in assessing the
severity of the illness than your visual assessment of the patient.
• Develop your clinical skills. Never depend on the laboratory to make a clinical
diagnosis. Train your brain to be better than a machine.
• History, examination findings, clinical diagnosis, and the laboratory investi-
gations should be internally consistent. Otherwise, something is wrong
somewhere. It is most probably a laboratory error (if your brain is smart enough).
• It is good to follow guidelines, but that should not limit your thinking process.
• Learn to make a list of differential diagnoses after history taking and clinical
examination, not after viewing the results of blood investigations or imaging.
• Change is the only permanent thing in life. Be rational, question existing
protocols, and try to improve yourself, patient care, and the department.
• Strive for academic excellence through research. The ED is an untapped
goldmine for research.
Contents
Section 1: Basic Life Support and Management of Cardiac Arrest

1. Basic Life Support 3
2. Management of Cardiac Arrest 14
Section 2: Anaphylaxis, Shock and Airway

3. Anaphylaxis 29
4. Overview of Shock 32
5. Septic Shock 35
6. Airway Management 40
7. Respiratory Support 44
Section 3: Fluid and Electrolytes

8. Fluid Therapy 51
9. Sodium 53
10. Potassium 56
11. Calcium 59
12. Magnesium 62
13. Acid-base Abnormalities 64
Section 4: Infectious Diseases

14. Antibiotic Protocol for Common Conditions 71
15. Dengue 75
16. Scrub Typhus 78
17. Malaria 80
18. Community-acquired Pneumonia 82
19. Influenza and H1N1 84
20. COVID-19 86
21. Rabies 90
22. Food Poisoning and Acute Gastroenteritis 93
23. Urinary Tract Infections 95
24. Acute Central Nervous System Infections 98
25. Tetanus 101
26. Antibiotic Doses and Spectrum 103
xviii Contents
Section 5: Toxicology
27. General Measures 109
28. Drug Overdose 111
29. Insecticide Poisoning 116
30. Rodenticides 121
31. Plant Poisons 124
32. Snake Bites 128
33. Insect Envenomation 131
34. Substance Abuse 134
35. Miscellaneous 137
Section 6: Cardiac Emergencies

36. Acute Coronary Syndrome 147
37. Hypertensive Emergencies 154
38. Pulmonary Edema 157
39. Atrial Fibrillation 159
40. Atrial Flutter 162
41. Paroxysmal Supraventricular Tachycardia 164
42. Wide Complex Tachycardias 166
43. Valvular Emergencies 169
44. Basics of Electrocardiogram 171
Section 7: Respiratory Emergencies

45. Bronchial Asthma 179
46. Chronic Obstructive Pulmonary Disease 183
47. Pulmonary Embolism 186
48. Pneumothorax 188
49. Hemoptysis 190
Section 8: Neurological Emergencies

50. Cerebrovascular Accidents 195
51. Cerebral Venous Thrombosis 199
52. Intracranial Hemorrhage 202
53. Guillain–Barré Syndrome 205
54. Hanging 207
55. Seizures 209
56. Headache 213
Contents xix
57. Bell’s Palsy 216

58. Acute Dystonia 218
59. MRI Stroke Protocol 219
Section 9: Gastrointestinal and Hepatic Emergencies

60. Gastrointestinal Bleeding 225
61. Acute Pancreatitis 227
62. Spontaneous Bacterial Peritonitis 229
63. Hepatic Encephalopathy 231
64. Acute Cholangitis 233
Section 10: Hematological Emergencies

65. Anemia 237
66. Febrile Neutropenia 240
67. Acute Leukemia 241
68. Tumor Lysis Syndrome 243
69. Sickle Cell Crisis 245
70. Anticoagulants 247
71. Bleeding and Clotting Disorders 250
72. Hemophilia and von Willebrand Disease 253
73. Blood Products and Transfusion 255
Section 11: Endocrine Emergencies

74. Thyrotoxic Crisis 259
75. Myxedema Coma 261
76. Adrenal Insufficiency 263
77. Diabetic Emergencies 265
78. Pheochromocytoma 270
Section 12: Obstetric and Gynecological Emergencies

79. Ectopic Pregnancy 273
80. Bleeding Per Vagina 275
81. Hyperemesis Gravidarum 278
82. Pelvic Inflammatory Disease 279
83. Ovarian Torsion 280
84. Pregnancy Induced Hypertension (Preeclampsia and Eclampsia) 282
85. Postpartum Hemorrhage 284
xx Contents
Section 13: ENT Emergencies

86. Epistaxis 289
87. Stridor 291
88. Vertigo and Benign Paroxysmal Positional Vertigo 292
89. Deep Neck Space Infections 297
Section 14: Urological Emergencies

90. Nephrolithiasis 301
91. Torsion Testis 303
92. Epididymo-orchitis 305
93. Penile Emergencies 307
Section 15: Surgical Emergencies

94. Skin and Soft Tissue Infections 313
95. Duodenal Ulcer Perforation 315
96. Acute Appendicitis 317
97. Acute Cholecystitis 320
98. Intestinal Obstruction 322
99. Mesenteric Ischemia 324
100. Gas Gangrene 326
101. Nail Bed Emergencies 327
102. Anorectal Emergencies 331
103. Vascular Emergencies 334
104. Breast Disorders 338
Section 16: Trauma

105. Early Management of Trauma 341
106. Hemorrhagic Shock 345
107. Head Injury 348
108. Cervical Spine 350
109. Maxillofacial Trauma 355
110. Thoracic Injuries 358
111. Abdominal Injuries 361
112. Extremity Injuries 364
113. Wound Management 379
114. Scalp Laceration 381
115. Compartment Syndrome 383
Contents xxi
116. Trauma in Pregnancy 385

117. Pediatric Trauma 388
118. Geriatric Trauma 392
119. X-rays in Trauma 394
120. Eponyms in Trauma 396
Section 17: Pediatric Emergencies

121. Assessment of a Sick Child in the Emergency Department 405
122. Febrile Seizures 412
123. Acute Asthma and Status Asthmaticus 414
124. Acute Stridor and Epiglottitis 417
125. Pneumonia and Bronchiolitis 420
126. Acute Otitis Media and Otitis Externa 423
127. Acute Gastroenteritis 424
128. Drugs and Dosages in Pediatric Emergencies 426
Section 18: Disaster Management

129. Mass Casualty Incidents 435
Section 19: Medicolegal Cases

130. Medicolegal Cases 441
Section 20: Triage

131. Triage Priorities 445
Section 21: Miscellaneous

132. Heat-related Illnesses 451
133. Malignant Hyperthermia 453
134. Neuroleptic Malignant Syndrome 455
135. Electrical Injuries 457
136. Burns 459
137. Drowning or Submersion Injuries 462
138. Alcohol-related Emergencies 464
139. Sudden Visual Loss 466
140. Acute Red Eye 469
141. Dermatological Emergencies 471
142. Needle-stick Injuries 473
xxii Contents
143. Drugs in Pregnancy 476

144. Acute Arthritis 479
145. Procedural Sedation 481
Section 22: Procedures

146. Nerve Blocks 485
147. Central Venous Access 493
148. Chest Tube Insertion 495
149. Intraosseous Line 497
150. Cricothyroidotomy 499
151. Pericardiocentesis 502
152. Pleural Tap 504
153. Ascitic Tap (Paracentesis) 505
Section 23: Protocols

154. Intubation Protocol 509
155. Investigations Protocol 511
156. Pain Protocol in the Emergency Department 513
157. Polytrauma/Trauma Team Activation Protocol 515
158. Prophylactic Antibiotic Protocol for Trauma Patients in
the Emergency Department 517
Index 521
Section 1
Basic Life Support and
Management of
Cardiac Arrest
Basic Life Support 1
CHAPTER
INTRODUCTION
Basic life support (BLS) is the component of the immediate care provided for the
victims of life-threatening conditions, leading to cardiac arrest, and injuries till the
patient can be shifted to a hospital. It can be given by doctors, nurses, paramedics,
or even by a trained bystander.
The brain is very sensitive to hypoperfusion. Therefore, the main objective of
BLS is to restore cerebral perfusion at the earliest.
The American Heart Association (AHA) periodically revises the guidelines for
BLS and Advanced Cardiac Life Support (ACLS). The 2020 AHA guidelines laid
emphasis on the following:
• Sequence of BLS: Circulation–Airway–Breathing (C–A–B)
• High-quality cardiopulmonary resuscitation (CPR)
• Use of naloxone (intramuscular or intranasal) in suspected opioid overdose
• Use of defibrillator for witnessed cardiac arrests as soon as possible
• Early epinephrine as soon as possible
• Monitoring arterial waveform with ETCO2
• Real-time audio–visual feedback to improve team performance.
BASIC LIFE SUPPORT/CARDIOPULMONARY

RESUSCITATION FOR ADULTS
Basic life support consists of the following main parts:
• Chest compressions
• Airway
• Breathing
• Defibrillation
Overview of Initial Basic Life Support Steps (Table 1)

• Assessment and scene safety.
• Remove victim from the hazardous environment to a place where care may be
provided without putting the victim or BLS provider at a risk of harm.
• Look for response and breathing pattern. If there is no response and the victim
is not breathing or is gasping, shout for help.
• Check the victim’s carotid pulse (take at least 5 seconds but no more than
10 seconds) (Fig. 1).
4 SECTION 1: Basic Life Support and Management of Cardiac Arrest
TABLE 1: Steps of basic life support.

Step 1 Assessment and • Make sure that the scene of the incident is safe for
scene safety you and for the victim
• Relocate victim from hazardous environment
Step 2 Recognize the cardiac arrest
Look for response • Tap the victim’s shoulder and shout, “Are you all
and breathing right?”
• If there is no response, no breathing or gasping,
shout for help
Check the victim’s • Take at least 5 seconds but no more than 10 seconds
pulse to check for pulse
• Locate the trachea using two or three fingers
• Feel the carotid pulse between trachea and the
muscles of the neck (lateral to the thyroid cartilage).
If no pulse is felt, activate the emergency response
system
Step 3 Activate the • If you are alone with an unresponsive victim and do
emergency response not have a mobile phone: Activate the emergency
system response system, get an AED, if available and then
begin the CPR
• If you have help at hand: Send them to get the AED
and begin CPR
Step 4 Start CPR with 30 chest compressions and 2 breaths
Chest compressions • Position yourself beside the victim
• Keep the victim in supine position and on a firm
surface
• Place the heel of one hand on the lower half of the
victim’s sternum
• Place the heel of the other hand on the top of the
first hand and interlock your fingers
• Straighten your elbows and position your shoulders
directly over your hands
• Push hard and fast
• Allow for complete chest recoil
• Minimize interruptions
Rescue breaths • Head tilt, chin lift to open the airway
• In case of suspected cervical spine injury, use only
jaw thrust. Avoid head tilt and chin lift
• Provide two rescue breaths keeping the nose
pinched after every 30 compressions
• Use an improvised mask device, if available
• Look for a chest rise with each rescue breath
• If unable to provide breaths, continue with chest
compressions
(AED: automated external defibrillator; CPR: cardiopulmonary resuscitation)
CHAPTER 1: Basic Life Support 5
FIG. 1: Carotid pulse check.
• Activate the emergency response system and get an automatic external

defibrillator (AED), if available and return to the patient.
• Start CPR. Perform five cycles of chest compressions and breaths (30:2),
starting with compressions (C–A–B sequence).
Chest Compressions
High-quality CPR improves a victim’s chance of survival. The BLS provider should
follow these critical characteristics of chest compressions while providing high-
quality CPR (Fig. 2).
• Start compressions within 10 seconds of recognition of cardiac arrest.
• Push hard, push fast: Compress at a rate of at least 100–120/min with a depth of
at least 5 cm (2 inches) for adults, approximately 5 cm (2 inches) for children,
and approximately 4 cm (1½ inches) for infants.
• Allow complete chest recoil after each compression.
• Minimize interruptions in compressions (try to limit interruptions to <10 s).
• In case of lay rescuer or sole rescuer present, compression only CPR is
sufficient.
• Give effective breaths that make the chest rise. With an advanced airway in
place, deliver 10 breaths/min or 1 breathe every 6 seconds.
Airway Maneuvers
In an unresponsive patient, the airway may be occluded due to decreased tone
of the tongue and pharyngeal muscles. There are two methods of opening the
airway to provide rescue breaths (Table 2 and Figs. 3A and B).
Use only jaw thrust in cases of suspected head injury or cervical spine injury. Avoid head
tilt–chin lift maneuver in these circumstances.
B C
FIGS. 2A TO C: Technique of chest compressions.
TABLE 2: Two methods of opening the airway.

Method Description
Head tilt–chin lift This maneuver lifts the tongue off the posterior pharynx thus
opening up the airway. Avoid in cases of suspected cervical injury
• Place your palm on the victim’s forehead and apply downward
pressure thus, tilting the head backward
• Place the tips of the index and middle fingers at the mentum of the
mandible and lift the chin upward
Jaw thrust Jaw thrust is indicated if the victim has a head or neck injury
• Place one hand on each side of the victim’s head, resting the
elbows on the surface on which the victim is lying
• Place the fingers under the angles of the victim’s mandible and
lift with both the hands, displacing the jaw forward
The jaw thrust displaces the mandible and tongue anteriorly, thus
preventing the lax tongue from occluding the airway
A B
FIGS. 3A AND B: (A) Head tilt–chin lift; and (B) Jaw thrust.
Caution
• Avoid pressing deeply into the soft tissue under the chin as this may block the
airway.
• Avoid using the thumb to lift the chin.
• Do not close the victim’s mouth completely.
Ventilation
Respiratory arrest is a condition where the patient’s respiratory efforts are either
inadequate to maintain oxygenation or completely absent.
Management of a respiratory arrest includes the following components:
• Administering oxygen
• Keeping the airway open using basic airway adjuncts
• Suctioning if necessary, to clear secretions
• Providing basic ventilation using bag mask equipment
• Securing an advanced airway
• Identifying the cause.
Basic Airway Adjuncts

In unresponsive patients, the tongue can fall back and obstruct the airway due
to loss of tone of the throat muscles. This can be prevented by the basic airway
opening techniques (head tilt–chin lift or jaw thrust). In addition to this, two
basic airway adjuncts (oropharyngeal airway or nasopharyngeal airway) can be
used to facilitate ventilation during resuscitation (Fig. 4). These are indicated
only in unconscious patients and come in various sizes. The correct size should
be chosen for each patient for maximum benefit and to minimize complications
such as oral trauma.
Oropharyngeal Airway
• Choose the correct size: It should be the distance between the first incisor and
the angle of the mandible.
• If it is too large, it may close the glottis and block the airway.
A B
FIGS. 4A AND B: Basic airway adjuncts: Oropharyngeal airway and
nasopharyngeal airway.
• In adults: Insert the tube with the concavity upward and then rotate it to 180
degree, when it touches the back of the throat.
• In children and infants: Insert the tube with the concavity downward while
using a tongue depressor to hold the tongue forward.
• It is contraindicated in conscious patients as it can induce a gag resulting in
vomiting.
Nasopharyngeal Airway
• Choose the correct size: It should be the distance between the tip of the nose
and the earlobe.
• It is inserted through one of the nostrils after lubricating it with an anesthetic
jelly. Push it till the flared end is at the nostril.
• It can be inserted in semiconscious patients.
• It is contraindicated in patients with base of skull fractures and nasal bleeds.
Rescue Breaths
• Ventilation may be provided mouth-to-mouth or mouth-to-nose.
• A mask or an improvised device (such as a rolled-up board) may be used.
• Give two rescue breaths after every 30 compressions.
• Give sharp rescue breaths, each over not more than 1 second.
• Provide enough tidal volume to see the chest rise, but avoid excessive ventilation.
• In an in-hospital setting, get a bag-mask for ventilation, if available.
Bag-mask Ventilation
Bag-mask ventilation (BMV) is a very efficient method of temporarily providing
positive pressure ventilation.
The BMV device consists of:
• Self-inflating reservoir bag along with a mask
• A one-way valve which prevents rebreathing the exhaled air
• Oxygen port for supplying supplemental oxygen.
Use the E–C clamp technique to bag-mask a patient (Table 3). If done properly,
it is as effective as a secured airway. Bag-mask ventilation can be done by one or
two people (Fig. 5).
TABLE 3: E–C clamp technique.

Single rescuer Use your thumb and first finger to form a C around the mask and place
your third, fourth, and fifth finger under the bony part of the mandible
forming an E to lift the jaw. Use the other hand to bag-mask
Two rescuers One person stands at the headend of the patient and holds the mask
bag mask firmly with both hands over the patient’s face using the E–C technique.
The other rescuer slowly squeezes the bag over for 1 s to provide an
effective chest rise
A B
FIGS. 5A AND B: E–C clamp technique: Single rescuer and double rescuer.
The following are the steps involved in bag-mask ventilation:

1. Place mask on the victim’s face. Use an airway adjunct if available.
2. The nasal end of the mask should cover the bridge of the nose, not extending
over the eyes; the body of the mask should cover the nose and mouth, and the
other end not extending beyond the chin.
3. Hold the mask using a single hand E–C technique or with both the hands
(preferred) if an additional rescuer is present.
4. Apply firm pressure, forming a good mask seal.
5. Ventilate using a volume just sufficient to cause chest rise (not more than 8–10
mL/kg).
6. Squeeze the bag steadily over a second. Avoid explosive squeezing.
7. Connect bag-mask device to reservoir bag with O2 supply, if available.
8. Give two ventilations after every 30 compressions for patients without an
advanced airway.
9. Give asynchronous ventilation every 8–10 seconds (6–8/min) to patients with
an advanced airway in place.
Basic life support for adults is explained in Flowchart 1.
FLOWCHART 1: Adult basic life support algorithm.

RESUSCITATION FOR CHILDREN (CHILDREN FROM
1 YEAR OF AGE TO PUBERTY)
The child BLS sequence is similar to the sequence in adults. Following are the key
differences:
• Compression–ventilation ratio for two rescuer CPR is 15:2 and for lone rescuer
is 30:2
• Compression depth: Compress at least one-third of the depth of the chest,
approximately 5 cm (2 inches).
• Compression technique: Can use one- or two-handed chest compressions for
very small children.
• Defibrillation dose: First shock: 2 J/kg, second shock: 4 J/kg, subsequent
shocks >4 J/kg, and maximum dose 10 J/kg or adult dose.
• To activate the emergency response system, following points are to be
considered:
cc In case of unwitnessed arrest and if the rescuer is alone, provide 2 minutes
of CPR before leaving the child to activate the emergency response system
and get the defibrillator.
cc In case of sudden and witnessed arrest, leave the child to activate the
emergency response system and get the defibrillator.


RESUSCITATION FOR INFANTS
The key points for infant BLS are:
• Pulse check: Feel the brachial artery in infants to check pulse.
• Technique of chest compressions: Two fingers for single rescuer and two thumb
encircling hand technique for two rescuers (Fig. 6).
• Compression depth: At least one-third the chest depth, approximately 4 cm
(1½ inches).
• Compression–ventilation ratio for two rescuers CPR is 15:2 and for lone
rescuer, 30:2.
• Defibrillation dose: First shock: 2 J/kg, second shock: 4 J/kg, subsequent
shocks >4 J/kg, and maximum dose 10 J/kg.
• To activate the emergency response system, follow the same steps as followed
for children.
Basic life support for children and infants is explained in Flowchart 2.
Defibrillation and Cardioversion

• Defibrillation is the nonsynchronized delivery of a shock that depolarizes
the entire cardiac tissue into a refractory period, making it unable to sustain
or propagate an aberrant circuit. It is performed during a cardiac arrest in a
pulseless patient.
• Cardioversion is the delivery of energy that is synchronized to the QRS
complex, thus only depolarizing the active circuit causing arrhythmia. It is
used to revert arrhythmias in awake patients (Table 4).
A B
FIGS. 6A AND B: Technique of chest compression in children.

FLOWCHART 2: Pediatric basic life support algorithm.
TABLE 4: Differences between cardioversion and defibrillation.

Cardioversion Defibrillation
Elective procedure Emergency procedure
Victim is awake but frequently sedated Victim is unconscious
Shock is synchronized with QRS Shock is not synchronized
Indications Indications
• Refractory supraventricular tachycardia Pulseless ventricular tachycardia
• Unstable atrial fibrillation/flutter Ventricular fibrillation
• Unstable ventricular tachycardia with pulse
50–200 J (biphasic) • 200 J (biphasic)
• 360 J (monophasic)
Monophasic versus Biphasic Defibrillators

• Defibrillators are machines that deliver electrical energy to the heart by
monophasic or biphasic waveform technology through paddles applied on
the chest wall.
• Monophasic defibrillators deliver the charge in only one direction, from one
electrode to the other. They use higher energy, typically 360 J and have many
disadvantages. They are no longer used in most emergency departments
(EDs).
• Biphasic defibrillators use lesser energy, are more efficient and cause lesser
damage to the heart. They deliver a charge in one direction in the first half and
the direction is reversed in the second half; hence a biphasic waveform.
• Currently, almost all the AEDs, manual and implantable defibrillators use the
biphasic waveform technology.
Using an Automatic External Defibrillator
• Read the instructions on the AED.
• Stick the pads on the chest wall.
• Place the right pad (white) below the right clavicle and the left pad (red) on the
left inferior-lateral chest, lateral to the apex.
• If the patient has an open thorax injury, respective pads may be placed on the
left and right axilla.
• Turn on the AED and follow the voice prompts.
• The AED will analyze the cardiac rhythm and will deliver defibrillation if a
shockable rhythm is present.
Using a Biphasic Defibrillator

• Turn on the defibrillator to the manual mode.
• Select the desired dose of energy (200 J in adults and 2 J/kg in children).
• Remove paddles, apply gel on the paddles.
• Charge paddles using the charge button on the paddles or on the device.
• Place paddles over the chest wall (Sternal paddle below the right clavicle and
apex paddle on left lateral chest wall).
• Resuscitation team should stay clear of contact, oxygen circuit should be
disconnected.
• Deliver shock by using the discharge button on the paddles or on the device.
• Resume CPR immediately; do not pause to check pulse/electrical rhythm
soon after the shock.
Cardioversion Using a Biphasic Defibrillator
• Obtain consent from the patient and administer sedation with ketamine
1 mg/kg or midazolam 2 mg plus fentanyl 50 µg.
• Turn on the defibrillator to the manual mode.
• Select the desired dose of energy (50–200 J).
• Remove paddles, apply gel on the paddles. Pads may also be used, if available.
• Place paddles/pads over the chest wall. (Sternal paddle below the right clavicle
and apex paddle on left lateral chest wall).
• Turn on the synchronized mode.
• Resuscitation team should stay clear of contact and oxygen circuit should be
disconnected.
• Keep paddles on contact for at least 5 seconds while holding discharge till
shock is delivered.
• Check pulse and electrical activity immediately after the shock.
• If arrhythmia persists, repeat the cardioversion with higher doses.
Management of
Cardiac Arrest 2
CHAPTER
INTRODUCTION
To revive a victim of a cardiac arrest successfully, advanced technology and
equipment like defibrillator, intubation facilities, oxygen, and drugs are required
in most cases. Advanced life support can be effectively performed in a well-
equipped emergency department (ED). The ED team may include doctors, nurses,
and paramedics, who work together as a team with each member performing
their role seamlessly. The team leader should take charge of the resuscitation
team and assign roles to team members, make treatment decisions but respect
and give constructive criticism to the team members.
As soon as a cardiac arrest is identified, the emergency response system
should be activated as per basic life support (BLS) protocol and follows the
following steps (Flowchart 1):
1. Connect the patient to the monitor to determine the cardiac rhythm and take
necessary action.
2. Establish peripheral venous access. If two attempts fail, start an intraosseous
line. Endotracheal tube (ET) may also be used to administer drugs, if the
patient is already intubated.
3. If the patient is not already intubated, insert an oropharyngeal or
nasopharyngeal airway to maintain airway patency by keeping the tongue out
of the way, till intubation can be performed.
4. Remember the 5Hs and the 5Ts that are the reversible causes of a cardiac
arrest (Table 1).
The overview of drugs used in cardiac arrest and the drugs that can be given
through the ET tube are shown in Tables 2 and 3, respectively.
BRADYARRHYTHMIAS
Bradyarrhythmia is defined as a rhythm disorder in which the heart rate (HR)
is less than 60 per minute, e.g., third-degree atrioventricular (AV) block or sinus
bradycardia (Table 4; Figs. 1 to 3).
Symptomatic Bradycardia
Intervention is required when patients develop features of inadequate tissue
perfusion as a result of bradycardia. The HR is generally <50 per minute. The signs
and symptoms of unstable bradyarrhythmia are:
• Hypotension or other signs of shock
• Altered sensorium
CHAPTER 2: Management of Cardiac Arrest 15
FLOWCHART 1: Adult cardiac arrest algorithm.

TABLE 1: Reversible causes: 5Hs and 5Ts.

• Hypoxia • Tension pneumothorax
• Hypovolemia • Tamponade cardiac
• Hydrogen ion (acidosis) • Toxins
• Hypo/hyperkalemia • Thrombosis, pulmonary
• Hypothermia • Thrombosis, coronary
TABLE 2: Overview of drugs used in cardiac arrest.

Drugs Indications Dosage
Adrenaline • VF • 1 mg (1:1000) IV/IO diluted in 10 mL NS
• Pulseless VT every 3–5 minutes
• PEA • 0.1–0.5 µg/kg/min continuous infusion
• Asystole
Amiodarone • Refractory VF and VT • During cardiac arrest: 300 mg IV/IO first
• Stable VT dose. If VT persists 150 mg IV/IO push
• Polymorphic VT second dose
• WCT of unknown origin • In case of arrhythmias: 150 mg over
10 minutes followed by 1 mg/min
infusion for 6 hours
Lignocaine/ • Refractory VF and VT • First dose: 1–1.5 mg/kg
lidocaine • Stable VT • Second dose: 0.5–0.75 mg/kg
• Polymorphic VT
• WCT of unknown origin
Atropine • Symptomatic bradycardia 1 mg IV every 3–5 minutes, maximum
dose: 3 mg
Dopamine • Symptomatic bradycardia 5–20 µg/kg/min IV infusion
(refractory to atropine)
• Hypotension with signs
and symptoms of shock
Magnesium Torsades de pointes 1–2 g diluted in 5% dextrose over 20
sulfate minutes
(VF: ventricular fibrillation; VE: ventricular ectopics; PEA: pulseless electrical activity; IV/IO: intravenous/
intraosseous; WCT: wide complex tachycardia; NS: normal saline)
• Active ischemic chest pain

• Acute pulmonary edema.
The following drugs may be given via ET tube in case of difficult IV/IO access.
The dose required to be administered via ET tube is typically 2–3 times the usual
IV dose (Table 3).
TABLE 3: Drugs that can be given through the ET tube.

Dosage (triple the
Drugs recommended IV dose) When to administer?
Adrenaline 2–3 mg If you fail to secure an IV access in
Atropine 2–3 mg two attempts during a cardiac arrest,
proceed with IO/ET route
Vasopressin 80–120 mg
Naloxone 800 µg
Lignocaine 3 mg/kg
(ET: endotracheal; IO: intraosseous; IV: intravenous)
TABLE 4: Bradycardia rhythms (HR <60/min).

Rhythm P-wave P-R interval QRS
Sinus bradycardia Regular Before each QRS, 0.12–0.2 ms <0.12 ms
identical
First-degree AV block Regular Before each QRS, >0.20 ms <0.12 ms
identical
Second-degree Irregular Present Progressive Dropped in a
Mobitz type 1 AV prolongation repeating pattern
block (Wenckebach)
Second-degree Irregular Present Constant Intermittent
Mobitz type 2 AV dropping of QRS
block complexes
Third-degree AV Regular Present, regular Variable No relation with
block (complete P-P interval P-wave. Regular
heart block) R-R intervals
(HR: heart rate; AV: atrioventricular)
FIG. 1: Sinus bradycardia.
FIG. 2: First-degree AV block.

FIG. 3: Second-degree Mobitz type 1 AV block (Wenckebach).
FIG. 4: Second-degree Mobitz type 2 AV block.
FIG. 5: Third-degree AV block (complete heart block).
Management of Bradyarrhythmias
• Patients with symptomatic bradycardia should be administered atropine
1 mg intravenous (IV) bolus immediately (Table 5). The therapeutic options
are:
cc Atropine: first-line therapy
cc Infusion of a chronotropic agent (adrenaline or dopamine)
cc Transcutaneous pacing
cc Transvenous pacing.
• Look for and treat any reversible causes like hypoxia, hypokalemia, hyper-
kalemia, and other organ involvement (pneumothorax, raised intracranial
pressure).
• If symptomatic bradycardia persists despite administering atropine, start a
chronotropic agent infusion and prepare for a transcutaneous pacing.
• If neither option works, seek expert opinion and prepare for transvenous
pacing.
• Atropine is ineffective in patients with a high-degree AV block (second-degree
Mobitz type 2 or third-degree AV block; Figs. 4 and 5). Do not administer
TABLE 5: Therapeutic agents for symptomatic bradycardia.

Drugs/procedure Dosage/indications
Atropine 1 mg IV stat. The dose may be repeated every 3–5 minutes
up to a total dose of 3 mg
Chronotropic agent If refractory to repeated doses of atropine (total 3 mg/three
infusion doses):
• Dopamine infusion 5–10 µg/kg/min
• Adrenaline infusion 5–10 µg/min
Transcutaneous pacing • Unstable/symptomatic bradycardia
• Mobitz type 2 second-degree AV block
• Third-degree AV block
• New left, right, or alternating bundle branch block or
bifascicular block
• Bradycardia with symptomatic ventricular escape rhythms
Transvenous pacing Persistent symptomatic bradycardia despite atropine,
(temporary pacemaker dopamine/adrenaline infusion and transcutaneous pacing
insertion)
(IV: intravenous; AV: atrioventricular)
atropine in these conditions. Proceed with transcutaneous pacing and

chronotropic infusion directly (Flowchart 2).
TRANSCUTANEOUS PACING
These are devices that pace the heart by delivering an electrical stimulus, causing
electrical depolarization and subsequent cardiac contraction. Transcutaneous
pacing delivers pacing impulses to the heart through the skin by use of cutaneous
electrodes (Figs. 6A and B).
The goal is to stabilize the heart till the underlying problem is resolved or a
more permanent means of pacing is secured.
Technique of Transcutaneous Pacing

Positioning Pacing Electrodes/Pads
• Ideally, the heart should be sandwiched between the pacing pads to mimic
the heart’s normal electrical axis. They may be placed anterior–posterior
or anterior–lateral depending on the manufacturer. Anterior–posterior
placement of pads, with one pad on the anterior chest and the other on the
posterior chest is more commonly used.
• Connect the electrocardiogram (ECG) leads.
• Set the pacemaker rate to 60–80 per minute.
• Begin pacing with 10 milliamps and slowly increase by 10 milliamps till
capture is noted.
FLOWCHART 2: Adult bradycardia algorithm (with pulse).
A B
FIGS. 6A AND B: Transcutaneous pacing.
• Once pacing is captured (signified by characterized by a wide QRS complex

with tall, broad T-waves on the ECG, or a palpable pulse) set the current at
5–10 milliamps above the threshold.
• External pacing can be quite uncomfortable, if the patient is awake/responsive.
Consider sedation if > 50 milliamps is used for pacing.
The success of pacing is determined by evidence of improved cardiac output:
palpable pulse, rise in blood pressure, and improved level of consciousness.
• The site of application of the pads should be changed every 4 hours to prevent
skin burn and discomfort.
TACHYARRHYTHMIAS
Tachyarrhythmias are defined as abnormal heart rhythms with a ventricular rate
of 100 or more beats per minute (Table 6).
The most important clinical determination in a patient presenting with a
tachyarrhythmia is whether or not the patient is experiencing signs and symptoms
related to the rapid heart rate.
The following are signs of unstable tachyarrhythmia:
• Hypotension or other signs of shock
• Active ischemic chest pain
• Acute pulmonary edema.
Initial Management of Tachyarrhythmias (Flowchart 3)

• Identify the rhythm
• Look for signs of unstable tachyarrhythmia:
cc If unstable, synchronized cardioversion is indicated
cc If stable, administer appropriate medical therapy and monitor the patient.
Look for and treat reversible causes (5Hs and 5Ts)

• Refer to Chapters 39 to 42 for details of management of different tachyar-
rhythmias.
TABLE 6: Classification of tachyarrhythmias.

Tachyarrhythmia Narrow complex Wide complexa
Regular • Sinus tachycardia • SVT with aberrancy
• SVT • VT
• Atrial flutter with fixed
conduction
Irregular • Atrial fibrillation • VF
• Atrial flutter with variable • Atrial fibrillation with aberrancy
conduction • Polymorphic VT
• Multifocal atrial tachycardia • Torsades de pointes
aAny regular wide complex tachycardia can be treated as ventricular tachycardia.
(SVT: supraventricular tachycardia; VT: ventricular tachycardia)
FLOWCHART 3: Adult tachycardia algorithm (with pulse).
IMMEDIATE POSTCARDIAC ARREST CARE FOR ADULTS

Systematic postcardiac arrest care after return of spontaneous circulation (ROSC)
can improve the likelihood of patient survival as well as quality of survival:
• ROSC is defined as resumption of sustained cardiac activity with peripheral
perfusion associated with significant respiratory effort. When ROSC is
achieved, ET CO2 abruptly increases to >40 mm Hg indicating a substantial
increase in cardiac output and blood flow to the lungs.
The main objectives are:
• Control body temperature to optimize survival and neurological recovery
• Manage airway by early placement of ET tube
• Identify and treat acute coronary syndromes (ACS)
• Optimize mechanical ventilation to minimize lung injury
• Support organ function to reduce the risk of multiorgan injury.
The following are the steps to be followed for postcardiac arrest care:
1. Confirm ROSC.
2. Optimize ventilation and oxygenation:
•c Target oxygen saturation 92–98%
•c Intubate the patient (advanced airway), if not already done
•c Do not hyperventilate. Give breaths at the rate of 10 per minute

•c Confirm and monitor ET tube placement by waveform capnography.
3. Treat hypotension (systolic blood pressure < 90 mm Hg):
•c Give 1–2 L intravenous or intraosseous bolus of cold normal saline if
inducing hypothermia (use 4°C fluid)
•c Consider vasopressor infusion
•c Target SBP > 90 mm Hg or MAP > 65 mm Hg
•c Consider and treat the reversible causes (5Hs and 5Ts)
•c Take a 12-lead ECG.
4. Assess sensorium:
•c If the patient does not follow commands, induce therapeutic hypothermia
using cold saline infusion and shift the patient for advanced critical care.
•c Targeted temperature management (TTM): Mild therapeutic hypothermia
must be induced for unconscious patients after a cardiac arrest by cold
NS infusion and other cooling devices. Maintain a target temperature of
32–36oC for the first 24 hours post arrest. Monitor core body temperature
(esophageal or rectal)
•c If the patient follows commands, treat ST-elevation myocardial infarction
or ACS as needed and shift the patient for advanced critical care.
CARDIAC ARREST IN PREGNANCY

Cardiac arrest in a pregnant patient poses a unique challenge for resuscitation.
Though rare, ED physicians must be aware of features peculiar to the pregnant
state. Knowledge of anatomic and physiologic changes in pregnancy is important
(refer Chapter 116).
The main priority of resuscitation remains the mother, but it must be
remembered that another life is at stake. Estimate the gestational age to determine
the viability of the fetus. If deemed nonviable, resuscitation can be wholly focused
on the mother.
As soon as a cardiac arrest is anticipated, assemble the ‘maternal cardiac
arrest team’ that includes an obstetrician and a neonatologist (Flowchart 4).
Maternal Resuscitation
• Standard resuscitation algorithm should be followed with a few modifications
to factor in the anatomical and physiological changes of pregnancy.
• Establish intravenous access above the diaphragm so that drug delivery to the
heart is not impeded by the gravid uterus compressing the inferior vena cava
(IVC).
• During CPR, tilt the patient 15–30° to the left and gently pull the gravid uterus
to the left to relieve compression on the IVC, thus increasing venous return.
• The position and dosage of defibrillation remains the same. Remove fetal
monitors prior to defibrillation.
FLOWCHART 4: Maternal cardiac arrest algorithm.
• As pregnant patients are more prone to hypoxia, oxygenation and airway

management should be prioritized during resuscitation.
• Due to changes in gastrointestinal motility and changes in sphincter tone, the
risk of aspiration increases. Consider RSI early during resuscitation to secure
the airway and prevent aspiration. Provide adequate preoxygenation.
• The pregnant airway is more prone to injury, trauma and failed intubation.
Fetal Monitoring
Fetal monitoring should not be done during cardiac arrest in pregnancy after
maternal resuscitation, any fetus considered viable (GA > 20 weeks) should be
monitored with fetal tocodynamometry. Look for early signs of fetal distress:
tachycardia, loss of beat-to-beat variability or late decelerations.
Perimortem Cesarean Delivery

• In case of maternal mortality, perform a perimortem cesarean delivery within
5 minutes of no ROSC.
• If the mother attains ROSC and if signs of fetal distress persist, perform
perimortem cesarean delivery within 5 minutes. Delivery of the fetus not only
increases chances of fetal survival but also increases chances of maternal
recovery.
Potential Causes of Maternal Arrest

Consider the following causes of maternal cardiac arrest and address them, in
addition to the usual 5Hs and the 5Ts:
• Obstetric causes: Peripartum hemorrhage, pregnancy induced hypertension,
peripartum cardiomyopathy, amniotic fluid embolism.
• Nonobstetric causes: Pulmonary embolism, infection/sepsis, trauma, myo-
cardial infarction.
Targeted Temperature Management (TTM)

Maintain a target temperature of 32–36oC for the first 24 hours postarrest while
continuously monitoring fetal heart during this phase.
PEDIATRIC CARDIAC ARREST

• In contrast to adults, cardiac arrest in children usually results from progressive
respiratory failure or shock and often referred to as hypoxic/asphyxia/hypoxic-
ischemic arrest. A primary cardiac cause (arrhythmias) is seen in only 10% of
all pediatric arrests.
• During cardiac arrest resuscitation, the C-A-B sequence must be followed but
securing airway, oxygenation and ventilation should be given high priority
(Flowchart 5).
• Use a compression-ventilation ratio of 30:2 for single rescuer and 15:2 for 2 or
more rescuers.
• After an advanced airway is established, continue chest compressions at a rate
of 100–120/min and give 1 breath every 6 seconds (10 breaths/min).
• When available, use End tidal CO2 (ET CO2) to monitor the quality of chest
compressions. ET CO2 <10–15 mm Hg indicates inadequate cardiac output
during CPR resulting in inadequate delivery to the lungs. Target ET CO2 more
than 10–15 mm Hg during CPR.
• During defibrillation, allow at least 3 cm between the paddles. The recom-
mended paddle size based on weight and age is given below:
cc >1 year old/>10 kg: Large adult paddles (8–13 cm)
cc <1 year old/<10 kg: Small infant paddles (4.5 cm).

FLOWCHART 5: Pediatric cardiac arrest algorithm.

Section 2
Anaphylaxis,
Shock and Airway
Anaphylaxis 3
CHAPTER
INTRODUCTION
Anaphylaxis is defined as a serious allergic or hypersensitivity reaction that is rapid
in onset, mediated by immunoglobulin E (IgE) and may cause death. Anaphylaxis
is highly likely when any one of the three criteria given in Table 1 is fulfilled.
The following are the organ systems involved in anaphylaxis:
• Skin and integumentary system: 90% of episodes
• Respiratory system: 70% of episodes
• Gastrointestinal system: 45% of episodes
• Cardiovascular system: 45% of episodes.
TABLE 1: Criteria for diagnosis of anaphylaxis.

Criterion 1 Acute onset of an illness (minutes to several hours) involving the skin,
mucosal tissue, or both (e.g., generalized hives, pruritus or flushing,
swollen lips, tongue, or uvula) and at least one of the following:
• Respiratory compromise (e.g., dyspnea, wheeze, bronchospasm, stridor,
reduced peak expiratory flow, hypoxemia)
or
• Reduced blood pressure (BP) or associated symptoms and signs of
endorgan dysfunction (e.g., collapse, syncope)
Criterion 2 Fulfilled if two or more of the following occur rapidly after exposure to a
likely allergen within minutes to a few hours:
• Involvement of the skin-mucosal tissue (e.g., generalized hives, itch,
swollen lips, tongue, or uvula)
• Respiratory compromise (e.g., dyspnea, wheeze, bronchospasm, stridor,
reduced peak expiratory flow, hypoxemia)
• Reduced BP or associated symptoms and signs (e.g., collapse, syncope)
• Persistent gastrointestinal symptoms and signs (e.g., abdominal cramps,
vomiting)
Criterion 3 • Reduced BP after exposure to a known allergen (minutes to several
hours)
• Reduced BP in adults is defined as a systolic BP <90 mm Hg or >30%
decrease from the patients baseline
Source: Sampson HA, Muñoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A, et al. Second
National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium
definition and management of anaphylaxis. J Allergy Clin Immunol. 2006;117(2):391.
30 SECTION 2: Anaphylaxis, Shock and Airway
Caution: Concurrent administration of certain medications such as blockers,

angiotensin converting enzyme (ACE) inhibitors, and alpha adrenergic blockers
may increase the likelihood of severe or fatal anaphylaxis and may also interfere
with the patient’s ability to respond to treatment.
MANAGEMENT OF ANAPHYLAXIS
• Remove the trigger for anaphylaxis immediately (e.g., blood transfusion,
antibiotic, antisnake venom).
• Maintain airway. Intubate if angioedema is present. If intubation is expected
to be difficult, keep tracheostomy, or cricothyroidotomy set ready.
• Check SpO2. Start supplementary oxygen by mask to maintain a target SpO2
> 94–98%.
• Assess circulation. If the patient is hypotensive, start a rapid infusion of 1–2 litres
of normal saline (NS). Children should be given NS in boluses of 20 mL/kg,
each over 5–10 minutes, and repeated, as needed. Large volumes of fluid (up
to 100 mL/kg) may be required.
• Place the patient in the supine position with the lower extremities elevated,
unless there is evidence of upper airway swelling necessitating the patient to
remain upright (and often leaning forward). If the patient is vomiting, place
the patient semirecumbent with lower extremities elevated. Place pregnant
patients on their left side.
• Administer injection adrenaline 0.3–0.5 mg (0.3-0.5 mL) intramuscular (IM)
(1:1,000 dilution) in the anterolateral thigh. The dose can be repeated every
5–15 minutes, if hemodynamically stable up to a maximum of 3 doses.
The following are the dosages of adrenaline in children:
cc <6 years: 0.15 mg IM
cc 6–12 years: 0.3 mg IM
cc >12 years: 0.5 mg IM
• If hypotension persists, administer adrenaline bolus (0.1–0.5 mg IV in 1:10,000

dilution) followed by an infusion at the rate of 0.1 µg/kg/min (e.g., for a 60 kg
man start at 6 µg/min).
• Antihistamines:
cc H1 blockers: Injection avil (chlorpheniramine maleate) 1–2 mL slow
intravenous (IV)/IM; injection phenergan (promethazine): 25 mg IV/IM

stat; and
cc H2 blockers: Injection ranitidine 50 mg IV stat and q8h.
Other agents that may be used in anaphylaxis are given here:

• Injection hydrocortisone 100–200 mg IV. (Onset of action: 20 minutes. Not
useful in acute stage. Blocks late response). Should be considered in acute
stage only if adrenaline is not available or if the anaphylaxis is severe.
CHAPTER 3: Anaphylaxis 31
• Bronchodilators: Salbutamol nebulization (5 mg in 5 mL saline) if broncho-

spasm present despite adrenaline.
• Glucagon 1–5 mg IV over 5 minutes, followed by infusion of 5–15 µg/min is
useful in patients on regular blockers.
Observe patients with mild symptoms for 4–6 hours, discharge, if stable.
Steroids (Hydrocortisone) do not relieve the initial symptoms and signs of anaphylaxis
and is given to prevent the biphasic or protracted reactions that occur in some cases.
Epinephrine decreases mediator release from mast cells and is the only medication
that prevents or reverses obstruction to airflow in the upper and lower respiratory
tracts and prevents or reverses cardiovascular collapse.
Therefore, do not substitute epinephrine with hydrocortisone during the initial
management.
If the patient is stable, discharge on the following medications:

• Tablet levocetirizine 5–10 mg hs OD for 3–5 days
• Tablet ranitidine 150 mg BD for 3–5 days
• Tablet prednisolone 0.5 mg/kg OD for 3 days.
Overview of Shock 4
CHAPTER
DEFINITION
Shock is a state of hypoperfusion that causes cellular and tissue hypoxia. This
may be due to decreased oxygen delivery to the tissues or increased oxygen
consumption.
CLASSIFICATION AND EXAMPLES OF TYPES OF SHOCK

• Distributive shock: Septic shock, neurogenic shock, anaphylactic shock, toxic
shock syndrome, Addisonian crisis
• Cardiogenic shock: Myocardial infarction, atrial and ventricular arrhythmias,
valve, or ventricle septal rupture
• Hypovolemic shock: Hemorrhage, diarrhea, vomiting, heat stroke, burns
• Obstructive shock: Pulmonary embolism, pulmonary hypertension, tension
pneumothorax, constrictive pericarditis, restrictive cardiomyopathy.
STAGES OF SHOCK
• Preshock (compensated/cryptic shock): In this stage, compensatory responses
(tachycardia and peripheral vasoconstriction to blood loss) to decreased
tissue perfusion are initiated by the body. This stage can be reversed, if the
subtle signs are identified and timely and appropriate interventions are
initiated immediately.
• Shock: This stage is characterized by signs of organ dysfunction as the
compensatory mechanisms are overwhelmed. These include tachycardia,
hypotension, dyspnea, restlessness, oliguria, metabolic acidosis, diaphoresis,
cold, and clammy skin.
• End stage: Multiorgan failure and irreversible organ damage occurs, if the stage
of shock is prolonged. Patients become obtunded or comatose progressing to
death (Flowchart 1).
VASOPRESSORS AND INOTROPES

Vasopressors are drugs that cause vasoconstriction and improve the mean
arterial pressure in patients with shock. Inotropes are drugs that increase cardiac
contractility. There is an overlap in the inotropic and vasopressor effects of many
drugs.
• Vasopressors: Noradrenaline, adrenaline, and phenylephrine
• Inotropes: Dopamine and dobutamine (Table 1).
CHAPTER 4: Overview of Shock 33
FLOWCHART 1: Mechanism of shock.
TABLE 1: Inotropes and vasopressors.

Drug (receptors) Initial dose Maximum dose Indications Complications
Noradrenaline 5 µg/min 35–100 µg/min First-line agent in Hyperglycemia,
(α1, β1) in refractory septic, cardiogenic bradyarrhythmias
shock and hypovolemic
shock
Adrenaline 5 µg/min 35 µg/min First-line agent Tachyarrhythmias,
(α1, β1, β2) in anaphylactic ischemia,
shock. Add on to mesenteric
noradrenaline in ischemia,
septic shock hyperglycemia
Dopamine 5 µg/kg/ 50 µg/kg/min Second-line Tachycardia,
(D1, D2, α1, β1) min agent in septic, arrhythmia
cardiogenic and
hypovolemic shock
Dobutamine 5 µg/kg/ 20 µg/kg/min First-line agent Hypotension,
(β1, β2) min in cardiogenic tachyarrhythmia
shock. Add on to
noradrenaline in
septic shock for
augmentation of
cardiac output
in patients with
myocardial
dysfunction
Note:
• Indication for starting vasopressors/inotropes infusion in a patient with tissue
hypoperfusion (Table 2).
cc Mean arterial pressure ≤ 60 mm Hg or
cc Drop in systolic blood pressure ≥ 30 mm Hg from baseline.

• The efficacy of some subcutaneous injections like heparin and insulin can
come down due to cutaneous vasoconstriction.
Hypovolemia should be corrected with IV fluids before starting a vasopressor.
TABLE 2: Clinical algorithm to shock management.

Type of shock Peripheries Heart JVP SBP DBP Pulse Management
rate pressure
Hypovolemic Cold Normal • Attain hemostasis
in hemorrhage
• Aggressive fluid
resuscitation
• Blood products in
hemorrhage
Septic Warm Wide • Early empiric
or antibiotic therapy
• Fluid
resuscitation
• Vasoconstrictors
(noradrenaline,
vasopressin)
and inotropes
(adrenaline,
dopamine)
Cardiogenic Cold Narrow Inotropic support
or or (Adrenaline,
dobutamine,
or noradrenaline)
Obstructive Cold/ Narrow Therapeutic

normal or intervention (e.g.,
Pericardiocentesis,
thrombolysis
of PE, needle
thoracostomy, etc.)
Neurogenic Warm Wide Fluid resuscitation
or Vasoconstrictors
(Dopamine,
Noradrenaline)
Hypoadrenal Cold Normal • IV glucocorticoid
crisis replacement
• Fluid
resuscitation
Inotropic
support
(Dopamine,
adrenaline)
(JVP: jugular venous pressure; SBP: systolic blood pressure; DBP: diastolic blood pressure)
Septic Shock 5
CHAPTER
INTRODUCTION
Sepsis is a potentially life-threatening clinical condition characterized by systemic
inflammation due to an infectious etiology. The severity ranges from early sepsis
to fatal septic shock.
Systemic inflammatory response syndrome (SIRS) is an inflammatory
response that may be elicited by an infectious or a noninfectious etiology. SIRS
associated with a suspected infection constitutes sepsis.
DEFINITION OF SYSTEMIC INFLAMMATORY RESPONSE

SYNDROME
• Temperature > 38.3 or < 36ºC
• Heart rate > 90 bpm
• Respiratory rate > 20 breaths/min
• WBC count >12,000/mm3 or <4,000/mm3
Though this definition has been in use for many decades and is easy to use, it
lacks sensitivity and specificity and is now considered outdated.
The Third International Consensus Definitions for Sepsis and Septic Shock
2016 (Sepsis-3) defined sepsis as a life-threatening organ dysfunction caused by a
dysregulated host response to infection.
Organ dysfunction is defined as an acute change in total Sequential Organ
Failure Assessment (SOFA) score of 2 or more points as a result of infection. In
patients with no known organ failure, the baseline SOFA score can be taken as
0. Patients with organ dysfunction can be expected to have a hospital mortality
of 10%.
Septic shock is defined as a subset of patients with sepsis in whom circulatory,
cellular, and metabolic abnormalities are severe enough to significantly increase
mortality. Patients in septic shock have persisting hypotension requiring
vasopressors to maintain mean arterial pressure (MAP) >65 mm Hg and have a
serum lactate level >2 mmol/L (18 mg/dL) despite adequate volume resuscitation.
This condition is associated with a mortality rate >40%. The term severe sepsis is
currently considered redundant.
qSOFA (Quick SOFA) and SOFA Scores

These are predictive scoring systems that measure disease severity and are used
to predict outcomes, mainly mortality. All patients with suspected sepsis should
TABLE 1: Sequential Organ Failure Assessment (SOFA) score.

0 1 2 3 4
P/F ratio >400 ≤400 ≤300 ≤200 ≤100
BP No MAP < 70 Dopa < 5 Dopa > 5/ Dopa > 15/
hypotension mm Hg Adr < 0.1 Adr > 0.1
GCS 15 13–14 10–12 6–9 <6
Creatinine (mg%) <1.2 1.2–1.9 2–3.4 3.5–4.9 >5
Platelet count >150,000 100,000– 50,000– 20,000– <20,000
(cells/mm3) 150,000 100,000 50,000
Bilirubin (mg%) <1.2 1.2–1.9 2–5.9 6–11.9 >12
(Adr: adrenaline infusion µg/min; BP: blood pressure; Dopa: dopamine infusion µg/kg/min; MAP: mean
arterial pressure)
Source: Vincent JL, Moreno R, Takala J, Willatts S, De Mendonça A, Bruining H, et al. The SOFA (Sepsis-
related Organ Failure Assessment) score to describe organ dysfunction/failure. Intensive Care Med. 1996;
22(7):707-10.
have qSOFA score checked at triage. qSOFA score is a simple bedside score to
identify adult patients with suspected infection who are likely to have a poor
outcome. This should alert the ED physicians to further investigate for organ
dysfunction. SOFA score may then be calculated and used to initiate or escalate
appropriate therapy. This score may also be used to admit patients quickly in the
intensive care unit (ICU) or to referral to a higher center, if adequate facilities
are not available. The higher the SOFA score, the worse the outcome of patients
(Table 1; Flowchart 1).
qSOFA Criteria (>2 Suggests Sepsis)

• Respiratory rate > 22/min
• Systolic blood pressure < 100 mm Hg.
NATIONAL EARLY WARNING SCORE 2

National Early Warning Score 2 (NEWS2) is an aggregate score made up of six
physiological parameters, with the aim of improving detection and response to
clinical deterioration in acutely unwell patients (Table 2). Parameters measured
are:
• Respiratory rate
• Oxygen saturation
• Systolic BP
• Pulse rate
• Level of consciousness (ACVPU score)
• Temperature
CHAPTER 5: Septic Shock 37
FLOWCHART 1: Evaluation of a patient with suspected sepsis.
Sepsis should be considered in any patient with a NEWS2 score of ≥5 in

the presence of known infection, signs or symptoms of infection, or who are at
elevated risk of infection.
MANAGEMENT OF SEVERE SEPSIS AND SEPTIC SHOCK

Patients in septic shock should be managed aggressively in the resuscitation room.
The four main therapies to be immediately initiated are: (1) Fluid resuscitation,
(2) antibiotic administration, (3) control of septic focus, and (4) temperature
control.
Fluid Resuscitation
• Administer crystalloids (NS or RL) at a dose of 10–20 mL/kg per bolus
(maximum 30 mL/kg) over the first hour. Assess the patient after every fluid
bolus for increase in blood pressure and signs of fluid overload.
• In patients with ARDS or sepsis, a restrictive approach to IV fluid administration
has been shown to decrease the duration of mechanical ventilation and ICU
stay, compared to a more liberal approach.
• Vasopressor: Noradrenaline is the vasopressor of choice in septic shock.
Adrenaline or vasopressin can be added as second line vasopressors to
achieve the target MAP of 65 mm Hg.
TABLE 2: National Early Warning Score 2.

Physiological Score
parameter 3 2 1 0 1 2 3
Respiratory ≤8 9–11 12–20 21–24 ≥25
rate (per min)
SpO2 (%) ≤91 92–93 94–95 ≥96
Scale 1*
SpO2 (%) ≤83 84–85 86–87 88–92 93–94 on 95–96 on ≥97 on
Scale 2# ≥93 on oxygen oxygen oxygen
air
Air/Oxygen Oxygen Air
SBP (mm Hg) ≤90 91–100 101–110 111–219 ≥220
Pulse (per min) ≤40 41–50 51–90 91–110 111–130 ≥131
Consciousness Alert CVPU
Temperature ≤35 35.1–36.0 36.1–38.0 38.1–39.0 ≥39.1
(°C)
*Scale 1 is used in patients without risk of Type 2 failure.
#Scale 2 is used in patients with risk of Type 2 failure (COPD, neuromuscular disease) in whom target
saturation is 88%.
(CVPU: confusion, voice, pain, unresponsive; SBP: systolic blood pressure)
Source: Reproduced from Royal College of Physicians. National Early Warning Score (NEWS) 2:
Standardizing the assessment of acute-illness severity in the NHS. Updated report of a working party.
London: RCP, 2017.
• Inotrope: Adrenaline or dobutamine can be started, if the cardiac contractility

is low.
• Glucocorticoid therapy: In refractory shock not responding to fluids and
vasopressors, injection hydrocortisone 100 mg q6h should be initiated.
Antibiotic Therapy
• Broad-spectrum antimicrobial therapy should be started within 6 hours,
preferably 1 hour of ED admission after two blood cultures are taken from two
different sites.
• Injection Piperacillin–Tazobactam, if blood pressure is normal/injection
meropenem 1 g, if patient is in shock.
Control of Septic Focus

The probable focus of sepsis (e.g., diabetic foot, abscess, perforation) should be
removed.
Temperature Control
Fever control with external cooling and antipyretics.
CHAPTER 5: Septic Shock 39
Other Measures and Monitoring

• Management of hyperglycemia: Target blood glucose level < 200 mg/dL
• Transfuse blood products if hemoglobin < 7 g/day
• Lactate clearance: This is defined by the equation [(initial lactate – lactate > 2
hours later)/initial lactate] × 100. Lactate clearance every 6 hours has been
shown to a reliable marker for effective resuscitation.
• Arterial blood gas should be repeated at the end of 1 hour of resuscitation to
look for:
cc Partial pressure of oxygen or P/F ratio: Worsening gas exchange may
be to a clue to the presence of pulmonary edema from excessive fluid

resuscitation and also help to detect other complications including
pneumothorax from central catheter placement, acute respiratory distress
syndrome, or venous thromboembolism.
cc pH and lactates: Resolution of metabolic acidosis and development of
hyperchloremic acidosis.
Airway Management 6
CHAPTER
AIRWAY MANAGEMENT IN THE EMERGENCY

DEPARTMENT
Airway management in the emergency department (ED) is quite challenging as
patients are sick and the time for preparation is shortened. Hence, all airways
should be considered as difficult and difficult airway management cart should be
kept ready for usage.
ASSESSMENT OF AIRWAY
ED physicians can use certain pneumonics to assess a patient’s airway for
difficulty. MOANS is the pneumonic used for assessing difficult mask ventilation
and LEMON is a pneumonic used to predict a difficult laryngoscopy.1
Difficult Mask Ventilation Assessment: MOANS

• M—Mask seal: Facial injuries, beard, blood make a mask seal very difficult
• O—Obesity/obstruction: It is difficult to bag mask obese patients
• A—Age >55 years: The elderly may have physiological conditions that decrease
compliance and hence are difficult to bag mask
• N—No teeth: Missing supporting structures that are necessary to seal the mask
make mask ventilation difficult in edentulous patients
• S—Stiff lungs: Patients with chronic obstructive pulmonary disease or asthma
have stiff lungs making mask ventilation difficult.
Difficult Airway Assessment: LEMON

• L—Look externally: Look for abnormal faces, burns, facial injuries, or a thick
beard
• E—Evaluate the 332 rule (Figs. 1A to C): Successful laryngoscopy depends
on normal relative anatomy. In patients with normal relative anatomy the
following applies:
cc Normal mouth opening is three fingerbreadths. It indicates good
temporomandibular joint mobility.
cc The distance between the mentum and the hyoid bone should be
three fingerbreadths. It indicates good mandibular space capacity to

accommodate the tongue during laryngoscopy.
cc Notch of the thyroid cartilage should be two fingerbreadths below the
hyoid bone. Absence indicates a high/anterior larynx, which would be

hard to visualize.
CHAPTER 6: Airway Management 41
A B C
FIGS. 1A TO C: Evaluating the 332 rule.
• M—Mallampati score: This evaluation of an awake patient in a sitting position

assesses the anatomical structures during mouth opening and classifies the
airway into four grades: 1 being easy airway and 4 being very difficult airway
• O—Obesity/obstruction: Look for signs of anatomical obstruction like stridor,
foreign bodies
• N—Neck mobility: Assess both flexion and extension of neck as it may be
difficult to align the airway structures during intubation in a patient with
limited neck mobility.
Diabetics have cervical mobility restriction, hence predicting difficult airway.
If a patient has dentures, they can be left in place for mask ventilation for better seal
and removed immediately before intubation to avoid displacement and aspiration.
Identification of Compromised Airway

Look for the following clinical signs that suggest a compromised airway
• Inspiratory stridor
• Gurgling
• Snoring
• Tracheal tug and subcostal retractions
• Hoarseness, expiratory phonation
• Paradoxical chest wall movement
• Rapid shallow breathing
• Central cyanosis
Expect a difficult airway in the following clinical scenarios:
• Maxillofacial trauma: Due to bleeding or fractured segments
• Burns: Due to acute edema of glottis or tracheobronchial mucosa, neck
contracture, mouth opening
• Neoplasms: Laryngeal or oral cancer-causing airway stenosis
• Arthritis: Temporomandibular joint or cervical spine (ankylosing spondylitis)
• Infections: Croup, supraglottitis, quincy, retropharyngeal abscess, Ludwig’s
angina, angioedema.
A B
FIGS. 2A AND B: Positioning of a patient during intubation.
Preparation for Endotracheal Intubation

Make sure that the following are in place before attempting endotracheal (ET)
intubation (Fig. 2)
• Position: Flexion of the neck, extension of the head
• Pillow: Below the occiput in adults (10 cm height)
• Drugs: Refer intubation protocol (Chapter 487)
• Equipment: Bag valve mask, suction catheter, ET tube, syringe, laryngoscope,
laryngeal mask airway, Bougie, and Stylet
• Communication with the team is important.
To intubate a patient, the path from the incisor teeth to the larynx should be in
a straight line. The angle of the axis of the mouth to the larynx is 90 degree. That of
the pharynx to the trachea is obtuse.
When an average, nonobese patient’s head is raised 10 cm off the bed by
placing a folded sheet under the head, the pharyngeal and laryngeal axes align.
Once the patient’s head is optimally positioned, tilt the head into the extension
with your right hand to bring all the axes into alignment.
• In patients with an unstable cervical spine, manual inline stabilization is
required.
• In obese patients, a ramped position may have to be used by placing pillows or
sheets under the patient’s shoulders and torso (Fig. 3).
Cormack and Lehane Grading

This is a commonly used grading system to describe laryngeal view during direct
laryngoscopy.
CHAPTER 6: Airway Management 43
FIG. 3: Ramped position.
Grade 1: Full view of the glottis (easy)

Grade 2A: Partial view of the glottis (easy)
Grade 2B: Arytenoids/posterior part of the cords are just visible (restricted)
Grade 3: Only epiglottis is visible (difficult)
Grade 4: No glottis structure is visible (difficult)
LARYNGEAL MASK AIRWAY

Laryngeal mask airway (LMA) is a supraglottic airway device that is designed to
rest inside the hypopharynx and thus allowing relative isolation of the trachea to
aid positive pressure ventilation. It can be used as an alternative to intubation in
the ED or during prehospital care for the following indications:
• For short duration procedures without requirement of neuromuscular
blockade
• As a means of airway rescue in cases of failed endotracheal intubation.
• For blind intubation of anticipated difficult airway, in the absence of alternate/
advanced equipment
LMA is available in sized 0 (infant) to 5 (adult >80 kg). Practically, use size 3 for
adult females or size 4 for adult males.
REFERENCE
1. Walls RM, Murphy MF. Manual of Emergency Airway Management, 3rd Edn. Philadelphia: Lippincott,
Williams and Wilkins; 2009; pp.. 9-10.
Respiratory Support 7
CHAPTER
INTRODUCTION
Oxygen can be administered conveniently by oronasal devices such as nasal
catheters, cannulae, and different types of masks:
• Use face masks with oxygen flow meter or venturi masks.
• FiO2 can be calculated by the formula 20 + [4 × O2 flow rate (L/min)].
• PaO2 of 60 mm Hg is equivalent to SpO2 of 90%. However, in patients with
metabolic acidosis, a higher PaO2 should be targeted.
• Oxygen flow rates must be adjusted and delivered using appropriate delivery
devices.
cc Nasal cannula: Oxygen flow rate up to 4 L/min.
cc Simple face mask: Oxygen flow rates 6–10 L/min.
cc Venturi mask: Oxygen flow rates 2–15 L/min.
cc Non rebreather mask/face mask with reservoir bag: Oxygen flow rates
10–15 L/min.
DANGERS OF OXYGEN THERAPY

• Physical risks: Oxygen being combustible, the risk of fire hazard and tank
explosion is always present. This is more with high concentration of oxygen.
Dry and nonhumidified gas can cause dryness and crusting of the oral and
nasal mucosa.
• Functional risks: Patients who have lost sensitivity to CO2 and depend upon
the hypoxic drive for inspiration are in danger of ventilatory depression as
seen in patients with chronic obstructive pulmonary disease (COPD).
• Cytotoxic damage: In the lungs, structural damage occurs from high FiO2 as
the oxygen can lead to the release of various reactive species, which attack the
DNA.
Respiratory support is needed for critically ill patients who have either
oxygenation problem or ventilation failure.
• Type 1 respiratory failure: This is most widely defined as PaO2 <8 kPa or 60 mm
Hg (equivalent to SaO2 of approximately 90%) with a normal or low PaCO2
level.
• Type 2 respiratory failure: This is most widely defined as presence of
hypercapnia with or without hypoxia. Hypercapnia is an elevated level of
PaCO2 (normal range: 34–46 mm Hg or 4.6–6.1 kPa).
CHAPTER 7: Respiratory Support 45
Two types of ventilation are used in the ED; noninvasive ventilation (NIV), if
the patient is conscious and cooperative or invasive ventilation in unconscious
patients or if a trial of NIV fails.
NONINVASIVE VENTILATION
Noninvasive ventilation is a mode of positive pressure ventilation delivered
through a noninvasive interface like nasal mask or face-mask rather than an
invasive interface like endotracheal tube or a tracheostomy. It can be delivered
using either a standard ventilator or continuous positive airway pressure (CPAP)/
bilevel positive airway pressure (BiPAP) machine. While on NIV, patients must
initiate all breaths.
When a ventilator is available, it can be used for delivering NIV, for both Type
1 and Type 2 respiratory failure. If ventilator is not available, patients with Type 1
respiratory failure can be managed by a CPAP machine.
Straps hold the interface in place and should be adjusted to avoid excessive
pressure on the nose or face. Generally, the straps should be loose enough to
allow one or two fingers to pass between the face and the strap. When nasal mask
or prongs are used, a chin strap is usually necessary to maintain closure of the
mouth.
Noninvasive ventilation can be delivered in two ways:
1. Noninvasive positive pressure ventilation (NIPPV)
•c NIPPV using a standard ventilator
•c BiPAP using BiPAP machine
•c CPAP using CPAP machine.
2. Noninvasive negative pressure ventilation (no longer used).
Indications for NIV include the following:
• Acute exacerbation of COPD with a respiratory acidosis (pH 7.25–7.35)
• Cardiogenic pulmonary edema unresponsive to medical management
• Hypercapnic respiratory failure secondary to chest wall deformity (scoliosis,
thoracoplasty) or neuromuscular diseases
• Weaning from tracheal intubation
• Decompensated obstructive sleep apnea.
Contraindications of NIV:
• Comatose patient (Glasgow Coma Scale <8)
• Upper airway obstruction
• Extensive facial surgery/trauma
• Respiratory failure: Needs immediate intubation
• Unstable hemodynamics on >1 inotropic support
• Extensive secretions (e.g., bronchiectasis)
• Recent upper gastrointestinal (GI) surgery
• Vomiting, upper GI bleed

• Patient in multiple organ dysfunction syndrome (MODS)
• Confused/agitated patients.
NIPPV Using a Standard Ventilator

The following should be set while initiating a patient in NIPPV using a standard
ventilator:
• Mode: NIPPV
• Pressure support: 12 cm H2O
• PEEP: 5 cm H2O
• FiO2: Start initially with 100% O2 and titrate to the response to maintain a
saturation of 94% for Type 1 failure and 88% in Type 2 failure.
cc In Type 1 failure, increase PEEP up to 10 cm H O to improve oxygenation.
2
Monitor hemodynamics as patient may develop hypotension or pneu-
mothorax on higher PEEP.
cc In Type 2 failure, if patient demonstrates “air hunger” , increase peak
inspiratory flow rate to compensate for minute ventilation.
Disadvantages
• Difficult suctioning
• Risk of aspiration.
Note: NG tube is essential in a patient on NIPPV to avoid gastric inflation. Select
appropriate size face mask for patient comfort and to prevent leak.
Discontinuation of NIPPV
• If there is inadequate improvement in 1 hour, intubate the patient and start
invasive ventilation.
• If there is satisfactory improvement both clinically and on arterial blood gas
(ABG), supports can be slowly titrated down and removed. The following
should be reached.
cc FiO < 40%
2
cc PEEP = 5
cc Pressure support of ≤7 cm H O
2
Bilevel Positive Airway Pressure

This mode is used in Type 2 respiratory failure (ventilator failure or CO2 retention).
Two settings have to be adjusted. These are:
1. IPAP: Equivalent to pressure support + PEEP in a standard ventilator
2. EPAP (Expiratory Positive Airway Pressure): Equivalent to PEEP in a standard
ventilator.
CHAPTER 7: Respiratory Support 47
Initial settings in BiPAP: IPAP 15 and EPAP 5.

Increase IPAP gradually up to 20 cm H2O, if tolerated.
Notes:
• On a BiPAP machine, increase in EPAP will decrease effective IPAP. Hence,
IPAP have to be increased to maintain desired ventilation.
• On a BiPAP machine, increase in IPAP will actually decrease the delivered
FiO2 as air is used to achieve the target pressure. In a standard ventilator,
oxygen blender is used and hence, FiO2 can be set and is stable. On a BiPAP
machine, increase the FiO2 while increasing IPAP.
Continuous Positive Airway Pressure

It is used for patients with Type 1 respiratory failure (only oxygenation failure) like
pulmonary edema:
• Start with FiO2 of 100% and PEEP of 5 cm H2O
• Increase the PEEP gradually up to 10 if tolerated to improve oxygenation.
Monitoring During Noninvasive Ventilation

• Clinical (every 30 minutes)
cc Patient comfort
cc Level of consciousness
cc Accessory muscle activity
cc Patient ventilator synchrony
cc Respiratory rate
cc Heart rate.
• Repeat an ABG after 1 hour of initiation of NIV and adjust the ventilator
settings.
(Rise in pH and fall in PaCO2 are good prognostic signs in Type 2 failure).
INVASIVE VENTILATION
Invasive ventilation should be initiated when a patient is not able to maintain
oxygenation or if the patient does not have spontaneous breathing or if a trial of
NIV fails.
Indications for Endotracheal Intubation

• Cardiac arrest
• Apnea
• Unconscious patient with SpO2 < 90%
• Type 2 respiratory failure with failure on NIV
• Impending respiratory arrest
• GCS < 8 in trauma
• Elective intubation for conditions like tetanus.
Initial Settings in a Standard Ventilator

• Mode: SIMV volume controlled with pressure support
• FiO2 100%
• PEEP: 5 cm H2O
• Tidal volume: Start with 6–8 mL/kg
• Rate: 10–15/min
• Pressure support: 12 cm H2O
The following needs to be monitored:
• If the expired tidal volume is less than the set tidal volume, look for leak in the
system.
• Monitor peak and plateau pressures (peak pressure should be <35 cm H2O/
plateau pressure should be <30 cm H2O). If these pressures are high, look
for patient discomfort, secretions, tube blockage, bronchospasm, tube bite,
pneumothorax.
• Do an ABG after 1 hour and adjust the settings.
• Titrate FiO2 to avoid oxygen toxicity. Keep it <50%.
Notes:
• Provide adequate sedation for all intubated patients. Midazolam infusion
4 mg/h can be started and titrated according to the response.
• Avoid neuromuscular paralyzing agents. Use it only if the patient is not
adequately oxygenating (PaO2 <60 mm Hg) on a FiO2 of 100% and a PEEP of
10. Sedate the patient adequately before giving paralyzing agent (vecuronium)
and patch the eyes to avoid exposure keratitis.
• Ensure adequate hydration before intubation as fall in blood pressure can
occur after intubation which is more marked in those with volume depletion
and autonomic neuropathy (Guillain–Barré syndrome). Treat hypotension
with fluids. In patients with fluid overload, use inotropes instead of fluids.
Vasopressors can be used to treat hypotension in volume overloaded patients.
• Oxygenation of a patient can be increased by:
cc Increasing FiO
2
cc Increasing PEEP
cc Physiotherapy and recruitment maneuvers to open the collapsed alveoli.
• Ventilation (regulating CO2) can be done by adjusting the tidal volume and
respiratory rate.
• Treat the primary cause (e.g., asthma—use of bronchodilators will improve
the ventilator parameters).
Section 3
Fluid and Electrolytes
Fluid Therapy 8
CHAPTER
INTRODUCTION
Water comprises approximately 60% of the human body weight and the other
40% being lean body mass. Water is distributed in the two main compartments
of the body: intracellular and extracellular compartments. The extracellular
compartment comprises of interstitial fluid and plasma (intravascular space).
These fluid compartments are in constant interchange with each other due to
movement of fluids and electrolytes across the membranes (Fig. 1).
CHOICE OF INTRAVENOUS FLUIDS

Many crystalloids and colloids can be used for fluid resuscitation in the emergency
department. The fluid administered is distributed between the intracellular
and extracellular compartments (Table 1). The composition of the different
crystalloids commonly used is shown in Table 2.
• 0.9% normal saline (NS): NS is an isotonic crystalloid and is the resuscitation
fluid of choice in trauma and in dehydrated patients. It expands extracellular
volume with no change in intracellular volume. Risks include hyperchloremic
acidosis.
• Ringer lactate (RL): RL is an isotonic crystalloid and is the resuscitation fluid
of choice for acute gastroenteritis (AGE). It expands extracellular volume with
minimum change in the intravascular volume. Avoid in patients with diabetic
ketoacidosis due to increase in serum lactate levels.
FIG. 1: Fluid compartments in the body.

52 SECTION 3: Fluid and Electrolytes
TABLE 1: The net effect of infusing 500 mL of each of the solutions.

Normal saline Glucose containing Colloid (albumin,
(NS, 0.9%) crystalloids (DNS/5%D) dextran, and haemaccel)
Intracellular Negligible 333 mL (2/3rd) Nil
fluid (ICF)
Extracellular 500 mL 167 mL (1/3rd) 500 mL
fluid (ECF)
Interstitial 375 mL Interstitial 125 mL Interstitial Negligible
Intra- 125 mL Intra- 42 mL Intra- 500 mL
vascular vascular vascular
TABLE 2: Profile of crystalloids (1 L).

Na (mmol/L) Cl (mmol/L) HCO3 (mmol/L) mOsm pH
0.9% NS 154 154 308 4.5–7
DNS 154 154 586 3.5–6.5
3% NS 512 512 1026 4.5–7
½ NS 77 77 154 4.5–7
RL 130 109 273 5.1
5% Dextrose 278 5
7.5% NaHCO3 1283 1283 2566 8.3
• Dextrose normal saline (DNS): A mixed crystalloid solution used for

resuscitation if sugars are low and the patient needs calorie replacement.
Usually used for postoperative patients.
• 5% Dextrose: Not the initial choice for resuscitation as majority of the fluid
goes into the intracellular and interstitial compartments. Only 10% is
retained in the intravascular space. Used for correction of free water deficit
in patients with hypernatremia. Also used as a solvent for IV infusions like
noradrenaline. Risks include hyponatremia, cerebral edema, pulmonary
edema, hyperglycemia and hypokalemia.
• 1/2 or 1/4 NS: These are hypotonic saline solutions used for correction
of free water deficit in patients with hypernatremia. Risks include hypo-
natremia, cerebral edema, pulmonary edema.
• 3% NaCl: A hypertonic crystalloid, it expands extracellular volume and
decreases intracellular volume. Used to treat severe hyponatremia and
cerebral edema. Risks include osmotic demyelination syndrome.
Sodium 9
CHAPTER
INTRODUCTION
This chapter discusses about the electrolyte, sodium. The normal level of sodium
is 135–145 mEq/L.
HYPONATREMIA
Hyponatremia is a condition that occurs when the serum sodium level is less
than 135 mmol/L. The causes and management of hyponatremia are given in
Table 1.
Symptoms
The symptoms of hyponatremia are headache, nausea, vomiting, fatigue, gait
disturbances, confusion, seizures, obtundation, coma, and respiratory arrest.
Management
Pseudohyponatremia: High concentration of intravascular protein or lipid may
falsely result in laboratory hyponatremia. This occurs with hyperglycemia,
TABLE 1: Causes and management of hyponatremia.

Volume status of the patient (ECF) Causes Management
True hyponatremia
Depletional • Gastrointestinal loss: • Mild: Oral correction
Both H2O and Na decreased Vomiting diarrhea • Severe: IV fluid correction
(Na > H2O) • Renal: Renal tubular with normal saline
disease, diuretic • Calculate Na replacement
therapy and correct over 48–72
• Cerebral salt wasting hours
Euvolemic • SIADH: Syndrome • Restrict fluids to
H2O increased and Na stable of inappropriate 500–800 mL/day
antidiuretic hormone • Increase salt intake
• Hypothyroidism
• Adrenal insufficiency
Dilutional • CHF • 3% NaCl IV
H2O increased and Na increased • Cirrhosis • Restrict fluids
(H2O > Na) • Nephrotic syndrome • Cautious use of diuretics
(IV: intravenous)
hyperproteinemia (multiple myeloma), uremia, and hypertriglyceridemia.

This must be considered before correcting hyponatremia. Apply the following
corrections for pseudohyponatremia:
• Every 100 mg/dL of glucose decreases serum Na by 1.6 mEq/L.
• Every 25 mg/dL increase of blood urea nitrogen (BUN) above the normal
value of 25 mg/dL decreases Na by 3.3 mEq/L.
Before initiating Na correction, calculate the total sodium deficit by the
following formula:
Total sodium deficit = Body weight × 0.6 × [Expected Na (135) − Measured Na].
• Hyponatremia correction should not rise by <10–12 mmol/L per 24 hours
because rapid correction can cause seizures or central pontine myelinolysis.
So, while calculating sodium deficit, correction for a day (expected Na –
measured Na) should be taken as 10–12 mEq/L.
Note: When hyponatremia is documented to have occurred within 12–24 hours, it is
safe to correct at a faster rate.
Indications for 3% NaCl intravenous correction in patients with euvolemic or

dilutional hyponatremia:
cc Seizure
cc Low sensorium
cc Very low serum Na (<120 mEq/L).
3% NaCl should be given ONLY to patients with euvolemic or dilutional hyponatremia.

Never give 3% NaCl to a patient who is dehydrated (check tongue and skin turgor) no
matter what the Na level is.
• 1000 mL of normal saline contains 154 mEq of Na.

• 100 mL of 3% NaCl contains 51.2 mEq of Na.
The following investigations are helpful in the evaluation of hyponatremia:
• Urine osmolality: To differentiate between conditions associated with
impaired free water excretion and primary polydipsia.
cc <100 mOsm/kg indicates primary polydipsia.
cc >100 mOsm/kg indicates syndrome of inappropriate antidiuretic hormone
secretion (SIADH) or depletional hyponatremia.

• Urine spot sodium: It helps to differentiate depletional hyponatremia and
SIADH.
cc 20–40 mEq/L indicates increased Na excretion (SIADH/diuretic use)
cc <20 mEq/L indicates renal conservation of Na (depletional).
• Serum osmolality: It differentiates between true hyponatremia and pseu

dohyponatremia.
cc High-serum osmolality (SOsm > 295): Hyperglycemia (pseudohypona
tremia).
CHAPTER 9: Sodium 55
cc Normal serum osmolality (SOsm: 280–295): Pseudohyponatremia from

elevated lipids or proteins.
cc Low-serum osmolality (SOsm <280): True hyponatremia.
HYPERNATREMIA
Hypernatremia is defined as serum sodium >145 mEq/L. Causes of hypernatremia
are given in Table 2.
Management
• Adrogue–Madias formula for calculating water deficit
(Measured serum Na – Normal serum Na)
Water deficit (L) = 0.6 × Body weight ×
Normal serum Na
The goal of hypernatremia correction is to lower the serum Na by a maximum
of 10–12 mEq/L in 24 hours. Therefore, (measured serum Na – Normal serum Na)
should be 10–12 mEq/L for calculating water deficit replacement for a day. The
following fluids may be used:
• 5% Dextrose if the patient is not a diabetic.
• ½ NS or ¼ NS may be used if sugars are high.
• Clear free water via nasogastric tube at 100 mL/h, if the airway is secure.
Rapid sodium correction can cause seizures and permanent neurological abnormalities
(central pontine myelinolysis).
So, serum Na should NOT be corrected >10–12 mmol/L over 24 hours.
TABLE 2: Causes of hypernatremia.

Excess Na Relative water deficit
Hypertonic saline, Inadequate fluid intake
NaHCO3 administration
Excess fluid loss
Lung/skin loss
Renal loss Reduced ADH level: Pituitary diabetes
insipidus (DI)
Reduced ADH action: Nephrogenic DI
Osmotic diuresis
Potassium 10
CHAPTER
INTRODUCTION
Potassium is predominantly an intracellular ion. The serum levels do not
accurately reflect the body stores of potassium. The normal potassium level is
3.5–5 mEq/L.
• Acidosis and hyperthermia cause hyperkalemia
• Alkalosis and hypothermia cause hypokalemia.
HYPOKALEMIA
Causes
• Deficit: Gastrointestinal loss: vomiting and diarrhea
• Renal loss: Diuretic use, Cushing syndrome, Bartter syndrome, and Liddle
syndrome
• Redistribution: Insulin, bicarbonate therapy, alkalosis, periodic paralysis, and
agonists.
Clinical Features
No symptoms at >3 mEq/L. Severe hypokalemia can cause muscle weakness,
fatigue, muscle cramps, and constipation.
Amount of potassium needed: The relationship between total body potassium
and serum potassium is not linear. At lower levels of measured potassium, much
more potassium is required to increase the serum level by 1 mEq/L than at a
higher level.
• If the serum potassium is >3 mEq/L, 100–200 mEq is required to increase it by
1 mEq/L.
• If the serum potassium is <3 mEq/L, 200–400 mEq is required to increase
it by 1 mEq/L assuming a normal distribution between the cells and the
intracellular space.
• 1 g of intravenous KCl contains 13 mEq of K.
• 5 mL of oral KCl contains 4 mEq of K.
ECG Changes
T wave inversion followed by QT prolongation, U waves, and mild ST depression.
CHAPTER 10: Potassium 57
Management
• Potassium replacement through peripheral line causes painful throm-
bophlebitis. Hence, use only 500 mL (with up to 3 g KCl) or 1 L (with up to
4.5 g KCl) of normal saline (NS) as the diluent.
• Administration through a central line can be given in 100 mL of fluid (3 g KCl
per 100 mL). Infusion rate should not exceed 1.5 g/h (20 mEq of KCl).
• Patients tolerating orally can be given syrup KCl (20 mL stat and repeat
dose after 2 h) in addition to the intravenous correction in case of severe
hypokalemia.
• Hypomagnesemia often coexists with severe hypokalemia. Add magnesium
to the infusate containing KCl (2–4 g MgSO4).
Always add MgSO4 2–4 g to the K correction for severe hypokalemia (K < 3 mEq/L)
• Patients on long-term diuretic therapy can have hypokalemia and this may
precipitate or aggravate digoxin toxicity. Correct hypokalemia aggressively in
patients on digoxin therapy.
• After correction, if the patient is stable to be discharged, advice the patient
to continue syrup KCl at a dose of at least 20 mL BD till the next OPD review.
Hypokalemic Periodic Paralysis

Attacks occur suddenly with generalized weakness. Consciousness is preserved
and bulbar and respiratory muscles are rarely involved. After correction, patients
may be discharged on syrup KCl and tablet acetazolamide 250 mg BD (to prevent
attacks).
HYPERKALEMIA
Causes
• Increased intake
• Reduced excretion: Renal failure, hypoadrenal state
• Drugs: Angiotensin-converting-enzyme (ACE) inhibitor, angiotensin-receptor
blockers (ARB), K-sparing diuretics (spironolactone, amiloride), nonsteroidal
anti-inflammatory drugs, cyclosporine, tacrolimus, and trimethoprim/
sulfamethoxazole (TMP–SMX)
• Shift out of cells: Acidosis, tissue damage
• Pseudohyperkalemia: Hemolyzed sample
ECG Changes
Peaked T waves, broad QRS, ST depression, and sine wave pattern.
TABLE 1: Treatment of hyperkalemia.

Goal Drug and dose Onset of action Duration of action
Cardio-protective 10 mL of 10% calcium 1–3 min 30–60 min
effect gluconate over 4 min
Intracellular shift Salbutamol nebulization 5 mg 30 min 2–4 hours
every 15 min × 3 doses
50 mL of 50% dextrose with 20 min 4–6 hours
8 units of short-acting insulin
over 10 min (if RBS is high, give
only insulin)
Elimination from Furosemide 40–80 mg IV stat 15 min 2–3 hours
the body and repeat after 4 hours if
blood pressure is normal
Potassium binding resin (Syrup >2 hours 4–6 hours
30 g of kayexalate with 12.5 g
mannitol in 100 mL water)
Hemodialysis Immediate
Clinical Features
Patients are usually asymptomatic, but may complain of fatigue, weakness,
paresthesias, paralysis, or palpitations.
False hyperkalemia is very common due to hemolyzed blood sample. If there
is no obvious predisposing factor, recheck serum K before intervention.
Management
The correction of hyperkalemia is shown in Table 1.
Potassium level may be repeated 2 hours after a correction. After correction, if
the patient is stable to be discharged.
• Make sure the offending drugs are stopped (e.g., ACI/ARB/TMP–SMX).
• Advice the patient to continue diuretics and K-binding resins (once/twice
daily) till the next OPD review.
Calcium 11
CHAPTER
INTRODUCTION
Calcium exists in three fractions in circulation:
1. Protein bound: 40–50%
2. Ionized form: 40–45%
3. Nonionized chelated complexes with anions: 10–15%.
Each gram of albumin binds 0.8 mg% (0.2 mmol/L) of calcium. Serum albumin
levels can alter total calcium without changing the ionized calcium levels. Ionized
form is the physiologically important form of calcium.
The normal range of ionized calcium is 4.65–5.25 mg/dL (1.16–1.31 mmol/L).
Corrected calcium = Measured calcium + (4 – serum albumin g%) × F
F = 0.8 if serum calcium value is in mg%
= 0.2 if serum calcium value is in mmol/L
HYPOCALCEMIA
Causes
• Hypoalbuminemia
• Acid-base disturbances: Acute respiratory alkalosis
• Hypocalcemia with low parathyroid hormone (PTH) (hypoparathyroidism)
cc Postoperative thyroid, parathyroid or radical neck surgery for head and
neck cancer
cc Autoimmune destruction of the parathyroid glands.
• Hypocalcemia with high PTH

cc Vitamin D deficiency or resistance
cc Chronic kidney disease: Due to decrease in renal production of

1,25-dihydroxy vitamin D
cc PTH resistance (impaired PTH action)
• Drugs: Bisphosphonates, Denosumab, Foscarnet, and Cisplatin.
Clinical Features
• Mild: Perioral numbness, paresthesias of the hands and feet, muscle cramps
• Severe: Carpopedal spasm, laryngospasm, and focal, or generalized seizures.
Trousseau’s Sign
Induction of carpopedal spasm by inflation of a sphygmomanometer above
systolic blood pressure for 3 minutes.
Chvostek’s Sign
Contraction of the ipsilateral facial muscles elicited by tapping the facial nerve
just anterior to the ear.
Management
• Severe/symptomatic hypocalcemia: 10% calcium gluconate 10 mL IV over
4 minutes
cc In persistent hypocalcemia, calcium gluconate 10 mL can be added in
500 mL normal saline over 4 hours and to be repeated till symptomatic

improvement
cc Treat concurrent hypomagnesemia if hypocalcemia is refractory. Add 4 g
MgSO4 to the infusate.

• Mildly symptomatic or chronic hypocalcemia: Oral calcium supplementation
(1,500–2,000 mg of elemental calcium as calcium carbonate or calcium citrate
daily, in divided doses) can be given.
HYPERCALCEMIA
Causes
Hypercalcemia is defined as increase in total serum calcium >10.5 mg% or ionized
calcium >1.4 mmol/L.
Clinical Features
Bones (painful), Groans (abdominal), Moans (depression, psychosis, apathy,
confusion), and stones (renal).
The clinical presentation depends on how fast and how high the calcium
level rises. Mild prolonged hypercalcemia may produce mild or no symptoms, or
recurring problems (renal calculi). Sudden-onset and severe hypercalcemia may
cause dramatic symptoms such as lethargy, confusion, or coma.
• Among all causes (Table 1), primary hyperparathyroidism and malignancy
are the most common, accounting for >90% of cases.
• Once hypercalcemia is confirmed, the next step is measurement of serum PTH.
An elevated or high-normal value indicates primary hyperparathyroidism.
TABLE 1: Causes of hypercalcemia.

Excess parathyroid hormone Primary, tertiary, and ectopic
Excess vitamin D Iatrogenic, tablet overdose, granulomatous disease
Malignancy Bone metastasis, lymphoma, myeloma
Endocrine Thyrotoxicosis, acromegaly, adrenal insufficiency
Medication Thiazide diuretics, lithium
CHAPTER 11: Calcium 61
Management
• Correct dehydration within the limits of comorbidities (cardiac/renal failure).
• Forced saline diuresis: Loop diuretics like furosemide intravenous (IV) 40–80 mg
2–4 hourly. Urine output should be replaced with normal saline. Maintain the
urine output at 100–150 mL/h.
• Administer calcitonin (4 IU/kg) S/C or intramuscular (IM) and repeat every
6–12 hours, if response is noted. Onset of action is 4–6 hours and lasts for
48 hours. Nasal sprays are not effective in reducing hypercalcemia.
• Bisphosphonates: Inhibit osteoclast activity
cc Zoledronic acid: 4 mg IV over 30 minutes (avoid in renal failure)
cc Pamidronate: 60–90 mg IV over 2–4 hours.
• Corticosteroids: If hypercalcemia is due to raised vitamin D3 (sarcoidosis,

lymphoma), then
cc Hydrocortisone IV 100–300 mg/day for 3–7 days
cc Tablet prednisolone 40–60 mg /day for 3–7 days.
• Dialysis: Low or no calcium dialysate considered as the last resort.

The administration of calcitonin plus saline should result in substantial
reduction in serum calcium concentrations within 12–48 hours. Bisphosphonates
will be effective by the second to fourth day, thereby maintaining control of the
hypercalcemia.
Magnesium 12
CHAPTER
INTRODUCTION
Magnesium is predominantly an intracellular ion, with 60% present in the bone.
The normal range in serum is 1.7–2.2 mg/dL.
HYPOMAGNESEMIA
Hypomagnesemia is a condition where the plasma level is <1.7 mg/dL
(<0.7 mmol/L).
Causes
• Gastrointestinal disorder: Malabsorption syndrome
• Renal loss: Renal tubular acidosis
• Alcoholism
• Endocrine disorder: Hyperparathyroidism, hyperthyroidism, and hyper-
aldosteronism
• Miscellaneous: Diuretics, aminoglycosides, amphotericin B, and cyclosporin.
Symptoms
• Neuromuscular hyperexcitability (tremors, tetany, seizures), weakness,
apathy, delirium, and coma.
ECG Changes
• QRS widening, peaking of T waves, PR interval widening, and ventricular
arrhythmias.
Management
• Symptomatic patients (tetany, arrhythmias, or seizures) should be given
intravenous magnesium with continuous cardiac monitoring. Treatment of
hypomagnesemia is given in Table 1.
HYPERMAGNESEMIA
Hypermagnesemia is associated with clinical features at plasma levels of
>4.8 mg/dL (>2 mmol/L).
CHAPTER 12: Magnesium 63
TABLE 1: Treatment of hypomagnesemia.

Symptomatic/very severe (<1 mg%) MgSO4 50% solution 2 g in 10 mL of NS IV over
10 min
Repeat up to 10 g in 6 hours, if needed
Symptomatic/less severe MgSO4 50% solution 6 g over 3 hours in NS,
(<1–1.4 mg%) followed by 3 g q 12 hours
Asymptomatic/mild (1.4–1.7 mg%) Oral replacement, Tablet MgO 250 mg 3–8
tablet/day
(Note: In CMC, we use 50% solution: 2 mL vial = 1 g = 4 mmol. Maximum concentration: 1 g in 5 mL)
Causes
• Chronic renal failure
• Oral ingestion: Commonly seen with some over the counter products like
Epsom salt and laxatives containing Mg.
• Magnesium enemas
• Miscellaneous: Familial hypocalciuric hypercalcemia, Milk-alkali syndrome,
adrenal insufficiency, dialysis with increased dialysate magnesium.
Symptoms
Symptoms are mainly neuromuscular, cardiovascular, and as a result of
hypocalcemia
• Plasma Mg 4.8–7.2 mg/dL: Nausea, headache, flushing, lethargy, drowsiness,
and depressed deep tendon reflexes
• Plasma Mg 7.2–12 mg/dL: Somnolence, absent deep tendon reflexes,
hypotension, bradycardia and ECG changes
• Plasma Mg >12 mg/dL: Muscle paralysis causing flaccid quadriplegia,
respiratory failure, complete heart block and cardiac arrest.
ECG Changes
• Prolongation of PR interval, QRS duration, and QT intervals
• Complete heart block and cardiac arrest usually occur at levels of >18 mg/dL
or 7.5 mmol/L.
Management
• Treat the underlying cause
• Dialysis may be required for severe or symptomatic hypermagnesemia
with advanced CKD. Intravenous calcium gluconate should be given as a
magnesium antagonist to reverse the neuromuscular and cardiac effects of
hypermagnesemia.
Acid-base Abnormalities 13
CHAPTER
INTRODUCTION
Evaluation of all acid-base problems must start with the history and examination
of the patient.
• Normal pH: 7.35–7.45
• Normal PaCO2: 35–45 mm Hg
• Normal HCO3: 22–26 mmol/L
• Normal PaO2 >60 mm Hg (80–100)
Correlation between SpO2 and PaO2—correlates till 90% SpO2, but below that
PaO2 drops faster than SpO2.
• Respiratory acidosis or alkalosis is compensated for by the kidneys and takes
more time.
• Metabolic acidosis and alkalosis is compensated for by the lungs and takes
less time.
Compensation never overshoots (e.g., a metabolic acidosis is compensated
for by increased CO2 wash out, but the compensation does not lead to a respiratory
alkalosis).
RULES OF COMPENSATION FOR A PRIMARY METABOLIC

PROBLEM
In any primary metabolic acidosis/alkalosis, the appropriate compensatory
response is a drop or increase in pCO2 value, respectively. The numerical value
of pCO2 should be within ±5 mm Hg of the number formed by the two digits after
the decimal point of the pH value. However, this does not apply if the pH is <7.1
or >7.6.
RULES OF COMPENSATION FOR A PRIMARY RESPIRATORY

PROBLEM
In any primarily respiratory problem, the compensation via the kidneys is slower.
Thus, an acute event is less compensated than a chronic event (Table 1).
If pH is normal and CO2 and HCO3 are abnormal, think of a mixed acid–base
problem.
CHAPTER 13: Acid-base Abnormalities 65
TABLE 1: Rules of compensation for a primary respiratory problem.

Change in HCO3 from 24 mmol/L
Every 10 mm Hg change in PaCO2 from 40 mm Hg Acute Chronic
PaCO2 increases (acidosis) 1 4
PaCO2 decreases (alkalosis) 2 5
HOW TO INTERPRET AN ARTERIAL BLOOD GAS

• Step 1: Ask for the basic history and determine the primary metabolic/
respiratory pathology.
• Step 2: Look at the PaO2. Calculate the PaO2/FiO2 ratio and optimize the
oxygen concentration.
• Step 3: Look at the pH
cc <7.3 = acidosis. >7.5 = alkalosis
cc If pH is normal but CO /HCO is abnormal, think of a mixed problem.

2 3
• Step 4: Look at the base excess (BE) if the patient is likely to have a metabolic
problem. Normal range is between –2 and +2. If BE is more negative, it means
that the patient has a primary metabolic acidosis. If the BE is more positive,
the patient has primary metabolic alkalosis.
• Step 5: Apply rules of compensation to look for compensation (metabolic/
respiratory).
• Step 6: If the basic pathology is a metabolic acidosis, calculate anion gap =
(Na + K) – (HCO3 + Cl). Normal range is 14 ± 4.
• Step 7: Check the electrolytes and sugars and correct them if abnormal.
• Step 8: Look at the lactate and methemoglobin levels for clues about the
underlying problem. Think of the underlying cause and correct the cause
(Flowchart 1).
Arterial Blood Gas versus Venous Blood Gas

• pH: The venous pH closely reflects arterial pH for most metabolic conditions
including diabetic ketoacidosis, uremia. pH value does not correlate well in a
cardiac arrest. As cardiac output decreases, the differences between arterial
and venous measurements increase. However, in clinical practice, knowledge
of either the arterial or venous pH or pCO2 during cardiac arrest does not alter
management.
Pooled mean difference is +0.035 pH units.
• Lactate: When lactates are elevated (>2), there is a close correlation between
arterial and venous lactate levels. A normal venous lactate measurement
predicts a normal arterial level. The bottom line is that venous lactate levels
are similar to those found in arterial samples.
Mean difference 0.08. (–0.27 to 0.42 95% CI).
FLOWCHART 1: Causes of acid-base disturbances.
• HCO3 : Similar in both ABG and VBG.

Mean difference −1.41 mmol/L (−5.8 to +5.3 mmol/L 95%CI).
• pCO2 : Venous pCO2 levels are significantly higher than arterial pCO2 levels
and hence presence or absence of clinically significant hypercarbia cannot
be decided by a VBG.
• pO2 : Venous pO2 levels do not reflect the arterial pO2 levels and therefore is a
poor surrogate to determine oxygen delivery to tissues.
Neither an ABG nor a VBG is required in most of the patients who present to the
ED. A good history and clinical examination gives much more information than any
laboratory test.
Do not be over dependent on ABG to make a diagnosis.
• When to do a VBG?
In our ED, a VBG is sufficient for most of the cases. Indications are:
cc Suspected DKA to determine the pH, lactate levels.
cc Acute severe pancreatitis in shock
cc Renal failure (acute/chronic) to determine the pH and need for dialysis.
cc To determine electrolyte abnormalities (K, Mg) in patients with arrhy-
thmias or impending cardiac arrest.

• When to do an arterial blood gas?
Venous blood gas is easier to perform and gives most of the essential
information for most cases. The following are the only indications when an
ABG is required.
CHAPTER 13: Acid-base Abnormalities 67
cc In a patient chronic obstructive pulmonary disease with exacerbation and

suspected type 2 failure, to decide on the need for noninvasive ventilation/
mechanical ventilation.
cc SpO
2 is usually sufficient for clinical decision making unless pulse
oximetry is unreliable for other reasons (shock, methemoglobinemia, etc.)
A VBG/ABG is not needed for any decision making in a patient on Venturi
mask (up to 8 L/min or 60% oxygen). An ABG may be warranted in some
patients who require high flow oxygen (>8 L/min)
cc In patients with type 1 respiratory failure on NIV/mechanical ventilation
to decide on adjusting the flow rate of oxygen.

To summarize, the only two indications to do an ABG and not a VBG in the
ED are:
• A patient suspected to have type 2 failure to know the pCO2 levels that may
determine the need to intubate or not
• A patient on high flow oxygen to determine the PaO2/FiO2 ratio and decide the
need for NIV/intubation.
Section 4
Infectious Diseases
Antibiotic Protocol for
Common Conditions 14
CHAPTER
INTRODUCTION
Febrile illnesses and infections are common presentations to the emergency
department (ED). Table 1 shows the antibiotic protocol for commonly seen
infections in the ED.
TABLE 1: Antibiotic protocol for commonly seen infections in the emergency

department.
Condition Etiology (most likely First choice Alternatives
pathogens)
Acute Viral entero- Not indicated
gastroenteritis toxigenic
Escherichia coli
Enteropathogenic
Escherichia coli
Cholera Vibrio cholerae Doxycycline 300 mg • Tablet azithromycin
PO × 1 dose 1 g × 1 dose
• Tablet ciprofloxacin
500 mg bd × 3 days
Bacillary Shigella species None needed for Ciprofloxacin 500
dysentery previously healthy mg PO bd × 3 days
patient with mild in patients with
symptoms severe symptoms or
immunocompromised
patients
Giardiasis Giardia lamblia Tinidazole 2 g PO ×
1 dose
Helminthiasis Ascaris, Enterobius, Albendazole 400 mg
and Ankylostoma PO × 1 dose
Repeat dose after
2 weeks for Enterobius
Typhoid fever Salmonella typhi Azithromycin 1 g PO × • Tablet cotrimoxazole
Salmonella 14 days or 1 ds tablet PO bd ×
paratyphi A Injection Ceftriaxone 14 days
2 g IV od × 14 days • Tablet
chloramphenicol
500 mg PO q6h ×
14 days
Continued
72 SECTION 4: Infectious Diseases
Continued

pathogens)
Cholangitis Enterobacteriaceae Piperacillin- Cefoperazone-
Tazobactam 4.5 g Sulbactam 3 g IV q12h
IV q6–8h × 7 days
Ertapenem 1 g IV od ×
7 days (if qSOFA ≥2)
Acute Enterobacteriaceae Piperacillin- Cefoperazone-
cholecystitis Tazobactam 4.5 g Sulbactam 3 g IV q12h
IV q6–8H × 7 days
7 days (if qSOFA ≥2)
Spontaneous Enterobacteriaceae Piperacillin- Cefoperazone-
bacterial (most often E. coli) Tazobactam 4.5 g Sulbactam 3 g IV q12h
peritonitis IV q6-8h × 7 days
7 days (if qSOFA ≥ 2)
Secondary Enterobacteriaceae Ertapenem 1 g IV od Cefoperazone-
peritonitis Anaerobes × 5–7 days Sulbactam 3 g IV q12h
(bowel (Bacteroides species)
perforation)
Intra- Enterobacteriaceae Ertapenem 1 g IV od × • Cefoperazone-
abdominal Anaerobes 5–7 days Sulbactam 3 g IV
abscess (Bacteroides species) q12h
• Tigecycline 100 mg
IV × 1 dose, then 50
mg IV q12h
Cellulitis Streptococcus Cloxacillin 1 g IV q6h Cloxacillin 500–1000
pyogenes, Cefuroxime 1.5 g IV mg PO q6H × 7–10
Staphylococcus q8h (for moderately ill days or Cephalexin
aureus patients) 500 mg PO q6h ×
7–10 days
Furunculosis S. aureus Cloxacillin 500 mg Cephalexin 500 mg PO
PO q6h × 7–10 days q6h × 7–10 days
Diabetic S. aureus Cefuroxime 1.5 g IV q8h Cloxacillin 500–1,000
foot— mild × 7–10 days mg PO q6h × 7–10 days
(localized OR Cephalexin 500 mg
cellulitis, no or PO q6h × 7–10 days
mild systemic
symptoms)
Continued
CHAPTER 14: Antibiotic Protocol for Common Conditions 73
Continued
pathogens)
Diabetic Polymicrobial—S. Piperacillin- Piperacillin-
foot— aureus, Group A Tazobactam 4.5 g IV Tazobactam 4.5 g IV
moderate-to- Streptococcus, q6-8h + Vancomycin q6-8h
severe (limb aerobic gram- 15 mg/kg IV q12h Ertapenem 1 g IV od
threatening) negative bacilli,
anaerobes
Necrotizing Group A Meropenem 1 g IV q8h Piperacillin-
fasciitis (life- Streptococcus + Vancomycin 15 mg/ Tazobactam 4.5 g IV
threatening kg IV q12h q6-8h + Clindamycin
infection) 900 mg IV q8h
Chickenpox Varicella zoster virus Valacyclovir 1,000 mg Acyclovir 800 mg PO
PO tid × 7 days 5 times/day × 7 days
Acute S. aureus Cloxacillin 2 g IV q4H Cefazolin 2 g IV q8h
osteomyelitis polymicrobial
Septic arthritis S. aureus Cloxacillin 2 g IV q6H Cefuroxime 1.5 g IV q8h
× 14–28 days
Acute Respiratory viruses Amoxycillin 500 mg PO Azithromycin 500 mg
pharyngitis Gb A Streptococcus tid x 10 days PO od × 5 days
Group A Benzathine penicillin Amoxicillin 500 mg PO
β-hemolytic 12 L units intra- q8h × 10 days
streptococci muscularly (IM) × 1 dose
For penicillin allergsic
patients: Erythromycin
500 mg PO q6h ×
10 days
Acute Haemophilus Ceftriaxone 1–2 g IV od
epiglottitis influenzae × 7–10 days
Ludwig’s Polymicrobial (oral Amoxicillin- Clindamycin 600 mg IV
angina anaerobes) clavulanate 1.2 g IV q8h × 2 weeks
Vincent’s q12h × 14 days
angina
Acute Viral Not required
bronchitis
Acute S. pneumoniae Amoxicillin clavulanate
bacterial H. influenzae 1,000 mg PO bd ×
rhinosinusitis Moraxella catarrhalis 7 days
Leptospirosis Leptospira Crystalline penicillin 15 L Ceftriaxone 1 g IV od
interrogans units IV q6H for 7 days × 7 days
Anicteric form (mild
disease): Doxycycline
100 mg PO bd × 7 days
Continued
Continued
pathogens)
Scrub typhus Orientia Doxycycline 100 mg PO Azithromycin 500 mg
tsutsugamushi bd × 7 days PO od × 7 days
Acute S. pneumonia Ceftriaxone 2 g IV If Listeria is suspected,
bacterial Neisseria q12H + Vancomycin add Ampicillin 2 g IV
meningitis meningitidis 15–20 mg/kg IV q8-12h q4h
(community + Dexamethasone10
acquired) mg IV q6h × 4 days; first
dose 15 minutes before
or along with the first
dose of antibiotic.
Bites (cat, dog, Pasteurella Amoxicillin-
human, and multocida clavulanate 625 mg
rat) Eikenella S. viridans PO tid for 3–5 days
Spirillum minus
Streptobacillus
Dengue 15
CHAPTER
INTRODUCTION
Dengue fever is an arthropod-borne (Aedes aegypti) viral infection caused by
dengue virus (DENV) endemic in many parts of India during the monsoon season
(July–November). Incubation period is 3–7 days. There are four serologically
distinct DENV types of the genus Flavivirus, called DENV-1, DENV-2, DENV-3,
and DENV-4 with transient cross-protection among the four types. Therefore, a
person can possibly get infected with DENV a maximum of 4 times.
The management of dengue is based on clinical assessment of severity. In the
absence of warning signs, management is mostly symptomatic and supportive.
The WHO case definition of dengue fever is shown in Table 1.
TABLE 1: Case definitions and grading.

Case definitions Tourniquet
and grading Clinical features HCT and platelet count test
Dengue fever Fever of 2–7 days with two May have mildly Negative
or more of the following— increased hematocrit
headache, retro-orbital pain, (HCT) and mild throm-
myalgia, arthralgia, and no bocytopenia, with or
evidence of plasma leakage without leukopenia
Dengue Above plus positive • HCT >20% of Positive
hemorrhagic fever tourniquet test and baseline
(grade I) evidence of plasma leakage • Platelets <100,000
Dengue Above plus some evidence • HCT >20% of Positive
hemorrhagic fever of spontaneous bleeding baseline
(grade II) (skin or other organs) and • Platelets <100,000
abdominal pain
Compensated Above plus circulatory • HCT >20% of Positive
dengue shock failure (weak rapid pulse, baseline
syndrome narrow pulse pressure, • Platelets < 100,000
(grade III) hypotension, cold clammy
skin, restlessness)
Uncompensated DHF with profound shock • HCT >20% of Positive
dengue shock syn with undetectable blood baseline
drome (grade IV) pressure or pulse • Platelets <100,000
Source: WHO. National Guidelines for Clinical Management of Dengue Fever. New Delhi: WHO; 2015.
Tourniquet test: Apply a blood pressure (BP) cuff, inflated for 5 minutes midway
between systolic blood pressure and diastolic blood pressure. Positive test is
petechiae >10/sq. inch on forearm.
WARNING SIGNS IN DENGUE FEVER

Look for the following warning signs of dengue fever. These signs and symptoms
indicate severity and disease progression and warrant aggressive resuscitation
and monitoring.
• Abdominal pain or tenderness
• Persistent vomiting
• Clinical or radiological fluid accumulation (ascites or pleural effusion)
• Mucosal bleeding
• Lethargy, restlessness
• Hepatomegaly
• Laboratory: Increase in hematocrit (HCT) associated with rapid decrease in
platelet count.
INVESTIGATIONS
Complete blood count, urea, creatinine, electrolytes, and liver function test.
Diagnosis is clinical. Tests such as reverse transcription–polymerase chain
reaction and NS1 antigen-based ELISA are helpful in early infection (days 1–5).
Dengue IgM and dengue IgG ELISA tests should be sent only after 5–7 days of
the onset of symptoms.
MANAGEMENT
Management of dengue fever depends on the grade of severity.
• Dengue fever:
cc Advice bed rest, tepid sponging, oral paracetamol, adequate oral hydration
with ORS
cc Avoid nonsteroidal anti-inflammatory drugs (NSAIDs)
cc Explain warning signs
cc Monitor HCT and platelets on an OPD basis.
• Dengue hemorrhagic fever (DHF) (Grade I and II):

cc Admit the patient, look for warning signs and signs of shock
cc Monitor HCT and platelet count
cc Start hydration with intravenous (IV) crystalloids and titrate therapy to
clinical improvement as evidenced by a fall in HCT, decrease in pulse rate,

stable BP, and good urine output
cc However, if HCT falls rapidly with signs of internal hemorrhage, transfuse
packed red cells.

CHAPTER 15: Dengue 77
• Dengue shock syndrome (DSS) with compensated shock (Grade III):

cc Start aggressive resuscitation with IV crystalloid infusion and titrate
therapy to clinical improvement

cc If the clinical condition deteriorates (rise in HCT, decrease in platelets
with signs of shock), continue aggressive fluid resuscitation and initiate

inotropic support
cc Transfuse packed red cells if there is evidence of hemorrhage.
• DSS with profound shock (Grade IV):

cc Assess and stabilize airway, breathing, circulation (ABC)
cc Start aggressive resuscitation with IV crystalloid bolus (10 mL/kg) and
titrate therapy to clinical improvement

cc Reassess and repeat fluid bolus, if necessary
cc If the shock is refractory to fluid resuscitation, initiate inotropic support
cc Transfuse packed red cells, if there is evidence of hemorrhage.
INDICATIONS FOR BLOOD PRODUCTS IN DENGUE

Severe bleeding in dengue shock may necessitate transfusion of packed red
cells or whole blood. Platelet transfusion has not been shown to be effective at
preventing or controlling hemorrhage but may be warranted in patients with
severe thrombocytopenia and shock. The following are the only indications for
transfusing platelets in dengue fever.
• For major or life-threatening hemorrhage, transfuse platelets regardless of
platelet count as there may be platelet dysfunction in DHF.
• Shock with coagulopathy.
• Prophylactic platelet transfusion may be considered in patients without
bleeding manifestations only if the platelet count is less than 10,000/mm3.
Scrub Typhus 16
CHAPTER
INTRODUCTION
Scrub typhus is a rickettsial infection, caused by Orientia tsutsugamushi, which is
spread by bite of the larva (chigger) of trombiculid mites, which thrives in scrub
vegetation. Ask for history of exposure to vegetation like working in the fields,
trekking, etc., which is essential for a person acquiring the infection.
EPIDEMIOLOGY
Scrub typhus is no longer restricted to the classical ‘Tsutsugamushi triangle’ with
cases being reported in South America, Africa, and Europe. In India, it is endemic
in many states, especially Tamil Nadu, Andhra Pradesh, Kerala, Maharashtra,
Rajasthan, Himachal Pradesh, the Himalayan belt, and the North–Eastern states.
CLINICAL FEATURES
The mean duration of fever before presentation is usually 8 days. Clinical features
include fever, myalgia, nausea, breathlessness, abdominal pain, headache, and
altered sensorium. Severe cases may be associated with multiple organ failure
(renal failure, hepatic failure, shock, acute respiratory distress syndrome,
meningitis, and meningoencephalitis).
The basic pathogenesis is vasculitis and perivasculitis of the small blood
vessels, resulting in multiple organ involvement.
Classical Finding
Eschar: A thorough search should be done as many eschars are found in the
genital region, inguinal region, axilla, and inframammary folds. An eschar may
be seen on any part of the body (Fig. 1). The finding of an eschar on the body
provides the most vital clue for diagnosing Scrub typhus.
INVESTIGATIONS
Complete blood count (CBC), electrolytes, creatinine, urea, and liver function
test (LFT).
The typical abnormalities are leukocytosis, thrombocytopenia, hyper-
bilirubinemia, low albumin, elevated liver enzymes, and alkaline phosphatase.
CHAPTER 16: Scrub Typhus 79
FIG. 1: Eschar of scrub typhus. (For colour version see Plate)
Cerebrospinal fluid analysis may show an aseptic meningitis picture with

elevated counts (Mean: 80 cells/cumm; range: 5–740) with a lymphocyte
predominance and elevated protein (Mean: 105 mg%; range: 13–640) and low
sugars.
DIAGNOSIS
Diagnosis can be confirmed by Scrub IgM ELISA positivity with or without a
pathognomonic eschar. However, ELISA test must be done only after 5–7 days
after onset of symptoms.
MANAGEMENT
• Severe cases: Doxycycline 200 mg intravenous (IV) stat in 100 mL normal
saline with 1 ampoule ascorbic acid over 30 minutes followed by 100 mg IV
q12h × 7 days.
• Mild cases: Tablet doxycycline 100 mg PO bd × 7 days.
• Alternate drug: Tablet/injection—azithromycin 500 mg od × 7 days.
Doxycycline is contraindicated in pregnancy. Azithromycin can be given.
• Supportive care for multi organ failure as indicated.
Malaria 17
CHAPTER
INTRODUCTION
Malaria is a protozoan infection cause by the bite of infected female Anopheles
mosquitoes. Four species of Plasmodium (P. vivax, P. falciparum, P. ovale and
P. malariae) cause malaria with most severe infections caused by P. falciparum.
Ask for history of travel to an endemic area.
Patients with one or more of the following clinical criteria are considered to
have “severe malaria” and should be treated with intravenous (IV) antimalarials.
• Impaired consciousness: GCS < 11
• Convulsions
• Metabolic acidosis: Base deficit > 8 mEq/L or HCO3 level < 15 mmol/L or
lactate ≥5 mmol/L
• Hypoglycemia
• Severe anemia: Hb < 5 g%
• Renal failure: Serum creatinine >3 mg% or serum urea >20 mmol/L
• Jaundice: Serum bilirubin >3 mg%
• Acute respiratory distress syndrome
• Shock
• Disseminated intravascular coagulation
• Plasmodium falciparum parasitemia: Parasitic index (PI) >5%.
HOW TO INTERPRET THE RESULT OF MALARIAL

PARASITE (MP) TEST?
• Look for the presence of ring forms or schizonts on the peripheral smear.
• Presence of only gametocytes (without ring forms or schizonts) on the smear
does not suggest active infection. It only means that the patient can pass on
the infection through mosquito bites. Radical cure with primaquine is then
warranted for Plasmodium vivax gametocytes or artesunate or artemether for
P. falciparum gametocytes.
• Look for PI in the case of falciparum malaria. A PI above 5% is indicative of
severe malaria.
Antigen-based rapid diagnostic tests (RDTs) are widely available and are used
in resource-poor settings. RDTs detect one or more of the following antigens:
histidine-rich protein 2 (HRP2), plasmodium lactate dehydrogenase (pLDH), and
aldolase. RDTs that detect HRP2 are somewhat more sensitive for P. falciparum
than those that detect pLDH.
CHAPTER 17: Malaria 81
MANAGEMENT
• Antimalarial therapy as per Table 1.
• Consider exchange transfusion for patients with parasitemia above 10%.
• Look for, and treat complications: Acute respiratory distress syndrome, renal
failure, shock, disseminated intravascular coagulation, and anemia.
• Uncomplicated malaria in pregnancy:
cc Chloroquine sensitive P. falciparum: All trimesters – Chloroquine
cc Chloroquine resistant P. falciparum: First trimester: Quinine + Clindamycin
Second and third trimesters: Artemesinin combination therapy

• Complicated malaria in pregnancy: All trimesters – Artesunate + Clindamycin.
Alternate options: Artemether or quinine
TABLE 1: Antibiotic therapy for P. vivax and P. falciparum.

Malaria P. vivax Chloroquine phosphate
• Day 1: 1,000 mg PO (600 mg base) (4 tablets)
• Day 2: 1,000 mg PO (600 mg base) (4 tablets)
• Day 3: 500 mg PO (300 mg base) (2 tablets)
• For radical cure: Primaquine phosphate 30 mg PO od
× 14 days
P. falciparum Artemether 20 mg + Lumefantrine 120 mg (co-formulated
tablets) 4 tablets bd × 3 days
Severe P. falciparum • Artesunate 2.4 mg/kg IV given as a bolus at 0, 12, and 24
malaria hours, and then once daily + Doxycycline100 mg PO
q12h or clindamycin 450 mg q8h
• Give IV Artesunate for a minimum of 24 hours and then
switch to oral therapy
DRUGS RECOMMENDED FOR TRAVELERS FOR

PROPHYLAXIS OF MALARIA
• Chloroquine: Prophylaxis only in areas with chloroquine-sensitive malaria.
300 mg base (500 mg salt) orally, once/week. Begin 1–2 weeks before travel.
Continue for 4 weeks after leaving the area.
• Mefloquine: 228 mg base (250 mg salt) orally, once/week. Begin 1–2 weeks
before travel. Continue for 4 weeks after leaving the area.
• Doxycycline: 100 mg orally, daily. Begin 1–2 days before travel. Continue for
4 weeks after leaving the area.
• Atovaquone (200 mg)–proguanil (100 mg): One tablet daily. Begin 1–2 days
before travel. Continue for 1 week after leaving the area.
Community-acquired
Pneumonia 18
CHAPTER
INTRODUCTION
Community-acquired pneumonia (CAP) is a lower respiratory tract infection. It
should be differentiated from hospital-acquired pneumonia (hospitalized in the
past 90 days) as the choice of antibiotics is very different.
ETIOLOGY
Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus,
gram-negative bacilli, Legionella species, Mycoplasma pneumoniae, Chlamydia
pneumoniae, and viruses.
CLINICAL FEATURES
Patients usually present with fever, cough with expectoration, breathing difficulty,
fatigue, or pleuritic chest pain.
Use the CURB-65 score to assess the severity of the pneumonia.
Assessment of severity: CURB-65 score: 6-point score (range 0–5). Gives one point
each for:
• Confusion (abbreviated mental test score <8 or new disorientation in person,
place, or time)
• Urea > 42 mg/dL
• Respiratory rate > 30 breaths/min
• Low blood pressure (systolic blood pressure < 90 mm Hg or diastolic blood
pressure <60 mm Hg)
• Age > 65 years.
The choice of antibiotics and the setting of care depends on the CURB-65
score (Table 1).
SETTING OF CARE
• CURB-65 score 0 or 1 (Low risk of death): Outpatient
• CURB-65 score 2 (moderate risk of death): Inpatient (ward)
• CURB-65 score >3 (high risk of death): Inpatient (ICU).
CHAPTER 18: Community-acquired Pneumonia 83
TABLE 1: Antibiotic management of community-acquired pneumonia.

CURB score Preferred Alternatives
CURB-65 Amoxicillin 500 mg PO q8h × Levofloxacin 750 mg PO od × 5–7days
score 0 or 1 5–7 days Azithromycin 500 mg PO od × 3 days
Doxycycline 100 mg PO bd × 5 days
CURB-65 Ceftriaxone 1g IV od + Crystalline Penicillin G 20 Lakh units
score 2 Azithromycin 500 mg IV od + IV q4h + Azithromycin 500 mg IV od +
Oseltamivir 75 mg PO bd × Oseltamivir 75 mg PO bd × 5–7 days
5–7 days
CURB-65 Piperacillin tazobactam 4.5 g IV
score 3 or q8h + Azithromycin 500 mg IV
more OD + Oseltamivir 75 mg PO bd
× 5–7 days
LUNG ABSCESS
Lung abscess (necrotizing pneumonia) refers to necrosis of the lung parenchyma
resulting in a localized collection of pus.
• Etiology: Oral anaerobes (peptostreptococcus, prevotella, bacteroides,
Fusobacterium)
• Antibiotic of choice: Amoxicillin clavulanate 1.2 g IV q8h
• Alternative choice: Clindamycin 600 mg IV q8h.
EMPYEMA THORACIS
Empyema thoracis refers to collection of pus in the pleural space often as a
complication of pneumonia, tuberculosis or a subphrenic abscess. May present
with fever, cough and pleuritic chest pain. Intercostal tenderness may be noted
with decreased breath sounds and dullness on percussion.
Etiology: Streptococcus milleri, Streptococcus pneumoniae, oral anaerobes
Empiric antibiotic: Amoxicillin clavulanate 1.2 g IV q8h or crystalline penicillin
20 lakh units IV q4h.
If MRSA suspected, add vancomycin 10–20 mg/kg IV q12h.
Çhest tube drainage is required to facilitate drainage of thick pus.
BIBLIOGRAPHY
1. Lim WS, van der Eerden MM, Laing R, Boersma WG, Karalus N, Town GI, et al. Defining community acquired
pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax.
2003;58(5):377-82.
Influenza and H1N1 19
CHAPTER
INTRODUCTION
• Seasonal influenza is an acute respiratory viral infection that is spread by
respiratory secretions. It is caused by influenza A or B viruses, members of
Orthomyxoviridae family. Influenza viruses are further subtyped on the basis
of the surface hemagglutinin (H) and neuraminidase (N) antigens.
• The H1N1 strain of influenza A is responsible for the 2008 pandemic flu. It
causes a mild self-limiting respiratory illness in the majority. However,
high-risk population may develop a severe respiratory illness with systemic
symptoms.
Incubation period: 1–4 days.
Period of infectivity: 3–5 days
CLINICAL FEATURES
Fever, coryza, sore throat, cough, breathlessness, myalgia, and pharyngeal
congestion may be seen. Patients with severe disease may have tachypnea, diffuse
crepitations, hypotension, hypoxemia, and signs of respiratory failure.
INVESTIGATIONS
Investigations include complete blood count, urea, creatinine, electrolytes, liver
function test, chest X-ray, and arterial blood gas (ABG).
Leukopenia, mild transaminitis, and azotemia may be noted.
Chest X-ray may show features of consolidation or diffuse fluffy alveolar
infiltrates. ABG may show hypoxemia and respiratory alkalosis in early disease
and mixed respiratory failure in very severe disease.
Confirmatory test: Influenza panel polymerase chain reaction on a nasal or throat
swab.
Caution: Do not wait for results to initiate treatment, if indicated.
HIGH-RISK CATEGORY FOR COMPLICATIONS OF

INFLUENZA/H1N1
• Pregnancy
• Underlying respiratory illness
• Extremes of age (<2 years and >65 years)
CHAPTER 19: Influenza and H1N1 85
• Underlying chronic debilitating illness such as congestive cardiac failure,

chronic liver disease, and chronic kidney disease
• Morbid obesity
• Patients on immunosuppression or HIV infection.
MANAGEMENT
• Nonhigh-risk category: Only supportive and symptomatic care such as
antihistamines and cough suppressants. Respiratory isolation and quarantine
are advisable to prevent the spread of infection. N95 face masks may be used
appropriately.
• High-risk category: If H1N1 infection is suspected clinically, then:
cc Start antiviral therapy with oseltamivir in patients who present within
48 hours of onset of symptoms:

– Capsule oseltamivir 75 mg bd × 5–7 days
cc Early invasive mechanical ventilation in case of hypoxemia or type 1
respiratory failure
cc Treat secondary bacterial infection if present appropriately with broad-
spectrum antibiotics.
Who should be Given Postexposure Prophylaxis with

Oseltamivir?
• Close contacts who have a high risk for complications of influenza (listed
before)
• Dose: Capsule oseltamivir 75 mg od × 7 days
• It should be started within 48 hours of contact with infected individuals.
Pre-exposure prophylaxis may be considered in settings with vulnerable high
risk population such as old-age nursing homes.
Who should be Advised Vaccination for Influenza Virus?

Annual vaccine is advisable for high-risk category patients and healthcare
workers, ideally in the months of October–November in the Northern hemisphere.
COVID-19 20
CHAPTER
INTRODUCTION
Coronavirus disease-2019 (COVID-19) is a viral infection caused by the novel
Coronavirus SARS-CoV-2, which probably originated from Wuhan, China in late
2019 and was declared a pandemic on March 11th, 2020 by the World Health
Organization.
It spreads from person to person via respiratory transmission and direct
contact.
Incubation period: 2–7 days, up to 14 days
Period of infectivity: 8–10 days, up to 14 days
CLINICAL PRESENTATION
• Majority of cases are asymptomatic to mild self-limiting disease. However,
high-risk* population may develop severe to critical illness. These include the
elderly, diabetic patients, hypertensive, obese, immunocompromised, and
those with multiple comorbidities.
• Initial symptoms may be nonspecific such as fever, sore throat, dry cough,
myalgias, diarrhea, and fatigue. Loss of smell and taste may also be noted.
• Breathlessness may preclude the onset of severe disease. Dyspnea may soon
progress to severe hypoxemia and respiratory failure due to ARDS.
• Procoagulant states have also been described with increased arterial
thrombotic events such as cerebrovascular accidents, cerebral venous
thrombosis, myocardial infarction, and pulmonary embolism.
EVALUATION
• COVID-19 can be confirmed by direct viral tests like by reverse transcription-
polymerase chain reaction (RT-PCR) test, which is considered to be the gold
standard or rapid antigen test (RAT).
• Chest X-ray: Multifocal and bilateral air-space opacities and/or consolidation
with peripheral and basal predominance.
• CT chest: Common findings include ground glass opacities (77.18%), reticu-
lation (46.24%), air bronchogram (41.61%), pleural thickening (33.35%), and
bronchial wall thickening (15.48%). Lesions are predominantly distributed
bilaterally (75.72%) and peripherally (65.64%).
CHAPTER 20: COVID-19 87
MANAGEMENT (TABLE 1)
The quintessential components of resuscitation (airway, breathing, and circula-
tion) with good supportive care are the cornerstone of acute management of
critically ill COVID-19 patients.
TABLE 1: Summary of evaluation and management of COVID-19 based on severity.

Severity category Evaluation Management
Mild illness No laboratory tests or • Home isolation recommended
• SpO2 > 94% on radiological imaging • Symptomatic management with
room air needed paracetamol
• RR < 20/min
Moderate illness • CBC profile • Home isolation can be considered with
• SpO2 > 94% on • Metabolic profile: pulse oximetry monitoring
room air Serum electrolytes, • Symptomatic management with
• RR < 24/min BUN, serum paracetamol
creatinine, LFT • Consider admitting high-risk patients
• One or more
high-risk factors* for monitoring
Severe illness • CBC profile, ABG, ECG • Corticosteroids: Dexamethasone 6 mg
• SpO2 < 94% on • Metabolic profile: IV OD or another equivalent steroid
room air Serum electrolytes, • Prophylactic thromboprophylaxis for
• RR > 24/min BUN, serum all patients. Change to therapeutic
creatinine, LFT dose, if evidence of thromboembolism
• Prognostication • Proning, if no contraindication
markers: Consider • Oxygen supplementation, targeting a
D-dimer, LDH, SpO2 of 94%. NIV/HFNC, if indicated
ferritin, CRP • Consider remdesivir or tocilizumab (if
• Radiological no contraindication)
imaging: CXR
Critical illness • CBC profile, ABG, • Corticosteroids: Dexamethasone 6 mg
• SpO2 < 94% on ECG IV OD or another equivalent steroid
room air • Metabolic profile: • Prophylactic thromboprophylaxis for
• RR > 30/min Serum electrolytes, all patients. Change to therapeutic
BUN, serum dose, if evidence of thromboembolism
• PaO2/FiO2 < 300
creatinine, LFT • Proning, if no contraindication
• Blood culture x 2 • Oxygen supplementation, targeting a
• Prognostication SpO2 of 94%
markers: Consider • NIV/HFNC if indicated
D-dimer, LDH, • Consider IMV if indicated
ferritin, CRP • Broad spectrum antibiotics if
• Radiological secondary infection
imaging: CXR • Consider remdesivir or tocilizumab
(if no contraindication)
(ABG: arterial blood gas; BUN: blood urea nitrogen; CBC: complete blood count; CRP: C-reactive protein;
CXR: chest X-ray; ECG: electrocardiogram; HFNC: high-flow nasal cannulae; IMV: invasive mechanical
ventilation; LDH: lactate dehydrogenase; LFT: liver function tests; NIV: noninvasive ventilation;
RR: respiratory rate)
Airway
In patients with a compromised airway, plan for rapid sequence induction (RSI)
and use a video laryngoscope, if available. Passively preoxygenate with 100% FiO2
for 3–5 minutes and avoid manual ventilation after paralysis to minimize potential
aerosolization of virus from the airways.
Breathing
Administer supplemental oxygen aiming to maintain target SpO2 > 92% by using
nasal prongs, venturi mask, nonrebreathing mask, high-flow nasal cannulae,
noninvasive ventilation, or invasive mechanical ventilation.
Oxygen flow rates must be adjusted and delivered using appropriate delivery
devices.
• Nasal cannula: Oxygen flow rate up to 4 L/min.
• Simple mask or Venturi mask: Oxygen flow rates 6–10 L/min.
• Non rebreather mask/face mask with reservoir bag: Oxygen flow rates
10–15 L/min
Patients with acute hypoxemic respiratory failure despite supplemental
oxygen therapy require additional respiratory support with either Hi Flow
Nasal Cannula (HFNC) or Non-invasive ventilation (NIV). This may reduce the
work of breathing and obviate the need for intubation and invasive mechanical
ventilation (IMV)
Circulation
COVID-19 patients requiring fluid resuscitation and hemodynamic support
should be treated and managed like patients with septic shock in accordance with
standard guidelines.
Drugs (Therapeutics)
The COVID-19 disease progression and lethality have a viraemic and inflam-
matory phases providing the biologic rationale for current strategies to reduce
morbidity and mortality associated with COVID-19.
• Corticosteroids: Corticosteroids are currently recommended only for patients
requiring supplemental oxygen to maintain SpO2 > 94%. The recommended
dose of dexamethasone, assuming no contraindications, is 6 mg once daily
(OD) IV/PO for 7–10 days or until discharge (if earlier), with blood glucose
monitoring, and concurrent proton pump inhibitor use for gastroprotection.
Prednisolone (40 mg OD PO) or methylprednisolone (32 mg OD PO or IV)
are suitable alternative recommendations for women who are pregnant or
breastfeeding.
• Anticoagulants: Recommended only for hospitalized patients
cc Enoxaparin: For < 80 kg, 40 mg subcutaneously OD; For > 80 kg, 60 mg
subcutaneously OD (consider dose adjustment in renal failure)

CHAPTER 20: COVID-19 89
cc Unfractionated heparin: 5,000 units subcutaneously BD

cc Fondaparinux 2.5 mg subcutaneously OD (consider dose adjustment in
renal failure)
• Antivirals, anti-inflammatory agents and antibiotics
cc Primary antivirals against SARS-CoV-2: Many drugs like hydroxychloro-
quine, ivermectin, ritonavir, remdesevir and favipiravir, have been tried for
their antiviral properties against SARS-CoV-2 and have now fallen out of
favor with most guidelines and recommendations.
cc Anti-inflammatory agents for host-directed therapy: Several targeted
immunomodulatory drugs have shown promise against SARS-CoV-2

induced cytokine storm. These include tocilizumab (IL-6 inhibitor),
Canakinumab (IL-1 inhibitor) and Baricitinib (Janus Kinase inhibitor).
cc Empiric antibiotics: Administer broad spectrum empiric antibiotics
(piperacillin-tazobactam/meropenem) only for patients with severe and

critical illness to cover secondary bacterial infections.
PREVENTION
• Good hand hygiene, wearing face masks, physical distancing, and contact
prevention. Quarantining and other public health measures advised.
• Appropriate PPE use for high-risk procedures to prevent transmission to
healthcare workers (HCW).
• Mass national vaccination campaigns from all over the world have shown a
clear benefit of vaccines preventing death and severe disease, and help attain
herd immunity.
• Vaccines currently available include mRNA vaccines (Pfizer, Moderna),
nonreplicating vector vaccines (AstraZeneca/Covishield, Sputnik), and
inactivated viral vaccines (Covaxin).
Rabies 21
CHAPTER
ANIMAL RESERVOIRS
• Dogs account for 90% or more of reported cases of rabies transmitted to
humans.
• Other animals that can transmit rabies are cats, bats, raccoons, skunks, and
foxes.
• Small rodents, such as gerbils, chipmunks, guinea pigs, squirrels, rats, mice,
and rabbits have not been conclusively proven to have transmitted rabies.
Incubation period: Average is 1–3 months after exposure, but can range from
several days to several years.
CLINICAL FEATURES
• Encephalitic (furious) rabies: (80%) fever, hydrophobia, pharyngeal spasms,
agitation with hyperexcitability, opisthotonos and autonomic hyperactivity
leading to paralysis, coma, and death.
• Paralytic (dumb) rabies: (20%) ascending paralysis, which can mimic Guillain-
Barré syndrome. Paralysis is usually more prominent in the bitten limb. It may
then spread either symmetrically or asymmetrically eventually resulting in
death.
MANAGEMENT
Management of a dog bite includes the following:
• Wound care
• Postexposure prophylaxis (PEP) for rabies [rabies immunoglobulin (RIG) and
rabies vaccine]
• Tetanus prophylaxis.
The classification of wounds and recommended therapy is shown in Table 1.
Wound Care
Wounds should be washed thoroughly. Flush and irrigate the wounds with
sterile water or saline using a 26-gauge needle to disinfect immediately.
• Wounds that are better managed by delayed primary closure after 72 hours:
cc Deep wounds
cc Wounds on the hand and feet
cc More than 12 hours old (24 h old on face)
cc Puncture wounds.
CHAPTER 21: Rabies 91
TABLE 1: Classification of wounds and recommended therapy.

Category Description PEP vaccine RIG
I Touching, feeding of animals No exposure, therefore, Not required
or licks on intact skin no prophylaxis (if history
reliable)
II Minor scratches or abrasions Patients NOT immunized Not required
without bleeding or nibbling previously: Full 5 dose
of uncovered skin schedule
Patients who have been Not required
immunized before*: 2
doses on day 0 and 3
III Single or multiple transdermal Patients NOT immunized Administer RIG
bites or scratches, licks on previously: Full 5 dose
broken skin, contamination schedule
of mucous membrane with Patients who have been Not required
saliva (i.e., licks) and suspect immunized before*: 2
contacts with bats doses on day 0 and 3
*Previously immunized patients include those who received pre-exposure prophylaxis and those who
completed a post-exposure vaccine regimen >3 months back.
• Wounds that can be considered for immediate primary closure:

cc Clinically uninfected wounds
cc Less than 12 hours old (24 h on the face)
cc Wounds on parts of the body other than on the hands or feet.
However, most studies do not show any difference in the rates of infection
between immediate suturing and late primary closure.
Wound care should be followed up by antibiotic prophylaxis (amoxicillin–
clavulanate 625 mg tid × 5 days).
Post-exposure Prophylaxis
• Pregnancy, infancy, and concurrent infections are not contraindications for
post-exposure prophylaxis (PEP).
• PEP vaccine must be provided regardless of duration since bite. Even if it has
been months after been bitten, the same PEP vaccination as for recent contact
must be administered.
• If the involved animal (dog or cat) remains healthy 10 days after the exposure
has occurred, PEP may be discontinued.
• Even immunized animals can transmit rabies because of the possibility of
vaccine failure. Therefore, immunization status of the animal is not a factor in
deciding administration of PEP.
• PEP includes rabies vaccine and/or RIG.
Rabies Immunoglobulin
• Maximum possible dose of RIG should be infiltrated into the depth and
around the wounds. If the wound is small, infiltrate as much as possible into
the wound and inject the remainder intramuscularly at a site (anterior thigh)
distant from that of the rabies vaccine.
• Dose of RIG: 20 IU/kg for human RIG or 40 IU/kg for equine RIG (ERIG).
• If the wounds are large or multiple, dilute the RIG two to threefold in sterile
normal saline to be able to infiltrate all the wounds. Make sure you do not
exceed the total recommended dose.
• If RIG is not available at presentation, it can be administered up to 7 days
from the date of the first dose of vaccination. After the seventh day, antibody
response to the vaccine would have occurred and the RIG is likely to be
ineffective. RIG is not indicated in previously vaccinated individuals.
• Even though the currently manufactured ERIG is highly purified and adverse
events are significantly less, it is safer to perform a skin sensitivity test prior
to its administration. Human RIG does not require any prior skin sensitivity
testing.
• Human monoclonal antibodies, with fewer side effects can also be adminis-
tered for the same indication at a recommended dose of 3.3 IU/kg.
Rabies Vaccine
• Postexposure prophylaxis for unvaccinated persons: Two intramuscular
schedules may be used for category 2 and 3 exposures:
cc The 5-dose intramuscular regime: One dose of the vaccine should be
administered on days 0, 3, 7, 14, and 28 in deltoid region or, in small

children, into the anterolateral area of the thigh muscle.
cc The 2 1 1 regimen may also be used. Two doses are given on day 0 in the
deltoid muscle, right and left arm. In addition, one dose is given on day 7
and one on day 21 in the deltoid muscle.
cc Vaccines should not be injected into the gluteal region.
• Postexposure prophylaxis for previously vaccinated persons:

cc Previously immunized patients includes those who have received pre-
exposure prophylaxis and those who have completed a post-exposure

vaccine regimen >3 months ago. For PEP, administer two intramuscular
doses of rabies vaccine; on day 0 or at the earliest and the second dose 3
days later.
cc RIG is not indicated for previously immunized people.
Tetanus Prophylaxis
• If the patient completed three doses of the primary series of tetanus-diphtheria
(Td) vaccine but the last dose/booster was <5 years ago: No need for a Td
vaccine or tetanus immunoglobulin (TIG).
• If the patient completed three doses of the primary series of Td vaccine but
the last dose was >5 years ago: Administer Td vaccine alone. No need for TIG.
• If the patient took less than three doses of the primary series of Td vaccine or
if the vaccine status is unknown: Administer Td and TIG. Advice the patient to
take two more doses of Td at least 2 weeks apart.
Food Poisoning and
Acute Gastroenteritis 22
CHAPTER
INTRODUCTION
Food poisoning is caused by the consumption of food or water contaminated with
bacteria and/or their toxins, parasites, viruses, or chemicals. The pathogenesis of
diarrhea in food poisoning is broadly classified into either non-inflammatory or
inflammatory types.
Noninflammatory diarrhea: It caused by the enterotoxin-producing organ-
isms [Vibrio cholerae, enterotoxigenic Escherichia coli (ETEC), Clostridium
perfringens, Bacillus cereus, and Staphylococcus organisms] or by organisms that
disrupt the absorptive and/or secretory processes of the enterocytes by attaching
to the mucosa (rotavirus, Norwalk virus, adenovirus, Giardia lamblia, and
Cryptosporidium). There is no mucosal inflammation or destruction.
Inflammatory diarrhea: This type of diarrhea can be caused by two types of
organisms: cytotoxin-producing noninvasive organisms [enteroinvasive E. coli
(EIEC), Yersinia enterocolitica, C. difficile] or by invasive organisms (Salmonella,
Shigella, Campylobacter, and Entamoeba histolytica).
MANAGEMENT
Oral hydration is the treatment of choice for mild-to-moderate dehydration. Oral
rehydration solution (ORS), 200 mL after each loose stool should be encouraged.
This may also be achieved by using sports beverages, fruit juices (orange, banana,
coconut), soups or a balanced clear liquid diet at home.
For severe dehydration or shock, insert a 18-G cannula in the antecubital fossa
and start IV infusion of Ringer lactate. Pediatric patients should be given a bolus
of 20 mL/kg of NS/RL and repeated as indicated.
• If vomiting is present, injection ondansetron 8 mg IV may be given along with
IV pantoprazole/omeprazole
• Monitor urine output. If decreased, suspect acute kidney injury. Monitor
electrolytes and correct any imbalance, especially sodium and potassium.
• Antibiotics are not indicated in most cases of acute gastroenteritis (AGE)

• Most cases of diarrhea settle down with just oral fluid rehydration
• If cholera is suspected (large volume, watery loose stools): Give doxycycline 300 mg
stat followed by 100 mg PO bd × 3 days, if hanging drop preparation is positive for
vibrio cholerae
• If bacillary dysentery is suspected (bloody diarrhea, fever, tenesmus, abdominal
pain)—Give tablet azithromycin 1g as a single dose or ciprofloxacin 500 mg bd for
3 days.
• If amoebic dysentery is suspected, send stool sample for ova and parasites and start
metronidazole therapy.
• Discharge the patient on ORS once frequency of loose stools or vomiting

decreases.
• Avoid anti-motility agents such as loperamide when infective or invasive
diarrhea is suspected.
ETIOLOGY OF FOOD POISONING/AGE BASED ON

INCUBATION PERIOD
Very Short Incubation Period (1–6 Hours)
• Bacillus cereus and staphylococcal species are the usual pathogens responsible
for food poisoning with a very short incubation period.
• Results from eating improperly refrigerated rice, meat, ham, poultry, eggs,
and salads.
• Severe nausea, vomiting, abdominal pain, and cramps are the usual symptoms.
Diarrhea is rare.
• Antibiotics are not indicated and treatment is mainly supportive care.
Short Incubation Period (10–48 Hours)

• Rotavirus, calicivirus, astrovirus, adenovirus, parvovirus, C. perfringens, and
C. botulinum are the usual pathogens.
• Watery diarrhea, nausea, and abdominal cramps are the usual symptoms.
• Treatment is mainly supportive.
Long Incubation Period (1–5 Days)

• Vibrio cholerae, Y. enterocolytica, Y. pseudotuberculosis, Salmonella, Shigella,
ETEC, enterohemorrhagic E. coli (EHEC), nontyphoidal Salmonella species,
and Campylobacter jejuni are the usual pathogens causing AGE with a longer
incubation period.
• Antibiotics are needed for cholera, salmonellosis, bacillary dysentery, and
severe ETEC infections.
Urinary Tract Infections 23
CHAPTER
INTRODUCTION
The term urinary tract infection (UTI) covers a heterogeneous group of conditions
with different etiologies, which have as their common factor the presence of
bacteria in the urinary tract, associated with variable clinical symptoms.
The first and the most important step after making a diagnosis of UTI is to
differentiate between cystitis and pyelonephritis (Flowchart 1).
• Lower UTI (cystitis): Infections that are localized to the lower urinary tract
(urethra, bladder). Symptoms are dysuria, frequency, urgency, and urinary
incontinence.
• Upper UTI (acute pyelonephritis): The most important symptom is fever. Other
symptoms include nausea and vomiting, loin and back (flank) pain. Costo-
vertebral angle tenderness may be elicited. The patient is systemically ill with
signs of sepsis and shock.
Cystitis presents only with lower urinary tract symptom. Fever is not a feature of cystitis.
Presence of fever with chills with urinary symptoms indicates acute pyelonephritis. Oral
antibiotics are adequate for cystitis; IV antibiotics are preferred for pyelonephritis.
FLOWCHART 1: Diagnosis and management of urinary tract infection (UTI).

ASYMPTOMATIC BACTERIURIA
Asymptomatic bacteriuria is defined as isolation of a specified quantitative count
of bacteria in an appropriately collected urine specimen from an individual
without symptoms or signs of UTI.
• In asymptomatic women or men, bacteriuria is defined as two consecutive
clean-catch voided urine specimens with isolation of the same organism in
quantitative counts of ≥105 cfu/mL.
• In asymptomatic catheterized men or women, bacteriuria is defined as a single
catheterized specimen with isolation of a single organism in quantitative
counts of ≥105 cfu/mL.
Whom to treat: Screening for and treatment of asymptomatic bacteriuria is
appropriate for pregnant women and for patients undergoing urologic procedures
in which mucosal bleeding is anticipated.
Whom not to treat: There is no role for screening for or treating asymptomatic
bacteriuria in populations other than pregnant women or patients undergoing
urologic procedures expected to cause mucosal bleeding.
Investigations to be sent: For lower urinary tract infections, confirm with urine
analysis and microscopy. Complete blood count, electrolytes, creatinine, liver
function test, blood culture and sensitivity (c/s), urinalysis, and urine c/s may be
sent for suspected pyelonephritis.
HOW TO INTERPRET URINALYSIS?

• Look for the urine white blood cell count: More than 5 cells in males and more
than 10 cells in females is significant.
• Leukocyte esterase may be used to detect more than 10 leukocytes per high-
power field (sensitivity of 75–96%; specificity of 94–98%).
• The nitrite test is fairly sensitive and specific for detecting ≥105 cfu of
Enterobacteriaceae per mL of urine.
ULTRASONOGRAPHY OF THE KIDNEYS

Acute pyelonephritis is a clinical diagnosis confirmed with results of urinalysis.
An ultrasonography (USG) of abdomen is not needed for most cases of community-
acquired pyelonephritis or for cystitis. The indications for an urgent USG are:
• Unresponsive to 48 hours of appropriate antibiotic therapy
• Patients with known urogenital tract abnormalities
• Catheter-acquired UTI
• Past history of renal calculi
• Elevated creatinine (acute worsening of renal functions).
Presence of renal angle tenderness without the above-mentioned conditions is not an

indication for requesting an USG abdomen.
CHAPTER 23: Urinary Tract Infections 97
A complicated UTI is defined as being associated with one of the following:

Diabetes mellitus, pregnancy, symptoms >7 days, renal failure, urinary tract
obstruction, renal transplantation, immunosuppression, nosocomial infection,
and indwelling urethral catheter or stent.
MANAGEMENT OF UNCOMPLICATED UTI

• Cystitis:
cc Oral antibiotics [nitrofurantoin, fluoroquinolones, and trimethoprim/
sulfamethoxazole (TMP/SMX)]
cc Amoxicillin–clavulanate, cefpodoxime, and cefaclor are alternatives but
are less effective

cc Ampicillin or amoxicillin should not be used (high-resistance rates).
• Pyelonephritis:
cc Outpatient management with oral fluoroquinolones is acceptable for
patients with mild-to-moderate illness. IV ceftriaxone is an alternative

cc Patients requiring hospitalization should receive beta lactams + beta-
lactamase inhibitor or carbapenems.
MANAGEMENT OF COMPLICATED UTI

• Cystitis:
cc Oral fluoroquinolones (ciprofloxacin 500 mg bd/levofloxacin 750 mg od)
cc Nitrofurantoin, TMP/SMX, oral beta-lactams are poor choices (high
resistance rates)
cc Parenteral therapy with once daily regimen of levofloxacin (500 mg),
ceftriaxone (1 g), ertapenem (1 g), or an aminoglycoside (3–5 mg/kg of

gentamicin) may be tried.
• Pyelonephritis:
cc Patients with complicated pyelonephritis should be managed as inpatients
with carbapenems (Table 1).
TABLE 1: Antibiotics for urinary tract infection (UTI).

Acute uncomplicated cystitis Escherichia Nitrofurantoin 100 mg Alternate
in women (dysuria and coli PO qid × 5–7days choice:
frequency in healthy, adult, Ciprofloxacin
non-pregnant women with 500 mg PO bd ×
normal urinary tract) 3 days
Pyelonephritis— E. coli Mild-to-moderate Severe illness
uncomplicated [no illness: Piperacillin (qSOFA ≥ 2):
underlying genitourinary tazobactam 4.5 g IV q6- Ertapenam 1 g
(GU) disease] 8h or Cefoperazone/ IV od
sulbactam 3 g IV q12h
Complicated UTI (underlying E. coli, Proteus Meropenem 1 g IV q8h;
GU disease) Pseudomonas de-escalate as per c/s
Acinetobacter
Acute Central Nervous
System Infections 24
CHAPTER
INTRODUCTION
Acute central nervous system (CNS) infections includes meningitis, encephalitis
and brain abscess. Meningitis refers to inflammation of the leptomeningitis
surrounding the brain, while encephalitis refers to inflammation of the brain
parenchyma itself.
ETIOLOGY
• Pyogenic meningitis: Streptococcus pneumoniae, Neisseria meningitidis; Group
B Streptococcus, Haemophilus influenzae, and Listeria monocytogenes.
• Viral meningitis or encephalitis: Herpes simplex virus (HSV), enteroviruses
(coxsackie, echovirus, other nonpoliovirus enteroviruses), varicella zoster
virus (VZV), mumps, HIV, lymphocytic choriomeningitis (LCM) virus.
MENINGITIS VERSUS ENCEPHALITIS

The presence or absence of normal brain function is the important distinguishing
feature between encephalitis and meningitis.
• Meningitis: Patients usually have fever, headache, lethargy, vomiting, and
neck stiffness.
Cerebral function remains normal initially in patients with meningitis.
• Encephalitis: Patients present with fever, altered mental status, motor or
sensory deficits, personality changes, speech or movement disorders or
seizures.
Abnormalities in brain function are common and an early feature of
encephalitis.
• Meningoencephalitis: The distinction between the two entities is frequently
blurred since some patients may have both a parenchymal and meningeal
process with clinical features of both.
Patients with pyogenic meningitis are usually toxic and clinically deteriorate rapidly within
3–5 days of onset of fever.
Patients with aseptic meningitis usually present later and have milder symptoms.
Patients with viral encephalitis present early but are usually nontoxic and have altered
mental status or seizures.
CHAPTER 24: Acute Central Nervous System Infections 99
CLINICAL EXAMINATION
Classic examination finding of meningitis is neck stiffness. Remember that
the elderly may have a significant amount of neck stiffness due to cervical
spondylopathy. Other classical signs of meningitis include Kernig's sign and
Brudzinski's sign.
Presence of papilledema on fundoscopy can be an indicator of raised ICP
and is a contra indication for a diagnostic lumbar puncture in resource limited
settings.
INVESTIGATIONS
• Complete blood count, electrolytes, creatinine, liver function test, blood
culture and sensitivity (c/s), and CT brain (plain).
• Chest X-ray if respiratory symptoms are present.
• Prothrombin time (PT), activated partial thromboplastin time (aPTT) if
patient is in systemic inflammatory response syndrome or shock.
• Cerebrospinal fluid (CSF) analysis: CSF total count (TC), differential count
(DC), protein, sugar, routine c/s, and multiplex polymerase chain reaction
(PCR) (if aseptic meningitis suspected). Check concomitant RBS during the
lumbar puncture (LP).
MANAGEMENT
Acute management of a bacterial CNS infection includes immediate administra-
tion of an empiric antibiotic with anti-epileptics if required and supportive care.
Most viral infections resolve without specific anti-virals but could lead to long
term sequelae. Empiric anti-viral drugs are warranted for herpes encephalitis/
meningitis. Empiric antibiotic therapy in the ED depends on the suspected
etiology.
• Pyogenic meningitis: Ceftriaxone 2 g IV q12h + vancomycin 15–20 mg/kg
IV stat
Dexamethasone 10 mg IV first dose 15 minutes before first dose of antibiotic
• Viral meningitis or encephalitis: Injection acyclovir 10 mg/kg IV stat and q8h
• Scrub typhus meningoencephalitis: Injection doxycycline 200 mg IV stat.
The approach to an acute CNS infection and the empiric antibiotic choice is
shown in Flowchart 1.
Before doing a LP, make sure that there is no papilledema or contraindication for LP on
CT scan.
In general, the presence of unequal pressures between the supratentorial and

infratentorial compartments is a contraindication for a LP.
FLOWCHART 1: Approach and empiric antibiotic choice in a patient with suspected

acute central nervous system infection.
CONTRAINDICATION FOR A LUMBAR PUNCTURE AS

DEFINED BY CT BRAIN
• Midline shift
• Cerebral hemorrhage/subarachnoid hemorrhage/epidural or subdural
hemorrhage
• Brain abscess
• Posterior fossa mass
• Loss of suprachiasmatic and basilar cisterns
• Loss of the superior cerebellar or quadrigeminal plate cistern.
Tetanus 25
CHAPTER
INTRODUCTION
• Tetanus is a nervous system disorder characterized by muscle spasms that are
caused by the toxin-producing anaerobe Clostridium tetani, which is found in
the soil.
• The incubation period of tetanus can be as short as 2 days or as long as 38 days,
with most cases occurring at a mean of 7–10 days following exposure.
• The severity of tetanus can be assessed by the Patel and Joag score (Table 1)
THERAPY
• Injection tetanus immunoglobulin (Tetglob) 500 U intravenous (IV) stat
• Injection tetanus immunoglobulin (Tetglob) 250 U intrathecal
• Injection crystalline penicillin 20 L U IV q4h × 10 days or injection
metronidazole 500 mg IV q6h × 7 days.
TABLE 1: Assessment of severity: Tetanus score (Patel and Joag score)

Parameter Score
Age >60 years 1
Postabortal 1
Incubation period <7 days 1
Period of onset <24 hours 1
Dysphagia 1
Rigidity 1
Reflex spasms 1
Spontaneous spasms 1
Autonomic hyper-reactivity (variable heart rate, 2
fluctuating blood pressure, diaphoresis)
Total score
<4 Mild
4–6 Moderate
>6 Severe (requires elective
intubation)
GENERAL MEASURES
• Secure airway and breathing. Intubate if necessary and possible or perform a
tracheostomy, if indicated (based on the scoring system).
• Isolate the patient to a quiet environment without triggers of spasm.
• Liberal sedation and muscle relaxation: Diazepam 10–20 mg IV/po q1–2 hours
(up to 500 mg/day).
• Supportive care.
ACTIVE IMMUNIZATION
Tetanus is one of the few bacterial diseases that do not confer immunity following
recovery from acute illness. All patients with tetanus should receive active
immunization with a total of three doses of tetanus ± diphtheria toxoid spaced
at least 2 weeks apart, commencing immediately upon diagnosis. Tetanus toxoid
should be administered at a different site than tetanus immunoglobulin.
TETANUS PROPHYLAXIS
Tetanus prophylaxis should be administered as soon as possible following a
wound but should be given even to patients who present after a few months for
medical attention (Table 2).
TABLE 2: Tetanus prophylaxis.

Previous doses of TT Clean and minor wound All other wounds
TT Human TIG TT Human TIG
<3 doses or unknown Yes* No Yes* Yes#
≥3 doses Only if last No Only if last No
dose given dose given
≥10 years ago ≥5 years ago
*The vaccine series should be continued and three doses at 2-week intervals should be completed.
#The dose of human TIG is 250–500 U intravenous stat with part infiltrated around the wound.
(TT: tetanus toxoid; TIG: tetanus immunoglobulin)
Antibiotic Doses and
Spectrum 26
CHAPTER
It is important to know the etiology of any infection and the antimicrobial

spectrum of commonly used antibiotics in order to be able to choose the most
appropriate empiric antibiotic in the emergency department (Table 1).
TABLE 1: Dosages of commonly used antibiotics and their antimicrobial spectrum.

Antibiotic Dose Antimicrobial spectrum
Crystalline 20 L U IV bolus • Gm-pos: Strep group A, B, C, G, Streptococcus
penicillin pneumoniae, Enterococcus, and Listeria
• Gm-neg: Neisseria meningitidis and Haemo-
philus ducreyi
• Anaerobes: Actinomyces, Prevotella,
Clostridium, and Peptostreptococcus
Amoxicillin/ 500 PO q8h • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
ampicillin Enterococcus, and Listeria
• Gm-neg: N. meningitidis and Proteus
• Anaerobes: Clostridium, Fusobacterium, and
Peptostreptococcus
Cloxacillin 500–1,000 mg PO • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
q6h Staphylococcus aureus (MSSA), and Staph
epidermidis
• Anaerobes: Peptostreptococcus
• Piperacillin– • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
tazobactam S. aureus (MSSA), S. epidermidis, and
• Cefoperazone– Enterococcus
sulbactam • Gm-neg: N. meningitidis, Moraxella,
H. influenzae, E. coli, Klebsiella, Enterobacter,
Serratia, Salmonella, Shigella, Proteus,
Citrobacter, Aeromonas, and Pseudomonas
• Anaerobes: Bacteroides, Prevotella, Clostridium,
Fusobacterium, and Peptostreptococcus
Amoxicillin- 625 mg PO TID or • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
clavulanate Augmentin duo Staph. aureus, (MSSA), and Enterococcus
1.2 g BD • Gm-neg: Neisseria gonorrhoeae,
N. meningitidis, Moraxella, H. influenzae,
E. coli, Klebsiella, Salmonella, Shigella, Proteus,
Aeromonas, and H. ducreyi
• Anaerobes: Actinomyces, Bacteroides,
Prevotella, Clostridium, Fusobacterium, and
Peptostreptococcus
Continued
Continued
Cefazolin (first 1–1.5 g IV q8h • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
generation) IV S. viridans, and Staph. aureus (MSSA)
• Gm-neg: Neisseria gonorrheae, H. influenzae,
E. coli, Klebsiella, and Proteus
Cefalexin (first 250–1,000 mg • Gm-pos: Strep group A, B, C, G, S.
generation) oral PO q6h pneumoniae, S. viridans, and S. aureus (MSSA)
• Gm-neg: H. influenzae, E. coli, Klebsiella, and
Proteus
Cefuroxime 125–500 mg • Gm-pos: Strep group A, B, C, G,
(second PO/IV q12h S. pneumoniae, S. viridans, S. aureus (MSSA)
generation) IV/ • Gm-neg: Neisseria gonorrheae, Moraxella,
oral H. influenzae, E. coli, Klebsiella, Proteus, and
Aeromonas
Ceftriaxone (third 1–2 g IV stat • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
generation) IV S. viridans, and S. aureus (MSSA)
• Gm-neg: Neisseria gonorrheae, N. meningitides,
Moraxella, H. influenzae, E. coli, Klebsiella,
Salmonella, Shigella, Proteus, Aeromonas,
Y. enterocolitica, and H. ducreyi
• Anaerobes: Actinomyces, Clostridium, and
Peptostreptococcus
Ceftazidime (third 1–2 g IV q8h • Gm-pos: Strep. group A, B, C, G, S. pneumoniae
generation) IV • Gm-neg: Moraxella, H. influenzae, E. coli,
Klebsiella, Salmonella, Shigella, Proteus,
Aeromonas, Pseudomonas, Burkholderia
cepacia, and H. ducreyi
• Anaerobes: Clostridium and Peptostreptococcus
Cefixime (third 200–400 mg • Gm-pos: Strep. group A, B, C, G,
generation) oral PO q12h S. pneumoniae, and S. viridans
• Gm-neg: Moraxella, H. influenzae, E. coli,
Klebsiella, Salmonella, Shigella, Proteus,
Aeromonas, Y. enterocolitica, and H. ducreyi
Vancomycin 1–2 g IV bolus in • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
100 mL normal Enterococcus, S. aureus (MSSA), S. aureus
saline (NS) and (MRSA), S. epidermidis, and Listeria
q12h • Anaerobes: Clostridium, Peptostreptococcus
Linezolid 600 mg q12h • Gm-pos: Strep group A, B, C, G, S. pneumonia,
PO/IV Enterococcus, S. aureus (MSSA), S. aureus
(MRSA), S. epidermidis, and Listeria
Continued
CHAPTER 24: 105
Continued
Ciprofloxacin 500–750 mg • Gm-pos: S. aureus (MSSA), S. epidermidis,
PO bd Listeria
200–400 mg IV • Gm-neg: N. meningitidis, Moraxella,
q8h H. influenzae, E. coli, Klebsiella, Enterobacter,
Pseudomonas, Y. enterocolitica, Legionella,
Chlamydia, and Mycoplasma pneumoniae
Levofloxacin 750 PO od • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
Enterococcus, S. viridans, S. aureus (MSSA),
S. epidermidis, Listeria
• Gm-neg: N. meningitidis, Moraxella,
Pseudomonas, Y. enterocolitica, Legionella,
Chlamydia, and Mycoplasma pneumoniae
• Anaerobes: Clostridium and Peptostreptococcus
Azithromycin 500 mg PO od • Gm-pos: Listeria

or 500 mg IV in • Gm-neg: Moraxella, H. influenzae, Legionella,
500 mL 5% D over Haemophilus ducreyi, Chlamydia, Mycoplasma
1 hour pneumoniae, Mycobacterium avium, and
Rickettsia
• Anaerobes: Actinomyces, Clostridium,
Prevotella, and Peptostreptococcus
Doxycycline 100 mg BD PO/IV • Gm-pos: Strep pneumoniae, Listeria
• Gm-neg: Neisseria meningitidis, Moraxella,
H. influenzae, Aeromonas, E. coli, Brucella,
Chlamydia, Mycoplasma pneumoniae, and
Rickettsia
• Anaerobes: Actinomyces, Clostridium,
Prevotella, and Peptostreptococcus
Meropenem 1 g IV in 100 mL • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
NS Enterococcus, S. viridans, S. aureus (MSSA),
S. epidermidis, and Listeria
Morganella, Citrobacter, and Pseudomonas
• Anaerobes: Bacteroides, Clostridium
(nondifficile), Prevotella, Fusobacterium, and
Peptostreptococcus
Continued
Continued
Ertapenem 1 g IV in 100 mL • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
NS bolus Enterococcus, S. viridans, S. aureus (MSSA),
S. epidermidis, and Listeria
Morganella, and Citrobacter
• Anaerobes: Bacteroides, Clostridium
(nondifficile), Prevotella, Fusobacterium, and
Peptostreptococcus
Gentamicin 1.5–2 mg/kg IV in • Gm-pos: S. aureus (MSSA)
100 mL NS bolus • Gm-neg: Moraxella, H. influenzae, E. coli,
and od Klebsiella, Enterobacter, Shigella, Serratus,
Proteus, Aeromonas, Pseudomonas, Y.
enterocolitica, and Francisella tularensis
Amikacin 15 mg/kg IV in • Gm-pos: S. aureus (MSSA)
100 mL NS bolus • Gm-neg: Moraxella, H. influenzae, E. coli,
and od Klebsiella, Enterobacter, Shigella, Serratus,
Proteus, Aeromonas, Pseudomonas,
Y. enterocolitica, Francisella tularensis, and
Mycobacterium avium
Clindamicin 15–20 mg/kg IV in • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
100 mL 5% od S. aureus (MSSA)
• Anaerobes: Actinomyces, Clostridium, Prevotella,
Fusobacterium, and Peptostreptococcus
Metronidazole 500 mg PO • Anaerobes: Bacteroides, Clostridium difficile,
q8h/400 mg Prevotella, and Fusobacterium
IV q8h
Nitrofurantoin 100 PO q6h • Gm-pos: Strep group A, B, C, G, S. pneumoniae,
Enterococcus, S. aureus (MSSA), and S. aureus
(MRSA)
• Gm-neg: Neisseria gonorrhoeae, E. coli, and
Salmonella
(Gm-pos: gram-positive; Gm-neg: gram-negative; Strep: Streptococcus; MSSA: methicillin-susceptible
S. aureus; MRSA: methicillin-resistant S. aureus)
All the above doses are for patients with normal renal function. Dose adjustments may be needed for
some of the antibiotics in the presence of renal failure.
Section 5
Toxicology
General Measures 27
CHAPTER
INTRODUCTION
History is often the most valuable tool because many patients (e.g., children,
suicidal or psychotic adults, patients with altered consciousness) cannot provide
the required reliable information; friends, relatives, and rescue personnel should
be questioned. Even, seemingly reliable patients or relatives may incorrectly
report the amount or time of ingestion. When possible, the patient’s living quarters
should be inspected for clues (e.g., partially empty pill containers, evidence
of recreational drug use). Pharmacy and medical records may provide useful
information. Decontamination is an emergency procedure done to decrease
and minimize absorption of toxins into the systemic circulation. These include
gastrointestinal (GI), skin and mucosal decontamination.
GASTRIC LAVAGE
Gastric lavage is a GI decontamination procedure in which toxic contents in the
stomach are removed by repetitive instillation and aspiration of small amounts of
fluid. Most patients present beyond the window period of 1–2 hours and hence
lavage may not be helpful in decreasing the gastric absorption. It must be done
only after ensuring that the airway is secured.
Indications
• Potentially life-threatening poisoning (or if history is not available) and
unconscious presentation
• Potentially life-threatening poisoning and presentation within 1 hour
• Potentially life-threatening poisoning due to drug with anticholinergic effects
and presentation within 4 hours
• Ingestion of sustained release preparation of significantly toxic drug
• Large amount of salicylate poisoning presenting within 12 hours
• Iron or lithium poisoning.
Do not perform a gastric lavage in drowsy or unconscious patients unless the airway is
secured because of the high risk of aspiration.
Technique
• Insert a large (16F) nasogastric tube and check its placement by air insufflations
and auscultating the epigastrium
110 SECTION 5: Toxicology
• Place the patient in the left lateral decubitus position

• Instill 100–200 mL of warm tap water slowly through the NG tube
• Drain the fluid with the stomach contents into a dependent bucket placed at
the head end
• Repeat the process of instilling and draining of the fluid till the draining fluid
is clear
• Usually, 500–3,000 mL of tap water is required to perform a good lavage.
ACTIVATED CHARCOAL
Activated charcoal is a highly adsorbent powder that is produced by pyrolysis of
organic material and steam cleaning (activation) to increase its surface area. It
adsorbs toxins in the gut lumen, thereby decreasing GI absorption.
It is indicated for poisonings that fulfill the following criteria:
• Drug ingested is adsorbed by charcoal and has significant potential for toxicity
• Time since ingestion is less than 1–2 hours
• Drug has significant enterohepatic circulation
• Drug delays gastric emptying and time with ingestion less than 4 hours
• Drug is in a controlled release preparation with ingestion less than
12–18 hours.
Dose: Mix 50 g of activated charcoal 100 mL of water and leave it in the stomach.
Multidose Activated Charcoal

The use of repeated activated charcoal is likely to produce a meaningful clinical
outcome for the following drugs: Carbamazepine, clonidine, colchicine,
dapsone, digitoxin, phenobarbitone, phenytoin, quinidine, salicylate, tricyclic
antidepressants (TCA), theophylline, verapamil, and warfarin.
Dose: 25–50 g (0.5 g/kg) mixed in 100 mL water every 4 hours.
Contraindications for Activated Charcoal

• Depressed mental status without airway protection (risk of aspiration)
• Late presentation
• Suspected esophageal or gastric perforation.
Drug Overdose 28
CHAPTER
INTRODUCTION
Drug overdose is usually intentional, but may be accidental in children. Many
self-poisonings involve multiple drugs or coingestion with alcohol. History may
be unreliable. Insist that the relatives go back and search for evidence such as
empty pill covers or bottles that may have been discarded by the patient near the
place of incident.
GENERAL MANAGEMENT OF DRUG OVERDOSE

• Assess airway, breathing and circulation (ABC)
• Obtain intravenous access and start fluid resuscitation
• Send the blood investigations including drug levels, if available
• Perform gastric lavage or activated charcoal if indicated (usually for patients
presenting within 1 hour of consumption)
• Provide supportive care.
• Administer specific antidotes, if available (Table 1)
ACETAMINOPHEN OVERDOSE
Acetaminophen (N-acetyl-p-aminophenol or paracetamol) is one of the most
widely used drugs for deliberate self-poisoning. Doses up to 4,000 mg per day
are considered therapeutic. The toxic dose is usually more than 150 mg/kg of
paracetamol (7.5–10 g in adults)
TABLE 1: Common specific antidotes.

Toxin Antidote
Acetaminophen N-Acetylcysteine
Benzodiazepines Flumazenil
Carbamates Atropine
Digitalis glycosides (digoxin, digitoxin, and oleander) Digoxin-specific Fab fragments
Ethylene glycol Ethanol
Methanol Ethanol and fomepizole
Opioids Naloxone
Organophosphates Atropine and pralidoxime
Tricyclic antidepressants NaHCO3
Clinical Presentation
The initial manifestations are often mild and nonspecific and include nausea,
vomiting or anorexia. Initial laboratory investigations may be normal. Acute liver
failure usually develops 24–36 hours after ingestion at which time laboratory
evidence of hepatotoxicity and occasionally nephrotoxicity become apparent.
Measure serum paracetamol levels 4 hours postingestion and then 4 hours
later to determine the ‘possible risk’ of hepatotoxicity using the modified Rumack-
Matthew treatment nomogram.
Management
• Gastric lavage ± activated charcoal if patient presents within 1 hour of ingestion
• If the patient likely ingested >7.5–10 g or has features of hepatotoxicity,
administer intravenous N-acetyl cysteine as an antidote
• Dose:
cc 150 mg/kg in 200 mL of 5% dextrose over 15 minutes, then
cc 50 mg/kg in 500 mL of 5% dextrose over 4 hours, then
cc 100 mg/kg in 1 L 5% dextrose over 16 hours
• Administer vitamin K1 10 mg IV stat
TRICYCLIC ANTIDEPRESSANT OVERDOSE

Tricyclic antidepressants (TCA) commonly used for DSP are amitriptyline,
imipramine, desipramine, lofepramine
Patients often present with anticholinergic symptoms like dry mouth, dilated
pupils, blurred vision, tachycardia, urinary retention, agitation, seizures or coma.
Cardiac conduction abnormalities are common due to inhibition of the fast
sodium channels in the His-Purkinje system and myocardium.
ECG changes: Sinus tachycardia, QRS prolongation>100 ms, prolongation of PR
and QT intervals, VT, VF
Venous blood gas analysis: Look for metabolic acidosis which indicates severe
toxicity
Management
• Monitor the patient closely for cardiac conduction delays, arrhythmias and
hypotension.
• If QRS prolonged/metabolic acidosis/hypotension/arrhythmias, NaHCO3 is
the primary initial therapy for cardiotoxicity. Administer NaHCO3 50–100 mL
IV bolus followed by 10 mL/h infusion.
CHAPTER 28: Drug Overdose 113
• Hypotension may be refractory, primarily secondary to peripheral alpha-1

adrenergic receptor antagonism: If present, rush in a fluid bolus and administer
Glucagon: 5 mg IV bolus, repeat after 10 minutes. Then start glucagon infusion
at 1–5 mg/h or vasopressors like nor-adrenaline
• Ventricular dysrhythmias unresponsive to alkalinization: MgSO4 2 g IV over
20 minutes
• Respiratory failure: Intubate and secure the airway
• Seizures/agitation: Midazolam/diazepam
• Lipid emulsion therapy may be considered in patients who do not respond to
the above standard therapies
The clinical features and management of some other common drug overdoses
are shown in Table 2.
TABLE 2: Clinical features and specific management of common drug overdose.

Symptoms and signs Specific treatment
Benzodiazepines Drowsiness, slurred Flumazenil
speech, nystagmus, • 0.2–0.3 mg bolus, repeat dose every
hypotension, ataxia, 5 min till patient is rousable up to a max
respiratory depression, of 3 mg, followed by
coma • 0.1–0.4 mg/h infusion
Barbiturates Respiratory depression, • Maintain airway and breathing. Intubate
hypotension, shock, and if severe respiratory depression
urinary retention • Fluid resuscitation and forced alkaline
diuresis
• Hemodialysis if renal failure/anuria
Beta-blockers Sinus bradycardia, • Bradycardia: Atropine 1 mg IV, repeat
hypotension, every 3–5 min. Max dose: 3 mg. If persists
bronchospasm, seizures, and in shock: cardiac pacing
cardiac failure, cardiac • Seizures: Midazolam 5 mg IV or diazepam
arrest drowsiness, • Bronchospasm: Salbutamol nebulization/
hallucinations, coma terbutaline infusion 0.05 µg/kg/min
• In severe cases, administer high dose
insulin therapy: 1 U/kg insulin bolus
followed by 1–4 U/kg/h insulin infusion
in 10% dextrose (improves myocardial
contractility and systemic perfusion).
Monitor sugars and potassium
• Hypotension: Glucagon 5 mg IV bolus,
repeat after 10 min. Then start infusion at
1–5 mg/h
• Calcium gluconate loading, then add
10 mL to the IV fluids every 4 hours.
Continued
Continued
Calcium channel • General: Nausea, • Calcium gluconate loading, then add
blockers (CCB) vomiting, dizziness, 10 mL to the IV fluids every 4 hours
• Nifedipine confusion, seizures • Glucagon: 5 mg IV bolus, repeat after
and • Metabolic: acidosis, 10 minutes. Then start infusion at
amlodipine hypocalcemia, and 1–5 mg/h
• Verapamil and hyperkalemia • Hypotension: elevate foot end of bed
diltiazem • Cardiac: hypotension, and give fluid challenge. Inotropes
bradycardia, AV block, (noradrenaline) if severe hypotension
complete heart block, persists
pulmonary edema • Bradycardia: Atropine 1 mg IV, repeat
every 3–5 min. Max dose: 3 mg. Consider
pacing if required
• In severe cases, administer ‘High dose
insulin therapy’: 1 U/kg insulin bolus
followed by 1–4 U/kg/h insulin infusion
in 10% Dextrose (improves myocardial
contractility and systemic perfusion).
Monitor sugars and potassium
• Correct acidosis (pH <7) with NaHCO3
Copper sulfate Acute: Nausea, • Corrosive esophageal burns: Early UGI
(powerful vomiting, hemorrhagic scopy. Treat like corrosive poisoning
oxidizing agent) gastroenteritis. • D-Penicillamine 1,000–1,500 mg/day in
After 24 hours: three divided doses for 1–2 weeks
Hemolysis, hepatic • If methemoglobinemia (MetHb): Give
failure, coagulopathy, methylene blue 1–2 mg/kg IV bolus.
cardiovascular collapse, Repeat dose after 1 hour if MetHb level
rhabdomyolysis, renal still elevated. Administer oxygen
failure, coma
Digoxin • Anorexia, nausea, • Digoxin specific antibody (Fab)
vomiting, any cardiac fragments, if available
arrhythmia, visual • Bradyarrhythmia’s: Atropine 1 mg IV,
changes, diplopia, repeat every 3–5 min. Max dose: 3 mg.
photophobia, Consider transcutaneous pacing
xanthopsia (objects • Hypotension: IV fluid bolus
appear yellow)
• Correct hypokalemia, hypomagnesemia
• Hypokalemia, or hypercalcemia if present
hypomagnesemia,
• Life-threatening ventricular arrhythmias:
renal failure
Manage as per ACLS protocol
precipitates toxicity
• ECG changes:
Down sloping
ST depression,
shortened QT
interval, Flat, inverted
or biphasic T waves
Continued
CHAPTER 28: Drug Overdose 115
Continued
Iron GI irritation, abdominal • Desferrioxamine IV 15 mg/kg/h for a
pain, hepatic failure, max dose of 80 mg/kg (5 h infusion)
coagulopathy, seizures, • Treat coagulopathy with blood products
shock • Hemodialysis for severe toxicity
• Consider early decontamination of the
gut by Whole bowel irrigation if X-ray
abdomen shows radio-opaque iron
tablets beyond the pylorus
Lithium Thirst, polyuria, • Li level <1.4 mmol/L: Supportive care
diarrhea, vomiting, • Li level >1.4 mmol/L: Hemodialysis is
tremors, seizures, indicated
arrhythmias, • Ensure adequate hydration
hypotension
• Do not give diuretics
Phenytoin • Rapid loading: • Stop the drug
therapeutic hypotension, • Supportive care
range: 20–40 bradyarrhythmias, • Treat seizures with barbiturates/
and asystole benzodiazepines
• Increased levels: • In severe cases: Dialysis may be helpful
nystagmus, ataxia,
slurred speech,
lethargy, confusion,
coma
(IV: Intravenous)
Insecticide Poisoning 29
CHAPTER
ORGANOPHOSPHORUS COMPOUNDS
There are more than a hundred organophosphorus (OP) compounds in common
use. These are classified according to their toxicity and clinical use.
• High toxicity (e.g., tetraethyl pyrophosphates and parathion): These are mainly
used as agricultural insecticides.
• Intermediate toxicity (e.g., coumaphos, chlorpyrifos, and trichlorfon): These
are used as animal insecticides.
• Low toxicity (e.g., diazinon, malathion, and dichlorvos): These are used for
household application and as field sprays.
Clinical Features of Organophosphorus Poisoning

• SLUDGE/BBB—salivation, lacrimation, urination, defecation, gastric emesis/
bronchorrhea, bronchospasm, bradycardia
• DUMBELS—defecation, urination, miosis, bronchorrhea/bronchospasm/
bradycardia, emesis, lacrimation, salivation (Table 1).
Neurological Manifestations
• Type I paralysis or acute paralysis.
• Type II paralysis or intermediate syndrome: This syndrome develops
24–96 hours after the poisoning. Following recovery from the acute cholinergic
crisis, and before the expected onset of delayed neuropathy, some patients
develop a state of muscle paralysis. The cardinal feature of the syndrome is
TABLE 1: Symptoms and features of organophosphorus poisoning.

Muscarinic receptors Nicotinic receptors Central receptors
• Cardiovascular: Bradycardia, • Cardiovascular: • General effects:
hypotension Tachycardia Anxiety, restlessness
• Respiratory: Rhinorrhea, Hypertension ataxia, convulsions
bronchorrhea bronchospasm, cough • Musculoskeletal: insomnia, dysarthria,
• Gastrointestinal: Nausea/vomiting, Weakness tremors
increased salivation, abdominal Fasciculations • Coma
cramps, diarrhea, fecal incontinence Cramps • Absent reflexes
• Genitourinary: Urinary continence Paralysis • Respiratory
• Eyes: Blurred vision, increased depression
lacrimation, miosis • Circulatory collapse
• Glands: Excessive salivation
CHAPTER 29: Insecticide Poisoning 117
muscle weakness affecting the proximal limb muscles and neck flexors. One
of the earliest manifestations in these patients is the inability to lift their head
from the pillow (due to a marked weakness in neck flexion).
• Type III paralysis or organophosphate-induced delayed polyneuropathy
(OPIDP): characterized by distal weakness occurring 2–4 weeks after OP
exposure with recovery in weeks to months.
Cardiovascular Manifestations
Seen in two-thirds of patients, common ECG manifestations include QTc
prolongation, ST-T segment changes and T wave abnormalities. Death due
to cardiac causes is either due to an arrhythmia or due to severe refractory
hypotension.
Diagnosis
• Diagnosis is confirmed by a low-plasma pseudocholinesterase levels.
• Red blood cells cholinesterase is more accurate, but plasma cholinesterase is
easier to assay and is more readily available.
• Cholinesterase levels do not always correlate with severity of clinical illness.
• Falsely depressed levels of plasma cholinesterase are observed in liver
dysfunction, low-protein conditions, neoplasia, hypersensitivity reactions,
use of certain drugs (succinylcholine, codeine, and morphine), pregnancy,
and genetic deficiencies.
Management
The treatment should be initiated immediately on clinical suspicion, without
waiting for blood investigations.
• Skin decontamination
• Airway protection, if indicated
• Gastric lavage if patient presents within 1 hour of ingestion
• Anticholinergics
cc Atropine: IV bolus of 2 mg, then double the dose every 5 minutes till
atropinization targets are achieved. Central nervous system (CNS) side

effects include psychosis and restlessness.
cc Glycopyrrolate: It is equally effective, with less CNS side effects than
atropine. The standard dose used is 100 µg as bolus every 2–5 minutes.
cc After all the above targets are achieved, start atropine infusion at a rate of
20–30% (mL/h) of the total dose required for atropinization.
Atropinization targets:
• Heart rate >80/min
• Pupils not constricted
• No secretions. Dry lungs (Note: Focal crepitations may suggest aspiration)
• Systolic blood pressure (SBP) >80 mm Hg.
• Cholinesterase reactivator (oximes): The use of oximes is controversial and

they are not widely used.
ORGANOCHLORIDE COMPOUNDS
Chlorinated hydrocarbon (organochlorine) compounds are used in pesticides,
solvents, and fumigants. Organic chlorines lower the seizure threshold or remove
inhibitory influences to produce CNS stimulation. Dichloro-diphenyl-trichlo-
roethane (DDT) is a commonly used organochloride.
Features of CNS stimulation, seizures, agitation, lethargy, nausea, vomiting,
hyperaesthesia of the mouth and face, tongue, extremities, headache, dizziness
or myoclonus.
Management
• General measures and gastric lavage, if patient presents within 1–2 hours
• Secure airway
• Seizure control with benzodiazepines, phenytoin, barbiturates or propofol
• Atropine is not indicated in organochloride toxicity.
CARBAMATES
OP and carbamates are the two groups of cholinesterase-inhibiting insecticides
commonly used that can cause cholinergic toxicity. Medical carbamate
compounds include physostigmine, pyridostigmine and neostigmine. However,
these agents are transient cholinesterase inhibitors, which spontaneously
hydrolyze from the cholinesterase enzymatic site within 48 hours. As such, the
duration of cholinergic symptoms in carbamate poisoning is <48 h. However,
severe complications may persist.
• SLUDGE/BBB—salivation, lacrimation, urination, defecation, gastric emesis,
bronchorrhea, bronchospasm, bradycardia
• DUMBELS—defecation, urination, miosis, bronchorrhea/bronchospasm/
bradycardia, emesis, lacrimation, salivation.
Management
• General measures and gastric lavage if patient presents within 1–2 hours
• Treatment is with atropine but smaller doses and shorter courses are adequate
• Carbamates do not produce intermediate and late syndromes.
CHAPTER 29: Insecticide Poisoning 119
PYRETHROIDS
Pyrethroids are synthetic derivatives of the natural pyrethrins extracted from the
flower Chrysanthemum. These are contact poisons and exert their toxicity on ion
channels by prolonging neuronal excitation. Two basic poisoning syndromes are
seen.
• Type I pyrethroids produce reflex hyperexcitability and fine tremor.
• Type II pyrethroids produce salivation, hyperexcitability, choreoathetosis,
and seizures. Both produce potent sympathetic activation.
Management
• General measures and gastric lavage if patient presents within 1–2 hours
• Seizure control with benzodiazepines, Phenytoin, barbiturates or propofol
• Atropine is not indicated in pyrethroid toxicity.
PARAQUAT POISONING
Paraquat (dipyridylium) is a highly lethal herbicide when ingested, while causing
only limited, localized injury on dermal exposure. It is a highly polar and corrosive
substance, which upon absorption, rapidly diffuses and concentrates in tissues
like lung, kidney, liver, and muscle. Swallowing about 30 mL of 20–24% paraquat
concentrate is usually lethal.
• Patients present with a painful mouth and difficulty in swallowing, nausea,
vomiting and abdominal pain.
• Respiratory symptoms suggest systemic toxicity.
• Patients who ingest large doses (50–100 mL) present with fulminant multi-
organ dysfunction syndrome (MODS) with pulmonary edema, cardiac,
hepatic, renal failure and central nervous system involvement with seizures
with a high case fatality rate.
Management
• There is no antidote and management is mainly supportive care addressing
airway, breathing and circulation.
• Gastric lavage is not recommended as paraquat is corrosive in nature. Naso-
gastric tube should be inserted early.
• Treat multi-organ dysfunction as indicated with supportive care like
ventilation, blood products, etc.
• Hemodialysis can reduce the plasma load of paraquat but may not reduce the
toxic effects on the target organs, with no evident mortality benefit.
The commonly available insecticide compounds and their trade names are
shown in Table 2.
TABLE 2: Commonly available compounds and trade names in India.

Chemical names Trade names
Organo Parathion, malathion, fenthion, ethion, Brahma, Chlorex,
phosphates fensulfothion, diazinon, trichlorfon, disulfoton, Chase, Cythion,
terbu fos, dichlorvos, monocrotophos, coumaphos, Ekalux, and Rogor,
chlorpyriphos, bromophos, triazophos, quinalphos, Kaycermal and
fenamiphos, cyanophos, azinphos, fonophos, Tarzen
mevinphos, dichrotophos, fenchlorphos, temaphos,
dimethoate, crufomate, phenthoate, phorate, TEPP,
acephate, demeton, thionazin, and schradan
Organo • DDT and related analogs Hildan and Thiodan
chlorides • Cyclodienes: Aldrin, dieldrin,endrin, heptochlor
and endosulfan
• Hexachlorocyclohexane (lindane)
• Mirex and chlordecone
Carbamates Aldoxycarb, aminocarb, asalum, barban, Furadan
bendiocarb, bufencarb, butacarb, benomyl,
Carbofuran, carbaryl, carbetamide, carbendazim,
chlorbufam, dochlormate, dimetilan, hoppcide,
methomyl, oxamyl, propoxur, propham, thiofanox,
terbucarb and thiophenateethyl
Pyrethroids Allethrin, bifenthrin, cyfluthrin, cyhalothrin, Ambush, All out,
cypermethrin, DPhenothrin, deltamethrin, Good Night, and
flumethrin, fenpropathrin, fenvalerate, Karate
flucythrinate, permethrin, resmethrin, tetramethrin
and transfluthrin (all out)
OP + Chlorpyriphos + Cypermethrin Prophenphos + Anaconda, Rocket,
Pyrethroid Cypermethrin Ethion + Cypermethrin Korasha
Other newer Imidacloprid, cartap hydrochloride, avermectin, Atom
compounds amitraz, fipronil, and azadirachtin (neem oil)
Rodenticides 30
CHAPTER
INTRODUCTION
Rodenticides are commonly used across India for deliberate self-harm.
Anticoagulant rodenticides are relatively innocuous while phosphorous-based
compounds are highly lethal to human beings.
TYPES OF RODENTICIDES
• Anticoagulants:
cc First-generation compounds: Warfarin, coumachlor, and coumatetralyl
cc Second-generation compounds: Chlorophacinone, diphacinone, broma-
diolone, difethialone, and brodifacoum.

• Inorganic rodenticides: Zinc phosphide, aluminum phosphide, yellow
phosphorus, and thallium.
• Others: Strychnine, cholecalciferol.
ANTICOAGULANTS (WARFARIN AND RELATED

COMPOUNDS, COUMARINS, AND INDANDIONES)
These compounds depress the hepatic synthesis of vitamin K-dependent blood-
clotting factors [II (prothrombin) and VII, IX, and X], which results in mucosal or
internal bleeding.
The second-generation compounds, also called super-coumarins, have a
longer half-life and hence may require monitoring of the PT with international
normalized ratio (INR) for many days. Some agents such as brodifacoum may not
show an elevation of PT with INR until 48 hours after ingestion.
Treatment
• Prolonged INR with no bleeding: Inj. vitamin K1 10 mg IV OD or 10–50 mg
orally, two to four times per day till INR normalizes. However, patients
ingesting large doses of second-generation coumarins may require higher
doses (100–400 mg oral) of vitamin K1 and a longer duration of treatment
(weeks to months).
• Prolonged INR with significant bleeding manifestations: Vitamin K1 and fresh
frozen plasma as required. Refer to Chapter 70 on Anticoagulation for details
of management.
PHOSPHORUS COMPOUNDS
Aluminum and Zinc Phosphides
• Aluminum and zinc phosphides are highly effective insecticides and
rodenticides.
• Commonly found in powder, pellet, or tablet form.
• Acute poisoning with these compounds may be direct due to ingestion of the
salts or indirect from accidental inhalation of phosphine generated during
their approved use.
• Both forms of poisoning are mediated by phosphine, which has been thought
to be toxic because it inhibits cytochrome c oxidase.
• Mortality often occurs rapidly within the first day of severe metallic phosphide
poisoning regardless of therapy. Death typically results from cardiac
arrhythmias or refractory shock and cardiac failure.
Clinical Features
There is usually only a short interval between ingestion of phosphides and the
appearance of systemic toxicity in case of aluminum phosphide toxicity while
there is a latent period in zinc phosphide toxicity.
• Cardiac: Impaired myocardial contractility leading to circulatory collapse
and shock
• Pulmonary: Pulmonary edema, either cardiac or noncardiac
• Hepatic: Hepatic necrosis and fulminant hepatic failure
• Hematological: DIC
• Metabolic: Severe metabolic acidosis
Management
• Supportive measures are all that can be offered and many patients die despite
intensive care.
• Correct electrolyte abnormalities, especially hypomagnesemia as this may
contribute to mortality.
• N-Acetyl Cysteine (NAC) has been proposed as an antidote and may be given
if the patient presents early (<12 h).
Dose: 150 mg/kg in 200 mL of 5% dextrose over 15 minutes then 50 mg/kg in
500 mL of 5% dextrose over 4 hours then 100 mg/kg in 1 L of 5% dextrose over
16 hours.
YELLOW PHOSPHORUS
Elemental phosphorus exists in two forms: red and white (yellow)
• The red form, used in match stick production is not absorbed and has minimal
toxicity.
• Compounds of yellow phosphorus are commonly used as everyday
rodenticides, fertilizers and in fire crackers and are easily available in Tamil
Nadu.
CHAPTER 30: Rodenticides 123
Phosphorus is readily absorbed via the gastrointestinal (GI) tract. Renal

and hepatic phosphorus concentrations are elevated within hours. Yellow
phosphorous is commonly commercially manufactured as RATOL: Rat killer.
Clinical Features
• Yellow phosphorus causes cardiac, hepatic, renal, and multi-organ failure
similar to zinc phosphide and aluminum phosphide poisoning
• However, patients with yellow phosphorus intoxication passes through three
stages:
i. First stage: 24 hours. Patient is either asymptomatic or has signs and
symptoms of local GI irritation
ii. Second stage: 24–72 hours. An asymptomatic period
iii. Third stage: >72 hours. Features of cardiac, hepatic, renal, and multi-organ
failure eventually resulting in death.
Management
• Supportive measures are all that can be offered and many patients die despite
intensive care.
• NAC may be given as an antidote if the patient presents early (<12 h).
Dose: 150 mg/kg in 200 mL of 5% dextrose over 15 minutes then 50 mg/kg in
500 mL of 5% dextrose over 4 hours then 100 mg/kg in 1 L of 5% dextrose over
16 hours
• Administer vitamin K1 10 mg IV stat
• Liver transplantation if possible, may be the only lifesaving option.
Plant Poisons 31
CHAPTER
OLEANDER
Yellow Oleander (Cerebra thevetia); Tamil name: Arali. The leaves, flowers, fruits,
and seeds of this plant are all poisonous. The main poisonous principles are
cardiac glycosides (oleandrin, neriin, thevetin, etc).
Ingestion of the plant components results in poisoning similar to digitalis toxicity.
Common symptoms include nausea, vomiting, abdominal pain, diarrhea, and
restlessness.
Hyperkalemia is the most dangerous complication that may precipitate
cardiotoxicity unless identified and corrected immediately
Cardiac toxicity may manifest as bradycardia with atrioventricular (AV) block,
atrial tachycardias, ventricular tachycardia or ventricular fibrillation. Cardiogenic
shock with myocardial depression can also occur.
Management
• Gastric lavage followed by the administration of activated charcoal and,
possibly, a cathartic, if patient presents within 1–2 hours.
• Bradycardia/heart blocks may require atropine or electrical pacing.
Ventricular arrhythmias could be treated with phenytoin [intravenous (IV)
infusion of 3.5–5.0 mg/kg, at a rate not greater than 50 mg/min], or lignocaine
(1 mg/kg slow IV bolus followed by continuous infusion of 2–4 mg/min).
• Treat hyperkalemia: Hyperkalemia is due to extracellular shift of K rather than
increase in total body K, best treated with insulin dextrose and salbutamol
nebulizations. DO NOT give calcium gluconate as calcium increases the risk
of cardiac arrhythmias.
• If patient has hypokalemia: Hypokalemia worsens toxicity of digitalis
glycosides and could be life threatening. Give KCl supplementation, oral/IV.
• Antidote: Digoxin-specific Fab antibody fragments have been used successfully
in adult patients intoxicated with nerium oleander. However, they are very
expensive and not available in India.
ODUVANTHALAI
Oduvanthalai (Cleistanthus collinus): Tamil name: Oduvan. Patients may consume
fresh leaves, freshly ground leaf paste, or boiled leaf extract. Mortality is highest if
CHAPTER 31: Plant Poisons 125
the patient boils the leaves or seeds, makes a decoction and consumes it. The toxic
active principles are Cleistanthin A and B.
Patients may present with gastrointestinal symptoms, chest pain, dyspnea,
tachypnea, bradypnea, tachycardia, bradycardia, hypotension, or acute renal
failure with distal tubular necrosis. Hypokalemia is the most common and
dangerous electrolyte abnormality and distal renal tubular acidosis has been
implicated to be the main pathogenesis of severe toxicity and mortality.
Management (Flowchart 1)
• Gastric lavage followed by the administration of activated charcoal, if patient
presents within 1–2 hours.
• Mainstay of treatment includes the correction of electrolyte imbalance
(hypokalemia) and metabolic administer sodium bicarbonate and consider
hemodialysis for severe metabolic acidosis.
• Cardiac pacing in the setting of cardiac rhythm abnormalities and QTc
prolongation.
FLOWCHART 1: Management of oduvanthalai poisoning.

DATURA
Datura stramonium is a widespread plant in India. Also known as thorn apples,
jimsonweeds and devils trumpets, the seeds and flowers have traditionally been
used over centuries as a psychoactive substance and also as a potent poison. The
active ingredients that cause cholinergic symptoms when ingested are atropine,
hyoscyamine, and scopolamine.
The classic description of anticholinergic intoxication is:
• Red as a beet (cutaneous vasodilation)
• Dry as a bone (anhidrosis)
• Hot as a hare (anhidrotic hyperthermia)
• Blind as a bat (nonreactive mydriasis)
• Mad as a hatter (delirium, hallucinations)
• Full as a flask (urinary retention).
Management
• Most patients with anticholinergic toxicity do well with supportive care alone,
but some may benefit from antidotal therapy with physostigmine 0.5–2 mg
slow IV push over 5 minutes. Additional, smaller doses may be repeated after
20–30 minutes.
• Physostigmine can induce a life-threatening cholinergic crisis (e.g., seizures,
respiratory depression, asystole).
• Therefore, physostigmine generally should be used only for patients for the
following:
cc Unresponsive to supportive measures
cc Tachydysrhythmias and subsequent hemodynamic compromise
cc Intractable seizures unresponsive to benzodiazepines
cc Extremely severe agitation or psychosis.
STRYCHNINE
The seeds of the plant Strychnos nux vomica contain the alkaloids, strychnine
and brucine. Commercially, strychnine is available as an odorless and tasteless
white powder, often used as rodenticides or for adulteration of street drugs like
cocaine, heroin, etc.
• Symptoms and signs occur within 10–20 minutes of ingestion. These include
anxiety, mydriasis, hyperreflexia, clonus and rigidity of facial and neck
muscles.
• The characteristic finding is an ‘awake seizure’ in which the patient is fully
awake during recurrent episodes of tonic-clonic seizures.
CHAPTER 31: Plant Poisons 127
• Patients may exhibit opisthotonos (truncal rigidity with arched back) and
risus sardonicus (rigid facial grimacing).
• Persistent rigidity of the skeletal muscles may result in tachycardia,
hyperthermia, rhabdomyolysis and severe metabolic acidosis.
• Immediate cause of death is respiratory paralysis due to involvement of the
diaphragm and thoracic muscles.
• Differential diagnoses to be considered are tetanus, epilepsy, acute dystonic
drug reactions, and hypocalcemia.
Management
• Control muscle activity: High doses of benzodiazepines (diazepam 5–10 mg
IV or lorazepam 2–3 mg IV) are the cornerstone of therapy. The dose may be
repeated every 15 minutes until rigidity is controlled. In severe cases, propofol
may be required to control muscle spasms.
• Airway management: Aggressive airway management is required as respiratory
paralysis could be fatal. Consider sedation, paralysis and endotracheal
intubation in severe cases.
• IV fluids: Administer adequate IV fluids to maintain urine output above
1 mL/kg/h to prevent complications of rhabdomyolysis, metabolic acidosis
and acute renal failure.
• There is no role for gastric lavage or activated charcoal.
Snake Bites 32
CHAPTER
INTRODUCTION
There are about 60 venomous snakes in India. However, most venomous bites are
caused by the “Big four” snakes against which the polyvalent antisnake venom
(ASV) is effective (Table 1).
• Russell’s viper is the only hemotoxic and neurotoxic snake in India.
• If a patient with neurotoxicity alone has significant local reaction at the bite
site, it is likely to be a Cobra bite.
• Krait bites are usually painless and often occur at night, especially to people
sleeping outdoors or on the ground. Consider krait bite as a differential on
any patient found unconscious lying on the ground in the early hours with no
other obvious history.
• Other poisonous snakes in India include King Cobra (Ophiophagus hannah),
Malabar Pit Viper (Trimeresurus malabaricus), sea snakes and coral reef
snakes.
TABLE 1: Common snakes in India and syndromes.

Snake Syndrome Local reaction
Indian Cobra (Naja naja) Neurotoxic Yes (significant)
Indian Krait (Bungarus caeruleus) Neurotoxic No
Russell’s viper (Daboia russelii) Hemotoxic + neurotoxic Yes (significant)
Saw scaled viper (Echis carinatus) Hemotoxic Yes (mild)
FIRST AID
• Apply a broad tourniquet above the site of the bite, preferably above the joint
to occlude the lymphatic flow. Pulses should be felt with the tourniquet in
place and one should be able to insinuate a finger under the tourniquet.
• Immobilize the limb by splinting and prevent walking, if the lower limb is
involved.
• No cooling/incision should be done at the bite site.
EXAMINATION AND INVESTIGATIONS

• Locate the fang marks and determine if the snake is venomous or not (two fang
marks indicate a venomous snake and multiple marks suggest a nonpoisonous
snake).
CHAPTER 32: Snake Bites 129
• Look for features of neurotoxicity.

cc Difficulty in lifting the neck suggests neck muscle weakness.
cc Ptosis
cc Single breath count: It is normally >20–30 numbers per minutes. A
decreased single breath count indicates neurotoxicity.

• Look for features of hemotoxicity: Bleeding manifestations like petechiae,
hematuria, gum bleed, melena, and hematemesis.
• Whole blood clotting time: Take 10 mL of whole blood in a glass tube and leave
it by the bed side. Clotting time >10 minutes suggests coagulopathy.
• Investigations: Complete blood count (CBC), electrolytes, creatinine, urea,
urinalysis, Prothrombin time (PT), activated partial thromboplastin time
(aPTT), Creatine kinase (CK), and ECG.
MANAGEMENT
• Analgesics for pain relief (avoid NSAIDs in patients with hemotoxicity).
• Antibiotics for infection: Anaerobic infections should be covered. Amoxicillin–
clavulanate is a good choice.
• Tetanus prophylaxis: Tetanus toxoid or diphtheria-tetanus (dT) vaccine 1 amp
intramuscular (IM) into the deltoid.
ANTISNAKE VENOM
Antisnake venom is prepared by hyperimmunizing horses against the
venoms of the ‘Big four’ poisonous snakes of India. Plasma obtained from the
hyperimmunized horses is enzyme refined, purified, and concentrated.
Remember that most bites are dry bites and do not require the polyvalent ASV.
It needs to be given only when there are features of envenomation.
• Premedication to decrease the risk of anaphylactic reactions
cc Premedication is not needed for most of the patients.
cc In those with history of atopy/reaction to equine antiserum, administer.
– Injection chlorpheniramine maleate (avil) 1 ampoule slow intra-

venous (IV).
– Injection Adrenaline 0.25 mg IM (1:1,000 dilution) in the anterolateral
thigh.
• Dose of ASV
cc Hemotoxic bite: 8–10 vials in 5% Dextrose over 30 minutes
– Reassess bleeding manifestation and whole blood clotting test after

6 hours and give four to eight vials, if needed depending on the severity
of symptoms.
cc Neurotoxic bite: 8–10 vials in 5% dextrose over 30 minutes
– Reassess after 2 hours and if neurotoxicity persists, give 4–8 vials

depending on the severity of symptoms.
• Treatment of early anaphylactic reaction

cc Stop the ASV infusion immediately
cc Injection Adrenaline 0.5 mg IM (1:1000 dilution) in the anterolateral thigh
cc Injection Chlorpheniramine maleate (Avil) 1 ampoule slow IV/IM
cc Restart the ASV slowly after 30–60 minutes after the reaction has settled.
• If respiratory failure develops, mechanical ventilation may be required.

• If significant bleeding continues despite giving ASV, send fibrinogen levels
and arrange for fresh frozen plasma/cryoprecipitate.
• Shock due to myocardial depression needs to be treated with fluid resuscitation
and inotropes.
• Renal failure due to rhabdomyolysis or shock may require hemodialysis.
• Ptosis due to neurotoxic snake bite may persist for 1–2 weeks. Without other
neurological manifestations, there is no indication to continue ASV for just
ptosis.
Each vial of lyophilized ASV costs more than Rs. 650. Administer ASV only when
indicated and use it judiciously.
Most of the venom used for the production of ASV in India is supplied by the
Irula tribal society snake catchers, who catch the big four snakes from the
districts of Kancheepuram and Thiruvalluvar in Tamil Nadu.
The venom of a Russell’s viper in North India is different from the venom of a Russell’s
viper from South India. Hence, the efficacy of ASV in other parts of India is questionable.
Though there is no evidence, smaller doses may be sufficient in Tamil Nadu.
• The currently available polyvalent ASV is not effective against King Cobra
envenomation, which is seen in the Himalayan belt, Eastern and Western
ghats. Monovalent antivenom against King Cobra is available in some places.
Insect Envenomation 33
CHAPTER
SCORPION STING
Among the 86 species of scorpions in India, Mesobuthus tamulus and Palamnaeus
swammerdami are venomous. The venom stimulates the sustained release
of acetylcholine and catecholamines resulting in initial cholinergic and late
adrenergic symptoms. Generally, the less venomous species cause more local
reaction.
Clinical Features
• Benign stings: Most stings are benign and cause severe local pain with no
progression of symptoms.
• Potentially dangerous stings:
cc 0 hours: Mild local pain, paresthesia, vomiting and salivation
cc 4 hours: (Autonomic storm) sweating, priapism, cool limbs, tachycardia,
hypertension, myocardial dysfunction, arrhythmias, and pulmonary

edema
cc 48 hours: Stage of shock and death, if untreated.
Investigations: Complete blood count (CBC), electrolytes, creatinine, and ECG.
Management
• First aid consists of applying an ice bag over the area of the sting.
• Benign stings need good pain relief with intravenous/intramuscular (IV/IM)
opiates or digital ring block with 2% xylocaine (without adrenaline).
• Administer diphtheria-tetanus (dT) toxoid intramuscularly if not adequately
vaccinated. (Refer chapter 25)
• Antibiotics if signs of infection are present (cloxacillin/augmentin)
• Potentially dangerous stings with autonomic storm
cc Prazosin: 0.25 mg for children and 0.5 mg for adults every 3 hours till
extremities become warm and dry. Usually, 2–6 doses of prazosin are
needed. Administer the first dose of prazosin even if blood pressure is low.
Start noradrenaline infusion concomitantly.
cc Benzodiazepines/phenobarbitones for seizures
cc Treat shock and cardiac failure with fluids and inotropes
cc Treat life-threatening arrhythmias.

CENTIPEDE BITE
Centipede bite mostly causes only local reaction, pain, anxiety, vomiting,
headache, and palpitations. Symptoms are usually mild.
Management
• Adequate pain relief with NSAIDs/opiates
• Local application of ice may reduce some of the discomfort
• Antitetanus prophylaxis if not adequately vaccinated. (Refer chapter 25)
• Antibiotics if signs of infection present (cloxacillin/augmentin)
• Antihistamines may be given for local pruritic reactions.
BEE AND WASP (HYMENOPTERA SPECIES) STINGS

Bees, wasps, hornets and fire ants belong to the order Hymenoptera and frequently
sting humans when disturbed. It may not always be possible to exactly identify
the culprit species, but the sting is always acutely painful. Most people only
develop minor local reactions (redness and swelling that usually resolves within a
few hours). However, some (0.3–3%) may develop anaphylaxis and could be fatal.
Bees and wasps have a similar mechanism of delivering venom. After a single
sting by a bee, the barbed venom apparatus detaches, eviscerating, and killing the
bee instantly. However, the unbarbed venom apparatus of a wasp remains intact
and hence a wasp can sting a person multiple times.
Management
• Uncomplicated local reactions may be treated with just cold compresses
• Large local reactions (exaggerated redness/swelling) can be treated with
cold compresses, antihistamines (levocetirizine 5 mg PO OD × 1–2 days)
and a nonsteroidal anti-inflammatory drug (NSAIDs). Persistent large local
reactions may require 1 or 2 days of oral prednisolone at a dose of 40–60 mg
PO od.
• Administer beta agonist (salbutamol) nebulizations for patients who develop
wheezing
• If symptoms of anaphylaxis are observed, treat with adrenaline, antihistamines,
H2 blockers and fluid resuscitation. (Refer chapter 3)
• After a sting, the barbed sting apparatus with the venom sac remains lodged
in the skin. Venom is released within seconds to minutes of the bite. Hence
removal of the embedded stingers from the skin by scraping the skin with a
23-G needle or scalpel (Fig. 1) is useful if done immediately after the sting.
However, if the patient presents after 5–10 minutes, removal of the sting
apparatus is not urgent as most of the venom would have already been
released into the body. All the stings should still be removed to prevent foreign
body reactions.
CHAPTER 33: Insect Envenomation 133
FIG. 1: Technique of Hymenoptera sting removal.
• Clean and disinfect the site of sting with soap and water followed by spirit
• Apply ice packs to slow down the spread of venom
• If the patient is stable to be discharged, advice calamine lotion to be applied
twice daily.
OTHER INSECT BITES

Beetles, Caterpillars, and Millipedes
Some species of these arthropods cause severe burning pain, numbness,
erythema, nausea, vomiting, and headache. Wash the area thoroughly with soap
and water and remove any spines or hairs by using adhesive tape or glue or facial
peel. Apply local ice packs and give analgesics for severe pain.
Spider Bites
Majority of spiders are non-venomous. Rate bites of Loxosceles and Poecilotheria
species have been reported from India. Symptoms of a bite may include mild
erythematous lesions with pruritis and swelling. The lesion may become necrotic
with eschar formation in a week. Management includes local ice pack application,
anti histamines and analgesics if required. Antibiotics (cloxacillin) are warranted
for severe local reactions.
Substance Abuse 34
CHAPTER
OPIOIDS
Opioids are prescribed legitimately for analgesia, especially for palliation.
Overdose of a legitimate prescription and illicit drug abuse result in a large
number of cases. Commonly abused opioids include morphine, heroin, tramadol,
methadone, and oxycodone.
Symptoms and Signs of Overdose

• Central nervous system (CNS) depression, respiratory depression, and miosis
are the characteristic features of opioid intoxication.
• Nausea, vomiting, orthostatic hypotension, localized urticaria, and
bronchospasm may also be seen.
• Diagnosis is purely clinical based on the classic triad of respiratory depression,
coma, and miosis.
Management
• Securing airway and breathing is crucial
• Antidote: Naloxone works by competitive inhibition of the OP3 recep-
tor and fully reverses the CNS and respiratory depression. Antidote can
be given intravenously/intramuscularly/subcutaneously (IV/IM/SC) or
intratracheally.
Intravenous Dose of Naloxone

• Adults: 0.4–2 mg IV bolus depending on the severity of symptoms. Repeat
doses of 0.4–2 mg IV may be given every 2–3 minutes till full reversal is
achieved. The maximum total dose is 10 mg.
• Children <5 years/<20 kg: 0.1 mg/kg.
• Children >5 years/>20 kg: 0.4–2 mg IV bolus.
• Depending on the severity of presentation, additional bolus doses may be
required every 30 minutes to 2 hours to maintain reversal.
CANNABIS (MARIJUANA)
• Natural marijuana contains over 60 cannabinoids and include delta-
9-tetrahydrocannabinol, the most psychoactive cannabinoid, cannabidiol,
and cannabinol.
CHAPTER 34: Substance Abuse 135
• Recreational use often consists of smoking the dried flower in the form of
rolled cigarettes (joints) and water bongs.
• Common slang terms include pot, grass, dope, MJ, Mary Jane, doobie, hooch,
weed, hash, reefers, and ganja.
• Synthetic cannabinoids are now widely available and are sold as K2, spice,
crazy monkey, chill out, spice diamond, spice gold, and chill X.
• Signs of intoxication: Tachycardia, tachypnea, elevated blood pressure (BP),
conjunctival injection, dry mouth, nystagmus, ataxia, and slurred speech.
• Complications associated with inhalation use: Acute exacerbations of asthma,
pneumomediastinum, pneumothorax, angina, and myocardial infarction.
Management of Acute Intoxication

• Mild symptoms of anxiety may be controlled with benzodiazepines
(lorazepam/midazolam)
• Cannabis hyperemesis syndrome (abdominal pain, nausea, and vomiting)
may be treated with IV fluids, antiemetics (ondansetron), and benzodiazepines
• If the patient complains of sudden onset chest pain, consider ACS/
pneumothorax/acute exacerbation of asthma and treat accordingly.
AMPHETAMINE
Amphetamine is widely abused for its CNS arousal effects. Complications include
vasospasm and intracranial hemorrhage secondary to hypertension.

• Sedate agitated patients with a benzodiazepine (diazepam 5–10 mg IV or
lorazepam 1–2 mg IV/IM). Haloperidol 5–10 mg IM may be useful in psychotic
patients.
• Control seizures with benzodiazepines.
• If the patient has seizures/focal deficits, get a computed tomography (CT)
scan is done to rule out intracerebral bleed/subarachnoid hemorrhage.
• Significant hypertension (diastolic blood pressure >120 mm Hg) may respond
to sedation. If not, treat as a hypertensive emergency.
COCAINE
Street names include coke, cola, dust, nose candy, etc.
Presentation: Seizures (common), hypertension, tachycardia, CNS depression,
ventricular arrhythmias, cardiorespiratory failure, and paranoid delusions
(chronic use).
Complications: Angina/myocardial infarction (vasoconstrictor effects on the
coronary circulation), cerebrovascular accident, and psychotic reactions.

• Sedate agitated patients with a benzodiazepine to control seizures.
• Treat hypertension as a hypertensive emergency and rapidly lower the BP
with antihypertensives.
• If the patient has seizures/focal deficits, do a CT scan to look for an intracranial
bleed.
• If the patient complains of sudden onset chest pain, consider an acute
coronary syndrome.
ECSTASY/3,4-METHYLENEDIOXYMETHAMPHETAMINE
3,4-Methylenedioxymethamphetamine (MDMA), commonly known as ecstasy
or molly, may cause life-threatening cardiac dysrhythmias, acute liver failure,
cerebral infarction, and hemorrhage. Severe hyperthermia (core temperature
>40°C), severe metabolic acidosis, muscle rigidity, DIC, and rhabdomyolysis may
also occur.
• Treatment is mainly supportive in a quiet environment. Stabilize ABC.
• If the patient presents within 1 hour of ingestion, perform a gastric lavage and
administer activated charcoal.
• Benzodiazepines can be given to control agitation, seizures, or panic reaction.
• Initiate cooling measures for hyperthermia.
• Monitor ECG and look for cardiac arrhythmias.
LYSERGIC ACID DIETHYLAMIDE (LSD)

LSD, commonly known as ‘acid’ is a hallucinogenic drug that causes altered
thoughts, feelings and awareness of one’s surroundings. Clinical features include
pupillary dilatation, sweating, acute anxiety state, tachycardia, depolarization,
and visual illusions. Large doses can cause convulsions, focal neurological deficit
(due to vasospasm), and coma.
• Treatment is mainly supportive in a quiet environment. Stabilize ABC.
• Benzodiazepines can be given to control agitation.
• LSD is rapidly absorbed through the gastrointestinal tract. Hence, gastric
lavage and activated charcoal are not beneficial and best avoided.
Miscellaneous 35
CHAPTER
CORROSIVE POISONING
A corrosive is a substance that erodes and destroys any surface it comes in contact
with. Acids and alkalis are the two primary types of agents which are most often
responsible for caustic exposures.
• Alkali ingestion: Causes liquefaction necrosis.
• Acid ingestion: Causes coagulation necrosis.
Commonly Used Corrosives

• Acids: Car battery fluid (sulfuric acid), descalers/toilet bowl cleaners
(hydrochloric acid), metal cleaners (nitric acid), rust removers (hydrogen
fluoride), acetic acid, phenol (carbolic acid), and oxalic acid.
• Alkalis: Bleach (hypochlorite) and sodium hydroxide (liquid lye and paint
remover/drain cleaner).
• Heavy metal salts (sublimate), formalin, and iodine tincture.
Investigations to be Sent
Complete blood count, electrolytes, creatinine, liver function test, ECG, rapid
blood-borne virus screen (BBVS), chest X-ray, and X-ray neck soft tissue AP/
lateral.
Management
• If the patient presents within 24 hours of ingestion
cc Do not give gastric lavage. Patients may aspirate and worsen stricture
cc Establish intravenous (IV) access and start IV fluid resuscitation
cc Remove contaminated clothes and continuously irrigate any ocular
injuries
cc Injection Pantoprazole 40 mg IV and injection metoclopramide 10 mg IV stat
cc Administer adequate analgesia
cc Refer to ENT for evaluation of oropharynx and clearance for upper
gastrointestinal (UGI) scopy.

cc Diagnostic endoscopy: Refer to gastroenterology for endoscopy-guided NG
tube insertion and further management. Endoscopy must be done within

6–24 hours of ingestion. If performed earlier than 6 hours, the lesions may
not manifest and if performed later than 24 hours, the risk of esophageal
perforation is very high.
cc If there is evidence of esophageal perforation, start extended spectrum
antibiotics: clindamycin 15–20 mg/kg IV stat or ertapenem 1 g IV stat.

• If the patient presents after 24 hours of ingestion

cc The role of endoscopic evaluation and intervention decreases, if the
patient presents to the ED after 24 hours of ingestion of corrosive.

cc If the patient already has a NG tube placed outside, refer to gastro-
enterology for further management plan.

cc If NG tube has not been inserted even after 24 hours of ingestion,
the primary treatment for severe corrosive injury is surgical. Feeding

gastrostomy or feeding jejunostomy tube needs to be inserted by general
surgery. The primary unit would be general surgery.
If endoscopy reveals only mild lesions, then the patient can be discharged
and clinical follow-up should be done at 1 month. If severe lesions are found on
endoscopy, then surgical gastrostomy is indicated, which should be followed by
repeat endoscopy and dilatation after 3 weeks.
METHANOL (METHYL ALCOHOL) POISONING

Methanol toxicity occurs most commonly due to consumption of illegally
produced alcohol products. It causes an initial syndrome similar to alcohol.
However, the formation of toxic metabolites leads to a profound metabolic
acidosis and there is also direct retinal toxicity from these metabolites (Fig. 1).
A dose of as little as 10 mL of pure methanol may cause significant toxicity or
death.
Clinical Features
• The initial effects of methanol resemble those of alcohol with central nervous
system (CNS) depression, ataxia, nausea, and vomiting. Subsequent CNS
effects may be secondary to the acidosis or to the activity of the metabolites
and include coma and convulsions.
FIG. 1: Metabolism of ethanol and methanol.

CHAPTER 35: Miscellaneous 139
• With the development of acidosis, tachycardia, tachypnea, and hypertension

may occur. However, more severe toxicity is manifested by hypotension and
cardiogenic shock.
• Blurred vision, photophobia, and decreased visual acuity may occur. About
25% of patients will have some degree of permanent visual loss.
• The major feature seen is a severe metabolic acidosis with a raised anion gap.
Management
• Supportive care: IV fluid hydration.
• Acidosis should be corrected with bicarbonate.
• Fomepizole (4-methyl pyrazole), if available should be given. Dose: 15 mg/kg
IV infusion over 30 minutes, then 10 mg/kg IV q12h for four doses. Treat until
ethylene glycol or methanol levels are <20 mg/dL.
• Ethanol has a higher affinity for alcohol dehydrogenase and competitively
inhibits the metabolism of methanol to more toxic metabolites. Hence,
ethanol should be given intravenously or orally if the IV preparation is not
available. A blood alcohol level of 100 mg/dL (21.7 mmol/L) is required to
maximally inhibit alcohol dehydrogenase.
Loading dose:
cc Four standard drinks (4 × 30 mL of spirits) orally.
cc 360–420 mL of 10% ethanol by IV infusion.
• Folate is a cofactor in the further metabolism of formic acid to nontoxic

metabolites. Folic acid 50 mg IV q4h (or folinic acid 50 mg q4h) should be
given to patients with severe toxicity.
• Hemodialysis: Methanol and its metabolites are cleared by hemodialysis.
Indications:
cc Renal failure
cc Severe metabolic acidosis (pH <7.1)
cc Methanol concentration >50–100 mg/dL.
KEROSENE POISONING
Pulmonary toxicity can occur within 1–8 hours of ingestion due to aspiration
into the respiratory tract (chemical pneumonitis). Symptoms may include
breathlessness, cough, nausea, vomiting, or abdominal pain. X-ray abnormalities
may be evident only after 72 hours.
Management
• Avoid emesis and gastric lavage.
• Supplemental oxygen if patient is tachypneic or saturation is low.
• Patients with acute lung injury may require prophylactic antibiotics
(piperacillin-tazobactam or meropenem)
• Refer to medicine for further management.
INHALATION INJURIES (CARBON MONOXIDE POISONING)

Common inhalation injuries are smoke inhalation and accompanying burns.
Smoke is a complex and variable mixture of solid, liquid, and gas constituents.
Components of inhalation injury are:
• Carbon monoxide poisoning (responsible for 85% of deaths)
• Direct thermal injury
• Soot particles that cause local injury to the cilia of the respiratory tract and
obstruct small airways
• Gas products of combustion: Oxides of sulfur, nitrogen, ammonia, chlorine,
phosgene, isocyanates, aldehydes, and ketones are highly irritative and cause
laryngospasm.
Clinical Features
Suspect smoke inhalation if any of the following features are present: exposure
to smoke or fire in an enclosed place without adequate ventilation, confusion,
altered sensorium, singed nasal hairs, oropharyngeal burns, hoarseness of voice,
wheeze, dysphagia, stridor.
Severe carbon monoxide poisoning can cause neurological manifestations
like seizures, syncope, or coma, myocardial ischemia, ventricular arrhythmias,
pulmonary edema, and profound lactic acidosis.
Delayed neuropsychiatric syndrome can be seen in up to 40% of patients
with severe CO poisoning and can occur 3 days–8 months after recovery, and
are characterized by variable degrees of cognitive deficits, personality changes,
movement disorders, parkinsonism features, and focal neurologic deficits.
Investigations
CBC, electrolytes, creatinine, LFT, CXR, ECG, ABG, carboxy-Hb (COHb) level.
COHb levels correlate poorly with clinical features and are not predictive of
delayed neurologic sequelae.
Management
• Prompt removal from the source of carbon monoxide.
• Administer high-flow oxygen by face mask. Give the highest possible
concentration of humidified oxygen. The use of hyperbaric oxygen remains
controversial.
• Protect the airway. Intubate early if necessary. However, mucosal swelling
in the upper airway and oropharynx can progress rapidly and necessitate a
surgical airway.
• IV fluid resuscitation depending on the extent of burns
• Salbutamol nebulization if bronchospasm occurs.
CYANIDE POISONING
Cyanide is a mitochondrial toxin, which is extremely lethal.
Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3,
inhibiting this final enzyme in the mitochondrial cytochrome complex. The cell
must then switch to anerobic metabolism of glucose to generate ATP and this
produces severe lactic acidosis.
Sources of Cyanide
• Industrial exposure: Plastics, photography, fumigation, metal polish,
electroplating, hair removal from hides
• Plants and fruits: Bamboo sprout, Rosaceae family (plum, peach, pear, apple,
bitter almond, cherry)
• Drugs: Sodium nitroprusside, laetrile
• Others: Artificial nail glue remover, phencyclidine synthesis.
Clinical Features
Clinical features of cyanide poisoning are dependent upon the route, duration,
and amount of exposure. The CNS and CVS are mostly affected.
Headache, anxiety, confusion, vertigo, initial tachycardia and hypertension,
then bradycardia and hypotension, vomiting, abdominal pain, hepatic necrosis,
renal failure, coma.
Clinical features are similar to carbon monoxide poisoning, which is a strong
differential for cyanide poisoning.
Management
General measures and ABC as for any poisoning. Three antidotal strategies may
be used:
• Direct cyanide binding using hydroxycobalamin, a precursor of vitamin B12
that contains a cobalt moiety that avidly binds to intracellular cyanide with
greater affinity than cytochrome oxidase.
• Induction of methemoglobinemia using amyl nitrite or sodium nitrite. The
formation of methemoglobin (MetHb) provides an attractive alternative
binding site for cyanide, in direct competition with the site on the cytochrome
complex. When cyanide binds MetHb, a relatively less toxic cyanmethemo-
globin is formed.
• Sulfur donors using sodium thiosulfate maximizes the availability of sul-
fur donors for rhodanese, a ubiquitous enzyme that detoxifies cyanide by
transforming it to thiocyanate.
Cyanide poisoning is common among jewelers as an occupational exposure or
intentional self-harm. They are usually provided the antidotes as a “cyanide kit”
when they buy cyanide compounds for commercial reasons. Administer the
antidote immediately, if available.
Dosages
cc Amyl nitrite: Inhaled by the patient (held under the patient’s nose or via
the endotracheal tube) for 30 seconds of each minute, for 3 minutes

cc Sodium nitrite: 10 mg/kg IV bolus
cc Sodium thiosulfate: 50 mL of a 25% solution (12.5 g) IV bolus
cc Hydroxycobalamin: 70 mg/kg IV bolus. A second dose of 35 mg/kg can be
given depending upon the severity of poisoning or the clinical response to

treatment.
METHEMOGLOBINEMIA
Methemoglobin is generated by oxidation of the heme iron moieties into ferric
state (Fe+3), causing a a characteristic bluish-brown muddy colour resembling
cyanosis. Methemoglobin has a very high affinity for oxygen and hence virtually
no oxygen is delivered to the tissues.
There are two types of methemoglobinemia: Congenital and acquired.
1. Congenital type: It is characterized by decreased enzymatic reduction of
methemoglobin back to functional hemoglobin. Affected patients have
lifelong cyanosis but are generally asymptomatic; e.g., cytochrome b5
reductase deficiency, hemoglobin M disease, cytochrome b5 deficiency.
2. Acquired type: Can be fatal and typically results from ingestion of specific
drugs or agents that cause an increase in the production of methemoglobin
(Table 1).
Clinical Features
Symptoms in patients with acquired methemoglobinemia result from an acute
impairment in oxygen delivery to tissues:
• Asymptomatic: (at levels <20%)
• Early symptoms: (at levels >20%) pale skin, lightheadedness, headache,
tachycardia, fatigue, dyspnea, and lethargy
• At higher levels of MetHb: (>30%) cyanosis, respiratory depression, altered
sensorium, coma, shock, seizures, and death.
TABLE 1: Common precipitating agents of acquired methemoglobinemia.

Drugs Dapsone, Clofazimine, Chloroquine, Metoclopramide, Primaquine,
Rasburicase, and Sulfonamides
Local anesthetics Benzocaine, Lidocaine, and Prilocaine
Nitrites Amyl nitrite, Farryl nitrite, Sodium nitrite, Nitroglycerin, Nitric oxide
Others • Acetanilide, p-Aminosalicylic acid, Aniline, aniline dyes, Benzene
derivatives, Chlorates, Naphthalene,
• Nitrobenzene, Paraquat, Phenacetin, Phenazopyridine, and Resorcinol
When to Suspect Methemoglobinemia?

• Sudden onset of cyanosis with symptoms of hypoxia after administration or
ingestion of an agent that can cause methemoglobinemia
• Hypoxia (low SpO2 on pulse oximeter) that does not improve with an increased
fraction of inspired oxygen
• Abnormal dark red, chocolate, or brownish coloration of the blood observed
during phlebotomy.
Management
• Asymptomatic patient with a MetHb level <20%: No therapy other than
discontinuation of the offending agent(s)
• Symptomatic patients or if the MetHb level is > 20%:
cc Methylene blue: Methylene blue 1–2 mg/kg IV bolus. Repeat dose after
1 hour if MetHb level is still elevated (>20%). The response is usually rapid
and one dose is sufficient in most patients. Repeated doses may cause
acute hemolysis and may worsen the methemoglobinemia.
cc Ascorbic acid: 10 g IV every 6 hours or 300–1,000 mg/day orally in divided
doses may be given if methylene blue is contraindicated (G6PD deficiency).

Ascorbic acid is slow to act and requires multiple doses over 24 hours for
the same effect as methylene blue.
Section 6
Cardiac Emergencies
Acute Coronary
Syndrome 36
CHAPTER
INTRODUCTION
The term acute coronary syndrome (ACS) refers to a spectrum of clinical
presentations ranging from myocardial ischemia to myocardial infarction (MI).
There are three types of ACS (Flowchart 1):
1. ST elevation (Q-wave) MI (STEMI)
2. Non-ST elevation (non-Q wave) MI (NSTEMI)
3. Unstable angina (UA).
Angina Pectoris
• Substernal discomfort precipitated by exertion
• Radiation to the shoulder, jaw, or inner aspect of the arm
• Relieved by rest or nitroglycerin in <10 minutes.
Unstable Angina
• Rest angina, >20 minutes in duration
• New onset angina that markedly limits physical activity
• Angina that is more frequent, longer in duration, or occurs with less exertion
than previous angina.
Angina Equivalents
Not all patients with ACS present with a typical chest pain. Many patients,
especially diabetic patients may present with symptoms other than chest pain
FLOWCHART 1: Spectrum of acute coronary syndromes.

148 SECTION 6: Cardiac Emergencies
that should arouse a suspicion of ACS. These symptoms, called angina equivalents
include breathlessness, epigastric pain with vomiting, palpitations, presyncope
and syncope.
EXAMINATION
• Look for features of hypoperfusion on examination, e.g., cold extremities,
sweating, hypotension, altered sensorium, thready pulse, focal deficits
• Look for features of cardiac failure.
ECG Criteria for Diagnosis

• STEMI: New ST elevation at the J point in two anatomically contiguous leads
with the following diagnostic cutoffs.
cc ≥1 mm elevation in all leads other than V and V
2 3
cc In leads V and V , the following ST elevation limits are needed for
2 3
diagnosis
– In women: ≥1.5 mm elevation
– In men >40 years: ≥2 mm elevation
– In men <40 years: ≥2.5 mm elevation
• NSTEMI/UA
c c New horizontal or down-sloping ST depression ≥0.5 mm in two
anatomically contiguous leads or

cc T inversion 1 mm in two anatomically contiguous leads with prominent R
wave or R/S ratio >1.

• Old MI (in the absence of LVH/LBBB)
cc Look for
– Q wave in leads V2 to V3 ≥0.02 s or

– QS complex in any 2 contiguous leads
– Q wave ≥0.03 s and ≥1 mm deep in any two contiguous leads or
– R wave ≥0.04 s in V1 to V2 and R/S ≥1 with a concordant positive
T wave in the absence of a conduction defect.
Contiguous leads are defined as pairs or groups of leads that reflect the
different walls of the heart. These are the inferior (II, III, aVF), lateral (I, aVL), and
anterior leads (V1–V6).
POSTERIOR WALL MYOCARDIAL INFARCTION

Posterior infarction usually occurs along with an inferior or lateral infarction
and is associated with an increased risk of LV dysfunction and death. Isolated
posterior infarction is an indication for emergent coronary reperfusion.
ECG criteria: Presence of ST elevation and Q waves in the posterior leads (V7–V9).
ST elevation of only 0.5 mm is required to confirm the diagnosis of a posterior
wall MI.
CHAPTER 36: Acute Coronary Syndrome 149
A B
FIGS. 1A AND B: (A) Position of the posterior leads; and (B) ECG changes of posterior
wall MI in the anterior leads.
Position of the posterior leads used to confirm posterior wall MI (Fig. 1A):
• V7: Left posterior axillary line, in the same horizontal plane as V6.
• V8: Tip of the left scapula, in the same horizontal plane as V6.
• V9: Left paraspinal region, in the same horizontal plane as V6.
Posterior MI is suggested by the following changes in V1-V3 (Fig. 1B):
• Horizontal ST depression
• Tall, broad R waves (>30 ms)
• Upright T waves
• Dominant R wave (R/S ratio >1) in V2.
Sgarbossa Criteria to Diagnose STEMI in the Presence

of LBBB
Three components of Sgarbossa criteria:
• ST elevation ≥1 mm in a lead with a positive QRS complex (concordance):
5 points
• ST depression ≥1 mm in lead V1, V2, or V3: 3 points
• ST elevation ≥5 mm in a lead with a negative (discordant) QRS complex:
2 points.
≥3 points = 90% specificity and 36% sensitivity for STEMI. The sensitivity may
increase, if serial or previous ECGs are available.
WELLENS’ SYNDROME
Wellens’ syndrome refers to the presence of deeply inverted or biphasic T waves
in V2–V3. This is a very highly specific sign for a critically stenotic proximal left
anterior descending (LAD) artery.
Patients may be pain free and asymptomatic by the time the ECG is taken.
Cardiac enzymes may be slightly elevated. However, they are at extremely high
risk for extensive anterior wall MI within the next few days to weeks.
B
FIGS. 2A AND B: Wellens’ syndrome type A and type B.
There are two patterns of Wellens’ syndrome based on the T wave

abnormalities:
1. Type A (seen in 25%): Biphasic, with initial positivity and terminal negativity
(Fig. 2A)
2. Type B (seen in 75%): Deeply and symmetrically inverted (Fig. 2B). The
T waves evolve over time from Type A to a Type B pattern.
Lead aVR: Augmented Unipolar Right Arm Lead

Lead aVR is often described as the ignored lead. Oriented to the right upper side
of the heart, it provides useful information on the right ventricular outflow tract
and basal septum.
• Acute coronary syndrome: ST changes in avR may signal left main coronary
artery (LMCA) occlusion. The typical ECG findings include:
cc ST elevation in aVR ≥1 mm
cc ST elevation in aVR ≥ ST elevation in lead V

1
cc Horizontal ST depression in leads I, II, V -V
4 6
When to Send Cardiac Enzymes for Suspected ACS?

• In patients with one episode of acute onset chest pain: Send only Troponin T
• In patients with recent onset chest pain (within 1 week) and presenting again
with acute worsening angina: Send Troponin T and CKMB
• In case of NSTEMI/UA: Repeat Troponin T after 3–6 hours of the first sample.
MANAGEMENT OF STEMI
Diagnose quickly—time is myocardium—if there is a high-clinical suspicion of
ACS, diagnose and start management simultaneously.
Nondiagnostic initial ECG: The initial ECG is often not diagnostic in patients with MI (up to
45% of cases in some series)
• In patients with strong suspicion of MI and ongoing chest pain, repeat an ECG in
10 minutes
• In patients with strong suspicion of MI, give 300 mg stat of Aspirin without any delay.
• Assess ABC. Administer oxygen only if SpO2 <94% (Target SpO2 94–98%).
Avoid hyperoxia.
• Relieve pain
cc Nitrates: Sublingual nitroglycerine 0.4 mg every 5 minutes up to three
doses
cc If pain is persistent, start GTN infusion 5 µg/min and titrate as per
symptoms while closely monitoring blood pressure (contraindicated in

IWMI). Stop if SBP <90 mm Hg
cc Morphine 3–5 mg IV stat to control pain and anxiety. Persistent pain
means persistent ischemia. A repeat dose of 3–5 mg IV can be given after

15 minutes.
• Give antiplatelets, statins and beta-blockers
cc Aspirin: 325 mg nonenteric coated to chew
cc Clopidogrel 300 mg loading dose PO, if <75 years old and 75 mg PO if
>75 years old

cc Atorvastatin 80 mg stat
cc Beta-blocker: Tablet Metoprolol 25 mg PO if no contraindications
(contraindicated in CCF, COPD, and high degree AV block). Start within

24 hours of admission.
• Anticoagulation
cc For primary PCI: Unfractionated heparin 70 units/kg bolus (maximum
5,000 units)/bivalirudin
cc For thrombolysis or if no reperfusion planned
– Unfractionated heparin 100 units/kg bolus (maximum 5,000) followed

by infusion at 12–18 units/h to maintain aPTT 1.5–2.5 times normal
(50–70); or
– Enoxaparin 30 mg IV bolus followed by 1 mg/kg IV q12 h.
• If patient has IWMI with hypotension: Start IV fluids; do not give nitrates
• If patient has anterior/lateral/septal MI with hypotension: Start inotropes
• Choice of reperfusion strategy in STEMI
cc Primary PCI: If the patient presents within 12–24 hours of onset of
symptoms
cc Thrombolysis: If the patient presents within 12 hours of onset of symptoms
and when PCI facility is not available. It may be considered an option for
up to 24 hours in symptomatic patients if PCI facility is not available and

ECG changes/chest pain persists
– Streptokinase: 1.5 million units IV infusion (diluted in 100 mL NS) over
60 minutes
– Tenecteplase: 30–50 mg IV bolus over 5 seconds.
Complications: Arrhythmias, hypotension, cardiac failure, acute MR, and
myocardial rupture with tamponade.
MANAGEMENT OF NSTEMI
• Assess ABC. Administer oxygen only if SpO2 <94% (Target SpO2 94–98%).
Avoid hyperoxia.
• Relieve pain
cc Nitrates—sublingual nitroglycerine 0.4 mg every 5 minutes up to three
doses
cc If pain is persistent, start GTN infusion 5 µg/min and titrate as per
symptoms while closely monitoring blood pressure (contraindicated in

inferior wall MI). Stop if SBP <90 mm Hg
cc Morphine 3–5 mg IV stat to control pain and anxiety. Persistent pain
means persistent ischemia. A repeat dose of 3–5 mg IV can be given after

30 minutes.
• Give antiplatelets, statins, and beta-blockers
cc Aspirin 325 mg nonenteric coated to chew
cc Clopidogrel 300 mg loading PO, if <75 years old and 75 mg PO if
>75 years old

cc Atorvastatin 80 mg tablet PO stat
cc Beta-blocker: Tablet Metoprolol 25 mg PO if no contraindications (contra-
indicated in cardiac failure, obstructive airway disease).

• Anticoagulate all patients with UA/NSTEMI
cc Unfractionated heparin 5,000 U IV stat and q6h or
cc Enoxaparin 1 mg/kg SC stat and q12h. Enoxaparin dose needs renal
adjustment.
• Do not thrombolyse patients with NSTEMI
• Determine risk in UA/NSTEMI to determine early/late reperfusion based on
TIMI score (TACTICS TIMI trial) (Table 1).
Note: If there is high clinical suspicion of ACS with no ECG changes or elevated
enzymes, monitor the patient for at least 12 hours with repeat ECGs.
TABLE 1: Thrombolysis in myocardial infarction (TIMI) score for unstable angina (UA)/non-
ST-segment elevation myocardial infarction (NSTEMI).
Characteristic Points
Age ≥65 years 1
Presence of at least three risk factors for coronary heart disease 1
(hypertension, diabetes, dyslipidemia, smoking, or positive family history
of early MI)
Prior coronary stenosis of ≥50% 1
Presence of ST segment deviation on admission electrocardiogram 1
At least two angina episodes in prior 24 hours 1
Elevated serum cardiac biomarkers 1
Use of aspirin in prior 7 days 1
Interpretation of the score Rate of death/new or recurrent MI or severe angina requiring
urgent revascularization in 14 days
• Low-risk score 0–2 • Score 0–1: 4–7%
• Intermediate risk score • Score 2: 8.3%
3–4 • Score 3: 13.2%
• High-risk score 5–7 • Score 4: 19.9%
• Score 5: 26.2%
• Score 6–7: 40.9%
Source: Antman EM, Cohen M, Bernink PJ. The TIMI risk score for unstable angina/non-ST elevation MI: a
method for prognostication and therapeutic decision making. JAMA. 2000;284(7):835-42.
Hypertensive
Emergencies 37
CHAPTER
HYPERTENSIVE EMERGENCY
This is defined as severe hypertension (HTN) [usually diastolic blood pressure
(DBP) >120 mm Hg] with evidence of acute end-organ damage. It can be a life-
threatening emergency and requires immediate treatment. Reduce BP within
minutes to hours.
HYPERTENSIVE URGENCY
Severe HTN (usually DBP >120 mm Hg) in asymptomatic patients is referred to
as hypertensive urgency. There is no evidence of acute end organ damage, unlike
in hypertensive emergency. Rapid reduction in BP in asymptomatic patients with
hypertensive urgency has not been proven to be beneficial. Reduce BP within
hours to days.
HISTORY AND EXAMINATION

• Hypertensive emergencies can develop in patients with or without pre-
existing chronic HTN.
• On history and examination look for features of end-organ damage and
secondary causes of HTN, e.g., projectile vomiting, focal neurological signs,
peripheral pulses, chest pain, pulmonary edema, and papilledema.
• An important history is past antihypertensive medications and compliance.
Remember that sudden withdrawal of antihypertensives can cause
rebound HTN.
INVESTIGATIONS
• Electrocardiogram: Look for features of left ventricular hypertrophy (LVH)
with strain, and acute coronary syndrome (ACS)
• Chest X-ray: Features of pulmonary edema
• Urinalysis: Casts and active sediment suggestive of acute glomerulonephritis
• Serum electrolytes and serum creatinine
• Cardiac enzymes (if an ACS is suspected)
• Computed tomography (CT) or magnetic resonance imaging (MRI) of the
brain (if head injury, neurologic symptoms, hypertensive retinopathy, nausea,
or vomiting are present)
• Contrast-enhanced CT or MRI of the chest or transesophageal echocardiog-
raphy (if aortic dissection is suspected).
CHAPTER 37: Hypertensive Emergencies 155
MANAGEMENT
Antihypertensive medications must be initiated as soon as uncontrolled
hypertension is diagnosed in the ED. In general, target a gradual reduction
of BP over 24 hours with oral antihypertensives for hypertensive urgency and
intravenous antihypertensives for hypertensive emergency. However, the
following conditions warrant a rapid control of BP.
• Acute aortic dissection to reduce aortic shearing forces
• Hemorrhagic stroke with high BP: Target SBP of 140–160 mm Hg.
Hypertensive Emergency
Acute rapid BP lowering should be done only in those with suspected end-organ
damage. Aim for a 10–20% decrease in mean arterial pressure (MAP) in the 1st
hour and 15% over the next 24 hours. However, in aortic dissection, MAP should
be reduced by 25% in the 1st hour and a further 25% over the next 24 hours.
MAP is calculated by the following formula:
MAP = DBP + 1/3 (SBP-DBP)
Use intravenous (IV) short-acting drugs so that titration is possible.
• Nitroglycerin 5–100 µg/min as IV infusion. Check BP every 10 minutes
• Labetalol (alpha plus beta-blocker): Initial bolus of 20 mg IV followed by
20–80 mg IV bolus every 10 minutes (maximum 300 mg) [avoid in heart failure
and chronic obstructive pulmonary disease (COPD)]
• Esmolol (beta-blocker): 250–500 µg/kg loading dose over 1 minute; then
initiate IV infusion at 25–50 µg/kg/min; titrate incrementally up to maximum
of 300 µg/kg/min (avoid in heart failure, and COPD)
• If pheochromocytoma is suspected, do not start a beta-blocker alone as the
alpha receptors will have more sympathetic activation
• Add oral antihypertensives while tapering IV antihypertensives:
cc Tablet amlodipine 10 mg od; or
cc Tablet nifedipine R 20 mg bd; or
cc Tablet metoprolol XL 25 mg bd; or
cc Tablet losartan 50 mg od; or
cc Tablet hydrochlorothiazide 25 mg pd.
• Observe the patient for 12 hours. Refer to medicine if BP is uncontrolled. If BP

is well-controlled, discharge the patient on at least two oral antihypertensives.
Hypertensive Urgency
Blood pressure lowering can be done with oral medications with BP monitoring
q2h. Aim for a 25–30% decrease in MAP or a BP recording of SBP <160 mm Hg or
DBP <100 mm Hg over 24 hours.
• In previously known and treated hypertensives:
cc Restart the prior medications (may be 1–3 antihypertensive) in
nonadherent patients
cc Increase the dose of existing antihypertensive medications, or add another

agent
cc Add a diuretic, and reinforce dietary sodium restriction.
• In hypertension diagnosed for the first time: The following drugs can be given:
cc Tablet nifedipine R 20 mg stat and bd; or
cc Tablet metoprolol 50 mg stat and od; or
cc Tablet losartan 50 mg stat and od; or
cc Tablet prazosin 1 mg stat and q4h or
cc Tablet hydrochlorothiazide 25 mg stat and od.
• Start one drug, check BP after 4 hours. Add another drug if BP is still high
• In patients with very high BP (>200/120 mm Hg) and confirmed by rechecking
the BP, two antihypertensives may be initiated at the same time
• If the BP reduction is achieved, the patient may be discharged on two of
the earlier medications and advice to follow-up in medicine outpatient
department (OPD).
Pulmonary Edema 38
CHAPTER
INTRODUCTION
Pulmonary edema is a common and potentially fatal cause of acute respiratory
distress. Patients with acute pulmonary edema need continuous cardiac
monitoring.
“Flash” pulmonary edema is a term that is used to describe an acute onset of
severe decompensated heart failure caused by acute increase in left ventricular
(LV) diastolic pressure with rapid fluid accumulation in the pulmonary interstitial
and alveolar spaces.
CAUSES
• Cardiogenic: Left ventricular failure, mitral stenosis
• Noncardiogenic: Infections (pneumonia), inhaled toxins, aspiration, acute
radiation pneumonitis, hypoalbuminemia,
• Unknown/incompletely understood: High-altitude pulmonary edema,
neurogenic pulmonary edema, narcotic overdose, postcardioversion
INVESTIGATIONS TO BE SENT
Complete blood count (CBC), electrolytes, creatinine, urea, troponin T,
electrocardiogram (ECG), chest X-ray (CXR), and arterial blood gas (ABG).
MANAGEMENT
• Sit the patient up in bed.
• Start oxygen (O2) therapy with 60–100% O2 by face mask. Target SpO2 94–98%
• Treat any hemodynamically unstable arrhythmia: Urgent synchronized
cardioversion may be required.
• Diuretics: Furosemide 40–120 mg intravenous (IV) or torsemide 20–60 mg IV.
Check systolic blood pressure (SBP) before giving furosemide. Administer
only if SBP >100 mm Hg
• If the patient has arrhythmia/acute coronary syndrome (ACS), start heparin/
antiplatelets. If SBP >90 mm Hg, give glyceryl trinitrate (GTN) 5 mg sublingual
or spray.
Start GTN infusion at 5–10 µg/min and increase infusion rate every
15–20 minutes [target mean arterial pressure (MAP) around 70].
• If SBP is <90 mm Hg, treat as cardiogenic shock with noradrena line

(0.1–0.5 µg/kg/min)/dopamine (5–20 µg/kg/min) infusion
• Consider dialysis if known oliguric renal failure or no response to furosemide
in 4 hours or with rising creatinine.
• Start continuous positive airway pressure (CPAP) if severe type 1 failure [Start
with FiO2 of 100; PEEP of 5]. Invasive ventilation may be needed, if the patient
deteriorates clinically.
HIGH ALTITUDE PULMONARY EDEMA (HAPE)

Exposure to high altitude (usually >2,000 meters) with physical exertion is a
common cause of noncardiogenic pulmonary edema in unacclimatized yet
otherwise healthy individuals. This condition is commonly seen in tourists visiting
hill stations and in mountaineering expeditions and could be fatal. Symptoms
include shortness of breath, nonproductive cough, headache, and decreased
effort tolerance. The mechanism is unknown but hypoxia seems to play major
role.
Acute mountain sickness (AMS) may manifest as nausea, vomiting, headache.
High altitude cerebral edema (HACE) with features of ataxia, confusion resulting
in coma may coexist with HAPE.
Management
• Descent to a lower altitude must be the highest priority
• For mild AMS, Tab. Acetazolamide 125–250 mg PO bd may help in speeding
acclimatization
• Administer oxygen if available (2–4 L to maintain SpO2 >90%)
• If oxygen is unavailable, nifedipine 10 mg PO q4-6h may be given for HAPE
• For HACE/HAPE, dexamethasone 4 mg PO/IV stat, then 4 mg q6h provides
symptomatic relief
• Prophylactic inhalation of -agonists like Salmeterol reduces the incidence
of HAPE
Atrial Fibrillation 39
CHAPTER
INTRODUCTION
Atrial fibrillation (AF) is one of the most common arrhythmias encountered in the
ED and is characterized by an irregularly irregular pulse.
Atrial fibrillation may present with palpitations, chest pain, breathlessness,
syncope, hypotension, and embolic episodes (stroke or peripheral embolus).
Management of the patient depends on the duration of the AF (if known).
There are four main types of AF:
1. Paroxysmal: Self terminating AF or with intervention within 7 days of onset,
with recurrent episodes of variable frequency
2. Persistent: AF lasting more than 7 days and not self-terminating
3. Long-term persistent: AF lasting more than 12 months
4. Permanent: AF lasting more than 12 months with unsuccessful rhythm control
interventions or decision made by patient and clinician not to pursue rhythm
control.
ELECTROCARDIOGRAM CHARACTERISTICS
Atrial rate of about 300 beats per minute (bpm).
• Irregularly irregular rhythm
• Absent P waves
• Presence of fibrillation waves.
CAUSES
• Underlying cardiac disease: Rheumatic heart disease (RHD), ischemic
heart disease (IHD), hypertension (HT), congestive cardiac failure (CCF),
cardiomyopathy, and pericarditis.
• Thyrotoxicosis
• Electrolyte imbalance: Hypokalemia, and hypomagnesemia
• Drugs: Alcohol, and sympathomimetics.
• Complete blood count (CBC), electrolytes, creatinine, magnesium (Mg),
thyroid-stimulating hormone (TSH), and chest X-ray (CXR)
• Cardiac enzymes and drug levels (digoxin), if needed

• Other investigations depend on suspected precipitant.
MANAGEMENT
• Stabilize airway, breathing, and circulation
• Correct any electrolyte abnormality and metabolic acidosis: Correct
hypokalemia or hypomagnesemia if present. Sodium bicarbonate (NaHCO3)
for severe metabolic acidosis
• Rate and rhythm control:
cc Patient with signs of unstable rhythm (hypotension/signs of shock/acutely
altered sensorium/ischemic chest pain/acute heart failure): Synchronized

cardioversion starting at 50 J, if no response, increase to 100 J, then 200 J,
with adequate sedation (midazolam 2 mg IV or ketamine 1–2 mg/kg IV).
– Do not attempt to cardiovert patients with known chronic AF, severe
mitral stenosis (MS) and severe left ventricular (LV) dysfunction as
chances of success are very low and risk of embolization is high.
– If DC shock fails initially:
c Attempt further DC shock with 200 J
c Give Amiodarone 150 mg over 10 minutes followed by 1 mg/min
infusion for 6 hours.
c Check and correct electrolyte abnormalities.
cc Hemodynamically stable patients or if cardioversion is contraindicated:
Rapid pharmacological rate control (target rate <110 bpm). Choose from
one of the following drugs:
– Metoprolol:
c Intravenous metoprolol 2.5–5 mg over 2 minutes. Repeat every
5 minutes up to a maximum of 15 mg, if the patient tolerates the
drug (no hypotension)
c Oral metoprolol XL 25 mg stat and bd may be started in asymp-
tomatic patients with mild tachycardia.
– Diltiazem:
c Intravenous diltiazem 20 mg over 2 minutes. If heart rate (HR) still
>110 bpm, give a 35 mg bolus over 2 minutes. This regimen usually
controls the ventricular rate within 4–5 minutes if the patient
tolerates the drug (no hypotension)
c Oral diltiazem 30 mg stat and q6h may be started in asymptomatic
patients with mild tachycardia.
– Verapamil:
c Intravenous verapamil 5–10 mg over 2 minutes. Repeat dose every
15–30 minutes, if the patient tolerates the drug (no hypotension)
c Oral verapamil 40 mg stat and tid may be started in asymptomatic
patients with mild tachycardia.
CHAPTER 39: Atrial Fibrillation 161
– Digoxin:
c Intravenous digoxin 0.5 mg in 50 mL normal saline (NS)/5%
dextrose over 30 minutes. Repeat a 0.25 mg IV dose twice if needed
(only in patients with AF due to RHD)
c Oral digoxin 0.125 mg stat and od may be started in asymptomatic
patients with mild tachycardia with pre-existent heart failure.
– Amiodarone:
c Can prevent recurrences in paroxysmal AF. Only used for rate
control in chronic/persistent AF.
• Assess the need for anticoagulation:
cc All patients with AF due to RHD need to be anticoagulated
cc Use CHADSVasc score for all nonrheumatic AF to decide the need for
anticoagulation (Table 1).

cc If indicated, start oral anticoagulation: Warfarin 5 mg od or sintrom
2 mg od
cc If anticoagulation not indicated, start aspirin 75 mg od
cc For chronic AF, oral anticoagulation needs to be given for 4 weeks prior
and 3 weeks post-DC cardioversion.
TABLE 1: CHADSVasc score.

Condition Points
• Congestive heart failure (or LV systolic dysfunction) 1
• Hypertension: BP >140/90 mm Hg (or treated hypertension on medication) 1
• Age 65–74 years 1
• Age ≥75 years 2
• Diabetes mellitus 1
• Sex category (i.e., female sex) 1
• Stroke in the past or TIA or thromboembolism 2
• Vascular disease (e.g., peripheral artery disease, MI, and aortic plaque) 1
Interpretation
Score Risk Anticoagulation therapy
• 0 (male) or 1 (female) Low No anticoagulant therapy
• 1 (male) Moderate Oral anticoagulant should be considered
• 2 or greater High Oral anticoagulant is recommended
(BP: blood pressure; LV: left ventricular; MI: myocardial infarction; TIA: transient ischemic attack)
Source: Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting
stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro
heart survey on atrial fibrillation. Chest. 2010;137(2): 263-72.
Atrial Flutter 40
CHAPTER
INTRODUCTION
Atrial flutter is an abnormal cardiac rhythm characterized by rapid, regular atrial
depolarization at a characteristic rate of approximately 300 beats per minute
(bpm) and a regular ventricular rate of about 150 bpm [2:1 atrioventricular (AV)
conduction] (Fig. 1).
CLINICAL MANIFESTATIONS
Palpitations, fatigue, lightheadedness, dyspnea, angina, hypotension, anxiety,
presyncope, or infrequently syncope.
ELECTROCARDIOGRAM CHARACTERISTICS
• Atrial rate of about 300 bpm.
• Typical P waves are absent, and the atrial activity is seen as a saw-tooth pattern
(also called F waves) in leads II, III, and aVF (Table 1).
• There is typically a 2:1 conduction across the AV node; as a result, the
ventricular rate is usually one-half the flutter rate in the absence of AV node
dysfunction.
FIG. 1: Atrial flutter showing 4:1 conduction.
TABLE 1: Electrocardiogram characteristics of atrial flutter.

Heart rate Rhythm Baseline QRS Diagnosis
>100 bpm Irregular/regular Saw-tooth nature <0.12 ms Atrial flutter
CHAPTER 40: Atrial Flutter 163
MANAGEMENT
• Hemodynamically stable patient: Amiodarone 5 mg/kg in 5% dextrose over
30 minutes followed by 10 mg/kg over 23 hours.
As in atrial fibrillation (AF), the major issues that must be addressed in atrial
flutter are:
cc Control of the ventricular rate: Same as in AF
cc Reversion to normal sinus rhythm: Pharmacological or radiofrequency
ablation
cc Prevention of systemic embolization: Same as in AF.
• Patient with signs of unstable rhythm (hypotension/signs of shock/acutely

cardioversion starting at 50 J, if no response, increase to 100 J, then 200 J, with
adequate sedation (midazolam 2 mg IV or ketamine 1–2 mg/kg IV).
Paroxysmal
Supraventricular
Tachycardia 41
CHAPTER
INTRODUCTION
The term paroxysmal supraventricular tachycardia (PSVT) is applied to
intermittent SVTs with abrupt onset and offset other than atrial fibrillation (AF),
atrial flutter, and multifocal atrial tachycardia (MAT). PSVTs are often due to
reentry, although the sites of reentry vary.
The major causes are:
• Atrioventricular nodal reentrant tachycardia: 60%
• Atrioventricular reentrant (or reciprocating) tachycardia: 30%
• Atrial tachycardia or sinoatrial nodal reentrant tachycardia: 10%.
The typical pattern of PSVT is shown in Figure 1 and characteristics are shown
in Table 1.
MANAGEMENT
Acute management of PSVT includes controlling the rate and preventing
hemodynamic collapse.
• Patient with signs of unstable rhythm (hypotension/signs of shock/acutely
• Hemodynamically stable patient:
cc Vagal maneuvers like breath-holding and the Valsalva maneuver (slow
conduction in the atrioventricular (AV) node and can potentially interrupt

the reentrant circuit).
FIG. 1: Paroxysmal supraventricular tachycardia.
TABLE 1: Electrocardiogram characteristics of PSVT.

Heart rate Rhythm P wave QRS Diagnosis
>100 bpm Regular Absent <0.12 ms Supraventricular
tachycardia (SVT)
CHAPTER 41: Paroxysmal Supraventricular Tachycardia 165
Carotid Massage
• External pressure on the carotid bulb stimulates baroreceptors in the carotid
sinus, which triggers a reflex increase in vagus nerve activity and sympathetic
withdrawal. The result is a temporary slowing of sinoatrial (SA) nodal activity
and AV nodal conduction.
• The carotid sinus is usually located inferior to the angle of the mandible at the
level of the thyroid cartilage. Apply steady pressure over one carotid sinus for
5–10 seconds.
• If there is no response, the procedure may be repeated on the other side after
1–2 minutes.
• This is generally safe and well-tolerated, but potential complications include
profound hypotension, bradycardia, transient ischemic attack (TIA)/stroke,
and arrhythmias.
• Do not perform the procedure if a carotid bruit is heard.
Adenosine
• Adenosine is a purine nucleoside base that markedly decreases heart rate and
prolongs atrioventricular (AV)—nodal conduction.
• This drug is administered by rapid intravenous (IV) injection over 1–2 seconds
through a peripheral line (preferably brachial) followed by a normal saline
flush using a three-way stopcock.
• The patient should be supine and should have electrocardiogram (ECG) and
blood pressure (BP) monitoring.
• The half-life of adenosine is very short (10–20 s) as it is rapidly cleared from
plasma by rapid intracellular metabolism. Hence the need for a normal saline
flush after administration to reach the heart faster.
• Dose of adenosine:
cc The usual initial dose in adults is 6 mg (100 µg/kg in children)
cc If not successful, administer a second dose of 12 mg (200 µg/kg in children)
after 1–2-minutes
cc If not successful, administer a third dose of 12 mg (300 µg/kg in children)
after 1–2 minutes

Note: If a central IV access site is used, the initial dose should not exceed 3 mg.
• Contraindications: Sinus node disease, second- or third-degree heart blocks,
long QT syndrome, hypotension, bronchial asthma/COPD
• Side effects: Mild side effects include flushing, chest discomfort, dyspnea,
metallic taste, and a sense of “impending doom”
cc Magnesium may also be given both to correct a deficiency and also as a
therapeutic agent for cardiac arrhythmias. Dose is 2 g IV over 5–10 minutes.

cc Alternatives to adenosine for the acute treatment of SVT include calcium
channel blockers (CCBs) (verapamil/diltiazem) and beta-blockers

(metoprolol or esmolol).
– In cases of recurrent PSVT—attempt radiofrequency ablation (high
success rates).
Wide Complex
Tachycardias 42
CHAPTER
INTRODUCTION
Wide complex tachycardias (WCT) refer to dysrhythmias at a ventricular rate >100/
min and are characterized by QRS >0.12 seconds. WCT are usually associated with
ischemic heart disease or acute myocardial infarction and include ventricular
tachycardia (VT) and ventricular fibrillation (VF) (Table 1). These WCT originate
in the ventricles, but a supra-ventricular tachycardia (SVT) can also produce a
WCT if associated with a conduction abnormality/aberrancy.
Ventricular Tachycardia
Ventricular tachycardia may be classified as monomorphic or polymorphic.
• Monomorphic VT: The QRS complexes are regular in pattern and at a rate
of 150–200/min. Monomorphic VT can be classified as sustained and non-
sustained.
cc Sustained VT: Defined as WCT lasting >30 seconds in duration or causing
hemodynamic instability
cc Non-sustained VT: Defined as WCT >3 beats and lasting <30 seconds in
duration
• Polymorphic VT: The QRS complexes vary in shape and structure in the same
lead.
cc Torsades de pointes: This is a specific variant of polymorphic VT in which
the QRS axis swings from a positive to negative direction in a single

lead. Drugs that prolong repolarization (prolong QT interval) such as
quinidine, disopyramide, procainamide, phenothiazines, and tricyclic
antidepressants can trigger this arrhythmia.
Ventricular Fibrillation
Ventricular fibrillation refers to a totally disorganized depolarization and
contraction of a small area of the ventricular myocardium. ECG shows a fine or
TABLE 1: Characteristics of wide complex tachycardias.

Condition Heart rate (HR) Baseline P wave QRS
Ventricular tachycardia >100 bpm Regular Lost in QRS >0.12 ms
complex
Ventricular fibrillation No pulse Wavers unevenly Absent Absent
Torsades de pointes >100 bpm Varying amplitude Lost in QRS >0.12 ms
and axis complex
CHAPTER 42: Wide Complex Tachycardias 167
a coarse zigzag pattern without distinguishable P waves or QRS complexes. It is

never associated with a pulse or blood pressure.
MANAGEMENT
Ventricular Tachycardia (Fig. 1)
• Patient with signs of unstable rhythm (hypotension signs of shock/acutely
• Hemodynamically stable patient:
cc Monomorphic VT:
– Adenosine 6 mg intravenous (IV) rapid bolus followed by 12 mg IV

bolus. Consider Adenosine ONLY if regular and monomorphic.
– If no response, give Amiodarone 150 mg over10 minutes followed by 1
mg/min infusion for 6 hours.
– If no response, give Magnesium sulfate (MgSO4) 2 g IV over 3–5 minutes.
– If no response, give Lignocaine 100 mg IV push.
– If no response to the earlier drugs, try Synchronized cardioversion
with 100 J, with adequate sedation (midazolam 2 mg IV or ketamine
1–2 mg/kg IV).
cc Polymorphic VT with long QT (Torsades de pointes) (Fig. 2):
– Magnesium sulfate 2 g IV over 3–5 minutes

– Amiodarone 150 mg over 10 minutes followed by 1 mg/min infusion
for 6 hours.
– If no response, give Lidocaine 1–1.5 mg/kg IV.
FIG. 1: Ventricular tachycardia.
FIG. 2: Torsades de pointes.

– If no response to the earlier drugs, give Unsynchronized cardioversion

with 200 J, with adequate sedation (midazolam 2 mg IV or ketamine
1–2 mg/kg IV).
– Other drugs that may be tried in refractory cases are beta blockers,
calcium channel blockers, and phenytoin.
Ventricular Fibrillation (Fig. 3)

• Follow ACLS protocol for cardiac arrest and, defibrillate with 200 J
• Amiodarone 300 mg IV bolus after the third shock (refer ACLS guidelines)
FIG. 3: Ventricular fibrillation.
A summary of electrical energy dosage required for cardioversion of different

arrhythmias is shown in Table 2.
TABLE 2: Summary of electrical energy dosage.

Rhythm Monophasic Biphasic Synchronized
Initial energy (escalate if needed)
Narrow complex regular (SVT, 50–100 J 50–100 J Yes
atrial flutter)
Narrow complex irregular (AF) 200 J 120–200 J Yes
Wide regular (VT) 100 J 100 J Yes
Wide irregular (VF) 360 J 200 J No
(AF: atrial fibrillation; SVT: supraventricular tachycardia; VF: ventricular fibrillation; VT: ventricular
tachycardia)
Valvular Emergencies 43
CHAPTER
INTRODUCTION
Acute valvular emergencies can be divided into two primary categories:
1. Native valve emergencies
2. Prosthetic valve emergencies.
NATIVE VALVE EMERGENCIES

Native acute onset valvular emergencies are almost always regurgitant in nature.
However, patients with inadequately treated chronic mitral stenosis (MS) may
present to the ED with worsening of congestive cardiac failure.
• Acute aortic regurgitation:
c c Causes: Infective endocarditis, rupture of sinus of Valsalva, aortic
dissection involving the root of the aorta

cc Clinical features: Features of cardiac failure, loud P2, and left ventricular
(LV) third heart sound (S3). No cardiomegaly.

• Acute mitral regurgitation:
cc Causes: Chordal rupture, papillary muscle rupture, acute endocarditis,
and blunt chest trauma

cc Clinical features: Pulmonary edema, hypotension, and LV S3. No cardio-
megaly.
Investigations
Electrocardiogram (ECG), ECHO, chest X-ray (CXR), cardiac enzymes to rule out
acute coronary syndrome (ACS), electrolytes, creatinine, and complete blood
count (CBC).
Management
Regurgitant Lesions
• Manage cardiogenic shock and cardiac failure
• An intra-aortic balloon pump can be used in acute mitral regurgitation (MR)
to decrease aortic impedance and regurgitant fraction.
• Beta-blockers contraindicated in acute regurgitant lesions as the slower heart
rate increases the duration of diastole during which the regurgitation happens.
• Take blood cultures and empirically start treatment for infective endocarditis
(IE) if patient has fever with peripheral features suggestive of IE
• Definitive treatment is surgery and replacing the valve.
Mitral Stenosis
Medical management of MS includes diuretic therapy to alleviate pulmonary
congestion, control of atrial fibrillation and anticoagulation for patients at risk
of arterial embolic events. Primary treatment for symptomatic MS is mechanical
intervention by balloon mitral valvotomy (BMV), valve repair or valve replacement.
PROSTHETIC VALVE EMERGENCIES

Mechanical and biologic prostheses in any location are vulnerable to acute
paravalvular regurgitant disease as a result of either suture failure or valve
dehiscence related to endocarditis. Mechanical prostheses can have acute
stenosis due to either pannus or acute thrombosis.
• Acute valvular thrombus and embolism: High-risk period is up to 3 months
postoperative. Stroke or pulmonary embolism may occur and is usually seen
in those who are noncompliant with anticoagulation.
cc Treatment: Optimize anticoagulation to attain a therapeutic international
normalized ratio (INR) of 3–4.

• Acute obstructive valve thrombus: This is also seen in those with subtherapeutic
anticoagulation. The onset may be gradual or sudden onset with dyspnea and
fatigue. Embolic events may occur.
cc Clinical diagnosis: Auscultate for absence of prosthetic valve click, a strong
indicator of prosthetic valve stenosis/occlusion.

cc Diagnosis: Urgent ECHO, to look for gradient across the prosthetic valve
cc Treatment: Surgery if obstructive, thrombosed, left-sided prosthetic
heart valve causing New York Heart Association (NYHA) class III to IV
symptoms. Urgency of the surgical intervention depends on how acute
and how severe the presentation is.
– Fibrinolytic therapy if obstructive, thrombosed, left-sided prosthetic
valve caused recent onset (<14 days) NYHA class I to II symptoms, and
a small thrombus (<0.8 cm2).
– Emergency surgery if thrombosed, left-sided prosthetic heart valve
with a mobile or large thrombus (≥0.8 cm2).
– Fibrinolytic therapy for obstructive thrombosed, right-sided prosthetic
heart valves.
• Valve regurgitation or paravalvular regurgitation: This may be seen early
postoperative period or due to infective endocarditis. Presents with a change
in prosthetic sounds, dyspnea, or other signs of heart failure. Treatment
includes managing the failure and surgical correction.
Basics of
Electrocardiogram 44
CHAPTER
HOW TO CALCULATE HEART RATE?

• For regular rhythms: In Lead II
cc 300/number of big squares between RR or
cc 1,500/number of small squares between RR.
• For irregular rhythms: In Lead II, number of R waves in 30 consecutive big

squares × 10
WHAT IS A NORMAL SINUS RHYTHM?

The following are the characteristics of a normal sinus rhythm
• Regular rhythm at a rate of 60–100 bpm in adults
• Each QRS complex is preceded by a normal P wave.
• P waves should be upright in leads I and II and inverted in aVR (Normal
P wave axis)
• PR interval remains constant.
• QRS complexes are <100 ms wide
HOW TO INTERPRET THE AXIS?

Look at QRS in lead I and aVF and see if it is predominantly positive or negative.
• Lead I positive plus aVF positive: Normal axis (0° to +90°)
• Lead I negative plus aVF positive: Right axis deviation (+90° to +180°)
• Lead I positive plus aVF negative: Left axis deviation (0° to –90°)
• Lead I negative plus aVF negative: Extreme right axis deviation (–90° to +180°)
(Figs. 1A and B).
NORMAL DURATIONS
• P wave duration: <120 ms; It represents atrial depolarization
• PR interval: 120–200 ms; It represents the time taken for the electrical impulse
to be conducted through the AV node
• QRS complex: 70–100 ms; It represents ventricular depolarization
• QT interval: Up to 440 ms; It represents the duration of time taken for the
ventricles to depolarize and repolarize
FIGS. 1A AND B: (A) Electrocardiogram (ECG) axis

deviation diagram; (B) ECG axis.
P Wave
A P wave, by convention is the first positive deflection in the ECG complex. It
represents atrial depolarization. A normal P wave, P pulmonale and P mitrale are
shown in Figure 2.
A normal P wave shows the following characteristics:
• <120 ms in duration (3 small squares)
• <2.5 mm amplitude in the limb leads
• <1.5 mm amplitude in the chest leads
• Positive in lead II and negative in lead AVR
CHAPTER 44: Basics of Electrocardiogram 173
FIG. 2: Right and left atrial enlargements in lead II and lead V1.
P pulmonale: This is a typical finding of right atrial enlargement (e.g., COPD,

pulmonary hypertension, tricuspid stenosis) and is characterized by:
• P wave amplitude in inferior leads (II, III and AVF) >2.5 mm; or
• P wave amplitude in lead V1 and V2 >1.5 mm
P mitrale: This is a typical finding of left atrial enlargement (e.g., mitral stenosis)
and is characterized by:
• P wave duration in lead II >120 ms; or
• Biphasic P wave in lead V1
Q Wave
A Q wave, by convention is the first negative deflection in the ECG complex. It
represents the normal left-to-right depolarization of the interventricular septum.
A normal Q wave shows the following characteristics:
• <40 ms wide (1 small square)
• <2 mm in amplitude
• <25% of the depth of the QRS complex
Q waves can normally be present in leads III and aVR. They are considered to
be pathological, if they are >0.04 seconds (1 small square) in duration or >1/4 of
the height of the subsequent R wave.
R Wave
The first positive deflection in the QRS complex is called an R wave. It represents
depolarization of the thick ventricular walls and is the largest wave of the QRS
complex.
S Wave
A negative deflection after an R wave is called an S wave.
It represents depolarization of the Purkinje fibers and is usually a small wave.
T Wave
T wave is a positive deflection after a QRS complex. It represents ventricular
repolarization.
FIG. 3: Peaked T waves. FIG. 4: Hyperacute T waves.
T waves are upright in all leads except aVR and V1. T wave amplitude is
normally <5 mm in limb leads and <10 mm in precordial leads.
Peaked T waves: Tall, narrow and symmetrically peaked T waves are seen in
hyperkalemia (Fig. 3).
Hyperacute T waves: Broad, asymmetrically peaked T waves are seen in early
STEMI (Fig. 4).
LEFT VENTRICULAR HYPERTROPHY(LVH) DIAGNOSTIC

CRITERIA
Any of the following voltage criteria must be met to diagnose LVH.
• S wave in V1 + R wave in V5 or V6 >35 mm (Sokolov Lyon criteria)
• S wave in V3 + R wave in aVL >28 mm in men or >20 mm in women (Cornell
voltage criteria)
• R wave in aVL >11 mm
Additional ECG findings usually seen in LVH are left atrial enlargement and
left axis deviation.
LEFT BUNDLE BRANCH BLOCK (LBBB) DIAGNOSTIC

CRITERIA
• Broad QRS complex (>120 ms)
• Dominant S wave in lead V1
• Broad, monophasic ‘M’ shaped R wave in lateral leads (I, AVL, V5, and V6)
• Prolonged R wave peak time >60 ms in left precordial leads (V5–V6)
• Absence of Q waves in lateral leads (I, V5, and V6)
LBBB is almost always pathological, common causes being ischemic heart
disease, anterior wall MI, aortic stenosis, hypertension, dilated cardiomyopathy,
hyperkalemia, and digoxin toxicity.
CHAPTER 44: Basics of Electrocardiogram 175
RIGHT BUNDLE BRANCH BLOCK (RBBB) DIAGNOSTIC

CRITERIA
• Broad QRS complex (>120 ms)
• RSR’ pattern in leads V1–V3 (‘M’ shaped QRS complex)
• Wide, slurred S wave in the lateral leads – I, AVL, V5 and V6 (‘W’-shaped QRS
complex)
RBBB can be a normal finding in young, healthy people. Pathological
causes include ischemic heart disease, rheumatic heart disease, corpulmonale,
pulmonary embolism, myocarditis, and atrial septal disease.
BRUGADA SYNDROME
Brugada syndrome is a rhythm abnormality with a high incidence of sudden
cardiac arrest in people with structurally normal hearts. This syndrome results
from an inherited disorder of sodium channels and is usually seen in middle
aged people. The typical ECG pattern is a coved ST segment elevation >2 mm
in >1 of V1–V3 followed by a negative T wave (Brugada sign) (Fig. 5). Syncope
and sudden cardiac arrest due to Brugada syndrome can often be triggered by
fever, hypokalemia, hypothermia or drugs such as flecainide, propafenone, beta
blockers, alpha blockers, calcium channel blockers, nitrates, cocaine and alcohol.
The only definitive treatment is an implantable cardioverter defibrillator (ICD).
FIG. 5: Brugada sign.

Section 7
Respiratory Emergencies
Bronchial Asthma 45
CHAPTER
INTRODUCTION
Asthma is a chronic inflammatory disorder characterized by airway hyperres-
ponsiveness, variable airflow obstruction, and reversibility with bronchodilators.
CLINICAL FEATURES
Clinical features include recurrent episodes of chest tightness, breathlessness,
wheezing, and cough.
The following are the differences between asthma and chronic obstructive
pulmonary disease (COPD) (Table 1).
TABLE 1: Differences between asthma and COPD.

Asthma COPD
Age of onset Children and young adults Older age (>40 years)
Allergy/Atopy Common Uncommon
Family history Common Uncommon
Smoking association Not causal, but may Yes, usually >10 pack years
exacerbate
Chronic productive sputum Uncommon Common
Airway inflammation Eosinophilic Neutrophilic
Airflow obstruction on Reversible Minimal or no reversibility
spirometry
Disease course Stable with exacerbations Progressive worsening
with exacerbations
Role of bronchodilators Needed for immediate relief, Regular therapy warranted
can be taken as required
Response to steroids Essential for disease control Helpful in moderate to
severe disease, and for
acute exacerbations
180 SECTION 7: Respiratory Emergencies
CLASSIFICATION OF ACUTE ASTHMA

• Life-threatening asthma:
cc Peak expiratory flow rate (PEFR) less than 33% of best or predicted
cc Peripheral capillary oxygen saturation (SpO ) <92%, normocapnic

2
cc Silent chest, cyanosis, and poor respiratory effort
cc Bradycardia, arrhythmia, and hypotension
cc Exhaustion, confusion, and coma.
• Near-fatal:
cc Raised partial pressure of arterial carbon dioxide (PaCO ) requiring
2
mechanical ventilation.
• Acute severe asthma:
cc Peak expiratory flow 33–50% of best or predicted
cc Respiratory rate >25 breaths/min
cc Pulse rate >110 beats/min
cc Not able to talk in sentences (cannot complete sentence in one breath).
• Moderate exacerbation:
cc PEFR 50–75% of best or predicted
cc Talks in phrases
cc Respiratory rate <25 breaths/min
cc Pulse rate <110 beats/min.
All that wheezes is not asthma!! Think of:

• Upper airway obstruction
• Foreign body aspiration
• Endobronchial malignancy
• Pulmonary edema: Cardiac asthma
• Chronic obstructive pulmonary disease.
The interpretation of spirometry used to confirm the diagnosis of asthma is
shown in Flowchart 1.
INVESTIGATIONS
• Complete blood count (CBC)
• Creatinine
• Electrolytes
• Chest X-ray
• Electrocardiogram
• Arterial blood gas (ABG) only for moderate-to-severe asthma
• Do not do an ABG for mild cases of asthma.
MANAGEMENT OF ACUTE ASTHMA

• Stabilize airway, breath, and circulation (ABC)
• High-flow oxygen: Maintain SpO2 > 94%
CHAPTER 45: Bronchial Asthma 181
FLOWCHART 1: Interpretation of spirometry.
• Oral prednisolone 40–50 mg or IV hydrocortisone 200 mg stat, followed by

100 mg IV q6h.
• Oxygen driven nebulizer (salbutamol 5 mg mixed with ipratropium 0.5 mg ×
3 doses every 15 min).
• Give ipratropium nebulizer alone if patient has significant tachycardia (heart
rate >140 beats/min).
• Assess response after the three doses of nebulization and repeat three more
doses, if severe wheeze persists.
• If there is a good response, start metered dose inhaler (MDI) via spacer and
discharge the patient after a few hours.
• If there is no response in acute severe asthma, admit the patient.
• Start antibiotics if there is evidence of infection (fever, cough, and purulent
sputum) or if the patient is in septic shock.
Routine use of antibiotics is not indicated. Asthma is a hypersensitivity
reaction and total white blood cell count may be high. Most mild cases do not
require antibiotics.
Refractory Asthma (Not Responding to the Above Treatment)

• Consider single dose of IV magnesium sulfate 2 g infusion in 100 mL normal
saline over 20 minutes.
• Injection epinephrine 0.3–0.5 mg subcutaneously, or

• Injection terbutaline 0.25 mg subcutaneously every 20 minutes up to three
doses. Terbutaline infusion 0.05 µg/kg/min can also be tried in life-threatening
asthma.
• Assisted ventilation: Noninvasive ventilation should be started to decrease the
work of breathing.
• Do not delay intubation in life-threatening near-fatal asthma. Beware of
normocapnia or hypercapnia.
• Aminophylline infusion is no longer recommended for the management of
acute severe asthma.
Recommendation at Discharge
• Tab prednisolone 40–50 mg/day for 5–7 days.
• Inhaled steroid + long-acting agonist:
cc MDI formonide (formoterol + budesonide) 200 µg 2 puffs twice daily via
spacer or
cc MDI Seroflo (salmeterol + fluticasone) 125 µg/250 µg 2 puffs twice daily via
spacer.
cc MDI salbutamol 100 µg 2 puffs as and when required (reliever).
NOTE
• Acute exacerbations in pregnancy should be aggressively managed to avoid
fetal hypoxia. All medications used to treat asthma in normal patients can be
given in pregnancy.
• Peak expiratory flow rate: Maximal rate a person can exhale during a short
maximal expiratory effort after a full inspiration.
Chronic Obstructive
Pulmonary Disease 46
CHAPTER
INTRODUCTION
Chronic obstructive pulmonary disease (COPD) is a disease characterized by
persistent and progressive airway limitation caused by chronic inflammation as a
result of prolonged exposure to noxious particles or gases. Cigarette smoking and
chronic exposure to firewood cooking are the usual causes. Emphysema, chronic
bronchitis, and chronic obstructive asthma are considered subtypes of COPD.
These conditions are closely related and airflow limitation is the common factor
in the spectrum of these conditions.
Diagnosis is by demonstration of postbronchodilator irreversibility on
spirometry.
• Chronic bronchitis: It is defined as a chronic productive cough for at least
3 months in 2 successive years in a patient with other causes of chronic cough
(e.g., bronchiectasis) being excluded. Diagnosis is based on history.
• Emphysema: It is a pathological term that describes abnormal and permanent
enlargement of the airspaces distal to the terminal bronchioles and is
accompanied by destruction of the airspace walls, without obvious fibrosis.
PULMONARY FUNCTION TESTS

Spirometry is performed pre- and post-bronchodilator administration (e.g.,
inhalation of albuterol 400 µg) to determine whether airflow limitation is present
and whether it is partially or fully reversible. Airflow limitation that is irreversible
or only partially reversible with bronchodilator is the characteristic physiologic
feature of COPD. (postbronchodilator FEV1< 80% and FEV1/FVC<70% confirms
the diagnosis)
Investigations to be sent: Complete blood count (CBC), creatinine, electrolytes,
chest X-ray (CXR), electrocardiogram (ECG), and arterial blood gas (ABG).
MANAGEMENT OF ACUTE EXACERBATION OF COPD

• Assess airway, breathing, and circulation (ABC).
• Commence oxygen therapy and aim for a peripheral capillary oxygen
saturation (SpO2) of 88–92%. Uncontrolled oxygen therapy may worsen CO2
retention in some patients.
Do not give high-flow O2 in patients with COPD. Target maximum SpO2 of 88–92%.
• Treat bronchospasm and obstruction:

cc Nebulizer (salbutamol 5 mg mixed with ipratropium 0.5 mg × 3 doses
every 15 min). Avoid oxygen-driven nebulization to prevent hyperoxia

cc Assess response after three doses and repeat three more doses, if necessary
cc Give steroids: Hydrocortisone 200 mg IV stat, followed by 100 mg IV q6h
cc If no response, consider a single dose of IV magnesium sulfate 2 g infusion
over 20 minutes
cc Injection terbutaline 0.25 mg subcutaneously every 20 minutes up to
three doses. Terbutaline infusion 0.05 µg/kg/min can also be tried in life-
threatening COPD.
• Antibiotics: If there is evidence of infection (fever or purulent sputum), start
antibiotics based on CURB score.
• Noninvasive ventilation (NIV): This is the first-line treatment of choice for
patients with type 2 respiratory failure who failed to respond to initial therapy.
NIV reduces the need for intubation, decreases mortality and hospital stay.
cc Indications for NIV:
– Respiratory acidosis (pH <7.35 PaCO2 > 45 mm Hg)

– Severe breathlessness with signs of fatigue (use of accessory muscles,
paradoxical breathing or intercostal retraction)
– Persistent hypoxemia not responding to oxygen therapy (target
SpO2 >88%).
• Mechanical ventilation: This should be considered in patients unlikely or
unable to tolerate NIV.
The most important step before discharging a patient on metered dose inhalers is
checking and teaching the patient proper inhaler technique using a spacer. Most
patients do not know the proper technique and hence present to the emergency
department with recurrent exacerbations.
Metered Dose Inhaler Technique via Spacer

Step 1: Shake the metered dose inhaler (MDI) hard and attach it to the spacer
Step 2: Exhale gently to empty the lungs
Step 3: Keep the spacer in the mouth and press the MDI once
Step 4: Inhale deeply and hold breath for 5–10 seconds
Step 5: Take two more breaths slowly with the spacer still in the mouth
Step 6: Take the spacer out of the mouth, wait for 1 minute and repeat the steps
for the second puff.
SPIROMETRY
Spirometry is used to assess lung function to differentiate obstructive from
restrictive lung disease. Most lung volumes, except residual volume (RV) can be
measured using spirometry (Fig.1). Residual volume (and thus FRC and TLC) can
be measured using helium dilution or body plethysmography. The following are
some of the important volumes and capacities.
CHAPTER 46: Chronic Obstructive Pulmonary Disease 185
FIG. 1: Lung volumes on spirometry.

Source: Wikimedia Commons. (2011). LungVolume.jpg. [Online]. Available from: http://creativecommons.
org/licenses/by-sa/3.0. [Last Accessed April, 2021].
Tidal Volume (TV): Refers to the volume of air drawn into and out of the lungs
during normal breathing. Typically, 500 mL in a 70 kg man.
Inspiratory reserve volume (IRV): Refers to the additional volume of air that can
be inspired at the end of a normal inspiration. Typically, 3,300 mL in a 70 kg man.
Expiratory reserve volume (ERV): Refers to the additional volume of air that can
be expelled at the end of a normal expiration. Typically, 1,700 mL in a 70 kg man.
Residual volume (RV): Refers to the volume of air remaining in the lungs after a
maximal expiration. Typically, 1,800 mL in a 70 kg man.
Vital capacity (VC): Refers to the maximum tidal volume when an individual
breathes in and out as far as possible. Typically, 5,500 mL in a 70 kg man. VC =
IRV + TV + ERV.
Total lung capacity (TLC): Refers to the volume of air in the lungs after a
maximum inspiration. Typically, 7,500 mL in a 70 kg man. TLC = VC + RV.
Pulmonary Embolism 47
CHAPTER
INTRODUCTION
Acute pulmonary embolism (PE) is a form of venous thromboembolism to
the pulmonary artery or one of its branches and can be fatal. The source of the
embolus is usually a thrombus originating in the deep veins of the lower limbs or
pelvic veins. These emboli may lodge at the bifurcation of the main pulmonary
artery or in the smaller lobar branches.
The most common presenting symptom is dyspnea, followed by pleuritic pain,
cough, hemoptysis, and symptoms of deep venous thrombosis.
A high index of suspicion is needed in patients with risk factors and
unexplained hypoxia. Use the modified Wells scoring system to assess the
probability of pulmonary embolism (Table 1).
TABLE 1: Modified Wells scoring system for clinical assessment of suspected pulmonary
embolism (PE).
Parameter Points
Clinical symptoms of deep venous thrombosis (DVT) (leg swelling, 3
pain on palpation)
Other diagnosis less likely than pulmonary embolism 3
Heart rate >100 beats/min 1.5
Immobilization (≥3 days) or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Hemoptysis 1
Malignancy 1
Probability Score
PE likely > 4.0
PE unlikely ≤ 4.0
CHAPTER 47: Pulmonary Embolism 187
INVESTIGATIONS
• Electrocardiography: Sinus tachycardia is the most common finding. The
classical triad of S1Q3T3 is seen in only 5–10% of patients with PE.
• D-dimer: It has a high negative predictive value and can be used to exclude PE.
It is considered significant, if levels are more than 500 ng/mL.
• Chest X-ray: It usually shows no abnormality. Well established but rare
abnormalities include focal oligemia (Westermark’s sign) or a peripheral
wedge-shaped density above the diaphragm (Hampton’s hump).
• Echocardiography (ECHO): More than half the patients with PE may have a
normal ECHO. Right ventricular (RV) free-wall hypokinesis with normal RV
apical motion (McConnell’s sign) is specific for PE.
• CT pulmonary angiography (CTPA): It is the most specific test for confirmation
of diagnosis. Look for intraluminal filling defects.
MANAGEMENT
• Supplemental oxygen should be administered to target the peripheral
capillary oxygen saturation (SpO2) more than 90%.
• Intravenous fluids: Avoid fluid overload as it worsens RV functioning.
• Vasopressors: Norepinephrine for patients in shock. Dobutamine may be used
to increase myocardial contractility.
• Hemodynamically stable patients: Empiric anticoagulation—heparin 5,000
units IV bolus or enoxaparin 1 mg/kg subcutaneously stat if high suspicion
of PE.
• Hemodynamically unstable patients: Thrombolytic therapy is indicated
provided there is no contraindication.
cc Alteplase (recombinant tissue plasminogen activator): 100 mg IV over
2 hours.
cc Streptokinase: 250,000 units IV over 30 minutes, then 100,000 U/hr for
24 hours.
• Absolute contraindications for thrombolysis:
cc Prior intracranial hemorrhage
cc Known structural cerebral vascular lesion
cc Known malignant intracranial neoplasm
cc Ischemic stroke within 3 months
cc Suspected aortic dissection
cc Active bleeding or bleeding diathesis
cc Significant closed-head trauma or facial trauma within 3 months.
• Surgical or catheter embolectomy may be performed if thrombolysis is

contraindicated
Pneumothorax 48
CHAPTER
TYPES OF PNEUMOTHORAX
• Primary spontaneous pneumothorax: It occurs in patients without underlying
pulmonary disease or with undiagnosed lung condition. More common in
smokers.
• Secondary spontaneous pneumothorax: Occurs in patients with underlying
pulmonary disease like chronic obstructive pulmonary disease (COPD)
(rupture of a bleb or bulla).
• Traumatic pneumothorax: It is a common complication of penetrating or
blunt chest injuries.
• Iatrogenic pneumothorax: It is caused by medical interventions, including
transthoracic needle aspiration, thoracentesis, central venous catheter
placement, mechanical ventilation, and cardiopulmonary resuscitation.
SYMPTOMS AND SIGNS

Symptoms and signs include dyspnea (sudden or gradual) and pleuritic chest
pain.
DIAGNOSIS
• Chest X-ray (CXR): Radiolucent air and the absence of lung markings
• Ultrasonography: Absence of lung sliding.
How to Determine the Size of a Pneumothorax?

Measure the distance between the collapsed lung and chest wall on CXR:
• Small: ≤2–3 cm between the lung and chest wall on CXR.
• Large: >3 cm rim of air on CXR.
MANAGEMENT
• Immediate needle decompression by inserting a large bore needle in
the second intercostal space (ICS) at the midclavicular line for tension
pneumothorax (Fig. 1).
• Start supplemental O2 until CXR results are available because O2 accelerates
pleural reabsorption of air. The usual rate of absorption of a pneumothorax
is about 1% per day. If 100% oxygen is used, it increases to 6% per day as the
nitrogen in the pleural space is replaced by oxygen.
CHAPTER 47: Pneumothorax 189
FIG. 1: Needle thoracostomy for tension pneumothorax.
FIG. 2: Tube thoracostomy (underwater seal).
• Tube thoracostomy for secondary and traumatic pneumothorax (Fig. 2).

• Primary spontaneous pneumothorax that is <20% of the lung field and that
does not cause respiratory or cardiac symptoms can be safely observed
without treatment if follow-up CXRs done at about 6 and 48 hours show no
progression.
Tension pneumothorax is a medical emergency and should be diagnosed clinically;

time should not be wasted confirming the diagnosis with a CXR. It should be treated
immediately by inserting a 14- or 16-gauge needle with a catheter through the chest wall
in the second inter costal space at the midclavicular line. The sound of high pressure air
escaping confirms diagnosis.
Hemoptysis 49
CHAPTER
INTRODUCTION
Hemoptysis refers to expectoration of blood or blood-stained sputum. Severity of
hemoptysis can be graded as follows:
• Mild: <100 mL blood loss per day
• Moderate: 100–150 mL blood loss per day
• Severe: Up to 200 mL blood loss per day
• Massive: >500 mL blood loss per day or >150 mL/h or 100 mL blood loss per
day for more than 3 days
Massive hemoptysis that is potentially acutely life-threatening usually results
from bleeding from a bronchial artery in 90% of cases, most commonly due to
bronchiectasis, bronchogenic carcinoma, tuberculosis, and fungal infections.
In the emergency department (ED), it is important to clinically differentiate
hemoptysis from hematemesis. Table 1 shows the differences between the two.
TABLE 1: Differences between hemoptysis and hematemesis.

Hemoptysis Hematemesis
Bright red in color Dark brown or black in color
Frothy, mixed with sputum Not frothy, may be mixed with food particles
Cough precedes hemoptysis Nausea and vomiting usually precedes hematemesis
Malena absent Malena present
pH is alkaline pH is acidic
Past history of respiratory disease Past history of peptic ulcer disease or cirrhosis
CAUSES
• Bronchiectasis: Chronic airway inflammation causes hypertrophy and
tortuosity of the bronchial arteries that accompany the regional bronchial
trees.
• Tuberculosis: The cause of the bleeding is usually bronchiolar ulceration with
necrosis of adjacent blood vessels or rupture of a Rasmussen’s aneurysm.
• Fungal infections: Chronic necrotizing pulmonary aspergillosis, aspergilloma,
histoplasmosis, and blastomycosis.
• Bronchogenic carcinoma: Common with large, centrally located tumors,
especially squamous cell carcinoma.
CHAPTER 49: Hemoptysis 191
• Immunologic lung diseases: Goodpasture syndrome, Wegener’s granu-

lomatosis, systemic lupus erythematosus (SLE), and microscopic polyangiitis.
• Cardiac and vascular diseases: Pulmonary arteriovenous (AV) malformation,
pulmonary embolism, mitral stenosis (MS), and aortic dissection.
MANAGEMENT
Airway
The most lethal sequelae of hemoptysis is hypoxia due to ventilation-perfusion
match that occurs due to small airways and alveoli getting flooded with blood.
Administer supplemental oxygen to maintain SpO2 >94%.
If hemoptysis is life threatening, secure the airway by a large-diameter endo-
tracheal tube (ETT), 8 mm or larger to allow for bronchoscopy. If the bleeding
persists and the bleeding side can be localized, advance the ETT into the main
stem bronchus of the non-bleeding side to improve ventilation. The right main
stem bronchus is easier to enter than the left bronchus.
Breathing
In patients with a known lateralizing source of bleeding, a mitigating 'lung down'
approach can be employed in which the patient is positioned with the bleeding
lung in the dependant position. This promotes and protects the unaffected lung
and improves oxygenation.
Circulation
Massive hemorrhage can result in hemodynamic instability.
• Secure an IV access with a large bore cannula and administer crystalloids.
• Consider blood transfusions in patients with massive hemoptysis. Correct any
coagulopathy, if present
• Administer injection tranexamic acid 1 g intravenous (IV) bolus followed by
oral tranexamic acid 500 mg q6h
Antibiotics
Consider antibiotics for mild haemoptysis due to bronchitis or bronchiectasis if
there is any evidence of a bacterial infection
Bronchoscopy
Early bronchoscopy performed at the bedside facilitates direct visualization
of the central airways and allows therapeutic intervention. These include
injection of vasoactive agents, balloon and topical haemostatic tamponade and
thermocoagulation.
CT Chest
If the patient is hemodynamically stable, CT chest gives valuable information
in localizing the site of bleeding and can guide bronchial artery embolization, if
required.
Interventional Angiography
Bronchial artery embolization is the first line therapy for patients unable to
tolerate bronchoscopy or surgery. Massive bleeding due to tuberculosis and
bronchiectasis respond well. Rare complications include dissection and arterial
perforation.
Section 8
Neurological Emergencies
Cerebrovascular
Accidents 50
CHAPTER
INTRODUCTION
Cerebrovascular accidents include ischemic stroke and hemorrhagic stroke.
• Ischemic stroke: 80% of all strokes
• Hemorrhagic stroke: 20% of all strokes.
Transient ischemic attack (TIA) is a brief episode of neurologic dysfunction
resulting from focal temporary cerebral ischemia not associated with cerebral
infarction. In patients presenting with a TIA or stroke, use the ABCD2 score
to prognosticate and predict the recurrence of stroke within the next 2 days
(Table 1).
INVESTIGATIONS
A magnetic resonance imaging (MRI) stroke protocol or plain (computed
tomography) CT brain may be done to confirm the diagnosis (Flowchart 1).
TABLE 1: ABCD2 score.

Age older than 60 years 1 point
BP: Systolic blood pressure ≥140 mm Hg 1 point
or
Diastolic blood pressure ≥90 mm Hg
• Clinical unilateral weakness 2 points
• Speech impairment without weakness 1 point
Duration of TIA
• ≥60 minutes 2 points
• 10–59 minutes 1 point
• <10 minutes 0 point
Diabetes 1 point
Stroke risk (In the next 48 h):
Scores 0–3: Low risk 1%
Scores 4–5: Moderate risk 4%
Scores 6–7: High risk 8%
(TIA: transient ischemic attack; BP: blood pressure).
196 SECTION 8: Neurological Emergencies
FLOWCHART 1: Stroke protocol in the emergency department.
MANAGEMENT OF HEMORRHAGIC STROKE

• Antihypertensives: Lower the blood pressure aggressively to target SBP of
140–160 mm Hg. Injection Labetalol 20 mg IV bolus and repeat if needed or
tablet Nifedipine Retard 10–20 mg PO
• Start anticonvulsants (phenytoin or levetiracetam) if the bleed is in the
cerebral cortex or has extended into the ventricles.
• Consider antiedema measures if there is a significant midline shift. Use either
hypertonic saline or mannitol
cc 3% NaCl 100 mL over 30 minutes, then 100 mL infusion over 4 hours
cc 20% Mannitol 100–200 mL over 10 minutes followed by 100 mL every
8 hours
• Indications to refer neurosurgery for possibility of decompression surgery
cc Large bleed with midline shift
cc Cerebellar bleed greater than 3 cm
cc Intraventricular extension.
MANAGEMENT OF ISCHEMIC STROKE

Antihypertensives: Do not lower the BP aggressively unless the BP ≥185/110 mm Hg
(for patients eligible for reperfusion therapy) or ≥220/120 mm Hg (for patients not
eligible for reperfusion therapy).
Administer tablet Nifedipine Retard 10–20 mg PO or Injection Labetalol 10–
20 mg IV over 1–2 min and repeat once if needed. However, remember that a very
rapid reduction in BP may worsen the deficits by extending the infarct into the
surrounding ischemic penumbra.
If not eligible for reperfusion therapy or >4.5 h from onset of symptoms:
• Tablet Aspirin (chewable) 150 mg PO stat followed by 75 mg od
• Tablet Atorvastatin 40 mg PO stat followed by 20 mg HSOD
CHAPTER 50: Cerebrovascular Accidents 197
If eligible for reperfusion therapy (<4.5 h from onset of symptoms):

Fibrinolytic therapy: Intravenous thrombolysis with recombinant tissue
plasminogen activator (rtPA) at a doose of 0.9 mg/kg (10% as bolus and rest as
infusion over 1 h) remains the first choice therapy.
Endovascular therapy: Intra-arterial rtPA, percutaneous angiographic clot
removal (mechanical thrombectomy) and sonothrombolysis have all shown to
have clinical benefit and can be used when expertise is available.
Contraindications for thrombolysis:
• Coma with complete hemiplegia
• Systolic blood pressure (SBP) >180 mm Hg or diastolic blood pressure (DBP)
>110 mm Hg (consider thrombolysis if BP decreases)
• Clinical presentation suggestive of subarachnoid hemorrhage (SAH) even if
the CT scan is normal
• Presumed septic embolus
• Heparin medication within the last 48 hours and has an elevated activated
partial thromboplastin time aPTT
• International normalized ratio (INR) >1.7
• Known advanced liver disease and advanced right heart failure
• Platelet count <100,000 cells/mm3
• Serum glucose <2.8 mmol/L or >22.0 mmol/L.
Malignant middle cerebral artery (MCA) infarct: This denotes a large MCA
infarction, with or without involvement of the ipsilateral anterior cerebral artery
(ACA) or posterior cerebral artery (PCA) territories that results in cerebral edema
in the first 48 hours after a CVA, resulting in elevated intracranial pressure (ICP)
or brain herniation. An infarct larger than two thirds of the MCA territory usually
results in a malignant infarct.
If the patient has a malignant MCA infarct, do not give aspirin/clopidogrel. Approximately,
10% of ischemic strokes are classified as malignant or massive because of the presence of
space-occupying cerebral edema that is severe enough to produce elevated intracranial
pressure and brain herniation. Refer to neurosurgeon for decompressive craniotomy.
POSTERIOR CIRCULATION STROKE

Posterior circulation strokes are less common than anterior and middle
cerebral artery strokes. Because of the variation in presentation and frequent
transient nature of symptoms, posterior circulation strokes are often missed in
the emergency department (ED). Hence, a high index of suspicion is needed in
patients presenting with vertigo, cranial nerve deficits, especially sudden onset
visual field deficits, etc.
Areas Supplied by the Posterior Circulation

Areas supplied by the posterior circulation are brainstem (medulla, pons, and
midbrain), cerebellum, occipital cortex, inferior temporal lobe, and thalamus.
Symptoms
• Vertigo and nystagmus
• Ataxia and unsteadiness
• Crossed syndromes: Ipsilateral cranial nerve lesions with contralateral
pyramidal or sensory tract lesions
• Sensory deficits (numbness, paresthesia) in the limbs or face
• Visual field deficits: Homonymous hemianopia, gun barrel vision
• Cranial nerve deficits.
Management
Treatment of a posterior circulation stroke is the same as that of any ischemic or
hemorrhagic stroke. The important fact to remember is that the posterior fossa is
a very tight space. Hence, a large infarct or bleed in the cerebellum may result in
a significant increase in the intracranial pressure (ICP). Hence, a decompressive
craniectomy may be required. Refer to neurosurgeon.
When to Refer
• Activate stroke protocol (neurology, radiology, and vascular surgery) for any
patient presenting within 4.5 hours with a stroke or TIA
• In case of intracranial bleeds (parenchymal) inform both neurosurgery and
medicine. If surgical intervention is required, neurosurgery will be the primary
unit. If no surgical intervention is needed, medicine will be the primary unit.
Cerebral Venous
Thrombosis 51
CHAPTER
INTRODUCTION
• Cerebral venous thrombosis (CVT) refers to thrombosis of the dural sinus
and/or cerebral veins. It is a very challenging condition to diagnose in the
emergency department.
• Cerebral blood is drained by the superficial and deep venous systems into
the major dural sinuses (superior sagittal sinus, inferior sagittal sinus, lateral
sinus, cavernous sinus and straight sinus) and eventually into the internal
jugular vein (IJV).
• Symptoms of CVT depend on the location and acuity of thrombus formation
in the cerebral veins or dural sinuses.
RISK FACTORS
• Prothrombotic conditions (antithrombin III, protein C, and protein
deficiency, antiphospholipid and anticardiolipin antibodies, factor V Leiden
gene mutation, prothrombin G20210A mutation, hyperhomocysteinemia)
• Oral contraceptives pills (OCP)
• Pregnancy and the puerperium
• Malignancy
• Infections such as meningitis, sinusitis, otitis media, cellulitis of the face
• Head injury and mechanical precipitants
CLINICAL FEATURES
Symptoms and signs of CVT can be grouped in three major syndromes:
1. Isolated intracranial hypertension syndrome: Headache with or without
vomiting, papilledema, and visual problems
2. Focal syndrome: Focal deficits, seizures, or both
3. Encephalopathy: Multifocal signs, mental status changes, stupor, or coma.
Headache is the most common and prominent symptom of CVT and can vary
from a sudden onset severe headache to a gradual onset progressively worsening
type.
When to Suspect a CVT?

• Young/middle-aged women on OCP or in the peripartum period with severe
headache not relieved with regular painkillers
• Patients with known malignancy who develop severe throbbing headache

• An infarct or a bleed seen in an atypical location on computed tomography (CT)
brain.
DIAGNOSIS
Different techniques used for diagnosis are CT brain or magnetic resonance
imaging (MRI) with magnetic resonance venography (MRV) (Fig. 1).
A B
C D
FIGS. 1A TO D: CT and MRI findings of cerebral venous thrombosis. (A) CT brain non-contrast:
Hemorrhagic infarct in the right parietal region. (B) CT brain non-contrast: Hyperintensity
in the right transverse sinus. (C) CT brain non-contrast: Hyperintensity in the straight sinus
(cord sing). (D) MRI brain T1 weighted with gadolinium (sagittal): filling defect in superior
sagittal sinus.
CHAPTER 51: Cerebral Venous Thrombosis 201
CT Brain
• May be normal in up to 30% of CVT cases
• Direct signs of CVT seen in one-third of cases are:
cc Dense triangle sign (noncontrast CT): A hyperdensity with a triangular or
round shape in the posterior part of the superior sagittal sinus caused by
the venous thrombus
cc Empty delta sign (contrast CT): A triangular pattern of contrast
enhancement surrounding a central region lacking contrast enhancement
in the posterior part of the superior sagittal sinus
cc Cord sign (contrast CT): A curvilinear or linear hyperdensity over the
cerebral cortex caused by a thrombosed cortical vein.

• Indirect signs of CVT are more common
cc Hemorrhagic lesions include intracerebral hemorrhage and hemorrhagic
infarcts
cc Nonhemorrhagic lesions include focal areas of hypodensity caused by
edema or venous infarction, usually not respecting the arterial boundaries,

as well as diffuse brain edema.
MRI Brain with Venography

MRV is the most sensitive imaging method for demonstrating the thrombus and
the occluded dural sinus or vein. MRV features include nonvisualization of the
vessel (indicates absent flow), flow defect, and presence of collateral veins at the
site of occlusion.
MANAGEMENT
• Lower the intracranial pressure (ICP) with 3% NaCl infusion (0.5–1 mL/kg/h)
• Seizure control with phenytoin 10–20 mg/kg IV loading dose and 100 mg IV q8h
• Anticoagulation: Give unfractionated heparin 5000 U IV stat and q6h or low-
molecular-weight heparin (LMWH) (Enoxaparin 1 mg/kg s/c stat and q12h)
• Endovascular treatment: Direct endovascular interventions have been
used as an alternative treatment in those who worsen despite adequate
anticoagulation.
Intracranial Hemorrhage 52
CHAPTER
Intracranial hemorrhage encompasses four types of intracranial bleeds:

extradural hematoma (EDH), subdural hematoma (SDH), subarachnoid
hemorrhage (SAH), and intraparenchymal hemorrhage.
EXTRADURAL HEMATOMA
• Extradural/epidural hematomas are rare, but may form as a result of blunt
injury to the head associated with a skull fracture. Damage to the middle
meningeal artery results in blood collecting in the epidural space. Venous
epidural hematomas are common in children.
• These hematomas are biconvex/lenticular (Fig. 1) and are most often located
in the temporal or temporoparietal regions.
• Clinical features include loss of consciousness, headache, nausea, vomiting
or seizures. A lucid interval between the time of injury and neurological
deterioration is characteristic of an EDH.
• Management:
cc Stabilize airway, breathing, and circulation (ABC)
cc Antiepileptics: To prevent seizures. Administer phenytoin 10–20 mg/kg IV
or other antiepileptics
cc Refer to neurosurgery for urgent surgical evacuation of the hematoma and
stopping the bleeding source.
SUBDURAL HEMATOMA
• These are more common after a blunt injury to the head and result from the
shearing of small bridging vessels of the cerebral cortex.
• On a CT brain, SDH appears to adhere to the contours of the brain (Fig. 1). An
acute SDH is typically hyperdense while a chronic SDH appears hypodense.
• Parenchymal damage due to pressure effect is much more severe than that
caused by an EDH.
• An acute SDH usually presents with recent trauma, headache, nausea,
vomiting, altered sensorium, seizures or focal neurological deficits.
• Management:
cc Stabilize ABC
cc Antiepileptics: To prevent seizures (phenytoin 10–20 mg/kg IV or other
antiepileptics
cc Refer to neurosurgery for burr hole evacuation of the hematoma or a
craniotomy if required.
CHAPTER 52: Intracranial Hemorrhage 203
A B
C D
(EDH: extradural hematoma; SAH: subarachnoid hemorrhage; SDH: subdural hematoma)

FIGS. 1A TO D: Intracranial hemorrhage showing EDH, SDH, SAH, and intraparenchymal
hemorrhage.
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage (SAH) refers to bleeding into the subarachnoid space.
Most are caused by a ruptured saccular aneurysm. These aneurysms form at
bifurcations of large or medium-sized intracranial arteries and 85% of them are in
the anterior circulation, mostly in the circle of Willis.
• Sudden onset severe headache, typically described as a thunderclap headache
with or without focal neurological deficits is the most consistent symptom.
• Many patients describe it as “the worst headache of my life”. Other symptoms
include dizziness, loss of consciousness, seizures, diplopia or visual loss.
• Rebleeding and vasospasm are the two major complications of SAH and must
be addressed immediately. The risk of rebleed is highest in the first 24 hours.
• The mortality rate of SAH in the first month is almost 50%.
Diagnosis
• Noncontrast CT scan of the brain typically shows hyperdense material filling
the subarachnoid spaces around the brain, commonly around the circle of
Willis (Fig. 1). A contrast CT may obscure the SAH.
• In patients with a strong suspicion of SAH and a normal CT brain, a lumbar
puncture is mandatory. Look for an elevated opening pressure and an
increased cerebrospinal fluid (CSF) red blood cell (RBC) count.
• Once the diagnosis of SAH is made, the site of bleeding can be confirmed by a
digital subtraction angiography (DSA).
Management
• Stabilize ABC
• Blood pressure (BP) control: Target BP is SBP <160 mm Hg. Give Nifedipine R
10 mg stat or IV antihypertensives depending on the BP at arrival
• Antiepileptics: To prevent seizures. Administer phenytoin 10–20 mg/kg IV or
other antiepileptics
• Antifibrinolytic therapy: Oral tranexamic acid 500–1,000 mg q8h or IV
tranexamic acid 1,000 mg over 10 minutes, followed by 1,000 mg infusion over
8 hours has been shown to decrease the rate of rebleed in some studies
• Prevention of vasospasm and delayed cerebral edema: Give Nimodipine 60 mg
PO q4h
• Refer to Neurosurgeon for surgical management of an aneurysm or an arterio-
venous malformation.
• An external ventricular drain (EVD) may be required to prevent hydrocephalus
INTRAPARENCHYMAL HEMORRHAGE
• Intraparenchymal hemorrhage refers to bleeding into the brain parenchyma
usually as a result of a cerebrovascular accident, aneurysm rupture, trauma,
tumor, etc. The incidence increases with increasing age.
• Majority of the contusions occur in the frontal and temporal lobes.
• Patients typically present with focal neurological deficits, headache, altered
sensorium, or seizures.
• CT brain shows hyperdense lesions within the brain parenchyma (Fig. 1)
• Management:
cc Stabilize ABC
cc Antiepileptics: To prevent seizures. Administer phenytoin 10–20 mg/kg IV
or other antiepileptics
cc Lower the intracranial pressure (ICP) with 3% NaCl infusion (0.5-1 mL/kg/h)
cc Management depends on the etiology of the hemorrhage and could range
from aggressive surgical evacuation, craniectomy or just observation and

conservative management.
Guillain–Barré Syndrome 53
CHAPTER
INTRODUCTION
Guillain–Barré syndrome (GBS) is an acute autoimmune polyradiculoneuropathy
that is usually provoked by a preceding acute infection (Campylobacter jejuni,
human herpes virus, mycoplasma pneumonia, etc.).
CLINICAL FEATURES
• GBS manifests as a rapidly progressive, symmetric ascending paralysis of both
the lower limbs with or without sensory involvement. The disease course is
<4 weeks.
• The usual presentation is an ascending paralysis first noticed in the legs
and evolving over hours to a few days to the upper limbs and eventually the
diaphragm
• Almost 30% of patients require ventilatory support due to diaphragmatic
weakness.
• The lower cranial nerves are also frequently involved resulting in bulbar
weakness, difficulty in maintaining airway and handling secretions
• Deep tendon reflexes are typically absent. Bowel and bladder functions are
usually spared.
GBS Variants
• Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
• Acute motor axonal neuropathy (AMAN)
• Acute sensorimotor axonal neuropathy (AMSAN)
• Miller Fisher syndrome (MFS), characterized by ophthalmoplegia, ataxia and
areflexia.
DIAGNOSIS
Diagnosis of GBS is made by a combination of typical clinical features, examina-
tion findings, and supportive laboratory evidence.
Electrodiagnostic Tests
Electromyography (EMG) and nerve conduction velocity (NCV) studies typically
show acute polyneuropathy with demyelinating features (prolonged distal
latencies, conduction velocity slowing and evidence of conduction block) in
AIDP. A predominantly axonal pattern is seen in AMAN and AMSAN.
Cerebrospinal Fluid (CSF) Analysis

By the end of the first week of illness, cerebrospinal fluid (CSF) analysis typically
shows an elevated protein (100-1000 mg/dL) with a normal sugar and cell count
(albumin-cytologic dissociation). Sustained presence of leucocytes in CSF
suggests an alternate diagnosis.
Differential Diagnosis
• Acute myelopathy: Usually associated with back pain and sphincter
disturbances
• Diphtheria: Ascending paralysis with early oropharyngeal disturbances
• Lyme disease: distinguished by CSF pleocytosis, history of tick bite and
presence of CSF lyme antibodies
• Hypokalemic periodic paralysis: recurrent episodes of acute paralysis with
severe hypokalemia. Deep tendon reflexes typically intact.
• Tick borne paralysis: Mimics GBS; carefully examine for ticks. It is a non-
infectious condition caused by neurotoxins in the saliva of certain ticks
• Botulism: Caused by botulism neurotoxin secreted by Clostridium botulinum.
Starts with cranial nerve palsies and progresses to descending flaccid paralysis.
• Acute intermittent porphyria: Characterized by a triad of weakness, psychosis
and abdominal pain with or without seizures.
• Acute poisoning: Arsenic or thallium
MANAGEMENT
• The first step in the management of a patient with suspected GBS is assessment
of respiratory function in order to support the work of breathing if needed.
This can be best assessed by a single breath count at the best side. Secure
airway and stabilize breathing.
• Close respiratory monitoring: Up to 30% of patients develop neuromuscular
respiratory failure requiring invasive mechanical ventilation.
• Disease-modifying treatment: The main modalities of therapy for GBS include
plasma exchange (plasmapheresis) and administration of intravenous
immunoglobulin (IVIG).
cc IVIG is administered at a dose of 2 g/kg over 2 days.
cc In plasmapharesis, 200–250 mL/kg of plasma is exchanged during
5 sessions over 1–2 weeks.

Hanging 54
CHAPTER
INTRODUCTION
Hanging is a form of strangulation that is caused by the victim being suspended
from the neck.
• Complete hanging: When the whole body hangs off the ground and the
entire weight of the victim is suspended at the neck, the hanging is said to be
complete.
• Significant cervical spinal cord injuries usually result from hangings that
involve a fall from a height greater than the victim’s height.
• Incomplete hanging: This implies that some part of the body is touching the
ground and that the weight of the victim is not fully supported by the neck.
PATHOPHYSIOLOGY
In judicial hanging, the head is effectively decapitated from the neck and torso
due to fracture of the upper cervical spine.
In other mechanisms of strangulation injuries (nonjudicial hanging, incom-
plete hanging, and strangulation), the following mechanisms are postulated as
the cause of death:
• Venous obstruction, leading to cerebral congestion, hypoxia, and unconsciousness
• Arterial obstruction due to carotid pressure, leading to low cerebral blood
flow and collapse
• Vagal collapse due to pressure to the carotid sinuses resulting in increased
parasympathetic tone
• Airway obstruction due to compression on the trachea resulting in hypoxia
and death.
HISTORY
Victims are generally brought to the emergency department by friends, or family
members or strangers. Ask them about the height of the drop as the extent of
injury to the cervical spine increases in severity with increasing height.
EXAMINATION
• Look for any ligature mark, lacerations, abrasions, contusions or edema on
the neck
• Look for subconjunctival and skin petechiae above the site of choking
• If gentle palpation of the larynx causes severe pain, it may indicate laryngeal
fracture
• Look for features of stridor and respiratory distress
• Mental changes may be a sign of hypoxic damage to the brain.
INVESTIGATIONS
• In nonjudicial hangings, cervical spine injury is rare. Therefore, X-ray of the
cervical spine is not needed in most cases
• Soft-tissue X-ray of the neck anteroposterior (AP) and lateral should be
obtained in all strangulation victims. Look for hyoid bone fracture
• Noncontrast computed tomography (CT) scan of the brain is indicated when
the neurologic status is compromised
• Routine blood investigations and arterial blood gas (ABG).
MANAGEMENT
• Assess airway and breathing
• Remember the possibility of an unstable cervical spine while securing airway.
If in doubt, apply a cervical collar and avoid head tilt during intubation
• Secure the airway. Consider early endotracheal intubation if sensorium is
low, as this could be due to hypoxia. Early intubation and ventilation improve
neurological outcome. If endotracheal intubation is unsuccessful, consider
cricothyroidotomy.
• Keep the patient on continuous cardiac monitoring to identify and manage
dysrhythmias.
• Cerebral edema and raised intracranial pressure may require strategies like
hyperventilation, diuretics an fluid restriction.
Seizures 55
CHAPTER
INTRODUCTION
Seizure is defined as an abnormal neurological activity caused by excessive
electrical activity in the brain.
Epilepsy is defined as recurrent unprovoked seizures due to a genetically
determined or acquired brain disorder.
Less than one-half of epilepsy cases have an identifiable cause. Patient
may present to the emergency department with a new onset, recurrent or a
breakthrough seizure.
• New-onset seizures: First episode of a seizure
• Breakthrough seizures: Occurs if patient is noncompliant with antiepileptics
or if the serum drug levels are below the therapeutic range.
MANAGEMENT (TABLES 1 AND 2)

• Assess airway, breathing and circulation. Maintain and protect the airway,
including the use of a oropharyngeal airway if needed. Protect the patient
from self injury during this time.
• Identify and correct rapidly reversible ictal insults like hypoxia and
hypoglycemia.
• Hypoglycemia is a common reversible metabolic causes of seizures. Check
RBS for all patients and correct with 50% dextrose solution if indicated.
• If patient is noncompliant with antiepileptic medications:
cc Loading dose oral/IV of phenytoin or sodium valproate or levetiracetam
cc Do not send serum levels of antiepileptics
cc Restart regular dose of antiepileptics
cc Discharge and advice the patient to followup in epilepsy clinic.
TABLE 1: Summary of evaluation and management of seizures.

New-onset seizures Breakthrough seizures
Investigations to CBC, electrolytes, creatinine, LFT Hb, TC, DC, electrolytes, creatinine.
be sent CT brain (plain) Drug levels if patient is compliant
with medications
Management Loading dose of antiepileptics Discharge if sensorium normal.
Refer to neurologist Refer to neurologist/medicine if
drowsy or in status epilepticus
(CBC: complete blood count; LFT: liver function test; CT: computed tomography; Hb: hemoglobin; TC:
total count; DC: differential count)
TABLE 2: Doses of antiepileptic drugs.

Drug Loading dose Maintenance dose Side effects
Phenytoin IV: 10–20 mg/kg 300–400 mg/day Ataxia, nystagmus, rashes,
Oral: 10–20 mg/kg in 2–3 divided nausea, vomiting, blood
doses dyscrasias, gum hyperplasia,
hirsutism, vitamin K and
folate deficiency
Phenobar- IV: 10–20 mg/kg 30–180 mg/day in Drowsiness, sedation,
bitone Oral: 10–20 mg/kg 2–3 divided doses lethargy, ataxia, dystonia and
respiratory depression
Carbama- No loading dose. 800–2000 mg in 2 Dizziness, diplopia, nausea,
zepine Causes severe divided doses vomiting, ataxia, blurred
giddiness vision, aplastic anemia and
Steven–Johnson syndrome
Oxcarba- No loading dose 600–2400 mg/day Somnolence, headache,
zepine in 2 divided doses dizziness, rash and
hyponatremia
Sodium Oral: 30 mg/kg Valproate SR/ Nausea, vomiting, tremors,
valproate IV: 30 mg/kg Chrono 500–1,000 sedation and irritability
mg in 2 divided
doses
Levetirace- IV: 10–20 mg/kg 500 mg twice Somnolence, asthenia, and
tam (higher dose for daily dizziness
status epilepticus)
Oral: 500–1,000 mg
Clobazam No loading dose 10–20 mg in 1 or Sedation, dizziness, ataxia,
(Frisium) 2 divided doses blurred vision, diplopia,
irritability, and depression
• If patient is compliant with antiepileptic medications:

cc Loading dose oral/IV of phenytoin or carbamazepine or sodium valproate
or levetiracetam
cc Look for a precipitating factor (e.g., hypoglycemia, hyponatremia)
cc Send trough serum levels of the regular antiepileptic
– If serum levels are low: Increase the dose of the regular antiepileptics.
If already on a maximum dose, add on a new antiepileptic before
discharge
– If serum levels are normal: Add on a new antiepileptic and advice the
patient to followup in epilepsy clinic.
• Phenytoin loading should be monitored for electrocardiogram (ECG) changes,
bradycardia, and hypotension
• Avoid phenytoin and valproate in the first trimester of pregnancy. The drugs of
choice in pregnancy are levetiracetam or phenobarbitone
CHAPTER 55: Seizures 211
• Advice the patient to return to the emergency department if he/she notices

new onset of rash or discoloration at the injection site. Extravasation of
phenytoin can cause severe tissue necrosis.
STATUS EPILEPTICUS
Historically, status epilepticus was defined as a single episode of seizure lasting
more than 30 minutes or a series of episodes of seizures during which neurological
function is not regained between the episodes in a 30-minutes period.
Currently, the accepted operational definition of status epilepticus is:
• ≥5 minutes of continuous seizures, or
• ≥2 episodes of seizures between which there is incomplete recovery of
consciousness.
Etiology
• Acute structural brain injury (stroke, trauma, SAH, cerebral ischemia)
• Nonadherence to antiepileptic medications
• Metabolic abnormalities: Hypoglycemia, hepatic encephalopathy, uremia,
hyponatremia, hyperglycemia, hypocalcemia and hypomagnesemia
• Withdrawal syndromes associated with the discontinuation of alcohol,
barbiturates, or benzodiazepines.
Management of Status Epilepticus

• The steps in the management of status epilepticus are shown in Flowchart 1.
• Go to the next step only if seizures are not controlled after loading dose of first
antiepileptic
• At any stage, if the airway is compromised, or when midazolam infusion is
started, consider rapid sequence intubation
• Avoid propofol, if the patient is hypotensive.
FOSPHENYTOIN
Fosphenytoin is a water-soluble prodrug of phenytoin that can be used instead of
phenytoin for treatment of seizures in the ED.
• 1 mg Phenytoin = 1.5 mg; Fosphenytoin = 1 mg Phenytoin equivalent (PE)
• Loading Dose:
Adult: 18–20 mg PE/kg iv
Children: 10–20 mg PE/kg iv
• Maintenance Dose:
Adult: 4–6 mg PE/Kg iv twice a day
Children: 2–3 mg PE/Kg iv twice a day
• Infusion rate: 150 mg PE/min
FLOWCHART 1: Management of a patient with status epilepticus.
• Dilution: 100 mL normal saline or 100 mL 5% dextrose

• Advantages: Less hypotension, less pruritus, less arrhythmia as preservative
propylene glycol is not used
• Monitoring: Monitoring to be continued for half an hour post-infusion as
Maximum phenytoin dose reached after 20 minutes of infusion
Headache 56
CHAPTER
APPROACH TO A PATIENT WITH HEADACHE

• Take a detailed history on the onset, type, duration, aggravating, and relieving
factors, associated stressors and symptoms.
• Determine the need for a computed tomography (CT) scan of the brain.
History of projectile vomiting, diplopia, nystagmus, early morning increase in
headache and severe throbbing headache strongly suggests raised intracranial
pressure (ICP) and would warrant neuroimaging.
• If there is a strong suspicion of cerebral venous thrombosis (CVT), request for a
CT brain/magnetic resonance imaging (MRI) brain with magnetic resonance
venography (MRV).
• If any obvious stressor is identified, treat like a tension headache and
prescribe paracetamol and a low dose of tricyclic antidepressants (TCA)
(tablet Amitriptyline 10 mg hs od for 1 week). Refer the patient to psychiatrist
for counseling.
The following clinical situations may warrant neuroimaging:
• The worst headache ever
• Recent significant increase in the pattern, frequency, or severity of headaches
• New or unexplained neurologic symptoms or signs
• Headache always on the same side
• Headaches not responding to treatment
• New-onset headaches after age 50 years
• New-onset headaches in patients with cancer or human immunodeficiency
virus (HIV) infection.
MIGRAINE
Migraine is an episodic disorder characterized by severe headache generally
associated with nausea and/or light and sound sensitivity. A prodrome of blurred
vision, visual aura, malaise, anorexia, vomiting may be seen in one-third of
patients. This usually lasts for 5–30 minutes. The headache may last for 4–72 hours
and is usually throbbing and unilateral but may be generalized.
Treatment of Acute Attacks

• Mild-to-moderate attacks: Simple analgesics like Paracetamol 1 g stat and
prn with an anti-emetic (Metoclopramide 10 mg PO tid). Nonsteroidal anti-
inflammatory drugs (NSAIDs) also are effective for most episodes of migraine.
• Moderate-to-severe attacks:
cc Sumatriptan (5HT1 antagonist) dose of 25–50 mg PO prn or 6 mg s/c is
effective but can cause vasoconstriction and is contraindicated in ischemic

heart disease (IHD) and uncontrolled hypertension
cc NSAIDs may be added to Sumatriptan for severe attacks
cc Tablet Metoclopramide 10 mg PO tid for associated nausea and vomiting.
When to Start Prophylaxis for Migraine?

More than four headaches per month or headaches that last longer than 12 hours
are generally considered reasonable thresholds for starting preventive therapy.
The usual drugs are:
• Tablet Flunarizine10 mg hs od
• Tablet Amitriptyline 10–25 mg hs od
• Tablet Propranolol 10–20 mg bd.
CLUSTER HEADACHE
This distinctive vascular headache syndrome is characterized by 1–3 short lived
attacks of peri-orbital pain daily over a 1–2-month period followed by pain-free
interval of up to 1 year. Pain is strictly unilateral, affects the same side, typically
lasts 30 min–2 hours and is explosive in nature. Associated symptoms include
homolateral lacrimation, redness, nasal stuffiness, and nausea. Usually seen
in men aged 20–50 years, this episodic pattern may become established in the
chronic form.
Treatment is mainly prevention of attacks by drugs like prednisolone (60 mg
daily × 7 days and rapidly taper), lithium (600–900 mg daily), ergotamine and
sodium valproate.
TRIGEMINAL NEURALGIA
Also known as tic douloureux, it is a chronic pain syndrome characterized by
recurrent brief episodes of unilateral neuralgic pain in the sensory distribution of
the trigeminal nerve. The pain is often accompanied by facial spasms or tics. The
number of episodes may vary from 1 to 100 per day.
Etiology
Most cases (80–90%) are caused by compression of the trigeminal nerve root by an
aberrant loop of an artery or vein. Other causes include vestibular schwannoma,
meningioma, epidermoid or other cyst, saccular aneurysm or arteriovenous
malformation (AVM).
Neuroimaging
CT or MRI brain with contrast is used to look for structural lesions.
CHAPTER 56: Headache 215
Treatment
Start with tablet Carbamazepine 100–200 mg bd and increase to 600–800 mg daily.
Other drugs like baclofen (15 mg tid), lamotrigine (50–100 mg od) or gabapentin
(300 mg od/bd) may be added for refractory pain.
Refer to neurosurgeon for microvascular decompression or ablative procedures.
TEMPORAL ARTERITIS
Temporal arteritis (TA) also known as giant cells arteritis is a chronic systemic
vasculitis mainly involving large to medium vessels, especially branches of the
internal carotid artery and is seen exclusively in patients over 50 years of age.
Clinical features: The characteristic headache of TA is described as severe and
throbbing felt over the frontotemporal region with or without jaw claudication.
The involved temporal artery may be tender with a feeble pulse. Ischemic optic
neuritis with loss of vision is a dreaded complication.
Diagnosis: Diagnosis requires histopathological confirmation and is confirmed if
three of the following criteria are fulfilled:
• Age >50 years
• New-onset localized headache
• Temporal artery tenderness/decreased pulse
• Erythrocyte sedimentation rate (ESR) >50 mm/h
• Temporal artery biopsy finding of granulomatous inflammation with multi-
nucleated giant cells
Management: Corticosteroids are the mainstay of therapy and must be started
immediately on high clinical suspicion, especially if vision is compromised.
Start oral prednisolone 40–60 mg PO od and refer to neurology for
confirmation of diagnosis.
Bell’s Palsy 57
CHAPTER
INTRODUCTION
Bell’s palsy is the most common cause of sudden-onset lower motor neuron
(LMN) facial nerve palsy. It usually results from a viral infection [herpes simplex
virus (HSV), varicella zoster virus (VZV), human herpesvirus 6 (HHV-6), and
Lyme disease] that causes swelling of the facial nerve within the temporal bone.
EXAMINATION FINDINGS
LMN Facial Nerve Palsy
Deviation of the angle of the mouth to the opposite side, absence of forehead
wrinkling and inability to close the eye on the same side, hyperacusis on the
affected side (due to stapedius muscle paralysis), decreased lacrimation (greater
petrosal nerve involvement) and metallic taste (chorda tympani nerve).
Attempting to close the eye on the affected side results in upward gaze, known
as the Bells phenomenon.
DIFFERENTIAL DIAGNOSIS FOR BELL’S PALSY

Other Causes of LMN Facial Palsy
• Ramsay Hunt syndrome: Due to herpes zoster virus (HZV) infection of the
geniculate ganglion. In addition to LMN facial palsy, a painful herpetiform
vesicular eruption in the external auditory meatus and vestibulocochlear
dysfunction are characteristic findings. The pain is considerably mire severe
than that of Bells palsy with a poorer rate of recovery of facial nerve palsy.
Treatment is similar: Prednisolone and antiviral therapy for 7–10 days.
• Pontine tumors or vascular events: Other cranial nerves are also usually
involved.
• Middle ear infection and cholesteatoma: Acute otitis media can be treated with
antibiotics and may require myringotomy for decompression. Malignant otitis
externa, caused by Pseudomonas aeroginosa may cause facial nerve palsy and
requires prolonged anti-pseudomonal antibiotic therapy with or without
surgical debridement.
• Trauma
• Parotid gland tumors
• Sarcoidosis.
CHAPTER 57: Bell’s Palsy 217
MANAGEMENT
• If patient presents within 72 hours of onset of symptoms:
cc Tablet prednisolone 1 mg/kg in 2 divided doses × 5 days. Then decrease by
10 mg each day and stop by the 10th day.

cc Antivirals have not proven to be of much added benefit. If herpetic vesicles
are seen on the skin or inner ear, give tablet Valacyclovir 1,000 mg bd ×
5 days.
cc Refer to ophthalmologist: Artificial tears and an eye patch at night are
needed to prevent corneal ulceration.

cc Refer to ENT specialist: To assess the inner ear and to rule out other local
causes. In rare cases, surgical decompression of the facial nerve may be

indicated.
cc Refer to physiotherapist: Transcutaneous electrical nerve stimulation
(TENS) exercises have been used to try to promote motor recovery in

patients with Bell’s palsy, but strong evidence for its benefits is lacking.
• If patient presents after 72 hours of onset of symptoms:
cc Refer to ophthalmologist: Artificial tears and an eye patch at night are
needed to prevent corneal ulceration.

cc Refer to ENT specialist: To assess the inner ear and to rule out other local
causes.
cc Steroids are less effective if started after 72 hours of onset of symptoms.
May be given if the patient complains of ear pain suggestive of facial nerve
swelling in the temporal bone.
cc Antivirals are not beneficial if started late. Therefore, not indicated.
cc Refer to physiotherapist: TENS have been used to try to promote motor
recovery in patients with Bell’s palsy, but strong evidence for its benefits
is lacking.
Long-term outcome after 6 months for most patients with Bell’s palsy is good.
Many patients, especially those treated early have good functional recovery.
Acute Dystonia 58
CHAPTER
INTRODUCTION
Drug-induced dystonia (tardive dystonia; tardive dyskinesia; acute dystonic
reaction): A number of drugs are capable of causing dystonia. Most people
develop an acute dystonic reaction after a one-time exposure to the drug.
Drugs causing dystonic reactions are typical antipsychotics (chlorpromazine,
fluphenazine, haloperidol, perphenazine, prochlorperazine, thioridazine,
trifluoperazine), metoclopramide (perinorm).
• Symptoms may include intermittent spasmodic or sustained involuntary
contractions of muscles of the face, neck, trunk, pelvis, and extremities. The
symptoms are usually transient
• Painful forced extension of the neck is a common presentation and can be
quite distressing to the patient and relatives.
TREATMENT
For the treatment, any of the following drugs may be given:
• Diphenhydramine (Benadryl): Given for its anticholinergic effect
cc Can be given as a syrup (10–20 mL stat and repeat, if needed) or
cc Injection Diphenhydramine 25–50 mg IV over 2 minutes or 50 mg IM stat
cc Continue oral dosage (10 mL tid) for 3–4 days to prevent recurrence of
symptoms.
• Promethazine (Phenergan) 25–50 mg IV stat.
• Benztropine: Blocks striatal cholinergic receptors. Dosage: 1–2 mg IV, then
1–2 mg PO q12h to prevent recurrence.
• Benzodiazepines: Lorazepam or diazepam can be given intravenously.
• Trihexyphenidyl (pacitane): Dose of 2 mg PO stat; increase as necessary to
usual range: 5–15 mg/day in 3–4 divided doses.
Stop the drug precipitating dystonia and refer to neurology.
MRI Stroke Protocol 59
CHAPTER
INTRODUCTION
A full clinical multimodal stroke magnetic resonance imaging (MRI) study for
acute stroke takes 15–20 minutes.
• T1-weighted imaging (T1-WI): Cerebrospinal fluid (CSF) has a low signal
intensity in relation to brain tissue.
• T2-weighted imaging (T2-WI): CSF has high signal intensity in relation to
brain tissue.
Conventional (T1/T2) MRI sequences may not demonstrate an infarct for
6 hours, and small infarcts may be hard to appreciate on computed tomography
(CT) for days.
SEQUENCE OF ACUTE MRI STROKE PROTOCOL

Acute MRI stroke protocol includes the following sequences (Figs. 1A to D):
• Diffusion-weighted imaging (DWI): Most sensitive brain imaging method to
reliably demonstrate small and early infarcts within the first minutes to hours
after onset. An acute infarct appears as a hyperintensity in DWI.
• DWI with apparent diffusion coefficient (DWI/ADC): The appearance of DWI/
ADC depends on the timing. An acute infarct, which is seen as a hyperintensity
on DWI is seen as a hypointensity on DWI/ADC.
• T2-weighted fluid-attenuated inversion recovery (FLAIR)
cc FLAIR is a T2-weighted sequence in which the CSF signal is suppressed.
On traditional T2-weighted MRI, CSF appears bright, whereas on FLAIR

this fluid appears dark.
cc This is very useful in identifying subarachnoid hemorrhage (SAH) and
subdural hemorrhage (SDH).

cc Acute ischemic stroke produces no signs on FLAIR in the first 6 hours
from onset with areas of hyperintensity evolving thereafter. In those with

unwitnessed onset/wake-up strokes, a DWI lesion without a matching
hyperintensity on FLAIR suggests that the stroke occurred less than
6 hours previously.
• Magnetic resonance angiography (MRA): MRA is very sensitive to flow and
is based on the difference in signal between moving blood and stationary
brain tissue; angiographic-like images of the cervicocranial vasculature are
produced. This is a useful tool in identifying the site of occlusion or dissection.
A B
C D
FIGS. 1A TO D: MRI stroke protocol imaging findings of an acute infarct. (A) DWI 1000:
Large area of diffusion restriction (hyperintensity) seen in the right MCA territory. (B) ADC:
Corresponding area of hypointensity in the right MCA territory. (C) T2-FLAIR: In an acute
stroke <6 hours, the lesion is not visible on a T2-FLAIR. (D) SWI: Susceptibility artifact
(blooming) is not seen in an infarct
• Susceptibility-weighted imaging (SWI): This is a fully velocity-compensated

high-resolution 3D gradient-echo sequence. Intracerebral hemorrhage
appears as an isointense to hyperintense center with a hypointense periphery
(blooming).
Steps to Identify an Acute Infarct on a MRI Stroke Protocol
• DWI: Look for an area of uniform hyperintensity in the suspected territory
• DWI/ADC: Look for a hypodensity in the same area as hyperintensity on DWI
• MRA: Look for an area of stenosis/cut off
• T2W FLAIR: If a hyperintensity is seen, it means that the infarct is greater than 6 hours
old and hence beyond the time for thrombolysis
• SWI: Look for blooming (hypointensity) which suggests areas of hemorrhage (if present).
CHAPTER 59: MRI Stroke Protocol 221
An intracerebral bleed shows areas of hypointensities within the hyperintensity

on DWI and the reverse on DWI/ADC (Figs. 2A to D).
A B
C D
FIGS. 2A TO D: MRI stroke protocol imaging findings of a bleed. (A) DWI 1000: Central
hyperintensity in the right capsuloganglionic region. (B) ADC: Corresponding area of
hypointensity in the right capsuloganglionic region. (C) T2-FLAIR: Hyperintensity in the
right capsuloganglionic region. (D) SWI: Susceptibility artifact (blooming) in the right
capsuloganglionic region confirms a bleed.
Section 9
Gastrointestinal and
Hepatic Emergencies
Gastrointestinal
Bleeding 60
CHAPTER
INTRODUCTION
Blood loss from the gastrointestinal (GI) tract may occur in four ways:
(1) hematemesis, (2) hematochezia, (3) melena, and (4) occult loss.
Upper GI bleed is defined as bleeding originating proximal to the ligament of
Treitz, while lower GI bleed originates distal to it.
UPPER GASTROINTESTINAL BLEED

Causes of upper GI bleed: Peptic ulcer, esophagogastric varices, arteriovenous
malformation, GI tumor, Mallory-Weiss tear, etc.
History
• Ask for history of alcohol consumption and smoking.
• Drug history: Use of nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin,
anticoagulants, antiplatelet agents.
• Ask for previous GI bleed and other sites of bleeding.
Symptoms
• Abdominal pain, hematemesis, and melena.
• Melena is the usual presentation, but stool may be frankly bloody or maroon
with massive or brisk upper GI bleeding.
Examination
• Tachycardia or orthostatic hypotension changes suggest moderate-to-severe
blood loss; hypotension suggests life-threatening blood loss.
• Perform a rectal examination to assess stool color (black/red/normal) to
differentiate between melena and hematochezia.
• Look for features of chronic liver disease (ascites, jaundice) that could suggest
a variceal bleed.
• Significant abdominal tenderness accompanied by signs of peritoneal
irritation (e.g., involuntary guarding) suggests perforation.
Investigations to be sent:
• Complete blood count, electrolytes, creatinine, liver function test, rapid
blood borne virus screen, chest X-ray, electrocardiogram, prothrombin time,
activated partial thromboplastin time.
• Arrange cross-match for blood if hemoglobin (Hb) is less than 7 g%.
226 SECTION 9: Gastrointestinal and Hepatic Emergencies
Management
• Assess and stabilize airway, breathing, and circulation.
• Start two large bore intravenous (IV) cannulae and commence IV fluid
resuscitation.
• If the GI bleed is severe, arrange for cross-matched blood for transfusion.
• Acid suppression with proton-pump inhibitor (PPI): Injection pantoprazole
80 mg/omeprazole 40 mg IV stat.
• Prokinetics: Metoclopramide 10 mg IV stat and q8h.
• If a variceal bleed is suspected: Octreotide IV bolus of 100 µg followed by
100 µg IV q6h.
• Administer antibiotics (injection ceftriaxone 1 g IV stat) 2 hours prior to the
upper GI endoscopy.
• Initiate blood transfusions if the Hb is <7 g% (Box 1).
• Transfuse fresh frozen plasma for coagulopathy.
• Transfuse platelets for thrombocytopenia (platelets <50,000) or platelet
dysfunction (e.g., chronic aspirin therapy).
• Refer to gastroenterology for upper GI endoscopy.
BOX 1 Blood transfusion protocols for upper gastrointestinal bleed.

• If Hb is <6 g%, cross-match and transfuse two pints packed cells over 6 h
• If Hb is between 6 and 7 g%, cross-match and transfuse one-pint packed cells over 4 h
• If Hb >7 g% upper GI endoscopy can be done immediately
• Target Hb >8 g% for patients with ischemic heart disease
(Hb: Hemoglobin)
LOWER GASTROINTESTINAL BLEED

Causes of lower GI bleed: Diverticulosis, angiodysplasia, hemorrhoids, GI malig-
nancies, inflammatory bowel disease:
• Anal hemorrhoids are the most common cause of lower GI bleed. Proctoscopy
is often diagnostic. Refer to Chapter 102 for details of management.
• Other conditions like diverticulosis or angiodysplasia can be diagnosed by
colonoscopy.
• Primary treatment includes fluid resuscitation and blood product transfusion
for severe bleeding.
Acute Pancreatitis 61
CHAPTER
INTRODUCTION
It is critical to diagnose acute severe pancreatitis as soon as possible in the
emergency department (ED) as it can be associated with significant mortality.
According to the revised Atlanta classification (Table 1), the diagnosis of acute
pancreatitis is confirmed if two of the following three criteria are fulfilled:
1. Abdominal pain consistent with acute pancreatitis (acute onset of a persistent,
severe, epigastric pain often radiating to the back).
2. Serum lipase or amylase at least three times greater than the upper limit of
normal.
3. Characteristic findings of acute pancreatitis on ultrasonography (USG) or
computed tomography (CT) abdomen.
CLINICAL FEATURES
Patients typically present with epigastric abdominal pain but may also be diffuse.
The onset of pain is relatively rapid, increasing in severity over a few hours. The
constant and severe pain may radiate to the back, with patients wriggling to try
a position of comfort and is often relieved by leaning forward. Hypotension,
tachycardia, and shock indicate severe disease with complications.
ETIOLOGY OF ACUTE PANCREATITIS

• Gallstones (60%)
• Alcohol (20%)
• Others: Hypertriglyceridemia, hypercalcemia, trauma, iatrogenic, systemic
vasculitis, drugs [thiazides, nonsteroidal anti-inflammatory drugs (NSAIDs),
sulfonamides, azathioprine, tetracyclines, valproate], infections [mumps,
rubella, coxsackie B, Epstein–Barr virus (EBV), cytomegalovirus (CMV),
ascaris, Clonorchis sinensis].
TABLE 1: Modified Atlanta Grading (2012) of severity of acute pancreatitis.

Mild acute pancreatitis No organ failure, no local, or systemic complications
Moderately severe acute Organ failure that resolves within 48 h (transient organ
pancreatitis failure) and/or local or systemic complications without
persistent organ failure
Severe acute pancreatitis Persistent organ failure (>48 h) that may involve one or
multiple organs
INVESTIGATIONS
• Complete blood count (CBC), electrolytes, creatinine, liver function test
(LFT), calcium, amylase, lipase, chest X-ray (CXR), electrocardiogram (ECG).
• USG abdomen: The only indication of an USG abdomen during the acute
stage is to identify an impacted gallstone that may be relieved by endoscopic
retrograde cholangiopancreaticography (ERCP). The presence of an impacted
gallstone would reflect as an abnormal LFT (elevated ALP or transaminitis).
Urgent USG in the ED is indicated only in patients with a deranged LFT
suggestive of choledocholithiasis.
MANAGEMENT
• Fluid replacement: Establish intravenous (IV) access and start fluid
replacement. Patients are usually volume depleted and hence aggressive
fluid resuscitation is essential.
• Pain control:
cc Injection paracetamol 1,000 mg in 100 mL normal saline (NS) IV stat plus
cc Injection morphine 5 mg IV stat (reassess and repeat dose after 30 minutes,
if needed), or
cc Injection tramadol 50 mg IV stat
cc If pain persists after 4 hours, morphine 5 mg IV can be repeated every
4 hours.
• Administer injection pantoprazole 40 mg IV and ondansetron 8 mg IV.
• If evidence of infection/sepsis, administer empiric broad spectrum antibiotics
(ertapenem/meropenem).
• Keep the patient nil per oral (NPO) till pain relief is achieved. The benefit of
nasogastric (NG) tube placement is unproven. Oral feeds can slowly be started
in mild pancreatitis once pain subsides (usually after 12 h).
• Biliary pancreatitis: In patients with gallstone-induced pancreatitis, urgent
ERCP within 72 hours reduces complications and mortality.
Spontaneous
Bacterial Peritonitis 62
CHAPTER
INTRODUCTION
Spontaneous (primary) bacterial peritonitis (SBP) refers to ascitic fluid infection
as a result of bacteremic seeding without an obvious surgically treatable intra-
abdominal focus of infection. It almost always occurs in patients with cirrhosis
and ascites.
The diagnosis of SBP is confirmed by:
• Positive ascitic fluid bacterial culture
• Elevated ascitic fluid absolute neutrophil count (≥250 cells/mm3)
• Exclusion of secondary causes of bacterial peritonitis.
SBP must be differentiated from secondary peritonitis, where bacteria spread
into the peritoneum from an intra-abdominal focus or perforation of a viscus. The
diagnosis of SBP can be made only after ruling out a primary intra-abdominal
source of infection.
CLINICAL FEATURES
• Fever, diffuse abdominal pain/tenderness, altered mental status, diarrhea,
paralytic ileus, and hypotension.
• Renal failure develops in 30–40% of patients with SBP and is a major cause of
death.
ETIOLOGY
Gut bacteria such as Escherichia coli and Klebsiella, but entero-bacteriaceae
are the usual causes but streptococcal and staphylococcal infections can also
cause SBP.
INVESTIGATIONS
• Perform a diagnostic ascitic tap and send for ascitic fluid TC, DC and culture
sensitivity
• Complete blood count (CBC), electrolytes, creatinine, blood c/s.
INDICATIONS FOR ANTIBIOTIC THERAPY

• Empiric therapy for SBP should be started in a patient with ascites who has
any of the following findings:
cc Temperature >37.8°C (100°F)
cc Abdominal pain and/or tenderness
cc Altered sensorium
cc Ascitic fluid absolute neutrophil count ≥250 cells/mm3.
MANAGEMENT
• Stabilize airway, breathing, and circulation (ABC).
• Start broad spectrum antibiotics: Cefoperazone-sulbactam 1 g IV stat or
meropenem 1 g in 100 mL normal saline (NS) IV stat if the patient is in shock.
Most patients require a 5-day course of antibiotics.
• Refer to gastroenterology for further management.
HEPATO-RENAL SYNDROME
Hepato-renal syndrome is a potentially fatal complication in a patient with
cirrhosis and ascites. It is characterized by worsening uremia with oliguria and
sodium retention in the absence of a potentially identifiable cause of renal failure.
This condition may be precipitated by severe GI bleed, sepsis or aggressive
attempts at diuresis or paracentesis.
Diagnosis is confirmed by worsening renal failure and demonstration of avid
urinary sodium retention (urine spot sodium is typically <5 mmol/L).
Treatment is usually unsuccessful. Early albumin infusion may be tried, but
liver transplantation remains the only option.
Hepatic Encephalopathy 63
CHAPTER
Hepatic encephalopathy is a reversible impairment of neuropsychiatric function

associated with impaired hepatic function characterized by altered sensorium
and behavior, personality changes, asterixis and distinctive electroencephalo-
graphic (EEG) changes.
It is a recurring complication of cirrhosis of the liver and may be acute and
reversible or chronic and progressive. Elevated ammonia levels have been
implicated as the pathogenesis of this condition.
CLINICAL FEATURES
The clinical manifestations vary in severity from mild cognitive dysfunction,
irritability, confusion and profound coma.
Examination Findings
• Asterixis: Seen in mild-to-moderate encephalopathy. Asterixis is a low
amplitude, alternating flexion and extension of the wrist that occurs when the
hand is held in extension.
• Other features of cirrhosis: Palmar erythema, spider naevi, testicular atrophy,
loss of axillary and pubic hair, ecchymotic patches and ascites
• Fetor hepaticus: Seen in severe cases, it refers to a musty breath odour,
presumably due to ammonia and ketones in the breath.
Hepatic encephalopathy can be graded in severity as:
• Grade I: Changes in behavior, mild confusion, slurred speech, disordered
sleep.
• Grade II: Lethargy, moderate confusion.
• Grade III: Marked confusion (stupor), incoherent speech, sleeping but
arousable.
• Grade IV: Coma, unresponsive to pain.
INVESTIGATIONS
• Complete blood count (CBC), electrolytes (look for hypokalemia), creatinine,
LFT, RBS
• Perform a diagnostic ascitic tap and send for ascitic fluid TC, DC, and culture
sensitivity to rule out spontaneous bacterial peritonitis (SBP).
MANAGEMENT
The initial management of acute hepatic encephalopathy in patients with cirrhosis
involves two steps.
1. Identification and correction of precipitating causes: These include
• Gastrointestinal (GI) bleeding: Consider blood transfusion and urgent UGI
scopy for therapeutic interventions
• Infection: Commonly SBP/UTI. Administer broad spectrum antibiotics
• Hypokalemia and/or metabolic alkalosis: KCl supplementation
• Renal failure
• Hypovolemia: Careful administration of fluids
• Hypoxia: Administer supplemental oxygen
• Sedative or tranquilizer use: Consider naloxone for opioid use
• Hypoglycemia: Intravenous dextrose administration
• Constipation: Laxatives like Syrup lactulose
2. Measures to lower the blood ammonia concentration:
• Syrup lactulose 30 mL (mixed in a glass of water or fruit juice) PO stat and
q4h till two to three well-formed stools are passed per day. Lactulose, a
disachharide (galactose + fructose) is minimally absorbed and is degraded
into lactic acid in the colon. By acidifying the GI tract, ammonia is trapped
and excreted in the stools. It can be given orally or rectally.
• Oral antibiotics: These may be used as second line therapy among patients
who do not respond to a 48-hour therapy with disaccharides. Neomycin
(1 g PO bd), rifaximin (400 mg PO tid) or Ampicillin (500 mg PO bd) may
be effective in lowering blood ammonia.
• Bowel wash at the earliest. This decreases the absorption of protein and
nitrogenous products from the intestines.
Refer to gastroenterology for further management.
Acute Cholangitis 64
CHAPTER
INTRODUCTION
Acute cholangitis refers to bacterial infection of the biliary system (biliary ducts).
It requires the presence of 2 factors; biliary obstruction (usually by a stone) and
bacterial growth in the bile, resulting in inflammation and often dilatation of
the biliary ducts. It is often caused by choledocholithiasis, which refers to the
presence of one or more gall stones in the common bile duct (CBD) resulting in
obstruction of the flow of bile.
Cholangitis must be differentiated clinically from cholecystitis, which refers
to inflammation of the gall bladder, usually due to gall stones with or without
bacterial infection or involvement of the rest of the biliary system.
• The organisms causing cholangitis usually ascend from the duodenum.
• If the biliary tract obstruction persists, intraluminal pressure increases,
resulting in reflux of the bacteria into the hepatic veins and lymphatic vessels
and eventually into the systemic circulation, resulting in sepsis.
• The common causes of biliary obstruction are biliary calculi (30–70%), benign
stenosis (5–30%), malignancy (10–30%) and bile duct stent blocks.
BACTERIOLOGY (USUALLY POLYMICROBIAL)

• Escherichia coli (most common), Klebsiella species, Enterobacter, Entero-
coccus, Streptococcus, Pseudomonas aeruginosa.
• Anaerobes (Bacteroides/Clostridia) are usually present as part of a mixed
infection.
CLINICAL FEATURES
• The classic presentation is fever, jaundice, and right upper quadrant abdominal
pain (Charcot’s triad). Approximately 25% of patients with cholangitis may
not have all three symptoms.
• Suppurative cholangitis may cause hypotension and altered sensorium in
addition to the Charcot’s triad (Reynolds’ pentad).
INVESTIGATIONS
• Complete blood count (CBC), electrolytes, creatinine, liver function test (LFT),
blood culture/sensitivity (C/S), blood borne virus screen (BBVS), chest X-ray
(CXR), electrocardiogram (ECG), prothrombin time (PT), activated partial
thromboplastin time (aPTT) are needed, if intervention likely.
• Liver function test shows features of cholestasis [hyperbilirubinemia, elevated

alkaline phosphatase (ALP)].
• Ultrasonography (USG) abdomen: Look for:
cc Common bile duct (CBD) dilatation with or without intrahepatic biliary
radicle dilatation (IHBRD)

cc Evidence of an etiology for bile obstruction (stone, tumor, or stent).
DIAGNOSIS
The closest differential for a cholangitis is cholecystitis which also presents
with right upper quadrant pain. Patients with cholangitis have high fever and
appear more ill than those with cholecystitis. Another important feature is the
presence of jaundice and elevated bilirubin in cholangitis, which are uncommon
in cholecystitis. Ultrasonography evidence of dilated common and intrahepatic
ducts is required to distinguish cholangitis from cholecystitis.
MANAGEMENT
• Monitor and stabilize airway, breathing, and circulation (ABC).
• Obtain a blood culture and administer broad-spectrum parenteral antibiotics
(piperacillin-tazobactam/meropenem).
• Analgesics as needed (paracetamol/tramadol/morphine)
• The key to successful treatment is early decompression of the biliary tract
which can be achieved by the following:
cc Endoscopic sphincterotomy with stone extraction and/or stent insertion
(depending on the cause of the obstruction) is the treatment of choice for

restoring biliary drainage.
cc Percutaneous transhepatic cholangiography (PTC) can be considered
when endoscopic retrograde cholangiopancreatography (ERCP) is

unavailable, unsuccessful, or contraindicated.
Section 10
Hematological
Emergencies
Anemia 65
CHAPTER
INTRODUCTION
Anemia can be defined as a reduced absolute number of circulating red blood
cells (RBCs). The criteria for anemia in men and women are less than 14 g/dL and
less than 12 g/dL, respectively. Two general approaches can be used to identify
the cause of anemia: (1) kinetic approach and (2) morphologic approach.
1. Kinetic approach: According to this approach, anemia can be caused by three
independent mechanisms (Table 1).
2. Morphologic approach: In this approach, the causes of anemia are classified
according to measurement of RBC size, as seen on the blood smear. The normal
RBC has a volume [mean corpuscular volume (MCV)] of 80–96 femtoliters (fL)
(Table 2).
RETICULOCYTE COUNT
• Anemia with a high reticulocyte count reflects an increased erythropoietic
response to continued hemolysis or blood loss.
TABLE 1: Kinetic approach of the cause of anemia.

Cause Examples
Decreased • Lack of nutrients: Iron, vitamin B12, folic acid deficiency
RBC • Bone marrow disorders: Aplastic anemia, pure RBC aplasia, marrow
production infiltration
• Bone marrow suppression: Drugs, chemotherapy, irradiation
• Ineffective erythropoiesis: Alpha- and beta-thalassemia, myelodysplastic
syndrome, sideroblastic anemias
• Others: Chronic renal failure, hypogonadism, hypothyroidism
Increased • Inherited hemolytic anemias: Hereditary spherocytosis, sickle cell disease,
RBC thalassemia major
destruction • Acquired hemolytic anemias: Coombs-positive autoimmune hemolytic
anemia, thrombotic thrombocytopenic purpura, hemolytic uremic
syndrome, malaria, paroxysmal nocturnal hemoglobinuria
• Hypersplenism
Blood loss • Obvious bleeding: Trauma, melena, hematemesis, menometrorrhagia
• Occult bleeding: Slowly bleeding ulcer or carcinoma
(RBC: red blood cell)
238 SECTION 10: Hematological Emergencies
TABLE 2: Morphologic approach of the cause of anemia.

Type Examples
Macrocytic • Abnormalities of DNA metabolism: Vitamin B12 deficiency, folate
anemia MCV deficiency, drugs (hydroxyurea, zidovudine, methotrexate, azathioprine)
>100 fL • Shift to immature or stressed red cells: Aplastic anemia/Fanconi anemia,
pure red cell aplasia
• Primary bone marrow disorders: Myelodysplastic syndromes
• Others: Alcohol abuse, liver disease, hypothyroidism
Microcytic • Reduced iron availability: Iron deficiency, anemia of inflammation,
anemia MCV copper deficiency
<80 fL • Acquired disorders of heme synthesis: Lead poisoning, acquired
sideroblastic anemias
• Reduced globin production: Thalassemia, other hemoglobinopathies
• Rare congenital disorders: Sideroblastic anemias, porphyria, and defects
in iron absorption, transport, utilization, and recycling
Normocytic • Systemic disorders
anemia MCV • Cancer-associated anemia
= 80–100 fL • Anemia of chronic renal disease
(MCV: mean corpuscular volume)
• A stable anemia with a low reticulocyte count is strong evidence for deficient
production of RBCs.
• Normal range is 0.5–2.0%.
• Investigations to be sent: Complete blood count profile, reticulocyte count,
electrolytes, creatinine.
• If hemolysis is suspected: Liver function test, lactate dehydrogenase, urea, uric
acid, calcium, phosphate, urinalysis, chest X-ray (CXR).
• If patient is a pure vegetarian (get this history from all patients): Vitamin B12
and folate levels.
MANAGEMENT
• If the patient has signs of failure, transfuse one to two packed red cells urgently;
target hemoglobin (Hb) >7 g%.
• Identify and treat the underlying cause.
For Iron Deficiency Anemia

• Dietary: Advice increased dietary iron intake
• Deworm:
cc Tablet mebendazole 100 mg bd × 3 days. Repeat after 2 weeks (safe in
pregnancy), or
cc Tablet albendazole 400 mg stat. Repeat after 2 weeks, or
cc Tablet tinidazole 2 g stat.

CHAPTER 65: Anemia 239
• Oral iron therapy:

cc Tablet ferrous sulfate 200 mg (60 mg elemental iron) tid × 6 months, or
cc Tablet ferrous fumarate 152 mg + folic acid 1,500 µg (Livogen) bd ×
6 months, or
cc Tablet ferrous fumarate 350 mg + folic acid 2,000 µg + vitamin B
12 15 µg
(Autrin) od × 6 months.
After 6 months, if the Hb is normal, iron supplementation should be continued
for a further 6 months till iron stores are replenished.
• Parenteral iron therapy.
For Suspected B12/Folate Deficiency

• For pernicious anemia: Injection vitamin B12 1,000 µg intramuscular (IM)/
subcutaneous (SC) once daily for 1 week, followed by 1,000 µg every week for
4 weeks and then 1,000 µg every month for 6 months. Supplement this with
tablet folate 5 mg OD till complete hematological recovery.
• In pure vegetarians: Oral B12 and folate supplementation with neurobion/
multivitamin tablets may be tried. However, if the degree of anemia is severe,
initial 1 week of IM/SC vitamin B12 injections may be necessary.
The evaluation of a patient with anemia is shown in Flowchart 1.
(G6PD: glucose-6-phosphate dehydrogenase; MDS: myelodysplastic syndrome; MCV: mean corpuscular

volume; RBC: red blood cell; RDW: red blood distribution width; Chr: Chronic)
FLOWCHART 1: Evaluation of anemia.
Febrile Neutropenia 66
CHAPTER
INTRODUCTION
Patients with malignancies on cytotoxic chemotherapy that affects hemopoiesis
and integrity of gastrointestinal mucosa, frequently develop fever due to
colonizing bacteria or fungus. It is critical to recognize neutropenic fever early
and to initiate empiric antibiotics promptly to prevent progression to a sepsis
syndrome and possibly death.
Neutropenia is usually defined as an absolute neutrophil count (ANC)
<1,500 cells/µL, and severe neutropenia is usually defined as an ANC <500 cells/µL
or an ANC that is expected to decrease to <500 cells/µL over the next 48 hours.
MICROBIOLOGY
• Bacteremia is documented in only 10–25% of neutropenic fever episodes.
• Common organisms are:
cc Gram-positive: (60%) Staphylococcus epidermidis, coagulase negative
staphylococci, Staphylococcus aureus, Streptococcus viridans

cc Gram-negative: (30%) Escherichia coli, Klebsiella species, Pseudomonas
aeruginosa
cc Others: (10%) Acinetobacter, fungal infections (Aspergillus, Candida),
anaerobes, viruses.
INVESTIGATIONS
Investigations to be sent:
• Perform a thorough physical examination to identify any focus of infection:
cc Complete blood count (CBC), electrolytes, creatinine, liver function test
(LFT), blood culture/sensitivity (c/s)

cc If urinary symptoms are present: Urinalysis and urine c/s
cc If respiratory symptoms are present: Chest X-ray (CXR).
MANAGEMENT
• Empiric broad-spectrum antibacterial therapy should be initiated immedi-
ately after blood cultures have been obtained. Administer cefoperazone-
sulbactam 3 g intravenous (IV) stat plus amikacin 15 mg/kg IV stat.
• Refer to hematology immediately for further management.
Acute Leukemia 67
CHAPTER
INTRODUCTION
Acute leukemia may occur de novo or may transform from chronic myeloid
leukemia (CML) [70% to acute myeloid leukemia (AML) and 30% to acute
lymphoid leukemia (ALL)] or from myelodysplastic syndrome (MDS).
TYPES OF ACUTE LEUKEMIA

Types of acute leukemia have been shown in Table 1.
TABLE 1: Types of acute leukemia.

Acute lymphoid leukemia (ALL) Acute myeloid leukemia (AML)
World Health Organization (WHO) French–American–British (FAB)
classification: classification:
• B-lymphoblastic leukemia/ • M0: Undifferentiated acute myeloblastic
lymphoblastic lymphoma leukemia
• B-lymphoblastic leukemia/lymphoma, • M1: Acute myeloblastic leukemia with
not otherwise specified minimal maturation
• B-lymphoblastic leukemia/lymphoma • M2: Acute myeloblastic leukemia with
with maturation maturation
• T-lymphoblastic leukemia/lymphoma • M3: Acute promyelocytic leukemia
• M4: Acute myelomonocytic leukemia
• M5: Acute monocytic leukemia
• M6: Acute erythroid leukemia
• M7: Acute megakaryocytic leukemia
Patients with acute leukemia may present with problems due to:
• Red cells: Anemia, fatigue
cc White cells: Leukopenia may cause fever, while leukostasis due to high blast
count may result in myocardial infarction (MI), respiratory impairment,

renal failure, stroke or acute confusional state.
cc Platelets: Bleeding manifestations
cc Coagulopathy: Disseminated intravascular coagulation (DIC) and shock
due to sepsis is frequently seen in AML M3.

MANAGEMENT
• Assess and stabilize airway, breathing, and circulation (ABC).
• Treat anemia/bleeding with appropriate blood product transfusion.
• If the patient has fever or neutropenia, consult hematology immediately and
start antibiotics.
CHRONIC MYELOID LEUKEMIA

• Chronic myeloid leukemia is a myeloproliferative disorder associated with the
Philadelphia chromosome t(9;22)(q34;q11) and/or the BCR- ABL fusion gene.
• The course of CML has three phases:
1. Chronic phase: Approximately 85% of patients are in this phase at the time
of diagnosis. Blast cells comprise less than 10%
2. Accelerated phase: Blast cells in blood and marrow between 10% and 19%
3. Blast phase: Blast crisis, occasionally of sudden onset, is an ominous
clinical event that is difficult to treat. Peripheral blood or bone marrow
blasts comprise ≥20%.
• Transformation may be suggested clinically by the development of signs and
symptoms more typical of acute leukemia (e.g., night sweats, weight loss,
fever, bone pain, symptoms of anemia). The blast crisis may be lymphoid in
30% (to ALL) or myeloid in 70% (to AML).
• Patient with blast crisis may develop complications like fever, tumor lysis and
renal failure.
Treatment
• Treat fever and tumor lysis, if present.
• Treat anemia/bleeding with appropriate blood product transfusion.
• Tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib). Imatinib is generally
well-tolerated with side effects being nausea, vomiting, edema, neutropenia,
and thrombocytopenia.
Tumor Lysis Syndrome 68
CHAPTER
INTRODUCTION
Tumor lysis syndrome (TLS) is an oncologic emergency that is caused by massive
tumor cell lysis with the release of large amounts of potassium, phosphate, and
nucleic acids into the systemic circulation.
Catabolism of the nucleic acids to uric acid leads to hyperuricemia, and the
marked increase in uric acid excretion can result in the precipitation of uric
acid in the renal tubules. This can also induce renal vasoconstriction, impaired
autoregulation, decreased renal blood flow, and inflammation, resulting in acute
kidney injury. Hyperphosphatemia with calcium phosphate deposition in the
renal tubules can also cause acute kidney injury.
Tumor lysis syndrome most often occurs after the initiation of cytotoxic
therapy in patients with high-grade lymphomas (particularly the Burkitt subtype)
and acute lymphoid leukemia (ALL). However, TLS can occur spontaneously and
with other tumor types.
• The symptoms associated with TLS largely reflect the associated metabolic
abnormalities (hyperkalemia, hyperphosphatemia, and hypocalcemia).
• They include nausea, vomiting, diarrhea, anorexia, lethargy, hematuria, heart
failure, cardiac dysrhythmias, seizures, muscle cramps, tetany, syncope, and
possible sudden death.
CAIRO-BISHOP DEFINITION
• Laboratory TLS (LTLS) is defined as any two or more abnormal serum values
present within 3 days before or 7 days after instituting chemotherapy in the
setting of adequate hydration (with or without alkalinization) and use of a
hypouricemic agent.
• Clinical TLS (CTLS) is defined as LTLS plus one or more of the following that
was not directly or probably attributable to a therapeutic agent: Increased
serum creatinine concentration (≥1.5 times the upper limit of normal), cardiac
arrhythmia/sudden death or a seizure.
INVESTIGATIONS
Complete blood count (CBC), electrolytes, creatinine, urea, liver function test
(LFT), blood culture/sensitivity, calcium (Ca), phosphate (PO4), uric acid, lactate
dehydrogenase (LDH), urinalysis, arterial blood gas (ABG).
PREVENTION
Aggressive hydration [intravenous (IV) and oral] is the cornerstone of
preventing TLS.
MANAGEMENT OF ESTABLISHED TUMOR LYSIS

SYNDROME
• Aggressive hydration to induce high urine output to minimize the likelihood
of uric acid or calcium phosphate precipitation in the tubules. Administer
crystalloids (NS/RL) and monitor urine output to maintain a target of 2 mL/
kg/h. About 4–6 L of IV fluids may be required per day. Closely monitor
cardiovascular status to avoid fluid overload. Loop diuretics like furosemide
may be used to maintain target urine output but generally not required in
those with normal renal and cardiac function.
• Alkalinization of urine: Sodium bicarbonate (NaHCO3), 100 mL IV stat, is only
indicated in patients with metabolic acidosis. The aim is to keep urine pH >7.
• Management of electrolyte abnormalities associated with TLS:
cc Hyperuricemia: Allopurinol 300 mg PO stat and 100–200 mg q8h, or
Febuxostat 40–80 mg PO stat, or Rasburicase 0.2 mg/kg IV over 30 minutes

and od for 5 days
cc Hyperkalemia: Correct hyperkalemia (Refer Chapter 10)
cc Hypocalcemia: Administer 10 mL of 10% calcium gluconate IV over
4 minutes. Treat hyperphosphatemia first before correcting calcium.

cc Hyperphosphatemia: Oral phosphate binders containing aluminum
hydroxide (Syrup Digene gel 10 mL stat and q2h) can be given.
• In refractory cases Renal replacement therapy/hemodialysis can be
considered. Indications are:
cc Severe oliguria or anuria
cc Persistent hyperkalemia
cc Hyperphosphatemia-induced symptomatic hypocalcemia
cc A calcium-phosphate product ≥70 mg/dL2.

Sickle Cell Crisis 69
CHAPTER
INTRODUCTION
Hemoglobinopathies are disorders affecting the production, structure or function
of hemoglobin. Sickle cell syndromes are caused by a mutation of the β-globin
gene, resulting in HbS, which when deoxygenated results in the characteristic
sickle-shaped RBC. Sickled cells lose the pliability to traverse small capillaries, and
thus get sequestered in the spleen and other organs, causing acute complications.
Acute complications of sickle cell disease include:
• Infections: Common infections include bacteremia and meningitis due
to encapsulated organisms (Streptococcus pneumoniae and Haemophilus
influenzae), pneumonia due to Mycoplasma pneumoniae, Chlamydia
pneumoniae, and viruses (parvovirus, H1N1 influenza, Zika virus, SARS-
CoV-2).
• Severe anemia: Hemolytic anemia occurs as a result of splenic sequestration,
aplastic crisis, or hyperhemolysis.
• Vaso-occlusive phenomena: Vaso-occlusive phenomena and hemolysis are
the clinical hallmarks of sickle cell disease. Vaso-occlusion results in recurrent
painful episodes and a variety of serious organ system complications.
Hemolysis of red blood cell (RBC) causes chronic anemia and pigment
gallstones.
CLINICAL PRESENTATION OF SICKLE CELL CRISIS

• Painful (vaso-occlusive) crisis: Excruciating pain usually in long bone, ribs,
sternum, and vertebra.
• Chest crisis: The most common cause of mortality. Vaso-occlusion of
pulmonary microvasculature results in reduced perfusion and infarction.
Precipitated by pneumonia, pregnancy, and smoking.
• Cerebral infarction: Usually in children. High risk of recurrence.
• Splenic and hepatic sequestration: RBC trapped in spleen/liver may cause
organomegaly, severe anemia, and circulatory collapse.
• Aplastic crisis: It is caused by parvovirus infection, exacerbated by folate
deficiency.
• Hemolytic crisis: Can cause chronic anemia and pigment crisis
• Priapism: Prolonged, painful erection due to local vaso-occlusion. Major
crisis are often preceded by “stuttering” priapism episodes.
MANAGEMENT
• Give adequate analgesia. Oral NSAIDs may be sufficient for minor crises.
Administer parenteral opiates (injection morphine 5 mg IV) for moderate or
severe pain and titrate to response.
• Adequate hydration should be ensured (oral or IV).
• Administer oxygen, especially in severe chest crisis.
• Give tablet folic acid 5 mg PO od.
• If an infective etiology is suspected, start broad-spectrum antibiotics.
• Give thromboprophylaxis for deep vein thrombosis (DVT): Low-molecular-
weight heparin (LMWH)/unfractionated heparin (UFH)
• Exchange transfusion: This can be performed either by manual phlebotomy
or by automated red cell exchange. Indications include chest crisis, cerebral
infarction, severe persisting painful crisis, and priapism.
• Hydroxyurea is the drug of choice in the overall management of sickle cell
disease as it reduces the incidence of acute vaso-occlusive events.
• Hematopoietic stem cell transplantation remains the only life long cure for
sickle cell disease.
Anticoagulants 70
CHAPTER
INTRODUCTION
Anticoagulants include heparin, warfarin, direct thrombin inhibitors (DTIs),
direct factor Xa inhibitors, and fondaparinux.
ORAL ANTICOAGULANTS
• The commonly used oral anticoagulants are warfarin and acenocoumarol
(Sintrom).
cc Warfarin: “WARF”—Wisconsin Alumni Research Foundation; “ARIN”—
coumarin.
– It is a synthetic derivative of dicoumarol.
– It has a longer half-life (36 h), cheaper but has significant drug
interactions.
– Starting dose for anticoagulation: 5 mg od and increase by 2.5 mg after
3 days, if needed based on PT with INR.
cc Sintrom/Acenocoumarol:
– It is also a derivative of coumarin (generic).

– It has a shorter half-life (10 h), costlier and has lesser drug interactions.
– Starting dose for anticoagulation: 2 mg od and increase by 1 mg after
3 days, if needed based on PT with INR.
• They inhibit reduction of vitamin K to its active form and lead to depletion of
vitamin K-dependent clotting factors (II, VII, IX, X, and proteins C, S, Z).
• Therapeutic goals of anticoagulation have been shown in Table 1.
TABLE 1: Therapeutic goals of anticoagulation.

Indication International normalized ratio (INR) goal Duration
for anticoagulation
Proximal deep vein thrombosis 2–3 6 months
Calf deep vein thrombosis 2–3 3 months
Pulmonary embolism 2–3 6 months
Atrial fibrillation 2–3 Lifelong
Mechanical heart valve 2.5–3.5 Lifelong
Antiphospholipid antibodies 2.5–3.5 Lifelong
(APLA) with thrombosis
TABLE 2: Management of supratherapeutic international normalized ratio (INR).

INR Bleeding Recommended action
>Therapeutic No/minor • Withhold one dose and restart warfarin at a lower dose
range—5 bleeding • Check INR after 2 days and follow-up with primary unit
>5–9 No/minor • Withhold one dose and restart warfarin at a lower dose
bleeding • Administer 10 mg vitamin K1 IV stat
• Check INR after 1 day and follow-up with primary unit
(monitor INR more frequently to achieve therapeutic range)
>9 No/minor • Withhold warfarin for at least 3 days
bleeding • Administer 10 mg vitamin K1 IV od for 3 days
• Resume warfarin at a lower dose when INR is in therapeutic
range (monitor INR more frequently to achieve therapeutic
range)
Any INR Severe • Withhold warfarin
bleeding • Administer 10 mg vitamin K1 IV over 30 minutes, repeat at
12-hour intervals if the INR remains elevated
• Supplement FFP (15 mg/kg), depending on clinical urgency
• Monitor and repeat INR as needed
• Oral anticoagulant overdose (accidental or deliberate) results in prolongation

of prothrombin time (PT) with international normalized ratio (INR). Risk
factors for significant bleeding include local lesions (peptic ulcer, colon
angiodysplasia), higher levels of anticoagulation (INR >2.5) and coexistent
hematological abnormalities.
• Management of supratherapeutic INR has been shown in Table 2.
PARENTERAL ANTICOAGULANTS
• Heparins including unfractionated and low-molecular-weight heparin
(LMWH) products:
cc Unfractionated heparin:
– Unfractionated heparin (UFH) comes from porcine intestinal mucosa

and it directly inactivates thrombin and factor Xa, via antithrombin.
– UFH prolongs the thrombin time (TT) and activated partial thrombo-
plastin time (aPTT).
– The dose for prophylaxis is 5,000 U intravenous (IV)/subcutaneous
(SC) q6h. aPTT monitoring is not necessary.
– For therapeutic anticoagulation, UFH is administered as 80 U/kg IV
bolus, followed by 18 U/kg/h infusion. The rate of infusion is titrated
based on aPTT monitoring 6 hours later.
– Protamine sulfate is used as an antidote to reverse bleeding caused by
UFH. Approximately 1 mg protamine sulfate IV neutralizes 100 U of
CHAPTER 70: Anticoagulants 249
heparin, up to a maximum dose of 250 mg, the dose can be given as

25–50 mg IV over 10 minutes and the rest of the calculated dose as IV
infusion over 8–16 hours.
cc Low-molecular-weight heparins:
– LMWHs are produced by enzymatic cleavage of UFH, and they
indirectly inactivate thrombin and factor Xa via antithrombin.
– aPTT monitoring is not needed during treatment with LMWH.
– Peak factor Xa levels measured 4 hours after a SC dose may be used for
monitoring.
– Contraindicated in patients with a creatinine clearance <10 mL/min.
Patients with creatinine clearance <30 mL/min need renal dose adjust-
ment (“od” instead of “bd”).
– Protamine sulfate does not fully reverse the anticoagulant effect of
LMWH.
– Dose and indications of LMWH:
Enoxaparin: 1 mg/kg SC bd daily [unstable angina, non-ST segment
elevation myocardial infarction (NSTEMI), deep vein thrombosis
(DVT), pulmonary embolism (PE)]
Dalteparin: 200 IU/kg SC bd daily (DVT, PE).
cc Fondaparinux:
– It is a synthetic pentasaccharide factor Xa inhibitor.
– As it does not inhibit thrombin, it does not prolong the aPTT.
– Factor Xa level monitoring is not recommended, but may be necessary
in patients with renal failure, obesity, and cachexia.
– Dose of fondaparinux has been shown in Table 3.
cc Direct factor Xa inhibitors: Apixaban, rivaroxaban, and edoxaban.
cc Direct thrombin inhibitors: Argatroban and bivalirudin are synthetic DTI
used in patients with heparin-induced thrombocytopenia (HIT). These
are administered as IV infusions.
TABLE 3: Dose of fondaparinux.

Non-ST segment elevation myocardial 2.5 mg SC od
infarction (NSTEMI)
Deep vein thrombosis (DVT), pulmonary embolism (PE)
50 kg 5 mg SC od
50–100 kg 7.5 mg SC od
>100 kg 10 mg SC od
Bleeding and Clotting
Disorders 71
CHAPTER
INTRODUCTION
Normal regulation of bleeding is a complex process involving platelets and the
coagulation system.
• Bleeding related to platelets usually presents as petechial and mucosal
bleeding.
• Bleeding related to coagulation defects presents as spontaneous or deep bleeds.
CONGENITAL PLATELET DISORDERS

• Glanzmann’s thrombasthenia: Defect in the platelet integrin IIb 3.
• Bernard-Soulier syndrome: Giant platelet disorder.
Treatment: Platelet transfusion [10 platelet rich concentrate (PRCs) for
intracranial bleed/4 PRCs for other bleeds].
ACQUIRED PLATELET DEFECTS

• Decreased platelet production: Due to marrow infiltration (tumor, infec-
tion), viral infections [rubella, human immunodeficiency virus (HIV)], drugs
(heparin, sulfa antibiotics), radiation, vitamin B12/folate deficiency.
• Increased platelet destruction:
cc Idiopathic thrombocytopenic purpura (ITP): Platelet destruction is
mediated by production of autoantibodies that attach to circulating
platelets. The presence of lymphadenopathy, hepatosplenomegaly or
hyperbilirubinemia should suggest an alternate diagnosis like leukemia,
lymphoma, systemic lupus erythematosus (SLE), etc.
– Initial therapy for ITP is usually steroids (prednisolone 1 mg/kg/day).
– Platelets should be transfused only if needed, following the first dose
of steroids.
– Transfuse patients only if the bleeding is life-threatening.
– Avoid using antiplatelet medications such as aspirin or nonsteroidal
anti-inflammatory drugs (NSAIDs).
cc Thrombotic thrombocytopenic purpura (TTP) and hemolytic–uremic
syndrome (HUS): These are thrombotic microangiopathies caused by
platelet—von Willebrand factor (vWF) aggregates and platelet-fibrin
aggregates respectively, resulting in thrombocytopenia, microangio-
pathic hemolytic anemia and organ ischemia. The typical pentad of TTP
is seen in <30% of patients and includes thrombocytopenia, hemolytic
anemia, fever, renal dysfunction and fluctuating neurological deficits.
CHAPTER 71: Bleeding and Clotting Disorders 251
c Laboratory investigations show presence of schistocytes, normal

prothrombin time (PT) and activated partial thromboplastin time (aPTT),
elevated lactate dehydrogenase (LDH) and thrombocytopenia.
c Mainstay of treatment is plasma exchange. If not available, transfusion of
fresh-frozen plasma (FFP) or high-dose glucocorticoids may be tried.
cc Viral infections: HIV, mumps, varicella, Epstein–Barr virus (EBV).
• Platelet loss: Due to excessive hemorrhage or hemodialysis.

• Splenic sequestration: Due to sickle cell crisis or cirrhosis.
• Qualitative platelet abnormalities: Certain disorders can cause qualitative or
functional disorders of platelet function. These include uremia, liver disease,
disseminated intravascular coagulation (DIC), multiple myeloma, etc.
ACQUIRED COAGULATION DISORDERS

• Liver disease: Mainly due to decreased synthesis of clotting factors, including
vitamin K-dependent carboxylation of factors, II, VII, IX and X. FFP may be
required to correct the bleeding. If fibrinogen levels are less than 100 mg/dL,
cryoprecipitate may be used. Desmopressin may also be used.
• Renal disease: Hemostatic abnormalities are commonly present in patients
with renal failure due to abnormalities in clotting factors and quantitative and
qualitative platelet dysfunction. Retention of uremic toxins causes inhibition
of platelet aggregation. In uremic patients with prolonged bleeding times and
active bleeding, desmopressin (0.3 mg/kg, max 20 mg, SC or IV or 3 mg/kg,
max 300 mg, intranasal spray every 12 h up to three doses) may be given.
• Disseminated intravascular coagulation: DIC is an acquired syndrome,
characterized by inappropriate and widespread activation of the coagulation
system resulting in intravascular fibrin formation. Concomitant activation
of the fibrinolytic system also occurs, resulting in breakdown of fibrin clots,
consumption of coagulation factors, and bleeding.
cc DIC usually results in multiple organ dysfunction. Although bleeding and
thrombosis may occur simultaneously, one usually predominates.

cc Laboratory findings include thrombocytopenia, low fibrinogen level,
elevated D-dimer, prolonged PT and aPTT.

cc Treatment includes supportive measures and treatment of the under-
lying illness.
cc The differences between DIC, TTP/HUS are shown in Box 1.
BOX 1 Diagnosis of DIC, TTP/HUS.

• The presence of schistocytes on peripheral smear suggests DIC, TTP or HUS
• How to differentiate DIC from TTP/HUS:
{{In DIC, PT and aPTT will be prolonged
{{In TTP/HUS, PT and aPTT will be normal

CLOTTING DISORDERS
• Inherited clotting disorders: These disorders cause a hypercoagulable state.
cc Protein C and S deficiency: Autosomal dominant. These patients are at a
higher risk of developing skin necrosis.

cc Factor V Leiden mutation: Also called activated protein C resistance, it is
the most prevalent inherited hypercoagulable disorder. Usually presents

with venous thromboembolism and pregnancy-related complications
(preeclampsia, abruption, stillbirth).
cc Prothrombin gene mutation 20210A: Presents with venous thrombo-
embolism and pregnancy-related complications.

cc Antithrombin deficiency: Presents with venous thromboembolism and
pregnancy-related complications.
cc Hyperhomocysteinemia: Associated with both arterial and venous
thrombosis. Treatment is with folic acid 5 mg od, along with pyridoxine
and vitamin B12.
• Acquired clotting disorders:
cc Antiphospholipid syndrome: APS is an autoimmune condition that may
be associated with complications during pregnancy such as preeclampsia

and fetal loss or stroke.
cc Pregnancy and estrogen use: There is increased risk of venous
thromboembolism and cerebral venous thrombosis.
cc Malignancy: Many malignancies are associated with an increased risk of
venous thromboembolism.
Hemophilia and
von Willebrand Disease 72
CHAPTER
HEMOPHILIA
Hemophilia A and B are hereditary X-linked recessive disorders of bleeding that
present in male children. As these are X linked disorders, men are overwhelmingly
affected with women being asymptomatic carriers. These bleeding disorders
typically present early in life with spontaneous deep bruises, hemarthrosis,
retroperitoneal or intracranial bleeding.
• Hemophilia A: Deficiency of factor VIII.
• Hemophilia B: Deficiency of factor IX.
Clinical presentation depends on degree of factor deficiency:
• Mild: >5% factor activity. Bleeding is rare.
• Moderate: 1–5% activity. Spontaneous bleeding is rare.
• Severe: <1% activity. Serious bleeding diathesis may be seen. Acute
hemarthrosis, intramuscular bleeds, intracranial bleeding, hematuria, post-
trauma bleeding may be severe.
Investigations
• Complete blood count (CBC) profile, ultrasonography (USG) scan for muscle
hematomas, computed tomography (CT) scan for headache/focal deficits.
• Coagulation workup typically shows a prolonged activated partial thrombo-
plastin time (aPTT) with all other tests normal.
Management
• Mild-to-moderate hemophilia with minor bleeding: Desmopressin—DDAVP
(0.3 µg/kg IV in 50 mL NS over 30 min, or 300 µg intranasally q12h). Increases
factor VIII activity three to five times. DDAVP has no effect on factor IX activity.
• Mild-to-moderate hemophilia with major bleeding or severe hemophilia with
any bleeding: Factor VIII replacement is the mainstay of therapy. Every 1 U/kg
infused increases activity by 2%. A 50 U/L IV bolus increases factor VIII activity
by about 100% over baseline.
• Superficial mucosal bleeding may be controlled with anti-fibrinolytic therapy.
Administer oral tranexamic acid 500–1,000 mg q8h or IV tranexamic acid 10
mg/kg q8h.
• If factor VIII concentrate is not available, cryoprecipitate or FFP may be used
to control acute bleeding.
Hemophilia B is treated with factor IX replacement. Each 1 IU/kg of factor IX
replacement increases plasma factor IX activity by 1%.
VON WILLEBRAND DISEASE

von Willebrand disease (vWD) is the most common inherited bleeding disorder
in the world. vWD is characterized by reduced levels or abnormal function of
von Willebrand factor (vWF), which normally promotes platelet adhesion and
protects factor VIII from destruction. Hence, there is reduced factor VIII level in
severe disease.
Clinical Features
• The clinical presentation is less severe than hemophilia with hemarthroses
and muscle bleeds being rare.
• Epistaxis, prolonged bleeding from trivial wounds, oral cavity bleeding,
excessive menstrual bleeding.
Diagnosis
Diagnosis is confirmed by an assay of vWF activity by measurement of ristocetin
cofactor (RCoF) activity. Normal RCoF values are 50–200 IU/dL. Levels of <30 IU/
dL are considered definitive for vWD.
Management
• Desmopressin induces the release of vWF from storage sites in the endo-
thelium and is the mainstay of therapy. The dose is 0.3 µg/kg (max 20 µg) SC/
IV every 12–24 h for 3–4 doses.
• Plasma derivatives like cryoprecipitate that contains vWF and factor VIII can
also be used to control acute bleeding.
• Intermediate purity factor VIII concentrate or vWF plasma derived concentrate
transfusions, if available, may be used.
Blood Products and
Transfusion 73
CHAPTER
BLOOD COMPONENTS
Blood components are those products derived from whole blood:
• Packed red cells: Each pack is from a single donor. A transfusion of 4 mL/kg will
increase circulating hemoglobin (Hb) by 1 g/dL.
• Platelets: They may be either pooled or derived from a single donor by
plateletpheresis. Crossmatching is not necessary before transfusion.
• Fresh frozen plasma: FFP is plasma obtained after separation of whole
blood from RBC s and platelets and then frozen within 8 hours of collection.
It contains coagulation factors (fibrinogen, albumin, protein C, protein S,
antithrombin, tissue factor pathway inhibitor). It is free of erythrocytes,
leucocytes and platelets. 10–20 mL/kg (4–6 units in adults) will increase factor
levels by approximately 20%. FFP must be ABO compatible with the recipient’s
red cells.
FFP is indicated in patients with the following:
• Congenital or acquired deficiency of clotting factors with active bleeding
• For planned surgeries or invasive procedures in the presence of abnormal
coagulation tests
• For reversal of warfarin induced coagulopathy in the presence of active
bleeding
• Cryoprecipitate: Cryoprecipitate is the cold insoluble protein fraction of
FFP. One unit of cyoprecipitate (20–50 mL) contains fibrinogen (factor I),
antihemophilic factor (factor VIII), fibrin stabilizing factor (factor XIII) and
von Willebrand factor (vWF). Cryoprecipitate is indicated in bleeding due
to hemophilia, von Willebrand disease, hypofibrinogenemia (disseminated
intravascular coagulation). Crossmatching is not necessary before transfusion.
COMPLICATIONS OF BLOOD TRANSFUSION

• Immune-mediated reactions:
cc Febrile transfusion reaction: Most common reaction, presents with fever,
chills, and malaise. Usually caused by cytokines from leukocytes in

transfused red cell or platelet components.
cc Acute hemolytic reaction: Most serious reaction, presents with fever, chills,
pain at transfusion site, nausea, vomiting, and dark urine. Often a result of
ABO/Rh incompatibility due to administration error.
cc Allergic reaction: Presents with urticaria, pruritis, hives which may progress
to laryngeal oedema or bronchospasm. Anaphylaxis is rare.

cc Transfusion Related Acute Lung Injury (TRALI): Presents with sudden onset
of non-cardiogenic pulmonary oedema within 6 hours of transfusion.
Associated with the presence of antibodies in the donor blood to recipient
leukocyte antigens and may be fatal.
cc Graft-vs-Host Disease (GVHD): Presents with rash, fever, diarrhea, and
hepatic dysfunction 1–4 weeks after transfusion. There is no effective

treatment for GVHD.
• Nonimmune reactions:
cc Transfusion associated circulatory overload (TACO): Presents with acute
respiratory distress within 6 hours of transfusion of large volume of blood,

especially in the elderly. Slow the transfusion and administer diuretics.
cc Hypothermia: When large volume of freshly thawed fresh frozen plasma
(FFP) is transfused
cc Electrolyte toxicity: Hyperkalemia due to red blood cell (RBC) leak-
age during storage. Citrate, commonly used to anticoagulate blood

components chelates calcium and may cause hypocalcemia
cc Iron overload
cc Infections: Hepatitis C, B, human immunodeficiency virus (HIV), cytome-
galovirus (CMV), human T-cell lymphotropic virus (HTLV), parvovirus

B19, malaria.
MANAGEMENT OF SUSPECTED TRANSFUSION REACTION

• Immediately discontinue the transfusion.
• Check and monitor vital signs.
• Check if the right blood product has been given to the right patient.
• Treat the patient symptomatically:
cc For mild febrile reaction: Injection/tablet paracetamol
cc For mild allergic reaction: Injection chlorpheniramine (Avil) 1 amp IV stat
cc For severe anaphylactic reaction with stridor/wheeze/hypotension:
– Injection chlorpheniramine (Avil) 1 amp (22.75 mg/mL: 2 mL) IV stat

– Injection adrenaline 0.5 mg IM in the anterolateral thigh
– Treat like anaphylaxis (refer chapter 3).
• TRALI: Stop the transfusion. Administer oxygen and aggressive respiratory
support. Avoid diuretics.
• For mild reactions, discontinue transfusion for 30–60 minutes and restart
slowly.
• For severe reactions, stop the transfusion and send the blood product to blood
bank along with a patient’s blood sample in a ethylenediaminetetraacetic acid
(EDTA) tube and a urine sample.
Section 11
Endocrine Emergencies
Thyrotoxic Crisis 74
CHAPTER
INTRODUCTION
Thyrotoxic crisis or thyroid storm is a rare but potentially life-threatening
emergency induced by a sudden release of thyroid hormones in patients
with thyrotoxicosis. It occurs in 1–2% of patients with thyrotoxicosis and is
characterized by exaggerated symptoms, further distinguished by the presence
of fever, marked tachycardia, central nervous system (CNS) dysfunction, and
gastrointestinal symptoms.
CLINICAL FEATURES
The clinical presentation of a thyroid storm is quite dramatic with the common
triggers being infection, diabetic ketoacidosis, hypoglycemia, radioactive iodine
treatment, and thyroid hormone overdose.
Hyperthermia (104-106°C) and tachycardia (heart rate >150/min) are quite
prominent.
CNS dysfunction is a hallmark of thyroid storm and presents with restlessness,
agitation, delerium, seizures, and coma.
Gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain, and
sometimes cholestatic jaundice) are also pronounced.
Other features of thyrotoxicosis are quite evident in patients with thyroid
storm. These include fine tremors, muscle wasting, hyperreflexia, exophthalmos,
ophthalmoplegia, wide pulse pressure, congestive heart failure, atrial fibrillation
or flutter.
INVESTIGATIONS
Serum thyroid stimulating hormone (TSH): In primary hyperthyroidism, TSH
levels are low due to negative feedback mechanism of high thyroid hormone
levels, while TSH is increased in secondary hyperthyroidism because of increased
production in the pituitary.
Free thyroxine (FT4) and triiodothyronine (T3): A low TSH with elevated FT4 or T3
confirms the diagnosis of thyrotoxicosis.
Thyroid antibody titers: Thyroid stimulating antibodies (to thyroglobulin or
thyroid peroxidase) are detected in Graves disease.
260 SECTION 11: Endocrine Emergencies
MANAGEMENT
• Identify and treat the precipitating factor.
• Stop excessive thyroid hormone synthesis, action, and reduce enterohepatic
circulation. Remember the mnemonic 5Bs provided in Table 1.
TABLE 1: Medical management of thyroid storm.

5Bs Aim Drug and dose
Block synthesis Inhibit synthesis of thyroid • Propylthiouracil (PTU) 600 mg PO
hormones stat and 200 mg q4–6h or
• Carbimazole: 20–30 mg PO q4–6h
Block T4 into T3 Reduce T4 to T3 conversion, Hydrocortisone 100 mg IV q6h
conversio promote vasomotor (PTU also blocks peripheral T4 to T3
stability, and possibly conversion)
treat an associated relative
adrenal insufficiency
Block releasea Inhibit thyroid hormone • Iopanoic acid 1 g IV stat and q8h
release from the glands for 24 h, followed by 500 mg IV
bd; or
• Lugol’s solution: 5–10 drops PO
q6–8h; or
• Potassium iodide: 5–10 drops PO
q6–8h
Beta-blocker Symptomatic relief and • Propranolol:
blocking peripheral effects {{1–2 mg/min slow IV bolus,
of excess thyroid hormones repeat q15 min till maximum

dose of 10 mg/day is
reached. Use IV route only in
hemodynamically unstable
patients
{{Tablet propranolol 40–80 mg
q4–8h
• Metoprolol 100 mg PO q6h
Bile acid To decrease entero- Cholestyramine 4 g PO q6–12h
sequestrants hepatic recycling of thyroid
hormones
a To be given at least 1 hour after the administration of PTU.
Myxedema Coma 75
CHAPTER
INTRODUCTION
Myxedema coma is a state of severe hypothyroidism in which the functioning
of every organ system in the body slows down significantly, resulting in
altered sensorium, hypothermia, and other changes due to physiological
decompensation. Common causes of hypothyroidism are given below
• Primary hypothyroidism (intrinsic dysfunction of the thyroid gland): Auto-
immune etiology (Hashimoto thyroiditis), post-ablation (surgical, radio-
iodine), infiltrative diseases (lymphoma, sarcoidosis, amyloidosis,
tuberculosis), and drugs (amiodarone, lithium).
• Secondary hypothyroidism (disorders at hypothalamic-pitutary axis): Panhy-
popituitarism, pituitary adenoma, tumours impinging on hypothalamus,
infiltrative causes (sarcoidosis, hemochromatosis).
• Dermatological manifestations: Manifestations are puffiness of the hands and
face (due to deposition of mucopolysaccharides in the dermis), thickened
nose, swollen lips, and enlarged tongue. Nonpitting pedal edema is a classical
finding.
• Neurologic manifestations: These include decreased mental status with
confusion, lethargy, obtundation, or coma. Focal or generalized seizures may
occur. Atypical forms include myxedema madness (psychotic features).
• Hyponatremia: It is seen in 50% of cases and may cause seizures or worsen the
sensorium.
• Hypothermia: It is due to decrease in thermogenesis as a result of decrease in
metabolism.
• Hypoventilation: Contributing factors include central respiratory center
depression, respiratory muscle weakness, mechanical obstruction due to the
enlarged tongue, and sleep apnea.
• Hypoglycemia: It may be caused by hypothyroidism alone or, more often, by
concurrent adrenal insufficiency.
• Cardiovascular abnormalities: These include bradycardia, decreased myo-
cardial contractility, a low cardiac output, and sometimes hypotension.
DIAGNOSIS
Diagnosis is initially based upon the history, physical examination, and exclusion
of other causes of coma.
• Primary hypothyroidism is confirmed by a high TSH and low FT4 or T3 levels.
• Secondary hypothyroidism is confirmed by a low TSH and low FT4 or T3
levels.
MANAGEMENT
General supportive care includes securing airway and breathing. Supplemental
oxygen, respiratory support, cardiac monitoring for dysrhythmias, rewarming
for hypothermia, dextrose containing fluids for hypoglycemia and correction of
electrolyte abnormalities may be required.
Thyroid Hormone Replacement

• Tablet T4 (thyronorm/eltroxin) in a loading dose of 200–400 µg followed by a
daily dose of 1.6 µg/kg.
• Tablet T3 (Cytomel) may also be given in a dose of 5–20 µg stat, followed by
2.5–10 µg q8h, depending upon the patient’s age and coexistent cardiac risk
factors.
Note: The biologic activity of T3 (triiodothyronine and liothyronine) is greater
and its onset of action is more rapid than T4 (levothyroxine).
• Hydrocortisone 100–200 mg IV q6h because of associated hypopituitarism
and secondary adrenal insufficiency. Administer steroids before thyroid
hormone replacement.
• Intravenous thyroxine can be prepared (by pharmacy) in severe cases, if
requested during an emergency.
Intravenous Thyroxine Preparation Method

• 10 tablets of 100 µg thyroxine (LT4) crushed
• 14 mg of mannitol added
• Reconstituted to make 100 mL mixture with 7.4% NaHCO3
• So 100 mL will contain 1,000 µg of thyroxine (1 mL = 10 µg). The entire content
is filtered with 0.2 µg Vygon antibacterial filter.
Adrenal Insufficiency 76
CHAPTER
ADRENAL HORMONES
• Glucocorticoids: Cortisol is the main glucocorticoid produced by the adrenal
gland.
• Mineralocorticoids: Aldosterone helps to regulate the body’s sodium and
potassium levels, blood volume, and blood pressure.
• Androgens: Testosterone, dehydroepiandrosterone (DHEA), and DHEA
sulfate.
Conversion formula for various steroids for glucocorticoid effect:
20 mg of hydrocortisone = 6 mg of deflazacortisone = 5 mg of prednisolone = 4 mg of
methylprednisolone = 1 mg of dexamethasone/betamethasone
CAUSES
• Primary adrenal insufficiency: Also known as Addisons crisis, it is due to
intrinsic adrenal gland dysfunction and results in decreased cortisol and
aldosterone production.
cc Immune-mediated: Isolated or part of polyglandular syndrome
cc Infection: Tuberculosis, histoplasmosis, and cytomegalovirus
cc Vascular: Infarction or hemorrhage
cc Infiltration: Metastatic malignancy, hemochromatosis, sarcoidosis, and
amyloidosis
cc Iatrogenic: Ketoconazole, etomidate, rifampicin, and anticonvulsants.
• Secondary adrenal insufficiency: It is due to hypothalamic-pituitary

dysfunction leading to insufficient adrenocorticotropic hormone (ACTH)
production by the pituitary. This results in cortisol deficiency only.
cc Pituitary cause: Tumor/apoplexy/infiltration/infection
cc Chronic exogenous steroid intake (>2 weeks): This is the most common
cause of adrenal insufficiency. The dose implicated is variable (even

dose <10 mg Prednisolone equivalent over 2 weeks is sufficient to cause
secondary adrenal insufficiency).
CLINICAL FEATURES
The symptoms are generalized fatigue, marked orthostatic hypotension, loss
of appetite, weight loss, nausea, vomiting, and skin hyperpigmentation (skin
creases, pressure areas, mucous membranes, and nipples seen only in primary
insufficiency).
DIAGNOSIS
• A history of chronic steroid abuse may give a clue to the diagnosis of secondary
adrenal insufficiency.
• Hyponatremia and hyperkalemia are the two major electrolyte abnormalities
of primary adrenal insufficiency.
Demonstration of inappropriately low cortisol production is the first step in
establishing the diagnosis. Send a random serum cortisol level. Plasma ACTH
level should also be sent if suspicion of adrenal insufficiency is high. Both samples
should be sent before initiating glucocorticoid therapy.
• If serum cortisol is low and plasma ACTH is high, the patient has primary
adrenal insufficiency (i.e., primary adrenal disease).
• If both serum cortisol and plasma ACTH are low, the patient has secondary
(i.e., pituitary disease) or tertiary (i.e., hypothalamic disease) adrenal
insufficiency.
MANAGEMENT
The treatment is replacement of deficient hormones.
• Injection hydrocortisone 100–200 mg IV stat followed by 100 mg q6h or
injection dexamethasone 8 mg IV q8h.
• Fluid resuscitation with crystalloids (NS/RL).
• Correct hypoglycemia and start 10% Dextrose infusion if necessary.
• Replace mineralocorticoids (fludrocortisone 100 µg PO od) after adequate
hydration. Not required when hydrocortisone is used, because hydrocortisone
has sufficient mineralocorticoid effect.
• Look for an underlying infection: If suspected, start broad-spectrum antibiotics.
Diabetic Emergencies 77
CHAPTER
HYPOGLYCEMIA
Patients are usually symptomatic at glucose levels of 50–55 mg/dL (hypoglycemic
thresholds are variable).
Causes
• Most common cause is a relative imbalance of administered versus required
insulin or oral hypoglycemic agents (OHAs).
• Alcohol
• Addison’s disease
• Pituitary insufficiency
• Insulinoma
• Liver failure
• Postgastric surgery.
Symptoms
• Neurogenic symptoms:
cc Tremors, palpitations, and anxiety or arousal (catecholamine-mediated
and adrenergic)
cc Sweating, hunger, and paresthesia (acetylcholine-mediated and
cholinergic).
• Neuroglycopenic symptoms:
cc Cognitive impairment, behavioral changes, psychomotor abnormalities
and at lower plasma glucose concentrations, seizure, and coma.
Management
• Conscious patient: Oral simple carbohydrates (sugar and glucose powder).
• Unconscious patient: Administer 50% Dextrose 100 mL intravenous (IV) stat
followed by 10% dextrose 500 mL over 4 hours till hypoglycemia is corrected.
• In cases of OHA overdose or refractory hypoglycemia, continue 10% Dextrose
infusion for 8–12 hours.
• Monitor general random blood sugar (GRBS) every 2 hours.
• Look for the etiology of hypoglycemia, evaluate and treat it.
Discharge Recommendation
• If due to OHA or insulin excess, stop OHA for 2 days or decrease the dose of
insulin for the next 2 days
• Advice the patient to always keep simple sugars with them at all times and
take it as soon as symptoms start
• Refer the patient to follow up in Medicine OPD with AC/PC and HbA1C.
DIABETIC KETOACIDOSIS
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of
diabetes that mainly occurs in patients with type 1 diabetes mellitus (T1DM),
but it is not uncommon in some patients with type 2 diabetes mellitus (T2DM).
Three ketone bodies are produced and accumulate in DKA: Acetoacetic acid (true
ketoacid), beta-hydroxybutyric acid and acetone. Nitroprusside test commonly
used for urine ketones detects only acetoacetic acid; hence may be falsely negative
in DKA and also can not be relied upon to quantify the severity of acidosis. Direct
serum assays for beta-hydroxybutyrate have become the preferred diagnostic
tests.
Clinical Features
• The most common early symptoms of DKA are insidious increase in polydipsia
and polyuria.
• Malaise, generalized weakness, fatigability, altered sensorium, and associated
symptoms of infections may be seen.
• Patients would be extremely dehydrated with a fluid deficit of at least 6 liters.
Examination: If the GRBS is high, look for dryness of tongue and start IV fluids immediately
before performing any test. Fluid resuscitation is lifesaving.
Precipitating Cause
• Look for any precipitating cause and address it
• Common precipitating causes—The 5Is
cc Insulin—nonadherence
cc Infection or inflammation
cc Ischemia or infarction
cc Intra-abdominal process—pancreatitis, cholecystitis, appendicitis,

splenic injury, and ischemic bowel
cc Iatrogenic—steroid use.
Diagnostic Triad
• High plasma sugar level (>250 mg%)
CHAPTER 77: Diabetic Emergencies 267
• Ketosis: Urine ketones positive (2+ or 3+. Remember that ketone 1+ positive
is a common finding and does not mean ketosis). If available, serum ketones
>3 mmol/L is more accurate and diagnostic of diabetic ketosis.
• Acidosis: Serum bicarbonate < 18 mEq/L or ABG pH < 7.30.
Management
The order of therapeutic priorities is fluids first, then potassium correction and
then insulin administration.
Fluid Resuscitation
This is the most important step. Start normal saline (NS) at the following rate
(Rule of diminishing of ½)
• NS 1,000 mL over 30 minutes
• NS 500 mL over 30 minutes
• NS 500 mL over 60 minutes
• NS 500 mL every 2 hours till fluid deficit is corrected.
Tailor the above rates with the patient’s cardiopulmonary status. Reassess
every 2 hour and look for fluid overload.
Restrict fluids in those with congestive cardiac failure or pulmonary edema.
Type of Fluid
• Initial replacement: NS
• If serum Na+ >155 mEq/L, use ½ NS
• Once GRBS is <250 mg%, change the infusate to 5% Dextrose. Do not stop
insulin infusion.
Insulin Administration
• Administer a bolus of 10 units IV regular insulin.
• Insulin infusion at 6 units/h and check the GRBS q1h.
• The expected decline of the glucose per hour is 50 mg/dL. If not, increase
the infusion by 2 units/h (consider a bolus of 4 units insulin if the GRBS is
persistently high and does not show a decreasing trend).
• If significant hypokalemia exists (K+ <3 mEq/L), do not start insulin infusion
or give the bolus dose until IV KCl supplementation is initiated urgently.
• When blood glucose levels reach 250 mg%, decrease insulin infusion to 4 units
per hour and change infusate to 5% Dextrose. Do not stop insulin infusion. If
blood sugars continue to drop, change infusate to 10% Dextrose.
Potassium Correction
• Metabolic acidosis results in pseudohyperkalemia and the actual K levels may
be lower than the result shown.
• Start K+ correction unless K level is >5 mEq/L.
• If K+ is <5 mEq/L, add 1.5–4.5 g KCl in 1,000 mL NS over 4 hours as a parallel

infusion.
• Decrease the amount of KCl supplementation in patients with renal failure.
Treat the Precipitating Cause

If there is any evidence of infection, start broad-spectrum antibiotics, i.e.,
carbapenems.
Correct Severe Metabolic Acidosis

• Administer NaHCO3 only if the serum pH is less than 6.9. Give 100 mL bolus
followed by 10 mL/h infusion.
• There is no role for dialysis in patients with DKA.
Correct Other Electrolyte Abnormalities

Serum phosphate usually falls during treatment as it moves intracellularly with
potassium. Supplement with Syrup Neutral phosphate 30 mL stat and repeat dose
based on serum phosphorus levels.
Every patient with DKA should have at least three IV lines. One each for IV fluids, insulin
infusion, and K correction. Additional lines for antibiotics or NaHCO3 may be needed.
Start a central line at the earliest.
HYPEROSMOTIC HYPERGLYCEMIC NONKETOTIC STATE

(HHNK)
The HHNK is characterized by progressive hyperglycemia and hyperosmolarity
typically in debilitated elderly patients with undiagnosed or poorly controlled
diabetes mellitus, limited access to water and a precipitating illness. This
condition, unlike DKA, evolves over days or weeks and the patient complaints of
fatigue, anorexia, dyspnea, chest or abdominal pain or a neurological complaint.
This condition is characterized by hyperglycemia, dehydration, and serum
hyperosmolarity without ketosis or significant acidosis.
Diagnosis
• Very high plasma glucose levels
• High plasma osmolality: >350 mOsm/kg
• No metabolic acidosis.
Differences between DKA and HHNK

• The amount of fluid deficit is much higher in HHNK (average deficit 10–12 L).
• Glucose levels are usually very high in HHNK.
CHAPTER 77: Diabetic Emergencies 269
• Hypernatremia is common in HHNK. If present, use ½ NS or ¼ NS as the

replacement fluid.
• Use lesser doses of insulin (typically half the dose used in DKA) in HHNK as
these patients may be more sensitive to insulin action.
Management
Management is similar to DKA management, except the above-mentioned
differences.
SLIDING SCALE FOR INSULIN ADMINISTRATION

Intravenous infusion of short-acting actrapid insulin, 1 mL (40 units) in 39 mL of
NS, to be adjusted according to GRBS every 2 hours (Table 1).
TABLE 1: Sliding scale for insulin infusion.

GRBS (mg%) Insulin infusion rate
<80 No insulin
81–150 0.5
151–200 1
201–250 1.5
251–300 2
301–350 2.5
351–400 3
401–450 4
451–500 5
>500 6.0
(GRBS: General random blood sugar)
Pheochromocytoma 78
CHAPTER
INTRODUCTION
Catecholamine-secreting tumors that arise from chromaffin cells of the adrenal
medulla and the sympathetic ganglia are referred to as “pheochromocytomas”
and “catecholamine-secreting paragangliomas” (extra-adrenal pheochromo-
cytomas), respectively.
The classic triad of symptoms in patients with a pheochromocytoma consists
of episodic headache, sweating, and tachycardia. About 50% have paroxysmal
hypertension. Patients are usually volume depleted at presentation and should
be rehydrated prior to initiation of therapy.
LABORATORY INVESTIGATIONS
• 24 hours urine measurement of catecholamines (metanephrine and
normetanephrine).
• If the biochemical results are abnormal, abdominal imaging with CT/MRI is
needed to locate the tumor.
MANAGEMENT
• Adequate fluid replacement.
• Acute hypertensive crisis: Phentolamine 2–5 mg intravenous bolus and repeat
every 15–20 minutes as necessary. Alternate drug is nitroprusside infusion
(0.5–1.5 µg/kg/min and titrate).
• To prepare a patient for surgery, initiate alpha-blockade with prazosin XL
2.5 mg PO daily and increase to 10 mg PO over 1 week. Phenoxybenzamine
10 mg PO daily and increase gradually to 40 mg PO tid may also be tried. Once
blood pressure is controlled with alpha-blockade, add propranolol 10–20 mg
PO tid.
• Do not administer beta-blocker without adequate alpha-blockade as
unopposed alpha receptor stimulation can precipitate a hypertensive crisis.
Section 12
Obstetric and
Gynecological Emergencies
Ectopic Pregnancy 79
CHAPTER
INTRODUCTION
Ectopic pregnancy is an extrauterine pregnancy and is the most common cause
of maternal mortality in the first trimester. There must be a high risk of suspicion
of ectopic pregnancy among young women presenting with abdominal pain or
vaginal bleeding especially, if associated with syncope.
• Almost all ectopic pregnancies occur in the Fallopian tube (98%).
• Other possible types include cervical, interstitial, hysterectomy scar, intramural,
ovarian, or abdominal. Rare cases of multiple gestations may include both
uterine and extrauterine pregnancy.
Clinical presentation includes first trimester vaginal bleeding and/or abdominal
pain. It can manifest as syncope or may also be asymptomatic.
Ruptured versus unruptured ectopic pregnancy: At the time of presentation, an
ectopic pregnancy may be ruptured or unruptured.
The typical findings of a rupture are abdominal pain, shoulder pain (due
to diaphragmatic irritation by blood in the peritoneal cavity) and eventually,
hypotension or shock. Abdominal examination findings include tenderness and
possible peritoneal signs.
DIAGNOSTIC EVALUATION
• History of amenorrhea: Ask for last menstrual period (remember sometimes,
there may not be a period of amenorrhea)
• Confirm that the patient is pregnant: Urine pregcolor test
• Send blood investigations: Complete blood count, electrolytes, creatinine,
rapid blood borne virus screen (BBVS).
• Serum beta-human chorionic gonadotropin (β-hCG): Serum β hCG levels
approximately doubles every 2 days in a normal pregnancy and a longer
doubling time indicates a pathologic pregnancy, Hence, a single serum β hCG
level cannot be used to reliably distinguish between a normal pregnancy and
an ectopic pregnancy and a repeat test after 48 hours is required to confirm
the diagnosis. In an ectopic pregnancy, β hCG levels typically decrease or
plateau after 48 hours.
274 SECTION 12: Obstetric and Gynecological Emergencies
• Transabdominal ultrasonography (USG): The primary role of a transabdominal

USG in suspected ectopic pregnancy is to determine if an intrauterine
pregnancy (IUP) is present. An embryo with cardiac activity seen within the
uterine cavity is called a 'viable IUP'.
• Transvaginal ultrasound (TVUS): TVUS typically shows an extrauterine
gestational sac with a yolk sac or embryo with or without a heartbeat. There
would be no evidence of an intrauterine pregnancy.
• An empty uterus with embryonic cardiac activity visualized outside the uterus
is diagnostic of ectopic pregnancy.
• Differential diagnosis includes spontaneous abortion, subchorionic hema-
toma, gestational trophoblastic disease, cervical polyp.
MANAGEMENT
• Start large bore intravenous cannula and resuscitate the patient with
crystalloids.
• Send crossmatch for blood if bleeding is severe.
• Refer to Obstetrician/Gynecologist for TVUS or ultrasonography of abdomen
and for further management.
Medical management: Methotrexate as a single dose or in a multiple dose protocol
can be used for medical management. It inhibits cell division in rapidly growing
cells like in the trophoblast. Methotrexate may be administered as a systemic
intramuscular injection or by direct injection into the ectopic gestational sac by
laparoscopy or under USG guidance. Lower abdominal pain (75%), flatulence
and stomatitis are side effects of local methotrexate therapy. Complications
include tubal rupture that may present with vaginal bleeding, abdominal pain,
weakness or syncope after treatment.
Surgical management: Surgical options include laparoscopic salpingostomy or
salpingectomy. The products of conception are removed and the fallopian tubes
are left open to heal by secondary intention.
Alloimmunization: There is a potential risk of Rh seroconversion if a small amount
of fetal blood mixes with the mother's after 6 weeks of gestation. Hence, all Rh
negative women with ectopic pregnancy must be administered 300 microgram
of anti-RhD immunoglobulin.
Bleeding Per Vagina 80
CHAPTER
INTRODUCTION
Bleeding per vagina (PV) may occur in the pregnant and the nonpregnant women.
This chapter deals with management of bleeding PV in the nonpregnant patient.
A normal cycle is between 21 and 35 days. Blood loss is usually >80 mL and
lasts <7 days. About 60% of those who complain of heavy bleeding actually have
normal bleeding.
Etiology of bleeding PV can be classified as follows:
• Gynecological: Heavy menstrual bleeding, adenomyosis, endometrial
hyperplasia, uterine fibroids, pelvic inflammatory disease, polycystic ovarian
syndrome, sexual abuse, cervical cancer, cervical polyps, and intrauterine
contraceptive device.
• Hematological: Thrombocytopenia (immune thrombocytopenic purpura or
dengue), coagulopathy, disseminated intravascular coagulation, and hemo-
philia/von Willebrand factor deficiency.
• Obstetric: Ectopic pregnancy, threatened abortion, abruptio placenta or
placenta previa (later trimester).
ABNORMAL UTERINE BLEEDING

Evaluation of a patient with abnormal uterine bleeding (AUB) involves good
history taking and clinical examination, which includes per speculum examina-
tion and vaginal examination.1 AUB can be classified based on the PALM-COEIN
classification as follows
Structural Causes
Polyps: Endometrial polyps are epithelial proliferations arising from the endo-
metrial stroma and glands. The majority are asymptomatic. Polyps may occur on
their own or may coexist with leiomyomas.
Adenomyosis: Typically, adenomyosis occurs with increasing age and is associated
with dysmenorrhea. Adenomyosis may be focal or diffuse and may coexist with
leiomyomas.
Leiomyomas: Often referred to as uterine fibroids/myomas, they can be classified
based on location as intramural, submucosal, subserosal, and cervical myomas.
Malignancy or hyperplasia: Endometrial hyperplasia and malignancy should
be ruled out especially in the perimenopausal age group and in those with risk
276 SECTION 12: Obstetric and Gynecological Emergencies
factors such as obesity and diabetes. Cervical cancer as well as other gynecological
cancers must also be kept in mind during evaluation of a patient.
Nonstructural Causes
Coagulopathy: Often due to von Willebrand disease, coagulopathy can be
assessed by history regarding bleeding tendencies such as postsurgical bleeding,
especially dental procedures, easy bruisability, gum bleeding, and family history
of bleeding disorders.
Ovulatory: An ovulatory cycle may contribute to AUB by unopposed estrogen
effects on the endometrium causing marked proliferation and thickening resulting
in heavy menstrual bleeding along with an altered frequency of menstruation.
This is observed at the extremes of reproductive age; however, impact on the
hypothalamic-pituitary-ovarian axis along with endocrinopathies is also present.
The latter include polycystic ovarian syndrome (PCOS), hyperprolactinemia,
hypothyroidism as well as factors such as obesity, anorexia, weight loss, mental
stress, and extreme exercise.
Endometrial: AUB that occurs in the context of a structurally normal uterus with
regular menstrual cycles without evidence of coagulopathy is likely to have an
underlying endometrial cause. Perturbations of local glucocorticoid metabolism,
aberrant prostaglandin synthesis, and excessive plasminogen (resulting in pre-
mature clot lysis) have all been implicated in AUB.
Iatrogenic: These include exogenous hormone therapy, which can cause
unscheduled menstrual bleeding. The use of an intrauterine device may also
cause endometritis leading to spotting.
Not otherwise classified: These include arteriovenous malformation, endometrial
pseudoaneurysm, etc.
MANAGEMENT OF VAGINAL BLEEDING IN A

NONPREGNANT PATIENT
• Tranexamic acid: Administer tranexamic acid 500 mg stat and q6h as an
antifibrinolytic agent.
• Progestogen therapy: Tablet norethisterone (Primolut N) 10 mg or medroxy-
progesterone 10 mg q6h for 24–48 hours till bleeding stops. Then:
cc 10 mg q8h × 3 days
cc 10 mg q12h × 3 days
cc 10 mg OD × 15 days and stop
• Estrogen therapy: Ethinyl estradiol 50 mcg od can be used for 5 days.

When bleeding stops, add medroxyprogesterone or an estrogen progestin
combination in the usual dose for the rest of the cycle. Stop for synchronized
withdrawal bleed.
CHAPTER 80: Bleeding Per Vagina 277
• High-dose oral contraceptive pills: OCPs containing 30 mcg ethinyl estradiol

given 8th hourly for 48–72 h until bleeding stops and can then be tapered by
giving twice a day for 5 days followed by once a day for 2 weeks.
• Blood products: If the patient has severe anemia in failure, transfuse packed
red cells. Correct any obvious coagulopathy or thrombocytopenia with fresh
frozen plasma/cryoprecipitate/platelets as indicated.
• If the patient is hemodynamically stable and bleeding is mild, discharge on
tranexamic acid with or without progestogens and advice to follow up in
obstetrics OPD with an USG abdomen.
• Perform a pregnancy test for any patient with bleeding PV in the reproductive
age group, if there is a recent history of sexual activity. If a threatened abortion
is suspected, perform a vaginal examination and an ultrasound in order to
decide plan of management.
REFERENCE
1. Munro MG, Critchley HO, Fraser IS, FIGO Menstrual Disorders Committee. The two FIGO systems for normal
and abnormal uterine bleeding symptoms and classification of causes of abnormal uterine bleeding in the
reproductive years: 2018 revisions. Int J Gynecol Obstet.2018;143:393-408.
Hyperemesis
Gravidarum 81
CHAPTER
INTRODUCTION
Nausea with or without vomiting is a common symptom in the first trimester of
pregnancy, seen in about 60–80% of all pregnancies. Hyperemesis gravidarum, seen
in about 2% of all pregnancies, refers to severe nausea and vomiting resulting in
dehydration, ketosis, weight loss, electrolytes and acid-base imbalances, nutritional
deficiencies, and even death. These symptoms usually resolve spontaneously
by mid-pregnancy. The presence of abdominal pain, however, is highly unusual
and suggests an alternate diagnosis such as cholelithiasis or cholecystitis (more
common in pregnancy), pancreatitis, gastroenteritis, pyelonephritis, hepatitis or
ectopic pregnancy.
EVALUATION
Physical examination is usually normal except for signs of dehydration. Laboratory
investigations include complete blood count (CBC), electrolytes, creatinine,
urea, and urine ketone. The presence of ketonuria is an important finding as it
an early sign of starvation. Serial measurements of urine ketones may be done to
determine adequacy of rehydration therapy.
MANAGEMENT
• Assess hydration status and start intravenous (IV) fluids [normal saline/
Ringer’s lactate (NS/RL)]. If ketones are positive, use 5% Dextrose or DNS
instead of RL. Initially, keep the patient nil per oral till symptoms of nausea
subsides.
• Proton pump inhibitor (pantoprazole) and antiemetic (metoclopramide/
ondansetron).
• If the patient is experiencing persistent vomiting, it is important to replenish
low levels of vitamins like thiamine (100 mg IV stat and od for 2–3 days).
• If there is no dehydration and nausea resolves with symptomatic treatment,
the patient can be discharged on antiemetics (doxylamine succinate +
pyridoxine + folic acid twice daily: Commonly available as doxinate tablet)
and to follow-up in OPD.
Pelvic Inflammatory
Disease 82
CHAPTER
INTRODUCTION
Pelvic inflammatory disease (PID) is primarily a disease of sexually active women.
It includes a spectrum of acute infections of the upper genital tract structures
in women (salpingitis, endometritis, myometritis, parametritis, oophoritis,
and tubo-ovarian abscess). Any one or all of the genital tract structures may be
involved. The minimum criteria required to make a presumptive clinical diagnosis
of PID in sexually active young women are:
• Lower abdominal tenderness
• Adnexal tenderness, and
• Cervical motion tenderness.
ETIOLOGY
Most common sexually transmitted organisms that cause the disease are
Chlamydia trachomatis and Neisseria gonorrhoeae. These originate in the lower
genital tract and ascend to the upper tract. Other organisms include herpes simplex
virus, trichomonas vaginalis, mycoplasma genitalium, Ureaplasma urealyticum,
Gardanella vaginalis, Bacteroides species, etc.
Complications include tubo-ovarian abscess, scarring and adhesions of the
fallopian tubes, infertility, chronic pelvic pain, and dyspareunia.
MANAGEMENT
There is no single diagnostic test for PID. Evaluation of any woman in the
reproductive age group in the ED should include a pregnancy test. Consider the
possibility of an ectopic pregnancy or septic abortion.
• Analgesics: (Mefenamic acid 500 mg + dicyclomine 20 mg), NSAIDs and
paracetamol if required for pain relief.
• Antibiotics: Empiric antibiotic therapy is recommended to patients with
suspected PID. The regimen must be tailored to local antibiotic resistance
pattern. Doxycycline 100 mg PO BD/azithromycin 500 mg PO od plus
metronidazole 500 mg PO q8h × 5–10 days is the most commonly used
regimen. Injection ceftriaxone 250 mg IM single dose plus doxycycline 100 mg
PO BD × 14 days is an alternate option.
• Patients who do not respond to 72 hours of antibiotic therapy may require
laparoscopic or surgical interventions like drainage of tubo-ovarian abscess
or pus loculations
• If an intra-uterine device (IUD) is present, it should be removed after initiation
of antibiotics.
Ovarian Torsion 83
CHAPTER
INTRODUCTION
Ovarian torsion is a gynecological emergency where the ovary either partially or
completely twists on its ligamentous supports. This often results in impedance of
its blood supply.
When the fallopian tube twists along with the ovary, it is referred to as adnexal
torsion.
• Torsion is commonly seen in young girls in the reproductive age group
because of regular formation of a corpus luteal cyst during the menstrual
cycle. Up to 80% of cases of ovarian torsion are associated with a benign
ovarian malignancy.
• Acute onset of moderate to severe pelvic pain, adnexal mass, often with
nausea, vomiting, and fever. A recent vigorous activity (often intercourse) may
be an inciting event.
• Fever may be a marker of adnexal necrosis, particularly in the setting of
leukocytosis.
INVESTIGATIONS
The investigations to be sent are complete blood count (CBC), electrolytes,
creatinine, and urea.
• Urine Pregcolor test should carried out in the reproductive age group to rule
out an ectopic pregnancy.
• If surgical intervention is required: Rapid blood borne virus screen (BBVS)
• Arrange for an USG of the abdomen and pelvis. USG findings include enlarged
ovary with a heterogeneous stroma and small peripherally displaced follicles,
ovarian mass or evidence of hemorrhage.
• Doppler ultrasound scan is inconsistent due to dual blood supply of the
ovary from both ovarian and uterine arteries. Despite this limitation, doppler
may still be useful if abnormal venous flow is demonstrated. Visualization of
the twisting of the pedicle with coiled vessels, known as 'whirlpool sign' is an
accurate sign of adnexal torsion.
CHAPTER 83: Ovarian Torsion 281
DIFFERENTIAL DIAGNOSIS
• Ectopic pregnancy: A negative serum human chorionic gonadotropin (HCG)
and a pregcolor test excludes ectopic pregnancy.
• Ruptured ovarian cyst: Pelvic pain is often at midcycle. May have a history
of vigorous physical activity as an inciting agent. Can be differentiated by
sonography.
• Tubo-ovarian abscess: The clinical course is usually indolent and associated
with fever.
• Appendicitis: Can be difficult to differentiate clinically. Sonography required
to confirm ovarian torsion.
• Renal calculi: Typical pain starts in either flank and is colicky in nature.
• Pyelonephritis: Associated with fever and dysuria. Urinalysis findings of
leucocytes or pyuria in this setting can confirm the diagnosis of pyelonephritis.
MANAGEMENT
• Administer analgesics for pain relief. Administer morphine 5 mg IV/SC or
tramadol 50 mg IV and repeat doses as required.
• The mainstay of treatment of ovarian torsion is swift operative evaluation to
preserve ovarian function and prevent other adverse effects (e.g., hemorrhage,
peritonitis, and adhesion formation).
• Most torsed ovaries are considered potentially viable, unless there is a clearly
necrotic appearance. Ovaries are usually salvageable if the patient is taken up
to the operating room within 8 hours of onset of symptoms.
• Refer to Obstetrician/Gynecologist.
Pregnancy Induced
Hypertension (Preeclampsia
and Eclampsia) 84
CHAPTER
INTRODUCTION
Hypertensive disorders occur in 6–8% of pregnancies with various grades of
severity.
• Gestational hypertension characterized by elevated blood pressure (BP) of
>140/90 mm Hg that starts in pregnancy and usually resolves within 6 weeks
of the postpartum period.
• Preeclampsia is a gestational hypertension associated with proteinuria
(>300 mg/24 h).
• Eclampsia is a severe complication of preeclampsia characterized by the
occurrence of new onset generalized tonic-clonic seizure (GTCS) or coma.
It occurs after the 20th week of gestation or in the immediate postpartum
period, for up to 3 weeks.
• HELLP syndrome (Hemolysis, Elevated liver enzymes and low platelets) is a
variant of pre-eclampsia often seen in multi-gravid patients. It is characterized
by epigastric or right upper quadrant pain and must be considered in any
pregnant or postpartum patient presenting to the ED with abdominal pain as
the chief complaint.
• Gestational hypertension presents with elevated systolic or diastolic blood
pressure with no proteinuria or evidence of organ damage.
• Preeclampsia is associated with proteinuria and evidence of vasospastic
effects in end organs. Symptoms include headache, right hyochondrial or
epigastric pain, visual disturbances (scotoma, loss of vision, diplopia, visual
field defects). Laboratory abnormalities include thrombocytopenia, elevated
creatinine and LFT derangement.
• Eclapmsia is characterized by the occurrence of seizures (usually GTCS) or
coma in the setting of preeclampsia. One third of eclampsia seizures occur
in the 28 day postpartum period, but usually in the first 48 hours of delivery.
Complications of preeclampsia, eclampsia and HELLP syndrome include
fetal death, abruptio placentae, neurological damage from recurrent seizures,
intracranial bleeding, hepatic or splenic hemorrhages, and acute renal failure.
CHAPTER 84: Pregnancy Induced Hypertension (Preeclampsia and Eclampsia) 283
DIAGNOSIS
Eclampsia is a purely clinical diagnosis made in a patient with pre-eclampsia
presenting with new onset GTCS with or without an elevated BP. All patients with
a sustained BP of >140/90 mm Hg with any symptom secondary to hypertension
need to considered for hospitalization and evaluation by an obstetrician.
MANAGEMENT
• Prevention of maternal hypoxia and trauma: Place the patient in left lateral
position and administer supplemental oxygen (4–5 L/min).
• Treatment of hypertension, if present: Injection labetalol 20 mg intravenous
(IV) is given over 2 minutes and the dose may be repeated at 10-minute
intervals. If not available, tablet nifedipine R 10 mg may be given orally. The
drug of choice for chronic hypertension is methyldopa (250 mg q6h and
titrated higher) due to its safety profile to the fetus.
• Active seizures: The anticonvulsive drug of choice is magnesium sulfate.
cc Loading dose: 4 g IV over 15–20 minutes (20% solution)
cc Maintenance dose: 1 g/h as a continuous IV infusion.
• Recurrent seizures in patients on maintenance MgSO4 therapy can be treated

with an additional bolus of 2 g MgSO4 over 5–10 minutes, with frequent
monitoring for signs of Mg toxicity (e.g., loss of patellar reflex, respiratory rate
<12/min and oliguria).
• If seizures persist, midazolam or lorazepam infusion may be started. If patient
is in status, mechanically ventilate and treat like status epilepticus.
• Evaluation for prompt delivery: The treatment of pre-eclampsia is delivery of
the fetus. This decision is more complicated in mild pre-eclampsia and when
the fetus of <37 weeks of gestation.
Postpartum Hemorrhage 85
CHAPTER
INTRODUCTION
Postpartum bleeding or hemorrhage is defined as the loss of >500 mL of blood
within the first 24 hours postpartum in a woman who has had a normal vaginal
delivery or >1,000 mL in a woman who has had a cesarean section.
It may also be defined as a decrease in hemoglobin of 10% from baseline
within the first 24 hours postpartum. It is one of the leading causes of maternal
mortality. Most cases are due to uterine atony, the remainder is due to traumatic
causes.
CLINICAL FEATURES
Orthostatic hypotension, fatigue, and anemia result from moderate bleeding.
In severe cases, the hypovolemic shock may cause anterior pituitary necrosis
(Sheehan’s syndrome). Myocardial ischemia and dilutional coagulopathy may
also occur. The risk of postpartum depression is increased in these patients
making the care of the newborn more difficult.
In patients with significant coagulopathy, consider other possibilities like
abruptio placenta, HELLP (hemolysis, elevated liver enzyme levels, and low
platelet levels) syndrome, and fatty liver of pregnancy or septicemia.
INVESTIGATIONS
The investigations to be sent are complete blood count (CBC), electrolytes,
creatinine, cross-match for packed cells, and rapid blood borne virus screen
(BBVS).
• If coagulopathy is suspected: Prothrombin time (PT), activated partial
thromboplastin time (aPTT), and fibrinogen.
MANAGEMENT
• Fluid resuscitation: Secure IV access with 2 large bore peripheral IV cannulae
and start fluid resuscitation with crystalloids (NS/RL)
• Blood transfusion:
cc Packed red blood cells depending on the degree of blood loss
cc Fresh frozen plasma and cryoprecipitate are required if the patient has
dilutional coagulopathy.
cc Consider activating massive transfusion protocol for significant bleeding
CHAPTER 85: Postpartum Hemorrhage 285
• Determine if the cause of postpartum hemorrhage (PPH) is an atonic uterus

or a traumatic cause. Uterine atony can be determined by placing the hand on
the uterine fundus and finding a boggy, soft uterus.
cc If the uterus is atonic, medical management should be initiated
immediately.
– Commence bimanual massage: Place one hand on the fundus and the
other hand anterior to the cervix in the vagina and massage.
– Administer oxytocin 20 units IV in 500 mL RL/NS bolus followed by a
10 units IM dose. Then, add 40 units in 1 L NS and run as an infusion
over 4 hours.
– If bleeding continues, methylergometrine (methergine) 0.2 mg IM
and repeat the dose every 30 minutes up to a maximum of three doses
(contraindicated in hypertension and ischemic heart disease).
– If bleeding continues, give prostaglandin F2 alpha. 250 µg IM q15
minutes up to a maximum of eight doses.
– Misoprostol 800 µg rectally can be given in severe cases.
cc If the PPH is likely to be traumatic in origin:
– Explore the uterine cavity and control bleeding by packing the uterine
cavity rolled gauze to create a tamponade effect.
– Look for any bleeding vessel in the cervix and vagina and ligate it.
– After delivery, if pain and uterine bleeding is persistent despite the use
of uterotonic agents, consider the possibility of uterine rupture with or
without intra-abdominal bleeding. Palpation of the uterine cavity may
reveal the opening which may be anterior, posterior, fundal or lateral.
Consider uterine arterial embolization or surgical intervention, if the
bleeding is uncontrolled.
– If a mass is seen in the vaginal vault and the uterus cannot be palpated
per abdominally, consider the possibility of an uterine inversion.
• Administer tranexamic acid for its anti-fibrinolytic activity in controlling
hemorrhage. Dose: 1 g IV over 10 minutes, followed by IV infusion of 1 g over
8 hours.
Section 13
ENT Emergencies
Epistaxis 86
CHAPTER
INTRODUCTION
Epistaxis is a common problem, occurring in up to 60% of the general population.
ANATOMY
Epistaxis may be classified as anterior or posterior, depending upon the source of
bleeding.
Anterior Bleeds
Anterior bleeds are by far the most common source of bleeding. Up to 90% occur
within the vascular watershed area of the nasal septum known as Kiesselbach’s
plexus (Fig. 1). Anastomosis of four primary vessels occurs in this area:
• Septal branch of the anterior ethmoidal artery
• Lateral nasal branch of the sphenopalatine artery
• Septal branch of the superior labial branch of the facial artery
• Greater palatine artery.
FIG. 1: Kiesselbach’s plexus.

290 SECTION 13: ENT Emergencies
Posterior Bleeds
Posterior bleed arises most commonly from the posterolateral branches of the
sphenopalatine artery and Woodruff’s venous plexus in hypertensives, but may
also arise from the carotid artery.
MANAGEMENT
• Grasp and pinch the nose and maintain continuous pressure.
• Apply a few cubes of ice wrapped in a cloth over the bridge of the nose.
• Maintain airway. If patient is conscious, maintain a propped up position
leaning forward to prevent aspiration.
• Start IV line. Start crystalloids if there is evidence of hemodynamic shock.
• If the patient is a hypertensive, control blood pressure (BP) aggressively.
However, patients frequently have elevated BP due to stress, adequate
analgesia, and mild sedation helps to lower BP.
• If the patient is on anticoagulants, check prothrombin time/activated partial
thromboplastin time and correct the coagulopathy.
• Refer to ENT for further management.
Nasal Packing
Nasal packing is most easily accomplished with a nasal tampon. These are usually
made of Merocel, a synthetic open-cell foam polymer that appears to provide a
less hospitable medium for Staphylococcus aureus than traditional gauze packing.
It is inserted as follows:
• Ask the patient to sit and look directly ahead and attempt the sniffing position.
Patients often try to tilt the head back to facilitate a nasal examination, but the
nasopharynx lies in the anteroposterior plane and extension of the neck will
obscure most of the cavity from view.
• After positioning the patient properly, pretreat with a topical anesthetic (e.g.,
2% Lidocaine) and topical vasoconstrictor (e.g., Oxymetazoline).
• Coat the tampon with bacitracin ointment to facilitate placement, and possibly
decrease the risk of toxic shock syndrome.
• Insert the tampon by sliding it directly along the floor of the nasal cavity until
nearly the entire tampon lies within the nasal cavity.
Stridor 87
CHAPTER
INTRODUCTION
Stridor is an abnormal, high-pitched sound produced by turbulent airflow through
a partially obstructed airway at the level of the supraglottis, glottis, subglottis, or
trachea.
It can occur during inspiration, expiration, or both, although it most typically
occurs with inspiration.
• Inspiratory stridor suggests a laryngeal obstruction
• Expiratory stridor implies tracheobronchial obstruction
• Biphasic stridor suggests a subglottic or glottic anomaly.
ETIOLOGY
In Children
Stridor occurs due to the following: Laryngotracheobronchitis, foreign body
aspiration, bacterial tracheitis, retropharyngeal abscess, peritonsillar abscess,
epiglottitis, and laryngomalacia.
In Adults
Stridor may be due to the following reasons:
• Malignancies of larynx, trachea, or esophagus.
• Superior vena cava (SVC) syndrome may cause stridor due to secondary
interstitial edema of the head and neck, which may narrow the lumen of the
nasal passages and larynx.
• Patients on radiotherapy for malignancies of the head and neck.
• Tracheal stricture due to previous endotracheal intubation or tracheostomy.
• Foreign body aspiration.
MANAGEMENT
• Maintain airway: If possible, perform endotracheal intubation. Tracheostomy
may be required for laryngeal abnormalities.
• Start oxygen supplementation.
• Corticosteroids: Inj. Hydrocortisone 100–200 mg IV stat.
• Adrenaline nebulizations: 1 in 10,000 dilution (1 mL Adrenaline in 9 mL NS).
Take 1 mL for nebulization every 10 minutes till definite treatment is done.
• Antibiotics: For epiglottitis, bacterial tracheitis, retropharyngeal abscess, and
peritonsillar abscess (Amoxicillin-Clavulanate/Ceftriaxone).
• Refer to ENT urgently.
Vertigo and Benign
Paroxysmal Positional
Vertigo 88
CHAPTER
VERTIGO
Vertigo is a symptom of illusory movement (feels as if the person or the objects
around them are moving when they are not).
It arises because of asymmetry in the vestibular system due to damage to or
dysfunction of the labyrinth, vestibular nerve, or central vestibular structures in
the brainstem. The evaluation of a patient with vertigo is shown in Flowchart 1.
The common causes of vertigo are shown in Table 1 and the clinical features of
the common causes are shown in Table 2.
FLOWCHART 1: Evaluation of a patient with vertigo.

CHAPTER 88: Vertigo and Benign Paroxysmal Positional Vertigo 293
TABLE 1: Causes of vertigo.

Peripheral causes Central causes
• Benign paroxysmal positional vertigo • Vestibular migraine
• Vestibular neuritis • Brainstem ischemia
• Ménière's disease • Cerebellar infarction and
• Herpes zoster oticus hemorrhage
• Labyrinthine concussion
• Otitis media
TABLE 2: Clinical features of common causes of vertigo.

Time course Suggestive Associated Auditory Other
clinical neurologic symptoms diagnostic
setting symptoms features
Benign Recurrent, Predictable None None Dix–Hallpike
paroxysmal brief head maneuver is
positional movement/ diagnostic
vertigo positions
precipitate
symptoms
Vestibular Single Accompa- Falls toward Usually none Head thrust
neuritis episode, nying viral side of lesion test usually
acute onset, syndrome and no abnormal
may last brainstem
days signs
Ménière's Recurrent Spontane- None May be Audiometry
disease episodes, ous onset preceded by shows U/L
last minutes ear pain, U/L sensorineu-
to several hearing loss, ral hearing
hours and tinnitus loss
Vestibular Recurrent History of Migraine Usually none Between
migraine episodes, migraine headache episodes,
(peripheral)/ last several and/or other tests are
central minutes-to- migrainous usually
nystagnus) hours symptoms normal
BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)

It is most commonly attributed to calcium debris within the posterior semi-
circular canal, known as canalithiasis. This debris likely represents loose otoconia
(calcium carbonate crystals) within the auricular sac. These are normal structures
that are displaced from the utricle. There are three variants:
1. Posterior canal (prototype/classical)
2. Anterior canal (superior canal)
3. Horizontal canal.
Posterior Canal Benign Paroxysmal Positional Vertigo

(Prototype/Classical)
Recurrent episodes of vertigo lasting 1 minute or less. Although individual
episodes are brief, these typically recur periodically for weeks-to-months without
therapy.
Episodes are provoked by specific types of head movements, such as looking
up while standing or sitting, lying down or getting up from bed, and rolling over in
bed. The spells may wax and wane over the time.
The vertigo may be associated with nausea and vomiting.
Examination
Nystagmus is optimally provoked by the Dix–Hallpike (sensitivity 50–88%) or
Barany maneuvers.
Nystagmus is an involuntary movement of the eye characterized by a smooth
pursuit eye movement followed by a rapid saccade in the opposite direction of the
smooth pursuit eye movement.
Dix–Hallpike Maneuver
• With the patient sitting, the neck is extended and turned to one side.
• The patient is then placed supine rapidly, so that the head hangs over the edge
of the bed.
• The patient is kept in this position until 30 seconds have passed if no nystagmus
occurs.
• The patient is then returned to upright, observed for another 30 seconds for
nystagmus, and the maneuver is repeated with the head turned to the other
side.
Diagnostic Criteria
Diagnostic criteria employing the Dix–Hallpike maneuver have been proposed
for posterior canal BPPV.
• Nystagmus and vertigo usually appear with a latency of a few seconds and last
less than 30 seconds.
• It has a typical trajectory, beating upward and torsionally, with the upper
poles of the eyes beating toward the ground.
• After it stops and the patient sits up, the nystagmus will recur but in the
opposite direction.
• The patient should then have the maneuver repeated to the same side; with
each repetition, the intensity and duration of nystagmus will diminish.
Management of Peripheral Vertigo

Epley’s maneuver (Fig. 1 and Table 3) should be performed for all patients
with confirmed BPPV. This procedure alone provides significant symptom
relief in many patients. Oral medications may then be added for symptomatic
management.
CHAPTER 88: Vertigo and Benign Paroxysmal Positional Vertigo 295
FIG. 1: Epley’s maneuver for right-sided benign paroxysmal positional vertigo.
TABLE 3: Particle repositioning maneuver (Epley’s maneuver).

The Epley’s Maneuver for Right Side BPPV
Step 1 Patient is made to sit facing forward
Step 2 Turn the head 45° to the right and then rapidly bring the patient into supine
position with the head extending just beyond the examining table with the
right ear down
Step 3 Examiner should move to the head end of the table
Step 4 Turn the head quickly to the left side with the right ear upward and hold
this position for 30 seconds
Step 5 Roll the patient to the left lateral position and rotate the head until the nose
faces the floor. Hold this position for 30 seconds
Step 6 Rapidly lift the patient into sitting position
Entire sequence is repeated until no nystagmus can be elicited
Medications for Vertigo

The neurons involved in the vestibular system are mediated by acetylcholine.
Anticholinergic drugs or antihistamines with anticholinergic activity are
extremely useful in treating vertigo.
• Tablet Cinnarizine 25 mg tid; or
• Tablet Betahistine (Vertin) 16 mg tid; or
• Tablet Prochlorperazine (Stemetil) 10 mg tid; or
• Tablet Flunarizine 10 mg tid; or
• Tablet Promethazine (Avomine/Phenergan) 25 mg bd.
Acute bacterial labyrinthitis: Patients may require admission , IV antibiotics and if
severe, surgical drainage and debridement.
Meniere's disease (classic triad of episodic vertigo, tinnitus and hearing loss):
Dietary restrictions (low sodium and caffeine) and lifestyle modifications
(cessation of smoking and alcohol) are helpful in decreasing the frequency of
episodes. Acute episodes should be managed with vestibular suppressants and
antiemetics with or without additional diuretics. Glucocorticoid therapy may be
required for patients with refractory and disabling symptoms.
Deep Neck Space
Infections 89
CHAPTER
RETROPHARYNGEAL ABSCESS
Once almost exclusively a disease of children, retropharyngeal abscess (RPA) is
observed with increasing frequency in adults. Patients who present at an early are
often misdiagnosed as pharyngitis and are treated inadequately.
Clinical Features
Clinical features include fever, sore throat, dysphagia, odynophagia, neck pain,
and stridor. Patients may present with signs of airway obstruction. Physical signs
prior to this stage include posterior pharyngeal edema, cervical adenopathy,
drooling, and neck stiffness.
Causes
Retropharyngeal abscess usually occurs through contiguous spread from upper
respiratory or oral infections. Pharyngeal trauma from endotracheal intubation,
nasogastric tube insertion, endoscopy, foreign body ingestion, and foreign
body removal may cause a subsequent RPA. Common organisms include
Streptococcus species, Staphylococcus aureus, Klebsiella, Bacteroides, and
Escherichia coli.
Investigations
If a RPA is suspected, ask for X-ray soft tissue neck lateral view. Widening of the
retropharyngeal soft tissues is seen in most cases. This is defined as soft tissue
swelling.
• >7 mm at C2, or
• >22 mm at C6, or
• More than two-thirds of the width of the vertebral body.
Management
• Initiate antibiotics: Amoxicillin-Clavulanate
• Refer urgently to ENT
• Urgent incision and drainage may be required, if airway is compromised.
PERITONSILLAR ABSCESS (QUINSY)

• Peritonsillar abscess is usually a complication of acute tonsillitis and is the
most common deep space infection of the neck.
• It is a collection of pus in the peritonsillar space (between the tonsillar capsule
and the superior constrictor and palatopharyngeus muscles). The infection
begins as a cellulitis and progresses to abscess formation, most commonly
near the superior pole of the tonsil.
• Symptoms and signs include fever, odynophagia, foul breath, ‘hot potato
voice,’ earache, and trismus.
• Microbial etiology includes S. pyogenes (group A Streptococcus) and oral
anaerobes like Fusobacterium.
• Start antibiotics (Amoxicillin-Clavulanate) and refer to ENT for needle
aspiration or incision and drainage of the abscess.
• Complications include airway obstruction, cavernous sinus thrombosis,
rupture and aspiration of the contents, epiglottitis, septicemia.
LUDWIG’S ANGINA
• Ludwig’s angina is a bilateral infection of the submandibular space. Infection
usually begins in the 2nd or 3rd mandibular molar teeth.
• It is typically a polymicrobial infection involving the flora of the oral cavity
(alpha-hemolytic streptococci, staphylococci, and Bacteroides).
• Clinical features include odynophagia, fever, and brawny cellulitis without
lymphadenopathy.
• Airway compromise due to rapid posterior displacement of the tongue is a
potential complication.
• Treatment includes urgent surgical drainage and antibiotic therapy. Injection
clindamycin 600 mg IV q6–8h 2 weeks or injection Amoxicillin/Clavulanate
1.2 mg IV q12h 2 weeks.
• Difficulty in managing secretions and stridor may necessitate emergency
airway management.
Section 14
Urological Emergencies
Nephrolithiasis 90
CHAPTER
INTRODUCTION
Kidney and ureter stones commonly present as emergencies with acute
abdominal pain.
Types of Stones
• Major cause (80%): Calcium stones (mostly calcium oxalate or, less often,
calcium phosphate). Predisposing conditions include primary hyperpara-
thyroidism and distal renal tubular acidosis (RTA).
• Minor causes (20%): Uric acid, struvite (magnesium ammonium phosphate),
and cystine stones.
Symptoms
The typical colicky pain starts in the one of the flanks, radiates inferiorly around
the abdomen towards the ipsilateral testes or labium majora. Ureteral distension
and peristalsis cause the acute severe pain that lasts 20–60 minutes with patients
unable to find a comfortable position to lie in. Other symptoms include hematuria,
nausea, vomiting, dysuria, urgency, penile pain, or testicular pain.
Diagnosis
• Urinalysis: Send a urinalysis for all patients with suspected renal calculi.
Presence of hematuria supports the diagnosis of renal calculi. If urinalysis
shows bacteria/pyuria or if the leucocyte esterase/nitrate is positive, send a
urine c/s to confirm etiology of urinary tract infection.
• X-ray KUB (kidney, ureter, and bladder): Can identify sufficiently large
radiopaque stones such as calcium, struvite, and cystine stones, but may miss
radiolucent uric acid stones.
• Ultrasonography: Sensitivity 57%. Procedure of choice to avoid radiation.
• Noncontrast CT: This is a very sensitive test (88%) in diagnosing renal calculi
without the use of contrast.
Differential Diagnosis
Renal: Pyelonephritis (presence of fever unlike a renal calculi which is not
associated with fever).
Gastrointestinal: Mesenteric ischemia, biliary colic (right upper quadrant pain),
pancreatitis (epigastric pain), perforated peptic ulcer, appendicitis or diverticulitis.
302 SECTION 14: Urological Emergencies
Vascular: Aortic dissection, aortic abdominal aneurysm.

Gynaecologic: Ectopic pregnancy (perform a urine pregcolor test in patients of
reproductive age), torsion ovary, salpingitis.
Genitourinary: Testicular torsion, epididymitis.
Acute Therapy
• Pain relief:
cc Inj. Paracetamol 1,000 mg in 100 mL normal saline intravenous (IV) stat
plus Injection Hyoscine (Buscopan) 20 mg IV stat.

cc Nonsteroidal anti-inflammatory drugs (NSAIDs) are preferred over
opioids for pain management: Injection Diclofenac 75 mg IM (reassess and
repeat dose after 30 min, if needed) and can also be combined with oral
Diclofenac 75 mg stat. NSAIDs have the added advantage of decreasing
ureteral smooth muscle tone, thereby directly treating ureteral spasm.
cc Injection Morphine 5 mg IV stat (reassess and repeat dose after 30 min, if
needed) or injection Tramadol 50 mg IV stat.

cc If pain persists after 4 hours, Morphine 5 mg IV can be given every 4 hours.
• Hydration: Encourage the patient to take plenty of fluids orally. Oral hydration
is adequate, if tolerated. Start IV fluids, if patient is not able to tolerate orally.
• Urology consultation: Warranted in patients with urosepsis, acute renal failure,
anuria, and/or unyielding pain.
• Facilitating stone passage: Alpha-blockers like Tamsulosin (0.4 mg PO od)
for up to 4 weeks increase the spontaneous passage rate of ureteral stones of
diameter 5–10 mm and may be prescribed to stable patients at discharge from
the ED.
Torsion Testis 91
CHAPTER
INTRODUCTION
Torsion testis is a common urological emergency among neonates and young
adults (<40 years). It results from inadequate fixation of the lower pole of the testis
to the tunica vaginalis:
• The spermatic cord twists on itself, thereby obstructing the blood supply to
one testis. This results in ischemia and the affected testes becomes tender and
pushed superiorly due to shortening of the spermatic cord on that side.
• The ischemic changes become irreversible and gangrene sets in within
6 hours of the onset of symptoms.
• It can also occur several hours after vigorous physical activity or minor trauma
to the testicles.
CLINICAL FEATURES
• The clinical presentation of torsion testes is that of acute onset of severe
unilateral scrotal pain.
• Patients with a bell clapper deformity (inappropriately high attachment of the
tunica vaginalis to the testes) are at a higher risk of torsion.
• Most torsions twist inward and toward the midline.
• Hence, immediate recognition and urgent intervention is required in
the ED.
• While examining the testes, it is often possible to detorse a testis by gently
rotating it away from the midline (outward and laterally). Relief of pain with
detorsion indicates likely testicular torsion.
• Ipsilateral absence of cremasteric reflex is a sign of testicular torsion. In other
causes of scrotal pain like epididymitis, the reflex is typically intact.
Diagnostic test of choice: Doppler ultrasonography of the scrotum.
MANAGEMENT
• In the emergency department, manual detorsion of the testes may be at-
tempted and if successful, converts an emergency into an elective procedure.
• Manual detorsion: Most testes twist/torse in a lateral to medial manner.
Hence, detorsion must be done in medial to lateral motion including one and
a half rotations (540 degrees). In other words, while standing at the food end
of the bed facing the patient, the patient's right tested must be twisted in an
anti-clockwise fashion and the left testes in a clockwise fashion in order to
detorse. Occasionally, patients may require manipulation beyond the one and
a half rotations. Immediate relief of pain is a positive sign of success, which
can be confirmed by demonstration of restoration of blood flow on a doppler
ultrasound.
• Immediate surgical exploration with intraoperative detorsion and fixation of
the testes is the definitive treatment.
Suspected torsion of the testes is a surgical emergency. Refer to urology as soon as the
clinical diagnosis is made. Do not wait for results of blood investigations/USG scrotum.
Torsion of the Appendages

The four testicular appendages: appendix testis, appendix epididymis, paradidymis
and vas abberans are all capable of torsion, especially in pre-pubertal boys. The
pain is more intense near the head of the epididymis and a tender nodule can
often be palpated. A blue spot may be seen on trans illuminating the scrotum.
This 'blue dot sign' is characteristic of torsion appendix testes or epididymis.
Most appendages calcify or degenerate on their own in 2 weeks and surgical
intervention is mostly not required.
DIFFERENTIAL DIAGNOSIS FOR ACUTE SCROTAL PAIN IN

ADULTS
• Epididymo-orchitis
• Testicular torsion
• Fournier’s gangrene (necrotizing fasciitis of the perineum)
• Torsion of the appendix testis
• Testicular cancer (hemorrhage and infarction)
• Inguinal hernia
• Henoch–Schönlein purpura (IgA vasculitis)
• Mumps.
Epididymo-orchitis 92
CHAPTER
INTRODUCTION
Epididymitis refers to inflammation of the epididymis. If the infection extends
to the scrotum, it is called “epididymo-orchitis”. It causes significant morbidity
among men in the age group 18–60 years. The clinical presentation of epididymitis
is similar to torsion testes, but it is critical to identify torsion testes since torsion is
a true urologic emergency and requires immediate intervention.
ETIOLOGY
• Bacterial:
cc Sexually active age group: Chlamydia trachomatis and Neisseria gonor-
rhoeae.
cc Older men: E. coli, other coliforms, and Pseudomonas species.
• Viral: Mumps (may cause isolated orchitis) and cytomegalovirus.

• Others: Epididymitis may also be caused by noninfectious causes such as
trauma and autoimmune diseases, but these usually present as subacute or
chronic epididymitis.
CLINICAL FEATURES
Epididymo-orchitis may be acute (lesser than 6 weeks) or chronic (≥6 weeks):
• The clinical features are fever, testicular pain and swelling, and tenderness.
• Epididymitis is characterized by local testicular pain tenderness on the
posterior part of the scrotum where the epididymis is located.
• In contrast to torsion testes, manual elevation of the scrotum relieves pain
(positive Prehn’s sign) due to epididymo-orchitis.
• In epididymo-orchitis, the cremasteric reflex is positive, in contrast to torsion
testes where it is typically absent.
• The above two clinical findings help in differentiating torsion testes from
epididymo-orchitis.
LABORATORY INVESTIGATIONS
The following examinations should be done:
• Complete blood count (CBC) and renal function tests
• Urinalysis and urine culture to confirm the infective etiology
• Doppler ultrasonography to rule out testicular torsion.
MANAGEMENT
• Most patients can be managed on an outpatient basis with oral antibiotics,
local application of ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and
opioids if necessary.
• Antibiotics: Empiric antimicrobial therapy should be started in the ED pending
culture sensitivity results and depends on the risk of acquiring sexually
transmittable diseases (STD)
• Patients at high risk of acquiring STDs: Empiric antibiotics should cover
N. gonorrhoeae and C. trachomatis
Injection Ceftriaxone 500 mg IV stat plus Tab. doxycycline 100 mg bd × 10 days
(Tab Azithromycin 1g stat single dose is an alternate to doxycycline)
• Patients at low risk of acquiring STDs: Empiric antibiotics should cover enteric
gram negative bacteria
Tablet levofloxaxin 500 mg od × 10 days
or
Tablet trimethoprim-sulfamethoxazole double strength bd × 10 days
• Scrotal elevation is a very useful adjunct and must be advised to all patients
till symptomatic relief. Ambulatory patients must be advised to wear scrotal
supporter and be careful not to do maneuvers that increase intra-abdominal
pressure like lifting heavy objects or straining while passing stools.
• Complications include scrotal abscess, testicular infarction, testicular
atrophy, and infertility.
Penile Emergencies 93
CHAPTER
PHIMOSIS
Phimosis is a condition seen in uncircumcised males in which the foreskin
(prepuce) cannot be retracted over the glans penis (Fig. 1). The foreskin may
normally be nonretractile up to 5 years of age.
Pathologic phimosis may present with painful erections, painful prepuce,
recurrent urinary tract infections, hematuria, or a weakened urinary stream.
Management
• Patients with phimosis rarely requires any emergency intervention and can
be managed by conservative therapy by application of dexamethasone cream
thrice daily for 1 week and referring to Urology.
• If the patient has severe symptoms, refer to Urology. A dorsal slit can be
performed for immediate relief.
PARAPHIMOSIS
Paraphimosis is a urologic emergency in which the retracted foreskin cannot be
reduced back to is normal position. It is seen in uncircumcised males.
It is often caused by medical professionals (during examination and
procedures like catheterization) and parents who retract the foreskin improperly
for a long period. This may result in painful swelling of the glans penis. Decreased
blood supply eventually results in gangrene and amputation of the glans penis
(Fig. 1).
FIG. 1: Phimosis and paraphimosis.

Management
• Administer a penile ring block, which is similar to a digital ring block.
• Apply gentle and constant pressure for 5 minutes to reduce the edema and
then attempt manual reduction to reduce the glans back into the preputial
fold.
• Before attempting manual reduction, soak the penis in a glove full of ice. This
helps to reduce the edema around the glans.
• If manual reduction fails, an emergency dorsal slit may have to be performed.
Refer urgently to Urology.
PENILE FRACTURE
• A penile fracture refers to an acute tear or rupture of the tunica albuginea of
one or both corpus cavernosa. It occurs in young adults from trauma during
sexual intercourse or other sexual activities.
• A typical snapping sound occurs followed by loss of erection, rapid swelling,
bruising and deviation of the penis. The penis appears acutely swollen,
discolored, flaccid, and tender.
• Ultrasonography is useful to delineate the exact location and extent of the tear.
• Management: Surgical intervention is required in most cases and may require
hematoma evacuation and suture opposition of the ruptured tunica albuginea.
PRIAPISM
Priapism is a urological emergency characterized by a persistent, pathological,
painful erection of the penis. Both the corpora cavernosa are engorged with
stagnant blood. It is classified as follows:
• Low flow (ischemic) priapism: The most common type is very painful and
results from impaired venous drainage, thus increasing cavernosal pressures.
If prolonged, it can result in irreversible ischemic changes and permanent
erectile dysfunction. It is commonly caused by intracavernosal injection
of vasoactive substances (papaverine, prostaglandin E) for impotence,
prothrombotic disorders (sickle cell anemia) or some oral medications
(hydralazine, prazosin, chlorpromazine, trazodone).
• High flow (nonischemic) priapism: Usually, nonpainful and results from
dysregulation of penile blood flow (traumatic fistulae) secondary to trauma
or surgery.
Management
Low flow priapism is a urological emergency.
• Administer adequate analgesia. Systemic analgesia like morphine/tramadol
can be given but may not be adequate. Consider a dorsal penile nerve block
by landmark technique or under ultrasound guidance (Fig. 2).
CHAPTER 93: Penile Emergencies 309
FIG. 2: Dorsal-Penile-Nerve-Block.
FIG. 3: Intracorporal-Injection.
• Apply warm compress for vasodilation that would improve blood flow and
relieve pain
• Priapism due to sickle cell disease can be reversed by adequate hydration and
if required, a simple exchange transfusion.
Invasive management: Intracorporal injection of an alpha-adrenergic agonist
(phenylephrine) can cause cavernous smooth muscle contraction, thus allowing
venous outflow. Phenylephrine (250–500 µg diluted in 1 mL NS) or Adrenaline
(0.1 mg diluted in 1 mL NS) can be injected at either ‘2 o'clock’ or at ‘10 o'clock’
position at the base of the penis using a 25 or 26 guage needle. Advance nedle
at 45 degrees angle to the skin till blood is aspirated (Fig. 3). A repeat injection
can be given after 30 minutes. Bilateral injection is not necessary as the corpora
cavernosa communicate.
Definitive management incudes aspiration and irrigation with a vasoactive
substance such as phenylephrine or adrenaline using a 19 guage butterfly needle
at the same site described above. Irrigation is done if inadequate blood returns on
aspiration or detumescence is not achieved.
Section 15
Surgical Emergencies
Skin and Soft Tissue
Infections 94
CHAPTER
CELLULITIS
Cellulitis and erysipelas are superficial infections of the skin and soft tissue that
are caused by bacteria (Staphylococcus and group A streptococci) breaching the
skin barrier through open wounds.
Erysipelas: Infection of the upper dermis and superficial lymphatics, with an area
of erythema and well-demarcated, raised borders, usually involving the lower
extremities or the face.
Cellulitis: Infection of the deeper dermis and subcutaneous fat, with ill-defined
borders, most commonly involving the extremities.
Necrotizing fasciitis (NF): NF is characterized by infection of the deep fascia
and necrosis of the subcutaneous tissues. This represents the other end of the
spectrum of skin and soft tissue infections and results from untreated cellulitis
or erysipelas.
Investigations
Investigations include complete blood count (CBC), electrolytes, creatinine, and blood
culture and sensitivity (c/s).
Management
• MgSO4 dressing twice daily to reduce edema. Treat skin dryness with topical
agents like moisturizers.
• Limb elevation for drainage of edema.
• Antibiotics:
cc Cefazolin 1 g IV q8h × 7–10 days; or
cc Cloxacillin 500–1,000 mg PO q6h × 7–10 days; or
cc Cephalexin 500 mg PO q6h × 7–10 days.
• Refer to general surgery.

It is important to differentiate cellulitis and necrotizing fasciitis (NF) clinically
• Cellulitis is a superficial infection of the skin and requires only conservative management.
• Necrotizing fasciitis is a deeper infection of the subcutaneous tissues, has skin
discoloration/blebs/necrosis. Urgent surgical debridement is essential.
• Do not send preoperative tests [prothrombin time (PT), activated partial
thromboplastin time (aPTT), and blood borne virus screen (BBVS)] for clinical diagnosis
of cellulitis.
314 SECTION 15: Surgical Emergencies
NECROTIZING FASCIITIS
Necrotizing fasciitis is an acute bacterial infection involving the skin and deeper
layers of the fascia, resulting in necrosis of the skin and subcutaneous tissue. It is
a rapidly progressive condition characterized by skin color changes, blisters, and
gangrene and requires urgent surgical intervention.
Fournier gangrene: Necrotizing fasciitis involving the scrotum, penis and
perineum is called Fournier gangrene. It typically presents abruptly with severe
pain and may rapidly spread to the anterior abdominal wall or the gluteal muscles.
Microbiology
• Type I infection: It is the most common type and is a polymicrobial infection
caused by obligate and facultative anaerobes like Bacteroides, Clostridium, or
Peptostreptococcus. It usually involves the trunk and perineum with diabetes
mellitus being the risk factor.
• Type II infection: It is monomicrobial, most common organism being Group A
beta-hemolytic Streptococcus. It usually affects the extremities.
• Type III infection: It is also monomicrobial caused by Clostridium species,
gram-negative bacteria, Vibrio vulnificus, or Aeromonas hydrophila.
• Type IV infection: It is usually caused by fungi (Candida species and
Zygomycetes) in the immunocompromised host.
Investigations
The investigations include CBC, electrolytes, creatinine, blood c/s, chest X-ray,
ECG, PT, aPTT, and BBVs rapid.
Management
• Limb elevation for drainage of edema
• Antibiotics: Piperacillin-Tazobactam 4.5 g IV stat and q6–8h, or
Crystalline penicillin 20 L Units IV q4h + Clindamycin 600 mg IV q6h
• Refer to general surgery for urgent surgical debridement.
In large tertiary care hospitals with high rates of antibiotic resistance, the
following protocol may be followed:
cc Moderate infection (local infection with erythema >2 cm or involving
structures) involving skin and subcutaneous tissues (e.g., abscess,

osteomyelitis, septic arthritis, fasciitis): Piperacillin tazobactam 4.5 g IV
q8h plus Vancomycin 15 mg/kg IV q12h.
cc Severe infection (life-threatening/gangrene/septic shock): Meropenem 1
g IV q8h plus Vancomycin 15 mg/kg IV q12h.

• Surgical debridement is a limb and life-saving intervention and must be
performed as soon as possible. Debridement, necrosectomy, or fasciotomy
may have to be repeated till fresh viable tissue starts appearing. Any delay in
surgical intervention may lead to irreversible necrosis and gangrene resulting
in amputation of the limb or death due to septic shock.
Duodenal Ulcer
Perforation 95
CHAPTER
INTRODUCTION
Peptic ulcer disease is a common condition that may be complicated by bleeding,
perforation, or gastric outlet obstruction.
Duodenal ulcer perforation should be suspected in patients who suddenly
develop severe, diffuse abdominal pain. It is important to take history of chronic
antiplatelets, nonsteroidal anti-inflammatory drugs (NSAIDs) and steroid use in
patients suspected to have duodenal perforation.
Consider the differentials shown in Table 1 while evaluating a patient with
acute abdominal pain.
• Initial phase (within 2 h of onset): Abdominal pain is usually sudden, some-
times producing collapse or syncope. Usually, localized to the epigastrium.
• Second phase (usually 2–12 h after onset): Abdominal pain may lessen, usually
generalized, often markedly worse upon movement. Abdomen shows marked
board-like rigidity.
• Third phase (usually >12 h after onset): Abdominal distension increases but
abdominal pain, tenderness, and rigidity may be less evident. Hypovolemia
and shock may result due to third spacing into the peritoneal cavity.
TABLE 1: Causes of acute abdominal pain in adults.

Surgical Gynecological Medical
• Acute appendicitis • Ectopic pregnancy • Acute pancreatitis
• Acute cholecystitis • Pelvic inflammatory • Inferior wall myocardial
• Biliary colic disease infarction
• Duodenal ulcer perforation • Rupture/torsion of • Peptic ulcer disease
• Intestinal obstruction ovarian cyst • Acute hepatitis
• Ureteric colic • Endometriosis • Diabetic ketoacidosis
• Testicular torsion • Mittelschmerz • Urinary tract infection
• Aortic dissection • Gastroenteritis
• Diverticulitis • Irritable bowel
• Mesenteric ischemia syndrome
• Large bowel perforation
• Nonspecific abdominal pain
FIG. 1: Air under the diaphragm.
INVESTIGATIONS
The investigations include complete blood count (CBC), electrolytes, creatinine,
urea, blood culture and sensitivity, rapid blood borne virus screen (BBVS),
prothrombin time, activated partial thromboplastin time (aPTT), ECG, chest
X-ray erect, and X-ray abdomen supine. Look for air under the diaphragm (Fig. 1).
If clinical diagnosis is doubtful, amylase, lipase, or cardiac enzymes may have
to be sent depending on the history and examination findings.
MANAGEMENT
• Obtain IV access and start fluid resuscitation.
• Insert a nasogastric (NG) tube and keep the patient nil per oral (NPO)
• Prove adequate analgesia (Morphine/Tramadol).
• Give proton pump inhibitor and antiemetics (Injection Pantoprazole 40 mg +
Injection Metoclopramide 10 mg IV stat.)
• Administer empiric antibiotics:
cc In hemodynamically stable patients: Cefazolin 1 g IV + Gentamicin
1.5–2 mg/kg IV + Metronidazole 500 mg IV stat.

cc In patients with systemic inflammatory response syndrome/shock:
Piperacillin-Tazobactam 4.5 g IV or Injection Ertapenem 1 g IV stat.
• Refer to general surgery for further management.
Acute Appendicitis 96
CHAPTER
INTRODUCTION
Appendicitis is one of the most common causes of acute abdomen presenting to
the emergency department. It refers to an inflammation of the vestigial vermiform
appendix.
The clinical presentation is characterized by the following symptoms:
• Abdominal pain: Classically, pain starts in the periumbilical region and
migrates to the right lower quadrant (right anterior iliac fossa) with increasing
inflammation.
• Anorexia
• Nausea and vomiting
PHYSICAL EXAMINATION
Palpate gently for areas of tenderness. It is unnecessary and unkind to attempt to
repeatedly elicit rebound tenderness. Tenderness on percussion or palpation is
ample evidence of peritonitis.
Common physical signs include:
• McBurney’s sign is described as maximal tenderness at the McBurney’s point
(Fig. 1), which lies at one-third of the distance from the anterior superior iliac
spine (ASIS) to the umbilicus (sensitivity 50–94%; specificity 75–86%).
• Rovsing’s sign: Palpation of the left lower quadrant elicits pain in the right
lower quadrant. This sign is also called “indirect tenderness” and is indicative
of right-sided local peritoneal irritation.
• The psoas sign is associated with a retrocecal appendix, which may manifest
by right lower quadrant pain with passive extension of the right hip.
• The obturator sign is associated with a pelvic appendix. In this sign, right
lower quadrant pain is elicited on flexing the patient’s right hip and knee
followed by internal rotation of the right hip.
Rectal examination, although often advocated, has not been shown to provide
additional diagnostic information in cases of appendicitis.
FIG. 1: McBurney’s point.
INVESTIGATIONS
• The investigations include complete blood count (CBC), electrolytes,
creatinine, liver function test (LFT), chest X-ray (CXR) (to rule out hollow
viscus perforation), and urinalysis (to look for RBC in urine s/o renal calculi).
• Acute appendicitis is a clinical diagnosis. Ultrasonography (USG) of abdomen
is only indicated in female patients with nonspecific abdominal pain to
rule out a gynecological cause. An inflamed appendix may be seen as a
noncompressible tubular structure of 7–9 mm in diameter on a USG.
• In women of reproductive age group, perform a pelvic examination and do a
pregnancy test (urine precolor) to rule out obstetric causes.
• Send rapid blood borne virus screen (BBVS) and prothrombin time (PT), and
activated partial thromboplastin time (aPTT), if surgical intervention is likely.
Calculate the probability of acute appendicitis by using the modified Alvarado
score (Table 1)
MANAGEMENT
• Commence IV fluids if there is evidence of dehydration.
• Give IV opioid and antiemetic (Tramadol 50 mg IV/Morphine 0.1 mg/kg IV
stat plus Metoclopramide 10 mg IV stat. Repeat if necessary).
• If appendicectomy is planned, start antibiotics: Piperacillin-Tazobactam
4.5 g IV stat. Preoperative administration of antibiotics decrease postoperative
wound infections.
• Insert a nasogastric (NG) tube and keep the patient nil per oral (NPO)
• Management depends on whether the appendix is perforated or nonper-
forated at the time of presentation.
CHAPTER 96: Acute Appendicitis 319
TABLE 1: Modified Alvarado score for acute appendicitis.

Conditions Score Interpretation
M Migratory right iliac fossa pain 1 0–3: Low risk
A Anorexia 1
N Nausea or vomiting 1 4–6: Probable
T Tenderness in the right iliac fossa 2
R Rebound tenderness in the right iliac fossa 1 7–9: Very probable
E Fever >37.5°C 1
L Leukocytosis 2
S Shift to the left 1
cc Nonperforated: This refers to simple/uncomplicated appendicitis without

clinical or radiological signs of perforation. Appendectomy is the standard
of care for most patients, either by laparoscopic or by open approach.
cc Perforated appendix: About 10–20% of patients with acute appendicitis
may have a perforation and would require emergency appendectomy.

• Refer to General surgery for further management
Acute Cholecystitis 97
CHAPTER
INTRODUCTION
The term cholecystitis refers to inflammation of the gallbladder.
• Acute cholecystitis: Acute cholecystitis refers to inflammation of the gall-
bladder, usually caused by a gallstone obstructing the biliary drainage
(Fig. 1). It is characterized by right upper quadrant abdominal pain, fever, and
leukocytosis.
• Acalculous cholecystitis: This is clinically similar to acute cholecystitis but
is not associated with gallstones. It usually occurs in critically ill patients or
severe trauma.
HISTORY
Right upper quadrant or epigastric pain that is steady and severe is the typical
presentation. The pain may radiate to the right shoulder or back. Episodes of
biliary pain keep recurring in most patients. Approximately, 60–70% of patients
report a previous episode of biliary pain that resolved spontaneously.
Patients with acute cholecystitis are usually ill appearing, febrile, and tachycardic.
FIG. 1: Anatomy of the pancreaticobiliary drainage.

CHAPTER 97: Acute Cholecystitis 321
Murphy’s sign: Right hypochondrial tenderness on deep inspiration in sitting

position.
INVESTIGATIONS
• Complete blood count (CBC), electrolytes, creatinine, and liver function test.
• Ultrasonography abdomen: To look for gallstones, CBC dilatation. Ultrasonic
Murphy’s sign may be elicited to confirm the diagnosis.
• Rapid blood borne virus screen (BBVS) and prothrombin time (PT), and
activated partial thromboplastin time (aPTT), if surgical intervention likely.
DIAGNOSIS
Diagnosis of acute cholecystitis is generally made on the basis of typical history
and examination findings. The classical triad of sudden onset right upper quadrant
(hypochondrial) pain, fever and leukocytosis (WBC count: 10–15,000/mm3) is
highly suggestive of acute cholecystitis.
MANAGEMENT
• Intravenous (IV) fluid resuscitation
• Provide analgesia (Tramadol 50 mg IV/Morphine 0.1 mg/kg IV stat plus
Metoclopramide 10 mg IV stat). Repeat if necessary.
• Start broad-spectrum IV antibiotics after taking a blood culture
• Refer urgently to general surgery
• Percutaneous cholecystostomy tube placement (for surgically high risk
or critically ill patients) or cholecystectomy (definitive treatment) may be
required if there is no clinical improvement with antibiotics and supportive
care.
What Causes Elevation of Alkaline Phosphatase Levels?

Alkaline phosphatase level (ALP) is produced from only four sites in the body.
It is usually elevated due to cholestasis. If ALP is elevated, think of the following
sources.
• Liver:
cc Mild elevation: Hepatitis, heavy alcohol consumption, and sepsis.
cc High levels: Biliary obstruction, infiltrative process (malignancy, tuber-
culosis, amyloidosis, and sarcoidosis), and primary biliary cirrhosis.

• Gastrointestinal (GI) tract: GI malignancies and GI tuberculosis.
• Bone: Fractures, Paget’s disease, and osteomalacia.
• Placenta: Pregnancy.
Gamma-glutamyl transpeptidase (GGT) also reflects cholestasis and is rarely
elevated in conditions other than liver disease. If ALP and GGT are both elevated,
the source of ALP is the liver. If ALP is elevated and GGT is normal, the source of
ALP is the GI tract/bone/placenta.
Intestinal Obstruction 98
CHAPTER
INTRODUCTION
Intestinal obstruction may be mechanical or paralytic in nature. The causes of
intestinal obstruction are shown in Table 1.
HISTORY
• Classic symptoms are abdominal pain, distension, vomiting, and constipation.
• Ask for history of previous surgery.
• Severe pain suggests strangulation and developing ischemia in a closed loop.
EXAMINATION
• Look for evidence of dehydration and shock.
• Carefully examine the hernial orifices and inspect for scars of previous
surgery.
• Look for distension and areas of tenderness.
• Perform a per rectal examination. Impacted stools may be the cause for obstruction
especially in theelderly.
INVESTIGATIONS
The investigations include:
• Complete blood count (CBC), electrolytes, creatinine, and liver function test
(LFT)
TABLE 1: Causes of intestinal obstruction.

Mechanical causes Paralytic causes
• Adhesions after previous surgery • Postoperative ileus
• Obstructed hernia • Electrolyte disturbance: Hypokalemia
• Tumors (gastric, pancreatic, and large • Pseudo-obstruction
bowel)
• Volvulus (sigmoid, gastric, and cecal)
• Inflammatory mass (diverticular and
Crohn’s)
• Peptic ulcer disease
• Gallstone ileus
• Intussusception
CHAPTER 97: Intestinal Obstruction 323
• Chest X-ray (CXR) erect and X-ray abdomen supine

• Rapid blood borne virus screen (BBVS), prothrombin time (PT), and activated
partial thromboplastin time (aPTT), if surgical intervention is likely.
• The site and nature of the bowel loops may suggest the site of obstruction.
MANAGEMENT
• Insert an intravenous (IV) cannula and start IV fluid resuscitation.
• Insert a nasogastric tube and keep the patient nil per oral.
• Give an antiemetic (Metoclopramide/Ondansetron).
• Refer to surgical team for further management.
INTESTINAL PSEUDO-OBSTRUCTION
This is due to chronic impairment in gastrointestinal (GI) motility, especially seen
in the elderly taking tricyclic antidepressants or other anticholinergic drugs. Any
part of the GI tract may be involved, but colonic distention is the most common.
Treatment of acute colonic pseudo-obstruction is decompression using a
colonoscopy.
When to do a CT Abdomen?
In patients with intestinal obstruction and signs of peritonitis who require
immediate intervention and in postoperative patients where the etiology is
known, computed tomography (CT) abdomen is not needed.
CT scan of the abdomen is useful to identify:
• Specific sites of obstruction (transition points)
• Severity of obstruction (partial vs. complete)
• Determining the etiology like hernias, masses, or inflammatory changes
• Identifying complications like ischemia, necrosis, or perforation.
Do not ask for CT abdomen with oral contrast in a patient with signs of perforation.
Mesenteric Ischemia 99
CHAPTER
INTRODUCTION
Acute mesenteric ischemia refers to the sudden onset of small intestinal
hypoperfusion, which is usually due to acute embolic occlusion of the intestinal
blood supply, most commonly the superior mesenteric artery (SMA).
Mesenteric ischemia can be divided into arterial and venous. Arterial disease
can be further sub divided into non occlusive (low flow state) and occlusive
(embolic or thrombotic).
OCCLUSIVE MESENTERIC ARTERIAL DISEASE

1. Mesenteric arterial embolism: The source of emboli is the heart (left atrium,
left ventricle, and valves) or a dislodged thrombus from the proximal aorta.
Increased risk among patients with cardiac arrhythmias, valvular heart
disease, infective endocarditis, recent myocardial infarction, ventricular
aneurysm and aortic aneurysm.
2. Mesenteric arterial thrombosis: Acute thrombosis of the mesenteric
circulation usually occurs in patients with chronic mesenteric ischemia due
to progressively worsening atherosclerotic plaque in the mesenteric arteries.
It may also occur in patients with vascular injuries due to abdominal trauma,
infection, or mesenteric dissection.
CLINICAL FEATURES
Usually presents with sudden onset severe diffuse abdominal pain. Typically, the
severity of the pain initially far exceeds the associated physical signs. Pain due to
embolism to the proximal superior mesenteric artery is typically sudden, severe,
peri-umbilical and associated with nausea or vomiting. Pain due to thrombotic
etiology is usually insidious in onset with post-prandial worsening.
• Initially there may only be mild diffuse abdominal tenderness. Shock, absent
bowel sounds, abdominal distension, and tenderness are late signs.
• Carefully examine the cardiovascular system for any embolic source (atrial
fibrillation and valvular heart disease).
• Perform a per rectal examination to look for altered blood in stools that
suggests progression of the ischemia.
CHAPTER 99: Mesenteric Ischemia 325
DIAGNOSIS
Diagnosis may be difficult as the clinical presentation mimics other acute intra-
abdominal emergencies. A high index of suspicion is required for diagnosis,
especially in the elderly (>60 years) and those with atrial fibrillation, myocardial
infarction or congestive heart failure.
• Arterial blood gas typically reveals a severe metabolic acidosis and elevated
lactate. These findings in a patient with severe abdominal pain should arouse
a strong suspicion of mesenteric ischemia.
• A computed tomography (CT) angiography confirms the diagnosis. It
can differentiate between embolic and thrombotic etiologies and provide
information for operative planning, such as distal arterial reconstitution and
choice of inflow vessel for surgical bypass.
MANAGEMENT
• Resuscitate with intravenous fluids and oxygen, if required
• Nasogastric tube and keep the patient nil per oral
• Prove adequate analgesia. Administer Morphine 5 mg IV/SC or Tramadol
50 mg IV and repeat doses as required.
• Administer proton pump inhibitors (Pantoprazole 40 mg IV stat) and an
antiemetic (Metoclopramide 10 mg IV stat)
• Consider broad-spectrum antibiotics (Meropenem/Piperacillin-Tazobactam)
• Administer anticoagulants (unfractionated heparin or low molecular heparin)
to limit thrombus propagation
• Refer to general surgery for urgent surgical intervention. Immediate surgery is
indicated for patients with acute mesenteric ischemia with clinical symptoms
or signs of bowel gangrene (e.g., peritonitis, septic shock, pneumatosis
intestinalis). Surgery consists of abdominal exploration/damage control and
revascularization (embolectomy/mesenteric bypass). Despite best efforts,
prognosis remains poor with a high mortality rate.
Gas Gangrene 100
CHAPTER
INTRODUCTION
Gas gangrene or clostridial myonecrosis is a rapidly progressive infection of the
muscles caused by Clostridium species and can be fatal.
It may develop at the site of trauma or may get seeded in the muscle by
hematogenous spread from the gastrointestinal (GI) tract. Clostridial gas gangrene
may therefore present in two ways: Traumatic and spontaneous.
1. Traumatic gas gangrene: Most common etiology is C. perfringens. Some
conditions that predispose to traumatic gas gangrene include crush injuries,
gun shot wounds, knife wounds, bowel and biliary tract surgery, abortion, and
retained placenta.
2. Spontaneous gangrene: Most common etiology is C. septicum.
CLINICAL FEATURES
• Sudden onset of severe pain at the site of surgery or trauma.
• The mean incubation period is <24 hours (range 6 h to several days).
• Characteristic yellowish-brown or bronze appearance of the skin, followed by
blebs or hemorrhagic bullae. The skin becomes tense and exquisitely tender.
• Serosanguinous exudate with a characteristic foul odor.
• Signs of systemic toxicity develop rapidly including tachycardia and fever,
followed by shock and multiorgan failure.
DIAGNOSIS
• Pain at a site of traumatic injury together with signs of systemic toxicity and
gas in the soft tissue support the diagnosis of gas gangrene. The most specific
finding to confirm gas gangrene is demonstration of crepitus in the soft tissue.
• Gas within the soft tissue can be detected by X-ray, CT scan, or MRI scan.
• Definitive diagnosis of gas gangrene requires demonstration of large, gram-
variable rods at the site of injury. Tissue culture and blood culture (aerobic
and anaerobic) should be obtained.
MANAGEMENT
• Resuscitate with intravenous (IV) fluids and oxygen if required
• Isolate the patient in side observation area after resuscitation
• Antibiotic therapy: Injection crystalline penicillin 40 L units q4h plus injection
clindamycin 600 mg IV q8h. Carbapenems are an alternative.
• Surgical debridement: Extensive debridement of devitalized tissue is life-
saving. The affected limb may have to be amputated.
Nail Bed Emergencies 101
CHAPTER
INTRODUCTION
The most common nail bed emergencies are injuries (crush injury or subungual
hematoma) and infections (paronychia).
NAIL BED INJURIES

Fingertip and nail bed injuries are common components of hand injuries. Nail
bed is the soft tissue below the nail and helps in nail growth. Crush injuries of the
nail bed and fractures of the distal phalanx result in stunted, deformed, or absent
nail growth.
Subungual hematomas are frequently associated with nail bed injuries and
can be excruciatingly painful. The nail bed has a rich vascular supply and bleeding
results in increased pressure under the nail and can cause significant discomfort.
Management
• Administer digital ring block (with 2% lignocaine without adrenaline) for
immediate pain relief. Assess the neurological status of the finger before
administering anesthesia.
• If the nail plate is mobile, remove it and inspect the matrix for nail bed
lacerations.
• Irrigate the nail bed with sterile normal saline (NS) using a 26-G needle.
• Clean and remove debris.
• Reinsert the nail plate and reappose the nail folds.
• Apply sterile nonadherent dressing and splint.
• Small subungual hematomas resolve spontaneously and hence require no
treatment. However, painful and large hematomas should be evacuated via
nail trephination (i.e., making a hole in the nail for drainage of blood).
Nail Trephination (Fig. 1)

• Paint the nail with 10% povidone-iodine (Betadine) solution.
• Puncture the nail with a hot metal wire (e.g., an electrocautery device or
a carbon dioxide laser). The hole should be large enough (3–4 mm) for
continued drainage, which may occur for 24–36 hours after the injury.
• Alternatively, insert an insulin syringe needle (29-G) underneath the nail at
the distal hyponychium and advance it proximally and parallel to the nail
A B
C D
FIGS. 1A TO D: Nail trephination.
plate with gentle suction on the syringe until the hematoma begins to drain.
Apply light pressure to the nail to complete evacuation.
• Cover the puncture site with sterile gauze dressing while the wound continues
to drain.
PARONYCHIA
Paronychia is the most common infection of the hand, occurring along the edge
of the finger nail or toe nail. The infection is most often caused by Staphylococcus
aureus or Streptococcus species. Mixed bacterial and gram-negative etiology is
common in diabetic patients.
CHAPTER 101: Nail Bed Emergencies 329
Management
• Early acute paronychia without abscess formation can be treated with warm
water soaks, oral antibiotics (Cloxacillin) and analgesics.
• Incision and drainage is required, if an abscess develops.
Paronychia Drainage (Fig. 2)

• Prepare the skin with 10% povidone-iodine (Betadine) solution.
• Administer mid-dorsal digital block with 2% lignocaine without adrenaline.
• Using a small blunt instrument like the back of a sterile blade or a metal probe,
gently elevate the lateral eponychial fold and allow the pus to drain.
• If required, make a longitudinal incision using a No. 11 or No. 15 blade away
from the nail fold. This drains the pus without disturbing the eponychial folds.
• Irrigate the cavity with NS using a 24-G syringe.
• Excise the lateral nail if pus has tracked under the nail, such as in ingrown toe
nail.
• Removal of the entire nail is usually not indicated.
• Oral antibiotics (Cloxacillin 500 mg q6h or Cefazolin 500 mg q6h for 1 week).
• Administer adequate analgesia (nonsteroidal anti-inflammatory drugs or
Tramadol).
• Review and change dressing after 48 hours.
A B
FIGS. 2A AND B: Paronychia drainage.
FELON
• A felon is a subcutaneous pyogenic infection or abscess of the pulp space of
the distal finger or thumb that may cause increased pressure and ischemic
necrosis of the surrounding tissue, osteomyelitis, flexor tenosynovitis or septic
arthritis of the distal interphalangeal joint.
• Infection begins with minor trauma and patients present with severe throbbing
pain and a tense, red pulp space.
• The infection may spread between septae of the pulp space, forming
compartmental abscesses.
• Management:
cc In the early stages, patients may respond to warm soaks, elevation, rest
and oral antibiotics (Cloxacillin 500 mg PO q6h or Cephalexin 500 mg PO

q6H × 5–7 days)
cc Severe cases require incision and drainage or even debridement of the
abscess cavity (Fig. 3).
FIG. 3: Incision and drainage of a felon.

Anorectal Emergencies 102
CHAPTER
HEMORRHOIDS
Hemorrhoids or piles refer to enlarged or swollen veins in the anal canal and
rectum and increase in incidence with age. They are of two types: External and
internal.
1. External hemorrhoids form at the anus and protrude out. They may be
complicated by thrombosis, hygiene-related problems, infection, or bleeding
per rectum. They are usually associated with significant pain, itching, and
incomplete bowel movements. A skin tag is usually a sign of a healed external
hemorrhoid.
2. Internal hemorrhoids arise in the lower rectum and may not protrude out
though the anus. As they do not have any cutaneous innervations, they
typically cause painless, bright red bleeding associated with defecation, but
blood is not mixed in stools.
A thrombosed hemorrhoid may present as an acute emergency and is usually
quite painful. It may necessitate immediate surgical intervention to remove the
thrombosed vessel.
Management
• Advice high-fiber diet.
• Prescribe stool softeners (naturolax powder 2 teaspoon od/bd) and analgesics.
• Warm sitz baths: Advice the patient to sit in a shallow tub filled with warm
water and soak the rectal area for 10–15 minutes, 2–3 times daily.
• Refer to general surgery for surgical intervention or conservative management.
ANAL FISSURE
Anal fissures may cause severe pain on defecation and for a few hours afterward.
Most fissures are located posteriorly in the midline just inside the anal orifice.
Management
• Advice high-fiber diet.
• Prescribe stool softeners and analgesics.
• Topical analgesic jelly or creams (e.g., 2% lidocaine jelly) may be prescribed.
• Topical vasodilators like nifedipine (0.2–0.3% ointment, 2–4 times daily) or
topical nitroglycerine (0.4% rectal ointment twice daily) increase the local
blood flow and reduce the anal sphincter pressure.
• Warm sitz baths: Advice the patient to sit in a shallow tub filled with warm
water and soak the rectal area for 10–15 minutes, 2–3 times daily.
• Most heal spontaneously but the presence of significant ulceration,
hypertrophied tissue, skin tags suggests chronicity and needs surgical follow
up.
PILONIDAL ABSCESS
• Pilonidal cysts usually form in young individuals (15–35 years), probably due
to impacted hair follicles in the natal cleft. They may be itchy and painful and
cause discomfort while sitting.
• A pilonidal sinus is formed when a pilonidal cyst ruptures through the skin
forming a tract that discharges material or pus from the cyst. This may become
chronic.
• A pilonidal abscess is formed when a pilonidal cyst or a sinus becomes
infected. This requires immediate surgical intervention as patients present
with a fluctuant swelling in the natal cleft, which is extremely painful and
tender.
Etiology of a Pilonidal Abscess

Most common pathogens are anaerobic bacteria such as Bacteroides, but
Enterococci, Staphylococci, and hemolytic Streptococci have also been implicated.
Anaerobes are usually associated with postoperative wound reinfections.
Management
Broad-spectrum antibiotics (Metronidazole/Piperacillin-Tazobactam) and
immediate surgical drainage of the abscess.
ANORECTAL ABSCESS
An anorectal abscess (perineal abscess) is formed if an anal crypt and gland gets
infected. The infection can easily spread through the loose intersphincteric space,
ischiorectal space, or the supralevator space. These are more common in young
and middle-aged males.
The types of anorectal abscess shown in Figure 1 are:
• Perianal (60%)
• Ischiorectal (20%)
• Intersphincteric (5%)
• Supralevator (4%)
• Submucosal (1%)
CHAPTER 102: Anorectal Emergencies 333
FIG. 1: Location of anorectal abscesses.
Symptoms
Persistent dull, throbbing pain made worse by walking or sitting and prior to
defecation. Pain is a prominent symptom followed by signs of local inflammation.
Examination shows a localized fluctuant red tender swelling close to the anus.
Management
Administer analgesics (NSAIDs or opiates). Definitive treatment is incision
and drainage. Isolated, simple, superficial, fluctuant perianal abscesses may be
drained in the ED under local analgesia or procedural sedation.
FISTULA IN ANO
• Fistula in ano refers to an abnormal tract lined with epithelium and granu-
lation tissue, connecting the anal canal with the skin.
• These tracts usually result from perianal or ischiorectal abscesses and may
also be associated with Crohn’s disease, colonic malignancies, anal fissures or
sexually transmitted diseases.
• Goodsall’s rule: Anterior opening fistulas follow a simple direct course to the
anal canal while posterior opening fistulas often follow a devious, curving
path including horseshoe-shaped tracks.
• Patients present with persistent, blood-stained, foul smelling discharge.
Recurrent abscesses may form due to blockade of the tracts due to
inflammation.
• Analgesics, antipyretics, antibiotics (metronidazole) may be started for
patients with significant symptoms awaiting surgical consultation.
• The only definite treatment is surgical excision of the fistula.
Vascular Emergencies 103
CHAPTER
RUPTURED ABDOMINAL AORTIC ANEURYSM

Rupture of an abdominal aortic aneurysm (AAA) carries significant mortality.
Early diagnosis, prompt resuscitation, and early surgical intervention are of
paramount importance.
Most AAA is saccular and found in the infrarenal part of the aorta.
• The presentation is highly variable ranging from severe pain to syncope or
cardiac arrest. The pain is usually sudden onset, severe, and located to the
central abdomen or low back.
• Examination may show tachycardia, hypotension, one or both absent femoral
pulse or a tender pulsatile abdominal mass.
Diagnosis
• Diagnosis of a ruptured AAA is confirmed by CT angiogram. In patients with
a known AAA, an emergency USG may be sufficient and safer rather than
shifting the unstable patient for a CT scan.
• Close differentials are ureteric colic and acute pancreatitis.
Management
• Obtain intravenous (IV) access and start fluid resuscitation.
• Send cross match for blood products.
• Provide adequate analgesia (Morphine if BP is normal, else Tramadol).
• Give Pantoprazole and an antiemetic (Ondansetron 8 mg IV stat).
• Refer to vascular surgery immediately if clinical suspicion is high.
AORTIC DISSECTION
Aortic dissection is caused by a circumferential or transverse tear of the intima of
the ascending aorta or the descending thoracic aorta. According to the Stanford
classification, they can be of two types:
• Type A/Proximal dissection involving the ascending aorta
• Type B/Distal dissection involving the descending aorta only
CHAPTER 103: Vascular Emergencies 335
Clinical Features
• Abrupt onset of severe pain in the chest or between the scapulae is the most
common presentation
• Examination findings may include hypertension or hypotension, loss of distal
(lower limb) pulses, or pulmonary edema
• Dissection into the carotid artery may result in syncope or hemiplegia
• Paraplegia may result if arterial supply to the spinal cord is interrupted
• Aortic regurgitation, hemopericardium, and cardiac tamponade may
complicate a proximal dissection
Diagnosis
• Chest X-ray: CXR findings of a thoracic dissection usually are, a widening of the
mediastinum, pleural effusion, deviation of the trachea, mainstem bronchi or
esophagus.
• Echocardiography: Transesophageal ECHO is quite sensitive at identifying
dissections involving ascending and descending thoracic aorta. Aortic
regurgitation and pericardial effusion can also be visualized.
• CT/MRI angiography: These are the diagnostic tests of choice for identifying
intimal flap and extent of the dissection.
Management
• Medical management: In the ED, initiate medical management as soon as
diagnosis is suspected
• Treat like a hypertensive emergency and rapidly lower the blood pressure.
Administer a beta blocker (injection labetolol 20 mg IV stat or injection
esmolol 250–500 µg loading dose over 1 min) refer Chapter 37.
• Add a vasodilator like nitroprusside (0.5 µg/kg/min IV) for further antihy-
pertensive effect
• If the patient presents with hypotension, administer fluids and blood
products if required
• Surgical management: Urgent open or endovascular surgical intervention is
the definite treatment of an aortic dissection. Refer to cardiothoracic surgery
and vascular surgery.
ACUTE LIMBISCHEMIA
Acute limb ischemia secondary to a thrombus or embolism requires immediate
intervention for limb salvage. The term 'critical limb ischemia' is used when
chronic progressive peripheral arterial disease results in ischemic pain at rest,
ulceration or gangrene. The following are common causes of arterial occlusion:
• Thrombus (most common): Atherosclerosis or thrombus of native vessels and
bypass grafts
• Embolic: Cardiac source (atrial fibrillation, RHD, mechanical valves, infective

endocarditis)
• Others: Vasculitis (rheumatoid arthritis, lupus, polyarteritis nodosa), Raynaud
disease, thromboangiitis obliterans (Buergers disease), Takayasu arteritis
Clinical Features
The cardinal features of acute limb ischemia are summarized by the six Ps.
1. Pain
2. Paresthesia
3. Pallor
4. Pulselessness
5. Paralysis (due to muscle damage)
6. Poikilothermia
Pain may be either constant or elicited by passive movement of the involved
extremity.
The history should include a history of intermittent claudication, previous leg
bypass or other vascular procedures, and history suggestive of embolic sources,
such as cardiac arrhythmias and aortic aneurysms.
Examination
• Look for skin changes. A clear demarcation between normal and ischemic
skin suggests an embolic cause.
• Palpate all pulses carefully. The presence of normal pulses in the contralateral
limb suggests an embolic source, whereas absent or weak contralateral pulse
makes thrombosis more likely.
• Look for potential sources of emboli (irregular pulse, murmurs, clicks, or
bruits).
Investigations
Investigations include complete blood count (CBC), creatinine, urea, electrolytes,
prothrombin time (PT), activated partial thromboplastin time (aPTT), ECG, chest
X-ray (CXR), rapid blood borne virus screen (BBVS), and hand Doppler screening.
Administer unfractionated heparin (80 U/kg bolus followed by 18 U/kg/h infusion)

immediately, if acute limb ischemia is suspected clinically (unless there is a
contraindication for heparin).
Administer heparin before sending any blood investigation or referring to vascular surgery.
Management
• Unfractionated heparin 80 U/kg bolus followed by 18 U/kg/h infusion.
CHAPTER 103: Vascular Emergencies 337
• Refer to vascular surgery immediately. Revascularization is required within

6 hours to prevent muscle necrosis and complications like renal failure.
• If the etiology is embolus, embolectomy is required.
• If the etiology is thrombosis, angiography is needed to define the site and
extent of the lesion. Thrombolysis with or without reconstructive surgery
would then be required.
ACUTE DEEP VEIN THROMBOSIS

Deep vein thrombosis (DVT) results due to abnormal clotting in the deep venous
system of the legs (popliteal) or pelvis (femoral or iliac). Acute mortality is due to
pulmonary embolism. About 50% of those with DVT will develop post-thrombotic
syndrome with lifelong pain and swelling of the leg.
Risk Factors for DVT

• Recent surgery (especially orthopedic, abdominal, spinal, or obstetric done
under general anesthesia)
• Pregnancy
• Obesity
• Smoking
• Malignancy
• Prothrombotic states: Antithrombin III deficiency, protein C or protein S
deficiency, factor V Leiden mutation, and prothrombin gene mutation.
Clinical Features
Classical symptoms of DVT include leg pain, swelling, warmth, tenderness, and
dilated superficial veins in the affected leg. However, clinical signs depend on the
size and extent of the thrombus and are highly variable.
Investigations
Investigations include CBC, creatinine, electrolytes, D-dimer, PT, aPTT, ECG,
CXR, and venous Doppler.
Administer unfractionated heparin (80 U/kg bolus followed by 18 U/kg/h infusion)

immediately, if acute DVT is suspected clinically (unless there is a contraindication for
heparin).
Administer heparin before sending any blood investigation or referring to vas cular surgery.
Management
• Unfractionated heparin (80 U/kg bolus followed by 18 U/kg/h infusion)
• Prove adequate analgesia (Morphine/Tramadol)
• Refer to vascular surgery.
Breast Disorders 104
CHAPTER
ACUTE MASTITIS AND BREAST ABSCESS

Acute inflammation of the breast tissue (mastitis) may or may not be accompanied
by infection and presents with erythema, edema, and tenderness with or without
fever.
• Lactational mastitis:
cc This condition is most common in the first 3 months of breastfeeding.
Most episodes are caused by Staphylococcus aureus.

cc Initial management of mild lactational mastitis consists of symptomatic
treatment to reduce pain and swelling (nonsteroidal inflammatory agents,

cold compresses). The mother should be encouraged to completely empty
the breast of milk via ongoing breastfeeding, pumping, or hand expression.
cc Moderately severe cases with fever require a course of antibiotics
(Cloxacillin 500 mg PO q6h or Cephalexin 500 mg PO q6H × 5–7 days)

cc Patients with an organized breast abscess will require incision and
drainage or surgical debridement.

• Nonlactational mastitis:
cc Periductal mastitis (mammary duct ectasia) is an inflammatory condition
of the subareolar ducts resulting in periareolar inflammation. Secondary

infection of inflamed ducts may result in duct rupture or abscess formation.
cc This condition is seen in women over 40 years of age and presents with
constant mastalgia associated with nipple retraction and discharge.

cc Management includes pain relief and a course of antibiotics. Refer to
general surgery for definitive management.
MASTALGIA
• Mastalgia (mastodynia) is a common cause of breast pain among men-
struating women and must be differentiated from acute mastitis.
• Cyclical mastalgia usually presents in the immediate premenstrual phase and
resolves completely after menstruation.
• The pain is usually bilateral, but may be more severe in the upper outer
quadrants of the breasts
• Symptoms are relieved by occasional use of nonsteroidal anti-inflammatory
drugs (NSAIDs).
Section 16
Trauma
Early Management of
Trauma 105
CHAPTER
PRIORITIES IN EARLY MANAGEMENT OF TRAUMA

Certain caveats in the early management of a trauma victim are:
• Treat it as the greatest threat to life first.
• Lack of a definitive diagnosis should never impede the application of an
indicated treatment.
• A detailed history is not a prerequisite to begin the evaluation of an acutely
injured patient.
The main steps in the early management of trauma are:
1. Primary assessment
2. Resuscitation: Perform primary assessment and resuscitation together
3. Reassessment of airway, breathing, and circulation (ABC)
4. Secondary assessment
PRIMARY ASSESSMENT
The purpose of a primary assessment is to identify life and limb-threatening
injuries. It should be conducted in a sequential manner as follows:
A—Airway with in-line cervical spine immobilization
B—Breathing with oxygen supplementation
C—Circulation with hemorrhage control
D—Disability: Neurological status, as expressed by the patient
E—Exposure of the entire body, looking for occult injuries
RESUSCITATION
Resuscitation should follow the ABC pattern of the primary assessment, and
should be performed simultaneously.
• If the airway is compromised, the primary assessment should be suspended
till the airway is secured.
• If breathing is compromised, then that should be dealt with. This may require
decompression of a tension pneumothorax or a massive hemothorax. It may
also involve endotracheal intubation and mechanical ventilation in a patient,
who is not breathing adequately.
• Resuscitation of circulation includes insertion of two large bore cannulae and
infusing 2 L of normal saline/Ringer’s lactate solution. At the same time, take
a blood sample for crossmatch, electrolytes, and hemoglobin (Hb).
342 SECTION 16: Trauma
A B
FIGS. 1A AND B: Manual in-line stabilization of the spine.
• While examining or intubating a trauma victim, ask an assistant to perform a

manual in line stabilization of the neck in order to minimize un-intentional
movement of the cervical spine.
This maneuver is performed by an assistant standing at the head end or side of
the trolley and using the fingers and palms of both hands stabilizes the patient’s
occiput and mastoid processes. This should be done while moving a trauma
victim, performing a logroll and during intubation (Figs. 1A and B).
REASSESSMENT OF THE ABC

Reassessment of the ABC is an integral component to ensure that there has been
no decompensation after initial resuscitation. This should be done as each step of
the primary assessment is completed or if there is a time lag between components.
By the end of the primary assessment and resuscitation, the following should
be achieved.
• Airway established and maintained
• Supplemental oxygen initiated
• Cervical spine immobilized
• Two large bore intravenous lines started
• Blood drawn for baseline investigations and crossmatch
• External hemorrhage control achieved
• ECG, BP, and saturation of oxygen (arterial blood) (SpO2) monitoring
• Brief neurological examination completed
• Full exposure and environmental control done.
SECONDARY ASSESSMENT
The secondary assessment should be performed after the completion of primary
assessment. It is a head-to-toe systematic and comprehensive evaluation of all
CHAPTER 105: Early Management of Trauma 343
organ systems. It is during this phase of management that the patient’s detailed
history should be elicited. A useful system for history elicitation is the AMPLE:
A—Allergies
M—Medications (especially anticoagulants, insulin, and cardiovascular
medications)
P—Previous medical or surgical history
L—Last meal (time)
E—Event: Details regarding the biomechanism of injury
Examination of the Head and Face

Immobilize the neck with a hard cervical collar until cervical spine X-ray is
done and cleared. With an assistant immobilizing the head, remove the cervical
collar and examine the neck for any lacerations, tenderness, bogginess, or step
deformities indicating the possibility of a cervical spine injury.
• Scalp lacerations tend to bleed profusely because of abundant vascular
supply. Apply direct pressure to control any bleeding. Check the continuity of
the cranium with a gloved hand, palpating gently with the fingertips. Beware
of small puncture wounds of the scalp, which may indicate penetrating injury
of the brain.
• Assess the Glasgow Coma Scale.
• Examine the nose and ears for bleeding and leakage of cerebrospinal fluid.
• Inspect the mouth for lacerations, broken teeth, or vomitus, since they could
jeopardize the airway.
Examination of the Thorax

Although assessed during primary assessment, the thorax should again be
reviewed for injuries. Check SpO2 to assess peripheral oxygen saturation.
Examination of the Abdomen

• Abdominal assessment includes inspection for contusions, abrasions, and
distension. Discoloration of the flanks may indicate retroperitoneal bleeding.
Any wound above the umbilicus may have penetrated the thorax.
• Femoral pulse should be simultaneously palpated bilaterally and assessed for
equality.
• The integrity of the pelvis should be evaluated by pushing on the wings of the
iliac bone to determine, if this action elicits pain.
• Examine the urinary meatus for the presence of blood, which may indicate
ruptured urethra.
• Perform a digital pelvic examination in females to look for the presence of
vaginal bleeding.
• The patient should be logrolled with the head aligned to the body and the
spine evaluated for asymmetry and the presence of tenderness (Fig. 2).
FIG. 2: Logrolling of the patient.
• During the logroll, perform a rectal examination to evaluate sphincter tone

and presence of blood.
Examination of the Extremities

• Palpate the extremities for tenderness, crepitus, and deformities.
• Evaluate for quality and integrity of pulses. Diminished pulses suggest
disrupted blood vessels. Traction generally restores blood flow.
• If the patient is conscious, assess sensory and motor functions.
• Suspected fractures and dislocations should be splinted for further
radiographic and diagnostic evaluation.
Adjuncts to Secondary Assessment

• Urinary catheter is a vital adjunct for polytrauma management. The urine
output is an excellent way of assessing perfusion in patients with an intact
renal function. Moreover, blood in the urine may indicate renal trauma.
Urinary catheter should be inserted only after ensuring that there are no
pelvic fractures that could have injured the urethra. Blood in the meatus,
perianal hematoma or a high riding prostate on rectal examination should
raise suspicion of a urethral injury. Under these circumstances, urinary
catheterization should only be attempted after an ascending urethrogram.
• Nasogastric tube needs to be inserted, to avoid stomach distension and to
reduce the risk of aspiration. When a base of skull fracture is suspected, the
gastric tube should be inserted orally to prevent intracranial passage.
• If available, obtain an arterial blood gas test to assess the hematocrit, partial
pressure of arterial oxygen and the degree of acidosis.
Mandatory X-rays in trauma evaluation for all high velocity accidents includes
chest, lateral cervical spine, and pelvis. Focused assessment with sonography for
trauma (FAST) is indicated, if intra-abdominal injury is suspected.
Hemorrhagic Shock 106
CHAPTER
INTRODUCTION
The blood volume is 7% of an adult body weight. It is slightly higher in children at
80–90 mL/kg body weight. Clinically, it is possible to estimate the volume of blood
lost in a patient. Four classes of hemorrhagic shock are recognized as tabulated
in Table 1.
From Table 1, it is evident that fall in blood pressure occurs only when more
than 30% of blood loss has occurred.
MANAGEMENT OF HEMORRHAGIC SHOCK

Hemorrhagic shock in trauma is one of the potentially preventable causes of
death. The first step in treatment is recognition of shock, as bleeding may often
be covert. The average amount of blood lost with some common fractures is as
follows: Humerus (750 mL), tibia (750 mL), femur (1,500 mL) and pelvis (>3 L).
Tachycardia is often the first abnormal vital sign of hemorrhagic shock. BP may
be normal till 30% of the blood volume is lost (750–1,500 mL). Hence, prolonged
capillary refill time (normally <3 s) is a very useful test to identify early decrease
in peripheral perfusion due to hemorrhagic shock.
TABLE 1: Blood loss and hemodynamic compensation due to hemorrhagic shock.

Parameter Class I Class II Class III Class IV
Blood loss <750 mL 750–1,500 mL 1,500–2,000 mL >2,000 mL
Blood volume lost <15% 15–30% 30–40% >40%
Heart rate <100/min 100–120/min 120–140/min >140/min
Capillary refill time Normal Delayed Delayed Delayed
Systolic BP Normal Normal Low Low
Diastolic BP Normal Raised Low Often
unrecordable
Respiratory rate Normal 20–30/min 30–40/min >35/min
Urine output >30 mL/h 20–30 mL/h <20 mL/h <20 mL/h
Mental state Mildly anxious Anxious Confused Confused/
drowsy
Resuscitation Crystalloid Crystalloid Crystalloid and Crystalloid
blood and blood
• In the acute phase, the therapeutic priority is control of hemorrhage by

pressure bandage or ligation of bleeders.
• Start 2 large bore IV cannulae (14/16G) in the antecubital fossa and start
fluid resuscitation with ringer lactate. In severe trauma, do not give >1 L of
crystalloids due to the risk of dilutional coagulopathy.
• For significant hemorrhage, transfuse O negative blood followed by type
specific blood.
Tranexamic Acid: Early administration in trauma victims with significant
hemorrhage has been of proven benefit and should be administered to patients
who present within 3 hours of the incident.
Dose: 1 g intravenous (IV) over 10 minutes, followed by IV infusion of 1 g over
8 hours.
Evaluating the type of response to initial resuscitation is important to deter-
mine further management of the patient.The response to the initial resuscitation
may be of three types.
1. Rapid responders: These are patients in whom bleeding has either been
contained or controlled and the initial resuscitation fluid restores the lost
volume.
2. Transient responders: These patients show a good response to the initial
resuscitation but deteriorate when fluids are slowed. They require group
specific blood in addition to crystalloids. A search for the source of bleeding
should be made and a surgical opinion sought.
3. Non-responders: These are patients who continue to deteriorate despite
resuscitation and indicate an ongoing hemorrhage. These patients require
immediate blood transfusion and surgical intervention.
MASSIVE TRANSFUSION PROTOCOL

Severe bleeding results in dilutional anemia and dilutional coagulopathy and
hence, plasma substitutes are required in addition to packed red cells. The “lethal
triad” of trauma is acidosis, hypothermia, and coagulopathy. In patients with
trauma presenting with severe bleeding and expected to require large amount
of blood product transfusion, massive transfusion protocol (MTP) should be
initiated (Flowchart 1).
Massive blood transfusion is most practically defined as:
• Transfusion of >4 units of packed red blood cells (PRCs) in 1 hour when on-
going need is foreseeable
• Replacement of 50% of total blood volume within 3 hours.
When to Activate?
• Polytrauma or severe crush injuries or multiple long bone injuries with
hemorrhagic shock despite fluid resuscitation.
• Thoracic or abdominal trauma with persistent hypotension due to blood loss.
CHAPTER 106: Hemorrhagic Shock 347
(aPTT: activated partial thromboplastine time; FFP: fresh frozen plasma; MTP: massive
transfusion protocol; PCV: packed cell volume; PT: prothrombin time)
FLOWCHART 1: Massive transfusion protocol.
Massive transfusion protocol should be activated by the senior emergency

department physician when the need for massive transfusion is perceived
and usually after 2–3 units of PRCs are transfused. The most acceptable
recommendation for MTP is a predefined ration of 1:1:1 of PRCs:Fresh frozen
plasma (FFP)/cryoprecipitate:Platelets. Once activated, the blood bank should
ensure rapid supply of these blood products for transfusion.
• Packed red cells: 4 mL/kg body weight
• FFP: 10–15 mL/kg body weight
• Cryoprecipitate: 1 unit for every 5–10 kg body weight
• Platelets: 1 unit
Complications of Massive Transfusion

• Volume overload
• Hypothermia (monitor temperature)
• Excessive citrate may cause metabolic acidosis and hypocalcemia (monitor
pH and calcium)
• Hyperkalemia
Head Injury 107
CHAPTER
INTRODUCTION
Traumatic brain injury may be primary or secondary:
• Primary injury occurs at the time of head injury with axonal shearing and
disruption and areas of hemorrhage. The primary damage may be widespread
(diffuse axonal) or localized.
• Secondary injury occurs later and may be due to hypoxia, hypovolemia and
cerebral hypoperfusion, seizures, or infection.
Many of the secondary injuries are preventable with aggressive resuscitation.
GLASGOW COMA SCALE

This scale is now almost universally used to assess the severity of brain injury,
and also to guide management and prognosticate. It has three components with a
total of 15 points. The minimum score of 3 points indicates maximal severity, and
a score of 15 is considered normal. In children, the Glasgow Coma Scale (GCS)
is slightly modified. The total GCS is used to classify the severity of head injury
(Table 1).
• Severe: 8 or less
• Moderate: 9–13
• Mild: 14–15
A cervical spine X-ray before a CT brain is mandatory for all patients with
suspected head injury.
MANAGEMENT
• Initial assessment of a patient with head injury includes airway, breathing,
and circulation management. Airway and breathing may be compromised
due to low sensorium and/or bleeding. Patients with GCS of <8 with airway
compromise will require urgent intubation and those with normal oxygenation
and stable airway will need elective intubation.
• Examine the scalp for lacerations. Scalp wounds can result in significant
blood loss and should be managed by full thickness interrupted suturing at
the earliest.
• Palpate the skull for deformities or tenderness. Signs of base of skull fracture
such as Battle's sign (Mastoid hematoma), bilateral racoon eyes, and CSF
otorrhea or rhinorrhea should be noted.
CHAPTER 107: Head Injury 349
TABLE 1: Glasgow Coma Scale (GCS).

Eye opening Score Verbal response Score Motor response Score
GCS: Adult
Spontaneous eye 4 Oriented 5 Obeys commands 6
opening
Opens eyes to call 3 Confused 4 Localizes painful 5
stimuli
Opens eyes to 2 Inappropriate 3 Withdraws to pain 4
painful stimuli words
No eye opening 1 Incomprehensible 2 Abnormal flexion to 3
sounds pain
No verbal 1 Abnormal extension 2
response to pain
No motor response to 1
pain
GCS: Infant (<1 year)
Spontaneous 4 Coos and babbles 5 Moves spontaneously 6
To verbal stimuli 3 Irritable cries 4 Withdraws to touch 5
To pain only 2 Cries to pain 3 Withdraws to pain 4
No response 1 Moans to pain 2 Abnormal flexion 3
No response 1 Abnormal extension 2
No response 1
• Observe for bleeding or cerebrospinal fluid leak from the ear or nose.
• Start fluid resuscitation and oxygen therapy if saturation is low.
• Decrease intracranial pressure if there is evidence of intracranial herniation
or a dropping GCS. Start 20% mannitol 100 mL stat and q8h.
• Start antiepileptics (phenytoin) if there is any parenchymal injury or a
depressed skull fracture.
• Administer tetanus-diphtheria (Td) vaccine for open injuries if not adequately
vaccinated. At discharge, advice the patient to complete the vaccination
schedule (2 more doses 4 weeks apart).
Cervical Spine 108
CHAPTER
INTRODUCTION
Significant spinal cord injuries are caused by road traffic accidents, heavy weights
falling on a person, fall from a height, etc.
Injudicious movement after trauma and inadequate immobilization during
transportation can cause “secondary spinal cord injury”. In fact, about 10–25% of
neurological deficits occur because of improper prehospital handling.
Principles of Assessment and Management of Suspected

Cervical Spine Injuries
• Assume that all trauma victims have spinal cord injury until proven otherwise,
especially in unconscious patients.
• During transportation of a trauma victim, total spinal immobilization along
with the head, neck, chest, pelvis, and lower extremities should take utmost
priority.
• In spinal cord injuries, there is a high probability of cord edema, which may
cause respiratory arrest. Hence, airway and ventilation must be adequately
addressed during transportation of a trauma victim.
• C-spine immobilization: This can be achieved by using a rigid cervical orthosis,
sandbags, strapping, or a spine board.
• Immobilize spine in the same position the victim presents to you. Do not
attempt to straighten or manipulate the neck.
• General examination of any suspected case of spinal injury must be carried
out with patient in a neutral position and without any movement of the spine.
No spinal segment should be mobilized until it has been specifically cleared
by appropriate radiography.
• A conscious patient with paralysis is usually able to localize the site of an
injury because of tenderness or loss of sensation below that level.
• Paralysis and loss of sensation mask severity of intra-abdominal and lower
extremity injuries.
Classification of Spinal Injuries

• Unstable: Subluxation, bilateral facet dislocation, atlanto-occipital dislocation,
odontoid fracture with lateral displacement, posterior neural arch fracture
(C1), Jefferson’s fracture (C1), and Hangman’s fracture (C2).
• Stable: Unilateral facet dislocation, wedge fracture, Clay Shoveler’s fracture
(C7), and transverse process fracture.
CHAPTER 108: Cervical Spine 351
HOW TO CLEAR A C-SPINE CLINICALLY

History and physical examination can be sufficient in clearing the cervical
spine. Notable clinical prediction rules to determine the need for radiological
imaging are:
1. National Emergency X-Radiography Utilization Study (NEXUS) criteria
2. Canadian C-Spine rules (more sensitive and specific)
However, we recommend the following SMART-D assessment of patients with
suspected cervical spine injuries. (Table 1).
Follow Flowchart 1 to determine indications for C-spine imaging and for
clinical clearance of cervical spine.
RADIOLOGICAL EVALUATION OF CERVICAL SPINE

• Plain radiography is the basic investigation (Lateral/Swimmers cervical spine
X-ray). If the lateral view is inadequate and does not show C7 lower end plate,
then traction can be given to the hand or a swimmers view (the arm closer to
the cassette over the head and the other arm depressed) can be performed.
• This is a crucial investigation as early cord injury, which requires surgery for
good prognosis can be picked up on basis of fractures.
• Delayed recognition may lead to irreversible injury
• All radiographs must be taken with the cervical collar in situ.
TABLE 1: SMART-D assessment of C-spine in the emergency department (ED).

S SENSORIUM • Alertness—whether fully awake and conscious
• Alcohol intoxication
M MECHANISM OF • Painful distracting injury: Refers to any injury to the
INJURY body producing pain sufficient enough to distract the
patient from neck injury. (long bone fractures, visceral
injuries, crush and degloving injuries, burns)
• Dangerous mechanism of injury (Fall from height
>3 feet/5 stairs, axial load to the head, high velocity
motor vehicle accidents, rollover, or ejection motor
vehicle injuries)
A AGE • Age >65 years
R ROTATION OF NECK • Ability to rotate the neck 45 degree left and right (This
step must be performed ONLY if all the other factors of
SMART-D assessment are negative)
T TENDERNESS OVER Assess posterior midline cervical tenderness (from occiput
NECK to T1)
D DEFICITS • Paresthesia in extremities
• Focal neurological deficits
(GCS: Glasgow Coma Scale)

FLOWCHART 1: C-spine assessment.
INTERPRETATION OF THE CERVICAL SPINE X-RAY

Carefully look for the following components while interpreting a cervical spine
X-ray.
• A: Adequacy and Alignment:
cc Adequacy of a spine X-ray is determined by the clear visibility of C7/T1
junction. If this is not visible on a lateral X-ray, a simmers view may be

performed.
cc In a normal C-spine X-ray, all four longitudinal lines shown in Fig. 1B
would be aligned. The four longitudinal lines are

a. Anterior contour line
b. Posterior contour line
c. Spinolaminal line
d. Spinous process line
CHAPTER 108: Cervical Spine 353
• B: Bones:
cc Look for normal bony outline of the vertebrae and bone density. Subtle
changes in bone density should be noted, as it may indicate a compression

fracture.
• C: Cartilage (Disc Spaces):
cc Atlas-dens-space: Distance between the anterior arch of C1 and odontoid
process should be less than 3 mm in adults and 5 mm in children. (Fig. 1A)

cc An increase in any intervertebral disc space suggests regional injury and
hematoma/ ligamentous injury.

cc A good lateral view should show uniform intervertebral disc spaces. Facet
joints are best visualized when a proper lateral view is taken.
B
FIGS. 1A AND B: (A) Normal cervical spine X-ray; and (B) Normal
structural relationship in a lateral view.
• S: Soft Tisssue:
cc Prevertebral soft tissues can be used as an indicator of acute swelling or
hemorrhage resulting from an injury.

cc Air within soft tissue could suggest rupture of the esophagus or trachea
Normal soft tissue thickness as shown in Fig. 1B are as follows:

• At C1 level: 10 mm
• At C2 level: 4–7 mm
• Retrotracheal space (C5–C7): 20 mm
Maxillofacial Trauma 109
CHAPTER
INTRODUCTION
Facial trauma is also known as maxillo-facial trauma. Fractures of the facial bones
can be classified as follows:
• Major fractures: Le Fort I, II, III, and mandibular.
• Minor fractures: Nasal, sinus wall, zygomatic, orbital floor, antral wall, and
alveolar ridge.
Le Fort Fractures
Le Fort fractures are complex fractures of the midface determined by areas of
structural weakness of the maxilla. These fractures are classified into three types,
based on the direction of the fracture: Horizontal, pyramidal or transverse (Fig. 1).
The pterygoid plate is involved in all the three types.
Le Forts fractures can be clinically differentiated by pulling forward on
maxillary teeth:
• Le Fort I: Only the maxilla moves. Also called horizontal maxillary fracture, the
maxilla is separated from the palate. Clinically presents with swollen upper
lip, malocclusion of the teeth and palatal ecchymosis.
• Le Fort II: Maxilla and base of nose move. Also called pyramidal fracture,
the fracture line crosses the nasal bones and the orbital rim. Clinically
FIG. 1: Le-Fort-classification-of-maxillary-fractures.
presents with significant facial deformity, swelling, malocclusion of the teeth,

intercanthal space widening, epistaxis, raccoon eyes.
• Le Fort III: The whole face moves. Also called craniofacial dysjunction or
transverse facial fracture. Clinically present with bilateral raccoon eyes,
elongation and flattening of the face (dish-face deformity), enopthalmos, CSF
rhinorrhea/otorrhea and hemotympanum.
Nasal Fractures
• Often diagnosed clinically: X-ray not needed
• Prime concerns are epistaxis and septal hematoma.
Septal hematomas are associated with necrosis of the septum if left untreated
and should be drained as soon as possible. Simple incision and expression of the
clot followed by anterior packing is sufficient. Pack is kept in place for 2–3 days.
The patient should follow up with an otolaryngologist for nasal pack removal and
reassessment.
Temporomandibular Joint Dislocation

The temporomandibular joint (TMJ) consists of the articulation of the temporal
and mandibular bones. TMJ dislocation occurs when the condyle travels anteriorly
along the articular eminence and becomes locked in the anterior superior aspect
of the eminence, preventing closure of the mouth.
Dislocation results in stretching of the ligaments, and is associated with severe
spasm of the muscles that open and close the mouth (i.e., the masseter, medial
pterygoid, and temporalis). The resultant trismus prevents the condyle from
returning to the mandibular fossa.
Anterior TMJ dislocation commonly follows:
• Extreme opening of the mouth (e.g., during eating, yawning, laughing, and
dental treatment)
• Trauma
• Dystonic reactions to drugs
• Seizures
Steps in the manual reduction of anterior dislocation of TMJ (Fig. 2).
1. Massage the masseter muscles in order to relax and fatigue them which may
facilitate manual reduction.
2. Sedation and muscle relaxation (Injection Midazolam 5 mg IV + Injection
Morphine 5 mg IV).
3. The emergency department registrar should face the patient and an assistant
should hold the head from behind to prevent movement of the head.
4. Grasp the mandible with both hands; the thumbs resting on the occlusal
surfaces of the teeth and the fingers wrapped around the outside of the jaw.
5. Apply downward pressure to the mandible to free the condyles from the
anterior aspect of the eminence; then guide the mandible posteriorly
(backward) and superiorly back into the temporal fossa.
CHAPTER 109: Maxillofacial Trauma 357
FIG. 2: Reduction of anterior dislocation of temporomandibular joint.
6. Refer to maxillofacial surgeon (dental surgery) for further follow up.
Downward Backward Upward
After successful reduction of a TMJ dislocation, do an orthopantomogram

(X-ray mandible lateral view) to ensure adequate reduction and to exclude an
avulsion fracture.
Following reduction, the patient should receive the following instructions:
• Avoid extreme opening of the jaw for 3 weeks
• Support the lower jaw when yawning
• Apply warm compresses to the TMJ area for 24 hours
• Take nonsteroidal anti-inflammatory drugs as needed for pain and swelling.
The following patients should be urgently referred to an oral and maxillofacial
surgeon:
• Patients with an anterior TMJ dislocation in association with a fracture
• Patients who fail reduction of an anterior TMJ dislocation despite multiple
attempts
• Patients who have had more than two prior TMJ dislocations
• Patients with superior or posterior dislocations.
Thoracic Injuries 110
CHAPTER
INTRODUCTION
• About 25% of deaths due to trauma are a result of thoracic injuries.
• Majority of deaths (60–70%) occur after patient reaches a hospital.
• The following are the five immediately life-threatening chest injuries that
should be identified in the primary assessment. Failure to identify these could
be immediately fatal (Table 1).
cc Tension pneumothorax
cc Open pneumothorax
TABLE 1: Clinical features and management of common thoracic injuries.

Tracheal Chest wall Breath Percussion Treatment
position movement sounds
Tension Away Decreased Decreased Hyper- • Immediate:
pneumothorax or absent resonant Needle
thoracostomy
• Definitive: Tube
thoracotomy
Open Midline Decreased May be May be • Immediate:
pneumothorax decreased hyper- Occlusive
resonant dressing over
Usually the wound,
normal which is taped
on three sides
• Definitive: Tube
thoracotomy
• Massive Midline Decreased Dimini- Dull, • Fluid
hemothorax shed, especially replacement
• Defined as if large posteriorly • Tube
accumulation Normal, if thoracotomy
of >1,500 mL small • Surgical
of blood in thoracotomy,
the thoracic if initial blood
cavity loss via chest
tube >1,500 mL
or a persistent
need for blood
transfusion
Continued
CHAPTER 110: Thoracic Injuries 359
Continued
Tracheal Chest wall Breath Percussion Treatment

position movement sounds
Flail chest + Midline Paradoxical Normal Normal • Adequate
pulmonary movement may have ventilation,
contusion of the flail crackles humidified
segment O2, analgesics
and fluid
resuscitation
• Endotracheal
intubation
in case of
impending
respiratory
failure
cc Flail chest
cc Massive hemothorax
cc Cardiac tamponade
TENSION PNEUMOTHORAX
If the air leak occurs through “one-way valve” from the lung or through the chest
wall, the air is forced into the thoracic cavity completely collapsing the affected
lung. This condition, known as tension pneumothorax causes cardio-respiratory
collapse by shifting the mediastinum to the contralateral side and compression of
the great vessels of the thorax. Immediate decompression by needle thoracostomy
is warranted. Common causes of tension pneumothorax are mechanical
ventilation with positive end-expiratory pressure, ruptured emphysematous
bullae, blunt trauma, in which parenchymal leak which has not sealed.
OPEN PNEUMOTHORAX
Open pneumothorax is caused by a large wound in the chest wall, that remain
open. Equilibrium between intrathoracic and atmospheric pressure occurs
almost immediately. If the opening is greater than two-thirds the diameter of
the trachea, air passes through the defect from the atmosphere thus impairing
ventilation.
Emergency management: If a patient has an open wound in the thorax causing
tension pneumothorax, apply a sterile occlusive dressing over the wound and
tape it on 3 sides (Fig. 1). The 3 way occlusive dressing provides a flutter type valve
and prevents air from entering from outside.
FIG. 1: 3 way occlusive dressing.
FLAIL CHEST + PULMONARY CONTUSION

These occur when there are fractures of two or more ribs at two or more sites.
A bony segment moves independent of the rest of the thoracic cavities. The
pathophysiology arises from underlying lung injury, along with impaired
pulmonary mechanics. The flail segment does not move with the rest of the lung
during respiration. Although chest wall instability leads to paradoxical motion of
the chest wall with inspiration and expiration, this defect alone does not cause
hypoxia. Associated pain with restricted chest wall movement and underlying
lung injury contribute to the patient’s hypoxia. The injured lung in flail segment
is sensitive to both under and over hydration and hence adequate care must be
taken during fluid resuscitation.
Tension pneumothorax is a clinical diagnosis. Do not wait for radiological confirmation to

intervene.
CARDIAC TAMPONADE
Relatively small amount of blood (150 mL) in the pericardial sac can increase
the pressure around the heart leading to impaired cardiac filling and decreased
cardiac output. The classic Becks triad of cardiac tamponade includes distended
neck veins, muffled heart sounds, and hypotension. Most patients will have
at least one of these signs; all three rarely appear simultaneously. Urgent
pericardiocentesis is warranted and the removal of as little as 10–15 mL of blood
from the pericardial cavity results in remarkable improvement.
Abdominal Injuries 111
CHAPTER
INTRODUCTION
• Abdominal trauma is a cause of preventable deaths, which can easily go
unnoticed if one does not search for it.
• When assessing the “C” in trauma, the abdomen and pelvis are important
areas to rule out bleeding.
• Any mechanism of injury involving the torso, such as blunt or penetrating
injuries or deceleration injuries can cause abdominal injuries.
cc Blunt trauma occurs in 85% while penetrating trauma accounts for only
15% of all abdominal traumas.

cc Large amounts of blood can accumulate in the peritoneal and pelvic
cavities without any significant or early changes in the physical examination

findings.
• In the case of blunt injuries, the following is the incidence:
cc Spleen: 40–55%
cc Liver: 35–45%
cc Bowel: 5–10%
• In the case of stab injuries, the following is the incidence:

cc Liver: 40%
cc Small bowel: 30%
cc Diaphragm: 20%
cc Colon: 15%
• In the case of gunshot injuries, the following is the incidence:

cc Small bowel: 50%
cc Colon: 40%
cc Liver: 30%
EVALUATION
• Assessment of hemodynamic stability is the most important initial concern in
the evaluation of a patient with abdominal trauma.
• Chest X-ray to look for diaphragmatic hernia, hemothorax, or air under the
diaphragm.
• Extended focused assessment with sonography in trauma (eFAST) (Fig. 1) is
the dominant imaging modality used in the early assessment of abdomino-
thoracic trauma. In a hemodynamically unstable patient with a negative
eFAST, it may be prudent to repeat it after 10 minutes. If a hemodynamically
stable patient has a positive eFAST, a CT thorax and abdomen needs to be
performed.
(eFAST: extended focused assessment with sonography in trauma)

FIG. 1: The sequence of 8 views that make up the eFAST examination.
• A CT scan though has the highest positive yield rate, should be reserved only
for persistently stable patients.
Do not shift a hemodynamically unstable patient for a CT scan.
MANAGEMENT
Emergency Department Management
• Secure airway and breathing
• Start 2 wide bore IV lines above the diaphragm and start fluid resuscitation
• Avoid femoral central line
• Tranexamic acid 10 mg/kg IV (1 g in adults) over 10 minutes, if the patient
presents within 3 hours of trauma
• If the penetrating object is still in place, DO NOT ATTEMPT TO REMOVE IT
• Avoid palpating the prostate by digital rectal examination (DRE). It must be
done only to assess bleeding PR, or anal tone
Surgical management may involve either operative intervention (laparotomy)
or conservative management.
Indications for Emergency Laparotomy

• Bowel or bladder rupture
• Peritonitis
• Uncontrolled shock despite adequate resuscitation
• Penetrating injuries: Relative indication
• Air under the diaphragm
• Massive intra-abdominal bleed.
CHAPTER 111: Abdominal Injuries 363
Nonoperative Management
This involves frequent monitoring of hemodynamic status and bleeding
manifestations.
• Hemodynamically stable patients with positive eFAST findings require a CT
scan to define the nature and extent of their injuries and thus augment the
decision to manage by nonsurgical intervention.
• Operative treatment is not indicated in every patient with positive eFAST
results, since this could result in an unacceptably high laparotomy rate.
Most pediatric patients can be resuscitated and treated nonoperatively.
Hemodynamically stable adults with solid organ injuries, primarily those to
the liver and spleen, may be candidates for nonoperative management.
Extremity Injuries 112
CHAPTER
FRACTURES
Definition
A fracture is any break in the continuity of the bone.
• Open versus Closed: Open fractures occur when either the fractured bone
communicates with the exterior by breaching the muscle planes and skin or
as a result of an external injury exposing the bone at the fractured site. Open
injuries need to be prioritized over closed fractures to limit infection.
• Based on pattern: Fractures can be radiologically described as transverse,
oblique, segmental, comminuted, or with bone loss.
Signs and Symptoms

Signs and symptoms can be as overt as gross deformity of the limb, restriction of
movements of joints with pain or as subtle as tenderness with limb shortening.
Gustilo and Anderson Classification

This is a useful tool for assessing open fracture severity (Table 1).
TABLE 1: Gustilo open fracture classification.

Gustilo grade Definition
I Open fracture, clean wound, and wound <1 cm in length
II Open fracture, wound >1 cm but <10 cm in length without extensive soft-
tissue damage, flaps, and avulsions
III Open fracture with extensive soft-tissue laceration (>10 cm), damage, or
loss or an open segmental fracture. This type also includes open fractures
caused by farm injuries, fractures requiring vascular repair, or fractures
that have been open for 8 h prior to treatment
III A Type III fracture with adequate periosteal coverage of the fracture bone
despite the extensive soft-tissue laceration or damage
III B Type III fracture with extensive soft-tissue loss, periosteal stripping, and
bone damage. Usually associated with massive contamination. Will often
need further soft-tissue coverage procedure (i.e., free or rotational flap)
III C Type III fracture associated with an arterial injury requiring repair,
irrespective of degree of soft-tissue injury
Source: Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open
fractures: A new classification of type III open fractures. J Trauma. 1984;24:742-6.
CHAPTER 112: Extremity Injuries 365
Compound or open fractures occur when a fracture is open through a skin

wound. These may be associated with gross soft tissue damage, hemorrhage, or
vascular injuries.
Basic Principles of Management of Fractures

• Obtain proper history of the mechanism of injury.
• Administer analgesia prior to handling the wound.
• Administer tetanus-diphtheria (Td) vaccine as prophylaxis, if not adequately
immunized.
• Start antibiotics only in open injuries.
• Realign limb to minimize deformity and pain.
• Document any neurovascular deficit.
• Using sterile techniques, wash the wound with normal saline and apply sterile
padding.
• Immobilize the affected limb one joint above and below the fracture site with
appropriate splint or traction.
• Keep the limb elevated to minimize swelling.
X-rays
• Order only minimal, relevant imaging to clinch a diagnosis.
• X-rays of a fractured limb should involve one joint above and below the
fractured site.
• Always order two views of a limb [anteroposterior (AP) and lateral].
• In children, order X-rays of the normal limb too, for comparison and to avoid
confusion over growth plates.
Investigations
The investigations include packed cell volume (PCV), creatinine, electrolytes, and
rapid blood borne virus screen (BBVS) (if surgery is required).
Preservation of Amputated Part

Remember only clean cut amputations can be salvaged; crushed, or ragged body
parts are nonsalvageable.
• Wash part in isotonic solution
• Wrap in sterile gauze soaked in penicillin (100,00 units in 50 mL of Ringer’s
lactate)
• Wrap this in a sterile moist towel
• Place in a plastic bag
• Keep in crushed ice and avoid freezing
• Call the hand surgery team on arrival of patient itself, as time to surgery is the
key to a good prognosis.
COMMON FRACTURES SEEN IN THE EMERGENCY

DEPARTMENT
Hand Fractures
Hand fractures are commonly seen but commonly missed.
• Initial treatment: Follow basic principles of management.
• Fingers can be buddy-splinted by strapping the injured finger to a neighboring
unaffected finger (Fig. 1).
• X-rays: Anteroposterior and oblique views for full hand.
• For isolated finger injuries: AP and lateral views focusing on the specific finger.
FIG. 1: Buddy taping of fingers.
Colles Fracture
It is the most common distal radius injury (fracture at the base of the ulnar
styloid process). This results from a fall on the out stretched hand with the wrist
in dorsiflexion. Carefully examine the median nerve and motor function of the
finger flexors.
• Intra-articular fractures require an orthopedic intervention.
• Extra-articular fractures can be close reduced and sent to outpatient
department in a cast or splint.
Reduction Technique (Figs. 2A to C)

• Administer a hematoma block; allow it to take effect.
• Then reduce the fracture by giving a sustained linear traction, with one
assistant pulling on the proximal part at the elbow while another assistant
holds the thumb separately with one hand and the rest four fingers with the
other giving a counter traction distally in 30 degree of ulnar deviation and
10 degree of palmar flexion.
A B
C
FIGS. 2A TO C: Reduction of Colles fracture.
• Placing your hands on the fracture site, manually realign the fracture by
reversing the position of the displaced fragments.
• Then maintaining the traction-countertraction, now apply a padded Colles
cast to maintain the reduction.
X-rays
Anteroposterior and lateral of the wrist with forearm; repeat check X-rays after
reduction.
Pelvic Fractures
This is a potentially life-threatening condition which should be recognized
immediately. An “open book” fracture with diastasis of more than 2 cm is
considered unstable.
When to Suspect?
• High-velocity trauma
• Falls from height
• All trauma patients presenting with unexplained hypotensive shock.
Pelvic Compression Test

This test is done to confirm a pelvic fracture. This is done by giving downward and
inward compression to both iliac crests simultaneously. If one feels a “give” it is
considered to be positive for an unstable pelvis. Perform this test only once.
X-rays
Pelvis anteroposterior view.
Treatment
• Avoid moving the patient unnecessarily
• Apply a pelvic binder (any broad sheet or cloth can be used for this purpose)
• Fluid resuscitation as required and maintain the blood pressure
• Avoid catheterization till urethral injury has been ruled out.
Hip Fractures
These are very common in the elderly and mostly result from fall on the level
ground. This can be associated with acetabular fractures.
Neck of Femur versus Intertrochanteric Fractures

These can be easily diagnosed clinically by observing the attitude of the lower limb.
• Neck of femur fracture: Being an intracapsular fracture, patients present with
slight shortening and mild external rotation of the lower limb.
• Intertrochanteric fractures: Being an extracapsular fracture, patients present
with ecchymosis of the overlying skin, shortening and gross external rotation
of the lower limb.
X-rays
Pelvis with both hips (in 10 degree of internal rotation)—anteroposterior and
lateral view of affected hip. Follow the Shenton’s line for finding obscure fractures
(Fig. 3).
FIG. 3: Shenton’s line.

Treatment
Initial treatment consists of immobilizing the lower limb with skin traction. There
is no role for splints.
Shaft of Femur and Tibia Fractures

Both these injuries are common in road traffic accidents. Always assess the
neurovascular status in these limbs, as the incidence of neurovascular injuries is
quite high. Monitor for compartment syndrome.
X-rays
Anteroposterior/lateral views visualizing both the joint above and below the shaft.
Always request for an additional X-ray of the pelvis with both hips, as fracture
dislocation is often associated with these injuries.
Treatment
Immobilize with a Below Knee (B/K) splint for a tibia fractures and Above Knee
(A/K) splint for a femur fracture.
Alternately, a Thomas splint may be used for these fractures, which is also the
best way to transfer a patient.
DISLOCATIONS
• Dislocation is a complete loss of articular contact between two opposing joint
surfaces.
• Subluxation is a partial loss of articular contact between two opposing joint
surfaces.
Signs and Symptoms

A dislocation is more painful than sustaining a fracture and therefore needs
immediate attention. However, they are often associated with a fracture.
Based on the joint involved, the presentation is usually classical for that joint.
Always check the neurovascular status of the limb.
Investigations
No routine blood investigations are required for dislocations.
Role of X-ray
X-ray is not needed in habitual or recurrent dislocations. In first time dislocations,
an X-ray may be warranted to rule out other injuries as well. However, do not delay
getting it done as one needs to reduce the dislocation soon after.
The following are some of the more common dislocations one would
encounter in the emergency department (ED).
SHOULDER DISLOCATIONS
Anterior glenohumeral (AGH) (Fig. 4) dislocations are the most common, while
posterior (PGH) accounts less than 1%. Luxatio erecta (inferior dislocation) and
superior are extremely rare (Table 2).
Clinical Examination (Focused)

• Anterior glenohumeral dislocation: Arm is usually held in abduction and slight
external rotation with shoulder appearing “squared off”, i.e., loss of normal
rounded contour. Humeral head (HH) is palpable and anterior to shoulder
joint.
• Posterior glenohumeral dislocation: Arm is usually adducted and internally
rotated making the anterior shoulder appear flat. Prominence of the coracoid
and HH is palpable posterior to the shoulder joint.
• Inferior dislocation: HH is palpable in the lateral chest wall with the arm fully
abducted, elbow flexed, and forearm lying behind or on the head.
• Look for axillary nerve injury by checking sensation over the deltoid region.
• Check for brachial and radial artery pulsation.
A B
C D
FIGS. 4A TO D: Types of anterior glenohumeral dislocation.

TABLE 2: Types of shoulder dislocation.

Types Subtypes Description of injury Associated injuries
Anterior (MOI: Subcoracoid HH displaced anterior Fracture greater
Indirect blow with (most common) to glenoid and tuberosity, humeral
arm in abduction, inferior to coracoid neck, anterior glenoid
extension, and rim (Bankart fracture),
external rotation) and axillary artery
injury
Subglenoid HH lies inferior
and anterior to the
glenoid
Subclavicular HH displaced medial
to coracoid below the
clavicle
Intrathoracic HH lies between the
ribs and thoracic
cavity
Posterior (MOI: Subacromial HH posterior to Fracture of posterior
Indirect forced (most common) glenoid and inferior glenoid rim, humeral
internal rotation to acromion head, and shaft and
and adduction) lesser tuberosity
Subglenoid HH lies inferior and
posterior to glenoid
Subspinous HH lies inferior to
spine of scapula
Inferior (MOI: Neck of humerus is Severe soft tissue
Continuous levered against the injury, rotator cuff tear,
hyperabduction acromion and inferior neurovascular injury,
force at shoulder) capsular tear and fracture proximal
humerus
(HH: humeral head; MOI: mechanism of injury)
X-rays
• X-ray of anteroposterior view of the shoulder.
• X-ray of scapular Y view—to classify the dislocation further.
Treatment
• Posterior and inferior glenohumeral dislocations need expertise and should
be reduced and managed only by orthopedicians.
• Anterior dislocations are commoner and may be reduced in the ED. Under
sedation, all attempts to reduce the dislocation should be done by one of
the following techniques available. Most techniques use either leverage or
traction-countertraction mechanisms.
Stimson’s Technique
This is very useful in a busy ED where one cannot attend to the patient immediately
or in a situation where an anticipated difficult reduction (as in a dislocation which
occurred many hours earlier) is expected (Fig. 5).
• Administer a good dose of analgesic before the procedure.
• Place the patient in prone position with the affected arm hanging down by the
side of the table.
• Place a folded sheet under the clavicle of the affected side and attach a weight
of approximately 3–5 kg to the wrist of the affected hand.
• The muscles will slowly relax and gravity helps to reduce the dislocation in
20–30 minutes.
• In addition to above steps, a manual rotation of tip of the dislocated scapula
medially with one hand and stabilizing upper scapula with the other hand
help in much easier reduction with a success rate close to 96% (Scapular
manipulation).
• Monitor the neurovascular status periodically.
Kocher’s Technique
This technique was first described in 1870 as a painless procedure and since then
many modifications have been proposed. This method uses leverage alone and
does not involve traction (Figs. 6A to D).
• Place the patient supine and stand by the side of the affected arm.
• Bend the arm at 90 degree at the elbow and adduct it against the body.
• Grasp the wrist and the point of the elbow.
• Externally rotate the arm by 70–85 degree until a resistance is felt.
• Lift the externally rotated arm in the sagittal plane as far forward as possible.
FIG. 5: Stimson’s technique for shoulder.

A B
C D
FIGS. 6A TO D: Kocher’s technique for shoulder reduction.
FIG. 7: Matsen’s traction—countertraction method.
• Now internally rotate the shoulder to bring the patient’s hand toward the
opposite shoulder.
• This should result in the femoral head slipping into the glenoid fossa.
• Patient can be discharged after a check X-ray, on an arm pouch.
Matsen’s Traction—Countertraction Method

This technique employs the traction-countertraction principle and requires an
assistant (Fig. 7).
• Place the patient in the supine position.
• Wrap a sheet around the patient’s thorax under the axilla that is held by the
assistant standing on the other side to provide countertraction.
• With the elbow of the affected arm flexed at 90 degree, grasp the forearm, lean
back, and apply traction at 30–40 degree abduction.
• The assistant should pull on the sheet toward the opposite shoulder to provide
countertraction.
• This usually unhinges the dislocated shoulder back into its normal position.
HIP DISLOCATIONS
Hip dislocations are classified into anterior hip dislocation (AHD), posterior hip
dislocation (PHD), central, and inferior (luxatio erecta) (Table 3) and are usually
associated with motor vehicle accidents without seat belt usage.
TABLE 3: Types of hip dislocation.

Types Subtypes and description of Associated injuries
dislocation
Anterior (10%) (MOI— Epstein classification of anterior • Fracture and impaction
forceful extension, hip dislocation (Fig. 8) of femoral head
abduction and external • Superior dislocation (pelvis) • Fracture of acetabulum
rotation of the leg. • Inferior dislocation (obturator) • Femoral artery and
Femoral head levers out nerve injury
of the acetabular cup)
Posterior (90%) [MOI— Thompson and Epstein 10% incidence of sciatic
axial force over the classification of posterior hip nerve injury especially
femur with knee and dislocation (Fig. 9) the peroneal branch
hip flexed, adducted, • Simple dislocation with or
and internally rotated without an insignificant
(dash board injury)] posterior wall fragment
• Dislocation associated with
a single large posterior wall
fragment
• Dislocation associated with a
comminuted posterior wall
fragment
fracture of the acetabular floor
fracture of the femoral head
Central (rare) Entire femoral head is forced Acetabular fracture
centrally through comminuted
acetabular fracture
Inferior (very rare) Exclusively in children <7 years
(MOI: mechanism of injury)
A B
FIGS. 8A AND B: Epstein classification of anterior hip dislocations.
A B C
D E
FIGS. 9A TO E: Thompson and Epstein classification of posterior hip
dislocations.
Examination (Focused)
• Anterior hip dislocation—the dislocated limb lies in abduction, external
rotation, and in slight flexion.
• Posterior hip dislocation: The dislocated limb lies flexed, adducted, and
internally rotated such that the knee rests on the unaffected limb. There
is shortening of the dislocated limb, prominence of greater trochanter, and
buttock.
• Do not forget to examine for distal pulsation, especially in AHD.
• Check peroneal nerve injury by dorsiflexion of the ankle and extension of
extensor hallucis longus against resistance (PHD).
X-rays
• X-ray of the pelvis with both the hip joints’ AP and lateral view (if the patient
cooperates).
• X-ray of Judet view of the pelvis—look for acetabular and rim fractures.
Treatment
Hip dislocations should be reduced in less than 6 hours in order to prevent
avascular necrosis.
Reduction of a Posterior Hip Dislocations

Allis Technique
• After adequate procedural sedation, place the patient on the floor from the
trolley or bed.
• Ask the assistant to stabilize the pelvis by applying pressure over both the
anterior and superior iliac spine and the physician should flex patient’s
dislocated hip and knee to 90 degree with inline continuous traction as
demonstrated in the Figure 10.
• The reduction is achieved by slight internal and external rotation at the hip.
Anterior hip dislocation is relatively rare and earlier referral to orthopedic team for
reduction is ideal.
Complications
• Osteonecrosis, the incidence of which is directly proportional to the time
taken for reduction.
• Post-traumatic osteoarthritis on long term
FIG. 10: Allis technique for reduction of posterior dislocation.

• Recurrent dislocation (2%)

• Neurovascular injury.
PATELLAR DISLOCATIONS
Patellar dislocations occur due to twisting injury on an extended knee resulting
in severe pain and deformity of the knee. Without exception, patellar dislocations
are lateral due to the pull of the stronger lateral ligaments. Habitual or recurrent
dislocations can also occur.
Attitude
Knee is semiflexed with a bony prominence seen or felt usually lateral to the knee
joint.
Treatment
Under sedation all attempts to reduce the dislocation should be attempted by the
technique described (Fig. 11).
• Flex the hip, hyperextend the knee and slide the patella medially back into
place.
• This maneuver results in immediate relief of pain.
Perform an X-ray to rule out a fracture or an intra-articular loose body. Apply
a knee brace for primary dislocations after the relocation procedure to allow
healing.
FIG. 11: Reduction of patellar dislocation.

CASTS AND SPLINTS

• Plaster of Paris (POP): POP is cheap and easily available. Disadvantages are
susceptibility to damage or disintegration and longer time (<48 h) for large
casts to dry fully after the application of cast.
• Resin casts: These are costlier, but lighter and stronger than POP. They are also
more resistant to water. They set in 5–10 minutes and gain maximum strength
after 30 minutes. However, they are more rigid and harder to mold and hence
more difficult to apply and remove.
Steps in Applying a POP Slab

• Prepare the cotton base: Apply a 6-inch bandage roll to the desired length and
apply to a thin layer of nonabsorbable cotton over the bandage.
• Prepare the POP roll: Spread the POP roll to the exact length of the limb. Layer
the POP roll over itself 9–10 times for the upper limb and 10–11 times for the
lower limb.
• Prepare the slab: Soak the plaster roll in a pail containing water for 5 seconds.
Squeeze gently without twisting or wrinkling to remove excess water and
stretch out the roll. Place the POP layer over the cotton base and fold the edges
of the base over it.
• Apply the slab: Place the slab over the posterior aspect of the limb with the
cotton base in contact with the skin and the limb in the desired position. Apply
2–3 layers over the slab and await setting and to hold the slab in position. It
sets firmly in position in about 30 minutes.
Complications
• Local irritation
• Excessive tightness and pain leading to vascular compromise
• Pressure necrosis
• A loose slab may cause the fracture to worsen.
FAT EMBOLISM SYNDROME

Presence of fat globules in pulmonary circulation 24–72 hours following an initial
insult like long bone fractures and multiple fractures.
Triad of Fat Embolism

• Early pulmonary symptoms (Hypoxemia, dyspnea, tachypnea, and ARDS)
• Neurological symptoms (Minor global dysfunction, seizures, and focal deficits)
• Cutaneous manifestations (Petechial rash on conjunctiva, neck and axilla)
Management
• Early immobilization of fracture reduces incidence of fat embolism syndrome
• Early fixation (External fixation/Open reduction and Internal fixation)
• Administer oxygen if the patient is hypoxic (SpO2 <94%). There is no role for
prophylactic oxygen administration
Wound Management 113
CHAPTER
INTRODUCTION
Instructions to be followed as part of wound management are:
Wound Wash
• All open wounds should be thoroughly washed before and after wound
debridement as it clears the debris and hematoma whilst providing optimal
exposure, reducing contamination, and bacterial load.
• Wound irrigation should be done before and after wound debridement
as it clears the debris, hematoma and provides optimal exposure, reduces
contamination and bacterial load. It should be a part of routine wound
management.
• Low pressure irrigation can be performed in the emergency department (ED)
using a syringe/bulb and is usually adequate to remove material from the
surface of most wounds.
• Warm, isotonic, normal saline is typically used for wound irrigation. There is
no advantage of adding soap/antiseptics/antibiotics to lavage fluid.
• Use of hydrogen peroxide, alcohol solution, povidone iodine, and other
chemical agents may impair osteoblast function, inhibit wound healing and
cause cartilage damage and hence should not be used.
• Adequate quantity of lavage fluid must be used for cleaning the wound based
on the principle “the solution for pollution is dilution”. Typically, >9 L of fluid is
required for Gustillo type IIIb injuries.
Tetanus Prophylaxis
• Diphtheria-tetanus (dT) vaccine and human tetanus immunoglobulin (TIG)
should be administered to all patients with open wounds.
• At discharge, advice the patient to complete the full course of tetanus
vaccination with 2 more doses of dT given at 4 weekly intervals.
Analgesia
Be generous in administering analgesics like opioids as soon as the patient
presents to the ED.
SUTURE MATERIALS
Suture materials are classified as absorbable or nonabsorbable, natural or
synthetic, and braided or monofilament.
• Absorbable suture materials: Defined by the loss of most of their tensile
strength within 60 days after placement. These are best suited for closure of
deep structures such as dermis and fascia.
cc Natural absorbable sutures: Catgut (made from sheep or cattle intestines)
cc Synthetic braided sutures: Polyglycolic acid (Dexon) and polyglactin 910
(Vicryl)
cc Synthetic monofilament sutures: Polydioxanone (PDS), polytrimethy lene
carbonate (Maxon), poliglecaprone (Monocryl), glycomer 631 (Biosyn),

and polyglytone 6211 (Caprosyn).
• Nonabsorbable suture materials: Defined by their resistance to degradation by
living tissues. These are most often used to close the outermost layers of the
skin or for repair of tendons.
cc Natural absorbable sutures: Silk, cotton, and linen
cc Synthetic braided sutures: Composed of nylon and polyester (infrequently
used)
cc Synthetic monofilament sutures: Nylon (Ethilon), polypropylene (Prolene),
and polybutester (Novafil).

• Monofilament synthetic sutures (nylon or polypropylene) have the lowest
rates of infection.
• Braided sutures are usually easier to handle and tie, but can harbor bacteria
between strands and cause higher infection rates.
The higher the number of zeros (1-0 to 10-0), the smaller the size and the lower
the strength:
• Hand and finger lacerations: 5-0 sutures
• Facial laceration: 5-0 or 6-0 sutures
• Scalp lacerations: 3-0 or 4-0 sutures
• Other lacerations: 4-0 sutures
SUTURE NEEDLES
• Cutting: Have opposing cutting edges.
• Conventional cutting: Have a third cutting edge on the inside concave
curvature of the needle.
• Reverse cutting: Have a third cutting edge located on the outer convex curvature
of the needle. It is used for thick skin like the palm and soles.
Scalp Laceration 114
CHAPTER
INTRODUCTION
Scalp laceration is a common injury presenting to the emergency department (ED).
The scalp consists of five layers, best remembered by the mnemonic SCALP:
• S: Skin
• C: Subcutaneous tissue
• A: Aponeurosis and muscle (contains the middle meningeal artery)
• L: Loose areolar tissue and subgaleal fascia
• P: Periosteum
In lacerations, separation usually occurs at the layer of loose areolar tissue.
Clinical evaluation should identify associated serious head injury, laceration of
the galea, or bony defect of the skull. Removal of all foreign debris and blood will
allow for proper assessment.
MANAGEMENT
Hemostasis
Bleeding may be profuse and substantial blood loss can occur with scalp
lacerations. Hemostasis should be achieved by applying direct pressure for
5–15 minutes with or without local injection of lidocaine and adrenaline. If this
fails, the edges of the laceration should be everted and rapidly closed with simple
interrupted sutures.
Wound Debridement and Cleansing

After hemostasis is achieved and the wound should be irrigated using a syringe
with 26-G needle, administer local or regional anesthesia prior to initiating
irrigation and wound cleansing to improve patient comfort.
• Small and clean wounds can be irrigated with isotonic 0.9% normal saline (NS).
• Larger, more extensive laceration (animal or human bites and contaminated
wounds) should be irrigated with a mixture of 10% povidone iodine solution
(Betadine® solution) and 0.9% NS.
Wound Closure
It is not necessary to shave or cut scalp hair prior to wound closure; shaving
increases the likelihood of a wound infection.
• Small scalp lacerations may be closed with 3-0 or 4-0 nonabsorbable or
absorbable (Vicryl) simple, interrupted sutures.
• Deep scalp lacerations may also benefit from the placement of a pressure
dressing for the first 24 hours to prevent hematoma formation.
• Scalp wounds should be left open to air unless they require a pressure dressing
to prevent hematoma formation.
• After 24–48 hours, wounds closed with staples or nonabsorbable sutures can
be cleansed gently with soap and water.
• Staples or nonabsorbable sutures should be removed after 7–14 days.
• Administer tetanus-diphtheria (Td) vaccine for open injuries, if not adequately
vaccinated. At discharge, advice the patient to complete the vaccination
schedule (2 more doses 4 weeks apart).
Compartment Syndrome 115
CHAPTER
DEFINITION
In general, compartment syndrome is a condition in which the circulation within
a closed compartment of one of the extremities is compromised by an increase
in pressure within the compartment, causing necrosis of muscles and nerves and
eventually of the skin because of excessive swelling.
Any injury or insult that causes a decrease in compartment size or increase
in compartment pressure can initiate compartment syndrome. Compartment
syndrome may be acute or chronic.
CAUSES OF COMPARTMENT SYNDROME

• Acute:
cc Closed fractures
cc Crush or compression injuries
cc Burns
cc Tight or constricting casts
cc Intra-arterial injections
cc Infections
cc Snakebites
• Chronic:
cc Excessive exercise
cc Anomalous insertions of the foot muscles
CLINICAL FEATURES
Severe pain (out of proportion to findings) on passive extension is the most
important sign. In addition, look for paresis, pallor, tense swelling, and pulse-
lessness (late sign).
COMMON SITES
The common sites are forearm and leg; and the less common sites are foot, hand,
thigh, and abdomen.
DIAGNOSIS
• It is essentially based on clinical judgment of signs and symptoms.
• Bedside invasive measurement of compartment pressures (>30 mm Hg of
the diastolic pressure of the patient) is an adjunct. This in invasive and not
performed in the ED. Unilateral swelling with severe pain and/or pulselessness
should alert the physician of the possibility of compartment syndrome.
• In unconscious patients, it may be useful to assess with serial girth
measurements of the limb.
• Bedside doppler and/or USG can also be done to look for subcutaneous
edema and/or reduced pulsatility of arteries.
Other investigations include routine blood tests, serum creatine phos-
phokinase (CPK), and X-ray of affected limb.
MANAGEMENT
Refer to the treating department immediately without any delay:
• Medical: Keep limb slightly elevated up to heart level:
cc Administer adequate analgesia (Morphine/Tramadol)
cc Remove any constricting padding
cc Serial measurements of limb circumference
cc Start mannitol: 100 mL intravenous stat and q8h till improvement in limb
swelling.
• Surgical: The definitive treatment of compartment syndrome is urgent
fasciotomy, preferably done within 12 hours of onset of symptoms. Make a
surgical incision along the length of the compartment to relieve the pressure
and leave the wound open. After a few days, once the edema resolves, the
patient may be take to the operating room for wound closure.
Trauma in Pregnancy 116
CHAPTER
INTRODUCTION
Trauma is a leading cause of non-obstetric morbidity and mortality in pregnant
women where two lives are at stake instead of one. Pregnancy causes major
anatomical and physiological changes in almost every system of the body. The
initial treatment and stabilization are the same as for non-pregnant patients. The
best initial resuscitation of the fetus is the optimal resuscitation to the mother.
ANATOMICAL CONSIDERATIONS FOR NORMAL

PREGNANCY
• The major anatomical considerations are due to the enlarged gravid uterus.
The enlarging uterus reaches the umbilicus by 20 weeks and the costal margin
by 34–36 weeks. As the bowel gets pushed cephalad, the risk of intestinal
injuries decreases. But complex intestinal injuries can occur, in the case of
penetrating upper abdominal trauma. The gravid uterus can also cause
compression of major vessels, thereby decreasing cardiac return.
• The placenta, which is not as flexible as the uterine myometrium, is highly
susceptible to abruption when shearing forces are involved. Pelvic injuries
and fractures can cause direct fetal injuries in late gestation.
PHYSIOLOGICAL CONSIDERATIONS FOR NORMAL

PREGNANCY
• Cardiovascular changes:
cc Blood volumes increase in pregnancy till the 34th week with a smaller
increase in RBC volume, resulting in physiological anemia of pregnancy.

cc Due to increased intravascular volume, healthy pregnant patients can lose
up to 1.5 L of blood volume before developing tachycardia or hypotension,

resulting in delayed recognition of shock. However, due to decreased
perfusion of the placenta, the fetus may show signs of distress early.
cc Hypotension can be precipitated by the compression of the inferior vena
cava (IVC) by the gravid uterus, whereas hypertension may represent

preeclampsia.
cc When supine, compression of the vena cava by the gravid uterus results in
decreased venous return to the heart, and can decrease the cardiac output
by up to 30%.
cc Heart rate increases by 10–15/min in pregnancy. Consider this factor while

assessing a tachycardic response to hypovolemia.
• Pulmonary changes:
cc Due to increase in tidal volume, minute ventilation increases in pregnancy,
hence hypocapnia is relatively common in late pregnancy. Therefore, a

PaCO2 of 35–40 mm Hg may indicate impending respiratory failure.
cc Due to elevation of the diaphragm, chest tubes must be placed in the
midaxillary line, but 2 cm higher than usual, to avoid damage to the liver
or spleen.
• Other systems:
cc Due to delayed gastric emptying during pregnancy, early gastric
decompression by a nasogastric tube is recommended to prevent
aspiration.
cc By the 7th month, the symphysis pubis widens to 4–8 mm and the sacroiliac
joint spaces widen. Consider these factors while interpreting X-rays of the
pelvis.
cc Blunt trauma to the abdomen may result in massive retroperitoneal
hemorrhage due to the large, engorged pelvic vessels surrounding the

uterus.
RESUSCITATION AND MANAGEMENT

• Standard trauma algorithm (primary survey and secondary survey) must be
followed for evaluation of a pregnant patient with trauma. Obstetric team
should be called along with the trauma team.
• Secure the airway early to prevent aspiration, provide adequate ventilation
and effective circulation to the mother.
• In an unconscious patient, gently palpate the abdomen and measure fundal
height to estimate the gestational age.
• Displace the uterus manually to the left side to relieve compression on the
IVC.
• IV access should be above the diaphragm, avoiding femoral lines. At least
2 wide bore IV lines should be placed. Initiate crystalloid fluid resuscitation
and early type specific blood administration. Vasopressors should be the last
resort as they reduce uterine blood flow and cause fetal hypoxia.
• Fibrinogen and other clotting factors level are higher than normal in
pregnancy. A normal level in cases of trauma could be suggestive of early
disseminated intravascular coagulation (DIC).
• Perineal examination and per vaginal examination by an obstetrician are
indicated in all cases of trauma to rule out abruption or early onset of labor.
• The main causes of fetal death are maternal shock, maternal death, abruption,
and uterine rupture. Identify if present and address these immediately
cc Abruptio placenta: This should be suspected even in minor trauma
especially in late pregnancy. Presence of vaginal bleeding, uterine

tenderness, uterine contractions or uterine tetany suggests an abruption.
CHAPTER 116: Trauma in Pregnancy 387
cc Uterine rupture: Abdominal tenderness, guarding, rebound tenderness

may suggest a uterine rupture if associated with shock. Other signs of
rupture include inability to palpate the fundus (due to fundal rupture),
easy palpation of fetal parts (due to extrauterine location).
• Monitor the fetal heart continuously by tocodynamometer. The normal range
for fetal heart rate is 120–160 beats/min. The following are signs of impending
fetal distress and warrants urgent obstetric consultation
cc Abnormal fetal heart rate
cc Repetitive decelerations
cc Absence of beat-to-beat variability or accelerations
cc Frequent uterine activity
• Fetomaternal hemorrhage results in isoimmunization if the mother is Rh

negative. Administer Rh immunoglobulin (300 microgram) to all pregnant Rh
negative trauma patients with suspected abdominal trauma (within 72 h of
injury).
• If a pregnant mother has a cardiac arrest, perimortem cesarean section can be
a lifesaving intervention for both mother and fetus. In case of maternal death,
perform perimortem caesarian section within 5 minutes of the arrest.
Pediatric Trauma 117
CHAPTER
INTRODUCTION
Evaluation and management of injuries in children have the same principles as
for adults. Due to unique anatomical and physiological characteristics, children
sustain a distinct pattern of trauma.
• Smaller body mass, lesser fat, lesser subcutaneous tissue, and close proximity
of vital organs often result in multiple injuries.
• Due to a proportionately larger head in smaller children, head injuries are
more common. Blunt injuries to the head often result in apnea, hypoven-
tilation and hypoxia with hypovolemia and hypotension being much less
common. Hence, the need for more aggressive management of airway and
breathing.
AIRWAY MANAGEMENT
• If the airway is partially obstructed, use jaw-thrust maneuver with bimanual
inline stabilization of the spine to open the airway. Clear the mouth and
oropharynx of secretions or debris and administer supplemental oxygen.
• Oral airway: If the child is unconscious, insert an oral airway directly into the
oropharynx. Do not perform the maneuver of inserting the airway backward
and rotating 180 degrees as in adults, as this could result in trauma to the soft
tissue structures of the oropharynx in children.
• Preoxygenation: Before attempting to mechanically establish an airway, all
children must be adequately preoxygenated.
• Infants: Infants (<1 year) have a profound vagal response to laryngeal
stimulation during endotracheal intubation, resulting in bradycardia.
Consider pretreatment with atropine (0.01–0.03 mg/kg) for infants 1–2 minutes
before intubation. Atropine also dries oral secretions, enabling visualization of
landmarks for intubation
• Endotracheal (ET) tube: A simple way to determine the size of the ET tube is to
approximate the diameter of the tube to the child’s nares or the tip of the small
finger. A cuffed ET tube can be used even in infants as the currently available
ET tubes are safe and do not cause tracheal necrosis. However, check the cuff
pressure after intubation and <30 mm Hg is considered safe.
• Intubation: Orotracheal intubation with manual in line stabilization of
the spine is the preferred method of securing the airway. Do not perform a
nasotracheal intubation due to the relatively acute angle in the nasopharynx
in children, making the procedure very difficult. Position the ET tube 3–4 cm
CHAPTER 117: Pediatric Trauma 389
below the level of the vocal cords. For correct ET tube placement, it should be
fixed at the gums/teeth at the number 3 times the size of the ET tube.
Breathing and Ventilation

• Use a pediatric bag mask for children <30 kg as an adult bag mask can cause
significant barotrauma in children.
• Hypoxia due to hypoventilation is the most common cause of cardiac arrest
in children and hence must be addressed by providing optimum oxygenation
and ventilation.
• Tension pneumothorax must be decompressed at the 2nd intercostal space in
the midclavicular line as in adults.
• Chest tubes, when required are proportionately smaller and should be
inserted in the 4th to 5th intercostal space, just anterior to the midaxillary line
as in adults.
Circulation
• Normal parameters in children: The mean normal systolic blood pressure
(SBP) in children is 90 mm Hg plus twice the age in years. The lower limit
of normal SBP is 70 mm Hg plus twice the age in years. The diastolic blood
pressure (DBP) should be two-thirds the SBP. A child’s blood volume is 70 mL/
kg while an infant’s blood volume is 80 mL/kg.
• Children have increased physiological reserve and hence can maintain BP
even in the presence of shock. Hypotension manifests only after a 30% decrease
in circulating blood volume. Tachycardia and decrease skin perfusion may be
the only early markers of hypovolemia in children, and must be recognized to
initiate appropriate fluid resuscitation.
• Other subtle signs of blood loss in children include weakening of the pulse,
narrow pulse pressure (<20 mm Hg), cold extremities, decreased sensorium,
and dulled response to pain.
• If two attempts at peripheral percutaneous venous access fail, obtain an
intraosseous line at the anteromedial tibia or distal femur (refer Chapter 149).
• Fluid resuscitation: Crystalloid administration is based on the weight of the
child. Administer three boluses of 20 mL/kg (total of 60 mL/kg) to replace the
estimated 25% blood loss. Consider the use of packed red blood cells (pRBC)
while administering the third fluid bolus. Administer pRBC at boluses of
10 mL/kg and consider additional products like plasma and platelets.
• Response to fluid resuscitation: The following are indicators of adequate fluid
response.
cc Slowing of heart rate (age dependent)
cc Improving sensorium
cc Increased strength of the pulse
cc Increased warmth of extremities
cc Return of normal skin color

cc Increased blood pressure and pulse pressure

cc Improving urinary output
• Urine output: If the child requires substantial fluid resuscitation, insert a
urinary catheter to accurately measure urine output. The target urine output
for infants (<1 year) is 2 mL/kg/h, for younger children is 1.5 mL/kg/h and for
older children is 1 mL/kg/h.
• Hypothermia: Significant blood loss results in hypothermia which in turn
worsens trauma associated coagulopathy and makes resuscitation ineffective.
Initiate warming measures like thermal blankets, warming the intravenous
fluids, and room heaters.
DISABILITY AND EXPOSURE

Chest Trauma
In children, mobility of the mediastinal structures often results in tension
pneumothorax, which is the most common immediately life-threatening injury.
Abdominal Trauma
• Most children swallow large amounts of air due to the stress and pain of
trauma. If the upper abdomen is distended, insert a nasogastric tube to
decompress the stomach.
• Avoid deep, painful forceful palpation of the abdomen that may induce
voluntary guarding from the child, hence confusing the findings.
• Isolated intraparenchymal bleed which account for one third of solid organ
injuries in children can not be identified by an E FAST. Hence, bedside
ultrasonography alone cannot be relied upon as the sole diagnostic test for
intra-abdominal injuries in children.
Head Trauma
• Hypotension from hypovolemia and hypoxia can have a devastating
combination on an injured child’s brain and hence must be addressed as
priority.
• Vomiting and amnesia are common in children, post-head trauma and do not
necessarily indicate raised intra cranial pressure (ICP). However, persistent
or more frequent vomiting is an alarming sign and warrants a CT imaging of
the head.
• Infants with open fontanelles and uncalcified cranial sutures have more
tolerance for a large intracranial hematoma and may not show signs of raised
ICP early on. They may present with a bulging fontanelle or suture diastases,
which must be treated as signs of raised ICP due to an intracranial bleed.
CHAPTER 117: Pediatric Trauma 391
• The following drugs can be used to decrease cerebral edema and ICP:
Hypertonic saline 3% (3–5 mL/kg) or Mannitol (0.5–1 g/kg). However, diuresis
with mannitol may worsen hypovolemia and hence should not be given in the
early stages of resuscitation of head trauma.
Spinal Cord Injury

• Pseudosubluxation (anterior displacement of C2 on C3) may be seen on
a lateral X-ray in 20–40% of children. This radiographic abnormality can be
corrected by placing the child’s head in a neutral position (place a 2.5 cm thick
padding under the body from shoulders to the hips, but not the head). True
subluxation will persist on the X-ray with this maneuver.
• Spinal cord injury without radiographic abnormalities (SCIWORA) is
more commonly seen in children than in adults. Therefore, if history and
neurological examination suggest spinal cord injury, and if X-ray imaging of
the spine is normal, continue spinal immobilization till further imaging with
CT/MRI can be done and obtain neurosurgical consultation.
Musculoskeletal Trauma
• In children, crush injuries to the physis (growth plates) have the worst
prognosis with significant long-term disability.
• Long bone and pelvic fractures result in proportionately less blood loss in
children than in adults.
• Green stick fractures: Fractures of long bones often result in incomplete
fracture with angulated bones, due to immature, pliable nature of bones in
children.
• Simple splinting of fractured extremities in children usually is sufficient until
definitive orthopedic evaluation can be performed.
Geriatric Trauma 118
CHAPTER
INTRODUCTION
The geriatric age group (>65 years) is vulnerable to trauma and has a higher
mortality rate due to physical impairment, degenerative diseases, cognitive
decline, and the presence of comorbidities. Hence, the above factors must be
considered during assessment and management of geriatric trauma.
Remember that minimal trauma may result in fractures and significant
disability. The common locations of fractures among the elderly are the ribs, hip,
proximal femur, wrist, and the humerus.
The following are important points to note during early management of
geriatric trauma.
AIRWAY
• Factors that affect management of the airway in the elderly include dentition,
nasopharyngeal fragility, microstomia, macroglossia, and cervical spine
arthritis.
cc Remove any broken dentures. If the dentures are intact and well-fitted, it is
best to leave them in place till airway is secured.

cc Be careful while placing a NG tube as nasopharyngeal friability, especially
around the turbinate, may result in profuse bleeding.

cc Arthritis of the temporomandibular joints and the cervical spine may
make endotracheal intubation difficult and even dangerous with a risk of

spinal injury during manipulation of the arthritic spine.
BREATHING AND VENTILATION

• Ageing and chronic inhalation of pollutants and smoking results in decreased
compliance of the lungs and chest wall and increased work of breathing. This
alteration places elderly trauma patients at high risk for respiratory failure.
• Chest wall injuries, rib fractures, and even simple pneumothorax are not well-
tolerated by the elderly and need close monitoring.
• Aging causes a suppressed heart rate response to hypoxia; respiratory failure
may present insidiously in older adults.
• Adequate pain control with analgesics and opioids is crucial for pain relief,
but must be balanced with the increased risk of respiratory depression.
CHAPTER 118: Geriatric Trauma 393
CIRCULATION
• Ageing heart and coronary artery stenosis results in progressive loss of
function. The maximum tachycardia response decreases with age. The
maximal heart rate can be calculated by the formula: 220 minus current age.
• With aging, total blood volume decreases and circulation time increases. In a
hypertensive elderly, a systolic blood pressure (SBP) of about 110–120 mm Hg
post-trauma may actually represent hypotension.
• Early stages of shock may be masked by the absence of tachycardia and
hypotension. Hence, in the elderly, “normal BP” and “normal heart rate” DO
NOT necessarily indicate normovolemia.
• Elderly on chronic medications like diuretics may be volume contracted and
more prone for serious electrolyte imbalances and to volume overload during
resuscitation.
• As the kidneys lose mass after the age of 50 years, creatinine clearance
decreases in the elderly, and the aged kidney is more susceptible to damage
from hypovolemia, nephrotoxins, and medications.
• Consider the early use of advanced monitoring [e.g., central venous pressure
(CVP), echocardiography and ultrasonography] to guide optimal resusci-
tation, given the risks of preexisting cardiovascular disease.
DISABILITY
• In the elderly, brain mass shrinks causing the dura to become more adherent
to the skull, thereby increasing the risk of subdural and intraparenchymal
hematomas with injury. Hence, liberal use of imaging of the brain is advised
in the elderly.
• Take a detailed history of antiplatelet and anticoagulant use as these increases
the risk and severity of intracranial hemorrhage.
• Age related changes that predispose the elderly to injuries include reduced
cerebral blood flow due to atherosclerosis, auditory and visual decline,
demyelination, memory loss, and other preexisting medical conditions.
• In the spine, age related degeneration of the intervertebral discs, osteoporosis
and osteoarthritis increases the likelihood of injuries.
EXPOSURE AND ENVIRONMENT

• Age related decrease in skin integrity, results in decreased thermal regulation,
decreased barrier function, and impaired wound healing.
• Hypothermia significantly worsens outcome and care must be taken to
prevent this complication.
X-rays in Trauma 119
CHAPTER
INTRODUCTION
Prompt and focused imaging of trauma victims must be planned in the ED based
on a thorough clinical examination through primary and secondary surveys. The
standard trauma series is composed of X-rays of the chest, pelvis, and cervical
spine. Following is a comprehensive list of X-rays required to assess the extent of
injury in trauma victims.
TABLE 1: X-rays in trauma.

Region X-rays Comments
Clavicle and rib Chest AP In case of suspected clavicular fracture, include
the acromioclavicular and sternoclavicular joints
Cervical spine Lateral • Look for alignment—integrity of the anterior
and posterior spinal lines, the spinolaminar
line and the spinous process line
• Look for cortical breaks in the outline of
cervical vertebrae
Swimmers view If C7-T1 intervertebral disk space is not
visualized on lateral view
AP If one of the spinous processes is misaligned, a
facet dislocation may be seen
Open-mouth If predentate space is >3 mm in adults and
odontoid view 5 mm in children on lateral X-ray
Shoulder AP and lateral In case of shoulder dislocation
(Y-view)
Elbow AP and lateral Supracondylar fracture, radial head fracture or
elbow dislocation
Wrist AP and lateral Include forearm if fracture of radius or ulna is
suspected
Scaphoid series In case of suspected scaphoid bone fracture
(oblique and PA with ulnar deviation)
Hand AP and oblique For entire hand
Lateral Isolated finger injury in addition to AP view
Continued
CHAPTER 118: X-rays in Trauma 395
Continued
Region X-rays Comments

Pelvis with hip AP with both hip Neck of femur fracture or intertrochanteric
joints fracture
Lateral hip joint
view
Femur AP and lateral Proximal and distal joints to be included
Knee AP and lateral Include distal femur and proximal tibia
Skyline For suspected patellar dislocation or fracture
Ankle AP and true lateral For suspected ankle fracture
Mortise view To visualize the lateral malleolar joint space
Foot AP To visualize 1st and 2nd metatarsal, medial, and
intermediate cuneiforms, tarsometatarsal joint
and metatarsophalangeal joints
Oblique To visualize 3rd, 4th, and 5th metatarsals, lateral
cuneiform, navicular, cuboid, phalanges, and
interphalangeal joints
(AP: anteroposterior; PA: posteroanterior)
Eponyms in Trauma 120CHAPTER
The following are the common eponyms of fractures/dislocations in trauma

(Table 1).
TABLE 1: Eponyms in trauma.

Eponym Description Bones/Joints Comment
involved
ARM
Bankart fracture Avulsion fracture of the Scapula Associated with
anteroinferior glenoid rim (glenoid rim) recurrent anterior
shoulder dislocation
Hill–Sachs Compression fracture of Humeral Associated with
fracture posterolateral humeral head recurrent anterior
head shoulder dislocation
when glenoid rim hits
the posterior part of
humeral head
Holstein–Lewis Spiral fracture of the distal Shaft of Radial nerve entrapment
fracture third of shaft of humerus humerus
FOREARM
Barton fracture Fracture-dislocation of Radiocarpal Distal radius intra
radiocarpal joint involving joint articular fracture. Fall on
the volar or dorsal lip outstretched hand
(volar/reverse Barton or
dorsal Barton fracture)
Hume fracture Fracture of the olecranon Elbow joint Usually seen in children.
with an associated Hyperextension of
anterior dislocation of elbow with pronation of
radial head forearm
Colles fracture/ Fracture of the distal radial Distal radius Extra articular distal
Pouteau fracture metaphyseal region with radius fracture. Fall on
dorsal angulation and outstretched hand
impaction
Smith fracture Fracture of the distal radial Distal radius Extra articular distal
metaphyseal region with radius fracture. Fall on
volar angulation flexed wrist
Continued
CHAPTER 120: Eponyms in Trauma 397
Continued

involved
Essex-Lopresti Fracture of the radial Radial head, Longitudinal force on the
fracture- head, dislocation of DRUJ outstretched hand with
dislocation the distal radioulnar joint the elbow in extension
(DRUJ) and rupture of the
antebrachial interosseous
membrane
Galeazzi Distal third radial shaft Distal Radius, Surgical fixation
fracture- fracture with associated DRUJ
dislocation/ DRUJ injury
Piedmont
fracture
Monteggia Proximal third Proximal ulna Common in children.
fracture ulna fracture with and radial Posterior interosseous
dislocation of radial head head nerve (PIN) neuropathy
Chauffeur Intra-articular fracture of Radial styloid Forced ulnar deviation
fracture/ the radial styloid process of the wrist causing
Hutchinson avulsion of the radial
fracture/backfire styloid
fracture
Nightstick Isolated fracture of Ulna Direct blow to the medial
fracture the ulnar shaft, typically forearm
transverse and located in
the mid-diaphysis
Golfer's elbow Medial epicondylitis Medial An overuse syndrome of
epicondyle of the flexor-pronator mass
humerus origin
Tennis elbow Lateral epicondylitis Lateral Overuse injury involving
epicondyle of at the origin of common
humerus extensor tendon
HAND
Bennett fracture An intra-articular, Base of first Axial force applied to the
simple, oblique fracture metacarpal thumb in flexion
at the base of the first bone
metacarpal. Usually, a
2-part fracture
Rolando fracture Three-part or Base of first Axial force applied to the
comminuted intra- metacarpal thumb in flexion
articular fracture- bone
dislocation of the base of
the 1st MCP
Continued
Continued

involved
Boxer's fracture Minimally comminuted, Neck of fifth Direct trauma to a
transverse fractures of the metacarpal clenched fist
5th metacarpal neck bone
Gamekeeper's Avulsion or rupture of the First MCP Valgus force on the
thumb/Skier's ulnar collateral ligament abducted MCP joint,
thumb/Break- (UCL) of the first MCP joint leading to a ruptured
dancer's thumb UCL
Mallet finger/ Finger deformity caused Extensor Traumatic impaction
Baseball finger by disruption of the tendon injury blow (sudden forced
terminal extensor tendon of DIP joint flexion) to the tip of the
distal to DIP joint finger in the extended
position. Lack of active
DIP extension
Jersey finger/ Avulsion injury of flexor Flexor tendon Hyperextension of
Rugby finger digitorum profundus injury of DIP finger at DIP joint while
(FDP) from insertion at joint proximal portion of
base of distal phalanx finger is flexed. Inability
to flex at DIP joint
PELVIS
Duverney Isolated iliac wing Ilium Direct blow to the ilium
fracture fracture. Stable injury
Malgaigne's Unstable pelvic ring Pelvic bone Due to high energy
fracture fracture. Vertical impact to pelvis (front to
shear injury causing back)
vertical orientation of
pubic rami fracture,
disruption of SI joints,
vertical displacement of
hemipelvis
KNEE
Stieda fracture Bony avulsion injury of MCL Valgus knee loading and
the medial collateral forceful shifts of direction
ligament (MCL) at the (e.g., skiing, football, ice
medial femoral condyle hockey)
Segond fracture Lateral tibial plateau ACL Due to internal rotation
avulsion fracture with ACL and varus stress of the
tear knee
Continued
Continued

involved
LEG
Gosselin V-shaped fracture of distal Tibia Axial loading of weight
fracture tibia with extension into bearing surface of tibia
the tibial plafond dividing
it into anterior and
posterior segments
Pilon fracture Articular fracture of distal Tibia Axial loading of weight
tibia involving the tibial bearing surface of tibia
plafond
Toddler's Undisplaced spiral Tibia Common in children in
fracture fracture of distal tibia in early years of walking
children (9 months to 3 years)
Bumper fracture Compression fracture of Tibia Forced valgus of knee
lateral tibial plateau when struck from side by
car bumper
Runner's Stress fracture of Fibula Due to repeated axial
fracture distal fibula 3–8 cm above stress on fibula
the lateral malleolus
ANKLE
Bosworth Bimalleolar fracture Ankle joint Extreme external
fracture dislocation of the ankle rotation
with entrapment of fibula
behind the posterior
tubercle of distal tibia
Chopart Fracture dislocation Midtarsal Fall from height/MVA/
fracture- of mid-tarsal joints joint twisting injuries
dislocation (Talonavicular and
Calcaneocuboid joints)
Cotton fracture Fracture of the ankle Ankle joint Trimalleolar ankle
involving both malleoli fracture
and posterior process of
the tibia
Dupuytren Fracture of the distal Ankle joint Type of bimalleolar ankle
fracture portion of the fibula fracture causing ankle
above the lateral instability
malleolus, with rupture
of distal tibiofibular and
deltoid ligaments
Continued
Continued

involved
Lisfranc Dislocation of the TMT joint Direct crush injury or
fracture- articulation of the tarsus indirect load onto a
dislocations with the metatarsal bases plantar flexed foot
Maisonneuve Spiral fracture of the Fibula Pronation-external
fracture proximal third of fibula rotation injury
with distal tibiofibular
syndesmotic disruption
Pott's fracture Fracture affecting one or Tibia/fibula Twisting injury while
both of the malleoli walking/running
Shepherd Fracture of the lateral Posterior Inversion or extreme
fracture tubercle of the posterior process of equinus
process of the talus Talus
Stieda process Fracture of elongated Posterior Inversion or extreme
fracture lateral tubercle of the process of equinus
posterior process of the Talus
talus
Cedell fracture Fracture of the medial Posterior Forced dorsiflexion and
tubercle of the posterior process of pronation
process of the talus Talus
Tillaux fracture Fracture through the Tibia Abduction-external
anterolateral aspect of the rotation force on foot
distal tibial epiphysis causes ATFL to avulse the
anterolateral corner of
distal tibial epiphysis
Aviator fracture Coronal fracture of the Talus Forced dorsiflexion of the
neck of the talus ankle. Proximal avascular
necrosis is a potential
complication of neck
fractures
Paratrooper's Fracture of posterior Distal tibia Injuries sustained due
fracture malleolus or posterior lip to improper landing
of distal tibia techniques from height
FOOT
Jones fracture Extra-articular fracture 5th Significant adduction
at the base of the metatarsal force to the foot with
fifth metatarsal heel raised and foot in
plantar flexion
Continued
Continued

involved
Pseudo jones Tuberosity avulsion 5th Inversion and plantar
fracture fractures metatarsal flexion of foot
Dancer's Long spiral fracture 5th Dancer rolling over their
fracture extending into the distal Metatarsal foot/while landing a
metaphyseal area jump
March fracture Metatarsal fracture caused Most Repetitive stress/fatigue
by repetitive stress commonly
2nd, 3rd
metatarsals
Nutcracker Cuboid Cuboid Forced plantar flexion
fracture impaction fracture, and abduction, crushing
associated with navicular the cuboid between
avulsion fracture calcaneus and 4th, 5th
metatarsals
SPINE
Jefferson Burst fracture of the C1 vertebrae Axial compression injury
fracture ring of C1 with lateral
displacement of both
articular masses
Hangman's Traumatic anterior C2 vertebrae Hyperextension injury
fracture spondylolisthesis of
the axis (C2) due to
bilateral fracture of pars
interarticularis
Clay-shoveler Avulsion-type spinous Most Direct trauma to
fracture process fracture in the commonly posterior spinous
lower cervical or upper C7, but can process or sudden
thoracic spine affect C6 to muscular/ligamentous
T3 pull in flexion or
extension
Chance/seatbelt Flexion-distraction type Most Flexion distraction
fracture injuries of the spine that commonly injury. Associated with
extend to involve all three lower intra-abdominal injuries.
spinal columns thoracic and Unstable fracture: All 3
upper lumbar columns involved
spine
Continued
Continued

involved
Holdsworth Unstable fracture Thoraco- Flexion-rotation injury
fracture dislocation of the thoraco- lumbar
lumbar junction of the junction
spine
FACE
Le Fort fractures Fractures of the midface. Mid face Divided into Le Fort I, II
Separation of all or a and III
portion of the midface
from the skull base
Section 17
Pediatric Emergencies
Assessment of a Sick
Child in the Emergency
Department 121
CHAPTER
INTRODUCTION
A sick child in the emergency department (ED) is a unique challenge to the
emergency physicians as the age group varies from newborns to adolescents.
The purpose of this assessment is to quickly identify whether the sick child is
in respiratory distress, respiratory failure, shock, or cardiopulmonary failure.
Assessment should focus on identifying and recognizing a child who is likely to
deteriorate. Use the following four steps to assess sick children.
1. Initial assessment
2. Primary assessment
3. Secondary assessment
4. Tertiary assessment
INITIAL ASSESSMENT (TABLE 1)

• Observe the child’s consciousness, breathing pattern, and color. This visual
and auditory assessment would not take longer than 30 seconds and helps to
identify, if the child is sick or not.
TABLE 1: Initial assessment: Consciousness, breathing, and color.

Consciousness Level of consciousness: For example, unresponsive, irritable,
or alert
Breathing Increased work of breathing, absent or decreased respiratory
effort, or abnormal sound heard without auscultation
Color Abnormal skin color, such as cyanosis, pallor, or mottling
PRIMARY ASSESSMENT
After a quick initial assessment (30 s), begin the primary assessment by evaluating
the following components sequentially.
• A: Airway
• B: Breathing
• C: Circulation
• D: Disability
• E: Exposure.
406 SECTION 17: Pediatric Emergencies
Airway
Upper airway obstruction can be identified by the following signs:
• Increased inspiratory effort with intercostal retraction
• Snoring or stridor
• Absent breath sounds despite respiratory effort (suggests complete upper
airway obstruction).
If there is evidence of airway obstruction, open and maintain airway by using
simple maneuvers. Use advanced interventions, if needed.
The following are simple maneuvers that can be used to open and maintain the
airway:
• Head tilt–chin lift
• Jaw thrust (in head or neck injury)
• Heimlich maneuver
• Airway adjuncts: For example, nasopharyngeal airway (NPA), oropharyngeal
airway (OPA).
Advanced interventions to maintain airway patency are:
• Noninvasive ventilation [continuous positive airway pressure (CPAP)]
• Laryngeal mask airway
• Invasive ventilation (Endotracheal intubation)
• Needle or surgical cricothyrotomy.
Breathing
Breathing evaluation focuses on respiratory rate and effort, chest expansion, lung
and airway sounds and oxygenation. The normal respiratory rate by age is shown
in Table 2.
TABLE 2: Normal respiratory rate by age.

Age Breaths/min
Birth till 2 months <60/min
2 months till 1 year <50/min
1–5 years <40/min
School age (6–12 years) <30/min
Abnormal respiratory rate: Tachypnea, bradypnea, apnea
Lung and airway sounds: Stridor, grunting, gurgling, wheezing, and crackles
CHAPTER 121: Assessment of a Sick Child in the Emergency Department 407
Oxygen Saturation by Pulse Oximetry

Perform pulse oximetry and identify hypoxemia if present or if cyanosis or
bradycardia develops. Monitor oxygen saturation by continuous pulse oximetry
in children with respiratory distress/failure or during transport and during
postresuscitation care.
Signs of increased respiratory effort include:
• Flaring of alar nasae
• Chest indrawing or intercostal retractions
• Seesaw respiration
• Head bobbing
• Increased duration of inspiration or expiration
• Open mouth breathing
• Use of accessory muscles
• Grunting
• Gasping
Circulation
Circulation is assessed by the evaluation of:
• Heart rate and rhythm
• Peripheral and central arterial pulses
• Capillary refill time at the palms, soles, or forehead
• Skin color and body temperature
• Blood pressure (Table 3).
cc Circulation is considered normal if skin color is normal, capillary refill
time is less than 2 seconds and all pulses (peripheral and central) are
strong with regular rhythm.
cc Circulation is considered abnormal if child is cyanosed, mottled, or pale or
if central and peripheral pulses are weak, BP is low or if capillary refill time
is more than 2 minutes.
TABLE 3: Definition of hypotension by systolic blood pressure (SBP).

Age SBP (mm Hg)
Term neonates (0–28 days) <60
Infants (1–12 months) <70
Children (1–10 years) <70 + (Age in years × 2)
Children >10 years <90
Disability
The disability assessment by using either AVPU (alert, voice, pain, unresponsive)
scale or Glasgow Coma Scale (GCS) is a quick way of evaluating neurological
function. The AVPU scale is a simple clinical tool to assess the disability or
neurological status of the child.
• A: Alert
• V: Responsive to voice
• P: Responsive to pain
• U: Unresponsive.
The GCS is the most widely used method of evaluating a child’s level of
consciousness and neurologic status but is time consuming. The GCS has been
modified for preverbal or nonverbal children.
Disability can be assessed by following neurologic signs:
• Decreased level of consciousness
• Loss of muscle tone
• Generalized seizures
• Size of pupils (in millimeters)
• Irregularities in pupil size or response to light.
Exposure
In this final component of primary assessment, expose the child with assistance
of the parents in a neutral thermal environment to avoid hypothermia. Make sure
you maintain the modesty and respect of the child.
SECONDARY ASSESSMENT
After primary assessment and initial stabilization, perform the secondary
assessment. Components of secondary assessment are:
• Focused history
• Focused physical examination.
A mnemonic of this brief focused history is SAMPLE:
• S: Signs/Symptoms of the injury
• A: Allergies (NSAIDs, antibiotics like penicillin)
• M: Medications (regular medications for comorbid conditions)

• P: Past medical history (comorbidities, previous surgery)
• L: Last meal (time of last meal for administration of anesthesia if needed)
• E: Events preceding the injury/illness.
Focused Physical Examination

Infants and toddlers are always most comfortable and cooperative when
examined in the parent’s lap.
TERTIARY ASSESSMENT
Tertiary assessment is mainly done by “doing diagnostic tests” to identify the
problems. The following diagnostic tests can be done in pediatric emergency.
• Random blood sugar
• Urine analysis
• Hemoglobin, complete blood count (CBC)
• Chest X-ray (CXR), ultrasonography (USG)
• ECG, ECHO
• Arterial/Venous blood gas.
The formulas for estimating the weight for age is shown in the Table 4. The
emergency department should have an adequate supply of the resuscitative
equipment as shown in the Table 5.
TABLE 4: Formula for estimating weight for age for normal children.
Age Weight (kg)
3–12 months Age in months + 9
2
1–6 years (Age in years × 2) + 8
7–12 years (Age in years × 7) + 5
2
410
TABLE 5: Pediatric resuscitative equipment.
Equipment Newborn/Small Infant Toddler Small Child Child Child Large Child Adult
infant (3–5 kg) (6–9 kg) (10–11 kg) (12–14 kg) (15–18 kg) (19–22 kg) (24–30 kg) (≥32 kg)
Resuscitation bag Infant Child Child Child Child Child Child/adult Adult
O2 mask Newborn Newborn Pediatric Pediatric Pediatric Pediatric Adult Adult
Oral airway Infant/Small Infant/Small Small child Child Child Child/Small Child/Small Medium
child child adult adult adult
Laryngoscope 0–1 straight 1 straight 1 straight 2 straight 2 straight 2 straight 2–3 straight 3 straight
blade (size) or curved or curved or curved or curved
Tracheal tube (mm) Premature infant 3.5 uncuffed 4.0 uncuffed 4.5 5.0 5.5 6.0 cuffed 6.5 cuffed
2.5 term infant uncuffed uncuffed uncuffed
3.0–3.5 uncuffed
SECTION 17: Pediatric Emergencies
Tracheal tube 10–10.5 10–10.5 11–12 12.5–13.5 14–15 15.5–16.5 17–18 18.5–19.5
length (cm at tip)
Stylet (F) 6 6 6 6 6 14 14 14
Suction Catheter (F) 6–8 8 8–10 10 10 10 10 12
BP Cuff Newborn/Infant Newborn/Infant Infant/Child Child Child Child Child/Adult Adult
IV catheter (G) 22–24 22–24 20–24 18–22 18–22 18–20 18–20 16–20
Butterfly (G) 23–25 23–25 23–25 21–23 21–23 21–23 21–22 18–21
Nasogastric tube (F) 5–8 5–8 8–10 10 10–12 12–14 14–18 18
Urinary catheter (F) 5–8 5–8 8–10 10 10–12 10–12 12 12
Defibrillation/ Infant paddles Infant paddles Adult paddles Adult Adult Adult Adult Adult
Cardioversion until 1 year or when ≥1 year paddles paddles paddles paddles paddles
external paddles 10 kg or ≥10 kg
Chest tube (F) 10–12 10–12 16–20 20–24 20–24 24–32 28–32 32–40
Source: Adapted from the Broselow pediatric resuscitation tape.
KEY POINTS
• Begin your initial assessment by CBC then continue with the ABCDEs
• Begin management based on the CBC and ABCDs
• Focused history using SAMPLE
• Once child is stabilized, do a detailed physical examination
• Perform ongoing assessment throughout the stay
• For etiology, plan the required laboratory tests and imaging.
Febrile Seizures 122
CHAPTER
INTRODUCTION
Febrile seizures usually occur between 6 months and 6 years of age with a peak
incidence between 12 and 18 months. It is usually a single episode of seizure,
which is associated with fever. An active central nervous system (CNS) infection
or a developmental delay should be ruled out before making this diagnosis.
Febrile seizures occur on the 1st day of illness in most children. In some cases, a
febrile seizure may be the first manifestation of the illness.
• Risk factors for febrile seizures
cc A positive family history of febrile seizures
cc High fever
cc Electrolyte abnormalities (hyponatremia and hypernatremia)
cc Recent immunization [measles, mumps and rubella (MMR), diphtheria,
pertussis (whooping cough), and tetanus (DPT), and tetanus toxoid (TT)]
• Simple febrile seizures: This is the most common type. Characterized by one
episode of generalized tonic-clonic seizures (GTCS) lasting <15 minutes
without recurrence.
• Complex febrile seizures: Seizures may be of focal type, may recur and last
longer (>15 min).
Investigations: Complete blood count (CBC) profile, electrolytes, random blood
sugar (RBS), calcium, urinalysis, lumbar puncture, CT/MRI brain.
MANAGEMENT
• Assess airway, breathing and circulation. Maintain and protect the airway,
including the use of a nasopharyngeal airway, if needed. Protect the patient
from self injury during this time
• Hypoglycemia and hypocalcemia are common metabolic causes of seizures,
especially in infants. Check RBS and Calcium and correct, if indicated.
• Administer an antiepileptic either through the buccal, rectal intramuscular or
intravenous route route (Table 1).
• Prophylaxis: For simple febrile seizures, clobazam prophylaxis 1 mg/kg PO
divided in two doses × 2 days may be given with the next episode of fever.
CHAPTER 122: Febrile Seizures 413
TABLE 1: Antiepileptics, route and dose for febrile seizures.

Antiepileptic Route Dose
Midazolam Buccal 0.2 mg/kg (max: 10 mg)
Intranasal 0.2 mg/kg (max: 5 mg/nare)
Intramuscular 0.1–0.2 mg/kg (max: 10 mg)
Intravenous 0.15 mg/kg (max: 10 mg)
Lorazepam Buccal 0.1 mg/kg (max: 4 mg)
Rectal 0.1 mg/kg (max: 4 mg)
Diazepam Rectal 0.5 mg/kg (max: 20 mg)
Complications
• The postictal phase can be associated with confusion or agitation and
drowsiness. Prolonged drowsiness is unusual.
• Transient hemiparesis (Todd’s paresis), usually of complex or focal type, is
seen in 0.4–2% of cases.
• Febrile status epilepticus.
Acute Asthma and
Status Asthmaticus 123
CHAPTER
INTRODUCTION
Acute exacerbation of asthma is a very common emergency among children.
If a severe acute exacerbation of asthma does not respond to initial treat-
ment with steroids and bronchodilators, it is termed “status asthmaticus”. The
classification of asthma based on severity of the episode as shown in Table 1.
TABLE 1: Severity score: Classification of mild, moderate, and severe asthma.

Parameter* Mild Moderate Severe Respiratory
arrest
imminent
Activity Normal or Decreased activity. Decreased activity Unable to
dyspnea on (Infants may have (Infants stop eat
exertion softer, shorter cry; feeding). Hunched
difficulty feeding) forward
Speech Normal Phrases Words Not able to
speak
Alertness Alert Might look Usually agitated Drowsy or
agitated confused
Respiratory Increased Increased Often >30
rate breaths/min
Age Normal rate
<2 months <60 breaths/min
2–12 months <50 breaths/min
1–5 years <40 breaths/min
6–8 years <30 breaths/min
Accessory Minimal Intercostal Significant Marked
muscles and intercostal and substernal respiratory respiratory
suprasternal retractions retractions distress. All distress.
retractions accessory muscles Paradoxical
usually involved thoraco-
abdominal
movement
Wheeze Moderate, Loud Usually loud Absent
often only
end-expiration
Continued
CHAPTER 123: Acute Asthma and Status Asthmaticus 415
Continued
Parameter* Mild Moderate Severe Respiratory
arrest
imminent
PEF after initial >80% Approximately <60% predicted Not able to
broncho- 60–80% or personal best perform
dilator % (<100 L/ min
predicted or adults) or response
personal best lasts <2 h
SpO2% >94% 91–94% <90% <90%
* The presence of several parameters, but not necessarily all, indicates the general classification of the
attack.
(PEF: peak expiratory flow)
MANAGEMENT OF ACUTE ASTHMA

• Mild-to-moderate:
cc Administer humidified O
2 at high concentration, keep O2 saturation
≥94%
cc Administer salbutamol by a metered-dose inhaler (MDI) or nebulizer
solution
cc Administer oral corticosteroids.
• Moderate-to-severe:
cc Administer humidified O
2 at high concentrations to keep O2 saturation
≥94%. Use a nonrebreathing mask, if needed.
cc Administer salbutamol by MDI (with spacer) or nebulizer solution. If not
responding, try continuous salbutamol administration.

cc Administer ipratropium bromide by nebulizer solution. Salbutamol and
ipratropium may be mixed for nebulization.

cc Administer corticosteroids PO/IV.
cc Consider administering magnesium sulfate by slow (15–30 min) IV bolus
infusion while monitoring heart rate and blood pressure.

• Impending respiratory failure:
cc In addition to the above therapies, the following are indicated:
– Administer O2 at high concentrations

– Administer salbutamol by continuous nebulizer
– Administer corticosteroids IV if not already given.
– Consider giving terbutaline subcutaneously or by continuous infusion
– Consider subcutaneous or IM epinephrine as an alternative
– Consider bilevel positive airway pressure (noninvasive positive-
pressure ventilation), especially in alert, cooperative children
– Consider endotracheal intubation for children with refractory
hypoxemia (low O2 saturation), worsening clinical condition (e.g.,
decreasing level of consciousness and irregular breathing), or both

despite the aggressive medical management described above.
Intubation in an asthmatic child carries significant risk for respiratory
and circulatory complications. Consider using a cuffed endotracheal
(ET) tube.
KEY POINTS
• Recognize asthma since all the wheezes are not asthma.
• Determine severity of the asthmatic exacerbation on arrival.
• Primary treatment of asthma exacerbation: Oxygen, inhaled salbutamol, and
systemic corticosteroids.
• In severe exacerbations, consider: Anticholinergic agents, IV magnesium
sulfate, and IV terbutaline.
At discharge, prescribe: MDI salbutamol, oral prednisolone × 3–5 days, and
consider initiating inhaled corticosteroids to prevent future exacerbations.
Acute Stridor and
Epiglottitis 124
CHAPTER
ACUTE STRIDOR
Introduction
Stridor is a high-pitch harsh inspiratory sound produced due to airflow through
a narrowed or obstructed airway (oropharynx, subglottis or trachea). In severe
obstruction, stridor may occur during expiration also.
Causes of stridor are shown in Table 1. The most common cause is acute
laryngotracheobronchitis or croup.
Laryngotracheobronchitis is an acute viral infection of the larynx and
subglottic region and is caused by parainfluenza virus type 1. It is insidious in
onset and presents with hoarseness of voice, stridor, and a peculiar brassy cough.
Stridor is an acute medical emergency. The emergency department
management is shown in Table 2.
Note:
• Give dexamethasone 0.6 mg/kg IV/oral stat. Most of the time for Grade-1
and -2 stridor, one dose is sufficient. Alternatively, oral prednisolone 1 mg/kg
may be used.
• Dexamethasone 0.15 mg/kg/dose 12 hourly can be continued if stridor
persists.
• Nebulized adrenaline: For Grade III and IV croup—0.5 mL/kg up to maximum
5 mg of 1 in 1,000 adrenaline solution via nebulizer. Constitute the solution to
4 mL for nebulization. Can be repeated 0.5–1 hourly, if necessary.
TABLE 1: Causes of stridor.

Infectious Congenital Acquired Allergic
• Laryngotracheitis • Laryngomalacia • Laryngeal • Acute
• Acute epiglottitis • Vocal cord paralysis granuloma angioneurotic
• Bacterial tracheitis • Congenital subglottic • Foreign body edema
• Retropharyngeal stenosis • Neoplasms
abscess • Vascular ring
TABLE 2: Classification of stridor at arrival and management in the emergency department.

Grade I Grade II Grade III Grade IV
• No stridor at rest • Stridor at rest • Stridor at rest • Marked respiratory
• Stridor only on without sternal with sternal distress
crying and chest wall and chest wall • Tachycardia
retractions and retractions • Sweating, pallor/
no distress cyanosis
Management Algorithm of Acute Laryngotracheobronchitis/Croup
• Do not upset • Dexamethasone • Oxygen and IV • Oxygen and IV fluids
the child IV/oral stat fluid • Dexamethasone IV
• Gentle handling • Dexamethasone • Dexamethasone stat abd prn
• Oral q12h can be IV stat and prn • Maintenance
prednisolone/ continued if • Maintenance dexamethasone
dexamethasone stridor persists dexamethasone • Nebulized adrenaline
stat and observe • Nebulized • ICU admission
in ED adrenaline • If needed consider—
BMV and RSI
• Call for ENT help
for tracheostomy if
required
(BMV: bag-mask ventilation; ED: emergency department; RSI: rapid sequence intubation)
ACUTE EPIGLOTTITIS
Introduction
Acute epiglottitis is a life-threatening inflammation of the supraglottic structures
(arytenoids, aryepiglottic folds, and epiglottis) that may be complicated by severe
laryngospasm, stridor, and irreversible airway obstruction. It has become a very
rare occurrence after introduction of the H. influenzae vaccine.
Etiology
• S. pyogenes, S. pneumoniae, S. aureus, and H. influenzae.
• H. influenzae was responsible for most of the cases in the preimmunization era.
Clinical Features
Acute onset fever, throat pain and discomfort, excessive drooling and stridor.
Symptoms may progress rapidly (few hours) or subacutely (1–2 days). Cough is
usually not a typical feature.
The child appears sick and typically assumes the “tripod position” or “sniffing
position” in which the chin is pushed forward with the neck slightly extended.
CHAPTER 124: Acute Stridor and Epiglottitis 419
Diagnosis
Diagnosis is mainly clinical. Lateral X-ray soft tissue of the neck (neck extended
during inspiration) may show the characteristic “thumb sign” of the swollen
epiglottis.
Management
• Assess and protect the airway. Ensure that facilities to provide a surgical
airway are readily available, if intubation is difficult.
• Adrenaline nebulizations and steroid (budesonide) nebulizations are helpful
in relieving the edema.
• Antibiotics: Second or third generation cephalosporins for 7–10 days.
Pneumonia and
Bronchiolitis 125
CHAPTER
RESPIRATORY INFECTIONS AND PNEUMONIA

IN CHILDREN
Pneumonia: It may be classified as lobar pneumonia, bronchopneumonia, or
interstitial pneumonia.
Clinical Assessment
• Check temperature, respiratory rate, and the type of cough
• Chest in drawing, low saturation, and cyanosis
• Stridor, wheeze, crepitations, and bronchial breath sounds
• Assess the sensorium of the child
• Assess the nutritional status
Investigations
• Complete blood count, blood culture
• Chest X-ray for severe pneumonia and very severe disease.
Criteria for Hospitalization

• Children less than 3 months of age irrespective of severity of pneumonia
• Moderate-to-severe respiratory distress
• Respiratory failure, hypoxemia SpO2 < 90% on room air
• Dehydration or inability to feed orally
• Recurrent pneumonia
• Toxic appearance
• Underlying conditions that may predispose to serious course of pneumonia:
Cardiac conditions, genetic syndromes, neurocognitive disorders, immuno-
compromised host, and metabolic conditions
• Complications (effusion/empyema)
• Failure of outpatient therapy.
The classification of illness and the ED management of patients with
pneumonia are shown in Table 1.
CHAPTER 125: Pneumonia and Bronchiolitis 421
TABLE 1: Classification of illness and management.

Severity Features Management
No • Respiratory rate: Symptomatic management
pneumonia {{<2 months: <60 breaths/min
{{2–12 months: <50 breaths/min
{{1–5 years: <40 breaths/min
Pneumonia • Fast breathing without chest in • Amoxicillin 50–100 mg/kg/day PO

not severe drawing in three divided doses × 5–7 days
• Respiratory rate: • Ensure that the child receives
{{<2 months: >60 breaths/min adequate fluids
{{2–12 months: >50 breaths/min • Encourage breastfeeding and oral
{{1–5 years: >40 breaths/min
fluids
Severe • Fast breathing with chest • Crystalline penicillin IV 200,000

pneumonia indrawing units/kg/day q6h
• Nasal flaring • OR Ampicillin IV 100–150 mg/kg/
• Grunting day q6h
• OR Co-amoxiclav 25–40 mg/kg/
day PO (of Amoxicillin) three
divided doses × 5–7 days
• Intravenous fluid: ±
• Monitor and ensure oxygen
saturation >94%
• Suspecting S. aureus: Add injection
Cloxacillin 100–200 mg/ kg/day IV
in four divided doses
Very severe • Vomiting or unable to drink • Ceftriaxone 100 mg/kg IV once a
disease • Convulsions day (may give IM if no IV access)
• Stridor OR
• Malnutrition • Cefuroxime-axetil
• Central cyanosis 75–100 mg/kg/day IV in three
doses (change to oral Cefuroxime
• Head nodding
at dose of 20–30 mg/kg/day when
child improves)
• IV fluids
• Monitor and ensure oxygen
saturation >94%
• Suspecting S. aureus: Add injection
Cloxacillin 100–200 mg/kg/day IV
in four divided doses
INDICATIONS OF INTENSIVE CARE

• Signs of impending respiratory failure (lethargy, increased work of breathing,
hypercarbia, saturation <90% with 100% FiO2).
• Recurrent apnea or slow irregular respiration, altered mental status
• Cardiovascular compromise with progressive tachycardia and hypotension
• Need for ventilatory support: Individualized based on clinical, laboratory and
radiological findings.
KEYPOINTS
• Tachypnea is the most reliable predictor for lower respiratory tract infection
(LRTI)
• Drug of choice for uncomplicated pneumonia: Amoxicillin
• If hypoxia persists despite 100% FiO2, consider respiratory failure
• Do not perform a routine chest X-ray to confirm uncomplicated pneumonia.
Acute Otitis Media and
Otitis Externa 126
CHAPTER
ACUTE OTITIS MEDIA

Introduction
Acute otitis media refers to inflammation of the middle ear and is characterized
by ear pain, discharge, fever, irritability, vomiting, and anorexia.
Etiology
• Bacteria: S. pneumoniae (40–50%), H. influenzae (30–40%), M. catarrhalis
(10–15%), S. aureus and C. pneumoniae (1–2%).
Clinical features: Ear discharge, otalgia, headache, fever, and anorexia.
Management
• Antibiotics: Syrup Amoxicillin × 7–10 days
• Nasal decongestants:
cc Xylometazoline nasal drops (3 drops q8h) × 3 days
cc Normal saline nasal drops (3 drops q6h) × 7 days
cc Syrup Chlorpheniramine + Phenylephrine (T-Minic) 1–2 mg/mL
– 2–5 years: 1 mL PO q6h

– >6 years: 2 mL PO q6h
• Keep the ear dry: Advice the patient to keep cotton soaked in vaseline in the
ears while having a bath.
ACUTE OTITIS EXTERNA

Introduction
Acute otitis externa, also referred to as Swimmer's ear, is an inflammation of the
external auditory meatus. Children exposed to water for long periods are at risk.
• Symptoms: Ear pain, aural fullness, and itching.
• Signs: Tragal tenderness, diffuse aural canal edema, erythema, and ear
discharge.
• Etiology: Staphylococcus aureus is the usual organism. Malignant otitis externa
is caused by P. aeruginosa.
Management
• Ear canal cleaning
• Antibiotics: Syrup/Tablet Cloxacillin q6h × 7 days
• Keep the ear dry: Advice the patient to keep cotton soaked in vaseline in the
ears while having a bath.
Acute Gastroenteritis 127
CHAPTER
INTRODUCTION
The term “acute gastroenteritis” denotes infections of the gastrointestinal tract
caused by bacterial, viral, or parasitic pathogens.
Bloody diarrhea with visible blood and mucus is called dysentery and is
usually bacterial in etiology.
When a child presents to the emergency department, assess the hydration
status of the child to classify the severity of diarrhea (Table 1).
TABLE 1: Classification of dehydration.

No dehydration Some dehydration Severe dehydration
Appearance Well and alert Restless/irritable Lethargic/unconscious/floppy
Thirst Drinks normally Thirsty Unable to drink
Skin pinch Goes back quickly Goes back slowly Goes back very slowly
Tongue Moist Dry Very dry
Eyes Normal Sunken Sunken
Vital signs Normal Tachycardia, may Tachycardia, weak peripheral
have delayed CRT pulses, delayed CRT, cold
peripheries, with or without
hypotension
(CRT: capillary refill time)
COMMON PATHOGEN CAUSING ACUTE

GASTROENTERITIS IN CHILDREN
• Viruses (70%): Rotaviruses, adenovirus, calicivirus, astrovirus, and enterovirus.
• Bacteria (10–20%): Campylobacter, E. coli, Shigella, V. cholerae, Yersinia,
S. typhi, and S. paratyphi.
• Protozoa (<10%): Giardia, E. histolytica, and Cryptosporidium.
MANAGEMENT
• Fluid resuscitation with ORS or IV/IO fluids should be initiated immediately
(Table 2).
• Zinc supplementation: Zinc supplementation is shown to reduce duration and
severity of diarrhea.
CHAPTER 127: Acute Gastroenteritis 425
TABLE 2: Management of acute watery diarrhea.

No dehydration: Plan-A Some dehydration: Plan-B Severe dehydration: Plan-C
Exclusively breastfed • The approximate • Start IV/IO fluids immediately
(give ORS in addition amount of ORS: • If central pulse weak—give
to breast milk) 75 mL/kg over 4 h 20 mL/kg fluid of RS/NS over
• <2 years: • After 4 h, reassess the 20 min
50–100 mL with child and classify the • Then, give 100 mL/kg RL or normal
each loose stool child for dehydration saline divided as follows:
• >2 years: {{Age <12 months: 30 mL/kg over
100–200 mL with 1 h, then 70 mL/kg over 5 h
each loose stool, or {{Age >12 months: 30 mL/kg over
• 10 mL/kg ORS with 1/2 h, then 70 mL/kg over 2.5 h
each loose stool Reassess the patient after 6 h. As soon
as child can drink, give ORS, usually
after 3–4 h for infants and 1–2 h for
older children
cc Children 2–6 months: 10 mg/day of elemental zinc for 14 days.

cc Children >6 months: 20 mg/day of elemental zinc for 14 days.
• Antibiotics:
cc Diarrhea in children is mostly of viral etiology and hence does not warrant
antibiotics.
cc Administer antibiotics only if the child has the following symptoms
– Bloody diarrhea with visible blood and mucus

– High fever with suspected sepsis
– Traveler’s diarrhea.
cc Antibiotic of choice: Syrup Cefixime 8 mg/kg/day in two divided doses for
5 days.
Special Instructions to the Mother

• Recommend longer duration of breastfeeding to the mother at each feed
• Teach the mother how to prepare and give ORS. If the child vomits, tell her
to wait for 5–10 minutes and then retry giving ORS slowly. Tell her to give
more ORS if the child wants more.
• In addition to ORS, food-based fluids like soup or rice water may be given to
children who are not exclusively breastfed.
• Older children can be encouraged to continue to take their usual diet.
Drugs and Dosages in
Pediatric Emergencies 128
CHAPTER
INTRODUCTION
The wide spectrum of drug dosages based on age is a challenge in the emergency
department. Commonly used drugs in pediatric emergencies and their dosage
are given in Table 1.
TABLE 1: Drugs and dosages in pediatric emergencies.

Drug Route Recommended pediatric dosage
Activated NG • Up to 1 year: 10–25 g or 0.5–1 g/kg
charcoal • 1–12 years: 25–50 g or 0.5–1 g/kg
• Adolescents and adults: 25–100 g
Acyclovir IV HSV infection, encephalitis: 10 mg/kg/dose q8h
• Max dose: 1,500 mg/m2/day
Oral • <2 years: 100 mg five times a day
• 2–18 years: 200 mg five times daily
Adenosine IV • Neonate: 0.05 mg/kg
• Infant/child: 0.1 mg/kg (maximum 1st dose 6 mg, by
rapid bolus) followed by 0.2 mg/kg/dose (maximum
12 mg)
Adrenaline IV, IM, ET, • IV: 0.1 mL/kg 1:10,000 dilution
IO, SC • ET: 0.1 mL/kg 1:1,000 dilution
• IM: For anaphylaxis 1:1,000 dilution
{{<6 years: 150 µg (0.15 mL)
{{6–12 years: 300 µg (0.3 mL)
{{>12 years: 500 µg (0.5 mL)
Albendazole PO • 1–2 years: 200 mg single dose

• >2 years: 400 mg single dose
Repeat dose after 2 weeks for roundworms
Amikacin IV, IM • Preterm: 7.5 mg/kg IV OD
• Neonates: 10 mg/kg/day IV OD
• Infant and child: IV/IM: 15–22.5 mg/kg/day q8h
Amiodarone IV • For pulseless VF/VT: 5 mg/kg IV/IO by rapid bolus (can
repeat 5 mg/kg bolus to a total of 15 mg/kg/24 h)
• Maximum single dose 300 mg
• For SVT/stable VT: 5 mg/kg given over 60 min. Maximum
total dose 15 mg/kg per 24 h
Continued
CHAPTER 128: Drugs and Dosages in Pediatric Emergencies 427
Continued
Amoxicillin PO • Standard dose: 50 mg/kg/day in 2–3 divided doses
• High dose (resistant S. pneumoniae): 80–90 mg/kg/ day in
2–3 divided doses
• Maximum dose: 2 g/day
Amoxicillin/ IV/PO 45 mg/kg/day q8h
Clavulanic acid
Ampicillin IV • Neonates:
{{<7 days: 50 mg/kg/dose IV q12h
{{7–21 days: 50 mg/kg/dose IV q8h
{{21 days: 50 mg/kg/dose IV q6h
For suspected meningitis with group B Steptococcal infection:

100 mg/kg/dose
• Infant/child: 25 mg/kg/dose (maximum: 1 g) IV q6h
{{1 month–2 years: 12.5 mg/kg/dose PO q6h
{{2–12 years: 250 mg/dose PO q6h
{{12–18 years: 500 mg/dose PO q6h
Aminophylline IV For bronchospasm: 5 mg/kg IV loading dose over

20–30 min
Atropine IV, ET, IO • ET: 0.02 mg/kg/dose, q5 min × 2–3 doses
• Maximum single dose: 0.5 mg
• Minimum dose: 0.1 mg
Azithromycin PO/IV • 6 months–12 years: 10 mg/kg/day PO od
• Maximum dose:
{{3–7 years: 200 mg
{{8–11 years: 300 mg
{{12–14 years: 400 mg
{{>14 years: 500 mg
• Enteric fever: IV/oral: 20 mg/kg/day q12h

Benzathine IM For rheumatic fever prophylaxis:
Penicillin • <27 kg: 6 lakh units IM single dose after test dose
• >27 kg: 12 lakh units IM single dose after test dose
Calcium IV • Hyperkalemia: 1 mL/kg with equal volume of water slow
gluconate 10% IV over 10 min
• Hypocalcemia: 2 mL/kg with equal volume of water for
slow IV over 10 min
* Stop injection if symptomatic bradycardia occurs.
Extravascular administration can result in severe skin
injury.
• Maximum 10 mL as a stat dose
Continued
Continued
Cefoperazone IV 50–200 mg/kg/day q8H
Cefazolin IV 25–100 mg/kg/day divided every 6–8 h
• Maximum: 6 g daily
Cefixime PO • Infant and child: 8 mg/kg/day in 2 divided doses
• Adolescents: 400 mg/day in 1–2 divided doses
Cefotaxime IV, IM • Neonates: IV/IM 150 mg/kg/day q8h
• Infant and child:
{{Sepsis:100 mg/kg/day IV q6h
{{Meningitis: 200 mg/kg/day IV q6h
• Maximum dose: 12 g/24 h

Ceftazidime IV 100–150 mg/kg/day IV q8h
Ceftriaxone IV, IM • Mild-to-moderate infection: 50–75 mg/kg/dose once
daily; maximum daily dose: 1,000 mg
• Severe infection: 100 mg/kg/day divided every 12–24 h;
maximum daily dose: 4,000 mg
Cefuroxime IV, PO • Neonate: 50–100 mg/kg/24 h IVq12h
• Child:
{{Mild-to-moderate infection:
– Oral: 20–30 mg/kg/day divided twice daily;

maximum single dose: 500 mg
– IM, IV: 75–100 mg/kg/day divided in 3 doses;
maximum single dose: 1,500 mg
{{Severe infection: IM, IV: 100–200 mg/kg/day divided in
3–4 doses; maximum single dose: 1,500 mg

Cefoperazone IV 40–80 mg/kg/day in 2–4 divided doses
+ Sulbactam • Maximum: 160 mg/kg/day
Cephalexin PO 25–100 mg/kg/day q6h
Chlorampheni- IV • Neonates <14 days: 12.5 mg/kg/dose IV q12h
col • Neonates >14 days: 12.5 mg/kg/dose IV 2–4 times
• Children: 50 mg/kg/day in 4 divided doses (double dose
for meningitis and septicemia)
Ciprofloxacin PO, IV • Neonates: 10 mg/kg PO/IV q12h
• Children: 15–30 mg/kg/day IV/PO q12h
• Maximum dose: 800 mg/24 h
Clindamycin IV • Neonates: 15–20 mg/kg/day IM/IV divided q6–8h
• Infants, children, and adolescents: 20–40 mg/kg/day IM/IV
divided q6–8h
• Maximum dose: 450 mg/dose
Continued
Continued
Clobazam PO 0.5–1 mg/kg/day q12h
Cloxacillin PO, IV • 50–100 mg/kg/day q6h
• High dose 200 mg/kg/day q6h
Cotrimoxazole IV, PO • 6–20 mg TMP/kg/day PO q12h
• 15–20 mg TMP/kg/day IV q12h
Crystalline IV • Neonates: 1 lakh unit/kg/dose IV q12h
Penicillin • Infant and child: 50,000 units/kg/dose IV q6h
Dexamethasone IV • Croup: 0.6 mg/kg/dose
• Meningitis: 0.15 mg/kg/dose
Digoxin Oral IV • Maintenance dose: 0.01 mg/kg/day, once a day, 5/7
• Atrial fibrillation (rate control): Total digitalizing dose (TDD):
8–12 µg/kg IV; administer half of TDD over 5 min with the
remaining portion as 25% fractions at 4–8 h intervals
Dobutamine IV Infusion 15 mg/kg in 50 mL NS (1 mL: 5 µg/kg/min)
Dopamine OV Infusion 15 mg/kg in 50 mL NS (1 mL: 5 µg/kg/min)
Doxycycline PO • Cholera: Oral 6 mg/kg/dose stat
• Rickettsial infection: 4 mg/kg/day q12h
• Maximum dose: 300 mg/day
Erythromycin PO • 0–7 days: 20 mg/kg/day q12h
• >7 days: 30 mg/kg/day q8h
• Infant–child: 30–50 mg/kg/day q6h
• Maximum dose: 4 g/24 h
Fentanyl IV 1–2 µg/kg/dose
Fluconazole Oral • Mucosal candidiasis: 3-6 mg/kg/day PO od
• Systemic candidiasis/Cryptococcosis: 6–12 mg/kg/day
PO od
Furosemide IV • 0.5–1 mg/kg/dose
(Lasix) • For infusion: 3–4 mg/kg/day in 24 mL of NS, at 1 mL/h
Gentamicin IV, IM • Neonates <7 days: 2.5 mg/kg IV/IM q12h
• Neonates >7 days: 2.5 mg/kg IV/IM q8h
• Children <12 years: 7.5 mg/kg/day IV/IM in 3 divided doses
• 12–18 years: 3–6 mg/kg/day IV/IM in 3 divided doses
Hydrocortisone IV • Infants: 10–25 mg IV stat followed by 10–25 mg/day in
divided doses q6h
• Children <5 years: 25–50 mg IV stat followed by
25–50 mg/day in divided doses q6h
• Children ≥5 years: 50–100 mg IV stat followed by
50 mg/day in divided doses q6h
• Adolescents: 100 mg IV stat followed by 100 mg/day in
divided doses q6h
Continued
Continued
Hydroxyzine Oral • Pruritus:
(Atarax) {{6 months–6 years: 5–15 mg PO hsod
{{7–12 years: 10–15 mg PO hsod
{{12–18 years: 25 mg PO hsod
• Anxiety:
{{<6 years: 50 mg/day PO in 3–4 divided doses
{{>6 years: 100 mg/day PO in 3–4 divided doses
Hyoscine PO, IM, IV • PO: 5–12 years: 10 mg/dose, 12–18 years: 20 mg/dose
(Buscopan) 3–4 times/day
• IM/IV: <6 years: 5 mg/dose, 6–12 years: 5–10 mg/dose,
>12 years: 20 mg/dose 3–4 times/day
• Maximum dose: 1.2 mg/kg/day
Kayexalate PO, • PO: 1 g/kg every 6 h
(Sodium rectal • Rectal: 1 g/kg/dose every 2–6 h
polystyrene
sulfonate)
KCl PO 2–5 mEq/kg/day in divided doses; not to exceed
1–2 mEq/kg as a single dose
Ketamine IM, IV IV: 1–2 mg/kg/dose
Lidocaine IV 1 mg/kg/dose
Lorazepam IM, IV 0.1 mg/kg/dose
Levetiracetam IV, PO 10–20 mg/kg/dose stat, followed by 10 mg/kg/dose bd for
1 week, then increase by 10 mg/kg/day up to maximum of
60 mg/kg/day
Mannitol (20%) IV 2.5 mL/kg (0.5 g/kg given over 15 min)
Magnesium 0.1 mL/kg of 50% MgSO4 as slow infusion with NS over 30
sulfate min
Meropenem IV • Neonates:
{{Sepsis: 20 mg/kg/dose q12h
{{Meningitis: 40 mg/kg/dose q12h
• Children:
{{Moderate infection: 20 mg/kg/dose IV q8h
{{Meningitis: 40 mg/kg/dose IV q8h
• Maximum dose:
{{Moderate infection: 3 g/day
{{Severe infection: 6 g/day
Continued
Continued
Metronidazole IV, PO • Neonates:
{{Loading dose: 15 mg/kg
{{Maintenance:
– 7.5 mg/kg/dose q24h for VLBW

– 7.5 mg/kg/dose q12h for weeks 1–4
– 7.5 mg/kg/dose q8h over 4 weeks
• Child: 7.5 mg/kg/dose IV/PO q8h
* Maintenance dose should begin 48 h after loading dose
for VLBW and 24 h after loading dose for term babies
Midazolam IV, IM IV/IM: 0.1 mg/kg/dose
• For infusion: 0.5 mg/kg in 50 mL NS
• Seizure dose infusion: 3 mg/kg in 50 mL NS: Start at
1 mL/h
Morphine IV, IM, SC 0.1–0.2 mg/kg/dose
Nifedipine Oral • HT urgency: 0.1–0.25 mg/kg/dose. Can be repeated
every 4–6 h
• Chronic treatment: 0.25–0.5 mg/kg/day in 1 or 2 divided
doses
• Maximum single dose: 10 mg
Noradrenaline IV Add 0.3 mg/kg in 50 mL NS, 1 mL/h = 0.1 μg/kg/min,
2 mL/h = 0.2 μg/kg/min
Pancuronium IV • Neonates: 0.05–0.10 mg/kg/dose
• Children: 0.05–0.15 mg/kg/dose
Pantoprazole IV/oral 1 mg/kg/dose od
• Maximum dose: 40 mg/day
Pheniramine IM, IV, PO 0.5 mg/kg/day q8h
maleate (Avil)
Phenobarbitone IV 20 mg/kg loading dose slow IV over 20 min followed by
5 mg/kg/day in 2 divided doses
• Maximum dose: 30 mg/kg/day
Phenytoin IV Loading 15–20 mg/kg in 50–100 mL NS slow infusion
sodium over 20 min and then 3–4 mg/kg/day in 2 divided doses
in neonates and 5–6 mg/kg/day in 2 divided doses in
children
Piperacillin- IV • Infant: 300 mg/kg/day in 3 divided doses
Tazobactam • Child: 400 mg/kg/day in 3 divided doses
• Maximum single dose: 4.5 g
Propranolol IV, oral • Oral: 0.5–1 mg/kg/day q6–12h
• IV: 0.15–0.25 mg/kg/dose slow IV push (TOF)
Continued
Continued
Ranitidine IV, PO 1 mg/kg/dose q8h
Salbutamol PO 0.1 mg/kg/dose q8h
Sodium IV 1 mEq/kg/dose or 0.3 × kg × base deficit
bicarbonate
Spironolactone PO 1–3 mg/kg/day in 2 divided doses
Succinylcholine IV 1–2 mg/kg/dose
* Increases ICP, contraindicated in burns, massive trauma,
hyperkalemia
Thiopental IV 1–5 mg/kg/dose
Tranexamic acid PO, IV 10 mg/kg/dose
Tramadol IM, IV 1–2 mg/kg/dose 6th hourly
• Maximum single dose: 100 mg
UDCA PO 5–10 mg/kg/dose twice a day
Valproate PO, IV • IV: 20 mg/kg loading dose followed by
5–10 mg/ kg/dose
• Maximum dose: 60 mg/kg/day
Vancomycin IV • Neonates: 15 mg/kg/dose IV
{{<28 weeks: Once daily
{{29–35 weeks: Twice daily
{{>35 weeks: Thrice daily
• Children: 15 mg/kg loading dose followed by 10 mg/kg/

dose q6h
Vecuronium IV 0.1 mg/kg/dose
Vitamin K1 IM, SC, IV • Infant and child: 2.5–5 mg/24 h, PO od
• Infant and child: 1–2 mg/dose, IM, SC, IV, od
• Adolescent and adult: 10 mg/dose, PO, SC, IV, IM, od
Ipravent (Neb) • <12 years: 250 µg/dose, q20 min × 3 then q6–8h
• >12 years: 500 µg/dose, q30 min × 3 then q6–8h
Salbutamol • <2 years: 0.3 mL in 3 mL of NS
(Neb) • 2–5 years: 0.5 mL in 3 mL of NS
• >5 years: 1 mL in 3 mL of NS
Adrenaline (Neb) 0.5 mL/kg 1 in 1,000, diluted in 3 mL of NS
• Maximum dose:
{{<4 years 2.5 mL/dose
{{>4 years 5 mL/dose
(HSV: herpes simplex virus; ICP: intracranial pressure; NS: normal saline; SVT: supraventricular tachycardia;
TOF: tetralogy of Fallot; UDCA: ursodeoxycholic acid; VF/VT: ventricular fibrillation/ventricular
tachycardia; VLBW: very low birth weight baby)
Section 18
Disaster Management
Mass Casualty Incidents 129
CHAPTER
DISASTER MANAGEMENT: HOSPITAL PREPAREDNESS

Disaster, mass casualty, and catastrophe have all become household terms in
this 21st century by virtue of the global change in environment and lifestyle.
The impact of these disasters not only imply on life but also on the functional
status of the individual and the society. Disaster management is no more a topic
of discussion but a field of specialty called disaster medicine and nursing. This
chapter focuses on the hospital preparedness and response for disaster and mass
casualties.
Objectives of Hospital Preparedness

To ensure that the healthcare team is able to:
• Be prepared in disaster risk reduction (DRR)
• Respond appropriately to mass casualty/disaster management
• Document the response toward disaster management.
Definitions of Terminology Used in Hospital Disaster

Management Center for Research on the Epidemiology of
Disasters (CRED)
• Disaster: A situation or event, which overwhelms local capacity, necessitating
a request to national or international level for external assistance [definition
considered in emergency events database (EM-DAT)]; an unforeseen and
often sudden event that causes great damage, destruction, and human
suffering. Though often caused by nature, disasters can have human origins
(EM-DAT).
• Hazard: Threatening event, or probability of occurrence of a potentially
damaging phenomenon within a given time period and area.
• Risk: Expected loss (of lives, persons injured, property damaged, and
economic activity disrupted) due to a particular hazard for a given area and
reference period. Based on mathematical calculations, risk is the product of
hazard and vulnerability.
• Transport accident: Disaster type term used in EM-DAT to describe
technological transport accidents involving mechanized modes of transport.
• Vulnerability: Degree of loss (0–100%) resulting from a potential damaging
phenomenon.
436 SECTION 18: Disaster Management
Classification of Hospital Disasters

• Internal disasters: Events that result in loss of resources used for regular
hospital activities.
Examples: Fire, earthquake, loss of utilities, worker strikes, release of
chemicals, or radiation.
• External disasters: Events that occur in the community outside the hospital
that may affect the hospital’s ability to carry out regular activities.
Examples: Road, rail accidents, and technological hazards.
This chapter focuses on the response of the emergency department toward external
disaster, which means, response to mass casualty incidents reporting to the hospital.
MASS CASUALTIES IN THE EMERGENCY DEPARTMENT

A mass casualty incident (MCI) is any incident in which emergency medical
services resources, such as personnel and equipment, are overwhelmed by
the number and severity of casualties. The mass casualty management (MCM)
depends upon the policy of the institution and is based on the capacity and the
resources.
The success of MCM system depends on the following:
• Pre-established procedures, to be used in daily emergency activities and to
be adapted to meet demands of a major incident, such as an event in which
there may be large number of patients reporting to the ED at the same time
(Disaster plan).
• Optimal use of existing resources (Logistics).
• Multidimensional preparation and response (Capacity building).
• Strong preplanned and tested coordination (Mock drill).
Management of a MCI in the ED of CMC, Vellore (Flowchart 1)

Step 1: Verification of the MCI: On receiving information/arrival of first patient
of an MCI, the ED registrar and nurse in-charge should confirm the authenticity
of the information from the public relations officer (PRO) or the administration.
Step 2: Notification of MCI: The ED registrar or nurse should inform the on-call
trauma coordinator (TC) and trauma nurse coordinator (TNC). The TC and
TNC should inform the head of the department and arrive in the ED within
5–10 minutes.
Step 3: Activation of the MCM team: This is done by the TC and TNC through
telephone exchange (Ph. No. 2500). The TC is the incident commander of the
MCM team.
Step 4: Team members reporting to the ED: All team members should report to the
ED at the earliest and perform their roles as described.
CHAPTER 129: Mass Casualty Incidents 437
(ED: emergency department; TC: trauma coordinator; TNC: trauma nurse coordinator; HOD: head
of the department; MS: medical superintendent; GS: general superintendent; MCM: mass casualty
management; MRD: medical records department; CSSD: central sterilization and supply department;
NS: nursing superintendent)
FLOWCHART 1: Mass casualty management (MCI) protocol at CMC, Vellore.
Step 5: Deactivation of MCI: This is done when all the patients are attended to and
stabilized.
The MCM Team Members Responding to an MCI in CMC

• Emergency department: TC, TNC, additional doctors and nurses, paramedics,
social worker, and housekeeping staff.
• Other departments: Medical superintendent (MS), general superintendent
(GS), nursing superintendent (NS), orthopedics, neurosurgery, general
medicine, general surgery, pharmacist, medical records, central sterile supply
department, PRO, additional security, blood bank, ICU, and chaplain.
JOB DESCRIPTION OF THE TEAM MEMBERS

The TC and TNC should wear color-coded aprons for easy identification.
438 SECTION 18: Disaster Management
Trauma Coordinator
Upon arrival in the ED, the TC should take charge of the scene. The TC should
ensure that all the team members have been informed of the MCI. The TC should
make trolleys available by:
• Transferring the existing patients, if needed
• Making stable patients to wait outside, and
• Discharging the patients.
In case of a large disaster, the TC should identify the surge capacity area in the
Trauma Bay. All patients should be managed in collaboration with the involved
specialties.
Trauma Nurse Coordinator

The TNC, after taking charge of the scene should ensure that all the team members
respond to the call. In coordination with the TC, the TNC should ensure that
trolleys are available at triage and nondisaster patients requiring admission are
shifted to the wards.
ED Registrars and Nurses

They have to ensure continuity of care of patients in their bays and quickly
discharge or shift out stable patients to priority 3. At least three trolleys should be
made available in each bay for receiving MCI patients. They have to take up the
area of management as advised by TC and TNC.
Others
• The pharmacist should report in person within the department with the
stipulated drugs needed for MCM.
• The medical records person should bring patient charts with predesignated
hospital numbers so that investigations may be sent without waiting for
registration.
• The PRO coordinates with the Head of ED, MS, and GS to update the press. The
PRO also provides needed support to the relatives through volunteers.
• A minimum of five security officers, including two sergeants report to the TC
for crowd control. They take charge of patient’s valuables in prelabeled MCM
bags and look after the safety of the hospital staff involved in patient care.
• Attenders and housekeeping staff support the medical and nursing staff to
mobilize patients to the wards and to priority 3 and arrange equipment as
needed in consultation with TNC.
A debriefing of the MCM should be done by the head of the ED on the next
working day.
Section 19
Medicolegal Cases
Medicolegal Cases 130
CHAPTER
INTRODUCTION
A medicolegal case (MLC) is any case of injury or ailment, etc., in which
investigations by the law-enforcing agencies are essential to fix the responsibility
regarding the causation of the injury or ailment. An MLC has not been explicitly
defined anywhere in the law. It depends more or less upon the judgment of the
doctors.
LIST OF COMMON MEDICOLEGAL CASE

The following are the common MLCs for which an incident report has to be filed:
• All vehicular, railway, airplane, ship, boat accidents, or other unnatural
accidents where there is likelihood of death or grievous hurt
• All thermal and electrical injuries
• All workplace injuries/accidents
• All deliberate self-harm attempts (Indian Penal Code, IPC: 309)
• Suspected or evident sexual assaults
• Suspected or evident criminal abortion
• Suspected or evident homicide attempt (assault)
• Drowning/hanging/strangulation
• Domestic violence causing grievous injury
• Unconscious cases where the cause is not natural or not clear
• Animal-related injuries
• Snake bite (only when requested by relatives for claiming compensation)
• Dead on arrival cases where an unnatural cause is suspected
• Any other case not falling under the above mentioned category but has legal
implications.
GRIEVOUS AND NONGRIEVOUS INJURIES

Section 320 in the IPC defines grievous hurt. The punishment is enhanced when
the injury is grievous. The wound certificate issued should include the grievous
or nongrievous nature of injury; the following are the guidelines to designate an
injury as grievous:
• Emasculation
• Permanent privation of the sight of either eye
• Permanent privation of the hearing of either ear
• Privation of any member or joint
442 SECTION 19: Medicolegal Cases
• Destruction or permanent impairing of the powers of any member or joint

• Permanent disfiguration of the head or face
• Fracture or dislocation of a bone or tooth
• Any injury which endangers life or which causes the sufferer to be during the
space of 20 days in severe bodily pain, or unable to follow his ordinary pursuits
• Any intra-abdominal injury can be considered as grievous.
INCIDENT REPORTING
All MLCs who present to the hospital should be directly reported to the police. If
a patient has been treated elsewhere and referred, it is the responsibility of the
referring doctor to inform the police. However, in our ED, we report all MLC that
present acutely after the incident (<48 h). The incident report has to be filled online
through the ED module. The report will be sent to the police station through the
Medical Superintendent office.
DEATH OF AN MEDICOLEGAL CASE

In case of a brought dead MLC, the nearest police station has to be informed
immediately through the “brought dead MLC form”. The body may be kept in
mortuary for the investigation to take place. However, if the relatives are aggressive
and insist on releasing the body, to ensure safety of the healthcare workers first,
the police should first be informed and the body may be released after taking
informed signed con sent from the relatives on the “release of body” form.
Section 20
Triage
Triage Priorities 131
CHAPTER
INTRODUCTION
Triaging is a process by which victims are classified according to the severity and
nature of their injuries. The purpose of triage is to ensure prioritization so that
the “right patient gets the right treatment at the right time”. When more than one
victim is brought into the emergency department (ED), it is essential to assess and
identify those who require immediate care. This process of prioritizing the patient
facilitates appropriate care. The primary objectives of triage are:
• Identification of immediate life-threatening situations
• Reducing severity of the condition by ensuring immediate intervention
• Reducing delay in the treatment.
The commonly used color coding of triage categories are as follows:
• Red: Priority 1, most urgent
• Yellow: Priority 2, urgent
• Green: Priority 3, nonurgent
• Black: Dead
Many different triaging systems are used across the World with 3–5 triage
categories. Some of the commonly used ones are Australasian Triage System
(5 categories), Canadian Triage and Acuity scale (5 categories), Manchester
Triage Scale (5 categories) and the Emergency Severity Index (5 categories).
Though triaging is based on physiological parameters of the patient at
presentation, it is better to incorporate common regional medical and surgical
emergencies into the triaging criteria. This is the strength of the 4-category CMC
Vellore triage guidelines which were the first triage system developed in India
in 1999. This has been further revised every 2 years with the latest revision in
January, 2021 (Tables 1 to 4).
TABLE 1: CMC Triage guidelines (Revised edition, January 2021: Priority I).
Trauma Non-trauma
ABC compromised ABC compromised
GCS ≤ 8 GCS ≤ 8/altered sensorium
Penetrating ocular trauma RR < 12 or > 40/min or SpO2 < 94%
Hemodynamically unstable abdominal HR < 50/min or >150/min
and pelvic injuries Palpitations with HR > 150/min
Hemodynamically unstable SBP < 80 mm Hg
Continued
446 SECTION 20: Triage
Continued
Trauma Non-trauma
Limb injuries with vascular compromise Acute onset fever with altered sensorium
Obvious dyspnea with chest pain (post- Hypertensive emergency: SBP > 180 mm Hg
trauma) with any of the following: and/or DBP > 120 mm Hg with evidence of
• RR < 12 or > 30/min end organ failure like altered sensorium, chest
• SpO2 < 94% pain, breathing difficulty, visual disturbance,
and oliguria
• Subcutaneous emphysema
• Open pneumothorax
• Penetrating chest/neck wound
Hypovolemic shock (SBP < 90 mm Hg or Poisoning with h/o consumption < 2 h or GCS
HR > 130/min) < 13 or hemodynamically unstable
Active seizures
Cerebrovascular accidents < 4.5 h
Chest pain < 8 h (back, shoulder, and
epigastric pain)
(ABC: airway, breathing, and circulation; GCS: Glasgow coma scale; RR: respiration rate; HR: heart rate;
SBP: systolic blood pressure; DBP: diastolic blood pressure)
TABLE 2: CMC Triage guidelines (Revised edition, January 2021: Priority II).
Trauma Non-trauma
ABC not compromised ABC not compromised
• RR: 12–30/min • Dyspnea with RR 28–40/min, SpO2 > 94%, use of
• SpO2 >94% accessory muscles, and comorbid conditions
• GCS ≥9 • Hemoptysis or hematemesis within 24 h.
• All dislocations • Chest pain more than 8 h or ongoing chest pain
• Ear, nose, and throat (ENT) >24 h
bleed • Palpitations with HR < 150/min and
• All long bone fractures with hemodynamically stable
no vascular compromise • Acute gastroenteritis with HR > 120/min
• Treated and referred open • High sugars with acetone positive
fractures • High sugars with acetone negative but with
• Compartment syndrome dehydration and fever
• Foreign body in the eyes • Severe pain which requires immediate attention or
• Subcutaneous emphysema analgesics including acute abdominal pain
with no dyspnea • Poisoning without ABC compromise and normal
• Hemodynamically stable sensorium
abdomen and pelvic injuries • Scorpion sting/bee sting/unknown bite/ snake bite
• Pregnant women with stable • Hematological illness with active bleeding
vital signs (following trauma) • Giddiness with associated features
Continued
CHAPTER 131: Triage Priorities 447
Continued
Trauma Non-trauma
• Altered sensorium of any cause with vitals stable
• Hyperemesis gravidarum with urinary ketones
positive
• Pregnant patient with bleeding per vaginal (PV)/
abdomen pain/spotting PV
• Acute deep vein thrombosis
• Fever ≥ 103°F
• Fever with vomiting and not tolerating orally and
dehydration
• Fever with neck stiffness
(ABC: airway, breathing, and circulation; GCS: Glasgow coma scale)
TABLE 3: CMC Triage guidelines: Revised edition, January 2021: Priority III (Patients with
acute problems and stable vital signs).
Trauma Non-trauma
• GCS 15/15 with no loss of • Mild abdominal pain, passed stool, and
consciousness (LOC), stable vital signs, flatus
and no history of vomiting • Acute gastroenteritis with stable vitals
• Isolated closed forearm fractures • Acute urinary retention (fast track)
without neurovascular deficit • Fever without high-risk factors and no
• Lacerations with no active bleed features of sepsis
• Hand injury (fast track) • Localized cellulitis
• Closed ankle and foot injuries (fast • Isolated facial palsy
track) • Toothache
• Burns <9% and peripheral in location • Dog bite
• Trauma in children without vomiting, • Patients with incidentally detected high
LOC, and child being active blood sugars
• Any patient in pain (fast track) • Giddiness with no associated illness
• Any patient in pain (fast track)
TABLE 4: CMC Triage guidelines: Revised edition, January 2021: Priority IV

Trauma Nontrauma
Patients with chronic trauma with no Patients with chronic problems with no acute
acute worsening worsening
Section 21
Miscellaneous
Heat-related Illnesses 132CHAPTER
INTRODUCTION
Heat-related illnesses have a spectrum of severity.
• Heat cramps: Core temperature is between 37°C and 39°C. Characterized by
brief cramps usually after exertion. Mental function is normal.
• Heat exhaustion: Core temperature is between 37°C and 40°C. Symptoms
include weakness, fatigue, headache, vertigo, nausea, vomiting, giddiness,
and syncope. Mental status remains normal. Most patients recover with
adequate rest and fluid replacement.
• Heat stroke: Core temperature is more than 40°C (104°F). Many patients with
heat-related illnesses may have a core temperature greater than 104°F. However,
only patients with central nervous system (CNS) dysfunction (irritability,
confusion, hallucinations, ataxia, seizures, focal deficits, or coma) are classified
as having a heat stroke. All thermoregulatory function is lost.
DIAGNOSIS
The diagnosis of classic (non-exertional) heat stroke is made clinically with the
following triad:
• An elevated core body temperature (generally > 40°C/104°F)
• CNS dysfunction (e.g., altered mental status)
• Exposure to severe environmental heat. This should be determined through
history of type of house, place of work, and availability of cooling facilities like
air conditioning.
There are two types of heat stroke:
1. Classic (nonexertional) heat stroke: Usually, affects the elderly with underlying
chronic medical conditions. Bedbound patients left in a hot environment at
home and patients on anticholinergics are especially vulnerable.
2. Exertional heat stroke: Young healthy people like athletes, military training
recruits who perform rigorous exercises in a hot and humid environment may
develop exertional heat stroke.
DIFFERENTIAL DIAGNOSIS
Consider the following as the differentials; otherwise you may miss the diagnosis:
• Infections: Cerebral malaria, leptospirosis, septic shock, CNS infections
• Noninfectious causes: Neuroleptic malignant syndrome (NMS), malignant
hyperthermia, thyroid storm, serotonin syndrome.
452 SECTION 21: Miscellaneous
Complete blood count, liver function tests, electrolytes, creatinine, Urea,
prothrombin time, activated partial thromboplastin time, creatine phospho-
kinase, blood c/s, arterial blood gas, ECG, chest X-ray, urinalysis.
MANAGEMENT
• Secure circulation, airway, and breathing
• Fluid resuscitation: IV crystalloids to be rushed in
• Cooling measures: The target of cooling at the end of the golden hour
(1st hour) should be a core body temperature of 39°C.
cc Move to a cool environment
cc Start internal cooling via cold NS, nasogastric tube ice cold saline/water
cc Evaporative cooling: Undress the patient, spray tepid water (not cold) and
cool by fans blowing parallel to the body to maximize evaporative heat loss
cc Keep ice packs in the axilla, groin, head and neck (Fig. 1)
cc Apply wet sheets loosely over the patient.
• Correct electrolyte abnormalities

• Control shivering with injection promethazine (phenergan) 12.5–50 mg IV
• Anti-epileptic of choice for seizures is phenobarbitone. Avoid phenytoin.
• Identify and treat complications (e.g., CNS dysfunction, rhabdomyolysis, acute
kidney injury, acute liver failure, disseminated intravascular coagulation).
Monitor sugars for hypoglycemia.
Drugs to be avoided: Anticholinergics, antipyretics (will not help), α adrenergics (increases

peripheral resistance), salicylates (may worsen platelet dysfunction), large dose of
paracetamol (may worsen hepatic injury).
FIG. 1: Ice pack application.

Malignant Hyperthermia 133CHAPTER
INTRODUCTION
Malignant hyperthermia (MH) is a rare inherited life-threatening condition
characterized by excessive oxidative metabolism in the skeletal muscles resulting
in hyperpyrexia, circulatory collapse, and even death upon exposure to certain
drugs. It usually occurs in the operating theater or during the immediate post-
operative period.
Susceptible patients have genetic skeletal muscle receptor abnormalities
(abnormal RYR1 or DHP receptors) that allow excessive myoplasmic calcium
to accumulate when exposed to certain anesthetic triggering agents. This
leads to unregulated passage of calcium from the sarcoplasmic reticulum into
the intracellular space, resulting in sustained muscle contraction, change to
anaerobic metabolism, rhabdomyolysis, and hyperthermia.
DRUGS IMPLICATED AS POTENTIAL TRIGGERS

These are:
• Halothane
• Isoflurane
• Enflurane
• Sevoflurane
• Desflurane
• Succinylcholine.
The earliest sign is an increase in end-tidal carbon dioxide (ETCO2)
• Early signs: Sinus tachycardia, masseter muscle rigidity, generalized muscle
rigidity
• Late signs: Hyperthermia, ECG changes of hyperkalemia, ventricular fibril-
lation/ventricular tachycardia (VF/VT), myoglobinuria, bleeding.
DIAGNOSIS
The diagnosis must be considered in all patients receiving triggering agents.
An increased ETCO2, generalized muscle rigidity, hyperkalemia (K > 6 mEq/L),
arterial blood gas pH <7.25, base excess (BE) < –8 mEq/L, creatine phosphokinase
>20,000 IU and myoglobinuria strongly suggest the diagnosis.
MANAGEMENT
It includes:
• Stabilize airway and breathing. Optimize oxygenation and ventilation
• Circulation: Ensure adequate hydration by administering cold crystalloids
• Discontinue triggering agents
• Dantrolene bolus dose of 2.5 mg/kg IV followed by boluses every 5 minutes
of 1 mg/kg IV until acute symptoms abate. Dantrolene binds to the RYR1
receptor and inhibits release of calcium from the sarcoplasmic reticulum;
thus reversing the negative cascade of effects
• Monitor and treat hyperkalemia
• Cooling measures:
cc Start internal cooling via cold normal saline (NS), nasogastric (NG) ice
cold saline or water

cc Evaporative cooling: Undress the patient, spray tepid water and cool by
fans blowing parallel to the body to maximize evaporative heat loss.

• For ventricular dysrhythmias: Procainamide loading dose 20–50 mg/min or
100 mg every 5 minutes until arrhythmia is controlled or hypotension occurs.
Neuroleptic Malignant
Syndrome 134
CHAPTER
INTRODUCTION
Neuroleptic malignant syndrome (NMS) is a life-threatening emergency caused
by an adverse reaction to certain neuroleptic agents. It is characterized by
hyperthermia, generalized muscular rigidity, altered sensorium, and autonomic
dysfunction.
Drugs that can cause NMS:
• Neuroleptic agents:
cc Highly potent neuroleptics: Haloperidol, fluphenazine, and prochlor-
perazine
cc Low potency neuroleptics: Chlorpromazine and promethazine
cc Newer “atypical” antipsychotics: Clozapine, risperidone, and olanzapine.
• Antiemetic agents: Domperidone and metoclopramide.
The classical tetrad of NMS symptoms usually evolve over 1–3 days.
• Mental status change in the form of an agitated delirium with confusion or
pyschosis is seen in the majority of patients
• Generalized muscular rigidity characterized by “lead pipe rigidity”
• Hyperthermia >38°C
• Autonomic instability in the form of tachycardia, labile or high BP, tachypnea,
dysrhythmias, or diaphoresis.
DIAGNOSIS
There is no diagnostic test for NMS. Diagnosis is purely clinical. The differential
diagnosis for NMS includes heat stroke, malignant hyperthermia, and severe
sepsis. Laboratory abnormalities include leucocytosis (10,000–40,000/cumm),
elevated creatine phosphokinase (CPK), electrolyte abnormalities (hypo/
hypernatremia, hyperkalemia, hypocalcemia, hypomagnesemia), hepatic
transaminitis, and myoglobinuria.
MANAGEMENT
• Discontinue any neuroleptic agent or precipitating drug
• Obtain IV access and start fluid resuscitation. Ensure adequate hydration
• Maintain cardiorespiratory stability
• Cooling measures:
cc Start internal cooling via cold normal saline (NS), nasogastric (NG) ice
cold saline or water

cc Evaporative cooling: Undress the patient, spray tepid water and cool by
fans blowing parallel to the body to maximize evaporative heat loss.

• Benzodiazepines (lorazepam 0.5–1.0 mg) may be needed to control agitation.
• Specific therapy:
cc Dantrolene: A direct-acting skeletal muscle relaxant. Doses of 1–2.5 mg/kg
IV is typically used in adults and can be repeated every 5–10 minutes to a

maximum dose of 10 mg/kg/day, or
cc Bromocriptine: A dopamine agonist. Doses of 2.5 mg (through nasogastric
tube) q6-8h and titrate up to a maximum dose of 40 mg/day, or

cc Amantadine: It has dopaminergic and anticholinergic effects. Initial dose
is 100 mg orally.
Electrical Injuries 135CHAPTER
INTRODUCTION
An electric shock may cause cardiac or respiratory arrest. Thermal injury from the
electrical current can result in burns and muscle damage. Muscle spasms from
a shock may result in dislocations or fractures or precipitate a fall causing major
trauma.
• An electrical short circuit near a person may cause sudden vaporization of
metal and deposition of a thin layer of hot metal on the skin, without any
electricity passing through the body. These are often superficial and heal
uneventfully.
• In contrast, an electrical arcing through the body produces high temperatures
and may cause deep dermal or full-thickness burns, especially if clothing
catches fire.
• If electricity passed through the patient, there are usually two or more entry or
exit wounds that are typically painless, gray to yellow depressed areas. Tissue
damage will be more extensive than the visible burns.
• Myoglobinuria and renal failure may be caused by damage to deeper layers of
skeletal muscles.
• Cardiac injury may result in arrhythmias in up to 30% of victims. Low voltage
alternating current (AC) may trigger ventricular fibrillation, while high voltage
AC or direct current (DC) are likely to induce transient ventricular asystole.
• Neurological effects, seen in up to 50% of patients include transient loss of
consciousness, seizures, coma, headache, transient paralysis, and peripheral
neuropathy.
• Other common injuries include spinal cord injuries (due to vertebral fractures),
orthopedic injuries (due to associated falls or tetanic muscle contractures),
blast injuries, inhalation injuries, ocular injuries (cataract, retinal detachment,
corneal burns, intraocular hemorrhage), auditory injuries, and disseminated
intravascular coagulation.
INVESTIGATIONS
Complete blood count (CBC), electrolytes, creatinine, urea, serum myoglobin,
creatine kinase, urinalysis, ECG, chest X-ray.
MANAGEMENT
• Assess and stabilize airway, breathing, and circulation.
• Examine thoroughly for head, chest, abdomen, and skeletal injuries.
• Examine all over for skin entry or exit burns. Cleanse the skin, and dress the
burns with silver sulfadiazine or mafenide acetate.
• Monitor ECG for arrhythmias, conduction defects, and ST and T wave
changes. Continuous cardiac monitoring should be instituted for all high-
voltage injuries.
• Begin fluid resuscitation with crystalloids (NS/RL). Administer an initial fluid
volume of 20–40 mL/kg over the first 1 hour and titrate to urine output of
0.5–1 mL/kg/h in patients with significant burns or myoglobinuria.
• Extremities with significant burns should be splinted in a functional
position (35–45-degree extension at the wrist, 80–90-degree flexion at the
metacarpophalangeal, and full extension of the proximal interphalangeal and
distal interphalangeal joints) to minimize edema and contracture formation.
• Check for compartment syndrome locally. Perform a fasciotomy if needed
and debride necrotic tissue.
When to Refer
• Asymptomatic patients with minor low-voltage burns, normal ECG, no
palpitations, and no myoglobinuria may be observed for 6–8 hours and
discharged.
• All patients with electrical burn injuries need to be referred to plastic surgery.
• Patients with no or minimal external burns but having arrhythmias or renal
failure need to be referred to medicine.
Burns 136
CHAPTER
INTRODUCTION
Burns is a traumatic injury to the skin cause by excessive heat. They may be caused
by heat (flames, hot liquid, steam or hot solid objects), electrical discharge,
friction, chemicals (acid/alkali) or radiation.
The severity of burns is determined by the burned surface area, depth of burns
(Table 1) and presence of co-morbidities. The ‘Rule of 9's’ is commonly used to
estimate the burned surface area in adults and in children (Table 2 and Fig. 1).
• If there is no airway compromise and burns area is greater than 20%, refer to
plastic surgery immediately for admission to the burns unit.
• If there is airway compromise or if the burns area is less than 20, admit the
patient in the ED and initiate resuscitation as described below.
TABLE 1: Evaluation of depth of burns.

Superficial burn Partial thickness burn Full-thickness burn
Superficial Deep
Appearance Pink or small Red to white Red and mottled Waxy, leathery,
blisters large blisters blisters charred
Sensation Painful Pinprick feels Pinprick feels Anesthetic
sharp dull
Capillary return Present Delayed Absent Absent
Spontaneous 5–10 days 10–14 days 14–21 days Requires grafting
healing
TABLE 2: Percentage of burns by rule of 9 in adults and children.

Adults Children
Upper limbs 9% each (18%) 9% each (18%)
Lower limbs 18% each (36%) 14% each (28%)
Back of trunk 18% 18%
Front of trunk 18% 18%
Head and neck 9% 18%
Perineum 1% 0
FIG. 1: Rule of 9 in adults.
EMERGENCY DEPARTMENT MANAGEMENT OF BURNS

1. Maintain airway: Look for inhalational or facial injuries. Suspect airway
compromise and secure the airway.
2. Secure venous access: Start 2 large bore (16-G or 18-G) IV lines and send sample
for complete blood count (CBC), urea, creatinine, electrolytes, creatine
phosphokinase, and liver function test.
3. Start IV fluids based on modified Parkland formula.
Initial 24 hours: NS/RL 2–4 mL/kg/% burn (adults)
Next 24 hours: Begin colloid infusion of 5% albumin 0.3–1 mL/kg/% burn/16/h
During the first period of 8 hours since the incident, give one half of the above
volume. During the second period of 16 hours, give the other half of the total
volume.
4. Provide pain relief:
• Injection morphine 0.1 mg/kg IV in small boluses
• Injection paracetamol 1 g in 100 mL NS
• Avoid nonsteroidal anti-inflammatory drugs.
5. Antibiotics: Prophylactic antibiotics are not indicated in the early postburns
period.
6. Wound management:
• Administer diphtheria tetanus (dT) toxoid
• Debride large blisters and just puncture the small ones with a 25-G needle
CHAPTER 136: Burns 461
• Apply sterile dressings if other unit registrar is going to open the wound
initially to allow for repeat examination
• If no further review is required and the wound is clean and dry, apply
occlusive dressing which is to be removed after a week.
• Do not use Paraffin gauze or Sofra-tulle.
• Silver sulfadiazine (SSD):
cc To be used only in full-thickness and in infected burns
cc Do not use SSD for partial thickness burns
cc Do not wrap SSD dressings circumferentially. Apply them longitudinally.
Admission Criteria/Referral to Plastic Surgery

• More than 15% burns in children
• More than 20% burns in adults
• Involvement of face, hands, feet, genitalia, perineum, and major joints
• Electric burns
• Chemical burns
• Suspected inhalational injury
• Circumferential burns
• Burns in the extreme age groups.
Drowning or
Submersion Injuries 137
CHAPTER
INTRODUCTION
In nonfatal drowning, the victim survives at least temporarily after being
immersed or submersed in a liquid medium. Drowning may be classified as wet
and dry drowning.
• Wet nonfatal drowning: Aspiration of fluid into the lungs occurs resulting in
pulmonary edema.
• Dry nonfatal drowning: No aspiration occurs but patient has a period of
asphyxia due to severe persistent laryngospasm. This is triggered by a small
amount of water entering the larynx and results in asphyxia with immediate
outpouring of thick mucus and froth.
END-ORGAN EFFECTS
• Pulmonary: Fluid aspiration may result in varying degrees of asphyxia. Both
salt water and fresh water wash out the surfactant in the lungs causing acute
respiratory distress syndrome or noncardiogenic pulmonary edema. Some
patients may develop dry drowning as described earlier.
• Cardiovascular: Arrhythmias may occur secondary to hypothermia and
hypoxemia.
• Neurological: Hypoxemia and ischemia cause neuronal damage, which may
cause cerebral edema and raised intracranial pressure.
• Metabolic: A metabolic and/or respiratory acidosis is a common finding.
• Renal: Usually due to acute tubular necrosis resulting from hypoxemia, shock,
hemoglobinuria, or myoglobinuria.
• Other injuries and disorders that are associated with submersion injuries are
spinal cord injuries, hypothermia, panic, seizures and worsening of premorbid
conditions.
MANAGEMENT
• Maintain the airway. Remove regurgitated fluid or debris by suction. If the
patient is apneic or gag reflex is absent, ventilate with bag and mask and
proceed with early endotracheal intubation.
• Ensure adequate ventilation and correct hypoxia with supplemental oxygen.
• Keep the patient on continuous cardiac monitoring. Ventricular dysrhythmias
(ventricular tachycardia/ventricular fibrillation), bradycardia, and asystole
may occur as a result of acidosis and hypoxemia rather than electrolyte
imbalance.
CHAPTER 137: Drowning or Submersion Injuries 463
• If patient has a cardiac arrest, commence cardiopulmonary resuscitation.

Begin mouth to mouth assisted ventilation at the earliest, even before the
victim is extricated from the water. Manoeuvres such as Heimlich and
Patrick to remove water from the lungs are ineffective and increase the risk of
aspiration. As such, these manoeuvres are not recommended unless airway
occlusion by a foreign body is suspected.
• Remove all wet clothing. Check core body temperature and correct
hypothermia with with rapid core rewarming techniques (warmed IV fluid
infusion, warming adjuncts like blankets and other devices). Defibrillation will
not be effective unless hypothermia is corrected and core body temperature
is >30°C.
• Insert nasogastric tube to relieve gastric distension.
• Consider the possibility of alcohol or drug overdose.
• Prophylactic antibiotics (carbapenems/piperacillin-tazobactam) may be
warranted, if the incident occurred in contaminated water.
• Inhaled particles may have to be removed by bronchoscopy.
Remember that cervical spine trauma may be present in any victim of
shallow or rocky water immersion injury. Apply a cervical collar till C spine
injury is ruled out.
Alcohol-related
Emergencies 138
CHAPTER
ALCOHOL WITHDRAWAL
Alcohol withdrawal symptoms may occur with stopping alcohol consumption
or even with decreasing in the daily dose in chronic alcohol consumers. Genetic
predisposition may have a role in the fact that some patients develop much severe
withdrawal symptoms than others.
Minor withdrawal symptoms: Symptoms include insomnia, tremors, anxiety,
gastrointestinal upset, anorexia, headache, diaphoresis, palpitations, and occur
due to central nervous system (CNS) hyperactivity.
Withdrawal seizures: These are generalized tonic-clonic seizures that typically
occur within 12–48 hours after the last drink, but may occur after only 2 hours of
abstinence.
DELIRIUM TREMENS
• Occurs in some alcoholics who undergo withdrawal and carries significant
mortality.
• Symptoms of delirium tremens (DT) include hallucinations, disorientation,
agitation, hypertension, hyperthermia, tachycardia, and diaphoresis in the
setting of acute reduction or abstinence from alcohol.
• Delirium tremens usually manifests between 48 to 96 hours after the last drink
and symptoms may last up to 5 days.
• Death occurs from arrhythmias, infection, seizures, or cardiovascular collapse.
WERNICKE’S ENCEPHALOPATHY
This is an acute syndrome that occurs in chronic alcohol consumers who are
thiamine deficient. It is characterized by degenerative changes surrounding the
third ventricle, aqueduct, and mammillary bodies.
The classic triad of Wernicke’s encephalopathy (WE) includes:
• Encephalopathy: Profound disorientation, indifference, and inattentiveness
• Oculomotor dysfunction: Nystagmus, lateral rectus palsy, and conjugate gaze
palsies
• Gait ataxia: Ataxia typically affects the trunk and lower extremities.
CHAPTER 138: Alcohol-related Emergencies 465
KORSAKOFF’S PSYCHOSIS
This refers to a chronic neurologic condition that usually occurs as a consequence
of thiamine deficiency. Patients suffer from severe impairment of memory
(profound retrograde and anterograde amnesia) with relative preservation of
other intellectual abilities.
MANAGEMENT OF ALCOHOL WITHDRAWAL/WE/DT

• Rule out alternative diagnoses: Metabolic causes, infections, and CNS bleed.
• Supportive care: Intravenous (IV) fluids, nutritional supplementation, and
frequent clinical reassessment. Thiamine and glucose should be administered
in order to prevent or treat WE:
cc Parenteral thiamine 500 mg infused in 1 pint NS over 30 minutes. This can
be repeated three times daily. Alternatively, 1 ampoule of multivitamin

infusion can be added to dextrose normal saline in each subsequent
maintenance fluid.
cc The notion that thiamine must be given prior to dextrose to avoid
precipitating WE is largely unsupported.

cc In the ED, do not withhold administration of dextrose for hypoglycemia, if
thiamine is not available. However, do not forget to administer thiamine

at the earliest.
• Symptom control: Benzodiazepines are used to decrease psychomotor
agitation. IV lorazepam (2–4 mg IV every 15–20 min) or diazepam (5–10 mg
IV every 5–10 min) until the appropriate level of sedation is achieved. Oral
chlordiazepoxide (25–100 mg q1h) may also be given till agitation is controlled.
• Patients with severe withdrawal symptoms need admission.
• Patient with mild-to-moderate symptoms may be discharged after controlling
agitation on the following medications.
cc If no liver failure: Chlordiazepoxide 25 mg PO q6-8h for 5 days and taper.
cc In patients with chronic liver disease: Lorazepam 2 mg PO q8h for 5 days
and taper.
• Oral thiamine replacement (100 mg od) should continue along with
multivitamin supplementation for the next 6 months.
• Refer to psychiatry for further rehabilitation.
Sudden Visual Loss 139
CHAPTER
INTRODUCTION
• Acute transient visual loss is defined as a sudden onset of visual loss in one
or both eyes lasting less than 24 hours. It is caused by a transient vascular
occlusion in the circulation to the eye or visual cortex, or by neuronal
depression after a seizure or migraine.
cc Amaurosis fugax: Unilateral temporary loss of vision within a few seconds
to minutes. The cause is a small embolus to the retinal, ophthalmic or

ciliary artery and the patient describes it as “a curtain coming down”. There
is complete recovery.
• Acute persistent visual loss may be defined as visual loss lasting at least
24 hours and is typically not caused by transient ischemia. This can be divided
into three categories:
i. Media problems: Keratitis, corneal edema, hyphema, lens changes,
vitreous hemorrhage, and uveitis.
ii. Retina problems: Vascular occlusion, retinal detachment, and acute
maculopathy.
iii. Visual pathway problems: Optic nerve disease, chiasmal, and retro-
chiasmal visual pathway pathology.
COMMON CAUSES OF SUDDEN ONSET PERSISTENT

PAINLESS LOSS OF VISION
• Central retinal artery occlusion (CRAO):
cc Due to arterial emboli. There may be a history of amaurosis fugax
cc Look for atrial fibrillation (AF), murmurs or carotid bruit
cc Examination of the eye shows a sluggish or absent direct pupil reaction
and a normal consensual reaction (afferent pupillary defect)

cc Fundoscopy shows pale retina with swollen optic disk and “cherry red
macula spot”.
cc Treatment:
– Gentle digital massage for 5–15 seconds may dislodge the emboli.
– Acetazolamide 500 mg IV stat (to decrease intraocular pressure).
• Central retinal vein occlusion:
cc More frequent cause of painless visual loss than CRAO
cc Risk factors: Diabetes mellitus (DM), hypertension (HT), old age, chronic
glaucoma, and hyperviscosity syndromes

CHAPTER 139: Sudden Visual Loss 467
cc Examination shows decreased visual acuity and afferent pupillary defect

cc Fundoscopy shows a “stormy sunset appearance” (hyperemia, flame-
shaped hemorrhages)
cc Outcome is variable. There is no specific treatment refer to ophthalmology
to salvage the other eye.

• Temporal arteritis:
cc Seen in those aged more than 50 years and is associated with polymyalgia
rheumatica
cc Visual loss may be preceded by headaches, jaw claudication, malaise and
myalgia
cc Fundoscopy shows a pale disk
cc Pathology: Inflammation of the posterior ciliary artery causing optic
neuritis
cc If suspected, give 200 mg hydrocortisone IV stat.
• Vitreous hemorrhage:
cc Risk factors: DM, patients with bleeding disorders
cc Small bleeds may cause vitreous floaters with little visual loss, large bleeds
cause visual loss

cc Elevate the head end of the bed to allow blood to collect inferiorly.
• Retinal detachment:
cc Occurs in myopes, diabetics, post-trauma and in the elderly
cc Patients may report premonitory flashing lights or a “snow storm” before
developing clouding of vision

cc Retina is dark and opalescent but may be difficult to visualize by
fundoscopy.
• Optic neuritis:
cc Optic nerve inflammation causing visual loss occurs over a few days
Usually occurs in young women

cc Most recover untreated, some develop multiple sclerosis.
• Other causes: Methanol poisoning, quinine overdose, optic atrophy, and

cataract.
APPROACH TO A PATIENT WITH SUDDEN PAINLESS

LOSS OF VISION
• Consider ophthalmological pathology and refer to ophthalmologist, if any
obvious cause is found.
cc Examine: Visual acuity, pupillary reactions, eye movements, fundoscopy.
• Consider and rule out a central cause of blindness:

cc History of recurrent headaches (temporal arteritis), risk factors for an
occipital infarct (smoking, DM, HT, etc.), and history of substance abuse
(methanol poisoning).
cc Examination:
– Palpate temporal artery for tenderness (temporal arteritis)
– Look for any obvious source of emboli: AF, cardiac murmurs or carotid
bruit
– Look for cortical blindness (patient is aware of his/her blindness and
does not deny it) or
– Anton syndrome (patient is unaware of being blind and denies the
problem even when it is pointed out).
cc Investigations: CT brain or MRI brain and other routine tests.
cc Treatment:
– If an occipital infarct is found, give aspirin and statins
– If temporal arteritis is suspected, give steroids and refer to medicine
– If no obvious central cause is found refer the patient to ophthalmology.
Acute Red Eye 140
CHAPTER
INTRODUCTION
Acute red eye is a common presentation to the emergency department (ED). The
common causes include:
• Foreign body
• Conjunctivitis: Allergic, chemical, viral, or bacterial
• Subconjunctival hemorrhage
• Corneal ulceration
• Acute angle closure glaucoma
• Iritis, episcleritis, uveitis.
History
Ask for history of unilateral/bilateral involvement, trauma, visual changes,
amount and type of discharge, pain, photophobia, use of contact lens, and
presence of systemic disease.
Examination
• Assess vision and visual fields
• Evert the eyelids and inspect the undersurface
• Check pupil size and reflexes
• Examine the cornea, conjunctiva, and iris using a slit lamp, if available.
CHEMICAL OCULAR INJURY

Chemicals including acids and alkalis can cause severe ocular injury and requires
immediate intervention right at the site of the incident. These incidents typically
occur in industrial settings.
• Irrigate the eye with at least 2 L of normal saline (NS) or ringer lactate (RL).
Use an intravenous infusion line to direct a steady controlled flow of NS or RL
on to the ocular surface, for atleast 10–15 minutes.
• The goal of irrigation is to remove the offending chemical and restore
physiological pH. Monitor the pH using a litmus paper till the target of 7–7.4
is achieved.
• Continue irrigation with up to 8–10 L of NS or RL depending on the chemical
and till target pH is achieved.
• Topical cycloplegic (homatropine 5% or cyclopentolate) to alleviate ciliary
spasm.
• Topical erythromycin ointment 0.5% every 1–2 hours.
The clinical features and management of common causes of acute red eye is
shown in Table 1.
TABLE 1: Clinical features and management of acute red eye.

Etiology Clinical features Management
Conjunctival Feeling of foreign • Eye irrigation
foreign body body sensation • Evert the eyelid and use a sterile cotton bud to
remove the foreign body
Allergic Itching, watery • Remove inciting agent
conjunctivitis discharge, chemosis, • Artificial drops 5–6 times per day
history of allergy • Antihistamine (pheniramine) eye drops 4 times
daily
• Lubricant (hydroxypropyl methylcellulose) eye
drops 4 times daily in both eyes
• In severe cases: Steroid (fluorometholone) eye
drops 4 times daily
• Cold compress 4 times daily
Viral • Watery discharge, • Antihistamine (Pheniramine) eye drops 4 times
conjunctivitis chemosis, daily
conjunctival • Steroid (fluorometholone) eye drops 4 times daily
inflammation • Lubricant (hydroxypropyl methylcellulose) eye
• May have viral drops 4 times daily in both eyes
respiratory • Cold compress 4 times daily
symptoms
Bacterial Mucopurulent • Antibiotic eye drops: Chloramphenicol or
conjunctivitis discharge, lomefloxacin or ofloxacin or ciprofloxacin eye
eyelash matting, drops 4–6 times daily in both the eyes
conjunctival • Antibiotic ointment should be applied on the
inflammation lower fornix and smeared along the lids at bed
time. This prevents the eyelids from sticking
together
• Lubricant (hydroxypropyl methylcellulose) eye
drops 4 times daily in both eyes
Glaucoma Eye pain, headache, • Refer urgently to ophthalmology
(Acute angle cloudy vision, visual • Acetazolamide 500 mg PO stat
closure halos, vomiting, • Topical timolol 0.5%
glaucoma) conjunctival
• Topical pilocarpine 1% 1 drop q15 min for 2
injection, fixed mid-
doses
dilated pupil, corneal
clouding, raised • If intraocular pressure does not decrease and
intraocular pressure vision does not improve, start mannitol IV
100 mL IV stat
Dermatological
Emergencies 141
CHAPTER
URTICARIA
Urticaria (hives) is a common allergic cutaneous reaction characterized by
pruritic, erythematous fleeting wheals of various sizes. Angioedema is a similar
but more severe edematous reaction involving deeper dermis of the face, neck,
and extremities.
Management
• Identify and immediately remove the offending agent
• Antihistamines (Tablet levocetirizine 5–10 mg od × 3–5 days plus tablet
ranitidine 150 mg bd × 3–5 days) with or without steroids are the mainstay of
treatment
• Advice the patient to apply cold compresses and calamine lotion locally for
soothing effect
ERYTHEMA MULTIFORME
• This is an acute self-limited condition characterized by sudden appearance of
erythematous or violaceous macules, papules, vesicles, or bullae, distributed
in a symmetrical pattern on the palms, soles and back of the hands, arms, legs,
or feet.
• Characteristic skin lesions include “target lesions” with three zones of
color (a central dark papule or vesicle, surrounded by a pale zone and an
erythematous halo)
• Common precipitants include infections (mycoplasma, herpes simplex virus),
drugs (antibiotics, anticonvulsants), and malignancies.
• This condition may remain localized to the skin or may evolve into a multi-
system disease with mucosal involvement into Stevens–Johnson syndrome
(SJS), which could be fatal.
Management
• The most important step is identification and immediate discontinuation of
the offending agent
• Supportive care includes fluid and electrolyte replacement, maintenance of
thermal regulation, maximizing protein nutrition, meticulous wound care,
and aggressive infection control.
• Mild forms may resolve spontaneously in 2–3 weeks. Severe cases with
systemic involvement may require a short course of systemic steroids
(prednisolone 60–80 mg in divided doses for 3–5 days)
cc Blisters and bullous lesions may be treated with cool, wet soaks of 1:16,000
solution of KMnO4 or 5% aluminum acetate.

Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis

• Stevens–Johnson syndrome/Toxic epidermal necrolysis (TEN) represents
opposite ends of a spectrum of the same rare life-threatening mucocutaneous
reaction characterized by erythema, epidermal necrosis, and desquamation.
• The percentage of body surface area (BSA) affected determines whether the
reaction is classified as SJS or TEN. In SJS <10% BSA is involved, whereas
10–30% BSA is involved in SJS/TEN overlap and >30% BSA epidermal
detachment is seen in TEN.
• Common medications responsible for SJS/TEN are allopurinol, NSAIDs,
sulfonamide antibiotics, and anticonvulsants (phenytoin, phenobarbitone,
and carbamazepine).
• SJS/TEN usually occurs 1–3 weeks after starting the causative drug. Initial
manifestations are typically nonspecific. There may be a prodrome of fever,
malaise, sore throat, skin tenderness, followed by development of dusky
erythematous macules that may progress to flaccid blisters. Buccal, genital
and ocular mucosa are commonly involved. Epidermal detachment may
result in massive fluid loss and electrolyte imbalance, while severe ocular
involvement may result in permanent scarring and visual loss.
• Management:
cc The most important step is identification and immediate discontinuation
of the offending agent

cc Supportive care includes fluid and electrolyte replacement, maintenance
of thermal regulation, maximizing protein nutrition, meticulous wound

care, and aggressive infection control.
BULLOUS DISEASES
• Pemphigus vulgaris is a generalized, autoimmune, mucocutaneous eruption
common in the 40–60-year age group.
• The typical skin lesions are small, flaccid bullae that break easily forming
superficial erosions and crusted ulcerations, which heal slowly and are prone
to secondary infections.
• Nikolsky sign (easy dislodgment of the superficial epidermis from the dermal–
epidermal junction by a lateral shearing force) is a characteristic finding of
this condition
• Bullous pemphigoid is a generalized mucocutaneous blistering disease of
the elderly (average age: 70 years) with deeper blisters (below the epidermal
basement membrane), better prognosis and more rapid response to therapy
than pemphigus vulgaris.
• Management:
cc Local wound care and pain control are essential components of manage-
ment.
cc Refer to dermatology for initiation of steroid therapy or other immuno-
suppressants.
Needle-stick Injuries 142
CHAPTER
INTRODUCTION
Needle stick injuries refer to penetration of the skin by a sharp object, usually
hypodermic needles that has been in contact with blood, tissue or other body
fluids before the exposure. These injuries increase the risk of blood borne
infections and hence extreme caution must be exercised during venesection and
while performing major and minor surgical procedures.
Potentially Infectious Exposures

• A percutaneous injury (hollow needles are more infectious than solid needles)
• Contact of mucous membrane or nonintact skin.
The rate of transmission of HIV, HCV, and HBV through needle-stick injuries
(NSI) is 0.3%, 10%, and 30%, respectively.
Body Fluids of Concern

• Body fluids definitely proven to be infective: Blood, semen, and vaginal
secretions.
• Potentially infectious fluids of undetermined risk: Cerebrospinal fluid, synovial,
pleural, peritoneal, pericardial, and amniotic fluids.
• Fluids that are NOT considered infectious: Tears, saliva, nasal secretions,
gastric secretions, sweat, urine, vomitus, and feces.
When to Test for HIV after Exposure?

With or without prophylaxis, testing must be done at baseline, 6 weeks, 3 months,
and 6 months.
POSTEXPOSURE PROPHYLAXIS: GENERAL MEASURES

• Needle-stick injuries: Wash for 10 minutes with soap and water. Small wounds
and punctures can be washed with alcohol (alcohol is virucidal to HIV,
hepatitis B virus, and hepatitis C virus).
• Mucosal exposure: If eye is involved, irrigate with 500 mL of running NS over
10 minutes with the eye being held open by another person.
PROTOCOL FOR PEP FOR HIV

• Healthcare worker with percutaneous, mucous membrane or non-intact skin
exposure to body fluids of concern from a known HIV patient: Follow post
exposure prophylaxis (PEP) as shown in Table 1.
TABLE 1: Categorization of exposure and recommended prophylaxis.

Exposure Features Recommended PEP
Low risk Solid needles, superficial wound, Tenofovir 300 mg + Emtricitabine
and low-risk source 200 mg × 4 weeks
Mucocutaneous Small volume Same as low-risk PEP
High risk Hollow needle, device with visible Tenofovir 300 mg + Emtricitabine
blood, needle from artery or 200 mg + (Lopinavir 400 mg +
vein of the source and high-risk Ritonavir 100 mg) × 4 weeks
patient
(PEP: postexposure prophylaxis)
• Healthcare worker with exposure from a source with unknown HIV status. The
source should be tested for HIV and PEP can be stopped if the test is negative
unless the source is suspected to have acute HIV infection.
• Contamination from an unknown source.
PEP for HIV should be started as soon as possible. Those who started PEP
should complete a full 4-week course of the drugs.
PROTOCOL FOR PEP FOR HEPATITIS B

After exposure to hepatitis B virus, timely prophylaxis can prevent acute infection
and development of chronic complications. The mainstay of prophylaxis against
hepatitis B is the hepatitis B vaccine and in certain situations, hepatitis B immune
globulin for added protection.
Infants born to HBV-positive mothers should be given hepatitis B vaccine and
hepatitis B immunoglobulin within 12 hours of birth.
The protocol for PEP for hepatitis B is shown in Table 2.
• If the patient presents after 72 hours, administer only hepatitis B virus vaccine
(0, 1, and 2 months).
• Check hepatitis B surface antigen status after 6 months and 12 months.
PROTOCOL FOR PEP FOR HEPATITIS C

• Hepatitis C is a major infectious cause of cirrhosis and is associated with high
morbidity and mortality.
• Wash the affected area thoroughly (refer general measures for PEP).
• Though many directly acting anti-HCV antiviral (DAA) regimens are currently
available, there is insufficient evidence to recommend them as PEP.
• Immunoglobulin is not effective.
CHAPTER 142: Needle-stick Injuries 475
TABLE 2: Protocol for PEP for hepatitis B (when presenting within 72 hours of exposure).
Exposed person Exposure source
HBsAg positive HBsAg negative Status unknown
Unvaccinated Administer HBIG Initiate the HBV Initiate the HBV vaccine
0.06 mL/kg vaccine
intramuscularly and
initiate the HBV vaccine
Vaccinated Check anti HBs titer, if No PEP Check anti-HBs titer, if
available: recommended available:
• >100 million IU: No • >100 million IU: No
therapy therapy
• 10–100 million IU: • 10–100 million IU:
Administer 1 dose of Administer 1 dose of
HBV vaccine HBV vaccine
• <10 million IU: • <10 million IU: Give 1
Administer HBIG + 1 dose of HBV vaccine
dose of HBV vaccine
(HBsAg: hepatitis B surface antigen; HBIG: hepatitis B immune globulin; HBV: hepatitis B virus; PEP:
postexposure prophylaxis)
Drugs in Pregnancy 143 CHAPTER
SAFETY RATING OF DRUGS IN PREGNANCY AND

LACTATION (TABLE 1)
• Category A: Controlled studies in women did not show any risk to the fetus in
the first trimester or later. Drugs can be used freely in pregnant and lactating
mothers.
• Category B: Animal reproduction studies have not demonstrated a fetal risk
but there are no controlled studies in pregnant women. Drugs can be used
freely in pregnant and lactating mothers.
• Category C: Animal studies revealed adverse effects on the fetus. There are
no controlled studies among women. Drugs can be administered only if the
potential benefit justifies the potential harm to the fetus.
• Category D: Evidence of human fetal risk has been demonstrated. However,
benefit to the mother from usage in pregnancy significantly outweighs the risk
to the fetus. To be used only in life-threatening situations.
• Category X: Studies in humans and animals have demonstrated fetal
abnormalities and the risks clearly outweigh any possible benefits. These
drugs are contraindicated in women who are or may become pregnant.
TABLE 1: List of drugs and their safety during pregnancy.

Pregnancy Lactation
Antibiotics
Amoxicillin, ampicillin, penicillin Yes (A) Yes
Augmentin (amoxicillin + clavulanate) Yes (A) Yes
Azithromycin Yes (B) Yes
Ceftriaxone, cephalexin, cefazolin, Yes (A) Yes
ceftazidime
Metronidazole Yes (B) Yes
Clindamycin Yes (A) Yes
Acyclovir, valacyclovir Yes (B) Yes
Amikacin Avoid (D) Yes
Ciprofloxacin, levofloxacin Avoid (B) Yes
Piperacillin-Tazobactam Yes (B) Avoid
Continued
CHAPTER 143: Drugs in Pregnancy 477
Continued
Pregnancy Lactation
Ertapenem, imipenem, meropenem Yes (B) Yes
Trimethoprim/sulfamethoxazole Avoid (C) Yes
Doxycycline Avoid (D) No
Albendazole Avoid (D) No
Linezolid Yes (B) Caution
Rifampicin Yes (C) Yes
Chloroquine Yes (D). Do not Yes
withhold in malaria
Artemether No data. Do not Yes
withhold in malaria
Antacids
Ranitidine, omeprazole, pantoprazole Yes (A) Yes
Antiemetics
Doxylamine, metoclopramide, Yes (A) Yes
ondansetron, promethazine
(phenergan)
Antihistamines/nasal decongestants
Chlorpheniramine (Avil), Yes (A) Yes
diphenhydramine (Benadryl),
fexofenadine (Allegra)
Cetirizine, loratadine Yes (B) Yes
Oxymetazoline, phenylephrine Avoid (D) Avoid
Antiepileptics
Phenytoin, phenobarbitone Yes (D) Yes
Sodium valproate Avoid Avoid
Carbamazepine Yes (D) Yes
Levetiracetam, clobazam Yes (B) Yes
Antihypertensives
Amlodipine, nifedipine Yes (C) Yes
Diltiazem, verapamil Yes (C) Yes
Enalapril, losartan Avoid (D) Yes
Hydrochlorothiazide Yes (C) Avoid
Metoprolol, atenolol, propranolol Yes (C) Yes
Prazosin Yes (B) Yes
Continued
Continued
Pregnancy Lactation
Others
Warfarin Avoid (D) Yes
Statins No (C) Avoid
Enoxaparin Yes (C) Yes
Gabapentin Yes (B) Yes
Methotrexate Avoid (D) Avoid
Ibuprofen, naproxen, diclofenac Yes (C) Yes
Ketamine Yes (B) Avoid
Acute Arthritis 144CHAPTER
ACUTE MONOARTHRITIS
Presentation
Acute monoarthritis presents as a hot, swollen red joint, joint line tenderness,
decreased range of movements, and systemic symptoms (fever and malaise).
Examination
Look for evidence of a multisystem disease (rash, ocular involvement, orogenital
ulcers, and gastrointestinal symptoms).
Causes
• Traumatic: Fracture and hemarthrosis (hemophilia)
• Infective: Septic arthritis
• Crystal arthropathy: Uric acid (gout), calcium pyrophosphate (pseudogout),
and hydroxyapatite.
Synovial fluid analysis: This is done to confirm the diagnosis. Send the aspirate
for:
• Synovial fluid white blood cells (WBC)
• Synovial fluid gram smear and culture (if frank pus aspirated)
• Polarized microscopy for crystals.
SEPTIC ARTHRITIS
It is due to direct invasion of joint space by various microorganisms. Common
pathogens are Staphylococcus aureus, Neisseria gonorrhoeae, Streptococcus and
gram-negative bacteria. Most septic joints have a synovial fluid WBC count more
than 50,000/μL, with more than 75% neutrophils.
Management
• Strict bed rest. No weight bearing on the joint
• Administer adequate analgesia [opioids and nonsteroidal anti-inflammatory
drugs (NSAIDs)]
• Antibiotics: (Injection cefazolin 1 g IV stat or injection cloxacillin 1 g IV stat).
Continue for 2–4 weeks
• Refer to Orthopedics.
GOUT
Gout refers to deposition of monosodium urate (MSU) crystals in joints, most
commonly the great toe, tarsal bones, ankles, knees. Though hyperuricemia
is associated, diagnosis can only be confirmed from aspiration of strongly
birefringent needle shaped MSU crystals from the inflamed joints or tophi.
• Prompt administration of analgesics is helpful. NSAIDs are the first choice.
• Tablet colchicine is an alternative for acute episodes. Give 1 mg initially
followed by 0.5 mg every 4 hours until pain is relieved or vomiting or diarrhea
occurs.
• Intra-articular steroid injections may be given to those who cannot take
NSAIDs or colchicine.
• Systemic steroids (prednisolone 20–40 mg) for 1–2 days may be given in severe
cases.
• Allopurinol and probenecid are not useful for acute attacks of gout.
ACUTE POLYARTHRITIS
Polyarthritis that resolves within 6 weeks is generally associated with viral
infections. If symptoms last >6 weeks, it is classified as chronic polyarthritis
and warrants a detailed evaluation. Common causes are rheumatoid arthritis,
seronegative arthritis (psoriatic arthropathy, ankylosing spondylitis, enteropathic
arthritis, and reactive arthritis), systemic lupus erythematosus, crystal
arthropathy, and infections.
REACTIVE ARTHRITIS (REITER SYNDROME)

It comprises a triad of:
• Seronegative arthritis
• Nonspecific urethritis
• Conjunctivitis.
It has been associated with:
• Gastrointestinal infections, caused by Shigella, Salmonella, Yersinia,
Campylobacter, and others
• Genitourinary infections, caused by Chlamydia trachomatis.
The arthritis begins about 2 weeks after infection and the lower limb joints are
most commonly affected. Joint involvement is usually asymmetrical and resolves
over months. NSAIDs are the mainstay of therapy.
Procedural Sedation 145
CHAPTER
INTRODUCTION
• Procedural sedation involves the use of short-acting analgesic and sedatives
to perform procedures effectively, while monitoring for potential adverse
effects.
• Propofol, benzodiazepines (midazolam), etomidate, ketamine, fentanyl, and
ketofol (ketamine + propofol) are usually used.
KETAMINE
It provides sedation, analgesia, and amnesia.
Dissociative anesthesia: Acts by causing dissociation between the thalamocortical
and limbic systems. It provides analgesia and amnesia without loss of
consciousness.
Contraindications:
• Raised intracranial pressure (ICP)
• Severe systemic hypertension
• Raised intraocular pressure
• History of seizures or psychosis
Onset of action is 1–2 minutes and duration of action is 10–20 minutes.
Dose:
• Usual induction dose is 1–2 mg/kg over 1–2 minutes
• Doses of 0.25–0.5 mg/kg may be repeated every 5–10 minutes thereafter.
Side effects: Tachycardia, hypertension, laryngospasm, emergence reactions
(disorientation, hallucinations, nightmares), hypersalivation, nausea, and vomiting.
• Glycopyrrolate (5 µg/kg) or atropine (0.5–1 mg) may be given for hyper-
salivation.
• Midazolam 1–2 mg may be used for treating or preventing emergence
reactions.
• Laryngospasm: If a patient develops laryngospasm, attempt to break
it by applying a painful inward and anterior pressure at the “Larson’s
point”/“laryngospasm notch”, which is located near the top of the ramus of
the mandible (Fig. 1). Also consider deepening the sedation with a low dose
of propofol to reduce laryngospasm.
FIG. 1: Larson’s point/laryngospasm notch.
MIDAZOLAM
Midazolam is a short acting benzodiazepine that provides anxiolysis and amnesia.
No analgesia.
Dose:
• 0.02–0.03 mg/kg slow intravenous (IV) bolus
• Repeat doses may be given every 2–5 minutes as necessary
• Maximum single dose is 2.5 mg and maximum cumulative dose is 5 mg.
• Onset of action is 1–2 minutes and duration of action is 30–60 minutes.
Side effects: Respiratory depression and hypotension. Action reversed by flumazenil.
FENTANYL
It is a synthetic short-acting opioid that has 75–125 times the potency of morphine.
It provides analgesia. No amnesia or anxiolysis.
• Onset of action is 1–2 minutes and duration of action is 30–60 minutes.
Dose:
• 0.5–1 µg/kg slow IV push every 2 minutes, until an appropriate level of sedation
and analgesia is achieved
• The maximum total dose is 5 µg/kg or approximately 250 µg.
Side effects: Respiratory depression and hypotension (rare). Naloxone may be
used to reverse respiratory depression.
Section 22
Procedures
Nerve Blocks 146
CHAPTER
INTRODUCTION
Nerve blocks should be administered to all patients requiring emergency
procedures such as debridement, dressing, fracture reduction, and wound wash
with or without procedural sedation. Digital nerve block, wrist block, and ankle
block are the most commonly administered blocks and do not require ultrasound
guidance.
• The choice of the local anesthetic (LA) depends on the desired duration of
the block. 2% lignocaine is used for shorter duration of blockade, while 0.5%
bupivacaine is used for longer blockade (Table 1).
• Ensure IV access, monitoring, and full resuscitation facilities are available
prior to the procedure, due to possibility of anaphylaxis/systemic toxicity.
TABLE 1: Characteristics of local anesthetics.

Local anesthetic Onset of action Anesthesia (hours) Analgesia (hours)
(minutes)
2% lignocaine 10–20 2–5 3–8
0.5% bupivacaine 15–30 5–15 6–30
DIGITAL NERVE BLOCK (FINGER WEB SPACE BLOCK)

This is administered for conditions like finger or toe lacerations, nail bed injuries,
paronychia drainage, and nail avulsion.
Contraindications
• Infection at the site of block
• Allergy to the anesthetic agent
• Compromised digit circulation.
Techniques (Fig. 1)
• Prepare the area with chlorhexidine solution
• Place the hand flat with palmar side down on a sterile drape.
• Inject 2 mL of 2% lignocaine or 0.5% bupivacaine into the subcutaneous tissue
of web space at the base of finger just distal to metacarpophalangeal joint
using a 26-G hypodermic needle
486 SECTION 22: Procedures
FIG. 1: Web space block.
• Withdraw the needle completely and repeat the procedure on the web space
of the opposite side of the finger.
Precautions
• Avoid using an anesthetic with adrenaline for webspace blocks
• Aspirate before injecting the drug to rule out intravascular injection
• Avoid injecting directly into the nerves.
WRIST BLOCK
A wrist block is a procedure by which the terminal branches of the ulnar nerve,
median nerve, and radial nerve are blocked separately by administering an LA.
Indications
Surgeries of the hand and finger, carpal tunnel.
Contraindications
• Infection at the site of block
• Allergy to the drug.
Radial Nerve Block

Anatomy
Radial nerve emerges between the brachioradialis tendon and the radius just
proximal to the styloid process and becomes superficial to supply the dorsum
of hand. Because the radial nerve has a less predictable anatomic location and
divides into multiple smaller cutaneous branches, a more extensive infiltration
is required.
CHAPTER 146: Nerve Blocks 487
FIG. 2: Radial nerve block.
Procedure (Fig. 2)
• Position: With the patient supine or sitting, keep the arm abducted, fore arm
pronated, and wrist in slight dorsiflexion.
• Insert a 26-G needle just proximal to the styloid process of the radius in the
anatomical snuff box and aim medially
• After negative aspiration, inject about 3 mL of 2% lignocaine
• After that, direct the needle laterally and inject an additional 3 mL of LA
subcutaneously in a fan-shaped manner.
Median Nerve Block

Anatomy
Median nerve is located in the flexor retinaculum between tendons of palmaris
longus and flexor carpi radialis. The palmaris longus can be identified by asking
the patient to oppose the thumb and the little finger.
Procedure (Fig. 3)
• Insert a 26-G needle between the tendons of palmaris longus and flexor carpi
radialis until it hits the bone.
• Withdraw the needle slightly and inject about 3–5 mL of LA after ruling out
intravascular injection by negative aspiration.
Ulnar Nerve Block

Anatomy
The ulnar nerve runs between the ulnar artery and the flexor carpi ulnaris tendon
(the most medial tendon palpable).
Procedure (Fig. 3)
• Insert a 26-G needle under the flexor carpi ulnaris tendon and advance about
5–10 mm laterally
• After negative aspiration, inject about 3 mL of LA.
The cutaneous nerve supply of the hand is shown in Figure 4.
FIG. 3: Median and ulnar nerve blocks.
FIG. 4: Cutaneous nerve supply of the hand.
ANKLE BLOCK
The ankle block is used for surgery of the foot and toes and is a purely sensory
block. It consists of separate blocks of five nerves (Figs. 5 to 7):
1. Four branches of the sciatic nerve
i. Superficial peroneal (fibular) nerve
ii. Deep peroneal (fibular) nerve
iii. Tibial nerve
iv. Sural nerve
2. One cutaneous branch of the femoral nerve
i. Saphenous nerve.
FIG. 5: Cutaneous nerve supply of the foot.
FIG. 6: Axial view showing the plane of the nerves at the

level of the ankle.
Positioning
Position the patient supine, with the foot elevated and supported on blankets or
pillows, and the ankle is rotated as necessary for needle placement.
Deep Peroneal Nerve Block

• Palpate the dorsalis pedis artery between the tendons of extensor hallucis
longus and extensor digitorum longus. Extensor hallucis tendon can be
identified by having the patient extend the great toe.
FIG. 7: Nerves around the ankle and ankle block injection sites.
• At the mid-tarsal portion of the foot, insert the needle just lateral to the
extensor hallucis tendon and advance until bone is encountered.
• Inject 2–3 mL of LA in the deep plane as the needle is slowly withdrawn.
Superficial Peroneal Nerve Block

• The superficial peroneal nerve innervates the dorsum of the foot and is
blocked by subcutaneous infiltration of LA.
• Insert the needle at the injection site for deep peroneal nerve block.
• Inject about of 5–10 mL of LA subcutaneously over the dorsum of the foot
medially and then laterally from the site of needle insertion to the level of the
malleoli.
Posterior Tibial Nerve Block

• The distal tibial nerve provides sensation to the calcaneus and plantar surface
(sole) of the foot and is blocked at the level of the medial malleolus
• Palpate the posterior tibial artery behind the medial malleolus
• Insert the needle posterior to the artery, and advance until the bone is reached
while aiming toward the malleolus at a 45 degree angle
• After negative aspiration, inject 2–3 mL of LA
• To increase the success rate of the block, inject an additional 1–2 mL of LA
using a fan technique, medially and laterally.
Sural Nerve Block

• The sural nerve innervates the lateral ankle and foot, as well as the fifth toe. It
runs within the subcutaneous tissues behind the lateral malleolus
• Insert the needle subcutaneously just behind the lateral malleolus
• Inject 2–3 mL of LA behind the lateral malleolus directed toward the Achilles
tendon as a subcutaneous wheal.
Saphenous Nerve Block

• The saphenous nerve innervates the medial aspect of the ankle and foot. It is
blocked at the ankle using anatomic landmarks
• Insert the needle medial and superior to the medial malleolus and direct it
posteriorly toward the Achilles tendon
• After negative aspiration, inject 2–3 mL of LA as a subcutaneous wheal.
Deep peroneal nerve and posterior tibial nerves lie deep and need to be injected deep
for nerve block.
Superficial peroneal nerve, sural nerve and saphenous nerve lie superficially and need
to be injected subcutaneously for nerve block.
SYSTEMIC TOXICITY OF LOCAL ANESTHETICS

(BUPIVACAINE/LIGNOCAINE)
While generally safe, local anesthetic agents can be toxic. The toxicity of local and
infiltration anesthetics can be local or systemic. Systemic toxicity of anesthetics
most often involves the central nervous system (CNS) or the cardiovascular
system (CVS). Manifestations of local anesthetic toxicity typically appear
1–5 minutes after the injection, but onset may range from 30 seconds to as long
as 60 minutes.
• CNS manifestations: Systemic toxicity begins with symptoms of CNS
excitement (circumoral and/or tongue numbness, metallic taste,
lightheadedness, dizziness, muscle twitching, convulsions, etc.) followed by
CNS depression (unconsciousness, coma, respiratory depression, and arrest)
• Cardiovascular manifestations: Chest pain, shortness of breath, palpitations,
diaphoresis, hypotension, syncope
• Hematologic manifestations: Methemoglobinemia (benzocaine, lidocaine,
prilocaine, etc.)
• Allergic manifestations: Rash, urticaria, anaphylaxis (very rare), etc.
Management of Systemic Toxicity

Treatment of local anesthetic toxicity includes the following:
• Stop injecting more local anesthetic
• Stabilize airway
• Seizure suppression: Benzodiazepines/barbiturates for seizures

• Management of cardiac dysrhythmias: Look for prolonged PR, QRS, and QT
intervals potentiating reentrant tachycardias with aberrant conduction,
which may herald CVS toxicity. Follow advanced cardiac life support (ACLS)
guidelines for management of arrhythmias.
• Use Amiodarone as first line drug for arrhythmias in usual doses.
• Lipid emulsion therapy: Cardiac resuscitation may be difficult and prolonged
(>30 min) because some anesthetics are very lipid soluble and require a
long time for redistribution. Lipid emulsion therapy is performed with an
intravenous (IV) infusion of a 20% solution.
cc Administer a bolus of 1.5 mL/kg over 1 minute. (If patient >70 kg then give
a maximum dose of 100 mL IV bolus)

cc Then convert to an infusion at a rate of 0.25 mL/kg/min for 30–60 minutes
or until hemodynamic stability is restored

cc After that, the infusion should be continued for at least 10 minutes longer.
cc Repeat the bolus dose and double the rate of infusion in case of persistent
or recurrent cardiovascular collapse.

cc Maximum dose of lipid emulsion: 12 mL/kg
• Treatment of allergic reactions: Antihistamines or epinephrine as needed.

Central Venous Access 147
CHAPTER
SUBCLAVIAN LINE
• It is associated with the lowest rate of thrombosis.
• Position a sheet roll between the shoulder blades and keep the head down.
• If the patient is on a chest tube, insert the line on the same side.
• Site of insertion of the needle: 2 cm inferior to the junction of the middle and
medial third of the clavicle.
• Advance the needle under and along the inferior border of the clavicle toward
the suprasternal notch until the vein is entered.
• Fix the line at 14 cm for females and 16 cm for males.
• Postprocedure X-ray check is mandatory and should be followed up by the
person inserting the central line.
INTERNAL JUGULAR LINE

• Place the patient in Trendelenburg position with the head down.
• Site of insertion of the needle: Locate the apex of the triangle formed by the
sternal and clavicular heads of the sternocleidomastoid (SCM) muscle and
the clavicle. The internal jugular vein (IJV) lies 1 cm lateral to the internal
carotid artery.
• Insert the needle at the apex of this triangle, lateral to the carotid pulsation
and directed toward the ipsilateral nipple at an angle of 30–45 degree to the
skin.
• The IJV should be reached no deeper than 2.5 cm.
• Ensure good dilatation of the SCM before inserting the central venous catheter.
• Postprocedure X-ray check is mandatory and should be followed up by the
person inserting the central line.
FEMORAL LINE
• Consider this in a patient with bleeding risk, and bleeding parameters not
available. It is the safest site to start a central line.
• This is also the route of choice for an inexperienced person in an emergency
• The point of insertion is 1 cm below the inguinal ligament and 1 cm medial to
the pulsating femoral artery.
• Drawback of a femoral approach is an increased incidence of venous
thrombosis.
Technique of Insertion of a Central Line

• Seldinger technique is used for placement of the central venous catheter.
• Clean and drape the site of catheter insertion. Identify the target vessel and
anesthetize the site with lignocaine by creating a subcutaneous wheal.
• Connect a wide bore introducer needle in the central venous set to a 5 cc
disposable syringe. Insert the needle at the anesthetized site and advance
gradually with negative pressure on the syringe to aspirate venous blood.
Disconnect the syringe once there is free flow of venous blood and occlude
the needle hub to avoid air being drawn by the negative intrathoracic pressure.
• Then, insert the blunt tipped guidewire through the introducer needle and
remove the introducer needle while holding the guidewire in place.
• Enlarge the insertion site with a stab using 11-size blade or using a dilator.
Thread the dilator over the guidewire while holding the guidewire in place
during insertion and removal of the dilator.
• Then thread the central venous catheter over the guidewire while withdrawing
the guidewire until it protrudes from the infusion port of the catheter. Hold
the guidewire firmly and place the catheter at the desired depth. Remove the
guidewire.
• Aspirate and confirm free flow of blood from all lumens, secure the catheter
with appropriate sutures.
SURGICAL PEARLS
• Wear appropriate PPE including mask, cap, gown, and gloves.
• Make sure that all the required equipment is in place, sterile area secured,
towels clamped, all lines flushed and guidewire ready for access before
starting the procedure.
• Anesthetize the suture site as well as the insertion site.
• Watch out for ectopic beats on the monitor while inserting guidewire during
IJV and subclavian cannulation, readjust guidewire to prevent arrhythmias.
• Look out for a return of red pulsatile blood, which indicates that the needle is
in an artery. Remove the needle immediately and apply firm pressure for at
least 2 minutes or longer, if required to prevent hematoma formation.
Chest Tube Insertion 148
CHAPTER
REQUIREMENT
• 1% or 2% lidocaine with epinephrine
• Syringes and needle for local
• Blade No. 10 or No. 11
• Large and medium Kelly clamps
• Large straight suture scissors
• Chest tube of appropriate size
cc Adult male: 28–32F
cc Adult female: 24–28F
cc Child: 12–28F
cc Infant: 12–16F
cc Neonate: 10–12F.
• Silk or nylon suture, 0 or 1-0 needle holder

• Chest tube drainage device with water seal.
• Personal protective equipment (PPE)
• Sterile drapes, sponges, gauze and elastic tape.
PROCEDURE
• The arm on the affected side should be abducted and externally rotated,
simulating a position in which the palm of the hand is behind the patient’s
head.
• Identify “safe triangle” formed (Fig. 1):
cc Anteriorly by the lateral border of the pectoralis major
cc Laterally by the lateral border of the latissimus dorsi
cc Inferiorly by the line of the fifth intercostal space
cc Superiorly by the base of the axilla.
• Make a 1-cm skin incision in between the midaxillary and anterior axillary
lines over the lower rib in the fifth intercostal space.
• Direct the drain track over the top of the lower rib to avoid the intercostal
vessels lying below each rib. The incision should easily accommodate the
operator’s finger.
• Using a curved clamp, deepen the track by blunt dissection only. Insert the
clamp into muscle tissue and spread to split the fibers. The track should be
developed with the operator’s finger.
• Once the track comes onto the rib, angle the clamp just over the rib and
continue dissection until the pleura is entered by puncturing it.
FIG. 1: Site of chest tube insertion (safe triangle).
• Insert a finger into the pleural cavity and explore the area for pleural adhesions.
• Mount the appropriate size chest tube on the clamp and pass it along the
track into the pleural cavity. Direct the tube superiorly for pneumothorax and
inferiorly for pleural effusion/hemothorax.
• Connect the tube to an underwater seal and suture or secure it in place.
• Reexamine the chest to confirm effect.
• Perform a chest X-ray (CXR) to confirm the placement and position.
COMPLICATIONS
• Improper placement: Make sure that all the holes in the chest tube are inside
the pleural cavity. Subcutaneous position of the holes may cause subcutane-
ous emphysema.
• Bleeding: Local bleeding usually responds to direct pressure. Intercostal artery
injury might require thoracotomy.
• Hemoperitoneum (liver or spleen injury): This may require urgent laparotomy.
• Tube dislodgement.
• Infection: Local (site of insertion) or empyema.
Intraosseous Line 149
CHAPTER
INTRODUCTION
An intraosseous (IO) line is as effective as an intravenous (IV) route for emergency
drugs and fluid administration. It can be inserted much faster than a peripheral
line in patients in shock or cardiac arrest in whom IV access may be difficult.
Fluids and drugs should be administered under pressure using a syringe and
stopcock manually, using pressure bag or infusion pumps
PROCEDURE
• Palpate the tibial tuberosity. Locate one finger’s breadth below and medial to
the tuberosity. (The bone can be felt under the skin at this site).
• Clean the skin over and surrounding the site with an antiseptic solution.
• Stabilize the proximal tibia with the left hand by grasping the thigh and knee
above and lateral to the cannulation site, with the fingers and thumb wrapped
around the knee but not directly behind the insertion site (Fig. 1).
• Insert the needle at a 90-degree angle with the bevel pointing toward the foot.
Advance the needle using a gentle but firm, twisting, or drilling motion.
• Stop advancing the needle when you feel a sudden decrease in resistance.
• Aspirate 1 mL of the marrow contents (looks like blood); using a 5 mL syringe,
to confirm that the needle is in the marrow cavity.
FIG. 1: Intraosseous needle insertion.

• Attach a 5 mL syringe filled with normal saline. Stabilize the needle and slowly
inject 3 mL while palpating the area for any leakage under the skin. If no such
infiltration is seen, start the infusion.
• Apply dressings and secure the needle in its place.
Note: IO infusions should not continue for >24 hours. It is usually removed within 8 hours
once a central venous access is established.
COMPLICATIONS
• Incomplete penetration of the bony cortex: This happens if the needle is not
well fixed; infiltration occurs under the skin. Push in the needle further to
overcome this problem.
• Penetration of the posterior bone cortex (more common): Suspect this if
infiltration occurs (calf becomes tense), with the needle well fixed. Remove
the needle and repeat at another site. This problem may be avoided by placing
the index finger against the skin to prevent the needle from going in too deeply.
• Blockage of the needle by marrow: Suspect this if the infusion stops. The line
must then be flushed by 5 mL of normal saline.
• Infection: This is rare if the infusion is left for less than 24 hours, osteomyelitis
is very rare. Cellulitis may be seen at the site of the infusion. Remove the IO
needle unless it is essential; give local skin care and antibiotic treatment.
• Necrosis and sloughing of the skin at the site of the infusion: This occurs
particularly when drugs such as adrenaline or sodium bicarbonate pass into
the tissues. Avoid by infusing gently and not under pressure.
Cricothyroidotomy 150CHAPTER
INTRODUCTION
Cricothyroidotomy is performed as a last resort in cases of airway compromise
where intubation is impossible. This procedure is easier and quicker to perform
than tracheostomy, does not require manipulation of the cervical spine, and is
associated with fewer complications.
INDICATIONS
• Facial and oropharyngeal swelling from severe trauma, or due to inhalational
burns
• Angioneurotic edema
• Foreign body obstruction
• Facial, oropharyngeal, and laryngeal edema from anaphylaxis (insect bites,
bee stings, drugs, etc.)
• Infection (epiglottitis).
ANATOMY OF THE CRICOTHYROID MEMBRANE

The cricothyroid membrane, as the name suggests, is bounded by the cricoid
cartilage inferiorly and the thyroid cartilage superiorly. The key anatomic land-
marks are hyoid cartilage, thyroid cartilage, cricothyroid membrane, cricoid
cartilage, and the tracheal rings.
• In adults, the laryngeal prominence at the upper border of the thyroid cartilage
is easily felt. The thyroid cartilage can then be followed inferiorly to locate the
cricothyroid membrane.
• In children, the laryngeal prominence is not developed, making it difficult to
identify the thyroid cartilage. Instead, it is easier to follow the tracheal rings
superiorly to locate the prominence of the cricoid cartilage.
The cricothyroid arteries and veins usually overlie the apical portion of the
membrane and proceed from the sides, anastomosing in the midline. Hence,
cricothyroidotomy should be performed in the central, lower portion of the
membrane.
NEEDLE CRICOTHYROIDOTOMY (FIG. 1)

This is a temporary measure, to be adapted when surgical cricothyroidotomy
cannot be performed due to lack of equipment or experience. It may be
performed on patients of any age but is considered to be preferable to surgical
FIG. 1: Needle cricothyroidotomy.
cricothyroidotomy in children up to 12 years of age because of less potential

damage to the larynx and surrounding structures. It is important to remember
that effective ventilation cannot be established by this maneuver, since it provides
very limited airflow.
Equipment: 12G or 14G intravenous (IV) cannula, 2 mL syringe.
• Fix a 2 mL syringe with 1 mL of saline or water for injection in it, on the end of
the wide bore IV cannula.
• Identify the cricothyroid membrane
• Introduce the cannula through the cricothyroid membrane at 90 degree with
the needle pointing inferiorly.
• Aspirate gently as the cannula is introduced. Bubbles of air escape through the
saline in the syringe.
• Advance the cannula forward off the needle until its hub is at the skin surface
and then remove the needle.
• Take the plunger out of the 2 mL syringe and then force the oxygen tubing
down the end of the barrel of the 2 mL syringe and connect to the oxygen
source.
• The patient can be adequately oxygenated for about 45 minutes. Because
of inadequate exhalation, there will be progressive accumulation of carbon
dioxide.
• Establish more definite airway.
SURGICAL CRICOTHYROIDOTOMY (FIG. 2)

Equipment needed: Scalpel with no. 10 blade, bougie and cuffed tracheostomy
tube size 6.
CHAPTER 150: Cricothyroidotomy 501
FIG. 2: Surgical cricothyroidotomy.
• Stand on right side of the patient if you are right-handed. Stabilize the larynx
with the left hand by using thumb and middle finger over the thyroid cartilage.
Identify the cricothyroid membrane by palpation using the index finger.
• Make a 4 cm vertical incision over the skin in the midline at the level of the
membrane and use blunt dissection till the membrane. Make a horizontal
stab in the membrane using the blade and rotate the blade by 90-degree
(sharp end caudally) to create a stoma.
• Use blade to stent the opening and insert the bougie. Direct the bougie
caudally and feel for tracheal clicks or resistance if the carina is reached to
confirm position into the trachea. Avoid forcing the bougie.
• Insert the tracheostomy tube or size 6 endotracheal tube over the bougie into
the trachea and remove the bougie
Complications of surgical cricothyroidotomy:
• Bleeding
• Placement of the tube anterior to the trachea in the subcutaneous plane
resulting in a subcutaneous emphysema.
Pericardiocentesis 151
CHAPTER
INTRODUCTION
Pericardiocentesis is the aspiration of fluid from the pericardial space that
surrounds the heart. In case of tamponade, even a small amount of fluid aspirated
can cause a significant improvement to the hemodynamic status of the patient.
The classic Becks triad of cardiac tamponade includes distended neck veins,
muffled heart sounds, and hypotension. Most patients will have at least one of
these signs; all three rarely appear simultaneously.
INDICATIONS
• Emergency pericardiocentesis: Suspected cardiac tamponade with life-
threatening hemodynamic changes.
• Nonemergency pericardiocentesis: For diagnostic, palliative, or prophylactic
reasons, performed under ultrasonography.
TECHNIQUE (FIG. 1)
• Subcostal (subxiphoid) approach
cc Prepare the skin by applying a chlorhexidine-based solution to the chest
and upper abdomen and drape the region to maintain sterility

cc Anesthetize the puncture site and needle track in alert patients via
infiltration of local anesthetic
FIG. 1: Pericardiocentesis (subxiphoid approach).

CHAPTER 151: Pericardiocentesis 503
cc Introduce the needle substernally 1 cm inferior to the left xiphocostal angle

cc Aim the needle toward the left shoulder at an angle of 30–45 degree to the
chest wall and advance it slowly while continuously aspirating
cc If no fluid is aspirated, the needle should be withdrawn promptly and
redirected. In the absence of ultrasound guidance, withdraw the needle to

the skin and redirect it along a deeper posterior trajectory
cc In most cases, a 7–9 cm needle is adequate, but longer needles (up to
12 cm) may be needed for obese patients

cc When you strike blood, withdraw the stylet and leave the cannula behind
cc Observe for improvement in hemodynamic status. If cardiac tamponade is
present, there is instant relief even with aspiration of 10 mL of blood.

• Parasternal approach: Insert the needle perpendicular to the skin and over
the cephalad border of the fifth or sixth rib immediately adjacent to the sternal
margin.
• Apical approach: Insertion site is at least 5 cm lateral to the parasternal
approach within the 5th, 6th, or 7th intercostal space. Advance the needle
over the cephalad border of the rib and towards the patient’s right shoulder.
There is a higher risk of pneumothorax with this approach.
COMPLICATIONS
• Cardiac dysrhythmia
• Cardiac puncture
• Pneumothorax
• Hemothorax
• Coronary vessel injury
• Left internal mammary artery injury
• Peritoneal puncture, liver or stomach injury, diaphragmatic injury (with the
subxiphoid approach).
Pleural Tap 152CHAPTER
PROCEDURE
Site: Insert the needle midway between the spine and posterior axillary line in the
6th, 7th or 8th intercostal space based on fluid level, based on percussion. Direct
the needle above the upper border of lower rib to avoid injury to neurovascular
bundle that lies on the lower border.
• Routine: Pleural fluid TC, DC, protein, sugar, lactate dehydrogenase (LDH), etc.
• Other tests in specific situations: pH, triglycerides (chylothorax), amylase
(pancreatic effusion), cytology, routine culture, acid-fast bacillus (AFB) culture, etc.
Send serum protein (liver function test, LFT) and LDH along with other blood
investigations.
INTERPRETING THE PLEURAL FLUID ANALYSIS:

LIGHT’S CRITERIA
If any one of the following is present, the fluid is an exudate:
• Pleural fluid protein/serum protein >0.5
• Pleural fluid LDH/serum LDH >0.6
• Pleural fluid LDH >2/3 of the upper limit of normal serum range.
Note: This misclassifies 25% of transudates. If there is a mismatch between clinical
and laboratory parameters, look at serum-pleural fluid protein and albumin
gradient. If protein gradient is >3.1 g% or albumin gradient is >1.2 g% it indicates
transudative fluid.
If the pleural fluid is hemorrhagic, consider malignancy or pulmonary
embolism, tuberculosis, traumatic or catamenial.
If the pleural fluid is grossly hemorrhagic look at the pleural fluid hematocrit (Hct)
Pleural fluid Hct >50% of blood Hct suggests a hemothorax (refer to thoracic surgery).
Ascitic Tap (Paracentesis) 153
CHAPTER
INTRODUCTION
Paracentesis is a procedure in which a needle or catheter is inserted into the
peritoneal cavity to obtain ascitic fluid for diagnostic or therapeutic purposes.
INDICATIONS
• Diagnostic tap
cc New onset ascites to determine etiology, to differentiate portal hyper-
tension versus other pathologies and to detect the presence of malignant

cells
cc Suspected spontaneous or secondary bacterial peritonitis.
• Therapeutic tap
cc Respiratory compromise secondary to ascites
cc Abdominal pain or pressure secondary to ascites (tense ascites).
TECHNIQUE
Site of insertion of the needle: Right or left lower quadrant of abdomen. Two finger
breadth above and medial to anterior superior iliac spine (ASIS). Left lower
quadrant is preferred due to thinner abdominal wall and avoidance of cecum or
appendicectomy scar as on right.
Insert the needle in an angle or using Z track technique (traction on skin
during initial needle insertion) to create a displaced track which will help prevent
leakage of fluid after procedure.
Note: Avoid scars on abdomen as bowel may be tethered. Avoid needle introduction
medial to rectus muscle to prevent bleeding from injury to inferior epigastric artery.
THERAPEUTIC PARACENTESIS
There is no volume limit for paracentesis under monitoring. For practical purposes,
remove 500 mL to 2 L of ascitic fluid, if indicated. If large volume is removed, give
normal saline (NS) or albumin to replace intravascular volume loss.
Routine tests
• Ascitic fluid TC, DC: Neutrophil count ≥250 cells/mm3 suggests spontaneous
bacterial peritonitis (SBP).
• Ascitic fluid culture: In bactec medium (blood culture bottle)
• Ascitic fluid albumin: Send concomitant serum albumin to determine the
serum ascites albumin gradient (SAAG)
cc SAAG >1.1 suggests portal hypertension as the etiology [chronic liver
disease (CLD), Budd-Chiari syndrome, etc.]

cc SAAG <1.1 suggests peritoneal pathologies as the etiology [tuberculosis
(TB), malignancy, pancreatitis, etc.].
OTHER TESTS DONE IN SPECIFIC SITUATIONS

• Ascitic fluid lipase: Elevated in pancreatitis.
• Ascitic fluid acid-fast bacilli (AFB) culture: If TB abdomen is suspected. Collect
sample in a culture tube.
• Ascitic fluid cytology for malignant cells: Collect sample in a cytology bottle
and send to the laboratory immediately for centrifugation and processing.
• Ascitic fluid creatinine: When a “urinoma” is suspected. A urinoma is
a collection of extravasated urine in the peritoneal cavity or it may be
encapsulated. Usually seen after a blunt trauma to the abdomen or after a
laparotomy, if the ureter is injured.
Ascites: Serum creatinine ratio of >1.0 is suggestive of intraperitoneal urinary
leak/urinoma.
• Ascitic fluid triglyceride: Chylous ascites has triglyceride content more than
200 mg/dL.
Section 23
Protocols
Intubation Protocol 154 CHAPTER
INTRODUCTION
• Rapid sequence intubation (RSI) is the standard of care in emergency airway
management for intubations not anticipated to be difficult
• Rapid sequence intubation is the virtually simultaneous administration of
a sedative and a neuromuscular blocking agent to render a patient rapidly
unconscious and flaccid in order to facilitate urgent endotracheal intubation
and to minimize the risk of aspiration.
RAPID SEQUENCE INTUBATION PROTOCOL (TABLE 1)

• Midazolam and fentanyl can cause hypotension and hence should be avoided
in hemodynamically unstable patients.
• Succinylcholine induces rapid, complete, and predictable paralysis with
spontaneous recovery in about 5 minutes. However, in certain situations,
it causes potassium release from the muscles and can cause dangerous
hyperkalemia, especially in patients with extensive burns and soft tissue
injuries.
• Succinylcholine is contraindicated in patients with hyperkalemia. Avoid
succinylcholine/check K before intubation in patients with the following
conditions:
cc Known case of chronic kidney disease
cc Extensive burns (can be given if patient presents within 24 hours of
incident)
cc Patients with spinal shock presenting 24 hours after the incident.
• If succinylcholine is absolutely contraindicated in hemodynamically unstable

patients, a small dose of midazolam (2 mg) can be given during RSI.
TABLE 1: Rapid sequence intubation protocol.

Hemodynamically stable Hemodynamically unstable
• Preoxygenate with 100% oxygen • Preoxygenate with 100% oxygen
• Midazolam 5 mg (0.1 mg/kg) • Ketamine 100 mg (1–2 mg/kg)
• Fentanyl 100 µg (2 μg/kg) • Succinylcholine 100 mg (2 mg/kg)
• Succinylcholine 100 mg (2 mg/kg) • Wait for 60 s, then intubate
• Wait for 60 s, then intubate
510 SECTION 23: Protocols
Difficult Airway
For all intubations in the ED, be prepared for a difficult airway and seek help
when needed. Refer Chapter 6 for Assessment of Airway.
• Plan A: Direct/video laryngoscopy
• Plan B: Bag and mask ventilation with/without viral filter /LMA
• Plan C: Surgery–cricothyroidotomy
Postintubation Checklist
• Confirm position by 5-point auscultation
• Check ETCO2 and wave form capnography
• Check the cuff pressure (optimal range: 20-30 cm H2O)
• Optimize ventilator settings
• Check blood pressure
• Monitor SpO2
END-TIDAL CARBON DIOXIDE (ETCO2)

The ETCO2 measured by wave form capnography indicates the concentration
of CO2 at the end of expiration ('end-tidal'). Normal value is 35–45 mm Hg and
correlates closely with PaCO2.
Uses:
• Confirms tracheal placement of endo-tracheal tube
• Is a dynamic marker for chest compressions during CPR of intubated patients
(should be >10 mm Hg)
• Is a reliable indicator of ROSC (>40 mm Hg)
Flat ETCO2 trace: Esophageal intubation, ventilator disconnection, cardiac arrest.
Increased ETCO2: Fever, increased cardiac output, increased BP, hypoventilation,
bronchial intubation.
Decreased ETCO2: Hypothermia, reduced cardiac output, hypotension,
hyperventilation, pulmonary embolism, cardiac arrest.
Investigations Protocol 155CHAPTER
Basic investigations to be sent by emergency department (ED) registrars for

common conditions are shown in Table 1.
TABLE 1: Basic investigations to be sent by emergency department (ED) registrars for

common conditions.
General medicine
Acute febrile CBC, electrolytes, creatinine, LFT, If dysuria: Urinalysis, urine c/s
illness blood c/s × 2, malarial parasite If neck stiffness/altered
sensorium: CT brain
If cough/breathlessness: CXR
Poisonings CBC, electrolytes, creatinine, LFT, Organophosphorous/unknown
ECG, CXR (if cough/breathlessness/ poison: Pseudocholinesterase
risk of aspiration) Drug overdose: If known drug,
phenytoin, phenobarbitone,
valproate, paracetamol levels If
fever/aspiration: Blood c/s
Gastroenterology
Acute CBC, electrolytes, creatinine, LFT, If fever: Blood c/s
pancreatitis amylase, lipase, CXR, ECG If chest pain/ECG changes: Trop
USG abdomen if LFT abnormal T
UGI bleed CBC, electrolytes, creatinine, LFT,
rapid BBVS, CXR, ECG, PT, aPTT
DCLD with CBC, electrolytes, creatinine, LFT,
suspected SBP CXR, ECG, rapid BBVS (if not done
before)
Ascitic fluid TC, DC, c/s (protein and
albumin if new case), PT, aPTT
Corrosive CBC, electrolytes, creatinine, LFT, ENT consult for airway
poisoning ECG, rapid BBVS, PT, aPTT to be sent assessment
CXR, X-ray neck soft tissue AP/
lateral
Continued
Continued
Neurology
CVA/TIA CBC, electrolytes, creatinine, ECG, CXR
CT brain (Plain)/MRI stroke protocol
(<4.5 h)
Seizures CBC, electrolytes, creatinine, CT
brain (plain), CXR
Surgery
Abdominal pain CBC, electrolytes, creatinine, LFT Suspected ureteric colic: Urea,
urinalysis, urine c/s, X-ray KUB,
USG abdomen
Suspected ovarian torsion: USG
abdomen
Suspected DU perforation: CXR
erect, X-ray abdomen supine
Suspected pancreatitis:
Amylase, lipase
If chest pain: ECG, Trop T
If fever: Blood c/s
Cellulitis/ CBC, electrolytes, creatinine, blood Consider X-ray of the limb,
necrotizing c/s D-dimer
fasciitis If surgery required: CXR, ECG,
PT, aPTT, rapid BBVS
Others
COPD/asthma CBC, electrolytes, creatinine, ECG, CXR If fever: Blood c/s
exacerbation ABG (priority 1 and 2 patients) If chest pain/ECG changes: Trop T
Febrile CBC, electrolytes, creatinine, LFT,
neutropenia blood c/s, MP, CXR, urinalysis
CKD CBC, electrolytes, creatinine, urea, If dialysis required: PT, aPTT,
urinalysis, ABG, ECG, CXR rapid BBVS (if not done before)
Suspected MI/ CBC, electrolytes, creatinine, Trop T, If abdominal pain: Amylase,
ACS ECG, CXR lipase
(UGI: upper gastrointestinal; CBC: complete blood count; LFT: liver function test; CT: computed
tomography; CXR: chest X-ray; ECG: electrocardiogram; ABG: arterial blood gases; USG: ultrasonography;
BBVS: blood borne virus screen; PT: prothrombin time; aPTT: activated partial thromboplastin time;
DCLD: decompensated chronic liver disease; SBP: spontaneous bacterial peritonitis; TC: total count;
DC: differential count; AP: anteroposterior; ENT: ear, nose, and throat; CVA: cerebrovascular accident;
MRI: magnetic resonance imaging; KUB: kidneys, ureters, bladder; DU: duodenal ulcer; COPD: chronic
obstructive pulmonary disease; CKD: chronic kidney disease; MI: myocardial infarction; ACS: acute
coronary syndrome).
Pain Protocol in the
Emergency Department 156
CHAPTER
SCALE TO ASSESS SEVERITY OF PAIN

• Verbal numeric rating scale (VNRS): 0–10.
• No pain-0. Worst pain-10.
The universal pain assessment tool is illustrated in Figure 1. Use the tool to
assess pain score at admission and 30 minutes after administration of analgesics.
Target pain score <4.
TIME TO ASSESS PAIN

• At the time of initial presentation to emergency department (ED) or respective
bays or at acute change of character of pain.
• Every 30 minute after intravenous (IV) analgesic till target score is achieved.
• Then every 1 hour for 4 hours.
Analgesics
Be generous with administration of analgesics to trauma victims.
• IV morphine:
cc 0.1 mg/kg bolus.
cc 0.05 mg/kg every 30 minutes for a maximum of 3 doses.
cc Avoid in traumatic brain injury, biliary colic, and history of allergy.
cc Watch for sedation, decrease in respiratory rate, hypotension, and
vomiting.
• IV fentanyl:
cc 1–2 µg/kg bolus
cc 1 µg/kg every 30 minutes for a maximum of 3 doses.
FIG. 1: Universal pain assessment tool.

ccAvoid in traumatic brain injury, biliary colic, and history of allergy.

ccWatch for: sedation, decrease in respiratory rate, and vomiting.
• IV tramadol:
cc 2–3 mg/kg bolus (maximum 150 mg)
cc Avoid in patients on antidepressants or with history of seizures, biliary
colic, and history of allergy.

cc Watch for: Seizures and vomiting.
• IV paracetamol:
cc Use in all patients without renal and hepatic injury.
cc 15–20 mg/kg bolus in 100 mL normal saline (NS).
cc Dose to be repeated every 6 hours (without hepatic injury).
• IV ketamine:
cc Use for procedural analgesia with midazolam.
cc 0.5–1 mg/kg bolus.
• Local anesthetic (lignocaine) infiltration:

cc To be used for all procedures.
cc 1–60 mL (0.5–1% solution).
Always administer an antiemetic (ondansetron) along with any opioid.
Discharge Plan for Pain Relief

• For adults: Oral tramadol (50 mg) + paracetamol (500 mg) combination three
times/day (if no contraindication to any of the drugs).
• If creatinine is normal, give a 3–5 day course of NSAIDs.
Polytrauma/Trauma
Team Activation Protocol 157
CHAPTER
INTRODUCTION
Patients with polytrauma need urgent attention by many people (ED physician,
paramedics, nurses, and the specialty registrars) in order to perform primary and
secondary surveys and resuscitate at the same time. Hence, a polytrauma team
should be activated through the telephone exchange.
Criteria to activate polytrauma team:
• Unexplained shock
• More than one system involvement
• Mass casualty incident, i.e., more than 10 patients with significant injuries
from the same accident.
MEMBERS OF THE TRAUMA TEAM

• Senior registrars of general surgery, orthopedics, neurosurgery (trauma),
radiology
• Duty radiographer
• Trauma coordinator (TC) of the ED
• Duty consultant of ED
• Duty chaplain
TRAUMA TEAM CALL OUT PROCEDURE

• Call telephone exchange (2,500) and say, “please activate the trauma team”.
• The telephone exchange will activate trauma team members by a priority call.
• The team members should report to the resuscitation room (RR) of ED
immediately in person. If they do not arrive within 20 minutes, the head of the
respective departments should be contacted.
Subspecialty consultation, i.e., thoracic surgery, plastic surgery, ENT,
urology, etc., should be subsequently carried out by the TC, if necessary.
• All trauma victims below the age of 15 years should be assessed by the pediatric
surgery team.
• If there is a delay or uncertainty in assuming primary responsibility by the
clinical units, the ED on call consultant will decide the primary unit and admit
the patient under that unit in the concerned ward/intensive care unit (ICU).
This decision of the ED consultant is final and binding.
ROLE OF TRAUMA COORDINATOR

• The TC should take control of the situation and coordinate the trauma team
in resuscitation.
• Documentation regarding progress in resuscitation and MLC should be done
by the TC.
• The first two units of blood should be arranged. Call blood bank duty doctor
and arrange crossmatched blood or Onegative blood, if patient is in shock.
• If necessary, the TC should activate massive transfusion protocol. (Refer
Chapter 106)
Prophylactic Antibiotic
Protocol for Trauma Patients in
the Emergency Department 158
CHAPTER
INTRODUCTION
It is important to administer appropriate prophylactic antibiotic protocol for
trauma patients in the emergency department. Table 1 gives the prophylactic
antibiotics protocol for trauma victims used in Christian Medical College (CMC),
Vellore.
TABLE 1: Prophylactic antibiotics protocol for trauma patients in the Emergency

department (ED).
Trauma sites Antibiotics
1. Scalp 1a. Abrasion Neosporin/Fusidic acid local application
1b. Laceration (clean) Daily cleaning and dressing, if needed
1c. Laceration Capsule cloxacillin 500 mg q6h × 3 days
(contaminated) or
Capsule cephalexin 500 mg q6h × 3 days
+
Tablet metronidazole 400 mg tid × 3 days
(only if severely contaminated)
1d. Laceration with Injection cloxacillin 1 g IV stat and q6h
underlying fracture of or
skull bones Injection cefazolin 1 g IV stat and q8h
or
Injection cefuroxime 1.5 g stat and q8h
+
Injection metronidazole 500 mg IV stat and
q8h (only if severely contaminated)
If discharged from ED:
Capsule cloxacillin 500 mg q6h × 3 days
or
+
Continued
Continued
2. Face 2a. Abrasion Neosporin/Fusidic acid local application
2b. Superficial laceration Capsule cloxacillin 500 mg q6h × 3 days
(involves epidermis, or
dermis, and fascia) Capsule cephalexin 500 mg q6h × 3 days
2c. Superficial laceration Capsule cloxacillin 500 mg qid × 3 days
involving dangerous area
of face
2d. Superficial laceration Capsule cloxacillin 500 mg qid × 3 days
involving dangerous +
area of face + intraoral Tablet metronidazole 400 mg tid × 3 days
laceration
2e. Deep laceration (involves Injection cloxacillin 1 g IV stat and q6h
epidermis, dermis fascia, or
and muscle) Injection cefazolin 1g IV stat and q8h
or
+
2f. Deep laceration with Injection cloxacillin 1 g IV stat and q6h
facial bone fractures or
Injection cefazolin 1 g IV stat and q6h
or
+
or
+
Continued
CHAPTER 158: Prophylactic Antibiotic Protocol for Trauma Patients... 519
Continued

2g. Deep laceration + facial Injection cloxacillin 500 mg IV stat and q6h
bone fractures + intraoral or
extension Injection cefazolin 1 g IV stat and q6h
or
+
q8h
or
+
3. Thorax, 3a. Abrasion Neosporin/Fusidic acid L/A
abdomen, 3b. Superficial laceration Capsule cloxacillin 500 mg q6h × 3 days
back, and (involves epidermis, or
pelvis dermis, and fascia) Capsule cephalexin 500 mg q6h × 3 days
3c. Deep laceration (involves Injection cloxacillin 1 g IV stat and q6h
epidermis, dermis, fascia, or
and muscle) Injection cefazolin 1 g IV stat and q6h
or
+
or
+
3d. Penetrating injuries (stab Injection piperacillin-tazobactam 4.5 g IV
entering parietal pleura stat and q8h
or peritoneum)
Continued
Continued

4. Animal/ 4a. Human bite Tablet augmentin 625 mg tid × 3–5 days
human 4b. Dog/cat/rat bite Tablet augmentin 625 mg tid × 3–5 days
bites
4c. Bull gore injury Injection piperacillin-tazobactam 4.5 g IV
(penetrating) stat and q8h
5. Appendi- 5a. Abrasion Neosporin/Fusidic acid local application
cular 5b. Superficial laceration Capsule cloxacillin 500 mg q6h × 3 days
injuries (involves epidermis, or
Without dermis, and fascia)
fractures Capsule cephalexin 500 mg q6h × 3 days
5c. Deep laceration (involves Injection cloxacillin 500 mg IV stat and q6h
epidermis, dermis, fascia, or
muscle, and tendon) Injection cefazolin 1g IV stat and q8h
or
+
or
+
Appendicular 5d. No or minimal Injection cloxacillin 500 mg IV stat and q6h
injuries with contamination or
fractures Injection cefazolin 1 g IV stat and q8h
or
5e. Heavily contaminated Injection cefuroxime 1.5 g stat and q8h
wound +
q8h
or
Injection piperacillin-tazobactam 4.5 g IV
stat and q8h
Index
Page numbers followed by f refer to figure, fc refer to flowchart, and t refer to table.
A Acute pancreatitis 227, 511

etiology of 227
Abdomen 519 modified Atlanta grading of severity
examination of 343 of 227t
ultrasonography of 96, 321 Acute red eye 469
Abruptio placenta 282, 386 causes of 470
Abscess 314 management of 470t
intra-abdominal 72 Acute respiratory distress syndrome 80
peritonsillar 298 Acyclovir 73, 426, 476
pilonidal 332 Adenomyosis 275
retropharyngeal 297 Adenosine 165, 426
Absolute neutrophil count 240 Adenovirus 93
Absorbable suture materials 380 Adrenal disease, primary 264
Acetaminophen 111 Adrenal insufficiency 263
overdose 111 causes 263
Acid-base clinical features 263
abnormalities 64 diagnosis 264
disturbances 59, 66fc management 264
Acid-fast bacillus 504 primary 263
Acidosis 16, 56, 267 secondary 263
metabolic 64, 80 Adrenaline 16-18, 33, 38, 426, 432
respiratory 45, 64 infusion 36
severe metabolic 268 nebulized 417
Acinetobacter 240 Adrogue–Madias formula 55
Activated charcoal 110, 426 Advanced cardiac life support 3
contraindications for 110 Aedes aegypti viral infection 75
multidose 110 Agitation 113
Activated partial thromboplastin time Air under diaphragm 316f, 362
99, 233, 336, 347, 512 Airway 3, 88, 111, 183, 191, 202, 392,
Acute angle closure glaucoma 470 406, 446, 447
Acute asthma 414 assessment of 40
classification of 180 management 40, 127, 388
management of 180, 415 maneuvers 5
Acute coronary syndrome 22, 147, 154, oropharyngeal 7, 8f
512 Albendazole 71, 426, 477
spectrum of 147fc Albumin 255
Acute exacerbation 45, 182 Alcohol 227
management of 183 withdrawal 464
Acute obstructive valve thrombus 170 management of 465
522 Index
Alkaline phosphatase 234 Ankle 399, 490f

levels, causes of 321 block 488, 490f
Alkalosis 56 level of 489f
acute respiratory 59 Ankylosing spondylitis 41, 480
metabolic 64, 232 Ankylostoma 71
respiratory 64 Anorectal abscess 332
Allergic reaction 255 location of 333f
mild 256 types of 332
treatment of 492 Anorectal emergencies 331
Allis technique 376, 376f Anorexia 317
Alloimmunization 274 Antacids 477
Alpha plus beta-blocker 155 Anterior dislocation
Aluminum 122 reduction of 357f
phosphide 121 temporomandibular joint 357f
Amantadine 456 Anterior glenohumeral dislocation 370
Amaurosis fugax 466 types of 370f
Amenorrhea, history of 273 Anterior hip dislocation 374, 375
American Heart Association 3 Epstein classification of 375f
Amikacin 106, 426, 476 Antibiotic 30, 103-106, 184, 191, 279,
Aminoglycosides 62 291, 306, 423, 425, 460, 476
Aminophylline 427 doses 103
Amiodarone 16, 161, 426 empiric 83, 89
Amlodipine 114, 477 protocol 71
Amoxicillin 73, 74, 83, 103, 291, 297, therapy 38, 81, 326
427, 476 indications for 230
Amphetamine 62, 135 Anticoagulants 88, 121, 247
Ampicillin 103, 427, 476 parenteral 248
Amyl nitrite 142 Antidotes 111t, 124, 134
Amylase 228 Antiemetic agents 455
Anal fissure 331 Antiepileptics 204, 413t, 477
Analgesia 379 drugs, doses of 210t
Analgesics 279, 513 Anti-fibrinolytic activity 204, 285
Anaphylactic reaction, severe 256 Antigen-based rapid diagnostic tests 80
Anaphylaxis 29 Antihistamines 30, 477
diagnosis of 29t Antihypertensives 196
management of 30 Antimalarial therapy 81
Androgens 263 Antimicrobial spectrum 103, 103t, 104,
Anemia 237 105, 106
cause of 237t, 238t Antiphospholipid syndrome 252
evaluation of 239fc Antipsychotics, atypical 455
microangiopathic hemolytic 250 Antisnake venom 30, 128, 129
pernicious 239 Antithrombin 255
severe 80, 245 deficiency 252
Anesthesia, dissociative 481 Anton syndrome 468
Angina Anxiolysis 482
pectoris 147 Aortic aneurysm, abdominal 334
unstable 147, 153t Aortic dissection 191, 334
Angiography, interventional 192 Apathy 60, 62
Index 523
Aplastic crisis 245 Attacks

Apnea 47 acute 213
Appendages, torsion of 304 mild-to-moderate 213
Appendicitis 281, 301, 317, 318, 319t moderate-to-severe 214
Appendicular injuries 520 Attitude 377
Areflexia 205 Augmentin 476
Arm 396 Automated external defibrillator 4, 5, 13
Arrhythmia 32, 33, 165 Aviator fracture 400
Artemesinin combination therapy 81 Avomine 296
Artemether 477 Azathioprine 227
Arterial blood gas 39, 46, 65, 84, 87, 325 Azithromycin 71, 73, 74, 105, 279, 306,
Arteriovenous malformation 191, 214 427, 476
Arteritis, temporal 215, 467, 468 Azotemia 84
Arthritis 41
acute 479 B
enteropathic 480
reactive 480 Bacillary dysentery 71
septic 73, 314, 479 Bacillus cereus 93, 94
Ascaris 71, 227 Backfire fracture 397
Ascites 506 Bacteremia 240
Ascitic fluid Bacteria 424
acid-fast bacilli culture 506 Bacteriology 233
creatinine 506 Bacteriuria, asymptomatic 96
cytology 506 Bacteroides 297, 298
lipase 506 Bag-mask ventilation 8
triglyceride 506 Balloon mitral valvotomy 170
Ascitic tap 505 Bankart fracture 396
indications 505 Barbiturates 113
technique 505 Baricitinib 89
Asthma 179, 179t Barton fracture 396
acute 180, 414 Baseball finger 398
bronchial 179 Basic life support 1, 3, 10, 10fc, 11, 14
life-threatening 180 steps of 4t
mild 414t Battle’s sign 348
moderate 414t Bee and wasp stings 132
refractory 181 Bell’s palsy 216
severe 414t differential diagnosis for 216
AstraZeneca 89 Bennett fracture 397
Ataxia 198, 205 Benzathine penicillin 73, 427
Atenolol 477 Benzocaine 491
Atrial fibrillation 159, 163, 164, 168 Benzodiazepines 111, 113, 131, 218,
Atrial flutter 162, 162f, 162t 456, 465, 481
Atrioventricular nodal reentrant Benztropine 218
tachycardia 164 Bernard–Soulier syndrome 250
Atropine 16-19, 111, 117, 427 Beta-blocker 113, 155, 260
Atropinization targets 117 Betahistine 296
524 Index
Bile acid sequestrants 260 Bradypnea 125

Bile duct, common 233, 234 Brain
Bilevel positive airway pressure 45, 46 abscess 98
Biliary system, bacterial infection of 233 computed tomography of 200, 201,
Biphasic defibrillator 12, 13 213
Bisphosphonates 59, 61 function, abnormalities in 98
Bites 74, 520 injury, traumatic 348
Bladder 512 magnetic resonance imaging of 213
rupture 362 Break-dancer’s thumb 398
Bleeding Breast
disorder 250 abscess 338
gastrointestinal 225, 232 disorders 338
intracranial 202 tissue 338
normal regulation of 250 acute inflammation of 338
per vagina 275 Breathing 3, 88, 111, 183, 191, 202, 389,
etiology of 275 392, 406, 446, 447
postpartum 284 Breathlessness 84, 86
Blockade, shorter duration of 485 Bromocriptine 456
Blood Bronchiectasis 45, 190
ammonia concentration 232 Bronchiolitis 420
borne virus screen 233, 280, 318, 365, Bronchitis
512 acute 73
components 255 chronic 183
culture 233 Bronchodilators 31
loss 225, 345t Bronchoscopy 191
pressure 36, 76, 155, 161 Bronchospasm 134
control 204 Brudzinski’s sign 99
diastolic 34, 154, 389, 446 Brugada sign 175f
systolic 23, 34, 36, 38, 389, 393, 407, Brugada syndrome 175
446 Bullous diseases 472
products 255, 277 Bumper fracture 399
transfusion 30, 255, 284 Bungarus caeruleus 128t
complications of 255 Bupivacaine 485, 491
protocols 226 Burns 32, 41, 459
urea nitrogen 54, 87 depth of 459t
Body fluids 473 full-thickness 459
Bone 60, 353 management of 460
cortex, posterior 498 partial thickness 459
Bony cortex 498 percentage of 459t
Bosworth fracture 399 superficial 459
Botulism 206 Buscopan 302
Bowel perforation 72
Boxer’s fracture 398 C
Bradyarrhythmias 14, 33
management of 18 Cairo–Bishop definition 243
Bradycardia 20fc, 124, 125 Calcium 59, 228
rhythms 17t channel blockers 114
symptomatic 14, 19t gluconate 427
Index 525
Campylobacter jejuni 94, 205 Central retinal

Canadian C-spine rules 351 artery occlusion 466
Canakinumab 89 vein occlusion 466
Candida 240, 314 Central venous
Cannabis 134 access 493
Carbamates 111, 118, 120 pressure 393
Carbamazepine 210, 215, 477 Cephalexin 72, 313, 338, 428, 476, 517,
Carbapenems 463 520
Carbon monoxide poisoning 140 Cerebra thevetia 124
Carcinoma, bronchogenic 190 Cerebral blood 199
Cardiac arrest 15fc, 23, 47 Cerebral edema 204
management of 1, 14 high-altitude 158
maternal 23, 24fc Cerebral function 98
Cardiac diseases 191 Cerebral infarction 245
Cardiac dysrhythmias, management of Cerebral venous thrombosis 199, 200f,
492 213
Cardiac tamponade 359, 360 Cerebrospinal fluid 204
Cardiomyopathy, restrictive 32 analysis 79, 99, 206
Cardiovascular system 29 Cerebrovascular accidents 195
Cardioversion 11 Cervical spine 350
Carotid injuries 350
massage 165 radiological evaluation of 351
pulse check 5f trauma 463
Cartilage 353 X-ray
Casts 378 interpretation of 352
Catabolism 243 normal 353f
Cetirizine 477
Catecholamine-secreting tumors 270
CHADSVasc score 161t
Cedell fracture 400
Chance fracture 401
Cefalexin 104
Charcot’s triad 233
Cefazolin 73, 104, 313, 428, 476, 479,
Chauffeur fracture 397
517, 518
Chest
Cefixime 104, 428
compressions 3, 5
Cefoperazone 72, 103, 428 technique of 6f, 11, 11f
Cefotaxime 428 computed tomography of 86, 192
Ceftazidime 104, 428, 476 crisis 245
Ceftriaxone 71, 73, 74, 99, 104, 279, 291, pain 125
428, 476 active ischemic 16, 21
Cefuroxime 72, 73, 104, 428, 517, 518, trauma 390
520 tube insertion 495
Cells, shift out of 57 site of 496f
Cellulitis 72, 313 wall injuries 392
investigations 313 X-ray 84, 86, 87, 154, 187, 188, 228,
management 313 233, 335, 336
Centipede bite 132 Chickenpox 73
Central nervous system 117, 134, 451 Chlamydia
dysfunction 259 pneumonia 82, 245
infection 98, 100fc, 412 trachomatis 279, 480
526 Index
Chloramphenicol 71, 428 Colonic malignancies 333

Chlordiazepoxide 465 Coma 53, 62
Chlorinated hydrocarbon 118 Combustion, gas products of 140
Chloroquine 81, 477 Common drug overdose, specific
Chlorpheniramine 477 management of 113t
Chlorpromazine 218, 455 Common medicolegal case, list of 441
Cholangiography, percutaneous Common thoracic injuries
transhepatic 234 clinical features of 358t
Cholangitis 72, 233 management of 358t
Cholecystitis 72, 278, 320 Compartment syndrome 383
acalculous 320 causes of 383
Cholelithiasis 278 Complete blood count 78, 84, 87, 209,
Cholera 71 228, 229, 231, 233, 244, 336, 512
Cholesteatoma 216 Computed tomography 86, 154, 192,
Cholinesterase reactivator 118 200, 201, 209, 213
Chopart fracture 399 pulmonary angiography 187
Chronic obstructive pulmonary disease Confusion 38, 53, 60
44, 155, 179, 183, 188, 512 Congestion, pharyngeal 84
Chvostek’s sign 60 Conjunctivitis 469
Chylothorax 504 allergic 470
Cinnarizine 296 bacterial 470
Ciprofloxacin 71, 105, 428, 476 viral 470
Circulation 111, 183, 191, 202, 388, 389, Consciousness, level of 36
393, 407, 446, 447 Constipation 232
spontaneous 22 Continuous positive airway pressure 45,
Cisplatin 59 47
Clavulanate 73, 74, 83, 103, 291, 297, Contusion, pulmonary 359
476 Convulsions 80
Clavulanic acid 427 Copper sulfate 114
Clay–Shoveler fracture 401 Coral reef snakes 128
Cleistanthus collinus 124 Cord sign 201
Clindamycin 73, 81, 83, 106, 428, 476 Cormack and Lehane grading 42
Clobazam 210, 429, 477 Coronavirus disease-2019 86
Clonorchis sinensis 227 Corpora cavernosa 309
Clostridium 326 Corrosive poisoning 137, 511
botulinum 206 Corticosteroids 61, 88, 291
perfringens 93 Coryza 84
tetani 101 Cotrimoxazole 71, 429
Clotting disorder 250, 252 Cotton fracture 399
Cloxacillin 72, 73, 103, 313, 329, 338, Cough 84
429, 517, 518 Countertraction method 373, 373f
Clozapine 455 Covaxin 89
Coagulation disorders, acquired 251 COVID-19 86, 88
Coagulopathy 241, 276 management of 87t
Cobra bite 128 Covishield 89
Cocaine 135 Coxsackie 98, 227
Colles fracture 366, 396 C-reactive protein 87
reduction of 367f Creatine phosphokinase 384
Index 527
Creatinine 78, 84, 228, 233, 336, 452, 457 Denosumab 59

Cricothyroid arteries 499 Dense triangle sign 201
Cricothyroid membrane 499 Depression 60, 134
anatomy of 499 respiratory 134
Cricothyroidotomy 499, 500 Desflurane 453
indications 499 Dexamethasone 99, 264, 429
surgical 500, 501f Dextrose
Critical limb ischemia 335 infusion 264
Crohn’s disease 333 normal saline 52
Crush injury 327 Diabetes mellitus
Cryoprecipitate 255 type 1 266
Cryptosporidium 93 type 2 266
Crystal arthropathy 479 Diabetic foot 72, 73
Crystalline penicillin 73, 83, 103, 429 Diarrhea 32
Crystalloids, profile of 52t inflammatory 93
C-spine noninflammatory 93
assessment 352fc Diazepam 113, 413
immobilization 350 Dichloro-diphenyl-trichloroethane 118
smart-D assessment of 351t Diclofenac 478
Cyanide Dicyclomine 279
poisoning 141 Difficult airway assessment 40, 510
sources of 141 Difficult mask ventilation assessment 40
Cyanosis, central 41 Digital nerve block 485
Cyclosporin 62 Digital subtraction angiography 204
Cyst 214 Digitalis glycosides 111
Cystitis 95, 97 Digitoxin 111
Cytomegalovirus 227 Digoxin 111, 114, 161, 429
Cytotoxic damage 44 specific fab fragments 111
Diltiazem 114, 160, 477
D Diphenhydramine 218, 477
Diphtheria 206
Daboia russelii 128 Diplopia 282
Dancer’s fracture 401 Direct cyanide binding 141
Dantrolene 456 Direct thrombin inhibitors 247, 249
Datura 126 Disability 390, 393, 408
D-dimer 187 Disaster 435
Deep neck space infections 297 management 433, 435
Deep peroneal nerve block 489 Disc spaces 353
Deep vein thrombosis, acute 337 Disseminated intravascular coagulation
Defibrillation 3, 11 80, 251, 386
Dehydration, classification of 424t Distal phalanx, fractures of 327
Delirium 62 Diuretics 62
tremens 464 Diverticulitis 301
Dengue 75 Dix–Hallpike maneuver 294
fever 75, 76 Dobutamine 33, 38, 429
management of 76 Dog bite, management of 90
warning signs in 76 Domperidone 455
hemorrhagic fever 75, 76 Dopamine 16, 18, 33, 429
shock syndrome 75, 77 infusion 36
528 Index
Dorsal-penile-nerve-block 309f Electrocardiogram 87, 154, 159, 162,

Doxycycline 71, 74, 81, 105, 306, 429, 165, 172f, 210, 228, 233
477 basics of 171
Doxylamine 477 Electrodiagnostic tests 205
succinate 278 Electrolyte 49, 53, 78, 84, 228, 233, 336,
Drowning 462 452, 457
management 462 abnormalities 268
Drugs 59 toxicity 256
list of 476t Electromyography 205
overdose 111 Elevated ascitic fluid absolute
general management of 111 neutrophil count 229
therapeutics 88 Embolectomy 325
Dry nonfatal drowning 462 Embolism, pulmonary 32, 186, 186t, 191
Ducts, biliary 233 Emergency laparotomy, indications for
Duodenal ulcer 512 362
perforation 315 Emphysema 183
Dupuytren fracture 399 Empty delta sign 201
Duverney fracture 398 Empyema thoracis 83
Dysentery 424 Enalapril 477
Dyspnea 86, 125 Encephalitic rabies 90
Dysrhythmias, ventricular 113 Encephalitis 98, 99
Dystonia early feature of 98
acute 218 Encephalopathy 199, 231, 464
drugs-induced 218 Endocrine
reaction, acute 218 disorder 62
emergencies 257
E Endometritis 279
Endoscopic retrograde
E-C clamp technique 9f, 9t cholangiopancreaticography 228,
Echis carinatus 128 234
Echocardiography 187, 335, 393 Endotracheal intubation 42
Echovirus 98 indications for 47
Eclampsia 282, 283 Endotracheal tube 14, 191, 388
Ectopic pregnancy 273, 278, 281 End-tidal carbon dioxide 510
clinical presentation 273 Enflurane 453
diagnostic evaluation 273 Enoxaparin 88, 478
management 274 Entamoeba histolytica 93
ruptured 273 Enterobacteriaceae anaerobes 72
unruptured 273 Enteroviruses 98
Edema Epididymitis 305
acute pulmonary 16, 21 Epididymo-orchitis 304, 305
cardiogenic pulmonary 45 clinical features 305
pulmonary 157 etiology 305
Electrical injuries 457 laboratory investigations 305
clinical presentation 457 management 306
investigations 457 Epiglottitis 73, 417, 418
management 458 Epilepsy 209
Index 529
Epinephrine 31 reaction, mild 256

Episcleritis 469 seizures 412, 413t
Episodic vertigo 296 transfusion reaction 255
Epistaxis 289 Felon 330
anatomy 289 drainage of 330f
anterior bleeds 289 incision of 330f
management 290 Femoral line 493
nasal packing 290 Femur
posterior bleeds 290 neck of 368
Epley’s maneuver 294, 295f, 295t shaft of 369
Epstein–Barr virus 227 Fentanyl 429, 481, 482
Ertapenem 72, 73, 106, 477 Fetal monitoring 24
Erysipelas 313 Fetor hepaticus 231
Erythema multiforme 471 Fever 84
Erythromycin 429 Fexofenadine 477
Escherichia coli 229, 233, 240, 297 Fibrillation, ventricular 16, 166, 168,
enteropathogenic 71 168f, 432, 462
enterotoxigenic 71, 93 Fibrinogen 255
Esmolol 155 Finger’s breadth 497
Essex–Lopresti fracture-dislocation 397 Fistula in Ano 333
Estrogen therapy 276 Flail chest 359
Ethanol 111 Fluconazole 429
metabolism of 138f Fludrocortisone 264
Ethylene glycol 111 Fluid 49
Ethylenediaminetetraacetic acid 256 compartments 51f
Etomidate 481 replacement 228
Exacerbation, moderate 180 resuscitation 37, 267, 389
Expiratory phonation 41 therapy 51
Expiratory positive airway pressure 46 Flumazenil 111
Extracellular fluid 52 Flunarizine 296
Extremity Fluphenazine 218
examination of 344 Focal syndrome 199
injuries 364 Folic acid 278
Fomepizole 111
F Fondaparinux 249
Face 402, 518 dose of 249t
mask 44, 88 Food poisoning 93
Facial surgery, extensive 45 etiology of 94
Factor V Leiden mutation 252 Foot 400, 489f
Fasciitis 314 Forearm 396
necrotizing 73, 313, 314 Foscarnet 59
Fat embolism Fosphenytoin 211
syndrome 378 Fournier’s gangrene 304, 314
triad of 378 Fractures 327, 364, 396
Fatigue 53 intertrochanteric 368
Febrile management of 365
illness 71, 511 Free thyroxine 259
neutropenia 240 Fresh frozen plasma 255, 347
530 Index
Fungal infections 190, 240 Goodsall’s rule 333

Furosemide 429 Gosselin fracture 399
Furunculosis 72 Gout 480
Fusobacterium 298 Graft-vs-host disease 256
Guillain–Barré syndrome 48, 90, 205
G Gustilo and Anderson classification 364,
364t
Gabapentin 478 Gynecological emergencies 271
Gait
ataxia 464
disturbances 53
H
Galeazzi fracture-dislocation 397 H1N1 84
Gallstones 227 influenza 245
Gamekeeper’s thumb 398 Haemophilus influenzae 73, 82, 98, 245
Gamma-glutamyl transpeptidase 321 Haloperidol 218
Gangrene, spontaneous 326 Halothane 453
Gardanella vaginalis 279 Hand Doppler screening 336
Gas gangrene 326 Hand fractures 366
clinical features 326 Hangman’s fracture 401
diagnosis 326 Hazard 435
management 326 Head
traumatic 326 and face, examination of 343
Gastric lavage 109, 124, 125 injury 348
Gastroenteritis 51, 71, 93, 278, 424 trauma 390
Gastrointestinal Headache 53, 213, 214, 282
disorder 62 Hearing loss 296
emergencies 223 Heart
symptoms 125, 479 block 124
system 29 complete 18f
tract 123, 225, 321, 424 disease, ischemic 285
Gentamicin 106, 429 rate 14, 34, 35, 171, 446
Geriatric trauma 392 Heat
Giardia lamblia 71, 93 cramps 451
Giardiasis 71 exhaustion 451
Glanzmann’s thrombasthenia 250 stroke 32, 451
Glasgow coma scale 45, 343, 348, 349t, classic 451
408, 446, 447 exertional 451
Glaucoma 470 HELLP syndrome 284
Glenohumeral dislocation, posterior Helminthiasis 71
370 Hematemesis 190t, 225
Glucagon 31 Hematochezia 225
Glucocorticoid 263 Hematoma
metabolism 276 epidural 202
therapy 38 extradural 202, 203
Glucose-6-phosphate dehydrogenase mastoid 348
239 subdural 202, 203
Glycopyrrolate 117 subungual 327
Golfer’s elbow 397 Hemodynamics, unstable 45
Goodpasture syndrome 191 Hemoglobin 209
Index 531
Hemoglobinopathies 245 Holdsworth fracture 402

Hemolytic crisis 245 Holstein–Lewis fracture 396
Hemolytic reaction, acute 255 Hormone
Hemolytic-uremic syndrome 250 adrenal 263
Hemoperitoneum 496 therapy, exogenous 276
Hemophilia 253, 479 Hospital disasters, classification of
A 253 436
B 253 Human herpesvirus 205, 216
investigations 253 Human immunodeficiency virus 473
management 253 Hume fracture 396
mild-to-moderate 253 Humeral head 371
severe 253 Hutchinson fracture 397
Hemoptysis 190, 190t Hydrochlorothiazide 477
Hemorrhage 32, 284 Hydrocortisone 31, 61, 264, 429
fetomaternal 387 Hydrogen ion 16
intracranial 202, 203f Hydroxycobalamin 142
intraparenchymal 202, 203f, 204 Hydroxyurea 246
postpartum 284 Hydroxyzine 430
subarachnoid 202, 203, 219 Hymenoptera sting removal, technique
subconjunctival 469 of 133f
subdural 219 Hyoscine 302, 430
vitreous 467 Hyperacute T waves 174f
Hemorrhagic infarct 200f Hyperaldosteronism 62
Hemorrhoids 331 Hypercalcemia 60, 227
external 331 causes of 60t
internal 331 Hypercapnic respiratory failure 45
Hemostasis 381 Hyperemesis gravidarum 278
Hemothorax, massive 358, 359 evaluation 278
Hemotoxic bite 129 management 278
Henoch–Schönlein purpura 304 Hyperglycemia 33
Heparin, unfractionated 89, 246, 248 management of 39
Hepatic encephalopathy, acute 232 Hyperhomocysteinemia 252
Hepatitis 278 Hyperkalemia 16, 56, 57, 124, 244
B 473-475, 475t treatment of 58t
C 474 Hypermagnesemia 62
Hepato-renal syndrome 230 Hypernatremia 55
Herpes simplex virus 98, 216, 432 causes of 55t
Herpes zoster Hyperosmotic hyperglycemic nonketotic
oticus 293 state 268
virus infection 216 Hyperparathyroidism 62
High-flow nasal cannula 87, 88 Hyperphosphatemia 244
Hill–Sachs fracture 396 Hyperplasia 275
Hip endometrial 275
dislocation 374 Hypertension 481
posterior 374, 375 gestational 282
types of 374t pregnancy induced 282
fractures 368 pulmonary 32
Histidine-rich protein 2 80 severe 154
Hoarseness 41 treatment of 283
532 Index
Hypertensive Iliac fossa, right anterior 317

crisis, acute 270 Imipenem 477
disorders 282 Immunization 102
emergency 154, 155 Immunoglobulin E 29
Hyperthermia 56 Inactivated viral vaccines 89
malignant 453 Indian cobra 128
Hyperthyroidism 62 Indian krait 128
Hypertriglyceridemia 227 Infections 41, 232, 245, 256, 314, 498
Hyperuricemia 244 bacterial 314
Hypoalbuminemia 59 middle ear 216
Hypocalcemia 59, 244 respiratory 420
chronic 60 viral 251
severe 60 Infectious diseases 69
symptomatic 60 Influenza 84
Hypoglycemia 80, 232, 261, 264, 265 A virus 84
causes 265 B virus 84
discharge recommendation 266 complications of 84
management 265 virus 85
symptoms 265 Infusion pumps 497
Hypokalemia 16, 56, 232 Inhalation injuries 140
Hypokalemic periodic paralysis 57, 206 Inherited clotting disorders 252
Hypomagnesemia 62 Injuries
treatment of 63t abdominal 361
Hyponatremia 53, 261 electrical 457
causes of 53t evaluation of 388
correction 54 grievous 441
management of 53t hepatic 514
symptoms of 53 management of 388
Hypoparathyroidism 59 mechanism of 371
Hypoperfusion 32 needle-stick 473
Hypotension 14, 21, 23, 33, 113, 125, 407t nongrievous 441
orthostatic 134, 284 penetrating 362
Hypothalamic disease 264 submersion 462
Hypothalamic-pituitary axis 261 thermal 457
Hypothermia 16, 56, 256, 261, 390, 510 Inorganic rodenticides 121
Hypothyroidism Inotropes 32, 33t, 38
primary 261 Insecticide poisoning 116
secondary 261 Inspiratory reserve volume 185
Hypoventilation 261 Inspiratory stridor 41
Hypovolemia 16, 34, 232 Insulin
Hypoxia 16, 232 administration 267
maternal 283 sliding scale for 269
infusion 267, 269t
Intensive care, indications for 422
I Internal jugular vein 199, 493
Ibuprofen 478 Intestinal obstruction 322
Ice pack application 452f causes of 322t
Idiopathic thrombocytopenic purpura examination 322
250 history 322
Index 533
investigations 322 Kiesselbach’s plexus 289f

management 323 King cobra 128
Intoxication, acute 135, 136 Klebsiella 297
Intracellular fluid 52 Knee 398
Intracranial pressure 201, 204, 432 Kocher’s technique 372, 373f
Intraosseous line 497 Korsakoff’s psychosis 465
complications 498
procedure 497 L
Intraosseous needle insertion 497f
Intravenous fluids 187 Labetalol 155
choice of 51 Labyrinthine concussion 293
Intravenous thyroxine preparation Labyrinthitis, bacterial 296
method 262 Lactate 65
Intubation 388 clearance 39
protocol 509 dehydrogenase 87, 504
Invasive mechanical ventilation 47, 87, Larson’s point 482f
88 Laryngeal mask airway 43
Iritis 469 Laryngospasm 481
Iron 115 notch 481, 482f
deficiency anemia 238 Le-Fort fractures 355, 402
overload 256 Left ventricular hypertrophy 154
Ischemia 33 diagnostic criteria 174
mesenteric 33, 324 Leg 399
Isoflurane 453 Leiomyomas 275
Isolated intracranial hypertension Leptomeningitis 98
syndrome 199 Leptospira interrogans 73
Leptospirosis 73
Leukemia
J acute 241, 241t
Janus kinase inhibitor 89 lymphoid 241, 243
Jaundice 80 myeloid 241
Jaw thrust 6 chronic myeloid 241, 242
Jefferson fracture 401 Leukocyte esterase 96
Jersey finger 398 Leukopenia 84
Jones fracture 400 Levetiracetam 210, 430, 477
Jugular venous pressure 34 Levofloxacin 105, 476
Liberal sedation 102
K Lidocaine 16, 290, 430, 491
Lignocaine 16, 17, 485, 491, 514
Kayexalate 430 Limb ischemia, acute 335
Kernig’s sign 99 Linezolid 104, 477
Kerosene poisoning 139 Lipid emulsion therapy 113, 492
Ketamine 430, 478, 481, 509 Lisfranc fracture dislocations 400
Ketoacidosis, diabetic 266, 268 Listeria monocytogenes 98
Ketosis 267 Lithium 115
Kidneys 512 Liver
disease, chronic 59, 512 disease 251
ultrasonography of 96 failure 465
534 Index
function test 78, 84, 209, 228, 233, Malignant hyperthermia 453
318, 452, 512 clinical presentation 453
injury 496 diagnosis 453
Local anesthetics management 454
characteristics of 485t Mallampati score 41
infiltration 514 Mallet finger 398
systemic toxicity of 491 Mammary duct ectasia 338
toxicity, treatment of 491 Mannitol 430
Loop diuretics 61 March fracture 401
Loratadine 477 Marijuana 134
Lorazepam 413, 430, 456 Mass casualty 436
Losartan 477 incidents 435
Low flow priapism 308 management protocol 437fc
Lower gastrointestinal bleeding 226 Massive intra-abdominal bleed 362
causes of 226 Massive transfusion
Lower motor neuron complications of 347
facial nerve palsy 216 protocol 346, 347, 347fc
sudden-onset 216 Mastalgia 338
Low-molecular weight heparin 201, cyclical 338
248, 249 Mastitis 338
Ludwig’s angina 73, 298 acute 338
Lumbar puncture 100 lactational 338
Lung nonlactational 338
abscess 83 periductal 338
diseases, immunologic 191 Mastodynia 338
injury, acute 256 Matsen’s traction 373, 373f
Lyme disease 206, 216 Maxillary fractures, Le-Fort
Lymphocytic choriomeningitis virus classification of 355f
98 Maxillofacial trauma 41, 355
Lysergic acid diethylamide 136 McBurney’s point 318f
McBurney’s sign 317
M Mean arterial pressure 35, 36, 155
Mean corpuscular volume 237, 239
Magnesium 62, 165 Mechanical ventilation 184
sulfate 16, 430 Median nerve block 487, 488f
Magnetic resonance Medicolegal cases 439, 441
angiography 219 death of 442
imaging 154, 200, 213 Mefenamic acid 279
venography 213 Mefloquine 81
Maisonneuve fracture 400 Melena 225
Malabar pit viper 128 Ménière’s disease 293, 296
Malabsorption syndrome 62 Meningitis 98
Malaria 80, 81 bacterial 74
complicated 81 viral 98, 99
prophylaxis of 81 Meningoencephalitis 98, 99
severe 81 Meropenem 73, 105, 325, 430, 477
Malarial parasite test 80 Mesenteric arterial
Malgaigne’s fracture 398 embolism 324
Malignancy 199, 337 thrombosis 324
Index 535
Mesenteric artery, superior 324 Musculoskeletal trauma 391

Mesenteric ischemia 33, 324 Myalgia 84
clinical features 324 Mycoplasma pneumonia 82, 205, 245
diagnosis 325 Myelodysplastic syndrome 239, 241
management 325 Myelopathy, acute 206
physical examination 324 Myocardial infarction 32, 147, 148, 161,
Mesobuthus tamulus 131 512
Metered dose inhaler technique 184 Myometritis 279
Methanol 111 Myxedema coma 261
metabolism of 138f clinical presentation 261
poisoning 138, 467 diagnosis 262
Methemoglobinemia 142, 143 management 262
acquired 142t
induction of 141 N
Methergine 285
Methotrexate 478 N-acetylcysteine 111
Methyl alcohol poisoning 138 N-acetyl-P-aminophenol 111
Methylene blue 143 Nail bed
Methylenedioxymethamphetamine 136 crush injury of 327
Metoclopramide 213, 218, 318, 455, 477 emergencies 327
Metoprolol 160, 477 injuries 327
Metronidazole 106, 333, 431, 476, 517, Nail trephination 327, 328f
518 Naja naja 128
Midazolam 113, 413, 431, 481, 482, 509 Naloxone 17, 111
Migraine 213, 214 intravenous dose of 134
vestibular 293 Naproxen 478
Miller Fisher syndrome 205 Nasal cannula 44, 88
Mineralocorticoids 263 Nasal decongestants 423, 477
Miosis 134 Nasal fractures 356
Mitral regurgitation, acute 169 Nasogastric tube 344
Mitral stenosis 169, 170, 191 Nasopharyngeal airway 8, 8f
Moderna 89 National Early Warning Score 2 36, 38t
Monoarthritis, acute 479 National Emergency X-radiography
Monophasic defibrillators 12 Utilization Study Criteria 351
Monosodium urate 480 Native valve emergencies 169
Monteggia fracture 397 Natural absorbable sutures 380
Moraxella catarrhalis 73 Nausea 53, 134, 278
Morphine 431 Neck mobility 41
Motor axonal neuropathy, acute 205 Necrotizing fasciitis 73, 313, 314
Mountain sickness, acute 158 investigations 314
Multifocal atrial tachycardia 164 management 314
Multiple organ dysfunction syndrome Needle
46 cricothyroidotomy 499, 500f
Mumps 98, 227 thoracostomy 189
Murphy’s sign 321 Neisseria
Muscarinic receptors 116 gonorrhoeae 279, 305, 479
Muscle meningitidis 74, 98
damage 336 Neoplasms 41
relaxation 102 Nephrolithiasis 301
536 Index
Nerve Ondansetron 477

blocks 485 Oophoritis 279
conduction velocity 205 Opening airway, methods of 6t
Nervous system disorder 101 Ophiophagus hannah 128
Neuralgia, trigeminal 214 Ophthalmoplegia 205
Neuritis, vestibular 293 Opioids 111, 134
Neuroleptic malignant syndrome 451, intoxication 134
455 Optic neuritis 467
clinical manifestations 455 Oral airway 388
diagnosis 455 Oral anaerobes 73, 83
management 455 Oral antibiotics 232
Neuropathy, peripheral 457 Oral anticoagulants 247
Neurotoxic bite 129 Oral contraceptive pills 199
New York Heart Association 170 high-dose 277
Nicotinic receptors 116 Oral hydration 93
Nifedipine 114, 431, 477 Oral iron therapy 239
Nightstick fracture 397 Oral rehydration solution 93
Nitrite test 96 Organ
Nitrofurantoin 106 dysfunction 35
Nonabsorbable suture materials 380 ischemia 250
Noninvasive ventilation 45, 47, 88, 184 Organochlorides 120
Nonpoliovirus enteroviruses 98 compounds 118
Non-rebreather mask 44, 88 Organochlorine 118
Nonsteroidal anti-inflammatory drugs Organophosphates 111, 120
213, 227, 302, 306, 315, 338, 479 Organophosphorus compounds 116
use of 225 Organophosphorus poisoning
Non-ST-segment elevation myocardial clinical features of 116
infarction 153t features of 116t
management of 152 Orientia tsutsugamushi 74, 78
Noradrenaline 33, 431 Orogenital ulcers 479
Norwalk virus 93 Oseltamivir 85
Nutcracker fracture 401 Osteomalacia 321
Nystagmus 198, 293 Osteomyelitis 73, 314
Otitis externa 423
O Otitis media 293, 423
Ovarian cyst, ruptured 281
Obesity 40, 41, 337 Ovarian torsion 280
Obstetric emergencies 271 clinical presentation 280
Obstruction 40, 41 differential diagnosis 281
Obtundation 53 investigations 280
Occlusive mesenteric arterial disease management 281
324 Oxcarbazepine 210
Oculomotor dysfunction 464 Oxygen 44
Oduvanthalai poisoning, management flow rates 44
of 125fc saturation 36, 407
Olanzapine 455 therapy, dangers of 44
Omeprazole 477 Oxymetazoline 290, 477
Index 537
P Parvovirus 245
Patellar dislocation 377
P mitrale 173 reduction of 377f
P pulmonale 173 Peak expiratory flow rate 182
P wave 171, 172 Peaked T waves 174f
Packed cell volume 347, 365 Pediatric
Packed red cells 255 basic life support 12fc
Paget’s disease 321 cardiac arrest 25, 26fc
Pain 336 emergencies 403
abdominal 315t, 317, 512 drugs and dosages in 426
control 228 resuscitative equipment 410t
epigastric 282, 301 trauma 388
lower abdominal 274 Pelvic
relief 302, 460 compression test 368
discharge plan for 514 fractures 367
severity of 513 inflammatory disease 279
Painful crisis 245 etiology 279
Palamnaeus swammerdami 131 management 279
Pallor 336 Pelvis 398, 519
Pamidronate 61 Penicillin 476
Pancreatic effusion 504 Penile
Pancreaticobiliary drainage, anatomy emergencies 307
of 320f fracture 308
Pancreatitis 278 Peptic ulcer disease 315
acute 227, 511 Pericardiocentesis 502, 502f
biliary 228 complications 503
mild acute 227 emergency 502
moderately severe acute 227 indications 502
severe acute 227 nonemergency 502
Pancuronium 431 technique 502
Pantoprazole 278, 431, 477 Pericarditis, constrictive 32
Paracentesis 505 Peripheral capillary oxygen saturation
therapeutic 505 183
Paracetamol 111, 302 Peritonitis 325, 362
Paradoxical chest wall movement 41 bacterial 72, 229, 231, 512
Paralysis 90, 336 secondary 72
transient 457 Perphenazine 218
Parametritis 279 Pfizer 89
Paraphimosis 307, 307f Pharyngitis, acute 73
management 308 Phenergan 218, 296, 477
Paraquat poisoning 119 Pheniramine maleate 431
Parathyroid hormone 59 Phenobarbitone 131, 210, 431, 477
Paratrooper’s fracture 400 Phenylephrine 309, 477
Paresthesia 336 Phenytoin 210, 211, 477
Paronychia 327, 328 sodium 431
drainage 329, 329f therapeutic range 115
Parotid gland tumors 216 Pheochromocytoma 270
Paroxysmal supraventricular laboratory investigations 270
tachycardia 164, 164f management 270
538 Index
Phimosis 307, 307f Posterior hip dislocations 374, 375

management 307 reduction of 376
Phosphorus compounds 122 Thompson and Epstein classification
Piedmont fracture 397 375f
Piles 331 Posterior tibial nerve block 490
Pilon fracture 399 Postexposure prophylaxis 90, 91, 473-
Piperacillin 72, 73, 103, 314, 316, 318, 475
325, 431, 463, 476 Postpartum hemorrhage 284
Pituitary disease 264 clinical features 284
Plant poisons 124 investigations 284
Plasmodium management 284
lactate dehydrogenase 80 Potassium 56
vivax 80 Pott’s fracture 400
Plaster of Paris 378 Pouteau fracture 396
Plastic surgery 461 Pralidoxime 111
Platelet 241, 255 Prazosin 131, 477
defects, acquired 250 Prednisolone 61, 471
destruction 250 Preeclampsia 282
disorders, congenital 250 Pregnancy 84, 199, 252, 337
loss 251 drugs in 476
production 250 ectopic 273, 278, 281
Pleural fluid analysis 504 Preoxygenate 509
Pneumatosis intestinalis 325 Preoxygenation 388
Pneumonia 420 Pressure
community-acquired 82, 83t bag 497
necrotizing 83 support 46
Pneumothorax 188 Priapism 245, 308
iatrogenic 188 management 308
open 358, 359 Prilocaine 491
primary spontaneous 188 Prochlorperazine 218, 296
secondary spontaneous 188 Progestogen therapy 276
traumatic 188 Promethazine 218, 296, 455, 477
types of 188 Prophylactic antibiotic protocol 517,
Poikilothermia 336 517t
Poisonings 206, 511 Prophylaxis 474t
Polyangiitis, microscopic 191 Propranolol 431, 477
Polyarthritis 480 Prosthetic valve emergencies 170
Polycystic ovarian syndrome 276 Protein
Polymicrobial 73 bound 59
Polyps 275 C 255
Polyradiculoneuropathy, acute deficiency 252
inflammatory demyelinating 205 S 255
Polytrauma 515 deficiency 252
Pontine tumors 216 Prothrombin
Porphyria, acute intermittent 206 gene mutation 252
Positive ascitic fluid bacterial culture 229 time 99, 233, 336, 347, 512
Index 539
Protozoa 424 Regurgitant lesions 169

infection 80 Regurgitation
Pseudo Jones fracture 401 aortic 169
Pseudohyperkalemia 57 paravalvular 170
Pseudohyponatremia 53 Reiter syndrome 480
Pseudomonas aeroginosa 216, 233, Renal calculi 281
240 Renal disease 251
Psoas sign 317 Renal failure 80, 125, 282
Psychosis 60 Renal loss 56, 62
Puerperium 199 Renal replacement therapy 244
Pulmonary edema, high-altitude 158 Renal tubular acidosis 62
Pulmonary function tests 183 Rescue breaths 8
Pulse Reservoir bag 44, 88
check 11 Resin casts 378
oximetry 407 Respiratory arrest 53
rate 36 Respiratory failure 44, 45, 47, 113
Pulseless electrical activity 16 Respiratory rate 35, 36, 38
Pyelonephritis 95, 97, 278, 281 Respiratory system 29
Pyogenic meningitis 98, 99 Respiratory viruses 73
Pyrethroids 119, 120 Resuscitation 341, 386
Pyridoxine 278 cardiopulmonary 3, 4, 10, 11
maternal 23
Q Reticulocyte count 237
Retina problems 466
Q wave 173 Retinal detachment 467
QRS complex 171 Retropharyngeal abscess 297
Quinine 81 causes 297
clinical features 297
R investigations 297
R wave 173 management 297
Rabies 90 Reverse transcription-polymerase chain
immunoglobulin 91 reaction test 86
vaccine 92 Rhinosinusitis, bacterial 73
Radial nerve block 486, 487f Rifampicin 477
Raised intracranial pressure 213, 390 Right bundle branch block diagnostic
Ramsay Hunt syndrome 216 criteria 175
Ranitidine 432, 477 Right upper quadrant pain 301
Rapid antigen test 86 Ringer lactate 51
Rapid blood borne virus screen 336 Risperidone 455
Rapid sequence induction 88, 509 Rodenticides 121
protocol 509, 509t types of 121
Rapid shallow breathing 41 Rolando fracture 397
Rash 479 Rotavirus 93
Red blood Rovsing’s sign 317
cell 237, 239 Rubella 227
count 204 Rugby finger 398
distribution width 239 Runner’s fracture 399
Red eye, acute 469 Russell’s viper 128
540 Index
S Sexually transmitted diseases 333

Sheehan’s syndrome 284
S wave 173 Shenton’s line 368, 368f
Saccular aneurysm 214 Shepherd fracture 400
Salbutamol 432 Shigella 71, 480
nebulization 31 Shock 32, 80
Salmonella 480 anaphylactic 32
paratyphi 71 cardiogenic 32
typhi 71 classification of 32
Salpingitis 279 compensated 77
Saphenous nerve block 491 distributive 32
Sarcoidosis 216 electric 457
Saw scaled viper 128 hemorrhagic 345, 345t
Scalp 517 hypovolemic 32, 284, 446
laceration 381 management 34t
Scorpion sting 131 mechanism of 33fc
Scotoma 282 neurogenic 32
Scrotal pain, acute 304 obstructive 32
Scrub typhus 74, 78, 99 overview of 32
Eschar of 79f septic 32, 35, 88, 325
Sea snakes 128 signs of 14, 21
Seasonal influenza 84 stages of 32
Seatbelt fracture 401 types of 32, 34
Sedation, procedural 481 Shoulder
Segond fracture 398 dislocation 370
Seizures 53, 62, 113, 131, 209, 512 types of 371t
active 283 reduction, Kocher’s technique for
complex febrile 412 373f
management of 209t Sickle cell
new-onset 209 crisis 245
simple febrile 412 clinical presentation of 245
suppression 492 disease, acute complications of 245
withdrawal 464 Silver sulfadiazine 461
Seldinger technique 494 Sinoatrial nodal reentrant tachycardia
Sensorimotor axonal neuropathy, acute 164
205 Sinus
Sensorium, altered 14, 21, 36 bradycardia 14, 17, 17f
Sepsis 35, 37, 37fc rhythm, normal 171
Septic focus, control of 38 Skier’s thumb 398
Septic shock 32, 35, 88, 325 Skin
management of 37 and integumentary system 29
Sequential organ failure assessment hyperpigmentation 263
score 36t infection 313
Sequestration, hepatic 245 Smith fracture 396
Serum beta-human chorionic Snakes 128t
gonadotropin 273 bites 128
Sevoflurane 453 Snoring 41
Index 541
Sodium 53 Stroke 165

bicarbonate 432 hemorrhagic 196
nitrite 142 ischemic 195, 196
polystyrene sulfonate 430 Strychnine 126
thiosulfate 142 ST-segment elevation myocardial
valproate 210, 477 infarction, management of 151
Soft tissue 354 Subclavian line 493
infection 313 Substance abuse 134
Sore throat 84 Succinylcholine 432, 453, 509
Sphincterotomy, endoscopic 234 Sulbactam 103, 428
Spider bites 133 Sulfamethoxazole 306, 477
Spinal cord injury 391 Sulfonamides 227
Spinal injuries, classification of 350 Sulfur donors 141
Spine 401 Superficial peroneal nerve block 490
manual in-line stabilization of 342f Supratherapeutic international
Spirometry 184 normalized ratio, management of
interpretation of 181fc 248t
lung volumes on 185f Sural nerve block 491
Spironolactone 432 Surgical cricothyroidotomy 500, 501f
Spleen injury 496 complications of 501
Splenic sequestration 245, 251 Suture
Splints 378 materials 380
Sputnik 89 needles 380
Staphylococcus Synovial fluid analysis 479
aureus 72, 82, 240, 290, 297, 328, 338, Synthetic braided sutures 380
479 Synthetic monofilament sutures 380
epidermidis 240 Systemic inflammatory response
organisms 93 syndrome 35
Statins 478 Systemic lupus erythematosus 191
Status asthmaticus 414 Systemic toxicity, management of 491
Status epilepticus 211, 212fc
management of 211 T
Steroids 31 T wave 173
Stevens–Johnson syndrome 472 T2-weighted fluid-attenuated inversion
Stieda fracture 398, 400 recovery 219
Stiff lungs 40 Tachyarrhythmias 21, 33
Stimson’s technique 372, 372f classification of 21t
Stones, types of 301 initial management of 21
Streptococcus Tachycardia 22fc, 33, 125, 259, 481
milleri 83 atrial 164
pneumonia 82, 83, 98, 245 supraventricular 21, 168, 432
pyogenes 72 ventricular 21, 166, 167, 167f, 168,
viridans 240 432, 462
Stridor 291, 417 Tachypnea 125
acute 417 Tardive
causes of 417t dyskinesia 218
classification of 418t dystonia 218
etiology 291 Tazobactam 72, 73, 103, 314, 316, 318,
management 291 325, 431, 463, 476
542 Index
Temporary pacemaker insertion 19 Tidal volume 185

Temporomandibular joint 356 Tigecycline 72
dislocation 356 Tillaux fracture 400
Tennis elbow 397 Tinidazole 71
Tense ascites 505 Tinnitus 296
Tension pneumothorax 16, 32, 189f, Tissue factor pathway inhibitor 255
358, 359 Tocilizumab 89
Testicular cancer 304 Toddler’s fracture 399
Testicular torsion 304 Torsades de pointes 166, 167f
Tetanus 101 Torsion
prophylaxis 90, 92, 102, 102t, 129, 379 higher risk of 303
Tetany 62 testis 303
Tetracyclines 227 clinical features 303
Tetralogy of Fallot 432 management 303
Thallium 121 Total lung capacity 185
Thiazides 227 Tourniquet test 76
Thioridazine 218 Toxic epidermal necrolysis 472
Third-degree atrioventricular block 14 Toxic shock syndrome 32, 290
Thompson and Epstein classification Toxins 16
375f Tracheal tug 41
Thoracic injuries 358 Tramadol 318, 432
Thorax 519 Tranexamic acid 276, 285, 432
examination of 343 Transaminitis 84
Three-way occlusive dressing 360f Transcutaneous electrical nerve
Thrombocytopenia 250 stimulation 217
heparin-induced 249 Transcutaneous pacing 18, 19, 20f
Thrombolysis in myocardial infarction Transfusion reaction 256
score 153t Transient ischemic attack 161, 165,
Thrombosis 195
coronary 16 Transvenous pacing 18, 19
pulmonary 16 Trauma 216, 227, 283, 385, 515, 517
Thrombotic thrombocytopenic purpura abdominal 390
250 early management of 341
Thrombus 335 Tremors 62
Thyroid Tricyclic antidepressants 111-113
antibody titers 259 overdose 112
gland, intrinsic dysfunction of 261 Trifluoperazine 218
hormone replacement 262 Triglycerides 504
stimulating hormone 259 Trihexyphenidyl 218
storm 259 Triiodothyronine 259
medical management of 260t Trimeresurus malabaricus 128
Thyrotoxic crisis 259 Trimethoprim 306, 477
clinical features 259 Trousseau’s sign 59
investigations 259 Tube thoracostomy 189f
management 260 Tuberculosis 190
Tibia fractures 369 Tubo-ovarian abscess 279, 281
Tick borne paralysis 206 Tumor lysis syndrome 243, 244
Index 543
Tunica vaginalis 303 Vascular diseases 191

Typhoid fever 71 Vasculitis, systemic 227
Vaso-occlusive
U crisis 245
phenomena 245
Ulnar nerve block 487, 488f
Vasopressin 17
Ultrasonography 96, 188, 234, 393
Vasopressors 32, 33t, 187
Universal pain assessment tool 513f
Vasospasm, prevention of 204
Upper airway obstruction 45
Vecuronium 432
Upper gastrointestinal
Vena cava, inferior 385
bleeding 46, 225, 226b
Venous blood gas 65
causes of 225
analysis 112
surgery 45
Ventilation 7, 389
Urea 84, 336
Ventricle septal rupture 32
Ureaplasma urealyticum 279
Venturi mask 44, 88
Ureters 512
Verapamil 114, 160, 477
Urinary catheter 344
Vertigo 198, 292, 292fc
Urinary tract infection 95
benign paroxysmal positional 292,
antibiotics for 97t
293, 295f
diagnosis of 95fc
causes of 293t
lower 95
medications for 296
management of 95fc
peripheral 294
upper 95
posterior canal benign paroxysmal
Urine
positional 294
alkalinization of 244
Vibrio cholerae 71, 93, 94
osmolality 54
Vincent’s angina 73
output 390
Viral infection, arthropod-borne 75
precolor 318
Viridans spirillum minus Streptobacillus
spot sodium 54
74
Urological emergencies 299
Viruses 240, 424
Ursodeoxycholic acid 432
Vision
Urticaria 471
loss of 282
Uterine
painless loss of 466
bleeding, abnormal 275
sudden painless loss of 467
rupture 387
Visual disturbances 282
Uveitis 469
Visual field defects 198, 282
Visual loss, sudden 466
V Vital capacity 185
Vaginal bleeding, management of 276 Vitamin
Valacyclovir 73, 476 D deficiency 59
Valproate 227, 432 K1 432
Valve regurgitation 170 Vomiting 32, 46, 53, 134
Valvular emergencies 169 von Willebrand disease 253, 254
Valvular thrombus, acute 170 clinical features 254
Vancomycin 99, 104, 432 diagnosis 254
Varicella zoster virus 73, 98, 216 management 254
544 Index
W Wrist block 486
Warm sitz baths 331, 332

Watery diarrhea, acute 425t
X
Weakness 62 X-rays 365-369, 371, 376, 394, 395
Web space block 486f role of 369
Wegener’s granulomatosis 191
Wellens’ syndrome 149, 150f Y
Wells scoring system, modified 186t Yellow
Wernicke’s encephalopathy 464 oleander 124
White blood cell count 96 phosphorus 121, 122
Whole blood clotting time 129 Yersinia 480
Wide complex tachycardia 16, 166 enterocolitica 93
characteristics of 166t
Wound
care 90
Z
classification of 91t Zika virus 245
cleansing 381 Zinc
closure 381 phosphide 121, 122
debridement 381 supplementation 424
management 379, 460 Zoledronic acid 61
wash 379 Zygomycetes 314
PLATE
FIG. 1: Eschar of scrub typhus. (Chapter 16)

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CMC Vellore Handbook of

CMC Vellore Handbook of Emergency Medicine, previously called

JAYPEE BROTHERS MEDICAL PUBLISHERS

Corporate Office Overseas Office

Inquiries for bulk sales may be solicited at: [email protected]

CMC Vellore Handbook of Emergency Medicine / KPP Abhilash

Dr Shubhanker Mitra (1981–2016) who was a fantastic colleague and friend, an

Priya G MD (Anesthesiology) Sandeep David MD (Anesthesiology)

There has been a perceived need to have comprehensive

• Treat the patient’s symptoms. Do not treat the monitors or laboratory

Section 1: Basic Life Support and Management of Cardiac Arrest

Section 2: Anaphylaxis, Shock and Airway

Section 3: Fluid and Electrolytes

Section 4: Infectious Diseases

Section 6: Cardiac Emergencies

Section 7: Respiratory Emergencies

Section 8: Neurological Emergencies

57. Bell’s Palsy 216

Section 9: Gastrointestinal and Hepatic Emergencies

Section 10: Hematological Emergencies

Section 11: Endocrine Emergencies

Section 12: Obstetric and Gynecological Emergencies

Section 13: ENT Emergencies

Section 14: Urological Emergencies

Section 15: Surgical Emergencies

Section 16: Trauma

116. Trauma in Pregnancy 385

Section 17: Pediatric Emergencies

Section 18: Disaster Management

Section 19: Medicolegal Cases

Section 20: Triage

Section 21: Miscellaneous

143. Drugs in Pregnancy 476

Section 22: Procedures

Section 23: Protocols

BASIC LIFE SUPPORT/CARDIOPULMONARY

Overview of Initial Basic Life Support Steps (Table 1)

TABLE 1: Steps of basic life support.

FIG. 1: Carotid pulse check.

• Activate the emergency response system and get an automatic external

FIGS. 2A TO C: Technique of chest compressions.

TABLE 2: Two methods of opening the airway.

Basic Airway Adjuncts

TABLE 3: E–C clamp technique.

The following are the steps involved in bag-mask ventilation:

FLOWCHART 1: Adult basic life support algorithm.

BASIC LIFE SUPPORT/CARDIOPULMONARY

emergency response system and get the defibrillator.

BASIC LIFE SUPPORT/CARDIOPULMONARY

Defibrillation and Cardioversion

FIGS. 6A AND B: Technique of chest compression in children.

FLOWCHART 2: Pediatric basic life support algorithm.

TABLE 4: Differences between cardioversion and defibrillation.

Monophasic versus Biphasic Defibrillators

Using a Biphasic Defibrillator

FLOWCHART 1: Adult cardiac arrest algorithm.

TABLE 1: Reversible causes: 5Hs and 5Ts.

TABLE 2: Overview of drugs used in cardiac arrest.

• Active ischemic chest pain

TABLE 3: Drugs that can be given through the ET tube.