Approach To Pediatric Emergency

Approach to
Pediatric Emergency
Approach to
Pediatric Emergency
Jaydeep Choudhury
Assistant Professor
Department of Pediatrics
Institute of Child Health
Kolkata, West Bengal, India
Jayanta Bandyopadhyay
Senior Consultant, Pediatrician, Durgapur, West Bengal, India
Former Fellow, Pediatric Cardiac Critical Care
Madras Medical Mission, Chennai, Tamil Nadu, India
Senior Registrar, Pediatric Emergency Medicine
Mater Childrens Hospital, Brisbane, Australia
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Approach to Pediatric Emergency
2011, Jaypee Brothers Medical Publishers
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First Edition: 2011
ISBN 978-93-5025-386-1
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Dedicated to
Our respected teachers
who trained us and our special friend
Dr Biswajit Bandopadhyay
Contributors
Amitabha Chattopadhyay
Fellow, Pediatric Cardiology
Childrens Hospital Westmead
Consultant Pediatric Cardiologist
Rabindranath Tagore International
Institute of Cardiac Sciences
Amiya Kumar Mukhopadhyay
Consultant Dermatologist
Asansol, West Bengal, India
Anirban Chatterjee
Associate Professor
Department of Pediatric
Orthopedics
Biswajit Bandopadhyay
Head, Department of Pediatrics
Cardiology
Rabindranath Tagore International
Institute of Cardiac Sciences
Senior Consultant, Pediatrician
Durgapur, West Bengal, India
Former Fellow, Pediatric Cardiac
Critical Care
Madras Medical Mission
Chennai, Tamil Nadu, India
Senior Registrar, Pediatric
Emergency Medicine
Mater Childrens Hospital
Brisbane, Australia
Jaydeep Choudhury
Assistant Professor
Joshi Anand Karketta
Consultant Pediatrician
The Mission Hospital
Lav Kochgaway
Consultant Pediatric
Ophthalmologist
Mahasweta Chaudhuri
Consultant Pediatrician
BC Roy Technology Hospital
IIT, Kharagpur, West Bengal, India
Saheli Misra
Assistant Professor
Sudipta Sekhar Das
Consultant and Head
Department of Transfusion
Medicine
The Mission Hospital
Tapan Kumar Ghosh
Scientific Coordinator
Institute of Child Health, Kolkata
Past Chairperson
IAP Infectious Diseases Chapter
Member, APCRI and ASAP, India
Preface
Pediatric emergency is relatively a new discipline. It is taking its shape
worldwide for the last few years as a new specialty dealt with by specialists
interested in this discipline. Approach to Pediatric Emergency is an endeavor
towards building up such an interesting field of pediatrics wherein the first
few golden moments at presentation to emergency department, a rational,
step-wise and correct approach can not only save the child but also reduce
the morbidity to a minimal.
This is neither a textbook nor a book dealing with cases in intensive
care or critical care. The effort starts at trying to understand the severity
and gravity of each individual case, resuscitate at emergency department,
order some investigations to come to a working diagnosis, then manage
appropriately according to the diagnosis and refer to the appropriate specialty either as out-patient or admitting to ward or ICU after stabilization.
Not being a textbook, the book is more approach-based, algorithmic
and naturally ready to use. Even with sound knowledge, working in a busy
emergency may be stressful and tiresome. Going through a textbook or
descriptive text may be time consuming and mind boggling too. We need
at a glance format which can be accessed by emergency physicians, emergency fellows, trainees, pediatric postgraduates and even practicing
pediatricians.
The book deals with ideas which can be practised in any reasonably
good hospital set-up. It also covers emergency situations that can be dealt
with both by emergency physicians and pediatricians. Chapters on Ophthalmology, Dermatology, Orthopedics even Psychiatry discuss topics where
there is a clear boundary what as a pediatrician and emergency specialist
should do and when he should refer to other specialists. A lucid approach
has also been made for relatively new pediatric trainee or emergency trainee
in chapters like Neonatal Collapse or approach to a crying baby, croup,
bronchiolitis so that hesitation can be brought down to minimum.
It was an absolute pleasure for us writing this book. We are grateful to
all the contributing authors for their valuable inputs. We are indebted to
our alma mater the Childs Trust Hospital, Chennai, Tamil Nadu where
during our postgraduation we used to encounter innumerable cases during our long hours in the emergency room. Perhaps, it was the driving
force for this venture.
With a heavy heart, we remember Dr Tapan Kumar Ghosh. The chapter on Animal Bites was his last scientific article, written exactly a week
before his untimely demise.
We express our sincere gratitude to Shri Jitendar P Vij (Chairman and
Managing Director), Mr Tarun Duneja (Director-Publishing), Mrs Samina
Khan (PA to Director), Mr Mohit Ghai and the team of M/s Jaypee Brothers
Medical Publishers (P) Ltd, New Delhi and Mr Sabyasachi Hazra and the
team from Kolkata Branch for their whole-hearted effort and cooperation.
A supportive family is the backbone of any work. We are fortunate to
have understanding parents, wives and children. We are grateful to our
parents Arun and Anjali Bandyopadhyay, Ashish and Jaya Choudhury,
spouse Munmun Bandyopadhyay and Sudarsana Choudhury, children
Chandrika Bandyopadhyay and Sayondeep Choudhury for their constant
help and encouragement.
We are also indebted to Dr Robyn Brady, Deputy Director, Pediatric
Emergency Department, Mater Childrens Hospital, Brisbane, Australia
for his impetus and support.
We are open to suggestions and criticisms. Feel free to mail us at
drjaydeep_choudhury@yahoo.co.in and sendjayanta@yahoo.com
Jaydeep Choudhury
Contents
SECTION 1: GENERAL EMERGENCY
1.1. Setting-up Pediatric Emergency Department .............................. 3
Pediatric Resuscitation Equipment ........................................... 3
Monitoring and Recording Vital Functions .............................. 6
Transferring the Patient ........................................................... 6
Documentation in ED ............................................................... 8
1.2. Approach to a Child in Pediatric Emergency Department ......... 9
Jayanta Bandyopadhyay, Jaydeep Choudhury
Warning Symptoms in History .................................................. 9
Warning Signs in Examination ................................................. 9
Decision-making in Pediatric Emergency ................................ 9
Normal Vital Signs .................................................................. 10
Things to be done in Emergency Room ................................. 10
1.3. Early Assessment and Emergency Triage ................................. 12
Priority 1Severe Life-threatening Emergency ..................... 12
Priority 2Acute Medical Problems or Distress ..................... 12
Priority 3Semiurgent Acute Medical Problems ................... 13
Priority 4Nonurgent Acute Medical Problems .................... 13
Priority 5Condition is Stable and will not Deteriorate
as a Result of Waiting .............................................................. 13
SECTION 2: RESUSCITATION
2.1. Cardiopulmonary Resuscitation ................................................ 17
Jayanta Bandyopadhyay, Joshi Anand Karketta, Jaydeep Choudhury
Airway ..................................................................................... 17
Breathing ................................................................................ 18
Circulation .............................................................................. 19
2.2. Shock ........................................................................................... 24
Joshi Anand Karketta, Jayanta Bandyopadhyay, Jaydeep Choudhury
Types of Shock ........................................................................ 24
Clinical Features ..................................................................... 24
Investigations .......................................................................... 25
Management ........................................................................... 26
xii
2.3. Coma ............................................................................................ 28

Mahasweta Chaudhuri, Jayanta Bandyopadhyay, Jaydeep Choudhury
Etiology ................................................................................... 28
History .................................................................................... 29
Physical Examination .............................................................. 29
Neurological Examination ...................................................... 30
Investigations .......................................................................... 32
Management ........................................................................... 33
Emergency Management of Raised Intracranial Pressure ...... 34
Antiseizure Medications in Coma ........................................... 34
Choice of Empiric Antimicrobials ........................................... 36
Prognosis ................................................................................. 36
2.4. Syncope ....................................................................................... 37
Basic Vascular Pathophysiology .............................................. 37
Causes ..................................................................................... 37
History .................................................................................... 38
Goals ....................................................................................... 38
Physical Examination .............................................................. 39
Differential Diagnosis ............................................................. 39
Investigations .......................................................................... 39
Treatment ............................................................................... 39
2.5. Anaphylaxis ................................................................................ 40
Common Known Causes of Anaphylaxis ................................ 40
Different Types of Presentation .............................................. 40
Management ........................................................................... 40
2.6. Oxygen Administration .............................................................. 44
Mahasweta Chaudhuri, Jayanta Bandyopadhyay
Drawbacks of SpO2 ................................................................. 45
Humidification of Oxygen ...................................................... 45
Administration of Oxygen ...................................................... 45
Measurement of Delivered Oxygen ........................................ 46
Practice Points ........................................................................ 46
Disadvantages of Oxygen Therapy ......................................... 46
2.7. Fluid and Electrolyte Balance .................................................... 47
Joshi Anand Karketta, Jaydeep Choudhury, Jayanta Bandyopadhyay
General Guidelines for Rehydration ...................................... 47
Rehydration in Acute Gastroenteritis ..................................... 47
Hyponatremic Dehydration .................................................... 50
Hypernatremic Dehydration .................................................. 51
Hyperkalemia ......................................................................... 53
Hypokalemia ........................................................................... 54
Hypocalcemia ......................................................................... 55
Contents
xiii
2.8. Blood Component Transfusion .................................................. 56

Sudipta Sekhar Das
Red Blood Cell ........................................................................ 56
Platelets ................................................................................... 58
Plasma ..................................................................................... 59
Cryoprecipitate ....................................................................... 60
Granulocytes ........................................................................... 61
Blood Component Administration ......................................... 61
Complications of Transfusion ................................................ 62
Current Controversies and Unresolved Issues ....................... 62
Use of Non-Cross-matched Blood in Emergency
Situations ................................................................................ 64
Emerging Technologies .......................................................... 64
SECTION 3: SEDATION, ANALGESIA, INTUBATION AND PROCEDURES

3.1. Sedation, Analgesia, Paralysis and Drug Dilutions .................. 69
Goals of Sedation in the ER .................................................... 69
Classes of Drugs Commonly Used in the ER ......................... 69
Basic Pharmacologic Principles .............................................. 70
Opioids ................................................................................... 70
Benzodiazepines ..................................................................... 72
Ketamine ................................................................................. 73
Propofol .................................................................................. 75
Muscle Relaxants .................................................................... 77
3.2. Basics of Intubation .................................................................... 84
Jayanta Bandyopadhyay, Mahasweta Chaudhuri
Indications for Intubation ...................................................... 84
Equipment .............................................................................. 86
Preparing for the Procedure ................................................... 87
Positioning the Patient ............................................................ 87
Procedure ................................................................................ 87
3.3. Rapid Sequence Intubation ........................................................ 89
Fundamental Concept ............................................................ 89
Indications .............................................................................. 89
Contraindications ................................................................... 89
Technique ............................................................................... 90
3.4. Intraosseous Access .................................................................... 94
Jaydeep Choudhury
Contraindications ................................................................... 94
Procedure ................................................................................ 94
xiv
3.5. Chest Tube Drainage and Needle Thoracocentesis .................. 97

Points to Remember ............................................................... 97
Chest Tube Placement ............................................................ 97
Procedure ................................................................................ 97
Complications ......................................................................... 99
3.6. Needle Pericardiocentesis ........................................................ 100
Indications ............................................................................ 100
Contraindications ................................................................. 100
Equipment ............................................................................ 101
Procedure .............................................................................. 101
Post-procedure Monitoring ................................................... 102
Complications ....................................................................... 102
3.7. Cricothyrotomy ......................................................................... 103
Procedure .............................................................................. 103
Complications ....................................................................... 103
SECTION 4: NEONATAL EMERGENCIES

4.1. Neonatal Emergencies .............................................................. 107
Jaydeep Choudhury
Severe Hypothermia ............................................................. 107
Seizures ................................................................................. 108
Hypoglycemia ....................................................................... 109
Neonatal Hemorrhage .......................................................... 110
Neonatal Apnea .................................................................... 110
Air Leak ................................................................................ 111
4.2. Prolonged Neonatal Jaundice .................................................. 113
Jaydeep Choudhury, Jayanta Bandyopadhyay
Common Causes of Unconjugated
Hyperbilirubinemia in Children .......................................... 113
Clinical Assessment of Unconjugated Hyperbilirubinemia .. 113
Approach to Patients Presenting with Jaundice
at Emergency Room .............................................................. 114
Factors Increasing Effectiveness of Phototherapy ................ 115
Treatment of Unconjugated Hyperbilirubinemia ................ 115
Treatment of Conjugated Hyperbilirubinemia .................... 115
4.3. Bleeding Neonate ..................................................................... 123
Few Points in History ............................................................ 123
Examination ......................................................................... 123
Baseline Investigations ......................................................... 123
Management ......................................................................... 124
Contents
xv
4.4. Neonatal Collapse ..................................................................... 126

Causes ................................................................................... 126
Associated Clinical Features ................................................. 127
Investigations ........................................................................ 127
Hyperoxia Test ..................................................................... 127
Management ......................................................................... 128
Practice Points ...................................................................... 129
SECTION 5: RESPIRATORY EMERGENCIES

5.1. Respiratory Distress and Noisy Breathing .............................. 133
Evaluation of a Child with Respiratory Distress ................... 133
Noisy Breathing .................................................................... 134
Approach to Noisy Breathing ............................................... 135
5.2. Croup ......................................................................................... 136
Clinical Presentation ............................................................. 136
Practice Points ...................................................................... 136
5.3. Acute Epiglottitis ...................................................................... 139
Saheli Misra, Jaydeep Choudhury
Etiology ................................................................................. 139
Symptoms ............................................................................. 139
Signs ...................................................................................... 139
Caution ................................................................................. 139
Management ......................................................................... 140
Recommended Antibiotics .................................................... 140
5.4. Bronchiolitis ............................................................................. 142
Etiology ................................................................................. 142
Risk factors............................................................................ 143
Social Risk Factors ................................................................ 143
Diagnosis ............................................................................... 143
Management ......................................................................... 143
Practice Points ...................................................................... 144
5.5. Acute Severe Asthma ................................................................ 145
Evaluation of Severity of an Acute Episode of
Asthmain Children above 2 Years ..................................... 145
Caveat ................................................................................... 145
Criteria for Hospital Admission ........................................... 146
Management ......................................................................... 146
Good Response Group .......................................................... 147
xvi
Signs of High Risk ................................................................ 148

Poor Response Group ........................................................... 148
First Attack of Status Asthmaticus ......................................... 149
SECTION 6: CARDIOVASCULAR EMERGENCIES

6.1. Cyanotic Spell ........................................................................... 153
Mahasweta Chaudhuri, Jaydeep Choudhury, Jayanta Bandyopadhyay
Pathophysiology .................................................................... 153
Management ......................................................................... 154
Practice Points ...................................................................... 155
6.2. Heart Failure ............................................................................. 156
Common Causes of Heart Failure ........................................ 156
Physical Examination ............................................................ 156
Investigations ........................................................................ 156
General Management ........................................................... 157
Specific Management ........................................................... 157
Practice Points ...................................................................... 157
6.3. Abnormal Pulse Rate or Rhythm ............................................. 160
Amitabha Chattopadhyay, Biswajit Bandopadhyay
Bradyarrhythmia................................................................... 161
Tachyarrhythmia ................................................................... 161
History .................................................................................. 162
Clinical Scenario ................................................................... 162
ECG ...................................................................................... 162
General Management of Arrhythmia ................................... 163
Bradycardia ........................................................................... 164
Tachycardia ........................................................................... 165
Supraventricular Tachycardia ............................................... 167
Management ......................................................................... 169
Wide-complex Tachycardia ................................................... 170
Defibrillator for Cardioversion ............................................. 174
6.4. Chest Pain ................................................................................. 175
Assessment ............................................................................ 176
Management ......................................................................... 177
6.5. Cardiac Emergencies in a Noncardiac Set-up ......................... 179
Clinical Evaluation ................................................................ 180
Clinical Scenario ................................................................... 181
Interpretation of Chest X-ray when Heart
Disease is Suspected ............................................................. 181
Features Suggestive of a Duct Dependent Lesion ................ 181
Time of Presentation ............................................................ 182
Contents
xvii
Presentation .......................................................................... 182

Duct Dependent Systemic Lesions ....................................... 182
Management ......................................................................... 182
Prolonged QT Syndrome ...................................................... 182
Drugs that Prolong QT Interval ........................................... 183
SECTION 7: GASTROINTESTINAL EMERGENCIES

7.1. Acute Abdominal Pain .............................................................. 187
Jaydeep Choudhury
Red Flags .............................................................................. 187
Initial Clues for Severe Abdominal Pain .............................. 187
Acute Lower Abdominal Pain ............................................... 188
Pediatric Gynecological Emergencies ................................... 190
Investigation ......................................................................... 192
Midgut Malrotation .............................................................. 192
7.2. Acute Scrotum ........................................................................... 194
Torsion of the Testis .............................................................. 194
Torsion of the Hydatid of Morgagni ..................................... 195
Idiopathic Scrotal Edema ..................................................... 196
Testicular Trauma ................................................................. 196
Epididymo-orchitis ............................................................... 196
7.3. Upper Gastrointestinal Bleeding ............................................. 198
Jaydeep Choudhury
Investigations ........................................................................ 199
Management ......................................................................... 199
7.4. Fulminant Hepatic Failure ....................................................... 202
Etiology ................................................................................. 202
Clinical Manifestations ......................................................... 202
Investigations ........................................................................ 202
Red Flag Signs ...................................................................... 204
Management ......................................................................... 204
Follow-up and Monitoring .................................................... 206
Temporary Hepatic Support ................................................. 206
SECTION 8: RENAL EMERGENCIES

8.1. Acute Renal Failure .................................................................. 209
Jaydeep Choudhury
Causes of ARF ....................................................................... 209
Presentations in Emergency ................................................. 209
Assessment of Severity .......................................................... 209
xviii
Determination of Underlying Cause .................................... 210

Investigations ........................................................................ 210
Points to Ponder ................................................................... 211
Management ......................................................................... 211
Diet ....................................................................................... 211
Infection................................................................................ 211
Indications of Dialysis in ARF .............................................. 213
8.2. Hypertensive Crisis .................................................................. 214
Saheli Misra
Immediate Evaluation .......................................................... 216
Evaluation for Identifiable Cause ......................................... 216
Features of End Organ Damage............................................ 216
Basic Investigations .............................................................. 216
Advanced Investigations ....................................................... 216
Management ......................................................................... 217
8.3. Hematuria ................................................................................. 220
Indications for Prompt Evaluation ....................................... 220
History .................................................................................. 220
Family History ....................................................................... 221
Basic Investigations .............................................................. 221
Practice Points ...................................................................... 221
SECTION 9: NEUROLOGICAL EMERGENCIES

9.1. Headache ................................................................................... 225
Headache with Fever ............................................................ 225
Headache without Fever ....................................................... 225
Migraine ............................................................................... 225
Pseudotumor Cerebri ............................................................ 227
Raised Intracranial Pressure ................................................. 227
Hydrocephalus with Shunt ................................................... 228
Arteriovenous Malformation and Subarachnoid
Hemorrhage ......................................................................... 229
Hypertension ........................................................................ 229
Trauma .................................................................................. 229
Tension Headache ................................................................ 229
Indications for a CT Scan in a Child with Headache ........... 229
9.2. Status Epilepticus ..................................................................... 231
Etiology ................................................................................. 231
Management ......................................................................... 231
Practice Points ...................................................................... 233
Contents
xix
9.3. Rapid Onset Limb Weakness ................................................... 235

Jaydeep Choudhury
Indications for Hospitalization ............................................. 236
Investigations ........................................................................ 236
Management ......................................................................... 238
SECTION 10: HEMATOLOGICAL EMERGENCIES

10.1. Sickle Cell Disease and Crisis .................................................. 243
Vaso-occlusive Crises ............................................................. 243
Acute Splenic Sequestration Crisis ....................................... 244
Aplastic Crisis ....................................................................... 245
SECTION 11: ENDOCRINAL EMERGENCIES

11.1. Diabetic Ketoacidosis ............................................................... 249
Jaydeep Choudhury
Assessment ............................................................................ 249
Intervention .......................................................................... 249
Investigations ........................................................................ 249
Treatment ............................................................................. 250
Monitoring Initial Progress .................................................. 252
Complications During Treatment ........................................ 252
Cerebral Edema .................................................................... 252
Further Care ......................................................................... 253
11.2. Hypoglycemia in Neonates and Children ............................... 254
Joshi Anand Karketta, Jaydeep Choudhury, Jayanta Bandyopadhyay
Clinical Features ................................................................... 254
Optimum Time to Screen for Hypoglycemia ....................... 256
Blood Sampling .................................................................... 256
Clinical Clues Leading to High Risk Group for
Hypoglycemia ....................................................................... 256
Investigations ........................................................................ 257
Hyperinsulinism ................................................................... 257
Causes of Hyperinsulinism ................................................... 257
Neurodevelopmental Outcome of Hypoglycemia ................ 258
Management ......................................................................... 258
Tapering ................................................................................ 258
Drugs Causing Hypoglycemia .............................................. 259
Practice Points ...................................................................... 260
11.3. Adrenal Insufficiency and Addisonian Crisis ......................... 262
High-risk Group for Adrenal Insufficiency .......................... 263
Signs and Symptoms ............................................................. 263
xx
Investigations ........................................................................ 263

Treatment ............................................................................. 264
SECTION 12: ENVIRONMENTAL PROBLEMS

12.1. Animal Bites .............................................................................. 267
Tapan Kumar Ghosh, Jaydeep Choudhury
Etiology ................................................................................. 268
Clinical Types ....................................................................... 269
Modes of Transmission ......................................................... 269
Diagnosis ............................................................................... 270
WHO Classification of Bites ................................................. 270
Management ......................................................................... 270
Rabies Immunoglobulin (RIG) ............................................. 271
Antirabies Vaccines ............................................................... 272
Pre-exposure Schedule ......................................................... 274
Canine Rabies ....................................................................... 274
12.2. Snake Bite .................................................................................. 276
Clinical Effects ...................................................................... 276
Laboratory Findings and Monitoring ................................... 277
Management ......................................................................... 277
Who should be given Antivenin? .......................................... 278
Neuroparalysis ...................................................................... 279
Supportive Treatment .......................................................... 279
12.3. Scorpion Sting ........................................................................... 281
Indian Scorpions................................................................... 281
Effects of Scorpion Envenomation ....................................... 281
Grading of Clinical Manifestations ....................................... 282
Clinical and Laboratory Monitoring .................................... 282
Management of Grade III Patients in ICU .......................... 282
Advantages of Prazosin ......................................................... 283
Adverse Effects of Prazosin ................................................... 283
12.4. Near Drowning .......................................................................... 284
Etiology ................................................................................. 284
History and Clinical Findings ............................................... 284
Complications ....................................................................... 285
Laboratory Investigations ..................................................... 285
Prehospital Intervention ....................................................... 285
Emergency Department Management ................................. 286
Hospital Admission Criteria ................................................. 286
Contents
12.5.
12.6.
12.7.
12.8.
xxi
Hypothermia ........................................................................ 287

Cerebral Edema .................................................................... 287
General Measures for Management ..................................... 287
Practice Points ...................................................................... 287
Prognosis ............................................................................... 287
Orlowskis Prognostic Scoring System .................................. 288
Burn ........................................................................................... 289
Jaydeep Choudhury
First Aid: To be done at the Site of Burn .............................. 289
Life Support .......................................................................... 289
Degree of Burn ..................................................................... 289
Admission Criteria for Pediatric Burns Patients .................. 290
Fluid Resuscitation ............................................................... 290
Sedation ................................................................................ 290
Infection................................................................................ 291
Stress Ulcer ........................................................................... 291
Topical Treatment ................................................................ 291
Complications ....................................................................... 291
Electrical Burn .......................................................................... 292
Jaydeep Choudhury
Management ......................................................................... 292
Admission Criteria ................................................................ 292
Discharge after Emergency Management ............................. 292
Hyperpyrexia and Hyperthermia ............................................ 294
Jaydeep Choudhury
Common Causes of Hyperpyrexia ........................................ 294
Effective Cooling .................................................................. 294
Drugs and Sympathetic Treatment ...................................... 294
Care of the Unconscious Patient .......................................... 294
Hyperpyrexia or Hyperthermia ............................................ 294
Management ......................................................................... 295
Accidental Hypothermia .......................................................... 296
Factors Influencing Thermoregulatory Balance in
Pediatric Age Group ............................................................. 296
Common Complications of Severe Hypothermia ................ 296
Laboratory Findings and Investigations ............................... 296
Management ......................................................................... 298
Rewarming Techniques ........................................................ 298
Dysrhythmias ........................................................................ 299
Sepsis .................................................................................... 299
Prognosis ............................................................................... 299
Frostbite ................................................................................ 299
xxii
SECTION 13: POISONING

13.1. General Management Principles and Approach to
Unknown Poisoning .................................................................. 305
Management ......................................................................... 305
13.2. Various Poisonings .................................................................... 307
Jayanta Bandyopadhyay, Joshi Anand Karketta
Paracetamol .......................................................................... 307
Iron ....................................................................................... 309
Salicylates .............................................................................. 314
Acid ....................................................................................... 315
Alkali ..................................................................................... 318
Hydrocarbons ....................................................................... 320
Moth Balls (Naphthalene) .................................................... 322
Organophosphorus Compound............................................ 323
Phenothiazines ...................................................................... 325
Tricyclic Antidepressants ...................................................... 327
Beta Blockers ........................................................................ 327
Digoxin ................................................................................. 328
SECTION 14: FOREIGN BODY

14.1. Airway Foreign Body ................................................................ 333
Usual Foreign Bodies Aspirated ........................................... 333
Management ......................................................................... 334
Management of Partial Airway Obstruction ......................... 336
Practice Points ...................................................................... 336
14.2. Foreign Body in GI Tract ......................................................... 339
Predisposing Factors ............................................................. 339
Signs and Symptoms ............................................................. 339
Complications ....................................................................... 339
Investigation ......................................................................... 340
Management ......................................................................... 340
Practice Points ...................................................................... 340
14.3. Button Battery Ingestion .......................................................... 341
Mode of Action ..................................................................... 341
Clinical Effects ...................................................................... 343
Contents
xxiii
Treatment ............................................................................. 344

Battery in the Nose or Ear .................................................... 345
SECTION 15: PSYCHIATRIC BEHAVIORAL AND SOCIAL ISSUES

15.1. Psychiatric Assessment for Nonpsychiatrists ......................... 349
Jaydeep Choudhury
Mental State Examination .................................................... 351
15.2. Nonaccidental Self-Harm ......................................................... 352
Common Predisposing Factors ............................................. 352
Goals of Assessment Interview .............................................. 352
Assessment ............................................................................ 352
15.3. Aggressive Behavior and Violent Child ................................... 355
Few Donts .......................................................................... 355
Few Dos ............................................................................. 355
Management ......................................................................... 355
Practice Points ...................................................................... 356
15.4. Abuse of Children ..................................................................... 357
Indicators of Physical Abuse ................................................. 357
Dating Fractures ................................................................... 358
Further Tests ......................................................................... 358
Indicators of Sexual Abuse ................................................... 358
Medical Management ........................................................... 359
Medicolegal Perspective ....................................................... 360
SECTION 16: TRAUMA AND ORTHOPEDICS

16.1. Head Trauma ............................................................................ 363
Type of Injury ....................................................................... 363
Immediate Priority ............................................................... 363
Practice Points ...................................................................... 366
16.2. Acute Neck Stiffness ................................................................. 367
Life-threatening Conditions ................................................. 367
Causes of Acute Stiff Neck .................................................... 367
16.3. Acute Painful Hip ..................................................................... 369
Transient Synovitis ................................................................ 369
Septic Arthritis ...................................................................... 370
Acute Osteomyelitis .............................................................. 371
xxiv
16.4.
16.5.
16.6.
16.7.
Slipped Upper Femoral Epiphysis (SUFE) .......................... 372

Other Conditions .................................................................. 372
Pulled Elbow ............................................................................. 374
Investigation ......................................................................... 374
Management ......................................................................... 374
Spinal Cord Injury and Spinal Cord Injury without
Radiographic Abnormality (SCIWORA) ................................. 375
Initial Assessment ................................................................. 375
Spinal Immobilization .......................................................... 375
Cervical Spine Injuries ......................................................... 376
Spinal Cord Injury ................................................................ 380
SCIWORA ............................................................................. 382
Blunt Trauma ............................................................................ 384
Basic Principles of Trauma Management ............................. 384
Management ......................................................................... 384
Chest Trauma ....................................................................... 384
Abdominal Trauma ............................................................... 386
FracturesInitial Stabilization and Management .................. 388
Anirban Chatterjee
Management Goals ............................................................... 389
Injuries in the Appendicular SkeletonCommon
Upper Extremity Injuries ..................................................... 389
Immobilization Methods and Optimum Position
for Injuries to the Upper Limb ............................................ 394
Injuries in the Appendicular SkeletonCommon
Lower Extremity Injuries ...................................................... 394
Immobilization Methods and Optimum Position
for Injuries to the Lower Limb ............................................. 394
Injuries to the Axial Skeleton ............................................... 397
SECTION 17: OPHTHALMOLOGICAL EMERGENCIES

17.1. Ophthalmological Issues .......................................................... 401
Lav Kochgaway
Leukocoria ............................................................................ 401
Congenital Cataract .............................................................. 401
Red Eye ................................................................................. 403
Trauma .................................................................................. 405
Periocular Infections ............................................................. 407
Buphthalmos ........................................................................ 408
Shaken Baby Syndrome ........................................................ 408
Contents
xxv
SECTION 18: OTOLARYNGOLOGICAL EMERGENCIES

18.1. Otolaryngological Issues .......................................................... 411
Jaydeep Choudhury
Acute Otitis Externa ............................................................. 412
Acute Otitis Media (AOM) .................................................... 413
Foreign Body in the Nose and Ear ....................................... 414
Epistaxis ................................................................................ 416
Sinusitis ................................................................................. 417
Oral Cavity Lesions ............................................................... 417
SECTION 19: DERMATOLOGICAL EMERGENCIES

19.1. Fever with Rash ......................................................................... 421
History .................................................................................. 421
Evolution of Rashes .............................................................. 425
Diagnosis ............................................................................... 425
Management ......................................................................... 425
19.2. Urticaria and Angioedema ....................................................... 428
Amiya Kumar Mukhopadhyay, Jayanta Bandyopadhyay
Etiology ................................................................................. 429
Risk Factors ........................................................................... 429
19.3. Stevens-Johnson Syndrome (SJS) ............................................. 432
Etiology ................................................................................. 432
Diagnosis ............................................................................... 432
Management ......................................................................... 432
19.4. Toxic Epidermal Necrolysis ..................................................... 435
Etiology ................................................................................. 435
Management ......................................................................... 437
SECTION 20: INFECTIONS

20.1. Fever without Focus .................................................................. 441
Stabilization .......................................................................... 441
Symptoms and Signs of a Child with Serious
Bacterial Infection (SBI) ....................................................... 441
Common Organisms Causing SBI in 0 to 3 Months ............ 442
xxvi
20.2.
20.3.
20.4.
20.5.
20.6.
Common Causes above 3 Months ........................................ 442

Factors that Increase the Predilection of SBI
Infants Less than 3 Months .................................................. 442
Severe and Complicated Malaria ............................................. 445
Jaydeep Choudhury
Clinical Assessment ............................................................... 446
Investigations ........................................................................ 446
Management ......................................................................... 446
Management of Complications ............................................ 448
Dengue ...................................................................................... 450
Jaydeep Choudhury
Undifferentiated Fever ......................................................... 450
Dengue Fever (DF) ............................................................... 450
Dengue Hemorrhagic Fever (DHF) and Dengue
Shock Syndrome (DSS) ......................................................... 451
Clinical Examination ............................................................ 451
Investigations ........................................................................ 451
Dengue Serology ................................................................... 451
Criteria for Hospitalization .................................................. 452
Monitoring DSS .................................................................... 452
Management ......................................................................... 453
Community Acquired Pneumonia ........................................... 454
Jaydeep Choudhury
Age Related Etiology ............................................................ 454
Investigations ........................................................................ 454
Management ......................................................................... 457
Acute Meningitis ....................................................................... 458
Etiology ................................................................................. 458
Investigations ........................................................................ 458
Antibiotic Therapy ................................................................ 459
Prophylaxis ........................................................................... 461
Urinary Tract Infection ............................................................ 462
Jaydeep Choudhury
Etiology ................................................................................. 462
Classification and Clinical Manifestations ............................ 462
Treatment ............................................................................. 464
Antibiotic Therapy ................................................................ 464
SECTION 21: MISCELLANEOUS EMERGENCIES

21.1. Crying and Irritable Child ....................................................... 469
Normal Cry in Infants .......................................................... 469
Pathological Cry Indicating Organic Cause .......................... 469
Contents
xxvii
Approach to Diagnosis .......................................................... 470

Management ......................................................................... 471
Indications for Admission ..................................................... 474
21.2. Penis and Foreskin Problems ................................................... 475
Jaydeep Choudhury
Balanitis ................................................................................ 475
Phimosis ................................................................................ 476
Paraphimosis ......................................................................... 476
Penile Zipper Entrapment Injury ......................................... 477
21.3. Toxic Shock Syndrome ............................................................. 479
Management ......................................................................... 482
21.4. Biochemical Genetic EmergencyInborn Errors of
Metabolism ................................................................................ 484
Jaydeep Choudhury
History .................................................................................. 486
General Principle of Management of Acute Illness .............. 490
Acute Management of Hypoglycemia .................................. 490
Acute Management of Hyperammonemia ........................... 493
Long-term Treatment of IEM .............................................. 493
Metabolic Autopsy ................................................................ 494
SECTION 22: MEDICOLEGAL ISSUES

22.1. Medicolegal Issues in Emergency Room ................................ 499
Jaydeep Choudhury
Documentation in Emergency Ward .................................... 499
Consent in Emergencies ....................................................... 499
Medical Negligence .............................................................. 500
Informing the Police ............................................................. 500
Breaking Bad News ............................................................... 500
Death Certificate ................................................................... 500
Index ..................................................................................................... 503
GENERAL
EMERGENCY
1.1
Setting-up Pediatric
Emergency Department
Pediatric Resuscitation Equipment

Airway
1. Laryngoscope with stylets
i. Straight pediatric blades.
ii. Adult curved blades.
2. Endotracheal tubes Sizes 2.5 to 8.
3. Magill forceps.
4. Suction devices.
5. Soft suction catheters Sizes 6 to 14.
6. Oral, nasal and nasopharyngeal airways.
7. Tracheostomy kit.
8. Needle cricothyroidotomy set.
9. Humidity moisture exchange unit.
Breathing
1. Oxygen masks with reservoir.
2. Self-inflating resuscitation bags with reservoir
i. 240 ml infant size.
ii. 500 ml child size.
iii. 1600 ml adult size.
3. Portable ventilator.
4. Face masks
i. Infant Circular 01, 1, 2.
ii. Child Anatomical 2, 3.
iii. Adult Anatomical 4, 5.
5. Catheter mount and connectors.
6. Ayres T-piece.
Circulation
1. ECG monitor Defibrillator with pediatric paddles.
2. Noninvasive blood pressure (NIBP) monitor With infant and child

size cuffs.
3. Pulse oximeter With infant and child size probes.
4. Capnogram.
5. Intravenous access requirements
i. Intravenous cannulae 18 to 25 g.
ii. Intraosseous infusion needles 16 to 18 g.
iii. Gradual burette.
iv. Intravenous drip sets.
v. Syringes 1 to 50 ml.
6. Intravenous drip monitoring devices, syringe pumps.
7. Cut down set.
8. Central venous catheter set-up with CVP.
9. Pericardiocentesis instruments.
10. Temporary external pacemaker.
Special Trays
1.
2.
3.
4.
Lumbar puncture (LP) set.

Newborn kit including umbilical vessel cannulation devices.
CPAP set.
Urinary catheters Sizes 5 to12.
Fluids
1.
2.
3.
4.
5.
6.
Normal saline (0.9%).

Ringers lactate.
Dextrose infusions 5 percent, 10 percent, 25 percent.
Colloid.
Albumin 5 percent.
Sodium bicarbonate 8.4 percent.
Drugs
1. Oxygen.
2. Anticonvulsants:
i. Phenobarbitone.
ii. Phenytoin.
iii. Diazepam.
iv. Midazolam.
3. Antibiotics: Penicillin, ampicillin, gentamicin, cefotaxime, cefuroxime.
4. Analgesics:
i. Inj. Morphine.
ii. Inj. Pethidine.
iii. Paracetamol tablets, suspension, drops and suppository.
5. Drugs for raised ICP:
i. Frusemide.
ii. Mannitol 20 percent.
Chapter 1.1: Setting-up Pediatric Emergency Department
6. Antiarrhythmic:
i. Lignocaine 1 percent.
ii. Amiodarone.
iii. Adenosine.
iv. Calcium chloride.
7. Vasoactive drugs:
iv. Adrenaline (Epinephrine) 1:10,000.
v. Adrenaline (Epinephrine) 1:1000.
vi. Atropine 0.6 or 1 mg/ml.
vii. Dopamine.
viii. Dobutamine.
ix. Milrinone.
8. Common antidotes:
i. Inj. PAM.
ii. Activated charcoal.
iii. Inj. Desferroxamine.
iv. Inj. Methylene blue.
v. Inj. Flumazenil.
9. Paralyzing agents:
i. Inj. Pancuronium.
ii. Inj. Vecuronium.
iii. Inj. Succinylcholine.
10. Antihypertensive agents:
i. Inj. Sodium Nitroprusside.
ii. Inj. Labetalol.
11. Miscellaneous:
i. Insulin.
ii. Potassium chloride.
iii. Hydrocortisone.
iv. ORS.
v. Inj. Td/TT.
vi. Tetanus and rabies immunoglobulin.
vii. Antisnake venom.
viii. Sodium bicarbonate.
ix. Inj. Magnesium sulfate.
x. Nebulization solutions Salbutamol.
Others
1.
2.
3.
4.
5.
6.
7.
Thermometer.
Sphygmomanometer with various sizes of cuffs.
Measuring tape.
Otoscope, ophthalmoscope.
Weighing machine.
Radiograph view box.
Stick test for glucose.
8.
9.
10.
11.
Chest drain set with under water seal system.

Gloves, sterile gowns, gauze pads, tapes, scalp vein, venous cannula.
Garbage and biohazard collecting bags and bins.
The batteries should regularly be checked.
Location, design and infrastructure of emergency room

Emergency department (ED) should have a wide approach road. Clear and
prominent directions of the way leading to the department should be displayed. ED should be on the ground floor with wide spaced corridor and
car parking.
Radiology department, procedure room, operation theater (OT) at least
for minor procedures and day care OT should be adjacent to the ED.
Plan and way for rapid transfer to the ICU and major OT should be
ready. Dedicated phone line, elevator, electricity back-up (UPS) and internet
access are now a day a must for a busy ED. Admission desk and pharmacy
are the other facilities which should be in close proximity.
The department itself should be spacious to receive patient, segregated accordingly to place them in cubicles, general beds or waiting areas
as per the necessity. The doors should easily accommodate trolleys, portable USG, echocardiography and X-ray machines. There should be separate
work station, resuscitation area, preferably a room, attendants meeting area
and an area separately kept for instruments, gadgets and drugs.
The department should have adequate electrical outlets, oxygen outlet, vacuum outlets and compressed air outlets depending on the capacity
of the ED. Department staff including nurses and paramedical staff should
be dedicated only to the department round the clock and nowhere else.
Separate space should be allotted for toilets, doctors and nurses room.
ED should never be used as a thoroughfare route to other departments.
Nice and attractive cartoons and pictures should be mounted on the walls
to distract and pacify the children.
Drinking water, bank ATM, public telephone booth, public toilet, snack
bar and cloakroom should be arranged by the hospital authority in the
best interest of the patients attendants.
Monitoring and Recording Vital Functions

1.
2.
3.
4.
5.
6.
Respiratory rate.
Heart rate and ECG.
Oxygen saturation.
Noninvasive blood pressure (NIBP).
Temperature (Core and peripheral).
End tidal CO2.
Transferring the Patient

It requires maintaining ABCDE.
Chapter 1.1: Setting-up Pediatric Emergency Department
Airway and Breathing

1. The airway must be patent and secure before moving and throughout
the transfer of the patient.
2. Nasal endotracheal tubes are better secured than oral.
3. The length of the endotracheal tubes must be known before moving
the child.
4. Suction must be working and available throughout the transfer.
i. Portable suction should be there for transporting ventilated babies.
ii. A condenser and humidifier should be used to reduce blockage.
5. Appropriate analgesics, sedatives and muscle relaxants should be used
to transfer the patient safely.
6. Full intubation equipment and drugs should be taken for emergent
intubation or reintubation.
7. Ventilation should be provided by mechanical ventilator rather than
manually.
8. A fully pressurized E sized oxygen cylinder contains 600 liters of gas.
Amount of oxygen required for the journey is calculated as below.
Number of cylinders =
2 duration of journey flow (L/min)

cylinder capacity in L
Circulation
1. Stabilize and optimize perfusion before moving the child.
2. Two separate good intravenous access.
3. Central venous access is necessary for transport of a hemodynamically
unstable or potentially unstable patient.
4. Blood pressure monitoring throughout the transfer either indirectly
or direct invasive method.
5. Heart rate and rhythm.
6. Inotrope infusion pumps.
7. Correction of shock, hypoglycemia, acidosis and electrolyte imbalances.
Disability
1. The development of rising intracranial pressure should be anticipated
and treated.
2. Spinal board in a case of suspected spinal injury.
3. Fractured limbs to be immobilized.
Exposure
1. Use blankets to prevent hypothermia.
2. Ensure the transport vehicle is adequately heated.
3. Do not use cold intravenous infusions, warm them before using.
Documentation in ED
1.
2.
3.
4.
5.
6.
Name, age, sex and weight.

All clinical findings, treatments and procedures should be documented.
All details of resuscitation.
All investigations: (with results or pending).
Notes, X-rays and cross matched blood.
Consent for management and transfer.
Bibliography
1.
2.
Macknay-Jones K, Molyneux ER, Philips B, Susan W Editors. Advanced Pediatric Life Support, 4th edition, Blackwell publishing, 2003.
Singhi S, Bharti B. Setting-up a pediatric emergency room. Indian J Pract
Pediatr 2006;8:6-13.
1.2
Approach to a Child in Pediatric
Emergency Department
Children present to the emergency department more often than adults.

Smaller children are more difficult to assess as most of the time they present
with nonspecific signs and symptoms. A strong clinical judgement is the
cornerstone for determining the severity of the condition in children.
Warning Symptoms in History

1.
2.
3.
4.
5.
6.
Child with persistent lethargy, not smiled over a few hours.

Child with prolonged irritability or inconsolable child.
Child taking less than 50 percent of normal fluids.
No urine output for six hours.
Seizure, cyanosis, pallor or apnea.
Parental concern out of proportion to childs illness.
Warning Signs in Examination

1. Respiratory distress, grunting
2. Tired or looks sicker than usual illness
3. High pitched cry
4. Drowsy
5. Floppy
6. Pale
7. Alteration in vital signs
8. Low saturation
9. Signs of shock
10. Full or bulging fontanelle
11. Nonblanching petechiae or purpura
12. Bilious vomiting.
Decision-making in Pediatric Emergency

It is the synthesis of the whole process of balance of history, examination,
knowing when to trust the parents, intuition and maintaining objectivity.
Sometimes the features are glaring and decision making is very easy, at
10
other times there is no definite pointer but somehow one feels that everything is not right and these are the difficult situations. But in pediatric
emergency probably a bit of over doing is better that taking a chance. When
in doubt it is better to admit a patient for observation.
Normal Vital Signs

The vital signs like respiratory rate and heart rate are crucial points in
examination. Unlike adults the children are unique in this sense as both
this parameters change with age. The normal weight, respiratory and
heart rate for children of different age groups and the differentiating
features between sick and well children are shown in Tables 1.2.1 and
1.2.2 respectively.
Things to be done in Emergency Room

1. Get the relevant history from the parents or the reliable informers
only.
2. Do not allow a crowd to gather it jeopardises the whole process and
management.
TABLE 1.2.1: Normal weight, respiratory and heart rate in children of different age groups
Age
Birth
3 months
6 months
1 year
2 years
4 years
6 years
8 years
10 years
12 years
14 years
Weight (kg)
RR / min
HR/ min
2.5 3.5
6
8
10
12
15
20
25
30
40
50
40 60
30 50
30 50
30 40
20 30
20
16
16
16
16
16
100-160
100-160
100-160
100-160
100-150
80 130
70 120
70 110
60 100
60 100
60 100
TABLE 1.2.2: Differences between sick and well children

General behavior
Mood
Wakefulness
Tone
Vital signs
Well child
Sick child
Plays with toys

Interacts with parents
Normal
Alert, smiles
Consolable if cries
Awake
Normal sleep pattern
Normal
Afebrile
RR and HR normal
Not playful
Not much interaction
Irritable
Unhappy
Cries more than usual, inconsolable
Sleepy
Difficult to waken
Floppy
Fever
Tachypnea
Tachycardia
Chapter 1.2: Approach to a Child in Pediatric Emergency Department
11
3. All the children attending the emergency department should be attended as an emergency situation at least immediately by the nurses
if the doctor is busy with some other patient.
4. Competent nurses are as important in an emergency department as
the doctors.
5. Most of the time the seriousness of the condition can be assessed immediately by a gross inspection.
6. None of the children should be dismissed without proper assessment.
7. If there is any doubt after clinical assessment, it is always better to
admit a child brought to the emergency department. If beds are not
available, the child should be stabilized first before referring to other
hospital.
8. Emergency equipment should be available, such as oxygen supply,
sucker apparatus, bas and mask ventilation.
Bibliography
1.
Royal Childrens Hospital 2003 Clinical practice guidelines resuscitation:

Emergency drug and fluid calculator. Melbourne, Australia. URL: http:// www.
rch.org.au/ clinical guide/
1.3
Early Assessment and
Emergency Triage
Triage includes early patient assessment, priority rating, first aid, control of
patient flow, assignment of correct area of care, initiation of diagnostic measure and liaising with relatives and health care professionals. Many early
hospital deaths can be prevented by an accurate triaging and thus instituting
quick treatment. Following is an example of triage categories though the
process may be never perfect leaving the chance of patients having more
serious illness than the category suggests.
Priority 1Severe Life-threatening Emergency

Management should start immediately and needs to be shifted to resuscitation area equipped with resuscitation backup.
1. Cardiac or respiratory arrest.
2. Hypovolemic shock.
3. Severe trauma (pediatric trauma score 8 or below).
4. Coma (GCS 10 or below).
5. Status epilepticus.
6. Anaphylaxis with cardiorespiratory decompensation.
Priority 2Acute Medical Problems or Distress

Management should start within 10 minutes and should be shifted to acute
care area with arrangement for basic life support.
1. Severe respiratory distress.
2. Febrile child with signs of sepsis.
3. Developing petechial rash.
4. Venomous bite.
5. Fractured shaft of femur.
6. Fractured cervical spine with cord damage.
7. Multiple fractures.
8. Burn more than 10 percent.
Chapter 1.3: Early Assessment and Emergency Triage
13
Priority 3Semiurgent Acute Medical Problems

Should be attended in 10 to 30 minutes. Also should be kept in acute care
area.
1. Moderate respiratory distress.
2. Potentially venomous bite in asymptomatic patient.
3. Febrile infant younger than 3 months.
4. Febrile child with irritability, drowsiness or pallor.
5. Moderate dehydration.
6. Limb fractures.
Priority 4Nonurgent Acute Medical Problems

Should be attended in 30 to 60 minutes.
1. Recent seizure activity.
2. Mild dehydration.
3. Suspected limb fractures with no deformity and minimal pain.
4. Nontraumatic limp.
Priority 5Condition is Stable and will not Deteriorate as a

Result of Waiting
1. Uncomplicated laceration.
2. Febrile older child in absence of signs of sepsis.
3. URTI in absence of fever.
Though this is an outline, the list can not be exhaustive and each patient needs individual assessment. A continuous assessment and monitoring
of already categorized patient is also necessary by triage station from patient deteriorating into more urgent category while waiting for treatment.
Remember, watchful trained eyes looking for basic signs of life like respiratory rate, heart rate, work of breathing, sensorium, pulse volume, capillary
refill, cyanosis and saturation combined with clear idea about differential
diagnoses and potential outcome of early institution of treatment are the
essence of successful triage program.
Bibliography
1.
Pediatric Emergency Medicine: Departmental policy manual; January 2005,

Mater Health Services, Brisbane, Australia.
RESUSCITATION
2.1
Cardiopulmonary
Resuscitation
Jayanta Bandyopadhyay, Joshi Anand Karketta,
Jaydeep Choudhury
A sudden cardiac arrest is uncommon in children. Cardiac arrest is usually

the terminal event of progressive respiratory failure or shock. Any emergency set up should be well equipped with procedures for cardiopulmonary
resuscitation (CPR).
Airway
1. Mild neck extension is preferable (Childs head and occiput are proportionately large causing neck flexion). One can use a folded towel
placed under the neck and shoulder.
2. Open the airway by head tilt-chin lift method. If cervical injury is suspected, open the airway using a jaw thrust without head tilt.
3. Clear airway from secretions, vomits and remove foreign bodies. In
neonates and infants this can be effectively done with bulb mucus sucker
(Figure 2.1.1).
FIG. 2.1.1: Bulb mucus sucker
18
4.
Oropharyngeal and nasopharyngeal airways for maintaining an open airway.

i. Oropharyngeal airway in unconscious patient, i.e. with no gag
reflex. The size is determined by the distance from the central
incisors to the angle of the mandible.
ii. Nasopharyngeal airway is better tolerated than oral airway by
patients who are not deeply unconscious. The size is determined
by the distance from the tip of the nose to the tragus of the ear.
Breathing
1. Use 100 percent oxygen during resuscitation.
2. Bag-mask ventilation can be as effective as endotracheal intubation:
i. Use a self-inflating bag with a volume of 450 to 500 ml (Figure 2.1.2).
ii. Maintain oxygen flow of 15 L/min into a reservoir attached to a
bag.
iii. The mask should fit over the mouth and nose to provide a tight
seal and avoid any air leakage.
3. Ventilation through an endotracheal tube (ETT) (Figure 2.1.3).
Size for children 1 to 10 years of age is determined as ETT internal
diameter (mm) = (age in yrs/4) + 4.
FIG. 2.1.2: Bag and mask ventilation
FIG. 2.1.3: Endotracheal tube
Chapter 2.1: Cardiopulmonary Resuscitation
19
4. Laryngeal Mask Airway (LMA): When endotracheal intubation is not

possible LMA is an acceptable adjunct for experienced providers.
To Minimize Gastric Inflation

i. Avoid excessive peak inspiratory pressures (e.g. ventilate slowly and
watch chest rise, deliver only the volume needed to produce visible
chest rise).
ii. Apply cricoid pressure to obstruct the esophagus.
iii. Pass NG tube after intubation because a gastric tube interferes with
the gastroesophageal sphincter, allowing possible regurgitation.
Excessive Ventilation is Detrimental Because:
i. It impedes venous return and therefore decreases cardiac output,
cerebral blood flow and coronary perfusion by increasing intrathoracic pressure.
ii. Causes air trapping and barotraumas in patients with small airway
obstruction.
iii. Increases the risk of regurgitation and aspiration.
Circulation
1. Check pulse (Brachial artery in infantscarotid or femoral artery in
children).
2. Start cardiac compressions when heart rate <60 beats/min with signs
of poor perfusion. Two thumbencircling hands chest compression
and bag and mask ventilation is shown in Figure 2.1.4.
Characteristics of Good Chest Compressions

1. Push fast at a rate of 100 compressions/min.
2. Push hard to depress the chest 1/3 to 1/2 of the anterior-posterior
diameter of the chest.
FIG. 2.1.4: Two thumbencircling hands chest compression and bag-mask ventilation
20
3. Release completely to allow the chest to fully recoil after each compression.
4. Minimize interruptions in compressions.
Recommended Chest Compression-ventilation Ratio

1. One rescuer: Cycles of 30 compressions and two breaths.
2. Two rescuers: Cycles of 15 compressions and two breaths.
3. When an advanced airway is established (e.g. ETT or LMA):
i. Give continuous chest compressions without pauses for breaths.
ii. Give 8 to 10 breaths/minute.
iii. Check rhythm every two minutes and change the compressor
role to prevent fatigue and deterioration in quality and rate of
chest compressions.
iv. The switch should be done in less than five seconds to minimize
interruption in chest compression.
v. If the pulses are present but no breathing, give 12 to 20 breaths
per minute (1 breath every 3 to 5 seconds).
The method of chest compression is shown in Table 2.1.1.
Vascular Access
If one cannot achieve a reliable access quickly, an intraosseous (IO) access
should be established.
Fluids
1. Isotonic crystalloid solution to treat shock (20 ml/kg of normal saline
as quickly as possible). Repeated boluses may be necessary.
2. HypotensionSystolic blood pressure less than 5th percentile of normal for age:
i. <60 mm Hg in term neonates.
ii. <70 mm Hg in infants.
iii. <70 mm Hg + (2 age in yrs) in children 1 to 10 years
iv. <90 mm Hg in children >10 years of age.
3. Glucose containing fluids are not indicated during CPR unless hypoglycemia is present.
TABLE 2.1.1: Method of chest compression in infants and children
Cardiac compressions
Infants
Children
Rate/min
Depth
Site
100
1/3 of AP chest diameter
Lower half of the sternum not
over the xiphoid (below
intermammary line)
2 fingers technique. OR
2 thumbencircling hands
technique (preferred).
100
1/3 to 1/2 of AP chest diameter
Lower half of the sternum not
over the xiphoid
Technique
Heel of one hand or two hands

technique
21
Drugs
1. Drugs are preferably administered through IV or IO route than by
ETT.
2. If vascular access cannot be established, the following drugs can be
given via ETT LEAN lidocaine, epinephrine, atropine and naloxone. Flush with a minimum of 5 ml normal saline followed by 5 assisted
manual ventilations. If CPR in progress, stop chest compressions briefly
during administration of medications.
3. Epinephrine dose in cardiac arrest = 0.01 mg/kg of 1:1000 epinephrine as the first and subsequent IV doses.
Medications for pediatric resuscitation and arrhythmias that should be
available in pediatric emergency and medications to maintain cardiac output and for postresuscitation stabilization are shown in Tables 2.1.2 and
2.1.3 respectively.
* flush with 5 ml of normal saline and follow-up with 5 ventilations
Sodium bicarbonate
Procainamide
Naloxone
Magnesium sulfate
Lidocaine
Glucose
Calcium chloride (10%)

Epinephrine
Atropine
Bolus 1 mg/kg IV/IO

Maximum dose 100 mg
Infusion 20-50 g/kg/min ET* 2-3 mg
25-40 mg/kg IV/IO over 30 min, may be given faster in
Torsades pointes
Maximum dose 2 g
<5 y or 20 kg 0.1 mg/kg IV/IO/ET*
5 y or >20 kg 2 mg IV/IO/ET*
15 mg/kg IV/IO over 30-60 min adult dose 20 mg/min IV infusion
up to total maximum dose 17 mg/kg
1 mEq/kg/dose IV/IO slowly
Adenosine
Amiodarone
Dose
0.1 mg/kg (max 6 mg)
Repeat dose 0.2 mg/kg (max 12 mg)
In pulseless VT or VF 5 mg/kg IV/IO
Repeat up to 15 mg/kg, maximum 300 mg.
Infusion 25 mcg/kg/min for 4 hrs followed by
5-15 mcg/kg/min continuous.
0.02 mg/kg IV/IO 0.03 mg/kg ET* repeat once if needed
minimum dose 0.1 mg maximum single dose in child 0.5 mg,
in adolescent 1 mg
20 mg/kg IV/IO (0.2 ml/kg)
0.01 mg/kg (0.1 ml/kg 1:10 000) IV/IO 0.1 mg/kg
(0.1 ml/kg 1:1000) ET* maximum dose 1 mg IV/IO; 10 mg ET*
0.5-1 g/kg IV/IO
Medication
TABLE 2.1.2: Medications for pediatric resuscitation and arrhythmias

Remarks
Use lower doses to reverse respiratory depression associated with

therapeutic opioid use (1-15 g/kg)
Monitor ECG and BP use
caution when administering with other drugs that prolong QT
After adequate ventilation
10% dextrose diluted with 5-10 ml/kg 25%

dextrose diluted with 2-4 ml/kg
50% dextrose diluted with 1-2 ml/kg
Slowly
May repeat every 3-5 min
Higher doses may be used with organophosphate poisoning
Monitor ECG
Rapid IV/IO bolus
Monitor ECG and BP
Use with caution when administering with
other drugs that prolong QT
22
23
TABLE 2.1.3: Medications to maintain cardiac output and for postresuscitation stabilization
Medication
Dose
Comment
Dobutamine
Dopamine
2-20 g/kg/min IV/IO

2-20 g/kg/min IV/IO
Epinephrine
0.1-1 g/kg/min IV/IO*
Norepinephrine
Sodium nitroprusside
0.1-2 g/kg/min*
1-8 g/kg/min
Inotrope, vasodilator
Inotrope, chronotrope; renal and splanchnic vasodilator in low doses; pressor in
high dose
Inotrope, chronotrope, vasodilator in low
doses; pressor in higher doses
Inotrope, vasopressor
Vasodilator; prepare only in D5W
6 body weight (in kg) = mg of drug to add to 100 ml D5W then, an IV rate of 1 ml/h delivers 1 g/
kg/min of drug.
*0.6 body weight (in kg) = mg of drug to add to 100 ml D5W, then, an IV rate of 1 ml/h delivers 0.1
g/kg/min of drug.
Bibliography
1.
2.
3.
4.
American Heart Association in collaboration with International Liaison

Committee on Resuscitation and European Resuscitation Council. From the
2005 International Consensus Conference on Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care Science With Treatment Recommendations, Part 6.
American Heart Association. Part 12: Pediatric Advanced Life Support.
Circulation. 2005;112:IV-167-IV-187.
American Heart Association. Part 11: Pediatric Basic Life Support. Circulation.
2005;112:IV-156-IV-166.
Pediatric Basic and Advanced Life Support. Circulation 2005;112: III-73-III90.
2.2
Shock
Joshi Anand Karketta, Jayanta Bandyopadhyay,
Jaydeep Choudhury
Shock results from inadequate blood flow and oxygen delivery to meet
tissue metabolic demands.
Types of Shock
1. Hypovolemic: Results from intravascular volume loss, hemorrhage and
interstitial loss. (e.g. gastroenteritis, burns, GI bleeding, sepsis and intestinal obstruction).
2. Distributive: Due to vasodilation, resulting in a relative hypovolemia.
(e.g. anaphylaxis, spinal shock and sepsis).
3. Cardiogenic: Due to impairment of cardiac contractility (e.g. congestive heart failure, cardiomyopathy, sepsis).
4. Septic: Sepsis can lead to systemic vasodilation, intravascular fluid leak
into tissue third spaces and depress myocardial function. Mainly caused
by Gram negative bacteria (endotoxic shock).
5. Obstructive: It is due to mechanical obstruction to ventricular flow causing primary circulatory derangement (e.g. tension pneumothorax, cardiac
tamponade, coarctation of the aorta and severe valvular stenosis).
Clinical Features
If not recognized early and treated promptly, the child will progress from
compensated to decompensated to irreversible shock and ultimately cardiopulmonary arrest. Recognition of cardiopulmonary deterioration
requires rapid physical examination in less than 30 seconds.
The three vital determinants for assessment of a child in shock are
peripheral perfusion, pulse rate and blood pressure.
Compensated Shock
The vital organ functions like brain and heart are conserved by sympathetic reflexes which increase the systemic arterial resistance and divert
blood from nonessential tissues:
1. Tachycardia.
2. Cool extremities.
Chapter 2.2: Shock
25
3. Prolonged capillary refill (despite warm ambient temperature).

4. Weak peripheral pulses compared with central pulses.
5. Normal blood pressure.
Decompensated Shock
It is a state of inadequate end-organ perfusion. Manifested with signs of
compensated shock and in addition the following may be present:
1. Depressed mental status.
2. Decreased urine output.
3. Metabolic acidosis.
4. Weak central pulses and undetectable peripheral pulses.
5. HypotensionSystolic blood pressure <5th percentile of normal for
age:
i. <60 mm Hg in term neonates.
ii. <70 mm Hg in infants.
iii. <70 mm Hg + (2 age in yrs) in children 1 to 10 years.
iv. <90 mm Hg in children >10 years of age.
Irreversible Shock
It occurs as a consequence of decompensated shock not managed properly
and at right time. Damage to the vital organs is severe and recovery does
not occur even with adequate restoration of circulatory volume.
A dehydrated child is shown in Figure 2.2.1.
Investigations
Laboratory tests are useful in assessment of the severity of physiological
derangement, determining the cause and monitoring, but it is not essential for initial evaluation.
Blood: CBC, electrolytes, HCO3, renal and liver function test, blood culture, ABG.
Chest X-ray: May be helpful to determine cardiomegaly and hemorrhage.
FIG. 2.2.1: A dehydrated child (For color version see Plate 1)
26
Management
The treatment priorities and stepwise assessment of a child in shock is
shown in Flow chart 2.2.1.
Treatment
1. Ensure the ABCs and administer 100 percent supplemental oxygen,
2. Secure 2 large-bore IV lines. If vascular access is not available insert
intraosseous route,
3. Intravenous fluids: Administer 20 ml/kg of 0.9 percent NS over 10-15
minutes. If no improvement may repeat the cycle. If no response to
fluids, colloid can be used (5% albumin, or blood products).
4. In severe hypovolemia or sepsis more than 60 ml/kg of volume may be
required in the first hour of resuscitation. Consider central venous pressure (CVP) monitoring.
5. If CVP <10 mm Hg, continue fluid therapy CVP >10 mm Hg with
poor perfusion, give vasoactive agents.
6. Place urinary catheter and maintain urine output 1-2 ml/kg/h. Can use
furosemide 1 mg/kg/dose IV after restoring intravascular volume.
7. If hypoglycemia is present, give IV dextrose 0.5-1 g/kg.
8. If the patient has refractory central hypotension or a cardiogenic shock
inotropic agents must be employed. Acidosis usually is corrected with
volume supplementation and optimal ventilation. In persistent shock
Flow chart 2.2.1: Treatment priorities and stepwise assessment
Chapter 2.2: Shock
27
or severe acidosis (PH<7.15 or HCO3 <10 mEq/l) give NaHCO3

1 mEq/kg IV over 10 to 15 min before correcting acidosis correct hypocalcemia and assure adequate ventilation). Initial coverage with
empiric antibiotics is essential in critical patients. Corticosteroid is
debated. It is lifesaving in adrenal cortical insufficiency.
Bibliography
1.
2.
American Heart Association. Part 12: Pediatric Advanced Life Support.

Circulation 2005;112:IV.
Barkin R, Rosen P. Emergency Pediatrics: A Guide to Ambulatory Care, 1999.
5th edition.
2.3
Coma
Mahasweta Chaudhuri, Jayanta Bandyopadhyay,
Jaydeep Choudhury
Clinical status of a patient can be divided into four typesalert, lethargy,

stuporous and coma. Coma is defined as the state of unarousable unresponsiveness; patient lies without spontaneous movement and intelligible
speech. May respond to noxious stimuli by purposeful withdrawal but not
localize pain with discrete, defensive movements. A patient presenting with
coma should be considered a medical emergency.
Etiology
Cerebral Hypoxemia/Ischemia
Severe anemia, apnea, asphyxia, CO poisoning, drowning, respiratory failure, shock, cerebrovascular event.
Epilepsy
Postictal state, status epilepticus.
Traumatic
Concussion, contusion, intracranial hemorrhage, shaken baby syndrome.
Vascular
Hypertensive encephalopathy, venous sinus thrombosis.
Infectious Diseases
Encephalitis, meningitis, cerebral malaria, septic shock, acute disseminated
encephalomyelitis (ADEM).
Raised Intracranial Pressure

Mass lesions (abscess, empyema, hemorrhage or pressure tumor), cerebral
edema, hydrocephalus, malfunction of a ventriculoperitoneal shunt.
Chapter 2.3: Coma
29
Metabolic and Endocrine Disorders

Diabetic ketoacidosis, adrenal insufficiency, hypopituitarism, hypo/hyperglycemia, hyper/hyponatremia, hypocalcemia, hypomagnesemia, liver
failure, renal failure, uremia, inborn errors of metabolism, Reyes syndrome.
Toxic
Substance abuse (alcohol, hallucinogens, opiates, volatile agents), clonidine,
paracetamol, salicylates, lead, other toxins.
History
Clues to the causes of coma should be sought by interviewing the attendants:
1. Time: Course of changes in mental state (behavior, feeding,
schoolwork)It can be sudden in case of ruptured intracranial
aneurysm, cardiac arrest or hemorrhage. Gradual, progressive onset
favors a metabolic problem, including neurometabolic diseases.
2. History of fever in the recent past, accompanying focus of infection,
ear discharge may indicate CNS infection or a parainfectious process.
3. Recent infectious illness should lead to consideration of ADEM, Reyes
syndrome or mitochondrial disorders.
4. Headache may suggest raised intracranial pressure.
5. Episodic coma suggests drug ingestion, epilepsy, inborn errors of metabolism.
6. Family historyEpilepsy or migraine.
7. Drugs or toxins present in the house.
8. History of head trauma.
9. Past historyChildren with diabetes mellitus can present with hypo or
hyperglycemic coma. One can present with uremic encephalopathy in
renal failure. A child with cyanotic heart disease may suffer from cerebral abscess or infarction.
Physical Examination
1. TemperatureHypothermia is noticed in sepsis, hypothyroidism, or
environmental exposure. Hyperpyrexia is present in infectious causes,
thyrotoxicosis or toxin exposure.
2. Smell Alcohol, glue, ketones, bitter almonds (cyanide), phenol.
3. CardiovascularBlood pressure, pulse rate and rhythm, peripheral
perfusion. Bradycardia is encountered in raised ICP and hypothyroidism.
4. Hypotension is seen in massive hemorrhage, septic shock or dissecting aneurysm. Hypertension is a feature of raised ICP.
5. SkinAbnormal pigmentation (Addisons disease), anemia, bruising,
jaundice, needle marks, petechiae, sweating. Petechial rashes point to
a diagnosis of meningococcemia.
30
6. Neurological posture, evidence of a ventricular shunt, level of consciousness, localizing signs, papillary responses, examination of the
fundi, signs of trauma to the head.
7. Respiration, color (cyanosis), rate and pattern of breathing.
Neurological Examination
1. Level of Consciousness: Modified Glasgow coma scale (GCS) as shown
in Table 2.3.1 has been used in children and infants to assess the duration and depth of altered consciousness.
2. Attitude and posturing: Resting position and spontaneous movements
should be documented. Hemiparesis, focal motor seizure, or any asymmetrical finding indicates structural brain lesion, whereas symmetrical
lesion is usually seen in metabolic coma. Decorticate rigidity indicates
structural lesion of cerebral hemisphere or diencephalons whereas
decerebrate rigidity indicates upper brainstem lesions. Medullary lesions cause flaccidity.
3. Respiration: Abnormal respiratory pattern in coma helps in localization:
i. Cheyne-Stokes respirationBilateral hemispheric or diencephalic lesions.
ii. Apneustic respirationUpper pontine lesions.
iii. Cluster breathingLower pontine or upper medullary lesions.
iv. Ataxic respirationLower medullary lesions.
v. Central neurogenic hyperventilationMidbrain or upper pontine lesion.
vi. Kussmaul breathingMetabolic acidosis.
TABLE 2.3.1: Modified GCS
Response
Eye opening
(i)
Spontaneous
(ii) To speech
(iii) To pain
(iv) None
Best verbal response
(i)
Smiles, oriented to sound, follows object, interacts
(ii) Consolable cry
(iii) Inconsistently consolable cry
(iv) Inconsolable cry, restless, agitated, unaware of environment or parents
(v) No response
Best motor response
(i)
Spontaneous movement/obeys verbal command
(ii) Localizes to supraocular pain
(iii) Withdraws
(iv) Abnormal flexion to pain
(v) Abnormal extension to pain
(vi) None
Grading 13-14 Mild, 9-12 Moderate, <8 severe
Score
4
3
2
1
5
4
3
2
1
6
5
4
3
2
1
Chapter 2.3: Coma
31
4. Brainstem function:
i. Pupillary response: Assuming the visual pathways to the lateral geniculate body are intact, assessment of the pupillary responses is
important in localizing the site of coma and separating structural from toxic/metabolic causes, as pupillary responses in the
latter are intact.
a. Unilateral fixed dilated pupilUncal herniation or rupture
of posterior communicating artery aneurysm.
b. Unilateral constrictionHorners syndrome.
c. Bilateral pinpoint pupilsPontine lesion or opiate poisoning.
d. Bilateral midpositionNonreactive in midbrain lesion and
Reactive in metabolic causes.
e. Bilateral dilated and fixedSevere midbrain damage.
ii. Ocular motility: It is an important clinical indicator of the site of
lesion in coma.
If there is spontaneous eye movement, look for the following.
a. Conjugate spontaneous roving movements indicate an intact
brain stem.
b. Conjugate lateral deviationLook towards the lesion indicates cerebral hemispheric lesion and away from the lesion is
seen in brainstem damage.
c. Ocular bobbing indicates bilateral pontine or cerebellar lesion
d. Skew deviation occurs with posterior fossa lesions.
e. Persistent adduction in paresis of VI cranial nerve.
f. Persistent abduction in paresis of III cranial nerve.
g. Dysconjugate gaze in horizontal plane indicates intoxication.
h. Downward deviation of the eyes indicates bilateral thalamic
or subthalamic lesions and metabolic coma.
If there is no spontaneous eye movements, then ocular motility can be tested by oculocephalic reflex (Dolls eye
maneuver) and oculovestibular reflex (Caloric testing). The
methods of the tests are shown in Table 2.3.2.
iii. Fundoscopic examination: Assess for papilledema and any hemorrhage.
TABLE 2.3.2: Methods of testing oculocephalic and oculovestibular reflexes
Oculocephalic reflex
Oculovestibular reflex
- Eyes move conjugately to the opposite

direction to head movement: Normal
- Lateral gaze palsy: Brainstem lesion
- No movement: Pontine lesion
- Nystagmous with fast component away

from site of stimulation: Normal
- No nystagmus or dysconjugate response:
Brainstem lesion
- Full deviation towards the stimulated side:
Cerebral hemispheric lesion with intact
brain stem
32
iv. Other cranial nerve reflexes: Corneal reflexes (V and VII cranial
nerves); gag and cough reflexes (IX and X cranial nerves) should
also be assessed. Corneal reflex is retained until coma is very
deep.
5. Signs of meningeal irritation: Presence of meningeal signs indicates
meningitis or subarachnoid hemorrhage and parenchymal bleed with
intraventricular extension.
Clinical differentiation of toxic, metabolic or infectious causes of coma
from structural causes of coma like supratentorial and infratentorial coma
are shown in Table 2.3.3.
Investigations
1. Blood sugarIn all patients presenting with coma or altered sensorium, blood sugar or blood glucose should be tested with Dextrostix.
Treatment should not be delayed of symptomatic hypoglycemia awaiting this result.
2. Full blood count, malarial parasite in peripheral smear.
3. Blood culture.
4. Consider coagulation screen before considering a lumbar puncture.
5. If hypoglycemicMeasure blood ketones. Insulin, growth hormone
and cortisol may be measured if possible.
6. Urea and electrolytes.
7. Blood Gas, including arterial lactate.
8. Liver function testsConsider serum ammonia in case of suspected
hepatic coma, Reyes syndrome or urea cycle defect.
9. Thyroid function tests.
10. UrinalysisConsider toxicology screen of urine and blood if indicated.
11. CT scan or MRI brainIf trauma or clinical suspicion of child abuse,
focal neurodeficit. Initial normal CT does not rule out an evolving
lesion of an infection or metabolic disorder.
12. CSF analysisLumbar puncture (LP) is contraindicated in presence of
coma (GCS <9), raised intracranial pressure or unstable clinical state. If
meningitis is suspected but LP is contraindicated, start antibiotics.
13. Cervical spine imaging Protect neck until injury has been excluded
by standard criteria in cases of trauma or possible trauma. It is often
not possible to exclude cervical spine injury in a comatose child. May
need to CT scan of upper cervical spine in trauma.
TABLE 2.3.3: Differences between metabolic and structural coma
Toxic/metabolic/infectious
Supratentorial lesions
Infratentorial lesions
i. Confusion precedes motor signs

ii. Pupillary reactions
preserved.
iii. Symmetrical motor responses
iv. Asterixis, myoclonus
v. Hyper/hypoventilation
i. Initial focal signs

ii. Rostral to caudal
progression
i. Preceding brainstem
dysfunction
ii. Sudden onset
iii. Cranial nerve palsies
iv. Early respiratory
disturbances
Chapter 2.3: Coma
33
14. MRI provides better visualization of brainstem and cerebellar structures, venous sinuses, diffuse disorders, for example in inborn errors
of metabolism or hypoxic encephalopathy.
15. EEGSerial EEG is more useful. Relatively specific in herpes simplex
encephalitis. It helps in detection of nonconvulsive stats epilepticus as
a cause of coma.
Management
Early appropriate supportive care is essential to avoid preventable secondary insults and optimize the neurological outcome. Evaluation and
stabilization of the patients airway, breathing and circulation (ABCs) must
proceed simultaneously with assessments of the depth of coma and the
presence of raised intracranial pressure (ICP). Any rapidly correctable cause
of coma must be immediately corrected.
Airway
Ensure adequate airway. Use airway adjunct oropharyngeal airway, nasopharyngeal airway, LMA or intubate if unable to maintain airway. If
GCS <8 and clinical circumstances do not suggest improvement or imminent herniation, then intubation is indicated to secure airway. Even if
spontaneously breathing with normal gas exchange, many comatose children will benefit from intubation, especially if they have intracranial
hypertension.
Breathing
Give oxygen, monitor oxygen saturation, and assess rate and pattern of
breathing. Supplemental oxygen is indicated for hypoxia, but should not
be given routinely to comatose children with normal circulation and oxygen saturation.
Circulation
Assess for signs of shock and treat as indicated. The aim of fluid therapy
in raised ICP is to maintain adequate cerebral perfusion pressure (CPP).
CPP = Mean arterial pressureIntracranial pressure. Give normal saline or Ringers lactate to maintain BP and perfusion. What must be
restricted are hypotonic fluids such as 1/5th normal saline in 5 percent
dextrose (Isolyte P). The dextrose will be metabolized with a resultant
hypotonic fluid that can exacerbate cerebral edema and ICP. Enteral feeds
should be started at the earliest.
Hypoglycemia
Bolus of 10 percent dextrose 5 ml/kg IV, followed by a 10 percent dextrose
infusion at 4 ml/kg/hour (7 mg/kg/min) with close monitoring of blood glucose.
34
Hyperglycemia
Due to stress or diabetic ketoacidosis.
Drugs
If opioid toxicity is suspectedNaloxone 0.1-0.8 mg /kg IV (maximum
dose 2 mg). Avoid flumazenil, which may induce convulsions in mixed overdoses, particularly if tricyclic antidepressants have been taken. Isolated
benzodiazepine overdose does not cause significant respiratory depression
and children are best managed with simple observation.
Specific Therapy
After stabilization, a rapid approach to diagnosis is imperative so that specific therapy can be given.
1. Known poisoningSpecific antidotes.
2. Hypertensive encephalopathyAntihypertensives.
3. Space occupying lesionsNeurosurgery.
The stepwise approach to diagnosis and management of coma in children is shown in Flow chart 2.3.1.
Emergency Management of Raised Intracranial Pressure

GCS <9 and Cushings triad of hypertension, bradycardia, abnormal respiration and/or fixed, dilated pupil(s).
1. AirwayOxygenate and intubate.
2. VentilationAvoid hypercapnea with an aim to maintain a pC02 of 30
to 35 mm Hg.
3. Osmotic therapy: Use 3 percent NaCl, 3 ml/kg IV given as a rapid
infusion or Use mannitol 0.5g to 1.0g/kg (2.5 to 5ml/kg of 20% mannitol). Mannitol is indicated acutely for patients in whom there is a strong
clinical suspicion of raised ICP or imminent herniation. In the hypotensive/hypoperfused patient, hypertonic saline may be the
osmotherapy of choice for reducing ICP while maintaining MAP/CPP.
4. Sedation and pain reliefFor example, morphine and midazolam.
5. Elevate head to 30.
6. Control feverGive paracetamol intragastrically or rectally 10 to
15 mg/kg q 4 hrly.
7. In raised ICP refractory to medical measures, surgical decompression
has been shown to improve survival and functional outcome.
Antiseizure Medications in Coma

Convulsions can cause massive increases in CBF, consequent increase in
ICP, can lead to secondary brain damage and may precipitate or be precipitated by cerebral herniation. Apart from generalized tonic clonic
seizures, some comatose children may have nonconvulsive seizures mani-
Chapter 2.3: Coma

Flow chart 2.3.1: Algorithm for the diagnosis and management of coma in children
35
36
festing with subtle signs such as eyelid twitching, eye deviation or nystagmus. If in doubt, empiric treatment of seizures may be justified and can
result in improvement of consciousness.
Choice of Empiric Antimicrobials

If a CNS infection is suspected in a febrile child presenting in acute coma
and seizures, empiric antimicrobial should include acyclovir in addition to
a third generation cephalosporin until further confirmatory tests are available. The need for empiric antimalarials should be carefully assessed.
Prognosis
Recovery from coma depends primarily on the cause rather than depth.
Metabolic coma carries the best prognosis, while prolonged stupor following global hypoxic event has a poor prognosis. Early rehabilitation in most
cases is often very much rewarding.
Bibliography
1.
2.
3.
4.
5.
6.
Avner JR. Altered state of consciousness. Peds Rev 2006;27:331-7.

Bansal A, Singhi SC, Singhi PD. Nontraumatic coma. Indian J Pediatr
2005;72:467-73.
Fleisher GR. Textbook of paediatric emergency medicine, 355:207-8.
Larsen GY, Vernon DD, Dean JM. Evaluation of the Comatose Child. In: Rogers
MC (Ed). Textbook of Pediatric Intensive Care. 3rd edition Baltimore: Williams and Wilkins:1996,735-45.
Mayer SA, Chong JJ. Critical care management of increased intracranial pressure. J Intensive Care Med 2002;17:55-8.
Pauline CL. Approach to an unconscious child. IJPP 2005;7(1):38-45.
2.4
Syncope
Syncope is a transient loss of postural tone and consciousness resulting

from an acute reduction in blood flow to the brain.
Basic Vascular Pathophysiology

1. Blood pressure is the product of cardiac output (heart rate X stroke
volume) and total peripheral resistance.
2. Blood flow to the brain depends on the mean arterial blood pressure
and the intracranial pressure.
3. Blood flow in the brain is maintained by autoregulation in response to
minor changes in systemic blood pressure.
4. However, sudden, dramatic reduction in blood pressure below a mean
arterial BP of about 60 mm Hg results in a parallel fall in brain perfusion, resulting in a gradual loss of consciousness.
Causes
1. Altered heart rate:
Bradyarrhythmia:
Primary:
a. Complete heart block (Stokes-Adam attack)
b. Atrial fibrillation
c. Sinus arrest.
Secondary:
a. Carotid sinus hypersensitivity (head turning, neck massage)
b. Cold food (Ice cream syncope), swallow (swallow syncope), rectal
exam (prostatic syncope) can activate vagal reflex.
Tachyarrhythmia:
Supraventricular tachycardia:
a. WPW syndrome
b. Prolonged QT syndrome
Ventricular tachycardia.
38
2. Reduced stroke volume:

Acute reduction:
Low blood volume:
a. Acute fluid lossburns, vomiting, diarrhea, dehydration
b. Hemorrhage
c. Addisons disease
d. Diuretics.
Obstruction to venous return:
a. Cough, micturition, defecation
b. Cardiac temponade.
Chronic reduction:
Impaired outflow from heart:
a. Dilated cardiomyopathy
b. Congenital heart disease.
Obstruction to the outflow from heart:
a. Hypertrophic obstructive cardiomyopathy (HOCM)
b. Aortic stenosis (syncope on exertion)
c. Atrial myxoma.
3. Reduced peripheral resistance:
a. Spinal cord injury
b. Guillain-Barr syndrome
c. Others: Vasovagal (commonest cause, even emotion can precipitate), heat (cutaneous vessel dilatation), large meal (splanchnic
vessel dilatation), anemia, drugs (prazosin, hydralazine, calcium
channel blocker, phenothiazines, diuretics).
History
Interview both the patient and witness if available.
Goals
Confirming the event and finding the cause.
1. Precipitating/contributory factors: Acute pain, emotional shock, heat,
prolonged standing, drugs, straining, change in posture (standing after prolonged lying), large meal.
2. Presyncopal symptoms: Light headedness, dizziness, dimming of vision, muffled sound, nausea, sweating, weakness. Palpitation and chest
pain may indicate cardiac cause.
3. Associated features during attack: Pale, clammy, floppy.
4. Duration: Seconds to 1-2 minutes, if patient assumes recumbent position and not held upright.
5. Sequelae: Very little confusion and almost no difficulty recalling the
warning symptoms.
Chapter 2.4: Syncope
39
Physical examination is usually normal. Look for pigmentation if Addisons
disease is suspected.
Cardiovascular
1.
2.
3.
4.
Pulse (rate, rhythm, character)

BP (supine and standing)
JVP (low in hypovolemia and raised in cardiac failure)
Heart (features of aortic stenosis, outflow obstruction).
Neurological
Sign of peripheral neuropathy.
Differential Diagnosis
1. Seizure and pseudoseizure
2. Hypoglycemia
3. Drop attacks.
Investigations
In any child presenting with syncope, the following baseline investigations
should be done:
1. Full blood count (anemia).
2. Urea, electrolytes, glucose, calcium, magnesium (common metabolic
problems).
3. Chest radiograph.
4. ECG, Holter monitor, stress ECG (arrhythmias).
5. Electrophysiology study (recurrent syncope, abnormal ECG, clinical
suspicion of arrhythmia, arrhythmia on Holter monitor).
6. Echocardiography (Vulvular heart disease, outflow obstruction, cardiomyopathy).
7. EEG (focal neurological sign, history suggestive of seizure, postictal
behavior, recurrent syncope of unknown origin.
Treatment
1. Reassurance: In most of the cases where common predisposing factors
are obvious (dehydration, hot weather, tired).
2. Attend to heart disease (Pacemaker in complete heart block).
3. Correct metabolic or hormonal disturbances.
4. Stop drugs causing postural hypotension.
5. Psychiatric assessment: Patient with otherwise unexplained frequent
syncope. Anxiety, panic attacks, somatization disorder may report as
repeated syncope
Bibliography
1.
Hankey G J, Wardlaw JM. Clinical Neurology 2002;59-64.
2.5
Anaphylaxis
Jaydeep Choudhury
Anaphylaxis is a rapidly evolving multisystem allergic reaction which is

potentially life-threatening and may progress to shock lower and upper
airway obstruction or all of them. The classic anaphylaxis is IgE-mediated
and triggered by an exposure to an allergen in a sensitized individual.
Clinical features may be as mild as simple urticaria to upper airway obstruction, hypotension and death.
Common Known Causes of Anaphylaxis

1. Ingestants: Food, milk products, coloring agents.
2. Drugs: Antibiotics, NSAIDs, neuromuscular blocking agents, contrast
medium.
3. Stings and bites: Bee, wasps.
4. Foreign proteins: Vaccines.
5. Blood products.
6. Others: Rubber and latex.
Different Types of Presentation

1. Begin within 30 min of exposure and resolve within a few hours. Usually follow injection of an allergen.
2. Biphasic reaction: Recurrence of signs and symptoms 1-8 hours after
initial resolution.
3. Protracted anaphylaxis: Continue for many hours or days despite aggressive treatment. Usually follow oral medication.
The clinical features of anaphylaxis are shown in Table 2.5.1.
Management
A, B and C
In case of anaphylaxis, maintenance of patent airway and oxygenation is of
utmost importance. The child should lie flat on a firm surface with raised
foot end to facilitate blood supply to vital organs.
Chapter 2.5: Anaphylaxis
41
TABLE 2.5.1: Clinical features of anaphylaxis

System
Features
Cutaneous
Upper respiratory
Urticaria and angioedema.

Hoarseness, dysphonia, feeling of lump in throat( features of laryngeal edema and upper airway obstruction).
Wheezing, dyspnea.
Hypotension, shock, cardiovascular collapse and arrhythmia.
Sneeze, itch, rhinorrhea, nasal and palatal pruritis, watery eyes diaphoresis.
Lower respiratory
Cardiovascular
General
Treatment of Choice
Injection Aqueous Epinephrine 1:1000 dilution, 0.01 ml/kg deep intramuscular. The maximum dose should not exceed 0.3 to 0.5 ml. The same
dose may be repeated every 15 min. Though, subcutaneous route may also
be employed but skin perfusion is often poor due to peripheral vasoconstriction and hence deep intramuscular route is preferred. The same may
be given via endotracheal tube.
In case of serious reaction an intravenous infusion of epinephrine may
be started at 0.1 gm/kg/min to sustain a systolic blood pressure of 80 mmHg.
Hypotension
Rapid intravenous infusion of normal saline, sometimes colloids may be
required. Dopamine may sometimes be used for maintaining the blood
pressure. Infusion of epinephrine and norepinephrine may be used to
counter widespread vasodilatation and capillary leak.
Antihistaminics
Diphenhydramine 1 mg/kg intravenous, intramuscular or per oral may be
given and repeated 4 hourly along with ranitidine 3-6 mg/kg/day in 2 or 3
divided doses.
Systemic Corticosteroid
Its role is debatable and questionable. It may be of help in the late phase of
allergic reaction. The following drugs may be used:
Methylprednisolone 2 mg/kg intravenous followed by 1 mg/kg every 6
hourly.
Hydrocortisone 10 mg/kg intravenous followed by 5 mg/kg every 6
hourly.
Salbutamol
Nebulized salbutamol 0.15 mg/kg with normal saline may be repeated every 20 min to counter the bronchospasm.
42
The doses of various drugs in anaphylaxis is shown in Table 2.5.2 and

the Flow Chart 2.5.1 shows the step-wise management of anaphylaxis.
The algorithm for management of anaphylaxis is shown in Flow chart
2.5.1.
TABLE 2.5.2: Pharmacotherapy of anaphylaxis
Medication
Dose
Epinephrine (1: 1000)

Norepinephrine
Hydrocortisone
Dopamine
Diphenhydramine
10 gm /kg IM and 0.1-1 g/kg/min IV as infusion

0.1-1 g/kg/min
4 mg/kg
2-20 g/kg/min IV
5 mg/kg/day PO in 3-4 divided doses
Flow chart 2.5.1: Algorithm for anaphylaxis treatment
Chapter 2.5: Anaphylaxis
43
Bibliography
1.
2.
3.
4.
ASCIA 2004. ASCIA is the peak professional body of clinical immunologists

and allergy specialists in Australia and New Zealand.
Linzer JF. Anaphylaxis. Pediatr 2006;2. URL: www. emedicine.
The diagnosis and management of anaphylaxis, An updated practice parameter. J Allergy Clin Immunol. 2005;115:S483-523. Established by the American
Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Asthma and Immunology (ACAAI).
Understanding Anaphylaxis: Defining, Identifying and Treating Severe Allergic Reactions. Infectious Disease in Childhood 2004;4.
2.6
Oxygen Administration
Oxygen is probably the maximally used drug in either emergency department or ICU all over. Whenever body tissues face stress, the first
physiological response is an increased metabolic demand, which in turn
increases oxygen demand.
Tissue oxygenation is determined by the following equation:
O2 delivered = O2 carrying capacity of the blood Cardiac output
= (Hb in gm 1.34 % O2 saturation of Hb) (stroke
volume heart rate)
Indications for oxygen supplementation:
1. Significant airway obstruction: Upper or lower airway due to various causes.
2. Lung parenchymal disease: Pneumonia, ARDS.
3. Arteriovenous shunting of the blood: Intra or extra cardiac.
4. Cardiac failure, e.g. in septic shock, neurogenic shock
5. Sepsis, burns, i.e. increased oxygen demands by various tissues.
Hypoxia indicates underoxygenation, while hypoxfemia indicates decreased oxygen content of blood. A patient may be hypoxic, but not
hypoxemic as in severe septic shock and vice versa as in hemodynamically
stable cyanotic heart disease. Hypoxia is always a medical emergency.
Oxygenation can be determined by the following:
Signs and symptoms:
i. CNS: Lethargy, confusion, delirium, seizures, coma.
ii. Cardiac: A progressive shock state with multiorgan failure.
iii. Central symmetrical cyanosis.
Investigations:
i. Arterial blood gases: It determines dissolved oxygen in plasma (PaO2)
and correlates well with Hb saturation except in few conditions with
abnormal Hb.
ii. Pulse oxymetry: It determines hemoglobin oxygen saturation (SpO2).
iii. Transcutaneous oxygen monitor: Used extensively in units with High
Frequency ventilation to determine any rapid change in PaCO2.
iv. Tissue oxygenation can be detected by in direct parameters like
plasma. HCO3 and lactate levels.
Chapter 2.6: Oxygen Administration
45
Drawbacks of SpO2
1. Hyperoxia cannot be identified.
2. False readings in shock states due to low peripheral perfusion.
3. Skin, nail coats will hinder the infrared rays and will give wrong readings.
4. Motion artifacts.
5. Proximity to electrocautery will give wrong reading.
Humidification of Oxygen
Nonhumidified, unwarmed oxygen will cause hypothermia, mucociliary
dysfunction, drying of secretions and airway obstruction. Optimum requirement is 80 to 100 percent humidity with 32 to 37C temperature.
Administration of Oxygen
Various devices are used depending upon age, dose of oxygen, convenience
of the patient and type of disease. The flow rate is set at 3-4 times the
calculated minute volume. Minute volume (MV) = Tidal volume respiratory rate.
Table 2.6.1 shows oxygen percentage with different systems.
Low Flow Devices

1. Nasal canula: It will provide low FiO2 between 30 to 40 percent. Fitting
a nasal canula in a neonate will give almost 90 percent FiO2 at 1L/min.
2. Simple mask: Should not to be used for conditions of hypoxemia.
3. Partial rebreathing mask: This is a simple mask with an additional
reservoir that allows accumulation of oxygen enriched gas for
rebreathing. Upto 60 percent FiO2 can be delivered.
4. Nonrebreathing mask: It is similar but has a valve which allows only
oxygen from the source to enter the reservoir and not allowing the
exhaled air. Hence, 80 to100 percent O2 can be provided.
The oxygen percentage in different devices is shown in Table 2.6.1.
TABLE 2.6.1: Oxygen percentage with different systems
Lt/min
5
6
8
10
12
15
Simple mask
<40%
45-50%
Partial rebreathing mask

35%
45-50%
60%
60%
60%
Nonrebreathing mask
55-60%
60-80%
80-90%
90%
90-100%
46
High Flow Devices

1. Nonrebreathing mask: It has a valve at the exhalation port that allows
only exhaled gases to enter the reservoir. A well fitting mask can provide up to 100 percent oxygen.
2. Venturi masks: These are dilutional masks where oxygen is delivered
through a narrow orifice at a high flow. There are openings near the
nozzle that allows room air to be sucked in, diluting the oxygen. Changing the size of the nozzle, the flow rates, as well as ports, allows control
of the amount of oxygen.
3. Oxyhood: Adequate flow of humidified oxygen allows mixing of delivered gases and flushing out of CO2. O2 gradient can vary as 20 percent
from top to bottom and continuous flow of 6 L/min avoids this problem. Cold airs causes heat stress and condense on babys head, which is
mistaken as perspiration.
Measurement of Delivered Oxygen

Oxymeter or FiO2 meter is used to measure concentration of oxygen. A
sensor which is connected to the instrument digitally converts the sensed
concentration into a reading that is displayed. The oxyhood is the ideal
place to use it.
Practice Points
1. During physiotherapy, increase FiO2 by 5 percent.
2. Oxygen requirement is reduced by maintaining thermo-neutral environment, minimal handling, correction of anemia and acidosis.
3. Oxygen requirement is increased by: any stress, hypothermia, sepsis,
infection, post-trauma, congenital cardiac or lung malformation.
4. To improve oxygenation in a ventilated patient:
Increase FiO2.
Increase mean airway pressure (MAP) increases proportionately to PEEP,
PIP, inspiratory time and flow rate.
Disadvantages of Oxygen Therapy

1.
2.
3.
4.
Direct lung injury: If FiO2 is >60 percent and used for a long-time.
Alveolar collapse.
Retinopathy of prematurity.
Hyperbaric oxygen causes severe cerebral vasoconstriction and epileptic fits.
Bibliography
1.
Lieh-Lai MW, Ling-McGeorge KA, Asi-Bautista MC. Pediatric Acute Care, 2nd
edition. Philadelphia: Lippincott Williams and Wilkins, 2003.
2.7
Fluid and Electrolyte Balance
Joshi Anand Karketta, Jaydeep Choudhury,
Fluid and electrolyte balance is a very important aspect of pediatric emergency management. A large number of children present to the emergency
department with dehydration due to various etiology. The commonest cause
of dehydration in children is acute gastroenteritis.
General Guidelines for Rehydration

1. Better under hydrate than over hydrateDo not exceed 100 ml/kg for
deficit replacement.
2. Care for the kidney is crucial; it will care for minor miscalculations.
This is by providing 20 ml NS/kg in case of hypovolemia.
3. An overweight infant is misleading:
i. Signs of dehydration are late and can be missed.
ii. They may be already in shock when recognized.
iii. Hypernatremia is a risk.
4. An underweight infant:
i. Has poor tolerance to the usual calculations.
ii. Needs calories more than water and sodium.
iii. Signs of dehydration are exaggerated.
5. A drowsy child with gastroenteritis is critical:
i. Associated CNS infection.
ii. Brain edema (Hyponatremia).
iii. Brain dehydration (Hypernatremia).
6. Abdominal distension with gastroenteritis is always abnormal:
i. Perforated appendix.
ii. Intussusception.
iii. Septicemia, late NEC.
iv. Hypokalemia.
Rehydration in Acute Gastroenteritis

While managing a dehydrated child, appropriate fluid therapy is vital. Various intravenous fluids are available. It is important to use that intravenous
fluid which is closest to physiological milieu. Thus, one should be familiar
48
with the compositions of commonly used rehydration solutions as shown

in Table 2.7.1.
The type of rehydrating solution is chosen according to its sodium
content. Carbonated drinks and apple juice should not be used for rehydration as they do not contain sodium and have 10 to 12 percent sugar
concentration.
Principles
1.
2.
3.
4.
5.
Correction of hypovolemia or shock.

Replacement of deficit. .
Provision of maintenance.
Allowance for ongoing losses (if any).
Attention to the sodium status.
Hypovolemia or Shock
20 ml/kg NS over 30 to 60 minutes can be repeated if there is no response.
For adolescents 10 ml/kg.
Deficit Replacement
Volume replacement depends on degree of dehydration as shown in Table
2.7.2. Sodium loss in various states of dehydration is shown in Table 2.7.3.
TABLE 2.7.1: Composition of commonly used rehydration solutions and plasma
Normal saline (NS)
0.45 NS 5% D
0.22% NS
8.4% NaHCO3
Human plasma
WHO-ORS
Content
Osmolality
Na = 150 mmol/L
Cl = 150 mmol/L
Na = 75 mmol/L
Cl = 75 mmol/L
Glucose = 50 g/L
Na = 37 mmol/L
Cl = 37 mmol/L
HCO3 = 1 mmol/ml
Na = 1 mmol/ml
Na = 145 mmol/L
K = 4.5 mmol/L
Na = 90 mmol/L
K = 20 mmol/L
Citrate = 30 mmol/L
Glucose = 110 mmol/L
300 mOsmol/kg
428 mOsmol/kg
290 mOsmol/kg
320 mOsmol/kg
TABLE 2.7.2: Volume replacement in dehydration

Mild
Moderate
Severe
Younger children
Older children
50 ml/kg
75 ml/kg
100 ml/kg
30 ml/kg
50 60 ml/kg
70 90 ml/kg
Chapter 2.7: Fluid and Electrolyte Balance
49
Apart from hypernatremia the sodium content of a rehydrating solution for deficit replacement is 80 to 100 mmol/L
Maintenance Requirements
Following deficit replacement, fluid balance is continued by maintenance
therapy.
Volume
Water or calorie requirement is shown in Table 2.7.4.
Sodium
Requirement is 2 to 4 mmol/kg/day.
Potassium
Requirement is 2 to 3 mmol/kg/day.
Ongoing Losses
If IV hydration is considered, you can successfully rehydrate most children
with the following solutions.
1. Normal saline (150 mmol Na/L).
2. 0.45 NS in D5 percent (75 mmol Na/L) and add 4 percent KCl (0.5 mmol/ml).
Start with 20 ml NS in any child with more than moderate dehydration, discount them from the deficit. Then, as per following calculation.
1. 6 to 8 hoursDeficit + 1/3 maintenance.
2. 6 hoursDeficit + 2/3 maintenance.
It has to be remembered that Na content in deficit fluid is 80 to 120
mmol/L and that in maintenance fluid is 30 mmol/L. The following solution is satisfactory.
0.45 NS = 75 mmol/L sodium.
TABLE 2.7.3: Sodium loss in various states of dehydration
Status
Approximate sodium loss
Isonatremia (Acute)
Isonatremia (Chronic)
Hyponatremia
Hypernatremia
100 mmol/L
70-80 mmol/L
120 mmol/L
40-60 mmol/L
TABLE 2.7.4: Water or calorie requirement

Weight
Water (or calorie) requirements
Birth-10 kg
11-20 kg
21-30 kg
100/kg
1000 + 50 /kg above 10
1500 + 20 /kg above 20
50
To each liter add 20 to 30 mmol K = 40-60 ml 4% KCl. Which comes to

each 500 ml fluid add 10-15 mmol
K = 20-30 ml 4% KCl.
Example
A 12 months old child with acute gastroenteritis is admitted with severe
dehydration. His weight is 10 kg.
Total fluid needed is as follows.
Deficit = 10 100 = 1000 ml.
Maintenance = 10 100 = 1000 ml.
Step 1: IV 0.9% NS 200 ml over 60 minutes.
Step 2: IV 0.45 NS in 5% D 500 ml + 4% KCl 25 ml. Volume 700 ml over
7 hours.
This provides the remaining deficit (400) + 1/3 of the maintenance
(300) = 700 ml.
Step 3: IV 0.45 NS in 5% D 500 ml + 4% KCl 25 ml.
Rate 60 ml/h over 16 hours. This provides 1000 ml (approx.), which
covers the remaining deficit + 2/3 of the maintenance.
Hyponatremic Dehydration
By definition serum sodium less than 130 mEq/L is hyponatremia. Low
sodium concentration in serum may be due to water retention, sodium
retention or both. Consequently, the extracellular fluid volume may be
low, normal or high.
Serum sodium less than 125 mEq/L is associated with lethargy, nausea
and vomiting. When serum sodium is less than 115 mEq/L neurological
manifestations like seizures and coma develop.
Asymptomatic Hyponatremia
It is better to explain with an example. A 12 months old child with acute
gastroenteritis is admitted with severe dehydration. His weight is 10 kg.
Step 1: IV 0.9% NS 200 ml over 60 minutes (same as in isonatremia).
Step 2: IV 0.45 NS in 5% D 500 ml + 25 ml 4% KCl (Rate/duration as in
isonatremia).
Step 3: IV 0.45 NS in 5% D 500 ml + 4% KCl 25 ml (Rate/duration as in
isonatremia).
Symptomatic Hyponatremia
1. Acute symptomatic hyponatremia (120 mEq/L) is treated by 3% NaCl
(513 mEq/L) over 4 hours. The requirement is calculated as follows:
Na requirement in mEq/L = (Desired Na Actual Na) 0.6 weight
(kg).
The desired Na is usually 125 mEq/L.
51
2. Clinical assessment should be done to look for vital signs, hydration

status, fluid loss or underlying disease.
3. Laboratory assessment of serum electrolytes, urea, creatinine, glucose,
serum osmolality and urine analysis for sodium, creatinine and osmolality should be done.
4. Serum sodium should be estimated and further correction if required
is done over 24 to 48 hours. The possible course of events, cause and
management is described in Table 2.7.2.5.
Management of other conditions like adrenal insufficiency with steroid, cardiac failure, cirrhosis.
True hyponatremia must be distinguished from factitious hyponatremia.
Factitious Hyponatremia
1. When nonpermeable substances (Glucose, mannitol) are added to infusion, redistribution of water occurs from intra to extracellular space
leading to hyponatremia.
2. Hyperlipidemia.
3. Hyperproteinemia.
4. Measured plasma osmolality is high.
The two syndromes presenting with hyponatremia are Syndrome of
Inappropriate Antidiuretic Hormone Secretion (SIADH) and Cerebral Salt
Wasting (CSW).
Hypernatremic Dehydration
Normal serum sodium concentration is 138 to 145 mEq/L. Hypernatremia
is present when serum sodium concentration exceeds 150 mEq/L. Serum
sodium concentration more than 158 mEq/L is critical and may produce
severe signs and symptoms.
Hypernatremia relfects a deficiency of water relative to total body sodium. It is actually a disorder of water balance rather than sodium. Serum
sodium level estimation in hypernatremia does not reflect the total body
sodium content. It may be high, low or normal depending on the total
body water content and the cause of hypernatremia.
TABLE 2.7.5: Etiology and management of hyponatremia
Status
Hypovolemic
hyponatremia
Euvolemic
hyponatremia
Hypervolemic
hyponatremia
Etiology
i. Renal loss
ii. Extrarenal loss
(Gastrointestinal,
sweat, third space)
Isotonic saline
i. SIADH
ii. Water intoxication
iii. Drugs
(Mineralocorticoids)
Water restriction
i. Renal loss
ii. Edematous state
Salt and water restriction
Frusemide, hypertonic
saline
Hypertonic saline,
dialysis
Initial
management
Further
5% Dextrose with
management 0.45% saline
52
Rapid increase in intravascular osmolality draws water from intracellular space to extracellular space causing intracellular dehydration. This
altered water balance affects central nervous system also and results in brain
shrinkage and blood vessel tear. It may lead to intracerebral bleeding, pulmonary edema and systemic arterial hypertension.
Hypovolemic Hypernatremia
Hypotonic fluid loss: This is the most common cause of hypernatremic dehydration in pediatric patient. It results from excessive loss of hypotonic
fluid with inadequate water intake, like diarrhea with decreased water intake or vomiting. Osmotic diuresis in diabetes mellitus and osmotic diuretics
like mannitol can induce hypernatremia secondary to excess hypotonic
urine. In these conditions, the total body sodium is decreased but the total
body water is reduced much more.
Water deficit: This is a condition of pure renal water loss secondary to
diabetes incipidus, isolated renal water loss in excessive sweating, fever
and hyperventilation.
Euvolemic Hypernatremia
This is the physiological state of sodium excess. Pure sodium excess is unusual in human biophysical milieu. It can occur as a result of feeding
improperly mixed ORS solution or concentrated artificial feed to infants.
Rarely does it occur due to excess intravenous sodium administration, like
excess sodium bicarbonate administration during resuscitation.
Clinical Features
1. Shock doughy consistency of skin usually occurs with >10 percent
dehydration.
2. Lethargy, irritability, coma and seizures.
3. Central nervous system dysfunction is severe and often leaves permanent sequelae.
Management
Initial Resuscitation
1. Severe dehydration and/or imminent shock should be corrected with
isotonic fluid like NS or Ringers lactate solution 20 ml/kg boluses till
blood pressure becomes normal. Intravenous fluid containing sodium
concentration at physiological level is ideal despite hypernatremia as
it will drive water to the intracellular space. The aim is to correct intracellular dehydration.
2. Subsequently, 0.33 or 0.45 percent saline infusion is used till the child
voids urine.
3. The aim is to correct dehydration over 48 hours.
53
Subsequent Management
Hourly fluid rate = Maintenance + Deficit/48
The fluid to be used is 0.33 or 0.25 percent saline in 2.5 percent Dextrose with adequate potassium. The sodium content of the fluid is adjusted,
based on subsequent serum levels. The rate of fluid correction is more
important than the sodium content.
If serum sodium falls >0.5 mEq/hr, then intravenous fluid infusion
rate is to be slowed down.
If serum sodium falls <0.5 mEq/hr the infusion rate has to be increased.
Rate of fall in serum sodium level should ideally be 10 to 15 mEq/l/day.
Too rapid correction of hydration and fall in serum sodium may cause
cerebral edema, hypovolemia, pulmonary edema and central pontine myelinolysis.
1. Hypernatremic patients have predilection for hyperglycemia. Intravenous fluid after initial resuscitation should contain 2.5 percent Dextrose,
insulin is not required.
2. Hypocalcemia may require appropriate treatment.
3. Once the child voids urine potassium may be added at 40 mEq/L, it
aids water entry into cells.
4. Diabetes incipidus may be treated accordingly.
5. Severe hypernatremia, serum sodium around 200 mEq/L may require
peritoneal dialysis with high glucose (7.5%) and low sodium dialysate.
Hyperkalemia
Hyperkalemia is defined as serum potassium more than 5.5 mEq/L in children and more than 6.5 mEq/L in infants.
Etiology
1. Increased intake.
2. Decreased renal excretionRenal failure, potassium sparing dugs like
spironolactone, ACE inhibitors, NSAIDs and mineralocorticoid deficiency.
3. Increased movement into extracellular fluid like acidosis.
4. Cell death or tissue necrosis.
Clinical Features
1. Muscle weakness.
2. Cardiac arrhythmia.
ECG Changes
1. Tall T-wave.
2. Long PR-interval, wide QRS.
3. Absent P-wave, sinusoidal wave.
54
Management
1. Ensure sample not hemolyzed.
2. Stop all exogenous potassium (IV, oral, drugs, blood product transfusion).
3. Cardiac monitor.
Serum K >7 mEq/L or any hyperkalemia with ECG changes:
i. Calcium (cardioprotective) with ECG monitoring10 percent calcium gluconate 0.5 to 1 ml/kg/dose IV over 5 to 10 min. or 10
percent calcium chloride 0.2 ml/kg/dose IV over 5 to 10 min. It
can be repeated up to 4 times or until serum calcium increases or
ECG normalizes. Its effect lasts about 30 minutes.
ii. NaHCO3 1 to 2 mmol/kg/dose IV over 30 min. every 2 to 4 hourly.
Do not mix with calcium in same IV line (Results in precipitation).
iii. Glucose 0.5 g/kg IV with insulin 0.1 unit/kg IV over 30 min. May
be repeated in 30 to 60 min.
iv. Salbutamol nebulization.
v. Consider dialysis if above measures unsuccessful.
Hypokalemia
Hypokalemia is a state when serum potassium concentration is less than
2.5 mEq/L.
Etiology
1. Inadequate intake
2. Conditions when potassium is transferred into the cellsAlkalosis, insulin.
3. Increased lossDiuretics, renal tubular acidosis, Bartters syndrome, gastrointestinal loss, loss through skin like sweating or burns, excess steroid.
Clinical Features
Skeletal muscle weaknesses, abdominal distension with paralytic ileus are
the most prominent features. Ployuria and polydipsia are secondary to loss
of concentrating ability of the kidneys.
ECG Changes
ST segment depression, low and sometimes flat T-wave, in extreme cases
U-wave. Increased risk of arrhythmia.
Management
1. Acute: Enteral replacement is preferable 1 to 4 mEq/24 hr in 2 to 4
divided doses. If parenteral replacement have to be given then 0.3 to
0.5 mEq/kg/hr infusion by pump with cardiac monitoring. Central line
is preferred. Serum potassium should be monitored closely.
2. Chronic: The daily dose to be calculated and replaced with potassium
chloride or gluconate.
55
Hypocalcemia
Hypocalcemia is defined as serum calcium less than 2 mmol/L.
Clinical Features
Lethargy, poor feeding, vomiting, abdominal distension, twitching, tetany,
seizures, apnea, stridor, laryngospasm.
ECG Changes
Prolonged Q-Tc interval. (Normal <0.45 sec).
Management
Asymptomatic hypocalcemia: 100 mg/kg/d elemental calcium orally in divided every 6 to 8 hourly.
Symptomatic hypocalcemia:
i. 10 percent calcium gluconate 0.5 to 1.0 ml/kg/IV (diluted) over 5 to
10 min followed by 10 percent calcium gluconate 1 to 2 ml/kg/dose
every 4 to 6 hourly bolus infusion diluted to 2 percent (Mix 10 ml of
10 percent calcium gluconate in 40 ml NS to obtain 2 percent solution). Or else continuous IV infusion 5 to 8 ml/kg/day of 10 percent
calcium gluconate diluted to 2 percent. All patients on IV calcium
should be on cardiac monitor.
ii. Integrity of the intravenous site should be ascertained before administering calcium through a peripheral vein.
iii. Adjust infusion rate q 4h based on plasma calcium level. Reduce infusion rate slowly once desired level reached then start oral calcium.
iv. Monitor IV site for extravasation burns and venous thrombosis.
v. Correct hypomagnesemia (Mg <0.6 mmol/L) because hypocalcemia
does not respond until magnesium level is corrected.
vi. Magnesium sulfate 50 percent 0.2 ml/kg/dose IM/IV slowly.
vii. Consider starting vitamin D.
Bibliography
1. Barkin R, Rosen P. Emergency Pediatrics: A Guide to Ambulatory Care. 5th
edition, 1999.
2. Colin R, Abraham R, Margaret H, George E, Norman S. Rudolphs Pediatrics.
21st edition.
3. Crain E, Gershel J, Gallager E. Clinical Manual of Emergency Pediatrics. 4th
edition, 2002.
4. Harry E, Zimmerman J. Hyperkalemia. March 2005. www.emedicine.com.
5. Jarvis D, Greenway K, Venturelli J. Pediatric Advanced Life Support. 5th edition.
6. Shefler A. The HSC Handbook of Pediatrics. 9th edition, 1997.
7. Singhal A, Campbell D. Hypocalcemia. October 2002. www.emedicine.com.
8. Vellaichamy M. Hypernatremia. January 2003. www.emedicine.com.
9. Vellaichamy M. Hyponatremia. January 2003. www.emedicine.com.
10. Verive M, Jaimovich D. Hypokalemia. August 2004. www.emedicine.com.
2.8
Blood Component Transfusion
Sudipta Sekhar Das
Refinements in cross-match techniques and the development of sophisticated screening tests for transmissible diseases have made blood
transfusiona safe and often lifesaving form of therapy. Because of the
wide range of potential adverse effects of transfusion therapy, the clinician
must have a clear understanding of the indications, efficacy, and complications of blood component therapy. The available blood components are
shown in Table 2.8.1.
Preparation and storage methods have been kept out of discussion in
this chapter for obvious reason.
Red Blood Cell

A dose of one unit of compatible red blood cells will increase the hemoglobin level in those who is not bleeding or hemolysing by approximately 1g/dl
or hematocrit by 3 percent. In neonates and older children, a dose of 10 to
15 ml/kg is usually given.
The cause of the anemia must be considered because alternative therapy
(e.g. iron sulfate, vitamin B12, folate, or erythropoietin) may eliminate the
need for transfusions altogether.
Indications
1. Chronic hypoproliferative anemia: Chronic anemia is accompanied by
several physiologic adaptations that enhance oxygen delivery despite
a reduced red blood cell oxygen carrying capacity. Therefore, transfusions are rarely necessary for patients with chronic anemia who have
hemoglobin concentrations above 7 g/dL unless significant cardiopulmonary disease is present, and transfusions may result in circulatory
overload, if given rapidly or in excessive quantity.
2. Acute blood loss: Intraoperative blood loss may require red blood cell
transfusion to maintain hemodynamic stability, and burn patients often require vigorous blood component support because of volume
depletion through denuded body surfaces.
Chapter 2.8: Blood Component Transfusion
57
TABLE 2.8.1: Blood components available

Products available
1. Red blood Cells (RBC)
Homologous packed RBC
Leukocyte-poor RBC
Irradiated RBC
Washed RBC
Frozen RBC
Neocytes
Directed donor RBC

Autologous RBC
Preparations
Prepared from potential donors, are transfused most often.
Promote oxygen delivery for patients with active bleeding or
severe anemia.
Prepared by a variety of techniques to remove more than 99%
of leukocytes. Reduce febrile reactions; Prevent HLA
alloimmunization and CMV infection in potential transplant
recipients or those requiring chronic platelet transfusions.
Reduces transfusion associated graft-versus-host disease
(TAGVHD).
Washing red blood cells in saline removes most plasma proteins and some leukocytes and platelets. Substitute for
homologous RBC in patients sensitive to a plasma component; Avoid transfusion of anti-A and anti-B antibodies when
O-negative blood is used in patients who are type A, B, or AB.
Not often used today.
RBCs frozen in liquid nitrogen with glycerol as a cryoprotective agent, can be stored for up to 10 years.Preserve
autologous RBC; maintain store of rare blood types.
Prepared by differential centrifugation or cell separators and
have a longer circulating life span than standard red cells, but
they are rarely used. Increase efficacy of individual transfusion for patients with transfusion-dependent anemia,
thalassemia, etc.
After screening and informed consent, may be substituted
for volunteer RBC at patient request. Reduces multiple donor
exposure in chronically transfused patients.
May be collected preoperatively, by perioperative blood salvage, or by acute normovolemic hemodilution to decrease
homologous red blood cell use.
2. Platelets
Random donor platelets (RDP) Obtained from whole blood.
Platelet pheresis
Obtained by apheresis technology. Also known as single donor platelet (SDP). It has advantages over RDP.
Leukocyte-poor platelets
Various techniques to prepare are available. It can remove
>99% of leukocytes. It reduces febrile reactions and HLA
alloimmunization and CMV transmission.
Irradiated platelets
Reduces transfusion associated graft-versus-host disease.
HLA matched platelets
Treat bleeding associated with thrombocytopenia in patients
who are refractory to platelet transfusions due to HLA
alloimmunization.
3. Plasma and derivatives
Fresh frozen plasma (FFP)
Prepared by separating plasma from whole blood and freezing it within 6 hours after collection at 18C or colder. It can
be stored for up to 1 year and is thawed prior to administration. It is very effective in coagulopathies.
Contd...
58
Contd...
Fresh plasma (liquid plasma)
Cryoprecipitate-poor plasma
Cryoprecipitate
4. Granulocytes
Leukapheresis
Same as FFP, except does not contain factors V and VIII. Used
for preparation of plasma derivatives (e.g. immunoglobulin,
cryoprecipitate, albumin, coagulation factor concentrates).
Supernatant plasma remaining after preparation of cryoprecipitate and contains adequate quantities of all coagulation
factors except Fibrinogen, factors VIII and XIII, and vwf. Correct coagulation factor deficiencies other than VIII, XIII,
fibrinogen, vwF; may be indicated for treatment of refractory
TTP.
Formed by thawing FFP at 4C. This cryoprecipitate is separated from the supernatant plasma and resuspended in a small
volume of plasma. It is then refrozen at 18C and kept for up
to 1 year.
Granulocyte concentrates are prepared by automated
leukopheresis from ABO-compatible donors stimulated several hours before collection with corticosteroids, G-CSF or
both.
3. Hemolytic anemia: Patients with markedly symptomatic antibody-mediated hemolytic anemias may require red blood cell transfusion until
definitive therapy is effective. It requires series of immunohematological tests before planned transfusion therapy.
4. Sickle cell anemia: Patients with sickle cell anemia may require red
blood cell transfusion for management of specific complications, including splenic sequestration and aplastic crises. Exchange transfusion
is also indicated in the management of acute central nervous system
infarction or hemorrhage.
5. Perioperative transfusion: Transfusion is rarely indicated for patients
undergoing noncardiac surgery who have hemoglobin values greater
than 7-8 g/dL and no risk factors for myocardial ischemia.
Unacceptable indications: Red blood cell transfusions should not be used to
enhance a patients general sense of well-being, to promote wound healing,
or to expand vascular volume when oxygen-carrying capacity is adequate.
Platelets
Whenever possible, ABO type specific platelets should be used in children.
If type specific platelets are not available, plateletpheresis is a good option.
Although platelets do not carry Rh antigens, platelets from Rh-negative
donors should be used for transfusion in Rh-negative women of childbearing years to prevent sensitization from contaminating red blood cells.
Platelets are always transfused in a dose of 5 to 10 ml/kg considering
the source of the platelets, the cause and degree of thrombocytopenia, and
the observed response to transfusions. Each platelet units of approximately
50 ml should contain a minimum of 3.5 to 4.5 1010 platelets.
59
The response to platelet transfusions should be determined by obtaining a platelet count 1 hour after transfusion and daily thereafter and by
observing the effect on control of bleeding. The 1 hour count should increase by about 5000 to 10,000/L per unit of random-donor platelets or
30,000 to 50,000/L per unit of single-donor platelets. Stored homologous
platelets survive 3-5 days in thrombocytopenic patients.
Indications
1. Treatment of bleeding associated with thrombocytopenia or intrinsic
platelet dysfunction.
2. Patients undergoing cardiopulmonary bypass may require platelet transfusions if excessive bleeding occurs because of thrombocytopenia and
decreased platelet function induced by the bypass procedure.
3. Other surgical procedures in thrombocytopenic patients generally require prophylactic platelet transfusions to maintain adequate
perioperative platelet counts for at least 3 days. More than 50,000/L
for most major procedures except neurologic, ophthalmic and cardiac
procedures where platelet count of more than 100,000/L is preferred.
4. Severely thrombocytopenic (e.g. <10,000/L platelets) patients undergoing intensive chemotherapy for acute leukemia; the threshold for
transfusion may be higher in the presence of fever, infection, or drugs
that cause platelet dysfunction.
Platelet transfusions may be harmful in patients with TTP-HUS despite the presence of thrombocytopenia, presumably owing to accelerated
thrombosis in vital organs. Patients with heparin-associated thrombocytopenia also may suffer increased thrombotic complications if platelets are
transfused.
Plasma
The average child with multiple factor deficiencies requires 10-15 ml/kg of
plasma acutely to control bleeding, with smaller quantities given at periodic intervals as necessary to maintain adequate hemostasis. Control of
bleeding and measurement of coagulation times (prothrombin time and
partial thromboplastin time) should be used to determine when and if to
give repeated doses of plasma. The therapeutic products derived from
plasma and their therapeutic uses are shown in Table 2.8.2.
Indications
1. Active bleeding due to deficiency of multiple coagulation factors, or
risk of bleeding due to deficiency of multiple coagulation factors (DIC,
Liver disease).
2. Severe bleeding due to warfarin therapy, or urgent reversal of warfarin
effect.
3. Massive transfusion with coagulopathic bleeding.
60
TABLE 2.8.2: Therapeutic products derived from plasma

Plasma derivative
Therapeutic use
Albumin (heat-treated)
Plasma-derived factor VIII concentrate
Humate-P
Prothrombin complex concentrate
Hypoalbuminemia in nephrotic syndrome

Hemophilia A
Von Willebrands disease
Coaugulation inhibitors, factor X and prothrombin deficiencies
Factor VIII inhibitors
Hemophilia B*
Hypofibrinogenemia
Factor VII,XI,XII deficiency
Thrombosis in antithrombin III deficiency
Angioedema
Prevent lung damage in 1-AT deficiency
Severe protein C or S deficiency
Immunodeficiency states; immune cytopenias,
Kawasaki syndrome, Guillain-Barr syndrome,
dermatomyositis
Passive immunization against hepatitis A
measles, poliomyelitis, varicella, rubella
Activated factor IX concentrates

Plasma-derived factor IX concentrate
Fibrinogen concentrate
Factor VII,XI,XIII concentrate
Antithrombin III concentrate
C1 esterase inhibitor concentrate
1-Antitrypsin concentrate
Protein C and S concentrate
Intravenous immunoglobulin
Immune serum globulin
4. Bleeding or prophylaxis of bleeding for a known single coagulation

factor deficiency for which no concentrate is available.
5. TTP-HUS, cryoglobulinemia, Goodpastures syndrome, Guillain-Barr
syndrome and post-transfusion purpura.
6. Rare specific plasma protein deficiencies, such as C1 inhibitor.
7. Plasma exchange may be of value in some patients with chronic inflammatory demyelinating polyneuropathy, cold agglutinin disease,
autoimmune thrombocytopenia, rapidly progressive glomerulonephritis, and systemic vasculitis.
Plasma should not be administered for reversal of volume depletion or
to counter nutritional deficiencies (except severe protein losing enteropathy in infants) because effective alter natives are available.
Cryoprecipitate
Each bag of cryoprecipitate (about 20 ml) contains approximately 150 to
250 mg of fibrinogen, 80 to 100 IU of factor VIII, 40 to 70 percent of the
plasma vWF concentration, 50 to 60 mg of fibronectin, and factor XIII at
one and one-half to four times the concentration in FFP.
Two to three bags per 10 kg of body weight will increase the fibrinogen
concentration by about 100 mg/dL. Maintenance doses of one bag per 15
kg of body weight can be given daily until adequate hemostasis is achieved.
Indications
1. Severe hypofibrinogenemia (<100 mg/dL) for treatment of bleeding
episodes or as prophylaxis for invasive procedures.
61
2. Severe bleeding in uremic patients unresponsive to desmopressin and

dialysis.
3. Used to make topical fibrin glue for use intraoperatively to control
local bleeding and has been used in the removal of renal stones when
combined with thrombin and calcium.
4. Widely used in developing countries including India for treatment of
hemophilia A.
Granulocytes
Granulocytes have decreased function if refrigerated or agitated, so these
concentrates should be given as soon as possible after collection (preferably within 6 hours; never after 24 hours).
The minimal dose recommended is 2 to 3 1010 granulocytes per
transfusion, infused slowly under constant supervision. Daily transfusions
should be administered for at least 4 days and perhaps longer until the
infection is controlled.
Indications
The indications for granulocyte transfusions are controversial:
1. In patients with documented bacterial or fungal infections unresponsive
to antibiotics accompanied by prolonged severe neutropenia (<500/cmm)
when bone marrow recovery is expected in 7 to 10 days.
2. In patients with congenital severe granulocyte dysfunction complicated
by life-threatening fungal infections.
3. Neonatal sepsis, although this remains controversial.
Granulocyte transfusions should be used with caution in patients receiving amphotericin B and in those with pulmonary infiltrates because of
the potential for adverse pulmonary events.
Blood Component Administration

1. Informed consent: Before elective transfusion of any blood component
is undertaken, the patient should be informed of the benefits of transfusion, the potential risks of transfusion, and the alternatives to
transfusion.
2. Patient identification: Identification of the patient and proper documentation of the blood product is very important.
3. Preparation of blood components: Potential donors are screened with a
questionnaire prior to donation to eliminate donors with identifiable
risk factors for complications in both the donor and the recipient. After
collection, donor blood is screened for the presence of infectious diseases or their markers, including VDRL, HBsAg and core antibody,
hepatitis C, HIV-1 and 2, malaria and occasionally, CMV antibody. The
ABO and Rh types of donor and recipient red blood cells are determined, and the sera of both donor and recipient are screened for clinically
significant alloantibodies to the major red blood cell antigens.
62
4. Administration: All blood components should be administered through

a standard blood filter to trap clots and other large particles into any
accessible vein or central venous catheter. When leukocyte-depleted
red blood cells or platelets are desired, third-generation leukoreduction
filters may be used.
Blood components should be administered slowly for the first 5 to10
minutes while the patient is under observation, and the patient should be
reassessed periodically throughout the transfusion process for adverse effects. Blood components should not be kept at room temperature for more
than 4 hours after the blood bag has been opened. If a slower infusion rate
is necessary to avoid circulatory overload, the unit may be divided into
smaller portions. Each portion should be refrigerated until used.
Complications of Transfusion
The infectious and noninfectious causes of complications of transfusion
are shown in Tables 2.8.3 and 2.8.4 respectively.
Nonhemolytic, noninfectious transfusion reactions account for more
than 90 percent of adverse effects of transfusions and occur in approximately 7 percent of recipients of blood components.
Current Controversies and Unresolved Issues

1. Perioperative transfusion: The need for transfusion in the perioperative
period should be determined by individual patient characteristics and
by the type of surgical procedure rather than by hemoglobin level alone.
2. Directed donations: Transfusions from ABO and Rh-compatible family
members or friends are frequently requested because of concerns about
the safety of homologous transfusion. There is no evidence that directed donations are safer than volunteer donations. However, some
evidence exists that they may be less safe because blood from directed
donors has a higher prevalence of serologic markers of infections than
blood from volunteer donors.
3. Massive transfusion: Administration of a volume of blood and blood
components equal to or exceeding the patients estimated blood volume
within a period of, 24 hour is accompanied by complications not often
seen during transfusion of smaller volumes. Deficiencies of platelets and
TABLE 2.8.3: Infectious complications of transfusion therapy
Viruses
Bacteria
Spirochetes
Parasites
Prion
Hepatitis A, B, C
Parvovirus B19
Cytomegalovirus
Epstein-Barr virus
HTLV 1 and 2
HIV
West Nile virus
-Environmental
contaminants
-Donor transmitted:
Yersinia, Salmonella,
Klebsiella
Serratia
Staphylococcus
Syphilis
Lyme disease
Malaria
Babesiosis
Chagas disease
Toxoplasmosis
Variant
CreutzfeldtJakob
disease
63
TABLE 2.8.4: Nonhemolytic, noninfectious complications

Complication
Clinical manifestations, pathogenesis, prevention, and treatment strategies
Febrile-nonhemolytic
transfusion reaction (FNHTR)
Occurs in 0.53% of transfusion. Rigors or chills followed by

fever during or shortly after transfusion due to prior sensitization to WBC or platelet antigens, or to pyrogenic cytokines
released during storage. Prevent with antipyretics or leukocyte depletion of blood components before storage.
Noncardiogenic pulmonary edema with fevers, chills, tachycardia, and diffuse pulmonary infiltrates shortly after transfusion,
due to leukocyte incompatibility. Resolves in 14 days; rarely
results in respiratory failure. Occurs in approximately 1:5000
transfusions.
Occurs in 13% of transfusions. Urticaria, pruritus, bronchospasm, or frank anaphylaxis due to recipient sensitization to a
cellular or plasma element. If severe, evaluate recipient for
IgA deficiency. Leukocyte depletion or washed red cells may
be necessary for subsequent transfusions.
Common following transfusion for chronic anemia or when
patient has impaired cardiovascular reserve. Prevent by transfusing only when clearly indicated, using the minimum amount
of blood required to reverse symptoms. Treat with oxygen,
diuretics, and, rarely, phlebotomy (save units for reinfusion if
necessary).
Transfusing with more than one blood volume or red blood
cells with dilute platelets and coagulation factors. Replacement indicated only for clinical bleeding.
Due to citrate intoxication following massive transfusion. Treat
only if symptomatic.
May occur in patients with preexisting renal insufficiency and
hyperkalemia or in neonates. Use of fresh blood or washed
red cells decreases potassium load for these patients.
After massive transfusion of refrigerated blood, hypothermia
may cause cardiac arrhythmias. Refrigerated blood may accelerate hemolysis in patients with cold agglutinin disease.
Prevent by warming blood.
Immunocompetent donor T lymphocyctes may engraft if the
recipient is markedly immunosuppressed or if closely HLArelated. Symptoms and signs include high fever, maculopapular
erythematous rash, hepatocellular damage, and pancytopenia, 230 days after transfusion. Usually fatal despite treatment
with immunosuppressives. Prevent by irradiating all blood
components with 2500 cGy for immunocompromised recipients or when donor is first-degree relative.
Multiple transfusions in the absence of blood loss lead to excess accumulation of body iron with cirrhosis, heart failure,
and endocrine organ failure. Prevent by decreasing total
amount of red cells given, using alternatives whenever possible, using neocytes, and modifying diet to decrease iron
absorption. Iron chelation indicated for patients with chronic
transfusion dependence if prognosis is otherwise good.
Transfusion-related acute
lung injury (TRALI)
Allergic reactions
Transfusion-associated
circulatory overload (TACO)
Dilutional effects
Hypocalcemia
Hyperkalemia
Hypothermia
Transfusion associated
Graft-versus-host disease
Iron overload
Contd...
64
Contd...
Post-transfusion purpura
Miscellaneous
Acute severe thrombocytopenia about 1 week after transfusion

due to alloantibodies to donor platelet antigen, usually human
platelet antigen 1A (HPA 1A). Self-limited, but treatment with
steroids, high-dose IgG, plasmapheresis, or exchange transfusion recommended to prevent CNS hemorrhage. Platelet
transfusions are ineffective even with compatible platelets.
Increased supply of complement may accelerate hemolysis in
paroxysmal nocturnal hemoglobinuria or make angioedema
worse in patient with C1 esterase inhibitor deficiency. Increased
blood viscosity may occur in patients with Waldenstrms macroglobulinemia, polycythemia, or leukemia with high WBC count.
clotting factors may occur, especially if extensive tissue injury or DIC is

present.
Clinically significant citrate (anticoagulant) intoxication is rare even
with massive transfusions. Prophylactic calcium administration is not indicated, with the possible exception of patients with severe hepatic dysfunction
or heart failure in whom citrate metabolism may be impaired. Hyperkalemia occurs rarely following even massive blood transfusion. There appears
to be no advantage in transfusing fresh red blood cells over stored cells.
Hypothermia may result from massive transfusion of refrigerated blood
and may impair cardiac function. Warming of blood prior to transfusion is
recommended to prevent this complication. A significant potential hazard
of massive transfusion is unrecognized acute hemolytic transfusion reaction.
Use of Non Cross-matched Blood in Emergency Situations

In the absence of unusual antibodies, complete cross-matching takes approximately 30 to 60 minutes. In most cases of acute hemorrhage,
transfusion with noncross-matched type O, Rh-negative blood or ABO
compatible blood tested with an abbreviated cross-match (5-20 minutes)
may be necessary. If the recipients blood type is known, unmatched blood
of the same group may be used. Patients with group AB blood may receive
either group A or group B cells.
Emerging Technologies
Blood substitutes (e.g. cell-free Hb solutions and perfluorocarbon emulsions) may serve as alternative oxygen carriers in patients undergoing
surgery, following massive trauma, or for patients who refuse blood products. New erythropoiesis stimulants may offer more rapid correction of
anemia. Embryonic stem cells have the capacity to produce all blood cells
and eventually may lead to a new source of cells for blood transfusion.
65
Bibliography
1.
2.
3.
4.
Boshkov LK. Transfusion-related acute lung injury and the ICU. Crit Care
Clin 2005;21:47995.
Davenport RD. Pathophysiology of hemolytic transfusion reactions. Semin
Hematol 2005;42:1658.
Goodnough LT. Risks of blood transfusion. Crit Care Med 2003; 31(Suppl
12):S67886.
Goodnough LT, Shander A, Brecher ME. Transfusion medicine: Looking to
the future. Lancet 2003;361(9352):1619.
SEDATION, ANALGESIA,
INTUBATION AND
PROCEDURES
3.1
Sedation, Analgesia, Paralysis
and Drug Dilutions
Many times children need to be sedated in the emergency room (ER) for
proper assessment and various procedures.
Goals of Sedation in the ER

1.
2.
3.
4.
5.
Analgesiafor painful diseases and procedures.

Compliancewith controlled ventilation and routine intensive care.
Amnesiaduring the periods of sedation.
Reduce the physiology of sedation.
Avoid complications.
Classes of Drugs Commonly Used in the ER

1.
2.
3.
4.
5.
6.
7.
8.
Narcotics.
Benzodiazepines.
Nonsteroidal anti-inflammatory agents (ketorolac).
Ketamine.
Propofol.
Neuroleptics.
Barbiturates.
Paralyticsdepolarizing and nondepolarizing.
Situations in which some combination of the above drugs are commonly needed
1. Mechanical ventilation, postoperative.
2. Mechanical ventilation, ARDS.
3. Mechanical ventilation, asthma.
4. Mechanical ventilation, epiglottis or croup.
5. Head injury.
6. Postoperative.
7. Chest syndrome.
8. Intubationin various scenarios.
9. Painful procedureschest tubes, lumbar puncture, bone marrow aspirate, dressing changes, endotracheal tube suctioning.
70
Basic Pharmacologic Principles

1. Onset of action: T1/2 reflects initial distribution from blood to highly
perfused tissues. Clinical onset of action is the time necessary to see
effect of the drug.
2. Half-life (T1/2): The time it takes for the concentration of the drug to
decrease by half Elimination constant, Kel = 0.693 T1/2 (T1/2 = redistribution and metabolic clearance).
3. Volume of distribution (Vd): Relates the amount of drug in the body to
the concentration of drug in the blood or plasma, the fluid volume
that would be needed to account for the entire drug in the body. Small
Vd implies that the drug is retained within the vascular compartment,
large Vd implies distribution throughout the body of sequestration in
certain tissues. Vd (ml/kg) = Dose (mg/kg) /concentration at time 0
(mg/ml).
4. Clearance (Cl): The ability of the body to eliminate a drug, expressed
as a volume of blood cleared of drug per unit time. Cl = Vd Kel.
5. Metabolism: Mostly renal and/or hepatic for most drugs.
6. Bioavailability: The percent of the dose reaching the systematic circulation as unchanged drug following administration by any route.
Opioids
Opiates provide both pain relief and sedation. They are the most commonly used class of drugs for analgesia in the ER. In addition to their
analgesic properties, narcotics decrease responsiveness to external stimulation and reduce the level of consciousness. Nevertheless, the sedative
properties of narcotics are inferior to those of the benzodiazepines, and
amnesia following narcotic administration is incomplete. The various opioids are listed in Table 3.1.1.
The characteristic features of various opioids are as below:
Morphine
i. Minimal direct effect on myocardial performance.
ii. Histamine releasemay induce hypotension if large doses are given
rapidly.
iii. Dose-related analgesia, sedation and euphoria.
iv. Dose-related respiratory depression.
TABLE 3.1.1: The relative doses, elimination half lives and clearance of various opioids
Morphine
Meperidine
Fentanyl
Methadone
Relative dose
Elimination t1/2
Clearance (ml/kg/min)
0.1 mg
1.0 mg
1-5 mcg
0.1 mg
114 min
222 min
202 min
15 hours
14.7
15.1
11.6
Chapter 3.1: Sedation, Analgesia, Paralysis and Drug Dilutions
71
Meperidine
i.
ii.
iii.
iv.
v.
Respiratory depression similar to other opioids.

Normeperidine (metabolite of meperidine) is epileptogenic.
Mild vagolytic.
Histamine release and myocardial depression on high doses.
Less biliary tract spasm.
Fentanyl
i. Synthetic opioid, highly lipid soluble, shot distribution T1/2 but long
elimination T1/2.
ii. Metabolized almost exclusively in the liver, that may accumulate with
altered hepatic blood flow.
iii. Provides hemodynamic stability, even in very high doses, and blunts
pulmonary vascular responses.
iv. May produce muscle rigidity if given as large fast bolus.
v. Commonly causes lowering of heart rate (unrelated to pain relief or
sedation).
Methadone
i.
ii.
iii.
iv.
Potent analgesic effects, minimal hemodynamic effects.

Long half-life.
Absorption after oral administration reliably 50 to 70 percent that of IV.
Sedative and euphoric properties may be less pronounced than those
of morphine.
v. Useful for pain control as well as for treating abstinence phenomena.
Untoward Effects of Opioids

Respiratory depression: All opioids cause dose-related respiratory depression
by shifting the CO2 response curve to the right, and abolishing the ventilatory
response to hypoxemia. Depending on the drug, one can see decreased ventilatory rate or tidal volume (thus, the rate may be normal, but the tidal volume
may be inadequate). Respiratory depression may occur at any age.
Reversal
Done with naloxone.
Full reversal0.1 mg/kg body weight. 2.0 mg for >20 kg.
Partial reversalsTitrate to effect. Start with 2 to 10 mcg/kg. Easiest way
to do this is to take 0.4 mg (i.e. 1 cc of 0.4 mg/cc vial) and dilute in 10 cc NS
= 40 mcg/cc. Thus, 1 cc per 4 kg body weight equals 10 mcg/kg. Most
useful for patients who have significant residual pain (i.e. surgical, chest
syndrome, sickle cell crisis and oncology).
The half-life of naloxone is significantly shorter than morphine,
demerol or fentanyl. If there has been a significant overdose, more than
one dose will be necessary. A continuous infusion may be needed.
72
Pruritus
Several of the opioids cause itching, and there is significant interpatient
variability in susceptibility. It may be alleviated by diphenhydramine.
Tolerance and Dependence

Tolerance generally develops after 2 to 3 days of frequent or continuous
usage. Dependence (i.e. the potential for withdrawal symptoms) generally
develops after 5 to 7 days of frequent or continuous use. Tolerance is treated
by increasing the dose as needed for pain relief. Dependence is treated
with gradual withdrawal of the drug, either using the initial drug, or converting to methadone for convenient dosing. Treatment of withdrawal can
be difficult if the patient has been receiving narcotics for prolonged periods. In general, the longer the period of treatment, the longer the period
of withdrawal needed. Alternatively, one can treat symptoms with alternative drugs (A method usually reserved for those who have a psychological
as well as physical dependence on the drug).
Benzodiazepines
Benzodiazepines provide hypnosis, anxiolysis, antegrade amnesia and anticonvulsant activity. They do not provide analgesia. They are useful for
providing sedation and treating seizures, but one must remember to treat
pain with an analgesic. The various benzodiazepines are listed in Table 3.1.2.
Midazolam
It has a short onset of action, short duration of action, and relatively short
elimination half-life. For these reasons, it is useful for short procedures,
but inconvenient for prolonged sedation. It may be used as a constant
infusion. Continuous administration may result in prolonged sedation even
after the infusion is discontinued if the rate of administration is too high.
There have also been reports of dystonia and choreoathetosis after
midazolam infusion and may represent benzodiazepine withdrawal,
persistent effects of the drug, or the combined effect of multiple drugs.
Diazepam
It has a short onset of action, like midazolam, and slightly longer duration
of action, but a long elimination half-life. Thus, with repeated doses, it
may accumulate.
TABLE 3.1.2: The relative doses, elimination half lives and clearance of various benzodiazepines
Diazepam
Lorazepam
Midazolam
Relative
dose
T1/2
(redistribution)
(min)
T1/2
(elimination)
(hours)
Vd
(liter/kg)
Clearance
(ml/kg/min)
0.3-0.5
0.05
0.15-0.30
30-60
21-37
10-20
1-4
1.0-1.5
0.8-1.3
1.0-1.5
0.2-0.5
0.7-1.0
6-8
6-15
73
Lorazepam
It is less lipid-soluble, and has a longer duration of action, but a long elimination half-life. Thus, it is more appropriate than diazepam for prolonged
sedation. (Longer duration of action but less risk of accumulation with
repeated dosing).
Untoward Effects of Benzodiazepines

Tolerance
As with the narcotics, dose may need to be increased after 2 to 3 days.
Dependence
Dependence and withdrawal phenomena can be severe. Withdrawal needs
to be done carefully, looking for signs for withdrawal (tremor, tachycardia,
high BP). Too rapid withdrawal in severely dependent, patient can cause
seizures.
Choreoathetoid Movement Disorder

Usually improves with time.
Personality Changes
Usually improves with time, though after long-term, high dose use, personality changes may remain apparent to family members for weeks to
months.
Respiratory Depression
Dose related.
Reversal
Flumazenil: It is a benzodiazepine receptor antagonist. 0.2 mg over 30 sec
may increase dose up to 0.5 mg/minute. Up to 5 mg total. Contraindicated
where benzodiazepines have been used to treat seizures, chronic benzodiazepines use, TCAs present, mixed drug overdose.
Ketamine
Ketamine is chemically related to phencyclidine or cyclohexamine.
Ketamine hydrochloride is water soluble at commercial concentrations, but
is quite lipid soluble as well and quickly crosses the blood-brain barrier.
Pharmacokinetics is very similar in children and adults. With intravenous administration, the distribution half-life is less than 30 seconds, the
redistribution half-life 4.7 minutes, and the elimination half-life 2.2 hours.
Clinically, one sees peak concentrations within one minute of IV administration, with rapid absorption by the brain and early immediate induction of
74
clinical effects. With redistribution to peripheral tissues, the decrease in CNS

levels correlates with resolution of the clinical effect, generally within 15-20
minutes.
The anesthetic state produced by ketamine has been classically described as a functional and electrophysiological dissociation between the
thalamoneocortical and limbic systems. Ketamine is a potent analgesic at
sub-anesthetic concentrations, and the effects may be mediated by different mechanisms. Ketamine blocks NMDA receptors, and there is some data
that it interacts with opiate receptors as well as CNS muscarinic receptors.
Clinical Effects of Ketamine

CNS
Ketamine produces a dissociative state. Its effect on intracranial pressure
remains controversial in practice, but controlled studies in which ventilation was controlled showed no effect on intracranial pressure. It probably
does, however, increase CMRO2, and hence, use in patients with intracranial injury should probably be avoided if possible.
Emergence phenomena are frequently reported after the use of
ketamine in older adolescents. Concordant treatment with a benzodiazepine has been shown to prevent the development of unpleasant emergence
phenomena.
Cardiovascular System
Ketamine inhibits reuptake of catecholamines in both the peripheral circulation and the CNS in a dose-dependent fashion. It has a negative inotropic
effect on the myocardium, and a direct vasodilatory action on vascular
smooth muscle. This is generally overwhelmed by central sympathetic stimulation that occurs, however, leading to increase in heart rate, systematic
arterial pressure, and possibly systematic vascular resistance. The cardiovascular effects of ketamine are attenuated by alpha and beta blocking
agents, verapamil, benzodiazepines, and high epidural blockade.
Respiratory Effects
Ketamine is a mild respiratory depressant, and there is a dose-related increase in respiratory depression with incremental dose of ketamine. In
children, respiratory rate, tidal volume, and minute ventilation are unaffected, but the CO2 response curve is shifted to the right. Ketamine generally
preserves airway patency, and proactive airway reflexes are not repressed.
Transient bronchospasm or laryngospasm are rarely reported, and are associated with coincident respiratory infection. Ketamine increases oral
secretions, and this may be more clinically important in those children with
upper respiratory infections. Laryngospasm and the potential for emesis/
aspiration are more pronounced in infants and patients with a full stomach,
hence, these patients should be considered at risk for airway compromise.
75
Ketamine is a potent bronchodilator. The mechanisms of this response

is considered to be a combination of drug induced increase in circulating
catecholamines, direct smooth muscle dilatation, and inhibition of vagal
tone.
Neuromuscular Effects
Ketamine increases skeletal muscle tone, and there are frequently random
movements of the head or extremities. Ketamine also appears to potentiate the effects of neuromuscular blocking agents, both depolarizing and
nondepolarizing.
Intraocular Pressure
The effects of Ketamine on IOP are controversial, and the literature contains various contradictory reports regarding the potential for increased
IOP during ketamine anesthesia.
Dosage Recommendations
In the intensive care unit all anesthetic/analgesics/sedative agents should be
titrated to effect, with the unique physiology of each patient kept in mind.
This makes dosage recommendations difficult. These children may be compromised from a pulmonary, hemodynamic, or neurologic perspective, and
judicial use of any agent is warranted. Ketamine, for example, while supporting hemodynamics in the majority of patients, can cause hypotension if
the patients myocardial reserve is limited. Thus, these recommendations
are NOT to be interpreted as policy, but as simple guidelines.
Analgesia0.25 to 0.75 mg/kg IV
Dissociation/anesthesia 1.02.0 mg/kg IV in a well-hydrated patient with
good hemodynamics, 0.251.0 mg/kg in a severely dehydrated patient
with compromised myocardial function.
Continuous infusion1 mg/kg IV followed by 0.5 to 1.0 mg/kg/hour
Tolerance develops with repeated doses, and the optimal dose will need to
be increased.
Coadministration of benzodiazepines reduces the incidence of emergence phenomena in older children, but will prolong the duration of
sedation. This is not generally problematic in the intensive care setting,
but should be considered.
Propofol
Propofol (2, 6-disopropyl phenol) has low aqueous solubility, and the commercial preparation is a 1 percent (i.e., 10 mg/ml) solution in intralipid
(i.e. 1.2% egg phosphatide, 2.25% glycerol). It has a rapid onset and short
duration of action, and produces respiratory and cardiac depression that is
dose related. It is most useful for short procedures or short continuous
infusions.
76
Propofols unique pharmacokinetics is its rapid onset of hypnosis and

rapid resolution of effects after discontinuation of the drugs. The distribution of propofol is described by an open three-compartmental modelrapid
initial distribution from blood to highly perfused tissues (brain, heart, lung,
liver), t1/2 1.8 to 4.1 min, redistribution and metabolic clearance is t1/2 21 to
69 min, and slow return from poorly perfused tissues to blood t1/2 (184-834
min). Propofol has a large central volume of distribution, is highly protein
bound, and has an apparent high volume of distribution at equilibrium.
Propofol is extensively metabolized in the liver and possibly other sites
to inactive glucuronide and sulfate conjugates which are excreted in the
urine. In adults with renal or hepatic disease, propofol pharmacokinetic
parameters are not significantly altered.
Clinical effects are realized within 40 seconds of administration, and
emergence occurs within 10 to 30 minutes, depending partially on the
length of administration.
Clinical Effects of Propofol

CNS
IV administration of propofol produces hypnosis with minimal excitation, usually within 40 seconds. Propofol is not an analgesic. It appears to decrease ICP,
presumably by reducing cerebral blood flow (CBF) and increasing cerebrovascular resistance. CPP may be reduced to unacceptable levels. Propofol may be
effective anticonvulsants for status epilepticus unresponsive to other drugs.
Cardiovascular
Propofol may produce hypotension by a direct vasodilatory effect on both
arterial and venous beds and by reducing sympathetic tone. High concentration of propofol has a direct negative inotropic effect. Propofol is thus
more likely to induce hypotension in patients with hypovolemia, compromised myocardial function, or vasomotor instability.
Respiratory
Propofol acts as a moderate respiratory depressant, that blunts both hypoxic and hypercapnic ventilatory drive. Minute ventilation, tidal volume
and FRC are all decreased during its use. As well as high levels, airway
protective reflexes are blunted. Propofol is a mild bronchodilator and pulmonary dilator, but does not affect hypoxic vasoconstriction.
Metabolic
Propofol is significantly decreased VO2 and VCO2 in excess of its sedative
effects, possibly due to a decrease in cellular metabolism. Serum and urine
cortisol levels are decreased, but the adrenal response to ACTH is preserved. Hypothalamic function, thyroid function, or glucose metabolism
have not been shown to be affected.
77
There have been a number of reports of profound metabolic acidosis

in children who have received propofol for long-term (>24 hours) sedation. The etiology of the metabolic acidosis remains unclear, but probably
precludes routine use of propofol for long-term sedation in the PICU.
Immunologic
Anaphylaxis has been reported with propofol use. Because of its carrier, it
is contraindicated in patients with known hypersensitivity to egg.
Untoward Effects
1. Pain Pain on injection is relatively common and can be ameliorated
by concomitant injection of 1 percent lidocaine, generally in a ratio of
1 cc lidocaine to 10 to 20 cc propofol.
2. Hyperlipidemia may occur with long-term use.
3. Green urine (No clinical significance).
4. Ability to support bacterial growth due to carrier media. Thus, should
be treated as a sterile injection.
5. In vitro evidence of inhibition of neutrophil chemotaxis.
6. Excitatory phenomena when there are low serum levels of drugs.
Dosage Recommendations
1. As with all anesthetics, keep hydration status, vascular tone and inotropic state in mind.
2. If patient is not intubated, have available equipment to secure an airway.
3. For induction (intubation)0.5 to 1.0 mg/kg (i.e. 0.5-1.0cc/10 kg).
4. Bolus method for short procedure0.1 to 0.5 mg/kg/bolus, every 3 to
10 minutes.
5. Maintenance (sedation)15 to 100 mcg/kg/min, (i.e. 0.075 to 0.6 ml/
kg/hour) start with low dose, increase as necessary. Occasionally need
to use upto 300 mcg/kg/min.
6. ICU sedationInitial 5 to 10 mcg/kg/min, increase as necessary in 10
mcg/kg/min increments, up to 100 mcg/kg/min.
Muscle Relaxants
Muscles relaxants are used when one needs to have the patient motionless
with muscle activity. They do not provide any sedation or analgesia.
Indications for Muscle Relaxants

The indications are always relative.
1. Intubation.
2. Mechanical ventilation where risk of extubation is great or risk of baro/
volutrauma is high.
3. Procedures such as central line placement of biopsy in the intubated
patients.
78
4. Intractable intracranial hypertension (if ICP being monitored).

5. Reduction of CO2 production or O2 consumption.
Classification of Neuromuscular Blockers

Depolarizing Neuromuscular Blocker
Succinylcholine.
Nondepolarizing Neuromuscular Blockers

i.
ii.
iii.
iv.
Pancuronium, vecuronium.
Atracurium, cis-atracurium.
Doxacurium.
Rocuronium.
Succinylcholine
Sux is both loved and hated. One must understand why before one uses
it safely. It is a depolarizing neuromuscular blockerit depolarizes the
neuromuscular junction by binding the Ach receptor and further transmission of nerve impulses cannot be propagated. It has a rapid onset of action
average 45 seconds to achieve incubating conditions and short duration
of actiongenerally 5 to 8 minutes. It is vagotonic, thus bradycardia is
common and may be hemodynamically significant, necessitating premeditation with atropine in most cases.
Fasciculation occurs in children and adults and rare in infants. There is
a rise in serum K+ of 0.5 mEq in normal patients (those with history of
muscle disease), and hence is to be avoided in states of hyperkalemia. The
rise in serum K+ is massive in certain pathology statesburn injury, crushes
injury, spinal cord injury and certain neuromuscular diseases. It is also a
triggering agent for malignant hyperthermia (which may be fatal), and
patients who are known to have methemoglobinemia, who have a family
history of methemoglobinemia, or who have a condition that puts them at
risk for methemoglobinemia should never receive succinylcholine.
Risk of hyperkalemia: Burn injury, tetanus, spinal cord injury, encephalitis,
crush injuries, certain neuromuscular diseases and intra-abdominal sepsis.
Risk of malignant hyperthermia: Positive family history, muscular dystrophies (Duchenne muscular dystrophy), central core myopathy and
unknown myopathies.
Other untoward effects of succinylcholine
i. Jaw stiffness, usually masseter muscle spasm.
ii. Arrhythmiasusually vagal in origin. Premedicate with atropine.
iii. Myoglobinemiarelatively frequent (40% if given succinylcholine and
halothane), occasionally significant enough to produce myoglobinuria.
iv. Increased intraocular pressureavoid in the presence of eye injury.
v. Inability to intubateeven 5 minutes can be a long time. Short duration of action is not a license to use succinylcholine in a situation
when the patient should not be paralyzed.
79
Nondepolarizing Neuromuscular Blockers

These drugs have a longer onset of action and longer duration of action than succinylcholine. They act as competitive antagonists of Ach at
the neuromuscular junction. They do not affect potassium and are not
methemoglobinemia triggering agents. They differ in their chemical
structure, route of metabolism and elimination, onset and duration of
action. The various nondepolarizing neuromuscular blockers are listed
in Table 3.1.3.
Problems associated with neuromuscular blocker use
i. Loss of a valuable patient monitorwithout muscle activity one must
depend on vital changes to assess pain and anxiety, as well as abdominal assessment.
ii. Fluid retention without muscle activity to stimulate venous and lymphatic drainage.
iii. Long-term weakness has been associated with continuous infusions
of neuromuscular blocking agents, most commonly the steroid based
NMBs (vecuronium) used in conjunction with steroids.
iv. There are now reports of significant myopathy associated with
atracurium, however, so the implication of the steroid base as etiologic may not be valid. Excessive blockade should be avoided. This
may be accomplished by Train of Four testing, giving drugs as intermittent boluses, or by stopping paralysis on a regular basis and
observing the time needed for return of functions.
v. Many antibiotics, especially than aminoglycosides, have neuromuscular blocking properties (complex and varied mechanisms).
Aminoglycosides should be avoided if possible if continuous infusions of NMBs are used. If not avoidable, depth of paralysis should
be monitored.
The standard dilutions and infusions of comman drugs used in emergency are shown in Table 3.1.4
TABLE 3.1.3: Nondepolarizing neuromuscular blockers
Dose
(mg/kg)
Onset
Duration
effects
Side
Metabolism
Pancuronium
0.1
2 min
4-6 min
Tachycardia
with bolus use
Vecuronium
0.1-0.3
1.5-2 min
20-30
(children)
60-80
(infants)
Atracurium
0.3-0.6
2-3 min
15 min
Rocuronium
0.6-1.2
60 sec
60 min
Renal (60-80%)
and biliary excretion
Hepatic
metabolism,
biliary (80%)
and renal (20%)
excretion.
Hoffman degradation
Histamine
release (mild)
200 mg/20 ml
(1ml = 10mg)
4 mg powder
IV
IV
IV
Propofol
Vecuronium
Antibiotics
Acyclovir
250 mg powder
5 mg/5 ml
100 mg/2 ml
500 mg powder
Midazolam
IV
Suxamethonium IV
Thiopentone
IV
10ml
1 ml
2 ml
2 ml
Fentanyl
100 mcg/2 ml
1 ml
Rapid sequence induction agents

Ketamine
IV
500 mg/10 ml
Phenobarb
Phenytoin
IV
2 ml
Nil
1 ml
1 ml
5 ml
10 mg/2 ml
5 mg/5 ml
5 mg/1 ml
200 mg/1 ml
250 mg/5 ml
Midazolam
2 ml
Amount to
draw up
WFI 10 ml
+ NS 40 ml
WFI 4ml
NS 4 ml
NS 8 ml
WFI 20 ml
Can then
portion into
5 ml syringe
NS 8 ml
NS 9 ml
NS 8 ml
Nil
Nil
NS 9 ml
NS 20 ml
NS 8 ml
Diluent and
volume
WFI: Water for injection,
PR
IV
IM
IV
IV
Initial
concentration
10 mg/2 ml
Intended
route of
delivery
Antiepileptic drugs
Diazepam
IV
Drug
TABLE 3.1.4: Emergency Drugs: Standard Dilutions and Infusions
5 mg/ml
1 mg/ml
10 mg/ml
1 mg/ml
10 mg/ml
25 mg/ml
10 mcg/ml
5 mg/ml
1 mg/ml
1 mg/ml
5 mg/ml
20 mg/ml
10 mg/ml
1 mg/ml
Final
concentration
of drug
NS: Normal Saline
D: 5% Dextrose
10 mg/kg
0.1 mg/kg
2-3 mg/kg
0.1-0.3 mg/kg
1-1.5 mg/kg
4 mg/kg
less if low
BP or GCS
2 mcg/kg (less in infants)
1-2 mg/kg
0.5 mg/kg
0.1 mg/kg increments
0.1 mg/kg
Load 15-20 mg/kg
Load 15-20 mg/kg
0.2 mg/kg (0.1-0.3 mg/kg)
Suggested
dose
range
Over 1 hr
Rapid IV
Over 10 sec
Over 10-30 sec

Give over 2-3 min
Second dose if reqd
Over >30 sec
Over 15 min
Over 15-20 min
Give slowly
Give slowly
Infusion
rate
Fridge
Beware hypotension.
Contd...
Do not use in child < 6 monthsBeware

laryngospasm if too rapid injection
Use with caution under 6 months
Brief muscle rigidity high doses
Fridge
Avoid extravasation
Beware hypotension
Use Dilantin filter cardiac monitor
Beware hypotension and respiratory

depression. Antidote flumazenil
Other
comments
80
IV
IV
Metoprolol
Lignocaine
Hydralazine
Frusemide
Nitroprusside
IV
IV
IV
Antihypertensive agents
Diazoxide
IV
IV
Digoxin
2 ml
2 ml
Amount to
draw up
20 mg/2 ml
20 mg/2 ml
50 mg powder
+ reconstituent
300 mg/20 ml
2 ml
2 ml
3 mg/kg
10 ml
500 mcg/2 ml
2 ml
(0.25 mg/ml)
5 mg/5 ml
5 ml
40 mg/2 ml (2%) 2 ml
6 mg/2 ml
IV
Adenosine
1 g powder
1 g powder
1 g powder
80 mg/2 ml
500 mg/100 ml
600 mg powder
500 mg powder
0.6 mg/ml
IV
IV
IV
IV
IV
IV
IV
Amoxicillin
Cefotaxime
Ceftriaxone
Gentamicin
Metronidazole
Penicillin G
Vancomycin
Initial
concentration
Cardiac drugs: Single use

Atropine
IV
Intended
route of
delivery
Drug
Contd...
NS 18 ml
Nil
Make up to
50 ml with NS
Nil
NS 5 ml
NS 6 ml
NS 4 ml
(infants)
None
(adolescents)
NS 8 ml
WFI 9.3 ml
WFI 9.6 ml
WFI 9.7 ml
NS 6 ml
Nil
WFI 5.6 ml
WFI 10 ml
Diluent and
volume
10-50 mg/kg
25-50 mg/kg
25-50 mg/kg
2.5-5 mg/kg
7.5 mg/kg
25-50 mg/kg
10 mg/kg
Suggested
dose
range
1 mg/ml
10 mg/ml
1 ml/hr =
1 mcg/kg/min
15 mg/ml
500 mcg/ml
5 mg/ml
50 mcg/ml
0.1-0.3 mg/kg/hr
1 mg/kg
0.5-6.0 mcg/kg/min
1-3 mg/kg/dose
0.1 mg/kg
1 mg/kg
15 mcg/kg (1/2 load)
20 mcg/kg
max 0.6 mg/dose
1 mg/ml (infants)3mg/ml (older)
0.6 mg/ml
100 mg/ml
100 mg/ml
100 mg/ml
10 mg/ml
5 mg/ml
100 mg/ml
50 mg/ml
Final
concentration
of drug
Over >5 min

Slow push
Over 30 sec
Over > 5 min

Rapid push
Over > 5 min (30 min)
0.05 mg/kg
Rapid push
Slow push
Slow push
Slow push
Over 30 min
Over 20 min
Over 15-30 min
Over 60 min
Infusion
rate
Contd...
Maximum 150 mg/dose may repeat

every 5-15 min
Adjust rate every 30 min as needed
Beware hypokalemia
Protect from light
Monitor cyanide levels
Beware bradycardia, CCF, asthma
Rapid pushthen flush

Repeat every two minutes at higher
dose to max 0.25 mg/kg or version
Once dose drawn up dilute further

to give concentration < 5 mg/ml
Protect from light in storage
Other
comments
81
Intended
route of
delivery
Initial
concentration
0.3 mg/kg
IV infusion 2 mg/ml
Noradrenaline
30 mg/kg
3 mg/kg
3 mg/kg
0.3 mg/kg
2.5 g/5 ml (50%) 5 ml
1 ml
1 ml
10 ml
5 ml
30 mcg/kg
IV
Magnesium
sulfate
400 mcg/1 ml
500 mcg/1 ml
1 g/10 ml(10%)
4 mg/ml
500 mcg/5 ml
Amount to
draw up
Cardiac support drugs: Infusions

Adrenaline
IV
1 mg/1 ml
infusion
(1:1000)
Dobutamine
IV
250 mg/20 ml
infusion
Dopamine
IV
200 mg/5 ml
infusion
Lignocaine
IV
40 mg/2 ml (2%)
infusion
500 mcg/ml
Prostaglandin E1 IV
IV
IV stat
IV
IV
IV
Naloxone
Salbutamol
Calcium
Gluconate
Others
Dexamethasone
Flumazenil
Gastrointestinal decontamination drugs

Activated
NG
50 g/300 ml
charcoal/
sorbitol
35% pre-mix
Drug
Contd...
Make up to
50 ml with NS
Make up to 50
ml with NS
Make up to 50
ml with NS
Make up to 50
ml with NS
Make up to 50
ml with NS
Make up to 50
ml with NS
20 ml NS
Nil
NS 19 ml
Nil
Nil
NS 5 ml
Diluent and
volume
1 ml/hr =
0.1 mcg/kg/min
1 ml/hr =
1 mcg/kg/min
1 ml/hr =
1 mcg/kg/min
1 ml/hr =
10 mcg/kg/min
1 ml/hr =
0.01 mcg/kg/min
1 ml/hr=
0.1 mcg/kg/min
100 mg/ml
0.4 mg/ml
25 mcg/ml
100 mg/ml
50 mcg/ml
1 g/6 ml slurry
Final
concentration
of drug
0.05-0.5 mcg/kg/min
0.01-0.1 mcg/kg/min
10-50 mcg/kg/min
1-20 mcg/kg/min
1-20 mcg/kg/min
0.05-1.0 mcg/kg/min
25-40 mg/kg Max 1.2 g
0.1 mg/kg
10 mcg/kg
20 mg/kg/hr =
0.2 ml/kg/hr Max 20 ml
0.1-0.2 mg/kg
5 mcg/kg
1-2g/kg =
6-12 ml/kg
Suggested
dose
range
Over 30 min
Over 10 min
Over 60 minutes
Over 1 min
Infusion
rate
May cause apneas.

Cardiac consult.
Central line only
ICU consult
May be given in
peripheral IV
Need central IV usually
Repeat every 60 sec as needed to max

2 mg (0.04 mg/kg or 8 doses)
Max 2 mg/dose + repeat PRN
Cardiac monitor
Eg Ca channel blocker overdose
orunstable hyperkalemia
Cease if bradycardia
Cardiac monitor
May need repeat doses of

charcoal
Do not use in ileus
Other
comments
82
83
Bibliography
1.
2.
3.
Barkin R, Rosen P. Emergency Pediatrics: A Guide to Ambulatory Care. 5th

edition, 1999.
Crain E, Gershel J, Gallager E. Clinical Manual of Emergency Pediatrics. 4th
edition, 2002.
Lieh-Lai M W, Ling-McGeorge KA, Asi-Bautista M C. Pediatric Acute Care,
2nd edition. Philadelphia: Lippincott Williams and Wilkins, 2003.
3.2
Basics of Intubation
Jayanta Bandyopadhyay, Mahasweta Chaudhuri
Intubation is the definitive advanced life support technique for airway

management. The purpose is to either secure the airway or to ensure
adequate ventilation and oxygenation. The pediatric airway is particularly
challenging due to the small patient size, differences in anatomy, and
relatively high oxygen demand in pediatric patients. The characteristics of
pediatric airway and the associated implications during intubation is
summarized in Table 3.2.1. Figures 3.2.1A and B shows technique of bag
and mask ventilation.
Indications for Intubation

One should be aware that intubation may be difficult and expert hands
should be ready. Oropharyngeal airway and position is shown in Figures
3.2.2A and B.
1. Provide airway in functional or anatomic airway obstruction (chest
trauma with flail chest, maxillofacial injury, epiglottitis, peritonsillar
abscess).
2. Protect airway in patients with loss of cough and gag reflexes and copious tracheal secretions as a result of inadequate CNS control or
neuromuscular diseases (Apnea, head injury, GB syndrome and poliomyelitis).
TABLE 3.2.1: Pediatric airway and its implications during intubation
Characteristics
Implications
Infant epiglottis is omega () shaped and

angled away from the axis of trachea.
Relatively larger tongue, which can
obstruct airway
Larynx is more rostral and anterior
This anatomy necessitates use of straight blade

laryngoscope
Commonest cause of airway obstruction.
May necessitate better head positioning.
Difficult to visualize the cord, a shoulder roll may
be needed, may have to visualise the cord at 45
angle or greater
Uncuffed tube are used in children up to 8 yrs,
however, present studies show cuffed tube may be
used safely if needed
Narrowest part of pediatric airway is

cricoid cartilage
Chapter 3.2: Basics of Intubation
FIGS 3.2.1A and B: Bag and mask ventilation
FIGS 3.2.2A and B: Oropharyngeal airwayproper size and position
85
86
3. Instituting positive pressure ventilation (Pneumonia, ARDS, pulmonary edema, bronchiolitis).

4. Circulatory disorder (Cardiac arrest, shock, pulmonary artery hypertension).
5. ElectiveBefore any major and/or extensive surgery, till hemodynamically stable.
Equipment
1.
2.
3.
4.
5.
6.
7.
8.
9.
Suction apparatus and tracheal suction catheter.

Oxygen.
Appropriate ET tubedifferent sizes.
Bag valve mask device.
Laryngoscope, preferable straight blade.
Tincture benzoin, tape.
Medications.
Monitoring equipment.
Experienced medical and paramedical assistants.
Selection of Laryngoscope Blade

Miller blade is preferred for infants and younger children. It facilitates
lifting of the epiglottis and exposing the glottic opening. Care must be
taken to avoid using the blade as a fulcrum with pressure on the teeth and
gums. Macintosh blades are generally used in older children.
ET Tube Size
The appropriate ET tube, laryngoscope blade and suction catheter details
are represented in Table 3.2.2.
Nasal intubation should not be tried in the following:
1. Need for immediate airway access.
2. Fracture at the base of skull, faciomaxillary trauma.
3. Coagulopathy.
Pharmological Control Over Intubation

1. Without any premedication: Done in a moribund patient with impending cardiorespiratory arrest where a delay to paralyze may be
detrimental. Access may be difficult due to struggle, bite and may cause
trauma to airway, laryngospasm, deteriorating vital signs during the
procedure. This is the commonest situation in emergency room.
2. With sedation: This should be attempted by the most experienced hand.
Sedation may be used where patient has a low or moderate oxygen requirement (using fentanyl and midazolam followed by suxamethonium
and then vecuronium). Avoid using ketamine if suspecting raised intracranial tension. But intubation using sedation runs the risk of compromised
airway reflexes and hence chance of aspiration.
87
Chapter 3.2: Basics of Intubation

TABLE 3.2.2: ET tube, laryngoscope blade and suction catheter details
Body
Tube size Depth of
Laryngoscope Laryngoscope
Tracheal suction
weight / age (mm)
insertion (cm) blade (Miller) blade (Macintosh) catheter (F)
15003000 gm
Neonate
6 months
6 18
months
2 years
>2 years
(8-10 yrs)
Adult
3.0
7-9
3.5
10
4.0
11
6-8
4.5
Age (yrs)/
4+4
12
Age (yrs)/
2+ 12
21-23
2
2
2-3
3-4
4
8
10-12
8-8.5
(Men)
7.5- 8
(Women)
1
2-6 yrs = 1
6-10 yrs = 2
>11 yrs = 2-3
3
14
3. Anesthetized: Done in totally controlled and elective situation like prior

to major surgery (using thiopentone, propofol/ketamine according to
individual choice and case to case basis).
Preparing for the Procedure

While intubating a patient, there are certain basic essentials that must be
present to ensure a safe intubation. They can be remembered by the mnemonic SALT.
Suction: It is the first and an extremely important step in the whole procedure. Often patients may have secretions in the pharynx that make
visualization of the vocal cords difficult.
Airway: Oxygen source with proper delivery mechanism (bag and mask)
must be available. Medication and monitoring equipment should be ready.
Laryngoscope: Proper size with good batteries should be ready for placing
an endotracheal tube.
Tube: Endotracheal tubes of appropriate sizes.
Positioning the Patient

1. Child above 2 yrsA folded towel to be placed under the occiput to
align the pharyngeal and tracheal axis.
2. Child below 2 yrsA folded sheet to be placed under shoulder to align
airway.
Procedure
1. The child should be assessed, vital signs, level of consciousness, and
oxygen saturation should be recorded. Gastric content should be aspirated to avoid aspiration during intubation.
88
2. Preoxygenate and ventilate with 100 percent O2 using bag-valve mask.

Premedicate as per requirement.
3. Airway is visualized directly using laryngoscope.
4. When vocal cords have been visualized, the endotracheal tube is passed
through the cords.
5. Ventilation is initiated and tube placement is confirmed.
6. Proper tube placement should be confirmed by the following:
i. Auscultate to confirm equal breath sounds in axilla and no sound
over gastric area.
ii. Water vapor in the tracheal tube during exhalation.
iii. Pulse oximetry to confirm O2 saturation.
Endotracheal tube should be secured. Head immobilization should be
done to prevent tube dislodgement. Chest x-ray should be taken to check
tube placement, and also obtain arterial blood gas measurements to assess
the adequacy of ventilation.
Bibliography
1.
2.
3.
Barkin R, Rosen P. Emergency Pediatrics: A Guide to Ambulatory Care. 5th

edition, 1999.
Crain E, Gershel J, Gallager E. Clinical Manual of Emergency Pediatrics. 4th
edition, 2002.
Lieh-Lai M W, Ling-McGeorge KA, Asi-Bautista MC. Pediatric Acute Care, 2nd
3.3
Rapid Sequence Intubation
Rapid sequence intubation (RSI) is the administration of a potent induction

agent followed immediately by a rapidly acting neuromuscular blocking
agent to induce unconsciousness and motor paralysis for tracheal intubation.
Fundamental Concept
The technique is predicted on the fact that the patient was not fasting
prior to intubation and there is a risk of aspiration of gastric contents.
Therefore, administration of drugs is preceded by a preoxygenation phase
to permit a period of apnea to occur safely between the administration of
drugs and intubation. Bag and mask positive pressure assisted ventilation
should not be performed as it may cause gastric distension and increase
the risk of aspiration.
Indications
RSI is indicated in pediatric patients who require tracheal intubation but
are considered at high risk for aspiration of gastric contents.
i. Recent oral intake.
ii. Comatosed patient.
iii. Swallowed blood in stomach.
iv. Head injury.
RSI is the cornerstone of emergency airway management. The superiority of RSI in terms of success rate, low complication rate and control of
adverse effects makes it procedure of choice for most emergency department intubations.
Contraindications
i.
ii.
iii.
iv.
Anticipated difficult airway.

Untreated shock.
Facial, trauma, fracture or edema.
Inexperienced physician.
90
Technique
The following 7 Ps are the stepwise procedures for RSI.
Preparation
Assess carefully for presence of difficult airway. Predictors of a difficult airway include the following:
i. Small mouth, facial trauma, limited mouth opening or short
interincisor distance.
ii. Short neck or limited neck mobility.
iii. Receding mandible or mandibular hypoplasia.
iv. High arched and narrow palate.
v. Prominent upper central incisor with overriding maxilla.
vi. Temporomandibular dysfunction.
vii. Rigid cervical spine.
viii. Obesity.
ix. Infants with associated congenital anomaly, tumor, subglottic stenosis, extrinsic tracheal compression.
Escape plans in the event of failed intubation must be ready with all
necessary equipments at hand. These include laryngeal mask ventilation,
anesthesist and surgical consult or conscious intubation.
The following arrangements are must for proper preparation:
i. Patient should be in an area of emergency department properly
equipped and organized for resuscitation.
ii. Cardiac monitoring, BP monitoring and pulse oximetry.
iii. At least one well functioning secured IV line, advised to have another line before induction.
iv. All pharmacolgic agents drawn up and properly labelled and arranged
according to planned sequence.
v. Two functioning laryngoscope handles and variety of blades (2 different sized curved and straight blades).
vi. Light bulbs on each laryngoscope should be handtightened to ensure they are firmly seated.
vii. Proper sized endotracheal tube (ETT). Keep a size bigger and a
smaller (0.5 mm) ready.
viii. ETT cuff (generally used 8 years and above) should be checked for
proper inflation and any leak thereafter.
ix. Use stylet and take care that the proximal end does not protrude
beyond the ETT.
x. Suction source, Yankauer suction, tape, bag-valve-mask device, oxygen source.
Preoxygenation
It is the establishment of oxygen reservoir within the lungs and body tissue
to allow several minutes of apnea to occur without arterial desaturation.
Chapter 3.3: Rapid Sequence Intubation
91
The principal reservoir is functional residual capacity (FRC) in the lungs

which is 30 ml/kg. Administration of 100 percent oxygen for 5 minutes
replaces predominantly nitrogenous mixture of room air with oxygen allowing several minutes of apnea before saturation falls below 90 percent.
Always use pulse oximetry to monitor saturation and avoid guess work.
Pretreatment
It is the administration of drugs to mitigate the adverse effects associated
with intubation. The primary benefits of these agents are to add the depth
of anesthesia, modify succinylcholine side effects or permit a reduced dose
of induction agent.
Intravenous lidocaine (1-1.5 mg/kg) for reactive airway disease or raised
ICP or fentanyl (2 mg/kg) to blunt the sympathetic response 3-5 minutes
before induction is advocated by many authors. Topical lidocaine 5 mg/kg
as aerosol or 3 mg/kg as direct topical application minimizes the risk for
systemic toxicity.
Atropine (10 mg/kg) is recommended in infants for reducing the risk
of arrhythmias and reflex bradycardia from laryngoscopy and succinylcholine.
Paralysis with Induction

Induction agent is given as a rapid IV push followed immediately by rapid
IV push of neuromuscular blockade by succinylcholine. The patient will
begin to loose consciousness and respiration will decrease. After 20 to 30
seconds, apnea universally sets in.
Common Induction Agents

One should be cautious with the first three drugs if there is associated
hypotension:
i. Thiopentone 4 mg/kg (Lower dose to 2-3 mg/kg if hypotensive),
ii. Propofol 2 to 3 mg/kg.
iii. Midazolam 0.1 to 0.3 mg/kg.
iv. Ketamine 1 to 2 mg/kg. It is the preferred drug in hypotensive and
asthmatic patient. It should be avoided if raised ICT or IOP is suspected or there is uncontrolled hypertension.
v. Etomidate 0.2 to 0.4 mg/kg. It lacks analgesic property and minimally
alters hemodynamic effects. Experience in children still is limited.
Muscle Relaxant
Succinylcholine (1-2 mg/kg) is the only depolarizing agent clinically available and only agent with fastest onset of action (30-45 secs) and recovery
(5-10 minutes). It remains the drug of choice for RSI of pediatric patient in
emergency department unless specifically contraindicated for the following reasons. Though rare, the conditions should be always remembered
for its devastating consequences.
92
i. Malignant hyperthermia or associated conditionCentral core disease, muscular dystrophy (Duchenne, Becker, myotonia, others),
King-Denborough syndrome.
ii. Chronic myopathy or denervating neuromuscular disease.
iii. 48 to 72 hrs after acute phase denervating injury and burns.
iv. Pre-existing hyperkalemia.
v. Known cholinesterase deficiency (Prolonged duration of action).
Rocuronium, a relatively new nondepolarizing agent with similar onset of action (35-60 secs) but late recovery(30-45 minutes) becomes the
next drug of choice in such cases.
Protection and Positioning

Sellicks maneuver, the application of firm pressure on the cricoid cartilage
to prevent regurgitation of gastric contents should be started immediately
on the observation that the patient is loosing consciousness. The maneuver should be continued throughout the entire intubation sequence until
ETT has been placed correctly, position checked and cuff inflated. In few
compromised patients where bag-mask ventilation is necessary to be continued before, during and after intubation, Sellicks maneuver should be
applied throughout to minimize the likelihood of aspiration.
Placement and Proof

Check the jaw flaccidity about 45 seconds after administrating succinylcholine. Proceed gently taking care of dentition and airway to cause
minimum trauma. Take out stylet and inflate the cuff after successfully
placing the ETT. Tape and tie, look for equal bilateral chest expansion and
auscultate equal air entry in the midaxilla and their absence in epigastrium. Chest radiograph should be obtained to check the pulmonary status
and position of the ETT. Monitor saturation.
Postintubation Management
i. Bradycardia: Assumed to be due to esophageal intubation with hypoxia until proved otherwise. Succinylcholine induced bradycardia
responds well to premedication with atropine.
ii. Hypertension: Indicates inadequate sedation. Long-term sedation
should be started using morphine-midazolam/fentanyl-midazolam
as continuous infusion and a competitive neuromuscular blocking
agent (pancuronium 0.1 mg/kg or vecuronium 0.1mg/kg) and should
be repeated 1/3 of original dose every 45 to 60 minutes or any motor
activity detected.
iii. Hypotension.
The various complications are summarized in Table 3.3.1.
Chapter 3.3: Rapid Sequence Intubation
93
TABLE 3.3.1: Complications of RSI

Cause
Detection
Action
Tension pneumothorax
PIP, desaturation, difficulty in

bagging, breath sound
PIP secondary to high
intrathoracic pressure.
Immediate thoracocentesis
Decreased venous return

Cardiogenic
Induction agents
Cardiac compromised
Other causes excluded
Fluid bolus, expiratory time,

bronchodilators
( airway resistance)
Pressor agents
Fluid bolus
Bibliography
1.
2.
McAllister JD, Gnauck KA. Rapid sequence intubation of the pediatric patient.
Pediatric Clinics of North America, 1999;1249-75.
Walls RM. Rapid sequence intubation. Manual of Emergency Airway Management, London: Lippincott Williams and Wilkins 2000;8-15.
3.4
Intraosseous Access
Jaydeep Choudhury
Peripheral venous cannulation is sometimes difficult and time consuming.

The small veins may collapse during shock. Intraosseous (IO) access is required in life-threatening situations, particularly in a critically ill, injured
or severely dehydrated child. IO access is indicated when intravenous access fails (3 attempts or >90 seconds).
It can be used for administration of crystalloids, colloids, blood products and drugs. IO may be left in place for 72 to 96 hours, though it is
better to attempt and establish an intravenous line as soon as the child is
stabilized and remove the IO cannula.
Contraindications
i. Ipsilateral fracture (risk of extravasation and compartment syndrome).
ii. Previous attempt or placement of IO in the same leg (risk of extravasation).
iii. Osteogenesis imperfecta (risk of fracture).
iv. Osteopetrosis (risk of fracture).
v. Obvious overlying infection (a relative contraindication).
Procedure
Proximal Tibia
The procedure is illustrated in Figure 3.4.1.
1. Strict aseptic technique.
2. Local infiltration with 1 to 2 ml of 1 percent lignocaine.
3. Flex the knee and put a towel roll or a sandbag as support behind the
knee.
4. Hold the stylet ball in the palm of your hand, and place the tip of your
index finger 1 to 1.5 cm from the tip of the needle.
5. Insert the IO needle 1 to 3 cm below the tibial tuberosity on the
anteromedial surface of the tibia at 90 degrees to the skin (perpendicular) and slightly caudal (towards the foot) to avoid the epiphyseal
growth plate.
Chapter 3.4: Intraosseous Access
95
FIG. 3.4.1: IO in proximal tibia
6. Advance the needle using a screwing motion until a give is felt when
the needle penetrates the cortex of the bone.
7. Correct placement of IO needle is confirmed by the aspiration of blood
and marrow, if it stands upright without support and the infusion flows
smoothly.
Other Sites
i. Distal tibiaAs shown in Figure 3.4.2.
ii. Distal femurAs shown in Figure 3.4.3.
Complications
i.
ii.
iii.
iv.
v.
Local infection (cellulitis, osteomyelitis).

Compartment syndrome secondary to fluid extravasations.
Local hematoma.
Pain.
Potential for growth plate injuries in rare instances.
FIG. 3.4.2: IO in distal tibia
96
FIG. 3.4.3: IO in distal femur
Bibliography
1.
2.
Barkin R, Rosen P. Emergency: A Guide to ambulatory Care, 5th edition; 1999.

Eric V, Anamaria B, Peter R, Xavier L. Update in Anesthesia 2000;10:1.
3.5
Chest Tube Drainage and
Needle Thoracocentesis
Thoracocentesis is used to treat pneumothorax, pleural effusion, empyema and hemothorax. In case of tension pneumothorax, needle
thoracocentesis is performed as an emergency procedure.
Points to Remember
1. Do not delay for an X-ray if one is certain about the diagnosis.
2. Insert a cannula or green butterfly needle (in neonates) in the 2nd
intercostal space, midclavicular line on the same side as the tension
pneumothorax.
3. Connect to a 3-way stop cock and syringe and aspirate air.
4. When things are more stable, insert a chest drain and perform the
chest X-ray.
Chest Tube Placement

Requirements
i. Full aseptic technique with gloves, gown and patient skin preparation and sterile drapes.
ii. Monitoring of oxygen saturation and heart rate.
iii. Chest drain.
iv. Scalpel, blunt dissection forceps.
v. Needle holder and suture material.
vi. Under water seal equipment.
Procedure
1. Support the child supine or with affected side up.
2. Aim for 4th or 5th intercostals space in the mid-axillary line. The position should be guided by ultrasound when there is empyema.
3. Infiltrate local anesthetic. In apprehensive child, IV midazolam and
fentanyl may act as a good sedative and analgesic.
98
4. Make an incision just above and parallel with the rib, avoiding the
intercostals vessels and nerve that lie inferior to each rib. With fine
forceps, bluntly dissect down to the pleura.
5. Do not use the trocar in the chest drain; use the forceps to insert it.
After initial resistance, it will pop through the pleura. Advance it so
that all the holes are inside the chest.
6. Connect the drain to the seal or valve. Stitch the incision closed. Secure the tube with a stitch and use an occlusive dressing over the whole
site.
7. Confirm drain position with a chest X-ray.
8. If the drain is not bubbling, applying a small amount of suction will
help.
9. The drain can be removed once it has stopped bubbling for 24 hours.
Remove it on expiration or while the child is crying. Close the incision
and perform a chest X-ray after 2 to 4 hours.
Tables 3.5.1 and 3.5.2 shows common causes and criteria for differentiation between transudative and exudative pleural effusion and analysis of
pleural fluid respectively.
TABLE 3.5.1: Common causes and criteria for differentiation between transudative and exudative
pleural effusion
Variable
Common causes
Pleural fluid protein/

serum protein
Pleural fluid LDH/serum
LDH
Pleural fluid LDH
Transudate
i.
ii.
iii.
iv.
Congestive heart failure

Cirrhosis
Nephrotic Syndrome
Pulmonary embolism
Exudate
i.
ii.
iii.
iv.
v.
vi.
<0.5
Pneumonia
Trauma
Tuberculosis
Rheumatoid arthritis
SLE
Malignancy
>0.5
<0.6
< 2/3 upper limit of serum
LDH
>0.6
>2/3 upper limit of serum
LDH
TABLE 3.5.2: Analysis of pleural fluid

Containers
Primary study
Plain red top tube
Protein, LDH, amylase, glucose and triglycerides if

needed
Cell count, differential
Fluid pH
Gram staining and culturing (for aerobic and anaerobic
organisms, mycobacteria, fungi)
Cytologic analysis
EDTA, lavender top tube

Heparin treated blood gas syringe
Sterile container
Green top tube, heparinized
Chapter 3.5: Chest Tube Drainage and Needle Thoracocentesis
99
Complications
1.
2.
3.
4.
Pain, coughing or infection at local site.

Hemothorax, intra-abdominal injury.
Air embolism, postexpansion pulmonary edema.
Pneumothorax.
Bibliography
1.
Lieh-Lai MW, Ling-McGeorge KA, Asi-Bautista MC. Pediatric Acute Care, 2nd
3.6
Needle Pericardiocentesis
Pericardiocentesis is a needle procedure for either life-saving decompression of acute cardiac tamponade or for diagnostic evaluation of pericardial
effusion.
Indications
Therapeutic
1. Cardiac tamponadeHemodynamic compromise due to large or rapidly developing pericardial effusion.
2. Management of a large pericardial effusionMore than 20 mm separation of pericardial membranes on echocardiography.
3. Palliative in cases of metastatic, neoplastic disease involving pericardium.
Diagnostic
1. Obtaining pericardial fluid for analysis.
2. Pericardioscopy.
3. Epicardial or pericardial biopsy.
Contraindications
1. Aortic dissection producing pericardial effusion.
2. Uncorrected bleeding diathesis, including drug causes, such as anticoagulants.
3. Marked thrombocytopeniaPlatelet count less than 50 109/L.
4. Loculated pericardial effusion, or small pericardial effusion or posteriorly located pericardial effusion.
5. Where the effusion is caused by cardiac trauma, a surgical approach is
preferred. Pericardiocentesis may be used as an emergency procedure.
6. PyopericardiumSurgical drainage is preferred as fluid is likely to be
viscous and difficult to drain.
Chapter 3.6: Needle Pericardiocentesis
101
Equipment
1.
2.
3.
4.
ECG monitor.
Resuscitation facilitiesDefibrillator and emergency medications.
Preferably under ECHO guidance.
Equipments for central line insertion:
i. Sterile drapes, antiseptics.
ii. 10 ml syringe and fine-gauge needle with 5 to 10 ml 2 percent
lidocaine for local anesthesia.
iii. 22/25 G needles, scalpel and blade.
iv. Pericardiocentesis needle with guide wire and dilators.
v. Pigtail catheter with many holes.
vi. Drainage bag, 3-way tap.
Procedure
1.
The child should sit at 3045 angles (This allows pericardial fluid
to pool inferiorly).
2. The entry site should be selected closest to pericardial space as revealed by echocardiography, avoiding important.
3. Clean the procedure site and administer local anesthesia.
4. The needle should be introduced towards pericardial space using
echocardiographic guidance towards left shoulder at 15 to 20 angle
from abdominal wall as shown in Figure 3.6.1.
5. Intermittently instil local anesthesia as the needle is advanced.
6. Confirm gaining of pericardial space by echocardiographic guidance. Once pericardial space gained and confirmed, the soft-tipped
guide wire should be inserted, then the needle should be removed
and the dilators passed over to enlarge the track.
7. After this the soft-tipped cannula with multiple side-holes is passed
over the guide wire.
8. Then remove the guide wire and connect to drainage tubing and
secure with sutures.
9. Obtain samples of fluid for analysis, e.g. cytology, biochemistry, culture, etc.
10. Cannula may be left in situ for up to 24 hrs to drain large effusions.
Routine tests on pericardial fluid are often indicated including cell
count with differential, lactate dehydrogenase (LDH), protein, glucose,
Gram-stain, and routine bacterial cultures. Smear for acid-fast bacilli staining, adenosine deaminase, tuberculosis culture, viral cultures, and cytology
are indicated depending on the degree of suspicion of tuberculosis, specific viral, or cancer etiology. Further specific tests on pericardial fluid usually
depend on the results of the initial test.
102
FIG. 3.6.1: Procedure for pericardiocentesis
Post-procedure Monitoring
1. Vital signs should be monitored.
2. ECG monitoring during and after procedure.
3. Post-procedure chest X-ray and echocardiography to confirm position
of cannula.
4. Hypotension, pulseless electrical activity, pneumothorax and liver laceration should be assessed.
Complications
1.
2.
3.
4.
5.
Myocardial laceration, perforation.

Coronary artery or vein laceration or perforation.
Pneumothorax.
Cardiac arrhythmias, particularly bradycardia.
Peritoneal puncture, laceration or puncture of abdominal viscera, particularly liver.
6. Acute cardiac decompensation and pulmonary edema.
Bibliography
1.
Prajapati B. Essential Procedures in Pediatrics, 1st edition. New Delhi: Jaypee

Brothers, 2003.
3.7
Cricothyrotomy
Cricothyrotomy is an ultimate life saving procedure. It is indicated when

other airway methods are unsuccessful.
Procedure
1. Performed with the patients head in neutral position, with adequate
spine stabilization.
2. Prepare and drape the area.
3. Use one finger to palpate the cricothyroid membrane in the midline
between the thyroid and cricoid cartilages. It is critical to say precisely
in the midline during the procedure to ensure the airway is cannulated
appropriately and significant bleeding is avoided.
4. Once the membrane is identified clearly, attach a 10 ml syringe to a
large bore needle (14 gauge) or an over-the-needle catheter device.
5. Insert the needle with the catheter just below the mid point of the
cricoid membrane with the needle angled 45 degrees caudally.
6. Rapid aspiration of the air into the syringe indicates entry into the
tracheal lumen.
7. Withdraw the needle carefully advancing the catheter caudally into the
trachea taking care not to perforate the posterior tracheal wall. Recheck the position of the catheter through aspiration of the syringe.
8. Attach the hub of the catheter to an adapter to connect between the
oxygen source and the cannula. Oxygen flow to be more than15 liters/
min.
9. Ventilation can be provided by a jet ventilator or by occluding the open
port of the Y connector with the thumb placed on for 1 second and off
for 4 seconds.
10. This technique allows 30 to 40 minutes of oxygenation and is a temporary measure until a surer airway can be obtained.
Complications
1. Hemorrhage.
2. Carbon dioxide narcosis.
104
Bibliography
1.
2.
Textbook of Pediatric Critical Care, 3rd edition. Philadelphia: Mosby Elsevier,

2006; 505-6.
Thompson AE. Pediatric airway management. In: Furham BP, Zimmerman J,
Editors.
NEONATAL
EMERGENCIES
4.1
Neonatal Emergencies
Jaydeep Choudhury
Identifying a sick neonate is always a challenge. More so is the determination of neonatal emergencies. It is crucial for pediatricians and emergency
doctors to be alert particularly because of early discharge policies followed
in most newborn nurseries. The mothers impression is often invaluable in
this regard.
A neonate presenting with altered mental status is a common entity.
The history usually reveals only a change in feeding pattern or subtle behavioral changes. A high index of suspicion is the key. The following causes
as per the mnemonic THE V SEPSIS may be remembered as a basic guide.
Causes of a neonate presenting altered mental status: THE V SEPSIS
T Trauma
H Heart diseases
E Electrolyte imbalance
V Volume imbalance (hypovolemia, inappropriately prepared formula)
S Seizures
E Endocrine (congenital adrenal hyperplasia, thyrotoxicosis)
P Poison and toxins
S Surgical (volvulus, intussusception, necrotizing enterocolitis)
I Inborn errors of metabolism
S Sepsis
Assessment of a newborn right after birth in the delivery room is crucial. The standard practice is assessment of Apgar score at 1 and 5 minutes
after birth. A score of 10 at 1 minute indicates the newborn in perfect
condition, but it is unusual as most babies have some acrocyanosis. If 5
minute, Apgar score is 6, the score continue to be noted at 5 minutes
intervals till it is above 6. The Apgar scoring system is shown in Table 4.1.1.
Severe Hypothermia
All babies should be in thermoneutral environment. Ideally, a rectal temperature should be measured and the thermometer should be kept for 3
min in neonates, 2 min in infants and children.
108
TABLE 4.1.1: Apgar scoring system

Sign
Score 0
Score 1
Score 2
Heart rate
Respiratory effort
Muscle tone
Reflex irritability
Color
Absent
Absent
Limp
No response
Blue, pale
Under 100 beats/min

Slow (irregular)
Some flexion of extremities
Grimace
Pink body, blue extremities
Over 100 beats/min

Good crying
Active motion
Cough or sneeze
All pink
Temperature Range
Normal temperature:
Cold stress:
Moderate hypothermia:
Severe hypothermia:
36.537.5C
3636.5C
3236C
<32C
Management
Moderate Hypothermia
1. Skin to skin contact (Kangaroo method in neonate).
2. Frequent monitoring, every 15 minutes.
3. Frequent feeding.
Severe Hypothermia
Severe hypothermia is a life threatening condition and needs immediate
care. The management comprises of the following:
1. Radiant warmer which can provide extra heat and cause rapid rewarming. Temperature should be rapidly raised to 34oC and then slowly.
2. Room heater.
3. Oxygen.
4. Dextrose 10 percent IV 2 to 4 ml/kg bolus, blood glucose should be
checked regularly.
5. Intravenous fluid infusion.
Seizures
Typical frank seizures are often not present in neonates. It is very important to identify subtle seizures like abnormal eye movements, lip smacking,
abnormal tongue movements, repetitive chewing, drooling, yawning,
pedalling, apnea, focal or multifocal clonic, tonic posturing of limbs and
myoclonic seizures.
Management
1. Stabilization: T, A, B, C.
2. An intravenous line should be established. If possible blood sample
should be collected for sugar, calcium, magnesium, electrolytes, blood
Chapter 4.1: Neonatal Emergencies
3.
4.
5.
6.
7.
8.
109
cell count and CRP. The following management is continued one step
at a time till seizure is controlled, throughout taking care of the vital
functions.
If situation permits rapid screen of blood sugar should be done with
Dextrostix. The correction of hypoglycemia (40 mg/dl) should be
corrected immediately. Intravenous injection 10 percent dextrose 2 to
4 ml/kg over 3 min. If the seizure gets controlled then intravenous
infusion is started with dextrose at the rate of 6 to 8 mg/kg/min.
Lorazepam 0.1 mg/kg IV is the initial drug of choice. Lorazepam has
got smaller volume of distribution and longer half-life than diazepam.
Diazepam 0.1 to 0.3 mg/kg may also be given.
Phenobarbitone is the second choice, 15 to 20 mg/kg is given slow
intravenous. If the seizure is not controlled after 15 minutes, a second
loading dose 10 to 20 mg/kg can be given. Maximum total phenobarbitone loading dose is 50 to 60 mg/kg. Maintenance dose is 5 mg/kg in
two divided doses.
Phenytoin 15 to 25 mg/kg loading dose diluted in normal saline is
given slow intravenous over 15 minutes. Maintenance dose is 5 mg/kg
in two divided doses.
If hypocalcemia is present (7 mg/dl), calcium gluconate 10 percent
solution, 2 ml/kg is injected slowly over 5 to 10 minutes under cardiac
monitor.
Hyponatremia (125 mg/dl) should be corrected with 3 percent saline.
The replacement calculation is as follows.
(125 Serum Na) weight 0.6 mEq of Na+ (1 ml = 0.5 mEq), slowly
over 4 hours.
Hypoglycemia
By definition blood glucose <30 mg/dl is hypoglycemia. But neonates with
blood glucose between 30 and 40 mg/dl may be symptomatic. Thus any
blood glucose less than 40 mg/dl should be treated.
Management
1. Intravenous injection 10 percent dextrose 2 to 4 ml/kg over 3 minutes.
2. Followed by intravenous infusion started at the rate of 6 to 8 mg/kg/min.
3. If the seizure is not controlled infusion may be hiked to 12 mg/kg/min.
the maximum allowed tonicity by a peripheral line is 12 percent. A
central venous line is necessary to give glucose at 15 to 20 percent.
4. If the seizure gets controlled the rate of infusion is continued for next
24 hours.
5. Hydrocortisone5 mg/kg injection twice daily is given, if the seizure
is controlled, the same dose may be continued for 3 to 5 days.
6. Glucagon0.1 mg/kg, maximum 1 mg may be given intramuscularly.
7. Diazoxide5 to 15 mg/kg/day in 3 divided doses oral.
110
Neonatal Hemorrhage
Hemorrhage in neonates is always life-threatening. The hemorrhage may
be either internal or external.
Management
1. Stabilization is the cornerstone. Blood from mouth and nose should
be sucked and cleaned to prevent aspiration. It also keeps the airway
patent. Oxygen may be administered to facilitate breathing. An intravenous fluid should be started to safeguard from circulatory
compromise.
2. Blood sample to be collected for Hb, PCV, cell type and count, platelet
count, prothrombin time, partial thromboplastin time, sugar and CRP.
3. Vitamin K2 mg intravenous or intramuscular.
4. Ranitidine1 mg/kg stat, followed by 12 hourly.
5. Packed cell transfusion 10 ml/kg.
6. At this stage further assessment has to be done and laboratory reports
analysed. The following are the possibilities:
i. Normal platelet count, elevated prothrombin time: Vitamin K
injection to be repeated and prothrombin time repeated after 12
hours.
ii. Low platelet countSick child with positive tests for sepsis then
the condition has to be treated according to the etiology like
congenital infection, disseminated intravascular coagulation or
congenital heart disease.
iii. Low platelet countMothers platelet count has to be checked.
iv. If mothers platelet count is normalCongenital anomalies like
giant haemangioma has to be looked for.
v. If mother has low platelet countMaternal ITP, SLE, drugs like
sulphonamide or quinine intake. Baby born to mother suffering
from ITP or SLE should be given intravenous immunoglobulin
400 mg/kg/day for 2 to 5 days and prednisolone 2 mg/kg/day.
Neonatal Apnea
Neonatal apnea is a frequent manifestation of respiratory control disorder.
Preterm infants are more prone to apnea due to immaturity in all or any of
the components of respiratory control: central or peripheral.
Apnea if present for 20 sec produces fall in PaO2. Cyanosis develops
after 30 sec and after 45 sec there is bradycardia, pallor, hypotension and
unresponsiveness.
Management
1. Temperature maintenance, control of sepsis if any, normoglycemia and
control of polycythemia are important aspect as hypothermia may trigger apnea.
Chapter 4.1: Neonatal Emergencies
111
2. A particular head neck posture may also trigger apnea, which should
be avoided.
3. All infants less than 34 weeks of gestational age should be monitored
for apneic spells for at least the first week of life. Along with impedance apnea monitors heart rate should also be monitored.
4. Most apneic spells in premature infants respond to tactile stimulation.
5. Unresponsive patients should be ventilated during spell with bag and
mask with a FiO2 under 0.4.
6. PharmacotherapyIndications are 2 or more episodes in an 8 hour
interval that require physical stimulation or a single episode that requires bag and mask ventilation. The following drugs may be used:
Aminophylline 68 mg/kg loading dose intravenous followed by
2 to 6 mg/kg/day in 2 divided doses.
Theophylline 5.57 mg/kg loading dose orally followed by 2.5 to
8 mg/kg/day in 3 divided doses.
Caffeine 10 mg/kg loading dose oral or intravenous followed by
2.5 mg/kg/day.
The drugs may be discontinued at 37 weeks postnatal age.
7. Nasal CPAPA pressure of 34 cm H2O reduces mixed and obstructive apnea.
8. VentilationIndications are total respiratory failure, failure of pharmacotherapy and CPAP.
Air Leak
It is usually an outcome of mechanical ventilation particularly in the background of meconium aspiration syndrome.
Management
1. Conservative therapyIt may be adequate in infants with noncontinuous air leak, no underlying lung disease, no distress and not on
mechanical ventilator. Close observation is necessary.
2. Needle aspirationIt may be employed as diagnostic and therapeutic
procedure in distressed neonate. A 23 or 25 gauge needle with a 3-way
stop cock is inserted through the second intercostals space through the
midclavicular line grazing the upper border of the rib. A continuous
suction should be applied as the needle is inserted. A rapid flow of air
will occur when the pneumothorax is entered. Once airflow ceases,
needle should be withdrawn.
3. Chest tube insertionIt is necessary in neonate with continuing air leak.
No. 10 or 12 French chest tubes are most commonly used. A small
incision should be made along the 6th rib in the anterior axillary line.
The tube should be inserted bluntly guided by a hemostat through the
3rd or 4th intercostals space. The tube should be secured well and
connected to a water seal. Chest X-ray should be frequently taken to
112
see the progress. The tube is removed when the lung disease has improved and the tube has drained no air for 24 to 48 hours.
Bibliography
1.
2.
3.
4.
Brousseau T, Sharieff GQ. Newborn emergencies: the first 30 days of life. Pediatr
Clin North Am 2006;53:69-84.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J Editors. Textbook of Paediatric Emergency Medicine, 1st edn, 2006. Philadelphia: Churchill Livingstone.
81-7.
Cloherty JP, Eichenwald EC, Stark AR Editors. Manual of Neonatal Care, 6th
edition. Philadelphia: Lippincott Williama and Wilkins, 2008.
Mondkar J, Pejaver RK Editors. NNF Manual of Neonatal Care, 1st edition.
Bangalore: Prism Books, 2004.
4.2
Prolonged Neonatal Jaundice
Neonatal hyperbilirubinemia is mostly a benign condition barring few cases

showing persistent elevation causing a concern and requiring detailed
investigations. Visible jaundice beyond 2 weeks in a term neonate and 3
weeks in a preterm neonate are taken as prolonged jaundice.
Common Causes of Unconjugated Hyperbilirubinemia in Children

1. Prematurity
2. Fetomaternal blood group incompatibilities (ABO and Rh), are the commonest varieties
3. Breast milk jaundice
4. Hypothyroidism
5. Concealed hemorrhage
6. Pyloric stenosis, conditions causing functional bowel obstruction
7. Criglar-Najjar disease
8. Trisomy 21.
Common causes of conjugated hyperbilirubinemia are:
1. Idiopathic neonatal hepatitis.
2. InfectionsTORCH, Hepatitis A, B, C, Coxsackie, etc.
3. Bacterial sepsis.
4. Extrahepatic biliary atresia.
5. Inspissated bile syndrome.
6. Total parenteral nutrition.
7. Intrahepatic biliary atresia.
8. Metabolic disorders (Alpha1antitrypsin deficiency, galactosemia, cystic fibrosis).
Clinical Assessment of Unconjugated Hyperbilirubinemia

i. Blanching the skin with digital pressure.
ii. Jaundice progresses in cephalocaudal direction (face first to get involved), Cremar index is a reasonable guide.
Jaundice of face5 mg percent
114
Face and trunk 10 to 15 percent

Face, trunk, palms and soles >15 mg percent
Approach to Patients Presenting with Jaundice at Emergency Room

History
1. Mothers blood group and previous sibling with neonatal jaundice.
2. Instrumental deliveryConcealed hemorrhage.
3. Familial jaundice, history of liver disorderCrigler-Najjar disease,
Gilberts disease, Dubin-Johnson syndrome.
4. Any drug administered which might have caused hemolysis due to G6PD
deficiency.
5. Delayed passage of meconiumHypothyroidism, Hirschsprungs disease.
6. VomitingPyloric stenosis, intestinal obstruction, sepsis.
7. Breast feedingBreast milk jaundice.
8. Color of stool and urine.
Pale stool and dark urineconjugated hyperbilirubinemia
Yellow stool and normal colored urineunconjugated hyperbilirubinemia.
9. Lethargy, poor feeding, seizuremetabolic disorder, sepsis.
Examination
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Cephalhematoma, caputExtravasation of blood.

Pallor, anemia, shockHemolytic anemia.
HepatosplenomegalyIU infection, hemolytic anemia, neonatal
hepatitis.
Umbilical herniaHypothyroidism.
Facial dysmorphismChromosomal anomalies.
SGA/microcephalyIU infection.
Bleeding tendency, petechaieHepatocellular failure, IU infection.
Cataract, chorioretinitisIU infection.
OmphalitisSepsis.
Cystic mass below liverCholedochal cyst.
Investigations
1. Serum bilirubinConjugated and unconjugated (Bilirubin 1 mg/
dl=17 moles/l).
2. Coombs test on neonates blood.
3. Peripheral smear, reticulocyte count.
4. Blood and urine culture.
5. G6PD level.
6. Thyroid function test.
7. Karyotyping (If chromosomal disorder is strongly suspected).
Chapter 4.2: Prolonged Neonatal Jaundice
115
8. Blood grouping Mother and infant.

9. Abdominal ultrasound (also to look for situs inversus and polysplenia
found in extrahepatic biliary atresia).
Special investigations in cases of documented conjugated hyperbilirubinemia
1. Complete liver function test including coagulation profile.
2. Serum glucose and electrolytes.
3. TORCH panel and Viral hepatitis markers (Hepatitis A, B, C, E).
4. Septic screen including CSF study.
5. Urine and blood for screening of metabolic disease.
6. Hepatobiliary imaging (MRCP, HIDA scan).
Factors Increasing Effectiveness of Phototherapy

1.
2.
3.
4.
5.
Blue lamps (peak output at 435-475 nm).

Irradiance (> 5 W/cm/nm to 9 uW/cm/nm).
Distance between baby and lamp < 50 cm.
Nursing the infant naked except eye patches and diaper.
Turning every 2 hours.
Treatment of Unconjugated Hyperbilirubinemia

1.
2.
3.
4.
Phototherapy with blue light (Figure 4.2.1) or biliblanket.

Phototherapy and exchange transfusion.
SurgeryObstructive lesions.
Hormonal replacementHypothyroidism.
Other specific therapy if any.
Treatment of Conjugated Hyperbilirubinemia

1. Promotion of bile flowApplication of UDCA and cholestyramine.
FIG. 4.2.1: A neonate under phototherapy (For color version see Plate 1)
116
2. Prevention of malnutrition and vitamin deficiencyVitamin A, D, E,

K supplement, medium chain triglyceride based diet.
3. Surgical interventionKasai procedure (hepatic portoenterostomy) for
extrahepatic biliary atresia, choledochal cyst, liver biopsy.
4. Orthoptic liver transplant.
Jaundice in first 24 hours are always pathological and cause should
be thoroughly searched. Causes include hemolytic diseases of the newborn due to fetomaternal incompatibility, red cell enzymes defect,
administration of large amount of vitamin K, salicylates to mother,
Crigler-Najjar disease, Lucey-Driscol syndrome, homozygous alpha
thalassemia.
Failure of phototherapy means decline of bilirubin less than 1 to 2 mg/
dL/4-6 hours and inability to keep below exchange transfusion level.
Table 4.2.1 shows management of unconjugated hyperbilirubinemia
in is healthy term babies and Table 4.2.2 shows indications for exchange
transfusion and phototherapy in preterm babies.
High risk factors include hemolysis, sepsis, perinatal distress factor
like birth asphyxia, hypothermia, hypoglycemia, and acidosis. Start phototherapy at a level lower by 5 mg/dL than exchange level due to increased
risk if bilirubin brain damage and managed more aggressively.
Side Effects of Phototherapy

1. Fluid and electrolytes:
Term infantsincreased insensible water loss by 40 percent (normal
insensible water loss 30 ml/kg/day),
TABLE 4.2.1: Management of unconjugated hyperbilirubinemia in healthy term babies
(Total serum bilirubin in mg/dL)
Age in hours
Consider phototherapy
Institute phototherapy
Exchange transfusion if
phototherapy fails
12
15
17
15
18
20
20
25
25
24
2528
4972
72
TABLE 4.2.2: Indications for exchange transfusion and phototherapy in preterm babies
(Total serum bilirubin in mg/dL)
Birth weight (gram)
Upto 1000
10001250
12511500
15012000
20012500
>2500
Normal neonates
1012
1214
1416
1618
1820
2022
High risk neonates

810
1012
1214
1416
1618
1820
2.
3.
4.
5.
6.
7.
8.
117
Preterm infantsincreased insensible water loss by 80 percent (normal insensible water loss VLBW is 40 ml/kg/day and VVLBW is 50 ml/
kg/day).
Neo Blue Cool Light may not require fluid increase.
Hyperthermia and irritability.
Opening of ductus arteriosus.
Diarrhea and watery loose stools.
Decrease calcium levels.
Retinal damage (shield the eyes).
Cellular DNA damage (shield the genitalia).
Bronze baby if mistakenly phototherapy applied on babies with liver
parenchymal disease.
Frequency of Monitoring Bilirubin

1. Every 8 to 12 hours while on phototherapy.
2. Check one level 12 hours after therapy is stopped.
Double Phototherapy and Triple Phototherapy

The number of lights are increased to give higher irradiation may be up to
12 uW/cm /nm.
High dose IV immunoglobulin in hemolytic disease of newborn:
1. It is recommended for use in Rh, ABO, and minor group incompatibility causing hemolytic disease.
2. Criteria for use In the presence of a positive direct Anti-Globulin test
(DCT) with:
i. Jaundice in day one close to exchange level (in the double phototherapy range).
ii. Significant rise in bilirubin > 0.5 mg/dL/hour in spite of 4 hours
of phototherapy.
iii. Anemia (Hb < 13 g/dL) progressive and a high reticulocyte count
> 80 percent.
Recommended dose:
i. 500 to 1000 mg/kg/day (maximum daily dose of 2.5 gm).
ii. Total number of doses should not exceed 3 doses.
iii. Continue PT as per recommended schedule.
iv. Perform exchange transfusion as per recommended schedule.
Figures 4.2.2 to 4.2.6 shown the management of hyperbilirubinemia
in neonates.
118
FIG. 4.2.2: Management of hyperbilirubinemia in the heathy term infants
119
FIG. 4.2.3: Management of hyperbilirubinemia in the sick term newborn infant or with hemolytic
disease
120
FIG. 4.2.4: Management of hyperbilirubinemia in the preterm infant 20002500 gm
121
122
Bibliography
1.
2.
AAP Subcommittee on Hyperbilirubinemia. Pediatrics 2004;114 (7).

Systematic review of intravenous immunoglobulin in hemolytic disease of the
newborn. Arch Dis Child Fetal Neonatal edition 2003;88:F6-10.
4.3
Bleeding Neonate
Both term and preterm neonates may present with bleeding due to various
problems of blood disorders. Quick assessment is very important as these
children may quickly go into shock.
Few Points in History

1. Age of the baby and sites of bleeding.
2. Whether the neonate is sick or healthy.
3. Family historyHemophilia A or B, platelet disorders like Wiskott Aldrich
syndrome, von Willebrands disease, clotting factors deficiencies.
4. Maternal diseasesITP, SLE, excessive bruising, pre-eclampsia.
5. Maternal infections during pregnancy.
6. Maternal drug ingestionAspirin, thiazide, phenobarbitone.
7. Birth trauma and complicated delivery.
8. Administration of vitamin K at birth.
Examination
1.
2.
3.
4.
5.
Sick or healthy baby.

Assessment of pulse, BP, respiration and perfusion.
Sites of bleeding.
Presence of hepatosplenomegaly.
Presence of seizure.
Baseline Investigations
1. Complete blood count, RBC morphology.
2. Platelet count.
3. Prothrombin time (PT), Partial thromboplastin time (PTT), thrombin
time (TT) and fibrinogen.
4. Sepsis screenBlood culture, CRP.
124
Management
Supportive Care
1. StabilizationA, B, C and thermoneutral environment.
2. Monitoring for shock and appropriate fluid resuscitation.
3. Injection vitamin K1 mg IV.
Neonate in Shock
1.
2.
3.
4.
Transfusion on O negative blood, 10 to 15 ml/kg over 5 to 15 minutes.

The above can be repeated once if the neonate is still in shock.
Monitoring BPAim is to keep above 40 mm Hg.
Transfer to NICU for management.
Neonate not in Shock

Transfusion of matched blood.
Specific Treatment
1.
2.
3.
4.
Vitamin K injections.
Fresh frozen plasma.
Platelet transfusion.
Whole blood transfusion.
A child with neonatal purpura and the diagnostic approach to a bleeding neonate are shown in Figure 4.3.1 and Flow chart 4.3.1 respectively.
FIG. 4.3.1: A child with neonatal purpura (For color version see Plate 1)
Chapter 4.3: Bleeding Neonate
125
Flow chart 4.3.1: Diagnostic approach to bleeding disorder in neonates
Bibliography
1.
2.
Clapp DW, Shannon KM, Phibbs RH. Hematologic problems. In: Klaus MH,
Fanaroff AA Editors. Care of High-risk Neonate, 5th edition. New Delhi:
Saunders Hardcourt India, 2001.
Irani SF, Kanhere S. Bleeding newborn. In: Mondkar J, Pejaver RK Editors NNF
Manual of Neonatal Care, 1st edition. Bangalore: Prism Books, 2004;302-9.
4.4
Neonatal Collapse
This is a state where a neonate in a very short span of time or in other

words almost suddenly becomes pale, limp, ashen gray with cold extremities, absent peripheral pulses and apneic or has shallow respiration and
rapidly nosedives to cardiorespiratory arrest. This is always attributable to
sudden changes in hemodynamic status secondary to the causes discussed
below. Many times frank clinical evidence of the precipitating cause is absent due to its sudden onset and rapid fulminant course.
Causes
Cardiac
1. Duct dependent outflow obstruction (Mitral atresia, tricuspid atresia,
pulmonary atresia with intact ventricular septum).
2. Critical aortic stenosis, pulmonary stenosis.
3. Hypoplastic left heart.
4. Coarctation of aorta.
5. TAPVC.
6. Transposition with intact atrial and ventricular septum.
7. Cor triatrium.
8. Other cardiac causesCardiomyopathy, myocarditis, arrhythmias, cardiac tamponade, PPHN.
Respiratory
1. Bronchiolitis (Severe and presenting with apnea, specially in preterm
neonates).
2. Diaphragmatic hernia.
3. Chest trauma and injury, pneumothorax.
Endocrine
1.
2.
3.
4.
Congenital adrenal hyperplasia (CAH).

Addisons disease.
Hyperaldosteronism (Pseudohypoaldosteronism).
Hypoglycemia.
Chapter 4.4: Neonatal Collapse
127
Metabolic Diseases
1.
2.
3.
4.
Galactosemia.
Urea cycle disorder.
Fatty acid oxidation disorder.
Electrolyte imbalances, acidosis.
Sepsis, Meningitis
Gastrointestinal
1. Enterocolitis (NEC or Hirschsprungs disease).
2. Duodenal atresia, malrotation, volvulus.
3. Gastroenteritis with severe dehydration.
Sudden Infant Death Syndrome (SIDS)

Others
Perinatal hypoxia, ruptured spleen, liver or adrenal hemorrhage, or bleeding anywhere in the body secondary to trauma, hemorrhagic disease of the
newborn.
Associated Clinical Features

Apart from looking pale, lethargic, hypotonic, extremities becomes cold
and capillary refill time gets prolonged. Sclerema develops in the late stage
along with oliguria or anuria. Seizure may occur due to hypoglycemia,
hypocalcemia, meningitis, IEM or hypoxic ischemic damage.
Investigations
1.
2.
3.
4.
5.
6.
ABG.
CXR.
ECG.
Hyperoxia test.
Echocardiography.
Blood glucose, metabolic work up, serum lactate, ammonia, electrolytes.
7. Urinary ketones.
8. Intestinal contrast study for obstruction.
9. CSF study.
Hyperoxia Test
The purpose of hyperoxia test is to identify cardiac cause of cyanosis.
Method
Administer 100 percent O2 for 10 minutes. Measure PaO2 (Arterial) before or
after O2 administration and take blood from radial artery. PaO2 >150 mmHg
128
excludes structural heart disease and almost always due to lung disease
except TAPVD with obstruction which may respond to O2. Cyanotic heart
disease is usually associated with PaO2 50 mmHg.
Management
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Initiate CPR, check blood glucose.

Maintain a thermoneutral environment to minimize oxygen and
glucose requirement.
Intubate if primary apnea, HR <100/min after initial airway maneuvers and start mechanical ventilation. Assess ABG.
Tracheal adrenaline or injection via umbilical vein.
Volume expansion with normal saline, fresh frozen plasma, packed
cell (As condition necessitates) 10 ml/kg and repeat according to the
clinical condition.
Bicarbonate for acidosis diluted and slowly to be corrected.
Calcium gluconate 2 ml/kg of 10 percent solution slowly IV both for
hypocalcemia and more so for its positive inotropic action.
IV glucose injection for hypoglycemia.
PGE1If proved duct dependent circulation.
InotropesDopamine 5 to 10 mcg/kg/min.
Add dobutamine if low cardiac output but normal or increased peripheral vascular resistance.
Neonate with cardiogenic shockIsoproterenol (0.1- 0.5 mcg/kg/
min) and digoxin with be helpful.
Milrinone and inamrinone (3 mg bolus and then 5-20 mg/kg/min)
reduce after load by their vasodilator effect.
Antibiotics according to institutional protocol for sepsis, NEC and
meningitis.
Central venous pressure and arterial blood pressure should be monitored to guide therapy though technically may be difficult in
newborns.
Naloxone for opiate induced respiratory depression.
During salt loosing period or when vomiting is present in congenital adrenal hyperplasia, apart from fluid rescitation, hydrocortisone
50 mg/m stat followed by 100 mg/ m/day every 6 hourly IV till
stabilizes then 20 mg/ m/day and add fludrocortisone 0.15 mg/m/
day. Maintain hydrocortisone at 9.5-15 mg/ m/day as it causes least
growth inhibition compared to dexamethasone and prednisolone.
Continue fludrocortisone 0.15 mg/m/day lifelong.
Management algorithm for neonatal collapse is shown in Flow chart
4.4.1.
Special Investigations
After stabilizing the initial period of catastrophe.
1. Adrenal hormones.
2. Urine 17 ketosteroids 17 OH progesterone.
Chapter 4.4: Neonatal Collapse
129
Flow chart. 4.4.1: Neonatal collapse algorithm
*Cardiac causes
TDuct dependant CirculationStart PGE1, consult pediatric cardiologist for BAS
Severe valvular stenosis and COAConsult pediatric cardiologist for balloon dilatation of valve and
balloon angioplasty respectively
TOF physiologyConsult surgeon for BT shunt
Other medical causesSpecific treatment as per guidelines.
3. DHEA.
4. GonadotrophinsFSH, LH.
5. Sex hormonesTestosterone and ostrogen, plasma cortisol (ACTH,
renin, aldosterone).
6. Karyotype.
Practice Points
1. Dose of PGE10.01-0.1 mcg/kg/min, may be started with 0.02 mcg/
kg/min.
130
2. Side effectsApnea if unintubated, bradycardia, pyrexia, seizure, cutaneous vasodilatation.

3. ContraindicationsHMD, PPHN, dominant L to right shunt (Large
VSD, truncus arteriosus).
Bibliography
1.
Klaus MH, Fanaroff AA Editors. Care of High-risk Neonate, 5th edition. New
Delhi: Saunders Hardcourt India, 2001.
RESPIRATORY
EMERGENCIES
5.1
Respiratory Distress and Noisy Breathing
Acute respiratory distress is a common presentation in emergency room. It

is a potential life-threatening condition. Frequently a child suffering from
asthma presents for the first time with respiratory distress. As a whole respiratory distress may be due to upper airway, lower airway or sometimes
due to a nonrespiratory cause.
Evaluation of a Child with Respiratory Distress

There is no scope for detailed history taking in such a situation. A definite
history of foreign body aspiration should always be obtained. The caregiver
should be asked whether the child was playing with small objects. Few important points are listed below:
1. Breathing difficulty:
i. Rapid breathing.
ii. Orthopnea.
iii. Retractions Supraclavicular, intercostals, subcostal.
iv. Accessory muscle use.
v. Use of abdominal wall muscles.
2. Change of color: Cyanosis or pallor.
3. Noisy breathing: Wheeze, stridor, grunt.
Nonspecific symptoms: Fever, poor feeding and failure to suck, inability to
speak in sentences, diaphoresis and pain may contribute in determining
the underlying cause.
(a) Respiratory rate: Fifty or more in 1 to 12 months and 40 or more in 1
to 5 years old is significant. A fast sleeping respiratory rate is more
significant as respiration is normally faster in awake child. Metabolic
acidosis should be suspected in a tachypneic child without distress.
(b) Chest indrawing: Suprasternal indrawing is a sign of respiratory distress present in both upper and lower airway diseases and signifies
active accessory muscles of respiration. Subcostal indrawing suggests a
more severe distress, it indicates that the diaphragm is working hard.
134
(c)
(d)
(e)
(f)
Intercostal indrawing suggests parenchymal lung disease like pneumonia where there is decreased lung compliance.
Heart rate, blood pressure, perfusion and temperature: Aids in identifying early cardiorespiratory compromise.
Sensorium: Hypoxic children can either be drowsy or irritable.
Oxygen saturation: Pulse oximetry is a very useful measure in a child
with respiratory distress.
Respiratory sounds: Stridor are an inspiratory sound and is an indicator of upper airway disease. Wheeze is an expiratory sound produced
by obstructed lower airways. Grunting is a serious condition produced
in alveolar diseases.
Nonrespiratory Causes of Respiratory Distress

Cardiac condition should always be assessed in a child with respiratory
distress. Heart failure may present with distress. Acidosis may produce respiratory distress. Renal failure, liver disease also cause distress. Drug history
may be useful as overdose may cause respiratory distress.
Noisy Breathing
Noisy breathing in children is usually due to the various causes of upper
airway obstruction.
Above the Larynx

1.
2.
3.
4.
5.
6.
Choanal atresia or stenosis.

Mid-face hypoplasia (typically, ex-premature infants).
Pharyngeal cysts.
Retropharyngeal abscess.
Tonsillar or adenoidal hypertrophy (the most common cause).
Epiglottitis (supraglottitis).
At the Larynx
1.
2.
3.
4.
5.
6.
7.
Laryngomalacia.
Laryngeal papillomata.
Vocal cord palsy.
Laryngeal cysts.
Foreign body.
Laryngeal diphtheria.
Laryngeal spasm.
Below the Larynx

1. Croup (laryngotracheitis).
2. Tracheal compression (vascular ring, mediastinal masses).
3. Tracheal malformation (tracheomalacia, webs, stenosis).
Chapter 5.1: Respiratory Distress and Noisy Breathing
135
TABLE 5.1.1: Differences between croup, epiglottitis and foreign body aspiration
Parameters
Croup
Epiglottitis
Foreign body
Age
Onset
Prodromal features
Temperature
Stridor
6 18 months
Gradual, over 24 48 hours
Present
May be mildly elevated
High pitched loud
2 5 years
Sudden
Nil
High
Low pitched soft
> 6 months
Sudden
Nil
Normal
Variable, depends on
location of foreign
body
Variable
Variable
Depends on degree
of obstruction
Barking cough
Present
Hoarse voice
Present
General appearance Noisy and playful
No cough
Voiceless
Anxious, sits still
4. Tracheal hemangioma.
5. Foreign body (tracheal, esophageal).
Approach to Noisy Breathing

Diagnosis and management of various emergency situations of noisy breathing in children is discussed in other sections. Few important points for
noisy breathing are as follows:
1. Focused and detailed history.
2. Examination of noseSeptum, adenoid, foreign body.
3. Throat and larynxTonsils, diphtheritic patch, foreign body.
4. Pharynx and epiglottis.
5. Lymphadenopathy.
6. ENT consultation at the earliest.
Differentiating features between croup, epiglottitis and foreign body
aspiration.
The differences are shown in Table 5.1.1.
Bibliography
1.
2.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J Editors. Textbook of Paediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill
Livingstone. 135-8.
Mellis C. Respiratory noises: How useful are they clinically? Pediatr Clin North
Am 2009;56:1-17.
5.2
Croup
Viral laryngotracheobronchitis or croup is the commonest cause of acute

upper airway obstruction.
Clinical Presentation
1.
2.
3.
4.
5.
Harsh barking cough (Seal bark cough).

Inspiratory stridor, sometimes expiratory stridor also.
Variable degree of respiratory distress.
With or without hoarse voice (Due to laryngitis).
Often associated with mild fever and coryzal symptoms.
Practice Points
1. Accompanying stridor often begins at night awakening infants and toddlers from sleep.
2. No role of antibiotics in viral croup.
3. Blood gases are usually not necessary (May precipitate still worse obstruction) and little to be gained from chest and neck X-rays in typical
cases (Shifting to radiology room may be risky idea).
TABLE 5.2.1: Clinical Scoring System. By Westley CR, Cotton EK, Brooks JG
Level of consciousness
Cyanosis
Stridor
Air entry
Retraction
Normal (including sleep)

Disoriented
None
Cyanosis at agitation
Cyanosis at rest
None
When agitated
At rest
Normal
Decreased
Markedly decreased
None
Mild
Moderate
Severe
0
5
0
4
5
0
1
2
0
1
2
0
1
2
3
Chapter 5.2: Croup
137
4. Pulse oxymetry is on the other hand reliable noninvasive way of monitoring.

5. Assessment of severity using Westley Clinical Scoring System in emergency department, as shown in Table 5.2.1 is very useful to plan for
staying at observation unit, hospital admission, ICU admission.
6. Agitation, exhaustion, cyanosis, severe retractions, markedly decreased
air entry are signs of impending danger of airway obstruction.
7. Endotracheal intubation if planned must be performed by a specialist
preferably an anesthesiologist because of the risk of laryngospasm precipitated by instrumentation.
The step wise management of croup is shown in Flow chart 5.2.1.
Flow chart 5.2.1: Croup management plan
138
Bibliography
1.
2.
3.
Barkin, (Ed). Pediatric Emergency Medicine: Concepts and Clinical Practice,

2nd edn, RG: Mosby1997;1091-4.
Everard M L. Acute bronchiolitis and croup. Pediatr Clin North Am 2009; 56:
119-33.
Westley CR. Am J Dis Child 1978; 132(5): 484-7.
5.3
Acute Epiglottitis
Acute epiglottitis is a life-threatening bacterial infection of the epiglottitis

and aryepiglottic folds.
Etiology
Hemophilus influenzae type B (Hib) is the cause in more than 75 percent of
cases, though the incidence of acute epiglottitis has decreased considerably due to Hib vaccination.
Other causes are Group A Streptococci, Pneumococcus, Staphylococcus aureus, H. parainfluenzae.
Age incidence
Most common between 2 to 6 years, mean being 40 months.
Symptoms
1.
2.
3.
4.
5.
Abrupt onset.
Fever Often more than 103oF.
Voice Aphonia, hoarseness, muffled voice.
Look Anxious appearance.
Posture Prefer sitting position, with jaw thrust forward.
Signs
1.
2.
3.
4.
5.
6.
Sore throat.
Drooling.
Stridor and labored respirations, retractions.
Tachycardia.
Tachypnea (but respiratory rate is rarely above 40/min).
Cyanosis in later stages.
Caution
Visualization of the epiglottitis is hazardous and should not be done in
the child with suspected epiglottitis. Agitating the child may precipitate
140
complete airway obstruction. A tongue depressor should not be used on

these patients.
Management
The algorithm for management of acute epiglottitis is shown in Flow chart
5.3.1.
Recommended Antibiotics
1. Cefotaxime 200 mg/kg/day IV divided every 8 hours, or Ceftriaxone
100 mg/kg/day IV divided every 12 to 24 hours. First dose stat.
2. If bacterial tracheitis is suspected add better gram-negative coverage.
Respiratory isolation for 24 hours after initiation of antibiotics should
be ordered.
Indications and guidelines for rifampicin chemoprophylaxis for contacts of index cases of invasive Hemophilus influenzae type b (Hib) disease
Dose of rifampicin 20 mg/kg orally once daily for 4 days, maximum
600 mg/day.
Flow chart 5.3.1: Management of acute epiglottitis
Chapter 5.3: Acute Epiglottitis
141
Chemoprophylaxis Recommended
1. All household contacts (Except pregnant women), irrespective of age,
with at least 1 contact younger than 4 years of age who is unimmunized
or incompletely immunized. The index patient also should receive
chemoprophylaxis.
2. All members of a household with a child younger than 12 months of
age, even if the primary series has been given.
3. All occupants of a household with an immunocompromised child, irrespective of the childs Hib immunization status.
4. Nursery and child care center contacts, irrespective of age, when 2 or
more cases of invasive disease have occurred within 60 days.
5. Index case, if treated with regimens other than cefotaxime or
ceftriaxone. Chemoprophylaxis usually is provided just before discharge.
Chemoprophylaxis not Recommended

1. Occupants of households with no children younger than 4 years of age
other than the index patient.
2. Occupants of households when all household contacts younger than
48 months of age have completed their Hib immunization series.
3. Nursery and child care center contacts of one index case, especially
those older than 2 years of age.
4. Pregnant women.
Bibliography
1.
Kirsch EA. Acute Epiglottitis. Pediatric Emergency Manual 2000.
5.4
Bronchiolitis
Bronchiolitis is inflammation of the lower respiratory tract due to an infection.
Etiology
1. Respiratory syncytial virus is the commonest.
2. Other important viral causes include adenovirus, influenza virus, parainfluenza virus, human metapneumovirus, and rhinovirus.
3. Mycoplasma pneumoniae may occasionally be associated with bronchiolitis.
Bronchiolitis is most common in the first year of life.
Initially coryzal symptoms, followed by cough and respiratory distress.
Fever is not a constant feature. If present, fever may range from mild to
markedly elevated temperature.
The presenting signs include tachypnea, hyperinflation of the chest,
audible wheeze, with signs of accessory muscle use in breathing. Auscultation will reveal widespread crepitations and rhonchi. Bronchiolitis
assessment tool (BAT) is shown in Table 5.4.1.
The illness peaks at 2 to 3 days and improves by 5 to 7 days. Cough
may persist for several weeks.
TABLE 5.4.1: Bronchiolitis assessment tool (BAT)
Mild
Moderate
Severe
Wheeze
None or end expiratory
Entire expiration
Feeding
Normal
Less than usual
Oxygen
Chest indrawing
No oxygen requirement
Nil/mild
Behavior
Normal
May require oxygen

Intercostal and/or
tracheosternal
Irritability/lethargy
Inspiratory and expiratory

Not interested, gasping/
coughing
Requires oxygen
Severe with nasal flaring
Irritability/lethargy
Chapter 5.4: Bronchiolitis
143
Risk Factors
1.
2.
3.
4.
5.
6.
Underlying medical condition.

Apnea in less than 4 weeks or ex-preterms.
Chronic respiratory or cardiac disease.
Lethargy indicating risk of impending respiratory failure.
Severity of illness.
Day of illness (if early in illness they may get worse before they get
better).
Social Risk Factors

Poor parental support or parents lack confidence to manage infants at home.
Diagnosis
Chest X-rayHyperinflation with variable opacities.
Nasopharyngeal aspirate (NPA)Immunofluorescence for causative
respiratory viruses.
Management
1. Small frequent feeds. In moderate and severe cases nasogastric feeds
may be needed. In severe respiratory distress it may be safest not to
feed and give IV fluids.
2. Saline nasal drops may facilitate feeding if there is a problem with
nasal obstruction.
3. Oxygen should be administered as necessary to maintain adequate saturation (>92%). O2 is usually administered via a nasal cannula.
4. Infants who are not maintaining satisfactory oxygenation with nasal
O2 or who are having apneic episodes require PICU assessment.
5. Most children with bronchiolitis do not benefit from bronchodilators
and there is some evidence that nebulized bronchodilators can cause
babies to deteriorate. Some older infants may benefit from
bronchodilators.
6. Antibiotics are of no benefit in bronchiolitis. A small number of children with bronchiolitis may develop secondary bacterial chest infection.
This should be considered if there is a deterioration associated with a
fever.
7. Steroids are not indicated for bronchiolitis.
8. Ribavirin is indicated in immunocompromised patients.
The management plan of bronchiolitis is shown in Flow chart 5.4.1.
Progress
The illness usually peaks on the second or third day with gradual resolution over 7 to 10 days. Cough may persist for several weeks.
144
Flow chart 5.4.1: Management of bronchiolitis
Practice Points
1. Bronchodilators and corticosteroids are of no proven value.
2. Antibiotics are not routinely used unless secondary bacterial pneumonia.
3. A single dose of trial nebulized salbutamol may be considered in older
infants where asthma is considered a possibility.
Bibliography
1.
Gavin R. Bronchiolitis. Bronchiolitis Pathway Group. General Paediatrics 2005.

16. www.starship.org.nz
5.5
Acute Severe Asthma
Ideally all known asthma patients should have a proper home management plan that will minimize the incidence of development of acute
exacerbations. If exacerbations do occur, the patient should receive inhaled short acting agonists like salbutamol or levosalbutamol. A good
response is characterized by resolution within an hour with no further
symptoms in the next 4 hours.
Evaluation of Severity of an Acute Episode of Asthma

in Children Above 2 Years
Acute Severe
1. Cannot complete sentences in one breath or too breathless to talk or
feed.
2. Pulse rate >30 in 2 to 5 years or >20 beyond 5 years.
3. Respiratory rate >50/min in 2 to 5 years or >30 beyond 5 years.
4. Peak expiratory flow (PEF) 33 to 50 percent of self best or predicted
value.
Life-threatening
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Poor respiratory effort.

Exhaustion.
Cyanosis.
Confusion.
Coma.
Silent chest.
Hypotension, bradycardia.
PEF <33 percent best or predicted.
Oxygen saturation <92 percent in room air.
PaO2<55 mm Hg, normal PaCO2.
146
Caveat
1. Children with life-threatening attacks may not be distressed, may not
have all these abnormalities.
2. Assessment in very young children may be difficult.
3. The presence of any of the above features should alert the physician.
Criteria for Hospital Admission

1.
2.
3.
4.
5.
6.
7.
Life-threatening attack (Criteria as listed above).

Severe attack persisting after initial treatment.
Previous life-threatening attack.
Concerns about compliance.
Comorbid conditions.
Physical disability.
Presentation at night and coming from far off place.
The first two criteria require ICU admission.
Management
The main aim of acute severe asthma management is to provide adequate
oxygen through a bronchospasm free respiratory passage. The first move
should be to relieve the bronchospasm by nebulization or inhaler therapy.
1. Oxygen by mask at 5 liter/min to achieve SpO2 >90 percent.
2. Metered dose inhaler Figure 5.5.1This is a very effective device to:
control acute exacerbation of asthma. Inhaler therapy may be started at
home even before bringing the child to the hospital. If the child is a
known asthmatic, the parents and the child should be educated about its
use in emergency situations and they should always carry an inhaler with
them. Salbutamol 100 gm per dose or levosalbutamol 50 gm per dose.
The recommended schedule in different age groups is as follows:
i. Children less than 6 years6 puffs at 20 minutes intervals, 3
times, that is over the first hour.
FIG. 5.5.1: Metered dose inhaler with spacer and baby mask
Chapter 5.5: Acute Severe Asthma
147
ii. Children more than or equal to 6 years12 puffs at 20 minutes

intervals, 3 times, that is over the first hour.
With proper usage like using spacer device in older children or spacer
with mask in small child most of the cases may be controlled effectively.
3. Nebulization: Salbutamol 0.15 mg/kg/dose with 2 to 3 ml normal saline.
2.5 mg (0.5 ml) in children <20 kg body weight
5 mg (1 ml) in children >20 kg body weight
May be repeated every 20 min for 3 doses
Continuous salbutamol nebulization may be applied 10 mg in 10 ml
normal saline via a jet nebulizer.
4. Corticosteroid: A single oral corticosteroid, prednisolone 1 to 2 mg/kg
may be given early. In older children as the body weight is more even
0.5 mg/kg dose is sufficient.
The management algorithm of acute asthma is shown in Flow chart 5.5.1.
Good Response Group

If the child improves with the above measures and SpO2 >90 percent in
room air the child may be discharged and advised to take inhaled
Flow chart 5.5.1: Management of severe asthma
148
bronchodilators and oral corticosteroid like prednisolone 1 to 2 mg/kg/day

in 2 divided doses for 3 days.
If the child does not respond to the above measure, a thorough
evaluation and need to transfer to intensive care set up has to be considered.
Signs of High Risk

1.
2.
3.
4.
5.
Altered sensorium (either drowsy or irritable).

Bradycardia.
Poor pulse volume.
Cyanosis (With 60% oxygen).
Exhaustion (vocalization limited to 12 words) and excessive use of
accessory muscles of respiration.
6. Excessive diaphoresis.
7. Silent chest on auscultation.
8. ABG: pCO2 > 55 mm Hg, pO2 < 60 mm Hg, rate of rise of pCO2 > 5
mm Hg/hr, metabolic acidosis (Base deficit > 710).
Poor Response Group

1.
2.
3.
4.
5.
6.
7.
8.
Continue oxygen.
Nebulizationsalbutamol every 20 min.
Intravenous fluid.
Corticosteroid: If the child tolerates oral medicines, then steroid may
be given orally. Parenterally methylprednisolone 2 mg/kg followed by
1 mg/kg every 6 hourly or hydrocortisone 10 mg/kg followed by 5 mg/
kg 6 hourly intravenous.
It is ideal to use corticosteroid early as it limits morbidity. With
clinical improvement intravenous corticosteroid may be tapered after
48 hours. Inhaled corticosteroids are of not much benefit in acute
asthma.
Ipratropium bromide: When used along with salbutamol it offers additional bronchodilator benefit. Dose is 0.5 ml in <1 year and 1 ml in
>1 year nebulisation along with normal saline.
2 agonist: Terbutaline or salbutamol may be used. Terbutaline 5 to 10
gm/kg intravenous bolus over 10 min followed by 2 to 10 gm/kg/
hour. The infusion should be under continuous ECG monitor. In case
of tachycardia, arrhythmia, ST changes the infusion should be reduced
and nebulization stopped.
Aminophylline: 5 to 6 mg/kg loading dose slow intravenous infusion
followed by maintenance dose 0.5 to 1 mg/kg/hour. Dose of terbutaline
should be halved if aminophylline is concurrently administered.
Magnesium sulfate 50 percent solution: 25 to 50 mg/kg diluted with
normal saline and infused over 30 min.
Chapter 5.5: Acute Severe Asthma
149
Same management should be continued for at least 4 hours. Hourly

clinical assessment has to be done to detect any improvement or deterioration.
Improvement at the end of 6 hours
1. Decrease 2 agonist every 1 to 4 hourly.
2. Stop injection aminophylline.
3. Continue corticosteroid for 3 days.
Condition Unchanged
Consider mechanical ventilation.
Clinical Deterioration
Indications for mechanical ventilation
1. Exhaustion, shallow respiration and drowsiness at presentation.
2. Not responsive to above treatment.
3. Severe respiratory distress, silent chest.
4. Cardiorespiratory arrest.
5. Comatosed child.
6. ABGPCO2 >55 mm Hg, PO2 <60 mm Hg, rate of rise of PCO2
>5 mm Hg/hr, metabolic acidosis (base deficit >7 10).
First Attack of Status Asthmaticus

The diagnoses to be considered are the following:
1. Foreign body.
2. Massive aspiration.
3. Pulmonary edema.
4. CNS disorder (central hyperventilation).
5. Metabolic acidosis (DKA, inborn error of metabolism).
Bibliography
1.
Robinson PD, Asperen PV. Asthma in childhood. Pediatr Clin North Am 2009;
56:191-226.
CARDIOVASCULAR
EMERGENCIES
6.1
Cyanotic Spell
Mahasweta Chaudhuri, Jaydeep Choudhury,
The cyanotic spell (also called hypoxic spell, tet spell, hypercyanotic
spell, paroxysmal dyspnea) most frequently occurs in young infants with
tetralogy of Fallot but may be associated with other congenital heart defects that have decreased pulmonary blood flow or a manifestation of shunt
malfunction in whom palliative procedure (e.g. BT shunt, which is a systemic-pulmonary connection) has been done. Cyanotic spell can occur at
any age.
It is characterized by the following:
1. Period of uncontrollable crying/panic
2. Rapid and deep breathing (hyperpnea), deepening of cyanosis
3. Decreased intensity of heart murmur
4. Limpness, convulsions and rarely, death.
Common precipitating factors include the following:
1. Crying, feeding, defecation, waking from naps (low systemic resistance).
2. Fever, dehydration, tachypnea, tachycardia due to any cause.
3. Medications (e.g. ACE inhibitors).
4. They tend to occur in those with mild-to-moderate cyanosis at rest and
are more common in children who are iron deficient.
Hypercyanotic spells need to be recognized quickly and effectively controlled to prevent the development of serious complications from prolonged
hypoxia. While medical intervention is indicated, many episodes are selflimiting.
Pathophysiology
Hypercyanotic spell is best thought of as an imbalance between pulmonary
and systemic vascular resistance favoring decreased pulmonary flow and
increased right-to-left shunting.
Hypoxemia, metabolic acidosis, hyperpnea, increased systemic venous
return, catecholamines and pulmonary vasoconstriction are thought to be
involved in an interaction that results in a self-perpetuating cycle. Infundibular spasm is not an absolute requirement.
154
Management
Acute Care
Treatment of spells involves the following procedure. The algorithmic approach to management of cyanotic spell is shown in Flow chart 6.1.1.
1. Knee chest position: To increase systemic vascular resistance. This can
be easily done in older children. Infants and small children can be
picked up in the lap with legs folded at the knees to obtain similar
result.
2. Oxygen: To be given at highest possible concentration though result
may not be proportionate.
3. Morphine: 0.1 to 0.2 mg/kg subcutaneously. Also can be given IV 0.05
to 0.1 mg/kg slowly over 10 minutes. Morphine depresses respiratory
center which in turn decreases systemic venous return. While giving
morphine, facilities for ventilation should be available.
4. IV fluids: Preferably initially as bolus of 10 to 20 cc/kg which may be
increased to 60 cc/kg. Bolus fluid should be isotonic saline or colloid.
Extra volume can be given in cyanotic spell as the physiology is not
inductive to CCF and also because of a restrictive RV physiology.
5. Sodium bicarbonate injection: 1 to 2 mcg/kg slowly intravenous. This
is to correct metabolic acidosis.
Flow chart 6.1.1: Algorithm for management of cyanotic spell
Chapter 6.1: Cyanotic Spell
155
6. Propanolol: 0.1 to 0.2 mg/kg intravenously over 5 min. Propanolol

reduces dynamic RV outflow obstruction, slows heart rate which in
turn decreases right to left shunting. It also causes slight increase in
systemic vascular resistance and blocks hyperpnea response.
7. Metoprolol injection: 0.1 mg/kg over 5 min, repeat every 5 min to
max 3 doses , then start infusion 1 to 5 mcg/kg/min. Metoprolol is
only used when intravenous propranolol is not available.
8. Another short acting Beta-blocker that can be used is esmolol injection 0.5 mg/kg over 1 min then 50 mcg/kg/min over 4 min.
9. Transfuse packed red blood cell 5 to 10 ml / kg IV over 5 hrs.
10. Treat sepsis if there is any evidence.
11. Mechanical ventilation if refractory to above treatment and perpetuating to bradycardia and/or spiralling desaturation, coma, convulsion.
If ultimately ventilated, ketamine has a good role to play. Ketamine
0.25 to 1.0 mg/kg IV, has dual benefit. It causes sedation and increases
systemic vascular resistance. Ketamine without ventilation may be tried
but all arrangement to intubate and ventilate must be ready.
12. Consult a cardiac surgeon for emergency surgical intervention (BT
shunt).
Ongoing Care
If there is a single severe or frequent minor spells, commence oral propranolol 0.5 mg/kg/dose TDS. This should be done in hospital, watching for
hypotension and hypoglycemia. Increase gradually to 1.0 to 1.5 mg/kg/
dose TDS (3.0-4.5 mg/kg/day).
Practice Points
1. Peak between 2 to 4 months.
2. Usually occurs in morning.
3. In refractory cases phenylephrine hydrochloride has been advocated
at a dose of 0.01 mg/kg IV (slowly) or 0.1 mg/kg SC or IM ( SVR and
reducing right to left shunt dose to be titrated to BP response).
Bibliography
1.
2.
3.
4.
American Heart Association Guidelines 2001.

Moss, Adams. Heart Disease in Infants, Children and Adolescents, 6th edition.
Park M K. Pediatric Cardiology for Practitioners, 3rd edition.
The Harriet Lane Handbook, 16th edition.
6.2
Heart Failure
Jaydeep Choudhury
Common Causes of Heart Failure

1. Congenital heart disease
i. Large left to right shunt (VSD, ASD, PDA)
ii. Obstructive lesions (Coarctation of aorta, AS)
iii. Anomalous left coronary artery from the pulmonary artery
(ALCAPA).
2. Acute myocarditis.
3. Dilated cardiomyopathy (familial, metabolic).
4. Restrictive cardiomyopathy.
1.
2.
3.
4.
5.
6.
7.
Tachycardia.
Tachypnea with respiratory distress.
Weak peripheral pulses and/or delayed capillary refill.
Jugular venous distension may be observed in older children.
Heart sounds are often muffled with or without gallop rhythm.
Murmurs of the original disease.
Pulmonary and systemic venous congestion are manifest by crepititions
and hepatomegaly.
8. Arrhythmia particularly ventricular ectopy.
Investigations
1. ECG
i. Low amplitude.
ii. Sometimes abnormal axis.
iii. Atrial or ventricular enlargement according to the original disease.
2. Chest X-rayCardiomegaly with pulmonary venous congestion.
3. EchocardiogramTo check for cardiac anomalies and ventricular function.
4. Complete blood count with differential counts.
5. Blood culture and ESR if fever and infection are evident.
Chapter 6.2: Heart Failure
157
6. Creatinine kinase (CK-MB).

7. Viral IgM antibody titers (in suspected viral myocarditis).
8. Serum carnitine, lactase, pyruvate in suspected metabolic or familial
cardiomyopathy.
General Management
1.
2.
3.
4.
5.
6.
7.
8.
ABC, oxygen inhalation.

Connect to a cardiac monitor.
Secure an IV line.
If in shock intubate and ventilate.
Keep fluid input/output chart.
Fluid restriction 70 percent ml/kg/day.
If the baby is tachypneic consider feeding via NG tube.
Monitor serum electrolytes frequently (especially potassium).
Stepwise management of heart failure is shown in Flow chart 6.2.1 and the
management of heart failure with shunt lesions is shown in Flow chart 6.2.2.
Specific Management
1. Dopamine is not used as first line inotropes unless the baby is hypotensive, it causes tachycardia and subsequently reduced tissue perfusion.
2. Milrinone Produces inotropic, vasodilator effect and after load reduction. Best used as infusion in combination with dobutamine.
3. Monitor electrolytes for hypokalemia during frusemide administration.
4. Captopril can be increased weekly if necessary by 25 mg/dose to maximum 450 mg/day. Contraindicated in left ventricular outflow
obstruction, e.g. critical aortic stenosis.
If captopril is given with digoxin and diuretics, then spironolactone
should be reduced or stopped according to potassium level.
Practice Points
1. When starting digoxin with diuretics (frusemide and spironolactone),
the dose given as 0.01 mg/kg/day every 12 hourly.
2. If captopril is given with digoxin and diuretics, then spironolactone
should be reduced or stopped according to potassium level.
3. Digoxin toxicity can occur if the above 4 drugs are given and lower
doses of digoxin should be given (0.0075 mg/kg/day every 12 hourly).
4. It is advisable that antifailure therapy be started by cardiologist initially in conditions of large left to right shunt lesions and in obstructive
lesions.
Management of chronic heart failure (with dilated cardiomyopathy and left
ventricular dysfunction)
1. Stable patients should be maintained on ACE inhibitors (e.g. Captopril,
enalapril) on for long-term. The doses are adjusted according to BP.
158
Flow chart 6.2.1: Management of heart failure due to acute myocarditis
2. Diuretics are given in some patients as adjunctive therapy when left

ventricular ejection fraction is <40 percent.
3. Long acting Beta blockers have proven efficacy in patient with chronic
heart failure. The drug used nowadays is carvedalol 0.1 mg/kg/dose
every12 hourly. Increase slowly and monthly by 0.1 mg/kg/dose to
maximum dose of 6.25 mg every12 hourly.
Chapter 6.2: Heart Failure
159
Flow chart 6.2.2: Management of heart failure due to shunt lesions (VSD, PDA, AVSD)
Bibliography
1.
2.
3.
4.
Pediatric Cardiac Intensive Care. Anthony Chang 1999.

Pediatric Cardiology. Robort Anderson. Second edition, 2002.
The Harriet Lane Handbook 2002.
Treatment of heart failure in children. Current Paediatrics 2005;15,539-48.
6.3
Abnormal Pulse Rate or Rhythm
Arrhythmia is definitely not as common in pediatric patients as in adults.

But strong clinical vigilance is required for correct acute assessment and
management of arrhythmia which will have a significant long-term consequence. Detection and identification of pediatric cardiac arrhythmias is a
diagnostic challenge. Most children with cardiac arrhythmias present with
vague and nonspecific symptoms. Feeding difficulty or fussiness is the
common presenting features in infants and young children. They even
present in shock. Older children often presents with nonspecific discomfort. Sometimes older children present early, in a stable condition with a
perception of palpitations. It is critical to identify and manage cardiac
arrhythmias on children despite the rarity of the condition and vague presentation. Cardiac arrhythmias may lead to cardiopulmonary compromise
and arrest if left untreated.
Most tachyarrhythmias in children are due to re-entrant congenital
conduction pathway abnormality. Some are due to poisoning, metabolic
disturbances, following cardiac surgery and in the course of cardiomyopathy. In tachyarrhytmias the rate is fast but the rhythm is largely regular.
Majority of bradyarrhythmias are due to hypoxia and shock and are
pre-terminal events. They almost always present with respiratory failure
and shock. A few are due to conduction pathway damage during cardiac
surgery. The rate is slow and the rhythm usually irregular.
The most common pediatric cardiac arrhythmias are sinus tachycardia
(50%), supraventricular tachycardia (13%), bradycardia (6%) and atrial fibrillation (4.6%).
The normal respiratory rate and heart rate in children are shown in
Table 6.3.1.
The Most Common Indications for Obtaining ECG in Children
1. Suspected arrhythmia.
2. Chest pain.
3. Electrolyte abnormalities.
4. Seizures.
5. Syncope.
Chapter 6.3: Abnormal Pulse Rate or Rhythm
161
TABLE 6.3.1: Normal respiratory and heart rate in children of different age groups
Age
RR / min
HR/ min
Birth
3 months
6 months
1 year
2 years
4 years
6 years
8 years
10 years
12 years
14 years
40-60
30-50
30-50
30-40
20-30
20
16
16
16
16
16
100-160
100-160
100-160
100-160
100-150
80-130
70-120
70-110
60-100
60-100
60-100
6. Drug exposure.
7. Electrical burns.
8. Confirmation of abnormal physical examination findings.
The most life-threatening findings are caused by
1. Electrolyte disturbances
2. Drug exposure
3. Burns
A systematic approach to ECG interpretation is always advisable. ECG
should be evaluated in rate, rhythm, axis, chamber hypertrophy (ventricular and atrial), T-wave morphology, evidence of ischemia and repolarization
abnormalities.
Bradyarrhythmia
Bradyarrhythmias in children have a slow rate for age and the rhythm
usually irregular. An abnormally slow pulse rate is defined as less than 60/
min or a rapidly falling heart rate associated with poor systemic perfusion.
This will almost always be in a child who requires major resuscitation.
Causes
1.
2.
3.
4.
5.
Hypoxia or shock as a preterminal event.

Raised intracranial pressure.
Postcardiac surgery due to conduction pathway damage.
Congenital or acquired heart block (Myocarditis, dyselectrolytemia).
Long QT syndrome.
Tachyarrhythmia
Tachyarrhythmias in children are characterized by a fast heart rate for age
but the rhythm remains regular in majority of the cases.
In practice, most serious disease or injury states are associated with a
sinus tachycardia. In infants this may be as high as up to 220/min, and in
162
children up to 180/min. Heart rates over these values are highly likely to be
tachyarrhythmias, but in any case of significant tachycardia, 200/min in an
infant and 150/min in a child, one should obtain an ECG rhythm strip and
a full l2-lead ECG if possible.
Very high heart rates may be impossible to count manually and the
pulse oximeter is unreliable as well in counting the fast heart rate exactly.
Causes
1. Re-entrant tachycardia through a congenital conduction pathway abnormalityit is relatively a common cause.
2. Metabolic disturbance.
3. Poisoning.
4. Cardiomyopathy.
5. Postcardiac surgery.
6. Genetic proarrhythmic conditions (Long QT syndrome and Brugada
syndromes).
History
Obtain a detailed history of the childs health and activity over the previous 24 hours. Children with arrhythmias usually present with the following:
1. History of palpitations, chest pain, dyspnea.
2. History of syncope.
3. Poor feeding, nausea, vomiting, abdominal discomfort.
4. Heart failure or shock.
Certain key features which will be identified clinically in the following:
1. Focused history.
2. Primary assessment.
3. Initial blood tests.
4. Rhythm strip and l2-lead ECG.
These can point the clinician to the likeliest working diagnosis for emergency treatment.
Clinical Scenario
The clinical scenario and presentation may be the following:
1. A pulseless arrest.
2. Bradycardia with inadequate cardiac output.
3. Tachycardia with hemodynamic stability.
4. Tachycardia with hemodynamic instability.
ECG
From the ECG the arrhythmia can be categorized by the following simple
questions:
1. Is the rate too fast or too slow?
2. Is the rhythm regular or irregular?
3. Are the QRS complexes narrow or broad?
163
Bradycardia
It is usually a preterminal rhythm as the final response to profound hypoxia
and ischemia.
i. Precipitated by vagal stimulation (intubation, suctioning, in
postoperative cardiac patients). The rhythm is usually irregular.
ii. In raised intracranial pressure.
iii. Overdose of digoxin or beta-blockers.
iv. Congenital or acquired heart blocks.
Tachycardia
i. Narrow QRS complex on the ECG is supraventricular tachycardia.
The rhythm is usually regular.
ii. Wide QRS complex on the ECG is ventricular tachycardia which can
be provoked by hyperkalemia, tricyclic antidepressants,
macrolidecisapride combination, genetic proarrhythmic conditions
(long QT syndrome).
General Management of Arrhythmia

Whatever may be the presenting feature, the basic approach remains almost the same. As with any other emergencies in children, the management
starts with the primary assessment following the algorithm of ABCDE.
Airway
Maintain an open airway, may require intubation.
Breathing
Assess the effort of breathing, the efficacy of breathing, and the effects of
respiratory failure on other systems.
Features Suggesting Cardiac Cause of Respiratory Inadequacy

i.
ii.
iii.
iv.
v.
vi.
Cyanosis, not correcting with oxygen therapy.

Tachycardia out of proportion to respiratory difficulty.
Raised jugular venous pressure.
Gallop rhythm or murmur.
Enlarged liver.
Inequality of pulses.
Circulation
Assessment of circulatory status is very important. An abnormal pulse rate
is defined as one falling outside the normal range.
Important Considerations
i. If there is shock and the heart rate <60/min, start chest compressions.
164
ii. ECG shows ventricular tachycardia then give up to 1 to 2 synchronous electrical shocks at 1and 2 joules/kg. Use sedation or anesthesia
for the child who is responsive to pain. Synchronous shocks for VT
may be ineffectual if the defibrillator cannot recognize the abnormally shaped QRS complex. In such a situation one may have to
deliver asynchronous shock, because without conversion the rhythm
may deteriorate to VF and asystole. Synchronization avoids shock
delivery at a point in the cardiac cycle likely to precipitate ventricular fibrillation.
iii. Gain intravenous or intraosseous access.
iv. If the tachyarrhythmia is SVT then give intravenous/intraosseous adenosine 100 mcg/kg to a maximum single dose of 500 mcg/kg (300
mcg/kg under one month) if this can be administered more quickly
than a synchronous electrical shock.
v. Send blood for CBC, urea, creatinine, glucose and other laboratory
tests.
vi. Give a bolus of 20 ml/kg IV of crystalloid to a patient with bradycardia who is in shock.
Disability
i. Mental status or consciousness level.
ii. Posture.
iii. Pupils.
Exposure
i. Features suggestive of hypo or hyperthyroidism or other metabolic
abnormalities.
ii. Rash or fever.
iii. Sweating, raised JVP, gallop rhythm, murmur, hepatomegaly.
Bradycardia
Bradycardia in children is almost always a preterminal finding in patients
with respiratory or circulatory insufficiency. Airway, breathing and circulation should always be assessed before any other forms of treatment.
Treatment if there is hypoxia and shock:
1. High concentration of oxygen, bag mask ventilation, intubation and
IPPV.
2. Volume expansion (20 ml/kg of 0.9% saline repeated as recommended
in the treatment of shock).
3. If ineffective give bolus of adrenaline 10 mcg/kg IV.
4. If ineffective give infusion of adrenaline 0.05 to 2 mcg/kg/min IV.
Adrenaline induces vasoconstriction increasing aortic diastolic pressure and thus the coronary perfusion pressure, a critical determinant of
successful resuscitation.
165
Treatment if there has been vagal stimulation

1. Adequate ventilation.
2. Atropine 20 mcg/kg IV/IO (Minimum dose 100 micrograms maximum
dose 600 micrograms). It is actually a parasympatholytic drug that accelerates sinus or atrial pacemakers and increases AV conduction. Small
doses of atropine (0.1 mg) may produce paradoxical bradycardia, hence
the minimum dose is required.
3. It may be repeated in 5 minutes (maximum total dose of 1.0 mg in a
child and 2.0 mg in an adolescent).
4. If IV/IO access is unavailable, atropine (0.04 mg/kg) may be administered intratracheally (unreliable absorption).
5. If there has been poisoning, seek expert toxicology help.
If the rhythm does not return to a sinus rhythm after the initial resuscitative efforts and the patient remains hemodynamically unstable, one
may have to transfer the patient to a specialist cardiac center where facilities of a temporary pacemaker insertion is available, pending further
investigations regarding the exact cause of the bradycardia .
PALS bradycardia protocol is cited below in Flow chart 6.3.1 as a guide.
Tachycardia
If there are no palpable pulses, proceed with the PALS Pulseless Arrest
Algorithm. If pulses are palpable and the patient has signs of hemodynamic compromise (poor perfusion, tachypnea, weak pulses), ensure that
the ABC is maintained, administer supplementary oxygen, and attach an
ECG monitor or defibrillator to assess the rhythm and QRS duration.
QRS Complexes
Based on duration of QRS complexes, tachycardia may be classified as narrow-complex or wide-complex tachycardia. QRS duration is 0.08 second
is narrow-complex tachycardia. Narrow complex tachycardias are universally of supraventricular origin.
QRS duration 0.08 second is wide-complex tachycardia.
Narrow Complex Tachycardias

The common narrow complex supraventricular arrhythmias are the following.
1. Atrial flutter.
2. Atrial fibrillation.
3. Atrial tachycardia.
4. Atrioventricular re-entrant tachycardia (AVRT).
5. Atrioventricular nodal re-entrant tachycardia (AVNRT).
Evaluate a 12-lead ECG (best in lead II and V1) and the patients clinical presentation and history to differentiate probable sinus tachycardia from
probable supraventricular tachycardia (SVT). If the rhythm is sinus tachycardia, search for and treat reversible causes.
166
Flow chart 6.3.1: PALS bradycardia protocol
If the patient is very unstable or IV, access is not readily available, provide electrical synchronized cardioversion. Consider sedation if possible.
Starting dose of electrical cardioversion 0.5 to 1 J/kg. If unsuccessful, repeat using a dose of 2 J/kg.
167
If a second shock is unsuccessful or the tachycardia recurs quickly, consider antiarrhythmic therapy (amiodarone or procainamide) before a third
shock. Consult a pediatric cardiologist.
Consider amiodarone or procainamide for SVT unresponsive to vagal
maneuvers and adenosine.
If the presentation is of a pulseless condition with shock, the preferable
guideline is the PALS pulseless arrest protocol, as cited in Flow chart 6.3.2.
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is the most common non-arrest arrhythmia during childhood and is the most common arrhythmia that produces
cardiovascular instability during infancy. SVT in infants generally produces
a heart rate >220/min. Lower heart rates may occur in children during
SVT.
It is important to differentiate SVT from sinus tachycardia Table 6.3.2
in both of which the QRS complex is narrow and both of them may be
present in a clinical scenario of shock and poor perfusion. P waves may be
difficult to identify in both sinus tachycardia and SVT once the ventricular
rate exceeds 200/min.
Clinical Features
Older children usually complain of:
1. Lightheadedness.
2. Dizziness.
3. Chest discomfort.
4. Palpitations.
Infants may remain undetected with very rapid rates for a long time
until they develop a low cardiac output state and shock.
This deterioration in cardiac function occurs because of increased myocardial oxygen demand and limitation in myocardial oxygen delivery during
the short diastolic phase associated with very rapid heart rates.
TABLE 6.3.2: Characteristics to distinguish between sinus tachycardia and SVT
Sinus tachycardia
Supraventricular tachycardia
Infants and children usually have a

HR <220/min
P waves if visible usually upright in
leads I and AVF
Beat-to-beat variability of HR present,
which is often responsive to stimulation
HR slows gradually in response to treatment.
Clinical scenario of shock with preceding
history of AGE, blood loss, septicemia, etc.
Usually HR >220/min
P waves if visible are usually negative in leads
II, III and AVF in SVT
No beat-to-beat variability of HR in SVT
Termination is abrupt
Clinical scenario usually points towards some
pre-existent or co-existent cardiac disorders.
168
Flow chart 6.3.2: PALS pulseless arrest protocol
169
If baseline myocardial function is impaired (e.g. in a child with a cardiomyopathy), SVT can produce signs of shock in a relatively short time.
Figure 6.3.1. shows an ECG of supraventricular tachycardia.
Management
Reassess ABC
Vagal Stimulation
It should be done with ECG monitoring. The following are the maneuvers
to increase the vagal tone which slows the atrioventricular conduction to
interrupt the tachycardia.
i. Application of ice or iced water over the face to elicit the Diving
reflex.
ii. One-sided carotid body massage
iii. Older children can try a Valsalva maneuver. Some children may become experienced to know that a certain position or action will usually
cause a return to sinus rhythm. Blowing hard through a partially
obstructed straw may be effective for some children.
Ocular pressure in an infant or child is contraindicated as retinal damage may result.
Adenosine
If the tachycardia does not terminate with these maneuvers and IV access
is readily available, then intravenous adenosine should be given. Adenosine is the drug of choice for supraventricular tachycardia as it is highly
efficacious and safe. Adenosine causes a temporary atrioventricular (AV)
nodal conduction block and interrupts re-entry circuits that involve the AV
node. Adenosine is a very rapidly acting drug with a half-life of less than 10
seconds.
Dose: 100 mcg/kg rapid intravenously. If there is no response, 200 mcg/kg
and then 300 mcg/kg may be given. The effect is short lasting and the
FIG. 6.3.1: ECG showing supraventricular tachycardia
170
tachycardia might recur. It should be rapidly injected into a large peripheral vein, using a 3 way stopcock followed by a rapid saline flush before it is
taken up by the RBCs for metabolism.
The maximum total dose is 500 mcg/kg (300 mcg/kg under 1 month)
up to a maximum of 12 mg in total.
Cardioversion
The patient can be treated by cardioversion with a general anesthesia or
sedation or a rapid atrial overdrive pacing, if pacing wires are in place in a
post operative patient or by help of transcutaneous pacing pads.
To start with a dose of 0.5 to 1 J/kg may be used and repeated using a
dose of 2 J/kg.
Further Management
If the SVT does not terminate by these methods, one of the following may
be suggested but it is preferable to consult a pediatric cardiologist before
doing so.
1. Amiodarone: Loading dose of 5 mg/kg over at least 1 to 2 hours, followed by a continuous infusion of 5 to15 microgram/kg/min.
2. Procainamide and flecainide: These can be used but preferably at a
specialized center.
3. Propranolol: Dose of 50 mcg slowly intravenously. This may be tried
only if pacing is available, as asystole may occur. Propranolol and
verapamil should not be given to the same patient. It can be combined
with digoxin.
4. Verapamil: This drug has been associated with irreversible hypotension and asystole when given to infants. It therefore should not be used
in children under first year of age and with caution in children as may
cause hypotension and myocardial depression.
Wide-Complex Tachycardia
Wide-complex tachycardia with poor perfusion is probably ventricular in
origin but may be supraventricular with aberrancy. All wide-complex
tachycardias should be considered as ventricular tachycardias unless proved
other-wise.
It is important to differentiate wide-complex tachycardia from SVT
with aberrant conduction.
The factors favoring ventricular tachycardia (VT) are the following:
1. Clinical situation: Pre-existing myocardial disease, post MI, LV dysfunction.
2. Physic examination: Hemodynamic collapse or near collapse with cool
peripheries and hypotension favors VT, though SVT may also have the
similar features.
3. Intermittent cannon waves in the JVP.
4. Independent P wave activity on the ECG.
171
5. Capture or fusion beats.

6. Broader the QRS complex, more likely it is VT.
7. The precordial leads (V1V6) are either all positive or all negative (Precordial concordance) VT is likely.
ECG of ventricular tachycardia is shown in Figure 6.3.2.
Approach to a Child with VT

Hemodynamically Stable
Obtain a history to identify an underlying cause.
Underlying causes
i. Congenital heart disease and surgery.
ii. Poisoning with tricyclic antidepressants, procainamide, quinidine,
cisapride and macrolide antibiotics, or terfenadine with grapefruit juice.
iii. Renal disease or other cause of hyperkalemia.
iv. Genetic proarrhythmic conditionsLong QT syndrome.
ECG features
Characteristic ECG indicative of torsade de pointes. Seen in conditions
characterized by a long QT interval Quinine, quinidine, disopyramide,
amiodarone, tricyclic antidepressant and digoxin poisoning and cisapride
with erythromycin.
Is it really a ventricular tachycardia?
i. Wide-QRS SVT (i.e. SVT with aberrant conduction) though uncommon in infants and children may be a confounding factor. Careful
analysis of an l2-lead ECG should be done.
FIG. 6.3.2: ECG showing ventricular tachycardia
172
ii. A dose of adenosine may help identify the underlying etiology of the
arrhythmia, but should be used with extreme caution in hemodynamically stable children with wide-complex tachycardia as because
acceleration of the tachycardia and significant hypotension can occur.
iii. Check serum Na, K, Mg and Ca levels.
Emergency Treatment of VT
1. Reassess ABC.
2. Hemodynamically stable child with ventricular tachycardiaearly consultation with a pediatric cardiologist is preferred.
3. Amiodarone (5 mg/kg over minutes to over an hour depending on the
urgency) or intravenous procainamide (15 mg/kg over 30-60 minutes,
monitor ECG and BP). Amiodarone slows AV conduction, prolongs
the AV refractory period and QT interval, and slows ventricular conduction (thus widening the QRS). Complications include bradycardia,
heart block, and torsades de pointes ventricular tachycardia (VT). Be
careful when administering with another drug causing QT prolongation. Procainamide works by prolonging the refractory period of the
atria and ventricles and depressing the conduction velocity. Both of
them can cause hypotension, through vasodilatation, which should be
treated with volume expansion.
4. In cases, where the ventricular arrhythmia has been caused by drug
toxicity, DC shock after sedation/anesthesia may be the safest approach.
Use synchronous shocks initially, which are less likely to produce ventricular fibrillation. If synchronous shocks are ineffectual (If the
instrument fails to identify the abnormal QRS complexes), try asynchronous if the child is in shock.
5. For torsade de pointes ventricular tachycardia: Magnesium sulphate
as IV infusion (Over several minutes) of 25-50 mg/kg (up to 2 g). Magnesium produces vasodilatation and may cause hypotension if
administered rapidly.
6. Amiodarone 5 mg/kg may be given over a few minutes in ventricular
tachycardia if the child is in severe shock.
7. Lidocaine decreases automaticity and suppresses ventricular
arrhythmias.
Hemodynamically Unstable
Treat with synchronized electrical cardioversion (0.5 to 1 J/kg). If it does
not delay cardioversion, try a dose of adenosine. Then a second shock with
2 J/ kg may be given.
If a second shock (2 J/kg) is unsuccessful or if the tachycardia recurs
quickly, consider antiarrhythmic therapy (Amiodarone or procainamide)
before a third shock.
It is important not to delay a safe therapeutic intervention for longer
than necessary in VT as the rhythm often deteriorates quite quickly into
pulseless VT or VF.
173
Shown in Flow chart 6.3.3 is the PALS tachycardia algorithm, which

should be observed as a guide.
Flow chart 6.3.5: PALS tachycardia algorithm
174
Defibrillator for Cardioversion

One should be well equipped with working instruments and should be
confident about its use at the appropriate and demanding moment.
Defibrillators are either manual or automated (AED), with monophasic or
biphasic waveforms. The energy adjustment of the machine should be appropriate for children.
Paddle Size
Use the largest paddles or self-adhering electrodes that will fit on the chest
wall without touching (leave about 3 cm between the paddles). The best
paddle size for adults and children weighing more than 10 kg is 8 to 10 cm.
Infant paddles are for infants weighing less than10 kg.
Interface
The electrode-chest wall interface can be gel pads, electrode cream, paste,
or self-adhesive monitoring-defibrillation pads. Saline-soaked pads, ultrasound gel, bare paddles, or alcohol pads should not be used.
Energy Dose
The lowest energy dose for effective defibrillation and the upper limit for
safe defibrillation in infants and children are not known. Energy doses
4 J/kg (Up to 9 J/kg) have effectively defibrillated children.
Technique
1. Apply firm pressure on the paddles (manual) placed over the right
side of the upper chest and the apex of the heart (to the left of the
nipple over the left lower ribs). Alternatively place one electrode on
the front of the chest just to the left of the sternum and the other over
the upper back below the scapula.
2. Provide CPR until the defibrillator is ready to deliver a shock, and
resume CPR, beginning with chest compressions, immediately after
shock delivery. Minimize interruptions of chest compressions.
3. Give 1 shock (2 J/kg) as quickly as possible and immediately resume
CPR, beginning with chest compressions. Biphasic defibrillators have
a first shock success rate that exceeds 90 percent.
4. CPR may provide some coronary perfusion with oxygen and substrate
delivery, increasing the likelihood of defibrillation with a subsequent shock.
5. Continue CPR for about 5 cycles (about 2 minutes).
Bibliography
1.
2.
3.
American Heart Association. Part 12: Pediatric Advanced Life Support. Circulation. 2005;112(IV):167-87.
Doniger S J, Sharieff GQ. Pediatric dysrhythmias. Pediatr Clinics North Am
2006;53:85-106.
Park MK Pediatric Cardiology for Practitioners, 3rd edition.
6.4
Chest Pain
The majority of children presenting with chest pain as a primary complaint do not have a cardiac or other serious underlying disorder. The
priorities of assessment are firstly to exclude these disorders or provide
appropriate emergency treatment and then subsequently form a diagnosis
and management plan for the remainder of patients.
Causes of chest pain in pediatric patients include:
1. Cardiac:
i. Coronary artery diseaseischemia/ infarction:
Anomalous coronary arteries
Kawasaki disease (coronary arteritis)
ii. Arrhythmias:
Supraventicular tachycardia
Ventricular tachycardia
iii. Structural abnormalities of heart:
Hypertrophic cardiomyopathy
Severe pulmonic stenosis
Aortic valve stenosis
2. Infection:
Pericarditis
Myocarditis
3. Gastrointestinal disorders:
Reflux esophagitis
Drug induced esophagitis
Esophageal foreign body
4. Musculoskeletal disorders:
Chest wall trauma/contusion
Rib fracture
Costochondritis
5. Pulmonary disorders:
Severe cough
Asthma
Pneumonia
176
Pneumothorax/Pneumomediastinum
Pulmonary embolism
6. Psychological disorders:
Stress related
7. Idiopathic
8. Miscellaneous:
Sickle cell crisis
Abdominal aortic aneurysm (Marfans syndrome)
Pleural effusion (Collagen vascular disease)
Shingles
Pleurodynia (Coxsackievirus)
Breast tenderness
Chest mass
Assessment
As chest pain covers a wide spectrum of disease ranging from innocuous
conditions to severe life-threatening diseases, one has to be very meticulous in assessment of the children.
History
1. Onset of painAcute pain is more likely to be organic.
2. Pain wakes child from sleepMore likely to be organic.
3. Pain associate with exertion and syncopeCardiac or exercise induced
asthma.
4. FeverPneumonia, myocarditis, pericarditis.
5. Midsternal burning pain, worsens when recumbentGastroesophageal
reflux, acute gastritis.
6. History of existing heart diseaseRelated to underlying condition.
7. Serious associated conditionsMarfans, lupus, diabetes mellitus,
Kawasaki disease.
8. Stressful events in lifeConsider psychogenic causes.
Examination
1. Respiratory distress, abnormal vital signsConsider monitoring at
emergency department till diagnosis and or stabilization achieved.
2. Decreased breath sounds, palpable subcutaneous air: consider pneumonia, pneumothorax.
3. WheezingConsider asthma and pain related to complications like
pneumomediastinum, pneumothorax.
4. Abnormal auscultation of heart (rub, murmur, arrhythmia Consider
pericarditis, myocarditis, SVT, structural heart disease).
5. FeverPneumonia, myocarditis, pericarditis.
6. Evidence of traumaConsider pneumothorax.
7. Reproducible painConsider musculoskeletal pain, costochondritis.
177
Chapter 6.4: Chest Pain
8. Drooling in young childFB ingestion.

9. Tall, thin patientConsider pneumothorax.
The presence of certain worrisome signs and symptoms to prompt further work-up are as shown in Table 6.4.1.
Consider further following investigations:
1. D-dimer, CT chest: If patient has increased risk of pulmonary embolism (coagulation disorder, recent abortion, trauma, takes contraceptive
pills, neoplasm and central venous catheter).
2. Echocradiogram: If cardiac disease suspected.
3. Holter monitor: If arrhythmia suspected.
4. Exercise stress test, pulmonary function test: If pain is related to exercise.
5. Troponin level: If acute myocardial infarction suspected.
6. Drug screen: If cocaine abuse is strongly suspected.
Management of pediatric chest pain is shown in the algorithm Flow
chart 6.4.1.
Management
1. Bronchodilators for asthma related pain.
2. Antibiotics for pneumonia.
3. H2 blocker and proton pump inhibitors for midsternal burning pain
or in few selected cases as therapeutic trial.
4. Analgesia for musculoskeletal pain other undiagnosed pain. Arrange
follow-up.
5. Referral to cardiologist, pulmonologist, trauma surgeon or pediatrician in other cases as diagnosis made.
TABLE 6.4.1: Work-up for important symptoms and signs
Work-up
History/ symptoms
Sign
Chest X-ray
Fever
Cough
Shortness of breath
History of trauma
Pain wakes from sleep
H/o drug abuse( cocaine)
Associated with exercise
Serious medical problem (Marfan
syndrome, Kawasaki disease, lupus)
Foreign body ingestion
(coin, button battery)
Acute onset of pain
Associated with exercise
Associated with syncope
History of drug abuse
Fever
Tachypnea, distress, rales
Sick looking
Significant trauma
Extreme tachycardia
Pathological auscultation of heart
Absent/decreased breath sound
tall, thin
ECG
Drooling, gagging
Palpation of subcutaneous air
Pathological auscultation of heart
Tachycardia >80/minute
Sick looking
178
Flow chart 6.4.1: Pediatric chest pain algorithm
Bibliography
1.
Chang BA, editor. Pediatric Clinics of North America 2009;56:49-65.
6.5
Cardiac Emergencies in a
Noncardiac Set-up
In the emergency department one often faces emergencies which are

either directly or remotely connected to cardiac issues. The present discussion is just an outline of the ways by which one can think and act when
faced with these emergencies in a noncardiac set-up, before further help
arrives or the patient is referred to a specialist cardiac set-up.
The discussion has been presented in the form of a few clinical scenarios, which we encounter daily.
It is important to remember
1. Timely diagnosis is important.
2. There may be lack of classic cardiac symptoms like chest pain, palpitations and shortness of breath.
3. It is important to identify whether the symptoms are cardiac in origin,
the definitive diagnosis is not so important in this situation.
4. Certain cardiac emergencies presenting to the emergency department
in the neonatal period may require immediate definitive intervention.
5. Arrhythmias, often less appreciated, may be seen in children even in
those who have not undergone cardiac surgery.
How to suspect a cardiac emergency in a child not known to have cardiac problem?
1. Breathlessness or tachypnea where airway or lung cause is unlikely.
2. Cyanosis.
3. Cardiac murmur.
4. Signs of heart failure.
5. Unexplained failure to thrive.
6. Phenotypic abnormality.
7. Family history of structural heart disease.
Initial approach to a patient where diagnosis is not known
1. Airway, breathing, circulation to be attended as required.
2. IV accessgive volume 10 to 20 mL/kg NS or Ringers lactate.
3. Saturation assessment by pulse oximetry.
4. Carotids should be palpated.
5. Consider coarctation of aorta, interrupted aortic arch.
180
6.
7.
8.
9.
10.
11.
Connect the cardiac monitor.

BP 3 extremities (both arms and leg).
Chest X-ray as soon as possible.
12 lead electrocardiogram.
Finger prick test for capillary blood glucose.
Blood examinationcomplete blood count, Na, K, glucose, blood
cultures.
12. ABGright arm.
13. Catheterization of urinary bladder.
14. If the child is in shock, the child should be managed accordingly.
Clinical Evaluation
Cardiac Specific History
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Poor feeding, lethargy.

Sweating.
Respiratory distress.
Frequent cough and cold.
Edema.
Oliguria.
Bluish discoloration and cyanotic spells.
Chest pain.
Palpitations.
Syncope.
Hemoptysis.
Cardiac Specific Examination

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Respiration.
Femoral pulses.
Liver Size, tenderness.
Cardiac murmur.
Poor perfusion, cyanosis.
Cyanosis.
Tachycardia.
Poor peripheral pulses.
Blood pressure.
Pulse oximetry.
ECG and chest X-ray.
Other Investigation if Facilities Permit

1.
2.
3.
4.
Holter monitor.
Echocardiogram, in various forms.
Cardiac catheterization.
CT angiogram, cardiac MRI and perfusion scans.
Chapter 6.5: Cardiac Emergencies in a Noncardiac Set-up
181
Clinical Scenario
Newborn with subtle distress, cyanosis, born in a district hospital, did not
require resuscitation in delivery room. At present not improving to oxygen
therapy. Planned for referral to a higher center.
The differential diagnosis would include the following
1. Congenital heart disease.
2. Pneumonia.
3. Sepsis.
4. Inborn error of metabolism.
Initial approach to all patients with unknown diagnosis
1. IV accessvolume infusion10 to 20 ml/kg.
2. Complete blood counts, CRP, blood glucose estimation by Dextrostix
or blood sugar estimation, Na, K, urea, creatinine, cultures.
3. ABGright arm.
4. Catheterize the bladder.
5. 12 lead ECG, cardiac monitor if available.
6. BP3 extremities, palpate carotids, consider coarctation of aorta, interrupted aortic arch.
7. Antibiotics if indicated.
Interpretation of Chest X-Ray when Heart Disease is Suspected

The possible findings are as follows:
1. Small heart, normal pulmonary vascular markings: Probably noncardiac cause.
2. Small heart, enhanced pulmonary vascular markings: TAPVC with obstruction is a possibility.
3. Large heart, enhanced pulmonary vascular markings: Stiff lungs secondary to large shunt like VSD, PDA, truncus arteriosus, AV canal defect.
These are due to pulmonary recirculation. Other possibilities are obstructive low output lesions like corrected TGA, TAPVC.
4. Large heart, decreased pulmonary vascular markings: Right to left shunt
as in TOF, PA, TGA, VSD, PS, Ebsteins anomaly. Usually these are not
low output lesions.
Features Suggestive of a Duct Dependent Lesion

1. Sudden onset cyanosis and collapse in first few weeks of life.
2. Abnormal cardiac examination: Differential pulses, differential cyanosis, abnormal S2.
3. Poor response to oxygen, fluids, antibiotics.
4. Abnormal cardiac silhouette on CXR.
5. Abnormal ECG for age.
182
Time of Presentation
1. Duct dependent pulmonary blood flow (PBF) usually presents in the
nursery.
2. Duct dependent systemic blood flow (SBF) usually present within the
first 3 weeks of life with shock.
3. After the anatomical closure of the ductus at 2 to 3 weeks of age baby suddenly becomes ill, develops sudden cyanosis and/or cardiovascular collapse.
Presentation
1.
2.
3.
4.
Sudden onset of decreased perfusion.

Mottling.
Altered mental status.
Oliguria.
Duct Dependent Systemic Lesions

1. Critical coarctation of aorta or interrupted arch.
2. Critical aortic stenosis.
3. Hypoplastic left heart.
Duct dependent pulmonary lesions with inadequate pulmonary blood

flow
1.
2.
3.
4.
Pulmonary atresia with intact ventricular septum.

Tricuspid atresia.
Critical pulmonary stenosis.
Transposition of great arteries.
Management
1. Maintenance of ABC.
2. Sepsis should be ruled out.
3. Prostaglandin E1 (PGE1) is a potent vasodilator; it has immediate effect on the ductus. PGE1 infusion should be started without delay at
0.01 to 0.1 mcg/kg/min. Improvement usually seen within 15 minutes.
Complications of PGE1 Use

1.
2.
3.
4.
Apnea.
Fever.
Hypotension.
Seizures.
Prolonged QT Syndrome
Patients commonly present between the ages of 9 and 15 years. Recurrent
episodes of resyncope or frank syncope episodes may be precipitated by
Chapter 6.5: Cardiac Emergencies in a Noncardiac Set-up
183
intense emotion, loud noise or vigorous exercise. It may be hereditary or

acquired. Approximately 10 percent of children with prolonged QT syndrome will present with sudden death due to malignant ventricular
arrhythmias.
Drugs that Prolong QT Interval

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
AntiarrhythmicsClass 1A and 3.
AntiemeticDroperidol.
AntifungalKetoconazole.
AntihistaminesAstemizole, terfenadine.
AntimicrobialsErythromycin, co-trimoxazole.
AntipsychoticsHaloperidol.
Organophosphorus compounds
Phenothiazines
Promotility agentsCisapride.
Tricyclic antidepressantsAmitriptyline.
Treatment
1. Stabilization and ABC.
2. Patients presenting with an episode of polymorphic ventricular tachycardia should receive magnesium 25 to 50 mg/kg IV, maximum 2 gm.
3. -blockers may be useful in suppressing catecholamine surge. -blockers
significantly reduce episodes of syncope and sudden death.
4. Serum electrolytes and toxicology screen should be done.
5. Patients with recurrent ventricular tachycardia may require temporary
ventricular pacing.
6. The child should be admitted for further management. All these patients should have thorough assessment and long-term follow-up.
Bibliography
1.
Park MK. Pediatric Cardiology for Practitioners, 3rd edition.
GASTROINTESTINAL
EMERGENCIES
7.1
Acute Abdominal Pain
Jaydeep Choudhury
The first task in the management of a child with acute abdominal pain is to
determine whether assessment by a surgeon is required. It is also worthwhile to remember that not only abdominal but also extra-abdominal
emergencies produce acute abdomen. Children presenting with acute abdominal pain should be thoroughly evaluated before labeling them as a
nonspecific or nonorganic disorder.
Red Flags
1. Surgical abdomen (abdominal distension, guarding, rigidity, absent
peristalsis, lump).
2. Persistent vomiting or bilious vomiting.
3. Dehydration or shock.
Initial Assessment
1. The vital parameters should be assessed first.
2. The volume status of the child is a very important determinant, so
appropriate volume replacement should be done.
3. A child in shock should be resuscitated and stabilized first.
Initial Clues for Severe Abdominal Pain

1.
2.
3.
4.
Toxic look.
Decubitus: Curled up or supine without any movement.
Skin: Tense or red abdomen.
Blood in stool and persistent or bilious vomiting.
It is often very difficult to distinguish between organic and non-organic pain in children. The differentiating points are shown in Table 7.1.1.
Tests to Look for Peritoneal Irritation

1. Sit up straight from lying position.
2. Voluntary coughing or pushing the abdominal wall out and drawing
it in.
188
TABLE 7.1.1: Differentiation of non-organic from organic pain

Organic
Nature of pain
History
Examination
Any time in day and night

i.
ii.
iii.
iv.
v.
vi.
vii.
Weight loss
Lack of energy
Fever
Change in bowel habit
Urinary symptoms
Intestinal symptoms
Vomiting: continuous,
bile stained, hematemesis
viii. Rectal bleeding
Various manifestations
Non-organic
Periodic, usually in day, good
in-between. Often peri-umbilical.
i. Migraine
ii. School and family problem
iii. Isolated vomiting, not bile stained
Usually normal and thriving
3. Straight leg rising.

Inability to do these activities suggests pain due to peritoneal irritation.
Acute Lower Abdominal Pain

Acute lower abdominal pain is more common and more likely to indicate
surgical pathology. Similarly, right sided pain is more significant. The differential diagnoses of acute lower abdominal pain are:
1. Acute appendicitis.
2. Mesenteric adenitis.
3. Intussusception.
4. Meckels diverticulitis.
5. Primary peritonitis.
6. Ruptured luteal cyst, torsion of ovarian cyst or ovary in female.
7. Intestinal obstruction.
8. Acute painful scrotum/ deep iliac lymphadenitis.
9. Constipation.
10. Gastroenteritis.
11. Urinary tract infection.
Acute Appendicitis (with or without Peritonitis)

Acute appendicitis must be considered in every abdominal emergency in
childhood. Classically central abdominal pain, anorexia, later nausea with
subsequent shift of pain to right iliac fossa which is persistent, associated
sick look, tachycardic, often mildly febrile and having involuntary abdominal guarding, rebound tenderness are diagnostic of appendicitis.
Peritonitis is a frequent complication of appendicitis that may be difficult to recognize in infants and young children. Tenderness may be diffuse
rather than localized and rigidity may be absent even when advanced general peritonitis.
Chapter 7.1: Acute Abdominal Pain
189
Mesenteric Lymphadenitis
It presents in the same way as acute appendicitis. But preceding or concurrent URTI, abdominal tenderness in two or more areas, absence of guarding
and failure of the signs to progress suggest the condition. Normal blood
count and enlarged lymphnodes with normal looking appendix in ultrasound makes the diagnosis more confident. Treatment is supportive and
symptomatic.
Intussusception
Intermittent inconsolable cry, sick looking, tachycardic often dehydrated and
exhausted child should raise the suspicion. Red stool is often a late sign.
Absence of palpable mass and normal abdominal X-ray does not exclude the condition. USG abdomen often proves the diagnosis Figure 7.1.1.
Air contrast enema followed by pneumatic reduction is nowadays highly
successful treatment and reduced surgical correction, which is reserved for
unsuccessful and more advanced cases with suspected bowel loss.
Meckels Diverticulitis
Commonest cause of major gastrointestinal bleeding in childhood, also
suspected in a patient with intestinal obstruction who has not undergone
previous abdominal operation. Sometimes indistinguishable from appendicitis, true diagnosis becomes apparent only at operation.
Intestinal Obstruction
The common cause of obstruction is strangulation of an inguinal hernia, if
looked for, it presents few problems in diagnosis. Most cases of obstruction
FIG. 7.1.1: Target sign of intussusception in abdominal USG
190
in older children are due to bands or adhesions following a previous abdominal operation.
Recurrent pain and vomiting with distended loops of gut, visible or
palpable, air-fluid level in the X-ray will confirm the diagnosis. Figure 7.1.2
shows visible peristaltic wave in a child with intestinal obstruction, Figure
7.1.3 shows abdominal distension with right inguinal hernia in a neonate
and Figure 7.1.4 shows multiple air-fluid levels in straight X-ray abdomen.
Children who have not had a previous abdominal operation, obstruction may be due to volvulus, Meckels band or diverticulum.
Primary Peritonitis
Caused by Pneumococcus, mainly occurs in immunocompromised patients
or patients on steroid therapy, e.g. nephrotic syndrome. Background of
the patient and clinical suspicion are necessary. Treatment is intravenous
penicillin and supportive care.
Pediatric Gynecological Emergencies

In pubertal girl, exaggerated intraperitoneal bleeding at normal time of
ovulation (Mittelschmertz bleeding) or rupture of luteal cyst may be unsuspected and not recognized. Torsion of ovary, acute salpingitis, ovarian tumor,
ectopic pregnancy are uncommon and rarely diagnosed before operation.
Typically, extreme tenderness in pelvis contrasts with the relative absence
of abdominal signs.
FIG. 7.1.2: Visible peristaltic waves
191
FIG. 7.1.3: Abdominal distension with right inguinal hernia in a neonate
FIG. 7.1.4: Multiple air-fluid levels in straight X-ray abdomen
Distinction between rupture of a follicular or luteal cyst and acute pelvic appendicitis can be difficult. Pelvic ultrasound can detect small ovarian
cyst and can save exploration than a laparoscopy.
192
Investigation
X-ray abdomen may be helpful in intestinal obstruction or intussusception
and investigation is not necessary to diagnose constipation which is more
a clinical diagnosis.
Ultrasound abdomen can be helpful to diagnose intussusception, ovarian cyst and torsion, tumor, deep iliac lymphadenitis and also appendicitis
though retrocecal and retropelvic appendicitis may be missed and only
picked by CT scan.
High blood count and acute phase reactant are more corroborative in
appendicitis and deep iliac lymphadenitis, do not replace clinical judgement in acute appendicitis. Always rule out no UTI exists.
Acute upper abdominal pain is generally less common and less likely
to have significant underlying problem. However, the following conditions
should be always considered:
1. Viral gastritis/drug induced gastritis/reflux esophagitis
2. Pneumonia
3. Diabetic ketoacidosis
4. Acute pyelonephritis
5. Malrotation of midgut/ volvulous
6. PUJ obstruction
7. Pancreatitis.
While a good history and clinical examination and simple investigations can diagnose first three conditions. Acute pyelonephritis is diagnosed
in pyrexial and ill patient with marked renal angle tenderness and evidence of UTI in laboratory test.
PUJ obstruction and pancreatitis require high index of suspicion. Recurrent lateralised severe colic and associated vomiting is the usual history
in PUJ obstruction confirmed by renal ultrasound. Pancreatitis is diagnosed
by raised pancreatic enzymes, a not so rare condition in pediatric age group.
Midgut Malrotation
Bile stained vomiting associated with a soft nondistended abdomen is early
feature. The diagnosis should be made at this early stage before widespread
ischemic gut damage occurs. Signs vary depending on the degree of intestinal obstruction versus ischemia. Signs of shock, pallor and a vague mass
may be palpable at the center of abdomen in strangulation. Blood or blood
tinged mucus may be present rectally. Distension is variable and often absent or confined to epigastrium when duodenum is obstructed, for a large
vomit can empty the stomach and proximal duodenum.
Investigation: Radiocontrast fluoroscopy is the most reliable confirmation
which shows the duodenojejunal flexure is located at a lower level than the
pylorus. The contrast may show the spiral twist of the volvulus as well.
Treatment: Urgent laparotomy is required to salvage from ischemia of the
gut as much as possible. The malfixation is corrected by Ladds operation.
Approach to acute abdominal pain is shown in Flow chart 7.1.1.
193
Flow chart 7.1.1: Approach to acute abdominal pain
Bibliography
1.
2.
Hutson JM, Woodward AA, Beasley SW Editors. Joness Clinical Paediatric Surgery: 5th edition, Blackwell Science Asia.
McCollough M, Sharieff GQ. Abdominal pain in children. Pediatric Clinics of
North America 2006;53:107-38.
7.2
Acute Scrotum
Some of the acute scrotal swellings are dire medical emergencies. They
have to be assessed early and referred to the Pediatric Surgeon for management. The differential diagnosis of acute scrotum in pediatric age group
includes:
1. Torsion of the testis.
2. Torsion of the hydatid of morgagni.
3. Idiopathic scrotal edema.
4. Testicular trauma.
5. Epididymo-orchitis.
Torsion of the Testis

Torsion of the testis is one of the most severe acute conditions of the testis.
It occurs as a result of high attachment of the visceral layer of the tunica
vaginalis on the spermatic cord. The testis hangs horizontally and freely
within the tunica. The muscle of the cord spirals downward while contraction leads to a twist of the testis, compromising its blood supply. Neonatal
tunica vaginalis is not adherent to the rest of the scrotum allowing testicle
and tunica vaginalis to twist on the neurovascular pedicle.
Two distinct peak ages are neonatal and prepubertal. While unsettled cry
and red scrotum may be the only clinical presentation in neonatal period,
other group experience sudden severe scrotal, groin and often lower abdominal pain with associated nausea and vomiting. The child looks pale
and sweaty. Testis exquisitely tender, swollen; lies high and horizontally.
The cord is also tender.
After 8 to 12 hours, the overlying scrotal skin is reddened and often a
secondary hydrocele ensues Figure 7.2.1.
Investigations
Investigations are rarely indicated. Ultrasound with Doppler may be helpful
only in ambiguous cases. No blood flow to the testis clinches the diagnosis.
Chapter 7.2: Acute Scrotum
195
FIG. 7.2.1: Torsion testis (For color version see Plate 2)
Management
Urgent surgical exploration and correction. The other testis also should be
fixed as a precaution. Testicular loss approaches 2 out of 3 if surgery is
delayed beyond 12 hours after the onset of pain.
Torsion of the Hydatid of Morgagni

It is also called Torsion of the Testicular Appendage.
Mild pain over weeks, days or hours precedes the acute onset of the pain.
Blue dot sign is seen in 40 percent of the cases at the upper pole of the
testis at the early stage and is a classical sign. Tender nodule at the upper
pole of the testis with otherwise low lying free testis is diagnostic of this
condition. Reactive hydrocele occurs within 12 to 24 hours. But diagnosis
becomes difficult after 24 hours of the onset with pain, hydrocele and absence of blue dot sign, often necessitating surgical exploration. No
abdominal pain or constitutional symptoms unlike testicular torsion are
present.
Investigations
Ultrasound will demonstrate nodule at the upper pole, normal testis and
secondary hydrocele.
196
Management
Analgesia and rest if diagnosis is certain, pain resolves in 2 to 3 days. Expert opinion should be sought if uncertain and surgery if symptoms are
severe.
Idiopathic Scrotal Edema

Rapidly developing edema of one side of the scrotum may spread to the
opposite side, inguinal region and perineum. Cause is unknown but has
been attributed to possible allergy, insect bite.
Usually toddlers, discomfort rather than acute pain and swelling may not
be noticed until bath time. Scrotum is pink or pale red and swelling anterior to the testis. Nontender testis of normal size and easily palpable normal
cord.
Investigations
Test for proteinuria as nephrotic syndrome may present with isolated scrotal edema with or without penile edema.
Management
It resolves spontaneously in 3 to 5 days.
Testicular Trauma
Hematoma within or around the testicle, traumatic hydrocele or fracture
of testicle.
Investigations
Ultrasonography is the investigation of choice.
Management
Always get experts opinion about diagnosis and surgical exploration if
concerned about testicular viability.
Epididymo-orchitis
Rare in children and should not be considered until testicular torsion has
been excluded. Epididymo-orchitis may be associated with ascending UTI
or urinary tract abnormality like duplex kidneys. Though the condition
may also occur in the absence of pyuria and with negative urine culture.
Acute scrotal pain in the presence of normal testicular exam.
Chapter 7.2: Acute Scrotum
197
Management
Sterile acute epididymo-orchitis is self-limiting without any sequelae. Mild
infective cases treated with amoxycillin while more severe may require IV
antibiotics.
Bibliography
1.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J Editors Textbook of Paediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill
Livingstone. 817.
7.3
Upper Gastrointestinal Bleeding
Jaydeep Choudhury
Gastrointestinal (GI) bleeding manifests in the following ways:

1. Hematemesis is the passage of vomited material that is coffee grounds
in color or contains frank blood.
2. Melena is the passage of black tarry stool, results from bacterial degradation of hemoglobin.
3. Hematochezia is passage of bright red color blood from the rectum.
This can occur in lower as well as upper GI bleeding.
The age wise etiological agents are shown in Table 7.3.1 and the grades
of GI bleeding are shown in Flow chart 7.3.1.
Severe bleeding means the following:
1. Shock.
2. 20 percent of blood volume required immediately or
3. 40 percent or more of blood volume needed in 24 hours to stabilize.
4. Fall in Hb 8 gm/dL or less.
5. Signs of heart failure, kidney, liver or bowel ischemia and dysfunction.
TABLE 7.3.1: Etiology according to age
Neonates
i. Swallowed maternal
blood
ii. Hemorrhagic
disease of newborn
iii. Gastritis
iv. Stress ulcer
v. Esophagitis
vi. Congenital blood
dyscrasias
vii. Vascular
malformation
viii. Idiopathic
1 month to 1 year
1 year to 12 years
Adolescents
i. Gastritis
i. Esophageal varices
i. Esophageal varices
ii. Stress ulcer
ii. Gastritis
ii. Gastritis
iii. Esophagitis
iv. Mallory-Weiss
syndrome
v. Vascular
malformation
vi. GIT duplication
iii. Stress ulcer

iv. Esophagitis
iii. Stress ulcer

iv. Esophagitis
v. Mallory-Weiss
syndrome.
vi. Peptic ulcer
v. Mallory-Weiss
syndrome
vi. Peptic ulcer
vii. Foreign body
Chapter 7.3: Upper Gastrointestinal Bleeding
199
Flow chart 7.3.1: Management plan according to severity and bleeding
Investigations
1.
2.
3.
4.
Complete blood count, ESR.

Coagulation profile.
Liver function test, renal function test.
Blood grouping and cross matching.
Management
Immediate
1.
2.
3.
4.
5.
6.
7.
Double IV access.
Oxygen inhalation.
Nasogastric tube in situ.
Blood drawn for investigations as detailed above.
Urinary bladder catheterization to measure urine output.
CVP line and keep pressure of 5 to 8 cm of water.
Endotracheal intubation and ventilation if required.
Restore and Maintain Intravascular Volume

1. Fluid bolus10 to 20 ml/kg of normal saline or Ringers lactate rapidly over 30 to 60 minutes.
2. Repeat fluid boluses till urine output is normal and pulse, BP, CFT
improves.
3. Monitor and maintain hematocrit of 30 percent.
200
Re-establish a Normal Oxygen Carrying Capacity

Transfuse whole blood initially to maintain intravascular volume. Once bleeding stops and specific components are available, change to packed cell.
Determination of Source and Site of Bleeding

If possible determine source and site of bleeding and steps should be taken
to stop bleeding. After initial stabilization and review of whole clinical
situation, emergency endoscopy should be planned and approached as
shown in Flow chart 7.3.2. The management plan of acute variceal bleed is
shown in Flow chart 7.3.3.
Abbreviations used
EST Endoscopic sclerotherapy.
EVL Endoscopic variceal ligation.
TIPS Transjugular intrahepatic portosystemic shunt.
Treatment Options Available for Acute Variceal Hemorrhage

1. Endoscopic technique: Sclerotherapy, band ligation.
2. Pharmacological intervention
i. Vasopressin.
ii. Terlipressin.
iii. Somatostatin.
iv. Octreotide.
3. Balloon tamponade
Less preferred if pharmacological intervention or endoscopic sclerotherapy can be applied effectively.
i. Sengstaken-Blakemore tube.
ii. Minnesota tube.
Flow chart 7.3.2: Endoscopic evaluation of GI bleed
Chapter 7.3: Upper Gastrointestinal Bleeding
201
Flow chart 7.3.3: Management plan for acute variceal bleeding
4. Surgical technique:
i. Portacaval shunt.
ii. Distal splenorenal shunt.
iii. Devascularization.
iv. TIPS (Limited pediatric experience).
Bibliography
1.
2.
3.
4.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J, editors. Textbook of Paediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill
Livingstone. 81-7.
Krebs H, Seidman, Sokol, et al. Pediatric Clinical Gastroenterology 1995. 4th
edition.
Walker, Durie, Hamilton, Walker Smith, Watkins. Pediatric Gastrointestinal
Disease, 2000.
Wyllie, Hyams. Pediatric Gastroentestinal Disease, 1999.
7.4
Fulminant Hepatic Failure
Fulminant hepatic failure is the development of signs of advanced liver

failure such as hepatic encephalopathy which present within 8 weeks of the
onset of liver disease in the absence of previous liver disease.
Etiology
1. Infections: Hepatitis A, B, C, E, herpes, adenovirus, toxoplasmosis,
CMV, EBV, leptospirosis and others.
2. Metabolic: Galactosemia, tyrosinemia, Wilsons, mitochondrial disease,
bile acid disorders.
3. Toxins and medications: Paracetamol, halothane, phenytoin, isoniazide,
valproate, tetracycline.
4. Autoimmune hepatitis: Liver, kidney and microsomal antibodies in serum.
5. Ischemia: Congenital heart disease, post cardiac surgery, Budd-Chiari
disease.
6. Others: Malignancy.
Clinical Manifestations
Fever, jaundice, vomiting, poor feeding, abdominal pain, bleeding, ascites,
hepatosplenomegaly, encephalopathy. Figure 7.4.1 shows a child with advanced liver failure. The clinical staging of hepatic encephalopathy is shown
in Table 7.4.1.
Investigations
Advise the following minimum investigationsliver function tests, sugar,
electrolytes (Na, K, HCO3), urea, creatinine, prothrombin time, partial
thromboplastin time and serum ammonia. The battery of full investigatory
workup is as below.
Biochemical
Bilirubin, transaminases, alkaline phosphatase, albumin, urea, creatinine,
calcium, phosphate, ammonia, acid-base, lactate, glucose.
203
Chapter 7.4: Fulminant Hepatic Failure
FIG. 7.4.1: A child with advanced liver failure

TABLE 7.4.1: Clinical staging of hepatic encephalopathy
Stage
Asterixis
EEG changes
Clinical manifestations
Stage 1 Prodrome
Slight
Minimal
Stage 2 Impending
coma
Easily elicited
Generalized slowing
of rhythm
Stage 3 Stupor
Present if patient
is cooperative
Grossly abnormal
slowing
Stage 4 Coma
Usually absent
Appearance of delta
waves, decreased
amplitudes
Mild intellectual impairment, disturbed sleep

wake cycle
Drowsiness, confusion,
inappropriate behavior,
mood swing
Drowsy, unresponsive
to verbal commands,
markedly confused,
delirious
Hyperreflexia, extensor
plantar response,
unconscious, decerebrate
or decorticate response to
pain (4a) or absent (4b)
Hematology
Full blood count, platelet, smear and reticulocyte count, MP, PT, APTT,
FDP, factor V or VII.
Radiology
Abdominal USG, X-ray and CT or MRI if indicated.
Septic Screen
Blood and urine culture. Lumbar puncture should be avoided.
204
Neurophysiology
EEG.
Diagnostic Investigations
Serum hepatitis A-IgM, hepatitis E-IgM, hepatitis CV-Ab, HbsAg, Hbc IgM,
Leptospira serology, CMV, HSV, EBV serology, paracetamol level if indicated, serum copper, ceruloplasmin, autoantibodies, aminoacids for
metabolic disorder screening.
Urine
24 hours copper, aminoacids, organic acids screening, reducing sugar.
Red Flag Signs

Clinical
1.
2.
3.
4.
5.
Below 1 year of age.

Stage 4 encephalopathy.
Need for dialysis.
Spontaneous bleed.
Ascites.
Biochemical
1.
2.
3.
4.
5.
PT >5 sec difference despite vitamin K.

Persistent hypoglycemia.
Low serum albumin.
SGPT >3000.
Serum bilirubin >20 mg/dl.
Management
1. Position: Head in the midline raised at an angle of 30o. Neck flexion
should be avoided.
2. A, B, C and admit in ICU. Gastroenterologist should be consulted early.
3. It is ideal to go for the minimum investigations.
4. Tubes: One nasogastric tube, two intravenous lines and one indwelling
bladder catheter should be in situ.
5. Assess neurological status and level of consciousness. GCS 7 need
intubation and ventilation.
6. Intravenous fluid: Two-third maintenance fluid with the following additions:
i. Intravenous glucose solution concentration should be >12 to 15
percent, for which a central line may be required. These children are prone to hypoglycemia, blood sugar must be maintained
between 100 and 150 mg/dL.
Chapter 7.4: Fulminant Hepatic Failure
7.
8.
8.
9.
10.
11.
12.
13.
14.
15.
205
ii. Protein free or <0.5 gm/kg/day and amino acid mixture rich in
branched chain amino acid.
iii. Sodium should be given at 1 to 2 mEq/kg/day. These children
are prone to dilutional hyponatremia. Rehydration fluid should
be 0.33 to 0.25 percent saline. Serum sodium need to be corrected to >125 mEq/L.
iv. Potassium should be given at 2 to 3 mEq/kg/day and serum K to
be maintained between 3.5 to 4.5 mEq/L.
v. Calcium should be given as 10 percent calcium gluconate solution
10 ml diluted in intravenous solution.
Feeding should be started early with low protein containing feed.
Gut clearance:
i. Lactulose 10 to 15 ml every 2 to 4 hourly till atleast 3 loose stools/
day.
ii. Constant nasogastric tube suction to remove any blood from stomach.
iii. Bowel wash and enema with 50 percent magnesium sulphate.
Cerebraledema: Positioning, hyperventilation, mannitol.
Bleeding manifestations:
i. Vitamin K 0.2 mg/kg/day (maximum 10 mg/day) injection daily
for 3 consecutive days.
ii. Ranitidine 2 to 4 mg/kg/day injection every 12 hourly.
iii. Fresh frozen plasma 10 ml/kg for control of coagulopathy.
iv. Hematocrit >30 percent and platelet count >30,000/cmm to be
maintained.
Infection: Broad spectrum antibiotics are indicated to combat nosocomial pneumonia, bacteremia and urinary tract infection. Antifungal
agents may be required.
Anticonvulsants: Phenytoin is the anticonvulsant of choice. Lorazepam
is the preferred sedative, as it is not metabolized through hepatic P450
pathway.
Respiratory failure: In stage 3 or 4 encephalopathy and with profound
respiratory compromise mechanical ventilation may be needed.
Renal failure: Hepatorenal syndrome is a known complication of liver
failure in a previously normal kidney. Early peritoneal or hemodialysis
is the preferred treatment.
Hypotension and shock: Appropriate fluid management with inotropes
as required under CVP monitor.
Other modalities:
i. Flumazenil, the benzodiazepine antagonist.
ii. N-acetyl cysteine in paracetamol induced liver damage.
iii. Branched chain amino acid: L-ornithine l-aspartate if serum ammonia is high.
iv. Glucagon.
206
Follow-up and Monitoring

1. Hourly: Pulse, BP, RR, temperature, GCS, fluid balance with indwelling catheter. Every 4 to 6 hourly blood glucose.
2. Every 12 to 24 hourly: Serum electrolytes and renal function.
3. Daily: Hemoglobin, PCV, TC, platelet count, coagulation profile.
4. Every 2 to 3 days: Liver function test (including glucose, albumin, coagulation, ammonia, bilirubin, ALT, AST, ALK, GGT) depends on
clinical situation.
5. CT head if suspecting cerebral edema.
6. EEG for encephalopathy grading.
7. Abdominal ultrasonography.
Temporary Hepatic Support

1. Hemodialysis, hemoperfusion, exchange blood transfusion and
plasmaphresis have been tried with mixed results.
2. Extracorporeal liver assist device (ELAD).
3. Finally liver transplantation is the treatment.
Bibliography
1.
2.
3.
4.
Krebs H, Sokol S, et al. Pediatric Clinical Gastroenterology. 4th edition1995.

Suchy FJ, Jsokol R, Balistreri WF. Liver Disease in Children. 2nd edition 2001.
Walker, Durie, Hamilton, Smith W, Watkins. Pediatric Gastrointestinal Disease.
2002.
Wyllie, Hyams. Pediatric Gastrointestinal Disease.1999.
RENAL
EMERGENCIES
8.1
Acute Renal Failure
Jaydeep Choudhury
Acute renal failure (ARF) presents in various ways and relates to the underlying disorder.
Causes of ARF
Prerenal
Decreased cardiac output (cardiogenic shock) or decreased intravascular
volume (dehydration, hemorrhage, third-spacing).
Renal
Renal parenchymal disease (acute glomerulonephrosis, hemolytic uremic
syndrome, pyelonephritis, drug induced).
Postrenal
Obstructive uropathy (posterior urethral valve, intra-abdominal tumor).
Presentations in Emergency
1. Absolute anuria: No urine output in the last 12 hours with empty urinary bladder.
2. Anuria: Urine output less than 0.5 ml/kg/hr.
3. Oliguria: Urine output less than 1 ml/kg/hr.
4. Hypertensive crisis.
5. Cardiorespiratory compromise.
Assessment of Severity
1. CVS: Blood pressure, low BP may suggest dehydration or shock and
high BP signifies renal disease.
2. CNS: Sensorium may be altered in uremia, seizure may be present.
3. Respiratory system: Hyperventilation signifies acidosis.
4. Abdomen: Palpable kidneys suggest hydronephrosis, distended bladder may be due to urinary obstruction.
210
Determination of Underlying Cause

The typical signs and symptoms of ARF in different situations are summarized in Table 8.1.1. A quick assessment of the child will help in determining
the etioligy of ARF. The differentiating features of renal and prerenal causes
of ARF are shown in Table 8.1.2.
Investigations
1.
2.
3.
4.
5.
Blood biochemistry: Ceatinine, serum electrolytes ,Ca, Mg, PO4.

Full blood count, red cell morphology, differential counts (HUS).
Chest X-ray (Cardiomegaly, pulmonary edema).
Renal ultrasound: If post renal causes suspected.
Renal indices: Urine specific gravity, osmolality, sodium, urea, creatinine, FENa.
(To differentiate prerenal and intrinsic renal failure).
Fractional excreation of sodium (FENa)
Urine Na (mEq/L) Plasma creatinine (mg/dL)
100
=
Plasma Na (mEq/L) Urine creatining (mg/dL)
Plasma osmolality 275295, urine osmolality >700 is normal.
TABLE 8.1.1: Typical signs and symptoms of ARF in different situations

History/Symptoms
Signs
Diagnosis
Vomiting, diarrhea, hemorrhage

Falciparum malaria, G6PD
deficiency, snake bite, mismatched
blood transfusion
Fever
Recent H/O diarrhea. Melena/
sudden pallor/seizure
High fever
Sore throat / pyoderma
H/O nephrotoxic drugs
Variable urine output
Dehydration, shock
Variable, depending on
individual condition
Gastroenteritis, hypovolemia
Petechiae, bleeding
Sepsis, DIC
Suspect HUS, confirm with
laboratory results
Pyelonephritis
Acute glomerulonephritis
Drug induced ARF
Obstructive uropathy
Flank tenderness
Hypertension/edema
Suprapubic mass
Acute tubular necrosis
TABLE 8.1.2: Differentiating features of renal and prerenal causes of ARF

Prerenal
Renal
History/clinical features
Dehydration, hypovolemia
Yes
No. may be normal or over

hydration
Renal indices
Specific gravity
Urinary sodium
Urine/plasma osmolality
FENa
Diuretics and fluid challenge
> 1020
< 20 mEq/L.
>1:3
<1(< 2 in newborn)
Positive response
normal
>20 mEq/L
<1:3
>1(>2 in newborn)
No response
Chapter 8.1: Acute Renal Failure
211
Points to Ponder
1. Is it prerenal so that ARF can be prevented by fluid therapy?
2. Are there any associated life-threatening complications that must be
treated immediately?
3. Is there any obstruction that must be relieved immediately?
4. Any indication for peritoneal dialysis?
5. Any nephrotoxic drug that needs discontinuation or dose adjustment?
Management
1. Normal saline infusion 20 to 30 ml/kg over 30 to 60 mins to correct
hypovolemia.
2. Monitoring of vital parameters.
3. Measurement of central venous pressure (CVP).
4. Check over hydration and measure urine output (UOP).
5. Electrolytes, dietProtein, salt that need appropriate adjustments and
monitoring.
Stepwise management and fluid management of ARF is summarized
in Flow charts 8.1.1 and 8.1.2 respectively.
The various complications of acute renal failure and their management are described in Table 8.1.3.
Diet
1. Protein should not be restricted. 0.6 gm/kg/day in children and 1gm/
kg/day in infants.
2. Liberal amount of carbohydrate and fat.
3. Vitamin and mineral supplementation.
4. Salt restriction, if there is hypertension.
Infection
Diuretic phase of ARF is characterised by increased urine output, with high
blood urea and creatinine. The urine output has to be replaced by 0.45
percent saline infusion.
Flow chart 8.1.1: Stepwise management of ARF
Anemia
Hypertension
Metabolic acidosis
Hyponatremia (Na <120 mEq/L)
Hypocalcemia (Total Ca <8 mg%

or ionized Ca <0.8 mmol%)
10% Ca gluconate 1-2 ml over 10 minutes with cardiac monitor

i. Fluid restriction (dilutional hyponatremia)
ii. 3% NaCl correct up-to 125 mEq/L over 30-60 min (1ml = 0.5 mEq)
If pH <7.2 then, bolus NaHCO3 may be administered
(base excess weight 0.3 ) over 30 minutes
nifedepine, Nitroprusside, diazoxide (avoid betablocker in fluid
retention and ACE inhibitor causes potassium retention)
Packed cell transfusion
vi.
iv.
v.
i.
ii.
iii.
Fluid overload (Intrinsic renal failure)
Pulmonary edema
Hyperkalemia (K>5.5 mEq/L)
Treatment
5% Dextrose for insensible water loss (400 ml/mt square/day)
+ 0.45% saline for previous days urine output.
O2, frusemide, consider intubation and ventilation
K containing fluid to be avoided
Kayexalate (Sodium polysterene sulfate) 1 gm/kg enema or oral
10% Ca gluconate 0.51 ml/kg over 510 min, to be discontinued
if heart rate falls by 20
Salbutamol 5-10 mg nebulization
7.5% Sodium bicarbonate 13 mEq/kg
IV over 30 minutes
Dextrose (0.5-1 mg/kg) + Insulin 0.1 unit/kg over 1 hour
Complication
TABLE 8.1.3: Complications of ARF and their management

Remarks
Should be lowered gradually
Latter binds phosphate so that serum

Ca Premains <70 mmol
Other losses to be monitored and replaced

accordingly
CVP to be monitored
Calcium stabilizes cell membrane and
salbutamol facilitates K entry into cells
212
Chapter 8.1: Acute Renal Failure
213
Flow chart 8.1.2: Fluid management of ARF
Indications of Dialysis in ARF

1. Clinical course suggesting prolonged period of oliguria/anuria likely
2. Uremia: Altered sensorium, abnormal behaviour, seizure, nausea, pericarditis.
3. Hyperkalemia: K>6.5 mEq/L or K 5.5 to 6.5 mEq/L with ECG hanges.
4. Hyponatremia: Na<120 mEq/L
5. Fluid overload: Pulmonary edema, hypertension, CCF resistant to diuretics.
6. Uncontrolled metabolic acidosis: pH<7.2 despite NaHCO3.
7. Hypercatabolic state: Sepsis, tissue injury, burns.
Bibliography
1.
Nammalwar BR, Vijayakumar M editors. Principles and Practice of Pediatric

Nephrology, 1st edition, New Delhi: Jaypee Brothers 2004;225-32.
8.2
Hypertensive Crisis
Saheli Misra
Hypertension being not so common in children often goes undetected. So,

blood pressure (BP) should be routinely checked in children presenting to
the emergency department. By definition, the following are the types of
hypertension. The common causes of hypertension in children in different
age groups are shown in Table 8.2.1. The etiology of hypertensive emergencies in children is shown in Table 8.2.2.
1. Prehypertension: Systolic and/or diastolic blood pressure (BP) levels
are 90th but <95th percentile.
2. Hypertension: Defined as systolic and/or diastolic BP 95 percent percentile on three or more occasions.
3. White-coat hypertension: BP >95th percentile in a physicians office or
clinic, who is normotensive, outside a clinical setting.
4. Severe hypertension: BP >99 percent for age, sex, and height percentile.
5. Hypertensive emergency: Severely elevated blood pressure with evidence
of target organ injury to the central nervous system, kidneys or cardiovascular system.
Hypertensive emergencies occur rarely in children. It is usually
seen in those with underlying renal disease. It is a severe, symptomatic
hypertension with BP well above the 99th percentile and requires
prompt treatment. They manifest as hypertensive encephalopathy with
neurological symptoms of lethargy, coma, and/or seizures. The absolute degree of BP elevation is less important than whether symptoms
and/or target end organ damage is present.
6. Hypertensive urgency: Severely elevated blood pressure with no current evidence of secondary organ damage, although it left untreated,
target organ injury may result imminently. Hypertensive urgencies are
accompanied by less serious symptoms, such as severe headache or
vomiting.
7. Rebound hypertension: It occurs with abrupt withdrawal of clonidine,
angiotensin converting enzyme inhibitors or beta-blockers.
Chapter 8.2: Hypertensive Crisis

TABLE 8.2.1: Common causes of hypertension in children
Age Group
Cause
Newborn
Renal vessel thrombosis

Renal artery stenosis
Congenital renal anomalies
Coarctation of the aorta
Renal parenchymal disease
Renovascular disease
Coarctation of the aorta
Essential hypertension
Essential hypertension
Early childhood (infancy to 6 years)
School age (610 years)
Adolescence
TABLE 8.2.2: Common causes of pediatric hypertensive emergencies

Renal disease: (80%)
i. Nephritides:
ii. Vascular:
iii. Congenital malformations:
Miscellaneous:
Endocrine:
Cardiovascular:
Drugs:
Henoch-Schnlein purpura
Postinfectious glomerulonephritis
Systemic lupus nephritis
Rapidly progressive glomerulonephritis
Hemolytic-uremic syndrome
Renal artery stenosis and thrombosis
Renal vein thrombosis
Sickle cell nephropathy
Polycystic kidney disease
Tuberous sclerosis
Hydronephrosis
Renal hypoplasia
Obstructive uropathy
Iatrogenic fluid overload
Renal failure with fluid overload
Reflux nephropathy
Renal tumors
Pheochromocytoma
Congenital adrenal hyperplasia
Aortic thrombosis
Aortic coarctation
Aortic insufficiency
Subacute bacterial endocarditis
Corticosteroids
NSAIDs
Oral contraceptive pills
Theophylline
Phenylephrine
215
216
Immediate Evaluation
1. First, it should be ensured that BP is truly elevated. Any errors in cuff
size or the instrument should be excluded.
2. Standard percentile charts for BP in various ages should be followed
before starting any medication.
3. Reactive increase in BP should be excluded: Pain from any cause, various
emotional causes and time of the day.
4. Pre-existing hypertension and renal diseases, presence of cardiac, neurological symptoms, and medication history.
Evaluation for Identifiable Cause

1. Assessment of the patients volume status: Volume overload needs diuretics,
volume depletion stimulates renin-angiotensin system.
2. Assessment of end organ involvement.
3. Fundus examination: Look for papilledema and hard exudates.
4. Cardiac examination: Cardiomegaly, S3, S4, cardiac murmur.
5. Neurological examination: Any neurodeficit .
Features of End Organ Damage

1.
2.
3.
4.
5.
6.
CNS: Encephalopathy, seizures, facial palsy, hemiplegia.

Visual: Blurred vision, diplopia and findings of retinopathy.
CVS: LVH, CHF, chest pain.
Renal: Polyuria or polydipsia, acute renal failure.
Gastrointestinal: Abdominal pain, GI bleeding.
Hematological: Microangiopathic hemolytic anemia.
Basic Investigations
1.
2.
3.
4.
5.
6.
7.
Complete blood count.

Urea, creatinine, electrolytes, calcium.
Lipid profile.
Urine analysis and culture.
Renal ultrasonography.
ECG.
DMSA before and after ACE inhibitors.
Advanced Investigations
Done in selected patients only.
1. Plasma renin and aldosterone.
2. Urine catecholamines.
3. Thyroid function test, FSH (To rule out polycystic ovary).
4. Renovascular imaging studies: Ultrasonography with Doppler, contrast
tomography angiography CTA, magnetic resonance angiography MRA,
arterial angiography.
217
Management
1. Hypertensive emergencies should be treated by an intravenous antihypertensive that can produce a controlled reduction in BP, aiming to
decrease the pressure by 25 percent or less over the first 8 hours after
presentation and then gradually normalizing the BP over 24 to 48
hours.
2. Hypertensive urgencies can be treated by either intravenous or oral
antihypertensives, depending on the childs symptomatology.
3. Consider intra-arterial continuous blood pressure monitoring. Continuous parental therapy for BP control should not be administered
without continuous monitoring.
4. Provide adequate control of pain and anxiety.
5. When BP is under control with parenteral medications, gradually switch
to oral antihypertensives.
The drugs to treat severe hypertension are shown in Table 8.2.3.
The stepwise management protocol of hypertension in children is shown
in Flow chart 8.2.1. Management of hypertensive emergency and urgency
are depicted in Flow charts 8.2.1 and 8.2.2 respectively.
TABLE 8.2.3: Drugs to treat severe hypertension
Drug
Class
Dose
Route
Comments
Esmolol
blocker
100-500 g/kg/min
IV infusion
Hydralazine
Vasodilator
0.2-0.6 g/kg/min
IV/IM
Labetalol
and blocker Bolus: 0.2-1.0

mg/kg/dose
up to 40 mg/dose
infusion: 0.25-3.0
mg/kg/hr
Calcium channel 1-3 mcg/kg/min
blocker
Vasodilator
0.53-10 mcg/kg/min
Very short acting.

Constant infusion
preferred. May cause
profound bradycardia
Should be given every
4 hours when given IV
bolus.
Recommended dose is
lower than FDA label.
Asthma and overt heart
failure are relative
contradiction
Nicardipine
Sodium
Nitroprusside
IV bolus or
infusion
IV infusion
IV infusion
May cause reflex

tachycardia
Monitor cyanide levels
with prolonged (>72
hr) use or in renal
failure; or coadminister
with sodium thiosulfate
218
Flow chart 8.2.1: Step-wise management of hypertension
Flow chart 8.2.2: Management of hypertensive emergency

Hypertensive emergency
1. Take a quick history and physical examination.

2. Admit to ICU.
3. Monitor BP (Preferably arterial line).
4. Place the patient on cardiac monitor.
5. Draw blood for CBC, electrolytes, RFT.
6. Chest X-ray and ECG.
7. Start IV medication.
1. The goal for BP reduction is to achieve controlled reduction in BP to minimize the

risk of hypoperfusion in cerebral, coronary, and renovascular beds.
2. Controlled reduction = Rate of reduction
1/3 of total amount to be reduced over 6 hrs,
Further 1/3 over 24 -36 hrs,
Final 1/3 over 48-72 hrs.
There are no absolute recommendations regarding which agent to use.

1. Use the one you are familiar with and most comfortable using.
2. Use agent with short half-life.
3. Treatment with constant infusion gives steadier, more controlled, and dependable
response.
Following drugs may be used:
1. Labetolol
(i) Onset of action: 2-5 min.
(ii) Duration: 2-4 hrs.
(iii) Starting dose: 0.41 mg/kg/hr, followed by continuous infusion0.253.0 mg/kg/
hr.
(iv) Contraindicated in asthma, uncompensated cardiac failure.
(v) Recommended for hypertension with high ICP.
2. Sodium nitroprusside
(i) Onset of action: Seconds to 2 min.
(ii) Duration: 1-10 min.
(iii) Starting dose: 0.3 0.5 g/kg/min (Titrate dose to get the desired effect).
(iv) Usual maintenance dose: 3 4 g/kg/min.
(v) Maximum dose: 10 g/kg/min.
(vi) Contraindicated in coarctation of aorta, AV shunt.
(vii) Monitor cyanide level in patient with hepatic dysfunction.
3. Hydralazine
(i) Onset of action in IV use: 5-20 min.
(ii) Duration of action of IV medication: 2-6 hrs.
(iii) Bolus doses only.
(iv) Starting dose: 0.1-0.2 mg/kg/dose IV (Maximum 20 mg/dose) every 4-6 hrs.
(v) Faster reduction rate (within minutes) would be recommended in cases of pulmonary edema and dissecting aorta.
219
Flow chart 8.2.3: Management of hypertensive urgency

Hypertensive urgency
1. Admit to the general ward.

2. Take history and physical examination.
3. IV access is not needed.
4. Blood for CBC, electrolytes, renal function test.
5. Chest X-ray.
6. ECG.
7. Start oral medication with one of the following:
1. Captopril:
(i) Initial dose: 0.3-0.5 mg/kg/dose every 6-12 hours.
(ii) Maximum: 6 mg/kg/day. If a maximum dose reached and the blood pressure still
high add a calcium channel blocker.
2. Amlodipine:
(i) Starting dose 0.1 mg/kg/dose every 6-12 hourly.
(ii) May increase to maximum 0.6 mg/kg/day up to 20 mg/day.
3. Hydralazine:
(i) Starting dose 0.75-1 mg/kg/day every 6-12 hourly.
(ii) Increase over 3-4 weeks to a maximum dose 7.5mg/kg/day.
Other oral antihypertensive drugs:
Propranolol:
1-2 mg/kg/day every 6-12 hourly, maximum 8 mg/kg/day. It is the best for pheochromocytoma.
Nifedipine:
It can be used if amlodepine not available.
Initial dose is 0.25-0.5 mg/kg/day orally every 6-12 hourly.
Maximum dose 3 mg/kg/day up to 180 mg/day.
Sublingual route is not recommended.
The goal is to reduce BP over longer perioddays not hours.
Bibliography
1.
2.
3.
4.
Advances in the Pathogenesis and Management of Hypertensive Crisis. Current Opinion in Pediatr 2005;17:210-4.
Constantine E, Linakis J. The assessment and management of hypertensive
emergencies and urgencies in children. Paediatr Em Care 2005;21:391-6.
Fourth Report on the diagnosis, evaluation and treatment of high blood pressure in children and adolescent. NIH Publication September1996. Revised May
2006.
Hypertensive crises: Diagnosis and management in the emergency room. Eur
Rev Med Pharmacol Sci 2004;8:143-52.
8.3
Hematuria
Macroscopic hematuria is visible to the naked eye but microsopic hematuria is defined as more than 5 RBC/hpf. For obvious reason patients with
symptomatic and macroscopic hematuria turn up in the emergency department. Microscopic and asymptomatic hematuria hence is beyond the
scope of this discussion.
Indications for Prompt Evaluation

Evaluation is directed towards potentially life-threatening causes of hematuria who has any of the following in addition to hematuria:
1. Hypertension.
2. Edema.
3. Oliguria.
4. Significant proteinuria (More than 500 mg/24h).
These children should be referred to pediatric nephrologist after initial
evaluation and stabilization.
The common diseases presenting with hematuria include the following:
1. Postinfectious glomerulonephritis.
2. Henoch-Schnlein purpura.
3. Hemolytic uremic syndrome.
4. Membranoproliferative glomerulonephritis.
5. IgA nephropathy.
6. Focal segmental glomerulonephritis.
History
1. Trauma: Recent bladder catheterization or blunt abdominal trauma.
2. Recent sore throat, skin infection (pyoderma, impetigo): Acute post Streptococcal glomerulonephritis.
3. Viral illness: Adenovirus induced UTI, preceeding IgA nephropathy.
4. Dysuria, frequency, urgency, enuresis: UTI or nephrolitiasis.
5. Urine color: Stream discolored at initiation, throughout or at termination.
Chapter 8.3: Hematuria
221
6. Abdominal pain, costovertebral angle pain, suprapubic pain IgA nephropathy.

7. Medication: Cyclophosphamide, coumadin, aspirin.
8. Passage of calculus.
9. Joint or muscle pain: SLE, HSP.
Family History
1.
2.
3.
4.
5.
6.
7.
Hematuria.
Deafness: Alport syndrome .
Hypertension.
Coagulopathy: von Willebrands disease.
Hemoglobinopathy: Sickle cell anemia.
Calculi.
Renal failure, dialysis, transplant.
1.
2.
3.
4.
5.
Fever: UTI, HUS, secondary infection.

Arthritis, rash: SLE, HSP.
Blood pressure.
Edema: Nephrotic syndrome.
Nephromegaly, costovertebral angle tenderness: Tumor, hydronephrosis,
polycystic kidney.
Basic Investigations
1. Complete blood count: Hemolytic uremic syndrome, thrombocytopenia.
2. Throat swab culture, ASO, Anti strepto DNAse activity, serum C3
Acute post streptococcal glomerulonephritis (APSGN).
3. Serum potassium and urea, creatinine: To detect any renal insufficiency.
4. Renal ultrasound: Tumor, structural and congenital anomalies, polycystic kidney, renal vein thrombosis.
Special Tests
24 hours urine for protein, creatinine and calcium.
The Algorithm for approach to macroscopic hematuria is shown in
Flow chart 8.3.1.
Practice Points
1. Painful gross hematuria is caused by infection, calculi and urological
conditions.
2. Most common causes of painless hematuria in children are APSGN
and IgA nephropathy.
3. Schistosoma hematobium is often diagnosed by finding an ova in the
urine of an unexplained macroscopic hematuria.
222
Flow chart 8.3.1: Algorithm for approach to macroscopic hematuria
Bibliography
1.
2.
Meyers Kevin EC. Evaluation of hematuria in children. Pediatr Clin North Am

2004;31:559-73.
Nammalwar BR, Vijayakumar M, Editors. Principles and Practice of Pediatric
Nephrology, 1st edition, New Delhi: Jaypee Brothers 2004:225-32.
NEUROLOGICAL
EMERGENCIES
9.1
Headache
A child presenting with headache in the emergency calls for a thorough

evaluation before starting any treatment. It is unjust to label any headache
as psychogenic without excluding other more common causes of headache
in children. A very important consideration in children is whether headache is associated with fever or not.
Headache with Fever

1. Systemic febrile illnesses: Several systemic viral infections are commonly
associated with headache.
2. Intracranial infections: Meningitis presents with fever, headache and
signs of meningeal irritation. Meningism may be a false localizing sign
in pneumonia, pharyngitis and pyelonephritis.
3. Extracranial infections: Sinusitis, otitis media and dental infection may
be associated with headache.
Headache without Fever

1.
2.
3.
4.
5.
6.
7.
8.
Migraine.
Pseudotumor cerebri.
Raised intracranial pressure.
Hydrocephalus with shunt.
Arteriovenous malformation and subarachnoid hemorrhage.
Hypertension.
Trauma.
Tension headache.
Migraine
It is a well-recognized cause of headache in children. Family history of
migraine is often present. Physical examination shows no focal neurological deficit.
226
The diagnostic criteria (International Headache Society, 1988) are the

following:
Migraine without Aura (Common Migraine)

Five attacks with an untreated duration of 4 to 72 hours.
Characteristics (2 out of the following 4):
1. Unilateral.
2. Pulsating.
3. Moderate or severe.
4. Aggravated by physical activity.
Concomitant features:
1. Nausea and/or vomiting,
2. Photophobia and phonophobia may be associated.
Migraine with Aura

Two attacks are the feature.
Characteristics (3 out of following 4)
1. Aura indicating focal cerebral or brainstem dysfunction.
2. Aura developing gradually over 4 minutes or several in succession.
3. Aura lasting<60 minutes.
4. Headache developing before, with or within 60 minutes of the aura.
Classification of Migraine with Aura

1. Classic: Visual aura like scotoma, blurring, flashing lights, hemianopsia.
2. Complicated: Neurological symptoms that precede, accompany or follow
migraine, and requires thorough neurodiagnostic studies. These are
hemiplegic (Hemiparesis or hemisensory loss followed by contralateral
headache), ophthalmoplegic (Diplopia, ptosis or mydriasis associated
with III cranial nerve palsy during or after headache), basilar artery
migraine (Bilateral visual problems and dimming of vision, vertigo,
ataxia, dysarthria, drop attacks, loss of consciousness, quadriparesis,
paresthesia) acute confusional state (Restlessness, hyperactive,
combative), Alice in wonderland syndrome (Macropsia, micropsia,
auditory/gustatory/olfactory hallucination).
Management
1. Analgesics:
i. Acetaminophen10 to 15 mg/kg/dose oral every 4 hourly.
ii. Ibuprofen5 to 10 mg/kg/dose oral every 6 hourly.
2. Codeine: 0.5 to 1 mg/kg/dose oral every 4 to 6 hourly.
3. Antiemetics:
i. Metoclopramide0.5 to 2 mg/kg/dose oral or IV every 4 to 6
hourly
Chapter 9.1: Headache
227
ii. Promethazine0.25 to 1 mg/kg/dose oral, IM or IV every 4 to 6

hourly.
4. Specific therapy:
i. Dihydroergotamine0.5 to 1 mg/dose IM or IV, may be repeated
after 1 hour.
ii. Sumatriptan6 mg SC or 100 mg oral in children above 12 years.
Pseudotumor Cerebri
Also known as idiopathic intracranial hypertension, it should be diagnosed
only by exclusion. The distinguishing features are the following:
1. Headache of variable severity and duration typically worse in the morning.
2. Nausea, vomiting and visual abnormalities.
3. Papilledema is seen virtually in all cases.
4. Cranial nerve palsies particularly VI nerve may be present.
Neuroimaging like CT scan or MRI should be done to exclude intracranial tumors. LP may be done if no mass lesion is present. The CSF opening
pressure is high but cell count, protein and sugar are normal.
Management
1. Removal of CSF.
2. Acetazolamide 60 mg/kg/day in 4 divided doses.
Raised Intracranial Pressure

Raised intracranial pressure is a possibility in a child presenting with unexplained headache, vomiting and irritability.
Examination of the head may be described as 8S:
1. Size
2. Sutures
3. Skin
4. Sound
5. Shunt
6. Sunset sign
7. Squint
8. Spine.
Size: Macrocephaly is diagnosed when head circumference is above two
standard deviations of the expected mean for age, sex, height and weight.
Sutures: In infants sutures may be separated in raised intracranial pressure.
Two fontanels are commonly palpated, anterior and posterior fontanel.
Normal feel of fontanel is slightly depressed and pulsatile.
Skin: In hydrocephalus, skin is shiny and tense. The superficial veins may
be visible.
Sound: The soft skull bones can be indented, known as craniotabes. A Percussion over the skull with one finger produces cracked pot sign.
Shunt: The location of shunt and the shunt tubing should be traced and
followed up to the drainage site in chest (VA shunt) or abdomen (VP shunt).
Sunset sign: It is due to paralysis of upward gaze center in tectum of midbrain due to pressure effect.
Squint: Usually 3rd and 6th cranial nerve palsy.
Spine: Neural tube defect including postoperative scar.
228
In any critically ill child, it is the prime aim of the physician to maintain
a normal cerebral perfusion pressure (CPP), which is an indirect indicator
of cerebral blood flow (CBF). CPP is determined by subtracting intracranial
pressure (ICP) from mean arterial pressure. CPP = MAP ICP.
It is obvious that raised ICP will lower CPP. MAP cannot be increased
excessively in order to raise CPP. The critical determining factor in
maintenance of CPP is control of ICP to an acceptable level. Three
compartments contribute to ICP: brain, intracranial blood volume and CSF.
According to Monro-Kellie doctrine, a small change in the volume of any
compartment must be accompanied by an equal and opposite change in
another compartment or ICP must rise because cranium is a closed box.
Brain is the least compressible. ICP is regulated by controlling the cerebral
blood flow and CSF.
Investigation
Plain CT scan of head.
Management
Head elevation: Head should be in neutral position (midline). The elevation
of 30 to 45o of head above horizontal plain decreases intracranial pressure
by improving jugular venous drainage. Systemic blood pressure is not affected, so the overall result is increased cerebral perfusion.
1. Normothermia should be maintained (35.537oC).
2. Sedation with or without muscle paralysis.
3. Blood pressure and blood volume should be normal.
4. Blood sugar should be in the normal range, hyperglycemia should
be avoided.
5. Serum electrolytes should be normal, hyponatremia should be
avoided.
6. Prevention of seizure.
7. Mild hyperventilation (PCO2 3035 mm Hg) to decrease cerebral
blood flow.
8. Measures to decrease brain volume:
i. Osmotic diuretics: Mannitol 0.25 to 1 gm/kg/dose.
ii. Loop diuretics: Frusemide 1 to 2 mg/kg.
iii. Corticosteroids is useful only in vasogenic edema around a mass
lesion: Dexamethasone 0.1 to 0.2 mg/kg every 6 hourly.
9. Measures to decrease CSF volume: CSF withdrawal via external ventricular drain.
Hydrocephalus with Shunt

Patient with shunt malfunction commonly present with manifestations of
raised ICP. Other than signs of raised ICP, a swelling from CSF tracking
along the shunt tract is indicative of obstruction.
Chapter 9.1: Headache
229
Investigations
Radiographic shunt series and plain CT scan of head.
Management
Depends on the patients status and the site of shunt obstruction. If the
distal end of the shunt is blocked, the ICP, can be lowered by removing
CSF through a shunt tap.
Arteriovenous Malformation and Subarachnoid Hemorrhage

It should be suspected when headache is of abrupt onset and often bilateral. It may be accompanied by seizure and loss of consciousness. Meningeal
signs are usually positive. A CT scan of brain is confirmatory.
Hypertension
Though this is not a common cause in children but definitely a very important cause. Blood pressure should always be measured in a child presenting
with headache.
Trauma
Headache may be due to underlying skull fracture or acute extradural or
subdural hematoma.
Tension Headache
A careful history may reveal stress in the school or in the family. Tension
headache typically starts at the end of the day and are dull aching type.
Indications for a CT Scan in a Child with Headache

1. Abnormal neurological signs (unexplained reduction in visual acuity,
enlarged head circumference; 95 percent risk of tumor).
2. Headache awakens child during sleep, early morning headache, with
increased frequency and severity.
3. Migraine and seizure phenomena occurring in same episode and vascular symptoms preceding the seizure (2050% risk of tumor and
AVM). Repeat in 4 to 6 months if first study is negative.
4. Cluster headache in child, any child <5 yrs whose principal complaint is headache.
5. Focal neurological signs or symptoms develop during a headache
(Complicated migraine).
6. Focal neurological signs or symptoms develop during aura with fixed
laterality. Also focal signs of aura persisting or recurring in the headache phase.
7. Periodic headaches and seizures coincide, especially if seizure has a
focal onset.
230
8. Visual greying out occurring at the peak of a headache instead of the

aura.
9. Symptoms such as recent school failure, behavioral change (Anorexia,
apathy) and fall off in linear growth rate.
10. Brief cough headache in a child or adolescent (raised intracranial
tension).
Bibliography
1.
Cameron P Jelink G, Everitt I, Browne G, Raftos J Editors. Textbook of Paediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill
Livingstone.
9.2
Status Epilepticus
An episode of continuous seizure or intermittent seizures without recovery

of consciousness lasting for more than 30 minutes is status epilepticus. The
most common cause of status epilepticus is febrile seizure lasting for more
than 30 min in a child less than 3 years age.
Etiology
Majority of patients with status epilepticus are not known to be epileptics.
30 to 50 percent are complications of an acute CNS insult like CNS infection, glucose or electrolytes disturbance especially in young children.
Management
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
A, B, C Airway, breathing and circulation should be taken care of

with continuous monitoring.
Clear airway and suction, insert an airway.
The child should be kept in lateral prone position to prevent aspiration.
NG tube insertion to decompress and empty stomach.
100 percent O2 by face mask.
In case of difficult vascular access an intraosseous route is acceptable. Once a vascular access is established, blood should be collected
for sugar, electrolytes, calcium, magnesium, ammonia, sepsis workup
and ABG. Blood anticonvulsant levels and toxicology screen may be
done in appropriate cases.
In neonates and infants convulsion due to hypoglycemia or
hypocalcemia is common. These should be detected and treated
accordingly. Thereby it reduces the chance of administration of
several anticonvulsants.
Bedside capillary blood glucose should be checked early. If blood glucose is less than 40 mg/dL then 10 percent dextrose 2 to 4 ml/kg IV.
If hypotensive with poor peripheral perfusion treat as in shock.
Pulse oximetry and blood pressure monitoring should be started
early.
232
Initial Control of Seizure

Short acting benzodiazepines are the preferred first line drugs. Initially
before any vascular access is established, diazepam or lorazepam may be
given per rectal. The drugs may be given via 6 or 8 Fr feeding tube, 6 cm
into the rectum, a 2 ml syringe fitted to the other end of the tube. This may
be tried even before the child is transferred to the hospital.
1. Diazepam 0.3 mg/kg/dose mixed in 3 ml 0.9 percent NaCl every 10
min, 3 doses may be given.
2. Lorazepam 0.05-0.1 mg/kg/dose mixed in 3 ml 0.9 percent NaCl every
10 min, 3 doses may be given.
3. Instead of the above two, midazolam may be given 0.2 mg/kg intramuscular,
intravenous or intraosseous every 10 min, 3 doses may be given.
Stage I
Lorazepam0.05 to 0.1 mg/kg IV (maximum 4 mg) or
Diazepam0.3 mg/kg IV (maximum 10 mg) undiluted over 2 minutes.
If IV access could not be established
Diazepam rectal 0.5 mg/kg or
MidazolamIM 0.2 mg/kg.
If seizure does not stop within 5 to 10 minutes

Go to stage II
If seizure stops:
Adjust previous antiepileptic medications or start oral anticonvulsants if
required. (The decision depends on the likelihood for seizure recurrence).
If patient is shocked or cyanosed with dilated pupils at any stage of management or has been convulsing an hour or more, go straight to stage IV.
Stage II
Repeat lorazepam0.05 to 0.1 mg/kg IV (maximum 4 mg) or
Diazepam0.3 mg/kg IV (maximum 10 mg) undiluted over 2 minutes.
Then start
Phenytoin15-20 mg/kg (maximum dose 1000 mg) IV infusion at the rate
1 mg/kg/min under ECG monitor. Prepare infusion as 10 mg phenyton/ml
NS or
Fosphenytoin30 mg/kg IV infusion at the rate 3 mg/kg/min.
Consider pyridoxine100 mg IV for children <2 years of age.
Start 20 percent mannitol5 ml/kg over 20 minutes.
If still convulsing 10 minutes after starting phenyton a 3rd dose of diazepam may be given.
If there is response; continue phenytoin 5 mg/kg/day qevery12 hours

Follow blood level
If no response 5 minutes after the end of phenytoin infusion.
Chapter 9.2: Status Epilepticus
233
Stage III
PhenobarbitoneLoading dose 15 to 20 mg/kg IV, slowly over 10 minutes.
Be prepared for ventilation and if there is response continue maintenance
Phenobarbitone5 mg/kg/day every 12 hours.
If no response in 5 to 10 minutes after end of infusion or seizure already
more than 60 minutes or unstable vital signs.
Stage IV (ICU)
Intubation and ventilation muscle relaxant (use short acting muscle relaxant in repeated doses to monitor seizure when EEG monitoring is not
available).
Midazolam0.2 mg/kg IV bolus.
Then infusion 1 to 2 mcg/kg/minute titrated up to10 mcg/kg/min
(During infusion maintain phenytoin and phenobarbitone at high therapeutic level) or propofol 1 to 2 mg/kg followed by 2-10 mg/kg/hour. If
seizure is not controlled in 1 to 2 hours induce barbiturate coma.
Thiopentone2 to 8 mg/kg loading then reduce infusion to 1 to 10 mg/kg/
hour when needed, titrating for best control.
Monitor for BP, hypoglycemia, electrolytes imbalance, hypocalcemia, acidosis consumptive coagulopathy (PT, APTT) and hyperpyrexia.
Restrict fluid to 60 percent maintenance (Unless low BP) and continue
treatment for brain edema with mannitol every 6 hours dexamethasone
(With IV ranitidine).
After stabilization consider CT scan brain and work-up for possible causes.
Treat for CNS infection if indicated (LP after brain CT scan).
Practice Points
1. Intravenous valproaic acid is also used in status epilepticus at 10 to 15
mg/kg IV at stage 3 along with or instead of phenobarbitone.
2. Each vial of thiopentone contains 500 mg, dilute with 25 ml of distilled water to make 1 ml = 20 mg.
3. 1.5 mg phosphenytoin =1 mg phenytoin equivalent.
Bibliography
1. Appleton R, Sweeney A, Robson J, Molyneux E. Lorazepam versus diazepam
in the treatment of epileptic seizures and status epilepticus. Developmen Med
Child Neurol 1995;37:682-8.
2. Brown JK, Hussain IH. Status epilepticus: Treatment. Developmental Med
Child Neurol 1991;33:97-109.
3. Browne TR. The Pharmacokinetic of agents used to treat status epilepticus.
Neurol 1990;40:S28-S32.
4. Gross-Tsur V, Shinner S. Convulsive status epilepticus in children. Epilepsia
1993;34:S12-S20.
5. Hanhan U, Orloski J. Status epilepticus. Pediatr Clin North Am 2001;48:683-94.
234
6. Knapp LE, Kugler AR. Clinical experience with fosphenyton in adults:

Pharmacokinetice safety and efficacy. J Child Neurol 1998;13:S15-S18.
7. Morton LD . Clinical experience with fosphenyton in children. J Child Neurol
1998;13:S19-S22.
8. Pellock JM. Use off midazolam for refractory status epilepticus. J Child Neurol
1998;13:581-7.
9. Ramsay ER. Treatment of status epilepticus. Epilepsia 1993;34:S71-S81.
10. Shorvon S. Tonic clonic status epilepticus. J Neurol Neurosurg Psychiatr
1993;56:125-34.
11. Treiman DM. The role of benzodiazepines in the management of status
epilepticus. Neurol 1990;40:S32-S42.
9.3
Rapid Onset Limb Weakness
Jaydeep Choudhury
Acute onset limb weakness represents a vast area that requires accurate
assessment. Trauma as the cause should be ruled out early. In infant and
young child non-accidental injury can present as acute weakness also.
Limb weakness due to flaccid paralysis evolving over a few hours or
days suggests lower motor neuron complex involvement. The following
are the important causes as per the anatomical distinction of lower motor
neuron:
1. Anterior horn cells of spinal cord Poliomyelitis and transverse myelitis.
2. Nerve trunks (polyneuritis) Guillain-Barr syndrome, toxins like diphtheria and porphyria.
3. Neuromuscular junction Tick or botulinum toxin.
4. Metabolic Periodic paralysis.
5. Inflammatory muscle disease Myositis.
Compressive lesion of the spinal cord usually does not present as acute
flaccid paralysis but is should also be ruled out.
The child should be assessed and airway, breathing, circulation should
be established first. Optimum posture should be maintained for pain relief, if any. Blood pressure should be checked. If there is any obvious trauma,
it should be taken care of.
After stabilization, the detailed course of illness should be obtained
along with the pattern and evolution of weakness. The important points in
history are the following:
i. Onset of symptoms.
ii. Recent trauma.
iii. Presence of fever, headache, nausea or vomiting.
iv. Ascending paralysis: Whether the weakness initially started distally
and progressing proximally.
v. History suggesting respiratory muscle involvement: Difficulty in
breathing, decreased chest movements, cyanosis, whether the child
was put on ventilator.
vi. Bulbar palsy: Drooling of saliva, pooling of secretions, nasal regurgitation, dysphagia.
236
vii.
viii.
ix.
x.
Bladder dysfunction.
Infection or immunization.
Past history of epilepsy, congenital heart disease, bleeding disorder.
Family history of similar disorders.
Examination should be performed to establish the level and nature of
lesion. The typical features of different levels of weakness are as follows:
Muscular
i.
ii.
iii.
iv.
Usually more proximal than distal weakness.

Reflexes preserved until late.
Muscular tenderness may be present.
Gowers sign may be positive.
Neuromuscular Junction
i. Easy fatigability.
ii. Reflexes preserved.
Lower Motor Neuron

i. More distal than proximal.
ii. Reflexes absent.
Upper Motor Neuron

i. Tone and reflexes increased following initial acute flaccid phase.
ii. Sensory levels in spinal cord lesion.
iii. Sensorium, speech may be affected.
Cardiac abnormalities, hematologic disorders and intracranial infections should be ruled out in all children presenting with acute limb weakness.
Transient hemiparesis may be due to seizure, hemiplegic migraine and
diabetes mellitus.
A brief outline of the approach is given in Table 9.3.1. The four common
causes of acute onset weakness of lower limbs are poliomyelitis, GuillainBarr syndrome (GBS), transverse myelitis and traumatic neuritis.
Indications for Hospitalization

1.
2.
3.
4.
5.
6.
Progression of paralysis.
Respiratory distress.
Bulbar involvement.
Paralysis of upper limbs of less than 3 days.
Marked drowsiness.
Other complications.
Investigations
It is mandatory to examine each case of AFP within 48 hours or as soon as
it is reported.
Poliomyelitis
Less than 4 days, max. 7 days
Present
Proximal, asymmetrical
Diminished
Decreased or absent
Myalgia, back ache
Only when bulbar or bulbospinal
Only when bulbar or bulbospinal
Transient retention
Severe asymmetric atrophy
High
Normal or slight increase
Normal then slight decrease
Abnormal
Signs and symptoms
Progression of paralysis
Fever at onset
Flaccidity
Muscle tone
DTRs
Sensation
Cranial nerve
Decreased respiration
Bladder dysfunction
Sequele
CSF: WBC
CSF: Protein
NCV (3 wks)
EMG (3 wks)
TABLE 9.3.1: Approach to rapid onset weakness of lower limbs

GBS
From hours to 20 days
Absent
Distal, symmetrical
Diminished
Absent
Cramps, tingling, hyposthesia
Often present
In ascending paralysis
Sometimes
Absent or minimal
Less than 10
High
Abnormal demyelination
Normal

Absent
Lower limbs, symmetrical
Diminished in lower limbs
Absent in lower limbs
Anesthesia of lower limbs, root pain
Absent
Absent
Present
Moderate atrophy
Normal
Normal or slight increase
Normal
Normal
Transverse myelitis
Traumatic neuritis
Variable
Asymmetric limb
Diminished in limb
Decreased or absent
Pain in gluteal region
Absent
Absent
Absent
Peroneal atrophy
Normal
Normal
Abnormal in sciatic nerve
Normal
Chapter 9.3: Rapid Onset Limb Weakness
237
238
1. Stool: Collect two stool samples 8 gram each (approx. one thumb size)
24 to 48 hrs apart and send it maintaining reverse cold chain at below
8oC for culture of poliovirus as positive result is most probable within 2
weeks of onset of AFP.
2. Complete blood count, platelet count, prothrombin time and partial
thromboplastin time, serum glucose, electrolytes.
3. Nerve conduction velocity (NCV): Abnormal in GBS.
4. Electromyography (EMG) Abnormal in poliomyelitis (better result
after 3 weeks).
5. CSF: Albumino-cytological dissociation in GBS.
6. X-ray spine: Trauma.
7. Serum potassium: Hypokalemia.
8. MRI of spine with contrast: Transverse myelitis.
Management
Immediate Management
1. Complete bed rest: Change of posture in bed every 2 to 3 hours. The
child should be placed on stomach for short period every day to avoid
the risk of pneumonia.
2. Correct positioning of affected limbs: The limbs should be kept in optimum position with pillows and rolled towels. The optimum positions
arehip slight flexion, knee 5o flexion, ankle 90o (support against the
sole), both legs supported from the lateral side to prevent external
rotation.
3. Passive movement of the joints: 10 minutes 2 to 3 times a day.
4. Warm water fomentation: 10 minutes 2 to 3 times a day.
5. Symptomatic treatment for fever and pain.
6. No restriction for diet if the patient can take.
7. No massage or intramuscular injection.
8. If the paralysis progresses, immediate action to be taken.
9. Mechanical ventilation may be required in some children with progressive paralysis.
Specific Management
1. GBS: Intravenous immunoglobulin 400 mg/kg daily for 5 days or 1 gm/
kg for 2 days. Plasmapheresis is the most effective therapy.
2. Transverse myelitis: Complete immobilization, care of the bladder.
Recovery is usually complete within weeks to months.
Long-term Management
1. Physical rehabilitation: In poliomyelitis usually there is wasting, weakness of the limbs; proper physiotherapy with exercise like swimming is
encouraged. Callipers and braces are used and occasionally wheelchair
is required.
Chapter 9.3: Rapid Onset Limb Weakness
239
Flow chart 9.3.1: Management of acute onset limb weakness
2. Social rehabilitation.
3. Economic rehabilitation.
An approach to the management of acute onset limb weakness is shown
in Flow chart 9.3.1.
Bibliography
1.
2.
Lieh-Lal MW, Ling-McGeorge KA, Asi-Bautusta MC, Editors. Pediatric Acute

Care, 2nd edition, 2003. Philadelphia: Lippincott Williams and Wilkins.
Moe PG, Benke TA. Neurologic and muscular disorders. In: Hay WW, Levin
MJ, Sondheimer JM, Deterding RR, Editors. Currant Pediatric Diagnosis and
Treatment, 7th edition. New York: Lange Medical Books 2005;732-809.
10
HEMATOLOGICAL
EMERGENCIES
10.1
Sickle Cell Disease and Crisis
Sickle cell crises are any new syndrome that develops rapidly in patients
with sickle cell disease due to its inherited abnormality. The following are
various types of sickle cell crises:
1. Vasoocclusive.
2. Sequestration.
3. Aplastic.
Vasoocclusive Crises
Vasoocclusive crises are acute painful episodes results from intravascular
sickling and tissue infarction. These are most common complications and
are seen in bone, lungs, liver, spleen, brain and penis.
Painful Crisis
It is typically seen with deep throbbing pain and local tenderness, swelling,
erythema and warmth. Bone marrow ischemia leading to infarction has
been identified as the cause. Knee, shoulder, elbow, femur, lumbosacral
spine and less commonly sternum, ribs, iliac crest are seen to be involved.
Management is symptomatic, mainly hydration and intravenous analgesia.
Hand-Foot Syndrome
Mainly affects children below 5 years and in small bones of hand and feet.
White blood cell count goes up to 20,000 to 60,000/cumm and child refuses
to bear weight, cries with pain. Bone changes specially destruction are seen
after 2 weeks. Early symptoms of hand-foot syndrome below 1 year, high
blood count and low Hb below 7 are predictors of bad prognosis.
Management is symptomatic, mainly hydration and intravenous analgesia.
Acute Chest Syndrome

Episodes of acute pain chest, fever, cough, tachypnea, and hypoxia along
with lung infiltrates are known as acute chest syndrome and leading cause
244
of mortality in sickle cell disease. The common etiologies of acute chest

syndrome are fat embolus and infection with chlamydia, mycoplasma or
virus.
Though most patients recover only with supportive treatment, these
patients should be managed in hospital settings. Oxygen, analgesia and
mechanical ventilation may be required along with antibiotics,
bronchodilators and blood transfusion.
Acute Abdominal Pain

Often presents with fever, guarding, rebound tenderness, leukocytosis indistinguishable from surgical abdomen. Mesenteric or intrahepatic sickling
and vertebral nerve root compression have been forwarded as the cause.
Intrahepatic cause present often with jaundice, hepatomegaly and abnormal liver enzymes. A simple exchange tranfusion may help to improve the
situation.
Acute CNS Event

Infarction in internal carotid artery or often in middle cerebral artery or
anterior cerebral artery may cause devastating stroke. Old intimal damage
leading to hemorrhage may result in subarachnoid bleed. They present
with headache, syncope, vertigo, ptosis, nystagmus, neck pain. Carotid
angiography should be done earlier if any prior symptoms are present.
Priapism
It can occur in male in all age groups. Clinical variants may be acute prolonged (more than 24 hours), chronic, stuttering (short 2-3 hours) or
multiple episodes. Patient should be instructed to urinate frequently, increase fluid intake, soak in warm tub, give analgesia and prepare for
transfusion.
Acute Splenic Sequestration Crisis

Typical presentation is sudden, rapid, massive enlargement of spleen with
trapping of considerable portion of red cell mass. The rapidity may be so
severe that often patient may die even before presentation to emergency
department. Clinically there is profuse hypotension and cardiac decompensation. Hematocrit is often halved, with brisk reticulocytosis, moderate
thrombocytopenia and nucleated RBC.
Treatment
1. Immediate intravascular volume restoration and packed cell transfusion.
2. Meticulous monitoring of hemodynamic state and early detection of
shock.
3. Supportive care.
Chapter 10.1: Sickle Cell Disease and Crisis
245
4. Later splenectomy may be required because of the possibility of recurrence.
Aplastic Crisis
Decreased red cell survival (15-50 days) in sickle cell anemia in normal
steady state is compensated by 6 to 8 fold increase in bone marrow output.
Intercurrent viral or bacterial illness may suppress the bone marrow activity temporarily causing hematocrit to fall 10 to 15 percent per day with no
compensatory reticulocytosis. Spontaneous recovery is usually achieved by
markedly elevated NRBC, followed 1 to 2 days by vigorous reticulocytosis.
Bibliography
1.
2.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J Editors. Textbook of Pediatric

Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill Livingstone.
Sachdev A Editor. Hemoglobinopathies, 1st edition. New Delhi: Jaypee
Brothers, 2006.
11
ENDOCRINAL
EMERGENCIES
11.1
Diabetic Ketoacidosis
Jaydeep Choudhury
Diabetic ketoacidosis (DKA) results from a state of relative or absolute insulin deficiency and is a life-threatening complication of diabetes. Many
children with type 1 insulin dependent diabetes mellitus present for the
first time with DKA. It is the commonest cause of death in adolesecents
with type 1 diabetes mellitus and should be treated seriously and promptly.
As a dictum blood sugar should be routinely checked in any children presenting with coma.
Children can die from DKA due to
1. Severe dehydration and shock.
2. Cerebral edema.
3. Hyperkalemia.
4. Sudden unexplained death.
Assessment
1.
2.
3.
4.
5.
6.
Airway
Vital signspulse, respiration, blood pressure, temperature.
Level of consciousness using Glasgow coma scale.
Weight (if comatose, estimate from age and old records).
Bedside glucose reading.
Degree of dehydration (as a rough guide, 5% just detectable and 10%
severe dehydration).
Intervention
Intravenous access as soon as possible, intraosseous if intravenous could
not be established due to shock.
Investigations
1. To be done urgentlyblood glucose, blood gas, serum electrolytes and
urea, creatinine.
2. Urine analysis.
250
3. Other tests and investigations may be necessary depending on the precipitating cause. Blood count and culture, chest X-ray, urine culture
for suspected sepsis, respiratory tract or urinary infection.
4. A new patient with type 1 diabetes presenting for the first time with
DKAcholesterol, triglycerides, LDL, HDL, thyroid function tests, liver
function tests, calcium, phosphate and HbA1c.
5. Following tests may be done if facilities permitautoantibodies (Islet
cell, insulin, GAD), celiac antibodies (Antigliadin, endomysial), C-peptide,
insulin, IGF1, IGF-BP3, immunoglobulins.
Treatment
Treatment of DKA encompasses several aspects.
Fluid
1. If severe dehydration and shock is present with tachycardia and decreased perfusion, administer 10 to 20 ml/ kg plasma expander, like 5
percent albumin or equivalent (0.9% saline) IV rapidly. The same fluid
is to be repeated if no obvious improvement is seen.
2. Aim is to replace calculated fluid deficit slowly over first 48 hrs + required daily maintenance + continuing losses keeping IV infusion rate
as even as possible.
3. Maintenance (based on weight): 100 ml/ kg for first 10 kg
50 ml/kg for next 10 kg
20 ml/kg for every kg of weight thereafter.
A 45 kg male requires 1000 + 500 + 500 = 2000 ml maintenance fluid
in 24 hrs.
4. Deficit formulae (for 45 kg male): If estimated dehydration is 5 percent then
volume to be replaced is 50 percent of weight in grams. 45 kg male with 5
percent dehydration is 4500/2 = 2250 ml, this should be replaced in 48
hrs. Therefore, in first 24 hrs body requires maintenance 2000 ml + deficit
1125 ml ( of 2250 ml)= 3125 ml, which is at the rate of 130 ml/hr.
(Note: Recalculate and deduct the fluid from 3125 ml that has been
given initially as bolus fluid resuscitation)
5. Nil by mouth until clinical improvement is observed.
Electrolytes
Potassium
1. Add 10 to 20 mEq/lt KCl with IV fluid with commencement of rehydration and before insulin has been started unless:
i. K+ above 5 mEq/L.
ii. Peaked T-wave in ECG.
iii. Previously known to have renal failure.
In dwelling catheter may be necessary to measure urine output in
shocked and comatosed patient.
Chapter 11.1: Diabetic Ketoacidosis
251
2. When blood glucose has dropped between 200 to 220 mg/dL change the
ongoing fluid to 5 percent dextrose and normal saline with added KCl
(50 ml of 50% dextrose to 450 ml of normal saline makes 5% dextrose).
Sodium
1. The measured Na+ concentration is depressed by the dilutional effect
of coexistent hyperglycemia. An approximate corrected sodium can be
calculated as:
Corrected sodium = Sodium measured + 1.6 mEq Sodium for every
100 mg glucose above 100 mg.
2. If corrected sodium still shows hypernatremia, correction of dehydration and electrolyte imbalance is advocated over 48 to 72 hr to minimize
risk of cerebral edema as an independent glucose hyperosmolar state
also exists.
Bicarbonate
1. The role of bicarbonate in correcting acidosis in DKA remains controversial. It should not be given routinely and should be considered with
severe acidosis when PH< 7.0 and bicarbonate <5 mEq/L.
Dose of bicarbonate = base deficit weight (kg) 0.3.
Initially, administer 50 percent of this dose over 1 to 2 hrs, added to IV
fluids then repeat pH and bicarbonate and reassess.
2. Cardiac monitoring should continue in these patients and the risk of
hypokalemia to be kept in mind. KCl needs to be added to the rehydrating fluid if bicarbonate is being administered. These patients should
be admitted in ICU.
Insulin
1. Only soluble (short acting) insulin should be used initially. Frequent
assessment of insulin dose is mandatory. Ensure that insulin infusion is
clearly labeled. Insulin is added to normal saline in a syringe pump so
that solution contains 1unit/1 ml normal saline (add 50 units insulin to
49.5 ml normal saline). This makes further adjustments easy as serious
errors occur when calculating dose of insulin.
2. Adjusting insulin dose Commencement dose = 0.1 unit /kg/hr (>6
yrs) and 0.05 unit/kg/hr (<6 yrs).
Reduce dose once blood glucose < 220 mg/dL (0.05 unit/kg/hr if blood
glucose 160 to 220 mg/dL.
Stop insulin when blood glucose is below 160 mg/dL.
3. Aim for fall in blood glucose 100 mg/dL/hr.
4. Occasionally when acidosis is severe or fluids are restricted, the amount
of dextrose in IV fluid is increased instead of reducing insulin.
5. Once the blood glucose has fallen, acidosis corrected and patients condition has stabilized, IV insulin infusion should be switched to
subcutaneous insulin injections.
252
Monitoring Initial Progress

1. Vital signs: For first 24 hours monitor hourly heart rate, respiratory
rate, blood pressure, level of consciousness using Glasgow Coma Scale.
Temperature 4 hourly and daily weights.
2. Blood glucose: Hourly capillary blood glucose until IV insulin stopped.
3. Electrolytes: As a minimum, at admission and again in 4 hrs but frequency depends on patients status. Severe cases, electrolytes and even
blood gas analysis may be necessary as frequently as 1 to 2 hourly. Acidosis may worsen initially alerting the underlying severity of dehydration.
If patient is still poorly perfused, fluid regimen should be revised.
4. Fluid balance: Strict and careful assessment is mandatory. It may be
necessary to catheterize the patient if drowsy, unconscious or severely ill
toddlers. Input and output must be interpreted in the context of hydration and blood electrolytes. It may be necessary to increase fluids if large
volume of dilute urine is passed and patient is still clinically dry.
5. Urine analysis: All urine should be tested for ketones. The continued
presence of heavy ketonuria suggests either inadequate insulin doses
(if blood glucose is high) or inadequate carbohydrate replacement (if
blood glucose is low).
6. Level of consciousness: All patients with DKA should be assessed neurologically using GCS hourly. If score is falling, cerebral edema should
be assumed unless another cause is obviously more likely.
Complications During Treatment

1.
2.
3.
4.
Cerebral edema.
Acute gastric dilatation.
Acute respiratory distress syndrome.
Venous thrombosis.
Cerebral Edema
It is a life-threatening and unpredictable complication, may relate to
overhydration with hypotonic fluids. Cerebral edema can occur suddenly
usually between 6 to 12 hours (range 224 hrs) after commencement of
treatment. Mortality and morbidity is high if not treated early. It is most
likely to occur at the first presentation in children under 5 yrs of age.
Warning signs: Failure of sodium level to rise as blood glucose level declines or development of hyponatremia during therapy.
Early signs: Headache, confusion, irritability, decreased consciousness.
Late signs: Bradycardia, hypertension, seizures.
Treatment must be instituted without waiting for CT scan to confirm
the diagnosis.
Treatment of Suspected Cerebral Edema

i. Raise the head end of the bed.
ii. Administer 1.25 ml/kg of IV 20 percent mannitol (equal to 0.25 gm /
kg). Repeat in 15 to 20 minutes if the patient has not improved.
Chapter 11.1: Diabetic Ketoacidosis
253
iii. Intubation and hyperventilation helps reducing raised intracranial

tension.
iv. Transfer to ICU.
v. Reduce IV fluid to maintenance rate.
vi. Opinion of Neurologist to be sought and CT scan arranged.
Further Care
Once the nausea and vomiting associated with ketosis have settled, diet
can be introduced. This also must correspond to stable metabolic status
(normal blood glucose, pH and serum bicarbonate level).
Once the oral intake has been established, change over to subcutaneous insulin is usually possible. Plasma half-life of insulin is only few minutes.
Subcutaneous insulin takes 4 to 6 hrs to be completely absorbed. It is necessary to continue the insulin infusion at least 1 hour after the first
subcutaneous insulin injection.
1. Combined subcutaneous insulin: A mixture of short acting (soluble) and
intermediate acting insulin twice daily (prebreakfast and predinner) is
the preferred method. This is because waiting for satisfactory control
using sliding scale with 6 hourly insulin before change to twice daily will
delay discharge for some days. The dose used is dependant on patients
weight and insulin requirement over previous 24 hrs (IV soluble). In
general starting total daily doses of 0.4 to 1.0 unit/kg are used.
Prescribe 2/3rd of the total daily dose for morning and 1/3rd for
the evening with 2/3rd of each dose as intermediate acting insulin and
1/3rd as short acting insulin.
2. Sliding scale subcutaneous insulin: Administer soluble (short acting)
insulin before breakfast, lunch, evening meal and dinner according to
the following scale:
Blood glucose > 350 mg/dL
0.4 unit /kg
0.3 unit/kg
0.2 unit/kg
Blood glucose <180 mg/dL
0.1 unit/kg
Monitoring of blood glucose before main meals and 0300 hrs should continue though urine monitoring for ketones and glucose should be stopped
once urine is ketone free. Ketosis causes insulin resistance for several days
even after insulin treatment has commenced in newly diagnosed type 1 diabetes mellitus. Some initial recovery of natural insulin secretion is also common
once treatment is instituted decreasing exogenous insulin requirement rapidly. Frequent hypoglycemic episodes indicate need to reduce dose of insulin.
Bibliography
1.
2.
Diabetes, Endocrine and Metabolic protocols, 2004, Queensland Diabetes Center, Australia.
Dunger B, et al. Arch Dis Child 2004;89:18-19.
11.2
Hypoglycemia in Neonates and Children
Joshi Anand Karketta, Jaydeep Choudhury,
A blood glucose concentration at/or above 40 mg/dL, preferably in the 54

to 72 mg/dL range represents a more acceptable euglycemic value. The
common causes of pediatric hypoglycemia based on age are shown in
Table 11.2.1.
Clinical Features
Neonates
There is no pathognomonic sign or symptom of hypoglycemia. The following are nonspecific features seen in the neonates with hypoglycemia.
1. Lethargy.
2. Apathy.
3. Irritability.
4. Apnea.
5. Tachypnea.
6. Bradycardia.
7. Cyanosis.
8. Jitteriness.
9. Seizures.
10. Coma.
11. Asymptomatic high-risk infant.
Children
Hypoglycemia in older children may present with the following features:
1. Decreased cognitive ability.
2. Agitation and emotional lability.
3. Sensation of warmth (despite cool clammy skin).
4. Blurred vision.
5. Slurred speech.
6. Lethargy.
7. Confusion.
8. Unresponsiveness.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Small for gestational age

Premature infant
Neonatal asphyxia or fetal distress
Hypothermia
Fetal-alcohol syndrome
Mother taking hypoglycemia-inducing drugs
Diabetic or pre-eclamptic mother
Congenital heart disease
Beckwith-Wiedemann syndrome
Erythroblastosis fetalis
Infection
Adrenal hemorrhage and adrenal insufficiency
Perinatal
TABLE 11.2.1: Causes of pediatric hypoglycemia based on age
13.
14.
15.
16.
Idiopathic ketotic hypoglycemia

Drug-induced (salicylate, alcohol)
Islet cell adenoma
Islet cell hyperplasia
Factitious insulin or sulfonylurea use
Infection
Hypothermia
Large non-beta cell tumors
Fulminant hepatic disease
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Starvation
Idiopathic ketotic hypoglycemia
Hypopituatrism
Hypoadrenalism
Hypothyroidism
Growth hormone deficiency
Inborn error of metabolism
Amino acid metabolic abnormality
Islet cell adenoma
Islet cell hyperplasia
Functional beta cell secretory defect
Factitious insulin use or sulfonylurea
use
Infection
Hypothermia
Congenital heart disease
Childhood
Infancy
Chapter 11.2: Hypoglycemia in Neonates and Children
255
256
9. Psychotic behavior.
10. Focal neurological deficits.
11. Seizures.
High-Risk Group for Hypoglycemia

1.
2.
3.
4.
5.
6.
7.
8.
9.
Preterm neonates.
Small for gestation (SGA).
Macrosomic.
Infants of diabetic mother (IDM).
Asphyxiated babies.
Rhesus hemolytic disease.
Hypothermia.
Polycythemia.
Beckwith-Wiedeman syndrome
Intrapartum Risk Factors for Hypoglycemia

1.
2.
3.
4.
5.
Maternal uncontrolled diabetes.

Maternal glucose infusion.
Maternal tocolytic therapy.
Maternal use of propronolol, chlorpropamide, salicylates, benzothiazide.
Perinatal asphyxia. (Cord blood arterial pH<7.20).
Optimum Time to Screen for Hypoglycemia

Physiologically, the nadir in blood glucose in newborn takes place at 2 to 4
hours after birth. Hence this would be an ideal time for screening an asymptomatic high-risk newborn. However, intrapartum risk factors would
warrant early screening.
Blood Sampling
For screening purposes reagent strips are commonly used on capillary
samples by heel prick, with the help of dextrometer. Reagent strips measure whole blood glucose.
Clinical Clues Leading to High Risk Group for Hypoglycemia

1. PlethoraPolycythemia.
2. Midline defects, cholestatic jaundice, micropenisHypopitutarism.
3. Ambiguous genitalia, hyperpigmentationCongenital adrenal hyperplasia.
4. CataractsIU infections, galactosemia, hereditary fructose intolerance.
5. Foul smelling cordInfection.
6. Hydrops fetalisRh hemolytic disease.
7. Visceromegaly, umbilical hernia, microcephaly, macroglossia
Beckwith-Wiedemann syndrome.
257
8. Hairy pinna, macrosomiaIDM.

9. HepatomegalyGlycogen storage, galactosemia, fructose intolerance,
gluconeogenic defect.
10. FundusIUGR.
11. Sweet odor of urineMaple syrup urine disease.
12. JaundiceGalactosemia, hereditary fructose intolerance.
13. Features of myopathy, cardiomyopathyGlycogen storage disease.
Investigations
1.
2.
3.
4.
Blood sugar.
Serum electrolytes.
Urine for nonglucose reducing substances and ketone.
Sepsis screen.
Further Evaluation
1.
2.
3.
4.
Serum insulin levels.

Endocrine profilegrowth hormone, cortisol, glucagons, ACTH.
Serum lactate.
Inborn errors of metabolismUrine aminoacidogram, urine for organic acid, plasma aminoacidogram.
5. USG abdomen.
Hyperinsulinism
Hyperinsulinism is the most common cause of intractable hypolycemia in
neonates.
Causes of Hyperinsulinism
1.
2.
3.
4.
5.
6.
7.
8.
Small for gestation baby.

Infant of diabetic mother.
Glucose infusion in mother.
IV bolus of glucose.
Autosomal recessive hyperinsulinism.
Autosomal dominant hyperinsulinism.
Nesidioblastosis.
Perinatal asphyxia.
Confirmatory Tests
i. Insulin level > 6 IU/ml
ii. C-peptide level > 0.2 mmol/L
iii. Pro-insulin level > 5 micromol/L
A rise in plasma glucose greater than 25 mg/dL strongly suggests hyperinsulinism in response to glucagon.
Recessively inherited hyperinsulinism is not responsive to diazoxide.
Autosomal dominant hyperinsulinism is responsive to diazoxide and most
258
infants are not large for gestation. Insulin (IU/ml) to glucose (mg/dL) ratio
0.4 or greater suggests hyperinsulinemia.
Neurodevelopmental Outcome of Hypoglycemia

1. There is no single value below which brain injury definitely occurs.
2. The absence of overt symptoms at low glucose levels does not rule out
CNS injury.
3. More the depth of hypoglycemia and longer its duration more adverse
is the neurologic sequele.
Management
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Ensure thermoneutral environment.

Secure an IV access.
Collect blood for basic investigations.
If symptomatic give a bolus of 2 to 4 ml/kg IV 10 percent dextrose.
If asymptomatic do not give bolus as it may cause rebound hypoglycemia.
Start glucose infusion with 10 precent dextrose at 6 mg/kg/min preferably using an infusion pump.
Check blood glucose level after 30 min.
If low, increment glucose infusion rate as protocol given below. Following changes in infusion rate check glucose after 30 min.
Calculate separately glucose infusion rate (mg/kg/min) and fluid requirement (ml/kg/day).
Need for glucose >12 mg/kg/min or >12.5 percent dextrose to maintain euglycemia suggests refractory (intractable) hypoglycemia. Put a
central line to deliver glucose of higher concentration to avoid thrombophlebitis.
Approach to hypoglycemia in neonates is shown in Flow chart 11.2.1.
Management for Refractory Hypoglycemia

1. Start hydrocortisone 5 mg/kg/dose, IV, 12 hourly. Collect sample for
insulin and cortisol before giving hydrocortisone.
2. Glucagon 0.1 mg/kg/ dose, IV or IM as a temporary measure to raise
blood glucose or when IV access is difficult.
3. Diazoxide l0 mg/kg/day, 8 hourly or octreotide 2 to 4 mg/kg/day 12 hourly.
4. Evaluate for underlying etiology and treat underlying specific cause.
Tapering
1. When glucose level crosses 60 mg/dL glucose infusion rate is gradually
tapered with decrements of 2 mg/kg/min every 12 hourly, till glucose
infusion rate comes down to 6 mg/kg/min with satisfactory blood glucose values more than 50 mg/dL.
259
Flow chart 11.2.1: Approach to hypoglycemia in neonates
2. Oral feeds are gradually introduced when glucose infusion is being

tapered depending upon infant condition.
3. The infant is completely weaned off intravenous infusion when blood
glucose values are stable at an infusion of 4 mg/kg/min.
4. Continue hydrocortisone until the infant is stable for 48 hours off IV
fluid. This usually takes for 5 to 7 days.
Diagnostic approach to hypoglycemia in children is shown in Flow chart
11.2.2.
Drugs causing Hypoglycemia

1. Insulin, oral hypoglycemic agents.
2. AntibioticsSulfonamides, isoniazid, pentamidine, trimethoprim, quinine, ketoconazole.
3. AnalgesicsPhenylbutazone, salicylates, propoxyphene, stanazol.
4. Cytotoxic agentsMethotrexate, 6 mercaptopurine.
5. AnticoagulantsBishydroxycoumarin.
6. Psychotropic drugsEthanol, methanol, lithium haloperidol, tricyclic
antidepressants, chlorpromazine, fluoxetine.
260
Flow chart 11.2.2: Diagnostic approach to hypoglycemia in children
7. InsecticidesVapor rodenticide, carbamates, organophosphates.

8. Cardiac drugsDisopyramide, propanolol, thiazide diuretics, clofibrate, ACE inhibitors.
Practice Points
1. Monitor carefully any neonate or infant with a blood glucose concentration less than 50 mg/dL.
2. Seizures occur in a minority of babies with hypoglycemia. When they
do occur, however, they usually imply long standing hypoglycemia.
3. Infants with glycogen storage disease can tolerate very low blood glucose concentrations without having significant symptoms.
4. There is a normal dip in blood glucose in first 2 to 4 hours postnatally.
The maximum risk for hypoglycemia is in first 24 hours and definitely
not after 72 hours, unless it is multifactorial in at risk group. Moni-
5.
6.
7.
8.
9.
261
toring for glucose should be done 4 hourly in first 24 hours or whenever baby is symptomatic.
Earliest marker for predicting hypoglycemia in the first few hours of
life would be cord blood glucose.
Do not perform blood glucose determination by reagent strip at temperature below 18C or above 35C.
The glucose level can fall by 14 to 18 mg/dL per hour in a blood sample
that awaits analysis.
Oral glucose or feeding alone are not enough once hypoglycemia has
occurred because oral glucose is more likely to stimulate insulin release as compared to intravenous glucose infusion.
In all other cases of hypoglycemia with the exception of galactosemia
and fructose intolerance, ketonemia and ketonuria are present at the
time of fasting hypoglycemia.
Bibliography
1.
Cameron P, Jelink G, Everitt I, Browne G, Raftos J Editors. Textbook of Pediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill Livingstone.
11.3
Adrenal Insufficiency and
Addisonian Crisis
The following are the causes of adrenal insufficiency:

A. Hypothalamic pituitary related
1. Hypothalamic lesion.
2. Hypopituitarism.
3. Isolated adrenocorticotrophin deficiency.
4. Adenoma.
5. Iatrogenicsteroid induced suppression.
B. Adrenal related
Defective steroidogenesis:
1. 21 hydroxylase deficiency.
2. 3 hydroxysteroid dehydrogenase deficiency.
Anatomical defect:
1. Surgery.
2. Trauma.
3. Hypoplasia.
C. Autoimmune
D. Hemorrhage
1. Waterhouse Freiderichsen syndrome.
2. Bleeding disorder.
E. Infection
1. Tuberculosis.
2. CMV infection.
3. HIV infection.
F. Genetic
1. Adrenoleukodystrophy.
2. Wolmans disease.
G. Drugs
1. Rifampicin.
2. Phenytoin.
3. Phenobarbitone.
4. Ketoconazole.
Chapter 11.3: Adrenal Insufficiency and Addisonian Crisis
263
High-Risk Group for Adrenal Insufficiency

1.
2.
3.
4.
5.
Hypoparathyroidism.
Pernicious anemia.
Secondary hypothyroidism (low TSH).
Growth hormone deficiency.
Central diabetes insipidus.
Signs and Symptoms

1.
2.
3.
4.
5.
6.
7.
8.
Weakness.
Fever.
Abdominal pain.
Seizure.
Dehydration.
Hypotension.
Shock.
Hypoglycemia.
Undiagnosed primary adrenal insufficiency causes chronic fatigue,
weakness, abdominal pain, anorexia, weight loss, vomiting, diarrhea,
salt craving and skin pigmentation. One should not wait for results of
investigations to start treatment if one suspects adrenal crisis. Features
of adrenocortical failure caused by adrenal or CNS disease is shown in
Table 11.3.1.
Investigations
1. Serum electrolytes and glucose, urine electrolytes and ABG. The typical findings are as follows: SerumNa, K, Glucose; UrineNa,
K, metabolic acidosis.
TABLE 11.3.1: Features of adrenocortical failure caused by adrenal or CNS disease
Adrenalcortical
Disease
HypothalamicPituitary Disease
Biosynthetic Defect
(CAH 21-O Hase)
Deficient hormone(s)
Cortisol
Aldosterone
Cortisol Aldosterone
(Salt wasting variant)
Hyperpigmentation
Serum Na+
Yes
Low (salt wasting)
Serum K+
Serum ACTH
Cortisol response
to IV ACTH
17-OH progesterone
response to IV ACTH
High
High
None
ACTH/CRF Cortisol
(Aldosterone pathway
intact)
No
Mildly low when
patient well (unable
to excrete free water
load)
Normal
Low
Increase
High if salt waster

High
Increase
None
Increase
Exaggerated
Yes
Low if salt waster
264
2. Creatinine, BUN, urinalysis, complete blood count with differential count.

3. Draw 5 to 10 ml extra clotted blood to measure cortisol level.
4. ACTH levels require prechilled purple top tube sent immediately to
laboratory.
Investigations to Determine Etiology

1.
2.
3.
4.
Contrast enhanced CT adrenal glands.

Chest X-ray, Mantoux test, ESRto rule out tuberculosis.
MRI brain.
Thyroid function test, GH stimulation.
Treatment
1. ABC should be maintained.
2. Cardiac monitor.
3. Patient will virtually always have significant volume contraction. So fluid
should be replaced with isotonic crystalloid with added dextrose at 20
ml/kg rapid infusion. The child may need to repeat bolus.
4. IV glucocorticoids to be given if possible, after diagnostic blood tests
are drawn. Hydrocortisone 50 mg/m stat followed by 100 mg/ m/day
every 6 hourly IV till stabilizes then 20 mg/m/day and add
fludrocortisone 0.15 mg/m/day. Maintain hydrocortisone at 9.5 to 15
mg/m/day as it causes least growth inhibition compared to dexamethasone and prednisolone. Continue fludrocortisone 0.15 mg/m/day
life-long.
5. Ongoing care:
i. Admit to PICU.
ii. Close monitoring of hydration and blood glucose and correction
of hypoglycemia.
iii. Check electrolytes every 2 to 4 hourly depending on degree of
illness.
iv. Replace 50 percent of fluid deficit in first 8 hours, using 0.9 percent saline with 5 percent glucose.
v. Replace remaining fluid deficit over 8 to 24 hours.
vi. Add potassium to IV if required, depending on serum K+ level.
vii. Taper glucocorticoid to physiological dose over 1 to 3 days as
patient condition allows.
viii. Parents should be advised IM injectable steroid for home emergency use (e.g. hydrocortisone).
Bibliography
1.
Muir A. Management of children with adrenal crisis. Pediatric Endrocrinology,

2004.
12
ENVIRONMENTAL
PROBLEMS
12.1
Animal Bites
Tapan Kumar Ghosh, Jaydeep Choudhury
All warm blooded animals can be infected by rabies virus. Human rabies is
acquired by bites, licks or scratches of rabid animals. Dogs account for 90
to 96 percent of animal bites in India. Children are more vulnerable to
animal bites and consequent rabies due to the following reasons:
1. Children are curious and love to play with dogs and cats.
2. They often play provocatively with animals which results into bites.
3. Their relative short height makes them more vulnerable to bites to
head, face, neck and hands, as shown in Figures 12.1.1 and 12.1.2.
4. They do not have any knowledge about danger of animal bites and
possible outcome. Also they often fail to report animal bites to their
parents.
5. Traversing time of virus from periphery to central nervous system is
short.
FIG. 12.1.1: Dog bite over face (For color version see Plate 2)
268
FIG. 12.1.2: Dog bite over arm (For color version see Plate 2)
Etiology
Causative Virus
Rabies virus is a bullet shaped, single stranded RNA virus, belong to family
Rhabdoviridae and genus Lyssavirus. This virus causes acute encephalitis
in human being. This virus cannot penetrate intact skin but can penetrate
intact mucosa. This virus basically infects animals. Two cycles namely, sylvatic and urban cycles in the animals help this disease to exist in the world.
Unless both these cycles are totally stopped, rabies will continue to stay.
Transmitting Animals
Apart from dogs, which are the main culprits other warm blooded animals
like cat, fox, jackals, etc, transmit rabies. The domestic animals like cow,
buffalo, goat, pig, sheep can transmit rabies when they are bitten and get
infected by rabid animals. Raw milk from an infected cow can transmit
rabies virus as rabies virus can penetrate intact mucus membrane. Boiling
the milk kills the virus. Monkey can also transmit this disease if they are
infected. Domestic rats do not transmit rabies virus but wild rodents do
transmit. Man to man transmission is rare except in cases of cornea transplant from donors with undiagnosed rabies.
269
Chapter 12.1: Animal Bites
Incubation Period
Twenty to 180 days, peak 30 to 60 days, extreme 9 days and 1 year. Incubation period is shorter if the bite is closer to brain.
Clinical Types
Two types of clinical rabies are described. Furious type in 80 percent and
paralytic type in 20 percent (dumb rabies). Both types are common for
human and canine rabies.
The virus first multiplies in striated muscles, ascends along axons from
periphery to spinal cord and eventually to neurons in the brain. There is
neuronal destruction in the brainstem and medulla and severest changes
in pons and IV ventricles but cortex are spared.
Modes of Transmission
Common Modes
1. Bite and scratch from infected animals.
2. Lickon broken skin and intact mucus membranes.
Rare
1. Aerosol transmission.
2. Organ transplantation.
Bites by insectivorous bats can also transmit rabies and rabies can spread
also by aerosol infection in bat infested caves but these are not problems of
India.
Clinical Features
As stated earlier furious type of rabies is most common (80%) but dumb
type of rabies manifested by ascending paralysis (20%) is also reported.
The furious type of rabies presents with acute neurological phase characterized by hydrophobia, aerophobia, photophobia, dysphagia, etc. No
survival is so far reported in unvaccinated infected persons in the world
literature. The difference of the presenting features in these two types is
shown in the following Table 12.1.1.
TABLE 12.1.1: Clinical features in furious and paralytic type of rabies
Furious Type (80%)
Paralytic Type (20%)
Tingling/numbness at bite site

Nonspecific symptoms
(Fever, malaise, headache, etc.)
Hydrophobia, Aerophobia
Photophobia
Death in 35 days
(Cardiac and respiratory failure)
Tingling/numbness at bite site

Nonspecific symptoms
(Fever, malaise, headache, etc.)
Ascending paralysis
Coma
Death in 721 days
(Cardiac and respiratory failure)
270
Diagnosis
Diagnosis is mainly based on clinical signs of hydrophobia and aerophobia
in the furious type of rabies. Confirmation of diagnosis is based on the
followings.
1. Detection of Negri body in brain by Sellers stain
2. Detection of virus antigen by immunofluorescence
3. Mouse pathogenecity (Biological test)
Detection of antibodies in CSF or serum of unimmunized persons and
detection of viral nucleic acid from infected tissue is also possible. Virus
can be isolated from saliva.
WHO Classification of Bites

Before starting the treatment of animal bite cases in human being, classification of the exposure is most important. The following Table 12.1.2 shows
the WHO classification of animal bites cases.
Management
Treatment following an exposure (Bite, scratch or lick on broken wounds
in skin or directly on mucous membrane, i.e. on oral cavity or on anus by
suspected rabid animal) will consist of the following stages:
1. Proper wound management.
2. Infiltration of rabies immunoglobulin (RIG) in all category III exposures (vide the Table 12.1.2) rabies.
3. Antirabies vaccination with modern cell culture rabies vaccine (CCRV).
4. Antitetanus prophylaxis.
5. Supportive treatment with antipyretic/analgesics, local and/or systemic
antibiotic as required.
TABLE 12.1.2: Type of contact, exposure and recommended postexposure prophylaxis
Category
Type of contact
Type of
exposure
Recommended postexposure
prophylaxis
Touching or feeding of animals.

Licks on intact skin.
Nibbling of uncovered skin.
Minor scratches or abrasions
without bleeding.
Single or multiple transdermal
bites or scratches, licks on
broken skin.
Contamination of mucous
membrane with saliva (i.e, licks)
None
None, if reliable case history

is available
Wound management
+
Anti-rabies vaccine
Wound management
+
Rabies immunoglobulin
+
Antirabies vaccine
II
III
Minor
Severe
Note: After carefully assessing the category of exposure, the treating doctor should evaluate the course of
action to be taken, based on the following general considerations. He should also keep in the mind that with
the presently available safe cell culture rabies vaccines (CCRV), it is always safe to offer treatment rather
than withhold in doubtful situations.
271
The Steps of Management

STEP I Wound management
In wound management, the most important steps are the following:
i. Thorough washing of wounds under running tap water for at least 10
minutes with the aim of physical elimination/shedding of the viral
loads and application of soap/detergent for chemical treatment and
changing the pH of the wounds.
ii. Application of disinfectants like povidone iodine, spirit, household
antiseptics, etc. to remove the remaining virus particles and prevention of secondary infection.
STEP II Rabies immunoglobulin (RIG)

Infiltration of bases of wound(s) with rabies immunoglobulin (RIG): Neutralization of the virus and forming a coat around the virus thus obliterating
virus entry into the nerve endings.
STEP III Antirabies vaccination (ARV)

A course of postexposure prophylaxis (PEP) either IM or ID route with
modern cell culture ARV (CCRV).
STEP IV Antitetanus prophylaxis

Administration of tetanus toxoid (TT or Td) and/or tetanus immunoglobulin (TIG) as required.
It is to be noted that in wound management application of irritants,
cauterization and suturing, i.e. closing of wounds are to be avoided. If suturing is needed for the purpose of hemostasis, it can be done only after
administration of RIG.
Rabies Immunoglobulin (RIG)

The antirabies serum (ARS)/rabies immunoglobulin (RIG) provides passive immunity in the form of readymade antibody to tide over the initial
phase of the infection. Antirabies serum or RIG has the property of binding to rabies virus, thereby resulting in neutralization of the virus. Two
types of RIGs are available:
1. Equine rabies immunoglobulin (ERIG): ERIG is of heterologous origin
raised by hyperimmunization of horses. Currently manufactured ERIGs
are highly purified and enzyme refined. The dose of ERIG is 40 IU per
kg body weight of patient and is given after testing for sensitivity (Skin
test), up to a maximum of 3000 IU.
2. Human rabies immunoglobulins (HRIG): These are prepared from the
serum of people hyperimmunized with rabies vaccines. The dose of
HRIG is 20 IU per kg body weight (maximum 1500 IU). HRIG does
not require any prior sensitivity testing (Skin test).
272
RIG is to be infiltrated as much as possible into and around all the

wounds; remaining if any is to be given intramuscularly at a site away from
the site of vaccination. All the wounds are to be infiltrated with RIG. After
calculation of the dose of RIG if it is seen that RIG is insufficient by volume
to infiltrate all the wounds, it is to be diluted with normal saline to make it
2 or 3 times of its volume.
Antirabies Vaccines
Active immunization is achieved by administration of safe and potent CCRVs
or purified duck embryo vaccines (PDEV). In India, nerve tissue vaccine or
NTV (semple vaccine) was used for postexposure treatment in public sector.
However, as this vaccine was reactogenic (neuroparalyticogenic), the
production was stopped in December, 2004 in all centers. The dosage
schedule of cell culture rabies vaccine (CCRV) is same irrespective of the
body weight or age of the children.
Types of Antirabies Vaccines

1. Cell culture rabies vaccines (CCRV):
i. Human diploid cell vaccine (HDCV).
ii. Purified chick embryo cell vaccine (PCEC).
iii. Purified vero cell rabies vaccine (PVRV).
2. Purified duck embryo vaccine (PDEV): All CCRVs and PDEV used for
postexposure prophylaxis (PEP) should have potency (antigen content)
greater than 2.5 IU per dose.
Reconstitution and storage: The lyophilized vaccine should be reconstituted
with the diluent provided with the vaccine immediately prior to use. In
case of unforeseen delay it should be used within 6 to 8 hours of
reconstitution.
Presently liquid human diploid cell (HDCV) vaccine is also available.
Intramuscular (IM) Regimen of Cell Culture Antirabies Vaccine

The regimens for IM administration are described below. But the Essen
Schedule is only IM regimen to be practiced in India.
Essen scheduleFive dose intramuscular regimen (1-1-1-1-1): Total five
injections, single dose on Days 0, 3, 7, 14 and 28. Day 0 indicates date of
first injection.
Site of inoculationThe anterolateral thigh region is ideal in infants and
younger children whereas the older children can take in deltoid regions
safely. Gluteal region is not recommended because the fat present in this
region traps the vaccine, retards the absorption of antigen and hence impairs the generation of optimal immune response
Intradermal (ID) Regimen of Cell Culture Antirabies Vaccine

Intradermal regimens consist of administration of a fraction of intramuscular dose of CCRVs on multiple sites in the layers of dermis of skin. The
273
use of intradermal route leads to considerable savings in terms of total

amount of vaccine needed for full pre- or postexposure vaccination, thereby
reducing the cost of active immunization. But the regimen will not make
any economic meaning when one or two doses are used in private clinics. It
is better to be used in antirabies clinics and centers (ARCs) where a handful number of cases of animal bites/scratches will be available.
The following vaccines have been approved by Drug Controller General of India (DCGI) currently for use by intradermal route: (i) Purified
chick embryo cell vaccines, (ii) Purified vero cell vaccine.
As purified duck embryo cell vaccine is a suspension, its use is not
recommended for ID administration, similarly the liquid and adjuvanted
human cell culture vaccine is not suitable for ID use.
Potency of approved vaccines: The vaccines should have stated potency of
>2.5 IU per IM dose, irrespective of reconstituted volume. The same vaccine is used for ID administration as per stated schedule. 0.1 ml of vaccine,
irrespective of reconstituted volume, is administered per ID site as per
schedule below. Technique of ID administration and the resultant wheal
formation is shown in Figure 12.1.3.
ID Vaccine Regimen
Updated thai red cross (Updated TRC-ID) schedule (2-2-2-0-2): The most
ideal ID schedule. This involves injection of 0.1 ml of reconstituted vaccine
per ID site and on two such ID sites per visit (one on each deltoid area, an
FIG. 12.1.3: Intradermal injection and the resultant wheal formation
274
inch above the insertion of deltoid muscle) on days 0, 3, 7 and 28. The day
0 is the day of first dose administration of IDRV and may not be the day of
rabies exposure/animal bite. No vaccine is given on day 14.
Preexposure Schedule
As rabies is a cent percent fatal disease and children constitute a special
risk for getting the infection, it may be advisable to vaccinate children after
they attain the age of 3 years and start playing in the streets and a may
come in contact with street or pet dogs. This schedule is also practiced in
persons engages in rabies research and production of rabies vaccine units,
in municipality workers, in postmen, in persons going to forests where
there are bat infested caves, veterinary practitioners, taxidermists, etc. It
has been shown in several studies that a course of preexposure vaccination
will elicit a good immune response and the memory cells generated will
last for many years. In fact some studies have also shown that protective
levels of antibodies may persist for at least a decade. If such children are
exposed to rabies by animal bites, 2 booster doses given on Day 0 and on
Day 3 will elicit a rapid and stronger secondary immune response which
will neutralize the virus and prevents its ascent to the CNS. There is no
need for administration of rabies immunoglobulin in patients who had
taken a complete course of preexposure or postexposure course of CCRVs
in their previous exposure.
Schedule of Preexposurer Vaccination

Intramuscular: Three doses of any CCRV (1 ml or 0.5 ml depending on
the brand) administered on the anterolateral thigh or deltoid region on
days 0, 7 and 28.
Intradermal: The dose (0.1 ml) is same for all vaccine brands and 0.1 ml is
administered intradermally over the deltoid on days 0, 7 and 28.
Canine Rabies
All warm-blooded animals even bats are susceptible to rabies, the incubation period and symptoms had marked similarities in all of them. The
abnormal behaviors of the infected animals are seen commonly. Even rabies is reported in small percentage of bites by immunized dogs and also
by puppies. The observation period of 10 days is only true in dog and cat
bites. Antirabies vaccines should be started even when bitten by immunized domestic dogs and cats.
Dogs are the most important animal in spreading rabies, responsible
for 96 percent of the cases of human rabies deaths in India. But for several
reasons it is difficult to control stray dog population in this country. The
most friendly animal to human being, the dogs become restless, move to
other places of seclusion, sudden burst of excessive affection are seen in
the early stage with persistent attempts to lick, when the dogs are infected
275
by rabies virus. There are behavior changes, ultimately the dog develops
irresistible tendency to scratch and bite. The pupils dilate and salivation is
increased. The furious form which shows the classical symptoms gives the
concept of mad dogs. Dumb rabies is characterized by progressive development of paralysis.
It is to be accepted that stray dog population has to be reduced drastically, initiative to sterilize the male dogs in stray population and vaccination
with modern rabies vaccines by the Government Health Department and
NGOs combined are needed. Even the pet dogs must have municipality
licenses, and they have to be immunizes annually with rabies vaccines. All
these will help to reduce the incidence of human deaths due to rabies in
India.
Bibliography
1.
2.
3.
4.
5.
6.
7.
8.
Association for Prevention and Control of Rabies in India. WHO Sponsored

National Multicentric Rabies Survey, 2004. Bangalore: APCRI 2004:44-5.
Bompart F, Dutta AK, Wood SC. Rabies immunoglobulins in WHO category
III bites. Journal of Association for Prevention and Control of Rabies in India
2001;1(2):7-11.
Caplan K. Rabies: The Facts. Oxford: Oxford University Press, 1977;53-61.
Ghosh TK. Prevention of rabies by vaccination and immunoglobulin therapy:
Some controversies and solutions. In: Ghosh TK Editor Infectious Diseases in
Children and Newer Vaccines. New Delhi: Jaypee Brothers 2007:330-5.
Ghosh TK. Rabies and its prevention. Pediatr Clin India 2001;36:42-51.
Kundu R, Ganguly N, Ghosh TK. IAP Protocols on Infectious Diseases in Children. Kolkata: IAP Infectious Diseases Chapter. 2008;57-71
Madhusudana SN. Implementing intradermal vaccination : Why delay (Editorial). APCRI Newsletter 2003;3:3.
World Health Organisation. WHO Expert Committee on Rabies, 8th Report.
WHO Tech Rep Ser 1992;824:1-84.
12.2
Snake Bite
Snake bite is common in rural area. With rapid expansion of urban limits it
is seen in developing urban areas also. Most of the time people are scared
as they fail to distinguish between poisonous and nonpoisonous snakes
and come for medical management. It is heartening to note that most
snakes are nonpoisonous. At the same time the poisonous snakes should
also be identified for immediate management.
There are three classes of poisonous snakes available in India:
1. Cardiotoxic and neurotoxic: Cobra and krait. They are identified by
hood like head of cobra or small triangular head of krait, pit between
eye and nostril, large belly scale, compressed tail and characteristic
bite mark of two fangs with or without other teeth.
2. Hemolysis and severe local reaction: Viper. They have a V-shaped mark
on their head and white belly. They hiss loudly.
3. Myotoxic: Sea snake.
Clinical Effects
1. Local tissue: Pain, swelling, rhabdomyolysis and lymphadenopathy.
2. Systemic: Vomiting, nausea, abdominal pain, headache, tachycardia,
hypotension.
3. Neurological: Blurred vision, bulbar/facial weakness, ptosis (may be an
early sign of progressive muscle paralysis), lethargy and loss of consciousness.
4. Hematological: Defibrination, thrombocytopenia and clinical bleeding (like hematemesis).
5. Others:
a. Respiratory: Respiratory paralysis may occur due to neurotoxic component.
b. Genitourinary: Hematuria, dark urine may be from myoglobinuria.
Acute renal failure.
c. Musculoskeletal: Generalized muscle pain due to muscle destruction from myotoxins. Common with sea snake bites.
Chapter 12.2: Snake Bite
277
Laboratory Findings and Monitoring

Blood should be drawn for following tests before antivenom is started.
1. Clotting factors: Prothrombin time and partial thromboplastine time,
fibrinogen and platelet count
2. Full blood count, urea, creatinine.
3. Creatine kinase (CPK), d-dimer.
Monitor heart rate, BP and oxygen saturation. Gradual desaturation
may be indicator of respiratory muscle paralysis.
Management
First Aid
1. A wide bandage should be applied to cover the bitten area. The wound
should be cleaned with saline.
2. Immobilization of the bitten extremity with a splint or sling.
3. Tetanus prophylaxis as indicated by immunization status. Consider tetanus immunoglobulin according to standard national recommendations.
4. The pressureimmobilization bandage may be removed if there is no
clinical or laboratory evidence of envenomation or once envenomation administration has been commenced.
5. If there is no clinical evidence of envenomation and pressure-immobilization bandage has been removed, patient should be observed at least
for 4 hours, then clinical and laboratory assessment should be repeated.
Patient may be discharged, if the second clinical and laboratory assessment shows no evidence of envenomation. Periods of observation may
need to be longer in certain circumstances as shown in Flow chart 12.2.1
management plan .
6. Do not apply suction, arterial tourniquet or incise bitten area.
Local Wound Management

1. Wound should be cleaned and left open.
2. If swelling or tenderness is present, the proximal edge and time of
detection should be marked so that progression can be monitored.
3. Similarly the circumference of the limb at the level of edema should be
recorded.
4. Fasciotomy may be done to prevent compartment syndrome.
5. Wound debridement may be required after 3 to 5 days.
Optimize ABC
Assisted ventilation and fluid resuscitation may be required and are important components even before specific treatment is started.
278
Flow chart 12.2.1: Snake bite management plan
Specific Treatment
Polyvalent antivenin with venoms of four common snakescobra, krait
and two types of viper are available.
Who should be given Antivenin?

Bite by any species may show no specific systemic effect due to presence of
a dry bite where no venom is introduced. Some victims may not recall the
bite as there may be minimal pain. Bite marks are not a good predictor of
the degree of envenomation. Severe envenomations have occurred without obvious bite marks. These cause great dialemma in the management of
snake bite.
Indications
1. Weakness including ptosis, hypoventilation, bleeding, oliguria, myoglobinuria.
2. Collapse, shock or convulsion after confirmed bite.
3. Laboratory reports of coagulopathy, deteriorating renal function,
myolysis.
4. Where laboratory test facilities are not available, 20 minutes whole blood
clotting test (20 WBCT) has been advocated. It should be carried out
in a clean new and dry test tube. A few ml of fresh venous blood is left
undisturbed for 20 minutes and then gently tilted. If blood is still in
Chapter 12.2: Snake Bite
279
liquid state, it is an evidence of coagulopathy and confirms bite by

viperine. Cobras and krait dont cause antihemostatic symptoms.
Do not administer antivenom in patients who only have minor headache, abdominal pain, nausea or vomiting and lymphadenopathy.
Skin Test
It has been abandoned as it has no predictive value.
Pretreatment
Corticosteroid, antihistaminic and ranitidine should be administered before starting antivenin as there is risk of anaphylaxis. Adrenaline, oxygen,
fluid and equipments for airway management should be kept ready for
emergency. See chapter on anaphylaxis.
Antivenin
Each vial contains 10 ml of antivenin. The total dose necessary in children
ranges from 8 to 10 vials depending on the clinical progress and stability of
the patient. Maximum 25 vials may be required.
1. Initially 2 vials are diluted in 100 ml normal saline and infused over
1 hour.
2. The rest of the dose is repeated over 4 hours with continuous monitoring. Mainly the development of neurological or hematological
manifestations is to be looked for. This infusion may be repeated till
the child stabilizes both clinically and blood report wise.
3. After stabilization repeat coagulation profile and renal parameters.
4. Repeat doses of antivenin though rarely required depends on
antihemostatic condition and clinical improvement. It should be started
6 hours after finishing the first lot.
If indicated, antivenin should be started as soon as possible and should
not be withheld due to late presentation.
Neuroparalysis
Neurotoxin of cobra and krait may produce curare like neuromuscular blockade. Both neuroparalysis and respiratory paralysis may develop.
1. Neogstigmine 0.07 mg/kg intravenous, may be repeated 4 hourly.
2. Atropine 0.02 to 0.50 mg/kg before each dose of neostigmine.
Constant ECG monitoring should be done.
Supportive Treatment
1. Pain relief.
2. Broad spectrum antibiotic should be started prophylactically to prevent cellulitis, osteomylitis, septicemia and necrotising fascitis.
3. Renal failure, if develops should be managed appropriately. Sometimes
dialysis has to be commenced with caution in the context of
coagulopathy.
280
4. Bleeding manifestations and DIC are life-threatening and should be

controlled with blood products and heparin. FFP and platelet will not
help unless sufficient antivenom is also given.
5. Myoglobinuria: Diagnosed by red or brown colored urine, false positive
for occult blood with absent RBC, markedly elevated serum CPK. Forced
alkaline diuresis should be instituted and/or early dialysis if rapid elevation of potassium, creatinine occurs.
6. Surgical debridement if required.
Bibliography
1.
Lieh-Lal MW, Ling-McGeorge KA, Asi-Bautista MC Editors. Pediatric Acute

Care, 2nd edition. Philadelphia: Lippincott Williams and Wilkins, 2003.
Chapter 12.3: Scorpion Sting
283
3. Prazosin30 mcg/kg/dose orally or through NG tube along with H2

blocker like ranitidine to counter the excess gastric acid secretion.
Prazosin to be repeated every 3 to 4 hourly up to 4 doses or till improvement. Appearence of wide pulse pressure is an early indicator of
reduction of preload and afterload.
4. Insulin 0.1 U/kg subcutaneously 8 hourly for myocardial protection.
Check blood glucose 6 to 8 hourly.
5. Sodium nitroprusside 0.5 to 8 mcg/kg/min may also be used. Sodium
nitroprusside should be protected with an opaque cover. Prazosin has
to be repeated 1 hour before stopping sodium nitroprusside.
6. Dobutamine 5 to 15 mcg/kg/min may be required in hemodynamically
compromised patients. Sodium nitroprusside and dobutamine combination increases the cardiac output with significant left ventricular
afterload reduction.
7. Frusemide injection may be required for pulmonary edema.
8. Rarely assisted ventilation is required. Early institution of PEEP may
be helpful
9. Localinfiltration of lignocaine 2 percent for local pain relief. Consider IV opioid if not controlled.
10. Injection Td if the child is not already immunized.
Advantages of Prazosin
Highly selective 1 blocker: It is the direct physiological antidote.
Decreases peripheral resistance.
Blocks pressor action of adrenaline on heart.
Decreases sympathetic flow to the heart by central action, prevents
arrhythmia.
v. Corrects metabolic changes.
vi. It is an oral drug and can be easily monitored.
i.
ii.
iii.
iv.
Adverse Effects of Prazosin

i.
ii.
iii.
iv.
v.
vi.
Postural hypotension.
Palpitation.
First dose effect: Hypotension.
Headache, drowsiness.
Dry mouth.
Skin rash.
Bibliography
1.
2.
Mahadevan S. Scorpion sting. Indian Pediatr 2000;37:504-11.

Mahadevan S. Scorpion sting. In: Pediatric and Neonatal Emergencies, 2nd
edition. New Delhi: Jaypee Brothers 2004;409-13.
12.4
Near Drowning
Drowning refers to death from asphyxia within first 24 hours of submersion in a liquid. Near drowning is defined as submersion in which survival
is greater than 24 hours regardless of morbidity or mortality.
Pathophysiology
As the child sinks into water, he/she holds the breath until reflex respiratory effort occurs. As the victim begins to panic or become hypoxic, water
may be swallowed into the stomach. The victim becomes unconscious secondary to hypoxia. Hypoxia leads to cardiac arrest unless there is
intervention.
In fresh water drowning the surfactant is inactivated and alveolar basement membrane is damaged. The resulting alveolitis and transudation of
proteinaceous material produces pulmonary edema. Functional loss of surfactant results in alveolar collapse. In hypertonic sea water submersion,
there is movement of water from intravascular space to alveolar space. Surfactant is diluted and effluted from alveolar space. Additional alveolar
basement membrane is also damaged.
Etiology
Fresh water: Accounts for about 90 percent of drowning. The usual places
are swimming pools, rivers, ponds, during bath or boat capsize.
Hypertonic sea water: Accounts for about 10 percent cases, usually due to
boat capsize, or ship sinking.
History and Clinical Findings

1.
2.
3.
4.
5.
6.
7.
Episode and mechanism of injury.

Evidence of trauma, seizures, intoxication, exhaustion.
Time of submersion.
Time until CPR begins.
Loss of consciousness.
History of seizure.
Medication used.
Chapter 12.4: Near Drowning
285
8. Drug or alcohol ingestion.

9. Prehospital treatment given, if any.
Complications
1.
2.
3.
4.
5.
6.
7.
8.
9.
Hypoxia.
Acidosis.
Hypoperfusion.
Hypothermia.
Respiratory insufficiency.
Aspiration pneumonia.
Coagulopathy leading to DIC.
Hemolysis.
Myoglobinuria, hemoglobinuria, hypoxia, acidosis leading to renal failure.
10. Brain injury following trauma or hypoxia.
11. Cardiac dysrrhythmmias and cardiogenic shock.
12. Significant electrolyte disturbanceUncommon until large amount of
sea water is swallowed.
Laboratory Investigations
1. ABG.
2. Blood: Complete blood count, serum electrolytes, glucose, urea, creatinine, LFT. Screen for DIC including PT, PTT, platelet count, fibrinogen
and fibrin split products.
3. Urine RE.
4. Chest X-ray: Serial X-rays may be required to monitor progression.
Prehospital Intervention
1. Treatment begins with search, location or removal of patient from
water.
2. Warming and drying.
3. 100 percent O2 administration.
4. Cervical spine immobilization.
5. The child should be intubated in the following situations:
i. Airway not maintainable
ii. Apnea
iii. Inadequate respiration or excessive work of breathing
iv. Cardiopulmonary arrest
v. Inadequate assisted ventilation
vi. Prevention of aspiration
vii. Neurological deterioration.
6. Venous or intraosseous access.
7. Nasogastric tube, if patient intubated.
8. Cardiac monitoring.
286
9. Pulse oximetry, if available.

10. Adrenaline if patient is in cardiac arrest.
Emergency Department Management

1.
2.
3.
4.
5.
6.
7.
8.
9.
Warming and drying as necessary.

Immobilize neck if cervical spine injury suspected.
Vital signs including core temperature.
Venous access.
Arterial line or central line if indicated.
Intubation if indicated.
Nasogastric tube, Foleys catheter in all unconscious patients.
Cardiac monitor.
Pulse oximeters.
The specific management algorithm in emergency department is shown
Hospital Admission Criteria

1. Tachypnea, retractions.
2. Hypoxia.
Flow chart 12.4.1: Specific management of near drowing in emergency department
Chapter 12.4: Near Drowning
287
3. Abnormal ABG.
4. Abnormal Chest X-ray.
5. Any neurological impairment.
Hypothermia
See treatment in respective chapter.
Cerebral Edema
1. Elevate head end to 30 degree.
2. Maintain PCO2 25 to 30 mm Hg.
3. Minimize procedure which can increase ICP (NG tube, Foleys catheter).
4. Restrict fluid to 50 to 60 percent of maintenance, once vascular stability achieved keeping CVP8 to 10 mm Hg and urine output 0.5 ml to
1.0 ml/kg/hr.
5. Mannitol 0.5 gm/kg over 30 min every 3 to 4 hourly, IV may be used if
patient is symptomatic.
6. If arrangement is there monitor ICP.
7. Induce anesthesia with thiopentone in a dose of 3 to 20 mg/kg IV and
maintain 1 to 2 mg/kg/hr while monitoring blood pressure and ICP.
Maintain muscle paralysis with pancuromium bromide 0.1 mg/kg IV.
General Measures for Management

1. Correct electrolytes and acid base abnormalities.
2. Control seizures with phenytoin 10 to 20 mg/kg IV followed by maintenance 5 mg/kg/day.
3. Aspirate stomach content with NG tube.
4. Insert Foleys catheter subsequently.
5. Cardiac monitoring for any dysrhythmias.
6. No role of steroid has been documented.
7. No role of prophylactic antibiotics though empiric antibiotic therapy is a
common practice because of chance of streptococcal pneumonia sepsis.
Practice Points
Hypotension and shock in near drowning may be due to ischemic cardiomyopathy, acidosis, CNS insult, vascular shunting and blood loss associated
with trauma, cervical spine injury and hypothermia.
Prognosis
Victims submerged in nonicy water, the reliable predictor of death or severe neurological sequele are the following:
1. Unresponsiveness on arrival at hospital.
2. Elevated blood glucose levels.
288
3. Fixed pupils in emergency room.

4. Cardiac arrest requiring more than 25 minutes of advanced life support.
5. Initial GCS <5.
6. Seizures or flaccidity.
Orlowskis Prognostic Scoring System

One point for each of the following criteria. A score of 2 or less has 90
percent likelihood of good recovery with standard therapy, where as patient with score 3 or more has only 5 percent likelihood of good recovery.
1. Age <3 years.
2. Immersion time longer than 5 minutes.
3. No resuscitation for 10 minutes.
4. Coma at initial presentation.
5. Arterial pH less them 7.1.
Bibliography
1.
2.
Livingstone.
Lieh-Lal M W, Ling-McGeorge K A, Asi-Bautista M C Editors. Pediatric Acute
Care, 2nd edition. Philadelphia: Lippincott Williams and Wilkins, 2003.
12.5
Burn
Jaydeep Choudhury
Children are prone to burn due to various factors. They are inquisitive, they
play with inflammable objects which they get from parents and care givers,
people in the kitchen often fail to notice children approaching from behind
and above all children do not realize the consequences of fire and flames.
First Aid: To be done at the Site of Burn

1. Flames should be extinguished first. A very effective mode is falling
and rolling over the ground. A blanket cover may be applied.
2. Airway: Should be cleaned and patency to be established.
3. Clothing and constricting items to be removed. The burns should be
covered with water soaked sterile cloth. Recently sustained minor burns
should be cooled under running water.
4. Chemical injury: It should be washed off with plain water.
5. Electrical burns: First the source of electrical current should be switched
off. If it is not possible then the affected person should be touched
with a nonconducting material and separated from the source.
Life Support
1. Breathing: Humidified oxygen by mask or endotracheal tube.
2. Circulation: Intravenous fluid should be started in all children with
>15 percent body surface area (BSA) burn, inhalation injury and electrical injury. Ringers lactate 10 to 20 ml/kg/hr intravenous should be
started.
3. Any associated injury should be looked for and evaluated.
4. Wounds should be covered.
5. A nasogastric tube and a urinary catheter should be kept in situ.
Degree of Burn
1 burn: Epidermis only (swelling, erythema and pain).
2 burn: Entire epidermis and variable portion of dermis (vesicle, blister).
3 burn: Entire epidermis and dermis (lack of pain and capillary filling).
290
1 and 2 burns are called partial thickness burn where as 3o burn is called
full thickness burn.
The calculation of body surface area of different parts of the body in
children is detailed in Table: 12.5.1.
Admission Criteria for Pediatric Burns Patients

1.
2.
3.
4.
5.
6.
7.
Partial thickness burns involving more than 20 percent BSA.

Full thickness burns involving more than 5 to 10 percent BSA.
Suspected smoke inhalation.
Hands, feet, face, perineum and joints burns.
Burns less than 20 percent BSA in children less than 1 year.
Comorbidity and other injuries.
Suspected child abuse.
Fluid Resuscitation
Parkland Formula
1st 24 hours: Ringers lactate 4 ml/kg/% BSA burned the amount in 1st
8 hours over next 16 hours.
2nd 24 hours: 0.45 percent saline with 5 percent dextrose: of the 1st
days fluid.
5 percent albumin may be used to maintain serum albumin above 2 gm/dL
Packed cell transfusion, if Hb is less than 8 to 10 gm/dL.
Monitor: Pulse rate, blood pressure and urine output should be at least
1 ml/kg/hr.
Injection Td if the child is not already immunized.
Sedation
Should be kept at minimum. The choices are the following:
i. Pethidine 1 mg/kg.
ii. Morphine 0.1 mg/kg.
iii. Pentazocine 0.1 mg/kg.
TABLE 12.5.1: Surface area of different parts of the body in children expressed as percentage of
total body surface area (BSA)
Body part
Newborn
3 years
6 years
12 + years
Head
Trunk
Arms
Legs
18%
40%
16%
26%
15%
40%
16%
29%
12%
40%
16%
32%
6%
38%
18%
38%
Chapter 12.5: Burn
291
Infection
i. Wound swab should be collected for culture, blood sample should be
taken for culture and sensitivity.
ii. Pseudomonas prophylaxis should be started.
Stress Ulcer
Curlings ulcer in the stomach is a known complication. All the burn cases
should be given H2 blocker or other antacids.
Topical Treatment
i. Silver nitrate
ii. Silver sulfadiazine
Complications
Early: Shock, respiratory tract injury, ARDS, infection, Curlings ulcer,
thrombophlebitis, nutritional deficiencies.
Delayed: Post burn scar, contracture, Marjolins ulcer.
Bibliography
1.
2.
Yurt RW. Burns. In: Mandell G Editor. Principles and Practice of Infectious
Diseases, 5th edition. New York: Churchill Livingstone 2000:3198-206.
12.6
Electrical Burn
Jaydeep Choudhury
These are usually seen in toddlers and male adolescents involved in risk
taking behaviors. Electrical currents preferentially flow along low resistance
tissues such as blood vessels, nerves and muscles. There is usually an entrance and exit burn. The internal injury is more than the surface injury.
Management
1. The initial priority is assessment of childs A, B and C.
2. Examination for skin burn and potential internal injuries. A search for
entrance and exit wound to determine the potential for deeper burns.
3. Baseline 12-lead ECG, unless a very minor exposure.
4. Cardiac monitoring continues, if the initial ECG is abnormal or the
child is symptomatic (chest pain, impaired consciousness).
5. Analgesia for the burn and muscle pain.
6. Fluid therapy: It is difficult to calculate fluid requirement by using
Parkland formula as most of the injury is internal. The aim is to maintain urine output of 2 ml/kg/hour.
7. Myoglobinuria: Muscle involvement may lead to myoglobinuria, which
may cause renal failure. Forced diuresis with diuretics and alkalinization prevent renal damage.
The electrical outputs should always be protected and kept out of reach
of children Figure 12.6.1.
Admission Criteria
1. Any high voltage injury.
2. Child with evidence of cardiac or neurological abnormality.
3. Other complications.
Discharge after Emergency Management

Asymptomatic child with low voltage injury with normal ECG.
Chapter 12.6: Electrical Burn
293
FIG. 12.6.1: Covered electrical outputs
Bibliography
1.
81-7.
12.7
Hyperpyrexia and Hyperthermia
Jaydeep Choudhury
Core body temperature more than 41C is hyperpyrexia.
Common Causes of Hyperpyrexia

1. Infections: Bacterial, viral and parasitological.
2. CNS: Infection, hemorrhage, trauma, surgery, hypothalamic malfunction.
Effective Cooling
1. Tepid sponging in warm water, cold water or ice pack may produce
shivering, which produces more heat is better avoided.
2. Switching on the fan to facilitate evaporative heat loss.
Drugs and Sympathetic Treatment

1. Dehydration should be corrected by normal saline 20 to 30 ml/kg in
the first hour.
2. Chlorpromazine 0.5 to 1 mg/kg intravenous every 4 hourly.
3. NSAIDs like paracetamol 15 mg/kg oral or rectal suppository.
Care of the Unconscious Patient

If the child is having altered sensorium, general care of an unconscious
child should be carried out. The primary condition producing hyperpyrexia should be taken care of.
Hyperpyrexia or Hyperthermia?
The hypothalamic set point of temperature regulatory mechanism is altered in hyperpyrexia and set at a higher point. So pharmacologic
interventions including the use of antipyretics are effective in bringing the
temperature down.
The thermoregulatory center is unaltered in hyperthermia. The set
point of temperature is not elevated despite high temperature. The in-
Chapter 12.7: Hyperpyrexia and Hyperthermia
295
crease in temperature exceeds the bodys ability to loose heat. Here

antipyretics are not effective. Here treatment of the precipitating factor is
more important.
Features of Hyperthermia
History: Family history of malignant hyperthermia.
Fever: High with profuse sweating.
Early sign: Masseter spasm.
Other features: Mottled skin, tachycardia, hypertension, arrhythmia, tachypnea, grunting, whole body rigidity.
If the precipitating cause is heat stroke, then the child should be removed from the heat and general care given to cool the body. Sometimes,
it is due to the effect of some drugs like inhaled anesthetic agent, mainly
halothane or neuromuscular blocking agent succinylcholine, which should
be discontinued. Hyperthermia due to its effects on various organs is a
more serious condition.
Management
1.
2.
3.
4.
Ensure A, B and C.
100 percent oxygen inhalation.
Pulse oximetry.
End tidal CO2: Increase in ET CO2 is the earliest sign of malignant
hyperthermia.
5. ECG monitor.
6. IV access Bolus with cold Normal Saline 10 to 20 ml/ kg.
7. Iced saline to stomach by NG lavage and ice packs to groin and axilla.
It is ideal to shift the child to ICU for further management.
Further Management Includes

1. Dantrolene as muscle relaxant.
2. Management of acidosis by hyperventilation or sodium bicarbonate.
3. Ventricular arrhythmias: Procainamide is the preferred antiarrhythmic.
4. Myoglobinuria: Normal saline bolus, mannitol, frusemide.
5. Other complications like hyperkalemia, DIC.
Bibliography
1.
12.8
Accidental Hypothermia
Accidental hypothermia occurs either by cold water immersion or by continuous non-immersion exposure to cold environment.
Hypothermia is defined as core body temperature 35C (95F).
Profound hypothermia is generally <28C (82F).
Moderate hypothermia is 30C (86F) to 32C (89F).
Factors Influencing Thermo Regulatory Balance in

Pediatric Age Group
1.
2.
3.
4.
Large surface area/body weight ratio.

Minimal subcutaneous fat.
Thin skin with increased permeability.
Delayed shivering and inefficient ability to generate heat compared to
adult.
5. Immature or inappropriate behavioral response to environment.
6. However, brown fat cells, found abundantly in certain infants bodies in
areas like neck and shoulder region allows for a tripling of heat production may be advantageous to young children or infants.
Common Complications of Severe Hypothermia

1.
2.
3.
4.
5.
6.
7.
Dysrryhthmia.
GI bleeding.
Acute renal failure.
Pancreatitis.
Deep vein thrombosis.
DIC.
Pulmonary edema.
Laboratory Findings and Investigations

1. ABG: ABG correction according to temperature variation is given in
Table 12.8.1.
297
Chapter 12.8: Accidental Hypothermia

TABLE 12.8.1: ABG correction according to temperature variation
pH Unit
PCO2 (mm Hg)
PO2 (mm Hg)
Above 37C
Below 37C
Change/C>37C
-0.015 unit
+4.4%
+7.2%
Change/C<37C
+0.015 unit
-4.4%
-7.7%
2. Hyperkalemia May be secondary to metabolic acidosis, renal failure,

rhabdomyolysis.
3. Blood glucose (Hyperglycemia is common due to low glucose metabolism), calcium, magnesium.
4. PT, PTT, platelet count, and fibrinogen level (Thrombocytopenia is
common, hypercoagulability may exist with DIC syndrome).
5. Urea, creatinine, amylase, hematocrit.
6. Radiography and CT Scan Brain particularly not helpful unless fracture and trauma suspected.
7. ECG:
i. J wave or Osborne wave when core temperature near 30C (It is
a positive deflection on the RT segment).
ii. Bradycardia, atrial fibrillations are common and often unmanageable with medication until core temperature reaches 30C.
Clinical Features
The clinical findings with progressive hypothermia is shown in Table 12.8.2.
TABLE 12.8.2: Clinical findings with progressive degree of hypothermia
State of hypothermia
Core temp in
F (Rectal)
Core temp in
C (Rectal)
Mild
99.6
95
37.6
35
Moderate
89
32
86
30
82
28
79
77
26
25
68
59
20
15
Severe
Clinical findings
Normal homeothermic state
Maximal shivering and slurred
speech
Change in consciousness and blood
pressure. Muscle rigidity and incoordination. Shivering ceases. Pupils
fixed but reacts to light.
Respiratory rate decreases, stuporous state begins, many resuscitation
drugs inactive
Bradycardia refractory to atropine,
Osborne wave, voluntary motion
ceases, pupils nonreactive to light
Areflexic, loss of consciousness
Pulmonary edema, ventricular fibrillation, appears dead, no respiration
Cardiac asystole
Lowest core temp infant to survive
298
Management
Mild hypothermia does not require hospitalization or special care other
than prevention of further heat loss. Patient progressing to moderate to
severe hypothermia may become physically, mentally and metabolically
incapable of reversing the situation unless intervened.
Prehospital Phase
1. No one is dead though may look that way until they are warm.
2. Initial assessment should focus on cervical spine or traumatic injury,
hypoglycemia, near drowning management, removal of wet clothes.
3. Measure core temperature, 1 minute respiratory rate, as apneic patient should be intubated, if facilities available.
4. O2 may be single most important medicine in prehospital set-up if
patient is in metabolic ice box.
5. Dont consider active means of external re-warming unless patient is
conscious or in prehospital set-up.
6. Initial CPR if in collapse rhythm (Ventricular fibrillation or asystole).
Hospital Phase and Treatment

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Humid oxygen preferably warm to 40 to 42C (103105F).

Definitive airway stabilization.
IV support.
Injury and cervical spine precaution.
Accurate vital signs and monitoring.
Doppler ultrasound may be necessary to locate pulse.
Remove remaining clothing and cut off from wet body parts. Insulate
properly with warm clothing and warm room environment.
CVP line to monitor volume status. Aggressive but controlled fluid resuscitation is often required. Arterial line for repeated ABG.
NG tube and Foleys catheter to be inserted.
Resuscitation fluid may be warmed by a blood warmer (hemotherm) if
rate of infusion is not rapid. Counter current inline warmers and rapid
infusion of prewarmed saline could be used for required transfusion.
NS and Dextrose-NS are preferable and Ringers lactate should not be
used as liver cannot metabolize lactate as it is in the metabolic ice box.
Frozen extremities should not be thawed until all control means are in
place or core temperature >32 to 34C.
Rewarming Techniques
External Techniques
1. Warm clothing and warm ambient temperature.
2. Rewarming jackets and cushion (e.g. provided by Baer-Hagger machine).
299
Internal Rewarming by Extracorporeal Techniques

1. Rewarming hemodialysis or bypass (warm blood pretreated in a
hemotherm is circulated through hemodialysis technique).
2. Other techniques includesperitoneal, gastric, rectal lavage or heated
intravenous fluid.
Rewarming is discontinued once core temperature is approximately
36C to avoid over heating. Advantages of extracorporeal technique include rapid return to normal temperature and reduction of blood viscosity
despite cardiac instability.
Common resuscitation drugs especially dopamine has deleterious effects as they accumulate and produce potential toxity after rewarming and
hence should be avoided except O2.
Dysrhythmias
It is common but it in self-correcting once returns to normothermnia. Both
asystole and atrial or ventricular fibrillation are documented. Recent studies have shown bretyllium is better choice than lidocaine both in prophylaxis
and therapy of ventricular fibrillation in hypothermia. Chemical therapies
not recommended below core temp to 30C and electrical cardioversion is
rational to attempt 3 standard defibrillation before resuming CPR though
may be unsuccessful. Magnesium is another benign drug has been used
with success. There is no advantage of pacing and have actually precipitated VF.
Sepsis
Hypothermia induced depression of immune systems and hence predisposed to sepsis. Prophylactic broad spectrum antibiotics are recommended
in patients with moderate or severe hypothermia.
Management of other complicationssee respective chapters.
Prognosis
Survival is unlikely if
1. Core temp <15C (59C).
2. K+ >10 mEq/L.
3. Fibrinogen <50 mg/dl.
4. Total environmental exposure >24 hours.
5. No cardiac rhythm.
Frostbite
Frostbite is associated with tissue freezing and vascular disruption is produced by a significant cold stress associated with a decrease in blood flow to
involved skin and different body areas. The impaired blood flow does not
deliver sufficient heat to the tissue, resulting in freezing injury.
300
Pathophysiology
First mechanism is ice crystal formation in the tissue and skin especially in
the extracellular space. It draws water from the cells resulting in intracellular hyperosmolality reaching to toxic levels. Second issue is vascular stability
and abnormal blood flow in the distal parts of involved skin and surface
organ systems.
Diagnostic Findings
Frostbite occurs on the most distal or exposed skin areas. The early stage of
freezing injury, frost nip is reversible stage of the progressive disorder. Progression of frostbite beyond frost nip occurs in two stages:
1. Superficial frost bite: Involves skin and immediate underlying layer of
subcutaneous tissue.
2. Deeper frost bite: Involves skin, subcutaneous tissue and deeper structure such as muscle, tendon or bone.
Clinical Features
Depends on depth of injuries and area involved.
Frost nip: Sensation of intense cold and numbness.
Superficial Frost Bite

i. No pain or sensation.
ii. Pain starts during thawing process.
iii. Skin has white or paraffin like appearance with no or little capillary
refill.
iv. Edematous, erythematous, purplish or mottled affected area.
v. Eschar can form, may be mistaken for gangrene.
Deeper Frost Bite

i. No pain, even painless after rewarming because sensory nerve ending may be damaged.
ii. Even after thawing color of skin is mottled or grayish.
iii. Blister formation doesnt occur but if formed are generally hemorrhagic.
Management
1. Rapid rewarming or rapid thawing of the frozen body part by immersion in water warmed between 38 to 43C (100110F). The process
takes 20 to 30 minutes.
2. Do not warm slowly as can result in further tissue damage. Never warm
in a situation where refreezing can occur and can cause maximum tissue damage.
3. Patient may require analgesic IV due to intense pain.
301
4. After rapid thaw next focus will be on preventing infection, aiding circulation and tetanus prophylaxis.
5. Hyperbaric O2 has been advocated by some clinicians.
Disposition
Frost bite is best managed in a burn unit with strict use of aseptic techniques. Growth plate injury has been reported, though there is no method
to prevent this injury at present and parents need to be warned against it.
Bibliography
1.
13
POISONING
13.1
General Management Principles and
Approach to Unknown Poisoning
Poisoning in children is usually unintentional, involves a single substance

found in the household and results in minimal toxicity. It is related to their
natural inquisitive, exploratory behavior parental underestimation of the
capabilities of the children.
Management
Three basic aspects have to be remembered regarding management of poisoning. When a child presents with unknown, or any poisoning, the child is
most likely to recover if ABC is taken care of, timely and adequate gut
decontamination is done and complications are effectively managed.
ABC
This is true for any poisoning. Adequate airway and breathing are priority.
Circulatory compromise should be managed with fluid resuscitation.
Surface Decontamination
Exposure and contamination of skin requires thorough irrigation with water. Particular attention should be given to hair, fingernails and skin folds.
Soap water washing is indicated for hydrocarbons and oily substances. Eye
exposure should also be washed with saline water.
Gastrointestinal Decontamination
Ideally should be done within 1 hour of ingestion, but should not be denied if the child presents late. Largest possible orogastric tube should be
inserted. Patient in left lateral position, normal saline at 15 ml/kg aliquots
should be used to wash the stomach contents. The first return sample should
be preserved for forensic testing. Lavage should be continued till clear
fluid returns. If the patient is obtunded, airway should be protected with
an endotracheal tube.
Emesis should not be induced in pediatric patients.
Activated charcoal: It should be administered before removal of the lavage
tube. It absorbs poison even distal to pylorus and interrupts enterohepatic
306
circulation. Dose is 1 gm/kg diluted 1:4 with water or juice. Acids, alkalis,
essential oils, cyanide, alcohol, metals like iron, lead, mercury and pesticides like malathion and DDT are not bound by charcoal.
Whole bowel irrigation (WBI): Iso-osmolar polyethylene glycol electrolyte
solution (PEGLEC, Tablets, India) is used at a dose of 30 ml/kg/hour for 6
8 hours until the fecal effluents are clear. It flushes out the gastrointestinal
tract without causing fluid and electrolyte shifts. This technique is useful in
cases of delayed presentation.
Enhanced Elimination
This is reserved for severe toxicity and deterioration in vital function despite adequate supportive therapy.
Alkalinization of urine: Useful for elimination of weak acids like salicylates
and barbiturates. The aim is to achieve urine pH of 7.0 to 8.0. Sodium
bicarbonate is given 2 ml stat followed by 1 to 2 ml/kg infusion over 6
hours.
Hemodialysis and peritoneal dialysis: Both are effective in removal of absorbed toxins, former is more effective.
Antidotes
Most of poisoning cases respond well to general measures, specific antidotes are rarely required.
Bibliography
1.
2.
Bates N, Edwards N, Roper J, Volans G Editors. Pediatric Toxicology: Handbook of Poisoning in Children. McMillan Reference Ltd, 1997.
Tenenbein M. Recent Advances in Pediatric Toxicology. Pediatric Clinics of
North America 1999;46:1179.
13.2
Various Poisonings
Jayanta Bandyopadhyay, Joshi Anand Karketta
Paracetamol
Paracetamol overdose in pediatric population may be either unintentional,
usually up to school going age or intentional in adolescent or sometimes
following depression. Hepatocellular damage is life-threatening and the
main cause of concern but fortunately it is less frequent.
Risk Factors for Hepatotoxicity

1.
2.
3.
4.
5.
Presentation to the emergency department more than 24 hrs ingestion.

Age range 10 to 17 years.
Intentional overdose.
Caucasian race.
Ingestion of 100 mg/kg or more in known liver disease, cystic fibrosis,
alcohol abuse or on anticonvulsant or barbiturate therapy or recent
high intake of paracetamol.
Manifestations
Paracetamol overdose manifests with multisystem involvement.
Gastrointestinal
Nausea, vomiting and abdominal pain may develop soon after ingestion
and also may recur 12 to 24 hrs later. Serum amylase may be high though
clinical sign of pancreatitis may not be obvious.
Hepatic
Laboratory evidence of deteriorating LFT starts within 24 to 48 hrs and
peaks 3 to 4 days post ingestion. Vomiting, right sided abdominal pain,
jaundice, coagulopathy, hypoglycemia and finally encephalopathy ensues
slowly on day 3 to 4 after paracetamol ingestion. Metabolic acidosis is common in patients 3 to 4 days after ingestion with evolving hepatic failure.
308
Genitourinary
Transient nephrotoxic effects include acute tubular necrosis, flank pain
and hematuria.
Monitoring and Laboratory Investigations

1. Ideally a 4 hour post-ingestion plasma acetaminophen level should be
obtained. It should be plotted on the Rumack-Matthew nomogram to
determine potential risk of hepatotoxicity and need for NAC (N-acetyl
cysteine) therapy. Check you are using the correct units (1 mg/L = 6.5
micromol/L).
a. Levels drawn earlier may not reflect complete absorption and
cannot be used to predict risk of hepatotoxicity and need for
NAC therapy.
b. The nomogram is designed to be used for single acute ingestion
and not helpful in determining the need for NAC in chronic ingestion.
c. NAC treatment should not be started unless the nomogram indicates a potentially toxic paracetamol level.
Rumack-Matthew nomogram is shown in Figure 13.2.1.
FIG. 13.2.1: Rumack-Matthew nomogram
Chapter 13.2: Various Poisonings
309
2. Determine LFT, coagulation profile on admission as baseline and daily

for 3 days or until levels begin to return to normal. If significant abnormalities in LFT develop then renal function, electrolytes, glucose,
amylase, full blood count, urinalysis, ECG should be followed as clinically indicated.
Management
1. Activated charcoal: 1 gm/kg immediately if less than 1 hour since ingestion in the proportion 240 ml water/30 gram charcoal.
2. N-acetyl cysteine (NAC): According to FDA/Prescott protocol, NAC
therapy should preferably be initiated within 8 hours of ingestion, but
is effective when given even more than 24 hours postingestion.
a. Loading dose: 150 mg/kg NAC in 200 ml of 5 percent dextrose over
15 minutes,
b. Second infusion: 50 mg/kg NAC in 500 ml of 5 percent dextrose
over next 4 hours,
c. Third infusion: 100 mg/kg NAC in 1000 ml of 5 percent dextrose
over next 16 hours.
In young children to avoid excessive amount of free water, prepare a
NAC solution of 40 mg/ml (50 ml of 20% NAC + 200 ml of 5% dextrose = 40 mg/ml) and administer as below:
i. Loading infusion: 150 mg/kg (3.75 ml/kg) infused over 15 minutes.
ii. Second infusion: 50 mg/kg (1.25 ml/kg) over 4 hrs (0.31 ml/kg/hr).
iii. Third infusion: 100 mg/kg (2.5 ml/kg) over 16 hrs (0.16 ml/kg/hr).
In patients who develop hepatic injury secondary to paracetamol, NAC
therapy (0.16 ml/kg/hr) should be continued until liver function improves.
Adverse event: Anaphylactoid reactions to NAC may manifest with wheeze
and rash. In such situations, infusion should be stopped for 30 minutes and promethazine 0.2 mg/kg IV should be given and infusion
should be started at half the previous rate. Increase the rate slowly
over time until the desired rate is again reached.
Oral NAC is available as 10 percent and 20 percent solution. It
should be diluted to 5 percent solution with fruit juice.
a. Loading dose: 140 mg/kg orally as a 5 percent solution,
b. Maintenance dose: 70 mg/kg orally as a 5 percent solution every 4
hours for a total of 17 doses. No change in the dose is necessary in
patients who have received activated charcoal.
3. Hepatic failure: Supportive measures for hepatic failure should be
started and NAC continued until hepatic function improves.
Management of paracetamol overdose is shown in Flow chart 13.2.1.
Iron
Oral iron preparation may be tablets, capsules in immediate release or
modified release form or liquid. Toxicity depends on the elemental iron in
310
Flow chart 13.2.1: Management plan of paracetamol overdose
the compound. Overdose with parenteral preparation and other industrial

poisoning is out of the scope of this book. The elemental iron content of
different iron salts and toxic doses of iron are shown in Tables 13.2.1 and
13.2.2 respectively.
Mode of Action of Iron

1. Early features are due to corrosive and vascular effects while later are
largely due to disruption of cellular process.
2. Iron tablets may adhere to the stomach or duodenum causing irritation, hemorrhagic necrosis and perforation of gastric and jejunal
mucosa.
3. Consequent fluid and blood loss can be enormous and compounded
by post arteriolar dilation, venous pooling and increased capillary permeability leading to hypovolemia and decreased cardiac output. This
ultimately results in tissue hypoxia, lactic acidosis, shock and cardiac
failure.
4. Iron is rapidly cleared from extracellular space by parenchymal cell
uptake mainly in liver causing mitochondrial damage, interfering cellular respiration, metabolic acidosis and cell death.
311

TABLE 13.2.1: Elemental iron content of different iron salts
Iron salts
Ferrous sulfate
Elemental iron (%)
Ferrous gluconate Ferrous fumerate Ferrous succinate
20
12
33
35
TABLE 13.2.2: Toxic doses of iron

Toxicity
Elemental iron
mg/kg of body weight
Serum iron at
4 hours (gm/dL)
Serum iron at 4
hours (mol/L)
Mild
Moderate
Severe
Lethal
<30
>30
>60
>150
110-300
300-500
500
1000
20-55
55-90
>90
>180
5. Widespread organ damage follows, liver being chiefly affected. Hepatic failure with hypoglycemia, coagulopathy often turns fatal.
Laboratory Monitoring
1. Complete blood count, blood glucose, electrolytes, blood group and
cross match, baseline liver function and coagulation profile.
2. Abdominal radiograph may show undissolved iron tablets as they are
radiopaque
3. 4 hours serum iron level. Earlier, if dexferroxamine therapy planned
before 4 hours.
4. Further tests depending on the clinical status (LFT, coagulation profile, serum iron level, etc.).
5. If serum iron level not available: Vomiting and/or diarrhea, blood glucose >150 mg/dL, leukocytosis (>15,000 cell/mm3) signify high serum
concentration. Abdominal X-ray can give clue to amount of iron ingested provided X-ray taken almost immediately. Presence of coma,
leukocytosis, metabolic acidosis, elevated anion gap is associated with
iron concentration >90 mol/l (500 g/dL).
Clinical Features
The clinical course of iron poisoning is described in Table 13.2.3.
TABLE 13.2.3: Clinical course of iron poisoning in various phases
Phase
Onset and duration
Clinical features
I.
0.56 hours
II.
624 hours
Nausea, vomiting, abdominal cramps, dark red vomitus

and stool. Leukocytosis and hyperglycemia. Drowsy, lethargic, comatosed, convulsive, in shock and metabolic
acidosis in severe cases.
Latency. Apparent recovery and false sense of security.
May not be so in severe toxicity.
Contd...
312
Contd...
Phase
Onset and duration
III.
1248 hours
IV.
24 days
V.
28 weeks
Clinical features
Severe lethargy, coma, convulsions, shock, GI hemorrhage,
metabolic acidosis, cardiovascular collapse, hepatic and
renal failure, pulmonary edema.
Hepatic failure, encephalopathy, acute lung injury. Monitor liver functions and bilirubin closely.
Stricture formation, gastric and pyloric scarring. Small intestinal necrosis and obstruction in sustained release
preparations. Evaluate with barium contrast studies.
Management
Iron ingestion management plan is shown in Flow chart 13.2.2.
1. Stabilization and support: Shock should be treated accordingly. Blood
products may be necessary. Control any seizure and protect airway.
Initiate baseline investigations.
2. Decontamination:
i. Repeated gastric lavage may be undertaken to remove all tablets
if they are proximal to pylorus. Perform after airway protection
is assured.
ii. If iron tablets are beyond pylorus whole bowel irrigation is the
method of choice.
iii. Few clinicians prefer to perform endoscopic removal of retained
tablets in the stomach.
Polyethylene glycol balanced electrolyte solution (PEGLEC) orally
or by nasogastric tube is used for whole bowel irrigation. Patient should
be seated and/or the head of the bed elevated at least at 45 degree
angle.
9 months to 6 years500 ml/hr continue until rectal effluent is clear.
6 to 12 yrs1000 ml/hr continue until rectal effluent is clear.
>12 yrs2 liters initially followed by 1.5 to 2 liters/hr continue until
rectal effluent is clear.
3. Chelation therapy: The decision to use desferroxamine (DFO) should
be based on clinical status and laboratory value. DFO chelates free iron
removing from cellular binding sites and imparts a pink-brown color
(Vin-Rose color) to the urine.
Indication: Serum iron concentration up to 55 to 90 mol/L (300-500
gm/dL) should be observed for 24 to 48 hours and gastric lavage/
bowel irrigation/endoscopic removal are enough if asymptomatic or
have nonbloody diarrhea or vomiting.
IV desferroxamine is urgently needed in patients with hypotension
shock, lethargy, coma or convulsion or serum iron concentration
>90 mol/L.
Dose: 15 mg/kg/hour (may be reduced after 24 hours).
Adverse effects: Faster rates, IV boluses or higher doses cause hypotension but infusion rates up to 35 mg/kg/hr has been used in children.
313
Flow chart 13.2.3: Iron ingestion management plan
Discontinuation: End point is adjusted when symptoms subside and urine

color is clear. This generally corresponds to 8 to 12 hours in moderate
toxicity and 24 hours or longer with severe toxicity.
4. Hemodialysis: Only useful to remove iron-desferroxamine complex in
renal failure.
Practice Points
1. Ranitidine does not have any clear benefit as iron causes direct mucosal injury, sloughing and hemorrhage.
2. Oral desferroxamine is no longer recommended.
3. Activated charcoal does not bind iron to any significant amount and
makes endoscopy difficult should it be required later.
4. Iron tablets that have already dissolved and liquid preparations are
not radiopaque.
5. Patient should be advised to come back in the following 2 to 6 weeks if
recurrent vomiting due to risk of pyloric stenosis or stricture formation.
314
Salicylates
Despite relatively less use, salicylate poisoning in pediatric age group is
still quite common. Many times the outcome is fatal.
Clinical Features
1. General features: Profuse sweating, red and swollen face, paresthesia
and muscle weakness.
2. Central nervous system: Headache, vertigo, lethargy, mental confusion,
convulsion and coma.
3. Cardiovascular: Tachycardia is the characteristic feature.
4. Gastrointestinal: Nausea, vomiting, epigastric pain, hematemesis and
malena.
5. Respiratory: Tachypnea and hyperpnea followed by acidotic breathing, pulmonary edema.
6. Renal: Oliguria or anuria.
7. Vision and hearing: Tinnitus, deafness and blurring of vision.
8. Others: Dehydration, hypo or hyperglycemia, fever, bleeding tendency
due to defective platelet aggregation, hypo or hypernatremia.
Severity of Intoxication
The severity of intoxication is determined by blood salicylate level as depicted in Table 13.2.4.
Fatal Dose
The minimum acute toxic dose is 150 mg/kg. Usually symptoms appear
within 1 to 3 hours of ingestion.
Investigations
1.
2.
3.
4.
5.
6.
7.
8.
CBC.
Blood salicylate level.
Blood glucose.
Serum electrolytes.
Pyruvate, lactate (Generally elevated).
Coagulation profile, liver function.
Renal function.
ABGmixed acid base disturbance where a metabolic acidosis follows
a respiratory alkalosis.
TABLE 13.2.4: Severity of intoxication as per blood salicylate level

Blood salicylate level (mg/dL) at 6 hours
<50
50-100
> 100
Level of severity
Mild
Moderate
Severe
315
Management
1. General supportive care like airway, breathing, circulation.
2. Gastric wash and activated charcoal (As soon as possible).
3. Repeated dose of activated charcoal is advisable till salicylate level is
falling; whole bowel irrigation is also helpful.
4. Obtain serum salicylate level at presentation and 6 hrs after ingestion.
5. Treat shock with plasma or 5 percent albumin at 10 ml/kg.
6. Ensure adequate urine output by boluses of 20 ml/kg of fluids. (at least
1 ml/kg/hr of urine). The fluid should contain Na 75, K 40, HCO3 25,
Cl 50 mEq and glucose of 5 to 10 percent solution per liter. The aim is
a urine output of 3 ml/kg/hr with a urine pH of >7.5.
7. After ensuring adequate urine output, alkalinize urine by infusing a solution of 5 percent dextrose with Na 40, K 35, HCO3 20, Cl 50 mEq/L.
8. Even with normal glucose, brain may suffer from neuroglycopenia,
so administer glucose.
9. Keep serum potassium level in higher normal range (both sodium
bicarbonate and tachypnea lower potassium level).
10. Treat fever by tepid sponging.
11. Control seizure with phenobarbitone, hypocalcemic tetany with 10
percent calcium gluconate, prolonged PT with vitamin K, respiratory
failure with ventilatory care.
Indication of Dialysis
1. Salicylate over 100 mg/dL, as this level is usually associated with severe
toxicity.
2. Severe acidosis, oliguria or anuria.
3. Pulmonary edema.
4. Intractable seizures.
Acid
Acids are used in various day-to-day utilities. The common acids found are
the following:
Household Products
1. Toilet bowl cleaner (Sulfuric acid, hydrochloric acid, oxalic acid, sodium
bisulfate).
2. Drain cleaner (Sulfuric acid), metal cleaner and antirust compounds (Phosphoric acid, oxalic acid, sulfuric acid, hydrochloric acid, chromic acid).
3. Pool sanitizer (Calcium and sodium hypochloride).
4. Automobile battery fluid (Sulfuric acid).
Industrial Uses
1. Plating, photography, cement manufacturing, leather tanningchromic anhydride.
316
2.
3.
4.
5.
6.
7.
Bleaching, metal refining, plumbinghydrochloric acid.

Disinfectant, metal cleaning, rust proofingphosphoric acid.
Tanning band blueprint paperoxalic acid.
Preservative in foodcitric acid.
Print, dye and rayon manufacturingacetic acid.
Fertilizer manufacturingsulfuric acid.
Acids According to Strength and Effect

Weak Irritant
Strength 5 to 10 percent.
Acetic acid, aluminium sulfate, ammonium nitrate, calcium chloride anhydrous.
Strong Irritant
Strength 10 to 50 percent.
Acetic acid, phosphoric acid, hydrochloric acid, sulfuric acid, zinc chloride.
Corrosive
Strength >50 percent.
Sulfamic acid, sulfuric acid, zinc sulfate, glycolic acid.
Clinical Features
Contact and ingestion of acid may affect various systems of the body.
Gastrointestinal
GI bleeding, gastritis, perforation, edema, necrosis, vomiting, stenosis, fistula, acute hepatic injury. Esophageal, pyloric or laryngeal stricture are
late sequelae after 3 to 4 weeks.
Respiratory
Dyspnea, pleuritic chest pain, pulmonary edema, upper airway edema,
bronchospasm, pneumonitis.
Cardiovascular
Cardiovascular collapse.
Genitourinary
Renal failure, hemoglobinuria, nephritis (Following hydrochloric acid poisoning).
Acid Base Balance and Fluid

Metabolic acidosis, hyperkalemia after hemolysis, fluid shift following extensive burn.
317
Hematologic
Hemolysis.
Dermatological
Cellulitis, sepsis, contracture, osteomyelitis.
Eye
Pain, swelling, corneal erosion and blindness.
Investigations
1. Baseline CBC, electrolytes, renal and hepatic function including coagulation study.
2. Chest X-ray should be done in children with pulmonary symptoms.
Management
As with any acute care management, airway and breathing should be maintained by intubation, cricothyrotomy or tracheostomy if required.
Circulation should be taken care of. Hypotension and shock if any should
be treated with IV bolus fluid.
Dermal
Remove contaminated clothing and wash the exposed area with copious
amount of water.
Eye
Irrigate the eyes with normal saline at least for an hour or until cul-de-sac
are free of particulate matter and returned to neutrality (It can be confirmed by testing with pH paper). If pain, swelling, lacrimation, photophobia
persists, consult ophthalmologist.
Inhalation Exposure
Move to fresh air, provide oxygen if breathing difficulty, assisted ventilation if situation worsens, treat bronchospasm with 2 agonist and oral/
parenteral steroid.
Oral/Parenteral Exposure
i. Mucosal decontamination: Dilute with water or milk if no respiratory
distress is present.
ii. Gastric decontamination: Use of emetic is contraindicated. Consider
flexible NG tube to suction gastric content if large ingestion but risk
of further mucosal injury must be weighed against potential benefit.
Oral fluid is started if patient can swallow saliva, otherwise gastrostomy feeding or hyperalimentation are other choices.
318
iii. Endoscopy: Evaluation recommended within 24 hours even in asymptomatic children and follows-up 10 to 20 days later with barium swallow.
iv. Pharmacologic treatment: Corticosteroids are controversial, consider
where no GI bleed or perforation. Antibiotics in suspected perforation, infection and patients receiving steroids.
v. Surgical options: If esophageal burn is found, a string may be placed in
stomach to facilitate dilatation later. Dilatation is indicated after
2 to 4 weeks if stricture is confirmed. If unsuccessful, colonic intraposition
or gastric tube placement later may be performed. Consider early laparotomy in patients with severe esophageal or gastric burn.
Alkali
Different alkali preparations are also used in various household materials
and cleaning items. Common alkalis are found in the following:
1. Bathroom and household cleaningsodium hypochloride.
2. Cementcalcium oxide.
3. Automobile airbagssodium hydroxide.
4. Electric dishwasher soapsodium tripolyphosphate.
Clinical Features
Alkali affects all the systems of the body.
Cardiovascular
Tachycardia, hypotension.
Respiratory
Dyspnea, stridor, pulmonary edema, upper airway edema especially with
vapourized caustic.
Gastrointestinal
GI bleeding, gastritis, perforation, edema, necrosis, mediastinitis, stenosis, fistula and much later gastric carcinoma. Esophageal, pyloric or laryngeal
stricture are late sequelae after 3 to 4 weeks.
Acid Base Balance and Fluid

Metabolic acidosis following extensive burn.
Dermatological
Severe skin irritation and burn.
Face and Eye

Pain, swelling of lips, tongue, oral mucosa. Loss of corneal, conjunctival
and lens epithelium and loss of endothelium of cornea and blood vessels.
319
Investigations
1. Baseline CBC, electrolytes, renal parameters and coagulation profile.
2. Chest X-ray in children with pulmonary symptoms.
Treatment
Airway should be maintained by intubation, cricothyrotomy or tracheostomy if required. Hypotension and shock if present should be treated with
IV bolus fluid.
Dermal
Promptly remove contaminated clothing and wash the exposed area with
copious amount of water.
Eye
Irrigate eye with normal saline at least for an hour or until cul-de-sac are
free of particulate matter and returned to neutrality (It can be confirmed
by testing with pH paper). If pain, swelling, lacrimation, photophobia persists, consult ophthalmologist.
Inhalation Exposure
Move to fresh air, provide oxygen if breathing difficulty, assisted ventilation if situation worsens, treat bronchospasm with 2 agonist and oral/
parenteral steroid.
Oral/Parenteral Exposure
i. Mucosal decontamination: Dilute with water or milk if there is no
respiratory distress.
ii. Gastric decontamination: Use of any emetic is contraindicated. Consider flexible NG tube to suction gastric content if large ingestion
but risk of further mucosal injury must be weighed against potential
benefit. Oral fluid is started if patient can swallow saliva, otherwise
gastrostomy feeding or hyperalimentation are other choices.
iii. Endoscopy: Evaluation recommended within 24 hours in children
with stridor, vomiting, drooling, dysphagia, refusal to swallow, abdominal pain and follow 10 to 20 days later with barium swallow.
iv. Pharmacologic treatment: Corticosteroids are controversial, consider
where no GI bleed or perforation. Antibiotics in suspected perforation, infection and patients receiving steroids.
v. Surgical options: If esophageal burn is found, a string may be placed in
stomach to facilitate dilatation later. Dilatation is indicated after
2 to 4 weeks if stricture is confirmed. If unsuccessful, colonic intraposition
or gastric tube placement later may be perfomed. Consider early laparotomy in patients with severe esophageal or gastric burn.
Point to note: Significant corrosive injury is unlikely to occur from a
substance with a pH less than 11.
320
Hydrocarbons
Hydrocarbons may be of the following types:
1. Low viscosity, unsubstituted: Most likely to cause aspiration pneumonitis.
Vapor inhalation can cause CNS depression. Examples are kerosene,
mineral seal oil, gasoline, petroleum naphtha.
2. High viscosity, unsubstituted aliphatic: Poorly absorbed from GI and
less likely to cause lipoid pneumonia. Examples are motor oil and petroleum jelly.
3. Terpenes: In addition to aspiration may cause CNS depression. Examples are pine oil and turpentine oil.
4. Aromatics: High-risk for CNS depression, mild-risk for cardiac irritation and little risk of aspiration. Examples are benzene and xylene.
5. Halogenated-chlorinated: Can produce CNS effect, arrhythmias, renal
and hepatic effect. Examples are chloroform, carbon tetrachloride and
trichloroethylene.
Clinical Features
Respiratory
Coughing, choking, tachypnea, dyspnea, cyanosis, crepitations in chest,
hemoptysis, pulmonary edema, pneumatocele, lipoid pneumonia, respiratory arrest is the ultimate consequence.
Gastrointestinal
Nausea, vomiting, abdominal pain and diarrhea.
Neurologic
Mild CNS depression to excitement is common after ingestion or vapor
inhalation. CNS effects are secondary to hydrocarbon pneumonitis and
hypoxia. Some hydrocarbons are simple asphyxiants.
Hepatic
Elevated hepatic transaminases. Carbon tetrachloride is a potent hepatotoxin.
Genitourinary
Acute tubular necrosis, proteinuria, hematuria though infrequent. Acute
renal failure has been reported from chronic glue, solvent, halogenated
hydrocarbons.
Hematologic
DIC, hemolytic anemia, pancytopenia. Benzene is bone marrow toxin, associated with acute leukemia.
321
Cardiovascular
Various dysrhythmias.
Musculoskeletal
Rhabdomyolysis, thrombosis, tissue necrosis following high pressure injection.
Investigations
Investigations are indicated when patients are symptomatic with wheeze,
dyspnea, retractions, tachypnea and persistent coughing.
1. ABG: Documents hypoxemia and hypercarbia.
2. Chest X-ray: To be done at least 6 hours after ingestion, to look for
perihilar opacities, basilar infiltrates and atelectasis. Other documented
complications of hydrocarbon aspiration include pneumatocele, pleural effusion, empyema, pneumothorax.
3. ECG.
4. Pulse oximetry.
5. Also CBC, urinalysis, liver and kidney function, electrolytes depending on the situation.
6. Check methemoglobin where exposure to nitrobenzene and aniline is
suspected and not responding to supplemental oxygen.
Lethal Dose
Severe pneumonitis has been observed in animals even when less than 1
ml of some hydrocarbons are directly aspirated.
Criteria for Hospital Admission

1. Respiratory distress or abnormal chest radiograph.
2. Significant CNS depression or seizure.
3. Any progressively worsening symptoms (Vomiting, abdominal pain, tachypnea) after a period of observation.
Management
Pure Petroleum Distillates
Gastric decontamination not indicated as systemic toxicity is unlikely.
Other Hydrocarbons
i. Decision to decontaminate the stomach depends on toxicity of the
agent, volume ingested, time since ingestion and patients clinical
status.
ii. The potential for rapid CNS depression, seizure, respiratory depression and aspiration must be considered.
322
iii. Gastric emptying may increase the risk of aspiration. Many prefer
activated charcoal alone than gastric lavage for those who require
decontamination.
iv. Gastric aspiration may be done after endotracheal intubation using
a small flexible nasogastric tube.
v. Activated charcoal is ideal in cases of large amount of ingestion and
very toxic additives. Dose for children is 25 to 50 gm (1 to 12 years)
and 1 gm/kg for <1 year.
Inhalation Exposure
Move to fresh air, administer oxygen, assisted ventilation if required. Evaluate for RTI, treat bronchospasm with 2 agonist and oral or parenteral
corticosteroid.
Eye Exposure
Irrigate eye with room temp water at least for 15 minutes. Consult eye
specialist if pain, swelling, irritation or lacrimation persists.
Moth Balls (Naphthalene)

Naphthalene balls are small, white and children often mistake as things to
play with Figure 13.2.2. It may cause severe hemolysis in patient with G6PD
FIG. 13.2.2: Naphthalene balls
323
deficiency. Newborns, if they ingest accidentally are more susceptible to

complications resulting in kernicterus. Hemolysis and jaundice have occurred after dressing infants in clothing stored with moth balls.
Clinical Features
1.
2.
3.
4.
Acute intravascular hemolysis especially in G6PD deficiency.

Fever, jaundice, anemia, hemoglobinuria, dermatitis.
Headache, nausea, vomiting, abdominal pain.
Excitement, coma, acute renal failure, pulmonary edema, kernicterus
(In neonates) in extreme cases.
Lethal dose5 to 15 gm.
Investigations
1.
2.
3.
4.
CBC and reticulocyte count, serum bilirubin.

Urine for hemoglobin.
Methemoglobin estimation.
G6PD screening.
Management
1.
2.
3.
4.
Activated charcoal as slurry, most effective within 2 hours.

Ask for packed RBCs if there are symptoms of hemolysis.
Exchange transfusion to halt progression to kernicterus.
Forced alkaline diuresis with sodium bicarbonate orally 5 gm every 4
hourly and frusemide 1 mg/kg once.
5. Avoid milk and fatty food.
6. Hydrocortisone IV for prevention of hemolysis.
7. IV methylene blue for methemoglobinemia.
Organophosphorus Compound
Toxicity is usually associated with products formulated for outdoor use.
Household products rarely cause significant toxicity.
Muscarinic Effects
The manifestations can be effectively summarized by the mnemonics SLUDGE
and DUMBELS. SSalivation, LLacrimation, UUrination,
DDefecation, GGastrointestinal cramps, EEmesis and DDiarrhea,
UUrinary incontinence, MMiosis and muscle fasciculation,
BBronchorrhea, bronchospasm and bradycardia, EEmesis.
Nicotinic Effects
Tachycardia, hypertension, fasciculation, mydriasis, muscle cramps and
weakness, respiratory paralysis.
324
Central Effects
Confusion, seizure and coma.
Onset
Within few minutes up to 12 hours depending on dosage, inherent toxicity,
rate of absorption.
System Wise Effects

Cardiovascular
Bradycardia, tachycardia, hypotension, hypertension, dysrhythmia.
Respiratory
Bronchorrhea, bronchospasm, dyspnea and pulmonary edema.
Eye
Miosis, lacrimation, blurred vision are common but mydriasis, opsoclonus
may also occur.
Gastrointestinal
Nausea, vomiting, abdominal cramps, diarrhea.
Genitourinary
Increased urinary frequency; urinary incontinence may occur.
Neurologic
i. Early effects: Giddiness, ataxia, drowsiness, seizure, coma.
ii. Intermediate effect: Development of proximal weakness, 12 hours to 7
days after exposure, unresponsive to pralidoxime. Treatment is
supportive.
iii. Distal sensory-motor polyneuropathy may develop 6 to 21 days after
exposure, recovery may be slow or incomplete.
Electrolytes/acid-base
Metabolic acidosis, hypokalemia.
Psychiatric
Anxiety, depression, defects in expressive language, cognitive function,
impaired memory, psychosis.
Lethal dose 0.1 mg/kg.
Investigations
1. Plasma cholinesterase and RBC cholinesterase activities. Depression
more than 50 percent is associated with severe symptoms.
325
2. ECG, electrolytes, pancreatic amylase. Patients with high amylase, prolonged QTc interval in ECG are more likely to develop respiratory
insufficiency and indicates a bad prognosis.
Management
1.
2.
3.
4.
5.
6.
7.
8.
9.
Maintain ABCs and secure airway and an IV line.

Remove all clothes, wash skin with soap and water.
Administer activated charcoal.
Atropine: Antagonizes the muscarinic symptoms. 0.01 mg/kg every 5
to 10 minutes (0.5 mg for toddlers and 2 mg in adolescents) given by
IV, oral, subcutaneous or endotracheal route. IV is the preferred route.
Tachycardia is not a contraindication. The end point is satisfactory gas
exchange, not pupil size or heart rate.
Pralidoxime (PAM): It regenerates cholinesterases and ameliorates the
nicotinic symptoms. It must be given with atropine. Most effective if
given within 24 to 48 hours. Dose is 20 to 40 mg/kg (Maximum 1 gm/
dose) IV over 30 min as 5 percent dextrose in NS. The dose to be
repeated after 1 hour and every 3 to 8 hours if symptoms are not relieved or begin continuous infusion of 10 to 20 mg/kg/hr.
Seizures: Diazepam 0.2 to 0.5 mg /kg, repeat every 5 minutes as needed.
Consider phenobarbitone if uncontrolled.
Acute lung injury: Maintain ventilation, assess with ABG frequently.
Hypotension: Isotonic fluid 10 to 20 ml/kg, if persists, dopamine 5 to20
mcg/kg/min titrate to desired response.
Personal protection: Rescuer should avoid dermal contact to avoid poisoning themselves.
Phenothiazines
Phenothiazines are widely used as antiemetic and tranquilizer. Symptoms
may occur not only after overdose but also during normal course of treatment. Examples are chlorpromazine (Largactil ), prochlorperazine
(Stemetil), and thioridazine.
Clinical Effects
Cardiovascular
Tachycardia, hypotension, complete heart block and ventricular arrhythmia.
Central Nervous System

Lethargy, apathy, convulsion, hypothermia, hyperthermia.
Extrapyramidal Symptoms
Dystonia, choreiform movement, pseudoparkinsonism, tardive dyskinesia,
neuroleptic malignant syndrome.
326
Autonomic Nervous System

Tachycardia, hypertension, diaphoresis, dyspnea, incontinence.
Respiratory
Tachypnea, respiratory depression.
Gastrointestinal
Nausea, vomiting, decreased bowel movement.
Eye
Blurring of vision, miosis.
Skin
Dry and pigmented skin, dermatitis.
Others
Jaundice, leukopenia, agranulocytosis.
Investigations
1. ECG: Flattening and inversion of T wave, prominent U wave, ST depression, prolonged PR, QRS and QT intervals.
2. Estimation of the drug level, if facilities available.
Management
1. Supportive care.
2. Activated charcoal (If less than 4 hrs).
3. Treat hypotension with bolus normal saline 1020 ml/ kg. Dopamine,
dobutamine contraindicated.
4. Diphenhydramine: 0.5 to 1 mg/kg (Up to 50 mg IV or IM). Use same
dose orally every 4 to 6 hrs for 2 to 3 days to prevent recurrence.
5. Benztropine mesylate0.02 mg/kg IV/IM in children 3 years, maximum 1 mg, repeat in 15 min if no response. Benzatropine mesylate is
not recommented below 3 years of age. Use it if there is no response
to diphenhydramine.
6. Treat seizures with diazepam and IV loading dose of phenytoin.
7. Respiratory insufficiency to be managed with ventilatory care.
8. Control hypothermia or hyperthermia accordingly.
9. Arrhythmias: Put the patient on cardiac monitor. Sodium bicarbonate
IV to normalize the pH.
10. Lidocaine: 1 mg/kg IV bolus followed by 0.03 mcg/kg/min.
11. Phenytoin: 0.1 mg /kg to a maximum of 1 mg may be repeated after
5 minutes.
Cardiac pacemaker for complete heart block.
327
Tricyclic Antidepressants
It should be suspected in any child with disturbed sensorium, and/or seizures that are associated with prolonged QRS. Examples are imipramine,
amitriptyline and doxepin. It has a direct myocardial (quinidine like) depression, and anticholinergic (atropine like) activity.
Clinical Features
CNS: Depressed level of consciousness, seizures, delirium, lethargy and
coma. Myoclonus and choreoathetosis occur in few cases.
Anticholinergic (atropine-like) effect: Tachycardia, mydriasis, dryness of
mucous membrane, urinary retention, hallucination and flushing. Fever
may be present.
Cardiovascular: Manifestations include tachycardia, various arrhythmia and
hypotension. Arrhythmias include RBBB, LBBB, AV block. ECG changes
include widening of QRS complex, prolonged QT interval, flattening of T
wave and ST depression.
Lethal dose: 5 to 20 mg/kg but may be as low as 5 to 6 mg /kg.
Investigations
1. ABG to document hypoxemia and acidosis.
2. Blood level of the drug if facilities available.
Management
1.
2.
3.
4.
5.
General supportive careICU care may be needed in severe cases.

Activated charcoal.
Continuous ECG monitor.
Hypertension is transient, usually needs no treatment.
For prolonged QRS and hypotension give 20 ml/kg NS and sodium
bicarbonate 1 to 2 mEq/kg, repeat to keep pH between 7.45 to 7.55.
6. Give IV diazepam and loading dose of phenytoin for seizures.
7. Treat life-threatening ventricular arrhythmias with lidocain or phenytoin. Supraventricular arrhythmias usually need no treatment.
Beta Blockers
In pediatric population, beta blockers are used to mainly treat hypertension, thyrotoxicosis and migraine.
Clinical Features
CVS
Bradycardia (Sinus, AV nodal or ventricular), bradyarrhythmias, conduction delays, severe hypotension.
328
CNS
Depressed sensorium, delirium, coma and convulsions.
Others
Bronchospasm, hypoglycemia.
Investigations
1. ECG continuous and also 12 lead.
2. Chest X-ray.
3. Blood glucose level.
Management
1.
2.
3.
4.
5.
6.
7.
8.
9.
General supportive care.

Continuous ECG and blood pressure monitoring.
Obtain serum electrolytes and blood glucose level.
Gastric decontamination with orogastric lavage and activated charcoal
or whole bowel irrigation.
Correct hypotension with a bolus of IV normal saline.
Treat bradycardia with atropine 0.5 to 1 mg IV, give isoprotrenol if no
response.
High dose glucagons is recommended as first line therapy for
cardiotoxicity produced by beta blockers, given as a bolus dose of 50 to
150 mcg/kg over 1 to 2 minutes . This will have transient effect within 5
minutes. If benefit is seen, a continuous infusion at a rate of 2 to 5 mg/hr
(Maximum 10 mg/hr) diluted in 5 percent dextrose injection. This infusion can be tapered as patient improves.
Treat hypoglycemia, hyperkalemia accordingly.
Treat seizures with IV diazepam.
Digoxin
Digitalis toxicity occurs mostly due to overdose during chronic maintenance therapy or accidental ingestion.
Manifestations
CVS
Dysrhythmia of every known type may occur including bradycardia, varying
degree of heart block, junctional tachycardia, PVC, ventricular fibrillation,
ventricular tachycardia, hypotension and asystole. Nonocclusive mesenteric
ischemia and infarction has been associated with cardiac glycoside toxicity.
CNS
Drowsiness, lethargy, asthenia, muscle weakness. Signs of psychosis including hallucination, paranoia, agitation, confusion and delirium.
329
Gastrointestinal
Nausea and vomiting.
Fluid and Electrolytes

Hypokalemia especially with concomitant diuretic use. Toxicity increases
with hypokalemia, hypercalcemia, and hypomagnesemia.
Psychiatric
Visual and auditory hallucination.
Lethal dose: 10 mg of digoxin in adult and 4 mg in child may produce
serious toxicity including cardiac arrest.
Investigations
1. Collect serum digoxin and electrolyte level.
2. Obtain an ECG, determine PR interval.
Management
1. Basic measures including ABC followed by activated charcoal. Child
up to 12 years, 25 to 50 gm of initial activated charcoal then subsequent doses at 1 to 4 hours interval at a rate of 6.25 gm/hr. Continue
till clinical and laboratory parameters are improving. Consider gastric
lavage with recent ingestion, preferably within 1 hour.
2. Hyperkalemia: Treat aggressively. If serum potassium is more than 5.5
mEq/L use IV sodium bicarbonate (1 mEq/kg), IV glucose (0.5 gm/kg)
and insulin (0.1 U/kg) infusion. Oral kayxalate not recommended as it
lowers total body potassium.
3. Dysrhythmias: Continuous ECG monitoring. Treat clinically significant
arrhythmia.
i. Bradycardia due to AV or SA block should be treated with atropine 0.02 mg/kg IV every 5 minutes, minimal single dose 0.1 mg
and maximum single dose of 0.5 mg, adolescent 1 mg; maximum total dose 1 mg child and 2 mg adolescent.
ii. Heart block: Dose of atropine as above. Phenytoin 15 mg/kg up
to 1 gm IV not to exceed a rate of 0.5 mg/kg/min followed by 2
mg/kg every 8 hourly. Consider pacemaker for 2 and 3 heart
block or symptomatic and refractory bradycardia.
iii. Ventricular arrhythmia: Evaluate hypoxia, acidosis, electrolyte
disorder and correct properly. Hemodynamically dysrhythmia
should be treated with digoxin.
iv. Phenytoin 2 mg/kg IV slowly over 20 min. Repeat every 5 minutes till arrhythmia stops or maximum of 15 to 20 mg/kg.
v. Lidocaine can also be used, 1 mg IV bolus then 20 to 50 gm/kg/
min. continuous infusion.
Do not use calcium as it may worsen ventricular arrhythmia.
330
Digoxin immune Fab: Digoxin antibodies or Digibind. Indications are manifestations of severe toxicity, e.g. ventricular dysrhythmias, progressive
bradyarrhythmias, 2 or 3 heart block, hemodynamically significant supraventricular tachydysrhythmias and hyperkalemias. One vial = 38 mg,
each mg can bind 12.5 mcg of digoxin.
Dose calculated from the estimated body load using equations below.
Digoxin body load = dose ingested 0.8 OR
Digoxin body load
Steady state serum level in nanogm/ml 5.6 wt in kg
=
1000
body load (mg)
Now digibind dose = number of vials =
or
0.5
Number of vial
Serum digoxin concentration (ngm/ml) patient wt (kg)
=
100
Practice Points
1. Despite best effort, patient may die of malignant ventricular
arrhythmias.
2. If neither the dose ingested nor the plasma digoxin level is known 380
mg of digibind should be given taking into mind that each vial bind
approximately 0.5 mg of digoxin.
3. Fab should be diluted as 1 mg/ml in 5 percent dextrose or normal
saline. Administer total dose over 30 minutes.
4. Avoid coadministering with other drugs or electrolytes. Use 0.22 micron filter to restrict undissolved particulate matter.
Bibliography
1.
2.
3.
4.
Bates N, Edwards N, Roper J, Volans G Editors. Pediatric Toxicology: Handbook of Poisoning in Children. Macmillan Reference Ltd. 1997.
Jayanthi R. Corrosive Poisoning. Indian J Pract Pediatr 2009;11:37-40.
Rajendran C, Ravi G, Subramanian PT. Organophosphate, Carbamate and
Rodenticide Poisoning. Indian J Pract Pediatr 2009;11:6-14.
Singh UK, Layland FC, Suman S, Prasad R. Poisoning in Children, 2nd
edition. New Delhi: Jaypee Brothers, 2001.
14
FOREIGN BODY
14.1
Airway Foreign Body
Foreign body (FB) in the airway can be a life-threatening event. From the
management point of view it is necessary to determine the FB is in which
anatomic position (Supraglottic, infraglottic or distal to carina) and the
effect is a complete or an incomplete obstruction.
Usual Foreign Bodies Aspirated

Organic
1.
2.
3.
4.
5.
Peanuts (probably the commonest).

Seeds.
Bones.
Vegetables.
Bread.
Inorganic
1.
2.
3.
4.
Parts of toys.
Crayons.
Coins.
Pins and needles.
Clinical Features
Many times, the parents suddenly discover that their child is suddenly
coughing profusely, making some strange sounds or choking while playing. Rarely the parents come up with definite foreign body aspiration.
Foreign body aspiration should definitely be considered if a previously
healthy child presents suddenly with choking, stridor, gagging, coughing,
wheezing with or without cyanosis, inability to vocalize or respiratory arrest in life-threatening total airway obstruction. Foreign bodies may lodge
at any place along the airway from the pharynx to the segmental bronchus.
The most common site of aspiration is right main bronchus, followed by
left main bronchus.
Commonest age for occurrence1 to 3 years but can occur at any age.
334
Is it an incomplete obstruction?
Symptoms arestridor, difficulty in breathing, cough.
Is it a complete obstruction?
Symptoms are that of inability to move air or phonate. Subsequently and
as a result of complete airway obstruction, patient is terrified fearing impending doom, making attempts to inspire, will often hold his anterior
neck with one or both hands in universal choking sign. Once complete
obstruction ensues, patient may go into apnea, may or may not be unconscious in a short while. Total airway obstruction will eventually lead to
hypoxic loss of consciousness and ultimately cardiorespiratory arrest. Basic life support should be initiated at the site of occurrence or as soon as
possible.
The typical X-ray features are shown in Figures 14.1.1, 14.1.2 and 14.1.3.
Management
The step-by-step management algorithm of airway foreign body is shown
in Flow charts 14.1.1 and 14.1.2. The rigid bronchoscope used for foreign
body removal are shown in Figures 14.1.4 and 14.1.5.
FIG. 14.1.1: Normal chest X-ray
Chapter 14.1: Airway Foreign Body
335
FIG. 14.1.2: Expiratory film showing marked air trapping in right lung with right-to-left mediastinal
shift
FIG. 14.1.3: Radiopaque foreign body in upper airway
336
Flow chart 14.1.1: Management of airway foreign body
Management of Partial Airway Obstruction

Partial airway obstruction should be approached with extreme caution as
one needs to avoid the potential to convert the situation to one of complete obstruction.
Practice Points
1. If the obstruction is incomplete, move slowly to ensure that incomplete obstruction is not converted into a complete obstruction.
2. Call for early help.
3. If the obstructing FB is above the vocal cords and can not be removed,
immediate cricothyroidotomy is indicated.
4. If the obstructing foreign body is distal to the vocal cords and can not
be visualized from above by direct laryngoscopy, cricothyroidotomy will
be of no benefit and should not be performed.
Chapter 14.1: Airway Foreign Body
337
Flow chart 14.1.2: Management of complete airway obstruction
5. Heimlich maneuver is a reasonable first-step in any case of complete

obstruction.
338
FIG. 14.1.4: Rigid fiberoptic bronchoscope
FIG. 14.1.5: Foreign body removal by fiberoptic bronchoscopy (For color version see Plate 3)
Bibliography
1.
2.
3.
4.
Bloom DC, Christenson TE, Manning SC. Plastic laryngeal foreign bodies in
children: A diagnostic challenge. Int J Pediatr Otorhinolaryngol 2005;69(5):65762.
CDC: Nonfatal choking-related episodes among childrenUnited States, 2001.
MMWR Morb Mortal Wkly Rep 2002;51(42):945-8.
Eren S, Balci AE, Dikici B. Foreign body aspiration in children: Experience of
1160 cases. Ann Trop Paediatr 2003;23(1):31-7.
Walls RM. Manual of Emergency airway management, 2nd edition. Philadelphia: Lippincot Willims and Wilkins, 2003. 190-4.
14.2
Foreign Body in GI Tract
Foreign body (FB) ingestion is common in children. The following are some
characteristic:
1. It can occur at any age, peak age being 6 months to 3 years.
2. Most commonly reported FB is coins.
3. Radiopaque FB found in 60 to 88 percent, most often due to coins.
4. Most nonopaque FB is due to retained food.
5. Most of the ingested FB pass through the GI tract spontaneously and
excreted without serious consequences.
Predisposing Factors
1. Anatomical abnormality like esophageal stricture secondary to GERD,
caustic ingestion and post esophageal atresia repair.
2. Mental retardation, psychiatric disorder, and child abuse specially in
older children.
Prominent esophageal narrowing and sites of probable FB impaction
1. Cricopharyngeus muscleat the level of C6 spine.
2. Thoracic inletat the level of T1 spine.
3. Aortic arch and tracheal bifurcationat the level of T4 spine.
4. Gastroesophageal junctionat the level of T10 to 11 spine.
Signs and Symptoms

Many a time FB ingestion goes unnoticed as it passes out without causing
any obstruction. Following are the typical presentations:
1. Initial choking episode.
2. Dysphagia, drooling, and sudden change in feeding habit.
3. Excessive salivation and regurgitation of food.
4. Sore throat, can not breath, substernal pain.
Complications
1. Aspiration, asphyxiation, perforation.
2. Coins and button batteries eroding and or bleeding after 72 hours are
not very uncommon.
340
Investigation
X-ray chest, abdomen, lateral view of soft tissue neck.
Management
1. Check ABCs and stabilize the patient if in distress.
2. Observe if asymptomatic for 12 to 24 hours and if no previous operative site.
3. Repeat X-ray after observation to check clearance through gastric passage.
4. Immediate esophagoscopy if upper airway compromise, otherwise.
5. Planned esophagoscopy if FB does not move in 12-24 hours.
6. Decision for surgical removal of button battery in some specific situation, as detailed in chapter on button battery ingestion.
Practice Points
1. Large object larger than 5 cm in diameter will not pass through esophagus.
2. Open safety pins or needle will not pass.
3. Objects that have passed though stomach can be expected to pass safely.
4. Refer to an ENT specialist for fish/chicken bones in pharynx/upper
esophagus.
Bibliography
1. Krebs H, Seidman, Sokol, et al. Pediatric Clinical Gastroenterology.
4th edition. 1995.
2. Walker, Durie, Hamilton, Walker Smith, Watkins. Pediatric Gastrointestinal Disease: 2000.
3. Wyllie, Hyams. Pediatric Gastroentestinal Disease 1999.
14.3
Button Battery Ingestion
With the advent of newer technologies we have invited newer medical problems too. Button batteries are now indistinguishable part of modern
electronic gadgets like calculators, watches, electronic games, pagers, remote control devices, digital diaries. The number of button battery ingestion
is also increasing in last two decades. Button batteries are small, smooth
and easy to swallow Figure 14.3.1.
Mode of Action
The majority of batteries traverse the gastrointestinal tract uneventfully
but complications arise if the battery becomes lodged. This occurs most
commonly in esophagus. The compositions of various types of batteries
are described in Table 14.3.1.
FIG. 14.3.1: Button batteries
Zinc metal 32 %
24.8%
Manganese dioxide
Zinc/Air
16%
Manganese dioxide
AlkalineManganese
LithiumManganese
0.3%
5%
3%
Mercuric oxide 40%

Silver oxide 39%
Mercury
Silver
Manganese dioxide
Main constituent
Types
TABLE 14.3.1: Battery types and composition
10%
12%
7%
8%
Potassium hydroxide
7%
14%
13%
Zinc powder amalgum
1.8%
3%
1.5%
Graphite
0.5%
0.5%
0.15%
Zinc oxide
Propylene carbonate 6%,

Lithium
perchlorate
1%, Lithium
metal anode
2%, Ethylene
glycoldimethyl
ether 4.3%
Carbon black
2%, Mercury
metal 1%
Sodium aluminate 0.05%

Cement 1.5%
Others
342
Chapter 14.3: Button Battery Ingestion
343
1. Corrosive effect: Damage to the battery casing may occur in the gastrointestinal tract from acidic attack by gastric contents and/or
electrolytic attack due to its own electrical properties, causing leakage
of contents. Leakage and/or production of alkali may cause severe caustic
injury and local liquefaction. Thus tissue damage may occur from prolonged contact at a single site as the electrical activity of battery cause
local short circuit through the tissue, as well as a rise in pH.
2. Toxic metal effect: Leakage of metal salts may result in systemic toxicity. A single mercury battery contains potentially lethal quantity of
mercury for a child.
Theoretically, used batteries are less hazardous as they are less likely to
leak and cause electrical damage and metal salts are reduced to relatively
harmless elemental state though existence of some residual charge and
unreduced metal salt with its damaging potential can never be ruled out.
Clinical Effects
1. Esophageal impaction: Irritability, difficulty in swallowing, vomiting,
hematemesis, nausea and burn. Complication (may be delayed for few
days) includes tracheoesophageal fistula, aortoesophageal fistula, esophageal burns, perforation and stricture.
2. Lower intestine impaction: Vomiting, tarry or bloody stools, abdominal pain and fever. Acute gastroenteritis in heavy metal poisoning few
days after ingestion. Intestinal ulcers, perforation, adhesion and obstruction and necrosis are few rare but known complications. Figure
14.3.2 shows a button battery in the intestine.
FIG. 14.3.2: Button battery in the intestine
344
Treatment
Plan of management for button battery ingestion is summarized in Flow
chart 14.3.1.
1. Whole bowel irrigation may be considered following ingestion of multiple batteries. The brand and type of battery should be determined
from spare battery kept at home.
2. Chest and abdominal X-rays both postero-anterior and lateral to confirm ingestion and position. Button battery can be distinguished from
coin ingestion by their lateral view. Coins are usually left to pass spontaneously.
Flow chart 14.3.1: Management plan for button battery ingestion
Chapter 14.3: Button Battery Ingestion
345
3. If the battery is still in esophagus, urgent removal by endoscopy is

essential.
4. If the battery is intact and in stomach, admit for observation. Osmotic
laxatives may be given to reduce transit time in gastrointestinal tract.
Abdominal X-ray should be taken every 48 hrs (24 hours for mercury
or unidentified batteries) until battery is passed in the stools or absent
on X-rays.
5. Discharge if battery is intact and beyond pylorus and repeat X-ray after 24 hrs.
6. If the battery is in the stomach and shows signs of leakage, it should be
removed by endoscopy or by fluoroscopy using magnet.
7. Surgical removal is indicated if endoscopy fails or facility unavailable
in the context of signs of leaking, no movement in 48 hrs (24 hours for
a mercury or unidentified battery) or bloody/tarry stool and /or gastroenteritis.
8. Mercury concentration in blood should be measured in case of mercury battery ingestion.
Emesis and lavage are not recommended, unlikely to evacuate and
runs the risk of lodgment into esophagus. Charcoal is also of no benefit as
may obscure detection of button cells and discolor stool.
Battery in the Nose or Ear

Extensive corrosive damages have been reported. While swelling, pyrexia,
foul smelling discharges are common, and perforation of nasal septum
and tympanic membrane are on record. Other complications include hearing loss, facial nerve paralysis.
Battery should be removed immediately and area thoroughly irrigated.
Patients with evidence of secondary infection should receive antibiotics.
Bibliograhpy
1.
Bates N, Edwards N, Roper J, Volans G Editors. Pediatric Toxicology, Handbook of Poisoning in children, Macmillan Reference Ltd. 1997;103-8.
15
PSYCHIATRIC
BEHAVIORAL AND
SOCIAL ISSUES
15.1
Psychiatric Assessment for
Nonpsychiatrists
Jaydeep Choudhury
While suspecting any psychiatric illness, one should be conspicuous in approach. If the patient suspects that the doctor is delving into personal
problems then they either become very aggressive or go into a shell and
refuse to give any history. Thus, one should start with a standard comprehensive medical history and physical examination.
Ask about the presenting complaint (Emotional or psychiatric)
1. Duration, severity, what makes it worse and what helps?
2. What effect has it on family?
3. What would the parents like to see happen?
Extend the family history to include
1. Physical and psychiatric family history (including suicide or other
deaths).
2. Personality, upbringing and schooling of parents and siblings.
3. Drug and/or alcohol abuse; criminal history.
Take special note of
1. Problems during pregnancy with the child.
2. How the mother felt towards the child before and after birth and subsequently.
3. Any problems in development.
4. Problems reported by preschool teachers, teachers and peers.
Ask about interpersonal relationships
1. With family members, peers.
2. Any physical or sexual abuse?
3. Sexual orientation, anxieties, practices, problems and puberty.
Ask specifically about (if appropriate)
1. Attentiveness, activity level, clumsiness, weakness, tics and gait.
2. Sleepnightmares, night terrors, sleep walking.
3. Habitsincluding nail biting, thumb sucking, head banging or rocking, repetitive habits, comforting behaviors and favorite routines.
4. Speechnormal progression? Delay? Problems with comprehensions?
Usually suggests
Croup
Anxiety
Many potential medical and surgical causes
Idiopathic abdominal pain of later childhood
Gastroenteritis, other medical or surgical conditions
Wide variety of medical problems
Epilepsy
Gynecological cause
Systemic disease
Acute neurological problem
Drug overdose, acute neurological condition
Hypocalcemia
Epilepsy variant
Glue ear, congenital deafness
Organic cause
Major systemic illness
Symptom / sign
Acute stridor
Hyperventilation
Acute abdominal pain

Recurrent abdominal pain (older child)
Acute vomiting
Chronic pain
Seizures
Amenorrhea
Diffuse muscle pain
Limb paralysis
Confusional state
Carpopedal spasm
Complex partial seizure
Deafness
Mutism
Inanition, inability to walk, speak
TABLE 15.1.1: Symptoms and signs which may indicate both medical and psychiatric conditions
May be an indication of
Hysterical stridor (in a child of 7 years or older)
Asthma. Could be due to either or both in a child or
adolescent with asthma
Aerophagy due to anxiety
Peptic ulceration, renal disease, gall stones
Somatization of psychological symptoms
Underlying depression
Pseudoseizures, associated with psychological
problems
Anorexia nervosa
Hyperventilation due to long standing anxiety
Conversion disorder
Hysterical fugue
Hyperventilation from anxiety
Masturbatory habit disorder, in 3 5 year olds
Autism spectrum disorders
Selective mutism
Pervasive refusal disorder
350
Chapter 15.1: Psychiatric Assessment for Nonpsychiatrists
351
5. Vision and hearing including hallucinations, frightening dreams while

awake.
6. Thought processconcentration, day dreaming, delusions, muddled
thoughts.
7. Personality and behavioremotional expression, worries, fears, phobias, aggression, excitability, adaptability, disobedience.
8. Antisocial behaviorlying, stealing, fighting, alcohol/drugs, trouble
with school authorities/police/courts.
9. Fantasy lifegames played and their content, imagination, imaginary
friends, transitional objects, times when in a world of their own.
10. Attack disordersbreath holding, fits, fainting.
Mental State Examination

In addition to the neurological examination, following should be noted.
1. Appearance and behavior: Attire, cleanliness, self-care, appropriateness
of clothing, general health, injuries, nonverbal communication, language, motor function, interaction with interviewer.
2. Speech: Rate, quantity, pattern, perseveration, articulation, vocabulary.
3. Ability to read and write.
4. Thought: Content, avoided subjects, preoccupations, thought flow, unusual use of language, hallucinations, delusions, obsessions, phobias,
paranoia.
5. Apparent intellectual ability.
6. Mood and affect: Is the child happy? Sad? Fearful? Angry? Suicidal?
Observe the child for appropriate affectis he/she blunted? Labile?
Perplexed? Suspicious?
7. Attitude to family, friends and school. Fantasy life (the childs three
magical wishes, the three most wanted people in a deserted island).
8. Observed playcontent, concentration, distractibility, imagination; significance or symbolism demonstrated?
9. Consider use of mini-mental state examination.
It is important to distinguish between certain medical conditions and
those psychiatric conditions which may mimic medical conditions. Symptoms and signs which may indicate both medical and psychiatric conditions
are shown in Table 15.1.1.
Bibliography
1.
Kilham H, Isaacs D Editors. The New Childrens Hospital Handbook, 1999.

Westmead NSW Australia.
15.2
Nonaccidental Self-Harm
The topic includes suicide attempts or lesser degree of self-harm which

may indicate widely variable range of psychiatric disturbances and therefore ineffective way of coping with the problems.
Common Predisposing Factors

1.
2.
3.
4.
5.
Chronic physical illness.

Poor school achievement or peer relationship.
Family conflict and/or psychiatric illness.
Drug or alcohol problems in self and/or in family.
Unusual life stress such as sexual abuse.
Goals of Assessment Interview

1. Establish contact: Listen carefully, be calm, take control and show realistic hope.
2. Understand the attempt: Get details of what happened.
3. Explore the plan and idea: How intense, how long, evidence of premedication, details of plan, anger at being found.
4. Assess previous attempts.
5. Current problems.
6. Method of coping.
7. Future safety issues: Where can the patient go to get enough support,
protection and supervision?
8. Plan of action.
Assessment
1. Demographics:
i. Name/age/sex.
ii. Cultural background.
iii. Educational level/school/attendance/current grade.
iv. Current living circumstances.
v. Family tree.
Chapter 15.2: Nonaccidental Self-Harm
353
2. Medical history: Including current medication, allergy, adverse reaction, substance abuse history and physical examination.
3. Presenting complaint:
i. Duration, onset, severity (how fatal/lethal), stressors, precipitants,
relieving factor, injuries sustained.
ii. Safety risk-self and others-intent, plans, means (? still current),
remorse.
iii. Helplessness, hopelessness, plan for future.
iv. Effects on the family.
4. Pastpsychiatric history:
i. Self-harm/suicidal attempts/aggression.
ii. Outpatient/inpatient care needed.
5. Family history:
i. Psychiatric and physical illness in the family including suicide.
ii. Drug and /or alcohol abuse and criminal history.
iii. Personality, upbringing and schooling of parents and siblings.
iv. Interpersonal relationship with family members.
v. Physical/sexual abuse, problems with puberty, family practices.
6. Collateral history: Should be obtained from parents, care giver, accompanying person to confirm or high light inconsistencies. Also get the
following history from parents:
i. Problem during pregnancy.
ii. Problem during development.
iii. Lying, stealing, fighting.
iv. Problem reported by school teachers, peers, police, court.
7. Mental status:
i. Appearance and behavior: Attire, cleanliness, appropriateness
of clothing, self-care, general health, injuries, language, nonverbal communication, interaction with interviewer.
ii. Attentiveness: Activity level, orientation, concentration, distractibility, clumsiness, weakness, gait.
iii. Attitude: To family, friends, school. Fantasy life, imagination and
description of a life of their own.
iv. Speech: Rate, quantity, pattern, perseveration, articulation, vocabulary, comprehension.
v. Thought: Content, preoccupation, avoided subjects, thought flow,
unusual use of language, hallucinations, delusions, obsessions,
phobias, paranoia.
vi. Mood and affect: Happy, sad, fearful, irritable, anxious, angry,
blunted, labile, perplexed, suspicious.
vii. Habits: Nail biting, thumb sucking, head banging/rocking, repetitive habits and comforting behavior.
viii. Intellectual ability, reading, writing.
8. Miscellaneous: Fits, fainting, frightening dreams while awake, nightmares, night terrors, sleep walking.
354
Before summing up the assessment and developing a plan about referral to psychiatrist/hospital admission/arrangement of care at other place
once again some key issues should be addressed:
1. Priority treatment: Management of poisoning, injury (Burn, fracture, laceration, etc.).
2. Relevant questions:
i. Suicidal tendency still present?
ii. Have you ever just wanted to get away from it all?
iii. Do you ever feel like going to sleep and not waking up?
iv. Have you ever wished you could die?
v. What ways have you thought about hurting yourself?
vi. Do you want to hurt yourself now/die now?
3. Support:
i. Who knows you best who could make you feel better?
ii. Who is most worried about what you have done?
iii. Who would have you missed most if you had succeeded?
4. Safety/security:
i. Is the patient disruptive and can run away?
ii. Is there a place of safety with appropriate people to supervise?
5. Coping:
i. If problem sorted out, would you still hurt yourself?
ii. Part of life which still is impetus for living?
iii. Can you think back when life was all right?
These children may require admission to a special ward and round the
clock supervision. Early assessment by psychiatrist is essential.
Bibliography
1.
2.

Sachdev HPS, Choudhury P, Bagga A, Chugh K, Ramji S, Puri RK Editors.
Principles of Pediatric and Neonatal Emergencies, 2nd edition. New Delhi:
Jaypee Brothers. 354-63.
15.3
Aggressive Behavior and Violent Child
Encountering a violent child in the emergency department is a challenge.

It is much more difficult to assess them when other normally behaving
children and curious onlookers are there. The violent children have to be
managed differently.
Few Donts
1. Dont accept the assessment and admission of a violent patient over
the phone without consulting a psychiatrist first.
2. Dont admit a violent patient in the general ward.
3. Dont admit a violent patient without considering that intravenous sedation may be required.
4. Dont deal with difficult interactions with multiple spectators.
Few Dos
1. Do warn staff if a known potentially violent patient is to be admitted.
2. Do make sure others are around when you interview, including the
security staff.
3. Do avoid confronting, make or break interactions and shouting.
4. Do have one person in charge and avoid everyone getting involved
into it.
5. Do get children and noninvolved families out of the way.
Management
1. Seek a quiet location where there is no audience.
2. Avoid confinementat least initially.
3. Ask individuals who may inflame the patient to leave and who calm to
stay.
4. Consider what examination must be done and what examinations
can be done.
5. If restraint is necessary it must be planned, decisive, effective and speedy.
6. Use the routine observations for a comatose patient.
356
7. If sedation is required have the medications drawn up out of view prior

to attempting restraint. Drug therapy to consider:
Diazepam up to 0.2 mg/kg/dose to a maximum of 20 mg. Dilute
with water for injection to 1 mg/ml. Give over 5 minutes, continuously
monitoring the rate of respiration and the level of consciousness.
Lorazepam or midazolam may also be given.
Droperidol 0.1 to 0.3 mg/kg/dose to a maximum dose of 10 mg.
Dilute with water for injection to 1 mg/ml. Give over 5 minutes, continuously monitoring pulse rate and regularity.
8. The restraint may need to be in place for 20 to 30 minutes pending the
onset of action of medication.
9. Arrange for psychiatric assessment after you have dealt with the crisis.
10. Recheck if there are any medical issues you may have missed or that
the psychiatry team should be alerted to.
Practice Points
1. IM droperidol is very effective in 20 minutes. Rarely laryngeal spasm
may cause respiratory obstruction.
2. IM diazepam is absorbed over many hours and may cause tissue damage, hence, should be best avoided.
3. IV diazepam may lead to acute respiratory depression, especially if
given as a bolus.
Bibliography
1.

15.4
Abuse of Children
Child abuse in India is indeed a social problem but under reported and
moreover under recognized. Children are abused physically, sexually or
emotionally and emergency department becomes the point of first contact
after a serious physical injury or harm. Suspected cases of child abuse should
be reported to the police after emergency medical treatment.
Indicators of Physical Abuse

1. Inconsistent, bizarre, vague or variable history which do not tally with
physical findings.
2. An unexplained delay between injury and presentation for medical
attention.
3. General features suggestive of long standing neglect and emotional
abuse like:
i. Nonorganic failure to thrive.
ii. Hypervigilance.
iii. Unusual withdrawal.
iv. Physical signs of injury in nonambulant child.
4. Pattern of injury.
i. Soft tissue-bruises like the following:
a. Age under 1 year.
b. Bite mark more than 3 cm.
c. Slap marks.
d. Bruises over pinnae or behind.
e. Instrumental outlines (shoe, stick).
f. Grabmarks over chest or shoulder.
g. Face or head bruising.
h. Multiple sites affected.
i. Bruises not overlying bony prominences.
ii. Soft tissue-burn:
a. Forced immersion pattern (linear edge, flexure spared).
b. Instrumental outlineCigarette burn (over dorsum of hand,
back, buttock).
358
iii. Abdominal injuryunexplained rupture of solid or hollow viscous.

iv. Skeletal injury:
a. Metaphyseal or epiphyseal corner fractures.
b. Rib fractures.
c. Humeral other than supracondylar fracture in children less
than 3 years.
d. Femoral fracture in children less than 1 year.
e. Multiple or bilateral fractures of varying ages.
v. Head injury:
a. Unexplained coma, seizures or neurological signs.
b. Depressed, basilar, bilateral skull fracture with history of fall
from more than 4 feet.
c. Intracranial hemorrhage (other than epidural) with history
of minor injury.
d. Retinal hemorrhage.
Dating Fractures
Abused children are often brought for medical care several days after the
injury. Dating the fractures are essential in such situations.
i. Resolution of soft tissue change4 to 10 days.
ii. Periosteal new bone formation (earliest sign)10 to 14 days.
iii. Loss of fracture line definition: 14 to 21 days.
iv. Soft callus14 to 21 days.
v. Hard callus21 to 42 days.
vi. Remodelling1 year.
Further Tests
1. Full skeletal survey:
i. AP chest, AP abdomen/pelvis/upper femur.
ii. AP both arms (shoulder to legs), AP both legs (femur to feet).
iii. AP and lateral skull and full spine and special views or additional views as necessary.
2. Coagulation profile to document coagulation parameters in cases with
multiple bruises, urine microscopy for RBC to detect covert abdominal trauma.
3. Detailed ophthalmology examination in all patients with head injury.
4. CT scan brain and abdomen as clinically indicated.
5. Medical photography, if facility is available.
Indicators of Sexual Abuse

1. A story of sexual interference by child herself, particularly if consistent.
2. Inadequately explained genital and perianal trauma or bleed.
3. Age inappropriate behavior and/or persistent sexualized behavior.
Chapter 15.4: Abuse of Children
359
4. Sexual activity between children which involves coercion and a power

imbalance.
5. Recurrent vaginal discharge, STD, pregnancy.
6. Depression, unexplained emotional disturbance.
7. Drug dependency, self-harming behavior, run away from home.
What should be Recorded?

Keep a record of who asked to see the child, who accompanied him or her,
who raised the question of abuse, who gave the history, who was present
during examination.
The history should also include details of incident causing suspicion,
full pediatric history, with particular emphasis on genitourinary and bowel
symptoms, details of previous abuse or sexual offence within family or household or else.
Who should Examine?

1. A person with skill in pediatric examination, familiar with normal genital
and anal appearance of children should conduct the exam.
2. When physical abnormalities are expected from the history a forensic
physician should be invited or referred to.
3. Junior medical staff should not examine suspected victims unless the
child needs urgent medical attention.
What should be and should not be done?

1.
2.
3.
4.
5.
Take a female witness while taking history and carrying out physical examination. This should be done with privacy, sensitivity and calmness.
Internal examinations are rarely necessary but if needed is preferable
to perform under anesthesia. Remember forensic evidence can be collected up to 7 days following an assault and serious genital injury forensic
evidence should not be compromised when abuse is thought to have
occurred recently (with in 6-7 days).
Consent for examination should be obtained from a parent or person
with parental responsibility.
It is usually counterproductive to examine a resistant child and examination should be deferred for optimal arrangement and to avoid
repetitive examination in case forensic experts examination, diagnostic tests and adequate equipments are necessary. But if the child is
unstable and needs urgent medical attention, examination and treatment as appropriate and necessary should continue.
Nobody should remove clothing or attempt to clean or bath the child.
Medical Management
1. Wound care as necessary.
2. Pregnancy prophylaxis.
360
3. Screening and treatment for STD. Screening tests include the following:
i. Endocervical swab for gonorrhea, chlamydia culture.
ii. High vaginal swab for Candida, Trichomonas.
iii. Blood test for syphilis serology, hepatitis B antigen.
iv. HIV only after careful history and counseling.
v. Anal and throat swabs depending on sexual practice.
4. Psychological counseling.
Medicolegal Perspective
1. Document clinical notes in detail, clearly and legibly with date, time,
proper signature and name written in bold capital letters.
2. Enter the medicolegal register clearly stating why child abuse was suspected.
3. Inform local police in the form provided, signed by the doctor examined.
4. Affix medicolegal seal on all related documents.
Bibliography
1.
2.
3.
American Academy of Pediatrics: Diagnostic imaging of child abuse. Pediatr

87:262-64.
Hudson M, Kaplan R. Clinical response to child abuse. Pediatric Clinics of
North America 2006;53:27-40.
Meadow R. ABC of Child Abuse, 3rd edition. BMJ publishing group, 1997.
16
TRAUMA AND
ORTHOPEDICS
16.1
Head Trauma
Head injury remains the leading cause of accidental deaths in our country
in pediatric age group.
Type of Injury
Primary Insult
It is the injury to the brain that occurs at the time of impact. The brain
injury results from translational or rotational forces.
i. Translational force: It produces compressive and tensile strains on
skull and brain leading to focal brain injuries (linear skull fractures,
cerebral contusions, epidural hematomas, acute subdural hematomas and contrecoup cerebral contusions).
ii. Rotational force: It results in shearing stress that causes diffuse brain
injuries and can be more devastating (cerebral concussion, diffuse
cerebral injuries).
Secondary Insult
It is the progressive deficit caused by cerebral ischemia, hypoxia,
hypercarbia, hypotension and intracranial hypertension. Prevention of rapid
deterioration from this secondary injury becomes the high priority of the
management of severe brain trauma. Quick assessment, establishing the
priorities, planning the acute phase can only deliver good outcome with
minimum long-term insult and morbidity.
Immediate Priority
Establishment of airway, breathing, circulation and cervical spine stability.
Airway
1.
2.
3.
4.
Establishment of patent airway with adequate ventilation takes priority.

High flow oxygen support with bag mask ventilation.
Jaw thrust and no chin lift to avoid cervical damage.
Aspiration of gastric content to assist ventilation.
364
5. Suction and maintenance of upper airway (e.g. Guedels airway).

6. Orogastric (not nasogastric) intubation if fractured cibriform plate is
suspected in maxillofacial or forehead trauma.
7. Use rapid sequence intubation technique if intubation indicated.
Atropine (0.02 mg/kg), midazolam (0.1-0.2 mg/kg), suxamethonium
(1mg/kg) are perhaps the best choice for less experienced clinician.
Alternative is vecuronium (0.1mg/kg) instead of suxamethonium for
theoretically more advantageous in raised ICT. Ketamine is contraindicated in raised ICT.
Circulation
1. Treat hypotension urgently and maintain normal blood pressure and
cardiac output to prevent cerebral hypoperfusion. Traumatic head injury with shock has a grave prognosis. Attribute other organ trauma to
shock than head injury. Significant intracranial blood loss to cause shock
is rather uncommon. Hb, PCV and blood group should be checked.
2. Select isotonic nonglucose containing fluid, e.g. normal saline (to prevent cerebral edema). Arrange for colloids, e.g. Hemaccel, FFP and blood.
Cervical Spine
1. Any patient with head trauma must be considered to have spinal trauma
and associated injuries until they are excluded. Neutral position should
be maintained by use sandbag and semirigid cervical collar. Use logroll technique to locate tenderness, deformity or to assess cervical spine.
2. Maintain cervical stabilization until radiological clearance.
Assess
1. Level of consciousness: GCS should be monitored. Minor head trauma
is associated with score of 13 to 15, moderate 9 to 12 and severe 3 to 8
according to few authors, though this simplification is never absolute
and only a guideline.
2. Mechanism of injury: To assess whether there is any major impact.
3. Circumstances of accident: Motor vehicle, sports, diving, fall or blow.
Child abuse should also be considered.
4. Chronology: Loss of consciousness (immediate or afterwards) and period of lucidity.
5. Associated findings: Amnesia, disorientation, dizziness, vomiting or
nausea, seizure, sensorimotor abnormalities and visual disturbances.
6. Posturing (decerebrate posture or flaccidity have worst prognosis), pupils (size, reaction) eye movement (dolls eye reflex), fundus, sensory
responses, refelexes (presence, absence, equality or presence of
Babinskis reflex).
7. Other important findings include bulging fontanelle, palpable depression or crepitus of skull, evidence of basilar skull fracture (Battles sign
ecchymosis posterior to ear, raccoo n signbilateral black eyes, CSF
rhinorrhea, hemotympanum).
Chapter 16.1: Head Trauma
365
8. Simultaneous chest, abdomen, limb, pelvis injury and their severity in

relation to priority to their treatment.
Major impact to head includes fall from a height of over 2 meters where
there is a reason to suspect that the child has sustained a blow to head or a
blow to head as a pedestrian run down or as a motor vehicle passenger in
a vehicle traveling at high speed. Head trauma management plan is shown
Flow chart 16.1.1: Head trauma management plan
366
Practice Points
1. No prospective role of mannitol infusion. Indications of mannitol are
evidence of herniation (pupillary dilation, bradycardia), mass effect
(hemiparesis). No role of steroid either.
2. Assess neurological status frequently to monitor trends.
3. Pain, struggle causing procedures are detrimental to already raised
ICT.
4. The child must be hemodynamically stable before CT scan.
5. Consider prospective anticonvulsants if seizures are prolonged and
recurrent which are markers of poor prognosis.
6. Cushings reflex (bradycardia, hypertension and irregular respiration)
is usually a late finding of raised ICP.
7. X-ray study of skull is usually not needed (except suspected depressed
fracture with palpable defect, crepitus or history of blunt injury with
head of hammer or heel of high heeled shoe) as a linear undisplaced
skull fracture is not a critical injury.
Bibliography
1.
Pons PT, Barkin RM, Rosen P Editors. Head trauma: A Guide to Ambulatory
Care. Emergency Pediatrics, 6th edition. Mosby 2001;417-30.
16.2
Acute Neck Stiffness
Neck stiffness is caused acutely by discomfort resulting from various cervical

spine motions. The most common causes being minor trauma, inflammation or infection (Usually viral myositis, cervical adenitis, meningitis),
oculogyric crisis and congenital muscular torticollis (Seen only in infants).
Life Threatening Conditions

The following conditions should be excluded first as these are life threatening:
1. Meningitis.
2. Cervical spine injuryfracture or dislocation.
3. Retropharyngeal abscess.
Causes of Acute Stiff Neck

1. Trauma: Cervical subluxation, muscle injury, hematoma, fracture of
clavicle or cervical spine.
2. Inflammation or infection: Meningitis, cervical adenitis, vertebral osteomyelitis, viral myositis, retropharyngeal abscess, arthropathy
asoociated with pharyngitis.
3. Tumor: Nerve, muscle or bone tumor with swelling or nerve compression causing pain.
4. Oculogyric crisis: Usually painless.
5. Hysteria: Mainly in adolescent girls.
6. Down syndrome and acute atlanto-occipital subluxation: Children with
Down syndrome are more at risk of atlanto-occipital subluxation.
The diagnostic approach to acute neck stiffness is shown in Flow chart
16.2.1.
368
Flow chart 16.2.1: Diagnostic approach to stiff neck
Bibliography
1.
Doughty RA, Fleisher G, Ludwig S Editors. Neck Stiffness. Textbook of Pediatric Emergency Medicine, 2nd edition, Williams and Wilkins 1988; 219-22.
16.3
Acute Painful Hip
Acute painful hip is a common condition in childhood but sometimes correct diagnosis of the underlying cause poses a great challenge to clinicians.
The common differential diagnoses are as below:
1. Transient synovitis.
2. Septic arthritis.
3. Acute osteomyelitis.
4. Slipped upper femoral epiphysis (SUFE)sudden slip in 30 percent cases.
5. Other less common conditions are epiphyseal-metaphyseal fracture,
trochanteric avulsion fractures, cellulitis of the soft tissue around hip.
Few other conditions like reactive arthritis, acute rheumatic fever, juvenile rheumatoid arthritis, Henoch-Schonlein purpura, viral arthritis
(Rubella, Parvo virus B19, Epstein-Barr virus) also may present with acute
onset pain. But most often presents with polyarticular often migratory pain
and involving other joints of the lower limbs than a single hip joint in
particular, additionally other more obvious systemic features. Perthes disease on the other hand is an important condition of hip pain and limp in 5
to 10 years of age of subacute or chronic onset. This chapter restricts our
discussion with suspected single painful hip presenting with acute onset
(<2 weeks) and unable to weight bear.
Transient Synovitis
It is a nonspecific inflammation of the synovium of hip, it is usually of short
duration with resolution within two to five days. Trauma is often coincidental. It is a diagnosis of exclusion.
Typically presents in 2 to 10-year-old male with history of recent viral low
grade upper respiratory tract infection or otitis media and fever or malaise. Looks otherwise well with lying supine and hip flexed but limping or
often refusal to walk. Hip pain often referred to knee.
On examination, hip is flexed, slightly abducted and externally rotated. Range of movement proportionate to the degree of pain.
370
Investigations
1. Complete blood count, ESR is generally normal and blood culture sterile.
2. Hip X-rays are normal in most cases, but in a few more pronounced
cases joint space may be widened.
3. Ultrasound shows hip effusion more efficiently if present but does not
differentiate from septic arthritis.
Management
1. No antibiotics are needed.
2. Simple analgesia and rest for 7 to 10 days brings complete resolution.
3. Admit and treat as septic arthritis if ESR is high, any sign of bacterial
infection, local warmth and significant restriction in joint movement.
4. Transient synovitis is usually one-time affair. However, recurrence do
occur and then one should consider Legg-Perthes disease (2% of cases).
Septic Arthritis
Infection of the joint capsule by hematogenous origin or due to spread
from a neighboring bone lesion caused by Group A streptococcus, E.coli
(neonates) Hemophilus influenzae (below 2 years and nonimmunized), Staphylococcus aureus (older children) and salmonella (in sickle cell anemia).
Febrile child (Temperature 3840 celcius) with tender, swollen and
erythematous joint should be treated as septic arthritis until proved otherwise. The joint movement may be severely restricted. Patients looks more
toxic than transient synovitis but absence of sick look does not exclude
septic arthritis. Position of the hip is similar to transient synovitis. Neonates may present with fever without any apparent source while infants
screams only during handling like change of nappy.
Investigations
1. Complete blood count, ESR, CRP are generally elevated and blood
culture may be positive in 40 percent of cases.
2. X-ray shows widening of the joint space due to lateral displacement of
the femoral head and upper femur and soft tissue swelling.
3. Ultrasound shows distension of the joint space, joint effusion occasionally even debris and thickening of the joint capsule.
4. Flouroscopy guided aspiration by orthopedic surgeon both for diagnostic and therapeutic purposes performed under sterile condition, in
an operating theater under general anesthesia. Polymorphoneuclear
leucocytes 10,000 to 100,000/cmm, positive gram staining (75%) and
positive culture (60%) are diagnostic.
Chapter 16.3: Acute Painful Hip
371
Management
1. Early surgical drainage by arthrotomy or arthroscopy will decrease the
risk of late degenerative arthritis.
2. Also admit for IV antibiotics (Flucloxacillin with Cefotaxime) with upper limit of dosage. Appropriate changes are made according to the
bacteriological reports and antibiotics changed to oral (except neonates and infants) once response to treatment is evident. If treatment
is commenced early, 3 weeks treatment is sufficient.
Acute Osteomyelitis
An inflammatory process with nidus in the metaphysis due to hematogenous spread by Group A streptococcus, E.coli (neonates) Hemophilus
influenzae (below 2 years and nonimmunized), Staphylococcus aureus (older
children and commonest) and salmonella (in sickle cell anemia).Trauma to
metaphysis enables infection to establish in the tortuous blood vessels. It
may then track to the surface as periosteal abscess or to epiphysis in infants. Moreover it may spread simultaneously as septic arthritis as joint
capsule in infants insert low on the femoral neck.
Sudden onset pain or limp in an otherwise normal child, usually but not
always becomes febrile and toxic. Pain often localized (finger tip tenderness) to the metaphysis of femur and is an important sign of early
osteomylitis. Limitation of the movement and with or without swelling and
redness are important other clinical features.
Investigations
1. Complete blood count, ESR and CRP are elevated, blood culture positive in 50 percent of cases.
2. X-ray may be normal in first 10 days. However, absence of joint space
widening plus obliteration of iliopsoas fat pad serve to differentiate
from septic arthritis. Patchy rarefaction of metaphysis and periostitis
are late changes. Sclerosis, new periosteal bone and sequestrum follow
much later. Bone scan should be arranged quickly if doubt exists.
3. Ultrasound shows soft tissue swelling, periosteal thickening, subperiosteal fluid collection and cortical breach or destruction corresponding
to the duration of infection.
4. Technetium 99c bone scan detects the hot spots or even photopenic or
cold spots (820%). Sensitive but less specific, less expensive than MRI.
5. MRI is also very sensitive in acute phase.
Management
1. Admit for IV antibiotics (Flucloxacillin with Cefotaxime) with upper
limit of dosage.
372
2. Appropriate changes are made according to the bacteriological reports

and antibiotics changed to oral (except neonates and infants) once response to treatment is evident (afebrile, local swelling and tenderness
subsides and CRP decreases). Uncomplicated cases, 3 to 4 weeks treatment is sufficient whereas bone changes in X-ray require more
prolonged treatment (56 weeks).
3. Surgery is indicated when collection of pus develops-intraosseous, subperiosteal, intra-articular that means when diagnosis has been delayed.
Antibiotics are not effective in the presence of pus and failure to drain
leads to chronic osteomylitis.
Slipped Upper Femoral Epiphysis (SUFE)

It is a condition of late childhood, male: female 4:1. Females 11 to 14 years
and male 13 to 16 years mostly affected. Two-thitrds of them are overweight and sexually immature, 50 percent have history of trauma. Systemic
conditions associated with SUFE include hypothyroidism, panhypopituitarism, hypogonadism, ricket and exposure to radiation. Only in 30 percent
slip occurs suddenly, though in 70 percent slip is gradual.
Limp with moderate pain in hip, thigh or groin, often misdiagnosed as
sprain but pain comes back with exercise. Decreased abduction and internal/medial rotation while external rotation is a late sign.
Investigations
1. Hip radiograph AP (straight and frog leg) as well as lateral.
2. Trethowan sign: Line drawn along superior surface of neck remains
superior to the head of the femur instead of passing through it. Lateral view demonstrates the posterior displacement and step-off of the
epiphysis on the femoral neck.
Management
Regarded as orthopedic emergency, admitted for prompt surgery.
1. Modest displacement (<1/3) is percutaneously pinned to stabilize the
epiphysis and precipitate closure of proximal growth plate.
2. Greater displacement (>1/3) requires reduction and pinning.
Other Conditions
Depends on the history of trauma and X-ray findings. Cellulitis of the soft
tissue around hip may mimic septic arthritis or osteomyelitis. Most often
cellulitis is due to inflammation of the inguinal lymphnodes and can be
differentiated from others by ultrasound by showing increased blood flow
with inflammatory adenopathy in cellulitis against joint fluid in septic arthritis.
Chapter 16.3: Acute Painful Hip
373
Flow chart 16.3.1: Management plan of acute painful hip
The overall management plan of acute painful hip is shown in Flow

chart 16.3.1.
Bibliography
1.
Swischuk LE. Emergency Imaging of the Acutely Ill or Injured child, 3rd edition, Williams and Wilkins 1994;472-88.
16.4
Pulled Elbow
Pulled elbow is the most common upper limb injury in one to five-yearsold children. Most commonly caused by axial traction on an extended and
pronated arm and rarely after a fall. It is often falsely attributed to shoulder
injury or elbow fracture if the clinician is unaware of the condition.
Refusal to use arm with arm held in pronation and slightly flexed at elbow.
Usually tenderness over the radial head at the elbow.
Investigation
X-ray is not necessary with typical presentation. But significant tenderness, swelling or bruise suggest more serious condition (supracondylar
fracture) and should be excluded.
Management
Reduction by simultaneous extension and supination of the affected arm
with gentle pressure over radial head, often confirmed by a click.Typically
child starts using arm within 10 minutes.
16.5
Spinal Cord Injury and Spinal Cord Injury

without Radiographic Abnormality
(SCIWORA)
Injuries to the spines and spinal cord are less in children than adults. Children account for up to 10 percent of all spinal injuries.
The incidence of spinal cord injury amongst spine injured children is
probably about 1 percent. In neurologically impaired survivors the injuries
are most commonly at the C1-C2 levels, or in the lower cervical or thoracic
spine. The common causes of spine and spinal cord injuries in children are
motor vehicle crashes, falls, diving accidents, sport injuries and occasionally nonaccidental injury.
The thoracolumbar junction is the most commonly injured area outside the cervical spine, with the thoracic and lumber spines having roughly
equal incidence of about 25 percent.
Initial Assessment
All patients with significant trauma should be assumed to have a spine or
spinal cord injury and appropriate precautions must be taken to prevent
further exacerbating any possible injury. The initial assessment of patients
with potential spine or spinal cord injury should be directed at the airway,
beathing and circulation, in line with trauma resuscitation guidelines. The
patient should be stabilized and a thorough secondary survey performed.
At this point all possible spine and spinal cord injuries should be identified. The lateral cervical spine X-ray will be done at this stage in patients
with major trauma. Thorough radiological assessment of the injuries should
be completed once resuscitation and stabilization and the secondary survey have all been accomplished.
A thorough history of mechanism of injury, previous spinal injury, other
illness particularly respiratory illness (acute or chronic), cardiac illness, bone
disorders, medication and allergies is needed to determine the patients
premorbid physiological status.
Spinal Immobilization
Traditionally the spine has been immobilized in a rigid cervical collar with
a head immobilizer and straps, and a spine board to which the patient is
strapped, thus providing adequate control of the entire spine.
376
Indication for initial immobilization of the spine

1. Impaired levels of consciousness.
2. Inability to give history of pain.
3. Neck or back pain.
4. Neurologic signs and symptoms.
5. History of significant trauma:
i. Fall from height >3 meters.
ii. Pedestrian or cyclist hit by car.
iii. Unrestrained passenger in motor vehicle crash.
iv. Diving accident.
6. History of spinal abnormality.
Problems associated with spinal immobilization in children
1. Incorrect fitted c-spine collar causing distraction of the spine of the
spine or allowing movement.
2. Flexion of the spine in children under 8 years of age.
3. Reduction in tidal volume and limitation of respiratory effort.
4. Discomfort.
5. Distress and anxiety.
6. Pressure sores.
A number of different cervical collars are available and satisfactory to
use. The clinician must be familiar with the method of sizing and applying
the collar available.
The back should be examined by log rolling the child. This requires at
least three people in the smallest of child and up to five in the larger patients.
The child is freed from the head immobilizer and any strapping to the spinal
board removed. One person must stabilize the cervical spine by supporting
the head and neck in neutral position throughout movement. No traction
should be applied to the neck. The other team members control the shoulders,
hips and legs, and one person must be free to inspect and palpate the back.
The back is inspected for bruised, abrasions, wounds or deformity of the
spine. The spinous processes are palpated for tenderness. The back of the
neck and head and the buttock and anus should be inspected.
Cervical Spine Injuries

As the cervical spine is the most common region injured and accounts for
the majority of spinal cord injuries a thorough knowledge of injuries in
this region and the appropriate assessment of the spine both clinically and
radiographically is mandatory. In children, younger than 8 years of age,
the majority (but not all) injuries occur above the fourth cervical vertebra.
After 8 years the pattern of injuries is similar to that seen in adults (the
majority of injuries below C4).
Mechanisms of Injury
The mechanism of injury is an important historical factor, as it will determine the type and possibility in stability of the underlying injury.
377
Chapter 16.5: Spinal Cord Injury
Flexion: The most common mechanism of injury seen is hyper flexion.

This type of injury produces a compressive force on the anterior segment
of the vertebraleading to a compression fracture or tear drop fracture.
Extension: Hyperextension injuries produce distracting forces anteriorly,
while compressing the posterior vertebral structures.
Rotation: In the cervical spine isolated injuries are uncommon.
Vertical compression: These injuries are due to axial compression of the
cervical spine. This can produce a burst fracture of any vertebra, with a
lesion at C1 being most unstable.
In many instances not one but a combination of these mechanisms of
injury are involved. The classification and stability of cervical spinal injuries is shown in Table 16.5.1.
Clinical Assessment
After immobilization and resuscitation of the injured child and as part of
the secondary survey the neck should be examined. This is done to look
for neck abrasions and signs of injury to other structures in the neck as well
as to examine the cervical spine.
The cervical collar should be removed while another person holds the
head midline. No traction should be applied to the neck. The cervical
spine is palpated for tenderness over the spinous processes. If there is
tenderness over a specific region the collar should be reapplied and the
spine evaluated with X-ray. If there is no tenderness (or only soft tissue
tenderness) the child should be allowed to gently move the head side to
side. If this produces pain posterior in the neck the collar should be reap-
TABLE 16.5.1: Classification of cervical spine injuries

Mechanisms of injury
1. Flexion
i. Flexion tear drop fracture
ii. Bilateral facet joint dislocation
iii. Atlanto-occipital dislocation
iv. Displaced odontoid fracture
v. Anterior subluxation
vi. Anterior wedge fracture
vii. Clay Shovelers fracture
2. Extension
i. Atlantoaxial dislocation
ii. Hangmans fracture C2
iii. Extension tear drop fracture
3. Rotation
i. Rotary atlantoaxial dislocation
ii. Unilateral facet dislocation
4. Vertical compression
i. Jefferson fracture (burst fracture C1)
ii. Burst fracture vertebral body
Stability
Very unstable
Unstable
Unstable
Unstable
Unstable
Stable
Very stable
Very unstable
Unstable
Unstable (in extension)
Unstable
Stable
Very unstable
Stable
378
plied and the spine X-rayed. If there is not pain on movement the collar
and cervical spine protection can be removed.
Young children represent a difficult subgroup. They are preverbal and
cannot follow commands or communicate easily. If palpation of the posterior cervical spine does not cause distress the neck should be let free, if the
child spontaneously moves the neck without discomfort the neck can be
cleared.
Radiographic Images
Radiographic evaluation is required for all children who do not meet all
the criteria for clinical clearance of the cervical spine. All patients who
require radiological evaluation require a full cervical spine series.
The cervical spine series consists of a lateral film, an anterior-posterior film and an odontoid view. Using these three views all abnormal cervical
spines will be detected, allowing further investigations to fully delineate
the individual injuries.
CT scan of the cervical spine: There has been a number of indications for
routine CT scan. The most widely accepted being for further evaluation
and elucidation of fractures identified or to view suspected lesions which
are not seen adequately on the initial cervical spine series. Other suggested
indications are for the assessment of the unconscious patient with normal
initial radiographs, and for patients having a CT scan of brain.
MRI brain and spine: It is the imaging method of choice for assessing
ligamentous injuries and for spinal cord injuries. In many instances MRI
will alter the specifics of surgical management in those who require surgical stabilization. MRI provides prognostic information in children with
spinal cord injury.
Radiographic Evaluation
Evaluation of the lateral cervical spine radiograph begins with assessment
of the four linescorresponding to the anterior vertebral bodies, the posterior vertebral bodies, the spinolaminar line, and the tip tips of the spinous
processes. All four of these lines should follow a smooth, even contour. The
articular facets should be parallel, the intervertebral disc spaces, at the
posterior margin, of the vertebral bodies, should be similar, and the distances between spinous processes should show no significant widening
(fanning). Review of the soft tissue shadow should show a retropharyngeal
space of not more than one half the AP diameter of the vertebral body at
C2 and no wider than the full width of the vertebral body at C6. As mentioned this may be difficult to interpret in the crying child.
Assessment of these areas of possible abnormality has been made easier
by the formulation of a series of normal measurements. For the atlantoaxial relationship (C1-C2) a measurement of the distance (on the lateral
film) from the posterior border of the anterior arch of C1 to the anterior
margin of the odontoid should be less than 5 mm in children under 8 yrs
379
of age, and 3 mm in older children and adults. To assess the relationship

of the bastion of the skull to the atlas the most reliable measurement in
children is Harriss posterior axial line which should lie within 12 mm of
the bastion of the skull.
Indications for thoracolumbar spine X-rays in multitrauma:
1. Pain in the thoracic or lumber region.
2. Tenderness of the spine in the thoracic or lumber region.
3. Significant bruising or deformity of the spine.
4. Altered conscious state.
5. Proven fracture in another region of the spine.
The standard views for both areas are the anterior-posterior radiograph and the lateral film. In the thoracic region the radiographs need to
be overexposed compared to a normal chest X-ray to allow adequate views
of the spine.
The films should be evaluated by following the anterior and posterior
vertebral body lines and the spinolaminar line on the lateral view. These
three lines should have a parallel course. The height of each vertebral
body should be assessed anteriorly and posteriorly, and a difference of
more than about 3 mm treated as pathologic. On the AP view the paraspinal
lines should be closely inspected to detect evidence of paraspinal hematoma.
The posterior elements should be visible through the vertebral body and
should be in alignment. Each vertebra should be inspected; an apparent
empty or invisible vertebral body indicated a fracture dislocation with distraction.
While most thoracic and lumber spine fractures are diagnosed on the
initial plain radiographs, these films often do not provide enough information on the extent of the injury and a CT scan of the region is usually
obtained elucidate the full extent of the injury. MRI will be needed to visualize all ligamentous and spinal cord involvement.
Management
Management must start with care of the airway, breathing and circulation. Only once these areas have been stabilized should management of
the spine proceed. However, while the patient is being stabilized the spine
should be maintained in alignment and patient moved via log rolling. A
thorough assessment and investigation of the abdomen and chest is mandatory for all patients with significant thoracic and upper lumbar spine
injuries, and injuries to the pelvic must not be forgotten with lumber
spine injuries. As many of these injuries are associated with intra-abdominal injuries an ileus is common and nasogastric or orogastric tube should
be inserted. Consultation with a pediatric orthopedic surgeon or neurosurgeon should be sought for definitive care of the injury. Surgical
stabilization is usually requred for unstable fractures and those fractures
associated with neurological injury.
380
Spinal Cord Injury

The goal of management of injury to the spinal cord or cauda equina is to
minimize the resulting neurological deficit. This commences with adequate
immobilization of the spine and complete and thorough investigation to
detail the anatomy of the injury.
Spinal cord injury should be suspected in any child who has multisystem trauma, minor trauma associated with spinal pain, sensory or motor
symptoms, and any patient with altered consciousness. The patient must
be adequate immobilized such as on a spinal board with a cervical collar
and head immobilizer and any assessment of the back or patient movement accomplished with by log rolling. Up to 50 percent of patients with
spinal cord injury will have at least moderate head injury.
Spinal Cord Injury Syndromes

A number of patterns of neurological deficit are seen in with spinal cord
injury, with the deficit dependent on the portion of the spinal cord damaged.
1. Neurogenic shock: The manifestations of loss of sympathetic output to
the cardiovascular systems. It is seen immediately after complete cord
injury at the level of T6 or above. This should not be confused with
spinal shock, which is the reversible dysfunction of the spinal cord associated with injury. It is concussion of the cord without permanent
damage. It may exist alone or in combination with permanent cord
injury. Its resolution is responsible for the improvement in neurological function seen in the first few days post injury.
2. Complete or partial cord injury: The distinction between a complete
injury and a partial injury is done by preservation of some motor or
sensory function below the lesion. Many patients with partial injury
will regain much or all of the neurological function.
Complete cord injury is usually seen in injuries of the thoracic
spine and thoracolumbar junction. The spinal cord is large in relation
to the size of the spinal canal at this level. Complete cord injuries that
remain at 24 hours rarely regain any significant function.
3. Cauda equina lesions: Injuries at or below L2. It involves the peripheral nerves rather than the spinal cord and can show significant
recovery of lower limb. The sphincter function even gets weakened
after the injury.
4. Central cord syndrome: It is usually seen in hyperextension injury resulting in herniation of the intervertebral disc into the spinal cord.
The resulting injury causes a motor deficit that is greater in the arms
than legs more extensive in the small muscles of the hand. The sensory
deficit is variable.
5. Brown-Sequard syndrome: It is hemi section of the cord which causes a
contralateral loss of pain and temperature sensation and an ipsilateral
motor paralysis and loss of proprioception below the level of injury.
381
Approximately two thirds of those with central cord syndrome and onethird with Brown-Sequard syndrome shows good recovery.
Clinical Assessment
The most immediate threats to life and spinal cord function of patients
with spinal cord injury remain hypoxia and hypotension.
1. Initial steps in the management of a patient with a suspected spinal
cord lesion are the assessment, resuscitation and maintenance of the
airway, breathing and circulation. Spinal cord lesion in the upper cervical spine may impair respiratory function and require early intubation
and mechanical ventilation.
2. The unstable cervical spine must be maintained in alignment without
traction during treatment of the airway.
3. The loss of sympathetic vasomotor tone after the cervical spine cord
injury will result in vasodilatation, venodilatation and reduced venous
return to the heart causing hypotension. Usually there is an associated
relative bradycardia for age and existing blood pressure, which will
help distinguish this response from hemorrhagic shock.
4. Initial fluid resuscitation with 10 to 20 ml/kg should adequately replace the relative hypovalemia. If hypotension persists, measurement
of central venous pressure (CVP) may be needed to guide fluid replacement. Excessive fluid replacement that pushes central venous and
pulmonary artery pressures above the normal range will result in pulmonary edema.
5. In patients who are significantly bradycardic inotropic agents such as
dopamine or adrenaline may be useful. Patients requiring more than
40 ml/kg of fluid replacement and having a low CVP must be assumed
to have other injuries causing blood loss.
Examination of the neurological impairment is done as apart of the
secondary survey. A thorough examination of the motor function of the
limbs and assessment of reflexes should be performed and a level of sensory deficit sought.
Radiographic Evaluation
In all patients with suspected spinal cord injury the spine should be
X-rayed. The radiographs should include the entire spine a multiple levels
of injury are common.
MRI should be performed as soon as possible after identification of
spinal cord injuries it will allow identification of remedial intraspinal problems in patients with a partial neurological deficit. The appearance of spinal
cord on MRI also allows prediction of neurological outcome. Cord transection and major hemorrhage have a poor outcome, minor hemorrhage and
edema have a moderate to good outcome, and a normal MRI is associated
with complete recovery.
382
Treatment
Most of the treatment available for spinal cord injuries is supportive.
1. The breathing and circulation must be supported as needed.
2. As there will be a neurogenic bladder catheterization is necessary and
a nasogastric tube is needed.
3. For transport, antiemetic is useful to prevent and vomiting and spine
movement or airway compromise.
4. Subcutaneous low molecular weight heparin should be instigated once
the patient is stable to prevent deep venous thrombosis.
Once the patient has been stabilized and investigated and transferred
to a spinal cord injury unit should be expedited. These unit and associated
intensive care units are geared to manage the cardio-respiratory compromise that may occur in the ensuing weeks, the psychosexual issues that
accompany spinal cord injury, the urological problems, and the potential
for skin breakdown that are exaggerated in these patients.
SCIWORA
Spinal cord injury without radiographic abnormality (SCIWORA) is defined as objective signs of myelopathy as a result of trauma with no
evidence of fracture and ligamentous instability on plain X-rays or tomography. SCIWORA is most frequently seen in younger children,
especially below 8 years of age and in injuries of the cervical spine.
Postulated causes includes ligamentous laxity and bony immaturity allowing excessive, transient movement during trauma causing distraction
or compression of the spinal cord or cord ischemia due to vascular injury or hypoperfusion. The incidence reported in children ranges from
1 to 10 percent of all spinal cord injuries.
Younger children tend to have more profound neurological injury and
hence less long-term improvement. A number of children will present with
minor neurological injury and progress to complete or partial spinal cord
injury. Because of these diverse presentations all children with history of
neurological symptoms of any neurological deficit should be treated as a
patient with a potential spinal cord injury.
After primary resuscitation and radiographic evaluation any patient
with any neurological deficit should remain immobilized until all bony,
ligamentous and spinal cord injury is excluded or treated. Further investigation with a CT scan focused at the level of symptoms and possibly MRI
to view the cord should be performed. Delayed flexion and extension radiographs can be used to determine ligamentous stability of the cervical
spine. MRI provides the same prognostic information in SCIWORA injuries as in other spinal cord injuries.
Management of the potentially injured cervical spine is shown in Flow
chart 16.5.1.
383
Flow chart 16.5.1: Guideline to management of the potentially injured cervical spine
Bibliography
1.
2.
3.
Brandser EA. El-Khoury GY. Thoracic and lumbar spine trauma. Radiologic
Clinics North Am 1997;35:53357.
Jaffe DM. Evaluation of children for cervical spine injuries. In: Strange GR,
editor. Pediatric emergency medicine: A comprehensive study guide. Ohio:
McGraw Hill, 2002.
Oakley ED. Spinal injury. In: Cameron P, Jelink G, Everitt I, Browne G, Raftos
J Editors. Textbook of Paediatric Emergency Medicine, 1st edition, 2006. Philadelphia: Churchill Livingstone. 63948.
16.6
Blunt Trauma
Trauma is a common cause of death in children above 1 year age. Majority

of the injuries are blunt in nature. Motor vehicle collisions, automobile
versus pedestrian accidents, bicycle injuries and falls are associated with
the greatest risk of blunt trauma. Childhood sports and recreational activities can also sometimes produce blunt trauma.
Other than immediate history regarding the nature of trauma, history
of bleeding disorder is very important. Thorough examination is invaluable but most important is the assessment of vital parameters. Tachycardia
is the most significant parameter.
Basic Principles of Trauma Management

1. Do not waste timeeven a well looking child may deteriorate rapidly.
2. Occult injury should be suspectedinternal injury may not be manifest always.
3. Each child should be approached systematically.
Management
1. Urgent investigations: CBC, LFT, X-rays and urinalysis.
2. Fluid resuscitation: Particularly in unstable children. Normal saline or
Ringers lactate 20 ml/kg initially.
3. Blood: Continued hemodynamic instability even after 2 boluses should
be treated with 10 ml/kg packed RBC.
4. CT scan: As a part of initial assessment if the child is stable and facility
is available. Unstable children should be stabilized first before going
for CT scan.
5. Surgical referral.
Chest Trauma
Several vital structures are in the thorax. Diaphragm, lungs, heart, great
vessels, esophagus and thoracic spine are prone to injury in severe trauma.
In any chest trauma chest X-ray should be done promptly.
Chapter 16.6: Blunt Trauma
385
Lung Contusion
In children significant lung injury can occur without chest wall injury or rib
fractures. It may also present insidiously hours after trauma. Chest X-ray
may show pulmonary opacity, CT scan may reveal contusion. Rib fractures
or pneumothorax may also be associated.
Management
i. Oxygenation: High flow mask or positive pressure ventilation.
ii. Pain relief.
iii. Restricted fluid therapy.
Pneumothorax
Though pneumothorax varies in their size and clinical significance, they
should be considered as having the potential to cause cardiorespiratory
compromise. Chest X-ray is diagnostic.
Management: Oxygen should be administered and intravenous line started.
All children with traumatic pneumothorax should be admitted. Depending on the clinical presentation, chest tube should be inserted after
stabilization.
Pericardial Tamponade
In this rare complication the child presents with dyspnea and tachycardia.
Echocardiography is confirmatory.
Flail Chest
This uncommon injury in children results in multiple rib fractures that
destabilize the chest wall and result in ineffective ventilation.
Management: Strapping or external stabilization of chest wall is not required in children. These children require intubation and mechanical
ventilation.
Tracheobronchial Injury
They typically present with respiratory distress and subcutaneous
emphysima. This injury is also rare.
Management: Urgent chest tube placement. Chest X-ray shows large air
leak and failure of lung expansion. Cardiothoracic surgical consult should
be obtained.
Mediastinal Injury
It may occur in adolescents due to high speed motor vehicular accident.
Aortic rupture is very serious and often fatal. Diagnosis depends on clinical suspicion.
Management: ABC and stabilization should be started as soon as possible.
Management is surgical.
386
Abdominal Trauma
There are some unique features in children which make them more vulnerable
to abdominal injuries. The rib cage does not extend as far down as in adults,
the ribs are more compliant and the abdominal wall musculature is thinner.
Consequently the upper abdominal viscera are more at risk of injury.
Liver Trauma
Spleen and liver are the two organs commonly injured by blunt trauma in
children.
Abdominal CT scan, particularly contrast CT scan is helpful in
determining the extent of injury. Hemodynamic assessment is most
important in any child with trauma. Management of liver trauma is outlined
Splenic Trauma
Splenic trauma should be suspected in children with left upper quadrant
tenderness, left lower rib fractures or evidence left lower abdominal or
chest contusion. The spleen is a commonly injured organ in blunt
abdominal trauma. CT scan finding of splenic rupture is shown in Figure
16.6.1 and management of splenic trauma is shown in Flow chart 16.6.2.
Pancreatic Trauma
Though pancreatic trauma is rare in children but it should be suspected in
children who falls on the horizontal handle bar of a bicycle and sustains a
crush injury. It is often very difficult to diagnose clinically. CT scan abdomen may be helpful.
Flow chart 16.6.1: Management of liver trauma
Chapter 16.6: Blunt Trauma
387
FIG. 16.6.1: CT scan showing splenic rupture
Flow chart 16.6.2: Management of splenic trauma
Renal Trauma
Most renal trauma is the result of motor vehicle accident. Presence of visible or microscopic hematuria following abdominal trauma should raise
the suspicion of renal injury. Most renal trauma heals with conservative
management. The overall management is similar to liver trauma.
Bibliography
1.
2.
Livingstone. 6558.
Wegner S, Colletti JE, Van Wie D. Pediatric blunt abdominal trauma. Pediatric
Clinics of North America 2006;53:24356.
16.7
FracturesInitial Stabilization
and Management
Anirban Chatterjee
Musculoskeletal injuries in children are fairly common accounting for 10

to 15 percent of all childhood injuries. These include fractures, dislocations and soft tissue injuries. Childrens bones are malleable and weaker
than adult bone. The long bones have physes and epiphyses, which being
centers of growth are also weak points in the appendicular skeleton and
are therefore prone to injury. Ossification in the epiphysis increases with
age, thus imparting rigidity to the epiphysis. This is why epiphyseal injuries are encountered more often in older children, while younger children
sustain plastic deformation and greenstick type fractures.
The most common sites for fractures are the distal forearm and hand,
accounting for 50 percent of pediatric fractures. The peak incidence is
during adolescence.
The eyes do not see what the mind does not knowtherefore one
must be aware of the commonest fractures, epiphyseal injuries and dislocations that occur in children so that, one can institute early and proper care
to the injured part and the child.
Glossary of some common terms used in pediatric musculoskeletal injuries
1. Greenstick fracture: Failure of cortical bone due to bending forces. One
cortex (tensile) surface fails first while the other (compression) cortex
remains in plastic deformation, just like a green twig.
2. Torus fracture or buckle fracture: Derived from Latin tori meaning swelling or protuberance. Essentially a greenstick fracture resulting
from compression failure of the long bone. The force being transmitted axially along the long bone and therefore occurs at the junction of
the metaphysis with the diaphysis, where there is a transition from the
weaker cortical bone of the metaphysis with the stonger cortical bone
of the diaphysis. The metaphyseal cortex buckles or deforms without complete failure due to its less rigidity. This creates a relatively
stable injury. Commonly seen at distal radius, distal femur and proximal humerus.
3. Plastic deformation: The bone deforms under the applied load but
does not return to its original shape. This is due to microfractures
Chapter 16.7: FracturesInitial Stabilization and Management
4.
5.
6.
7.
389
occurring within the osteons causing changes in the ultrastructure of

bone. Common bones involved areradius and ulna, humerus and
fibula.
Displacement: It refers to the position of the fragments of the fracture.
Usually the distal fragment determines the nomenclature with respect
to the position.
Fracture pattern: Transverse, oblique, spiral, etc. are terms used to
describe the fracture configuration as seen on the X-rays. These usually refer to complete diaphyseal fractures.
Diaphysis, metaphysis, physis and epiphysis: Different parts of a long
bone.
Open fracture or compound fracture: It refers to a fracture which communicates with the external environment, i.e. there is associated soft
tissue injury overlying the fracture site. Grades of severity exist ranging from simple inside out compounding to extensive soft tissue loss.
Management Goals
1. Suspicion of fractureget relevant history of trauma. Try to judge velocity of injury: high/low.
2. Examine the child without further jeopardizing the fracture.
3. Splint the limb.
4. Order relevant X-rays in two orthogonal planes.
5. Provide analgesia and sedation to calm the child and thus the agitated
family.
6. Send appropriate referral.
7. Suspect (Red flag) for child abuse, pathological fractures, e.g. osteogenesis imperfecta, when multiple fractures seen, or fractures through
bone tumors when fractures occur spontaneously or after trivial injury
Figure 16.7.1, or in metabolic derangements like rickets, scurvy, etc.
Injuries in the Appendicular Skeleton

Common Upper Extremity Injuries
Fall on the Outstretched Hand
The usual mechanism is a fall on the outstretched hand with the hand or
volar aspect of the wrist hitting the ground first. In such cases suspect the
following:
1. Distal radius and or distal ulna fracture Figures 16.7.2 and 16.7.3.
2. Diaphysis of radius and ulna fracture.
3. Fracture with dislocation:
i. Monteggia type: Fracture of proximal ulna with dislocation of the
radial head Figure 16.7.4.
ii. Galleazi type: Fracture of distal radius with dislocation of distal
radio-ulnar joint.
390
FIG. 16.7.1: Pathological fracture through a simple bone cyst in the humeral diaphysis
FIG. 16.7.2: Displaced distal end radius and ulna fracture
391
FIG. 16.7.3: Angulated greenstick fracture of the distal radius with a buckle (Torus) fracture of the
distal ulna
FIG. 16.7.4: Monteggia fracture dislocation. Note the ulnar fracture associated with dislocated radial head. The associated dislocation necessitates early manipulative reduction, hence
early referral is indicated
392
4. Fractures around the elbow:

i. Supracondylar humerus fractures Figure 16.7.5.
ii. Lateral condyle humerus fractures Figure 16.7.6.
5. Proximal humerus fracture Figure 16.7.7.
6. Fracture clavicle Figure 16.7.8.
Fall Directly on the Elbow

If the injury is with a fall directly on the elbow, then suspect the following:
1. Supracondylar humerus fractures.
2. Lateral condyle of distal humerus fractures: This is a fracture of necessity,
i.e. it requires urgent attention if displaced due to its intra-articular
and physeal extension of the fracture pattern.
If the injury is due to a sudden pulling of the arm/hand of the child,
then suspect the following.
Pulled elbow synonym nursemaids elbow: It is essentially a partial tear of
the annular ligament around the neck of the radius, resulting in subluxation of the proximal radio-ulnar joint.
Check for radial pulse and sensorimotor deficit especially for median
and ulnar nerve dysfunction. Urgent referral is necessary as delay can cause
vascular compromise. Avoid tight bandaging as that may lead to compartment syndrome and later Volkmanns ischemic contracture in the forearm.
Lateral condyle fractures are epiphyseal injuries and displaced ones
require urgent operative reduction, so as to obtain union and good elbow
function.
FIG. 16.7.5: Displaced supracondylar fracture of distal humerus
FIG. 16.7.6: Displaced lateral condyle humerus fracture
FIG. 16.7.7: Displaced proximal humerus fracture
393
394
FIG. 16.7.8: Clavicle fracture
Immobilisation Methods and Optimum Position for

Injuries to the Upper Limb
1. A simple cuff and collar sling or a triangular swathe around the neck to
support the involved side elbow in flexion can be used for clavicular
fractures, fractures of the humeral shaft, the distal humerus.
2. An Above elbow posterior back slab with the elbow in flexion and forearm in the mid prone position is most suitable for fractures around the
distal humerus, for fractures of the shaft of the radius and ulna, and
for the fracture-dislocations in the forearm.
3. A Below elbow posterior back slab is suitable for fractures around the
distal radius, and in hand fractures.
Injuries in the Appendicular Skeleton

Common Lower Extremity Injuries
The tibia is the most commonly fractured bone, followed by the femur.
Fractures around the hip and pelvis account for less than 1 percent of pediatric fractures and hence have not been included in this chapter. Figures
16.7.9 to 12 are showing various fractures of the lower limb.
Femur fractures entail a significant amount of blood loss, hence the
child should be admitted for observation, ruling out other injuries and
hemodynamic stabilization. Splintage with a Thomas splint or surface skin
traction helps relive the muscle spasm associated with the injury.
Immobilization Methods and Optimum Position for Injuries to

the Lower Limb
1. An above knee posterior back slab with the knee in 15 degrees of flexion and ankle in 90 degree position is suitable for fractures of the
diaphysis of the tibia and fibula, as well as distal femur.
2. A Thomas splint or surface skin traction is required for immobilization
of fractures of the femur shaft, as well as proximal femur.
3. A Below knee posterior back slab is suitable for fractures around the
distal tibia, ankle injuries and in foot fractures.
395
FIG. 16.7.9: Transverse fracture of the femoral diaphysis in a 4-year-old child, with bone overlap
FIG. 16.7.10: Greenstick fracture of tibia and fibula with valgus angulation
396
FIG. 16.7.11: Undisplaced spiral fracture of the tibia, the fracture line is not visualized on the lateral
projection but is well visualized on the anteroposterior projection. This highlights
the need for X-rays in two orthogonal planes
FIG. 16.7.12: An epiphyseal fracture separation of the lower end of tibia in an adolescent child
397
Injuries to the Axial Skeleton

Injuries to the spine extending from the cervical to the lumbosacral region
and fractures of the rib cage are included in this section. Such fractures
need to be suspected in children who have sustained high velocity trauma,
e.g. polytrauma due to road accidents, falls from height, etc. In such situations head injury and associated visceral injuries and their management
take priority.
Definitive fracture management is usually deferred and the axial skeleton often immobilized with collars, belts till the child is treated for the
head injury and/or visceral injuries.
Injuries to the children need to be treated properly at the earliest opportunity so as to ensure optimum results. A high index of suspicion should
be maintained to come to a conclusive diagnosis and appropriate treatment or referral instituted.
Bibliography
1.
2.
Hatch E, Saunders C. Fracture Management for Primary Care, 1998.

Rockwood CA, Wilkins Editors. Fractures in Children, 6th edition. Philadelphia: Lippincott Williams and Wilkins, 2007.
17
OPHTHALMOLOGICAL
EMERGENCIES
17.1
Ophthalmological Issues
Lav Kochgaway
Pediatricians being the primary health care provider for infants and children need to be aware of the basics of ocular emergencies. In this chapter
we would try to explain the conditions in a simple pattern. It would help
the pediatricians to identify the condition and provide basic treatment before they are referred to a pediatric ophthalmologist.
Leukocoria
Leukocoria or white pupillary reflex is an ocular emergency in children.
The underlying etiology for white pupillary reflex may lead to vision threatening or even life-threatening consequences if left unattended.
Causes of White Pupillary Reflex

1.
2.
3.
4.
5.
6.
Congenital cataract.
Retinoblastoma.
Retinopathy of prematurity.
Intraocular infection (Toxoplasma, Toxocara).
Retinal detachment.
Coat disease.
Figures 17.1.1 and 17.1.2 show white pupillary reflex.
Diagnosis
1. White pupillary reflex with torch light.
2. Absence of red glow on distance direct ophthalmoscopy.
3. Presence of central opacity on distance direct ophthalmoscopy.
Congenital Cataract
Congenital cataract needs a special mention, since the etiology of the cataract
may be due to underlying general health problem of the child. Unilateral
congenital cataract is a definite emergency situation which needs to be
identified and operated upon as soon as possible. Bilateral congenital cataract
too needs to be operated within the first few weeks of life. This would prevent
the child from developing severe stimulus deprivation amblyopia.
402
FIG. 17.1.1: White pupillary reflexpediatric cataract (For color version see Plate 3)
FIG. 17.1.2: Leukocoriaretinoblastoma (For color version see Plate 3)
Etiology
Unilateral
i.
ii.
iii.
iv.
v.
vi.
Idiopathic.
Persistent hyperplastic primary vitreous.
Anterior segment dysgenesis.
Posterior lenticonus.
Trauma.
Masked bilateral cataract.
Chapter 17.1: Ophthalmological Issues
403
Bilateral
i.
ii.
iii.
iv.
v.
vi.
Idiopathic.
Hereditary.
TORCH infection.
Syphilis.
Galactosemia.
Other genetic metabolic disorders like hypoglycemia, pseudohypoparathyroidism, Lowes syndrome, Downs syndrome, myotonic
dystrophy, etc.
Investigations
Coexisting systemic illness need to be ruled out when a patient reports
with congenital cataract. Some of the investigations which may be helpful
in finding the cause are as follows:
i. TORCH titer.
ii. VDRL.
iii. Urine for reducing substance (especially after feed).
iv. Red cell galactokinase.
v. Urine for amino acids.
vi. Calcium and phosphorus levels.
Role of Pediatrician
i. White pupillary reflex is one of the sign which is almost invariably
associated with poor visual or life-threatening complications. As soon
as a white pupillary reflex is diagnosed the child should be referred
to a pediatric ophthalmologist.
ii. The parents should be explained regarding the urgency of the situation and need for an early intervention.
iii. These children should never wait for appointment of the pediatric
ophthalmologist. If required they should walk in for emergency consultation.
Red Eye
Common Causes
i. Acute conjunctivitis (viral/bacterial),
ii. Injury (Corneal abrasion or sub-conjunctival hemorrhage),
iii. Corneal ulcer.
History
i. History of trauma (Corneal abrasion, subconjunctival hemorrhage).
ii. Trauma with vegetable matter (Fungal corneal ulcer).
iii. Recent fever or upper respiratory tract infection.
404
A child with red eye can be approached in the following four categories
as shown in Flow chart 17.1.1. A child with red eye is shown in Figure 17.1.3.
Trivial Trauma with Red Eye

Without photophobia: Likely diagnosis would be subconjunctival hemorrhage without corneal involvement. The parents can be reassured but needs
an eye check up to rule out other effects of trauma like macular edema.
With photophobia: Likely diagnosis would be subconjunctival hemorrhage
with corneal abrasion. The diagnosis can be confirmed with simple application of a fluorescein on anesthetized cornea. The abrasion on cornea
would get stained. If present, the eye can be patched after applying antibiotic eye ointment and referred for further management.
Conjunctival Congestion with Watery/Blood Stained Discharge

i. Likely diagnosis would be viral conjunctivitis.
ii. Lid swelling with boggy conjunctival congestion may make examination of eyeball difficult.
iii. Photophobia may give a hint regarding involvement of cornea.
iv. Can give prophylactic broad spectrum antibiotic to prevent superimposed bacterial infection.
Flow chart 17.1.1: Approach to a child with red eye
FIG. 17.1.3: Red eye (For color version see Plate 4)
405
v. Donot apply steroid eye drops as it may aggravate the condition,

vi. Donot patch the eye if there is suspicion of viral/bacterial infection.
Conjunctival Congestion with Mucopurulent Discharge

i. Look for photophobia, if positive then likely to have corneal ulcer as
well.
ii. Ask for injury with vegetable matter (especially patients with rural
background)likely to be fungal ulcer.
iii. Can start broad spectrum antibiotic drops before referringl
iv. Donot apply steroid eye drop or patch the eye.
Only Congestion and Pain, no Discharge

i.
ii.
iii.
iv.
History of hypodermic needle injury or recent fever,

Endophthalmitis due to above causes need to be ruled out,
Urgent referral,
Antibiotic drops can be started.
Trauma
Ocular trauma is one of the most common pediatric ocular emergencies.
What makes it most challenging is the variety of presentation that these
children may have. The common clinical presentations of children with
history of trauma are the following. Traumatic cataract with sphincter tear
due to blunt trauma is shown in Figure 17.1.4.
1. Hypodermic needle (especially in rural settings).
2. Injury with sharp tip of pencil or pen.
3. Injury with sharp household items like broom sticks.
FIG. 17.1.4: Blunt traumatraumatic cataract with sphincter tear (For color version see Plate 4)
406
4. Chemical injuryacid or alkali.

5. Blunt trauma with or without perforation.
6. Corneal foreign bodypartial or full thickness.
Penetrating/blunt Injury with Ocular Perforation

i.
ii.
iii.
iv.
History regarding the cause of injury,

Possibility of intraocular foreign body? Extent of perforation?
Prolapsed iris or intraocular contents?
Any ocular perforation should be repaired within 6 hours of primary
injury.
Pediatricians Role
a.
b.
c.
d.
Patch the eye,

Dont apply any eye drop or ointment in a perforated globe,
Injection Tetanus Toxoid can be administered,
Advice the patient to be nil oral in case there is access to facility
where emergency wound repair can be done,
e. Dont try to clean the eye with prolapsed ocular tissue; it may lead to
auto evisceration.
Hypodermic Needle Injury

i.
ii.
iii.
iv.
Look for entry wound.

Eye may not be soft as in globe perforation.
Antibiotic drops can be started.
Need early referral as have very high chances of developing
Endophthalmitis or traumatic cataract.
Chemical Injury
Lime used with beetle leaves is one of the common causes. Figure 17.1.5
shows eye affected by chemical injury.
a.
Immediate irrigation with ringer lactate solution connected to IV tube

(full bottle).
b. Can be done after applying local anesthetic to the eye.
c. Both the fornix to be washed thoroughly to wash out any coagulated
particle or the granules.
d. Eye to be patched after application of antibiotic ointment.
e. Immediate referral.
Corneal Foreign Body

Assessment regarding the depth of the foreign body to be done, preferably
by an ophthalmologist. The injury may be full thickness, if it was a flying
particle that pierced the eye.
407
FIG. 17.1.5: Chemical injury affected eye (For color version see Plate 4)
a. In case of any doubt regarding the depth, refer.
b. If sure of it being very superficial, it can be removed using cotton tipped
applicator or a 23 to 26 G needle. The direction of the stroke of needle
should be away from the pupillary area.
c. Eye to be patched after application of antibiotic ointment and referred
to pediatric ophthalmologist.
Blunt Trauma without Perforation

i. Will need assessment for the effects of the trauma like angle recession, traumatic cataract, macular edema, zonular weakness, etc.
ii. No immediate treatment required from the pediatrician.
iii. Word of cautionbullous subconjunctival hemorrhage with soft eyeball may have an underlying perforation globe.
Periocular Infections
Patients with periocular infection may have a variety of presentation
depending on the site involved. The common periocular infections in
children are hordeolum externum (Stye), hordeolum internum (Chalazion), prespetal orbital cellulitis and nasolacrimal duct obstruction
with acute dacryocystitis. Hordeolum externum and internum would
present with infection in the eyelids. Preseptal cellulitis would lead to
diffuse swelling of the periocular soft tissue, while acute dacryocystitis
would involve the area near nasal canthus.
Most of the periocular infections would require systemic antibiotics.
Depending on the severity these children would require either parenteral
408
FIG. 17.1.6: Buphthalmos (For color version see Plate 5)
or oral antibiotics. These children could be started on treatment before

being referred to an ophthalmologist.
Do not wait to see an ophthalmologist if the child is responding to
therapy. They need evaluation in terms of the structures involved, as an
orbital cellulitis may progress to cavernous sinus as well. One of the ways to
assess depth of infection is to assess ocular motility. If the motility is full,
then it would most likely not have involved the deeper structures.
Buphthalmos
A congenital glaucoma or buphthalmos is identified by large eyeball, bluish sclera and the child would have photophobia and lacrimation. It may
be unilateral or bilateral. These children need urgent referral because if
untreated they may end up with irreversible blindness due to optic atrophy
and cloudy cornea. Figure 17.1.6 shows a child with buphthalmos.
Shaken Baby Syndrome

Any child who on examination is suspected to have shaken should have an
emergency eye check up. These children may have ocular associations like
retinal hemorrhages or vitreous hemorrhage. These patients if admitted
can be examined bedside initially.
Bibliography
1.
Wright KW, Spiegel PH. Pediatric Ophthalmology and Strabismus, 2003. The
Wills Eye Manual, 5th edition.
18
OTOLARYNGOLOGICAL
EMERGENCIES
18.1
Otolaryngological Issues
Jaydeep Choudhury
Pain in the ear is a very common complaints in children. This often causes
incessant cry and disturbed sleep. The common causes of ear pain or otalgia are listed in Table 18.1.1.
TABLE 18.1.1: Common causes of ear pain in children
Source of pain
Causes
Intrinsic to external ear
Otitis externa
Foreign body
Trauma
Perichondritis infected preauricular cyst or sinus
Acute otitis media
Middle ear effusion
Barotrauma
Mastoiditis
Via trigeminal nerve:
i. Dental
ii. Temporomandibular joint
iii. Jaw
iv. Oral cavity
Via facial nerve:
i. Herpes zoster
ii. Bells palsy
Via glossopharyngeal nerve:
i. Tonsil
ii. Oropharynx
iii. Nasopharynx
Via vagus nerve:
i. Laryngopharynx
ii. Esophagus
iii. Thyroid
Via cervical nerves:
i. Lymphnodes
ii. Cervical spine
iii. Neuralgia
Others:
i. Migraine
ii. Sinuses
iii. Salivary gland
iv. CNS
Intrinsic middle ear and mastoid
Referred
412
Acute Otitis Externa

Acute otitis externa is an inflammatory condition, anatomically which involves external auditory canal and external surface of the tympanic
membrane. Pathologically there is a compromise of the lining of the canal.
Etiology
1. Hot and humid conditions and in swimmingin these conditions the
ear canal is exposed to water for long periods. The canal becomes
macerated and desquamates.
2. Local trauma due to various causesforeign bodies, cotton swabs, insect bites and eczema.
3. Ear plugs.
4. Immunocompromised host.
Clinical Features
1. Ear acheranging from initial pruritus to severe pain. Pain is worse
with motion or chewing. Pain aggravates on pulling the auricle or tragus.
2. Aural fullnesscanal becomes erythematous and increasingly swollen.
3. Hearing loss in some cases.
Management
1. Cleaning and debridement of the ear canal with cotton swab and hydrogen peroxide.
2. An acidifying agent like 2 percent acetic acid is useful to inhibit growth
of bacteria and virus.
3. Topical preparationsmixed antibiotics, anti-fungal and steroid drops
or antibiotics alone atleast for 3 days after resolution of symptoms.
Steroids decrease inflammation.
4. For pain reliefnonsteroidal anti-inflammatory drugs (NSAIDs).
Prevention
1. Drying the ear canal after bathing and swimming.
2. Use of ear plugs while swimming.
3. Instillation of 2 percent acetic acid solution in the ear.
Various Types of Otitis Externa

Furunculosis
Relatively localized form of otitis externa, usually occurs in the outer
portion of the ear canal. Abscess develops in a hair follicle with spread of
the infection to the surrounding skin. Staphylococcus aureus is the most
common agent.
Chapter 18.1: Otolaryngological Issues
413
Treatment: Incision and drainage followed by application of antistaphylococcus

antibiotics.
Diffuse Bacterial Otitis Externa

This is the most common form of otitis externa. It is most commonly seen
in swimmers. The commonest pathogen is Pseudomonas aeruginosa.
Initially there is intense pruritus. With progress of infection it becomes
increasingly painful. There may be conductive hearing loss. On examination the external ear may be red and edematous. Secretions may be present,
which is sometimes purulent.
Otomycosis
It is a chronic superficial infection of ear canal and may extend up to tympanic membrane. It occurs more commonly in humid weather, after
prolonged steroid application or in immunocompromised.
Pruritus is the most prominent feature. Pain may also be present. Debris may seen in the external ear.
Treatment: Topical antifungal agents like clotrimazole or itraconazole. A
combination of antifungal, steroids and acidifying agents may also be applied.
Malignant or Necrotizing
It is usually caused by Pseudomonas aeruginosa and as a complication of persistent otitis externa.
The characteristic features are severe erythema, edema and tenderness of the ear canal and the surrounding area with otorrhea. The pain is
often severe. Facial nerve palsy is sometimes present.
Treatment: Prolonged systemic therapy is required with antipseudomonal
drugs like quinolones. Intravenous antibiotics may also be required. CT
scan imaging may be required to see bone involvement.
Acute Otitis Media (AOM)

Acute otitis media is characterized by acute onset of pain in the ear, fever
and otorrhea with middle ear effusion.
Middle ear effusion is indicated by any of the following:
1. Bulging of the tympanic membrane.
2. Limited orabsent mobility of the tympanic membrane.
3. Air fluid level behind tympanic membrane.
4. Otorrhea.
Middle ear inflammation is characterized by
1. Direct erythema of the tympanic membrane.
2. Distinct otalgia that interferes with normal activity or sleep.
414
Causative Organisms
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis make
85 percent of total incidence and rest 15 percent includes Staphylococcus
aureus, gram negative organisms and respiratory viruses.
Management
Treatment algorithm of AOM is shown in Flow chart 18.1.1.
In children with penicillin allergy, erythromycin 50 mg/kg/day 6 hourly
or cotrimoxazole 6 to 12 mg trimethoprim, 30 to 60 mg sulfamethoxazole
kg/day 12 hourly.
Foreign Body in the Nose and Ear

Children love to play with small objects and put those in their nose and
ears. The foreign bodies found in nose and ears are parts of toys, various
food particles, pieces of papers, beads and sometimes small insects.
Flow chart 18.1.1: Treatment of acute otitis media
415
Clinical Features
Sometimes, children present with a definite history of self-insertion of the
foreign body. Some children present with complains of impairment of hearing or olfaction. Many children are asymptomatic and the foreign body is
discovered by parents or the physician during physical examination.
The physical examination findings are variable depending on various
factors like size of the object, duration since its impaction and physical
characteristics of the foreign body. A small foreign body in nose or ear may
be asymptomatic whereas a large one may cause trauma and bleeding. A
foreign body which is present in either ear or nose for a long duration may
present with unilateral nasal or ear discharge, bad odor or epistaxis.
An insect in the ear canal presents with irritation, intense constant
pain in the ear and a sensation of movement inside.
Most of the electronic toys are powered by button batteries. Children
may swallow these button batteries. The button batteries release small amounts
of chemicals and voltage that may lead to alkaline chemical burns, necrosis
and perforation. Button batteries should be removed to as soon as possible.
Management
The following are the prerequisites for foreign body removal in an emergency department:
1. The child should be restrained properly or adequately sedated, otherwise the attempts will cause unnecessary trauma.
2. A good light source is very important for proper visualization.
3. The following instruments should be availablenasal speculum, alligator forceps, curette and suction apparatus.
The following techniques may be adopted for foreign body removal.
1. Manually grasping the object with forceps.
2. Getting behind the object with a curette, when there is room for advancing the curette.
3. Irrigation by water.
4. Applying suction to the surface of the foreign body.
One should attempt foreign body removal in the emergency only if
one is confident for removal because repeated failed attempts result in
increased swelling and trauma. It may also push the object to such a location from where it will be very difficult to remove. An attempt for removal
is based on the characteristic of the foreign body and anatomic location.
1. A live insect: It should first be killed with either 2 percent lidocaine or
mineral oil.
2. Vegetable matter or sponges: Irrigation should be avoided because the
added water will make the foreign body swell.
3. Smooth round: Suction should be applied.
4. Large occlusive nasal foreign body: Bag and mask ventilation over
mouth and manually occluding the noninvolved nostril.
416
If attempted removals are unsuccessful, one should refer to an otolaryngologist.
Epistaxis
The rich blood supply and thin mucus membrane makes the nose vulnerable to bleed spontaneously following minor trauma. Most of the time
bleeding from nose or epistaxis is mild and self-limited.
Etiology
1. The commonest causes in children are local trauma due to nose picking and upper respiratory infection.
2. Other causes arefacial trauma, foreign body and sinusitis.
3. Systemic causesliver disease, leukemia, ITP and coagulopathies.
Bleeding disorders or coagulopathies may be congenital like von
Willebrands disease, hemophilia and Osler-Weber-Rendu disease or
acquired due to NSAIDs and aspirin.
Clinical Features
According to the site of bleeding, it may be of the following types:
1. Anterior: It is more common and accounts for approximately 90 percent of the cases. The commonest age of epistaxis is 2 to 10 years. It
usually arises from the venous Kiesselbachs plexus. As the bleed is
mostly of capillary or venous origin, it is characteristically slow and
persistent oozing.
2. Posterior: It arises from artery and bleeds more profusely. Posterior
bleeding may manifest as hemoptysis, hematemesis or blood in the
posterior pharynx. It carries a higher risk of airway compromise, aspiration of blood and life-threatening hemorrhage.
Management
Minor Bleeding
1. Pinching the nostrils together for 5 to 10 minutes nonstop. One should
not release the grip in between.
2. A piece of gauze soaked with nasal decongestant epinephrine 1:10,000
or phenylephrine induces local vasoconstriction.
Major Bleeding
1. When anterior nasal bleeding is difficult to control: Cautery or anterior nasal packing with petroleum jelly may be done.
2. Posterior nasal bleeding: It is less amenable to cautery. It requires urgent admission for posterior nasal packing or epistaxis balloon. These
interventions should be done by an otolaryngologist.
417
Sinusitis
Sinusitis is a common form of upper respiratory tract infection in children.
Children usually do not present with classical features of sinusitis like the
adults. It is very difficult to distinguish between simple viral sinusitis,
rhinosinusitis and acute bacterial sinusitis.
Acute Bacterial Sinusitis

Among the various causes of sinusitis in children acute bacterial sinusitis
requires urgent treatment. Upper respiratory tract infections with symptoms persisting for more than 10 days without much improvement are more
likely to be bacterial sinusitis. Viral sinusitis presents with fever, constitutional symptoms and mucoid nasal discharge. But bacterial sinusitis
classically presents with high fever and purulent nasal discharge. Children
often have cough which is worse at night or on lying down.
Treatment
Antibiotics are the mainstay of treatment. Initially broad spectrum antibiotics like high dose amoxicillin or amoxicillin-clavulanic acid should be
started. If penicillin resistance is suspected azithromycin or cefuroxime
may be started. The duration of treatment should be 10 to 14 days.
Oral Cavity Lesions

Lesions in the oral cavity can be very distressing in children. It causes severe discomfort and pain. Children refuse to eat and may cry incessantly.
Herpetic Gingivostomatitis
It is caused by Herpes simplex virus (HSV). Commonly seen in children 6
months to 5 years.
Clinical Features
1. Systemic: Abrupt onset of fever, malaise and irritability.
2. Oral: Clusters of vesicles which coalesce to form large painful ulcers in
the oral and perioral region. Gingival region becomes erythematous
and edematous.
The duration of the symptoms is usually less than a week, but may last
for about 3 weeks.
Treatment
1. Topical: Anesthetics like diphenhydramine syrup mixed 1:1 solution
with magnesium hydroxide. This should be applied to the affected
area every 2 hours. Topical acyclovir has no role.
2. Paracetamol and ibuprofen for fever and pain relief.
418
3. Acyclovir: Should be started within 72 hours of the onset of lesions.

4. Due to severe pain children often refuse oral intake and they are at risk
of dehydration. Oral intake of fluid should be encouraged or else intravenous fluid may be given.
Herpangina
It is an oropharyngeal lesion caused by coxsackieviruses A and B. Commonly seen in children 3 to 10 years. It is highly contagious. Skin infected
with coxsackieviruses A manifests as hand, foot and mouth (HFM) disease.
Systemically there are flu-like symptoms of fever, sore throat and headache. The painful vesicles and ulcerations occur over the posterior pharynx
and tonsils.
The disease is self-limited, resolving within 3 to 7 days. Treatment is
symptomatic with systemic antipyretics and topical analgesics.
Bibliography
1.
2.
3.
AAP Guidelines for management of acute otitis media. American Academy of

Pediatrics. Pediatrics 2004;113:1451.
Bernius M, Perlin D. Pediatric ear, nose and throat emergencies. Pediatr Clin
North Am 2006;53:195-214.
Riding KH. Ear, nose, and throat disorders. In: Baldwin GA Editor. Handbook
of Pediatric Emergencies. Philadelphia: Lippincott Williams and Wilkins; 3rd
edition, 2001:146-64.
19
DERMATOLOGICAL
EMERGENCIES
19.1
Fever with Rash
Rash with fever in children refers to an eruption of the skin, usually, but
not always as a result of communicable diseases. The common causes of
fever and rashes in children is summarized in Table 19.1.1.
History
1. Age of the child: Roseola in infancy, Kawasaki disease under 5 years,
infectious mononucleosis in older children and adolescents.
2. Duration of the rash: Chronic inflammatory disease tends to follow
prolonged fever with rashes in variable stages of illness.
3. Associated with or preceded by fever and cold, irritability and malaise.
4. Accompanied by intense itching/pain.
5. History of known allergy or any exposure to an index case of contagious disease in the preceding 2 to 3 weeks period.
6. Is on particular drug recently: Mostly implicated drugs are antibiotics, sulphonamides and anticonvulsants.
TABLE 19.1.1: Conditions associated with fever and rashes
Cause
Conditions
Viral
Varicella, measles, rubella, roseola, erythema infectiosum, HFM

(Hand, foot and mouth disease usually due to coxsackie B virus),
enteroviral exanthem, HSV infection, infectious mononucleosis, viral hemorrhagic fever (like dengue), hepatitis B
Scarlet fever, scalded skin syndrome, toxic shock syndrome, meningococcemia, infective endocarditis, spirochetal infections
(syphilis), leptospirosis, Lyme disease
Systemic lupus erythematosus, systemic onset juvenile rheumatoid arthritis, vasculitis syndrome (Kawasaki disease, HenochSchnlein purpura), inflammatory bowel disease
Leukemia, lymphoma
Rickettsial, fungal, helminthic and protozoal infections. StevensJohnson syndrome, toxic epidermal necrolysis, histiocytosis
syndrome
Bacterial
Inflammatory diseases
Malignancy
Miscellaneous
422
7.
8.
9.
10.
Vaccination history.
History of travel recently.
Underlying illness: Heart disease, immunodeficiency.
Prodrome: Fever, associated symptoms, sequence of events. Rubella
and varicella with short prodrome, meningococcemia with short but
rapidly evolving constitutional symptoms.
Location and characteristics of rash, like color, size, pattern, secondary
changes in the form of crusting.
Different Forms of Skin Rash

i. Maculeflat and impalpable.
ii. Papuleraised and circumscribed, palpable.
iii. Vesicleraised, circumscribed, filled with fluid, less than 0.5cm diameter.
iv. Pustuleraised lesions filled with pus.
v. Petechiaeflat or raised hemorrhagic, up to 0.5 cm diameter, nonblanching.
vi. Purpuraflat or raised hemorrhagic spots over 0.5 cm in diameter.
vii. Ecchymosislarge, irregular discoloured areas, resulting from extravasated blood.
Figures 19.1.1 to 19.1.3 show children with measles, chicken pox and
meningococcal rash respectively. The conditions presenting with various
characteristic rashes is shown in Table 19.1.2.
FIG. 19.1.1: A child with measles (For color version see Plate 5)
Chapter 19.1: Fever with Rash
423
FIG. 19.1.2: A child with chickenpox (For color version see Plate 5)
FIG. 19.1.3: A child with meningococcal rash (For color version see Plate 6)
Distribution
i.
ii.
iii.
iv.
v.
Generalizedmeasles, scarlet fever, disseminated HSV.

Centralvaricella, roseola, Stills disease.
Peripheralgionatti Crosti syndrome, HMF, late stage of Kawasaki.
Flexural areasscarlet fever, SSS.
Extensor surfaceHSP, erythema nodosum, late stage of erythema
infectiosum.
vi. LocalizedLyme disease, herpes zoster, anthrax, streptococcal erysipelas, pseudomonal ecthyma gangrenosum.
424
Typical Facies
Malar rash in SLE, flushed cheek in scarlet fever, slapped cheek in erythema
infectiosum.
Other Features
i. General condition, temperature, altered sensorium (encephalopathy with convulsion in viral and rickettsial disease).
ii. Signs of shock (dengue shock syndrome, meningococcal disease and
gram-negative sepsis, TSS).
iii. Involvement of mucocutaneous junctions:
a. Koplik spotmeasles.
b. Conjunctivitismeasles, Kawasaki, SJS.
c. Congested pharynx and strawberry tongueKawasaki disease,
scarlet fever.
d. Involvement of eye, mouth and genitalia mucous membrane
HSV1 (oral), HSV2 (genitalia), SJS, TEN, TSS.
e. Oral ulcerHFM disease.
f. Exudative tonsillitisscarlet fever, infectious mononucleosis.
iv. Cervical lymphadenitisrubella, infectious mononucleosis, Kawasaki
disease, Stills disease, syphilis.
v. Hepatomegaly (with or without splenomegaly)infectious mononucleosis, leptospirosis, Stills disease.
vi. Arthropathyconnective tissue disorder, parvovirus B19 infection.
vii. PolyserositisSLE, dengue, Stills disease.
viii. NephropathySLE, HSP, leptospirosis.
ix. Multisystem involvementdisseminated varicella, HSV, leptospirosis, TSS.
TABLE 19.1.2: Differential diagnosis of rashes
Erythematous
Maculopapular
Petechiae or Purpura
Vesico-bullous
Staphylococcal SSS
Toxic shock syndrome
Anaphylaxis
TEN
Scarlet fever
Viral exanthem
(measles, roseola,
rubella)
Urticaria
Lyme disease
Pityriasis
Drug reaction
Erythema multiforme
Stevens-Johnson
syndrome
Meningococcemia
Rocky Mountain
spotted fever
Eczema, Psoriasis
Meningococcemia
ALL
HSP
TTP
ITP
Vasculitis
Varicella Zoster
HSV
DIC
Pemphigus vulgaris
Bullous pemphigus
Necrotizing fascitis
Contact dermatitis
HFM disease
Stevens-Johnson
syndrome
425
Evolution of Rashes
Few individual but typical examples:
i. Varicella: Rapid evolution in 24 to 48 hours through macule, papule,
vesicle and pustule, umbilication and scab. Lesions appear in crops
over 3 to 4 days in pleomorphic appearance.
ii. Measles: Commencing in hairline of the forehead and progress caudally over face, trunk, upper and lower limbs, finally desquamation
and brown staining in convalescing stage.
iii. Erythema infectiosum: 3 stage rash, cheek, generalized maculopapular
rash which fades centrally to leave a reticulated lacy pattern over limbs.
iv. Dengue: Biphasic fever with transient generalized macular erythema
at onset and then in secondary phase. Purpura who develop hemorrhagic dengue.
Diagnosis
Mostly Clinical
Measles, varicella, roseola, erythema infectiosusm, HMF disease.
Diagnostic Criteria Combining both Clinical and Laboratory Results

Rheumatic fever, SLE, Kawasaki disease.
1. Complete hemogram and peripheral smear study:
a. Cytopenias in viral infections.
b. Neutrophilia in KD, Stills disease, bacterial infections.
c. Thrombocytosis in KD.
d. Thrombocytopenia and deranged coagulation profile in dengue
hemorrhagic fever.
2. Serology for viral exanthematous fever if any diagnostic confusions.
Serology for dengue illness, spirochetal and rickettsial diseases.
3. Blood culture and CSF study.
4. Imaging, bone marrow or biopsies in unexplained prolonged fever
with rash and suspected malignancies.
Management
Most viral exanthematous fevers are self-limiting and hence symptomatic
and supportive measures are enough.
Life-threatening conditions in meningococcal disease, dengue illness
and toxic shock syndrome needs coordinated, multipronged approach to
save life and reduce morbidity resulting from multiorgan dysfunction.
Unwell Child with Fever and Petechiae/Purpura

At least 90 percent of children with fever and petechiae will not have meningococcal disease. TSS has been dealt separately in other chapter. However,
426
recognition and early treatment of the child with meningococcal disease is

paramount. Clinical signs and laboratory investigations will help determine those who should be treated for suspected meningococcal disease.
Indicators of meningococcal disease (or other serious bacterial infection)
include:
i. Unwell child with abnormal vital signs and poor peripheral perfusion.
ii. Altered conscious state.
iii. Purpura more than 2 mm, nonblanching, maculopapular rash becomes apparent within first 24 hours of disease; sparsely distributed
on face, trunk and lower extremities. Later the petechiae in center of
macules become hemorrhagic.
iv. Abnormal blood indices (including WCC >15 109/L and <5
109/L and raised CRP >8 mg/dl). Though blood culture and CSF
analysis including culture should be sent but one should not wait for
reports. It is ideal to send baseline serum cortisol level.
Principles in the Management of Meningococcal Disease

i. Immediate fluid resuscitation, early administration of antibiotics (third
generation cephalosporincefotaxime 200 mg/kg/day or ceftriaxone
100 mg/kg/day or penicillin 2.5 to 4 lakh U/kg/day) and involvement
of intensive care staff.
ii. Any child with meningococcal disease, including one who appears
nontoxic, may deteriorate rapidly.
iii. Endotracheal intubation to be considered early.
iv. Give methylprednisolone 30 mg/kg before (or within 30 minutes)
first dose of antibiotics.
v. Consider hydrocortisone 1mg/kg 6 hourly if cortisol level is low, otherwise may cause Addisonian crisis.
vi. Contact chemoprophylaxis: It is important that prophylaxis be given
within 24 hours to all intimate, household or day care contacts who
have been exposed to index case within 10 days of onset:
a. Infants and children >1 month of agerifampicin 10 mg/kg
orally 12 hourly (max 600 mg) for 2 days.
b. Adultsrifampicin 600 mg 12 hourly for 2 days.
c. Infants less than 1 month of agerifampicin 5 mg/kg 12 hourly
for 2 days.
d. Pregnancy/contraindication to rifampicinceftriaxone 125 mg
(less than 12 years)/250 mg (more than 12 years) intramuscularly
as a single dose.
Bibliography
1.
2.
Ashton R, Leppard B. Differential Diagnosis in Dermatology. 3rd edition.

United Kingdom: Radcliffe Publishing, 2005.
Braunwald E, et al. Harrison's Principles of Internal Medicine. 15th edition.
New York: McGraw Hill, 2001.

3.
4.
5.
427
Harwood-Nuss A, et al. The Clinical Practice of Emergency Medicine. 2nd

edition. Philadelphia: Lippincott-Raven, 1996.
Nguyen T, et al. Dermatologic Emergencies: Diagnosing and Managing LifeThreatening Rashes. Emergency Medicine Practice: An Evidenced-Based
Approach to Emergency Medicine. 2002.
Sauer G, Hall J. Manual of Skin Diseases. 7th edition. Philadelphia: LippincottRaven, 1996.
19.2
Urticaria and Angioedema
Amiya Kumar Mukhopadhyay, Jayanta Bandyopadhyay
Urticaria manifests as transient smooth slightly elevated erythematous and

edematous patches (wheals) often associated with severe pruritus. The typical
features are shown in Figures 19.2.1 and 19.2.2. In acute form it may last
for few minutes to hours, rarely longer than 2 days, disappears spontaneously leaving a normal skin. Chronic urticaria is recurrent episodes for
more than 6 weeks.
Angioedema manifests as localized swelling of skin and mucosa with
characteristic stinging sensation.
FIG. 19.2.1: Urticaria (For color version see Plate 6)
Chapter 19.2: Urticaria and Angioedema
FIG. 19.2.2: Typical wheal in urticaria (For color version see Plate 6)
Etiology
1.
2.
3.
4.
5.
Viral exanthems.
Insect bites Figure 19.2.3.
Food allergy.
Drugs.
Physical factorsexercise, heat.
1.
2.
3.
4.
5.
6.
7.
Pruritus.
Wheal.
Erythema.
Dermographism.
Sometimes may be painful.
May leave pigmentationurticarial vasculitis.
Stay for few minutes to hours.
Risk Factors
1. Laryngeal edema.
2. Bronchial constriction.
3. Multiple drug intake.
429
430
FIG. 19.2.3: Insect bite (For color version see Plate 7)
Management
1. Remove the responsible agent. Drugs like aspirin, NSAID, sulfonamides,
penicillins, etc. Foods like nuts, chocolates, seafood, etc.
2. Hospitalize children with acute urticaria and angioedema as they may
suffer from respiratory obstruction. One should be ready for tracheostomy if severe laryngeal edema develops.
3. If severe utricaria develops with low blood pressure, tachycardia and
features of shock, management should be like anaphylaxis.
4. Counseling and reassurance is an important aspect of management.
Moderate to Mild Urticaria

1. Oral antihistamincs are the mainstay; sometimes injectable
antihistaminics may be required. Antihistaminics used in children are
highlighted in Table 19.2.1. In acute urticaria, 5 to 10 days course is
needed.
2. H2 blocker,
3. Oral or parenteral steroid. Methylprednisolone, prednisolone or dexamethasone may be used.
4. Topical soothing agents like calamine lotion.
Chronic Urticaria
1.
2.
3.
4.
Antihistaminics, may be given for 3 to 6 months.

H2 blocker.
Cyproheptadine especially in cold urticaria.
Montelukast.
Chapter 19.2: Urticaria and Angioedema
431
TABLE 19.2.1: Antihistaminics used in children for urticaria and angioedema

Drug
Sedative
1. Promethazine
2. Chlorpheniramine
3. Hydroxyzine
4. Cyproheptadine
Mild sedative Cetrizine
Nonsedative
1. Fexofenadine
2. Loratadine
Dose
0.5 mg/kg/dose every 8 hourly
0.35 mg/kg/day
1-2 mg/kg/day
0.2 mg/kg/day
0.25 mg/kg/day
30 mg 12 hourly (6-12 years)
5 mg/day (used above 2 years)
5. Doxepine hydrochloride.
6. Calcium channel blockers.
7. Desensitization of allergens.
Bibliography
1.
2.
3.
Buxton PK. ABC of Dermatology, 4th edition. London: BMJ Books, 2003;38.
Dhar S. Colour Atlas and Synopsis of Paediatric Dermatology, 2nd edition.
New Delhi: Jaypee Brothers, 2007;111-2.
Thomas J. Pediatric Dermatology Ward Rounds, 1st edition. New Delhi: Jaypee
Brothers, 2007;172-4.
19.3
Stevens-Johnson Syndrome (SJS)
Stevens-Johnson Syndrome (SJS) compromises extensive erythema

multiforme (EM) of the trunk and mucous membrane accompanied by
fever, myalgia and arthralgia.
Etiology
1. Following drugs are the common offending agentsco-trimoxazole,
penicillins, NSAIDs, fluconazole, phenobarbitone, phenytoin,
carbamazepine, azithromycin.
2. Immunologic.
3. InfectionsMycoplasma pneumoniae. Also following infections with herpes simplex virus, influenza, mumps, cat-scratch fever, histoplasmosis,
Epstein-Barr virus.
4. SJS is more common in systemic lupus erythematosus and HIV/AIDS.
Clinical Features
1. Erythema multiforme like lesions, typically known as target lesions
Figures 19.3.1 and 19.3.2 .
2. Oral and mucosal erosion and ulcerationsseen in 100 percent cases.
3. Skin blisters and erosion affecting 10 percent of body surface area.
4. Fever may be present.
5. Myalgia.
Diagnosis
The clinical features are typical, history is often corroborative. Skin biopsy
proves the diagnosis.
Management
1. All the children should be hospitalized.
2. If any drug is the precipitating factor, it should be stopped. This is the
most important step.
Chapter 19.3: Stevens-Johnson Syndrome (SJS)
433
FIG. 19.3.1: Erythema multiforme (For color version see Plate 7)
FIG. 19.3.2: Target lesion (For color version see Plate 7)
3. Basic investigationscomplete blood count, electrolytes, liver and renal function tests.
4. Thermoneutral environment should be maintained. Ideal temperature is environmental temperature at 30 to 32C.
5. Due to extensive skin and mucus membrane involvement, these children may not be able to take adequate fluid and are prone to
dehydration. They should be given intravenous fluids. Minimum urine
output in children should be 1 ml/kg/hour.
6. Role of corticosteroid is controversial. Injection methylprednisolone
or dexamethasone may be given.
7. Antihistaminics and analgesics may give some symptomatic relief.
8. Healing process may take about 2 weeks, so proper skin care is very
important. Topical emollients and antibiotics may give some relief, but
topical silver sulfadiazine should be avoided because of its causative
association. Use topical agents such as 0.5 percent silver nitrate solu-
434
tion or 0.05 percent chlorhexidine solution to cleanse the skin. Warm

these solutions before application.
9. H2 blockers like ranitidine should be given to prevent stress ulcer.
Bibliography
1.
2.
Dhar S. Colour Atlas and Synopsis of Pediatric Dermatology, 2nd edition. New
Delhi: Jaypee Brothers 2007;146-8.
Brothers 2007;44-6.
19.4
Toxic Epidermal Necrolysis
Toxic epidermal necrolysis (TEN) is a severe life-threatening disorder with

rapidly progressive eruption of the skin usually following drug intake which
leads to generalized loss of epidermis and mucosa, resembling burn.
Etiology
Usually one of the following drugs:
1. Sulfonamides.
2. Co-trimoxazole.
3. Aminopenicillins.
4. Quinolones.
5. Cephalosporins.
6. Carbamazepine.
7. Phenytoin.
8. Phenobarbitone.
9. NSAID.
Rarely infection is the cause:
1. Mycoplasma.
2. Viral.
3. Postimmunization.
Clinical Features
Drug induced TEN usually develops within 48 to 72 hours after intake of a
drug. It may develop 2 to 3 weeks after intake of anticonvulsants or antitubercular drugs. The typical features are the following. The condition may
become life-threatening within hours of onset. The features are shown in
Figures 19.4.1 and 19.4.2.
1. Sudden onset diffuse macule or erythema with rapid progression.
2. Prompt transformation to peeling of skin in sheets.
3. Blister formation.
4. Skin is tender.
5. Positive Nikolskys sign.
436
FIG. 19.4.1: Typical features of TEN (For color version see Plate 8)
FIG. 19.4.2: TEN affecting face (For color version see Plate 8)
Chapter 19.4: Toxic Epidermal Necrolysis
437
6. Fever, malaise, arthralgia.

7. Mucosal involvement is uncommon.
Management
1. Early hospitalization, ideally in a burn unit.
2. The suspected drug should be stopped and structurally related compound is to be avoided.
3. Adequate IV fluid and maintenance of fluid and electrolyte balance.
4. Oral prednisolone, though controversial, may be given at 2 to 4 mg/
kg/day for 3 to 4 days.
5. IV Immunoglobulin or cyclosporin A may be given.
6. Prophylactic antibiotic may be given if large area is involved. But one
should be careful about selection of antibiotic as many antibiotics may
precipitate
7. Skin and ophthalmologic care should be taken. Skin is a protective
barrier. Large scale affection of skin may cause improper thermoregulation. Topical antibiotics may also cause allergic reaction and produce
fever. One should be very cautious in selection of topical agents. The
crucial factor is maintenance of strict asepsis without much intervention.
Bibliography
1.
2.
Dhar S. Colour Atlas and Synopsis of Pediatric Dermatology, 2nd edition. New
Delhi: Jaypee Brothers 2007;149-50.
Brothers 2007;44-6.
20.1
Fever without Focus
Fever is the most common indicator of illness. Parents are often worried by
high rise of temperature, but in children the magnitude of fever is often
out of proportion to the stimulus, it may be high in mild illness. Infants
and children are often brought to the emergency department with fever as
the only complain.
Stabilization
Any febrile child should be stabilized first and then clinically evaluated
before a decision is taken to send them home. Approach to a small child
having fever is shown in Flow chart 20.1.1.
i. Child should be made comfortable by removing clothing and excess
blankets and clothing.
ii. Antipyretic like paracetamol 10 to 15 mg/kg may be given orally.
iii. Oral fluid intake should be encouraged.
iv. Children who have high temperature and those who run the risk of
having febrile convulsion may be given tepid water sponging to bring
down the temperature.
Symptoms and Signs of a Child with

Serious Bacterial Infection (SBI)
General: Reduced activity, weak cry, poor eye contact andent smile.
Body temperature: Unstable, fever, hypothermia.
Signs of shock: Clammy, mottled skin, reduced CRT.
Respiratory: Apnea, tachypnea, shallow respiration and grunting.
Gastrointestinal: Poor feeding, vomiting, abdominal distension and diarrhea.
CNS: Drowsiness, irritability, bulging fontanelle in meningitis.
442
Common Organisms Causing SBI in 0 to 3 Months

Developed Countries
Early onset: Group B Streptococci (GBS), E. coli.
Late onset: E. coli, GBS, coagulase negative Staphylococcus, N. meningitides,
Streptococcus pneumoniae, Salmonella, Listeria monocytogenes.
Developing Countries
Klebsiella, E. coli, Pseudomonas, Salmonella, Staphylococcus aureus,
H. influenzae, Streptococcus pneumoniae, Streptococcus pyogenes.
Common Causes above 3 Months

Streptococcus pneumoniae, N. meningitides, Salmonella.
Diagnostic approach to a child 0 to 3 months age with fever without
any focus is shown in Flow chart 20.1.1. The observation items to identify a
child with SBI are shown in Table 20.1.1.
Factors that Increase the Predilection of SBI

Infants less than 3 Months
Temperature
Neonates: Any degree of fever.
Older children: >39oC, particularly >40oC.
Pre-existing Disorder
Neonates: Prematurity, PROM, maternal infection, GBS.
Older children: Sickle cell disease, immunosuppression, neoplastic syndrome, splenectomy, HIV infection.
Others: Various catheters, skin puncture.
TABLE 20.1.1: Observation items to identify a child with SBI
Item
Unwell
Appearance
Sick looking (lethargy, reduced activity) Absent eye contact, doesnt

recognize parents, no activity
Whimpering
Weak cry, high pitched cry
Slow response, unwilling
Too weak to respond
Drowsy
Frequently falls sleep, difficult
to wake
Slightly dry mouth.
Dry mouth, sunken fontanelle, doughy skin
Peripheral cyanosis or pallor
Mottled pale face or ashen
Briefly smiles and responds
Not smiling, anxious face,
expressionless
Quality of cry
Response to cuddling
Alertness
Hydration
Color
Sociability/stimulation
Very unwell
Chapter 20.1: Fever without Focus
443
Flow chart 20.1.1: Approach to fever with no focus in 0 to 3 months
Laboratory Findings
i.
ii.
iii.
iv.
v.
vi.
WBC >15000/cmm.
CSF >10 (neonates), >40 (older children).
CSF >8 WBC/cmm
Urinepositive nitrate in dipstick, urinalysis showing >10 WBC/hpf.
Chest X-rayinfiltrates.
Stool>5 WBC/hpf.
Approach to a child with fever without focus 3 to 36 months is shown in
Flow chart 20.1.2.
444
Flow chart 20.1.2: Approach to a child with fever without focus 3 to 36 months
Bibliography
1.
El-Radhi AS, Carroll J, Wigel K Editors. Fever in children, 1st edition. Springer
2009;125.
20.2
Severe and Complicated Malaria
Jaydeep Choudhury
Severe malaria is almost always due to Plasmodium falciparum, though recently

some Plasmodium vivax cases are also presenting with complications.
Complicated malaria is a medical emergency with high mortality. However
appropriate timely management can limit morbidity and mortality.
Irrespective of etiology all complicated malaria with severe manifestations
should be treated with injectable antimalarials.
WHO has laid down criteria for severe falciparum malaria as shown in
Table 20.2.1. By definition severe falciparum malaria is one or more of the
criteria in the presence of a sexual parasitemia.
Anticipation and high degree of suspicion is vital for diagnosis and
management of severe malaria. The unique feature in children is that the
progression to cerebral malaria is rapid in children compared to adults.
WHO modified general danger signs of malaria are as follows:
TABLE 20.2.1: Features of severe malaria
Prognostic valuea
Clinical manifestation
+
Prostration
+++
Impaired consciousness
+++
Respiratory distress (acidotic breathing)
+
Multiple convulsions
+++
Circulatory collapse
+++
Pulmonary edema (radiological)
+++
Abnormal bleeding
++
Jaundice
+
Hemoglobinuria
Laboratory findings
+
Severe anemia
+++
Hypoglycemia
+++
Acidosis
+++
Hyperlactatemia
+/Hyperparasitemia
++
Renal impairment
a
On a scale from + to +++; +/- indicate infrequent occurrence.
Frequencya
+++
+++
+++
+++
+
+/+/+
+/+++
+++
+++
+++
++
+
446
1.
2.
3.
4.
5.
Not able to drink or breastfeed.

Vomiting everything.
Recent history of convulsion.
Lethargic or unconscious state.
Unable to sit or stand up.
Management of complicated malaria in children are three pronged
antimalarial chemotherapy, supportive management and management of
complications. All the three interventions should proceed simultaneously.
Clinical Assessment
Any child with fever and altered sensorium in malaria endemic area is a
probable case of severe malaria. The following aspects should be assessed:
1. Level of consciousness.
2. Temperature.
3. Hydration status.
4. Rate and depth of respiration.
5. Blood pressure.
6. Pallor.
Investigations
1. Blood smear examination: Thick and thin blood films should be sent for
detection of malarial parasite is still the gold standard. Blood should
be collected as soon as malaria is suspected irrespective of fever. Blood
should preferably be collected from the finger tip or earlobe as these
capillary rich areas contain a relatively greater density of parasites.
Both thick and thin smear should be prepared as soon as possible.
2. Rapid diagnostic tests: These tests may be of help in emergency department as the results may be obtained early and on spot, but it has some
limitations as it is not sensitive in low parasite load.
3. Hemoglobin and PCV.
4. Blood glucose.
5. Lumbar puncture for CSF study particularly in cerebral malaria. Secondary infection is a common feature of cerebral malaria. If lumbar
puncture is delayed, appropriate antibiotic cover for meningitis must
be given.
Management
Supportive
1.
2.
3.
4.
Maintenance of ABC. Proper positioning with attention to airways.

Oxygen should be given and respiratory support if necessary.
Care of eyes, mucosa and skin.
IV fluid. In case of shock, fluid resuscitation with normal saline or
Ringers lactate should be done. Under or over hydration should be
Chapter 20.2: Severe and Complicated Malaria
5.
6.
7.
8.
9.
447
avoided. Blood sugar should be monitored and appropriate dextrose

containing fluid should be given and corrections made if required.
Nasogastric tube should be placed in situ to minimize the risk of aspiration.
Convulsion should be treated appropriately.
Hyperpyrexia should be managed accordingly.
Monitoring of vital signs: Preferably 4 hours till the patient is out of
danger. Intake output chart should also be maintained.
Antibiotic coverage should be given as these children prone to septicemia.
Antimalarial Chemotherapy
1. Child should be weighed and dose of antimalarials should be calculated according to body weight.
2. Initially antimalarials should be given as injections and it should be
replaced by oral preparations as soon as the child is able to take oral
medicines.
3. If intravenous preparations are not available, crushed tablets may be
given through nasogastric tube, but it may cause vomiting and inadequate drug absorption.
4. Antimalarial chemotherapyartesunate or artemether.
Artesunate: 2.4 mg/kg IV stat dose and then at 12, and 24 hours, followed
by once daily for 7 days. Artesunate, 60 mg per ampoule is dissolved in
0.6 ml 5 percent sodium bicarbonate diluted to 3 to 5 ml with 5 percent
dextrose and given immediately after reconstitution by IV bolus. If the
child is able to swallow, the daily dose may be given orally. As soon as the
child is able to swallow tetracycline 4 mg/kg/dose 4 times daily in children
above 8 years or doxycline 3.5 mg/kg once daily in children above 8 years
should be given for 7 days. In children below 8 years, clindamycin 20 mg/
kg/day in 2 divided doses should be given for 7 days.
Artemisinin based combination therapy (ACT): Those who can swallow, a
fixed dose of artemether lumefantine can be given orally for 3 days as
Monitoring
Monitoring of the response to treatment should be carried out simultaneously. Blood smear examination should be done every 6 to 12 hours for
the first 48 hours to look for parasitemia.
TABLE 20.2.2: Arteminsinin based combination therapy (ACT)
Body weight
Dose of artemether + lumefantine
515 kg
>1525 kg
>2535 kg
above 35 kg
20 mg + 120 mg
40 mg + 240 mg
60 mg + 360 mg
80 mg + 480 mg
448
In case of artemisin in therapy parasitemia comes down within 5 to 6

hours of starting the therapy. In case of quinine therapy, parasite count
falls by 24 hours and disappears by 5 days. But initially parasite count may
rise for 18 to 24 hours.
Poor Prognostic Indicators

i. High parasite densitymore than 5 percent RBC infected or parasite density >250000/L.
ii. If mature parasites are moremore than 20 percent parasites contain visible pigments.
iii. More than 5 percent peripheral leukocytes contain visible malaria
pigment.
Management of Complications
There may be several complications of falciparum malaria. Mortality is
high unless these complications are managed early.
Severe Anemia
Anemia develops due to acute destruction of red blood cells, this is more
common with hyperparasitemia. The following conditions warrant packed
cell transfusion:
i. PCV less than 12 percent or hemoglobin below 4 gm/dl.
ii. Transfusion is indicated in less sever anemia associated with respiratory distress, impaired consciousness and high parasite load (>20%
RBC infected).
Hypoglycemia
The following situations may precipitate hypoglycemia:
i. Children below 3 years with hyperparasitemia or having seizures.
ii. Children treated with quinine.
Blood sugar should be monitored frequent as the features of hypoglycemia may be difficult to distinguish clinically.
Cerebral Malaria
It may evolve gradually or occasionally, it may progress very rapidly to
convulsion or coma. Convulsion may be subtle also. Good supportive care
is essential along with management of coma. Children may also present
with features of raised intracranial tension. These children should be managed with general measures like head end elevation, fluid restriction and
hyperventilation by mechanical ventilation. Mannitol is not indicated.
Hyperpyrexia
It is common in children and may lead to convulsion. Tepid sponging,
paracetamol and cool ambient temperature are the mainstay of treatment.
Chapter 20.2: Severe and Complicated Malaria
449
Hyperparasitemia
This is typically seen in nonimmune children with severe disease. Exchange
transfusion or cytapheresis may be considered is parasite load is high.
Lactic Acidosis
Clinically deep breathing with chest retractions without much auscultatory
findings are characteristic. It usually accompanied cerebral malaria, anemia and dehydration. Acid-base status should maintained and hypovolemia,
anemia, seizure should be controlled.
Circulatory Collapse
Gram-negative septicemia should be excluded in case of circulatory collapse and should be treated accordingly with fluids and antibiotics.
DIC
Should be treated with vitamin K and blood.
Bibliography
1.
2.
3.
Kapse A, Kundu R, Ganguly N. Management of severe and complicated malaria. In: Ganguly N, Kundu R, Ghosh TK Editors. Multidrug Resistant Pediatric
Infections, 1st edition. New Delhi: CBS Publishers 2009;166-71.
World Health Organization: Guidelines for treatment of malaria. Geneva: WHO,
2006. URL: who/html/mal/2006. 1108.
World Health Organization: Management of severe malaria. A Practical Hand
Book. 2nd edition. Geneva: WHO, 2000.
20.3
Dengue
Jaydeep Choudhury
The clinical presentation of dengue is a large spectrum which extends from

asymptomatic infection to dengue shock syndrome. The following are the
four clinically recognized syndromes:
1. Undifferentiated fever.
2. Dengue fever (DF).
3. Dengue hemorrhagic fever (DHF).
4. Dengue shock syndrome (DSS), it is actually a severe form of DHF.
Dengue is endemic in most parts of the country. Any child presenting
with fever with or without rash and thrombocytopenia should be suspected
to suffer from dengue infection.
Undifferentiated Fever
It mimics any other viral fever and is the commonest presentation of dengue infection. Most of the time it is treated as simple viral illness without
any investigations.
Dengue Fever (DF)

The typical manifestations are sudden onset with a sharp rise in temperature. It is usually associated with severe headache and flushed face. The
rash in dengue fever is flushing or fleeting particularly over the face, neck
and chest. It is maculopapular or scarlatiniform and classically appears on
the third or fourth day. Gradually the rash fades and clusters of petechiae
may appear over the extremities. Skin hemorrhage can be demonstrated
by tourniquet test. This may progress to retro-orbital pain, photophobia,
backache and pain in the muscles, bones and joints of the extremities.
There may be abdominal pain and sore throat also. These symptoms may
persist for several days.
Tourniquet Test
The blood pressure cuff around the upper arm is inflated to a point midway between the systolic and diastolic blood pressure for five minutes. The
Chapter 20.3: Dengue
451
test is positive if 10 or more petechiae appear in a 2.5 cm 2.5 cm square

area over the forearm. This test is particularly useful in children above 4
years.
Dengue Hemorrhagic Fever (DHF) and

Dengue Shock Syndrome (DSS)
DHF is a syndrome of increased vascular permeability accompanied by abnormal hemostasis. The following is the WHO case definition for clinical
diagnosis of DHF and DSS. All of the following criteria must be presebted:
1. Fever (high and continuous of 2-7 days duration).
2. Hemorrhagic diathesis (at least a +ve tourniquet test, except in shock).
3. Thrombocytopenia (less than 100,000/mm3).
4. Hemoconcentration (20% or more relative to baseline) or evidence of
plasma leakage (i.e. pleural effusion, ascites and/or hypoproteinemia).
The first two clinical criteria along with thrombocytopenia and a rising
hematocrit establish the diagnosis of DHF.
Clinical Examination
1.
2.
3.
4.
5.
6.
7.
8.
9.
Pulse.
BP.
CFT.
Skin rash.
Conjunctival injection.
Muscle tenderness.
Hepatosplenomegaly.
Pleural effusions, ascites.
Hess test (tourniquet test).
Investigations
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Complete blood count.

Hematocrit, platelet count.
SGPT.
PT, APTT.
Urea, creatinine.
Serum protein.
Electrolytes and ABG.
X-ray chest.
USG abdomen and chest.
Dengue antibodies.
Dengue Serology
The following are the tests:
1. The ELISA tests (IgM capture ELISA and IgG capture ELISA).
2. Rapid immunochromatographic card tests.
452
Primary Dengue Infections

IgM: Positive in 80 percent by day 5 and 99 percent by day 10 to 20. It
peaks by 2 weeks and declines over the next 2 to 3 months.
IgG: IgG antibodies rise later and to lower levels but persist at low levels
for life.
Secondary Dengue Infections

IgG: Characterized by brisk and rapid response. The levels rise much higher
than that seen in primary dengue infection. It peaks at 2 weeks and then
declines slowly over the next 3 to 6 months.
IgM: The response is slower and lower than IgG. It may be undetectable in
some individuals.
The interpretation of dengue IgM and IgG in various dengue infections are shown in Table 20.3.1.
Criteria for Hospitalization

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Lethargy or restlessness.
Cold extremities.
Rapid weak pulse.
Capillary refill >2 seconds.
Hypotension or pulse pressure <20 mm of Hg.
Oliguria.
Bleeding in any form.
Hematocrit 40 or rising hematocrit.
Platelet count less than 100,000/mm3.
Acute abdominal pain.
Evidence of plasma leakagepleural effusion, ascites.
Monitoring DSS
1. Every 30 minutespulse, BP, respiration.
2. Hematocrit and hemoglobin every 2 hours for first 6 hours and then
every 4 hours until the patient is stable.
3. Fluid balance sheettype, volume and rate.
4. Urine outputfrequency and volume.
Parents must bring the child back immediately to the nearest hospital
in the presence of any one of the following situations:
TABLE 20.3.1: Interpretation of dengue IgM and IgG
IgM
IgG
Interpretation
Negative
Negative
Negative
Positive
Positive
Positive
Negative
Positive (Low titer)
Positive (High titer)
Negative
Positive (Low titer)
Positive (High titer)
Early sample
Postdengue infection
Secondary dengue infection
Primary dengue infection
Current or recent dengue infection
Secondary dengue infection
Chapter 20.3: Dengue
453
Flow chart 20.3.1: Volume replacement flow chart of dengue fever and dengue hemorrhagic fever
i.
ii.
iii.
iv.
v.
vi.
vii.
Not drinking/feeding poorly.

Passing less urine than usual.
Abdominal pain.
Bleeding in any form.
In older children, inability to sit up, giddiness.
Irritability, drowsiness, restlessness.
Child continues to be unwell.
Management
Volume replacement of dengue fever and dengue hemorrhagic fever in
minimal set up is shown in Flow chart 20.3.1. For further information,
refer to the chapter on shock.
Bibliography
1.
2.
Halstead SB. Dengue and dengue hemorrhagic fever. In: Feigin, Cherry,
Demmler, Kaplan Editors. Textbook of Pediatric Infectious Diseases, 5th edition. 2004; 2178-200.
World Health Organization. Dengue hemorrhagic fever: Diagnosis, treatment,
prevention and control. Geneva: WHO, 1997.
20.4
Community Acquired Pneumonia
Jaydeep Choudhury
Inflammation of lung parenchyma which occurs in previously healthy child

and the infection is acquired outside hospital environment is community
acquired pneumonia (CAP).
Age Related Etiology

Birth to 20 Days
Group B streptococcus, Gram-negative enteric cocci, Chlamydia trachomatis
and Listeria monocytogenes.
3 Weeks to 3 Months
Respiratory viruses (RSV, influenza, parainfluenza, adeno, boca, rhinovirus), Chlamydia trachomatis, Streptococcus pneumoniae, Haemophilus influenzae,
Bordetella pertussis, Staphylococcus aureus, Mycobacterium tuberculosis.
4 Months to 4 Years
Respiratory viruses, Mycoplasma pneumoniae, Streptococcus pneumoniae, Streptococcus pyogenes, Haemophilus influenzae, Staphylococcus aureus, Mycobacterium
tuberculosis.
5 to 15 years
Mycoplasma pneumoniae, Streptococcus pneumoniae, Staphylococcus aureus, Mycobacterium tuberculosis.
Investigations
1. Complete blood count and differential count, ESR, CRP, blood culture.
2. Chest X-ray.
3. ABG if in distress.
4. USG chest to determine small pleural effusion and differentiation from
consolidation.
Chapter 20.4: Community Acquired Pneumonia
455
5. If required nasopharyngeal aspirates for immunofluorescence for respiratory viruses.

6. Mycoplasma or Chlamydia serology, if facilities are available.
The typical chest X-rays of pneumonia are shown in Figures 20.4.1 to 20.4.3.
FIG. 20.4.1: Bilateral upper lobe consolidation
FIG. 20.4.2: Right basal lobe consolidation
456
FIGS 20.4.3A and B: Bronchopneumonia
Chapter 20.4: Community Acquired Pneumonia
457
TABLE 20.4.1: Antibiotics for outpatient treatment of CAP

Age
First line
Second line
3-5 months
>5 months
Amoxicillin
Amoxicillin
Co-amoxyclav
Macrolides / co-amoxyclav
TABLE 20.4.2: Injectable antibiotics for inpatient treatment of CAP

Age
First line
Second line
<3 months
3 months 5 years
Cefotaxime/ceftriaxone
Co-amoxyclav/ampicillin
>5 years
Ampicillin/co-amoxyclav/macrolide
Add aminoglycoside
Co-amoxyclav/cefotaxim/
ceftriaxone
Cefotaxime/ceftriaxone/
macrolide
Ceftriaxone/cefotaxime/
vancomycin/linezolid
Suspected staphylococcus Cefuroxime/co-amoxyclav/3rd

generation cephalosporin
Management
1. Check O2 saturation. Aim is to keep more than 92 percent saturation.
2. Antibiotics: The choice of antibiotic is mainly empirical depending on
the age, severity of illness, etiology, local epidemiology and possible
drug resistance pattern. The choice of antibiotics for outpatient and
injectable medications are shown in Tables 20.4.1 and 20.4.2 respectively.
The duration of treatment should be 7 to 10 days. Staphylococcus pneumonia without complications should be treated for 2 weeks and those with
complications for 4 to 6 weeks.
Neonatal pneumonia and any pneumonia below the age of 3 months
should always be admitted and treated with injectable antibiotics.
The dose of various antibiotics is as follows.
1. Ampicillin 100 to 200 mg/kg/day every 6 hourly.
2. Amoxicillin 30 to 50 mg/kg/day every 8 hourly, high dose 60 to 80 mg/
kg/day.
3. Cefotaxime 150 mg/kg/day every 8 hourly.
4. Ceftriaxone 100 mg/kg/day every 12 hourly.
5. Erythromycin 40 mg/kg/day every 6 hourly.
6. Clarithromycin orally 15 mg/kg/day every 12 hourly.
7. Azithromycin orally 10 mg/kg/day once daily for 5 days.
Bibliography
1.
2.
Jadavji T, Law B. Label MH, et al. A practical guide for the diagnosis and
treatment of paediatric pneumonia. Can Med Asso J 1996;156:S703-11.
Macintosh K. Community acquired pneumonia in children. N Eng J Med
2002;346:429-37.
20.5
Acute Meningitis
Pyogenic meningitis in children is associated with considerable morbidity

and mortality. It has to be suspected early, diagnosed early and treated
promptly. The initial management approach of a child with suspected acute
pyogenic meningitis depends on early recognition, rapid diagnostic evaluation, antimicrobial and adjunctive therapy.
Etiology
Neonates
Group B streptococcus, E. coli, Listeria monocytogenes.
1 to 3 Months
Streptococcus pneumoniae, N. meningitidis, H. influenzae, Group B streptococcus,
Listeria monocytogenes.
Beyond 3 Months
Streptococcus pneumoniae, N. meningitidis, H. influenzae.
Postcraniotomy, V-P Shunt

Coagulase negative staphylococci, Staphylococcus aureus, Pseudomonas
aeruginosa.
Investigations
1. Complete blood count, ESR, CRP, blood culture, serum electrolytes,
glucose.
2. FDP, coagulation profile if suspecting DIC.
3. Lumbar puncture for CSF study.
4. CT scan brain when required.
CSF Study
1. Gram stain.
2. Cell countWBC and differential.
Chapter 20.5: Acute Meningitis
459
3. Biochemistryglucose (compared with blood), protein.

4. Culture and sensitivity.
5. The basis of other tests is detection of bacterial antigens or antibodies
against the bacteria. These tests are particularly relevant in those
who have received prior antibiotics which reduces the yield of both
CSF Gram stain and culture. Latex agglutination for antigen
detection.
6. If tuberculosis is suspectedacid fast bacilli stain and mycobacterium
and culture.
7. If viral meningitis is suspectedviral PCR to (HSV, VZV, CMV and
enteroviruses).
The interpretation of CSF result is shown in Table 20.5.1.
Lumbar puncture should be deferred under the following circumstances:
i. Evidence of increased intracranial pressure (ICP), with clinically manifestations of obtundation, anisocoria, papilledema, Cushing triad of
hypertension, bradycardia and irregular respiration.
ii. Presence of focal neurological signs.
iii. Cardiopulmonary instability.
Contraindications of lumbar puncture (LP) are the following:
i. Clinically significant cardiorespiratory compromise.
ii. Infection in the area the LP needle would traverse.
iii. Platelets <20,000 or bleeding diathesis.
Signs of increased ICP are a relative contraindication.
Indications of CT Brain
1.
2.
3.
4.
Focal neurological signs.

Prolonged convulsions.
Impaired level of consciousness.
Evidence of increased intracranial pressure.
Management
1.
2.
3.
4.
Maintenance of ABC.
Restore circulating volume and urinary output.
Monitor vital signs, hydration and neurological status.
If impaired consciousness keep patient on parenteral fluid and nutrition only.
5. Start antibiotics after collecting CSF report as soon as possible.
Antibiotic Therapy
Full Term Neonates <1 Week
Ampicillin 150 mg/kg/day IV every 8 hourly with cefotaxime 150 to 200
mg/kg/day IV every 8 to 12 hourly.
>75%
lymphocytes
>50
20-45 mg/dL
Predominant cells
Protein
Glucose
<5
WBC
Normal child
TABLE 20.5.1: Interpretation of CSF result
84 45 mg/dL
Polymorphs +
lymphocytes
46 10 mg/dL
<22
Normal neonate
Low, <50%
of serum
100-500 mg/dL
Polymorphs
300-2000
Bacterial
50-200 mg/dL
Increased
rarely >1000
Early: Polymorphs
then lymphocytes
Normal
viral
Very high,
100-3000 mg/dL
Low
Lymphocytes
10-500
TB
High,
100-500 mg/dL
Polymorphs or
lymphocytes
Low or normal
5-10000
Partially treated
460
Chapter 20.5: Acute Meningitis
461
1 Week to 3 Months
Ampicillin 200 mg/kg/day IV every 6 hourly with cefotaxime 150-200 mg/
kg/day IV every 6 hourly.
Children >3 Months

Cefotaxime 200 mg/kg/day IV every 6 hourly.
Add Vancomycin
60 mg/kg/day IV every 6 hourly in the following situations:
1. Gram stain showing gram positive cocci.
2. Very ill child with hemodynamic instability.
Once the organism and sensitivities are recognized switch to appropriate and narrowest spectrum antibiotic.
Duration of Antibiotics
Neonates2 weeks (3 if gram-negative organism).
S. pneumoniae10 to 14 days.
H. influenzae 710 days.
N. meningitides 57 days.
Gram-negative infections3 weeks.
Supportive Care and Monitoring

1.
2.
3.
4.
5.
Input and output chart and daily weight.

Daily head circumference.
Watch for SIADHurine specific gravity and serum sodium.
IV fluidsmaintenance (If SIADH restrict to 2/3 maintenance).
Anticonvulsant if convulsions.
Prophylaxis
1.
2.
3.
4.
5.
S. pneumoniaeNot indicated.
H. infuenzaeRefer to chapter on acute epiglottitis.
N. meningitidisRefer to chapter fever with rash.
Contact with patients oral secretions (within 7 days of presentation).
Health care workers: Only if mouth resuscitation, endotracheal intubation or has been in direct contact with the patients oral secretions.
No prophylaxis for indirect contact.
Bibliography
1.
2.
3.
Tunkel AR. Bacterial meningitis. 1st edition, Philadelphia: Lippincott Williams and Wilkin 2001.
Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clinical Infect Dis 2004:39;1267-84.
WHO. Pyogenic meningitis. In: Guidelines on Standard Operating Procedures
for Microbiology 2007.
20.6
Urinary Tract Infection
Jaydeep Choudhury
Urinary tract infection (UTI) is diagnosed when urine culture report reveals a colony count more than 105 colony forming unit (CFU) per ml of
clean catch urine. This signifies significant bacteriuria.
Etiology
Bacterial Pathogen
1. Nearly 90 percent of the first UTI and 70 percent of recurrent infections are caused by Escherichia coli.
2. Other organisms like Klebsiella, Staphylococci epidermidis and Streptococcus
faecalis are occasionally incriminated.
3. UTI following instrumentation and nosocomial infections may be due
to Proteus and Pseudomonas.
Other Causes
1. Fungal UTI should be suspected in hospitalized newborns and infants
who are either immunocompromised or have received prolonged
parenteral antimicrobials.
2. Tuberculosis of the urinary tract is extremely rare in children.
Classification and Clinical Manifestations

Acute Pyelonephritis
Abdominal or flank pain, fever, vomiting and diarrhea are the typical features. Some newborn and infants may show jaundice, poor feeding,
irritability and weight loss.
Acute Cystitis
Dysuria, urgency, frequency, suprapubic pain, incontinence, malodoros urine
and usually without fever.
Chapter 20.6: Urinary Tract Infection
463
Asymptomatic Bacteriuria (ABU)

Individuals who have a positive urine culture without any manifestations of
infection and occurs almost exclusively in girls.
Complicated UTI
Presence of fever >38.5oC, toxicity, persistent vomiting, dehydration and
renal angle tenderness.
The following aspects should be looked into:
1. Growth parameter.
2. Temperature (fever in pyelonephritis).
3. Blood pressure.
4. Abdomen (kidneys, bladder, hard stool).
5. Neurological examination.
6. Spinal examinationsacral dimple, sinus, tuft of hair, etc.
7. External genitalia (features suggestive of sexual abuse).
Urine Analysis
Occasionally it may be normal in children due to various reasons.
Microscopy
i. WBC >10 cells/HPF, hematuria and bacteriuria.
ii. Leukocyte esterase test.
iii. Nitrite test.
Urine Culture
Suprapubic aspiration: It is the best specimen to come to a diagnosis that
can be obtained from an infant, in case of labial adhesion, tight foreskin
and anatomical abnormality. Even a single colony is significant.
Midstream clean catch: Possible in children with urinary control, significant colony count >105 CFUs is significant.
Bladder catheterization: Children without urinary control. Here also colony
count >105 CFU is significant.
Bagged urine best to be discouraged and discarded.
Other Investigations
1. Complete blood count, ESR and CRP should be done in all children.
2. Ultrasonography of abdomen should be done in a child as a routine
measure.
464
Treatment
Indication for Admission
1.
2.
3.
4.
5.
6.
Neonates and infants.

Children of any age with high fever and/or flank pain, sepsis or shock.
Known complex underlying urological pathology.
Persistent vomiting, dehydration or inability to take oral medication.
Known/suspected causative organism resistant to oral medication.
Psychosocial issues: inability of family to care for child appropriately.
Antibiotic Therapy
Bacterial antibiotic resistance patterns are geographically determined and
should be reviewed at each hospital to determine the best initial oral antibiotics. Using broader spectrum antibiotics might contribute in emergence
of resistant organisms.
Agents that are excreted in the urine but do not achieve therapeutic
concentrations in the bloodstream, such as nalidixic acid or nitrofurantoin, should not be used to treat UTI in febrile infants and young children
in whom renal involvement is likely. The recommended antibiotics for treatment of UTI in children are shown in Tables 20.6.1 and 20.6.2.
Intravenous antibiotics can be switched to oral antibiotics once the causative agent and the antibiotic sensitivities were identified. The patient can
be discharged home in the following circumstances:
1. More than 2 months of age.
2. Afebrile for >24 hours.
3. Tolerating oral fluids.
TABLE 20.6.1: Antimicrobial for oral treatment of UTI
Antimicrobial
Dosage
Trimethoprim-sulfamethoxazole
Amoxicillin/co-amoxyclav
Cephalexin
Cefixime
Cefuroxime axetil
Cefpodoxime
4-6 mg TMP, 20-30 mg SMX/kg/day q12 hours

20-40 mg of amoxicillin/kg/day in 3 doses
50-100 mg/kg/day in 4 doses
8 mg/kg/day in 2 doses
TABLE 20.6.2: Antibiotics for parenteral treatment of UTI

Antibiotic
Daily Dosage
Ceftriaxone
Cefotaxime
Ceftazidime
Gentamicim
Amikacin
Ampicillin
75 mg/ kg/day every 12 hours

150 mg/kg/day divided every 6 hours
150 mg / kg/ day divided every 6 hours
7.5 mg/kg/day every 12-24 hours
15 mg/kg/day divided every 12 hours
100 mg / kg/ day divided by every 6 hours
Indication
All children following UTI
i. Acute pyelonephritis
ii. First UTI in a boy or girl <2 years age
iii. First UTI in a child of any age with family
history of UTI, urinary tract abnormalities or
abnormal voiding pattern
Suspected pyelonephritis at young age
Recurrent UTI evidence of vesicoureteric reflux
Used to follow up vesicoureteric reflux after
initial traditional MCUG
Rationale
Dosage
2 mg TMP once daily
1 mg/ kg dose once daily
25 mg/kg/dose once daily
Trimethoprim-sulfamethoxazole
Nitrofurantoin
Cephalexin
Advantage: Less radiation Disadvantage:

Not as sensitive as MCUG does not show
urethral Or bladder abnormalities
Rule out renal scarring.
To rule out major urinary tract structural pathology

To rule out vesicoureteric reflux
Posterior urethral valve in boys Anatomical
or functional bladder abnormalities
Prophylactic antibiotics
TABLE 20.6.4: Prophylactic antibiotics for prevention of UTI
Radionuclide cystogram
DMSA Scan
Ultrasound abdomen
MCUG
Investigation
TABLE 20.6.3: Follow-up investigations of UTI
Chapter 20.6: Urinary Tract Infection
465
466
Duration of Therapy
Seven to ten days treatment regimens are recommended for UTI, longer
duration up to 14 days might be necessary in complicated UTI.
The follow-up investigations are shown in Table 20.6.3.
MCUG can be performed once infection is cleared. DMSA should be
done 4 to 6 weeks after an UTI episode.
Prophylactic Antibiotics
Although the evidence of benefit of long-term low-dose antibiotic prophylaxis for prevention of UTI is not strong, it is the most widely used strategy
to prevent UTI in clinical practice. Antibiotic prophylaxis is recommended
in the following:
i. Infants with UTI pending completion of evaluation.
ii. Children with VUR and
iii. Those with recurrent febrile UTI even if the urinary tract is normal.
Medications used for prophylaxis are usually given as single bedtime
dose Table 20.6.4.
Bibliography
1.
2.
3.
4.
American Academy of Pediatrics, Committee on Quality Improvement, Subcommittee on Urinary Tract Infections. Pediatrics 1999;103:843-52.
Bagga A. Urinary tract infections. In: Ghosh TK, Yewale V, Parthasarathy A,
Shah NK Editors. Pediatric Infectious Diseases, 1st edition. Mumbai, Indian
Academy of Pediatrics, 2006;138-45.
Consensus Statement on Management of Urinary Tract Infections. Indian Pediatric Nephrology Group: Indian Academy of Pediatrics. Indian Pediatr 2001;
38:106-1115.
Srivastava RN, Bagga A. Urinary tract infection. In: Pediatric Nephrology, 3rd
edition. New Delhi, Jaypee Brothers 2001;185-207.
21
MISCELLANEOUS
EMERGENCIES
21.1
Crying and Irritable Child
Crying is a way of communication for infants. Mothers are the best judge
about the childs cry. When mothers express genuine concern about her
childs abnormal cry then it has to be looked into.
Normal Cry in Infants

1. Hours of cry: 2 hrs/ day 1 hr at 4 weeks
3 hrs/day 1 hr at 6 weeks
1 hr/day by 12 weeks
These are mostly due to hunger cry, uncomfortable environment
(too hot, too cold environment, wet nappy, not-so-soft couch, unattended for a while), and imminent sleep.
2. Concurrent patterns of cry: Within 9 months most infants cry in late
afternoon and between 4 to 8 pm.
Increased daily cry peaks at 6 to 8 weeks followed by rapid decline.
3. Variation in temperament: Few infants are intrinsically more demanding, it may signify misfit mother and child.
Pathological Cry Indicating Organic Cause

1.
2.
3.
4.
5.
Paroxysmal screaming.
Crying interrupting feeding.
Interrupted sleep.
Abnormal movementsbody arching and head nodding.
Crying associated with regurgitation and vomiting.
Causes of Pathological Cry

1. CNS:
a. Infectionmeningitis, meningoencephalitis, brain abscess.
b. Hypoxiasecondary to pneumonia, bronchiolitis, asthma and cyanotic heart diseases.
c. Head injury and raised intracranial tension due to any cause.
2. Systemic infection: Bacterimia, retroperitoneal and pelvic abscess.
470
3. Musculoskeletal system:
a. Infectionseptic arthritis.
b. Fracture limbs.
c. Otherspulled elbow, caffeys disease
4. Urogenital system:
a. InfectionUTI, cystitis.
b. Acute scrotum including torsion testis.
c. Posterior urethral valve.
d. Paraphimosis, pelviureteric junction obstruction (PUJ).
5. Gastrointestinal tract:
a. Emergencies: Appendicitis, strangulated hernias (inguinal, umbilical, epigastric), Meckels diverticulum, intussusception,
malrotation,
b. Others: GE reflux, milk protein allergy, infantile colic, diarrhea,
constipation, anal fissure.
6. Perioral and adnexal areas:
a. Oral thrush and ulcers, dental caries, gingivitis and angular stomatitis, tonsillitis, herpangina, FB nose.
b. Cervival lymphadenitis, mastoiditis.
7. Ears: ASOM, foreign body (FB) ear.
8. Eyes: Eye discharge, conjunctivitis, FB in eyes.
9. Skin: Miliaria and other pruritic rashes, perianal excoriation, pruritus ano, pruritus valvae, insect bite.
10. Cardiology: Supraventricular tachycardia (SVT), cyanotic heart disease, myocarditis and chronic heart failure (CHF).
11. Miscellaneous: Nasal congestion, multiple scalp boils, diaper pin, tight
clothes, strangulation of digits.
Approach to Diagnosis
History
Crying is the commonest mode of communication in infants. It is often
very difficult to get a proper history or examine the child thoroughly while
he is crying. A high index of suspicion is the key to success. A good history
and nature of symptoms from parents may be helpful.
a. Fever: If there is a fume, there must be a fire. Mostly it denotes infection. The higher the fever more is the chance of serious bacterial
infection. Neonates may be hypothermic.
b. Cry: High pitched, intermittent, often inconsolable cry.
c. Vomiting: Projectile, biliary, possetting.
d. Feeding: Poor intake of feeds, dribbling from mouth, dysphagia.
e. Discharges: Rectal bleed, discharge from ear, nose, eyes and other natural orifices.
f. Trauma: Fall from height and history of injury, child abuse.
g. Neurological: Lethargy, sleep disorder, abnormal posturing and back
arching.
Chapter 21.1: Crying and Irritable Child
471
h. Respiratory: Recurrent cough and wheeze, apnea, cyanosis, recurrent

pneumonia.
i. Miscellaneous: Worms seen in stool, recent weight loss, hard irregular
stool.
Examination
Head to toe exam is the dictum.
a. General examination and parameters: Weight, heart rate, rhythm, respiratory rate, oxygen saturation, BP, temperature, CFT, pulse volume,
anemia, cyanosis, jaundice, edema, features of dehydration and shock.
b. Head: Fontanelle, hematoma, bruise and laceration, boils, mastoids.
Eyes, ears, neck, nose and oral cavity.
c. Skin.
d. Hernial sites.
e. Joints and limbs: Swelling, local temperature, tenderness, effusion and
range of movement. Each joint and digits should be examined. Clavicles
should always be examined.
f. Abdomen: Liver, spleen, any mass, distension, classical triad of pain,
mass and rectal bleed signifies intussusception. Hernial orifices should
also be checked.
g. Chest: Wheeze, crepitations, air entry, tracheal and chest retraction,
respiratory excursion.
h. Anorectal area: Balanoposthitis, perianal excoriation, anal fissure, paraphimosis, vulvovagintis.
i. Cardiac: Heart sounds, murmur and gallop rhythm.
Some sites are often missed and must be looked into in an irritable
child, as shown in Figures 21.1.1 to 21.1.5.
Investigations
Only to support the diagnosis as diagnosis is mostly made clinically.
a. CBC, CRP, blood and urine culture.
b. CSF analysis and culture (as and when required).
c. X-rays if anticipating fractures, pneumonia.
d. CT scan brain and other organs.
e. USG: appendicitis, intussusception, acute scrotum, PUV, PUJ obstruction, intra-abdominal abscess.
f. Echocardiography: Congenital heart disease, myocarditis.
Management
1. ABC.
2. Fluid resuscitation for dehydration and shock.
3. Oxygen for pneumonia and bronchiolitis. Nebulization and oxygen
for asthmatics.
4. Nasal suction, antiemetics, skin emollients, mild antispasmodics for
symptomatic relief.
472
FIG. 21.1.1: Bee sting in the finger (For color version see Plate 8)
FIG. 21.1.2: Herpetic gingivitis (For color version see Plate 9)
Chapter 21.1: Crying and Irritable Child
FIG. 21.1.3: Herpangina (For color version see Plate 9)
FIG. 21.1.4: Dental caries (For color version see Plate 9)
473
474
FIG. 21.1.5: Anal fissure (For color version see Plate 10)
5. Oral and rectal local anesthetics and analgesia in concerned conditions as discussed before.
6. Good analgesia for fractures including nerve block and digital block.
Splinting the limbs as required.
7. FB removal in cases of FB impaction.
Indications for Admission

a.
b.
c.
d.
e.
f.
Severe dehydration and shock due to any cause.

Suspected meningitis, brain abscess, encephalopathy.
Mastoiditis.
Septic arthiritis.
Pneumonia, bronchiolitis, asthma requiring oxygen, IV antibiotics, frequent oropharyngeal suctioning, NG feeding.
Surgical cases: Appendicitis, torsion testis, strangulated hernias, malrotation, intussusception, fracture reduction under GA.
21.2
Penis and Foreskin Problems
Jaydeep Choudhury
Balanitis
Balanitis arises when phimosis of the foreskin is present and infection sets
in the space under the foreskin. The infection spreads by migration of
cutaneous or enteral bacteria. It is usually subacute or chronic, but sometimes it may present as an acuter infection.
In the emergency the child may present with acute pain and swelling
of the penis and he may refuse to pass urine. Figure 21.2.1 shows the typical balanitis.
FIG. 21.2.1: Balanitis (For color version see Plate 10)
476
Management
A sample of urine and swab of the foreskin should be obtained. But relief
of pain is most important as the child may refuse to pass urine due to pain.
Paracetamol or ibuprofen may be given for pain relief. The commonest
organism for balanitis is Staphylococcus and Streptococcus, hence the suitable
antibiotics are co-amoxyclavulanic acid or cephalexin. Antibiotics, intravenous or oral should be started as per the situation. Recurrent balanitis is an
indication for circumcision or prepucioplasty.
Phimosis
Phimosis is a condition when the foreskin cannot be retracted. In acute
condition it may present with obstruction to the flow of urine, dribbling,
straining and ballooning during micturition or balanitis. In 97 percent
cases prepuce is retractile by 3 years of age.
Specific Management
Circumcission or prepucioplasty. Analgesic for immediate pain relief, if
any. Severe infection like balanitis has to be treated first before surgery.
Paraphimosis
Edema of the foreskin distal to the tight ring that develops due to forceful
retraction of the foreskin not returned to its normal position. The foreskin
becomes painfully swollen and is difficult to reduce Figure 21.2.2.
FIG. 21.2.2: Paraphimosis (For color version see Plate 10)
Chapter 21.2: Penis and Foreskin Problems
477
Management
It is easier to reduce the foreskin as early as possible when the edema is
minimal. The child should be given analgesics like ibuprofen and gentle
digital pressure should be used on the foreskin through saline soaked gauze.
This may reduce the foreskin edema to some extent attempt should be
made to replace the foreskin to its normal position.
If this method fails then the child should be referred to a pediatric
surgeon. The same procedure may be tried under general anesthesia or he
may puncture the edematous foreskin with hypodermic needle to evacuate
the edema.
Penile Zipper Entrapment Injury

It is the most common cause of penile entrapment. Usually occurs while
the boy is zipping up the pants. Once entrapped, attempts of unzipping
for self-extrication complicates the situation. This condition is extremely
painful. The movable zipper head may catch the soft tissue and the interlocking teeth may entrap some soft tissue.
Management
A thin median bar is the only structure separating the two tracks on the
zipper-sliding device and interlocking them. This median bar should be
cut with a bone or wire cutter Figure 21.2.3.
FIG. 21.2.3: Technique of cutting the median bar of the zipper
478
The external genitalia should be soaked with mineral oil for lubrication. Local anesthesia in the form of 1 percent lignocaine without adrenaline
should be injected. Once the median bar is broken, the front and back
plates fall apart releasing the entrapped skin. When the external genitalia
is entrapped in the interlocking teeth, the zipper should be cut just inferior to the entrapment site. With gentle manipulation, the interlocking
will separate from one another and release the skin.
Bibliography
1.
2.
3.
Livingstone. 655-8.
Choe JM. Paraphimosis: Current treatment options. American family Physician 2000;62:2623-8.
Lundquist JT, Stack LB. Diseases of the foreskin, penis, and urethra. Emergency Medicine Clinics of North America 2001;19:529-46.
21.3
Toxic Shock Syndrome
Toxic shock syndrome (TSS) is a multisystem disease manifested by sudden onset of fever, chills, hypotension, and rash with multisystem
involvement. Todd et al, first described staphylococcal toxic shock syndrome in 1978. The association of toxic shock syndrome with menstruation
and tampon use was established in 1980.
Pathophysiology
Staphylococcal toxic shock syndrome is caused by certain toxin-producing
strains. Toxic shock syndrome toxin-1 (TSST-1) is implicated in 75 percent
of patients with TSS, enterotoxin B is implicated in 23 percent and enterotoxin C is implicated in 2 percent of patients with toxic shock syndrome.
TSST-1 and the enterotoxins are superantigens. They result in nonspecific
T-lymphocyte stimulation without normal antigenic recognition. This massive activation of lymphocytes leads to release of cytokines that contribute
to the development of toxic shock syndrome.
Streptococci that produce streptococcal pyrogenic exotoxin A (SPEA)
and/or streptococcal pyrogenic exotoxin B (SPEB) cause streptococcal TSS.
The predominant streptococcal serotype that produces toxic shock syndrome is M-1, although other serotypes, such as M-2, M-3, M-12, and
M-28en reported. Differences between Staphylococcal and Streptococcal
TSS are shown in Table 21.3.1. The diagnostic criteria of Staphylococcal
and Streptococcal TSS are shown in Table 21.3.2.
Clinical Features
1. Abrupt onset of fever, headache, vomiting and diarrhea.
2. Associated sore throat, myalgia.
3. Sunburn like macular rashes followed by hyperemia of conjunctival,
pharyngeal and vaginal mucous membranes.
4. Strawberry tongue is common.
5. May quickly lead to altered sensorium, oliguria, hypotension, DIC and
shock.
Local invasive disease

Generalized erythroderma
Nausea, vomiting, or diarrhea
Bacteremia
Toxins implicated
Mortality rate
Age
Sex
Causes
Findings
Absent
Present
>90% of patients
Uncommon
TSST-1; enterotoxins B and C
3.3%
15-35 yrs
More common in females
i. Menstruation.
ii. Nonmenstrual conditions: Surgical wounds,
such as hernia repair and arthroscopy, respiratory
infections, varicella infection, nasal packing.
Staphylococcal TSS
TABLE 21.3.1: Differences between Staphylococcal and Streptococcal TSS
i.
ii.
iii.
iv.
v.
vi.
20-50 yrs
Males and females
Skin infections
Surgical wounds
Pharyngitis
Varicella infection
Influenza virus infection
NSAIDs:
Present
Absent
Uncommon
60% of patients
Streptococcal pyrogenic exotoxins A and B
30%
Streptococcal TSS
480
Major criteria (all required)

i. Temperature >38.8C
ii. Hypotension (orthostatic/shock)
iii. Rash (erythroderma with late desquamation)
Minor criteria (any three)
i. Mucous membrane inflammation
ii. Vomiting, diarrhea
iii. Liver abnormalities
iv. Renal abnormalities
v. Muscle abnormalities
vi. Central nervous system abnormalities
vii. Thrombocytopenia
Exclusionary criteria
i. Absence of another explanation
ii. Negative for blood cultures (except for S. aureus)
i.
ii.
iii.
iv.
v.
vi.
Streptococcal TSS
Hypotension plus two or more
Impairment
Coagulopathy
Hepatic involvement
Adult respiratory distress syndrome
Generalized erythematous macular rash
Soft tissue necrosis
Definite case
Clinical criteria plus group A streptococcus
from a normally sterile site (blood, CSF,
pleural/peritoneal fluid, tissue biopsy specimen)
Probable case
Clinical criteria plus group A streptococcus
from a nonsterile site (throat, vagina, sputum
or superficial skin lesions)
Staphylococcal TSS
TABLE 21.3.2: Diagnostic criteria of Staphylococcal and Streptococcal TSS
Chapter 21.3: Toxic Shock Syndrome
481
482
Complications
Acute respiratory distress syndrome, myocardial dysfunction, renal failure,
desquamation specially in palms and soles later in recovery period, loss of
hair and nails.
Differential Diagnosis
1.
2.
3.
4.
5.
6.
7.
Kawasaki disease.
Adenovirus infection.
Toxic epidermal necrolysis.
Meningococcal infection.
Scarlet fever.
Leptospirosis.
Rocky mountain spotted fever.
Work-up
1. Microbiologic studies should be performed to recover the organisms
from appropriate samples, such as blood, surgical wounds, vagina,
throat, or soft tissue aspirates.
2. Hematology, biochemical, electrolyte, renal and liver profile.
3. Urine examination to see sediments and hemoglobinuria.
4. Coagulation studies should be obtained, including prothrombin time,
activated partial thromboplastin time, platelet count, fibrinogen split
products and D-dimer assay.
5. If CNS infection is possible, the CSF should be analyzed and cultured.
6. Appropriate serologic analysis may be necessary to evaluate other possible differential diagnoses
7. Soft tissue radiography, CT scanning, or MRI may help delineate the
deeper tissue involvement in patients with necrotizing fasciitis and streptococcal toxic shock syndrome.
Management
Seriously ill patients may require care in the ICU, including dialysis for renal
failure, ventilatory support for acute respiratory distress syndrome (ARDS),
and correction of coagulopathy using plasma and blood products as necessary.
Treatment regimens for toxic shock syndrome (TSS) includes the following:
Staphylococcal Toxic Shock Syndrome

1. Aggressive fluid support with normal saline or colloids.
2. Vasopressor/inotrope infusion as necessary.
3. Antistaphylococcal antibiotics (penicillin and clindamycin or vancomycin and clindamycin in patients with penicillin allergy).
4. Removal of tampons, nasal packing, and other foreign objects.
5. Intravenous immunoglobulin (IVIG) therapy.
6. Aggressive supportive care in an ICU.
Chapter 21.3: Toxic Shock Syndrome
483
Streptococcal Toxic Shock Syndrome

1. Normal saline or colloids may be used. Intractable hypotension that
results from diffuse capillary leaking may require large amounts of these
fluids. Albumin replacement may be necessary in patients in whom
albumin levels drop lower than 2 g/dL.
2. Vasopressor/inotrope infusion as necessary.
3. Surgical debridement is mandatory in the presence of tissue necrosis.
4. Use penicillin plus clindamycin for antibiotic treatment. Clindamycin
therapy for streptococcal toxic shock syndrome produces better results
than penicillin alone.
5. Studies have suggested a salutary effect of IVIG therapy.
6. Aggressive supportive care in an ICU is needed.
7. The role of hyperbaric oxygen in streptococcal toxic shock syndrome
remains uncertain in the absence of any comparative clinical trials.
Bibliography
1.
2.
3.
4.
5.
6.
Baxter F, McChesney J. Severe group A streptococcal infection and streptococcal toxic shock syndrome. Can J Anaesth 2000;47(11):129-40.
Chuang YY, Huang YC, Lin TY. Toxic shock syndrome in children: Epidemiology, pathogenesis, and management. Paediatr Drugs 2005;7(1):11-25.
Davis JP, Osterholm MT, Helms CM, et al. Tri-state toxic-shock syndrome study.
Clinical and laboratory findings. J Infect Dis 1982;145:441-8.
Hackett SP, Stevens DL. Superantigens associated with staphylococcal and streptococcal toxic shock syndrome are potent inducers of tumor necrosis factor-beta
synthesis. J Infect Dis 1993;168(1):232-5.
Kaul R, McGeer A, Norrby-Teglund A, et al. Intravenous immunoglobulin
therapy for streptococcal toxic shock syndromea comparative observational
study. The Canadian Streptococcal Study Group. Clin Infect Dis. 1999;28:8007.
Todd J, Todd AS. Twenty years of toxic shock syndrome: Evolution of an emerging disease. Royal society of medicine: Int Congress Symp series
1998;229:201-04.
21.4
Biochemical Genetic EmergencyInborn
Errors of Metabolism
Jaydeep Choudhury
Inborn Errors of Metabolism (IEM) comprise a group of disorders in which

a single gene defect leads to a clinically significant block in a metabolic
pathway resulting either in accumulation of substrate behind the block or
deficiency of the product. All IEMs are genetically transmitted typically in
an autosomal recessive or X-linked recessive fashion.
IEM is one of the most neglected entities in clinical practice but the
diagnosis of IEM remains one of the most challenging areas of pediatric
clinics. There is varied clinical presentation. The signs and symptoms are
nonspecific and more often than not mimic more common conditions such
as infections, failure to thrive, heart diseases and asphyxia. The key to
early diagnosis is high index of suspicion. Most IEMs manifest in the newborn period or in early infancy. Due to the advancement in medical science
it is also possible to screen and detect many of these disorders in utero.
When should a genetic metabolic disorder be considered?
The presence of any of the following should prompt the clinician to consider the possibility of an inborn error of metabolism in any neonate, infant
or child:
1. Unexplained cardio-respiratory collapse.
2. Acute encephalopathy.
3. Acute liver failure.
4. Hypoglycemia.
5. Metabolic acidosis (with or without ketosis).
6. Lactic acidemia.
7. Hyperammonemia.
The major categories are the following:

Aminoacidopathies
The characteristic presentations of these disorders are metabolic acidosis
with ketosis, mild to moderate hyperammonemia and often with elevated
lactate.
1. Aromatic amino acidsexamples are phenylketonuria (PKU), tyrosinemia.
Chapter 21.4: Biochemical Genetic Emergency
485
2. Lysine groupexamples are glutaric aciduria.

3. Glycine groupexamples are nonketotic hyperglycinemia.
Organic acidemias
Caracterized by marked metabolic acidosis with ketosis, often with elevated
lactate and mild to moderate hyperammonemia. Examples are: Maple syrup
urine disease (MSUD), methylmalonic or propionic acidemia, isovaleric
academia, holocarboxylase deficiency.
Urea cycle disorders
Catabolism of amino acids results in the production of free ammonia, which
is highly toxic to the central nervous system. Ammonia is detoxified to
urea through a series of reactions known as Krebs-Hensleit or urea cycle.
Five enzymes are required for synthesis of urea. These defects are characterized by severe hyperammonemia and respiratory alkalosis, with a typical
onset after 24 hours of age.
1. Ornithine transcarbamoylase deficiency.
2. Carbamoyl phosphate synthase deficiency.
3. Citrullinemia.
4. Argininosuccinic aciduria
5. Argininemia.
Fatty acid oxidation defects
These disorders are characterized by hypoketotic hypoglycemia,
hyperammonemia, and cardiomyopathy. Medium-chain acyl-CoA dehydrogenase deficiency (MCAD) is among the most common of all IEMs and
may account for 5 percent of SIDS cases.
1. Carnitine uptake defects.
2. Fatty acid entry defects: For example, carnitine palmitoyltransferase
deficiency.
3. Defects of beta-oxidation: For example, VLCAD, MCAD and LCHAD
deficiency.
Carbohydrate metabolism defects
These are a heterogeneous group of disorders caused by inability to
metabolise specific sugars, aberrant glycogen synthesis, or disorders of gluconeogenesis. They may manifest with hypoglycemia and hepatosplenomegaly. Lactic acidosis or ketosis often accompanies.
1. Glycogen storage diseases (GSD)types I to IX.
2. Galactose metabolism defectsexamples are galactosemia,
galactokinase deficiency, epimerae deficiency.
Disorders of pyruvate metabolism
The typical presentation of these groups of disorders is severe lactic acidosis.
1. Pyruvate dehydrogenase deficiency.
2. Pyruvate carboxylase deficiency.
3. Cytochrome oxidase deficiency.
486
Storage disorders
1. Peroxisomal storage disorders: These disorders result from failure of
the peroxisomal enzymes. Examples are: Zellweger syndrome,
adrenoleukodystrophy.
2. Lysosomal storage defects: These are caused by accumulation of Glycoproteins, glycolipids, or glycosaminoglycans within lysosomes in
various tissues. Examples are: Mucopolysaccharidosis, Tay-Sachs,
Niemann-Pick disease, Gauchers disease.
3. Mucopolysaccharidoses: They may manifest with hypoglycemia,
hepatosplenomegaly, lactic acidosis or ketosis. Examples are: Galactosemia, hereditary fructose intolerance, fructose 1, 6-diphosphatase
deficiency and the glycogen storage diseases.
History
1. Pregnancy and maternal health: Perinatal history in most instances
does not reveal anything significant. Children with IEMs are usually
born of normal birth weight and in good condition. The exceptions
are nonketotic hyperglycinaemia and disorders of pyruvate metabolism, which have intra-uterine or immediate effects following birth. A
history of maternal acute fatty liver of pregnancy (AFLP) or hemolysis elevated liver enzymes and low platelets (HELLP) is associated
with several fatty acid oxidation disorders.
2. Family history.
3. Consanguinity.
4. Unexplained neonatal or infantile deaths.
5. Past medical history of developmentally delayed child.
6. Unexplained hypoglycemia: Useful clues to an underlying IEM are a
history of hypoglycemia, an episode of unexplained encephalopathy,
or an extreme reaction requiring hospitalization to an otherwise supposed mild illness such as gastroenteritis.
7. Encephalopathy.
8. Protein aversion: This typical phenomenon is seen most commonly
in the urea cycle disorders.
9. Self-injurious behavior: A history of self-injurious or self-mutilation
behavior can be seen in Lesch-Nyhan syndrome and hyperammonemia.
10. Psychiatric symptoms: Various other psychiatric abnormalities may
be associated with disorders of cobalamin and later onset lysosomal
storage disorders.
11. Seizure disorder: A severe seizure disorder in the newborn period
occurs in non-ketotic hyperglycinemia, peroxisomal disorders and in
sulphite oxidase/molybdenum cofactor deficiency.
12. Type of developmental delay or regression: Any suggestion of regression of acquired skills makes an IEM much more likely and merits
intensive investigation.
487
13. Hypotonia: Hypotonia causing gross motor delay is seen in the organic acidurias, fatty acid oxidation disorders (FAOs) and urea cycle
defects. Generalized delay with associated sensori-motor hearing loss
suggests a mitochondrial disorder. Seizures may occur in association
with developmental delay.
14. Speech delay: Speech delay is often the first sign of Sanfilippo syndrome (mucopolysaccharidosis type III).
Clinical Features
1. Dysmorphism:
i. Smith-Lemli-Opitz syndrome.
ii. Other cholesterol synthesis disorders.
iii. Congenital disorders of glycosylation.
iv. Peroxisomal disorders.
v. Lysosomal disorders.
2. Hepato (spleno) megaly: Lysosomal storage disorders, glycogen storage disorders.
3. Cardiomyopathy: Lysosomal storage disorders, fatty acid oxidation
defects, mitochondrial disorders.
4. Smell in organic acid disorders: A characteristic odour is associated
with certain organic acidurias such as maple syrup urine disease (sweet)
and isovaleric aciduria (sweaty feet) but is rarely a leading sign.
5. Neurological signs:
i. Dystonia: Mitochondrial disorders, organic acidurias, pterin defects.
ii. Macrocephaly: Canavans disease, Tay-Sachs, L-2-hydroxyglutaric
aciduria, glutaric aciduria type I.
iii. Microcephaly: Sulphite oxidase deficiency, maternal PKU offspring, previous hyperammonemia, previous hypoglycemia,
GLUT-1 deficiency, neuronal ceroid lipofuscinosis 1.
6. Failure to thrive, short stature: Many IEMs, e.g. organic acid, amino
acid, and urea cycle disorders present with failure to thrive.
7. Hair: Coarse, kinky Menkes disease, MPS disorders, arginino-succinic aciduria.
8. Skin: Coarse, ichthyosis, eczema LSD, Conradi-Hunermann, biotinidase
deficiency.
The various causes of IEM according to the time of onset of IEM in
neonates are shown in Table 21.4.1. It is often not possible to pin point the
exact diagnosis of IEM causing developmental delay from the clues in history and clinical examination. In such situations laboratory investigations
should be done in a serial logical manner. The first, second and third line
investigations are shown in Tables 21.4.2 to 21.4.4 respectively. Table 21.4.5
shows the methods of sample collection for various IEM diagnoses. Table
21.4.6 shows the clues to IEMs from initial few investigations.
Results that may suggest an IEM

Metabolic acidosis/respiratory alkalosis
Hypoglycemia
Increased anion gap (normal 12-16 mmol/L)
Raised transaminase
Usually negative (but sepsis common in some IEM)
Aminoacidopathies
Organic acedemias
Disorders of carbohydrate metabolism
Blood gas
Blood sugar
Electrolyte
Liver function tests
Infection screen
Galactosemia
Holocarboxylase synthase deficiency
Methylmalonic academia
Phenylketonuria tyrosinemia
Isovaleric academia
Glycogen storage disease type I
Organic acedemias
Fatty acid oxidation disorders
Aminoacidopathies
Urea cycle disorders
Aminoacidopathies
Organic acedemias
Disorders of pyruvate metabolism
Organic acedemias
Peroxisomal disorders Syndromic
Category
Investigation
TABLE 21.4.2: First line investigations in IEM
Late neonatal period
1-4 weeks
First few weeks
Maple syrup urine disease

Propionic academia
CPT deficiency type II
Glycogen storage disease type II
Zellweger syndrome
Neonatal adrenoleukodystrophy
Menkes disease
Smith-Lemli-Opitz syndrome
Glutaric academia type I
Glutaric academia type II
Nonketotic hyperglycemia
VLCAD deficiency
Birth
Hours to day 7
1-3 days
1-5 days
3-5 days
First week
Disease
Age of onset
TABLE 21.4.1: Time of onset of IEM in neonates
488
Encephalopathy, acidosis, unexplained multi-system

disorder
Hypoglycemia
Blood lactate
Encephalopathy, hyperammonemia, hypoglycemia,

metabolic acidosis
metabolic acidosis
Hyperammonemia
Liver disease
Liver disease
Liver disease
metabolic acidosis, cardiomyopathy, liver disease
Encephalopathy, fits
Unexplained neurological disease, particularly if associated with dysmorphic features
Unexplained multi-system disorder
Chronic progressive neurological disease,
organomegaly, certain dysmorphic features
Acylcarnitines by tandem mass spectrometry
Beutler test
Urine succinylacetone
Alpha1 antitrypsin
Plasma carnitine
OCT: Ornithine carbamoyltransferase, DHAP-AT: Dihydroxyacetone phosfate acyl tranferase.
Very long-chain fatty acids, DHAP-AT

Transferrin iso-electric focusing
Urine mucopolysaccharides and oligosaccharides
CSF lactate, glucose and amino acids
Urine organic acids

Urine orotic acid
Urine/Plasma amino acids
Liver renal disease

Encephalopathy, hypoglycemia, metabolic acidosis
Encephalopathy, Hyperammonemia, Hypoglycemia,
metabolic acidosis
Urine reducing substances

Urine ketones
Carbohydrate deficient glycoprotein syndrome

Screening test for some lysosomal disorders
Peroxisomal disorders
Normal <80 mol/l (usually >200 mol/L in organic

acidemia, >500 mol/L in urea cycle disorders)
Normal <2.5 mmol/L (exclude poor tissue perfusion and cardiac disease)
Endogenous hyperinsulinism, surreptitious insulin
injection and other endocrine causes of hypoglycemia
Unreliable for diagnosis of galactosemia
Marked ketosis unusual in newborn, suggest IEM,
hypoketosis in older infants with hypoglycemia
suggests disorder of fatty acid oxidation or hyperinsulinism
Organic acidemiasfat oxidation defects
Aminoacidopathies, characterization of urea cycle
disorders
Fat oxidation defects (only reliable during acute
metabolic decompensation) and organic acidemias
OCT deficiency
Screening test for galactosemia, unreliable if blood
transfusion within 3 months
Specific test for tyrosinemia
Primary and secondary carnitinine deficiency
Unexplained neurological disease
Encephalopathy
Blood ammonia
Insulin, c-peptide, growth hormone, cortisol
Comments
Indications
Investigations
TABLE 21.4.3: Second line investigations in IEM
489
490
TABLE 21.4.4: Third line investigations in IEM

Investigation
Results that may suggest an IEM
DNA analysis
For specific mutation analysis (if available)

Consult specialist laboratory
For specific disorders. Tissue required dependent upon suspected disorder
Consult specialist laboratory.
Enzymes assays
General Principle of Management of Acute Illness

Supportive Care
1. Intensive care is often necessary.
2. Establish arterial and central venous access.
3. Maintain adequate respiratory support (Assisted ventilation should be
considered early).
4. Correct hypothermia, hypoglycemia and dehydration.
5. Treat cerebral edema if present.
6. Correct significant metabolic acidosis with intravenous sodium bicarbonate (0.5-0 mmol/kg/hr).
7. Monitor electrolytes and blood gases.
8. Treat with antibiotics as septicemia is commonly associated with metabolic decompensation.
Reduce Load on the Affected Metabolic Pathway

1. Stop all exogenous protein.
2. Give IV glucose at 5 to 10 mg/kg/min (central lines are usually required
for >10% dextrose).
3. Give insulin at 0.05 to 1 I U/kg/hr (maintain blood sugar at 7-11 mmol/L).
Removal of Toxic Metabolites

1. Give IV L-carnitine at 100-200 mg/kg/day (but may be contraindicated
in certain fat oxidation defects).
2. Maintain adequate urine output if possible.
3. Dialysis may be required if poor urine output, hypernatremia, metabolic acidosis, or in order to remove, specific toxic substrates or
metabolites (for example, ammonia in urea cycle disorders or organic
acidemias, leucine in maple syrup urine disease, propionate in propionic acidemia). Hemodialysis is usually the most effective method.
Acute Management of Hypoglycemia

1. Insert IV cannula (central venous access is required for persistent hypoglycemia).
2. Collect 5 ml blood for investigations (1 ml fluoride, 2 ml heparin, 2 ml
clotted, blood spot).
Blood 2 ml in fluoride
Blood 2 ml in perchlorate
Blood 7 ml heparinized in
EDTA
WBC pellet
Blood 0.5 ml heparinized or heparinized capillary tubes
2 ml plasma heparinized
Blood 3 ml heparinized
Plasma 5 ml EDTA
1015 ml
5 ml on a thick filter paper
Newborn screening card
MPS electrophoresis
Urine amino acids
Sugar chromatography
TLCX for oligosaccharides
Plasma amino acids
Qualitative
Quantitative
Serum lactate
Serum pyruvate
Lysosomal enzymes
Plasma acylcarnitines
Beutler test
Biotinidase assay
Carnitine
Very long chain fatty acids
Urine organic acids
Fresh, without preservative in an airtight container

Air-dry thoroughly
Free flowing blood, without squeezing spreading uniformly and soaking to the reverse side of the paper,
allowed to get dry for 4 hours
Collect without applying tourniquet, transported on

ice and analyze immediately within 15 minutes
Arterial sample, collected as above, transport within
30 minutes on ice
As for serum lactate
4C, within 6 hours
Within 48 hours
-20C, on dry ice
Can be stored at room temperature in a week
Fresh
Transport on dry ice, within 24 hours
Fresh
Room temp, within 24 hours
2 hours after milk feed
Fresh
Preferably fasting
On ice
15 ml urine
50 ml aliquot of 24 hours sample
Urine 10 ml
Urine 24 hours
Urine 5 ml
Urine 10 ml
2 ml heparinized blood
2 heparinized capillary tubes
Blood 3 ml heparinized
Plasma 1 ml deproteinized
Blood 2 ml
MPS screen
Serum ammonia
Comments
Sample
Test
Table 21.4.5: Sample collection for IEM diagnosis
491
No++
++
++
++
No++
No+
No
++
No++
+
No+
No+
Normal
Normal
Normal
Normal
Blood
glucose
Normal
Blood
NH4
Cataract (galactosemia), raised

AFP (tyrosinemia), history of
fructose intake (HFI)
Relationship to dietary protein

intake and catabolic episodes
Relationship to dietary protein
intake and catabolic episodes
Often precipitated by fasting or
catabolic illness liver/cardiac
symptoms
Respiratory alkalosis tachypnea
Other clinical and

biochemical clues
N Normal, PDH Pyruvate dehydrogenase deficiency, PC Pyruvate carboxylase deficiency, TCA Tricarboxylic acid cycle, CBC Completel blood count.
Normal
Normal
No
No
Normal
Normal
Normal
Hemolysis,
consumption
N or
N or
No+
Fatty acid oxidation

or ketogenesis
defects
Urea cycle defects
Primary lactic defects
i. PDH deficiency
ii. PC deficiency
iii. Gluconeogenesis defects
iv. TCA defects
v. ETC defects
Acute hepatic failure
(including galactosemia, tyrosinemia
type 1, HFI
N or
No+
++
++
platelets
WCC
Normal
Normal
Organic acidopathies
Normal
No++
No++
Blood
lactate
Normal
Anion
gap
Metabolic
acidosis
Ketosis
Amino acidopathies
CBC and
coagulation
TABLE 21.4.6: Clues to IEMs from initial few investigations
492
493
3.
If symptomatic give bolus dose of 10 percent dextrose 2 ml/kg (200 mg/kg)

at the rate of 1 ml/min.
4. Start infusion of 10 percent dextrose at 4 ml/kg/h (~ 7 mg/kg/min).
5. Recheck glucose after 15 mins. Increase rate to 8 ml/kg/h of 10 percent
dextrose (~ 13 mg/kg/min of glucose) if still hypoglycemic (higher rates
will be required for hyperinsulinism).
Acute Management of Hyperammonemia

Hyperammonemia ia defined as serum ammonia (NH4) above 120 mol/L).
The management outline is shown in Table 21.4.7.
TABLE 21.4.7: Acute management of hyperammonemia (NH4 > 120 mol/L)
1. Stop all exogenous protein.
2. Inhibit endogenous catabolism.
3. Correct metabolic acidosis if present.
4. Give maintenance fluids as 10 to 15 percent glucose (aim for blood sugars of 7-11 mol/L).
5. Combine with continuous insulin infusion at 0.05 to 0.1 IU/kg/hour.
Intravenous medication,
start if ammonia
> 150 mol/L.
Sodium
benzoate
(mg/kg)
Sodium
phenylbutyrate
(mg/kg)
Arginine
10% (mg/kg)
L-cartinine
(mg/kg)
Priming infusion :
Make up in 30 ml/kg
of 10% glucose and
give over 90 mins
Maintenance:
Make up up to 30 ml/kg
10% glucose and give
as continuous infusion
over 24 hours
250
250
200
250
250
200 (600 in
citrullinemia and
argininosuccinic
aciduria)
100200
Monitor NH4+, sodium, potassium and blood gases 4 to 8 hourly

Dialysis: For ammonia levels >400 mol/l, or if <400 V abut with no decrease after 4 hours of intravenous medication. Hemodialysis is preferable
(better clearance of NH4+) but if not available hemofiltration should be
used. Peritoneal dialysis is less effective but can be used if it is the only
form of dialysis available. Dialysis will also remove toxic metabolites that
accumulate in organic acidemias.
Patients with urea cycle disorders will need to continue on oral medication following recovery.
Long-term Treatment of IEM

Dietary Treatment
This is the mainstay of treatment in phenylketonuria, maple syrup urine
disease, homocystinuria, galactosemia and glycogen storage disease. Types
I and III. Special diets for PKU and MSUD are commercially available in
494
the west. These are not just available in India, but can be imported. These
special diets are however very expensive, and cannot be afforded by most
Indian patients.
Enzyme Replacement Therapy (ERT)

ERT is now commercially available for some lysosomal storage disorders.
However, these disorders do not manifest in the newborn period, an exception being Pompes disease (glycogen storage disorder Type II) which
may present in the newborn period and fro which ERT is now available.
Cofactor Replacement Therapy

The catalytic properties of many enzymes depend on the participation of
nonprotein prosthetic groups, such as vitamins and minerals as obligatory
co-factors. The following cofactors may be beneficial in certain IEM as
TABLE 21.4. 8: Cofactor therapy in IEM
Disorder
Vitamin/cofactor
Dose (mg/day)
Amino acid
supplement
Neonatal trysinemia
Classical homocytinuria
50-100
100-500
10-20
100-250
100-150
10-20
1.0-3.0
5-10
-
Cystine
Hartnup disease
Mitochondrial disorder
Maple syrup urine disease
Methylmalonic acidomias
Multiple carboxylase deficiency
Isovaleric acidemia
Vitamin C
Pyridoxine and
Folic acid
Niacin
Riboflavin
Thiamine
B12
Biotin
-
Hawkinsinuria
Vitamin C
1000
Bicarbonate
Glycine and
L-cartinine
-
Metabolic Autopsy
The following samples are to be obtained in infant with suspected IEM
when diagnosis is uncertain and death seems inevitable.
1. Blood5 to 10 ml; frozen at 20oC; both heparinized (for chromosomal studies) and EDTA (for DNA studies) samples to be taken.
2. Urinefrozen at 20oC.
3. CSFstore at 20oC.
4. Skin biopsyincluding dermis in culture medium or saline with glucose. Store at 4 to 8oC. Do not freeze.
5. Liver, muscle, kidney and heart biopsy as indicated.
6. Clinical photograph in cases of dysmorphism.
7. Infantogram in cases of skeletal abnormalities.
495
Bibliography
1.
2.
3.
4.
5.
6.
7.
8.
9.
Chaves-Carballo E. Detection of inherited neurometabolic disorders; a practical clinical approach. Pediatr Clin North Am 1992;39:801-20.
Cleary MA, Green A. How to investigate for an inborn error of metabolism
Developmental delay: when to suspect. Arch. Dis. Child 2005;90:128-32.
Geene CL, Thomas JA, Goodman SI. Inborn error of metabolism. In: Hay WV,
Levin MJ, Sandheimer JM, Deterding RF Editors. Current pediatric diagnosis
and treatment. New York. Lange Medical Books 2005;17 edition:1014-31.
Kumta NB. Inborn errors of metabolism (IEM); An Indian perspective. Ind J
Ped 2005;72(2):325-32.
Losty H. UK National Metabolic Biochemistry Network Guidelines for the Investigation of Hyperammonaemia for Inherited Metabolic Disorders. 2004.
www.metbio.net
Muranjan M, Agarwal R. Inborn errors of metabolism: An overview. Ind J of
Prac Ped 2005;7(3):206-19.
National Metabolic Biochemistry Network Guidelines for the Investigation of
Hypoglycemia in Infants and Children. The National Metabolic Biochemistry
Network. 2004. URL: www.metbio.net
Rama Devi R, Naushad SM. Newborn screening in India, Indian J Pediatr
2004;71:157-60.
Verma IC, Bijarnia S, Puri RD. Screening for inborn errors of metabolism.
J Neonatol 2005;19:107-24.
22
MEDICOLEGAL
ISSUES
22.1
Medicolegal Issues in Emergency Room
Jaydeep Choudhury
Emergency room services actually deals with patients whose life is at risk.
Thus, it is potentially a volatile area, particularly when the patient is a
child. Here the children are brought with some acute symptoms and the
caregivers expect prompt action and relief. On the other hand, sometimes,
it is not possible to pinpoint a diagnosis. In such a situation the attending
doctor is expected to be gentle, caring and confident. A good emergency
duty doctor not only treats the disease well but also counsels the parents
avoiding any misunderstanding or communication gap. It is imperative
that doctors are answerable for the outcome of the patients and are bound
to justify the actions taken by them. Most of the time more than medical
mismanagement, it is the lack of communication and improper dealing of
the situation that leads to litigation. In such a scenario the medicolegal
aspect of emergency services should always be protected.
Documentation in Emergency Ward

Proper documentation with date, time, name and signature is evidence
which justifies that the patient was attended to at the emergency, treatment
given and diagnosis was attempted. Documentation is of utmost importance in clinical practice.
Consent in Emergencies
In emergency situations consent may not be taken for providing life-saving
treatment, even though the nature of treatment may amount to adventure.
Even emergency operations like tracheostomy may be performed without
consent if it saves the life of the patient. But the doctor should do only that,
which is necessary to save the life, ensures improvement and prevent deterioration. Nonurgent problems should not be dealt with in the emergency.
Whenever possible consent should be obtained from the parents or
relative. Indian Penal Code states that a consent given by a child under 12
years of age is invalid. Indian Majority Act states that a person who has
attained the age of 18 years may give legally valid consent for medical or
surgical procedures.
500
Medical Negligence
It is failure on part of a doctor to exercise skill and diligence which are required of a professional. It may be either an act of omission or an act of
commission which an emergency doctor of average skill is not supposed to do.
Criminal negligence is the act of negligence on part of the practitioner
who is so careless or reckless that it almost results in severe damage to the
health of the individual.
In emergency situations patients are brought in critically ill, often moribund condition. In such a situation the priority is to save the life without
bothering about complications. A typical example, is rib fracture following
cardio-respiratory resuscitation. Here the relatives cannot sue the treating
doctor for rib fracture.
Informing the Police

Police should be intimated in the following situations:
i. Unnatural death and sudden death after treatment or reaction to
medicine.
ii. Unknown, unconscious patient.
iii. Any poisoning.
iv. Motor vehicular and other accidents that account for fractures, head
injuries, accidental falls needing inpatient treatment.
v. Burns.
vi. Drowning.
vii. Tetanus, gas gangrene, significant violence needing inpatient treatment.
viii. Attempted suicide, poisoning and attempted homicide. In attempted
poisoning the doctor should collect the stomach wash and blood
samples clotted and in EDTA and hand it over to police.
ix. Human, animal or snake bite.
x. Abandoned child.
xi. Suspected child abuse.
xii. Rape, minors pregnancy, MTP, battered baby.
Breaking Bad News

If a junior doctor is on duty it is better to call a senior colleague for breaking a bad news. The parents should be taken to a separate room or place
and make them sit before breaking the news. The communication should
be made as reassuring as possible. A second opinion is always welcome in
such a situation. Often the parents become very emotional and angry. Both
the extremes of situation should be dealt calmly and with empathy.
Death certificate
Proper judgement for issue or denial of death certificate is often very crucial.
Chapter 22.1: Medicolegal Issues in Emergency Room
501
Child Brought Dead who was Under Treatment at the Hospital

1. If the child was under treatment at the hospital for some chronic and
potentially fatal disease and has been brought dead to the emergency,
death certificate has to be issued if the death seems to be a logical
outcome of the disease.
2. Death certificate can be issued if no foul play is suspected.
3. But if the cause of death seems unnatural then the police has to be
informed.
Child Brought Dead by the Parents

After initial assessment and attempts for resuscitation death has to be declared. Police has to be informed and postmortem advised.
Child Brought Dead by a Mob

1. Rapid assessment whether the child is really dead.
2. It is prudent to start an attempt for resuscitation as this will not only
help the physician to buy time but also pacify an anxious crowd.
3. The signs of death should be reassessed infront of a few members of
the crowd and death declared. Police has to be informed and postmortem advised.
4. If the mob seems to be rowdy, the police should be informed and asked
for protection before declaring death.
Caution has to be exercised, if a child is suddenly brought dead or
succumbs in the emergency department shortly after initiating treatment.
Doctor should not yield to pressure or comply on sympathetic ground. It is
prudent to plead helplessness to the relatives and inform the police. Here
again proper communication and tact is of utmost importance. If the situation is such that it is not possible to tackle the situation alone, then help of
colleagues should be taken.
In an emergency department, treatment cannot be refused to any child.
Not only the attending physician, but the whole paramedical team should
be motivated to get involved. Confusion arises when two or more critically
ill children are brought to the emergency at the same time. One should be
careful to assess and attend to all of them. It is important to quickly examine and assess who is the most critical of them and treat him or her, still not
denying the basic management to the rest of the sick children. Here the
paramedical team plays a crucial role. The accompanying family members
should not feel that basic treatment is being denied to their child.
Bibliography
1.
2.
3.
4.
Indian Penal Code, 1860. Sections 299, 309, 319-338, 375, 376.
The Consumer Protection Act, 1986 as amended up to date in 2002.
The Criminal Procedure Code, 1973. Sections 154, 173.
Tiwari S, Tiwari M, Baldwa M Editors. Medico-legal Issues in Pediatric Practice, 1st edition. Mumbai: Indian Academy of Pediatrics 2007.
Index
A
Abdominal
distention 191f
trauma 386
Abnormal pulse rate or rhythm 160
Abuse of children 357
Accidental hypothermia 296
Acid base balance and fluid 316, 318
Acute
abdominal pain 187, 193, 244
appendicitis 188
bacterial sinusitis 417
care 154
chest syndrome 243
CNS event 244
epiglottitis 139
lower abdominal pain 188
management of
hyperammonemia 493, 493t
hypoglycemia 490
medical problems or distress 12
meningitis 458
neck stiffness 367
osteomyelitis 371
otitis
externa 412
media 413
painful hip 369
renal failure 209
scrotum 194
severe asthma 145
splenic sequestration crisis 244
variceal hemorrhage 200
Addisonian crisis 262
Adenosine 169
Administration of oxygen 45
Adrenal insufficiency 262, 263
Airway foreign body 333
Anal fissure 474f
Analysis of pleural fluid 98t
Anaphylaxis 40, 41t

Angioedema 428
Angulated greenstick fracture of
distal radius 391f
Animal bites 267
Antibiotic therapy 461, 464
Antidotes 306
Antimalarial chemotherapy 447
Antirabies vaccination 271
Antiseizure medications in coma 34
Antitetanus prophylaxis 271
Apgar scoring system 108t
Aplastic crisis 245
Arrhythmia 163
Artemisinin based combination
therapy 447t
Arteriovenous malformation 229
Asymptomatic hyponatremia 50
Autonomic nervous system 326
Axial skeleton 397
B
Bag and mask ventilation 18f, 85f
Balanitis 475
Battery in nose or ear 345
Bee sting in finger 472f
Benzodiazepines 72, 72t, 73
Beta blockers 327
Bicarbonate 251
Bilateral upper lobe consolidation 455f
Biochemical genetic emergency 484
Bleeding
disorder in neonates 125
neonate 123
Blood
component
administration 61
transfusion 56
sampling 256
stained discharge 404
504
Blunt trauma 384, 405f

Bradyarrhythmia 161
Bradycardia 163, 164
Breathing 18, 33, 163
Bronchiolitis 142
Bronchopneumonia 456f
Buckle fracture of distal ulna 391f
Bulb mucus sucker 17f
Buphthalmos 408, 408f
Burn 289
Button
battery
in intestine 343f
ingestion 341
C
Canine rabies 274
Carbohydrate metabolism defects 485
Cardiopulmonary resuscitation 17
Cardiovascular emergencies 151
Causative virus 268
Causes of
acute stiff neck 367
ARF 209
chest pain 175
hyperinsulinism 257
pediatric hypoglycemia based
on age 255t
white pupillary reflex 401
Cell culture antirabies vaccine 272
Central nervous system 325
Cerebral
edema 252, 287
hypoxemia/ischemia 28
malaria 448
Cervical spine 364
injuries 376
Chemical injury affected eye 407f
Chest
pain 175
trauma 384
tube
drainage and needle
thoracocentesis 97
placement 97
Child with
advanced liver failure 203f
chickenpox 423f
measles 422f
meningococcal rash 423f
neonatal purpura 124f

red eye 404
Choice of empiric antimicrobials 36
Choreoathetoid movement disorder 73
Chronic urticaria 430
Classification of
cervical spine injuries 377t
migraine with aura 226
neuromuscular blockers 78
Clavicle fracture 394f
Cofactor replacement therapy 494
Coma 28
Common causes of
ear pain in children 411t
heart failure 156
hyperpyrexia 294
hypertension in children 215t
pediatric hypertensive
emergencies 215t
unconjugated hyperbilirubinemia
in children 113
Common
complications of severe
hypothermia 296
lower extremity injuries 394
migraine 226
upper extremity injuries 389
Community acquired pneumonia 454
Compensated shock 24
Complete obstruction 334
Complications of RSI 93
Composition of commonly used
rehydration solutions and
plasma 49t
Confirmatory tests 257
Congenital cataract 401
Conjugated hyperbilirubinemia 113
Conjunctival congestion 405
Contraindications of lumbar
puncture 459
Corneal foreign body 406
Cricothyrotomy 103
Croup management plan 137
Cyanotic spell 153
D
Dating fractures 358
Decision-making in pediatric
emergency 9
Decompensated shock 25
505
Index
Deeper frost bite 300
Degree of burn 289
Delivered oxygen 46
Dengue 450
fever 450
hemorrhagic fever 451, 453
serology 451
shock syndrome 451
Dental caries 473f
Diabetic ketoacidosis 249
Dialysis in ARF 213
Diazepam 73
Diffuse bacterial otitis externa 413
Digoxin 328
Disadvantages of oxygen therapy 46
Disorders of pyruvate metabolism 485
Displaced
distal end radius and ulna
fracture 390f
lateral condyle humerus
fracture 393f
proximal humerus fracture 393f
supracondylar fracture of distal
humerus 392f
Dog bite over
arm 268f
face 267f
Drugs to treat severe hypertension 217t
Duct dependent systemic lesions 182
Duration of antibiotics 461
Dysrhythmias 299
E
Electrical burn 292
Electrolytes 250, 324
Elemental iron content of different
iron salts 310t
Emergency treatment of VT 172
End organ damage 216
Endocrine disorders 29
Endoscopic evaluation of GI
bleed 200
Endotracheal tube 18f
Enzyme replacement therapy 494
Epididymo-orchitis 196
Epilepsy 28
Epiphyseal fracture separation of lower
end of tibia in adolescent
child 396
Epistaxis 416
Erythema multiforme 433f

ET tube 87t
Euvolemic hypernatremia 52
Extracorporeal techniques 299
Eye exposure 322
F
Factitious hyponatremia 51
Fatty acid oxidation defects 485
Fentanyl 71
Fever
with rash 421
without focus 441
Fiberoptic bronchoscopy 338
First
aid 277, 289
attack of status asthmaticus 149
Flail chest 385
Fluid 20, 250
and electrolyte balance 47
management of ARF 213
resuscitation 290
Foreign body in
GI tract 339
nose and ear 414
Fractures 388
Frequency of monitoring bilirubin 117
Frostbite 299
Fulminant hepatic failure 202
Furunculosis 412
G
Gastrointestinal
decontamination 305
emergencies 185
Granulocytes 61
Greenstick fracture of tibia and fibula
with valgus angulation 395f
Guideline to management of potentially
injured cervical spine 383
H
Hand-foot syndrome 243
Head trauma 363
Headache 225
with fever 225
without fever 225
Heart
disease 181
failure 156
506
Hematuria 220
Hemolytic disease of newborn 117
Hepatic encephalopathy 203t
Herpangina 418, 473f
Herpetic
gingivitis 472f
gingivostomatitis 417
Heterometrus bengalensis 281
Humidification of oxygen 45
Hydrocarbons 320, 321
Hydrocephalus with shunt 228
Hyperbilirubinemia 113
Hyperglycemia 34
Hyperkalemia 53
Hypernatremic dehydration 51
Hyperoxia test 127
Hyperparasitemia 449
Hyperpyrexia 294, 448
Hypertension 229
Hyperthermia 294, 295
Hypocalcemia 55
Hypodermic needle injury 406
Hypoglycemia 33, 109, 256, 258, 448
Hypokalemia 54
Hyponatremia 50, 51t
Hyponatremic dehydration 50
Hypotension 41
Hypothermia 287
Hypovolemia 48
Hypovolemic hypernatremia 52
I
Idiopathic scrotal edema 196
Incomplete obstruction 334
Incubation period 269
Indian
red scorpion 281
scorpions 281
Infectious
complications of transfusion
therapy 62t
diseases 28
Inhalation exposure 317, 319, 322
Injuries in appendicular
skeleton 394, 389
Insect bite 430f
Insulin 251
Interpretation of dengue IGM and
IGG 452t
Intestinal obstruction 189
Intracranial
pressure 34
injection 273
Intraocular pressure 75
Intraosseous access 94
Intussusception 189
IO in
distal
femur 96f
tibia 95f
proximal tibia 95f
Iron 309
ingestion management plan 313
Irreversible shock 25
K
Ketamine 74
L
Lactic acidosis 449
Laryngoscope blade 87t
Larynx 134
Left ventricular dysfunction 157
Leukocoria 401, 402f
Liver trauma 386
Lorazepam 73
Lower motor neuron 236
Lung contusion 385
M
Macroscopic hematuria 222
Management of
acute
epiglottitis 140
illness 490
onset limb weakness 239
airway foreign body 336
bronchiolitis 144
chronic heart failure 157
complete airway obstruction 337
cyanotic spell 154
heart failure due to
acute myocarditis 158
shunt lesions 159
hyperbilirubinemia in
healthy term infants 118f
in preterm infant 120f-122f
sick term newborn infant 119f
507
Index
hypertensive emergency 218
liver trauma 386
severe asthma 147
splenic trauma 387
Management plan
for acute variceal bleeding 201
for button battery ingestion 344
of acute painful hip 373
of paracetamol overdose 310
Meckels diverticulitis 189
Mediastinal injury 385
Medications for pediatric resuscitation
and arrhythmias 22t
Meningitis 127
Meningococcal disease 426
Meperidine 71
Mesenteric lymphadenitis 189
Mesobuthus tamulus 281
Metabolic
and structural coma 32t
autopsy 494
diseases 127
Methadone 71
Midazolam 72
Middle ear
effusion 413
inflammation 413
Midgut malrotation 192
Migraine 225
with aura 226
without aura 226
Moderate hypothermia 108
Modified GCS 30t
Monteggia fracture dislocation 391f
Morphine 70
Moth balls 322
Mucopurulent discharge 405
Multiple air-fluid levels in straight
X-ray abdomen 191f
Muscle relaxants 77, 78, 91
N
Naphthalene 322
Narrow complex tachycardias 165
Nasal intubation 86
Needle pericardiocentesis 100
Neonatal
apnea 110
collapse 126
collapse algorithm 129
hemorrhage 110
Neonate under phototherapy 115f

Neuromuscular blocker use 79
Neuroparalysis 279
Noisy breathing 134, 135
Nondepolarizing neuromuscular
blockers 78, 79, 79t
Nonrespiratory causes of respiratory
distress 134
Nonurgent acute medical problems 13
Normal
chest X-ray 334
vital signs 10
O
Opioids 70
Optimize ABC 277
Organic acidemias 485
Organophosphorus compound 323
Orlowskis prognostic scoring
system 288
Oropharyngeal airway 85f
Otitis externa 412
Otomycosis 413
Oxygen
percentage with different
systems 45t
supplementation 44
P
Paddle size 174
Painful crisis 243
Pancreatic trauma 386
Paracetamol 307
Paralytic type of rabies 269t
Paraphimosis 476
Parkland formula 290
Partial airway obstruction 336
Pediatric
airway 84t
burns patients 290
cataract 402f
chest pain algorithm 178
musculoskeletal injuries 388
resuscitation equipment 3
Penile zipper entrapment injury 477
Penis and foreskin problems 475
Pericardial tamponade 385
Periocular infections 407
Peritoneal irritation 187
Pharmacotherapy of anaphylaxis 42t
Phenothiazines 325
508
Phimosis 476
Pneumothorax 385
Poisoning 303, 305
Postcraniotomy 458
Postexposure prophylaxis 270t
Potassium 49, 250
Prazosin 283
Primary
dengue infections 452
peritonitis 190
Procedure for pericardiocentesis 102f
Progressive degree of
hypothermia 297t
Prolonged
neonatal jaundice 113
QT syndrome 182
Prophylaxis 461
Propofol 76
Proximal tibia 94
Pruritus 72
Pseudotumor cerebri 227
Pulmonary blood flow 182
Pure petroleum distillates 321
Q
QRS complexes 165
R
Rabies immunoglobulin 271
Radiopaque foreign body in upper
airway 335
Raised intracranial pressure 28, 227
Rapid
onset limb weakness 235
sequence intubation 89
Red
blood cell 56
eye 403, 404f
flag 187
Refractory hypoglycemia 258
Rehydration 47
in acute gastroenteritis 47
Renal trauma 387
Respiratory
depression 73
distress 133
Resuscitation 15
Retinoblastoma 402f
Rewarming techniques 298
Right
basal lobe consolidation 455f
inguinal hernia in neonate 191f
Rigid fiberoptic bronchoscope 338
Rumack-Matthew nomogram 308f
S
Salbutamol 41
Salicylates 314
SCIWORA 382
Scorpion
envenomation 281
sting 281
Secondary dengue infections 452
Seizures 108
Selection of laryngoscope blade 86
Septic
arthritis 370
screen 203
Serious bacterial infection 441
Severe
abdominal pain 187
and complicated malaria 445
anemia 448
bleeding 198
hypothermia 107, 108
malaria 5, 44t
Severity of intoxication 314, 314t
Sexual abuse 358
Shaken baby syndrome 408
Shock 24, 48
Sick and well children 11t
Sickle cell disease and crisis 243
Simple bone cyst in humeral
diaphysis 390f
Sinus tachycardia and SVT 167t
Sinusitis 417
Skin
rash 422
test 279
Slipped upper femoral epiphysis 372
Snake bite 276
Sodium loss in various states of
dehydration 49t
Spinal
cord injury 375, 380
immobilization in children 376
Splenic trauma 386
509
Index
Staphylococcal
and streptococcal TSS 480t, 481t
toxic shock syndrome 482
Status epilepticus 231
Stepwise management of
ARF 211
hypertension 218
Stevens-Johnson syndrome 432
Streptococcal toxic shock
syndrome 483
Stress ulcer 291
Subarachnoid hemorrhage 229
Succinylcholine 78
Suction catheter 87t
Sudden infant death syndrome 127
Superficial frostbite 300
Supraventricular
tachycardia 167, 169f
Syncope 37
T
Tachyarrhythmia 161
Tachycardia 163, 165
Target
lesion 433f
sign of intussusception in
abdominal USG 189f
Technique of cutting median bar of
zipper 477f
Ten affecting face 436f
Tension headache 229
Testicular trauma 196
Therapeutic products derived
from plasma 60t
Thoracolumbar spine X-rays in
multitrauma 379
Three classes of poisonous snakes 276
Torsion of testis 194
Tourniquet test 450
Toxic
doses of iron 311t
epidermal necrolysis 435
shock syndrome 479
Tracheobronchial injury 385
Transient synovitis 369
Transverse fracture of femoral
diaphysis 395f
Trauma 229, 405

Traumatic cataract with sphincter
tear 405f
Treatment of
acute otitis media 414
conjugated hyperbilirubinemia 115
Treatment priorities and
stepwise assessment 26
Tricyclic antidepressants 327
Types of
antirabies vaccines 272
injury 363
shock 24
Typical
features of ten 436f
wheal in urticaria 429f
U
Ulnar fracture 391f
Unconjugated hyperbilirubinemia 115
Undisplaced spiral fracture
of tibia 396f
Upper
gastrointestinal bleeding 198
limb 394
motor neuron 236
Urea cycle disorders 485
Urinary tract infection 462
Urine 204
Urticaria 428, 428f
V
Vagal stimulation 169
Vancomycin 461
Ventricular tachycardia 171, 171f
Visible peristaltic waves 190f
Volume replacement
flow chart of dengue fever 453
in dehydration 48t
W
Water or calorie requirement 49t
White pupillary reflex 402f
WHO classification of bites 270
Wide-complex tachycardia 170

Approach To Pediatric Emergency

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Approach to Pediatric Emergency

Approach to Pediatric Emergency

2.3. Coma ............................................................................................ 28

2.8. Blood Component Transfusion .................................................. 56

SECTION 3: SEDATION, ANALGESIA, INTUBATION AND PROCEDURES

Approach to Pediatric Emergency

3.5. Chest Tube Drainage and Needle Thoracocentesis .................. 97

SECTION 4: NEONATAL EMERGENCIES

4.4. Neonatal Collapse ..................................................................... 126

SECTION 5: RESPIRATORY EMERGENCIES

Approach to Pediatric Emergency

Signs of High Risk ................................................................ 148

SECTION 6: CARDIOVASCULAR EMERGENCIES

Presentation .......................................................................... 182

SECTION 7: GASTROINTESTINAL EMERGENCIES

SECTION 8: RENAL EMERGENCIES

Approach to Pediatric Emergency

Determination of Underlying Cause .................................... 210

SECTION 9: NEUROLOGICAL EMERGENCIES

9.3. Rapid Onset Limb Weakness ................................................... 235

SECTION 10: HEMATOLOGICAL EMERGENCIES

SECTION 11: ENDOCRINAL EMERGENCIES

Approach to Pediatric Emergency

Investigations ........................................................................ 263

SECTION 12: ENVIRONMENTAL PROBLEMS

Hypothermia ........................................................................ 287

Approach to Pediatric Emergency

SECTION 13: POISONING

SECTION 14: FOREIGN BODY

Treatment ............................................................................. 344

SECTION 15: PSYCHIATRIC BEHAVIORAL AND SOCIAL ISSUES

SECTION 16: TRAUMA AND ORTHOPEDICS

Approach to Pediatric Emergency

Slipped Upper Femoral Epiphysis (SUFE) .......................... 372

SECTION 17: OPHTHALMOLOGICAL EMERGENCIES

SECTION 18: OTOLARYNGOLOGICAL EMERGENCIES

SECTION 19: DERMATOLOGICAL EMERGENCIES

SECTION 20: INFECTIONS

Approach to Pediatric Emergency

Common Causes above 3 Months ........................................ 442

SECTION 21: MISCELLANEOUS EMERGENCIES

Approach to Diagnosis .......................................................... 470

SECTION 22: MEDICOLEGAL ISSUES

Pediatric Resuscitation Equipment

Approach to Pediatric Emergency

2. Noninvasive blood pressure (NIBP) monitor With infant and child

Lumbar puncture (LP) set.

Normal saline (0.9%).

Chapter 1.1: Setting-up Pediatric Emergency Department

Approach to Pediatric Emergency

Chest drain set with under water seal system.

Location, design and infrastructure of emergency room

Monitoring and Recording Vital Functions

Transferring the Patient

Chapter 1.1: Setting-up Pediatric Emergency Department

Airway and Breathing

2 duration of journey flow (L/min)

Approach to Pediatric Emergency

Name, age, sex and weight.

Children present to the emergency department more often than adults.

Warning Symptoms in History