(Am-medicine.com)

READY RECKONER
for
Treatment in Pediatrics
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READY RECKONER
for
Treatment in Pediatrics
Sumitha Nayak
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MD(Ped) DNB(Ped) PGDMLS PGDGC
(Consultant Pediatrician)
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The Children’s Clinic
Bengaluru (Karnataka), India
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Foreword
Padmaja Aradhya MD
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®
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

New Delhi • Panama City • London
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®
Jaypee Brothers Medical Publishers (P) Ltd.

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All rights reserved. No part of this book may be reproduced in any form or by any means
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This book has been published in good faith that the contents provided by the author contained
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Ready Reckoner For Treatment in Pediatrics

First Edition: 2012
ISBN : 978-93-5025-804-0
Printed at Ajanta Press
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To
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All my little patients, who have helped me
through the years, to hone my skills as a pediatrician
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To all my teachers, who taught me the intricacies of pediatrics
To my close friends and colleagues
who have inspired me to achieve my goals
Above all, to my family, that stood behind me at all times, in all my
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endeavors, and constantly encouraged me to reach for the stars
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Foreword
“If you hear hoofbeats, look for horses, not zebras.” Common medical
conditions are what we need to look for rather than looking for unusual
conditions. This is what we were taught, when we were in medical
school. When we walk into a crowded hospital emergency room and
we are encountering patients, we need to be quick, thorough and
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accurate, so that treatment is delivered immediately and relief is
provided to the suffering patient. This book is about common conditions
in children. It is also about opening a chapter and getting to know the
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signs and symptoms as well as differential diagnosis with a quick
treatment guide. This will also enable a physician to be vigilant about
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mimickers. Being a neurologist, status epilepticus has been my bane of
life. A young child seizing in the casualty is something a physician gets
to see quite often. It is very distressing for the parent to watch this.
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Getting this under control is very gratifying not only to the physician
but also to the parents. Juvenile rheumatoid arthritis is another
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condition, which used to have a very catastrophic outcome as there
was really not much treatment available for this condition. With the
tumor necrosis factor blockers and various immunosuppressant
therapies, which are now available, treating this condition is very
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gratifying. However, to know is one thing and to treat is another. This
book will be of great help to physicians all over the world to treat
common conditions. On a personal note, Dr Sumitha Nayak has been a
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childhood friend of mine. Her thoroughness and her obvious brilliance
are not unknown to me. I know of no better person, who is suited to be
a pediatrician than Dr Nayak. This book is something you can slip into
your white coat and it will be a very helpful guide to your day-to-day
routine with patients.
Padmaja Aradhya MD
Diplomate American Board of Psychiatry and Neurology (Neurology)
Diplomate American Board of Electrodiagnostic Medicine
Diplomate American Board of Psychiatry and Neurology
(Neuromuscular Medicine)
Diplomate American Board of Psychiatry and Neurology (Vascular Neurology)
Island Neuro Care
4230 Hempstead Turnpike, Suite106 Bethpage, New York 11714, USA
Phone (516) 520-5507, Fax (516) 520-5493
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Preface
The Ready Reckoner for the Treatment in Pediatrics is written with the idea
of providing a concise handbook for a practitioner who, when
confronted with a patient whose diagnosis has been made, will have at
his fingertips all that he needs to know to manage his patient. At the
galloping rate of science today, it may not be possible for a busy
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practitioner to keep himself abreast with all the new developments
taking place around him. At the same time, due to increase in the
medico-legal problems faced by practitioners, one can never be in
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position of compromise.
This book has attempted to provide easy-to-follow guidelines,
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including a brief overview of the etiology and pathogenesis, and
protocols for management, including the current investigations available
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for each condition, and the latest treatment modalities to be followed. I
have extensively researched the materials available, including online
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sites to get the latest updates for each chapter, at the time of publication.
Easy-to-follow diagrams, flowcharts and pictures make it convenient
for the practitioner to follow his case. I have also included requirements
related to immunization, patient education and follow-up requirements
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that the practitioner needs to address, as related to each disease
condition. The chapters are listed in alphabetical order for easy
reference.
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I recommend a quick look at the chapters of this book, while treating
patients in a busy OPD.
Sumitha Nayak
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Acknowledgments
I express my gratitude to Prakash, my dear husband, who has always

stood by me through all my trials in life and has always encouraged me
to follow my dreams.
My sincere thanks to Nikhil and Nishant, my dearest and loving
sons, who have always been my best critics and who have taught me
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the nitty-gritty of computers and technology.
I am greatly indebted to my darling mom, who has been a source of
inspiration and support to us, her children, at all times.
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And above all, I am extremely grateful to my beloved dad, who taught
me to stand on my own feet and to follow the path of righteousness
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always.
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Contents
1. Asthma in Children .......................................................................... 1

Asthma 1
Definition 1
Etiology 2
Risk Factors 2
Symptoms 3
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Signs 3
Investigations 4
Classification of Asthma 4
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Management of Asthma 6
Types of Inhalation Devices Available 6
Reliever Medications 7
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Controller Medications 8
Leukotriene Inhibitors 9
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Suggested Treatment Protocol 10
Status Asthmaticus 11
Treatment 11
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2. Atopic Dermatitis in Children ..................................................... 14
Predisposing Factors 14
Types of Atopic Dermatitis 15
Symptoms 15
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Signs 15
Investigations 16
Treatment 16
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Complications 18
Prognosis 18
Prevention 18
3. Anaphylaxis in Children ............................................................... 21

Causes of Anaphylaxis 21
Symptoms 22
Signs 23
Treatment 24
Patient Education 25
4. Bronchiolitis .................................................................................... 26
Etiology 27
Pathology 28
Treatment 29
Prognosis 30
Prevention 30
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xiv Ready Reckoner for Treatment in Pediatrics
5. Bronchomalacia and Tracheomalacia ......................................... 32

Causes 32
Symptoms 33
Signs 33
Investigations 33
Treatment 33
Prognosis 34
6. Croup (Laryngotracheobronchitis) .............................................. 36

Causes 36
Incidence 37
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Symptoms 37
Signs 38
Investigations 38
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Treatment 38
Complications 40
Prognosis 40
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7. Infections .......................................................................................... 41
Typhoid in Children 41
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Mode of Transmission of Infection 42
Pathogenesis 42
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Investigations 43
Complications 44
Carrier State 46
Treatment 46
Role of Steroids in Typhoid Fever 47
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Diet in Typhoid Fever 47
Prognosis 47
Prevention 47
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Tuberculosis in Children 48
Methods of Transmission of Infection 49
Factors Aiding Spread of Infection 49
Time Interval between Infection and Clinically
Apparent Disease 49
Pathogenesis 50
Clinical Features 51
Investigations 56
Treatment 59
Viral Hepatitis in Children 63
Hepatitis A 64
Route of Transmission 64
Pathology 64
Investigations 65
Treatment 66
Complications 66
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Contents xv
Prevention 66
Prognosis 67
Hepatitis B 67
Pathogenesis 68
Investigations 70
Treatment 70
Complications 71
Prevention 71
Hepatitis C 73
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Pathogenesis 73
Investigations 73
Treatment 74
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Complications 74
Hepatitis D 74
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Pathogenesis 75
Investigations 75
Treatment 75
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Complications 75
Hepatitis E 76
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Pathogenesis 76
Investigations 76
Treatment 76
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Prevention 76
Dengue Fever 77
Etiology 77
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Investigations 80
Treatment 81
Complications 82
Prognosis 82
Prevention 82
8. Gastroenteritis ................................................................................. 86
Diarrhea 86
Definition 86
Common Causes of Diarrhea 86
Pathophysiology of Rotavirus Diarrhea 86
Symptoms of Rotavirus Diarrhea 87
Signs of Rotavirus Diarrhea 87
Assessment of Dehydration 88
Danger Signs 89
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xvi Ready Reckoner for Treatment in Pediatrics
Algorithm to follow While Treating a

Child with Diarrhea 90
Investigations 90
Treatment 91
Types of Dehydration based on Electrolyte Imbalance 94
Feeding in Gastroenteritis 96
Drugs in Gastroenteritis 96
Prognosis 97
9. Juvenile Rheumatoid Arthritis ..................................................... 99

Types of Juvenile Rheumatoid Arthritis 99
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Criteria for Diagnosis of Juvenile Rheumatoid Arthritis 99
Causes of Juvenile Rheumatoid Arthritis 100
Pathogenesis 100
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Symptoms of Juvenile Rheumatoid Arthritis 101
Signs of Juvenile Rheumatoid Arthritis 101
Investigations 103
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Treatment 105
Physiotherapy 105
Vaccinations in JRA 106
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Complications 106
Prognosis 107
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10. Reactive Arthritis .......................................................................... 109
Causes of Reactive Arthritis 109
Symptoms of Reactive Arthritis 110
Signs of Reactive Arthritis 110
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Investigations 111
Treatment 111
Prognosis 112
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11. Kawasaki Disease ......................................................................... 113
Causes of Kawasaki Disease 113
Pathogenesis 113
Symptoms and Signs of Kawasaki Disease 114
Diagnostic Criteria 116
Investigations 116
Treatment 117
Complications 117
Treatment of Complications 118
Vaccinations in Kawasaki Disease 118
Prognosis 118
Poor Prognostic Indicators 118
12. Otitis Media in Children ............................................................. 121

Etiology 122
Types of Otitis Media 122
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Contents xvii
Pathogenesis 123
Symptoms 123
Signs 124
Tympanometry 124
Treatment 125
Prevention 126
Prognosis 126
13. Pneumonia in Children ............................................................... 128

Causes 128
Clinical Features 129
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Signs 130
Investigations 132
Treatment 132
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Indications for Admission to Hospital 132
Response to Treatment 134
Non-response to Treatment 134
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Complications 134
Prevention 134
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Prognosis 134
14. Rheumatic Fever ........................................................................... 137
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Etiology 137
Symptoms 138
Major Criteria 138
Minor Criteria 138
Laboratory Evidence 139
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Supportive Evidence 139
Carditis 139
Arthritis 140
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Chorea 140
Erythema Marginatum 140
Subcutaneous Nodules 141
Minor Criteria and Laboratory
Criteria help to make a Diagnosis of Rheumatic Fever 141
Investigations 142
Treatment 144
Prevention 145
Prognosis 146
15. Status Epilepticus ......................................................................... 149

Definition 149
Causes 149
Classification of Seizures 150
Convulsive Status 150
Non–convulsive Status 150
Investigations 150
Management of Status Epilepticus 152
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xviii Ready Reckoner for Treatment in Pediatrics
16. Urinary Tract Infection in Children .......................................... 156

Symptoms 156
Signs 157
Investigations 157
Treatment 158
17. Vulvovaginits in Children .......................................................... 160

Etiology 160
Symptoms of Vulvovaginitis 161
Signs of Vulvovaginitis 162
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Investigations 162
Treatment 163
Prevention of Recurrence 163
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Prognosis 164
Index ......................................................................................................... 165
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Asthma in Children 1
Asthma in
1 Children
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ASTHMA
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Definition
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Asthma is a chronic inflammatory condition of the lung airways resulting
in episodic airflow obstruction. This chronic inflammation results in airway
hyper-responsiveness (AHR) to allergens or other inhaled substances. In
case of recurrent and long-standing episodes, there is resultant airway
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remodeling, which could result in compromised airways.
By using the predictive test for asthma, it may be possible to predict
the occurrence of asthma in a child with wheezing. The criteria can be
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divided into major and minor.
Major Criteria
1. History of asthma in parents
2. Eczema associated with wheezing
3. Inhaled allergen sensitivity.
Minor Criteria
1. Allergic rhinitis, especially recurrent
2. Wheezing other than with cold symptoms
3. Food allergen sensitivity
4. Increased eosinophils in blood (>/=4%).
The occurrence of one major criteria or two minor criteria provides
a 77 percent chance of the persistence of wheezing into adulthood.
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2 Ready Reckoner for Treatment in Pediatrics
Etiology
Genetic predisposition: Familial disposition to hyper-reactive airways
Environmental factors: Asthma can be triggered by some environmental
allergens like pollen, nuts, foods, chocolate
• Recurrent respiratory infection
• Smoke inhalation
• Environmental tobacco smoke.
All these factors (Fig. 1.1) trigger airway hyper-reactivity, which
eventually results in airway remodeling. This is a single important factor
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in the progress to asthma in adulthood.
Risk Factors
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Risk factors in childhood which could be predictive of asthma; are the
following:
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1. Recurrent wheezing episodes
2. Allergic rhinitis
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3. Allergic dermatitis
4. Allergy
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5. Food sensitization
6. Inhaled allergen sensitization
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Fig. 1.1: Etiopathogenesis of bronchial asthma with treatment modalities
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7. Familial history of asthma in parents

8. Recurrent lower respiratory infection
9. Bronchiolitis
10. Environmental tobacco smoke inhalation (Fig. 1.2).
Symptoms
• Recurrent cough with expectoration of mucoid sputum
• Preceded by cold, runny nose or non-specific viral infection
• Difficulty in breathing not relieved by usual cough medications
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• Recurrent cough
• Cough increases during the late night and early morning
• Cough increases on exposure to aeroallergens
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• Cough increases with exercise
• Chest pain—non-focal
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• Skin rash and itching associated with cough
• Flexural eczematous skin patches, more on elbows and knees.
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Signs
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• Dyspnea
• Respiratory distress
• Expiratory wheeze on auscultation
• Eczematous skin lesions
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• Reduced breath sounds may indicate airway obstruction
• SPO2 may be reduced on auscultation.
In case of absent breath sounds, it indicates severe airway
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obstruction and needs urgent treatment.
Fig. 1.2: Narrowed bronchial lumen due to edema, as seen in bronchial asthma
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Investigations
No definitive investigation is available. However, when a strong
background history of allergy is present, the following tests may aid in
the diagnosis:
1. *CBC, ESR, Absolute eosinophil count (AEC)
2. Sputum test for eosinophils
3. Chest X-ray—to rule out any superadded/underlying infections. In
asthma, the X-ray shows increased airway markings.
4. Therapeutic test—response to inhaled short-acting beta-agonists
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(SABA)—instant improvement is seen in case of hyper-reactive
airway disease.
5. Pulmonary function tests aid in the diagnosis, by showing the extent
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of airway obstruction and residual airway function. Spirometry is
essential to outline the patient’s lung function. At times of distress,
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the peak flow meter reading gives an indication of the airway
obstruction.
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6. Lung function tests
7. Spirometry tests—shows airflow obstruction
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Low FEV1
FEV1/FVC less than 0.8.
After broncodilator (SABA) inhalation, improvement is noted.
FEV1 greater than or equal to 12 percent
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Exercise challenge shows worsened functions:
FEV1 shows lowered levels , over 15 percent of pretest level
Diurnal variation in FEV1noted.
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*CBC-complete blood count
ESR-Erythrocyte sedimentation rate
FVC-Forced vital capacity
FEV-Forced expectorant volume
Classification of Asthma
Depending on the degree of control of the asthma, it can be divided
into four:
1. Well controlled
2. Partly controlled
3. Uncontrolled
4. Exacerbation
Well-controlled Asthma
• No day/night time symptoms.
• No exacerbations
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Fig. 1.3: Inflammation in asthma
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• No need for reliever medication
• Normal lung functions—peak expiratory flow (PEF) and FEV1.
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Partly Controlled Asthma
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• Symptoms more than two times/week
• Limitation of activities present
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• Nocturnal symptoms present
• Need for reliever medications, more than two times/week
• Impaired lung functions as measured by FEV1 of best less than 80
percent
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• Exacerbations one or more per year.
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Uncontrolled Asthma
• Over three features of the above mentioned, in any one week
• Impaired lung function measured by less than 60 to 80 percent of
personal best
• Exacerbations—one in any one week.
Exacerbation
• Continuous symptoms, requiring frequent reliever medications
• May need hospitalization and oxygen therapy
• Lung functions poor.
As can be observed from Figure 1.3, inflammation in the airways
play a major role in the pathogenesis of asthma. Hence an anti-
inflammatory drug is essential in the management. However, for quick
relief, most children need a short-acting bronchodilator (SABD).
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BOX 1.1: Asthma Management

• Regular assessment and monitoring
• Control of factors contributng to severity
• Asthma pharmacotheraphy
• Patient education
Management of Asthma
Management of asthma, includes all the four aspects, as mentioned in
Box 1.1.
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1. The child needs to be assessed regularly, at least every 3 to 4 weeks,
to check for control of symptoms, compliance with medication,
avoidance of allergens, etc.
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2. Control of aggravating factors include avoidance of allergens and
precipitating factors and prevention of viral infections.
3. Asthma pharmacotherapy is extremely important to keep the
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symptoms under control.
4. Patient education must be an ongoing process to educate and
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sensitise the parents to the child’s condition, what they must do in
an exacerbation and how they can help to prevent exacerbations.
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5. The treatment modalities can be broadly divided into:
a. Reliever medication
b. Controller medication.
Inhaler therapy is the mainstay of treatment in case of childhood
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asthma.
Types of Inhalation Devices Available
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Nebulizer
Nebulizer is power driven, hence it does not require patient effort to
take the medication. Useful when child is severely dyspneic, and also
in infants and young children who are unable to coordinate the
respiratory effort.
MDI (metered-dose inhaler)

MDI (metered-dose inhaler) with or without spacer has the same effect
and rapidity of action as the nebulizer. However, patient effort is
required, hence may not be useful when child is severely dyspneic
usually recommended for those above the age of 6 years, as patient
compliance without the spacer can be assured.
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Dry Powder Inhaler

Dry powder inhaler (DPI) is recommended for children above 3 to 4
years, as they can be trained to blow as in blowing candles or a whistle.
Inhalation devices are available as rotahaler, diskhaler, turbuhaler. Type
of device selected depends on the child’s acceptance and age.
Optimal inhalation technique for each puff of MDI-delivered medication
is a slow (5 sec) inhalation, then a 5 to 10 sec breath hold. No waiting
time between puffs of medication is needed. Young pre-school-age
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children cannot perform this inhalation technique; MDI medications
can then be delivered with a spacer and mask, using a different
technique: Each puff administered with regular breathing for about 30
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sec or 5 to 10 breaths, a tight seal must be maintained, and talking,
coughing, or crying will blow the medication out of the spacer. This
technique will not deliver as much medication per puff when compared
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with the optimal MDI technique used by older children and adults.
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Reliever Medications
The reliver medications are short-acting and gives immediate relief of
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symptoms (Box 1.2).
Recommended use
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1. During exacerbations of asthma
2. In case of persistent cough
3. To give rapid relief of symptoms
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BOX 1.2: Reliever Medications
• Rapid-acting inhaled 2-agonists
• Systemic glucocorticosteroids
• Anticholinergics
• Methylxanthines
• Short-acting oral 2-agonists
Rapid-acting beta-2-agonists
Salbutamol/Albuterol—Dose: 0.15 mg/kg/dose.
In case of use in the nebulizer, it should be diluted with normal
saline to give a total volume of 3 ml.
Can be repeated every 20 minutes for maximum of three doses in
case of severe bronchospasm.
SPO2 to be maintained above 92 percent.
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Oxygen inhalaton may be needed to avoid ventilation: perfusion

mismatch.
Anticholinergics
Ipratropium bromide may be added to the salbutamol. It provides both
mucolytic and bronchodilator functions. It must not be used without
salbutamol.
Dose: 0.5 mg/dose every 6 to 8 hourly as needed. Can be mixed in
the nebulizer with salbutamol and ICS.
Methylxanthines
Methylxanthines like theophylline have been used as reliever
medication. However, the therapeutic levels of the drug need to be
monitored, as the therapeutic window is very narrow. It is not
recommended for use as monotherapy in children for this reason. The
absorption of the drug varies with different preparations.
Oral Corticosteroids
These corticosteroids have an anti-inflammatory effect. Its use is
indicated in severe asthma or in exacerbations not responding to inhaled
medications.
Prednisolone dose: 0.5 to 1 mg/kg every 6 to 12 hourly for 48 hours,
then 1 to 2 mg/kg every 12 hourly till symptoms subside. Dosing
preferred at 8 am to reduce the effect of adrenal suppression.
Prednisolone is available as 5 mg tablets.
Oral beta-2-agonists
Not routinely recommended as the dose is difficult to adjust and the
risk of side effects is high due to the narrow therapeutic range.
Controller Medications
These are the mainstay of asthma control.
Inhaled Corticosteroids (ICS)

Inhaled corticosteroids are the most potent and effective medications
for the treatment of asthma in children.
Dose: depends and varies with the type of ICS.
Beclomethasone: 100 to 200 microgram every 6 to 8 hourly. Maximum
600 microgram per day.
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Budesonide: 200 to 400 microgram every 6 to 8 hourly. Maximum 800

microgram per day.
Fluticasone: 100 to 200 microgram per day every 8 to 12 hourly.
Long-acting Beta Agonists

Not to be used without ICS. It can be combined with ICS for inhalation
therapy.
Salmeterol MDI: 1 to 2 puffs every 12 to 24 hourly
Formoterol DPI: 1 capsule every 12 to 24 hourly
Salmeterol and Fluticasone combined MDI available. To be used 1
to 2 puffs every 12 hourly.
Daily ICS therapy is the treatment of choice for all patients with
persistent asthma. ICS therapy has been shown to improve lung function
and reduce AHR, ‘rescue’ medication use asthma symptoms and, most
importantly, reduce urgent care visits, hospitalizations, and prednisone
use for asthma exacerbations by about 50 percent. ICS therapy may
lower the risk of death due to asthma.
Leukotriene Inhibitors
Leukotrienes are known to aggravate bronchospasm, induce mucus
secretion and have inflammatory effects on the airways. Hence,
leukotriene inhibitors can reverse these effects and have been known
to help in asthma control in children.
Two-types of leukotriene inhibitors are currently available:
Zafirlukast and Montelukast
Zafirlukast and Montelukast of the two, montelukast has found

widespread acceptance and use in children. It is recommended to be
used as a first-line drug along with ICS in those children who have
mild to moderate symptoms. For those with severe disease, it needs to
be combined with LABA + ICS to give optimal benefits.
As the leukotrine receptor antagonists (LTRAs) have specific actions
on the leukotrienes produced in the system, the side effects of the drug
are practically non-existent.
LTRAs are useful in viral-induced as well as exercise-induced asthma
and also in intrinsic asthma.
Dose: 0–1 year : 4 mg sachets/4 mg tablets
1–6 year : 4 mg tablets
6–12 year : 5 mg tablets
> 12 year : 10 mg tablets
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All tablets are chewable, hence acceptance is easy. Alternatively, it

may be crushed or the sachets may be mixed with the foods that are
consumed by the child. Treatment duration of 3 to 6 months is
recommended.
Sometimes, the child who has recurrent attacks of wheezing, may
need the leukotriene inhibitor to be administered for slightly longer
duration of time. This has practical implications, as the frequency of
use of rescue medications are definitely reduced.
Some children may need repeated courses of administration of
leukotriene inhibitors. Hence, on a seasonal requirement, the drug may
be administered every year for durations of 3 to 6 months, to keep the
child symptom free.
Suggested Treatment Protocol

A suggested protocol for treatment of asthma is schematically shown
in Figure 1.4.
Follow-up
All asthma patients must be followed up regularly to ensure drug
compliance and to stabilize the treatment. As it is a chronic disease, the
child needs long-term treatment. As such, once the child becomes
symptom free, the dose of inhaled medication is reduced to the lowest
level which keeps the child comfortable and symptom free.
Step-down treatment: This implies that once control has been achieved,
the drug is gradually reduced to the lowest recommended dose that
can keep the child asymptomatic.
Step-up treatment: This indicates that in case a child who had been
maintained on the lowest recommended dose, develops a breakthrough
exacerbation, the dose of the inhaled medication needs to be increased
Fig. 1.4: Suggested treatment protocol
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to the level at which symptom control can be achieved. It is better to go

for an aggressive approach to obtain symptom control faster and then
step-down the therapy.
Avoidance of Triggers
• Regular follow-up and counseling is needed to avoid contact with
triggers—environmental smoke, tobacco smoke, pollens, dust, etc.
• Regular follow-up is essential to check drug compliance and
appropriate use of MDI.
• Regular follow-up is needed to maintain adequate drug dosage and
maintain the child symptom free.
• Recommend vaccination with seasonal influenza vaccine. This is
particularly helpful in viral-induced asthma, by reducing the number
of viral infections.
Prognosis
Thirty to thirty-five percent of children suffer from recurrent cough
and wheezing in childhood. Of these, one-third go on to become
persistent wheezers in adulthood, while two-third recover.
The extent and severity of wheezing and the lung functions are a
guide to predict if the child will go on to become a wheezer in adulthood.
Spontaneous improvement is known to occur at the age of 5 to 6 years
and again by 12 to 13 years of age.
STATUS ASTHMATICUS
Status asthmaticus is defined as an exacerbation of asthma, not
responding to regular antiasthmatic medication. The patient needs to
be attended to immediately and the airway obstruction reversed at the
earliest.
Treatment
1. Monitor SPO2. If it is below 92 percent, administer O2.
In case of hypoxemia, oxygen inhalation is required and may be
given at levels of 5 to 6 litres/min. While ongoing SABA treatments,
it is essential to administer oxygen to avoid ventilation/perfusion
(V:Q) mismatch which may occur during recovery.
2. Short-acting beta-agonist (SABA) by nebulization. Repeated doses
(salbutamol/albuterol) may be given every 15 to 20 minutes, for a
maximum of three times, until the airway obstruction improves.
Then it may be recommended every 4 to 6 hourly. Dose 0.15 mg/kg.
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3. Ipratropium may be added to the SABA. This helps in relieving the

bronchoconstriction. It reduces mucus secretion and undergo
synergistic interactions with the SABA.
4. ICS to be administered. In severe cases, budesonide is recommended.
Dose—200 microgram per kg to be given every 4 to 6 hourly,
depending on the severity.
5. In case of suspected underlying lung pathology, IV antibiotic is
recommended, preferably a broad-spectrum drug.
6. IV corticosteroid as a short course is recommended to hasten
recovery and to reduce the airway inflammation. Hydrocortisone
IV is fast acting. Once the child is better, it may be changed to oral
steroid for three days.
7. IV maintenance fluids to be given as the child would be dyspneic
and unable to eat/drink sufficiently.
Once a patient has developed status asthmaticus, the patient needs
to be closely monitored with regard to compliance with drugs. The child
needs careful titration of the administered drugs to ensure that the
symptoms are adequately controlled and no breakthrough symptoms
develop.
Patient counseling needs to be done on a regular basis and a written
protocol must be given for action to be taken during worsening of
symptoms.
FURTHER READINGS
1. Bacherior LB, Boner A, Corlsen KH, et al. Diagnosis and treatment of asthma
in childhood: a PRACTALL consensus report. European Pediatric Asthma
Group. Department of Pediatrics, Washington University, St Louis, MO, USA.
Allergy. 2008;63(1):5-34.
2. Becker A, Gie RP, Chan-yeeing M. Management of childhood asthma. Int J
Tuberc Lung Dis. 2006;10(6):592-99.
3. Berger WE. New approaches to managing asthma: a US perspective. Ther
Clin Risk Manag. 2008;4(2):363-79.
4. Bousquet J, Demoly P, Godard P. Recommendations for the management of
asthma: Rev Prat. 2001 15;51(5):533-7. [Article in French]. Service des maladies
respiratoires, CHU Monptellier, INSERM U454, Hôpital Arnaud-de-
Villeneuve 34 295 Montpellier.
5. Centers for Disease Control and Prevention. National Center for Health
Statistics. Asthma Prevalence, Health Care Use and Mortality: United States,
2003-05. January 2007.
6. Centers for Disease Control and Prevention. National Center for Health
Statistics, National Health Interview Survey, 2005. Analysis by the American
Lung Association, Research and Program Services Division using SPSS and
SUDAAN.
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7. Expert Panel Report 3 (EPR-3): Guidelines for the diagnosis and management
of asthma-summary report 2007. J Allergy Clin Immunol. 2007;120
(5 Suppl):S94-138.
8. Fuhlbrigge AL, Guilbert T, Spahn J, et al. The influence of variation in type
and pattern of symptoms on assessment in pediatric asthma. Pediatrics.
2006;118:619-25.
9. Galant SP, Morphew T, Amaro S, et al. Current asthma guidelines may not
identify young children who have experienced significant morbidity.
Pediatrics. 2006;117:1038-45.
10. Janson S. National Asthma Education and Prevention Program, Expert Panel
Report. II: Overview and application to primary care. School of Nursing,
University of California, San Francisco, USA. Lippincotts Prim Care Pract.
1998;2(6):578-88.
11. Morgan WJ, Stern DA, Sherrill DL, et al. Outcome of asthma and wheezing in
the first 6 years of life: follow-up through adolescence. Am J Respir Crit Care
Med. 2005;172:1253-58.
12. National Asthma Education and Prevention Program. Expert panel report:
Guidelines for the diagnosis and management of asthma. Update on selected
topics-2002. J Allergy Clin Immunol. 2002;110(5 Suppl):S141-S219.
13. Ng D, Salvio F, Hicks G. Anti-leukotriene agents compared to inhaled
corticosteroids in the management of recurrent and/or chronic asthma in adults
and children. Cochrane Database Syst Rev. 2004;(2):CD002314.
14. Rachelefsky G, Fitzgerald S, Page D, et al. An update on the diagnosis and
management of pediatric asthma. Based on the National Heart, Lung and
Blood Institute expert panel report. Nurse Pract. 1993;18(2):51-2, 55, 59-62.
15. Robert M Kleigman, Richard E Behrman, Hal B Jenson, et al. Nelson Textbook
of Pediatrics. 18th edition. Elsevier- Health sciences division. 2007.
16. Sheffer AL, Taggart VS. The National Asthma Education Program. Expert
panel report guidelines for the diagnosis and management of asthma. National
Heart, Lung, and Blood Institute. Med Care. 1993 Mar;31(3 Suppl):MS20-8.
17. Thomas M. Breaking new ground: challenging existing asthma guidelines.
Department of General Practice and Primary Care, University of Aberdeen,
Foresterhill Health Centre, Westburn Road, Aberdeen AB25 2AY, UK. BMC
Pulm Med. 2006 30;6 Suppl 1:S.
18. Warman KL, Silver EJ, Stein RE. Asthma symptoms, morbidity, and anti-
inflammatory use in inner-city children. Department of Pediatrics, Albert
Einstein College ege of Medicine, Bronx, New York 1046, USA. Pediatrics.
2001;108(2):277-82.
19. Watts B. Outpatient management of asthma in children age 5-11 years:
guidelines for practice. Tri-County Internal Medicine, 807 Jackson Trace Road,
Wetumpka, AL 36092, USA. J Am Acad Nurse Pract. 2009;21(5):261-9.
20. William T Basco AAP 2006: New Research in asthma, eczema, and urticaria.
21. Williams PV. Rhinitis, sinusitis, and asthma. Program and abstracts of the
American Academy of Pediatrics 2006 National Conference and Exhibition;
October 7-10, 2006; Atlanta, Georgia. Session H142.
22. Williams SG, Schmidt DK, Redd SC. Key clinical activities for quality asthma
care. Recommendations of the National Asthma Education and Prevention
Program. MMWR Recomm Rep. 2003 28;52(RR-6):1-8.
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Atopic Dermatitis
2 in Children
ATOPIC DERMATITIS
Atopic Dermatitis is a manifestation of allergy in the skin. It is a chronic
and relapsing skin condition and commonly manifests in infancy.
Incidence varies between 10 to 20 percent and no sex predominance
is seen. Approximately 30 percent develop the disease between 6 to 12
months or after 1 year of age, when newer foods and solids are
introduced in the diet.
Atopic dermatitis (AD) is a complex genetic disorder with an
exaggerated T-cell response to allergens, which manifest as a defective
skin barrier. It is associated with T-cell infiltration, mast cells in different
stages of degranulation and increased IgE levels. In chronic stages,
lichenification of the skin occurs, associated with spongiosis,
hyperkeratosis, and hypertrophied epidermis.
Predisposing Factors
1. Family history of allergic rhinitis
2. Family history of asthma
3. Family history of skin allergy
4. Formula feeds
5. Recurrent skin irritation
6. Excessive skin dryness
7. Use of skin irritants like soaps, moisturizers, perfumes, etc.
8. Excessive use of air-conditioning system
9. Early introduction of allergenic weaning foods
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Atopic Dermatitis in Children 15
10. Excessive sweating

11. Family history of gastrointestinal allergy.
Types of Atopic Dermatitis
Atopic Eczema
Atopic eczema is associated with IgE-mediated skin sensitization. Here,
the memory T-cells produce increased levels of Th2-type cytokines,
with exaggerated interleukin response, especially IL4 and IL13 cells.
Eosinophilia is seen as the levels of IL5 are also increased.
Non-Atopic Eczema
In this type, there is no associated IgE response seen. Levels of IL4 and
IL13 are low.
Symptoms
• Intense skin itching
• Periorbital itching and rubbing the eyes
• Pruritus increased at night and during sleep
• Symptoms occur due to the excessive itching includes skin
excoriation, ulcers, oozing skin, etc.
• Symptoms appears initially and are pronounced in the skin folds,
flexures of the arms and legs (Fig. 2.1), groin, behind the ears,
periorbital areas
• Due to chronic pruritus, skin thickening may be noticed.
Signs
• Evidence of itching in the form of scratch marks
• Dry exfoliating skin
• Thickened skin folds
Fig. 2.1: Thickened and ichthyotic skin over flexural (ventral aspect) area of the knee joint
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Fig. 2.2: Flaky skin with erythematous papules on the cheek
• Erythematous papules with flaky skin

• In chronic cases, with severe atopy, the skin is extremely thickened
and pigmented, with no dermal lines visible
• Bacterial superimposition results in secondary skin infection, with
purulent, foul-smelling exudates
• Due to recurrent rubbing of the skin around the eyes, lines may be
observed in the infraorbital area—these are known as Dennie-
Morgan lines
• Occasionally, there may be associated subcapsular cataract and
keratoconus.
Investigations
1. Complete blood count—reveals increased eosinophil count. May
help to detect bacterial contamination of the eczema.
2. Absolute eosinophil count—may show increased levels—above the
normal range of 40–440 cells/cumm
3. Serum IgE levels increased in atopic eczema
4. Allergy test: Blood levels of the various antigen may reveal what
the child is sensitive to. Recommended to do the food panel as well
as the dust panel . Hence, avoidance of the allergen can help alleviate
symptoms.
Treatment
1. Avoidance of allergen
2. Skin care—completely avoid soap, other skin moistening products
and creams, especially perfumed products.
3. Adequate hydration—drink plenty of water, avoid excessive
exposure to air-conditioning.
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4. Avoid excessive heat and sweating

5. Skin hydration—use emollient cream, non-perfumed and gentle,
containing aloe vera, paraffin, etc. preferably with a thick base that
can keep the skin moist for longer periods. Use this moisturizer at
least twice daily.
6. Use soap-free cleansers for the skin if required. Preferably avoid
use on the face.
7. For active skin lesions, mild potency steroid is the drug of choice.
Use mometasone once daily, which is safe even in neonates, or,
hydrocortisone skin cream 0.1 to 0.2 percent. Duration—until the
skin lesions heal and pruritus is decreased.
8. Oral antipruritic—in case of severe itching—chlorpheniramine
maleate (0.2–0.3 mg/kg/day in 3 divided doses) or cetirizine (5 mg
once daily) is useful to control the symptoms. Also in case of
exaggerated nocturnal itching, the sedative action may be useful
to calm the child.
9. Oral montelucast is known to reduce the symptoms of allergy and
pruritus, as it is a leukotriene blocking agent. May be given as
early as 2 months of age. Dose—2 months to 5 years, 4 mg once
daily; 5 to 12 years, 5 mg once daily; 12 to 18 years, 10 mg once
daily. Duration of treatment is from 3 to 6 months. Minimum
duration of 3 months is required to see a clinical response. Helps
to reduce associated symptoms of allergic rhinitis and asthma also.
10. Oral corticosteroids—in severe cases, a short course of prednisone
orally may give dramatic results. However, there is always the
potential for rebound increase in the lesions after stopping
treatment.
11. Topical non-steroidal calcineurin inhibitors—pimecrolimus 1
percent cream (Elidel) is useful in mild to moderate cases.
Tacrolimus 0.1 to 0.3 percent (protopic) is indicated in moderate to
severe AD. Indicated for use above two years age, may be used for
long term.
Indications for use of calcineurin inhibitors: in cases not responding
to steroids, steroid phobia, in face and neck involvement where
patient is hesitant to use steroids.
12. Antibiotics—in case of superadded bacterial infection—most
common organism is Staphylococcus aureus. In mild cases, topical
mupirocin is adequate to control the infection. In more severe cases,
use of systemic antibiotic is indicated—amoxicillin, azithromycin,
or erythromycin. In case of sensitivity, cephalosporins may be used.
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13. Superimposed fungal or viral infection may occur and needs to be

adequately treated to reduce the AD symptoms.
Complications
1. Secondary bacterial infection
2. Secondary fungal infection
3. Secondary viral infection
4. Pyoderma
5. Corneal scarring and visual impairment—from recurrent/chronic
eyelid dermatitis
6. Keratoconus—from recurrent rubbing of the eyes—cornea takes on
a conical shape
7. Anterior cataract—may be due to recurrent use of systemic steroids
or steroid eyedrops.
Prognosis
• Atopic dermatitis tends to follow a chronic recurrent course
• Spontaneous resolution may occur around the age of 5 years
• Resolution may occur as the child grows older—may outgrow it by
adolescence
• Relapse may occur in adulthood.
Predictive Factors for Severe and Chronic Disease

1. Early onset of AD
2. Family history of AD
3. Extensive AD in childhood
4. Associated history of asthma and allergic rhinitis
5. Family history of asthma and allergic rhinitis
6. High levels of IgE.
Prevention
1. Breastfeeding
2. Hypoallergenic formula feeds
3. Identify and eliminate allergens
4. Regular use of skin emollients and avoidance of harsh skin-debriding
agents (Fig. 2.3).
5. Avoid skin dryness and exposure to excess heat.
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Fig. 2.3: Preventive methods to be adopted in children with atopic dermatitis
FURTHER READINGS
1. Akdis CA, Akdis M, Bieber T, et al. Diagnosis and treatment of atopic
dermatitis in children and adults: European Academy of Allergology and
Clinical Immunology/American Academy of Allergy, Asthma and
Immunology/PRACTALL Consensus Report. J Allergy Clin Immunol.
2006;118:152-69.
2. Amy E Gilliam, Ilona J Frieden. Treatment of atopic dermatitis: Optimizing
management and implications of the new labeling for topical calcineurin
inhibitors. Medscape. 2006.
3. Boguniewicz M, Fiedler VC, Raimer S, et al. for the Pediatric Tacrolimus Study
Group. A randomized, vehicle-controlled trial of tacrolimus ointment for
treatment of atopic dermatitis in children. J Allergy Clin Immunol.
1998;102:637-44.
4. Fonacier L, Spergel J, Charlesworth EN, et al. Report of the topical calcineurin
inhibitor task force of the American College of Allergy, Asthma and
Immunology and the American Academy of Allergy, Asthma and
Immunology. J Allergy Clin Immunol. 2005;115:1249-53.
5. Irani A. Atopic dermatitis, urticaria, and angioedema. Program and abstracts
of the American Academy of Pediatrics 2006 National Conference and
Exhibition; October 7-10, 2006.
6. James E Gern. Update on atopic dermatitis: Medscape. 2000.
7. Kramer MS, Kakuma R. Maternal dietary antigen avoidance during pregnancy
or lactation, or both, for preventing or treating atopic disease in the child.
Cochrane Database of Systematic Reviews 2006, Issue 3. Art. No.: CD000133.
DOI: 10.1002/14651858.CD000133.pub2.
8. Kreth HW, Hoeger PH. Safety, reactogenicity, and immunogenicity of live
attenuated varicella vaccine in children between 1 and 9 years of age with
atopic dermatitis. Eur J Pediatr. 2006; 165:677-83.
9. Laurie Barclay. Therapeutic options for pediatric atopic dermatitis reviewed:
Medscape. 2008.
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10. Paul C, Cork M, Rossi AB, et al. Safety and tolerability of 1% pimecrolimus
cream among infants: experience with 1133 patients treated for up to 2 years.
Pediatrics. 2006;117:e118-e128.
of Pediatrics. 18th edition. Elsevier-Health sciences division. 2007.
12. Ruzicka T, Bieber T, Schopf E, et al, for the European Tacrolimus Multicenter
Atopic Dermatitis Study Group. A short-term trial of tacrolimus ointment for
atopic dermatitis. N Engl J Med. 1997;337:816-21.
13. Schneider LC. Atopic dermatitis. Program and abstracts of the 56th annual
meeting of the American Academy of Allergy, Asthma and Immunology;
March 3-8, 2000.
14. William T Basco. AAP 2006: New Research in asthma, eczema, and urticaria.
2006.
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Anaphylaxis in Children 21
Anaphylaxis
3 in Children
ANAPHYLAXIS
Anaphylaxis is an acute severe allergic reaction that requires immediate
and aggressive therapy to avoid any fatality. It is a potentially life
threatening condition and needs to be managed on an urgent emergency
basis.
Anaphylaxis occurs due to the sudden release of potent biological
mediators from the mast cells and basophils giving rise to skin, GIT,
respiratory and cardiovascular symptoms.
Causes of Anaphylaxis
Common causes of anaphylaxis in children are foods, medicines, latex,
insect stings, vaccination, inhaled allergens and other miscellaneous
factors.
Foods
Nuts—peanuts, hazelnuts, walnuts, cashewnuts, pistachios, brazil nuts,

etc.
Sea foods—shrimps, crabs, shellfish and other varieties of fish.
Milk—cheese, yogurt
Fruits—pineapple, peach, strawberry, apple, melon.
Chocolate
Coffee
Grains—wheat, ragi, rice, millet
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Medicines—antibiotics, anti-inflammatory, non-steroidal anti-

inflammatory drugs (NSAIDs), muscle relaxants, vitamin B12 insulin,
anesthetics
Latex
Insect Stings—Stings of insects like bees, wasps, ants, scorpion, hornet,
etc.
Vaccinations—vaccines for measles, tetanus, influenza, etc.
Miscellaneous—cold exposure, blood products, radiocontrast dyes.
Inhaled allergens—pollen, dust, animal furs, dander, strong perfumes,
smoke, tobacco smoke, etc.
Major routes of exposure to allergens is given in Table 3.1.
Symptoms
The symptoms may be immediate or delayed. It depends on the type of
allergen. In case of injected allergens like stings or vaccinations the
reactions are immediate.
Manifestation of Symptoms
Runny nose, nasal itching, urticaria (hives), perioral tingling, (Fig. 3.1)
sense of faintness, local edema, backache, severe myalgia, tightness of
Table 3.1: Routes of Exposure to Allergens

Routes Allergens
Oral Foods
Medicines
Nuts
Chocolate
Cheese
Milk
Inhaled Animal furs
Danders
Smoke
Perfumes
Food odors
Environmental tobacco smoke
Injected Vaccines
Antibiotics
Anti-inflammatory—drugs diclofenac
Blood
Contact Insect bites
Wasp stings
Plant latex
Latex gloves
Soaps and detergents
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Fig. 3.1: Symptoms indicating anaphylaxis
the throat, choking sensation, wheezing, difficulty in breathing, etc. are

the main symptoms. With ingested allergens, the interval may be
between several minutes to 2 hours after consumption. Abdominal pain,
nausea, vomiting, severe colic, and diarrhea are common with ingested
allergens.
Severe bronchospasm may develop suddenly and could be fatal.
Patient may collapse suddenly. Giant urticarial patches will be seen on
trunks and limbs (Fig. 3.2).
Signs
• Child appears suddenly pale, hypotensive, with low blood pressure
(BP) and, pulse is rapid
Fig. 3.2: Giant urticarial patches seen on trunk and limbs
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Fig. 3.3: Edema and swelling of lips and mucosa: erythema of the ear lobes
• Child may feel itching due to severe pruritus

• Wheezing and cough. Flushing may occur
• The diagnosis is apparent due to the dramatic nature of the events
• Can develop angioneurotic edema (Fig. 3.3).
Treatment
Anaphylaxis is a medical emergency and must be treated urgently.
1. Administer epinephrine—IM or Subcutaneous.
Dose 0.01 ml/kg of 1:1000 dilution. Maximum dose 0.3 ml.
Can repeat epinephrine every 15 minutes until the patient is stable.
2. Maintain airway. Use an oropharyngeal airway if necessary.
3. Administer 100 percent oxygen 4 to 6 L/min.
4. Secure the IV line. Administer normal saline fast, in case of low
BP—give a bolus of up to 30 ml/kg in half an hour.
5. Monitor blood pressure.
6. Maintain the patient in the supine position with the feet elevated.
7. Administer hydrocortisone 10 mg/kg . In case of shock or laryngeal
edema give 35 to 50 mg/kg.
8. Antihistamine diphenhydramine 1 mg/kg IM or chlorpheniramine
(CPM) 0.25 mg/kg IV/IM.
9. Nebulize with salbutamol/albuterol to relieve airway obstruction.
10. In case of persistent hypotension administer dopamine/
noradrenaline drip.
11. Administer ranitidine (25 mg/ml), dose 1 mg/kg slow IV maximum
50 mg.
Post Emergency Treatment

1. Administer cetirizine 5 to 10 mg or loratadine 5 to 10 mg daily for 3
days orally—antihistamine H1 receptor antagonist.
2. Prednisone 1 mg/kg—maximum 75 mg for 3 days, orally.
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Fig. 3.4: Avoid allergens like pets
Patient Education
1. Instruct the patient on the most likely causative agent.
2. Avoid the allergen at all times especially foods, plants, pets, (Fig. 3.4)
etc.
3. Explain the early signs—pruritus, tingling, so that the patient may
recognize the symptoms and take immediate medical help.
FURTHER READINGS
1. Assessment of patients who have experienced anaphylaxis: A 3-year survey:
Hugh A. Sampson In Pediatrics. 1995;96:384.
2. Liberman DB, Teach SJ. Management of anaphylaxis in children: Pediatr Emerg
Care. 2008;24(12):861-66; quiz 867-69.
4. Russell S, Monroe K, Losek JD. Anaphylaxis management in the pediatric
emergency department: opportunities for improvement. Pediatr Emerg Care.
2010 Feb;26(2):71-76.
5. Sicherer SH, Simons FE. Self-injectable epinephrine for first-aid management
of anaphylaxis: Section on Allergy and Immunology, American Academy of
Pediatrics. Pediatrics. 2007;119(3):638-46.
6. Susan D Dibs, M Douglas Baker. Anaphylaxis in children: A 5-year experience.
Pediatrics. 1997; 99: e7.
7. Y Tse, G Rylance. Emergency management of anaphylaxis in children and
young people: new guidance from the Resuscitation Council (UK). Arch Dis
Child Educ Pract Ed 2009;94:97-101.
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Bronchiolitis
4
BRONCHIOLITIS
Bronchiolitis indicates inflammation of the airways involving the small
bronchioles and results in edema, swelling and airway obstruction.
It is common in the younger ages between 2 to 6 months up to 2
years. Maximum incidence is below 1 year age when the children need
hospitalization most often. This is due to the smaller airways (Fig. 4.1)
and immature immune system.
Fig. 4.1: Smallest airways affected in bronchiolitis
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Bronchiolitis 27
Etiology
Commonly Caused by Viruses

The most common organism is (respiratory syncytial virus) (RSV). Other
viruses include influenza, parainfluenza, adenovirus (Fig. 4.2), etc.
Human metapneumovirus (hMPV) may be superadded on RSV.
No bacterial causative agent found.
Common Causative Agents

Bronchiolitis is common in overcrowded homes, and usually for the
child who is not breastfed (Fig. 4.3). Often the infected adults are the
source of infection for the babies.
Fig. 4.2: Viruses causing bronchiolitis
Fig. 4.3: Predisposing factors in bronchiolitis
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Pathology
There is bronchial airway narrowing due to edema, mucus secretion
and epithelial desquamation caused by the viral infection. As the
resistance to airflow is inversely proportional to the fourth power of
the airway diameter, even a small obstruction to the infant’s airways
will cause wheezing and difficulty in breathing.
Symptoms
• Preceding history of runny nose and cold
• Mild fever
• Reduced appetite, irritabilty
• Sudden onset of wheezing and difficulty in breathing.
Signs
• Appears tachypneic
• Mild/subnormal body temperature
• Poor feeding
• Tachycardia
• Progressive increase in the work of breathing and increasing
respiratory rate
• Wheezing on auscultation with prolonged expiratory phase
• With more severe disease, cyanosis and grunting may appear
• Pulse oximetry may reveal reduced saturation
• Usually, the severity of respiratory distress does not go on par with
the respiratory signs. In this situation, a diagnosis of bronchiolitis is
recommended.
Investigations
1. Complete blood count to confirm viral origin—mild leukocytosis
may be seen between 12,000-16,000/cu mm.
2. Chest X-ray—hyperinflated, hyperlucent lung fields (Fig. 4.4) due
to air trapping beyond the obstruction. Patchy atelectasis may be
observed. Associated pneumonia may be visualized.
3. Viral culture and polymerase chain reaction (PCR) tests to detect
the causative virus.
4. Therapeutic trial of inhaled bronchodilator—improvement seen in
patient with brochiolitis and asthma as against children with
obstruction due to foreign bodies.
5. Chest computed tomography (CT) scan—to confirm the absence of
any associated structural abnormality. Helps in the diagnosis of
inhaled foreign bodies.
vip.persianss.ir
Bronchiolitis 29
Fig. 4.4: Showing hyperlucent lung fields
Treatment
1. Check the SPO2 using pulse oximetry. In case of reduced saturation,
administer cold humidified oxygen by mask or nasal prongs. Start
at 5 l/min to ensure adequate aeration of the terminal airways.
Minimum 2 l/min.
2. Nebulized bronchodilator—salbutamol/albuterol will help to relieve
the airway obstruction. Short duration of action.
3. Inhaled steroid—Budesonide may be useful but not clinically proven.
4. Frequent nasal and oral suction to remove secretions.
5. IV fluids for maintenance, as the child has poor feeding. Use one-
fifth dextrose normal saline (DNS) preferably. Maintenance dose to
be administered.
6. Paracetamol 10 to 15 mg/kg in case of fever.
7. No role of antibiotics.
8. In case of proven RSV infection, ribavirin, the specific antiviral agent,
may be used.
A scoring system can be used to asses the severity of the patient’s
condition, which is as given in Table 4.1.
Table 4.1: Scoring system to assess the severity of the patient’s condition
Score Breath rate Retractions Nasal flaring Wheezing General status
(respirations/ during
min.) inspiration
0 < 30 No No No Normal
1 30–45 Only intercostal Mild and rarely Heard only wth Moderately uneasy
stethoscope and occasionally
crying
2 45–60 Intercostal, Moderately severe Heard in both Very uneasy, crying
subcostal and and intermittently expiration and continuously
supraclavicular inspiration wth
stethoscope
3 < 60 Abdominal Severe and Heard in both Lethargic
respiration continuously expiration and
accompanying inspiration wthout
stethoscope
Grade 0-1 : Mild bronchiolitis, good prognosis
Grade 2-3 : Moderate-to-severe bronchiotitis with respiratory distress.
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Fig. 4.5: Correlation between RSV infection and wheezing
Prognosis
• Improvement seen usually after first 48 to 72 hours of treatment.
• 30 to 35 percent of children with bronchiolitis persist into adult
wheezers, especially if there is a strong family history of atopy and
bronchial asthma.
• Median duration for complete recovery is 12 to 15 days.
• Longer duration in children with underlying pathology like
congenital heart diease (CHD), bronchopulmonary dysplasia,
prematurity, etc.
Prevention
Prevention of RSV infection (Fig. 4.5) during the season is recommended.
This is done by administering Palivizumab, a monoclonal antibody to
RSV (Box 4.1). To be given before the onset of the RSV season, to offer
protection. Available as injection Synagis, 50 mg or 100 mg.
BOX 4.1: Indications for Palivizumab

1. Age > 2 year
2. Hemodynamically unstable cyanotic CHD.
3. Acyanotic CHD
4. Chronic lung disease
5. Preterm/low-birth weight (LBW) infants.
FURTHER READINGS
1. Garzon LS, Wiles L. Management of respiratory syncytial virus with lower
respiratory tract infection in infants and children. AACN Clin Issues.
2002;13(3):421-30.
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Bronchiolitis 31
3. Romero JR. Palivizumab prophylaxis of respiratory syncytial virus disease

from 1998 to 2002: results from four years of palivizumab usage. Pediatr Infect
Dis J. 2003;22(2 Suppl):S46-54.
4. Van Woensel J, Kimpen J. Therapy for respiratory tract infections caused by
respiratory syncytial virus. Eur J Pediatr. 2000;159(6):391-98.
5. Wright M, Piedimonte G. Respiratory syncytial virus prevention and therapy:
Past, present, and future. Pediatr Pulmonol. 2010.
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Bronchomalacia and
5 Tracheomalacia
BRONCHOMALACIA AND TRACHEOMALACIA

Bronchomalacia and tracheomalacia refers to the softening of the
bronchial and tracheal airway respectively, which gives rise to
symptoms. This contributes to persistent wheezing in childhood—the
wheezing sound may be so severe as to suspect stridor in the child.
Causes
The usual cause of this condition is the softness of the supporting
cartilage of the trachea and bronchi. This may be primary or secondary
(Fig. 5.1)
Primary
Primary bronchomalacia or tracheomalacia occurs as a congenital
weakness/absence of the cartilage surrounding the airways.
Secondary
Secondary bronchomalacia/tracheomalacia occurs due to obstruction
of the cartilaginous part. This may be caused by vascular rings, pressure
due to any mediastinal masses, aberrant blood vessels, etc.
Fig. 5.1: Causes of Bronchomalacia/tracheomalacia
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Bronchomalacia and Tracheomalacia 33
Symptoms
• Persistent wheezing in the absence of respiratory infection
• Wheeze more in the supine position
• Symptoms disappear during feeding
• Symptoms increase when child is playing or vigorously active.
Signs
• Monophonic wheezing, low-pitched, heard more over the trachea
in case of tracheomalacia and over one side in case of involvement
of a bronchus.
• There is no evidence of involvement of the lower airways and
respiratory distress.
Investigations
1. Chest X-ray—may not show any abnormality. In case of associated
vascular abnormalities, like right-sided aortic arch, these may be
visualized in the plain X-ray. In case of associated lung pathology,
like pneumonia, atelectasis, the X-ray findings may be helpful.
2. Fluoroscopy—shows dynamic collapse of the affected part. If this
test is positive, there is no need for further invasive tests.
3. Bronchoscopy (rigid or flexible)—may give a definitive diagnosis
of the cause.
4. Pulmonary function tests—may show some flattening of the flow-
volume loop. These tests are not diagnostic.
5. Magnetic resonance imaging (MRI) of the chest is diagnostic and
needs to be done especially when vascular rings or vascular causes
of obstruction are suspected. This is mandatory when a right-sided
aortic arch is seen on the X-ray.
Treatment
Mode of treatment depends on the severity of the condition.
• In mild to moderate cases, postural drainage to clear the secretions
is adequate. Normally as the baby grows, the condition tends to
improve as the airway diameter increases.
• Nebulized ipratropium bromide may be useful in case of severe
wheeze, by drying up the secretions.
• Beta agonists are to be avoided in the absence of asthma.
• In case of associated lung infections, appropriate treatment and
antibiotics are needed.
• In case of associated asthma, supportive care is required.
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• In severe cases, tracheostomy is needed to maintain adequate

respiratory function.
• Airway stenting is indicated for severe cases. There are no clear-cut
guidelines for each of these treatment modalities. However, the
severity of each case guides the therapy.
• Continuous positive airway pressure (CPAP) for severe cases after
tracheostomy will maintain the air exchange. It may be indicated as
a long-term therapy in case of severe respiratory distress; also in
perioperative phases and in severe intercurrent illness, necessitating
intensive care treatment.
• In severe cases, ventilator support is indicated, especially in case of
life-threatening intercurrent illness.
• Surgery—indicated only in very severe cases with associated
complications like apnea, bradycardia or cyanosis, due to the severe
airway obstruction. Surgical aortopexy has been found to be the most
common, long-term curative therapy for malacia, especially
involving the lower third of the trachea, with/without extension into
the mainstem bronchi.
Prognosis
Excellent—wheezing reduces as the baby grows, due to increase in the
airway diameter in primary cases. Usually, by the age of 3 years, there
is no evidence of the wheeze. In secondary cases, the prognosis depends
on the causative factors.
FURTHER READINGS
1. Altman KW, Wetmore RF, Marsh RR. Congenital airway abnormalities in
patients requiring hospitalization. Arch Otolaryngol Head Neck Surg.
1999;125:525-28.
2. Beasley SW, Qi BQ. Understanding tracheomalacia. J Paediatr. Child Health.
1998;34:209-10.
3. Boogaard R, Huijsmans SH, Pijnenburg MW, et al. Tracheomalacia and
bronchomalacia in children: incidence and patient characteristics. Chest
2005;128:3391-97.
4. Burden RJ, Shann F, Butt W, et al. Tracheobronchial malacia and stenosis in
children in intensive care: bronchograms help to predict oucome. Thorax.
1999;54:511-17.
5. Campbell AH. Definition and causes of the tracheobronchial collapse
syndrome. Br J Dis Chest. 1967;61:1-11.
6. Carden KA, Boiselle PM, Waltz DA, et al. Tracheomalacia and
tracheobronchomalacia in children and adults: an in-depth review. Chest.
2005;27:984-1005.
vip.persianss.ir
Bronchomalacia and Tracheomalacia 35
7. Chang AB, Gaffney JT, Eastburn MM, et al. Cough quality in children: a
comparison of subjective vs bronchoscopic findings. Respir Res. 2005;6:3.
8. Chen JC, Holinger LD. Congenital tracheal anomalies: pathology study using
serial macrosections and review of the literature. Pediatr Pathol. 1994;14:513-
37.
9. Ian Brent Masters, Anne Bernadette Chang. Tracheobronchomalacia in
Children. Expert Rev Resp Med. 2009;3(4):425-39.
10. Landing BH, Dixon LG. Congenital malformations and genetic disorders of
the respiratory tract (larynx, trachea, bronchi, and lungs). Am Rev Respir Dis
120,151-85 (1979).
11. Masters IB. Congenital airway lesions and lung disease. Pediatr Clin North
Am. 2009;56:227-42.
12. Murgu SD, Colt HG. Tracheobronchomalacia and excessive dynamic airway
collapse. Respirology. 2006;11:388-406.
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Croup
6 (Laryngotracheobronchitis)
CROUP
Croup or laryngotracheobronchitis refers to inflammation of the glottis
and subglottic regions of the upper respiratory tract. Croup constitutes
an emergency, as, if it is left untreated, there may be severe lower airway
obstruction.
Causes
Most common etiologic agents are viruses—Parainfluenza A virus
constitutes approximately 75 percent case. Influenza A virus may cause
severe disease. Other viruses, like respiratory syncytial virus (RSV),
adenovirus, measles virus, etc. have been known to be associated, but
cause milder disease (Fig. 6.1).
Haemophilus influenzae type B (HiB) was a noted causative agent
of croup. However, after the introduction of HiB immunization, the
incidence of this as a causative agent has reduced.
Fig. 6.1: Frequency of causative viruses
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Croup (Laryngotracheobronchitis) 37
Fig. 6.2: Mouth and throat anatomy
Incidence
Croup occurs due to the movement of air against a closed glottis. It is
usually of subglottic pathology. Postural change of croup indicates a
supraglottic pathology. (Please refer to Figure 6.2 for details of mouth
and throat anatomy).
Croup is common in the younger ages, from 6 months to 3 years.
Male predominance is seen. However, it may occur in older children,
especially males.
Symptoms
• Common in the night when the air temperature is low
• Prodromal symptoms include runny nose, fever, cough and non-
specific symptoms. This may be present for 1 to 2 days prior the
condition
• The child suddenly develops barking cough, hoarseness and
difficulty in breathing
• Fever may or may not be present
• Crying and agitation aggravates the symptoms
• Drooling may be present. However, if significant, it indicates
likelihood of epiglottitis
• Child prefers to sit upright
• Classically the child is awakened from sleep by the barking cough
and hoarseness
• Symptoms may persist for up to 1 week despite reduction with
medication
• No dysphagia, or facial edema.
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Signs
• Child appears agitated
• Barking cough
• Hoarseness of voice
• Throat appears congested
• Stridor is usually inspiratory due to the turbulent airflow
• Fever may be high or loub—high grade fever over 102 to 103°F
suggests epiglottitis
• Mild coryza present
• Other family members may be suffering from runny nose and
respiratory infection
• Signs of mild respiratory distress like flaring of alae nasi, subcostal
retractions may be seen
• Occasionally, severe respiratory distress may occur in case of lower
airway obstruction
• Do not move the child unnecessarily.
Investigations
Croup is a clinical diagnosis.
However, some investigations may be done to help in differentiation
between bacterial and viral infection, which are as follows:
1. Complete blood count (CBC)
2. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)
3. Blood culture
4. X-ray of the neck—shows the narrowing of the epiglottis—seen as
the ‘steeple’ sign (Fig. 6.3)
Associated signs include
a. Dilatation of the ventricle
b. Dilatation of the hypopharynx
c. Narrowing/haziness of the subglottic space (Fig. 6.4).
Treatment
1. Check the SpO2 using a pulse oximeter and ensure that the saturation
is maintained above 92 percent in room air.
2. Nebulized racemic epinephrine is the drug of choice.
Dose: 0.25 to 0.75 ml of 2.25 percent racemic epinephrine dissolved
in 3 ml of normal saline. Duration of action is 2 hours. To be given
only if the patient can be observed for this time. May be repeated
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Croup (Laryngotracheobronchitis) 39
Fig. 6.3: X-Ray of the neck showing the ‘steeple’ sign
Fig. 6.4: Schematic representation of narrowing of the subglottic space
again after 20 to 30 minutes. It is not recommended to use more

than 2 doses, as rebound increase in stridor may be noted. Peak
effect seen in 10 to 30 minutes and fades after 2 hours. Always,
observe the child for at least 2 to 3 hours after administration of
epinephrine.
3. In case of non-availability of racemic epinephrine, the regular L-
isomer of epinephrine may be used. Dose: 5 ml of 1:1000 dilution in
2 to 5 ml of normal saline solution. This is safe and has no side effects.
4. Nebulized steroids may be given in case of non-availability of
epinephrine. It acts by reducing the inflammatory fluid in the
airways. Needs to be repeated at 4 to 6 hourly intervals until the
child shows improvement. If given alongside racemic epinephrine,
it may be useful to reduce the rebound stridor.
5. IV fluids for maintenance, in case the child is not able to accept oral
feeds or progressive airway obstruction occurs.
6. Oral steroids help in reducing airway edema and inflammation.
Dexamethasone 0.15 mg/kg day for 1 to 3 days may be used. It reduces
the requirement of epinephrine as well as the need for hospitalization.
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It is useful in viral croup, as it has a strong anti-inflammatory activity,

over ten times that of budesonide. In the absence of dexamethasone,
nebulized budesonide may be administered.
7. It is always worth asking for an ENT specialist’s opinion, in case of
worsening croup (Box 6.1), which may require tracheostomy and
intubation subsequently.
8. No role of antibiotics in viral croup.
BOX 6.1: Indications for Hospitalization

1. Worsening stridor
2. Reduced SPO2 in room air.
3. Increasing respiratory distress indicative of progressing lower airway obstruction.
4. Cyanosis
5. Hypoxia
6. Poor oral intake
7. Decreased sensorium
After hospitalization, when the patient recovers from the symptoms

he can be discharged (Box 6.2).
Complications
The patient may develop viral pneumonia. This is common in immuno-
compromised children.
BOX 6.2: Indications to discharge the patient from hospital

1. No stridor at rest
2. Accepting oral feeds
3. Adequate SPO2 in room air. No sign of respiratory distress
4. Normal color
5. Normal consciousness
Prognosis
Viral croup has an excellent prognosis.
Some children may have recurrent episodes of croup. In these children,
it is essential to ensure up-to-date immunization, early treatment of
upper respiratory tract infections (URTI), avoidance of sudden cold
exposure, avoidance of contact to others with URTI infections.
FURTHER READINGS
1. Alexander KC Leung, James D Kellner, David W Johnson. Viral Croup: A
Current Perspective: J Pediatr Health Care. 2004;18(6).
3. W Steven Pray. Croup and Its Treatment. US Pharmacist. 2006;31(7).
4. www. uptodate.com
vip.persianss.ir
Infections 41
Infections
7
TYPHOID IN CHILDREN
Typhoid is a foodborne bacterial infection caused by a gram negative
non-encapsulated bacilli belonging to the Salmonella group of organisms.
There are various serotypes of Salmonella that infect animal and
human host. However, by far the most virulent and dangerous serotypes
are Salmonella typhimurium and Salmonella enteritidis that affect human
beings.
Salmonella organisms are heat-resistant and are capable of facultative
anaerobic growth. They can survive at reduced temperatures for long periods
in sewage, animal products, fecal matter, etc. Hence they are transmitted
from animals to the human host via contaminated meat products and meat.
Fecal contamination of food, unhygienic food preparation, storage and
handling favor the spread of disease and maintenance of the cycle of
transmission in the society (Fig. 7.1). However, the bacteria can be destroyed
by heat at 140°F for 15 minutes or 130°F for 1 hour.
Fig. 7.1: Cycle of transmission of typhoid
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Salmonella has a somatic ‘O’ antigen and a flagellar ‘H’ antigen. The
presence of the ‘O’ antigen in the blood is indicative of an ongoing
infection with Salmonella, while the presence of the ‘H’ antigen indicates
a previous infection.
Mode of Transmission of Infection

Fecal-oral transmission is the route of transmission of the organisms
into the human host. Improper and unhygienic food production,
contaminated and unclean food machines, improper food storage with
varying temperature controls, infected food handlers all contribute to
the spread of disease. Contamination in chicken is a potent source of
contaminated eggs and can cause a major outbreak of infection
especially in schools and closed communities.
Pathogenesis
The organism enters the host via the oral cavity and reaches the stomach.
The dose of inoculum, the rapidity of transit through the stomach, the
acidity of the stomach environment and the immune status of the child
dictate the occurrence and severity of the disease. When the organisms
transit through the stomach and reach the intestines, they produce
inflammation and edema of the mucosa. They penetrate the lamina
propria of the terminal ileum and migrate to the lymphoid tissues and
mesenteric lymph nodes, where they can cause hypertrophy which may
obstruct the blood supply. Lymphohematogenous spread may occur,
and the organisms can lodge in the liver and spleen causing gland
enlargement. This is called the primary bacteremia. They also spread
via the blood stream to other parts of the body where they multiply
within the reticuloendothelial system, within the macrophages. Once
again they are disseminated via the blood stream to various parts of
the body. This is the secondary bacteremia, which is symptomatic and
marks the end of the incubation period. Multiplication of the organisms
in the deeper layers of the mucosa can cause ulceration and result in
intestinal bleeds. They can penetrate the muscularis as well as the serosal
layer and produce perforation in the intestine.
Incubation Period
The incubation period for typhoid is 4 to 14 days, depending on the
host immunity. Inoculating dose of organisms is 105 to 109 organisms.
vip.persianss.ir
Infections 43
The organisms are known to colonize and multiply in the gall bladder
wall, from where they are periodically discharged into the blood stream.
Symptoms
• Fever—high grade, spiking or persistent and associated with chills
Classical presentation of stepladder pattern of fever may not be seen
in children
• Myalgia
• Loose motions in the early stages, which are indistinguishable from
acute gastroenteritis
• Later on, the child develops constipation
• Pain abdomen and abdominal discomfort
• Vomiting
• Skin rash on the lower part of the chest—usually at the end of first
week of fever.
Signs
• High grade fever
• Appearance of toxicity
• Coated tongue
• Macular or maculopapular skin rash called rose spots found on the
lower part of the chest—diagnostic of typhoid fever
• Hepatomegaly
• Splenomegaly
• Pain abdomen
• Ileus
• Perforation—late sign.
Investigations
1. Complete blood count—shows generalized neutropenia. In younger
children, there may be leukocytosis noticed. Thrombocytopenia is a
poor prognostic marker.
2. ESR elevated—in acute phase reaction.
3. CRP – elevated.
4. Widal test—usually positive if done after the fifth day of fever.
The test shows the titers of the ‘O’ and the ‘H’ antigen of the
organism (Box 7.1). Elevated levels (> 1:80 titer) of ‘O’ antigen is
indicative of an active ongoing infection. Futher dilutions with
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positive samples of O-antigen and the test result of those are

indicative of more pathogen load in the body. This is a time-tested
diagnostic tool, but is neither specific nor sensitive. Hence false
positive results may be found. Rising titer of ‘O’ antigen in paired
sera is diagnostic. Vi antigen positivity indicates a carrier state.
BOX 7.1: Interpretation of Widal Test

‘H’ antigen positive – Typhoid vaccination
– Previous infection with Salmonella
‘O’ and ‘H’ antigen positive – Active typhoid infection
“Vi “antigen positive – Typhoid carrier
5. Blood culture – done early in the course of illness, during the stage
of bacteremia will show growth of Salmonella organisms. The
organism is hence needs to be grown on blood containing agar
plates. This test is the mainstay in the diagnosis of typhoid fever.
Alongside the culture, the drug sensitivity patterns reveal the most
sensitive antibiotic that can be used to treat the disease.
6. Stool culture—positive during the second week of the illness, when
fecal shedding of the organism commences.
7. Chest X-ray—done to rule out Salmonella pneumonia which may
be silently present.
8. USG abdomen—Ultrasonography (USG) of abdomen is essential
to document the size of the hepatosplenomegaly. At the same time,
it gives an idea about any coexisting gastrointestinal (GIT)
pathology like ileus, perforation, etc.
9. Rapid diagnostic PCR tests—which are able to locate the specific
areas of the Salmonella antigens, even in cases of low bacterial load.
It is more sensitive and specific test.
10. Liver function tests—mild elevation in the liver enzymes may be
seen during the active stage of typhoid. Persistence of elevated
levels could indicate the onset of hepatitis as a complication of
typhoid fever.
Complications
As the organism can enter any organ system in the body, it can give rise
to a wide variety of complications involving several organ systems,
which are as follows:
 Conjunctivitis
Eye  Optic neuritis
 Retinitis
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Infections 45
 Meningitis
 Encephalitis
 Cerebral abscess
 Cerebral edema
CNS  Seizures
 Ataxia
 Aphasia
 Motor neuron disease
 Guillain–Barre syndrome
 Psychosis
 Nerve deafness
ENT  Otitis media
 Tinnitus
 Pericarditis
 Myocarditis
CVS  Endocarditis
 Congestive heart failure
 Arteritis
 Pneumonia
RS  Empyema
 Bronchopleural fistula
 Pyogenic abscess
Skin  Psoas abscess
 Dermatitis
 Cutaneous vasculitis
 Cholecystitis
 Hepatitis
 Hepatic abscess
 Splenic abscess
GIT  Intestinal ulcers
 Intestinal perforation
 GIT hemorrhage
 Paralytic ileus
 Peritonitis
Genitourinary system  Renal abscess
 Urinary tract infection
 Epididymitis
 Prostatitis
 Pelvic abscess
 Septic arthritis
Bone and joints  Osteomyelitis
Dactylitis
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 Anemia
Hematological  Leukopenia
 Thrombocytopenia
 Thrombosis
Abbreviations: CNS-Central nervous system, ENT-Ear-nose-throat
system, CVS-cardiovascular system, RS-Respiratory system, GIT-
Gastrointertinal tract.
Carrier State
When a patient continues to excrete the Salmonella typhi organisms in
the stools for over 3 months after initial infection, it is called carrier
state. This is uncommon in children, with an incidence if less than 2
percent, but it increases in older children. They test positive for the Vi
antigen in the serum.
Treatment
1. IV fluids—to correct the ongoing fluid losses. Also helps to reduce
the intensity of fever by improving the hydration. Administer 5
percent dextrose with electrolytes, preferably one-fifth DNS.
Calculate fluid required for correction of moderate dehydration and
reduce it as the oral intake improves.
2. Isolate the patient and his personal belongings, to prevent the spread
to other family members.
3. Paracetamol—15 mg/kg every 6 hourly, to reduce the fever spikes
and keep the child more comfortable, reduces myalgia.
4. Cough suppressant—in case of mild cough. Preferably use herbal
soothers.
5. Antibiotics—oral medication to be used in case child can accept
orally. Chloramphenicol is the drug of choice. Dose 50 to 75 mg/kg
in three to four divided doses for 14 to 21 days.
Alternate drugs of choice include:
a. Amoxicillin 75 to 100 mg/kg/day for 14 days
b. Fluoroquinolones: ciprofloxacin or ofloxacin 15 mg/kg/day in two
divided doses for 7 days.
c. Cefixime 20 mg/kg/day for 7 to 14 days.
In toxic patients or in patients who are unable to accept orally due
to GIT symptoms, Ceftriaxone injection IV 50 to 100 mg/kg/day once
daily is recommended.
Usually the patient shows remission from fever and symptoms
within 48 to 72 hours after the start of therapy. In case of persistence of
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Infections 47
symptoms, look out for the possibility of complications or any other

associated symptoms.
Role of Steroids in Typhoid Fever

Steroids have a role in the treatment of typhoid fever, but needs to be
used with caution and under continuous supervision. Hence it is
recommended only in hospitalized children. Indications for the use of
steroid in this condition is given in Box 7.2.
BOX 7.2: Indications for use of steroids in typhoid fever

1. Severely ill child
2. Toxic patient
3. Shock
4. Comatose patient
5. Aphasia
6. Cerebellitis
Diet in Typhoid Fever

Recommend a home-cooked diet. Diet should be soft and nutritious.
Avoid use of raw fruits and vegetables. Ensure that vegetables are well
washed before cooking. Avoid use of raw eggs. Avoid use of extra spicy
foods. Plenty of oral fluids are recommended.
Prognosis
Prognosis of typhoid is usually excellent if treatment is started early
and with adequate antibiotic coverage. However, chances of relapse
are there, hence caution must be advised to the family.
Recommend administration of Vi typhoid vaccine after 4 to 6 weeks
of recovery from typhoid fever to all patients, to reduce the occurrence
of relapse.
Prevention
Patient and family must be counseled on strict hand washing, proper
care in food preparation, handling and storage, avoid raw foods and
eggs. Avoid use of cut fruits from outside. Use always boiled water or
mineral water.
Recommend the Vi typhoid vaccine, to be administered every 3 years
to all members of the family of the patients.
Isolate and treat the chronic carriers, till the test shows negative for
the Vi antigen.
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TUBERCULOSIS IN CHILDREN
Tuberculosis is a common infection in children, especially in the tropical
countries.
According to WHO estimates one third of the world’s population is
infected with tuberculosis. This indicates the extent of the problem the
world faces from this disease. They normally suffer from paucibacillary
disease and hence do not contribute to disease transmission in the
community.
Tuberculosis is caused by Mycobacterium tuberculosis. There are other
organisms in this family—M. bovis, M. africanum, M. microti and M.
canetti. They are gram-positive, curved rods, which are non-motile and
non-spore forming. They are obligate aerobes, which require special
media for growth. Lowenstein-Jensen medium is used which contains
glycerol and ammonium that provides the carbon and nitrogen required
for bacterial growth. They are fastidious organisms, slow growing and
require around 3 to 4 weeks for isolation from culture. However, slightly
faster isolation is possible in a liquid medium BACTEC, which has
radiolabeled nutrients. Isolation from this medium is possible in 3
weeks. Currently, polymerase chain reaction (PCR) tests using DNA
probes may be able to identify the presence of Mycobacterium with in
several hours. Restriction fragment length polymorphism (RFLP) of
Mycobacterium is another useful tool to diagnose infection and aids in
epidemiological studies to make faster diagnosis.
Primary complex disease involves disease at the primary portal of entry
into the body along with the local lymph nodes. This is common in the
lungs, where there is associated mediastinal lymphadenopathy.
Drug-resistant tuberculosis is mycobacterial infection that does not
respond to the usual antitubercular drugs. It requires the second line of
drugs for control of disease.
Disseminated tuberculosis occurs when the tubercle bacilli are spread
to distant organs of the body from the site of primary infection in the
lungs. This shows usually a slow spread.
Miliary tuberculosis occurs when a large number of tubercle bacilli are
released into the bloodstream and seed several organs, at least two
organs, usually simultaneously and rapidly.
Reactivation tuberculosis occurs when the endogenous bacilli present
in the encapsulated foci are reactivated and causes disease symptoms.
This commonly occurs when the body immunity is suppressed from
various reasons.
vip.persianss.ir
Infections 49
Latent tuberculosis occurs when the child has been infected with
mycobacterium tuberculosis, but there are no clinical or radiological
features of the disease. The tuberculin test is positive and could be the
only feature suggestive of infection in the child.
Methods of Transmission of Infection

1. Droplet infection—smaller droplet size, i.e. 1 to 5 microns, spread
infection to a larger distance.
2. Contact with contaminated secretions—nasal, sputum, vomitus, etc.
Factors Aiding Spread of Infection

1. Close contact with an infected individual
2. Poor air circulation and poor hygiene levels favour spread of
infection
3. Poor immunity—makes the child more susceptible to infection.
4. Protein energy malnutrition—makes the child more susceptible to
infections like tuberculosis
5. After viral infection—like measles, varicella, etc. where the body
immunity is lowered and the child is susceptible to mycobacterial
infection.
6. Long course of steroids—for any associated pathology like
nephrotic syndrome, rheumatoid arthritis, etc.
7. Associated HIV infection—which reduces the body resistance.
8. Ongoing treatment with any other immunosuppressives—
cyclophosphamide, antimalignancy drugs, etc.
9. After organ transplantation—due to the immunosuppression.
10. Drug abusers, especially injecting drug users.
11. Persons of foreign origin, especially from areas of high prevalence.
Time Interval between Infection and Clinically Apparent Disease

1. Primary complex and conversion from tuberculin negative to
tuberculin positive state—occurs in approximately 6 weeks from
infection.
2. Lymph node disease—usually takes between 3 to 9 months after
infection to show signs of the disease.
3. Endobronchial tuberculosis—usually takes approximately 5 to 6
months after exposure to infection.
4. Disseminated disease—may take between 2 to 6 months after
primary infection.
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5. Meningeal infection—may be an early manifestation, occurring 2 to

6 months after exposure.
6. Bone and joint disease—is a slow disease and may take several years
to manifest the symptoms.
7. Renal and GIT tuberculosis—are late manifestations and may occur
several years after primary infection.
These clinically apparent diseases are classified under three main
category—early onset, intermediate and late manifestation (Box 7.3).
BOX 7.3: Clinically apparent diseases

Early onset disease— Primary complex
Progressive primary complex
Intermediate disease— Endobronchial tuberculosis
Lymph node disease
Meningeal infection
Disseminated disease
Late manifestation— Bone and joint disease
Renal and GIT disease
Pathogenesis
After inhalation of the tubercle bacilli, by the susceptible host, the
organism travels via the bronchioles, to reach the terminal bronchioles,
the smallest part of the airway. Here it lodges in the subpleural location,
which is usually a single site and is called the ‘primary focus’. The bacilli
multiply here, in the alveolar ducts and terminal alveoli. Most may be
destroyed by the macrophages, but some that escape are transported
by the lymphatics and reach the lymph nodes, draining the area. Here,
they may lodge and multiply, forming the pathological ‘tubercle’ with
a central area of necrosis, called ‘caseation’. This triad of the primary
focus plus regional lymphatics plus affected lymph nodes is together
called the ‘primary complex’.
Usually, as the lung is the primary focus, the hilar lymph nodes are
involved. However, in cases of involvement of the upper lobe of the
lung, the paratracheal lymph nodes may be the affected one.
Once the tubercle develops, it is enclosed in fibrous tissue, which
prevents the spread of the organism. The lesion may thus heal by
fibrosis, and subsequently calcification may occur. However, the central
caseation may progress and the necrotic material then may be spilt out
via the bronchioles, resulting in a cavitary lesion left behind, leading to
cavitation in the lungs. Occasionally, there may be a pleural reaction,
especially when the primary focus is subpleural in position. This could
result in pleural effusion or pleurisy.
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Infections 51
The tubercles may extend causing a pneumonitis in the lung

parenchyma. The enlarged lymph nodes may obstruct the draining
bronchus and cause a partial obstruction, which can lead to
hyperinflation of the distal lung parenchyma. In case of complete
obstruction of the bronchus by the enlarged lymph nodes or by the
caseous material, there may result a collapse or atelectasis of the distal
lung parenchyma. This together is called collapse-consolidation of the
lung parenchyma which results in a segmental lesion. The inflamed
caseous material may erode through the bronchial wall and spill out its
contents into the bronchus. This results in endobronchial tuberculosis.
A fistula tract may result between the bronchial wall and the
parenchyma.
Once in the bronchus, the caseous material or the tubercles may
spread via the lymphatics and result in distant organ seeding called
disseminated tuberculosis.
After primary infection, the child is at greatest risk of dissemination
during the initial 3 months. At this time, any compromise in the child’s
immune status, will facilitate a spread of the infection and the
development of disseminated tuberculosis.
Clinical Features
Usually the child presents with a history of fever, which may be high
grade, persistent and/or recurrent, along with symptoms of cough, loss
of appetite, general malaise and weakness. Sometimes they present with
the typical history of fever with night sweats. There may be failure to
gain weight and may present as a failure to thrive in long standing
cases.
Many of the children have no specific symptoms.
Primary Pulmonary Disease

The diagnosis of primary pulmonary disease is usually made only after
radiological investigation. As most of the primary lesions are located
subpleurally, there may be some associated pleurisy manifested as a
pleural pain, again this may be non-specific (Fig. 7.2). The initial
parenchymal infection is not seen by X-ray. However, once the lymph
nodes are involved , they are visualized radiologically. The parenchymal
involvement may spread to adjacent segments of the lung. The hilar
lymph nodes are most commonly affected and are seen to be larger
than normal by X-ray. This obstruction results in distal hyperinflation
of the airways, followed by obstruction and then collapse of the airways.
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Fig. 7.2: Complications of pulmonary tuberculosis
Together with the parenchymal lesions, the X-ray shows a picture of

collapse/consolidation in the affected segment of the lung. Occasionally,
the caseated material may be extruded via the draining bronchus,
resulting in endobronchial tuberculosis, leaving behind an empty cavity
in the parenchyma. Sometimes, the pressure caused by the caseated
material may result in a fistula formation. The enlarged subcarinal
lymph nodes may compress on the trachea and produce a broncho–
tracheal fistula. Most of the lesions heal on treatment, without scarring.
Occasionally, there is calcification in the lymph nodes and in the affected
segments, which takes around 6 to 12 months to develop, which are
then visualized radiologically. Occasionally, there may be scarring of
the affected bronchus, which results in segmental bronchiectasis.
The primary tubercle may rupture into the blood stream and cause
dissemination to all parts of the lung. This is seen as small nodules
spread through out the lungs and is known as miliary tuberculosis.
Progressive Primary Tuberculosis

Progressive primary tuberculosis (Fig. 7.3) is a rare complication,
occurring in children with further compromise in the immune system.
Fig. 7.3: Progressive primary tuberculosis
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Infections 53
The primary focus enlarges steadily resulting in a tubercle with central

caseation. This contains large numbers of viable bacilli and is potentially
highly infective. It may rupture, releasing plenty of bacteria into the
adjacent bronchus, with further spread of the disease. There may be
extra thoracic lymph node involvement, as in the cervical or mesenteric
lymph nodes. The child is symptomatic with high grade fever, night
sweats and weight loss, with cough and sputum. Clinically, there may
be rales and bronchial breathing heard over the cavitary lesion. Slow
recovery occurs with appropriate therapy.
Lymphohematogenous Spread of Tuberculosis

Spread of the bacteria are dependent on the child’s immune status and
the quantity of the infecting organisms. In case of large quantity, or
poor immune response, the bacteria may seed to various organs via the
blood stream and lymph. This may be asymptomatic. However, in
indolent cases, with recurrent or prolonged release of the bacteria into
the blood stream, the child may have recurrent lymph nodes and
abscesses skin wherein papulonecrotic lesions may be visualized. Renal
disease may occur from lodgment in the kidneys. Bone and joint disease
may also occur. This condition is commonly mistaken for malaria, as
the child has intermittent spiking fever, with associated splenomegaly.
Miliary Tuberculosis
Miliary tuberculosis, occurs when there is a sudden influx of a large
number of bacteria into the blood stream, resulting in disease in two or
more distal organ systems. This is common in younger children and
infants with poor immune systems, as a complication of the primary
infection, but may also occur in older children and adolescents due to
the breakdown of the healed primary focus.
Due to the sudden release of a large number of organisms into the
blood stream, the child suddenly falls sick, with high spiking fever,
loss of appetite, weight loss and cough. At this time, the clinical signs
are minimal and the chest X-ray may be normal. However, with
persistence of the symptoms, the child develops breathlessness with
increase in cough, due to the lungs getting filled with tubercles.
Lymphadenopathy and hepatosplenomegaly may develop after some
more weeks. At this time, the chest X-ray may show the typical miliary
mottling, which are small speckled areas approximately 2 to 3 mm in
diameter. The lesions may coalesce to form larger lesions and
subsequently infiltrates which may extend through the lung fields.
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Pleural Effusion
The pleural effusion is caused by the rupture of a subpleural primary
focus, resulting in the release of tubercle bacilli into the subpleural space
and causing a pleural effusion. This may also be caused by release of
bacilli from a caseating lymph node. Pleural effusion may be
asymptomatic, in many cases. It is rare in children of 2 to 6 years age. In
long-standing pleural effusion, the child becomes symptomatic. The
appearance of sudden spiking fever, difficulty in taking deep inspiration
and pain of the affected side of the chest should be an indicator of the
possibility of pleural effusion.
It is usually detected on radiological examination of the chest and is
most commonly unilateral. The pleural fluid is an exudate, yellowish
in color and shows high levels of protein. The sugar level in the fluid is
low or normal, plenty of white blood cells may be seen in the fluid,
predominantly neutrophils in the early stages and lymphocytes later
on. Gram stain for acid-fast bacilli (AFB) may be negative. Tubercle
bacilli may be isolated from culture of the pleural fluid. Biopsy of the
pleural membrane may show AFB and will grow the organism in the
culture. It shows a dramatic response on treatment with antituberculous
drugs. However, radiological clearing may take a longer time.
Pericardial Effusion
Pericardial effusion is a rare complication of tuberculosis in children.
The symptoms may be non-specific with vague fever and chest
discomfort. The child may or may not complain of chest pain. Clinically,
there is pulsus paradoxus and the heart sound appear faint and distant.
Electrocardiogram will show low volume QRS complexes.
Echocardiogram will reveal the presence of fluid in the pericardial cavity
(Fig. 7.4).
The pericardial fluid is serosanguinous and usually small in quantity.
It is exudative and culture could reveal the presence of Mycobacterium
tuberculosis. Response to treatment with antituberculous drugs is
excellent.
Central Nervous System Disease

The disease of central nervous system is potentially the most dangerous
complication of tuberculosis and may be fatal if not treated rapidly
and aggressively. It occurs early in the course of the disease, may be
within 3 to 6 months of primary infection. It is common in the younger
age groups, below 4 to 5 years of age, probably due to the lower levels
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Infections 55
Fig. 7.4: Pericardial effusion
of immunity in these ages. The incidence reduces after one year, after
the primary infection.
It is usually caused by seeding of the meninges or the cerebral cortex
during the stage of the lymphohematogenous dissemination of the
bacilli. The bacilli lodge and multiply there and are released in small
quantities into the subarachnoid space. It causes an exudative effusion
here and also the cerebrospinal fluid acts as a vehicle to transfer the
organisms to all parts of the meninges. The gelatinous exudates infiltrate
the blood vessels and causes vasculitis, obstruction and later infarction
of the cerebral cortex. The brain stem suffers the maximum damage,
hence involvement of the cranial nerves II, IV, VI is common.
Additionally, the thick exudates obstructs the flow of cerebrospinal fluid
in the basal cisterns, causing a communicating hydrocephalus. The signs
may progress rapidly causing sudden severe symptoms and serious
disability. In cases where the progression is slower, the disease may be
divided into three stages:
First stage: The first stage which is the earliest stage with non-specific
symptoms such as fever, headache, drowsiness, irritability, malaise, etc.
There are no CNS deficits at this stage, however, there may be a loss of
developmental milestones at this stage. The child may appear to be
more lethargic and disinterested in his surroundings. If untreated, the
child proceeds to the next stage.
Second stage: The second stage which begins abruptly, with the
manifestation of CNS symptoms. The child may start vomiting
profusely, projectile and complain of neck stiffness and rigidity,
convulsions. There may be hypertonia in the limbs and one or more
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cranial nerve involvement may be seen. On examination at this stage,

there is found to be neck rigidity, cranial nerve involvement and signs
of meningeal irritation as in positive Kernig’s and Brudzinski’s signs.
The child has electrolyte disturbances which may be a manifestation of
SIADH antidiceretic (syndrome of inappropriate antidiuretic hormone).
Third stage: The child may rapidly progress to the third stage, which is
the stage of CNS deficits with coma, decerebrate posturing, hemiplegia
or paraplegia, and may rapidly progress to death.
In children, treated early in the course, the signs may be completely
reversible while in the later stages there may be neurological deficits
like persistent cranial nerve deficits, deafness, hemi- or paraplegia,
recurrent convulsions, hydrocephalus, etc.
A high degree of suspicion is essential to diagnose the child with
tuberculous meningitis (TBM), especially in the early stages. Contact
tracing is extremely important in these children and treatment of the
infective adult is essential.
According to WHO classification, patients with tuberculosis can be
classified as:
a. Suspected cases of tuberculosis
b. Probable cases of tuberculosis
c. Confirmed cases of tuberculosis.
This classification is based on the available symptoms, chest X-ray
evidence and history of exposure to a known case of tuberculosis.
Investigations
1. Complete blood counts—show a lymphocytic predominance
during the disease course. Platelet count to be monitored, especially
after start of therapy.
2. ESR—may be elevated. Grossly elevated in cases of TBM.
3. Mantoux skin test—is an important tool to show the skin
hypersensitivity to the tubercle antigen. It is also called the
tuberculin skin test (TST).
Mantoux test done by injectiong 0.1 ml of 5 tuberculin units of
purified protein derivative (PPD) stabilized with Tween 80
intradermally into the anterior cubital area usually on the left arm.
The test is read after 48 to 72 hours to notice the induration at the
site of injection. The reading must be taken by the person who has
given the test. Positive reaction, means induration with or without
associated erythema and vesicles at the site of injection.
Interpretation of mantoux test and the features contributing to false
negative and false positive tubercullin test are given in Boxes 7.4,
7.5 and 7.6 respectively.
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BOX 7.4: Interpretation of mantoux test

0–5 mm induration—negative tuberculin test
6–9 mm induration—borderline
> 10 mm induration—positive test
> 10 mm induration + vesiculation or necrosis—strongly positive tuberculin test.
Tuberculin test usually becomes positive within 4–8 weeks after exposure to the tubercle
bacilli.
BOX 7.5: False Negative Tuberculin Test

1. Malnutrition
2. After viral infection like measles, chickenpox
3. Associated HIV infection
4. Disseminated tuberculosis
5. Tubercular meningitis
6. After corticosteroid therapy
7. After immunosuppressive therapy
8. Improper administration of the test
9. Children below the age of 4 years.
BOX 7.6: False Positive Tuberculin Test

1. Infection with atypical mycobacteria
2. Following BCG vaccination
4. BCG Test—this is given to those children in whom a false negative

reaction is anticipated or is found. The BCG vaccine is administered
intradermally into the left deltoid area and the reaction is noted:
Classical reaction: seen after 3 to 6 weeks, associated with induration,
erythema and ulceration followed by scab formation and drying
over the next 2 to 4 months, leaving behind a puckered scar.
Accelerated reaction: the reaction is fast and the child shows papule
formation within a few hours, followed by ulceration in 3 to 4 days,
and scab formation within a week.
An accelerated BCG reaction is definitive diagnosis of the presence
of tuberculosis.
Negative BCG reaction rules out tuberculosis in the child. It also
plays an important role as a protection against infection.
5. Chest X-ray—helps to detect the presence of lung involvement in
tuberculosis. There may be evidence of pneumonia, pleural effusion,
calcification of the primary complex, collapse/consolidation,
subcarinal lymph node enlargement, etc. Additionally, in cases of
pericarditis, there may be some evidence of increase in the cardiac
diameter. This investigation is absolutely essential in all cases of
suspected tuberculosis.
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6. IgG and IgM levels in blood—the elevated IgM levels specific to

tuberculosis, will indicate the occurrence of active disease in the
child. Elevated IgG levels indicate some exposure of the body to
the mycobacteria, but is not indicative of active disease. Normal
level of IgG is 780 to 1500 mg/dl and that of IgM is 70 to 250 mg/dl.
7. QuantiFERON—TB gold test measures the level of interferon
gamma in the child’s body. This is a rapid diagnostic test and gives
results in a matter of a few days. Has high specificity and sensitivity.
No cross reaction between other types of mycobacteria and
Mycobacterium tuberculosis.
8. Culture of the mycobacteria—detection of mycobacteria on growth
in L-J or BACTEC medium is diagnostic of tuberculosis infection.
The organism may be isolated from body secretions like sputum,
gastric lavage, pleural aspirate, pericardial aspirate, pus from
caseating lumph nodes, etc. However, it takes at least 6 to 12 weeks
to isolate the organism, as they are slow growers.
9. CSF examination—obtained by lumbar puncture in suspected cases
of TBM. It is an invaluable test in diagnosis. CSF is an exudate,
appears cloudy and on standing at room temperature overnight,
has a cobweb formation on the surface. If this is harvested, it shows
acid-fast bacilli on staining.
The CSF protein levels are grossly elevated (400 to 5000 mg/dl),
while the sugar levels are reduced, below 40 mg/dl. Microscopic
examination reveals elevated cell count (> 10–500 cells/hpf),
predominantly lymphocytes. In the early stages, neutrophilic
dominance may be noted.
10. CT scan of the brain—is essential in all cases of suspected TBM. In
the early stages, focal ischemia seen as areas of hypodensity may
be observed. Later, there may be evidence of cerebral edema, as
observed by areas of increased density in the scan. Hydrocephalus,
which is a late manifestation, may be observed. Tuberculomas, if
any, may also be seen in the CT scan.
11. MRI scan of the brain—will show all the features of TBM, as in
exudates, ischemia, inflammation in the different areas of the cortex
and meninges. All the areas of the brain are outlined and any
tuberculomas can be easily picked up. Hydrocephalus, seen as the
widening anywhere along the ventricular system can be observed.
12. Lymp hnode examination—any excised material from the affected
lymph nodes can be examined under the microscope. It will reveal
the typical tubercular node with central caseation and tubercle
formation. If this is observed, it is diagnostic of tuberculosis.
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Infections 59
13. Liver function tests—need to be done as a baseline, to look for any

liver involvement. This is also essential as the child needs to be
followed up during therapy for side effects of the anti-tubercular
drugs on the liver. In particular, liver enzymes, serum glutamic-
oxaloacetic transaminase (SGOT), serum glutamic pyruvic
transaminase (SGPT) and alkaline phosphatase need to be closely
monitored.
14. Blood urea—to be done as a baseline, before commencing treatment
with antitubercular drugs, as some drugs are nephrotoxic.
15. Eye test—to rule out any underlying ocular disease. Also regular
follow-up to pick up early optic neuritis that may develop during
the course of treatment.
Diagnosis of tuberculosis is made based on the presence of the
following triad (Fig. 7.5):
1. History of contact with a known case of tuberculosis
2. Positive tuberculin skin test (TST)
3. Chest X-ray suggestive of tuberculosis
This triad is extremely useful in non-endemic areas.
Treatment
As soon as a diagnosis of tuberculosis is made, the child needs to be
started on antitubercular therapy to avoid further spread of the disease
and to avoid any complications.
Usually short course chemotherapy is recommended in pulmonary
tuberculosis, using four drugs. There are various regimens, with
different combinations of drugs. It is always best to stick with a familiar
regimen, in most cases. However, in patients who do not respond, the
alternate combinations using the second line of drugs can be used.
Fig. 7.5: Diagnostic triad for tuberculosis
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The initial therapy consists of 2 months course of three drugs—

isoniazid, rifampicin and pyrazinamide followed by 4 months treatment
with two drugs only—isoniazid and rifampicin.
DOTS
Directly observed treatment short-course (DOTS) involves the patient
taking medication under the direct supervision of health care worker
twice weekly. This ensures proper drug compliance and provides
adequate treatment. To be initiated after 2 weeks of daily treatment.
Isoniazid: Dose 10 mg/kg once daily. Incase of DOTS, 20 to 30 mg/kg
twice weekly. Maximum dosage is 300 mg/day. Highly effective and
bactericidal against the rapidly growing and dividing organisms, but
has bacteriostatic effect against the slow dividing organisms.
Side effects: hepatic enzyme elevation, mild hypersensitivity, peripheral
neuritis.
Rifampicin: Dose 10 mg/kg once daily. In case of DOTS, give 10 to 20
mg/kg twice weekly. Maximum dosage is 600 mg/day. Highly
bactericidal against intracellular organisms, semidormant and persistent
organisms. Hence a very useful drug. Acts by inhibiting the DNA-
dependent RNA polymerase enzyme, resulting in suppression of nucleic
acid synthesis and hence bacterial destruction.
Side effects: Rifampicin has several side effects, the most notorious being
staining of the urine and body secretions like sweat, etc. which have an
orange tinge. Also, thrombocytopenia, elevated liver functions, vomiting
and hypersensitivity may occur.
Pyrazinamide: Dose 20 mg/kg once daily. Incase of DOTS, give 50 mg/
kg twice weekly. Maximum dose is 2 g/day. Has a bactericidal action
against the Mycobacterium tuberculosis present within the macrophages,
in the inflamed tissues and in the acidic environment.
Side effects: hepatotoxicity, vomiting, arthralgia, etc.
Ethambutol: Dose 15 to 20 mg/kg. In case of DOTS, give 50 mg/kg.
Maximum dose is 2.5 g/day. Is effective against the rapidly growing
organisms in the cavity walls. Also effective against slow growers and
some atypical mycobacteria.
Side effects: ocular disturbances in visualizing red and green colors,
reversible optic neuritis, vomiting, etc.
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Usually the initial regimen consists of 2 months of intensive therapy

with three or four drugs, followed by 4 months of treatment with two
drugs. In this way, the likelihood of developing resisitance to the drugs
is much lesser, while at the same time, the initial intensive therapy
ensures adequate arrest to the spread of the organisms. The reason for
using ethambutol with pyrazinamide is that this drug does prevent the
development of resistance to rifampicin.
Treatment Modalities Recommended in Children

There are two stages in the treatment: initial, intensive phase and later
continuation phase.
- New sputum positive cases/seriously ill sputum negative/
extrapulmonary cases: give 2H 3 R 3 Z 3 E 3 (intensive) + 4H 3 R 3
(continuation)
- Relapse after treatment/treatment failure: give 1H3R3Z3 (intensive)
+ 5H3R3Z3 (continuation)
- In TBM, use HRZS instead of HRZE in intensive phase. Continue
treatment for total 9 months.
H = isoniazid, R = rifampicin, z = pyrazinamide, E-ethambutol, S-
streptomycin
Alternate Drugs used in Tuberculosis

These drugs are used in cases of drug-resistant tuberculosis and is better
administered by a chest physician:
1. Ethionamide: Dose 15 to 20 mg/kg in two or three divided doses orally
daily, maximum dose is 1 g/day.
Side effects: hepatotoxicity, can induce hypothyroidism, GIT upset,
vomiting.
2. Amikacin: Dose 15 to 30 mg/kg injection given IM or IV. Maximum
dose is 1 g/day
Side effect; is nephrotoxic, as well as ototoxic. Can disturb the liver
functions.
3. Para-amino salicylic acid (PAS): Dose 200 to 300 mg/kg orally per day.
Maximum dose is 10 g/day.
Side effects: hepatotoxic, GIT disturbances, hypersensitivity.
4. Cycloserine: Dose 10 to 20 mg/kg in two divided doses, orally.
Side effects: may cause personality disorders and psychosis, skin rash
and seizures.
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5. Streptomycin: Dose 20 to 40 mg/kg intramuscular once daily.

Side effects: can cause skin rash, can cause hearing loss, loss of balance
due to vestibular impairment, nephrotoxic and can cause acute renal
failure.
Role of Corticosteroids in Tuberculosis

Paradoxical as it may seem, corticosteroids do have a role in the
treatment of tuberculosis. Most often, they are administered for short
durations.
Indications for use of steroids in tuberculosis is given in Box 7.7.
BOX 7.7: Indications for Steroids

1. TBM
2. Pleural effusion
3. Pericardial effusion
4. Endobronchial tuberculosis
5. Tubercular arthritis
6. Optic neuritis
7. Tuberculoma
8. Miliary tuberculosis
9. Tuberculous ascites
In all these cases, the steroid helps in reducing the inflammation,

vasculitis and aids in faster healing of the disease.
Dose: Prednisone 1 to 2 mg/kg given for 4 to 6 weeks, followed by
tapering gradually.
Supportive Treatment
1. Administer antipyretics, in case of fever.
2. IV fluids in case of TBM or incase of inadequate oral intake. Use
dextrose-free solutions.
3. IV mannitol 20 percent to reduce the cerebral edema in case of TBM—
to be given for 3 days, upto a maximum of 5 days. Dose 7.5 ml/kg
every 6 to 8 hourly, rapid infusion.
4. Control of seizures—to abort—use diazepam 0.3 to 0.5 mg/kg start
up to a maximum of 10 mg.
For prevention of recurrence of seizures use IV diphenylhydantoin.
Loading dose 15 to 20 mg/kg, followed by maintenance dose of 5 mg/kg.
5. Maintain the nutrition: children with tuberculosis require a high-
protein diet.
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Infections 63
6. Frequent vision check to monitor development of optic neuritis

during the course of therapy.
7. Passive physiotherapy—especially in case of TBM, to prevent the
development of strictures, muscle wasting and loss of motor
functions.
Immunization in Tuberculosis
All attenuated and killed vaccines can be safely administered to the
child on treatment for tuberculosis.
Live virus vaccines need to be postponed in children on treatment
with corticosteroids, in those with miliary tuberculosis, tubercular
meningitis and those with severe disseminated tuberculosis. In these
children, the vaccine needs to be postponed until the end of treatment,
and the child is tuberculin negative. Vaccines to be temporarily withheld
include measles mumps and rubella (MMR), varicella, influenza and
BCG vaccines.
VIRAL HEPATITIS IN CHILDREN

Viral hepatitis is caused by a wide variety of viruses, but the most
important are the hepatitis viruses A, B, C, D and E. Other viruses may
cause liver damage (Fig. 7.6) and hepatitis as part of their disease
spectrum-these include, cytomegalovirus (CMV), Epstein-Barr virus
Fig. 7.6: Liver in hepatitis
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(EBV), varicella—zoster virus (VZV), human immunodeficiency virus

(HIV), rubella virus, etc.
Hepatitis G virus (HGV) is another virus that has hepatotropic
effects, but cannot cause disease on its own.
HEPATITIS A
Of all the viruses, Hepatitis A virus (HAV) is the most prevalent
throughout the world and causes the most benign form of the disease.
It is an RNA virus, which is heat stable. It is a highly contagious virus,
causing acute hepatitis in man.
Incubation period: 2 to 3 weeks
Route of Transmission
Route of transmission is fecal-oral. It is transmitted via contaminated
food, water, especially sea food, improperly cooked foods, raw
vegetables and cut and exposed fruits and vegetables.
Viral shedding in the feces begins during the incubation period
before the patient becomes symptomatic, peaks with the onset of
symptoms and continues until approximately 2 weeks after the patient
shows symptoms. Hence, the patient is highly contagious before the
onset of symptoms and until the complete resolution of symptoms.
Pathology
HAV infection causes cytopathic injury to the liver cells. This results in
damage to the liver cells manifested as a rise in serum bilirubin levels
and also the liver enzymes being elevated—alanine aminotransferase
(ALT) and aspartate transaminase (AST). There is minimal obstruction
so, the enzymes related to the biliary ducts are normal or marginally
elevated. The elevated levels of enzymes return to normal at the end of
the active stage, but any increase or persistence of elevated ALT and
AST have poor prognosis.
Symptoms
• Malaise, lethargy
• Vomiting
• Pain abdomen
• Low grade fever
• Anorexia
• Nausea
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Infections 65
• Passing high-colored urine

• Diarrhea.
Signs
• Jaundice is noticeable usually after 1 week of the onset (Fig. 7.7) of
symptoms
• Mild hepatomegaly
• Spleen just palpable
• Dehydration in case of persistent and severe vomiting.
Investigations
1. Complete blood count—may show leukocytosis
Platelet counts normal.
2. ESR—elevated.
3. Urine examination—elevated bile salts and bile pigments.
Urobilinogen levels may be also elevated.
4. Total serum bilirubin—elevated (normal 0.4–1.2 mg/dl). Levels
mildly elevated in HAV infection.
Direct bilirubin—elevated, indicative of liver damage (normal up
to 0.4 mg/dl).
5. Liver enzymes—ALT and AST are elevated early in the course and
reduce to normal levels with subsidence of symptoms (normal AST
5–32 mU/ml or 10–40 units: ALT 7–33 mU/ml or 10–40 units).
6. Detection of anti-HAV IgM—indicates an acute infection (Fig. 7.8).
Done by radioimmunoassay or by PCR technique. Is a diagnostic
test for HAV infection.
Detection of anti-HAV IgG—is indicative of a past infection or HAV
vaccine administration.
7. Serum albumin—normal level (normal 3.5–5 g/dl).
8. Prothrombin time—normal level.
9. Ultrasound of abdomen—essential to rule out any other underlying/
associated liver pathology, ascites, spleen size, etc.
Fig. 7.7: Jaundice visible in the conjunctiva
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Fig. 7.8: Time interval for appearance of antibodies in Hepatitis A
Treatment
1. Isolate the patient’s personal belongings, as the virus is shed in stools
and patient is highly contagious.
2. IV fluids—in case of poor oral intake, persistent nausea, vomiting
and dehydration. Use dextrose containing solutions. Assess the
hydration status and calculate the requirements—usually
maintenance fluids are adequate.
3. In case patient is accepting adequate oral feeds, he can be managed
without IV fluids. Advise plenty of oral fluids, especially dextrose
containing.
4. Oral paracetamol—in case of fever, myalgias, etc. use 10 mg/kg/dose.
5. Oral multivitamins, as the absorption of the fat soluble vitamins
may be impaired.
6. Role of Liv 52—a herbal preparation, which is known to aid in
regeneration of liver cells, may be useful. Individual choice may
guide its usage.
Complications
1. Bleeding diathesis—due to malabsorption of the fat-soluble vitamins.
2. Cholestatic syndrome—rare. Due to persistence of viral
multiplication and duct obstruction. Resolves spontaneously, but
may persist for many months.
3. Acute liver cell failure—is rare with HAV infection. May occur in
immunocompromised and those with associated underlying liver
disease.
Prevention
Hepatitis A vaccine is available as an inactivated, immunogenic vaccine.
Recommended to children above 1 year age. Two doses to be
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Infections 67
administered, 6 to 12 months apart. Given deep IM into the anterolateral

thigh or into the deltoid muscle.
Prognosis
Usually good with HAV infection. No residual damage.
HEPATITIS B
Hepatitis B a more serious form of viral hepatitis.
It is caused by a DNA virus belonging to the hepadnaviridae group.
It is circular with a double stranded DNA and contains a surface or an
‘S’ (HBsAg) antigen and a core or ‘C’ (HBcAg) antigen. There is also a
non-structural ‘E’ (HBeAg) antigen, which is formed from the cleavage
of the B antigen. Its presence gives an indication of viral replication.
Hepatitis B has six genotypes, ranging from A to H, of which B and
C are the most widely found in Asia (Fig. 7.9).
This virus is transmitted by contact with body fluids like blood, serum,
semen, vaginal secretions, saliva, other body secretions, vaginal fluid,
etc (Fig. 7.10). Hence person-to-person transmission can occur after
contact with infected person’s saliva, by sexual contact, tattoos, injectable
drug users, after blood transfusion and during birth. Placental
transmission is known to occur in the fetus. The newborn may acquire
the virus during its passage through the vaginal canal and may test
positive for hepatitis B antigen in the newborn period. Breast feeding is
not known to cause an increased risk of disease transmission.
Incubation period- 1 ½ to 4 months.
Fig. 7.9: Hepatitis virus associations
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Fig. 7.10: Important routes of transmission of Hepatitis B virus
Pathogenesis
Hepatitis B virus is hepatotropic, but does not cause a direct cell necrosis.
The cell injury is immune mediated. After cell infection, the cells express
the viral antigens, especially HBcAg and HBeAg on the surface. The
MHC proteins in the cells combine with these antigens, making the
cells more susceptible to lysis by the T-cells. In this manner, the liver
cell destruction is immune mediated. This reaction varies in intensity—
it may be minimal giving rise to clinical features that may recover over
time, or cause a massive liver cell destruction resulting in acute liver
failure. There may also be a chronic carrier state that develops as the
lymphocytes are unable to recognize the MHC proteins along with the
viral antigen, resulting in a chronic infection in the tissues. This is
common with in utero or periuterine acquisition of the disease, in
neonates and infants.
Circulating immune complexes may be found to damage other organs
in the body, notably the kidneys, blood vessels, skin and blood cells.
Symptoms
• May be asymptomatic, as evidenced by a large number of HBsAg
positive carriers in the community
• Lethargy
• Myalgia
• Passing dark-colored urine
• Skin rash
• Joint pain.
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Infections 69
Signs
• Jaundice may or may not be visible, as in chronic carriers
• Hepatomegaly
• Splenomegaly
• Lymph node hypertrophy
• Increased tendon reflexes
• Altered sensorium
• The last two signs are indicative of a fulminant hepatic failure.
Associated Features
• Skin rash-papular, maculopapular, urticarial or purpuric
• Papular acrodermatitis—Gianotti-Crosti syndrome
• Arthralgia
• Membranous or membranoproliferative glomerulonephritis
• Polyarteritis nodosa
• Polymyalgia rheumatica
• Leukocytoclastic vasculitis
• Guillain–Barre syndrome.
Chronic carrier is one who remains HBsAg positive for over 6
months. The patient continues to carry the virus in his blood stream
and is highly contagious to others.
Understanding the antigen changes that occur during the course of
infection with hepatitis B virus is important to arrive at a correct
diagnosis of the state of the infected person.
1. Early in the course of infection, HBsAg and HBeAg are positive,
together with HBV DNA, which may be isolated via PCR technique
(Fig. 7.11). The HBeAg levels fall before the HBsAg levels, which
also reduce as the symptom reduce.
2. Elevated levels of ALT enzyme indicate the onset of symptoms.
Fig. 7.11: Time interval for appearance of antibodies in the serum
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3. Anti-HBc IgM—is present during the acute stage and indicates active
infection. It remains positive for several months.
4. Anti-HBc IgG—starts to rise towards the end of the symptomatic
period, but remains elevated for many years.
5. Anti-HBs—appears towards the time the anti-HBc levels begin to
fall. It indicates clinical recovery from disease.
6. Anti-HBe—rises later in the course of illness and marks a stage of
improvement, especially in chronic carriers.
Investigations
1. Complete blood count—anemia may be found. Leukocytosis,
usually lymphocytic. Platelets are usually adequate—reduced
levels indicate poor prognosis.
2. Peripheral smear—important to look for associated aplastic anemia.
3. CRP—usually elevated, as an acute phase reaction.
4. ESR—grossly elevated.
5. HBsAg level to be checked. If positive, indicative of infection, which
may be acute or chronic.
6. Anti-HBc IgM antibody—if positive, indicates an acute infection.
It rises early in the course and remains positive for many months,
hence is invaluable in diagnosis.
7. Liver function tests: elevated enzyme levels, especially ALT occurs
early in the course of the disease, serve as an indicator of the
progress of the disease in the child.
8. Serum albumin level—may be reduced in case of severe liver damage.
If grossly reduced, is a poor prognostic indicator. Normal: 3.5 to 5 g/dl
9. Prothrombin time: essential to estimate the liver functions in
production of coagulation factors.
10. Ultrasound abdomen—shows the extent of hepatomegaly,
splenomegaly, any associated lymph node enlargement, etc. Also
useful to pick up any associated renal damage, that can occur due
to the infection.
11. MRI scan—may be done to delineate the extent of liver damage, any
associated tumors, etc. It is not required as a routine investigation.
Treatment
No specific treatment available. Some measures which can be adopted
are:
1. Rest during the acute stage.
2. Fluid replacement—in case of evidence of dehydration, inadequate
oral intake, etc.
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Infections 71
3. Interferon alpha-2b has been proven to be beneficial in confirmed

cases of hepatitis B.
4. Refer to the gastroenterologist—who can follow-up the patient in
case of development of chronic carrier state and plan for further
management.
Complications
1. Chronic carrier
2. Acute fulminant liver failure
3. Hepatic encephalopathy
4. Hepatic fibrosis
5. Cirrhosis
6. Hepatocellular carcinoma
7. End-stage liver disease, etc. (Fig. 7.12).
Prevention
Prevention is the best way of curbing the spread of disease.
1. Isolate the patient’s personal belongings.
2. Avoid hugging, kissing and body contact, as infected serum may
transmit virus particles through small abrasions.
3. No needle sharing, sharing of toothbrushes, blades, razors and
stationery items.
4. In cases where the hepatitis B status is known, it is advisable to
administer passive immunization to the other family members.
Fig. 7.12: Clinical outcomes of acute HBV infection
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Administer hepatitis B immunoglobulin (HBIG). This provides

temporary protection for up to 3 to 6 months.
5. Always administer hepatitis B vaccine-recombinant vaccine,
alongside the hepatitis B immunoglobulin (HBIG). This provides
active immunity and long-term protection.
Dosage Schedule for Immunization

• Universal immunization:
Recommended three doses—0, 1, 6 schedule. Start first dose at birth.
Occasionally a fourth dose may be given at 12 months (Fig. 7.13).
• HBsAg positive mother:
At birth—administer HBIG plus HB vaccine, first dose Box. Follow-
up with two more doses at 1 and 6 month intervals.
• Contact with infected person:
At contact—administer HBIG plus HB vaccine, first dose, followed
by two more doses at 1 and 6 month intervals.
• Contact with contaminated blood, body fluids or sexual exposure:
At contact—administer HBIG plus HB vaccine, first dose followed
by two more doses at 1 and 6 month intervals.
Dosage of vaccine is given in Box 7.8.
BOX 7.8
Dosage of vaccine
< 19 year—10 microgram of Engerix B
> 19 year—20 microgram of Engerix B
Dose of HBIG—100 units in children
Adminster the HBIg and HB vaccine at different sites on the same day.
Fig. 7.13: Dosage schedule for immunization
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Infections 73
HEPATITIS C
Hepatitis C is caused by an RNA virus belonging to the Flaviviridae
family. There are several genotypes and subtypes of the virus, which
cause disease.
Hepatitis C is commonly transmitted via infected blood transfusion.
As the current screening trends for blood transfusion have improved,
this route of transmission of infection is uncommon. However, it can
be spread perinatally from an infected mother. The other routes of
transmission include shared syringes in drug abusers and via sexual
contact. In HIV-infected women, coinfected with hepatitis C virus
(HCV), the chance of transmission to the child is very high.
Incubation period: 2 weeks to 24 weeks.
Pathogenesis
Damages the liver cells through direct cell injury. Immune-mediated
injury is rare. HCV infection is commonly seen in chronic hepatitis
patients.
Symptoms
• Insidious onset of jaundice
• Mild symptoms
• Usually develop chronic infection.
Signs
• Icterus
• Usually chronic hepatitis
• Long-term morbidity common in these children.
Investigations
1. Liver function tests—shows elevated levels of AST, ALT, and total
serum bilirubin (TSB).
2. Urine—shows presence of bile salts and bile pigments.
3. Anti-HCV antibody levels—by enzyme immunoassay (EIA) tests.
Positive report indicates infection. However false negative report
may be due to the antibody becoming positive only after 3 months
of infection. It is useful to follow-up the patient during its chronic
course.
4. Ultrasound abdomen—to check for hepatic fibrosis, development
of hepatocellular carcinoma, and signs of acute liver failure.
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5. Serum alpha-fetoprotein (AFP) levels—to monitor development of

hepatocellular carcinoma.
Treatment
Supportive treatment only.
• Interferon treatment along with ribavirin is useful in adults, but not
recommended for use in children
• Avoid unnecessary drug usage in children
• Provide adequate nutrition
• Maintain adequate fluid balance
• Immunize with hepatitis A and hepatitis B vaccine to prevent
superinfection with these viruses, which may cause severe liver
disease
• Refer to pediatric gastroenterologist.
Complications
1. Hepatic fibrosis
2. Hepatic cirrhosis
3. Liver failure
4. Hepatocellular carcinoma.
These patients need to be followed up regularly, as they tend to
remain positive with HCV for long duration of time. Serial tests will
help to follow-up these patients. Viral clearing may be found after 3 to
6 months. Usually, clearing is common in children, who have less
associated comorbid conditions.
HEPATITIS D
Hepatitis D virus (HDV) is the smallest viral particle that causes infection
in man. It is considered as an incomplete virus, as infection by this
virus is not possible unless there is simultaneous infection with hepatitis
B virus. This is because the outer coat of the virus is composed of the
excess amount of HBsAg from the HB virus. This is because the virus is
incapable of producing the protein coat to cover the core antigen. Once
the hepatitis B infection is reduced, due to vaccination procedures, the
incidence of hepatitis D infection is naturally reduced. Hepatitis D
infection can be divided into two—coinfection and superinfection.
Coinfection: Infection of hepatitis D virus with simultaneous infection
with hepatitis B virus is called coinfection. The incubation period is the
same as that of HBV (1½ to 4 months).
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Infections 75
Superinfection: Infection with hepatitis D virus in a person already

infected with hepatitis B virus is called superinfection. (Incubation
period 2 to 8 week).
Pathogenesis
Hepatitis D virus causes damage to the liver cells by direct cytopathic
injury to the liver cells. The liver injury may be quite severe, resulting
in severe liver damage.
Symptoms
Same as for hepatitis B. However, the symptoms may be more severe.
Signs
Same as for hepatitis B, but more severe.
In case of coinfection, the acute symptoms and signs are more severe,
but the chance of developing chronic hepatitis is less. In superinfection,
acute illness is less, but the chance of developing chronic infection is
more.
Investigations
1. Liver function tests—abnormal.
2. Test to detect IgM Anti-HDV antibody by PCR, is available. If
positive, indicates HDV infection. If negative, does not rule out
infection with HDV. Always suspect HDV infection in patients who
are HBV positive with severe disease.
3. USG abdomen—to assess the liver status.
Treatment
• Supportive
• No specific treatment available
• Provide immunization against HBV in case of non-immunized
patient.
Complications
1. Chronic liver disease.
2. Acute liver failure.
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HEPATITIS E
Hepatitis E virus (HEV) an RNA virus. It causes epidemic outbreaks of
enterically transmitted hepatitis. Incubation period is 2 to 8 weeks.
Transmission of HEV infection occur via the fecal-oral route.
Pathogenesis
Cytopathic liver damage.
Symptoms
Symptoms are some as that of acute liver disease.
Signs
• Same as hepatitis A virus disease
• Causes severe disease in pregnant women
• May even cause fatal disease in them.
Investigations
1. Liver function tests—may be disordered.
2. HEV antibodies—IgM levels elevated within 7 to 10 days of infection.
Indicates acute, active infection.
3. HEV IgG antibodies—elevated later in disease.
4. Viral RNA particles—detected by PCR technique. Confirmatory of
infection with HEV.
Treatment
• Symptomatic.
• No specific treatment available.
Prevention
1. Improved personal hygiene.
2. Hand washing, strictly enforced.
3. Recombinant vaccine available for use in endemic areas.
4. No role of immunoglobulin in treatment.
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Infections 77
DENGUE FEVER
Dengue fever is a viral infection caused by the viruses of the family
Flaviviridae.The virus is transmitted by the mosquito bites, hence it is
a vector-borne disease (Fig. 7.14).
Etiology
Flaiviridae group of viruses have distinct antigenic types, of which at least
four types are known. Other related viruses of the family Flaviviridae
cause West Nile fever, which is also an arthropod-borne disease.
The virus is transmitted by the mosquito vector belonging to the
Stegomyia family. The carrying insect, the Aedes aegypti (Fig. 7.15) is a
Fig. 7.14: Virus transmission into the human host from the vector
Fig. 7.15: Aedes aegypti mosquito
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highly urbanized mosquito. It breeds in stagnant water collections in

urban areas, rainwater pools, ponds, storage water, cesspools and any
other water bodies that remain stagnant for long durations. They have
been shown to carry all the four antigenic variants of the virus.
Dengue outbreaks are common as epidemics in the temperate parts
of the world. It has become endemic in the tropical parts of the world
where mosquito breeding is facilitated due to the climatic conditions.
Antigenic response, in the body, occurs to the viral antigens.
Enhancing antigens in the body make the person more susceptible to
severe disease. Infants may be protected from disease by the maternally-
transmitted antibodies. Usually first infections are mild. First infection
provides immunity to the particular infecting serotype. Second infection
could result in massive antigenemia, which may manifest as dengue
hemorrhagic fever (DHF) or dengue shock syndrome (DSS) (Fig. 7.16).
This is related to antibody-dependent enhancement. Other factors have
been postulated to be important in the pathogenesis of DHF, including
viral virulence, host genetic background, T-cell activation, the viral
burden, and autoantibodies.
Early in the course of infection, there is complement activation. The
levels of C1q,C3, C5 to C8, and C3 proactivators are reduced while the C3
catabolic rates are elevated. All factors interact to produce increased
vascular permeability, resulting in the leakage of fluid, electrolytes,
proteins and sometimes the red blood cells leaking into the extracellular
spaces. This redistribution of fluids, together with the ongoing fluid loss
due to the associated vomiting and poor oral intake, lead to electrolyte
imbalance, hypovolemia, hemoconcentration and metabolic acidosis.
Fig. 7.16: The extent of viremia indicates the disease severity
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Infections 79
Fig. 7.17: Transient skin rash in dengue fever
Dengue hemorrhagic fever is an extremely severe form of the viral

infection. There is sudden deterioration and drop in the blood platelet counts,
which can cause sudden massive hemorrhage in any organ and result in
immediate collapse and death. It occurs in non-immune individuals and
also when there is infection with multiple antigenic strains of the virus.
Symptoms
• Incubation period 1 to 7 days
• Fever which may be moderate to high degree, lasting 1 to 3 days.
Follows a biphasic or humpback pattern
• Associated with severe retro-orbital or frontal pain especially with
application of pressure over the region
• Associated rhinitis, sore throat, cough may occur
• Severe back pain may precede the onset of fever (back-break fever)
• Transient rash (Fig. 7.17) maculopapular seen in the first 24 to 48
hours of fever
• Nausea, vomiting, usually later in the course of the disease
• Anorexia
• Followed by 1 to 2 days of defervescence
• Rash, maculopapular seen on the trunk and limbs. Reduces in 1 to 4
days, followed by desquamation
• Slight increase in temperature noted along with the appearance of
the skin rash.
Signs
• Moderate to high degree fever up to 104 to 106°F
• Skin rash, initially transient, that blanch on pressure. Maculopapular
not associated with itching, more on the trunk. Usually spares the
palms and soles
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• Severe back pain.

• Retro-orbital pain increased on pressure
• Altered taste sensations
• Cutaneous hyperesthesia
• Generalized lymphadenopathy
• In dengue hemorrhagic fever, there occurs, spontaneous bruising,
petechiae, bleeding from the site of venipuncture, circumoral pallor,
peripheral cyanosis, with cold, clammy extremities. The pulse is
thready, rapid and heart sounds appear faint. The respirations are
shallow, rapid and labored. The child may appear unduly drowsy.
If this crisis period is rapidly volume-corrected, the child responds
with a rapid recovery.
Investigations
1. Complete blood count: May show anemia, in case of bleeds. Is a
good way to monitor the likelihood of occurrence of internal
bleeds.
Pancytopenia common after 3 to 4 days of fever. Total count is
below 2000 to 3000/cu mm and may remain so even during
convalescence.
Thrombocytopenia is a hallmark of dengue fever and dengue
hemorrhagic fever. Counts are usually found below 100,000/cu mm
2. Hematocrit over 20 percent indicates likelihood of dengue shock
syndrome.
3. Bleeding time—within normal range (1–4 min, Duke method).
4. Clotting time—within normal range (6–8 min, Lee-White method).
5. Prothrombin time—usually within the normal range with regard
to the control. However, in case of severe disease, the levels may
be less than 40 percent of the control (12–14 sec Quick method).
6. INR (international normalized ratio)—is a standardization for
prothrombin time from different laboratories. Gives an indication
of the likelihood of bleeding (Normal 1–1.2%).
7. Fibrinogen level—reduced.
8. Fibrin split Products (FSP)—elevated (Normal < 10 microgram/
ml).
9. Serum electrolytes: Sodium levels may be reduced due to
hyponatremia (135–145 mEq/L).
Chloride levels—may be reduced especially with associated
metabolic acidosis.
10. Blood urea nitrogen—may show slight elevation. Normal 10 to 20
mg/dl.
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Infections 81
11. Serum albumin—may be reduced, due to extravasation of proteins

into the tissues (Normal 3.5 to 5 g/dl).
12. Chest X-ray—presence of bilateral pleural effusion, especially with
dengue shock syndrome (DSS).
13. Electrocardiogram—shows sinus bradycardia, prolonged PR
interval and ventricular ectopics.
14. Ultrasound of the abdomen—hepatomegaly seen in DSS. Peritoneal
fluid collection may be noted in severe cases.
15. CT of brain—rarely required. In case of suspected intracranial
bleeds.
16. Virus isolation—At present, the three basic methods used by most
laboratories for the diagnosis of dengue virus infection are
a. viral isolation and characterization
b. detection of the genomic sequence by a nucleic acid
amplification technology assay and
c. detection of dengue virus-specific antibodies.
After the onset of illness, the virus is found in serum or plasma,
circulating blood cells and selected tissues, especially those of the
immune system, for approximately 2 to 7 days, roughly corresponding
to the period of fever. At this time, virus isolation is relatively easier, if
suspected.
Virus isolation by cell culture and from mosquitoes remain the ‘gold
standard’. This has however been replaced by the RT-PCR as a rapid
diagnostic test.
Treatment
1. Bed rest—in case of dengue fever helps to keep the child comfortable
during the acute febrile stage.
2. Antipyretics—paracetamol 15 mg/kg in three to four divided doses
will keep the temperature under control, especially with high grade
fever.
3. Oral hydration—when the child is able to accept and retain the oral
fluids.
In case of DHF/DSS, rapid intravenous fluids are required to correct
the intravascular dehydration. Treat the child as a case of severe
dehydration and administer electrolyte containing fluids rapidly.
Normal saline infusions are preferred to Ringer’s lactate.
4. In cases of hypotension with labored breathing, administer plasma
or other colloid solutions. Indicated when serum albumin remains
low despite fluid replacement continued, elevated hematocrit or with
a wide pulse pressure more than 20 mm Hg.
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5. Transfusion with platelets—when the blood tests show thrombo-

cytopenia. Dose 10 ml/kg.
6. Sedation with chloral hydrate or paraldehyde—when the child is
agitated or restless.
Complications
• Rare in uncomplicated dengue fever
• Febrile convulsions during high grade fever may occur in young
children
• Epistaxis, purpuric bleeds and ecchymosis may occur at any stage
during the illness
• During recovery, ventricular extrasystoles may occur
• Fatality may occur in case of DHF and DSS.
Prognosis
Depends on the immune status of the child at the time of infection.
First infections are usually mild.
In case of DSS and DHF, the rapidity of fluid replacement and
electrolyte correction guides the prognosis. If rapid correction is
achieved, the child recovers and progresses back to normal.
Massive GIT bleeds, or intracranial bleeds carry a poor prognosis.
Prevention
Prevention of infection is basically related to avoidance of mosquito
bites. Use of personal protection and mosquito repellants and steps
taken to reduce and clear out the mosquito breeding areas will help to
reduce disease transmission by eradicating the vector.
At all times of likely mosquito exposure, it is advised to wear
protective clothing that will reduce the likelihood of mosquito bites.
Ultimately eradication of mosquito vectors will help to completely
eradicate the disease (Fig. 7.18).
Fig. 7.18: Complete eradication of mosquito vectors recommended
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Infections 83
FURTHER READINGS
Typhoid in Children
1. Anju Sinha, Sunil Sazawal, Ramesh Kumar, et al. Typhoid fever in children
aged less than 5 years: Lancet. 1999 28;354(9180):734-37.
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study. NIMHANS Journal 1990; 8:111-26.
3. Gulati S, Marwaha R, Singh S, et al. Ciprofloxacin in children with enteric
fever due to multi-drug resistant. S. Typhi 1992 Abst. TB/24, Abstract Booklet
of 29th The National Conference of Ind Aad Ped, Nagpur. 103.
4. Gupta BL, Bhujwala RA, Shriniwas. Multi-resistant Salmonella Typhi in India.
Lancet 1990;336:252.
5. Jesudasan MV, Jacob John T. Multi-resistant Salmonella Typhi in India. Lancet.
1990;336:252.
6. John A Crump, FouadG, Youssef Stephen P, et al. Estimating the incidence of
typhoid fever and other febrile illnesses in developing countries: Emerging
Infectious Diseases:2003:9(5):539-44.
7. Kanungo S, Dutta S, Sur D. Epidemiology of typhoid and paratyphoid fever
in India. J Infect Dev Ctries. 2008 1;2(6):454-60.
8. Kathryn M, Edwards. Vaccination against typhoid after natural disease:
Medscape.
9. Liging Zhou, Andrew J Pollard. A fast and highly sensitive blood culture PCR
Method for clinical detection of Salmonella enteric Serovar Typhi.Ann Clin
MicrobiolAntimicrob 2010:9(1):14.
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fever in children. Ind J Child Health. 1959;8:273.
11. Osuntokun BO, Bademosi O, Ogunremi K, et al. Neuropsychiatric
manifestations of typhoid fever in 959 patients. Arch Neurol. 1972;27:7-14.
12. Pohwala J, Ghai OP. Typhoid fever. Neurological complications quoted by
Udani. Ind J Child Health. 1957;25.
14. Sharma A, Ghathwala G. Clinical profile outcome in enteric fever. Ind Pediat
1993;30:47-50.
15. Sinha A, SazawalS,Kumar R, et al. Typhoid fever in children aged less than
five years: Lancet 1999:354:734.
16. Taneja PN, Sood SC. Typhoid Fever. Role of corticosteroids and ACTH in
treatment. 1957;6:123-31.
17. Udani PM. Typhoid fever in Textbook of Pediatrics with special references to
problems of child health in developing countries. Ed. PM Udani, Pub. Jaypee
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18. Verma PS, Malik P, Ghosh S. Neurological manifestations of enteric fever, clinical
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Tuberculosis in Children
1. API Consensus Expert Committee API TB Consensus Guidelines 2006:
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Viral Hepatitis in Children

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15. Previsani N, Lavanchy D. World Health Organization. Hepatitis B (WHO/
CDS/CSR/LYO/2002.2). 2002;[Full Text].
16. Previsani N, Lavanchy D. World Health Organization. Hepatitis C (WHO/
CDS/CSR/LYO/2003.). 2002;[Full Text].
17. Previsani N, Lavanchy D. World Health Organization. Hepatitis D. (WHO/
CDS/CSR/NCS/2001.1). 2001;[Full Text].
18. Previsani N, Lavanchy D. World Health Organization. Hepatitis E. (WHO/
CDS/CSR/EDC/2001.12.). 2001;[Full Text].
20. Salama II, Samy SM, Shaaban FA, et al. Seroprevalence of hepatitis A among
children of different socioeconomic status in Cairo. East Mediterr Health J
2007;13:1256-64.
21. Velu V, Saravanan S, Nandakumar S, et al. Transmission of "a" determinant
variants of hepatitis B virus in immunized babies born to HBsAg carrier
mothers. Jpn J Infect Dis 2008;61:73-76.
22. Wasley A, Grytdal S, Gallagher K. Surveillance for acute viral hepatitis-United
States, 2006. MMWR Surveill Summ. 2008;57:1-24.
23. Wasley A, Grytdal S, Gallagher K. Surveillance for acute viral hepatitis-United
States, 2006. MMWR Surveill Summ. 2008;57(2):1-24. [Medline]. [Full Text].
24. Williams I, Wasley A, Darling N, et al. Hepatitis A vaccination coverage among
children aged 24-35 months-United States, 2004-2005. Morb Mortal Wkly Rep.
2007;56:678-81.
25. www. medscape.com
26. www. uptodate.com
Dengue Fever
1. A Trout, G Baracco, M Rodriguez, et al. Locally Acquired Dengue-Key West,
Florida, 2009-2010. Morbidity & Mortality Weekly Report. 2010;59(19):577-81.
2. CDC. Dengue fever at the US-Mexico border, 1995-1996. MMWR 1996;45:841-44.
3. CDC. Dengue hemorrhagic fever-US-Mexico border, 2005. MMWR
2007;56:785-89.
4. CDC. Underdiagnosis of dengue-Laredo, Texas, 1999. MMWR 2001;50:57-59.
5. Effler PV, Pang L, Kitsutani P, et al. Dengue fever, Hawaii, 2001-2002. Emerg
Infect Dis. 2005;11:742-49.
6. Freedman DO, Weld LH, Kozarsky PE, et al. Spectrum of disease and relation to
place of exposure among ill returned travelers. N Engl J Med. 2006;354:119-30.
7. Gibbons RV, Vaughn DW. Dengue: an escalating problem. BMJ. 2002;324:1563-66.
9. Wilder-Smith A, Schwartz E. Dengue in travelers. N Engl J Med. 2005;353:924-32.
vip.persianss.ir
Gastroenteritis
8
Gastroeneteritis is the inflammation of the musous membrane of the

stomach and intestines, manifesting as diarrhea, nausea and vomiting.
DIARRHEA
Definition
Frequent passage of watery stools, over four to five times per day for
about 2 to 3 days is defined as diarrhea. It may be associated with other
symptoms like fever, pain in abdomen, vomiting, etc.
Common Causes of Diarrhea

1. Bacterial causes: Escherichia coli, Shigella, Salmonella, are the common
organisms.
2. Viral causes: Rotavirus, enterovirus, adenovirus are some of the agents
that can cause symptoms.
3. Parasitic causes: Helmenths, especially roundworms, pinworms, etc.
4. Drug–induced causes: Some drugs like co-amoxyclav, macrolides,
cephalosporins may be the cause for frequent loose stools.
5. Systemic Causes: Underlying pneumonia, appendicitis, any other
systemic infection, etc.
Figure 8.1 shows the common etiology of gastroenteritis.
Of all the viral particles causing diarrhea in children, the rotavirus
(Fig. 8.2) causes the most severe symptoms and high degree of
dehydration requiring urgent medical care.
Pathophysiology of Rotavirus Diarrhea (Fig. 8.3)

As can be seen from the above figure, rotavirus causes disease by various
mechanisms. The net result is severe gastroenteritis in children.
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Gastroentritis 87
Fig. 8.1: Common etiology of gastroenteritis
Fig. 8.2: Electron microscope view of rotavirus particle
Symptoms of Rotavirus Diarrhea

• Frequent passage of watery stools
• Associated with pain in abdomen, vomiting
• May be associated with passage of blood and mucus in the stools
• Fever associated may be indicative of an infective pathology
• Severe and persistent vomiting usually associated with rotavirus
diarrhea in children
• Decreased urination or not passed urine for over 4 to 5 hours.
Signs of Rotavirus Diarrhea

General condition of the child: Alert, active, appears to be thirsty, etc.
Eyes: Moist/Dry
Tongue: Moist/Dry—early indicator of dehydration
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Fig. 8.3: Pathophysiology of rotavirus diarrhea
Skin turgor: By pinching the skin fold of the child over the abdomen or
the upper arm and let go, the skin fold should return immediately. Any
persistence of tenting is indicative of dehydration and requires urgent
and immediate rehydration.
Per abdomen: Check for tenderness, which could be generalized in
gastroenteritis. Localized tenderness should make one aware of the
possibility of underlying pathology.
Respiratory system (RS): To rule out any systemic respiratory infection,
etc.
Central nervous system (CNS): Mental status needs to be assessed. Any
evidence of drowsiness or altered mental status is an indicator for
immediate rehydration which needs to be instituted.
Assessment of Dehydration (Table 8.1)
No Dehydration
Early in the course of the disease, the child may be seen without any
dehydration. However, the child may rapidly progress to dehydration
in case of persistent diarrhea and vomiting. Hence, the child needs to
be periodically reassessed and the parents need to be informed about
the danger signs.
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Gastroentritis 89
Table 8.1: Clinical Criteria for Assessing Severity of Dehydration

Particulars Mild (3%–5%) Moderate (6%–9%) Severe (> 10%)
Mental status Well Ill appearing Lethargic, toxic
Heart beat Normal/Increased Increased Marked tachycardia
Breathing Normal Increased Increased, deep
Pulse Normal Normal-decreased Poor quality
Capillary refill Normal (< 2 sec) Normal/Slightly Markedly prolonged
prolonged
Perfusion Warm Cool Cool, mottled
Blood pressure Normal Normal Hypotension
Eyes Normal Slightly sunken Very sunken
Tears Normal Decreased Absent
Mucous Moist Sticky Very dry
membranes
Skin turgor Normal recoil Delayed (> 2 sec) Very delayed
Urine output Normal/Slight Decreased Minimal/Absent
reduction
Danger Signs
• Reduced alertness, drowsiness
• Thirsty all the time
• Persistent vomiting—unable to accept/retain oral fluids
• Not passed urine for over 5 to 6 hours
• Persistent severe diarrhea.
Mild Dehydration (1 to 6% loss of body fluid)

• Eyes and tongue are dry. Extremities are warm with normal capillary
refill
• Pulse, BP, heart rate normal
• Skin turgor normal. Urine output normal/slightly reduced
• Accepts ORS and other oral fluids and feeds
• Treatment—ORS, other oral fluids and solids recommended.
Moderate Dehydration (6 to 9% loss of body fluid)

• Eyes and tongue are dry. Delayed capillary refill in extremities
• Skin turgor lost. Anterior fontanelle sunken
• Rapid low-volume pulse. BP normal, pulse rate increased
• Urine output reduced
• May or may not appear drowsy
• Accepts ORS but may vomit/pass loose stools immediately in large
amounts
• Requires intravenous (IV) fluids and observation.
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Severe Dehydration (9 to 12% loss of body fluid)

• Eyes and tongue are dry. Cold mottled peripheries
• Skin turgor absent. Skin-fold tenting seen
• Rapid thready pulse. BP low, tachycardia, cyanosis and sometimes
hyperpyrexia
• Reduced/Absent urine output
• Appears obtunded and drowsy or comatose.
• Needs immediate and rapid rehydration with IV fluids.
Algorithm to follow While Treating a Child with Diarrhea
Eyes  Moist  No/Mild Dehydration

 Dry  Dehydration Present
Tongue  Moist  No/Mild Dehydration

 Dry  Dehydration Present
Skin Turgor  Normal  No/Mild Dehydration

 Reduced  Dehydration—Moderate/Severe
Mental Status Alert  Severe Dehydration Ruled Out

 Drowsy  Severe Dehydration/Electrolyte Imbalance
Vomiting  Occasional  May/May not Need IV Fluids

 Persistent  Need IV Fluids
Accepts Oral Feeds  Yes  May Not Need IV Fluids

 No  Need IV Fluids
 Good  Mild—Moderate Dehydration
Urine Output
 Reduced/Absent  Severe Dehydraton and
Needs Rapid Rehydration
Investigations
1. Complete blood count (CBC), C-reactive protein (CRP), Erythrocyte
sedimentation rate (ESR): Indicates possibility of bacterial/viral
infections.
2. Stool exam: routine examination to look for the presence of pus cells
which would give a clue to bacterial infection, presence of helminths,
etc.
Test to check whether rotavirus is positive
Culture and sensitivity test—gives an accurate indication of a
bacterial infection. Normally 48 hours is required for report.
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Gastroentritis 91
3. Serum electrolytes: Sodium, Potassium, Chloride and Bicarbonate –

which could be of help for guiding the fluid management. Normal
levels:Serum sodium (135–145 mEq/L), Serum potassium (3.5–5.0
mEq/L)
4. Blood Urea and Creatinine: To be done only if more than 5 percent
dehydration is assessed. BUN (Blood urea nitrogen) 20–40 mg/dl,
Serum Creatinine (0.5—1.3 mg/dl)
5. Urine examination: include is specific gravity
6. Blood gases: to determine acidosis, in case of sever dehydration.
7. Ultrasound Abdomen: To rule out any intra-abdominal pathology
associated.
Treatment
Oral rehydration solution (ORS) is the mainstay in the treatment of
gastroenteritis.
Dosage 10 ml/Kg for each watery or loose stool passed.
If the child is able to accept and retain orally, ORS must be advocated
immediately. It is also recommended that children who are given IV
fluids may simultaneously be offered oral feeds (see Fig. 8.4).
Oral rehydration solution (ORS) was the major breakthrough in the
1970s which reduced the diarrheal deaths in children considerably.
Composition of ORS
Standard ORS recommended by WHO has the following constituents
(Table 8.2).
Fig. 8.4: Oral feeds of ORS
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Table 8.2: Composition of ORS recommended by WHO

Molecule/Ion Standard ORS solution (mEq or mmol/L)
Glucose 111
Sodium 90
Chloride 80
Potassium 20
Citrate 10
Osmolarity 311
However, it was found that by using a solution with reduced

osmolarity, the results seen in children was much better. Hence, the reduced
osmolar ORS (Table 8.3) has been formulated and recommended in
children.
Advantages of Reduced Osmolar ORS

1. Reduced stool output by 25 to 30 percent.
2. Reduced vomiting by 30 percent
3. Reduced requirement for IV therapy by > 30 percent.
In case of non-availability of ORS sachets, homemade ORS is advised.
This is a sugar-salt solution that can be prepared as follows (Fig. 8.5):
• 8 level teaspoons of sugar
• 1 level teaspoon of salt
• 1 liter of clean drinking water.
Mix all the ingredients. If possible, add ½ orange juice to improve
the palatibilty.
Alternative fluids that may be administered during gastroenteritis:
1. Tender coconut water
2. Weak tea
3. Fresh fruit juice
4. Rice gruel
Intravenous Fluids
Required to replace the accumulated losses and to compensate ongoing
fluid losses
Table 8.3: Composition of Reduced Osmolar ORS
Reduced osmolar ORS gram/liter Reduced osmolar ORS mmol/liter
Sodium chloride 2.6 Sodium 75

Glucose, anhydrous 13.5 Chloride 65
Potassium chloride 1.5 Glucose, anhydrous 75
Trisodium citrate, dihydrate 2.9 Potassium 20
Citrate 10
Total Osmolarity 245
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Gastroentritis 93
Fig. 8.5: Homemade ORS solution
Deficit Correction
In Severe Dehydration: Rapid infusion of fluids with electrolytes: 20 ml/
kg over half an hour to 1 hour. Recommended Ringer’s lactate or normal
saline. Do not use dextrose containing fluids.
Reassess the patient’s condition. May repeat 20 ml/kg boluses until
BP, pulse and perfusion return to normal. Watch for urine output.
Then calculate the fluid requirement as follows:
Deficit correction is done using the uncorrected body weight,
depending on the extent of dehydration. This is corrected along with
the maintenance requirement over the next 12 to 24 hours.
In case of hypertonic dehydration, the correction is done over 24
hours. Fluid used during resuscitation is to be deducted from this.
For Maintenance Therapy
0 to 1 year: 120–150 ml/kg/24 hours
Above 1 year: First 10 kg: 100 ml/kg/24 hours
Next 10 kg (10 to 20 kg) : 1000 ml + 50 ml/kg/day
Subsequent kg (> 20 kg) : 1500 ml + 20 ml/kg/day
Divide the entire fluid requirements into two parts. The first part
correction should be completed in the first 12 hours, after which the
child must be reassessed. The remainder fluid is for the ongoing losses
and must be administered over the next 12 hours. After 24 hours,
reassess the patient.
After the patient has passed urine, 10 mmol of KCl/500 ml may be
added to the fluid (Table 8.4).
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Table 8.4: Types of Fluids for Infusion

Fluids Na+ Cl- K+ Ca2+ Lactate
Normal Saline (NS) 154 154

½ Normal Saline 77 77
(0.45% NaCl)
Ringer’s Lactate 130 109 4 3 28
0.2% Normal Saline 34 34
Maintenance fluids usually contain 5 percent dextrose (D5), which

provides 17 calories/100 ml and nearly 20 percent of the daily caloric
needs. This is enough to prevent ketone production and helps to minimize
protein degradation. However, prolonged treatment with this regimen
will result in weight loss and hence, early introduction of oral feeds/TPN
(total parenteral nutrition) wherever indicated, is recommended.
Maintenance Fluids
Children typically receive either D5 ½ NS + 20 mEq/L KCl or D5 0.2 NS
+ 20 mEq/L KCl. The other maintenance fluids like isolyte P, etc. consist
of 1/5 DNS with potassium and sodium, hence the need for extraneous
potassium is avoided.
Types of Dehydration based on Electrolyte Imbalance (Fig. 8.6)
Isotonic Dehydration
The loss of fluids and electrolytes is proportional, hence rehydration
may be done with electrolyte containing fluids as mentioned before.
Fig. 8.6: Child with diarrhea, dehydration and pain abdomen
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Gastroentritis 95
This normally occurs with continued loose stools and vomiting, wherein
the child has been fed with regular electrolyte solutions. Serum sodium
levels are within the normal range.
Hypertonic Dehydration
In this condition, the loss of fluid is more than the loss of electrolytes
hence in the body, level of electrolyte is high. Serum sodium levels are
elevated well above the normal upper range of 140 mEq/L, usually over
150 mEq/L. This occurs in cases where the child with gastroenteritis
has been fed hyperosmolar ORS or homemade ORS, where the salt
levels are more than normal. It may also occur when the child has
received concentrated formula milk feeds. On examination, the child
appears lethargic, dry tongue and seems thirsty. Skin turgor has a
doughy feel and urine output may be reduced. The anterior fontanelle
may be bulged. The child needs to be rehydrated with IV fluids, but
avoid the use of hyperosmolar fluids. Use ½ normal saline, until the
serum sodium level falls below 150 mEq/L then change over to 0.18
and normal saline. Do a slow fluid correction over 48 hours. The rate of
fall of sodium should be not more than 10 mmol/L/24hours.
Complication: Due to the hyperosmolar cellular milieu, the patient is in
potential danger of developing intracranial hemorrhage. Hence seizures
may occur as complication and needs to be actively prevented. During
rehydration, cerebral edema may be a complication due to rapid
reduction in serum sodium levels.
Hypotonic Dehydration
In this condition, the loss of electrolytes is more than the loss of fluids.
Hence, there is a state of fluid overload in the cells. The child may not
appear thirsty, but the eyes may be dry, skin turgor could be normal.
Serum sodium is below the normal range of 125 to 140 mEq/L. This
occurs when the child has been given very dilute ORS in large quantities,
or hypotonic IV fluids in large amounts and rapidly. Gradual
rehydration with electrolyte containing solutions is indicated.
Na+ deficit (mmol) = (desired Na+ level – measured Na+ level) × 0.6 ×
bodyweight in kg.
Replace volume with ½ normal saline with 5 percent dextrose.
Complications: The patient is in potential danger of developing cerebral
edema and seizures due to this.
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Acidosis
Causes: Dehydration, infection, shock, starvation and gastrointestinal
losses.
Usually mild and corrects with the fluid correction. However,
sometimes in sick children, soda bicarb needs to be administered.
Ideally, blood gas analysis needs to be done before administration.
Bicarb for correction = 1/3 × base deficit × body weight in kg.
Repeat blood gas analysis after half the amount has been administered.
Feeding in Gastroenteritis
1. Continue breastfeeds.
2. Formula feed may be given once the vomiting has stopped. No need
to change formula unless intolerance is proved.
3. Soft solid diet to be recommended, including rice, potato, lean meat
fruits like apple, pomegranate, banana, cereals and vegetables.
4. Avoid fatty and sugary foods.
5. Malnourished and low birth weight babies are at further risk of losing
weight, hence early institution of oral feeds is recommended.
Drugs in Gastroenteritis
Antidiarrheal drugs are not recommended.
Antiemetics may be administered in case of persistent uncontrollable
vomiting. Domperidone (1mg/kg) is the recommended drug. Currently,
ondansetron has been found to be the preferred drug to use in children
with persistent vomiting. The vomiting usually settles with 1 to 2 doses
of the medication and seldom requires to be continued for maximum
of 3 to 4 days.
Dose: orally: < 0.3 m2 : 1 mg/dose
0.3–0.6 m2 : 2 mg/dose
0.6–1 m2 : 3 mg/dose
2
>1m : 4 mg/dose
Parenteral dose: IV: 0.15 mg/kg/dose. Dose may be repeated every 8th
hourly, as required.
Probiotics
Play a role especially in viral diarrhea and antibiotic-induced diarrhea
in reducing the volume of stool, frequency of stool, and help with
digestion of ingested food.
Lactobacillus sps is useful in infective diarrheas, while the
Saccharomyces sps are of value in antibiotic-induced diarrhea.
vip.persianss.ir
Gastroentritis 97
Antibiotics (Rarely used)

Recommended only in case of dysentery or bacterial diarrhea, proved
by culture (blood and mucus in stool)—usually Salmonella, Campylo-bacter
or E. Coli diarrhea. Drug of choice: Cefixime once daily (10 mg/kg) for
5 days is adequate.
In case of Giardiasis and amoebiasis, Metronidazole is the drug of
choice for 7 to 10 days.
Prognosis
Good, adequate and rapid fluid correction is the mainstay of treatment
in gastroenteritis.
Counseling regarding hand hygiene, cleanliness, food preparation
and storage are recommended to prevent recurrence of gastroenteritis.
FURTHER READINGS
1. Alfredo Guarino, Andrea Lo Vecchio, Roberto Berni Canani. Current Opinion
in Gastroenterology. 2009;25(1):18-23.
2. Bass ES, Pappano DA, Humiston SG. Pediatr. Rev. Rotavirus. 2007;28(5):183-91.
3. Bernstein DI: Rotavirus overview. Pediatr. Infect Dis. 2009;28(Suppl.3):550-53.
4. Elliott EJ: Acute gastroenteritis in children. BMJ. 2007;334(7583):35-40.
5. Freidman JN, Goldman RD, Srivastava R, et al. Development of a clinical
dehydration scale for use in children between 1 and 36 months of age.
Pediatrics. 2004;145:201-7.
6. Goldman RD, Freidman JN, Parkin PC. Validation of the clinical dehydration
scale for children with acute gastroenteritis. Pediatrics. 2008;122:545-9.
7. Gorelick MH, Shaw KN, Murphy KO. Vaildity and reliability of clinical signs
in the diagnosis of dehydration in children. Pediatrics. 1997;99:E6.
8. King C, Glass R, Bresee J, et al. Managing acute gastroenteritis among children.
Oral rehydration, maintenance, and nutritional therapy. MMWR
Recommendations and Reports. 2003;52(RR16):1-16.
9. King CK, Glass R, Bresee JS, et al. For the Centers for Disease Control and
Prevention: Managing acute gastroenteritis.
10. Leung AK, Robson WL. Pediatrics Child Health. In children with vomiting
related to acute gastroenteritis, are antiemetic medications an effective adjunct
to fluid and electrolyte therapy? Part A: evidence-based answer and summary.
2008;13(5):391-4.
11. Levine DA. Current opinion in Pediatrics. Antiemetics for acute gastroenteritis
in children. 2009. (Epubahead of print).
12. Malek MA, Curns AT, Holman RC et al. Pediatrics. Diarrhea- and rotavirus-
associated hospitalizations among children less than 5 years of age: United
States: 2006;117(6):1887-92.
13. Matty de wit AS, Marion PG, Laetitia Kortbeek M, et al. Gastroenteritis in
Sentinel General Practices, the Netherlands. National Institute of Public Health
and the Environment, Bilthoven, the Netherlands. Emerging Infectious
Diseases. 2001;7(1) [© 2001 Centers for Disease Control and Prevention (CDC)].
vip.persianss.ir
14. Nelson Textbook of Pediatrics 18th Edition.

15. Ozuah PO, Avner JR, Stein RE. Oral rehydration, emergency physicians, and
practice parameters: a national survey. Pediatrics. 2002;109(2):259-61.
16. Ozuah PO, Avner JR, Stein RE. Oral rehydration, emergency physicians and
practice parameters: a national survey. Pediatrics 2002;109:259-61.
17. Parashar UD, Hummelman EG, Bresee JS, et al. Global illness and deaths
caused by rotavirus disease in children. Emerg. Infect. Dis. 2003;9(5):565-72.
18. Payne DC, Staat MA, Edwards KM et al. Pediatrics. Active, population-based
surveillance for severe rotavirus gastroenteritis in children in the United States.
2008;122(6):1235-43.
19. Practice parameter: the management of acute gastroenteritis in young children.
American Academy of Pediatrics Provisional Committee on Quality Improvement,
Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-36.
20. Szajewska H, Setty M, Mrukowicz J, et al. Probiotics in gastrointestinal diseases
in children: Hard and not-so-hard evidence of efficacy. Pediatr. Gastroenterol
Nutr. 2006;42:454-75.
21. Van Niel CW, Feudtner C, Garrison MM, et al. Pediatrics. Lactobacillus therapy
for acute infectious diarrhea in children: A meta-analysis. 2002;109:678-84.
22. Vreeman RC. Pediatric health. Role of Antiemetic Drugs for the Treatment of
Acute Gastroenteritis in Children. 2009;3(4):337-341.
23. Wendy L. Woolley; John H. Burton. Pediatric health. Pediatric Acute
Gastroenteritis: Clinical Assessment, Oral Rehydration and Antiemetic
Therapy. 2009;3(2):191-7.
vip.persianss.ir
Juvenile Rheumatoid Arthritis 99
Juvenile Rheumatoid
9 Arthritis
Juvenile rheumatoid arthritis (JRA) is a common childhood disease. It

primarily involves the joints and causes a chronic joint disability. It
usually affects the peripheral joints and is associated with joint pain,
effusion, swelling and synovitis. JRA may involve the extra-articular
areas giving rise to systemic symptoms and disease.
Types of Juvenile Rheumatoid Arthritis (Fig. 9.1)
Pauciarticular JRA
Involving four or less than four joints.
Polyarticular JRA
Involving five or more joints.
Systemic Onset JRA
Arthritis associated with systemic manifestations.
Criteria for Diagnosis of Juvenile Rheumatoid Arthritis

1. Age below 16 years.
2. Arthritis associated with joint pain, swelling, limitation of range of
movement, increased local heat.
3. Oligoarticular/pauciarticular type involving less than or equal to
four joints.
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Fig. 9.1: Types of juvenile rheumatoid arthritis
4. Polyarticular type involving greater than or equal to 5 joints.

5. Systemic onset disease with fever and extra-articular involvement.
6. Absence of any other cause of the arthritis.
Causes of Juvenile Rheumatoid Arthritis

1. Genetic susceptibility to disease: Increased incidence associated
with—Human leukocyte antigen (HLA-DR 4), HLA-DR 5 and HLA-
DR 8 variants.
2. External trigger factors, such as viral infections with epstein-barr
virus EBV, parvovirus B19, rubella virus, etc. altered immunogenicity
to self-antigens, increased reactogenicity of T-cells and B-cells to
antigens.
3. Recurrent trauma to the joint can be considered a possible cause.
Pathogenesis
T-cell activation and recruitment into the synovium occurs due to altered
antigen recognition. This results in widespread proliferation of the
T-cells causing inflammatory changes, synovial thickening, with
hypertrophy and hyperplasia of the villous surface of the synovium
and edema in the subsynovial tissues. Mononuclear and plasma cells
infiltration may occur in the vascular endothelium.
T-cell activation results in a cascade of events leading to tissue
damage in joints and other affected tissues, including B-cell activation,
complement consumption and immune-complex formation, and, in
particular, release of tumor necrosis factor (TNF)–-interleukin-6 (IL-6),
IL-1 and other proinflammatory cytokines, possibly under the control
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of specific genetic alleles. All this results in the variety of inflammatory

changes seen in JRA.
Symptoms of Juvenile Rheumatoid Arthritis

• Acute onset of pain
• Swelling in the joints
• Limitation of movements in the affected joints
• Pain and swelling, more in the morning, on waking up from sleep
• Interference with normal daily activities
• Usually asymmetrical involvement of the distal small joints—hands,
feet, wrist, ankles, etc (Fig. 9.2). In polyarticular types, the larger joints
are affected along with the small joints like knee, shoulder, elbow,
cervical joints, etc. (Fig. 9.3)
• Fever, malaise, myalgia more towards the evening, in the systemic
onset type
• Affected joints are warm to feel.
Signs of Juvenile Rheumatoid Arthritis

Pauciarticular JRA
Usually affects smaller joints, commonly of the lower limb but may
affect upper limb also in isolation. Commonly involved are toes, ankle,
fingers, wrist joints.
Polyarticular JRA
Several joints are involved, sometimes up to 20 to 40 joints larger like

the hip maybe involved early. Larger joint involvement indicates a
poorer prognosis.
Fig. 9.2: Small joint swelling and deformity
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Fig. 9.3: Joint changes seen in JRA
Rheumatoid nodules may be seen in the extensor surface of elbows,

achilles tendon, shins, etc. indicate a poor prognosis.
Atlantoaxial subluxation may occur from involvement of the small
joints of the cervical column. The risk of neurologic sequelae could be
potentially life-threatening.
Chronic temperomandibular joint involvement may manifest as
micrognathia, difficulty in opening the mouth and chewing food.
Gait may be affected due to involvement of lower limb joints, hip
joint and cervical column.
Systemic onset JRA

Associated with high fever, over 39oC, recurring on a daily basis. Fever
more towards the evenings.
Associated with systemic involvement, like hepatosplenomegaly,
lymphadenopathy, and serous effusion around organs, like pleural/
pericardial effusion.
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Fig. 9.4: Macular skin rash in systemic juvenile rheumatoid arthritis
Skin rash (Fig. 9.4), macular, rosaceous occuring in linear or circinate

patterns may be seen if carefully observed. The rash is non-pruritic.
Skin hypersensitivity known as Koebner’s phenomenon occurs,
wherein superficial trauma results in appearance of the rash, indicates
a systemic onset disease.
Eye involvement resulting in chronic uveitis may occur in systemic
onset or polyarticular disease.
Investigations
1. Hemoglobin is reduced due to chronic inflammatory condition.
Usually, normocytic, normochromic picture is seen.
2. Total and differential white blood cell counts are increased.
3. Platelet count—increased acute phase reactant.
4. ESR is increased due to chronic inflammatory process. It is an acute
phase reactant. Helps in following the disease course.
5. CRP—Increased: acute phase reactant.
6. Serum immunoglobulins increased.
7. Rheumatoid arthritis factor (RA factor) may be elevated, but may
be normal in some patients. RA factor positive patients tend to
have a more prolonged and severe course and disability than the
RA factor negative patients.
8. Antinuclear antibodies (ANA) may be positive in some patients
with pauciarticular and polyarticular disease. It is usually negative
in systemic onset disease. Could be an indicator for development
of uveitis in the patient.
9. Serum creatinine, blood urea—to detect any associated renal
involvement. Also acts as a baseline during treatment.
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10. Serum electrolytes—sodium, potassium, serum calcium, vitamin D,

phosphorus levels.
11. X-ray of the affected joint shows soft tissue swelling, periarticular
edema and periosteal new bone formation (Fig. 9.5). The bone
density may be reduced. Early fusion of the epiphysis may be
stimulated due to chronic inflammation.
Local bone growth may be decreased. In large joints, linear growth
may be accelerated and limb length discrepancy, especially with
involvement of the knee, becomes prominent. Continued active
disease may lead to subchondral erosions and narrowing of
cartilage space, especially in small tubular bones with varying
degrees of bony destruction.
Characteristic radiographic changes in cervical spine, most
frequently in the neural arch joints at C2-3 may progress to
atlantoaxial subluxation.
12. Examination of the eye to rule out ocular involvement, chronic
uveitis, cataract, etc. Periodic examinations are essential to check
progression during active disease and to see the effects caused by
the medications administered.
13. Charting the range of movement of the joints affected at every
hospital visit to give an accurate picture of the course and
progression of the disease.
14. MRI of the affected joint shows soft tissue and joint involvement
and is more sensitive early in the course than the plain X-ray and
in doubtful cases to confirm the diagnoses.
Fig. 9.5: X-Ray of the hand showing soft tissue swelling bony
deformity and narrow cartilaginous space
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Treatment
Treatment is a multi-pronged approach as the child needs to be treated
for his symptoms together with the rehabilitation for his altered lifestyle.
In case of pauciarticular JRA administer NSAID’s—usually start with
ibuprofen 10 mg/kg in divided doses, for 1 to 2 weeks. Check for
improvement. If better, continue for 4 to 6 weeks
If no improvement, consider intra-articular triamcinolone injection
for the affected joint.
Oral steroids may help to reduce disease during serious flare-ups.
In polyarticular JRA, if RA factor is positive, treat the child as an
adult type JRA and administer NSAID’s.
If RA factor is negative, administer NSAID’s for 6 weeks and reassess.
If no improvement, consider intra-articular triamcinolone for
selected joints like hip, knee, shoulder, etc. which would affect the child’s
activities and mobility considerably.
If no improvement, consider oral methotrexate 10 to 15 mg/m2/week
for 6 weeks.
If no improvement, consider subcutaneous methotrexate 10 to 15 mg/
m2/week. If still insufficient response, consider cyclosporine. If still
unresponsive, add an anti–tumor necrosis factor (TNF) alpha agent.
At each step, oral corticosteroids, 1 to 2 mg/kg/day prednisone may
be considered to be added to control the flare-ups.
In sytemic onset JRA, if child presents with arthritis, treat as pauci
or polyarticular disease depending on the presentation. In case of fever,
start with NSAID’s for 1 to 2 weeks and follow the response. If no
improvement, add oral corticosteroid—prednisone 1 to 2 mg/kg/day
until remission occurs then taper the dose.
In case of non response, introduce parenteral steroid IV prednisone.
In case of non response, consider cyclosporin administration.
Newer drugs like humaira given subcutaneously are being
recommended in severe cases, non-responsive to regular medications.
It has been found to be safe though long term studies and availability
of the drug act as serious restrictions impediments to its use.
Physiotherapy
Physiotherapy is extremely important, once the acute symptoms reduce.
Graded muscle strengthening exercises are recommended to ensure
patient mobility.
Walking must be encouraged to avoid development of stiffness and
limb contractures. Swimming, preferably in a warm pool, helps to
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reduce pain and aids in joint mobility without increasing joint damage.
Swimming is an extremely good exercise modality, as the joints may be
moved causing minimal damage and the weight bearing on the joint is
practically reduced.
Hot water bath to immerse the affected joint and limb will reduce
pain, inflammation and impaired mobility.
Wax baths may help in case of restricted mobility or contractures,
especially of the digits.
Treatment of the Eye Lesions
Local steroid drops help to reduce the uveitis and prevent development
of ocular complications. Regular ophthalmic follow-up with slit lamp
is recommended.
Diet Management
To ensure adequate intake of calories, vitamin D and calcium. In absence

of this, oral supplementation of vitamin D and calcium is recommended.
Vaccinations in JRA
All vaccinations are recommended in these patients to prevent vaccine
preventable diseases.
While the patient is taking immunosuppressive drugs like steroids
for long term over 3 months, cyclosporine, methotrexate or other
immunosuppressives, it is recommended to avoid live virus vaccines—
measles, MMR, varicella, oral polio, parenteral polio vaccines. BCG is
also not recommended, in case the child has not received it.
To give these vaccines, the child should not be taking any of the
immunosuppressives for at least 3 to 6 months.
Pneumococcal vaccine is recommended to avoid severe life
threatening pneumococcal infections in these children.
Complications
1. Limb length discrepancy
2. Short stature due to disease activity and long-term steroid therapy
3. Limb contractures
4. Impaired limb movements
5. Shortened spinal column
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6. Ocular complications- posterior synechiae, cataract, etc.

7. Psychosocial problems—adjustability, social acceptance, poor school
attendance, resulting in poor academic performance.
Prognosis
RA factor positive, female patients with pauci or polyarticular JRA, have
a poor prognosis.
Antinuclear antibodies (ANA) positive have a good prognosis except
in case of ocular involvement in pauciarticular types.
Systemic onset with polyarticular types have a poor prognosis.
All other types have excellent prognosis.
FURTHER READINGS
1. Alexaa Adams, Thomas Lehman. Current opinion in rheumatology. Update
on the pathogenesis and treatment of systemic onset: Juvenile rheumatoid
arthritis. 2005; 17(5):612-6.
2. American college of Rheumatology Ad Hoc committee on clinical guidelines.
Guidelines for the management of rheumatoid arthritis. Arthritis Rheum. 1996
(May);39(5):713-22. (Medline).
3. American college of rheumatology Ad Hoc committee on clinical guidelines.
Guidelines for the management of rheumatoid arthritis. Arthritis Rheum. 2002
(Feb);46(2):328-46. (Medline).
4. Arnett FC, Edworthy SM, Bloch DA, et al. Arthritis Rheum. The American
Rheumatism Association 1987 revised criteria for the classification of
rheumatoid arthritis. Arthritis Rheum. 1988 (Mar);31(3):315-24.
5. Cassidy JT. Juvenile rheumatoid arthritis. In: Ruddy S, Harris JR, Sledge CB
(Eds). Kelley's Textbook of Rheumatology. 6th edition. Philadelphia: WB
Saunders co 2001; 1297-1313.
6. Emery HM, Bowyer SL, Sisung CE. Rehabilitation of the child with a rheumatic
disease, Pediatr Clin North Am. 1995;42:1263-83.
7. Emery P. Treatment of rheumatoid arthritis. BMJ. 2006 (Jan 21);332(7534):152-
5. [Medline (full text)].
8. Hafner R, Truckenbrodt H, Spamer M, et al. Rehabilitation in children with
juvenile chronic arthritis. Baillieres Clin Rheumatol. 1998;12:329-61.
9. Howard R Smith. Rheumatoid Arthritis. (Medscape).
10. Jacqueline Oliver E, Alan Silman J: What epidemiology has told us about risk
factors and etiopathogenesis in rheumatic diseases: Arthritis research and
therapy. 2009;11.
11. Klippel JH. Biologic therapy for rheumatoid arthritis. N Engl J Med. 2000
(Nov 30 ); 343(22):1640-1. [Medline]
12. Kremer JM. Rational use of new and existing disease-modifying agents in
rheumatoid arthritis. Ann Intern Med. 2001 (Apr 17);134(8):695-706. [Medline].
13. Malleson PN. Management of childhood arthritis, II: Chronic arthritis. Arch
Dis Child 1997;76:541-4.
14. Nelson textbook of pediatrics 18th edition.
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15. O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J Med. 2004
(Jun 17 ); 350(25):2591-602. [Medline].
16. Oliver JE, Silman AJ. Risk factors for the development of rheumatoid arthritis.
Scand J Rheumatol. 2006;35:169-74.
17. Pincus T, Callahan LF. What is the natural history of rheumatoid arthritis?
Rheum Dis Clin North Am. 1993 (Feb);19(1):123-51. [Medline].
18. Prieur AMF. Juvenile chronic arthritis: management. In: Klippel JH, Dieppe
PA (Eds). Rheumatology. 2nd edition. London: Mosby. 1998;pp5.21.1-10.
19. Sawhney S, Woo P. Diagnosis and management of juvenile idiopathic arthritis:
Current statistics. Indian Pediatr 2001;38:1083-90.
20. White PH. Juvenile chronic Arthritis, clinical features. In: Klippel JH, Dieppe
PA (Eds). Rheumatology. 2nd edition. London: Mosby. 1998;pp 5.18.1-10.
vip.persianss.ir
Reactive Arthritis 109
Reactive Arthritis
10
Arthritis associated with infection is called reactive arthritis.

Reactive arthritis indicates infection outside the joint, usually in the
gastrointestinal, genitourinary tract or systemic infection like typhoid,
which result in effusion into the joint.
Nonviable, immune portions of the organism may be isolated from
the joint fluid.
Suppurative arthritis indicates infection within the joints. Infective
organisms may be isolated in the joint fluid obtained by aspiration of
the joint.
Post-infectious arthritis indicates a sterile synovitis that follows systemic
infection.
Causes of Reactive Arthritis

Reactive arthritis may be caused by enteric infection with Salmonella
species, Shigella, Yersinia Enterocolitica, Camplylobacter jejuni Giardia
lamblia
Genitourinary organisms like Neisseria gonorrhea, Chlamydia trachomatis,
etc. Systemic viral infections like Parainfluenza, Enterovirus, Adenovirus,
Mumps Varicella, EBV, Hepatitis, etc.
There appears to be an immunologic cross reaction between the
antigens of the target organ and the antigens in the joint space, resulting
in a cross reaction and joint space effusion and symptoms. It appears
that the T- lymphocytes engage in antigenic cross reaction and increase
inflammation. Remnants of bacterial or viral tissues may be found in
the synovium, indicating incomplete clearing of systemic infections.
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Certain carriers of HLA – Human leukocyte antigen B27, are found

to be more susceptible to reactive arthritis. They may have associated
uveitis, and some may develop spondyloarthropathy. Some common
infections that can trigger reactive arthritis is given in Fig. 10.1.
Symptoms of Reactive Arthritis

• Fever
• General malaise
• Prodromal/associated infections- like gastroenteritis, urinary tract
infection, etc.
• Followed by appearance of joint swelling, severe pain in the joints,
difficulty in movement
• No local increase in temperature
• Mono/polyarticular joint involvement seen
• May be involvement of tendons, commonly Achilles tendon.
Signs of Reactive Arthritis

• Fever
• Evidence of associated systemic infection may be present
• May follow after 1 to 2 months of systemic infection
• Usually large joints like hip, shoulder, elbow and knee joints
involved. Occasionally, small joints are also affected
• Joint swollen, restricted mobility
• Depending on the affected joint, there could be gait alterations,
limping, inability to place the feet on the ground, difficulty in holding
the pencil, wearing the clothes, etc.
Fig. 10.1: Common infections that can trigger reactive arthritis
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Reactive Arthritis 111
• No evidence of local inflammation – no erythema

• In case of tendon involvement, local tenderness may be noted
• Sausage toes
• Associated back pain
• Congestion in conjunctiva and eye inflammation
• Flaky patches on skin and genitalia (Fig. 10.2).
Investigations
1. Complete blood count—increased total and differential count may
indicate associated/concurrent infection. May also help to
differentiate suppurative arthritis from reactive/post-infectious
arthritis.
2. ESR may be increased in acute stage. It is an acute phase reactant,
hence is a non-specific indicator. May be used to follow-up the course
of the arthritis.
3. Joint fluid aspiration—examination of the joint fluid will confirm
the diagnosis. In suppurative arthritis, the effusion fluid may be
turbid and may show polymorphs on microscopic examination.
Culture of the fluid will grow the causative organism. Sterile fluid
with no evidence of polymorphs and no growth in culture go in
favor of reactive arthritis.
4. X-ray of the joint shows increase in joint space due to collection of
edema fluid. No evidence of joint destruction seen.
5. CT scan of the affected joint shows increased fluid in the joint space.
No evidence of cartilage or bony damage found.
Treatment
No specific treatment. It is usually self-resolving. During the acute stage,
immobilization of the joint and restricted activities is recommended. In
case of severe pain, administer anti-inflammatory medication—
Ibuprofen 10 mg/kg/day till the acute symptoms subside.
No indication for antibiotics unless proven suppurative arthritis.
Fig. 10.2: Associated signs in reactive arthritis
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Prognosis
Good. Usually no residual deficits. Recurrent episodes may occur with
recurrent infections.
FURTHER READINGS
1. Alexander JE, Fitz Randolph RL, Mc Connell JR et al. The limping child.
Current Problems in diagnostic radiology 1987;16:229-70.
2. Alexander KC, Leung, Jean Francois Lemay. The Limping Child. Pediatric
Health Care. 2004;18(5).
3. Hart JJ. Transient synovitis of the hip in children. American Family Physician
1996;54:1587-91.
4. Kost S. Limp. In: Fleisher GR, Ludwig S, Henretig FM (Eds). Textbook of
pediatric Emergency Medicine. 2000;369-74.
5. Lawrence LL. The limping child. Emergency medical clinics of North America.
1998;16:911-29.
6. Marjatta Leirisalo Repo. Current opinion in Rheumatol. 2005;17(4):433-9.
7. Nelson textbook of pediatrics. 18th edition.
8. Sawhney S, Woo P. Diagnosis and management of juvenile idiopathic arthritis:
current statistics. Indian Pediatr. 2001;38:1083-90.
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Kawasaki Disease 113
Kawasaki Disease
11
Kawasaki disease is also known as infantile polyarteritis or muco-

cutaneous lymph node syndrome.
It was first described by a Japanese scientist Dr Tomisaku Kawasaki
in 1967. It has since been described in children all over the world, with
Asians being at an increased risk.
Causes of Kawasaki Disease

The exact etiology is unknown. However, there is evidence that some
kind of infective agent acts on those children who are immunologically
predisposed to the disease to cause the symptoms.
Kawasaki disease is common in groups of children who attend child
care. It is also frequent in children whose parents had suffered from
the disease in their childhood. It is uncommon in children below 3
months, probably owing to the presence of maternal protective
antibodies.
Pathogenesis
There is a severe vasculitis of the medium-sized arteries in the body.
An inflammatory infiltrate of the endothelial and smooth muscle cell
wall, initially by polymorphs and later by macrophages, plasma cells
and T lymphocytes, associated with edema is seen. This has a
predilection for the coronary blood vessels. There is a resultant thinning
of the blood vessel wall, with destruction of the internal elastic lamina.
The loss of integrity of the vessel wall leads to weakness, dilatation and
aneurysm formation. Thrombi may occlude the blood flow in the vessel.
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During the healing phase , due to fibrosis, scar formation may cause
further obstruction to blood flow in the affected vessel.
The non-vascular tissues may also be affected by Kawasaki disease.
Here, an inflammatory infiltrate of plasma cells, may be noted in tissues
like the respiratory tract, myocardium, biliary tree, pancreas, etc.
Immunoglobulin levels are elevated during the acute stage of the
disease.
Classical Kawasaki Disease
Fever plus four of the five criteria mentioned below are present.
Diagnosis confirmed.
Atypical Kawasaki Disease
Fever criteria plus greater than four mentioned below are found.
Diagnosis difficult. More likelihood of developing coronary aneurysms.
Symptoms and Signs of Kawasaki Disease

There are five characteristic features which need to be present before
diagnosis of Kawasaki disease can be made. These features are usually
associated with fever.
1. Fever—high grade, generally over 104°F, unresponsive to antibiotics.
The fever is intermittent, and may last up to 2 weeks, but may persist
longer, up to 4 weeks.
2. Bilateral bulbar conjunctival congestion (Fig. 11.1). Usually, there
are no associated exudates.
Fig. 11.1: Bulbar conjunctival congestion—non-exudative
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Fig. 11.2: Strawberry tongue in Kawasaki disease
3. Strawberry tongue (Fig. 11.2) red, congested tongue and mucous

membranes in the oral cavity.
4. Cracked lips, dry with no ulceration.
5. Redness and erythema of the hands and feet. More pronounced in
the tips. Usually results in desquamation of the skin (Fig. 11.3) as
the disease progresses. It is an important diagnostic aid.
6. Cervical lymphadenopathy [node size (over 1.5 cm)].
7. Skin rash, which is usually scarlet, erythematous and maculopapular.
More pronounced in the skin folds and groin area. Perineal
desquamation may be seen.
Coronary artery disease manifested as dilatation, aneurysms, is late
features and indicates a poorer prognosis. Child is extremely irritable
arthritis involving the large lower limb joints is common. It may occur
by early, in the first week itself, or after the 2nd week. It is usually self-
limiting.
Fig. 11.3: Skin peeling noted in the digits
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Diagnostic Criteria
Fever plus any four out of the five mentioned features must be present
to make a diagnosis of Kawasaki disease (KD), in the absence of any
other associated disease.
Acute Febrile Stage

First 1 to 2 weeks of disease is associated with high fever. May have
features of myocarditis, with minimal pericardial effusion. Clinical
features are non-specific.
Sub-acute Phase
Fever settles last 1 and 3 to 4 weeks. However, child is persistently
irritable, anorexic and lethargic. Skin desquamation, thrombocytosis
and development of aneurysms are likely at this stage. Evidence of
aneurysm may be seen in Echo. Sudden death may occur in those with
aneurysms.
Convalescent Stage
Last 4 to 6 weeks, with healing of cardiac lesions, skin lesions. Acute
phase reactants return to normal (Fig. 11.4).
Investigations
No specific diagnostic test. Clinical findings are the guide to diagnosis.
1. Complete blood count may show polymorphonuclear leucocytosis
and increased number of immature forms. Anemia may be associated.
2. ESR (Erythrocyte sedimentation rate) elevated > 40 mm/hr. Indicates
ongoing inflammation.
Fig. 11.4: Stages in the development of Kawasaki’s disease
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3. CRP increased > 3.0 mg/dl. It is an acute phase reactant.

4. Thrombocytosis > 400,000/cumm—acute phase reactant. Increased
levels seen during the sub-acute phase.
5. Urine examination shows increased number of pus cells. However,
the urine culture is normal, showing no growth.
6. 2 D Echocardiogram needed to detect the presence of cardiac
abnormalities—dilatation of the artery, myocardial damage and
aneurysm formation, which could be fatal. Repeat test is recommended
after 2 to 3 weeks, and again at 6 to 8 weeks as follow-up. In case of
normal studies also, it is recommended to do follow-up Echo at 6 to
12 months after the illness.
Treatment
1. IV fluids—calculate maintenance requirements + 10 percent to cover
ongoing loss from high grade fever.
2. Keep the child comfortable and free from anxiety.
3. Intravenous Immunoglobulin (IVIG) IV Immunoglobulin is the drug
of choice once the diagnosis is made. Dose: 2 g/kg over 10 to 12
hours. Results in rapid defervescence and reduction of all symptoms
in over 90 percent of patients. Reduces the incidence of coronary
abnormalities and aneurysms. Mode of action-possibly anti-
inflammatory effect. Single infusion usually adequate.
In case of inadequate response, second infusion of IVIG is recommended.
4. Aspirin, as an anti-inflammatory, to be given together with IVIG.
Dose: 80–100 mg/kg divided, every 6th hourly. Reduce the dose to
anti-thrombotic doses of 3-5 mg/kg on the 14th day of treatment. Or
when the child has been asymptomatic for at least 3 to 4 days.
Duration: 6 to 8 weeks after disease onset, in case of no coronary
anomalies.
5. Seek opinion from a cardiologist at the earliest.
6. Local skin emollients to counter the skin peeling and reduce the
skin irritation.
7. Bland diet and small frequent feeds to counter the reduced oral intake
from the strawberry tongue.
Complications
1. Coronary aneurysms.
2. Coronary thrombosis.
3. Coronary artery stenosis.
4. Aneurysmal stenosis, especially in giant aneurysms.
5. Sudden death from rupture of aneurysms.
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Treatment of Complications
Children with small aneurysms need aspirin continuously at anti-
thrombotic doses.
In children with large or multiple aneurysms, clopidogrel 1 mg/kg
upto a maximum of 75 mg/day. Alternatively, low molecular weight
heparin may be used at prophylactic doses of 1–1.5 mg/kg divided every
12th hourly, administered subcutaneously.
VACCINATIONS IN KAWASAKI DISEASE

1. Recommended Influenza vaccine annually to reduce risk of Reye’s
disease.
2. Varicella vaccine to reduce risk of Reye’s disease in children on
aspirin.
3. In children who have received IVIG, delay admnistration of MMR
for 11 months, as the vaccine uptake is interfered with and reduced
by the immunoglobulin.
Prognosis
Prognosis depends on the stage of diagnosis and stage of administration
of IVIG.
In case of early diagnosis and administration of IVIG, the prognosis
is excellent in approximately 90 percent of children. In patients with
myocarditis, the likelihood of sudden death due to coronary artery
involvement is very high. Frequent Echo tests need to be performed for
at least up to 1 year after completion of treatment.
Poor Prognostic Indicators

1. Persistent, long-standing fever
2. Delayed administration of IVIG
3. Associated coronary aneurysms
4. Severe skin excoriation and peeling
5. Large tender lymph nodes
6. Multiple aneurysms.
FURTHER READINGS
1. American Academy of pediatrics. Kawasaki syndrome. In: Pickering LK (Ed).
Red book, Report of the Committee on Infectious Diseases, 28th edition, Elk
Grove Village. 2009;413.
2. Ayusawa M, Sonobe T, Uemura S, et al. Revision of diagnostic guidelines for
Kawasaki disease (the 5th revised edition). Pediatr Int. 2005;47:232.
vip.persianss.ir
3. Barron, KS. Kawasaki disease in children. Curr Opin Rheumatol. 1998;10:29.

4. Burns JC, Glodé MP. Kawasaki syndrome. Lancet 2004;364:533.
5. Burns, JC, Glodé MP. Kawasaki syndrome. Lancet 2004;364:533.
6. Curtis N, Levin M. Kawasaki disease thirty years on. Curr Opin Pediatr.
1998;10:24.
7. Durongpisitkul K, Gururaj VJ, Park JM, Martin CF. The prevention of coronary
artery aneurysm in Kawasaki disease: a meta-analysis on the efficacy of aspirin
and immunoglobulin treatment. Pediatrics. 1995; 96:1057.
8. Egami, K, Muta, H, Ishii, M, et al. Prediction of resistance to intravenous
immunoglobulin treatment in patients with Kawasaki disease. J Pediatr.
2006;149:237.
9. Fukushige J, Takahashi N, Ueda K, et al. Long-term outcome of coronary
abnormalities in patients after Kawasaki disease. Pediatr Cardiol. 1996;17:71.
10. Furusho K, Kamiya T, Nakano H, et al. High-dose intravenous gammaglobulin
for Kawasaki disease. Lancet. 1984;2:1055.
11. Germain BF, Moroney JD, Guggino GS, et al. Anterior uveitis in Kawasaki
disease. J Pediatr. 1980;97:780.
12. Hsieh KS, Weng KP, Lin CC, et al. Treatment of acute Kawasaki disease:
aspirin's role in the febrile stage revisited. Pediatrics. 2004;114:689.
13. Inoue Y, Okada Y, Shinohara M, et al. A multicenter prospective randomized
trial of corticosteroids in primary therapy for Kawasaki disease: clinical course
and coronary artery outcome. J Pediatr. 2006;149:336.
14. Kato H, Sugimura T, Akagi T, et al. Long-term consequences of Kawasaki
disease. A 10- to 21-year follow-up study of 594 patients. Circulation.
1996;94:1379.
15. Kobayashi T, Inoue Y, Takeuchi K, et al. Prediction of intravenous
immunoglobulin unresponsiveness in patients with Kawasaki disease.
Circulation 2006;113:2606.
16. Melish ME. Kawasaki syndrome: a 1986 perspective. Rheum Dis Clin North
Am. 1987;13:7.
17. Morens DM, Anderson LJ, Hurwitz ES. National surveillance of Kawasaki
disease. Pediatrics. 1980;65:21.
18. Nelson textbook of pediatrics 18th Edition.
19. Newburger JW, Takahashi M, Beiser AS, et al. A single intravenous infusion
of gamma globulin as compared with four infusions in the treatment of acute
Kawasaki syndrome. N Engl J Med. 1991;324:1633.
20. Newburger JW, Takahashi M, Burns JC, et al. The treatment of Kawasaki
syndrome with intravenous gammaglobulin. N Engl J Med. 1986;315:341.
21. Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and
long-term management of Kawasaki disease: a statement for health
professionals from the Committee on Rheumatic Fever, Endocarditis and
Kawasaki Disease, Council on Cardiovascular Disease in the Young, American
Heart Association. Circulation. 2004; 110:2747.
22. Oates-Whitehead RM, Baumer JH, Haines L, et al. Intravenous
immunoglobulin for the treatment of Kawasaki disease in children. Cochrane
Database Syst Rev 2003; :CD004000.
23. Petty RE. Kawasaki disease. In: Cassidy JT (Eds). Textbook of pediatric
rheumatology. 4th edition. Philadelphia: WB saunders. 2001;pp580.
24. Shinohara M, Sone K, Tomomasa T, et al. Corticosteroids in the treatment of
the acute phase of Kawasaki disease. J Pediatr. 1999;135:465.
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25. Smith LB, Newburger JW, Burns JC. Kawasaki syndrome and the eye. Pediatr
Infect Dis J 1989;8:116.
26. Tse SM, Silverman ED, McCrindle BW, Yeung RS. Early treatment with
intravenous immunoglobulin in patients with Kawasaki disease. J Pediatr.
2002;140:450.
27. Wang S, Best BM, Burns JC. Periungual desquamation in patients with
Kawasaki disease. Pediatr Infect Dis J. 2009;28:538.
28. Wei CM, Chen HL, Lee PI, et al. Reye's syndrome developing in an infant on
treatment of Kawasaki syndrome. J Paediatr Child Health. 2005;41:303.
29. Yellen ES, Gauvreau K, Takahashi M, et al. Performance of 2004 American
Heart Association recommendations for treatment of Kawasaki disease.
Pediatrics. 2010; 125:234.
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Otitis Media in Children 121
Otitis Media
12 in Children
OTITIS MEDIA
Otitis media indicates an infection of the middle ear.
The middle ear begins at the tympanic membrane and extends until the
inner ear. There is a normal amount of fluid in the middle ear, which aids
in the transmission of the sound waves into the inner ear. The three ear
bones, the malleus, incus and stapes are located in the middle ear and
can be visualized beyond the normal tympanic membrane, which is
translucent and pearly white in color (Fig. 12.1).
Fig. 12.1: Anatomy of the ear
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Otitis media is an acute disease, associated with inflammation and

middle ear effusion. The diagnosis requires the presence of an acute
infection, middle ear effusion together with signs of inflammation in
the middle ear.
Etiology
Bacteria
Haemophilus influenzae, Streptococus pneumoniae, Escherichia coli, Klebsiella
Pseudomonas, Staphylococci, Streptococci, Enterobacteriacee, etc.
Virus
Rhinovirus, influenza, para influenza, RSV, adenovirus, other
respiratory viruses.
Viral pathogens are commonly associated or superimposed with
bacterial infection.
Types of Otitis Media

Infective/suppurative otitis media, also called acute otitis media
Non-infective/secretory/otitis media with effusion—no evidence of
aute infection.
In both the conditions (Fig. 12.2) middle ear effusion is a common
feature. It indicates underlying middle ear inflammation.
1. Younger ages: Higher incidence between 6 months to 2 years.
2. Male sex: Higher incidence statistically.
3. Seasonal variation: Lower incidence in the summer months.
4. Lower socioeconomic status: Due to overcrowding, poor hygiene,
frequent and untreated respiratory infections.
5. Formula fed babies have more incidence of otitis media as against
breast fed.
6. Environmental tobacco smoke inhalation.
Fig. 12.2: Types of otitis media
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7. Congenital abnormality: Cleft palate, cranio-facial abnormalities,

Down’s syndrome.
8. Pneumococcal vaccination status: Lower incidence in immunized
children.
Pathogenesis
The eustachian tube is normally closed and is opened only by the
contraction of the tensor veli palatini muscle. The most important
function of the tube is ventilation. It is dependent on the nasopharynx
for aeration and ventilation. In case of nasal obstruction, eustachian
tube obstruction occurs, which in turn results in inflammatory changes
like metaplasia, impaired clearance and aeration of the middle ear and
fluid secretion into the middle ear behind the tympanic membrane.
This pathology is central to both types of otitis media. Obstruction of
the eustachian tube most commonly may be due to infection, otherwise
it may be enlarged adenoids, tumors, etc.
In infants, the short eustachian tube is more prone to regurgitation
from the nasopharynx, together with impaired gravitational clearance
in the supine position. This explains the increased incidence of infection
in younger children.
As the child grows, the increased diameter of the eustachian tube
counters the effects of mild obstruction. Also, the improved immunity
aids in reducing the incidence of infection in older children.
As the fluid in the middle ear increases due to the inflammatory
changes, the pathologic organisms have a favorable medium for growth
and multiplication. Hence, unless complete eradication is aimed for,
the disease process can recur frequently.
In children with recurrent otitis media, do suspect underlying Ig G
subgroup defects.
In children left at daycare, due to repeated exposure to respiratory
viruses, the mucociliary clearance may be impaired and favors the
occurrence of recurrent otitis media.
Symptoms (Fig. 12.3)

• Fever
• Sudden onset of excessive crying
• Pulling/tugging the ear
• Ear pain of sudden acute onset
• Altered eating and behavior pattern
• Altered sleeping pattern
• Hearing loss
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Fig. 12.3: Common symptoms of otitis media
Signs
• Irritable and agitated child
• Crying excessively
• Tugging/rubbing the ear
• Fever.
Tympanometry is the diagnostic test, which gives an idea of the
mobility of tympanic membrane. Its findings confirm the diagnosis of
otitis media. Hence, it is essential to perform this test before coming to
the diagnosis of otitis media.
Apart from this test, the visualization of the tympanic membrane is
absolutely important in making the diagnosis of otitis media.
The normal tympanic membrane is slightly concave, pearly grey in
color and shows a light reflex. It is translucent and some degree of
opacification is normal in younger ages.
Erythema of the membrane, loss of the light reflex, bulging tympanic
membrane (Fig. 12.4) fluid in the middle ear are indicative of otitis media.
Impaired membrane mobility is an early finding. Structural changes may
include scars, perforations, thickening and later, cholesteatoma formation.
In middle ear effusion, air bubbles or distinct air-fluid levels may be
seen behind the ear drum. This may indicate impending resolution.
Tympanometry
Tympanometry is a simple test which gives an idea about the mobility
of the tympanic membrane and helps in differentiation between acute
otitis media (AOM) and middle ear effusion (MEE). The tympanometer
measures and records the volume of the external auditory canal and if
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Fig. 12.4: Shows bulging and erythema of tympanic membrane
a tympanic membrane perforation or a patent tympanostomy tube is

present, the volume of the middle ear and mastoid air cells as well is
measured and recorded. A volume reading of > 1.0 ml should suggest
the presence of either a perforation or a patent tympanostomy tube.
The volume reading is indicative of the fluid behind the tympanic
membrane.
A normal tympanogram shows a sharp peak followed by a gradual
gradient and indicates normal fluid pressure and volume in the middle
ear.
When there is a shallow peak with a flat/negative gradient, it is
indicative of fluid in the middle ear canal and may be diagnostic of
MEE. This is a simple and sensitive test that may be done in a clinical
setting to differentiate between AOM and MEE.
Treatment
1. Antibiotic treatment is indicated in confirmed cases of AOM , at all
ages.
The drug of choice is amoxicillin-clavulanic acid at 90 mg/kg/day in
two divided doses for 7 to 10 days depending on the severity of the
otitis media. In case of sensitivity to this drug, alternatives may be
used like cefdinir, cefuroxime or cefpodoxime.
2. Ibuprofen at 10 mg/kg/day for 2 to 3 days for pain relief.
3. Antihistamines—loratidine or cetrizine will help to reduce associated
nasal symptom.
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4. Nasal decongestant drops will reduce the eustachian catarrh. To be

used for maximum 3 days only, to avoid rebound increase in
symptoms.
5. Ensure the ear is kept dry at all times, to prevent development of
recurrent otitis media.
6. Steam inhalation helps by decongesting the eustachian tube and
reducing the catarrh.
Prevention
1. Vaccination with Hib vaccine and pneumococcal conjugate vaccine
helps to prevent infection in the middle ear by bacterial and viral agents.
2. Protecting the child from recurrent influenza and viral infections
by administration of seasonal influenza vaccine.
3. Avoiding swimming and other activities that may cause water entry
to the ear.
4. Keeping the ears dry at all times.
5. Early treatment of upper respiratory infections.
6. Avoid feedings in the supine position.
Prognosis
Usually self-limiting and hence good prognosis.
FURTHER READINGS
1. American Academy of Pediatrics Subcommittee on Management of Acute
Otitis Media. Diagnosis and management of acute otitis media. Pediatrics.
2004;113:1451.
2. American Academy of Pediatrics Subcommittee on Management of Acute
Otitis Media. Diagnosis and management of acute otitis media. Pediatrics.
2004;113:1451.
3. Arguedas A, Loaiza C, Soley C. Single dose azithromycin for the treatment of
uncomplicated otitis media. Pediatr Infect Dis J. 2004;23:S108.
4. Barry B, Gehanno P, Blumen M, Boucot I. Clinical outcome of acute otitis
media caused by pneumococci with decreased susceptibility to penicillin.
Scand J Infect Dis. 1994; 26:446.
5. Bertin L, Pons G, d'Athis P, et al. A randomized, double-blind, multicentre
controlled trial of ibuprofen versus acetaminophen and placebo for symptoms
of acute otitis media in children. Fundam Clin Pharmacol. 1996;10:387.
6. Bluestone CD. Clinical course, complications and sequelae of acute otitis
media. Pediatr Infect Dis J. 2000;19:S37.
7. Bluestone CD. Epidemiology and pathogenesis of chronic suppurative otitis
media: implications for prevention and treatment. Int J Pediatr
Otorhinolaryngol. 1998;42:207.
8. Chonmaitree T, Saeed K, Uchida T, et al. A randomized, placebo-controlled
trial of the effect of antihistamine or corticosteroid treatment in acute otitis
media. J Pediatr. 2003; 143:377.
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9. Finkelstein JA, Stille CJ, Rifas-Shiman SL, Goldmann D. Watchful waiting for
acute otitis media: are parents and physicians ready? Pediatrics. 2005;115:1466.
10. Flynn CA, Griffin GH, Schultz JK. Decongestants and antihistamines for acute
otitis media in children. Cochrane Database Syst Rev. 2004;CD001727.
11. Hoberman A, Paradise JL, Burch DJ, et al. Equivalent efficacy and reduced
occurrence of diarrhea from a new formulation of amoxicillin/clavulanate
potassium (Augmentin) for treatment of acute otitis media in children. Pediatr
Infect Dis. J 1997;16:463.
12. Hotomi M, Yamanaka N, Samukawa T, et al. Treatment and outcome of severe
and non-severe acute otitis media. Eur J Pediatr. 2005;164:3.
13. Klein JO. Review of consensus reports on management of acute otitis media.
Pediatr Infect Dis J. 1999;18:1152.
14. Kozyrskyj A, Klassen TP, Moffatt M, Harvey K. Short-course antibiotics for
acute otitis media. Cochrane Database Syst Rev. 2010;9:CD001095.
15. Lee D, Youk A, Goldstein NA. A meta-analysis of swimming and water
precautions. Laryngoscope. 1999;109:536.
16. Nelson textbook of pediatrics. 18th edition.
17. Robson WL, Leung AK. Swimming and ear infection. J R Soc Health.
1990;110:199.
18. Rosenfeld RM, Vertrees JE, Carr J, et al. Clinical efficacy of antimicrobial drugs
for acute otitis media: meta-analysis of 5400 children from thirty-three
randomized trials. J Pediatr. 1994;124:355.
19. Siegel RM, Kiely M, Bien JP, et al. Treatment of otitis media with observation
and a safety-net antibiotic prescription. Pediatrics. 2003;112:527.
20. Sox CM, Finkelstein JA, Yin R, et al. Trends in otitis media treatment failure
and relapse. Pediatrics. 2008;121:674.
21. Spiro DM, Tay KY, Arnold DH, et al. Wait-and-see prescription for the
treatment of acute otitis media: a randomized controlled trial. JAMA.
2006;296:1235.
22. Takata GS, Chan LS, Shekelle P, et al. Evidence assessment of management of
acute otitis media: I. The role of antibiotics in treatment of uncomplicated
acute otitis media. Pediatrics. 2001;108:239.
23. Takata GS, Chan LS, Shekelle P, et al. Evidence assessment of management of
acute otitis media: I. The role of antibiotics in treatment of uncomplicated
acute otitis media. Pediatrics. 2001;108:239.
24. Teele DW, Klein JO, Rosner BA. Epidemiology of otitis media in children.
Ann Otol Rhinol Laryngol Suppl. 1980;89:5.
25. Uhari M, Mäntysaari K, Niemelä M. A meta-analytic review of the risk factors
for acute otitis media. Clin Infect Dis. 1996;22:1079.
26. Wald ER. To treat or not to treat. Pediatrics. 2005;115:1087.
vip.persianss.ir
Pneumonia
13 in Children
Pneumonia is an inflammation of the parenchyma of the lungs.
Causes
The causative organism varies with the age of the child
It is essential to have an idea of the causative organism (Fig. 13.1) which
varies with age, as the drug of choice could be different for each
organism.
The highest frequency of viral pneumonia occurs between the ages
of 2 and 3 years, decreasing slowly thereafter.
Recurrent pneumonia is defined as two or more episodes in a single
year or three or more episodes ever, with radiographic clearing between
Table 13.1: Etiology of pneumonia in children

Age of the child Causative organism
0–20 days Commonly Escherichia coli, Group B Streptococci,

listeria bacteria
Cytomegalovirus, herpes Simplex virus
3 weeks–3 months Chlamydia trachomatis, Streptococci bacteria
adenovirus, influenza, parainfluenza virus
4 months–5 years Mycoplasma Pneumoniae
S. pneumoniae, Haemophilus influenzae B bacteria
adenovirus, influenza, parainfluenza, rhinovirus,
respiratory syncytial virus, occasionally varicella
zoster virus
5 years–adolescence Pneumococci, S. pneumoniae, staphylococci,
Haemophilus Influenza B Mycoplasma Pneumoniae-
epstein–barr virus
Adenovirus, EBVirus, influenza, parainfluenza virus
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Pneumonia in Children 129
Fig. 13.1: Common etiological agents
occurrences. An underlying disorder should be considered if a child

experiences recurrent bacterial pneumonia.
Slowly resolving pneumonia refers to the persistence of symptoms or
radiographic abnormalities beyond the expected time course.
Afebrile pneumonia may occur in babies between 1 to 3 months. Here,
there are radiological signs of pneumonia, but the baby is afebrile. The
common causative organisms here are Chlamydia trachomatis,
Mycoplasma hominis, Ureaplasma urealyticum and cytomegalovirus.
Pneumonitis
Inflammation of the lung with/without parenchymal consolidation.
Bronchopneumonia
Inflammation mainly involving bronchioles, resulting in mucopurulent

exudation that obstructs small airways causing patchy consolidation
of the adjoining lobules.
Interstitial Pneumonitis
This is an inflammation of the interstitium, which includes the walls of the

airways, bronchioles, alveoli, ducts and alveolar sac.
Clinical Features
Usually a brief period of cough and fever is preceded, followed by a
sudden worsening.
• Fever, high grade lasting for over 3 to 4 days, may be associated
with chills and shaking. Poor appetite
• Cough, which could be productive with expectoration of copious
sputum
• Cyanosis, especially perioral
• Chest pain
• Signs of respiratory distress, intercostals indrawing, flaring of alae
nasi
• Drawing up the legs to reduce the pleuritic pain.
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Staphylococcus aureus pneumonia manifests in confluent

bronchopneumonia, which is often unilateral and characterized by the
presence of extensive areas of hemorrhagic necrosis and irregular areas
of cavitation of the lung parenchyma, resulting in pneumatoceles,
empyema or at times, bronchopulmonary fistula.
Pneumonia in the newborn period may manifest only as poor feeding,
fever along with signs of respiratory distress and decreased activity.
Signs (Fig. 13.2 to 13.5)

• The child appears sick and toxic. Signs of dehydration may be
present
Fig. 13.2: Early pneumonia
Fig. 13.3: Pneumonia: well-developed consolidation in right upper zone
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• Tongue is coated and dry

• Febrile. High grade fever > 38oC
• SPO2 low below 92 percent in room air/unable to maintain saturation
above 92 percent without supplemental oxygen
• Flaring of alae nasi, intercostals and subcostal retractions, rapid
respiratory rate are evidence of respiratory distress
• Bronchial breathing with coarse crepitations may be heard on
auscultation, which are due to the secretions in the alveoli
• Rhonchi may be heard due to airway narrowing from the fluid and
secretions
• Associated gastrointestinal disturbances characterized by vomiting,
anorexia, diarrhea and abdominal distention secondary to a paralytic
Fig. 13.4: Pneumonia with interlobar fissure effusion
Fig. 13.5: Resolving lobar pneumonia
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ileus. Rapid progression of symptoms is characteristic in the most

severe cases of bacterial pneumonia.
Investigations
1. Complete blood count, erythrocyte sedimentation rate (ESR),
C-reactive protein (CRP) may help to differentiate the bacterial
etiology from viral etiology.
2. Chest X-Ray will aid in clinching the diagnosis by showing the area
of consolidation. In early cases, there may not be well-demarcated
areas on the X-ray.
3. Serologic testing may be valuable as an epidemiologic tool to define
the incidence and prevalence of the various respiratory viral pathogens.
4. Mycoplasma IgM may be useful to detect Mycoplasma infection.
5. Blood culture will be definitive evidence of bacterial infection.
However, results require at least 48 to 72 hours, hence start empirical
antibiotics based on the current sensitivity pattern in the area. May
need to change the drugs in case of different sensitivities or in case
of non-response to treatment.
Treatment
In case of a sick, toxic looking child, immediate hospital admission is
indicated.
If the child is not too sick, able to accept and tolerate oral feeds with
the X-ray not showing very gross lobar involvement and with no signs
of respiratory distress, the child may be treated as an outpatient with
oral antibiotics.
Indications for Admission to Hospital

1. Age below 6 months
2. Supplemental oxygen required
3. Dehydration
4. Persistent vomiting
5. Toxic appearance
6. Non-response to oral antibiotics
7. Multiple lobar involvement
8. Severe respiratory distress.
Correct the Dehydration
Administer IV Fluids using maintenance fluids containing 5 percent

dextrose. Additional 10 percent fluid in case of high fever.
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Oxygen supplementation to be started. Start at higher levels to

maintain the saturation above 92 percent (usually at least 5 to 6 l/min).
Antipyretcis
Paracetamol to be given every 6th hourly at 15 mg/kg/dose. This will

help to keep the child afebrile and reduce the oxygen requirements.
Administer IV Antibiotics
Cefuroxime 150 mg/kg/day in three divided doses or ceftriaxone

75–100 mg/kg/day in a single dose may be administered after skin
testing.
In case of suspicion of Mycoplasma infection, a macrolide is usually
added. Erythromycin (40 mg/kg/day every 8th hourly) is used above 3
weeks, while clarithromycin may be given in older children in the dose
of 7.5–10 mg/kg/dose every 12th hourly. In case of intolerance,
azithromycin is recommended at 10 mg/kg/day once daily for 5 days.
Duration of Treatment
It is 7–10 days, usually it is suggested to give 10 days of treatment.
In case the child is treated as an outpatient, the drug of choice is
amoxicillin- clavulanic acid (100–150 mg/kg/day) or cefuroxime
20–30 mg/kg/day in two divided doses may be given.
In case of neonates below 3 weeks, IV antibiotics are mandatory.
Preferred drugs are ampicillin 50–100 mg/kg/day in divided doses every
6 to 8th hourly along with gentamicin 2.5 mg/kg/day every 8 to 12th
hourly. Cefotaxime may or may not be added depending on the baby’s
condition (100-150 mg/kg/day in divided doses every 8–12th hourly).
Repeated nebulization may be needed in case of airway obstruction.
The role of steroids in case of pneumonia has been extensively discussed,
however, fluticasone may be used to reduce the airway inflammation
and edema, along with the SABA (short-acting beta agonist)- usually,
salbutamol.
Cough syrups, which may act as sootheners may be used to relieve
the disturbing cough. It is safer to use a herbal or a non-sedating cough
syrup.
Probiotics
Lactobacillus to be given along with the antibiotics.
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Response to Treatment
Usually seen after 48 to 72 hours. Hence the child needs to be reviewed
at this time.
X-ray clearing may lag behind the clinical signs of improvement.
Check X-ray is advised at the end of treatment period usually, after
10 days, to document complete clearing of the consolidation patch.
Non-response to Treatment
If child shows no signs of improvement after 48 to 72 hours

1. Could indicate the onset of complications.
2. Incorrect drug/organism not responding
3. Incorrect dosage of the drugs used.
4. Non-compliance with the medications.
5. Associated lesions like immotile cilia syndrome, cystic fibrosis,
foreign bodies, mucus plugs, etc.
Complications
1. Pleural effusion
2. Empyema
3. Spreading pneumonia
4. Atelectasis
5. Myocarditis
6. Meningitis
7. Bacteremia
8. Recurrent pneumonia
Prevention
1. Administration of pneumococcal and conjugate/Hib vaccination.
2. Seasonal influenza vaccine.
3. Early and adequate treatment of upper respiratory tract infections.
Prognosis
Usually complete recovery, as documented by complete clearing of the
lung fields in the check X-ray. However, some children have a tendency
to have repeated attacks of pneumonia. In these patients, always suspect
an underlying disorder related to the immune system, immotile cilia
syndrome, alpha-1 antitrypsin deficiency, etc.
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FURTHER READINGS
1. American Lung Association. Trends in pneumonia and influenza morbidity
and mortality. 2008 (Sep).
2. Burke Cunka A. Pneumonia, community-acquired. (Medscope)
3. Falsey AR, Walsh EE. Viral pneumonia in older adults. Clin Infect Dis. 2006
(Feb 15); 42(4):518-24. [Medline]
4. Forgie S, Marrie TJ. Healthcare-associated atypical pneumonia. Semin Respir
Crit Care Med. 2009 (Feb);30(1):67-85. [Medline].
5. Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am. 2001
(Nov); 85(6):1461-91, x. [Medline].
6. Grant CC, Scragg R, Tan D. Hospitalization for pneumonia in children in
Auckland, New Zealand.: J Paediatr Child Health. 1998 (Aug);34(4): 355-9.
7. Hui DS. An overview on severe acute respiratory syndrome (SARS). Monaldi
Arch Chest Dis. 2005 (Sep );63(3):149-57. [Medline].
8. Hussain AN, Kumar V. The Lung. In: Robbins and Cotran (Eds). Pathologic
Basis of Disease. 7th edition Elsevier, Saunders; 2005:Ch 15.
9. Ketai L, Jordan K, Marom EM. Imaging infection. Clin Chest Med. 2008
(Mar);29(1):77-105, vi. [Medline].
10. Kim EA, Lee KS, Primack SL, et al. Viral pneumonias in adults: radiologic
and pathologic findings. Radiographics. 2002 (Oct);22 Spec No:S137-49.
[Medline].
11. Leventhal JM. Clinical predictors of pneumonia as a guide to ordering chest
roentgenograms. Clin Pediatr (Phila). 1982 (Dec);21(12):730-4. [Medline].
12. Levine OS, Farley M, Harrison LH, et al. Risk factors for invasive pneumococcal
disease in children: a population-based case-control study in North America.
Pediatrics. 1999(Mar);103(3):E28. [Medline].
13. Louie JK, Kajon AE, Holodniy M, et al. Severe pneumonia due to adenovirus
serotype 14: a new respiratory threat?. Clin Infect Dis. 2008 (Feb 1);46(3):421-
5. [Medline].
14. Mark I Neuman, Harvard Medical School; Pediatrics, Pneumonia. (medscape).
15. Murphy CG, van de Pol AC, Harper MB, Bachur RG. Clinical predictors of
occult pneumonia in the febrile child. Acad Emerg Med. 2007 (Mar);14(3):243-
9. [Medline].
17. Nicholas John Bennett Joseph Domachowske Isabel Virella-Lowell,
:Pneumonia: medscape.
18. Peter G. The Child with Pneumonia: Diagnostic and Therapeutic
Considerations. 7. 1988:453-6.
19. Schidlow DV, Callahan CW. Pneumonia. Pediatr Rev. 1996 (Sep);17(9):300-9;
quiz 310. [Medline].
20. Shah S, Mathews B, Neuman MI, Bachur R. Detection of occult pneumonia in
a pediatric emergency department. Pediatr Emerg Care. 2010 (Sep);26(9):615-
21. [Medline].
21. Smith NM, Bresee JS, Shay DK, et al. Prevention and Control of Influenza:
recommendations of the Advisory Committee on Immunization Practices
(ACIP). MMWR Recomm Rep. 2006 (Jul 28);55:1-42. [Medline].
22. Tarver RD, Teague SD, Heitkamp DE, Conces DJ. Radiology of community-
acquired pneumonia. Radiol Clin North Am. 2005 (May);43(3):497-512, viii.
[Medline].
vip.persianss.ir
23. Tsolia MN, Psarras S, Bossios A, et al. Etiology of community-acquired

pneumonia in hospitalized school-age children: evidence for high prevalence
of viral infections. Clin Infect Dis. 2004 (Sep 1);39(5):681-6. [Medline].
24. Waris ME, Toikka P, Saarinen T, et al. Diagnosis of Mycoplasma pneumoniae
pneumonia in children. J Clin Microbiol. 1998 (Nov);36(11):3155-9. [Medline].
25. Whitney CG, Harper SA. Lower respiratory tract infections: prevention using
vaccines. Infect Dis Clin North Am. 2004 (Dec);18(4):899-917. [Medline].
26. Wubbel L, Muniz L, Ahmed A, et al. Etiology and treatment of community-
acquired pneumonia in ambulatory children. Pediatr Infect Dis J. 1999
(Feb);18(2):98-104. [Medline].
vip.persianss.ir
Rheumatic Fever 137
Rheumatic Fever
14
Rheumatic fever is a complication that could arise subsequent to throat

infection caused by Group A beta-hemolytic streptococcus (GAS). These
organisms are notorious for causing sore throat (Fig. 14.1) and recurrent
sore throat could result in rheumatic fever.
ETIOLOGY
Human beings are natural reservoirs of GAS organisms. These
organisms are highly invasive and pathogenic and can cause disease in
normal individuals with no prior immunity. Infection spreads through
salivary droplets and infected nasal secretions. Hence, disease is
common in closed communities, daycare, crowded homes, etc.
Rheumatic fever could develop in children with recurrent
streptococcal sore throat that has been inadequately treated. There occurs
Fig. 14.1: Streptococcal sore throat
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an antigenic cross reaction between the Group A streptococci and the

cardiac muscles. Certain serotypes of the streptococci are considered
rheumatogenic and infection with these organisms can produce rheumatic
fever. These serotypes are M type—1, 3, 5, 6, 18, and 24.
The possible pathogenesis is partly explained by a cytotoxin
hypothesis, whereby it is presumed that the cytotoxins, especially
streptolysin O produced by the GAS organisms cross reacts with the
cardiac muscle tissue to produce damage to the tissues of the heart.
The other possible explanation is the immunogenic cross reactivity
between the GAS antigens and the tissues of the body, notably the heart
muscle. There could also be a possibility of involvement of the GAS
superantigens, in producing disease.
Symptoms
There is no definite symptom apart from fever.
However, in 1944, Duckett Jones suggested the occurrence of certain
criteria, which could aid in the diagnosis of rheumatic fever.
This has been subsequently modified as the ‘MODIFIED JONES’
criteria. There are five major criteria plus four minor criteria.
For the diagnosis to be made, a patient must have two major criteria,
two or one major plus two minor criteria (Fig. 14.2).
Major Criteria
• Carditis
• Polyarthritis
• Chorea
• Subcutaneous nodules
• Erythema marginatum
Minor Criteria
• Fever
• Arthralgia
Fig. 14.2: Major criteria in rheumatic fever
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Rheumatic Fever 139
Laboratory Evidence
• Elevated acute phase reactants—erythrocyte sedimentation rate
(ESR) and C-reactive protein (CRP)
• Prolonged P-R interval in the ECG
Supportive Evidence
Supportive evidence of preceding streptococcal infection:
• Elevated antistreptolysin O titre
• Positive throat swab culture for GAS organism
• Positive streptococcal test
CARDITIS
Carditis is potentially the most dangerous complication of GAS
infection. All the three heart layers could be affected—pericardium,
moycaridum and the endocardium. The acute phase is manifested as
myocarditis. There could be presence of murmur, tachycardia, sleeping
heart rate disproportionate to the extent of fever and change in the nature
of pre-existing murmur, if present.
Pericarditis could be manifested as minimal effusion, visualized on
echocardiogram, to a fulminant pericardial effusion (Fig. 14.3) causing
sudden death.
Endocardial involvement commonly affects the valves of the heart,
(valvulitis), especially the left-sided valves—mitral and aortic, making
them non-plaint resulting in regurgitation or stenosis. Endocarditis is a
common feature of rheumatic fever, while the occurrence of myocarditis
and pericarditis is variable. They do not occur without endocarditis in
rheumatic fever. 2D Echocardiogram will reveal the valve impairment.
However, for the criteria to be fulfilled, it is essential to have auscultatory
findings alongside the echo findings.
Fig. 14.3: X-ray showing pericardial effusion
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In fulminant rheumatic fever, all three layers of the heart may be

involved as pancarditis.
ARTHRITIS
Arthritis could be the earliest manifestation of rheumatic fever.
Typically, a polyarthritis of the flitting nature, involving the bigger
joints of the body like ankle, knee, shoulders, elbows, wrist, etc. There
is swelling of the joint due to edema in the joint spaces. The joints are
exquisitely tender and the child does not tolerate movement of even
the clothes on the joints. The pain and inflammation in one joint totally
subsides when the next joint is involved. The severity of the arthritis
has been found to be inversely related to the severity of carditis.
Involvement of the hip, spine and small joints of the extremities is
rare in rheumatic fever. The joint pain, if left untreated could persist for
as long as 6 to 8 weeks.
CHOREA
Chorea is usually a late manifestation of rheumatic fever and may occur
after all the other features have subsided. Occasionally, it may be an
isolated occurrence, but its presence alone can make the diagnosis of
rheumatic fever.
The child could suddenly develop difficulty in walking, unsteady
gait and show emotional lability—sudden bursts of spontaneous,
unprovoked crying, laughing, etc. aggravated by stressful situations.
Dropping objects from the hand or excessively tight grip or alternate
gripping and loosening called the milkmaid’s grip occurs. This is due
to the alternate contraction and relaxation of the hand muscles. The
handwriting may suddenly change and become unreadable or shaky.
On extension of the hands, tremors are noted distally and the hands
are kept pronated. On protrusion of the tongue, tremors are noted there,
called the “bag of worms” appearance. The head may make sudden jerky
movements to change direction—“jack -in –the- box appearance”.
All the above mentioned features are aggravated by stress, such as
talking to the patient while examination, etc. but disappear completely
during sleep.
ERYTHEMA MARGINATUM
Characteristic erythematous rash (Fig. 14.4) is seen during the acute
stage of the disease. It is difficult to notice, especially in the dark skinned
patients and is transient. It has a serpiginous erythematous pattern,
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Rheumatic Fever 141
Fig. 14.4: Erythema marginatum
with central clearing and is not itchy. It is predominant on the trunk

and extremities and does not occur on the face. If it is observed, it is
characteristic of rheumatic fever.
Subcutaneous Nodules
Subcutaneous nodules is a rare finding. Small tender nodule (Fig. 14.5)
approximately 1 cm in size occur on the extensor surfaces of the elbows,
shin, etc. They are noted at the insertion of the tendons along the bony
prominences. Could persist for some time during the course of the
disease and gradually fade away and are thought to be due to
immunological reactions in the body.
Minor Criteria and Laboratory Criteria help to make a Diagnosis

of Rheumatic Fever
Arthralgia—joint pain, in the absence of joint swelling, which may be
flitting in nature.
Fig. 14.5: Subcutaneous nodules
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Fever—high grade, over 102oF especially early in the course of the illness.
Elevated acute phase reactants—ESR (Erythrocyte sedimentation rate),
CRP (C-reactive protein) are supportive.
Elevated ASO (Antistreptolysin O) Anti-DNase B
Prolonged P-R interval in the ECG is indicative of first degree heart
block (Fig. 14.6).
Investigations
1. Sleeping pulse rate to be documented at least for 3 to 4 days, until
the diagnosis can be confirmed. Usually, pulse rate is higher than
expected for the height of fever—disproportionate elevation noted.
2. Complete blood count—may show polymorphonuclear
leukocytosis in arthritis and acute disease.
3. ESR elevated over 40 mm/hr may be in hundreds.
4. CRP elevated over 3 mg/dl
5. Anti-streptolysin O elevated > 250 Todd units
6. Anti-DNase B, anti-hyaluronidase levels elevated
Fig. 14.6: Clinical manifestations of acute rheumatic fever
Fig. 14.7: Frequency of occurrence of major symptoms in rheumatic fever
vip.persianss.ir
Rheumatic Fever 143
7. Chest X-ray may show cardiomegaly in case of cardiac failure with

pancarditis.
8. X-ray of the involved joints will show joint effusion and soft tissue
swelling. Helps to rule out other causes that may be associated
with rheumatic fever.
9. ECG in all 12 leads could show the prolonged P-R interval. Any
other associated cardiac arrhythmias may be noted. Evidence of
cardiac hypertrophy (Fig. 14.8), left ventricular hypertrophy, right
ventricular hypertrophy, which could suggest the underlying
valvular disease. Varying degrees of heart block may be noted.
Pericardial effusion may be suspected with low voltage complexes.
10. Echocardiogram gives a picture of the structural damage to the heart.
Cardiomegaly, pericardial effusion, decreased cardiac contractility,
Fig. 14.8: Increased transverse diameter of cardia
Fig. 14.9: Myocarditis with fast small PQR complexes on the ECG
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may be observed. Ventricular wall hypertrophy, valvular regurgitation

(Fig. 14.10) or stenosis may also be confirmed by Echo.
11. Synovial fluid aspiration in cases of arthritis,could show normal
glucose, increased protein levels > 4 g/dl, cell count is increased
10,000–100,000/cumm with a predominance of polymorphs.
Treatment
Bed Rest
Recommended during the acute stage, until the sleeping pulse rate is
normal.
Antibiotics
Penicillin is the drug of choice. Orally administered phenoxymethylpenicillin
125–250 mg orally 3 to 4 times per day for 10 days, or a single injection of
1,20,000 units of benzathine penicillin to eradicate associated GAS infection.
Alternative drug that may be used is erythromycin 40 mg/kg in four divided
doses for 10 days.
Aspirin
Given in patients with polyarthritis, carditis without cardiomegaly or
cardiac failure. Dose 100 mg/kg in four divided doses, orally, for 3 to 5
days, until the fever resolves and arthritis subsides. Normally, arthritis
shows a dramatic response to a single dose of aspirin.
Maintenance therapy with aspirin 75 mg/kg in four divided doses
for 4 to 6 weeks.
Prednisone
Indicated in patients with carditis with/without cardiomegaly and cardiac
failure: Dose 2 mg/kg in four divided doses for 2 to 3 weeks, till the
Fig. 14.10: Aortic regurgitation
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Rheumatic Fever 145
symptoms subside. Then gradually taper the dose with 5 mg/day every 2
to 3 days. Start aspirin at 75 mg/kg/day at the start of the tapering.
Additional therapy with digoxin- in case of cardiac failure.
Dose: 30–50 gm/kg is the total digitalising dose. Administer half
the amount at start, followed by ¼ after 8 hours and the remaining ¼
after 8 hours. Maintenance dose ¼ of the total digitalizing dose to be
given once daily 24 hours after the initial digitalizing dose.
Diuretics- Frusemide, (Lasix) – in case of heart failure. Dose
1–2 mg/kg/day once daily.
Oxygen inhalation
5. In chorea, sedation with phenobarbitone 16–32 mg every 6–8th hourly
orally is recommended. Alternatively, chlorpromazine 0.5 mg/kg every
4-6 hourly orally, or Haloperidol 0.01-0.01mg/kg in 12 hourly divided
doses, orally may be given (Fig. 14.11).
Prevention
Primary Prevention
To prevent the occurrence of rheumatic fever in a patient with GAS
infection. This is achieved by appropriate antibiotic therapy instituted
before the 9th day of infection in the patient.
Secondary Prevention
To prevent re-infection with GAS organisms in a patient who has
recovered from rheumatic fever. This is achieved by continuous
antibiotic prophylaxis.
Fig. 14.11: Drugs used in the treatment of rheumatic fever
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Drugs used for Antibiotic Prophylaxis

1. Inj benzathine penicillin 600,000–1,200,000 IU every 21 days
2. Tablet erythromycin 250 mg twice daily.
3. Sulfadiazine 0.5 mg once daily for children< 30 kg and 1 mg once
daily for children > 30 kg. Useful in children allergic to penicillin.
Alternate Drugs
1. Amoxicillin 125 mg orally thrice daily.
2. Cefadroxil 15 mg/kg/day orally.
Duration of Prophylaxis
1. Children with only rheumatic fever: Give for at least 5 years for
symptom free period, or until the age of 21 years
2. Children with rheumatic fever + carditis: Give for 10 years or until
adulthood, whichever is the longer period.
3. Children with rheumatic fever + carditis with residual heart disease:
For 10 years since the last episode or at least till the age of 40 years.
Prognosis
1. Only rheumatic fever—good prognosis. Ensure early treatment of
Group A streptococcal disease infections. Recurrence may occur, but
usually not associated with carditis.
2. Rheumatic fever + carditis—prognosis depends on the severity of
the carditis. If there is no residual heart damage, the prognosis is
good. The child needs continuous chemoprophylaxis.
3. Rheumatic fever + carditis + valvular disease/heart failure—
prognosis depends on the severity of the valve lesions. Usually prone
to recurrent GAS infections and recurrent rheumatic fever attacks.
FURTHER READINGS
1. Abernethy M, Bass N, Sharpe N, et al. Doppler echocardiography and the
early diagnosis of carditis in acute rheumatic fever. Aust N Z J Med. 1994
(Oct);24(5):530-5. [Medline].
2. AHA. Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992
update. Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease
of the Council. on Cardiovascular Disease in the Young, the American Heart
Association;JAMA 1992 (Oct 21);268(15):2069-73. [Medline].
3. Braunwald E. Rheumatic fever. In: Heart Disease: A Textbook of Cardiovascular
Medicine. 5th ed. Philadelphia, Pa: WB Saunders Co; 1997.
4. Carapetis JR, McDonald M, Wilson NJ. Acute rheumatic fever. Lancet. 2005
(Jul 9-15); 366(9480):155-68. [Medline].
vip.persianss.ir
Rheumatic Fever 147
5. Cilliers AM, Manyemba J, Saloojee H. Anti-inflammatory treatment for carditis

in acute rheumatic fever. Cochrane Database Syst Rev. 2003;CD003176.
[Medline].
6. Clinical trial. The natural history of rheumatic fever and rheumatic heart
disease. Ten-year report of a cooperative clinical trial of ACTH, cortisone,
and aspirin. Circulation. 1965 (Sep);32(3):457-76. [Medline].
7. Cotran RS, Kumar V, Collins T, et al. Robbins Pathologic Basis of Disease. 6th
ed. Philadelphia: WB Saunders Co; 1999.
8. Dajani A, Taubert K, Ferrieri P, et al. Treatment of acute streptococcal
pharyngitis and prevention of rheumatic fever: a statement for health
professionals. Committee on Rheumatic Fever, Endocarditis, and Kawasaki
Disease of the Council. on Cardiovascular Disease in the Young, the American
Heart Association;Pediatrics 1995 (Oct); 96(4 Pt 1):758-64. [Medline].
9. Gerber M, Baltimore R, Eaton C, et al. Prevention of rheumatic fever and
diagnosis and treatment of acute streptococcal pharyngitis. A scientific
statement from the American Heart Association Rheumatic Fever,
Endocarditis, and Kawasaki Disease Committee of the Council on
Cardiovascular Disease in the Young, the Interdisciplinary Council on
Functional Genomics and Translational Biology, and the Interdisciplinary
Council on Quality of Care and Outcomes Research. Circulation. 2009.
10. Guilherme L, Ramasawmy R, Kalil J. Rheumatic fever and rheumatic heart
disease: genetics and pathogenesis. Scand J Immunol. 2007;66(2-3):199-207.
[Medline]. [Full Text].
11. Jaine R, Baker M, Venugopal K. Acute rheumatic fever associated with
household crowding in a developed country. Pediatr Infect Dis J. 2010 (Oct
13) [Epub ahead of print].
12. Jaine R, Baker M, Venugopal K. Epidemiology of acute rheumatic fever in
New Zealand 1996-2005. J Paediatr Child Health. 2008 Oct;44(10):564-71.
13. Laurie Barclay. Once-Daily Oral Amoxicillin Effective for Streptococcus
Pharyngitis in Children: (medscape).
14. Lisa Nainggolan. AHA updates advice on strep throat, Preventing Rheumatic
Fever: (medscape).
15. Marijon E, Ou P, Celermajer DS, et al. Prevalence of rheumatic heart disease
detected by echocardiographic screening. N Engl J Med. Aug 2 2007;357(5):470-
6. [Medline].
16. Massell BF, Fyler DC, Roy SB. The clinical picture of rheumatic fever: diagnosis,
immediate prognosis, course, and therapeutic implications. Am J Cardiol.
1958 (Apr); 1(4):436-49. [Medline].
17. Minich LL, Tani LY, Pagotto LT, et al. Doppler echocardiography distinguishes
between physiologic and pathologic "silent" mitral regurgitation in patients
with rheumatic fever. Clin Cardiol. 1997 (Nov);20(11):924-6. [Medline].
18. Narula J, Virmani R, Reddy KS, et al. Rheumatic Fever. Washington DC:
American Registry of Pathology; 1999.
20. Pickering LK, et al. 2009 Red Book: Report of the committee on infectious
diseases. 28th ed. Elk Grove Village, IL: American Academy of Pediatrics;
2009:616-628.
21. Richard P Barthel, : PANDAS in Children - current approaches. (medscape).
22. Robertson KA, Volmink JA, Mayosi BM. Antibiotics for the primary prevention
of acute rheumatic fever: a meta-analysis. BMC Cardiovasc Disord. 2005 (May
31);5(1):11. [Medline].
vip.persianss.ir
23. Thomas K Chin, Eric M Chin, Tariq Siddiqui, et al Rheumatic Heart Disease.
(medscape).
24. Update on pediatric rheumatic diseases from ACR 2008.
25. Veasy LG, Wiedmeier SE, Orsmond GS, et al. Resurgence of acute rheumatic
fever in the intermountain area of the United States. N Engl J Med. 1987 (Feb
19);316(8):421-7. [Medline].
26. WHO. Rheumatic fever and rheumatic heart disease. 2004. WHO technical
report series. [Full Text].
27. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis:
guidelines from the American Heart Association: a guideline from the
American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki
Disease Committee, Council on Cardiovascular Disease in the Young, and
the Council on Clinical Cardiology, Council on Cardiovascular Surgery and
Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary
Working Group. Circulation. 2007 (Oct 9);116(15):1736-54. [Medline]. [Full
Text].
vip.persianss.ir
Status Epilepticus 149
Status Epilepticus
15
Definition
Status epilepticus is defined as a continuous convulsion lasting longer
than 20 to 30 minutes or the occurrence of serial convulsions between
which there is no return of consciousness. Generalized tonic-clonic
seizures predominate in cases of status epilepticus. Status epilepticus
is a medical emergency that requires an organized and skillful approach
to minimize the associated mortality and morbidity.
Causes
There are three major, common causes of status epilepticus in children.
1. Prolonged febrile seizures
2. Idiopathic status epilepticus
3. Secondary-status epilepticus due to underlying metabolic or
neurologic disorder.
Status epilepticus may occur in children with febrile seizures,
especially below 3 years of age. This is an unusual occurrence.
Idiopathic status epilepticus refers to those children who have no
underlying abnormality. This commonly occurs in children when
anticonvulsants are administered irregularly or in case of sudden
withdrawal of anticonvulsants, especially benzodiazepines.It may also
herald the onset of epilepsy in children.
The secondary group usually have an underlying structural
abnormality of the brain like hippocampal sclerosis. It may herald the
onset of encephalitis. It may be a complication of meningitis.
Status epilepticus in newborns may be an indication of underlying
metabolic disorders. This requires aggressive treatment to abort the
seizure, so as to prevent prolonged hypoxia and brain damage.
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Classification of Seizures (Fig. 15.1)

However, for the sake of convenience they are divided as follows:
Convulsive Status
Generalized Tonic-clonic
Tonic
Myoclonic
Partial Partial motor seizures
Non–convulsive Status
Generalized Absence seizures
Petit mal
Partial Complex partial seizures
Investigations
Complete Blood Count
Indicator of any underlying infective etiology, malignancy, chronic
infections, etc.
CRP (C-reactive Protein)

Acute phase reactant. Indicator of underlying bacterial infection or
inflammation. Non-specific.
Fig. 15.1: Any of the above mentioned seizure types may result in status epilepticus
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ESR (Erythrocyte Sedimentation Rate)

Acute phase reactant may indicate underlying disease like tuberculosis,
salmonella meningitis, intracranial tumors, etc. Non-specific.
Serum Electrolytes as follows:

a. Serum sodium: Alterations may indicate hypernatremia, or hyponatremia,
which can give rise to prolonged seizures.
b. Serum calcium: Lowered levels may be associated with tetany.
c. Serum magnesium: Low levels are associated with seizures, which
may be non-responsive to other medications.
d. Serum potassium: Needs to be monitored during treatment, hence
baseline values are invaluable.
Blood Gas Analysis

Important, especially in cases of prolonged status epilepticus. It gives
an indication of the metabolic status during therapy. Monitor levels of
PaO2,,PaCO2,,HCO3 levels.
Blood Glucose Levels

May be reduced in prolonged status.
Blood Urea and Serum Creatinine Levels

Especially indicated in children with vomiting, prolonged diarrhea with
dehydration and in young children.
Serum Phenytoin Levels, or Serum Valproate Levels

In case if known epileptic on treatment.
Blood Culture and Sensiitivity

To confirm presence or absence of bacterial infection.
Blood for PCR (Polymerase Chain Reaction) and Viral Cultures

In cases of suspected viral encephalitis.
Chest X-Ray
To rule out any associated chest infections, pneumonia, primary
complex, etc.
X-ray Skull
At least two views to locate any calcification, abnormalities visible
radiologically, etc.
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EEG
It is recommended in all patients. It will help to diagnose the underlying
etiology of the seizures.
CT scan Brain
Recommended to do the scan without the use of contrast dyes. Helps
in the identification of tumors, infections, congenital anomaly,
hydrocephalus, head trauma, etc.
MRI Scan
For a proper visualisation of the soft tissue structures, ventricular system, all
the cranial nerves and vascular system. Essential in younger patients with
partial seizures and in prolonged status epilepticus. Also recommended in
children with a history of delayed developmental milestones.
Lumbar puncture is not recommended when the child is in status
epilepticus as the chances of a traumatic tap are extremely high. To be
done only in case of suspected meningitis or CNS (Central nervous
system) dysfunction.
Management of Status Epilepticus

1. Assess heart rate and respiratory status—BP, heart rate, pulse (SPO2).
Keep the patient on a flat surface, preferably turned to one side.
2. Secure oral airway, clear oral and nasal passages of secretions.
3. Start oxygen infusion at 10 l/min. Consider intubation and assisted
ventilation, if required.
4. Insert IV cannula to maintain IV access.
5. Check random blood sugar (RBS) by glucometer. Administer
10 percent glucose at the rate of 5 ml/kg in case of low blood sugar
level. Administer thiamine 100 mg IV.
6. Collect blood sample for complete blood count (CBC) electrolytes
including sodium, calcium, phosphorus, magnesium, C-reactive
protein (CRP). In case of suscipion of infection, sample may be
collected for blood culture and sensitivity.
7. In case of normal RBS, start IV maintenance fluid containing
5 percent dextrose.
8. Administer drugs (Fig. 15.2).
Diazepam –––– 0.1–0.3 mg/kg IV. Maximum three doses may
be given.
0.3–0.5 mg/kg per rectaum
OR
Lorazepam–––– 0.005–0.1 mg/kg IV slow (0.05–0.1 mg/kg per
rectaum)
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Fig. 15.2: Important drugs used in status epilepticus
OR
Midazolam–––– 0.15-0.3 mg/kg IV slowly.
9. In case of persistence of status epilepticus, despite these drugs
administer:
Phenytoin–––– 15–30 mg/kg IV. Administer with normal saline
under cardiac monitoring. Do not use dextrose
solution.
10 mg/kg increments may be given at the rate
of 1 mg/kg/min
Phenobarbitone 15–20 mg/kg IV (10 mg/kg increments maybe
given over 10 to 30 minutes.
No use of IM injections in case of status epilepticus.
10. Consider elective intubation/mechanical ventilation in case of
persertence of status.
IV Infusion–Midazolam 0.2 mg/kg bolus, 20–40 g/kg/hr infusion

11. If still no improvement, intubation and ventilation with barbiturate
coma required.
Monitor EEG, ECG and SPO2 levels
Needs intensive care management.

12. Consider neurological opinion and further investigation.
FURTHER READINGS
1. Appleton R, Choonara I, Martland T, et al. The treatment of convulsive status
epilepticus in children. The Status Epilepticus Working Party, Members of
the Status Epilepticus Working Party. Arch Dis Child. 2000;83:415.
vip.persianss.ir
2. Appleton R, Macleod S, Martland T. Drug management for acute tonic-clonic

convulsions including convulsive status epilepticus in children. Cochrane
Database Syst Rev. 2008; CD001905.
3. Bleck TP. Management approaches to prolonged seizures and status
epilepticus. Epilepsia. 1999;40 Suppl 1:S59-63; discussion S64-6.
4. Chin RF, Neville BG, Peckham C, et al. Treatment of community-onset,
childhood convulsive status epilepticus: a prospective, population-based
study. Lancet Neurol. 2008;7:696.
5. Dardis C, Farid S, Doherty C. Re: New lessons: classic treatments in convulsive
status epilepticus. Ir Med J. 2008 (Feb);101(2):61.
6. Diagnosis and Management of non-convulsive status epilepticus in children
: Nature Clinical Practice Neurology:Christian M Korff; Douglas R, Nordli Jr
7. Early, Aggressive Treatment Warranted in Pediatric Status Epilepticus:
Caroline Cassells:Lancet Neurol. 2008;7:696-703 Abstract, 667-66.
8. Freeman JM. Status epilepticus: it's not what we've thought or taught.
Pediatrics. 1989; 83:444.
9. Hanhan UA, Fiallos MR, Orlowski JP. Status epilepticus. Pediatr Clin North
Am. 2001; 48:683.
10. Husain AM et al. (1999) Generalized periodic epileptiform discharges:
etiologies, relationship to status epilepticus, and prognosis. J Clin
Neurophysiol 16: 51-58.
11. Johnson J, Wrenn K. Inappropriate fosphenytoin use in the ED. Am J Emerg
Med. 2001; 19:293.
12. Khurana DS. Treatment of status epilepticus. Indian J Pediatr. 2000 (Jan);67(1
Suppl):S80-7.
13. Lowenstein DH (1999) Status epilepticus: an overview of the clinical problem.
Epilepsia 40 (Suppl 1): S3-S8.
14. Lowenstein DH and Aminoff MJ (1992) Clinical and EEG features of status
epilepticus in comatose patients. Neurology 42: 100-104.
15. Maytal J, Novak G, Ascher C, et al. Status epilepticus in children with epilepsy:
the role of antiepileptic drug levels in prevention. Pediatrics 1996;98:1119.
16. McIntyre J, Robertson S, Norris E, et al. Safety and efficacy of buccal midazolam
versus rectal diazepam for emergency treatment of seizures in children: a
randomised controlled trial. Lancet 2005;366:205.
18. Rivera R, Segnini M, Baltodano A, et al. Midazolam in the treatment of status
epilepticus in children. Crit Care Med. 1993;21:991.
19. Riviello JJ Jr, Ashwal, S, Hirtz, D, et al. Practice parameter: diagnostic
assessment of the child with status epilepticus (an evidence-based review):
Report of the Quality Standards Subcommittee of the American Academy of
Neurology and the Practice Committee of the Child Neurology Society.
Neurology 2006;67:1542.
20. Singh RK, Gaillard WD. Status epilepticus in children. Curr Neurol Neurosci
Rep. 2009 (Mar);9(2):137-44.
21. Singh RK, Stephens S, Berl MM, et al. Prospective study of new-onset seizures
presenting as status epilepticus in childhood. Neurology 2010;74:636.
22. Singh, BM, Strobos, RJ. Epilepsia partialis continua associated with nonketotic
hyperglycemia: clinical and biochemical profile of 21 patients. Ann Neurol.
1980;8:155.
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23. Singhi S, Dass R, Singhi P: Status epilepticus: emergency management. Indian

J Pediatr. 2003 (Mar);70 Suppl 1:S17-22.
24. Sofou K, Kristjánsdóttir R, Papachatzakis NE, et al. Management of prolonged
seizures and status epilepticus in childhood: a systematic review. J Child
Neurol. 2009;24:918.
25. The treatment of convulsive status epilepticus in children:the status epipelticus
working party: R Appleton, I Choonara, TM Artland, B Phillips, R.Scott,
W.Whitehouse,: Ir Med J. 2007 (Nov-Dec); 100 (10):618-20.
26. www. medscape.com
27. www.ilae-epilepsy.org
vip.persianss.ir
Urinary Tract
16 Infection in Children
URINARY TRACT INFECTION

Urinary tract infection (UTI) is diagnosed when the urine culture shows
a colony count of over 105 organisms after 48 hours of incubation. In
case of the culture showing 104 organisms and the child is symptomatic,
it is considered to be a UTI. In the absence of culture positivity, UTI
cannot be documented.
Incidence of UTI in infancy shows a male : female ratio of 3–5:1, but
beyond 2 years, the incidence is higher in females showing 1:10 ratio.
1. Female sex
2. Uncircumcised male
3. Improper toilet training
4. Poor perineal hygiene
5. Bubble bath
6. Vesicoureteiral reflux
7. Urinary tract obstruction
8. Pinworm infestation
9. Constipation
Symptoms (Fig. 16.1)

• Increased frequency of micturition
• Painful micturition
• Burning micturition
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Urinary Tract Infection in Children 157
• Passing high colored urine

• Passing blood with urine
• Fever
• Passing reduced amount of urine
• Dribbling of urine.
Signs
• Non-specific
• May be febrile
• Unable to pass urine without pain.
Investigations
1. Complete blood count will show leukocytosis with neutrophilic
predominance.
2. CRP (C-reactive protein), ESR (Erythrocyte sedimentation rate)
increased indicates bacterial infection. Non-specific.
3. Peripheral blood smear shows leukocytosis.
4. Urine midstream sample is recommended. Routine exam will show
increased number of pus cells.
5. Urine nitrites and leukocyte esterase will be positive in case of
infection.
6. Urine culture and sensitivity after 48 hours incubation will be
positive. Over 105 organisms/ml will indicate definite UTI.
The sensitivity pattern will guide the treatment.
7. Ultrasound scan of the kidney-ureter-bladder (KUB) area is
recommended in male children after the first episode of documented
UTI and after the second episode in female children. This is done to
confirm the presence of urinary obstruction, hydronephrosis, renal
scars, calculi or any other structural renal abnormality.
Fig. 16.1: Important symptoms of urinary tract infection
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8. Voiding cystourethrogram (VCUG) is needed to rule out the presence

of vesicoureteral reflux (VUR), as the ultrasound is not sensitive and
is able to pickup only 40 percent VUR. VCUG is done after the first
episode of UTI in males. In females, in case of recurrent UTI (> 4 – 5
episodes in 6 months). Radionuclide labeled VCUG is preferred to a
contrast VCUG as it gives more accurate results.
9. DMSA is the scan dimereaptosuccinic acid most sensitive test to
demonstrate renal scarring. Also useful in cases of VUR, pyelonephritis
and other renal abnormalities.
Treatment
1. Plenty of oral fluids is recommended. Water, barley water, juice,
milk, tender coconut water, etc.
2. Antibiotics to be started immediately in case of suspected UTI.
Empirical antibiotics may be used depending on the prevalent
strains and may be changed once the culture reports are available.
Amoxicillin-clavulanic acid acts as a broad spectrum antibiotic
50–70 mg/kg/day in divided doses.
Nitrofurantoin 5–7 mg/kg/day in 3–4 divided doses is useful against
E scherichia coli and Klebsiella organisms also.
Duration of treatment is 10 to 14 days.
3. Avoid tight fitting underwears.
4. Improve local hygiene, especially in females and provide improved
toilet training.
5. Treat associated worm infestations.
Once the antibiotic course is complete, it is recommended to repeat
a urine culture test to ensure complete sterilization of the urine.
In case of recurrent UTI, close follow-up and frequent urine test
once in three months is recommended.
FURTHER READINGS
1. Alon US, Ganapathy S. Should renal ultrasonography be done routinely in
children with first urinary tract infection? Clin Pediatr (Phila). Jan
1999;38(1):21-5. [Medline].
2. Barnett BJ, Stephens DS. Urinary tract infection: an overview. Am J Med Sci.
1997;314:245-9.
3. Craig JC, Simpson JM, Williams GJ, et al. Antibiotic prophylaxis and recurrent
urinary tract infection in children. N Engl J Med. 2009 (Oct 29);361(18):1748-
59. [Medline].
4. Dick PT, Feldman W. Routine diagnostic imaging for childhood urinary tract
infections: a systematic overview. Dialysis. 1996 (Jan);128(1):15-22. [Medline].
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Urinary Tract Infection in Children 159
5. Girardet P, Frutiger P, Lang R. Urinary tract infections in pediatric practice. A

comparative study of three diagnostic tools: dip-slides, bacterioscopy and
leucocyturia. Paediatrician. 1980;9(5-6):322-37. [Medline].
6. Goldsmith BM, Campos JM. Comparison of urine dipstick, microscopy, and
culture for the detection of bacteriuria in children. Clin Pediatr (Phila). 1990
(Apr);29(4):214-8. [Medline].
7. Hellerstein S. Recurrent urinary tract infections in children. Pediatr Infect
Dis. 1982;1:271-81.
8. Hellerstein S. Urinary tract infections. Old and new concepts. Pediatr Clin
North Am. Dec 1995;42(6):1433-57. [Medline].
9. Hoberman A, Wald ER. Urinary tract infections in young febrile children.
Pediatr Infect Dis J. 1997 (Jan );16(1):11-7. [Medline].
10. Mårild S, Jodal U. Incidence rate of first-time symptomatic urinary tract
infection in children under 6 years of age. Acta Paediatr. 1998;87:549-52.
11. Merguerian PA, Sverrisson EF, Herz DB, et al. Urinary tract infections in
children: recommendations for antibiotic prophylaxis and evaluation. An
evidence-based approach. Curr Urol Rep. 2010 (Mar);11(2):98-108. [Medline].
13. Nuutinen M, Uhari M. Recurrence and follow-up after urinary tract infection
under the age of 1 year. Pediatr Nephrol. 2001;16:69-72.
14. Roberts KB, Akintemi OB. The epidemiology and clinical presentation of
urinary tract infections in children younger than 2 years of age. Pediatr Ann.
1999;28:644-9.
15. Rushton HG. Urinary tract infections in children. Epidemiology, evaluation,
and management: Pediatr Clin North Am. 1997 (Oct);44(5):1133-69.
16. Shah G, Upadhyay J. Controversies in the diagnosis and management of
urinary tract infections in children: Paediatr Drugs. 2005;7(6):339-46.
17. Stanley Hellerstein, Urinary tract infections in children, pathophysiology, risk
factors and management. [online] Available from www.medscape.com.
18. Winberg J, Andersen HJ, Bergstrom T, et al. Epidemiology of symptomatic urinary
tract infection in childhood. Acta Paediatr Scand Suppl. 1974;(252):1-20.
19. Zaffanello M, Malerba G, Cataldi L, et al. Genetic risk for recurrent urinary
tract infections in humans: a systematic review. J Biomed Biotechnol.
2010;2010:321082. [Medline].
20. Zamir G, Sakran W, Horowitz Y, et al. Urinary tract infection: Is there a need
for routine renal ultrasonography? Arch Dis Child. 2004;89:466-8. [Medline].
21. Zelikovic I, Adelman RD, Nancarrow PA. Urinary tract infections in children.
An update. West J Med. 1992 (Nov);157(5):554-61.
22. Zorc JJ, Levine DA, Platt SL, et al. Clinical and demographic factors associated
with urinary tract infection in young febrile infants. Pediatrics. Sep
2005;116(3):644-8. [Medline].
vip.persianss.ir
Vulvovaginitis
17 in Children
VULVOVAGINITIS
Vulvovaginitis is a common condition in children. It is characterized
by vaginal discharge associated with pruritus, erythema and tenderness.
The proximity of the vagina to the anal orifice makes it an easy source
of infection. This, together with the low estrogen levels in the
prepubertal child makes the vagina, a susceptible location. The thin
labial folds are inadequate to protect the delicate internal structures
which are exposed on squatting.
Prolonged use of bubble baths, tub baths, poor local hygiene, shared
toilets and use of medicated toiletries, enhance the chances of
vulvovaginitis.
Helminthic infestations, especially pinworms which cause extreme
pruritus, can act as precursors for vulvovaginitis.
Recurrent vulvovaginitis is common in cases of poor perineal hygiene.
Etiology
Bacteria
Staphylococci, especially from the local skin area, streptococci,
Escherichia coli, occasionally shigella.
Helminths
Enterobiasis (pinworm) is associated with increased incidence.
vip.persianss.ir
Vulvovaginitis in Children 161
Protozoa
Giardiasis is common in children.
Viral
Molloscum contagiosum can cause umbilicated lesions in the vulval
area resulting in itching and discharge.
Sarcopties Scabeii
Rarely but especially with gross and widespread scabies
Other causes
Candida, anaerobic bacteria like peptococci, peptostreptococci,
Gardneerella vaginalis, etc. (Fig. 17.1).
Symptoms of Vulvovaginitis
Vaginal discharge is the presenting symptom in over 75 to 80 percent
of cases. The discharge is initially minimal, but tends to be troublesome
and could increase in untreated cases. Most often, the mild discharge is
ignored initially, but presents in the clinic when it causes a significant
staining of the underclothes.
The discharge is usually thin, translucent, and not foul smelling,
unless there is an infective etiology. Tends to be increased upon exercise,
straining or excessive sweating.
Pruritus or intense itching is associated with the discharge. It may
be so intense that it may result in bleeding.
Erythema or redness of the vulval area (Fig. 17.2) may be associated
with symptoms of burning especially more during micturition. The child
may find it extremely difficult to pass urine and this may be
misinterpreted as dysuria. This can also result in increased frequency
of micturition as the child is unable to evacuate the bladder completely
at a stretch, due to the severe pain.
There may also be nocturnal enuresis, with bedwetting.
Fig. 17.1: Common etiology of vulvovaginitis
vip.persianss.ir
Fig. 17.2: Red and inflamed vulval and vaginal mucosa
Signs of Vulvovaginitis (Fig. 17.3)

1. Vaginal discharge
2. Erythema in the vulval region
3. Local scratch marks may be noted
4. Localized bleeding in the vulval and genital region.
Investigations
1. Physical inspection of the local area is of utmost importance. The
diagnosis can be made most often by physical examination alone.
2. Vaginal discharge smear shows the presence of bacteria, pus cells,
giardia, or any other infective organisms.
Fig. 17.3: Commonest symptoms and signs of vulvovaginitis
vip.persianss.ir
Vulvovaginitis in Children 163
3. Vaginal swab culture and sensitivity will grow the infecting organism
and show its sensitivity pattern.
4. Urine exam routine to rule out associated urine infection, diabetes
mellitus, etc.
5. Urine culture and sensitivity in case if any evidence of urine infection.
Culture positivity documents the organism responsible.
6. Stool examination in cases suspected to be caused by Giardia lamblia.
7. Blood sugar test is recommended in cases of recurrent vaginitis, to
rule out underlying diabetes mellitus.
Treatment
1. Local hygiene- frequent washing, especially after micturition. Avoid
use of irritant soaps, use of mild vaginal wash is recommended.
2. Frequent changing of underclothes, use of only cotton underwear.
3. Avoid use of tubs, bubble baths, shared pools, etc.
4. Avoid tight fitting clothes, jeans, leotards, etc. adequate vulval airing
is extremely important for healing of the vulvovaginitis.
5. Treat the specific causative organism in case of bacteria, topical
antibiotic cream are normally adequate to clear the infection. Topical
bacitracin is an excellent antibiotic. In case of non-response or in
case of associated systemic symptoms like fever, etc. use of a systemic
antibiotic penicillin, amoxicillin is recommended. In severe cases,
cephalosporin is recommended.
6. In case of giardiasis, use of metronidazole 10 mg/kg in two divided
doses is recommended for 7 to 10 days.
7. In case of Candida infection, topical antifungal like canesten is usually
adequate for clearing.
8. In case of Molluscum contagiosum, thermal curettage of the lesion is
recommended.
9. In case of Enterobiasis, the child needs to be given anthelminthic.
Single dose albendazole gives as good results as mebendazole for 3
days. The dose may need to be repeated after 2 to 3 weeks.
Prevention of Recurrence
• Improved local hygiene
• Frequent changing of underwear.
• Use of cotton underwear only
• Regular deworming
• Avoiding use of tubs and areas of stagnant water during bath.
vip.persianss.ir
Prognosis
Excellent. With improved local hygiene, the chances of recurrence is
minimal.
FURTHER READINGS
1. Angotti L, Lambert L, Soper D. Vaginitis: making sense of over-the-counter
treatment options. Infect Dis Obstet Gynecol. 2007;97424. [Medline].
2. Biggs WS, Williams RM. Common gynecologic infections. Prim Care. Mar
2009;36(1):33-51, viii. [Medline].
3. Eckert LO. Clinical practice. Acute vulvovaginitis. N Engl J Med. 2006 (Sep
21); 355(12):1244-52. [Medline].
4. Emans SJ. Vulvovaginitis in the child and adolescent: Pediatrics in Review
1986;8:1,12-9.
5. Freeto JP, Jay MS. "What's really going on down there?" A practical approach
to the adolescent who has gynecologic complaints. Pediatr Clin North Am.
2006 (Jun ); 53(3): 529-45, viii. [Medline].
6. Jasper J. Vulvovaginitis in the prepubertal child. Clin Pediatr Emerg Med.
2009 (Mar);10.
7. Jones R. Childhood vulvovaginitis and vaginal discharge in practice. Family
Practice 1996;13:369-72.
8. Katz. Vaginitis. In: Katz (Ed). Comprehensive gynecology. 5th edition. Elsevier.
2007;588-96.
9. Mark Leber J, Anuritha Tirumani: Vulvovaginitis, [online] available from
www.medscape.com
10. Nelson's textbook of pediatrics 18th edition.
11. Nyirjesy P. Vulvovaginal candidiasis and bacterial vaginosis. Infect Dis Clin
North Am. 2008 (Dec);22(4):637-52, VI [Medline].
12. Owen MK, Clenney TL. Management of vaginitis. Am Fam Physician. 2004
(Dec 1); 70(11):2125-32. [Medline].
13. Szumigala JA, Alveredo R. Vulvovaginitis. In: Ferri: Ferri's clinical advisor,
Elsevier. 2009;155:1008-12.
14. Vulvovaginitis in children, [online] available from www.rch.org.au.
vip.persianss.ir
Index
Page numbers followed by f refer to figure
A Bronchopneumonia 129
Acidosis 96 Bulbar conjunctival congestion 114f
Active typhoid infection 44 Bulging and erythema of tympanic
Acute membrane 125f
febrile stage 116 C
HBV infection 70
rheumatic fever 142f Carditis 139
Acyanotic CHD 30 Causes of
Adenovirus 128 anaphylaxis 21
Advantages of reduced osmolar ORS 92 bronchomalacia/tracheomalacia 32f
Aedes aegypti mosquito 76f diarrhea 86
Alternate drugs used in tuberculosis 61 juvenile rheumatoid arthritis 100
Anaphylaxis 21 Kawasaki disease 113
Anatomy of ear 121f reactive arthritis 109
Antibiotics 23, 97, 144 Central nervous system disease 54
Anticholinergics 7, 8 Cerebellitis 47
Anti-inflammatory drugs 23 Chest X-ray 151
Antipyretics 133 Chlamydia trachomatis 128
Aortic regurgitation 144f Chorea 140
Aphasia 47 Chronic lung disease 30
Arthritis 110f, 111f, 140 Citrate 92
Aspirin 144 Classical Kawasaki disease 114
Assessment of dehydration 88 Classification of
Asthma 1 asthma 4
pharmacotheraphy 6 seizures 150
Atopic Complete
dermatitis 14, 18f blood count 150
eczema 15 eradication of mosquito vectors 83f
Atypical Kawasaki disease 114 Complications of pulmonary
tuberculosis 53f
B Composition of ORS 91
Bacteria 122, 160 Control of factors contributing to
BCG vaccination 57 severity 6
Bed rest 144 Corticosteroid therapy 57
Blood 23 C-reactive protein 150
culture and sensitivity 151 Cyanosis 40
for PCR 151 Cycle of transmission of typhoid 41f
gas analysis 151 Cytomegalovirus 128
glucose levels 151
urea and serum creatinine levels 151 D
Bone and joint disease 50 Decreased sensorium 40
Bronchial asthma 2f, 3f Dengue fever 85, 77
Bronchiolitis 26, 26f Diarrhea 86
Bronchomalacia 32 Diet in typhoid fever 47
vip.persianss.ir
Disseminated Hyperlucent lung 28f

disease 50 Hypertonic dehydration 95
tuberculosis 57 Hypotonic dehydration 95
Dosage of vaccine 72 Hypoxia 40
Dosage schedule for
immunization 72, 73f I
Drugs Immunization in tuberculosis 63
in gastroenteritis 96 Immunosuppressive therapy 57
used in treatment of rheumatic Incubation period 42
fever 145f Infection with atypical mycobacteria 57
Dry powder inhaler 7 Inflammation in asthma 5f
Inhaled corticosteroids 8
E Insect bites 23
Early pneumonia 130f Intermediate disease 50
Edema and swelling of lips and Interstitial pneumonitis 129
mucosa: erythema of Intravenous fluids 92
ear lobes 25f Isotonic dehydration 94
Endobronchial tuberculosis 50, 62
Erythema marginatum 140, 141f J
Erythrocyte sedimentation rate 151 Jaundice visible in conjunctiva 64f
Exacerbation 5 Juvenile rheumatoid arthritis 99
F K
False Kawasaki disease 114
negative tuberculin test 57
positive tuberculin test 57 L
Feeding in gastroenteritis 96 Leukotriene inhibitors 9
Flaky skin with erythematous Liver in hepatitis 62f
papules on cheek 17f Low-birth weight infants 30
Frequency of causative viruses 37f Lower airway obstruction 40
Lymph node disease 50
G Lymphohematogenous spread of
Gastroenteritis 86f tuberculosis 53
Giant urticarial patches 22f
M
H Macular skin rash in systemic juvenile
Haemophilus influenzae B bacteria 128 rheumatoid arthritis 103f
Helminths 160 Malnutrition 57
Hemodynamically unstable Management of
cyanotic CHD 30 asthma 6
Hepatitis status epilepticus 152
A 64 Mantoux test 57
B 67 Meningeal infection 50
C 73 Metered-dose inhaler 6
D 74 Methods of transmission of infection 49
E 76 Methylxanthines 7, 8
virus 66f Mild dehydration 89
Herpes simplex virus 128 Miliary tuberculosis 53, 62
HIV infection 57 Mode of transmission of infection 42
Homemade ORS solution 93f Moderate dehydration 89
vip.persianss.ir
Index 167
Mouth and throat anatomy 37f Role of

Mycoplasma pneumoniae 128 corticosteroids in tuberculosis 62
Myocarditis with fast small PQR steroids in typhoid fever 47
complexes on ECG 143f Rotavirus
diarrhea 89f
N particle 87f
Nebulizer 6 Route of transmission 64, 67, 76
Non-atopic eczema 15 Routes allergens 23
Non-convulsive status 150
Normal saline 94 S
Sarcopties scabeii 161
O Severe
Occasionally varicella zoster virus 128 and chronic disease 18
Optic neuritis 62 of dehydration 89, 90
Oral Shock 47
corticosteroids 8 Short-acting oral beta 2-agonists 7
feeds of ORS 91f Signs of
Otitis media 121, 124f juvenile rheumatoid arthritis 101
reactive arthritis 110
P rotavirus diarrhea 87
Palivizumab 30 vulvovaginitis 162
Parainfluenza virus 128 Small joint swelling and deformity 101f
Partly controlled asthma 5 Smallest airways affected in
Pathophysiology of bronchiolitis 26f
rotavirus diarrhea 86 Soft tissue swelling bony
Pauciarticular JRA 99, 101 deformity and narrow
Pericardial effusion 54 cartilaginous space 104f
Pneumonia 130f Stages in development of
in children 128 Kawasaki's disease 116f
with interlobar fissure effusion 131f Status
Pneumonitis 129 asthmaticus 11
Polyarticular JRA 99, 101 epilepticus 153f
Polymerase chain reaction 151 Steeple sign 39f
Prednisone 144 Steroids in typhoid fever 47
Previous infection with salmonella 44 Strawberry tongue in
Primary pulmonary disease 51 Kawasaki disease 115f
Progressive primary Streptococcal sore throat 137f
complex 50 Streptococci bacteria 128
tuberculosis 52, 53f Subcutaneous nodules 141, 141f
Protozoa 161 Symptoms of
juvenile rheumatoid arthritis 101
R reactive arthritis 110
Red and inflamed vulval and rotavirus diarrhea 87
vaginal mucosa 162f vulvovaginitis 161
Regular assessment and monitoring 6 Systemic glucocorticosteroids 7
Renal and GIT disease 50
Resolving lobar pneumonia 131f T
Respiratory syncytial virus 128 Tracheomalacia 32
Rheumatic fever 138f, 141f, 142f Transient skin rash in dengue fever 78f
Ringer's lactate 94 Transmission of hepatitis B virus 69f
vip.persianss.ir
Treatment of eye lesions 106 U

Trisodium citrate 92 Urinary tract infection 156, 157f
Tubercle bacilli 57
Tubercular V
arthritis 62
Vaccinations in
meningitis 57
JRA 106
Tuberculin test 57
Kawasaki disease 118
Tuberculoma 62
Tuberculosis 58f Viral hepatitis in children 63, 84
in children 48, 84 Virus transmission into human host 76f
Tuberculous ascites 62 Viruses causing bronchiolitis 26f
Tympanometry 124 Vulvovaginitis 160, 161f, 162f
Types of
W
atopic dermatitis 15
dehydration 94 Wasp stings 23
fluids for infusion 94 Widal test 44
inhalation devices available 6 Worsening stridor 40
juvenile rheumatoid
arthritis 99, 100f X
otitis media 122, 122f X-ray
Typhoid of hand 104f
in children 41, 83 of neck 39f
vaccination 44 skull 151
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Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com

Ready Reckoner For Treatment in Pediatrics

I express my gratitude to Prakash, my dear husband, who has always

1. Asthma in Children .......................................................................... 1

3. Anaphylaxis in Children ............................................................... 21

5. Bronchomalacia and Tracheomalacia ......................................... 32

6. Croup (Laryngotracheobronchitis) .............................................. 36

Algorithm to follow While Treating a

9. Juvenile Rheumatoid Arthritis ..................................................... 99

12. Otitis Media in Children ............................................................. 121

13. Pneumonia in Children ............................................................... 128

14. Rheumatic Fever ........................................................................... 137

15. Status Epilepticus ......................................................................... 149

16. Urinary Tract Infection in Children .......................................... 156

17. Vulvovaginits in Children .......................................................... 160

Fig. 1.1: Etiopathogenesis of bronchial asthma with treatment modalities

7. Familial history of asthma in parents

BOX 1.1: Asthma Management

Types of Inhalation Devices Available

MDI (metered-dose inhaler)

Dry Powder Inhaler

Oxygen inhalaton may be needed to avoid ventilation: perfusion

Inhaled Corticosteroids (ICS)

Budesonide: 200 to 400 microgram every 6 to 8 hourly. Maximum 800

Long-acting Beta Agonists

Zafirlukast and Montelukast

Zafirlukast and Montelukast of the two, montelukast has found

All tablets are chewable, hence acceptance is easy. Alternatively, it

Suggested Treatment Protocol

Fig. 1.4: Suggested treatment protocol

to the level at which symptom control can be achieved. It is better to go

3. Ipratropium may be added to the SABA. This helps in relieving the

10. Excessive sweating

Types of Atopic Dermatitis

Fig. 2.2: Flaky skin with erythematous papules on the cheek

• Erythematous papules with flaky skin

4. Avoid excessive heat and sweating

13. Superimposed fungal or viral infection may occur and needs to be

Predictive Factors for Severe and Chronic Disease

Fig. 2.3: Preventive methods to be adopted in children with atopic dermatitis

Nuts—peanuts, hazelnuts, walnuts, cashewnuts, pistachios, brazil nuts,

Medicines—antibiotics, anti-inflammatory, non-steroidal anti-

Table 3.1: Routes of Exposure to Allergens

Fig. 3.1: Symptoms indicating anaphylaxis

the throat, choking sensation, wheezing, difficulty in breathing, etc. are

Fig. 3.2: Giant urticarial patches seen on trunk and limbs

• Child may feel itching due to severe pruritus

Post Emergency Treatment

Fig. 3.4: Avoid allergens like pets

Fig. 4.1: Smallest airways affected in bronchiolitis

Commonly Caused by Viruses

Common Causative Agents

Fig. 4.2: Viruses causing bronchiolitis

Fig. 4.3: Predisposing factors in bronchiolitis

Fig. 4.4: Showing hyperlucent lung fields

Fig. 4.5: Correlation between RSV infection and wheezing

BOX 4.1: Indications for Palivizumab

3. Romero JR. Palivizumab prophylaxis of respiratory syncytial virus disease

BRONCHOMALACIA AND TRACHEOMALACIA

Fig. 5.1: Causes of Bronchomalacia/tracheomalacia