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Essence of Pediatrics

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Prof. MR KhanMBBS, DTM&H, DCH, FCPS, FRCP

National ProfessorDirector & Professor (Honorary) of Child Health

Institute of Child Health & Shishu Shasthya Foundation Hospital, DhakaVisiting Professor, International Centre for Diarrheal Disease

Research, Bangladesh (ICDDR,B)

Prof. M Ekhlasur RahmanMBBS, FCPS, FRCP Edin

Professor and Head Department of Pediatrics

Dhaka Medical College & Hospital, Dhaka

ELSEVIERA division of

Reed Elsevier India Private Limited

Essence of PediatricsFourth Edition

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Essence of Pediatrics, 4/eKhan and Rahman

ELSEVIERA division ofReed Elsevier India Private Limited

Mosby, Saunders, Churchill Livingstone, Butterworth-Heinemann and Hanley & Belfus are the Health Science imprints of Elsevier.

© 2011 Elsevier

All rights are reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise without the prior permission of the publisher.

ISBN: 978-81-312-2804-3

Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The authors, editors, contributors and the publisher have, as far as it is possible, taken care to ensure that the information given in this text is accurate and up-to-date. However, readers are strongly advised to confi rm that the information, especially with regard to drug dose/usage, complies with current legislation and standards of practice. Please consult full prescribing information before issuing prescriptions for any product mentioned in this publication.

Published by Elsevier, a division of Reed Elsevier India Private Limited.Registered Offi ce: 622, Indraprakash Building, 21 Barakhamba Road, New Delhi–110 001.Corporate Offi ce: 14th Floor, Building No. 10B, DLF Cyber City, Phase II, Gurgaon–122 002, Haryana, India.

Managing Editor (Development): Shabina NasimDevelopment Editor: Shravan Kumar Manager Publishing Operations: Sunil KumarProduction Executive: Arvind Booni

Typeset by Chitra Computers, New Delhi.

Printed and bound at Sanat Printers, Kundli, Haryana.

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Dedicated to our mothers:Jaira Khanam

Ameena KhatoonFor the continued aff ection & inspiration they have fl owing non-stop

in the stream of their blood for their children

Dedicated to our wives:Anwara Khan

Rehana RahmanFor their inherent inquisitiveness and intense enthusiasm that had

made the delivery of this book less painful

“Every time a child is born, it brings with it the hope that God is not yet disappointed with man”—Rabindranath Tagore

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Contributors

Prof. MN IslamMBBS, FCPS, FRCPProfessor and Head, PediatricsGanoshasthya Samajvittic Medical College, Dhaka

Professor Nazmun NaharMBBS, FCPS, FRCPProfessor of PediatricsAdditional Director General, BIRDEM, Dhaka

Prof. Md Moazzem HossainMBBS, FCPS, FRCPProfessor of Pediatric Nephrology & Treasurer, Bangabandhu Sheikh Mujib Medical University, Dhaka

Prof. AFM SelimFCPS, PhDProfessor of PediatricsDeputy Director, Institute of Child Health & SSF Hospital, Dhaka

Dr. AN AlamMBBS, PhDConsultant PhysicianICDDR,B, Dhaka

Prof. Md Nazrul IslamMBBS, FCPSProfessor of PediatricsCommunity Based Medical College & Hospital, Mymensingh

Prof. ASM Bazlul KarimMBBS, FCPSProfessor of Pediatric Gastroenterology & NutritionBangabandhu Sheikh Mujib Medical University, Dhaka

Prof. Md Habibur RahmanMBBS, FCPS, MDProfessor of Pediatric NephrologyBangabandhu Sheikh Mujib Medical University, Dhaka

Prof. M Q-K TalukderMBBS, DIP NUTR, DCH, PhD, FRCPChairman, Centre for Women & Child Health, Dhaka

Prof. MA MannanMBBS, FCPS, M Phil, FRCPEx. Pro-VC & Professor of Pediatric Hematology & OncologyBangabandhu Sheikh Mujib Medical University, Dhaka

Prof. Shafi qul HoqueMBBS, FCPSChairman, Department of Pediatric SurgeryBangabandhu Sheikh Mujib Medical University, Dhaka

Prof. Md Abul Kashem SarkarMBBS, DCH, MRCPProfessor of PediatricsBangladesh Institute of Child Health (BICH), Dhaka

Prof. ARM Luthful KabirMBBS, FCPSProfessor of PediatricsSir Salimullah Medical College & Mitford Hospital, Dhaka

Dr. Md Mesbah Uddin AhmedMBBS, D Ortho, MSConsultant, Orthopedic SurgerySquare Hospital, Dhaka

Prof. Soofi a KhatoonMBBS, FCPSProfessor & Head, PediatricsShahid Suhrawardy Medical College & Hospital, Dhaka

Dr. Sajal Kumar MazumderMBBS, MSAssistant Professor of Pediatric SurgeryShahid Suhrawardy Medical College & Hospital, Dhaka

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ESSENCE OF PEDIATRICS

Dr. MA RoufMBBS, MD, FCPSAssistant Professor of NeonatologySylhet MAG Osmani Medical College & Hospital, Sylhet

Prof. Md Abid Hossain MollahMBBS, FCPS, FRCP, M Med, FCCPProfessor of PediatricsDhaka Medical College & Hospital, Dhaka

Prof. Afi qul IslamMBBS, FCPS, MDChairman, Pediatric Hematology and OncologyBangabandhu Sheikh Mujib Medical University, Dhaka

Dr. Narayan Chandra SahaMBBS, FCPSAssociate Professor of PediatricsDhaka Medical College & Hospital, Dhaka

Dr. Selina Husna BanuMBBS, DCH, PhDAssociate Professor of Neuroscience, Department of PediatricsInstitute of Child Health and Shishu Shasthya Foundation Hospital, Dhaka

Dr. Rehana Perveen MBBS, FCPSAssociate Professor of Obstetrics & GynaecologyShahid Suhrawardy Medical College & Hospital, Dhaka

Dr. Ahmed Murtaza ChoudhuryMBBS, FCPSAssociate Professor of PediatricsMymensingh Medical College & Hospital, Mymensingh

Dr. Shakil AhmedAssistant Professor of PediatricsShahid Suhrawardy Medical College & Hospital, Dhaka

Dr. Monirul Islam Khan RanzuMBBS, MDConsultant, PediatricsMymensingh Medical College, Mymensingh

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Preface to the Fourth Edition

In United States of America, reduction of infant & neonatal mortality was identifi ed as two of ten important achievements during the last century. Th e ten countries of South-East Asia Region (SEAR) contribute to 40% of neonatal deaths and 40% of deaths due to tuberculosis; 30% of U5 child deaths occur in SEAR.

Although globally U5 mortality has decreased by almost a third since 1970s, this reduction has not been evenly distributed throughout the world. According to the 2005 World Health report, about 10.5 million children die before they reach their 5th birthday—60% of them die of malnutrition, 20% of pneumonia, 12% of diarrhea, and 22% of perinatal causes.

We are really amazed by the overwhelming acceptance of “Essence of Pediatrics”, Th ird Edition by the under- and post-graduate students, pediatricians, and teachers in countries of South-East Asia region. We are very much thankful and grateful to them.

Th is edition contains detailed and updated coverage of all the systems. Th ere is also addition of a new chapter named “Drug Th erapy in Children”. All the topics have been thoroughly revised, corrected, and expanded.

We gratefully acknowledge the publications and books from where information has been taken; reference lists have been cited at the end of each chapter, but if some have been left out through oversight, we off er our sincere apologies.

We hope that the fourth edition of “Essence of Pediatrics” will continue to stimulate the under- and post-graduate medical students, doctors, and pediatricians of Bangladesh, India, Nepal, Pakistan & other countries, and will prove to be as useful to readers as the third edition had been.

Our heartiest thanks are due to Dr. Abu Sadat Mohammad Saleh, Dr. UKM Nazmun Ara, and Dr. Nazmul Huq of Department of Pediatrics, Dhaka Medical College & Hospital for their untiring eff orts in preparation of manuscript and proof reading; they worked smilingly to complete this Himalayan task early. We are also thankful to Dr. Mohammad Mohsin, Dr. Abu Sayeed, Dr. Mehdi Pervez and Dr. Monir Hossain of Department of Pediatrics, Dhaka Medical College & Hospital whose hard work and co-operation have made delivery of this book less painful.

We acknowledge gratefully the contributions made by Dr. Shishir Ranjan Das, Assistant Professor of Neonatology, Dhaka Medical College and Dr. Imnul Islam, Assistant Professor of Pediatrics, Bangabandhu Sheikh Mujib Medical University, Dhaka.

Any constructive criticism and structured suggestion will be thankfully acknowledged.For the fi rst time, Elsevier, a division of Reed Elsevier India Pvt. Ltd. has taken the responsibility of editing, printing, and

publishing the fourth edition of “Essence of Pediatrics”; we express our heartiest thanks and felicitation to all the staff members of Elsevier.

Dhaka MR KhanJuly, 2011 M Ekhlasur Rahman

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Preface to the First Edition

It has long been felt that a book dealing with practical pediatric problems is urgently needed; in this small volume, we have discussed briefl y the recent management of commoner childhood diseases consulting the available current literatures. Protein–energy malnutrition, acute respiratory infections and diarrheal diseases are written a bit elaborately, since these are the major killer diseases of children here. One chapter, in this book, is devoted for practical procedures and another one for pediatric dose calculation; so it is presumed that this volume will be very much helpful in pediatric practice. We hope this book will meet up some of the demands of under- and post-graduate medical students, general practitioners, and pediatricians.

References have been cited at the end of each chapter, but if some have been left out through oversight, we off er our sincere apologies.

We are deeply thankful to Prof. Maleka Khatoon, Prof. M Q-K Talukder, and Dr. CA Kawser of Department of Pediatrics, IPGM&R; Prof. Md Nurul Islam and Dr. Shafi ur Rahman of Sir Salimullah Medical College; Prof. Nazmun Nahar, Dr. Munimul Hoque, and Dr. Quazi Monzurul Moula of Dhaka Medical College; Prof. FH Nazir and Dr. ABM Siddique of Rajshahi Medical College; Dr. MA Rab of Sylhet Medical College, Dr. SA Hamid of Mymensingh Medical College, Prof. Shahadat Hussein and Dr. Chowdhury B Mahmood of Chittagong Medical College; Dr. Hamidur Rahman of Rangpur Medical College, Dr. BD Shaha of Sher-e-Bangla Medical College and Prof. MS Akbar, Dr. AFM Salim of Dhaka Shishu Hospital for their chronic encouragement and inspiration in writing a book on pediatrics.

Our sincere appreciations and thanks are due to Dr. Bazlul Karim, Dr. Azizur Rouf, Dr. ARM Luthful Kabir, Dr. Afi qul Islam, Dr. Shahnewaz-bin-Tabib, Dr. Manajjir Ali, Dr. Md Ruhul Amin, and Dr. Mohammad Shahidullah for their spontane-ous help in writing this book.

We owe a great deal to Mr. Motior Rahman Khan (Moti) for his frequent persuation in timely completion of this book, and to Mr. Hawladar for his secretarial assistance. We wish to thank to the staff s of Messrs BRAC Printers whose hard work and co-operation had made this endeavor possible.

Any suggestion or criticism for updating this volume will be thankfully acknowledged.

Dhaka MR KhanJanuary, 1989 M Ekhlasur Rahman

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Contents

Contributors ......................................................................................................................................................vii

Preface to the Fourth Edition ...............................................................................................................................ixPreface to the First Edition ..................................................................................................................................xi

Pictorial Diagnosis ............................................................................................................................................. xv

Chapter 1 HistoryTaking and Physical Examination ...............................................................................1Chapter 2 Neonatology .............................................................................................................................7Chapter 3 Infant and Young Child Feeding ............................................................................................49Chapter 4 Growth and Development ......................................................................................................56Chapter 5 Nutritional Problems ..............................................................................................................72Chapter 6 Community Pediatrics ............................................................................................................85Chapter 7 Respiratory Diseases .............................................................................................................104Chapter 8 Diseases of Gastrointestinal System ......................................................................................130Chapter 9 Cardiovascular Diseases ........................................................................................................152Chapter 10 Renal Diseases ......................................................................................................................195Chapter 11 Fluid Electrolytes and Acid–Base Disturbances ....................................................................212Chapter 12 Endocrine and Metabolic Diseases .......................................................................................219Chapter 13 Neurology .............................................................................................................................252Chapter 14 Muscle Disorders ..................................................................................................................286Chapter 15 Hematology ..........................................................................................................................291Chapter 16 Oncology ..............................................................................................................................303Chapter 17 Connective Tissue Diseases ...................................................................................................317Chapter 18 Child Psychiatry and Developmental Disorders ...................................................................330Chapter 19 Dermatology .........................................................................................................................347Chapter 20 Poisoning ..............................................................................................................................357Chapter 21 Immunization and Infectious Diseases .................................................................................370Chapter 22 Genetic Disorders .................................................................................................................423Chapter 23 Common Surgical Problems .................................................................................................444Chapter 24 Procedures in Practice ...........................................................................................................455Chapter 25 Some Selected Syndromes ....................................................................................................465Chapter 26 Laboratory Medicine ............................................................................................................469Chapter 27 Drug Th erapy in Children ...................................................................................................473Chapter 28 Growth Charts ......................................................................................................................508

Index ..............................................................................................................................................................531

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Diseases of Ear, Nose, and Throat

DISEASES OF THE EAR

Otitis MediaAnatomic feature that makes children younger than 5 years susceptible to ear infections include shorter, more horizontally placed complaint Eustachian tubes, which permits refl ux of nasopharyngeal secretions into the middle ear. Other risk factors include exposure to cigarette smoke, over-crowding, bottle-feeding, cleft palate, and allergic rhinitis. Th e same risk factors are operative in the pathophysiology of the two common varieties of otitis media seen in children—acute sup-purative otitis media (ASOM) and otitis media with eff usion (OME).

Acute Suppurative Otitis MediaChildhood acute otitis media tends to occur in a bimodal age distribution, with children between ages 6 and 24 months and between ages 5 and 6 years at greatest risk. Streptococcus pneumoniae and Haemophilus infl uenzae are the two most common causative organisms of ASOM, accounting for approximately 65% of all cases. About 15% of the cases are due to Branhamella catarrhalis, Streptococcus pyogenes, and Staphylococcus aureus infection. Respiratory viruses may play an important role in initiating otitis media and may be the only pathogens involved in some cases, as up to 20% of middle ear aspirates are sterile.

Clinical Features Acute otitis media presents with a history of ear discomfort or pain lasting anywhere from a few hours up to several days. Th ere is often a history of recent upper respiratory tract infection. Infants may present with irritability, otalgia, and incessant crying. A child with acute otitis media may also pull or rub the aff ected ear(s). Older children may report impaired hearing in the aff ected ear. Fever is frequently present, particularly in younger children. Dramatic relief of pain, irritability, and crying indicates perforation of ear drum; pus discharge is seen at this stage.

Otoscopic examination generally reveals a red and bulging tympanic membrane, decreased mobility with loss of normal landmarks. Suppuration (rupture of the drum with ear dis-charge) may be seen fi lling the ear canal. Cleaning of this fl uid usually reveals an intact drum, as the rupture is small and closes promptly after spontaneous perforation.

Treatment Antimicrobial therapy is the mainstay of treatment. Adjuvant treatment with oral decongestant drugs has not been shown to be of any signifi cant value, but may be used selectively to provide symptomatic relief of nasal blockage from co-existing cold. Topical decongestants, though frequently prescribed, are detrimental due to rebound congestion and nasal and nasopharyngeal mucosal irritation. Another frequently misused class of drugs is antihistamines, which contribute little to the resolution of otitis media and may precipitate sinus infections due to their drying eff ect on mucosal secretions.

Amoxicillin should be the fi rst-line therapy for acute otitis media. Higher doses (60–90 mg/kg/d) may be considered

CHAPTER 7Respiratory Diseases

Diseases of ear ........................................................................104 Otitis media ..........................................................................104 Otitis externa ........................................................................105 Hearing loss .........................................................................106Diseases of the nose and sinuses ......................................106 Rhinitis ...................................................................................106 Sinusitis ..................................................................................107 Nasal obstruction ................................................................108 Sleep disordered breathing ............................................108 Epistaxis .................................................................................108 Choanal atresia ....................................................................109Diseases of the throat ...........................................................109

Acute pharyngitis ................................................................109 Acute laryngotracheitis ......................................................110 Acute spasmodic laryngitis ...............................................110 Croup (Laryngotracheobronchitis) .................................110 Acute epiglottitis ..................................................................111Bronchiolitis ..............................................................................112Bronchiolitis obliterans ..........................................................113Asthma .......................................................................................114Pneumonia ...............................................................................119 Viral pneumonia ..................................................................121 Pneumococcal pneumonia ...............................................121 Staphylococcal pneumonia ..............................................121

Haemophilus infl uenzae pneumonia ............................122 Primary atypical pneumonia ............................................122 Hospital-acquired pneumonia .........................................122Summary of physical signs in the common

respiratory diseases ............................................................123Lung abscess ............................................................................124Bronchiectasis ..........................................................................124Pleural effusion ........................................................................126Empyema thoracis ..................................................................126Pneumothorax .........................................................................127Subcutaneous emphysema ..................................................128Respiratory failure ...................................................................128

Chapter Contents

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RESPIRATORY DISEASESC

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where streptococcal resistance is endemic. Drugs such as co-trimoxazole, amoxicillin–clavulanic acid, cefaclor, cefu-roxime, or other newer cephalosporins are useful second-line agents for unresponsive infections.

Some dissent exists regarding the routine use of antibiotic for uncomplicated ASOM, because at least 50% of uncom-plicated cases experience spontaneous resolution within 24–48 hours. Antibiotics are reserved for those children who show continued symptoms after 48 hours. Initial antibiotic therapy should last at least 7 days in uncomplicated cases, with re-examination indicated after 3–4 days and at 3 weeks. Current evidence does not support use of decongestant and antihistamine in ASOM. Myringotomy/tympanocentesis is indicated in children with severe refractory pain, hyperpy-rexia, and complications (i.e., mastoiditis, facial paralysis, labyrinthitis, or CNS infection).

Many children present with recurrent episodes of ASOM. If particularly troublesome, this condition may be treated either with prolonged antibiotic prophylaxis (e.g., amoxicillin 20 mg/kg for 3–6 months) or insertion of tympanostomy tubes. Th ere are preliminary data that adenoidectomy may be eff ective as well.

Complications Extracranial complications include acute mas-toiditis, subperiosteal and neck abscesses, and facial palsy. Acute mastoiditis should initially be treated with parenteral antibiot-ics, e.g., chloramphenicol. Surgery in the form of a cortical mastoidectomy is reserved for cases with poor response to par-enteral antibiotic therapy, subperiosteal abscess, an intracranial complication, or acute mastoiditis in a chronic ear. Intracranial complications are meningitis or intracranial abscess.

Otitis Media with Eff usionFollowing an episode of ASOM, serous middle ear eff usions may be seen in a number of children. Eff usion has been found to persist in up to 40% of children 1 month after their fi rst episode of otitis media and usually subsides within 3 months. Treatment is warranted in cases lasting for 3 months or more. However, many children with fl uid eff usion in the middle ear do not have any history of acute middle ear infections in the past. Pathogenesis of this condition has not been clearly established, but infectious, allergic, or immunologic mecha-nisms may be at play.

Diagnosis Mild to moderate hearing loss and sensation of ear blockage are the chief complaints, although the condition may also be asymptomatic. Otoscopy reveals a dull tympanic membrane, loss or distortion of cone of light with or without a fl uid level. Diagnosis is established by demonstrating reduced mobility of the tympanic membrane with insuffl ation, or more reliably, by fi nding a type B pattern on tympanometry. Audi-ometry may reveal varying degree of hearing loss.

Treatment Since 50% of serous middle ear eff usions resolve spontaneously within 3 months, newly diagnosed eff usions

should be observed for this period in nearly all cases. If eff usion persists beyond 3 months, tympanostomy tube insertion may be considered for signifi cant hearing loss (>25 dB). Improvement in hearing as well as ear discomfort is immediate and quite gratifying, but lasts only as long as the tubes are in place. Mean time before extrusion is usually between 6 and 9 months. Th e majority of the ears recover by the time the tubes extrude, but some children require repeated tube placements. Insertion of tubes (of T-tube design) for long term or adenoidectomy may be considered in cases of persistent symptomatic eff usion. It is probably safe for children to avoid swimming altogether to prevent contamination of the middle ear space.

CSOM: The Draining EarPersistent or recurrent ear discharge is generally due to chronic infection of the middle ear space. Such infection invariably presents with chronic perforation of the tympanic membrane, which allows egress of the suppurative material. Chronic sup-purative otitis media (CSOM) most often results from neglected acute middle ear infections.

Pseudomonas aeruginosa, S. aureus, Proteus species, E. coli, and anaerobic streptococcal organisms are the organisms identifi ed commonly in chronically draining ears.

Less frequently, CSOM may be seen with cholesteatoma, which is a sac of squamous epithelium extending from the tympanic membrane into the middle ear. Most cholesteatoma is acquired, rarely, congenital. Th ough not malignant, cholesteatoma may cause serious complications by slow expansion and local destruction. Such complications include mastoiditis, mastoid and neck abscesses, inner ear infection resulting in sensory hearing loss, facial palsy, meningitis, and intracranial abscess.

Treatment Medical therapy consists primarily of topical anti-biotics, though oral or parenteral administration may be necessary in selected cases. Ear drying by wicking is helpful. Instructions to parents to avoid water entry in the aff ected ear should also be given. Otolaryngology referral is mandatory for ruling out cholesteatoma.

Surgical therapy is primarily directed towards creating a “safe ear”. If cholesteatoma is suspected, ear exploration and cholesteatoma removal is mandatory. In simple tympanic membrane perforations without cholesteatoma, surgical repair is now considered appropriate treatment in children older than 8 years of age. Tympanic membrane repair (tympanoplasty) protects the ear from further contamination and infection, often improves hearing, and may have a positive eff ect on the quality of the child’s life.

Otitis ExternaAcute diff use otitis externa (“swimmer’s ear”) presents with itching, pain, and fullness in the aff ected ear. Pain is severe and precludes otoscopic examination. Tympanic membrane is usually normal, if it is visualized. Erythema and edema of the


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canal skin and tenderness on moving the pinna and pressing over tragus are diagnostic features. Cerumen is soft and white instead usual fi rm-yellow. Preauricular lymph node may be tender and palpable. P. aeruginosa and S. aureus are the most common organisms isolated in diff use otitis externa. Treatment consists of ear canal cleaning by experienced personnel and topical antibiotic (neomycin based preferable). Oral or even parenteral antibiotics may be needed for severe cases.

Localized otitis externa or furunculosis presents as an exquisitely painful, superfi cial abscess in the outer portion of the ear canal. Such infection is commonly staphylococcal in origin. Oral anti-staphylococcal antibiotics and analgesics bring about prompt relief. Occasionally, incision and drainage of a pointing abscess may be necessary.

Eczematous or psoriatic otitis externa describes a group of infl ammatory conditions in which there is drainage, pruritus and/or scaling of the ear canal skin. Underlying causes include contact dermatitis, atopic dermatitis, and seborrheic dermatitis. To treat this condition eff ectively, the primary dermatologic disorder must be addressed.

Otomycosis or fungal otitis externa is most common in humid weather and presents with pain and pruritus of the aff ected ear. Examination reveals fungal spores and fi laments along with cloudy discharge. Aspergillus is the most common pathogen, though other fungi may be implicated. Aural toilet and application of clotrimazole are curative.

Hearing LossConductive hearing loss: Any process that interferes with the conductive mechanism of the ear canal, tympanic membrane, or ossicles may cause a conductive hearing loss. Th e most common cause of conductive deafness in children is otitis media with eff usion. Several congenital syndromes may also be associated with middle ear abnormalities, such as Apert, Crouzon, and Treacher–Collins syndromes.

Sensorineural hearing loss: Sensorineural hearing loss (SNHL) is caused by a lesion of the cochlea, auditory nerve, or central auditory pathways. SNHL can be acquired or congenital. Th e majority of pediatric SNHL falls into the acquired category.

Th e most common cause of acquired sensorineural hearing loss is meningitis. Other causes include perinatal infections (TORCH, mumps, measles), neonatal hyperbilirubinemia, perinatal asphyxia, and ototoxic medications (aminoglycosides, loop diuretics).

Congenital causes of sensorineural hearing loss can be further divided into hereditary (i.e., Alport, Pendred syndromes) and non-hereditary types. Causes of non-hereditary congenital hearing loss include neonatal sepsis, prematurity/low birth weight, and congenital infections.

ScreeningNeonatal screening: All neonates with risk factors for hearing loss must be screened with an auditory brainstem response

(ABR) to exclude hearing impairment. It must be recognized, however, that use of clinical indicators to focus hearing screens will miss as many as 50% of all cases of impairment, while universal ABR testing would be ideal.

Screening in older children: It has been shown that parental assessment of the child’s hearing, while helpful, is not always reliable. Unrecognized hearing loss of even a mild to moderate severity can lead to speech and language delays and academic under-achievement. Examination should include otoscopy with attention to middle ear pathology, such as OME and CSOM. Any doubtful cases must be referred for detailed audiologic evaluation at the earliest opportunity in order that timely intervention for hearing rehabilitation may begin. Multiple techniques exist to assess hearing sensitivity and are selected based on the age and the abilities of the child. For younger children unable to understand instructions, behavioral or play audiometry is usually performed. Pure-tone audiometry is usually possible in children >5 years of age. Tympanometry may be performed in nearly all children to assess ear drum mobility.

TreatmentOnce the diagnosis of hearing loss has been established, treat-ment is based on the extent of defi cit and on the underlying pathology. For very mild or unilateral hearing loss, treatment includes preferential seating in school. For signifi cant conduc-tive hearing loss, treatment may consist simply of tympanos-tomy tubes or tympanoplasty.

Sensorineural hearing loss, in contrast, is generally more diffi cult to correct than conductive hearing loss. Treatment of signifi cant SNHL may require the use of assistive hearing devices such as hearing aids from as early as 3 months of age. Cochlear implants are indicated only for profound (>90 dB) sensorineural deafness that is unresponsive to a 3–6 month trial with the most powerful hearing aid available.

Lip reading, sign language, and deaf education programs should be considered for children who are not candidates for or cannot aff ord cochlear implantation.

DISEASES OF THE NOSE AND SINUSES

Allergic RhinitisAllergic rhinitis is an infl ammatory disorder characterized by sneezing, itching, nasal blockage, and clear rhinorrhea; symptoms may be seasonal (“hay fever”) or perennial. Th is occurs mainly in children older than 5 years; but diagnosis may be made in infants. Symptoms in younger ones are sniffi ng, snorting, and rubbing of nose; while older children tries to clear nose with repeated blowing. Repeated allergic salute (rubbing nose with open palm) creates nasal crease over the bridge of the nose. Nasal congestion and blockage are severe enough at night to cause sleep disturbance, irritability, and snoring. Asthma, sinusitis, allergic conjunctivitis, and otitis media are comorbid conditions often associated with


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allergic rhinitis. Examination reveals an edematous nasal mucosa, boggy-hypertrophied inferior terbinates, mucoid discharge, hyper-trophic pharyngeal lymphoid follicles (cobblestone appearance), and postnasal drainage. Conjunctival itching and redness are sometimes present. Inhaled allergens (pollen, spores, dust mites) are the most common cause; food allergy (e.g., to cow’s-milk) is rarely implicated.

Th ough the above symptomatology is characteristic, accu-rate diagnosis may require demonstration of raised eosinophil counts in blood and nasal mucus, and skin and serologic tests to show specifi c IgE response to a variety of allergens (allergy tests). High nasal eosinophil indicates allergic diagnosis, while higher neutrophil count supports bacterial infection

Treatment Avoidance of known allergens, use of topical cromolyn

sodium and intranasal steroid sprays for prevention, oral montelukast, and antihistamines for relief of symptoms.

Topical decongestants should generally be discouraged as they cause rebound congestion (short-term) and chemical rhinitis or rhinitis medicamentosa (long-term). However, it can be used in severe nasal blockage interfering daily life. Use should be restricted to 5 days and once in a month.

Immunotherapy may be benefi cial for refractory cases, but its application is now infrequent owing to the success of steroid sprays.

Viral Rhinitis (Common Cold) Viral infections of the nose are very common in the pediatric age group. Parents often need reassurance that such frequent colds are not abnormal, provided their child has an otherwise normal growth pattern. Malaise, low to moderate grade fever, nasal congestion, and rhinorrhea are the presenting symptoms.

TreatmentTreatment is symptomatic and requires paracetamol for fever. For nasal blockage, normal saline can be instilled in nostrils every 4–6 hours. Plenty of fl uid should be advised. Home remedies (honey, tulshi, lemon juice) are benefi cial for cough and cold. Antihistamines are contraindicated. Otitis media and sinusitis are frequent complications.

SinusitisEthmoid and maxillary sinuses are the earliest to develop and are the ones most commonly involved in infancy and early childhood. Maxillary sinusitis may be associated with ethmoidal infection in children older than 1 year, and frontal sinuses may become involved only after 4–5 years of life. Ethmoidal pathology is now recognized to be the primary site of origin of infl ammation in most cases of sinusitis.

Th e most common isolates are S. pneumoniae, H. infl uenzae, B. catarrhalis, and S. pyogenes.

Clinical FeaturesAcute sinusitis typically follows an episode of viral rhinitis and presents with nasal discharge, nasal congestion, moderate fever, foul breath (halitosis), cough and postnasal discharge. Fever of moderate severity may be present in younger children. Tenderness over the involved sinuses is present in adolescent and adults; a purulent nasal and postnasal discharge may be entirely negative. Children seldom complains of headache and facial pain.

Diagnosis CT scanning, when available and aff ordable, is far superior to plain x-ray PNS OM view in the diagnosis of sinusitis. Opacifi cation, mucosal thickening, and air-fl uid level are the imaging fi ndings of sinusitis, but do not point towards the etiology.

Complications Preseptal cellulitis, orbital cellulitis, and abscess are more common. Infections behind the orbital septum can occur in infants as well as older children, and present with proptosis, chemosis, and painful ocular movement. In addition, ophthal-moplegia, loss of vision, and severe toxemia indicate a spread of infection to the cavernous sinus. Intracranial complications such as meningitis and abscesses may also occur.

Treatment Amoxicillin given for 10 days should be the fi rst-line of

medical therapy for acute sinusitis. Second-line agents, such as amoxicillin-clavulanic acid, clarithromycin, or cefuroxime, should be reserved for unresponsive infections or suspected antibiotic resistance. Longer courses are indicated for refrac-tory infections. Treatment of frontal sinusitis should be initiated with parenteral antibiotic, because it can rapidly progress to intracranial infection.

Other adjuvant measures that may have a possible benefi t include oral decongestants, mucolytic agents, and topical nasal saline. Antihistamines are detrimental due to their drying eff ect on mucosal secretions and are best avoided.

An additional consideration in treating chronic or recur-rent acute sinus infections is the presence of underlying infl ammation, such as that caused by allergy, passive smoke inhalation, or exposure to environmental pollut-ants. Control of such processes may help to eliminate the infection. In refractory cases, a CT scan must be ordered to identify anatomical abnormalities requir-ing surgical correction. Surgery in chronic or recurrent sinusitis should be directed towards opening the natural sinus ostia (“functional” sinus surgery); however, with aggressive medical therapy, the need to resort to sinus surgery in children should be rare.


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Nasal ObstructionChronic mouth breathing in children is generally caused by blockage of nasal air-fl ow. Th e site of nasal blockage is more often in the nasopharyngeal area, i.e., adenoid hypertrophy. Intranasal causes of obstruction include allergic rhinitis, recur-rent sinusitis, nasal septum deviation, turbinate hypertrophy, and antrochoanal polyp. Certain tumors (such as sarcomas or angiofi bromas) and congenital lesions (such as choanal atresia or meningoceles) also belong in the diff erential diagnosis.

DiagnosisAdenoid enlargement should be suspected in children, usually older than 2 years, who present with nasal blockage, mouth breathing, sleep disturbance, and chronic nasal discharge. Examination must rule out nasal pathology. X-ray of naso-pharynx (lateral view) will confi rm the presence of soft tissue enlargement in the nasopharynx.

TreatmentTonsillectomy is often recommended for recurrent attacks of sore throat. It does not prevent recurrence of pharyngeal infections. Tonsillectomy should be advised only if there are more than six signifi cant attacks of tonsillitis in a year for two consecutive years or if there is tonsillar or peritonsillar abscess. It may reduce the incidence of group A beta-hemolytic strep-tococcal infection (GABHS). Tonsillectomy is recommended in diphtheria carriers. Tonsils may be removed only if these are acting as foci of infection for suppurative otitis media. Tonsil-lectomy should not be done during epidemics of poliomyelitis. Th ere is no indication for tonsillectomy after rheumatic fever or glomerulonephritis.

Other indications include obstructive sleep apnea or suspi-cion of malignancy. History of previous peritonsillar abscess may also be a relative indication.

Tonsillar hypertrophy alone is not an indication. Recurrent otitis media with eff usion and deafness may be an indication for tonsillectomy.

Adenoidectomy should be recommended for symptomatic younger children. In older children, it is useful to remember that pubertal growth of the mid-face and regression of adenoid size tends to result in relief of adenoid-related nasal obstruction from around the age of 9 years.

Generally speaking, surgery on the nasal septum should be avoided in prepubertal children, as it may lead to retardation in mid-face growth and saddling of the nasal dorsum. Turbinate hypertrophy usually responds to treatment of allergy, though in refractory cases, electrocautery may be used for reduction of turbinate size.

Sleep Disordered BreathingObstructive sleep apnea (OSA) has been increasingly recognized in children. Snoring is the hallmark of sleep apnea. Adenotonsillar

hypertrophy is the main cause of OSA in children. During sleep, muscle tone reduces and there is critical obstruction of already compromised upper airway (by adenotonsillar hypertrophy), obstruction causes awakening from sleep and the airway again opens. Th is goes on cyclically throughout the night, and there is repeated hypoxemia-sympathetic hyperactivity.

Clinical Features Childhood OSA is a disorder of breathing during sleep, char-acterized by prolonged upper airway resistance and partial or complete airway obstruction disrupting pulmonary ventila-tion and oxygenation. Night-time manifestations are snoring, snorting, mouth breathing, increased respiratory eff ort, upper torso sweating, choking, restless sleep, sleeping with hyperex-tended neck and frequent awakening. Some children present with secondary nocturnal enuresis. Daytime symptoms are sleepiness school hours, early morning headache, tiredness, fatigue, hyperactivity, poor attention span, poor school per-formance, aggressiveness, failure to thrive, below average IQ, and pulmonary hypertension. Physical fi ndings are mid-facial hypoplasia, receding chin, high arched palate, hypertension, FTT, adenotonsillar hypertrophy, large tongue, and nasal block. OSA is associated with Down syndrome, hypothyroidism, and mucopolysaccharidoses (MPS).

Diagnosis Gold standard: Overnight polysomnography (PSG)—>1.5

apnea-hypopnea index is diagnostic of OSA. X-ray nasopharynx (lateral view): Enlarged adenoid with

compression of the air column.

Treatment Topical nasal steroid (Fluticasone) use for 6 weeks has been

found to demonstrate moderate improvement in a double-blind study in children.

Adenotonsillectomy is found to be curative in 85% cases, even if they are obese.

CPAP is used as second-line treatment, especially where adenotonsillectomy is contraindicated or failed.

EpistaxisMost epistaxis occurs in the antero-inferior portion of the nasal septum due to the rich capillary vasculature in this region known as Little’s area (also known as Kiesselbach’s plexus). Minor trauma, vigorous rubbing of the nose, use of nasal steroid, and dry winter air are frequently the cause of bleeding. Daytime bleeding occurs without warning and is spontaneous, while night-time bleeding may be swallowed and bloody vomiting or melena frequently causes diagnostic confusion.

Examination reveals prominent capillaries in Little’s area that bleed promptly when touched with a cotton-tipped probe.


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Treatment Digital pressure by pinching the nose invariably stops

bleeding. Avoidance of nose picking, application of an antibiotic

ointment for lubrication and antimicrobial protection, and for refractory cases, cautery (with silver nitrate or electro-cautery), packing (anterior or posterior nasal packing), or surgery (ligation of anterior ethmoidal artery) can be done.

Control of allergy may be important in atopic children. Hematinics to improve hemoglobin status.

Bleeding disorders must be suspected in children with a suggestive family history, a history of frequent bleeding from other sites, or any nasal bleeding that does not respond in the usual fashion.

Nasopharyngeal angiofi broma is a tumor occurring exclu-sively in adolescent males that can cause brisk bleeding in a young boy.

Choanal AtresiaFailure of the nasal cavities to open posteriorly into the naso-pharynx (choanae) during fetal development is called choanal atresia. Th is process may be unilateral or bilateral. Bilateral choanal atresia usually presents in the neonate immediately after birth with respiratory distress, which is due to the fact that most infants are obligate nose-breathers. Th e aff ected baby cycles between spells of cyanosis and crying. Attempts at suckling immediately precipitate cyanosis.

Bilateral choanal atresia requires urgent management. Th e airway may be established immediately by inserting a fi nger in the baby’s mouth; this can be replaced with a plastic oropha-ryngeal airway or a McGovern nipple. Failure of these measures to secure a satisfactory airway may necessitate endotracheal intubation or tracheostomy. Once the airway is established, diagnostic evaluation to confi rm the presence of this condi-tion and delineate its severity must be initiated. Passage of an 8 French catheter or, preferably, a narrow gauge fi breoptic endoscope will be diagnostic. A CT scan will demonstrate the thickness of the atretic plate and reveal whether it is bony or membranous.

Unilateral choanal atresia is a more indolent process and may present later in infancy or early childhood with unilateral nasal discharge or blockage.

TreatmentTreatment is surgical. A variety of approaches is available and includes transpalatal, transnasal, and trans-septal techniques. Drilling may be required to create a new passage for bony atresia. Stents are placed in the nasal passages to prevent reste-nosis. Th ese are left in place for 3–6 weeks and require close nursing care to prevent blockage.

DISEASES OF THROAT

Acute PharyngitisAcute pharyngitis includes infections of pharynx and tonsils. Most of the times, it is associated with rhinitis, sinusitis, and occasionally laryngitis.

Commonly caused by viruses such as rhino, corona, infl u-enza, parainfl uenza and adenoviruses; 15–30% of sore throats are caused by bacteria. Th e important bacterial pathogen is group A beta-hemolytic Streptococcus and C. diphtheriae.

Clinical FeaturesChildren with acute pharyngitis may have fever, sore throat, pain during deglutition, nasal discharge, conjunctival conges-tion, and discomfort in throat. Th ere may be enlargement of tonsils with congestion and exudates over pharynx, tonsils, and palate. Enlarged tonsils and soreness in throat may cause blockade of oropharynx, leading to poor intake by children and occasionally may present with drooling of saliva. Cervical lymph nodes may be enlarged and tender.

Viral pharyngitis is self-limiting and recovers in 5–7 days. Pharyngitis caused by group A beta-hemolytic Streptococcus may lead to suppurative complications such as retropharyngeal and peritonsillar abscess. Presence of these complications may be indicated by high-grade fever, severe dysphagia, and bulge in the posterior wall of pharynx or around tonsils.

Th e non-suppurative complications due to streptococcal pharyngitis include rheumatic fever and acute glomerulonephritis. For prevention of these complications, it is important to treat streptococcal pharyngitis with penicillin, as early as possible.

It is very diffi cult to diff erentiate viral from bacterial phar-yngitis. Presence of exudates on pharynx with enlarged cer-vical nodes and absence of nasal discharge suggest bacterial pharyngitis.

DiagnosisAcute pharyngitis is a clinical diagnosis. At times, it is very diffi cult to diff erentiate nasopharyngitis from pharyngitis. Pos-sibility of streptococcal pharyngitis can be made with presence of exudates, enlarged tonsils, and absence of nasal discharge. Th e diagnosis can be confi rmed by throat swab culture. Now, a rapid diagnostic test based on latex agglutination is also available for diagnosis of streptococcal pharyngitis.

Treatment Th e major consideration in the treatment of acute pharyn-

gitis is to prevent rheumatic fever. If a clinical diagnosis of streptococcal pharyngitis is made, a throat swab should be


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taken to demonstrate streptococci, and penicillin should be administered.

Penicillin can be given orally or by intramuscular route. Th e duration of oral penicillin is for 10 days. If compli-ance is a problem, single injection of benzathine penicil-lin can be given.

Th e other alternative antibiotics are ampicillin, amoxicil-lin, or oral cephalosporins. If an individual is sensitive to penicillin, he or she may be treated with erythromycin. Th e newer macrolide such as roxithromycin, clarithromycin, and azithromycin may be alternative to erythromycin in future. At present, they are not recommended as fi rst-line drugs due to less experience of these drugs in children.

If diphtheria is suspected, the child should be managed accordingly.

Acute LaryngotracheitisIs the most common of the clinical entities termed “croup”. Acute laryngotracheitis is caused primarily by respiratory viruses, most commonly parainfl uenza virus. Because of its viral cause, this croup syndrome is often referred to as viral croup.

Clinical FeaturesViral croup usually has a gradual onset and course. Symptoms are often worse at night and persist for several days.

Patients are initially seen with symptoms of upper respiratory tract infection, followed after several days by the characteristic barking cough, inspiratory stridor, and respiratory distress.

Fever is usually low grade, but temperature as high as 104° F have been noted.

Hoarseness and aphonia are common. Classic triad—hoarse voice, harsh barking cough, and

inspiratory stridor.

Diagnosis Diagnosis is clinical but can be aided by radiography of the larynx, which reveals subglottic narrowing. An anteroposte-rior view of the neck shows the classic narrowing of trachea (“Church steeple” or “wine bottle” sign). X-ray is not manda-tory, can diff erentiate from epiglottitis.

TreatmentTh erapy for viral croup is mainly directed at improving air exchange.

Humidifi cation: Home: Patients who have mild illness may be treated at

home with humidifi ed air from a hot shower or bath, hot steam from a vaporizer, or “cold steam” from a nebu-lizer. Respiratory distress may improve within minutes, but humidifi cation should be continued until the cough subsides, which usually is after 2 or 3 days.

Hospitalization: Patients who have moderate-to-severe illness should be hospitalized if any one of the following signs and symptoms is noted: cyanosis, decreased level of consciousness, progressive stridor, or a toxic appear-ance. Cold, humidifi ed oxygen should be provided, and the patient should be observed closely in case emergency intubation is needed. But otherwise the patient should be disturbed as little as possible. Pulse oximetry and ar-terial blood gas analysis are important in assessing the adequacy of air exchange.

Racemic epinephrine (2.5% solution diluted 1:8 with water in doses of 2–4 ml for 15 minutes delivered by nebulizer) has been shown to improve air exchange in these patients. Th is drug should be used in moderately ill, hospitalized patients, and it may eliminate the need for intubation during the 24–48 hours when the illness is most severe. Racemic epinephrine’s eff ects are transient and acts by reducing vascular permeability of the airway epithelium; therefore, diminishing airway edema and improving airway caliber.

Systemic corticosteroids are eff ective in reducing symp-toms within 6 hours and for at least 12 hours after initial treatment. Dexamethasone 0.6 mg/kg/dose IM, IV, PO; or prednisolone 1–2 mg/kg can be used.

Contraindications: Sedatives, opiates, expectorants, bron-chodilators, and antihistamines should not be given to these patients.

Acute Spasmodic Laryngitis or Spasmodic CroupIt refers to brief repeated attacks of symptoms that are clinically similar to those of viral croup but less severe. Spasmodic croup occurs most often in children who are between 1 and 3 years old.

Spasmodic croup is believed to be caused by viruses, although important allergic and psychological factors probably contribute to the illness in some patients.

Clinical Features Spasmodic croup is characterized by the sudden onset (usually at night) of croupy cough and respiratory stridor. Th e episodes usually last less than 1 day, but may recur several times per year.

TreatmentTreatment at home with humidifi ed air is generally suffi cient for this illness.

Croup (Laryngotracheobronchitis)Croup is characterized by a distinctively brassy cough combined with one or more of the following: hoarseness, inspiratory stridor, and signs of respiratory distress due to laryngeal obstruction.

Laryngotracheobronchitis is more severe, most commonly caused by viruses. Severe tracheal obstruction with copious, thick secretion is common.


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Laryngotracheobronchitis is caused by parainfl uenza or infl uenza viruses.

Laryngotracheobronchitis is usually similar in onset to laryngotracheitis but results in more serious illness.

TreatmentNebulized racemic epinephrine is recommended. Oral steroid (as described under laryngotracheitis) should be given in viral croup. A helium–oxygen mixture is eff ective. Intubation with vigorous suctioning of the airway to remove secretions may be necessary.

Acute EpiglottitisIt is rapidly progressive infection of the epiglottis and contigu-ous structures that may cause life-threatening airway obstruc-tion, which must be regarded as medical emergency. It may aff ect any age, but peak age is 3–6 years.

Almost all cases of acute epiglottitis in children are caused by H. infl uenzae type b.

Clinical Features Th e abrupt onset of high fever, moderate-to-severe respiratory distress, and stridor in a child who is sitting forward with his or her mouth open and drooling (because of the inabil-ity to swallow normally) are symptoms highly suggestive of acute epiglottitis. Classic “tripod position”—forward leaning posture with bracing arms and extension of neck that allows for maximal air entry.

Diagnosis Physical examination should be done quickly and with

care to minimize anxiety. Even a slight increase in

restlessness may cause complete obstruction of the airway by the swollen epiglottis. Th e diagnosis is based on fi nding a swollen, cherry-red epiglottis. It is essential to visualize the epiglottis with a laryngoscope or bronchoscope in an operating room with complete cardiorespiratory support. Visualization of the epiglottis in other settings by depressing the tongue is contraindicated because of the possibility of inducing airway obstruction. Support from otolaryngologist or anesthetist should be taken.

Radiography: In patients with mild stridor who are not acutely ill, radiographs (lateral neck views) of the nasopharynx and upper airway are useful in determin-ing whether epiglottitis is present. Th e presence of the “thumb printing” sign is a common radiographic marker for epiglottitis.

Culture of the epiglottic surface and blood should be obtained for identifi cation of the causative organism and its antimicrobial susceptibility pattern.

Treatment Ventilatory support: After visual confi rmation of epiglot-

titis, the patient should be intubated and given ventilatory support until edema subsides, usually after several days. O2 inhalation.

Antibiotic therapy is given for 7–10 days and is directed against H. infl uenzae type b. Ceftriaxone, cefotaxime, or chloramphenicol can be used, initially IV then orally.

Contraindications: Racemic epinephrine and corticosteroids should not be given to these patients.

Characteristics of three upper airway infections have been summarized in Table 7.1.

Table 7.1: Characteristics of Three Upper Airway Infections

Characteristics Viral Croup and Spasmodic Croup Bacterial Tracheitis Epiglottitis

Etiology Respiratory viruses, including parainfl uenza viruses and infl uenza viruses

Respiratory viruses and bacteria, including S. aureus, S. pyogenes, S. pneumoniae

Haemophilus infl uenzae type b

Common age of occurrence 3 months–3 years 3 months–5years 2–7 years

Clinical features Onset

Fever

Hoarseness and barking cough

Dysphagia

Course of obstruction

Variable (12–48 hr)

Variable (100°–105°F)

Yes

No

Variable progression

Gradually progressive (12 hr-7 days)

Variable (100°–105°F)

Yes

No

Variable progression, usually severe

Rapid (4–12 hr) High (>103°F)

No

Yes

Rapid progression

Leukocyte count Mildly elevated band form count Variable, possibly increased Usually markedly elevated with increased band forms

Roentgenogram Subglottic narrowing on PA radiograph

Subglottic narrowing on PA radiograph; irregular soft-tissue density within trachea on lateral radiograph

Swollen epiglottis on lateral radiograph

Treatment Humidifi cation, epinephrine, corticosteroid

Humidifi cation, antibiotic, intubation Antibiotic, intubation


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Bronchiolitis

Bronchiolitis is an acute viral infection of the bronchioles resulting in infl ammatory obstruction.

Common in children younger than 2 years (due to their small airways) with peak incidence at 6 months of age; male child, children who have not been breast-fed, who live in crowded conditions, whose mothers smoke cigarettes are at greater risk. Highest incidence is in winter and early spring, occurs sporadically and epidemically.

Respiratory syncytial virus (>50%), parainfl uenza virus, adenovirus, metapneumovirus, and mycoplasma are common pathogens.

CLINICAL FEATURES

Onset of bronchiolitis is characterized by mild upper respiratory tract symptoms (serous nasal discharge and sneezing), which last for several days and may be accompanied by mild fever (temperature of 101°–102° F), in a healthy child.

Lower respiratory tract involvement follows, with gradual development of respiratory distress (i.e., paroxysmal cough, wheez-ing, dyspnea) accompanied by irritability and decreased appetite.

Most aff ected infants have a history of exposure to older chil-dren/adult with minor respiratory diseases within the week preced-ing the onset of illness. Local endemicity is usually present.

Tachypnea, fl aring of alae nasi, and use of accessory muscles of respiration result in intercostal and subcostal retractions and occasionally cyanosis. Widespread bilateral rales and expiratory wheezes are characteristic. Breath sounds are barely audible in most severe cases. Liver and spleen may be palpable due to depression of diaphragms by hyperinfl ated lungs. Pulse oximetry is very helpful in detecting SpO2 and is a useful guide in treatment.

DIFFERENTIAL DIAGNOSIS

Diff erential diagnosis includes asthma, bronchopneumonia, congestive cardiac failure, foreign body inhalation, cystic

fi brosis. Refer Tables 7.2 and 7.3 for diff erentiating features of bronchiolitis, asthma, and bronchopneumonia.

INVESTIGATIONS

Diagnosis is clinical; investigations exclude diff erential diag-nosis and detect complications.

Total WBC count and diff erential count are usually within normal range unless associated with secondary bacterial infection.

X-ray chest is not mandatory, but reveals hyperinfl ation of lungs and occasional scattered areas of consolidation due to atelectasis (30%), peribronchial thickening, diff use interstitial infi ltrates, increased anteroposterior diameter on lateral view.

Blood gas analysis in severe cases. Virus isolation from nasopharyngeal secretions by antigen

detection using monoclonal antibodies against RSV or by PCR or culture.

TREATMENT

Mild cases can be cared for at home in humidifi ed atmosphere. If respiratory distress increases or feeding problem appear, child should be hospitalized. Indications for hospitalization include apnea, resting respiratory rate >70 breaths/min, SpO2 <95%, atelactasis on CXR, not able to feed, and age <2–3 months.

Treatment in hospital:

General measures Bed rest in propped up position with head and neck el-

evated at an angle of 30°–40° with humidifi ed oxygen in-halation (mainstay of treatment). Pulse oxymetry should be performed regularly to keep O2 saturation >95%.

Correction of dehydration, if any, orally or by perenteral fl uid.

Table 7.2 Differentiating Features of Bronchiolitis and Asthma

Features Bronchiolitis Asthma

Defi nition Acute viral infections of the bronchioles caused by respiratory syncytial virus, parainfl uenza and infl uenza virus, adenovirus, mycoplasma

Asthma is a chronic infl ammatory disorder caused hyper-responsiveness to certain stimuli resulting in recurrent airfl ow obstruction, presenting as wheezing, breathlessness, chest tightness, and coughing

Age of onset 2 months to 2 yr with peak incidence between 3 and 6 months

26% within fi rst year of life and 74% in children <5 years

Frequency of attack Usually single Recurrent attacks

Family history of allergy and asthma Infrequent Frequent

Concomitant allergic manifestation (eczema or atopy)

Absent Usually present

Response to bronchodilators, corticosteroids None Improvement occurs

Serum IgE and eosinophil count Normal Usually elevated, eosinophil in sputum is characteristic


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Maintenance of nutrition by oral or NG tube feeding. Sedatives should be avoided.

It is very diffi cult to diff erentiate between fi rst attack of asthma and bronchiolitis. Salbutamol with ipratropium inhalation may provide some benefi t. Aerosolized epineph-rine provides some benefi t.

Corticosteroid: Its use is controversial. Patients having a family history of atopy were found to be benefi ted with Prednisolone given orally for 3 days.

Antibiotics have no role. Antiviral agent. Ribavirin is indicated only in very sick

infants or in infants with congenital cyanotic heart disease, signifi cant bronchopulmonary dysplasia, severe immunodefi -ciency; Ribavirin is delivered by small particle aerosol, along with oxygen, for 20–24 hr/day for 3–5 days.

About 2–7% of infants progress to respiratory failure and need CPAP or assisted ventilation.

Extracorporeal membrane oxygenation (ECMO), when not controlled by mechanical ventilation.

PROGNOSIS

In most cases, patients recover spontaneously after the fi rst 48–72 hours of illness and do not require ribavirin therapy or hospitalization. Overall mortality rate is <1%. However, 30–50% of all patients with bronchiolitis develop asthma, and the incidence is higher if there is family history of asthma or other atopic disorders.

PREVENTION

Most important method of prevention is frequent hand-washing. Pooled hyperimmune sera (respiratory syncytial virus immune globulin intravenous [RespiGam]) given IV and respiratory syncytial virus monoclonal antibody (Palivizumab [Synagis]) given IM are administered monthly during the respiratory syncytial virus season.

Bronchiolitis Obliterans

In bronchiolitis obliterans, the bronchioles and smaller airways are injured, and the attempted repair produces a large amount of granulation tissue that causes airway obstruction. Eventu-ally, the airway lumens are obliterated with nodular masses of granulation tissue and fi brosis.

ETIOLOGY

Idiopathic. Infections by measles, infl uenza, adenovirus, myco-plasma; pertussis; connective tissue disease; and drugs.

CLINICAL FEATURES

Initially, cough, respiratory distress, and cyanosis may occur, followed by a brief period of apparent improvement. Progressive disease is characterized by increasing dyspnea, cough, sputum production, and wheezing.

INVESTIGATIONS

X-ray chest fi ndings ranging from normal to miliary mottling, in 10% cases unilateral hypertranslucency with decreased pulmonary vascular markings (Swyer James syndrome).

Bronchography reveals obstruction of the bronchioles. CT scan reveals bronchiectasis. Pulmonary function test variable, severe obstruction is most

common. Lung biopsy is confi rmatory.

TREATMENT

Supplemental oxygen should be given to patients with oxygen desaturation during normal activities or sleep.

Oral and inhaled bronchodilators may reverse airway obstruction if there is a reactive component to the disease.

Table 7.3 Differentiating Features of Bronchiolitis and Bronchopneumonia

Features Bronchiolitis Bronchopneumonia

Defi nition Acute viral infection of the bronchioles resulting in obstruction

Infl ammation of the lung parenchyma

Age of onset 2 mo to 2 yr with peak incidence between 3 and 6 months

Both infancy and childhood

Fever and cough Usually mild High fever and severe cough are common a few days after onset

Chest indrawing Sudden Gradual, if present

Signs Hyper-resonant percussion note. Widespread fi ne rales and rhonchi with prolonged expiratory breath sound. In severe cases, breath sound barely audible on auscultation

Impaired percussion note. Vesicular with prolonged expiration. Creps and rhonchi may also be heard on auscultation

Total WBC count Normal Usually increased (increased PMN)

Chest X-ray Hyperinfl ated lung fi eld along with scattered areas of consolidation

Widespread patchy opacities on both lung fi elds, pneumatocele (staphylococcal) may be present


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At least one course of corticosteroid treatment in an attempt to reverse the obstruction or present ongoing damage.

Antibiotics may be used.

PROGNOSIS

Some patients deteriorate rapidly within weeks of onset of initial symptoms, but most survive with chronic disability.

Asthma

Asthma is a chronic infl ammatory disorder causing hyper-responsiveness of airways to certain stimuli, resulting in recur-rent airfl ow obstruction, presenting as wheezing, breathlessness, chest tightness, and coughing; completely or partially reversible with bronchodilator or spontaneously resolving.

CLASSIFICATION

Pathophysiological Classification Extrinsic or atopic asthma: 90% of all asthma, common

in children, 80% with documented allergy. Intrinsic or non-atopic asthma: 10% of all asthma,

common in women after 30, follows upper respiratory infection, symptom persist, and diffi cult to treat.

Special variants: Exercise induced: Almost all asthma patients experience

it. Some patients have it as a precipitant. Reduction of FEV1 ≥10% is diagnostic.

Cough variant: Chronic cough and sputum eosinophilia. Mostly in young at night.

Drug induced: Aspirin, propranolol, timolol may induce in some patients.

Occupational: Agents inhaled in occupational settings—farmer, cigarette manufacturer, bakery worker, etc.

Seasonal.

Clinical Classification Intermittent: Two or less than two nocturnal symptoms in

a month. Between the episodes, the patient is symptom-free and PFT is normal.

Persistent: Frequent attacks, >2/month. In between, the patient may or may not be symptom-free and PFT is abnormal except in mild variety.

Severity of persistent asthma:— Mild: More than 2 times/month, and PEFR or

FEV1 is usually <80%–65%. — Moderate: Almost daily attack, and PEFR/FEV1 is

<65%–50%.— Severe: Dyspnea continuously for 6 months or

more, and PEFR or FEV1 <50%.

Diff erentiation: Refer Table 7.4.

Acute exacerbation: Loss of control of any class or variant may cause mild to life-threatening condition:

Mild: Patient is dyspneic but can complete sentences. Moderate: Patient is dyspneic and cannot complete sen-

tence in one breath. Severe: Patient is severely dyspneic, talks in words and

may be restless, even unconscious.

Diff erentiation: Refer Table 7.5.

Table 7.4: Clinical Features Differentiating Mild Intermittent, Mild Persistent, Moderate Persistent, and Severe Persistent Asthma

Clinical features

Mild intermittent

Mild persistent

Moderate persistent

Severe persistent

Days with symptoms

≤2/Week 3–6/Week Daily Continual

Nights with symptoms

≤2/Month 3–4/Month ≥5/Month Frequent

PEFR or FEV1

≥80% ≥80% >60–<80% ≤60%

PEFR variability

<20% 20–30% >30% >30%

Table 7.5: Symptoms, Signs, and Clinical Parameters Differentiating Mild, Moderate, and Severe Acute Exacerbation of Asthma

Mild ModerateSevere/life-threatening episode

Symptoms

Physical exhaustion No No Yes

Talk in Sentences Phrases Words/can’t talk

Feeding Able to feed

Feed with diffi culty

Too breathless to feed

Signs

Consciousness ±Agitated Usually agitated

Agitated to drowsy

Accessory muscle use: sternocleidomastoid retraction

No Yes Usually prominent

Pulse (/min) <100 100–160 >160

Cyanosis Absent Absent Likely to be present

Wheeze End expiratory

Throughout the expiration

Expiration+inspiration, may be silent chest

PEFR/FEV1 >60% 40–60% <40%

Pulsus paradoxus Normal May be present 20–40 mmHg

SaO2 (pulse oxymetry)

>95% 95–91% <91%


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(6.00 PM) in asthmatic patients. PEFR measurements on morning and afternoon (for ~1 week) before treatment can establish diurnal variability, increases in variability of >20–30%, on an average, indicate increased bronchial responsiveness and worsening asthma.

Laboratory criteria: Sputum eosinophilia, increased eosinophil count in

blood Blood gas analysis , pH

CXR: Shows bilateral symmetric air trapping. Patches of atelectasis of various sizes due mucous plaque is not unusual. Extensive areas of collapse, consolidation suggest an alterna-tive diagnosis. X-ray is also done to exclude TB. CXR may be normal in asthma.

Allergy test: Skin test and RAST (radioallergosorbent test) have limited usefulness, since the role of desensitization therapy is not fully established.


Pulmonary tuberculosis, bronchiolitis, bronchiolacia or tracheo-malcia, foreign body aspiration, hypersensitivity pneumonitis, cystic fi brosis, recurrent pneumonia, GERD.

MANAGEMENT PLAN

Management goal is to achieve clinical control. GINA revised guideline—Rule of ‘2’:

Day time symptoms <2/wk Nocturnal symptoms <2/mo Number of reliever drug <2/yr (salbutamol canister) No exacerbation Normal or near lung function No limitation of daily activities

Scoring system for step care management:

Criteria Score

1. Do you have dyspnea everyday? Yes = 1 No = 0

2. Do you have nocturnal attacks of dyspnea >2 times/month?

Yes = 1 No = 0

3. Have you suffered from dyspneic attacks severe enough to necessitate steroid tablets or injection, nebulization, Inj. aminophylline or hospitalization?

Yes = 1 No = 0

4. Do you have persistent dyspnea for the last 6 months or more or are you taking steroid tablets (prednisolone etc.) for any 1 year or more?

Yes = 3 No = 0

5. Is patient’s baseline (asymptomatic stage) PEF ≤60% of predicted value?

Yes = 1 No = 0

Total score 7–0

Classification on the Basis of ControlIt is important and relevant for management of asthma. On the basis of control, asthma can be classed as (i) controlled, (ii) partly controlled, and (iii) uncontrolled (Table 7.6).

PRINCIPLE OF DIAGNOSIS

Clinical criteria: Cardinal feature of asthma—paroxysmal respiratory distress, recurrent cough, wheeze, chest tightness, recurrent attacks due to multiple stimuli.

Pumonary function tests (PFT): Th e important parameters in spirometry include PEFR, FEV1, FVC and FEV 25–75.

In asthma, FEV1/FVC is <0.8 (normal, 0.8–1). In asthma, FEV1 is commonly used for assessing the severity of asthma.

FEV 25–75 is eff ort independent and is probably more sensitive indicator of airway obstruction.

PEFR can be measured with peak expiratory fl ow meter, while for other parameters spirometer is required. It may be used as a diagnostic tool as well as monitoring of treatment. Abnormality in PEFR suggestive of asthma include:

— A diurnal variation of >20%, ≤80% of predicted, and improvement of ≥20% after bronchodilator therapy.

— Bronchodilator reversibility test: It is done to diff er-entiate obstructive defect from restrictive defect and to diff erentiate asthma. Reversibility can be found out by FEV1 before and 30 minutes after administration of �2-agonist aerosol. An increase of >12% in PEFR or FEV1 after aerosol therapy is strongly suggestive of asthma. Failure to respond, however, does not exclude asthma.

— Variability tests: Th e PEFR is usually lowest in the morning (6.00 AM) and highest in the afternoon

Table 7.6: Levels of Asthma Control

Characteristic Controlled (all of the following)

Partly controlled (any measure present in any week)

Uncon-trolled

Daytime symptom

None (twice or less/wk)

More than twice/wk

Three or more features of partly controlled asthma present

Limitation of activities

None Any

Nocturnal symp/awakening

None Any

Need for reliever/rescue treatment

None (twice or less/wk)

More than twice/wk

Lung function(PEFR/FEV1)

Normal <80% predicted or personal best


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Step detection:

Children ≤5 years >5 years

Score Recommended step Score Recommended step

0 Step I 0 Step I

1 Step II 1 Step II

2 Step III 2 Step III

3–6 Step IV 3 Step IVA

4 Step IVB

5–7 Step V

Long-term Management of Asthma: Step Care Management

Step care plan for children <5 year:

Childhood asthma Medication Adult asthma

Step I As per need salbutamol inhaler Step I

Step II Full-dose cromolyn or nedocromil Step II

Step III Low-dose ICS

Step IV High-dose ICS Step III

Step VA High-dose ICS + LABA/theophylline Step IV

Step VB Step V + Oral corticosteroid Step V

Management of Asthma at HomeFirst aid for asthma—“Rule of 5” 1. Ensure the patient is sitting comfortably upright, be calm,

and reassuring

2. Give 5 puff s of reliever inhaler with spacer/direct through mouthpiece

3. Wait for 5 minutes 4. If no improvement, give another 5 puff s 5. Repeat the process for 5 times; if little/no improvement,

transfer to hospital with puff s every 5 minutes

Patient Education and Self ManagementTh e traffi c zone system of control:

Green zone: Indicated all is clear, PEF 80–100%, <15% variability, minimal symptom—patient has to continue treatment

Yellow zone: Indicated caution 60–80%, 5–25% variability, asthma symptom may occur—intensifi cation/stepping up of maintenance

Red zone: PEF <60% and symptom at rest—immediate β2-agonist use, follow yellow zone if improve or report to emergency department.

TREATMENT

Treatment of Mild Acute AsthmaInhaled salbutamol 1 puff stat, another one after 5 minutes; then 1–2 puff s 3–4 hourly for the next 12–24 hour. Spacer is preferable. If inhaled salbutamol is not available, give oral salbutamol 0.2–0.4 mg/kg/d 6–8 hourly for the next 12–24 hour.If no improvement after 24 hour, advise for hospitalization for further management.

Treatment of Moderate Acute AsthmaRefer Figure 7.1 for treatment of moderate acute asthma.

Treatment of Severe Acute AsthmaRefer Figure 7.2 for treatment of severe acute asthma.

General management:

1. Dehydration, if any, must be corrected by dextrose saline. Potassium may be given if hypokalemia develops. Usually, more than 1–1.5 times maintenance level of fl uid should be given. Care should be taken not to over-hydrate the patient.

2. Routine administration of antibiotics is not needed, but if there is consolidation on chest X-ray, blood neutrophilia, or presence of coarse crepitations or bronchial breath sounds, give antibiotics, such as erythromycin or amoxicillin.

3. Chest X-ray should be obtained in all severe cases or when mediastinal emphysema, Pneumothorax, or pneumonia is suspected.

4. Sedation is hazardous. Tranquillizers, morphine and other opiates are contraindicated because of their depressant eff ect on respiratory center.

Step care plan for >5 year and adult:

Step I Step II Step III Step IV Step V

Asthma education and Environmental control

As need rapid acting β2-agonist

Controller option

Select one: Select one: Add one/more: Add one/more:

• Low-dose ICS

• Low-dose ICS + LABA

• Medium/high-dose ICS + LABA

• Oral glucocort-icosteroid

• Leukotriene modifi er (receptor antagonist/ synthesis inhibitor)

• Medium/high-dose ICS

• Leukotriene modifi er

• Anti-IgG

• Low-dose ICS + Leukotriene modifi er

• Sustained-release theophylline

• Low-dose ICS + sustained-release theophylline

ICS, inhaled corticosteroid; LABA, long-acting beta2-agonist.After starting appropriate treatment, the patient should be seen every 4–12 weeks for

step up or step down.


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Salbutamol inhaler with spacer 2 puffs every 20 min

for 3 times

Continue Salbutamol inhaler 2 puffs 2-4 hourly

for 24-36 hr

Add oral prednisolone 1-2 mg/kg/d in

3 divided doses for 3 days

Nebulized Salbutamol 0.15–0.3 mg/kg

Hospitalization for further

management

Discontinue inhaler (relievers). Maintain other advice, e.g., preventer, avoid allergens.

No improvement or inhaler not available

Improvement but wheeze still pesists

after 24-36 hr.

Improved No Wheeze

Improved No Wheeze

No improvement

No improvement or deteriorationafter 3 doses

ImprovementImprovement

Fig. 7.1: Treatment of moderate acute asthma.

Rescue steroid therapy: During step care management, patient may lose asthma control at any step suddenly, for example, due to viral respiratory tract infection. No stepping up is required prior to it. Patient should follow the exist-ing step after ending the rescue course. Oral prednisolone 1–2 mg/kg/d in single morning dose or two divided doses for 3–14 days should be given. No tapering of this dose is needed.

Drugs Used in AsthmaRefer Table 7.7 for list drugs used in Asthma.

PEFR NomogramSee Figure 7.3 for nomogram relating PEFR to height. Th e nomogram is based on a study conducted among South Indian children.

PREVENTION

Avoid triggering factors (ASTHMA), i.e., Allergens (pollen, dander, dust, fungal spore), Sports (exercises, games, traveling), Temperature (cold weather, wet, windy weather), Heredity (environmental factors), Mites, Anxiety (stress, worries).


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Desensitization is not very eff ective, may sometimes be harmful.

Pneumonia

Pneumonia is defi ned as an acute infl ammation of lower respiratory tract (lung parenchyma) associated with recently developed radiological pulmonary shadowing.

CLASSIFICATION

Community-acquired pneumonia: Bacterial (Strep. pneumoniae, H. infl uenzae, Staph. aureus, Kl. pneumoniae), Viral (respiratory syncytial virus, seen mainly in infancy; infl uenza virus; parainfl uenza virus; measles virus; and varicella virus), Chlamydia (Chlamydia pneumoniae), Mycoplasma pneumoniae, Rickettsiae (Coxiella burnetii) can

Immediate Hospitalization

Add Ipratropium bromide 6 hourly—<2 yr, 250 �g;

>2 yr, 250–500 �g

Discontinue inhaler(relievers). Discharge with

advice, e.g., preventer, avoid allergens, follow-up after 3–7

days, etc.

Add Inj Aminophylline 5 mg/kg bolus over 20 min and then 0.5–0.7 mg/kg/hr

Or, Inj. Salbutamol 15 �g/kg bolus then –0.1 �g/kg/min

Available Not available

ICU care± ventilator support

Other drugs—epinephrine/MgSO4

Propped-up position Oxygen 4-6 L/min

Nebulized salbutamol 0.15–0.3 mg/kg/dose every 20 min3 times or continuously.

Inj. Hydrocortisone 3–4 mg/kg 4–6 hourly Or oral Prednisolone

2 mg/kg starting dose & then 1 mg/kg 6–12 hourly

Inj Hydrocortisone 3-4 mg/kg4-6 hourly OR Oral prednisolone2mg/kg single dose (max 60mg),

preferably morning dose(If patient can swallow)

If improved

No improvementOr deterioration

No improvementOr deterioration

No improvement

Complete Relief

If improved

ICU care

Fig. 7.2: Treatment of severe acute asthma.


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also give rise to primary pneumonia. See Table 7.8 for clinical features diff erentiating bacterial pneumonia from viral pneumonia.

Hospital-acquired pneumonia (pneumonia occurring at least 2 days after admission to hospital). Common organ-isms are E. coli, Pseudomonas, Klebsiella, Staph. aureus, and anaerobic organisms.

Pneumonia in the immunocompromised patient, e.g., Pneumocystis carinii, Aspergillus fumigatus, CMV, herpes virus, Myco. tuberculosis.

Pneumonia in damaged lung (including suppurative and aspiration pneumonia), e.g., Staph. aureus, Klebsiella, and anaerobic bacteria.

Table 7.7: Drugs Used in Asthma

Drug Dose Preparations available

1. Salbutamol a) Oral

b) Inhaler

c) Respirator solution (solution & nebule)

d) Injection

0.2–0.4 mg/kg/d

2 puffs qds. In EIB 1–2 puffbefore exercise0.15–0.3 mg/kg/dose<5 yr = 0.5 ml/dose>5 yr = 1ml/dose15 mg/kg bolus over 30 minThen 0.1 μg/kg/min.

Syrup, tablet1 tsf = 2mg; 1 tab = 2,4 mgMDI 100 μg/puff

1 ml Solution = 5mg1 Nebule = 2.5 mg

1 ml = 1mg

2. Salmeterol 2 puffs 12 hourly MDI 25 μg/puff

3. Hydrocortisone 3–4 mg/kg/dose 4–6 hourly 1 vial = 100 mg

4. Methylprednisolone Loading dose: 2 mg/kgMaintenance dose: 1–2 mg/kg/d qds

1 vial = 40, 125, 500, 1000, 2000 mg

5. Prednisolone 1–2 mg/kg/d tds 1 tab = 5 mg

6. Aminophylline Loading dose 5 mg/kg followed by0.5–0.7 mg/kg/hr

1 ml = 25 mg

7. Ipratropium bromide <2yr = 250 μg/dose; >2yr = 250–500 μg/dose6 hourly

Respirator solution 1 ml = 250 μg

8. Epinephrine (1:1000 dilution) 0.01 ml/kg/dose (highest 0.3 ml) Injection (1:1000) 1ml/ampule

9. Cromones a) Sodium cromoglycate b) Nedocromil sodium

1 puff qds1 puff qds & after control 1 puff bd

MDI 5 mg/puffMDI 2 mg/puff

10. Beclomethasone 1–2 puff tds–qds MDI 50,100,250 μg/puff

11. Budesonide 50–400 μg bd MDI 50,100,200 μg/puff

12. Fluticasone 50–100 μg bd MDI 25, 50,125,250 μg/puff

13. Triamcinolone 1–2 puff qds MDI 100 μg/puff

14. Theophylline 7–10 mg/kg/d bd Syrup 1 tsp-120 mg

15. MgSO4 25–50 mg/kg (max 2 g) Injection 5 ml = 2.5 mg (1g = 4 mmol)

16. Leukotrienes antagonists:Montelukast(Not recommend below 12 years of age).

>12 years: 20 mg twice daily, 1 hour before or 2 hour after meal.

Tab. Monas 4.5, 10 mg

17. Combination inhalers:Salmeterol + Fluticasone

≥4 years: One inhalation (50 μg salmeteroland 100 μg fl uticasone propionate) twice daily.Or one inhalation (50 μg salmeterol and 250 μg fl uticasone propionate) twice daily.

Fig. 7.3: Nomogram relating PEFR (on the ordinate) to height (on the abscissa). Mean and 95% confi dence limits are shown. (Based on a study among South Indian children.)

450

400

350

300

250

200

150

10090 100 110 120 130 140 150 160 170

+95%

Mean

–95%

Peak

flow

rate

(L\m

in)

Height (cm)

PEFR nomogram


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SOME DEFINITIONS OF PNEUMONIA

Bronchopneumonia: It is primarily a spreading infl ammation of the terminal bronchioles and their related alveoli.

Lobar pneumonia: It is a pathological state of the lung, where the alveolar air has been replaced by cellular exudate and transudate.

Pneumonitis: It is a localized infl ammation of the lung paren-chyma due to non-infectious causes.

Post-measles bronchopneumonia: It is a mixed pneumonia involving the alveoli, supporting tissue and bronchioles, usually manifest with or after the onset of measles. Radiologically, it is seen as peribronchial thickening, usually bilateral and often extensive.

Interstitial pneumonia: It is characterized pathologically by massive proliferation and desquamation of alveolar cells and thickening of alveolar walls. Chest skiagram may reveal a diff use, hazy, ground glass appearance, usually at the lung bases with poorly defi ned hilar densities.

Persistent pneumonia: It is defi ned as persistence of symptoms and roentgenographic abnormalities for >1 month.

Recurrent pneumonia: It is defi ned as two episodes of pneu-monia in 1 year or >3 episodes at any time with radiographic clearance between two episodes of illness.

RADIOLOGICAL DIAGNOSIS

A guide to radiological diagnosis of pneumonia:

Acute lobar pneumonia: Consider pneumococcal pneumonia

Right upper lobe pneumonia: Suspect aspiration, especially in neonates and infants

Upper lobe pneumonia with cavitation: Tuberculosis Recurrent right middle lobe pneumonitis: Consider partial

bronchial obstruction due to glands Lower lobe pneumonitis: Chemical pneumonitis Multiple small abscesses: Staphylococcal/Klebsiella pneu-

monia Severe bilateral interstitial pneumonia: Viral Bilateral interstitial pneumonia with malignancy: Pneumo-

cystis carinii

Note: Th e X-ray changes often lag behind clinical fi ndings, both at the onset of pneumonia and at the time of resolution.


Bronchiolitis, congestive heart failure (CHF), asthma, aspiration of foreign body, pulmonary tuberculosis, pulmonary abscess.

TREATMENT

Treatment plan of pneumonia:

Specifi c: Antimicrobial therapy Supportive

O2 inhalation Hydration (fl uid may be restricted, considering SIADH) Nutrition Antipyretics Bronchodilators Physiotherapy

VIRAL PNEUMONIA

In general, lower respiratory tract viral infections are much more common during winter months. Th e types and severity of illness are infl uenced by several factors including age, season of the year, immune status of the host and environmental factor such as over-crowding. Th e peak attack rate for viral pneumonia is between the age of 2 and 3 years and decreases slowly thereafter.

Clinical Features Rhinitis, cough, low-grade fever, cyanosis, respiratory distress, tachypnea accompanied by chest indrawing, and nasal fl aring, and use of accessory muscle is common. Hyper-resonant chest, wide-spread crackles, and wheezing may be present.

Diagnosis Total count of WBC tends to be normal or slightly elevated

(<20,000/mm3), with a predominance of lymphocytes.

Table 7.8: Clinical Differentiation of Bacterial Pneumonia from Viral Pneumonia

Feature Bacterial Viral

Onset Acute (Pry) Gradual

Epidemic pattern – +

Course Progressive Self-limiting

Temperature +++ +/–

Toxemia +++ -

Dyspnea ++ + (infants)

Associated URTI – +

Auscultation Creps Rhonchi/Wheeze

++++

+/–+/–

Radiological Confl uent infi ltrates Diffuse infi ltrates in perihilar areas

Hyperinfl ation +/- +(RSV Infection)

Pleural involvement + –

Pneumatocele + –


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Acute phase reactants (ESR or CRP) usually are normal or slightly elevated.

Chest x-ray reveals diff use infi ltrates. Hyperinfl ation is common. Isolation of organism from nasopharynx or throat by culture

or polymerase chain reaction. Rapid diagnostic test (fl uorescent antibody tests) that use

labeled virus-specifi c antibodies to detect viral antigens in respiratory secretions.

Treatment Specifi c measure: Antiviral agents, like aerosolized ribavirin

(for RSV). Oral amantadine or rimantadine (infl uenza virus). Supportive measures: As mentioned earlier.

PNEUMOCOCCAL PNEUMONIA

S. pneumoniae is still the most common cause of bacterial infection of the lungs. Th e classical four stages of conges-tion, red hepatization, grey hepatization, and resolution are well-known.

Clinical Features Th e onset is sudden, and high fever, cough, pain in the chest on the aff ected side, tachypnea, circumoral pallor, inspiratory dilatation of the alae nasi, expiratory grunt, diminished chest movement on the aff ected side, dullness on percussion, bron-chial breath sounds, increased vocal resonance, crackles, and pleural rub are found.

Diagnosis White blood cell count is usually elevated to 15,000–40,000/

mm3, with preponderance of PMN cells. Arterial blood samples usually show hypoxemia without

hypercapnia. Chest x-ray reveals consolidation. Pleural reaction with

presence of fl uid may be seen. Isolation of the bacteria from blood or lung aspirate is

diagnostic.

Treatment Specific: Th e drug of choice is crystalline penicillin G

(100,000 units/kg/24 hr). A third-generation cephalo-sporin (cefotaxime, 150 mg/kg/24 hr, or ceftriaxone, 75 mg/kg/24 hr) should be used if the isolate of S. pneumoniae is resistant to penicillin but sensitive to cephalosporin. Vancomycin (40 mg/kg/24 hr) should be used if the isolate is resistant to penicillin and third-generation cephalosporin.

Supportive: As mentioned earlier.

STAPHYLOCOCCAL PNEUMONIA

Pneumonia caused by S. aureus is a serious and rapidly progressive infection. It occurs less frequently than viral or pneumococcal pneumonia. Although it may occur at any age, 30% of all patients are younger than 3 months and 70% are younger than 1 year. Th e pulmonary lesion may be primary infection of the parenchyma; or may be secondary to generalized staphylococcal septicemia or may be a complication of measles, infl uenza, or cystic fi brosis of lungs or may follow minor staphylococcal pyoderma. Debilitating conditions including malnutrition predispose the infants to infection with staphylococci.

Clinical Features Th e illness usually follows upper respiratory tract infection, pyoderma, or other associated purulent disease. Th e infant becomes acutely ill with high fever, cough, respiratory dis-tress, tachypnea, grunting respirations, chest indrawing, nasal fl aring, cyanosis, reluctant to feed, toxic appearance, dullness on percussion with bronchial or diminished breath sounds, crepitations over the aff ected areas.

Diagnosis Chest x-ray reveals bronchopneumonia early in the illness.

Th e infi ltrate soon become patchy or may be dense and homogenous and involve an entire lobe or hemithorax. Th e involvement may be right sided (65%) or bilateral (<20%). A pleural eff usion or empyema may be found and pyopneumothorax in 25% of patients. Pneumatocele of various sizes are common.Rapid progression from bronchopneumonia to eff usion or pyopneumothorax with or without pneumatoceles is highly suggestive of staphylococcal pneumonia.

Total count of WBC: Leukocytosis usually occurs with predominance of the polymorphonuclear cells.

Gram stain of aspirated material (from trachea) or pleural tap reveals gram-positive cocci in clusters.

Blood culture may be positive.Pleural fl uid reveals an exudate with PMN cell counts of 300–100,000/mm3; protein >2.5 g/dl, and a low glucose concentration.

Treatment Specific: A suitable antibiotic combination is fl ucloxacil-lin (50–100 mg/kg/d) and ampicillin (50–100 mg/kg/d) in four divided doses. Cefuroxime (50 mg/kg/d) or Naf-cillin (200 mg/kg/d) is indicated if a favorable response is not obtained within 72 hours. Empyema should be drained by chest tube.Supportive: As mentioned earlier.


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HAEMOPHILUS INFLUENZAE PNEUMONIA

H. infl uenzae type b is an important cause of serious bacterial infection in infants and children who have not received H. infl uenzae type b vaccine (Hiberix).

Clinical Features Th e onset of the illness is gradual with nasopharyngeal infec-tion. Th e child has moderate fever, cough, dyspnea, grunting respiration, and chest indrawing. Th e course is subacute and prolonged. Th e localized dullness on percussion, crepitation, and bronchial breath sound may be noted.

Diagnosis Th e diagnosis is established by isolating the organism from

the blood, pleural fl uid, or lung aspirate. Moderate leukocytosis is usually found.

In the absence of a positive culture, a positive urine latex agglutination test result supports the diagnosis of this infection.

Treatment Specifi c: Ceftriaxone (75 mg/kg/24 hr) or cefotaxime (150

mg/kg/24 hr) is included in the initial antibiotic therapy. Chloramphenicol 50–100 mg/kg/d in four divided doses may also be given if one cannot aff ord ceftriaxone. If the strain is sensitive, ampicillin (100 mg/kg/d) may be administered. If the initial response to antibiotic is good, oral treatment can be instituted to complete a 10–14 days course. Pleural eff usion may require drainage.


PRIMARY ATYPICAL PNEUMONIA

Primary atypical pneumonia is mycoplasma pneumonia. Th e disease is transmitted by droplet infection. It occurs in epi-demics, chiefl y in winter months. Th e disease is common in children at age over 5 years.

Clinical Features Fever, cough, headache, sore throat, and myalgia. Onset is insidious or abrupt. Cough is usually dry at the onset and then it becomes productive. Mild pharyngeal congestion, cervical lymphadenopathy, dullness on percussion, rhonchi, rales, and decreased breath sounds may be present.

Diagnosis Total and diff erential WBC counts are usually normal.

Th e rising titer of cold agglutinins (which agglutinate human red cells in the cold) should be determined. A titer of 1:64 or higher supports the diagnosis. Acute and convalescent titers for M. pneumoniae demonstrating a four-fold or greater rise in specifi c antibody confi rm the diagnosis.

Chest x-ray usually demonstrates interstitial or bronchopneu-monic infi ltrate, frequently in the middle or lower lobes.

Treatment Specifi c: Spontaneous recovery usually takes place after an

illness of 1–2 weeks duration. Erythromycin (50 mg/kg/d), clarithromycin (15 mg/kg/d given in two divided doses for 10 days), or azithromycin (10 mg/kg on day 1, and 5 mg/kg/day on days 2–5), oxytetracycline (for children aged >8 years, 50 mg/kg/d in four divided doses) are eff ective in shortening the course of mycoplasmal illness.


HOSPITAL-ACQUIRED (NOSOCOMIAL) PNEUMONIA

Hospital-acquired or nosocomial pneumonia refers to a new episode of pneumonia occurring at least 2 days after admission to hospital. Th e term include post-operative and certain forms of aspiration pneumonia, and pneumonia or bronchopneumonia developing in patients with chronic lung disease, general debility or those receiving assisted ventilation. Th e mortality of hospital-acquired pneumonia is high (30%).

Etiology Th e majority of infections are caused by gram-negative bacteria. Th ese include Escherichia, Pseudomonas, Klebsiella, Staph. aureus(including multidrug-resistant MRSA forms), and anaerobic organisms.

Factors predisposing to nosocomial pneumonia: Reduced host defenses against bacteria:

Reduced immune defenses (e.g., corticosteroid treatment, diabetes, malignancy)

Reduced cough refl ex (e.g., post-operative) Disordered mucociliary clearance (e.g., anesthetic agents) Bulbar or vocal cord palsy

Aspiration of nasopharyngeal or gastric secretions: Immobility or reduced conscious level Vomiting, dysphagia, achalasia, or severe refl ux Nasogastric intubation

Bacteria introduced into lower respiratory tract: Endotracheal intubation/tracheostomy Nebulizers/bronchoscopes Dental or sinus infection

Bacteremia: Abdominal sepsis Intravenous cannula infection Infected emboli


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Clinical Features Cough, fever, rigors, vomiting or a febrile convulsion, loss of appetite, tachycardia, tachypnea, breathlessness, central cyanosis, pleural pain (uncommon), impairment of percussion note. In the early stages, the physical signs are those of acute bronchitis followed by development of crepitations.

Diagnosis CBC shows neutrophilic leukocytosis.

Chest x-ray shows mottled opacities in both lung fi elds, chiefl y in the lower zones.

TreatmentSpecifi c: Gram-negative coverage is usually obtained with third-generation cephalosporin (e.g., cefotaxime) plus an aminoglycoside (e.g., gentamicin) or imipenem. Aspira-tion pneumonia can be treated with co-amoxiclav plus metronidazole.


Summary of Physical Signs inCommon Respiratory Diseases

Refer Table 7.9 for summary of physical signs in common respiratory diseases.

Lung Abscess

A lung abscess is a suppurative process resulting in destruction of pulmonary parenchyma and formation of a cavity contain-ing purulent material. Th e causes of lung abscess (APISOCE) are as follows:

Aspiration: Aspiration of infected material when the local defense mechanisms are overwhelmed by a large number of virulent microorganisms or are compromised by factors such as recent surgery (e.g., tonsillectomy or adenoidectomy) or systemic disease. Aspirated material containing bacteria that are normal inhabitants of the nasopharynx and oropharynx reaches the most dependent portion of the lungs. Th e pos-terior segment of the upper lobe and the superior segment of the lower lobes are most frequently involved in the

Table 7.9: Summary of Physical Signs in Common Respiratory Diseases

Pathological process

Movement of chest wall

Mediastinal displacement

Percussion note

Breath sounds

Vocal resonance

Added sounds

Consolidation as in lobar pneumonia

Reduced on affected side

None Dull High-pitched bronchial

Increased; whispering pectoriloquy

Fine crepitations early; coarse crepitations later.

Collapse due to obstruction of a major bronchus (absorption collapse)


Towards lesion

Dull Diminished or absent

Reduced or absent None

Collapse due to peripheral bronchial obstruction


Towards lesion

Dull High-pitched bronchial

Increased; whispering pectoriloquy

None early; coarse crepitations later.

Localized fi brosis and/or bronchiectasis

Slightly reduced on affected side

Towards lesion

Impaired Low-pitched bronchial

Increased Coarse crepitation

Cavitation (usually associated with consolidation or fi brosis)

Slightly reduced on affected side

None, or towards lesion

Impaired Bronchial Increased; whispering pectoriloquy

Coarse crepitation

Pleural effusion Empyema

Reduced or absent (depending on size) on affected side

Towards opposite side

Stony dull Diminished or absent (occasionally bronchial)

Reduced or absent (occasionally increased)

Pleural rub in some cases (above effusion)

Pneumothorax Reduced or absent (depending on size) on affected side

Towards opposite side

Normal or hyper-resonant

Diminished or absent (occasionally faint bronchial)

Reduced or absent Tinkling crepitation when fl uid present

Bronchitis: acute or chronic

Normal or symmetrically diminished

None Normal Vesicular with prolonged expiration

Normal Rhonchi, usually with some coarse crepitations

Asthma Symmetrically diminished

None Normal Vesicular with prolonged expiration

Normal or reduced Rhonchi, mainly expiratory and high-pitched

Bronchopneumonia Symmetrically diminished

None May be impaired

Usually harsh vesicular with prolonged expiration

Normal Rhonchi and coarse crepitations


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recumbent position, and basilar segments of the lower lobes are the most likely to be aff ected when aspiration occurs during dental procedure (i.e., erect position); anaerobic bacteria including bacteroides, fusobacterium, and anaerobic streptococci are commonly isolated.

Pneumonia caused by aerobic pyogenic organisms (Staph. aureus and Klebsiella)

Infarction: Bacterial infection of a pulmonary infarct may produce a lung abscess.

Septicemia, pyemia: Metastatic lung abscess secondary to septic emboli from bacterial endocarditis in right side of the heart and septic thrombophlebitis.

Obstruction of bronchi due to enlarged lymph node, tumor, or foreign body may occasionally be complicated by abscess formation.

Collapse: Bacterial infection of a collapsed lobe from tubercular lymphadenopathy, foreign body, and adenoma may produce abscess.

Extension from subphrenic abscess (amebic or pyemic liver abscess) and mediastinal sepsis.

CLINICAL FEATURES

Onset: Acute or insidious Symptoms

Cough, productive of large amounts of sputum, which is sometimes fetid and blood-stained.

Pleural pain common. Sudden expectoration of copious amount of foul sputum

occurs if abscess ruptures into a bronchus.

Signs High remittent pyrexia Profound systemic upset Digital clubbing may develop quickly (10–14 days) Chest examination usually reveals signs of consolidation;

signs of cavitation rarely found Pleural rub common Rapid deterioration in general health with marked weight

loss can occur if the disease is not treated adequately.

LABORATORY FINDINGS

CBC—Anemia, raised ESR, PMN leukocytosis Gram staining, Z-N staining, and microscopy and culture

of sputum X-ray chest (P/A and lateral view): Homogenous opacity (if

abscess does not communicate with air passage) or a thick walled lung cavity with or without fl uid level (if commu-nication with bronchus present).

CT scan may provide better localization of the lesion and may be helpful in doubtful cases.

MT and BCG tests.


Loculated pleural eff usion, Echinococcus cyst, neoplasm, infected congenital cyst.

TREATMENT

Antibiotics: Should be chosen according to culture and sensitivity (C/S); sample may be taken from sputum, blood, or pleural fl uid for C/S. If organisms could not be identi-fi ed, antibiotics directed at Staph. aureus, H. infl uenzae, Pneumococcus and anaerobes (combination of ampicillin, cloxacillin, and metronidazole or a combination of ceftri-axone, cloxacillin, and metronidazole) can be used for 4–6 weeks. Antibiotic should be given parenterally for at least 2–3 weeks. Chloramphenicol can be used if a patient is allergic to penicillin. In non-response, TB should be considered.Postural drainage.

Bronchoscopy to identify and to remove a foreign body.Surgical resection should be considered only in children with recurrent hemoptysis, repeated episodes of infection or suspicion of malignancy.

PROGNOSIS

Although radiological resolution may be very slow, resolution occurs in most patients without risk factors.

Bronchiectasis

Bronchiectasis is a chronic suppurative disease, characterized by destruction of the bronchial and peribronchial tissues, dilata-tion of the bronchi, and accumulation of infected material in the dependent bronchi.

ETIOLOGY

Acquired: Infections: Recurrent lung infections, measles, pneumo-nia, pertussis, post-primary TBBronchial obstruction (followed by infection). Lymphadenopathy (e.g., tuberculosis), aspiration of foreign body, tooth or tonsil fragment, neoplasm, gastro-esophageal refl ux with repeated aspirations, congenital heart disease with compression of airway by abnormal vessels.Predisposing factors are cystic fi brosis, lung abscess, sar-coidosis, localized cysts, persistent lobar collapse, and emphysema with compression of lung parenchyma.

Immune defi ciency syndrome with repeated attacks of pneumonia and bronchitis.


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Congenital: Congenital bronchiectasis, tracheo-broncho-megaly, primary ciliary dyskinesia (Kartagener syndrome—bronchiectasis, sinusitis, transposition of viscera).

CLINICAL FEATURES

Bronchiectasis may produce no symptoms.

Symptoms:

Due to accumulation of pus in dilated bronchi: Chronic productive cough usually worse in mornings and often brought on by changes of posture. Sputum is often copious and persistently purulent in advanced disease.

Due to infl ammatory changes in lung and pleura surround-ing dilated bronchi: Fever and increased cough and sputum volume when spread of infection causes pneumonia, which is frequently associated with pleurisy. Recurrent pleurisy in the same site often occurs in bronchiectasis.

Hemoptysis: Can be slight or massive and is often recurrent, usually associated with purulent sputum or an increase in sputum purulence. It can, however, be the only symptom in the so-called dry bronchiectasis.

General health: Weight loss, anorexia, sleep sweating, and failure to thrive in children. In these patients, digital club-bing is common.

Signs:

When the disease is suffi ciently developed, the character-istic fi nding is that of persistent early and mid-inspiratory crackles. Th ese crackles are frequently described as “coarse” and are not shifted by coughing.

Clubbing of the fi ngers and/or toes is a feature of gross disease with prolonged bronchial infection.

Signs of collapse and fi brosis may be present in advanced cases. Th ere may also be cyanosis, with signs of pulmonary hypertension and right heart failure.

INVESTIGATIONS

X-ray chest (P/A) shows honey combing of the involved area indicating multiple small abscess cavities or marked linear streaking (“rail road tracks”) with loss of volume (“crowding”), which is highly suggestive.

Bronchoscopy is undertaken where there is a possibility of surgical intervention.

CT scan: High-resolution CT scan is replacing bronchos-copy and is safer.

Sputum should be sent for staining (Gram staining, AFB), culture and sensitivity.

MT, BCG tests. Sweat chloride test (by pilocarpine iontophoresis) is useful

in the diagnosis of cystic fi brosis.

COMPLICATIONS

Recurrent pneumonia, lung abscess, empyema, bronchopleural fi stula, hemoptysis, metastatic cerebral abscess, cor pulmonale, and rarely amyloidosis.

TREATMENT

Postural drainage: Th e aim of this measure is to keep the dilated bronchi emptied of secretions. It is of great value both in reducing the amount of cough and sputum and in preventing recurrent episodes of bronchopulmonary infec-tion. Postural drainage consist of adopting a position in which the lobe to be drained is upper most, thereby allowing secretions in the dilated bronchi to gravitate towards the trachea from where they can readily be cleared by vigorous coughing. Percussion on the aff ected side of the chest wall with cupped hands aid dislodgement of sputum, and a number of mechanical devices are available that cause the chest wall to oscillate, thus achieving the same eff ect as postural percussion and chest wall compression.Antibiotic therapy: Appropriate antibiotics are indicated only when there is acute exacerbation, which is evident by increase in quantity of sputum, sputum becoming yellow, purulent and foul smelling, and presence of systemic symp-toms such as fever. Choice of antimicrobials are co-amoxiclav, ampicillin–cloxacillin, second- or third-generation cepha-losporins, ciprofl oxacin (if pseudomonas) and metronidazole (if anaerobes). Anti-TB treatment, when indicated.Relief of atelectasis can be achieved by bronchoscopic aspiration of secretion or removal of foreign body.Surgical treatment: Indications are progression of localized severe disease despite adequate medical management, intrinsic anatomic obstruction of bronchus, life-threatening hemorrhage from a demonstrable source, and suppurative lesion from aspiration of fragmented foreign bodies that include bron-choscopic removal (e.g., grass fi ber or fragments of pea-nut).

Pleural Effusion

Pleural eff usion is the collection of fl uid in the pleural space. It may be unilateral or bilateral, transudative or exudative.

ETIOLOGY

Exudate: Result from infl ammation, or other diseases of the pleural surface; total protein is >3.0 g/dl, LDH > 200 IU/L.

PneumoniaTuberculosis

Malignant diseases—lymphoma, metastasesCollagen diseases—juvenile rheumatoid arthritis, SLE


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Subphrenic abscess: amebic or pyemic liver abscess, pan-creatitis

Pulmonary infarction (rare)

Transudate: Hydrothorax, result from mechanical factors infl uencing the rate of formation of pleural fl uid passively; total protein is <3.0 g/dl.

Nephrotic syndrome Cardiac failure Decompensated cirrhosis of liver Kwashiorkor

CLINICAL FEATURES

Clinical features depend on amount of eff usion. Onset is usually subacute with such manifestation as high fever, cough, chest pain on aff ected side that worsen on deep breathing and coughing, refl ex abdominal pain in case of basal eff usion, and weight loss.

On examination: reduced chest expansion, stony dull per-cussion note, absent or decreased breath sound (occasionally bronchial), with no added sound, and absent or decreased vocal resonance.

INVESTIGATIONS

Complete blood count. Sputum examination (Gram staining, Z-N staining). X-ray chest (P/A): Homogenous dense opacity obscuring

the underlying lung with a curved fl uid line above. Large eff usion may shift the mediastinum to the contralateral side. Small eff usion may only blunt the costophrenic angle. Occasionally, the fl uid is localized below the lower lobe (subpulmonary eff usion), loculated.

Ultrasonography: It is valuable to diff erentiate between a loculated pleural eff usion and tumor and also help to localize an eff usion prior to aspiration and pleural biopsy.

Aspiration of fl uid by a pleural tap confi rms the diagnosis. Pleural fl uid analysis and pleural biopsy. BCG, MT test(s), if TB is suspected.

TREATMENT

Specifi c: Chemotherapy depends on the etiology of pleural eff usion (e.g., anti-tubercular drugs for PTB, antibiotics for pneumonia).

Supportive: Th erapeutic thoracocentesis is indicated in case of large pleural eff usion causing respiratory distress.

Empyema Thoracis

Empyema is an accumulation of pus in the pleural spaces. It is most often associated with pneumonia due to staphylococci and less frequently with pneumococci and H. infl uenzae.

ETIOLOGY

Empyema is always secondary to infection in a neighboring structure, usually the lung. Th e principal infections liable to produce empyema are bacterial pneumonia, lung abscess, pulmonary tuberculosis, bronchiectasis, septicemia, metastatic spread of suppurative foci from distant lesion such as osteo-myelitis and rupture of a subphrenic abscess. It may follow traumatic or surgical wound.

PATHOPHYSIOLOGY

Pathophysiology of empyema has been described in three stages:

Exudative stage (1–3 days): Th is is parapneumonic eff usion with minimal cellular response and is usually culture negative.Fibrinopurulent stage (4–14 days): Eff usion at this stage contains PMN and fi brin. Gram stain and culture shows organism.

Organizing stage (after 14 days): An inelastic membrane is formed on both pleural and visceral surface.

CLINICAL FEATURES

Empyema is more common in younger children. High-grade fever, tachypnea, dyspnea, cough, chest pain, toxemia are usual presenting features. Long-standing cases develop clubbing, anemia, and malnutrition. Chest examination reveals clinical signs of pleural eff usion as mentioned earlier. Immunocom-promised patient may not have fever.

COMPLICATIONS

Bronchopleural fi stulas, pyopneumothorax, purulent pericar-ditis, pulmonary abscess, osteomyelitis of ribs, meningitis, arthritis, and septicemia.

INVESTIGATIONS

CXR: Indistinguishable from those of pleural eff usion. CT can detect loculated empyema and pleural thickening in non-responding patient.

Aspiration of pus: Confi rms the presence of empyema.

USG is recommended to identify the optimal site to undertake pleurocentesis.

Bacteriological examination: Gram staining and Z-N staining of pus may help to determine the cause of empyema.

PMN leukocytosis and elevated ESR may be found.

TREATMENT

Intercostal tube drainage should be done without any undue delay, as this is the single most important step that


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will bring relief. Tube with largest possible size should be used and connected to under water seal drainage. Intercostal drainage is kept inside till drainage is <30–50 ml per day.

Choice of antibiotic is based on suspected microorganisms. Staphylococcus responds to cloxacillin, nafcillin, vancomycin; Pneumococcus to penicillin, cefotaxime, or ceftriaxone; and H. infl uenzae responds to cefuroxime, ceftriaxone, or azithromycin or chloramphenicol. When organism is not identifi able, ampicillin with clox-

acillin or cloxacillin with third-generation cephalosporin is the right combination.

When anaerobic organisms are suspected, metronida-zole should be added. Systemic antibiotic therapy is re-quired for at least 3–4 weeks.

Anti-TB treatment, if indicated.

Supportive: O2 inhalation, nutrition, hydration, antipyretics. Fibrinolytic agent: Streptokinase and urokinase instillation

into the pleural cavity has been found to reduce adhesion in both uniloculated and multiloculated empyema thoracis

Physiotherapy. Surgical management is indicated in pleural thickening,

loculated empyema, non-expansion of lung with drainage tube, and bronchopleural fi stula. Surgical modalities are (i) decortication, (ii) lobectomy, and (iii) video-assisted thoracoscopic surgery (VATS).

Complications: Bronchopleural fi stula and empyema necessitans (cutaneous fi stula).

Pneumothorax

Pneumothorax (accumulation of air in the pleural cavity) is more common in term and post-term infants than in premature ones. Th e incidence is increased among infants with lung disease, such as meconium aspiration and HMD, in those who have had vigorous resuscitation or are receiving assisted ventilation.

ETIOLOGY

Neonate (usually following alveolar rupture):

Respiratory distress syndrome Positive pressure ventilation Vigorous resuscitation Meconium aspiration syndrome Spontaneous or idiopathic Rupture of a congenital cyst Traumatic Ball-valve type of bronchial or bronchiolar obstruction

resulting from aspiration

Children:

Idiopathic

Spontaneous Secondary to lung abscess, empyema, infarct, rupture of a

cyst or an emphysematous bleb (e.g., in asthma) Foreign bodies in lung Traumatic Post-pneumonic, especially staphylococcal Iatrogenic—thoracentesis, tracheotomy, transbronchial

biopsy

CLINICAL FEATURES

Clinical features depend on degree of lung collapse and on the extent of pre-existing lung disease. It ranges from asymptomatic to severe respiratory distress, chest pain, and cyanosis.

On examination, there is increased respiratory rate, reduced chest expansion, hyper-resonant percussion note, absent or decreased breath sound with no added sound, and decreased vocal resonance.


Large pulmonary cavities, diaphragmatic hernia, gaseous dis-tension of the stomach, and emphysema.

INVESTIGATIONS

X-ray chest (P/A) shows presence of air in the pleural space with sharply defi ned edge of defl ated lungs (better fi lm when taken in expiration). Complete translucency between this and chest wall with no lung markings. If pneumothorax is large and under tension, compressive atelectasis of the underlying lungs and shift of the mediastinum and trachea to the opposite side may be demonstrated.

TREATMENT

A small or even moderate sized pneumothorax in an otherwise normal child may resolve without specific treatment, usually within a week. A small (<5% collapse) pneumothorax complicating asthma may also resolve spontaneously.

If collapse >5% or in recurrent pneumothorax or in tension pneumothorax, a defi nitive treatment is necessary.

Administering 100% O2 may hasten resolution by increas-ing the nitrogen pressure gradient between the pleural air and the blood.

Pleural pain deserves analgesic treatment, but codeine may be justifi ed.

Closed thoracotomy (i.e., simple insertion of a chest tube) and drainage of the trapped air through a catheter, the external opening of which is kept in a dependent position under water seal, is adequate to re-expand the lung in most patients. Chest tube is usually removed


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24 hours after the lung has fully re-infl ated and bubbling has stopped. If bubbling in the underwater bottle stops prior to full re-infl ation, the tube is either blocked, kinked, or displaced.

Recurrent pneumothorax: Chemical pleurodesis by intro-duction of talc powder, tetracycline, or silver nitrate into the pleural space prevent recurrences. Open thoracotomy through a limited incision with plication of blebs, closure of fi stula, stripping of the pleura, and basilar pleural abrasion is also an eff ective treatment.

Treatment of the underlying lung disease (i.e., antibacterial or antitubercular drugs) should be given.

Advise not to fl y for 3 months in case of spontaneous pneumothorax.

Subcutaneous Emphysema

It is defi ned as free air in subcutaneous tissue.

ETIOLOGY

Air leaks from pneumomediastinum, fracture orbit (air leak from sinuses), tracheotomy, deep ulceration in the pharyn-geal region, esophageal wounds, any perforating lesion of the larynx, or trachea. It is occasionally a complication of thoracocentesis, asthma, or abdominal surgery. Air rarely may be formed in the subcutaneous tissues by gas produc-ing bacteria.

Interstitial emphysema from ruptured alveolus dissect along peribronchial perivascular connective tissue sheaths of the roots of lungs. If volume of air is great, then there is mediastinal emphysema, pneumomediastinum, pneumothorax, subcuta-neous emphysema. It may press pulmonary veins at hilum, interfering venous return and cardiac output.

CLINICAL FEATURES

Usually asymptomatic. On palpation, crackling under the skin. If air press on trachea or on pulmonary veins at hilum, venous return may be disturbed and cardiac output may be decreased, respiratory distress may develop.

INVESTIGATIONS

X-ray shows air in subcutaneous soft tissue.

TREATMENT

If the cause is air leak from the respiratory system, the problem is usually self-limited and requires no specifi c treatment. Resolu-tion occurs by resorption of subcutaneous air after elimination of its source.

Rarely, dangerous compression of the trachea by air in the surrounding soft tissue requires surgical intervention.

Respiratory Failure

Respiratory failure is defi ned as inability of the respiratory system to deliver adequate oxygen or to remove CO2 from the circulation, leading to arterial hypoxia (i.e., arterial PO2 <50 mmHg), hypercapnia (i.e., arterial PCO2 >50 mmHg), or both. Respiratory failure accounts for approximately 50% of deaths of children under 1 year of age.

CLASSIFICATION

Its classifi cation into type I and type II relates to the absence or presence of hypercapnia (raised PCO2) (Table 7.10).

CLINICAL FEATURES

Respiratory: Wheezing, expiratory grunting. Decreased or absent breath sounds, fl aring of alae nasi, retraction of chest wall, tachypnea, bradypnea or apnea, and cyanosis.Cerebral: Restlessness, irritability, headache, confusion, con-vulsion, coma.Cardiac: Bradycardia or excessive tachycardia, hypotension or hypertension, cardiac arrest.General: Fatigue and sweating.

TREATMENT

I. Acute type I respiratory failure:a. High-concentration oxygen (≥35%) by oronasal mask

or by oxygen tents.

Table 7.10: Causes of Respiratory Failure

Type and fi ndings Causes

Type-I(PO2<8.0 kPaPCO2<6.6 kPa)pH normal or low

AcuteSevere acute asthmaLVF and other causes of pulmonary edema.Acute respiratory distress syndromePneumoniaPneumothorax

ChronicRight to left shuntsLung fi brosis

Type-II(PO2<8.0 kPaPCO2>6.6 kPa)pH low

AcuteSevere acute asthma when life-threatening.Acute epiglottitisInhaled foreign bodyRespiratory muscle paralysis (polio, GBS)Brain stem lesionSleep apneaNarcotic drugs

ChronicKyphoscoliosisPrimary alveolar hypoventilation


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b. Immediate tracheal intubation and mechanical ventila-tion (if patient is very ill)

c. Close monitoring: Arterial blood gas analysis (blood should be taken within 20 minutes) to establish that treatment has achieved acceptable PaO2 levels

d. Prompt diagnosis and treatment of underlying causes. II. Chronic type I respiratory failure:

a. Long-term oxygenb. Treatment of underlying disorder

III. Acute type II respiratory failure:a. Rapid reversal of precipitating event, e.g., dislodge-

ment of foreign body or tracheostomy, reversal of narcotic poisons

b. Treatment of severe acute asthmac. Controlled low-concentration O2d. Mechanical ventilation if the condition causing respi-

ratory failure cannot be reversed immediately. IV. Acute on chronic type II respiratory failure:

Initial assessmenta. All patients may not appear distressed despite being

critically illb. Conscious level (response to commands, ability to

cough)c. CO2 retention (warm periphery, bounding pulses,

fl apping tremor)d. Airway obstruction (wheeze, intercostal indrawing,

pursed lips, tracheal “tug”)d. Right heart failure (edema, raised JVP, hepatomegaly,

ascites)e. Background functional status and quality of life

Investigationsa. Arterial blood gases (severity of hypoxemia, hypercap-

nia, and acidemia)b. Chest radiograph

Treatmenta. Maintenance of airwayb. Treatment of specifi c precipitating event c. Frequent physiotherapy± pharyngeal suctiond. Nebulized bronchodilators

e. Controlled oxygen therapy; start with 24% controlled-fl ow mask. Aim for a PO2 ≥7 kPa (a PO2 <5 is very dangerous)

f. Antibiotics Diuretics

Progressa. If PCO2 continues to rise or patient cannot achieve

a safe PO2 without severe hypercapnia and acidemia, respiratory stimulants (e.g., doxapram) or mechanical ventilation may be required.

V. Type II chronic respiratory failure:a. Treatment of underlying disorderb. Controlled long-term oxygen therapyc. Mechanical ventilatory support, if necessary

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