The Short Textbook of

Pediatrics
Incorporating National and International Recommendations
(MCI, IAP, NNF, WHO, UNICEF, CDC, IPA, ISTP, AAP, etc.)

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Twelfth Edition

Edited by
Suraj Gupte MD, FIAP, FSAMS (Sweden), FRSTMH (London)

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Professor and Head
Postgraduate Department of Pediatrics
Mamata Medical College/Mamata General and Superspeciality Hospitals
Khammam, Telangana, South India
E-mail:  drsurajgupte@gmail.com, recentadvances@yahoo.co.uk

Honorary Director: Pediatric Education Network

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Website: www.drsurajgupte.com

Editor: Recent Advances in Pediatrics (Series), Textbooks of Pediatric Emergencies, Neonatal Emergencies and Pediatric
Nutrition, Pediatric Gastroenterology, Hepatology and Nutrition, Pediatric Infectious Diseases, Perspectives in Influenza,
br
Influenza: Complete Spectrum, Nutrition in Neonatal ICU, etc.
Author: Differential Diagnosis in Pediatrics, Instructive Case Studies in Pediatrics, Pediatric Drug Directory, Speaking of
Child Care
Co-editor: Asian Journal of Maternity and Child Health (Manila, Philippines)
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Section and Guest Editor: Pediatric Today (New Delhi)

Editorial Advisor: Asian Journal of Pediatric Practice (New Delhi)
Editorial Advisory Board Member/Reviewer: Indian Journal of Pediatrics (New Delhi), Indian Pediatrics (New Delhi),
Synopsis (Detroit, USA), Indian Journal of Child Health (Gwalior) International Journal of Pediatric Gastroenterology,
Hepatology, Transplant and Nutrition (Jaipur), Maternal and Child Nutrition (Preston, UK), Journal of Infectious Diseases
(Turkey), etc.
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Examiner: National Board of Examinations (NBE) for DNB, New Delhi; All India Institute of Medical Sciences (AIIMS), New
Delhi; Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh; Sher-i-Kashmir Institute of Medical
Sciences (SKIMS), Srinagar; Indira Gandhi Open University (IGNOU), New Delhi; and several other universities.
Pediatric Faculty Selection Expert: All India Institute of Medical Sciences (AIIMS), Punjab Public Service Commission,
Jammu and Kashmir Public Service Commission, Union Public Service Commission, etc.
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Foreword
Dr Pramod Jog

  The Health Sciences Publisher

New Delhi | London | Philadelphia | Panama

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 How this Book is Useful ?
Features
Ÿ This is the latest edi on of this extensive guide to the field of paediatrics, featuring revised, updated
and brand new content.
Ÿ Bulleted format for easy learning.

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Ÿ Incorporates na onal and interna onal recommenda ons of MCI, IAP, NNF, WHO, UNICEF, IPA, ISTP,
AAP, etc.
Ÿ Blend with recent advances in pediatrics with special focus on the scenarios in the Indian subcon nent.

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Ÿ Eminently covers curriculum of Medical Council of India (MCI) for MBBS students and updated content
for postgraduate entrance examina on prepara on.
Ÿ Every chapter has been updated to accommodate new knowledge, changing concepts and fresh
concerns by the experts drawn from India and abroad.
Ÿ Divided into ten sec ons covering everything from core paediatrics to allied special es and unclassified

Ÿ
Ÿ
issues in paediatrics.

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The first sec on brings this edi on firmly up to date, with an introduc on to contemporary trends.
Other sec ons include neonatology, paediatric infec ons, subspecial es, procedures, syndromes, and
drug doses.
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Ÿ New chapters in this edi on include fever spectrum, fungal, protozoal, heliminthic, intrauterine, and
nosocomial infec ons and infesta ons, all in the paediatric infec ons sec on.
Ÿ Enhanced by over 815 full colour images, diagrams, algorithms, boxes and tables.
Ÿ Important points highlighted in colored boxes for last minute revision at the me of examina on.
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Ÿ Pearls include mul ple choice ques ons and clinical problems along with further reading at the end of
chapters for self-evalua on.
Ÿ Useful appendices have been added at the end.
Ÿ Tailor-made and student-friendly textbook with down-to-earth presenta on and easy-to-follow
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descrip ons.
Ÿ An ideal resource for undergraduates, compulsory rotator interns (CRIs) residents, junior pediatricians,
family physicians, prac cing physicians and established teachers.
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 IN THEIR ESTEEMED OPINION...
Prof NS Tibrewala (Mumbai) : “... occupies pride of the place as a standard textbook... an indispensable
companion...”
Prof PM Udani (Mumbai) : “An essential reading... a nice work.”
Prof NR Bhandari (Bhopal) : “A great gift to the students, both undergraduates and postgraduates.”
Prof DG Benakappa (Bengaluru) : “Very comprehensive and up-to-date... highly recommended.”
Prof N Sundravalli (Chennai) : “A work of special merit.”
Prof AB Desai (Ahmedabad) : “...effectively worded and illustrated, and of great value.”
Prof K Indira Bai (Annamalai) : “Comprehensive... extremely well written... ideal... strongly recommended.”
Prof Meharban Singh (Noida) : “Very informative.”

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Prof GP Mathur (Kanpur) : “Very useful for undergraduates, postgraduates and practitioners.”
Prof PK Misra (Lucknow) : “A very nice comprehensive textbook.”
Prof K Kalra (Agra) : “Strongly recommended to undergraduates and postgraduates.”
Prof Pinaki Banerjee (Kolkata) : “A very comprehensive book... ideal for students.”

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Prof SS Deshmukh (Nagpur) : “...fulfills a long awaited need... wonderful... very comprehensive.”
Prof Rafiq Ahmed (Kolkata) : “A book of outstanding merit.”
Prof KPS Sinha (Patna) : “A fine and appreciable work... clinical approach is commendable.”
Prof SK Khetarpal (Amritsar) : “Concise, comprehensive, up-to-date and to the point....”
Prof PS Mathur (Gwalior) : “Warmly recommended.”
Prof P Chaturvedi (Sewagram)
Prof Birendra Kumar (Darbhanga)
Prof BK Garg (Meerut)
Prof Shanta Karup (Kottayam) ot
: “Very helpful to students.”
: “A really very useful and precise volume for students.”
: “Ideal for students.”
: “A very good work.”
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Prof Ananthakrishna (Chennai) : “Excellent... covers every aspect of pediatrics.”
Prof NB Mathur (Sewagram) : “Highly useful... strongly recommended.”
Prof AK Dikshit (Jamshedpur) : “The book fulfills a very long-standing need.”
Prof AV Ramana (Warangal) : “Very useful for students as well as practitioners.”
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Prof SP Srivastava (Patna) : “Very up-to-date, comprehensive and appropriate for our students, both
under- and postgraduates.....”
Prof Neetu Raizada (Ludhiana) : “A highly recommended state-of-the-art textbook... an essential reading.”
Prof B Sharda (Udaipur) : “Most comprehensive and state-of-the-art textbook...”
Prof Madhuri Kulkarni (Mumbai) : “... tailor-made to the needs of the students.”
Prof A Parthasarthy (Chennai) : “A prototype of Nelson Textbook of Pediatrics.... modelled as per requirements
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in India...”
Prof AM Sur (Nagpur) : “... a boon for pediatric scholars in India in particular... warmly recommended.”
Prof Utpal Kant Singh (Patna) : “... profusely illustrated, clinical-oriented, most up-to-date and ideal to meet the
needs of students in India in particular.”
Prof BS Prajapati (Ahmedabad) : “An essential reading for all students of pediatrics... carries valuable information
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including much-sought-after statistical data... useful for teachers too.”

Prof VN Tripathi (Kanpur) : “A meritorious work... most suitable for undergraduates in particular and
postgraduates in general.”
Prof Javed Chowdhary (Srinagar) : “A textbook of extraordinary merit... An essential reading for the undergraduates
as well as postgraduates...”
Prof Masood-ul-Hassan (Srinagar) : “Most up-to-date, well-illustrated, clinical-oriented, very comprehensive and
student-friendly textbook... warmly recommended.”
Prof Praveen C Sobti (Ludhiana) : “For nearly 4 decades, Dr Suraj Gupte’s textbook has been popular with
undergraduates and postgraduates alike. The book contains all that the
students need to know about common childhood illnesses in the developing
world. It is a thoroughly readable book.”
Prof Vijay Sharma (Shimla) : “A highly recommended textbook of pediatrics...”
Prof DB Sharma (Jammu) : “Tailor-made for the needs of students in India... strongly recommended.”

Prelims.indd 1 03-02-2016 13:36:37

 ii The Short Textbook of Pediatrics

Prof (Col) VS Puri (Jammu) : “An outstanding clinical-oriented textbook... most useful... warmly recommended.”
Prof Pankaj Abrol (Rohtak) : “A very comprehensive and up-to-date textbook of Pediatrics... a nice Indian
response to Nelson’s Textbook of Pediatrics... can easily compete with best
textbooks of pediatrics... A “must” for all students of pediatrics in India.”
Prof MMA Faridi (Delhi) : “There are many books around in the specialty but The Short Textbook of
Pediatrics is unique... it makes the subject easy, interesting and understandable.”
Prof Rekha Harish (Jammu) : “This textbook of extraordinary merit eminently meets the requirements of
students, especially the undergraduates, and is warmly recommended...”
Prof B Vishnu Bhat (Puducherry) : “Well-written book covering all information needed by undergraduates and
postgraduates in pediatrics. Good reference book for practising pediatricians
as well...”

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Prof Ajay Gaur (Gwalior) : “…a genuinely good book for the undergraduate and postgraduate students
with the expertise of eminent academicians… The contents are well presented
in a uniform style and in keeping with the standard protocols and guidelines.....”
Prof Ghanshyam Saini (Jammu) : “…an extraordinary work... a very useful tool for the undergraduates,

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postgraduates and academicians.”
Prof RK Gupta (Jammu) : “An excellent textbook, full of latest updates… unique in itself, providing
concise but comprehensive information…. invaluable in pediatric education
for the undergraduates and postgraduates.’’
Prof E Chen (Malaysia) : “A complete textbook on tropical pediatrics… a “must possession” by each and

Prof Shaukat Sidiqui (Pakistan)

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every student of pediatrics in the region.”
: “Most valuable for the pediatric UGs, PGs, teaching faculty and practising
pediatricians as also for the GPs treating infants, children and adolescents in
the subcontinent…”
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Prof RN Koirala (Nepal) : “An exceptionally useful textbook of pediatrics, eminently meeting the needs
of our students and their teachers… most suitable for our settings.”
Prof JE Jaywardne (Sri Lanka) : “A warmly recommended pediatric textbook, focusing exactly on what is
needed by our medical students, emerging pediatricians and teachers…”
Prof AQ Bhashani (Bangladesh) : “The textbook is a spotlight on everything that we need to teach our students
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of pediatrics in Bangladesh and neighboring countries…”

Prof Panna Choudhury (New Delhi) : “A pediatric textbook of extraordinary merit and value… highly recommended…”
Prof Najma Khan (Maryland) : “ A treat to go through the excellent text and illustrations, especially diseases
prevalent in the underprivileged… a superb textbook.”
Prof RA Anderson (London) : “... unique textbook with down-to-earth clinical-orientation,.... wealth of up-to-
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date knowledge... ideal for students and scholars interested in child health and
disease in resource-poor settings.”
Prof Anupam Gandhi (Johannesburg) : “A commendable cocktail of excellence and much-needed information
presented in a most palatable manner... strongly recommended book.”
Ja

Prelims.indd 2 03-02-2016 13:36:38

 Preface to the Twelfth Edition

The much-awaited 12th edition of The Short Textbook of Pediatrics appears at a time when pediatrics has well established its
status as an independent subject in the undergraduate curriculum with a separate examination at university level in India
following the laudable endeavors of the Indian Academy of Pediatrics.
Since the last edition eminently succeeded in meeting the needs of the undergraduate students, here in the 12th edition

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we have made further strides to attain the enhanced excellence not only for them but also for the benefit of postgraduates,
residents, practitioners and teachers. The goal is to provide a blend of time-honored concepts along with new advances
with special emphasis on the needs in the Indian subcontinent.
Each and every chapter stands updated with extensive revisions and/or rewriting, reorganization and additional material.

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Besides a few new chapters, hundreds of fresh illustrations (clinical photographs, diagrams, algorithms/flow charts), boxes
and tables are added. An enlarged Index shall further facilitate easy retrieval of information.
In keeping with the changing needs, two new features have been incorporated at the end of each chapters in the form
of self-assessment Multiple Choice Questions (MCQs) and Clinical Problem-solving Reviews.
As a result, the new edition is yet more reader-friendly, state-of-the-art and practical-oriented. Yet, the hallmarks of

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the earlier editions, namely brevity with comprehensiveness, simple and straightforward style and easy to understand
expression have been retained and, in fact, further strengthened.
Without any shadow of doubt, the unique and enhanced value of the 12th edition is very much on account of the
expertise, hard work and command in the respective fields of the distinguished contributors. My hats off to them!
A multitude of colleagues, friends and readers, in India and abroad, made worthy suggestions for enhancing the utility
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of the book. Informed assistance from the faculty of the Postgraduate Department of Pediatrics, Mamata Medical College
and Hospitals, especially Dr G Somaiah, Dr MAM Siddiq and Dr G Arpitha, is particulary acknowledged. Also, the time-to-
time academic feedbacks from our residents/postgraduates deserve appreciation.
The Management and the Administration of Mamata Medical College and Hospitals, especially Mr P Nageshwara Rao
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(Founder), Mr P Ajay Kumar, MLA (Chairman), Dr G Venketeshwara Rao (Medical Director), Dr K Koteshwer Rao (Dean), and
Dr T Jaysree (Principal) have been gracious enough for blessing the project and for providing moral support and motivation
in successfully completing the project.
My wife, Shamma, graciously assisted me so much in taking the project to its logical conclusion. So did my daughter,
Dr Novy; son-in-law, Dr Gagan; son, Er Manu; and daughter-in-law, Er Shivani, in spite of their tight schedules and
preoccupation. My brothers, Dr Satish, Raji (alas, we lost him some months back!), Subhash and Rajendra’s continuing
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interest in this project and suggestions for the betterment of the book has all along been a support for my endeavors.
Dr Pramod Jog, President (2016), Indian Academy of Pediatrics, has been gracious enough to write a Foreword to this
edition. My hats off to him for warmly recommending the book.
Finally, I wish to thank Mr Jitendar P Vij (Group Chairman), Mr Ankit Vij (Group President), Ms Chetna Malhotra Vohra
(Associate Director-Content Strategy) Jaypee Brothers Medical Publishers (P) Ltd., and their dedicated staff for the skillful
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production qualities of the 12th edition.

Suraj Gupte
drsurajgupte@gmail.com, recentadvances@yahoo.co.uk
www.drsurajgupte.com

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 Foreword to the Twelfth Edition

I am really at a loss for words to write a Foreword for the 12th edition of The Short Textbook of Pediatrics,
a book which has such a track record and long history of excellence since its first release at the 15th
International Congress of Pediatrics in 1977, New Delhi. In fact, a book of this caliber does not need
introductions, forewords and endorsements for its continuous success.

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The publication of a book is a process as laborious as the process of delivering a baby. Maturity
(contents and the quality), weight gain (number of pages) and intact survival (final copy) all have to be
carefully looked after. Moreover, bringing out a new edition of a textbook is a tight-rope-walk. There is
a need to maintain a continuity in academic contents and advances without affecting the flavor of the

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earlier editions.
Mercifully, The Short Textbook of Pediatrics by Prof Suraj Gupte, an eminent educationist, researcher and author of
national and international repute, continues to remain a prestigious publication, highlighting the phenomenal and fast
explosion of knowledge in modern pediatrics in edition after edition.
The 12th edition of this book is an excellent combo of clinical pediatrics with recent advances in the field of child health.
The value of this textbook is largely due to its expert and authoritative contents by scores of knowledgeable contributors

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drawn from India and abroad. Every reader should be indebted to the dedicated authors for their hard work, knowledge,
thoughtfulness and good judgment in providing a wealth of information in the form of profusely-illustrated and state-
of-the-art chapters with spotlight on problems in the Indian subcontinent. In the formative stage of medical career, it is
important that a student gets authentic information about different topics.
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I am confident that the 12th edition of The Short Textbook of Pediatrics will act as a support system for medical teachers
and help medical students, especially undergraduates, to “Update Grey cells”! The new edition should be yet more
successful in improving the standard of pediatric education and child healthcare in the Indian subcontinent in particular.

Dr Pramod Jog MD, MNAMS, FIAP

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President (2016),
Indian Academy of Pediatrics
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 Contents

Section 1  Introduction to Pediatrics

1. Pediatrics: Contemporary Trends...................................................................................................................................................................3
Suraj Gupte

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Section 2  Core Pediatrics
2. Pediatric History-taking and Physical (Clinical) Examination............................................................................................................ 19

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Suraj Gupte, Rita Smith
3. Normal Growth.................................................................................................................................................................................................. 38
Suraj Gupte, EM Gomez
4. Growth Disorders.............................................................................................................................................................................................. 66
Suraj Gupte, EM Gomez

Gagan Hans, Suraj Gupte, EM Gomez

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5. Development...................................................................................................................................................................................................... 84

6. Developmental, Behavioral and Psychiatric Disorders........................................................................................................................ 96

Monika Sharma, Tejinder Singh, Gagan Hans, Suraj Gupte
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7. Adolescent Medicine.....................................................................................................................................................................................116
Suraj Gupte, AK Sahni
8. Pediatric-related Biostatistics......................................................................................................................................................................130
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G Somaiah, Suraj Gupte

9. Community Pediatrics...................................................................................................................................................................................135
Shaveta Kundra, Tejinder Singh, Suraj Gupte
10. Immunization...................................................................................................................................................................................................153
Suraj Gupte
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11. Nutritional Requirements.............................................................................................................................................................................173

Shashi Vani, Suraj Gupte
12. Infant and Young Child Feeding................................................................................................................................................................183
Satish K Tiwari, Suraj Gupte, EM Gomez
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13. Malnutrition......................................................................................................................................................................................................197
Suraj Gupte, EM Gomez
14. Vitamins..............................................................................................................................................................................................................225
Suraj Gupte
15. Micronutrients/Trace Elements/Minerals...............................................................................................................................................245
Suraj Gupte
16. Fluid, Electrolytes and Acid-base Balance and Disturbances..........................................................................................................253
MAM Siddiq, Suraj Gupte, Lalita Bahl

Section 3  Neonatology
17. Neonatology.....................................................................................................................................................................................................267
B Vishnu Bhat, Shashi Vani, Rajib Chatterjee, Suraj Gupte

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 xxii The Short Textbook of Pediatrics

Section 4  Pediatric Infections

18. Viral Infections..................................................................................................................................................................................................331

L Ranbir Singh, Suraj Gupte
19. Bacterial Infections.........................................................................................................................................................................................359
Ravinder K Gupta, Suraj Gupte
20. Fungal Infections.............................................................................................................................................................................................375
Utpal Kant Singh, Suraj Gupte
21. Protozoal Infections and Infestations......................................................................................................................................................379
Ajay Gaur, Suraj Gupte

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22. Heliminthic Infections and Infestations..................................................................................................................................................395
Suraj Gupte
23. Intrauterine Infections...................................................................................................................................................................................405
Kaiser Ahmed, Suraj Gupte

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24. Nosocomial, Anaerobic and Opportunistic Infections......................................................................................................................410
KV Raghava Rao, Novy Gupte, Suraj Gupte
25. Fever Spectrum................................................................................................................................................................................................416
Harmesh Singh Bains, Suraj Gupte

Section 5  Pediatric Subspecialties

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26. Pediatric Pulmonology..................................................................................................................................................................................425
Daljit Singh, Suraj Gupte
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27. Pediatric Cardiology.......................................................................................................................................................................................461
BP Karunakara, Suraj Gupte, Anil Grover
28. Pediatric Neurology........................................................................................................................................................................................506
Sheffali Gulati, L Ranbir Singh, Suraj Gupte, Bhavana B Chowdhary
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29. Pediatric Gastroenterology..........................................................................................................................................................................549

Ashok Patwari, Suraj Gupte, RA Anderson
30. Pediatric Hepatology and Pancreatology...............................................................................................................................................588
Suraj Gupte, RA Anderson
31. Pediatric Nephrology.....................................................................................................................................................................................612
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G Arpitha, Suraj Gupte, RM Shore

32. Pediatric Hematology....................................................................................................................................................................................633
Praveen Sobti, Jagdish Chandra, Suraj Gupte
33. Pediatric Oncology.........................................................................................................................................................................................665
AM Graham, Suraj Gupte
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34. Pediatric Immunology...................................................................................................................................................................................682

ML Kulkarni, Suraj Gupte, S Frank
35. Pediatric Rheumatology...............................................................................................................................................................................695
GS Latha, Suraj Gupte, DM Sharma
36. Pediatric Dermatology..................................................................................................................................................................................705
Suraj Gupte, NE Parsons
37. Accidental Poisoning.....................................................................................................................................................................................723
Edwin Dias, Suraj Gupte, RK Kaushal
38. Envenomation..................................................................................................................................................................................................734
Suraj Gupte, KV Raghava Rao, RK Kaushal
39. Pediatric Endocrinology...............................................................................................................................................................................739
Vandana Jain, Suraj Gupte, AW Koff

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 Contents xxiii

40. Genetics in Health and Disease..................................................................................................................................................................761

S Frank, Suraj Gupte
41. Inborn Errors of Metabolism.......................................................................................................................................................................773
S Frank, Suraj Gupte
42. Neuromuscular Disorders............................................................................................................................................................................784
B Vishnu Bhat, Suraj Gupte

Section 6  Allied Specialties

43. Pediatric Ophthalmology.............................................................................................................................................................................797
Vijay Wali, Suraj Gupte, G Somaiah

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44. Pediatric Ear, Nose and Throat (ENT) Problems....................................................................................................................................808
VM Rao, Suraj Gupte, G Somaiah
45. Pediatric Dental Problems............................................................................................................................................................................814

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NK Nagpal, Suraj Gupte, G Somaiah
46. Pediatric Surgery.............................................................................................................................................................................................818
Devendra K Gupta, Suraj Gupte
47. Pediatric Orthopedics....................................................................................................................................................................................831
Surya Bhan, Suraj Gupte

Section 7  Miscellaneous and Unclassified Issues

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48. Miscellaneous and Unclassified Issues....................................................................................................................................................845
Suraj Gupte
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Section 8  Pediatric Procedures
49. Pediatric Practical Procedures....................................................................................................................................................................857
Ravinder K Gupta, Suraj Gupte
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50. Pediatric Laboratory Procedures...............................................................................................................................................................870

Ghanshyam Saini, Anumodan Gupta, Suraj Gupte

Section 9  Pediatric Syndromes

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51. Pediatric Syndromes......................................................................................................................................................................................879

Bashir Ahmed Charoo, Javed Iqbal, Asif Ahmed, Suraj Gupte

Section 10  Pediatric Drug Dosages

52. Pediatric Drug Dosages.................................................................................................................................................................................889
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Novy Gupte, SS Prakash, Suraj Gupte

Appendices.....................................................................................................................................................................................................................899
Index ...............................................................................................................................................................................................................................925

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29 Pediatric Gastroenterology
BASICS OF GASTROINTESTINAL TRACT
The term, gastrointestinal tract (GIT), refers to the
alimentary tract extending from the mouth to the anus. It is
divided into mouth, oropharynx, esophagus, stomach, small
intestine (jejunum and ileum) and large intestine (colon).
On ingestion of food by the mouth, it is moved by the
oropharynx into the esophagus. The latter acts as a conduit
for transfer of food to the stomach, where it is stored
and mixed prior to its controlled passage into the small
intestine, where it is digested and absorbed. Then, it moves
to large intestine where salts and water are conserved prior
to excretion as feces.
Undoubtedly, the normal GIT function is the net result
is a breakdown of any one, intestinal function will be
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of combined action of many functional systems. If there
disturbed. For instance, diarrhea develops when there is
an enhanced overload of fluids from small intestines into
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the colon following maldigestion or active secretion, or
when the absorptive capacity of the colon is compromised
by disease. A defect of intestinal mucosal immunity may
lead to recurrent enteric infections. Intestinal obstruction
follows loss of normal intestinal motility. An insult to the
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digestive or absorptive capacity of the GIT may cause
digestive and abdominal complaints, failure to thrive
(FTT) and even weight loss. Diseases elsewhere may also
present with manifestations attributable to the GIT.
DIAGNOSTIC WORK-UP FOR
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GASTROINTESTINAL DISORDERS
Clinical Work-up
A good history and physical examination together
with skillful interpretation of the common symptoms
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and signs See Chapter 2 (Pediatric History-taking and
Clinical Examination) assist in deciding about the various
investigations to arrive at the final diagnosis in a child
suspected of a gastrointestinal disorder.
Special Investigative Work-up
For esophageal structure and function
„„ Barium meal studies for defining anatomy of upper
GIT and detecting advanced mucosal lesions, e.g.
varices and gastroesophageal reflux (GER).
„„ Endoscopy for varices.
„„ 24-hour pH monitoring is the most sensitive test for
GER.
„„ Esophagoscopy for esophagitis and mucosal biopsy.
Chapter 29.indd 549
RIGHT TEXT FOR YOU...
Ashok Patwari, Suraj Gupte, RA Anderson
For maldigestion/malabsorption
„„ Stool examination, including fat globules, reducing
substances, pH, and microscopy is advisable. In case
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of a strong suspicion of intestinal parasitosis, it is
advisable to carry stool microscopy by concentration
method for at least 3 (preferably 6) consecutive days
since ova and cysts frequently pass intermittently. For
details, See Chapter 49 (Pediatric Practical Procedures.)
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„„ 24-hour stool fat by fat balance studies and chemical
examination of stools or by a semiquantitative method
termed as steatocrit. A daily stool fat of greater than 5 g
is considered indicative of steatorrhea.
„„ D-xylose test consists in measuring excretion of xylose in
a 5-hour sample of urine after administering the pentose
in a dose of 1 g/kg body weight (BW). An excretion of
<20% points to malabsorption. A tolerance test too
is available for infants and small children in whom
collection of urine sample is quite cumbersome.
„„ Anti-tissue transglutaminase for celiac disease (CD)
„„ Lactose tolerance test.
„„ Breath test involving measurement of H+.
„„ Barium meal follow-through, employing a non-
flocculable medium, may reveal intestinal changes
indicative of malabsorption, such as intestinal
dilatation, flocculation, and atypical mucosal pattern,
plus anatomic defects.
„„ Endoscopic gastric or jejunal biopsy: The jejunal
biopsy provides vital histologic details as well as the
material for enzymes, disaccharidases, especially,
lactase, assay. It may also identify such pathogens
as Giardia lamblia and Helicobacter pylori. Gastric
biopsy may be employed for histopathology, culture
or rapid urea test for H. pylori.
„„ Schilling test measures the vitamin B12 absorption
from the gut. It consists in administering a tracer dose
of radioactive vitamin B12, after saturating body stores
with vitamin B12, and its urinary excretion measured
over the next 24 hours. An excretion of < 5% indicates
defective absorption from the ileum.
„„ Sweat chloride estimation by iontophoresis, using
pilocarpine, is important for assay of the exocrine
pancreatic function. A level of >60 mEq/L usually
establishes the diagnosis of cystic fibrosis.
DIARRHEAL DISEASES: AN OVERVIEW
Diarrheal diseases rank among the top three causes of
death in pediatric population of the developing world.
Globally, approximately 4–5 million deaths occur as
03-02-2016 11:34:39
 550 a result of diarrheal diseases every year. Eight out of
these 10 deaths are in the first 2 years of life, the most
susceptible period for malnutrition. As indicated in
Chapter 2 (Pediatric History-taking and physical (Clinical)
Examination) diarrhea accounts for about 20% of the
hospitalized pediatric cases in India.
On an average, a child suffers from around 12 episodes
of diarrhea, 4 such episodes occurring during the very
infancy (first year). Existence of malnutrition makes the
child very much vulnerable to diarrheal disease. It is
estimated that incidence of diarrhea in malnourished
children is five to seven times higher than in healthy
children. Likewise, its severity too is three to four times
greater.
By definition, diarrhea means passage of three or
more loose or watery motions per 24 hours, resulting in
excessive loss of fluid and electrolytes in stools. Secretory,
osmotic or motility abnormalities, singularly or in
combination, form the basis of all diarrheal episodes.
„„ Secretory diarrhea has a tendency to be watery,
voluminous and persistent even when no feeding
is given orally. It is usually caused by an external
or internal secretagogue (cholera toxin, lactase
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Section 5  Pediatric Subspecialties
deficiency).
„„ Osmotic diarrhea follows ingestion of a poorly
absorbed solute because of an inherent character of
the solute (magnesium phosphate, alcohol, sorbitol)
br
or a small bowel defect (lactose in lactase deficiency
in brush-border). It tends to be watery and acidic with
reducing substances.
„„ Motility diarrhea is associated with increased
(irritable bowel syndrome) or delayed motility
ee
(intestinal pseudo-obstruction).
„„ Acute diarrhea refers to diarrhea that begins acutely and
terminates within a week or so, only a small proportion of
cases passes to the second week or even beyond.
„„ Chronic diarrhea refers to diarrhea beyond 2
weeks. The term is best reserved for cases with an
yp
obvious malabsorptive disorder or, less frequently,
an underlying organic disease without obvious
malabsorption.
„„ The term persistent diarrhea denotes an episode of
acute diarrhea, presumably of infective origin, that
Ja
lasts for 2 weeks or more.
„„ The term intractable diarrhea of infancy should
be reserved for cases that have onset of protracted
diarrhea before the age of 3 months. These infants
start as an infective diarrhea, become dehydrated and
wasted and have high mortality. They need emergency
treatment.
ACUTE DIARRHEA
(Acute Gastroenteritis)
Acute diarrhea, often accompanied by gastritis manifesting
as vomiting, is called acute gastroenteritis. It is a leading
cause of morbidity and mortality in pediatric practice. The
incidence and mortality are especially high in infancy,
Chapter 29.indd 550
Box 29.1 Etiology of acute diarrhea
zz Enteric infections
„„ Bacteria: Escherichia coli, Shigella, Salmonella, Staphylococcus,
Cholera vibrio, Yersinia enterocolitica, Campylobacter jejuni,
Clostridium difficile, Aeromonas hydrophilia, Vibrio parahemolyticus,
Plesiomonas shigelloides
„„ Viruses: Rotavirus, Norwalk and allied viruses, Enterovirus.
Influenza virus, Measles virus
„„ Parasites: Entameba histolytica, Giardia lamblia, Cryptosporidium,
Cyclospora cayetanensis, Isospora, Hymenolepis nana, Trichuris
trichiura, malarial parasite
„„ Fungi: Candida albicans
„„ Parenteral: URI, otitis media, tonsillitis, pneumonia, urinary
tract infection
rs
zz Drugs: Antibiotics
Dietetic/Nutritional: Overfeeding, starvation, food allergy, food
zz
poisoning
zz Nonspecific.
he
Abbreviation:  URI, upper respiratory infection.
more so in the presence of malnutrition and erratic feeding
practices.
According to a conservative estimate, almost 500
million children suffer from acute diarrhea annually. Of
them, 5 million die every year. In India alone, nearly 1.5
million children die due to acute diarrhea every year.
Etiology
Box 29.1 lists various causes of acute diarrhea in infancy
and childhood. This acute diarrhea, mostly infectious in
origin in pediatric practice, is borne out by the following
points:
„„ Magnitude of diarrhea prevalence is directly
proportional to sanitary and personal hygiene
standards of the community.
„„ Acute diarrhea in the community behaves on the same
lines as other infectious diseases.
„„ Infants and children are more frequently and more
severely affected than older people, indicating poor
immunity in the former.
Viral Diarrhea
Recent evidence has indicated that viruses, such as
rotavirus and Norwalk and Norwalk-like agents, are
responsible for majority of the acute diarrhea in infants
and young children.
Rotavirus, also termed as gastroenteritis virus (GEV),
is the most frequently encountered virus in diarrheal
stools of children. Four established serotypes of rotavirus
account for 20–40% of acute diarrhea. Age 9–12 months
appears to show the peak incidence. Excepting newborns,
it has been observed to have a predilection for winter and
dry months in the Indian subcontinent. Transmission is by
feco-oral route.
The virus causes reversible patchy villous atrophy and
loss in the absorptive capacity of the intestinal mucosa
in a cephalocaudal direction. A marginal reduction in
disaccharidases with some reduction in carbohydrate
absorption is usually present such Brush border enzymes
03-02-2016 11:34:40
 such as alkaline phosphatase, sucrase and trehalase
are also reduced. The small intestinal morphology and
function revert to normal within 2–3 weeks. Incubation
period is usually < 48 hours (range 1–7 days). The average
duration of illness is 5–7 days.
An important clinical feature of rotavirus diarrhea
is the vomiting that usually precedes the onset of watery
motions. About 30–50% cases show slight fever, 25% mucus
in stools and, just an occasional case, blood in stools. It is
responsible for 10–20% of acute diarrheal cases.
Norwalk and Norwalk-like agents, are also associated
with outbreaks of generally mild gastroenteritis occurring
in school, community and family settings. Notwithstanding
minor histological insult to small intestinal mucosa, brush
border enzymes are reduced.
The incubation period is around 48 hours. The attack
is usually mild and self-limiting, lasting 12–24 hours in a
majority of the cases.
Vomiting, abdominal pain, anorexia, headache,
myalgia and malaise are important features of diarrhea,
secondary to this group of viruses. Other viruses
incriminated in the etiology of diarrhea include Hawaii
virus, adenovirus, astroid virus, calici-virus, coronavirus,
enterovirus and minirotavirus.
Bacterial Diarrhea
This constitutes the next major group. The most domi-
ot
nant pathogen in this category is Escherichia coli. Diar-
br
rheagenic E. coli have five classes—enteropathogenic
E. coli (EPEC), enterotoxigenic E. coli (ETEC), entero-
hemorrhagic E. coli (EHEC), enteroadherent E. coli
(EAEC) and enteroinvasive E. coli (EIEC). ETEC are noto-
rious for causing dehydrating diarrhea in developing
ee
countries. EIEC causes shigellosis-like illness. EPEC is
responsible for prolonged diarrhea (non-bloody) with
mucus and at times, pyrexia. EHEC is characterized
by abdominal pain and diarrhea which soon becomes
bloody (hemorrhagic colitis) as in case of shigellosis.
This is called EIEC illness. Risk of developing hemoly-
yp
tic-uremic syndrome in EHEC diarrhea with pyrexia is en-
hanced. EAEC usually causes dehydrating diarrhea which
often becomes prolonged as in case of EPEC.
Vibrio cholerae 01 and 0139, contrary to the widely-
held belief, cause severe watery diarrhea and vomiting
Ja
only in a minority of the children. In most cases, the
infection is mild with minor or no symptoms.
Shigella, Campylobacter jejuni and nontyphoidal
Salmonella account for about 10%, 12% and 3% of acute
diarrhea cases, respectively. These bacteria, along with
EIEC may cause damage to the mucosa of distal ileum and
colon through their toxins, leading to formation of ulcers
as also mucosal secretion of water and electrolytes, and
dysentery.
Parasitic Diarrhea
Giardia lamblia is an important cause of recurrent
diarrhea. Entameba histolytica is encountered relatively
less frequently in infants and children, Hymenolepis nana
(dwarf tapeworm) is common in some pockets only. These
Chapter 29.indd 551
three pathogens may infrequently cause even dysentery- 551
like manifestations.
Cryptosporidium, a coccidian protozoan parasite,
typically causes watery diarrhea, varying from mild to
severe, together with crampy epigastric pain, vomiting,
anorexia, malaise and loss of weight. In immunodeficiency
states (human immunodeficiency virus {HIV} infection,
congenital hypogammaglobulinemia, immunosuppr-
essant therapy in hematogenous malignancies), crypto-
sporidiosis may cause acute diarrhea that tends to become
persistent diarrhea, frequently ending up fatally.
Pathogenesis
rs
Diarrhea: Modus Operandi of Development
The delicate balance in the ecology of the GIT needs to
be broken down by one of the two situations in order that
diarrhea occurs:
he
„„ The conditions in which the defense weakens,
say malnutrition (both primary and secondary),
immunologic disorders, etc. so that even commensals
organisms with weak virulence, or opportunist
organisms overpower and cause diarrhea
Chapter 29  Pediatric Gastroenterology
„„ The known pathogens overcome the natural defense.
The pathogenic organisms produce diarrhea by one or
more of the mechanisms (Box 29.2).
Secretory and Osmotic Diarrhea
Secretory diarrhea results from activation of intracellular
mediators like cyclic adenosine monophosphate (cholera,
heat-labile E. coli, Shigella, Salmonella, Campylobacter
jejuni, Pseudomonas aeruginosa), hormones (vasoactive
intestinal peptides, gastrin, secretin, anion), surfactants (bile
acids, ricinoleic acid), cyclic guanosine monophosphate
(heat-stable E. coli, Yersinia enterocolitica), and intracellular
calcium (Clostridium difficile, acetyl choline, serotonin,
bradykinin).
Osmotic diarrhea results from excessive intake of
carbonated drinks or nonabsorbable solutes (sorbitol,
lactulose, magnesium hydroxide). These concentrated
substances (say, lactose, lactulose) are not absorbed from
the gut. They pull water from intestinal wall into stools.
Such a diarrhea subsides on fasting.
Modus operandi of production of diarrhea
Box 29.2 by pathogens
zz Adhesion to the intestinal mucosal wall, e.g. enteropathogenic
E. coli (EPEC) which are further categorized as class I EPEC
(showing localized adherence) and class II EPEC (showing diffuse
adherence).
zz Elaboration of an exotoxin, (secretory diarrhea), e.g. rotavirus,
enterotoxigenic E. coli (ETEC), Vibrio cholerae, Aeromonas
hydrophilia, Plesiomonas shigelloides, causes excessive secretions.
Fasting has no effect.
zz Mucosal invasion (exudative diarrhea), e.g. enteroinvasive
E. coli (EIEC), Shigella, Salmonella (nontyphi), Clostridium difficile,
Campylobacter jejuni, Yersinia enterocolitica, enteropathogenic
E. coli (EPEC), rotavirus, damage and exudative blood. Fasting
exerts no effect.
03-02-2016 11:34:40
 552 Diarrheal Dehydration: Modus operandi
In order to appreciate the modus operandi of diarrheal
dehydration and dyselectrolytemia, it must be noted that
diarrheal losses are drawn from extracellular fluid (ECF)
compartment constituted by circulating blood, interstitial
fluid and secretions. This compartment accounts for the
60% of the BW of the child.
Loss of water from the child’s body causes shrinkage in
the volume of the ECF compartment. In around one-half
cases with excessive sodium loss in stools, hyponatremia
develops as a result of fall in serum and ECF sodium levels.
Since sodium is the major determinant of osmolality, there
results fall in osmolality of ECF, then follows movement of
water from ECF to intracellular fluid (ICF) compartment.
Further shrinkage of the already shrunk ECF compartment
volume becomes inevitable. This is manifested in the form
of loss or impairment of skin elasticity.
In a small proportion of cases in which diarrheal
dehydration has been treated with fluids containing far
too much of sodium, osmotic pressure of ECF becomes
high, prompting water in ICF compartment to move
to ECF compartment. This is likely to camouflage the
existence of severe dehydration which may erroneously
ot
Section 5  Pediatric Subspecialties
be interpreted as mild dehydration. Depletion of ECF
compartment leads to reduction in blood volume, causing
peripheral circulatory failure and oliguria or anuria. Loss
of potassium in stools leads to hypokalemia, causing
br
abdominal distention, hypotonia and electrocardiogram
(ECG) changes in the form of ST depression and flat T
wave. Loss of bicarbonate in stools leads to acidemia,
causing acidotic respiration (Kussmaul breathing) which
is characteristically deep and rapid.
ee
Clinical Features
Clinical picture varies in mild, moderate and severe cases
(Tables 29.1 and Fig. 29.1).
„„ Mild diarrhea: In mild cases, onset is usually insidious
yp
with two to five motions, which may be loose, green,
offensive and contain mucus and milk curds. The
volume may be small or large. The attack usually
subsides in a day or two without any remarkable
constitutional manifestations or dehydrations.
Ja
Table 29.1:  Clinical features of viral versus bacterial diarrhea
Features Viral diarrhea
Noninvasive
Character of motions Watery Watery or semisolid with
mucus, but no blood
Vomiting Severe Only slight
Pyrexia Slight Nil
URI Usually present Nil
Seizures Nil Nil
Toxemia Nil Nil
Stool microscopy Moderate pus cells NAD
Abbreviations:  NAD, nothing abnormal detected; URI, upper respiratory infection.
Chapter 29.indd 552
Fig. 29.1: Severe diarrheal dehydration. Note the characteristic
rs
features, including moribund state with shock, acidosis and anuria.
Oral rehydration solution (ORS), hailed as the most important medical
advance of the 20th century, has the potential of saving 10,000
children each day—the child population that could otherwise die from
diarrheal dehydration.
he
„„ Moderate diarrhea: The number of motions is ten
or more and constitutional symptoms like fever,
irritability, anorexia and vomiting are usually present.
Mild dehydration (3–5%) is associated.
„„ Severe diarrhea: Here the child passes ‘too many’
loose motions and has severe vomiting to the extent
that nothing is retained and the oral intake becomes
virtually impracticable. Such cases are most often
characterized by sudden, rather than gradual, onset.
They may have marked constitutional symptoms.
Moderate (5–10%) to severe (> 10%) dehydration
further aggravates the clinical picture.
Table 29.2 summarizes the clinical picture seen in
different grades of dehydration.
Manifestations secondary to central nervous system
(CNS) disturbances are prominent in all types of severe
dehydration (Table 29.3). Hypertonic dehydration has
more of these. Early irritability, alternating with apathy,
may progress to restlessness, cloudiness or consciousness,
delirium or stupor, lethargy and coma. Convulsions may
occur at any stage. The high viscosity of blood may cause
as serious a complication as cerebral thrombosis.
In addition to cerebral thrombosis, conditions that
may cause seizures in acute diarrhea or AGE include
marked hyponatremia, rapid correction of hypernatremia,
Bacterial diarrhea
Invasive
Semisolid, small amount, very frequent, with mucus and
blood
Moderate
Moderate to high
Nil
Occasionally
Slight
Moderate pus and red cells
03-02-2016 11:34:40
 Table 29.2: Clinical picture of different grades of dehydration Table 29.4:  Clinical picture in certain special situations
553
Grade of Estimated Conditions Physical signs
dehydration fluid loss Clinical picture Acidosis Breathing increased in depth and rate
Mild (3–5% <50 mL/kg Irritability or drowsiness; pallor; Alkalosis Breathing decreased in depth and rate; latent
weight loss) somewhat sunken eyes. or manifest tetany
Moderate 50–100 mL/kg Sick-looking child, pallor, Hypokalemia Abdominal distention, paralytic ileus
(6–10% weight depressed anterior fontanel, hypotonia, hyporeflexia; mental apathy; ECG
loss) sunken eyes, dry mucos changes
membrane, dry and inelastic skin. Hyperkalemia Fibrillation or paralysis of skeletal muscles;
Severe (>10% >100 mL/kg Signs of superimposed shock ECG changes
weight loss) (coma, limpness, pallor, cold- Hypocalcemia Tetany; paralytic ileus
clammy skin, thin, rapid or almost
impalpable peripheral pulses), Hypercalcemia Hypotonia; fecal masses

rs
metabolic acidosis, oliguria/anuria. Hypomagnesemia Tetany; muscular twitching
Hypermagnesemia CNS depression; hyporeflexia

Table 29.3:  Clinical picture in isotonic, hypotonic and hyper- Abbreviations:  ECG, electrocardiogram; CNS, central nervous system.
tonic dehydration
home-made electrolyte solution (HES) may also be

he
Criteria Isotonic Hypertonic Hypotonic
used. There are distinct advantages in using a cereal-
Skin color Gray Gray Gray
based solution, such as rice-water electrolyte solution
Temperature Cold Cold or hot Cold (RWES), especially since it has a better tolerance
Turgor Poor Fair Very poor and provides greater energy. Each motion must be
Feel Dry Thickened Clammy (moist) followed by replacement with an equal amount of

Chapter 29  Pediatric Gastroenterology

ORS. Breastfeeding must not be discontinued. In fact,
Mucous
membrane
Eyes
Anterior
fontanel
Dry

Sunken and soft

Depressed
Parched

Sunken
Depressed ot
Slightly moist

Sunken and soft

Depressed
„„
it potentiates the usefulness of ORT.
Intravenous fluid therapy is indicated in cases with
severe dehydration (Fig. 29.2) and those who fail
to retain ORS persistently. It consists of deficit and
br
Sensorium Drowsy Very irritable Comatose maintenance therapy.
Pulse Rapid Moderately Rapid „„ Deficit therapy: A particular grade of dehydration,
rapid moderate for instance, may mean variation from 5 to
Blood Low Moderately low Very low 10% weight loss. It is, therefore, rather unrealistic to
pressure administer the same amount of fluid to all such children.
ee

Table 29.6 gives a modification of a popular scoring

hypocalcemia, hypomagnesemia, encephalitis and shige- system. It has yielded gratifying results in ours as well
llosis. Table 29.4 summarizes the clinical picture seen in as others’ experience in managing dehydrated infants
and children.
certain special situations.
The deficit therapy is obtained by the following:
yp

Clinical Assessment of Diarrheal Dehydration

Since laboratory investigations are most often not
available, it is advisable to make the best use of one’s
clinical knowledge in evaluating the grades and type of
dehydration (Table 29.5).
Ja
Score × weight in kg × 10
Thus, an 18-month-old, weighing 10 kg and scoring
8 points (8% dehydration or weight loss) requires 8 × 10
× 10 = 800 mL of fluids to cover the deficit as a result of
dehydration.

Management „„ Maintenance therapy: It is best calculated as already

outlined in Chapter 16 (Fluid, Electrolytes and Acid-
Conventional Rehydration Therapy
base Balance and Disturbances). Thus, again taking up
Replacement of the fluids as soon as possible is the sheet- the just-cited example, this 18-month-old needs 125 ×
anchor of management of acute diarrhea: 10 = 1250 mL of fluids/24 hours (Table 29.7).
„„ Oral rehydration therapy (ORT), is described in „„ Plan of therapy: Different centers employ different
detail later in this very chapter, is ideal for mild plans. The following lines of administering the fluids
dehydration and a majority of the children with are generally favored*:
moderate dehydration. Current recommendation zz Initial therapy: Of the total fluids calculated for
in infants and children is reduced osmolarity oral 24 hours, one-fifth is given rapidly in the form of
rehydration salts (ORS) (osmolarity 245 mOsm/L Ringer lactate in 2.5 or 5% glucose during the first
instead of 311 mOSm/L in WHO standard ORS). A 1–2 hours**.
* The vast majority of pediatric dehydration in India is ‘isotonic’. The regimen is, therefore, by far the best in our set-up.
** To determine number of drops per minute, apply this equation: No. of drops/minute = mL to be given in one hour/3

Chapter 29.indd 553 03-02-2016 11:34:40

 554 Table 29.5:  Assessment of diarrheal dehydration as per the World Health Organization
Area of clinical observation Actual observation(s)
No dehydration Some dehydration Severe dehydration
Look at
zz General condition Well alert Restless, irritable Lethargic, unconscious
zz Eyes Normal Sunken Sunken
zz Tears Present Absent Absent
zz Mouth and tongue Moist Dry Dry
zz Thirst Drinks normally, not thirsty Drinks eagerly, thirsty Drinks poorly/ unable to drink
Feel
zz Skin pinch Goes back quickly Goes back slowly Goes back very slowly

rs
Decide
The patient has no signs of Two or more signs denote Two or more signs denote severe
dehydration some dehydration dehydration
Treat Use treatment Plan A Use treatment Plan B Use treatment Plan C urgently

he
ot
Section 5  Pediatric Subspecialties

br
ee

Fig. 29.2:  Severe diarrheal dehydration. Note the classical features.

Table 29.6:  Dehydration scoring system Table 29.7:  Composition of important intravenous
yp

solutions (mEq/L)
Score 1 Score 2
Solution Na K Mg Cl HCO3
zz Irritability, drowsiness, or lethargy zz Shock/coma
zz Sunken anterior fontanel and/or eyes zz Acidosis Isotonic saline (0.9% NaCl) 154 – – 154 –
zz Dry mucus membrane and/or skin zz Anuria Ringer lactate 130 4 – 109 28
zz Loss of skin turgor zz Moribund state
Half-strength 61 18 3 52 27
Ja

zz Abdominal distention Darrow’s solution

zz Tachycardia
Sodium bicarbonate 892 – – – 892
zz Oliguria
(NaHCO3 7.5%)
Sodium lactate (N/6) 167 – – – 167
If anuria persists despite rapid flushing in of the
intravenous (IV) fluids, a bolus dose of frusemide plan of fluid therapy works well in a vast majority
may be administered. If the child passes urine, the of the cases. It takes care of potassium deficiency as
IV drip is continued. Else, the child is treated as for well as acidosis. Complications such as metabolic
acute renal failure (ARF)/injury, reducing the fluid
acidosis, paralytic ileus or hypocalcemic tetany are
intake considerably.
rare with this regimen.
zz Continuation therapy: For rest of the 24 hours,
remaining four-fifth fluid is administered slowly. Maintenance of fluids and electrolytes should continue
Here, half-strength Darrow’s solution which is over the second 24 hours even if diarrhea has stopped in
relatively rich in potassium is ideal. The aforesaid the very first 24 hours. In severe acidosis (CO2 <8 mEq/L),

Chapter 29.indd 554 03-02-2016 11:34:41

 it is advisable to give additional alkali (which should be
infused) in amounts as per the following formula:
mL of NaHCO3 (7.5%) = bicarbonate deficit (mEq/L) × body weight
(kg) × 0.5.
In situations where it is difficult to determine the base
deficit, sodium bicarbonate may be given in the dose of
2–3 mL/kg. It is advisable to review the child after 2 hours
to find if further correction is needed.
In case of severe hypokalemia, additional potassium in
the dose of 1–3 mEq/kg may be added to the drip. Contrary
to earlier recommendation, insistence on passing urine
freely before potassium is administered is not necessary. If
possible, an ECG should be done. In the event of occurrence
of hyperkalemia, exchange resins, or digoxin are of value.
IV NaCl and Ca are also helpful. For hyponatremia, full-
strength electrolyte solutions and even 3% NaCl may
be used. Significant hypernatremia requires solutions
with sodium content of around 30 mEq/L. Highly diluted
solutions may cause convulsions and other neurologic
manifestations. Rarely, very serious cases of hypernatremia
may need peritoneal dialysis as is done in the case of ARF.
Finally, it needs to be remembered that plain solutions,
like 5% glucose, should never be used for IV dehydration
correction.
World Health Organization (WHO) Guidelines on the
Management of Diarrheal Dehydration
ot
br
Plan A for—No dehydration
„„ Objective: Prevention of dehydration. It is carried at
home and consists of:
zz ORS administration, in amounts exceeding normal
ee
requirements:
−− <6 months 50 mL (1/4th glass)
−− 7 months to 2 years 50–100 mL (1/4–1/2 glass)
−− 2–5 years 100–200 mL (1/2–1 glass)
−− Later As much as the child accepts
zz Continuing normal feeding
yp
zz Asking the caretaker to bring back the child after
2 days (even earlier in the presence of danger signals
such as fever, repeated vomiting, dehydration,
blood in stools).
Plan B for—Some Dehydration
Ja
„„ Objective: Correction of dehydration and prevention
of malnutrition.
zz Correction of dehydration is carried out by
administering ORS, 75 mL (50–100 mL)/kg over a
period of 4 hours
zz Continuing breastfeeding/other feedings
zz Reassessment after 4 hours:
−− If adequately rehydrated, deal as in Plan A
−− If poor response to ORS, treat as in Plan C.
Plan C for—Severe Dehydration
„„ Objective: Quick correction of severe dehydration with
IV fluids (preferably Ringer’s lactate) in a hospital/
facility.
Chapter 29.indd 555
zz <1 year 30 mL/kg within first hour followed by 70 555
mL/kg over next 5 hours
zz >1 year 30 mL/kg within 1/2 hour followed by
70 mL/kg over next 2 ½ hours
zz Assess every 1–2 hours.
−− If no improvement, give IV fluid more rapidly
−− If improvement, complement with ORS as soon
as the infant starts accepting it
−− After 6 hours in infants and 3 hours in older
children, opt for the suitable plan A, B or C,
depending on the assessed hydration status.
Antibiotics
Bacterial or parasitic organisms are not isolated from a
rs
large majority of pediatric patients suffering from acute
diarrheal disease. Routine use of antibiotics is, therefore,
generally not favored by the experts. However, antibiotic
cover may be indicated in the following situations:
he
„„ Bloody diarrhea (bacillary dysentery)
„„ Cholera
„„ Amebiasis
„„ Giardiasis
„„ Malnutrition.
Chapter 29  Pediatric Gastroenterology
Pharmacotherapy for Symptomatic Control
In the past, nonspecific antidiarrheal agents, like codeine,
morphia, tincture opium, charcoal, chalk, anticholinergic
drugs, products of hydroscopic bulk (psyllium seed or
Plantago ovatum), kaolin, bismuth, pectin, diphenoxylate
hydrochloride and loperamide hydrochloride have been
used. These drugs are either not quite effective or their
use is accompanied by unpleasant/untoward side-effects.
These are no longer recommended.
The role of prostaglandin inhibitors and antisecretory
agents, such as aspirin, though theoretically significant,
needs detailed evaluation in the therapy. Racecadotril,
an antisecretory drug, claims to reduce stool output and
duration of diarrhea. However, its efficacy remains to be
convincingly proved. Its routine use in acute diarrhea is
not yet recommended.
Nutrition (Diet)
Prolonged starvation damages rather than helps and
should be discouraged. Even hypocaloric oral therapy
during an episode of diarrhea and vomiting may lead to
severe malnutrition. Lack of attention to nutrition during
diarrhea appears to be the largest contributing factor
to overwhelming problem of malnutrition in the Indian
subcontinent.
Banana, apple pulp, yoghurt, curd, potatoes, rice, wheat,
etc. should be given as soon as possible. Foods rich in fats or
sugar, including juices and soft drinks, should be avoided.
Current recommendations on nutritional manage-
ment of acute diarrhea are as follows:
„„ Since most nutrients are well-absorbed during diarrhea
and since diarrhea predisposes to malnutrition, it is
safe and desirable to continue breastfeeding as also
other feedings during a diarrheal episode. That rest to
gut promotes early recovery is no longer held true. It
has no physiologic basis at all.
03-02-2016 11:34:41
 556 „„ Optimally, energy-dense foods with minimal bulk,
given in small quantities every 2–3 hours, promote
better nutrition.
„„ Since staple foods do not provide optimal calories
per unit weight, these are best enriched with richer
sources of energy, like fats and oils, e.g. khichri with
oil, rice with milk or curd, mashed banana with milk or
curd, mashed potato with oil, etc.
„„ Foods with high fiber content (coarse fruits and
vegetables) as also soft drinks and juices with very
high sugar content may be avoided during an acute
diarrheal episode.
„„ In artificially-fed infants, milk should preferably be
given undiluted during all phases of acute diarrhea. If
the infant is over 4 months, milk cereal mixture (say
dalia-sago, rice-milk) is strongly recommended.
„„ Transient lactose intolerance, which is frequent in
acute diarrheal disease, does not warrant lactose-
free milk unless it persists beyond 8–10 days and is
accompanied by progressive weight loss.
„„ During convalescence from acute diarrhea, dietary
intake should be enhanced by at least 25% of normal
to make up for the losses during illness and to promote
ot
Section 5  Pediatric Subspecialties
rapid weight gain until the child attains normal
nutritional status.
Finally, it is most appropriate to re-emphasize the
WHO/United Nations Children’s Fund (UNICEF) slogan
that the full package for diarrhea therapy in a vast majority
br
of children is ORS and continued feeding.
Ancillary Measures
These include control of vomiting by sips of ORS, a mild
antiemetic or stomach wash, and treatment of any other
ee
accompanying problem.
„„ Zinc, 10–20 mg/day (O), in every child with diarrhea,
for 2 weeks is strongly recommended by the Indian
Academy of Pediatrics (IAP). It helps in cutting down
severity and duration of diarrhea. Furthermore, it
reduces the risk of developing persistent diarrhea.
yp
„„ Probiotics, may be helpful to restore the normal
intestinal flora (lactobacilli) which are likely to be
destroyed by the disease or by antibiotic therapy.
However, at present, routine use of probiotics is not
recommended by the IAP.
Ja
„„ Vitamin A supplements may, assist healing of the
damaged intestinal epithelium.
„„ If IV drip is to be prolonged, vitamins should be added
to the infusion.
„„ Abdominal distention, if mild and with normal bowel
sounds, warrants no intervention. Paralytic ileus,
manifested by gross abdominal distention and poor
or absent bowel sounds, is an indication for temporary
withdrawal of oral feeds, intermittent nasogastric
* Children with significant protein energy malnutrition (PEM) often suffer from hypotonic dehydration. This observation is in sharp contrast with
the picture seen in other children in whom dehydration is usually of isotonic type. Malnourished children, should, therefore, receive:
• Either isotonic or even hypertonic solution.
• Additional potassium.
• Additional sodium bicarbonate or sodium lactate to combat severe acidosis.
• Relatively less amount of fluids.
Chapter 29.indd 556
suction and administration of potassium chloride
with a parenteral fluid. The existence of septicemia
or enterocolitis should be seriously considered and
treated energetically.
„„ Seizures during acute diarrhea may result from
several factors, namely fever, hypo or hypernatremia,
hypoglycemia, hypocalcemia (consequent upon
administration of bicarbonate for correction of
acidosis), meningitis, encephalitis, cavernous sinus
thrombosis, etc. After symptomatic control of seizures
with IV diazepam/lorazepam (or another suitable
anticonvulsant) has been attained, attention should
be paid to treat the etiologic basis of seizures.
rs
Prognosis
„„ Age: Mortality is higher in newborns and infants than
in older children.
he
„„ Nutritional status: Diarrhea in malnourished children
carries poor prognosis*. Even mild-to-moderate diarrhea
in such subjects may cause almost irreversible metabolic
alterations, causing death. In one investigation, while
the mortality in well-nourished patients was 4.3%, it
was 22% in those suffering from marasmus.
„„ Causative organism and severity of illness: E. coli
resistant to most available antibiotics and Shigella
cause very severe illness.
„„ Associated illness/complications: Presence of profound
dehydration, electrolyte imbalance or bronchopneu-
monia definitely has adverse effect on the outcome.
„„ Management: Promptness and adequacy of treatment
also have great bearing on the ultimate outcome.
Prevention
„„ Improvement in the nutritional status of the
children: Malnutrition predisposes to diarrhea which
further aggravates the state of poor nutrition
„„ Improvement in community’s water supply,
sanitation and hygiene: Mothers must ensure proper
handwashing before serving, preparing or eating food,
using clean (potable), preferably boiled or filtered,
drinking water, protecting food from contamination by
flies, cockroaches and dirt, washing fruits and vegetables
before use, and proper disposal of excreta (Fig. 29.3).
„„ Breast (biological) feeding should be encouraged:
Those who are bound to stick to artificial feeding
should learn the hygienic preparation of the formula
and care of bottle, teats, etc.
„„ Mothers must be taught when to consult the doctor in
case of diarrhea.
„„ Standardized simple method of administering IV
fluids should be available not only in the cities but in
rural areas as well.
03-02-2016 11:34:41

Fig. 29.3:  Major gains of biological feeding.
„„ Easy availability of take-home ORS sachets.
„„ Rotavirus vaccine: Two doses of RV-1 is given in 10
and 14 weeks’ schedule. RV-5 is given in three doses in
6, 10 and 14 weeks’ schedule.
Complications/Sequelae
„„ Dehydration and dyselectrolytemia with its widespread
complications, including acute kidney injury, paralytic
ileus, thromboembolism, seizures, etc
„„ Superadded infections including thrombophlebitis at
the site of catheter/cutdown
„„ Overhydration and CCF
„„ Malnutrition
„„ Hypoglycemia
„„ Syndrome of inappropriate secretion of antidiuretic
hormone (ADH)
„„
„„
„„
Carbohydrate intolerance and persistent diarrhea
cause mental retardation in later life
Consumptive coagulopathy
ot
Subdural collection of fluid/blood that may possibly
br
„„ Toxic megacolon.
CHOLERA
This is a form of severe gastroenteritis characterized
by sudden onset of profuse effortless watery diarrhea
ee
followed by vomiting and severe dehydration. The most
severe form of cholera is termed as cholera gravis.
Etiology
The causative agent is labeled as Vibrio cholerae 01 or
yp
V. cholerae 0139 Group 1. The classical biotype is now by
and large replaced by the E1 T or biotype mostly belonging
to the serotype Ogawa.
In addition to the known 138 serotypes of V. cholerae, a
new serotype (non-01) identical to the Indian serotype has
been identified in Bangladesh. It behaves like V. cholerae
Ja
01 in causing a severe disease through production of a
large quantity of cholera toxin.
Epidemiology
Though epidemics are now infrequent (the July–August
1988 outbreak in Delhi and other parts of the country was
the most remarkable in the recent decades), cholera is
currently endemic in Maharashtra, Tamil Nadu, Madhya
Pradesh, Andhra Pradesh and Assam. These states account
for 80% of the total incidence in India. Bengal is no longer
considered as the home of cholera.
The disease is transmitted by the feco-oral route, the
channels of transmission being contaminated water,
contaminated foods or drinks, or direct person-to-person
Chapter 29.indd 557
contact. Poor environmental sanitation, thus, constitutes 557
the lifeline for spread of cholera.
Clinical Features
Incubation period is 1–2 days with a variation of few hours,
to 5 days. Clinical picture shows the following three stages:
1. Stage I (stage of evacuation) is characterized by
profuse, effortless watery diarrhea with rice-water
appearance (as many as 50 motions/day) followed by
vomiting and rapidly developing dehydration.
2. Stage II (stage of collapse) is characterized by severe
dehydration, eventually ending up in shock, which
may prove fatal.
rs
3. Stage III (stage of recovery) is characterized by signs
of clinical improvement in subjects who have escaped
death.
he
Diagnosis
In suspected cases needs to be confirmed by:
„„ Direct microscopy of samples of stool, vomitus, water
or food. Under dark field illumination, organisms
appear as several shooting stars in a dark sky
Chapter 29  Pediatric Gastroenterology
„„ Culture on peptone water tellurite (PWT) medium
„„ Biochemical tests.
Complications
These include acute renal shutdown, hypokalemic
nephropathy, paralytic ileus, pulmonary edema and
arrhythmias.
Management
Treatment consists in administering oral and/or IV
rehydration therapy along with chemotherapy to cut
short the duration of disease as also to reduce period of
vibrio excretion. Drug of choice is tetracycline but, in
view of its known adverse side-effects in children, the
choice should be out of erythromycin, azithromycin,
Furazolidone ciprofloxacin and cotrimoxazole. A 3-day
course is sufficient. Whereas V. cholerae 0139 is resistant to
cotrimoxazole, tetracycline-resistant strains of V. cholerae
01 have also occurred in many countries.
Attention must also be directed to sanitation measures
such as water control, excreta disposal, food sanitation
and disinfection. The innovative cholera cot developed
by the Diarrheal Disease Center, Dhaka, Bangladesh, is of
great utility. It is a portable cot with a hole in the middle,
leading to a bucket underneath.
Prophylaxis
Chemoprophylaxis (same drugs as for treatment and for
the same period) is recommended for household contacts
or for a closed community with outbreak of cholera. Oral
cholera vaccine is recommended in children > 1 year of
age in two doses 2 weeks apart, and in persons residing in
highly endemic areas or traveling in areas where risk of
transmission is very high, like Kumbh Mela.
03-02-2016 11:34:41
 558 „„ Blood counts reveal a marked leukocytosis with rise of
Box 29.3 Subdivisions of Shigella
polymorphonuclear cells in majority of the cases.
zz Group A: Shigella shiga or dysenteriae is the most important „„ Stool cultures for isolating the organism are essential
among the ten serotypes
zz Group B: Shigella flexneri or paradysenteriae is the most important
for establishing the diagnosis.
among the six serotypes Treatment
zz Group C: Shigella boydii
zz Group D: Shigella sonnei. Specific
Choice of antibiotic depends on the existing sensitivity of
ACUTE BACILLARY DYSENTERY the organism in the particular community. In the wake
of increasing resistance to ciprofloxacin, ampicillin,
(Bloody Diarrhea, Shigellosis) cotrimoxazole, nalidixic acid, etc. The following approach
Definition is most appropriate:
„„ Children with bacillary dysentery who are stable:
It is defined as the passage of loose stools containing

rs
Ciprofloxacin, cefixime or azithromycin
mucus, pus and visible blood, and accompanied by fever,
„„ Children with bacillary dysentery who are very sick:
tenesmus and crampy abdominal pain.
Ceftriaxone should be considered the current drug of
Etiopathogenesis choice.

The causative organism, Shigella, is subdivided into four
groups (Box 29.3).
Invasive strains of Shigella, after penetrating the
epithelial cells of the intestine, multiply in the submucosa
and lamina propria. This leads to local inflammation and
superficial ulcers which may bleed.
he
General Measures
These include correction of dehydration and electrolyte
imbalance and associated malnutrition, including hypo-
proteinemia and anemia. Antimotility drugs such as
diphenoxylate and loperamide may decrease frequency
of motions, but prolong excretion of Shigella, and are best

ot
Section 5  Pediatric Subspecialties

Epidemiology
Shigellosis occurs worldwide, usually towards the late
summer. The disease spreads chiefly by oral-fecal route.
br
The spread is boosted by the low level of personal hygiene,
environmental sanitation level causing breeding of flies,
and contamination of water, ice, milk and other foods.
Both sporadic and epidemic forms occur.
ee
avoided.
Prognosis
Institution of proper treatment well in time leads to a
favorable prognosis in a large majority of the cases. Factors
such as malnutrition and enclosed population (say, that of
mental institution) contribute to increased morbidity and
mortality.
Complications include anemia with hypoproteinemia,

rectal prolapse, arthritis, Reiter’s syndrome, vaginitis and

Clinical Features
Incubation period is usually 1–3 days. Onset is sudden with
fever, prostration, vomiting, bloody diarrhea, abdominal
pain and tenesmus. Dehydration and electrolyte loss may
yp
hemolytic uremic syndrome. A chronic form of shigellosis
may occur. In such a carrier state, a synthetic derivative of
lactose (lactulose) may transiently reduce the excretion of
the organisms.
Prevention

cause shock. Headache, drowsiness and even coma, neck

rigidity and convulsions may occur. This is by control of carrier and active states and attention
to personal, water and food hygiene and environmental
Differential Diagnosis standards. No vaccine is so far available against shigellosis.
Table 29.8 lists the major differential diagnosis of bloody
diarrhea in children.
ANTIBIOTIC-ASSOCIATED DIARRHEA
Ja

Definition
Diagnosis
Antibiotic-associated diarrhea (AAD) is defined as diarrhea
„„ Stool sample shows leukocytes (pus cell) and red that has no known cause other than antibiotic therapy
blood cells. given concurrently or, at the most, 4 weeks preceding it.

Table 29.8:  Major differential diagnosis of bloody diarrhea

Group Pathogens/Conditions
Invasive bacteria Shigella, coli (enteroinvasive, enterohemorrhagic, Campylobacter jejuni, Salmonella (nontyphoidal)
Protozoa/helminths Escherichia histolytica (both luminal and invasive), Giardia lamblia, Hymenolepsis nana, Strongyloides
stercoralis, hookworm
Miscellaneous/noninfectious Intussusception, vitamin K deficiency, ulcerative colitis, Crohn’s disease, blood dyscrasias (leukemia),
purpura (ITP).
Abbreviations:  ITP, idiopathic thrombocytopenic purpura; HSP, Henoch-Schӧnlein purpura.

Chapter 29.indd 558 03-02-2016 11:34:41

 Blood in stools is not mandatory. On the contrary, 559
stools may be frequent, watery and voluminous with or
without gross (visible) blood or mucus.

Etiopathogenesis
Any antibiotic is capable of causing diarrhea. However, the
following are considered the high-risk antibiotics for AAD:
„„ Clindamycin A
„„ Ampicillin
„„ Lincomycin
„„ Macrolides, especially azithromycin
„„ Cephalosporins.
Antibiotics are supposed to cause diarrhea through

rs
C. difficile which produces adverse effects on intestinal
mucosa through its toxins. Toxin A acts on the intestinal B
mucosa to produce diarrhea. Toxin B, a cytotoxin,
enhances vascular permeability in low doses, but in higher Figs 29.4A and B:  Pseudomembranous colitis. (A) Multiple yellow
plaques throughout colonic mucosa; (B) Flat raised lesions that vary
doses, it may prove lethal.

he
in size with intervening hyperemic mucosa.
Additional mechanisms (other than toxin) of
production of diarrhea by C. difficile are: Differential Diagnosis
„„ Suppression of the normal gut flora.
„„ Production of enzyme, beta-lactamase, by resistant Differential diagnosis is from:
pathogens, thereby inactivating antibiotics and „„ Diarrhea due to Shigella, Salmonella, E. coli, Yersinia,

Chapter 29  Pediatric Gastroenterology

facilitating growth of C. difficile. Helicobacter, E. histolytica, G. lamblia, S. stercoralis,

Clinical Features
„„ ot
Manifestations range from mild self-limited diarrhea
without pseudomembrane through explosive watery
T. trichiura, or H. nana
„„ Hemolytic uremic syndrome (HUS)
„„ Inflammatory bowel disease
„„ Neutropenic colitis
br
diarrhea with occasional blood to severe hemorrhagic „„ Typhilitis

colitis with classical picture of blood and mucus „„ Malabsorption states.

accompanied by toxemia in psedomembranous colitis.
„„ Toxic patient may have fever, cramps, crampy Treatment
ee

abdominal pain, nausea and vomiting, dehydration
with dyselectrolytemia, protein-losing enteropathy
and hypoalbuminemia.
„„ Serious complications such as toxic megacolon,
colonic perforation, peritonitis and shock may occur.
Diagnosis
yp
Discontinuation of the suspected drug and rehydration
therapy, if dehydration is present, results in remarkable
improvement within 48 hours and complete resolution
within 7–10 days in mild cases.
If response is unsatisfactory within 48–72 hours or in
case of a severe illness (pseudomembranous colitis), the

following drugs are recommended:

A high index of suspicion is the key in detecting cases of
antiepileptic drug (AED), including pseudomembranous
colitis. Diagnosis needs detection of the organism, C.
difficile (culture), as also the toxin A (enzyme-linked
immunosorbent assay {ELISA} or latex agglutination
Ja
„„ Oral metronidazole, ornidazole or nitazoxanide
OR
„„ Oral vancomycin (20–40 mg/kg/day) yet more critical
situations (toxic megacolon, adynamic ileus), a

combination of the two drugs intravenously (IV) is

assay) and toxin B (cytotoxicity to cultured fibroblasts).
Colonoscopy may be of value in visualizing the lesions
in atypical cases:
„„ Stage 1: Normal appearance
„„ Stage 2: Mild edema and erythema
„„ Stage 3: Granular friable or hemorrhagic mucosa
„„ Stage 4: Pseudomembranous colitis.
Typically, pseudomembranous nodules or plaques
occur in rectum, sigmoid and distal colon. In a proportion
of cases these may be found only in cecum and transverse
colon. The lesions appear as grayish-white exudates
that are surrounded by edematous and erythematous
inflammatory response (Figs 29.4A and B). These are
poorly adherent to the underlying tissue.
recommended.
If the patient fails to respond to one, it may be substi-
tuted by the other. In yet more critical situations (toxic
megacolon, adynamic ileus), the two drugs may well be
administered IV and simultaneously. Supportive measures
include use of probiotics for restoration of normal gut flora
and inhibition of growth of C. difficile.
Prognosis
Recurrences may occur in a proportion of the cases. Oral
cholestyramine, bacitracin, immune globulin, lactobacilli,
Baker’s yeast or instillation of fecal flora may work in such
subjects.

Chapter 29.indd 559 03-02-2016 11:34:41

 560 Prevention Table 29.9:  Low osmolarity ORS vis a vis standard oral
Prevention lies in judicious use of antibiotics plus good rehydration salts
food and personal hygiene, meticulous handwashing and Standard Low osmolarity
proper environmental cleaning. A vaccine is around the Component ORS ORS
corner. Algorithmic approach for antibiotic-associated Contents
diarrhea is shown in Figure 29.5. Sodium chloride 3.5 g 2.6 g
Sodium bicarbonate (citrate)* 2.5 g (2.9 g) 2.9 g
ORAL REHYDRATION THERAPY
Potassium chloride 1.5 g 1.5 g
Oral rehydration means drinking a solution of clean
water, sugar and mineral salts to replace the water and Glucose 20.0 g 13.5 g
salts lost from the body during diarrhea, especially when Osmolarity
accompanied by vomiting, the so-called gastroenteritis. Sodium 90 mOsm 75 mOsm
Studies conducted all over the world, particularly in

rs
Chloride 80 mOsm 65 mOsm
Bangladesh, India and Indonesia, have established the
Citrate 10 mOsm 10 mOsm
value of this revolutionary concept in counteracting
dehydration which is known to be the main cause of death Potassium 80 mOsm 20 mOsm
in acute diarrheal disease, a major public health problem. Glucose 111 mOsm 75 mOsm

he
ORS is now distributed internationally by the Total osmolarity 311 245
UNICEF in packets labeled ORS and also manufactured * Replacement of sodium bicarbonate by trisodium citrate dihydrite
commercially by several pharmaceutical houses for sale (2.9 g) undoubtedly enhances the shelf-life of the ORS but also makes
on prescription. it more expensive. The ORS thus prepared provides 10 mmol/L of
citrate in place of 30 mmol/L of bicarbonate (one mmol citrate =
Indications 3 mmol base).

ot
Section 5  Pediatric Subspecialties

Abbreviation:  ORS, oral rehydration salts.

ORS is beneficial in three stages of diarrheal disease,
namely: 1. Prevention of dehydration if initiated right at the
beginning of an episode of diarrhea.
2. Rehydration of the dehydrated child so that he does
br
not enter the phase of severe dehydration in which IV
fluids may become necessary
3. Maintenance of hydration after severely dehydrated
patient has been rehydrated with IV administration.
ee

Standard Formulation
The standard formulation, recommended by WHO until
recently has an osmolarity of 311 mOsm/L (Table 29.9).

Low Osmolarity ORS

yp

Recently, WHO has done well to introduce a low osmolarity

ORS (Table 29.9) to cut down risk of hypernatremia
which earlier restricted its wide usage in neonates and
infants. This formulation provides a total osmolarity of
245 mOsm/L compared to the standard WHO formulation
Ja

with 311 mOsm/L. It is supposed to lower stool output,

shorten diarrheal duration and reduce vomiting. It may be
given at all ages. IAP has pleaded for easy availability of yet
lower osmolarity oral rehydration salts (224 mOsm/L) for
infants <2 months.

ReSoMal (ORS in severely

Fig. 29.5:  Algorithmic approach for antibiotic-associated diarrhea.
malnourished children)
Oral rehydration salts for severely malnourished children
needs to be special in order to provide high potassium and
low sodium. WHO recommends ReSoMal for this purpose.
Though commercially available, it can be prepared by
diluting standard WHO, ORS in 2 liters of water rather
than one liter and adding 50 g sucrose (in place of 20 g)

Chapter 29.indd 560 03-02-2016 11:34:42

 561

rs
Fig. 29.6:  Oral rehydration salts sachets must bear logo and instructions for use as shown here.

he
and 40 mL of mineral mix which, among other minerals,
provides high content of potassium chloride. This solution
is administered in a dose of 70–100 mL/kg over 12 hours
(Fig. 29.6).

Chapter 29  Pediatric Gastroenterology

Home-made Preparations of ORS
Several studies with home-made preparations as also our
own experience with them have given gratifying results.
How to make ORS at home? The easiest approach is to ot
br
mix one three-finger-pinch (1/2 teaspoonful) of common
salt and two four-finger-scoops (5 teaspoonful) of sugar in
one liter of tap or boiled water. Addition of lemon or orange
juice, coconut water, mashed tomato, papaya or banana
to this solution brings it close to the recommended WHO
ee

formulation. Even if none of these can be procured, it

does not matter. It has been demonstrated that potassium
and bicarbonate may not be essential in the early stages
of dehydration. Also, there is nothing wrong in replacing
sugar or glucose with molasses (gur) (Fig. 29.7).
Substituting a polymeric form of glucose (starch) of the
yp

WHO ORS for the single molecule form results in solution

that may perform better than the standard ORS. Hence Fig. 29.7:  Preparing oral rehydration solution at home.
the designation super ORS. This has led to the concept of
cereal-based oral rehydration therapy (ORT) (Box 29.4),
Advantages of cereal-based oral rehydration
the best studied so far being RWES. RWES consists of Box 29.4 solution
Ja

decanted solution after cooking rice. Salt is added to it. This

zz More palatable
may also be prepared by dissolving 2-finger scoops of rice
zz Provides more energy
powder (boiled rice) in water and boiling for 3 minutes. To zz Reduces stool volume; hence less diarrheal fluid losses
it are added a pinch or two of salt and 1/4th medium size zz Controls/lessens vomiting during treatment
lemon juice. zz Shortens duration of diarrhea
Alternative home-made electrolyte solutions include: zz Ingredients (cereals, starchy vegetables) easily available in
„„ Dal and water solution, carrot juice, tender coconut households
water, Bengal gram kanji, weak tea, fruit juices, banana zz RWES is more palatable. Babies not responding to the standard
„„ Honey-based—one teaspoonful of honey + pinch of ORS may respond to it.
salt + one glass water
„„ Arrowroot kanji + salt with vitamin A, or, at least, linkage of distribution of vitamin
„„ Butter milk + salt + with or without sugar and lemon. A and ORS sachets has been advocated. This may prove an
Since diarrhea and vitamin A deficiency are beginning to effective strategy reducing the morbidity accompanying
be considered as risk factors for each other, fortification of ORS diarrheal dehydration and vitamin A deficiency.

Chapter 29.indd 561 03-02-2016 11:34:42

 562 Administration
Ideally, each motion should be followed by replacement
of as much fluids. Illiterate mothers, however, may not be
able to judge the amount of fluid loss. In such cases, let
them give the child as much ORS as he desires. But, it is
unwise to push the fluids if the child does not accept these
or if vomiting is persisting. Giving ORS in sips often helps
to tide over this difficult situation.
Limitations
„„ A common criticism of standard ORT is that it may
cause hypernatremia, resulting in convulsions,
cerebral hemorrhage and often death. The availability
of low osmolarity ORS has overcome this criticism.
„„ Glucose malabsorption may occur in a small
proportion of cases, thereby worsening the diarrhea
and dehydration.
„„ ORT may not the answer in a proportion of the cases
with severe dehydration leading to shock, anuria and
acidosis. It may also flop in severe vomiting and high
rate of stool loss.
PERSISTENT DIARRHEA
ot
Section 5  Pediatric Subspecialties
Definition
The term, persistent diarrhea, is employed when an
episode of acute diarrhea/gastroenteritis (invariably
infective in etiology) continues beyond 2 weeks period.
br
Invariably, it starts off as an acute infective episode that
stretches beyond 2 weeks in at-risk infants and children.
More than dehydration, these patients suffer from
deteriorating nutritional status.
According to conservative estimates, some 7–25%
ee
children in preschool age group who suffer from acute
gastroenteritis may end up with persistent diarrhea in the
resource-limited countries such as ours. Peak incidence
is around 1 year of age. It contributes considerably
to malnutrition. In subjects under 1 year, mortality is
particularly high. When persistent diarrhea develops
yp
before the age of 3 months, it is often termed as intractable
diarrhea of infancy.
Etiology
Persistent diarrhea is as yet an entity of obscure etiology.
Ja
Identifiable risk factors are listed in Box 29.5.
Clinical Features
Three clinical types are recognized:
1. Subjects with several motions/day, but without any
adverse fallout on nutritional status and growth and
development
2. Subjects with several motions (without dehydration),
and malnutrition and growth retardation
3. Subjects with several motions and dehydration that is
difficult to control by ORS.
In the subjects belonging to the second and third
categories, manifestations include progressive weight loss,
malnutrition, anorexia, malabsorption and secondary
infections.
Chapter 29.indd 562
Box 29.5 Risk factors for persistent diarrhea
zz Age between 6 months and 1 year; after 2 years of age, risk of
persistent diarrhea is reduced
zz LBW and malnutrition; vitamin A deficiency
zz Diarrheal episode with blood and mucus such as caused by
enteropathogenic or aggregative adherent Escherichia coli,
Shigella, Salmonella, Campylobacter jejuni, and rotavirus,
especially in infants <3 months of age
zz Excessive fluid intake, especially carbonated drinks and fruit
juices
zz Artificial feeding
zz Indiscriminate use of ORS, especially with high sugar content
zz Lactose intolerance
zz Systemic infections like septicemia
rs
„„ Irrational antibiotic use, causing bacterial/fungal overgrowth
and persistent diarrhea
zz Milk protein allergy
zz A preceding diarrheal episode in the recent past may make the
child vulnerable to yet another episode that becomes persistent.
he
The factors that contribute to persistent diarrhea in such a
situation include deterioration in nutritional status, damage
to small intestinal mucosa, contamination of animal milk and
osmotic diarrhea
zz Intestinal parasitosis.
Abbreviations:  ORS, oral rehydration salts; LBW, low birth weight.
Diagnosis
It is by and large clinical with support from screening
laboratory tests. The latter must include meticulous stool
microscopy, on at least 6 successive days for ova and cysts.
A stool culture is warranted. An acidic diarrheal stool is an
indication for demonstration of reducing substances in
stools, a highly fatty stool for fat balance studies, persistent
diarrhea with recurrent chest infection for sweat chloride
and persistent diarrhea with skin lesions for serum zinc level.
Treatment
Diet
Dietary manipulation along with rehydration therapy
is the backbone of management of persistent diarrhea.
Breastfeeding must continue. Though diarrhea may
continue despite breastfeeding, infant’s nutrition
remains maintained and he may even gain some weight.
Box 29.6 lists highlights of the three recommended diets
in management of persistent diarerhea.
1. Diet A: In case persistent diarrhea is mild, the infant
on artificial feed (should be given milk mixed with a
cereal (Table 29.10) or curd rather than milk as such.
2. Diet B: In case persistent diarrhea is severe, as
manifested by dehydration, high purge rate (over 7
mg/kg/hour) or very frequent large and watery stools,
total milk elimination in an artificially fed infant is
needed. Table 29.11 lists the composition of an egg-
based milk-free diet for persistent diarrhea.
Breastfeeding, reduced intake of other milk, or its total
withdrawal should be supplemented with enriched
gruels like khichri with oil, lentil with oil, mashed
potato with oil, curd mixed with mashed potatoes or
banana or rice with added sugar.
03-02-2016 11:34:42
 Three recommended diets in persistent Table 29.12:  Chicken-based diet with glucose (diet C) for 563
Box 29.6 diarrhea severe persistent diarrhea with likelihood of lactose and
Diet A (low lactose diet) other disaccharide intolerance
zz Reduced (not totally eliminated) lactose (milk), e.g. milk-rice Ingredients Amount/liter kcal (%) Protein (g%)
gruel, rice-curd, dalia; even milk-banana.
Chicken 100 g 110 26
zz Indication: Initial diet in persistent diarrhea.

Diet B (lactose, i.e. milk-free with reduced starch diet) Glucose 20–40 g 160 –
zz Cereals + glucose for carbohydrates; egg, chicken or commercial Coconut oil 40–50 g 450 –
protein hydrolysate
KCl (15%) 7.5 mL – –
zz No milk at all.

zz Indication: Lactose intolerance/malabsorption. NaHCO3 (7.5%) 20–30 mL – –

Diet C (monosaccharide-based) Total 1000 mL 720 26
zz Only glucose + egg white/chicken, oil

zz Total elimination of disaccharides, i.e. no milk, no cereals

Notes:

rs
zz Indication: Disaccharide intolerance/malabsorption.
zz It is prepared by grinding the precooked boneless chicken stuff in

a mixie. Glucose, oil and some water are added to it and the feed is
Table 29.10:  Composition of an initial milk-rice diet (diet A) brought to a boil. Additional water is added to make a final volume
for persistent diarrhea of 1 liter. Finally, KCl and NaHCO3 are added. To safeguard against
spoilage, it is stored in a refrigerator

he
Ingredient Amount (g)
zz Glucose is initially added in 2% concentration and then built upto
Puffed rice* 12.5 4% by increasing 1% every alternate day. To reduce osmolar load, a
Milk 40.0 mixture of glucose and sugar may be employed
zz Any vegetable oil may be employed in place of coconut oil.
Sugar 2.25
Oil 2.0

Chapter 29  Pediatric Gastroenterology

All disaccharides need to be eliminate. Table 29.12
Water
Egg density
Protein
Carbohydrate
100.0 mL
96 kcal/100 g
10.0%
55.87% ot gives details of a chicken-based diet for such a
persistent diarrhea.
Vitamins and Micronutrients
It is advisable to provide twice the maintenance
br
Lactose 1.73%
Fat 33.9%
requirements of vitamins, and trace elements like iron,
and folate for a minimum of 2–4 weeks. Iron is best started
Amino acid score 1.0%
after diarrhea has controlled. Zinc, 10–20 mg daily for
* Puffed rice is ground and appropriate quantities are mixed with sugar 2 weeks, should be given to all infants and children with
and oil. Boiled water is then added to make a thick gruel. This feed has
ee

persistent diarrhea on dietary manipulation.

a shelf life of around 3 hours.
Vitamin A in a single oral dose (<6 months 50,000 IU,
6–12 months 100,000 IU and 1–3 years 2000,000 IU) should
Table 29.11:  Composition of an egg-based milk-free diet also be given.
for persistent diarrhea
Ingredient Amount (g) Probiotics
yp

Puffed rice 13.5 Probiotics may be helpful in restoring the normal gut flora.
As yet, there is insufficient evidence favoring their routine
Egg* 11.0
use in persistent diarrhea.
Sugar/glucose 3.5
Antimicrobial Therapy
Oil 3.5
Water 100.0 mL
It is indicated in the presence of identifiable enteric
Ja

pathogens such as Shigella or E. coli, when persistent

Egg density 92.2 kcal/100 g
diarrhea is bloody but culture facilities are not available,
Protein 9.5% and when there is evidence of persistent diarrhea being
Carbohydrate 56.9% secondary to a systemic infection like septicemia. In the so-
Fat 33.29% called bacterial overgrowth syndrome, a combination of
Amino acid score 1.0%
oral gentamicin (50 mg/kg/day 4 hourly for 3 days) and oral
cholestyramine (l g 6 hourly for 5 days) may prove useful.
* Egg white is added to the mixture of weighed rice, sugar and oil. Antimotility drugs, kaolin and pectin are best left out.
Boiled water is added to make a thick gruel weighing 100 g.
Wormicidals
3. Diet C: In cases of severe persistent diarrhea that fails Metronidazole is recommended only for amebiasis,
to respond to the dietary management outlined above, giardiasis, or anaerobic infections. Finally, parenteral
intolerance to disaccharides (other than lactose as nutrition (partial or total) may be indicated in very
well) becomes quite likely. Mono or oligosaccharide advanced cases when small bowel mucosa is extensively
carbohydrates diet is well tolerated by these children. denuded, causing intolerance to even small amounts

Chapter 29.indd 563 03-02-2016 11:34:42

 564 of gruel (which moves out in stools) with significant
weight loss. An algorithmic approach to management of
persistent diarrhea is given in Figure 29.8.
Response to Therapy
Criteria for good response include:
„„ Reduction in frequency of diarrheal stools
„„ Improvement in appetite
„„ Improvement in dietary intake
„„ Weight gain.
Diet During Convalescence
During convalescence, most cases need relatively higher
intakes for the catch-up growth.
Prevention
Promotion of breastfeeding and safe weaning practices
together with prompt treatment of acute diarrhea with
ORS or IV fluid therapy and attention to child’s overall
nutrition, during and after the diarrheal episode, should
go a long way in safeguarding against development of

rs
he
ot
Section 5  Pediatric Subspecialties

br
ee
yp
Ja

Fig. 29.8:  Management algorithm for persistent diarrhea.

Chapter 29.indd 564 03-02-2016 11:34:43

 persistent diarrhea. Starvation therapy and exclusion of
lactose from diet for mild transient lactose intolerance
must be avoided, so should the indiscriminate use of ORS
and antimicrobial therapy.
Prognosis
Most children with persistent diarrhea recover following
stepped up dietary manipulation. Survivors are usually left
with moderate to gross malnutrition. Inadequately treated
or untreated persistent diarrhea causes high morbidity
and mortality, particularly in infants. Determinants of
poor outcome include:
„„ Systemic infections
„„ Severe lactose and/or monosaccharide intolerance.
CHRONIC DIARRHEA
Definition
Chronic diarrhea is defined as diarrhea of at least 2 weeks
duration or 3 attacks of diarrhea during the last 3 months,
usually due to obvious malabsorption or an organic or
other cause without obvious malabsorption.
Though cutoff point for both persistent and chronic
diarrhea remains 2 weeks, unlike persistent diarrhea,
significant malabsorption is a prominent feature of chronic
diarrhea. It is a common pediatric problem in tropical
countries and is responsible for considerable ill-health and
morbidity.
ot
br
Evaluation Protocol
Roughly diagnostic evaluation of the child with chronic
diarrhea should be step-by-step (Box 29.7) rather than by
ee
a large number of investigations at a time. The individual
Four phases of evaluation of the child with
Box 29.7 chronic diarrhea/malabsorption
zz Phase I: History and physical examination with special reference
to onset of diarrhea and its relationship with various factors
yp
(excessive carbonated drinks/fruit juices, supplementary milk
feeds, cereals), specific amount of fluids ingested/day, nutritional
status, etc.
„„ Meticulous stool examination (ova and cysts, pH, reducing
substances, fat globules)
„„ Stool culture
Ja
„„ Stool for C. difficile toxin
„„ Blood studies (CBC, ESR, electrolytes, BUN, creatinine).
zz Phase II: Fat balance studies for daily stool fat or steatocrit
„„ D-xylose test
„„ Sweat chloride test
„„ Stool osmolality and electrolytes, phenophthalein, magnesium
sulfate, phosphate
„„ Breath H tests.
2 factors. Note that the common causes occupying the top
zz Phase III: Barium meal/enema to exclude anatomic defects small
intestinal biopsy/colonic biopsy by endoscopic studies
„„ Sigmoidoscopy/colonoscopy.
zz Phase IV: Hormonal studies
„„ Neurotransmittal studies (vasoactive intestinal polypeptide,
gastrin, secretin, 5-hydroxyindoleacetic assays).
Abbreviations:  CBC, complete blood count; ESR, erythrocyte
sedimentation rate; BUN, blood urea nitrogen.
Chapter 29.indd 565
merits of each case and the proper application of 565
knowledge and experience of the attending pediatrician
contribute to deciding the necessary investigations.
Pathophysiologic Mechanisms
Osmotic diarrhea results from presence of malabsorption
of water-soluble nutrients (lactose intolerance) and
excessive intake of carbonated fluids or nonabsorbable
solutes (sorbitol, lactulose, magnesium hydroxide) which
cause an osmotic load in the colon. It shows good response
to simple fasting.
Secretory diarrhea results from activation of intra-
cellular mediators like cyclic adenosine monophosphate
rs
(cholera, heat-labile E.coli, Shigella, Salmonella, C. jejuni,
P. aeruginosa, hormones like vasoactive intestinal pep-
tide, gastrin, secretin, anion surfactants like bile acids and
ricinoleic acid), cyclic guanosine monophosphate (heat
stable E.coli, Y.enterocolitica and intracellular calcium
he
(C. difficile, acetylcholine, serotonin, bradykinin).
Mutation defects in apical membrane (ion) transport
proteins such as in chloride-bicarbonate exchange and
sodium-bile acid transporter result in secretory diarrhea
and FTT at birth.
Chapter 29  Pediatric Gastroenterology
Reduction in anatomic surface area in such
conditions as short bowel syndrome following surgical
resection in necrotizing enterocolitis, volvulitis or
atresia. Alteration in intestinal motility in conditions
such as malnutrition, diabetes mellitus, intestinal
pseudo-obstruction syndromes and scleroderma. Here,
diarrhea is of secretory type.
Etiologic Considerations
A large number of conditions, involving intraluminal
factors, mucosal factors, or both, can cause chronic
diarrhea (Box 29.8). Nevertheless, the scene is dominated
by a few conditions.
„„ Is the child consuming excessive amounts of
carbonated drinks or fruit juices (over 150 mL/kg/
24 hours) and yet has normal growth and height
parameters (nonspecific chronic diarrhea)? The
problem usually resolves following reduction in fluids
(under 90 mL/kg/24 hours).
„„ Is the child having excessive intake of nonabsorbable
nutrients such as sorbitol, Mg (OH)2 or lactulose?
A corrective action often controls the chronic diarrhea.
As a result of extensive studies in North India, it
has become exceedingly clear that etiology of chronic
diarrhea in tropical children is much different from what
is described in the textbooks from the western countries.
Box 29.9 gives the relative incidence of important etiologic
positions.
Chronic Diarrhea/Malabsorption:
A Practical Approach
The following approach is suggested for diagnosis and
management of a child with chronic diarrhea and/or
malabsorption in our set-up.
03-02-2016 11:34:43
 566
Box 29.8 Etiology of chronic diarrhea Box 29.9 Causes of chronic diarrhea in Indian children
Intestinal mucosal causes zz PEM
zz Altered integrity: zz Iron deficiency anemia
„„ Infections/infestations: Viral, bacterial, fungal, parasitic zz Excessive consumption of fluids (carbonated, fruit juices)
„„ Cow’s milk protein allergy/intolerance zz Intestinal parasites (Giardia lamblia, hookworm, roundworm,
„„ Soy protein allergy/intolerance
Entamoeba histolytica, Strongyloides stercoralis, Trichuris trichuria,
„„ Inflammatory bowel disease.
tapeworms)
zz Altered immune function:
zz Intestinal infection (enteropathogens, M.tuberculosis)
„„ HIV/AIDS
zz Celiac disease
„„ Autoimmune enteropathy
zz CF
zz Endemic tropical sprue
zz Altered function:
zz Carbohydrate intolerance
„„ Abetalipoproteinemia
zz Irritable colon syndrome
„„ Acrodermatitis enteropathica
zz Ulcerative colitis
„„ Tropical sprue
Miscellaneous (regional ileitis, anatomic defects, protein-losing

rs
zz
„„ Selective folate deficiency
enteropathy, etc.).
„„ Defects in Cl , HCO , Na /H .
– – + +
3
zz Altered digestive function: Abbreviations:  CF, cystic fibrosis; PEM, protein energy malnutrition.
„„ CF

zz Altered surface area: Is there a family history of chronic diarrhea (CF,

zz

he
„„ Celiac disease CD, hereditary lactose intolerance)?
„„ Malnutrition zz Is there any history of intolerance to an item of food,
„„ Iron deficiency anemia
i.e. wheat, barley, rye, oat (CD) or milk (lactose
„„ Endemic tropical sprue
intolerance)?
„„ Hookworm infestation.
zz Was the child failing to thrive from early infancy
zz Altered secretory function:

„„ Enterotoxin—producing bacteria
or started suffering from growth failure after

ot
Section 5  Pediatric Subspecialties

„„ Vasoactive peptides—secreting tumors. introduction of a solid food? The latter situation is

zz Altered anatomical structures: very much suggestive of CD.
„„ Congenital megacolon zz How is the appetite? It is generally increased in
„„ Partial small bowel obstruction.
CF and in some children suffering from giardiasis.
zz Altered motility:
br
In CD, it is almost always poor. Mothers of celiacs
„„ Malnutrition

„„ Diabetes mellitus
often express surprise ‘as to how children who eat
„„ Intestinal pseudoobstruction
so little can pass such voluminous stools’.
„„ Scleroderma. zz Does the mother feel that the child eats like a glutton
Intestinal intraluminal causes but, despite all that, he has not been growing well?
ee

zz Excessive intake of carbonated drinks This strongly suggests CF. We have encountered
zz Excessive intake of sorbitol, lactulose, magnesium salts
this situation in some children suffering from
zz Carbohydrate malabsorption
symptomatic giardiasis as well.
zz Congenital monosaccharide malabsorption.
zz What do the stools look like? Large, pale, frothy
Pancreatic causes
zz CF
and very foul-smelling stools are highly suggestive
zz Chronic pancreatitis. of steatorrhea. Characteristically white, fatty stools
yp

Bile-related disorders with plenty of undigested material are most often a

zz Chronic cholestasis feature of giardiasis.
zz Bacterial overgrowth
zz Was the persistent diarrhea preceded by an attack
zz Prolonged use of bile acid sequestrants
of acute gastroenteritis? The situation is highly
zz Terminal ileum resection.

Miscellaneous
indicative of secondary lactose intolerance. This
condition is fairly common and the stools in it are
Ja

zz Factitious diarrhea

zz Toddler’s diarrhea watery, profuse, accompanied by excess of flatus

zz Chronic nonspecific diarrhea.
Abbreviations:  HIV, human immunodeficiency virus; AIDS, acquired
immune deficiency syndrome; CF, cystic fibrosis.
„„ A good history—the importance of a carefully taken
history cannot be overemphasized. Most valuable
pointers and clues are likely to be obtained from
answers to the following questions:
zz Did the symptoms appear early in infancy (CF) or
after the first six months of life (CD)?
zz Was there any relationship between onset of
symptoms and introduction of supplementary milk
feeds (lactose intolerance) or cereals (CD)?
and have extremely foul smell. The perianal area
appears raw and red in a large majority of these
children.
„„ Stool microscopy: Microscopic examination of stools
for evidence of parasitic infestations is of definite
value. At least three meticulous stool examinations on
successive days are essential before one rule out the
presence of intestinal infestation.
The presence of numerous large fat globules, after
staining with Sudan-3 or eosin, is indicative of
steatorrhea. However, this is a rough screening test
„„ Daily stool fat: Chemical examination of stools for fat
content is the next important investigation.

Chapter 29.indd 566 03-02-2016 11:34:43

 The child is placed on a diet that provides at least 50g
of fat per day over a period of 6 days. During the last
3 days all the stools passed by the child are collected
and analyzed chemically. The 24-hour fat excretion is
calculated. The mean fat excretion in normal Indian
infants and children is 2.32 ± 0.73 g. A fat excretion
of more than 5 g/24 hours is regarded as indicative
of steatorrhea. Stool fat can also be measured by a
semiquantitative simple, cheap and accurate method,
steatocrit. It is a method of microcentrifugation of
fecal homogenate.
„„ D-xylose test: In older children, D-xylose excretion
in a 5-hour urine sample, after administration of
the pentose in a dose of 1.0 g/kg of BW, dissolved in
water, is estimated. An excretion of <20% indicates
malabsorption. Infants and young children present
difficulties in collection of urine. D-xylose tolerance
test is, therefore, preferred in their case. Here,
D-xylose is administered in the same dose and blood
samples are taken at 0, 30, 60, 90 and 120 minutes by
finger prick. Estimation of the pentose in these small
samples is done by a micromethod. The peak level of
<30 mg% is considered indicative of absorptive defect
of the small bowel. A child with steatorrhea but normal
D-xylose test is said to be suffering from steatorrhea of
ot
br
ee
yp
A B
Ja
C D
Figs 29.9A to D: Peroral jejunal biopsies showing significant villous atrophy in children suffering from celiac disease, protein energy
malnutrition (PEM), iron deficiency and hookworm infestation.
Chapter 29.indd 567
nonentrogenous origin as is the case with CF and, in 567
our experience, with giardiasis also
„„ Endoscopic/peroral jejunal biopsy: In view of the
nonspecific results obtained from this investigation,
its use may be reserved for difficult cases. Only in
a few conditions like intestinal lymphangiectasia,
abetalipoproteinemia, amyloidosis and intestinal
lymphoma is the intestinal histology pathognomonic.
In CD, endemic tropical sprue, protein energy
malnutrition (PEM), iron deficiency anemia and
ancylostomiasis, similar types of villous atrophy occur
and differentiation on the basis of histologic changes is
nearly impossible (Figs 29.9A to D).
rs
„„ Radiology: Barium meal examination, using a non-
flocculable medium may reveal abnormalities like
intestinal dilatation, flocculation, segmentation and
atypical mucosal pattern. These are indicative of
he
malabsorption but fail to differentiate one condition
from another, especially the ones that are responsible
for most of the tropical malabsorption in infants and
children. This investigation is of value in detecting
anatomic defects.
Chapter 29  Pediatric Gastroenterology
„„ Other investigations: Schilling test, sweat chloride
estimation, tryptic activity, lactose tolerance test,
etc. may be performed under special circumstances,
03-02-2016 11:34:43
 568 Usefulness of jejunal biopsy in evaluation of The diagnosis of CF is best confirmed by sweat chloride
Box 29.10 chronic diarrhea/malabsorption estimation (sweat chloride is very high in this condition,
zz Pathognomonic
always above 60 mEq/L) and tryptic activity.
„„ Intestinal lymphangiectasia
A patient with gross steatorrhea, in whom the diagnosis
„„ Abetalipoproteinemia of CF has been excluded, may be put on gluten-free diet.
„„ Amyloidosis If he shows amelioration of symptoms, this regimen is
„„ Intestinal lymphoma
continued and absorptive tests (and jejunal biopsy, if done
„„ Parasites: Giardia lamblia (sometime)

„„ Agammaglobulinemia
earlier) are repeated after a period of 10–12 weeks. If found
ŠŠ Crohn’s disease normal, the patient is challenged with gluten to see if the
ŠŠ Microvillous atrophy intestinal abnormality returns. This is now considered
ŠŠ Tufting enteropathy adequate to confirm the diagnosis of CD. If, on the other
zz Nonspecific hand, 3 months of gluten-free diet fails to benefit, the
„„ Celiac disease
patient’s record is reviewed to find, if he could be a case of
„„ Endemic tropical sprue

rs
„„ Iron deficiency
tropical sprue. A Schilling test is indicated in this situation.
„„ Ancyclostomiasis If it is abnormal, he should be put on folic acid and/or
ŠŠ Cow milk protein intolerance tetracycline therapy. Symptomatic control of diarrhea, as
ŠŠ Severe malnutrition the diagnostic tests are in progress, is desirable.
ŠŠ Radiation enteritis

depending on the individual merits of a case. These,
like jejunal biopsy (Box 29.10) and radiology, need
not to be done in every child suffering from chronic
diarrhea/malabsorption.
Despite the fact that the list of causes responsible for
he
Lastly, it is worthwhile to have a clear idea about the
pattern of chronic diarrhea/malabsorption in a particular
region. This, together with an individualized approach
and an adequate follow-up, solves a vast majority of the
diagnostic problems (Figs 29.10A to D).
Fig. 29.12 presents algorithmic approach to manage-

ot
Section 5  Pediatric Subspecialties

ment of chronic diarrhea in pediatric practice.

malabsorption is rapidly expanding, in practice only a
few of the conditions appear to monopolize the situation. CELIAC DISEASE
In our experience, stool fat signifying mild to moderate
steatorrhea is usually indicative of PEM, IDA or intestinal (Gluten-Induced Enteropathy)
br
parasitic infestation. Gross steatorrhea is generally due to It is one of the most common causes of malabsorption in
CF, CD or tropical sprue. the West. Until recently, it was believed to be practically
ee
yp

A B
Ja

C D
Figs 29.10A to D:  Peroral jejunal biopsies from the patients in Figs 29.9A to D after treatment. Note that the appearances are comparable to
the normal as shown in Fig. 29.11.

Chapter 29.indd 568 03-02-2016 11:34:43


Fig. 29.11:  Peroral jejunal biopsy showing normal histological
appearance.
nonexistent in the oriental population. Since 1960s, it has
emerged as one of the top causes of chronic diarrhea/
malabsorption in wheat-eating population in India as well.
Etiopathogenesis
It is an abnormal response to the gliadin fraction of gluten
present in wheat, barley, rye and oat. Varying degree of
villous atrophy, resulting in absorptive defect, is an essential
pathologic lesion. Without dietary manipulation, the small
intestinal mucosal damage is permanent. Elimination
of gluten from diet, however, leads to disappearance
br
of the changes. Reintroduction of gluten causes their
reappearance. This characteristic feature of CD has earned
it, such descriptive names as gluten-sensitivity and gluten-
induced enteropathy. The so-called transient gluten
ee
yp
Ja
Fig. 29.12:  Algorithmic approach to pediatric chronic diarrhea.
Chapter 29.indd 569
sensitivity that has been reported in several disorders is, 569
therefore, strictly speaking, not to be included under this
heading.
Clinical Features
The disorder generally manifests a few months after the
introduction of gluten-containing foods—often a wheat
preparation in the feeding program. Chronic diarrhea—
with large, pale, highly foul-smelling stools which stick
to the pangrowth failure, anemia and other vitamin
and nutritional deficiencies, abdominal distention,
irritability and anorexia are the usual presenting features
rs
(Figs 29.13A and B).
Diagnosis
In the presence of above mentioned clinical profile, the
diagnosis of CD must be seriously considered.
he
Conventional Approach
To establish existence of malabsorption, daily stool fat
excretion should be biochemically determined. D-xylose test
is another useful diagnostic tool. Histological abnormality
Chapter 29  Pediatric Gastroenterology
ot
of the small intestinal mucosa can be demonstrated
by endoscopic/peroral intestinal biopsy (Table 29.13).
Responses to removal of gluten from diet and, latter, to
gluten challenge are needed to establish the diagnosis.
Two immunoglobulin A (IgA) dependent tests are
currently recommended:
1. Serum IgA against tissue transglutaminase (tTG). It
is an ELISA based test with a very high sensitivity as
well as specificity varying between 90–100%
03-02-2016 11:34:44
 570 ESPGAN modified criteria for diagnosis of
Box 29.11 CD in children
zz Clinical profile in keeping with diagnosis:
„„ Jejunal biopsy in keeping with the diagnosis as such or with

serology.
„„ Unequivocal response to gluten-free diet within 12 weeks of

its introduction.
Abbreviations:  ESPGAN, European Society of Pediatric Gastroentero-
logy and Nutrition; CD, celiac disease.

Treatment
The cornerstone of management is gluten withdrawal
from diet which has to be strictly enforced. Gluten-free diet

rs
(GFD)* latter has got to be a life-long measure. Attention
to good nutrition with supplements of iron and folic acid
is important.
GFD leads to a prompt improvement in appetite,

he
weight gain, and control of chronic diarrhea, etc. Six
months of gluten-free diet should be followed with TTG
estimation for fall in titers to show compliance is adequate.
Repeat biopsies (post-therapy or postgluten challenge)
A B
are no longer recommended.
Figs 29.13A and B: Celiac disease. Note the growth retardation,

ot
Section 5  Pediatric Subspecialties

abdominal protuberance and irritability in this 3-year-old girl who Prognosis

suffered from chronic diarrhea since the age of 7 months with
investigations consistent with celiac disease. Untreated CD carries enhanced risk of:
„„ Lymphoma
„„ Cancers
Table 29.13:  Marsh criteria of histological changes in small
br
intestinal biopsy in celiac disease „„ Autoimmune disorders
„„ Osteoporosis.
Grade Histological picture Significance
1 Normal — CYSTIC FIBROSIS
2 Infiltrative with increased Nonspecific but
(Mucoviscidosis)
ee

intraepithelial lymphocytes compatible with CD

3 Hyperplastic, i.e. grade 1
changes + hyperplastic crypts
4 Hypoplastic (total villous
atrophy + hypoplastic crypts
yp
Characteristic of CD A common disorder in the Western countries, its
occurrence in India has only recently been recognized.
Characteristic of CD
Etiopathogenesis
Cystic fibrosis is a genetic disorder involving the exocrine

Abbreviation:  CD, celiac disease.

glands—not just the pancreas, but the sweat glands as also
2. Serum IgA antiendomysial antibody (EMA). It is the glands in the liver as well. As a rule, intestinal mucosa is
based on immunofluorescence technique, has an normal. Steatorrhea is, therefore, of extraintestinal origin.
equally high sensitivity and specificity. However, it is
expensive and not easily available.
Clinical Features
Ja

Antigliadin antibodies (AGA) and antireticulin
antibodies (ARA) are no longer recommended in view of
their high false positivity. Serology, though a very important
test for the diagnosis of CD, needs to be supported by an
abnormal intestinal biopsy and response to gluten-free
diet. Box 29.11 lists the modified diagnostic criteria for CD
as per the European Society of Pediatric Gastroenterology
and Nutrition (ESPGAN). The major change from the
old criteria is that gluten-challenge (an essential criteria
earlier) is no longer required. Coexistence of CD with CF
is known. Such a situation causes difficulties in arriving at
the exact diagnosis.
Chronic/recurrent diarrhea and recurrent respiratory
infections—especially since early infancy—FTT despite
exceptionally good appetite and multiple nutritional
deficiencies are the common presenting features (Fig.
29.14). Stools are characteristically steatorrheic but may
be loose. An obstinate catarrhal cough or frog in the throat
may be present ever since the first weeks of life. Abdominal
distention, a palpable liver, clubbing, higher incidence
of rectal prolapse and nasal polyps, and pseudotumor
cerebri are the other findings.
A noteworthy observation by the mother may be a line
of salt on the forehead after sweating or ‘the baby tastes

* GFD means not just wheat-free but also barley, rye and oat-free diet. Oat does not contain gluten, but the way it is stored renders it susceptible
to contamination with gluten-containing items.

Chapter 29.indd 570 03-02-2016 11:34:44


Fig. 29.14:  Cystic fibrosis. This 8-month-old baby had recurrent
diarrhea and respiratory infections since birth. His sweat chloride was
256 mEq/L.
salty when kissed’. At times, CF may manifest at birth as
meconium ileus, meconium peritonitis or ileal atresia.
Diagnosis
When clinical picture arouses suspicion, fat balance studies
ot
br
to establish steatorrhea and D-xylose test to establish that
steatorrhea is not enterogenous in origin are indicated.
Poor tryptic activity lends support to the clinical diagnosis.
But, a high sweat chloride* (in no case <60 mEq/L) is a must
to confirm the diagnosis. Sweat chloride test is considered
ee
the gold-standard for diagnosis of CF. Deoxyribonucleic
acid (DNA) testing for CFT mutations is now available.
Fetal screening of CF (F 508) is not feasible. Very
infrequently, CF may coexist with CD, posing difficulties
in arriving at the diagnosis.
yp
Treatment
„„ Every child with proved CF should receive pancreatic
enzymes replacement therapy (PERT). PERT effective-
ness is enhanced when administered in enteric-coated
Ja
microspheres form (mixed with acid foodstuff (say sour
fruit or fruit juice). Its dose is calculated either by weight
of the child or by weight of the fat consumed.
„„ Antibiotics are indicated to control respiratory infections.
„„ Maintenance of nutrition and symptomatic measures
are indeed important.
„„ Gene therapy (DNase), both bovine and human, is
now available for CF.
Complications
These include bronchiectasis, systemic amyloidosis, cor
pulmonale and cirrhosis. One-half of the CF subjects
* Sweat chloride may be high (not as much as in CF) in other conditions such as malnutrition, hypothyroidism, hypoparathyroidism, nephrogenic
diabetes insipidus, adrenal insufficiency, pancreatitis, G6PD deficiency, familial cholestasis, mucopolysaccharidosis, etc.
Chapter 29.indd 571
571
rs
he
Fig. 29.15: Endemic tropical sprue. Note the remarkable growth
retardation in this 9-year-old child with chronic diarrhea and moderate
dimorphic anemia.
Chapter 29  Pediatric Gastroenterology
who reach beyond 20 years, develop CF-related diabetes
(CFRD) due to a combination of insulin deficiency and
resistance.
ENDEMIC TROPICAL SPRUE
Contrary to the time-honored belief that the condition
affects adults only, its occurrence in childhood is being
increasingly recognized now.
A typical case is a grown-up child with chronic diarrhea,
malabsorption, considerable malnutrition and anemia
(Fig. 29.15). Steatorrhea is usually moderate to gross.
Partial or subtotal villous atrophy is present. D-xylose test
shows poor intestinal absorption. Schilling test is almost
always abnormal, indicating that the intestinal mucosal
atrophy and absorptive dysfunction are not limited to the
upper gut but are present in the ileum too. These patients
do not respond to gluten-free diet or to gluten challenge as
is remarkable of CD.
Endemic tropical sprue is considered a sort of folic acid
deficiency. Many patients show encouraging response to
10–20 mg/day of folic acid. A group of patients may need
a prolonged course of tetracyclines, favoring an infective
etiology. Yet, others may have to be given both, folic acid
and tetracyclines.
PROTEIN-LOSING ENTEROPATHY
The term refers to excessive loss of plasma proteins
(predominantly albumin) into the gut.
Etiology
A number of diseases may have associated protein-losing
enteropathy (Box 29.12).
03-02-2016 11:34:44
 572
Box 29.12 Etiology of protein-losing enteropathy
zz Gut
„„ Stomach: Giant hypertrophic gastritis
„„ Small gut: Malabsorption syndrome
„„ Large gut: Dysentery, ulcerative colitis, Hirschsprung disease.
zz Cardiac
„„ CCF, ASD, constrictive pericarditis
zz Miscellaneous
„„ Immunodeficiency.
Abbreviations:  CCF, congestive cardiac failure; ASD, atrial septal
defect.
Clinical Features
Besides the clinical picture of the primary disease, the
patient may have poor weight gain, hypoproteinemic
edema (with or without chylous ascites), anemia
(especially megaloblastic) and vitamin deficiency signs
(especially those of fat-soluble vitamins).
Diagnosis
Plasma albumin is usually below 2.5 g/dL. Nutritional,
hepatic and renal causes of hypoproteinemia need to be
excluded before labeling a case as that of protein-losing
ot
Section 5  Pediatric Subspecialties
enteropathy. For establishing the diagnosis, measurement
of spot stool alpha-1-antitrypsin (unlike albumin it resists
digestion) level is of value.
Treatment
br
Treatment is essentially that of the primary underlying
disorder. If there is gross hypoproteinemia from severe
losses, albumin infusions may be of temporary benefit.
ee
CARBOHYDRATE MALABSORPTION
It may be of two types—(1) disaccharide malabsorption,
and (2) monosaccharide malabsorption.
Disaccharide Malabsorption
It may be primary or secondary:
yp
„„ In primary disease, which is very rare, there is con-
genital deficiency of one or more of the disaccharidase
enzymes (lactase, isomaltase, invertase, maltase) in
the brush border of the small bowel epithelium.
„„ In secondary disease, the enzyme deficiency results
Ja
from such conditions as acute gastro enteritis, PEM,
cow milk protein (CMP) allergy, CF, gluten-induced
enteropathy or drugs like neomycin.
Clinical Features
Watery diarrhea with only little solid matter, acid character
of stool, excoriation of the perianal area and buttocks,
abdominal distention and pain are noticed. The abdominal
cramps are particularly a feature of lactose intolerance in
older children and result from excessive gas production.
Diagnosis
„„ Character of diarrhea and circumstances of its onset.
„„ Low pH of stools (under 6) while the patient is on
modest dietary intake of the offending sugar(s).
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Chapter 29.indd 572
„„ Presence of reducing substances in stools.
„„ Disaccharide (usually lactose) tolerance test.
„„ Breath test involving measurement of H+.
„„ Barium meal—the suspected sugar is added to a
barium meal. Defect in its absorption causes fluid
retention in intestinal lumen, intestinal hurry and
coarsening of the mucosal folds.
„„ Endoscopic/peroral jejunal biopsy for assay of the
enzymes offers the most definitive diagnosis.
In clinical practice, diagnosis is more often confirmed
by response to withdrawal of the offending sugar from the
diet rather than by cumbersome investigations.
rs
Treatment
It is by giving low-disaccharide diet. Soya milk is a good
substitute for milk in case of lactose intolerance. As
the child grows, symptoms often become less severe in
he
congenital deficiency. In acquired one, the phenomenon
is in any case transient and subsides in due course,
particularly with the restriction of the sugar.
Monosaccharide Malabsorption
„„ A rare congenital disorder, it is being increasingly
reported in association with PEM, gastroenteritis,
chronic diarrhea, gluten-induced enteropathy, or
following surgery.
Treatment consists of excluding glucose and galactose
„„
from diet. A period of intravenous feeding is usually
indicated in serious cases.
„„ Reintroduction of the sugars should be cautious.
COW MILK PROTEIN INTOLERANCE
(Cow Milk Protein Hypersensitivity/Allergy)
About 1–2% of infants may have hypersensitivity to cow milk.
Clinical Features
„„ Vomiting, diarrhea (usually watery), colic, rash (infantile
eczema or urticaria), rhinitis, otitis media, chronic
cough with wheeze (just as in bronchial asthma),
anemia and poor weight gain.
„„ Eosinophilia, glucosuria, sucrosuria, lactosuria,
aminoaciduria, renal tubular damage, acidosis and
pulmonary acidosis may occur in some cases.
„„ Smear from rectal mucus shows eosinophils.
Withdrawal of cow milk is followed by disappearance
of the manifestations. Its reintroduction leads to reappear-
ance of the symptoms within 48 hours.
Etiology
Allergy to beta-lactoglobulins appears to be the operative
cause in large majority of the cases. Allergy to casein,
lactalbumin, bovine serum globulin and bovine serum
albumin may also be present. Remember, the disorder is
no longer considered a sort of lactose intolerance due to
deficiency of lactase in the small intestinal mucosa.
03-02-2016 11:34:44
 Treatment
Management consists of omitting cow milk from the
feeding regimen. Soya milk or goat milk may well be a
good substitute. When the infant approaches the age
of 9 months, cow milk may be introduced drop by drop,
increasing the amount everyday until the desired intake is
reached.
Alternatively, if rapid reintroduction is desired, cow
milk may be given under the shield of 10 mg of prednisolone
daily. Once milk is tolerated, prednisolone should be slowly
tapered off to zero dose.
ACRODERMATITIS ENTEROPATHICA
(Brandt Syndrome)
This is a familial disorder with autosomal recessive inherit-
ance and with unique cocktail of clinical manifestations.
Etiology
The cause is zinc deficiency secondary to malabsorption
of zinc.
Clinical Features
The condition, manifesting at the time of weaning, is
characterized by chronic diarrhea (at times, together
with steatorrhea), symmetrical rash or vesiculobullous,
ot
eczematous, dry, scaly or psoriasiform lesions (Fig. 29.16),
paronychia, nail dystrophy, loss of hair (alopecia), stomatitis
br
and glossitis. The skin lesions are most marked over the
mucocutaneous junctions (buttocks, around the anus and
mouth), face (cheeks) and extremities (knees, elbows).
Blepharitis, conjunctivitis and photophobia are the frequent
ee
ocular accompaniments. Superadded Candida albicans
infection may modify the clinical profile. Left untreated, it is
accompanied by FTT.
Differential Diagnosis
Acrodermatitis enteropathica needs to be differentiated
yp
from a similar syndrome resulting from long-term total
parenteral nutrition (TPN) (unsupplemented with zinc)
and in chronic malabsorption, advanced PEM, CF, maple
Ja
Fig. 29.16: Acrodermatitis enteropathica. Note the symmetrical
rash and alopecia in an infant with diarrhea.
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Chapter 29.indd 573
syrup urine disease, organic aciduria, essential fatty acid 573
deficiency, biotinidase deficiency and methylmalonic
acidemia.
Diagnosis
It is by and large clinical. Serum zinc level and alkaline
phosphatase activity are reduced. Small intestinal biopsy
demonstrates Paneth cell inclusions with parakeratosis
and pallor of the upper epidermis.
Treatment
Zinc, 1–2 mg/kg/day (elemental) in divided doses, gives
dramatic response with improvement in diarrhea and
rs
prompt healing of skin lesions. With the availability of
zinc for therapeutic use, diiodohydroxyquin which was
supposed to yield good results but was likely to cause optic
neuritis in infants is no longer employed.
he
INFLAMMATORY BOWEL DISEASE
Definition
Inflammatory bowel disease is defined as a chronic inflam-
matory disease of the gut with overwhelming gastrointesti-
Chapter 29  Pediatric Gastroenterology
nal presentation and some systemic manifestations. Three
types are recognized:
1. Ulcerative colitis: Only colon is involved with
continuous lesions.
2. Crohn’s disease: The whole of gut is involved with
discontinuous lesions with normal intervening
mucosa (skip lesions).
3. Indeterminate colitis: Nonspecific manifestations not
fitting into ulcerative colitis or Crohn’s disease.
Ulcerative Colitis
It is characterized by recurrent bloody diarrhea and inflam-
mation of the colonic mucosa beginning in childhood and
adolescence and showing peak age at 15–25 years.
Etiology
The disease is now believed to be an immunologically
mediated reaction triggered in a genetically vulnerable
host. Identical twins, close family members, patients of
ankylosing spondylitis and Turner syndrome have greater
susceptibility to the disease. Incidence in Jews is 2–4 times
greater than in general population.
Clinical Features
„„ Bloody diarrhea with copious mucus, fecal urgency,
tenesmus and lower abdominal pain, especially just
before defecation, anorexia, weight loss, FTT and
nutritional deficiency and growth retardation.
„„ Occasionally, the onset may be acute with fulminant
bloody diarrhea, high pyrexia and progression to
peritonitis and even perforation.
„„ Abdominal examination reveals distention and tender-
ness, especially along the left side. Bowel sounds are
exaggerated.
„„ Rectal examination may reveal fissures and, at times,
fistulae and abscesses.
03-02-2016 11:34:44
 574 „„ Extraintestinal manifestations (less frequent in „„ Crohn’s disease
pediatric ulcerative colitis) include arthritis, erythema „„ Necrotizing enterocolitis
nodosum, pyoderma gangrenosa, iritis, hepatitis, „„ Intolerance of dietary protein
clubbing, peripheral hypoproteinemic edema, „„ Hemolytic uremic syndrome
phlebitis, hemolytic anemia, etc. „„ Hirschsprung disease, etc.
„„ The disease is characterized by recurrent exacerbations,
Treatment
most subjects remaining asymptomatic and well during
remissions that may stretch over months to years. „„ Diet: It is by and large supportive with special attention
to the nutrition, including supplements of vitamin D
Investigations and calcium to prevent osteoporosis
In addition to detailed history (including family and „„ Drugs: To reduce inflammatory activity, currently
treatment history), clinical examination (including rectal recommended agents are:
examination for tags, fissures and fistula), and such zz 5-aminosalicylic acid (5-ASA)

rs
tests as complete blood picture, serum protein, stool zz Steroids
examination for occult blood, C-reactive protein (CRP), zz Cyclosproine
etc. the following specific investigations should be done: zz 6-MP (mercaptopurine)
„„ Barium enema, less sensitive than colonoscopy, zz Azathioprine
reveals diffuse distal lesion that may extend proximally zz Methotrexate

to involve the whole colon only in later stages of disease
„„ Colonoscopic examination reveals that rectal and distal
colonic mucosa is inflamed, granular and very friable; „„
active bleeding may be there (Fig. 29.17). Ulcers,
unusual in pediatric ulcerative colitis, are diffuse.
„„ Serology—it is positive for perinuclear antineutrophil
he
zz Infliximab (monoclonal antibodies against tumor
necrosis).
Adjuvant therapy: In the wake of some recent
reports, probiotics may be considered as an adjuvant
therapy for added benefit in inducing and maintaining
remission

ot
Section 5  Pediatric Subspecialties

cytoplasmic antibody (p-ANCA). „„ Surgery: Surgical resection of the whole colon cures
It is of value to evaluate the small intestine as well by the disease. Its indications are:
barium meal follow through, computed tomography (CT) zz Acute colitis not responding to conservative measures
enteroclysis or magnetic resonance (MR) enterography zz Poorly controlled hemorrhage
br
for ascertaining extent of disease. Involvement of small zz Intestinal perforation
intestine favors diagnosis of Crohn’s disease. zz Megacolon
zz Intestinal obstruction
Differential Diagnosis
zz Abscess.
It is from:
ee

„„ Chronic intestinal infections such as Campylobacter Complications

jejuni, Yersinia enterocolitica, Edwardsiella tarda,
Aeromonas hydrophila, Plesiomonas shigelloides,
Mycobacterium tuberculosis, E. histolytica, Crypto-
sporidium, Isospora belli and Cytomegalovirus
yp
These include hemorrhage, perforation of colon, megaco-
lon and colonic cancer (3% risk in first decade and 20% in
subsequent years).
Crohn’s Disease

It is also termed as regional ileitis, granulomatous entero-

colitis, it has similar etiology, age incidence and certain
other features as in ulcerative colitis, is characterized by
segmental transmural bowel involvement, distal ileum
and colon being most commonly affected.
Ja

Clinical Features
These include crampy abdominal pain and diarrhea
that may be accompanied in one half of the patients by
pyrexia, malaise, anorexia, growth failure and arthralgia or
arthritis. Chronic perianal lesions like skin tags, fissures,
fistulas and abscesses even in an asymptomatic child
should be considered as early signals of Crohn’s disease.
Extraintestinal manifestations are more frequent in
Crohn’s disease than in ulcerative colitis.
Diagnostic Investigations
„„ Upper gastrointestinal endoscopy with biopsy which
Fig. 29.17: Ulcerative colitis. Colonoscopy showing severe colitis
with denuded mucosa and active bleeding. Such a severe ulcerative reveals an inflammatory lesion with polymorphonu-
colitis is an indication for resection of the colon. clear infiltration and crypt abscesses.
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 „„ Barium contrast roentgenograms reveal segmental 575
Table 29.14:  Distinguishing features of Crohn’s disease
distribution, irregular mucosa or a cobblestone-like and ulcerative colitis
pattern, thickened bowel and enteric fistulae.
Features Crohn disease Ulcerative colitis
„„ Rectal biopsy shows typical noncaseating granuloma
Bloody diarrhea/ Infrequent Common
with transmural inflammation. rectal bleed
„„ Fiberoptic colonoscopy rather than conventional Abdominal pain Common Variable
sigmoidoscopy defines the colonic involvement. The
Abdominal mass Common Absent
so-called skip lesions characterized by ulceration with
Failure to thrive/ Common Variable
normal intervening mucosa spread throughout the gut. growth failure
Treatment Perianal disease Common Infrequent
It is primarily supportive with special emphasis on Rectal involvement Infrequent Invariably present
maintenance of good nutrition and emotional support Stomatitis Common Rare

rs
to the patient and the family. For acute exacerbations, Colonic Variable (present Always present
prednisolone needs to be given for 6 weeks and then involvement in over one-half
tapered gradually over 8–12 weeks period. subjects)
In severe exacerbations, it may be given in conjunction Ileal involvement Common Absent

he
with azathioprine. Sulfasalazine, for colonic Crohn’s Strictures Common Unusual
disease, metronidazole for cases with fistulae and severe Fistulas Common Unusual
perianal problems, methotrexate and cyclosporine for Fissures Common Absent
some severe cases are also recommended. Toxic megacolon Absent Present
Surgical resection is of less value than in ulcerative Cancer risk Enhanced Greatly enhanced

Chapter 29  Pediatric Gastroenterology

colitis. The current recommendation is to resect as little as Histopathology Granuloma Transmural; cryptitis,
possible (scar removal) for improved results.
Prognosis
Prognosis is rather poor. Though incidence of intestinal ot
cancer is much < in ulcerative colitis, 1–2 decades after the
Typical lesions

Definition
Skip lesions
cryp abscesses
Continuous lesions
br
onset of the disease, most subjects with Crohn’s disease Currently, CAP is defined as the abdominal pain that is
develop obstructive problems in relation to the intestinal spread over a period of 3 months or more. Whether it is
lumen, especially in the ileal disease. recurrent with pain-free intervals or occurs every day has
no bearing on the present definition.
Crohn’s Disease Versus Ulcerative Colitis
ee

This definition replaces the Apley’s definition that

Distinguishing features between Crohn’s disease and
ulcerative colitis are listed in Table 29.14.
FUNCTIONAL GASTROINTESTINAL DISORDERS
The term, functional gastrointestinal disorders (FGIDS),
yp
described RAP as abdominal pain that is severe enough to
disturb daily activities, occurring at least three times over
a 3-month period.
Classification/Types

is an umbrella that includes a spectrum of disorders Chronic abdominal pain may be classified into two major
characterized by a combination of symptoms that are categories—1. nonorganic and 2. organic.
chronic or recurrent and are not explained entirely with 1. Nonorganic chronic abdominal pain:
current structural or biochemical investigations. zz It may be functional (psychogenic) or secondary

The use of the term, functional, implies that many of to irritable bowel syndrome (IBS), 3-months colic,
the symptoms may accompany normal development or nonulcer dyspepsia, etc.
Ja

may be a response to otherwise normal internal or external zz In case of functional CAP, the pain is periumbilical,

cues. Earliest description of a FGID was given by Apley nonspecific and inconsistent. There, usually, is
who coined the term recurrent abdominal pain in 1958 a secondary gain pattern (usually skipping the
which was revised by the Rome Pediatric Working Group school) and the child manages to seek the attention
on functional gastrointestinal disorders in 2006. of the parents, may the whole household
zz There is often evidence of parental conflict,

CHRONIC ABDOMINAL PAIN disturbed interpersonal relationship and parent(s)

frequently complaining of abdominal or other
(Recurrent Abdominal Pain) bodily pains.
Some 5–10% of school going children suffer from chronic Box 29.13 lists classical pain pattern in nonorganic
abdominal pain (CAP)—the new semantic for recurrent CAP. Rome II Group defines functional abdominal pain
abdominal pain (RAP). In quite a proportion of them, the syndrome as 12-week of continuous or nearly continuous
etiologic diagnosis remains elusive despite a battery of abdominal pain in a school-going child or adolescent
investigations. with no or occasional relationship with physiological
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 576
Box 29.13
Classical pain pattern in nonorganic chronic Box 29.15 Stepwise investigative protocol for CAP
abdominal pain
zz Level 1: Blood, urine and stool (at least on 3 successive days).
zz Gradual onset Extended investigations include screening for tuberculosis, LFT,
zz Periumbilical pain RFT, S. amylase and lipase, X-ray of abdomen and chest and
zz Paroxysmal with variable severity ultrasonography
zz No or vague relationship with food or defecation zz Level 2: Further investigations should depend on the clues
zz Clustering of pain
obtained from the clinical work-up and/or initial investigations
zz Failure to clearly describe location and nature of pain by the
These include:
child/parents.
„„ GI contrast studies

„„ Upper GI endoscopy is important for confirming GER

events like eating, defecation, and menstrual cycles. Some „„ Colonoscopy.

interference with daily functions may be seen. CAP in this zz Level 3: EEG for abdominal epilepsy, cyclic vomiting syndrome
case should neither be malingering nor fit into any other „„ Specific tests for porphyrias, lead poisoning, food allergy,

lactose tolerance, collagen vascular disorders, motility

rs
known functional GI disorder (functional dyspepsia, IBS,
disorders, etc.
abdominal migraine, aerophagia).
2. Organic recurrent abdominal pain Abbreviations:  LFT, liver function test; RFT, renal function test; S.
zz It may be secondary to conditions in relation with
amylase, serum amylase; GI, gastrointestinal; GER, gastroesophageal
reflux; EEG, electroencephalogram; CAP, chronic abdominal pain.
GIT (gastroesophageal reflux, intestinal parasitosis,

chronic constipation, lactose intolerance, food
allergy or lactose intolerance, Crohn’s disease,
ulcerative colitis, Helicobacter pylori infection,
recurrent intussusception, chronic appendicitis,
inguinal or abdominal wall hernia), gallbladder
(cholelithiasis, choledochal cyst), pancreas
he
on child’s emotional status, interpersonal relationship
with parents, siblings, school teacher and peers, school
performance, etc.
Investigative Work-up
A structured stepwise approach is needed, starting with

ot
Section 5  Pediatric Subspecialties

(recurrent pancreatitis), genitourinary tract, urinary
tract infection, urolithiasis, hydronephrosis), CNS
(abdominal migraine), hemopoietic system (sickle
cell crisis, Henoch-Schönlein purpura)
br
zz The pain invariably is away from the umbilicus,
usually in the dermatone that supplies innervation
to the involved viscera. It tends to be constant and
consistent, localized or diffused
ee
simple investigations and moving on more sophisticated
if the need be (Box 29.15).
Treatment
Management is dictated by the diagnosis. In a proportion
of cases, no specific diagnosis may be forthcoming in
spite of investigations. It is in order to reassure them and
carry deworming effective for the common infestations

zz Rebound tenderness may be present prevalent in the area. Deworming may well be repeated
zz Evidence of the primary disease supports the once in 3 months.
diagnosis of organic RAP. In psychogenic RAP, all efforts must be made to alleviate
Box 29.14 lists classical pain pattern in organic CAP. the child’s as well as parental anxiety and tension—
sometime, if the need be, with assistance from a psychiatrist.
Diagnosis
yp

Clinical Work-up CONSTIPATION

A detailed clinical work-up is mandatory in the evaluation Constipation is a common pediatric problem responsible
of the child with RAP. Information should also be obtained for physical and psychological morbidity and poor quality
of life (QoL).
Classical pain pattern in organic chronic As a normal physiological phenomenon, most
Box 29.14 abdominal pain
Ja

children after infancy (when stool frequency is around 4+/

zz Pain away from umbilicus day) slowly settle to a frequency of a single motion/day by
zz Localized pain 4 years. Some normal children may pass a normal motion
zz Associated fever not daily but every 3–4 days.
zz Associated weight loss
zz Radiating pain Definition
zz Well-defined pain, say stabbing, burning sensation
zz Pain severe enough to awaken the child from sleep It is defined as passage with difficulty of hard, dry stools
zz Tenderness accompanied by considerable discomfort and/or distress
zz Organomegaly to the child. More than duration, it is the troublesome
zz Anemia
zz Urinary symptoms
evacuation that is important.
zz High ESR/CRP As long as the child passes motion at least twice a
zz Arthralgia, rash or purpura. week, the motion is not dry and hard and no difficulty/
Abbreviations:  ESR, erythrocyte sedimentation rate; CRP, C-reactive distress is involved in passing it, it is need not to be labeled
protein. as constipation.
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Chapter 29.indd 576 03-02-2016 11:34:45