Spotters in Pediatrics

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(2) Spotters in Pediatrics. SUBASH/NMC15-1393.

(3) SUBASH/NMC15-1393.

(4) Spotters in Pediatrics Editor-in-Chief Anoop Verma. MD FIAP FIAMS. Swapnil Nursing Home and Research Center Civil Lines Raipur, CG 492001. Chapter Editors Navneet Jain MS. Neurology Sanjay Sharma DM (PGI Chandigarh) Consultant Neurologist Modern Medical Institute, Lalpur, Raipur, CG. Laparoscopy Surgeon Ramkinker Medical Institute Purani Basti, Raipur, CG. Neonatology Ramesh Bhatt MD. Infectious Diseases Ashok Gupta MD FIAP. Associate Professor Dept. of Pediatrics, KMC, Manipal. Associate Professor Pediatrics SMS Medical College, Jaipur. Pediatric Surgery Pulak Parag MS MCh (CMC Vellore). Dermatology Arun Agrawal MD FIAP FIAMS. Pediatric Surgeon Consultant Pediatric Surgeon, Raipur, CG. Chandra Laxmi Hospital Ghaziabad, UP. ®. JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD. New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad Kochi • Kolkata • Lucknow • Mumbai • Nagpur. SUBASH/NMC15-1393.

(5) Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3, EMCA House, 23/23B Ansari Road, Daryaganj New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: +91-11-32558559 Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected] Visit our website: www.jaypeebrothers.com Branches. ❑. 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015 Phones: +91-79-26926233, Rel: +91-79-32988717, Fax: +91-79-26927094 e-mail: [email protected]. ❑. 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001 Phones: +91-80-22285971, +91-80-22382956, +91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected]. ❑. 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089 Fax: +91-44-28193231 e-mail: [email protected]. ❑. 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095 Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929 Fax:+91-40-24758499 e-mail: [email protected]. ❑. No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala Phone: +91-484-4036109, +91-484-2395739, +91-484-2395740 e-mail: [email protected]. ❑. 1-A Indian Mirror Street, Wellington Square Kolkata 700 013 Phones: +91-33-22651926, +91-33-22276404, +91-33-22276415 Rel: +91-33-32901926, Fax: +91-33-22656075 e-mail: [email protected]. ❑. Lekhraj Market III, B-2, Sector-4, Faizabad Road, Indira Nagar Lucknow 226 016 Phones: +91-522-3040553, +91-522-3040554 e-mail: [email protected]. ❑. 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel Mumbai 400012 Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896 Fax: +91-22-24160828 e-mail: [email protected]. ❑. “KAMALPUSHPA” 38, Reshimbag, Opp. Mohota Science College, Umred Road Nagpur 440 009 (MS) Phone: Rel: +91-712-3245220, Fax: +91-712-2704275 e-mail: [email protected]. Spotters in Pediatrics © 2008 Anoop Verma All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the editor and the publisher. This book has been published in good faith that the material provided by contributors is original. Every effort is made to ensure accuracy of material, but the publisher, printer and editor will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi jurisdiction only.. First Edition : 2008 ISBN : 978-81-8448-249-2. Typeset at Printed at. JPBMP typesetting unit Replica Press. SUBASH/NMC15-1393.

(6) To My grandfather late Dr GP Shrivastava, MRCP, DTMH, from whom I imbibed the interest in clinical medicine and zeal to remain updated in officepractice. My father late Dr BBL Verma and mother late Suman Lata Verma from whom I learned to aim high and follow the path of voice within. My wife Rashmi, daughter Swapnil and son Shantanu and my whole family are my energy pillars, and my confidence. SUBASH/NMC15-1393.

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(8) Contributors Agrawal Anju Department of Pediatrics UCMS and GTB Hospital Shahdara, Delhi Agrawal Arun, MD FIAP Chandra Laxmi Hospital Ghaziabad, UP Agrawal Ashwani, DCH Pediatrician and Neonatologist Gudhiari, Raipur, CG Agrawal Sanjay, MD Mungeli, Bilaspur Bansal CP, MD FIAP Pediatrician and Neonatologist Shabda Pratap Nursing Home Gwalior, MP Barua Ankur Assistant Professor Department of Community Medicine Sikkim Manipal Institute of Medical College Gangtok, Sikkim Batra Prerna Ascociate Professor Department Pediatrics Mahatma Gandhi Institute of Medical Sciences Sewagram, Wardha. Budhwani KS, MCh Professor and Head Department of Pediatric Surgery Gandhi Medical College Bhopal, MP Chatterjee Pallabh Consulting Pediatricians Kolkata Chawda Arun Pediatrician Fafdeh, Raipur, CG Faridi MMA Professor Pediatrics Department of Pediatrics UCMS and GTB Hospital Shahdara, Delhi Gupta Ashok Associate Professor Pediatrics SMS Medical College, Jaipur Gupta Vinay, MS Surgeon / Andrologist Bilaspur, CG Gurudatta HS, MD Mahasamund Hariramani Suresh, MD Children Hospital Tilda. Bhatt Ramesh Associate Professor Department of Pediatrics KMC, Manipal. Jain Karuna, MD Laparoscopic and Obstetric Surgeon Raminker Hospital, Purani Basti Raipur, CG. Bopardikar Ranjan Pediatrician Sparsh Children Hospital Bhilai, CG. Jain Navneet, MS Laparoscopy Surgeon Ramkinker Medical Institute Purani Basti, Raipur, CG. Jain Nirved, MCh Plastic and Cosmetic Surgeon Jeevan Memorial Hospital New Shanti Nagar, Raipur, CG Jain Vijay, MD, FIAP Consulting Pediatrician Gaya, Bihar Kalda Sunil, MCh Cosmetic Surgeon Kalda Nursing Home, GE Road Raipur, CG Khanduja MK, MD, DCH Pediatrician Nehru Nagar, Bhilai, CG Khandwal Onkar, MD Assistant Professor Pt JNM Medical College, Raipur Madharia Arun, MS Orthopedic Surgeon Gayatri Hospital, Raipur, CG Madharia Nalini, MD Laparoscopic and Obstetric Surgeon Aashirvad Hospital, Sunder Nagar Raipur, CG Mandric SK Pediatrician Science College Colony, Raipur CG Menghani Jagdish, MD Katora Talab, Raipur, CG Menghani Kavita, MD Telebandha, Raipur, CG Mukhopadhyay Sagori JK Lon Hospital, SMS Medical Hospital, Jaipur. SUBASH/NMC15-1393.

(9) viii Nebhani Shyam, DCH Nebhani Nursing Home Ravigram, Raipur, CG Pal Ranbir Associate Professor Department of Community Medicine, Sikkim Manipal Institute of Medical College Gangtok, Sikkim Pardal Rakesh, MD Chief Medical Officer Mahasamund Patel GS, MD Professor Pediatrics Medical College, Indore, MP Patel Jyotish, MD Sickle Cell Anemia Foundation Bardoli, District–Surat, India Phulzhele NL Head, Department of Pediatrics Medical College, Raipur Pulak Parag, MS, MCH Pediatric Surgeon Consultant Pediatric Surgeon Raipur, CG Purohit Alok, MD Professor and Unit Head JK Lon Hospital, Sawai Man Singh (SMS) Hospital, Jaipur. Spotters in Pediatrics Rathi ML, MD, DCH Senior Pediatrician Budhapara, Raipur, CG. Sharma Shayam Resident Medical Officer Swapnil Nursing Home, Raipur. Saha Abhijeet Senior Lecturer in Pediatrics Government Medical College and Hospital, Chandigarh 160030. Shukla Lalit, MS Shree Netralaya, Ashirwad Towers Raipur, CG. Sahai KM, MD KMS Hospital Jaipur, Rajasthan Saify Rubina, MD Pediatrician and Neonatologist Indrawati Colony, Raipur, CG Sarbhai KP, MD Sarbhai Nursing Home Sunder Nagar, Raipur, CG Savant AP Senior Pediatrician District Hospital, Durg, CG Sethi Sidhartha Kumar Department of Pediatrics UCMS and GTB Hospital Shahdara, Delhi Shadangi Lokesh, MD District Hospital, Raigarh, CG Sharma Sanjay, DM Consultant Neurologist Modern Medical Institute Lalpur, Raipur, CG. Sur DK Senior Pediatrician Bayron Bazar, Raipur, CG Tamer SK, DM HOD Department of Neurology, JNM Institute, Bhilai, CG Thakur Vasudev, MD Bhatapara Uttamani Naresh, MD, DNB Pediatrician and Neonatologist Civil Lines, Raipur, CG Verma Amar MD, DCH, PhD, WHO Fellow. Associate Professor RIMS, Ranchi, Jharkhand Yadu Shirish, MS Consulting Surgeon Modern Medical Institute, Lalpur Raipur, CG. SUBASH/NMC15-1393.

(10) Foreword Dear Dr Anoop Verma, I congratulate you for an excellent work and here is my comment. “I am aware of your zest to capture images of patients including videos that I have myself witnessed during your academic presentations at various conferences. I am sure one stores what one sees more than what one just reads and that is how we learn better from patients rather than mere textbooks. This compilation of large number of images would certainly help all of us to memorise those conditions that in turn would help us to spot them quickly. I appreciate your efforts to disseminate knowledge in unique way. I strongly recommend for each one of us to make best use of such a ready reckoner. Short relevant text accompanying the images is a bonus.” With regards and best of wishes. Prof. YK Amdekar (Retd) Pediatrics Dept., JJ Hospital, Mumbai Hon. Prof of Pediatrics, Jaslok Hospital, Mumbai. SUBASH/NMC15-1393.

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(12) Foreword Childhood illnesses constitute as major public health problem in many developing countries including India. There are innumerable emerging and re-emerging diseases, genetic and metabolic disorders and rare syndromes, which are extremely difficult to diagnose. A large number of these diseases especially infectious if diagnosed early can save the lives of these babies. Genetic disorders always remain an enigma and diagnostic dilemma to majority of clinicians. There are innumerable dermatological conditions in children, which baffles the clinician. Normal physiological conditions in the newborn are often regarded as pathological and cause panics in the minds of the parents and some physicians. It is, therefore, important to differentiate normal from abnormal conditions in the newborn. I earnestly appreciate the sincere effort being done by Dr Anoop Verma in putting together excellent photographs of high quality in the book “Spotters in Pediatrics” which would prove to be a useful readymade armamentarium in the hands of Pediatricians and Physicians. I have known Dr Verma as one of the most dynamic and hardworking pediatrician in the country. He has excellent organizational capacity and in a short period of time attained various important positions in Indian Academy of Pediatrics in both State and at National level. This book will be an extremely useful guidebook for all clinicians. The book contains very useful chapters of infectious diseases, neonatology, genetic and metabolic disorders, nephrology, rare syndromes and dermatological conditions in children. By bringing out this important book, Dr Verma has made significant contribution in the field of Pediatrics bridging the gap of a near famine of relevant topics in this field. I am sure, the book will find a place in the desktop of many clinicians in the country. I wish Dr Anoop Verma all success in his further effort in this direction.. AK Dutta Vice-Principal, Director Professor and HOD, Pediatrics Kalawati Saran Children’s Hospital Lady Hardinge Medical College New Delhi. SUBASH/NMC15-1393.

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(14) Foreword It is a matter of great privilege and pride for me to learn about the launching of the publication Spotters in Pediatrics by Dr Anoop Verma, ex-National Vice-President of IAP. The field of pediatrics has tremendously expanded in the last decade with expertise in various sub-specialties. In addition the recent advances in the field of perinatology, newborn care, molecular biology, drug therapy, genetics and emerging-reemerging infection have added new dimensions in the understanding the childhood problems for the practicing pediatrician. Thus, it has become necessary for the medical professional to update himself with the recent know-how in the field of newborn and childhood diseases from the diagnostic and management point of view. This book is an excellent collection of clinical photographs of common to rare pediatric diseases along with short text for ready reference. It will definitely prove to be a guiding source of knowledge for the busy practicing pediatrician and will serve as ready reckoner. I would like to congratulate Dr Anoop Verma for this innovative academic venture. With personal regards and best wishes. Uday Bodhankar Deputy Secretary General CAMHADD UK International Council Member ASPR Japan Chairman ICMCH and INSPCAN India Hon. Prof. of Pediatrics – IGMC Nagpur Past President IAP / ISTP / SCM – IPA Ramdaspeth, Nagpur 440012 MS, INDIA Ph: (R) 0091- 712- 2425020 / 2445554 (H) 0091 -712- 2459090 / 2422505 FAX : 0091- 712- 2428145 / 2421017 Email : [email protected]. SUBASH/NMC15-1393.

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(16) Foreword One of the essential requirements of scientific progress and research is correct documentation of facts. In western countries scientific data and observation were meticulously recorded and stored. Out of 2.1 billion children below first year of life, the 3/4th are in developing countries, have very high under-five mortality. Pediatrician in India has contributed a lot in reducing infant mortality and in various childhood illnesses. Contributions of Indians in world literature are still below expectation. “Spotters in Pediatrics” by Dr Anoop Verma will fill this gap to great extent. Dr Anoop Verma is very hard working and sincere pediatrician with a habit of recording observations, which has given rise to this monograph for which he deserves great compliments. Spotters in Pediatrics should find its place in bookshelf of practicing pediatricians, graduates in pediatrics and general practitioners. It should stimulate them for good record and for bringing more books like this in future.. Padmashree AT Dabke MD PhD Dean, Professor and Head (Rtd) Department of Pediatrics Pt JNM Medical College, Raipur. SUBASH/NMC15-1393.

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(18) Preface Pediatrics is a fascinating branch, not because we deal with innocent patients but because we draw conclusions from what parents say and what we assess in examination of patient. It is more or less a role of detective. To become a good detective it is not only to read the text thoroughly but also to memorise and search the abnormalities. “A picture is worth a thousand words, and a video is worth a thousand pictures. I cannot define an elephant unless I have seen one.” A glimpse of clinical condition is sufficient to repercuss your brain later, when you come across similar condition in future. The art of making diagnosis by gestalt is not inherited; it needs repeated practice mixed with interest in it. The more you see a condition, the more you go through the text, less is the chance, the condition is escaped your recognition. Experience is not one day job, it is gradual building of memory of variety of cases you come across over the years. It is an old saying you are never late in medical practice. The journey to this fascinating subject can begin at any point of time, provided you have constant zeal and persistent interest in this subject. In clinical practice we must wear the spectacle of astute clinical observer and behave like assiduous and prolific recorder of observation. The syndromic child is most of the time considered a gift of God and hence, further treatment by parents comes to an end. It is on the part of treating physician to counsel such parents and make them aware of the condition and accordingly encourage future course of disease and its inheritance. There are certain conditions which have strong possibility and probability to recur in future generation, on the contrary, there are conditions which almost occurs once (sporadic mutation).The concept of counseling should spread to all parents of such children. Rarely do we find parents who are concerned of their child’s disease and its course. The usefulness of a clinical atlas in medicine is known since ages. The present shape of “Spotters in Pediatrics” is the result of years of devotion and hard work. With its classified and authoritative format this atlas supplies the answer to question that may arise during examination or consultation, giving advice on symptoms, diagnosis and therapeutic measures. We hope that the detailed but concise information given in this atlas will prove of value to students and experienced practitioners alike.. Anoop Verma. SUBASH/NMC15-1393.

(19) Acknowledgements One’s body may be handsome, wife beautiful, fame excellent and varied, and wealth like unto Mount Meru; but if one’s mind be not attached to the lotus feet of Guru, what thence, what thence, what thence ? Adi Shankara Guruvastakam, Verse 1 In my development as a pediatrician, apart from my destiny, there was huge share of my devoted teachers, who have virtually paved my way to clinical pediatrics. My deep regards and respect to my teachers Late Prof DS Dave, Prof NG Prasan, Padmashree Prof AT Dabke and Prof Ashok Rawat. I have got great encouragement and blessings from stalwarts in pediatrics Prof YK Amdekar, Prof AK Dutta, Prof Uday Bodhankar, Prof HP Singh. From my core of heart I convey my sincere gratitude to them. I convey my thanks to our inspirational National President of IAP 2007 Dr Naveen Thacker, who virtually introduced me to publisher, and given me the initial push. I am indebted to our past National Presidents Dr Raju Shah and Dr Nitin Shah for keeping me on track by their able guidance. My hearty thanks to my chapter editors Sanjay Sharma, Pulak Parag, Navneet Jain, Arun Agrawal, Ashok Gupta and Ramesh Bhatt. Their infectious interest has virtually lessened my workload. To come up with plethora of clinical photographs is not easy task, but due to important contributions from contributors. I convey my deep sense of regards to the contributors of this book. A sense of deep regards to my colleagues at Chhattisgarh and my friends, namely DK Sur, ML Rathi, KP Sarbhai, Vijay Makhija, Ashwani Agrawal, SK Mandrik, KW Deoras, Pradeep Sihare, Rakesh Sahu, Madhu Shree Deshpande, Ashok Mehta and Lokesh Shadangi their powerful support, encouragement and guidance has always lifted my morale. I am indebt to all of them. My due regards to M/s Jaypee Brothers Medical Publishers (P) Ltd., especially Shree Tarun Duneja, General Manager, (Publishing), for his interest and support. Last but not the least, my wonderful colleague and friend Shyam Sharma, who has kept me free to complete this life time work. Lastly, I am overwhelmed to convey my gratitude to my whole family Sudhir, Nalini, Manoj, Aarti, Soumiya, Anuj and Siddhi for creating encouraging milieu favorable to this work.. SUBASH/NMC15-1393.

(20) Contents CHAPTER 1 INFECTIOUS DISEASES ------------------------------------------------------ (1–14) Measles ---------------------------------------------------------------------------------------------------- 1 Mumps ----------------------------------------------------------------------------------------------------- 3 Chickenpox ----------------------------------------------------------------------------------------------- 4 Molluscum contagiosum -------------------------------------------------------------------------------- 7 Warts (Verrucae) ----------------------------------------------------------------------------------------- 7 Tubercular lymphadenopathy --------------------------------------------------------------------------- 8 Scrofuloderma -------------------------------------------------------------------------------------------- 9 Lupus vulgaris -------------------------------------------------------------------------------------------- 9 Tetanus ----------------------------------------------------------------------------------------------------- 9 Tetanus neonatorum ----------------------------------------------------------------------------------- 10 Kawasaki disease ----------------------------------------------------------------------------------------11 Hydatid disease ------------------------------------------------------------------------------------------11 Ascaris lumbricoides ---------------------------------------------------------------------------------- 12 Herpes zoster ------------------------------------------------------------------------------------------- 13 CHAPTER 2 DERMATOLOGY --------------------------------------------------------------- (15–44) Atopic dermatitis --------------------------------------------------------------------------------------- 15 Alopecia ------------------------------------------------------------------------------------------------- 16 Stevens-Johnson syndrome --------------------------------------------------------------------------- 18 Toxic epidermal necrolysis --------------------------------------------------------------------------- 20 Henoch-Schönlein purpura --------------------------------------------------------------------------- 20 Seborrheic dermatitis ---------------------------------------------------------------------------------- 22 Hemangioma and vascular malformation ----------------------------------------------------------- 23 Cutis marmorata telangiectatica congenita --------------------------------------------------------- 25 Nevus of Ota -------------------------------------------------------------------------------------------- 25 Epidermolysis bullosa --------------------------------------------------------------------------------- 26 Acrodermatitis enteropathica ------------------------------------------------------------------------- 27 Scabies --------------------------------------------------------------------------------------------------- 28 Head lice ------------------------------------------------------------------------------------------------ 30 Psoriasis ------------------------------------------------------------------------------------------------- 31 Collodion baby ----------------------------------------------------------------------------------------- 32 Harlequin fetus ----------------------------------------------------------------------------------------- 33 Ichthyosis vulgaris ------------------------------------------------------------------------------------- 34 Cutis laxa ------------------------------------------------------------------------------------------------ 35 Scleroderma --------------------------------------------------------------------------------------------- 36 Tinea corporis ------------------------------------------------------------------------------------------- 37 Urticaria ------------------------------------------------------------------------------------------------ `38 Dermatographism -------------------------------------------------------------------------------------- 39 Dermatofibroma ---------------------------------------------------------------------------------------- 40. SUBASH/NMC15-1393.

(21) xx. Spotters in Pediatrics Congenital melanocytic nevus -----------------------------------------------------------------------Juvenile xanthogranuloma ---------------------------------------------------------------------------Ectodermal dysplasia ---------------------------------------------------------------------------------Hypomelanosis of Ito ----------------------------------------------------------------------------------. 40 42 42 43. CHAPTER 3 NEONATOLOGY ----------------------------------------------------------- (45–70) Erythema toxicum -------------------------------------------------------------------------------------- 45 Mongolian spot ----------------------------------------------------------------------------------------- 46 Salmon patch ------------------------------------------------------------------------------------------- 46 Milia ----------------------------------------------------------------------------------------------------- 47 Junctional nevus ---------------------------------------------------------------------------------------- 47 Cutis marmorata ---------------------------------------------------------------------------------------- 48 Cephalohematoma ------------------------------------------------------------------------------------- 48 Mastitis neonatorum ----------------------------------------------------------------------------------- 50 Supernumerary nipples -------------------------------------------------------------------------------- 51 Neonatal teeth ------------------------------------------------------------------------------------------ 51 Neonatal hymenal tags -------------------------------------------------------------------------------- 51 Neonatal vaginal bleed -------------------------------------------------------------------------------- 51 Sternocleidomastoid tumor --------------------------------------------------------------------------- 52 Milia crystalline ---------------------------------------------------------------------------------------- 52 Miliaria rubra ------------------------------------------------------------------------------------------- 53 Acne neonatorum -------------------------------------------------------------------------------------- 53 Bullous impetigo --------------------------------------------------------------------------------------- 54 Baby of diabetic mother ------------------------------------------------------------------------------- 54 Beckwith-Wiedeman syndrome ---------------------------------------------------------------------- 56 Asymmetric crying facies ----------------------------------------------------------------------------- 57 Amniotic band ------------------------------------------------------------------------------------------ 58 Congenital syphilis ------------------------------------------------------------------------------------- 60 Oral thrush ---------------------------------------------------------------------------------------------- 60 Single umbilical artery -------------------------------------------------------------------------------- 60 Birth trauma --------------------------------------------------------------------------------------------- 62 Erb-Duchenne palsy ----------------------------------------------------------------------------------- 63 Hemorrhagic disease of newborn -------------------------------------------------------------------- 64 Twin to twin transfusion------------------------------------------------------------------------------- 65 Nonimmune hydrops ---------------------------------------------------------------------------------- 66 Epignathus ---------------------------------------------------------------------------------------------- 67 Sacrococcygeal teratoma ------------------------------------------------------------------------------ 68 Ophthalmia neonatorum ------------------------------------------------------------------------------- 68 Ear abnormality ---------------------------------------------------------------------------------------- 69 CHAPTER 4 ENDOCRINOLOGY ------------------------------------------------------------ (71–80) Gynecomastia ------------------------------------------------------------------------------------------- 71 Idiopathic precocious puberty ------------------------------------------------------------------------ 72 Cushing’s syndrome ----------------------------------------------------------------------------------- 73 Congenital hypothyroidism --------------------------------------------------------------------------- 74 Micropenis ---------------------------------------------------------------------------------------------- 77 Ambiguous genitalis ----------------------------------------------------------------------------------- 78. SUBASH/NMC15-1393.

(22) Contents. xxi. CHAPTER 5 PEDIATRIC SURGERY ------------------------------------------------------ (81–136) Abscess -------------------------------------------------------------------------------------------------- 81 Thyroglossal duct cyst --------------------------------------------------------------------------------- 82 Dermoid cyst -------------------------------------------------------------------------------------------- 83 Cystic hygroma ----------------------------------------------------------------------------------------- 84 Preauricular sinus -------------------------------------------------------------------------------------- 85 Cleft lip and cleft palate ------------------------------------------------------------------------------- 87 Inguinal hernia ------------------------------------------------------------------------------------------ 88 Umbilical hernia ---------------------------------------------------------------------------------------- 89 Lumbar hernia ------------------------------------------------------------------------------------------ 90 Omphalocele -------------------------------------------------------------------------------------------- 91 Gastroschisis -------------------------------------------------------------------------------------------- 92 Achalasia cardia ---------------------------------------------------------------------------------------- 94 Infantile hypertrophic pyloric stenosis -------------------------------------------------------------- 95 Duodenal atresia and stenosis ------------------------------------------------------------------------ 97 Disorders of rotation and fixation of intestine ------------------------------------------------------ 99 Pneumoperitoneum in newborn --------------------------------------------------------------------- 102 Intussusception ---------------------------------------------------------------------------------------- 104 Hirschsprung’s disease ------------------------------------------------------------------------------- 105 Anorectal malformations ----------------------------------------------------------------------------- 108 Rectal prolapse ---------------------------------------------------------------------------------------- 110 Congenital diaphragmatic hernia -------------------------------------------------------------------- 111 Eventration of diaphragm ---------------------------------------------------------------------------- 114 Phimosis ------------------------------------------------------------------------------------------------ 115 Paraphimosis ------------------------------------------------------------------------------------------- 116 Labial adhesion ---------------------------------------------------------------------------------------- 116 Hair-tourniquet syndrome ---------------------------------------------------------------------------- 117 Vesicoureteral reflux ---------------------------------------------------------------------------------- 119 Posterior urethral valve ------------------------------------------------------------------------------- 121 Bladder exstrophy—epispadias --------------------------------------------------------------------- 123 Rhabdomyosarcoma ---------------------------------------------------------------------------------- 125 Conjoint twins ----------------------------------------------------------------------------------------- 128 Empyema thoracis ------------------------------------------------------------------------------------- 132 CHAPTER 6 BONE DISORDERS ---------------------------------------------------------- (137–149) Rickets -------------------------------------------------------------------------------------------------- 137 Scurvy -------------------------------------------------------------------------------------------------- 139 Osteogenesis imperfecta ------------------------------------------------------------------------------ 141 Congenital club foot ---------------------------------------------------------------------------------- 143 Digital abnormalities ---------------------------------------------------------------------------------- 144 Polydactyly --------------------------------------------------------------------------------------------- 144 Syndactyly --------------------------------------------------------------------------------------------- 145 Brachydactyly ----------------------------------------------------------------------------------------- 145 Ectrodactyly (Lobster-Claw defect) ---------------------------------------------------------------- 146 Multiple cartilaginous exostosis --------------------------------------------------------------------- 147 Greenstick fracture ------------------------------------------------------------------------------------ 147 Congenital scoliosis ----------------------------------------------------------------------------------- 148. SUBASH/NMC15-1393.

(23) xxii. Spotters in Pediatrics. CHAPTER 7 NEUROLOGY ----------------------------------------------------------------- (150–178) Neurofibromatosis ------------------------------------------------------------------------------------ 151 Tuberous sclerosis ------------------------------------------------------------------------------------- 153 Sturge-Weber syndrome ------------------------------------------------------------------------------ 155 Ataxia telangiectasia ---------------------------------------------------------------------------------- 156 Parry-Romberg syndrome ---------------------------------------------------------------------------- 157 Cutis verticis gyrata ----------------------------------------------------------------------------------- 157 Klippel-Trenaunay-Weber syndrome --------------------------------------------------------------- 158 Waardenburg syndrome ------------------------------------------------------------------------------ 159 Neurocysticercosis ------------------------------------------------------------------------------------ 159 Bells palsy ---------------------------------------------------------------------------------------------- 161 Marcus Gunn phenomenon -------------------------------------------------------------------------- 162 Myasthenia gravis ------------------------------------------------------------------------------------- 163 Rett’s syndrome --------------------------------------------------------------------------------------- 164 Angelman syndrome ---------------------------------------------------------------------------------- 166 Duchenne muscular dystrophy ---------------------------------------------------------------------- 167 Neural tube defect ------------------------------------------------------------------------------------- 168 Spina bifida -------------------------------------------------------------------------------------------- 168 Sincipital meningoencephalocele ------------------------------------------------------------------- 170 Anencephaly ------------------------------------------------------------------------------------------- 171 Iniencephaly ------------------------------------------------------------------------------------------- 172 Microcephaly ------------------------------------------------------------------------------------------ 172 Agenesis of corpus callosum ------------------------------------------------------------------------ 173 Lissencephaly ------------------------------------------------------------------------------------------ 174 Joubert syndrome ------------------------------------------------------------------------------------- 175 Large head (macrocephaly) -------------------------------------------------------------------------- 176 Phenytoin-induced gingival overgrowth ----------------------------------------------------------- 177 Drug induced dystonia ------------------------------------------------------------------------------- 177 CHAPTER 8 GENETIC ----------------------------------------------------------------------- (179–219) Down syndrome --------------------------------------------------------------------------------------- 179 Edward’s syndrome ----------------------------------------------------------------------------------- 181 Patau’s syndrome -------------------------------------------------------------------------------------- 182 Saldino-Noonan syndrome --------------------------------------------------------------------------- 183 Majewski dysplasia ----------------------------------------------------------------------------------- 184 Thanatophoric dysplasia ----------------------------------------------------------------------------- 185 Achondrogenesis -------------------------------------------------------------------------------------- 186 Asphyxiating thoracic dysplasia -------------------------------------------------------------------- 188 Achondroplasia ---------------------------------------------------------------------------------------- 189 Turner’s syndrome ------------------------------------------------------------------------------------ 191 Noonan’s syndrome ----------------------------------------------------------------------------------- 193 Marphan’s syndrome --------------------------------------------------------------------------------- 194 Robin anomalad --------------------------------------------------------------------------------------- 195 Albinism ------------------------------------------------------------------------------------------------ 196 Hurler’s syndrome ------------------------------------------------------------------------------------ 197 Morquio’s syndrome ---------------------------------------------------------------------------------- 198. SUBASH/NMC15-1393.

(24) Contents. xxiii. Progeria ------------------------------------------------------------------------------------------------- 199 Goldenhar syndrome ---------------------------------------------------------------------------------- 200 Meckel-Gruber syndrome ---------------------------------------------------------------------------- 201 Charge syndrome -------------------------------------------------------------------------------------- 202 Apert’s syndrome ------------------------------------------------------------------------------------- 203 Disorganization-like syndrome ---------------------------------------------------------------------- 204 Kabuki make-up syndrome -------------------------------------------------------------------------- 205 Lesch-Nyhan syndrome ------------------------------------------------------------------------------ 205 Poland sequence --------------------------------------------------------------------------------------- 206 Osteopetrosis ------------------------------------------------------------------------------------------- 207 Potter syndrome --------------------------------------------------------------------------------------- 207 Fibular hemimelia ------------------------------------------------------------------------------------- 208 Proboscis lateralis ------------------------------------------------------------------------------------- 208 Bardet-Biedl syndrome ------------------------------------------------------------------------------- 209 Vater syndrome ---------------------------------------------------------------------------------------- 210 Blepharophimosis syndrome ------------------------------------------------------------------------ 211 Milroy-Hereditary lymphedema --------------------------------------------------------------------- 211 Macrodystrophia lipomatosa ------------------------------------------------------------------------ 212 MRKH syndrome ------------------------------------------------------------------------------------- 212 Genetic counseling ------------------------------------------------------------------------------------ 215 CHAPTER 9 MISCELLANEOUS CONDITIONS -------------------------------------- (220–240) Tetralogy of Fallot ------------------------------------------------------------------------------------ 220 Congenital ptosis -------------------------------------------------------------------------------------- 223 Congenital cataract ------------------------------------------------------------------------------------ 223 Periorbital cellulitis ----------------------------------------------------------------------------------- 223 Rhinosporidiosis--------------------------------------------------------------------------------------- 224 Vitamin A deficiency --------------------------------------------------------------------------------- 225 Geographic tongue ------------------------------------------------------------------------------------ 226 Fissured tongue ---------------------------------------------------------------------------------------- 226 Foreign body nose ------------------------------------------------------------------------------------ 227 Ingested foreign body -------------------------------------------------------------------------------- 227 Foreign body aspiration ------------------------------------------------------------------------------ 228 Palatal perforation ------------------------------------------------------------------------------------- 229 Extravasation injury ---------------------------------------------------------------------------------- 230 Intraosseous transfusion ------------------------------------------------------------------------------ 233 Sickle cell disease ------------------------------------------------------------------------------------- 234 Index ---------------------------------------------------------------------------------------------------- 241. SUBASH/NMC15-1393.

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(26) Chapter. 1. Infectious Diseases. MEASLES (Figs 1.1 to 1.3) DEFINITION  Measles (derived from Latin misellus meaning ‘miserable’) is a highly contagious viral disease sometime called as rubeola (Latin rubeolus = reddish) or morbilli (Latin morbus = disease). It is caused by an RNA virus called as paramyxovirus.  Human is the only known natural host for the measles virus. There is no natural animal reservoir of the virus, although monkeys can be infected following human contact.1 CLINICAL FEATURE  Its incubation period ranges from 10 to 12 days. It is most infectious during the early prodromal phase of the disease when large quantities of virus are present in nasopharynx secretion and rashes have yet to develop.  It is characterized by (3C), Cough, Coryza and Conjunctivitis. The exanthem of the disease is erythemetous papule (Morbilliform) is a significant feature of eruption. It starts along hairline and proceeds downward. Peak eruption occurs at third day coincides with peak of the fever and constitutional symptom. Rashes resolves by 5th and 8th day, later branny desquamation as brown staining of skin follows.  Enathem: Koplicks spot seen 2 days before and 2 days after the rash seen opposite lower molar. It is white popular dots on an erythematous buccal mucosa looks like ‘Salt grain’ sprinkled on a red background. A transverse line of conjunctival inflammation sharply demarcates along the eyelid margin called as Stibsons line.. SUBASH/NMC15-1393.

(27) 2. Spotters in Pediatrics. Fig. 1.1: A 6-year-old patient Fig. 1.2: Morbilliform rashes presented with cough, coryza, fever, photo-phobia and classical rash. Fig. 1.3: Conjunctivitis with peculiar rash. COMPLICATIONS  Complications of Measles is mainly respiratory, e.g. Otitis media, Pneumonias (Interstitial pneumonia and secondary bacterial pneumonia), Laryngotracheal bronchitis. NeurologicalFebrile seizures, SSPE, Encephalitis. Miscarriages, premature births and congenital malformations have been occasionally associated with measles.2 Other complications are diarrhea, hepatitis, appendicitis, corneal ulceration, and myocarditis.  Subacute Sclerosing Pan Encephalitis (SSPE) is chronic measles encephalitis, having 8 years average age of onset. As a rule past infection of measles at early stage is always there before the age of two years. It presents as personality change and declining school performance. Fundus examination at early stage shows pigmentary changes in the macula. Myoclonic seizures usually develops next, classical EEG changes are evident in the form of periodic burst of spike and wave complexes (approximately 5 to 7 seconds). Later there is rapid neurological deterioration to spasticity, dementia and involuntary movement develops and later dementia supervenes. Anti measles antibody in csf is usually positive. Intraventricular alpha interferon gives some improvement in few cases. Prognosis is usually poor. TREATMENT  Is always supportive. Bed rest, antipyretics and adequate fluid intake are indicated. Isolate from non-immune children until five days after the rash has appeared.  Pulmonary complications are usually due to secondary bacterial infections and has to be treated by antibiotics.  Currently UNICEF and WHO3,4 has recommended vitamin A supplementation to all cases of measles in developing country. Children 6 months-old to 1 year-old: 100,000 IU by mouth as a single dose, repeated the next day and again at 4 weeks. Children 1 year-old or older: 200,000 IU as a single dose, repeated the next day and again at 4 weeks.. SUBASH/NMC15-1393.

(28) Infectious Diseases. 3. PREVENTION5  Measles vaccine is given at age of 9 months, subcutaneously on the upper arm or anterolateral thigh. It can be given even at 6 months in measles outbreaks. This vaccine is a live attenuated virus vaccine, it results in actual infection and multiplication in the body, which mimics actual infection of measles but is usually asymptomatic. Point of precaution while reconstitution of multidose measles vaccine is to maintain strict asepsis has, since there is no antibacterial contents in the vial, some cases of staphylococcal sepsis/toxic shock syndrome is seen.  MMR vaccine is recommended to all children by IAPCOI. For infants given measles vaccine at 9 to 12 months MMR vaccine is given between 15 and 18 months. If measles vaccine was missed altogether then one dose of MMR vaccine is given at or after 12 months.. MUMPS (Figs 1.4 and 1.5) DEFINITION  Mumps (from an old English word meaning ‘Grimace’) or endemic parotitis is an acute infectious disease marked by a painful enlargement of one or both parotid salivary gland. RNA virus of genus paramyxovirus causes it. CLINICAL FEATURE  Clinical feature is characterized by pain and swelling in one or both parotid glands. The gland fill the gap between posterior border of mandible and mastoid and then extends downward and forward. The swelling pushes earlobe upward and outwards and the angle of mandible is no longer visible. The swelling subsides within 3 to 7 days.  The swelling is painful and tender especially elicited by tasting sore liquid such as lemon juice. There is redness and swelling in the opening of stensons duct. In severe cases swelling and edema may approach manubrium and upper chest because of lymphatic obstruction.  It is estimated that 20 to 40 percent of infection results in no symptoms, 40 to 50 percent is nonspecific symptoms and in only 30 to 40 percent in typical acute parotitis.6  Diagnosis is usually clinical. Elevated serum amylase, IgM and IgG Ab against mumps virus are detectable and lastly viral culture. COMPLICATION  Meningo encephalitis is most common, occurs in 5 to 15 percent6 cases. Ten percent of these cases seen over 20 yrs, mortality from this condition accounts to 2 percent.  Orchitis and epididymitis—less commonly seen in preadolescent boys, it accounts to 15-35 percent in adolescent boys. Orchitis follows parotitis after 8 days. It can occur without parotitis. Abrupt onset, fever with chills and rigors, nausea and vomiting, lower abdominal pain. Right testis is often involved. Infertility is rarely seen with bilateral involvement.  Pancreatitis: There is abdominal pain, persistent vomiting and fever. The pain is epigastric and steady, often resulting in the child assuming antalgic position with hips and knees. SUBASH/NMC15-1393.

(29) 4. Spotters in Pediatrics. Fig. 1.4: Enlarge parotid gland. Fig. 1.5: Two brothers suffering from mumps (Beware of spread of infection to unprotected ones). flexed, sitting upright, or lying on the side. The serum amylase is typically elevated for up 4 days. Ultrasonography and CT scan have major role in diagnosis. Other complication includes—oophoritis, myocarditis, arthritis, thyroiditis, deafness.  Recurrent parotitis: It is common to notice recurrent idiopathic enlargement of parotid gland. It is unilateral but can involve other side also. It produces mild pain and usually lasts 2 to 3 weeks. Commonly notice in spring. It starts at age of 6 years and persists for many years. Congenital or autoimmune defects of the duct are presumed to be the cause of recurrence. Each episode last for few days to 2 weeks before spontaneous resolution occurs. TREATMENT  Treatment is always symptomatic: Antipyretics/ acetaminophen/ibuprofen. Bed rest, diet. Local warm or cold pack in the region of swelling. Good oral hygiene.  Isolation of patient till swelling persists. The period of infectivity is 7 days before and 9 days after the onset of parotitis.  Sialogogue agents (vitamin C, lemon chewing gums). It is said it drain the saliva and prevents stagnation and later secondary infection. Sore items induces pain in parotid if it is discomforting to patient it can better avoided.  Antibiotic if ascending infection from mouth is suspected.  Orchitis should be treated by local support and bed rest. Mumps arthritis is treated with NSAID/Corticosteroid.  Pancreatitis: Pain relief, fluid and electrolyte balance to be maintained. Nil orally till serum amylase returns to normal and clinical symptoms has resolved. PREVENTION7 Mumps vaccine is given as component of MMR vaccine given between 15 and 18 months.. CHICKENPOX (Figs 1.6 and 1.7) DEFINITION  Varicella is highly contagious exanthemetous illness caused by varicella zooster virus, a member of herpes virus group.. SUBASH/NMC15-1393.

(30) 5. Infectious Diseases. Fig. 1.6: Neonate with chickenpox. Fig. 1.7: Chickenpox rashes.  Primary infection occurs by circulating virus in the nasopharynx through droplet inoculation. Local replication occurs here leading to viremia and dissemination by circulating mononuclear cells.  It is highly contagious 1 to 2 days before and shortly after onset of rash, but lesion are infectious until they have turned into dried crusts. CLINICAL FEATURES  Its incubation period is 14 to 16 days. The disease is characterized by mild fever and constitutional symptoms in children.  The rashes appear as crops and acquire a characteristic centripetal distribution (more lesion are found on torso than on face and extremities). It rapidly progresses from red macule to vesicle, pustule and crusts within 3 to 4 days. The rash produces intense itching. Lesion is also seen in scalp and mucous membrane. The classical lesion is a vesicle surrounded by erythematous base described as ‘a dew drop on rose petal’.  Varicella is most severe above 13 years.  The vesicles get secondarily infected by beta hemolyticus Streptococcus (GBHS) may result into streptococcal toxic shock syndrome, necrotising fasciitis Figs 1.8A and B, or purpura fulminance.  Apart from other complication acute cerebellar ataxia is common, but is transient and may improve of own.  Immunity following chickenpox is life long and hence, it doesn’t recur, but the virus may persists in the dorsal root ganglia after an acute infection and may get reactivated to cause shingles or herpes zooster. Its involvement is always unilateral dermatomal distribution and stops in the midline.. SUBASH/NMC15-1393.

(31) 6. Spotters in Pediatrics. A. B Figs 1.8A and B: (A) Necrotizing fasciitis (B) Spread of secondary bacterial infection leading to extensive necrotizing fasciitis. TREATMENT  In healthy children varicella is a benign, self-limiting disease with low rate of complication. It usually requires symptomatic treatment.  Analgesics/antipyretics/local soothing agents and antibiotics if secondary infection is suspected. Aspirin should not be used to avoid Reye’s syndrome.  Acyclovir is recommended for normal individual 13 years and above and for immunocompromised host. Acyclovir in dose of 20 mg/kg/dose 4 times a day for 5 days within 24 hours of onset of skin lesion will reduce the severity of the disease.  In uncomplicated varicella, acyclovir is not recommended but on choice can be used to modify the course of disease. Acyclovir doesn’t hampers development of immunity against varicella.  In complicated varicella like encephalitis and viral pneumonia, intravenous acyclovir (10 mg/ kg/dose 8 hrly) must be used. The treatment must be continued for 7 days or till no fresh lesions appears for 48 hours which ever is later. PREVENTION8 Active Immunization  Varicella vaccine (live attenuated).  IAPCOI opines that varicella vaccine is not recommended for universal immunization in India at present. One has to emphasize the benign nature of and rarity of complications with varicella in young children.  It may be offered to children of high socioeconomic status at 12 months to 12 years single dose and for person over 12 years of age, two doses, 4 to 8 weeks apart.  Other indications are children with chronic heart and lung diseases, HIV infection ( but with CD4 counts above 25% of age related norms), in leukemia (but in remission for at least 1 year), household contacts of immunocompromised children.. SUBASH/NMC15-1393.

(32) 7. Infectious Diseases Passive Immoprophylaxis.  Varicella zooster immunoglobulin (VZIG).  Given to susceptible at risk of developing severe varicella and in Immunocompromised children.8 To neonates whose mother experienced onset of varicella 5 days, or less before delivery or within 48 hours after delivery.. MOLLUSCUM CONTAGIOSUM (Fig. 1.9)  This is a skin infection caused by a poxvirus (DNA). It is a common infection in children. It is transmitted by skin contact with an infected person.  The infection presents as small discrete, round, pearly-white growths, with central umblication on the skin. There may be single or multiple growths on the skin. These growths are usually symptomless.  Common sites of infection are the eyelids, neck, trunk and Fig. 1.9: Molluscum contagiosum anogenital area.  Treatment- a) Trichloroacetic acid applications or b) Cryotherapy with liquid nitrogen applications or c) Light electrosurgery, d) Tretinoin gel for small lesion, e) Manual curettage of big lesions.. WARTS (VERRUCAE) (Figs 1.10A and B)  Warts are intraepidermal tumor of skin caused by human papilloma virus (HPV). TYPES  Common wart (Verruca vulgaris): They are discrete flesh colored, single or multiple papules with a rough surface more common in hands but may occur anywhere.  Flat wart (Verruca plana): They are grouped as flat topped, flesh colored or pigmented papules with smooth surface, common on the face.  Anogenital wart (Condylomata accuminata): It is cauliflower like or pink filiform sessile papule with rough surface. It can be acquired from birth canal or acquired from sexual abuse.  Plantar wart.  Periungual wart. TREATMENT  Conservative: No treatment spontaneous regression occurs within 2 years in most cases.  20 percent Podophylline is applied with a toothpick twice daily for 3 days. Podophylline is a plant extract, is a microtubule inhibitor that blocks the cell division. In excess doses it is neurotoxic and produces areflexic coma.. SUBASH/NMC15-1393.

(33) 8. Spotters in Pediatrics. A. B. Figs 1.10A and B: (A) Condylomata in 7 months old child (B) Venereal wart in an adolescent boy.  Use of salicylic acid and lactic acid locally.  Tretinoin gel locally at night.  Oral cimetidine 30 mg/kg/day in three divided doses for 3 months.. TUBERCULAR LYMPHADENOPATHY (Figs 1.11A to C)  Cervical and mediastinal glands are affected most commonly, followed by axillary and inguinal: in 5 percent more than one regional group is involved.  Significant constitutional disturbance and evidence of associated tuberculosis is lacking.  The lymph nodes are painless, initially mobile, and occasionally discharge through the skin causing a “Collar-stud” abscess.  Diagnosis • Ziehl-Neelsen microscopy (positive in only 25% cases). • Histology revealing caseating granuloma. • Culture on Lowenstein-Jensen or Bactec media.. A. B. C. Figs 1.11A to C: Tubercular lymphadenopathy. (A) Large solitary cervical lymph node proved to be tubercular on histopathological examination. (B) X-ray chest of the same patient depicting hilar adenopathy. (C) Scrufuloderma over cervical region. SUBASH/NMC15-1393.

(34) Infectious Diseases. 9.  Treatment and Prevention • Short course chemotherapy (as for Pulmonary TB). • Paradoxical enlargement as a result of hypersensitivity reaction occurs occasionally during or even after completion of therapy. • Surgical excision is sometime necessary. • Prevention as for pulmonary tuberculosis.  Scrufuloderma (Fig. 1.11C) results from enlargement, cold abscess formation, and breakdown of a lymph node, with extention to the overlying skin. Linear or serpiginous with dissecting fistulas and subcutaneous tracts studded with soft nodule may develop. Spontaneous healing may take years and eventually a cord like keloid scar results.. LUPUS VULGARIS (Figs 1.12A and B) It is a rare chronic progressive form of tuberculosis of the skin that develop in an individual with moderate to high degree of tubercular sensitivity induced by previous infection. It is due to direct skin involvement from underlying joint and nodes. A solitary lesion consists of brownish red, soft papule that has an apple-jelly color when examined by diascopy. Chronicity is characteristic, and persistence and progression to plaque over many years are common. Treatment consists of excision of small lesions and antitubercular drugs.. A. B. Figs 1.12A and B: Lupus vulgaris: (A) Lupus vulgaris in a nine-year-old boy. (B) Lupus vulgaris in different parts of the body. Courtesy-Dr Ranbir Pal, Dr Ankur Barua, Dr Pradeep Barua, Sikkim Manipal Institute of Medical Sciences. TETANUS (Figs 1.13A and B)  It is caused by C.tetani, which is a gram positive, spore forming anaerobic bacilli.  Although the incidence of tetanus is reducing due to wide coverage by vaccination, still tetanus neonatorum cases are seen in India due to practice applying mud and cowdung over cord.  From the contaminated wound the toxin tetanoplasmin travels proximally along the nerve to nervous system. It produces tetanus by two mechanisms; by blocking acetylcholine release. SUBASH/NMC15-1393.

(35) 10. Spotters in Pediatrics. A. B Fig. 1.13A and B: (A) Tetanus in grown-up child, note the facial expression during the spasm (B) Spasm in neonate. at myoneural junction and by countering the inhibitory influence on muscle reflex arc. It results in increased activity of lower motor neuron, which produces muscle rigidity and spasm. Once fixed the toxin cannot be neutralized by antitoxin. CLINICAL FEATURES  After an incubation period of 5 to 10 days painful stiff jaw muscle (trismus) appears followed by difficulty in opening the mouth (Lock jaw). Stiffness spreads to neck, back, chest and abdomen. This is rigid stage of the disease.  Intermittent painful contraction of the muscle then starts, the spasmodic stage. The spasm causes grimacing of face (risus sardonicus), and arching of neck and back (opisthotonus). Spasm of respiratory and laryngeal muscle causes respiratory failure. TREATMENT  Ideally should be treated in intensive care.  Human Tetanus Immunoglobulin (TIG) 3000 to 6000 IU IM followed by debridement of the wound. The role of ATS, i.e. antitetanus serum is now less important. It is only given when TIG is not available. It is given 50,000 to 100,000 units half IM and half IV.  Benzyl penicillin IV or IM for 10 days to eradicate the existing foci of infection and stop further toxin production.  Sedation by diazepam, but should be nursed in quit environment. Tracheostomy is indicated in severe cases, to guard against the life threatening laryngeal spasm.  Prevention: Tetanus is prevented by immunizing children by DPT under the age of five and by TT thereafter following the IAP immunizing schedule. TETANUS NEONATORUM (Fig. 1.13B)  Tetanus neonatorum is potentially serious and fatal disease. It usually begins between 3 and 10 days. There is progressive difficulty in sucking, swallowing and excess crying is there. The spasms and stiffness develops sometime opisthotonus posture is seen.  Prevention: It is prevented by immunizing pregnant mothers by two dose of tetanus toxoid between 16 and 36 week of pregnancy and only one dose of TT in the subsequent pregnancy.. SUBASH/NMC15-1393.

(36) Infectious Diseases. 11. KAWASAKI DISEASE (Figs 1.14A to C)  The etiology of this condition is unknown. Search for an infective agent has so far proved unsuccessful. It is claimed to be an abnormal immunological response to variety of microbial agent including streptococci, rickettsiae, viruses and house dust mite. The greatest prevalence is in Japan. It occurs predominantly in children below five years of age.  Clinical Features and Diagnosis • Five main features are recognized: fever for more than 5 days, non-purulent bilateral conjunctivitis, reddened lips and oral mucosa, raw red tongue, erythema of limbs including palms and soles, and edema may be present (later periungual or more generalized desquamation occurs), cervical adenopathy. • Persistent leucocytosis, high erythrocytic sedimentation rate (ESR) or plasma viscosity and thrombocytosis (2nd week onwards) are characteristic laboratory features. • Up to 20 percent of cases develops coronary aneurysm due to coronary arteritis during later phase of illness.  Diagnosis and Treatment • Diagnosis is by clinical and laboratory features. • Other diseases have to be ruled out like scarlet fever, TSS, erythema multiforme, juvenile stills. • IV Gamma globulin and aspirin during the early stage reduces the risk of coronary aneurysm formation. • Prolong follow-up should be advised.  Prognosis: usually benign, about one percent of cases ends fatally, mostly from cardiac complication.. A. B. C. Figs 1.14A to C: Kawasaki disease, note the exfoliation of palms and soles. Photographs by Dr KM Sahai, Jaipur. HYDATID DISEASE (Figs 1.15A and B)  The dog is the definitive host of the small tapeworm Taenia echinococcus that produces large number of eggs in the faeces, contaminating grass and infecting sheep, which are the usual intermediate hosts. The cycle is completed by the ingestion of infected raw sheep offal by dogs. Human becomes accidental intermediate host by close contact with dogs.. SUBASH/NMC15-1393.

(37) 12. A. Spotters in Pediatrics. B Figs 1.15A and B: Hydatid disease. (A) Contrast CT scan showing multiple hydatid cyst. (B) CT chest showing hydatid cyst in lungs.  In humans, the ingested ova develop to form embryo worms, which penetrate the gut wall and invade the tissues. Most of the embryos are destroyed, but one or more may survive and become encysted, usually in the liver.  Usually there is single cyst, but in 30 percent cases there are multiple cysts, usually in single organ. Cysts have been described in every organ but favored sites are liver, lungs, spleen, brain, eyes, heart, bone and genitourinary system.  Hydatid cysts reach a diameter of 1 cm in 5 months and continue to grow as large as 35 cm containing liters and ‘Hydatid sand’.  Clinical features: infection become manifest either because of expansion of cyst or by rupture and release of the cyst contents. Clinically the cyst present as a palpable, slowly growing liver tumor or as partially calcified lesion on chest X-ray. Large cysts in the liver may rupture spontaneously, causing sudden pain, fever allergic rash and eosinophilia. Cysts may calcify gradually with the death of all living worm tissue.  Diagnosis: Usually by radiography, ultrasongraphy and CT scan. Serological tests such as indirect hemogglutination or ELISA can be of value but false negatives occur, particularly in pulmonary disease and in children. The Casoni skin test is less reliable than serological test.  Treatment: Albendazole in three cycles of 28 days each may succeed in killing infective cysts. Hepatic Hydatid cysts are very slow growing and may not require any treatment unless large and causing compression. Operative removal of cyst under pre- and post albendazole treatment regimen is the mainstay of therapy. Calcified cysts should be left alone. Non-surgical aspiration of the cyst is dangerous and should be avoided.. ASCARIS LUMBRICOIDES (Figs 1.16A to C)  Ascaris lumbricoides is an intestinal round worm, and adult worm ranges from 20 to 35 cm long and is as thick as a pencil, although the male tends to be small. They are particularly more prevalent in condition of poor sanitation, with an individual patient harboring up to 1000 worms and mature female producing up to 20,000 eggs daily. The eggs need to. SUBASH/NMC15-1393.

(38) Infectious Diseases. A. B. 13. C. Figs 1.16A to C: Ascaris lumbricoides infestation. (A) Child harboring hundreds of roundworm (B) Adult worm in stool. (C) Abdominal USG revealed multiple horizontal streaks depicting worm body. . .  . mature for 2 to 3 weeks in the soil. The spread is fecal-oral with an incubation period of 4 to 8 weeks. The ingested embryonated eggs hatch in the duodenum and the larvae penetrates through the wall into the blood or lymphatics. They are carried to the liver, heart and thence to pulmonary circulation, here they penetrate through the capillaries into the alveoli. They then ascend the bronchial tree, enter the esophagus and pass down to the small intestine. Here they mature, mate and produces eggs 45 to 60 days after ingestion. The only symptoms in majority are the excretion of worms or eggs in the stool. In the small percentages of cases gastrointestinal or pulmonary symptoms may arise, probably related to the number of eggs. Loffler’s syndrome occurs when the larva migrates through the lungs. Cough, wheezing and breathlessness are the most important common presenting features. Heavy worm load in children may cause abdominal pain and features of intestinal obstruction and failure to thrive. Diagnosis is usually by passage of adult worm in stool, detection of ova in stool. Barium meal examination, occasionally adult worm can be picked up in abdominal ultrasonogram. Treatment consists of use of antihelminth drugs like albendazole, mebendazole, etc. No drug is effective in pulmonary phase of infection.. HERPES ZOSTER (Figs 1.17A and B)  Zoster results from reactivation of latent VZV in a dorsal root or extramedullary cranial nerve ganglion. The virus travels down the sensory nerve to the area of skin supplied by the nerve and produces the typical skin lesion. Zoster in the very young children is probably related to decreased CMI at the time of primary VZV infection.  Clinical features • Prodromal pain: it persists for 2 to 3 days. • Rashes initially red patches with vesicles progressing to pustule which scab and then separate. New lesions continue to occur for 3 to 5 days. Scabbing and separation are usually complete by 2 to 4 weeks. Single dermatome is usually involved, but lesion can be seen extending to adjoining dermatome due to overlapping innervations.. SUBASH/NMC15-1393.

(39) 14. Spotters in Pediatrics. A. B. Figs 1.17A and B: Herpes zoster. (A) Note the red patche with vesicle over anterior and lateral chest. (B) Note the same strip of vesicle on backside, the dermatomal distribution. • •. Dorsolumbar dermatomes are most frequently involved followed by trigeminal, cervical and sacral. Acute phase pain—common during rash evolution..  Complication depend on site of vesicles - ranging from skin infection, ocular, neuralgia, meningoencephalitis, Ramsay Hunt syndrome, cutaneous and visceral dissemination.  Treatment • Antiviral drugs (acyclovir, famiclovir,valaciclovir) shortens the duration of acute illness. • Analgesics • In PHN amitrytylene topical cool spray and transcutaneous nerve stimulation are often helpful. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.. Meyer HM et al. Am J.Dis. Child 1062; 103: 307. Jes Persen CS et al. Acta Pediatri Scand 1977; 66: 376. Measles: The urban Challenge, UNICEF NY. 1991. WHO/UNICEF: Wkly Epidemiol Rew 1987; 62: 133. IAP guide book on immunization 2004; 16-18. CDC Data. Mumps surveillance Jan 1977, Dec 1982. US Dept of Health and Human Service 1984. IAP guide book on immunization, 2004; 38. IAP guide book on immunization, 2004; 25-26.. SUBASH/NMC15-1393.

(40) Chapter. 2. Dermatology. ATOPIC DERMATITIS (Figs 2.1A and B) DEFINITION Atopic dermatitis or eczema is an itchy, dry, hypersensitive skin disorder affecting many people. It is common in children but can occur at any age. It is not infectious or contagious.  The exact cause of atopic eczema is unknown. It may be hereditary. The patient or some family members may have other hypersensitive conditions like asthma or hay fever. Infections like Staphylococcus aureus, herpes simplex virus help in flaring of the dermatitis.  The rash may appear red, wet and weepy or dry, thickened and scaly. Scratching often aggravates the rash. The skin thickens and becomes darker. It is a chronic condition. It can affect any part of the body, particularly the elbow bends, back of the knees and the neck. Infantile Type (seen from 2 months to 2 years). Classically cheeks and shin are involved. It produces intense itching, lesion is dry, erythematous, excoriated plaques may then become lichenified and hyperpigmented. Spontaneous remission is common by 2 years. Childhood Type—Seen above 5 years, seen at flexural area, neck, wrists antecubital and popliteal areas. PATHOGENESIS There are two hypotheses: 1. Increased in cyclic AMP phosphodiesterase activity, and 2. Decrease in cell mediated immunity both of these are responsible in over activity of the T-helper cell (TH2) subset of T-lymphocyte and thus, leads to significant inflammation.. SUBASH/NMC15-1393.

(41) 16. Spotters in Pediatrics. A. B. Figs 2.1A and B: (A) Atopic dermatitis. The lesions in childhood form are flexural in distribution as contrast to infantile form where there is axillary involvement. (B) antecubital areas involvement. MANAGEMENT 1. Care of dry skin by taking brief bathing with mild soap, and patting (not rubbing) the dry skin leaving moisture. Application of moisturizer or emollients after bath like hydrophilic petroleum, etc. 2. Steroids: Mild steroids like hydrocortisone is applied over face and in infants. Moderate potent steroid like (clobetasone butyrate 0.050%) for subacute lesion. The potent steroids like betamethasone dipropionate 0.050 percent, flucinolone acetornide and mometasone for chronic lesions. 3. Antibiotics are used for infected cases. Beta lactam antibiotics are best-suited drugs here for at least 2 to 3 weeks. 4. Antihistamines: Hydroxyzine 1mg/kg/day at bed time double the usual dose. Other drugs used are diphenhydramine, doxepin, loratidine, cetrizine.. ALOPECIA (Figs 2.2A and B) DEFINITION Hair loss, alopecia, is the result of changes in the hair follicle. If the changes are transient (as in alopecia areata) and non destructive of the hair matrix, there is eventual regrowth. Condition that causes destruction of the hair matrix (such as folliculitis decalvans or physical trauma) lead to the formation of scars or atrophy resulting in permanent alopecia. CLASSIFICATION It is classified into two groups: Non-scarring alopecia usually divided into localised or diffuse, and cicatricial or scarring alopecia. THE HAIR CYCLE To understand the pathogenesis of alopecia requires knowledge of the hair follicle cycle and its role in disorders of the hair and scalp.. SUBASH/NMC15-1393.

(42) 17. Dermatology. A. B. Figs 2.2A and B: Alopecia. (A) Alopecia areata in a 2-year-old boy. (B) Tinea capitis. Circumscribed area of hair loss without scalp change and hair broken off at the follicular orifice. Hair growth occurs in cycle. Anagen phase (Growing phase): In this phase hair grows about 2 mm a week for 2 to 5 years or longer. This is followed by short, involutional phase, the catagen phase. In this phase mitosis ceases at the hair bulb and the matrix is enveloped by shortening outer root sheath. Telogen phase: It is characterized by non-pigmented “club” hair. The new anagen hair pushes out the old telogen hair, beginning the new cycle. The human scalp has approximately 100,000 hair follicles of which some 5 to 10 percent are in the telogen phase. Since the telogen phase lasts for 3 months for each individual hair, the number of normally lost telogen hairs is 50 to 100 daily. In acutely stressful events, such as birth, auto accidents, illness with high fever, and acute psychiatric illness may results in a rapid conversion of growing hairs to resting hairs. Following the events by 2 to 4 months, the hairs are shed over 3 to 4 months. TELOGEN EFFLUVIUM (Fig. 2.3)  Telogen is the name given to the acquired diffuse alopecia that results from rapid conversion of scalp hairs from growing state to resting state.  Diagnosis: It is made by plucking atleast 50 hairs from the child’s scalp and examining the roots to determine whether they are growing or resting. In anagen phase, the hair will have a pigmented core and a bulbous root that is larger in diameter than the hair shaft. In telogen phase, the external root sheath is absent, or fragmented pigment is often absent, and the root of the hair is narrower than the caliber of the outer hair and frequently curved.  Treatment: Patient should be reassured that normal hair growth would return within 6 months. ANAGEN EFFLUVIUM It is an acute, severe diffuse inhibition of growth of anagen follicles; the loss is greater than 8090%. It is caused by radiation and cancer chemotherapeutic drugs and hypervitaminosis A.. SUBASH/NMC15-1393.

(43) 18. Spotters in Pediatrics.  Fig. 2.3: Telogen effluvium. Note acquired diffuse nonscarring alopecia. ALOPECIA AREATA (Fig. 2.2A)  It is characterized by complete or almost complete hair loss in circumscribed areas without scalp changes.  A positive family history is seen in 10 to 20 percent of patients.  Nail disease is seen in 46 percent cases ranging from pitting 1 to 2 mm in nail plate.  Prognosis for most children is excellent. Complete hair growth occurs within a year in 95 percent cases. Spontaneous remission is the rule.  Treatment • Anthralin used locally for its irritant effect (stimulate hair growth). • Intralesional injection of triamcinolone solution. • Topical corticosteroid.. STEVENS-JOHNSON SYNDROME (Figs 2.4 and 2.5) DEFINITION  It is a severe type of adverse reaction mostly due to drugs, some times due to infectious agent and is characterized by a distinct eruption and involvement of atleast two mucous membranes and the erosions involve more than 20 percent area. It is also called as erythema multiforme major. When mucous membrane are not involved it is called as erythema multiforme minor. The severe form of erythema multiforme spectrum is toxic epidermal necrolysis (TEN) here more than 30 percent of area is affected by erosion.  Etiology: Drugs like—Anticonvulsants- Barbiturate, diphenhydantoin, carbamazepine, Lamotrigene. Antibiotics—Penicillins, sulphonamides. Nonsteroidal anti-inflammatory drugsIbuprofen and naprosyn. Infectious agent like Mycoplasma pneumoniae, herpes simplex, etc. CLINICAL FEATURES  The skin lesions are seen of many types erythematous macule, purpuric macule, papules, blisters leading to erosions. Target or iris lesion are quite specific, individual erosions are < 3 cm in diameter.. SUBASH/NMC15-1393.

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