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100% found this document useful (7 votes)
257 views75 pages

Hutchison Paediatrics 2nd Edition by Krishna M Goel, Devendra K Gupta ISBN 9350257718 9789350257715 PDF Download

The document provides information about various medical textbooks available for download, including titles like 'Hutchison Paediatrics 2nd Edition' and 'Manufacturing Processes 2nd Edition.' It includes ISBN numbers, authors, and links for purchasing or downloading the books. Additionally, it features details about the publishers and contributors involved in the creation of these educational resources.

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HUtchison’s
Paediatrics
HUtchison’s
Paediatrics
Second Edition

Edited by
Krishna M Goel
MD DCH frcp (Lond, Edin and Glas) Hon frcpch
Formerly Honorary Senior Lecturer of Child Health
University of Glasgow and Consultant Paediatrician
at the Royal Hospital for Sick Children
Yorkhill, Glasgow, Scotland, UK

Devendra K Gupta
MS MCh Fams (Hon) FCSS frcs (Edin) frcs (glas) FAMS (Rom) DSc (Honoris Causa)
Vice Chancellor
Chhatrapati Shahuji Maharaj Medical University
Lucknow, Uttar Pradesh, India

Foreword
Professor Terence Stephenson

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD


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

Headquarter
Jaypee Brothers Medical Publishers (P) Ltd
4838/24, Ansari Road, Daryaganj
New Delhi 110 002, India
Phone: +91-11-43574357
Fax: +91-11-43574314
Email: [email protected]

Overseas Offices
J.P. Medical Ltd. Jaypee-Highlights medical publishers Inc.
83 Victoria Street, London City of Knowledge, Bld. 237, Clayton
SW1H 0HW (UK) Panama City, Panama
Phone: +44-2031708910 Phone: + 507-301-0496
Fax: +02-03-0086180 Fax: + 507-301-0499
Email: [email protected] Email: [email protected]

Website: www.jaypeebrothers.com
Website: www.jaypeedigital.com

© 2012, Jaypee Brothers Medical Publishers

All rights reserved. No part of this book may be reproduced in any form or by any means without the prior permission of the
publisher.

Inquiries for bulk sales may be solicited at: [email protected]

This book has been published in good faith that the contents provided by the contributors contained herein are original, and
is intended for educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the
editors specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the
contents of this work. If not specifically stated, all figures and tables are courtesy of the editors. Where appropriate, the readers
should consult with a specialist or contact the manufacturer of the drug or device.

Hutchison's Paediatrics
First Edition: 2009
Second Edition: 2012

ISBN : 978-93-5025-771-5
Printed at
Contributors
Alastair Turner David James Honorary Professor of Oral and
BSc Med Sci MBChB MRCPCH MBChB Dip Ed DCH DPM FRCPsych FRCP (Glas) Maxillofacial Surgery—Glasgow
Consultant Paediatric Intensive Care Retired Child Psychiatrist formerly University, Consultant Oral and
Honorary Senior Clinical Lecturer at Department of Child and Family Maxillofacial Surgeon­­­—West of Scotland
University of Glasgow Psychiatry Plastic and Maxillofacial Unit
Royal Hospital for Sick Children Royal Hospital for Sick Children Canniesburn Hospital
Glasgow, Scotland, UK Glasgow, Scotland, UK Glasgow Civilian Consultant
to the Royal Navy
Alison M Cairns Devendra K Gupta Scotland, UK
MSc BDS MFDS FRCS (Edin) M Paed Dent (RCPSG) MS MCh FAMS (Hon) FCSS FRCS (Edin) FRCS (Glas)
Clinical Lecturer in Paediatric Dentistry FAMS (Rom) DSc (Honoris Causa)
Kirsteen J Thompson
University of Glasgow Dental Hospital Vice Chancellor MSc FRCS (Edin)
and School, Glasgow, Scotland, UK Chhatrapati Shahuji Maharaj Medical Consultant Ophthalmologist
University Inverclyde Royal Hospital
Anne Margaret Devenny Lucknow, Uttar Pradesh, India Greenock, Scotland, UK
MBChB MRCP (UK) FRCPCH
Paediatric Respiratory Consultant Elizabeth A Chalmers Krishna M Goel
Royal Hospital for Sick Children MBChB MD MRCP (UK) FRCPath MD DCH FRCP (Lond, Edin & Glas) Hon FRCPCH
Glasgow, Scotland, UK Consultant Paediatric Haematologist Formerly Honorary Senior Lecturer of
Royal Hospital for Sick Children Child Health, University of Glasgow and
Beena Koshy Glasgow, Scotland, UK Consultant Paediatrician
MBBS MD (Paed) PDFDP
Royal Hospital for Sick Children
Assistant Professor of Developmental James Wallace Glasgow, Scotland, UK
Paediatrics, Christian Medical College BSc MR PharmS FRCPCH (Hon)
Vellore, Tamil Nadu, India Chief Pharmacist Louis Low
Yorkhill Hospitals MBChB MRCP (UK) FRCP (Lond, Edin & Glas)
Benjamin Joseph FRCPCH
Glasgow, Scotland, UK
MS Orth MCh Orth Honorary Clinical Professor in Paediatrics
Professor of Orthopaedics and Head of Jean Herbison Department of Paediatrics
Paediatric Orthopaedic Service MBChB MRCP FRCPCH DCCH MFFLM and Adolescent Medicine
Kasturba Medical College Consultant Paediatrician and Clinical The University of Hong Kong
Manipal 576104, Karnataka, India Director for Child Protection Services Queen Mary Hospital
Greater Glasgow and Clyde Health Board Pokfulam, Hong Kong
Christina Halsey Child Protection Unit
BM Bch BA (Hons) MRCP MRCPath PhD
Royal Hospital for Sick Children Lydia Edward Raj
Honorary Consultant Paediatric Glasgow, Scotland, UK
MSOT
Haematologist and Scottish Senior Reader (In-charge OT Education)
Clinical Fellow Judy Ann John Department of Physical Medicine
Department of Paediatric Haematology MD DipNB (PMR) and Rehabilitation
Royal Hospital for Sick Children Associate Professor Christian Medical College
Glasgow, Scotland, UK Department of Physical Medicine and Vellore, Tamil Nadu, India
Rehabilitation
Chikkanayakanahali Manjunatha Christian Medical College Margo L Whiteford
MD (Paed) DCH DNB (Paed) MRCP (UK) FRCPCH BSc FRCP (Glasgow)
Vellore, Tamil Nadu, India
Consultant Neonatologist Consultant Clinical Geneticist
Wishaw General Hospital Jugesh Chhatwal Ferguson-Smith Centre for Clinical Genetics
50, Netherton Road MD DCH Yorkhill Hospital
Wishaw ML2 0DP Professor and Head of Paediatrics Glasgow, Scotland, UK
Lanarkshire, Scotland, UK Christian Medical College
Mary Mealyea
Ludhiana, Punjab, India MBChB Diploma in Dermatology
Craig Williams
MD FRCP FRCPath Associate Specialist in Paediatric
Khursheed F Moos
Consultant Microbiologist MBBS (Lond) BDS (Lond) FRCS (Edin) FDS RCS (Eng
Dermatology
Royal Hospital for Sick Children and Edin) FDS RCPS (Glasg) FRCPS (Glasg) Honorary Royal Hospital for Sick Children
Glasgow, Scotland, UK FCPS (Pakistan) Honorary OBE Glasgow, Scotland, UK
vi Hutchison's Paediatrics 

Maya Mary Thomas Richard Welbury Sarada David


MBBS DCH MD (Paeds) DM (Neuro) BDS (Hons) MBBS PhD FDSRCS FDSRCPS MS DO
Associate Professor and Paediatric FRCPCH Professor and Head
Neurologist, Department of Neurological Professor of Paediatric Dentistry Department of Ophthalmology
Sciences, Christian Medical College University of Glasgow Dental Hospital Christian Medical College
Vellore, Tamil Nadu, India and School Vellore, Tamil Nadu, India
Glasgow, Scotland, UK
Michael Morton Shilpa Sharma
MPhil MA MBChB FRCPsych FRCPCH
Robert Carachi MS MCh DNB PhD
Consultant Child & Adolescent Psychiatrist MD PhD FRCS (Glas & Eng) FEBPS Associate Professor
In-patient & Liaison Child & Adolescent Professor of Surgical Paediatrics Paediatric Surgery
Psychiatry with Neuropsychiatry University of Glasgow 416 Administration Block
Department of Child & Family Psychiatry Royal Hospital for Sick Children PGIMER, Dr RML Hospital
Royal Hospital for Sick Children Glasgow, Scotland, UK Baba Kharg Singh Marg
Glasgow, Scotland, UK Connaught Place
Rosemary Anne Hague New Delhi, India
NV Doraiswamy
MD MRCP (UK) FRCPCH
MS FRCS (Edin & Glas) FICS FISS FFAEM FRCPCH
Consultant Surgeon (Retd) Consultant Paediatric Id/Immunology Syed Rehan Ali
Royal Hospital for Sick Children Yorkhill NHS Trust MB DCH MRCP FRCP
Royal Hospital for Sick Children Assistant Professor and Consultant in
Glasgow, Scotland, UK
Glasgow, Scotland, UK Neonatal Medicine
Paul Galea Director of Neonatal Services
MD DCH FRCP (Glas) FRCPCH Rosemary Sabatino Department of Paediatrics and Child Health
Consultant Paediatrician Trainer and Educator Aga Khan University Hospital
Royal Hospital for Sick Children Crisis Care Training International Karachi, Pakistan
Glasgow, Scotland, UK International Office
PO Box 517, Fort Mill Tahmeed Ahmed
Peter Galloway MBBS PhD
BSc DCH FRCP (Edin & Glas) FRCPath South Carolina, USA
Head, Nutrition Programme Scientist
Consultant Medical Biochemist
Samuel E Ibhanesebhor Clinical Sciences Division
Royal Hospital for Sick Children,
FWACP FMCPaed FRCPCH FRCP (Glasg) International Centre for Diarrhoeal
Glasgow, Scotland, UK
Consultant Neonatologist Diseases Research, B
Phyllis Kilbourn Wishaw General Hospital Dhaka, Bangladesh
International Director 50, Netherton Road
Crisis Care Training International Wishaw ML2 0DP Trevor Richens
MBBS BSc (Hons) MRCP (Lond)
International Office, PO Box 517 Lanarkshire, Scotland, UK
Fort Mill, South Carolina, USA Consultant Paediatric Cardiologist
Sandra J Butler Royal Hospital for Sick Children
Prabhakar D Moses BSc (Hons) MBChB MRCPCH FRCR Glasgow, Scotland, UK
MBBS MD (Paed) MRCP (UK) FRCP (Edin) FCAMS
Consultant Paediatric Radiologist
Professor and Head of Paediatrics Unit 111 Zulfiqar Ahmed Bhutta
Royal Hospital for Sick Children
Christian Medical College MBBS FRCP FRCPCH FCPS PhD
Glasgow, Scotland, UK
Vellore, Tamil Nadu, India The Husein Lalji Dewraj
Rajeev Srivastava Sanjay V Maroo Professor and Chairman
MBBS MS (Orth) FRCS (G) FRC Path MBChB M-Med FRCR Department of Pediatrics and Child Health
Consultant Medical Biochemist Consultant Paediatric Radiologist The Aga Khan University and
Royal Hospital for Sick Children Royal Hospital for Sick Children Medical Center
Glasgow, Scotland, UK Glasgow, Scotland, UK Karachi, Pakistan
Foreword
The world moves at a frightening pace and sometimes I hear a view expressed that textbooks are a thing of the past. We
should be able to get all the information we need from the Internet and what is more, it is argued, it is more likely to be up-
to-date. I disagree. I think there is still a place for a well written, comprehensive textbook and I use the books on my shelves
most days. The reader can have confidence in the contents if they are familiar with the authors and editors and this is an
advantage that has to be set against the potential benefits of electronic information. Whilst the Internet is likely to be updated
in real time, there is very little peer review or filtering of the information placed on it and the reader can rarely be sure of
the provenance of the opinions expressed.
I am delighted that Krishna M Goel and Devendra K Gupta have produced the second edition of their marvellous
textbook Hutchison’s Paediatrics. This will be of great value to all those who use it, whether students, or those preparing for
professional examinations, or simply (like myself) keeping up-to-date or finding the answers to difficult clinical problems in
daily practice.
James Holmes Hutchison graduated at the University of Glasgow. He served in the Second World War rising to the
rank of Lieutenant Colonel and was awarded an Order of the British Empire in 1945. He returned to the Hospital for Sick
Children in Glasgow and subsequently became the Samson Gemmel Professor in Paediatrics. He was President of the Royal
College of Physicians and Surgeons of Glasgow, then became President of the British Paediatric Association and then served
as Dean of the Faculty of Medicine in Glasgow. Following his time in Glasgow, he was appointed Professor of Paediatrics
at the University of Hong Kong.
I hope you enjoy reading Hutchison’s Paediatrics in this new edition as much as I have.

Professor Terence Stephenson


DM FRCP (Lon) FRCPCH
President
Royal College of Paediatrics and Child Health
University of Nottingham
Nottingham, UK
Preface to the Second Edition
The patterns of childhood disease throughout the world are changing with advancing knowledge, altering standards of living,
lifestyle and rising levels of medical care. The origins of physical and mental health and disease lie predominantly in the early
development of the child. Most of the abnormalities affecting the health and behaviour of children are determined prenatally
or in the first few years of life by genetic and environmental factors. The authors have summarised the current knowledge of
causation and have indicated where health education and prevention might reduce the burden of childhood ill health.
The more diverse authorship of chapters in this second edition reflects the growing dependence upon cooperative interests
of colleagues in paediatrics. In clinical practice, such collaborative work can only be accomplished within a large hospital
or a unit devoted to children. Both editors have been fortunate to work in such an environment and believe that the highest
standards of paediatric practice can only be attained in such circumstances. In this, the second edition, we welcome ten new
contributors. In this book we seek to provide practical advice about the diagnosis, investigation and management of the full
spectrum of childhood disorders, both medical and surgical. We have tried to indicate, and where appropriate to describe,
techniques and laboratory investigations which are necessary for advanced diagnosis and up-to-date therapy. Attention is
directed to the special problems which arise in the developing countries. The need for such a text has been confirmed by the
success of the first edition, published in 2009. As is often the case, space limitation demands some selectivity of content. It
is intended in a true apprenticeship fashion of teaching to provide a manageable, readable and practical account of clinical
paediatrics for medical undergraduates, for postgraduates specialising in paediatrics and for general practitioners whose
daily work is concerned with care of children in health and sickness. Knowledge within the field of paediatrics continues to
increase exponentially. Accordingly, many chapters in this edition were completely revised, updated and extended with an
additional four chapters. Many figures illustrating salient concepts summarising clinical findings and treatment results have
been added.
We are especially grateful to the parents and to the many children and their families who contributed to our knowledge
and understanding of paediatrics and willingly gave permission to reproduce photographs of their children. A book such as
this cannot be written without reproducing material reported in the medical literature. We acknowledge here, with gratitude,
the permission granted free of charge by individual publishers to reproduce material for which they hold the copyright.
We particularly wish to thank the Hutchison family for allowing us to use the name of the late Professor James Holmes
Hutchison, the author of 'Practical Paediatric Problems' to enable us to title this book Hutchison's Paediatrics. Even today,
Hutchison's name is highly respected in the paediatric world.
Finally, we are grateful to the various contributors to this second edition for their cooperation in its production.

Krishna M Goel
Devendra K Gupta
Preface to the First Edition
The patterns of childhood disease throughout the world are changing with advancing knowledge, altering standards of living,
lifestyle and rising levels of medical care. The origins of physical and mental health and disease lie predominantly in the
early development of the child. Most of the abnormalities affecting the health and behaviour of children are determined
prenatally or in the first few years of life by genetic and environmental factors. The range of contributors indicates that they
are all experts in their particular fields. The authors have summarised the current knowledge of causation and have indicated
where health education and prevention might reduce the burden of childhood ill health. We seek in this book to provide
practical advice about the diagnosis, investigation and management of the full spectrum of childhood disorders, both medical
and surgical. We have tried to indicate and where appropriate to describe, techniques and laboratory investigations which
are necessary for advanced diagnosis and up-to-date therapy. Attention is directed to the special problems which arise in the
developing countries.
It is intended in a true apprenticeship fashion of pedagogy to provide a manageable, readable and practical account of
clinical paediatrics for medical undergraduates, for postgraduates specialising in paediatrics and for general practitioners
whose daily work is concerned with care of children in health and sickness. The authors had to be selective in deciding what
to exclude in order to keep the book manageable and practical.
We would like to express our immense gratitude to our colleagues who have provided us with help and advice in writing
this book. The willingness with which they gave us their time in spite of many other commitments leaves us permanently in
their debt.
We are especially grateful to the parents and to the many children and their families who contributed to our knowledge
and understanding of paediatrics and willingly gave permission to reproduce photographs of their children. Also a book such
as this cannot be written without reproducing material reported in the medical literature. We acknowledge here with gratitude
the permission granted free of charge by individual publishers to reproduce material for which they hold the copyright.
Our deepest thanks go to Professor Forrester Cockburn, Professor Dan Young and Professor Robert Carachi, who most
kindly passed on to us their rights of the book entitled ‘Children’s Medicine and Surgery’ from which some material has been
used.
We particularly wish to thank the Hutchison family for allowing us to use the name of the late Professor James Holmes
Hutchison, the author of ‘Practical Paediatric Problems’ to enable us to title this book Hutchison’s Paediatrics. Even today
Hutchison’s name is highly respected in the paediatric world.
Finally, we would like to express our thanks to Jean Hyslop, Medical Artist, who created the line drawings and art work
and helped to integrate the text with the illustrations.

Krishna M Goel
Devendra K Gupta
Contents

1. Paediatric History and Examination 1 Cyanotic congenital heart disease 34


Krishna M Goel, Robert Carachi Neonatal jaundice 35
Intrauterine growth restriction or retardation 37
The history 1 Preterm 37
Clinical manifestations of disease 1 Chromosomal abnormalities 41
History and documentation 2 Haematology 42
Introduction 4 Inborn errors of metabolism 43
History of present complaint 4 Multiple gestation 46
Past medical history 5 Maternal substance and alcohol abuse 47
Mother’s pregnancy, labour, delivery and the neonatal Neonatal sepsis 47
period 5 Neonatal procedures 48
Dietary history 5 Vaccination and weaning 48
Developmental history 5 Nutrition 48
Family and social history 5 Discharge planning 50
Physical examination 6 Withholding and withdrawal of treatment 50
A guide to examination of a child-patient 12 • Newborn health in developing countries 50
Respiratory system 13 Introduction 50
Cardiovascular system 14 Birth asphyxia 51
Percussion of the heart is not normally undertaken in Neonatal infections 52
children 14 Term iugr/lbw 55
Gastrointestinal system 14 Congenital malformations and inherited disorders 56
Nervous system 14 Prematurity 57
Cranial nerve 14 Respiratory distress syndrome 57
Locomotor system 15
Developmental assessment 15 4. Paediatric Genetics 59
Margo L Whiteford
2. Growth and Development 18
Louis Low Introduction 59
History 59
Normal growth 18
Patterns of inheritance 60
Assessment and monitoring of growth 19
The growth hormone: igf 1 axis 21 Investigations 63
Genetics of stature 21 5. Nutrition 75
Puberty 21 Tahmeed Ahmed, Zulfiqar Ahmed Bhutta,
Child development 23 Krishna M Goel
Gross motor development 23
• Protein-energy malnutrition and micronutrient
Fine motor development in early childhood 24 deficiencies in childhood 75
Language and speech development in childhood 24 Protein-energy malnutrition 75
Social development 25 Causes of pem 75
Emotional and cognitive development 26 Classification of pem 75
Development assessment 26 Management of mild or moderate malnutrition 77
3. Neonatal Paediatrics 28 Facility-based management of severe acute malnutrition 77
Samuel E Ibhanesebhor, Chikkanayakanahali Phases of management of severe acute malnutrition 78
Manjunatha, Syed Rehan Ali, Zulfiqar Ahmed Bhutta Treatment of complications 81
Community-based management of severe acute
Introduction 28 malnutrition 83
Neonatal resuscitation 28 • Other disturbances of nutrition 83
Hypoxic ischaemic encephalopathy 30 Vitamin d deficiency 89
Whole baby hypothermia 31 Vitamin d metabolism 89
Routine newborn examination 32 Vitamin c (ascorbic acid) deficiency 92
Perinatal injuries 33 Vitamin b deficiencies 93
Meconium aspiration syndrome 34 Vitamin e (tocopherol) deficiency 97
Transient tachypnoea of the newborn Vitamin k deficiency 97
(or ‘wet lung’) 34 Biotin and pantothenic acid 97
xiv Hutchison's Paediatrics 

6. Respiratory Disorders 100 Cirrhosis of the liver 147


Anne Margaret Devenny Pancreas 148
Juvenile tropical pancreatitis 148
Introduction 100
Liver transplantation 148
History and examination 100
• Infectious diarrhoea in childhood 149
Respiratory investigations 100
Examination 101 8. Paediatric Cardiology 157
The respiratory tract in children 102 Trevor Richens
Other congenital lung abnormalities 104 Introduction 157
Acquired abnormalities 105 General principles of diagnosis 157
Acquired lower respiratory tract problems 105 Examination 157
Aspiration pneumonia 108 • Congenital heart abnormalities 162
Asthma 108 Acyanotic congenital heart disease 162
Bronchiectasis 112 Cyanotic congenital heart disease 169
Cystic fibrosis 112 Acquired heart disease 176
Pulmonary tuberculosis 116 Heart rhythm abnormalities 181
Bronchiolitis obliterans 116 Case studies 183
Pneumothorax 116
Sleep disordered breathing in children 117 9. Care of the Paediatric Surgical Patient 186
Obstructive sleep apnoea 117 Shilpa Sharma, Devendra K Gupta
Neuromuscular causes of sleep disordered • Basic paediatric surgery 186
breathing 118 Introduction 186
Sudden infant death syndrome 118 History taking of paediatric surgical patients 186
Chest injury 118 Clinical examination 187
Foreign body inhalation 118 Pre- and postoperative care 188
Questions and answers 119 Fluid and electrolyte management 189
7. Gastroenterology and Hepatology 121 Blood transfusion 191
Krishna M Goel, Robert Carachi, Zulfiqar Ahmed Summary 192
Bhutta • Paediatric trauma and burns 192
Paediatric trauma 192
• Gastrointestinal and liver disease Physiological parameters 193
Introduction 121 Approach to the injured child 193
Gastro-oesophageal reflux disease (gord) 121 Emergency treatment 195
Gastrointestinal haemorrhage 122 Child abuse 197
Oesophageal varices 123 Burns 197
Peptic ulcer 123 Emergency room management 200
Blood per rectum 124 Surgical management of the burn wound 202
Rectal prolapse 124 Complications and rehabilitation 203
Intestinal polyps 125 Long-term complications 204
Infantile colic 125
Recurrent abdominal pain in children 125 10. Neonatal Surgery 205
Appendicitis 125 Devendra K Gupta, Shilpa Sharma
Foreign bodies 128 Congenital diaphragmatic hernia 205
Necrotising enterocolitis 129 Oesophageal atresia 206
Toddler’s diarrhoea 130 Infantile hypertrophic pyloric stenosis 209
Infectious diarrhoea in childhood 130 Malrotation 210
Fermentative diarrhoea (disaccharide intolerance) 130 Hirschsprung’s disease 212
Parasitic intestinal infection 131 Anorectal malformations 214
Nematodes 131 Neural tube defects 220
Cestodes 133 Hydrocephalus 223
Inflammatory bowel disease 134
11. General Paediatric Surgery 228
Coeliac disease (gluten-sensitive enteropathy) 137
Devendra K Gupta, Shilpa Sharma
Cystic fibrosis 139
Idiopathic childhood constipation 141 Cleft lip and palate 228
Protein-losing enteropathy 143 Branchial arch anomalies 230
Wilson’s disease (hepatolenticular degeneration) 144 Thyroglossal cyst 233
Jaundice 145 Umbilical hernia 234
Viral infections of the liver 145 Intussusception 235
 Contents xv

Surgical jaundice in children 235 Von willebrand disease 316


Choledochal cyst 238 Disseminated intravascular coagulation
Inguinal hernia and hydrocoele 241 consumption coagulopathy 317
12. Paediatric Urology 244 Acute leukaemias 318
Devendra K Gupta, Shilpa Sharma Meningeal and testicular leukaemia 319
Hydronephrosis 244 16. Paediatric Rheumatology 323
Exstrophy of bladder 247 Paul Galea, Krishna M Goel
Undescended testis or cryptorchidism 249 Introduction 323
Phimosis 253 Causes of arthralgia and arthritis in children 323
Paediatric intersex disorders 253 Juvenile idiopathic arthritis 323
13. Paediatric Oncology 258 Treatment of juvenile idiopathic arthritis 327
Devendra K Gupta, Shilpa Sharma, Robert Carachi Physiotherapy and occupational therapy 329
Juvenile reactive arthritis 329
Wilms' tumour 258
Benign joint hypermobility syndrome 330
Neuroblastoma 261
Limb pains of childhood with no organic disease
Rhabdomyosarcoma 265
(idiopathic limb pains) 330
Hepatoblastoma 268
Juvenile dermatomyositis 331
Hepatocellular carcinoma 270
Paediatric systemic lupus erythematosus 333
Germ cell tumours 271
Neonatal lupus erythematosus 334
14. Dermatology 279 Juvenile scleroderma 335
Mary Mealyea Juvenile systemic sclerosis 336
Introduction 279 Vasculitic syndromes 336
Common terms used 279 17. The Urinary System 340
History 280 Krishna M Goel
Vascular anomalies 280
Introduction 340
Disorders of pigmentation 283
Acute post-streptococcal glomerulonephritis 340
Café au lait macules 284
Primary iga nephropathy 342
Dermal melanocytosis 285
Nephrotic syndrome 342
Epidermal naevi 285
Congenital nephrotic syndrome 343
Blistering disorders 286
Urinary tract infections 344
15. Haematological Disorders 299 Renal tuberculosis 346
Krishna M Goel Hypertension in children 346
Haematopoiesis 299 Renal vein thrombosis 350
The normal blood picture in infancy 299 Renal calculi (urolithiasis) 350
Iron deficiency or nutritional anaemia of infancy 300 Hypophosphataemic vitamin d-resistant rickets
The megaloblastic anaemias (folate deficiency, (phosphaturic rickets) 351
vitamin b12 deficiency) 302 Renal fanconi syndrome (cystinosis) 352
The haemolytic anaemias 303 Nephrogenic diabetes insipidus 353
Autoimmune haemolytic anaemia 309 Renal tubular acidosis 354
Paroxysmal nocturnal haemoglobinuria 310 Nocturnal enuresis 354
Microangiopathic haemolytic anaemia 310 Haemolytic uraemic syndrome (d+hus, d –hus) 356
Aplastic and hypoplastic anaemia 310 Acute renal failure 356
Congenital hypoplastic anaemia (blackfan Chronic renal failure 358
diamond anaemia) 310
18. Diseases of Nervous System 360
Fanconi-type familial aplastic anaemia 311
Prabhakar D Moses, Maya Mary Thomas, Beena Koshy
Acquired hypoplastic anaemia 312
Albers-schönberg disease (osteopetrosis, marble Introduction 360
bones) 312 • Congenital malformations of cns 360
The thrombocytopaenic purpuras 312 Microcephaly 360
Idiopathic thrombocytopaenic purpura 313 Craniosynostosis 361
Neonatal thrombocytopenic purpura 314 • Infections of the nervous system 361
Wiskott-aldrich syndrome 315 Pyogenic meningitis 361
Henoch schönlein purpura 315 The waterhouse-friderichsen syndrome 363
Blood clotting defects 315 Aseptic meningitis 363
Haemophilia a 316 Acute encephalitis and encephalopathy 364
Haemophilia b (christmas disease) 316 Sclerosing panencephalitis 365
xvi Hutchison's Paediatrics 

Acute encephalopathy 365 Acute carbon monoxide poisoning 410


Tuberculosis of the central nervous system 366 Snake bite 410
Brain abscess 367 Insect stings 411
Neurocysticercosis 367 Marine stings 411
• Acute flaccid paralysis 368 Plant and mushroom poisoning 411
Acute postinfectious polyneuropathy Drowning and near drowning 411
(guillain-barre'syndrome) 369 20. Metabolic Diseases 413
• Convulsions in infancy and childhood 370 Peter Galloway, Rajeev Srivastava, Krishna M Goel
Febrile seizures 375
• Childhood stroke 375 Inborn errors of metabolism 413
• Movement disorders 378 Common aetiological principles 413
Rheumatic chorea (sydenham’s chorea, st. Vitus Treatable disorders 414
dance) 379 Clinical approach to diagnosis 415
• Neurocutaneous syndromes 379 • Specific common disorders 416
Neurofibromatosis (von recklinghausen’s disease) 379 Disorders of amino acid metabolism 416
Tuberous sclerosis (epiloia) 380 Other disturbances of amino acid metabolism 419
Sturge-weber syndrome (encephalofacial Disorder of branched-chain amino acid
angiomatosis) 380 metabolism 420
Ataxia–telangiectasia (louis-bar syndrome) 381 • Urea cycle disorders 420
Von hippel-lindau disease 381 Disorders of the sulphur-containing amino acids 421
• Neurodegenerative disorders 381 • Disorders of specific sugars 421
Neuronal ceroid lipofuscinoses 382 Pathogenesis 421
• Neuromuscular disorders 382 Clinical features 422
Spinal muscular atrophy (sma) 382 Diagnosis 422
Muscular dystrophy 383 Treatment 422
Myasthenia gravis 384 Disorders of purine and pyrimidine metabolism 423
Congenital mysathenic syndromes 385 • Congenital methaemoglobinaemia 424
• Autonomic nervous system 385 Aetiology 424
Familial dysautonomia (riley-day syndrome) 385 Pathogenesis 424
• Brain tumour in children 386 Clinical features 424
• Cerebral palsy 386 Diagnosis 424
• Learning disorders 392 Treatment 424
Learning disability (developmental retardation) 392 Glycogen storage disorders 424
Management of children with learning Inborn errors of lipid metabolism (the lipidoses) 427
impairment 398 The mucopolysaccharidoses 429
19. Accidental Poisoning in Childhood 399 Mitochondrial defects 431
Krishna M Goel Peroxisomal disorders 432

Introduction 399 21. Endocrine Disorders 434


Assessment of the child and management 399 Louis Low
Poison identification and assessment of the Hypopituitarism 434
severity of overdose 401 Disorders of the posterior pituitary 435
Salicylate poisoning 403 Short stature 436
Paracetamol poisoning 403 Tall stature 438
• Ibuprofen 404 Obesity 438
Acute iron poisoning 404 Thyroid gland 439
Barbiturate poisoning 405 Parathyroid glands 445
Poisoning by antihistamines 405 Rickets 447
Poisoning by tricyclic and related antidepressants 405 The gonads 448
Atropine poisoning 405 Adrenal gland 450
• Antimalarials 406 Disorders of sex development 455
Poisoning by digoxin 406 Diabetes mellitus 456
Poisoning by petroleum distillates, insecticides Hypoglycaemia 460
and weed-killers 406
22. Paediatric Orthopaedics 462
Acute alcohol poisoning 407
Benjamin Joseph
Lead poisoning 407
Caustic ingestion 408 Introduction 462
Swallowed foreign bodies 409 Deformities 462
 Contents xvii

Gait abnormalities 462 Shigellosis 541


Musculoskeletal pain 465 Streptococcal infections 541
Paralysis and pseudoparalysis 465 Pneumococcal infections 543
Joint stiffness 466 Meningococcal disease 543
Congenital anomalies 466 Haemophilus influenzae 544
• Developmental problems 472 Staphylococcal infections 545
Flatfoot 472 Tuberculosis 546
Paralytic conditions 475 Directly observed treatment short course (dots) 549
Infections of bone and joints 478 Leprosy 549
Inherited disorders of bone 479 Syphilis 551
Tumours of bone 481 Leptospirosis 552
Hip pain in children and adolescence 482 Measles 552
Mumps 555
23. Paediatric Dentistry 484 Rubella 556
Richard Welbury, Alison M Cairns Varicella virus (chickenpox) 556
Dental anatomy 484 Poliomyelitis 558
Caries 486 Rabies 558
Oral pathology/oral medicine 487 Japanese encephalitis 558
Infection 495 Dengue fevers 559
Bacterial infection 496 Human immunodeficiency virus infection (aids) 561
Anomalies 498 Associated infections 562
Dentoalveolar trauma 502 Perinatal transmission 562
Oral manifestations of systemic disease 507 Malaria 563
Toxoplasmosis 565
24. Immunity and Allergy 508 Amoebiasis 566
Rosemary Anne Hague Giardiasis 567
Components of the immune system 508 Kala azar (visceral leishmaniasis) 567
The next line of defence: innate 27. Paediatric Ophthalmology 569
(non-specific) immunity 509 Sarada David, Kirsteen J Thompson
Cells of innate immune system 510
Visual assessment in children 569
The adaptive (acquired) immune system 510
Nystagmus 573
Why are neonates and infants prone to infection? 512
Intrauterine infectious diseases 574
Nutrition and immunity 513
Orbital cellulitis 578
Problems with the immune system 513 Allergic conjunctivitis 578
Tests of cell mediated immunity 515 Lacrimal system 579
Test for humoral immunity 515 Cornea 580
Primary immunodeficiency disorders 515 Systemic diseases with corneal manifestations in
• Allergy 517 childhood 584
The immunology of allergic diseases 518 Childhood lens disorders 585
Mediators of the allergic response 519 Paediatric glaucoma 587
Epidemiology 519 Uveitis in children 588
Food allergy 520 Retinoblastoma 591
Diagnosis of allergy 522 Retinopathy of prematurity 593
Management of allergy 524 Traumatic retinopathy 594
Prophylactic medications 524 Preventive ophthalmology 594
Future developments 526 The child with visual impairment 595
25. Immunisation Against Infectious Diseases 527 28. Haematological Investigations in Children 596
Jugesh Chhatwal Christina Halsey, Elizabeth A Chalmers
Immunisation 527 Full blood count 596
Adverse events 528 Red cell indices 596
Travel immunisation 532 Blood film 596
26. Infectious Diseases 533 Reticulocyte count 597
Jugesh Chhatwal Normal ranges 597
Diphtheria 533 Investigation of low haemoglobin in infancy and
Pertussis (Whooping cough) 535 childhood 598
Tetanus 536 Hypochromic microcytic anaemia 598
Enteric fever (typhoid fever) 538 Tests to diagnose iron deficiency 601
xviii Hutchison's Paediatrics 

Tests to diagnose thalassaemia 601 Surgical causes 663


Macrocytic anaemia 602 A child with a mediastinal mass 665
Normocytic anaemia 602 Chest wall masses 668
Investigation of anaemia in neonates 604 Congenital heart disease 669
Polycythaemia 604 Cyanotic child with congenital heart disease 672
White cell disorders 604 Other cardiac and related conditions 673
Bone marrow examination 606 • Abdomen 675
Platelet disorders 607 A neonate with bilious vomiting 675
Coagulation testing in infants and children 607 Other abdominal conditions in children 678
When to perform a coagulation screen 608 The child with an abdominal mass 682
Coagulation tests 608 • Paediatric neuroradiology 685
Monitoring of anticoagulant therapy 610 Congenital brain malformations 685
29. Biochemical and Microbiological Investigations Holoprosencephaly 686
Trauma, hypoxiaischaemia and haemorrhage 689
in Paediatrics 611
Infections, tumours and hydrocephalus 694
Peter Galloway, Craig Williams
Congenital spine lesions 700
Introduction 611 • Paediatric skeletal radiology 702
What are the roles of diagnostic tests? 611 Skeletal dysplasias 702
What factors are important in interpreting data? 612 Mucopolysaccharidoses 704
What is normal? 612 Paediatric hip abnormalities 707
What do you need to know about biochemical tests? 613 Metabolic bone disorders 710
What do you need to know about microbiology Inflammatory joint and muscle conditions 711
tests? 614 Bone infections 712
30. Paediatric Emergencies 618 Haemolytic anaemias 713
Alastair Turner, NV Doraiswamy Langerhans’ cell histiocytosis 714
Paediatric bone tumours 716
Introduction 618 Osteosarcoma 716
Differences between adults and children in the • Paediatric renal imaging 717
emergency department 618 Congenital anomalies 717
Basic structured approach to management 619 Renal ectopia 719
Cardiac arrest 620 Urinary tract stones and nephrocalcinosis 722
Paediatric emergencies 628 Dilatation of urinary tract 722
31. Disorders of Emotion and Behaviour 639 Neoplastic diseases 724
Michael Morton, David James 33. Paediatric Maxillofacial Surgery 727
An introduction to child and adolescent Khursheed F Moos
psychiatry 639 Introduction 727
Problems in early childhood 641 Congenital deformity 728
Working with physically ill children 642 Craniofacial microsomia 732
Emotional disorders and medically Clinical features 733
unexplained symptoms 643 Treacher collins syndrome 736
Elimination disorders 646 Infection 738
Behaviour disorders 647 Trauma 740
Eating disorders 649 Pathology of the jaws and adjacent structures 748
Psychotic disorders 650 Vascular anomalies 751
Communication disorders 650
34. A Prescription for Play 753
Disorders with motor presentations 651 Phyllis Kilbourn, Rosemary Sabatino
Problems of learning 652
Working with social services and police 653 Introduction 753
Defining play 753
32. Paediatric Radiology 655 Importance of play 753
Sanjay V Maroo, Sandra J Butler
Description of forms of play 753
General considerations in paediatric radiology 655 Play: an essential element in child development 755
Radiation effects on children 655 The dangers of play deprivation 757
Imaging modalities used in paediatric imaging 655 Advice for parents (or caregivers) 757
Respiratory and cardiac 657 Play’s role in emotional health 758
Medical causes 660 Emotional issues stemming from trauma 758
 Contents xix

Defining organised play activities (play therapy) 758 Legal system 801
Play: a medium of communication 759 Section 1 803
Methods of play therapy 759 Section 2 803
Benefits of organised play 759 Section 3 803
35. Paediatric Rehabilitation 763 Child protection process for all staff 804
Judy Ann John, Lydia Edward Raj Standard operating procedure in relation to child
protection concerns 814
Introduction 763
The rehabilitation programme 764 38. Practical Paediatric Procedures 821
Alastair Turner, Robert Carachi, Krishna M Goel
36. Prescribing for Children 780
James Wallace Introduction 821
Preparation for practical procedures 821
The challenge 780 Restraint 821
Pharmacokinetics 780 Sedation and analgesia for clinical procedures 822
Compliance and concordance 781 Routine practical procedures 824
The issues in practice 782 Other practical procedures 838
Prescribing in paediatrics 783
Other issues 785 Appendices 855
37. Child Abuse and Neglect—How do We Protect Appendix a: guide to biochemical values 855
these Children? 786 Appendix b: a guide to normal ranges for the
Jean Herbison fbc in infancy and childhood 857
Introduction 786 Appendix c: surface area nomograms in
Various forms of abuse 786 infants and children 858
Emotional abuse and neglect 792 Appendix d: percentiles of age specific blood
Physical abuse 793 pressure measurements in boys and girls 859
Child sexual abuse 798 Appendix e: childhood myositis assessment
Fabricated and induced illness 799 scale (cmas) scoring sheet 863
Child trafficking 799
Child protection standardised procedures 801 Index 865
Krishna M Goel, Robert Carachi

C H A P T E R
Paediatric History and
Examination 1
THE HISTORY How is Knowledge Acquired?
Semeiology • Reading: 10–20% retention
• Taught by others: 10% retention, e.g. lectures, tutorials,
The study of symptoms. computer programs
• Personal experience: 80% retention, e.g. bedside
Disease
teaching.
“A condition in which, as a result of anatomical change or
physiological disturbance, there is a departure from the normal A Description of the Disease
state of health.” There is a lot of variation in normal people. • Knowledge of the causation (aetiology)
• Pathological, anatomical and functional changes which
CLINICAL MANIFESTATIONS OF DISEASE are present (morphology)
Symptoms • Assembly of all the relevant facts concerning the past and
present history (symptoms)
Something the patient feels or observes which is abnormal,
• Full clinical examination and findings (signs)
e.g. pain, vomiting, loss of function. A good history provides
• Simple laboratory tests, such as an examination of the
a clue to the diagnosis in 80% of patients.
urine or blood and X-rays (investigations).
Signs
Prognosis
Physical or functional abnormalities elicited by examination,
Depends on:
e.g. tenderness on palpation, a swelling, a change in a reflex
picked up on physical examination. Always inspect, palpate, • Nature of the disease
percuss then auscultate. • Severity
• Stage of the disease.
The Patient Statistical statements about prognosis can often be made,
e.g. the average expectation of life in chronic diseases or
Why do patients go to the doctor? the percentage mortality in the acute cases. These must be
• They are alarmed. They believe themselves to be ill and applied with great caution to individual patients. Patients
are afraid
expect this more and more with internet access. Often
• Relief of symptoms
information has to be interpreted. They may be testing your
• Cure
knowledge and comparing it to other doctors or information
• Prognosis.
obtained.
The Doctor
Syndrome
• Helps to diagnose the disease
A group of symptoms and/or signs which is commonly occur
• Symptoms + signs → differential diagnosis → D
together, e.g. Down’s syndrome and Beckwith-Wiedemann
definitive diagnosis
syndrome (*).
• Acquired knowledge allows recognition + interpretation
+ reflection → therapy + prognosis. * Oxford dysmorphology database
2 Hutchison's Paediatrics 

Warning! Flatulence (16, 26): Eructation (belching) and passage of


flatus.
When discussing medical matters in a patient’s hearing,
certain words with disturbing associations should be Bowels (25): Constipation (recent or long standing and
avoided. This is so, even if they are not relevant to the severity); diarrhoea (frequency and looseness of motions);
particular individual. presence of blood and mucus in faeces; altered colour of
faeces—black from altered blood (melaena); clay coloured in
HISTORY AND DOCUMENTATION obstructive jaundice; bulky and fatty in steatorrhoea, piles.
History of Present Condition Tenesmus painful sensation and urgent need to defecate
(Rectal pathology).
General Description
Appetite and loss of weight (17): Recent looseness of clothing.
The taking of an accurate history is the most difficult
Types of food in diet and amounts eaten.
and the most important part of a consultation. It becomes
progressively simpler as the physician’s knowledge of Difficulty in swallowing (18a): Food hard or soft, fluids,
disease and experience increases, but it is never easy. As level at which food ”sticks”. Pain, regurgitation. Progression
far as possible the patients’ complaint list should be written from solid food to liquid.
(in order of relevance), unaltered by leading questions,
but phrased in medical terms. When the patient’s own Heartburn, acid eructations “and belching”.
phraseology is used, the words should be written in inverted Jaundice (17): Constant or fluctuating.
commas, e.g. “giddiness”, “wind”, “palpitation” and an
attempt should be made to find out precisely what they mean Note: Steatorrhoea: Bulky pale foul smelling and greasy
to the patient. stools due to:
• Depressed fat digestion (pancreatic lipase and bile)
Onset: The order of onset of symptoms is important. If there
• Depressed fat absorption (small intestine mostly
is doubt about the date of onset of the disease, the patient
jejunum).
should be asked when he last felt quite well and why he first
consulted his doctor. Cardiovascular System Questions
Therapy: Notes on any treatment already received and of its Breathlessness (11): Dyspnoea on exertion [DOE (degree)],
effect, if any, must be made as it might alter disease states, dyspnoea at rest (DAR), time especially if wakes at night,
e.g. appendicitis masked by drug treatment for a urinary position, relieving factors, gradual or sudden onset,
tract infection (UTI).
change, duration [paroxysmal nocturnal dyspnoea (PND)],
Symptomatic Enquiry precipitating factors, number of pillows used.

After the patient has given a general description of his Pain in chest (19): Site on exertion or at rest, character,
illness, the system mainly involved will usually, but by radiation, duration, relief by drugs, etc. accompanying
no means always, be obvious. The patient should then be sensations, e.g. breathlessness, vomiting, cold sweat, pallor,
questioned about the main symptoms produced by diseases frequency, other relieving factors.
of this system. This should be followed by enquiries directed
Swelling of ankles (23): Time of day.
towards other systems. Remember different systems may
produce similar symptoms. Swelling of abdomen (27): Tightness of trousers or skirt and
This systematic enquiry runs from the “head to the toes” bloatedness.
(32 questions). However, relevant questions are grouped
together under systems. Here are some examples. Palpitation (20): Patient conscious of irregularity or
forcefulness of heart beat.
Alimentary Tract Questions Dizziness and faints: Hypertension pain.
Abdominal pain or discomfort (24): Site, character, e.g. Pain in the legs on exertion (22): Intermittent claudication at
constant or colicky, radiation, relationships to food and
rest, or exertion and other vascular problems.
bowel actions. Shift in site.
Coldness of feet (23): Raynaund’s phenomenon.
Nausea and vomiting (15): Frequency and relationship to
food, etc. (positive vomiting), amount of vomitus, contents, Dead fingers or toes (22): Pain, sensation, ulceration and
colour, blood (haematemesis), etc. diabetes.
 Paediatric History and Examination 3

Respiratory System Questions Speech disturbance (9): Duration, onset, nature. Problems in
reading or understanding.
Cough (12): Character, frequency, duration, causing pain
and timing. Productive. Genitourinary System Questions
Sputum (13): Quantity, colour (frothy, stringy and sticky
Micturition (29): Frequency during day and night, retention,
odour), colour when most profuse (during the day and the
dribbling, and amount of urine passed. Pain on micturition
year and the affect of posture (bronchiectasis) presence of
(dysuria). Stress incontinence, urgency incontinence.
blood haemoptysis. Is the blood red or brown? Is it pure
blood or ‘specks’? e.g. acute or chronic bronchitis. Urine (30): Colour and amount—smell, blood, colour, frothy.
Breathlessness (11): On exertion or at rest. Expiratory Lumbar pain (28): Radiation, history of trauma and
difficulty, precipitating factors, cough, fog, emotion, change mechanical.
of environment and wheezing.
Swelling of face or limbs (23): Presence on rising, drugs,
Pain in chest: Location, character, affected by respiration, improve with movement and pain.
coughing, position (↑↓pain) and weight loss.
Menstruation (31): Age of onset (menarche) and age of
Hoarseness (10): With or without pain (involvement of cessation (menopause). Regularity, duration, amount of
recurrent laryngeal nerve) and other associated features, e.g.
loss and pain (dysmenorrhoea). Inter-menstrual discharge—
neurological.
character, blood or otherwise. Vaginal discharge, quantity,
Throat (10): Soreness, tonsillitis, ulcers, infection. colour (normally clear), smell and irritation. Any hormone
Nasal discharge or obstruction (7): replacement therapy (HRT) and child bearing age.

Bleeding from nose (8): Epistaxis. Periods: Time of menopause


• Post-menopausal bleeding
Sweating (14): Day or night, associated symptoms and
• Last normal menstrual period (LNMP)
amounts.
• Menstrual cycle; number of days or interval, e.g. 4/28
Wheezing (12): Asthma, chest infection, relieving factor, • Regular or irregular
chronic obstructive pulmonary disease (COPD) • Interval longest or shortest, e.g. 21–49
Smoking. • Increase or decrease in flow.

Central Nervous System Questions Locomotor System Questions


Loss of consciousness (1): Sudden, warning, injuries, passage Swelling: One joint or multiple joints.
of urine, duration and after effects. Precipitating factor and • Pain—back (22)
witnesses? • When worse during day. Effects of exercise, lifting, etc.

Mental state (3): Memory, independent opinion of relative or Stiffness: Effect of exercise.
friend sought. Orientation. Previous bone or joint injury: Pain in joints. Where pain is
Headache (2): Character, site, duration, associated symptoms, worse in the morning or later during day or night. Whether
e.g. vomiting, aura and timing. it radiates from one joint to another.
Weakness or paralysis of limbs or any muscles (21): Sudden, Skin Questions
gradual or progressive onset, duration and visual disturbance.
Occupation (32): Exposure to irritants and drugs.
Numbness or ‘pins and needles’ in limbs or elsewhere (22):
Paraesthesia, back pain, diabetes. Rashes: Type, situation, duration, any treatment, painful and
itching (psoriasis).
Giddiness or staggering (5): True vertigo, clumsiness,
staggering and ataxia. Past history:
• Diabetes
Visual disturbance (4): Seeing double (diplopia) dimness, zig • Hypertension
zag figures (fortification spectra). • Rheumatic fever
Deafness or tinnitus (6): Discharge from ears, pain and • Heart disease
hearing loss. • Cystic fibrosis (CF)
4 Hutchison's Paediatrics 

• Spina bifida Table 1.1: History-taking—The paediatric patient


• Other illnesses. • Presenting problem
Illnesses, operations, injuries. Routine X-ray exami­
• History of the presenting problem
nations. In female—obstetrical history: (1) number of
deliveries and abortions, e.g. 3 + 1; (2) type of delivery, • Previous history
spontaneous vertex delivery (SVD), forceps, caesarean; (3) • Pregnancy and delivery
complication of puerperium or pregnancy. • Neonatal period and infancy
• Subsequent development
Family History • Other disorders or diseases
Married, number and health of children, health of partners, • Dietary
any illnesses in parents, grandparents, brothers, sisters, • Immunisation
longevity or short lives, any illnesses similar to patients.
• Family history

Drug History • Parents


• Siblings
• Social and personal history
• Occupation. • Others
• Draw a family tree if indicated
INTRODUCTION
and the parent-child relationship by simply observing the
At all times the doctor must show genuine concern and interest parent(s) and child during the history-taking and physical
when speaking with parents. The parents and the child must examination. Therefore watching, listening and talking are
feel that the doctor has the time, interest and competence of paramount importance in paediatric practice and are
to help them. A physician who greets the child by name invaluable in arriving at a working diagnosis.
irrespective of age will convey an attitude of concern and
interest. Parents tell us about the child’s signs and symptoms Key Learning Point
although children contribute more as they grow older. à Useful information may be obtained by observing the infant
The doctor-patient relationship gradually develops during and young child during the history-taking.
history-taking and physical examination. Considerable tact
and discretion are required when taking the history especially
in the presence of the child: questioning on sensitive subjects History of Present Complaint
should best be reserved for a time when the parents can be Even before language develops in the infant (Latin—without
interviewed alone. It may therefore be necessary to separate speech) parents can detect altered behaviour and observe
the parent and the child-patient when taking the history abnormal physical signs. It is sensible to commence with
especially when the problems are related to behaviour,
the history of the presenting observations because that is
school difficulties and socioeconomic disturbances in the
what the parents have come to talk about. In the newborn
home environment.
infant the history from the attending nurse and medical staff
The medical student having been instructed in the
is important.
history-taking and physical examination of adults needs to
Every endeavour should be made to ask appropriate
appreciate the modifications necessary when dealing with the
questions and discuss relevant points in the history in order
child-patient. A basic template for history-taking is useful
to identify the nature of the child’s problems and come to
and serves as a reminder of the ground to be covered (Table
a tentative diagnosis. Ask what the child is called at home
1.1). Initially the medical student may be confused because
and address the child with this name since otherwise he/she
of the need to obtain information from someone other than
may be less forthcoming. Let the parents give the history
the patient, usually the mother. Useful information may be
obtained by observing the infant and young child during in their own way and then ask specific questions. Ask,
the history-taking. The older child should be given an how severe are the symptoms; have the symptoms changed
opportunity to talk, to present their symptoms and to tell how during the past days, weeks or months; has there been any
they interfere with school and play activities. change recently in the child’s appetite, energy or activities;
The simple act of offering a toy, picture book or pen- has the child been absent from school; has anyone who
torch is often an effective step toward establishing rapport. cares for the child been ill; has the child been thriving or
Rigid adherence to routine is both unnecessary and counter- losing weight; what change in behaviour has there been;
productive. A lot may be learned of the family constellation has there been a change in appetite, in micturition or bowel
 Paediatric History and Examination 5

habits. An articulate older child can describe feelings and should be recorded. Details of any intrapartum or perinatal
symptoms more accurately, as the child’s memory for the problems should be recorded.
time and sequence of events may be more precise, than the
Dietary History
parents.
The duration of breastfeeding should be recorded or the type
Key Learning Point of artificial feed and any weaning problems. The dietary
history can be of major importance in paediatric history-
Establishing rapport
taking. If the patient is neither thriving nor has vomiting,
à The paediatrician should start the interview by welcoming and
diarrhoea, constipation or anaemia then the physician must
establishing rapport with the parent(s) and the child. Always
obtain a detailed dietary history. The dietary history should
refer to the infant or child by name rather than by “him”, “her”
not only include solid foods, but also the consumption of
or “the baby”. Also ask children about their clothes, siblings’
liquid foods and any other supplements, such as vitamins. In
name, friends’ name, their toys, what book, games or TV
this way the quality of the diet and the quantity of nutrients
programers they enjoy. Thus spending sometime at the start of
can be assessed and compared to the recommended intake.
the interview would put both the child and the parents at ease.
Any discrepancy between the actual and recommended intake
may have a possible bearing on the diagnosis.
Past Medical History
Developmental History
The past history is the documentation of significant events
Inquiries about the age at which major developmental
which have happened in the child’s life, and which may be
milestones in infancy and early childhood were achieved
of relevance in coming to a diagnosis. Therefore the doctor are necessary when faced with an infant or child who is
should try to obtain relevant information concerning the past suspected of developmental delay. On the other hand the
from the family and any other sources that are available. child who is doing well at school and whose physical and
It is useful, if the events are recorded in the sequence of social activities are normal, less emphasis on the minutiae
their occurrence. A careful history should contain details of development is needed. Some parents are vague about the
of pregnancy, delivery, neonatal period, early feeding, the time of developmental achievements unless, very recently
child’s achievement of developmental milestones and details acquired, but many have clear recall of the important events
of admissions to hospital, with date, place and reason for such as smiling, sitting and walking independently. It can be
admission. A complete list of current medication including helpful to enquire whether this child’s development paralleled
vitamins and other supplements should be obtained. An that of other children.
enquiry should be made of any drug or other sensitivity
which should always be prominently recorded. Details of Family and Social History
immunisation and all previous infectious diseases should be The health and educational progress of a child is directly
elicited. related to the home and the environment. Medical, financial
and social stresses within the family sometimes have a direct
Key Learning Point
or indirect bearing on the child’s presenting problem. It is,
à Dietary history is of vital importance in paediatric history- therefore, essential to know about the housing conditions and
taking especially if the child is neither thriving nor has some information of parental income and working hours, as
vomiting, diarrhoea, constipation or anaemia. well as the child’s performance in school and adjustment to
playmates.
The family history should be thoroughly evaluated.
Mother’s Pregnancy, Labour, Delivery
The age and health of the close relatives are important to
and the Neonatal Period
record. Height and weight of parents and siblings may be of
The younger the child, the more important is the information help especially when dealing with children of short stature,
about the period of intrauterine life. The history of obesity, failure to thrive, or the infant with an enlarged head.
pregnancy includes obstetric complications during the Consanguinity is common in some cultures and offspring
pregnancy; history of illness, infection or injury and social of consanguineous marriages have an increased chance of
habits, e.g. smoking of the mother are important. Drug or receiving the same recessive gene from each parent and thus
alcohol ingestion and poor diet during pregnancy may have developing a genetically determined disease. Therefore, it is
an adverse effect on the foetus and lead to problems. The important to draw a family tree and to identify children at
estimated length of gestation and the birth weight of the baby high-risk of genetic disease, and to make appropriate referrals.
6 Hutchison's Paediatrics 

Key Learning Point are outwith the 3rd to 97th centile for children of that sex and
age further study is indicated. If previous records of height,
à A history of recent travel abroad, particularly in tropical areas,
weight or head circumference are available for comparison
is important as the child may have a disorder uncommon in
with the current measurements this may provide considerable
his/her own country, but having been contracted in another
help towards diagnosis and management. Inquiry of parental
country where disease may be endemic.
height, weight or head size may also be important, e.g.
familial macrocephaly or constitutional short stature.
Physical Examination
Key Learning Point
The physical examination of the paediatric patient requires
à Allow the child-patient to see and touch the stethoscope,
a careful and gentle approach. It should be carried out in
auriscope, ophthalmoscope and other tools, which are going
an appropriate environment with a selection of books or
to be used during examination. Ask the child, which ear or
toys around, which can be used to allay the apprehension
which part of the body the child would like to be examined
and anxiety of the child. More can be learned by careful
first. It is vital to use the reassuring voice throughout the
inspection than by any other single examination method. The
examination of the child.
baby should be examined in a warm environment in good
light. Nappies must be removed to examine the baby fully.
The doctor must look first at the baby as a whole noting General Inspection
especially the colour, posture and movements. Proceed to a The general appearance of the child may suggest a
more detailed examination starting at the head and working particular syndrome. Does the child look like the
down to the feet “Top to Toe”. rest of the family? The facies may be characteristic in
It is important to realise that the child may be apprehensive Down’s syndrome and other chromosomal disorders
with a stranger, especially when faced with the unfamiliar or in mucopolysaccharidoses. Peculiar odours from an
surroundings of a surgery or hospital outpatient department. infant may provide a clue to diagnosis of aminoacidurias,
It is essential that the doctor be truthful with the child such as maple syrup disease (maple syrup like odour),
regarding what is going to be done. The child should never phenylketonuria (mousy odour), or trimethylaminuria
be made to face sudden unexpected manoeuvres and should (fishy odour). A more detailed examination should then
be allowed to play with objects such as the stethoscope. It be performed. The most valuable of the doctor’s senses
may be useful to let him or her examine a toy animal or doll are his eyes as more can be learned by careful inspection
to facilitate gaining confidence. Infants and young children and also on watching the patient’s reactions than any other
are often best examined on the mother’s lap where they feel single procedure.
more secure. The doctor should ensure that his hands and
instruments used to examine the child are suitably warmed. Colour
It is not always mandatory to remove all the child’s clothes, Should be pink with the exception of the periphery, which
although it is often essential in the examination of the acutely may be slightly blue. Congenital heart disease is only
ill child. Procedures, which may produce discomfort, such as suggested if the baby has central cyanosis. A pale baby may
examination of the throat, ears or rectal examination should be anaemic or ill and requires careful investigation to find
be left until towards the end of the examination. The order of the cause. A blue baby may have either a cardiac anomaly
the examination may be varied to suit the particular child’s or respiratory problems and rarely methaemoglobinaemia.
needs. Awareness of the normal variations at different ages
is important. Key Learning Point
A thorough physical examination is a powerful Central cyanosis
therapeutic tool especially if the problem is one primarily à Central cyanosis in a child of any age should always raise
of inappropriate parental anxiety. Understandably parents the possibility of congenital heart disease. Ideally, the best
do not usually accept reassurance, if the doctor has not areas to look for central cyanosis are the tongue and buccal
examined the child properly. Examination of the infant or mucosa, not the limbs and the nails.
child is often preceded by recording the patient’s height,
weight and head circumference on the growth chart. This
may have been done by a nurse before the doctor sees the Posture and Movements
family. These measurements are plotted on graphs or charts, A term baby lies supine for the first day or two and has
which indicate the percentiles or standard deviations at the vigorous, often asymmetric movements of all limbs. In
various ages throughout childhood. If these measurements contrast a sick baby adopts the frog position with legs
 Paediatric History and Examination 7

abducted, externally rotated and is inactive. Older infants


and children should be observed for abnormal movements,
posture and gait.

Key Learning Points


à Always leave the most upsetting parts of the examination until
the end, such as inspection of the throat or taking the blood
pressure.
à If epiglottitis is a possibility do not examine the throat because
obstruction may be precipitated

Skin
The skin is a major body organ which, because of the
larger surface area in relationship to weight, of the young
means that the skin is relatively more important in the
immature. It forms a barrier against environmental attack Fig. 1.1: Top of head anterior fontanelle and cranial sutures
and its structure and function reflects the general health of
the child, i.e. in states of malnutrition and dehydration. Head
The presence of any skin rash, its colour and whether there The head should be inspected for size, shape and symmetry.
are present macules, papules, vesicles, bullae, petechiae Measurement of the head circumference [occipitofrontal
or pustules should be recorded (Table 1.2). The skin circumference (OFC)] with a non-elastic tape by placing
texture, elasticity, tone and subcutaneous thickness should it to encircle the head just above the eyebrows around
be assessed by picking up the skin between the fingers. maximum protuberance of the occipital bone should be
Pigmented naevi, strawberry naevi, haemangiomata or performed and charted. In the infant the skull should be
lymphangiomata may be present and may vary in size and palpated to determine the size and tension in the fontanelles
number. They may be absent or small at birth and grow in and assess the skull sutures (Fig. 1.1). Premature fusion of
subsequent days or weeks. sutures suggests craniostenosis. In the neonate the posterior
fontanelle may be very small and subsequently closes by
Key Learning Point
3 months of age, but the anterior fontanelle is larger, only
Port-wine stain closing at around 18 months. A tense and bulging fontanelle
à Unilateral port- wine stain over the distribution of the ophthalmic suggests raised intracranial pressure and a deeply sunken one
division of the trigeminal nerve is usually a manifestation of suggests dehydration.
Sturge-Weber syndrome. It may be associated with seizures, Large fontanelles, separation of sutures, delayed closure
glaucoma, hemiparesis and mental retardation. of the fontanelles may be associated with raised intracranial

Table 1.2: Dermatological terminology

Terminology Definition
Macule Area of discoloration, any size, not raised-flat with skin
Papule Small raised lesion (< 5 mm)
Petechiae Haemorrhage in skin, non-blanching (< 1 mm)
Purpura Haemorrhage in skin, non-blanching (2–10 mm in diameter)
Ecchymoses Large bruise, non-blanching
Vesicle Small blister, elevated, fluid-filled (< 5 mm)
Bullae Large blister, elevated, fluid-filled (> 5 mm)
Weal Elevation in skin, due to acute oedema in dermis, surrounding erythematous macule
Pustule Elevated, pus-filled
Lichenification Thickened skin, normal lines in skin more apparent
8 Hutchison's Paediatrics 

Key Learning Point


Hearing deficit
à A number of children with hearing deficits may not be
diagnosed until they are 2 years of age. The main pointers
to hearing deficits include parental concern about their child’s
hearing, speech delay, and lack of developmental markers of
hearing.

Eyes
These should be inspected for subconjuctival haemorrhages
which are usually of little importance, for cataracts,
for papilloedema and congenital abnormalities, such as
colobomata (Figs 1.3A and B). ‘Rocking’ the baby from the
supine to vertical position often results in the eyes opening
so they can be inspected. Squint is a condition in which early
diagnosis and treatment is important. There are two simple
tests which can be carried out to determine whether or not a
Fig. 1.2: Method of restraining a child for examination of the ear squint is present.
pressure or other systemic disorders, such as hypothyroidism 1. The position of the “corneal light reflection” should
and rickets. normally be in the centre of each pupil if the eyes are both
aligned on a bright source of light, usually a pen torch.
Key Learning Point Should one eye be squinting then the reflection of the light
Occipitofrontal circumference from the cornea will not be centred in the pupil of that
à An abnormally “large head” (more than 97th centile or 2 eye. It will be displaced outwards, if the eye is convergent
SD above the mean) is due to macrocephaly, which may and inwards towards the nose, if the eye is divergent. It
be due to hydrocephalus, subdural haematoma or inherited may be displaced by such a large amount that it is seen
syndromes. Familial macrocephaly (autosomal dominant) is a over the iris or even over the sclera, where of course it
benign familial condition with normal brain growth. may be rather more difficult to identify, but with such
obvious squints the diagnosis is usually not in doubt.
Ears 2. In the “cover test” one chooses an object of interest
for the child, e.g. a brightly coloured toy with moving
Position and configuration of the ears should be observed. components. When the child is looking at the object of
Whilst abnormalities, such as low setting of the ears is
interest the eye thought to be straight is covered with
frequently associated with renal tract anomalies absence
an opaque card and the uncovered eye is observed to
of an ear or non-development of the auricle will require
see whether it moves to take up fixation on the object
early referral to an otolaryngologist. It often requires
of interest. If the child has a convergent squint then the
the parent to hold the child on his or her lap and provide
reassurance during the examination. Methods of doing eye will move laterally to take up fixation, and this is the
this are illustrated in Figure 1.2. Parents are usually very usual situation, since convergent squints are four times
competent in detecting hearing impairment. The exception more common than divergent squints. If the eye were
to this is where the child is mentally retarded. All infants divergent it would move medially.
should be given a screening test for hearing at 6 months of The most common cause for apparent blindness in young
age. Simple testing materials are required, e.g. a cup and children is developmental delay. Assessment of whether a
spoon, high and low pitched rattles, and devices to imitate young baby can see is notoriously difficult, fixation should
bird or animal sounds, or even snapping of finger tips are develop in the first week of life, but an early negative
usually effective if hearing is normal. The sounds should response is of no value as the absence of convincing evidence
be made quietly at a distance of 2–3 feet out of view of the of fixation is not synonymous with blindness. The failure
child. By 6 months of age a child should be able to localise to develop a fixation reflex results in ocular nystagmus, but
sound. To pass the screening test the child should turn and these roving eye movements do not appear until the age of
look directly at the source of the sound. 3 months.
 Paediatric History and Examination 9

Fig. 1.4: Gingival hyperplasia caused by phenytoin

Face
A Abnormalities of facial development are usually obvious and
an example is the infant with cleft lip. Associated with this
there may be a cleft palate, but full visual examination of
the palate including the uvula is necessary to ensure that the
palate is intact and there is not a submucous cleft of the soft
palate or a posterior cleft. Submucous and soft palate clefts
cannot be felt on palpation.

Mouth
Inspection of the mouth should include visualisation of the
palate, fauces, gum disease and the dentition (Fig. 1.4).
A cleft lip is obvious, but the palate must be visualised to
exclude a cleft. The mouth is best opened by pressing down
in the middle of the lower jaw. A baby is rarely born with
teeth, but if present these are almost always the lower central
incisors. The soft palate should be inspected to exclude the
possibility of a submucous cleft which could be suggested
by a bifid uvula. Small fibromata are sometimes seen in the
B gums. They are white and seldom require treatment. These
Figs 1.3A and B: (A) Congenital cataract and (B) Papilloedema are normal. The lower jaw should be seen in profile as a
receding chin (micrognathia) may be the cause of tongue
A misleading response may be obtained when a bright swallowing or glossoptosis (Pierre Robin syndrome) and it
light stimulus is applied to a child preferably in a dimly may be associated with a cleft palate.
lit room. The normal response is a blinking or “screwing
up” the eyes and occasionally by withdrawing the head. Neck
This is a subcortical reflex response and may be present
Examination of the neck may reveal congenital goitre and
in babies despite them having cortical blindness. The
midline cysts which may be thyroglossal or dermoid in
absence of this response increases the probability of
origin. Lateral cysts, which may be of branchial origin or
blindness.
sometimes there may be extensive swellings, which may
Key Learning Point be cystic hygroma or lymphangiomata. In early infancy a
Distraction and play sternomastoid tumour may be palpable in the mid region of
à If the doctor cannot distract the infant or make the awake the sternomastoid muscle. Associated with this there may
“infant” attend to an object, look at the paediatrician’s face, or be significant limitation of rotation and lateral flexion of the
a sound, consider a possible visual or hearing deficit. neck. Palpation along the clavicle will define any tenderness
or swelling suggestive of recent or older fractures.
10 Hutchison's Paediatrics 

collapse of the right lung. All areas should be auscultated


while the baby is quiet systolic murmurs may be very harsh
and can be confused with breath sounds.

Lungs
Small children frequently cry when the chest is percussed
and when a cold stethoscope is applied. If the mother holds
the child over her shoulder and soothes him, it is often easier
to perform a thorough chest examination. Light percussion
can be more valuable than auscultation in some situations,
but the basic signs are similar to those found in an adult.
Breath sounds are usually harsh, high pitched and rapid. Any
adventitious sounds present are pathological. Percussion of
the chest may be helpful to pick up the presence of a pleural
Fig. 1.5: Pectus excavatum (funnel-chest) effusion (stony dull), collapse, consolidation of a lung (dull)
or a pneumothorax (hyper-resonant). These pathological
Chest
states are usually associated with an increase in the respiratory
The shape, chest wall movement and the nature and rate of rate, as well as clinical signs of respiratory distress.
the breathing (30–40 per minute) as well as the presence
of any indrawing of the sternum and rib cage should be Abdomen
noted. In a normal baby without respiratory or abdominal In the infant the abdomen and umbilicus are inspected and
problems the abdomen moves freely during breathing and attention should be paid to the presence of either a scaphoid
there is very little chest movement. Most of the movements abdomen, which in a neonate may be one of the signs of
of the breathing cycle are carried out by the movement of the diaphragmatic hernia or duodenal atresia or a distended
diaphragm. The nipples and axilliary folds should be assessed abdomen, which suggests intestinal obstruction, especially
to exclude conditions, such as absent pectoral muscles. In if visible peristalsis can be seen. Peristalsis from left to right
Poland syndrome there is amastia, associated with ipsilateral suggests a high intestinal obstruction whereas one from the
absence of sternal head of pectoralis major. Ten per cent right to the left would be more in keeping with low intestinal
may have dextrocardia, dextroversion, or syndactyly. obstruction. Any asymmetry of the abdomen may indicate
Anterior chest wall deformities, such as pectus excavatum the presence of an underlying mass. Abdominal movement
(funnel chest) and pectus carinatum (Pigeon chest) should be should be assessed and abdominal palpation should be
recorded (Fig. 1.5). performed with warm hands.
Palpation of the abdomen should include palpation for the
Cardiovascular liver, the edge of which is normally felt in the new born baby,
Examination of the cardiovascular system of infants and the spleen which can only be felt if it is pathological and the
children is carried out in a similar manner to that of adults. The kidneys which can be felt in the first 24 hours with the fingers
examiner should always feel for femoral pulses and ascertain and thumb palpating in the renal angle and abdomen on each
whether there is any radiofemoral or brachiofemoral delay as side. The lower abdomen should be palpated for the bladder
this would suggest the possibility of coarctation of the aorta. and an enlargement can be confirmed by percussion from a
The most important factor in recording the blood pressure of resonant zone, progressing to a dull zone. In the baby with
children is to use a cuff of the correct size. The cuff should abdominal distension where there is suspicion of perforation
cover at least two-thirds of the upper arm. If the cuff size and free gas in the abdomen, the loss of superficial liver
is less than this a falsely high blood pressure reading may dullness on percussion may be the only physical sign present
be obtained. In small infants relatively accurate systolic and early on. Areas of tenderness can be elicited by watching
diastolic pressures as well as mean arterial pressure can be the baby’s reaction to gentle palpation of the abdomen.
obtained by use of the Doppler method. The apex should be There may be areas of erythema, cellulitis, and oedema of
visible and palpable and the position noted. The precordial the abdominal wall and on deeper palpation crepitus can
areas should be palpated for the presence of thrills. If the occasionally be felt from pneumatosis intestinalis (intramural
apex beat is not obvious look for it on the right side of the gas in the wall of the bowel).
chest as there could be dextrocardia or a left-sided congenital Auscultation of the abdomen in the younger patients
diaphragmatic hernia with the heart pushed to the right or gives rather different signs than in the adult. The infant even
 Paediatric History and Examination 11

Limbs
Upper and lower limbs are examined in detail. Hands and
feet should be examined for signs and those experienced in
dermatoglyphics may define a finger print pattern which is
consistent in various syndromes. The presence of a simian
palmar crease may suggest trisomy 21 (Down’s syndrome) and
thumb clenching with neurological disease. The feet, ankles
and knees should be examined for the range of movement in
the joints and tone of the muscles. The femoral head may be
outside the acetabulum at birth in true dislocation of the hip or
it may be dislocated over the posterior lip of the acetabulum
by manipulation, in which case the hip is described as
unstable, dislocatable or lax. There are conditions in which
Fig. 1.6: Ambiguous genitalia in a 10-year-old girl (clitromegaly, labial the acetabulum is hypoplastic and shallow and the femoral
fusion and empty scrotal folds of virilised female) head itself is distorted. Congenital dislocation of the hip is
more common after breech deliveries in girls and in certain
in the presence of peritonitis may have some bowel sounds parts of the world. All newborn infants should be screened
present. However, in the presence of ileus or peritonitis shortly after birth. The infant is placed supine with the legs
breath sounds become conducted down over the abdomen to towards the examiner and each hip is examined separately.
the suprapubic area and in even more severe disorders the The knee and hip of the baby are flexed to 90% and the
heart sounds similarly can be heard extending down over the hip fully abducted by placing the middle finger over the
abdomen to the suprapubic area. greater trochanter and the thumb on the inner side of the
Perineal examination is important in both sexes. thigh opposite to the position of the lesser trochanter. When
Examination of the anus should never be omitted. the thigh is in the mid-abducted position, forward pressure
Occasionally the anus is ectopic, e.g. placed more anteriorly is exerted behind the greater trochanter by the middle finger.
than it should be, stenotic or even absent. The rectal The other hand holds the opposite femur and pelvis steady. A
examination is an invasive procedure and should be carried dislocated femoral head is felt to slip over the acetabular ridge
out in a comfortable warm environment, preferably with the and back into the acetabulum as a definite movement. This
child in the left lateral position and the mother holding the part of the test is called the Ortolani manoeuvre. The second
hand of the child at the top end of the bed. part of the test is the Barlow procedure. With the infant still
The testes in boys born at term should be in the scrotum. on his back and the legs and hands in the same position the
The prepuce cannot be and should not be retracted. It is hip is brought into the position of mid-abduction with the
several months or years before the prepuce can be retracted thumb exerting gentle pressure laterally and posteriorly; at
and stretching is both harmful and unnecessary. In girls the the same time the palm exerts posterior and medial pressure.
labia should be separated and genitalia examined. If a hip is dislocatable the femur can be felt to dislocate over
The presence of a swelling in the scrotum or high in the posterior lip of the acetabulum. There is need for caution
the groin may suggest torsion of a testis and requires in performing this test and no force should be employed.
urgent attention. The testis which cannot be palpated in the Caution is particularly required in infants born with neural
scrotum and cannot be manipulated into the sac indicates the tube defects and paralysis of the lower limbs.
presence of an undescended testis which needs to be explored The knees, ankles and feet should be examined.
and corrected before the age of 2 years. A swelling in the Dorsiflexion of the feet should allow the lateral border to
scrotum which has a bluish hue to it suggests the presence come in contact with the peroneal compartment of the leg.
of a hydrocoele due to a patent processus vaginalis and one Failure indicates a degree of talipes equinovarus (TEV)
can get above such a swelling in most children. Palpation which is of concern to the parents although with simple
of the scrotum is initially for testes but if gonads are not physiotherapy there are seldom long-term problems in the
present then palpation in the inguinal, femoral and perineal absence of underlying neurological abnormality.
regions to determine presence of undescended or ectopic
Spine
testes should be carried out.
Conditions, such as hypospadias, epispadias, labial With the baby held face-downwards fingers should be run
adhesions or imperforate hymen or ambiguous genitalia along the spine excluding spinal defects, such as spina bifida
should be diagnosed on inspection (Fig. 1.6). occulta and noting the presence of the common post-anal
12 Hutchison's Paediatrics 

dimple, a tuft of hair, a pad of fat and haemangioma. A so that his feet are touching a firm surface he will raise one
Mongolian blue spot is commonly seen over the sacrum in leg and hesitatingly put it down in front of the other leg,
Asian babies. The presence of a posterior coccygeal dimple taking giant strides forwards. This is the “primitive walking
or a sacral pit is common in babies and is due to tethering reflex”.
of the skin to the coccyx. When one stretches the skin and Tendon reflexes, such as the biceps and knee jerks
the base of the pit can be seen then nothing needs to be are easily obtainable but the ankle and triceps jerks are
done about it. Very rarely there is communication with the not readily elicited. Important as an indication of nervous
spinal canal which could be the source of infection and cause system malfunction are muscle tone, posture, movement
meningitis. and the primitive reflexes of the newborn that have been
described. Plantar reflex is usually extensor and is of
Stool and Urine Examination
little diagnostic importance in the first year. Delay in
Examination of a stool which is preferably fresh is often disappearance of the primitive reflexes suggests cerebral
informative. The colour, consistency and smell are noted as damage.
well as the presence of blood or mucus. Urine examination
is also important in children since symptoms related to the A GUIDE TO EXAMINATION OF A CHILD-PATIENT
urinary tract may be nonspecific.
Checklist of Bodily Systems
Neurological Examination
General Examination
The neurological examination of the young infant and child is
different from that routinely carried out in the adult. Muscle • Is the child unwell, breathless or distressed?
tone and strength are important parts of the examination. In • Level of consciousness
infants muscle tone may be influenced by the child’s state • Is the child cyanosed, pale or jaundiced (in carotinaemia
of relaxation. An agitated hungry infant may appear to be the sclerae are not yellow)?
hypertonic, but when examined in a cheerful post-prandial • ENT examination: Child’s ears, nose and throat
state the tone reverts to being normal. The examination of • Is the child dehydrated?: Skin turgor, sunken eyes,
the neurological system cannot be complete without the sunken fontanelle
evaluation of the child’s development level relating to gross • Nutritional state
• Peripheral perfusion: Capillary refill time should occur
motor, fine motor and vision, hearing and speech and social
within 2 seconds
skills. All older children should be observed for gait to detect
• Does the child have any dysmorphic features, i.e. an
abnormal coordination and balance.
obvious syndrome?
Older children may be tested for sense of touch and
• Check blood pressure, temperature and pulses, i.e. radial
proprioception as in adults. Tests of sensation as well as
and femoral
motor power must be performed in the paediatric patient,
• Hands: For clubbing (look at all fingers), peripheral
but are difficult to assess in the very young child. The
cyanosis, absent nails (ectodermal dysplasia), pitted nails
normal newborn has a large number of primitive reflexes
(psoriasis), splinter haemorrhages (Fig. 1.7).
(Moro, asymmetric tonic neck, glabellar tap, sucking and
rooting process). The “Moro-reflex” is a mass reflex,
which is present in the early weeks after birth. Its absence
suggests cerebral damage. It consists of throwing out of the
arms followed by bringing them together in an embracing
movement. It can be demonstrated by making a loud noise
near the child. The “sucking reflex” is present at birth in
the normal baby as is the “swallowing reflex”. If the angle
of the baby’s mouth is touched by the finger or teat the baby
will turn his head towards it and search for it. It is looking
for its mother’s nipple and is known as the “rooting or
searching reflex”.
The grasp reflex is illustrated by gently stroking the back
of the hand so that the fingers extend and on placing a finger
on the palm of the baby it takes a firm grip. Similar reflexes
are present in the toes. If the baby is held up under the arms Fig. 1.7: Finger clubbing in cystic fibrosis
 Paediatric History and Examination 13

A
A

B B
Figs 1.8A and B: (A) Hyperextensible skin and (B) Genu recurvatum Figs 1.9A and B: Goitre in Hashimoto’s thyroiditis:
in Ehlers-Danlos syndrome (A) AP neck and (B) Lateral view neck

• Height, weight and head circumference (OFC): Plot • Head circumference: Measure the child’s OFC and
these on a percentile chart plot it on a growth chart (if not done under general
• Rash: Generalised or localised, bruises, petechiae, examination).
purpura, birth marks (learn dermatological terminology
(Table 1.2) Neck
• Abnormal pigmentation: Café au lait spots, Mongolian • Short, webbed (Turner syndrome), torticollis
blue spots, elasticity of skin and hypermobility of joints • Thyroid: Enlarged, bruit
(Figs 1.8A and B) • Swellings:
• Palpate for lymph nodes in the neck (from behind), • Midline: Thyroglossal cyst, goitre (Figs 1.9A and B)
axillae, groins any subcutaneous nodules • Lateral: lymph nodes, branchial cyst, cystic hygroma,
• Teeth: Any dental caries, a torn lip frenulum (physical sternomastoid tumour.
abuse)
• Genitalia: Injuries to genitalia or anus—sexual abuse RESPIRATORY SYSTEM
• Head shape: Normal, small (microcephaly, large
(macrocephaly), plagiocephaly, brachycephaly, oxycephaly Inspection
(turricephaly). Feel the sutures. Is there evidence of • Use of accessory muscles of respiration
craniostenosis? • Intercostal recession, any stridor, audible wheeze
• Hair: alopecia, seborrhoea of the scalp • Shape: Normal, zpectus carinatum (undue prominence of
• Eyes: subconjunctival haemorrhage, ptosis, proptosis, the sternum-pigeon chest, pectus excavatum (funnel chest),
squint, nystagmus, cataract, aniridia, optic fundi Harrison’s sulci, hyperinflation (increased anteroposterior
• Mouth: thrush, fauces, tonsils, teeth, palate diameter)
• Ears: normal, low-set, shape, pre-auricular skin tags • Count the respiratory rate
• Anterior fontanelle: diamond shaped, open, closed, • Scars of past surgery (look at the front and the back of the
sunken, bulging, tense chest).
14 Hutchison's Paediatrics 

Palpation GASTROINTESTINAL SYSTEM


• Chest wall movement: Is it symmetrical?
Inspection
• Feel the trachea: Central or deviated
• Tactile vocal fremitus (over 5 years of age—ask the child • General distension
to say 99). • Superficial veins—direction of flow, striae, umbilicus
• Masses, scars, visible peristalsis.
Percussion
Palpation and Percussion
• Percuss all areas: Normal, resonant, hyper-resonant, dull
(collapse, consolidation), stony dull (pleural effusion). • First lightly palpate the entire abdomen, keep looking at
the child’s face all the time
Auscultation • Localised tenderness, rebound tenderness and rigidity
• Air entry, vesicular (normal), absent breath sounds • Masses
(pleural effusion) and bronchial (consolidation) • Ascites—percuss for the shifting dullness
• Added sounds: Wheeze, inspiratory or expiratory, • Spleen, liver and kidneys
crackles (fine versus coarse), pleural friction rub • Hernial orifices
• Vocal resonance. • Genitalia (testes) and anus (site).

CARDIOVASCULAR SYSTEM Auscultation


Bowel sounds: absence implies ileus.
Inspection
• Are there features of Down’s (ASD, VSD), Turner’s NERVOUS SYSTEM
(coarctation of the aorta), or Marfan’s (aortic
• Level of consciousness
incompetence)
• Right or left handed
• Cyanosis: peripheral and central
• Orientation, memory (past and present)
• Hands: clubbing and splinter haemorrhages (endocarditis)
• Speech
• Oedema: praecordium, ankles and sacrum • Posture.
• Praecordium for scars of past surgery.
Cranial Nerve
Palpation
1st Smell-ability of each nostril to different smells
• Pulses: radial/brachial/femoral—radiofemoral delay (syn­
2nd Visual acuity, visual fields, pupils (size, shape,
chrony of the two pulses), rate
reaction to light and consensual); Fundoscopy:
• Character of pulse—collapsing, volume
papilloedema, optic atrophy, cataract
• Heart rate—rhythm 3rd Palsy: Unilateral ptosis, fixed dilated pupil, eye
• Apex beat: Position (normal position in children 4th–5th down and out
left intercostal space in the mid-clavicular line), beware 4th Palsy: Diplopia on looking down and away from
of dextrocardia the affected side
• Palpate for a parasternal heave and for precordial thrills. 5th Palsy: motor-jaw deviates to the side of lesion
Sensory: corneal reflex lost
PERCUSSION OF THE HEART IS NOT NORMALLY 6th Palsy: convergent squint
UNDERTAKEN IN CHILDREN 7th Facial nerve lesions: weakness
Only the lower two-thirds is affected in UMN
Auscultation
lesions, but all of one side of the face in LMN
• Listen to all four valve areas (apex, lower L sternal edge, lesions. Ask the child to screw-up eyes, raise
upper L sternal edge, and upper R sternal edge eyebrows, blow out cheeks, and show teeth
• Quality of heart sounds 8th Hearing, balance and posture
• Additional sounds, i.e. clicks, murmur (timing of the 9th and
murmur) 10th Gag reflex: look at palatal movement
• Blood pressure—use a cuff that covers at least two-thirds 11th Trapezii: shrug your shoulders
of the upper arm or use Doppler. 12th Tongue movement: deviates to the side of lesion
 Paediatric History and Examination 15

Cerebellar Function DEVELOPMENTAL ASSESSMENT


• Jerk nystagmus (worse on gaze away from midline) This should be carried out under four headings: gross
• Truncal ataxia (if worse when eyes closed then lesion is motor, fine motor and vision, hearing, and speech and social
of dorsal columns; not cerebellum) behaviour. These milestones are based for a child who is
• Intention tremor: ask the child to pick up a small object aged 6 weeks to 5 years.
and watch for tremor
• Past pointing: ask the child to cover one eye with one Birth to Six Weeks
hand and with the index finger of the other hand ask him
to touch his nose and then touch your finger Gross Motor
• Gait: ask the child to walk normally and then walk Marked head lag at birth on pulling to sit. By 6 weeks moderate
heel—toe look for ataxic gait. head lag on pull to sit prone, brings chin momentarily off
couch.
LOCOMOTOR SYSTEM
Fine Motor and Vision
Arms • Can see at birth
• Tone, muscle bulk, muscle power—oppose each move­ • By 6 weeks, can fix and follow across to 90°.
ment
• Joints: hands swollen/tender metacarpophalangeal Hearing and Speech
(MCP)/proximal interphalangeal (PIP) joints, test joints • Can hear at birth
for hypermobility • Startles and quietens to a soothing voice.
• Reflexes: biceps (C5, 6) and triceps (C7, 8)—compare
both sides Social Behaviour
• Hand: ask child to squeeze fingers or spread fingers
• Stops crying when picked up
• Coordination: finger-nose touching
• By 6 weeks, smiling to familiar noises and faces.
• Sensation: test light touch.

Legs Three to Six Months

• Tone, quadriceps or gastrocnemius bulk Gross Motor


• Power—oppose each movement • By 3 months, on ventral suspension brings head above
• Coordination—rub heel up and down shin (“heel-shin test”) level of back
• Joints: Swollen, tender, patella tap test (effusion in • Prone lifts head and upper chest off couch
knee) • By 6 months, sits with support or tripod sits
• Reflexes: Knee (L3, 4), ankle (S1, 2), plantar reflex—the • Beginning to weight bear. Rises to stand when supported.
plantar is normally up-going in infants until they begin to
walk Fine Motor and Vision
• Feet: Any deformity are arches high or low. • By 3 months, holds hands loosely open and has hand
regard
Sensation • By 6 months, reaches for toys with palmar grasp
• Joint position sense • Transfers hand-to-hand and hand-to-mouth.
• Fine touch discrimination.
Hearing and Speech
Gait • Can laugh, gurgle and coo
Ask the child to walk normally across room. • Starts to babble around 6 months. Will turn when called.

Gower’s Sign Social Behaviour


Ask the child to stand from supine. A child will normally • Holds on to bottle or feeding cup when fed
sit up from lying, and then stand. In Duchenne muscular • Frolics when played with
dystrophy, the child will have to roll over onto their front • Examines and plays with hands and places feet in
and then climb up their legs. mouth.
16 Hutchison's Paediatrics 

Six to Nine Months Social Behaviour


Gross Motor • Enjoys imitative games, such as clapping hands and
• By 6 months can roll from front to back waving goodbye
• Sits unsupported with a straight back • Shy with strangers until the end of the first year.
• Begins to pivot around on arms and legs into the crawling
Twelve to Eighteen Months
position.
Gross Motor
Fine Motor and Vision • By 12 months, can walk with hands held and begins to
• Small objects picked up between index finger and thumb stand alone
in a pincer grasp • By 18 months, climbs onto chair and up stairs. Holds on
• Transfers from hand-to-hand. to toys while walking.

Hearing and Speech Fine Motor and Vision


• By 9 months, shouts to gain attention • Pincer grip refined. Tiny objects can be picked up
• Vocalises nonspecific syllables such as “dada” and delicately
“mama”. • Points at objects with index finger
• Can be persuaded to give objects to another on request
Social Behaviour • Builds a tower of two or three bricks.
• Turns when talked to Hearing and Speech
• Resists when objects taken away
• Tries to reach for objects out of reach • Vocabulary of several words
• Likes to feed with fingers. • Comprehension is more advanced than speech at this age
• Enjoys looking at pictures on a book and points and
Nine to Twelve Months babbles while doing this.

Gross Motor Social Behaviour


• By 9–10 months most infants are crawling • By 12 months indicates wants, usually by pointing
• Of 10% normal infants never crawl, but move around by • Drinks from a cup and helps to feed themselves
rolling, padding or bottom shuffling. These children are • Begins to help with dressing
often late walkers and may not walk alone until 2 years • Learns to throw
of age • Enjoys simple games such as peek-a-boo.
• By 9–12 months, begins to pull to standing and cruise.
Two Years
Key Learning Point
Gross Motor
à Delayed walking could be due to the fact that the child
is a bottom shuffler. There is a family history of bottom Can walk, run, squat and climb stairs two feet per step.
shuffling. It is autosomal dominant in inheritance. Rest of the
developmental milestones is within the normal range. Fine Motor and Vision
• Builds tower of six or seven cubes
• Spontaneous scribbling
Fine Motor and Vision
• Hand preference
• Will bang two cubes together • Holds pencil with thumb and first two fingers
• Looks for fallen objects. • Imitates vertical lines.

Hearing and Speech Hearing and Speech


By 9–12 months, usually have 1 or 2 recognisable words in Uses 50 or more recognisable words and understands many
addition to “mama” and “dada”. more
 Paediatric History and Examination 17

• Forms simple sentences • Picks up very small objects and threads beads
• Carry out simple instructions. • Knows four primary colours.

Social Behaviour Hearing and Speech


• Feeds with a spoon, drinks from a cup • Intelligible speech
• Usually dry through day (variable) • Knows name, address and usually age
• Demands mother’s attention • Listens to and tells stories
• Tantrums when frustrated • Enjoys jokes.
• Instant gratification.
Social Behaviour
Three Years
• May wash, dress, undress, but not yet manage laces
Gross Motor • Understand taking turns, as well as sharing
• Climbs stairs one foot per step • Appreciates past, present and future time.
• Pedals a tricycle
• Kicks a ball. Five Years
Gross Motor
Fine Motor and Vision
• Catches a ball.
• Copies a circle, imitates a cross
• Builds a tower of nine cubes
• Threads beads. Fine Motor and Vision
• Draws triangle and detailed man.
Hearing and Speech
• Speaks in sentences and may know a few colours Hearing and Speech
• Recites nursery rhymes • Clear speech.
• Counts to 10.
Social Behaviour
Social Behaviour
• Comforts others
• Eats with fork and spoon
• Group play.
• Dry through night
• Likes to help in adult activities
Primitive Reflexes
• Vivid imaginary play
• Joins in play with others. • Rooting reflex: Appears at birth, disappears at 4
months
Four Years • Palmar/plantar reflex: Appears at birth, disappears at 4
Gross Motor months
• Stepping reflex: Appears at birth, disappears at 4
• Walks up and down stairs one foot per step months
• May hop. • Moro reflex: Appears at birth, disappears at 4 months
• Tonic neck reflex: Appears at 1 month, disappears at 6
Fine Motor and Vision months
• Copies cross (also VTHO) • Delay in disappearance of the primitive reflexes suggests
• Draws a man with head, legs and trunks cerebral damage
Louis Low

C H A P T E R
Growth and Development 2
NORMAL GROWTH any single intervention. Nutritional deprivation during
pregnancy can have an epigenetic effect on foetal growth
Human growth is determined by an interaction of genetic extending over many generations. Studies from Netherlands
and environmental factors. The infancy-childhood-puberty have shown that maternal smoking and cannabis use in
(ICP) growth model breaks down the human linear pregnancy results in significant foetal growth retardation,
growth curve into three additive and partly superimposed which is progressive through gestation. Cytokines are
components (Fig. 2.1). There are different growth essential for implantation and insulin-like growth factor
promotion systems for each component. The infancy phase 2 (IGF-2) is important for placental growth. Apart from
describes the period of rapid growth in utero and in infancy nutrition, hormones and growth factors have an important
and this phase of growth is predominantly nutritionally role in the control of foetal growth. Foetal insulin secretion
dependent. Maternal nutrition before and during pregnancy is dependent on the placental nutrition supply and foetal
are important determinants of foetal growth and low hyperinsulinaemia, which stimulates cell proliferation and
pre-pregnancy weight increases the risk of intrauterine foetal fat accumulation from 28 weeks gestation onwards.
growth retardation (OR 2.55). An additional intake of 300 Thyroid hormone, which affects cell differentiation and
Kcal and 15 g of protein per day are recommended for brain development, is also regulated by nutrition. Cortisol
pregnant mothers above the recommended intake for non- is essential for the pre-partum maturation of different
pregnant women. Nutrient supply to the growing foetus is organs including the liver, lung, gut and pituitary gland.
the dominant determinant in foetal growth, which is also Although growth hormone (GH) is important in post-natal
dependent in placental function. Multiple approaches of growth, it plays an insignificant role in foetal growth except
nutritional intervention, control of infection and improved for an effect on foetal fat content. Animal knockout studies
antenatal care to pregnant women are more effective than and human observations have shown that IGFs are most
important for metabolic, mitogenic and differentiative
activities of the foetus. Insulin-like growth factor-2 is more
important in early embryogenesis. In humans, foetal body
weight is more closely correlated with the concentration of
foetal serum IGF 1 than IGF 2.
In the childhood phase of growth, hormones like growth
hormone, thyroid hormone and growth factors like IGF
begin to exert their influence from the end of the first year of
life. A delay in the onset of the childhood phase of growth
results in faltering of growth during this critical period.
The growth faltering commonly observed between 6 and 18
months of life in children from developing countries are due
to nutritional and socioeconomic factors rather than ethnic
differences. The importance of the growth hormone and
Fig. 2.1: Analysis of linear growth using a mathematical model IGF 1 axis and other hormones in the childhood phase of
(Courtesy: J Karlberg, et al. Acta Paediatrica Scand. 1987;76:478) growth is described in a subsequent section of this chapter.
 Growth and Development 19

Short-lived growth acceleration between 7 and 8 years of age in Asia in 2005. With the improvement in socioeconomic
can be observed in two-thirds of healthy children followed conditions and healthcare in most countries, there is a
by a fall in growth velocity before the onset of puberty. The dramatic secular increase in mean stature of populations
pubertal phase of growth is controlled by nutrition, health, from Asia and other developing countries, while the positive
GH-IGF 1 axis and pubertal secretion of adrenal androgens secular trends in growth have slowed or even plateaued in
and sex steroids. The onset of the childhood component has developed countries in Europe and North America.
been known to be positively associated with the magnitude Although, malnutrition remains a problem in some parts
of the foetal or infancy component. The height at onset of of the world, there is now a worldwide obesity epidemic
puberty is an important determinant of the final adult height. in both developing and developed countries. The reason for
The onset of puberty component is negatively correlated with the increase in body weight in children in the community
the height at onset of puberty. is multifactorial including genetic, cultural differences and
The United Nations Children’s Fund (UNICEF) has dietary changes especially increase in intake of high fat
identified access to nutritionally adequate diet, health care energy dense foods, but most importantly the increasing
for mothers and children, and environmental health factors sedentary lifestyle adopted by different sectors of the
as conditioning factors of child growth worldwide. The population. The decrease in daily physical activity is due to
care required includes care of women in the reproductive mechanisation and computerisation. Time spent in watching
age, breastfeeding and feeding practices, psychological television and playing or working on the computer is now
care, food preparation, hygiene and home health practices. regarded as a surrogate marker of inactivity in children.
Low food intake and the burden of common childhood The health burden of excessive weight gain in childhood
infectious diseases, diarrhoea, respiratory infections and will be amplified in the years to come and urgent action by
infestations limit the full realisation of the genetic potential international organisations, governments and all national and
in children from developing countries. As more and more region stake-holders is needed.
women join the workforce, their duration of time spent in
child care and income generation determines whether child
care is compromised. Quality child care is not affordable or
ASSESSMENT AND MONITORING OF GROWTH
accessible to low-income working mothers. Environmental A clinician should take the opportunity to assess the growth of
pollution (air, heavy metals and smoking) can affect the each child at each clinical encounter. The head circumference
growth of children especially those living in developing should be measured as the biggest circumference between
countries undergoing rapid economic transition. The negative the frontal region and the occipital prominence using a non-
effects of active and passive smoking in mothers on foetal stretchable measuring tape. The body weight should be
growth and growth in early life have been well characterised.
measured with a calibrated electronic scale, without shoes
Environmental exposure to lead in children has been linked
or socks and the child wearing light clothing. In infants and
to impaired physical growth, neurodevelopment and delayed
puberty. Mercury poisoning from industrial pollution and young children, the supine length should be measured with
teething powder and drugs are less common. There are an infant stadiometer (Fig. 2.2). Children older than 2 years
claims of association of increased mercury exposure with of age should be measured standing using a wall-mounted
neurodevelopment deficits. No significant association of stadiometer (Fig. 2.3) without shoes or socks, with the eyes
prenatal and postnatal exposure to methylmercury from and external auditory meatus held in the same plane, and a
fish consumption with childhood neurodevelopment has slight upward pressure exerted on the jaw and occiput. The
been found in populations with high fish consumption. A anthropometric measurements should be plotted accurately
negative association between environmental sulphur dioxide, on the appropriate chart.
total suspended particulates and exposure to herbicide, and Monitor of growth in children and adolescents has been
birth weight has been consistently reported in the literature. widely used by paediatricians as a marker of their general
Impaired growth in infancy and childhood is associated with well-being. The normal pattern of growth in children is
short adult stature and impaired cognitive development. The traditionally described in an up-to-date ethnic specific
World Health Organisation (WHO) global database on child
growth and malnutrition provides information on growth
and nutrition worldwide (www.who.intnutgrowthdb) based
on the National Centre for Health Statistic (NCHS)/WHO
international growth reference. The prevalence of wasting
in preschool children in Cambodia, Indonesia, Indian
subcontinent, some island states in the Indian Ocean and some
countries in Africa, and Middle East has remained above
10%. According to WHO, 110 million stunted children live Fig. 2.2: Stadiometer for measurement of supine length
20 Hutchison's Paediatrics 

had completed [Acta Paediatr. 2006;95 (Suppl 450):1-106]


and is consider as the gold standard for assessing growth of
children worldwide.
Despite widespread acceptance of routine growth
monitoring of children as the standard of care, a recent meta-
analysis questioned the benefits of growth monitoring in
childhood, as there have been very few trials that evaluated
the impact of this practice on child health. Infants should
be weighed at birth and at times of their immunisation.
Surveillance of children’s weight above one year is only
recommended in children whose growth causes clinical
concern. Clinicians should pay more attention to growth
parameter collected during clinical consultations. Length
measurement should only be done in children under 2 years
of age, if there is a concern in their growth or weight gain.
In a normal population, less than 5% of the infants will
drop their weight through two centile lines and less than
1% of infants will have a fall in weight across three centile
Fig. 2.3: Wall mounted stadiometer for height measurement
lines in the first year of life. A baby would be regarded as
failing to thrive, if there is a fall in weight across more than
two centile lines in infancy. In the United Kingdom, it has
growth chart. Growth references are valuable tools for been recommended that primary care physicians should refer
accessing the health of individuals and for health planner to children for assessment, if their heights falls below the 0.4th
assess the well-being of populations. In a survey involving percentile (-2.67 SD) and a single height measurement at
178 countries, growth monitoring in the first six years of school entry using this criteria that has been found to be
life is an integral part of paediatric care in most countries a sensitive marker for undiagnosed organic disease. The
worldwide. Two-thirds of these countries use the NCHS or sensitivity of this recommended height screening test can
WHO growth reference, while more developed countries be improved by making a correction for the height of the
use their own national growth reference. In developing parents. Height measurements taken during other clinical
countries, health care workers monitor growth to detect encounters during childhood are further opportunities for
and intervene when children have growth faltering. In referral using the 0.4th percentile as the cut-off for action.
developed countries, growth monitoring has been regarded Clinicians have long placed a lot of emphasis on growth
as a useful tool for detecting unrecognised organic diseases, assessment using height velocity, which is calculated from
provision of reassurance to parents and for monitoring the the difference between two height measurements, thereby
health of children in the population. Understanding the combining the imprecision of the two readings. Successive
ethnic differences in childhood and pubertal growth helps measurements of height over time in an individual are highly
doctor in interpretation of results of surveillance of child correlated, whereas successive annual growth velocities are
growth based on the NCHS or WHO growth standard, which not. This suggests that growth velocity estimates are not
has a number of limitations. A WHO multicentre growth reliable and does not have a useful role in routine growth
reference has been developed, based on a longitudinal study monitoring. Despite its imprecision, a grossly abnormal
of exclusively breastfed children from birth to 24 months growth velocity can still be regarded as an indicator of
and a cross-sectional study of children from 18 to 71 months disease. Whether routine height screening every 2–3 years
from six countries (Brazil, Ghana, India, Norway, Oman and between 5 and 12 years of age will be cost-effective in
the United States). Babies in the Euro-Growth study who detecting silent disease without the capacity to cause harm
were breastfed according to the WHO recommendations within the paediatric population remains to be proven.
showed higher weight gain in the first 3 months of life and However, routine monitoring of the height and weight in
were lower in weight and length between 6 and 12 months both developing and developed countries is likely to continue
as compared to the NCHS or WHO growth reference. No in the years to come.
significant differences in growth from the NCHS reference In the monitoring of overweight and underweight, both
in these children were noted between 12 and 36 months. the WHO and the International Obesity Task Force (IOTF)
The finding was similar to that of the WHO multicentre have suggested the use of different body mass index [BMI
growth reference. The WHO multicentre growth reference derived from weight (kg)/height2 (in meters)] cut-offs for
 Growth and Development 21

identifying these problems in the clinical and public health of serum IGF 1 to two to three times of the adult serum
setting. The WHO has adopted the updated BMI reference concentrations as the children progress through puberty.
based on the United States NHANES I data collected in 1971– The serum IGF 1 level in childhood is also dependent on
1974 (www.cdc.gov/growth charts), while IOTF has adopted nutrients availability. It has now been shown that the local
an international BMI reference derived from six population generation of IGF 1 in tissues in response to GH rather than
growth studies (Cole TJ et al. BMJ. 2000;320:1270) as the circulating IGF 1 is essential for normal growth; liver-
the gold standard for international comparison. The WHO specific IGF 1 knockout mice have low circulating IGF 1
proposed a BMI below the 5th percentile, above 85th levels and yet they have near normal growth. Short stature
percentile and 95th percentile as cut-offs for underweight, has been reported in humans with mutations in the genes of
overweight and obesity respectively. The IOTF established GHRH, GH, GH receptor, STAT5b, IGF 1, ALS and IGF
BMI percentile cut-offs at different ages based on extrapolation 1 receptor.
of adult BMI cut-offs of 25 kg/m2 and 30 kg/m2 for overweight
and obesity. In addition, national BMI references are now GENETICS OF STATURE
available in many developed countries. The cut-offs based
on the United States reference data are related to some Fisher RA proposed in 1918 that many genetic factors, each
measures of morbidity, but the newly developed IOTF BMI having a small effect, explain the heritability of height.
cut-off points for children still require validation with data on This is still true in the genome era. From five genome wide
morbidity measures like blood pressure, serum lipids, insulin association studies using single nucleotide polymorphisms
resistance and diabetes. In a meeting organised by WHO or analysis, investigators have identified over 50 chromosome
International Association for the Study of Obesity (IASO)/ locations (implicating nearby genes), which appear to be
IOTF in Hong Kong in 1999, the experts were of the opinion partially responsible for the regulation of adult stature in
that a lower BMI cut-offs might need to be set for adult humans. Collectively, these genes account for about 4% of
Asian populations because of their predisposition to deposit adult stature. One gene LIN28B on chromosome 6q21 which
abdominal fat. The proposed revised BMI cut-off is 23 kg/m2 is shown to be important in the determination of stature
and 25 kg/m2 for overweight and obesity respectively (www. is also found to be associated with the age at menarche.
idi.org.au). Heterozygous carriers of mutations of natriuretic peptide
receptor B (NPR2) have a mean height of –1.1 ± 0.8 SD and
THE GROWTH HORMONE: IGF 1 AXIS the carrier frequency is 1 in 5–700 and some short children
may be NPR2 mutation carriers. Heterozygous insulin-like
The pulsatile secretion of growth hormone from the pituitary growth factor acid labile subunit gene (IGFAL S) mutation
gland is under the control of the stimulatory action of growth
carriers have –0.9 ± 1.51 SDS loss in height compared with
hormone releasing hormone (GHRH) and the suppressive
the normal population. It is possible that carriers of some
effect of somatostatin. Multiple neurotransmitters and
of these single gene defects can be the cause of some short
neuropeptides are involved in the hypothalamic release of these
children in the population. It is likely that more and more
hormones. Growth hormone is essential for normal human
height determining genes will be described in future.
growth in childhood and adolescence. The liver is the organ
with the highest GH receptor concentrations and is the main
PUBERTY
source of GH binding protein (cleaved extracellular portion of
the GH receptor) found in the circulation. After binding to its Puberty is defined as the maturational transition of an
receptor and inducing dimerisation, GH activates the JAK2/ individual from the sexually immature state to adulthood
STAT pathway to bring about the stimulation of epiphyseal with the capacity to reproduce. The hypothalamic-pituitary-
growth, osteoclast differentiation, lipolysis and amino acid gonadal axis is active in utero and at birth. After this period
uptake into muscles. The more important growth promotion of activation, the axis undergoes a long period of relative
action of GH is mediated by IGF 1. Circulating IGF 1 comes quiescence from 3 to 6 months after birth until late childhood
predominantly from the liver and is associated with IGF when pubertal development occurs. The onset of puberty is
binding protein 3 (IGFBP 3) and the acid labile submit (ALS) the result of decreasing sensitivity of the regulatory system
to form a ternary complex. The action of IGF 1 is modified of gonadotropin secretion (gonadostat) in the hypothalamus
by six binding proteins in the circulation. Although IGF 1 is to the negative feedback of the small amounts of gonadal
important in foetal growth, serum concentration of IGF 1 is steroids secreted by the pre-pubertal gonads, as well as a
low in foetal life and in early infancy. A significant rise in IGF decrease in the central neural inhibition of gonadotrophin
1 and IGFBP 3 concentrations is observed in normal children releasing hormone (GnRH) release. Disruption of genes
from 10 months onwards. There is further progressive rise controlling the migration of GnRH neurons from the olfactory
22 Hutchison's Paediatrics 

epithelium to the forebrain can result in delayed puberty. to develop and the Leydig cells to produce testosterone.
The initiation of puberty is associated with a decrease in Testosterone production increases progressively and is
trans-synaptic inhibition by GABAergic neurons and an responsible for the metabolic changes and the development
activation of excitatory glutamatergic neurotransmission of secondary sexual characteristics. Both LH and FSH are
in the control of GnRH secretion. There is also evidence required for the development and maintenance of testicular
that glial to neuron signalling through growth factors function. In early puberty in girls, circulating FSH level
is important in the neuroendocrine control of puberty. increases disproportionately to the LH level in response
Evidence for genetic regulation of the timing of puberty is to GnRH stimulation. Gonadotropin stimulation leads
suggested by the correlation of the age of onset of puberty to a rapid rise in ovarian oestrogen production before
in mother and their offsprings and also in twin studies. It menarche. When the concentration of oestradiol rises
has been suggested that 50–80% of the variance in pubertal above 200 pg/ml for a few days, the negative feedback on
onset may be genetically controlled. Kisspeptin, which is GnRH and gonadotropin release turns to positive feedback
encoded by the KISS 1 gene on chromosome 1q31, is cloned leading to the ovulatory LH surge. In humans, the ability
as a tumour metastasis suppressor gene. Kisspeptin-G of the hypothalamus to stimulate gonadotropin secretion in
protein coupled receptor 54 (GPR54) signalling complex response to positive feedback effects of oestrogen does not
is important in the control of puberty. Inactivating GPR 54 occur until after menarche. In adult females, the GnRH
mutations lead to hypogonadotropic hypogonadism and an pulse frequency starts at 90 minutes in early follicular
activating mutation of GPR54 has been described in a girl phase, increases to one pulse every 60 minutes in mid-
with slowly progressive precocious puberty. Genomewide follicular phase and slows to one pulse every 4–6 hours in
association studies (GWAS) and age at menarche (AAM) the lateral phase.
identified a significant association of LIN28B and AAM. From the age of 6–8 years onwards, there is a progressive
A meta-analysis of 32 GWAS identified 30 loci associated rise in adrenal androgens secretion up to 20 years of age.
with AAM and these genetic loci explained 3.6–6.1% of This process of maturation of the adrenal gland, referred
the variance in the AAM, equivalent to 7.2–12.2% of its to as adrenarche, is responsible for pubic and axillary
heritability. hair development and this event occurs independent of the
Light dark rhythm and climatic conditions have little effect maturation of the hypothalamic-pituitary-gonadal axis,
on the AAM. Children adopted from developing countries to although the timing of the two processes are usually related
live in a developed country have early puberty as a general in normal puberty. Adrenarche is coincident with the mid-
rule. Exposure to endocrine-disrupting chemicals can childhood adiposity rebound and there is evidence that
affect timing of puberty and, for example, isomers of DDT nutritional status measured as a change in the body mass
have oestrogen agonistic and androgen antagonistic effect. index (BMI) is an important physiological regulator of
Mycoestrogenic zearalenone was reported to be elevated in adrenarche.
35% of girls with central precocious puberty in a study from The progressive changes in the secondary sexual
Italy. Zearalenone is a nonsteroidal mycotoxin produced characteristics have been described in a standardised format
by Fusarium species on grains and causes contamination of by Tanner (Figs 2.4 and 2.5). There is considerable variation
grains and animal feeds. Brominated flame retardant and in the age of onset and the tempo of progression of puberty
dichlorodiphenyl-dichloroethylene (DDE) have been found to among normal children. Over the last century, children have
have an association with earlier puberty in girls. The timing tended to be taller in stature and reach sexual maturity at
of puberty is also influenced by nutrition and metabolic cues. an earlier age. In a recent population study from the United
A direct relationship between a particular ratio of fat to lean States, 5% and 15% of the white and African American girls
body mass and onset of puberty has been described. Leptin had breast development before the age of 7 years. Since
plays a role in informing the brain of peripheral energy stores the mean age of menarche in these American girls have not
and body composition and may act as a permissive signal for changed significantly over time, puberty in American girls is
the onset of puberty. associated with earlier onset of breast development, but with
With the onset of puberty, there is increasing pulsatile a slower tempo of pubertal progression. An age of onset of
secretion of luteinising hormone (LH) and to a lesser puberty before the age of 9 years in boys and before 7 years
extent follicle-stimulating hormone (FSH), mainly at night in girls is regarded as premature. Girls and boy without signs
through gradual amplification of GnRH pulse frequency of puberty by the age of 13 years and 14 years should be
and amplitude. In pubertal boys and girls, sleep-entrained monitored carefully and considered for evaluation of delayed
pulsatile GnRH secreted every 60–90 minutes progressing puberty. The mean age of onset on menarche can vary from
to become more regular throughout the day. In boys, 11.2 years in African Americans, 11.27 years in China and
the pulsatile gonadotropin secretion stimulates the testes 13.4 years in Denmark.
 Growth and Development 23

Fig. 2.4: Standards for breast development (From Tanner, 1969) Fig. 2.5: Standards for pubic hair ratings in boys and girls
(Courtesy: Endocrine and Genetic Diseases of Childhood and Adoles- (From Tanner, 1969)
cence by Gardner, Lytt.I. WB Saunders Company. 1975) (Courtesy: Endocrine and Genetic Diseases of Childhood and
Adolescence by Gardner, Lytt.I. WB Saunders Company. 1975)

CHILD DEVELOPMENT childhood and adolescence allow us to recognise global or


specific developmental delay beyond the normal acceptable
Development in children is predominantly determined by age, disordered developmental sequence or developmental
genetic factors, but a significant contribution comes from regression.
environmental factors (maternal nutrition during pregnancy,
birth, socioeconomic factors, nutrition and health after birth). GROSS MOTOR DEVELOPMENT
Intellectual development in childhood and adolescence is a
complex and dynamic process with the interaction between Motor development progresses in a cephalocaudal direction
genes and the environment continuously changing over time. with suppression of primitive reflexes and development of
Antenatal and postnatal depression, maternal malnutrition, postural tone and secondary protective reflexes. The primitive
maternal smoking during pregnancy, antenatal exposure reflexes including the Moro, grasp, stepping and asymmetric
to organic pollutants and adverse child care practice can tonic neck reflexes must have disappeared by 3–6 months of
disrupt the development of different psychomotor domains age before head control (4 months) and independent sitting
in infancy and childhood. Home environment, parent- at 6–8 months can occur. Prior to walking, an infant can
child relationship, parenting style and discipline practices crawl on all four limbs, bottom shuffle, commando creep or
and school environment can have a major influence in the roll along the ground. Shufflers, creepers and rollers tend to
socioemotional and cognitive growth of an individual in attain independent walking at a later age than infants who
childhood and adolescence. Traditionally, early childhood crawl on all fours. Thus early locomotor patterns can result
development can be described in stages in four functional in significant variation in the age of achieving independent
skill areas: gross motor, fine motor, language and speech, walking. A delay in walking beyond 18 months of age is a
social and emotional development. It is also important for warning sign in children who have been crawling as the early
paediatricians to be familiar with the development of the locomotor pattern. An infant stands holding on furniture by
special senses, like hearing, vision, taste, smell, sensation and 9 months of age, cruise round furniture by 12 months and
proprioception. Timing of achievement of major milestones walk independently by 13–15 months. At 18 months of age, a
in the various domains of development can vary enormously child can climb onto a chair and walk up and down stairs two
in normal children. Sound knowledge of development in feet per step by 24 months of age. By two and half years of
24 Hutchison's Paediatrics 

age, a child should be able to stand on tip-toes, jump on both


feet and kick a ball. A 3-year-old child can walk backwards
and can ride a tricycle. There is further development of
gross motor skill and balance with age and most children can
participate in a variety of activities like swimming, skating,
gymnastics and ball games by 6–7 years of age.

FINE MOTOR DEVELOPMENT IN


EARLY CHILDHOOD
The development of fine motor skills in childhood is
condition upon the development of normal vision. Voluntary
movements and fine motor manipulations require the co-
ordinated development of nervous system and visuomotor
coordination. Visual fixation can be demonstrated in babies
by 4–6 weeks of life. The grasp reflex is usually inhibited by
3 months of age and babies can be seen to open their hands,
clasp and unclasp their hands at the midline of the body.
Between 3 and 5 months, babies find their hands interesting
and persistence of “hand regard” beyond 5 months is unusual. Fig. 2.6: Build cubes
By 6 months of age, babies can reach and grasp an object
(one inch cube) with the palm of their hands (palmar grasp). verbally, then the action is referred to as speech. Language
Putting objects to the mouth is a common activity at this age.
acquisition is a complex process integrating interaction
Transfer of objects from one hand to the other can be seen at
between many factors. Genetic factors possibly play an
6 months. By 9 months of age, babies can hold a cube in each
important role early in the developmental process, but
hand and bring them together for comparison. Grasping of
neurological (cerebral palsy, neuromuscular disorders,
small objects with the thumb and index finger (pincer grasp)
hearing impairment, autism), cognitive (mental retardation,
can be achieved between 9 months and 12 months. Casting
specific learning disabilities and specific developmental
of objects is frequently observed towards the end of the first
language impairment), environmental (psychosocial
year of life, but voluntary release of an object on command
deprivation, bilingual or multilingual environments, cultural
only takes place at 15 months. By 15 months of age, a child
differences, maternal depression and large sibship) factors
can hold a pen in his/her palm and scribble. The child can
are important determinants of speech development. Impaired
build a tower of 2–3 cubes between 15 and 18 months. At
hearing is associated with impairment in language and speech
2 years of age, a child’s ability to manipulate small objects
development and the prevalence of severe hearing loss has
continues to improve (Fig. 2.6). Hand dominance can be
been estimated to be between 1:900 and 1:2500 in newborn
observed at 2 and half years of age and the child can scribble
infants. It has been shown that universal newborn hearing
and draw a line or circle with a tripod pen grip. At 3 years
screening, using auditory brainstem response (ABR) or
of age, a child can build a tower of 8 to 9 cubes and copy
two-step screening (ABR–ABR) and otoacoustic emissions
building patterns using three to four cubes. A child can eat
(OAE), enables the early identification of infants with
with a fork or spoon. By 4 years, a child can draw a man
moderate to severe hearing impairment. There is evidence
showing body parts and copy some alphabets. Between 5 and
that early diagnosis of impaired hearing and intervention
6 years, a child can write well and eat properly with knife
can be associated with a better-improved language and
and fork.
communication skills by 2–5 years of age. Cochlear implant
is an alternative for children with severe sensorineural
LANGUAGE AND SPEECH
hearing loss who do not benefit from conventional hearing-
DEVELOPMENT IN CHILDHOOD
aids. Early cochlear implantation before 3 years of age has
Language can be defined as an arbitrary set of symbols, been associated with a better outcome in terms of speech
which when combined in a particular sequence, allows an and language development as compared to children receiving
individual to convey a specific message or conceptualisation cochlear implants in later life.
and transmit them to another individual. When the A one-month-old baby startle to sound, but location of the
transmission of messages between individuals is performed source of sound presented at ear level is present at 6 months
 Growth and Development 25

of age. At 3 months, they respond to the call of their names, close approximation to the syntactic structure characteristic
smile and laugh or are comfortable in response to the sound of adult speech. After the age of 6 years, children are able
of the mother’s voice. Babies can make consonant sounds to engage in a long conversation with family members and
at 3 months of age (e.g. ba, ka and da) and deaf infants are their peers. They can perform simple tasks in command. At
usually referred to as quiet babies at this stage. Babbling in 7 years of age, children are able to express their thoughts in
strings usually occur after 6 months of age. At 12 months of speech and writing.
age, the baby understands some simple commands and uses As the number of children raised in bilingual or
increasing variety of intonation when babbling. At one year multilingual families increases, paediatricians should
of age, an infant understands simple commands like “blow a have some knowledge of the normal patterns of bilingual
kiss” or “wave bye-bye”. They are able to say a few words language acquisition. A child may acquire two languages
with meaning and have at least 6 recognisable words with simultaneously with an initial undifferentiated simple
meaning by 18 months. At 18 months of age, they can name language composed of elements from both languages. By 2–3
body parts on request and start to use word combinations. By years of age, the child begins to be able to differentiate the
2 years of age, children have a vocabulary of many words and two languages. The child can use the appropriate language
can speak in simple sentences. A 9-month-old child can look when speaking to a particular person or in a particular
for an object after being hidden, demonstrating their grasp of environment (e.g. home or school). Normal children in
the concept of object permanence. Before the development of bilingual families can also acquire the two languages in a
expressive speech, infants of one year age can indicate their sequential manner. In this situation, the first or dominant
desire by pointing or gesture. They demonstrate definition language is acquired first in the usual manner and then the
by use of common objects like cup, brush, comb and spoon. children develop an understanding of the second language
Symbolisation occurs at 18 months with the child imitating drawing on the experience with the first language. There may
the mother’s household chore or feeding a doll. Between 18 be a period of selective mutism before the child can switch
months and 22 months, children can engage in constructive from one language to the other proficiently. Bilingualism
symbolic play with toys of miniature. may contribute to delay in language development, but is not
Both expressive and receptive language involves three a cause of disorder of language or cognitive development.
important aspects, namely, phonology and articulation, Parents should be consistent in setting the boundaries for
semantics and syntax. The coordinated neuromuscular where each language is spoken.
mechanisms, which produce the desire sequence of phonemes,
constitute expressive phonology. The neurological process SOCIAL DEVELOPMENT
involved in the identification of the phonemes in a spoken
message is referred to a receptive phonology. Semantics By 4 weeks of age, babies show social smile in response to
refers to the process involved in relating a spoken word to the caregiver and enjoyment to cuddling, bathing and the
its meaning. In most cases, a thought cannot be expressed voice of the mother. At 6 months of age, a baby is able to
simply by a single word. In constructing a spoken message, finger feed and is more wary of strangers. A child can drink
syntax governs the particular order of words as they appear from a cup with help and enjoy songs and nursery rhymes
sequentially in speech. Syntax also governs the use of tense, at 9 months of age. They also desire a comfort object (like a
plurality, grammar and the relationship between the different soft toy, cloth or blanket) and become anxious when they are
words. Syntactic process works in conjunction with the separated from their caregivers (separation anxiety). Babies
semantic process in deriving the meaning conveyed by a can play pat-a-cake or wave bye-bye and show affection to
sequence of words. The use of two to three word combinations family members towards the end of the first year. At 18
in young children involves the omission of function words, months, they can feed themselves with a spoon and they can
which are used in the more complex adult speech. The feed themselves properly using knife and fork at 4 years. The
simple word combinations also reflect the reduced memory age of achievement of bladder and bowel control is variable,
capacity of young children. By 3 years of age, a child can use but is usually towards the end of the 2nd year of life, but
plurals, pronouns and prepositions (e.g. under, behind, in bedwetting at night can persist into mid or late childhood.
front of) in their speech. Most young children are disfluent, Beyond 2 years of age, children are increasing mobile and
but a child should be wholly intelligible and have few are curious and interested in exploring their environment.
infantile substitutions or consonant substitutions at the age of They can help with dressing and bathing. They can manage
4 years. As children become older and with experience, they to use the toilet indepen­dently by age of three years. At
incorporate new rules and expand rules already acquired, the age of 4 years, they can groom and dress themselves
in such a fashion that their speech becomes progressively a and brush their teeth. At age of 18 months, children are
Other documents randomly have
different content
shearing stresses act, there also occur compressive and tensile
stresses. The magnitude of these normal stresses is equal to that of
the shear. Therefore, when torsional loading is combined with other
types of loading, the maximum stresses occur on inclined planes and
can be computed by the methods of Arts. 5.3.3 and 5.3.6.
STRUCTURAL THEORY 5.29 Circular Sections. If a circular
shaft (hollow or solid) is twisted, a section that is plane before
twisting remains plane after twisting. Within the proportional limit,
the shearing unit stress at any point in a transverse section varies
with the distance from the center of the section. The maximum
shear, psi, occurs at the circumference and is given by v = y (5.43)
where T = torsional moment, in-lb r = radius of section, in / = polar
moment of inertia, in4 Polar moment of inertia of a cross section is
defined by J = J p2 dA (5.44) where p = radius from shear center to
any point in the section dA = differential area at the point In
general, / equals the sum of the moments of inertia above any two
perpendicular axes through the shear center. For a solid circular
section, J — irr4/2. For a hollow circular section with diameters D
and d, J — tt(D4 — d4)/32. Within the proportional limits, the
angular twist between two points L inches apart along the axis of a
circular bar is, in radians (1 rad = 57.3°): 77 6 = GJ (5-45) where G
is the shearing modulus of elasticity (see Art. 5.2.4). Noncircular
Sections. If a shaft is not circular, a plane transverse section before
twisting does not remain plane after twisting. The resulting warping
increases the shearing stresses in some parts of the section and
decreases them in others, compared wit the sharing stresses that
would occur if the section remained plane. Consequently, shearing
stresses in a noncircular section are not proportional to distances
from the share center. In elliptical and rectangular sections, for
example, maximum shear occurs on the circumference at a point
nearest the shear center. For a solid rectangular section, this
maximum may be expressed in the following form: v = Wd (5-46)
where b = short side of rectangle, in d = long side, in k = constant
depending on ratio of these sides; dlb = 1.0 1.5 2.0 3 4 5 10 k =
0.208 0.231 0.246 0.258 0.267 0.282 0.291 0.312 0.333 (S.
Timoshenko and J. N. Goodier, "Theory of Elasticity," McGraw-Hill
Publishing Company, New York.)
5.30 SECTION FIVE Hollow Tubes. If a thin-shell hollow
tube is twisted, the shearing force per unit of length on a cross
section (shear flow) is given approximately by H = X (5.47) where A
is the area enclosed by the mean perimeter of the tube, in2, and the
unit shearing stress is given approximately by M T v = - = — (5.48)
t lAt where t is the thickness of the tube, in. For a rectangular tube
with sides of unequal thickness, the total shear flow can be
computed from Eq. (5.47) and the shearing stress along each side
from Eq. (5.48), except at the corners, where there may be
appreciable stress concentration. Channels and I Beams. For a
narrow rectangular section, the maximum shear is very nearly equal
to v = Wd (5-49) This formula also can be used to find the
maximum shearing stress due to torsion in members, such as I
beams and channels, made up of thin rectangular components. Let J
= l/3Zb3d, where b is the thickness of each rectangular component
and d the corresponding length. Then, the maximum shear is given
approximately by V = ^y- (5.50) where b' is the thickness of the
web or the flange of the member. Maximum shear will occur at the
center of one of the long sides of the rectangular part that has the
greatest thickness. (A. P. Boresi, O. Sidebottom, F. B. Seely, and J. O.
Smith, "Advanced Mechanics of Materials," 3d ed., John Wiley &
Sons, Inc., New York.) 5.5 STRAIGHT BEAMS Beams are the
horizontal members used to support vertically applied loads across
an opening. In a more general sense, they are structural members
that external loads tend to bend, or curve. Usually, the term beam is
applied to members with top continuously connected to bottom
throughout their length, and those with top and bottom connected
at intervals are called trusses. See also Structural System, Art. 1.7.
5.5.1 Types of Beams There are many ways in which beams may be
supported. Some of the more common methods are shown in Figs.
5.11 to 5.16.
STRUCTURAL THEORY 5.31 Jl_1 FIGURE 5.11 Simple
beam. Li FIGURE 5.12 Cantilever beam. ^ FIGURE 5.13 Beam with
one end fixed. FIGURE 5.14 Fixed-end beam. 1 1 1 FIGURE 5.15
Beam with overhangs. .I.1.1.1. a a a a A FIGURE 5.16 Continuous
beam. The beam in Fig. 5.11 is called a simply supported, or simple
beam. It has supports near its ends, which restrain it only against
vertical movement. The ends of the beam are free to rotate. When
the loads have a horizontal component, or when change in length of
the beam due to temperature may be important, the supports may
also have to prevent horizontal motion. In that case, horizontal
restraint at one support is generally sufficient. The distance between
the supports is called the span. The load carried by each support is
called a reaction. The beam in Fig. 5.12 is a cantilever. It has only
one support, which restrains it from rotating or moving horizontally
or vertically at that end. Such a support is called a fixed end. If a
simple support is placed under the free end of the cantilever, the
propped beam in Fig. 5.13 results. It has one end fixed, one end
simply supported. The beam in Fig. 5.14 has both ends fixed. No
rotation or vertical movement can occur at either end. In actual
practice, a fully fixed end can seldom be obtained. Some rotation of
the beam ends generally is permitted. Most support conditions are
intermediate between those for a simple beam and those for a fixed-
end beam. In Fig. 5.15 is shown a beam that overhangs both is
simple supports. The overhangs have a free end, like cantilever, but
the supports permit rotation. When a beam extends over several
supports, it is called a continuous beam (Fig. 5.16). Reactions for the
beams in Figs. 5.11, 5.12, and 5.15 may be found from the
equations of equilibrium. They are classified as statically determinate
beams for that reason. The equations of equilibrium, however, are
not sufficient to determine the reactions of the beams in Figs. 5.13,
5.14, and 5.16. For those beams, there are more unknowns than
equations. Additional equations must be obtained on the basis of
deformations permitted; on the knowledge, for example, that a fixed
end permits no rotation. Such beams are classified as statically
indeterminate. Methods for finding the stresses in that type of beam
are given in Arts. 5.10.4, 5.10.5, 5.11, and 5.13.
5.32 SECTION FIVE 5.5.2 Reactions As an example of the
application of the equations of equilibrium (Art. 5.2.1) to the
determination of the reactions of a statically determinate beam, we
shall compute the reactions of the 60-ft-long beam 2,000" W-200^1
4,000* 6£00* 3,000 -12-I2'-H ^nimniinningEsi 36'•-I2-H FIGURE
5.17 Beam with overhangs loaded with both uniform and
concentrated loads. with overhangs in Fig. 5.17. This beam carries a
uniform load of 200 lb/lin ft over its entire length and several
concentrated loads. The supports are 36 ft apart. To find reaction i?,,
we take moments about R2 and equate the sum of the moments to
zero (clockwise rotation is considered positive, counterclockwise,
negative): -2000 X 48 + 36R, - 4000 X 30 - 6000 ■200 X 60 X 18 =
0 18 + 3000 X 12 R, 14,000 lb In this calculation, the moment of the
uniform load was found by taking the moment of its resultant, which
acts at the center of the beam. To find R2, we can either take
moments about R, or use the equation 2V = 0. It is generally
preferable to apply the moment equation and use the other equation
as a check. 3000 X 48 - 36R2 + 6000 X 18 + 4000 X 6 - 2000 X 12
+ 200 X 60 X 18 = 0 R2 = 13,000 lb As a check, we note that the
sum of the reactions must equal the total applied load: 14,000 +
13,000 = 2000 + 4000 + 6000 + 3000 + 12,000 27,000 = 27,000
5.5.3 Internal Forces Since a beam is in equilibrium under the forces
applied to it, it is evident that at every section internal forces are
acting to prevent motion. For example, suppose we cut the beam in
Fig. 5.17 vertically just to the right of its center. If we total the
external forces, including the reaction, to the left of this cut (see Fig.
5.18a), we find there is an unbalanced downward load of 4000 lb.
Evidently, at the cut section, an upward-acting internal force of 4000
lb must be present to maintain equilibrium. Again, if we take
moments of the external forces about the section, we find an
unbalanced moment of 54,000 ft-lb. So there must be an internal
moment of 54,000 ft-lb acting to maintain equilibrium. This internal,
or resisting, moment is produced by a couple consisting of a force C
acting on the top part of the beam and an equal but opposite force
T acting on
STRUCTURAL THEORY 5.33 2,000' 4,000* 6,000*
1w»2Q0*/' I mssmm 4 R,»14,000* 1V VI Jj « c V it (a) (b) FIGURE
5.18 Portions of a beam are held in equilibrium by internal stresses.
the bottom part (Fig. 18b). The top force is the resultant of
compressive stresses acting over the upper portion of the beam, and
the bottom force is the resultant of tensile stresses acting over the
bottom part. The surface at which the stresses change from
compression to tension — where the stress is zero — is called the
neutral surface. 2,000* 4,000* 6QO0* wax)*/' | I ' R,}|4,000* 3,000'
5.5.4 Shear Diagrams KMXIIIZIZIIZtllXIIIIflTXX ■"-I27-* X|*-I2{*j*"
18'— ► -H2*- 1 3fi' 36(o) R2' 13,000' 9,600 3,000 The unbalanced
external vertical force at a section is called the shear. It is equal to
the algebraic sum of the forces that lie on either side of the section.
Upward acting forces on the left of the section are considered
positive, downward forces negative; signs are reversed for forces on
the right. A diagram in which the shear at every point along the
length of a beam is plotted as an ordinate is called a shear diagram.
The shear diagram for the beam in Fig. 5.17 is shown in Fig. 5.1%.
The diagram was plotted starting from the left end. The 2000-lb load
was plotted downward to a convenient scale. Then, the shear at the
next concentrated load — the left support — was determined. This
equals -2000 - 200 X 12, or —4400 lb. In passing from must to the
left of the support to a point just to the right, however, the shear
changes by the magnitude of the reaction. Hence, on the right-hand
side of the left support the shear is -4400 + 14,000, or 9600 lb. At
the next concentrated load, the shear is 9600 — 200 X 6, or 8400 lb.
In passing the 4000-lb load, however, the shear changes to 8400 -
4000, or 4400 lb. Proceeding in this manner to the right end of the
beam, we terminate with a shear of 3000 lb, equal to the load on
the free end there. It should be noted that the shear diagram for a
uniform load is a straight line sloping downward to the right (see
Fig. 5.21). Therefore, the shear diagram was completed by
connecting the plotted points with straight lines. FIGURE 5.19 .Shear
diagram for the beam with loads shown in Fig. 5.17.
5.34 SECTION FIVE 6,000* 9,000* kio'^^io'-4*-io'-" 7,000
"R|= 4,000* R,» 4,000*' 4,000 S W»400*" gnmnnnB -L*20(a)LOAD
DIAGRAM 3 R|-wx«4,Q00-400x (b) SHEAR DIAGRAM -8,000 ■4j000
(c) BENDING MOMENT DIAGRAM FIGURE 5.20 Shear and moment
diagrams for a simply supported beam with concentrated loads. (c)
BENDING MOMENT DIAGRAM FIGURE 5.21 Shear and moment
diagrams for a simply supported, uniformly loaded beam. Shear
diagrams for commonly encountered loading conditions are given in
Figs. 5.30 to 5.41. 5.5.5 Bending-Moment Diagrams The unbalanced
moment of the external forces about a vertical section through a
beam is called the bending moment. It is equal to the algebraic sum
of the moments about the section of the external forces that lie on
one side of the section. Clockwise moments are considered positive,
counterclockwise moments negative, when the forces considered lie
on the left of the section. Thus, when the bending moment is
positive, the bottom of the beam is in tension. A diagram in which
the bending moment at every point along the length of a beam is
plotted as an ordinate is called a bending-moment diagram. Figure
5.20c is the bending-moment diagram for the beam loaded with
concentrated loads only in Fig. 5.20a. The bending moment at the
supports for this simply supported beam obviously is zero. Between
the supports and the first load, the bending moment is proportional
to the distance from the support, since it is equal to the reaction
times the distance from the support. Hence the bending-moment
diagram for this portion of the beam is a sloping straight line.
STRUCTURAL THEORY 5.35 The bending moment under
the 6000-lb load in Fig. 5.20a considering only the force to the left is
7000 X 10, or 70,000 ft-lb. The bending-moment diagram, then,
between the left support and the first concentrated load is a straight
line rising from zero at the left end of the beam to 70,000 ft-lb,
plotted to a convenient scale, under the 6000-lb load. The bending
moment under the 9000-lb load, considering the forces on the left of
it, is 7000 X 20 - 6000 X 10, or 80,000 ft-lb. (It could have been
more easily obtained by considering only the force on the right,
reversing the sign convention: 8000 X 10 = 80,000 ft-lb.) Since there
are no loads between the two concentrated loads, the bending-
moment diagram between the two sections is a sloping straight line.
If the bending moment and shear are known at any section of a
beam, the bending moment at any other section may be computed,
providing there are no unknown forces between the two sections.
The rule is: The bending moment at any section of a beam is equal
to the bending moment at any section to the left, plus the shear at
that section times the distance between sections, minus the
moments of intervening loads. If the section with known moment
and share is on the right, the sign convention must be reversed. For
example, the bending moment under the 9000-lb load in Fig. 5.20a
could also have been obtained from the moment under the 6000-lb
load and the shear to the right of the 6000-lb load given in the shear
diagram (Fig. 5.20£>). Thus, 80,000 = 70,000 + 1000 X 10. If there
had been any other loads between the two concentrated loads, the
moment of these loads about the section under the 9000-lb load
would have been subtracted. Bending-moment diagrams for
commonly encountered loading conditions are given in Figs. 5.30 to
5.41. These may be combined to obtain bending moments for other
loads. 5.5.6 Moments in Uniformly Loaded Beams When a bean
carries a uniform load, the bending-moment diagram does not
consist of straight lines. Consider, for example, the beam in Fig.
5.21a, which carries a uniform load over its entire length. As shown
in Fig. 5.21c, the bending-moment diagram for this beam is a
parabola. The reactions at both ends of a simply supported,
uniformly loaded beam are both equal to wL/2 — W/2, where w is
the uniform load in pounds per linear foot, W = wL is the total load
on the beam, and L is the span. The shear at any distance x from
the left support is R1 wx — wL/2 — wx (see Fig. 5.2lb). Equating
this expression to zero, we find that there is no shear at the center
of the beam. The bending moment at any distance x from the left
support is I x\ wLx wx2 w , „ M = RlX-wx[-\=— — = - x(L - x) (5.51)
Hence: The bending moment at any section of a simply supported,
uniformly loaded beam is equal to one-half the product of the load
per linear foot and the distances to the section from both supports.
The maximum value of the bending moment occurs at the center of
the beam. It is equal to wL2/8 = WL/8.
5.36 SECTION FIVE 5.5.7 Shear-Moment Relationship The
slope of the bending-moment curve for any point on a beam is equal
to the shear at that point; i.e., V-f (5.52) ax Since maximum bending
moment occurs when the slope changes sign, or passes through
zero, maximum moment (positive or negative) occurs at the point of
zero shear. After integration, Eq. (5.52) may also be written M1 -
M2= \ Vdx (5.53) 5.5.8 Moving Loads and Influence Lines One of
the most helpful devices for solving problems involving variable or
moving loads is an influence line. Whereas shear and moment
diagrams evaluate the effect of loads at all sections of a structure,
an influence line indicates the effect at a given section of a unit load
placed at any point on the structure. For example, to plot the
influence line for bending moment at some point A on a beam, a
unit load is applied at some point B. The bending moment is A due
to the unit load at B is plotted as an ordinate to a convenient scale
at B. The same procedure is followed at every point along the beam
and a curve is drawn through the points thus obtained. Actually, the
unit load need not be placed at every point. The equation of the
influence line can be determined by placing the load at an arbitrary
point and computing the bending moment in general terms. (See
also Art. 5.10.5.) Suppose we wish to draw the influence line for
reaction at A for a simple beam AB (Fig. 5.22a). We place a unit load
at an arbitrary distance of xL from B. The reaction at A due to this
load is 1 xL/L = x. Then, RA — x is the equation of the influence
line. It represents a straight line sloping upward from zero at B to
unity at A (Fig. 5.22a). In other words, as the unit load moves
across the beam, the reaction at A increases from zero to unity in
proportion to the distance of the load from B. Figure 5.22b shows
the influence line for bending moment at the center of a beam. It
resembles in appearance the bending-moment diagram for a load at
the center of the beam, but its significance is entirely different. Each
ordinate gives the moment at midspan for a load at the
corresponding location. It indicates that, if a unit load is placed at a
distance xL from one end, it produces a bending moment of Vi xL at
the center of the span. Figure 5.22c shows the influence line for
shear at the quarter point of a beam. When the load is to the right
of the quarter point, the shear is positive and equal to the left
reaction. When the load is to the left, the shear is negative and
equal to the right reaction. The diagram indicates that, to produce
maximum shear at the quarter point, loads should be placed only to
the right of the quarter point, with the largest load at the quarter
point, if possible. For a uniform load, maximum shear results when
the load extends from the right end of the beam to the quarter
point.
STRUCTURAL THEORY 5.37 CURVE OF MAX. MOMENTS (x-
x2)L (y
5.38 SECTION FIVE A & Wa=SP ! ,PS fi' |Wb=SP' C 1 ■f3 E
4 ^ a i o W=ZP 2 L. 2 ^ FIGURE 5.23 .Moving loads on simple beam
AB ae placed for maximum bending moment at point C on the beam.
FIGURE 5.24 Moving loads are placed to subject a simple beam to
the largest possible bending moment. at midspan. Then shift the
loads until the load P2 that was at the center of the beam is as far
from midspan as the resultant of all the loads on the span is on the
other side of midspan (Fig. 5.24). Maximum moment will occur
under P2. When other loads move on or off the span during the shift
of P2 away from midspan, it may be necessary to investigate the
moment under one of the other loads when it and the resultant are
equidistant from midspan. 5.5.10 Bending Stresses in a Beam To
derive the commonly used flexure formula for computing the
bending stresses in a beam, we have to make the following
assumptions: 1. The unit stress at a point in any plane parallel to the
neutral surface of a beam is proportional to the unit strain in the
plane at the point. 2. The modulus of elasticity in tension is the
same as that in compression. 3. The total and unit axial strain in any
plane parallel to the neutral surface are both proportional to the
distance of that plane from the neutral surface. (Cross sections that
are plane before bending remain plane after bending. This requires
that all planes have the same length before bending; thus, that the
beam be straight.) 4. The loads act in a plane containing the
centroidal axis of the beam and are perpendicular to that axis.
Furthermore, the neutral surface is perpendicular to the plane of the
loads. Thus, the plane of the loads must contain an axis of
symmetry of each cross section of the beam. (The flexure formula
does not apply to a beam loaded unsymmetrically. See Arts. 5.5.18
and 5.5.19.) 5. The beam is proportioned to preclude prior failure or
serious deformation by torsion, local buckling, shear, or any cause
other than bending. Equating the bending moment to the resisting
moment due to the internal stresses at any section of a beam yields
STRUCTURAL THEORY 5.39 M 11 C (5.54) tuiiuiL
COMPRESSIVE STRESSES Ke iV~\ TENSILE STRESSES NEUTRAL
AXIS FIGURE 5.25 Unit stresses on a beam cross section caused by
bending of the beam. M is the bending moment at the section, / is
the normal unit stress in a plane at a distance c from the neutral axis
(Fig. 5.25), and / is the moment of inertia of the cross section with
respect to the neutral axis. If / is given in pounds per square inch
(psi), / in in4, and c in inches, then M will be in inch-pounds. For
maximum unit stress, c is the distance to the outermost fiber. See
also Arts. 5.5.11 and 5.5.12. 5.5.11 Moment of Inertia The neutral
axis in a symmetrical beam is coincidental with the centroidal axis;
i.e., at any section the neutral axis is so located that y dA = 0 (5.55)
where dA is a differential area parallel to the axis (Fig. 5.25), y is its
distance from the axis, and the summation is taken over the entire
cross section. Moment of inertia with respect to the neutral axis is
given by /= y2 dA (5.56) Values of / for several common types of
cross section are given in Fig. 5.26. Values for structural-steel
sections are presented in manuals of the American Institute of Steel
Construction, Chicago, 111. When the moments of inertia of other
types of sections are needed, they can be computed directly by
application of Eq. (5.56) or by braking the section up into
components for which the moment of inertia is known. If / is the
moment of inertia about the neutral axis, A the cross-sectional area,
and d the distance between that axis and a parallel axis in the plane
of the cross section, then the moment of inertia about the parallel
axis is I' = I + Ad2 (5.57) With this equation, the known moment of
inertia of a component of a section about the neutral axis of the
component can be transferred to the neutral axis of the complete
section. Then, summing up the transferred moments of inertia for all
the components yields the moment of inertia of the complete
section. When the moments of inertia of an area with respect to any
two perpendicular axes are known, the moment of inertia with
respect to any other axis passing through the point of intersection of
the two axes may be obtained through the use
The text on this page is estimated to be only 17.15%
accurate

5.40 SECTION FIVE y\ d l\ \ t X --2 \ « — b — ► S


RECTANGLE A=bd c, ■ d/2 c2sd Si« Al» JPt s 6(bz + dz) 6 2rf2 bd
5=T*(b*td4) ~b'A'bd-bd' c = d/2 L i-bd»-b'd'» -- bd^-b'd'3 6d rJBd*
Ifabd-t/d') HOLLOW RECTANGLE TRIANGLE A 2
STRUCTURAL THEORY 5.41 of Mohr's circle, as for stresses
(Fig. 5.10). In this analog, Ix corresponds with fx. Iy with / , and the
product of inertia / with v^ (Art. 5.3.6). xy dA (5.58) The two
perpendicular axes through a point about which the moments of
inertia are a maximum and a minimum are called the principal axes.
The products of inertia are zero for the principal axes. HORIZONTAL
UNIT SHEARING STRESSES 5.5.12 Section Modulus The ratio S = lie
in Eq. (5.54) is called the section modulus. I is the moment of inertia
of the cross section about the neutral axis and c the distance from
the neutral axis to the outermost fiber. Values of S for common types
of sections are given in Fig. 5.26. 5.5.13 Shearing Stresses in a
Beam The vertical shear at any section of a beam is resisted by
nonuniformly distributed, vertical unit stresses (Fig. 5.27). At every
point in the section, there is also a horizontal unit stress, which is
equal in magnitude to the vertical unit shearing stress there [see Eq.
(5.34)]. At any distances y ' from the neutral axis, both the
horizontal and vertical shearing unit stresses are equal to VERTICAL
UNIT SHEARING STRESSES FIGURE 5.27 Unit shearing stresses on a
beam cross section. z*-> (5.59) where V = vertical shear at the
cross section t — thickness of beam at distance y ' from neutral axis
7 = moment of inertia about neutral axis A' = area between the
outermost fiber and the fiber for which the shearing stress is being
computed y = distance of center of gravity of this area from the
neutral axis (Fig. 5.27) For a rectangular beam with width b and
depth d, the maximum shearing stress occurs at middepth. Its
magnitude is 12V bd2 bd3b 8 3V_ 2bd That is, the maximum shear
stress is 50% greater than the average shear stress on the section.
Similarly, for a circular beam, the maximum is one-third greater than
the average. For an I beam, however, the maximum shearing stress
in the web is
5.42 SECTION FIVE not appreciably greater than the
average for the web section alone, if it is assumed that the flanges
take no shear. 5.5.14 Combined Shear and Bending Stress For deep
beams on short spans and beams made of low-strength materials, it
is sometimes necessary to determine the maximum stress /' on an
inclined plane caused by a combination of shear and bending stress
— v and /, respectively. This stress /', which may be either tension
or compression, is greater than the normal stress. Its value may be
obtained by application of Mohr's circle (Art. 5.3.6), as indicated in
Fig. 5.10, but with / = 0, and is ''=Wy2+ 2 (5'60) 5.5.15 Beam
Deflections When a beam is loaded, it deflects. The new position of
its longitudinal centroidal axis is called the elastic curve. At any point
of the elastic curve, the radius of curvature is given by FT R = -
(5.61) where M = bending moment at the point E = modulus of
elasticity / = moment of inertia of the cross section about the
neutral axis Since the slope dyldx of the curve is small, its square
may be neglected, so that, for all practical purposes, \IR may be
taken equal to d2yldx2, where y is the deflection of a point on the
curve at a distance x from the origin of coordinates. Hence, Eq.
(5.61) may be rewritten ,d^y dx2 M = EI^-2 (5.62) To obtain the
slope and deflection of a beam, this equation may be integrated,
with M expressed as a function of x. Constants introduced during the
integration must be evaluated in terms of known points and slopes
of the elastic curve. Equation (5.62), in turn, may be rewritten after
one integration as B M - dx (5.63) i El in which 6A and 6B are the
slopes of the elastic curve at any two points A and B. If the slope is
zero at one of the points, the integral in Eq. (5.63) gives the slope of
the elastic curve at the other. It should be noted that the integral
represents the area of the bending-moment diagram between A and
B with each ordinate divided by EI.
STRUCTURAL THEORY 5.43 The tangential deviation t of a
point on the elastic curve is the distance of this point, measured in a
direction perpendicular to the original position of the beam, from a
tangent drawn at some other point on the elastic curve. B Mx i EI dx
(5.64) Equation (5.64) indicates that the tangential deviation of any
point with respect to a second point on the elastic curve equals the
moment about the first point of the Ml El diagram between the two
points. The moment-area method for determining the deflection of
beams is a technique in which Eqs. (5.63) and (5.64) are utilized.
Suppose, for example, the deflection at midspan is to be computed
for a beam of uniform cross section with a concentrated load at the
center (Fig. 5.28). Since the deflection at midspan for this loading is
the maximum for the span, the slope of the elastic curve at the
center of the beam is zero; i.e., the tangent is parallel to the
undeflected position of the beam. Hence, the deviation of either
support from the midspan tangent is equal to the deflection at the
center of the beam. Then, by the moment-area theorem [Eq.
(5.64)], the deflection yc is given by the moment about either
support of the area of the M/EI diagram included between an
ordinate at the center of the beam and that support. }V 1 PL L2L
PV_ 2 AEI 2 3 2 ~ 48£7 Suppose now, the deflection y at any point
D at a distance xL from the left support (Fig. 5.28) is to be
determined. Referring to the sketch, we note that the distance DE
from the undeflected point of D to the tangent to the elastic curve at
support A is given by FIGURE 5.28 Load and Ml EI diagrams and
elastic curve for a simple beam with mispan load.
5.44 SECTION FIVE y + tAD = xtA where tAD is the
tangential deviation of D from the tangent at A and tAB is the
tangential deviation of B from that tangent. This equation, which is
perfectly general for the deflection of any point of a simple beam, no
matter how loaded, may be rewritten to give the deflection directly:
y = xtAB ~ tAD (5.65) But tAB is the moment of the area of the Ml
EI diagram for the whole beam about support B. And tAD is the
moment about D of the area of the Ml EI diagram included between
ordinates at A and D. Hence 1 PL L (2 l\ 1 PLx xL PL* y=X24EJ2{3 +
3)L-2 2EIxLJ = 48E-Ix(3-4x) It is also noteworthy that, since the
tangential deviations are very small distances, the slope of the
elastic curve at A is given by 6A = *f (5.66) This holds, in general,
for all simple beams regardless of the type of loading. The procedure
followed in applying Eq. (5.65) to the deflection of the loaded beam
in Fig. 5.28 is equivalent to finding the bending moment at D with
the Ml EI diagram serving as the load diagram. The technique of
applying the Ml EI diagram as a load and determining the deflection
as a bending moment is known as the conjugate-beam method. The
conjugate beam must have the same length as the given beam; it
must be in equilibrium with the Ml EI load and the reactions
produced by the load; and the bending moment at any section must
be equal to the deflection of the given beam at the corresponding
section. The last requirement is equivalent to requiring that the
shear at any section of the conjugate beam with the Ml EI load be
equal to the slope of the elastic curve at the corresponding section
of the given beam. Figure 5.29 shows the conjugates for various
types of beams. Deflections for several types of loading on simple
beams are given in Figs. 5.30 to 5.35 and for overhanging beams
and cantilevers in Figs. 5.36 to 5.41. When a beam carries a number
of loads of different types, the most convenient method of
computing its deflection generally is to find the deflections
separately for the uniform and concentrated loads and add them up.
For several concentrated loads, the easiest solution is to apply the
reciprocal theorem (Art. 5.10.5). According to this theorem, if a
concentrated load is applied to a beam at a point A, the deflection it
produces at point B is equal to the deflection at A for the same load
applied at B(dAB = dBA). Suppose, for example, the midspan
deflection is to be computed. Then, assume each load in turn
applied at the center of the beam and compute the deflection at the
point where it originally was applied from the equation of the elastic
curve given in Fig. 5.33. The sum of these deflections is the total
midspan deflection. Another method for computing deflections of
beams is presented in Art. 5.10.4. This method may also be applied
to determining the deflection of a beam due to shear.
STRUCTURAL THEORY 5.45 ACTUAL BEAM ±a Lk i_L (a) 3
F i I LU (b) H i Liilli (c) 11 u I t a t t n t u. td) 4-0-H4 L — *H-b-*
CONJUGATE BEAM iSlttlftih^ (bO ^ ^ ■|itlfYnErniif-wBB— (*o*|>«
— L — »4*H V) FIGURE 5.29 Various types of beams and
corresponding conjugate beams. 5.5.16 Combined Axial and Bending
Loads For stiff beams, subjected to both transverse and axial
loading, the stresses are given by the principle of superposition if the
deflection due to bending may be neglected without serious error.
That is, the total stress is given with sufficient accuracy at any
section by the sum of the axial stress and the bending stresses. The
maximum stress equals / P Mc A + T (5.67) where P = axial load A
— cross-sectional area M = maximum bending moment c — distance
from neutral axis to outermost surface at the section where
maximum moment occurs / = moment of inertia of cross section
about neutral axis at that section
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