Key To Diagnosis in Paediatrics

Clinical Methods
A Key to Diagnosis in Paediatrics

Clinical Methods
A Key to Diagnosis in Paediatrics
Dilip Mukherjee
MD (Paed), DCH, PhD, FIAP, FAMS
Professor of Paediatrics
Ex-Dean, Vivekananda Institute of Medical Sciences
Ramakrishna Mission Seva Pratishthan
Kolkata-700 026, India
Indraneel Banerjee
MD (Paed), MRCPCh (UK)
Consultant Paediatric Endocrinologist
Department of Paediatric Endocrinology
Royal Manchester Children’s Hospital (UK)
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Clinical Methods—A Key to Diagnosis in Paediatrics
© 2008, Dilip Mukherjee
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or
by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the
authors and the publisher.
This book has been published in good faith that the material provided by authors is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and authors will not be held responsible for any inadvertent error(s). In case
of any dispute, all legal matters are to be settled under Delhi jurisdiction only.
First Edition: 2008

ISBN 81-8448-193-4
Typeset at JPBMP typesetting unit
Printed at Replica
This book is dedicated to all who are
involved in the care of the children and
specially the residents and the
postgraduate students in paediatrics
Foreword
Standard textbooks serve as reference material but are no substitutes for books that deal with
practical aspects of clinical paediatrics. There are few books that focus on clinical approach to
childhood diseases but this book titled “Clinical Methods – A Key to Diagnosis in Paediatrics” is unique
in many ways.
Opening chapter emphasizes systematic approach to detailed history taking that nearly offers
clue to probable diagnosis. Importance of each point in the history is analysed with probable
interpretations. Physical examination follows in the next chapter that is aimed at sharpening clinical
skills. Subsequent chapters deal with individual systems. Appropriate stress on anatomy is a special
feature in the chapter on Neurology. Endocrinological and metabolic system is a welcome addition
that universally lacks in most of the publications. Special mention must be made for inclusion of
child behaviour and psychology that is often neglected though extremely relevant. Each chapter
includes many tables that provide useful information.
Another unique feature of this book is the Appendices that include growth charts, body surface
area chart, ECGs and radiological images. This adds significantly to the academic value of the
book. The book also includes many clinical photographs that offer visual impressions of various
conditions.
This book is authored by two experienced paediatricians — Dr. Dilip Mukherjee and
Dr. Indraneel Banerjee who have very thoughtfully presented their ideas on clinical methods.
Never before such a complete book was published on clinical methods and I strongly
recommend it to all the students and practitioners alike.
YK Amdekar MD, DCH

Former Professor of Paediatrics
Grant Medical College and J.J. Group of Hospitals
Mumbai
President of Indian Academy of Paediatrics 1995
Consultant Paediatrician Jaslok Hospital and Breach Candy Hospital
Mumbai
Preface
Clinical Paediatrics is a very challenging and interesting subject. Clinical medicine in adults has
been more or less standardised but in children there are wide variations across ages and individuals
which make it more complex. Further, we faced everyday with new knowledge of disease states
and better understanding of pathology. We therefore need to constantly refine our clinical methods
to account for this recent acquisition of information.
Our humble endeavour in this regard has been chiefly aimed at the postgraduate students and
all those involved in the care of the child. It shall be our greatest reward if this book can be of any
service to them.
A word of caution–clinical paediatrics is an eminently practical subject. The many cases you
see, the variety you come across, the better will be your insight to diagnose and treat. However
quality can never be compromised for quantity. Examine each case thoroughly, searching for all
possibilities with an observant eye and trained ear. Do not take things for granted – your meticulous
approach will be handsomely rewarded. This book is not meant to be armchair reading, rather it
is for practice, discussion, comparison and criticism.
It is important to follow-up a case and see through the natural progression. Examine the same
case periodically for differences of symptoms and sign, no matter how subtle. Do not be
disheartened if your provisional diagnosis does not always tally with the actual diagnosis made
after performing investigations. Remember to make a clinical diagnosis as would be expected of a
clinician. In most cases the clinical diagnosis would fit in with the real diagnosis, but not always.
In such situations be satisfied that your approach and rationality are justified in the formulation
of a working diagnosis.
Develop a sense of regard for the child or newborn baby. Never take a patient as a mere name
or a diagnosis. Cultivate a rapport with the patient and the guardian and you will positively find
your history taking and examinations less bumpy and more satisfying. Happy reading!
Dilip Mukherjee
Indraneel Banerjee
Acknowledgements
We express our great sense of gratitude to Dr Prachi, Clinical Psychologist and Stress Counsellor,
UN Department of Safety and Security (UNDSS), New Delhi for kindly contributing as guest author
for chapter on Psychological Assessment of Children. We are really indebted to her for her
contribution which as added a new dimension to this book. We are grateful to Prof YK Amdekar,
Ex-Prof of JJ Hospital, Mumbai and renowned consultant paediatrician and a versatile genius in
the field of paediatrics for kindly agreeing to write the foreword for this book. We express our
gratitude to him for his generosity.
We are also grateful to Prof AK Dutta the Director Professor of the Department of Paediatrics
of Lady Hardinge Medical College, New Delhi for kindly going through the manuscript and
encouraging us very much.
Dr Debjani Das and Dr Sutapa Halder the postgraduate students of the department of paediatrics
of Ramakrishna Mission Seva Pratisthan, Vivekananda Institute of Medical Sciences have kindly
drawn all the sketches for this book. Dr Anindya Saha, Dr Arpan Agarwal and Dr Suparna Guha
(MD, Paed) of our department who has taken all the photographs for this book. Dr Surajit Santra
has taken the arduous trouble to incorporate and edit the photos and the sketches in the CD for
the book. Dr Taraknath Ghosh, MD (Paed) and Ex-registrar of our department, and Dr Soumitra
Masani our PGT have gone through the entire book and did the primary editing job for us. We are
grateful to all of them and also to other residents and the senior colleagues of our department for
their suggestions and comments.
We are really grateful to Parimal Kar for doing the composing and typing of this manuscript.
We are also grateful to M/s. Jaypee Brothers Medical Publishers (P) Ltd for their cooperation
and help to publish this book.
Contents
1. History .................................................................................................................................. 1
2. General Survey ................................................................................................................. 15
3. Examination of the Gastrointestinal System ............................................................. 55
4. Respiratory System.......................................................................................................... 71
5. Cardiovascular System ................................................................................................... 83
6. Neurology .......................................................................................................................... 95
7. Examination of the Endocrinological and Metabolic Systems ............................ 133
8. Haematology – Oncology ............................................................................................. 136
9. Neonatal Examination .................................................................................................. 138
10. Assessment of Child Behaviour ................................................................................. 152
11. Psychological Assessment ........................................................................................... 155
Appendices ......................................................................................................................... 163
Index .................................................................................................................................. 213

HISTORY
INTRODUCTION The doctor, in an interview with the child

and parents, must have a well balanced attitude.
Obtaining a good history is an art and gets better
It would be unwise to allow your feelings to
with practice. A sound history is vital to
surface into confrontation. Barriers of language,
diagnosis as this is the structure on which to
culture or manners may tend to put you on the
build upon. A problem history is most often
wrong track, and in such situations evaluation
from parents and not directly from the child.
and re-evaluation of what has been said and
This entails a degree of bias which should not what has been missed, is essential.
be ignored but rather weighed for its true worth. Let the informant unfold the story in his own
Communication is most essential in this process. words. Only when he or she has done so should
The doctor-parent or doctor-patient relationship he or she be asked to expand on what appears
is not one way, rather it is a two-way process to be the more important aspects of the story.
involving two people studying each other. The Specific leading questions should only be asked
doctor must put the informant at ease and after you have reached the heart of the problem
encourage him or her to talk freely. and have framed in your own mind a possible
History is not just limited to questions and diagnosis and a differential diagnosis list.
answers. It helps to start a conversation by It is important that you practice this art over
greeting the patient, addressing him or her by and over again so as not to miss the salient
name, identifying a common town of origin or points of interest. Time is important and often
a mutual interest in pets. All this while, watch at a premium. In an unstructured setting, for
the parent’s and patient’s gestural language. The example, in a busy emergency, you have to get
eyes and hands may tell you more than what is all the details in a few minutes. This takes a lot
actually said. of practice and practice builds on premonition.
Concentration is very important in a conver- The following headings are relevant in history
sation. Your undivided attention must be (Table 1.1):
devoted to hearing the complaint; otherwise the
Table 1.1: History taking
response from the patient’s end will be
Name, age, sex and address
incomplete. Gentleness is all-important, more so Presenting complaint
in a physical examination. The patient should History of present illness
be reassured and not frightened or put off. History of prior illnesses/past illness
Behavioural problems often make it more Family history
Social history
difficult for the interviewer. It helps to strike up
Past medical/surgical treatment history
a communication directly with the patient, be it Antenatal and birth history
verbal or non-verbal. Establishing a rapport with Postnatal history
the distressed child relieves much anxiety Dietary history
relating to the disease. Immunization history
2 Clinical Methods—A Key to Diagnosis in Paediatrics
PRESENTING COMPLAINT • Aggravating factor: What brings it on and

what worsens it?
Try to define the main complaint and its
• Relieving factor: What makes it better?
duration. The presenting complaint is simply the
Likewise, symptoms of fever can be des-
problem that makes the patient seek medical
cribed as:
help. This is usually confined to one or two key
• Duration of illness
points. Multiple presenting complaints them-
• Height of temperature
selves represent the problem rather than the
• Type of fever (remittent, intermittent,
diagnosis. The timing and duration of sympto-
continued - Chap 2, page 28)
matic events is important since the chronology
• Character (i.e., quotidian) — associated with
provides clues to the underlying pathology.
chills or rigor
Sometime the duration of actual presenting
• Associated convulsions
complaints is bypassed and the onset taken at
• Associated malaise, headache
the point of trivial complaints. This error has to
• Descriptions of related symptoms.
be corrected as you go on taking the history.
Similar analysis of the other illness com-
plaints will help us draw a pen picture of the
THE HISTORY OF THE PRESENT ILLNESS
child’s problems. Relating one symptom to the
Ask the informant to give you a detailed account other will then help you towards a differential
of the illness from the beginning. A history may diagnosis. The pattern of evolution of the
not always start with a chief complaint, and may complaints tells you of the natural history of a
start with other relatively minor complaints. disease. Find out if the illness began insidously
Ideally you should allow the narrator to and gradually worsen or was it intermittent?
continue without any interruption, but for Was the onset acute, then slowly getting better,
people who are either quite reticent or too but not fully disappeared? Is there a relation to
talkative and deviating from the symptoms, you a previously diagnosed illness? Of the
will need to gently encourage them to stay on symptoms presented, which ones are more
track. relevant than others? Are there pieces of
information that appear out of place? Do you
Symptom Analysis need to revisit those issues and work out the
Each symptom has to be analysed thoroughly connection, if at all? A good history is like an
and qualified suitably. As an example, an illness intricate network – it is your job to set this up so
starting with pain should be described as: that you can make sense of it all.
• Timing and duration: When did the pain An outline of the questions related to
start? Does it come and go? How long does individual systems is given below:
it last on average?
• Character: What the pain feels like stabbing, General
burning, pricking, dull aching, colicky
Weight
• Severity: Whether it interferes with daily
activities or keeps the child awake at night • Is it increasing, decreasing or stationary?
• Radiation: Whether it stays at one place or • If the child has lost weight recently – has the
spreads along the distribution of a nerve child been unwell? Has he or she strenuously
• Referral: Whether the pain at a site originates exercised to lose weight?
at a different site • Is there a family history of obesity, type 2
• Shifting: Whether the pain shifts from the diabetes mellitus or early cardiovascular
original site to a new location morbidity?
History 3
Sleep • What is its relation to meals (if any)?

• Does it wake the patient at night? Does the
• Has the sleeping pattern changed?
child wake up in the night screaming with
• Is there difficulty in getting to sleep or unsual
pain?
early waking?
• What things aggravate it? What affords relief
• Does the child snare at night?
(food, anatacid, vomiting)?
• Is the patient sleepy and tired during the
• Does any particular posture relieve the pain?
day?
• Is it relieved by defaecation or by the passage
• Have the parents noticed any convulsions
of flatus?
during sleep?
• Is there underlying anxiety or tension
• Any odd behaviour during sleep?
suggesting a functional non-organic aetio-
• If the child is of an age of bladder continence,
logy?
does he or she have nocturnal enuresis?
• What medication does the child have for the
pain?
Energy
• Is it loss of energy or boredom? Appetite
• Is it part of a general malaise? • Is it increased or reduced?
• Is there unusual fatiguability? • Does the child dislike certain foods?
• What time of the day is there lethargy? • Does the child eat good size portions at
• Can the child play with his/her friends? mealtimes?
• Is the child so tired that he/she does not
want to be with his/her friends? Vomiting
• How serious a problem is this?
The Gastrointestinal System (Table 1.2) • Does the child throw up after milk feeds
(gastro-oesophageal reflux)?
Gastrointestinal symptoms can be of upper or • Is abdominal pain relieved by vomiting
lower tracts. The following questions should (gastritis)?
help you get to the bottom of the problem. • Is there vomiting in the morning (raised
intracranial pressure)?
Table 1.2: GI system
• What does the child throw up?
• Pain • Check if the vomitus is bilious (intestinal
• Appetite
• Vomiting
obstruction)
• Water brash • Does it ever contain fresh blood (mucosal
• Heart burn tear)?
• Dysphagia • Does it ever look like coffee grounds (gastric
• Diarrhoea mucosal haemorrhage)?
• Constipation
• Is the child having regular intermittent
vomiting episodes as in intermittent
Pain
malrotation?
• What site is the pain? • Is the child passing urine? Large fluid loss
• Judge the severity may result in dehydration
• Is it localized or diffuse? Is it persistent or • Is the child on any medication that is
intermittent? emetogenic, for example opioids?
• Does it radiate in any particular direction? • Is this is gastroenteritis, or is there a more
• For how long has the patient had it? serious underlying illness like diabetic
• Are there intervals of freedom? If so, for how ketoacidosis, pyelonephritis or metabolic
long? disorder?
Water Brash Constipation

• Does the patient ever experience excessive • How often does the child “go” to the toilet?
secretion of saliva into the mouth, with • Get the parents or child to describe the
regurgitation of mouthfuls of clear, tasteless motions—small, dry, hard and pellety,
fluid? elongated but hard or tubular and formed
• Is this a long standing problem (habit
Heartburn constipation, megacolon)?
• Does the child avoid the toilet because it is
• Does the patient suffer from pain behind the
painful to defaecate?
sternum?
• Does the child consume reasonable amounts
• Does it come on especially when lying
of fruit, vegetables and greens?
down?
• Can this be explained by change in
circumstances, medicines, etc.?
Dysphagia
• Is the child constantly wearing nappies and
• Record the child’s words—what does he/she will not pass motions if taken off (habit)?
mean by difficulty of swallowing? • Is there soiling of clothes suggestive of
• Where does the food appear to stick? overflow incontinence of stools secondary to
• Is it worse with liquids or with solids? constipation?
• Is swallowing painful? • Did the child open his or her bowels in the
• Is there underlying anxiety that itself could first day of life (Hirschprung disease)
be responsible for difficulty of swallowing? • Is the child taking medication to relieve
constipation? If so, what dose?
Diarrhoea • Is there any colicky pain? Is the pain
aggravated when using laxatives like senna?
• What is the duration of diarrhoea?
• Is there blood in the stools (anal fissure)?
• How frequent and at what times are the
motions during the day?
Liver and Gallbladder
• What is their relation to meals?
• Does the child have loose motions after Jaundice
eating certain types of food?
• Has the child eaten unusual food in the • Has the child noticed any yellow discoloura-
recent past? tion of conjunctivae or skin, or high coloured
• Is there a possibility of food poisoning? urine?
• What colour are the motions? • Are the motions pale or dark?
• Has the patient ever passed any blood or • Does the skin itch?
mucus with stool (dysentery, inflammatory • Any bruises or unusual skin marks?
bowel disease)? • Have there been any other cases of jaundice
• Are they unformed, porridge-like, frothy, or among family or friends?
watery (chronic diarrhoea, malabsorption)? • Any foreign travel?
• Do they float in the lavatory pan or are they • Was any injection given in the last 3 or 4
difficult to flush away (malabsorption)? months?
• Is the diarrhoea painless?
Pain
• Is there colicky abdominal pain, suggestive
of colitis? • Where is it?
• Does the patient use laxatives? • Has the patient ever had attacks of very
• How is the child’s appetite? severe pain, coming on suddenly and lasting
• Is the child gaining weight appropriately? for a few hours?
History 5
• If so, did the pain radiate and in what • Is there a past history of rheumatic fever or
direction? chorea?
• Was there any jaundice after the pain
subsided? Haemopoietic System
• Did the pain radiate to the tip of the shoulder
If the clinical features suggest a blood disorder,
or the middle of the back?
enquire about the following:
• Tiredness, lethargy, feeling miserable
The Cardiovascular System (anaemia)
If the symptoms point to disease of the • Infections involving the mouth, skin, lungs,
circulatory system, enquire about the following: urinary tract and perianal area (bone marrow
aplasia)
Dyspnoea • Blood loss from gums, nose, bruising, rectum
as well as malaena (black stools) and
• When does this come on? Is it present at rest menstrual irregularity (bleeding disorder)
or only on exertion? • Is bleeding or bruising out of proportion to
• What degree of exertion is necessary to degree of trauma (bleeding or clotting
produce it? diathesis)?
• Judge the severity of dyspnoea. Does it • Does the child appear to be pale?
impede routine daily activity? • Are there red skin spots (purpura, petechiae)
• Are there attacks of breathlessness at night and changes in skin colour?
(paroxysmal nocturnal dyspnoea)? • Is bleeding or skin rash associated with
• Does the patient have to sleep sitting up pallor?
(orthopnoea)? • What about diet–ask for consumption of
• Does the child have palpitations and how meat and green vegetables
long do they last? • If the child is drinking far too much milk
• Does the heart give an occasional thump there may be iron deficiency anaemia
now and then? • Does the child go about barefoot–hook-
• Is the pulse rate increased on occasion and worms can cause enough blood loss to cause
is it regular or irregular? significant anaemia
• Any excessive bleeding after dental
Cough extraction or tonsillectomy
• Enquire about cough, sputum and • Has the child ingested drugs known to cause
haemoptysis, as detailed in the section on the bone marrow aplasia or haemolytic
respiratory system anaemia?
• Is there a family history of blood disorders
Oedema (haemolytic disease)?
• Has the child noticed any glandular
• Do the heels or ankles swell? enlargements (lymphoma, leukaemia)?
• Does the face also swell up?
The Respiratory System
Other Symptoms
Parents will often tell you that their child has
• Are there cramp-like pains in the calves been coughing for some time or been rather
when walking relieved by rest? Or wheezy. Asthma is a common problem, so
• Is there undue coldness, redness or blueness explore atopy and allergy. Do think about
of the extremities? tuberculosis as a possible diagnosis, even though
this may not be very obvious. You should also • Is it ever blood-stained, and if so whether
ask for possible exposure to animal, mineral or with streaks or clots (tuberculosis, bron-
vegetable dusts to search for an explanation for chiectasis, trauma, pulmonary sequestration,
chronic cough. haemosiderosis)?
• Does the child do chest physiotherapy to
Cough help produce sputum (bronchiectasis)?
• What is the duration of the cough?
• Did the cough start recently or is it present Breathing
for weeks or even months? • Is there increased work of breathing?
• Is it chronic persistent (tuberculosis, • Is the child unusually tachpnoeic?
bronchiectasis) or chronic episodic (asthma)? • Does dyspnoea occur at rest, or after varying
• Is it dry or productive? degrees of exertion?
• In the child less than a year, is the cough • Describe the level of activity that brings out
“fruity” (bronchiolitis)? dyspnoea
• If this a baby, does the cough sound like a • Does the child snare at night?
“whoop” (pertussis)? • Does he or she fall asleep easily during the
• Enquire if the child had surgery (tetralogy day, suggesting obstructive sleep apnoea?
of Fallot repair) – viral upper respiratory tract
infections can trigger a “TOF” cough
Wheeze
• At what time of the day or night is it worst?
• Has the child used inhalers (relievers like • Is it wheeze or stridor?
salbutamol) and do they help? • Is it constant or intermittent?
• Are there family members who smoke • Is the child a “happy wheezer” (viral
around the child? wheeze)?
• Does the child have eczema or family history • Does anything provoke it?
of atopy, suggesting a predisposition to • Does the child become wheezy with viral
asthma? upper respiratory infections?
• Is it worsened by any particular conditions, • Is it worse at any particular time of day or
such as cold or dust? night?
• Is it painful or not? • What relieves it?
• Is the child taking medication (like captopril) • Is there a history suggestive of foreign body
that may aggravate the cough? inhalation?
• Are there associated symptoms to worry • What is the dose of inhaled reliever
about pulmonary tuberculosis? medication?
• Are there family members with a chronic • What about the technique of inhaler use?
coughing illness suggesting tuberculosis? • Is the child growing well (severe asthma)?
• Is there a functional element in the history • Is the child missing a lot of school days?
(habit cough)? (severity of asthma)?
• Can the child play a full game (assess
Sputum functional ability)?
• How much? (in children more than 6 years
Chest Pain
of age).
• When is expectoration maximal? • Where is it – all over the chest or central and
• What is the consistency, colour, and odour? retrosternal?
• Is it purulent (bacterial infection)? • Is the pain unilateral (pleural effusion)?
History 7
• Is it aggravated by deep breathing or • Is there a record of fluid intake-output? Have

coughing? the nappies been weighed to estimate urine
• Describe the pain character – sharp, stabbing output?
(pleuritic) or dull, aching (haematoma, • Is the child losing fluid elsewhere (e.g.
trauma, neuralgia). diarrhoea, vomiting)?
• Is it associated with an increase in cough, • Is urine output disproportionate to the oral
sputum or dyspnoea (pneumonia)? intake?
• Is the onset sudden and sharp and • Is there a history of diarrhoea preceding
accompanied by significant dyspnoea oliguria (haemolytic uraemic syndrome)?
(spontaneous pneumothorax)? • Does the face or ankles swell (nephrotic
syndrome, renal failure)?
The Urinary System • What medications is the child on?
• Is the child on long term steroids?
Pain on micturition, haematuria, oliguria and
• Are the side effects from medication
oedema are pointers in the direction of a renal
(Cushingoid appearance, infections from
or urology problem. Probe further if you feel that
steroid use)?
the waterworks are at fault.
• Is the child on dialysis? If so, what type?
• Is there less urine (oliguria)?
• Has the child had a renal transplant?
• Is the child passing urine too frequently
• What immunosuppressives is the child
(polyuria—diabetes mellitus, insipidus)?
using?
• Is the child drinking large amounts of fluids
• Is the child on antihypertensives?
(polydipsia)?
• If so is hypertension well controlled?
• Will the child drink water instead of juice
• Has the child been admitted to intensive care
(compulsive juice drinking)?
with headaches, blurring of vision,
• Does the child wake up often through the
drowsiness or fits (hypertensive encephalo-
night for a wee (polyuria)?
pathy)?
• Is the child at an age of continence?
• Is the child gaining weight and growing well
• Is there nocturnal enuresis? If so, how many
(poor growth and inadequate weight gain in
nights a week?
renal failure)?
• Is there day time incontinence and accidents
when the child is awake (bladder detrusor
weakness)? Skin Diseases
• What methods have the parents tried to
Itch
make the child continent?
• Explore the child’s social circumstances • Has the child got an itchy skin problem
• What is the colour of the urine? (eczema, contact dermatitis, scabies)?
• Is there blood in urine? • Whereabouts is the itch (between fingers in
• If there blood in urine, at what stage of the scabies, flexures in eczema)?
micturition is it (upper renal tract – constant, • Does the child have jaundice (obstructive
lower tract—end of micturition)? jaundice)?
• Is micturition painful? Does the child have a • Enquire carefully into the patient’s hygiene
burning or stinging sensation (cystitis)? – clothing, cleanliness etc (scabies)
• Any pain shooting down to the groin or • Is there any exposure to chemical substances
genitalia (calculi)? or other irritants? Ask about recent drug
• Is the child passing less urine (oliguria)? therapy.
• Is there a history of asthma, hay fever or any Neurology

other allergic disorder (atopic dermatitis)?
Headaches, convulsions, limb weakness, altered
• Is there contact with animals, insects, or
consciousness should alert you to investigate the
plants (contact dermatitis)?
child’s neurology.
• Does the child have dry skin (eczema)?
• What topical medications have been used?
Headache
• Is there a family history of skin disease,
asthma, hay fever, urticaria (atopy)? • How often does the child have headaches?
• How long do they last?
Rash • Is it one side only (migraine)?
• Are the headaches relieved by sleep
• Where is the rash?
(migraine)?
• What colour is the rash (red—measles,
• Do the headaches occur in the evening after
enterovirus, meningococcal infections)?
coming back from school (tiredness)?
• Is the rash vesicular (chicken pox, folliculitis,
• What exactly does the child mean by the term
burns)?
“headache” (headache an attention seeking
• Is the rash associated with joint swelling
device in preschool children)?
(Henoch-Schonlein purpura, juvenile
• Do headaches occur early in the morning and
idiopathic arthritis, vasculitis, inflammatory
improve by the end of the day (space
bowel disease)?
occupying lesions)?
• Is the rash brought on by specific food
• Any associated visual perceptions (acute –
ingestion (cow’s milk protein intolerance)?
migraine, chronic—craniopharyngioma,
optic nerve glioma)?
Pigmentation
• Any family history of headaches with or
• Are there patches of skin depigmentation without visual disturbances (migraine)?
(vitiligo, psoriasis, pityriasis)? • Is there loss of balance (cerebellar astro-
• Is there generalised pigmentation of the skin cytoma)?
with associated mucosal pigmentation • Does the child have an intracranial shunt? If
(Addison disease)? so when it was last revised?
• Are there leathery, dark patches over the • Was there weakness of the limbs at any stage
neck and axillae (acanthosis nigricans)? (migraine, stroke, vasculitis, tumours)?
• What medication does the child take to
Hair relieve the headaches?
• Is there loss of hair (alopecia)?
Convulsion
• Is the child on cytotoxic chemotherapy
(alopecia)? • Is it a convulsion—get a first hand account
• Is the child on sodium valproate (hyper- (jerking of limbs, incontinence, biting of
trichosis)? tongue, eyes rolling back—suggest tonic
• Is there excess hair in a girl (hypertrichosis clonic seizures)
or hirutism)? What is the distribution • Any post ictal symptoms (headaches,
(forearm, arm, legs—hypertrichosis; mous- paralysis)?
tache, sideburns, chest—androgenic) • Was the child standing when it happened
• Is there irregularity of periods associated (syncope)?
with excess hair (polycystic ovarian • Was the episode brought about by exercise
syndrome)? (hypertrophic cardiomyopathy)?
History 9
• Is there a family history of sudden death • Is the weakness generalized (malnutrition,

(hypertrophic cardiomyopathy)? chronic illness) or localized (nerve or muscle
• Does the child have episodes where he or she lesions)?
appears vacant and inattentive (behavioural, • Is there weakness in the lower limbs with
absence seizures)? sphincter incontinence (transverse myelitis)?
• Does the child show abnormal behaviour • Any paraesthesia (Guillain-Barre syn-
(complex partial seizures)? drome)?
• Is it a morning seizure with numbness of the • Any history of trauma to back or surgical
face, drooling and garbled vocalization intervention (spinal injury)?
(Rolandic seizure)? • Was the child treated for tuberculosis (spinal
• Was the convulsion triggered off by flashing tuberculosis)?
lights (photosensitive epilepsy) or accom- • Is weakness associated with headaches or
panied by lauging bouts (gelastic seizure)? dizziness (brain tumour, vasculitis)?
• Is there warning or aura (focal seizures)? • Any associated mouth ulcers and skin rash?
• Was there loss of consciousness (generalized (Behcet syndrome).
epilepsy) or not (partial epilepsy)? Locomotor System
• What is the treatment history?
Symptoms related to this system are covered
• Assess the compliance with anticonvulsants.
elsewhere. However, you may find to it impor-
tant to ask a few pertinent questions.
Dizziness • How far can the child walk (functional
ability)?
• Is dizziness induced by moving the head in
• Can the child run without hindrance
a particular way or assuming a particular
(excludes major abnormalities)?
posture (positional vertigo)?
• Is there swelling of one or more joints
• Did it follow an injury or a presumed viral
(juvenile idiopathic arthritis, vasculitis)?
infection (inner ear abnormality)? • Is joint swelling accompanied by high
• Is there a history of long standing amino- temperatures (osteomyelitis, vasculitis,
glycoside use (inner ear toxicity)? juvenile idiopathic arthritis)?
• Does the child appear unusually anxious • Was joint swelling preceded by gastro-
(panic attack)? enteritis (reactive arthritis)?
• Was the episode following intake of medi- • Is the child’s walking distance getting
cation (hypotension following antihyper- progressively short (Duchenne dystrophy)?
tensive ingestion)? • Does the child receive physiotherapy?
• Did dizziness precede headaches (migraine)? • Is there use of pain relieving medication?
• Does the child use orthopaedic devices
Weakness (ankle foot orthoses for Charcot Marie Tooth
disease, special boots for talipes equino-
• Is the weakness transient? (atypical varus)?
hemiplegic migraine) • Was there any surgery to limit the child’s
• Is the weakness present from birth (spinal movement?
muscular atrophy, cerebral palsy, congenital
myopathies)? HISTORY OF PRIOR
• Was the onset of weakness acute (vasculitis, ILLNESS/PAST ILLNESS
injury, infections) or chronic (tumours, Search for any past illness and whether it bears
degenerative disease)? a relation to the present illness. A history of fever
and sore throat is relevant in the context of acute Table 1.3: Socio-economic class as per BJ Prasad
glomerulonephritis. Children with immune Class Per capita income in Rs per month
deficiency often have recurrent hospital
I 1536 and above
admissions. Children with inadequate weight II 770-1535
gain may have had chronic illnesses in the past. III 360-769
Diseases like juvenile idiopathic arthritis or IV 150-359
chronic renal failure can lead to growth failure. V Less than 150
Prior steroid use may be the cause of later
problems of obesity. Always consider the child’s FAMILY HISTORY
current problems in the context of previous
Note the patient’s position in the family and the
episodes of illness and treatment. Do not,
ages of siblings if any. Also record the state of
however, assume that the present and past
health, important illnesses and cause of death
problems are associated all the time. The child
of immediate relatives. Draw a family tree going
may have different pathologies at different
back three generations. Ask about consanguinity
points in time.
as this is important for autosomal recessive
conditions. Document diseases in each family
SOCIAL HISTORY
member—a detailed description will help you
No history will be complete without a thorough understand if the child is likely to be a carrier
evaluation of the child’s social and economic or case of an autosomal recessive condition.
background. Many diseases are borne out of the Often the child is the index case and diagnosis
child’s circumstances. Malnutrition occurs in in other family members may be made after the
children of families of meagre income. Obesity diagnosis in the child. In a child with Langer
occurs relatively commonly where the family mesomelia, check the heights of the parents,
income has received a boost. Diseases may be uncles and aunts as they may have undiagnosed
spread by poor quality of housing and sanita- Leri-Weill dyschondrosteosis (haploinsuffi-
tion. Hookworm infestation, giardiasis, scabies ciency of SHOX). Very often a child will have
are typical examples. died in the family from an unknown disease. It
It is important to estimate the living may be relevant to know the circumstances
condition of the family. Ask about the number leading to death. For example, a child may have
of family members, the number of rooms, water died of thalassaemia major and secondary
supply and waste disposal facilities. It helps to infections prior to actual diagnosis. This
understand the family’s economic structure. indicates that the parents are carriers and hence
This is often a delicate matter and not all families exclusion of thalassaemia in the other children
will be keen to discuss their financial status. If is important.
you manage to extricate this information you Enquire about associated diseases in other
may compare this against a socio-economic scale family members – coeliac disease in a child with
such as that given in Table 1.3. You should type 1 diabetes mellitus, tumours in multiple
remember this table holds little relevance in real endocrine neoplasia and stillbirths in congenital
life as burgeoning costs and inflation have adrenal hyperplasia. Further, enquire about
rendered it obsolete. You could devise a scale close relations with persons outside the family.
along similar lines depending upon the It may be important to know of a next door
economic prosperity and average income of neighbour with tuberculosis who may have
people of your region. infected the child.
History 11
Treatment History Developmental History

Document medical or surgical treatment, if any. Gather information from the parents on the
Record details of medicines—their dose, child’s play, speech and social interactions. You
duration, complications and efficacy. Previous should be able to assess the age at which the
surgical intervention is important to know in the child functions in gross motor, fine motor,
context of a child with possible intestinal personal-social and speech-language areas. You
obstruction. Chemotherapy and craniospinal can calculate the Development Quotient (DQ)
radiation can damage the hypothalamus and as ratio of developmental age for chronological
pituitary gland resulting in hypopituitarism. age. A DQ of less than 70 is taken as deve-
Sodium valproate for epilepsy can lead to lopmental delay. You can quantify the child’s
weight gain in puberty. Carbamazepine can give developmental age with the aid of an inventory
rise to Stevens-Johnson syndrome acutely. Long (a screening test like the Denver Development
term steroids in nephrotic syndrome lead to Screening Test or a comprehensive Griffith
obesity and stunting of height. Previous Development Assessment) but in the bedside
treatment for urinary tract infection is important situation it helps to be aware of the common
in the child with chronic renal failure. milestones as given below.
You should remember that there is
ANTENATAL, BIRTH AND considerable variation in individuals and that
POSTNATAL HISTORY you should allow for social and cultural
situations. A child with limb weakness will
Data on any untoward event in pregnancy
perform below par in gross motor skills. A child
(rubella) may be important as a causation of
with recurrent otitis media may lag behind in
disease in the infant (congenital rubella). Equally
speech and language areas. Children with
important is the history of drugs taken which
chronic illnesses may falsely appear to have
may adversely affect the fetus (fetal hydantoin,
global developmental delay.
fetal alchol syndromes). Record if the antenatal
scan was normal. What was the growth of the
fetus in utero? Was the baby born premature? MILESTONES OF DEVELOPMENT
Was there any perinatal asphyxia? Document
Neonatal Period (1st 4 weeks)
the treatment if the child was in the neonatal
unit. Intraventricular haemorrhage may have a Prone : Lies in flexed attitude, turns head
bearing in a child with dystonic cerebral palsy. from side to side, head sags on
Extrahepatic portal vein thrombosis may be due ventral suspension.
to umbilical venous catheterization in the Supine : Generally flexed and a little stiff.
newborn period. A child with metabolic Visual : May fixate face or light in line of
syndrome may have been born small for vision, ‘Doll’s eye’ movement of eyes
gestational age. on turning head.
Reflex : Moro response active, stepping and
IMMUNIZATION HISTORY placing reflexes, grasp reflex active
Social : Visual preference for human face.
Note whether the child received oral polio, BCG,
triple antigen and measles as per the immuni-
4 Weeks
sation programme. Ask the mother whether a
BCG left a scar or not. A BCG vaccine without a Prone : Legs more extended, holds chin up
scar is best taken as having had no conversion. momentary, lifts head from plane of
Also enquire about the other vaccines namely body on ventral suspension.
hepatitis B, rabies, MMR. Ask for any serious Supine : Tonic neck posture predominates,
side effects after the first triple antigen dose. head lags on pull to sit position.
Visual : Watches person, follows moving Standing : When held erect, pushes with feet
object. Adaptive : Sees pellet, but makes no move to it
Social : Body movements in cadence with Social : Laughs aloud, may show dis-
voice of other in social contact, pleasure if social contact is broken,
beginning to smile. excited at sight of food.
8 Weeks 28 Weeks
Prone : Raises head slightly further, head Prone : Rolls over, pivots.
sustained in line of body on ventral Supine : Rolls over (Back to stomach - 6 mon),
suspension. squirming movements.
Supine : Tonic neck posture predominates, Sitting : Sits briefly with support of pelvis,
head lags on pull to sit. leans forward on hands, back
Visual : Follows moving objects. rounded.
Social : Smiles on social contact, listens to Standing : May support most of weight,
voice and coos. bounces actively.
Adaptive : Reaches out for and grasps large
12 Weeks object (voluntary grasp at 20 wk),
Prone : Lifts head and chest arms extended, grasps using radial palm, rakes at
head above plane of body on ventral pellet, transfers object from hand to
suspension. hand, bangs cubes on table.
Supine : Tonic neck posture predominates, Language: Polysyllabic vowel sounds formed
reaches towards and misses objects, (Da, Ma, Ba, Ka).
waves at toy, shows hand regard. Social : Prefers mother, babbly, enjoys
Sitting : Head lag partially compensated on mirror, responds to changes in
pull to sit, early head control with emotional content of social contact.
bobbing motions, back rounded,
leans forward. 40 Weeks
Reflex : Moro disappears, makes defensive Sitting : Sits up alone and indefinitely
movements or selective withdrawal without support, back straight.
reactions. Standing : Pulls to standing position, ‘cruises’
Social : Sustained social contact, listens to or walks holding to furniture.
music, says “aah, ngah.” (hatching Motor : Crawls (creeps—44 wk)
socially). Adaptive : Grasps objects with thumb and
forefinger, pokes at things with
16 Weeks
forefinger, picks up pellet with
Prone : Lifts head and chest, head in assisted pincer movement, uncovers
approximately vertical axis, legs hidden toy, atttempts to retrieve
extended. dropped object (object constancy),
Supine : Symmetric posture predominates, releases object grasped by other
hands in midline, reaches and person, clicks 2 cubes in imitation.
grasps objects and brings them to Language: Repetitive consonant sounds
mouth. (mama, dada).
Sitting : No head lag on pull to sit, head Social : Responds to sound of name, plays
steady, enjoys sitting with full trunk peek-a-boo (‘tuki’) or pat-a-cake
support. (‘tai-tai’), waves bye - bye (‘ta-ta’).
History 13
52 Weeks (1 year) 24 months

Motor : Walks with one hand held (48 wk), Motor : Runs well (walks backward - 21
rises independently, takes seveal mon), walks up and down stairs, one
steps. step at a time, opens door, climbs on
Adaptive : Picks up pellet with unassisted furniture, jumps.
pincer movement of forefinger and Adaptive : Tower of 7 cubes, circular scribbling,
thumb, releases object to other imitates horizontal stroke, folds
person on request or gesture, may paper once imitatively, parallel play
kiss on request, rings a bell. but not playing with other children.
Language: A few words besides ‘mama, dada.’ Language: Puts 3 words together (subject, verb
Social : Plays simple ball game, makes object), vocabulary of 100 words or
postural adjustment to dressing. more.
Social : Helps undress, listens to story with
15 months pictures, dry at night if lifted out late
Motor : Walks alone, crawls up stairs. in the evening.
Adaptive : Makes tower of 3 cubes, makes a line
with crayon, inserts pellet in bottle. 30 months
Language: Jargon, follows simple commands,
Motor : Goes upstairs alternating feet, jumps
may name a familiar object (ball),
on both feet.
looks with interest at coloured
Adaptive : Tower of 9 cubes, makes vertical and
pictures.
horizontal strokes, but generally will
Social : Indicates some desires or needs by
not join them to make a cross,
pointing, hugs parents.
imitates circular stroke, forming
closed figure.
18 months
Language: Refers to self by pronoun “I,” knows
Motor : Runs stiffly, sits on small chair, name.
walks up stairs with one hand held, Social : Helps put things away, pretends in
explores drawers and waste baskets, play.
manages spoon without rotating
near mouth, turns 2-3 pages of book 36 months
at a time.
Adaptive : Makes a tower of 4 cubes, imitates Motor : Rides tricycle, stands momentarily
scribbling, imitates vertical stroke, on one foot.
dumps pellet from bottle. Adaptive : Tower of 10 cubes, imitates
Language: Ten words (average), names pictures construction of “bridge” of 3 cubes,
(4), identifies one or more parts of copies circle, imitates cross.
body, identifies 3 parts on doll. Language: Knows age, sex, counts 3 objects
Social : Feeds self, a seeks help when in correctly, repeats 3 numbers or a
trouble, may complain when wet, or sentence of 6 syllables.
soiled, kisses parents with pucker, Social : Parallel play with other children,
alternates between clinging and unbuttons clothing, puts on shoes,
resistance. washes, handedness established.
48 months daily intake of food in terms of calories and

Motor : Hops on one foot, throws ball grammes of protein. A rigorous dietary assess-
overhand, uses scissors to cut out ment is crucial to evaluating the extent of mal-
pictures, climbs well. nutrition. In infants, note the the duration of
Adaptive : Copies bridge from model, imitates breast feeding, weaning foods and weight gain.
construction of “gate” of 5 cubes, A list of commonly used food items and their
copies cross and square, draws a calories and proteins are given in Table 1.4.
man with 2-4 parts besides head, Table 1.4: Calorie and protein value
names longer of 2 lines. of commonly used foods
Language: Counts 4 coins, tells story. Kcal Protein
Social : Goes to toilet alone plays with
1 Medium chapati (25g) 85 3
several children. 1 Medium katori Rice (25g) 86 2
1 Slice bread (25g) 60 2
60 months 1 Medium katora bread (25g) 86 6
Motor : Walks easily on narrow line, runs 1 Medium sized egg 60 6
lightly on toes, skips on alternate 1 Piece fish 60 9
2 Pieces Meat 60 10
feet.
Cow’s milk (250 ml) 165 8
Adaptive : Draws triangle form copy, names Curd (100 gm) 60 3
heavier of 2 weights. Leafy vegetable (100 gm)
Language: Names 4 colours, repeats sentence of 1/3 cup (cooked) 28 3
10 syllables, counts 10 coins 1/2 cup cooked potato (100 gm) 100 2
correctly, fully, nine-letter vision 1 Medium sized apple (100 gm) 60 -
1 Medium sized orange (100 gm) 48 -
chart at 6 meters and near-vision
1 Medium sized Banana (100 gm) 120 -
testing card (Stycar), delights at Oil and ghee 2 tsp 90 -
reciting, gives full birthday, home Sugar (25 gm) 5 tsp 100 -
address. Jaggery (15 gm) 1 small cup 96 -
Social : Dresses and underesses, asks
questions about meaning of words, Plan of Diagnosis (Table 1.5)
domestic role play, chooses own
A careful history will help you piece together a
friends, enjoys jokes and riddles.
credible story. There will be positive pointers as
SCHOOL PERFORMANCE well as important negative attributes that will
you build a multi-layered pen picture. A good
School is often the window to judge a child’s history will be multidimensional and allow you
overall health. Check if he or she finds it difficult to choose the thread to follow further with your
with numbers and concepts (Turner syndrome). examination.
Is there a problem with inattention, hyper-
activity or impulsiveness (attention deficit Table 1.5: Plan of diagnosis
disorder)? Has there been a recent steady decline History - Suggest something
in school work (autoimmune hypothyroidism)? General survey - Suggest specific system for
Is the child missing school frequently (chronic clinical diagnosis
illness)? Is the child isolated and avoiding Specific system - Points toward clinical
contact with other children (autism spectrum)? diagnosis
Investigation - Probable diagnosis
Dietary History Successful specific
A proper dietary history is important to assess treatment/
Surgery/Autopsy - Final diagnosis
the nutritional state. Record the child’s average
GENERAL SURVEY
The general survey is essential to form an perfusion and blood pressure. Whilst you are
opinion about the child before proceeding to the going from a distal to proximal aspect you will
systemic examination. You should pick up clues have noted any scars, wasting, venous
as you go along. Think of the examination as a prominences, lymph nodes and spider naevi. At
jigsaw puzzle and how you can fit the pieces. the neck, note lymph node enlargements,
The more meticulous you are the better. jugular venous engorgement, carotid pulsation
However, not all pieces of information will make and the thyroid gland. Look at the mouth for
sense at the same time. It may be that you will the health of teeth, gums, pallor, cyanosis,
come back to a sign or a lesion and understand jaundice, granulomas, mucositis and general
its meaning in retrospect. hygiene. The face is a vast source of information.
Observe the child’s appearance and activity There will be clues for anaemia, syndromes,
and note how the child adjusts to his or her facies, and a whole lot more. These will be dealt
environment. Simple observation can give you with in greater detail through the text.
vital clues, so it is important that you observe Whilst examining a child, always keep an eye
the child at play or in the way he walks or out for anything noteworthy. It may be a
interacts. Like the interview, establish a rapport ventriculoperitoneal shunt, a pleural drain or a
with the child and do appear non-threatening central venous catheter. These adjuncts are
in your approach. Record height, weight and crucial that you do not miss them, for they will
head circumference as detailed in the section on add up to the final diagnosis. As you perform a
anthropometry. general survey, you should think through the
Note the apparent age of the child and positive points in your examination. At the end
whether it tallies with the stated age. A of your survey, chalk out a plan of the system
‘nutritional dwarf’ will pass off as a normal for which is likely to be affected. This may not be
a lower age – anthropometry should resolve this. all that clear, so be prepared to examine a
Is the child cooperative, alert, playful, retracted number of systems, often in a certain order.
or anxious? Look for the following points in general survey:
It is useful to have a system by which you
can assess systematically in order - anaemia,
PALLOR
cyanosis, jaundice, oedema, clubbing and the tell
tale signs of any disease. One-way would be to Look for pallor with the child facing sunlight
start with examination of the hands and to and not in a room lit by artificial light. Look at
proceed upwards. In the hands you could note the lower palpebral conjunctiva, tip and dorsum
the presence of pallor, asymmetry, muscle of tongue, oral mucosa, creases of the palm and
weakness, liver, palms, clubbing, pulse, sole and the skin in general.
Table 2.1: Causes of pallor also peripheral sites). The common causes
• The “unwell” child (Table 2.2) are:
• Anaemia
• Shock states Table 2.2: Central cyanosis—causes
• Nephrotic syndrome Lung Causes
• Congestive cardiac failure • Respiratory failure
• Pneumothorax
It may sometimes be difficult to differentiate • Severe pneumonia
anaemia from other causes of pallor (Table 2.1). • Lobar collapse
Heart causes:
Pallor is also difficult to assess in the presence
• Fallot’s Tetralogy
of icterus. Pallor due to anaemia may be graded • Persistent fetal circulation
roughly in clinical terms as mild, moderate, and • Transposition of great arteries
severe: • Eisenmenger’s syndrome
• Mild—slightly less than normal Abnormal Haemoglobins:
• Abnormal haemoglobins such as sulphalemoglo-
• Moderate—conjunctival capillaries appear
binaemia and methaemoglobinaemia also give rise
prominent on a pale base to central cyanosis
• Severe—capillaries appear as pale as those
in the conjunctive; pallor evident in the b. Peripheral cyanosis: This occurs in the
palmar creases. presence of normal arterial oxygen satura-
tion (Table 2.3) and is due to pronounced
Icterus oxygen desaturation of the venocapillary
and capillary beds. Peripheral cyanois occurs
Like pallor, look for jaundice in daylight. The
in the tip of nose and nails, lips and ear
sites are the sclera, palate, under surface of
lobules.
tongue, palms and soles. A lemon yellow tint
indicates haemolytic anaemia; dark yellow or Table 2.3: Peripheral cyanosis
orange tint suggests obstructive jaundice (also
• Fever and rigor
look for scratch marks and shiny nails). In the • Cold exposure
neonate, discolouration of the face (= 5 mg/dl), • Shock
trunk (= 10 mg/dl), knee onwards (15 mg/dl) • Local vasomotor disturbance
and soles (20 mg/dl) gives a rough estimate (not
In newborns, cyanosis of the acral parts
to be relied on) of the degree of juandice.
(acrocyanosis) is common and is a variety of
peripheral cyanosis. A number of neonates have
Cyanosis
“perioral cyanosis,” due to prominent super-
This is the bluish discolouration of the skin and ficial venous plexuses in that region.
mucous membrane due to the presence of c. Differential cyanosis: It is as follows
reduced haemoglobin in the blood. Clinically • Hands blue, feet pink–Coarctation of aorta
cyanosis is present when the oxygen saturation with transposition of great arteries
is bellow 85 percent. Normal saturations are • Hands pink, feet blue–Patent ductus
greater than 93 percent—a child who is arteriosus with reversal of shunt due to
cyanosed is at serious risk of hypoxia. pulmonary hypertension.
Types Pigmentation
a. Central cyanosis (due to excessive oxygen Look for abnormal pigmentation on the face,
desaturation of the arterial blood): This is back, spinal prominences, buccal mucosa, gums
examined in all warm mucosal surfaces (and and on the palmar creases (Table 2.4).
General Survey 17
Table 2.4: Pigmentation

• Hyperpigmentation
– Ethnic
– Mongolian spot
– Kwashiorkor
– Cafe-au-lait spots
– Polyposis coli
– Addison’s disease
– Kala-azar
• Hypopigmentation
– Albinism
– Protein energy malnutrition
– Phenylketonuria
– Pityriasis versicolor
– Pityriasis alba
Fig. 2.1: Pitting oedema
Oedema The tissues at the base of the nail are thickened

An excess of fluid in the subcutaneous tissue and the angle between the nail base and the
causing swelling of the tissues is known as adjacent skin of the finger is obliterated. The nail
oedema. The best place to examine for this is loses its longitudinal ridges and becomes convex
over the medial malleolus of the tibia. In the from above downwards as well as from side to
supine child, it may be more useful to examine side. In extreme cases, the terminal segment of
over the sacral alae. Press over the area firmly the finger becomes bulbous like a drumstick.
with the ball of thumb for 20-30 seconds and You can assess clubbing by different ways
allow a depression to form (if there is a swelling). as follows:
Wait for the same duration of time and allow i. Keep the nail bed at the level of the eye
for the dimple to disappear. Palpate and make and look for the angle at the nail bed.
sure that the dimple persists (Fig. 2.1). Oedema Clubbing is present if this angle is lost.
due to fluid accumulation pits on pressure and Once clubbing is established, you can test
the skin returns to its previous state when time fluctuation. Stabilize the child’s finger
is allowed. Oedema due to lymphatic obstruc- distally with your thumbs and steady the
tion does not pit on pressure (Table 2.5). proximal phalangeal joint with the middle
fingers. Test for fluctuation using your
Table 2.5: Types of oedema index fingers. Then test for subperiosteal
a. Generalized (Due to changes of hydrostatic pressure,
thickening (hypertrophic pulmonary
osmolality or renal malfunction) osteoarthropathy) by palpating the bones
– Nephrotic syndrome of the wrist and ankle.
– Congestive cardiac failure ii. In normal nails, when both thumbnails are
– Kwashiorkor placed in apposition, there is a diamond
– Fulminant hepatic failure
– Cirrhosis
shaped gap, which is obliterated in
b. Localized (Due to local changes in capillary clubbing (Schamroth’s window test) (Figs
permeability) 2.2A and B).
– Angioneurotic oedema iii. The comparison of the depth of the index
– Urticaria finger at the base of the nail with its depth
– Cellulitis
at the distal interphalangeal joint is a good
method to recognize digital clubbing. The
Clubbing (Figs 2.2A and B)
depth at the base of the nail is normally
This physical sign is characterized by swelling smaller. A depth at the nail base equal to
of the terminal phalanges of the fingers and toes. that at the distal interphalangeal joint is
Table 2.6: Causes of clubbing

• Cardiac
– Cyanotic congenital heart disease
– Infective endocarditis
• Pulmonary
– Lung abscess
– Bronchiectasis
– Cystic fibrosis
– Chronic lung disease
– Empyema
– Tuberculosis
– Pleural mesothelioma
• Gastrointestinal
– Coeliac disease
– Inflammatory bowel disease
– Polyposis coli
Figs 2.2A and B: Clubbing – Chronic active hepatitis
• Others
– Familial
– Hodgkin lymphoma
said to be 2.5 standard deviations above – Thyrotoxicosis
normal.
Hypervascularity and opening of anastamo-
Types
tic channels in the nail bed occurs due to anoxic
(Fallot’s tetralogy), toxic (infective endocarditis) a. Of choice–comfortable in all positions.
influences, alteration of local prostaglandin b. Propped up–due to dyspnoea (congestive
metabolism, growth factors and other unknown cardiac failure due to rheumatic valvular
mechanisms. Clubbing is a slow process and is disease, pneumonia, bronchial asthma, huge
unlikely to be an acute event. You can use this ascites).
information to judge if the process has been c. Trepopnoea–a child with pleural effusion
going on for some time. Some clinicians grade and/or hydropneumothorax lies comfor-
clubbing but this is of little practical signi- tably on the affected side (splints the
ficance. Say if clubbing is present or absent. hemithorax) and becomes dypnoeic if lies on
When commenting on clubbing, also make the opposite side.
a note of cyanosis. You can home in on the d. Curled up–biliary colic, meningitis.
diagnosis in a child who is cyanosed and also e. Opisthotonus–kernicterus, tetanus, rabies,
has clubbing. Familial clubbing is by far the cerebral palsy.
commonest cause of clubbing in a well child. f. Listless–encephalopathy.
Compare with the hands of the parents in cases
of confusion. Here are some other causes of Facies
clubbing that you may come across (Table 2.6).
This refers to the expression on the face of the
child. Some diseases are thought to take on a
Decubitus
typical facial appearance. It is more sensible to
This is the posture of the patient in bed. This describe the appearance than label as a certain
does not apply to infants and young children facies. For example, in a child with thalassaemia
(who may be judged as to whether they are lying major, describe the (high cheekbones), maxillary
comfortably in the mother’s lap or not). protuberance and mild discolouration of the
General Survey 19
conjunctivae. It may also appear to be insen- a dull uninterested look suggest hypo-
sitive to speak of a “Down’s facies” when you thyroidism or mucopolysaccharidosis.
can convey the same information in your vi. Moon face–steroid therapy, nephrotic
description of a rounded face, almond shaped syndrome, Cushing syndrome, pulmonary
eyes and protruding tongue. However, you stenosis (Fig. 2.4).
should be familiar with some “typical” facies vii. Facies of bilateral facial palsy (loss of facial
and their associations with syndromes or expression) may occur with Guillain-Barre
diseases. You should look out for the following syndrome.
possibilities: viii. Malar flush–high colour on the cheeks is
i. Anxiety and apprehension may be due to said to be associated with mitral stenosis
pain, fear of the examiner or impending (an oestrogen effect, due to unmetabolized
respiratory failure. oestrogens in circulation)
ii. A child with a vacant look who is not ix. Risus sardonicus–raised eyebrows and
interacting with the environment may drawn out angles of the mouth (tetanus).
have severe learning difficulties and x. Congenital cry facies–deviation of the
mental retardation. angle of the mouth to one side due to an
iii. Down’s syndrome–upward slant of absent depressor anguli oris. A facial palsy
eyes, prominent epicanthic fold, small needs to be excluded.
nose, with depressed nasalbridge, wide xi. Conotruncal facies–hypertelorism, narrow
palpebral fissures small oral cavity with palpebral fissure, bloated eyelids, small
fissured, protuberant tongue. In Down’s mouth, deformed ear lobes. Examples are
syndrome the widest part is at the centre Fallot’s tetralogy, transposition of great
of the eye. This is in contrast to ethnic arteries and the chromosome 22-deletion
variants where the widest part is at the syndromes (like di George syndrome).
junction of middle and inner thirds (Fig. xii. Haemolytic facies–pallor, prominent malar
2.3). bones, depressed bridge of the nose,
iv. “Hepatic facies”– shrunken eyes, hollowed frontal bossing (Fig. 2.5).
out temporal fossa, pinched up nose, xiii. Anhidrotic ectodermal dysplasia– frontal
parched lips, muddy complexion and bossing, malar hypoplasia, recessing
icteric tinge. columella, lack of eyebrows, absent/
v. Thickened facial outlines (coarse features), conical teeth, wrinkled and hyper-
wrinkling of eyebrows, thick tongue and pigmentated periorbital skin.
Fig. 2.3: Facies of Down syndrome Fig. 2.4: Moon facies

A cry is sometimes accompanied by stridor as

in acute laryngotracheobronchitis.
Infants often hold their breath at the height
of crying. They may go blue or white in what is
described as a breath holding spell. A child with
Tetralogy of Fallot (without repair) may end up
with a cyanotic spell when crying.
Pulse
Pulse is the lateral expansion of the arterial wall
imparted by the column of blood due to
ventricular systole. Clinically there are different
areas to feel for a pulse (Table 2.7) (Figs 2.6 and
Fig. 2.5: Facies of haemolytic anaemia 2.6a). They are:
1. Radial pulse: Keep the child’s forearm in
slight pronation and wrist in mild flexion.
xiv. Williams’ syndrome–broad upper lip,
Feel with the tips of 3 fingers of your hand,
small mandible, prominent maxilla, up-
compressing the vessel against the bone of
turned nose and a “cocktail party chatter.”
the radius.
xv. Noonan’s syndrome–triangular face,
2. Brachial pulse: It is felt just medial to the
posteriorly rotated ears, ptosis, down-
tendon of the biceps brachii in the lower part
slanting palpebral fissures, deep grooved
of the arm.
philtrum.
3. Carotid pulse: The carotid may be gently
xvi. Russell-Silver syndrome – triangular face,
compressed against the transverse process of
pseudohydrocephalic appearance, down-
the cervical vertebrae. For quick localisation
turned corners of the mouth, lateral
(as in a cardiac arrest), palpate the thyroid
asymmetry.
cartilage (the most prominent point in the
neck) and slide the fingers down to the
Cry
groove in front of the sternocleidomastoid.
Babies normally cry and this is not always a Care should be taken not to palpate both
distress signal. With practise you will be able to carotids simultaneously (danger of critically
differentiate the cry of a well baby from that of reducing cerebral arterial supply). It is good
the sick newborn. The neonate with an infection practice to palpate the carotid whilst
has an irritable cry and may be difficult to listening to the heart. A carotid thrill with a
console. He or she will not generally be pacified murmur in the right second intercostal space
by measures like feeding. Irritable cry also is almost always an aortic stenosis.
occurs in other causes of cerebral irritation and 4. Femoral pulse: The femoral arteries lie
painful conditions of the skeletal system midway between the antero-superior iliac
(osteomyelitis, arthritis, periostitis).
Table 2.7: Pulses to check
A high-pitched shrill cry is heard in
conditions of raised intracranial tension (like 1. Radial
2. Brachial
meningitis) and tetanus. Hoarse cry is a feature
3. Carotid
of hypothyroidism, laryngotracheobronchitis or 4. Femoral
left recurrent laryngeal nerve paralysis. A weak 5. Popliteal
cry is heard in neuromuscular paralysis of the 6. Post-tibial
respiratory muscles as in diaphragmatic palsy. 7. Dorsalis pedis
General Survey 21
spine and pubic tubercle. They are easily examine the carotid artery, which is the closest
palpated against the underlying femur. pulse to the ascending aorta (the true arterial
Newborn femoral arteries should be waveform may be modified as one moves to the
routinely checked for coarctation of the aorta. periphery). The pulse rate is counted in beats
5. Popliteal pulse: They are not routinely per minute. Ensure that the child is relaxed (so
checked and are difficult to detect. They are as to eliminate tachycardia due to nervousness)
examined with the patient’s knees flexed at and note the pulse for a full minute. In emer-
an angle of 120 degrees. The fingertips of gency situations, one minute is a luxury. A
both hands are placed in the popliteal fossa, pragmatic way is to count beat for six seconds
with the thumbs restng on the child’s and multiply the figure by ten to arrive at the
patellae. pulse rate in beats per minute.
6. Posterior tibial pulse: This is detected 1 cm Normal pulse rates for various ages are given
behind the medial malleolus of the tibia. in Table 2.9.
7. Dorsal pedis pulse: You can feel this over the
dorsum of the foot by compressing over the Table 2.9: Normal pulse rate
tarsal bones. Age Pulse rate/min
Once a pulse has been localized, make Newborn 100 - 170
observations about the following (Table 2.8). <1 yr 80 - 160
2 yrs 80 - 130
Table 2.8: Peripheral pulse 4 yrs 80 - 120
6 yrs 75 - 100
Presence or absence (palpability) 8-10 yrs 70 - 90
• Rate
Adolescent 55 - 90
• Rhythm
• Volume
• Tension Tachycardia is an unusually fast pulse rate
• Equality when the rate exceeds the normal limits for age.
• Delay Tachycardia is usually sinus tachycardia, as with
• Character anxiety or fever. Bradycardia is when there is
unusual slowing of the heart rate. These can
Palpability occur with heart blocks and conduction defects.
When you feel for a pulse, be sure that you are There is some usage of a term called relative
not feeling the pulsation in the tips of your own tachycardia. In this case the pulse rate rises by
fingers. Absence of a femoral pulse may signify more than 10 beats per minute per degree rise
coarctation of the aorta. Hypoplastic left heart of temperature (oC) e.g., in rheumatic carditis,
syndromes may present with left outflow tract thyrotoxicosis.
obstruction and absence of a femoral pulse. A
child in shock may have a pulse that is difficult Rhythm
to palpate. In such a situation palpate a bigger
The pulse rhythm is either regular or irregular.
vessel like the carotid artery. Absent femorals
If it is irregular, try to assess if it is completely
can also be iatrogenic - umbilical artery catheters
irregular (the so called “irregularly irregular”
can lead to ileal/femoral artery spasm or
pulse) or is there any pattern to the regularity.
thrombosis.
Commonly an entirely normal rhythm is
occassionally interrupted by some slight
Rate
irregularity. This occurs with atrial ectopics that
Use one of the radial pulses to assess the rate. may be conducted to the ventricles or premature
For the character and volume, we should ventricular beats (extrasystoles). The pulse of
atrial fibrillation is completely irregular. Sinus first see what the normal arterial pulse looks like
arrythmia (heart rate increases with inspiration on a diagram.
and decreases with expiration) is a normally Abnormalities of different parts of the
occurring rhythm disturbance with no under- waveform occur with different conditions (Table
lying heart condition. 2.10). They are:
Table 2.10: Abnormal pulses
Volume
1. Slow rising pulse
The volume of a pulse gives an idea of the pulse 2. Hyperkinetic pulse
pressure. Pulse pressure in turn depends on the 3. Bisferiens pulse
stroke volume and compliance of the vessel wall. 4. Dicrotic pulse
5. Pulsus alternans
Low volume pulse is associated with shock, 6. Pulsus bigeminus
cardiomyopathy and significant aortic stenosis. 7. Pulsus paradoxus
High volume pulse occurs typically with fever 8. Collapsing pulse
or high output states like anaemia and
thyrotoxicosis. i. Slow rising pulse: There is slow upstroke
with a delayed peak. The pulse in aortic
Tension stenosis is classically ‘parvus et tardus’ - a
low volume and a prolonged systolic peak
Feel the ‘tension’ of a pulse by rolling the artery
(Fig. 2.6b).
and gauging the elasticity of its walls. However
ii. Hyperkinetic pulse: There is a quick rise
this is a very subjective test and has been largely
with good amplitude and is associated
replaced by the use of the sphygmomanometer.
with an increased stroke volume
Blood pressure recording is a more reliable
(congenital heart block, anxiety, anaemia,
measurement of tension.
fever, patent ductus arteriosus, aortic
regurgitation) (Fig. 2.6c).
Equality
iii. Bisferiens pulse: There are 2 systolic peaks,
Compare both radial pulses for equality. Suspect as occurs in aortic regurgitation, with or
a coarctation if a pulse is absent on one side. without aortic stenosis. The first systolic
Some types of anastamoses (for a primary peak is called the ‘percussion wave.’ A
coarctation) leave an absent pulse. It is also brief decline in pressure (mid-systolic
common to find an absent pulse in a Blalock- increase of obstruction) is followed by a
Taussig shunt (not a modified shunt) on that smaller, slow rising positive pulse wave
side. (tidal wave). The latter is produced by
continued ventricular ejection and
Delay reflected waves from the periphery (Fig.
2.6d).
Compare the femorals with the radials to
iv. Dicrotic pulse: This is due to 2 palpable
ascertain any radio-femoral delay. There should
waves, one in systole, and another in
normally be no delay (in fact the femoral pulse
diastole and occurs in those with low
arrives faster than the radial) unless there is any
stroke volume, some adolescents, cardiac
obstruction like a coarctation.
tamponade, severe heart failure and
hypovolaemic shock (Fig. 2.6e).
Character
v. Pulsus alternans: Alternating strong and
Occasionally, a pulse is assigned a special weak pulse occurs in left ventricular
character. To understand the character, let us failure. Unlike dicrotic pulse, each beat is
General Survey 23
separate with no quantitative difference in • Restrictive cardiomyopathy

systole and diastole (Fig. 2.6f). • Bronchial asthma
vi. Pulsus bigeminus: Regular alteration of • Severe cardiac failure
pressure pulse amplitude caused by • Superior mediastinal syndrome.
premature ventricular contraction that The mechanism of a paradoxic pulse is as
follows each regular beat. The larger wave follows. Normally, during inspiration, the
is followed by a small premature contrac- right atrium is at a lower pressure and this
tion and then by a pause. It usually occurs sucks in blood from the vena cavae. At the
with digoxin toxicity or ischaemic states of same time the pulmonary veins dilate
the myocardium as in hypoxia. leading to a marginal decrease of left atrial
vii. Pulsus paradoxus: It is an alteration of the volume. This in turn leads to lesser left
decrease in systolic arterial pressure ventricular filling. Thus, with inspiration
accompanying the reduced amplitude of there is a relative volume overload on the
the pulse that normally occurs during right compared with the left. As space is
inspiration (pulsus normalis exaggeratus). at a premium, bulging of the right side
Thus, a pulse is paradoxic if there is compresses the left side of the heart and
quickening during inspiration and slowing decreases the left ventricular output even
down in expiration. Some causes giving further. As cardiac output drops, blood
rise to a paradoxic pulse are: pressure falls and there is a compensatory
• Rapidly developing pericardial effusion, rise of pulse rate. The reverse takes place
cardiac tamponade in expiration. In states of constrictive
• Chronic constrictive pericarditis pericarditis or cardiac tamponade, the
a: Normal arterial pulse d: Bisferiens pulse
S = Systole, D = Diastole
b: Parvus et tardus pulse e: Dicrotic pulse
c: Hyperkinetic pulse f: Pulsus alternans
Fig. 2.6: Arterial pulse tracing

right ventricle further compresses the left caused by aortic regurgitation, patent ductus
ventricle, as the thickened pericardial sac arteriosus, arterio-venous fistula and other
allows no room to expand. In states of conditions where there is a run-off of blood from
bronchial asthma, bronchiolitis, the one vessel to the other. Mitral regurgitation and
negative intrathoraic pressure allows ventricular septal defect can sometime give rise
greater right atrial return and less of left to low volume collapsing pulse.
atrial filling. Also hyperinflation stretches The underlying mechanism of a high volume
the pericardium resulting in a rise of intra- collapsing pulse is as follows. An increased
pericardial pressure. stroke volume leads to the abrupt upstroke in
Pulsus paradoxus can be effectively the pulse wave. The collapsing character is a
demonstrated using a sphygmomano- result of two factors: a diastolic run-off into the
meter. Ask the child (who has to coope- left ventricle, and a rapid run-off to the
rate) to breathe normally without exagge- periphery because of low systemic vascular
ration. Push up the mercury and then resistance.
allow it fall. The first Korotkoff sound will In mitral regurgitation there is rapid run-off
be heard intermittently (varying with of blood into the left atrium. Similarly, blood
respiration). Note the first point and allow flows into the right ventricle in a ventricular
the mercury to fall until the first Korotkoff septal defect. In both instances there is rapid
sound is heard continously. This will run-off without an increase in stroke volume.
appear to be a “doubling” of the previous This leads to a low volume collapsing pulse.
sounds heard. Note the pressure at this
point. The difference between the two PERFUSION
points noted is known as the pulsus Capillary refill is a useful means of assessing
paradoxus. A 10-20 mm Hg change is skin perfusion. Press lightly for five seconds
equivocal but a value of more than 20 mm with the ball of the thumb in a central site, for
Hg is suspicious of a significant aetiology. example over the manubrium sterni. The area
viii. Collapsing (water-hammer) pulse: A of the skin should blanch with pressure. Count
collapsing pulse is characterized by a rapid how long it takes for the colour to return. The
upstroke and descent of the pulse wave. central capillary refill time should be less than
A water-hammer is a Victorian toy in the two seconds. It may be prolonged if the child is
shape of a club. It contains half water and underperfused from dehydration, septicaemia
half vacuum. On inverting the toy, a or cardiogenic shock. You may check capillary
sudden thud is felt on the palm due to the refill in the nailbeds, but do this only when you
falling column of water. A similar feeling are certain that the child’s circulation is intact
is obtained with a water-hammer pulse. and that the hands and feet are warm.
Hold the child’s wrist and feel the radial At the time that you check the child’s
pulse with your palm at the finger bases. capillary refill time, it is also useful to examine
Then lift the hand upwards quickly. In the for the state of hydration. Check the skin turgor,
normal individual, the pulse appears mucous membranes and anterior fontanelle to
feebler. In the high volume collapsing estimate the state of hydration. Enquire if the
pulse, the pulse is felt to slow initially child has passed urine–this gives you clues to
followed by an increased intensity. the state of renal perfusion. Do also note if the
Collapsing pulses can be of high volume or child is alert and well orientated–a pointer for
low volume. Highvolume collapsing pulse is cerebral perfusion.
General Survey 25
BLOOD PRESSURE and lower the pressure slowly. Listen

The blood pressure is recorded by a sphygmo- carefully for the first sound, which
manometer. An occlusion cuff is tied around the indicates the systolic pressure. As you
uper arm (right, by convention) and pressure in continue to lower the pressure, the sounds
the manometer is increased. As the pressure is suddenly become faint and then disappear
slowly reduced, Korot koff sounds are heard (diastolic pressure). The blood pressure
should ideally be measured in the resting
with the stethoscope over the brachial artery.
(static) and ambulatory phases. Record
The first sounds that occur (phase I) indicate the
should also be kept of the blood pressure
peak systolic pressure. The second and third
in the lower limb. This is useful in cases of
phases are due to turbulent flow of blood
suspected coarctation of the aorta. Tie the
through a partially occuluded vessel. The fourth
cuff over the thigh and auscultate the
phase occurs when the sounds become muffled
popliteal artery. Normally lower limb
and the fifth is when they disappear. The fifth
pressure is higher by 10-30 mm Hg in both
phase corresponds more accurately to true
systolic and diastolic pressures. This is due
diastolic pressure. These are following:
to the relatively smaller cuff size (trying
There should be some specifications that you
to occlude the greater muscle bulk of the
should ensure. thigh). In coarcation, the recorded pressure
i. Patient should be sitting or lying at ease. is low and in aortic regurgitation it is
ii. The manometer is placed so as to be at the higher by 40 mm Hg (Hill sign).
same level as the cuff on the arm and the iii. Flush method: Squeeze the palm of the
observer’s eye. limb with the cuff tied on the same arm.
iii. The cuff should be applied closely to the Inflate the cuff while the pressure on the
right upper arm, with the lower border not palm is maintained. The palm should look
less than 2.5 cm from the cubital fossa. pale when you have the cuff inflated. Now
iv. Cuff size should be correct for the arm. A reduce the pressure in the cuff slowly
narrow cuff will spuriously raise the blood while observing for the first flush. The
pressure. A variety of sizes are available. reading on the manometer at this point is
The inflatable bag should be long enough somewhere between systolic and diastolic.
to encircle the full circumference of the This test can also be done by holding up
upper arm and should be of a width the arm and applying a tight bandage from
roughly equal to two-third of the arm the hand up to the cuff and inflating. The
length. For general use, cuffs are made as bandage is then removed to reveal a white
neonatal, infant, child and adult sizes. limb. The pressure is slowly reduced to
You can use one of the many techniques of note the point of first flush.
blood pressure measurement. iv. Doppler: Automated oscillometric
i. Palpatory method: Palpate the arterial methods like “Dinamap” are a more con-
pulse while the mercury in the manometer venient way of measuring blood pressure
is allowed to fall. Note the point where than the flush method. This is especially
there is a return of pulsation. This gives useful in neonates, where any of the above
you the systolic blood pressure. methods are unreliable (in the absence of
ii. Ausculatory method: Palpate the radial an arterial catheter). This also comes in
artery and inflate the cuff to a pressure of handy in continuous recording of blood
30 mm Hg above the level at which the pressure in an intensive care setting.
pulse can no longer be felt. Place the v. Invasive arterial recording: An arterial
stethoscope lightly over the brachial artery catheter is introduced and the arterial trace
recorded. A pressure transducer can then ii. To detect pulsus paradoxus (see page 24).
read off the systolic and diastolic pressure iii. Hess test for thrombocytopenia/capillary
from the pressure wave. They are fragility: Draw a 2.5 cm circle on the
invaluable in umbilical or peripheral lines forearm and inflate a blood pressure cuff
in sick newborns or ill children who may to a pressure between systolic and diastolic
often need inotrope support. for 5 minutes. Normally less than 5-10
For a quick calculation, the median (50th petechiae should erupt.
percentile) systolic blood pressure for children
older than 1 year may be approximated by the Respiration
formula 90 mm Hg + (2 × age in years). The
Examine a child’s respiration in the following
corresponding diastolic blood pressure is
categories:
55 mm Hg + (2 × age in years). The lower limit
• Rate
(5th percentile) of systolic blood pressure (below
• Rhythm
which the child could well be in decompensated
• Depth
shock) is 70 mm Hg + (2 × age in years) (Table
• Type
2.11).
• Work of breathing
A child is said to have significant hyper-
• Adventitious sounds
tension if the blood pressure is at or above the
• Saturation.
95th centile for age. Blood pressure is normally
about 2-5 mm Hg higher for boys than girls.
Rate
Here are some figures from children in western
children to denote hypertension (Table 2.12). Count the rate for a minute when the child has
You may have noticed other uses of the been at rest for a few minutes or whilst sleeping.
sphygmomanometer apart from pure measure- Note also for rhythm, depth, position of
ment of blood pressure. They are: discomfort, dypnoea, adventitious sounds, and
i. To detect orthostatic hypotension (Chap. odour in breath. The normal respiratory rates
6, page 130). in children are given in Table 2.13.
Table 2.11: A guide to the normal Table 2.13: Normal respiratory rate in children
blood pressure values Age Respiration per minute
mm Hg Newborn 40-60
Birth (12 hours, less than 1000 g) 50/25 1-6 months 30-40
Birth (12 hours, 3 kg) 60/30 6 month - 2 years 20-30
Neonate (96 hrs) 65/45 Adolescents 12-20
1 year 75/50
4 years 85/60 Rhythm
8 years 95/65
10 years 100/70 Normal newborns (especially preterms) exhibit
alternate periods of progressively deeper
Table 2.12: Criteria for hypertension in western children respiration until a pause is reached. This is
Age Blood pressure (mm Hg) at 95th centile known as periodic breathing. Cheyne-Stoke
respiration is similar in older children with left
Newborn systolic 96
7 days systolic 104 ventricular failure or cerebral oedema. Biot’s
Child < 2 years 112/74 breathing is characterised by periods of apnoea
3-5 years 116/76 alternating with 4-5 breaths of normal depth,
6-9 years 122/78 and is associated with raised intracranial
10-12 years 126/82
tension.
General Survey 27
Depth distal airways (by virtue of the negative pressure

of the pleural lining) cannot collapse and
Shallow breathing is observed with ventilatory
continue to expand. During expiration air is
failure (narcotic overdose, cervical cord lesions).
pushed out of the lungs but no pressure gradient
Rapid, deep breathing is seen in cases of
exists for the subglottic tissues.
metabolic acidosis (salicylate poisoning, diabetic
Adventitious sounds are suggestive of
ketoacidosis).
pathology but their absence should not make
you assume normality. A child with a severe
Type of Respiration
asthma may not shift enough air to wheeze.
In older children, this is abdomino-thoracic. In Similarly, a child who is seriously ill with
newborns, the respiration is almost entirely epiglottitis may not produce an audible stridor.
diaphragmatic, and thus predominantly
abdominal. During inspiration, the compliant Oxygen Saturation
chest wall is sucked in (instead of expanding)
Pulse oximetry is being used increasingly as
giving rise to ‘paradoxic’ breathing.
bedside observation equipment. It incorporates
the principle of the oxygen dissociation curve.
Work of Breathing
A red and infra-red rich light source is used
You should assess the effort it takes the child to across an area rich in capillaries, like the pulp
breathe. The child without a respiratory problem of the finger or the ear lobule. The light is then
has quiet breathing. The child with a chest analysed at the other end after it passes through
infection has tachypnoea and has a noticeable the tissue. Depending on the state of the
effort in his breathing. Look at his or her chest oxygenation of haemoglobin in that tissue,
for recessions–subcostal, intercostal and certain parts of the red-rich light gets absorbed.
suprasternal. Check if the alae naesi are flaring. What comes out at the receiving end of the probe
A child with severe acute asthma will often find is analysed by a microprocessor into a
it difficult to speak. waveform. The machine then reads out a
percentage of oxygen saturation.
Adventitious Sounds Normal saturations are more than 93
percent. Saturations less than this indicate a
Sounds audible to normal ears are due to
degree of hypoxia but are rarely clinically
pathology in the upper airway (sniffling as in
detectable. Herein comes in the use of the pulse
nasal obstruction, snaring noise of soft palate
oximeter. It is a useful tool in any child with
weakness, rattling sound of loose mucous in the
tachypnoea and increased work of breathing.
trachea). The noise of stridor is typically
However, you must be aware that oximetry does
inspiratory but in severe cases may be both
not record the partial pressure of oxygen and is
inspiratory and expiratory. The expiratory noise
not a substitute for monitoring blood gases.
of wheezing may also be audible in a child with
Saturations can give false readings if there is a
asthma.
motion artefact (moving probe) or improper
Wheezing is expiratory because the smaller
signal quality (as in poor pickup from cold
airways collapse (patent in inspiration) during
surfaces).
expiration forcing air through them. Stridor is
inspiratory because the compliant subglottic
Temperature (Table 2.14)
tissue collapses due to negative pressure as a
result of the air travelling through the narrow Normal body temperature is considered to be
glottis at a high speed. On the other hand the between 36.6ºC (97.7ºF) and 37.2ºC (99.0ºF).
Table 2.14: The temperature ranges When the higher temperature has been reached,
at different conditions heat loss becomes apparent, the skin vessels
Centigrade Fahrenheit dilate and the body feels warm.
Normal 36.6-37.2 98-99 An infant with a high body temperature may
Subnormal < 36.6 < 98 be febrile or overheated. A febrile infant has a
Hypothermia < 35 95 high set point temperature and behaves as if
Febrile > 37.2 > 99 cold. Some infants can feel warm from a warm
Hyperpyrexia > 41.6 > 107
environment. In this situation he/she then
makes an effort to lose that extra-heat. The
When measuring temperature you should
clinical difference of the two is given in Table
ensure:
2.15.
i. The thermometer must be accurate.
Mercury thermometers are the standard Table 2.15: Clinical difference of overheated and
but sometimes cumbersome. Ear sensors febrile infant
are quick and reliable, provided they have Overheated infant Febrile infant
been calibrated. Skin probes are handy in
High rectal temperature High rectal temperature
situations that demand a continous skin
Warm hands and feet Cold hands and feet
temperature (as in a child with shock) but
Abdominal exceeds hand Abdominal exceeds hand skin
cannot always be relied upon.
skin temperature by temperature by more than
ii. Mercury thermometers must be kept in the less than 2oC 3 oC
oral cavity or under the axilla for 2-3 Pink skin Pale skin
minutes. Ear thermometers (which
Extended posture Lethargic
measure core temperature to a degree)
Healthy appearance Looks unwell
automatically read off when the signal is
complete. There are textbook descriptions of fever—
iii. Rectal temperatures (bulbous tip com- continued, remittent and intermittent. However,
pared to the long tip of the oral thermo- in practice the descriptions are less typical.
meter) are to be taken carefully as the glass Antipyretics will alter temperatures, especially
may break. Rectal temperatures are a if used on a regular basis. You should be more
useful method of measuring core tempe- keen on describing the spikes and duration of
rature but may not always be practical. fever than worry about the pattern it fits. The
Remember that axillary temperature is less classical fever patterns are:
than the rectal temperature by 1ºC, which a. Continued: Fever does not fluctuate more
in turn is less than the oral temperature by than 1ºC (1.5ºF) during 24 hours, and at no
0.5ºC. time touches normal.
iv. Before inserting the thermometer, wash it b. Remittent: Daily fluctuations exceed 2ºC and
with an antiseptic or in cold water and does not touch the base line.
see that the mercury is well shaken c. Intermittent: Fever present for several hours
down. Wash it again before replacing in daily with return to normal. Three patterns
its case. of intermittent fever exist (and in connection
In fever, the ‘thermostatic’ mechanism with malaria) which are:
controlling heat gain and loss is set at a level – Quotidian: Paroxysm occurs daily
higher than normal. While temperature is rising – Tertian: Paroxysm occurs on alternate
to this new level, heat is conserved, the skin days.
vessels are constricted so that the body feels cold – Quartan: Paroxysm occurs every two
and the patient may shiver violently (rigor). days.
General Survey 29
Fever may also be described in other ways. Table 2.16: Mechanisms of individual waves of JVP
i. Hectic: Temperature characterized by a a Due to atrial contraction
great swing with return to normal, as in c Coincides with the onset of ventricular systole and
septicaemia, empyema. results from the movement of the tricuspid valve ring
ii. Crisis/lysis: A temperature falling quickly into the right atrium as the right ventricular pressure
rises
within 6-12 hours is known as crisis (lobar
x Due to atrial relaxation and downward displacement of
pneumonia). Alternately the fever subsides the tricuspid value towards the apex of the right ventricle
gradually over several days by lysis in in systole
infections untreated by antibiotics and in v Due to passive rise in pressure as venous return to the
bronchopneumonia. atrium continues during ventricular systole whilst the
tricuspid value is closed
iii. Pel-Ebstein temperature: Regular altera-
y As the tricuspid valve opens, blood enters the right
tion of recurrent bouts of pyrexia with a ventricle rapidly and thus there is lowering of right atrial
period of apyrexia (lymphomas). pressure
iv. Relapsing fever: Characterised by cyclic
periods of fever and normal temperatures
(Borrelia recurrentis). does not exceed 2 cm vertically above the sternal
angle with the patient reclining at 45º. The
Jugular Venous Pressure (JVP) sternal angle is taken as the reference point
because the centre of the right atrium is at a
The internal jugular vein is in direct communi- depth of 5 cm from it in any position of the body.
cation with the right atrium and reflects pressure This means in a healthy child reclining at an
changes within the heart. The external jugular angle of 45º, the mean level will be invisible.
vein is more readily visible but is a less reliable When reclining at a 90º angle the venous level
means of predicting pressure changes in the should not be visible beyond the clavicle
right atrium. There are venous valves in the normally (Figs 2.7A to C).
external jugular vein that do not allow accurate If there is venous engorgement at the level
transmission of the pressure in the atria in the of the middle of the neck at 45º inclinaton, or at
heart. Further the external jugular system passes the root of the neck at 90º, jugular venous
through more fascial planes than the internal pressure is likely to be elevated. The venous
system and is more likely to be affected by pulse will normally be exaggerated (but not
extrinsic compression from other structures in beyond the lower third of the neck) when firm
the neck and upper thorax. In theory, therefore, and gentle pressure is applied below the right
the internal jugular venous pressure is an costal arch (hepato-jugular reflux).
accurate marker of atrial venous pressure. Note the vertical height of the pulsation
However, the relatively short neck of infants above the sternal angle. Venous pulse is often
makes detection of venous pulse extremely confused with an arterial pulse. In general, the
difficult in smaller children. characteristics of a venous pulse are given in
The venous pulse has 3 positive waves a, c Table 2.17. They should help you distinguish
and v and 2 negative waves (descents) x and y. true venous from arterial pulsations.
The mechanisms of the individual waves are
discussed in Table 2.16. Table 2.17: Characteristics of jugular venous pulse
To examine the jugular venous pressure, i. Soft, undulating, sinous
adopt the following procedure. Make an incline ii. Better seen in soft diffuse light e.g., a torch beam
of 45º on the bed with the examiner’s hand/back held tangentially across the neck
rest and allow the child to recline on it. The neck iii. Upper level falls with inspiration
should be supported so that the neck muscles, iv. Changes with posture
v. y-descent is seen as a dominant inward motion
especially the sternocleidomastoids are relaxed. (whereas the arterial pulse has an outward motion)
In normal children, the top of the venous column
lymphadenopathy in the child. The palpable

lymph node systems are given below:
i. Cervical lymph nodes: You can either exa-
mine from behind (with the neck slightly
flexed) or from the front. The lymph node
chains that you should palpate are:
occipital and suboccipital, post auricular,
Figs 2.7A to C: (A) Jugular venous pressure in normal
subject; (B) Reclining at 45°-point of transition between
anterior auricular, tonsillar, submandi-
distended and collapsed vein; (C) Upright-upper part of vien bular and submental groups, glands of the
collapsed and transition points obscured by sternum anterior and posterior triangles and lastly
the supraclavicular group.
ii. Axillary lymph nodes: Raise the patient’s
arm and insert the examining hand high
The JVP can be elevated due a number of into the axilla. Lower the arm into a flexed
reasons. They are as follows: position to rest across your examining arm.
i. Right heart failure Palpate individually for anterior, posterior,
ii. Superior vena caval obstruction medial, lateral and apical groups of lymph
iii. Pulmonary hypertension nodes. This is possible if only the child is
iv. Tricuspid stenosis, atresia not too ticklish.
v. Tricuspid regurgitation – A large c-v wave iii. Inguinal lymph glands: These are found
is formed by the regurgitation of blood into bilaterally along the groin creases. They are
the right atrium during right ventricular normally palpable (especially in children
systole. This wave is followed by a parti- who go barefeet) and are likely to be of no
cularly prominent y descent. significance on their own.
vi. Complete heart block–Regular ‘a’ waves iv. Other groups: Epitrochlear (behind the
occur while carotid pulsation occurs at a medial condyle of the humerus), popliteal
slower independent rate. Occasionally (back of the knee), retroperitoneal (deep
atrial contraction occurs when the atrio- palpation of the abdomen).
ventricular values are still closed, resulting Lymph nodes are thought to be significant
in a ‘canon wave.’ if the size of any of the lymph nodes (other than
vii. Constrictive pericarditis (JVP raised, but inguinal) is more than 1 cm in diameter. The
not pulsatile). corresponding size for the inguinal group is
viii. Cardiac tamponade (x descent only, no y more than 1.5 cm. Lymphadenopathy can be
descent). localized or generalized. If two or more lymph
node groups are enlarged, the term generalized
Lymph Nodes lymphadenopathy is used. When you detect
Examination of the lymph nodes is important lymphadenopathy, look for the associated
in the context of infection and malignancy. features:
Lymph nodes may be palpable due to minor 1. Matted–Typically found in tuberculosis but
abrasions or viral infections. A viral sore throat may also be present in lymphoma, bacterial
can give rise to large tonsillar nodes. A cut in lymphadenitis and secondary deposits.
the toes can track up to the inguinal nodes. To 2. Mobility–Malignant nodes may be fixed to
complete the picture, include a description of deeper structures. Any large adenopathy
what you think are the possible causes of appears to immobile.
General Survey 31
3. Tender, fluctuant, inflamed skin–These are deposition in the same area. Not the thyroid as
the tell tale signs of lymphadenitis, with or the child swallows—it should move up and
without absess formation. down with swallowing. Palpate the gland if
4. Draining areas–Commonly seborrhoea over enlarged (minor degrees of enlargement are
scalp, poor oral hygiene, tonsillitis. often better seen than felt). Comment on the
You should be wary of lymphadenopathy following aspects of the thyroid gland:
having a wider clinical significance. It is, a. Feel–solid, cystic, irregular.
therefore important to recognize the charac- b. Symmetry–enlarged on one side or smooth
teristics of lymph nodes when palpating them. and symmetrical.
Bear in mind the following diagnoses whenever c. Pressure effects–difficulty of swallowing,
you come across lymphadenopathy (Table 2.18). hoarseness.
You can consider lymphadenopathy to be d. Abnormal site–ectopic thyroids are often
either local or generalised. The causes for each lingual (look at the back of the tongue).
of the categories are given in Table 2.19. e. Associated features–exophthalmos, tachy-
cardia, sweating, warmth (thyrotoxicosis),
Thyroid learning difficulties, lethargy, dry skin,
delayed ankle reflex (hypothyroidism).
Inspect the neck for any general or local
If you have hypo or hyperthyroidism as a
enlargement of the gland. The thyroid gland is
possible diagnosis, do comment on the height
normally sited just below the Adam’s apple and
and weight of the child. Hypothyroidism may
should not be obviously visible in the healthy
lead to relative weight gain and poor growth.
child. Sometimes it may be confused with fatty
Hyperthyroidism can manifest itself as relative
tall stature. Remember to check for medication
Table 2.18: Important diagnoses
before commenting on the state of the thyroid.
associated with lymphadenopathy
Is the child taking thyroxine? Is he or she already
• Leukaemia–generalised lymphadenopathy with pallor
on anti-thyroid medication like carbimazole?
and bleeding
• Tuberculosis–“matted” nodes, failure to thrive and
history of contact with TB Skin, Hair, Nails
• Hodgkin lymphoma–isolated location, “rubbery” feel,
fever, night sweats Skin
• Kawasaki disease–marked cervical lymphadenopathy,
fever, rash, mucositis, skin peeling Run your hand over the skin in general and look
for dryness, pigmentation, scars, hydration and
Table 2.19: Causes of localised and signs of nutritional deficiency. You need to
generalised lymphadenopathy define skin lesions according to the site, size,
Causes of localised lymphadenopathy character and terminology. A useful description
• Local infection – throat, gums, hair follicles, wounds is given in Table 2.20.
• Lymphadenitis In practice, it is not so easy to distinguish
• Atypical mycobacteria between petechiae and purpura. More often
• Hodgkin lymphoma
• Infectious mononucleosis
than not, a child with a bleeding disorder will
Causes of generalised lymphadenopathy have a combination of petechiae and purpura.
• Acute leukaemias
• Lymphomas Hair
• Leishmaniasis
• Tuberculosis The pattern and distribution of hair is vital as
• Autoimmune disorders an adjunct in coming to a diagnosis in many
• HIV conditions. Look not only for scalp hair but also
Table 2.20: Skin lesions Table 2.21: Causes of hirsutism

Skin lesions Description Gonadal
• Polycystic ovary syndrome
Macule Non-palpable area of altered colour
• Ovarian tumour
Papule Palpable elevated area of skin < 0.5 cm
Adrenal
Plaque Palpable discoid lesion > 2 cm
• Cushing syndrome
Nodule Solid palpable lesion within the skin
• Congenital adrenal hyperplasia
> 0.5 cm
• Adrenal tumour
Vesicle Small fluid filled blister < 0.5 cm
Drugs
Bulla Large fluid filled blister > 0.5 cm
• Minoxidil, Phenytoin
Pustule Blister containing pus
• Danazol, androgenic steroids, oral contraceptives
Urticaria Elevated lesion, reddish or white with
• Acetazolamide, penicillamine, phenothiazines
red margin due to dermal oedema
Congenital
Telangiectasia Dilatation of superficial blood vessels,
• Trisomy 18
blanches on pressure
• Corelia de Lange syndrome
Petechiae Subdermal bleed, size about 2 mm
• Hurler syndrome
(pinhead)
• Hypothyroidism
Purpura Subdermal bleed, size about 3 mm
(larger than a pinhead)
Ecchymosis Large extravasation of blood size >5 mm Table 2.22: Causes of hypertrichosis
(bruise) Intrinsic factors
• Ethnic, familial traits
Extrinsic factors
hair over the body and genitalia. You should be • Local trauma
conversant with the Tanner staging of pubic and • Malnutrition
• Anorexia nervosa
axillary hair in boys and girls. Hypertrichosis • Phenytoin, corticosteroids, minoxidil, psoralen,
and hirsuitish are terms used to define excessive penicillamine, streptomycin
and abnormal hair growth, but they are not Naevi
synonymous. Hirsutism is an androgen • Congenital pigmented naevi, hamartomas
dependent male pattern of hair growth in Congenital disorders
• Mucopolysaaccharidoses
females. The common sites of hirsutism are the • Cornelia de Lange syndrome
moustache, sideburns, beard area and back • Lipodystrophy
(Table 2.21). Hypertrichosis is excessive hair • Hemihypertrophy
growth in non-androgenic areas. Causes of • Fetal hydantion and alcohol syndromes
hypertrichosis is given in Table 2.22. • Trisomy 18
• Porphyrias
Hypotrichosis is deficient hair growth,
whereas hair loss (partial or complete) is called
alopecia. Alopecia areata involves a patch of hair evidence to corroborate with your findings in
loss - if you look closely, you will find other systems. It is often a good idea to use a
“exclamation mark” hairs in that part of the magnifying glass to observe the nails. A handy
scalp. Tineasis, trichotillomania and idiopathic clinical tool is the auroscope if you do not have
alopecia are generally cited as the reasons. Other a magnifying glass. You could describe nails as
causes of scanty hair (alopecia and hypo- per Table 2.24.
trichosis) are as follows (Table 2.23).
REGIONAL EXAMINATION
Nails
Head
Nails are useful diagnostic markers in many
chronic disorders. Look for clubbing, cyanosis, Record the head circumference using standard
whitening, splinter haemorrhages and use the methods outlined (see anthropometry). An
General Survey 33
Table 2.23: Causes of alopecia Table 2.24: Different types of nail and its causes
From birth/inherited Small/absent–Ectodermal dysplasia, nail-patella
• Autosomal recessive anomaly, ectodermal dysplasia, syndrome, cartilage-hair hypoplasia, incontinentia
Moynahan syndrome, aplasia cutis, epidermal naevus, pigmenti, trisomy 13, trisomy 18, Turner syndrome, fetal
progeria, hereditary hypotrichosis, keratosis pilaris, hydantoin and alcohol syndromes
phenylketonuria, Menkes kinky hair syndrome, Large–Hemihypertrophy, Rubenstein-Taybi syndrome,
dyskeratosis congenita, Seckel dwarf, cartilage-hair pachyonychia congenita
hypoplasia, incontinentia pigmenti, Treacher-Collins White nails–Trauma, pallor, cirrhosis, hypoalbuminaemia,
syndrome tuberculosis, chronic arsenic poisoning, malignancies
Endocrine Terry nails (white nail, with distal normal pink colour) –
• Hypopituitarism, hypothyroidism, hypoparathyroidism, Hypoalbuminaemia of cirrhosis
diabetes Muehrcke lines (parallel white bands)–Hypoalbuminaemia
Nutritional Lindsay nails (proximal part white, distal part pigmented)
• Protein energy malnutrition, iron and zinc deficiency, –normal variant, renal failure
essential fatty acid deficiency, gluten-sensitive Onycholysis (separation from nail bed)–Trauma, fungal
enteropathy infection, psoriasis, contact dermatitis, vincristine,
Toxic bleomycin, chloramphenicol
• Cytotoxic chemotherapy, radiation therapy, heparin, Pitting–Psoriasis, alopecia areata, dermatitis, fungal
hypervitaminosis A infections
Auto immune Beau lines (transverse grooves in nail plate)–Systemic
• Alopecia areata, dermatomyositis disease (chronic illnesses), zinc deficiency (acrodermatitis
Traumatic enteropathica)
• Traction, trichotillomania Pigmentation–Lichen planus, black and Asian children
Cicatricial (melanonychia striata)
• Lupus erythematosus, dermatomyositis, tinea, Green pigmentation–Pseudomonas infection of nail
cicatricial pemphigoid, acne, leishmaniasis Yellow nails–Icterus, carotinaemia, yellow nail syndrome
• Trichodystrophies Azure half moons–Wilson’s disease
• Trichorrhexis nodosa, pili torti, pili annulati Red half moons–Chronic renal failure
Splinter haemorrhages–Minor trauma, dermatomyositis,
infective endocarditis, vasculitis, peptic ulcer disease,
abnormally big head is called macrocephaly. hypertension, chronic glomerulonephritis, cirrhosis, scurvy,
Similarly, microcephaly is a head circumference neoplasms
that is small by 3 standard deviations from the Clubbing–See section on clubbing
expected normal for age and sex (use a head
circumference growth chart). Common causes
fontanelle is closed. If normal, it is unlikely to
are described in Table 2.25.
be a fusion problem. Look for clues that will
There are many abnormal head shapes, not
point you in the right direction. The abnormality
all of which are related to disease conditions
may be the result of a localised swelling like a
(Fig. 2.8). The flat occiput of plagiocephaly,
cephalhaematoma, a dermoid or an abscess.
where the skull seems asymmetrical is a normal
Search for surgical scars and ventriculo-
variant in infants. Plagiocephaly is commoner
peritoneal shunts. Some abnormalities that
nowadays because of the advice given to
should alert to you a serious problem are given
mothers to lay their babies on the back (the
in Table 2.26.
“Back to Sleep” campaign to prevent cot death).
Plagiocephaly, however, can also be related to
Fontanelles
craniosynostosis that needs surgical interven-
tion. Palpate the sutures to see if they have fused There are 6 fontanelles at birth, all of which may
prematurely in craniosynostosis. Overriding of or may not be palpable. The most important
the skull bones may lead you to believe that ones are the anterior and posterior fontanelles.
there is prominence of a suture. Check if the The fontanelles may be measured by joining the
head circumference is small and if the anterior mid points of the 4 sides to form 2 diameters.
Table 2.25: Abnormal head circumferences

Microcephaly
Primary
Autosomal recessive
Autosomal dominant
Trisomies
Cornelia de Lange syndrome
Smith Lemli Opitz syndrome
Secondary
Intrauterine infections–CMV, Rubella, toxo-
plasmosis
Neuronal injury from meningitis, encephalitis,
perinatal hypoxia
Malnutrition
Fetal alcohol syndrome
Macrocephaly
Hydrocephalus, hydranencephaly
Cranial thickening–Chronic anaemia, rickets,
osteogenesis imperfecta
Subdural effusion–Secondary to meningitis, non-
accidental injury
Metabolic–Mucopolysaccharidosis, Tay-Sachs,
Alexander disease
Sotos syndrome
Neurofibromatosis
Table 2.26: Abnormal head shapes

• Dolicho/scaphocephaly–Head elongated in the Fig. 2.8: Different types of abnormal head shapes:
anteroposterior diameter (children born prematurely) oxycephaly, brachycephaly, macrocephaly, scaphocephaly,
• Prominent occiput (trisomy 18) hydrocephalus, plagiocephaly
• Frontal bossing (thalassaemia, rickets, Hurler’s
syndrome, hydrocephlaus, malnutrition)
• Acrocephaly/oxycephaly/turricephaly – conical head meningitis needs to be considered. Some
(Apert’s syndrome) conditions give rise to a wide anterior fontanelle.
• Brachycephaly–Anteroposterior flattening (Down’s Common causes are hydrocephalus, achondro-
syndrome)
plasia, prematurity, osteogenesis imperfecta,
• Trigonocephaly–Pointed metopic suture (cranio-
synostosis) trisomies and vitamin D deficiency rickets.
• Caput quadrantum–hot cross bun appearance (rickets) Normally, a fontanelle is pulsatile because
of transmitted pulsation of the CSF secretion
from the choroid plexus. In raised intracranial
The anterior fontanelle usually measures 2.5 cm
tension, the normal pulsation is lost. The
× 2.5 cm at 3 months and closes by 9-18 months
fontanelle then appears to be abnormally “full”
of age. The posterior fontanelle is small at birth
and tense. Contrast the depressed fontanelle that
(usually the size of a fingertip) and closes
you see in a child with significant dehydration.
rapidly by 6 weeks of age.
It is best to examine the fontanelle when the
Scalp
baby is quiet and the head upright. You may find
a bulge if he/she is crying and in the lying We discussed about the significance of hair in
position. In such instances, change position and the chapter headed “skin, hair, nails.” Here are
re-examine. You should always worry if the a few additional features of scalp hair that you
fontanelle feels tense and bulging in which case could comment in Table 2.27.
General Survey 35
Table 2.27: Scalp hair Table 2.28: Scalp abnormalities

Colour a. Caput succedaneum–Diffuse, boggy, soft swelling of
The colour of hair is genetically determined. Some the scalp that disappears by the end of the first or
conditions like phenylketonuria, albinism lead to uniformly second day
hypopigmented hair. Children with kwashiorkor have b. Scalp abscess, pyoderma
alternating periods of relatively improved nutrition and this c. Seborrheic dermatitis (cradle cap)–Adherent scales
gives rise to an alternating pattern of hypopigmentation and crusts that are large, moist, greasy and dirty yellow
called the ‘flag sign.’ Partial hypopigmentation of the hair d. Mastocytosis–Small brown to scales, crusting and
may also be found in Wardenberg, syndrome, Chediak- petechial lesions
Higashi syndrome and pili anulati. e. Distension of the scalp veins associated with raised
Texture intracranial tension
Fine thin hair is a feature of homocytinuria and Weaver’s f. Scalp defects as in focal dermal hypoplasia,
syndrome. Dry coarse hair is found in hypothyroidism and incontinentia pigmenti, Wolf-Hirschhorn syndrome
fetal alcohol syndrome. g. Subcutaneous nodules over occupital areas -
rheumatic fever or rheumatoid arthritis
Curled hair h. Cutis verticis gyrata–Characterized by 10-12 (1-2 cm
This hair is an Afro-Caribbean characteristic, but twisted thick) anteroposterior or transverse gyrate folds, often
hair along its long axis (pili torti) along with fragility is found accompanied by mental retardation
in Menkes syndrome.
Beaded appearance
This may be due to constriction at regular intervals particularly important when you are dealing
(monilethrix) and nodular swellings along the shaft
with dysmorphic syndromes. Look carefully at
(trichorrhexis nodosa). More commonly look for lice and
nits if the hair appears beaded. the size and shape of the forehead and comment
Aberrant pattern
on the frontal hairline. Vertical height of the
The normal pattern is characterized by a parietal whorl, forehead is increased in hydrocephalus,
located anterior to the position of the posterior fontanelle, Crouzon’s disease and Apert’s syndrome.
from which the hair stream progresses outward covering A pointed forehead is seen in trigonocephaly
the extent of scalp hair. Usually a single whorl is present and midline brain defects. Low frontal hairline
to the left of the midline. Abnormal patterns are:
1. Absent parietal whorl or location more central or
is common in Hurler’s syndrome, de Lange’s
posterior (microcephaly) syndrome and is often a feature in children with
2. Low hairline, often related to a short or webbed neck severe learning difficulties.
(Turner syndrome, Klippel-Feil anomaly) In a child with a large forehead and suspec-
3. Excess projection of hair into cheek (Treacher-Collins ted hydrocephalus you could percuss for a
syndrome)
“crackpot” sign (MacEwan’s sign), which feels
like a crumbling eggshell under your fingers.
Run your hand through the child’s hair and
The sign is positive when sutures are separated
look under the hair for any scalp abnormalities.
due to raised intracranial tension. It is physio-
You may pick up scars from neurosurgical
logically present during infancy as long as the
procedures that lie neatly hidden under locks
anterior fontanelle is open.
of hair. You may also palpate the tube coming
Translucency is a test for subdural effusion,
out of a ventriculoperitoneal (VP) shunt. Here
hydrocephalus, hydranencephaly and porence-
are some abnormalities which you may come
phaly. Use a flashlight, preferably with rubber
across in your examination (Table 2.28).
foam encircling the end, and place it snugly over
the frontal and occipital areas in a dark room.
Forehead
Look for a rim of translucency extending beyond
You may want to describe the forehead when 2.5 cm in frontal area and over 1 cm in the
commenting of the face of the child. This is occipital region.
Intracranial bruit may be auscultated over upper third of the neck. Observe if the carotids
the scalp. It may be present in 10 percent of are ‘dancing’ and if there is a thrill or a venous
normal children, some conditions of raised hum. If there is a swelling, ascertain if it arises
intracranial tension and artriovenous malfor- from a lymph node, muscle, bone or the skin.
mations. If you see a child with cardiovascular
features of high output failure but no obvious Eyes
lesion, it is good practice to put the stethoscope
The eyes are a storehouse of information and
over the scalp. An A-V malformation involving
you should reserve considerable time and effort
the vein of Galen is a noteworthy example.
in the eye examination. Whilst talking to or
observing the child you may have picked up
Neck
some features like squints, epicanthic folds or
Children normally have relatively shorter necks abnormal pigmentation. Make a mental note of
compared to adults. A neck length (occipital these findings and correlate them when you test
protruberance to the C7 vertebral spine) of less the eyes more formally.
than 1/13 of the occiput-heel length is defined It may be easier to have a system whereby
as a short neck in children. Shortness of the neck you test all aspects of the eye in sequential
in clinical practice is, however, a subjective term. fashion. A system is handy for practical
The neck may appear short in webbing due to purposes as it will enable you to cover most
Turner syndrome. Short neck occurs in children aspects the examination. With practice you
with vertebral anomalies, platybasia and should do this quickly and accurately. Before
Klippel-Feil deformity. Other causes include commencing your systematic examination you
chondrodystrophic congenital calicification, should make sure that the child can see well,
hypothyroidism, Sprengel deformity, Gold- otherwise it is meaningless to give him/her a
enhar, Hurler and Morquio syndromes. command. To do this, use a Snellen chart to test
The neck is a midline structure, but appears visual acuity in children older than seven years
to be positioned to one side in a child with (and possibly adapted to a local vernacular). In
tortiocollis. To differentiate between tilting and the absence of a formal chart, roughly test for
tortiollis have the child lie on his back and visual acuity by asking the child to count the
examine from the head end of the table. In number of rails (at a distance) or the number of
torticollis, the occiput is tilted to one side and fingers (near vision). Also satisfy yourself that
the chin tilted to the other. In head tilting both the child has some sense of colours. The Ishihara
the occiput and chin are tilted to the same side. chart is not standardized for children less than
Sternomastoid tumours commonly present with 11 years, so it is not helpful in those younger.
torticollis. In opisthotonus (tetanus, dystonic Use common primary colours on dresses, books,
cerebral palsy) the occiput is tilted markedly etc and ask the child “what colour is this?” This
backward. Neuromuscular disorders with question presumes that the child’s development
altered curvature of the spine may also affect is appropiate to understand the command.
the appearance of the neck. In Caries spine, the Look carefully at the eyes and note if they
child holds his neck stiff and walks carefully are normally spaced out. Are they too far apart
avoiding jarring movements. or are they too close to each other? Is there any
Look out for any abnormality that catches obvious squint (manifest squint)? Is there any
your eye. There may be lymph node enlarge- abnormality of the palpable fissure, eyelid,
ment, thyroid swelling, thyroglossal cyst, conjunctivae, cornea or iris? Do the eyes
branchial cyst or fistula. Branchial fistulas are move equally in all directions? Is one eye
located in the lower part of the neck and completely static in movement in all directions
thyroglossal fistula situated higher up in the (glass eye)?
General Survey 37
Comment on all visible structures in each eye 1.85 +/– 0.13 cm (whites), 2.00 +/– 0.22 cm
and say if they are normal. Next use a pen torch (blacks) or 1.95 +/– 0.20 cm (Hispanics).
and use it from a distance. The light should fall Local data in Indian children is not available
equally (almost) on the pupils of both eyes. This but these figures should give you a rough
is known as corneal reflection. If the spot of light guide of what to expect. Short palbebral
appears wide of the centre, a squint is likely. Do fissures are found in the fetal alcohol,
the cover-uncover test if there is any suspicion. William’s, whistling face syndromes and
Bring the light to one eye (whilst you put the with microphthalmia.
ulnar aspect of your hand over the nose to b. Squint, ptosis–Discussed in neurological
prevent light getting into the other eye) and examination.
observe for direct and consensual light reflexes. c. Eyepopping–When an examining light is
Repeat the same with the other eye. Move back removed, some infants show a transient
and ask the child to follow the light source. You widening of the palpebral fissure.
are now testing for extra-ocular muscle d. Colobomas (gap or discontinuity of a
movement. Let the child know what you are structure) of eyelids–Lower eyelid colo-
about to do and encourage him/he to say if he/ bomas occur in Treacher Collins syndrome
she sees double (diplopia) at any point. Define whilst those with upper lid defects occur in
(with your pen torch) movements in vertical, Goldenhar syndrome.
horizontal, temporal and nasal directions in the e. Excessive blinking–Eye strain, tic
shape of an “H” or an “X.” Observe for f. Belpharospasm–Congenital glaucoma,
nystagmus and corroborate with symptoms of corneal ulceration, conjuctivitis, keratitis
diplopia. You should also be able to watch for g. Upward slant of eyes–Down, Zellweger,
signs of lid lag or ptosis. Aarskog syndrome
You could now test for field of vision. Sit in h. Downward slant of eyes–Treacher-Collins,
front of the child (at one metre distance) with whistling face, cri-du-chat, Pfeiffer and 10p
one eye closed. Use the child’s own hand (or the deletion syndromes
parent’s) to cover his/her corresponding eye i. Hordeolum (stye), chalazion (meibomian
(opposite to you). Keep the head still and cyst), haemangioma, dermoid cyst
encourage fixing his/her eye on your nose. Do j. Eyelashes–Absent in premature babies,
the same for yourself. Wiggle your finger and Treacher Collins syndrome (inner 2/3 of
bring it from outside inwards and compare lower lid). Long eyelashes can be inherited
against your own field of vision. Make a game or are associated with chronically ill children
of this to see if the child can see better than you and in those with Cornelia de Lange
can. Test in different directions and for each syndrome. Pediculosis can occur in the
eye separately. Lastly use the ophthalmoscope eyelashes. Hypopigmented eyelashes (in
to see the fundi of both eyes (see chapter on non-Caucasians) occur with albinism and
neurology). You should have by now assessed uveomeningitis.
the 2nd, 3rd, 4th and 6th cranial nerves, k. Eyebrows–May be absent in premature
while also commenting on the structural babies and appears less in amount in
aspects. cartilage hair hypoplasia and Hallerman-
Let us now discuss a few abnormalities that Streiff syndromes. Eyebrows are bushy in
you are likely to encounter. Hurler syndrome and meet in the midline
a. Palpebral fissure length - Hold a ruler (synophrys) in de Lange and Waardenburg
across the eye’s greatest horizontal axis syndromes. Hypertrichosis of eyebrows can
from the medial to lateral canthus. At 40 be present with hypotrichosis of scalp in the
weeks gestation the palpebral lengths are Coffin-Siris syndrome.
l. Swelling around eyes–Slight puffiness of the Table 2.29: Conjunctival lesions

eyes and dark circles may be seen in those • Subconjunctival haemorrhage–pertussis, trauma, toxic
with nasal allergy (allergic shiners). shock syndrome, haemorrhagic diseases, Henoch
m. Lid oedema–Conjunctivitis, pertussis, Schonlein purpura, post normal delivery in neonates
measles, infectious mononucleosis, acute • Conjunctivitis–infective, allergic, phlyctenular
• Conjunctival xerosis–vitamin A deficiency
nephritis
• Pinguecula–elevated, yellowish lesion that extends
n. Epicanthus–A fold of skin extending down from the outer canthus: occurs in Gaucher’s disease.
from the upper lid to cover the medial • Pterygium–triangular membranous fold (whose apex
canthus of the eye may be noted in normal involves the cornea, the base being continuous with
newborns and disappears in 1-3 months. the conjunctiva) is often the result of exposure to wind,
dust and sun
Prominent epicanthic folds occur with Down
• Epibulbar dermoids–Goldenhar syndrome
syndrome, congenital ptosis and Pompe’s
disease. Epicanthic folds can also occur in a
variety of syndromes include the cerebro- q. Conjunctival lesions–You should look for the
hepatorenal, cri-du-chat, de Lange, fetal following lesions given in Table 2.29.
alcohol, fetal hydantion, leopard, Mobius, r. Sclera–Sclera of infants and young children
Noonan, Turner, Smith-Lemli-Opitz, Patau, are normally bluish. Pathological states with
Williams and Potter syndromes. blue sclerae are the following: Osteogenesis
o. Spacing–Spacing between the eyes are imperfecta, congenital glaucoma, Russel-
estimated, but to confirm hypertelorism Silver syndrome, Ehlers-Danlos syndrome,
(wide spacing) or hypotelorism (close Marfan syndrome, melanin deposits (naevi/
spacing), you should take measurements. freckles).
The interpupillary distance is the best s. Cornea–The cornea in newborn infants has
indicator of ocular hypertelorism (with the a diameter of 9-10 mm. Megalocornea (>13
exception of the Waardenberg syndrome). It mm) occurs in hereditary abnormal eye
is hard to measure interpupillary distance enlargement and congenital glaucoma. The
particularly in infants. You may obtain cornea is normally clear but can be clouded
special graphs to plot the distance between in a number of metabolic disorders like
inner and outer canthi in different ages. Hurler, Morquio, Scheie and Maroteaux-
You could think of ocular hypertelorism Lamy syndromes, GM1 gangliosidosis,
as putting a third eye between the eyes. Some mannosidosis, mucolipidosis, tyrosinosis as
causes of hypertelorism are: Apert, Aarskog, well as in interstitial keratitis (congenital
Sotos, cerebrohepatorenal, chromosome 4p syphilis). Corneal ulceration is a feature of
deletion, cri du chat, Crouzon, di George, keratomalacia (vitamin A deficiency) and
fetal hydantion, Noonan, orofaciodigital, herpes simplex (dendritic ulcer). Loss of
whistling face, Williams and Turner corneal sensation occurs with familial
syndromes. Ocular hypotelorism occurs in dysautonomia. A ring called the corneal
arhinencephaly, cyclopia and holopro- arcus is often present by age ten in those with
sencephaly. familial hypercholesterolaemia. The Kayser-
p. Tearing–Epiphora (excessive tearing) is Fleischer ring associated with Wilson disease
found is conjunctivitis, corneal ulcer, is characteristically different (Table 2.30). It
nasolacrimal duct obstruction, allergic is unilateral or bilateral, complete or
reaction and exophthalmos. Absence of tears incomplete, golden brown or greyish-green
occurs in the familial dysautonomia ring at the limbus of the cornea. KF rings may
syndrome. also be seen in some familial cholestatic
General Survey 39
syndromes and in chronic active hepatitis Table 2.31: Iris abnormalities and pathologies
with cirrhosis. It may not be obvious to the 1. Ciliary infection – usually associated with uveitis and
naked eye and you, therefore, should use a iridocyclitis. The iris may also appear dull and
slit lamp to visualize this. discoloured and sluggishly reacting. Slit lamp shows
keratitic precipitates and cloudy appearance of the
Table 2.30: A few corneal abnormalities aqueous humour. Common conditions are
pauciarticular juvenile chronic arthritis, tuberculosis,
Megalocornea Corneal Arcus inflammatory bowel disease, Reiter disease,
Clouded KF ring sarcoidosis and Vogt-Koyanagi-Harada syndrome.
Ulceration 2. Hypopigmented iris in albinism, Chediak Higashi
Loss of sensation syndrome
3. ‘Salt and pepper’ speckling of the iris (Brushfield spots)
t. Lens–Any opacity of the lens is called a in Down syndrome
cataract. A red fundal reflex surounds the 4. Iris nodules (Lisch nodules) in Neurofibromatosis
5. Heterochromia–Hetrochromic iridocyclitis of Fuchs,
opaque density if the cataract is not
Waardenburg syndrome
complete. Congenital cataracts are associated 6. Iridodonesis (quivering movement of the iris)–
with TORCH infections, galactosaemia, Homocystinuria, Marfan’s syndrome
homocystinuria, hypoparathyroidism, 7. Iris coloboma–Autosomal disorder, trisomy 13, focal
aspartyl glycosaminuria, osteopetrosis, dermal hypoplasia, CHARGE associations, Wolf-
Hirschhorn syndrome
Refsum syndrome, cerebro-hepato-renal
8. Aniridia–Autosomal dominant, association of Wilm’s
syndrome, Marfan syndrome, incontinentia tumour, Rieger anomaly
pigmenti, trisomies and the Smith Lemli
Optiz syndrome. Cataracts can be inherited
as an autosomal dominant condition. Radia-
tion therapy, hypoparathyroidism and long-
term steroid use are also common offenders.
u. Retrolental membranes–Retinopathy of
prematurity, persistent hyperplastic primary
vitreous, persistent pupillary membrane,
retinal dysplasia.
v. Uveal tract–The only part of the uveal tract
that you can see is the iris. Isolated abnor-
malities of the iris are rare in children and
you should, therefore, consider in your mind
the following pathologies given in Table 2.31.
w. Retina (Chap. 6).
x. Strabismus, diplopia, opsoclonus, nystagmus
(Chap. 6, page 104-107).
Fig. 2.9A: Position for examination of ear and throat
Ears (Fig. 2.9A)
1. Hearing - See section on neurology thirds of the ear by 38-40 weeks gestation.
2. Pinna - In the premature infant the cartilage The anatomic landmarks of the fully
is not fully developed. The pinna lies flat developed ear pinna are shown in Figures
against the scalp with only slight incurving 2.9A and B.
of the superior part at 33-34 weeks gestation. The external ear is often abnormal and
By 36 weeks gestation, the pinna springs “simple” in the dysmorphic child (Figs 2.9A
back after folding. Incurving occurs in two- and B). There may also be structural changes
c. Pre-auricular papillomas or tubercles –

Commonly these are due to maldevelopment
of the first branchial arch. These can be
isolated or occur as part of the Goldenhar
syndrome.
d. Congenital aural fistulas – Usually isolated
but can give rise to recurrent meningitis if
leading into the cranium.
e. Darwinian tubercle (small prominence or
thickening along the posterior segment of the
Fig. 2.9B: Anatomic landmarks of fully developed ear helix near the tip of the auricle)–normal
children, Marfan’s syndrome.
f. Microtia–Treacher-Collins, Goldenhar syn-
around the ear that make it appear abnormal. dromes.
Mastoiditis, lymph node enlargement and g. Linear indentations of the ear lobes (or
haemorrhage (Battle sign) from basal skull anterior/posterior lobule) - Beckwith Wiede-
fracture are some examples. In the pinna itself, mann syndrome.
observe for the following: h. Notched ears - Di George syndrome.
a. Low set ear – Consider a plane connecting 3. Tympanic membranes and external auditory
the medial and lateral canthi of the eyes. The canal: No examination is complete without
insertion of the ear to the scalp lies normally visualizing the tympanic membranes. First
on the same plane. The top of the ear is about you have to restrain the child so that he/she
1/10 (of the height of the pinna) above a does not get hurt when you insert the
horizontal line drawn from the medial auroscope. Sit the child (facing sideways) on
canthus. The ears may appear to be low-set the mother’s lap. Ask her to put one hand
(when in fact they are not) when the neck is over the child’s head and forehead to hold
short, cranial vault is high, the mandibular him/her down on her chest. Instruct her to
ramus is short or the auricles are rotated. In put the other hand across the child’s chest
Down syndrome, the child has low-set small to restrain him/her. Once you are satisfied
ears. The following table gives you some with the arrangement, insert an auroscope
causes associated with low set ears (Table to see the tympanic membrane (Fig. 2.10). In
2.32). newborns and infants, the direction of the
b. Prominent ear – Occurs in Fragile X ear canal is upward whereas in older
syndrome, Potter syndrome (low set, large, children it is downward and forward. Hold
floppy ear), lop ear (loss of superior crus, the pinna of the ear by the fingers of one
antihelix). hand and gently pull up and back in older
children and downward in infants. Before
inserting your auroscope, make note of the
Table 2.32: Causes of low set ears following observations:
• Trisomy syndromes – External otitis
• Apert syndrome – Foreign body
• Camptomelic dwarfism
– Cerumen
• Noonan syndrome
• Turner syndrome – Herpes-zoster lesions
• Hallerman-Streiff syndrome – Discharge
• Di George syndrome It is useful to hold the handle of the
• Fetal hydantoin syndrome auroscope between the thumb and index finger,
General Survey 41
rather like a pen. Insert the earpiece of the retracted drum usually does not move inward
auroscope whilst manipulating the pinna to get with positive pressure, but it moves somewhat
a good view of the tympanic membrane (Fig. outward with negative pressure. A hand held
2.10). Do the same with the other side. A sketch instrument that measures stapedial reflex (and
of the normal tympanic membrane is shown in gives graphical trace of tympanic compliance)
Figure 2.11. is often of use. Normal reflex appears as a sharp
Normally the ear dum is slightly concave conical curve, whilst an effusion makes it look
and translucent (pearly grey or ground glass in flat.
infants). Slight injection along the drum
periphery may be noted normally and slight Nose
generalized erythema is normally induced by
The size and shape of the nose may give many
crying. Describe the tympanic membrane with
clues to diagnosis. Here are some examples
reference to the points given below (Fig. 2.11).
(Table 2.33):
i. Continuity of the membrane–Intact/
perforated Table 2.33: Different shapes of nose
ii. Normal or dull in colour (otitis media with
1. Small nose–Down’s syndrome, trisomy 18, Apert’s
effusion) syndrome
iii. Loss of light reflex–Inflammation 2. Misshapen nose–Normal newborn, cleft lip
iv. Membrane bulging and convex (pus, 3. Large nose–Seckel dwarf, 13q deletion syndrome
blood, air in middle ear) or retracted 4. Depressed bridge of nose–Chondrodystrophy,
(Eustachian tube obstruction) cleidocranial dysostosis, congenital hypothyroidism,
Conradi syndrome, cranio-metaphyseal dysostosis,
v. Bubble or air–Fluid column behind Down syndrome, Hurler syndrome, Larsen syndrome,
membrane (otitis media with effusion). osteopetrosis, syphilis
If you have a pneumatic auroscope, gentle 5. Low nasal bridge with short, upturned nose–Fetal
squeezing of the bulb will allow observation of alcohol, fetal hydantoin
the mobility of the membrane in response to 6. Small nose and anteverted nares–Aarskog syndrome
7. Hypoplastic alae nasi and broad nasal tip–Infant of
positive pressure. Similarly, releasing the bulb diabetic mother (with femoral hypoplasia)
allows evaluation of the response to negative 8. Thin beak like nose–Progeria, Apert syndrome,
pressure. The tympanic membrane moves pyknodysostoiss, Hallermann-Streiff syndrome, Pfeiffer
inward with positive pressure and outward with syndrome, Rubinstein Taybi syndrome, Saethre-
negative pressure. Fluid in the middle ear, Chotzen syndrome
9. Rudimentary nose (proboscis-like)–Holoprosencephaly.
scarring or adhesions impede drum mobility. A
Fig. 2.10: Examination of ear by auroscope Fig. 2.11: Diagram of tympanic membrane
Tilt the tip of the nose and look for foreign wide mouth with prominent lips occurs in
bodies, swelling, purulent or bloody discharge, the fetal hyndantion syndrome. A fish
nasal obstruction, septal deviation and mouth (downturned corners) appearance
perforation. Nasal poyps are associated with is associated with idioathic hyper-
cystic fibrosis. Choanal atresia is a condition calcaemia and the Russell-Silver syn-
where there is no patency of the nasal passage. drome. Small mouths are associated with
If you suspect this in a newborn baby, pass a Hallermann Streiff, oropalatodigital and
firm catheter first through one nostril and then whistling face syndromes.
through the other and demostrate the patency. 2. Sucking and swallowing–This is more of
Another way to check for nasal patency is to use relevance in the newborn baby. Babies at
the back of a metal spoon. Hold the back of a 34 weeks gestation start sucking and
clean spoon (preferable cold) against the nostrils. swallowing, albeit rudimentarily. At 36
If the child is breathing through the nostril, there weeks they are considered to have a
should be condensation moisture on the metal mature suck and swallow reflex. At this
surface. If you suspect nasal obstruction, look time, about 30 rapid sucks are followed by
for signs of the CHARGE association. one swallow. Infants with oropharyngeal
incoordination due to neuromuscular
Mouth and Pharynx impairment feed slowly and often choke.
Inspection of the oral cavity and pharynx is You will note that preterm infants in the
usually unpleasant for young children and neonatal intensive care unit need to be tube
should be done quickly and with minimal fed for considerable lengths of time. These
discomfort. Some examiners prefer to leave this infants need further time to establish
till the end of the examination, which is satisfactory breast or bottle feeding. In
reasonable. First you may ask to see the teeth. term infants, botulism can impair sucking
Next instruct the child to open the mouth widely and swallowing and lead to pooling of
and protrude the tongue. If the pharynx is not saliva.
visible, use a tongue depressor for a better view. 3. Drooling of saliva–Little salivation occurs
In the infant who keeps his mouth highly closed, in the newborn infant and is minimal until
you should wait until he relaxes his clenched 2-4 months of age. Newborns with
jaws or cries. Make sure you restrain the child excessive mucus and saliva coming out of
during the examination. Good intra-oral lighting the mouth suggests oesophageal atresia.
is essential. If you suspect epiglottitis, do not Infants commonly drool if they have an
attempt to examine the pharynx, as it will upper respiratory tract infection or they are
precipitate laryngeal spasm and respiratory teething. Be wary of drooling in the child
arrest (Fig. 2.9B). with other serious problems–cerebral
At the beginning of the chapter, we palsy, familial dysautonomia, Wilson
discussed a “system” for the general survey and disease, acute epiglottitis, scorpion stings,
you will remember that examination of the organophosphorus poisoning, peritonsillar
mouth comes at the end. This is not to say that abscess and foreign body in airway or
this should be done in haste or in cursory oesophagus. The reverse of drooling is
fashion. The mouth and pharynx holds many xerostomia due to decrease in salivary
important clues to assist your diagnosis. flow. This occurs in Sjogren, Mikulicz and
1. Size–Assess the size of the mouth in uveoparotid syndromes.
relation to the size of the face and other 4. Sucking pads–A fullness of the cheeks
structures. A large mouth is said to be part anterior to the masseter muscle occurs in
of Morquio’s and Beckwith syndromes. A malnourished children.
General Survey 43
5. Mouth breathing–Adenoidal hypertrophy, • Erythema–Kawasaki disease, herpes

nasopharyngeal obstruction. simples gingivostomatitis, mucositis
6. Risus sardonicus–It occurs in some from chemotherapy (dactinomycin,
children with tetanus, in which the corners daunorubicin)
of the mouth are pulled outward and • Cherry coloured lips and mucous
downward and the lip is stretched across membranes-carbon monoxide poisoning.
the upper incisors to produce a sardonic 11. Buccal mucosa: Note the following when
grin. examining the oral mucosal lining (Table
7. Congenital cry facies–This occurs due to 2.34).
absence or hypoplasia of the depressor 12. Gingivae:
anguli oris. One corner of the mouth fails • Congenital epulis - In newborns, this is a
to move downward and outward, and is benign, pedunculated, smooth, soft tissue
noticeable especially when the child cries. growth arising from the gingival edge
The lateral part of the lower lip may feel • Unerupted molars appear pale or
thinner on the involved side. colourless
8. Bad breath (halitosis)–Common causes are • Pearly white retention cyst - may persist
poor oral hygiene, caries teeth, dry mouth, for months in infants
tonsillitis, nasal foreign body, sinusitis, • Abscess - periapical abscess occurs at the
adenoidal hypertrophy, Vincent stomatitis, base of the tooth, either in lingual or labial
enteric fever and lung abscess. positions
9. Circumoral pallor–Newborns, scarlet • Hypertrophy–Hydantion therapy, mouth
fever. breathers, poor dental hygiene
10. Lips–Note if any of these problems are • Gingivitis–neutropaenia, acute mono-
present. cytic or myelomonocytic leukemia.
• Large lips–Ethnic, Hurler’s syndrome,
angio-neurotic oedema
Table 2.34: Examination of oral mucosa
• Cleft lip/palate
• Pits or fistulas • Dehydration–Dry, little saliva
• Thrush–White, raised, membranous patches that
• Sucking pad/tubercle–Middle of the
resemble milk curds on the buccal surfaces, lips,
upper lip in normal newborns tongue and pharynx. The patches are removed with
• Fusion of lip to underlying gum– some difficulty and leave mucosal lesions slightly
Chondroectodermal dysplasia oozing with blood. Chronic oropharyngeal candidiasis
• Short philtrum–Di George, orofacio occurs in HIV, T-cell disorders, type 1 autoimmune
digital, Williams syndromes polyglandular syndrome and severe combined
immunodeficiency.
• Long philtrum–Femoral hypoplasia,
• Stomatitis–Commonly in cytotoxic chemotherapy,
gangliosidosis, Aarskog, Hurler, fetal chronic granulomatous disease, Vincent stomatitis,
alcohol and hydantoin syndromes herpes simplex and cyclic neutropaenia
• Cheilitis (drying, wrinkling, cracking, • Aphthous ulcers–Inflammatory bowel disease,
scaling of lips)–acute febrile illness, unexplained
chapping, contact sensitivity • Diffuse erythema–Kawasaki disease
• Red erythematous spots–leukaemia, thrombo-
• Angular stomatitis–Riboflavin deficiency
cytopaenia, Forscheimer spots (rubella), trauma
• Perleche (fissuring, scaling, maceration, • Koplik spots–First appearing on the buccal mucosa
crusting of the angles of the mouth) - opposite the lower molars, they appear as greyish or
candida or streptoccal infection bluish-white opalescent specks surrounded by a light
• Rhagades–Moist, radiating lesions about red, blotchy areola.
the corners of the mouth, found in cong- • Bullous eruptions–Epidermolysis bullosa, pemphigus
vulgaris, Steven-Johnson syndrome
enital syphilis
13. Palate: The palate is a good site to look for or with Apert, di George, orofaciodigital
pallor and jaundice. Petechiae may be and Treacher-Collins syndromes.
present in immune thrombocytopaenia or 14. Tongue: The tongue seems large in con-
leukaemia. Structural defects can be a cleft genital hypothyroidism, gylocogenosis
palate, high arch palate and cysts. Clefts type 2, Hurler syndrome, neurofibro-
are of four varieties. They can be: matosis, Beckwith syndrome, haeman-
i. Limited to soft palate gioma, lymphangioma and angioneurotic
ii. Cleft extends through both the soft and oedema. In contrast it is small in hypo-
hard palates up to the alveolar process glossal nerve lesions and in association
iii. Soft and hard palates are both involved with multiple cranial nerve palsies such as
with a unilateral cleft of the alveolar the Moebius syndrome. You should be
process vigilant for the following (Table 2.35).
iv. Same as above but with bilateral 15. Tonsils: Use a tongue depressor and have
alveolar clefts. the child say ‘aah’. Look for areas of pus
Ask the child to open the mouth and Table 2.35: Tongue – major abnormalities
inspect for a gap. In submucous cleft
• Dryness–Dehydration, mouth breathing
palate, there is no overt defect, but the • Colour–Pale in anaemia, blue in cyanosis, purple in
midline of the palate feels thin on palpa- the Eisenmenger syndrome, magenta in Riboflavin
tion. In newborns it is always preferable deficiency
to examine the oral cavity digitally so as • Cyst–Thyroglossal cyst at the base of the tongue
not to miss a small cleft. Cleft palate may • Pigmentation–Recent ingestion of coloured food and
lozenges
occur as an isolated defect or as a • Coating (white, greyish or brownish-white)–Occurs in
component or the following syndromes: febrile illness such as enteric fever
Trisomy 13, 18, mandibulofacial dysosto- • Strawberry tongue (raw red tongue with prominent
sis, Wolf-Hirschhorn, orofaciodigital, fungiform papillae)–Febrile illnesses, scarlet fever,
velocardiofacial (submucous cleft) and toxic shock syndrome, Kawasaki disease
• Black hairy tongue –A V-shaped brown to black area,
Pierre Robin syndromes. anterior to circumvallate papilla, seen in haemophilia
High arched palate is a common and purpura (hypertrophy of filiform papillae)
occurrence in neonates who have been • Protrusion– Occurs in infants with mental retardation,
ventilated (with oral endotracheal tubes) Down syndrome, congenital hypothyroidism, puppet-
for a considerable length of time. They are like syndrome of Angelman and Nieman-Pick
syndrome. In the neonate, a rhythmic protrusion of the
also said to be associated with mouth tongue suggests intracranial haemorrhage or cerebral
breathers, cerebral gigantism, Ehlers- oedema. Tongue thrusting is often noted in infants who
Danlos, Marfan, Down and Treacher- later demonstrate athetosis. In Syndenham chorea, the
Collins syndromes. Note that high arched tongue is often undulating and cannot be held still on
or cleft palates can often be associated with protrusion.
• Tremor–Werdnig Hoffman disease (fasciculations and
other midline abnormalities such as septo- atrophy of tongue)
optic dysplasia (hypopituitarism). • Fissures–Characterized by irregular fissures or
In newborns, small localised accumu- grooves in a cerebriform or scrotal patern (Down
lations of epithelial cells or cysts are syndrome)
common on each side of the median raphe • Geographic tongue–Annular smooth red patches with
slightly grey margins. They begin posteriorly on the
of the hard palate (‘Epstein pearls’) or dorsum and spread anteriorly and laterally. They are
along the alveolar ridge (‘Bohn nodules’). usually of no clinical significance.
When looking at the palate do also observe • Tongue tie (ankyloglossia)–Occasionally the frenum
the uvula. A bifid uvula may be normal, may be short and this appears as a notch at the tip of
or may occur with a submucous cleft palate the tongue. True tongue tie is a rare phenomenon.
General Survey 45
on the surface of the tonsils (streptococcal adenoidal hypertrophy. The pharynx is

pharyngitis). A grey or yellowish mem- usually swollen and congested with a
brane should indicate diphtheria, cherry red epiglotis in epiglottitis (Fig.
agranulocytosis, and infectious mono- 2.9B).
nucleosis. Tonsils may be normally large 17. Teeth: Count the number of erupted teeth.
due lymphoid tissue growth and may be Although eruption of teeth follows a
mistaken for tonsillitis. Displacement of developmental pattern, much individual
the tonsil to one side with painful swallow- variation occurs. A guide to the eruption
ing occurs with peritonsillar abscess of teeth is given in Tables 2.36 and 2.37
(quinsy). In Tangier disease, the tonsils are (Figs 2.12A and B).
hugely enlarged, yellow-grey in colour and Rarely the newborn may present with natal
honeycombed in pattern. teeth, usually mandibular central incisors. Natal
16. Pharynx: The pharynx looks red in viral teeth are attached to the gingival margin with
infections, bacterial pharyngitis or abscess. little root formation or bony support. Super-
You may be able to palpate a smooth tense numerary teeth on the other hand occur in the
swelling in the lateral parts in a retro- area of the maxillary central incisors and have
pharyngeal abscess. Hyperplasia of the bony support (demonstrated by X-ray). Natal
lymphoid folicles of the post pharyngeal teeth are associated with cleft palate, Pierre-
wall occurs with recurrent pharngitis and Robin, Ellis-von-Creveld, Hallermann-Strieff
Table 2.36: Age of appearance of teeth

Primary teeth Age of appearance (months) Secondary teeth Age of appearance (years)
Central incisors 6-7 1st molar 6
Lateral incisors 7-10 Central incisor 7
1st molar 12 Lateral incisor 8
Canine 18 1st premolar 9
2nd molar 24 2nd premolar 10
Canine 11
2nd molar 12
3rd molar 18
Table 2.37: Number of teeth in different ages in boys and girls

Number of Age in years Number of Age in years
primary teeth secondary teeth
Boys Girls Boys Girls
1 0.55 0.60 2 6.21 5.94
2 0.65 0.70 4 6.40 6.22
4 0.82 0.86 6 6.54 6.24
6 0.97 1.03 8 7.47 7.20
8 1.12 1.18 10 7.70 7.34
10 1.27 1.33 12 8.67 8.20
12 1.43 1.50 14 10.40 9.86
14 1.62 1.70 16 10.79 10.03
16 1.85 1.97 18 10.82 10.18
18 2.13 2.35 20 11.18 10.88
22 11.47 10.89
24 11.69 10.98
26 12.12 11.66
28 12.68 12.27
A B
Figs 2.12A and B: (A) Primary dentition, (B) Permanent dentition (Left upper quadrant)
syndromes and pachyonychia congenita. Peg shaped teeth have notches on the distal
Supernumerary teeth are associated with cleft border of the upper central incisors. They are
lip and palate, Gardner, orofaciodigital, classically seen in congenital syphilis. The
Hallermann-Streiff syndrome and cleidocranial Hutchinson tooth is shaped like the tip of a
dysplasias. Children with ectodermal dysplasia screwdriver, and also occurs in congenital
have poor dentition or conical central incisors. syphilis. Mulberry molars have irregularly
Milk teeth are white in colour and have a formed crowded cusps on a small occlusal
smooth edge in contrast to permanent teeth surface.
which have an ivory (off-white) colour and a The abnormalities can also be see in teeth. A
serrated edge. Black teeth are seen in children few abnormalities have been show in Table 2.38.
taking oral iron preparations. Yellowish
Chest, abdomen: See relevant chapters in exami-
discolouration is seen in those given tetracycline
nation of respiratory and gastrointestinal
in infancy. Brownish discolouration with pitting
systems.
and mottling occurs in dental fluorosis. Excess
plaque formation over the teeth is due to poor
Hands and Fingers
oral hygiene. Brown teeth may also with
amelogenesis imperfecta. Pink or reddish brown The examination of the hand provides a lot of
teeth occur with chronic porphyria. Caries teeth information relevant to all systems. Look for the
are extremely common and occur on the occlusal following in the hand:
(biting) surfaces or on the contact surface i. Handendess–Handedness develops by
between two teeth. Lesions may go deeper to 3 years of age but age variations occur. A
reach the alveoli and may give rise to dental or
periapical abscess. Table 2.38: Teeth – A few abnormalities
Check the alignment of teeth–ask the child Black teeth - Oral iron tonic
to bite down and then examine by separating Yellowish teeth - Tetracyclines
the lips. The occlusal surfaces of the teeth should Brownish teeth with - Dental fluorosis
Pitting + Mottling
appose with good alignment with the posterior Excess plaque - Poor oral hygiene
mandibular teeth slightly ahead of the Brown teeth - Amelogenosis imperfecta
corresponding maxillary teeth. Prognathism Pink/Reddish brown - Porphyria
may occur as a racial trait. Protuberant spaced teeth
out teeth occurs in children with thalassaemia Hutchinson teeth/ - Congenital syphilis
Pegshaped teeth
major.
General Survey 47
child with a consistent approach with one Table 2.39: Shape of hands and fingers
hand suggests a ‘hemisyndrome’. • Syndactyly–Apert syndrome, Carpenter syndrome,
ii. Tremor–Essential tremor, Wilson’s disease, focal dermal hypoplasia, Poland, Smith-Lemli-Opitz
anxiety, cerebellar disease, thyrotoxicosis, syndromes
asterixis. • Polydactly–Chondroectodermal dysplasia, short rib-
polydactyly syndrome, Lawrence-Moon-Biedl
iii. Grasp–This reflects power of individual
syndrome, Trisomy 13
muscles. An ill-sustained grip is seen in • Aplasia of thumb/radius–Holt-Oram syndrome,
chorea (alternate squeezing and relaxing). thrombocytopenia-absent radii (TAR) syndrome
iv. Size • Short broad terminal phalanges of thumb - Rubinstein-
• Small in achondroplasia, Down’s syn- Taybi syndrome, Carpenter syndrome, Apert
syndrome, Weaver syndrome, Peiffer syndrome
drome, de Lange syndrome, Prader-Willi
• ‘Hitchiker’ thumb–Diastrophic dwarfism
syndrome • Flexion of fingers with overlapping of digits–Trisomy
• Large in gigantism, Sotos syndrome 18
• Long hands with arachnodactyly– • Contractures–Insulin dependent diabetes mellitus with
Marfan syndrome, homocystinuria micro-vascular angiopathy, juvenile chronic
arthropathy, mucolipidosis, Whistling face syndrome
• Macrodactyly–neurofibromatosis, Ollier
• ‘Policeman receiving tip’–upper branchial palsy
disease, Mafucci syndrome, Proteus • Proximally placed thumb–Trisomy 22, diastrophic
syndrome dwarfism, Cornelia de Lange syndrome
• Shortening of digits–Down’s syndrome, • Distally placed thumb–Trisomy 18, orocraniodigital
pseudohypoparathyroidism, Turner syndrome
• Clinodactyly (incurving little finger due to shortening
syndrome
of the radial aspect of the middle phalanx)–Down
• Digital hypoplasia of digits and nails syndrome, Silver-Russel syndrome, normal individuals.
(more on the ulnar aspect)–Fetal
hydantoin syndrome.
v. Shapes of hand and fingers are given in viii. Dermatoglyphics
Table 2.39. a. Flexion creases: Usually there are 3 palmar
vi. Colour changes creases. When the two distal creases are
• Red–dactylitis, hand-foot-mouth syn- fused and run as a single crease across the
drome, reflex sympathetic dystrophy, high entire palm reaching the ulnar border of
output failure, liver failure the palm, it is called a “simian crease”
• Blue–cyanosis, Raynaud’s phenomenon (Down’s syndrome, 2-5 percent of normal
• Yellow–Icterus children). A Sydney line (congenital
• Pigmentation–Addison’s disease. rubella syndrome) is one in which the
vii. Rash proximal crease runs across the entire palm
• Macules–Erythema multiforme, viral rash, while the distal crease is normally present
SLE, dermatomyositis (Fig. 2.13).
• Papules–Eczematous dermatitis, scabies b. Ridge arrangement on palms: The ridges of
• Vesicles–Scabies, herpes simplex, the palm meet at certain places. These
molluscum contagiosum, staphylococcal places where the individual ridge systems
scalded skin syndrome, burns, epider- are confluent are known as triradii. Figure
molysis bullosa, congenital syphilis 2.14 shows the terminology of the triradii
• Nodules– Juvenile chronic arthritis, as a, b, c, d and t. The angle formed by
rheumatic fever joining the points a, t, d is known as the
• Purpura– Meningococcaemia, Henoch- atd angle and is normally about 40º. In
Schonlein purpura, Rocky-Mountain Down syndrome, the proximal point is
spotted fever. shifted distally resulting in an obtuse atd
Fig. 2.13: Transverse crease (simian) Fig. 2.14: Decrease of atd angle in Down’s syndrome
angle. Other conditions with obtuse atd Table 2.40: Examination of joints - Inspection
angle are Turner’s syndrome and • Swelling–Ill defined or well delineated
congenital rubella syndrome. • Pain–painless or painful
c. Finger print patterns: The characteristic • Redness–Local, widespread, any suggestion of
patterns over the fingertips are loop, abscess
• Scar–drain, muscle biopsy from adjacent area, intra-
whorl, arch and combined. The usual
osseous needle introduction
distribution is - ulnar loop on little finger, • Muscle bulk around joint–normal, atrophy, contracture,
radial loop on index finger, whorl or arch hypertrophy
on the middle finger. Ulnar loops occur in • Associated subcutaneous nodules–rheumatic fever
Down’s syndrome on all fingers. The • Pallor–leukaemia, systemic infection
• Bleeding sites–Haemophilia
congenital rubella syndrome is associated
• Rash–Henoch-Schonlein purpura, Still’s disease,
with a greater number of whorls whereas systemic lupus erythematosus, dermatomyositis
trisomy 18 children have more arches.
Spinal pathology is not common with
Joints
systemic conditions, although they can occur
Joint problems in children are either primary or with the juvenile chronic arthropathies.
secondary. Common arthropathies in childhood Tuberculous disease of the spine is common,
are the juvenile chronic arthritis (JCA) group of even in this day and age, and needs to be
joint disorders. Joints (and bones) are also considered as a possible diagnosis. Look for
involved in osteomyelitis, septic arthritis, scars, muscle wasting, scoliosis and kyphosis.
trauma or malignancy. Systemic problems may Palpate the joint on the affected site as well
present with arthropathy; some examples are as the joint on the opposite side. Examination
rheumatic fever, collagen vascular diseases, of the normal joint gives you a yardstick for
leukaemias and septicaemia. comparison. Feel the temperature (warm in
To examine the joint (usually a limb) in inflammation), and look for signs of tenderness.
question, expose the arm or leg. You will look, Is the overlying skin tense and shiny? This may
feel and move the joint that you are examining indicate an acute inflammatory process. Are
(Table 2.40). First inspect the part of the limb there any nodules to feel (rheumatic fever)? Is
from all around. the muscle atrophied around the joint? If so is it
General Survey 49
localised to one area? If a joint is chronically Finally, establish the degree of mobility of
inflamed over a period of time, the muscles may the child. Does he/she use crutches or orthoses?
lose their function. Intra-articular steroid What activities of daily living can he/she do?
injection can give rise to local skin and muscle What is the degree of pain relief? How far can
atrophy. the child walk without pain?
Move the joints passively unless the
movement is too painful for the child. Establish Anthropometry
the degree of unrestricted movement possible
It is absolutely crucial to measure physical
in that joint. Here are some joints that you will
growth in all children. Growth is a sensitive mar-
examine commonly (Table 2.41).
ker of the well being of the child and may well
Table 2.41: Movements of the joints to be examined
be an indicator of an underlying illness. Growth
(synonymous with height) may also be impaired
1. Interphalangeal and metacarpophalangeal joints of
the hand–Handwriting, grip, button-unbutton shirt, tie
as a primary process in which case you have to
shoelace, opposition of thumb to each of the fingers, be aware of endocrine causes as well as genetic
thumb adduction, abduction mechanisms. In this chapter, we shall deal with
2. Wrist–Extension, flexion various anthropometric measurements like
3. Elbow–Extension, flexion weight, height and head circumference.
4. Shoulder–Extension, flexion, abduction (lift your arms
like the wings of an aeroplane or a bird), adduction, Weight: This should preferably be measured by
touch with both hands the small of your back a beam type of weighing machine. Spring
5. Neck–Extension (look up at the ceiling), flexion (touch
the chin on your chest), sideways flexion (touch your
balances are not accurate and dependent on the
chin on your left or right shoulder) elasticity of the spring which varies with the age
6. Thoracic and lumbar spine–Flexion, extension (bend of the machine and temperature of the environ-
down to touch your toes, bend backwards) ment. The measurement should be done with
7. Interphalangeal joint of toes–Flexion/extension child wearing minimum clothing (ideally in the
(“wiggle” your toes)
8. Metatarsophalangeal joints–Flexion, extension of
nude). The balance should be balanced first by
toes bringing the lever to zero to see the oscillation
9. Subtalar joints–Inversion, eversion of the fulcrum. The child is then put on the
10. Ankle joint–Flexion, extension weighing machine and the levers are adjusted
11. Knee joint–Flexion, extension till the fulcrum is in the middle. The weight is
12. Hip–Flexion, extension, adduction, abduction,
circumduction
measured nearest to 25 gm accuracy and
recorded. Electronic weighing scales are
Check the joints above and below the joint accurate and easy to use and have replaced the
that you have just examined. If you suspect an cumbersome beam balance in many centres
arthropathy, it is preferable to do a full (Fig. 2.15).
examination of all the joints in the body, as For a quick calculation of expected weight
outlined above. Is there a pattern emerging? from the age, the following formula may be
How many joints are affected? Oligoarthritis is used: weight in kg = (age in years + 4) × 2. This
usually involvement of four or less joints in the is a rough guide and does not take into account
body. They commonly occur in girls and are any interethnic variation. It is, therefore,
associated with iridocyclitis. It is good to ask for essential to plot the child on a growth chart
a history of eye pain and lacrimation. If in doubt, (preferably drawn from local data) and check
you should send the child for a formal slit lamp on his/her pattern of growth.
examination by the ophthalmologists to check The weight for age is a reliable indicator of
for uveitis. the nutritional status of a child. The severity of
Pediatrics: Grade I (71-80%), grade II (61-70%),

grade III (51-60%) and grade IV (50% or less).
Below is a table that gives the figures for grading
of malnutrition for Indian children upto the age
of 14 years (Table 2.42).
Length (Crown-heel length): The length is
measured on a measuring board, with a fixed
head piece and a movable foot piece that has
wooden scales fixed to both sides. You will need
at least one other person to help you do this.
Make sure that the child is looking upwards
when lying on the measuring board. Your
Fig. 2.15: Weight measurement in a beam balance
assistant should check if the knees are perfectly
undernutrition can be assessed on the basis of extended and you can then flush the foot piece
the classification of the Indian Academy of against both feet (Fig. 2.16).
Table 2.42: Grading of malnutrition suggested by the Indian Academy of Pediatrics (weight in kg)
Age 50th percentile of
NCHS Standard Grade I Grade II Grade III Grade IV
Birth 3.4 2.4-2.7 2.1-2.3 1.7-2.0 1.6 or less
3 months 5.7 4.0-4.5 3.5-3.9 2.9-3.4 2.8 or less
6 months 7.6 5.4-6.1 4.6-5.3 3.9-4.5 3.8 or less
9 months 9.1 6.5-7.3 5.5-6.4 4.6-5.4 4.5 or less
12 months 10.1 7.2-8.1 6.2-7.1 5.1-6.1 5.0 or less
15 months 10.7 7.6-8.6 6.5-7.5 5.4-6.4 5.3 or less
18 months 11.4 8.1-9.1 6.9-8.0 5.8-6.8 5.7 or less
2 years 13.4 9.5-10.7 8.2-9.4 6.8-8.1 6.7 or less
2.5 years 14.6 10.4-11.7 8.9-10.3 7.4-8.8 7.3 or less
3 years 15.6 11.1-12.5 9.5-11.0 7.9-9.4 7.8 or less
3.5 years 16.6 11.8-13.3 10.1-11.7 8.5-10.0 8.4 or less
4 years 17.7 12.6-14.2 10.4-12.5 9.0-10.7 8.9 or less
4.5 years 18.8 13.3-15.0 11.5-13.2 9.6-11.4 9.5 or less
5 years 20.0 14.2-16.0 12.2-14.2 10.2-12.1 10.1 or less
5.5 years 20.7 14.7-16.6 12.6-14.6 10.5-12.5 10.4 or less
6 years 21.9 15.5-17.5 13.3-15.4 11.2-13.3 11.1 or less
6.5 years 23.2 16.5-18.5 14.1-16.4 11.8-14.0 11.7 or less
7 years 24.5 17.4-19.6 14.9-17.3 12.5-14.8 12.4 or less
7.5 years 25.9 18.4-20.7 15.8-18.3 13.2-15.7 13.1 or less
8 years 27.3 19.4-21.8 16.6-19.3 13.9-16.6 13.8 or less
8.5 years 28.6 20.3-22.9 17.4-20.2 14.6-17.3 14.5 or less
9 years 29.9 21.2-23.9 18.2-21.1 15.2-18.1 15.1 or less
9.5 years 31.3 22.2-25.0 19.1-22.1 16.0-19.0 15.9 or less
10 years 32.6 23.1-26.1 19.9-23.0 16.6-19.8 16.5 or less
10.5 years 33.9 24.1-27.1 20.7-24.0 17.3-20.6 17.2 or less
11 years 35.2 25.0-28.4 21.5-24.9 17.9-21.4 17.8 or less
11.5 years 36.7 26.1-29.4 22.4-26.0 18.8-22.3 18.6 or less
12 yeras 38.3 27.2-30.6 23.4-27.1 19.5-23.2 19.4 or less
13 years 42.2 30.0-33.8 25.7-29.9 21.5-25.6 21.4 or less
14 years 48.4 34.6-39.0 29.8-34.5 24.9-29.7 24.8 or less
General Survey 51
Fig. 2.16: Length measurement Fig. 2.17: Chest circumference measurement
In a child above the age of five years, it is ment is done midway between inspiration and
better to take the same reading standing up. A expiration and recorded nearest to 0.1 cm. The
stadiometer that has been calibrated should be tape should not be passed through the nipple
used. Make sure that the child looks straight line, as the nipple lines may be variable (Fig.
ahead with the lower margins of the eyes in the 2.17).
same horizontal plane as the external auditory
Cranial circumference: The cranial circumference
meatus. Ask the child to “breathe in and stand
is measured by the same tape, and is passed over
tall.” Use gentle upward traction over the
the supra-orbital ridges in front and that part of
mandibles to straighten the cervical spinal
the occiput which gives the maximum diameter.
curvature. Ensure that the heels are not lifted
Usually it is over the occipital protruberance, but
from the ground. The head board can then be
not always. Therefore only the maximum
placed horizontally on the top of the head and
diameter is to be considered. It is recorded
the height measurement taken.
nearest to 0.1 cm. Figure 2.18 shows the techni-
For a quick estimation of height/length, the
que of cranial circumference measurement.
following aide memoire is useful: Length at
The usual head circumference at birth is
birth = 50 cm; length at 1 year = 75 cm; length
36 cm in boys and 34 cm in girls, but indigenous
from 2-12 years = (age in years × 6) + 77 cm.
Indian values are probably 1 cm lesser. An easy
Remember this is only a rough guide and the
way to remember the values for head growth in
best way to record the child’s length is to plot it
childhood is given in Table 2.43.
on a suitable growth chart.
Chest circumference: The chest circumference is Table 2.43: Head circumference - Measurement
measured ideally by a fibre glass tape; if not First 3 months Growth 2 cm/month
available, an ordinary linen measuring tape, Second 3 months Growth 1 cm/month
standardized against a wooden scale from time Next 6 months Growth 0.5 cm/month
At 1 year, head circumference 47 cm
to time, may be used. The tape is first laid At 2 years head circumference 49 cm
stretched on the measuring board with reverse At 4 years head circumference 51 cm
side upwards. The child is then put on the At 11 years head circumference 52 cm
reversed tape on the measuring board. The tape
is passed through the xiphisternal junction and Mid-Arm circumference: The midpoint of the arm
surrounds the chest in that plane. The measure- is first determined by passing the tape from the
Fig. 2.19: Mid-arm circumference
child of the same height. Combinations of

these measurements have been used to
distinguish different types of malnutrition.
Fig. 2.18: Cranial circumference measurement
Waterlow suggested that weight/height
could be used to distinguish between
acromial end of the clavicle to the olecranon
malnutrition of recent origin (wasting) and
process of the ulna. At the midpoint (half of the
malnutrition due to a considerable period of
length of the arm) the circumference is
months. In chronic malnutrition the child is
measured by passing the tape around the arm
stunted, that is the weight-for-age and
in that plane. It is recorded nearest to 0.1 cm
height-for-age are low. In acute malnutrition,
(Fig. 2.19).
height-for age is normal but weight-for age
is low, and is called wasting. Thus, the
Age Independent Anthropometry
weight and height measurements are useful
a. Mid arm circumference: The midarm circum- together to understand the dynamics of
ference is relatively constant between malnutrition and enable us to distinguish
16.5 cm to 17.5 cm in children 1-5 yrs of age between acute malnutrition and chronic
and therefore this measurement may be malnutrition. In nutritional dwarfs, the
considered as an age independent variable weight/height is equal as there is chronic
in that age group. Any child with an MAC adaptation. The child may pass off as a
less than 12.5 cm (< 5 yrs of age) is considered normal child for lower age if the chrono-
malnourished. It is a useful method of logical age is not known.
assessment of nutritional status. In a comm- c. Quac stick: Quaker’s midarm circumference
unity setup, Shakir’s tape is a replacement measuring stick is a height-measuring rod
for MAC measurement. The red area (12.5 calibrated in MAC rather than height. Values
cm) denotes malnutrition, the yellow (13.5- of 80 percent MAC for height are marked on
12.5 cm) denotes impending malnutrition, the stick at corresponding height levels. If a
while the green area (above 13.5 cm) child is found taller than his arm circum-
represents children who are normal. ference level on the stick, he is considered
b. Weight for height: The degree of wasting can malnourished. The ‘Quac stick’ was devised
be measured by comparing the child’s in Mexico and has since been adapted in
weight with the expected weight of a healthy Africa and India.
General Survey 53
d Mid arm to head circumference ratio: It is a obesity. You must remember however these are
simple and useful ratio to quantify mal- Western standards and unlikely to be suitable
nutrition. A ratio 0.280 to 0.314 indicates for application in the Indian context. Indians
malnutrition. Values between 0.250 and have a greater amount of fat than the BMI ratio
0.279 denote moderate malnutrition, whilst suggests. In adult Indians, the World Health
those less than 0.249 indicate severe Organisation has lowered BMI cut-offs from 25
malnutrition. and 30 to 20 and 25 to represent overweight and
e. Quetlet’s index: It is based on the relationship obesity respectively.
between weight and height and is expressed The chief value of BMI is in the follow-up of
as weight (kg)/height (cm) × 100. Normal obese children. You should be able to determine
values vary between 0.14 and 0.16. In gross trend over time when plotted on a BMI centile
malnutrition the value is less than 0.14. chart. You may consider measuring waist
f. Mid upper arm to height ratio: This is another circumference as an adjunct to quantify visceral
useful indicator of nutritional status. A ratio fat mass. However, in obese children, measure-
of less than 0.29 indicates gross malnutrition, ments are rather erratic as it is often difficult to
while the normal value ranges from 0.32 to localize the point at which the tape should be
0.33. passed. Ideally you should select the midpoint
g. Bangle method: This is another age indepen- between the iliac crest and lower end of the ribs
dent anthropometric parameter where you on either side. It is often difficult to palpate the
slip a bangle with an internal diameter of iliac crest due to excess fat deposition.
4 cm up the forearm. The bangle should be i. Ponderal Index (PI): This is another index
made to move up without squeezing the similar to BMI and is often used in defining
hands. In case the bangle slips over the IUGR babies.
elbow, malnutrition is said to be present. Body weight (gm)
This is really an mid arm circumference that PI = __________________________ × 100
is meant for use in the community. Though Length (cm)3
simple to use, is not very reliable. ii. Sex Maturity Rating (SMR): This is often
h. Body mass index (BMI) missed out but remains an integral part of
Weight (kg) growth assessment of the child. It is
BMI = __________________ important to be aware of the maturation
Height (m) 2 of the secondary sex characters and their
This ratio is somewhat like the Quetlet’s relation to physical growth. Examining the
index. BMI represents adiposity in a child but genitalia can be slightly awkward in the
does not discriminate between fat free (lean) older child, so you should be duly sensitive
mass and fat mass. However, in practice this is and explain the procedure first. If the child
a relatively easy and reproducible tool to assess disagrees to the examination, you could
obesity. BMI values have been used to draw show him/her pictures depicting sexual
standardized percentile curves in children and development and ask him/her of the likely
adolescents. A child is overweight if the BMI is stage. The Tanner pubertal staging in
> 85th centile (NCHS). A BMI at or above 95th children is given in Tables 2.44 and 2.45
percentile for age is considered to represent (Figs 2.20A and B).
A B
Figs 2.20A and B: (A) SMR girls, (B) SMR boys
Table 2.44: Tanner pubertal staging–Girls

Girls
Pubic Hair SMR Breast
Preadolescent 1. Preadolescent
Sparse, lightly pigmented, straight, medial 2. Breast and papilla elevated as small mound, areolar
border of labia diameter increased
Darker, beginning to curl, increased amount 3. Breast and areola enlarged, no countour separation
Coarse, curly, abundant but less amount than adult 4. Areola and papilla form secondary mound
Adult feminine triangle, spread to medial thighs 5. Mature; nipple projects, areola part of general breast
contour
Table 2.45: Tanner pubertal staging–Boys

Boys
Pubic Hair SMR Penis Testes
None Preadolescent 1. Preadolescent
Scanty long, slightly pigmented 2. Slight enlargement Enlarged scrotum, pink, texture
altered
Darker, starts to curl, small amount 3. Longer Larger
Resembles adult, amount less, coarse, 4. Larger, breadth Larger, scrotum dark
curly increases in size
Adult distribution, spreads to 5. Adult size Adult size
medial surface of thighs
EXAMINATION OF THE
GASTROINTESTINAL
SYSTEM
The gastrointestinal tract extends from the so if the child is not putting on weight. A number
mouth to the anus. It is not just a passageway of the symptoms are subjective, so ask questions
for food, but is also connected to an intricate set to clarify your doubts. Some mothers will
of secretory glands that control the processing, complain that their child does not eat, where in
absorption and elimination of ingested material. fact the child is thriving well. There are also
The abdomen contains a large part of the GI tract those who find it difficult to provide proper
and also other organs (kidney, adrenals, testes) nutrition but maintain that their child is eating
that can be examined alongside. “all the time.” You could ask what the child likes
You may divide the abdominal wall by to eat instead of “what the child eats everyday.”
imaginary lines into nine compartments. There Do not appear to be threatening, as this will
are two vertical lines, each starting from the rarely give you the right answers. Build on the
midpoint of the groin (femoral artery) on either rapport to ask, “How many times a week can
side and passing upwards to cross the costal
margin at the tip of the ninth costal cartilage.
The two horizontal lines are called the subcostal
and interiliac lines. They pass horizontally
across the lowest points on the costal margin and
tubercles of the iliac crests respectively. The four
lines intersect and form nine quadrants: right
and left hypochondria, epigastrium, right and
left lumbar, umbilical, right and left iliac and
hypogastrium or suprapubic. It is useful to know
the quadrants as symptoms and signs relating
to the abdomen can be conveniently localised
(Fig. 3.1).
HISTORY
Ask the symptoms with regard to onset,
evolution and response to treatment. Common
symptoms of gastrointestinal disease are
Fig. 3.1: Compartments of the anterior abdominal wall:
abdominal pain, bowel disturbances (diarrhoea,
1. Epigastrium, 2. Left hypochondrium, 3. Left lumbar
constipation), vomiting, distension, jaundice, region, 4. Left iliac fossa, 5. Hypogastrium, 6. Right iliac
anorexia and failure to thrive (Table 3.1). It is fossa, 7. Right lumbar region, 8. Right hypochondrium,
important to take a good history of the diet, more 9. Umbilical region
you afford to give him this.”, Or “where do you disease, giardiasis and disaccharidase defi-
get your milk and eggs from?” Once you are sure ciency. First ascertain that the stools are truly
of a clear dietary history, put down an average ‘loose’. Is the stool so watery that it trickles down
diet and work out the calories and protein from the side of the child’s legs? Are the motions oily,
such a diet. Refer to the chapter on nutritional sticky and floating on water? The latter suggests
values to work out if the diet is appropriate. malabsorption. Is there blood in the stool? What
is the consistency? Are there any undigested
Table 3.1: Chief complaints of gastrointestinal system
food particles, as in children with toddler
• Abdominal pain diarrhoea?
Diarrhoea
• Bowel disturbance
Constipation is the relative increase in
Constipation consistency, decrease of frequency or difficulty
• Blood in stool in passing motions. Children may be consti-
• Vomiting, jaundice pated due to a poor diet. The bowel often loses
• Abdominal distension its habit to ‘go’ everyday. There are potentially
• Loss of appetite
• Weight loss
more serious causes—Hirschprung disease,
hypothyroidism, cerebral palsy, hypokalemia,
Pain hypercalcaemia, vincristine ileus, narcotic drugs
and coeliac disease. Enquire about the number
Abdominal pain is an important part of of times the child will open his bowels. Is the
gastrointestinal symptoms. Unfortunately motion rock solid? Do they cause bleeding? Is
visceral pain is rarely well localized and may there tummy ache associated with this? Do you
be misleading. Common causes of acute tummy think that there is secondary faecal soiling?
aches are gastroenteritis, appendicitis, urinary
tract infection, gastritis and peritonitis. Blood in Stool
Functional causes of abdominal pain are
common and difficult to differentiate from Parents are often alarmed when the child has
organic aetiology (Table 3.2). Look up the section blood in the stools. Often it is a mucosal tear of
on pain (history) for a fuller description. the anal or rectal mucosa. Bleeding per rectum
is a common association of gastroenteritis,
Table 3.2: Common causes of abdominal pain mostly bacterial. Do think of worrying condi-
• Gastroenteritis
tions like intussusception if there are other
• Appendicitis symptoms. Amoebic dysentery is common in the
• Urinary tract Infection slightly older population. Inflammatory bowel
• Gastritis disease and coeliac disease are not very
• Peritonitis common, but not all that rare either. More often
• Functional
than not, you will end up with no clear
diagnosis. In such situations it is best to be
Diarrhoea/constipation
pragmatic. If the child in unwell and has
Disturbance of bowel movement results in diarrhoeal stools, look for signs of intussuscep-
diarrhoea or constipation. Diarrhoea is an tion and infection. If the child is very well in
excessive loss of fluid and electrolytes in stool. himself, eating and drinking and without
Dysentery is described as frequent passage of abdominal tenderness, then it is reasonable to
stool mixed with blood and often associated wait and watch. The mother may rush to the
with tenesmus and urgency. Diarrhoea may be doctor alarmed at the sight of blood in stool.
caused by gastroenteritis, systemic infection, Here is a list of the causes of gastrointestinal
food poisoning, milk protein intolerance, coeliac bleeding in an infant or child (Table 3.3).
Examination of the Gastrointestinal System 57
Table 3.3: Causes of gastrointestinal haemorrhage Table 3.4: Common causes of vomiting
Common Neonate
• Acute bacterial gastroenteritis Swallowed air (inadequate burping), gastro-oesophageal
• Swallowed maternal blood (newborn) reflux, the ‘mucusy’ baby, systemic infection, gut
• Amoebic dysentery dysmotility in the premature infant, intestinal obstruction,
• Food poisoning adrenal hyperplasia
• Hookworm infestation One-month baby
• Intussusception Congenital hypertrophic pyloric stenosis, systemic
• Anal fissure infection, metabolic disorder, gastro-oesophageal reflux,
• Cow’s milk protein intolerance duodenal atresia
• Lymphonodular hyperplasia
Rare Older child
• Necrotising enterocolitis Gastroenteritis, drug side effects, gastritis, appendicitis,
• Volvulus urinary tract infection, hepatitis, raised intracranial
• Meckel’s diverticulum pressure, cyclical vomiting, migraine, chronic renal failure,
• Coeliac disease inborn errors of metabolism, bleeding varices
• Inflammatory bowel disease
• Stress ulcer with a poor appetite. Some causes can be related
• Coagulation disorder
to the treatment offered. Drugs like metro-
nidazole or chloroquin take away the desire to
Vomiting
eat. The child may be emotionally stressed to
The child who is sick may have problems with have an appetite. On the contrary, children may
his/her gastrointestinal tract or any other have a rather good appetite if they have ascaris
systemic disorder. You could have vomiting infestation, uncomplicated marasmus, receive
along with the diarrhoea of gastroenteritis. corticosteroid treatment or have hypothalamic
Equally the child may vomit when given disorders.
cytotoxic chemotherapy. Or there may be
vomiting along with retching shortly after the Fever
irritation of a cough spasm. Bile stained vomitus
Common causes of pyrexia with gastrointestinal
signifies obstruction below the ampulla of Vater.
problems are: viral hepatitis, parenteral
There are exceptions to this – often children who
diarrhoea, malaria, kala-azar, and liver abscess.
are vomiting at frequent intervals bring up a
Evaluate fever as in the section in general
little bile as part of normal regurgitation into
survey.
the stomach. A bloodstained vomitus (haema-
temesis) is due to swallowed maternal blood,
Potbelly
epistaxis, ruptured varices as in extrahepatic (or
cirrhotic) portal hypertension or stress ulcers. It This is a common complaint of parents who
is useful to note the child’s age - some conditions suppose that the child is suffering from a ‘liver’
present at certain ages and their knowledge will disorder. A potbelly contour in toddlers is
allow you to home you on the right cause. Here common and normal (unless examination
are some causes of vomiting as per age group reveals organomegaly, ascites) and therefore the
(Table 3.4). patients must be reassured. The appearance is
secondary to the exaggerated lumbar lordosis
Appetite in children of this age.
Quite a few alimentary disorders produce
Jaundice
anorexia. The child who is unwell will find it
difficult to eat or drink. Debilitating conditions In newborns physiologic jaundice is common.
like tuberculosis and kwashiorkor are associated Be aware of other causes of neonatal icterus. If
jaundice is prolonged to the second week, ask it difficult to eat from loss of appetite. Some have
yourself the question if there is a surgical cause systemic diseases like tuberculosis, chronic
that is being missed. Obstructive jaundice occurs haemolytic anaemias or worm infestation that
with biliary atresia, intrahepatic biliary paucity, siphon off the body’s energy stores. Malignancy
Alagille syndrome, prolonged parenteral can lead to cachexia if nutrition is not dealt with
nutrition, choledochal cysts and congenital adequately.
hypopituitarism. Unconjugated jaundice is The term failure to thrive (FTT) is used
common in the breast fed baby. Hypo- commonly to denote that the child fails to grow
thyroidism, galactosaemia, sepsis, urinary tract normally up to his/her full potential. Quanti-
infection, prolonged intestinal stasis and tatively the child should be moving away from
haemolysis are other common causes. his/her growth centile and possibly have had
In the neonate the appearance of jaundice crossed two major centiles (i.e., 75th, 50th, 25th).
according to the age in days may sometimes be If the child is progressing at the same rate on a
helpful in making a diagnosis (Table 3.5). lower centile, it does not count as FTT.
Table 3.5: Causes of jaundice in neonatal period Examination

Day 1 Rhesus or ABO incompatibility
Day 2 Crigler Najjar syndrome, early physiological
Start the examination doing a thorough general
jaundice survey. It is important to know the state of
Day 3 Physiological jaundice, early sepsis anaemia, clubbing, jaundice and vital signs.
Day 4 Sepsis Examine the mouth and pharynx carefully for
Day 7 Neonatal hepatitis, biliary atresia, galactosaemia ulcers, bleeding, dental hygiene and any distinct
pathology. Offer the older child a glass of water
In the older child, ask for the onset, pro- to drink. Observe if there is a problem with
gression and presence of features of obstruction deglutition. Come down to the neck and search
(clay coloured stools, skin itching, dark urine). for dilated veins, scar marks from previous
What drugs did the child have? Is there a close central lines and spider naevi. You can now
contact with viral hepatitis? What is the sleep proceed to examination of the abdomen. Note
pattern of this child? Is the child sleeping more your findings under the following headings:
during the day and waking up at night? Has the inspection, palpation, percussion and
child been behaving in an odd way? The last few auscultation.
symptoms are related to developing hepatic It may seem easier to you to have a method
encephalopathy. Jaundice is common due to of examination – the so-called “system.” Here
haemolytic anaemia, viral hepatitis, Wilson is one way: inspect the abdomen while the child
disease and Indian childhood cirrhosis. Look for lies on the bed. You ought to be positioned on
the signs of fulminant hepatic failure if you have the right side of the child. While the child lies
spotted jaundice. on his back, do the palpation, fluid thrill and
percussion for shifting dullness. You need to
Weight Loss turn the child on to one side for the fluid to drain
It is a feature of the body’s negative energy down to that side. If you choose to turn the
balance. Malabsorption (persistent diarrhoea, patient on to his left, you will have a good view
coeliac disease, protein losing enteropathy) is a of the back. Use this opportunity to inspect the
recognisable cause but first exclude inadequate back and palpate for renal angle tenderness. You
nutrition. Most children who are not thriving can also feel the spine and make suitable
well are undernourished both from poor comments. Finish doing the shifting dullness
quantity and quality of food. Some children find test. Lay the child back again and complete your
examination with auscultation and examination Venous filling is from below upwards in the
of the hernial orifices. Offer to examine the lower half of the abdomen in inferior vena
genitalia – be gentle with the child when you cava and hepatic vein obstruction. In
are doing this. Do not offer to do a per-rectal extrahepatic portal obstruction the veins in
examination (unless you suspect Hirschprung the lateral flank are more prominent.
disease) as it does not add on to the already • Shape—There is no ‘normal’ shape of the
existing information. Some consider it abdomen. An abnormally scaphoid
unpleasant, and therefore it is best avoided. abdomen in a newborn suggests diaphrag-
matic hernia. If the tummy appears full and
a. Inspection distended, the following may be the
possibilities: fat, fluid, flatus or faeces.
Ideally you should expose the abdomen from
Localised distension may suggest appendi-
just above the xiphisternum to the mid-thigh.
cular lump, a tumour from the abdominal
You should inspect the abdomen not only from
wall, a ‘phantom’ tumour (poliomyelitis) or
the anterior, but also from the posterior and both
distended urinary bladder. Look also for the
sides.
change of shape with breathing. In the
• Visible peristaltic waves—Gastric outlet
newborn it is normal for the abdomen to
obstruction, malrotation of gut, duodenal
bulge with inspiration. In the older child this
stenosis, adrenal insufficiency, prune-belly
may suggest weakness of the diaphragmatic
syndrome
muscles of respiration.
• Superficial abdominal veins—They are
• Scars—The presence of scars may tell you
normal in infancy but may be pathological
about previous surgical procedures. A scar
in the older child if they appear distended
in the right iliac fossa is likely to be due to
and engorged. The normal direction of
appendicectomy. Midline longitudinal scars
venous flow is away from the umbilicus,
are from exploratory laparotomy or other
both below and above it and the same
major abdominal surgery. A small scar over
pattern is exaggerated in portal hypertension
the epigastrium may mean a previous
(Fig. 3.2). Select a straight vertical segment
pyloromyotomy. A big scar over the right
of a vein with no tributaries in that segment,
hypochondrium could be from a Kasai
one below and one above the umbilicus.
procedure or a hepatic transplant. Search for
Place two fingers horizontally, side by side,
lateral and posteriorly placed scars of renal
on the vein above the umbilicus. Move the
operations. They may be associated with
lower finger away thus emptying part of the
scars of renal transplants in one of the iliac
vein. Remove the lower finger if there is
filling from below, the vein should fill up
easily. If filling from above, the vein should
remain empty during this procedure. Now
do the same procedure, this time removing
the upper finger. If the blood flow is away
from the umbilicus, the vein will remain
relatively empty. If the blood flow is toward
the umbilicus, the vein will distend quickly.
This gives a fair idea of the direction of
venous filling around the umbilicus.
Remember to test for veins below the
umbilicus as well (Fig. 3.2). Fig. 3.2: Method of detection of blood flow in veins
fossae. You should also look carefully at the vii. Omphalitis: Characterised by a red, warm,
umbilicus. This may reveal a scar from a moist periumbilical inflammation with or
previous gastroschisis repair. It is sometimes without a foul, purulent discharge.
difficult to spot the cosmetic scar of a viii. Prominent venous circulation around the
pyloromyotomy performed through an umbilicus: Collateral circulation may be
umbilical approach. associated with localised venous hum
• Umbilicus—Normally the umbilicus is and thrill, portal hypertension and sple-
slightly retracted and inverted and placed at nomegaly.
the centre of the abdomen. If everted, an • Oedema, erythema and tenderness of
umbilical hernia may be present. You can abdominal wall–Necrotising enterocolitis,
confirm this by feeling an expansile impulse perforation of gut, peritonitis
over the swelling when you ask the child to • Local lesions–Abscess, haemangioma, burns
give a short cough. The following are some • Striae–White striae with sudden weight loss,
of the abnormalities that you might find: purple striae with Cushing syndrome
i. Omphalocele: It is a defect of the umbilical • Fullness of flanks–Hirschprung disease
ring, containing liver and intestines and • Paradoxical respiration–Diaphragmatic
covered by peritoneum and amnion. palsy
Associations are the Beckwith-Weideman • Epigastric pulsation–Thinly built individual,
syndrome, trisomies and other congenital right ventricular hypertrophy, tumour
gastrointestinal, genitourinary and cardiac overlying the abdominal aorta
anomalies. • Hernial sites–Inguinal, femoral, umbilical
ii. Gastroschisis: This is a paraumbilical, full • Hydrocele–Hydrocele of the tunica vaginalis
thickness abdominal wall defect, usually of the testis is a fluctuant smooth or tense
a few centimetres in diameter, usually to swelling. The swelling in the scrotum shows
the right of the umbilicus and between the positive transillumination. A hydrocele at
recti. There is evisceration of bowel birth is benign and goes away on its own.
through the defect. Note that the umbilicus • Hydrocele of the cord–Here the swelling is
and umbilical cord are present to one side above the testis or in the inguinal canal but
of the defect. is not reducible, unlike a hernia
iii. Delayed separation of the umbilical cord: • Examination of the genitalia (Chap. 3, page
Causes can range from local sepsis, 66).
leukocyte adhesion defect and prolonged • Anything else that may be obvious – stoma
stay of umbilical artery catheters. (ileostomy, colostomy), nasogastric feeding
iv. Single umbilical artery: The normal tube, gastrostomy feeding tube, drain,
distribution of vessels at birth is one vein peritoneal dialysis catheter.
and two arteries. Single umbilical artery
can be an isolated finding or else associated b. Palpation
with renal and other congenital anomalies.
v. Diastasis/divarication of the recti: There are two very important aspects to a good
Commonly occurs in infants and small palpation. One, you should make the child feel
children. relaxed so as to avoid muscle guarding. Two,
vi. Patent omphalomesenteric (vitello- you should look at the child’s face to see if there
intestinal) duct: May present as a weeping is a response indicating tenderness. Palpate
umbilical granuloma. In infants with lightly to start with, and then proceed to deep
patent urachus, urine may leak from the palpation, if necessary. Make sure you have your
umbilicus. fingernails trimmed, your hand is warm, and
the child is comfortable. Palpate with the

cushion of the fingers rather than the tips. Do
not poke or hurt the child as it may cause
resentment if a tender area exists. Palpate all the
other sites first before you turn your attention
to the area of tenderness. Approach gently and
reassure the child when you do this. Sometimes
children can be ‘ticklish’ and that makes
examination difficult. Place the child’s hand on
the abdomen and your hand on top and use this
combination for palpation. It is useful to perform
a logical routine in palpating the abdomen. Here
is a scheme you could follow:
• Start in left iliac region, go anticlockwise to
end in the suprapubic region (first light then Fig. 3.3A: Correct method of superficial palpation – hand
deep palpation) should be held flat and moulded to abdominal wall
without any dipping or poking
• Palpate for left kidney, spleen, right kidney,
liver and urinary bladder. Palpate deeply for
retroperitoneal structures in the abdomen.
Do also palpate the groins and examine the
genitalia.
Technique
Sit down on the right side on the child. The only
exception is when you palpate for a pyloric lump
in congenital pyloric stenosis. It is best to palpate
from the left with the left hand. You should talk
to the child and allay all anxiety. The more
cooperative he or she is, the better for the
examination. Remember that palpation is not a
test of force and will not yield anything Fig. 3.3B: Deep palpation of abdomen
substantial if you have to ‘restrain’ a child by
force. Let the child lie on the bed in his/her own
preferred position. There is no need to flex the
hips so as to relax the abdomen. It helps to a
cover for the lower part of the tummy, especially
the genitalia. Children can often be put off if
examined completely in the nude (Figs 3.3A
to E) (splenomegaly).
Keep the fingers of your right hand straight
with slight flexion at the metacarpophalangeal
joints. For a left handed individual, you are
permitted to stand to the left of the child and
use your left hand. Gently palpate each
quadrant noting for rigidity, tenderness or
obvious lump (Figs 3.3A and B). Fig. 3.3C: Palpating of liver
Fig. 3.3D: Classical method of palpation of spleen Fig. 3.3E: Alternate method of palpation of spleen
Left kidney (Figs 3.3F and G) In the newborns the lower pole of the kidney
may normally be palpable.
Place the right hand anteriorly in the left lumbar
region whilst placing your left hand posteriorly
Spleen
in the left loin. Ask the child to draw a deep
breath in and press the left hand forwards and The spleen has to be enlarged to three times the
right hand backwards. If the left kidney is normal size to be palpable below the left
enlarged it is bimanually palpable and can be subcostal margin. Once the spleen has appeared
pushed from one hand to another (ballotable). in this position, it enlarges down towards the
Fig. 3.3F: Palpation of left kidney from same side Fig. 3.3G: Palpation of left kidney from opposite side
right or left iliac fossa. Place the flat of the left Table 3.6: Difference between splenic
hand over the lower ribs postero-laterally. Place and renal mass on palpation
the flat of the right hand on the anterior i. A notch in the lower medial border
abdominal wall in the right iliac fossa and ii. Not bimanually palpable
palpate upwards to the left subcostal arch. All iii. Dull on abdominal percussion (band of colonic
the while, ask the child to breathe deeply (if he/ resonance over kidney)
iv. Upper border cannot be felt (one cannot ‘get above
she can cooperate). With your left hand support
it’)
the rib cage so that the spleen may appear more
prominent. Repeat the palpation starting from Complete the examination of the enlarged
the left iliac fossa in the same way. Make sure spleen by listening for a splenic rub
to palpate below the left subcostal arch in both (perisplenitis). Whilst examining the liver on the
lateral and medial parts. If the spleen is palpable, right side, bear in mind that the child may have
it should come and touch your hand as a soft or situs inversus and associated polysplenia.
firm swelling during the phase of inspiration. Therefore, it is good practice to examine the liver
It is sometimes difficult to appreciate the feel and spleen as a whole before drawing your
of a ‘just palpable’ splenomegaly. You may try conclusions.
Short’s manoeuvre to feel the small spleen. Turn Here are some common causes of splenic
the child to the right lateral position and put the enlargement (Table 3.7).
left hand on the left lower ribs. Place the flat of
the right hand lightly over the abdomen below Table 3.7: Splenomegaly – Causes
the left subcostal arch. As the child breathes
• ‘Normal’ children – 15 percent newborns, 15 percent
deeply the spleen tip should just touch the tip children, 10 percent adolescents
of the fingers. In another method you may sit • Infectious diseases (typhoid fever, malaria,
on the left side of the child and place your tuberculosis, kala-azar, infectious mononocleosis,
right palm over the left subcostal arch with endocarditis, septicaemia, brucellosis, toxoplasmosis,
HIV)
the fingers resting lightly on the abdominal
• Haematological disorders (haemolytic anaemias,
wall: the spleen should come and touch your extramedullary haematopoiesis as in thalassaemia,
fingers, if it is palpable. Practise examining for osteopetrosis)
the spleen on all children and after a while you • Neoplasms (leukaemia, lymphoma)
will get used to the feel of a soft, small spleen • Infiltration and storage diseases (Niemann Pick,
Gaucher disease, mucopolysaccharidosis, histiocyto-
(Figs 3.3D and E).
sis)
A percussion technique is also used to detect • Congestion (portal hypertension due to cirrhosis, or
splenic enlargement. Percuss over the anterior extra-hepatic causes, congestive cardiac failure)
axillary lines in the lower intercostal spaces • Cyst (congenital or acquired)
(normally resonant). If the spleen is enlarged, • Other–lupus erythematosus, juvenile chronic arthritis
• Pseudosplenomegaly (elongated splenic mesentery,
you will find dullness in inspiration and
enlarged left lobe of liver)
resonance during expiration.
A large splenomegaly is easy to identify – it Right Kidney
is hard and will have anterior notches. There
may, however, be confusion between a very Palpate for the right kidney in the same manner
large spleen and large kidney mass. Watch out as the left. Place the flat of the right hand hori-
for the following features to distinguish an zontally in the right lumbar region anteriorly.
enlarged spleen from a kidney. It has to be said Push upwards with the left hand in the right loin
that these features are not absolute and there and ask the child to breathe deeply. Press down
may still be doubt at the end of the examination. the right hand and feel the lower pole of the
An ultrasound examination is the best way out kidney if it is palpable. Renomegaly is present
to differentiate the two (Table 3.6). in hydronephrosis, polycystic kidneys, Wilm’s
tumour, trauma to the loin and renal vein Measure the liver edge in centimetres from
thrombosis. You may have trouble delineating the subcostal margin. In children the normal
a liver mass from a kidney swelling. In general liver edge can be felt up to 2 cm below the ribs.
you should be able to feel the liver edge. The In newborns, a liver edge of up to 3.5 cm may
kidney appears as a deep-seated structure and be normal. Measurement of ‘liver span’ is a
more rounded in its feel. However, confusion useful concept and takes account of enlargement
may well remain if either is excessively enlarged. both upwards and downwards. Percuss the
upper border of liver dullness and mark that
Liver point. Mark the lower edge of the liver in the
right midclavicular line in the abdomen. Now
You normally palpate the liver margin in the
join these two points and measure the distance
right subcostal region. That is assuming that the
to give you the liver span.
child does not have situs inversus. Make
Below is a table showing average liver span
yourself comfortable first and sit on a couch on
at different ages (Table 3.8).
the right side of the patient. In the two handed
technique, place the flat of both hands side by Table 3.8: Average liver span
side below the right subcostal region, fingers
Age (years) Span (cm)
pointing towards the ribs. Ask the child to
breathe in deeply. At the height of inspiration 1 6
2 6.5
(as the liver is pushed down) press the fingers 3 7
firmly inwards and upwards. The liver border, 4 7.4
if palpable should rise beneath the fingers (Fig. 5 8
3.3C). 12 9
Alternatively place the flat of the right hand
parallel to the right costal arch. The liver edge Table 3.9: Points to note in a palpable liver
is then felt against the radial border of the index • Liver span
finger. Press lightly in the right hypochondrium • Consistency
• Movement with respiration
if the liver border is indistinct. • Surface
Check the lower border of liver dullness. • Edge
Percuss over the lower part of the chest wall on • Tenderness
the right side from above downwards. The • Pulsation
normal dullness appears in the 4th-5th • Upper margin of liver dullness
• Bruit
intercostal space. An enlarged liver may have a • Gallbladder
higher upper border of liver dullness. It also
helps to percuss for the liver over the abdomen. Note the following in a palpable liver (Table
If there is a suspicion of hepatomegaly, you may 3.9).
percuss in the subcostal region with resultant i. Is it abnormal? Measure the liver span and
dullness. have an estimate.
In ascites of considerable size, the liver is ii. Consistency – hard, firm or soft
palpated by the ‘dipping’ method. Thrust the Soft—Congestive cardiac failure, infective
tips of fingers quickly but gently into the hepatitis, malaria
abdomen so as to feel the organs below when Firm—Lymphoma, chronic haemolytic
you are displacing the ascitic fluid below your anaemia, repeated malarial attacks,
hands. In neonates and young children, you can amoebic hepatitis, fatty liver, Indian
palpate the liver if you place the palm of the childhood cirrhosis
right hand at the subcostal area and allow Hard—Malaria, myelofibrosis, metastasis
normal respiration. The liver, if enlarged, will iii. Movement with respiration–normally
touch your palm. mobile 1-3 cm with respiration
iv. Surface–smooth (congestive cardiac Table 3.10: Causes of bladder distension

failure, malaria, kala-azar, viral hepatitis) • Post-operative period
or irregular (malignancies, metastasis, • Posterior urethral valve
nodular cirrhosis) • Encephalopathy
v. Edge – a firm liver has sharp margins, a • Neurogenic bladder
soft liver has rounded margins • Transverse myelitis
• GB syndrome
vi. Tenderness–infective hepatitis, peri-
hepatitis, congestive cardiac failure, An exostrophy of the bladder is characterised
amoebic hepatitis by the absence of an abdominal wall over the
vii. Pulsation–haemangioma, tricuspid bladder area with complete or partial exposure
stenosis (presystolic) tricuspid incompe- of the bladder mucosa. An exostrophy of the
tence (systolic) cloaca is characterised by a stoma or prolapsed
viii. Upper border of liver dullness – lowering terminal ileum over the opening of the colon
occurs in hyperinflation (bronchiolitis), (accompanied by an omphalocele).
right sided pneumothorax, gas under
diaphragm (perforated viscus, pneumo- Retroperitoneal Structures
peritoneum) and cirrhosis (shrinkage). The
Use both hands to palpate deeply. Feel the aorta,
upper border may be raised in amoebic
retroperitoneal lymph nodes, faecal masses and
liver abscess, subdiaphragmatic abscess,
deep-seated masses. Retroperitoneal lumps may
right-sided pleural effusion and basal
be due to tumours arising from the peritoneum,
pneumonia.
kidneys, adrenals, or lymph nodes. It may help
ix. Bruit–hepatitis, arteriovenous malfor-
to have the child on all fours in a crawling
mations, haemangioma.
posture. You can then palpate the abdomen
x. Left lobe–palpate in the epigastrium to
from below – retroperitoneal structures may be
outline the left lobe of the liver. Riedel’s
better defined this way.
lobe, a congenital variant of the right lobe,
results in a tongue shaped process, best felt
Points of Tenderness
in the epigastrium.
xi. Gallbladder–a smooth, globular swelling The Mc Burney point in the right iliac fossa is a
moving with respiration (mucocele, point on the outer two-thirds of a line joining
choledochal cyst). the umbilicus and the anterior superior iliac
spine. Tenderness at this point is said to be
Urinary Bladder associated with appendicitis. Children generally
Distension of the bladder may be evident on have right iliac fossa tenderness (rather than a
inspection (swelling in the hypogastrium), typical Mc Burney point localisation) as a sign
percussion or palpation. In childhood the of appendicitis. Be wary of appendicitis
bladder is an intra-abdominal organ and this presenting in many different ways. Retro-
means that the bladder is more easily palpable peritoneal appendicitis is particularly notorious
than in the adult. A bladder of considerable for getting missed out. Examine for rebound
dimension may be confused with some other tenderness if there is a suspicion of appendicular
suprapubic lump. A spontaneous voiding or inflammation. Press on the abdominal wall and
catheterisation will easily distinguish the two. release your hand quickly. If the child has
Here are some causes of bladder distension: peritoneal involvement, he/she will feel pain
postoperative period, posterior urethral valves, when the hand is released. Guarding is also a
encephalopathy, neurogenic bladder dysfunc- sign of inflammation of the peritoneum. Whilst
tion, transverse myelitis and Guillain-Barre palpating the tummy you will have noticed a
syndrome (Table 3.10). rigidity of the muscles on that side. This is the
body’s natural mechanism to contain inflam- cylindrical. A physiological phimosis is a normal

mation. Get the child to turn the face away and finding. Small, white epithelial pearls or
give a short cough. Where does it hurt? Is it over inclusion cysts may be transiently present on the
the right iliac fossa? Ask the child to blow out distal portion of the prepuce in the newborn.
his tummy like a balloon and watch for his Pearly white papules are often normally present
reaction. He will fail to do so if there is a degree on the adolescent penile corona in 1-5 rows and
of peritonitis. In advanced cases of acute are not to be confused with venereal warts.
inflammation, pressure on the left iliac fossa The scrotum is highly pigmented in the
may cause pain in the right lower quadrant newborn. This is due to the surge in testosterone
(Rovsing sign). Flexion and internal rotation of in the perinatal period. Both testes should be
the right thigh may also cause abdominal pain located in the scrotal sac (unless premature) each
(obdurator sign). measuring about 1 cm in length. A hydrocele is
You should remember that there could be often present at birth that disappears
many other causes of right iliac fossa pain other spontaneously. In the adolescent growth spurt,
appendicitis. They may be gastroenteritis, the testes and penis increase in size and
urinary tract infection, constipation, typhlitis secondary sexual characteristics mature to that
(inflammation of caecal wall), twisted ovarian of the adult (see sex maturity staging).
cyst and inflammatory bowel disease. Note the following abnormalities while
Examine other parts of the abdomen for examining the penis:
tenderness – the left iliac fossa, right and left i. Enlargement of penis (with or without
renal angles, epigastrium and subcostal region. testicular enlargement)–Precocious
Left iliac fossa pain may be related to gastro- puberty (gonadotrophin dependent or
enteritis, amoebic dysentery or constipation. independent).
Renal angle tenderness could mean perinephric ii. Micropenis–Micropenis is an abnormally
abscess. Epigastric tenderness may be a result small penis, the stretched length of which
of gastritis. Similarly duodenal inflammation or deviates from the mean by more than 2.5
cholelithiasis may be responsible for pain in the SD. The full term neonate has a mean
right subcostal region. penile length of 2.5 cm. Retract the penis
is measure along the dorsum to the top of
the glans penis without including the
Groin
foreskin. Causes of small penile length are
Inspect the groins and palpate the inguinal canal hypogonadotrophic hypogonadism
for any expansile impulse on coughing. Perform (Kallmann syndrome, Prader-Willi
this test in the supine and later in the standing syndrome, congenital hypopituitarism,
position. Palpate the femoral artery on two sides septo-optic dysplasia), rudimentary testes
(see section on pulse) and along the artery for syndrome, 3 beta hydroxysteriod dehydro-
enlarged inguinal nodes. The presence of genase deficiency congenital adrenal
inguinal lymph nodes is normal in barefoot hyperplasia, 5 alpha reductase deficiency,
children. There may also be small cuts and partial androgen insensitivity, gonadal
scratches in the foot or the leg and cause the dysgenesis, and Noonan syndromes.
nodes in the groin to be prominent. iii. Erection–Transient erection of infancy,
priapism (local irritation, urethritis,
Male Genitalia urethral or bladder calculi, spinal cord
lesions, sickle cell disease, leukaemia,
A full term newborn male should have a well- Fabry disease).
formed penis and scrotum. The urethra opens iv. Chordee–Refers to abnormal ventral
at the tip of the penis, which is normally curvature of the penis as in hypospadias
v. Hypospadias–Urethral meatus opens on ii. Torsion of the spermatic cord–Swelling

the ventral surface of the penis. The meatus and ipsilateral bluish or erythematous
may be near the glans or anywhere on the discolouration of the involved side with
ventral surface of the penis and rarely in pain and tenderness. In the young infant,
the perineum (glandular, penile, peno- the only evidence may be an erythematous,
scrotal, perineal). Hypospadias may occur warm, tender groin mass.
alone or as part of undervirilisation in con- iii. Orchitis–Following viral fever (Coxsackie,
genital adrenal hyperplasia, or the Smith- mumps, rubella) the scrotum appears
Lemli-Opitz or Denys-Drash syndromes. swollen, painful and tender and the skin
vi. Epispadias–Urethral opening on the dorsal red and shiny.
surface of the penis. iv. Leukaemic infiltration–Firm swelling, with
vii. Stenosis of urethral meatus–observe the or without pain.
urinary stream for impedance or deflection v. Epididymitis–Painful, red scrotum with
(in posterior urethral valve obstruction, the thickened tender epididymis.
stream is lost and urine often comes out in vi. Torsion of the appendix of the testis or
drops) epididymis–Sub-acute onset or sudden
viii. Meatal redness–Local trauma, diaper pain and oedema of the scrotum. A ‘blue
dermatitis, Stevens-Johnson syndrome,
dot’ discolouration may be visible through
Kawasaki disease.
the skin and a tender mass may be
Next examine the scrotum and testes for any
palpated near the superior pole of the tests.
of the following defects:
The testis itself is non-tender.
i. Hernia – Check for:
vii. Henoch-Schonlein purpura–scrotal
a. Impulse on coughing, reducibility (unless
oedema, bleeding into scrotum, acute
obstructed)
b. Hernial sac in relation to pubic tubercle severe testicular pain and swelling along
(lateral and below–femoral; medial, and with other classical features.
above–inguinal) viii. Varicocele–In pubertal boys, appears as a
c. Contents - bowel gurgles, omentum feels ‘bag of worms’; increases on standing and
soft and doughy reduces with recumbent posture.
d. Exclude other causes ix. Undescended testes–Palpate for absence of
• Hydrocele, cyst of epididymis testes in each side of the scrotum. Fre-
- can get above swelling, transillumi- quently the testes in a newborn are in the
nant inguinal canal and so examine the root of
• Undescended or ectopic testes the scrotum for lumps. Most undescended
- empty scrotum on that side testes are of the migratory or retractile
• Saphenous varix types (well-formed scrotum with testes
- swelling disappears on lying down, that cannot be felt). Such testes may be
venous hum pulled down gently into the scrotum.
• Aneurysm of femoral artery Another method is to have the child sit
- expansile pulsation cross-legged so that the cremasteric reflex
• Psoas abscess is inactivated and testes are not retracted
- Fluctuant, may be compressible upwards. Testes that cannot be palpated
from below to appear in iliac fossa in the scrotum or in the inguinal canal may
• Inguinal lymph node be intra-abdominal or absent. Search for
- Search for source for site of infection ectopic sites above the superficial inguinal
in feet, legs, thigh, scrotum, ring, in the femoral area, at the base of the
perineum and perianal region. penis or in the perineum.
x. Small or absent testes–Congenital anorchia, from non-specific vaginitis, bacterial

rudimentary testes syndrome, post vaginosis and pinworm infestations.
radiation, Noonan syndrome, Klinefelter iv. Erythema–Trichomonas, candida infection,
syndrome, XX males, Kallmann syndrome, toxic shock syndrome, trauma, vulvo-
Biedl-Bardet syndrome, and constitutional vaginitis.
delay of puberty. v. Vesicles–Herpetic vulvovaginitis.
xi. Macro-orchidism–(testicular volume vi. Cyst, caruncle, prolapse of urethra
larger than that expected for age) Fragile vii. Foreign body.
X syndrome, tumour. viii. Clitoris–Small (gonadal dysgenesis,
xii. Unilateral testis–Mixed gonadal dys- hypopituitarism), large (precocious
genesis, undescended testis, unilateral puberty with virilisation).
anorchia, atrophy. ix. Imperforate hymen.
x. Condyloma acuminata–Filiform, clustered,
Female Genitalia soft lesions in the perineal and genital
areas.
It is easier to inspect the female genitalia rather
xi. Sarcoma botyroides–Moist, grape like
than do a digital vaginal or rectal examination.
fleshy masses at the vulva
The intact hymen makes a formal examination
xii. Examination for sexual abuse–Abrasion
unlikely. In the adolescent girl, you sometimes
and bruising of thigh, genitals, scarring of
can feel the cervix and uterus by doing a
fossa navicularis, injury to posterior
bimanual abdomino-rectal examination. This is
fourchette, tear of labia minora.
rarely indicated. Examination of the genitalia is
a traumatic experience for the child and needs
Anus and Rectum
a lot of prior preparation. Do not do a genital
examination unless there is a definite indication. Rectal examination is distressing to the child –
In this age, it may be better to perform invasive Be gentle and reassuring. Make the child lie in
internal examination only under general the left lateral position and inspect the anal
anesthesia. Nevertheless, do not delay opening for:
preliminary examination in instances where it i. Meconium–The normal newborn should
is clearly indicated - child abuse, Lichen sclerosis have passed meconium by the first day.
or vulvovaginitis. Explain to the child and the Passage of meconium through the vagina
parents and reassure them. Remember to have suggests a rectovaginal fistula.
a female attendant at all times. The smaller child ii. Location–In congenitally malformed
is best kept on the mother’s knee. rectum, the location may be far too
Sit in front of the mother and support the forward, close to the genitalia.
child’s feet on your knees. Place the soles of the iii. Pinworms or segments of tapeworm close
feet together to abduct the thighs. Now spread to the anal opening.
out the labia majora to expose the labia minora, iv. Rectal prolapse–The prolapsed rectum
urethral meatus, and vagina. Forward retraction appears as a bright red tube like protrusion
of the labia majora usually permits visualization with or without a history of blood in the
of the hymen. Observe for: stool. Causes are constipation, chronic
i. Secondary sexual development (see diarrhoea, cystic fibrosis, urinary
pubertal staging). obstruction, pertussis, malnutrition, spinal
ii. Personal hygiene, lice, scabies. cord lesions, polyps and hypothyroidism.
iii. Vaginal discharge – Whitish/blood stained v. Anorectal fistula–These fistulas develop
discharge is common up to the first week from perianal abscesses and open on the
of life. Discharge in the older infant can be perineum near the anus.
vi. Anal fissure–This may be an important e. Tone of sphincter –

cause for unexplained crying in infants. • Lax sphincter–Myelomeningocele, spinal
There may be a history of bright red blood cord injury
on the stools. A fissure near the muco- • Grips finger–Hirschprung disease is
cutaneous junction may not be evident typically associated with a loaded
unless the knees are curled well into the rectum. The anal sphincter grips the
chest and a good light used. Sometimes a finger; on release there is explosive
speculum may have to be used for lesions passage of flatus and faeces.
not seen on external inspection.
vii. Bruise, tears, laxity of sphincter suggests Percussion
sexual abuse.
Use the same technique as for percussion of the
viii. Perianal cellulitis–It is characterised by a
chest. This time you need to percuss over the
sharp demarcated, intensely red erythema
liver, spleen, bladder and other masses. More
of the perianal tissues.
importantly shifting dullness by percussion is
To perform a per-rectal examination in the
used to test for free fluid in the abdominal
young child, it is best to use the little finger. In
cavity.
older children you may use the index finger. Put
a generous amount of lubricant on the gloved
Shifting Dullness
finger and place the pulp of the finger (not the
tip) flat on the anus, and press firmly and slowly Lay the child supine after making sure that he/
in a slightly backward direction. After initial she has passed urine recently. Palpate the
resistance, the sphincter relaxes and the finger abdomen for liver and spleen to avoid
is passed into the anal. Rotate the finger through percussion over a lump and thereby receiving
360º and feel the anatomy of the rectum. Instead the wrong information. Percuss from below the
of putting the child in the left lateral position, xiphisternum downward till the maximum
you may put him in a lithotomy position. point or resonance is reached. At this point
Examine for the following. percuss laterally to one side from the midline
a. Anorectal stenosis–A ring or diaphragm till a point of dullness is reached. Mark the point
about 1.5-2 cm above the anus. In imperfo- and continue percussion in the same direction
rate anus, the proximal rectal pouch ends up to the lateral muscle wall to make that sure
blindly somewhere above the skin. The site that the dullness is not localized. Ask the child
is revealed by dimpling or increased to roll over and lie on the opposite side without
pigmentation of the skin (but not always). taking off the pleximeter finger. Allow some
This may occur alone or as part of the time for the fluid to settle in the dependent
VATER association (vertebral defects, anal position and percuss again. The note which was
atresia, tracheo-oesophageal fistula with previously dull should appear resonant if ascites
oesophageal atresia, radial and renal is present. Continue percussion from the flank
dysplasia) or the cat’s eye syndrome (ocular medially till an area or dullness (previously
coloboma, pre-auricular tags or pits, resonant) is reached. Percuss as far as the hand
congenital heart disease, ocular malfor- would allow. This shows continuity of dullness.
mation). Repeat the same procedure for the other side
b. Anal papillae–Small smooth rounded anal (Figs 3.4A and B).
tags. To detect minimal ascites, place the child in
c. Intussusception–A mass resembling the a knee-elbow position to ensure gravitation of
uterine cervix may be palpable. fluid to mid abdominal position (puddle sign).
d. Tenderness–Right sided tenderness may Percuss from the lateral to the periumbilical
occur in appendicitis or pelvic abscess. area, where you will expect to find dullness. In
A B
Figs 3.4A and B: Procedure to elicit shifting dullness
another method, the chest piece of the stetho- Auscultation

scope is placed over the mid-abdomen and the
Bowel sounds tell you if the intestines are
abdominal wall is gentle tapped (or scratched)
moving normally. Place the diaphragm of the
with the index finger from outside inward. A
stethoscope firmly on the abdominal wall
change of note is heard at the edge of the fluid
pocket. (usually to the right of the umbilicus) to listen
for bowel sounds. Note in the process if the chest
Fluid Thrill piece marks out an area of parietal oedema
Fluid thrill is present when the free fluid is gross (indentation on the abdominal wall). Listen
and under tension. Lay the child flat on his back. patiently and carefully to the bowels gurgling.
Place one hand flat over the lumbar region of Gastric peristalsis occurs about one in twenty
one side. Get an assistant to put the ulnar side seconds. The intestines in children move faster
of his/her hand firmly in the midline of the than this. Bowel sounds are excessive and
abdomen (the child’s own hand will not suffice exaggerated in acute mechanical obstruction.
in this regard). Tap or flick the opposite lumbar ‘Sluggish’ sounds occur in postoperative states,
region and feel the definite and unmistakable premature babies with slow gut motility or ileus
impulse on your hand in the opposite lumbar and peritoneal inflammation. Listen for a few
region. The purpose of the assistant’s hand is to minutes before commenting on a ‘silent’
dampen transfer of the impulse through the fat abdomen. Prolonged intestinal obstruction,
of the abdominal wall (Figs 3.4A and B). generalised peritonitis, and paralytic ileus may
give rise to this condition.
Hydatid Thrill Use your stethoscope to listen to other
This is found during percussion of an enlarged sounds as well. You may detect a renal bruit
liver or spleen. As the plexor taps the pleximeter from a renal artery stenosis or a venous hum
finger, the scolices and hydatid sand in a cyst over the epigastrium. It is common to auscultate
gets displaced. They come up again and touch a bruit in the iliac fossa in a child with a
the pleximeter soon after the tap. transplanted kidney.
RESPIRATORY SYSTEM
The respiratory system consists of the upper A line drawn from the second thoracic spine
airway and the lower respiratory tract. The to the sixth rib in the mammary line represents
upper tract starts from the nose up to the larynx the major interlobar fissure or the oblique
and includes the nose, sinuses and nasopharynx fissure. On the right side, a horizontal line from
and larynx. The lower tract includes the trachea, the sternum at the level of the fourth costal
bronchi, bronchioles and alveoli. cartilage, drawn to meet the line of the major
Before we proceed to the examination interlobar fissure marks the boundary between
proper, it would be helpful to undersand a few the upper and middle lobes (minor interlobar
anatomic landmarks. The bifurcation of the fissure, transverse fissure) (Figs 4.1A and B).
trachea corresponds in front with the lower To interpret a chest X-ray it is wise to know
border of the manubrium sterni (angle of Louis) the anatomy of the bronchopulmonary seg-
and behind with the disc between the 4th and ments. Most of the lower segments are situated
5th thoracic vertebrates. The ribs are counted posteriorly. The middle and upper lobes on the
from the second rib downward. The second rib right side and the upper lobe on the left occupy
is that one whose costal cartilage articulates most of the area in front. The axilla is that part
with the sternum at the angle of Louis in which all the lobes are accessible (Figs 4.2A
(manubriosternal junction). and B).
Fig. 4.1A: Respiratory segments supplied by Fig. 4.1B: Respiratory segments supplied by
segmental bronchi—anterior aspect segmental bronchi—posterior aspect
Cough
Infants do not have well-developed pathways
for the cough reflex. For this reason their
coughing is mostly ineffective. Expectoration
occurs only after about 6 years of age; therefore,
productive cough takes place only after that age.
Enquire about the following:
• How long has it been present?
A cough lasting for a few days may be due
to coryza while a prolonged history would
suggest pertussis or tuberculosis. There may
be other causes of a persistent cough which
are listed in Table 4.1.
Table 4.1: Different types of cough and their causes

Types of cough Conditions
1. Loose, productive Bronchitis, cystic fibrosis,
bronchiectasis
2. Brassy Tracheitis, habit cough
3. With stridor Laryngeal obstruction, pertussis
4. Paroxysmal Pertussis, cystic fibrosis, foreign
body
5. Staccato (machine Chlamydia pneumonia
gun burst)
6. With vigorous Exercise induced asthma,
exercise cystic fibrosis, bronchiectasis
7. Tight (wheezy) Reactive airways
8. Disappears with Habit cough, hysteria
sleep
Figs 4.2A and B: The Upper, mid and lower zone of
lung in X-ray chest: (A) PA view, (B) Lateral view • Worse at any particular time?
A dry cough at night may be an early
symptom of asthma. It is true however that
all types of cough seem to be exacerbated at
The upper border of the lung extends 2.5 cm
night. A cough, which is most severe on
(in the older child) above the medial third of the
awakening in the morning, is often
clavicle. The lower border on the midclavicular,
attributed to cystic fibrosis or bronchiectasis.
midaxillary and scapular lines are at the 6th, 8th,
• Is the cough aggravated by dust, pollen or
10th ribs respectively. The pleura extends to 2
cold air?
spaces below and parallel to each of these
The increased reactivity of the airways seen
landmarks.
in asthma and in some normal children after
viral respiratory infections may present in
History
this way. Severe coughing, whatever may be
Ask specifically for cough, sputum production, the cause may be followed by vomiting. In
stridor, breathlessness (dyspnoea) and chest pertussis, a spasm of cough is followed by a
pain. You should make detailed assessments on characteristic forced inspiration through a
each of the symptoms given below. narrowed glottis creating a ‘whoop’
Respiratory System 73
• Is there strong evidence to suggest asthma? croup, papilloma, cyst, webs, abductor palsy,
Parents quite often ask this question if the foreign body, tracheomalacia, thyroid enlarge-
child is wheezy for the first time. It is difficult ment, tracheo-oesophageal fistula, gastro-
to label a child as having “asthma” with the oesophageal reflux, Arnold-Chiari type II
first few wheezy episodes. Look for malformation and hysteria (Table 4.2).
associated clues which may turn the tables
one-way or the other. A strong family Table 4.2: Causes of stridor
history, maternal smoking in pregnancy and A. Acute B. Recurrent
atopic illness in siblings tend to favour • Laryngotracheobronchitis • Laryngomalacia
asthma. Eczema in the child also goes on to • Acute epiglottitis • Allergic croup
• Foreign body obstruction • Papilloma, cyst, webs,
add to the atopic predilection. A reasonably • Diphtheritic laryngitis abductor palsy
good response to inhaled bronchodilators • Foreign body
also seems to linked more to asthma than to • Tracheomalacia
viral wheeze. • Thymus enlargement
• Tracheoesophageal
fistula
Grunt • Gastroesophageal reflux
It is the body’s protective mechanism of closing • Arnold-Chiary type II
malformation
the glotttis during expiration to build up a • Hysteria
positive end expiratory pressure. This protects
the alveoli from collapse. Grunt is common Haemoptysis
in hyaline membrane disease, transient
tachypnoea of the newborn and children with Blood in the sputum is haemoptysis. First be sure
collapse-consolidation due to infection. The if it is haemoptysis or a haematemesis (or
grunt signifies an increase in the work of epistaxis). Haemoptysis is preceded by a bout
breathing, and therefore, potentially serious in of cough that brings up a small quantity of bright
the older child. red blood. Haemoptysis in children may occur
with bronchiectasis, lung abscess, pulmonary
Sputum sequestration, idiopathic pulmonary haemo-
siderosis, pulmonary oedema, tuberculous
If the child can bring up sputum, ask for a cavity or a bleeding disorder (Table 4.3).
description of the colour and consistency.
Yellow or green sputum generally signifies Table 4.3: Causes of haemoptysis
lower respiratory infection but eosinophils in the • Bronchiectasis
sputum in asthma may also colour it yellow. • Lung abscess
Foetid sputum suggests foreign body inhalation • Pulmonary sequestration
or lung abscess. • Idiopathic pulmonary haemosiderosis
• Pulmonary oedema
• Tubercular cavity
Stridor • Bleeding disorder
A predominantly inspiratory noise, this is

Epistaxis
caused by air being forced through a narrowed
glottis and subglottic space. Stridor can occur Epistaxis occurs with blood flowing freely
acutely in laryngotracheobronchitis, acute usually from one nose (or both) without
epiglottitis, foreign body obstruction and warning. Nose picking, trauma and foreign
diphtheritic laryngitis. A recurrent or persistent body are common causes. Other causes are
stridor occurs with laryngomalacia, allergic adenoidal hypertrophy, allergic rhinitis,
sinusitis, polyps, acute nasopharyngitis, a consolidation. Conversely you may interpret

paroxysmal cough (pertussis, cystic fibrosis), conducted sounds from the throat as ‘crackles’.
thrombocytopaenia, bleeding disorder, hyper- Listen in when the child is not making upper
tension, and renal failure, angiofibroma and airway noises. Do the sounds seem to come from
sometimes during menarche. When bleeding a superficial source?
occurs at night the child swallows the blood and
the epistaxis masquerades as a haematemesis (as Inspection
he/she vomits) or melaena (blood in stools).
a. Count the respiratory rate and comment on
the rhythm and chararacter of breathing (see
Dyspnoea
general survey). Look for signs of dyspnoea.
Dyspnoea is the subjective sensation of breath- Lift the tip of the nose to see the inside of the
lessness or the awareness of the presence of nostrils. Observe for a dull grey mucosa
breathing. Intermittent dypnoea may be due to (allergic rhinitis), blood, foreign body and
asthma. Dyspnoea without an organic cause polyp.
may present as the hyperventilation syndrome. b. Compare the size of the chest against the
In the smaller child and infant, look for measurement of the head circumference. At
tachypnoea, suprasternal or subcostal suction, birth, the head circumference is bigger than
chest retractions, cyanosis and audible the corresponding chest size. The chest
wheezing. should overtake the head size at 6-9 months
of age. If the head is bigger by the end of the
Chest Pain first year, think of malnutrition and
hydrocephalus. At birth (term baby) the
Pleuritic pain is sharp and stabbing (stitching)
chest circumference is 33 cm; that at one year
and is made worse by deep breathing or
is 48 cm and that at 3 years is approximately
coughing. The pain is often severe but may be
52 cm. This is a broad generalisation. If in
mild. The pain improves when an effusion
doubt, look up centile charts for head
develops to separate the inflamed surfaces. A
circumference to assess if the chest is truly
constant severe pain may follow rib fractures.
small in comparison to the head
An aching pain may be due to spontaneous
c. Look also at the shape of the chest. In
pneumothorax on the same side. Chest pain may
infancy, the transverse diameter and the
arise as a cause of pain referred from the
anteroposterior diameter of the chest are
abdomen.
equal so that the chest appears round. After
2 years, the transverse diameter increases so
Physical Examination
that the appearance is transversely oval. A
The anatomical and physiological differences round chest in an older child is often due to
between the child and adult mean that there will chronic obstructive lung disease. Here are
be some differences in physical signs. The chest some abnormal shapes that you may come
wall of the infant and young child is more across.
compliant. This explains the signs of intercostal • Bulging precordium—left ventricular
and subcostal recession seen during severe hypertrophy, complex congenital
respiratory illness. The chest wall is also thinner anomalies, pneumomediastinum
and the distance between the stethoscope and • Intercostal bulging—large pleural
bronchi smaller. Thus there is less alteration in effusion, marked expiratory effort
the quality of breath sounds in each cycle. A • Retractions—mild retractions are normal;
number of signs may be variable in the small more marked retractions occur with
child. You may not hear crackles in a child with atelectasis, pneumonia, bronchiolitis,
cystic fibrosis, asthma, laryngeal obstruc-

tion and choanal atresia. Inspiratory
retraction of the sternum does not always
signify insufficient pulmonary aeration
but may be a normal phenomenon in
small premature infants. Rib crowding
may be present on the same side in
collapse or fibrosis.
• Funnel chest (pectus excavatum) -
characterised by depression of the
sternum and costal cartilages. The defect Fig. 4.3: Pectus excavatum
usually begins in the 2nd intercostal
region and becomes more prominent
toward the xiphoid. They may be asso-
ciated with absent pectoralis muscles,
Marfan’s syndrome, Noonan syndrome
and in some normal children (Fig. 4.3).
• Pigeon breast (pectus carinatum) -
characterised by a prominent, protruding
sternum with vertical depressions along
the costochondral junction lateral to the
sternum. This deformity is found in
Fig. 4.4: Pectus carinatum
patients with the rickets Morquio,
Noonan and Schwartz-Jampel syn-
dromes (Fig. 4.4).
• Harrison groove - a horizontal depression
of the rib cage along the attachment of
the diaphragm extending from the lower
end of the sternum to the mid axillary
line. It may be congenital or may occur
as sequelae of rickets or severe chronic
respiratory infection in early childhood.
• Barrel shaped chest - the sternum appears
to be pushed out and the ribs more Fig. 4.5: Kyphoscoliosis
horizontal than usual. This occurs with
chronic obstructive lung diseases
(asthma, bronchopulmonary dysplasia).
• Narrow fixed thorax — occurs in
asphyxiating thoracic dystrophy as part
of a generalised skeletal abnormality.
• Rachitic rosary - rounded knob like
prominences or beading at the costo-
chondral junctions (rickets). This condi-
tion should not be mistaken for the
normally palpable costochondral junc-
tions in many normal infants (Fig. 4.7). Fig. 4.6: Kyphosis
Palpation
a. Chest palpation: Feel a swelling for warmth,
size, shape, tenderness and consistency.
Bony tenderness resulting in sternal pain
may be a feature of leukaemia. Tenderness
of the chest wall may be due to injury,
muscular (intercostal) pain, costochondritis,
herpes zoster (pre-eruption) and pleurisy.
You can measure chest expansion measured
at the nipple line between full inspiration
and expiration. In the cooperative older child
this should be at least 4 cm. You should
examine the chest systematically for:
Fig. 4.7: Rachitic rosary • Swelling pain/tenderness
• Scorbutic rosary—This is characterised • Trachea
by a sharp edge like depression at the • Apex beat
costochondral junction (scurvy). • Respiratory excursions
• Agenesis or hypoplasia of pectoralis • Vocal, rhonchial, friction fremitus
major and minor - this is accompanied by b. Palpation of trachea: This can be done in either
hypoplasia or absence of the breast and sitting or supine positions. Align the head,
nipple (Poland’s syndrome). neck and shoulders so that no one side is
• Precordial pulsation—in states of unduly prominent. Gently place the tip of the
hyperdynamic circulation (anaemia, left index finger in the suprasternal notch and
to right shunt, aortic regurgitation, mitral extend slightly upwards to touch the trachea.
regurgitation), thin chest wall, pul- Now move your finger to the right and left
monary hypertension. of the tracheal prominence. On each side of
• Epigastric pulsation—right ventricular the trachea is a depression between the
hypertrophy. trachea and the sternomastoid. You will have
d. Scars—midline sternotomy scars indicate to judge if the depression is more on the right
major cardiac surgery. They are often or the left. If the finger indentation is more
associated with scars around the xiphis- on the right, then the trachea is deviated
ternum and epigastrium (pericardial drains). more to the left (Figs 4.8 and 4.9). A slight
Lateral thoracotomy scars indicate Blalock deviation of the trachea to the right is within
Taussig shunts, repair of patent ductus normal limits. Marked deviation to any one
arteriosus, repair of coarctation and pulmo- side signifies a pull (collapse, fibrothorax) to
nary artery banding. They may be present that side or a push (pleural effusion,
along with abdominal scars that suggest pneumothorax empyema, lobar emphysema,
repair of diaphragmatic hernia or oesoph- tumour) to the other. Remember that a
ageal atresia. slowly developing effusion (tuberculosis)
e. Movement of chest with respiration (see does not cause a mediastinal shift. An
section of respiration under general survey). effusion low down or a small isolated
f. Note features that are obvious – a Hickman collapse of a segment may not alter tracheal
central line or the button of a portacath, scars position.
and chest drains. They may add up to give c. Cardiac impulse: Refer to apex beat (cardio-
you the whole picture. vascular system)
Fig. 4.8: Palpation of trachea conventional method Fig. 4.9: Palpation of trachea easier method
d. Asymmetry: Palpate for asymmetry of palpable wheezing or a pleural rub with your
excursion of movement. Lay the palms of the hand. Increased vocal fremtus can be caused
hands on the chest symmetrically on the by consolidation and a big cavity with patent
posterior surface of the chest with the bronchus. A word of caution – these signs
thumbs touching each other in the midline. are unreliable in children and therefore do
In the upper part, the chest moves vertically. not jump to conclusions without corrobo-
So if there is restriction of movement, the rative evidence.
thumb on that side will have move less in a f. Transillumination: Darken the room and
vertical direction. Now place the palms shine a bright light object (it is best to use a
encircling the chest with the thumbs in the fibreoptic cold light source) on to the chest
midline. This can either be done in the wall. The side of the pneumothorax in the
mammary and submammary area anteriorly neonate will show up transilluminant. This
or in the infrascapular area over the back. test is of little or no use in the older child.
Note the lateral excursion of thumbs.
e. Tactile vocal fremitus: Place the palm of the Percussion
hand in different areas of the chest and ask
the child to say ‘one-one’ or ‘ninety-nine’. You should have a fair idea of which areas to
You may use similar repetitive sounds in the percuss. The anterior aspect of the chest wall is
local vernacular. Use the same hand in all divided into the presternal area and right and
the areas (do not use both hands simul- left anterior portions. Each side, left or right, is
taneously as the sensation in the 2 hands may subdivided from above downward into
be different). In increased vocal fremitus you supraclavicular, infraclavicular (up to 2nd rib),
should be able to feel distinct vibrations such mammary (up to 5th rib) and infra mammary
that the sounds seem to be present just under regions. On the lateral aspects, there are 2 areas,
your hand. You may also be able to detect the axillary region (up to the 4th rib) and infra
axillary region. Over the back on either side, the so (Figs 4.11A and B). Percussion in the child
regions from above downward are supra- less than two years of age is of no great value –
scapular, interscapular and infrascapular. so do not spend too much time in tapping on a
The basic technique of percussion for a right- frightened toddler. It may be useful in the sick
handed clinician is as follows: child to examine the anterior aspect of the chest
Place the left hand on the chest wall, palm in its entirety (movement, percussion and
downwards and fingers slightly separated, so auscultation) before moving on to examine the
that the second phalanx of the middle finger is back. This way you will not have to go
precisely over the area to be percussed. The backwards and forwards to complete your
middle finger of the left hand is called the examination.
pleximeter finger. Press this finger down on the The principle of percussion is to set into
chest wall while all the other fingers are lifted vibration a body of air in a cavity of sufficient
up (so as to avoid dampening). The right middle size and appropriate shape so as to produce a
finger is called the plexor. With the plexor, strike resonant noise. There is also a characteristic
the pleximeter sharply at right angles like a feeling in the pleximeter finger. The sound and
hammer. The whole movement must be at the feel of resonance over a healthy lung has to be
wrist joint and not at the elbow. Note also that learnt by practice. In general it is low pitched
as soon as the blow has been given, the striking and clear in character.
finger must be raised. The blow should be no The normal degree of resonance varies from
heavier than is necessary to elicit the resonance individual and from region to region. The chest
of the part being percussed and the wrist joint wall below the clavicle is thin and hence more
should move loosely (Fig. 4.10). resonant. The percussion over the scapulae is
Percuss from above downward keeping the necessarily dull. The lower limits of lung
pleximeter parallel to the ribs (except for resonance are determined in quiet respiration
eliciting mediastinal dullness when the and light percussion. The lower border of the
pleximeter finger is kept vertical and percussed right lung lies in the mammary line at the 6th
from lateral to medial). Compare bilaterally for rib, in the mid-axillary line at the 8th rib, and in
qualitative and quantitative difference of note. the scapular line at the 10th rib. On heavier
Percuss both the front and the back. There is no percussion, the liver and diaphragm contribute
singular advantage of direct percussion over the to dullness two spaces higher up. On the left
clavicle and it is probably not worthwhile to do side, the lower border overlaps the stomach, so
that there is a transition from lung resonance to
tympanitic stomach resonance. The other areas
Figs 4.11A and B: Areas of percussion:

Fig. 4.10: Method of percussion (A) Front, (B) Back
are more or less similar to the corresponding intensity when inflating normally but will be
areas on the right side. reduced if there is localised airway narrowing,
Abnormal percussion notes are produced in or if there is intervening pleural thickening.
diseased states and are given in the Table 4.4. Breath sounds may be of increased intensity in
children with thin chest walls. There are
Table 4.4: Type of percussion note different types of breath sounds–vesicular,
and the diseased state bronchial and broncho-vesicular. A brief
Type Interpretation description for each is given below.
Tympanitic Hollow viscus 1. Vesicular breath sounds are quiet, low-
Hyperresonant Pneumothorax pitched rustling sounds. There is no pause
Resonant Normal lung between the end of inspiration and the
Impaired Consolidation, collapse, fibrosis
Dull Consolidation, collapse, pleural
beginning of expiration. When airway
thickening, pleural effusion obstruction is present the expiration is
prolonged.
Auscultation 2. Bronchial breathing sounds harsher and
seems to arise from the larger airways. In
It is difficult to auscultate the smaller child lying conditions of collapse, consolidation or
down. Most often he or she will resent having fibrosis, the breath sounds are transmitted
to lie on a bed away from the security of his to the surface through an intervening airless
mother’s lap. It is therefore prudent to auscultate zone from the underlying large airways
while the mother or father holds the child without attenuation. Listen with your
upright against the shoulder. You may find that stethoscope over the trachea to get used to
you have to seize the opportunity and listen in hearing brochial breath sounds. The ‘hollow’
when the child is quiet. The rest of the or ‘tubular’ character is more important than
examination including palpation and percussion the loudness, as often the intensity can be
can come later. diminished in overlying effusion. Histori-
Use the diaphragm of the stethoscope to cally bronchial breathing were classified into
listen representative areas anteriorly, posteriorly the following categories:
and over the axilla. Note the following on • Tubular : high-pitched
auscultation: • Cavernous : low pitched (cavity)
• Breath sounds–vesicular, bronchial, bron- • Amphoric : high pitched, resembles the
chovesicular sound produced by blowing
• Vocal resonance–bronchophony, whispering air across the mouth of a jar
pectoriloquy, aegophony (tension pneumothorax,
• Added sounds–pleural rub, wheezes, large superficial cavity with
crackles. patent bronchus)
It has to be said that there is very little to be
Breath Sounds gained by making such fine differentiation
In infancy and early childhood the breath in a child who is probably crying and
sounds are relatively louder and harsher than miserable. Nevertheless it helps to sharpen
in older children and adolescents. Examine the your clinical acumen and refresh your skills
breath sounds starting from the supraclavicular when you remember to look for such signs
fossae and proceed downward one intercostals in cases of florid chest pathology.
space at a time, comparing findings on both 3. The third variety of breath sounds is called
sides of the chest. Breath sounds are of normal bronchovesicular but in reality they are
vesiculobronchial in character. They are mislead you with artefactual adventitious

vesicular breath sounds with a more sounds. The various added sounds can be as
bronchial character during expiration. In a follows:
healthy child they are typically heard near • Crackles
the roots of the lung at the back or in the right • Pleural rub
infraclavicular region. • Wheeze
4. Vocal resonance (Table 4.5): This is like vocal a. Crackles/crepitations:
fremitus except that you auscultate, not These are short, explosive sounds perceived
palpate over the chest. Normally when the as bubbling or clicking noises. When the large
child says ‘one-one’ or ‘ninety-nine’, you will airways are full of sputum, a coarse rattling
not be able to perceive distinct syllables. In sound may be heard even without a stethoscope.
conditions where the resonance is increased, It is a common idea that crackles are produced
the sounds appear to originate from just by air bubbling through moist secretions. This
under the chest piece of the stethoscope and is the exception (pulmonary oedema) rather than
the syllables are more distinct. In some the rule. Crackles are actually caused by sudden
situations, the vocal resonance seems to be changes in gas pressure related to the sudden
nearer the earpiece (more intense) and is opening of previously closed small airways.
termed ‘bronchophony’. A ‘whispering Expiratory crackles are low pitched, scanty
pectoriloquy’ is an increased resonance and loud and may clear with coughing. They
where the words spoken become clear and occur with airflow obstruction. Inspiratory
seem to be spoken right into the listener’s ear. crackles can be end-inspiratory and occur with
A high-pitched nasal intonation or bleating pulmonary oedema, interstitial pulmonary
character (resembling the bleating of a goat) fibrosis and resolving pneumonia. Late inspi-
is called ‘aegophony’. Do not spend too ratory crackles heard particularly at the bases
much time in evaluating the type of indicate delayed airway opening (stiff lungs in
bronchial breathing. They are extremely interstitial pulmonary fibrosis) or oedema of the
subjective and more of academic interest smaller bronchi (pulmonary oedema).
than of real value. Fine crackles sound like the rustling of paper
and are related to consolidation, acute pulmo-
Table 4.5: Vocal resonance and their causes
nary oedema or bronchopneumonia. Coarse
Vocal resonance Cause crepitations are much louder and are heard in
Diminished Pleural effusion consolidation, lung abscess, bronchopneumonia
Pneumothorax and cystic diseases of the lungs. Bronchiectasis
Thickened pleura
Increased
is responsible for coarse crepitations with a
Whispering Consolidation leathery creaking quality (‘leathery rales’). In
pectoriloquy Superficial big cavity with most situations it is important to be aware of the
patent bronchus overall clinical condition and how your
Collapse with patent bronchus observations fit into a diagnosis. If you have an
Bronchophony/ Consolidation above the level of
Aegophony pleural effusion
infant with a fluffy cough and diffuse crackles
(more than wheezes), the likely diagnosis is
5. Added sounds: These are abnormal sounds bronchiolitis.
that arise in the pleura or lung. Make sure Crackles can be confused with pleural rub
that the sounds are not artefacts due to the (see below) and with pharyngeal sounds. In the
chest piece rubbing over the skin. Make sure latter, the noise is heard without a stethoscope
you do not auscultate over the clothes as this and a change of position or a cough will lead to
will not only be erroneus but will also disappearance of the sound.
b. Pleural rub: • Friction test: Place the chest piece on the

A creaking, grating or rubbing noise, it is centre of the chest and rub your fingernail
characteristic of pleural inflammation. It usually on on either side of the chest wall. The sound
occurs with chest pain and may on occasion be of scratching is heard well on the side having
palpable. A pleural rub occurs at the end of pneumothorax.
inspiration and the beginning of expiration • Ewart’s sign: Bronchial breathing may be
when the surfaces of the visceral and parietal audible over the left lower interscapular area
pleura are in contact. The inspiratory or in a patient with pericardial effusion
expiratory components are distinct and separate (compression of left main bronchos leading
in crackles. Unlike crepitations, the pleural rub to collapse).
does not change character with coughing. • D’ Espian’s sign: There is bronchial breathing
c. Wheezes: and increased vocal resonance in the midline
These refer to the older terminology of over the back below the level of the 4th
‘rhonchi’ and are musical sounds associated thoracic vertebra in case of a mediastinal
with airway narrowing. A wheeze is chiefly mass.
expiratory (collapse of the smaller airways) but • Hamman’s sign (mediastinal crunch):
may also be inspiratory in more severe cases Systolic crunching noises are auscultated
when the larger airways are also involved. In over the left sternal border from 3rd to 5th
severe asthma the obstruction may be so great interspaces in mediastinal emphysema with
that air entry is very poor – in such cases, no left sided pneumothorax.
wheeze is heard (silent chest).
A ‘monophonic’ wheeze is generated by Reconciliation
localised narowing of a single bronchus (foreign
This is not part of the clinical examination but
body, endobronchial tuberculosis). ‘Polyphonic’
is crucial to formulating an opinion on the
wheezes are particularly heard in expiration and
child’s diagnosis. As you proceed through the
are characteristic of diffuse airway obstruction
various tests you will pick up signs that may be
(asthma, bronchiolitis). There is dynamic com-
contradictory. Accumulate all your information
pression of the bronchi, which is accentuated in
and come to a decision as to the most likely
expiration when narrowing of the airway
diagnosis. Analysis of your findings will also
occurs. Some clinicians prefer to classify
mean that you have a list of differential
wheezes into sibilant and sonorous types. The
diagnoses.
former is said to be of high pitched, squeaky,
Clinicians work on a best-fit principle. Use
and originates in the smaller bronchi. The latter
the collected information and rationalise your
is low pitched and originates in larger bronchi.
thought on the possibilities. Now rank them
This differentiation has no clinical significance
according to the probability of occurrence. Here
from a management point of view.
are some hints to help you along.
d. Other sounds:
a. Left pleural effusion
• Succussion splash: Affix the chest piece to the
Chest expansion reduced on left
upper border of dullness in a suspected
Trachea shifted to right
pleural effusion and shake the child to elicit
Percussion note stony dull
splash of the fluid (hydropneumothorax).
Breath sounds absent or decreased
• Coin test: Place a coin in front of the chest
Added sounds none
and tap with another coin and auscultate at
Vocal resonance absent or decreased
an identical spot on the back. A loud bell like
b. Right upper lobe consolidation
tinkle is audible in patients with pneumo-
Chest expansion reduced
thorax.
Trachea central or slightly to Breath sounds absent or decreased

right Added sounds none/crackles/
Percussion note dull wheezes
Breath sounds bronchial Vocal resonance decreased/normal
Added sounds crackles d. Large right pneumothorax
Vocal resonance whispering Chest expansion reduced on right
pectoriloquy Trachea shifted to left
c. Collapse of right lower lobe Percussion note hyperresonant
Chest expansion reduced on right Breath sounds absent or decreased
Trachea central Added sounds usually none
Percussion note dull lower right Vocal resonance decreased
CARDIOVASCULAR
SYSTEM
The cardiovascular system is a central feature disease increases from a background 0.8 (2-6%).
in a good examination. Signs and symptoms What was the antenatal scan result? Did the
pertaining to this system often depend upon the mother have any fever and rash during the first
age of the child. You should therefore develop part of her pregnancy? If so think of rubella as a
your skills of examination so that they can be possibility.
suited to each age group. The more practice you Children with migratory joint pain, fever and
get the better. With practice, you will not miss skin nodules may have had rheumatic fever.
the subtle signs associated with neonatal What are the home conditions and sanitation
cyanotic congenital heart disease or the older facilities? Kawasaki disease may present with
child with cardiomyopathy. pyrexia, cervical lymphadenopathy, oral mu-
Dyspnoea is a measure of the child’s cositis and rash. Have a low threshold for
subjective sensation of breathlessness. You will diagnosing this if you think the symptoms fit
appreciate that the well child either plays or the criteria.
sleeps and rarely is inactive. The child who is
quiet and lethargic is obviously unwell. For the Cyanotic Spells
older child, you could consider grading
Ask for a history of cyanotic episodes. Does the
dyspnoea as one does for an adult (Table 5.1).
child go “blue around the lips and mouth”? The
Table 5.1: Grading of dyspnoea (NYHA grading)
parents may have noticed the excess colouring
when the child was playing or crying. Breath
Grade I Dyspnoea while performing heavy unaccus-
tomed exercise (running)
holding spells may be confused with cyanosis
Grade II Dyspnoea while performing accustomed due to congenital heart disease. Both are
exercise (daily routine activity) and against provoked by rapid (and deep) breathing. In the
gravity former, the cyanosis tends to appear somewhat
Grade III Dyspnoea on performing light work (going from later. In cyanotic spell, the child may adopt a
one room to another)
Grade IV Dyspnoea at rest (orthopnoea)
typical posture in an effort to minimise blood
supply to the heart, the so called “squatting”
posture with hips and elbows flexed. This helps
Background
to constrict the arteries by increasing systemic
Obtain a background to the child’s presenting resistance, and shunting off more blood toward
symptoms. Is there a family history of congenital the lungs. The posture also constricts the veins,
heart conditions? Is a sibling affected with a thereby preventing excess venous return. There
similar condition? If a first degree relative is may be variations of the posture adopted during
affected, the recurrence risk of congenital heart a cyanotic spell. In one variation, the child flexes
the hips while resting on the mother’s shoulders. • Cardiac impulse

In another, the child drops to the ground and • Scars (see section on respiratory system).
curls up into a ball. The hypoxia associated with 2. Palpation
such an episode may trigger off secondary • Corroborate findings on inspection
seizures. • Apex beat.
The apex beat is the down most and outer
EXAMINATION most point of definite cardiac impulse. To
examine this, put the child lie on his back (or
Examination is based upon five principles - some consider sitting and leaning forward) and
inspection, palpation, percussion, auscultation place the palm of the hand over the precordium
and ‘reconciliation’ (Table 5.2). The last is really on the left side. Put your hand also on the right
not an examination, but rather an analytical side, otherwise you may miss dextrocardia.
overview of the findings. As with the other Localise the apex beat with the tip of a finger.
systems, you will find signs that seem to have Count the ribs starting from the sternal angle,
variable interpretations in different situations. which serves as a landmark for the 2nd rib. The
Use the best-fit principle to explain your space below is the 2nd intercostal space. Count
examination findings. down to the space where you have localised the
No cardiovascular examination can be apex beat and note the space. Next measure the
complete without a thorough general survey. Of horizontal distance of the apex beat from the left
particular note are the facial appearance, pulse, midclavicular line. In children up to 3 years of
blood pressure, cyanosis, perfusion and neck age, the apex is usually in the 4th intercostal
veins. The regional examination is of crucial space, outside the midclavicular line. In children
importance to proceed towards a correct aged 4-7 years, the apex is in the same (or in
diagnosis. You should use such background some on the 5th) space inside the midclavicular
information to build a pen picture of your case. line. From 7 years of age, the position of the apex
Remember that you do not necessarily have to is 1 cm inside the left midclavicular line on the
be precise about the diagnosis in the cardio- 5th space. The apex beat shifts further to the left
vascular examination and that it is acceptable if examined in the left lateral position, and is
to have a reasonable differential diagnosis list. spread over an area of approximately 3 cm
Very often you will gather enough clues from (Table 5.3).
the general survey and regional examination to The point of maximum cardiac impulse
make up this differential. You should never have (MCI) is not the same as the apex beat. This can
the presumption that examination of the be helpful in determining the dominance of a
cardiovascular system is all about heart sounds. ventricle–right or left. In left ventricular
Auscultation is important but forms only a part dominance, the MCI is close to or coincides with
of the whole. the apex. Those with right ventricular pre-
dominance have the MCI over the lower left
Table 5.2: Scheme of examination sternal border.
• Inspection • Thrill
• Palpation A palpable murmur is called a thrill and
• Percussion
• Auscultation
transmits to the hand placed lightly over the
• Reconciliation chest, very much like the sensation of a purring
cat. Thrills may be systolic or diastolic or both.
1. Inspection of the chest wall – look at the chest 1. A systolic thrill in the left 2nd intercostal
for space is likely to be due to pulmonary
• Shape of the chest (Chap. 4, page 75) stenosis, while a diastolic thrill means
• Precordial bulge probable pulmonary regurgitation.
Cardiovascular System 85
Table 5.3: Variations of the apex beat pulmonary hypertension. A left ventricular
a. Difficult to palpate or locate apex–Infants, obesity, heaving apex beat with parasternal lift can be
pneumomediastinum, pericardial effusion, pleural due to biventricular hypertrophy. You can grade
effusion. parasternal impulse as:
b. Cardiomegaly–Location of the apex beat more than
1 cm lateral to the midclavicular line in the 4th Grade 1 : Mildly lifts the hand, but can be
intercostal space in young children and outside the obliterated
midclavicular line in the 5th space in older children. Grade 2 : Lifts the hand but does not stay with
c. Displaced apex–Cardiomegaly, dextrocardia,
it
mediastinal shift.
d. Type of apex–Normal, left or right ventricular. The Grade 3 : Lifts the hand and stays with it
normal apex is one that is most difficult to define. It is
• Other pulsations
located on the normal position and is akin to the right
ventricular (RV) apex except that it is much less – Suprasternal (coarctation of the aorta,
forceful. The RV apex is more out than down and may aortic regurgitation, unfolding of aortic
have a “tapping” nature. The LV apex is more down arch).
and is forceful in nature. Such an apex may be due – Left 2nd intercostal space (palpable
to ‘pressure overload’ (aortic stenosis), which causes
second sound known as diastolic shock,
a forceful sustained heave, or due to ‘volume
overload’ (aortic or mitral regurgitation) which results due to pulmonary hypertension).
in an ill sustained impulse. – Right sternal edge (huge right atrium as
in Ebstein disease).
– Interscapular and infrascapular region
2. A to and fro thrill is the same area is possibly (Suzman’s sign in coarctation of the
due to patent ductus arteriosus. That on the aorta).
right may well be as a result of a Blalock- • Other relevant areas
Taussig shunt. – Palpate other relevant areas-joints in
3. A diastolic thrill in the left 3rd space suggests rheumatic fever, liver edge and pedal
aortic regurgitation, whereas that situated oedema in congestive cardiac failure,
over the apex suggests mitral stenosis. A trachea and spine if the apex beat is
systolic thrill in the apical region is sugges- displaced.
tive of mitral regurgitation. A continuous 3. Percussion
thrill at the apex is probably due to mitral Percussion of the heart is rarely done, as it
stenosis and regurgitation. does not add much to the clinical assessment. It
4. The thrill of aortic stenosis is palpated in the may be hazardous in the child with cyanotic
right 2nd intercostal space and is transmitted heart disease where it may dislodge an embolus.
up to the carotid artery. Remember, Dullness beyond the apex suggests pericardial
therefore, to put your finger over the left effusion. In this condition the 2nd intercostal
carotid artery every time when you search space is also dull in the lying position. This
for a thrill. A thrill is always pathological; disappears as the patient sits up. In pulmonary
functional murmurs are never associated artery dilation and pulmonary hypertension,
with a thrill. dullness (Gerhardt’s dullness) is present both in
• Parasternal impulse lying and sitting positions.
Place the ulnar side of your hand lightly to 4. Auscultation
the left of sternum. The finding of a parasternal Auscultation for the beginner can seem
impulse indicates enlargement or hypertrophy frustrating, as you will often seem to have the
of the right ventricle or left atrium. A similar test incorrect findings. With practice and per-
is to put the ulnar side of your hand over the severance you will be able to train yourself to
left 2nd intercostal space. Such a sign indicates listen with growing confidence. You may have
to improvise your examination to catch the child areas. For example, say, “the first heart sound
in a good mood. Use any trick you have up your is normal (you have listened to the mitral area),
sleeve to make sure that the child is not crying. with mobile, close split of the second heart
Use distraction techniques using an interesting sound; there is a soft, grade 2/6 ejection systolic
toy or a set of colours. Sometimes it is best that murmur best heard in the left second intercostal
you go away and come back to examine when space, and this radiates through to the back”.
the child is sleeping. Over time you will be able You should know which areas to auscultate and
to listen correctly, correlate with regional they are given in Figure 5.1 and Table 5.4.
examination findings and draw appropriate
Table 5.4: Areas of auscultation
conclusions.
The stethoscope used for auscultation should i. Mitral area–corresponds to the apex beat
ii. Tricuspid area–lies just to the left of the lower sternum
combine both a bell-type chest piece and a
iii. Aortic area–right of the sternum in the 2nd intercostal
diaphragm. High-pitched sounds (1st and 2nd space
heart sounds, aortic diastolic murmur, systolic iv. Pulmonary area–left of the sternum in the 2nd
murmurs, opening snap) are heard well with the intercostal space
diaphragm. Low pitch sounds (3rd or 4th heart v. Other areas–
• Back-murmur of collaterals (pulmonary atresia,
sounds, mitral stenosis murmurs) are best heard
coarctation of the aorta, Blalock-Taussig shunt)
with the bell. Palpate the carotid artery as a time • Abdomen-renal artery bruit (renal artery stenosis),
reference (systolic or diastolic) and also to check bruit over transplanted pelvic kidney
if there is any thrill. • Carotids-carotid bruit (aortic stenosis)
It is best to auscultate all the areas of the chest • Liver–haemangioma, arteriovenous malformations
• Scalp–vein of Galen malformation
first and then formulate an opinion of the quality
and character of heart sounds and murmurs.
Heart Sounds
There is little point in commenting on the heart
sounds and murmurs in each individual area. The events of the cardiac cycle are shown in the
Instead you should reserve your judgement for Figure 5.2. The mitral and tricuspid valves close
heart sounds and murmurs in the ‘best heard’ to give the 1st heart sound. Next the aortic and
Fig. 5.1: Areas of auscultation of heart sounds (A) Mitral area;

(B) Pulmonary area; (C) Aortic area; (D) Tricuspid area
Fig. 5.2: Cardiac cycle
pulmonary valves open inaudibly. The closure disease. Abnormally loudness is also a
of the aortic and pulmonary valves gives rise to feature of tachycardia, short PR interval
the second sound. Closure of the pulmonary and mitral prolapse. Conversely heart
valves occurs after aortic valve closure because sounds normally appear faint in the obese
the pressure in the right ventricle is lower than child, as well as in pericardial effusion.
the left. Soon after this the mitral and tricuspid ii. Splitting: The mitral valve closes slightly
valves open inaudibly. The first heart sound is before the tricuspid valve and this gives
short and sharp (hence the onomatopoiesis– rise to splitting of the first sound. The
‘lup’); the second sound slightly low pitched splitting is of a very short span of time and
(‘dub’) and is normally split (aortic and the human ear cannot detect the small
pulmonary components). difference. When audible, splitting of the
Record any deviation from normal as: first sound is not always a sign of heart
i. Alterations in intensity: This is rather a soft disease. The chief importance lies in
sign – use this in relation to other features avoiding confusion with an atrial sound
of the disease. A loud first heart sound is (S4). The first sound should be preceded
normal in an infant with a thin chest wall by S4 and followed by an ejection click. It
but pathological in rheumatic mitral valve may difficult to define clearly which is
which. Time the sounds with the carotid A reversed split or paradoxical split is one in
pulse - the S4 (low frequency, soft sound) which P2 occurs earlier than A2. Reverse
appears just prior to the first heart sound splitting is caused by:
(or the carotid pulse). Very often the click 1. Delayed aortic closure
is accompanied by a murmur and appears a. Delayed electrical activation of LV (LBBB,
relatively distant to the first sound. RV ectopics).
The first heart sound is rarely split in the b. Prolonged LV mechanical systole (LV
normal state. More commonly split is associtated outlet obstruction).
with tricuspid stenosis, Ebstein’s anomaly and c. Reduced impedance of systemic vascular
right bundle branch block (RBBB). bed (post stenotic dilatation of aorta,
Splitting of the second sound is much easier PDA).
to understand because the two sounds (A2 and 2. Early pulmonary closure
P2) are more widely separated. Splitting is best a. Relative early activation of RV (Wolf-
appreciated in the 2nd left intercostal space (P2 Parkinson-White syndrome)
normally not audible in other areas). A The second sound may be heard as single
physiological split is that in which A2 is (either A2 or P2 inaudible) or closely split in the
followed by P2. Normally a split of 0.06 second following conditions:
during inspiration and 0.02 seconds (close split) 1. A2 inaudible
in expiration is normal for a child. a. Calcific aortic stenosis.
During inspiration, blood is drawn into the b. Synchronous with P2 in Eisenmenger’s
thorax and the right ventricular stroke volume syndrome.
increases. The right ventricle has to account for c. Concealed by
an extra volume of blood. The duration of right i. Loud P2 in pulmonary area (pulmo-
ventricular systole therefore lengthens and P2 nary hypertension).
is slightly delayed. In inspiration, the left ii. Loud pansystolic murmur of MR/
ventricular inflow falls due to a stasis in the VSD.
pulmonary veins associated with a negative iii. Loud prolonged ejection systolic
intrathoracic pressure. As left ventricular murmur (pulmonary stenosis).
volume falls, the systolic time is shortened and 2. P2 inaudible
A2 occurs earlier resulting in a split. The a. Diminished intensity (Fallot, tetralogy,
opposite mechanisms occur in expiration. Split pulmonary atresia, hyperinflation of
heart sounds are better appreciated in the supine lungs).
position. b. Synchronous with A2 (Eisenmenger’s
Causes of normal split S2 are: syndrome).
1. Delayed pulmonary closure c. Concealed by systolic murmur (aortic
a. Delayed electrical activation of RV stenosis).
(RBBB, LV ectopics). A split that is easily heard is for all practical
b. Prolonged RV mechanical systole purposes a wide split. This is found in atrial
(pulmonary stenosis). septal defect (ASD) and partial or total
c. Reduced impedance of vascular bed anomalous pulmonary venous drainage
(prolonged hangout interval) - ASD, (PAPVD/TAPVD). A wide split occurs in ASD
idiopathic dilatation of pulmonary artery, because of RV overload and also an associated
mild pulmonary stenosis. RBBB. This split is sometimes fixed if the ASD
2. Early aortic closure is large and the right atrium cannot distend
a. Shortened LV systole (mitral regurgi- further in inspiration to accommodate the
tation, VSD) enhanced venous return. Other causes of fixed
split are severe right heart failure, pulmonary • The opening snap (OS) is a high-pitched
embolism and cardiomyopathy impairing RV sound heard in mitral stenosis and is
function. followed by the typical rumbling mid-
diastolic murmur. A shorter A2-OS interval
iii. Third and fourth heart sounds signifies a more severe obstruction. It is best
These low frequency sounds are heard in heard slightly more parasternal to the apex,
diastole (after S2). You will be listening to a set where the rumbling diastolic murmur is less
of three beats, and when the heart rate is rapid, prominent.
this seems like a gallop rhythm. A gallop with • The pericardial ‘knock’ in constrictive
S1, S2 and S3 is known as a triple gallop. If the pericarditis is a loud but low frequency
fourth heart sound is added, it becomes a diastolic sound that is due to an abrupt stop
quadruple gallop. Sometime the diastole is in the phase of early diastolic filling.
shortened and the third and fourth heart sounds • An ejection click is a sharp high-pitched
coincide. This is known as a summation gallop. sound heard immediately after S1. An aortic
You will be hard pressed to distinguish the triple click (systemic hypertension, aortic stenosis,
gallop from a summation gallop, but in the latter bicuspid aortic value) is best heard over the
the amplitude is greater. aortic area of the apex. A pulmonary ejection
The 3rd and 4th heart sounds originate in the click (valvular pulmonary stenosis, pulmo-
ventricles. The S3 occurs early in diastole at the nary hypertension, tetralogy of Fallot) is best
time of rapid ventricular filling (0.15 second after heard over the pulmonary area. A pulmo-
S2). The S4 occurs later in diastole and is caused nary click differs from an aortic click in
by a bolus of blood delivered to the ventricle by becoming quieter or absent during inspi-
atrial contraction. An S3 occurs normally, in ration (in contrast to all other right heart
states of hyperdynamic circulation and sounds).
abnormal LV filling (LV failure, MR, anaemia). Murmurs
An S4 is due to a stiff and non-compliant
ventricular wall. Murmurs are audible adventitious sounds due
Listen to these sounds with the bell of the to turbulent flow across a value or an abnormal
stethoscope and the child turned to the left communication within the heart. Listen to a
lateral side. An S3 may be confused with a split murmur only after you are sure about the
S2. The differences between S3 and split S2 are character of the heart sounds. Always comment
given in Table 5.5. on a murmur in conjunction with the heart
sounds. For a start, define the murmur by type
Table 5.5: Differences between S3 and split S2
– systolic or diastolic. You can further qualify it
as being ejection, long systolic, pansystolic, early
Split S3
diastolic, mid-diastolic or continuous. Grading
Location Pulmonary area Usually apex a murmur is a measure that helps to compare
Intensities of the loudness. Intensity is useful for comparison
components Equal intensities Different
intensities
in time in the same patient. Sometimes the inten-
Interval between sity can give you an idea of the type of patho-
components Short Relatively long logy. A loud murmur of VSD is due to a small
opening (Maladie de Roger). A soft murmur of
Other diastolic sounds that may cause aortic regurgitation is due to a large opening.
confusion are the opening snap of mitral stenosis Check the grading in the section “intensity” of
and pericardial ‘knock’. murmurs.
Do not automatically jump to the conclusion system. It is generally heard in the right side of
that a murmur signifies pathology. A number the neck or anterior portion of the upper chest.
of children have murmurs without pathological Listen over the neck when the child is sitting
significance. It is important to be able to up and head turned to one side. The hum should
distinguish between innocent and pathological diminish in the lying position, and with light
sounds. Innocent murmurs (also called ‘flow’ or compression of the jugular veins. A mammary
‘functional’ murmurs) are commonly heard in soufflé and cephalic murmur can also be
the setting of fever, anxiety, infection and states continuous.
of increased cardiac output (Table 5.6). It is easy When listening to a murmur, you should be
enough to refer a child for an echocardiogram methodical in making your observations. The
with any murmur. Remember that a diagnosis murmur has to be evaluated in the light of other
of an innocent murmur can often be made on findings and therefore a full description is
clinical grounds. It is only when you are in doubt helpful. Take note of the following (Table 5.8):
that you should proceed for further investi-
gation. Table 5.8: What to note in a murmur
• Timing
Table 5.6: The clinical characteristics • Character
of such an innocent murmur • Intensity
i.Usually soft (grade 1-2), ejection systolic • Conduction
• Behaviour with respiration
ii.Not associated with thrill
iii.Localised • Valsalva maneuver
iv. Often musical • Positional changes
• Change with exercise
v. Intensity increased by physiological manoeuvres
that increase cardiac output • Transient arterial occlusion
vi. No symptoms attributed to cardiovascular system
1. Timing
The most common innocent murmur is the Palpate the carotid to say if the murmur is
medium pitched, vibratory (almost musical) systolic, diastolic or continuous. Note whether
Still’s murmur. It is short and ejection systolic the systolic murmur occurs throughout the
in character, and is best heard along the left mid systole and overlaps the first heart sound
and lower parasternal border. Innocent (pansystolic). Do you think that there is a
murmurs are almost always systolic. The typical diamond shaped configuration to the murmur,
innocent systolic murmurs are (Table 5.7): building to a peak in mid-systole (ejection
systolic)? A long ejection systolic murmur occurs
Table 5.7: Example of innocent murmur in moderately severe pulmonary stenosis. A
1. Vibratory systolic murmur (Still’s murmur) pansystolic murmur occurs in conditions like
2. Pulmonary systolic murmur (flow across pulmonary VSD or mitral regurgitation. Differentiate the
trunk)
3. Peripheral pulmonary systolic murmur (common in
long systolic from the pansystolic by noting the
neonates, thought to be branch pulmonary stenosis) distinct first sound and a small gap between S1
4. Systolic mammary soufflé and the murmur (period of isovolumetric
5. Supraclavicular/brachiocephalic systolic murmur contraction) in the former. It’s difficult to be
6. Aortic systolic murmur absolutely certain if the murmur that you hear
7. Cardiorespiratory murmur
is ejection systolic or long systolic without an
There are also a few innocent noises (though ejection character (that is different from a
not strictly murmurs) that are biphasic or pansystolic murmur). Murmurs of pulmonary
continuous. A venous hum is produced by stenosis and that of a VSD (not typically
turbulent blood flow in the jugular venous pansystolic) can appear alike. The site should
give you a clue – ejection murmurs occur in the 4. Conduction

2nd intercostal space, while VSD murmurs are Pulmonary and tricuspid valve lesions are
best heard lower down. generally well localized to their respective areas.
2. Character (Table 5.9) Aortic and mitral murmurs however often
radiate extensively. Localize the site of
Table 5.9: Characters of murmur
maximum intensity and then slowly ‘inch’ your
differences from one another
stethoscope to other areas (axilla, back, second
• Low pitched rumbling–mitral stenosis
spaces). In this respect two terms are used (often
• Soft blowing, high pitched early diastolic decrescendo
- aortic regurgitation interchangeably) - ‘radiation’ and ‘conduction’.
• To and fro (systolic component ends before S2, then A murmur at two distinct points on the chest
diastolic component starts)–mitral regurgitation and wall is ‘radiated’ from one to the other, if there
stenosis is no drop of intensity of the murmur along a
• Continuous (murmur ‘spills’ into diastole)– patent
line joining the two. A conducted murmur is one
ductus arteriosus
• High pitched blowing murmur at apex radiating towards in which there is drop of intensity progressively
the axilla–mitral regurgitation outward from the site of maximum intensity.
• Loud, rough, rasping ejection systolic murmur in aortic The murmur of mitral regurgitation (MR)
area–aortic stenosis selectively radiates to the axilla and left
• Low pitched diastolic murmur at apex–Austin Flint
infrascapular area of the chest. The murmurs of
murmur (severe aortic regurgitation due to opposing
directions of blood flow across aortic orifice and mitral patent ductus arteriosus and pulmonary stenosis
orifice) conduct to the back.
The murmur of mitral stenosis (MS) is
3. Intensity localised to the apex. In MS, the blood flow
Murmurs vary from the very faint to the very during the murmur is from the left atrium to the
loud. Auscultate the area having the maximum LV (i.e., from the posterior to a relatively anterior
intensity and base your grade of the murmur site). Hence, the murmur is localised to the apex.
according to the Table 5.10. Remember that the An MR due to posterior chordal rupture also
grading is for both systolic and diastolic radiates anteriorly but that of an anterior chordal
murmurs. Therefore with dual murmurs, assign rupture goes posteriorly. Aortic systolic
individual grades for each. murmurs may be as loud (or louder) at the apex
than they are in the aortic area. Systolic
Table 5.10: Grading of murmur murmurs that radiate into the carotid arteries
Grade 1 :
soft, picked up only by trained ears are usually aortic in origin.
Grade 2 :
soft, but clearly audible 5. Behaviour with respiration
Grade 3 :
loud murmur, not associated with thrill Murmurs originating in the right heart increase
Grade 4 :
loud murmur, associated with thrill
with inspiration (Carvallo’s sign in tricuspid
Grade 5 :
very loud murmur, heard even when one edge
of the stethoscope is lifted from the chest murmur) and that of the left side decrease with
Grade 6 : very loud murmur, heard even without a inspiration.
stethoscope 6. Valsalva maneuver
Ask the child to blow against a closed glottis (as
It helps to know that a heart without a if trying to pass stool) so that intrathoracic
murmur does not automatically mean that it is pressure goes up. Most murmurs decrease in
normal. Transposition of the great arteries, length and intensity except that of hypertrophic
double outlet right ventricle, cardiomyopathy, obstructive cardiomyopathy (HOCM) and
arrhythmias and many other defects may cause mitral valve prolapse (MVP). Following release,
serious haemodynamic disturbances without right-sided murmurs return to control intensity
producing murmurs. earlier than left-sided murmurs.
7. Positional changes You may hear a rub in the immediate post-

Most murmurs diminish with standing. The two operative state or following rheumatic fever.
exceptions are HOCM and MVP. The reverse
occurs with squatting. You may find that getting Other Areas of Auscultation
a child to stand up from the lying position (about
Auscultation need not be restricted to the chest
10 times or so, if the condition permits) will
only. In fact there are other places which also
bring out a soft systolic murmur associated with
provide vital clues (Table 5.11).
the acute phase of rheumatic fever.
8. Exercise Table 5.11: Areas of auscultation other than heart
Murmurs due to blood flow across normal or i. Lung fields for basal crackles (pulmonary oedema)
obstructed valves (PS, MS) become louder with ii. Systolic bruit over renal artery (renal artery stenosis)
both isotonic (free hand exercise) and isometric iii. Systolic bruit over right or left iliac fossa
(handgrip, lifting weights) exercise. Murmurs of (transplanted pelvic kidney)
MR, VSD and AR also increase with handgrip iv. Pistol shot sounds over the femoral artery in patients
with high pulse pressure (AR)
exercise but that of HOCM decrease with the v. Distal diastolic murmur (AR) – press the femoral
same. artery distally with the chest piece (proximal
9. Transient arterial occlusion pressure causes systolic murmur); other ‘peripheral’
You can inflate blood pressure cuffs on both signs include head bobbing (‘de Musset’ sign),
arms to a few millimetres of mercury more than visible capillary pulsation in nail beds (‘Quincke’
sign), water hammer pulse, wide pulse pressure,
the systolic pressure. This occludes the arteries dancing carotids (‘Corrigan’ sign), systolic pulsation
bilaterally and raises peripheral arterial of enlarged liver and spleen, pupillary changes with
resistance. This procedure augments the systole.
murmurs of MR, VSD and AR. vi. Suzman sign (pulmonary atresia, coarctation of
aorta)–continuous murmur of interscapular
collaterals at inter and infrascapular region
Pericardial Rub vii. Systolic bruit over a thyroid (thyrotoxicosis)
This is a characteristic high-pitched noise viii. Murmur over an arteriovenous malformation (cirsoid
aneurysm, caroticocavernous fistula)
likened to the creaking made by compression
of new leather. Pericardial rubs occur in systole
Reconciliation
(louder) and diastole and are still present when
the respiration is stopped voluntarily. Pausing Gather all your information and try and make
breathing is difficult in children and therefore sense of everything. With any other system of
not practical in the younger ones. Listen examination, you could talk of the findings as
carefully to the heart sounds and the breathing you go about examining. In the cardiovascular
at the same time. You will find that the rub is system, it is wise to stand back and hold your
like a ‘crunch’ that occurs with every heartbeat. breath for a minute. Reflect on the positive signs
If you are careful enough, you will notice that and symptoms. What important negative signs
the breathing is out of step with this noise. It is have you got? What is most plausible diagnosis?
however more complicated when you suspect If you do not have enough evidence to narrow
a pleuropericardial rub. The presence of a the diagnosis to a specific condition (which is
friction rub indicates contact of the inflamed certainly possible), be truthful and say that you
layers of parietal and visceral pericardium. The would rather offer a differential only.
development of an effusion separates the layers You may have other tools given to you at this
and eventually results in disappearance of the stage. A chest X-ray may be made available to
rub. Pericardial rubs signify pericarditis which you. Corroborate clinical signs of heart failure
is usually bacterial, or sometimes tuberculous. (tachycardia, tachypnoea and hepatomegaly)
with pulmonary plethora (pulmonary vascular Table 5.13: Cyanosis without heart failure
shadows extending to more than the outer third a. RV predominance
of the lung fields) on the X-ray film. The same i. Tetralogy of Fallot
applies for an ECG as well. Look for evidence ii. TGA with PS
of right axis deviation and bundle branch block iii. Moderate to severe PS
with a presumptive diagnosis of ASD. iv. Pulmonary atresia with VSD
v. Eisenmenger syndrome
In general terms you should not worry about vi. DORV with PS
the final diagnosis from your clinical exami- vii. TAPVD with obstruction
nation. It is rarely possible (and unsafe) to be b. CV/LV predominance
exact (like Ebstein disease or TAPVD) from i. Tricuspid atresia
bedside clinics alone. You should have a logical ii. Persistent arteriosus with PS
working diagnosis (usually the commoner ones)
and a set of differentials. The group of congenital Table 5.14: Heart failure without cyanosis
heart diseases is a good example of this princi- a. RV predominance
ple. From your examination you should be able i. Coarctation of aorta (till 1½ yrs of age)
to say if the child has cyanosis with heart failure ii. Cor triatriatum
b. CV/LV predominance
and therefore fits into the ‘transposition physio- i. Myocarditis
logy.’ That is your diagnosis falls under the ii. Myocardial ischaemia (hypoxic ischaemia)
broad umbrella of conditions that have similar iii. Anomalous coronary artery
haemodynamics. Similarly the cyanosed child iv. Endocardial fibroelastosis
without heart failure has the ‘Fallot physiology’. v. Common ventricle with L - transposition
vi. VSD, PDA critical AS
This pertains to a group of conditions with
restricted blood flow to the lungs. Here is a
logical approach to the congenital heart diseases.
Cyanosis should set off alarm bells ringing
This approach takes into account three factors:
– note the time of onset of clinical cyanosis. Early
cyanosis, heart failure and type of apex (right,
onset of cyanosis (first week) indicates one of
left or combined ventricular preponderance)
the ‘T’ diseases: TGA, TAPVC, tricuspid atresia,
(Tables 5.12 to 5.14).
truncus arteriosus, total (critical) PS and
Table 5.12: Cyanosis with heart failure tricuspid regurgitation with the Ebstein
anomaly. The Tables 5.12 and 5.13 should help
a. Right ventricular (RV) predominance
i. TGA you provide a suitable model to fit your patient.
ii. Double outlet right ventricle (DORV) without However, bear in mind that other conditions
pulmonary stenosis (PS) also give rise to cyanosis. Do not discount the
iii. Single ventricle without PS possibility of lung conditions (surfactant
iv. Hypoplastic left heart syndrome (HLHS)
deficient lung disease) that may present as a
v. Ebstein disease with right bundle branch block
(RBBB) cyanosed neonate. There may also be some
vi. TAPVD complicated situations where your clinical
vii. Persistent pulmonary hypertension (PPHN) judgement will not appear to follow any model.
b. Left ventricular (LV) or combined ventricular (CV) You should keep an open mind about the
predominance
occurrence of dual pathology in such cases. For
i. TGA with VSD/PDA
ii. Persistent truncus arteriosus example, a cyanosed child with the apex in the
iii. Complex defects with PDA (duct dependent right side of the chest can have asplenia,
circulation) methaemoglobinaemia (with dextrocardia) and
iv. Pulmonary atresia with intact ventricular septum situs inversus with cyanotic congenital heart
v. Atrioventricular canal defects
disease.
The onset of heart failure may give you some needing high concentrations of oxygen may well
clues to the aetiology. have persistent pulmonary hypertension. The
a. Very early onset (first few days) presentation blood gase may give you a clue. It is likely in
of heart failure is common to the following this condition to have low oxygen levels with
defects: asphyxia, sepsis, supraventricular normal or low carbon dioxide.
tachycardia, AV fistula, myocarditis, The ‘hyperoxia’ test has similar connotations.
anaemia, hypocalcaemia, congenital heart This is not done as a routine, but can often be
block, persistent pulmonary hypertension useful in the setting of the ventilated neonate
and tricuspid regurgitation (Ebstein who has either a lung condition or a cyanotic
anomaly). heart disease. If you give a child 100 per cent
b. Failure at the end of the first week may be oxygen for 20 minutes, the partial pressure of
due to HLHS, TAPVC, critical AS, PS, arterial oxygen should go up to 20kPa. If
coarctation of aorta, truncus arteriosus, oxygenation is compromised, in conjunction
DORV without PS, AV canal defect, AV with low or normal carbon dioxide levels, the
fistula, premature PDA, renal failure and likelihood of a heart lesion increases. For lung
hypertension, thyrotoxicosis and adrenal conditions like respiratory distress syndrome,
insufficiency. oxygenation is poor and the carbon dioxide is
c. Congestive cardiac failure can occur at any also high. This test is more easily done when the
time with supraventricular tachycardia, child is ventilated and therefore you can ensure
cardiomyopathy and myocarditis. sustained 100 per cent oxygenation. You can do
There are some pieces of information that a variation of this test by holding a mask tightly
you will pick up as the natural history unfolds. over the face and using 100 per cent oxygen.
They should be invaluable in formulating your ‘Hyperoxia’ is not commonly done and the
final diagnosis. For example, a preterm baby information it provides can reasonably be
who is fluctuating between saturations of the obtained from collateral evidence. It is also a
high nineties and dips down to the seventies dangerous test – duct dependent circulations
without change of oxygen concentration is likely may deteriorate rapidly when given too much
to have a shunt (ductus arteriosus or pulmo- of oxygen. It is therefore standard practice to
nary). start the neonate on intravenous prostaglandin
A cyanosed child with a normal heart (to keep the duct patent) if congenital cyanotic
anatomy and reasonably mature lungs and heart defect is suspected.
NEUROLOGY
If you are new to children, examination of the Table 6.1: Scheme of neurology examination
nervous system can seem daunting. But given 1. Higher functions and speech
the right attitude and practice, you should 2. Examination of the spine, nuchal rigidity, shunts
gather the relevant information from your and scars
3. Cranial nerves
examination without too much trouble. There 4. Gait, motor functions and cerebellum
will always be relatively difficult cases - children 5. Sensory system
who have severe communication disorders who 6. Autonomic system
will not understand what you say, or children
who are too little to obey your commands. In Table 6.2: Higher function
such situations, observe what you can and then • Consciousness
deduce logical (but limited) conclusions. • Position of child
As in the general survey, it helps if you have • Awarness of environment
a system of examination which you can apply • Response to stimuli
• Activity
for all children. There is no one universal fit, but • Behaviour
a sequential system is good as a starting point. • Emotional stability
Once you gather experience, you may choose to • Handedness
do the examination in a different order. This is • Memory
acceptable as long as you do not miss out any

important step. Let us discuss a system of exami-
nation that you could start off with (Table 6.1). Consciousness
The term consciousness is rather vague and has
Higher Functions a wide spectrum. For the well child who is alert
and running around, defining “full conscious-
It is best to talk to the child as in a general
ness” is not a problem. It does get difficult when
conversation. Find out the things that he can do you have a child coming from the emergency
and those he can not. It’s good to ask some with poor verbal response and intermittent
relevant questions about the development at this moans. Scales have, therefore, been defined to
stage because it ties in very well. You could give do away with the confusion of words like ‘coma’
the child a puzzle to solve or pictures to colour. and ‘stupor,’ which are often used inter-
Simple tasks give you a lot of information – so changeably. However, for the sake of complete-
be on the lookout for clues. Whatever you do, ness, ‘coma’ is a state in which a child is unable
judge the child in the following categories (Table to be aroused and is completely unaware of self
6.2). and surroundings even in the presence of strong
physical stimuli. ‘Stupor’ is a state that simulates and can maintain his airway, then it is
sleep and can be reversed by vigorous stimu- reasonable to wait and watch. Always
lation. The quickest and simplest way to assess remember to check the child’s blood glucose
the level of consciousness is to use the AVPU level if there is deterioration of consciousness
scale: before proceeding to any other examination.
A = Alert Hypoglycaemia is an emergency that is easily
V = Responds to voice reversible.
P = Responds to pain
U = Unresponsive
Position of the Child
This is a rough tool to judge the depth of
coma in the child till the time a modified Comment on the way the child lies on his/her
Glasgow Coma Scale (GCS) (Table 6.3) can be bed or chair. The bed may be padded with side
done. Children on the ‘P’ part of AVPU correlate rails for the immobile child. There may be a
to a GCS of about 8. The GCS is a handy yet wheelchair, which he/she uses for moving
comprehensive tool. The total maximum score around. The child may be sleeping upright with
is 15. The minimum for no response in any a backrest if he/she has impending respiratory
category (eye opening, best motor response, best failure from ascending peripheral neuropathy.
verbal response) is 3. Children who have meningitis may not like to
It’s good practice to record the GCS from be handled and are generally irritable. They can
time to time. A child’s GCS will fluctuate and lie with their eyes tightly closed and head turned
the trend can often be a useful clinical clue. away from the light. In severe meningeal
When managing the child, treat the child, not irritation and in tetanus, the child is in
the GCS. For example, an isolated GCS of eight opisthotonus with the occiput burrowed into the
or less does not always mandate that the child pillow. A floppy neonate with poor tone lies
needs ventilation. If the child is post-convulsive helplessly in a position called the ‘pithed frog’
Table 6.3: Glasgow Coma Scale

Eye opening
Score > 1 year < 1 year
4 Spontaneous Spontaneous
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best motor response
6 Obeys Spontaneous
5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Abnormal flexion(decorticate rigidity) Abnormal flexion(decorticate rigidity)
2 Extension(decerebrate rigidity) Extension(decerebrate rigidity)
Best verbal response
5 Orientated, converses, appropriate words Smiles, coos, babbles
4 Disoriented, confused Irritable
3 Inappropriate words Cries to pain
2 Incomprehensible sounds Grunts, moans to pain
Neurology 97
posture. A child with decerebrate rigidity shows compromised? Is this is in keeping with your
extension of the lower limbs, the upper limb in overall impression of the child? Are the higher
extension at the shoulder and elbow and the functions at odds with the degree of disability?
forearm pronated. In decorticate rigidity, the If so, is there a physical reason for disability –
lower limbs are in extension, the shoulders in limb paralysis in cerebral palsy, poliomyelitis or
external rotation, but the elbows flexed and the joint inflammation.
thumb adducted into the palm.
Behaviour
Awareness of the Environment
You should get a feel for childhood behaviour
How does the child interact with the environ- at different ages. You are really looking for gross
ment around him/her? Does he/she communi- differences from normal. The child of two will
cate with you or the parents? Does he appear to normally say ‘no’ to every question you ask
watch his/her toys or the television with him/her (it is therefore prudent in the two year
interest? Children with moderate learning old to say ‘do this,’ rather than ask ‘can you do
difficulties will change expression at something this’). A child of five or six is socially interactive
of their interest. Those with encephalopathy will and plays with his/her mates. The child who is
take no notice of the surroundings. Be wary of not should make you worry about autism or
the child with severe visual impairment—he/ Asperger syndrome. The child with impul-
she will not appear to take notice of any visual siveness and short attention span may have
cues that you may use. Look for a blank stare attention deficit hyperactivity disorder. Note
and roving nystagmus in such a child. also the shy and withdrawn boy or girl who may
have suffered neglect in his/her family.
Response to Stimuli
Emotional Stability
A child who is verbally communicating is
obviously responding to the stimuli around him. This is useful to gauge the age appropriateness
For those who with poor verbal communication, of the child’s mental state. Emotional instability
you will have to try other stimuli, for example occurs in children with learning difficulties,
an interesting toy. Watch for behaviour changes where the overall intelligence performance is
(like a cry or a smile) in response to the stimulus. below par. Children with behavioural disorders
Once you have demonstrated responsiveness, like conduct disorder or oppositional defiant
ascertain if that is age appropriate. Children disorders often have associated emotional
between 15-24 months often have stranger problems. Child abuse, be it in the past or the
anxiety and are afraid of being handled by new present, may adversely affect the child’s mood
faces. An autistic child does not make contact and behaviour.
with the examiner and regards objects as if
detached from humans. A child with a painful Handedness
condition of the bones or joints (osteomyelitis,
Dominance of a hand is governed by the
juvenile chronic arthritis, scurvy) does not like
dominant cerebral hemisphere. For right-
being handled.
handed individuals, this is on the left side of the
brain. Sixty percent of left-handed children have
Activity
also their dominant centres in the left.
How active is the child and is there a restriction Handedness develops over the first year and is
in his movements? Is there any clue to suggest prominent at three years. The child will draw a
that the functional activity of the child is circle with his right or left hand consistently.
Hand preference in the early months should months of age. He will have one word with
make you suspicious of a hemi-syndrome. This meaning at age one. At fifteen months, he/she
may be a subtle feature of hemiplegia from uses jargon and at eighteen months picks up on
intrauterine events. doll vocabulary. At two, he/she should put two
words in a sentence and at two and a half
Memory understand the implications of prepositions like
‘over’ and ‘under.’ At three, speech comes on in
Memory can be either short term or long term.
leaps and bounds—he/she will have a good
Test for short-term memory by giving the child
vocabulary and understand three step
a set numbers (say 1, 2, 3) and asking him to
commands. At four the child is likely to tell you
repeat it forwards, then backwards. The
a story or detail the activity in a complex picture.
backward repetition is more affected in organic
You should be on the look out for speech
brain disorders. For long-term memory, ask the
delay. Refer for audiology evaluation and
child to give his address, his school and the
consideration of speech therapy, if by:
names of his friends, and also some past
incidences that the child should remember (like 12 months - no differentiated babbling
festivals or birthday parties). You may see failure or vocal imitation
of long-term memory with degenerative brain 18 months - no use of single words
disorders. 24 months - single word vocabulary of
You could at this juncture test for intelli- less than 10 words
gence, but this is best left for the clinical 30 months - no evidence of 2 word
psychologists. Intelligence Quotient (IQ) testing combinations
is rigorous and is time consuming. There are 36 months - no use of telegraphic
some scales in use—Wechsler, Stanford-Binet, sentences
Peabody vocabulary and Bayley scales, to name 48 months - no use of simple sentences.
a few. Very few of these tests are standardized
for use in Indian children.
The presence or absence of speech does not
tell you the whole story. The quality of speech
Speech
is equally important. Volume of speech is related
The conversation will provide good clues if the to the amount of air pressure generated across
child has a speech problem. You should have the vocal cords. You could ask the child to blow
made out from the history if the child has a out a lighted match at a distance of 5 cm or ask
hearing problem. Hearing impairment can him to count from one to hundred.
impede the development of speech. Therefore, ‘Aphasia’ is disturbance of the ability to use
when talking to the child, make allowances for language (not only speaking, but also writing
possible hearing failure. Note if the child is and comprehension). Aphasia has been
wearing a hearing aid (sensorineural deafness). traditionally classified as motor (Broca’s area),
As you talk and listen to the child, tease out the sensory (Wernicke’s area), conductive (conduc-
following components: tive fibres between motor and sensory areas)
a. Absence or presence of speech and nominal (angular gyrus). However each of
b. Quantity of speech—age appropriateness the areas in the frontal, Rolandic, parietal,
c. Quality of speech—volume, phonation, temporal and occipital regions subserve certain
articulation, content, rhythm. common functions. The disturbances in their
You should have a fair idea of the normal functions are not just restricted to one site, and
development of speech. The infant says ‘ma ma,’ therefore anatomical delineation is not possible.
‘ba ba’ without meaning at seven to eight It is best to describe the lesions as those of
Neurology 99
articulation, fluency, naming, repetition, reading Examination of the Spine, Skull

and writing.
Examine the spine at the beginning of the
Phonation is a function of the vocal cords.
examination because it is a common tendency
Vocal paralysis may give rise to aphonia or
to forget doing this at the end. First look at the
dysphonia (bulbar paralysis). To judge
child from the back and note any obvious
articulation, content and rhythm of speech,
deformity – kyphosis, scoliosis or a combination.
listen to the child speak in long meaningful
sentences. See how he/she interacts with his/ Is there a lump in the spine or an adjoining
her parents. Defects of articulation occur in region? Run your hand down the curvature and
cerebellar, pseudobulbar and bulbar lesions. In feel for defects or any tenderness. Search for
cerebellar dysarthria, the patient speaks slowly scars in the lumbosacral region – they may be
and deliberately, syllable by syllable, as if from repair of a meningomyelocele. Next ask the
scanning a line of poetry. In pseudobulbar palsy, child to bend down, as if to touch his/her toes.
the pronunciation is slurred as if under the In postural scoliosis, there is exaggeration of a
influence of alcohol. Bulbar palsy also causes hump on the abnormal side.
nonspecific slurring. In cortical dysarthria there Come up to the skull and feel for any lumps
is irregular hesitancy in word production or patches of hair loss. There may be a scar from
associated with orofacial apraxia. Fluency can a surgical procedure. Ventriculo-peritoneal
be impaired in the child who has a stuttering shunts are often hidden under cover of the hair.
problem. The same applies for a reservoir, if one has been
Defects of articulation of individual words put in.
(depending on coordination and intelligibility) It is important to test for nuchal rigidity in
may results in lisping, rhotism and certain the child with suspected meningitis. Elicit neck
lexical syntactic disorders. In lisping the ‘th’ rigidity by flexing the head upon the chest. Any
sound replaces the ‘s’ sound. In rhotism, ‘w’ resistance is suggestive of meningeal irritation.
replaces ‘r’ (‘wun’ for ‘run’). Children, when A frightened child may not allow movement of
they start speaking, often have speech imma- the neck, thereby confusing the examiner. In
turities. Consonant deletions and substitutions such cases, bring the child to the edge of the bed,
like ‘bue’ for ‘blue’ and ‘yow-yow’ for ‘yellow’ and extend the neck over the edge. Then flex
are part of normal speech development. It is not the head from extension to neutral. Limitation
normal, however, for a child to repeat the first confirms meningeal irritation (Fig. 6.1A).
syllable of a polysyllabic word (‘gaga’ for Kernig’s sign tests for meningeal irritation
‘garage’) at the age of three years. Also the use is a slightly different way. Lie the child flat on
of back sounds, like ‘k’ instead of ‘g’ (‘koe’ for the bed and flex the hip and knee to 90o. Then
‘toe’) is clearly abnormal at this age. extend the knee further to 180o. In meningitis,
A child who has trouble understanding the due to irritation of the nerves and nerve roots,
language of others has problems in receptive the muscles will go into spasm and prevent
language. Does the child respond to speech extension. Local injury to the spinal cord or
inconsistently? Does he have difficulty with muscles of the back may cause difficulties. To
abstract language? Does he often give test the Brudzinski sign, flex the neck as you
inappropriate answers? Is there a lack of would to test neck rigidity. Flexion of the neck
understanding of riddles and jokes? If there is a causes flexion of the hips and vice versa (Fig.
‘yes’ then you have to watch out for commun- 6.1B).
ication disorders, perhaps the pervasive Another method to test minimal neck
developmental conditions. rigidity is to make the patient sit up with knees
Fig. 6.1A: Examination neck rigidity Fig. 6.1B: Elicitation of Kernig’s sign
extended. The neck is then flexed. Normally Test

flexion should be at least 45º. If minimal
It is not customary to test for smell in the
meningism is present, flexion will be limited to
younger child. You could ask the parents if they
less than 45º. Bear in mind that these signs can
have noted any deviation from what is
only be elicited in the older child. In the toddler
perceived as normal smell. In the older
and infant, you may not be able to pick up the
cooperative child inspect the nostrils first for
classic signs of meningism. In this age group
nasal catarrh. Explain to the child what you are
undue irritability and reluctance to move may
about to do. Ask him/her to close his/her eyes
point towards a meningeal aetiology.
and sniff whatever substance if laid out in front.
The “kiss the knee” test is another refined
One nostril is tested at one time. Ask the child
test for meningeal irritation. Put the child in the
to name the odour. Use common aromatic
supine position and ask him to get up and kiss
substances such as oil of cloves or almonds,
the knee on any one side. Make sure that he/
coffee, vanilla or even toothpaste or soap. Strong
she does not put his hands on the bed to do this.
irritant odours are best avoided.
This maneuver puts the meninges on stretch and
In ‘anosmia’, which can occur with head
therefore a good test for minimal meningism.
injury, the sense of smell is absent. It is important
You can utilise this test in cases of viral
to test for anosmia in a child with delayed
meningitis and early poliomyelitis.
puberty (Kallman syndrome). ‘Parosmia’ is a
rare abnormality in which pleasant odours seem
EXAMINATION OF THE CRANIAL NERVES
offensive. Olfactory ‘hallucinations’, usually of
Olfactory an unpleasant nature, are characteristic of
complex partial seizures in the aura stage.
Anatomy
The receptors of the olfactory nerve, responsible Optic Nerve
for the sense of smell, are situated high in the
Anatomy
nasal cavity. From these receptors, thin filaments
pass centrally through the cribriform plate of the The fibres of the optic nerve originate from the
ethmoid to the olfactory bulbs, containing the retina and pass back to the optic chiasm (Fig.
second order of neurons. These neurons project 6.2). Here the fibres from the inner nasal half of
to the olfactory area of the cerebral cortex (uncus each retina (representing the temporal field)
and parahippocampal gyrus). decussate, whilst those from the outer temporal
Neurology 101
Fig. 6.2: Optic nerve pathway
half (nasal field) remain on the same side. The acuity, colour vision, field of vision and
optic tract is formed after this chiasmal fundoscopy.
decussation and passes posterior to the lateral
geniculate body of the same side. Some pre- Cortical vision: A child following a bright object
geniculate fibres project to the superior colliculi. of light usually has intact cortical vision. To
The optic radiation starts in the lateral geniculate show that a patient has intact cortical vision, one
body, goes backwards through the posterior approach would be to make a gesture so as to
limb of the internal capsule to the calcarine poke the eye. In children after 10 months of age,
cortex of the occipital lobe. In the calcarine this will provoke a blinking reaction. An
cortex, the left half of field of vision is inconsistent response suggests that vision is
represented on the right and vice versa. The intact but its interpretation (e.g. parietal lobe
most peripheral part of the visual fields is most lesions) is impaired. This is not a very sensitive
anterior here. The macular area is represented test and one that can be perceived as menacing.
at the occipital pole (Fig. 6.2). Acuity: The best way to test this is by using the
Snellen chart, but this is only possible only in
Test children who know their letters (usually those
We discussed a method to examine the “eyes” who are literate and above the age of six). Ensure
as a whole in the section on general survey. This that the room you are testing is adequately lit
method will test for the optic nerve and also go up, and that the distance from the chart to the
on to test for the 3rd, 4th and 6th cranial nerves. child is exactly six metres. Ask the child to read
To examine the optic nerve in isolation, you from the top downwards. The letters of the
have to go through the following: cortical vision, alphabet are designed to subtend an angle at the
eye. This can be translated into visual acuity by In the young infant, acuity is difficult to test
noting the number on the last line read by the but ophthalmologists use several methods. They
child. This number appears on the deno- are: follow face test, optokinetic nystagmus and
minator—for example 6/12 or 6/6. test for fixation behaviour.
For children between the age of three and Field of vision: We discussed the method in the
six, a slightly different approach is used. The section “Eye” in general survey.
matching card letter test employs the same
principle as the Snellen chart. However, it does Colour vision: This may be judged by coloured
not rely on the child’s ability to identify letters. objects or by using Holmgren’s wools. A formal
A chart with letters is positioned at three metres testing using Ishihara chart is only possible in
from the child. Make the child sit up on the the older child.
mother’s lap and give her a card with the same Examination of the fundus: To do this you need
letters as they appear on the chart in the an ophthalmoscope. It consists of a head, handle
distance. Tell the child “show me the same” and batteries. The numbers that appear on the
when you point to a letter on the chart – the child head indicate minus lenses in the viewing
should point to the same letter on his/her card. aperture (red numbers or numbers with a minus
There are variations to this matching letter in front) or plus lenses (black or plain numbers).
test. The system called STYCAR has single Myopia in the patient’s lenses is neutralized by
letters on the chart to match against. The the minus lens and hyperopia by the plus lens
Sonksen-Silver cards have lines of letters, and of the ophthalmoscope. At the top of the head
this tests the child’s ability to differentiate letters is a control to give different kinds of beams. Two
in the periphery of the line (as opposed to test round apertures (one large, one small), a slit, a
centrally). Children with amblyopia can be grid, and a red free filter are usually provided.
missed if only single letters are used. Normally, The slit is used to determine convexity or
children are far-sighted up to six or seven years concavity of retinal lesions (in whether they are
of age. A three-month infant has acuity of 6/60, raised from the surface or are indented). The red
whereas at one year it is 6/18. free filter is used to detect small aneurysms and
Below the age of 2½ years, the STYCAR haemorrhages.
graded balls test may be used. Ten white balls Shine the widest beam of the ophthalmo-
are either rolled on a dark strip horizontal to the scope at a distance of two metres. The circle of
line of the infant’s gaze at 3 metres, or mounted light will catch both the corneas. As a result, the
on sticks for presentation behind a dark screen. corneal reflex and the pupillary red reflex are
Near vision may be tested by placing small both visible at one sitting (Bruckner’s test). Next
objects like ‘hundreds and thousands’ (cake use a +8 lens and focus the light to see any scars
dressings) on a piece of felt on a tabletop. See if or deposits on the cornea. Change to +10 or +12,
the child reaches for them. You can get the so that the iris becomes visible. Determine the
child’s interest in one of them and drag it along edge of the iris, whether it is regular and
the felt. At one point let go of the object and carry rounded. Now move back to ‘0’ and look for the
your hand in a smooth line. Watch if the child red reflex. Try to focus the fundus and move
follows your hand or stops when the object was from the periphery towards the optic disc, by
released. You can do this test for infants under following the vessels. The macula is situated
a year, but this is really is a test for visual approximately 2 disc diameters temporal to the
behaviour not that of acuity. For slightly older disc.
children, you can use the “Kay picture” test, In the fundoscopic examination, the
which aims to check acuity using standardised following need to be looked at: optic disc,
picture cards. vessels, peripheral retina and macular area. The
Neurology 103
macula appears as a dark, yellow-orange area Niemann-Pick disease, mucolipidosis

lateral to and slightly below the optic disc. A type 1
bright light reflex is present around the fovea. viii. Lipaemia retinalis (milky white, pink,
In infants, the optic disc is pale and grey, an waxy appearance of retinal vessels)—
appearance similar to optic atrophy in later life. Familial hypercholesterolaemia, diabetes
Optic nerve hypoplasia can be diagnosed if the mellitus
disc is less than half of the normal size. The ix. Retinoblastoma—Unilateral or bilateral,
macular light reflex is absent up to 4 months of gray or yellow-white, glistening vitreous
age. The normal ratio of the calibre of the mass
arterioles to that of the veins is 3:5. x. Rubella retinitis—Unilateral or bilateral
Pulsation in the retinal veins (artery = central involvement of the posterior pole, espe-
stripe, vein = darker) as they enter the optic cially the macula with small, black,
nerve head indicates normal intracranial irregular masses or fine to gross pig-
pressure (disappearance of venous pulsation is mentary speckling.
an early sign of papilloedema). The temporal xi. Retinal astrocytomas (glistening, nodular,
(lateral) portion of the disc is frequently pale. A mulberry—Like mass or oval, gray flat
partial or complete brown or black-pigmented areas in the retina)–Tuberous sclerosis
ring is commonly present around the disc xii. Retinal angiomatosis—von Hippel-Lindau
border. The nasal (medial) edge of the disc may syndrome.
appear slightly blurred. xiii. Retinitis pigmentosa (degeneration,
atrophy and pigmentation)—Laurence-
You may come across the following: Moon-Biedl syndrome, Refsum disease,
i. Retinal haemorrhages—Commonly in nor- neuronal ceroid lipofuscinosis, Cockayne
mal newborns (1/3 of vaginal deliveries), syndrome, abetalipoproteinaemia, Kearns-
childhood physical abuse, haemorrhagic Sayre syndrome, Hurler syndrome.
disorders, sickle cell disease, cardio- xiv. Exudative retinitis—Coats disease
pulmonary resuscitation, trauma, raised xv. Papilloedema—Space occupying lesions
intracranial tension. (tumour, tuberculoma, abscess, haema-
ii. Medullated nerve fibres (focal white patch toma), pseudotumour cerebri, encephalitis,
with brush stroke appearance)—Normal, meningitis, Guillain-Barre syndrome,
though myelination generally terminates hypertensive encephalopathy.
at optic disc margin. xvi. Optic atrophy —Primary (well-delineated
iii. Choroid tubercles—Elevated spots, often rim of disc) or secondary (rim may not be
better visible on direct ophthalmoscopy, well delineated), though the difference
typical of tuberculous meningitis may not always be possible to distinguish
iv. Retinal colobomas—Aicardi syndrome, on fundoscopy.
trisomies, CHARGE association, Golden-
har syndrome, linear sebaceous naevus, Oculomotor, Trochlear
focal dermal hypoplasia and Abducens Nerves
v. Retinal laser burns—Retinopathy of
prematurity, Coats disease Anatomy
vi. “Cotton-Ball” areas—chorioretinitis, The external ocular muscles are supplied by the
candida endophthalmitis 3rd, 4th and 6th cranial nerves in the following
vii. Cherry red spot—GM1 gangliosidosis, fashion-all muscles (including sphincter
Tay-Sach disease, Sandhoff disease, pupillae and levator palpebrae superioris) are
sialidosis, infantile Gaucher disease, supplied by the 3rd nerve except the superior
passes forward to enter the lateral wall of the

cavernous sinus. The 4th nerve emerges on the
rostral part of the roof of the 4th ventricle. They
decussate between their nucleii and emerge
from the brainstem dorsally. The 6th nerve
emerges between the medulla and pons after a
Fig. 6.3: Movements of extraocular muscles long intracranial course.
SR (Superior rectus); MR (Medial rectus);
IR (Inferior rectus); SO (Superior oblique); Test
LR (Lateral rectus); IO (Inferior oblique)
We test the extraocular muscles (as in the
chapter on “eyes” in general survey) by moving
oblique (supplied by the 4th cranial nerve) and a finger or a torch (and asking the child to
the lateral rectus (by the 6th cranial nerve). The follow) in different directions—superior,
medial rectus is the strongest of all the muscles— inferior, medial and lateral. Note all the while
its function is to adduct the eye. The opposite the position of the eyes, the movements, any
function (abduction) is performed by the lateral weakness, deviation, ptosis or abnormal motion.
rectus. The obliques act in the directions Palsy of the 3rd nerve results in lateral and
opposite to which their names suggest. Thus, the slight downward deviation of the eye. Palsy of
superior oblique depresses the eye (with the 6th nerve produces medial deviation of the
adduction and in-torsion) while the inferior affected eye. That of the 4th nerve produces little
oblique elevates the eye (with abduction and ex- change at rest. There is slight upward deviation
torsion) (Fig. 6.3) (Table 6.4). The nucleii of the in the abducted position. The eye fails to move
3rd, 4th, 6th cranial nerves are located in the when abducted. This is often accompanied by a
brainstem at the level of the superior head tilt.
quadrigemina and extend as far caudally as the The ‘setting sun’ sign, a forced downward
eminentia teres in the floor of the 4th ventricle. deviation of the eyes at rest with paresis of
The nucleus of the 3rd nerve is the most anterior. upward gaze, is an indication of raised
Its rostral part (Edinger-Westphal nucleus) intracranial tension. Here the pressure on the
supplies parasympathetic fibres to the ciliary quadrigeminal plate causes impairment of the
muscles and iris. Its caudal part chiefly supplies visual gaze centres. Normally this may be
the extraocular muscles. The nucleus of the 4th present in infants less than 4 weeks if the
nerve lies below the 3rd nerve nucleus. The 6th position of the head is suddenly changed.
nerve nucleus is situated in the floor of the 4th Normal newborns may show downward
ventricle at the level of the pons. deviation of the eyes, skew deviation and inter-
The 3rd nerves exits on the inner aspect of mittent opsoclonus (irregular chaotic oscillation
the cerebral peduncles between the superior of the eye in horizontal, vertical or oblique
cerebellar and posterior cerebral arteries, then directions).
Table 6.4: Movement of extraocular muscle
Squint
Medial rectus - Adduction
Lateral rectus - Abduction Squints are common in childhood and are
Superior oblique - Depression, broadly of two types: paralytic and non-
abduction intorsion
paralytic. The paralytic lesions are those of the
Inferior oblique - Elevation, abduction
extorsion cranial nerves as described above. Non-paralytic
Superior rectus - Elevation squints are the result of abnormal pulling of
Inferior rectus - Depression the eyes in one direction. They may be mani-
Neurology 105
fest (tropia) or latent (phoria). They can result evident pupillary inequality. Such physiologi-
from refractive errors giving rise to accommo- cally unequal pupils react normally. The causes
dative esotropia (hypermetropes) or exotropia of unequal pupils are given in Table 6.5.
(myopes). Making a diagnosis of squint can be There are a few other tests that are mainly
a challenge in the non-cooperative child. This is of academic interest. The cilio-spinal reflex is
how you can test for manifest non-paralytic tested by pinching the skin of the neck and leads
(concomitant) squint: to dilatation of the pupils. In Bryne’s reflex,
Sit the child on the mother’s knee. In the pinching one lower extremity causes dilatation
older child, it’s best to let them slouch as they of the pupil on the other side.
sit. This puts the head in a fixed position. Have
a tongue depressor with interesting stickers at Accommodation Reflex
both ends. These allow the child to engage his/
We did not test for accommodation-convergence
her attention when trying to fix.
in our examination of the “eyes,” but it is helpful
Use an occluder to cover one eye. Hold the
to do so if focussing on the cranial nerves alone.
object at a distance of 33 cm (and slightly tipped
Ask the older child to look at a distant object
upwards) and ask the child to look at it. Move
(theoretically infinity) and then bring a finger
the object from side to side and make sure that
(without a menace) within the point of near
he/she is actually looking at the object (the child
vision and instruct him to look at it. The pupils
should move his/her eyes along with your
become smaller on accommodating for a near
movement). Your concentration should be on
object. The ‘Adie’ pupil is an abnormality
the uncovered eye. Look for any movement
characterized by poor pupillary constriction to
inward (esotropia) or outward (exotropia) when
light and loss of accommodation/convergence.
the cover is removed. Repeat the test with the
object at a distance of six metres.
Ptosis
To test for latent squint (phoria), you have
to do the cover-uncover test. The idea is to cut The upper eyelid margin comes down and
off the binocularity of the eyes. This will allow covers more than 2 mm of the cornea. This is
the eyes to come to their natural position of rest. usually caused by a lesion of the third cranial
The cover-uncover test should be done quickly, nerve, but may also be due to other causes—
but not too quickly for the child to lose focus of congenital, myasthenia gravis and the Marcus
the object. There is, however, no great value in Gunn pupil. In the latter, there is reflex elevation
proving that the child has a latent squint – it or closure of the ptotic lid in response to
needs no management. swallowing or movements of the jaw. Pseudo-
ptosis may be due to inferior rectus palsy in
Pupils which the eye is rotated upward giving the false
impression of the eyelid covering the cornea. In
You have already noted the size and shape of
such cases there is no obstruction to vision and
the pupils and reactivity to light (direct and
so transverse furrows on the forehead (the child
consensual light reflex) when examining the
eyes. In infants less than 30 weeks gestation, Table 6.5: Causes of small and large pupil
pupils are large and there is no reaction to light. Small Large
After 32 weeks gestation, light shone on one eye
Normal Oculomotor palsy
should constrict the pupil on that side (direct) Head injury Fear, anxiety
along with constriction of the other pupil Horner syndrome Ipsilateral hippocampal
(consensual). The reverse happens when the herniation
light is removed. Approximately 12 percent of Deep coma Atropine medication
Organophosphorus poisoning Drug toxicity
normal individuals have a slight but clinically
with ptosis tries to over-ride the defect by using impaired. In neonates, absence of Doll’s eye
his orbicularis oculi) are absent. Partial ptosis response on one side indicates abductor palsy.
may be present in myopathies like myotonic Shortly after birth the eyes start getting
dystrophy, myasthenia gravis. In Horner’s conjugated and by two weeks of age, the infant
syndrome there is ptosis with constricted pupils, will move his eyes towards light and fixate.
anhidrosis and enophthalmos. Following movements are complete in all
You should spot ptosis when you look at the directions by four months. Depth perception
child from a distance. Is the ptosis unilateral or based on binocular vision appears at 2-4 months.
bilateral? Bilateral ptosis suggests a more Internuclear ophthalmoplegia (syndrome of
generalized disease such as myasthenia or medial longitudinal fasciculus) consists of
myotonic dystrophy. Unilateral disease paralysis of adduction of the contralateral eye
indicates local pathology—orbital cellulites, on lateral gaze with nystagmus of the abducting
cavernous sinus thrombosis or a third nerve eye and preservation of convergence.
palsy. It may be difficult to detect ptosis in Impairment or paralysis of movement of
myasthenia unless the muscles are tired enough both eyes in one direction occurs in conjugate
to droop. Use your pointed index and ask the gaze paralysis. Paralysis of lateral conjugate
child to look at the finger. Bring your finger up gaze is characteristically found with lesions of
and then down and make sure that the child the pons (Pontine Paramedian Reticular
moves his eyes up and down in conjunction. Formation or PPRF). Bilateral lateral conjugate
After a few attempts, the child’s eyelids may gaze paralysis is caused by centrally placed
droop if he/she has myasthenia gravis. pontine lesions above the level of the abducens
Complete third nerve palsy results in ptosis, nucleii. Upward conjugate gaze paralyses are
pupillary dilatation and loss of all movements associated with lesions in central midbrain,
(except lateral deviation). The eyes tend to rest inferior thalamic region, or near the oculomotor
in a lateral and downward direction. Partial nucleii.
damage to the third nerve, however, will not In tonic conjugate deviation, the eyes are
result in the full constellation of signs. persistently turned to one side (usually toward
the side of the lesion). Tonic conjugate deviation
Proptosis may also arise as a result of irritative cortical
lesions (deviation toward the healthy side),
Abnormal protrusion of the eyeball is proptosis.
which are usually accompanied by nystagmoid
Unilateral proptosis may be due to thyroto-
jerks to that side (a form of focal epilepsy). In
xicosis, retro-orbital tumours, neuroblastoma,
the pons, irritative lesions are rare and a
retinoblastoma, leukaemia, carotico-cavernous
structural lesion causes deviation in the reverse
fistulae, cavernous sinus thrombosis, or orbital
direction (eyes towards the healthy side). Skew
cellulitis. Bilateral proptosis (also called exoph-
deviation of the eyes occurs in cerebellar
thalmos) may be due thyrotoxicosis, cavernous
diseases and lesions so the inner ear—one eye
sinus thrombosis or histiocytosis.
is directed upward and the other downward.
Conjugate Movements of the Eyes Nystagmus
Doll’s eye movements are normally present up These are involuntary movements of the eyeball
to 10 days of age in the full term neonate, but that may be rhythmic or non-rhythmic. Less
there is little or no conjugation. The pheno- commonly, nystagmus is symmetrical with to
menon refers to the apparent turning of the eyes and fro oscillation called ‘pendular’ nystagmus.
to the opposite direction in response to rotation Nystagmus may be in different directions—
of the head. Besides neonates, it is also seen in horizontal, vertical, rotatory or mixed. Fine
coma and in conditions where optic fixation is nystagmus is where eye movement is less than
Neurology 107
1 mm, while coarse nystagmus means move- nystagmus is congenital and caused by poor
ment more than 3 mm. Generally nystagmus has visual acuity. This is characterised by absence
fast and slow components. You could grade of the rapid phase and the presence of slow
nystagmus as: first degree (nystagmus on searching movements.
looking towards the direction of the fast compo-
nent), second degree (moderate nystagmus Diplopia
in the medial position) and third degree
Whilst checking eye movements, it is helpful to
(nystagmus on looking in the direction of the
ask the child if he/she “sees double.” A false
slow component) Table 6.6.
image appears in the direction towards which
When you test for eye movement, you are
the paralysed muscle usually pulls. For example,
also looking for possible nystagmus. Be cautious
in medial rectus palsy, diplopia is present on
that nystagmus at the extremes of lateral gaze
looking towards the nose. In inferior oblique
may be physiological. If nystagmus does
paralysis, the direction will be upwards and
happen, you should ensure that your finger is
inwards, whereas in superior oblique paralysis
not any further than 45º from the centre. Re-
it will be downwards and inwards. Be wary of
member also that nystagmus must be sustained
the child with mono-ocular diplopia. There are
for more than a few beats to be significant.
really very few causes to account for such a
Nystagmus may also be elicited by caloric
phenomenon. If there are no local lesions in the
testing using warm and cold water. This is the
eye (like a lens subluxation), consider an element
principle of caloric testing for the semicircular
of functionality to the diagnosis.
canals in the inner ear. Vestibular nystagmus
Causes of diplopia are: Space occupying
occurs only in one direction of gaze (away from
lesion of the brain, refractory errors, Guillain-
the side of the lesion) and may be horizontal or
Barre syndrome, Fisher syndrome, myasthenia
rotational. Positional nystagmus occurs in
gravis, pseudotumour cerebri, botulism,
benign positional vertigo, viral labyrinthitis and
Sydenham chorea.
head injury. Central nystagmus results from
brainstem disease. It may be in any direction
TRIGEMINAL NERVE
including vertical. Up-beat nystagmus is asso-
ciated with lesions in the floor of the fourth Anatomy
ventricle, pontine tegmentum and anterior
cerebellum. Downbeat nystagmus is associated This is a mixed nerve having motor and sensory
with extrinsic compression of the foramen components. Those are three divisions of the
magnum. fifth nerve-ophthalmic, maxillary and mandi-
Nystagmus can be due to a cerebellar cause bular. The first two are sensory, the third has a
where it occurs towards the side of the lesion. sensory and a motor component (Table 6.7).
Ataxic nystagmus occurs in internuclear
ophthalmoplegia. See-saw nystagmus is found Test
in parasellar tumours. Here as one eye rises and a. Motor – Ask the child to clench the teeth and
turns, the other falls and turns out. Pendular palpate over the masseters and temporalis
Table 6.6: Nystagmus—Various types muscles bilaterally. Ask him to open and
close the mouth. A paralysis of one side will
A. Horizontal, vertical, rotatory, mixed
lead to a deviation of the jaw to the non-
B. Fine nystagmaus, coarse nystagmaus
paralysed side when the mouth is open. Test
C. First degree, second degree, third degree
the pterygoids individually by asking the
D. Upbeat nystagmus, Down beat nystagmus
patient to move the lower jaw to each side
E. Ataxic, pendular, see-saw
(which tests the opposite muscle).
Table 6.7: Trigeminal nerve
Branch Sensory Motor

Ophthalmic Conjunctiva (except lower lid) None
Lacrimal gland
Tip of the nose and skin over medial part of the nose
Upper eyelids – forehead and scalp up to the vertex
Maxillary Cheek, front of temple
Lower lids, conjunctiva None
Side of nose
Upper lip, teeth
Upper pharynx, roof of mouth, soft palate
Mandibular Lower part of face
Lower lip
Tongue, lower teeth part of ear salivary glands All muscles of mastication
except buccinator
b. Sensory – The sensory component (touch and d. Jaw Jerk–Ask the patient to open the mouth.
temperature) may be tested in the individual Place your index finger at the tip of the
regions supplied by the 3 divisions as shown mandible and tap gently with a percussion
in Figure 6.4. hammer. An exaggerated reflex indicates an
c. Corneal reflex The sensation of the cornea is upper motor lesion above the 5th cranial
carried by the 5th cranial nerve while the 7th nerve nucleus.
nerve mediates the effector response. It is not
standard practise to test for corneal reflex FACIAL NERVE
and will not give you any more information
Anatomy
than any of the other tests for the individual
nerves involved. However for the sake of The motor nucleus of the facial nerve is found
completeness, you could use a wisp of cotton in the pons medial to the descending nucleus of
and touch the sclero-corneal junction. Ask the 5th nerve. Efferent fibres loop round the
the child to look in one direction while nucleus of the 6th cranial nerve before leaving
approaching from the other (to avoid a visual the pons on its lateral aspect. At the cerebello-
blink reflex). This will cause a blinking action pontine angle, it is joined by the nervus
in both eyes. Test both sides. An easier (but intermedius. The two then enter the facial canal
crude) method would be to blow into the and then onto the geniculate ganglion. The
patient’s eye, and notice the blinking. nervus intermedius carries taste sensation from
the anterior 2/3 of the tongue via the lingual and
the chorda tympani nerve. The afferent fibres
have their cells of origin in the geniculate
ganglion and terminate in the upper medulla.
From the geniculate ganglion, secretory fibres
pass via the petrosal nerves to the lacrimal
glands (Fig. 6.5).
Leaving the ganglion, the facial nerve runs
through the facial canal in the temporal bone. It
lies in close proximity to the aditus of the
tympanic antrum where it gives off a branch to
Fig. 6.4: Trigeminal sensory nerve distribution the stapedius muscle (which limits the
Neurology 109
Fig. 6.5: Facial nerve nucleus
movement of the ear drum and ossicles in

response to loud noise). It is next joined by the
chorda tympani about 6 mm above the
stylomastoid foramen. In this part of its course
in the facial canal it is enclosed by a bony tube
and thus susceptible to trauma and oedema. Fig. 6.6: Distribution of facial nerve
After leaving the stylomastoid foramen, the
facial nerve passes anteriorly through the
eyelashes are generally buried (to some
substance of the parotid gland and is divides
extent) in the eyelids. Note that the child also
into a number of branches to all the musculature
lifts the corners of his mouth upwards.
of the face (Fig. 6.6).
In facial paralysis, the eyeball rolls
upward during attempted forced eye closure
Test
(Bell’s phenomenon). The eyelashes are not
Motor buried in the closure. The angle of the mouth
either does not move at all or moves much
It is helpful to observe the child’s face and facial
less than on the affected side.
expression. In case of unilateral facial paralysis,
2. Ask the child to whistle, if he can under-
the facial furrows are obliterated on the affected
stand.
side with accumulation of saliva and widening
3. Ask him to blow out one cheek. Tap with the
of palpebral fissure. The eyeball rolls up under
finger on the inflated cheek—if air can be
the upper eyelid rather than the upper lid
made to escape from the mouth, that is the
moving down on the eyeball and blinking may
weaker side.
be less forceful on the affected side.
4. Ask the child to smile or show his teeth. An
Facial palsy can be confused with the
easier way out is to say, “pull a tiger face”
‘congenital cry facies’ of the absence of depressor
and show him how it is done. The angle of
anguli oris. In this case, only the lower half of
the mouth is drawn to the healthy side.
the face below the angle of the mouth is
5. If possible, ask the child to frown, the action
involved. Bilateral facial weakness may be part
of which tests the action of the corrugator
of the Guillain-Barre syndrome, some myo-
supercilli muscles.
pathies and the Moebius syndrome.
The following are the tests are done to
Sensory
evaluate the motor function of the 7th cranial
nerve. The facial nerve carries the fibres for taste
1. Have the child close the eyes as tightly as sensation from the anterior two-third of the
possible. Say “can you scrunch (shut) your tongue. Have the child put out the tongue as far
eyes very tight and don’t let me open them”. as possible and use the following solutions—5
Normally, the upper lid will descend with percent glucose (sweet) 3 percent sodium
some movement of the eyeball upward. The chloride (salty), 1 percent citric acid (sour) and
0.1 percent quinine hydrochloride (bitter). The UMN innervation of the facial nerve nucleus.
child should not draw his tongue in but indicate Hence, UMN lesions will not affect the upper
with finger clues or point to cards with the half.
names of the tastes written on them. Taste is lost The nerves carrying taste sensation run
in lesions of the 7th nerve along its course from alongside the facial nerve for some part of the
the internal auditory meatus to the place where LMN course. Therefore, you will appreciate that
the chorda tympani branches off. UMN lesions of the facial nerve do not affect
taste. Further in UMN lesions, facial weakness
Autonomic may disappear on volition but is accentuated on
emotion. Facial reflexes, elicited by lightly
In recent lesions of the facial nerve, increased
tapping the facial muscles around the mouth are
lacrimation and salivation are common.
increased.
In infranuclear (LMN palsies) lesions, both
Reflexes
the upper and lower parts of the face are
The ‘glabellar reflex’ and ‘snout reflex’ indicate involved. The lesion may be in the nucleus or
a regression to infantile status or a frontal lobe the facial nerve itself. A lesion inside the facial
lesion. To elicit the glabellar reflex, tap gently canal (unless it is toward the outer end) involves
and repeatedly over the root of the nose. Normal the fibres of the chorda tympani and therefore
response is brisk closure of the eyes after the first causes loss of taste sensation in the anterior two
two or three stimuli. Persistent response thirds of the tongue. If the stapedius is
(without extinction) with closure of the eyes is paralysed, a sound on the side of the facial palsy
abnormal. Puckering of the lips in responses to may seem unusually loud (hyperacusis). A
a tap over the upper lid is called the ‘snout persistent LMN lesion will cause atrophy of the
reflex.’ This is not elicited in normal individuals facial muscles. LMN weakness is accentuated on
and is a frontal release sign. volition and disappears on emotion. Tapping
The Chvostek sign is not a reflex but a sign over the supraorbital region may produce
that indicates hypocalcaemia. Ask the child to ipsilateral blinking (McCarthy reflex).
open the mouth slightly. Tap gently on the facial It may be difficult at times to be certain of
nerve in front of the ears—there should be facial nerve paralysis. Bilateral facial palsy may
abrupt closure of the mouth. In normal indivi- be present but usually one of the sides is
duals, you will elicit only a flicker of movement. comparatively stronger. Minimal facial paralysis
may also be missed unless specifically looked
Pathology for. When asked to shut his eyes tightly, the
child’s eyelashes should normally be buried in.
Lesions of the facial nerve may be supranuclear
If they are not, you may consider a partial lesion.
(upper motor neuron, UMN), nuclear (lesion in
However, you should remember that this is only
the nucleus) or infranuclear (lower motor
possible in the older child who is capable of
neuron, LMN). The supranuclear facial palsy
responding to your command. Another sign of
(UMN lesions) chiefly affects the lower part of
minimal facial palsy is excessive watering and
the face. This is because the muscles of the upper
loss of prominence of the nasolabial furrow.
part of the face are bilaterally innervated. A
unilateral lesion, therefore, will cause only
partial paralysis of the upper part of the face, VESTIBULO-COCHLEAR NERVE
including eye closure, on one side. Movements
Anatomy
of the mouth (lower part of the face) on that side
will appear much more severely affected. One There are two components of this nerve—one
school of thought believes that there is little supplying the cochlea and serving auditory
Neurology 111
functions and the other supplying the be the method, make sure that you are out of
semicircular canals and serving functions of the child’s visual field as this might give him/
equilibrium. Auditory fibres reach the vestibular her unnecessary clues.
nuclei in the pons and medulla. Secondary Start the test with the distracter getting the
pathways arise from these locations and child’s attention. At one point the distracter
terminate in the inferior colliculi and medial should stop and hide the toy. You are required
geniculate bodies and at the cortical centre for to produce the sounds at this stage. Watch for
hearing in the temporal lobe. the child’s expression. A clear pass is when the
child clearly turns to the source of sound. For
Test for the Auditory Nerve the other side, the distracter has to start all over
again and you have to go to the other side. Doing
In neonates and infants, hearing tests are
a distraction test needs patience—for the child
difficult to perform. There may be clues that
as well as for the examiners. Very often the child
point to the problem. A normal newborn will
will not cooperate and lose attention. Get some
pause briefly during sucking on ringing a bell.
toys to play with the child and work hard to
After several stimuli the pauses will cease as
achieve a result. Some children with viral upper
habituation occurs. The neurologically abnormal
respiratory infections may score below par. A
infant will not habituate. It is best, however, to
middle ear effusion may occur transiently
test for hearing by auditory evoked potentials
secondary to a viral infection. A hand held meter
or otoacoustic emissions at this age. In the older
to assess tympanic compliance, if you have one,
child with hearing impairment, inappropriate
shows a damped trace. It is best to repeat the
speech and temper tantrums are common.
hearing test in a short while to make sure that
Suspect nerve deafness if there is failure to
the discrepancy is not real.
respond to normal sounds (turns the television
The hearing test is scored on an “audio-
on very loud), excessive response to visual
gram.” This is a graph with varying frequencies
stimuli, delayed speech and monotonous voice
(kHz) and intensities (decibels). There can be
with normal motor development.
patterns of conductive loss or sensorineural
hearing impairment or both.
Infant
The best method to check hearing in the infant Toddler
around 8-9 months of age is the “distraction
It is quite difficult to do a distraction test on a
test”. Sit the baby on his/her mother’s lap,
toddler, as he/she will not easily conform to the
facing the distracter. The setting ideally should
rules. A modified distraction may be a way
be a sound proof room with no extraneous noise.
forward. Get the child to play with the distracter
The distracter has a table in front of the child
while you produce the sounds. A useful toy is
with a toy to distract the child’s attention. The
“men in a boat.” When the child hears the
toy should not too attractive and should not
sound, he/she puts the man in the boat. For the
make a noise of its own. You should be behind
older child ask specifically “put the man in the
the child and one side at a time. You are required
boat when you hear something.”
to produce a series of sounds of varying
frequencies and intensities. You can either use
Older Child
a device called a “warbler” or tune your own
voice to high, mid and low frequencies (pitch A child above the age of five will tolerate the
or shrillness) and adjust the loudness (intensity) use of headphones. Headphones mask external
accordingly. Some people use a high frequency sounds and you can use pure tone (instead of
rattle to produce the high pitch noises. Whatever warbles tones as before). A pure tone audio-
metry can then be performed using the same posture, imbalance and nystagmus. The child
principles as the “men in the boat” test. For the may want to bury his face and not open the eyes.
school going child put a stick in the child’s hand You can test for vertigo by changing the position
and ask him to tap on the chair as soon as he of the head in the semi-reclining or horizontal
hears anything. position. This test is positive for disease in the
semicircular canal that is situated low down.
Rinne’s Test The caloric test is a more objective method
but requires the child’s full cooperation. It is
This can only be done on the co-operative child
unwise to attempt this in the younger child as
to assess air and bone conductions. Place a
he/she may start to panic. Make sure at the
vibrating tuning fork near the ear. If the child
beginning that there is no perforation of the
hears it, put the base of tuning fork on the
tympanic membrane and that the external
mastoid process. If it can be heard again,
meatus is clear. The child is kept in a semi-
compare to see which sound is heard louder and
reclining position (30º with pillows) and held
longer. Normally air conduction is louder and
steady. Inject 10 ml of cold water (30ºC) slowly
heard longer. In middle ear disease, bone con-
over 30 seconds directed at the tympanic
duction is louder and heard for longer periods.
membrane and observe the eyes for nystagmus.
Rinne’s test has now largely been replaced by
Normally this should produce slow deviation
audiometry, which is more accurate (Fig. 6.7).
of the eyes toward the side of injection with the
rapid phase of nystagmus away from the side
Weber’s Test
of injection. Warm water (44ºC) produces the
Put a vibrating tuning fork on the centre of the opposite effect. The above responses may be
forehead and ask the child to comment on which remembered by the acronym ‘COWS.’ That is
side he/she hears better. In conductive deafness, cold–away and warm–same. This response is
Weber’s test is lateralized to the deafer side. In lost in vestibular damage. Peripheral lesions
sensorineural deafness, the reverse occurs. This tend to cause a diminished response on the side
test, like the one before, is subject to significant (auditory canal paresis), although a directional
subjective variation. It is better to do tympano- preponderance (where nystagmus in one
metry and audiometry where there is suspicion direction is more prominent than the other) may
about hearing (Fig. 6.8). also be observed. The latter finding is most likely
to occur with central disorders, especially in the
Vestibular Function brainstem.
Children find it difficult to express vertigo.
Benign paroxysmal vertigo may present as
unexplained crying, vomiting with change of
Fig. 6.7: Rinne’s test Fig. 6.8: Weber’s test

Neurology 113
GLOSSOPHARYNGEAL, VAGUS AND Table 6.8: Defects of 9th and 10th cranial nerve
ACCESSORY CRANIAL NERVES
1. Stridor in the absence of mechanical obstruction
Anatomy suggests recurrent laryngeal nerve paralysis (10th
cranial nerve)
The 9th, 10th and 11th cranial nerves are situated 2. Hoarseness of voice, aphonia (10th cranial nerve)
in the floor of the 4th ventricle, above down- 3. Loss of swallowing reflex and dysphagia (to fluids in
ward, in succession. They emerge by several LMN lesions; to solids in UMN lesions)
roots along the lateral aspect of the medulla. The 4. Nasal regurgitation when swallowing liquids
5. Ineffective cough, ‘bovine cough,’ slurred speech -
spinal part of the accessory nerve emerges from
features of recurrent pharyngeal paralysis
the lateral column of the cord, passes up through 6. Inability to pronounce words such as ‘Egg’ (sounds
the foramen magnum to join its medullary part as ‘Eng’) and words ending with a ‘K’ sound
and emerges with it through the jugular
foramen. After emerging, the medullary part wide and introduce a tongue depressor. The
joins the vagus nerve while the spinal part position of the uvula at rest is variable, even in
supplies the sternomastoid and upper part of the health. You should watch the movement of the
trapezius muscle. palate during phonation. Ask him/her to say
The glossopharyngeal nerve is sensory. It ‘Aah’ (loud and clear) and observe whether both
carries sensation from the posterior third of the sides of the palate arch upwards. In unilateral
tongue and the mucous membrane of the paralysis, the palate on that side will be
pharynx. It supplies motor fibres to the middle immobile and the median raphe will be pulled
pharyngeal sphincter and the stylopharyngeus towards the healthy side. In bilateral paralysis,
muscle. It also carries taste fibres from the the whole palate is immobile.
posterior third of the tongue.
The vagus is motor for the soft palate (with Gag Reflex
the exception of the tensor palati), pharynx and The afferent of the pathway is the 9th nerve
larynx. It is sensory and motor for the respiratory while the efferent is the 10th. While testing for
tract, the heart and, by the parasympathetic the palate, touch the base of the tongue, soft
ganglia, most of the abdominal viscera. The palate or the pharyngeal wall with your tongue
vagal fibres to the soft palate, pharynx and depressor. You could use a swab stick instead.
larynx originate in the nucleus ambiguous and The normal response is elevation of the pharynx
traverse through the accessory nerve. The and retraction of the tongue. When there is no
visceromotor and cardio-inhibitory fibres are reflex, ask the child if the pharyngeal stimulus
derived from the dorsal nucleus of the vagus in was felt. Presence or absence of sensation will
the floor of the fourth ventricle. differentiate interruptions of the afferent or
Test for the 9th and 10th Nerves efferent limb of the reflex arc.
It may not always be practical to distinguish 11th Cranial Nerve

between lesions of the 9th and 10th cranial
The 11th cranial nerve (or the cranial part of the
nerves. The only clue to ipsilateral paralysis of
spinal accessory) is purely motor in function,
the 9th nerve may be a slight flattening of the
contributing to the innervation of the larynx and
arch of the palate on the affected side at rest. In
pharynx, as well as the sternomastoid and
general the following should alert you to the
trapezius muscles.
possibility of 9th and/or 10th nerve problems
(Table 6.8).
Test for the 11th Cranial Nerve
Palatal Paralysis Ask the child to shrug his/her shoulders, first
To examine the soft palate, place the child facing on his own and then against resistance. This tests
a light source. Instruct him/her to open mouth the upper part of the trapezius muscle. To test
the lower part of trapezius, have the patient Fibrillation is noticed when the tongue lies
prone with arms adducted to 90º and rotated relaxed in the mouth. These are worm like
laterally. Ask him to adduct the scapula against movements, associated with spinal muscular
resistance. The movement should take place atrophy and are seen on the under surface of
between the scapula and the thorax. Next test the tongue. Test for the power of the muscles of
the sternomastoid by asking the child to rotate the tongue. Look for signs of wasting. Ask the
the head to one side when resistance is applied child to move the tongue from side to side and
against this movement at the chin. This tests the protrude it into each cheek in turn, while you
muscle of the opposite side. To test muscles of press against the tongue from the outside. You
both sides at the same sitting, have the child are looking for asymmetry, wasting and reduced
bend his chin down while you apply resistance power.
to this movement.
Torticollis implies rotation of the chin in a Motor System
direction opposite to that of the direction of
Examination of the motor system entails the
rotation of the occiput. Torticollis and head
following: muscle mass, abnormal movements,
tilting are seen in athetoid cerebral palsy, hiatus
tone, power, reflexes, gait and coordination.
hernia, rheumatoid arthritis with cervical spine
However it may be cumbersome to perform the
involvement, cervical lymphadenopathy,
examination in the strict order. It is, therefore,
retropharyngeal abscess, mastoid abscess,
simpler to have a “system” of examination that
paralytic torticollis and as compensatory
covers all the aspects. We shall discuss about the
mechanisms in diplopia. Gastro-oesophageal
individual points in greater detail. For now, you
reflex is occasionally associated with inter-
could have a system that is as follows (Table 6.9).
mittent torticollis (Sandifer’s syndrome).
Talk to the child and put him/her at ease.
There may be vital clues to be obtained—a child
HYPOGLOSSAL NERVE
with Friedreich ataxia will have characteristic
This is a pure motor nerve and arises from a cerebellar speech. Look for such clues that will
nucleus in the lower part of the floor of the help you fit the pieces of the jigsaw puzzle. Make
fourth ventricle, close to the midline. It emerges a note of anything that catches your eye and try
from the brain stem between the anterior and correlate these with your findings.
pyramid and the olive. Expose the lower limbs to get a good view
of the shape and symmetry on both sides. There
Test may be scars (from muscle biopsy), wasting or
pseudohypertrophy. If the child is on the bed,
Look at the normal position of the tongue in the
make him sit up. Be careful not to walk a child
floor of the mouth, with the mouth slightly open.
If the tongue is in the midline, ask the child to Table 6.9: Scheme of motor
put out the tongue as far as possible. If there is examination of lower limbs
any paralysis, the tongue is pushed to the • Inspection of lower limbs
paralysed side, because of the mechanical • Sitting up
• Swinging leg side by side
positioning and peculiarities of the origins and
• Standing
insertions of the muscles of the tongue. This • Standing eye closed
deviation to the weaker side may be difficult to • Walking
interpret in the presence of facial weakness. • Walking on instep, outer edge of the feet, toes
Therefore, in such situations it is better to and heels
• Running
compare the position of the tongue in relation
• Gower test
to the tip of the nose.
Neurology 115
who has paraplegia. Then ask him to swing his Examine power in the different muscle
legs to the side of the bed and stand up slowly. groups of the upper and lower limbs. For
Be patient – the child may have Charcot-Marie- convenience, divide the muscles as flexors and
Tooth disease with lower limb wasting; he needs extensors, abductors and adductors. Ask the
an effort to stand up. When the child is up on child to do the movement on his own and then
both feet, you can use the opportunity to test for against resistance. Grade the power (Table 6.12).
ataxia—the Romberg test. Ask him to put two Explain to the child that you are about to use
feet together and then close his eyes. A child a patellar hammer and that it does not hurt.
with cerebellar ataxia will sway even with his Examine the different reflexes, superficial and
eyes open. In contrast in sensory ataxia the child deep, and note aberrance, if any. You can then
will be stable with eyes open (he uses visual go on to examine the cerebellar signs – upper
sense to compensate for loss of sensation from and lower limb coordination.
his feet) but not when they close. Let us now discuss about the individual
When you are certain that the child can be components in more depth.
steady on his feet, make him walk and assess
his gait. Allow him to walk up to the door and Muscle Mass
turn back. Use different techniques to bring out Wasting of muscles is usually caused by lower
minimal weakness—walking on the instep, motor neuron type lesions. Inspection gives us
outer edge of the feet, toes and heels. Watch for an idea of asymmetry. Corroborate this with
signs of minimal asymmetry and weakness. limb circumference measurements on two sides
Does the child swing his hands? Does he bend (at identical sites). Wasted muscles are not only
more on one side? Ask him to run—this is a good smaller, but also softer and flabbier on contrac-
way of assessing gait if you do not have time to tion. When muscle wasting is accompanied by
do the above manoeuvres. In a clinic situation, fibrosis, they become shortened. They then
a quick way of estimating power and function develop contractures—it may be difficult to
is to make the child hop on each leg (provided stretch them passively to a normal degree.
he is of the age to do so). Wasting may be proximal (myopathies) or
Now play a game with the child—the distal (peripheral neuritis). Generalized wasting
modified Gower test. Sit down on the floor and is not only seen in neurological conditions –
ask the child to do the same. Now tell him “let’s cachexia and malnutrition may confuse the
see who can get up faster.” This tests the picture. Hypertrophy occurs with excessive use
proximal muscle strength—you are observing if (athletic training) and can be a possibility in a
he demonstrates the Gower sign. The child who child with good physique. On the other hand,
has Duchenne dystrophy will “climb up,” pseudohypertrophy is more local and due to
holding on to his knees and thighs. pathological changes in the muscles them-
You can next go on to examine the tone, selves—the calves, buttocks and infraspinati are
power and reflexes. Talk to the child when you involved. There is fat deposition in the muscles
are checking tone. This keeps the child’s that are rendered ineffective. The muscles
attention distracted and does not affect the tone appear rounded and the feel is firm and rather
of the muscles. Examine tone by moving the woody.
joints passively and feel the resistance against
your movement. Examine pronation-supination, Involuntary Movements
flexion-extension of the wrists and forearm. Do Observe for the following movements. Some of
similar flexion-extension at the knees and elbows. them can be exacerbated by volitional activities
Roll the knees from side to side for resistance. (Table 6.10).
Table 6.10: Some involuntary movements one of the limbs (hemiballismus). They are
• Tics
sometimes to be associated with tuber-
• Fasciculation culous meningitis.
• Chorea More commonly the movement of
• Myoclonus chorea is associated with athetosis and is
• Athetosis therefore termed choreo-athetoid. Typical
• Dystonia
• Myokymia
examples are dystonic cerebral palsy,
• Asterixis tuberculous meningitis, glutaric aciduria
• Tetany and paroxysmal kinesogenic choreo-
athetosis. The last mentioned disease is
i. Tic—Purposeless, repetitive movements, rare but has a typical manifestation. The
that usually affect the ocular, facial and child with this condition acts and behaves
upper limb muscles. They disappear in normally but will tell you that he/she finds
sleep and do not interfere with the child’s irresistible episodes of abnormal move-
day-to-day activities. Tics can be a problem ments which get better on their own. Have
with the Tourette syndrome. the child lie down on the couch and
ii. Fasciculation-This is due to twitching of instruct him to start running at a signal.
groups of muscle fibres. It occurs in slow You will see a dramatic representation of
dysfunction of anterior horn cells as in the movement. The child will get up, run
Werdnig–Hoffman disease. Besides a few steps and fall to the ground and
skeletal muscles, the tongue is also a good show frank choreoathetoid movements.
place to observe for such movements (no iv. Myoclonus—Rapid, irregular jerking
submucus coat) where it is termed movement of a group of muscles in a limb
fibrillation. or even of the whole body constitutes
iii. Chorea—The term means a ‘dance’ and is myoclonus. A sudden start when surprised
defined as semi purposive, non-repetitive or bodily jerks when falling asleep (or
movements affecting the face, limbs or waking) are examples of benign myoclo-
trunk. The movements are often very brief nus. Myoclonus can be part of major
and difficult to discern. Ordinary volun- generalised epilepsy. Myoclonus also
tary movements such as walking or occurs in association with lesions of brain
picking up a cup and may be embellished stem nucleii and reticular formation.
with smooth, rapid extra little flourish of v. Athetosis—Slow writhing movements,
movement. Sydenham chorea can be a more pronounced in distal muscles,
result of rheumatic fever, still a common brought on by voluntary activity and
condition. To diagnose this, ask the child emotional stimuli.
to stretch out his arms above his head. The vi. Dystonia—This is an abnormally main-
arms and palms turn outward to give a tained posture, resulting in strange
“pronator” sign. If you ask the child to positions and torsion spasms. It disappears
stretch his arms in front, you may see a in sleep. This commonly occurs with the
spooning of the extended hand by flexion conditions with choreoathetosis. Other
of the wrist and extension of the fingers causes are Wilson disease, drugs (pheno-
(“choreic hand”). They are increased by thiazines, metoclopramide, chloroquin)
agitation or nervousness. and dopa-responsive dystonia.
Unilateral chorea may occur with deeply vii. Myokymia—Persistent twitching, often
placed lesions in one hemisphere such as rhythmical affecting the periorbital
the subthalamic nucleus of Luys. They may muscles. This is often a benign response
appear as violent, flinging movements of to fatigue.
Neurology 117
viii. Asterixis—An irregular, abrupt, brief loss

of posture evident in the outstretched
hand. It occurs in decompensated hepatic
failure (hepatic flap), viraemia, poisoning
with hypnotic drugs and respiratory
failure.
ix. Tetany—This characteristic posture is due
to hypocalcaemia or alkalosis. The fingers
and thumbs are held stiffly adducted and
the hand is partially flexed at the meta-
carpophalangeal joints; the toes may be
similarly affected (carpopedal spasm). You
can inflate a sphygmomanometer cuff and
hold the pressure above the systolic for
2 to 3 minutes with a similar result
(Trousseau sign). Light tapping in the Fig. 6.9A: Movements of the neck
region of exit of the facial nerve from skull
(about 3-5 cm below and in front of the
ear), results in twitching of facial muscles
with each tap (Chvostek sign).
Power
A quick and preliminary assessment of muscle
power is by watching the child lie, sit, stand,
walk, dress or undress. These movements
involve proximal and distal strength and
coordination to a certain degree and thus
observing such routine behaviour can provide
us with important clues. It is good practice to
Fig. 6.9B: Movements of the shoulder
comment on the functional ability of the child.
This acquires great importance in the child with
severe physical disability. Testing the muscle
power in such a child has little practical
implication. Activities of daily living are more
useful to judge the independence of the child.
Ascertain from the history if he can dress or
undress, eat and drink and care for himself
independently.
Test
There are two principles to testing groups of
muscles—active movements without resistance
and then against resistance. Try and test as many
groups of muscles as possible (Figs 6.9A to C).
They are given in Table 6.11. Fig. 6.9C: Movement of the lumbar and dorsal spine
Table 6.11: Movement of different joints Table 6.12: Grading of muscle power
• Neck: Flexion, extension, sideways rotation 0 - Complete paralysis
• Shoulder: abduction, adduction, flexion, extension 1 - A flicker of contraction only
• Elbow: Flexion, extension 2 - Power detectable only when gravity is excluded
• Wrist: Flexion and extension of the wrist, by appropriate postural adjustment
pronation and supination of the forearm 3 - The limb can be held against the force of gravity
• Fingers: Abduction, adduction of the fingers, but not against the
opposition of thumb and little finger, hand grip examiner’s resistance.
• Trunk muscles: Flexion, extension, lateral flexion 4 - There is some weakness, usually described as
• Hips: flexion, extension, abduction, adduction poor, fair or moderate strength (4-, 4, 4+)
• Knees: Flexion, extension 5 - Normal power is present
• Ankle: dorsiflexion and plantar flexion, inversion
and eversion
• Toes: Flexion, extension 4. Interossei and lumbricals—The lumbricals
flex the metacarpophalangeal joints and
When testing for power, it helps to have a extend the distal interphalangeal joints.
uniform command to give to the child for each The interossei adduct and abduct the
step. For example say to the child “lift your leg fingers. Instruct the child to button his shirt
in to the air and hold in there, don not let me to test the lumbricals. To test the interossei,
push it down.” Or say “push my hands away,” spread out the fingers and try to appose
or “pull your legs towards your bottom.” For them (and vice versa).
testing power at the shoulder girdle say “fold 5. Flexors of the fingers—Allow the child to
your arms like the wings of an aeroplane – do squeeze your index and middle fingers.
not let me push it down.” As you examine more This tests for strength of grip, and also tests
and more children you will start developing a other associated muscles.
system of your own. Practise the commands so 6. Flexors and extensors of the wrist—Ask the
that the examination looks slick and you miss child to make a fist and try to forcibly flex
little of vital importance. At the end, grade or extend the wrist.
muscle power as per the grading recommended 7. Brachioradialis—Place the arm midway
by the medical research council (MRC) (Table between the prone and supine position and
6.12). ask the child to bend up the forearm while
The tests of individual muscles are given opposing the movement by grasping the
below: hand. The muscle will stand out promi-
nently in the upper part.
Upper limb 8. Biceps—Ask the child to bend up the
forearm against resistance, with forearm in
1. Abductor pollicis brevis–Ask the patient to full supination.
abduct the thumb in a plane at right angles 9. Triceps—Ask the patient to straighten out
to the palmar aspect of the index finger. the forearm against resistance.
The muscle in the thenar eminence can be 10. Supraspinatus, deltoid—Instruct the child
seen and felt to contract. to lift his arm straight out at right angles
2. Opponens pollicis–Ask the child to touch to the side. The first 30º of movement are
the tip of the little finger with the point of by the supraspinatus, and the remaining
the thumb. Oppose the movement with 60º by the deltoid. This movement may be
your thumb or index finger. resisted to gauge the power.
3. First dorsal intraosseous–Ask the patient 11. Infraspinatus—Keep the forearm at a right
to abduct the index finger against your angle and then ask the child to tuck the
resistance. elbow into the side. With the elbow held
Neurology 119
against the side, ask him to rotate the 8. Rotators of the thigh—Ask the patient to
forearm like a lever, during which the rotate the limb outside or inside against
muscle may be seen and felt to contract. resistance.
12. Pectorals—Ask the patient to stretch the Sometimes it becomes difficult to decide
arms out in front and then to clap their whether weakness is real or feigned. Functional
hands together. You can resist the move- weaknesses can piggy back real weakness. It
ments by separating the hands. may be helpful to assess the child’s functional
13. Serratus anterior—Have the child push ability in these circumstances. A child who can
(with the hands) against a wall. A dress himself and yet shows motor weakness in
weakness of the serratus anterior may take his upper limb (with normal muscle bulk and
the shape of a ‘winged’ scapula. reflexes) is likely to have functional paresis.
14. Latissimus dorsi—The process is similar to Another test (Hoover sign) is applicable to h
that of testing the pectorals except that the emiplegics in older children. With the child lying
child has to clap behind his back. on his back, place your hands beneath the heels
on the bed. Ask the child to lift one leg and then
Lower Limb another. In case or true hemiplegia, when the
1. Intrinsic muscles of the foot—These are patient attempts to lift the paralysed leg off the
difficult to test and a paralysis of the above bed, you will feel a counter pressure on the non-
muscles may be inferred from the foot defor- paralysed heel. In ‘hysterical’ hemiplegics, the
mity. For example, in familial peripheral child is not making any effort at all to raise his
neuropathies, a hollow wasted foot defor- leg and so you will feel no pressure on your
mity ‘pes cavus’ is characteristic. Note also hands.
that normal children, especially avid
swimmers, also have hollow arches. Tendon Tone
reflexes will help in the differentiation. Muscle tone is the state of tension or partial
2. Dorsiflexors and plantar flexors—Test by contracture of a muscle at rest. It may be thought
elevation or depression of the foot against of as the readiness, steadiness and awareness of
resistance. a muscle waiting to contract. Tone can be
3. Flexors and extensors of knee—Bend the normal, hypotonia or hypertonia. Normal tone
knees and ask the child to push his feet pull is difficult to describe and requires experience
toward himself (flexion) as you resist. Then to define. Hypotonia occurs in sleep, use of
ask him to push your hand away (extension) certain drugs, lower motor neuron lesions,
against your resistance. neurogenic shock and cerebellar disease. You
4. Extensors of the hip—With the knee will come across the ‘floppy’ infant with
extended, ask the child to lift the leg off the differentials of spinal muscular atrophy,
bed. Push down while the child tries to hold congenital myopathies and congenital myotonic
in the same position. dystrophy. In these conditions, note that the
5. Flexors of the hip—As above, but now ask child is weak as well as being ‘floppy.’ The
the child to push down on the bed while you ‘floppy’ but strong child can have hypotonic
try to keep the leg elevated. cerebral palsy or Down syndrome. Sudden and
6. Adductors of the thigh—Abduct the limb episodic hypotonia signifies akinetic attacks or
and then ask the patient to bring it back to syncope. Lesions of either corticospinal or
the midline against resistance. extrapyramidal pathways cause hypertonia.
7. Abductors of the thigh—Keep the legs Upper motor neuron lesions of the corticospinal
together in the midline and try to separate tract give rise to ‘spasticity.’ The limb involved
against resistance. shows a ‘clasp knife’ character when flexed or
extended fairly rapidly. Note that the resistance the sensory endings of the muscle spindles in
to stretch increases during the initial phase and the stretched muscle, the nerve pathways and
then suddenly gives way, just like opening a synapses leading up to and through the spinal
penknife. cord and the efferent motor response. There is
Spasticity due to cerebral or brain stem also the influence of the corticospinal tract above
lesions result in typical postures. The upper the anterior horn cells of the nerve roots being
limbs are flexed and the lower limbs extended tested—the so-called upper motor neurons.
and feet in plantar flexion (think of a quadruped Depending on the pathology, reflexes can be
that has predominance of forefoot flexors and hyper-reflexia (upper motor neuron lesions) or
hind foot extensors). This distribution is most hypo-reflexia (lower motor neuron lesions)
evident in the erect posture and may be reversed (Table 6.13).
if the patient is lying head down, hinting that it Use a patellar hammer to elicit tendon
may as a result of labyrinthine or vestibular reflexes. The head should be well padded with
activity. rubber, so that you do not hurt the child. Explain
Hypertonia resulting from extrapyramidal the procedure, as otherwise this can lead to
disturbance is ‘rigidity.’ The resistance to apprehension. As you strike the tendon, there
passive movement in this disorder is described is brief contraction of the stretched muscle. Look
as ‘cog-wheel’ (like a lever rubbing on the teeth for this contraction in the muscle belly. The
of a cogwheel). The resistance is intermittent and movement of the relevant joint is secondary.
jerky. Rigidity can also be of the ‘lead-pipe’ type, In the event of absence of reflexes, there are
where the resistance is present throughout the two possibilities. The reflexes may be truly
range of movement. Extrapyramidal signs are absent, or else there is difficulty in trying to elicit
present with dystonic cerebral palsy, metabolic them. Differentiate the two by using reinforce-
disturbances, tuberculous meningitis, hypoxic ment (Jendrassik’s maneuver). Instruct the child
ishaemia and Wilson disease. to clench his teeth tightly or to hook one hand
with the other, and pull apart. This should make
Test a reflex prominent (if truly present).
Hyporeflexia may be as a result of lesion in
Tone is measured passively and therefore
the reflex arc in afferent or efferent limbs.
patient effort has to be minimized. Talk to the
Examples are poliomyelitis, peripheral neuro-
child about his friends, his school and his
pathies and primary muscle disease. Hyper-
hobbies. Divert attention whilst you are moving
reflexia occurs with upper motor neuron lesions
the various joints passively. If this does not help,
at levels above the anterior horn cells. It is
ask the child to let his muscles go floppy. The
proposed that the higher control over the muscle
tone of a particular group of muscles is felt while
spindles responsible for the reflex is lost. If
performing the opposite function—that is the
symmetrical and generalised, it does not always
tone of the biceps is felt while extending the
indicate neurological pathology. There may be
elbow.
elements of anxiety, hyperthyroidism or drug
Reflexes toxicity if there are generalised brisk reflexes.
For practical purposes, these are of two types – Table 6.13: Deep tendon reflexes
deep tendon reflexes and superficial reflexes. can be graded as follows:
The so called developmental reflexes will be 0 Absent
described at the end of the chapter. We shall 1 Present (as a normal ankle jerk)
describe the tendon reflexes first. Tendon 2 Brisk (as a normal knee jerk)
reflexes or jerks test for the entire path of a spinal 3 Very brisk
4 Clonus
reflex. This includes the afferent impulses from
Neurology 121
Table 6.14: Root value reflexes problems of the cervical spine. Unusually brisk
triceps reflexes may mean a spinal lesion above
• Biceps—C5, C6
• Tricpes—C6, C7 the level of the sixth cervical segment. Con-
• Supinator—C5, C6 versely, the absence of a triceps reflex may
• Knee—L2, L3, L4 herald ascending spinal paralysis and possible
• Ankle—S1 diaphragmatic involvement (Fig. 6.10C).
• Plantar—S1, S2
• Abdominal—T8 - T12 Biceps jerk: The fifth and sixth cervical segments
are concerned in this reflex. Flex the elbow at a
The following are the reflexes you will be right angle in the semi prone position. Place your
expected to examine (Table 6.14). thumb or index finger on the biceps tendon and
tap with the hammer. The result is a contraction
Knee jerk: The quadriceps contract when the
of the biceps and flexion of the elbow. The biceps
patellar tendon is tapped. The second, third and
jerk is useful like the triceps in delineating the
fourth lumbar spinal roots are involved. You can
level of a cervical spinal cord lesion (Fig. 6.10D).
put the child in the sitting (with legs dangling
from the side of the bed) or supine position. In Supinator jerk: Like the biceps jerk, this also is
the supine state, bend the knees and pass a hand dependent on the fifth and sixth cervical
underneath the knee to be tested. Tap the segments. A tap on the styloid process of the
patellar tendon midway between its origin and radius with forearm in the mid prone position
insertion. This should be followed by a causes supination of the elbow. Lesions of the
contraction of the quadriceps and brief extension cervical 5th and 6th spinal segments are often
of the knee. Knee jerks are normally brisk. In associated with hyperexcitability of the anterior
unusually hyper-reflexic states (UMN lesions), horn cells below the C5/C6 level. This gives rises
you will find a progression reception area of the to brisk flexion of the fingers, even though the
knee jerk. You may well see that tapping and elbow supination is lacking. This phenomenon
even touching other distant areas (like the shin) is known as ‘inversion’ of the supinator reflex.
will lead to a brisk response. This type of You may not find the supinator reflex to be great
response is particularly common in pyramidal practical use in your day-to-day practice and it
cerebral palsy and hypoxic ischaemic can be threatening to the child because of the
encephalopathy (Fig. 6.10A). pain. However if cervical lesions are on your
agenda, then do check this, by all means (Fig.
Ankle jerk: The segments concerned are the first
6.10E).
and second sacral. Place the foot in such a way
that it lies everted on the bed. Dorsiflex the foot Jaw jerk This test for the fifth cranial nerve the
slightly and tap on the Achilles tendon with jerk is sometimes absent in health and is
your hammer. There should be contraction of increased in upper motor neuron lesions above
the calf muscles and plantar flexion of the foot. the trigeminal nerve nucleus. Open the patient’s
(Fig. 6.10B). mouth lightly, not too wide. Put a finger
horizontally on the chin and tap on your finger.
Triceps jerk: This reflex depends upon the sixth
There results a muscle contraction closing the
and seventh cervical segments. Flex the elbow
jaw. Cortical lesions can give rise to a brisk jaw
and rest the forearm across the chest. If the child
jerk (Fig. 6.10F).
is sitting, you could rest the weight of the
forearm on your hand. Feel the triceps tendon Clonus: Clonus is the regular oscillation of
above the olecranon process of the humerus and contraction and relaxation on sustained stretch
tap on it gently. There should be contraction of of a muscle group. Sustained clonus (usually
the belly of the triceps muscle. The triceps jerk more than 6 oscillations) is evidence of an upper
is important to ascertain the level of lesion in motor neuron lesion. Unsustained clonus may
A D
B E
C F
Figs 6.10A to F: Jerks: (A) Knee jerk; (B) Ankle jerk; (C) Triceps jerk;
(D) Biceps jerk; (E) Supinator jerk; (F) Jaw jerk
Neurology 123
Fig. 6.11: Ankle clonus Fig. 6.12: Plantar reflex
occur in anxious persons. The places to look for of the thigh and sartorius. With a slightly
clonus are the ankle and the knee (Fig. 6.11). stronger stimulus, there is flexion of the outer
To test for ankle clonus, bend the child’s knee four toes. This flexion increases with the strength
slightly with your hand as support beneath it. of the stimulus and leads to dorsiflexion and
Hold the forefoot with the other hand and inversion of the ankle (Fig. 6.12).
dorsiflex in a quick movement. Keep the foot in In upper motor neuron lesions there is
dorsiflexion without putting too much pressure extension of the big toe instead of flexion. This
to achieve this. There is a brief reflex contraction response is however normal in infants under a
of the calf muscles that then relax; continued year of age. In a child with upgoing plantars,
stretch causes a regular oscillation called clonus. the first response is extension of the great toe
To test for patellar clonus, put the patient in followed by spreading out and extension of the
the supine position with knees extended. Pull a other toes. This is better elicited by stroking the
portion of skin proximal to the upper part of the more outer edges of the foot. A more medial
patella, upward. Then quickly push downward stimulus evokes flexion of the toes as part of the
toward the feet (and also a degree towards the ‘grasp response’ and can be quite misleading.
bed). You will notice the patella to move up and In major corticospinal lesions, the area of
down in patellar clonus. receptivity enlarges, spreading inward and over
Let us now come to the superficial reflexes. the sole of the foot and then spreads upward
They are elicited by sensory stimulation of the along the leg to the knee or higher. The following
skin and are not carried by afferents of the stimuli may then elicit a Babinski response:
muscle spindles. The plantar reflex is clinically
Oppenheim sign—Squeeze the calf or press along
the most important, and has great relevance in
the inner border of the tibia.
distinguishing upper and lower motor neuron
lesions. Gordon reflex—Pinch the calcaneus tendon.
Plantar reflex (Babinski response): Stroke the outer Gonda’s method—Flex and twist any toe.
edge of the sole of the foot from the heel gently
towards the little toe and then medially across Bing’s method—Stroke the big toe along the
the metatarsus (without touching the ball of the lateral side.
little toe). Minimal stimulus should cause Flexor spasms (Sherrington’s nociceptive flexion
contraction of the tensor fascia lata, accom- withdrawal response) - Sometimes while testing
panied by a slight contraction of the adductors for the plantar reflex, the whole limb is suddenly
drawn up into flexion and the great toe and have the tummy uncovered. Use a light
extended. This occurs particularly in spinal cord stimulus (key, wooden stick) and pass across the
disease and in some patients with bilateral UMN abdominal skin from the outer aspect towards
lesions at a higher level. the midline. The usual response is a ripple of
contraction of the underlying muscle. The level
Plantar equivalent (Hoffmann sign): Hold the
of the umbilicus is the thoracic tenth segment.
child’s hand is held at the level of the wrist.
As you stroke above and below this line, you
Grasp the tip of the middle finger with your
test for two cord segments superior and inferior
thumb and index finger. Flex the distal
to the T10 segment (Fig. 6.13).
interphalangeal joint and let go suddenly, so as
In UMN lesions above the spinal level, the
to snap the tip back to its normal position. There
abdominal reflex is absent. In thoracic cord
should be no movement of the thumb. In an
lesions, absence of this reflex indicates seg-
abnormal response the thumb flexes and
mental involvement of the cord below that level.
adducts. The other fingers may also flex in a
In cerebral palsy this reflex is preserved till late.
more widespread lesion.
You would normally test for plantar reflex Anocutaneous reflexes: The perianal skin should
in children (with sensitive skin) with your ideally be stimulated by a sharpish object. The
thumbnail. Quite often in children who go normal response is a contraction of the external
barefoot, you may find it difficult to get a res- anal sphincter with resultant in-drawing of the
ponse. Use the end of a key (make sure that it anal opening. A loss of this reflex indicates lesion
not too sharp) and go to the outer aspect of the at the levels of the sacral segments S2, S3 or S4.
foot for a try. The skin of the feet can be thick These lesions can be of importance with lesions
and keratinised to impair response. If you use like spina bifida and cauda equina. You could
too much of a pressure, the child may ‘with- at this juncture corroborate the sensation in the
draw’ by showing a flexor response of his knees perianal area by using the cold metal end of your
with a false up going of the plantars. Equally patellar hammer.
you may be at a loss to be absolutely certain if
Palmomental reflex: Normally, tapping the thenar
the plantars are up or down. In such cases, it is
eminence or the hand should not result in
best to call the response ‘equivocal’. Use
movements of the face. A bilateral frontal lobe
corroborative evidence to judge if the patient has
lesion results in contraction of the mentalis and
an upper or lower motor neuron lesion.
orbicularis oris muscles on the ipsilateral side.
Always test both sides and look for
asymmetry. Up going plantars on one side may
be indicative of spinal cord lesions on the
opposite side. This may not hold true for those
higher up. Cortical lesions can occur with a
crossed plantar response. Further the reflex may
be in evolution (of appearance or disappearance)
and this may be reflected in the absence on one
side and the presence on the other.
Abdominal reflex: This tests for the reflexes from
the different quadrants of the abdomen. You
elicit a muscle contraction by stimulating the
skin in that particular quadrant. You should not
attempt to do this in the younger child as he/
she will be frightened by it. Lie him/her down Fig. 6.13: Superficial abdominal reflexes
Neurology 125
Cremasteric reflex: This is mediated through the Test for Coordination

1st and 2nd lumbar segments. Stroking the skin
Upper Limbs
of the upper and inner part of the thigh from
above downward (or pressing the sartorius in • Finger-nose test—Ask the patient to touch the
the lower third of the Hunter’s canal) results in nose with one forefinger and then with
upwards movement of the testicle. Children can another. Alternatively have him touch your
be put off by this reflex – so don’t venture to do finger (kept at a distance) and then his nose
this unless you suspect spinal cord lesions at the in a sequence. Instruct him to do so quickly.
level of L1 or L2. In cerebellar ataxia, the errors of movement
occur at right angles to the direction of
movement (Fig. 6.14).
Coordination
Coordination of a group of muscles involves
recruitment, interaction and cooperation among
the individual muscles (and also the cere-
bellum). Ataxia results from imperfect coordi-
nation and is defined as an abnormality of the
rate or extent of movement of muscles or muscle
groups. The following are important in defining
coordination:
1. Afferent impulses from muscle and joint Fig. 6.14: Finger-nose test
receptors. • Dysdiadochokinesia—Alternate supination
2. Cerebellar function—The cerebellum develops and pronation of the forearm as rapidly as
predominantly in the postnatal period and possible. In cerebellar incoordination,
full cerebellar activity may not be evident movements are clumsy and awkward (Fig.
until 9 to 10 years of age. You will not be able 6.15).
to say with certainty if a child who cannot Minor degrees of ataxia can be evidenced by
walk in tandem (heel to toe gait) at the age noticing clumsiness of movements like
of five has cerebellar dysfunction. The same buttoning up, tying shoelaces or dropping
applies for hopping on one foot before the objects from the hand. Dyspraxia is a term used
age of seven. These signs (soft neurological for minor degrees of motor incoordination and
signs) ought to be taken with the full picture is often present in children born prematurely.
in view, and you should not lay too much
on them alone. Lower Limbs
3. State of tone and power of the muscles— • Tandem gait—Show the child how to walk
Children with paresis find it difficult to along a straight line with the heel of one foot
coordinate. Make allowances also for the touching the toes of the other. It is a sensitive
child with hypertonicity leading to contrac- test for lower limb incoordination. Making
tures.
4. Vision—This in itself is not directly connec-
ted with maintenance of coordination but
sight is important to control and direct the
movements that constitute the motor act.
When there is loss of joint or position sense,
the child uses his/her eyes as a compen-
satory mechanism. Fig. 6.15: Dysdiadochokinesia
a child walk can actually bring out other • Romberg sign—It is a test for sensory ataxia
useful information. Not only will it test for and not cerebellar ataxia. We however use
ataxia and cerebellar function, but it may also the principles of this test to detect both when
amplify minor degrees of limb weakness. we make the child stand up to examine the
Children with minimal hemiplegia will be motor system. If a child cannot stand with
find it hard to do the test and may flex the his eyes open (and feet close together), then
elbows as an associated movement (Fog he has sensory ataxia. Closing his eyes will
sign). exaggerate the unsteadiness. With cerebellar
• Heel-knee test—Show the child how to lift one lesions, the child can be steady with his eyes
leg high in the air, to place the heel of this open but not when they are closed (Fig. 6.17).
leg on the opposite knee and then slide the
heel down the skin towards the ankle. Gait
Instruct him/her to do this on his/her own
Understanding gait is central to any effort to
and rapidly. The child with lower limb
examine the motor system. Gait tells us about
coordination problems will clearly find it
the aspects mentioned before—tone, power,
impossible to do the test without help (Fig.
coordination, and much more. If you have a
6.16).
careful eye, gait will guide you the source of the
problem. For example a child with an asymme-
tric gait make you worry about hemiplegia.
Ataxic gait should make you suspicious of
Friedreich ataxia.
Gait itself is a cycle and consists of events
occurring between heel strike on one side and
the subsequent heel strike on the same side. In
each cycle, the lower limb goes through 2 phases
—stance and swing. The stance phase occurs
Fig. 6.16: Heel-knee test between heel strike and toe-off, while the swing
Fig. 6.17: Romberg’s test

Neurology 127
phase is between toe-off and heel strike. To test Table 6.15: Causes of waddling gait
gait, have the child walk a few steps forward
• Bilateral dislocation of hips
(ask the mother at a distance to call her child,
• Duchenne muscular dystrophy
who walks up to her) and observe for the • Polymyositis
following: • Bilateral slipped epiphysis
a. Can the child walk at all? • Bilateral coxa vara
b. Is help needed? • Glycogen storage disease - acid maltase deficiency
• Achondroplasia
c. Does the child walk in a straight line or
• Morquio disease
waver to one side? • Progressive diaphyseal dysplasia
d. Look at the ankle, knee, hip and spine? • Myelodysplasia
e. Look also at the movement of the hands for • Exostrophy of bladder - separation of the pelvic bones
the period of the gait.
Here are some examples that you may come Ataxic gait: Walking with a wide-based gait in
across. staggering unsteady fashion: Guillain-Barre
Trendelenburg gait – In the stance phase, lateral syndrome, posterior fossa tumours, Friedreich
trunk bending toward the side bearing weight ataxia, and phenytoin toxicity.
suggests abductor weakness (gluteus medius In-toeing gait: Associated with metatarsus varus,
and minimus) of that side (Fig. 6.18). tibial torsion, femoral neck anteversion,
Posterior trunk bending: Gluteus maximus pronated feet.
paralysis. Limping gait: Trauma, fractures, thigh con-
Waddling gait: This is comparable to that of a tusions, improper fitting shoes, periostitis,
duck. The body is usually tilted backwards with Perthes’ disease, arthritis, slipped femoral
an increase in lumbar lordosis. The feet are epiphysis, transient synovitis of hip, leukaemia,
planted wide apart; the body sways from side osteosarcoma, leg length discrepancy, peri-
to side. As each step is taken, the heel and toe pheral neuropathy, spinal cord tumour,
are almost brought down simultaneously. This muscular dystrophy, cerebral palsy, appen-
disorder suggests proximal muscle weakness as dicitis.
in myopathies and muscular dystrophies. The
Toe-walking (equinus gait): Normal up to 3 years
causes of waddling gait are given in Table 6.15.
of age, and is often as a result of habit. More
serious causes need evaluation: cerebral palsy,
dislocation of hip, Duchenne muscular dys-
trophy, contracture of Achilles tendon, glycogen
storage disease (acid-maltase deficiency),
intraspinal tumours, filum terminale tumours.
Check if there are abnormalities in the anatomy
of the foot. Examination of the power and
reflexes will give you clues as to the exact
aetiology.
Sensation
It is often very difficult to examine the sensory
system in children partly because they cannot
cooperate and also because they are easily
Fig. 6.18: Trendelenburg’s sign distracted or fatigued. It may be necessary to test
on more than one occasion to avoid confusion. Normally 2 mm of separation of points can be
The following forms of sensation can be tested recognized as 2 separate stimuli on the finger-
(Table 6.16). tips. The separation is slightly wider on the
pulps of the toes. This test is useful in cases of
Test posterior column disease or parietal cortical
lesions.
It is better to start testing for touch and position
sense and later use a pin (if at all) when you have Position sense: This is essentially a posterior
gained the child’s confidence. Apply the sensory column sensation. Explain to the patient that
stimulus first to an area of impaired sensation you will move part of a finger (or toe, or elbow)
and then to the area of normal sensation (the up or down and that he must respond by telling
patient readily notes the change). Explain clearly you which way it had been moved.
to the child the procedure and instruct him/her Movement sense: The appreciation of movement
to close the eyes. Whilst applying your stimulus, is closely related to the sense of position. With
make sure that you test bilaterally. Ignore small the patient’s eyes closed, gradually move a digit
differences as they may seem to upset the or limb into a new position and ask him to
broader picture. Use some dummy tests (no respond as soon as the movement is perceived
stimulus applied) to test if the child’s responses (Fig. 6.19).
are genuine.
Recognition of size, shape, weight and form: In the
Light touch: Use a wisp of cotton wool (or the tip older child, have the eyes closed and place in
of the index finger) and touch over a certain his palm familiar objects such as coins, a pencil,
area. Ask the child to indicate if he/she felt and a marble. Ask him to identify the objects or
anything. Compare with other areas and the to describe their form. Loss of this faculty
opposite side if that felt any more or less than (astereognosis) occurs in parietal lesions.
normal. Areas of diminished sensation should Vibration sense: Place the foot of a vibrating
be marked out. Use a map for the dermatomes tuning fork (frequency 128 Hz) on a bony
of the skin. Instead of testing sensation on all prominence (e.g. the patella) and ask the child
areas represented by a certain dermatome, it is to comment on the feeling. He/she will
easier to test a certain predetermined part e.g. generally describe it as a buzzing feeling.
the tip of the thumb tests for C6, the tip of the Perception of the cessation of vibration is a more
middle finger for C7 and that of the little finger sensitive marker than perception of the
for C8. Device a way to test all the dermatomes presence. Put the base of the tuning fork on a
- be selective but not exhaustive (Figs 6.12A
and B).
The ability to discriminate between 2 points
is tested by the use of blunt dividers. Ask the
child whether one or both points can be felt.
Table 6.16: Sensory system examination
1. Tactile sensibility—light touch, pressure, tactile

localization, discrimination
2. Position sense—appreciation of passive movement
3. Recognition of size, shape, weight and form of
objects
4. Vibration
5. Pain
6. Temperature Fig. 6.19: Testing for joint sense
Neurology 129
bony prominence and ask the child to close his/ Spatial summation: In other types of parietal lobe
her eyes. Ask him/her when the buzzing stops. lesions, the child will perceive a stimulus only
Repeat the tests from distal to proximal joints, if an area of skin larger than a certain critical
bilaterally. Testing for vibration sense may have area is stimulated.
significance in posterior column lesions as in
Temporal summation: Here rapidly repeated
Friedreich ataxia (Fig. 6.20).
stimuli applied to the same point are perceived
Pain: Pain can be either superficial (skin, but not the application of a single stimulus.
subcutaneous tissue) or deep (muscles, bones).
For superficial pain a pin (the tip should be Agnosia: This is a term to denote a condition
reasonably blunt) can be used. For deep pain, arising out of higher perceptual defects. The
press the calf muscle or press over a bony child loses perception of part of his/her body
surface. Do not test for pain unnecessarily – you e.g., finger agnosia.
will appear intimidating in your examination Apraxia: The patient fails on constructional tests
(Figs 6.21A and B). like copying a map, a complex diagram or a
Temperature: You can test this with two test tubes human face. Constructional apraxia occurs in
– one containing warm and the other cold water. right parietal lesions, and is an early marker of
Ask the child to comment on the sensation hepatic encephalopathy.
perceived. In syringomyelia, temperature sense
is lost so that the child may get a burn without Neurodevelopmental Examination—
feeling it. Developmental Reflexes
Other disturbances of sensation: Sensory inatten- Please see Neonatal examination (Chapter 9).
tion/sensory extinction/sensory neglect – have
the child close his eyes and stimulate homo- Autonomic Function (Table 6.17)
logous points on opposite sides of the body by
These consist of sympathetic and para-
touch or pinprick. Ask the child to indicate
sympathetic systems with a small degree of
which side or sides are touched. In sensory
voluntary control. They are concerned with
inattention, the stimulus on the pathological side
modulating the functions of the cardiovascular
is not felt, though on separate testing, no
system, gastrointestinal system, temperature
difference can be elicited. Sensory inattention
regulation, pupillary and respiratory reflex
occurs chiefly with parietal lobe lesions.
control mechanisms.
Table 6.17: Autonomic function

1. Heart rate
2. Pupillary reflex
3. Micturition, defaecation – history of abnormality
4. Blood pressure – hypotension, transient rise
5. Sweating
6. Deglutition
7. Deep breath test
8. Orthostatic hypertension
The following are tested:

Deep breath test: Do this in the older child. With
the patient flat on the back, count the pulse rate
Fig. 6.20: Testing for vibration sense during maximal deep breaths. In normal
Fig. 6.21A: Sensory nerve distribution in front

Neurology 131
Fig. 6.21B: Sensory nerve distribution at back

subjects, the pulse rate should fall by more than Autonomic dysfunction: can occur as part of a
15 beats per minute. In autonomic dysfunction, bigger problem. Head injury and brain tumours
the pulse rate slows by less than 10 per minute. can present with such a picture. So also can
Orthostatic hypotension: Check resting blood spinal lesions like poliomyelitis or the Guillain-
pressure with the child initially lying down, then Barre syndrome. You should know that some
in the sitting and finally in the standing position. conditions are termed as autonomic neuro-
Note the blood pressure at one minute and three pathies—familial dysautonomia, Hirschsprung
minutes after standing. A systolic blood pressure disease and reflex sympathetic dystrophy.
drop of more than 10 mm Hg indicates auto-
nomic disturbance.
EXAMINATION OF THE
ENDOCRINOLOGICAL AND
METABOLIC SYSTEMS
The examination of the system is not a separate • Pain in the extremities, skin eruption around
entity, rather it incorporates parts from the umbilicus - Fabry disease
general survey and from each of the 4 major • Joint pain with swelling - Farber disease,
clinical systems—gastrointestinal, neurological, Mucolipidosis
cardiovascular and respiratory. It is therefore • Family history of early myocardial
essential to perform accurately the clinical infarction, pancreatitis - Lipid disorders
examination in the above system to form an (familial combined hyperlipidaemi, lipase
opinion of the endocrinological status of the deficiency)
child. • Abdominal pain, skin changes, psychiatric
manifestations - Porphyrias
HISTORY • Polyuria, Polydipsia - Insulin dependent
diabetes mellitus (IDDM), Hyperparathy-
• Poor weight gain, failure to suck, lethargy,
roidism, Compulsive water drinking,
convulsion without evidence of septicaemia
Diabetes inspidus
in the infant—metabolic dysfunction (urea
• Tremor, palpitation, neck swelling -
cycle defects, aminoacidopathies, organic
thyrotoxicosis
acidaemias, galactosaemia)
• Deteriorating scholastic performance, failure
• Abnormal body odour-Maples-syrup urine
to grow, excessively 'sleepy' - Juvenile
disease, isovaleric acidaemia
hypothyroidism
• Vomiting refusal to feed, dehydration and
• Obesity, hirsuitism - Cushing's syndrome,
skin manifestations—multiple carboxylase
Polycystic ovarian disease
deficiency
• Ambiguous genitalia - Congenital adrenal
• Seizures, enlarging head circumference—
hyperplasia, Maternal progestogen use,
Canavan disease, Alexander disease, Tay-
Maternal tumours, Defects of testosterone
Sachs disease
biosynthesis, Camptomelic dwarfism, Mixed
• Hypopigmentation, seizures, mental
gondal dysgenesis, Androgen insensitivity
retardaton—Phenyketonuria
syndromes
• Jaundice, irritability, vomiting - Galacto-
• Precocious puberty (Table 7.1).
saemia, Tyrosinosis Type I
• Tall stature, thin long hands and fingers,
INSPECTION
refractory errors—Marfan syndrome
homocystinuria Short stature—Measure accurately (see anthro-
• Abnormal startle response—Tay-Sachs pometry on page 140) (Table 7.2) for length, upper
disease segment, lower segment, span - height ratio.
• Strabismus, Trismus, Dorsiflexion of head- • Disproportionate short stature (abnormal
infantile Gaucher disease span - height and upper: lower body ratios)
Table 7.1: Common causes of precocious puberty Table 7.3: Common causes of delayed puberty
• Hypothalamic hamartomas • Constitutional delay of growth and puberty
• Post trauma, encephalitis • Gonadotropin deficiency
• Congenital adrenal hyperplasia • Space occupying lesion of the brain
• McCune Albright syndrome • Primary gonadal dysgenesis
• Adrenal tumours • Kallmann’s syndrome
• Ovarian tumours • Systemic illness
• Exogenous oestrogen/androgen • Proximal muscle weakness
Table 7.2: Common causes of short stature Table 7.4: Common causes of
proximal muscle weakness
Proportionate short Disproportionate short
stature stature • Cushing syndrome
• Glycogen storage disease
Constitutional delay of growth Rickets
• Hypokalaemic periodic paralysis
Hypothyroidism Skeletal dysplasia
• Kocher-Debré-Sémélaigne syndrome
Malnutrition Untreated congenital
Hypopituitarism IUGR baby hypothyroidism
Systemic illness • Coarse features—Hypothyroidism, Muco-
polysaccharidoses, mucolipidoses, GMI
- rickets, skeletal dysplasia, untreated gangliosidosis
congenital hypothyroidism • ‘Rosary’ at costochondral Junction—Rickets,
• Goitre—EU/Hypo/Hyperthyroid scurvy, chondrodystrophy.
• Needle marks - IDDM
• Moon facies, buffalo hump, central obesity— Examination
Cushing syndrome
Hypertension
• Male hypogonadism—Noonan, Kallmann’s
syndromes, XX, XYY males, X-linked • Cushing’s syndrome
congenital adrenal hyperplasia, Post- • Hyperparathyroidism
radiation • Phaeochromocytoma.
• Pigmentation, vitiligo—Addison’s disease
• Frontal bossing, small triangular facies, Hyperventilation
hemihypertrophy—Russell-Silver syndrome
• Organic acidaemias
• Tall stature—Cerebral gigantism, Sotos
• Diabetic ketoacidosis
syndrome, Klinefelter’s syndrome, Marshall
• Salicylate poisoning
and Weaver syndromes, XYY males, XXX
• Glycogen storage disease type 1
female, Marfan’s syndrome
• Subacute necrotizing encephalopathy
• Abnormal facies, hypertelorism, cleft
• Carnitine deficiency
palate— DiGeorge syndrome
• Tachycardia—Thyrotoxicosis, diabetic
• Doll facies—Glycogen storage disease type
ketosis, hypoglycaemia, Addison's disease
1, Hypopituitarism, Pseudoparathyroidism
• Warm flushed extremities—Thyrotoxicosis,
• Xanthelasma—Hyperlipidemia
hypoglycaemia.
• Late puberty (Table 7.3)
• Proximal muscle weakness (Table 7.4)
Ejection Systolic Murmur
• ‘Mongoloid’ appearance, high forehead,
hypoplastic supraorbital ridges - Zellweger’s • Williams syndrome (supravalvular aortic
syndrome. stenosis)
Examination of the Endocrinological and Metabolic Systems 135
• Noonan syndrome (Pulmonary stenosis) Hypotonia

• DiGeorge syndrome (conotruncal defects) • Canavan disease
• Thyrotoxicosis. • Tay-Sachs disease
Retinitis Pigmentosa Spasticity/Rigidity

• Late onset GMI gangliosidosis
Table 7.5: Important causes of retinitis pigmentosa
• Niemann-Pick disease
• Refsum syndrome • Neurogenic cretin
• Laurence-Moon-Bardet-Biedl syndrome
• Metachromatic leukodystrophy
• Hunter-Hurler syndrome
• Zellweger’s syndrome • Wilson disease
• Delayed tendon reflex—Hypothyroidism
Peripheral neuropathy • Visual field defect—Cranipharyngioma
• IDDM • Hepatomegaly - Glycogen storage diseae
• Metachromatic leukodystrophy types I, VI, IX, X.
Cherry Red Macula Hepatosplenomegaly
Table 7.6: Causes of cherry red spot in macula

• Glycogen storage disease types II, IV
• Gaucher disease
• Tay-Sachs disease
• Sandhoff’s disease • GMI gangliosidosis
• GMI Gangliosidosis • Rickets
• Mucolipidosis • Mucopolysaccharidoses
• Sialidosis • Mucolipidosis.
HAEMATOLOGY -
ONCOLOGY
Most components of examination of this system (quinine, primaquine, sulphamethoxazole),

have been discussed in the individual systems. naphthalene balls, graft versus host disease
Start by asking the relevant questions. Do a • Diarrhoea–post chemotherapy, gastro-
thorough general survey, with special emphasis enteritis, cryptosporidiosis
on pallor, lymph node examination, bleeding • Constipation–vincristine, mass effect
manifestations and swellings of any part of the • Blood in stool–hookworm induced iron
body. Look for central lines and old scars. Look deficiency anaemia, bleeding disorder
for the tell tale signs of drug side-effects – • Sore mouth–mucositis (dactinomycin,
alopecia, gum hyperplasia, obesity. Always bear anthracyclines), infectious mononucleosis,
in mind that the child with a cancer may be in herpetic gingivostomatitis
unbearable pain. Be sensitive to this and respect • Joint swelling–Haemophilia A or B, leu-
the parents’ feelings. This chapter provides a kaemia, osteosarcoma, Ewing’s sarcoma,
brief round up of the salient features you would synovial sarcoma, sickle cell disease
expect to see in a child with a malignancy or • Bleeding from umbilical cord–Factor XIII
haematological disorder. deficiency
• Epistaxis–von Willebrand disease, acute
HISTORY leukemia, juvenile angiofibroma, rhabdomy-
osarcoma
• Exercise intolerance–anaemia, leukaemia,
• Red urine–G6PD deficiency, Paroxysmal
solid cell tumour
Nocturnal haemoglobinuria, haemorrhagic
• Respiratory distress–mediastinal mass,
cystitis (cyclophosphamide, ifosfamide)
blood loss, gram-negative sepsis, Pneumo-
• Poor urine output–dehydration, tumour lysis
cystis carinii infection
syndrome, renal failure (nephrotoxic agents).
• Weight loss–malignancies, poor nutrition,
post chemotherapy
Examination
• Weight gain–steroid use in leukaemia/
lymphoma regimes, postoperative cranio- • Pallor–anaemia, sepsis
pharyngiomas • Cyanosis–methaemoglobinaemia, sulpha-
• Fever–pancytopaenia, leukaemia, febrile emoglobinaemia
neutropaenia, bacterial, viral and fungal • Swelling–superior vena cava syndrome, local
infections mass effects, inflammation, venous thrombo-
• Rash–leukaemia, immune thrombocyto- sis
paenia, herpes zoster, viral rash, HIV • Jaundice–haemolytic anaemias (Thala-
• Jaundice–glucose-6-phosphate dehydro- ssaemia major, autoimmune haemolytic
genase deficiency (G6PD) from drugs anaemia, G6PD deficiency)
• Bleeding into skin/mucous membranes –

Idiopathic thrombocytopaenic purpura
(ITP), acute leukaemias, disseminated
intravascular coagulation, scurvy, meningo-
coccaemia
• Erythema–radiation effects, red man
syndrome (vincristine), allergic reaction,
vasomotor response
• Eczema like rash–graft versus host disease,
radiation
• Vesicles–varicella, herpes zoster, extra-
vasation injury
• Hyperpigmentation–Fanconi anaemia,
dyskeratosis congenita, Leishmaniasis, post
chemotherapy pigmentation of skin, radia-
tion scars
• Bony tenderness–acute leukaemia, bone
marrow infiltration by lymphoma, scurvy,
extramedullary haematopoiesis
• Proptosis–retinoblastoma, rhabdomyo-
sarcoma, cavernous sinus thrombosis,
neuroblastoma, osteopetrosis
• Hepatomegaly–neuroblastoma, haemolytic
anaemia, hepatoblastoma, leukaemia, lym-
phoma, metastasis to liver Fig. 8.1: Huge splenomegaly
• Lymphadenopathy–leukaemia, lymphoma,
autoimmune diseases, infectious mono-
nucleosis, cat scratch disease • Abdominal mass–Wilm’s tumour, neuro-
• Patch over tonsils–acute leukaemia, infec- blastoma, lymphoma, ovarian cyst, rhabdo-
tious mononucleosis, agranulocytosis myosarcoma
• Splenomegaly–leukaemia, lymphoma, • Neurological dysfunction–brain tumours,
haemolytic anaemias, congenital hypoplastic neuroblastoma, raised intracranial tension,
anaemia, osteopetrosis (Fig. 8.1) haemophilia, leukaemia, vincristine.
NEONATAL EXAMINATION
Examining the neonate is different from the obstruction, duct dependent complex cardiac
child, but not necessarily more difficult. This malformations, convulsions, etc. The child may
chapter deals with the standard format of be ventilated on breathing on his/herself. The
examination, but you will find that you have to level of care required will depend on the severity
refer to the other systems for more clues. A lot of the illness. Your examination should take
of the examination hinges on whether the baby these factors into consideration. It is best to have
is “unwell.” Children in this age are very a problem list and address the issues in each.
susceptible to infection and therefore do think This enables you to cover all the problems from
of sepsis as a prime suspect. Newborns respond a diagnostic and management point of view
well to treatment, but only if instituted early on. (Table 9.2).
A baby with frank septicaemia in disseminated It is beyond the scope of the book to detail
intravascular coagulation is extremely difficult all aspects of neonatal care. We shall be limited
to salvage. Therefore, it is of paramount impor- to the basic ‘clinical’ examination of the
tance to look for early signs. With experience, newborn. The general system of examination is
you will develop a ‘nose’ for suspecting
problems, even when the baby seems to be Table 9.1: Checklist for the newborn
feeding and growing normally. • Date and time of examination
In your day to day practice, you will come • Age of the baby
across two broad types of babies - the apparently • Gestational age – dates, ultrasound examination, any
abnormalities
healthy baby on the postnatal ward who needs • Birth weight, length, and head circumference and
a first day examination or a discharge check and current anthropometry
the ill child in intensive care needing careful • Method of feeding
nursing support and monitoring. Although • Colour, perfusion, general well being
tedious and time consuming, you should aim • Scalp, hair, head shape
• Anterior fontanelle, posterior fontanelle
to get as much experience as possible in • Eyes – appearance, red reflex (ophthalmoscopy)
examining normal neonates. You will then be • Face, nose, ears, neck
able to contrast the normal from the subtly • Mouth – any clefts, other abnormalities
abnormal. It is helpful to have a ‘scheme’ of • Chest – respiration, chest wall, type of breathing
examination for each. Here is a typical checklist • Cardiovascular – femoral pulse, heart rate, rhythm,
murmurs
for the newborn in the postnatal ward (Table • Abdomen – appearance, organomegaly, feed tolerance,
9.1). meconium, urine, anal orifice, umbilicus, genitalia,
You will come across a range of conditions hernial sites
on the intensive care unit—prematurity, • Extremities – digits, symmetry, movement
respiratory distress syndrome, necrotising • Hips
• Behaviour, reflexes, ‘handling’
enterocolitis, perinatal asphyxia, intestinal
Neonatal Examination 139
Table 9.2: Problem list of early neonatal deaths? These can be

• Date and time of examination
from conditions like early septicaemia,
• Age of the child in days congenital adrenal hyperplasia, genetic
• Gestation of the baby, corrected gestation for age defects, transposition of great arteries and
• Birth weight, current weight, head circumference, rate hypoplastic left heart syndrome. It is
of weight gain, growth chart important that you remain vigilant of the
• List set of problems – most important first
• Overall progress in the last 24 hours
possibility of recurrence of the previous
• Ventilation – type, parameters, blood gases, surfactant, problem in the current pregnancy. Also
chest movement, breath sounds, work of breathing, note the Rh and blood group of the mother.
chest X-ray, drains, oxygenation index ii. Pre-pregnancy health state: Diabetes
• Cardiovascular system – heart rate, blood pressure, mellitus, smoking, hypertension, tuber-
inotropes, heart sounds, regularity, murmurs, femoral
pulse
culosis and anticonvulsant use are
• GI system – feed tolerance, aspirates, abdominal associated with adverse outcomes in the
distension, tenderness, umbilicus, organomegaly, baby.
genitalia, urine, stool, bowel sounds iii. Antenatal history: Ask about illnesses
• Neurology – ‘handling’, fontanelles, reflexes, behaviour, suggestive of the intrauterine infections—
cranial ultrasound examination, retinopathy of
prematurity screen, audiology screen
toxoplasma, cytomegalovirus and rubella
• Skin – colour, ulcers, breakdown, maturity (fever, rash, cervical lymphadenopathy).
• Infection – organism, sensitivities, antibiotics, blood Ask about the use of medication during the
markers duration of pregnancy. Drugs like valproic
• Fluids – intake and output acid, alcohol, diethylstilbestrol, phenytoin,
• Medication – drugs, doses, day of treatment, side
effects
oestrogen-progesterone combinations are
• Lines – peripheral, central, arterial catheters liable to cause congenital malformations.
• Investigation – glycaemia, blood counts, biochemistry, Platelet disorders arise from thiazides,
jaundice quinine and salicylates. Seizures may
• Parents – awareness, involvement, breast feeding result from drug withdrawal syndromes
• Vaccination status
• Home conditions, social environment
and accidental injection of local anaesthetic
into the fetal scalp. Deafness may be due
to quinine, streptomycin or chloroquin.
Enquire about maternal Grave’s disease as
not too different from the older child. The
antibodies may cross the placenta and
principles of examination are the same with
cause neonatal thyrotoxicosis.
some modifications and adaptations. Some
Ask the mother about the quality of foetal
aspects like neurology have a slightly different
movements, if she had fever and whether
approach— we shall make note of these changes.
there was meconium-stained liquor at
birth. Get information on the antenatal
HISTORY
ultrasound scans to assess the well being
Start at the antenatal period and the events of of the foetus. Was there any comment
pregnancy and labour. Detail the obstetric about a congenital anomaly like hydro-
history on the following aspects: cephalus, cleft palate, diaphragmatic
i. Previous obstetric history: Ask for the hernia or major cardiac anatomic malfor-
maternal age, consanguinity, abortions, mation? “Soft” signs on antenatal scans
still birth, marital status, parity, diabetes like that of a dilated pelvi-calyceal system
mellitus, syphilis, malnutrition, immuni- or left ventricular “pea” (associated with
sation status, birth weight, gestational age, Down syndrome) need to have follow-up
perinatal complications. Is there a history in the post-natal period.
Ask for rupture of membranes and It is best to document in detail the baby at
whether the baby was preterm. Check birth, at one minute, five minutes, ten minutes
whether there was prolonged rupture of and if necessary, at twenty and thirty minutes.
the membranes, instrumentation, emer- Your descriptions should cover the headings of
gency caesarean section and the use of respiration, heart rate, perfusion, colour, tone
anaesthetic agents (spinal or general). Was and movements. Write down resuscitation
there foetal distress before delivery? Were procedures—cardiac compressions, what
antenatal steroids prescribed in anticipa- volume of fluid bolus given, whether ventilated
tion of a premature delivery? Is there a hint and if epinephrine was used. What were the
that the mother had chorioamnionitis? oxygen saturations? Collate results including
iv. Events at delivery: Note whether baby cried blood gas (acidosis) and blood counts
at birth or suffered hypoxia. Check the (antepartum haemorrhage, septicaemia). This
notes for details of resuscitation. Note the will build up a composite picture of the exact
details of the Apgar score (at 1, 5, 10 and condition of the baby at birth.
20 minutes) – does it support a possibility v. Neonatal progress: Determine if the baby
of perinatal asphyxia? The score is given was roomed in or transferred to the
in Table 9.3. intensive care unit. Was the baby
ventilated? Did the baby need intensive
Table 9.3: Apgar score monitoring? Was the child fitting and put
on anticonvulsants? What were the events
Sign 0 1 2
in the first few days of life? It is important
Heart rate Absent Below 100 Over 100
to ask about neonatal care—ventilation,
Respiratory Absent Slow, Good, crying
cardiovascular status, bowel movements,
effort irregular
neurological progress, jaundice, glycaemic
Muscle tone Limp Some flexion Active
of extremities motion status, resuscitation, feeding and growth.
Response to Response Grimace Cough or Summarise your information and associate
catheter in sneeze this with your examination findings.
nostril
Colour Blue, Body pink, Completely Examination
pale extremities pink i. Anthropometry: Measure the weight,
blue length, chest and head circumferences
(Table 9.4). The head circumference is
The score is useful to assess hypoxia but you preferably measured a day after birth but
should not rely fully on this as false positives which time caput succadaneum will have
and false negatives can occur. A low Apgar score subsided. By this time there will also be
(less than 3 at 20 minutes) is associated with a less overriding of the cranial bones from
poor outcome but higher scores do not moulding at birth. Record the weight on a
necessarily indicate normal outcomes. Judge the growth chart at the appropriate gestation.
score in the context of the events at delivery. A Subsequent weight records should be
child may have low Apgar scores, but have a corrected for prematurity. For example if
perfectly normal outcome. Conversely, a baby the child was born at 28 weeks of gestation,
who suffered intrauterine anoxia and has low then you should allow for 12 weeks of
Apgar scores is likely to have some neurological correction every time you plot his/her
dysfunction. Events with poor outcomes are weight or height (till the age of 2 years).
prolonged resuscitation and the use of Babies over 38 weeks of gestation need not
epinephrine at delivery. have this correction.
Table 9.4: Anthropometry to be done in all newborns few years. Documentation of catch up is
• Weight
important – IUGR babies who are otherwise well
• Length but do not exhibit adequate catch up to the target
• Head circumference centiles need consideration of growth hormone
• Chest circumference treatment at 4 years of age.
It is now well established that infants born
Categorise the baby as large for date,
IUGR are more likely to develop cardiovascular
appropriate for date or small for date. A large
complications, type 2 diabetes mellitus and the
for gestational age (LGA) baby is one whose
insulin resistance (metabolic) syndrome in later
birth weight is more than the 90th centile for age
life if given energy dense calorie intake in the
(large parental build, infant of diabetic mother,
postnatal period. You may therefore want to
transposition of great arteries, Marshall, Sotos’,
Weaver-Bottom syndromes). An intrauterine outline the calorie and fat intake after birth as
growth retardation (IUGR) baby is one whose also the pattern of weight gain.
birth weight is less than the 10th centile for age ii. Assessment of gestation: Check the dates of
(malnutrition, intrauterine infections, smoking, the mother’s last menstrual cycle. This
genetic defects, multiple pregnancies, hyper- should give you an expected date of
tension, long standing diabetes, heart disease, delivery that you can use to calculate the
working mothers). The terms IUGR and small gestation of the child. Ultrasound exami-
for gestational age (SGA) are often used nation for gestational age is in some ways
interchangeably. Strictly speaking, a baby less a more reliable indicator. It is helpful to
than the 10th centile in weight (or length) should note the two readings if both are available.
be classified as SGA. An IUGR baby has You can also assess the gestational age by
decreasing growth velocity in the uterine period clinical examination. The Dubowitz,
but may not be less the 10th centile at birth, and Ballard and other scoring systems utilise
therefore not SGA. For example, a baby growing the assessment of certain external features
normally along the 90th centile may drop to the and neuromuscular maturity. When
25th centile over a period of 2 weeks when he/ ultrasound assessment of gestation is
she stopped growing in utero. Technically this available, such scores are more of academic
child is not SGA but is clearly a case of IUGR. interest. However, one should know the
Measuring the occipito-frontal circumference principles and application of such a
helps you determine if the IUGR neonate has scoring system for use in the event of a
“symmetric” or “asymmetric” growth retarda- conflict between the scan age and
tion. Those children on the lower centiles for gestational age calculated from the last
weight, length and head circumference are menstrual period (Figs 9.1A and B).
“symmetric” IUGRs. Genetic causes are Knowing the gestational age is crucial in very
predominant in such children and their catch premature babies. Infants less than 23 completed
up is generally less than expected. On the other weeks of gestation are below the limits of
hand poor placental nutrition in the late stages viability. Babies more than 26 weeks of gestation
of pregnancy is the chief cause of “asymmetric” have a particularly good chance of survival and
IUGR. to be free of neurodisability. The chances of the
It is useful to determine the infant’s length baby needing surfactant at or below the 28th
and the target centile based on the midparental week are high. Gestation becomes relatively less
heights. Children born IUGR demonstrate a important as the baby becomes more mature
catch-up height (and weight) gain over the first than 33-34 weeks of gestation.
Physical maturity Score
-1 0 1 2 3 4 5
Skin Sticky friable, Gelatinous red, Smooth, pink, Superficial Cracking, Parchment like Leathery,
transparent translucent visible veins peeling and/or pale areas, deep cracking, cracked,
rash, few veins rare veins no vessels wrinkled
Lanugo None Sparse Abundant Thinning Bald areas Mostly bald
Plantar surface Heel-toe < 50 mm, no Faint red mark Anterior Creases on Creases over
40-50 mm : 1 crease transverse anterior 2/3rd entire sole
< 40 mm : 2 crease only
Breast Imperceptible Barely perceptible Flat areola, Stripped areola, Raised areola, Full areola,
no bud 1-2 mm bud 3-4 mm bud 5-10 mm bud
Eyes/ears Lids fused Lids open, Slightly curved Well-curved Formed and Thick cartilage,
loosely (-1) pinna flat, pinna; soft, pinna, soft but firm, instant ear stiff
tightly (-2) stays folded slow recoil ready recoil recoil
Genitals male Scrotum flat, Scrotum empty, Testes in upper Testes descending, Testes down, Testes pendulous,
smooth faint rugae canal, rare rugae few rugae good ragae deep rugae
Genitals female Clitoris Prominent clitoris, Prominent clitoris, Majora and Majora large, Majora cover
prominent, small labia minora enlarging labia minora equally minora small clitoris and
labia flat minora prominent minora
Fig. 9.1A: Assessment of gestational age by new Ballard score

Fig. 9.1B: Assessment of gestational age by new Ballard score
iii. Systemic examination: b. Recognition of major malformations -

a. Signs of acute illness anencephaly, hydrocephalus, myelomen-
The signs of infection may be very subtle. ingocele, extrophy of bladder, cleft lip
The baby may just be feeding marginally and palate, imperforate anus, Amelia.
slowly. The nurses may have noticed c. General survey–This is done in the same
him/her to be quieter than usual. He/she way as for children, except for some
may not be waking up at the right time modifications. Make additional notes to
looking for food. If any suspicion, it is best record the activity of the neonate. Does
to insert a cannula, check the baby’s the baby appear to be unusually quiet?
bloods, obtain a blood culture and start Is there abnormal movement of the limbs
antibiotics. You should have a low thres- and mouth? Does the baby pacify with
hold to treating sepsis. If sepsis is breast-feeding? Does he/she appear to be
advanced you will find that the baby is irritable despite your best efforts? Tone
less responsive to pain (like a venous is another important marker of the
cannula), lethargic and has a poor cry. neurological state of the infant. It is best
There may be tachypnoea, jaundice, to assess tone when the baby is in
apnoeas and bradycardias. Check the ‘Brazelton’ stage 3 or 4. Brazelton
temperature – the baby may have hypo- described different ‘states’ in the neonate,
thermia (core temperature less than which are given in Table 9.5.
35.5ºC). In severe cases you will come
across convulsions, an increased bleeding Table 9.5: Stages of Brazelton’s neurological state
tendency and skin thickening (sclerema). State 1 : Deep sleep, regular breathing, no movements
The signs of infection are rather non- State 2 : Light sleep, irregular breathing, rapid eye
specific and therefore often difficult movements (eyes closed)
State 3 : Drowsy, eyes open or closed, some activity –
to differentiate from other conditions. smooth
Look for signs of respiratory distress State 4 : Alert, minimal motor activity, mildly fussing
(tachypnoea, grunting, recession), pallor State 5 : Eyes open, considerable motor activity
and cyanosis for clues relating to State 6 : Crying
cardiorespiratory problems. Is there
abdominal distension suggesting ileus or Hypertonia (or hypotonia) signifies
intestinal obstruction? Have there been brain injury. This may be due to hypoxic
convulsions suggestive of intraventri- insult, intraventricular haemorrhage,
cular bleeds, meningitis or metabolic hypoglycaemia, hypocalcaemia, mito-
disturbance? chondrial defects, meningitis or meta-
Neonatal units have a low threshold bolic dysfunction.
for treating infections and you should d. Regional examination: Examine the
commence antibiotics pending the results different regions of the body, much like
of the sample for culture. You should that outlined in general survey for older
keep a record of how the child improves children. Some aspects are unique to
when treated. Hypoplastic left heart newborns and need to be addressed
syndrome and some of the metabolic differently. Asymmetry of the skull and
syndromes masquerade as septicaemia. overlapping of cranial bones at the
Be prepared to think laterally about these sutures are present shortly after birth.
conditions if the baby deteriorates inspite ‘Caput succedaneum’ overlies the
of treatment. presenting part of the head as a soft, non-
fluctuant oedematous swelling of the abdominal distension, umbilicus, peri-

scalp, the edge of which is ill defined. umbilical cellulitis, ambiguous genitalia,
‘Cephalohaematoma’ is characterised by perineal defects, hernia.
fluctuant swelling with clearly defined h. Neurodevelopmental examination –
edges that do not cross suture lines developmental reflexes
(except multiple cephalohaematomas or It is postulated that the child goes
subgaleal haematoma). Examine the through a process of developmental
scalp, fontanelles, head size, ears, eyes, maturation of the nervous system. The
face, nose, mouth and pharynx. child acquires and loses certain reflexes
Come down to the neck and search for (primitive reflexes) en route to the fully
swellings, fistula, neck size, intertrigo or functioning neurological state. Multiple
pustular melanosis. Next examine the centres in the brain and spinal cord are
chest starting from the clavicle (fracture responsible for posture and balance. They
in shoulder dystocia) downward. help the child progress to the charac-
Examine for asymmetry, movement, teristic human form of bipedal walking.
accessory nipples, apex beat and heart Normally at birth, spinal cord reflexes are
sounds. Examine the limbs for deformity, present and disappear within one or two
fractures, and movement. Palpate the weeks. Brain stem reflexes start appear-
abdomen for lumps and organomegaly. ing at about the second week of life and
Note if there is distension (intestinal should disappear by the 6th month.
obstruction, necrotising enterocolitis) or Midbrain reflexes start appearing at
tenderness. The liver is normally palpable about the 4th month but become
3 cm below the costal arch. The spleen tip suppressed by cortical influences after
and lower pole of left kidney may just be two years of age.
palpable. Examine the genitalia, look for It is often useful to have a practice of
hernial sites (common in preterm infants) the normal neurodevelopmental state in
and listen to bowel sounds. an infant. There are some postures and
Turn the baby prone to examine the reflexes that are normal for a certain age
back. Look for spinal defects (spina and not for others. Persistence of reflexes
bifida) at sites marked by a hollow in the beyond the normal time for disappea-
lumbosacral region. Check anal sphincter rance should make you worry about
tone and reaction. Check the skin in all brain damage in utero or in early life, as
regions for erythema toxicum, pustules, in cerebral palsy. Conversely the absence
bullae, melanocytic naevi, capillary of reflexes can imply states of hypotonia,
haemangioma and Mongolian spots. sensory dysfunction or motor paralysis.
e. Cardiovascular system: Count heart rate,
assess rhythm disturbances, check situs,
Test
femoral pulses, blood pressure, murmurs,
cyanosis, heart failure. It is good practice to comment on the attitude
f. Respiratory system: Observe for signs of of the child before rushing in to examine the
distress (tachypnoea, grunting, chest child. If you stand back and look you may pick
retraction), desaturation (drops in up vital clues. For example, the hypotonic infant
oximetry readings), chest transillumi- may be lying placidly on his back without
nation and adventitious sounds. making any movements. The spastic child with
g. Gastrointestinal system: Look for vomit- limb contractures may find it difficult to lie flat
ing, stools, feeding, sucking, swallowing, on a bed. Note the position of the limbs whilst
at rest and in motion. The hemiplegic child will order is given below, but it is best to leave the
display an asymmetry of one side. A good Moro and parachute reflexes till the very end as
neurodevelopmental examination will also take it may upset the child.
into account the child’s responses to you and the 1. Sucking and rooting: Birth to 4 months,
environmental stimuli. The child with until 6 months when asleep
nystagmus and looking ‘past’ you has visual 2. Palmar grasp: Birth until 3 months
cortical impairment. Do not ignore the padded 3. Flexor withdrawal: Keep the child in the
bed and the wheel chair. They speak volumes supine position with head in the midline
of the child’s inability to sit up or stand erect. and legs in extension. Pinch the sole of the
In the younger child (less than six months) foot – there should be slow response of the
you can do the ‘180 degree examination.’ The foot with uncontrolled flexion of the knee.
infant must be lying on a flat surface to start Persistence of this reflex beyond 2 months
with. Note the posture of the child and the way is abnormal. Do not confuse this reflex
that he/she lies on the bed. Is the face turned to with the brisk avoidance response seen in
one side with arm and leg extended on that side older children.
(the asymmetric tonic neck reflex)? Is there 4. Extensor thrust: One foot should be flexed
abnormal posturing as in chorea or athetosis? in the supine position. Pinch the sole of the
Next, draw the child into the sitting position,
flexed leg. There should be slow extension
by pulling on his/her arms. Note the degree of
(without attempting to kick the stimulus
head control or head lag. When the child has
away) in children up to 2 months of age.
been brought to the sitting position, note if there
5. Placing, stepping: Birth until 6 weeks –
is head and trunk control. Can the child sit
hold up the infant and place the plantar
unsupported? Next, hold up the child to check
aspect of the feet on a firm surface
weight bearing. This may bring out lower limb
scissoring (spastic diplegia) or help detect lower (stepping) when the feet are lifted up.
limb hypotonia (neuromuscular disorders). Touching the dorsum with an object also
Now, hold the child in the ventral suspension evokes a similar response.
(if the weight permits) and describe the position 6. Landau reflex: Hold the child in the prone
of the head, trunk and limbs. A hypotonic child position with your hand under the tummy.
may demonstrate a ‘C’ curve over your hand. The child should normally extend the
Conversely, the child with cerebral palsy may head, trunk and hips. Next flex the head
have an exaggerated extensor posture. Finally and neck—the response is flexion of the
lay the child prone. Put the child’s hands on trunk and hips. The first stage is from 4
either side of the shoulders with palms apposed months of age and the second stage is from
to the bed and elbows slightly flexed. Note the 9 months onwards. The reflex should be
ability of the child to raise the head and trunk gone by 2 years.
when prone. 7. Asymmetric tonic neck reflex (ATNR):
You can now check the primitive reflexes With the child in the supine position, rotate
(Figs 9.2A to I). These reflexes are important the head to one side. A ‘fencing’ posture
when trying to ascertain the neurodevelop- results. There is extension of the ipsilateral
mental age of the child. Their persistence or upper and lower limbs and contralateral
absence (allowing for a spectrum of normality) flexion. This reflex is said to be present
can tell you at what age the child functions. You normally between 2 and 6 months of age.
do not have to be exhaustive in testing the Persistence beyond the age of 6 months
primitive reflexes, but it is worthwhile to know may be indicative of upper motor neuron
a few, along with their chronology. A suggested lesions.
Fig. 9.2A: Sucking reflex Fig. 9.2B: Rooting reflex
Fig. 9.2C: Moro reflex Fig. 9.2D: Moro reflex

(viewed from side) (viewed from foot end)
Fig. 9.2E: Palmar grasp Fig. 9.2F: Symmetric tonic neck reflex
Fig. 9.2G: ATNR Fig. 9.2H: Gallant reflex
Fig. 9.2I: Crossed extensor reflex
Figs 9.2A to I: Neonatal reflexes
8. Symmetric tonic neck reflex: Support the suggestive of bearing weight. This reaction
child prone on your thigh whilst you are is present at birth and disappears by 3
seated on a chair. Flex the neck downward months. It later reappears at 6 months in
– the arms should flex and the legs should preparation for the child to walk around the
extend. Conversely when the neck is age of a year. Increased plantar flexion and
extended, the reverse happens. The adductor tone is abnormal (after 4 months)
response should normally disappear after and suggestive of lower limb spasticity.
6 months of age. 10. Negative supporting reaction: Try the
9. Positive supporting reaction: Pick up the same maneuver as above, but this time,
child by holding under the axillae and hoist him up into space. The child has
bounce his feet several times. When the feet increased flexion tone in the legs with
now touch the floor gently, there should be flexion at the knees. This reflex should
increased extensor tone in the legs, disappear after 4 months.
11. Neck righting reflex: Rotate the head to one Examine for possible deficits in the cranial
side and you will notice the trunk nerves. Test vision using a brightly coloured
following suit. This is normally present object (red wool). The examiner’s face may itself
between 6 months and 2 years. serve the purpose. The neonate fixes the object
12. Moro reflex: Birth to 4 Months – support of interest, in its line of vision. Note that visual
the child in the semi-sitting position and acuity at birth is 3/60, at 3 months is 6/60 and
suddenly drop the head and upper part of 12 months of age is 6/18.
the body (make sure your hands are Assess the third nerve by observing the
beneath to catch the fall). There will be pupillary reflex (present at 28-30 weeks of
sudden extension of the shoulders quickly gestation). The doll’s eye movement tests for
followed by flexion at the shoulder and ocular palsy. Tapping the nasion leads to closure
elbow in an embrace like movement. The of the eyes (5th and 7th nerves) and evaluates
fingers open during the reflex and also movements of the upper face. The rooting reflex
there is change of facial expression (watch gives information about the lower face. Look for
for this in hemiplegia). deviation of the angle of the mouth during
13. Parachute reflex: Hold the infant in the crying in a facial palsy. Clinical examination of
prone position with your hand under the hearing is not reliable. Watch the baby for a
tummy. Move the child, face downward startle response, blinking of the eyes and sudden
towards the floor. The child will extend changes in alertness at a noise. A negative
both upper limbs, as if to break the fall. The response does not automatically mean that the
reflex appears between 6 and 12 months child is deaf, as many other variables modify the
and persists. Absence of parachute reflex auditory response.
is abnormal, as is asymmetry (hemiplegia). Observe for nasal regurgitation and any
Neurological system: Examine the anterior abnormalities in sucking and swallowing.
fontanelle, head circumference, dysmor- Asymmetry of the tongue may be due to 12th
phic features, and abnormal movements. cranial nerve lesions.
The position of the child when lying on the To examine the motor system, start by
bed may provide clues to the underlying observing the normal range of spontaneous
diagnosis. For example, the hypotonic movements. Does the baby move both arms
neonate lies in a “pithed frog” position. spontaneously? There may be asymmetry on
Assess how the baby ‘handles.’ The child one side with an Erb’s palsy. Look at the posture
with clavicular fracture may be reluctant of the baby (elbows, hips, knees flexed) to have
to move the arm on that side. Does he/she an idea of the tone. In the lower limb, test for
desaturate or appear fretful whilst being the popliteal angle; in the upper limb test the
examined? Does he/she not respond, as ‘scarf’ sign. Use grading for post-asphyxial
you would expect for a baby of that encephalopathy as follows (Table 9.6).
gestation? Is there any abnormality on the Elicit deep tendon reflexes by tapping gently
recent cranial ultrasound examination? Is with a patellar hammer. It is sometimes easier
the baby encephalopathic? This may be to use the index finger for the knee and ankle
difficult to define especially in the context reflexes. In states of cerebral insult they appear
of mechanical ventilation and sedation brisk. Persistence of certain primitive reflexes
with morphine. In general, does the baby may be suggestive of neuronal insult. You
show any response to stimuli? Is this should be able to demonstrate asymmetry and
associated with abnormal movements and abnormal response, reflecting on neuromuscular
altered tone? Babies in stage 1 hypoxic immaturity. Here are some examples:
ischaemic encephalopathy have a ‘staring’ Asymmetric Moro–Brachial plexus injury
look. Depressed Moro–Cerebral ischaemia
Table 9.6: Clinical features for grading post-asphyxial encephalopathy

Mild Moderate Severe
Irritability Lethargy Coma
Hyperalert Seizures Prolonged seizures
Normal tone Differential tone:egs > arm, Severe hypotonia
neck extensors > flexors
Weak suck Poor suck, requires tube feeds No sucking reflex
Sympathetic dominance Parasympathetic dominance Coma, requires respiratory support
Incomplete Moro–Preterm less than 35 weeks of recommended. This applies for the other sensory
gestation examinations as well. However, in neural tube
Exaggerated startle–Tay-Sachs disease defects it is important to test the anal reflex as
Persistent palmar, plantar grasp–Cerebral palsy sphincter involvement denotes a poorer
Sensory testing, as part of the neurological prognosis.
examination, is of limited value in neonates. i. Hips: Use Barlow’s modification of
Nevertheless one must remember that neonates, Ortolani’s maneuver to identify dislocated
no matter how premature, are perfectly capable and dislocatable hips. Undress the baby
of feeling pain, but the response is not always and place him/her in the supine
consistently reproducible. Pain may be assessed position(Figs 9.3A and B). Steady the
by observing the behavioural response of the infant’s pelvis between the thumb resting
baby. The newborn in pain appears irritable and on the symphysis pubis and fingers under
unsettled. He or she may be desaturating more the sacrum. Use the other hand to test for
frequently than usual. Assessment of pain is dislocation. Alternatively, both hips can be
very subjective and cannot be relied upon. tested at the same time. Take a grip over
Routine testing for pain is, therefore, not the flexed hip with the thumb over the
femoral triangle and the middle finger
behind over the greater trochanter. Try to
bring the flexed thigh to the position of
mid-abduction. In congenital dislocation of
the hip, there is limitation of abduction to
that side. In the hip that can be brought to
Fig. 9.3A: Barlow’s maneuver for examination of hip Fig. 9.3B: Ortolani maneuver for examination of hip
mid-abduction, press over the greater • Pustular melanosis—Small benign

trochanter in a forward direction with the pustular lesions predominantly in many
middle finger. If a ‘clunk’ results with ethnic communities on the chin, neck,
movement of the femoral head anteriorly, back, extremities, palms and soles, and
then obviously the hip was already lasts typically 2-3 days
‘dislocated’ before pressure was applied. • Subconjunctival haemorrhage/retinal
If the above section of the test is haemorrhage—Normal variant
negative, then proceed to the next step. • Corneal size—Diameter more than 1 cm
Press gently with the thumb over the suggests congenital glaucoma
medial aspect of the thigh. If a ‘clunk’ • Erythema toxicum—Firm, yellow-white
results with the femoral head moving out papules or pustules with surrounding
of the acetabulum (and going back when erythematous flare (or occasionally only
the pressure is released), the hip is areas of blotchy erythema), sparing
probably ‘unstable.’ palms and soles, with peak incidence on
Some signs of minor significance: the 2nd day of life in normal newborns
• Jittery (metronomic movements with • Salmon patch—small, symmetric, pale,
equal amplitude, stops when part of limb pink, flat lesions of vascular ectasia on
is held)—Normal newborn, hypo- glabella, eyelids, upper lip, neck region,
glycaemia, hypocalcaemia prominent on crying and ultimately
• Pedal oedema—Prematurity, Turner fading away over a period of time
syndrome • Port wine stain (naevus flammeus)—
• Oedema of eyelids—Chemical irritation Unilateral, permanent, sharply circum-
by antiseptic scribed pink to purple lesions in head and
• Acrocyanosis—Normal in newborns neck region due to mature dilated dermal
• Harlequin colour change (division of the capillaries
body from forehead to pubis into red and • Capillary haemangioma (strawberry
pale halves)—A transient, harmless naevus)—Bright-red protuberant, com-
condition pressible, sharply demarcated lesions
• Lanugo hair—Fine, soft, immature hairs heralded by an erythematous mark or
over scalp and brow occur in the preterm area of pallor which develops into a area
infant and are replaced by vellus hair in of fine telangiectasia before undergoing
the term infant expansion.
ASSESSMENT OF
CHILD BEHAVIOUR
No assessment of a child is complete without a Table 10.1: Questionnaire interaction

behavioural and developmental assessment, the with environment
development of an infant and child has been • Is this a wanted child?
outlined in the chapter of history taking, • Is there marital discord or separation?
Chapter 1. Different scales are available to • Any parental experimental disruptions?
• Socioeconomic situation pressing?
quantify the defect (Denver developmental
• Abnormal health in antenatal period?
screening test, Baroda scales, Trivandrum • Prolonged maternal depression related to
development screening chart, etc.) and one may pregnancy?
proceed to use these screening tests to assess the • How she sees herself in mothering?
behavioural aspect or proceed to more • How helpful is the father in running the household?
• Does the mother work?
sophisticated scales (Rutter scales).
• If so who looks after the child?
• Father out of job?
HISTORY • Is he ill tempered, alcoholic?
• Any complaints of the child at school?
History is taken of the child’s problem and the • What do the parents think is wrong with the child?
interplay of the environment in shaping the • What do they expect to be done by the paediatrician?
child’s outcome and prognosis. Ask general and
informal questions like ‘what does he enjoy Table 10.2: Emotional development
playing with?’, ‘Does he play with his friends’?, Period of life Core problem being mastered
‘Can he tell a story’? to get an idea of the
Infancy Trust – Mistrust
developmental level. The current level of Toddler Autonomy – Shame
functioning is assessed under areas of play, Preschool Initiative – Guilt
language comprehension and expression, gross School Industry – Inferiority
motor, social skills and behaviour. Do not rely Adolescence Identity – Identify diffusion
on the parent’s interpretations as they may be
Behaviour
incorrect (e.g. reply to the question ‘can he
understand what you tell thy baby?’ is ‘He The core problem in each period of development
understands everything’). correlates with the major developmental task set
Ask the following questions (discreetly) to for that period.
obtain information about the environment in
Trust-Mistrust: In infancy the child is entirely
Table 10.1.
dependent on the mother. He needs a sense of
security and how secure he feels depends on
Emotional Development
how effective is the security provided by the
Erikson divided the emotional development of mother. He needs to develop his sense of trust
a child as shown in Table 10.2. before he can emotionally venture on his own.
Assessment of Child Behaviour 153
Autonomy-Shame: This equivalent of the A child with autism will not interact socially
Freudian Anal Stage is characterised by his or verbally with the examiner and hide in a shell
control of bowel and bladder functions, giving of his own, oblivious of the world round him. A
the child more independence. The negative child with attention deficit disorder cannot sit
feeling at this stage is ‘Shame’. still but is always impulsive and jumping at
Initiative-Guilt: As the child explores new objects things. A child with a physical handicap has
and activities, he also comes into contact with more ‘inferior’ feelings resulting in poorer
other children. The interaction gives vent to a performance.
sense of competition and resulting frustration
and guilt feeling. Cognitive Development
Industry-Inferiority: In the school years, he has It is important to have an idea of the cognition
considerable physical and mental energy in a child who may be physically normal but
(industry) he uses his newly acquired skills in parents are worried about unnatural or
all games and physical exercises. However, unseeming behaviour or deteriorating scholastic
though he believes he can be ‘a jack of all trades’ performance. Like Erikson, Plaget has devised
he fails in some and there develops the fear of a scheme development of intellectual function
failure (inferiority) he has to develop a sense of as given in Table 10.3.
pride in his industry without feeling inferior to
his peers. Table 10.3: Cognitive development stages
Identity-Identify diffusion: In adolescence, this is Period of Life Type

the biggest crisis with the child confused as to Infancy Sensory motor
his true worth. The parents want him timid and Toddler Sensory motor
Preschool Preoperational
docile, his peers would like him to be aggressive
School Concrete operations
and non-conformatory. Adolescent Formal operaitons
Each age has its own problems. Understand-
ing the core problems for each age period makes
Behaviour
it possible for the clinician to guide children and
parents appropriately. For example, in a child Sensor motor stages: In the first few years the child
of 3-6 years age, his problem is initiative versus is exposed to a world of different sights, sounds
guilt. At this time a marital discord makes the and experiences. Every day he stores new
child feels ‘guilty’ for the problem and thus he information through his sensory system
suffers an emotional setback. (explores own body, leaves mother to explore
If there is a crisis during a period the child the surrounding) as also he trains his motor
may not master the problem and get ‘stuck’ at system to help him gather the information for
that level (emotional developmental delay). The his senses.
paediatrician should be aware of these problems
and carefully observe the baby for: Preoperational: In this stage of pre-logical ideas,
• Contendedness the child is dominated by magical thinking,
• Interaction with mother egocentrism and thinking governed by
• Play with peers perception. Magical thinking is the thought of
• Activity unrealistic causation (e.g. power of wish turning
• Conversation true). Egocentrism is the inability to take
• Confidence another’s viewpoint.
Concrete operations: The pre-logical stage give Brainstorming skills – Original ideas to write a
way to the stage where logic and reason exert topic imaginatively.
sway over preconceived ideas. Critical thinking – Ability to compare and
contrast different views.
Formal operations: Upto the above stage the child
had to be dependent on someone else’s ideas, Metacognitive abilities – Refers to his capacity to
now he comes of his own and has the capacity think about thinking (whether the thinking is
to generate abstractions. Though there is no right or how to correct learning strategy).
structural change in the brain, cognitive process- Table 10.4: Common age related
ing has speeded up to include quantitative behavioural disorders
increases in knowledge, experience and Age Disorder
efficiency.
Infant and Toddler Feeding problem, 3 months colic,
Like the Eriksonian stages, these stages are stranger anxiety, breath holding spell,
important to understand the age differences in temper tantrum
cognition. A neurological insult to the deve- Preschool Head banging, body rocking, thumb-
loping brain may result in cerebral palsy with sucking, nail biting, masturbation
School Stuttering, pica, enuresis, encopresis
mental retardation. Repeated convulsions with Adolescence Juvenile delinquency, homosexuality
neuronal cell may cause a child to fare badly in
class. Observe the child carefully, talk to him to Behaviour Problems
know his viewpoints, tell him a story and see
A child often presents with behaviour problems
how he interacts, give him a riddle and see how
which are largely ignored in a bid to establish
he can solve it. To assess higher order cognition
organic origins for the complaint. Habit
the following parameters are used:
disorders, problems of eating, speech, sleep,
Concepts – His grasp of understanding the scholastic deterioration, sexual problems,
central point. antisocial activities are quite common in our
society and it is primarily the paediatrician’s
Problem solving skills – His ability in formulating responsibility to be alert to them. A list of
techniques. To meet a challenge and find out the common age-related behaviour problems is
best solution. given in Table 10.4.
PSYCHOLOGICAL
ASSESSMENT
ASSESSMENT: A DEFINITION However, studies indicate that psychological

problems in paediatric care are under-identified
Sundberg and Tyler (1962) defined assessment
(Costello, et al 1988, Brown, et al 2002).
as the process of bringing together relevant
Described below are the barriers to effective
information from a variety of sources, i.e. the
assessment.
systematic collection, organisation and inter-
• Inadequate training programme: Training
pretation of information about a person and his/
programmes do not provide specific
her situations that may be used for predicting
education, knowledge, training and skills to
his/her behaviour.
address psychosocial disturbance in patients.
• Time and financial pressures: The average visit
WHY ASSESS PSYCHOLOGICAL
is less than 15 minutes, barely enough time
FACTORS?
to assess and manage physical needs. The
In the holistic management of a child, financial pressures restrict their ability to
assessment of psychological factors is essential. devote sufficient efforts towards assessment
This is because: and management of patents psychological
• Illness (chronic as well as acute) have a functioning (American Academy of Paedia-
profound effect on the social, emotional, trics, 2002).
behavioural and academic functioning of the • Frequently, incorporation of mental health
child. issues is seen as a paradigm shift.
• Psychological factors (smoking, lack of • Resistance: Often paediatricians feel that
exercise, substance abuse, treatment non- patients would resist addressing psycho-
adherence) can be a major contributor to an logical issues and thus pediatricians are
illness, in terms of onset, maintenance and hesitant in inquiring about the child’s
treatment (Brown et al, 2002). behaviour, development and family
• Further psychological factors can interfere functioning (Perrin, et al 1999).
with procedures and complicate history- • Nondisclosure on patients/parents part: Often
making and symptom assessment. parents do not report psychological concerns
• In spite of the advancement in the medical due to stigma attached.
field, the inner world of children remains Considering the above-mentioned points, the
essentially unchanged (Rauch and Jellinek, present chapter is an attempt to provide an
2002). overview of psychological assessment with
Often paediatricians are considered as the children. The description of detailed clinical
ideal professionals to screen for psychological conditions and interventions is beyond the scope
disorders (Simonian and Tarnowski, 2001). of the present work.
This chapter outlines the role of psycho- be brief or chronic. The stressors or psychological
logical assessment under two categories: concerns commonly faced (and that should be
1. As part of medical conditions assessed) are highlighted in Table 11.1. The
2. Psychological assessment in general. stressors have been classified under three
categories, i.e. from the perspective of the child,
AS PART OF MEDICAL CONDITIONS the parents and the treating team. In cases where
Each medical condition carries its own unique the stressor is specific to a given condition, the
specific challenges. The stressors examined can same have been highlighted in brackets.
Table 11.1: Psychological concerns that need to be assessed

Child Parents Treating team
• Anxiety, Fear • Disruption of family routine and • A high stress environment
• Low mood, feeling sad lifestyle (e.g., absenteeism from • Long working hours
• Non-adherence/non- work, less time for each other) • Conflicts with other team
compliance • Coping with new anxiety- members (nurses, seniors/
• Frequent medical visits/ provoking information juniors)
Hospitalisation • Conflicting information by • Sense of helplessness
• Painful procedures different team members • Burn out
• Physical disability • Anger/Blame
• ↓Physical/exercise endurance • Uncertainty
(e.g., cystic fibrosis) • Guilt (e.g., passing defective
• Fear of death (e.g., Cancer, HIV) genes)
• Interruption of school and play • Emotional burst out
activities • Burnt out
• Monitoring symptoms (e.g., • Managing mealtime and
Glucose levels as in diabetes) medicines
• Adverse effects of medicines • Financial strain
• Change in lifestyle, eating
habits (e.g. Cancer, diabetes)
• Appear different from others
• Disclosure of diagnosis to peers
• Diminished self-esteem
• Decline in cognitive functions
(e.g. intelligence, concen-
tration, memory; in epilepsy,
cancer)
• Night awakening (e.g., asthma)
• Social isolation and rejection
• Compromised Quality of
Life (QOL)
• Unpredictable course of illness/
prognosis
• Stigma (e.g., cancer, HIV)
• Intense time consuming
medical regimen
While dealing with chronic illnesses, a age to adolescence. Psychological assessment is

developmental approach can be useful. It essential to help children cope with chronic
emphasises how psychosocial challenges and medical illness or painful procedures, as per
adjustment change from the preschool to school their developmental age.
Psychological Assessment 157
It is important to keep in mind that children • Children are less able to separate pain from
with chronic conditions may not have major emotions such as fear.
psychiatric disturbance but are at an increased • Children have fewer painful experiences
risk for psychological adjustment problems with which to compare the current event.
(Wallander, Thompson and Alriksoon-Schmidt, The commonly used assessment measures
2003). comprise of:
The following aspects although time a. Child Self-report and
consuming, are yet worth exploring: b. Observational methods.
• What is the hardest aspect of the illness from
the child's perspective? Child Self-Report
• How does it affect the child's image of him
or herself now and how has it changed? Visual analogue scale are the most common
• Does the child have worries about the future? forms of child pain intensity assessment. These
• How do the illness and treatment impact on scales involve the graphic representations of
peer relations and favourite activities? pain intensity by marking a point on a line and
• When and how does the child tell others can be used with children as young as 5-year-
about the illness and why? old (Dahlquist, 1990). Face Scales are also used
• Are there areas of conflicts between the child which consist of a set of line drawings or
and the parent or the child and the photographs of faces that depict pain states
physician? (Chambers, Giesbrecht, Craig, Bennett, and
• What are the child's perceptions of the Huntsman, 1999). Structured interviews with
parents' worries? (Rauch and Jellinek, 2002). children and their parents are commonly used
The author is well aware the sometimes, to assess the historial and contextual variables
despite the best intentions the paediatrician is contributing to pain experiences (Allen and
unable to assess these aspects in detail (due to Matthews, 1998).
various constraints). A well-trained Paediatric
Psychologist (as in West) or a Clinical psycho- Observational Methods
logist (as in India) can effectively assess these
aspects and his/her services should be availed Some researchers argue that behavioural
to provide holistic care to the child. observations are more reliable and valid than
In context of medical conditions, pain is one self-report measures because they are objective
of the most commonly assessed variables. It is in nature, recording the presence or absence of
challenging to measure pain due to its subjective discrete pain behaviours (Mcgrath, 1987).
nature and the important roles played by However, the behavioural observations capture
cognitive and emotional factors. With children only the overt expression of pain. Once can
the assessment of pain becomes even more observe for specific pain behaviours such as
difficult because of the following factors: limping, grimacing, sighing. It is also important
• Limited vocabulary to describe pain. to observe how the parents respond to child’s
• Pain scales require children to discriminate pain (e.g. ignore the pain, over-concerned,
constructs (e.g., intensity and duration) that minimise the pain by considering it as feigning,
may be sophisticated for their cognitive a ‘drama’, too critical/hostile).
development. To summarise, the choice of specific measure
• Further, in comparison to adults, children are should be determined by the child's develop-
less accurate in their estimates of pain; more mental level, the setting and whether the
susceptible to situational demands. assessment is for research or clinical purpose.
PSYCHOLOGICAL ASSESSMENT • Helps to build an aetiological hypothesis

IN GENERAL • Estimate the potential of the child and
The psychological concerns in children have • Provides information on child's assets and
broadly been classified under two domains: limitations.
Internalising and Externalising disorders
Assessment for Children: How is it
(Achenbach and Edelbrock, 1991). The interna-
Different from Adult Assessment?
lising disorders are also referred to as disorders
of emotions and are characterised by subjective • Unlike adults children rarely come to
distress in children, feelings of inferiority it, treatment on their own (Generally, referral
social withdrawal, self-consciousness, shyness, is initiated by significant others e.g., parents,
anxiety, crying, hypersensitivity, depression and teachers).
sadness (Quay, 1979). On the other hand, • Children and youth undergo behavioural,
Externalising disorders are marked by conflicts social, emotional and cognitive changes at a
with the environment and include aggressive- rapid pace than adults; and thus their
ness, temper tantrums, lying; which are behaviour must be viewed within a develop-
distressing to others. mental context.
The literature on psychological disorders is • The child assessment involves multiple
voluminous. To describe the diagnostic criteria persons in the child's life, unlike the adult
and assessment of each condition would defeat assessment, which involves only the adult
the purpose of the present work. The chapter client.
selectively focuses on the assessment pro- The most useful assessment tools for
cedures. A detailed account of diagnostic evaluating any child behaviour problem are
criterion and management of the psychological those that accurately describe the characteristics
conditions can be obtained in Walker and and impact of the concerned behaviour. For
Roberts (2001) and Rutter and Taylor. most childhood behaviour problems, a multiple
method of assessment is required, which obtains
Psychological Assessment information from at least two different
The psychological assessment is aimed at assessment methods.
evaluating the child's psychological and social According to Johnson and Bommarita, the
problems along with his/her limitations and assessment of children traditionally focuses on
capabilities. It also includes description and eight areas (Table 11.2). The commonly used
analysis of performance of a particular child. methods for assessment are also describe in the
table. It is essential to clarify that the methods
Psychological Assessment: are not corresponding to the areas being
Functions Served assessed. These are general methods and each
• Provides a picture of current phenome- area may be assessed using one or more of the
nology following methods.
Table 11.2: Areas and methods of assessment
Areas of assessment Methods of assessment
• Cognition • Psychological tests
• Personality • Clinical Interviews (with children and parents)
• Perception of environment • Direct observation
• Self-concept • Standard rating scales
• Environment
• Motor skills and brain injury
• Physical attributes and
• Social behaviour
A brief description of the assessment method have been adapted specifically for Indian
is illustrated below. children. The details of the same can be obtained
in Kapur (1995).
Psychological Tests
Broadly speaking, a test is any systematic and Clinical Interviews
quantified way of describing behaviour A. With Parents
(Sergeant and Taylor, 2002). It may be highly
standardised as an IQ test, or it may be Firstly, it is important to ask parents to clearly
developed and used for the unique problems of define the behavior that is of concern. A
an individual case. The traditional definitions statement that the child has a “bad attitude” or
of psychological tests focus on those procedures “never listens” is not enough to address the
and instruments that have been standardised problem. Parents should be asked to describe
through psychometric refinement, have the behaviour. Information on the course of
satisfactory reliability and are valid in describing problematic behaviour needs to be solicited (e.g.,
an individual child in relation to the rest of the duration; intensity; frequency; do factors such
population. Psychological testing makes mental as public setting, hunger, fatigue increase the
assessments more reliable and closer to what problematic behaviour). After defining the
they seek to measure. A large number of tests present problem, an assessment of antecedent
have been developed for assessing various and consequences is done. This is important
functions. It is difficult to enumerate all the tests. because it helps to establish the conditions under
Some of the most commonly used tests are which the child is having difficulty behaving or
depicted in Table 11.3. Details regarding the complying and they also provide targets for
administration, scoring and interpretation can interventions. Some of the probable questions
be obtained from test manuals. In general, to to determine Antecedents and Consequences
administer tests, one requires specific training are illustrated in Table 11.4. Characteristics
that needs to be learnt under expert guidance. (Family of origin, religious values, knowledge
Clinical psychologists are trained for this of child development), child characteristics
purpose and they can form a part of the team (temperament, handicaps, cognitive level),
involved in assessing the child. Some of the tests previous history with professionals (medical,
Table 11.3: Commonly used psychological tests for children

Area Commonly used tests
Cognition
• Intelligence Binet’s scale
Weschlers’ Intelligence Scale for Children (WISC)
Malin's Intelligence Scale for Indian Children (MISIC)
Raven’s Colored Progressive Matrices (CPM)
• Specific Learning Disabilities (SLD) NIMHANS Index of SLD
• Memory Cattell's Retentivity test
Benton's Visual Retention test
Personality Children's Personality Questionnaire
Rosenzweig Picture Frustration test
Children's Appreciation test
Roscharch Inkblot test
Draw A Person test
Perception of environment Preadolescent Adjustment Inventory
Self-concept Self Esteem Inventory
Table 11.4: Probable questions to determine antecedents and consequences

Antecedents Consequences
• Where does the behaviour occur and • Is the child praised/rewarded/ignored
with whom? for positive behaviour/compliance?
• What is the child generally doing before • Is the child sent for time out, reasoned with,
exhibiting the problematic behaviour? or begged to comply when she refuses
• How do the parents respond to the child to complete a task?
when she exhibits problematic behaviour? • Does the parent complete the task?
school), resources for family support (Relatives, clinician with an understanding of child's
friends, community) and overall stress level. perception of the current problem and his/her
Some of the other following family factors willingness to participate in treatment. The child
to be assessed while dealing with parents interviews also provide the opportunity to
include: evaluate any inconsistency of information
• The cultural background, provided by the parent versus the child.
• Socioeconomic status (income, education, A number of structured diagnostic tools have
living conditions), been developed. The most commonly used
• History of family disruption (shifting houses, instruments are: Diagnostic Interview for
illness), Children and adolescents-Revised (DICA-R,
• Parental psychopathology (substance abuse, Herjanic, et al 1975), Diagnostic Interview
anxiety, depression), Schedule for Children (DISC, Costello, et al
• Marital relationships (separation, divorce, 1984), Child Assessment Schedule (CAS,
conflicts), Hodges et al, 1981).
• Parenting characteristics (Family or origin,
religious values, knowledge of child Behavioural Observations
development),
• Child characteristics (temperament, handi- Behavioural observation has been an important
caps, cognitive level), method of assessing children. The child may be
• Previous history with professionals (medical, observed under Natural conditions (Naturalistic
school), observation) or in a structured situation (Struc-
• Resources for family support (Relatives, tured observation, e.g. school, clinic). During
friends, community) and observation, the focus is on verbal as well as
• Overall stress level. non-verbal cues (gestures and behaviour). While
observing the child, one can observe for the
B. Child Interviews following:
An interview with the child can provide • General appearance (dress, happy/
valuable information as well as an opportunity unhappy, tearful, afraid of being alone with
to observe his/her behaviour. Most interviews the examiner),
need to include a combination of questions that • Motor functions (slow/quick, clumsy, right-
require a knowledge base (e.g., what she left orientation, overactive/under active),
understands about illness and behavioural • Speech (talks freely/with hesitations, does
difficulties), the way the child relates to his not talk, stammering),
parents, sibs and peers and open-ended • Content of talk and thought (logical flow,
questions that have no right-wrong answers. expression),
The information gathered can provide the • Mood (happy, depressed, hostile, fearful).
It is also important to observe the interaction with the help of 10 overlapping parent and
between parents, attitude of the parents towards teacher items.
the child and interaction between the parents d. Developmental Psychopathology Checklist for
and child (answer for the child, provide cues, Children (DPCL): Has been devised for use
gets angry). with Indian children by Kapur, et al (1994).
It consists of 124 items classified under six
Rating Scales subsections:
i. Developmental history,
A number of standardised ratings scales are also
ii. Developmental problems,
used to obtain information from multiple
iii. Psychopathology,
informants, including the parents, teachers and
iv. Psychosocial factors,
the child. The rating scales provide an indicator
v. Temperament,
of child's conduct and emotional states. Rating
vi. Social support and asset of the child.
scales also provide a way to repeat assessment
during and after treatment and after medication
CONCLUSION
changes to monitor progress. Rating scales allow
for a child's score to be compared with scores of While working with children it is important to
children of similar ages, providing an important consider the behavioural/developmental
developmental reference for a child's emotional concerns medical/biological, and environ-
and behavioural functioning. The interpretation mental/psychosocial risk as well as protective
of rating scales requires knowledge of the factors. It is essential to keep in mind that a bi-
psychometric issues and how the various scales directional influence occurs between the infant
were developed. Some of the commonly used and the environment. Paediatricians should
behaviour rating scales are: focus on the patient's discomfort rather than on
a. Child Behaviour Checklist (CBCL): As deve- categorisation of clinical manifestations as either
loped by Achenbach (1991) is a commonly organically or psychologically determined.
used rating scale to assess internalising and Psychological factors have a role in the onset,
externalising problems in children. CBCL is maintenance and treatment of medical
documented to effectively discriminate illnesses/conditions. Further, psychological
between normal children and those referred difficulties may emerge as a result of the medical
to mental health clinics. condition and all these need to be dealt with in
b. Behaviour Assessment System for Children providing holistic care to the pediatric patients.
(BASC): Has been developed by Reynolds Only on the basis of a thorough assessment can
and Kamphaus (1991). It is available in three one plan individual and family interventions
forms: Parent rating scale, Teacher rating that are crucial in preventing mental health
scale and self-report of personality. Scores problems and exacerbating symptoms. To
are reported for behavioural symptoms, conclude, in order to provide quality care and
externalising and internalising problems, enhance quality of life, assessment of
school problems, adaptive skills and psychological factors is essential. For this
atypicality. purpose, a well-trained paediatric psychologist
c. Conners Rating Scale: developed by Conners needs to be an integral part of the paediatric
(1973) is commonly used to assess ADHD team.
APPENDICES
GROWTH CHARTS
• CDC
• ALL INDIA (IAP)
• ROAD TO HEALTH CHART
• RAINBOW CHART
Appendices 165
Appendices 167
Appendices 169
Appendices 171
Appendices 173
Appendices 175
Appendices 177
Appendices 179
Appendices 181
Appendices 183
Appendices 185
Road to health chart

Appendices 187
Rainbow chart
NOMOGRAM
SOME CLASSICAL
CLINICAL PICTURES
Fig. A.4: Choroid tubercle
Fig. A.1: Epiphyseal enlargement of wrist in rickets
Fig. A.2: Congenital cataract
Fig. A.3: Fissured tongue (Down syndrome) Fig. A.5: Ectopia vesicae
Appendices 191
Fig. A.8: Hypospedius
Fig. A.6: Hydrocephalus
Fig. A.9: Imperforate anus
Fig. A.7: Knock knee in ricket Fig. A.10: Lymphoma

Fig. A.11: Oral thrush
Fig. A.12: Prune belly syndrome Fig. A.13: Osteogenesis imperfecta
Fig. A.14: Turner syndrome

Appendices 193
Fig. A.15: Achondroplasia
Fig. A.16: Female with congenital adrenal hyperplasia Fig. A.17: Marfan syndrome
Fig. A.18: Down syndrome Fig. A.19: Fragile X-syndrome
Fig. A.20: Osteogenesis imperfecta Fig. A.21: Thyrotoxicosis

Appendices 195
Fig. A.22: Thalassaemic facies Fig. A.24: Russell-Silver syndrome
Fig. A.23: Congenital hypothyroidism Fig. A.25: Facial palsy

Fig. A.28: Corneal clouding in Hurler syndrome
Fig. A.26: Craniosynostosis
Fig. A.27: KF ring in Wilson disease Fig. A.29: Morquio syndrome

Appendices 197
Fig. A.30: Café au lait patch with neurofibroma Fig. A.31: Café au lait patch in
McCune-Albright syndrome
Fig. A.32: Ehlers-Danlos syndrome

X-RAYs
Fig. A.35: Eventration of diaphragm
Fig. A.33: Chronic hemolytic anaemia
Fig. A.34: Parthe’s disease Fig. A.36: Marble bone disease (Osteopetrosis)
Appendices 201
Fig. A.37: Pyopericardium Fig. A.39: Rickets
Fig. A.38: Achondroplasia Fig. A.40: Brock’s middle lobe syndrome

Fig. A.43: Cavity of right lung
Fig. A.41: Cardiomyopathy
Fig. A.42: Duplication of left ureter Fig. A.44: Eventration of diaphragm

Appendices 203
Fig. A.45: Hydatid cyst of left lung Fig. A.47: Lung abscess
Fig. A.46: Massive pleural effusion (left) Fig. A.48: Right upper lobe consolidation
ECG
Fig. A.49: Sinus arrhythmia Fig. A.52: Atrial fibrillation. Note the f waves
and irregular ventricular rhythm
Fig. A.53: Atrial extrasystoles. Note the abnormal (inverted)

P wave. The R-R interval is longer after the extrasystole than
in the normal cycle
Fig. A.50: Atrial flutter, 2:1 block. Atrial rate about 300. Note
the two spiked flutter waves to each ventricular complex
Fig. A.54: First degree heart block.

P-R interval = 0.42 second
Fig. A.51: Ventricular extrasystoles. Note that there is no P

wave before the second extrasystole, and there is an abortive Fig. A.55: Complete heart block. Atrial rate 55;
P wave just before the first extrasystole ventricular rate 39
EEG
Fig. A.56: Spikes, left temporal
Fig. A.57: Slow spike and wave complexes, generalised
Fig. A.58: 3-Hz spike-and-wave complexes, generalised

Appendices 209
Fig. A.59: Hypsarrhythmia, generalised
Fig. A.60: Burst suppression, generalised (Coma)

CT SCAN
Fig. A.61: Brain abscess Fig. A.63: Ring enhancing lesion
Fig. A.62: Hydrocephalus Fig. A.64: Sturge-Weber syndrome

INDEX
A C other disturbances of
sensation 129
Addison’s disease 134 Canavan disease 135 pain 129
Aicardi syndrome 103 Cardiovascular system 83 position sense 128
Alexander disease 135 cyanotic spells 83 recognition of size, shape,
Ankle clonus 123 examination 84 weight and form 128
Apgar score 140 scheme of examination 84 spatial summation 129
Areas of auscultation other than murmurs 89 temperature 129
heart 92 clinical characteristics 90 temporal summation 129
Assessment of child behaviour example of innocent vibration sense 128
152 murmur 90 test for coordination 125
history 152 other areas of auscultation 92 lower limbs
behaviour problems 154 pericardial rub 92 upper limbs 125
cognitive development 153 Causes of delayed puberty 134 Cushing syndrome 134
emotional development Causes of precocious puberty Cyanosis with heart failure 93
152 134 Cyanosis without heart failure
Causes of small and large pupil 93
B 105
Causes of waddling gait 127
Babinski response 123 Common causes of short stature D
Bing’s method 123 134 Defect of 9th and 10th cranial
Blood pressure 25 Coordination 125 nerve 113
jugular venous pressure (JVP) autonomic function 129 DiGeorge syndrome 134
29 deep breath test 129 Dysdiadochokinesis 125
lymph nodes 30 gait 126
measurement 25 ataxic gait 127
E
respiration 26 in-toeing gait 127
adventitious sounds 27 Trendelenburg gait 127 Examination of the cranial
depth 27 waddling gait 127 nerves 100
oxygen saturation 27 neurodevelopmental diplopia 107
rate 26 examination— nystagmus 106
rhythm 26 developmental reflexes oculomotor, trochlear and
type of respiration 27 129 abducens nerves 103
work of breathing 27 sensation 127 accommodation reflex 105
skin, hair, nails 31 agnosia 129 anatomy 103
temperature 27 apraxia 129 conjugate movements of
thyroid 31 light touch 128 the eyes 106
proptosis 106 technique 61 history of prior illness/past

ptosis 105 left kidney 62 illness 9
pupils 105 liver 64 history of the present illness
squint 104 right kidney 63 2
test 104 spleen 62 cardiovascular system 5
olfactory 100 urinary bladder 65 general 2
anatomy 100 haemopoietic system 5
test 100 F liver and gallbladder 4
optic nerve 100 locomotor system 9
anatomy 100 Facial nerve 108 neurology 8
test 101 anatomy 108 respiratory system 5
various types 107 pathology 110 skin diseases 7
Examination of the test 109 urinary system 7
endocrinological and autonomic 110 immunization history 11
metabolic systems 135 motor 109 developmental history 11
examination 134 reflexes 110 milestones of development 11
ejection systolic murmur sensory 109 presenting complaint 2
134 Fanconi anaemia 137 school performance 14
hepatosplenomegaly 135 Friedreich ataxia 126 dietary history 14
hypertension 134 plan of diagnosis 14
hyperventilation 134 G social history 10
spasticity/rigidity 135 Hunter’s canal 125
Gaucher disease 135
history 135 Hypoglossal nerve 114
Glasgow coma scale 96
inspection 135 involuntary movements 115
Glossopharyngeal, vagus and
Examination of the motor system 114
accessory cranial nerves
gastrointestinal system muscle mass 115
113
55 power 117
anatomy 113
examination 58 test 114
test for the 11th cranial nerve
inspection 59
113
palpation 60 K
test for the 9th and 10th
history 55 Kallmann’s syndromes 134
nerves 113
appetite 57 Kerning’s sign 99
11th cranial nerve 113
blood in stool 56 Klinefelter’s syndrome 134
gag reflex 113
diarrhoea/constipation 56 Kocher-Debré-Sémélaigne
palatal paralysis 113
fever 57 syndrome 134
Gonda’s method 123
jaundice 57
Gordon reflex 123
potbelly 57 M
Grading of muscle power 118
vomiting 57
weight loss 58 Marfan syndrome 135
percussion 69 H Marshall and Weaver syndromes
auscultation 70 Haematology-oncology 136 134
fluid thrill 70 examination 136 Moro reflex 147
hydatid thrill 70 history 136
shifting dullness 69 N
Heart failure without cyanosis
retroperitoneal structures 65 93 Neonatal examination 138
anus and rectum 68 History 1 examination 140
female genitalia 68 antenatal birth and postnatal anthropometry 140
groin 66 history 11 assessment of gestation
male genitalia 66 family history 10 141
points of tenderness 65 treatment history 11 systemic examination 144
Index 215
history 139 pigmentation 16 physical examination 74
antenatal history 139 pulse 20 auscultation 79
events at delivery 140 Perfusion 24 breath sounds 79
pre-pregnancy health state Plantar reflex 123 inspection 74
139 Psychological assessment 155 palpation 76
previous obstetric history as part of medical conditions percussion 77
139 156 reconciliation 81
test 145 child self-report 157 stridor 73
Neurology 95 observational methods 157 Romberg sign 126
examination of the spine, psychological assessment in Root value reflexes 121
skull 99 general 158 Russell-Silver syndrome 134
higher function 95 behavioural observations
activity 97 160 S
awareness of the clinical interviews 159
environment 97 different from adult Sandhoff’s disease 135
behaviour 97 assessment 158 Sensory nerve distribution 130
consciousness 95 functions served 158 at back 131
emotional stability 97 psychological tests 159 autonomic dysfunction
handedness 97 rating scales 161 132
memory 98 orthostatic hypotension
R 132
position of the child 96
response to stimuli 97 Regional examination 32 infront 130
scheme of neurology anthropometry 49 Sensory system examination 128
examination 95 bangle method 53 Sherrington’s nociceptive flexion
speech 98 body mass index (BMI) 53 123
Niemann-Pick disease 103 chest circumference 51 Sotos syndrome 134
Noonan syndrome 135 cranial circumference 51 Still’s murmur 90
mid arm to head
circumference ratio 53 T
O
mid-arm circumference 51
Oppenheim sign 123 Quetlet’s index 53 Tay-Sachs disease 135
weight for height 52 Trendelenburg’s sign 127
ears 39 Trigeminal nerve 107
P
eyes 36 anatomy 107
Pallor 15 forehead 35 test 107
clubbing 17 hands and fingers 46 Turner syndrome 151
cry 20 head 32
cyanosis 16 fontanelles 33 V
types 16 scalp 34 Vestibulo-cochlear nerve 110
decubitus 18 joints 48 anatomy 110
types 18 mouth and pharynx 42 test for the auditory nerve
facies 18 neck 36 111
icterus 16 nose 41 infant 111
oedema 17 Respiratory system 71 older child 111
palpability 21 haemoptysis 73
Rinne’s test 112
character 22 chest pain 74
toddler 111
delay 22 dyspnoea 74
vestibular function 112
equality 22 epistaxis 73
Weber’s test 112
rate 21 history 72
rhythm 21 cough 72
tension 22 grunt 73 W
volume 22 sputum 73 Wilms’ tumour 137

Key To Diagnosis in Paediatrics

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Clinical Methods

A Key to Diagnosis in Paediatrics

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Clinical Methods—A Key to Diagnosis in Paediatrics

© 2008, Dilip Mukherjee

First Edition: 2008

YK Amdekar MD, DCH

2. General Survey ................................................................................................................. 15

3. Examination of the Gastrointestinal System ............................................................. 55

5. Cardiovascular System ................................................................................................... 83

7. Examination of the Endocrinological and Metabolic Systems ............................ 133

8. Haematology – Oncology ............................................................................................. 136

9. Neonatal Examination .................................................................................................. 138

10. Assessment of Child Behaviour ................................................................................. 152

11. Psychological Assessment ........................................................................................... 155

Appendices ......................................................................................................................... 163

Index .................................................................................................................................. 213

INTRODUCTION The doctor, in an interview with the child

PRESENTING COMPLAINT • Aggravating factor: What brings it on and

Sleep • What is its relation to meals (if any)?

Water Brash Constipation

• Is it aggravated by deep breathing or • Is there a record of fluid intake-output? Have

• Is there a history of asthma, hay fever or any Neurology

• Is there a family history of sudden death • Is the weakness generalized (malnutrition,

Treatment History Developmental History

52 Weeks (1 year) 24 months

48 months daily intake of food in terms of calories and

Table 2.4: Pigmentation

Oedema The tissues at the base of the nail are thickened

Table 2.6: Causes of clubbing

Fig. 2.3: Facies of Down syndrome Fig. 2.4: Moon facies

A cry is sometimes accompanied by stridor as

separate with no quantitative difference in • Restrictive cardiomyopathy

a: Normal arterial pulse d: Bisferiens pulse

c: Hyperkinetic pulse f: Pulsus alternans

Fig. 2.6: Arterial pulse tracing

BLOOD PRESSURE and lower the pressure slowly. Listen

Depth distal airways (by virtue of the negative pressure

lymphadenopathy in the child. The palpable

Table 2.20: Skin lesions Table 2.21: Causes of hirsutism

Table 2.25: Abnormal head circumferences

Table 2.26: Abnormal head shapes

Table 2.27: Scalp hair Table 2.28: Scalp abnormalities

l. Swelling around eyes–Slight puffiness of the Table 2.29: Conjunctival lesions

c. Pre-auricular papillomas or tubercles –

5. Mouth breathing–Adenoidal hypertrophy, • Erythema–Kawasaki disease, herpes

on the surface of the tonsils (streptococcal adenoidal hypertrophy. The pharynx is

Table 2.36: Age of appearance of teeth

Table 2.37: Number of teeth in different ages in boys and girls

Pediatrics: Grade I (71-80%), grade II (61-70%),

Fig. 2.16: Length measurement Fig. 2.17: Chest circumference measurement

Fig. 2.19: Mid-arm circumference

child of the same height. Combinations of

Figs 2.20A and B: (A) SMR girls, (B) SMR boys

Table 2.44: Tanner pubertal staging–Girls

Table 2.45: Tanner pubertal staging–Boys

Table 3.5: Causes of jaundice in neonatal period Examination

the child is comfortable. Palpate with the

iv. Surface–smooth (congestive cardiac Table 3.10: Causes of bladder distension