Core Clinical Cases in Paediatrics 2nd Edition 2011

Core
Clinical
Cases in
Paediatrics
Second edition
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Core
Clinical
Cases in
Paediatrics
A problem-solving approach
Second edition
Andrew Ewer MD MRCP FRCPCH

Senior Lecturer, University of Birmingham; Honorary
Consultant Neonatologist, Birmingham Women’s
Hospital, Birmingham, UK
Rajat Gupta DCH MMedSci FHEA FRCP

(Ireland) FRCPCH
Consultant Paediatric Neurologist and Head of Clinical
Teaching Academy, Birmingham Children’s Hospital,
Birmingham, UK
Timothy Barrett PhD MRCP FRCPCH

Professor of Paediatrics and Honorary Consultant,
Paediatric Endocrinology and Diabetes, Department
of Endocrinology, Birmingham Children’s Hospital,
Birmingham, UK
Core Clinical Cases series edited by
Janesh K. Gupta MSc MD FRCOG

Professor in Obstetrics and Gynaecology, University
of Birmingham, Birmingham Women’s Hospital,
Birmingham, UK
First published in Great Britain in 2005 by Arnold
This second edition published in 2011 by Hodder Arnold, an imprint of Hodder Education, a
division of Hachette UK, 338 Euston Road, London NW1 3BH
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© 2011 Andrew Ewer, Rajat Gupta and Timothy Barrett
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generality of the preceding disclaimer) every effort has been made to check drug dosages;
however it is still possible that errors have been missed. Furthermore, dosage schedules are
constantly being revised and new side-effects recognized. For these reasons the reader is strongly
urged to consult the drug companies’ printed instructions before administering any of the drugs
recommended in this book.
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Contents
Acknowledgements vi
Series Preface vii
Foreword viii
Abbreviations ix
Chapter 1 Growth problems 1
Chapter 2 Developmental delay 13
Chapter 3 Weight faltering (failure to thrive) 23
Chapter 4 Acute severe illness 33
Chapter 5 Acute and chronic fever 47
Chapter 6 Respiratory problems 57
Chapter 7 Fits, faints and funny turns 69
Chapter 8 Headache 79
Chapter 9 Diarrhoea and vomiting 89
Chapter 10 Abdominal pain 99
Chapter 11 Jaundice 109
Chapter 12 Rashes 119
Chapter 13 Poisoning 129
Chapter 14 Emotional and behavioural problems 139
Index 149
Acknowledgements
The authors would like to acknowledge the work of Vin Diwakar as co-author of the first edition of this
book.
We would like to thank Rachel, Emma, Kate and Smriti, without whose constant support this book
would not have been written. We would also like to thank Ellen, Sophie, Alice, George, Joseph, Lydia,
Esha and Viraj for their wonderful drawings.
Series preface
‘A history lesson’
Between about 1916 and 1927 a puzzling illness appeared and swept around the world. Dr von
Economo first described encephalitis lethargica (EL), which simply meant ‘inflammation of the brain that
makes you tired’. Younger people, especially women, seemed to be more vulnerable but the disease
affected people of all ages. People with EL developed a ‘sleep disorder’, fever, headache and weakness,
which led to a prolonged state of unconsciousness. The EL epidemic occurred during the same time
period as the 1918 influenza pandemic, and the two outbreaks have been linked ever since in the
medical literature. Some confused it with the epidemic of Spanish flu at that time while others blamed
weapons used in World War I.
Encephalitis lethargica (EL) was dramatized by the film Awakenings (book written by Oliver Sacks,
an eminent neurologist from New York), starring Robin Williams and Robert De Niro. Professor Sacks
treated his patients with L-dopa, which temporarily awoke his patients giving rise to the belief that the
condition was related to Parkinson’s disease.
Since the 1916–1927 epidemic, only sporadic cases have been described. Pathological studies have
revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell)
infiltration. Recent examination of archived EL brain material has failed to demonstrate influenza RNA,
adding to the evidence that EL was not an invasive influenza encephalitis. Further investigations found
no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism. Magnetic
resonance imaging (MRI) of the brain was normal in 60 per cent but showed inflammatory changes
localized to the deep grey matter in 40 per cent of patients.
As late as the end of the 20th century, it seemed that the possible answers lay in the clinical
presentation of the patients in the 1916–1927 epidemic. It had been noted by the clinicians at that
time that the central nervous system (CNS) disorder had presented with pharyngitis. This led to the
possibility of a post-infectious autoimmune CNS disorder similar to Sydenham’s chorea, in which group
A b-haemolytic streptococcal antibodies cross-react with the basal ganglia and result in abnormal
behaviour and involuntary movements. Anti-streptolysin-O titres have subsequently been found to be
elevated in the majority of these patients. It seemed possible that autoimmune antibodies may cause
remitting parkinsonian signs subsequent to streptococcal tonsillitis as part of the spectrum of
post-streptococcal CNS disease.
Could it be that the 80-year mystery of EL has been solved relying on the patient’s clinical history of
presentation, rather than focusing on expensive investigations? More research in this area will give us
the definitive answer. This scenario is not dissimilar to the controversy about the idea that streptococcal
infections were aetiologically related to rheumatic fever.
With this example of a truly fascinating history lesson, we hope that you will endeavour to use the
patient’s clinical history as your most powerful diagnostic tool to make the correct diagnosis. If you do
you are likely to be right between 80 and 90 per cent of the time. This is the basis of the Core Clinical
Cases series, which will make you systematically explore clinical problems through the clinical history of
presentation, followed by examination and then the performance of appropriate investigations. Never
break those rules!
Janesh Gupta
2005
Foreword
As a paediatric student nearly 40 years ago, I went onto the children’s ward of my teaching hospital
for the first time, and picked up a small green textbook, which was mainly a series of lists. It helpfully
enumerated – without description – 200 causes of abdominal pain in children, 150 causes of failure to
thrive, and over 100 causes of short stature. Could this be what paediatrics was going to be about?
Fortunately not. Thankfully, fashions in clinical education have changed, and books of lists are no more.
This book represents a much more relevant, context-based approach to teaching paediatrics and
child health, and is one that has proven popular with students in Birmingham over a number of years.
Paediatric symptoms from infancy and childhood are presented, followed by a practical approach to
solving them. They have been assembled by a small, expert group of authors and chosen carefully,
because they are important – either because they are frequent, or because the symptom may indicate
a serious or dangerous underlying disorder. The content is relevant to both undergraduate medical
students and to postgraduates and probably to nurses in training too. It is not comprehensive – were it
to be, its point would be lost.
I am delighted to be able to commend this book to you. It contains a distillate of the authors’ clinical
acumen and wisdom. Consequently, there is hardly a list in sight.
Professor Ian Booth

Leonard Parsons Professor of Paediatrics and Child Health
The Medical School
Edgbaston
Birmingham
Abbreviations
AABR automated auditory brainstem response
ADHD attention deficit hyperactivity disorder
AOAE automated otoacoustic emission
BMI body mass index
CMV cytomegalovirus
CP cerebral palsy
CPAP continuous positive airway pressure
CRP C-reactive protein
CSF cerebrospinal fluid
CT computed tomography
EEG electroencephalography
FSH follicle-stimulating hormone
HIE hypoxic ischaemic encephalopathy
HSP Henoch–Schönlein purpura
IGF insulin-like growth factor
LH luteinizing hormone
LHRH luteinizing hormone-releasing hormone
LP lumbar puncture
LRTI lower respiratory tract infection
MRI magnetic resonance imaging
NAI non-accidental injury
PEA pulseless electrical activity
PEFR peak expiratory flow rate
RDS respiratory distress syndrome
RSV respiratory syncytial virus
SDLD surfactant deficient lung disease
SIDS sudden infant death syndrome
SSPE subacute sclerosing panencephalitis
TGA transposition of the great arteries
TORCH screen for Toxoplasma, rubella, cytomegalovirus, herpes simplex
TTN transient tachypnoea of the newborn
URTI upper respiratory tract infection
Growth problems
Questions
Clinical cases 2
OSCE Counselling cases 3
Key concepts 4
Answers
Clinical cases 6
Revision panel 11
2 Growth problems
Questions
Clinical cases
For each of the case scenarios given, consider the following:
Q1: What: is the likely differential diagnosis?

Q2: What issues in the given history support the diagnosis?
Q3: What additional features in the history would you seek to support a particular
diagnosis?
Q4: What clinical examination would you perform, and why?
Q5: What investigations would be most helpful, and why?
Q6: What treatment options are appropriate?
CASE 1.1 – My 6-year-old son is the shortest in his class.

A 6-year-old boy was seen in the paediatric outpatient department. His parents complained that he was
the shortest boy in his class, and he could not reach the coat pegs in school. On examination, the child’s
height was 106 cm (3rd centile).
CASE 1.2 – My 5-year-old daughter is developing breasts.

A 5-year-old girl was referred to outpatients because of early breast development. This had been present
since birth, but is increasing. She was on no medication. On examination, her height was 117 cm (98th
centile). Breast development was Tanner stage 2.
CASE 1.3 – My 14-year-old daughter has not yet started her periods.
A 14-year-old girl was referred for investigation of delayed puberty. She was born at full term, after a
normal pregnancy. Her general development was normal, and she attended a mainstream school. On
examination, she was prepubertal.
Questions 3
OSCE Counselling cases
OSCE COUNSELLING CASE 1.1 – My child has a diagnosis of

constitutional short stature. What does
this mean?
OSCE COUNSELLING CASE 1.2 – Why is my child overweight?

4 Growth problems
Key concepts
In order to work through the core clinical cases in this chapter, you will need to understand the
following key concepts.
PHASES OF CHILDHOOD GROWTH

Infancy phase: from birth to 2–3 years, the fastest period of growth. It is determined mainly by
nutrition.
Childhood phase: from 2–3 years to the onset of puberty, and is determined mainly by hormones,
including growth hormone, thyroxine and insulin.
Adolescent growth spurt: occurs from the onset of puberty to fusion of the epiphyses, and is
determined by the synergistic action of growth hormone and sex hormones (androgens and
oestrogens).
FUSION OF EPIPHYSES
A gradual process initiated by the secretion of oestrogen from the adrenals in boys and ovaries in girls.
Epiphyseal fusion limits final adult height.
PRECOCIOUS PUBERTY
The development of secondary sexual characteristics before the ages of 8 years in females and 9 years
in males. One example is thelarche, which is the isolated development of breast tissue without pubic or
axillary hair development.
DELAYED PUBERTY
The absence of pubertal development by 14 years of age in females and 15 years in males.
TANNER STAGING
The classification of pubertal development according to the appearance of pubic hair in males and
females, breast development in females, and external genital development in males. Stage 1 is
prepubertal, stage 5 is adult.
ORCHIDOMETER
A series of beads of increasing size from 2 mL volume to 24 mL volume used to assess testicular size.
Testicular volume increases in proportion to testosterone secretion. Volumes of 2–3 mL equates to
prepubertal testicular size; 12 mL volume is attained at the time of maximum height velocity. From 12 mL
upwards is normal for male adults.
MEASUREMENT OF HEIGHT AND HEIGHT VELOCITY

To determine the true height velocity, children should have their height measured on two occasions
at least 6 months apart. This reduces measurement inaccuracies due to observer error. The accuracy
of a single height measurement is ± 0.5 cm. Interobserver error is similar. To minimize these errors, the
height should be measured by the same person, on the same equipment, with a minimum interval of
6 months.
The height attained over a 6-month period can be doubled to express a height velocity in cm per year.
Centile charts exist for height velocity. A child’s height velocity needs to remain above the 25th centile
in order to maintain the centile on a linear growth chart.
Height velocity below the 25th centile for at least 18 months equates to a child drifting down the
centiles on a linear growth chart, and is one definition of growth failure.
Questions 5
ESTIMATION OF FINAL ADULT HEIGHT FROM PARENTS’ HEIGHT (MID-PARENTAL

HEIGHT)
To estimate a boy’s final height, add 12.5 cm to mother’s height and take the mean of the mother’s
adjusted height and the father’s height (mid-parental height). For a girl’s final height, subtract 12.5 cm
from the father’s height and take the mean of the adjusted father’s height and the mother’s height. The
95 per cent confidence limits for the child’s predicted adult height are the mid-parental height ± 8 cm.
TURNER’S SYNDROME
A common cause of short stature in girls, with a prevalence of about 1 in 5000. It is caused by the
absence of one of the sex chromosomes, giving a karyotype of 45XO.
Features include short stature, web neck, wide carrying angle at the elbow, convex nails, shield-
shaped chest, low posterior hairline, ovarian dysgenesis (defective development), and normal
intelligence (but sometimes difficulty in socialization).
Girls with Turner’s syndrome are relatively resistant to growth hormone, but they do benefit from
growth hormone treatment, which can increase their final height by about 5 cm.
These girls also need hormone replacement in the form of oestrogens to induce puberty.
Many children and parents benefit by getting in touch with a family support group such as the Child
Growth Foundation.
CHILDHOOD OBESITY
Obesity is now present in about 30 per cent of UK children, and is predicted to increase to 60 per
cent of children over the next 30 years.
There is no agreed definition of childhood overweight or obesity. Children should have their body
mass index (BMI) plotted on a UK BMI chart. These adjust for age and sex. The International Obesity
Task Force defines overweight and obesity by extrapolating back from a BMI at 18 years of 25
(overweight) and 30 (obese) (the adult cut-offs for overweight and obese). This definition is useful for
population studies. The commonly used UK definition is: overweight (above 90th centile for age and
sex) and obese (above 98th centile). The commonly used definition in North America is: overweight
(above 85th centile) and obese (above 95th centile).
Childhood obesity tracks into adulthood and is a risk factor for cardiovascular disease. Obesity in
childhood is associated with other cardiovascular risk factors including hypertension, dyslipidaemia,
and glucose intolerance.
The commonest cause of childhood obesity is an imbalance between calorie intake (food) and calorie
expenditure (exercise). There are genetic causes of obesity but these are rare (probably fewer than 10
per 1000 cases of childhood obesity).
The management of childhood obesity is focused on lifestyle changes, reducing calorie intake and
increasing exercise. There are no pharmacological treatments that are effective or that do not have
significant side effects.
6 Growth problems
Answers
Clinical cases
CASE 1.1 – My 6-year-old son is the shortest in his class.

A1: What is the likely differential diagnosis?
Familial short stature.
Constitutional delay of growth.
Psychosocial causes of short stature.
Isolated growth hormone deficiency.
A2: What issues in the given history support the diagnosis?

The boy is on the third centile for height, which means that 3 per cent of the population of 6-year-olds
are shorter than him. He is within the normal range of height for a UK population. Consequently, he is
likely to be a short, normal boy.
A3: What additional features in the history would you seek to support a
particular diagnosis?
Ask how long the parents have been worried, i.e. has he always been short or small; is there any
history of chronic illness? (e.g. coeliac disease [see p. 102], heart or kidney disease).
Was he a normal birth and delivery? (ask about birthweight). Was he born premature or growth
restricted? (constitutional short stature).
What ethnic group is the family from? (ethnic differences in height). How tall are his parents? (familial
short stature).
What is the social background and family relationships? (emotional neglect or other forms of child
abuse are causes of psychosocial short stature).
Is he falling behind his peers? (height falling off centiles as in growth hormone deficiency).
A4: What clinical examination would you perform, and why?

Measure his parents’ height and plot them on the growth chart.
Estimate mid-parental height.
A5: What investigations would be most helpful, and why?

Take serial height measurements at least 6 months apart.
Calculate height velocity. If height velocity is below 25th centile over 6 months, other investigations
would include:
measurement of insulin-like growth factor-1 (IGF1) as a surrogate marker of growth hormone;
X-ray of the left wrist to ascertain bone age or skeletal maturity. This is delayed in growth
hormone deficiency. Other causes of bone age delay include hypothyroidism and coeliac disease;
growth failure is an indication for formal pituitary testing with a dynamic growth hormone
stimulation test such as the insulin stress test in which a small dose of insulin is given to induce
hypoglycaemia. This is a potent stimulus for growth hormone secretion, and serial measurements
assess the peak secretion.
Answers 7
A6: What treatment options are appropriate?

The most likely diagnosis is familial short stature. No treatment is necessary, but reassurance that the
child is normal.
Children who are ‘short normal’, i.e. due to familial short stature or constitutional short stature,
do not need treatment other than reassurance that they are healthy. Constitutional short stature
refers to children who are usually born small and continue to grow slowly, but who have parents
who are usually normal height. Trials of growth hormone in short normal children have not shown
any appreciable increase in final adult height. Growth hormone is indicated for growth hormone
deficiency, Turner’s syndrome, Prader–Willi syndrome, Russell–Silver syndrome and in chronic renal
failure.
Psychosocial short stature will respond to elimination of the causes of emotional neglect or other
forms of child abuse. This may require removal of the child from the abusing environment.
CASE 1.2 – My 5-year-old daughter is developing breasts.

Isolated thelarche.
Thelarche variant.
Precocious puberty.

The child is not on any medication, and some breast development has been present since birth.
Ask whether parents have noticed any pubic hair or unusual mood swings (precocious puberty). In
addition, has the child been growing rapidly over the past 1–2 years, as in an adolescent growth
spurt?
Has anyone else in the family had early breast development? Did this progress to precocious puberty?

Plot the growth on a height and weight chart, together with previous measurements to gauge her
height velocity. A rapid height velocity would suggest an adolescent growth spurt, and precocious
puberty. Check mid-parental height.
Examine for pubic and axillary hair – again, signs of precocious puberty – and perform an abdominal
examination for masses.
Consider neurological examination. Intracranial tumours are a rare cause of precocious puberty,
more common in boys, and usually resulting in disconsonant puberty (pubic hair without testicular
enlargement).

If there are no other signs of puberty, then isolated premature thelarche is the most likely diagnosis.
This is a benign condition, and may not require follow-up. Parents can be instructed to contact the
doctor again if further signs of puberty develop.
If the child’s height is above the expected centile for the parents’ height, then serial measurements
of growth are required to detect a premature growth spurt. In addition, a bone age X-ray will give an
indication of possible advanced bone age. If the bone age is advanced in the absence of other signs
of puberty, the child fits into the category of thelarche variant. These children are at risk of developing
precocious puberty, and require follow-up.
8 Growth problems
The presence of other signs of puberty, such as pubic hair, warrants further investigations. These
include a pelvic ultrasound for ovarian follicles and uterine size, and a luteinizing hormone-releasing
hormone (LHRH) test. An injection of LHRH is given, and luteinizing hormone (LH) and follicle-
stimulating hormone (FSH) measured at time points after. The magnitude of the rise in LH and FSH
indicates whether the child is prepubertal, in early puberty, or established puberty. True precocious
puberty is usually of central origin at the level of the hypothalamus, and the cause is unknown.

The most likely diagnosis is isolated premature thelarche. In this situation, the parents can be
reassured and the child does not need to be followed-up.
If thelarche variant is present, the child needs follow-up as she is at risk of precocious puberty.
If precocious puberty is present, it is important to delay further progression to avoid compromising
final height, and to prevent the onset of menarche in primary school. The available treatment is
depot injection of a gonadotrophin-releasing hormone agonist such as goserelin. This acts by down-
regulating the release of LH and FSH from the anterior pituitary, and may regress pubertal signs.
CASE 1.3 – My 14-year-old daughter has not yet started her periods.
Familial delayed puberty.
Turner’s syndrome.
Systemic illness.
Anorexia nervosa.

This girl is presumably of normal development and intelligence as she attends a mainstream school. Age
at menarche has a large genetic component, and tends to run in families. However, Turner’s syndrome
must be excluded.
Ask about mum’s age at menarche, and the ages of menarche of any sisters.
Is the girl short compared to her peers? (Turner’s syndrome).
Does she have any chronic illness such as cystic fibrosis (see pp. 61–2) that would explain her delayed
puberty?
Are there any factors in the social history that would lead you to suspect anorexia (pressure of
examinations, unusual fixation with food, unwillingness to develop adult interests and behaviour).

Plot height and weight on a growth chart. Check the parents’ height.
Look for short stature in relation to parents’ heights (Turner’s) and underweight for height (anorexia).
Assess her pubertal stage. Is she prepubertal? (the commonest situation in Turner’s).
Does she have hypertelorism, web neck, wide carrying angle of the arms, shield chest, hypoplastic
nails, underdeveloped nipples, or other signs of Turner’s syndrome?

Chromosome karyotype. The normal female complement should be 46XX. Turner’s girls are usually
mosaic (i.e. they have a mixture of cells, some normal 46XX karyotype, some 45XO karyotype).
Answers 9
LHRH test (see p. 8). This will establish if the hypothalamo–pituitary–gonadal axis is intact, and
exclude primary gonadal failure.
X-ray the left wrist for bone age. Look for delayed bone age in most causes of delayed puberty.

If the diagnosis is familial delayed puberty, the girl can be reassured that she will achieve a final adult
height within the range predicted by her parents’ heights.
Girls with Turner’s syndrome need genetic counselling.
If a systemic illness is diagnosed, then specific treatment will be required.
Anorexia nervosa is a life-threatening condition that needs specialist child psychiatry input.
10 Growth problems
OSCE COUNSELLING CASE 1.1 – My child has a diagnosis of

constitutional short stature. What does
this mean?
This is a common term covering several possible diagnoses.
Constitutional short stature refers to children born small, with short stature but whose parents are
normal height. Possible causes include small for gestational age, intrauterine growth retardation
secondary to placental insufficiency, or certain syndromes. Constitutional short stature is usually not
amenable to treatment. One potential cause that is amenable to treatment with growth hormone is
Russell–Silver syndrome. This is a disorder of short stature, hemihypertrophy, incurved little fingers
and triangular shaped face. The underlying cause is genetic in many cases.
If growth hormone is indicated, the child and parents should be counselled about its use. Growth
hormone is administered by daily subcutaneous injection until the child’s height velocity falls below
2 cm per year (usually until mid-late teens).
The family may wish to contact a parent support group such as the Child Growth Foundation or
syndrome-specific family support organization.
Regular monitoring of the child’s growth is required to assess compliance and the effects of
treatment. In practice, this means 6-monthly measurements of height, weight and BMI. Some people
also measure IGF1 as a surrogate measure of growth hormone, to assess compliance with treatment.
Children with Russell–Silver syndrome or other causes of small for gestational age are growth
hormone resistant and require relatively large doses of growth hormone. Many children treated with
growth hormone during childhood are retested for growth hormone insufficiency at the end of their
growth period.
The benefits of exogenous growth hormone in growth hormone-insufficient adults is controversial;
there is some evidence that it improves general well-being and cardiac muscle contractility. However,
this must be balanced against the cost of this very expensive drug.
OSCE COUNSELLING CASE 1.2 – Why is my child overweight?

Children are often brought to general paediatric clinics because of obesity.
Find out in the history if there is any indication of pathology such as tiredness and lethargy in
hypothyroidism, growth failure in Cushing’s syndrome (very rare in children). Enquire about diet and
exercise, and look at the phenotype of the parents (are the parents overweight as well?).
Measure blood pressure, assess fat distribution (uniform in exogenous obesity), abdominal striae,
acanthosis nigricans (sign of insulin resistance).
The most likely diagnosis is exogenous obesity. This frequently induces more rapid growth and some
advance in bone age. The family needs to be reassured that there is no underlying pathology.
Explain that weight is determined by the balance of calorie intake and energy expenditure.
Give dietary advice to reduce the fat content in the diet, reduce salt and increase fibre.
Give exercise advice and suggest 30 min of exercise that makes the child breathless, every day.
Set realistic targets for weight, and give positive encouragement.
Answers 11
REVISION PANEL
Growth is determined by nutrition in the first 2 years of life, then predominantly by hormones
(growth hormone, thyroid hormone, insulin) in childhood, then by the synergistic effects of growth
hormone and sex hormones in puberty.
There are many causes of short stature; growth hormone deficiency is one of the rarer causes. You
should be able to identify the likely cause of short stature from a thorough history and examination.
Precocious puberty is relatively common in girls and often idiopathic, but rare in boys and
sometimes due to malignant causes (adrenal tumours). Learn the definitions of precocious puberty
and the warning signs to ask about.
Both precocious and delayed puberty need investigating to identify treatable causes and to avoid
compromising final height. Prompt treatment of precocious puberty to delay it can preserve final
height potential.
Childhood obesity is common but genetic causes are rare. Pointers to a genetic cause of obesity
include: obesity of onset in infancy; associated learning difficulties; delayed puberty; and sensory
deficits involving vision or hearing.
Developmental delay
Questions
Clinical cases 14
Key concepts 16
Answers
Clinical cases 17
Revision panel 21
14 Developmental delay
Questions
Clinical cases
Q1: What is the likely differential diagnosis?

diagnosis?
CASE 2.1 – My newborn baby is very ‘floppy’ (hypotonic).

A 2-day-old baby is noted to have very poor tone and is floppy (like a rag doll). He is feeding rather
slowly, but there are no other symptoms. The limbs move spontaneously.
CASE 2.2 – My 9-month-old baby is not yet sitting and has stiff arms
and legs.
A 9-month-old girl has been increasingly noted to hold her arms and legs out straight, with occasional
crossing-over of the legs at the ankles. She does not sit unsupported, nor does she roll over effectively.
She was born 12 weeks premature and was very ill during the neonatal period.
CASE 2.3 – My 2-year-old daughter does not say any recognizable

words.
A 2-year-old girl who is otherwise developing normally does not say any words which are recognizable.
She is a third child, and her siblings’ speech development was normal.
Questions 15
OSCE COUNSELLING CASE 2.1 – My 16-month-old son is not yet

walking.
OSCE COUNSELLING CASE 2.2 – My newborn baby has been diagnosed

with Down’s syndrome. What does this
mean for her?
Key concepts
NORMAL INFANT DEVELOPMENT

From birth, babies develop new skills as they get older.
These skills can be divided into five main groups:
gross motor (e.g. sitting, walking);
fine motor (e.g. holding an object, drawing a shape);
hearing and speech;
cognitive (thinking, understanding);
social (interaction with others).
DEVELOPMENTAL MILESTONES
These are specific skills that most infants will achieve by a certain age (e.g. smiling to social overtures
at 6 weeks of age, sitting unsupported at 8 months of age).
Milestones are subdivided into the major development groups described above. It must be
emphasized that although most infants will achieve milestones around the same time, some
milestones will have a significant variation (e.g. walking unsupported usually occurs around 13
months, but may be achieved as early as 11 months or as late as 18 months in normal children).
DEVELOPMENTAL DELAY
This is defined as a significant delay in achieving developmental milestones which is outside the
normal variation.
Delay may occur in one, some or all of the developmental skills groups.
CEREBRAL PALSY
Cerebral palsy (CP) is a chronic disorder of muscle tone and movement due to a non-progressive
injury to the developing brain.
CP can result from a number of conditions that result in brain injury which particularly affects the
motor areas of the brain.
The events which lead to injury usually occur before, during or shortly after birth, but may be
acquired at a later period following head trauma or meningitis. Most CP is due to brain injury which
is acquired before birth.
Infants may be floppy at birth and develop neonatal seizures. However, the diagnosis cannot be made
at birth; CP characteristically presents with motor delay and muscle stiffness (hypertonia or spasticity
which present in infancy). If only the legs are affected, this is called diplegia; if the arm and leg on
one side are affected, this is known as hemiplegia; and if all four limbs are affected the condition is
known as quadriplegia.
NEWBORN HEARING SCREENING

0.1–0.2 per cent of babies are born with some hearing loss, often with no family history of deafness. In
the UK all babies are screened shortly after birth using the automated otoacoustic emission screening
test (AOAE). Those not passing this test may go on to have the automated auditory brainstem response
(AABR) screening test.
Answers 17
Answers
Clinical cases
CASE 2.1 – My newborn baby is very ‘floppy’ (hypotonic).

Non-paralytic conditions (e.g. chromosomal disorders [Down’s syndrome], birth trauma or asphyxia,
metabolic disorders, benign congenital hypotonia).
Sepsis or other severe systemic illness.
Hypoglycaemia.
Paralytic conditions (e.g. spinal muscular atrophy, congenital myopathy, myotonic dystrophy,
myasthenia gravis).

This baby is moving the limbs spontaneously, and anti-gravity movements or maintenance of the posture
of an elevated limb would strongly suggest that the baby is not paralysed. Therefore, a non-paralytic
cause for the hypotonia is likely.
Check pregnancy history – did the baby move normally in utero, screening investigations (e.g. increased
risk of Down’s syndrome). Polyhydramnios (because of reduced swallowing of amniotic fluid).
Check birth history – fetal distress, Apgar scores, birth trauma, need for resuscitation. Past obstetric
history and family history – previous floppy babies or early neonatal deaths.
Parental consanguinity – autosomal recessively inherited conditions are more common in related
parents.

Examine limb movements and check tendon reflexes to exclude a paralytic condition.
Examine for dysmorphic features, e.g. those seen in Down’s syndrome (see OSCE Counselling
case 2.2) and cerebral irritability (e.g. jitteriness, seizures).
Is the baby unwell? – unresponsive, mottled skin, tachypnoeic, which may suggest sepsis or a
metabolic condition.

Karyotype (if dysmorphism noted).
Full blood count, blood glucose, electrolytes, blood culture, blood gas (? acidosis), urine culture,
lumbar puncture (if baby is unwell).
Cranial ultrasound (if birth trauma or asphyxia suspected).
Magnetic resonance imaging (MRI).
Note: In paralytic conditions other investigations such as muscle biopsy, nerve conduction studies and
electromyography may be required to establish the diagnosis.

Treatment depends on the underlying cause of the hypotonia.
CASE 2.2 – My 9-month-old baby is not yet sitting and has stiff arms
and legs.
CP.
Metabolic disorder.
Neuromuscular disorder.

The symptoms are suggestive of spastic quadriplegia (limb stiffness and scissoring of legs).
Preterm babies are much more likely to develop CP than those born at term.
Details of the neonatal course including labour and delivery, condition at birth, need for ventilation or
intensive care, episodes of sepsis (particularly meningitis), abnormal cranial ultrasound scans, seizures.
Family history (e.g. inherited disorder).
Subsequent progress – poor head control at term, delayed developmental milestones (e.g. sucking,
smiling, reaching for objects). Hearing loss, visual problems (including abnormal eye movements –
strabismus).

Assess posture and muscle tone (? hypertonia/spasticity).
Check tendon reflexes (? hyperreflexic).
Look for hand preference when reaching out for objects and head lag. Infants should use both hands
equally.
Preservation of primitive reflexes (e.g. Moro). The Moro reflex is characterized by abduction and
then adduction of the arms in response to gently allowing the head to fall a few centimetres (with
appropriate support). It is normal in newborns but should not persist beyond 4 months of age. Other
primitive reflexes include suck, grasp and asymmetrical tonic neck reflexes.

The diagnosis of cerebral palsy is usually made on clinical grounds.
MRI may be of use (particularly if the neonatal cranial ultrasound was abnormal).
If metabolic or myopathic disorders are suspected, then more specific investigations are warranted.

Physiotherapy: this is the mainstay of treatment in order to prevent limb deformities and promote, as
much as possible, maximal potential for motor development.
Drug treatment (e.g. baclofen) for severe spasticity.
Aids such as Piedro boots, walking frames or wheelchair may be necessary.
Further multidisciplinary input, e.g. from speech therapists, dieticians, surgeons, pre-school teachers,
educational psychologists, may be required as the child gets older.
Need for statement of special educational needs, and mainstream school inclusion.
Answers 19
CASE 2.3 – My 2-year-old daughter does not say any recognizable

words.
Maturational language delay.
Hearing impairment.
Developmental language disorder.
Mental retardation.
Psychosocial deprivation.
Autistic spectrum disorder.

The fact that she has otherwise normal development would make mental retardation and autism much
less likely.
Ask about pregnancy (? congenital infections), birth history (? birth asphyxia, sepsis) and early
development including responses to sounds and voices.
Ask about infant illnesses, especially meningitis and recurrent ear infections (e.g. otitis media) and
exposure to ototoxic drugs (e.g. gentamicin).
Did she pass the routine neonatal audiological screening? Is she socially responsive and does she
attempt to copy sounds?
Ask about family history of deafness and/or language delay. Enquire about potential psychosocial
stresses within the family.
Is there a failure of comprehension, e.g. can she follow a command?
Is there a problem with the production of sounds?
Can her parents understand her? Does she use non-verbal communication to demonstrate her
needs?

Plot height, weight and head circumference on centile charts.
Examine development milestones in other areas particularly social.
Examine tympanic membranes for evidence of chronic otitis media (glue ear).

Audiological assessment.
Speech and language therapy assessment.

Maturational delay is the most common cause of delayed speech, and the prognosis for this without
specific treatment is excellent.
If hearing impairment is detected, then treatment to improve hearing (e.g. grommets for otitis media
or hearing aids for sensorineural deafness) should be instituted urgently in order to facilitate language
development. Specific speech therapy may also be required.
OSCE COUNSELLING CASE 2.1 – My 16-month-old son is not yet

walking.
Delayed walking is not uncommon.
Children may employ alternative means of getting around (e.g. crawling, bottom shuffling). This may
run in families.
Occasionally, delayed walking may be related to problems such as muscular dystrophy or cerebral
palsy (see p. 16), but if other motor milestones (such as sitting, crawling and standing with support)
have been reached and the legs are normal on examination (muscle bulk and tone, reflexes) these
conditions are very unlikely.
Most children will be walking by 18 months of age.
OSCE COUNSELLING CASE 2.2 – My newborn baby has been diagnosed

with Down’s syndrome. What does this
mean for her?
Down’s syndrome (trisomy 21) is the commonest chromosomal abnormality.
Individuals with Down’s syndrome have an extra chromosome 21. This happened at some stage prior
to fertilization. Although it is more common in children born to older mothers, the precise cause is
not known.
Sometimes not all of the cells have an extra chromosome; this is called mosaicism.
Down’s syndrome is not preventable, but there are tests that can be done during pregnancy:
screening tests which may indicate an increased risk of the fetus having Down’s syndrome and
diagnostic tests which confirm the condition (karyotype).
Individuals with Down’s syndrome have certain physical characteristics which are usually recognizable
at birth. These include: characteristic facies (upslanting eyes, wide palpebral fissure, prominent
tongue); hypotonia; flattened occiput; single palmar creases, curved fifth finger, wide space between
first and second toes (sandal gap); white spots on the iris (Brushfield spots).
Associated with a degree of developmental delay (although most milestones are reached eventually).
Mild to moderate learning difficulties (IQ variable, but usually >80).
Early feeding difficulties may be encountered.
There is an increased incidence of congenital anomalies (particularly cardiac lesions and duodenal
atresia).
Some people with Down’s syndrome attend normal school initially and live fulfilling lives, including
employment and relationships.
Life expectancy is reduced (particularly if there are associated congenital anomalies), but people with
Down’s syndrome can now live into their fifties.
Answers 21
REVISION PANEL
Floppy (hypotonic) babies need thorough investigation.
CP cannot be identified at birth and should be suspected in infants with delayed development,
particularly if there is limb hypertonia.
Maturational delay is the commonest cause of delayed speech and does not usually require
treatment.
Delayed walking is common but most children walk by 18 months of age.
Although Down’s syndrome is associated with characteristic features, the only way to establish the
diagnosis with certainty is to perform karyotype analysis (chromosomes for trisomy 21).
Weight faltering
(failure to thrive)
Questions
Clinical cases 24
Key concepts 26
Answers
Clinical cases 27
Revision panel 31
24 Weight faltering
Questions
Clinical cases

diagnosis?
CASE 3.1 – My 2-year-old son is not gaining weight.

A 2-year-old boy was on the 25th centile at birth; his weight is now on the 0.4th centile. On visiting
the child’s home, the health visitor notes that the members of the family eat separately, with no regular
mealtimes. The child drinks 10–15 cups of orange squash per day. Food is put in front of him, but he
refuses to eat after two to three mouthfuls.
CASE 3.2 – My 18-month-old daughter is refusing to eat.

A mother is very concerned about her 18-month-old girl, who is refusing to eat. The child clamps her
mouth shut when offered food, and the mother often has to force-feed her, which makes her cough
and splutter. Her weight has fallen from the 50th centile at birth to the 3rd centile. The girl’s stools are
loose, green and mucus-covered.
CASE 3.3 – My 3-month-old is not gaining weight with breast-feeding.

A 3-month-old breast-fed baby’s weight was on the 25th centile at birth, but has dropped to the 10th
centile now. The baby’s length and head circumference are on the 10th centile.
Questions 25
OSCE COUNSELLING CASE 3.1 – My 18-month-old son refuses to eat.

An 18-month-old boy has a long history of refusing to eat. He takes one or two mouthfuls and then
refuses, and starts to have a tantrum. His weight has fallen from the 10th to below the 0.4th centile. His
parents say that they are at the end of their tether. A full history, physical examination and investigations
do not reveal an organic cause.
OSCE COUNSELLING CASE 3.2 – Should I bottle-feed my 3-month-old

who is not gaining weight on breast
milk?
A breast-fed 3-month-old baby’s weight has fallen from the 25th centile at birth to the 10th centile. He
is otherwise healthy and his head circumference and length are on the 10th centile. Clinical assessment
does not reveal an organic cause, and ‘catch-down’ growth is diagnosed.
26 Weight faltering
Key concepts
WEIGHT FALTERING (FAILURE TO THRIVE)

This is a descriptive term, not a diagnosis. No objective definition exists; the best available is: ‘a failure
of expected growth’. In clinical practice, classification usually rests on weight falling down two or more
centiles. However:
5 per cent of normal children will shift down two or more centiles between birth and 1 year of age.
5 per cent of children on the 98th centile at birth shift down three centiles by 6 weeks.
The commonest cause of weight faltering is under-nutrition. Organic causes are identified in only 5
per cent of cases.
5 per cent of cases involve child protection issues.
Though rare, organic causes include:
Inability to feed, e.g. cleft palate, oropharyngeal incoordination in neurodevelopmental delay.
Inadequate retention of intake, e.g. vomiting, gastro-oesophageal reflux (see pp. 92–3).
Malabsorption:
fat, e.g. cystic fibrosis (see pp. 61–2);
carbohydrate, e.g. coeliac disease (see p. 102), lactose intolerance;
protein, e.g. cows’ milk protein intolerance.
Chronic illness, e.g. cardiac, respiratory, renal, liver or thyroid disease, malignancy.
Answers 27
Answers
Clinical cases
CASE 3.1 – My 2-year-old son is not gaining weight.

Undernutrition due to poor feeding behaviour.
Poor feeding drive.
Gastro-oesophageal reflux.
Chronic illness:
cystic fibrosis;
renal disease;
congenital heart disease;
malignancy;
hypothyroidism.
Malabsorption, e.g. cows’ milk protein intolerance.
Social deprivation is not thought to be a factor in aetiology, although often stated in referrals.

A large intake of squash with lack of regular family mealtimes suggests undernutrition due to poor
feeding behaviour.
A fall through two or more centiles, or weight <0.4th centile, should trigger an evaluation at home by a
health visitor with observation of mealtimes with reference to:
Content and frequency of meals recorded in a food diary.
Interactions between different carers.
The child’s inherent feeding drive and appetite.
Any evidence of difficulty swallowing or chewing (oromotor dysfunction).
Medical staff need to take a detailed history, including a comprehensive systems review of any
cardiorespiratory, gastrointestinal, urinary or neurodevelopmental symptoms with a detailed family and
social history.

Look at the growth pattern and assess neurodevelopment.
Search for evidence of organic disease by performing a thorough physical examination.
Search for:
nutritional status;
dysmorphism, e.g. congenital infection;
clubbing, e.g. in cystic fibrosis;
pallor;
thyroid status;
signs of congenital heart disease, e.g. cyanosis, murmur;
28 Weight faltering
chest deformity, added sounds (cystic fibrosis);

abdominal masses (malignancy).

Investigations are only indicated if suggested by clinical assessment, and should be conducted early in
management to minimize hospital attendance. Investigations that might be considered include:
Full blood count and ferritin: for anaemia.
Urea and electrolytes, creatinine: for renal disease.
Thyroid function tests: for hypothyroidism.
Coeliac antibodies: for coeliac disease.
Urinalysis: for renal disease and urinary tract infections.

The multidisciplinary team is the key to dietary and behavioural management. The doctor’s role is to
identify and advise about coincident medical conditions, and particularly to reassure if none is found.
Dieticians and health visitors need to work with the family to:
Establish regular family mealtimes.
Encourage intake of high-energy foods.
Reduce fluid intake, especially of squash.
Discourage force-feeding.
CASE 3.2 – My 18-month-old daughter is refusing to eat.

Under-nutrition due to poor feeding behaviour.
Poor feeding drive.
Chronic illness (as in Case 3.1).
Malabsorption, e.g. cows’ milk protein intolerance.

Significant weight loss requires investigation. Force-feeding suggests poor feeding behaviour.
Cough and spluttering when fed suggests oromotor dysfunction, gastro-oesophageal reflux or a
tracheo-oesophageal fistula.
The consistency and colour of the stools suggests malabsorption or starvation stools.
Content and frequency of meals recorded in a food diary.
Interactions between different carers.
The child’s inherent feeding drive and appetite.
Any evidence of difficult swallowing or chewing (oromotor dysfunction).
Respiratory symptoms.
Vomiting.
Medical staff need to take a detailed history, including a comprehensive systems review of any
cardiorespiratory, gastrointestinal, urinary or neurodevelopmental symptoms with a detailed family and
social history.
Answers 29

Look at the growth pattern and assess neurodevelopment.
Search for evidence of organic disease by performing a thorough physical examination (see above).

Once again, investigations are only indicated if suggested by clinical assessment, and should be
conducted early in management to minimize hospital attendance and over-reliance on an organic
solution to the problem. Investigations that might be considered in addition to those listed above
include:
Stool analysis: for microscopy and culture, virology and faecal-1 elastase (a measure of fat
malabsorption).
Sweat test (see p. 62): to exclude cystic fibrosis in very young children or where a history of
malabsorption or respiratory symptoms exists.
Chromosome analysis: in girls, for Turner’s syndrome (see p. 5).
Contrast swallow or pH study: to rule out tracheo-oesophageal fistula and gastro-oesophageal
reflux (see pp. 92–3).

A community-based multidisciplinary team is the key to dietary and behavioural management.
In addition to a dietician and health visitor, this family may need a child psychologist to advise
on a feeding behaviour modification programme, and a speech therapist to assess and advise on
swallowing, oromotor skills, feeding technique and introduction of foods of different textures.
CASE 3.3 – My 3-month-old is not gaining weight with breast-feeding.

Normal growth pattern – ‘catch-down’ growth.
Under-nutrition – inadequate intake with breast-feeding.
Oromotor dysfunction – usually has an underlying cause, e.g. developmental delay, cleft lip and
palate.
Organic disease (see list in Key concepts).

The history and symmetrical growth suggest catch-down growth.
Breast-feeding and oromotor function needs further assessment.
Seek further information about:
Pregnancy, birth history.
Mother’s health and nutritional status.
Intercurrent symptoms – vomiting, diarrhoea, chest symptoms.
Feeding patterns and swallowing.
Neurodevelopmental milestones.
30 Weight faltering

Search for:
Growth pattern.
Nutritional status.
Dysmorphism.
Pallor.
Thyroid status.
Signs of congenital heart disease.
Chest deformity, added sounds.
Abdominal masses.
Neurodevelopmental assessment.

Investigations are only indicated if suggested by clinical assessment.
If catch-down growth is diagnosed clinically, urinalysis is the only investigation necessary.

Families often require much reassurance that the growth pattern is normal, and follow-up – ideally in a
community-based setting with the health visitor – is advised.
Answers 31
OSCE COUNSELLING CASE 3.1 – My 18-month-old son refuses to eat.

Weight faltering is usually a problem of feeding behaviour, and not due to serious illnesses which have
been excluded by a thorough examination and tests. The problem is not the parents’ or the child’s fault,
and is very common. Force-feeding makes the problem worse. Several members of the health team are
needed to help:
The dietician will assess what the boy does eat, and will advise on a variety of high-calorie foods.
The health visitor will visit the family at home and advise on establishing regular meal times, and on
the need for all family members to have a consistent approach to feeding the child.
A child psychologist may be useful to assess child development and advise on a behaviour
programme and on communication with children.
A speech therapist may be useful to assess swallowing, oromotor skills, feeding technique and
introduction of foods of different textures.
OSCE COUNSELLING CASE 3.2 – Should I bottle-feed my 3-month-old

who is not gaining weight on breast
milk?
Your baby is healthy.
Thorough assessment has ruled out a serious disease.
Tests would only be needed if we had concerns after checking your baby.
The baby’s growth pattern is called ‘catch-down’ growth.
Birth weight reflects placental function.
Weight in babies reflects nutritional intake, and if this if good – as it is in your case – it also reflects
genetic potential.
The baby’s growth needs to be monitored by the health visitor.
REVISION PANEL
Weight faltering is the failure to gain weight at a satisfactory rate.
The commonest cause of weight faltering is under-nutrition.
Organic causes of weight faltering are relatively rare but should be considered
Taking a full and detailed history is key when assessing a child for weight faltering.
Weight faltering is usually a problem of feeding behaviour and a multidisciplinary approach to
management is often needed.
Acute severe illness
Questions
Clinical cases 34
Key concepts 36
Answers
Clinical cases 37
Revision panel 45
34 Acute severe illness
Questions
Clinical cases

diagnosis?
CASE 4.1 – My 6-month-old baby has a cough, is burning up, and is

struggling to breathe.
A 6-month-old baby has had a cold for the past few days, but in the past 12 h has developed a high
fever, cough, poor feeding and loose stools. He has vomited twice and is restlessly sleeping more than
usual or is crying inconsolably.
CASE 4.2 – My 2-day-old baby is blue and can’t breathe.

A 2-day-old baby looks dusky and is having difficulty breathing. He has not been feeding well, and has
been sweaty. A murmur was heard at birth.
CASE 4.3 – My 5-month-old isn’t breathing.

A 5-month-old baby is found in the cot, not breathing, 1 h after being put down to sleep.
Questions 35
OSCE COUNSELLING CASE 4.1 – My child is hot; has she got meningitis?
A 14-month-old girl presents with a 1-day history of fever, coryza and cough. A physical examination
suggests an upper respiratory tract infection.
OSCE COUNSELLING CASE 4.2 – My toddler has diarrhoea and vomiting;

what should I do?
A 14-month-old boy has had diarrhoea and vomiting for 1 day. He has vomited twice today, and has
had about six loose bowel motions. Rotavirus has been identified in the stool. The baby is systemically
stable, without clinical evidence of shock or dehydration.
Key concepts
CHILDREN ARE NOT SMALL ADULTS

Key differences are:
Size: this changes rapidly in the first year of life. An average birth weight of 3 kg increases to 10 kg
by 1 year. Between the ages of 1 year and 10 years, weight can be predicted by the formula:
Weight (kg) = 2´(age [years] + 4).
Anatomy – younger children have a short, soft neck: the upper airway tends to obstruct if the neck
is overextended in resuscitation. In neonatal resuscitation the prominent occiput may cause airway
obstruction by flexion and a ‘neutral’ position is required.
Physiology – normal physiological parameters (pulse, respiratory rate, blood pressure) change with
age:
infants under 6 months are obligate nasal breathers; upper respiratory infections can cause
respiratory embarrassment and feeding difficulties;
small airways: resistance to flow is inversely proportional to the fourth power of the airway radius,
so minimal airway inflammation and swelling can cause significant obstruction.
Psychology: children fear illnesses and emergencies through a lack of prior knowledge, a magical
concept of illness (they may think illness has been caused by something they thought or did), picking
up on parental anxiety, and professional failure to communicate at the child’s level.
Parents find acute illnesses in children terrifying. Parents of young children, through an understandable
fear of meningitis and septicaemia, often seek medical reassurance for symptoms (e.g. fever, cough) that
professionals consider being minor and self-limiting.
Algorithms exist for recognition of the sick child, neonatal, basic and advanced paediatric life support
and choking.
INVESTIGATIONS IN ACUTE SEVERE ILLNESS

Specific investigations are guided by the history and examination, but often these are vague and/or non-
specific. In these circumstances it is appropriate to perform the following in an acutely unwell child:
Full blood count: risk of serious bacterial infection is increased if white cell count (WCC) is
>15 × 109/L or is reduced (especially in newborns), or there is an abnormal platelet count. In neonates
neutropenia may also indicate serious infection.
Urea and electrolytes – for electrolyte disturbance.
C-reactive protein (CRP) – an acute-phase protein, the levels of which may rise in serious bacterial
infection. However, the rise in CRP lags behind the onset of infection and therefore a low CRP does
not exclude infection.
Blood cultures.
Blood sugar – hypoglycaemia may suggest poor intake or inborn error of metabolism.
Urinalysis – positive nitrite test and/or urine stick testing is suggestive of urinary tract infection and
needs confirmation by urgent microscopy and subsequent culture.
Lumbar puncture (LP): cerebrospinal fluid (CSF) microscopy confirms or excludes meningitis in 80
per cent of cases. LP should be deferred if there are signs of cerebral herniation (raised intracranial
pressure cannot be excluded by computed tomography [CT] scan), focal neurological signs, or
cardiorespiratory compromise, but empirical antibiotic therapy should be given without delay. A
delayed LP can confirm the diagnosis of meningitis, as the cellular and biochemical changes remain
in CSF up to 44–68 h after the start of antibiotic treatment. CSF microscopy and polymerase chain
reaction (PCR) for Meningococcus and Pneumococcus from delayed LP can guide subsequent
treatment, although cultures may be negative within 2–6 h of antibiotic administration.
Answers 37
Answers
Clinical cases
CASE 4.1 – My 6-month-old baby has a cough, is burning up, and is

struggling to breathe.
Septicaemia.
Meningitis.
Lower respiratory tract infection.
Gastroenteritis and shock.
Urinary tract infection.
Hypoglycaemia.
Inborn error of metabolism.

An acute illness in young children often presents with non-specific symptoms. Septicaemia must
be considered in all infants presenting with fever, drowsiness and poor feeding. The baby’s clinical
condition has deteriorated rapidly during the previous 12 h.
Meningitis is suggested by irritability and inconsolable crying.
Vomiting and diarrhoea suggest gastroenteritis.
Urinary tract infection can present with non-specific symptoms.
Inborn errors of metabolism are rare, but should be considered.
Rapid clinical assessment of airway, breathing, circulation and disability (see Figure 4.1) may indicate
the need to intervene urgently before taking a detailed history.
Septicaemia, meningitis and urinary tract infection are difficult to diagnose on history in infants, and
should be considered in all young children with acute severe illness.
Diarrhoea and vomiting needs assessment of the duration and frequency of symptoms, fluid intake,
urine output and presence of bile or blood in vomit or stool.
A history of consanguinity or previous sudden death in childhood may suggest an inborn error of
metabolism.

Perform a rapid clinical assessment of airway, breathing (work of breathing, respiratory rate, stridor,
wheeze, cyanosis), circulation (tachycardia, weak pulse volume, prolonged capillary refill time,
pallor or cool peripheries, petechial rash) and conscious level. In the absence of cardiorespiratory
compromise or deterioration and a normal conscious level, a more detailed secondary examination is
undertaken seeking:
general inspection: fever, rashes;
cardiovascular: heart murmurs, signs of heart failure (tachycardia, gallop rhythm, palpable liver);
respiratory: wheeze, stridor, air entry ± added sounds on auscultation;
abdomen: hepatosplenomegaly (suggesting an inborn error of metabolism), abdominal

swelling or masses, increased or ‘tinkling’ bowel sounds (suggesting intestinal obstruction, e.g.
intussusception [see p. 93]);
neurology: the ‘classic signs’ of meningitis are absent under 1 year of age. Irritability and a bulging
fontanelle may suggest meningitis, but their absence does not exclude it.

Full blood count.
Urea and electrolytes.
CRP.
Blood cultures.
Blood sugar.
Urinalysis.
LP.

Maintain airway.
Oxygen in as high a concentration as can be delivered (in hospital, usually 15 L/min via a mask with a
rebreathe bag).
Intravenous access for intravenous antibiotics and fluids.
Rapid bolus of 0.9 per cent saline to correct shock.
Maintenance fluids plus deficit to correct dehydration infused over the next 24–48 h.
Admit to hospital for observation, supportive treatment and intravenous antibiotics, and observation
until culture results known.
CASE 4.2 – My 2-day-old baby is blue and can’t breathe.

Lower respiratory tract infection.
Neonatal septicaemia.
Congenital heart disease, e.g. transposition of the great arteries.
Inborn error of metabolism.

Lower respiratory tract infection is suggested by the history of difficulty breathing and cyanosis.
Murmur at birth, sweatiness, poor feeding, and cyanosis suggest congenital heart disease. The ductus
arteriosus closes within hours or a few days of age, suggesting a duct-dependent lesion (see p. 73).
There may be a relative lack of respiratory symptoms.
Neonatal sepsis is suggested by the age of the baby. Meningitis, septicaemia, urinary tract infection and
inborn error of metabolism may present with non-specific symptoms in newborns and young children.
Neonatal sepsis is suggested by history of maternal fever, prolonged rupture of membranes,
prematurity, maternal carriage of group B streptococci.
Seek antenatal history, including details of antenatal scans and family history of congenital heart
disease.
Birth history and a history of feeding from birth is important.
Answers 39

Rapid clinical assessment of airway, breathing, circulation and disability (see Figure 4.1) may indicate
the need to intervene urgently before taking a detailed history.
Seek clinical signs of congenital heart disease (cyanosis, tachycardia, gallop rhythm, heart murmur,
absent femoral pulses or bounding pulse volume, hepatomegaly, tachypnoea).
Measure oxygen saturation in air and in 100 per cent oxygen, using pulse oximetry.

In addition to investigations for sepsis (see Case 4.1, A5), consider:
Chest X-ray – for cardiomegaly, oligaemic or plethoric lung fields, signs of lower respiratory tract
infection.
Electrocardiogram – for signs of congenital heart disease.
Blood gas – in oxygen.
Echocardiogram – for congenital heart disease.

Maintain airway.
Oxygen.
Intravenous access.
Intravenous antibiotics.
Consider intravenous prostaglandin E2 to maintain patency of ductus arteriosus.
Intravenous fluids and stop feeds pending definitive diagnosis and management.
Consider transfer to regional paediatric cardiac unit (see also Chapter 7).
CASE 4.3 – My 5-month-old isn’t breathing.

Sudden infant death syndrome (SIDS).
Serious bacterial infection.
Electrolyte disturbance, e.g. due to dehydration.
Gastro-oesophageal reflux (see pp. 92–3).
Seizures (see pp. 72–3).
Upper airway obstruction.
Cardiac anomaly or arrhythmia.
Iatrogenic poisoning.
Non-accidental injury.

Sudden infant death syndrome (SIDS) is a diagnosis of exclusion; other causes may present in the same
way and must be considered.
Rapid clinical assessment of airway, breathing, circulation and disability (see Figure 4.1) may indicate the
need to intervene urgently before taking a detailed history. Paediatric resuscitation is usually conducted
by teams; one team member can be delegated to take a detailed history.
Review of intercurrent symptoms and prior illness.

Risk factors for SIDS should be reviewed and recorded, although identification of a single aetiology is
impossible in most cases:
modifiable factors:
® co-sleeping;
® bedding and clothing (evidence suggests increased risk from overheating but studies did not
investigate the relationship between bedding, ambient temperature and amount of infant
clothing);
® pre- and postnatal smoking.
non-modifiable risk factors:
® young mother;
® low birth weight;
® prematurity;
® no antenatal care;
® single mother;
® high parity;
® low socioeconomic class;
® admission to special care baby unit in infancy.
Past history should include a check of any previous injuries and antenatal/birth history.
Drug history should include a review of drugs which are kept in the home.
Family history should include consanguinity, family history of infant deaths.
Detailed social history, including review of housing and call to social services to check whether the
child is on a child protection register.
Answers 41

Rapid clinical assessment may indicate the need for immediate basic life support and advanced life
support.
Paediatric Basic Life Support

(Healthcare professionals with a duty to respond)
UNRESPONSIVE?
Shout for help
Open airway
NOT BREATHING NORMALLY?
5 rescue breaths
NO SIGNS OF LIFE?
15 chest compressions
2 rescue breaths
15 compressions
Call resuscitation team
Figure 4.1 Algorithm for paediatric basic life support. Redrawn with kind permission of the Resuscitation
Council (UK).
Paediatric Advanced Life Support
Unresponsive?
Not breathing or
only occasional gasps
CPR Call
(5 initial breaths then 15.2) resuscitation team
Attach defibrillator/monitor (1 min CPR first,
Minimise interruptions if alone)
Assess
rhythm
Shockable Non-shockable
(VF/Pulseless VT) (PEA/Asystole)
Return of
1 shock spontaneous
4J/kg
circulation
Immediately resume Immediate post-cardiac Immediately resume

arrest treatment
CPR for 2 min • Use ABCDE approach
CPR for 2 min
Minimise interruptions • Controlled oxygenation and Minimise interruptions
ventilation
• Investigations
• Treat precipitating cause
• Temperature control
• Therapeutic hypothermia?
During CPR Reversible Causes

• Ensure high-quality CPR: rate, depth, recoil • Hypoxia
• Plan actions before interrupting CPR • Hypovolaemia
• Give oxygen • Hypo-/hyperkalaemia/metabolic
• Vascular access (intravenous, intraosseous) • Hypothermia
• Give adrenaline every 3–5 min • Tension pneumothorax
• Consider advanced airway and capnography • Toxins
• Continuous chest compressions when advanced • Tamponade – cardiac
airway in place • Thromboembolism
• Correct reversible causes
Figure 4.2 Algorithm for paediatric advanced life support. VT, ventricular tachycardia; PEA, pulseless
electrical activity; CPR, cardiopulmonary resuscitation. Note: International resuscitation guidelines are
available from www.resus.org.uk. Redrawn with kind permission of the Resuscitation Council (UK).
Answers 43
Newborn Life Support
Birth
Dry the baby
Remove any wet towels and cover
Start the clock or note the time
AT
Assess (tone), breathing and heart rate 30 s
ALL
If gasping or not breathing:
Open the airway
Give 5 inflation breaths
Consider SpO2 monitoring 60 s
STAGES
Re-assess
If no increase in heart rate
look for chest movement
ASK
If chest not moving: Acceptable

Recheck head position pre-ductal SpO2
Consider 2-person airway control 2 min 60%
and other airway manoeuvres 3 min 70%
Repeat inflation breaths 4 min 80%
Consider SpO2 monitoring 5 min 85%
Look for a response 10 min 90%
DO
If no increase in heart rate
look for chest movement
YOU
When the chest is moving:
If heart rate is not detectable
or slow (<60 min–1)
start chest compressions
3 compressions to each breath
NEED
Reassess heart rate every 30 s

If heart rate is not detectable
or slow (<60 min–1)
HELP?
consider venous access and drugs
Figure 4.3 Algorithm for newborn life support. Note: Resuscitation of a newborn differs from paediatric
life support and therefore for completeness we include the algorithm for newborn life support. Redrawn
with kind permission of the Resuscitation Council (UK).
Physical examination following successful or during active resuscitation should include a search for
cataracts (may occur in inborn errors of metabolism), congenital abnormalities, hepatosplenomegaly,
presence of blood in nose or mouth, and signs of injury.

In addition to investigations for sepsis (see Case 4.1, A5), consider:
Urinalysis – collect urine for screening for inborn error of metabolism and toxicology.
Chest X-ray – for cardiomegaly, oligaemic or plethoric lung fields, signs of lower respiratory tract
infection.
Blood gas and pulse oximetry – in high-flow oxygen.
Blood lactate, ammonia – for evidence of inborn errors of metabolism.
Nasopharyngeal aspirate, throat swab – for evidence of viral or bacterial infection.
Skeletal survey – for unexplained injuries.
Skin biopsy and blood – for inborn errors of metabolism.
Electroencephalogram – for seizures.
Contrast swallow or pH study – for gastro-oesophageal reflux.
Cranial imaging – for intracranial trauma, bleeding, neoplasia, sepsis.

Basic and advanced paediatric life support.
Intravenous antibiotics.
Resuscitation is unlikely to be successful and is usually stopped if spontaneous circulation is not
restored within 30 min of cumulative life support, except in cases of poisoning or hypothermia.
Following the sudden unexpected death of an infant, families need:
counselling with verbal and written information about why their baby died;
to be encouraged to see and hold the baby;
to be informed that a coroner’s post-mortem investigation is required by law in all such cases, and
appropriate consent taken;
to be informed that the general practitioner, health visitor, police and social services will be
involved;
to be offered bereavement support from other agencies and a follow-up visit at home.
Answers 45
OSCE COUNSELLING CASE 4.1 – My child is hot; has she got meningitis?
Fear of meningitis is the commonest reason that parents of young children seek medical reassurance
for self-limiting illnesses. Doctors and parents approach such illnesses from different perspectives.
Doctors focus on diagnosis, whereas parents want to protect their children and alleviate symptoms.
Parents are often made to feel that their demands are inappropriate.
The doctor’s attitude is important if we are to reassure parents; a thorough history and examination
is essential. Parents are rightly suspicious if reassurance is given when the child hasn’t been seen and
examined.
Counselling should involve:
the opportunity for the parents and the child to express their specific concerns;
an explanation of each concern;
specific reassurance that serious illness has been ruled out;
a specific diagnosis, if one has been made;
advice about which symptoms and signs to be concerned about, and when and where to seek
medical help again.
OSCE COUNSELLING CASE 4.2 – My toddler has diarrhoea and vomiting;

what should I do?
The commonest causes of diarrhoea and vomiting in infants and small children is gastroenteritis (also
known as ‘tummy bug’). Most children with gastroenteritis will get better with no special treatment,
although it can continue for up to 2 weeks.
However, it is always taken seriously because babies and small children lose body fluid quickly and
can become dehydrated. It is important to prevent this by giving lots of clear drinks (juice or Dioralyte)
to replace the loss from the diarrhoea and vomiting. Give small sips frequently. (Dioralyte is a clear
drink which contains minerals and sugar to replace those lost because of diarrhoea and vomiting. It is
not a medicine and does not stop diarrhoea and vomiting.)
Normal feeds should be started again after 24 h.
You must watch out for the signs of dehydration and go to the doctor if you see:
sunken eyes and a glazed look;
mottled skin;
strong-smelling urine;
dry mouth.
Handwashing, after nappy changes and before making feeds or meals, is very important to stop other
family members from catching the virus.
REVISION PANEL
Children are not small adults.
Anatomy and normal physiological parameters change with age.
A rapid clinical assessment of airway, breathing, circulation and conscious level may indicate the
need to intervene urgently when a child presents with an acute illness.
Septicaemia, meningitis and urinary tract infection are difficult to diagnose on history in infants,
and should be considered in all young children with acute illness. If in doubt it is best to treat with
broad-spectrum antibiotics and await culture results.
Investigations are guided by the history and examination findings.
Acute and chronic fever
Questions
Clinical cases 48
Key concepts 50
Answers
Clinical cases 52
Revision panel 55
48 Acute and chronic fever
Questions
Clinical cases

diagnosis?
CASE 5.1 – My 18-month-old has developed a mild fever and a rash.

She has recently become quieter than usual. After 2 days of fever she broke out in a rash.
CASE 5.2 – My 4-year-old has developed a fever 2 weeks after

returning to the UK from abroad.
We have just returned from Africa, where we had been working when he was born. He had
uncomplicated chicken pox at 10 months, but has been otherwise well and is up to date with his
immunizations.
CASE 5.3 – My 3-year-old son has had a fever for 10 days, and his
fingers are peeling.
He was seen by his GP with a 4-day history of intermittent high fever above 39 oC, red eyes, sore throat
and cervical lymphadenopathy. He initially had a rash that has now faded.
Questions 49
OSCE COUNSELLING CASE 5.1 – My child has a rash and I am pregnant.

What if it is German measles?
OSCE COUNSELLING CASE 5.2 – All my friends are advising me not to

let my child have the MMR vaccine.
Key concepts
CHILDHOOD INFECTIOUS DISEASES

Infections are the most common cause of acute illness in children, and are responsible for about 14
million deaths in children worldwide each year.
Morbidity and mortality from infections has fallen dramatically in developed countries as a
consequence of improved living conditions, sanitation, immunization, antibiotic therapy and modern
medical care.
Some infections are still a major problem in some parts of the developed world, including
meningococcal disease and tuberculosis.
At birth, infants have a functioning immune system, but their circulating immunoglobulins, derived
from their mother, decrease during the first few months of life, leaving them susceptible to common
infections. These include the childhood exanthems (illnesses with fever and rash) measles, mumps,
rubella, varicella (chicken pox), and roseola infantum (see also Chapter 12).
RUBELLA (GERMAN MEASLES)

Rubella is usually a mild, self-limiting childhood illness.
The incubation period is 14–21 days, and infection spread is usually by the respiratory route. There is
a mild prodrome with a low-grade fever, followed by a maculopapular rash, starting on the face, then
spreading to the whole body, and fading in 3–5 days. There may also be cervical lymphadenopathy,
mild pharyngitis and conjunctivitis.
Complications may include arthritis, encephalitis, thrombocytopenia and myocarditis.
The major complication is infection during pregnancy, when it can give rise to the rubella syndrome
in the developing fetus. This is the triad of congenital deafness, cardiac defects and cataracts, and it
usually also includes severe mental retardation.
Maternal infection during the first trimester is the most serious, when organogenesis is occurring,
but the effects on the developing fetus progressively become less severe if infection occurs during the
second or third trimester.
MEASLES
Measles is a severe childhood illness with appreciable mortality, particularly in infants (see OSCE
Counselling case 5.2).
The incubation period is 10–12 days, and infection spread is by the respiratory route. The prodromal
illness includes symptoms similar to the common cold, leading to a severe dry cough, fever,
rhinorrhoea, conjunctivitis, and a macular rash starting behind the ears and progressing to the whole
body. The rash lasts for 5–7 days and turns brown as it fades.
Complications may include pneumonia and, rarely, subacute sclerosing panencephalitis (SSPE), a late
complication which can result in neurodegeneration and death.
Measles is making a resurgence in the UK in areas where the vaccination uptake has fallen below that
required for ‘herd immunity’.
KAWASAKI DISEASE
This condition affects children, mainly from the age of 6 months to 4 years.
Kawasaki disease is a vasculitic disease, affecting small and medium-sized vessels, including the
coronary arteries in about one-third of children, which can lead to aneurysms. Subsequent narrowing
of these vessels from scar formation can result in myocardial ischaemia and sudden death.
Questions 51
The diagnosis is made clinically, requiring the presence of a fever and four out of five other criteria, or
the presence of fever, three other criteria and coronary artery aneurysms on echocardiography.
The fever must be persistent and spiking, for more than 5 days.
The other criteria are: bilateral non-exudative conjunctivitis; oropharyngeal mucositis; a polymorphous
rash; cervical lymphadenopathy; and changes in the extremities. These changes involve erythema and
oedema on the wrists and ankles, desquamation of the skin round the nails, and peeling of the skin
which may include the perineum.
Thrombocytosis is a late feature of the disease.
Kawasaki disease is now known to be the result of a bacterial toxin acting as a superantigen.
Treatment is by intravenous human immunoglobulin and aspirin to reduce the risk of coronary artery
aneurysm and thrombus formation.
Echocardiography is now required for all cases of suspected Kawasaki disease.
UK IMMUNIZATION SCHEDULE
Active immunization (vaccination) is the administration of inactivated or attenuated live organisms or
their products to induce an immune response. Protection lasts for months or years, but takes weeks to
develop and may be dependent on receiving more than one dose. The UK schedule is as follows:
After birth: bacille Calmette-Guérin (BCG) (if family originate from an area where tuberculosis is
common or if there has been tuberculosis in the family in the previous 6 months); hepatitis B vaccine
if mother is hepatitis B positive.
2 months: diphtheria, tetanus, pertussis, polio and Haemophilus influenzae type b (DTaP/IPV/Hib);
pneumococcal conjugate vaccine (PCV).
3 months: DTaP/IPV/Hib; meningitis C (MenC).
4 months: DTaP/IPV/Hib; PCV; MenC.
Between 12 and 13 months: measles, mumps and rubella (MMR); PCV; Hib/MenC.
3 years and 4 months to 5 years: DTaP/IPV; MMR.
Girls aged 12–14 years: human papillomavirus (HPV) vaccination. Cervical cancer caused by human
papillomavirus (HPV) types 16 and 18.
13–18 years: tetanus, diphtheria and polio (Td/IPV).
Answers
Clinical cases
CASE 5.1 – My 18-month-old has developed a mild fever and a rash.

Rubella.
Measles.
Roseola infantum.
Kawasaki disease.
Other causes of childhood infection, e.g. streptococcal and meningococcal infection.

The child is mildly unwell, which would suggest rubella. Measles causes a particularly unpleasant
illness, with miserable, unwell children. A high fever and a toxic, unwell-looking child may occur with
meningococcal disease or streptococcal infection.
Does the child have a sore throat (pharyngitis), or red eyes (conjunctivitis)?
Is there any evidence of arthralgia, swollen glands in the neck, or history of a rash starting on the
face?

Check the temperature, heart rate and respiratory rate.
Look at the rash – is it blanching, is it maculopapular?
Look at the throat, eyes and tympanic membranes.
Feel for the cervical and occipital lymph nodes.
Assess the joints for pain and swelling.

Usually, rubella infection is a clinical diagnosis, and no investigations are necessary. If there were a risk
for a pregnant contact, then rubella serology would be appropriate.

Symptomatic measures only are appropriate, e.g. paracetamol for fever. The rash in children is not
usually itchy, unlike in adults.
CASE 5.2 – My 4-year-old has developed a fever 2 weeks after

returning to the UK from abroad.
Viral upper respiratory tract infection.
Childhood exanthems such as rubella.
Answers 53
Meningococcal disease.
Consider malaria.

Any history of recent travel abroad must raise the possibility of malaria. For a child from Africa, this is
likely to be severe Plasmodium falciparum infection, presenting acutely with high fever. Children from
South Asia tend to contract the milder Plasmodium vivax form, which may present with intermittent
fever. Ask about any evidence of severe infection, such as anorexia, not drinking, drowsiness, fits or
rigors, or meningococcal rash. Malaria may present with intermittent rigors as the sporozoites enter the
bloodstream.
Ask about a history of rigors. Find out whether the child and family took anti-malarial prophylaxis
before, during and after their visit, and whether their drugs covered the sensitivities of the malaria
parasites prevalent in their area. Look up the travel advice in the British National Formulary.

Look for a focus of infection, e.g.:
Respiratory/ENT: coryza, cough, noisy or fast breathing.
Gastrointestinal: vomiting, diarrhoea, abdominal pain.
Central nervous system: lethargy, irritability, photophobia.
Genitourinary: dysuria, smelly urine.
Skin: rash, conjunctivitis, skin lesions.
Musculoskeletal: joint pain.

Measure temperature.
Full blood count.
Thick blood films at the point of rigor to identify malarial parasites.
Blood culture.

Paracetamol to reduce fever. Also use physical measures to cool the patient down, e.g. strip down to
vest and pants, or use fan to circulate air in room but not directly on the child.
If malaria is confirmed, include an antimalarial drug such as chloroquine. Check with your local
microbiology service for guidance on the correct treatment depending on the sensitivities of the
malarial parasite strain.
CASE 5.3 – My 3-year-old son has had a fever for 10 days, and his
fingers are peeling.
Differential diagnosis of fever/rashes/sore throat:
Kawasaki disease.
Scarlet fever.
Glandular fever.
Group A streptococcal infection.
Measles.
Rubella.
Roseola.
Viral or bacterial tonsillitis.

A history of prolonged fever persisting for more than 10 days, the changes in the oral cavity, rash on
the skin, cervical lymphadenopathy, peeling of the skin on fingers and toes are strongly suggestive of
Kawasaki disease.
Ask how high the temperature has been; has it been continuous or spiking up and down?
What sort of rash, and where did it start?
Is there anyone else in the family affected (usually not with Kawasaki disease)?
Has the child been fully vaccinated (should make measles and rubella less likely)?

Examine the whole of the body for a rash.
Look for Koplik’s spots on the fauces (look like grains of salt on a red background; seen in the early
stages of measles).
Strawberry tongue (scarlet fever).
Palatal petechiae (may be seen in viral infections and meningococcal disease).
Swelling or erythema of extremities (Kawasaki disease).
Splenomegaly (glandular fever).

Full blood count: atypical lymphocytes in glandular fever; increased platelets – a late finding in
Kawasaki disease.
Monospot/Paul Bunnell test (for glandular fever).
Kawasaki disease is mainly a clinical diagnosis, but the following can be suggestive:
Raised platelet count (>500 000/mm3).
Blood culture.
Erythrocyte sedimentation rate very high.
Echocardiogram for coronary artery aneurysms.

Treatment of Kawasaki disease is intravenous human immunoglobulin and aspirin to reduce risk of
coronary artery aneurysm and thrombus formation.
Follow-up by a paediatric cardiologist is essential, with repeat echocardiography performed about 6
weeks after the original episode.
Answers 55
OSCE COUNSELLING CASE 5.1 – My child has a rash and I am pregnant.

What if it is German measles?
Rubella is a common childhood exanthem which is now very rare in the UK due to uptake of the
MMR vaccine. The child is likely to have a rash from some other infection if he has been immunized.
The mother is likely to have been vaccinated against rubella. All pregnant women have their rubella
status checked at the booking visit, so it should be possible to find out her status.
Check the child’s vaccination status; if not known, take blood from mother and child for rubella
serology.
If the child has rubella infection and the mother is non-immune, action depends on the stage of
pregnancy: the highest risk to the fetus is in the first trimester. The mother and father will require
specialist counselling and consideration of the option of termination of pregnancy.
OSCE COUNSELLING CASE 5.2 – All my friends are advising me not to

let my child have the MMR vaccine.
Measles infection is a childhood killer and cause of considerable mortality (1 in 1000 under 1 year of
age). It is also responsible for a rare fatal, degenerative disease – subacute sclerosing panencephalitis
(SSPE).
MMR is part of the UK immunization schedule, and over five million doses have been administered
since 1988 when it was introduced.
Measles vaccination rarely causes complications, including death in about one per million cases.
Concern has been expressed regarding a possible association between MMR vaccination and
autism in children. Several large-scale epidemiological studies have found no evidence for such an
association; consequently there is not thought to be any risk of developing autism due to MMR
vaccination.
Giving measles, mumps and rubella vaccines separately inevitably reduces the uptake of these
vaccines, increases the time for which children can contract these diseases, and exposes them to the
trauma of six extra injections. Some parts of London where the vaccination rate has fallen below 70
per cent are facing a measles epidemic.
REVISION PANEL
Learn the signs of meningococcal disease. Meningococcal septicaemia can present with a non-
blanching rash. This can be frankly purpuric or quite subtle with marks that look more like flea
bites. Always examine all the skin including perineum and legs and feet.
Meningitis can occur without meningococcal septicaemia, i.e. without a rash. Learn how to assess
neck stiffness. Remember that neck stiffness is an unreliable sign in children under 15 months. It is
not possible to exclude meningitis clinically below this age.
Revise the UK immunization schedule. This is regularly updated so check in the British National
Formulary for Children for the most recent version.
Kawasaki disease is a common cause of unremitting fever lasting 5 days or more. Perform a
thorough examination for the associated features and remember that skin peeling can occur in the
perineum as well as fingers and toes.
The commonest causes of infection in infants are: upper respiratory tract infection – often viral;
lower respiratory tract infection – pneumonia, again often viral; and urinary tract infection – usually
bacterial.
Respiratory problems
Questions
Clinical cases 58
Key concepts 60
Answers
Clinical cases 63
Revision panel 67
58 Respiratory problems
Questions
Clinical cases

diagnosis?
CASE 6.1 – My 6-month-old baby has developed a cough and noisy

breathing.
A 6-month-old baby has had a slight cold. Over the past day she has developed a mild temperature,
worsening cough and wheezing.
CASE 6.2 – My 4-year-old daughter has developed acute breathing

difficulties with cough and wheezing.
A 4-year-old girl has developed wheeze and acute shortness of breath. She has mild eczema, and her
brother needs an inhaler.
CASE 6.3 – My 11-year-old son with cystic fibrosis has developed

shortness of breath and a cough.
An 11-year-old boy who was diagnosed with cystic fibrosis as a neonate has increasing cough and
dyspnoea. He has a temperature and is producing more sputum.
Questions 59
OSCE COUNSELLING CASE 6.1 – My newborn baby has been taken to

the special care unit with breathing
problems. What is the cause?
OSCE COUNSELLING CASE 6.2 – My son has been diagnosed with cystic
fibrosis; what does this mean for him?
Key concepts
AIRWAY INFLAMMATION AND BRONCHOCONSTRICTION

Inflammation of the lining of the small airway can cause swelling which reduces the size of the
airway, making breathing more difficult.
Bronchoconstriction or bronchospasm is a reversible narrowing of the small airways (bronchioles) in
the lung which occurs as a result of contraction of the muscles surrounding the airway.
Airway inflammation can occur as a result of inhaled allergens (such as pollen, house dust mite) or
from viral infections (such as respiratory syncytial virus [see p. 61] and influenza virus).
Bronchoconstriction can be triggered by various factors, including exercise, cold air, smoke and dust.
Both airway inflammation and bronchoconstriction can occur singly or in combination, and can cause
shortness of breath, cough and wheeze.
Wheezing in infancy is very common, and about 50 per cent will experience some wheezing,
particularly after viral respiratory infections. Not all of these wheezy infants will develop asthma, and
two-thirds of children who have wheeze under 3 years of age will be wheeze-free at 9 years.
Some babies with more severe wheeze may benefit from treatment with inhaled bronchodilator
therapy (ipratropium bromide or b2 agonists via a face mask and spacer device may be of benefit in
the acute phase of the illness).
STRIDOR
A harsh, vibratory noise which occurs during the phases of breathing. Stridor can occur during
inspiration, expiration or both (biphasic).
Stridor is a sign of upper airway obstruction, and may be either acute or chronic.
Stridor from birth is usually due to a malformation at, or around, the larynx (e.g. laryngomalacia,
laryngeal cyst).
The commonest cause of acute-onset stridor is viral croup (laryngotracheobronchitis), which usually
affects children aged from 3 months to 5 years.
Mild croup usually manifests as a barking cough (sounding like a seal). Common viruses associated
with croup are parainfluenza virus (accounting for most cases), adenovirus, respiratory syncytial virus
(see p. 61), influenza and measles (see p. 50).
Viral croup is usually mild, and often can be alleviated by breathing moist or cool air. More severe
cases respond to nebulized adrenaline and corticosteroids.
Acute-onset stridor in a previously well child (particularly those over 1 year of age) should always raise
the suspicion of an inhaled foreign body.
Acute epiglottitis can cause severe, life-threatening stridor, but the incidence of this has fallen
dramatically since the introduction of Haemophilus influenzae type B vaccine (see p. 51).
BRONCHIOLITIS
Bronchiolitis is a common lower respiratory tract viral infection affecting children under 2 years of
age (peak age 3–6 months). It involves inflammation of the lower airway, resulting in breathing
difficulties.
Bronchiolitis is seasonal, and occurs mainly in the winter months.
Initial symptoms are similar to the common cold with congestion, runny nose and mild cough and
fever. These symptoms last for a day or two, and are followed by increasing breathing difficulty
characterized by wheezing, worsening cough, tachypnoea and dyspnoea with sternal and/or
subcostal recession (in-drawing of the chest wall at base of rib cage with each breath).
Questions 61
In mild cases, symptoms last 1–3 days. In severe cases, symptoms may progress more rapidly and
include poor feeding and the development of respiratory failure and/or apnoea.
A chest X-ray usually reveals hyperinflation and occasionally lobar infiltrates and/or atelectasis. Mostly
the clinical illness is mild with an uneventful recovery in 5–7 days, though coughing may persist for
up to 2 weeks.
Hospitalization may be necessary, and a small proportion of infants may need respiratory support. At
greatest risk are those with predisposing illness such as congenital heart disease or premature babies
(particularly those with chronic lung disease).
Respiratory syncytial virus (RSV) is the most commonly isolated agent in children aged less than 2
years and hospitalized for bronchiolitis. Other agents that cause bronchiolitis include influenza and
parainfluenza viruses and adenoviruses.
Treatment is mainly supportive – adequate hydration, oxygen if necessary. Monoclonal antibody
prophylaxis and a specific antiviral agent may be of use in high-risk infants such as those born
prematurely with chronic oxygen dependency.
RSV is highly contagious, and so strict measures to prevent cross-infection in hospitals are vital.
ASTHMA
Asthma is a chronic inflammatory disorder of the airways. The inflammation usually results in
widespread (but variable) airway obstruction and an increase in airway response to various stimuli.
Asthma is one of the commonest chronic illnesses in childhood, affecting up to 15 per cent of
schoolchildren.
The typical inflammatory response is characterized by mucosal oedema, increased mucus production
and contraction of bronchial muscles (bronchoconstriction).
Asthma attacks can be precipitated by various triggers, including respiratory infections, allergic
responses (e.g. to pollen, dust, animal dander), exercise, cold air and cigarette smoke.
Symptoms include cough (particularly at night), breathlessness, chest tightness and wheeze.
Clinical signs include wheeze on chest auscultation, chest wall recession and reduced peak expiratory
flow rate (PEFR).
Treatment includes avoidance of precipitating factors, short-acting bronchodilators (e.g. b2 agonists)
for mild disease; inhaled steroid prophylaxis, long-acting b2 agonists and leukotriene antagonists can
be used in more severe disease.
CYSTIC FIBROSIS
Cystic fibrosis is an inherited condition which affects the lungs and digestion.
Cystic fibrosis is the commonest inherited condition in white Caucasians, with an incidence in this
group of 1 in 2500 live births (carrier rate is 1 in 25). It is much less common in other ethnic groups.
A defective gene causes an alteration of the movement of sodium chloride across the membranes of
certain cells. This causes the lungs to produce thick, sticky mucus which blocks the small airways of
the lungs, causing breathing difficulties and predisposing the lungs to infection. Thick secretions also
block the enzymes which are normally produced by the pancreas to aid digestion. The reproductive
system can also be affected, and this results in sterility.
The commonest gene for cystic fibrosis (∆F508) is found on chromosome 7. This accounts for about
80 per cent of UK cystic fibrosis patients, but over 800 mutations have been discovered.
Symptoms include chronic, recurrent chest infections, poor absorption of fats from the diet which
leads to fatty stools (steatorrhoea), and failure to thrive. About 10–20 per cent of infants with
cystic fibrosis will present in the newborn period with meconium ileus, in which failure to pass thick
tenacious meconium leads to intestinal obstruction.
Treatment involves clearing the mucus from the lungs by means of postural drainage and chest
physiotherapy. Chest infections are prevented by prophylactic antibiotics, and exacerbations of
infections are treated aggressively with intravenous antibiotics. Dietary supplements are necessary to
allow adequate absorption of food (pancreatic enzyme supplementation).
The condition can be diagnosed before birth if the defective gene has been isolated from a previously
diagnosed affected sibling.
Blood spot screening at birth detects immunoreactive trypsin which is raised in cystic fibrosis. A sweat
test can then confirm the diagnosis
Treatment is lifelong, and at present no cure is available. Life expectancy is reduced, mainly as a
consequence of strain on the heart from the chronic lung damage (cor pulmonale), and heart–lung
transplantation may be the only option. However, adults with cystic fibrosis are surviving longer as
treatment regimens improve. The current median predicted survival is 35 years therefore currently half
of those with cystic fibrosis will live longer than this.
Answers 63
Answers
Clinical cases
CASE 6.1 – My 6-month-old baby has developed a cough and noisy

breathing.
Viral upper respiratory tract infection (URTI).
Laryngotracheobronchitis (croup).
Bronchiolitis; viral lower respiratory tract infection (LRTI).
Milk aspiration.
Bacterial pneumonia.
Cardiac failure.
Pertussis (whooping cough).

The baby has had coryzal symptoms prior to becoming unwell. Wheeze suggests lower respiratory tract
involvement. The baby is at the peak age for bronchiolitis.
Has the illness steadily worsened, or was there a sudden deterioration? (as in aspiration).
Ask about feeding and episodes of choking or coughing with feeds.
Has the baby turned blue or stopped breathing?
Have other family members (especially siblings) had similar symptoms? (spread of infection).
Past medical history of heart or lung disease, prematurity, immunocompromise.
Immunization history, including pertussis and RSV monoclonal antibody treatment.

Check temperature, heart rate and respiratory rate.
Assess cyanosis (check oxygen saturations), tracheal, sternal or subcostal recession (all of which would
suggest severe respiratory distress).
Auscultation of chest (wheezes ± crackles or stridor).
Abdominal palpation (hepatomegaly may occur in heart failure).

Nasopharyngeal aspirate for viral culture/immunofluorescence (RSV).
Consider per nasal swab (for Bordetella pertussis).
Consider a chest X-ray.

Fluid replacement – either by nasogastric tube or intravenous infusion if feeds not tolerated.
Oxygen – if cyanosis or low oxygen saturations occur (aim to keep oxygen saturations >94 per cent).
Blood gases – if respiratory failure suspected.
Respiratory support – if respiratory failure occurs.

Antibiotics – only if bacterial pneumonia is suspected
Antiviral agents – only in high-risk cases.
CASE 6.2 – My 4-year-old daughter has developed acute breathing

difficulties with cough and wheezing.
Asthma.
Inhaled foreign body.
Viral LRTI.
Bacterial LRTI.
Pneumothorax.

The symptoms are suggestive of asthma; there is a history of atopy and a family history of respiratory
problems.
Ask about onset – sudden or gradual and associated symptoms, e.g. coryza, fever.
Ask about small toys, nuts, etc. in the mouth (foreign body inhalation).
Previous history of wheeze in infancy or nocturnal cough.
Enquire further about family history of asthma or atopy. Exposure to potential precipitating factors –
cold air, exercise, dust, animal dander, etc.

Temperature, heart rate (? tachycardia) and respiratory rate (? tachypnoea).
Assess degree of respiratory difficulty – use of accessory muscles of respiration, intercostal and sub-
costal recession, cyanosis (check oxygen saturations), ability to talk – cyanosis and inability to talk
suggest severe respiratory compromise.
Auscultation of the chest – widespread inspiratory and expiratory wheezes? A silent chest, in which
the breath sounds are difficult to hear, suggests very poor air movement in the lungs and therefore
severe respiratory compromise.

Measurement of PEFR is important in older children, but children aged under 6 years are unlikely to
be able to use the peak flow meter effectively.
Blood gases and chest radiographs are rarely required.

Inhaled b2 agonist via spacer device or nebulizer.
Inhaled ipratropium bromide.
Oxygen (if O2 saturations <92 per cent).
Oral corticosteroids (prednisolone).
Consider continuous nebulized salbutamol, or intravenous aminophylline or intravenous salbutamol
(in refractory or life-threatening attacks, which may need to be given in the intensive care setting).
Answers 65
CASE 6.3 – My 11-year-old son with cystic fibrosis has developed

shortness of breath and a cough.
Acute LRTI.
Pneumothorax.

History of cystic fibrosis, fever, change in sputum production.
Ask about previous exacerbations, colonization with bacteria which are pathogenic in cystic fibrosis
(such as Pseudomonas aeruginosa and Stenotrophomonas maltophilia), haemoptysis and severe
dyspnoea.

Temperature, check for clubbing (chronic suppuration), assess chest expansion and oxygen
saturations. Auscultate for wheeze and crepitations.
Check weight and nutritional status.

Send sputum or cough swab for urgent microbiological analysis.
If possible, check spirometry.

Inhaled bronchodilator therapy.
Intravenous antibiotics as recommended by local cystic fibrosis centre.
Increase in physiotherapy regimen.
OSCE COUNSELLING CASE 6.1 – My newborn baby has been taken to

the special care unit with breathing
problems. What is the cause?
Breathing problems are very common immediately after birth and during the first few hours of life.
The symptoms of respiratory disorders in newborn babies are often the same despite the cause of the
problem. They include cyanosis, tachypnoea (rapid breathing >60/min), recession (sternal, subcostal,
suprasternal), grunting (expiratory noise), nasal flaring and head ‘bobbing’. The lack of specificity of
the symptoms means that all babies with respiratory difficulties should be carefully assessed.
The commonest cause of mild respiratory problems is transient tachypnoea of the newborn (TTN) which
occurs as a result of inadequate clearance of lung fluid immediately after birth. TTN is benign and usually
resolves within a few hours. Some babies may need additional oxygen until the condition settles.
More serious conditions include congenital pneumonia (such as group B streptococcus), surfactant
deficient lung disease (SDLD) or respiratory distress syndrome (RDS), meconium aspiration,
pneumothorax and congenital lung malformation (including congenital diaphragmatic hernia and
cystic adenomatous malformation).
Because of the potentially serious nature of the problems it is sometimes necessary in babies with
symptoms to admit them to the baby unit for assessment. This may include oxygen saturation
monitoring, blood tests and a chest X-ray to try to establish the cause of the symptoms.
The baby may need oxygen therapy or other forms of respiratory support such as continuous positive
airway pressure (CPAP) and ventilation depending on the severity of the illness.
OSCE COUNSELLING CASE 6.2 – My son has been diagnosed with cystic
fibrosis; what does this mean for him?
Cystic fibrosis is the commonest inherited condition in white Caucasians, and primarily affects the
lungs and the digestive system.
When a person has cystic fibrosis there is a problem with the movement of salt across the lining of
certain important cells in the lungs, pancreas and reproductive system. This causes a build up of thick,
sticky mucus which can block the tubes in these parts of the body, affecting how well they work.
The consequences of this build up of mucus is that the small airways of the lungs can become
blocked; this makes breathing difficult and the lungs more susceptible to infection. The blockage in
the pancreas means that important enzymes, which are necessary to digest fats, cannot get into the
intestines and so fats in the diet are poorly absorbed.
Common symptoms include poor growth and fatty stools as a result of poor absorption of fats; cough,
wheeze and chronic chest infections occur as a consequence of the mucus in the lungs. Sometimes,
babies with cystic fibrosis will have difficulty passing stool from birth and have a blocked intestine
which may require operation (meconium ileus). Blockages in the reproductive organs lead to sterility.
There is no cure for this condition, and individuals with cystic fibrosis have a shorter life expectancy.
However, developments in the management of cystic fibrosis have been made which reduce the
incidence of complications and increase the quality of life significantly.
The mainstay of treatment is chest physiotherapy and regular antibiotics to reduce infections and lung
complications, and enzyme supplements which help to improve fat digestion. Acute exacerbations of
chest infections are treated very promptly, usually with intravenous antibiotics.
Cystic fibrosis is an inherited condition, and the most common changes in the genetic material are
now known. Both parents are ‘carriers’ for the disease (i.e. they do not have the disease themselves,
but have the ability to pass it on to their children) There is a one in four risk of this occurring with
each pregnancy. It is now possible to detect whether an unborn baby has the disease if the genetic
defect of their brother or sister with cystic fibrosis is known.
Answers 67
REVISION PANEL
Wheezing in infancy is common but most wheezy infants will not become asthmatic as older
children.
Bronchiolitis is a seasonal viral lower respiratory tract infection which usually affects those under 2
years of age.
Asthma is one of the commonest chronic conditions of childhood which often needs regular
treatment.
Cystic fibrosis is the commonest inherited condition in white Caucasians. It is now routinely
screened for in the UK.
TTN is the commonest cause of breathing problems in newborns; however, symptoms of respiratory
disorders are often non-diagnostic and therefore the baby will require careful assessment in order
to avoid missing a potentially serious condition.
Fits, faints and funny turns
Questions
Clinical cases 70
Key concepts 72
Answers
Clinical cases 74
Revision panel 78
70 Fits, faints and funny turns
Questions
Clinical cases

diagnosis?
CASE 7.1 – My newborn baby is going blue.

After a normal birth and delivery, a baby is now 12 h old and has blue lips and tongue.
CASE 7.2 – My 3-day-old baby has had a fit.

She was a healthy term infant who is breast-fed. She has a nasty infected umbilical cord stump.
CASE 7.3 – My teenage son has just had a fit.

He stayed with friends at the weekend, and was found shaking all over this morning. He had a similar
episode 3 months ago.
Questions 71
OSCE COUNSELLING CASE 7.1 – My infant child has had his first febrile
convulsion; what does it mean?
OSCE COUNSELLING CASE 7.2 – My toddler has frightening breath-

holding attacks.
Key concepts
DEFINITIONS
An epileptic seizure is an intermittent, stereotyped disturbance of behaviour, emotion, motor function
or sensation that on clinical grounds results from cortical neuronal discharge.
Epilepsy is a condition in which epileptic seizures recur, usually spontaneously.
An epilepsy syndrome is a complex of signs and symptoms that define a unique epilepsy syndrome.
This involves more than just the seizure type.
Convulsion, seizure and fit are terms that are often used interchangeably to describe an unusual
episode during which there is a motor component such as stiffening, twitching, jerking or loss of
tone.
Epileptic seizures with a motor manifestation are often classified as myoclonic (rapid contraction
followed by rapid relaxation of one or more muscle groups), spasm (contraction with slow relaxation
of muscles), tonic (stiffening), clonic (rhythmical jerking), tonic-clonic (stiffening with rhythmical
jerking) or atonic/astatic (loss of tone/falling).
In childhood and adolescence there are numerous conditions in which there are intermittent
paroxysmal episodes and which are commonly confused with epilepsy. Such episodes include benign
neonatal sleep myoclonus, syncope, reflex anoxic seizures, hyperexplexia (exaggerated startle) and
self-gratification.
Epilepsy is a clinical diagnosis and it is essential to obtain a detailed history of the episodes concerned,
including how they begin, what happens during them and how they end.
Simple syncope or vasovagal attacks (faints) consist of a loss of consciousness, usually preceded by
a drop in peripheral vascular resistance and blood pressure, together with bradycardia, and are self-
limiting. This may be followed by a stiffening or anoxic epileptic seizure.
Breath-holding attacks or blue breath-holding is the end-expiratory apnoea that commonly
accompanies distraught crying in toddlers. It is the silent spell before the next loud inspiratory gasp
and subsequent cry. There may also be stiffening or unusual posturing but the children usually recover
quickly. However, rarely such episodes may be followed by anoxic epileptic seizures.
A febrile convulsion is a convulsion associated with fever (see OSCE Counselling case 7.1).
Reflex anoxic syncope or reflex anoxic seizure is a massive vagal bradycardia leading to transient
severe bradycardia or asystole which is 5–30 s in duration. The trigger may be a surprise or sudden
pain. Because there is severe bradycardia or asystole and impaired or no circulation, the child is white
and appears to be dead. The recovery from such episodes is usually relatively quick. These episodes
are very frightening, may continue for years, and often no trigger is identified.
Jitters which often occur in babies are fast twitches (faster than three per second) which are not
epileptic in nature, usually occur in response to an external stimulus, and can be stilled by touching
the limb.
THE PURPOSE OF ELECTROENCEPHALOGRAPHY

Electroencephalography (EEG) is the most commonly requested neurological test.
The electrical activity of the brain is recorded on paper in a number of channels (8 or 16).
Rhythms are described in terms of frequency, e.g. slow waves of 0.5–3 Hz.
EEG is indicated to clarify the type of epilepsy, once a clinical diagnosis of epilepsy has been made.
Common patterns include: a three per second spike and wave discharge in typical absence epilepsy;
hypsarrhythmia in infantile spasms; burst suppression and slow waves with encephalopathy.
Questions 73
NEONATAL SEIZURES
These are seizures occurring in the neonatal period; they usually have a cause.
Causes include hypoxic ischaemic encephalopathy (HIE), perinatal trauma (intracranial bleeding),
infection and metabolic abnormalities (e.g. hypoglycaemia, hypocalcaemia, hypomagnesaemia,
hyponatraemia and hypernatraemia).
Fits in neonates may present as cyanotic episodes or apnoeas, cycling limb movements or mouthing.
IDIOPATHIC EPILEPSIES
These are epilepsy syndromes in infancy and childhood, without an obvious precipitating cause.
These are classified by clinical features: generalized (e.g. tonic-clonic, typical absence and myoclonic);
and focal (e.g. focal sensory, focal motor, and focal sensorimotor).
Epileptic seizures are often not tonic-clonic in type, and may be subtle and easily missed.
CYANOTIC AND ACYANOTIC CONGENITAL HEART DISEASE

Most heart disease in children is congenital.
6–8 per 1000 live births have significant cardiac malformations.
Acyanotic heart lesions are not usually duct-dependent; that is, they may not rely on blood flow
through the patent ductus arteriosus, which closes soon after birth. Examples include ventricular
septal defect and atrial septal defect. The exceptions include critical aortic stenosis and coarctation of
the aorta, which may be duct-dependent.
Cyanotic heart lesions are often duct-dependent, and so present with central cyanosis soon after
birth. Examples include transposition of the great arteries (TGA) and Ebstein’s anomaly .
Peripheral cyanosis (blueness of the hands and feet) may occur when a child is cold or crying or ill
from any cause.
Central cyanosis is blueness of the tongue and lips, associated with a fall in arterial oxygen tension. It
is seen clinically if the concentration of reduced haemoglobin in the blood is at least 5 g/dL, so may be
difficult to spot in an anaemic child.
Pulse oximetry is useful in detecting mild cyanosis which may not be clinically apparent.
Answers
Clinical cases
CASE 7.1 – My newborn baby is going blue.

Cyanotic congenital heart disease, either from reduced pulmonary blood flow, or abnormal mixing of
systemic venous and pulmonary venous blood.
Persistent fetal circulation.
Respiratory causes, e.g. pneumonia, aspiration, transient tachypnoea of the newborn, surfactant
deficiency (respiratory distress syndrome), congenital abnormality.
Shock, such as blood loss, b-haemolytic streptococcal septicaemia.
Hypothermia.
Fits.

A diagnosis of cyanotic congenital heart disease would be supported by:
Central cyanosis (of the lips and tongue) as opposed to peripheral cyanosis (hands and feet).
Otherwise well infant.
Usually lack of respiratory distress unless coexisting respiratory disease (see above) or polycythaemia.
Ask about antenatal scans: many hospitals undertake a four-chamber view of the heart at around 20
weeks.
Does the infant get breathless on feeding? Any respiratory distress or apnoeas?
Ask if the infant ever looked pink.
Is there a family history of congenital heart disease?

Check for central or peripheral cyanosis.
Measure temperature.
Examine for signs of shock, e.g. delayed capillary return, rapid thready pulse, pallor.
Are there any other signs of systemic illness, e.g. hepatomegaly or rashes.
Are there any dysmorphic features, e.g. Down’s syndrome? (associated with increased incidence of
congenital heart lesions).
Check the pulses for brachio-brachial or brachio-femoral delay (coarctation of the aorta).
Is there an audible heart murmur or palpable thrill?

Measure oxygen saturation in right hand and lower limb (pre- and post-ductal). Normal arterial
oxygen saturation should be above 94 per cent. In cyanotic heart disease this can fall to the
saturation of venous blood, i.e. <75 per cent.
Answers 75
Nitrogen washout test. Place the infant in 100 per cent oxygen for 10 min. If the oxygen saturations
do not improve, it makes a respiratory cause for cyanosis much less likely, and a diagnosis of cyanotic
congenital heart disease is more likely.
Perform chest X-ray. Look for signs of an abnormal heart outline and/or oligaemic or plethoric lung
fields (congenital heart disease).
Electrocardiography.

In duct-dependent lesions, give a prostaglandin (PGE2) infusion. This is to maintain the patency of the
ductus arteriosus to allow mixing of venous and arterial blood.
Refer to a specialist paediatric cardiology unit for echocardiography and definitive diagnosis.
Definitive surgical treatment depends on the nature of the lesion. Some lesions are correctable
surgically (e.g. TGA); others are more complex, and may not be correctable.
CASE 7.2 – My 3-day-old baby has had a fit.

Most epileptic seizures in infants have an identifiable cause, as opposed to epileptic seizures in older
children, which are usually idiopathic.
Consider meningitis: this is usually associated with septicaemia in the first week.
Low serum levels of glucose, calcium, magnesium or sodium can all cause fits.
Drug withdrawal, for instance maternal opiate abuse in pregnancy.
Inborn errors of metabolism, such as organic acidaemias.
Epileptic seizures occurring in the first 48 h of life are most commonly due to perinatal hypoxia/
ischaemia, intracranial trauma or haemorrhage.

The infected umbilicus suggests infection but this may be coincidental.
Was there a history of difficult labour, i.e. prolonged, forceps (perinatal hypoxia, intracranial trauma)?
Did the baby need resuscitation? What were the Apgar scores?
Was there prolonged rupture of the membranes >18 h (sepsis)?
Was there a maternal history of drug abuse (drug withdrawal)?
Is there a family history of stillbirths or neonatal deaths (suggestive of inborn errors of metabolism)?
Poor feeding.

Examine the baby for signs of infection. A flare around or from the umbilicus would suggest a
bacterial infection.
Examine for signs of poor perfusion, e.g. sunken fontanelle, slow capillary refill and birth trauma (e.g.
bruising, fractures).
Observe conscious level and spontaneous movement. Is the baby irritable or drowsy?
Tense fontanelle may suggest meningitis.
Obtain a detailed description of the episode and if possible, observe or obtain a video recording of
further episodes.

Culture skin swabs, blood and cerebrospinal fluid for infection.
Consider a cranial ultrasound for evidence of intracranial haemorrhage.
Check blood glucose, serum electrolytes, calcium and magnesium.

Treat infection with systemic antibiotics.
Try to obtain control of seizures with anticonvulsants (phenobarbital and/or phenytoin are commonly
used to treat seizures occurring in the neonatal period. Benzodiazepines are used less frequently in
the neonatal period since they may cause respiratory depression).
If the cause is not clear consider rare causes and discuss with a paediatric neurologist and/or the
metabolic team.
Counsel the parents as to the cause.
CASE 7.3 – My teenage son has just had a fit.

Idiopathic epilepsy.
Syncope-related anoxic epileptic seizure.
Drug intoxication, e.g. alcohol.
Hypoglycaemic episode, possibly secondary to alcohol.
Trauma.
Space-occupying intracranial lesion.

Most epileptic seizures in teenagers are idiopathic, as opposed to epileptic seizures occurring in
infants, which usually are symptomatic (have an underlying cause).
The previous episode of a seizure makes the diagnosis of epilepsy more likely, and this is unlikely to
be simple syncope.
The history of shaking all over would be compatible with a generalized tonic-clonic seizure,
particularly if this was followed by a relatively long post-ictal phase (period of drowsiness, confusion
and or sleep).
Get a detailed description of the episode from his friends.
Was the son drinking with friends, or taking drugs?
Has there been a preceding history of headaches or visual disturbance? (intracranial lesion).
Does he regularly feel faint first thing in the morning? (hypoglycaemia, cortisol insufficiency, postural
hypotension).
Has he had a recent head injury, perhaps sports-related?
Is there a history of sleep deprivation or possible photosensitivity? (possible triggers for epileptic
seizures).
Is there a history of absence seizures/vacant episodes and/or myoclonic seizures/twitches/clumsiness
(occurring particularly in the mornings)? (If there is a history of absence seizures and/or morning
myoclonic seizures a possible diagnosis is juvenile myoclonic epilepsy.)
Answers 77

Look for signs of trauma.
Pale, clammy, with a bradycardia would suggest a faint.
Drowsiness, incontinence, tongue biting and reduced reflexes are more likely to occur in epileptic
seizures but may also occur in other conditions with intermittent paroxysmal episodes.
Pin-point pupils may suggest drug-taking.
Fundoscopy (for optic disc swelling), reflexes, full neurological examination.

Check capillary blood glucose for hypoglycaemia.
Consider blood or urine samples for drug levels if drug-taking is considered.
Check blood pressure, both lying and standing.
EEG to try to classify the seizure type and epilepsy syndrome.

Epilepsy should be treated with antiepileptic drugs (the choice of drug depends on the seizure
type, the likely epilepsy syndrome, gender, other health problems and interactions with any other
concomitant medications).
The patient should be advised to carry a MedicAlert bracelet or card with the diagnosis.
The patient should be encouraged to inform his close relatives, school, college and/or work
colleagues.
Advice should be given regarding lifestyle issues, e.g. avoiding sleep deprivation if felt to be a likely
trigger, drinking alcohol in moderation, avoiding flashing or flickering lights if have photosensitive
epilepsy and taking showers instead of baths due to the possible risk of drowning if has a seizure in
the bath.
Advice should be given regarding occupations (e.g. driving heavy goods vehicles), and sporting
activities such as swimming.
OSCE COUNSELLING CASE 7.1 – My infant child has had his first febrile
convulsion; what does it mean?
Febrile convulsions are common, and affect about 3 per cent of all children.
The commonest ages to be affected are between 6 months and 6 years.
The convulsions are usually brief, lasting under 5 min, and generalized tonic-clonic.
The precipitant is commonly a viral upper respiratory tract infection, with the convulsion occurring
when the temperature is rising rapidly.
Febrile convulsions often run in families.
In about 15 per cent of cases, another febrile convulsion will occur during the same episode of illness.
The risk of a further febrile convulsion with another illness is about 30 per cent.
This does not mean your child will have epilepsy; the risk for epilepsy after febrile convulsion is only
about 2–4 per cent.
The immediate management is to make sure your child is safe and breathing. Use simple measures to
reduce the temperature, e.g. anti-pyretic medication (paracetamol).
Do not place anything in your child’s mouth.
Call an ambulance if: the convulsion is atypical (i.e. prolonged more than 5 min), one-sided, your child
has a rash, or if your child goes blue.
OSCE COUNSELLING CASE 7.2 – My toddler has frightening breath-

holding attacks.
Blue breath-holding attacks are common and benign. They occur when your child breathes out and
pauses before breathing back in.
They can be set off by crying, upset or pain.
Your child may go blue and lose consciousness, but will rapidly recover.
No drug treatment is necessary, although these episodes have been linked to iron deficiency and it
would be worth checking your child is not anaemic.
Attacks will resolve by themselves, but behaviour modification therapy with avoidance of
confrontation may help.
REVISION PANEL
There are many different epileptic seizure types and epilepsy syndromes.
Neonatal seizures usually have a cause.
In childhood and adolescence there are many other conditions in which there are intermittent,
paroxysmal episodes which may be confused with epilepsy.
Epilepsy is a clinical diagnosis and the EEG may provide additional information which helps to
classify the seizure type and epilepsy syndrome.
Obtaining a detailed history of the episode, including how it begins, what happens during it and
how it finishes, is key to correctly diagnosing epilepsy or another condition with intermittent,
paroxysmal episodes.
Being able to review a video recording of the episode is often helpful in making a diagnosis.
Headache
Questions
Clinical cases 80
Key concepts 82
Answers
Clinical cases 83
Revision panel 87
80 Headache
Questions
Clinical cases

diagnosis?
CASE 8.1 – My 8-year-old daughter has started to get headaches and is

missing school.
An 8-year-old girl has started to get recurrent symmetrical headaches. They are of gradual onset and are
described thus: ‘like a band around my head’. She is having problems coping with the demands made by
her school and has missed a third of her schooling this term.
CASE 8.2 – My 11-year-old son is having recurrent headaches with

vomiting.
An 11-year-old boy is having recurrent headaches which are throbbing, over his left eye, and associated
with a visual aura. They are worsening in severity and frequency, but his school progress is good. His
mother gets migraines that respond to treatment with triptans.
CASE 8.3 – My 6-year-old girl has a headache and has gone off her legs.
A 6-year-old child presents with a 4-week history of a constant progressive headache which makes her
cry inconsolably, with a week’s history of an unsteady gait and slurred speech.
Questions 81
OSCE COUNSELLING CASE 8.1 – My 11-year-old son has migraine.

An 11-year-old boy has recurrent headaches which are throbbing, over his left eye, and are associated
with a visual aura. They are worsening in severity and frequency, but his school progress is good. His
mother gets migraines that respond to treatment with triptans. Clinical assessment suggests that the boy
also has migraine.
OSCE COUNSELLING CASE 8.2 – My 6-year-old girl needs an MRI head.

82 Headache
Key concepts
HEADACHE
Headache is common in schoolchildren and young people. Some 95 per cent of schoolchildren report
one headache per year.
Headache is uncommon in preschool children.
The following classification of headache is useful in diagnosis:
Acute:
febrile illness of any cause;
acute sinusitis;
intracranial sepsis (meningitis, encephalitis, abscess);
head injury;
space-occupying lesion;
intracranial bleed;
hypertension.
Recurrent:
tension headache;
migraine;
ocular headaches due to refractive errors;
space-occupying lesion;
raised intracranial pressure;
hypertension;
poisoning, e.g. drug abuse, carbon monoxide (see p. 135);
seizures (see pp. 72–3).
Answers 83
Answers
Clinical cases
CASE 8.1 – My 8-year-old daughter has started to get headaches and is

missing school.
Tension headaches.
Migraine.
Raised intracranial pressure.
Hypertension.
Sinusitis.
Benign intracranial hypertension.
Carbon monoxide poisoning.

The description of the headache as a ‘band’, its recurrent non-progressive nature, and the history of
school problems suggest tension headaches.
Seek symptoms of:
Migraine: aura, nausea, vomiting, pallor, focal neurology, abdominal pain, family history of migraine.
Raised intracranial pressure: worsening school progress, behavioural change, early morning
headaches, headaches at night, headaches worse on coughing, sneezing, laughing or bending over.

Plot height and weight.
Measure blood pressure.
Full neurological examination including conscious level, mentation, cranial nerves, e.g. visual fields
in craniopharyngioma, visual acuity problems in tension headaches and idiopathic intracranial
hypertension, other cranial nerve abnormalities in brainstem tumours, fundoscopy for papilloedema,
cerebellar signs and cranial bruits, e.g. in arteriovenous malformations.

Investigations are only conducted if indicated by clinical assessment. A diagnosis can often be made
without investigation. Urgent cranial imaging (computed tomography [CT] or magnetic resonance
imaging [MRI]) is indicated if there is evidence of:
Altered consciousness.
Focal neurological signs.
Hypertension.
Papilloedema.
Headaches worsening (e.g. waking at night).
84 Headache
Change in behaviour or personality.

Worsening school performance.

Tension headaches require reassurance and analgesia. School issues need to be addressed by working
with the school doctor and relevant teachers.
CASE 8.2 – My 11-year-old son is having recurrent headaches with

vomiting.
Migraine.
Tension headaches.
Raised intracranial pressure.
Hypertension.
Sinusitis.
Benign intracranial hypertension.
Carbon monoxide poisoning (see p. 135).

Recurrent headaches associated with nausea, an aura and a family history are suggestive of migraine.
Some 50 per cent of children with migraine have a first-degree relative with the same diagnosis.
Seek details of:
Amount of school missed.
Duration of each headache.
Severity.
Triggers, e.g. sleep deprivation, missing meals, poor fluid intake during the day, physical activity or
exercise, certain foods or drinks (caffeine as found in cola drinks and high energy drinks, chocolate
and coffee) are common triggers for migraines.
Treatment given so far.
Behaviour or personality change.
Nocturnal headache.

Full neurological examination including conscious level, mentation, cranial nerves, fundoscopy, cranial
bruits and cerebellar signs.

Investigations are only conducted if indicated by clinical assessment.
A diagnosis can often be made without investigation.
Indications for urgent cranial imaging are listed in Case 8.1, A5.
Answers 85

Management of migraine includes:
Diagnosis and explanation of cause.
Identification of triggers through a headache diary.
Avoidance of triggers.
Prompt treatment of early symptoms with analgesia such as paracetamol, which may be combined
with an anti-emetic.
Discussion about the pros of prophylaxis (reduced frequency of headaches) versus the cons (need to
take medication daily, side effects such as tiredness).
Triptans have not been used extensively in children, and are not licensed for this age group.
CASE 8.3 – My 6-year-old girl has a headache and has gone off her legs.
Brain tumour.
Intracranial infection, e.g. brain abscess, meningitis, septicaemia, encephalitis.
Trauma with intracranial injury.
Carbon monoxide poisoning (see p. 135).

The recent onset of a severe, progressive headache associated with focal neurological signs suggests
intracranial pathology.
Seek a history of:
Previous episodes.
Fever.
Onset of headache.
Behaviour and personality change.
School progress.
Contact with infectious diseases, travel (e.g. malaria).
Family history of migraine.

Examine skin for neurocutaneous signs (e.g. neurofibromas, café-au-lait spots in neurofibromatosis).
Full neurological examination including conscious level, mentation, cranial nerves, fundoscopy, cranial
bruits and cerebellar signs.

Urgent intracranial imaging (CT head or MRI).
Further investigations as indicted by clinical assessment and imaging:
full blood count: a raised white cell count suggests infection;
thick film for malaria parasites (see p. 53): if history of foreign travel;
urea and electrolytes: for syndrome of inappropriate antidiuretic hormone secretion (SIADH);
carbon monoxide levels: if history of contact;
lead levels.
86 Headache

Rapid clinical assessment may indicate need for urgent intervention before a detailed history can be
taken. Basic and advanced life support should be instituted as required.
Intravenous antibiotics and antivirals.
Management of raised intracranial pressure.
Urgent referral for neurosurgical opinion.
Answers 87
OSCE COUNSELLING CASE 8.1 – My 11-year-old son has migraine.

Families, children and young people with migraine require verbal and written information. They need to
know:
How their symptoms fit the diagnosis of migraine.
Fear of ‘brain tumour’ is a common reason for presentation; your careful and thorough assessment
has excluded this, and provided the reasons why.
The cause of migraine is not known; one theory is that blood vessels in one part of the brain
become narrowed when the sufferer gets altered sensations, then open wide so that may lead to
the headache. The blood vessels then return to normal. The theory does not explain the whole story
however, and chemicals in the brain may also play a part.
Commonly there is a family history of migraine.
Triggers are important in setting off migraine: diet (e.g. chocolate, cheese, caffeine-containing
foods and drinks), environment (e.g. smoke, bright lights), medication (e.g. the pill), hormones (e.g.
menstruation, anxiety). Sometimes, triggers can be identified and avoided by keeping a ‘headache
diary’.
Prompt treatment of early symptoms with an analgesic such as paracetamol is required; this may be
combined with an anti-emetic.
Discussion about the pros of prophylaxis (reduced frequency of headaches) versus the cons (need to
take medication daily, side effects such as tiredness).
OSCE COUNSELLING CASE 8.2 – My 6-year-old girl needs an MRI head.

MRI creates a detailed picture of the brain and the head.
Usually, you can go home on the same day as you have one.
The scanner looks like a small tunnel.
Sedation or a general anaesthetic may be needed if the child is too young to lie still. MRI scanners are
noisy and may frighten young children.
In order to see certain parts of the brain, you may need to be given a small amount of dye which
is harmless, but shows up on the pictures. The dye is given via a small needle which is inserted into
a vein on the back of the child’s hand. We will use a local anaesthetic cream to make sure that the
needle injection is not painful.
Play specialists should rehearse the procedure with children prior to the scan to ensure that they
understand what will happen.
REVISION PANEL
Headaches are common in schoolchildren and young people.
Headaches can be a symptom of an acute illness or may be recurrent.
History and examination are important in determining the cause for or type of headache.
Investigations such as cranial imaging are not usually needed in most children presenting with
headaches who otherwise appear well.
Cranial imaging is warranted if there are any signs or other symptoms to suggest possible raised
intracranial pressure or space-occupying lesion.
In migraines, there is often a family history and possible triggers can often be identified.
Diarrhoea and vomiting
Questions
Clinical cases 90
Key concepts 92
Answers
Clinical cases 94
Revision panel 97
90 Diarrhoea and vomiting
Questions
Clinical cases

diagnosis?
CASE 9.1 – My 6-month-old son started screaming with pain and

drawing up his legs. There is nothing I can do to console
him.
A previously well child has developed sudden-onset episodes of screaming and drawing up his legs; he
has not opened his bowels recently, and looks very pale.
CASE 9.2 – My toddler has developed sickness and diarrhoea. Most of

the other children at his nursery have developed it as well.
A 14-month-old boy has started vomiting and has loose watery stools up to eight times a day. He has a
slight fever and is rather quiet. Other mothers at the nursery report similar findings.
CASE 9.3 – My 4-week-old boy has suddenly started vomiting up all his
feeds and can’t stop, even though he still wants to feed.
This baby was born at term after a normal pregnancy. He fed well initially, but recently he has been
vomiting after every feed. Sometimes, the vomiting is forceful and shoots out of his mouth. He still
seems hungry and feeds vigorously.
Questions 91
OSCE COUNSELLING CASE 9.1 – My child cries all the time with colic;
what shall I do?
OSCE COUNSELLING CASE 9.2 – My baby keeps being sick after feeds, I
am changing clothes all the time; what
should I do?
Key concepts
ASSESSMENT OF DEHYDRATION
Dehydration is assessed clinically. The symptoms and signs to look for include:
Thirst, irritability, lethargy.
Dry mucous membranes.
Sunken eyes.
Rapid, thready pulse.
Sunken fontanelle (in babies).
Reduced tissue turgor (this is a reduction in the elasticity of the skin).
Reduced capillary return.
Pallor and mottled extremities.
Reduced urine output.
Reduced level of consciousness (in severe cases).
STOOL FREQUENCY AND DIARRHOEA

Newborn babies pass sticky black stools (meconium) after birth.
Breast-fed babies pass frequent, loose, seedy yellow stools.
Breast-fed infants may pass up to 8–10 stools a day. Bottle-fed babies usually pass stools less
frequently (2–3 times a day).
Stools that are watery or soak into the nappy with no solid material are abnormal.
The presence of blood in the stool indicates pathology, e.g. infection, mucosal tear, gastrointestinal
bleeding.
Diarrhoea is the passage of frequent, loose stools.
The causes of diarrhoea are acute (e.g. gastroenteritis, associated with antibiotic treatment) and
chronic (e.g. post-infectious malabsorption, coeliac disease and inflammatory bowel disease).
Treatment involves correction of any dehydration, and is then directed to the underlying cause.
Note: Oral rehydration therapy consists of a glucose and electrolyte powder which is reconstituted
with water. The principle is the linked active transport of sodium and glucose absorption in the small
intestine. Glucose and sodium are cotransported across the intestinal mucosa with water.
Give maintenance fluids plus replacement of deficit and ongoing losses. Aim to correct dehydration
within 4–12 h with 50–100 mL/kg oral rehydration fluid given as frequent small amounts.
INFANTILE COLIC
This is very common in infancy, and consists of paroxysmal, inconsolable crying or screaming together
with drawing up of the knees. This can occur several times a day, but it is more common in the evening.
The cause is unknown, but is benign, and it is not associated with other disease. Indeed, it is not
recognized in some countries.
Babies are well between episodes.
Management is by swaddling the child up for comfort, and cuddling.
It resolves usually by 3 months of age.
GASTRO-OESOPHAGEAL REFLUX
This is common in infancy, and ranges from the ‘posset’ of a mouthful of milk after a feed to
vomiting up most of the feed. If severe it may lead to failure to thrive, anaemia and aspiration
pneumonitis.
Most reflux resolves by 12 months of age.
Questions 93
Complications can include oesophagitis causing pain, bleeding and anaemia; dystonic movements of
the head and neck (Sandifer’s syndrome); apnoeas in preterm infants. It is more common in infants
with cerebral palsy (see p. 16).
The cause is thought to be functional immaturity of the lower oesophageal sphincter, leading to
inappropriate relaxation.
Diagnosis is usually made by the history, although a contrast swallow or 24 h oesophageal pH study
may be indicated in more severe cases.
Infants with mild uncomplicated reflux can be diagnosed clinically and managed with thickening
agents added to the feeds.
Sometimes, drugs which help to reduce acid in the stomach (e.g. ranitidine) or help bowel peristalsis
may be necessary.
The most severe cases are treated by fundoplication, where the stomach fundus is wrapped around
the intra-abdominal oesophagus.
INTUSSUSCEPTION
This is the invagination of one segment of bowel into an adjacent lower segment, cutting off the
blood supply to the invaginated segment as it progresses.
It usually begins proximal to the ileocaecal valve.
Intussusception is the commonest cause of bowel obstruction in infants after the neonatal period,
occurring most commonly at the age of 6–9 months.
It characteristically presents with paroxysmal, colicky abdominal pain and pallor. The infant draws up
the legs with the pain.
Vomiting and diarrhoea are common, and sometimes a sausage-shaped mass is palpable in the
abdomen.
Late presentations may include passage of ‘redcurrant jelly’ stools, which contain blood and mucus.
It is possible that viral infection leads to swelling of Peyer’s patches (lymph tissue in the small
intestine) from which the intussusception may begin.
An abdominal X-ray may show small bowel obstruction. Treatment is usually by reduction of the
intussusception with air per rectum; alternatively contrast medium may be used.
Profound shock may occur due to pooling of fluid in the gut. Intravenous fluids are usually required
to prevent circulatory failure.
PYLORIC STENOSIS
Affects infants between 2 and 8 weeks of age, more frequently males and first-born children.
There may also be a family history, especially in the mother.
The cause is hypertrophy of the pylorus muscle at the exit of the stomach.
There is persistent uncontrollable vomiting which is not bile-stained.
The vomiting is projectile, i.e. it shoots out with force.
Vomiting usually occurs within 30 min of a feed, and the infant is hungry afterwards.
The infant may be constipated and become dehydrated.
A hypochloraemic alkalosis develops from vomiting the acid stomach contents. Some infants are
mildly jaundiced.
On examination, gastric peristalsis may be visible in the epigastrium following a feed.
The diagnosis is made by palpation of an enlarged hard pylorus in the right upper quadrant during a
test feed (see below). An ultrasound scan of the pyloric region may also be diagnostic.
A test feed is performed as follows. Place the child on its mother’s lap and allow to feed, while
positioning yourself kneeling to the left side of the child’s abdomen. Observe the abdomen for signs
of peristalsis, particularly a wave occurring across the abdomen. Palpate using your left hand in the
infant’s right upper quadrant for a mass the size and consistency of the end of your nose.
The management is to correct the dehydration and electrolyte imbalance, and undertake a
pyloromyotomy: the pylorus is incised to divide the hypertrophied muscle fibres, but not the pyloric
mucosa.
Answers
Clinical cases
CASE 9.1 – My 6-month-old son started screaming with pain and

drawing up his legs. There is nothing I can do to console
him.
Acute infantile colic.
Acute intussusception.
Acute gastroenteritis.
Testicular torsion (in boys).
Strangulated inguinal hernia.
Other cause of intestinal obstruction.
Non-accidental injury.
Serious bacterial illness of any cause, e.g. meningitis, septicaemia.

Acute intussusception is supported by the sudden onset of the condition in a previously well child,
inconsolable pain, and drawing up of the legs. Infantile colic would have presented earlier and be
intermittent, with the child completely well between episodes.
Ask about any vomiting and diarrhoea which may occur in gastroenteritis and also intussusception.
What colour are the stools (i.e. is there blood present)?
Ask about pallor or any recent viral infection.

Assess the level of dehydration and shock (acute circulatory failure).
Examine the abdomen between bouts of pain for any tenderness or masses.
Listen for bowel sounds (in intestinal obstruction bowel sounds are characteristically tinkling).
Examine the hernial orifices and testes for erythema, tenderness or swelling.

Check a blood sample for acidosis, urea and electrolytes, and full blood count.
A plain abdominal X-ray would assist in the diagnosis of obstruction.
Urinalysis and blood culture.

If present, correct shock with intravenous fluids.
Reduction of the intussusception with air insufflation under radiological control.
An obstructed hernia will require urgent surgery.
Answers 95
CASE 9.2 – My toddler has developed sickness and diarrhoea. Most of

the other children at his nursery have developed it as well.
Acute viral gastroenteritis.
Bacterial gastroenteritis, e.g. Salmonella, Campylobacter, Shigella dysentery.
Lactose intolerance.
Coeliac disease.

The presence of diarrhoea and vomiting in the child’s nursery supports the diagnosis of an infective
cause (e.g. rotavirus). This also makes food-borne infections a possibility.
Ask about the frequency of dirty nappies. Up to four dirty nappies a day is probably normal.
Ask about the nature of the stools: profuse watery diarrhoea with little solid material suggests
gastroenteritis. Ask if there is any blood in the stools or vomit.
If the vomiting is bile-stained, consider obstruction.
Ask about any foreign travel (bacterial gastroenteritis more likely).

Examine the abdomen.
Assess the level of hydration.
moderate (5 per cent) dehydration gives the signs of irritability, dry lips and mouth, and eyes
slightly sunken;
severe (10 per cent) dehydration is suggested by altered consciousness, rapid thready pulse,
reduced skin turgor.

Consider checking serum sodium to look for hyponatraemic or hypernatraemic dehydration.
Take a stool sample for culture and microscopy for ova, cysts and parasites, and immunofluorescence
for rotavirus (the commonest cause of acute gastroenteritis in winter months).

Oral rehydration therapy rather than intravenous fluid therapy.
Reintroduce feeds as soon as possible when rehydrated. Do not stop breast-feeding.
CASE 9.3 – My 4-week-old boy has suddenly started vomiting up all his
feeds and can’t stop, even though he still wants to feed.
Pyloric stenosis.
Acute gastroenteritis.
Neonatal intestinal obstruction (e.g. malrotation, Ladd’s bands, duodenal web).

Pyloric stenosis is suggested by the timing of onset of vomiting (usually within 20 min of a feed), the age
(2–8 weeks at presentation) and the desire to continue feeding, which is present in the early stages but
is lost as the infant becomes dehydrated.
Birth history, early feeding and time to pass meconium.
Ask about any previous history of vomiting, particularly with feeds.
Enquire about stool frequency.
Is the child the first in the family and is there a family history of pyloric stenosis?

Assess level of dehydration.
Examine the infant’s abdomen before, during and after a test feed (see p. 93).

An ultrasound of the abdomen is most helpful to confirm the presence of pyloric hypertrophy.
Check urea, electrolytes and chloride for evidence of dehydration and hypochloraemic metabolic
alkalosis.

Correction of the metabolic abnormalities with intravenous fluids, including potassium.
Surgery: pyloromyotomy, only after correction of metabolic abnormalities.
Answers 97
OSCE COUNSELLING CASE 9.1 – My child cries all the time with colic;
what shall I do?
Colic is very common, and affects almost all babies at some point; the cause is unknown.
Colic is completely harmless and goes away by itself, usually by the age of 3 months.
Proprietary remedies may help some, but not all, babies.
Do not give alcohol in any form as the baby may become hypoglycaemic.
Wrap the baby up well and cuddle him.
If you just cannot cope any longer, seek help from family and friends, or your health visitor or general
practitioner (GP).
OSCE COUNSELLING CASE 9.2 – My baby keeps being sick after feeds, I
am changing clothes all the time; what
should I do?
Gastro-oesophageal reflux is common, and usually harmless.
It is more inconvenient than anything else as it involves lots of washing and makes the house smell.
It happens when food in the stomach gets pushed back up the gullet, due to immaturity of the
muscle at the base of the gullet that should stop this reflux.
The acid that comes up with the food may irritate the baby and cause discomfort.
Simple measures may help: nurse the baby upright or at 30o after feeds; try adding a proprietary
thickener to bottle feeds.
If necessary, there are drugs that will help.
Please let the doctor know if there is blood in the refluxed milk.
If it persists, further investigation and treatment may be necessary.
REVISION PANEL
Remember the signs of dehydration: (see also Chapter 10 revision panel); when calculating fluid
replacement, estimate the percentage dehydration; the normal maintenance requirements; and
any ongoing fluid losses. Add these together and replace over the required time (usually 24 h; in
diabetic ketoacidosis, over 48 h).
In an unwell child always consider the possibility of a child protection issue. Clues in the history
include: delayed presentation; a history that does not fit with the presenting signs; a history that
changes over time; and that changes between the carer who gives the history.
Always take abdominal pain seriously and get a surgical opinion if clinical signs. Children with acute
abdomens can rapidly progress to peritonitis.
Bloody stools usually but not always, suggests a bacterial infection such as Campylobacter, Shigella
or Salmonella.
Gastroenteritis is most commonly caused by viruses in infants and small children. Examples include
norovirus and rotavirus. Diarrhoea may persist for up to 10 days after an acute episode of viral
gastroenteritis. Persistence after 14 days merits further investigation.
Abdominal pain
Questions
Clinical cases 100
Key concepts 102
Answers
Clinical cases 103
Revision panel 108
100 Abdominal pain
Questions
Clinical cases

diagnosis?
CASE 10.1 – My 8-year-old son has abdominal pain with smoky-

coloured urine.
An 8-year-old boy presents to his general practitioner (GP) with acute abdominal pain. The pain is lower
abdominal and constant. He has been off his food for about 10 days, and has lost some weight. There
has been no vomiting. In addition, he recently had fever with a sore throat. His urine looks ‘smoky’ and
red, as if there is blood in it.
CASE 10.2 – My 9-year-old daughter has been thirsty for days and
passing lots of urine. Now she has tummy ache and is
drowsy.
A 9-year-old girl had a viral illness a week ago and has recently been drinking a large glass of water
every hour or so. She is passing a lot of urine, has to rush to the toilet, and wet the bed during the
previous night. Over the past few hours she has been very sleepy, and her breath smells funny.
CASE 10.3 – My 13-month-old child is getting thinner, with frequent

tummy aches and diarrhoea.
This child gained weight steadily during the first 6 months of life, but since then weight gain has slowed
down. He looks pale and skinny, and passes frequent bulky stools which have an offensive smell.
Questions 101
OSCE COUNSELLING CASE 10.1 – My 7-year-old son keeps getting

tummy ache on the way to school.
OSCE COUNSELLING CASE 10.2 – My 10-year-old daughter is

constipated, and this is very
distressing. Can you give her
something?
102 Abdominal pain
Key concepts
Problems arising in the gastrointestinal system can produce a wide variety of symptoms, and are
responsible for a high proportion of attendances at hospital accident and emergency departments.
Many non-gastrointestinal disturbances can also cause abdominal pain.
Abdominal pain is often non-specific, so it is important to keep an open mind regarding the cause
until a firm diagnosis is reached.
Medical causes of abdominal pain are common and include the following: acute post-streptococcal
glomerulonephritis; diabetic ketoacidosis; and coeliac disease.
ACUTE POST-STREPTOCOCCAL GLOMERULONEPHRITIS

Acute nephritis in childhood is a recognized complication of a streptococcal sore throat. Other
recognized complications include rheumatic fever and erythema marginatum.
Glomerular inflammation limits glomerular blood flow and reduces glomerular filtration rate. This
results in reduced urine output (oliguria) and volume overload. Other features include hypertension;
peri-orbital oedema and haematuria with proteinuria.
In the UK this is usually a mild illness, but it frequently causes abdominal pain.
The outlook is good, symptoms usually resolve within 2 weeks.
DIABETIC KETOACIDOSIS
Up to 45 per cent of children with type 1 diabetes will present with diabetic ketoacidosis.
Insulin production is insufficient to maintain normoglycaemia, or to suppress lipase activity. Glucose is
unable to enter cells, which consequently are starved of energy. Body metabolism is redirected from
an anabolic to a catabolic state. Lipase breaks down fats to fatty acids and glycerol. Fatty acids enter
the tricarboxylic acid cycle via acetoacetate, but are unable to be further metabolized due to a lack of
reducing power (NADH), and so are diverted towards ketone production. This leads to ketoacidosis.
The combination of dehydration and ketones is thought to be responsible for the acute abdominal
pain which occurs frequently in diabetic ketoacidosis.
COELIAC DISEASE
This is an enteropathy (inflammation of the lining of the gut) where the gliadin fraction of gluten
(found in wheat and wheat-based products) causes a damaging immunological response in the small
intestinal mucosa.
Villi become progressively shorter then absent, leading to a flat mucosa. This results in malabsorption
and can be demonstrated on a jejunal biopsy.
The prevalence of coeliac disease is about 1 in 3000, but this may be a considerable underestimate.
Children usually present in the first 2 years of life with failure to thrive following the introduction of
gluten to the diet.
Symptoms include failure to thrive (weight faltering, see Chapter 3), irritability, loose and frequent
stools, abdominal pain, and wasting of the buttocks.
Complete exclusion of gluten in the diet should result in resolution of symptoms within months.
Strict adherence to a gluten-free diet is also thought to reduce the long-term increased risk of bowel
lymphoma.
Children may undergo a follow-up biopsy to confirm that the villi have recovered. Nowadays,
compliance with treatment is monitored with autoantibody titres.
Answers 103
Answers
Clinical cases
CASE 10.1 – My 8-year-old son has abdominal pain with smoky-

coloured urine.
Causes of haematuria with abdominal pain include:
Trauma.
Acute post-streptococcal glomerulonephritis.
Henoch–Schönlein purpura.
Renal calculi.
Haemolytic uraemic syndrome.
Sickle cell disease.
Wilms’ tumour.
Bleeding disorders.
Bilharzia.

A diagnosis of urinary tract infection would be supported if there was a history of previous infections,
or unexplained low-grade fever, or dysuria.
Acute post-streptococcal glomerulonephritis would be supported by a history of sore throat in the
previous 3 weeks.
Ask about lethargy, dysuria, reduced urine output, and peri-orbital oedema in the days preceding
presentation.

Measure blood pressure and compare to age-standardized charts. Hypertension would make the
diagnosis of acute renal failure likely. Hypertension may also occur secondary to chronic renal failure
associated with recurrent urinary tract infections.
Examine the abdomen for tenderness and masses.

Examine the urine for protein, red cells and haemoglobinuria, and perform a stick test for nitrite
(indicative of infection).
Acute post-streptococcal glomerulonephritis is diagnosed by a raised anti-streptolysin O (ASO) titre
and low complement C3 levels that return to normal after 2–3 weeks.
Urea and electrolytes (these may show a raised urea and creatinine, and raised potassium in acute
renal failure).
Urine for microscopy, culture and sensitivity (to exclude urinary tract infection).
104 Abdominal pain

Urinary tract infections respond to appropriate antibiotics, depending on the sensitivity of the
organism cultured.
Acute post-streptococcal glomerulonephritis requires supportive management only. This includes
monitoring fluid balance, blood pressure and renal function; salt and water restriction to avoid fluid
overload; penicillin as prophylaxis against streptococcal infection; diuretics and anti-hypertensives to
treat the sequelae of renal failure.
Renal biopsy may be indicated only if the course of the disease is prolonged.
Dialysis may be required if renal failure and hypertension progress, or heart failure ensues.
CASE 10.2 – My 9-year-old daughter has been thirsty for days and
passing lots of urine. Now she has tummy ache and is
drowsy.
Diabetic ketoacidosis.
Mesenteric adenitis.
Urinary tract infection, pyelonephritis.
Acute post-streptococcal glomerulonephritis.
Acute appendicitis.

This child has a short prodromal illness, with weight loss. Diabetes at presentation can often be
precipitated by a prodromal viral illness such as a sore throat.
Other features include starting to wet the bed again after being dry at night (secondary enuresis),
polydipsia and polyuria and funny-smelling breath (ketones, which smell like pear drops).
Ask about lethargy.
Has there been any history of fungal infection (e.g. vaginal thrush in girls or balanitis [inflammation of
the glans penis] in boys).
Is there a family history of diabetes? (present in about 10 per cent of cases).

Look for signs of abdominal tenderness and guarding (may be present in both diabetic ketoacidosis
and acute appendicitis).
Ketones on the breath (smells like pear drops).
Examine for signs of dehydration (reduced skin turgor, dry mucous membranes, sunken eyes).
Examine for signs of shock (reduced capillary refill time, rapid thready pulse, pallor, cool peripheries,
altered consciousness).

Test the urine for glucose, ketones and nitrites.
Venous glucose estimation.
Check a capillary blood gas for metabolic acidosis.
Answers 105

Treat shock by restoring circulating blood volume. This involves intravenous administration of
physiological (0.9 per cent) saline.
Rehydrate slowly with 0.9 per cent saline, by calculating the fluid deficit, maintenance requirement,
and ongoing losses, and replace over 24–48h.
Add potassium to the fluid used to rehydrate, as there is a total body deficit of potassium.
Replace insulin via a continuous infusion initially, and then introduce a sliding scale when the blood
glucose falls below 12 mmol/L.
Change to subcutaneous insulin when the child is eating and drinking. This is usually in the form of a
mixture of short- and intermediate-acting insulin given as one injection, twice a day.
CASE 10.3 – My 13-month-old child is getting thinner, with frequent

tummy aches and diarrhoea.
Coeliac disease.
Other causes of malabsorption such as inflammatory bowel disease, lactose intolerance, milk allergy
and cow’s milk protein intolerance.
Feeding problems.
Parasitic infestation.
Malignancy such as Wilms’ tumour or neuroblastoma in a younger child.
Mesenteric tuberculosis.

Acquired malabsorption such as coeliac disease may present with failure to thrive in a previously
thriving child, so a history of getting thinner is not uncommon. Other causes include feeding
problems, lactose intolerance and cow’s milk protein intolerance.
In coeliac disease, increased bowel frequency occurs; this is usually combined with urgency and loose
stools.
Ask about symptoms of allergy: rashes, wheeze, swelling.
Ask about any family history of autoimmune disease such as diabetes, thyroid disease, alopecia.
Coeliac disease is commoner in some populations, e.g. the west of Ireland.
Ask about the onset of symptoms: are they related to the introduction of gluten products in the diet?

Plot height and weight on a growth chart.
Include previous measurements if possible, and see if the child has been crossing centiles downwards.
Look for signs of wasting, in particular in the buttocks. Look for pallor (anaemia).

Full blood count to check for anaemia. Consider measuring total IgA.
Check calcium, and alkaline phosphatase for evidence of rickets.
Blood test for anti-gliadin antibodies, anti-endomysial antibodies, and tissue transglutaminase
antibodies. If negative, consider allergy and breath testing.
If autoantibodies for coeliac disease are present, then a jejunal biopsy should be performed, to look
for flattened villi and inflammatory infiltrate.
106 Abdominal pain

Treatment of coeliac disease is by excluding gluten from the diet.
Answers 107
OSCE COUNSELLING CASE 10.1 – My 7-year-old son keeps getting

tummy ache on the way to school.
Recurrent abdominal pain which is sufficient to interrupt normal activities occurs in at least 10 per
cent of school-age children.
Less than 10 per cent of affected children will have a definable organic cause. In 90 per cent the
cause is functional abdominal pain.
Functional abdominal pain is characteristically peri-umbilical, worse on waking, associated with a
family history of abdominal pain or migraine, and not accompanied by any other features of ill health.
It is important that a full history and examination are performed to exclude other causes, such as
threadworms or constipation.
It may be helpful to explain the pain to the child and parent as ‘the intestine becoming so sensitive
that it is as if the child can feel the food going round the bends’.
About half of affected children have a rapid resolution of their symptoms, following referral.
About one-quarter resolve gradually.
About one-quarter go on to develop irritable bowel syndrome as adults.
No medical treatment is required.
OSCE COUNSELLING CASE 10.2 – My 10-year-old daughter is

constipated, and this is very
distressing. Can you give her
something?
Constipation is the infrequent painful passage of hard stools.
It is common in children, and is sometimes precipitated by a superficial perianal tear.
Sometimes it is exacerbated by stress, and children may withhold stool for fear of the associated
pain. The rectum then becomes full and distended and the sensation of needing to defecate is lost.
Involuntary soiling usually follows as the full rectum overflows.
Examination may reveal an abdominal mass which is indentable; on rectal examination the stool is
palpable down to the anal margin.
It is important to explain to the child and parents that constipation is common, soiling is involuntary,
and recovery of normal bowel habit takes as long as the constipation took to develop.
Mild cases of constipation may respond to mild laxatives (e.g. lactulose) and extra fluids.
In more severe cases, treatment begins with stool softeners for 2–3 weeks (e.g. docusate), followed
by large doses of powerful oral laxatives (picosulphate or senna) until the stools are liquid. This is
followed by regular doses of a stimulant laxative such as senna to prevent reaccumulation of stool.
Relapse is common, and positive encouragement by the child’s family and doctor are essential.
108 Abdominal pain
REVISION PANEL
Recurrent abdominal pain is common in children, 90 per cent due to functional abdominal pain,
and by definition has gone on for more than 3 months without an identifiable medical cause.
Chronic abdominal pain associated with weight loss or growth failure suggests an organic cause.
Coeliac disease is relatively common; inflammatory bowel disease is relatively rare in childhood.
Acute abdominal pain can be the presenting feature of both gastrointestinal and non-
gastrointestinal disease. Always take a full medical history and perform a thorough examination,
including urine.
The signs to look for of acute dehydration include dry mucous membranes, sunken eyes, sunken
fontanelle in infants, and decreased tissue turgor. More severe dehydration includes reduced
capillary refill time and low pulse volume tachycardia.
Learn how to describe an abdominal mass on examination: position (which quadrant of the
abdomen); associated with pain or guarding; size and consistency; indentable? (faecal mass); rising
up from the pelvis or down from beneath the ribs; ballotable.
Jaundice
Questions
Clinical cases 110
Key concepts 112
Answers
Clinical cases 113
Revision panel 117
110 Jaundice
Questions
Clinical cases

diagnosis?
CASE 11.1 – My newborn baby is yellow.

A 3-day-old term baby is noted to be yellow by his mother. He is breast-fed and is making slow progress.
CASE 11.2 – My 3-week-old baby is still jaundiced.

A 3-week-old girl was noted by the health visitor to have persisting jaundice. She is still breast-fed, but
has not yet regained her birth weight.
CASE 11.3 – My 7-year-old son has developed jaundice.

A 7-year-old boy was referred for investigation of malaise, fever and jaundice. He has dark urine and
pale stools.
Questions 111
OSCE COUNSELLING CASE 11.1 – Why is my newborn baby yellow?
OSCE COUNSELLING CASE 11.2 – I’m worried that my 3-week-old baby

is still jaundiced.
112 Jaundice
Key concepts
METABOLISM OF BILIRUBIN
Unconjugated bilirubin is formed following the break-down of erythrocytes, conjugated in the liver by
glucuronyl transferase and secreted in bile. In the gut, conjugated bilirubin is further metabolized to
urobilinogen (excreted in urine) and stercobilinogen (excreted in faeces). Some is deconjugated and
reabsorbed (enterohepatic circulation).
PHYSIOLOGICAL JAUNDICE
Common in newborn babies, and occurs usually between 3 and 7 days of age.
Precipitating factors include a high postnatal haemoglobin, shorter erythrocyte life span (due to fetal
Hb), reduced fluid intake and bruising. In addition, the neonatal liver is less efficient at conjugating
bilirubin.
The serum bilirubin is always >90 per cent unconjugated. This condition is self-limiting, and only
requires treatment if the serum bilirubin becomes very high (>300 mmol/L in term babies).
PATHOLOGICAL JAUNDICE
Any jaundice which is caused by a pathological process.
In the neonate, it can be subdivided into early (<24 h) and prolonged (>2 weeks) jaundice.
Early jaundice is likely to be due to erythrocyte haemolysis (e.g. Rhesus isoimmunization, ABO
incompatibility, spherocytosis). The serum bilirubin is unconjugated and may rise very rapidly. Breast
milk jaundice is a benign cause of prolonged jaundice. Sepsis may cause jaundice in the newborn.
Any baby who is jaundiced and unwell should be considered to have a pathological cause, until
proved otherwise.
A high conjugated component to the serum bilirubin (>15–20 per cent) suggests an obstructive cause
(see below).
OBSTRUCTIVE JAUNDICE
A high conjugated bilirubin, pale stools (lack of stercobilinogen) and dark urine (presence of bilirubin)
indicates an obstructive cause which may be either intrahepatic (e.g. hepatitis) or extrahepatic (e.g.
biliary atresia).
The conjugated component of total bilirubin should always be checked in any baby with jaundice at
more than 2 weeks of age. A delay in the diagnosis of biliary atresia beyond 6 weeks of age reduces
the likelihood of successful surgery for that condition (biliary drainage by a Kasai portoenterostomy).
It can be difficult to distinguish clinically between neonatal hepatitis and biliary atresia, and a
radionucleotide scan (or occasionally a liver biopsy) is usually indicated. Urgent referral to a specialist
paediatric hepatology service is advised.
HEPATITIS
Neonatal hepatitis can occur in a wide range of disease processes including congenital infections (e.g.
toxoplasmosis, cytomegalovirus [CMV]) and metabolic diseases (e.g. a-1-antitrypsin deficiency). In older
children, hepatitis A, B and C, glandular fever and CMV infection can cause acute liver inflammation.
Answers 113
Answers
Clinical cases
CASE 11.1 – My newborn baby is yellow.

Physiological jaundice.
Haemolysis.
Sepsis.
Congenital infection e.g. Toxoplasma, CMV.
Inherited metabolic disorder, e.g. glucose 6-phosphate dehydrogenase deficiency, galactosaemia.

The baby is at the age at which physiological jaundice is likely to present.
Breast-feeding may lead to reduced fluid intake initially. Some normal babies are slow to establish
breast-feeding, but this may indicate lethargy and suggest a pathological process such as sepsis.
Ask about feeding activity. Does he suck well? Is the baby pyrexial, excessively sleepy or lethargic?
Has he passed normal urine and stool? Clinical assessment of level of jaundice.
Check maternal blood group and presence of antenatal antibodies (e.g. anti-D).
Enquire about previous babies or family history of jaundice.

Assessment of baby’s well-being, plot growth on centile chart, check for pallor. Hepatosplenomegaly,
rashes (with congenital infections) and signs of sepsis (lethargy, high-pitched cry, mottling, tense
fontanelle).

Serum bilirubin, unconjugated and conjugated, to define degree of jaundice and exclude significant
conjugated component.
Full blood count (looking for anaemia, thrombocytopenia), blood group and direct antibody test
[DAT] or Coombs’ test (evidence of haemolysis due to ABO incompatibility or Rhesus disease).
Urine for reducing substances (Clinitest), including glucose, to exclude galactosaemia and
fructosaemia.
Urine culture (to exclude urinary tract infection).

In a well baby with no evidence of haemolysis, the most likely cause is physiological jaundice. If
the serum bilirubin is <300 mmol/L, no specific treatment is necessary other than encouraging fluid
intake.
If the bilirubin rises to >300 mmol/L, then treatment with phototherapy will break down the bilirubin
to harmless byproducts.
114 Jaundice
In haemolytic jaundice the bilirubin may rise rapidly to a level which is potentially dangerous (levels
>450 mmol/L may cross the blood–brain barrier and cause kernicterus). Phototherapy may be
insufficient in this case, and exchange transfusion may be required. An exchange transfusion removes
the baby’s blood which contains bilirubin ± antibodies and replaces it with transfused blood.
CASE 11.2 – My 3-week-old baby is still jaundiced.

Breast milk jaundice.
Neonatal hepatitis.
Extrahepatic biliary atresia.

The baby is receiving breast milk and is too old for physiological or haemolytic jaundice. The baby’s
weight gain is poor, which suggests either inadequate intake or a pathological process.
Ask about feeding activity and weight gain in more detail.
Is the baby pyrexial, excessively sleepy or lethargic?
Enquire about the colour of urine and stool (are the stools pigmented or are they pale? Is the urine
dark coloured?). Is the urine smelly? (a fishy smell may occur with urinary tract infection).
Clinical assessment of level of jaundice.
Enquire about previous babies or family history of jaundice.

General examination, assessment of well-being.
Re-check weight, examine for hepatosplenomegaly.

Serum bilirubin, unconjugated and conjugated, to define degree of jaundice and exclude significant
conjugated component.
If normal conjugated component and normal stools/urine, check urine for reducing substances and
culture.
If high conjugated component, check liver function tests (aspartate aminotransferase, alanine
aminotransferase, g-glutamyl transferase), TORCH screen (for Toxoplasma, rubella, CMV, herpes
simplex), a-1-antitrypsin phenotype.
Radionucleotide excretion scan to assess biliary excretion.

If normal conjugated component and normal stools/urine – advise regarding breast-feeding and milk
intake; re-weigh regularly until thriving.
Conjugated jaundice – urgent referral to paediatric hepatologist for further assessment and diagnosis.
Answers 115
CASE 11.3 – My 7-year-old son has developed jaundice.

Viral hepatitis (A, B or C).
Infectious mononucleosis (glandular fever).
CMV infection.
Wilson’s disease.
Chronic active hepatitis.

The combination of jaundice, dark urine and pale stools suggest acute liver inflammation.
Malaise and fever suggest an infective process.
Ask about prodromal illness with anorexia, abdominal pain, diarrhoea and vomiting.
Also ask about sore throat (glandular fever).
Check recent travel abroad, illness in close contacts and family history.

Examine skin for rashes and abdomen for tender hepatomegaly ± splenomegaly.
Examine eyes for Kayser–Fleischer rings (Wilson’s disease).
Check for lymph node enlargement (glandular fever).

Hepatitis A IgM antibodies – if negative consider:
hepatitis B sAg;
blood film for atypical mononuclear cells and monospot test for Epstein–Barr virus IgM antibodies
(glandular fever);
CMV IgM;
serum immunoglobulins and tissue autoantibodies (chronic active hepatitis);
serum caeruloplasmin and urinary copper (Wilson’s disease).

If the diagnosis is hepatitis A or B, glandular fever or CMV infection, then no specific treatment is
indicated.
The rare condition of Wilson’s disease may need treatment with penicillamine. This condition and
hepatitis C or chronic active hepatitis require the patient to be referred to a hepatologist.
116 Jaundice
OSCE COUNSELLING CASE 11.1 – Why is my newborn baby yellow?

The baby has physiological jaundice. This is a common condition, but it can cause parental anxiety.
Physiological jaundice is a self-limiting condition. Most babies with this condition do not need
treatment, but should be encouraged to drink plenty of fluid. Occasionally, the jaundice level reaches
a point which requires intervention, and the most usual treatment is phototherapy (blue light which
breaks down bilirubin into harmless metabolites), usually for a day or so.
The reasons that babies become jaundiced is usually because their blood count (haemoglobin) is
high and haemoglobin is broken down to bilirubin. Newborn babies’ blood cells are broken down
faster than those of adults, and their livers in the first few days of life cannot metabolize the bilirubin
as efficiently. Newborn babies also tend to take less fluid in the first day or so of life, and may have
bruises from the delivery. These factors may also contribute to jaundice.
A simple heel prick blood test will indicate the level of jaundice and the need for treatment. Other
simple routine tests may also be performed to exclude other causes of jaundice (e.g. urinalysis, blood
group and Coombs’ test).
If the baby is unwell, then the cause of jaundice is unlikely to be physiological and further urgent
investigations may be necessary.
OSCE COUNSELLING CASE 11.2 – I’m worried that my 3-week-old baby

is still jaundiced.
The baby is well, afebrile and breast-feeding well with good weight gain. Examination is normal and the
stool and urine are normal colour. The serum bilirubin is all unconjugated.
The commonest cause for prolonged jaundice is breast milk jaundice. However, there is not a specific
test that we can do to confirm this, so we need to consider other important causes. That is why we
have asked you about your baby and performed a blood test.
Bilirubin forms bile which is normally broken down in the intestines, and it is this that make stools
a yellow or brown colour. In a very serious condition where the bile cannot get into the intestines,
bilirubin builds up in the blood and can pass out in the urine, making it turn dark brown. The
combination of pale stools (like putty) and dark urine should alert us that there is a problem. It is
important that this condition (biliary atresia) is treated as soon as possible before irreversible damage
occurs in the liver. That your baby’s stools and urine are normal colour and the blood test shows only
one type of bilirubin (unconjugated) is very reassuring.
Sometimes an infection (particularly of the urine) can cause jaundice. The fact that your baby is well,
does not have a fever, is feeding well and thriving makes this unlikely.
By far the most likely cause is jaundice from breast milk. This is common, harmless and needs
no treatment. It usually resolves in 2–3 weeks. The presence of a substance (a-glucuronidase) in
the breast milk leads to a slight increase in the absorption of bilirubin back from the intestine (by
deconjugating bilirubin in the bowel and increasing enterohepatic circulation).
There is no need to stop breast-feeding to confirm the diagnosis. This will only deprive your baby of
the important nutrients and substances which improve immunity that breast milk contains.
Answers 117
REVISION PANEL
Physiological jaundice is common in newborn babies and is benign. The unconjugated bilirubin may
rise to a level which needs treatment with phototherapy.
Pathological jaundice is any jaundice caused by a pathological process. In neonates this may present
as early or prolonged jaundice.
Jaundice, dark urine and pale stools suggest liver inflammation. In a newborn baby this requires
urgent investigation. In adults the commonest cause is viral hepatitis but other important causes
may need to be excluded.
Prolonged unconjugated jaundice in newborn babies is usually caused by breast milk; however,
again careful assessment is required so the potentially serious conditions are not missed.
Rashes
Questions
Clinical cases 120
Key concepts 122
Answers
Clinical cases 124
Revision panel 128
120 Rashes
Questions
Clinical cases

diagnosis?
CASE 12.1 – My 6-month-old baby has dry, itchy skin with a red scaly
rash.
This baby has always had dry skin, but recently it has become worse and is now red and itchy. There is a
family history of asthma and allergies.
CASE 12.2 – My 18-month-old has bruising over his shins and knees.
This boy – who is otherwise well – has just started climbing upstairs. He is very adventurous, and recently
his mother has noticed more bruises on his legs.
CASE 12.3 – My 5-year-old son has dark red spots on his legs and
buttocks.
This boy had a viral illness a few days ago and has not recovered from this. He has a fever and is
miserable, but not particularly unwell. Today he has developed dark red spots on his legs and buttocks.
These spots do not blanch when pressed.
Questions 121
OSCE COUNSELLING CASE 12.1 – My newborn baby has a red rash in

the nappy area.
OSCE COUNSELLING CASE 12.2 – I am worried that there has been a

case of meningococcal disease at my
child’s school. Please could you tell me
about meningococcal disease and the
symptoms, including looking for skin
rashes?
122 Rashes
Key concepts
Erythematous (red) rashes are very common in infancy and childhood.
Most are not serious and resolve spontaneously or with simple treatment.
Serious infections may also present with rash, and it is important to differentiate between serious and
minor illness.
EXANTHEMS
Exanthems are widespread erythematous rashes which are usually associated with systemic symptoms
such as fever, malaise, myalgia and headache.
They are commonly caused by infectious agents, particularly viruses and occasionally bacteria.
Exanthems are very common in childhood. Examples include: measles (caused by a paramyxovirus),
chicken pox (caused by varicella zoster virus), rubella (caused by Rubivirus), scarlet fever (caused by
streptococcus A), fifth disease (caused by parvovirus B19) and hand, foot and mouth disease (caused
by Coxsackie virus A16).
Exanthems usually have a characteristic appearance to the rash and are associated with a pre-rash
prodromal period.
Some exanthems such as meningococcal disease can be life-threatening and require urgent diagnosis
and treatment; other exanthems follow a fairly benign course, but occasionally serious sequelae may
develop (e.g. encephalitis following measles).
Specific immunizations are available against certain exanthems such as measles and rubella (see
p. 50).
OTHER ERYTHEMATOUS RASHES

In addition to the exanthems, the commonest erythematous rashes which occur in childhood are
eczema, urticaria (or hives), candidiasis, ringworm, impetigo and scabies.
These conditions usually present with a red itchy rash.
Eczema is often scaly and may occur on any part of the body, particularly affecting the flexor creases
of the elbows and knees.
Urticaria occurs as a result of an allergic response, and is usually light red in colour with raised edges.
It can be very transient, and occurs more commonly on the trunk.
Candidiasis and ringworm are fungal infections. Candida normally affects the groin area, and appears
as red plaques. Ringworm can affect any part of the body, and appears as circular plaques.
Impetigo is a bacterial infection (caused by staphylococcal or streptococcal bacteria); although it can
occur on any part of the body, it usually appears around the mouth and nose as a golden crust over a
red base.
Scabies is an intensely itchy rash caused by a mite which burrows under the skin. Commonly
occurring on the hands or around the waistline, the rash appears as raised red spots which
occasionally crust over.
NON-BLANCHING RASHES (PURPURA, PETECHIAE AND ECCHYMOSES)

Purpura are reddish-purple lesions which occur as a result of extravasation of blood into the skin.
Petechiae are pin-point-sized purpura, and ecchymoses are >1 cm in size.
They can be differentiated from erythematous lesions in that they are non-blanching – that is, the
lesion does not blanch when pressure is applied to it. (Tumbler test: press a glass onto the lesion to
see if it blanches.)
These rashes can occur in a variety of conditions, including trauma, thrombocytopenia (low platelets),
vasculitic conditions and meningococcal disease.
Questions 123
Henoch–Schönlein purpura (HSP) is an allergic vasculitis of unknown aetiology which affects young
children. It typically presents with a low-grade fever and a purpuric rash on the legs and buttocks. It
is a self-limiting condition, but can result in more severe complications if haemorrhage occurs in the
joints, kidneys or intestine.
Childhood leukaemia may present with a purpuric rash or ecchymoses as a consequence of
thrombocytopenia.
The presence of a purpuric rash in an unwell child should always raise concerns about meningococcal
disease (see below).
Ecchymoses for which there is an inadequate explanation of cause, or those with an unusual
distribution (e.g. slap marks or finger-grip bruises), should always raise suspicion of non-accidental
injury (NAI) and a careful search for other injury (such as torn frenulum, burns, bite marks or
fractures) should be made.
MENINGOCOCCAL DISEASE
Meningococcal disease is a serious bacterial infection (septicaemia and/or meningitis) with a high
morbidity and mortality rate. Unless treated promptly, this condition is invariably fatal.
It occurs as a result of systemic infection with Neisseria meningitidis (meningococcus). Thirteen
serotypes (strains) of this bacterium exist; strains B and C are the commonest in the UK.
Symptoms include fever, headache, drowsiness, vomiting and confusion. The presence of any of
these symptoms and a purpuric (non-blanching) rash (press a glass against the lesion to confirm this if
necessary) warrants urgent medical attention and antibiotic treatment (intramuscular benzylpenicillin
if not in hospital).
A vaccine for meningococcus C is now available, and is given to all infants with diphtheria, tetanus,
pertussis, Haemophilus influenzae B and polio at 2, 3 and 4 months (see p. 51).
Vaccines against some (but not all) of the other serotypes are available.
Close contacts and people who live in the same house as a case are significantly more likely to
develop the disease than non-contacts. Chemoprophylaxis (antibiotics to prevent the disease
occurring: rifampicin in children and ciprofloxacin in adults) should be given to all significant contacts,
and then immunization (if the specific vaccine is available for the serotype causing the disease).
124 Rashes
Answers
Clinical cases
CASE 12.1 – My 6-month-old baby has dry, itchy skin with a red scaly
rash.
Infantile eczema (atopic dermatitis).
Scabies.
Fungal infection (candidiasis or ringworm).

Dry skin would suggest eczema.
The strong family history of atopy (asthma and allergy) would also fit with this diagnosis.
Confirm family history of allergy; ask about eczema in infancy in close family members.
Ask about localization of the rash (e.g. on face, trunk and in flexural creases).
Any other evidence of atopy, e.g. wheezing. Has there been a preceding prodrome and
symptomatology suggestive of an exanthem?

Examine the skin over the whole body. Is there dry skin and erythema over most of the trunk face
and limbs, particularly creases? Is it dry, or is it moist and weeping (suggesting infected eczema)? Is it
localized to the nappy area, and are the lesions well-circumscribed (suggestive of fungal infection)?
Are the lesions raised and localized to the fingers, wrists and groin (suggestive of scabies)?
Examine the chest for hyperinflation, Harrison’s sulci, sternal bowing and wheezes.
If candidiasis is suspected, check the mouth for typical white plaques on the inner cheek and tongue.

Specific investigations are not necessary if eczema is the most likely clinical diagnosis.
Skin scrapings from a suspected fungal lesion should be sent for mycology.
Scabies can be confirmed by extracting the mite from the skin burrows and examining it under a
microscope.

Eczema is treated in the first instance with regular, liberal application of emollients and use of bath oil
instead of soap.
Mitts may be helpful at night to reduce scratching.
More severe exacerbations will respond to sparing application of topical mild steroid ointment (e.g.
0.5–1 per cent hydrocortisone) in short courses (no more than 2 weeks at a time).
Fungal infections respond well to antifungal creams (see below). Scabies is treated with permethrin;
the whole family require treatment to prevent reinfection.
Answers 125
CASE 12.2 – My 18-month-old has bruising over his shins and knees.
Normal toddler bruising.
NAI.
HSP.
Clotting disorder (e.g. idiopathic thrombocytopenic purpura, haemophilia).
Leukaemia (or other conditions causing thrombocytopenia).

At 18 months of age children will be toddling, but may have frequent falls as they are learning. Active
adventurous children are more likely to tumble and acquire minor bruising as a consequence.
Enquire about the following:
Walking activity and frequency of falls.
Painful swollen joints (haemarthroses) which occur in coagulation disorders (e.g. haemophilia).
Abdominal pain, painful joints, preceding coryzal illness (e.g. as in HSP).
Lethargy, pallor, mucosal bleeding or other features of ill health (e.g. as in leukaemia).
Take a social history and enquire about carers and family dynamics.
Does the history fit the pattern of bruising observed, and was appropriate medical attention sought?
Are the histories of different care-givers consistent (if suspicious of NAI)?

Examine all the skin for bruising and/or petechiae. Are they extensive or large? Is the bruising
localized to the lower limbs (suggesting accidental bruising or HSP; bruising in HSP tends to be
localized to the extensor surfaces of the lower limbs and buttocks) or generalized and/or associated
with mucosal bleeding (suggesting a coagulopathy or leukaemia)?
Are the joints swollen or tender?
Are there any suspicious lesions which might suggest NAI? (e.g. slap or grip marks, burns or weals,
suspected fractures).
Check for lymphadenopathy, hepatosplenomegaly (suggestive of leukaemia).

If the child is well, the bruises are small and localized to parts of the body involved with falls (shins,
knees, occasionally head), the explanation is appropriate, and there are no other abnormal findings on
examination, then no further investigation is warranted.
However, if the bruising is excessive, widespread, associated with trivial accidents, swollen
joints, pallor or systemic signs of ill health, it would be appropriate to perform the following initial
investigations:
Full blood count (haemoglobin, white blood cell and platelet count) and blood film.
Coagulation screen (prothrombin time, partial thromboplastin time).
Consider bone marrow check if full blood count abnormal.
If in doubt, consider checking whether the child is on the child protection register and whether the
general practitioner (GP), health visitor or social services have any concerns, and discussing with a
paediatrician. If there are concerns about NAI, then the child protection process should be initiated.
This should involve a senior doctor and social services.
126 Rashes

Toddler bruising requires no treatment.
CASE 12.3 – My 5-year-old son has dark red spots on his legs and
buttocks.
HSP or anaphylactoid purpura.
Meningococcal disease.
Idiopathic thrombocytopenic purpura.

The localization of the purpuric rash to the legs and buttocks, and the preceding viral illness would
suggest HSP.
Enquire about fever, joint pain or swelling, abdominal pain and haematuria (these symptoms may be
associated with HSP).
Ask about photophobia, headache, neck stiffness and lethargy (which may be associated with
meningococcal disease).

Assess overall well-being. Are there features of serious illness?
Confirm that the rash is non-blanching. Examine joints and abdomen.

Check urine for blood and protein. Also, check blood pressure (25–50 per cent of patients with HSP
will have renal involvement, and a small proportion will develop renal impairment).
Check stool for occult blood if significant abdominal pain (haemorrhage into the gut can occur and
may occasionally cause intussusception).
Check platelet count and coagulation – to exclude idiopathic thrombocytopenic purpura and other
coagulopathies.
If doubt about diagnosis, perform a blood culture.

HSP is usually self-limiting, and no treatment is required except for analgesia for joint pain. If
complications occur (e.g. renal or gut involvement), then supportive therapy may be necessary.
Answers 127
OSCE COUNSELLING CASE 12.1 – My newborn baby has a red rash in

the nappy area.
Nappy rash usually occurs as a result of contact dermatitis (ammonia from urine) or fungal infection
(Candida or thrush). Occasionally, bacterial infection (e.g. staphylococcal) may occur.
Dermatitis usually presents as a widespread groin rash which spares the creases.
Candida usually appears as red plaques with occasional smaller spots (satellite lesions), and the
creases are involved. Sometimes, Candida can appear in the mouth as white plaques on the inner
cheek or tongue.
Nappy rash is very common, and not usually due to parental neglect.
Cleaning the area with water and cotton wool may be less irritating than disposable ‘baby wipes’
(which may contain alcohol or detergent).
Treatment of dermatitis involves barrier creams such as zinc oxide and exposure to the air (whenever
possible).
Candida responds to antifungal creams (e.g. miconazole, nystatin). The groin and the mouth may
both need treatment.
OSCE COUNSELLING CASE 12.2 – I am worried that there has been a

case of meningococcal disease at my
child’s school. Please could you tell me
about meningococcal disease and the
symptoms, including looking for skin
rashes?
Meningococcal disease is a serious infection caused by certain bacteria which may cause blood
poisoning (septicaemia) or inflammation of the lining of the brain and spinal cord (meningitis).
Neisseria meningitidis (meningococcus) is the bacterium responsible. It is found in the noses and
throats of 5–10 per cent of the population, but rarely causes serious disease unless it enters the
bloodstream or spinal fluid.
Meningococci can spread among people through the exchange of saliva and other respiratory
secretions during activities such as coughing and kissing, but they are not as contagious as the
common cold or influenza. They are not spread by simply breathing the same air as a person with
meningococcal disease.
Common symptoms of meningococcal disease include high temperature, headache, drowsiness
and vomiting. A stiff neck can occur with the meningitis, and an unusual rash occurs with the
septicaemia. Typically, this rash is dark red and does not blanch when pressure is applied. Use a glass
to see if the rash blanches when pressed.
If these symptoms occur – or if you are in any doubt at all – it is very important that medical advice
is sought urgently, because if the disease has developed it is very important to administer antibiotics
straight away. These should be given directly into a vein or a muscle, and not by mouth.
There are 13 different types (strains) of meningococcus, and vaccines are available against some, but
not all, of them. One is now given routinely with the other childhood vaccines.
Close contacts and people in the same house as a person who has the disease are more at risk
of developing it themselves. In this situation, antibiotics should be given to prevent this occurring
(antibiotic prophylaxis). These antibiotics can be taken by mouth, and do not need to be given into a
vein or muscle.
128 Rashes
REVISION PANEL
Erythematous rashes are very common in infancy and childhood. Most are not serious; however, it
is important to be able to differentiate between serious and minor illness.
The cornerstone of the treatment of eczema is regular liberal application of emollients. Steroid
creams may be used for severe cases but sparingly and only for short periods.
Any child with unexplained injury should raise the suspicion of NAI. If there are any concerns about
NAI the child protection process should be initiated.
A non-blanching rash in a child who has fever, drowsiness or headache should be treated as
meningococcal disease until proved otherwise. Urgent antibiotic treatment is indicated.
Nappy rash is common in babies and usually due to either contact dermatitis or fungal infection
with Candida. Once the cause is established the treatment is straightforward.
Poisoning
Questions
Clinical cases 130
Key concepts 132
Answers
Clinical cases 133
Revision panel 137
130 Poisoning
Questions
Clinical cases

diagnosis?
CASE 13.1 – My 22-month-old son may have ingested paracetamol

suspension.
A 22-month-old boy has been drinking from an open bottle of paracetamol suspension. The bottle was
previously half full, and is now nearly empty.
CASE 13.2 – My 4-year-old daughter has mistaken iron tablets for

sweets, and has eaten some.
A 4-year-old and her friends have mistaken iron tablets for sweets, and eaten a number of them. The
mother is uncertain how many were in the bottle, but there are quite a few left.
CASE 13.3 – My 11-year-old son is complaining of headaches,

confusion, nausea and vomiting and shortness of breath.
An 11-year-old boy presents with headaches, nausea and vomiting, confusion and shortness of breath.
The symptoms have been getting worse, but resolved during a few days’ stay with his cousins. He is
worse in the mornings, but improves when at school.
Questions 131
OSCE COUNSELLING CASE 13.1 – My toddler has ingested washing

powder. What will happen to him,
and how can I prevent this happening
again?
OSCE COUNSELLING CASE 13.2 – My 14-year-old daughter has

deliberately taken a paracetamol
overdose. What treatment does she
need?
132 Poisoning
Key concepts
The ingestion of a potentially toxic substance is relatively common, and can occur either deliberately
or accidentally.
The majority of children will be asymptomatic following ingestion and require no specific treatment.
A careful history is essential, paying particular attention to the precise nature and dose of the
substance ingested. An assessment of the potential maximum dose ingested should be made.
A careful examination, including full neurological assessment is also essential.
When treatments are necessary they usually involve delay in absorption or augmentation of
excretion. Examples of such treatments include activated charcoal, whole-bowel irrigation (e.g. in iron
ingestion), haemofiltration/haemodialysis (some drugs, e.g. theophylline, carbamazepine) and alkaline
diuresis (salicylate ingestion).
Supportive management including airway maintenance and treatment of the following is occasionally
required in serious poisoning: dehydration and shock, acidosis, hypoglycaemia and convulsions.
Many commonly ingested substances are relatively harmless and require no specific investigation
or treatment; these include oral contraceptives, silica gel, vitamin tablets (without iron), antibiotics,
cosmetics, paints, washing powder.
Some commonly ingested substances have a high toxicity; these include iron tablets, dishwasher
powder, toilet cistern blocks and antihistamines.
Some poisons have specific antidotes, e.g. N-acetylcysteine for paracetamol, naloxone for opiates,
and desferrioxamine for iron.
If there are any doubts about the management, the local poisons unit should be contacted promptly.
Answers 133
Answers
Clinical cases
CASE 13.1 – My 22-month-old son may have ingested paracetamol

suspension.
Possible paracetamol ingestion.
Normal child (i.e. no ingestion).

The child has been found with the bottle, and the contents are reduced.
Find out exactly how much was in the bottle, and what dose per mL of paracetamol is contained in
the suspension. Establish the maximum possible dose ingested.
Establish as precisely as possible the timing of the ingestion.
Was there any evidence of spillage? For example, on the floor or on the clothes.
Was anyone else with him at the time?
Has he vomited since being found?

Check his body weight (so that the maximum dose per kilogram can be established).

It is unlikely that a significant quantity of paracetamol will have been ingested. Paracetamol
suspension is usually 24 mg/mL, but a stronger preparation of 48 mg/mL is available. Significant
paracetamol ingestion is much more likely with tablets (usually 500 mg per tablet). However, given
the uncertainty it would be prudent to measure the serum paracetamol level (as described below) in
this case.
In all cases, if it is possible that more than 150 mg/kg has been ingested, a venous blood sample
for serum paracetamol level should be taken 4 h after ingestion. (It is important that the level is not
measured before this time, as interpretation is very difficult.)
Plot the blood result against time after ingestion treatment action chart.
If greater than 150 mg/kg has been ingested more than 8 h previously, do not wait for a serum level
before starting treatment. (It is also important to remember that paracetamol poisoning does not
cause symptoms in the early stages, and a delay in treatment may be fatal.) If a child has also drunk
alcohol or is taking anticonvulsants, this increases the risk of hepatotoxicity, and therefore a lower
threshold for treatment is warranted.
Paracetamol is hepatotoxic, and therefore clotting (international normalized ratio), creatinine and
alanine transferase levels should also be checked. Peak hepatotoxicity occurs at 72–96 h post-
ingestion.
134 Poisoning

Toxic levels of paracetamol are treated with N-acetylcysteine.
If the amount ingested is not greater than 150 mg/kg, then no treatment is required.
The parents should be advised about safe storage of medicines and other potentially harmful
substances, and the health visitor and general practitioner (GP) should be informed so that they can
reinforce safety in the home through child health surveillance.
CASE 13.2 – My 4-year-old daughter has mistaken iron tablets for

sweets, and has eaten some.
Iron toxicity.
Potential iron toxicity in the child’s friends.

The child has been playing with friends, but it is unclear how many tablets there were to start with, or
how many were ingested. It is therefore possible that none or all of the children may have ingested a
potentially toxic amount of iron. In view of this, the only safe option is to assume that they all may have
ingested a significant quantity.
Find out about the specific iron compound and the iron content of each tablet (this is vital, as the
amount of elemental iron per tablet varies with the type of preparation).
Find out about the maximum number of tablets in a full bottle, and how many are left. Were any
found on the floor, or in the children’s clothing or pockets?
Have any of the children vomited since the ingestion?
Have any of the children had any other symptoms which may suggest iron toxicity, e.g. diarrhoea,
abdominal pain or haematemesis? In severe cases there may be drowsiness, convulsions, metabolic
acidosis, shock and multi-organ failure.

Check the body weight of each child (so maximum dose per kilogram can be established). The
minimum toxic dose of iron in children is estimated to be anywhere from 20 to 60 mg/kg. Fatal
poisonings have rarely been reported with less than 60 mg/kg elemental Fe.
Pulse, respiratory rate and blood pressure.
Full examination, paying particular attention to the gastrointestinal tract and for evidence of central
nervous system depression.

If there is a risk of toxicity from iron ingestion, the following investigations should be performed in all
children:
Full blood count.
Serum iron level.
Plasma electrolytes, including chloride and bicarbonate (for anion gap).
Blood glucose.
Plain abdominal X-ray (may show evidence of radio-opaque pills or pill fragments in the
gastrointestinal tract).
Answers 135

Symptomatic and general supportive treatment is vital, with close monitoring of vital signs and
aggressive intravenous fluid resuscitation.
Patients who present early may benefit from whole-bowel irrigation using an osmotically balanced
polyethylene glycol-electrolyte solution (this forces the unabsorbed iron through the gastrointestinal
tract quickly and helps prevent further absorption of iron).
Severely affected patients may benefit from the use of intravenous desferrioxamine; this chelates iron,
allowing it to be renally excreted.
CASE 13.3 – My 11-year-old son is complaining of headaches,

confusion, nausea and vomiting and shortness of breath.
Viral illness (e.g. influenza or gastroenteritis).
Intracranial space-occupying lesion.
Carbon monoxide poisoning.

The chronic nature of the illness with improvement when out of the house should raise the suspicion of
carbon monoxide poisoning. The symptoms of carbon monoxide poisoning are often vague, and a high
degree of suspicion is required.
Enquire about the following:
The heating system in the house – does it use gas, oil, coal or wood? Also, fuels used in boilers,
engines, oil burners, gas fires, water heaters, solid fuel appliances and open fires.
The colour of the flame from gas appliances (may be yellow rather than blue if ventilation is
inadequate), and servicing of equipment and ventilation in the house, particularly in the boy’s room.
If any other members of the family have similar symptoms.

The consequences of carbon monoxide poisoning are related to damage from hypoxia and direct carbon
monoxide-mediated damage at a cellular level. The heart and brain are particularly susceptible. The
following should therefore be checked:
Pulse and respiratory rate (may be increased in carbon monoxide poisoning).
Blood pressure (may be reduced).
Check for cyanosis. Oxygen saturations may be unreliable in carbon monoxide poisoning.
Full assessment of the central nervous system – looking particularly for hyperreflexia, incoordination
and visual, hearing or sensory impairment.

Measure carboxyhaemoglobin (COHb) levels (a co-oximeter determines spectrophotometrically the
percentage of carbon monoxide-saturated haemoglobin).
Check acid–base status and arterial blood gases if severe poisoning is suspected.
Creatinine kinase levels may indicate the degree of rhabdomyolysis in severe cases.
136 Poisoning

Immediate treatment with 100 per cent oxygen.
Supportive therapy (e.g. fluids ± inotropic support, control of seizures, correction of acidosis, etc.).
Hyperbaric oxygen therapy should be considered in severe cases. Expert advice should be sought in
these circumstances.
Answers 137
OSCE COUNSELLING CASE 13.1 – My toddler has ingested washing

powder. What will happen to him,
and how can I prevent this happening
again?
Ingestions of household substances are very common, particularly in the 1- to 4-year age group.
The risk of serious consequences as a result of ingesting washing powder is low, and no hospital
admission or specific treatment is required.
However, some household substances are potentially very toxic, and it is important to be aware of
this. These substances include dishwasher powder, liquids or tablets, oven cleaners, button batteries
and toilet cistern blocks, all of which are very corrosive.
Prevention of ingestion of harmful substances is very important in homes with young children. All
potentially poisonous substances should be kept in tamper-proof containers, preferably in a high or
locked cupboard.
Do not store products in anything other than their original container.
Adequate adult supervision at all times is also required.
OSCE COUNSELLING CASE 13.2 – My 14-year-old daughter has

deliberately taken a paracetamol
overdose. What treatment does she
need?
Initial treatment of deliberate paracetamol ingestion should be the same as accidental ingestion (see
p. 133), although the likelihood of paracetamol toxicity is much greater.
The risk from paracetamol overdose occurs as a result of hepatotoxicity (liver damage).
If a significant quantity has been ingested, then treatment with intravenous N-acetylcysteine is
warranted.
Deliberate poison ingestion is a common presentation in older children, and can often be in response
to a precipitating factor (such as an argument with parent or friend) which may appear minor to
adults. However, it is important that these events are taken seriously, and not trivialized.
Individuals who attempt to self-harm have a much greater risk of psychiatric illness, and are therefore
at risk of repeating the attempt.
In view of this, all patients taking a deliberate overdose should undergo social, psychological and/or
psychiatric assessment prior to discharge.
This assessment can offer an opportunity for difficulties between adolescents and parents to be
discussed.
REVISION PANEL
Ingestion of potential poisons, either accidental or deliberate, is a common problem in paediatrics.
Ingestion of paracetamol suspension rarely results in toxicity; however, this is much more likely
following ingestion of tablets.
Many commonly ingested substances are relatively harmless; however, some such as iron and
antihistamine tablets, dishwasher powder and toilet cistern blocks have high toxicity.
The symptoms of carbon monoxide poisoning are often vague and a high degree of suspicion is
required. A careful history should always be taken.
Accidental poisoning by young children can be avoided by careful storage of potentially harmful
substances.
Emotional and
behavioural problems
Questions
Clinical cases 140
Key concepts 142
Answers
Clinical cases 143
Revision panel 147
140 Emotional and behavioural problems
Questions
Clinical cases

diagnosis?
CASE 14.1 – My 2-year-old girl refuses to eat, won’t go to sleep at

night, and hits other children.
A 2-year-old girl presents with a history of difficult behaviour since the age of 8 months. She hits other
children if they refuse to share their toys with her. She wakes frequently at night, and will not settle
unless taken into her parents’ bed. She refuses to eat at family meals, preferring to snack on chocolate,
crisps and biscuits. The family are asylum seekers, and their neighbours in a council property have been
complaining about the noise that the little girl makes. However, the local playgroup has told the health
visitor that she is a sociable little girl who interacts well with her peer group.
CASE 14.2 – My 6-year-old boy is disruptive in class, has no friends, and

is aggressive.
A 6-year-old boy has a long history of poor concentration and being disruptive in class, and has difficulty
in forming peer relationships. He is aggressive and his school progress is poor.
CASE 14.3 – My 2-year-old boy doesn’t play with other children, isn’t
speaking, and seems to be in a world of his own.
A 2-year-old boy has a long history of concerns over communication. He has never babbled or spoken
intelligible words. He plays alone, and is aggressive if his routines are disturbed.
Questions 141
OSCE COUNSELLING CASE 14.1 – My 9-year-old boy wets the bed.

It seems that this boy has always wet his bed at night. His bowel habit is normal, and he is otherwise
in good health. His father wet the bed until he was quite old. The physical examination, including
abdominal, spine, lower limb neurology and urinalysis, is normal.
OSCE COUNSELLING CASE 14.2 – My 2-year-old boy has nocturnal

screaming episodes.
This boy goes to bed without problems but wakes 2 h later, screaming. The parents find him sitting up
in bed, eyes open, disorientated, confused and distressed, but unresponsive to them. He settles back to
sleep after a few minutes, and shows no evidence of recall of the episode in the morning. Development
and growth history are normal, and physical examination reveals no abnormal signs.
Key concepts
Emotional and behavioural problems are common in children and young people. Up to 2 million
under-16-year-olds in England may require help from health services at some time, of whom about
half have definable mental health disorders, and a smaller number have severe mental illness.
Children’s behavioural and emotional responses are the result of genetic predisposition and
environment, of which the family is the major factor.
ATTENTION DEFICIT HYPERACTIVITY DISORDER

Attention deficit hyperactivity disorder (ADHD) is distinguished from the normal but very active child by
three key features:
Inattention (poor concentration with an inability to maintain attention without distraction): easily
distracted, easily moves from one incomplete task to the next, difficulty in following instructions.
Hyperactivity (difficulty in controlling the amount of physical activity appropriate to the situation):
difficult to sit quietly, can talk excessively, fidgets.
Impulsivity (lacks appropriate forethought): interrupts, difficult in turn-taking. Hearing, vision and
learning problems may also coexist with hyperactivity.
Definitive diagnosis is a specialist task for a neurodevelopmental paediatrician, or a child and adolescent
mental health multidisciplinary team.
PERVASIVE DEVELOPMENTAL DISORDER (AUTISM)

The following triad of features that affect function in all situations suggests a pervasive developmental
disorder:
Impairment of reciprocal social interactions (playing alone, failing to make eye contact, does not
come for comfort when hurt or upset).
Impairment of reciprocal communication (has never babbled or spoken intelligible words).
Restricted range of interests and activities (has marked routines or rituals, which produce violent
temper tantrums if disrupted).
Autism may be associated with cognitive impairment, unusual motor features (e.g. flapping hands,
walking on tiptoe), general learning disability, fears, phobias, sleeping and eating disturbance, tantrums,
self-injury and abnormal sensory responses (e.g. highly sensitive to noise).
Once again, definitive diagnosis is a specialist task for a neurodevelopmental paediatrician or a child
and adolescent mental health multidisciplinary team. Complex and often multiple mental and physical
health issues need specialist intervention.
Answers 143
Answers
Clinical cases
CASE 14.1 – My 2-year-old girl refuses to eat, won’t go to sleep at

night, and hits other children.
Preschool behaviour problem.
Disordered social background.
Hearing or visual problem.
Learning problem.
Hyperactivity.
Physical or sexual abuse.

Tantrums, waking at night and meal refusal are common behavioural problems in the preschool years,
and seem likely here in the light of good behaviour in other settings.
A full developmental history is needed to screen for hearing, vision and learning problems.
An account of what happens before and at mealtimes, bedtime and playtime is needed, together
with a description of the family’s responses to the child’s behaviour.
What are the family’s main concerns – lack of food/sleep or lack of discipline? In hyperactivity, the
child is overactive most of the time, and this seems unlikely here.

A full physical examination is required, with a particular emphasis on the developmental assessment.
An ear, nose and throat examination should be made for signs of visual, hearing or learning
problems.
The child’s behaviour in the consulting room can be informative.
Height and weight should be plotted on a growth chart, in view of the history of meal refusal.

Investigations may not be required.
A hearing or vision test, or a detailed formal interdisciplinary assessment in the family home or in a
child development centre, may be indicated by the history and examination.

Reassurance that the child does not have a major organic or mental health disorder, with empathy for
the family’s plight, is required.
The family needs advice and encouragement from the doctor, health visitor, social worker and
playgroup in order to adopt parenting strategies to modify the child’s behaviour.
Avoid confrontation at mealtimes, bedtime and playtime through avoidance of known antecedents to
behaviour; use distraction when confrontations arise.
Develop a relaxed routine for regular mealtimes and bedtime at the same time each night. Have
meals, bathtime and bedtime with other children.
Use favourite foods and toys as rewards.
Time out for difficult behaviour, e.g. walk away (return when the child quietens down), separate from
other children, remove from family meal, put in a ‘naughty corner’ for a few minutes.
CASE 14.2 – My 6-year-old boy is disruptive in class, has no friends, and

is aggressive.
ADHD.
Normal, but very active, child.
Hearing or visual problem.
Specific learning disability.
Autistic spectrum disorder.

Poor concentration and disruptive behaviour suggest ADHD, but may also be seen in normal active
children.
Ask about inattention and degree of physical activity, excessive fidgeting and talking. Is he easily
distracted? Can he follow instructions? Ask about social skills, e.g. turn-taking
A detailed history of relevant risk factors including details of a family history of hyperactivity, diet,
social adversity, and early childhood stresses such as abuse or hospitalization is also needed.

A full physical examination is required, including a neurodevelopmental assessment and ear nose and
throat examination.

Consider referral to a specialist team.

With ADHD, interprofessional work with parents, teachers and the child is required to build
concentration skills, enhance self-esteem, modify extreme behaviour through consistency and clarity
of approach.
In selected cases, medication such as methylphenidate has its place as part of a multiprofessional
behavioural programme.
CASE 14.3 – My 2-year-old boy doesn’t play with other children, isn’t
speaking, and seems to be in a world of his own.
Pervasive developmental disorder (autism).
Hearing or visual impairment.
Learning disability.
Physical or sexual abuse.
Answers 145

Poor communication, failure to mix with other children and development of routines are suggestive
of autism.
A full history is required. Ask about social interactions: eye contact, comfort-seeking, etc. Explore
routines and ritual behaviour in more detail.

A full physical examination is required as well as a comprehensive neurodevelopment assessment,
mental state examination and an assessment of cognitive function.

Consider referral to a neurodevelopmental paediatrician or a child and adolescent mental health
multidisciplinary team.

Specific interventions in all developmental disorders are aimed at enabling the young person to
achieve their potential, and supporting the family with a community-based multidisciplinary team.
Intervention to meet a child’s emotional, social and educational needs, including the provision of
special education.
OSCE COUNSELLING CASE 14.1 – My 9-year-old boy wets the bed.

Many treatments have been tried for bedwetting; no single treatment will cure all children, so the
important thing is to choose the right thing for each child. The consultation should identify both the
child’s and the parents’ concerns and objectives, and establish a way forward that is acceptable to all.
FACTS TO REMEMBER
Bedwetting is common at this age; 3 per cent of normal 10-year-olds wet the bed once a week, or
more.
There is often a family history of bedwetting.
Usually, children who wet the bed do not have physical or emotional problems.
Bedwetting can become a problem for many children and their families, particularly once children go
to junior school.
WHAT CAUSES BEDWETTING?

Bedwetting happens during a type of sleep in which sleep-walking and sleep-talking occur in younger
children. The cause is unknown.
Restricting drinks in the evening does not prevent the episode from occurring.
Because it happens during sleep, the child has no conscious control over it, so the problem is neither
the child’s nor the parents’ fault.
WHAT CAN PARENTS DO TO HELP?

Reassure your child, especially if they are upset. You need to be patient and understanding, even
though you may feel angry.
Encourage a good night’s sleep. Waking your child to go to the toilet during the night will not help
solve the problem.
Try absorbent pads. The pads go under the bottom sheet to keep the bed drier and more
comfortable.
Encourage your son to shower before he goes to school. The smell of urine is very strong and can
hang around. This may make your child feel embarrassed and lead to other problems, such as teasing
and name-calling at school.
WHAT TREATMENT MAY HELP?

Your local bedwetting clinic can supply or recommend a bedwetting alarm which wakes the child in
the night when he starts wetting. When a child begins to urinate, a sensor (either a bed pad or one
worn inside pyjamas) is moistened, and the alarm is triggered. Alarms work best with the professional
help of a bedwetting nurse. Alarms need lots of time and commitment on the part of both parents
and child to work! About half of all children who complete an alarm programme remain dry after the
programme is completed.
Alarms may be used in conjunction with a suitable reward systems (e.g. star charts) in which the
child might receive a star for every dry night, and a reward after a preset number of stars have been
earned.
Certain medications may help, but the problem often occurs again when the medications finish.
Thus, medication is most useful for specific events such as nights away from home. All drugs have
some side effects.
Most children grow out of the problem, even without treatment.
Answers 147
OSCE COUNSELLING CASE 14.2 – My 2-year-old boy has nocturnal

screaming episodes.
The history is typical of night terrors.
This is good news; they do not harm the child in any way, do not signify serious underlying problems,
and do not interfere with growth or development. Despite the child’s appearance they are not really
distressed, i.e. night terrors are not the same as nightmares.
A night terror is a disturbance of sleep pattern, where very rapid emergence from the first stage of
sleep produces a state of high arousal.
Sleep-walking is a similar phenomenon.
The child needs reassurance alone.
The problem settles with time.
Sometimes, waking the child 15 min before the phenomenon usually starts, each night for a week,
can cure the problem.
REVISION PANEL
Emotional and behavioural problems are common in children and young people.
Children’s behavioural and emotional responses are the result of genetic predisposition and
environment, of which the family is the major factor.
A detailed history as well as a full physical examination and developmental assessment are key to
determining the likely cause for emotional or behavioural problems.
It is important to explore the social/family circumstances and issues at school.
Often a multiprofessional approach with engagement of the school and family is required in the
management of children and young people with emotional and behavioural problems.
Index
Notes
Pages numbers in italics denote figures
a-1-antitrypsin deficiency 112 allergy 105

a-glucuronidase 116 aminophylline 64
abdominal masses 108 analgesia 84, 87, 126
abdominal pain 97, 99–108 anaphylactoid purpura (Henoch–Schönlein
acute 108 purpura) 123, 125–6
haematuria 103–4 anatomy 36
medical causes 102 androgens 4
non-specific 102 aneurysms, Kawasaki disease 50
abdominal tenderness and guarding 104 anorexia nervosa 8–9
abdominal X-ray 93, 134 anti-emetics 85, 87
abscess, brain 82, 85–6 anti-endomysial antibodies 105
absence epilepsy 72, 76 anti-gliadin antibodies 105
absorbent pads 146 anti-streptolysin O (ASO) 103
abuse 143, 144 antibiotics
accidental poisoning 137 acute severe illness 36
activated charcoal 132 cystic fibrosis 61, 65, 66
active immunization (vaccination) 51 meningococcal disease 127
acute appendicitis 104 neonatal seizures 76
acute circulatory failure 94 urinary tract infection 104
acute fever 47–55 anticonvulsants 76
acute gastroenteritis 94–6 antidotes 132
acute-onset stridor 60 antiepileptic drugs 77
acute post-streptococcal glomerulonephritis 102, antifungal creams 124, 127
103–4 antihistamines 132
acute renal failure 103 antimalarial drugs 53
acute severe illness 33–45, 36 antiviral agents 61
acyanotic congenital heart disease 73 apnoeas 93
ADHD (attention deficit hyperactivity disorder) appendicitis, acute 104
142, 144 arms, stiff 14, 18
adolescent growth spurt 4 arrhythmia 39, 44
adrenal tumours 11 asphyxia, at birth 17
advanced life support 42 aspiration 74–5
aggression 140, 143–4 aspirin 54
air insufflation 94 astatic episodes 72
airway asthma 61, 64, 67
breathing, circulation and disability assessment atonic episodes 72
37, 39, 41, 45 atopic dermatitis (infantile eczema) 124
inflammation 36, 60 atopy 124
obstruction 36, 39, 44 attention deficit hyperactivity disorder (ADHD)
alanine transferase 133 142, 144
alcohol, idiopathic epilepsy 77 autism 19, 140, 142, 144–5
alkaline diuresis 132 MMR vaccine 55
allergens 60 autoimmune disease 105
150 Index
automated auditory brainstem response (AABR) bowel lymphoma 102

screening test 16 bowel obstruction 93
automated otoacoustic emission screening (AOAE) brachio-brachial delay 74
16 brachio-femoral delay 74
average birth weight 36 brain
abscess 82, 85–6
b-haemolytic streptococcal septicaemia 74–5 injury 16
b2 agonists 60, 61, 64 tumour 85–6
babies breast development 2, 7–8
fits 70, 75–6 breast-feeding
respiratory disorders 66 reduced fluid intake 113
stools 92 stools 92
vomiting 90 under-nutrition 29–30
bacille Calmette–Guérin (BCG) vaccine 51 weight faltering 24, 25, 29–30, 31
baclofen 18 breast milk jaundice 112, 114, 116, 117
bacterial infection breath-holding attacks 71, 72, 78
breathing ceased 39, 44 breathing
fits 75 ceased 39–44
gastroenteritis 95 difficulties 34, 37–8, 58, 64
lower respiratory tract infection 64 noisy 58, 63–4
pneumonia 63–4 shortness 65, 130, 135–6
barrier creams 127 stopped 34, 39–44
basic life support 41 bronchioles 60
BCG (bacille Calmette–Guérin) vaccine 51 bronchiolitis 60–1, 63–4, 67
bedwetting 141, 146 bronchoconstriction 60
bedwetting alarm 146 bronchodilators 60, 61, 65
bedwetting nurse 146 bronchospasm 60
behavior modification therapy 78 bruising 120, 125–6
behavioural problems 139–47 Brushfield spots 20
benign congenital hypotonia 17 button battery ingestion 137
benzodiazepines 76
bereavement support 44 C-reactive protein (CRP) 36
bile 116 café-au-lait spots 85
bilharzia 103–4 caffeine 84
biliary atresia 112, 114, 116 calcium 75
biliary drainage 112 Campylobacter 95
bilirubin 112, 116 candidiasis 122, 124, 127
birth trauma 17 carbamazepine 132
bleeding disorders 103–4 carbohydrate malabsorption 26
blood gases 39, 63–4 carbon monoxide poisoning 83, 85, 135–6, 137
blood pressure 103 carboxyhaemoglobin (COHb) 135
blood spot screening 62 cardiac anomaly 39
blood sugar 36 cardiac failure 63–4
blue baby 34, 38–9, 70, 74–5 cataracts 44
blue breath-holding attacks 72, 78 ‘catch-down’ growth 25, 29–30, 31
body mass index (BMI) 5 centiles 4, 26
bone age central cyanosis 73, 74
delayed puberty 9 central nervous system assessment 135
premature growth spur 7 cerebral herniation 36
short stature 6 cerebral palsy (CP) 16, 18, 21, 93
thelarche variant 7 delayed walking 20
bottle-feeding 25, 31, 92 cerebrospinal fluid (CSF) microscopy 36
Index 151
chest auscultation, asthma 64 corticosteroids 60

chest physiotherapy 61, 66 cosmetics ingestion 132
chest X-ray 39, 44, 61, 75 cough
chicken pox 48, 122 acute breathing difficulties 64
child/adult differences 36 acute severe illness 34, 37–8
Child Growth Foundation 5, 10 cystic fibrosis 65
child health surveillance 134 noisy breathing 63–4
child protection 97, 125 cow’s milk protein intolerance 26, 105
child protection register 125 Coxsackie virus A16 122
childhood growth phases 4 cranial imaging 44, 87
childhood infectious diseases 50 creatinine 28, 133
chloride 96 creatinine kinase 135
chloroquine 53 croup (laryngotracheobronchitis) 60, 63
chromosomal disorders 17 CT (computed tomography) 83–4
chronic active hepatitis 115 cyanosis 63, 74–5, 135
chronic fever 47–55 cyanotic congenital heart disease 73, 74–5
chronic otitis media (glue ear) 19 cystic fibrosis 59, 61–2, 66, 67
chronic renal failure 103 breathing difficulties 58, 65, 66
ciprofloxacin 123 delayed puberty 8
Clinitest 113 cytomegalovirus (CMV) 112, 115
clonic seizure 72
clotting disorders 125 D F508 gene 61
CMV (cytomegalovirus) 112, 115 DAT (direct antibody test) 113
coagulation screen 125 deafness 19
coarctation of the aorta 73, 74 dehydration 45, 92, 95, 104, 108
coeliac disease 102, 105–6, 108 delayed puberty 2, 4, 8–9
colic 91, 92, 94, 97 delayed speech 14, 19, 21
communication impairment 142 delayed walking 15, 20, 21
complement C3 103 dermatitis 127
comprehension failure 19 desferrioxamine 132, 135
computed tomography (CT) 83–4 developmental delay 13–21
concentration 142 developmental language disorder 19
confusion 130, 135–6 developmental milestones 16
congenital heart disease 38–9 diabetic ketoacidosis 102, 104–5
acyanotic 73 dialysis 104
cyanotic 73, 74–5 diarrhoea 89–97
weight faltering 27–8 acute severe illness 35, 37, 45
congenital lung malformation 66 causes 92
congenital myopathy 17 coeliac disease 105–6
conjugated bilirubin 112 gastroenteritis 45, 97
conjugated jaundice 114 sickness and 90, 95
conjunctivitis 52 tummy ache and 100
consanguinity 17 dietary advice 10
constipation 107 dietary supplements 61
constitutional growth delay 6–7 dieticians 28, 29, 31
constitutional short stature 3, 6–7, 10 Dioralyte 45
contact dermatitis 127 diphtheria, tetanus, pertussis, polio and
continuous positive airway pressure (CPAP) 66 Haemophilus influenzae type b (DTaP/IPV/Hib)
contrast swallow 29 vaccine 51
convulsions 72 diplegia 16
Coombs’ test 113 direct antibody test (DAT) 113
cor pulmonale 62 disconsonant puberty 7
152 Index
dishwasher powder ingestion 132 ‘floppy’ (hypotonic) baby 14, 17, 21

disordered social background 143–4 fluid replacement 63, 97
distraction 142 follicle-stimulating hormone (FSH) 8
docusate 107 fontanelles 38, 75
Down’s syndrome (trisomy 21) 15, 20., 21 food diary 27, 28
drowsiness 100, 104–5 food refusal 24, 25, 28–9, 31, 140, 143–4
drug intoxication 76–7 force-feeding 24, 28, 31
drug withdrawal 75 foreign travel 48, 52–3, 95
ductus arteriosus 38 full blood count (FBC) 36, 85, 113, 125
dystonic movements 93 functional abdominal pain 107, 108
fundoplication 93
ecchymoses 122–3 fundoscopy 77
echocardiography 39, 51, 54, 75 fungal infection 104, 124, 127
eczema 58, 122, 128 funny turns 69–78
electrocardiography 39
electroencephalography (EEG) 72, 78 gastric peristalsis 93
electrolyte disturbance 36, 39, 44 gastro-oesophageal reflux 28, 29, 92–3, 97
emollients 124, 128 gastroenteritis 37, 45, 94, 97
emotional problems 139–47 acute 94–6
encephalitis 82, 85–6, 122 dehydration 45
encephalopathy 72 generalized tonic-clonic seizure 76, 78
enuresis, secondary 104 genetics
epiglottitis 60 cystic fibrosis 61, 66
epilepsy 70, 72, 76–7, 78 emotional and behavioural problems 142
epilepsy syndrome 72 German measles see rubella
epileptic seizure 72, 76 glandular fever (infectious mononucleosis) 53–4,
epiphyses fusion 4 115
erythema marginatum 102 glucose 75, 92, 102
erythematous (red) rashes 122, 128 glucuronyl transferase 112
erythrocyte haemolysis 112 glue ear (chronic otitis media) 19
ethnicity, height 6 gluten-free diet 102, 106
exanthems 122 gonadotrophin-releasing hormone agonist 8
exchange transfer 114 goserelin 8
exercise advice 10 grommets 19
extrahepatic biliary atresia 112, 114 group A streptococcal infection 53–4
growth 1–11
faecal-1 elastase 29 failure 4
failure to thrive see weight faltering first year of life 36
faints 69–78 phases 4
familial delayed puberty 8–9 spurts 4
familial short stature 6–7 growth hormone
fatty acids 102 deficiency 6–7
febrile convulsion 71, 72, 78 treatment 10
feeding Turner’s syndrome 5
behaviour modification programme 29 grunting 66
inability 26
refusal 24, 25, 28–9, 31, 140, 143–4 haemarthroses 125
ferritin 28 haematuria 103–4
fever 34, 37–8, 47–55, 72 haemodialysis 132
fidgeting 142 haemofiltration 132
fifth disease 122 haemolytic jaundice 113–14
fits 69–78 Haemophilus influenzae type B vaccination 51, 60
Index 153
hand, foot and mouth disease 122 infancy growth phase 4

hand preference 18 infant
handwashing 45 normal development 16
head bobbing 66 physiology 36
headache 79–87 infantile colic 91, 92, 94, 97
acute 82 infantile eczema (atopic dermatitis) 124
carbon monoxide poisoning 130, 135–6 infantile spasms 72
recurrent 80, 82, 84–5 infectious mononucleosis (glandular fever) 53–4,
unsteady gait 80, 85–6 115
headache diary 87 insulin 102, 105
health visitors 28, 29, 31 insulin-like growth factor-1 (IGF1) measurement 6
hearing aids 19 insulin resistance 10
hearing impairment 19, 143–4 insulin stress test 6
hearing test 143 intracranial infection 85–6
heart failure 37 intracranial pressure, raised 82, 83
heart–lung transplantation 62 intracranial tumours 7
heel prick blood test 116 intussusception 93, 94, 126
height involuntary soiling 107
final adult estimation 5 ipratropium bromide 60
measurement 4 iron tablet ingestion 130, 134–5
height velocity 4, 6–7 iron toxicity 134–5
hemiplegia 16 irritable bowel syndrome 107
Henoch–Schönlein purpura (HSP, anaphylactoid isolated premature thelarche 7–8
purpura) 123, 125–6
hepatitis 112, 114, 115 jaundice 109–17
hepatosplenomegaly 38, 113 jejunal biopsy 105
‘herd immunity’ 50 jitters 72
hives (urticaria) 122 juvenile myoclonic epilepsy 76
household substance ingestion 132
human papillomavirus (HPV) vaccination 51 karyotype
hydrocortisone 124 Down’s syndrome 20, 21
hyperactivity 142, 143–4 Turner’s syndrome 8, 29
hyperbaric oxygen therapy 136 Kasai portoenterostomy 112
hypernatraemic dehydration 95 Kawasaki disease 50–1, 53–4, 55
hyperreflexic reflexes 18 Kayser–Fleischer rings 115
hypertension 83–5, 102, 103 kernicterus 114
hypertonia 16 ketones 102, 104
hypoglycaemia 36, 76–7 Koplik’s spots 54
hyponatraemic dehydration 95
hypothermia 74–5 lactose intolerance 95, 105
hypothyroidism 27–8 lactulose 107
hypotonic (‘floppy’) baby 14, 17, 21 laryngotracheobronchitis (croup) 60, 63
laxatives 107
iatrogenic poisoning 39–44 learning problem 143–4
idiopathic epilepsies 73, 76–7 legs
idiopathic thrombocytopenic purpura 126 drawing up 90, 94
immunizations 51, 60, 122, 123 stiff 14, 18
immunoglobulins 50, 54 lethargy 113
impetigo 122 leukaemia 123, 125
impulsivity 142 leukotriene antagonists 61
inattention 142 liver function tests 114
inborn errors of metabolism 37, 38, 44, 75 liver inflammation 117
154 Index
lower respiratory tract infection 38–9, 64 N-acetycysteine 132, 134, 137

lumbar puncture (LP) 36 naloxone 132
luteinizing hormone-releasing hormone (LHRH) nappy rash 121, 127, 128
test 8, 9 nasal breathers 36
nasal flaring 66
magnesium 75 nasopharyngeal aspirate 44
magnetic resonance imaging (MRI) nausea 130, 135–6
head 81, 87 nebulized adrenaline 60
indications 83–4 neck stiffness 55, 127
maintenance fluids 92 Neisseria meningitidis (meningococcus) 36, 123,
malabsorption 26, 28, 102, 105–6 127
malaria 52–3, 85 neonatal hepatitis 112, 114
maturation delay 19 neonatal resuscitation 36
delayed speech 19, 21 neonatal seizures 73, 75–6, 78
measles 50, 52, 54 neonatal sepsis 38
epidemic 55 neurocutaneous signs 85
exanthems 122 neurodevelopment assessment 145
mumps and rubella (MMR) vaccine 49, 51, 55 neurological examination 83, 85
meconium 92 newborn hearing screening 16
meconium ileus 66 newborn jaundice 110
MedicAlert bracelet/card 77 newborn life support 43
meningitis 35, 37–8, 45, 123, 127 night terrors 147
diagnosis 36 nitrogen washout test 75
fear of 36, 45 nocturnal screaming episodes 141, 147
fits 75 noisy breathing 60, 63–4
meningitis C vaccine 51, 127 non-accidental injury (NAI) 123, 125–6, 128
meningococcal disease 52–3, 54, 122, 123, 126 non-blanching rashes 120, 122–3, 128
non-blanching rash 123, 127, 128 norovirus 97
symptoms 123, 126, 127 nystatin 127
vaccine 123
meningococcal septicaemia 55 obesity 5, 10, 11
meningococcus (Neisseria meningitidis) 36, 123, obligate nasal breathers 36
127 obstructed hernia 94
mental retardation 19 obstructive jaundice 112
metabolic disorders 18, 113–14 ocular headache 82
methylphenidate 144 oesophageal sphincter immaturity 93
miconazole 127 oesophagitis 93
mid-parental height 5 oestrogens 4, 5
migraine 80, 81, 84–5, 87 oligura 102
mitts 124 opiates 132
MMR (measles, mumps and rubella) vaccine 49, oral contraceptives ingestion 132
51, 55 oral rehydration therapy 92, 95
monoclonal antibodies 61 orchidometer 4
monospot/Paul Bunnell test 54 organic acidaemias 75
Moro reflex 18 oromotor dysfunction 27, 28, 29
mosaicism 20 oven cleaner ingestion 137
motor skills 16 overdose 131, 137
MRI see magnetic resonance imaging (MRI) overweight 3, 5, 10
mumps vaccine 49, 51, 55 oxygen therapy 38, 63
muscular dystrophy 20
myoclonic seizure 72, 76 paediatric advanced life support 42
myopathic disorders 18 paediatric basic life support 41
Index 155
paediatric resuscitation 39 polymerase chain reaction (PCR) 36

paint ingestion 132 poor feeding behaviour 28–9, 31
palatal petechiae 54 posset 92
pancreatic enzyme supplementation 61 post-mortem 44
paracetamol 52, 53, 78, 85, 133 post-streptococcal glomerulonephritis 102, 103–4
overdose 131, 137 postural drainage 61
paracetamol suspension ingestion 130, 133–4, potassium 105
137 precocious puberty 4, 7–8, 11
paralytic conditions 17 pregnancy, rubella 49, 50, 55
paramyxovirus 122 premature baby 14, 18
parental anxiety 36 preschool behavior problem 143–4
parvovirus B19 122 projectile vomiting 93
pathological jaundice 112, 117 prolonged jaundice 112, 116
peeling skin 48, 53–4 prostaglandin E2 39, 75
PEFR measurement 64 protein malabsorption 26, 105
penicillamine 115 proteinuria 102
penicillin 104 psychological short stature 6–7
perfusion, poor 75 psychology 36
peri-orbital oedema 102 puberty
perianal tear 107 delayed 2, 4, 8–9
peripheral cyanosis 73, 74 precocious 4, 7–8, 11
peristalsis 102 pubic hair 8
permethrin 124 pulse oximetry 73
pertussis (whooping cough) 63 purpura 122–3
pertussis vaccination 51 pyloric stenosis 93, 95–6
pervasive developmental disorder see autism pyloromyotomy 93, 96
petechiae 122–3
Peyer’s patches 93 quadriplegia 16
pH study 29
pharyngitis 52 radionucleotide excretion scan 114
phenobarbital 76 ranitidine 93
phenytoin 76 rashes 48, 52, 119–28
photosensitivity 76, 77 non-blanching 120, 122–3, 128
phototherapy 113, 116 red scaly 120, 124
physiological jaundice 112, 113–14, 116, 117 recession 66
physiology 36 reciprocal communication/interactions 142
physiotherapy 18 recurrent abdominal pain 108
picosulphate 107 recurrent headache 80, 82, 84–5
pin-point pupils 77 ‘redcurrent jelly’ stools 93
pituitary testing 6 reflex anoxic seizure (reflex anoxic syncope) 72
Plasmodium falciparum infection 53 reflex anoxic syncope (reflex anoxic seizure) 72
Plasmodium vivax infection 53 rehydration 92, 105
play specialists 87 renal biopsy 104
pneumococcal conjugate vaccine (PCV) 51 renal disease, weight faltering 27–8
Pneumococcus 36 renal failure 103–4
pneumonia 63–4, 66, 74–5 respiratory difficulty assessment 64
pneumothorax 64, 65 respiratory distress syndrome (RDS) 66
poisoning 39–44, 82, 129–37 respiratory problems 57–67
poisons unit 132 respiratory support 61
polio vaccination 51 respiratory syncytial virus (RSV) 61
polycythaemia 74 resuscitation 44
polyethylene glycol-electrolyte solution 135 reward systems 146
156 Index
rheumatic fever 102 small airways 36

rifampicin 123 small for gestational age 10
rigors 53 smoky-coloured urine 103–4
ringworm 122, 124 social deprivation 27
rituals 142 sodium 75, 92
rotavirus 35, 95, 97 soiling, involuntary 107
routines 142 sore throat 53–4
rubella 50, 52 spasm 72
exanthems 122 spastic quadriplegia 18
pregnancy 49, 50, 55 spasticity 16
vaccine 49, 51, 55 special care unit 59, 66
rubella syndrome 50 speech
Russell–Silver syndrome 10 delayed 14, 19, 21
slurred 80
salbutamol 64 speech therapy 19, 29, 31
salicylate ingestion 132 spinal muscular atrophy 17
Salmonella 95 splenomegaly 54
sandal gap 20 spots, dark red 120, 126
Sandifer’s syndrome 93 starvation stools 28
scabies 122, 124 steatorrhoea 61
scarlet fever 53–4, 122 stercobilinogen 112
schoolchildren stick test 103
disruptive 140 stool softeners 107
headache 82, 83–4 stools 24, 29
tummy ache 101 blood in 92, 97
screaming frequency 92
nocturnal 141, 147 loose 34
sudden-onset episodes 90, 94 malabsorption 28
seizure 44, 72–3 pale 110, 112, 115, 116
self-harm 137, 142 strawberry tongue 54
senna 107 streptococcal infection 52
sensorineural deafness 19 stress 107
sepsis 17, 113 stridor 60
septicaemia 36, 37–8, 45, 123, 127 subacute sclerosing panencephalitis (SSPE) 55
Shigella dysentery 95 sudden infant death syndrome (SIDS) 39–44
shock 74, 93, 104, 105 surfactant deficient lung disease (SDLD) 66
‘short normal’ 7 sweat test 29, 62
short stature 2, 6–7, 11 syncope attacks 72
SIDS (sudden infant death syndrome) 39–44
silent chest 64 tachycardia 64
silica gel ingestion 132 tachypnoea 64, 66
sitting, developmental delay 14, 18 Tanner staging 4
size 36 tantrums 25, 142
skeletal survey 44 teenage fits 76–7
skills development 16 temper tantrums 142
skin tension headaches 80, 83–4
dry, itchy 120, 124 test feed, pyloric stenosis 93
peeling 48, 53–4 testes
sleep deprivation 76, 77 size 4
sleep-talking 146 torsion 94
sleep-walking 146, 147 tetanus vaccination 51
slurred speech 80 thelarche 4, 7–8
Index 157
thelarche variant 7, 8 urine

theophylline 132 blood in 100, 103–4
thirst 104–5 dark 112, 115, 116
threadworms 107 jaundice 112, 115
thrombocytopenia 122, 123 lots of 100, 104–5
thyroid function tests 28 smoky-coloured 103–4
time out 144 urobilinogen 112
tinkling bowel sounds 38, 94 urticaria (hives) 122
tissue transglutaminase antibodies 105
tissue turgor 92 vaccination (active immunization) 51, 60, 123
toilet cistern block ingestion 132, 137 varicella zoster virus 122
tonic-clonic seizure 72 vasovagal attacks 72
tonsillitis 54 ventilation 66
topical steroids 124 video recordings, seizures 78
TORCH screen 114 viral croup 60, 63
toxic substance ingestion 132, 137 viral hepatitis 115, 117
toxoplasmosis 112 viral infection 60
tracheo-oesophageal fistula 28, 29 vision test 143
transient tachypnoea of the newborn (TTN) 66, 67 visual aura 80, 81
transposition of the great arteries (TGA) 73, 75 visual problems 143–4
tricarboxylic acid cycle 102 vitamin tablet ingestion 132
triptans 85 vomiting 89–97
trisomy 21 (Down’s syndrome) 15, 20, 21 acute severe illness 35, 37, 45
trypsin 62 after feeds 90, 91, 95–6, 97
tuberculosis 50, 105 carbon monoxide poisoning 130, 135–6
Tumbler test 122 recurrent headache 80, 84–5
tummy ache 100
‘tummy bug’ see gastroenteritis walking developmental delay 15, 20, 21
Turner’s syndrome 5, 8–9 washing powder ingestion 131, 132, 137
type 1 diabetes 102 weight faltering 23–31, 105–6
breast-feeding 24, 25, 29–30, 31
UK immunization schedule 51, 55 causes 26
ultrasound 96 weight prediction 36
unconjugated bilirubin 112 wheat 102
under-nutrition 26, 27–30, 31 wheezing 58, 60, 63–4, 67, 124
unsteady gait 80, 85–6 white cell count (WCC) 36
upper respiratory tract infection (URTI) 36, 63–4, white plaques 124
78 whole-bowel irrigation 132, 135
urea and electrolytes 85, 96, 103 whooping cough (pertussis) 63
urinalysis 28, 30, 36, 44 Wilms’ tumour 103, 105
urinary tract infection 37, 38, 45, 103–4, 114 Wilson’s disease 115
Core Clinical Cases
Core Clinical Cases is a series of guides that enable to you integrate
your knowledge with the realities of managing clinical problems,
and provide a basis for developing sound analytical and confident
decision-making skills. They are the ideal course companions that undergraduate
medical students turn to at various stages of clinical training.
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Gary Mires, Khalid S Khan and Janesh K Gupta
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Steve Bain and Jeffrey Stephens
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this book is written specifically for the medical
Paperback • May 2011 • £29.99
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Key Feaures: Review:
• Written in a succinct, user-friendly and Excellent…comprehensive,

informative style with clinical photographs yet does not include
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visualise key points information…the material
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• Highly structured and organised by body the student and junior
system, with chapters on subjects such as doctor market’
history and examination, development and
genetics Andrew Walker, F2 Doctor,
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What is the book about?

What is the book about?

What information is included in each chapter?

What information is included in each chapter?

Core

Andrew Ewer MD MRCP FRCPCH

Rajat Gupta DCH MMedSci FHEA FRCP

Timothy Barrett PhD MRCP FRCPCH

Core Clinical Cases series edited by

Janesh K. Gupta MSc MD FRCOG

© 2011 Andrew Ewer, Rajat Gupta and Timothy Barrett

British Library Cataloguing in Publication Data

Library of Congress Cataloging-in-Publication Data

ISBN-13: 978 1 444 12286 2

Commissioning Editor: Joanna Koster

Typeset in 9 on 11pt Frutiger by Phoenix Photosetting, Chatham, Kent

Professor Ian Booth

For each of the case scenarios given, consider the following:

Q1: What: is the likely differential diagnosis?

CASE 1.1 – My 6-year-old son is the shortest in his class.

CASE 1.2 – My 5-year-old daughter is developing breasts.

OSCE Counselling cases

OSCE COUNSELLING CASE 1.1 – My child has a diagnosis of

OSCE COUNSELLING CASE 1.2 – Why is my child overweight?

PHASES OF CHILDHOOD GROWTH

MEASUREMENT OF HEIGHT AND HEIGHT VELOCITY

ESTIMATION OF FINAL ADULT HEIGHT FROM PARENTS’ HEIGHT (MID-PARENTAL

CASE 1.1 – My 6-year-old son is the shortest in his class.

A2: What issues in the given history support the diagnosis?

A4: What clinical examination would you perform, and why?

A5: What investigations would be most helpful, and why?

A6: What treatment options are appropriate?

CASE 1.2 – My 5-year-old daughter is developing breasts.

A2: What issues in the given history support the diagnosis?

A4: What clinical examination would you perform, and why?

A5: What investigations would be most helpful, and why?

A6: What treatment options are appropriate?

A2: What issues in the given history support the diagnosis?

A4: What clinical examination would you perform, and why?

A5: What investigations would be most helpful, and why?

A6: What treatment options are appropriate?

OSCE Counselling cases

OSCE COUNSELLING CASE 1.1 – My child has a diagnosis of

OSCE COUNSELLING CASE 1.2 – Why is my child overweight?

For each of the case scenarios given, consider the following:

Q1: What is the likely differential diagnosis?

CASE 2.1 – My newborn baby is very ‘floppy’ (hypotonic).

CASE 2.3 – My 2-year-old daughter does not say any recognizable

OSCE Counselling cases

OSCE COUNSELLING CASE 2.1 – My 16-month-old son is not yet

OSCE COUNSELLING CASE 2.2 – My newborn baby has been diagnosed

NORMAL INFANT DEVELOPMENT

NEWBORN HEARING SCREENING

CASE 2.1 – My newborn baby is very ‘floppy’ (hypotonic).

A2: What issues in the given history support the diagnosis?

A4: What clinical examination would you perform, and why?

A5: What investigations would be most helpful, and why?

A6: What treatment options are appropriate?

A2: What issues in the given history support the diagnosis?

A4: What clinical examination would you perform, and why?