Clinical File-1 2

Secrets to Passing
MRCPCH Clinical Exam
Dr Ching Bih Hwa

Dr Yew Kian Teck
Secrets to Passing
A few observations and much reasoning leads to error,

many observations and a little reasoning to truth.
Alexis Carrel (1873 – 1944)
i
This book is dedicated to
Mr Ching Ah Yong (my father), Mdm Wee Nai Hiang (my mother),
Dr Goh Kwang Hwee (my husband), my daughter Goh Sin Yee and my son
Goh Kai Yang, for their patience while I was preparing for the book.
~ Dr Ching Bih Hwa
I would like to dedicate this book to both my wife, Li Peng and my family
members who have been supporting me unconditionally. With their
patience and love, I have finally walked through the wavy journey to be who
I wanted to be today.
~ Dr Yew Kian Teck
ii
Secrets to Passing
Dr Ching Bih Hwa

MBBS (Malaya), MRCPCH (UK)
Paediatrician,
Department of Paediatric,
Hospital Pakar Sultanah Fatimah, Muar
Dr Yew Kian Teck

MBBS (Malaya), MRCPCH (UK)
Paediatrician,
Department of Paediatric,
Hospital Pakar Sultanah Fatimah, Muar
HOSPITAL PAKAR SULTANAH FATIMAH, MUAR
MESRA BERSAMA MEMBINA KEUNGGULAN
We are what we repeatedly do.

Excellence, therefore, is not an act but a habit.
Aristotle
iii
All rights reserved. No part of this publication may be reproduced, stored
in a retrieval system or transmitted by electronic, mechanical,
photocopying, recording or other means, without the written permission
from the authors.
iv
Contents
Foreword viii
Preface ix
Acknowledgements x
General advice on how to pass MRCPCH clinical exam 1
Chapter 1: Approach to abdominal short cases 3

Abbreviations used in this chapter 4
How to prepare for abdominal short cases 6
Abdominal short cases 7
Abdominal scar 8
Abdominal mass 11
Causes of hepatomegaly 12
Causes of splenomegaly 13
Causes of hepato-splenomegaly 14
Causes of portal hypertension 15
Liver cirrhosis 16
Nutritional assessment 17
Management of malnutrition 19
Approach to renal mass 20
Approach to a child with chronic renal failure 21
Approach to a child with Beckwith-Wiedemann syndrome 22
Examples on how to present 23
Chapter 2: Approach to cardiovascular short cases 26

Cardiovascular short cases 28
How to prepare for cardiovascular short cases 29
Approach to cardiovascular short cases 31
Approach to a ‘pink’ child 34
Approach to a ‘blue’ child 35
Approach to dextrocardia 36
Example on how to present 37
Management of congenital heart disease 38
Chapter 3: Approach to developmental short cases 42

How to prepare for developmental short cases 43
Gross motor 45
Fine motor 48
Speech and language 52
v
Social 56
Key elements for short case presentation in developmental station 58
Chapter 4: Approach to endocrine short cases 60

Approach to Cushing’s syndrome 62
Approach to anterior neck swelling (Thyroid swelling) 63
Approach to short stature 64
Disproportionate short stature 65
Approach to tall stature 67
Marfan’s syndrome vs Homocysteinuria 68
Chapter 5: Approach to eyes examination 69

How to prepare for ophthalmological short cases 71
Examination of the eyes 72
Causes of blindness or severe visual impairment 74
Causes of corneal cloudiness 76
Pupils – Eye signs 77
Approach to a child with squint or strabismus 78
Fundoscopy examination – possible findings 82
Chapter 6: Approach to musculoskeletal short cases 83

How to prepare for musculoskeletal short cases 85
Musculoskeletal system examination 86
Paediatric Gait, Arms, Legs, Spine (pGALS) 88
Assess active movement of the specific joints 89
Approach to generalized joint hypermobility 91
Approach to scoliosis 93
Approach to unequal leg length 94
Chapter 7: Approach to neurological short cases 94

How to prepare for neurological short cases 96
Neurological short cases 98
Examination of the muscle power 101
Examination of the sensation 102
Root level of reflexes 103
Examination of the cranial nerves 104
Examination of the cerebellar system 106
vi
Approach to floppy infant 108
Approach to facial weakness 109
Approach to a child with ptosis 112
“Examine the gait.” 113
Approach to hemiplegic gait 114
Approach to spastic diplegic gait 116
Approach to ataxic gait 117
Approach to waddling gait 118
Approach to high stepping gait 119
Approach to spina bifida 120
Pes cavus, pes planus and bottom shuffling 121
Approach to microcephaly 122
Approach to macrocephaly 123
Approach to a child with Sturge Weber syndrome 124
Approach to a child with Neurofibromatosis Type 1 126
Approach to a child with Tuberous Sclerosis 128
Chapter 8: Approach to respiratory short cases 130

How to prepare for respiratory short cases 132
Approach to a child with bronchiectasis 133
Approach to a child with primary ciliary dyskinesia 135
Example on how to present 136
Chapter 9: Approach to history taking & management planning station 137

How to prepare for history taking & management planning station? 140
Possible cases for history taking & management planning station 143
Chronic constipation 146
Inflammatory bowel disease 147
Biliary atresia 149
Chronic renal failure 152
Approach to children with Type 1 diabetes mellitus 155
Duchenne muscular dystrophy 157
Sample scenarios 158
Appendix 163
Antiepileptic drugs and related side effects 164
Cytotoxic drugs and related side effecs 166
vii
Foreword
The Paediatric Department of Hospital Pakar Sultanah Fatimah, Muar

started conducting MRCPCH Preparatory courses in 2011 as an initiative to
address the shortage of Paediatricians in Johor. Thanks to the commitment
of all the Paediatricians and Medical Officers of the Department, over the
last 2 years, we have successfully conducted MRCPCH Part 1 and Part 2A
preparatory courses. These courses have not only benefited the Medical
Officers in Johor but have also received overwhelming responses from
around the country.
Following that, we are now taking on a new challenge – to organize the

MRCPCH Clinical preparatory course. I would like to congratulate Dr Ching
Bih Hwa and Dr Yew Kian Teck for producing this handbook “Secrets to
Passing MRCPCH Clinical Exam”. I hope this handbook would aid those
who are preparing for the Clinical Examinations in Paediatrics.
I would also like to thank all those who have contributed to the publication
of this handbook.
Dr Angeline Wan
Consultant Neonatologist and Head of Department
Paediatric Department
Hospital Pakar Sultanah Fatimah,
Muar, Johor.
viii
Preface
This book is published as a core reference material to supplement our

teaching in MRCPCH Clinical Exam Preparatory Course. The materials
presented here are the result of our effort during preparation for the
MRCPCH clinical exam.
The journey of preparing for the clinical exam is not easy. It is stressful and
tedious especially when there are so many things to read and learn in a
limited period of time. We are not full time medical students, and we have
to make time to study and continue our clinical practice. At the end of the
day, we have to prove to the examiners in 150 minutes that we deserve to
pass as a paediatrician! Many of us were lost, felt depressed in the exam
preparation and some gave up after multiple attempts.
By sharing our experiences, it is our sincere hope that it will provide a

guide for those who are planning to take the MRCPCH clinical exam.
Everyone who has gone through this exam would have their own secret
recipe. All will agree that “Although the path to success is not easy, the
reward is worth the struggle”.
This handbook is meant to provide a practical approach for the short case
examination station, history taking and management planning station in
MRCPCH clinical exam. It is not meant to provide details on management
strategies. It also includes tips to excel and possible exam cases in various
stations.
Lastly, we would like to thank all the consultants, specialists, medical

officers and house officers who have helped us in preparing this handbook.
Medicine is learned by the bedside and not in the classroom.

~ Sir William Osler (1849-1919)
Good luck!
Dr Ching Bih Hwa

Dr Yew Kian Teck
ix
Acknowledgements
We would like to express our greatest gratitude to the following

consultants who were kind enough to review the following chapters:
1. Dr Elaine Chiang (History taking and management chapter)

Consultant Community Paediatrician & Senior Lecturer
Newcastle University Medicine Malaysia
Johor Bahru.
2. Dr Gan Chee Chong (Ophthalmology chapter)

Ophthalmologist
Hospital Sultanah Aminah, Johor Bahru.
3. Dr Janet Hong Yeow Hua (Endocrinology chapter)

Consultant Paediatric Endocrinologist
Hospital Putrajaya.
4. Dr Khoo Teik Beng (Neurology chapter)

Consultant Paediatric Neurologist
Hospital Kuala Lumpur
5. Professor Lee Way Seah (Gastroenterology & hepatology chapter)

Senior Consultant Paediatric Gastroenterologist & Hepatologist
University Malaya Medical Centre
Kuala Lumpur
6. Dr Patrick Chan Wai Kiong (Respiratory chapter)

Senior Consultant Paediatrician and Paediatric Respiratory
Gleneagles Medical Centre.
7. Dr Ranjini Sivanesom (Development chapter)

Consultant Developmental Paediatrician
Hospital Kuala Lumpur.
x
8. Dr Tam Pui Ying (Cardiology chapter)
Consultant Paediatrician & Head, Dept. of Paediatrics
General Hospital Malacca.
9. Dr Tang Swee Ping (Rheumatology chapter)

Consultant Paediatric Rheumatologist
Hospital Selayang
Special thanks to the following doctors who helped us to type the texts and
algorithms:
1) Dr Azuan Muhafiz bin Abdul Karim 6) Dr Mohamad Afi Ifwan Hassan Adli
MBBS (UiTM) MB Bch BAO (Ireland)
2) Dr Evelyn Chia Wei Yen 7) Dr Nur’ Atiqah bte Mohd Jalil

MBBS (IMU), MRCPCH (UK) MBBS (USIM)
3) Dr Haslinda bte Rahaman 8) Dr Pavithira Devi Kailasam

MBChB, University of Sheffield, UK MBBS (MMMC)
4) Dr Jaiwant Singh 9) Dr Siti Soleha bte Bidin

MBBS (Monash) MD (UKM)
5) Dr Khairul Anuar bin Hassan 10) Dr Tee Chin Sien

MD. CSMU Ukraine MD (USM)
Thanks also to Dr Ngian Geok Hoon, Dr Tan Eva, Dr Jayavani Ettikan,

Dr Tan Hai Liang, Dr Gan Kai Ling and Dr Sia Yi Ping for proofreading, and Dr
Angeline Wan Seng Lian for encouraging the production of this handbook.
xi
General Advice on How to Pass the MRCPCH Clinical Exam
1. The decision to pass the exam lies within your hands, not the
examiners. Face the exam with positive attitude. Do not view it as a
disaster. Tell yourself, “I am here to pass, I can do it, I will make it!”
2. Knowledge is important, but with limited time for study, you have to
focus on vital topics. List down topics related to short cases
(differential diagnoses for various signs, diagnostic investigations and
principles of treatment), history taking and communication scenarios,
and read thoroughly on these topics. You will not pass by knowing the
whole of Nelson!
3. Practice makes perfect. You must practise repeatedly before the

exam. Choose an appropriate companion to practise with. Ask
him/her to question you and comment on your presentation. Also,
set a goal on the number of cases to see and practise every day. Make
a checklist of possible cases that may appear in the exam and
eliminate them after you have examined each case, rehearsed on the
presentation and discussion. This will ensure that you have adequate
exposure prior to the exam.
4. Gain adequate experience before the exam. Obtain as much clinical

experience as possible in your daily practice. Grasp every opportunity
to see different cases. Also, actively seek cases that you have no
experience with. Once you have seen a particular case, you will gain
confidence the next time you see it again. If you practice in a district
hospital, do clinical attachments in other hospitals with subspecialties
to have a more comprehensive exposure. Remember, the examiners
can tell if you are doing this for the first time or if you have done it on
a regular basis!
5. Clear and concise presentation. Look confidently at the examiner,

speak clearly and audibly. If you are less fluent in English, start
1
practising by communicating to patients in English every day.
Rehearse with a script for your presentations. You may fumble when
you are anxious, especially in exams!
6. Straight to the point. Listen carefully to the examiner’s question, and

answer the question asked. If you do not understand the question,
ask the examiner to repeat his/her question. Do not be vague. Do not
beat around the bush. Be proactive, elaborate on your answer and do
not wait for the examiner to ask you what is next.
7. Aim to give the most likely condition as your first diagnosis. Limit the
differential diagnoses to the child’s condition; do not give general
differential diagnoses. Common conditions appear commonly, so
mention the common things first. Don’t mention a very rare diagnosis
that you do not know much about. Lead the examiner to safe ground.
8. Look after the patient’s welfare. It is important to treat the child and
parents with respect at all times. Never hurt or cause distress to
them. You must make them feel comfortable throughout the
examination. Remember to thank them at the end of the
examination.
9. Do not give up after one failed station. While going through the
exam circuit, just concentrate on your current patient and give your
best to that patient. With that, you will do just fine.
10. Last but not least, make sure you are in good physical health and
have sufficient sleep prior to the exam. Dress well, do not under- or
overdress.
If success has an entry fee, the cost is TOTAL COMMITMENT.

~ Denis Waitley
2
Chapter 1
Approach to Abdominal Short Cases
Mnemonics used in this chapter: HIMGCM
Hematological causes
Infection
Malignancy
Gastroenterology/hepato-billary tract
Cardiac causes
Metabolic/miscellaneous/autoimmune disease
3
Abbreviations used in this chapter
ADPKD Autosomal dominant polycystic kidney disease

ARPKD Autosomal recessive polycystic kidney disease
AVF Arterio-venous fistula
a/w associated with
BP blood pressure
B/L bilateral
BWS Beckwith-Wiedemann syndrome
CF Cystic fibrosis
CLD Chronic liver disease
CMV Cytomegalovirus
CP Cerebral palsy
CRF Chronic renal failure
EBV Ebstein Barr virus
ESRF End stage renal failure
FTT Failure to thrive
GIT Gastrointestinal tract
GSD Glycogen storage disease
HBS Hepato-biliary system
H/O history of
HS Hereditary spherocytosis
IJVC Internal jugular venous catheter
IV intravenous
JIA Juvenile idiopathic arthritis
JVP Jugular venous pressure
LGA Large for gestational age
LIF Left iliac fossa
NG Nasogastric
OSA Obstructive sleep apnea
PD Peritoneal dialysis
PUJ Pelvic-ureteral junction
PUV Posterior urethral valve
RIF Right iliac fossa
RRT Renal replacement therapy
SAH Subarachnoid haemorrhage
SBE Subacute bacterial endocarditis
SCD Sickle cell disease
SLE Systemic lupus erythematosus
4
T° Temperature
TFT Thyroid function test
UFEME Urine full examination microscopy examination
VUJ Vesico-ureteric junction
VUR Vesico-ureteric reflux
5
How to prepare for Abdominal short cases?
Abdomen station is a relatively straight forward station that all candidates

should aim for a clear pass. Nothing much that you can palpate in the
abdomen, which includes
1) Enlarged liver
2) Enlarged spleen
3) Enlarged kidney/transplanted kidney
4) Enlarged bladder
5) Tumour arising from liver, kidney, adrenal gland (but unlikely to
be seen in exam)
6) Faecal mass in patient with constipation
Therefore, try to practice as much as you can, know

1. How to describe the mass you palpated
2. How to come out with the age-relevant differential diagnoses
3. How to assess complications related to the diagnosis
4. How to go on with the discussion on investigation and
management.
Other than that, be familiar with the abdominal scars and suggest the
possible surgery done based on the scar and the physical findings you
found. Some special scenarios like nutritional assessment (rare in exam),
approach to a child with Beckwith-Wiedemann syndrome are also
discussed in this chapter.
Be careful when you palpate the child abdomen. Make sure the exposure is
adequate. Cover areas not needed for examination with blanket.
Uncovering a child especially a teenager without good justification will
grant you a FAIL in exam. Make yourself comfortable by sitting on a chair
or squat down if the bed is too low before you start examining. Ask if there
is any pain before you start palpating the abdomen. Watch the patient’s
face as you palpating the abdomen. Be gentle and not to induce pain!
If you can master the above skills well, you should be able to score a clear
pass in this station.
6
Abdominal short cases
1) Thalassemia (major, intermediate) – more commonly seen in

Malaysia/Singapore
2) Hereditary spherocytosis – more commonly seen in UK

3) Sickle cell disease – more commonly seen in UK
4) Glycogen storage disease Type 1& 2
5) Infectious mononucleosis
6) Renal masses (unilateral or bilateral)
7) A child with chronic renal failure
8) A child with transplanted kidney
9) Neurogenic bladder
10) Fecal mass in a child with constipation
11) Biliary atresia, post Kasai procedure
12) A child with transplanted liver
13) Chronic liver disease
14) A child with cystic fibrosis and chronic liver disease – more commonly
seen in UK
15) A child with an abdominal scar – post intestinal surgery in Crohn’s

disease.
7
Abdominal scars
A: Midline laparotomy scar (any form of laparotomy)
B: Para-median scar (access to lateral structure eg: Kidney/spleen)
C: Kocher subcostal incision

Right – Gall bladder & billary tract
Eg.OTC (On Table Cholangiogram)
Cholecystectomy
Gallstone removal (in SCD, HS)
Left – Spleen
D: Upper abdomen midline incision (can be transverse)

Eg: Nissen’s fundoplication eg: Child with CP & gastrotomy scar
8
c
A: Rooftop
 Kasai procedure
 Extensive hepatic resection
 Total gastrectomy / Oesophagectomy
 Adrenalectomy eg: Neuroblastoma
 Operation for reno-vascular hypertension
B: Mercedes Benz Extension

 Liver transplantation
C: Transverse upper abdomen incision

 Left more than right
 Repair of congenital Diaphragmatic hernia
D: Small night upper transverse incision

 Eg :Ramstedt’s pyloromyotomy (more in males)
E: MC-Burney (Right iliac fossa)

 Appendicectomy
Note:
Transverse laparotomy scar often used for neonates & infants intra-
operatively as infant’s abdomen has a longer transverse than vertical
growth.
9
A: Lateral thoracolumbar scar
 Nephrectomy
 Cystic Dysplastic Kidney
(Prevent infection in redundant kidney, and development of
hypertension in adult life.)
B: Inverted J scar with transplanted kidney at RIF or LIF
C: Sub-umbilical / Umbilical scar

 Gastroschisis
 Exomphalos
 Umbilical hernia repair (after 2 years old)
D: Groin Scar
 Inguinal hernia repair
Note:
Be aware of liver biopsy scar as well (look carefully as it is small and often
missed!)
10
Abdominal mass
How to describe the abdominal mass?
Palpation
1) Site
2) Size
3) Shape
4) Consistency
 hard
 firm
 soft
 indentability
5) Surface
6) Edge
7) Tenderness
Percussion
- Dull / resonant
Auscultation
- Presence of bruit
11
Causes of Hepatomegaly
Infancy and Early

Neonate Older Children
childhood
Hematological Hemolytic Sickle cell disease
Disease of
newborn
Infection - Hepatitis Hepatitis
Malignancy -  Neuroblastoma  Secondary
 Hepatoblastoma infiltration
(<2y)  Hemangioma
GIT Neonatal Hepatic vein Hepatic vein
Hepatitis Thrombosis thrombosis
syndrome
(Including
biliary atresia)
Cardiac Heart failure Heart failure Heart failure
Metabolic Galactosaemia  GSD  GSD
Miscellaneous  Reye’s Syndrome  Wilson’s
Autoimmune ds  Fatty liver disease
 Autoimmune  Alpha 1
Hepatitis antitrypsin
deficiency
 Fatty Liver
 Autoimmune
hepatitis
Note:
LIVER SPAN
At birth: 5 – 6cm 3 years: 8 – 9cm
1 year: 6 – 7cm 12 years: 12cm
Note: It is better not to measure liver span if you can’t remember well the
different liver span for different ages. Generally, if the liver is palpable
more than 1 finger breath below the costal margin with normal positioned
upper border, then it can be considered as enlarged. It is easier and safer
to measure the span below the costal margin + ascertain the level of upper
border.
12
Causes of Splenomegaly
Infancy and Early Older Children

childhood
Hematological Sickle cell disease (young Hereditary
<1 year old child) Spherocytosis
Hereditary spherocytosis
Infection - SBE*
Malaria*
EBV,CMV
Malignancy Lymphoma Lymphoma
Cardiac - -
GIT Portal Hypertension Portal Hypertension
Metabolic Systemic JIA Systemic JIA
Miscellaneous SLE SLE
Gaucher’s disease Gaucher’s disease
Bold Commonly seen in exam (in UK)

* Uncommonly seen in exam
13
Causes of Hepato-splenomegaly
Neonate Infancy& early Older child

childhood
Haematological - Thalassemia Thalassemia
Infection Congenital Viral : Viral :
Infection ▪ CMV* ▪ CMV*
▪ CMV* ▪ EBV ▪ EBV
▪ Rubella* ▪ Hepatitis ▪ Hepatitis
▪ Toxoplasmosis* Bacterial Bacterial
▪ Septicemia ▪ Septicemia
Mycoplasma Mycoplasma
Malignant - Leukemia Leukemia
Lymphoma Lymphoma
GIT - Biliary atresia, Biliary atresia,
CLD & portal CLD & portal
hypertension hypertension
(post-Kasai) (post-Kasai)
Cardiac -
Metabolic/ -  MPS  MPS
Miscellaneous/  alpha 1  Alpha 1
Autoimmune ds anti-trypsin anti-trypsin
deficiency deficiency
 Cystic  Cystic
Fibrosis Fibrosis
 Systemic  SLE
JIA*  Systemic
 Gaucher’s JIA*
disease  Gaucher’s
disease
Bold Commonly seen in exam

(Thalassemia in Malaysia & Singapore, CF in UK)
* Uncommonly seen in exam
14
Causes of Portal Hypertension
Pre-hepatic
Portal Vein Thrombosis
(No stigmata of chronic level disease)
Idiopathic
Congenital abnormalities
H/o intra-abdominal sepsis eg: omphalitis
H/o umbilical catheterization
Hepatic
Cirrhosis
Infective
Metabolic
Surgical obstruction
Malignancy
Congenital hepatic fibrosis
Autosomal Recessive polycystic kidney disease
Large hard liver with normal liver function+ portal hypertension
Post Hepatic
Hepatic Vein Thrombosis (Budd-Chiari syndrome)
15
Liver cirrhosis
Clinical Features
 Splenomegaly with pancytopenia

 Cutaneous porto-systemic shunt
 Ascites
 FTT
 GIT bleeding( esophageal/ hemorrhoids)
 Hepatic encephalopathy
Causes of liver cirrhosis
1) Biliary tract Obstruction

 Billary atresia
 Alagille syndrome (Autosomal dominant)
 Choledochal cyst
2) Infection
 Hepatitis B & C
 CMV
3) Autoimmune
 Autoimmune hepatitis (ANA / Anti-SMC antibody / Anti-
mitochondrial)
4) Metabolic
 Wilson’s disease
 Alpha 1 anti-trypsin deficiency
 GSD type 3 & 4
 Iron deposition in Thalassemia patients
 Cystic fibrosis
 Progressive Familial Intrahepatic Cholestasis (PFIC)
Nutritional Assessment (Rare case in Exam)
General inspection
General well-being, obvious pathology, general growth, dysmorphism, NG
feeding tube, gastrostomy tube, IV TPN drip, pallor, jaundice, and edema.
16
Followed by head to toe examination…
Growth chart (needs to know how to do it or describe the method)

 height, weight, head circumference
 mid upper arm circumference (MUAC) → muscle bulk
(Circumferential measurement at mid-point between the
acromium and olecranon process)
 triceps skin fold thickness → s/c fat store
(Measure the pinch of skin fold thickness at the landmark similar
to taking MUAC with skin fold calipers.)
Head & hair

 thinning, sparse, brittle, easily fall off
 craniotabes
Rickets
 delayed closure of fontanelle (in young infants)
 eyes: xerophthalmia (vitamin A deficiency)
Mouth
 Tongue: glossitis, geographical tongue (folate), beafy tongue (B12)
 angular stomatitis (B12)
 oral ulcers
 unhealthy, swollen, bleeding gum → scurvy
 unhealthy teeth
Neck
 goitre → iodine deficiency
Hands
 nails: koilonychia → iron deficiency
Leuconychia → hypoalbuminaemia
 widened wrist joints → rickets
 pallor
 bruises → vitamin K deficiency
Upper Limbs
 skin → dry, keratitis, dermatitis
17
 bruises → vitamin K deficiency
Chest and trunk

 rickety rosary → rickets
 dry skin, keratitis
Abdomen
 abdominal distension + ascites → hypoalbuminaemia
 kwashiorkor
 hepatomegaly
Buttock
 gluteal wasting
Lower limbs
 genu varus / valgus → rickets
 dry skin, keratitis, acrodermatitis enteropathica (zinc deficiency)
 bruises
Reflexes
 hyporeflexia
 peripheral neuropathy → distal weakness, glove & stocking
sensory loss (beri-beri, vitamin B6 deficiency)
I would like to complete my examination by

1) Asking for possibility of night blindness ( by history – very rare )
2) Assessing the pubertal stage of the child
3) Examining the perianal area for evidence of excoriation and worm
infestations.
18
Management of Malnutrition
Factors contributing to malnutrition:
Reduce oral intake -LOA

-vomiting/regurgitation
-psychiatric problem with eating disorders
Malabsorption + -abnormal enzyme digestion
increase GIT loses -abnormal absorption
Increase energy needs -chronic illness

or basal metabolic rate -heart failure
-respiratory problems
-persistent systemic inflammation
Management
Multidisciplinary approach
Investigation
 identify the cause/ underlying disease
 determine the extent of nutrient deficiency & its severity
 assess the complications from malnutrition
 serve as baseline for monitoring of treatment progress
Management
 treat the underlying cause/illness with specialty input
 nutritional supplementation with paediatric-trained dietician:
Carbohydrate, fat, protein, micronutrients, vitamins supplements
 NG tube/gastrostomy tube feeding if necessary.
 Psycho-social support if needed.
19
Approach to Renal Mass
Renal Mass
 Ballotable
 Can get above it
 Does not move with inspiration
 Resonant on percussion
 Not indentable (fecal mass)
Bilateral Unilateral
Well child Child with signs 1. Unilateral

of CRF hydronephrosis 2° to
PUJ/VUJ obstruction or
VUR
ADPKD 1)ARPKD 2. Unilateral dysplastic
Association: - a/w hepatomegaly 2° to multicystic kidney
 cyst at congenital hepatic 3. Unilateral renal cyst
liver/pancreas fibrosis with portal HPT 4. Unilateral renal
 SAH 2° to 2)B/L hydronephrosis 2° to agenesis with
cerebral  Neurogenic bladder in compensated
aneurysm spina bifida contralateral renal
 B/L VUR hypertrophy
 PUV 5. Wilm ‘s tumour
3)BWS/ 6. Neuroblastoma (may
With
Storage mimic renal mass)
diseases visceromegaly 7. Renal vein
4)B/L dysplastic multicystic thrombosis Tender
Kidneys 8. Unilateral
(Some patients might not pyelonephritis
have signs of CRF yet for no
2 & 3)
Anything else?
1) Blood pressure
2) UFEME
3) T° chart.
4) Spine& lower limb examination, if there are palpable bladder & bilateral
renal mass (suspect spina bifida)
20
Approach to a Child with Chronic Renal Failure (CRF)
General examination
 Short stature (growth chart)
 Pallor/ uraemic – sallow looking
 Evidence of fluid overload: pedal edema, raised JVP, basal crackles
(unlikely to be seen in exam)
Abdomen
Beside routine abdominal examination, look hard for
 PD or Tenckhoff catheter
 AVF Indicate ESRF on RRT
 IJVC / Femoral catheter
 Transplanted kidney
 Renal biopsy scar
 Underlying cause for the CRF eg: Neurogenic bladder,
hydronephrosis etc
Musculoskeletal
 Signs of renal osteodystrophy
o Tibial bowing/ genu valgus
o Frontal bossing + craniotabes
o Rickety rosary + Harrison sulci
o Wrist for metaphyseal flare/widening
Complete examination by
1. BP/UFEME
2. Pubertal assessment (in teenager, chronic disease affects puberty)
3. Nutritional status
4. If patient has a transplanted kidney, assess complications related to
Rx (prednisolone, cyclosporine, azathioprine etc).
Note: Patient with rickets secondary to CRF can come as a patient in musculoskeletal
station. Your task is then to demonstrate to the examiner the musculoskeletal
abnormalities, and show that you find out CRF as the cause of rickets.
21
Approach to a child with Beckwith Wiedemann Syndrome
Tall & large for age child

(Although their final height is often <95th centile)
Macroglossia
(Can lead to speech problem, feeding difficulty, OSA)
Ear sign: Transverse ear crease

Facial naevus
Hemi-hypertrophy
Abdomen
 Look for scar around the umbilicus (suggest past history of
omphalocele)
 Examine for visceromegaly. Risk of:
Wilm’s tumour
Adrenocortical tumour Follow-up 3-4 monthly for abdominal
Hepatoblastoma palpation ±abdominal USG
Neuroblastoma
Anything else?
1. Neonatal history of hypoglycemia learning difficulty
2. Prematurity
3. LGA
4. Growth chart
Some conditions associated with Wilm’s tumour

1. BWS
2. Hemi-hypertrophy
3. WAGR ( Wilm’s, Aniridia, Genitourinary anomaly, mental Retardation)
4. DRASH syndrome (Genitourinary abnormality, renal disease, Wilm’s)
22
Examples of Presentation
1) Abdominal – GIT / HBS
I would like to complete my abdominal examination by examining the

hernia orifices and genitalia.I would also like to inspect the stool (for
melena, pale stool) & perianal region for hemorrhoids.
Jeffrey is a 10 years old boy with no dysmorphic features. He looks short

and thin for his age. I would like to plot him on a growth chart.
He has clubbing and palmar erythema. No scratch mark/bruises seen. He is

pink but jaundice. His mouth looks clean with no ulcers/ stomatitis. There
are a few spider naevi on the chest.
His abdomen is distended, with a roof-top scar seen. There are dilated
veins.
The abdomen is soft, no tenderness on superficial/deep palpation.

The liver is enlarged, measures _ cm below the right costal margin. The
upper border of the liver is at the right fifth intercostal space. The liver is
hard; surface is nodular, with an irregular edge, non tender. No bruit
heard. He has a large spleen, extending 5cm below the left costal margin.
Both kidneys are not ballotable. No renal bruit.
He has ascites, evidenced by positive shifting dullness with fluid thrill.

He has no significant lymphadenopathy, no pedal edema.
In summary, Jeffrey is a 10 year-old boy with hepato-splenomegaly and

stigmata of chronic liver disease and portal hypertension. The most likely
diagnosis is liver cirrhosis with portal hypertension secondary to billiary
atresia, post Kasai procedure.
23
2) Abdomen – Hematology / Renal
I would like to complete my abdominal examination by examining the

hernia orifices and genitalia (testicular metastasis in acute leukemia).
If renal…
I would like to measure her BP and does bedside urine dipstick test.
If haemato…
I would like to look at the T°chart.
Fatimah is a 16 year-old Malay girl who looks short and thin for her age. I
would like to plot her on the growth chart.
There is no clubbing, palmar erythema, scratch marks/ bruises seen. She

has a few scars suggestive of previous cannula insertion. Her PR is ….
She is pale, with tinge of jaundice. Her skin colour looks tan. She has mild
frontal bossing with malar prominences. Her mouth looks clear with no
ulcer/stomatitis. No spider naevi on the chest.
Her abdomen is distended, more prominent at the upper abdomen. There

are no surgical scars/ dilated veins (DFO injection marks?)
The abdomen is soft, no tenderness on superficial/deep palpation. The

liver is enlarged, measures _cm below the right costal margin. The upper
th
border of the liver is at the right 5 intercostals space. The liver is firm;
surface is smooth with a regular edge, non tender. No bruits heard.
She also has a large spleen, extending _cm below the left costal margin.
Both kidneys are not ballotable. No renal bruits
She has no ascites/ lymphadenopathy/ pedal edema.
24
In summary, Fatimah is a 16 year-old Malay girl with jaundice, pallor,
hepato-splenomegaly and evidence of extramedullary haemopoiesis. The
most likely diagnosis is Thalassemia major.
If time is permissible, I would like to assess her:

1) Pubertal status
2) CVS examination for dilated cardiomyopathy or flow murmur
3) Bedside glucose stick
4) Thyroid status
5) Eye assessment + hearing assessment (DFO)
25
Chapter 2
Approach to Cardiovascular Short Cases
26
AR Aortic regurgitation SBE Subacute bacterial

AS Aortic stenosis endocarditis
ASD Atrial septal defect TA Tricuspid atresia
AV Atrioventricular TAPVD Total anomalous
AVSD Atriventricular septal pulmonary venous drainage
defect TGA Transposition of great
bpm Beats per minute Arteries
BT shunt Blalock Taussig shunt TOF Tetralogy of Fallot
CXR Chest-X-Ray TR Tricuspid regurgitation
CoA Coarctation of Aorta TRO To rule out
ECG Electrocardiography ULSE Upper left sternal edge
Echo Echocardiography URSE Upper right sternal edge
EDM Early diastolic murmur VSD Ventricular septum defect
ESM Ejection systolic murmur
HPT Hypertension
ICS Intercostal space
Imp Important
IVS Intact ventricular
septum
JVP Jugular venous pressure
LLSE Lower left sternal edge
Max Maximum
MCL Midclavicular line
MDM Mid diastolic murmur
MR Mitral regurgitation
PA Pulmonary atresia
PDA Patent ductus arteriosus
PG Pressure gradient
PR Pulmonary regurgitation
PS Pulmonary stenosis
PSM Pansystolic murmur
Pulm Pulmonary
RHF Right heart failure
Rx Treatment
27
Cardiovascular short cases
1) VSD
2) ASD
3) PDA
4) Pulmonary stenosis
5) Aortic stenosis
6) Innocent murmur
7) Dextrocardia
8) Coarctation of aorta (with lateral thoracotomy scar and radio-femoral
delay)
9) TOF (post BT-shunt/ post BT-shunt & corrective surgery ± PR)
10) Complex cyanotic heart disease eg PA/IVS, PAVSD, DORV, single
ventricle with PA, TA (with BT-shunt/ palliative surgery done)
11) Eisenmenger syndrome
Very rarely :
12) Rhythms – bradycardia , irregular
13) Absent pulses – takayasu’s
14) AV fistulas
15) AV malformations – in failure
28
How to prepare for Cardiovascular short cases?
Cardiology station is the station that you should try to score a clear pass.
Often, the spectrum of diseases likely to come out in the exam is
predictable, and you should try to see all these patients while you are
preparing for the exam.
The following tips will help you in your cardiology station preparation:
1. If you are using a normal stethoscope, we suggest that you buy a

cardiology stethoscope, and use it at least 6 months before your
exam. The College allows candidates to bring their own
stethoscope. If you use a poor quality stethoscope, you are at risk
of missing important signs on auscultation. More importantly, you
should try to listen and appreciate as many murmurs as possible in
preparation for the clinicals.
2. When you approach a child with a cardiac problem, it is very

important to first decide if this child falls into the acyanotic or
cyanotic group. Mild cyanosis may be missed, therefore look hard
for clubbing ( both fingers and toes !)
3. Next, you need to assess whether this patient has any signs of
respiratory distress. This helps to narrow down the differential
diagnoses. Respiratory distress indicates that there is increased
pulmonary blood flow with pulmonary congestion, which can be
seen in patients with
 significant left to right shunt
 mixing of systemic and pulmonary blood flow, therefore
increased blood flow to the lungs and
 left ventricular failure
The lists of differential diagnoses for a child who is “pink, not
breathless”, “pink & breathless”, “cyanosed, not breathless” and
“cyanosed & breathless” are different.
4. The surgical scars often give valuable information on the possible

underlying cardiac lesion. Look carefully for the surgical scars, you
may miss it in patient with fair skin. Remember, most of the cases
29
put up in the exam would be stable patients who have undergone
cardiac surgery. Be familiar with post-operative cases.
5. Besides cardiac murmur, the second heart sound is equally

important in helping you to establish the diagnosis. A soft S2
indicates pulmonary valve stenosis or atresia; a loud S2 indicates
pulmonary hypertension; fixed splitting S2 with soft ESM suggests
ASD until proven otherwise. Learn how to appreciate a soft, normal
or loud S2.
6. If the patient is dysmorphic, and you can diagnose the

dysmorphism, look hard for commonly associated congenital heart
disease. Examples:
 Marfan syndrome: Aortic regurgitation, mitral valve
prolapse
 Turner syndrome: Coarctation of the aorta
 Noonan syndrome : PS
 Down syndrome: AVSD
 William’s syndrome: Supravalvular AS
However, do not create signs or be preoccupied with the
associated cardiac lesions, and try to fit in signs to suit your
diagnosis. Present what you find.
7. The oral presentation for cardiac cases is standard, as we follow the

steps and sequences in cardiovascular examination. Therefore, it is
good to have your own script for the presentation, and practise it
again and again. This helps you to present smoothly even when you
are under stress.
8. Be ready for discussion. Investigation comprises of CXR, ECG and

echocardiography. Make sure you know the expected findings for
the above investigations. Elaborate on your answer before the
examiner asks you. Be familiar with the principles of management
of paediatric cardiac diseases.
This chapter highlights the points illustrated above. A list of cardiac diseases
likely to be seen in the clinical exam is also attached. Last but not least,
examine as many patients with cardiac diseases as you can. Take the
initiative to go to cardiac clinic and IJN. Learn from the patients!
30
Approach to Cardiovascular short cases
General
 Dysmorphism (if present, what is the commonly associated cardiac
lesions?)
 FTT (commonly seen in patient with heart failure / cyanotic heart
disease)
 Pink / cyanosed + clubbing?
 In distress? → indicates heart failure (Pink? Blue?)
Hands
 Collapsing pulse  PDA/Aortic regurgitation
 Radial pulses unequal → Coarctation ± repair / BT shunt – classical
 Radio-femoral delay → Coarcation of aorta
Neck
 JVP (for bigger child)
Chest
Inspection:
Chest shape
Signs of heart failure
Visible pulsations
(See if you can locate the visible pulsation of the apex beat, left (normal) or right.)
Scar
 Median sternotomy scar  open heart surgery
 Right lateral thoracotomy scar + shunt murmur Right BT shunt with
 Left lateral thoracotomy scar + shunt murmur Left BT shunt cyanosis
Possible: TOF
PA + VSD / IVS
TA
 Left lateral thoracotomy scar + PS murmur in Down Syndrome child with
heart failure signs  possibility of PA banding (underlying AVSD)
 Left lateral thoracotomy scar + Radio-femoral delay, absent Left radial
pulse  Coarctation repaired
 Left lateral thoracotomy scar + No other abnormalities  Ligated PDA
31
Mid sternotomy scar Left and Right lateral thoracotomy scar
Palpation:
 Thrill
o ULSE  PS
o URSE  AS (+ suprasternal notch)
o LLSE  VSD/TR
o Mitral  MR
 Palpable P2 (You will expect to hear a loud P2 on auscultation) 

Pulmonary hypertension
 Parasternal heave
Cyanosed PS in TOF
PA
ASD
Pink
PS
 Don’t forget to look for any possible pacemaker (usual left shoulder or
epigastric area)
32
Auscultation:
Listen to the apex beat for possible dextrocardia (often missed)
 S2 Loud  Pulmonary hypertension

Fixed splitting  ASD/ RBBB
 Murmur
Site Systolic Diastolic Continuous

Apex PSM: MR MDM: MS
LLSE PSM: EDM: AR

VSD
TR  with a pulsatile
Liver & cyanosis
 Ebstein’s anomaly
ULSE ESM EDM: PR PDA

Still’s murmur (TOF repaired-
PS + soft S2 Post-
ASD + fixed splitting S2 augmentation)
URSE ESM: AS + Carotid

radiation +
Suprasternal thrill
Left PDA
infra- BT shunt
clavicular murmur
Posterior Coarctation (below left Collaterals

scapula)
33
Approach to a ‘Pink’ Child
PINK
Breathless Not breathless
* Significant Left to right shunt * Small Left to right shunt

from VSD from VSD
ASD ASD
PDA PDA
* AVSD *Coarctation
*PS
*AS
If the child is PINK with
Median sternotomy Median sternotomy Lateral thoracotomy +

scar + scar Median sternotomy scar
NO Murmur + PS murmur +PS murmur
VSD  PR murmur  PR murmur
ASD Repaired
AVSD
TGA post arterial Not likely to be PS only
switch  
 Large VSD + PA banding
 Large PDA + PA banding
 Large ASD + PA banding
 TOF post 2 staged corrective
surgery
(1) TOF post corrective surgery with
remnants of PS ± PR  Complex heart ( 2 pathology)
with residual PS/PR
(2) PS post surgical valvuloplasty with
remnants of PS ± PR
34
Approach to a ‘Blue’ Child
CYANOSED
Breathless Not Breathless

 TAPVD  TOF
 Truncus arteriosus  TA
 TGA + VSD or PDA  PA/IVS
 AVSD  PA/VSD or PDA ± collaterals
 Single ventricle
* NB: Collaterals are abnormal arterial connections direct from aorta to

pulmonary circulation
If the child is CYANOSED with
Lateral thoracotomy scar Lateral thoracotomy scar No scar

+ BT shunt murmur + median sternotomy
  
Possibilities: Possibilities: Possibilities:
1) TOF (with PS murmur) 1) PA / IVS* 1) TOF (with PS murmur)
2) PA / IVS (with Single S2 2) PA / VSD + collaterals* 2) TGA + VSD/ASD/PDA
 PSM / continuous 3) TA* (might be breathless)
murmur from collaterals) 4) Ebstein anomaly* 3) PA/VSD+collaterals
3) PA / VSD + collaterals * Operated, with BT (might be breathless)
(with Single S2  PSM/ shunt (later on closed), 4) AVSD (especially if Down
 continuous murmur) and had proceeded with syndrome, might be
4) TA Fontan/Glenn operation) breathless)
5) Ebstein’s anomaly 5) TAPVD (might be
 TR murmur,
(with breathless)
pulsatile liver & 6) Truncus arteriosus
cardiomegaly) 7) Eisenmenger syndrome
(Teenager with pulm
HPT)
35
Approach to Dextrocardia
Dextrocardia?
Trachea shifted to right side & lung Trachea centrally located

signs right side
Not ‘true dextrocardia’ Lungs: coarse crepts

Congenital right lung agenesis
Palpate abdomen
(Dullness left hypochondrium 
Liver; Resonant right hypochondrium
 Spleen)
Palpate for sinus tenderness +

otoscopy
Δ Kartagener Syndrome
36
Examples on How to Present
I would like to complete my examination by measuring his blood pressure

and spO2.
________ is a _____ year-old boy with no dysmorphic features. He looks

well-grown/thin for his age/ I would like to plot him on a growth chart.
He is pink in air/cyanosed @ rest with/without clubbing. He is not in

respiratory distress. There are no stigmata of infective endocarditis. The oral
hygiene is good.
His PR is ____ bpm, regular rhythm, good volume with normal character.
Both *radial pulses are present & his femoral pulses are normal with no
*radio-femoral delay (*or brachial-).
The chest shape is normal with no scars/ He has a prominent

sternum/hyperdynamic praecordium/visible pulsation/praecordial bulge
with ______ scars.
The apex beat is displaced/not displaced, located at the _____ ICS, MCL,
normal character /heaving / thrusting in nature. He has no thrills/has thrills
at ________, ± palpable second heart sound, ± parasternal heave.
st nd nd
The 1 & 2 heart sounds are present. The 2 heart sound is
soft/loud/normal/ He has fixed splitting of the S2.
There is a grade _________ murmur best heard at the ____________,

radiating to the __________ / with no radiation. The murmur is louder on
inspiration/expiration.
The lung bases are clear and there is no hepatomegaly/ He has crackles @
both lung bases, and a __________ cm hepatomegaly, and ± pedal oedema.
The most likely diagnosis is ____________________. But I would also

consider the following in my differential diagnoses.
37
Management of Congenital Heart Disease
(A) Investigations
1) CXR
2) ECG
3) 2D-echocardiography
 need to know the expected findings for CXR, ECG & Echo.
(B) Treatment
VSD
Small  watchful waiting, need TRO AV prolapse
Regular follow-up  80% close spontaneously
Moderate  If normal growth, no failure symptom, surgical closure by 5 yrs

of age
Large  Surgical closure by 6 months of age / PA banding + closure

(if failed max medical treatment with anti-failures or develop
pulmonary HPT (pulm : system flow ratio > 2:1)
ASD
Small  watchful waiting
Regular follow-up  will close spontaneously
Large  Closure by 5 years of age ideally, or

 if failed max medical Rx (earlier closure)
 pulm HPT (earlier closure)
 Risk of atrial arrhythmia, pulm HPT & RHF in adults!
Surgical options:
30% transcatheter closure device (> 5 yrs old)
Secundum 70% surgical closure (larger lesion)
ASD
Primum  all surgical closure by 5 years old
(Partial AVSD)
38
Pulmonary stenosis
 mainly conservative (PG < 50mmHg)
 Surgical intervention if PG > 60mmHg
Options Transcatheter balloon valvuloplasty (preferred)

Risk of PR
Corrective surgical valvuloplasty
* Critical PS with cyanosis  early transcatheter balloon valvuloplasty !!
Aortic Stenosis
Management as per pulmonary stenosis
 risk of AR
 to look for left heart lesions: CoA, VSD, MR
AVSD
Complete AVSD Primary surgical repair by 6/12 old
(may be conservative if severe AV valve regurgitation & older patients due
to poor surgical outcome.)
Coarctation of aorta
 all need intervention due to risk of HPT later on
 to look for left heart lesions: AS, VSD, MR
Transcatheter: balloon angioplasty & stenting (>10 years old)

Options
Surgical  Left lateral thoracotomy
1) Subclavian flap (absent pulses)
2) End to end anastomosis
3) Gore-tex graft (pulses present)
PDA
 Small with no murmur  conservative, will close spontaneously
 Small with murmur & no failure symptoms  transcatheter coil
closure by 1 year old
Transcatheter coil closure

Medium/large Depends on symptoms,
(Significant) Surgical ligation PDA size & body weight
39
 if failed medical Rx with anti-failures
 pulm HPT Early closure
Imp: ALL must close due to  risk of endarteritis & SBE
TOF
 Stable  single stage corrective surgery by 1 year old
 If
 hypercyanotic spell episodes
 severe cyanosis < 6/12 old BT shunt first, then
corrective surgery by
 unfavourable small pulm artery
1 year old
 abnormal coronary artery anatomy
TGA
Simple + IVS  maintain PDA  balloon atrial septostomy (BAS);
then arterial switch by 2/52 old
NB: Previously BAS by 1/52 old; then Mustard/Senning operation at 6-9
months old

TGA + VSD  anti-failure if needed, then single stage arterial switch + VSD
closure by 3/12 old
TGA + VSD + PS  BT shunt during first year, then Rastelli repair by 6 yrs old
TA/ PA/ Hypoplastic left heart

 BT shunt before PDA closure
 semi- Fontan at 6-9/12 old
 Fontan (total cavo-pulmonary anastomosis) at 3-5 yrs old
 further management depends on underlying anatomy of the cardiac
lesions!!
NB: May be conservative!
Truncus arteriosus
 surgical repair (VSD closure + RV- to -PA conduit ) before 3/12 old.
40
Management summary
In brief, if you are asked about the management of Congenital Heart Disease
or follow-up, always mention the following in your answer:
1) Left  Right shunt lesion

- Monitor for failure symptoms
- Medical treatment, if failed  Surgical intervention
2) Monitor growth, ensure adequate nutrition
3) Specific symptoms and management of complications if necessary
4) SBE prophylaxis
- With good oral care and hygiene
- Educate on symptoms of infective endocarditis
- Antibiotic prophylaxis *
*In local setting, but in UK not advocates antibiotic prophylaxis.
41
Chapter 3
Approach to
Developmental short cases
42
How to prepare for Developmental short cases?
You will enjoy the developmental station if you are adequately prepared for
it. In the MRCPCH clinical exam, the examiners are not looking for a
developmental paediatrician, but a general paediatrician who can recognise
a child with developmental delay and suggest an appropriate management
plan.
The examiners usually will not request for a full developmental assessment.
More often, they will tell you the child’s age in the lead-in statement and
request for the assessment of the child’s developmental age in a particular
domain, eg fine motor and vision or speech and language. However, if the
leading stem request to assess the child’s development without indicating a
particular domain, it will be useful to start with fine motor assessment and
to keep the gross motor assessment towards the end.
Here are some tips for developmental assessment:

1. Many candidates memorise the developmental milestones by
remembering what a child of a particular age can achieve in all 4
domains. For example, a 3 year old boy could ride a tricycle, copy a
circle, speak in 3 to 4 words sentence and dress himself with
supervision. However, this often leads to difficulty in performing an
examination smoothly when they are asked to assess the
developmental age of a particular domain. We would strongly
recommend approaching a developmental case by remembering the
skills in sequence that could be assessed in each domain. For instance,
in fine motor assessment, the candidate could assess the child’s ability
in turning pages in a book, build a tower using blocks, pencil grasp,
thread beads and cut a folded paper using a scissors.
2. In an exam, you should start the assessment from where the patient is
before you get them to a table task activity. Remember, if the child
cries, you will lose cooperation!
43
3. Start with a simple task before moving on to more complicated ones. If
the child successfully completes a given task, move on to subsequent
activities till the child meets his/ her ceiling.
4. Tasks that require demonstration will need the child’s attention

towards the item offered to him/ her. Will be good to do this as a table
task activity. Remember to remove the completed items prior to
moving on to the next task to avoid distraction.
5. If the child performs well, offer praise immediately. If the child is

unable to perform the required task, reassure him or her that “it’s
okay” and step down to a simpler task before getting the child to
attempt.
6. If you have difficulty in engaging the child, sought the parents’ help.
Involving the parents often encourages the child to engage with the
task at hand, particularly if it is interesting. You could then slowly join in
and take over the parent’s role.
7. When presenting, comment up to the child’s best potential and avoid

negative phrasing such as “he couldn’t…..” or “he was unable to….”
To be proficient in developmental assessment, you will have to diligently

practise on typically developing children. As you become more skilful in this,
you can then confidently start examining children with developmental
problems.
Last but not least, one has to have passion, patience and great enthusiasm
to be successful in this station. Good luck!
44
Gross Motor
Suggested gross motor developmental assessment approach:

1) Walk, tip toe
2) Run
3) Jump/hop
4) Stand on one leg
5) Climb up & down stairs
6) Ball (kick, throw, catch)
7) Tricycle/Bicycle
NB: Opportunistic observations and comments for toddlers
1) Walk
Age Gross motor milestones
12 mths Walk with feet wide apart or 1 hand held
Cruising
15 mths Walk alone, might sit down suddenly
18 mths Walk steadily and stop safely
2.5 yrs Stand on tip-toe when shown
3 yrs Stand & walk on tip-toe
Walk backwards & sideways
4 yrs Walk along a line
5 yrs Walk straight line for 20 steps
2) Run, tip-toe
18 mths Run steadily but unable to avoid obstacles
2 yrs Run safely, avoiding obstacles
4 yrs Stand, walk and run on tip-toe
3) Jump/hop
2 yrs Jump up
2.5 yrs Jump with both feet from a low step
3 yrs Jump from a low step
4 yrs Hop, jump across a line
5 yrs Hop 2-3m forwards, on each foot separately
45
4) Stand on one leg
3 yrs Stand on one foot ~ 3 sec
4 yrs Stand on one foot ~ 6 sec
5 yrs Stand on one foot ~ 10sec
5) Up & downstairs
“How does your child go up and down stairs?”
15 mths Crawl up stairs safely, come down stairs backwards
18 mths Climb up stairs with hand-held and 2 feet/step
Crawl backwards alone
2 yrs Walk up and down stairs, 2 feet/step, holding on rail
3 yrs Climb stairs one foot/step
Downward 2 feet/step
4 yrs Run up & down stairs, one foot/step (like adult)
6) Ball (Kick, throw & catch)

2 yrs Throw a ball
Walk into a large ball when attempting to kick it
2.5 yrs Kick a large ball gently
3 yrs Throw a ball overhead
Catch a ball with arms outstretched
Kick a ball with force
4 yrs Throw, catch, kick and bounce a ball
7) Tricycle/bicycle
2 yrs Propel tricycle
3 yrs Pedal tricycle
4 yrs Ride tricycle & make sharp turns easily
5 yrs Some may ride bicycle
46
Other relevant gross motor milestones:
12 mths Lying down to sitting position
Rise to standing without help/pulls to stand
Stand for few moments
Crawl on hands & knees
Bottom-shuffles
15 mths Kneel without support
18 mths Climb forward a chair, then turn around & sit
Kneel upright without support
Squat to pick up a toy
Move without support from squatting to standing
2 yrs Squat steadily
Climb furniture
4 yrs Bend at the waist to pick up objects from the floor
5 yrs Bend at waist & touch their toes
Dancing rhythmically
Play slide, swing, climbing frame
Special scenario
Bottom shuffler
Differential diagnoses:
1. Spine: Spina bifida
2. Neuromuscular: Muscular dystrophy, spastic diplegia/hemiplegia
3. Bone/joint: DDH, Osteogenesis imperfecta
4. Simple bottom shuffler (might have a +ve family history)
Complete your examination by

1. Full neurological examination
2. Examine the hips and the spine
3. Ask about family history of bottom shuffling/ late walking (18-24
months)
47
Fine Motor
Suggested fine motor developmental assessment approach:
1) Copying/drawing
2) Hold pencil/crayon
3) Turn pages in a book
4) Bricks
5) Thread beads
6) Hold scissors
1) Copying/Drawing
“Are you good at drawing? Can you draw…?”
Age Fine motor milestones
15 mths Imitate to-and-fro scribble
18 mths Scribble to-and-fro
2 yrs Circular scribble
Copy ‘│’
2.5 yrs Copy ‘ ‘
3 yrs Copy ‘O’
4 yrs Copy ‘X’ & ‘+’
4.5 yrs Copy ‘□’
5 yrs Copy ‘∆’
Draw a house with windows, door, roof, chimney
6 yrs Copy ‘◊’
NB: 1.Imitate usually 6 months earlier

Good enough
2. Mnemonic
Draw A Man Test:
LOXSTD
Vertical line
- Basal age: 3 yrs
2 yrs old Horizontal line - Each additional 4
2.5 yrs old criteria 1 year of age
O : Circle at 3 yrs old
is added
X : Cross at 4 yrs old
S : Square at 4.5 yrs old
T : Triangle at 5 yrs old
D : Diamond at 6 yrs old
48
2) Hold pencil/crayon
1 yr Hold crayon in palmar grasp
1.5 yrs Hold a pencil with primitive tripod grasp
2-2.5 yrs Hold pencil in their preferred hand with improved tripod grasp
Imp: Hand preference developed only after 18 mths!
3 yrs Dynamic tripod grasp
4 yrs Hold and use a pencil in adult fashion
5 yrs Good control of pencil & paintbrush
Palmar grasp Primitive tripod/ Static tripod grasp Dynamic tripod

digital grasp grasp
3) Turn pages in a book

1 yr Turn several pages of a book at once
2 yrs Turn pages singly and enjoy picture book
4) Bricks
“Let’s do some building, can you do this?”
Age Tower of bricks Shapes (Copy)
12 mths Bang bricks together with imitation
15 mths Build a tower of 2 cubes after this has been seen
18 mths 3
2 yrs 6
2.5 yrs 7-8 Train
3 yrs 9-10 Bridge
4 yrs >10 Steps (6 bricks)
5 yrs Steps (10 bricks)
49
Bridge Train 6 bricks steps 10 bricks steps
5) Thread beads
1.5 yrs Thread 3 large beads onto a lace/string
3 yrs Thread large beads onto a lace
4 yrs Thread small beads onto a lace
5 yrs Thread a large-eyed needle & sew with large stitches
6) Hold scissors
2 yrs Make a snip
3 yrs Cut along a straight line
4 yrs Cut along a circle
5 yrs Cut along a square
NB: All come 1 year later than the copying skill
Other relevant fine motor milestones:

12 mths Fine pincer grip
Can release small object into someone’s hand
Drop & throw toys deliberately & look to see where?
15 mths Can put small objects into a bottle
Casting (in play/rejection)
4 yrs Opposition of each finger with thumb
5 yrs Count finger on one hand using index finger of the other
Construct elaborate model eg Lego
Can do jigsaw puzzles
50
Special scenario
Handedness
 Abnormal before 18 months
 Usually develops in the 3 year
rd
Causes:
1. LMNL: Brachial plexus injury
2. UMNL: Hemiplegia
3. Visual field problems
4. Congenital abnormalities/musculoskeletal problems/Trauma
Complete your examination by:

1) Full neurological examination
2) Visual test
3) Ask about medical, surgical and past history
51
Speech and language
Start by asking mother

1) Whether there is any concern with hearing?
2) Does the child understand spoken language?
Suggested speech & language developmental assessment approach:

1) Personal details
2) Demands
3) Speech
4) Point/name body parts
5) Point/ name colours
6) Use a book – Name objects, tell story
7) Commands (steps, preposition)
8) Calculations
9) Opposites eg. Compare sizes/length
10) Nursery rhymes/songs
1) Personal details
Age Speech & language developmental milestones
12 mths Turn to their own name
18 mths Refer to themselves by name
2.5 yrs Know full name
3 yrs Name, sex
3.5 yrs Name, sex, age
4 yrs Name, sex, age, address
5 yrs Name, sex, age, address, birthday
Write name
2) Demands
15 mths Demand object out of reach by pointing with index finger
18 mths Indicate desire by pointing, urgent vocalisation/words
52
3) Speech
12 mths Babbling with high intonation
2 words
15 mths 2-6 recognisable words
Jargon
18 mths 6-40 recognisable words, especially ‘No’
Echolalia
Holophrase, eg ‘cat’ refers to all animals
2 yrs Combining 2 words
Speak > 200 words, accumulate new words rapidly
Often omit opening/closing consonants eg ‘bus’→’us’
Telegraphic speech
2.5 yrs Ask ‘what’, ‘who’
Use pronouns ‘I’, ‘me’, ‘you’ correctly
3 yrs Often ask ‘why’
Personal pronouns & plurals correctly
Simple conversation (3-4 words sentences, missing ‘is’, ‘the’ etc)
4 yrs Ask ‘why’, ‘when’, ‘how’
Talk fluently
Tell long stories, sometimes conflicting fact
5 yrs Fluent in speech, grammatically correct
Tell long stories
4) point/name body parts

15 mths Understand the names of various parts of the body
18 mths Point 2-3 body parts
2 yrs Point 4 body parts
2.5 yrs Point 6 body parts
5) Point/name colours
3 yrs Match 2-3 primary colours eg red
4 yrs 4 colours
53
6) Book – Name objects, tell story
15 mths Point to familiar people, animals, toys when requested
Identify pictures of a few named objects
18 mths Name 1 picture
2-2.5 yrs Identify 5 pictures
Name 3 pictures
3 yrs Name 8 pictures
4 yrs Letter recognition
7) Commands (steps, preposition)

12 mths Understand simple instruction ass/w a gesture eg Give it to me.
Hand objects to adults “Ball to mummy”
15 mths Understand “No”, “Show me” and “Look”
18 mths Obey one-step command eg “Shut the door.”
2 yrs Follow 2-step command
3 yrs Follow 3-step command
2 preposition
eg “Put ball on the table/under the chair.”
4 yrs 4 preposition
Eg: On, Under, Behind, Side
8) Calculations
3 yrs Count 1-10
4 yrs Count 1-20
Understand 1-3
5 yrs Count finger on one hand using index finger of the other
9) Opposites
3 yrs Big vs small
4 yrs Long vs short
5 yrs Left vs right
54
10) Nursery rhymes/songs
2 yrs Share songs, finger rhymes
2.5 yrs Few nursery rhymes
3 yrs Remember & repeat songs
4 yrs Repeat nursery rhymes & songs
NB:
1) If speech is delayed, refer to an Audiologist for a hearing
assessment!
2) If you were asked to assess the child’s cognitive function, assess the
child’s speech and language, personal social and fine motor skills
55
Social
Suggested social developmental assessment approach:

1) Play
2) Feeding
3) Dressing
4) Toileting
5) Emotion & Interaction
1) Play
Age Social developmental milestones
12 mths Play pat-a-cake
15 mths Can seek out a hidden toy
18 mths Solitary play
2 yrs Solitary/ spectator play
Symbolic/pretend/imaginative play
Parallel play
Role play
3 yrs Active pretend play with other children
Share toys & begin to take turns when playing
4 yrs Understand need to share & take turns
5 yrs Play alone/with others
Enjoy elaborate pretend play with others
Small-world play
Enjoy team games
2) Feeding
12 mths Holds bottle to feed
15 mths Drinks from a cup
18 mths Spoon-feed self (messy, but food get to mouth)
2 yrs Drinks from a cup with less spills,
Scoop with a spoon
2.5 yrs Eat skilfully with spoon
3 yrs Eat skilfully with spoon/fork
4 yrs Eat skilfully with spoon & fork
5 yrs Use knife & fork competently
56
3) Dressing
12 mths Help with dressing eg arms into coat
18 mths Takes off socks, hat, unzip
2 yrs Dress themselves with help
2.5 yrs Put on shoes, socks, underwear
3 yrs Dress with supervision, buttons with help
4 yrs Can dress & undress themselves, except for shoe laces, ties,
back buttons
5 yrs Dress & undress alone ± shoelaces
4) Toileting
18 mths Indicate toilet needs by restlessness/words
2 yrs Go to toilet independently, may need help with pulling their
pants
2.5 yrs Maybe dry by day
3 yrs Dry by day, often dry by night
4 yrs Dry by day & night
Wash & dry their hands
Brush their teeth
5) Emotion & Interaction

12 mths Still shy with strangers
Affectionate towards familial people
Wave bye-bye
Clap hands
18 mths Eager to be independent
Enjoy stories/rhymes that include repetition
2 yrs Like to help other
Tantrums when frustrated
3 yrs Like to do things unaided
Show affection for younger siblings
Gender role
4 yrs Show sensitivity to others
Like to be with other children
57
5 yrs Have definite likes & dislikes
Able to amuse themselves for longer periods of time eg reading
book, watching TV
Show sympathy & comforts friends who are hurt
Choose their own friends
* * * *
Key elements for short case presentation in Developmental Station
Key questions:
1) What is his/her first language?
2) Have you any concerns about your child’s vision/hearing?
3) Was your child born at term or premature?
Opening statement:
Comments on
1) Nutritional status
2) Dysmorphism
3) Social interaction
Example:
“Tony is a 3 year-old child who looks well, & appropriately grown for his age.
He is not dysmorphic with good interaction throughout the examination.”
“In the area of fine motor skills, he has a developmental age of _________,
because he demonstrated _____. But today he did not demonstrate ______.
His fine motor development is delayed for a 3 year-old child.”
Then suggest what to do next?

 Neurological examination, full developmental assessment,
vision/hearing where appropriate.
 Relevant investigations and referrals
 Multidisciplinary team approach
58
Reference:
C. Meggitt, G. Sunderland (2006) Child Development. An illustrated guide
(London: Heinemann Educational Publishers).
Note:
This chapter is meant to provide a brief targeted assessment for approach to
a child in the developmental station. Formal developmental assessment
training is available (Schedule of Growing Skills II, Bayley Scales of Infant and
Toddler Development (Bayley III) and Griffiths Mental Development Scales-
Extended Revised) for those who are keen.
59
Chapter 4
Approach to Endocrine Short Cases
60
AR Aortic regurgitation
BA Bronchial asthma
BP Blood pressure
CA Carcinoma
CF Cystic fibrosis
CHD Congenital heart disease
COH Circumference of head
CTDs Connective tissue diseases
CVS Cardiovascular system
F Female
GH Growth hormone
GIT Gastrointestinal tract
Ht Height
Ix Investigation
LN Lymph nodes
M Male
MPC Mid-parental centile
MPH Mid-parental height
MPS Mucopolysaccharidosis
MVP Mitral valve prolapse
RP Renal profile
TFT Thyroid function test
w/o without
Wt Weight
61
Approach to Cushing’s syndrome
Demonstrate to the examiner signs of Cushing’s syndrome

a) Moon face/ round face
b) Acne
c) Thin skin
d) Increased fat pad at the back of the neck (avoid the term
of Buffalo hum)
e) Truncal obesity with relatively thin limbs
f) Proximal myopathy and muscle wasting
g) Abdominal striae
Offer to check blood pressure, capillary blood sugar, cataracts
Find out the cause of Cushing’s syndrome

& proceed with full examination
1. Diseases that need steroid treatment (Iatrogenic, the commonest

cause)
 Hyperinflated chest with Harrison sulcus → Bronchial
asthma
 Nephrotic syndrome/ renal disease/ renal transplant
 GIT – Inflammatory bowel disease/ post liver transplant
 Musculoskeletal: JIA
 CTDs: SLE, dermatomyositis etc
2. Look for abdominal mass

 Adrenal gland tumour
 Wilm’s tumour → can produce ectopic ACTH
3. Look for signs of Cushing’s disease

Fundoscopy → Papilloedema
Visual field defect → Bitemporal hemianopia
62
Approach to anterior neck swelling (Thyroid swelling)
Inspection
General
a) Thin/ obese/ normal built/ presence of respiratory distress/ stridor/
hoarseness of voice
b) Presence of thyroid eyes sign – proptosis/ exophthalmos/ lid
retraction/ lid lag/ chemosis/ ophthalmoplegia
c) Presence of hypothyroid facial features – coarse facies/ dry skin/ dry
hair/ mental slowness.
The swelling
a) Surface overlying the swelling, surgical scar, extension of the swelling,
the edge
b) Measure the size
c) Movement – movement with swallowing/ movement with respiration
Goitre Thyroglossal cyst

Palpation
 Edge/ surface/ size/ consistency/
tenderness/ retrosternal extension  Proceed with
 Associated cervical LN palpation
 Then assess for
Auscultation complications:
 Thyroid bruit  From the cyst
itself
Assess the thyroid status  From the
 Euthyoid mass effect
 Hyperthyroid: warm & sweaty palms, fine
tremor, resting tachycardia, facial
flushings, high output cardiac failure Note:
Complete the
signs, check BP & hyper- reflexia.
examination by:
 Hypothyroid: dry coarse skin, coarse
a) Growth chart
facies, loss of outer 1/3 of eyebrow, b) Pubertal
mental slowness, pretibial myxedema, assessment (if
slow-relaxing ankle reflexes adolescent)
63
64
Disproportionate short stature
Spine Shortening
Normal Abnormal
B’>A’
Limb Shortening
Normal Abnormal
(B<A)
65
A = B (normal) A’ < B’ (Rhizomelic)
Eg. Achondroplasia
A’’ > B’’ (Mesomelic) A’’’= B’’’ (abnormal but symmetrical)
Eg: mesomelic dysplasia, Eg: Hypochondroplasia

Ellis Van Creveld syndrome
66
67
Marfan’s syndrome vs Homocysteinuria
Similarity:
 Tall stature
 High arched palate
 Dental crowding
 Elongated slender limbs (Dolichostenomelia)
 Arachnodactyly (wrist sign, thumb sign)
 Arm-span > height
 Pectus excavatum / carinatum
 Scoliosis
Differences:
Marfan
1. Long thin facies
2. Lens dislocated up and in
3. Normal IQ
4. Hyperlaxity of joints (palms touch floor on bending)
5. Pes planus
6. Normal bone density
7. Abnormal heart (aortic root dilation, AR, MVP)
8. No thromboembolic risk
9. Clinical diagnosis with a set of diagnostic criteria (Ghent)
Family history, skeletal, skin, eyes, CVS, lungs, dura features.
Homocystinuria
1. Ruddy complexion
2. Lens dislocated down and out
3. Subnormal IQ
4. Joint contracture (genu valgum)
5. Pes cavus
6. Osteoporotic bone
7. Normal heart
8. Risk of thromboembolic phenomenon
9. Urine for homocystine (high)
68
Chapter 5
Approach to Eyes Examination
69
AD Autosomal dominant
AR Autosomal recessive
BIH/IIH Benign/Idiopathic intracranial hypertension
CMV Cytomegalovirus
CN Cranial nerve
CP Cerebral palsy
DM Diabetes mellitus
HPT Hypertension
HSV Herpes simplex virus
HZV Herpes zoster virus
ICB Intracranial bleed
ICP Intracranial pressure
IEM Inborn error of metabolism
MG Myasthenia gravis
MPS Mucopolysaccharidosis
MS Multiple sclerosis
ROP Retinopathy of prematurity
70
How to prepare for Ophthalmological short cases
The Ophthalmology short case is an unusual encounter in the exam.

However, it can present as an exam scenario in the “Others” station.
Unfortunately, most candidates do not perform well because they are
unprepared for it.
In this chapter, we highlight some important techniques in approaching the

eye examination, as well as the discussion of differential diagnoses and the
principles for management of paediatric eye diseases.
The following tips are essential in the eye examination:

1. Ensure that the patient ‘can see’ before you proceed with other aspects
of the eye examination. Therefore, always start with a visual acuity
assessment. It would be terrible if you did not pick up that the patient
is actually blind after a 7-minute examination!
2. Ensure that you and your patient are comfortably positioned before
beginning your examination. This includes:
 Appropriate distance
 Appropriate height (at the same level as the patient)
 Appropriate lighting in the room
3. Give clear, simple instructions to your patient to ease your examination

process, and maintain professionalism.
eg. Ask the child to look at the teddy bear, explain that you are
going to look into his eyes. “Whenever I come between you and
the teddy bear, just look through me as if I were not there. If
you feel uncomfortable with the light, please let me know.”
4. Start practicing with normal, cooperative patients. Proceed & examine

patients with positive eye signs once you are familiar with the steps.
When you perform the examination smoothly in a station that most

candidates are unprepared for, you will shine!
71
Examination of the Eyes
“Do you have concerns about his/her eyesight?” Or “Do you wear glasses?”
General Inspection
 dysmorphism
 abnormal eyebrows
 ptosis
 rashes around the eyes
 microphthalmia
 abnormal sclera colour
 telangiectasia on the sclera /conjunctivae
 corneal opacity
 coloboma
 squint
 proptosis/enophthalmia
 Random, non-focusing eyeball movement → blindness?
Then, shine the ophthalmoscope light to elicit any “not so obvious” squints,
looking at the light reflexes on both corneas. Also check for the normal red
reflex in both eyes.
Pupillary reflexes: check direct and consensual pupillary light reflexes for
both eyes.
Now assess the eyes proper; ask the child put on glasses, if he/she normally
wears them!
Cranial nerve II
1) Visual acuity
 test each eye in turn
 far / distant (look at something far across the room)
 reading acuity
72
2) Visual field
 Make sure the child’s head is static
 Sit at the same level as the patient
 Ask child to close/cover one of his eye in turn
 The opened eye is focused on the examiner’s eye.
 Check 4 quadrants for each eye until child sees the red pin
3) Colour vision
 Check on primary colours: red, green, blue, (yellow).
Then movements of eyes: CN III, IV, VI (LR6, SO4)

 Test in “H” manner → Look for non-conjugate gaze, nystagmus, ask
for diplopia.
 CN III palsy: eye looks down and out with dilated pupils and ptosis.
 CN IV palsy: eye fails to look down when moved medially.
 CN VI palsy: eye fails to look laterally.
Then, test for accommodation reflex

 Ask the child to look at a far object, then look at your pen held
close to his/her nose.
 Look for:
1) Convergence of the eyes
2) Pupillary constriction
Then, do the cover/uncover test for subtle, manifest squints.
Finally, perform the fundoscopy examination.
73
Causes of blindness or severe visual impairment
1) Lens:
A. Cataract
 Familial
 Congenital infection (Rubella, Syphilis)
 Other less common causes
- Down’s syndrome
- Metabolic:
 Hypoparathyroidism /any cause of hypocalcaemia
 Galactosaemia (AR)
 Galactokinase deficiency (AR)
- Myotonic dystrophy (AD)
- Lowe’s syndrome (oculocerebrorenal syndrome)(X-linked
recessive)
- Aniridia
- Iatrogenic-prolonged steroid treatment
- trauma to the eyes
B. Subluxed lens (Marfan’s syndrome-AD, Homocystinuria-AR)
 Marfan’s (outward and upward)
 Homocystinuria (downward and inward)
2) Optic nerve pathology

 Optic atrophy 2° to
- CP
- Intracranial tumour (papilloedema)
- Hydrocephalus (papilloedema)
- Leber’s hereditary optic atrophy (rarely present in young child)
- MS –following papilloedema /optic neuritis.
 Septo-optic dysplasia (Absence of septum pellucidum with
hypopituitarism)
 Optic nerve glioma/meningioma
 Chronic posterior uveitis/scleritis
74
3) Retinal pathology
 ROP
 Retinoblastoma
- AD, gene mutation 13q14
- 40% inherited with affected parent, the rest are new
mutations
- 20-30% bilaterally
- Initial with squint alone; cardinal sign: loss of red reflex
 Pigmentary retinopathy
1) Retinitis pigmentosa
2) Leber’s amaurosis (AD, AR)
3) Laurence-Moon-Biedl Syndrome (AR)
4) MPS (AR)
5) Refsum disease (AR)
6) Abetalipoproteinaemia
 Choroidoretinitis
- TORCHES (Toxoplasmosis, CMV, Syphilis)
- Toxocariasis
4) Glaucoma
 Features: Buphthalmos, corneal cloudiness, photophobia
 Associated with Sturge weber syndrome, aniridia, cong. rubella
5) Others
 Nystagmus
 Albinism
 Trauma to any part of the eyes
 Cherry red macular degeneration in Tay-Sachs disease
Management
 Assess associated disabling conditions.
 Genetic counselling where indicated.
 Encourage use of any residual vision.
 Emotion, social, educational support.
75
Causes of Corneal Cloudiness
1) IEM
- MPS (except Hunter & Sanfilippo)
- GM 1 gangliosidosis
- Mucolipidosis
- Fabry’s disease
2) Keratitis
3) Post traumatic
4) Post infections eg. HSV, HZV
5) Congenital glaucoma
76
Pupils-Eye Signs
1) Ambylopic light reaction

 Afferent is affected
 Direct pupillary light reflex –ve
 Indirect pupillary light reflex +ve
2) Light near dissociation Pupillary light reflex –ve

Accommodation reflex +ve
Pupils
Constricted Dilated
Argyll Robertson pupils Holmes-Adie pupils

(Syphilis –midbrain lesion)
Ciliary ganglion lesion associated
with absent ankle jerk
(Holmes Adie syndrome)
3) Constricted pupils
 Horner’s
 Drugs eg, morphine/opiates
4) Dilated pupils
 CN III palsy
 Drugs
 Blindness
5) Non-reactive pupil(s)
 Prosthetic eye(s) – BEWARE!
* Pupillary reaction can still present even in cortical blindness (as long as
light reflex or accommodative pathway intact).
77
Approach to a child with Squint/Strabismus
General inspection and facial appearance

- Pseudosquint?
- Head posture?
Check visual acuity of each eye

- Near vision
- Far vision
Take out glasses if any
Corneal reflex
(Bright light held 30cm in front of the eyes)
Findings during corneal light reflection.

(A) Normal alignment: the light reflections are centered on
both corneas.
(B) Left esotropia: the light reflection is outwardly displaced
on the left cornea.
(C) Left exotropia: the light reflection is inwardly displaced on
the left cornea.
(D) Left hypertropia: the light reflection is downwardly
displaced on the left cornea
Eye Movements
Paralytic squints Non paralytic squint

Causes:
1) CN palsies 1) Cover/uncover test
 CN III 2) Alternating test
 CN IV (see next page)
 CN VI
2) Weakness of extraocular muscles Can be divided into
 Myogenic lesions, MG 1) Manifest squint
 Duane’s syndrome 2) Latent squint
 Brown’s syndrome (also convergent & divergent squint)
78
Manifest squint
Monocular and intermittent strabismus as demonstrated by cover-uncover testing.
79
Latent squint: Detecting phorias by cover-uncover testing.
80
Duane syndrome
 Congenital hypoplasia of VI nerve nuclei →CN III innervating both
medial and lateral rectus muscles
 Limitation in abducting / Failure to abduct
 Globe retraction on adduction
 Associated with narrowing of palpebral fissure
Brown’s syndrome
 Congenital developmental anomaly of the superior oblique tendon
 Torticolis. Limitation of elevation in adduction, but normal
elevation in abduction.
Non paralytic squint

- Causes
1) Refractive error
 hypermetropia (commonest)
 high/asymmetry refractive error
2) Eye diseases
 Cataract
 Retinoblastoma
 ROP
 Corneal scar
 Lesions of the optic nerve/macular
3) Congenital
Principles of management
 Squint persists after 6 months → Refer!
 To achieve the best possible vision each eyes
- Correct refractive error with glasses
- Removal of cataract
- Occlusion treatment (prevent ambylopia) of squinting eye
 Achieve best ocular alignment and stereopsis
- may need surgery
81
Fundoscopy examination – possible findings
1) Optic atrophy
2) Choroidoretinitis See “Blindness” for the

underlying causes
3) Pigmentary retinopathy
4) Cherry red spot

 A small red spot at the macula surrounded by a pale halo
 Seen in Sphingolipidoses:
1. Tay-Sachs disease
2. Niemann-Pick disease
3. Sandhoff disease
4. GM I gangliosidosis
5. Mucolipidosis
5) Papilloedema
 Raised ICP (late sign)
- Infection
- ICB
- Intracranial tumours
- BIH/IIH/pseudotumour cerebri
- Hydrocephalus
 Malignant HPT
 Craniosynostosis
82
Chapter 6
Approach to
Musculoskeletal Short Cases
Mnemonics used in this Chapter: DAMPSSS
Deformity
Asymmetry
Muscles and Soft Tissues (Joints & Swelling)
Posture
Scars
Skin
Stigmata
83
ADL Activity of daily living

AR Aortic regurgitation
CNS Central nervous system
CTD Connective tissue diseases
MCPJ Metacarpophalangeal joint
MSK Musculoskeletal
MVP Mitral valve prolapse
OM Osteomyelitis
pGALS paediatric Gait, Arms, Legs and Spine
PUD Peptic ulcer disease
ROM Range of movement
84
How to prepare for Musculoskeletal short cases?
Candidates often regard musculoskeletal station as a difficult station as the

majority of us are not familiar with musculoskeletal problems. In this
station, you must be able to describe what you see clearly, and examine
patient gently. Here are some tips to help you:
1. DO NOT use pGALS for every musculoskeletal short case. Listen

carefully to the examiner. If he/she has told you clearly that the
patient has difficulty walking, concentrate on “Gait” and “Legs”
assessment before zooming in to specific joint examination.
Blindly performing pGALS without tailoring it to the specific
question will result in “Clear fail”.
2. Remember the principles of MSK examination:

 Look (Mnemonics DAMPSSS)
 Feel
 Move
 Assess function
Always ask if the patient is in pain. Keep your eye on the patient’s
face when you move their joints.
3. Once you reach the diagnosis, assess the complications related to

the disease itself and with the treatment. Most connective tissue
and musculoskeletal disorders are chronic conditions. Doing this
will distinguish you as a good candidate.
4. A running commentary is a MUST in musculoskeletal assessment.

It prevents you from forgetting the signs that you have seen
especially if there is multiple joint involvement. Do not be afraid
of doing running commentary as the examiner is able to see what
you describe.
Lastly, remember to see and examine an adequate number of patients

with musculoskeletal problems before your exam. An attachment to the
Paediatric Rheumatology Clinic at Hospital Selayang will be very beneficial.
85
Musculoskeletal System Examination
 If the lead-in statement suggests pGALS screening, identify the

problematic joint from pGALS, then zoom in to the specific joint
examination.
 If the lead-in stem suggest specific joint assessment, go by LOOK, FEEL,

MOVE, and ASSESS FUNCTION approach.
1. LOOK
- General: Well? Thriving? (Growth) Any obvious clues?
(Eg: Orthosis, Splint)
- Specific to the joint: DAMPSSS
 Deformity
 Asymmetrical
 Muscles & soft tissues (swelling, joints)
 Posture (Claw hands, Wrist drop, Ulnar deviation)
 Scars
 Skin (Redness, Hyperpigmentation, Gottron’s papules)
 Stigmata
2. FEEL (Look at the patient’s face)

- Temperature (use the back of the hand to assess).
- Tenderness (over the joint line +/- enthesitic points)
- Swelling/ Effusion (do fluid bulge test, patella tap)
3. MOVE
- Active movement first (Pain? ROM? Stiffness?)
NB: Note all joints can do active movement
- Then check passive movement.
- Compare with the other normal joint or your own joint.
4. ASSESS FUNCTION:
- Lower Limb: Gait (Make the child squat, stand on one leg, heel
and toe walking).
- Spine: Stoop down and pick up object.
- Upper Limb (Hand Function):
* Grip power (Key).
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* Large object.
* Small object.
* ADL – Drink, eat, comb, button and unbutton clothes.
* Writing, drawing.
Anything Else?
1. Assess for other signs that might help to confirm the diagnosis or
exclude differential diagnoses.
- Skin (other connective tissue diseases): SLE, Dermatomyositis,
Psoriasis.
- Abdomen: Hepatosplenomegaly (Systemic JIA/ Leukemia)
- Lymph Nodes: Generalised lymphadenopathy (Systemic JIA/
Leukemia).
- Temperature Chart: Systemic JIA.
- Bruises: Hemophilia.
- CVS: Murmur (Acute Rheumatic Fever).
2. Assess complications of the disease

- Eyes: Uveitis (Visual Acuity), Pupillary irregularity
Request for slit lamp examination by ophthalmologist.
- Pallor: Anemia of chronic diseases/ Iron Deficiency Anemia.
- Growth, Delayed puberty.
- Limb length discrepancies (overgrowth, contracture).
3. Assess complications from treatment

- NSAIDS: Gastritis, PUD
- Steroids: Cushing syndrome
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Paediatric Gait, Arms, Legs, Spine (PGALS)
(2-minute screening approach)
Screening questions
1) Do you (or does your child) have any pain/stiffness in your (their)
joints, muscles or back?
2) Do you (or does your child) have any difficulty getting yourself
(him/herself) dressed without any help?
3) Do you (or does your child) have any problem going up & down stairs?
Sitting
1. Hold your hands out straight in front of you.
2. Turn your hands over and make a fist.
3. Pinch your index finger and thumb together.
4. Touch the tips of your fingers.
5. Squeeze MCPJ for tenderness.
6. Put your hands together palm to palm and put your hands together
back to back.
7. Reach up, “touch the sky” and look at the ceiling.
8. Put your hands behind your neck.
9. Try and touch your shoulder with your ears.
10. Open wide and put 3 fingers in your mouth.
Lying Supine
11. Feel for effusion at the knee (patella tap, cross effusion).
12. Active movement of knee (flexion+ extension) and feel for crepitus.
13. Passive movement of hip (internal rotation).
Standing Up
14. Observe the child standing (from front, back and sides).
15. Bend forwards and touch your toes.
16. Observe the child walking, “walk on your heels”, “walk on your tiptoes”
(check the medial longitudinal arch).
Note:
The “Hands On- Practical Advice on Management of Rheumatic Diseases. pGALS – A
Screening Examination of the Musculoskeletal System in School-aged Children” can be
downloaded as PDF file from the Arthritis Research Campaign website at
www.arthritisresearchuk.org.
88
Assess active movement of the specific joints
 Do pGAL then Sitting  Supine  Walking.

 Ask for pain before examination!
 If active movement is impaired proceed with passive movement
assessment.
 Demonstrate to the child how to perform the desired action.
1. Hands
- Make a claw wih your hand: Flexion of DIP and PIP.
- Make a fist: Flexion of each joint.
- Make a star: Extension of each joint.
- Make a circle and touch the tips of all fingers.
(Don’t forget to palpate the MCP joints).
2. Wrist
- Flexion and extension (as in pGALS).
- Ulnar and radial deviation.
(Swelling and effusion should be checked over the dorsal
surface).
3. Elbow
- Flexion and extension.
- Supination, pronation (with elbow flexed, radio-ulnar joint).
4. Shoulder
- Put your hands above your head.
- Put your hands straight at the back.
- Try to fly like a bird.
- Put your hands behind your neck.
- Scratch your back.
5. Jaw
- as in PGALS
6. Cervical spine
- Put your chin on your chest.
- Look up at the ceiling.
89
- Look over your shoulder.
- Put your ear on your shoulder.
7. Hip joint
- Flexion and extension.
- Abduction and adduction.
- Internal and external rotation.
8. Knee joint
- Flexion.
- Extension.
- Passive extension (normal < 10°)
9. Ankle and feet

- Look for ankle swelling from behind.
- Standing (check for pes planus, then tip toeing to look for pes
planus if it is not obvious initially).
- Movement (3 joints):
 Tibiatalar: Dorsi-flexion/ Plantar flexion.
 Subtalar: Inversion/ Eversion.
 Midtarsal: Supination/ Pronation
10. Spine
- Flexion.
- Extension.
- Lateral flexion.
- Lateral rotation.
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Approach to Generalised Joint Hypermobility
Confirm by assessing the Beighton Score

1. Touch palms on the floor with soles flat and straight leg (1
point).
th 0
2. Extend 5 MCPJ > 90 (1 point each side).
3. Oppose thumb to forearm (1 point each side).
0
4. Extend elbow > 10 beyond neutral (1 point each side).
0
5. Passive knee extension > 10 (1 point each side).
Total score ≥ 4/9  Generalised hypermobility
OI type I & IV Ehler-Danlos Syndrome

Marfanoid
 Paper- like scars

Full assessment Full assessment with easy bruising.
for OI ie. blue for Marfan’s  Skin
sclera, abnormal Syndrome. hyperelasticity
teeth, fractures. (snaps back into
place when
stretched).
 Examine the parents as well if present.

 CVS examination: MVP, AR. (for Marfan & EDS)
If it does not fit into either one diagnosis or Beighton score is <4 points,
1. Ask the parents or the child whether he/she has:

 Arthralgia post daily activity including sports
 Difficulty with daily activities eg: gripping for writing
 History of gross motor delay/ clumsiness in childhood.
(to assess the impact of joint hypermobility on child’s life)
91
Management for Benign Hypermobility Joint Syndrome is individualised
and requires a multi-disciplinary inputs which include:
 Advices:
o Avoiding high level ballet, cheerleading, dancing,
gymnastics and contact sports like rugby, football, etc is
necessary if it causes too much pain or joint dislocation.
o Avoid physical inactivity with sedentary lifestyle.
o Keeping an ideal body weight as overweight worsens the
problem.
o Reassure parents and child that most cases of BHJS are
self-limited as the children grow older, with a few having
lifelong hypermobility problem.
 Exercise & joint protection techniques:
o Assessment and treatment by a physiotherapist is
essential.
o Various guided exercise programs like postural,
proprioception, stability and balance training; muscle re-
education and strength training help to improve joint
strength.
o Use protective splints, braces or taping during exercise.
o Avoid sitting cross-legged.
o Not to perform those “entertaining” but unusual joint
movements.
o Stand with the knees slightly bend
o Wear the shoes with good arch supports.
o Assist with specific orthotics during physical activity if
there is too much pain or function is affected.
 Medications:
o NSAIDs provide only limited symptomatic relief on joint
discomfort/pain after activity.
92
Approach to Scoliosis
Scoliosis
 General inspection: Facial dysmorphism, growth, general well being.

 Examination in standing position
Look from the back
- Side of scoliosis (the side to which the spine is convex).
- Shoulder on the convex side is elevated.
- Abnormal skin creases.
- Position of the pelvic girdle
 Look from the side
- Associated kyphosis/ lordosis.
 Look from the front
- Chest wall deformity?
Ask patient to bend forward

“Can you touch your toes?”
Scoliosis disappear Scoliosis remains

(in 80% of cases) (remaining 20%)
Positional/ Postural Structural scoliosis
Lower Limb MSK system examination Well child with Dysmorphism/

no dysmorphism CNS disorders/
or no weakness MSK disorders.
Lower limb length Normal lower
discrepancy with limb length Idiopathic  Cerebral palsy.
secondary scoliosis No discrepancy scoliosis  SMA.
(Infantile,  Muscular dystrophy.
Juvenile or  Poliomyelitis.
Hip joint diseases Muscle weakness Adolescent  Friedrich’s ataxia.
 DDH - (Especially pelvic girdle/ type).  Marfan’s syndrome.
 Perthes - Proximal muscle group. Especially  Neurofibromatosis-1.
disease/AVN adolescent girl,  Osteogenesisimperfecta
 SUFE worsen during  Myelomenigocele.
Knee joint diseases puberty.  Klippel Feil syndrome.
 JIA  Sprengel’s shoulder.
 Tumour post-op  Vertebral abnormalities
 Haemophilia
Bone disease
 Tumour post-op
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Approach to Unequal Leg Length
Unequal leg length
True leg length discrepancy Apparent leg length discrepancy

(ASIS Medial malleolus) (Pubic symphysis Medial malleolus)
Causes:
Causes:
1. Undetected DDH
1. Secondary to scoliosis
2. Previous trauma/ bone surgery
2. CP with excessive spasm of muscles
(eg: OM)
3. Increase limb growth due to:
- Arthritis of knee.
- Hemihypertrophy
- Overgrowth (eg:
Neurofibromatosis,
hemangiomas)
4. Severe hemiparesis (atrophy
and contractures)
5. Osteogenesis imperfecta
6. Ollier’s disease
7. Polyostotic fibrous dysplasia
94
Chapter 7
Approach to Neurological Short Cases
Mnemonics used in this chapter:

1) VIPS
Vascular causes
Infections
Pressure
Space occupying lesions
2) DAMPSSS
Deformity
Asymmetry
Muscles & soft tissues (Joints, swellings)
Posture
Scars
Skin
Stigmata
94
AD Autosomal dominant
AHC Anterior horn cell
BP Blood pressure
CN Cranial nerve(s)
CNS Central nervous system
CP cerebellopontine, Cerebral palsy
Dev Development
DMD Duchenne muscular dystrophy
FA Friedreich’s ataxia
HC Head circumference
Ht Height
IEM Inborn error of metabolism
Ix Investigation
LL Lower limb
LMN Lower motor neurone
LMNL Lower motor neurone lesion
MR Mental retardation
MSUD Maple syrup urine disease
NF-1 Neurofibromatosis type-1
NMJ Neuromuscular junction
PN Peripheral neuropathy
Rx Treatment
SGA Small for gestational age
SUFE Slipped upper femoral epiphysis
UL Upper limb
UMN Upper motor neurone
UMNL Upper motor neurone lesion
Wt Weight
XLR X-linked recessive
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How to prepare for Neurological short cases?
Neurology station is often regarded as a difficult and challenging station

due to its complexity and the highly variable presentation of the
neurological disorders. Consequently, many candidates have a tendency to
“avoid” neurological patients. They often do not aim to “clear pass” the
station, but hope not to “clear fail” it.
In fact, neurological station is not that difficult to score, you can actually
enjoy and master it if you prepare adequately before your exam. The
following tips will help you excel in Neurology station:
1) For all neurological disorders, study them in group, ie

a) Central nervous system
Cerebrum, cerebellum, spinal cord
b) Peripheral nervous system
Anterior horn cell, peripheral nerve, neuromuscular junction,
muscle
Know the similarities and differences of each group of the diseases.
2) At postgraduate level, your task is not just to identify the diagnosis,

but you need to demonstrate to the examiner the site of lesion,
possible aetiology and associated complications (in 7 minutes), and
discuss on the relevant investigations and management (in the
remaining 2 minutes).
3) You need to have your ‘approach’ to all potential neurological short

cases in the exam, and rehearse it before the exam. Remember, you
have only 7 minutes for examination, you need to do it fast and
smooth!
4) General inspection plays a very important role. Often, before you start
touching the patient, you should have an idea what group of
neurological disorder you are dealing with. You can get various clues
from patient’s posture, movement, higher function, and some
96
neurocutaneous syndromes are spot diagnoses. Your task is then to
look hard and demonstrate to the examiner the signs that can help
you narrow down the provisional diagnosis and go on with the
discussion.
5) You need to give clear instruction to the patient to help you elicit the
most accurate neurological signs. This is particularly important when
you are
 Assessing the patient’s power
 Examining deep tendon reflexes with Jendrassik maneuver
 Performing cerebellar system examination
 Performing cranial nerves examination
If English is not your mother tongue, you need to rehearse it before
hand to make the whole exam smooth and easy.
6) Lower limb examination often gives you more signs unless upper limb
shows obvious pathology from inspection. Therefore, always examine
the lower limbs first if the lead-in statement is general, eg “Examine
this child neurological system.”
7) Gait assessment is very important. It is a very popular topic in clinical

examination. Make sure you have seen all form of gaits before your
real exam and know how to approach it. Go to neurology clinic, see it,
practice it!
8) Last but not least, do not tap the reflexes multiple times. Be confident
with your technique. If you can’t elicit the reflex in your first attempt,
do it again with Jendrassik maneuver the second time. If it is still
absent, that’s mean the patient is areflexia. Be professional.
This chapter highlights the points illustrated above. A list of neurological

disorders likely to be seen in the clinical exam is also attached. Happy
reading!
97
Neurological short cases
1) Large head/ Hydrocephalus
2) Small head
3) Cranial nerve palsy

- Opthalmoplegia
- Brainstem tumour
- Miller-Fisher syndrome
- Moebius syndrome
- Duane’s syndrome
- Ptosis
- Myasthenia gravis
- Horner’s syndrome
- Third nerve palsy
- Visual field defect
- Bitemporal hemiamopia
- Tunnel vision
- Facial palsy
- Bell palsy
4) Peripheral neuropathy
- SMA
- Hereditary sensory motor neuropathy
- Guillain-Barre syndrome
- Chronic inflammatory demyelinating polyneuropathy
- Brachial plexus injury (Erbs, Klumpke’s)
- Ulnar/ Median/ Radial nerve palsy
- Peroneal muscular atrophy
5) Floppy baby/Hypotonia/Arthrogyposis multiplex

 Without weakness
- Central
- Syndrome (Prader-Willi etc)
98
- Benign hypotonia of infancy
- Lax ligament (Ehler Danlos syndrome)
 With weakness
- Anterior horn cell ds
- Peripheral neuropathy
- Muscle disorders
6) Clumsy child
7) Monoplegia (hand preference)

- Demonstrate, level of lesion, cause
8) Abnormal gait
 Hemiplegic
- Demonstrate, level of lesion, possible cause
 Waddling
- Muscular dystrophy
- Myopathy
- Spina bifida
 Trendelenburg
- Developmental dysplasia of the hip
 High stepping gait
- Peripheral neuropathy (HSMN)
- Foot drop
 Ataxic gait
 Diplegic gait
- Spastic diplegia
- Spastic paraplegia
9) Cerebellar signs
 Demonstrate, aetiology
 Friedriech’s ataxia, SCA, Ataxia telangiectasia etc
10) Movement disorders (Describe, define, possible causes)

 Dystonia vs spasticity
 Chorea/ choreoathetosis
99
 Tics
 Myoclonus (Opsoclonus-myoclonus syndrome)
 Tremor
11) Myotonia
 Myotonic dystrophy
 Myotonia congenita (Thomson’s disease)
12) Foot deformities

 Pes cavus/planus
 Equinovarus/ equinovalgus
 Calcaneovalgus
 Dynamic spasticity vs contracture
13) Manoeuver in neurology

 Gower sign
 Fog test
 Tandem walking
 Romberg test
14) Neurocutaneous syndrome

 NF-1/2
 Tuberous sclerosis
 Sturge-weber syndrome
 Incontinentia pigmenti
 Hypomelanosis of Ito
100
Examination of the Muscle Power
“I’m going to test how strong you are.”
Upper limb
Ask the child to bend the arms and hold them up at 90° out to the side.
C5 (shoulder abduction) “Push your elbows away from your body.”
C6,7,8 (shoulder adduction) “ Pull your elbow into your body.”
Bend arms so that elbow is at right angle.

C5,6 (elbow flexion) “ Pull me towards you.”
C7, 8 (elbow extension) “ Push me away.”
Ask the child to make a fist

C6, 7 (wrist flexion/extension) “Don’t let me bend your wrist.”
Spread your fingers

T1 (finger abduction) “ Don’t let me squeeze them together.”
Lower limb
L1,2 “Lift your leg off the bed, keep it there and don’t let me push it
down.”
L5, S1 “Push your leg into the bed; don’t let me lift it off the bed.”
L3,4 “Bend your knee, now try to straighten your leg out as if you are
kicking me.”
S1 “Bend your knee and try to pull your heel up towards your bottom.”
L4,5 “Pull your toes up towards your head.”

L5 “Pull your big toe up towards your head.”
S1,2 “Point your toes towards the bed.”
L4,5 “Turn your foot inwards.”

L5, S1 “Turn your foot outwards.”
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Examination of the Sensation
You will not been frequently asked to assess the child’s sensation because
it is time-consuming and difficult to interpret if the child is too young.
Often, it is not done unless requested.
However, sensory examination is important in certain neurological

disorders like spinal cord disorders and peripheral neuropathy. Make sure
you know the dermatomes well.
Upper limb Lower limb

C5 Lateral arm L1 Inguinal ligament
C6 Tip of thumb L2 Middle of anterior thigh
C7
nd rd
Web between 2 & 3 finger L3 Medial aspect of knee
C8 Tip of little finger L4 Medial calf
T1 Medial forearm L5 Lateral calf
T2 Medial arm S1 Sole of foot
102
Root level of Reflexes
Upper limb
Biceps C5, 6
Triceps C7, 8
Supinator C5, 6
Lower limb
Knees L3, 4
Ankles S1, 2
How to elicit Jendrassik maneuver?

“Can you do this?” (Demo to patient how to pull your hands apart or
clench your teeth)
“Good. Now, I will count One, Two and Three. Can you do this again at the
count of three?”
“One…Two…Three (You tap the relevant deep tendon simultaneously),

thank you.”
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Examination of the Cranial Nerves
Hi, I am Dr Smith.
I am going to do some examination with you.
Is it alright for you to sit up and facing me? Thank you.
CN I : Do you have trouble with smells?
CN II : Do you have eye sights problem?
Do you wear glasses?
Visual acuity: Cover your right eye with this paper, then read with your left
eye. What alphabet/number is this?
o Do it with the other eyes.
o Check visual acuity (Snellen chart /alphabets /numbers
 counting fingers hand movements  perceive light)
Pupillary reflex: Keep your eyes looking ahead, I am going to shine my
torch to your eyes from the side.
o Direct light reflex for each eye.
o Consensual light reflex to be observed.
Accomodation reflex: Now can you look at the window/door (far object).
Then look at this object right in front of you?
Visual field: Keep your right eye looking at my nose. Cover your left eye
with this paper. I will bring this pen in between us from outside. Do tell me
“YES” when you first see the pen.
o Repeat for the left eye.
Fundoscopy: Dim the room lights and pull the curtains.
o “Let’s look ahead to the wall. I would like to look into
your eyes with this torch.”
o Whenever I come between you & the toy, just look
through me as if I were not there.”
CN III, IV, VI : I need you to follow my finger with your eye as I move. Do
keep your head straight ahead without turning. If you see
double images of my finger at any time, do tell me.
How many fingers do you see?
CN V : Please clench you teeth. Feel for both temporalis &
masseter muscle bulks.
Open your mouth wide and don’t let me close it.
Sensory: I am going to touch your face with a cotton ball.
Do tell me “YES” is you feel my touch onto your face.
104
CN VII : Can you raise your eye brows? / Can you open your eyes
wide?
Can you say “E”? / Show me your teeth? / Can you give me a
smile?
Please close your eyes tight, don’t let me open it.
Can you make your cheeks puff up?
Please close your mouth tightly, don’t let me open it.
CN VIII : Distracting the right ear with rambling sound, then whispers
after numbers. Then ask patient to repeat. Repeat for left ear.
CN IX & X : Open your mouth wide and then say “Ah”  Look for
position of uvula  central/deviated to one side.
CN XI : Can you shrug both of your shoulder?
CN XII : Please show me your tongue.
Alternative way of CN examination

 The above may be OK if the lead-in statement is “Would you like
to do cranial nerve examination?” and there is no obvious
external clue.
 However, in clinical setting and exam, a more common scenario is
a child with ptosis, squint or facial asymmetry or somebody with a
nasogastric tube. The lead-in statement may be:
“John was noted to have double vision/ droopy eyes etc, please
do cranial nerve examination to find out the cause.”
 Hence, in most of the ‘CN exam’ cases, the sequence of exam can
be examination of the motor CN from top down then sensory CN
after one has established that the child does not have visual
impairment. (i.e. check vision  (motor) CN III, IV, VI  VII, V
XII, IX, X  XI (sensory) hearing, sensation  (optional)
pupillary light reflex, visual fields, fundoscopy, smell).
 It is also useful to demonstrate what you want the child to do with
action. This is particular so, if there is language barrier especially
when you sit for exam locally (i.e. shrug you own shoulders as you
ask the child to shrug his shoulders)
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Examination of the Cerebellar System
Hi, I am Dr Smith.
I would like to do a few examinations with you.
General : How are you? How old are you? What is your school name?
 Listen for staccato speech.
Look for obvious nystagmus. Or
Could you please follow my fingerabduction of both eyes.
(Fast phase indicates the site of lesions)
If the patient is sitting initially:

 Can you sit upright for me? Put both of your hands on your lap.
Look for truncal ataxia.
 Can you stretch out your hands like me (Demo to the patient), and
then close your eyes?  Look for pronator drift (Upward -
cerebellar, Supinated - UMN lesion).
 Well done. I am going to bounce your hands.  Look for rebound
phenomena.
 Let us play some games alright. I will show you how to do it and
you just follow me. Then, keep up with my pace, alright?  Look
for dysdiadochokinesia.
 Very good. Now, I need you to touch your nose with your finger;
and then touch it to the tip of my finger (with demo).  Look for
intentional tremor and past pointing.
 Excellence. Can you sit near to the edge of the bed for me? Put
both of your legs down the edge of the bed. I am going to tap
your knee to see whether is swings.  Look for pendular knee
jerk.
Now, show me how you walk. I need you to walk to the door, and then
make a turn, and walk back here for me.
 Look for broad base, unsteady gait.
 Patient tends to swing to one side (side of lesion).
 Tandem gait if the ataxic gait is subtle.
Lastly, we do some exercise with your legs. Could you please lie down on
the bed. Thank you.
106
I need you to lift up your foot to touch my hand here, then touch the knee
with your heel and slide it down your leg (with demo).
 Heel-shin test: look for poor coordination.
Besides, checking and demonstrating the cerebellar signs, look out for
clues that may suggest underlying cause (eg, bulbar telangiectasia, pes
cavus, VP shunt and surgical scar etc)
Note:
 If the child is sitting initially, suggested sequence is to look for all
the cerebellar signs while sitting  walking  lying down.
 If the child is lying on the bed initially, suggested sequence is lying

 sitting  walking.
107
Approach to Floppy Infant
General inspection (DAMPSSS)

 Posture: Describe the child hypotonic posture
(avoid the term “frog-like” posture)
 Alertness/myopathic facies
 Any deformities? eg CTEV, contractures
 Muscle bulk, movements, fasciculations?
 Extras: Ryle’s tube gastrostomy, oxygen, orthosis
 Tone (Truncal / limbs)

 Power: Any anti-gravity limb movement?
 Reflexes (Important to narrow down your
differential diagnoses!)
o
180 test (Do it last, as this might provoke the child to cry), spine
No anti-gravity movement Good anti-gravity movement
Floppy weak Floppy strong
Peripheral causes Central causes
Look for underlying cause.

Diagnosis
 Head size/shape
*AHDPNNMJ*Muscle?  VP shunt
Ant horn cell ds (AHD): SMA  Dysmorphic features
Muscle: Congenital muscular dystrophy, o Down Syndrome
Myopathy, myotonic dystrophy o Prader Willi Syndrome
o Zellweger Syndrome
* Common in exam
108
Approach to Facial Weakness
Cranial nerve VII: Long intracranial course
Closely related to VI nerve in pons.

(Therefore Pontine lesion may  VI & VII nerves palsies)
Emerges from Cerebellopontine angle

(Lesions may affect V, VI, VII, VIII nerves)
Runs in petrous bone closely related to the middle ear
Near to parotid gland
Examination approach: Help you decide if it is unilateral/bilateral facial

1) Smile weakness, and if unilateral, which side with
2) Puff out the cheeks facial weakness?
3) Frown
4) Raise the eyebrows Help you to differentiate UMN/LMN facial
5) Close the eyes tightly weakness.
Patient can close both eyes Right eye does not close and eyeball
turns up (Bell’s phenomenon)
Patient can raise both eyebrows Patient can’t raise eyebrow on right
Right Upper Motor Neurone Right Lower Motor Neurone

(UMN) facial weakness (LMN) facial weakness/Right
facial nerve palsy
109
Facial weakness - Differential diagnoses:
Lower Motor Neuron Lesion Upper Motor Neuron Lesion

 Bell’s palsy(Commonest) Spares eyes & forehead (lesion
 Ramsay-Hunt Syndrome above pontine level)
 CSOMGradenigo  Cerebral palsy
syndrome  CNS infection
 Mumps  Hydrocephalus
 Moebius sequence  Intracranial tumours
 Congenital ± obstetric  Intracranial hemorrhage
forceps (CVA)
 Lyme disease Usually
UMN facial
 GBS bilateral
weakness
 Intracranial tumour
(CP angle/Pontine) Complete examination by
1) Full neurological
Facial nerve
examination
palsy (Ipsilateral hemiparesis)
Complete examination by: 2) Examine the scalp: Scar,
1) BP (Hypertension: VP shunt
mononeuritis multiplex,
affects vascularisation of
CNVII) Differential diagnosis:
2) Ears (vesicles), eardrum Absence of Depressor Angularis
mastoiditis (Ramsay- Oris
Hunt/ Gradenigo
syndrome)
3) Erythema migrans (Lyme
disease)
4) Parotid enlargement/
scar (Mump)
5) Cerebellar signs ±
contralateral hemiplegia
6) CN V, VI, VIII
(5&6: CP angle tumour)
7) Eyes (exposure keratitis
as complication)
8) Lymph nodes, abdomen
(Leukemia)
110
Bell’s palsy:
- Idiopathic: usually unilateral
- Diagnosis of EXCLUSION.
- Rx: Steroids (no evidence in children)
o Oral Acyclovir (within 72 hours of onset, if > 2 years old)
o Artificial eye drops
- Prognosis: >90% complete recovery. Shows sign of recovery by 4
weeks and complete recovery may take up to 3 months.
Moebius sequence:
- Very rare, sporadic, due to underdevelopment of cranial nerves
nuclei.
- Bilateral VI & VIII nerve paralysis (LMNL)
- Other lower cranial nerves may be affected.
- Maybe associated with micrognathia, CTEV
- 25% with learning difficulty
Bilateral facial weakness - Differential diagnoses:

1) Myotonic dystrophica
2) Fascioscapulohumeral muscular dystrophy
3) Congenital muscular dystrophy
4) Congenital myopathy
5) Mitochondrial myopathy
6) Myasthenia gravis
7) Gullain-Barre syndrome
111
Approach to a Child with Ptosis
Ptosis
Syndromic facies with Normal looking child

bilateral ptosis:
1. Noonan
2. Rubinstein-Taybi Unilateral/Bilateral ptosis
3. Smith-Lemli-Opitz
Bilateral
Unilateral
Check for fatiguability
No fatiguability
Pupils
+fatiguability Myopathic facies + facial weakness
+ophthalmoplegia
Constricted pupil & Dilated pupil & Myotonia +ve No myotonia

partial ptosis complete ptosis Myasthenia
Gravis
+Facial weaknes, Normal CNS
CN III palsy Myopathic facies examination
Horner’s syndrome
Divergent squint & myotonia
Enophthalmos
Diplopia similarly in parent
Ipsilateral anhydrosis
Familial
Heterochromia iridis
Congenital
(congenital Horner’s) - Examine CN IV, V,
Myotonic dystrophy Ptosis
VI(cavernous sinus
thrombosis)
Look for acquired causes +Upper limbs weakness
-Fundus examination -
of Horner’s syndrome +shoulder girdle weakness
Papilloedema in uncal
+winging of scapula
herniation secondary to
Examination of neck increased ICP
for swelling, scars,
Fascioscapulohumeral muscular dystrophy
lymph nodes
Head examination:
Look for median Gait
scars, VP shunt
sternotomy scar post
Waddling + Gower’s sign
cardiac surgery High stepping
Neurological
Examination of upper examination of upper >proximal weakness
>distal weakness
limb for Erb’s plasy & lower limbs
Congenital myopathy Generalised areflexia
post traumatic delivery
Mithochondrial myopathy
Causes: VIPS Congenital Muscular Dystrophy
+ataxia Gullain-
Barre
Miller Fisher Syndrome Syndrome
112
“Examine the Gait”
 Ask the patient & parents can the child walk?

 Look at the surrounding for walking aids – wheelchair/ rollator/
orthosis/ special shoes.
 “Can you walk to the front and turn back?” Ideally left with
shorts/underpants
 Observe the gait & arm swing
 Observe the turning
Then, ask the child to

 Walk in fast mode/ run Subtle hemiplegic/diplegic gait may
 Walk with foot in inversion - Fog test become more apparent
 Walk on tip-toe (Patient with spinal cord lesion below L5 will fail to do this)
 Walk on heel (Patient with foot drop/ spinal cord lesion below L4 will fail to do this)
 Tandem gait (Children 5 years and above, to elicit subtle ataxic gait)
Demo to the child whenever possible, & do necessary manoeuvre as
above until you can identify the abnormal gait.
Is this
1. Hemiplegic gait?
2. Spastic diplegic gait?
3. Ataxic gait?
4. Waddling gait?
5. High stepping gait?
6. Trendelenburg gait?
7. Antalgic gait?
If you can’t commit yourself what gait it is, describe what you see and
proceed with lower limb examination.
 If the child has waddling gait, ask the child to sit down on the floor and
stand up – look for Gower sign.
113
Gait Possible causes
1. Hemiplegic gait VIPS
2. Diplegic gait Spastic diplegia
Spastic paraplegia
3. Ataxic gait Cerebellar disease
Friedreich ataxia
Ataxia telangectasia
Angelman syndrome
Miller-Fisher syndrome
4. Waddling gait Muscular dystrophy (Duchenne,Becker)
Myopathy
Spina bifida
SMA type 3
5. High stepping gait Hereditary Sensory Motor Neuropathy
Foot drop (Peroneal nerve palsy)
Gullain-Barre syndrome
6. Trendeleburg gait DDH
Unilateral short limb
SUFE
Perthes Disease
114
Approach to Hemiplegic gait
Hemiplegic gait
(Ask child to run/ Perform fog test if subtle)
UL & LL examination
(To confirm and demonstrate the physical signs of hemiplegia)
Facial nerve examination

(To ascertain the level of the problem: Supratentorial/infratentorial)
supratentorial infratentorial
Hemiplegia ±ipsilateral UMN Hemiplegia + contralateral

facial weakness LMN facial weakness
Assess further site of lesion Look for underlying aetiology
CN V, VI, VIII assessment +
1) Visual field (homonymous
cerebellar signs
hemianopia – Site of lesion at internal
capsule or above)
2) Parietal lobe signs Cerebellopontine angle tumour
(Site of lesion ipsilateral to the facial weakness)
infer cortical lesions
Look for underlying * VIPS

aetiology Vascular
 Bleeding: AVM, MVA, NAI,
1) Head examination (5S) periventricular haemorrhage.
 Thromboembolism: Cyanotic
 Size
congenital heart disease, cardiac
 Shape surgery, infective endocarditis
 Suture (infant)  Vasculitis: SLE, Moya-moya, Takayasu
 Thrombosis: Homocystinuria, Anti-
 Scars Phospholipid Syndrome (SLE)
 Shunt  Family history of positive
2) CVS examination thrombophilic disease
(thromboembolic stroke as the Infections
underlying cause?)  Meningitis
3) Skin: NAI, SLE  Herpes Simplex Encephalitis
 Brain abscess
Pressure
Causes: VIPS*  Unilateral hydrocephalus
Onset of the problem/ clinical feature will SOL

determine the underlying aetiology  brain tumour
115
Approach to Spastic Diplegic Gait
Diplegic Gait (knock knee/scissoring gait)
Examine the LLs
Then ULs as well (MUST, TRO Spastic Quadriplegic Cerebral Palsy that can walk)
Spastic Diplegic Cerebral Palsy Spastic Quadriplegic Cerebral Palsy

1) Ex-prem with periventricular 1) Antenatal:
leucomalacia - Congenital cerebral
2) Periventricular leucomalacia malformations
o
2 to infection , ischaemia - TORCHES infection
3) IEM eg MSUD - Maternal substance abuse
- IEM ( more of dyskinetic
ΔΔ: Hereditary Spastic Paraplegia cerebral palsy) eg,
Spinal cord lesions mitochondrial disease/
- Check spine for scars glutaric aciduria
- Sensory level 2) Perinatal:
- Motor level Per abdomen - Perinatal asphyxia
- Bladder involvement examination 3) Postnatal:
- Bowel involvement - Meningitis
- Anal tone assessment - Severe IVH with severe
prematurity
- Hydrocephalus
 Check the head as well: look for scar, shunt, macrocephaly/

microcephaly.
 Look for complications: contractures, hip dislocation
 Onset of problem/clinical features will determine the possible
causes in each case!!
116
Approach to Ataxic Gait
Ataxic Gait
Romberg's Sign (RS)
RS positive RS Negative
- Teenager
- Distal muscle wasting Check Eyes
- Pes Cavus
Look hard for signs of FA Other CN involvement

(Especially CN V, VI, VII, VIII)
Friedreich Ataxia (AR) Head exam

Full UL&LL, CNS exam - Scar
- ↑ tone/ spasticity - VP shunt
- ankle areflexia - Abnormal occipital area
- Upgoing plantar response
- Loss of proprioception
+ve cerebellar signs
Others:
1) CVS: hypertrophied cardiomyopathy
2) Spine : kyphoscoliosis 1. Ataxic cerebral palsy
3) Glucostix : ↑ risk of DM 2. Post fossa/CP angle tumour
3. Dandy Walker Syndrome
Hypopituitarism
 Nystagmus (common Cx post CNS tumour Rx)
 Telangiectasia (ears, conjunctivae) - Assess growth, puberty,
 Children < 10y/o TFT
Cerebellar System Examination
+ve Cerebellar signs 1) Sitting Down
- Speech: Staccato/scanning
Ataxia Telangiectasia (AR) - truncal ataxia
- pronator drift
- Abd + LNs exam : TRO Lymphoreticular CA - Rebound phenomenon
- Full CNS exam : risk of brain tumour - Eyes: Nystagmus
- Ix: - Finger nose test: Pass pointing
& intentional tremor
1) DNA analysis
- Dysdiadochokinesia
2) Chromosomal fragility test - Pendular knee jerks
3) ↑ Se AFP 2) Lying Down
4) ↓ Se IgA & IgG - Heel shin test
- risk of infection 3) Standing
- walk in tandem gait
117
Approach to Waddling Gait
Waddling Gait
Myopathic facies +
myotonia
+ Gower Sign UL+LL examination
(Demonstrate proximal muscle
weakness, depressed reflexes)
-> Myotonia dystrophica
Calf hypertrophy Generalized
↑ Lumbar lordosis muscle wasting - assess mother!
Ix: 1) DNA analysis
2) EMG
ULs & LLs exam Facies
- DAMPSSS
- Proximal weakness
- Reflexes: Alert Looking Myopathic facies*
DMD: Knee -ve + fasciculation No fasciculation
Ankle +ve (tongue/fingers)
- No clonus, Babinski ↓
ULs & LLs exam
SMA type 3 - Hypotonia
Causes: - Proximal myopathy
1) DMD - Depressed reflexes
2) BMD ULs & LLs exam
3) Limb-girdle muscular - DAMPSSS
dystrophy - Demonstrate 1) Stigmata of
proximal weakness dermatomyositis?
- Generalized areflexia 2) Parent facies?
- Spine: scoliosis 3) Isolated
- CVS: Dilated hepatomegaly?
cardiomyopathy 1) Spine : scoliosis
- Spirometry/PEFR: 2) Spirometry/PEFR Causes:
Restrictive lung ds
1) Congenital myopathy
2) Dermatomyositis
Ix: 3) Late onset Pompe disease
Ix: 1) CK level
1) SMN gene DNA 4) Mitochondrial myopathy
2) DNA analysis
analysis 5) Muscular dystrophy
3) Muscle biopsy 2) Muscle biopsy
4) EMG 3) EMG
Ix: Muscle biopsy
* Myopathic facies is only obvious in congenital myopathies and myotonic dystrophy.
118
Approach to High Stepping Gait
High Stepping Gait
DAMPSSS
Deformity, Asymmetry, Muscles, Posture, Scars, Skin, Stigmata
No obvious joint deformity

- Pes cavus
- Champagne bottle legs
- hypotonia - +/- trophic ulcer
- distal weakness > proximal
- may have facial weakness
- Generalized areflexia Hereditary Sensory Motor
Acute
Neuropathy (HSMN)
aka Charcot Marie Tooth disease
Gullain Barre Syndrome - hypotonia
(GBS) - distal weakness > proximal
- areflexia
- Babinski ↓
GBS - +/- glove & stocking sensory loss
- PEFR/spirometry Chronic - loss of proprioception
- Blood pressure Ix:
- Neurogenic 1) Check parents and siblings
bladder/bowel (AD, AR or XLR)
- h/o preceding viral 2) Nerve conduction study (+ parents)
illness/immunization 3) Nerve biopsy (HMSN)
- Investigations:
CSF (↑protein)
Nerve conduction study
Chronic Inflammatory Demyelinating

Polyneuropathy (CIDP)
- Ix: same as GBS
119
Approach to Spina Bifida
Patient with spina bifida might walk with various abnormal gait, some could
be subtle depends on the level of lesion. If the lead in statement is “Please
examine this child’s gait”, look hard for
Waddling gait (mid or low lumbar lesions)
(Patient with thoracic or high lumbar lesions generally can’t walk independently.)
Spine examination
Inspections: DAMPSSS
LLs exam
Look for deformity eg CTEV, muscle wasting, abnormal posture, surgical scar,
trophic ulcers
Tone (hypotonia)
Most cases are = LMNL
If UMNL signs +ve, suspect associated hydrocephalus/cerebral malformation
Power & Reflexes

Determine neurosegmental level!!! (Based on myotome)
Defined as lowest level that gives a muscle power of at least 3/5, hence
Thoracic – complete paraplegia
High lumbar (L1/L2) – can flex hip but cannot extend the knee
Mid lumbar (L3) – good knee extension but unable to dorsiflex ankle
Low lumbar (L4/L5) – good dorsiflexion but no plantar flexion
Sacral – good dorsi-flexion/plantar flexion, may have foot deformity
Check sensory level with light touch (if you have adequate time to do this)
Others : Abdomen :Scar(VP shunt)/catheter(neurogenic bladder), hard stool

Orthosis
Mx:
- Multi-disciplinary approach
- Neurologist, paediatrician, rehab physician, nephro-urologist, dietitian,
occupational therapist, physiotherapist, educator, social worker
- Manage ds complications: contractures, scoliosis, UTI, constipation,
hydrocephalus
- Manage patient’s needs on ADL, education, diet, psychology
Approach to Pes Cavus, Pes Planus, Bottom shuffler
- Manage family needs: social supports & respite care, psychological help
120
Pes Cavus
Waddling gait/
Failed heel walking/ High stepping gait
Failed tip-toe walking Ataxic gait
HMSN
Check spine: Spinal bifida Friedreich Ataxia CIDP
Pes Planus
Demonstrated by absence of an arch
when standing on tip-toe
Benign flat feet Collagen ds Cerebral palsy

- Normal up to 6 years - Ehlers-Danlos syndrome
old - Marfan syndrome
- Child with joint hypermobility
Bottom Shuffling
Familial
(Most common)
Neurological disorder
Central causes
Joint Benign
- Spastic diplegia
disorder hypotonia
- Spastic hemiplegia
- DDH of infancy
- spina bifida
- OI
Peripheral causes
- Muscular dystrophy
121
Approach to Microcephaly
Microcephaly
-measures COH, Ht, Wt for patient & plot on growth chart
-measures parents & family members HC as well
All 3 parameters small HC small, Ht & Wt normal

- SGA
- Russell-silver
syndrome
- Parents same (microcephalic) - Parents normal
- Dev normal - Dev delayed/MR
Dysmorphic facies
Familial microcephaly
Possible diagnoses:
1) Angelman syndrome
2) Cornelia de lange syndrome
3) Smith-Lemli-Opitz syndrome
Not Dysmorphic 4) Rubinstein Taybi syndrome
1) Primary microcephaly + MR (AR) 5) Craniosynostosis
2) Secondary microcephaly
For craniosynostosis
a) Perinatal asyphyxia
b) Postnatal ischaemia
c) TORCHES infections
Syndactyly Exophthalmos
d) Fetal alcohol syndrome
(soft dysmorphism)
e) Infants of PKU mother
Alpert’s syndrome Crouzon's
(AD/sporadic) syndrome(AD)
Urgent neurosurgical referral

- to reduce ICP
122
Approach to Macrocephaly
Macrocephaly
- measures HC, Ht, Wt for patient & plot on growth chart
- measures parents & family members HC as well
All 3 parameters BIG HC big, Wt & Ht normal
Development - Parents same

- Dev normal Parents normal,
not macrocephalic
Normal Delayed
Familial
macrocephaly Ventriculoperitoneal
Big baby Soto’s syndrome
shunt (VP)?
+ VP Shunt No VP Shunt
- check spine
TRO spinal bifida
Normal Development Delayed Development
1) Big brain 1) Metabolic big brain
Hydrocephalus - NF-1 - MPS
2) Bony expansion - Glutaric aciduria
- Rickets type I
Causes: VIPS
- Achondroplasia - Canavan disease
1) Vascular
- Osteogenesis - Alexander disease
- Haemorrhage
imperfecta - Tay-Sach disease
(IVH, AVM, MVA, NAI)
- Osteopetrosis 2) Cerebral
2) Infection
3) Bone marrow malformations
- Post meningitis
expansion - Hydranencephaly
3) Pressure
- Thalassaemia - Holoproencephaly
- Cong. Aqueduct
Stenosis 3) Chronic subdural
- spinal bifida with Arnold effusion
Chiari malformations - NAI
4) SOL
- brain tumour
- Dandy Walker Syndrome
123
Approach to a child with Sturge-Weber Syndrome
General inspection:
- facial port-wine stain: unilateral/bilateral
- growth of the child
- interaction of the child with surroundings & persons
- behaviour of the child: appropriate for age?
- ipsilateral eye abnormalities
 Exophthalmos, coloboma or glaucoma
- contra-lateral limb weakness
Proceed with neurological examinations if limb weakness +ve

- Demonstrate UMNL signs for both UL & LL (often hemiplegia)
 Contractures across the joints
 ↑ Tone→ +/- spasticity: hip adductor; hamstring; ankle
 ↑ Reflex & +ve Babinski reflex, clonus
I would like to complete my examination by:

1) Asking about history of seizure
2) Perform a proper developmental assessment
3) Perform a fundoscopy; looking for retinal detachment
Discussion:
I would like to ask for:
1) MRI/CT brain scan: leptomeningeal angiomatosis & tram-line
intracranial calcifications
2) Proper eye assessment: glaucoma; retinal detachment
Management of the Port-wine Stain:

- It's a developmental defect of the mature dermal capillaries
- Mx: Camouflage/ pulsed dye laser therapy/ infrared coagulation
Supportive treatment for

 Seizure control
 Rehabilitative therapy if hemiplegia
 Eye assessment & management by Ophthalmologist
 Special education needs & supports
124
Example:
Anne is a 5 years old girl with Sturge Weber Syndrome, evidenced by
bilateral facial port-wine stain. She is interactive but her behaviour generally
inappropriate for her age. She is thin built; I would like to plot her growth
parameters onto the appropriate growth charts.
There are no gross eyes abnormalities. But her left upper limb is kept in
flexed posture. There is UMN signs over her left upper and lower limbs, in
keeping with left hemiplegia.
My diagnosis is Sturge-Weber Syndrome with left hemiplegia and

developmental delay.
I would like to perform a proper developmental assessment. And, I would

like to ask about history of seizure.
I would refer her for eye assessment looking for glaucoma & retinal
detachment.
A MRI brain scan is indicated looking for leptomeningeal angiomatosis &
tram-line intracranial calcification.
Her management will involve a multidisciplinary team approach:

1) Dermatologist for mx of port-wine stain
2) Physiotherapist & Occupational Therapist for hemiplegia
3) Ophthalmologist for mx of ophthalmic complications
4) Paediatrician & Neurologist for seizure control (hemispherectomy maybe
indicated)
5) Education authority for special education needs & support.
125
Approach to a child with Neurofibromatosis Type I
General inspection:
- growth of the child: short stature; macrocephaly
- interaction & behaviours of the child
Then, proceed with focused examinations:

(A) Making diagnosis:
1) Skin:
- ≥ 6 café-au-lait spots; ≥ 5mm in pre-pubertal child
≥ 15mm in post-pubertal child
- look for axillary/ inguinal freckling: ≥ 3mm hyperpigmented spots
- look for neurofibromas ≥ 2 or ≥ 1 plexiform neurofibromas
(pubertal age group)
2) Eyes:
- look for Lisch nodules ≥ 2 (iris hamartomas) - by slit lamp
- look for optic glioma (asymptomatic in early disease) →
abnormal afferent pupillary reflex/ visual impairment?
3) Bones:
- spine: kyphoscoliosis, scoliosis
- tibia: pseudoarthrosis, bowing
st
4) Presence of 1 degree relative with NF type-I (commonly
mother/father)
(B) Looking for complications:

1) Abdomen examination:
- possible renal mass of Wilm's tumour, renal bruit (Renal artery
stenosis)
2) Check blood pressure: hypertension

1) Asking about history of seizure & learning difficulty
st
2) Asking about family history of NF type I (if no bedside clue of 1
degree relative involvement)
I would refer for proper eyes assessment: to look for Lisch nodules/ optic
Glioma.
126
Example:
Ahmad is a 10 years old boy with Type I Neurofibromatosis as evidenced by ≥
6 cafe au-lait spots and axillary freckling. He is cooperative and well grown
for his age, but I would like to plot his growth parameters onto the suitable
growth chart. I did not see any neurofibromas. His spine is scoliotic towards
the right side. There is no bowing or pseudoarthrosis of his legs.
Palpation of his abdomen revealed no renal mass. There is no renal bruit
heard as well. I notice his mother has a few cafe au lait spots and
neurofibromas as well.
I would like to check his blood pressure to look for hypertension.

I would like to check his eyes to look for Lisch nodules on the iris; and
abnormal afferent pupillary reflex with visual impairment suggestive of the
optic glioma. I would also like to ask about history of seizure and learning
difficulty.
127
Approach to a child with Tuberous Sclerosis
General Inspections:
- growth of the child
- interaction & behaviour: intellectual impairment/GDD
- head protective helmet on the child
Then, proceed with focused examinations:

(A) Making diagnosis:
1) Skin:
- adenoma sebaceum over cheeks & malar area (onset>5y/o)
- Ash leaf spots/ hypopigmented macules on trunk (± wood’s lamp)
- Occasionally cafe au lait spots on trunk
- Shagreen patches over the lumbo-sacral area
2) Fingers: peri-ungual fibromas (onset @ puberty)
3) Eyes: retinal phakomata (with fundoscopy)
4) Teeth: enamel hypoplasia/ gingival fibromas
(B) Looking for associations:

1) CVS examination: - Rhadomyoma (infancy period only)
2) Abdominal examinations:
- ballotable renal mass: polycystic kidney ds, renal angiomyolipoma

1) Asking about history of seizure, developmental delay & learning
difficulties
2) Asking about family history of tuberous sclerosis (AD inheritance)
3) Examining patient’s parents/ siblings
I would like to refer the child for:

1) An ECHO : - Rhadomyoma in the heart (if < 1 years old)
2) An KUB USG: - renal angiomyolipomas/ polycystic kidney ds
3) A CT/MRI brain scan:
- intracranial calcifications / hydrocephalus
- subependymal nodules
- cortical tubers
- subependymal giant cell astrocytoma (SEGA)
4) Proper eye assessment: - retinal phakomata
128
Example:
Jane is a 7 years old girl. She is cheerful and well-grown. I would like to plot
her onto an appropriate growth chart. She wears a protective helmet.
She is interactive but her development is delayed for her age.
Jane has adenoma sebaceum, hypopigmented macules and a few cafe au lait
spots. There are shagreen patches at the back. No gingival abnormalities.
She has no peri-ungual fibromas. She has seizures frequently and learning
difficulty from mother's history.
My diagnosis is Tuberous sclerosis.
I would like to examine her abdomen for ballotable kidneys.

I would like to do a fundoscopy examination to look for retinal phakomata.
I would like to ask about family history of tuberous sclerosis and examine her
st
1 degree relatives for signs of tuberous sclerosis.
129
Chapter 8
Approach to Respiratory Short Cases
CCAM Congenital cystic adenomatoid malformation
CF Cystic fibrosis
CSOM Chronic suppurative otitis media
CVL Central venous line
ENT Ear, nose and throat
Ix Investigation
HPT Hypertension
NO Nitric oxide
PEFR Peak expiratory flow rate
Pulm Pulmonary
T⁰ Temperature
TB Tuberculosis
TOF Tetralogy of Fallot
TRO To rule out
130
How to prepare for Respiratory short cases?
The respiratory station is a station where you need to examine the patient
quickly, and interpret the signs accurately. The allocated time of 7 minutes is
often just adequate to fully examine a cooperative child’s respiratory system.
Therefore always listen carefully to the lead-in statement. If the examiner

asked you to examine the child’s respiratory system, then you need to
examine anteriorly and posteriorly. However, if the directions were only to
examine the child’s chest posteriorly, then just do so.
In either situation, always remember to do a good general examination.

Look carefully for clubbing, which may suggest bronchiectasis. Also, look
hard for other signs that suggest chronic diseases eg . failure to thrive,
multiple surgical scars, old branula insertion scars and the presence of
central venous lines. Position the child and yourself in a comfortable
position for examination. Organise your examination sequence properly and
avoid positioning the child repeatedly.
Do inspect for asymmetrical chest expansion prior to auscultation. The site

with reduced chest expansion is always the pathological site. This helps you
to concentrate on the subsequent percussion and auscultation findings to
reach a working diagnosis.
Once you have completed your examination, present your findings

systematically. You may present all your findings and conclude at the end.
You may also present the conclusion of your findings first, then justify it with
the supporting evidences. The second method is preferred as it is more time
saving, and candidates often appear more confident with this approach.
Lastly, the common respiratory short cases encountered in the postgraduate

clinical exam are listed as below:
1. Bronchiectasis
2. Cystic fibrosis
131
3. Primary ciliary dyskinesia with Kartagener syndrome
4. Ex-prem with chronic lung disease (± chest tube scars)
5. Congenital unilateral lung agenesis
6. Other congenital lung diseases eg CCAM, congenital lobar
emphysema (± lateral thoracotomy scars)
7. Resolving pleural effusion In recovering patients who are
8. Lobar pneumonia relatively stable
132
Approach to a child with Bronchiectasis
Clinical clues
 failure to thrive
 clubbing
 CVL /Portacath
 lateral thoracotomy scar => lobectomy
 ± respiratory distress
 lungs: coarse crepitations ± rhonchi
Differential diagnoses
1) Idiopathic (10%)
2) Congenital  CF
 1° ciliary dyskinesia / Kartagener syndrome
 Lobar sequestration
CCAM
Congenital emphysema
3) Acquired  Airway obstruction
- Foreign body aspiration
- Mediastinal Lymph node: TB, lymphoma
 Recurrent aspiration + pneumonitis
- H-type TOF
 Previous severe lung infections
- Pertussis
- Measles
- Adenovirus bronchiolitis obliterans
4) Immunodeficiency synd. + recurrent chest infections
 1° immunodeficiency
- X-linked agammaglobulinemia
- IgA deficiency., complement deficiency
- HyperIgE Syndrome
 2° Immunodeficiency
- HIV
133
 PEFR / Spirometry
 Sputum inspection
 T° chart
 SPO2 chart
 plot on growth chart
 CVS exam:
1) TRO pulm. HPT => cor pulmonale
2) Dextrocardia in Kartagener syndrome
Management
1) Regular chest physio with postural drainage + exercise
2) Prompt Ix & Rx of chest infection
3) Antibiotic prophylaxis if needed
4) Mucolytics
5) Bronchodilators
6) Immunization
7) Nutritional support
8) Surgical lobectomy
134
Approach to a child with Primary Ciliary Dyskinesia
Clinical features
- Bronchiectasis
- Sinusitis 50% with Kartagener Syndrome
- Nasal polyps  Dextrocardia
- CSOM Situs Inversus
Complete examination by
1) ENT
2) Abdominal examination  situs inversus
3) Sputum / T° chart
Investigation
1) Saccharin test (Normal: 11 minutes)
2) Measurement of NO exhalation
3) Nasociliary brushing Frequency (Motility)
Ultrastructure under electron microscope
Management
- same as bronchiectasis
- ENT & hearing assessment
- Genetic counselling (AR)
Male frequently infertile
135
Example on How to Present
I would like to complete my examination by measuring his SPO2, PEFR, look

at the T⁰ chart & sputum colour.
_________ is a ___ years old boy who looks _____ for his age & I would like
to plot him on a growth chart. He is pink / cyanosed, ± clubbing, no eczema.
He is in/not in respiratory distress, with respiratory rate of __, with/without
suprasternal recession, subcostal recession, intercostals recession.
His trachea is not deviated.

His chest shape is ______ . There is/ is no surgical scar. The apex beat is
displaced / not displaced.
1) His chest expansion is equal bilateral with resonant percussion notes

throughout both lung fields. Auscultation revealed bilateral equal vesicular
breath sound with/ without added sounds ________
Or
2) Examination of the lungs revealed findings consistent with _______

evidenced by
expansion
percussion
breath sound
vocal resonance
He has no palpable cervical lymph nodes.

With this, I think the most likely diagnosis is ____________
136
Chapter 9
Approach to History
Taking and
Management Planning Station
137
ACE-I Angiotensin-converting enzyme inhibitor

ADHD Attention Deficit Hyperactivity Disorder
ADPKD Autosomal dominant polycystic kidney disease
ALP Alkaline phosphatase
ARPKD Autosomal recessive polycystic kidney disease
5-ASA 5-amino-salicylic acid
a/w associated with
AZA Azathioprine
CAMHS Child and Adolescent Mental Health Services
CD Crohn’s disease
CF Cystic fibrosis
CLD Chronic liver disease
CMPI Cow’s milk protein intolerance
CRP C-reactive protein
Cx Complication
DIOS Distal intestinal obstruction syndrome
DKA Diabetic ketoacidosis
EBV Epstein Barr virus
EPO Erythropoietin
ESR Erythrocyte sedimentation rate
FBC Full blood count
FSGS Focal segmental glomerulosclerosis
FVC Forced vital capacity
GGT Gamma Glutamyl Transpeptidase
GH Growth hormone
GI (GIT) Gastrointestinal tract
GP General Practitioner
HBS Hepato-biliary system
HD Haemodialysis
Hep Hepatitis
HIDA Hepato-biliary iminodiacetic acid
CHO Carbohydrate
HOPI History of presenting illness
138
HPT Hypertension
HSP Henoch Schonlein purpura
HUS Haemolytic uraemic syndrome
Hx History
INR International normalised ratio
IO Intestinal obstruction
ITP Immune thrombocytopenic purpura
IV intravenous
LFT Liver function test
MCT Medium-chain triglycerides
MMR Mumps, measles, rubella
Mx Management
NG Nasogastric
NSAIDs Non-steroidal anti-inflammatory drugs
OGDS Oesophageal Gastric-duodenoscopy
OSA Obstructive sleep apnoea
OTC On Table cholangiogram
PD Peritoneal dialysis
PEG Percutaneous endoscopic gastrostomy
PMHx Past medical history
PUJ Pelvic-ureteric junction
PUO Pyrexia of unknown origin
RBS Random blood sugar
RP Renal profile
RRT Renal replacement therapy
Rx Treatment
SLE Systemic erythematosus
SVT Supraventricular tachycardia
Sx Symptom
TB Tuberculosis
TOF Tetralogy of Fallot
TSB Total serum bilirubin
UC Ulcerative colitis
UDC acid Ursodeoxycholic acid
USG Ultrasound
UTI Urinary tract infection
VBG Venous blood gas
WPW Wolff-Parkinson-White
139
How to prepare for the “History Taking & Management Planning”
Station
Some candidates think the ‘History taking and management planning’

station is a relatively ‘easy’ station, as the time allocated is longer than
short cases station, and we can get history and information from the
patient directly. However, this is not true without regular practice.
Good time management as well as a systematic approach are required. If

not, you may miss important details and possibly the hidden agenda. The
first 13 minutes require you to take a focussed history and the next 9
minutes require you to summarise the patient’s problems and make a
patient centred management plan.
It is vital to have a skeleton of your management plan for potential

scenarios, so that you can discuss it well with the examiner. The examiner
can ask you about various aspects of your patient based on their concerns.
A list of potential scenarios is included as a guide. A few examples for long
case discussion are also included.
Although learning the management of all potential cases that could occur
in the station is one option of preparing, it may be useful to bear in mind
what the examiners will be looking for as well. Examiners are indeed
looking at how you would approach seeing a patient in clinic; how you
interact with the patient & family, how you go about taking the history and
if you can make a sensible plan. Therefore you do not need to know how to
manage conditions according to a subspecialist. In fact, the cases often
revolve around a small aspect of the condition rather than the condition
itself. They want a safe doctor so know your limitations. It is acceptable to
check more complicated cases with a senior and get back to the parent,
although you should still give your opinion about the possible approach.
The following is the suggested approach:
Preparation (initial 4 minutes before starting the station)

 Read the scenario (often a referral letter from the GP) carefully.
 Decide what parts of the history you need to cover in this particular
case.
- Last time the child is well suitable for acute illness
140
- Onset of diagnosis in chronic well known illness
- Perinatal history in infants/conditions related to birth
 Anticipate which areas the examiner might be interested in.
 Confirm the child’s name, age & sex, and the carer’s name.
Consultation (13 minutes = 9 minutes + 4 minutes)

 Greet the child and carer at the start of consultation. Check how they
would like to be addressed.
 Example of opening sentence: “I understand you have come to see me
today because Adam has problem with…”
 Take a focused history. What you ask depends on what the problem is.
 Ask open questions and let the patient talk.
 Use closed question to clarify the issues.
(Often these patients have chronic conditions and the issue you need
to explore is how it is affecting their life, what they think is causing a
worsening of the condition, or how they are coping.)
 Check that your history includes:
1. Current problems
2. Relevant perinatal history
3. Relevant developmental history
4. Relevant immunisation history
5. Relevant past medical & surgical history
6. Relevant drug & allergy history
7. Relevant family history
8. Psycho-social history (4S: Social life, School, Sport, Sleep)
“What do you want to be/do when you grow up?” You can also
ask the parent “What would you like them to be?” and then this
should lead into a discussion about any concerns if they have any.
 Importantly, do not clerk the patient like a medical student.
 For worsening chronic illness, ask questions to check whether it is due
to:
1. Flare-up of the disease
2. Complication of the disease progression
3. Complications or side effects from the received treatment
4. New problem unrelated to the chronic illness
141
Once you get the warning (4 minutes before ending the consultation):
 Ask the child or parents if they have any concerns or expectations that
have not been covered?
Useful questions or concepts of ICE – Ideas, Concerns, Expectations:
1. What do you think might be causing the problem?
2. Are you concerned about anything in particular?
3. What is your biggest / main concern?
4. Is there anything else that you would like to tell me?
5. Before I go on to explain what I think we could do, is there anything
you were hoping to gain from this consultation?
 Summarise the main points back to the parent and child.
 Ask them “Is it right?”
 Thanks them before they leave the room.
 Organize your thoughts and list down the problems by priority and
management plan headings in your paper.
Discussion with the Examiner (9 minutes)

Presentation of the case
 Summarise your history succinctly with focus on:
o Personal data and reason for referral/admission if any.
o The active & main problem worrying the patient or parents.
o Other problems according to their priority (or list your differential)
o Psycho-social impact of the illness on the child & family.
 Don’t repeat the whole story again. The examiner watched you do it in
the last 13 minutes. He is more interested with how you summarise
the problems, and manage them accordingly.
Discussion on Management Plan
 Listen carefully to the examiner’s questions & lead in words.
 Discussion about appropriate management which could include
investigations, onwards referral or watch and wait.
 Mention the multidisciplinary team approach if relevant and be specific
on which services you would refer them to.
 Outline your management plan into
o Immediate, medium term and long term plan
o Management plan may involve medical, surgical treatment and
supportive care like rehabilitation, community care, patient
support group, etc.
 Follow up & reply to GP if appropriate
142
Possible cases for History Taking & Management Planning Station
Neurodevelopmental disorders
1. Headache
2. Epilepsy
3. Infantile spasms
4. “Funny turns”
5. Spina bifida
6. Duchenne muscular dystrophy
7. Cerebral palsy
8. Global developmental delay
9. Learning disability
10. Autistic spectrum disorder
11. ADHD
12. Speech delay
Cardiology
1. Heart failure
2. Cyanotic congenital heart disease eg TOF with hypercyanotic
spells
3. Cardiac arrhythmias eg. WPW syndrome, SVT
4. Kawasaki’s disease
Gastroenterology and Hepatology

1. Failure to thrive
2. Obesity
3. Recurrent abdominal pain
4. Chronic diarrhea
5. Coeliac disease
6. Cow’s milk protein intolerance
7. Chronic constipation
8. Inflammatory bowel disease
9. Prolonged jaundice
10. Chronic liver disease
11. Biliary atresia post Kasai procedure/liver transplantation
12. Gastro-oesophageal reflux disease
143
Infectious diseases
1. PUO
2. Immunodeficiency with recurrent infections
Nephrology
1. Nephrotic syndrome
2. UTI
3. Haematuria
4. Chronic renal failure
5. Nocturnal enuresis
Respiratory medicine
1. Cystic fibrosis
2. Bronchiectasis
3. Primary ciliary dyskinesia
4. Bronchial asthma
5. Chronic cough
6. Recurrent wheeze
7. Chronic stridor
8. Obstructive sleep apnoea
9. Chronic lung disease
Rheumatology
1. Joint pain
2. Juvenile idiopathic arthritis
3. Systemic lupus erythematosus
Haematology
1. Chronic anaemia
2. Thalassemia
3. Sickle cell anaemia
4. Hereditary spherocytosis
5. ITP
6. Haemophilia
144
Genetics
1. Down syndrome
2. Turner’s syndrome
3. Noonan’s syndrome
4. Prader Willi syndrome
5. William’s syndrome
6. Di George’s syndrome
7. Marfan’s syndrome
Endocrinology
1. Type 1 DM
2. Precocious puberty
3. Delayed puberty
4. Short stature
5. Thyrotoxicosis
Neonatology
1. Ex-premature baby with complications of prematurity
145
Chronic constipation (functional)
Clarify constipation
- Stool frequency
- Incontinence / soiling
- Presence of faecal mass per abdomen
- Large stool might obstruct toilet
- Painful defecation
- Straining at stool
Description of associated symptoms can be found in NICE guideline on

chronic constipation in children.
When? Infancy  weaning Transitional period

Common period Toddler  toilet training
School age
History of presenting illness:

- Clarify the problem of chronic constipation as mentioned.
- Associated symptoms or red flag symptoms eg: vomiting, blood in
stool, spurious diarrhoea
- Rule out organic causes :
1. Hirchsprung (ultra-short segment)
 Delayed in passing out meconium?
2. CF with DIOS
3. Spina bifida occulta
 ? Bladder problem / recurrent UTI (neurogenic bladder)
4. Hypothyroidism symptoms?
5. Crohn’s disease
6. Coeliac disease
7. CMPI (?recent change in diet) – often in infants
- Is the child thriving?
- Difficult experience in potty training? Toilet accessibility / phobia?
- Any behavioural problem?
- Dietary history: Balanced diet with adequate fluid & fibre intake?
146
Inflammatory Bowel Disease (IBD)
Differences in Crohn’s Disease (more common) & Ulcerative Colitis

 Anatomically
 Histo-pathological examination + Endoscopy findings
 Barium follow-through
 Clinically Intestinal Eye
Extra-intestinal Joint
Growth & nutrition Skin
Puberty Biliary tract & liver
Investigations
 CD: OGDS + colonoscopy, Barium meal & follow-through
 UC: Colonoscopy
 Both: FBC, CRP, ESR, albumin, LFT
Management
Aim 1. Induce remission and maintain it
2. Ensure normal growth and development
Medical Surgical Supportive

Induce remission Urgent - Diet
- Steroids - Toxic megacolon - Vitamin B12
- 5-ASA & iron
- AZA Elective supplement
- Enteral diet (80%) - Chronic disease not - Social
Elemental responding to maximum support
Whole protein medical Rx
Maintain remission - Recurrent /subacute IO
o
- 5-ASA 2
- AZA (if steroid-dependent/ stenosis
resistant) - UC: Reduce the risk of
Refractory cases malignancy → colectomy
- Cyclosporin (CD only) - Fistula/abscess not
- Infliximab (anti-TNFα responding to medical Rx
antibody)
147
Complications
 Emergency/acute
IV fluid
Toxic megacolon Broad spectrum antibiotics
eg: Cefotaxime/Ceftriaxone
+ Metronidazole
Fistulae/Abscess
-Metronidazole/ciprofloxacin
 Chronic
Risk of GI malignancy (UC > CD)  Endoscopy surveillance
6 monthly – yearly
8 – 10 years post diagnosis
Fistulae/abscess
GI tract stenosis
Liver cirrhosis & other extra-intestinal complications
148
Biliary atresia
Patients likely to be seen in exam

- Post Kasai procedure
- Post liver transplantation
Aetiology
- Prenatal (<common): a/w CVS/GIT abnormality & polysplenia /
asplenia
- Postnatal (acquired?) Infection: EBV, Rotavirus
Genetic
Ischemic / vascular injury
Immunological
Presentation
- Pale stool, dark urine with prolonged jaundice ± jaundice-free
period
- Hepato-splenomegaly
Investigations
- LFT: TSB (direct, indirect), Liver enzymes, ALP / GGT
- USG HBS  absent/ contracted gall bladder
- HIDA scan  Normal uptake, no excretion
- Liver biopsy  peri-portal oedema, fibrosis, cholestasis +++
- OTC  Failed to outline normal biliary tree  Kasai procedure
Treatment
Kasai When?
Success rate?
Complications - Ascending cholangitis
Rx: Ceftriaxone + Metronidazole
Prognosis
1/3: Failed, need transplant within 1 year
1/3: Need transplant by teen age
1/3: Not require transplant, but progress to CLD
149
Management: Multidisciplinary approach
 Treat the underlying cause

 Medical Rx
1. Portal HPT (Cx of cirrhosis)
- Propranolol
- Spironolactone, ↓ salt diet & fluid restriction for ascites
- OGDS surveillance & banding for varices
- Hypersplenism  Splenectomy (need to know post splenectomy
complications and Rx)
2. Cholestasis with pruritus
- UDC acid
3. Vaccination
- Hep B, Hep A
- Live vaccines : MMR, Chickenpox
4. Ascending cholangitis
rd
- 3 generation cephalosporin + metronidazole
5. Bacterial peritonitis
- Antibiotic Rx
 Non-medical Rx
1. Nutrition ( Dietician )
- Fat malabsorption
- MCT-based formula
- Adequate protein intake
- ↑ calorie diet
- Vitamin A, D, E, K supplements
2. Support group
- Social
- Financial
Also need to know the acute Mx of

GIT bleed
Hepato-renal syndrome
Hepatic encephalopathy
150
Liver transplant
Indication:
 End stage liver disease (death within 12 months)
 Unacceptable Cx
- Refractory oesophageal varices
- Refractory ascites
 INR > 4
 Unacceptable quality of life
 Encephalopathy
Other indications:
1. Liver tumour
2. Metabolic disease : Wilson’s disease, α-1-antitrypsin deficiency
3. Fulminant liver failure
151
Chronic Renal Failure
PMHx
“How the disease was diagnosed?”
Antenatal scan eg: PUJ obstruction, Infantile PKD
Postnatally symptomatic eg: FTT, anaemia, HPT, Bony deformities
Incidental eg: urine/RP
HOPI
Currently symptomatic of
- Uraemic Sx?
- Polyuria/polydipsia vs oliguria
- Rx PD? Related sepsis?
HD?  Effect on school & family life
Transplantation? → Effect of immunosuppression on
patient
Drug Hx
Prednisolone
Post transplant AZA
CRF supplement Cyclosporin
Personal Hx
- Diet Hx - Imp
- Immunisation – TB, MMR, Chicken pox (pre-renal transplant)
- Developmental Hx
- Birth Hx (Antenatal: oligohydromnios
Postnatal: Ventilation-pulmonary hypoplasia)
Social Hx
“What do you want to be / do in the future?”
Effect Social
School
Sports
Sleep & depression symptoms
152
Discussion on CRF
Definition
[Normal GFR 120ml/min]
60-80 : Mild
40-60 : Moderate
<40 : Severe  <10%: ESRF Dialysis
Renal transplant
(Minimum weight 10kg)
Causes
Dysplastic, agenesis, ARPKD
 Structural/congenital Reflux/obstructive
 Congenitally inherited  eg: Cystinosis, Alport syndrome, ADPKD
 Glomerulonephritis  eg: FSGS
 Acquired Vascular: HUS. HSP
Systemic: SLE
Iatrogenic: Aminoglycosides, NSAIDs
Management
Multidisciplinary approach
Aims Optimal growth & pubertal development
↓ Metabolic Cx
Preserve residual renal function
Healthier & normal life as possible
1) Nutrition & dietary modification (Dietician)

- Nutritional support
- Adequate protein & calorie intake
- Adequate salt supplement & water (unless oliguria)
- ↓phosphate (dairy product)
+
- ↓K (potatoes, fresh fruits)
- Infants / very poor appetite  NG / PEG feeding
2) Adequate supplements
- Haematinics
Anaemia
- Human recombinant EPO
3-
- CaCO3  binds PO4 ↓ Renal osteodystrophy
- HCO3  ↓acidosis
- Vitamin D (calcitriol / alfa-calcidol)
153
3) RRT
HD Good & bad points?
PD (preferable)
4) Psychosocial well being

Support group
Social welfare referral
Child psychiatry / adolescent specialist
5) GH replacement
154
Approach to children with Type I DM
Diagnosis of Type I DM
- Symptomatic?
- Blood Ix?
- Cx on presentation/presented initially with Cx?
Insulin Rx
- Co-managed by diabetic nurse, patient and family
- Understandings of insulin regime & dosage
- Monitoring of injections and compliance to Rx
- Local & systemic Cx from insulin injections
- Understandings of corrective dose of insulin Rx during hyper
/ hypoglycaemic state
- combined understandings of dietary + insulin Rx
Dietary management
- Co-managed with paediatrics dietician, diabetic nurse, patient &
family
- Dietary pattern and portion in details
- Understandings of carbohydrate calculation and exchange
- Presence of eating disorders / dieting?
Exercise
- Detail of physical activities that patient involves in
- Experience of hypoglycaemic episode post exercise
Hypoglycaemia episode
- Understandings of hypoglycaemia Sx
- Knowledge in handling hypoglycaemia
o Food Mx  HypoKIT Simple CHO / glucose
Complex CHO
o Insulin Mx + blood sugar monitoring
- Ability in identifying precipitating factors & relevant corrective
measures
- Understanding of short term & long term risks/complications of
recurrent hypoglycaemic episodes
155
Hyperglycaemic episode
- Understandings of hyperglycaemic Sx & DKA Sx
- Knowledge in handling hyperglycaemic state
o Insulin Rx
o Blood Ix (RBS + VBG + Blood ketone) + urine ketone
o Accessibility to diabetic care team for consultation
- Ability to identify precipitating factors & relevant corrective
measures
- Understandings of short term/long term risks/complications of
recurrent hyperglycaemic episodes
Sick-day rules
- Understanding of basic principle of sick-day rules
- Ability to adjust insulin therapy & increased frequency for blood
sugar monitoring
- Understands when to seek medical attentions if condition deems
unmanageable
Social implications Child

Family & siblings
1. To the patients
- Peer relationships & peer supports/ peer pressure
- Limitations to patient’s social lifestyle & modifications
- Patient’s smoking, alcohol intake, social drugs intake
- Referral to patient support group
- Registration of “Medic-alert bracelet”
- Patient’s emotional supports: CAMHS support
2. Patient’s schooling and school nurse support
- Problems with school
- School nurse and teachers involvement in caring of patient
- Understandings of DM and its emergency Mx among the teachers
3. To the parents & siblings
- How is the family structure & dynamic?
- Family understandings of DM & family supports
- How is the family coping with DM physically & emotionally?
- Requirement of financial support, psychologist/counsellor support
- Introduction of family support group/parent group
156
Duchenne Muscular Dystrophy
1. Prednisolone treatment
- Start early when patient is still ambulant (4-6 years old)
 monitor for long term steroid therapy complications
2. Physiotherapy + knee, ankle, foot orthoses (KAFO) (with orthotist)

- Gentle physiotherapy to promote walking & prevent contractures
- KAFO will help
- Avoid excessive, strenuous physiotherapy of which may accelerate
process of muscle fibres degeneration
3. Regular assessment of pulmonary functions & treats chest infection

aggressively
- May involve pulmonologist
- Monitor respiratory reserve with spirometry
 FVC is a good guide
 If FVC falls below 50%, to consider non-invasive ventilation (NIV)
Especially in those with nocturnal hypercapnia
- Monitor for sleep hypoventilation as well
 Sx similar to OSA
4. Regular assessment of cardiac Cx- Dilated cardiomyopathy (DCM)

- Need input from cardiologist
- May need ACE-i, β-blockers or diuretics in early stage of disease
with DCM
5. Mx of scoliosis
- Usually more progressive when patient is no longer ambulant
- May affect respiratory reserve, posture, feeding, comfort
- May need spinal fusion if feasible
- Spinal brace (jacket) does not prevent progression, but useful in
postural Mx
6. Nutritional supplementation
- Need dietician input for balanced diet & avoid obesity
- If develop problems with chewing/swallowing  Speech
therapist
- May need NG/gastrostomy feeding
NB: Gene therapy in DMD  still under research
157
Sample scenarios
Scenario 1: Cystic Fibrosis and Growth

Although cystic fibrosis is rare in Malaysia, it is fairly common in the UK.
And, the principles in this case can be transferred to other cases too.
Instructions to Candidate
Take a focussed history aiming to explore problem indicated as you would
in clinical situation. You may answer questions that the subject (role-
player) may pose to you. After the consultation the examiner will focus on
management planning.
Dear Doctor
RE: James Brown
Thank you for reviewing this 13yr old boy with Cystic Fibrosis. Over the last
year his parents are concerned that he has grown very little in height and
gained no weight and is now the smallest child in the class.
Yours sincerely
Dr Jones
GP
Suggested approach and management plan:

You should explore within your history whether the poor growth is related
to the cystic fibrosis
- Chronic respiratory problem (the actual disease)
- Malabsorption (complication of the disease)
- Diabetes (complication of the disease)
Or is it unrelated
- Constitutional
- Psychological
- Other
Within the history I would concentrate on:

 Number of exacerbations (courses of antibiotics, admission to
hospital for antibiotics)
 Cough (any cough in CF is significant)
 Organisms grown on sputum (previous pseudomonas or B.
cepacia indicates colonisation and is more difficult to treat)
158
 Current treatment (nebulisers, antibiotics, vitamins and
supplements, Creon, physio) – do they ever forget?
 Any symptoms suggesting malabsorption (stool consistency,
weight loss)
 Any symptoms of diabetes (polyuria, polydipsia)
 Any other symptoms (raised intracranial pressure)
 Diet history (are they eating enough? Is there enough
Creon)
 How tall is the family? (work out expected adult height
centile)
 What are the family’s concerns?
 What are the child’s concerns?
 Social history (school, development, puberty, stressors at
home, smoking, drugs, alcohol, relationships)
 Psychology (how do they feel about it all? What do they
want to do when they grow up, leave school? What A
levels, GCSEs are they taking? Do they have any signs of
depression? Are they self-harming? Eating disorder?)
 I.C.E of parents and child
Discussion with the examiner:

 Brief summary
 Give the problem list
 Then discuss how you might manage the case
Immediate management:
 Usually, the UK cystic fibrosis clinic is a multidisciplinary team
approach and therefore you could have immediate access to
dietician and physiotherapist
 Initially, fully examine the child including growth measurements
and plot
 Look for signs of puberty
 Calculate estimated adult height and compare with current
measurements
 Urine dipstick and blood pressure
 Faecal elastase (this is low if not enough enzyme)
 Check Creon dosage and other medications
159
 Refer to dietician
 Treat any exacerbations
 Cough swab (they cough onto a Petri dish)
Medium term:
 If constitutional, can watch and wait
 If pathological, will need further intervention eg insulin for
diabetes
 Ensure adequate support at home and at school (cystic fibrosis
nurses can liaise with staff)
 Financial support (disability living allowance in the UK)
 Psychological support (counsellor or CAMHS)
 Optimise management of cystic fibrosis (physio, treating
infections early, adequate Creon, adequate vitamin
supplementation, S. aureus prophylaxis, decolonise
Pseudomonas/B. cepacia if possible)
 Children usually have central venous access by this age
 Review in 1mth (or sooner if results suggest otherwise)
Long term:
 Continued follow up
 Support groups
 Optimise management of cystic fibrosis
 Discussion about alcohol, smoking, having a family if appropriate
 Preparing to hand over to adult team, therefore try seeing patient
by themselves to encourage independence.
 Ask the child directly about their medications and try to get them
to take charge of their condition.
 Other complications include obstruction which may include
surgery
 Discussion about possibility of heart lung transplant
160
Scenario 2: General Paediatrics Outpatient scenario
Instructions to Candidate
Take a focussed history aiming to explore problem indicated as you would
in clinical situation. You may answer questions that the subject (role-
player) may pose to you. After the consultation the examiner will focus on
management planning.
Dear Doctor,
Please can you see this 6 year old boy who has been lethargic over the last
few months. He was born prematurely at 27 weeks gestation and had a
pretty rough time in the NICU. He is under the growth clinic because of his
weight but this has been steady at the 0.4th centile. I have been unable to
identify any particular cause and would be grateful for your opinion. He
did suffer from shingles 2 months ago but I would have expected him to be
making some recovery by now.
Yours sincerely,
Dr Woo
GP
Suggested approach and management plan:

In this case, you should explore the nature of the lethargy and whether it is
related to his past medical history:
 What does the parents/child mean by lethargy? How is it
noticeable? Is it impacting on their lives?
 What are the main concerns?
 Review the past medical history in NICU (reason for premature
delivery, length of time in NICU, length of ventilation, any other
complications, home on oxygen, weight on discharge)
 Past medical history subsequently (admissions to hospital,
operations)
 Current health (diet, activity, growth, development, bowels, urine
output, recurrent infections, other symptoms eg polydipsia,
polyuria, fever, raised ICP) ie checking for any red flag symptoms
 Current medications if any
 I.C.E of parents and child
161
 Psychosocial (any major events, exams, school, house moves,
bereavement, depressive symptoms
Discussion with the examiner:

 Brief summary
 Give the problem list
 Then discuss how you might manage the case
Immediate management:
 These cases are difficult but can be a common reason for referral
to general paediatrics. However, don’t panic and think through
the problem carefully. If you haven’t identified an obvious cause,
then there may not be one. Your management should ensure that
you have rule out serious causes that might easily be excluded.
This may include anaemia, diabetes, immunodeficiency
 Full examination including growth measurements and plot on
growth chart
 FBC, blood film, immunoglobulins and antibodies to
immunisations
 Urine dipstick and microscopy examination, C+S
Medium term:
 Review in 1mth
 May consider further investigations if problem persists
 But need to be careful not to over investigate
 Consider chronic fatigue syndrome (but be aware that you will
probably be asked further questions about this if you raise it)
 Ensure school work not deteriorating and liaise with school to
monitor
 If no organic cause found, need to explain to parent and discuss
plan of further management
 Check what the family wants
Long term:
 Maintaining school attendance
 Healthy eating
 May consider CAMHS if persistent
162
Appendix
163
Antiepileptic drugs & related side effects
Anti-epileptics Side effects

Valproate  Transient hair loss
 Weight gain
 Tremor
 Gastric disorder
 sedation/ hyperactivity/ aggression
 Thrombocytopenia
 Severe liver damage (<3years old at risk, if undiagnosed
Inborn error of metabolism)
 Amenorrhoea /irregular periods
 Fetal malformation
Carbamazepine  Allergic skin reaction (Steven Johnson Syndrome/SJS)
 Agranulocytosis
 Accommodation disorders (blurred vision, diplopia,
ataxia)
Lamotrigine  Skin rashes (SJS)
 Headache
 Accommodation disorders
Topiramate  Fever 2° to anhydrosis
 Nephrolithiasis
 Memory/ word-finding difficulties
 Glaucoma
Levetiracetam  Somnolence, dizziness
 Aggressiveness
Phenytoin  Skin rash (SJS)
 Coarsening of facial features
 Ataxia, slurred speech
 Motor dyskinesia, tremor
 Rickets
Phenobarbitone  Skin rash (SJS)
 Drowsiness / mental depression
 Hyperkinesia/ hyperactivity
Clobazam  Drowsiness
 Tolerance
Clonazepam  Somnolence, fatigue
164
Anti-epileptics Side effects
Ethosuximide  Drowsiness
 Headache, nausea
Vigabatrin  Tunnel vision (1:3)
General Rules
1) All anti-epileptics can cause some drowsiness, headache / dizziness
2) SJS: Think of carbamazepine, Lamotrigine, phenytoin, phenobarbitone
3) Synergy Valproate & lamotrigine
4) Titration needed (slowly over 6-8 weeks)

- Lamotrigine
- Topiramate
5) Liver enzyme inducers:

-Carbamazepine
- Benzodiazepine group
-Phenytoin
-Phenobarbitone
-Topiramate
165
Cytotoxic Drugs & Related Side Effects
Cytotoxic drug Side effects

Cyclophosphamide - Bone marrow suppression
(eg, in difficult cases of - Haemorrhagic cystitis Monitor FBC
steroid sensitive nephrotic
- Hair thinning & UFEME
syndrome)
- Affects fertility > ♂ (if ↑ dose)
Cyclosporine - Hirsuitism, gum hypertrophy
(Need to monitor drug level) - Hypertension Monitor FBC, RP,
- Bone marrow suppression LFT weekly x1/12
- Renal & liver impairment then monthly
- seizures in patient with hypomagnesaemia &
hypercholesterolemia
Tacrolimus - Nephrotoxicity
Methotrexate - Nausea, Gastrointestinal upset
(in Juvenile Idiopathic - Liver impairment Monitor FBC, LFT
Arthritis)
- Bone marrow suppression
Azathioprine - Bone marrow suppression (Monitor FBC)
- Hepatotoxicity
- Pancreatitis (5%)
Infliximab - Anaphylactic reaction
- Increased pulmonary CXR pre-treatment
tuberculosis risk 4-5x Ask about BCG vaccine
- joint pain / stiffness
Contraindication: active sepsis
5-ASA - Headache
(5-amino salicylic acid) - Nausea, epigastric pain
eg: mesalazine - Diarrhoea
- Rash
- Infertility (sulfasalazine)
- Renal impairment (monitor RP)
166

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Secrets to Passing

MRCPCH Clinical Exam

Dr Ching Bih Hwa

A few observations and much reasoning leads to error,

~ Dr Ching Bih Hwa

Dr Ching Bih Hwa

Dr Yew Kian Teck

HOSPITAL PAKAR SULTANAH FATIMAH, MUAR

MESRA BERSAMA MEMBINA KEUNGGULAN

We are what we repeatedly do.

General advice on how to pass MRCPCH clinical exam 1

Chapter 1: Approach to abdominal short cases 3

Chapter 2: Approach to cardiovascular short cases 26

Chapter 3: Approach to developmental short cases 42

Chapter 4: Approach to endocrine short cases 60

Chapter 5: Approach to eyes examination 69

Chapter 6: Approach to musculoskeletal short cases 83

Chapter 7: Approach to neurological short cases 94

Chapter 8: Approach to respiratory short cases 130

Chapter 9: Approach to history taking & management planning station 137

The Paediatric Department of Hospital Pakar Sultanah Fatimah, Muar

Following that, we are now taking on a new challenge – to organize the

This book is published as a core reference material to supplement our

By sharing our experiences, it is our sincere hope that it will provide a

Lastly, we would like to thank all the consultants, specialists, medical

Medicine is learned by the bedside and not in the classroom.

Dr Ching Bih Hwa

We would like to express our greatest gratitude to the following

1. Dr Elaine Chiang (History taking and management chapter)

2. Dr Gan Chee Chong (Ophthalmology chapter)

3. Dr Janet Hong Yeow Hua (Endocrinology chapter)

4. Dr Khoo Teik Beng (Neurology chapter)

5. Professor Lee Way Seah (Gastroenterology & hepatology chapter)

6. Dr Patrick Chan Wai Kiong (Respiratory chapter)

7. Dr Ranjini Sivanesom (Development chapter)

9. Dr Tang Swee Ping (Rheumatology chapter)

2) Dr Evelyn Chia Wei Yen 7) Dr Nur’ Atiqah bte Mohd Jalil

3) Dr Haslinda bte Rahaman 8) Dr Pavithira Devi Kailasam

4) Dr Jaiwant Singh 9) Dr Siti Soleha bte Bidin

5) Dr Khairul Anuar bin Hassan 10) Dr Tee Chin Sien

Thanks also to Dr Ngian Geok Hoon, Dr Tan Eva, Dr Jayavani Ettikan,

3. Practice makes perfect. You must practise repeatedly before the

4. Gain adequate experience before the exam. Obtain as much clinical

5. Clear and concise presentation. Look confidently at the examiner,

6. Straight to the point. Listen carefully to the examiner’s question, and

If success has an entry fee, the cost is TOTAL COMMITMENT.

Approach to Abdominal Short Cases

Mnemonics used in this chapter: HIMGCM

ADPKD Autosomal dominant polycystic kidney disease

Abdomen station is a relatively straight forward station that all candidates

Therefore, try to practice as much as you can, know

1) Thalassemia (major, intermediate) – more commonly seen in

2) Hereditary spherocytosis – more commonly seen in UK

15) A child with an abdominal scar – post intestinal surgery in Crohn’s

A: Midline laparotomy scar (any form of laparotomy)

B: Para-median scar (access to lateral structure eg: Kidney/spleen)

C: Kocher subcostal incision

D: Upper abdomen midline incision (can be transverse)

B: Mercedes Benz Extension

C: Transverse upper abdomen incision

D: Small night upper transverse incision

E: MC-Burney (Right iliac fossa)

B: Inverted J scar with transplanted kidney at RIF or LIF

____ is a _ year-old boy with no dysmorphic features. He looks

There is a grade _ murmur best heard at the ____,