30 COMMON CHILDHOOD COMPLAINTS

1. The small child Fahad (received)

2. The obese child Fahad (received)
3. Child who is failing to thrive Peter
4. The child with cough/wheeze Muneera (received)
5. The child with stridor Dema (received)
6. The child with URI Muneera Ali
7. Child with recurrent headaches Muneera Ali (received)
8. The drowsy child Selverus
9. The child who has had a funny turn (Fits, faints and funny turns) Hassan (received)
10. The child who is slow to walk Omar M
11. The child who is slow to talk Hassan (received)
12. The child with a limp Selverus (received)
13. Child with an unsteady gait Imran
14. Child with a waddling gait Dorra (received)
15. The child with a swollen/painful joint Dema (received)
16. The child with chronic diarrhea Omar S received)
17. The child with chronic constipation Aysha (received)
18. The child with recurrent abdominal pain Sara (received)
19. The child with acute abdominal pain with/without vomiting Sara (received)
20. The child who is vomiting Mohammed (received)
21. Child with a heart murmur Dorra (received)
22. The cyanosed/dusky child Aysha
23. The child with an itchy rash Reem AW (received)
24. The child with a non-itchy rash Ahmed
25. The child who bruises easily Nusiebeh (received)
26. The pale child Mohammed (received)
27. The child who is bed-wetting Reem AW (received)
28. The child with an emotional/ behavior disorder (Irrelevant)
29. The child with neck swelling Nusiebeh (received)
30. The child with a squint Muneera (received)

1. THE SMALL CHILD

Short stature ! less than the 0.4th centile.
Important to measure the rate of growth as well.

Causes of Short Stature:

- Familial
o To measure the mid parental height in males: (Height of father + 12.5 + Height of mother)/2
o To measure the mid parental height in females: (Height of father 12.5 + Height of mother)/2
- Intrauterine Growth Restriction and Extreme Prematurity
o Ask about birth (Size and weight)
- Constitutional Delay
o Usually occurs in the parent of the same sex
o Has anyone else had a problem with height in the family? Were they short for a long time and
then suddenly grew?
- Endocrine
o The child is usually short and fat
Ask about /assess the weight!
o Hypothyroidism
Signs and symptoms:
Cardiac
o Bradycardia
Neurological
o Learning difficulties
o Slow relaxing reflexes
Metabolic
o Cold intolerance
o Constipation
o Weight gain despite decreased appetite
Thin, dry, hair
o Cushings
Are they taking any medication? (Corticosteroids)
o Growth Hormone deficiency
Either isolated or secondary to panhypopituitarism
Panhypopituitarism
Can be caused by carniopharyngioma
o Problems with vision (Bitemporal hemianopia)
Laron Syndrome ! growth hormone resistance
- Nutritional/Chronic renal disease
o What are their eating habits?
o Any chronic illnesses?
Crohns, Coeliac, chronic renal disease
o Assess nutrition on examination
- Psychosocial Deprivation
- Chromosomal Disorders
o Downs
o Turners
o Russel silver
o Prader Willi
- Idiopathic short stature
- Disproportionate Short Stature: Ex. storage disorder, scoliosis or achondroplasia.

Focused Questions:
- Compared to his siblings, have you noticed that he is significantly shorter? (Familial or not)
- Is this problem common in the family? And does it tend to resolve? (Constitutional delay. You
might have a father who says that all the men in the family tend to be short for the first few years
then they suddenly grow)
- Was he small from birth
- How is his eating habits? Is he able to put on weight normally? (Nutritional)
- Is he obese? (Obese and short tends to be metabolic)
- Ask about hypothyroidism symptoms
- Any known medical illnesses? Is he on any medication?
o Nephrotic syndrome, asthma or anything that requires corticosteroids)
o Crohns and Coeliac
- Developmental milestones
o Chromosomal abnormality
- Consanguinity ! Chromosome
Important to plot the child and see if there is any fall in the centile lines. If the child has a steady
growth but is just short, this is probably normal. If he has is falling in the centile lines, you would be
worried.

Quick recap:
History
Familial
General Health
Constitutional delay
Positive history if same condition is present in the same sex parent
Can be normal and all you need to do is reassure the parents.
Signs of hypothyroidism
Iatrogenic steroids
Psychological
IUGR
Chromosomal syndromes
Prader Willi
o Hypotonic
o Obesity
o Learning difficulty
Russel Silver
o Triangular face
o Very short
o Asymmetry of limbs
Laron syndrome
o GH resistance
o Midfacial hypoplasia
o Increased growth hormone and low IGF-1
o Does not respond to GH
Turners Syndrome
o 45 X, O
o Wide spaced nipples in adults
o Short stature
o Congenital cardiovascular defects (Especially coarctation of the oarta)
o Webbed neck
o Infertility

o Lymphodemia of the hands and feet

o Wide carrying angle
o Investigations
FBC ! Anemia
Coeliac, crohns, hypothyroidism
o Coeliac and crohns can also cause short stature
Thyroid function test
X ray to check bone age
You ask for an X ray of the left hand
Creatinine + Electrolytes (rule out chronic renal failure)
Karyotyping (For females to check for turners)
Hormones
IGF1, GH
o If IGF-1 is low and there is delayed bone age, you go for growth hormone stimulation
test.
Using either glucagon, insulin, clonidine or arginine
If GH is more than 20 units/L this is normal
If it is below that, you do an MRI to check the pituitary gland
To check for panhypopituitirism: TSH, LH, FH, ACTH (By checking cortisol),
Prolactin, ADH, Oxytocin
o Treatment of GH deficiency ! Once daily subcutaneous GH
o Other indications for subcutaneous growth hormone:
GH deficiency
Turners
Chronic renal failure
Idiopathic short stature


2. THE OBESE CHILD

Obesity ! 98th centile and above on BMI chart in young children.

Children who are 12 years and older, a BMI that is equal to or greater than 30 is considered obese.
If a child is obese and short, you would consider an endocrine or chromosomal cause.
The biggest problem that is brought to the clinic is obesity
If theyre tall and fat ! Too many calories
If theyre short and fat ! consider another problem, such as endocrine.

DDx:
- Diet and reduced exercise (Most common and increasing in prevalence)
- Endocrine (Rare)
o Hypothyroidism
o Cushings
- Chromosomal
o Prader Willi

Focused questions:
- How is his eating habits?
- Does he get the chance to move around and exercise?
- Signs and symptoms of Hypothyroidism
o Constipation
o Decreased appetite and increased weight
o Excessive tiredness
o Cold intolerance
o Dry skin and brittle hair
- Any known medical illnesses?
- Does he take any medication?
o Corticosteroids
- Developmental assessment
o Prader Willi ! Delayed development

Management depends on the cause.

4. THE CHILD WITH COUGH/ WHEEZE

Nature of the cough

Wet cough typically results from
excessive mucus production, mostly due
to infection or inflammation (eg,
bronchiectasis, cystic fibrosis, primary
ciliary dyskinesia, asthma, and chronic
aspiration). In contrast, pure
bronchoconstriction or structural causes
for airway narrowing (eg, asthma, airway
malacia or compression, foreign body,
vascular ring) are usually associated with
a dry cough.

Asthma History Features:

Intermittent episodes of wheezing
that usually are the result of a
common trigger (ie, upper
respiratory infections, weather
changes, exercise, or allergens)
Seasonal variation
Family history of asthma and/
or atopy
Good response to asthma
medications

Features that suggest a diagnosis

other than asthma include the
following
Poor response to asthma
medications
A history of neonatal or perinatal
respiratory problems and wheezing
since birth suggests a congenital
abnormality.
Wheezing associated with feeding
or vomiting can result from
gastroesophageal reflux or impaired
swallowing complicated by
aspiration.
A history of choking, especially
with associated coughing or
shortness of breath, suggests
foreign body aspiration, even if it
does not immediately precede
onset of wheezing symptoms.
Poor weight gain and recurrent
ear or sinus infections suggest
cystic fibrosis, immunodeficiency, or
ciliary dysfunction.
History of progressive dyspnea,
tachypnea, exercise intolerance,
and failure to thrive suggest
interstitial lung disease.

Differential:
Asthma( see table!)
Transient Early Wheezing
Non-topic Wheezing(Following RSV LRTI)
Atopic Asthma
Broncholitis: 1-9months.
Pneumonia
Cardiac Failure
Inhaled Foreign Body
Aspiration Feeds(NM disorder)

Focused History Questions: Age Is important to reach the appropriate diagnosis.

Describe the sound that you hear when your child is breathing? (whistling sound)
WHEN did you start hearing it? determine if acute or chronic.
DURATION constantly heard?
Is it associated with Cough?
Nature of cough? (wet versus dry).
Frequency
What brings the cough/ makes it worse?
What relieves it?
Is it constant throughout the day or increased in the morning or night?
Associated Symptoms:
Laboured breathing?
Fever?
Lethargy?
PMH Is this the first time he/she have these symptoms?
PMH Any known medical illness
PMH Previous admissions
PMH drugs(if uses inhaler, establish severity) + allergies
BIRTH HISTORY Complications/stay in NICU
NUTRITION Poor feeding? Vomiting?
FMH of Asthma
FMH of Eczema or allergy
SOCIAL Missing school if its a young child! establish impact of life.
SOCIAL Recent sick contact

Physical Examination:
1. Plot weight on Growth chart, vital signs including oxygen saturation.
2. General Inspection
3. Respiratory distress (calculate RR)+ listen for Audible sounds upon breathing, color,
hydration, nutrition, dysmorphic fx, paraphernalia.
4. Hands:
a. presence of cyanosis or clubbing.
b. Pulse
5. Face: Central cyanosis, nasal flaring,
6. Inspect Chest:

a. Skin: Scars, eczema( atopic patients)

b. Bone: deformities
c. Muscle Recession
d. Lung: symmetrical breathing, pattern of breathing( abdomino-thoracic in young/
thoracico-abdominal in older.
e. Shape of the lung(barrel shaped)
7. Palpate:
a. Trachea
b. chest expansion.

c. Liver: displaced in bronchiolitis.

8. Percussion: Any differences in resonance among lung regions?
9. Auscultation:
a. characteristics and location of wheezing, as well as variations in air entry among
different lung regions
b. Crackles can be present in conjunction with wheezing in asthma, pneumonia,
bronchiolitis, cystic fibrosis
c. Heart Sounds: Heart Murmur-> cardiac failure.

Response to treatment: For patients with diffuse wheezing, a trial of inhaled bronchodilators can be
used to confirm the presence of reversible airway disease. Decreased wheezing after bronchodilator
therapy is suggestive of asthma.

Laboratory investigations:In most cases, the probable diagnosis is suspected on the basis of the
clinical history and physical examination. The role of laboratory tests, when indicated, is either to
confirm the diagnosis or to rule out other less likely diagnoses [Complete blood counts are important
in patients with chronic or systemic symptoms and may reveal anemia, leukocytosis, or leukopenia.
Eosinophilia in this setting supports an underlying allergic process or possible parasitic infection.
Sputum stain and cultures may be useful in a setting suggestive of bacterial infections,
Sweat chloride testThe sweat chloride test allows clinicians to assess physiologic changes
associated with cystic fibrosis and is indicated in children with chronic lung problems, including
wheezing.
Immunoglobulin levels can be used to screen for immunodeficiency. Elevated IgE can be indicative
of an allergic process.

Treatment:
1. Bronchiolitis:
a. Humidified oxygen via nasal cannula
b. Nebulised bronchodilators (salbutamol and ipratropium bromide)
c. Mechanical ventilation in extremely severe cases (2%)

2. Pneumonia: Amoxicillin with Co-amoxiclav in those unresponsive.

3. Asthma:

Differential
Diagnosis

Findings

Asthma

5. THE CHILD WITH A STRIDOR: upper airway obstruction

History:
When did the stridor start?
- Age of onset: If it was since birth, then this is suggestive of laryngomalacia or a congenital
airway abnormality)
Is the stridor getting worse with time? Is it worse in the morning or at night?
What makes it worse? (E.g. feeding, crying)
Do you have difficulty breathing or swallowing?
Does it affect your speech?

How severe is it? Does the baby change colour? (Cyanosis)

Does the child have other symptoms such as fever, sore throat, drooling, and cough?
Perinatal history
Has the child been vaccinated?

Physical examination:
Inspection:
- Patient will look ill, with a fever. Check the oxygen saturation
-

See if the patient is in respiratory distress. You can hear the stridor

Color: cyanosis observe for signs of hypoxia

Mouth open with drooling saliva (suggestive of epiglottitis)

Comment on shape of chest

Tachycardia

Describe the cough (barking)

Chest recession (subcostal or intercostal)

NEVER examine the throat

Palpation:
- Deviation of trachea
Auscultate:
- Nose, neck and chest (to help locate the stridor)
Possible causes:
- Croup (most common)
-

Epiglottitis

Bacterial tracheitis

Inhaled foreign body

Laryngomalacia

7. CHILD WITH RECURRENT HEADACHES

Clinical Approach to a child with recurrent headache
1. History from the parent and child
Site
Onset
Character
Radiation
Association
Timing
exacerbating and relieving factors
severity
- Family history in first degree relative in migraine

2.
3.
4.
5.
6.

Red flags (wakes from sleep, in the morning, vomiting, neuro signs, change in behaviour)
Measure head circumference and BP
Look for skin markers (caf au lait spots) NF1 more prone for brain tumours
Examine ear, teeth, and sinuses
Examine eye (pupil, fields, visual)

Migraine
- Recurrent headache separated by symptom free intervals and 3 of the following:
Unilateral headache
Throbbing quality
Aura (visual, auditory, sensory)
Abdominal pain + N/V
Relieved after sleep
Family history
- Two main types:
Common migraine: most common (80%), not associated with aura
Classic migraine: less common, usually associated with aura (flashy lights)
- Migraine syndromes
Periodic syndrome: occurs in young children, presents with severe episodes of vomiting and
weakness, becomes dehydrated and requires IV hydration. Often misdiagnosed to having
abdominal pathology
Opthalmoplegic migraine: can occur in adults, complains of double vision
Hemiplegic migraine, acute confusion migraine, and footballers migraine
- Management
Acute attack: Paracetamol, Sleep
Prevention (must identify triggering factors by headache diary):
Decrease stress and adequate sleep
Good calorie intake
Avoid: Chocolate, caffeine, nuts, Citrus fruits, dairy products and bananas
Anti-migraine drugs: pizotifen (weight gain and sleepiness), clonidine, propranolol. These
drugs are used as prophylactic, however, they are not highly recommended.

Tension headaches
- Usually more than 10 years of age
-

Worsens as day ends, relieved by relaxation

Symmetrical band-like pressure

Psychogenic headaches
- Diffuse headaches
-

Persistent, not incapacitating

Difficult to describe by patient

Raised intracranial pressure headaches

- Diffused or localized
-

No symptom free intervals, just change in severity

Usually there is a change in frequency, quality, and pattern over time

Increase when laying down and in the morning

Usually associated with morning vomiting (causing relief)

Change in personality & school preformance

Could be associated with neurological signs:

Visual field deficits
CN abnormalities (squint and diplopia)
Ataxia
Tilting of the head
Papilloedema
Growth failure (eg.craniopharyngioma)

Could be associated with brain tumours, if in doubt CT and MRI must be performed (50% of those
with brain tumour will have neurological signs 2-3months after the onset of headache)

Management of headaches
1. Psychosocial support and relaxation techniques
2. Analgesics (Paracetamol and NSAIDs) as early as possible if the severity is increasing
3. Antiemetic (if vomiting): metoclopramide
4. Serotonin agonist: nasal preparation for children above 12 years

5. Prophylactic: pizotifen and propranolol

9. THE CHILD WHO HAS HAD A FUNNY TURN

Each has a distinctive identification character, trigger or symp. To be extractd from history
May mimic or be mimicked by seizures/ epilepsy.

DDx

Reflex anoxic seizures

mainly triggered by pain/
discomfort
Could involve tonic clonic
episode induced by
hypoxia

Seizures
Epilepsy
Meningitis
Breath holding attacks ! upset, tempered, cyanosed, loss
consciousness, recovers fully
Reflex anoxic seizures ! pain/ discomfort trigger, breath holding, cyanosis, tonic-clonic
seizure, Family Hx
Syncope ! long standing time, hot weather, fear
Migraine ! GI disturbances & light-headedness
Benign paroxysmal vertigo ! recurrent, Nystagmus, falling.
Cardiac arrhythmia !related to exercise
Fabricated ! observatory skills dependent

of

Hx Qs
Any Family history? V. Common
First episode? Similar triggers/ conditions to a previous episode if any?
Loss of consciousness?
Trauma? ! Reflex anoxic seizure
Was the child Upset/afraid previous to episode? Y! breath holding attacks/ reflex anoxic
seizures/ Syncope
Was the child cyanosed? breath holding attacks/ reflex anoxic seizure (tonic clonic component)
Loss of consciousness during? breath holding attacks/ reflex anoxic seizure
Symmetrical or asymmetrical tonic clonic? Asymmetric is not a funny turn (focal seizure! red
flag)
Cold food? ! Reflex anoxic seizure
Incontinence ! reflex anoxic seizure
Nystagmus! benign paroxysmal vertigo
Fall (unsteadiness) ! benign paroxysmal vertigo/ Syncope

PEx +ves:
Mainly a history diagnosis, if physical examination is remarkable along with an indicating history
EEG
Investigations: a history diagnosis, no investigations implicated
Treatment: no treatment for any of the funny turns, none of them is an actual limiting pathology

11. THE CHILD WHO IS SLOW TO TALK

Key in such history: must determine is cause if Delay or Disorder. The whole approach and subjects
of suspicion while progressing through your history depends on the age of the child.

DDx
Delay
o Hearing loss
o Global Dev Delay
o Difficulty in speech production- Anatomical anomaly (Cleft palate and lip)
o Environmental deprivation/ lack of social contact to learn the skill
o Normal variant of speech development in the family
Disorder in
o Comprehension of speech
o Language expression: knows what must be said just cant/ difficult
o Disordered phonation (stammering/ dysarthria)
o Pragmatics (the sentence meaning is different amongst the speaker and listener)
o Abnormal social/communication skills (autistic behave)

Hx Important Questions:
Any previous admissions? What for? (Also dig deep to preg and delivery history)
Determine which component of the speech production process is dysfunctional (initiation,
production or execution) by evaluating the communication and responsiveness of the case.
Any other related abnormality that can accompany a disorder will further re-direct you to the
correct system.
The severity of the disability can determine if its a mild deviation from the norm or a potentially
more global dilemma.
Any previous testing done? Result?
Emotional/ psychological distress associated? (Cause/ result of)

Physical +ves
Notice and dimorphic features or and detectable abnormality
The nature of any +ves on the Neurological Examination would further guide you towards a
more probable cause (motor/ sensory/ Cognitive/ severity/ systems involved)
Investigations:
Assess global and cognitive development
the symbolic toy test ! for v. early lang dev
the reynell test ! determine id receptive or expressive dysfunction is cause
Treatment
Fix anatomical deformity and restore velopharyngeal patency if indicated
Speech and language therapy
Cochlear implant
Psychological support (essential as it could be caused/ worsened by psychological influence)
Refer to an audiologist
Special schooling

12. THE CHILD WITH A LIMP

History key points
-AGE (some diseases only in a certain ages eg SCFE-> adolescence)
- ONSET (must determine acute vs chronic limp)
- PAIN ! hip pain ?
knee pain ?
if yes pain only on moving or even at rest ?
- recent cough/cold/flu ? (more likely to be transient synovitis)
- fever ? how high ? (really high could be septic arthritis/osteomyelitis)
-any trauma ? falls ?
- focused systemic qs :
rashes ?(HSP)
joint swelling ?
weight loss ? (tumours)
blood transfusions ? (sickle)
Weight ? (scfe if obese)

DDX for limp

pneumonic : STARTSS HOT
Septic arthritis
Trauma (VERY COMMON)
AVN (perthes)
RA (JIA)

Transient synovitis
SCFE
Sickle

HSP
Osteomyelitis
Tumours (bone tumours/leukemia)

NB. MUST DIFFERENTIATE BETWEEN TRANSIENT SYNOVITIS AND SEPTIC ARTHRITIS ! coz
both present with acute limp.
Transient synovitis
Septic arthritis

ACUTE ONSET, NON WEIGHT BEARING

No/mild fever Moderate/high fever

Child looks well
Child looks ill

Hip pain on movement Hip pain AT REST

ESR normal ESR raised


Some points about each differential:

In the really young (1-3 years) suspect DDH that wasnt caught on the normal screening and so now
presented with a limp. (no pain). Specially in females.

Transient synovitis
Commonest age : 2-12
Acute hip pain (on movement only !)

Usually follows a viral infection

Treatment ? Bed rest

SCFE
Look for the OBESE ADOLESCENT.

Physical : No way theyd get. Coz most are painful and they wont have 19 students inflicting pain on a
child.
Just a normal ortho exam, and ask about tenderness anywhere before touching. And comment on
posture of child before anything. (septic arthritis posture would have hip flexed and abducted + would
look really ill.)

14. CHILD WITH A WADDLING GAIT

Myopathic Gait (Waddling Gait)
Hip girdle muscles are responsible for keeping the pelvis level when walking. If you have weakness
on one side, this will lead to a drop in the pelvis on the contralateral side of the pelvis while walking
(Trendelenburg sign). With bilateral weakness, you will have dropping of the pelvis on both sides
during walking leading to waddling. This gait is seen in patient with myopathies, such as muscular
dystrophy.
Differential:
SMA
DMD-onset of waddling gat begins from 3-5 years old
Muscular dystrophies
more frequent in boys, delayed walking (>18 months), family hx (carrier
status)
proximal muscle weakness (Gower sign), Trendelenberg gait, inability to jump,
prominent but weak "pseudohypertrophied" calf muscles (symmetric), cardiomyopathy, scoliosis,
nonambulant by teenage years

Congenital hip dysplasia

Development hip dysplasia peak age 12 to 24 months; first-born females; breech birth; family history;
oligohydramnios; may present with delayed walking neonates: clicky hips, positive Barlow
maneuver, positive Ortolani maneuver; older child/toddler: leg length discrepancy (short ipsilateral
side), asymmetric skin creases (posterior thigh), positive and bilateral Trendelenberg gait (rollingwaddling gait)

History

What are the parent's concerns?

Take a detailed medical history including pregnancy, birth and development. Perinatal events
and motor development may reveal a diagnosis ofcerebral palsy.
Duration of complaint and progression. History should clarify if the problem began at birth, or
before or after walking. How has the problem changed during the past few months?
Family history; there is frequently a familial tendency.
Is there really concern about the gait or is it appearance? A toddler's gait and legs are different
from those of an adult. Parental concern often stems from a lack of understanding regarding the
maturation of the gait.
Signs and symptoms; ask about pain, limping, tripping and falling (Toe walking and falling
frequent in history of DMD case)
Sitting habits; internal tibial torsion is commonly associated with sitting on the feet, while
increased femoral anteversion is associated with sitting in a 'W' position.
Aggravating factors; torsional deformities become more apparent with fatigue.
Delayed achievement of motor milestones
Impact on life/school/daily activities

Diagnosis of DMD:

A positiveGowers' signreflects the more severe impairment of the lower extremities muscles.
The child helps himself to get up with upper extremities: first by rising to stand on his arms and
knees, and then "walking" his hands up his legs to stand upright.

Affected children usually tire more easily and have less overall strength than their peers.

Creatine kinase(CPK-MM) levels in the bloodstream are extremely high.

Anelectromyography(EMG) shows that weakness is caused by destruction of muscle tissue

rather than by damage tonerves.

Genetic testingcan reveal genetic errors in the Xp21 gene.

A musclebiopsy(immunohistochemistryorimmunoblotting) or genetic test (blood test)

confirms the absence ofdystrophin, although improvements in genetic testing often make this
unnecessary.

Management of DMD:
DMD is not curable, however treatment is available.
Predisone 0.75mg/kg/day to increase strength and function
Treatment goals: maintain function, prevent contractures and provide support to child and family.
Treatment is generally aimed at controlling the onset of symptoms to maximize the quality of life, and
include the following:
Corticosteroidssuch asprednisoloneanddeflazacortincrease energy and strength and defer severity
of some symptoms.

Randomised control trials have shown thatbeta2-agonistsincrease muscle strength but do not
modify disease progression. Follow-up time for most RCTs on beta2-agonists is only around 12
months and hence results cannot be extrapolated beyond that time frame.

Mild, non-jarring physical activity such as swimming is encouraged. Inactivity (such asbed
rest) can worsen the muscle disease.

Physical therapy is helpful to maintain muscle strength, flexibility, and function.

Orthopedic appliances (such as braces and wheelchairs) may improve mobility and the ability
for self-care. Form-fitting removable leg braces that hold the ankle in place during sleep can
defer the onset ofcontractures.

Appropriate respiratory support as the disease progresses is important.

15. THE CHILD WITH A SWOLLEN/PAINFUL JOINT:

HISTORY:
Pain:
- Location: where is the pain?
-

Radiation: does it go anywhere?

Characteristic: can you describe the pain?

Onset: when did the pain start

Periodicity: how often do you get the pain?

Duration: how long have you had the pain?

Severity: on a scale of 1-10 how bad is the pain?

Aggravating factors: what makes the pain worse?

Relieving factors: what makes the pain go away?

Associated symptoms: rash, fever

Is it worse in the morning?

Does it limit your everyday activity?
Does it limit sport activities?

Joint swelling:
- Has there been much swelling?
-

Was there any previous trauma?

Which joints are affected?

How long has it been swollen for? (acute vs chronic)

Stiffness:
- Is the patient stiff in the morning or evening
Systemic review:
- Any previous similar symptoms?
-

Other joints affected?

Have you noticed any rashes? Or any colour changes in skin?

Have you had any problems with your eyes?

Do you feel cold or warm?

Family history:
- Any musculoskeletal disorders running in the family?
Social history:
- If they live in a house one floor or more
-

Do you use walking aids

EXAMINATION:
Inspection:
- Any rash
-

Erythema

Scars

Specific to joint:
- Erythema
-

Swelling

Deformity

Around the area:

- Muscle wasting (E.g. knee check for quadriceps wasting)
Palpation: look for signs of discomfort on patients face while palpating
- Warmth
-

Tenderness

Swelling: joint effusion fluid can be shifted within the joint

Movement:
- Passive movement: check for limitation of movement, crepitus and joint stability
-

Active movement

Special knee tests:

- Patellar tap
Back examination:
- Check for scoliosis by 1. Comparing the two shoulder lengths 2. asking the patient to bend and
look for any deformity
-

Palpate the vertebrae

Shober test

Winging of the scapula

Differentiation between juvenile idiopathic arthritis, septic arthritis and osteomyelitis:

Septic arthritis:
- The kid looks generally ill (fatigue) with fever
-

Usually one joint is affected only swollen, tender and red

The affected joint cannot be moved as it will cause pain

If the hip is affected, the kid can present with a limp

Investigations:
- CBC (WBC, CRP, ESR)
JIA:

Blood culture (because hematogenous spread)

Prolonged joint swelling more than 6 weeks

Could be more than one joint affected

Fever and rash

Morning stiffness is common

Complain of pain after long hours of immobility of joint

Osteomyelitis:
- Remember it is an infection of the metaphysis and not the joint! However it can go on to affect
the neighboring joint

It can be a multi-focal loci so make sure to ask if other places have been affected

Painful immobile LIMB (not joint) in a child with fever (moving the limb causes severe pain)

Over the affected limb there could be swelling, tenderness and it is red

16. THE CHILD WITH CHRONIC DIARRHEA

Diarrheais increased stool volume, usually with looser consistency and increased frequency than
normal. Frequency may not change however. These qualitative attributes are relative to the persons
normal bowel pattern. Acute viral gastroenteritis, one of the most common causes, usually resolves in
2-5 days. Chronic diarrhea is defined as diarrhea lasting more than 2 weeks. With chronic diarrhea
there is often a cycle of infection, malabsorption and malnutrition which propagates the diarrhea.

Osmotic diarrhea usually will cease once the offending agent is stopped such as juice (Toddlers
diarrhea) or dairy products (Lactose intolerance). It has a low stool electrolyte content. Weight loss
and failure to thrive may be seen. Secretory diarrhea will continue even when taking nothing by
mouth. It has a high stool electrolyte content. Infectious diarrhea often is accompanied by fever,
nausea, emesis, prior antibiotic use and possibly bloody stools. More commonly it is an acute
problem. Inflammatory
diarrhea is generally chronic with other signs of disease such as failure to thrive, arthritis, perianal
lesions, and/or rash.
Diarrhea prevention includes high standards of hygiene include water, food and personal hygiene.
Vaccination against Rotavirus is available in many countries. Treatment for acute diarrhea
includesoral rehydration solutions, intravenous isotonic fluids, and early refeeding. Antimicrobials for
identified microorganisms depends on the organism and presenting problems. Treatment for chronic
diarrhea includes removal of the offending agent (e.g. cows milk, laxative, juice, etc.), and
appropriate evaluation to identify the disease process and its treatment.

Learning Point
Common causes of diarrheainclude:
Acute
Allergic enteritis cows milk allergy, soy allergy

Brush border deficiency Fructose, Isomaltose, Lactose, Sucrose

Infectious

Bacteria common organisms includeAeromonas, Campylobacter, Clostridium, E. coli,

Klebsiella, Plesiomonas, Salmonella, Shigella, Vibrio cholera, Yersinia

Parasite common organisms includeAmoeba, Cryptosporidium, Giardia, Strongyloides

Viral common organisms includeAdenovirus, Astrovirus, Calcivirus, Norovirus, Rotavirus

Medications laxative use or abuse, Magnesium-containing antacids, opioid withdrawal,

medication colorants and flavorings such as sorbitol

Methylxanthines caffeine, theophylline

Surgical problems Ascites, Appendicitis, Intussception, Malrotation, Necrotizing enterocolitis,

Peritonitis

Chronic
Allergic enteritis cows milk allergy, soy allergy, eosinophilic enteritis

Bile salt malabsorption

Brush border deficiency Fructose, Isomaltose, Lactose, Sucrose

Celiac disease

Endocrine Addisons disease, diabetes, hypoparathyroidism, pancreatic insufficiency (Cystic

fibrosis, Schwachman-Diamond syndrome), thyrotoxicosis

Fecal impaction including Hirshsprung disease

Infectious

Parasites common organisms includeCryptosporidium, Giardia,Tuberculosis

Viruses common organisms include HIV

Inflammatory bowel syndrome

Irritable bowel syndrome

Malnutrition failure to thrive, acrodermatitis entropathica

Medications alcohol, laxative use or abuse, medication colorants and flavorings such as
sorbitol, NSAID enteritis

Psychological secondary to stress

Surgical problems short gut syndrome, feeding tube problems

Toddlers diarrhea excessive intake of clear, sweet liquids

Tropical sprue

Vitamin

Deficiency Folate, Niacin

Toxicity Niacin

Stool colors
Red/Pink Stool
Blood

Diazepam syrup

Ampicillin

Viprynium

Phenophthalein

Red Jell-O

Dioralyteoral rehydration solution

Yellow Stool

Normal in formula-fed babies

Green/Greenish Gold Stool

Normally in fully breastfed babies

Stomach infection

Black Stool
Blood

Iron

Pepto-Bismol

Black licorice

Blueberries

Green-leafy vegetables

Lead

Charcoal

Coal

Dirt

White/Clay Colored Stools

Malabsorption

Biliary system blockage

Barium

Aluminum Hydroxide

Questions to Ask
A good history is crucial to gain a clinical picture of the patients problem. Generally, the history should
be directed to:
(1) ensure that the child is, in fact, experiencing an episode of diarrhea,
(2) determine the timing and severity, and
(3) lead you to a differential diagnosis.
The following questions may be helpful.
When did the current problem start?

How many bowel movements per day?

What is the normal pattern for this child?

Are the loose movements interspersed by normal ones?

Has the child ever experienced this before?

What is the childs dietary history (rule out overfeeding)?

What is the consistency of the stool?

What is the volume of stool that the child is passing?

Is there blood or pus contained within the stool?

Is it extremely foul-smelling or contain oil droplets (malabsorption)?

Bloody diarrhea may suggest specific infectious agents, inflammatory bowel disease, bowel
ischemia (or necrotizing enterocolitis) or cows milk protein allergy.

Does the child have a fever?

Has the child also been vomiting (very common and can exasperate dehydration)? What is the
childs current urine output (oliguria or anuria suggests a large volume deficit)? Has the child
been able to take in any fluids?

Do we have records of the childs weight (useful to compare these to the current to assess the
degree of dehydration)?

Is the child immunocompromised (if yes, think unusual infections)?

Has the child been exposed to anyone else with a similar illness?

Has the child been institutionalized?

Has there been any travel or has the child newly immigrated?

Has there been any recent use of antibiotics?

Are there any other concurrent problems or pertinent past medical history?

17. CHILD WITH CHRONIC CONSTIPATION

CONSTIPATION: infrequent passage of dry, hardened faeces often accompanied by straining or pain.
There may be abdominal pain which waxes and wanes. It really depends on the age of the patient.
Causes of constipation
Dietary
Dehydration
Anal fissure/stenosis
Hirschsprungs disease
Intestinal obstruction e.g. stricture post-necrotizing enterocolitis
Spinal cord lesion (abnormality below the lesion)

Cystic fibrosis (meconium ileus equivalent)
Cows milk intolerance
Drugs, e.g. opiates, vincristine, lead poisoning
Hypothyroidism
Sexual abuse
Anorexa Nervosa

HISTORY (important to know the AGE)

1. Duration
a. If acute- ask about any previous febrile illness
b.
2. What do you mean by constipation?
a. Hardness of stool
b. Painful defecation (maybe perianal fistula, fissure ! Crohns?)
c. Decreased frequency of defecation
d.
3. If decreased frequency ! Ask about the difference between now and before?
4.
5. Is this the first time?
6.
7. What was given to him at home/ health centre?
8.
9. Any abdominal pain?
a. Maybe abdominal pain which waxes and wanes with passage of stool
b. Overflow soiling????!!
c.
10. Vomiting
11.
12. Changes in weight
13.
14. Ask about the diet
15.
16. Any back pain
17.
18. Birth History trying to R/O Hx of Hirschsprung, NEC
19.
20. Any previous hospital admissions? Surgeries?
21.

22. Does the child have any medical condition?

23.
24. Any family history of
a. IBD
b. Cystic fibrosis
c. Thyroid problem
d.

Differential diagnosis of Constipation

BABIES-
Hirschsprung disease
Anorectal abnormalities
Hypothyroidisim
Hypercalcaemia
Coeliac disease (FTT)
CHILDREN-
Psychological
Problem with toilet training
Stress

Examination- palpable abdominal mass in a well-looking child. DRE done when pathological cause is
suspected.
WHAT ARE THE RED FLAG SYMPTOMS OR SIGNS IN THE CHILD WITH CONSTIPATION pg.237
Acute constipation (following febrile illness)
Resolve spontaneously
Dietary change, increase fluid intake
Use mild laxatives +extra fluid

Chronic constipation
(rectum would be over-distended with subsequent loss of feeling the need to defecate)
- Involuntary soiling (contractions of the full rectum will inhibit the internal sphincter leading to
overflow)
AIM: to evacuate overloaded rectum completely
Disimpaction regimen of stool softener
1. Macrogol laxative eg. Polyethylene glycol + electrolytes for 1-2 weeks until impaction resolves
2. IF NOT TOLERATED ! give osmotic laxatives (lactulose)
3. NOT SUCCESSFUL ! stimulant laxative eg. Senna or sodium picosulphate
4. Dietary interventions and sufficient fluid intakes (balanced diet with adequate fibre)
5. Encouragement
a. Sit in toilet following meals to utilise the physiological gastrocolic reflex.
b.

HIRSCHSPRUNG DISEASE: Loss of the ganglion cell from the myenteric and submucosal plexuses
of part of the large bowel results in a narrow, contracted segment. The abnormal bowel extends from
the rectum for a variable distance proximally, attached to a normally innervated dilated bowel.
CLINICAL SYMPTOMS/ SIGNS OF HIRSCHSPRUNG

Neonatal-
- Failure to pass meconium within 24 h of life
- Abdominal distension
- Later- bile stained vomiting

EXAMINATION- narrow segment and withdrawal of the examining finger ! releases a gush of liquid
stool and flatus. Causes delay in diagnosis because of temporary improvement.

Infants (few weeks of life)

- Present with severe life-threatening Hirschsprung enterocolitis due to infection with Cl.difficile.
Children
- Profound Chronic constipation
- Abdominal distension
- Growth failure
-

DIAGNOSIS
Suction rectal biopsy- demonstrating the absence of ganglion cells together with the presence of
large acetyl cholinesterase positive nerve trunk
Anorectal manometry or barium studies useful for the surgeon to give an idea of the length of the
aganglionic segment

TREATMENT OF HIRSCHSPRUNG DISEASE

SURGICAL
- Initial colostomy
- Anastomosing normally innervated bowel to the anus
-

18. CHILD WITH RECURRENT ABDOMINAL PAIN.

DDX: IBD, Abdominal migraine, PUD, UTI, gastritis, CRAP! (chronic recurrent abdominal pain).
HX: Pain aggravated or relieved by food?
loss of weight?
Fever?
Bowel habit? Vomiting?
Affects Quality of Life? Misses school because of this pain?
Mouth ulcers or peri-anal ulcers? (Crohns)
Hx of headaches?
Family hx of migraines or IBD

19. CHILD WITH ACUTE ABDOMINAL PAIN WITH OR WITHOUT VOMITING.

DDX: acute abdomen

Surgical
Medical
Extra-abdominal

Acute appendicitis Gastroenteritis
URTI

Intussusception (obstruction)
IBD (more of chronic..)
Lower lobe pneumonia

Inguinal hernia
DKA Torsion of the tests

Inflamed Meckels diverticulum Hepatitis
Hip and spine

Peritonitis UTI and pyelonephritis

Vomit

Hematemesis
Peptic ulcer

Projectile vomiting Pyloric stenosis

GIT

Abdominal distension
Intestinal obstruction

Blood in stool
Intussusception

Others

Severe dehydration Gastroenteritis, DKA

Failure to thrive
GORD, celiac disease

Bile stained Intestinal obstruction

Key questions to ask in History:-

When did the pain start? Where is it? Radiation? Severity?

Fever?
Vomiting? (blood or bile?)
Change in bowel habit? What is the stool like?
Urine (burning sensation, color)?
SOB? Cough?

20. THE CHILD WHO VOMITS

Causes:
1.GI (i.e., obstruction, pyloric stenosis, reflux, appendicitis, gatroenteritis, hEpatitis A)
2. CNS disease (tumours, migraine headaces, meninigtis)
3. pulmonary problems (astma-Children will cough up a fleck of sputum that initiates a gag
response, tumours again, inflammatory- eg pneumonia)
4. renal disease (kidney stone, peylonephritis, UTI, renal failure)
5. endocrine/metabolic disorders (DKA common)
6. drugs (either as side effects or in overdosages)
7. psychiatric disorders or stress.
Commonest causes:

Gastroenteritis:

Food allergies and irritations:Although any food can provoke a reaction, several in particular tend
to cause most food allergies, including eggs, milk, peanuts, shellfish, soy, tree nuts, wheat, and
fish. Nausea, vomiting, and abdominal pain can occur within minutes or hours after ingesting the
offending food.

Anxiety and stress:Worries about the new school year. all kinds of emotional upsets can lead to
nausea and vomiting, though this tends to happen more often with adults or older children.

flu and other illness:A few other common reasons kids might have nausea or vomiting include ear
infections, seasonal flu, swine flu, acid reflux, and reactions to medication, metabolic disorders.

Eating too much

Food poisoning

History:
-PC -when did it start
-how many times did the child vomit
-projectile or non-projectile
-colour
-blood or mucous
-after introducing food or drugs or not necessarily
-associated wit diahrrea or fever.
-recent take-away or undercooked food
- recent travel
-if no certain cause, then ask if stressed or not and how well they do in scool
-family diabetes, sickle cell

-Immunizations - hepatitis maybe.

-nutrition- wt loss, appetite, what they eat or drink.
-stress
Physical:
-look for general status of patient (alert or not)
-signs of dehydration (mucous membranes, skin turgor, capillary refill, sunken eyes and fontanelles)
Treatment:

ABC

Check vitals , cbc (metabolic alkalosis), growth,

Correct dehydration. Mild vs moderate vs severe

Mild- prevent dehydration, continue breast feeds, encourage fluid intake and dont give
carbonated drinks. ORS if needed

Moderate- ORS. give fluid deficit replacement+mainatinance fluid. Fluid deficit is 50 ml/k over
4 hours. Maintainance is first 10/100, second 10/50, 1/20.

Severe- IV therapy. Saline solution 0.9% NaCl. If shocked, fluid deficit given is 100 ml/k, 50 ml/
k if not. And maintain fluid with nacl and 5% glucose. Also give KCl.

Treat underlying cause.

21. CHILD WITH A HEART MURMUR

Heart murmurs are due to abnormalities of flow within the heart and great vessels. Innocent murmurs
are very common but it is essential to assess whether the murmur is haemodynamically significant
and whether appropriate antibiotic prophylaxis to prevent endocarditis is required.
History taking:
1. Ask about pre-natal and perinatal history, specifically focusing on infections, teratogenic exposure
and presence of gestational diabetes (all of these are risk factors that may have lead to congenital
defects)
2. Neonatal history including FTT, poor feedings, cyanosis
3. Age of onset-cardiac failure as a neonate
4. Past surgeries-corrections done after birth
5. In older children; ask about exercise intolerance, chest pain upon exertion, syncope or recurrent
URTIs.
6. Medical history to ask about diseases related with cardiac abnormalities.
7. Family history to rule out sudden death in family members, siblings/family members with similar
conditions or any genetic disorders such as Marfan,Noonan or Turner syndrome.
8. Impact on life- does the child miss school days, etc.

Presentation
Murmurs are described by location, intensity (grade 1-6 with grade 1 being virtually undetectable),
timing in the cardiac cycle, and radiation.

The absence of symptoms does not exclude important pathology. Certain features indicate that a
murmur is more likely to be pathological:

History: lethargy, tiredness, failure to thrive.

Inspection: cyanosis, clubbing, abnormal breathing (tachypnoea, intercostal recession).

Palpation: parasternal or apical impulse; abnormal pulses - diminished, absent or delayed

femoral pulses.

Abnormal heart sounds; second heart sound is accentuated and not variably split.

Systolic murmur which is pansystolic or is grade 3 or above.

Murmur which is purely diastolic.

Radiation of murmur to the back.

Presence of an early or midsystolic click.

Presence of cardiac failure or arrhythmia.

Innocent murmurs
Innocent murmurs are common in children and tend to become audible or louder when the heart
beats faster, such as with a raised temperature or excitement.
Still's murmur (or Fiddle string murmur) is the most common innocent murmur heard in children
aged 2 to 8 years old. It is a short, midsystolic murmur with a very characteristic low-frequency
buzzing or musical quality.It is localised to the lower left mid-sternal border and radiates to the
apex. The murmur is of short duration, low intensity and is loudest when the child is supine, often
varying markedly with posture. It is also provoked by fever and anaemia. It can be made to
disappear on hyperextension of the back and neck (Scott's manoeuvre). However, it is not

always possible to distinguish it from a smallventricular septal defect. Still's murmur usually
disappears at puberty.
Pathological systolic murmurs

Ejection systolic murmurs: reach a peak midway between 1st and 2nd heart sounds and don't
run into the 2nd heart sound. Usually maximal at the upper sternal borders, and possible
causes include:

Aortic stenosis.

Pulmonary stenosis.
Coarctation of the aorta: murmur is heard over the back, particularly in the interscapular region.

Hypertrophic obstructive cardiomyopathy.

Pansystolic murmurs have uniform intensity between 1st and 2nd heart sounds and merge
with the 2nd heart sound, which is therefore not distinguishable. Those at the lower sternal
border are more likely to be of regurgitant type due to:

Ventricular septal defect.

Atrial septal defect.

Mitral or tricuspid regurgitation.

Diastolic murmurs

Diastolic murmurs should always be regarded as pathological.

Early diastolic murmurs: occur just after the 2nd heart sound. They are high-pitched and easily
missed. Causes include aortic valve regurgitation (eg bicuspid aortic valve, Marfan's syndrome)
and pulmonary valve regurgitation (eg following surgery forFallot's tetralogyor pulmonary
stenosis), or with pulmonary hypertension.

Mid or late diastolic murmurs: are low-pitched and occur at the lower sternal borders in mitral
stenosis or tricuspid stenosis.

Continuous murmurs
These cross the 2nd heart sound and are a feature of:

Venous hum (otherwise they are always pathological).

Persistent ductus arteriosus.

Arteriovenous malformation.

Investigations

CXR, ECG and echocardiogram are often performed but add little or no information in a child
clinically assessed to have an innocent murmur.

Neonatologists and paediatric cardiologists are equally effective in diagnosing cardiac

pathology.

An echocardiogram is the gold standard for the diagnosis of a structural heart disease but is
not routinely required. Older toddlers who are asymptomatic when referred for echocardiogram,
are rarely found to have serious pathology.

Cardiac catheterisation is occasionally necessary.


23. THE CHILD WITH AN ITCHY RASH

Differentials:
-Acute:
Chicken pox: red vesicular rash over body caused by varicella zoster virus. Treatment: no
treatment necessary, fades away on its own.
Urticaria: flesh colored weals resulting from exposure to allergen or viral infection.
Treatment: no treatment necessary. Anti-histamines in some occasions.
Scabies: infestation with sarcoptes scabiei mite which burrows in epidermis. Papules and
vesicles occur between digits, axilla, buttocks, and in infants includes palms, soles, and trunk.
Treatment: permethrin cream. Must check all family members for infestation.
Impetigo (bullous): blistering form of impetigo due to staph aureus infection. Treatment:
systemic antibiotics.
Pityriasis rosea: viral origin, beginning with single oval scaly macule on trunk, upper arm,
neck, or thigh. Numerous small pink macules develop later. Treatment: no treatment required.
-Chronic:
Eczema: due to genetic deficiency of skin barrier function. Usually presents in 1st year of life
and uncommon in 1st two months. Rashes are itchy (key clinical feature) and excoriated
areas become weeping and crusted. Appear on face and trunk in infants, >2 months and on
flexor and friction surfaces in older children. Management: avoiding irritants, emollients,
topical corticosteroids, and immunomodulators.
Urticaria: chronic if persisting > 6 weeks, non-allergenic, due to local increase in permeability
of capillaries and venules.

Investigations: no investigations usually needed as diagnosis is clinical.

Rash terminology:
Macule: nonpalpable, circumscribed, flat lesion (<1 cm in diameter
Papule: palpable , elevated lesion (<1 cm in diameter)
Maculopapular: combination of macular and papular lesions
Vesicle: fluid-filled, elevated skin lesion (<1 cm in diameter)

Questions to ask:
When did the rash start?
Where did the rash start?
Where has the rash spread to?
Has there been any change in the rash (appearance, sensation, etc.)
What has been used to treat the rash?

25. EASY BRUISING AND BLEEDING

ETIOLOGY Summary:
1. Thrombocytopenia (reduced platelet count)
a. Disorders of platelet adhesion
b. Impaired platelet production
c. Platelet dysfunction
d. Destruction/Consumption of platelets
2. Non-Thrombocytopenia (normal platelet count)
3. Acquired disorders of coagulation

DIFFERENTIAL OF THROMBOCYTOPENIA
1. Disorders of platelet adhesion
a. Von Willebrand disease (vWD)
b. Bernard-Soulier syndrome (absence or dysfunction of GpIb/IX)
2. Impaired platelet production
a. Fanconi anemia
b. Wiskott-Aldrich syndrome
3. Platelet dysfunction
a. Glanzmann thromboasthenia (rare; (absence or dysfunction of GpIIb/IIIa))
4. Increased platelet destruction or consumption
a. Immune
i. Idiopathic thrombocytopenic purpura
ii. SLE
b. Non-immune
i. Hemolytic uraemic syndrome (HUS)
ii. Thrombotic thrombocytopenia purpura (TTP)
iii. DIC
iv. Congenital heart disease
v. Hypersplenism
c. Acquired
i. Aplastic anemia
ii. Leukemia (malaise, infection, pallor, splenomegaly, lymphoadenopathy)
iii. Drugs
Thrombocytopenia (Mnemonic: HELP ME ITS DIC)
H
Haemolytic uraemic syndrome/Thrombotic thrombocytopaenic purpura

E

L

P

M

E

I

T

Eclampsia/HEELP/Acute fatty liver

Liver disease/portal hypertension
Prosthetic heart valve
Malignancy/Marrow failure
Error (laboratory artifact)
Idiopathic thrombocytopaenic purpura
Transfusion

D

I

C

Storage diseases/hypersplenism
Drugs (heparin, antibiotics)
Infection/sepsis
Collagen vascular disease (especially lupus)

DIFFERENTIAL NON-THROMBOCYTOPENIC BRUISING

(Platelet count is NORMAL)
Vascular disorders
Congenital: Connective tissue disorders
o Marfan syndrome, Ehlers-Danlos, hereditary hemorrhagic telangiectasia
Acquired
o Meningococcal septicemia
o Vasculitis (i.e. Henoch-Schonlein Purpura (HSP), SLE, Scurvy)
o Trauma (accidental or non-accidental)

ACQUIRED COAGULATION DISORDERS

Vitamin K deficiency (mainly neonates or early infancy)
o Inadequate intake
o Malabsorption (celiac disease, cystic fibrosis, obstructive jaundice)
o Vitamin agonist (warfarin)
Liver disease
Idiopathic (ITP) immune thrombocytopenia
Disseminated intravascular coagulation (DIC)

ESSENTIAL QUESTIONS IN HISTORY TAKING:

1. Age of onset
a. 2-10 years: ITP
b. Adolescent: von Willebrand disease may present with menorrhagia
2. Duration between trauma and the signs of bleeding
a. Platelet disorder: bleeding comes on immediately after trauma
b. Coagulation disorder: bleeding occurs hours to days after injury
c. Meningiococemia: acute episode
3. Family hx
a. Autosomal dominant (Platelet defect)
b. Autosomal recessive (Coagulation defect)
c. X-linked recessive = all boys (Coagulation defect i.e. hemophilia)
4. Bleeding history
a. Previous surgical procedures; including dental extractions
b. After recent viral infection (ITP)
5. Pattern of bleeding
a. Mucous membrane bleeding (i.e. von Willebrand disease, thrombocytopenia)
i. Bleeding after brushing teeth
ii. Epistaxis
b. Skin hemorrhage (i.e. von Willebrand disease)
c. Distribution of petechiae or purpura
i. Lesion confined to buttocks, extensor surfaces of arms and legs (HSP)
ii. Wide spread: ITP
d. Bleeding into muscles or into joints (hemophilia)
e. Hematuria? (HSP)
6. Scarring and delayed hemorrhage (connective tissue disorders)
7. Blanching or non-blanching (meningococcal septicemia)
8. History of recent trauma
9. Concurrent disease
10. Diet: Does your child eat a lot of leafy greens i.e. spinach?
11. Drug history i.e. anticoagulants

12. Unusual pattern or inconsistent history ! Non-accidental injury = Abuse

a. Bruising to cheeks, orbits, hidden/healed fractures
b. Shape: whiplash, bite, pinch
EXAMINATION:
Skin lesion
o Purpura
o Petechiae
o Ecchymoses
Hepatosplenomegaly
Lymphadenopathy
Pallor
Distribution of purpura
Palpable or non-palpable lesions
Swollen tender joints

INVESTIGATIONS:
1. Full blood count
a. Evaluate for anemia, neutropenia
2. Blood film
3. Bleeding time
a. Prothrombin Time (PT) measures factors II, V, VII, X
b. Activated partial thromboplastin time (aPTT) measures II, V, VIII, X, XI, XII
4. Thrombin time: deficiency/dysfunction of fibrinogen
5. D-dimers: fibrin degradation products
6. Coagulation Screen
7. Platelet count
8. Liver Function test
9. Renal Function test
10. Bone marrow biopsy (Leukemia or if child is to be treated with steroids)
11. SLE screening
Disorder
PT aPTT Platelet Count
Bleeding Time

Haemophilia A
N


vWD N

N


DIC

Or N

ITP N
N

N

TTP N
N

N

Qualitative Defects
N

Liver Disease

Coag Pathophysiology Differential Diagnosis

1. Prolonged Prothrombin Time

The PT evaluates the extrinsic pathway of coagulation (II, V, VII
and X and fibrinogen).
Liver disease

2. Vitamin K deficiency
3. Warfarin
4. Factor VII deficiency

1. Prolonged aPTT (activated partial thromboplastin time) The aPTT evaluates the intrinsic
coagulation pathway (VIII, IX, XI and XII)
Heparin administration (this is the most common

2.
3.
4.
5.
a.
b.
c.
d.
e.

caused - blood drawn from a line flushed with heparin)

von Willebrand's disease
Lupus anticoagulant
Acquired factor inhibitors
Factor deficiencies:
Factor VIII (Haemophilia A)
Factor IX (Haemophilia B)
Factor XI
Factor XII

TREATMENT
Summary:
Usually supportive with colloid/blood transfusion if significantly anemia or hypovolemic.
Correct known coagulation or platelet abnormalities
Life-threating bleed! treat with blood (Fresh Frozen plasma)
Avoid IM injections, arterial puncture and NSAIDs
Seek hematologist and contact blood bank

1. Von Willebrand Disease

1. DDAVP
2. Plasma-derived F VIII concentrate (severe cases)

2. ITP
1. Acute
i. Oral prednisolone
ii. Intravenous anti-D
iii. Intravenous immunoglobulin
iv. Platelet transfusions (life-threatening hemorrhage)
2. Chronic =
i. Monoclonal antibodies i.e. rituximab
ii. Thrombopoietic growth factors
iii. Splenectomy (patients will require lifelong prophylactic antibiotics)

3. DIC
1. Treat underlying cause
2. Fresh frozen plasma
3. Cryoprecipitate

4. Platelets
5. Anti-thrombin and protein C concentrates

26. THE PALE CHILD

Pale child is a child whos skin colour is light. It is usually evident in te face/lips/hands. It is caused by
reduction in RBCs or decreased blood flow.

Causes/DDX of pale child:

Anemia (blood loss, poor nutrition or underlying condition eg sickle- most common)
Leukemia

Vitamin D deficiency
Illness (common cold, hypoglycemia,hypothyroid, etc.)

How to approach a child who is pale?

History:
age, sex, race, ethnic background
Duration of pallor
if child was sick, abdominal pain, wt loss, lethary,joint pain, bleeding..
nutrition (important)- type of milk if bottle-fed, duration of breastfeeding; timing of solids
introduction and whether an iron-fortified cereal was included after six months of age, cow's
milk can cause iron deficiency.
birth - preterm, child received supplements
Family history - should include any history of anaemia, jaundice, early onset of gallstones or
splenectomy (which may indicate hereditary spherocytosis). The mother's dietary history is
also important as a vegetarian mother deficient in B12 may have a B12-deficient child.

Physical:
- Look for palmar crease pallor and conjuctival pallor.
- Pallor and presence of jaundice can be assessed by an examination of the skin, conjunctiva
and creases of the palm. The presence of cafe-au-lait spots may indicate Fanconi's anaemia
- Bruising or petechiae may belie a low platelet count and suggests the possibility of leukaemia.
- Abdominal examination may reveal liver or spleen enlargement
- Heart rate, respiratory rate, temperature and BP.
- A cardiac flow murmur may be present if the child is anaemic.
- The child should also be examined for the presence of lymphadenopathy.

Treatment:
ABCs, assess severity of paleness and whether or not they require ventilation (o2 saturation). Then
check weight and height and plot on chart. Check vitals. Check if any dehydration present and give IV
fluids. If cause is anaemia then treat anemia (if iron def supplement iron, vit d def ) basically treat
underlying cause of paleness.

27. THE CHILD WHO IS BED WETTING

Also known as nocturnal enuresis, due to genetically determined delay in acquiring sphincter
competence. More common in males than females, usually with a first degree relative affected.
Organic causes:
Urinary tract infection
Polyuria from osmotic diuresis (e.g. DM)
Severe fecal retention causing a reduction in bladder volume and causing bladder neck
dysfunction
On examination: child is usually normal both physically and psychologically.
Differentials: UTI, constipation, DM
Investigations: Urinalysis is not recommended unless bedwetting is of recent origin, there are
daytime symptoms, or symptoms suggesting infection or DM. Investigate (and treat) daytime
symptoms before addressing enuresis, eg symptoms suggestive of diabetes, UTIs or constipation.
Treatment/management:
Considered usually after child is > 6 years old
1. Enuresis alarm: sensor placed in childs pants, sounds an alarm when it becomes wet to wake
child up to go to bathroom. Usually effective but requires time/patience.
2. Desmopressin: for short term relief from bed-wetting, the analogue of antidiuretic hormone is
given as tablets or sublingually.
Questions to ask:
1. Whether the bedwetting started in the last few days or weeks. If so, consider whether this is a
presentation of a systemic illness (DM)
2. How many nights a week does bedwetting occur?
3. How many times a night does bedwetting occur?
4. Does there seem to be a large amount of urine?
5. The presence of daytime symptoms in a child with bedwetting, including:
daytime frequency (more than 7 times a day)
daytime urgency
daytime wetting
passing urine infrequently (fewer than four times a day)
abdominal straining or poor urinary stream
pain passing urine.

29. A CHILD WITH NECK SWELLING

DIFFERENTIALS:
1. Infection
a. Bacterial (erythematous, warm, tender; most common cause)
i. Streptococcus, group A beta-hemolytic
ii. Staphylococcus aureus
iii. Toxoplasmosis (generalized lymphadenopathy)
iv. Cat Scratch disease (Bartonella henselae)
v. Haemophilus influenzae
vi. Peritonsillar abscess
vii.Tonsillitis
b. Viral (tender, non-erythematous/warm)
i. HIV
ii. CMV
c. Fungal
i. Actinomycosis
ii. Histoplasmosis
d. Tuberculosis
i. Mycobacterium tuberculi (cold, non-tender; systemic symptoms)
ii. Atypical Mycobacterium
2. Non-infectious inflammatory mass
a. Sarcoidosis
b. Sialadenitis
3. Tumor
a. Benign
i. Teratoma
ii. Desmoid tumor
iii. Lipoma
b. Malignant
i. Lymphoma (firm, non-tender cervical lymphadenopathy adherent to overlying
skin or underlying structures; systemic symptoms)
ii. Leukemia
iii. Rhabdomyosarcoma
iv. Neuroblastoma
4. Non-lymphadenomatous neck swellings
a. Sternocleidomastoid swelling
b. Thyroid gland enlargement
c. Thyroglossal cyst
d. Dermoid cyst
e. Branchial cyst (MC congenital neck mass)
f. Thymic cyst
g. Mumps
5. Vascular lesions
a. Hemangiomas
b. Cystic hygroma
6. Other
a. Head lice
b. Kawasaki Disease

IMPORTANT QUESTIONS FOR HISTORY TAKING:

Acute or Chronic Swelling
Symptoms:
o Painful or non painful?
o Fever?
o Night sweats?
o Weight loss?
o Does your child have difficulty breathing? (lesion causing compression)
Was the child immunized with BCG vaccine? MMR?
Family history of TB
History of contact with TB?
Recent upper respiratory tract infection?
Recent earache or toothache?
Recent head lice infestation or contact with already infested person?
o Tickling feeling of something moving in the hair
o Itchy scalp or sores on the head?
Travel in the last 6 months?

EXAMINATION:
Characteristics of the swelling
o Location
Midline: thyroglossal duct cyst, dermoid and epidermoid cyst, cervical clefts or
teratomas
Lateral neck: branchial cleft anomalies, lymphatic or vascular malformations
Supraclavicular: lymphoma
o Shape oval, hemispherical, irregular
o Size width, length and height
Cervical and axillary lymph nodes enlargement > 1 cm in diameter
Inguinal nodes enlargement > 1.5 in diameter
Supraclavicular enlargement (needs further investigation)
o Temperature warm vs. cold
o Surface smooth vs. irregular
o Consistency soft, firm, hard
o Translucency
o Fluctuation
o Color -erythema
o Tenderness
o Mobile
Moves with swallowing ! thyroglossal duct cyst
o Fluctuation (indicative of pus formation/abscess)
o Attached to the skin
o Pulsatility
o Compressibility
o Bruits
Torticollis?
Must check all lymph nodes
Systemic review:
o ENT
o Abdomen: Hepatosplenomegaly?

INVESTIGATIONS:
Full blood count and film
Coagulation study
Acute Phase reactants
o C-reactive protein
o ESR
Blood culture
Anti-streptolysin O titre
Paul-Bunnell test: tests for glandular fever (infectious mononucleosis)
Chest X-ray
Mantoux test
Viral serology

o HIV
o CMV
o Epstein-Barr virus (Infectious mononucleosis)
Fine Needle aspiration (gram stain, culture, acid fast stain, immunocytochemistry,
cytogenetics)
Biopsy of mass
Imaging
o Neck ultrasound (cystic vs. non-cystic)
o CT
o MRI
Thyroid function test
o TSH
o T3 and T4
Thyroid antibodies
o Thyroglobulin antibodies
o Thyroid peroxidase antibodies

TREATMENT:
Analgesia
Streptococcal/Staphylococcal infection: 10 day course of antibiotics i.e. co-amoxiclav
Complete surgical excision (i.e. branchial cleft cyst, thyroglossal duct cyst, dermoid cysts)
Pus/Abscess: surgical incision and drainage
TB treatment
o 6-9 months:
Isoniazid
Rifampin
Ethambutol
Pyrazinamide
o 2 months following above:
Isoniazid
Rifampin
Malignancy
o Chemotherapy
o Radiation
o Excision


30. The child with a squint (starbismus)

Background:
Common Condition, were there is misalignment of the visual axes.
May be associated with positive family history.
Newborn babies have transient misalignment up to 3 months of age.

Etiology:
Is caused by either failure to develop binocular vision due to refractive errors,(most common cause),
cataracts, and retinoblastoma.

Types:
1. Non paralytic: common: due to refractive error in both eyes, which is corrected with
glasses. Common in children with neurodevelopmental dely.
2. Paralytic: varies with gaze direction, and is due to paralysis of motor nerves.(may indicated
underlying space occupying lesion.

Focused History Questions:

WHEN? When is the deviation present? (eg, constantly? With fatigue? Only in certain positions
of gaze?)

DURATION AND SEVERITY What is the duration and severity of the deviation?

PMH as the deviation been present since early infancy?

PMH Is there any history of trauma?

PMH Is there any history of any other medical problems (eg, headaches)?

PMH Is there a history of exposure to toxins or medications?

PMH What is thedevelopmental/birthhistory?

FMH Is there a family history of strabismus?

Physical Examination: assessment of general health and

neurologic status, including an assessment of development. The
presence of a consistent head tilt or turn should be noted
4 main steps to look for squint:
1. LOOK 3x
2. Corneal light reflex test: Choose an accommodative target
(eg, a small toy) is held several feet in front of the child's
face, and a penlight is held next to the toy = Check if eye
reflection is symmetrical at same point in each eye.(refer
to supplementary diagram)
3. Do the Eye movement: The H.
4. Cover test: the good eye is covered with a piece of paper,
this will result in fixation of the squinting eye.
Treatment:
1. Glasses.
2. Eye patch on good eye, so the squint fixes
3. Surgery: mainly to prevent amblyopia(blindness)

The corneal light reflex test

involves shining a light onto
the child's eyes from a
distance and observing the
reflection of the light on the
cornea with respect to the
pupil. The location of the
reflection from both eyes
should appear symmetric
and generally slightly nasal
to the center of the pupil. A)
Normal corneal reflex. B)
Corneal light reflex in