Here is your full paediatric ward preparation guide. I've organized it by disease cluster so you can understand the "why" behind each diagnosis and be ready for any case.
Paediatric End-of-Posting Exam - Ward Prep Guide
CLUSTER 1: RESPIRATORY - BRONCHIAL ASTHMA & AEBA
Beds: 1A (Firas, 11y), 9A (Syuhadah, 8y), 15 (Ain Nadeera, 6y)
Why do these kids have asthma?
Asthma is a chronic inflammatory airway disease driven by the atopic triad: asthma + allergic rhinitis + eczema. All three are IgE-mediated Type I hypersensitivity reactions. When a genetically atopic individual (usually with FHx) is exposed to allergens (dust mites, mould, pet dander), B cells produce IgE. This IgE binds mast cells. On re-exposure, mast cells degranulate releasing histamine, leukotrienes (LTC4, LTD4), and prostaglandins - causing bronchoconstriction, mucus hypersecretion, and mucosal oedema.
The atopic march: eczema typically appears first in infancy, followed by allergic rhinitis, then asthma. These kids on the ward demonstrate this perfectly - Firas (Bed 1A) has all three.
Why AEBA now?
- Atypical pneumonia (Firas): Mycoplasma pneumoniae is the #1 trigger in school-age children. It produces a cytotoxin that directly damages airway epithelium AND drives Th2 immune response that worsens underlying airway hyperreactivity.
- URTI (Syuhadah, Ain Nadeera): Viral URTIs (rhinovirus, influenza) are the most common AEBA triggers. Viruses infect airway epithelium, causing neurogenic inflammation and increasing bronchial hyperresponsiveness.
- Sick contact with schoolmates - typical history for school-age kids.
AEBA Classification (GINA / Malaysian CPG)
| Severity | SpO2 | Breathlessness | PEFR | Treatment |
|---|
| Mild | ≥95% | Walking, can talk in sentences | >60% | Salbutamol MDI 2-4 puffs q20min x3, oral prednisolone |
| Moderate | 92-95% | At rest, phrases | 40-60% | Salbutamol nebuliser, IV hydrocortisone or oral pred |
| Severe | <92% | Words, accessory muscle use | <40% | Continuous nebulisation, IV hydrocortisone, consider Mg2+, ICU |
| Life-threatening | <90% | Silent chest, altered GCS | <25% | ICU, IV magnesium sulfate, IV salbutamol |
Firas (Bed 1A) is mild persistent asthma + AEBA + obstructive sleep apnea (from obesity). Key point: obesity causes restrictive mechanics + upper airway fat deposition = worsens OSA AND asthma control. Atypical pneumonia (Mycoplasma) causes low-grade fever, dry cough, minimal auscultatory findings ("walking pneumonia") but green sputum + worsening suggests secondary bacterial infection.
Ain Nadeera (Bed 15) - rhonchi with GOOD air entry, NO creps = pure bronchospasm/AEBA without consolidation. Moderate AEBA sec to URTI.
Syuhadah (Bed 9A) - rhonchi over LEFT lung + pneumonia = AEBA precipitated by pneumonia. The unilateral finding suggests the pneumonia is left-sided.
CLUSTER 2: PREMATURITY & BPD
Beds: 3A (Puteri Cahaya, 2y9m, 27+3 weeks), 8A (Azzhra, 1y5m, 26 weeks)
Why did these children get BPD?
Bronchopulmonary Dysplasia (BPD) is the most common severe complication of extreme prematurity. The mechanism:
- Immature lungs at 26-27 weeks: alveoli are at the saccular stage, surfactant deficient, fragile capillary-epithelial interface
- Respiratory distress syndrome (RDS) at birth requires mechanical ventilation + high O2
- Volutrauma + oxygen toxicity causes inflammatory injury to immature alveoli
- Arrested alveolar development: fewer, larger alveoli ("new BPD") rather than the fibrous scarring of old BPD
- Result: chronic lung disease (CLD), reduced gas exchange, airway hyperreactivity, pulmonary hypertension
New BPD definition (Jobe/Bancalari): Need for supplemental O2 at 36 weeks corrected gestational age.
Why PPHN in Puteri Cahaya?
At 27 weeks, the pulmonary vasculature is immature and hypoxia/acidosis from RDS/pneumothorax causes failure of normal postnatal drop in pulmonary vascular resistance - PVR stays high, blood shunts R→L through PDA and foramen ovale (bypassing the lungs). This is PPHN.
Why the left pneumothorax?
Mechanical ventilation with high pressures in fragile premature lungs can cause air leak syndrome - air ruptures alveoli, tracks to pleural space = pneumothorax. Left-sided in her case.
Other complications from extreme prematurity (Puteri Cahaya)
| Complication | Mechanism |
|---|
| Congenital hypothyroidism | Immature hypothalamic-pituitary-thyroid axis; iodine deficiency in NICU; thyroid dysgenesis. Screened by day 3 TSH/T4. |
| Bilateral ROP | Hyperoxia from O2 therapy suppresses VEGF → retinal vessel growth stops. When O2 is removed, VEGF spikes → abnormal neovascularization. Classified Zone I-III, Stage 1-5. |
| PVL (periventricular leukomalacia) grade 1 | Ischaemia/reperfusion injury to periventricular white matter (watershed zone in premature brain). Grade 1 = bilateral periventricular echodensities without cystic change. Risk of cerebral palsy and cognitive delay. |
| Subependymal cyst | Small haemorrhage or ischaemic injury in germinal matrix - the subependymal germinal matrix is highly vascular and fragile in preterm infants |
Why acute exacerbation of CLD now?
BPD lungs have:
- Reduced alveolar reserve
- Chronic airway hyperreactivity
- Intermittent pulmonary hypertension
Any respiratory insult (CAP, viral LRTI) causes disproportionate respiratory decompensation. Hence rhonchi + crepitations + rapid breathing with relatively minor precipitants.
Azzhra (Bed 8A): Similar profile - 26-weeker with BPD. Bibasal crepitations = bronchopneumonia on background of already-damaged lungs.
CLUSTER 3: PAEDIATRIC PNEUMONIA
Beds: 4A (Syafiatunnisa, 11m), 6A (Athif, DCM), 10 (Aish, 9m), 16 (Naqi, 4m, RSV), 23 (Kai Wen, 5m), 28 (Ayden, 1y9m, ALL)
Why do young infants get pneumonia so easily?
- Immature innate immunity (low IgG from transplacental transfer wanes by 3-6 months)
- Short, horizontal Eustachian tubes - nasopharyngeal organisms spread easily
- Narrow airways - small amounts of secretions cause disproportionate obstruction
- Obligate nose breathers (infants <3m) - any nasal congestion = respiratory distress
Pathogen by age (key for exams)
| Age | Most Likely Pathogen |
|---|
| 0-3 months | GBS, E. coli (neonatal), Chlamydia trachomatis (afebrile pneumonia) |
| 3m - 5 years | RSV, parainfluenza, rhinovirus (viral); Streptococcus pneumoniae (bacterial) |
| School age | Mycoplasma pneumoniae (#1 atypical), S. pneumoniae |
Naqi (Bed 16) - RSV Pneumonia
RSV is the #1 cause of lower respiratory tract infection in infants <2 years. It infects bronchiolar epithelium, causing:
- Mucosal oedema + necrotic debris plugs bronchioles
- Air trapping → hyperinflation
- V/Q mismatch → hypoxaemia
In infants, this causes bronchiolitis (wheeze, creps); in older children it causes pneumonia. The ward covers for secondary bacterial infection because RSV disrupts mucociliary clearance, allowing S. pneumoniae/S. aureus superinfection.
Athif (Bed 6A) - DCM with Bronchopneumonia
Why does DCM predispose to pneumonia? Dilated cardiomyopathy → low cardiac output → pulmonary venous hypertension → pulmonary oedema → fluid-filled alveoli are perfect culture medium for bacteria. Also, hepatomegaly from right heart failure elevates the diaphragm, worsening lung volumes. Key point: in any child with cardiac disease, pneumonia is more severe, harder to treat, and you must be cautious with IV fluids (risk of fluid overload).
Ayden (Bed 28) - Pre-B ALL with Bronchopneumonia
Why so immunocompromised? B-cell precursor ALL → bone marrow crowded with blasts → reduced neutrophil production (neutropenia) → bacterial/fungal susceptibility. Also chemotherapy itself causes further myelosuppression. Transaminitis here likely from: hepatic infiltration by blasts + chemotoxicity + possible viral hepatitis. Hepatosplenomegaly = extramedullary haematopoiesis + organ infiltration by leukaemic blasts.
CLUSTER 4: BRONCHIOLITIS
Bed 13 (Faiha, 5m)
Classic bronchiolitis presentation
Faiha is 5 months with noisy breathing (wheeze), recession, cough, rapid breathing, vomiting. This is textbook bronchiolitis.
Pathophysiology: RSV (most common) infects bronchiolar epithelium → inflammation, necrosis, mucus plugging → partial bronchiolar obstruction → air trapping (hyperinflation on CXR) + hypoxaemia. The wheezing is from partial obstruction, not bronchospasm per se - which is why salbutamol has limited benefit.
Why does bronchiolitis occur only in infants? Because bronchioles are relatively narrow in infants; the same degree of mucosal swelling causes critical obstruction. Older children/adults get the same virus but it stays as a URTI.
Management (GINA/Malaysian guidelines for bronchiolitis):
- Supportive: O2 to maintain SpO2 ≥92%, nasogastric feeds if can't suck
- NOT routinely recommended: nebulised salbutamol, nebulised adrenaline (may try once and assess), steroids, antibiotics
- Indication for ICU: apnoea, SpO2 persistently <92% on high flow O2
CLUSTER 5: FEBRILE SEIZURES & CNS
Beds: 20 (Qawiy, 2y7m, simple febrile fit), 31 (Al Fateh, 10m, complex febrile fit), 18 (Zahin, 11y, meningoencephalitis), Ps18 (Ayyash, 2y11m, G6PD + febrile seizure), Bed 29 (Aryan, 5m, afebrile seizure)
Simple vs Complex Febrile Seizure
| Feature | Simple | Complex |
|---|
| Duration | <15 min | >15 min |
| Type | Generalized | Focal OR |
| Recurrence in 24h | No | Yes (recurs in same illness) |
| Postictal state | Brief | Prolonged |
| Risk of epilepsy | ~1-2% (same as general population) | Higher |
Qawiy (Bed 20): Simple febrile fit + tonsillitis. The fever from acute tonsillitis rapidly crosses the threshold in a susceptible 2-year-old. Key: the "seizure threshold" is genetically determined and lower in children 6m-5y (peak 18m-2y). As the brain matures, threshold rises and fits stop.
Al Fateh (Bed 31): UNVACCINATED + complex febrile fit + transaminitis. The unvaccinated status immediately raises concern for measles, hepatitis A, pertussis. Complex fit = need to rule out bacterial meningitis/encephalitis. Cover for secondary bacterial infection = likely on IV ceftriaxone/cefotaxime pending LP.
Zahin (Bed 18): 11-year-old with fitting + fever. Meningoencephalitis until proven otherwise. Mother refused LP - this is a management dilemma. Without CSF analysis, you treat empirically:
- Bacterial meningitis cover: IV ceftriaxone 100mg/kg/day + dexamethasone (reduces hearing loss from pneumococcal meningitis)
- Viral/HSV encephalitis cover: IV aciclovir 10-15mg/kg/dose TDS
- Anti-epileptics for seizure control (IV levetiracetam or phenobarbitone)
Clinical pearl for exam: Kernig's and Brudzinski's signs are unreliable in children <18 months. In young infants, bulging fontanelle + irritability + paradoxical crying = meningism equivalent.
G6PD Deficiency (Beds 14, Ps18)
Why do these children have G6PD deficiency?
- X-linked recessive - more common in Malay/Chinese/African males
- G6PD is required in the hexose monophosphate shunt to generate NADPH, which regenerates glutathione (antioxidant)
- Without NADPH, oxidative stress from drugs/infection/food (fava beans) → Heinz body formation → intravascular haemolysis
In paediatric ward context: The G6PD-deficient children (Muhammad Iman Bed 14, Ayyash Ps18) with fever/infection are at risk of haemolytic crisis. Avoid:
- Primaquine, dapsone, nitrofurantoin
- High-dose aspirin
- Fava beans
- Naphthalene (mothballs)
Muhammad Iman (Bed 14): G6PD + multi-trigger wheeze + bronchopneumonia. "Multi-trigger wheeze" in a 2-year-old is distinct from asthma - it implies wheeze with every viral URTI (not interval symptoms), which may be viral-induced wheeze that resolves by age 6 rather than true persistent asthma.
CLUSTER 6: NEPHROTIC SYNDROME
Beds: 24 (Luth, 5y10m), 25 (Adam, 5y)
Why do children get nephrotic syndrome?
In children 1-8 years, 80-90% is Minimal Change Disease (MCD) - the most important thing to know. MCD is caused by T-cell dysfunction that releases a circulating factor damaging podocytes (the filtration slit diaphragm cells). The slit membrane is disrupted → massive protein leak → proteinuria >3.5g/day in adults, >40mg/m2/hr in children.
The consequences (pathophysiology chain)
Proteinuria → Hypoalbuminaemia → Low oncotic pressure → Fluid leaks into interstitium → Oedema (periorbital/facial first, then dependent, then ascites, pleural effusion, scrotal) → Reduced intravascular volume → Renin-Angiotensin-Aldosterone activation → Na and water retention → Worsens oedema (Underfill theory)
Anasarca = generalised oedema affecting all compartments - Luth (Bed 24) has this + right pleural effusion.
Why "frequent relapse steroid-dependent"?
- First episode: 4 weeks of daily prednisolone then 4 weeks alternate day = induction
- Relapse: proteinuria ≥2+ for 3 consecutive days after remission
- Frequent relapser: ≥2 relapses in 6 months, OR ≥4 in 12 months
- Steroid dependent: 2 consecutive relapses during steroid taper OR within 2 weeks of stopping
- These children eventually need steroid-sparing agents: levamisole, cyclophosphamide, mycophenolate mofetil, or calcineurin inhibitors (tacrolimus/ciclosporin)
Luth (Bed 24): Autism + nephrotic syndrome - the autism means medication compliance is harder to assess (child may not articulate symptoms). Faltering height from steroid toxicity is a major complication - chronic steroid use causes growth suppression (inhibit GH axis at multiple levels), adrenal suppression, osteoporosis, cushingoid features.
Complications you must know:
- Infection (most dangerous) - low IgG (lost in urine), low complement C3 → Streptococcus pneumoniae peritonitis/sepsis. Cover with phenoxymethylpenicillin prophylaxis.
- Thrombosis - loss of antithrombin III + high fibrinogen → hypercoagulable state → DVT, renal vein thrombosis
- Hyperlipidaemia - liver compensates protein loss by making lipoproteins
- Right pleural effusion (Luth) = fluid tracking along diaphragmatic lymphatics from ascites
CLUSTER 7: GROWTH HORMONE DEFICIENCY
Bed 26 (Muha Farha, 6y)
Why GH deficiency causes short stature
GH is secreted from anterior pituitary → stimulates liver to produce IGF-1 → promotes bone growth at growth plates. Without GH: reduced IGF-1 → reduced chondrocyte proliferation → slow linear growth. Presentation: height <-2SD for age, growth velocity <4-5cm/year, delayed bone age on wrist X-ray.
In exam: Must know GH stimulation tests (clonidine, glucagon, insulin tolerance test). GH <10mU/L (or <3.3 ng/mL on two separate stimulation tests) = deficiency. Treatment = recombinant human GH (rhGH) subcutaneous injection.
CLUSTER 8: TUBERCULOSIS
Bed 27
Why does paediatric TB present differently from adults?
- Children (especially <5 years) have immature cell-mediated immunity → cannot contain primary TB → more likely to progress to primary progressive disease, miliary TB, TB meningitis
- TB in children usually primary pulmonary TB with hilar lymphadenopathy (not cavitating adult-pattern disease)
- Key presentation in kids: prolonged fever >2 weeks, failure to thrive, night sweats, contact with TB adult
- Diagnosis in children: difficult because paucibacillary (can't spit sputum well), so rely on Mantoux/IGRA + CXR + gastric lavage/induced sputum
- Malaysia CPG: treat with 2HRZE/4HR (isoniazid, rifampicin, pyrazinamide, ethambutol for 2 months, then 4 months HR)
CLUSTER 9: OTHER HIGH-YIELD CASES
Bed 21 (Snake Bite - Nur Alisha)
- Management of alleged snakebite: ABC, immobilise limb, keep calm (slow lymphatic spread), observe for envenomation signs: local necrosis, coagulopathy (check PT/APTT/FBC), neurotoxicity (ptosis, ophthalmoplegia, respiratory paralysis)
- Antivenom (polyvalent or monovalent) indicated if: systemic envenomation OR progressive local swelling
Bed 24 (Alleged perfume ingestion - Hanania, 1y11m)
- Perfumes = ethanol + other hydrocarbons
- Ethanol ingestion in infants → rapid hypoglycaemia (limited glycogen stores + alcohol inhibits gluconeogenesis)
- Management: ABC, check glucose, observe for CNS/respiratory depression, activated charcoal NOT useful (alcohol absorbed too fast)
Ps19 (Bullous Impetigo - Nuha, 1y11m)
- Caused by S. aureus phage type 71 producing exfoliative toxin (epidermolytic toxin)
- Toxin cleaves desmoglein-1 in the superficial epidermis → intraepidermal split → flaccid bullae
- Treat: flucloxacillin/cloxacillin (cover S. aureus including methicillin-sensitive strains)
- Note: bilateral crepitations on lung exam = associated pneumonia/sepsis needs systemic antibiotics
Ps21 (Herpangina - Shaqqera, 1y11m)
- Caused by Coxsackievirus A (enterovirus)
- Herpangina: fever + painful ulcers on posterior oropharynx (tonsils, soft palate, uvula)
- Viral exanthem: maculopapular rash from viraemia
- Distinguish from HFMD (Coxsackie A16/EV71): HFMD has lesions on hands, feet AND mouth
- Treatment: supportive (oral hydration, analgesia)
Bed 32 (Cervical Lymphadenitis - Syazwana, 11m)
- In infants, most common cause is S. aureus or Group A Strep
- Mycobacterial (atypical) lymphadenitis is important differential - more indolent, unilateral, non-tender, violaceous skin
- Management: IV/oral antibiotics (amoxicillin-clavulanate or cloxacillin), US to rule out abscess, incision and drainage if fluctuant
CLUSTER 10: DILATED CARDIOMYOPATHY (Athif, Bed 6A)
Why does Athif have DCM?
In children, causes of DCM include:
- Viral myocarditis (most common acquired) - Coxsackievirus B, adenovirus
- Genetic/metabolic - LMNA mutations, dystrophin deficiency (Duchenne), metabolic storage diseases
- Dysplastic mitral valve - valve abnormality can be primary (congenital) OR secondary to DCM-related ventricular remodelling
DCM → volume overload → progressive ventricular dilation → wall stress → further dysfunction (Law of Laplace: T = P×r/2h)
Signs of heart failure in children: tachycardia, S3 gallop, hepatomegaly, FTT, poor feeding, respiratory distress (pulmonary oedema).
Management of DCM in children: ACE inhibitor (captopril/enalapril), diuretics (furosemide), beta-blocker (carvedilol in older children), digoxin for rate/inotropy.
EXAM QUICK-FIRE SUMMARY TABLE
| Bed | Child | Diagnosis | Key Mechanism |
|---|
| 1A | Firas 11y | AEBA + atypical pneumonia | Atopic triad, Mycoplasma trigger |
| 3A | Puteri 2y9m | CLD exacerbation (ex-27-weeker) | BPD from prematurity + MV injury |
| 4A | Syafiatunnisa 11m | Viral pneumonia | Immature immunity, RSV/viral |
| 6A | Athif | Bronchopneumonia + DCM | DCM → pulm oedema → infection risk |
| 8A | Azzhra 1y5m | Bronchopneumonia, ex-26-weeker BPD | Arrested alveologenesis |
| 9A | Syuhadah 8y | AEBA + pneumonia | Viral trigger, Th2 inflammation |
| 10 | Aish 9m | Bronchopneumonia + bronchospasm | Narrow infant airways, viral |
| 13 | Faiha 5m | Bronchiolitis | RSV, bronchiolar obstruction |
| 14 | Iman 2y | Bronchopneumonia + G6PD | Multi-trigger wheeze, X-linked G6PD |
| 15 | Ain Nadeera 6y | Moderate AEBA + URTI | IgE-mediated bronchoconstriction |
| 16 | Naqi 4m | RSV pneumonia | RSV viraemia → LRTI |
| 18 | Zahin 11y | Meningoencephalitis | Refused LP, treat empirically |
| 20 | Qawiy 2y7m | Simple febrile fit + tonsillitis | Low seizure threshold 6m-5y |
| 21 | Alisha 9y | Alleged snakebite | Rule out envenomation |
| 24 | Luth 5y10m | Nephrotic 6th relapse + anasarca | MCD, podocyte injury, steroid dependent |
| 25 | Adam 5y | Nephrotic relapse | Steroid dependent MCD |
| 26 | Farha 6y | GH deficiency | Low IGF-1, reduced linear growth |
| 27 | - | TB | Primary progressive TB in child |
| 28 | Ayden 1y9m | Bronchopneumonia + pre-B ALL | Neutropenia from leukaemia/chemo |
| 29 | Aryan 5m | Afebrile seizure + ptosis | Structural/metabolic seizure |
| 31 | Al Fateh 10m | Complex febrile fit | Unvaccinated, rule out meningitis |
| 32 | Syazwana 11m | Cervical lymphadenitis | Staph/Strep |
| 34 | Hanania 1y11m | Perfume ingestion | Ethanol → hypoglycaemia |
| Ps18 | Ayyash 2y11m | Febrile seizure + G6PD | Avoid haemolytic triggers |
| Ps19 | Nuha 1y11m | Bullous impetigo | S. aureus exfoliative toxin |
| Ps21 | Shaqqera 1y11m | Herpangina + viral exanthem | Coxsackie A |
TOP EXAM TIPS FOR ANY CASE YOU GET
- Always classify severity first (asthma, pneumonia, dehydration, seizure severity)
- Know the underlying condition cold - the examiner will always ask "why does this child have X?"
- Pathophysiology chain - for every diagnosis, know the full mechanism from cause to symptom
- Complications - know what can go wrong (especially in complex cases like DCM, ALL, nephrotic)
- For BPD/prematurity cases: know gestational age, birth weight, what interventions they had in NICU (surfactant, CPAP, O2, MV)
- For atopy cases: know the triad and the march - eczema → rhinitis → asthma
- For nephrotic: know the steroid protocol and relapse definitions by heart
- For febrile fits: ALWAYS rule out meningitis clinically before calling it simple febrile fit
Good luck with your exam! If you want me to do a deeper drill-down on any specific case or disease, just ask.
