🧠 MOCK OSCE · FCPS, MCPS, MD PAEDIATRICS ⏱ 10 min · NEUROMUSCULAR · AFP / GBS

Acute Flaccid Paralysis · Short Case

Candidate task: perform focused neuromuscular examination on a child with acute flaccid paralysis (AFP) / suspected Guillain-Barré syndrome (GBS).
Then discuss differential diagnosis, investigations, management & follow‑up.
Pre‑exam Protocol
· Wash, Warm, Introduce, Position, Expose, Approach

Standard pre‑examination protocol – must be demonstrated:

🖐 Wash hands with sterilizing solution.
🔥 Warm hands and stethoscope.
👋 Introduce yourself to child & parent.
🧍 Position child: supine, then sitting (if possible).
👕 Exposure — fully expose for neuromuscular exam, warm environment.
➡️ Approach from the right side.
CPSP marker: Pre‑exam Protocol is observed and scored.
1. Clinical Examination (≈6 min)
02 General Look (Inspection from end of bed)

Key observations – “Acute Flaccid Paralysis / GBS” clues:

  • Posture: flaccid, frog‑leg position (symmetrical or asymmetrical).
  • Movement: paucity of spontaneous movement, ascending weakness.
  • Facial features: bilateral facial weakness (lower motor neuron) – common in GBS.
  • Respiratory: shallow breathing, use of accessory muscles (respiratory failure risk).
  • Bulbar: drooling, weak cry, nasal regurgitation – bulbar involvement.
  • Autonomic: flushing, sweating, tachycardia, hypertension – dysautonomia.
👁 Red flags: ascending symmetrical weakness + areflexia + autonomic instability → GBS.
03 Neuromuscular Examination (Tone, Power, Reflexes, Cranial Nerves)

Systematic neuromuscular exam – focus on pattern of weakness:

  • Tone: hypotonia (flaccid) – lower motor neuron pattern.
  • Power: MRC grading; symmetrical ascending weakness (proximal & distal).
  • Reflexes: absent or diminished – early and hallmark sign.
  • Cranial nerves: facial palsy (bilateral in GBS), bulbar weakness (IX, X, XII).
  • Sensory: may be normal (AMAN) or diminished (AIDP).
  • Autonomic: BP variability, heart rate changes, urinary retention.
  • Respiratory: diaphragmatic weakness (paradoxical breathing).
🔍 Key: areflexia + ascending weakness + autonomic dysfunction → GBS.
04 General Physical Exam (Hands → Face → Chest → Abdomen → Limbs)

Systematic examination – identify aetiology & complications:

  • Hands: distal weakness, thenar wasting (late).
  • Face: bilateral facial palsy (GBS), dry mouth (autonomic).
  • Chest: respiratory rate, use of accessory muscles, vital capacity (bedside).
  • Abdomen: ileus (autonomic), constipation.
  • Limbs: symmetrical flaccid weakness, loss of deep tendon reflexes.
  • Back: spine tenderness (transverse myelitis).
  • Skin: tick bite (tick paralysis), rash (Lyme).
📏 Anthropometry: weight, length, head circumference – plot growth.
05 Developmental Assessment & Associated Signs

Assess:

  • Motor milestones: regression (loss of walking, sitting).
  • Speech: dysarthria, nasal speech (bulbar).
  • Feeding: poor suck, dysphagia, aspiration.
  • Behaviour: irritability, pain (myalgia, radicular pain).
  • Autonomic: orthostatic hypotension, sweating, bladder dysfunction.
🧠 Red flags: rapid progression to respiratory failure, dysautonomia → ICU admission.

📋 Case Presentation – (fill in during exam)

This is a _____-year-old _____ child, referred for _____ (acute weakness / inability to walk / respiratory distress). On examination, the child appears _____ (well / unwell / in distress), with _____ (symmetrical flaccid weakness / asymmetrical). Cranial nerves: _____ (bilateral facial palsy / bulbar weakness / normal). Tone: _____ (hypotonic / flaccid). Power: _____ (proximal > distal / distal > proximal / global). Reflexes: _____ (absent / diminished / brisk). Sensory: _____ (normal / glove & stocking). Autonomic: _____ (BP variability / tachycardia / normal). Respiratory: _____ (normal / shallow / using accessory muscles). GPE: _____ (rash / tick / hepatomegaly). Growth: weight _____ percentile, length _____ percentile.

2. Viva Discussion (≈4 min)
06 Viva · Differential, Investigations, Management, Follow‑up
🔹 Differential Diagnosis

Guillain-Barré syndrome (GBS) – AIDP, AMAN, AMSAN
Acute transverse myelitis – sensory level, bowel/bladder dysfunction
Acute flaccid myelitis (AFM) – viral (enterovirus D68), asymmetric
Tick paralysis – ascending paralysis, areflexia, tick found
Botulism (infantile / food-borne) – descending paralysis, dilated pupils, constipation
Spinal cord compression – trauma, tumour, abscess
Poliomyelitis / non-polio enterovirus – asymmetric, fever
Metabolic / toxic – porphyria, lead, organophosphates
Myasthenia gravis – fatigable, ocular/bulbar
Periodic paralysis – hypokalaemia, hyperkalaemia

🔹 Investigations – Diagnosis

Lumbar puncture (CSF): albuminocytological dissociation (high protein, no cells) – classic for GBS.
Nerve conduction studies (NCS) / EMG: demyelinating (AIDP) or axonal (AMAN).
MRI spine: nerve root enhancement (GBS), cord lesion (myelitis).
Pulmonary function: vital capacity, MIP, MEP – monitor respiratory failure.
Blood cultures / serology: Campylobacter jejuni, Mycoplasma, CMV, EBV.

🔹 Investigations – Aetiology

Stool for enterovirus / poliovirus: AFP surveillance.
Serum anti-ganglioside antibodies: GM1, GD1a (AMAN), GQ1b (Miller-Fisher).
MRI brain/spine: demyelination (ADEM, MS).
Tick check: entire body, scalp, skin folds.
Toxin screen: heavy metals, organophosphates.

🔹 Investigations – Exclude Others

MRI spine: exclude transverse myelitis, cord compression, syrinx.
Lumbar puncture: exclude meningitis (pleocytosis).
Serum electrolytes: K+, Ca++, Mg++ (periodic paralysis).
Creatine kinase (CK): myopathy (elevated) vs neuropathy (normal).
Toxicology screen: lead, arsenic, porphyrins.

🔹 Investigations – Rule Out Complications

Pulmonary function (Vital capacity): monitor for respiratory failure.
Autonomic function: BP monitoring, ECG (arrhythmias).
Swallow study: aspiration risk (bulbar weakness).
Ultrasound bladder: urinary retention.
DVT prophylaxis: Doppler if immobile.

🔹 Management – Across Organ Systems

Respiratory

Monitor vital capacity, early intubation if VC < 15-20 mL/kg or MIP < 30 cmH2O. Non-invasive ventilation (BiPAP).

Immunomodulation

IVIG (0.4 g/kg/day × 5 days) or plasmapheresis – within 2 weeks of onset. Steroids NOT effective.

Autonomic

Continuous BP/HR monitoring; treat hypertension (labetalol), bradycardia (atropine).

Nutrition

NG / gastrostomy for bulbar weakness. High-calorie, DVT prophylaxis.

Physiotherapy

Passive/active ROM, positioning, prevention of contractures.

Multidisciplinary

Neurology, physiotherapy, occupational therapy, speech therapy, dietitian, social work.

📈 Prognosis

  • GBS (children): excellent recovery in 80-90%; most walk by 6 months.
  • AMAN: slower recovery, more residual weakness.
  • Respiratory involvement: 15-20% require ventilation; usually recover.
  • Miller-Fisher: good prognosis, full recovery.
  • Acute flaccid myelitis: variable; may have permanent weakness.
  • Tick paralysis: rapid recovery after tick removal.

📋 Follow‑up Schedule

  • Acute phase: daily respiratory and neurological monitoring (ICU).
  • Post-acute: weekly / monthly for physiotherapy and functional recovery.
  • Long-term: 6-monthly to annually for residual weakness, fatigue.
  • Relapse: < 5% (acute-onset CIDP).
💡 Examiner expectation: logical differential (ascending vs transverse vs descending), systematic investigation (CSF, NCS, MRI), and a management plan with respiratory support, IVIG/plasmapheresis, and rehabilitation. Know the albuminocytological dissociation and NCS patterns for GBS.
Mock OSCE · Acute Flaccid Paralysis (AFP) / Guillain-Barré Syndrome · Based on Wyne‑Harris, Nelson & Pediatric Clinical Advisor