Standard pre‑examination protocol – must be demonstrated:
Action: Introduce yourself, explain the examination, and obtain verbal consent.
Key observations – “Acute Flaccid Paralysis / GBS” clues:
Systematic neuromuscular exam – focus on pattern of weakness:
Systematic examination – identify aetiology & complications:
Assess:
📋 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.
• 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
• 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.
• 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.
• 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.
• 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
Monitor vital capacity, early intubation if VC < 15-20 mL/kg or MIP < 30 cmH2O. Non-invasive ventilation (BiPAP).
IVIG (0.4 g/kg/day × 5 days) or plasmapheresis – within 2 weeks of onset. Steroids NOT effective.
Continuous BP/HR monitoring; treat hypertension (labetalol), bradycardia (atropine).
NG / gastrostomy for bulbar weakness. High-calorie, DVT prophylaxis.
Passive/active ROM, positioning, prevention of contractures.
Neurology, physiotherapy, occupational therapy, speech therapy, dietitian, social work.
📈 Prognosis
📋 Follow‑up Schedule