Synopsis
Localise rapidly evolving flaccid weakness across cord, roots, peripheral nerves, neuromuscular junction and muscle, anticipate respiratory and autonomic failure, and start cause-specific treatment without waiting for late tests.
- Acute flaccid paralysis describes rapid weakness with reduced tone and often reduced reflexes; it is not a final diagnosis and early spinal cord disease can also appear flaccid during spinal shock.
- Guillain-Barre syndrome commonly produces progressive, broadly symmetric limb weakness and areflexia after infection, with sensory symptoms, pain, facial weakness and autonomic instability.
- A sensory level, extensor plantar responses emerging later, early bladder dysfunction or a sharply asymmetric pattern favours spinal cord disease over uncomplicated Guillain-Barre syndrome.
Key red flags
Alternating hypertension and hypotension, bradycardia, tachyarrhythmia, ileus or urinary retention in GBS can deteriorate suddenly and needs monitored care.
Investigation priorities
Detect respiratory-muscle decline before gas exchange fails.
Management branches
Weakness evolves over hours to days with reduced tone or reflexes.
- Assess airway, cough, swallow, breathing pattern and circulation, obtain forced vital capacity and ECG and involve critical care early for any progressive bulbar or respiratory sign.
- Map cranial nerves, power, tone, reflexes, plantar responses, sensation and sphincter function, looking actively for a spinal level or descending pupillary syndrome.
Key medicines
Intravenous immunoglobulin for GBSA standard specialist course totals 2 g/kg, commonly divided as 0.4 g/kg daily for 5 days, using NHS weight, infusion and renal protocols.
Botulinum antitoxinUKHSA and the National Poisons Information Service arrange the current antitoxin product and adult administration as soon as clinical botulism is suspected.