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.
- Neuromuscular-junction disorders produce fatigable ocular, bulbar and respiratory weakness with preserved sensation; myasthenia often preserves reflexes, while botulism adds fixed pupils and descending paralysis.
- Hypokalaemia, hypophosphataemia, severe magnesium disturbance, porphyria, toxins, tick paralysis and acute myopathy belong in the early reversible differential.
- Assess forced vital capacity, cough, neck flexion, speech and swallow serially; normal saturation does not exclude neuromuscular hypoventilation.
- Autonomic Guillain-Barre disease can cause extreme blood-pressure variation, arrhythmia, ileus and urinary retention, making unmonitored ward care unsafe in a progressing case.
- Cerebrospinal fluid may show high protein with few cells after the first week, but early fluid can be normal and a marked pleocytosis should prompt infection or another cause.
- Nerve-conduction and electromyography classify demyelinating, axonal, junctional or muscle processes, but initial studies can be non-diagnostic and must not delay respiratory support.
- Intravenous immunoglobulin and plasma exchange are effective for non-ambulant or significantly progressing Guillain-Barre syndrome; corticosteroids do not improve GBS outcome.
- In England, suspected acute flaccid paralysis or acute flaccid myelitis is urgently notifiable: telephone the local UKHSA health-protection team within 24 hours and report online within 3 days without waiting for virology or neurophysiology; use equivalent devolved-nation routes elsewhere.
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.
- Correct dangerous glucose and electrolytes immediately while arranging urgent spinal imaging, infection work-up or neuromuscular testing from the localisation.
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.Assess thrombosis, renal impairment, haemolysis, fluid load and infusion reaction; do not routinely combine sequentially with plasma exchange. Current NHS England criteria state that a second GBS course is ineffective and may cause harm.
Botulinum antitoxinUKHSA and the National Poisons Information Service arrange the current antitoxin product and adult administration as soon as clinical botulism is suspected.It cannot reverse established paralysis and can cause hypersensitivity; airway, ventilation and wound or food-source management remain essential.