Synopsis
Recognise acute inflammatory polyradiculoneuropathy before respiratory collapse, monitor bulbar and autonomic function, and initiate IV immunoglobulin or plasma exchange without relying on late tests.
- Guillain–Barré syndrome usually causes rapidly progressive, relatively symmetrical limb weakness and areflexia reaching maximum severity within 4 weeks, often after respiratory or gastrointestinal infection.
- Paraesthesia and severe back or radicular pain are common, but a clear sensory level, early bladder paralysis or persistent marked asymmetry suggests an alternative diagnosis.
- Facial diplegia, dysphagia, weak neck flexion and inability to lift the head can precede respiratory failure and require frequent bedside reassessment.
Key red flags
Progressive bilateral leg then arm or cranial weakness with reduced reflexes over days strongly suggests GBS after cord compression and metabolic mimics are considered.
Investigation priorities
Detect declining inspiratory, expiratory and cough strength before gas exchange fails.
Management branches
Progressive bilateral weakness and areflexia raises possible GBS.
- Admit urgently, document time course and power, reflexes, cranial nerves, neck flexion, cough, swallowing, autonomic symptoms and an alternative central localisation.
- Measure FVC and inspiratory or expiratory strength promptly and serially, monitor ECG and blood pressure and obtain critical-care review for decline or bulbar weakness.
Key medicines
Intravenous human immunoglobulinA standard specialist course totals 2 g/kg, commonly 0.4 g/kg daily for 5 days, using the NHS commissioned weight and product protocol.
Low-molecular-weight heparin prophylaxisUse the local immobility prophylaxis dose adjusted for body weight, renal function, bleeding risk and planned lumbar or vascular procedures.