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.
- Measure serial forced vital capacity and inspiratory strength where available; pulse oximetry and arterial gases may remain normal until respiratory muscle failure is advanced.
- Autonomic involvement causes tachycardia, bradyarrhythmia, blood-pressure swings, ileus, urinary retention and sweating abnormalities and can be life-threatening.
- CSF often shows raised protein with few cells after the first week, but can be normal early; substantial pleocytosis should redirect investigation towards infection or inflammation.
- Nerve-conduction studies may show demyelination, conduction block or an axonal subtype and can also be non-diagnostic early, so repeat testing may be needed.
- Treat non-ambulant or significantly progressive GBS with IV immunoglobulin or plasma exchange through specialist protocols; routine corticosteroids do not improve outcome.
- Prevent venous thrombosis, pressure injury, contracture and aspiration, treat pain and provide rehabilitation and psychological support while axonal recovery evolves over months.
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.
Dysphagia, nasal speech, pooled secretions, weak cough or loss of head lift predicts aspiration and respiratory risk even before obvious breathlessness.
Large blood-pressure swings, resting tachycardia, episodic bradycardia, ileus or retention reflects dysautonomia and justifies monitored high-acuity care.
Ophthalmoplegia, sensory ataxia and areflexia with little limb weakness is a recognised GBS-spectrum variant requiring respiratory and bulbar vigilance.
Profound motor weakness with low compound muscle action potentials and less slowing can represent acute motor axonal or motor-sensory axonal neuropathy.
A sensory level, brisk reflexes, severe persistent asymmetry, early sphincter paralysis, fever or marked CSF pleocytosis should trigger investigation for cord, infection or another neuropathy.
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.
- Arrange CSF and neurophysiology without delaying treatment, adding spinal imaging and infection or metabolic tests when atypical features occur.
- Protect swallowing, secretions, pressure areas and venous circulation while a senior neurology team confirms the immune-treatment plan.