Acute inflammatory polyradiculoneuropathy (Guillain-Barré syndrome)

Acute inflammatory polyradiculoneuropathy (Guillain-Barré syndrome) typically presents as widespread weakness and sensory disturbance (often without sensory signs) that progresses rapidly. It usually starts peripherally, with impaired or lost tendon reflexes. Clinical presentations vary, and include the Miller Fisher variant (external ophthalmoplegia, ataxia, areflexia) and an uncommon bulbar presentation. Autonomic instability can occur (eg blood pressure variation, cardiac arrhythmia, urinary retention). Some cases are triggered by infection (eg with Campylobacter enteritis, Mycoplasma pneumoniae, Epstein-Barr virus, cytomegalovirus).

Tests to confirm the diagnosis include a cerebrospinal fluid examination—typically, the protein concentration is raised and the cellular response is absent or minimal. Early in the illness the only finding in nerve conduction studies may be the absence of F-waves, but later in the illness nerve conduction slows. Magnetic resonance imaging can exclude other causes and may show enhancement of nerve roots.

Manage patients in hospital. Monitor the vital capacity every 4 hours—if it falls to less than 20 mL/kg or declines rapidly, transfer the patient to an intensive care unit.

Intravenous immunoglobulin (IVIg) and plasma exchange are proven therapies of similar efficacy¹. However, plasma exchange:

• is not available at all sites
• needs good intravenous access
• has effects on fluids and blood pressure that may not be tolerated by older patients.

If acute inflammatory polyradiculoneuropathy is moderate to severe and onset was less than 2 weeks ago, use:

Prophylaxis for deep vein thrombosis is suggested for these patients, as the risk is increased by immobility and IVIg therapy.