Case #017

An ascending, symmetric, areflexic flaccid weakness developing over days after a diarrheal illness is the classic presentation of Guillain-Barré syndrome, most often triggered by Campylobacter jejuni through molecular mimicry between bacterial lipo-oligosaccharide and peripheral nerve gangliosides. The examination findings do the diagnostic work: global areflexia with flexor plantars and no sensory level argues against a spinal cord lesion such as transverse myelitis or compression, and preserved bladder function points the same way. Normal pupils, full eye movements and no fatigability argue against botulism and myasthenia gravis respectively. CSF showing markedly raised protein with a normal cell count, albuminocytologic dissociation, is characteristic, though it is often normal in the first week, so a normal early result does not exclude the diagnosis. Nerve conduction studies confirm a demyelinating process with conduction block and absent F waves, the latter reflecting proximal root involvement. The single most important management point is respiratory: the falling forced vital capacity is the reason this patient needs a monitored bed, since neuromuscular respiratory failure develops before hypoxia appears on pulse oximetry, and waiting for desaturation means intubating a patient in extremis. Treatment is IVIG or plasma exchange, equally effective, with nothing gained by combining them; IVIG is usually chosen on practical grounds and given over five days. Corticosteroids, notably, do not help in GBS. None of that addresses tonight, though. Elective intubation is indicated once the FVC falls to roughly 20 mL/kg, around 1.4 L in a man of his size, and at 1.9 L losing half a litre every eight hours he will reach it before morning.