• D W Zochodne, C F Bolton, G A Wells, J J Gilbert, A F Hahn, J D Brown, and W A Sibbald.
• Department of Clinical Neurological Sciences, Victoria Hospital, University of Western Ontario, London, Canada.
• Brain. 1987 Aug 1;110 ( Pt 4):819-41.

AbstractNineteen patients developed polyneuropathy complicating critical illness. They had been admitted to a critical care unit following intubation for cardiac or pulmonary disease and had developed sepsis and multiple organ failure. Approximately one month following intubation, failure to wean from the ventilator and limb weakness prompted neurological referral. Examination disclosed weakness and wasting of muscles and impaired tendon reflexes in most, but not all, patients. Electrophysiological studies in 17 patients revealed attenuated compound muscle and sensory nerve action potential amplitudes and widespread denervation on needle electromyography. Autopsy in 9 patients who died of their critical illness revealed widespread primary axonal degeneration of motor and sensory fibres, with extensive denervation atrophy of limb and respiratory muscles. Survivors recovered from the polyneuropathy three to six months following discharge. Seventeen of the patients were segregated by electrophysiological criteria into mild (8) and severe (9) polyneuropathy categories. An analysis of these two groups failed to reveal putative metabolic, drug, nutritional or toxic factors that might be responsible for the polyneuropathy. Our studies suggest that the mechanism may be a fundamental defect, still unknown, which causes dysfunction of all organ systems in this syndrome.

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