Ethylene glycol is the principal constituent in most motor vehicle “antifreeze” solutions. Reports of its potentially lethal effects if ingested first appeared soon after its widespread introduction in the 1930s. The principal toxic effect of ethylene glycol is renal failure due to deposition of oxalate crystals within tubules.1 This, together with metabolic acidosis and cardiopulmonary collapse, accounts for the high mortality. The lethal dose is estimated to be 100 ml. Although rare, neurological complications are well recognised.2 Cranial nerve palsies and optic atrophy are the most often reported. The mechanism of neuronal damage is unknown. Deposition of oxalate crystals in cranial nerves has been reported at necropsy and animal studies have shown evidence for a direct toxic effect of ethylene glycol on acetylcholinesterase positive neurons.3 We describe a case in which the ingestion of ethylene glycol led to a severe sensorimotor polyradiculoneuropathy.

A 43 year old man was transferred to the regional renal unit after presenting to a local casualty department in acute renal failure. Six days before admission he had deliberately ingested 250 ml antifreeze. There was a history of hypertension, acute myocardial infarction, atrial fibrillation, and a stroke, resulting in a left hemiparesis two years previously. He was taking digoxin, warfarin, and …