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Article

Delayed Neurologic Sequelae Resulting from Epidemic Diethylene Glycol Poisoning

, F.A.C.E.M. , M.B.B.S., , F.R.C.A.P. , M.B. , M.R.C.P.I., , F.R.A.C.P. , M.B.B.S., , F.R.C.A. , B.A. , M.A. , B.M. , B.Ch., , F.J.F.I.C.M. , M.B.B.S. , F.A.N.Z.C.A. & , F.A.C.E.M. F.A.C.M.T. , M.B.B.S. , Ph.D.
Pages 155-159 | Published online: 11 Aug 2009
 

Abstract

Background. Diethylene glycol (DEG) is a well-known metabolic and renal toxin usually ingested accidentally as an ethanol substitute or as a contaminant in various medicinals. To date, most poisonings have occurred in third-world countries where early death from renal failure is very common. We report a series of seven patients presenting with epidemic DEG poisoning from a correctional facility with varying degrees of metabolic acidemia and acute renal impairment responding to emergent hemodialysis (HD). Significantly, three patients developed delayed neurologic toxicity which has not been well characterized in the past. Case Series. Seven male patients (age range 19–55) presented over a 36 h period following ingestion of varying quantities of DEG. Initially three patients, ingesting the largest quantities of DEG, presented more than 24 h postingestion with severe metabolic acidemia (pH range 6.8–7.1) and anuric acute renal failure requiring HD. All three remained dialysis-dependent and developed significant cranial neuropathies with bulbar palsy in the second week postingestion. One patient died with cerebral oedema and a progressive encephalopathy. Two further patients presented within 24 h of ingestion with normal renal function and a moderate metabolic acidemia (pH range 7.2–7.28) requiring HD. They remained well. Finally, two further patients presented with a history of trivial DEG ingestion and did not require any therapy. Neurologic signs in the two surviving initial presenters improved over 4–6 months although they remained dialysis-dependent. Conclusion. Unrecognized DEG poisoning may present with metabolic acidemia and anuric acute renal failure. Established renal impairment may predict subsequent delayed neurologic toxicity.

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