Ethylene glycol is an osmotically active organic alcohol responsible for nearly 6000 intentional and accidental ingestions annually. It may be found in many industrial and household products including antifreeze and de-icing solutions, brake and hydraulic fluids, and window cleaners. Ethylene glycol, itself, has little toxicity but its metabolites can cause serious morbidity and mortality.
Initial effects from ethylene glycol ingestion may resemble intoxication from ethanol, and patients may exhibit dysarthria, ataxia, confusion, stupor and even coma. The parent compound is metabolized in the liver via alcohol dehydrogenase and aldehyde dehydrogenase resulting in the production of glycolic acid. This metabolite is chiefly responsible for the anion-gap acidosis that develops, and can exert significant cardiopulmonary toxicity. A small amount of glycolic acid is further metabolized into oxalate, which leads to calcium oxalate deposition in renal tubules and subsequent renal injury.
The diagnosis of ethylene glycol poisoning can be challenging, as patients may not be forthcoming, or may present too altered to provide a history of ingestion. Ethylene glycol levels may not be readily available at the treating institution. Either a high index of suspicion, or the presence of an unexplained osmolal gap or anion gap acidosis, should prompt empiric treatment to maximize favorable outcomes. Enzymatic inhibition of alcohol dehydrogenase through the use of fomepizole or ethanol is the cornerstone of successful management. In later presentations where a significant anion gap acidosis has developed, or when renal injury is apparent, hemodialysis must be considered.
Ethylene glycol Antifreeze Toxic alcohol Fomepizole Ethanol Glycolic acid Glycolate Oxalic acid Oxalate Anion gap Osmolar gap Osmolal gap Metabolic acidosis Overdose Acute renal failure
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