Current management of ethylene glycol poisoning

Ethylene glycol, a common antifreeze, coolant and industrial solvent, is re sponsible For many instances of accidental and intentional poisoning annual ly, Following ingestion, ethylene glycol is first hepatically metabolised t o glycoaldehyde by alcohol dehydrogenase. Glycoaldehyde is then oxidised to glycolic acid, glyoxylic acid and finally oxalic acid. While ethylene glyc ol itself causes intoxication, the accumulation of toxic metabolites is res ponsible for the potentially fatal acidosis and renal failure, which charac terises ethylene glycol poisoning. Treatment of ethylene glycol poisoning consists of emergent stabilisation, correction of metabolic acidosis, inhibition of further metabolism and enha ncing elimination of both unmetabolised parent compound and its metabolites . The prevention of ethylene glycol metabolism is accomplished by the use o f antidotes that inhibit alcohol dehydrogenase. Historically, this has been done with intoxicating doses of ethanol. At a sufficiently high concentrat ion, ethanol saturates alcohol dehydrogenase, preventing it from acting on ethylene glycol, thus allowing the latter to be excreted unchanged by the k idneys. However, ethanol therapy is complicated by its own inherent toxicit y, and the need to carefully monitor serum ethanol concentrations and adjus t the rate of administration. A recent alternative to ethanol therapy is fomepizole, or 4-methylpyrazole, Like ethanol, fomepizole inhibits alcohol dehydrogenase; however it does s o without producing serious adverse effects. Unlike ethanol, fomepizole is metabolised in a predictable manner, allowing for the use of a standard, va lidated administration regimen. Fomepizole therapy eliminates the need for the haemodialysis that is required in selected patients who are non-acidoti c and have adequate renal function.