Ethylene glycol (1,2-ethanediol) is used in car radiator antifreeze. It has a half-life of around 3 hours and is metabolized to three major toxic com- pounds: glycolaldehyde, glycolic acid, and glyoxylic acid. The oxidation of ethylene glycol to glycolaldehyde is catalyzed by liver alcohol dehydroge- nase. Both oxalic acid and formic acid are formed in smaller amounts. Oxalic acid itself is a highly toxic compound, which can rapidly precipitate as calcium oxalate crystals in various tissues as well as in urine. The formation of these crystals in urine, although not a constant finding, is an important diagnostic clue to ethylene glycol poisoning. The metabolite that accumulates in the highest concentrations in the blood is glycolic acid, and its concentration in blood and urine appears to correlate directly with symptoms and mortality. It is the major contributor to the high anion gap seen in metabolic acidosis. The fatal dose of ethylene glycol is around 100 g, and anuria and necrosis are the principal symptoms of acute poisoning. Other symptoms include nausea and vomiting, myoclonus, seizures, convulsions, depressed reflexes, and coma. Definitive diagnosis of ethylene glycol intoxication can be made by measuring serum ethylene glycol and glycolic acid by HPLC.
Treatment of ethylene glycol and methanol toxicity is similar and is based on symptoms and serum level. The mainstay of treatment is inhibition of the alcohol dehydrogenase enzyme, to minimize the formation of toxic metabolites, while the relatively nontoxic parent alcohol is eliminated renally. Although ethanol was originally used as a competitive inhibitor of alcohol dehydrogenase, the nonintoxicating agent fomepizole (4-methylpyrazole, Antizol, Paladin Labs, Montreal, Canada) is now gen- erally preferred (Brent, 2009). Dialysis, either hemodialysis or peritoneal dialysis, is utilized to remove either parent compound and its corresponding toxic metabolic products.