Ethylene glycol

In 2007 reported 5731 possible glycol exposures in the U.S.

Such poisonings are not mandatory reporting in the U.S.

A component of antifreeze, and it is the major source of ethylene glycol poisoning.

Confers a sweet taste to antifreeze.

Common source of childhood ingestions.

Poisoning associated with varying degrees of inebriation or alteration in mental status, metabolic acidosis, oxalate crystalloid and acute renal failure.

With severe cases may see clinical hypocalcaemia, multiple organ failure and death may occur (Jacobsen).

Death rate for untreated individuals is not known.

A metabolite, oxalic acid, can combine with ionized calcium in plasma to form calcium oxalate which precipitates in renal tubules and is the probable cause of ethylene glycol induced renal injury.

Poisoning associated with a prominent metabolic acidosis related to circulating glycolic acid.

Metabolism occurs mainly through the hepatic enzyme alcohol dehydrogenase.

Ethanol is a competitive substrate for alcohol dehydrogenase and can be given to inhibit ethylene glycol metabolism, followed by dialysis to remove the agent and its metabolites.

Use of ethanol for ethylene glycol or methanol poisoning can be associated with 2241atic pharmokinetic with changes in mental status, hypoglycemia and pancreatitis.

Poisoned patients often require intubation and ventilation and fluid resuscitation.

Intoxication and severe academia may require the use of bicarbonate.

For intoxication utilizing ethanol therapy it is recommended to have adjunctive hemodialysis for serum concentrations of ethylene glycol of at least 50 mg per dL, the presence of significant acidosis or a major drop in renal function.

Fomepizole approved for treating ethylene and methanol toxicity.

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