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Ethylene glycol, present in antifreeze products, may be ingested accidentally or for the purpose of inebriation or suicide. Ethylene glycol itself is relatively nontoxic, and its initial central nervous system (CNS) effects resemble those of ethanol. However, metabolism of ethylene glycol by alcohol dehydrogenase results in the formation of a number of acid metabolites, including oxalic acid and glycolic acid. These acid metabolites are responsible for much of the toxicity of ethylene glycol.
Three stages of ethylene glycol overdose occur. Within the first few hours after ingestion, there is transient excitation followed by CNS depression. After a delay of 4 to 12 hours, severe metabolic acidosis develops from accumulation of acid metabolites. Finally, delayed renal insufficiency follows deposition of oxalate in renal tubules.
Ethylene glycol toxicity is treated with 4-methylpyrazole (4-MP; fomepizole) or ethanol to saturate the enzyme alcohol dehydrogenase and prevent conversion of ethylene glycol to its toxic metabolites.
Confirming and monitoring ethylene glycol toxicity
Toxic concentrations greater than or equal to 20 mg/dL may cause intoxication, CNS depression, metabolic acidosis, renal damage and hypocalcemia. Ingestion of ethylene glycol can be fatal if patients do not receive immediate medical treatment.
Propionic acid produced in the rare inborn error of metabolism methylmalonic acidemia may be confused with ethylene glycol in the gas chromatographic assay.
Toxic concentration: > or =20 mg/dL
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