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For further information, see CMDT Part 38-44: Methanol & Ethylene Glycol Poisoning

Key Features

  • The toxicity of both agents is caused by metabolism to toxic organic acids

    • Methanol to formic acid

    • Ethylene glycol to glycolic and oxalic acids

Clinical Findings

  • Shortly after ingestion of either agent, patients usually appear drunk

  • After several hours, there is tachypnea, confusion, convulsions, and coma

  • Methanol intoxication frequently causes visual disturbances

  • Ethylene glycol often produces oxalate crystalluria and acute kidney injury


  • Initially, the serum osmolality is usually increased

  • After several hours, there is a severe anion gap metabolic acidosis

  • Ethylene glycol often produces oxalate crystalluria


  • Empty stomach by aspiration through a nasogastric tube if recent ingestion (within 30–60 minutes)

  • Folic acid, thiamine, and pyridoxine may enhance the breakdown of toxic metabolites

  • Ethanol blocks metabolism of the parent compounds by competing for the enzyme alcohol dehydrogenase

  • Fomepizole

    • Blocks alcohol dehydrogenase

    • Much easier to use than ethanol

    • If started before onset of acidosis, may be used as the sole treatment for ethylene glycol ingestion in some cases

  • Contact a regional poison control center for indications and dosing

  • For significant toxicity (manifested by severe metabolic acidosis, altered mental status, markedly elevated osmolar gap, or evidence of end-organ toxicity), perform hemodialysis as soon as possible

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