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

Diagnosis

• Initially, the serum osmolality is usually increased

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

• Ethylene glycol often produces oxalate crystalluria

• Differential diagnosis: alcoholic ketoacidosis also can cause a combined anion gap acidosis and osmolar gap

Treatment

• 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