Methanol & Ethylene Glycol Poisoning

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

• Methanol to formic acid

• Ethylene glycol to glycolic and oxalic acids

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

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

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