Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 38-44: Methanol & Ethylene Glycol Poisoning + Key Features Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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