In both methanol and ethylene glycol poisoning, elevation of the osmolar gap occurs after the development of a wide anion gap.
+A major route of elimination of methanol is the lungs.
+When you find a large anion gap metabolic acidosis and a large osmolar gap, you should immediately start treatment with intravenous ethanol or fomepizole.
+Treatment of methanol poisoning also includes intravenous thiamine and pyridoxine.
+Serum levels of ethylene glycol are readily available and should be used to determine which patients should be treated with hemodialysis.
Ethanol and fomepizole are used to competitively inhibit the metabolism of both methanol and ethylene glycol by alcohol dehydrogenase. Formic acid is the major toxic product of methanol metabolism. Glyoxylate and oxalate are the major toxic metabolite of ethylene glycol. In both types of poisoning CNS symptoms resemble those of ethanol intoxication. An increase in the osmolar gap is followed by an increased anion gap as metabolism occurs, then the development of a metabolic acidosis. Large quantities of intravenous bicarbonate may be needed to maintain a blood pH above 7.2. Ethanol or fomepizole should be given as soon as either diagnosis is suspected based on an increased anion or osmolar gap. Serum levels of ethylene glycol are not readily available. Thiamine and pyridoxine are cofactors in the metabolism of ethylene glycol to nontoxic metabolites. Folic acid is metabolized to the active cofactor folinic acid (leukovorin). Folinic acid is a cofactor used in the metabolism of methanol to inactive metabolites.