Methanol, also known as wood alcohol, is a potentially lethal substance when ingested and converted to toxic metabolites. Methanol is found in a variety of household products to include paint strippers, antifreeze, glass cleaner, automobile windshield washer fluid, and Sterno Canned Heat. The majority of intoxication cases are secondary to ingestion; however, contact with skin or via inhalation are other potential routes. The volume of distribution is 0.6 to 0.7 L/kg with peak serum levels obtained 30 to 90 minutes after contact.

Upon ingestion, methanol is oxidized to formaldehyde, which has a half-life of approximately 1 minute, by the enzyme alcohol dehydrogenase. Once formed, formaldehyde is then oxidized to formic acid, which has a much longer half-life than formaldehyde, by alcohol dehydrogenase. The rate-limiting step in formic acid metabolism is a folate-dependent mechanism; therefore, folate deficiency impedes formic acid clearance and leads to the accumulation of this toxic metabolite.

Symptoms of methanol toxicity usually begin between 12 to 24 hours after ingestion and include inebriation, lethargy, headache, vertigo, weakness, Kussmauls respirations, apnea, coma, seizures, and opisthotonos (posture of rigid hyperextension where the head and legs are bent backward while the trunk is bowed forward). Gastrointestinal symptoms include nausea, vomiting, and abdominal pain. Visual symptoms are characteristic of toxicity and include decreased visual acuity, blurred vision, photophobia, and hazy snow-like visions. On physical exam, pupils are dilated with poor light reflexes and hyperemia of the optic disk followed by retinal edema are noted. Dilated fixed pupils are a poor prognostic sign. Autopsy findings include cerebral edema, fatty liver infiltration, hemorrhagic pancreatitis, demyelinization of the optic nerve, and necrosis of the putamen.

Laboratory abnormalities include a high anion gap metabolic acidosis, which manifests as a low serum bicarbonate level. The measured serum osmolality is greater than the calculated osmolality yielding a significant osmolar gap. An elevated MCV is often noted. If no history is available to suggest the diagnosis, it is usually first entertained when an elevated anion gap metabolic acidosis is noted on ABG sampling in the unconscious patient. The diagnosis is confirmed by measuring the serum methanol level. It is important to note that mortality from methanol ingestion correlates best with how acidotic the patient is rather than with actual serum methanol levels. A serum bicarbonate level less than 10 mEq/L is a very poor prognostic indicator and has a high association with a fatal outcome.

The metabolism of methanol to formic acid is prevented when the competitive inhibitor of alcohol dehydrogenase, 4-methpyrazole is administer. In severe cases, hemodialysis may be required for refractory or severe acidosis or in cases or excessive ingestion (markedly elevated serum methanol levels).