Management: For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid. There is then a latent period lasting approximately 12–24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visual function becomes impaired, ranging from blurred vision and altered visual fields to complete blindness. Features: Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells. The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality. Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. Mechanisms of Toxicity: Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30–60 minutes. Epidemiology: Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption.
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