Wood alcohol poisoning

methyl-alcohol.gifMETHYL ALCOHOL. This simplest of alcohols, also called wood alcohol or methanol, is used as a solvent, antifreeze, paint remover, and as a denaturant in ethyl alcohol. Denatured ethyl alcohol preparations, such as Sterno or Solox, contain 5 to 15% methyl alcohol as well as other denaturants. Methyl alcohol poisoning results almost entirely from its ingestion as a substitute for ethanol or to the drinking of denatured ethyl alcohol. The toxic dose is quite variable: death has occurred after a dose of 20 mL, but 250 mL has been ingested with survival. As little as 15 mL methanol has caused permanent blindness.

Methanol is less inebriating than ethyl alcohol, and inebriation is not a prominent symptom of methyl alcohol intoxication. Methanol is oxidized in the body by alcohol dehydrogenase first to formaldehyde and then to formic acid; these metabolites cause the toxic mainfes-tations of methanol poisoning. At equivalent concentrations the rate
of its metabolism is only 15 percent that of ethanol for which alcohol dehydrogenase has a greater affinity and which can inhibit competitively the rate of metabolism of methanol. Formic acid and especially formaldehyde have toxic actions on many cells; the retina and optic nerve are damaged specifically. The toxic metabolites of methyl alcohol are also responsible for the severe acidosis which is the most prominent feature of methyl alcohol poisoning. This acidosis results partly from the accumulation of formic acid, but formate also appears to exert an inhibitory effect upon enzymes involved in the oxidation of carbohydrate with consequent accumulation of acid intermediates.
Symptoms of methanol poisoning usually do not appear until 12 to 24 h after ingestion, when sufficient toxic metabolites have accumulated. Manifestations include headache, dizziness, nausea, vomiting, vasomotor disturbances, central nervous system depression, and respiratory failure. Visual disturbance is almost universal and ranges from mild blurring of vision to total blindness. Impairment of vision may be transient, but permanent blindness may follow survival of the acute intoxication. The pupils are dilated and nonreactive, and there is hyperemia of the optic disc and retinal edema. Acidosis is commonly severe.
In the treatment of methyl alcohol intoxication emesis and gastric lavage are of use only within the first 2 h after ingestion. Intravenous administration of large amounts of sodium bicarbonate combats acidosis. Return of acidosis is frequent after initial correction, and additional alkali must be administered as indicated by close observation of the patient and laboratory determinations. It is most useful to obtain a blood methanol level as soon as possible. At any time after ingestion, levels between 20 and 50 mg/dL are associated with acidosis and significant symptomatology and are an indication for intravenous ethanol therapy (1 g ethanol per kilogram of body weight in 5% dextrose in water over 30 min to load, then 7 to 10 g/h in adults to maintain the blood ethanol level at about 100 mg/dL). Severely symptomatic patients should be treated even if a methanol level cannot be obtained. A methanol level exceeding 50 mg/dL is an indication for hemodialysis as well as ethanol therapy; dialysis also is indicated in the presence of severe acidosis with lower blood levels.