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Management of Methyl Alcohol Poisoning

Posted Feb 12 2010 12:00am
Methanol Poisoning

Methanol or Methyl Alcohol is a denaturant. It is a component of varnishes, paint removers, windshield wipers, anti-freeze solutions, copy-machine fluid and as a solvent.

Acute Methanol Poisoning is usually a consequence of ingestion of cheap, adulterated, illicit liquor. Methanol is very toxic and requires as little as 30 ml of 40% solution to be fatal. Poisoning is mostly stratified among the people of lower socioeconomic status. On ingestion, Methanol is metabolized in the liver to formaldehyde and formic acid by alcohol dehydrogenase. Although both are toxic, formic acid is what causes the more serious delayed effects. It is also readily distributed in the liver, gastrointestinal tract, eyes and kidneys.

Methanol is rapidly absorbed from the gastrointestinal tract, peak levels reaching within 1-2 hours. Onset of clinical manifestations is variable.

Early manifestations such as nausea, vomiting, headache, vertigo and gastritis are primarily caused by Methanol itself. High serum levels of Methanol (>40 mg/dl) is associated with obtundation, convulsions and coma.

Late manifestations such as visual disturbances, severe metabolic acidosis, seizures, coma and death are common after 30 hours after ingestion. The latent period is longer when Ethanol is ingested concurrently. Ocular toxicity is associated with diminished vision, flashing spots, dilated pupils, optic disc hyperemia, retinal edema and ultimately blindness.

Severe poisoning leads to myocardial depression, bradycardia and shock.

Apart from arterial blood gases which is essential, serum osmolality and anion gap assist in diagnosis. Renal and Liver function tests should be done and blood Methanol levels measured, if possible. CT scan of the brain may show bilateral putamen necrosis. A retrospective diagnosis of Methanol poisoning is sometimes based on this finding. Diagnosis is essentially clinical, but calculation of the osmolal and anion gap can help assess severity where serum methanol levels cannot be estimated.

1. Unabsorbed Methanol should be removed by gastric lavage.

2. Supportive Measures:

  • Correction of Acidosis
  • Control of seizures
  • Maintenance of nutrition
  • Alkalization of urine enhances excretion of formic acid

3. Specific Measures:

  • Administration of Ethanol to saturate alcohol dehydrogenase in the liver, preventing the formation of toxic metabolite, formaldehyde. A 5% solution of Ethanol is prepared and 15 ml/kg is given as loading dose and then 2-3 ml/kg/hour as maintenance dose orally. It can also be given intravenously.
  • Hemodialysis enhances elimination of Methanol and Formic acid and is indicated when Methanol levels exceed 50 mg/dl. In the absence of serum Methanol level measurements, the osmolar gap is useful to assess the indication for and duration of hemodialysis in Methanol-poisoned patients.
  • Folic acid has been used to enhance conversion of formate to carbon dioxide and water. The dose is 50 mg IV 4 hourly for 24 hours.
  • 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, has been successfully used as an alternative to Ethanol and Dialysis.
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