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It is metabolized and excreted at a rate approximately 1/5th of that of ethyl alcohol. After a single dose, the excretion may continue through the lungs and kidneys for at least four days.

Laboratory Findings

Thus, many specific laboratory tests for pancreatitis should be used before embarking on extensive investigations of the pancreas.

Initially, optic disc hyperaemia and peripappilary edema. When symptoms persist and scotomas or complete blindness develops, there is optic disc pallor and attenuation of arterioles.

Decreased pupillary response which has prognostic significance.


Sodium lactate and 5% glucose saline by intravenous drip to help in diuresis.

Correction of Acidosis
It is the main stay of the treatment.

Soda–bi–carb by mouth – 1–2 gm/15 min in 200 ml water. if the patient is unconcious, by stomach tube. The dose may be repeated 3–4 times keeping a to see that the plasma bicarbonate level is kept at about 20 mg/litre. Urinary reaction may be used as a guide towards administration of alkali. Oral treatment is not possible.

Care of Eyes
Eyes are covered to protect them from light.

Specific Therapy
It is directed towards slowing the metabolic degradation of methanol to its toxic metabolites. Ethanol has got a nine fold greater affinity for alcohol dehydrogenate compared to methanol. A serum ethanol concentration of 100mg/dl will fully inhibit alcohol dehydrogenate function and formic acid production. Ethanol may be administered either by means of IV or orally.

Loading Dose

Ethanol concentration should be maintained just over 100mg/dl

Maintenance Dose

The predictors of methanol toxicity and the need for hemodialysis are emperic and varied. Some indications for hemodialysis are

Methyl Pyrazole
It is a specific inhibitor of alcohol dehydrogenase and has been used as an antidote in experimental animals.

It enhances the rate of metabolism of formate.

Dose – 1 mg/kg – up to 50 mg/dose IV every 4 hours for a total of 6 doses. Alcoholic patients may be particularly susceptible to methanol poisoning because of their relative folate deficiency.

It relieves rigidity and hypokinesis caused due to neurological damage.

In Infants
The activity of alcohol dehydrogenase is 20–25% of mature levels and increases gradually to a maximum by five years of age. Thus, the relative inactivity of alcohol dehydrogenase in infants leads to long half life of methanol, which in turn results in a low rate of formate production. This reduces the risk of metabolic acidosis. Slow generation of toxic metabolites may also reduce the risk of sequele.