This occurs sporadically when industrial (methylated) spirit is consumed in the place of ethanol or epidemically when the supply of liquor is adulterated with methyl alcohol. Several outbreaks have occurred in closed communities from time to time. Minimum lethal dose is 30g. Methanol is metabolized in the system to formaldehyde and formates. In addition, derangement of hepatic metabolism results in the accumulation of lactate. Severe metabolic acidosis results after a latent period of 8-12 hours. Optic neuritis develops as a specific toxic reaction.
Clinical picture: Within hours of consuming methylated alcohol, patients develop restlessness, irritability, confusion, epigastric pain, vomiting and rapid loss of vision followed by metabolic acidosis. Visual loss is concentric. Ophthalmoscopy shows pale edematous discs. Coma may develop, which may become deep. Mortality in a large series is about 20%.
Treatment: Aims of treatment are:
1. Correction of acidosis.
2. Inhibition of methanol oxidation, and
3. removal of circulating methanol and its toxic products.
Acidosis is corrected by sodium bicarbonates given intravenously in adequate amounts. Hemodialysis helps to remove circulating methanol. Hemodialysis should be started without delay if the blood level of methanol exceeds 0.5g/liter or the total quantity ingested exceeds 0.5g/liters or the total quantity ingested exceeds 30 ml. Peritoneal dialysis is only 1/8th as effective as hemodialysis in removing methanol and therefore this should not be relied upon. Ethanol inhibits methanol oxidation when taken concurrently or given early after poisoning. Though this effect is demonstrable in experimental animals, clinical experience is variable. Folic acid or folinic acid in amounts of 10-15 mg intramuscular repeatedly is effective in reducing methanol toxicity in experimental animals. This is worth a trial in man. 4-Methyl pyrazole which inhibits methanol oxidation is found to be effective in experimental animals.
Till recently, barbiturates were the most common drugs used for suicide. Accidental poisoning is seen in epileptics, psychiatric patients and children who get regular prescriptions for these drugs. The most used barbiturate is phenobarbitone and it is used as an anticonvulsant. Absorption and metabolism of phenobarbitone are slow. About 10% of the drug is excreted in urine unchanged. The lethal dose of adults is about 5g. Simultaneous administration of alcohol aggravates its effects.
Clinical features: central nervous, respiratory and Cardiovascular systems are affected the most. Drowsiness, coma, slowing of respiration, and hypotension follow. Pupils are small but react to light. In severe poisoning when the medullary centers are depressed, the pupils are dilated and fixed and this indicates a poor prognosis. Tendon reflexes are sluggish or absent. Necrosis of sweat glands and bullous lesions over the skin develop in a few as a hypersensitivity reaction. These lesions heal slowly. Diagnosis can be confirmed by detection of barbiturates in the gastric contents and estimation of the barbiturate level in blood.
Treatment: In addition to general measures, forced alkaline diuresis and dialysis are helpful. Bemegride (magimide) was considered to be a specific antidote but subsequent research has disproved this assumption. Since Pneumonia is a fatal complication, these patients should be observed for a week till recovery is complete.
On a final note, Methanol and barbiturate poisoning are very common in Asia, most especially in India and these two poisoning agents account for more than 40% of cases of poisoning in India.