- 80% excreted unchanged through the lungs.
- 3% in Urine
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.
- Severe metabolic acidosis
- Moderate ketonemia
- Strongly acidic urine – containing albumin, acetone and formic acid
- Increased serum amylase – but this hyperamylasemia even when striking, should not be equated with pancreatitis because it is found to be mostly due to salivary type amylase.
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.
- First with plain water – to be preserved for chemical analysis
- Subsequently, with 4% NaHCO3 solution in warm water
- 500cc of this solution should be left in the stomach at the end.
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.
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.
- IV – 7.6 to 10.0 ml/kg 10% ethanol in 5% dextrose.
- PO – 0.8 to 1.0 ml/kg 95% ethanol diluted in orange juice.
Ethanol concentration should be maintained just over 100mg/dl
- IV – 1.4 ml/kg/hr – continuous drip of 10% ethanol in 5% dextrose.
- PO – 0.15 ml/kg/hr – 95% ethanol diluted in orange juice.
- The oral administration of ethanol is often preferable to the intravenous route because of the large volume of IV ethanol which may be required.
- Chronic drinkers will require considerably more than non–drinkers who need a lesser dose.
- The ethanol infusion should continue until the blood methanol concentration reaches undetectable levels.
- If hemodialysis is initiated, the ethanol infusion should be increased by about 6–7 gm/hr.
The predictors of methanol toxicity and the need for hemodialysis are emperic and varied. Some indications for hemodialysis are
- Patients with obvious toxicity (coma, ocular signs and acidosis).
- Blood ethanol concentration more than 100 mg/dl.
- Methanol concentration of 50 mg/dl; if more than 30 ml were ingested.
- Since acidosis and ocular toxicity accompany each other and are often delayed, several investigators have suggested using measures of acidosis (decreased bicarbonate and PH; and increased anion gap ) as indicators for the use of hemodialysis when methanol is known to be present.
- Several reports have suggested the determination of formate concentration to be a more direct indicator of toxicity because it is seen that the patient’s formate concentration correlates with his clinical condition but methanol concentration did not.
- Peritoneal dialysis has no place in the management of these patients, because it is only 1/8th times as efficient as hemodialysis. Methanol’s eight–hour half life observed at low doses is markedly prolonged (to 30–35 hours) with ethanol blocking. Hemodialysis reduces this half life to 2.5 hours.
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.
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.