Best method for methanol poisoning
treatment:
March 2007
a) Ethanol
b) Calcium gluconate
c) Desferroxamine
d) BAL
Correct Answer - A
Ans. A: Ethanol
When metabolized by hepatic alcohol and aldehyde dehydrogenase,
methanol forms formaldehyde and formic acid, both of which are
toxic.
Formic acid is the primary toxin that accounts for the majority of the
anion gap, metabolic acidosis, and ocular toxicity. Formic acid
inhibits cytochrome oxidase in the fundus of the eye. Swelling of
axons in the optic disc and edema result in visual impairment.
Degradation of formic acid is folate dependent. Thus, if a folate-
deficient person ingests ethanol, toxicity may be more severe due to
the increased accumulation of formic acid.
Approximately 90-95% of methanol metabolism occurs in the liver,
while 5-10% is excreted unchanged through the lungs and kidneys.
Methanol is primarily metabolized by alcohol and aldehyde
dehydrogenase.
Formaldehyde has a short half-life, lasting only minutes.
Formic acid is metabolized much more slowly, and it bioaccumulates
with significant methanol ingestion. Physical Sign
Ocular physical findings include sluggishly reactive or fixed and
dilated pupils.
Retinal edema or hyperemia
Edema of the optic disc may be seen.
Optic atrophy may appear in late stages (permanent blindness).
CNS signs include lethargy and confusion.
Respiratory signs include dyspnea (rare cases) or even Kussmaul
respiration, despite acidosis.
Cardiac signs (e.g., hypotension, bradycardia) are late signs
associated with a poor prognosis.
Lab studies
Methanol concentration: This study confirms ingestion and helps
guide treatment. Remember that low serum concentration do not
rule out significant toxicity; late presenters may have low methanol
concentrations but elevated formic acid levels and severe clinical
toxicity (e.g., severe metabolic acidosis, blindness, coma).
Treatment
Supportive measures
Attempted correction of acidosis using sodium bicarbonate is
indicated if pH is less than 7.20. An alkalemic pH makes it more
likely that formic acid will exist as its anion (formate), which cannot
access the CNS and optic nerve as readily.
Administer folic acid for several days to potentiate the folate-
dependent metabolism of formic acid to carbon dioxide and water.
Ethanol infusion is recommended: Ethanol is a competitive inhibitor
of alcohol dehydrogenase and, thereby, impairs the metabolism of
methanol and ethylene glycol. Ethanol has 10-20 times greater
affinity for alcohol dehydrogenase than methanol does.
Plasma formate concentration is of prognostic value