The symptoms of methanol poisoning may not appear for up to 12 to 18 h after ingestion because of the time it takes for methanol to be metabolized to its toxic metabolites. The delay in symptoms may be even longer if ethanol has been ingested. The cardinal clinical manifestations of methanol poisoning are central nervous system depression similar to that of ethanol, visual disturbances, abdominal pain, nausea and vomiting, and wide-anion-gap metabolic acidosis. As with isopropanol, the early phase of elation commonly seen in ethanol intoxication is absent.
On arrival at the hospital, the victim may be confused or, in severe cases, comatose. There may be complaints of headache or vertigo, and seizures may occur. Visual disturbances are seen in approximately 50 percent of patients. These include diplopia, blurred vision, decreased visual acuity, photophobia, descriptions of "looking into a snow field," constricted visual fields, and blindness. The clinician may find nystagmus, fixed and dilated pupils, retinal edema, and optic atrophy or hyperemia of the optic disk. Computed tomography of the brain may reveal basal ganglia infarcts consistent with the parkinsonian syndrome, which has been reported after methanol poisoning.7 Methanol is a potent mucosal irritant and causes severe abdominal pain as well as nausea and vomiting in over one half the cases; pancreatitis has also been commonly reported. However, serious ingestions may occur without subsequent gastrointestinal symptoms. Although an increased osmolal gap is usually present with serious methanol ingestion, methanol poisoning with a normal osmolal gap has been reported. This is due to complete metabolism of the methanol itself, while resultant toxic metabolites are exerting their effect.
Hypotension and bradycardia are late findings and suggest a poor prognosis. 7 Outcome is best correlated with the severity of the acidosis rather than serum methanol concentration.
Diagnosis of methanol poisoning rests on history, the presence of the characteristic clinical features outlined above, and the presence of a wide-anion-gap metabolic acidosis and osmolal gap. While confirmation of a tentative diagnosis depends on identification of the substance in the bloodstream, treatment should be initiated based on compatible clinical presentation to avoid morbidity resulting from delay. In any case, serum methanol determinations at many institutions depend on outside laboratories and may not be available for several hours. However if the ethanol level is known, the methanol level can be estimated from the osmolal gap ( Table
Normal methanol blood concentration from endogenous sources is 0.05 mg/dL. Asymptomatic individuals usually have peak levels below 20 mg/dL, while levels above 50 mg/dL indicate serious poisoning. Central nervous system symptoms usually appear when levels rise above 20 mg/dL; eye problems are associated with levels greater than 50 mg/dL, and the risk of fatality rises with levels greater than 150 to 200 mg/dL.
The differential diagnosis should include other potential causes of a wide-anion-gap metabolic acidosis—i.e., ethylene glycol, diabetic ketoacidosis, paraldehyde, isoniazid, salicylates, iron, lactic acidosis, phenformin, and uremia.
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