Methanol is a highly toxic alcohol commonly found in automobile windshield washer solvent, gas line antifreeze, copy machine fluid, fuel for small stoves, paint strippers, and as an industrial solvent (Budavari 1996B; Suit 1990). Many new uses for methanol, predominantly as an alternative energy source, have also been proposed. If these new applications are developed, methanol is likely to become even more accessible in the future and therefore, more available for misuse.
As with ethylene glycol, the clinical course of methanol poisoning occurs over a number of hours. While methanol itself is only mildly intoxicating, it is converted to highly toxic metabolites responsible for acidosis, blindness, and potentially death. Because the morbidity for methanol poisoning is related to delay in treatment, real or suspected methanol poisoning creates many challenges for clinicians because laboratory tests, antidotes and intensive care facilities are not always available.
The lethal dose of pure methanol is estimates to be 1-2 mL/kg ; however, permanent blindness and death have been reported with as little as 0.1 mL/kg (6-10 mL in adults)
Like ethylene glycol, methanol is relatively non-toxic; however, it is metabolized to highly toxic compounds that are responsible for the acidosis and blindness characteristic of methanol poisoning.
As in ethylene glycol poisonings, the initial step in the metabolism of methanol involves the enzyme alcohol dehydrogenase (ADH) (see Figure 2). First, methanol is slowly oxidized by ADH to yield formaldehyde. Next,formaldehyde is oxidized by formaldehyde dehydrogenase to yield formic acid (or formate, depending on the pH). This oxidation occurs rapidly so that little formaldehyde accumulates in the serum. FInally, formic acid is metabolized to carbon dioxide and water, which are excreted by the kidneys and lungs.
Initial symptoms of methanol poisoning may appear as soon as 12 hours post-ingestion, but usually develop 24 hours after ingestion. These may resemble ethanol intoxication and consist of drowsiness, confusion, and ataxia, as well as weakness, headache, nausea, vomiting, and abdominal pain. Collectively, these symptoms may mimic an alcohol hangover and are due to mild intoxication, caused by methanol itself.
As methanol metabolism proceeds, a severe anion gap metabolic acidosis will develop. Severe metabolic acidosis in conjunction with visual effects are the hallmark of methanol poisoning. Patients usually describe blurred or misty vision, double vision, or changes in color perception. There my be constricted visual field and, occasionally, total loss of vision. Characteristic visual dysfunctions include pupillary dilation and loss of pupillary reflex (Burkhart 1990; Suit 1990).
Further signs and symptoms may be shallow respiration, cyanosis, tachypnea, coma, seizures, electrolyte disturbances, and various hemodynamic changes including profound hypotension and cardiac arrest. There may be mild to profound loss of memory, confusion, and agitation, which may progress to stupor and coma as the severity of the acidosis increases (Suit 1990). In severe cases, death is possible. Surviving patients can be left with permanent blindness or with other neurological deficits
Treatment Objectives
As with ethylene glycol, the three primary goals of therapy include treatment of metabolic acidosis, inhibition of the methanol metabolism and enhanced elimination of the unmetabolized compound and existing toxic metabolites.
As with ethylene glycol, the three primary goals of therapy include treatment of metabolic acidosis, inhibition of the methanol metabolism and enhanced elimination of the unmetabolized compound and existing toxic metabolites.
Gastric decontamination is unlikely to be beneficial because methanol is rapidly and completely absorbed from the gut. Ipecac-induced emesis is contraindicated due to the risk of rapid loss of consciousness. It is doubtful activated charcoal has the ability to absorb significant amounts of methanol; however, it may be useful if a co-ingestant is suspected. Gastric lavage would need to be performed soon after ingestion to be beneficial.
Stabilization of the critical patient must be performed before other therapies can be instituted. Correcting acid/base status should be a priority because serious metabolic acidosis is common and a pH less than 7 is associated with poor prognosis. Sodium bicarbonate should be administered to correct serum pH. Fluid and electrolyte replacement, airway management and the treatment of serious cardiovascular and neurological signs, such as hypotension and seizures, should also be a primary concern.
The elimination of methanol may be enhanced by administering folic acid, a cofactor in the conversion of formic acid to carbon dioxide, and by performing hemodialysis
[source:antizol.com]
