Methyl alcohol (methanol, wood alcohol) is a component of antifreeze and many combustibles and is used in the manufacture of formaldehyde, as an industrial solvent, and as an adulterant of alcoholic beverages, the latter being the most common source of methyl alcohol intoxication. The oxidation of methyl alcohol to formaldehyde and formic acid proceeds relatively slowly; thus, signs of intoxication do not appear for several hours or may be delayed for a day or longer. Many of the toxic effects are like those of ethyl alcohol, but in addition severe methyl alcohol poisoning may produce serious degrees of acidosis (with an anion gap). The characteristic features of this intoxication, however, are damage to retinal ganglion cells—giving rise to scotomata and varying degrees of blindness, dilated unreactive pupils, and retinal edema—and bilateral degeneration of the putamens, readily visible on brain scans. Survivors may be left blind or, less often, with putamenal necrosis and dystonia or parkinsonism (McLean et al). The most important aspect of treatment is the intravenous administration of large amounts of sodium bicarbonate to reverse acidosis. Hemodialysis and 4-methylpyrazole (see later) may be useful adjuncts because of the slow rate of oxidation of methanol.
Ethylene glycol, an aliphatic alcohol, is a commonly used industrial solvent and the major constituent of antifreeze. In the latter form, it is sometimes consumed by alcoholics (5,000 cases of poisoning annually in the
United States) and in suicide attempts with disastrous results. At first the patient merely appears drunk, but after a period of 4 to 12 h, hyperventilation and severe metabolic acidosis develop, followed by confusion, convulsions, coma, and renal failure and death in rapid succession. Cerebrospinal fluid lymphocytosis is a common but not invariable feature. The metabolic acidosis is a result of the conversion of ethylene glycol by ADH into glycolic acid, thus producing an anion gap that reflects the presence of this additional substance in the blood. (The anion gap has been defined in different ways, but the most convenient is the difference between the positive ion Na+ and the sum of negative ions, Cl− plus HCO3− [venous CO2 is used for the latter]; a value greater than 12 is considered a gap.) The cause of the renal toxicity is less clear—probably it is a result of the formation of oxalate from glycolate and the deposition of oxalate crystals in renal tubules. (One of our recent patients had hippurate crystals in the urine, a finding that is more characteristic of toluene ingestions.) These crystals appear in the urine and sometimes in the cerebrospinal fluid and aid in diagnosis.
Treatment of Nonethanol Alcohol Intoxication