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Methanol (wood alcohol) is a common ingredient in many solvents, windshield-washing solutions, duplicating fluids, and paint removers. It sometimes is used as an ethanol substitute by alcoholics. Although methanol produces mainly inebriation, its metabolic products may cause metabolic acidosis, blindness, and death after a characteristic latent period of 6–30 hours.

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  1. Mechanism of toxicity

    1. Methanol is slowly metabolized by alcohol dehydrogenase to formaldehyde and subsequently by aldehyde dehydrogenase to formic acid (formate). Systemic acidosis is caused by both formate and lactate, whereas blindness is caused primarily by formate. Both ethanol and methanol compete for the enzyme alcohol dehydrogenase, and saturation with ethanol blocks the metabolism of methanol to its toxic metabolites.

    2. Pharmacokinetics. Methanol is readily absorbed and quickly distributed to the body water (Vd = 0.6–0.77 L/kg). It is not protein-bound. It is metabolized slowly by alcohol dehydrogenase via zero-order kinetics at a rate about one-tenth that of ethanol. The reported “half-life” ranges from 2.5 to 87 hours, depending on methanol serum concentration (the higher the serum level, the longer the half-life) and whether metabolism is blocked (eg, by ethanol or fomepizole). Only about 3% is excreted unchanged by the kidneys, and less than 10–20% through the breath. Endogenous formate half-life ranges from 1.9 to 9.3 hours; during dialysis, the half-life decreases to 1.5–3.1 hours.

  2. Toxic dose. The fatal oral dose of methanol is estimated to be 30–240 mL (20–150 g). The minimum toxic dose is approximately 100 mg/kg. Elevated serum methanol levels have been reported after extensive dermal exposure and concentrated inhalation. The ACGIH-recommended workplace exposure limit (TLV-TWA) for inhalation is 200 ppm as an 8-hour time-weighted average, and the level considered immediately dangerous to life or health (IDLH) is 6000 ppm.

  3. Clinical presentation

    1. In the first few hours after ingestion, methanol-intoxicated patients present with inebriation and gastritis. Acidosis is not usually present because metabolism to toxic products has not yet occurred. There may be a noticeable elevation in the osmolar gap (See Serum osmolality and osmole gap); an osmole gap as low as 10 mOsm/L is consistent with toxic concentrations of methanol.

    2. After a latent period of up to 30 hours, severe anion gap metabolic acidosis, visual disturbances, blindness, seizures, coma, acute renal failure with myoglobinuria, and death may occur. Patients describe the visual disturbance as blurred vision, haziness, or “like standing in a snowfield.” Funduscopic examination may reveal optic disc hyperemia or pallor, venous engorgement, peripapilledema, and retinal or optic disc edema. The latent period is longer when ethanol has been ingested concurrently with methanol. Visual disturbances may occur within 6 hours in patients with a clear sensorium. Findings on magnetic resonance imaging (MRI) and computed tomography (CT), such as putaminal necrosis and hemorrhage, may be present; however, these changes are nonspecific and can change over time and therefore are not diagnostic of methanol poisoning.

  4. Diagnosis usually is based on the history, symptoms, and laboratory findings because stat methanol levels are rarely available. Calculation of the osmolar and anion gaps (See ...

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