Methanol Poisoning: Clinical Aspects and Management

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What is methanol and what are its properties?

Methanol is a flammable, colorless, and slightly alcoholic solution. It is most commonly ingested through food.

What are the clinical signs and symptoms of methanol toxicity?

Methanol toxicity produces a raised anion-gap metabolic acidosis, ocular and central nervous system toxicity, blurred vision, decreased acuity, and the feeling of being in a snow field.

How is methanol metabolized?

Methanol is metabolized by alcohol dehydrogenase to formaldehyde, which does not accumulate to a significant degree, but is metabolized to formic acid. Formic acid is metabolized more slowly and accumulates, dissociating to formate and a hydrogen ion. The formate is then metabolized to CO2 and water by a folate-dependent mechanism.

What are the complications of methanol poisoning?

Complications of methanol poisoning include systemic acidosis, ocular toxicity, and central nervous system findings demonstrated on CT, MRI and at autopsy, including oedema and necrosis of the basal ganglia (particularly the putamen) and haemorrhages in the subcortical white matter.

What is the prognosis of methanol poisoning?

The prognosis for methanol poisoning is generally good, but a number of complications can occur. Follow up is important to ensure that patients are recovering well. A quantitative serum concentration of methanol may be useful to indicate the need for haemodialysis, and vitamins may be useful in the treatment of specific complications.

Study Notes

  • Methanol is a flammable, colorless, and slightly alcoholic solution.

  • Methanol is most commonly ingested through food.

  • Methanol toxicity produces a raised anion-gap metabolic acidosis, ocular and central nervous system toxicity.

  • Methanol is metabolized by alcohol dehydrogenase to formaldehyde, which does not accumulate to a significant degree, but is metabolized to formic acid.

  • Formic acid is metabolized more slowly and accumulates.

  • Formic acid dissociates to formate and a hydrogen ion.

  • The formate is metabolized to CO2 and water by a folate-dependent mechanism.

  • Systemic acidosis is produced through the production of formic acid and the generation of a lactic acidosis because of inhibition of cellular aerobic metabolism.

  • Formation of formic acid is the most likely cause of the early raised anion-gap metabolic acidosis seen following methanol exposure.

  • Consequent interruption of normal cellular respiration by formic acid then leads to the production of a lactic acidosis.

  • Ocular toxicity is caused by undissociated formic acid, which directly targets the optic disc and retrolaminar section of the optic nerve.

  • Acidosis worsens the ocular toxicity by promoting movement of formic acid into cells and decreasing the amount of undissociated formic acid.

  • Central nervous system findings demonstrated on CT, MRI and at autopsy following significant methanol poisoning include oedema and necrosis of the basal ganglia (particularly the putamen) and haemorrhages in the subcortical white matter.

  • The putamen is known to have high rates of oxygen and glucose consumption and for this reason is thought to be more vulnerable to the adverse effects of formic acid.

  • Methanol exposure can result in a number of clinical signs and symptoms, including blurred vision, decreased acuity, and the feeling of being in a snow field.

  • A quantitative serum concentration of methanol may be useful to indicate the need for haemodialysis.

  • Vitamins may be useful in the treatment of specific complications, including elimination enhancement, haemodialysis, and late complications.

  • The prognosis for methanol poisoning is generally good, but a number of complications can occur. Follow up is important to ensure that patients are recovering well.

Test your knowledge on the clinical aspects, toxic effects, and management of methanol poisoning. Understand the metabolic pathways, systemic effects, and complications associated with methanol toxicity.

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