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Methanol

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Charles Gomersall & Anna Lee

First posted June 2006

Source

  • paint remover
  • windscreen washing fluid
  • fuel for camping stoves
  • intoxication can occur by oral ingestion, inhalation or dermal absorption

Mechanism of toxicity

  • metabolized by alcohol dehydrogenase to formaldehyde
  • formaldehyde converted by aldehyde dehydrogenase to formic acid
  • formic acid primary toxin responsible for metabolic and ocular disturbance

Clinical features

Symptoms of intoxication usually limited to CNS, eye and GI tract. The co-ingestion of ethanol can delays the onset of symptoms beyond 24 hours

Initial phase

  • headache
  • inebriation
  • dizziness, ataxia
  • confusion
  • gastric irritation

Subsequently

  • 6-72 h
  • clinical features due to accumulation of formic acid
  • high anion gap metabolic acidosis
  • high osmolal gap
  • visual loss and papilloedema
  • pancreatitis

Treatment

Definitive therapy

  • gastric lavage in first hour post ingestion
  • infusion of sodium bicarbonate correct metabolic acidosis, reduce the ratio of formic acid to formate

  • inhibit formation of toxic metabolites by alcohol dehydrogenase
    • indications:

      • serum methanol >25mg/dl, or

      • osmolal gap >10mOsm/kg with recent history of ingestion

    • fomepizole
      • 15 mg/kg IV loading followed by 10 mg/kg IV 12 hourly
      • after 48 h increase dose to 15 mg/kg 12 hourly to account for increased metabolism
      • continue until methanol concentration <20 mg/dl
      • early administration avoid damage to kidney and prevent the need for ICU admission and dialysis

    • ethanol
      • 0.6 g/kg IV loading
      • followed by 66 mg/kg/h (non-alcoholic patients) or 154 mg/kg/h (alcoholic patients
      • double maintenance infusion rate for patients on dialysis
      • target serum ethanol concentration: 100-200 mg/dl
  • haemodialysis to remove methanol and metabolites. Indications:
    • serum methanol concentration >50 mg/dl
    • ingestion of a lethal dose of methanol (60-96 g; results in serum concentration of 80-100 mg/dl)
    • significant refractory metabolic acidosis (pH 7.25-7.3)
    • presence of ocular signs

    • evidence of other end-organ damage
    • ? serum methanol concentration >50 mg/dl

      • in the absence of ocular signs and significant metabolic acidosis, fomepizole should eliminate the need for hemodialysis in patients with serum methanol concentrations >50mg/dl

    Continue until serum methanol undetectable or for ≥36 hours

Supportive therapy

  • ± bicarbonate infusion
  • thiamine, folate, pyridoxine to promote the conversion of intermediate byproducts into nontoxic metabolites

Further reading

Mokhlesi B et al. Adult toxicology in critical care. Part II: Specific poisonings. Chest, 2003; 123:897-922

Me´garbane et al.Treatment of Acute Methanol Poisoning with Fomepizole.  Intensive Care Med. 2001, 27, 1370–1378

American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Methanol Poisoning


© Charles Gomersall & Anna Lee June 2006 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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