Medical Toxicology

, Volume 1, Issue 5, pp 309–334 | Cite as

Methanol and Ethylene Glycol Poisonings

Mechanism of Toxicity, Clinical Course, Diagnosis and Treatment
  • Dag Jacobsen
  • Kenneth E. McMartin
Toxicology Management Review


Methanol and ethylene glycol poisonings share many characteristics both clinically and biochemically. Both alcohols are metabolised via alcohol dehydrogenase to their toxic metabolites. Methanol is slowly metabolised to formaldehyde which is rapidly metabolised to formate, the metabolite mainly responsible for methanol toxicity. Formate metabolism depends upon the folate pool which is small in primates compared with other animals. Therefore, formate accumulates in primates during methanol intoxication and is mainly responsible for the metabolic acidosis in the early stage of intoxication. In late stages lactate may also accumulate, mainly due to formate inhibition of the respiratory chain. This tissue hypoxia caused by formate may explain the ocular as well as the general toxicity.

Ethylene glycol is metabolised more rapidly than methanol, via alcohol dehydrogenase to glycolaldehyde which is rapidly metabolised to glycolate, the metabolite mainly responsible for the metabolic acidosis in ethylene glycol poisoning. Glycolate is metabolised by various pathways, including one to oxalate which rapidly precipitates with calcium in various tissues and in the urine. Ethylene glycol toxicity is complex and not fully understood, but is mainly due to the severe metabolic acidosis caused by glycolate and to the calcium oxalate precipitation.

The clinical course in both poisonings is initially characterised by the development of metabolic acidosis following a latent period, which is more pronounced in methanol poisoning and is the time taken for both alcohols to be metabolised to their toxic metabolites. In methanol poisoning there are usually visual symptoms progressing to visual impairment, whereas ethylene glycol victims develop renal and cardiopulmonary failure.

Prognosis is excellent in both poisonings provided that there is early treatment with alkali to combat acidosis, ethanol as an antimetabolite, and haemodialysis to remove the alcohols and their toxic metabolites. Ethanol is also metabolised by alcohol dehydrogenase, but has a much higher affinity for this enzyme than methanol and ethylene glycol. Presence of ethanol will therefore inhibit formation of toxic metabolites from methanol and ethylene glycol. Due to competition for the enzyme, the therapeutic ethanol concentration depends on the concentration of the other two alcohols, but a therapeutic ethanol concentration around 22 mmol/L (100 mg/dl) is generally recommended.

Most patients are, however, admitted at a late stage to hospitals not capable of performing analyses of these alcohols or their specific metabolites on a 24-hour basis. Treatment is therefore often delayed because of delayed diagnosis, with fatal consequences. In situations where specific analyses are not available, the calculation of the anion and osmolal gaps in every case of metabolic acidosis of unknown origin can provide the diagnosis, allowing treatment to be started earlier. In ethylene glycol poisonings urine microscopy may also reveal the abundant presence of acicular calcium oxalate monohydrate crystals. Determination of the anion and osmolal gaps, along with the repetitive urine microscopy, is therefore mandatory whenever facing a metabolic acidosis of unknown origin.


Metabolic Acidosis Calcium Oxalate Glycolaldehyde Methanol Poisoning Glycol Poisoning 
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Copyright information

© ADIS Press Limited 1986

Authors and Affiliations

  • Dag Jacobsen
    • 1
  • Kenneth E. McMartin
    • 1
  1. 1.Department of Pharmacology and Therapeutics, Section of ToxicologyLSU Medical CenterShreveportUSA

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