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Ethylene glycol

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Anna Lee & Charles Gomersall

First posted June 2006


  • antifreeze
  • de-icers
  • industrial solvents

Mechanism of toxicity

  • Metabolized by alcohol dehydrogenase to glycoaldehyde and glycolic acid, which is the major cause of metabolic acidosis. Glycolic acid converts to glyoxylic acid, which eventually converts to oxalic acid and glycin

  • Accumulation and precipitation of oxalic acid as calcium oxalate crystals in renal tubules contributes to acute renal failure
  • Hypocalcaemia results from precipitation with oxalic acid
  • Myocardial depression

Clinical features

Traditionally was divided into three stages: progressive involvement of the CNS, the cardiopulmonary systems, and the kidneys

Stage 1

  • 0.5-12h after ingestion
  • inebriation
  • ataxia
  • seizures
  • high anion gap metabolic acidosis
    • variable severity
    • ± Kussmaul breathing
  • high osmolal gap
  • crystalluria
  • hypocalcaemia
  • cerebral oedema causing coma or death

Stage 2

  • 12h-24h post ingestion
  • myocardial dysfunction
  • pulmonary oedema
    • may be high or low pressure
  • death at this stage usually occurs as a result of myocardial dysfunction or aspiration pneumonia

Stage 3

  • 2-3 days
  • acute renal failure


Definitive therapy

  • gastric lavage in first hour post ingestion
  • infusion of sodium bicarbonate to correct metabolic acidosis, increase elimination of renal glycolic acid and prevent precipitation of calcium oxalate crystals

  • inhibit formation of toxic metabolites by alcohol dehydrogenase
    • indications

      • serum ethylene glycol >25mg/dl, or

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

    • fomepizole
      • early administration avoid damage to kidney, and prevent the need for ICU admission and dialysis

      • 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 ethylene glycol concentration <20 mg/dl
    • 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 ethylene glycol and metabolites. Indications:
    • significant refractory metabolic acidosis (pH < 7.25-7.3)
    • evidence of end-organ damage
    • ? serum ethylene glycol concentration >50 mg/dl
      • In the absence of renal dysfunction and significant metabolic acidosis, fomepizole should eliminate the need for hemodialysis in patients with serum ethylene glycol concentrations >50mg/dl

    Continue until ethylene glycol undetectable or for ≥36 hours

Supportive therapy

  • correct hypocalcaemia in patients with tetany or seizures
  • thiamine, folate, pyridoxine to promote the conversion of intermediate byproducts into nontoxic metabolites    


  • significant toxicity associated with serum concentration >50 mg/dl
  • ingestion of as little as 100ml can be lethal in an adult
  • fatal within 24 h if untreated

Further reading

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

Treatment of Ethylene Glycol Poisoning. American Family Physician, 2002; 66(5)

© Anna Lee & Charles Gomersall, 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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