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Anna Lee & Charles Gomersall
First posted June 2006
Source
- 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
Treatment
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
- 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
Prognosis
- 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
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