see also:

• toxicology
• methanol poisoning
• Wikitox

• ethylene glycol is used as a car radiator coolant and is not an uncommon agent used in intentional poisoning.
• one should suspect it as a cause of cases characterised by high anion gap metabolic acidosis with osmolal gap.
• a dose of over 1 mL/kg body weight may cause significant toxicity or death.
• it is rapidly absorbed with peak concentrations occurring within 1-2 hours.
• it has high water and lipid solubility and a volume of distribution similar to body water (0.6 L/kg).
• the initial effects of ethylene glycol resemble those of alcohol with CNS depression, ataxia, nausea and vomiting.
• the osmolal gap may be only mildly elevated in clinically significant poisoning (i.e. still be within the normal range). A concentration of 50 mg/dL produces a rise in the osmolal gap of only 10 mmol/kg. Some of the metabolites may also contribute to the osmolal gap
• it is metabolised by alcohol dehydrogenase to toxic metabolites (glycoaldehyde ⇒ glycolate ⇒ glyoxylate ⇒ oxylate) which form calcium oxylate crystals in the kidneys, acute tubular necrosis, and death from acute renal failure.

• Coma
• Seizures
• Renal failure
• Hypotension
• Ethylene glycol concentration > 50 mg/dL
• Calcium oxalate crystals in the urine
• Severe acidosis (pH < 7.1)
• Hyperkalaemia

¹⁾

• arterial pH < 7.109 or 7.25-7.30
• drop in arterial pH > 0.05 resulting in a pH outside the normal range despite bicarbonate infusion
• inability to maintain arterial pH > 7.30 despite bicarbonate therapy
• decrease in bicarbonate concentration > 5 mmol/L despite bicarbonate Rx
• renal failure (serum creatinine > 265 mmol/l or a rise of > 90 mmol/l)
• deteriorating vital signs despite intensive supportive care
• initial plasma ethylene glycol concentration > 0.5g/L (> 8.1 mmol/L)

• GIT decontamination NOT effective
• iv access, take bloods for FBE, U&E, Ca, Mg, acid-base, glucose, measured osmolality
• may require intubation and ongoing sedation, and the usual supportive care including iv fluids
• acidosis should be corrected with bicarbonate.
• hypocalcaemia should be corrected with intravenous calcium.
• assuming one does not have access to the alcohol dehydrogenase inhibitor, fomepizole, (approved for use in Australia in 2016)²⁾, then one should attempt to prevent metabolism of ethylene glycol by administering ethanol as the preferred substrate for alcohol dehydrogenase which will then allow the ethylene glycol to be cleared renally or by dialysis:
  • bolus dose iv ethanol:
    • 7.6-10ml/kg of 10% ethanol (v/v) in 5% dextrose given iv over 30min
    • this equates to 4 standard drinks for an adult or 0.6g/kg
  • place patient on haemodialysis (continuous venous-venous haemodialysis CVVHD) - may require this for ~ 1 week
  • ethanol infusion (5-10g/hr for adults) or add ethanol to dialysate, titrate to give a serum concentration of 100-150mg/dL (0.10-0.15%)
• encourage non-toxic metabolic pathways by giving thiamine 100mg qid and vitamin B6 (pyridoxine) 50mg qid
• watch for ethanol withdrawal seizures on ceasing ethanol administration, particularly if PH ethanol abuse
• 4-Methyl pyrazole (fomepizole):
  • a safer and more efficacious agent than ethanol but expensive (~$A8000 for course in Australia)
  • 15mg/kg iv loading dose over 30min then 10mg/kg 12hrly (4hrly if on dialysis) until ethylene glycol levels are low