Ethylene glycol is a type of alcohol used as a coolant or antifreeze.

After ingestion, ethylene glycol is metabolised by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase through the following key stages:

• Ethylene glycol → Glycolaldehyde
  • Toxic but short-lived intermediate.
• Glycolaldehyde → Glycolic acid (glycolate)
  • Most clinically important metabolite.
  • Responsible for severe high-anion-gap metabolic acidosis.
  • Causes CNS depression and cardiopulmonary toxicity.
• Glycolic acid → Glyoxylic acid (glyoxylate)
  • Another toxic intermediate
• Glyoxylic acid → Oxalic acid. Combines with calcium → calcium oxalate crystals
  • In blood → hypocalcaemia
  • In renal tubules → acute tubular necrosis and calcium oxalate stones

Features of toxicity are divided into 3 stages:

• Stage 1: symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness
• Stage 2: metabolic acidosis with high anion gap and high osmolar gap. Also tachycardia, hypertension
• Stage 3: acute kidney injury

Management has changed in recent times

• ethanol has been used for many years
  • works by competing with ethylene glycol for the enzyme alcohol dehydrogenase
  • this limits the formation of toxic metabolites (e.g. glycoaldehyde and glycolic acid) which are responsible for the haemodynamic/metabolic features of poisoning
• fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol
• haemodialysis also has a role in refractory cases

2. Ethylene glycol poisoning

found in coolant, anti-freeze, hydraulic brake fluids, etc.

toxic metabolite is Oxalic acid/ oxalate >> damage kidneys

usually has 3 distinct clinical phases-

• first stage- N, V, lethargy and CNS effects ( first 12 hours) s/a ataxia, nystagmus, slurred speech,
• second stage- CVS effects ( HTN, CCF, ARDS etc) metabolic acidosis with high anion gap and high osmolar gap (presents with Kussmaul's resp:) and