Ethylene Glycol Poisoning
Ethylene glycol is a toxic alcohol found in antifreeze, de‑icers and some industrial solvents. Much of the clinical harm arises from hepatic metabolism to glycolic and oxalic acids: glycolic acid produces a high anion‑gap metabolic acidosis and tissue injury, while oxalic acid chelates calcium and precipitates as calcium‑oxalate crystals that damage renal tubules and cause hypocalcaemia (UKHSA).
Pathophysiology and clinical phases
Ethylene glycol is rapidly absorbed and metabolised by alcohol dehydrogenase (ADH) to glycoaldehyde → glycolic acid → glyoxylic acid → oxalic acid. Clinical features evolve in overlapping phases (typical timings):
- Early / neurological (≈ 0.5-12 h): CNS depression - intoxication, dizziness, ataxia and coma that can mimic ethanol intoxication.
- Cardiopulmonary / metabolic (≈ 12-24 h): progressive high anion‑gap metabolic acidosis with compensatory tachypnoea, tachycardia and possible hypotension.
- Renal (≈ 24-72 h): acute kidney injury (oliguria/anuria), flank pain, haematuria; urine microscopy may show calcium‑oxalate crystals and hypocalcaemia may cause tetany or arrhythmias (UKHSA).
Timings are approximate and overlap; co‑ingested ethanol delays metabolism and alters the timeline.
Key investigations (ED priorities)
- Immediate: arterial or venous blood gas (pH, HCO3-), ECG, continuous monitoring and IV access.
- Bloods: sodium, potassium, chloride, bicarbonate, urea, creatinine, calcium, magnesium, glucose, measured osmolality, serum ethanol and, if available, ethylene glycol concentration.
- Calculate anion gap and osmolar gap - both help with timing/diagnosis (RCEM).