Ethylene Glycol Overdose
Overview
Ethylene glycol (EG) is a colourless, odourless, sweet‑tasting alcohol found in antifreeze, de‑icers and some industrial products. Toxicity follows ingestion (accidental in children, recreational or deliberate in adults).
Clinical harm results mainly from metabolism of EG by alcohol dehydrogenase (ADH) to acidic metabolites (glycolic, glyoxylic and oxalic acids) that produce a high anion‑gap metabolic acidosis, hypocalcaemia and acute kidney injury. Contact local poisons services and specialist toxicology/renal teams early.
Key points
- Lethal dose is product‑dependent; as an order‑of‑magnitude estimate for a 70 kg adult use ~100 g EG - calculate exact amounts from the product formulation.
- The biochemical picture evolves over time: an early raised osmolar gap (from the parent alcohol) is followed by a later rising anion‑gap metabolic acidosis as acidic metabolites accumulate. Never exclude poisoning on the basis of a single normal osmolar gap.
- Check serum calcium early - hypocalcaemia and calcium oxalate deposition in the kidney are common.
- Contact your local poisons service (NPIS/TOXBASE) and on‑call toxicology/renal teams early for advice on antidote use and dialysis thresholds.
Clinical features (staged)
- Early (0-12 h): ethanol‑like central nervous system depression (inebriation), nausea, vomiting, ataxia.
- Intermediate (6-24 h): progressive metabolic acidosis, tachypnoea, tachycardia, possible pulmonary oedema, symptomatic hypocalcaemia (perioral numbness, tetany), ECG changes.
- Late (>24 h): acute kidney injury (oliguria/anuria) from calcium oxalate deposition; possible prolonged...