ICU · toxicology
Acute Methanol and Ethylene Glycol Poisoning — Comprehensive ICU Management
Also known as Methanol poisoning · Ethylene glycol poisoning · Toxic alcohols · Fomepizole · 4-methylpyrazole · Formic acid toxicity · Calcium oxalate crystals · Osmolar gap · Anion gap acidosis · Wood alcohol · Antifreeze poisoning
Toxic alcohol poisoning = methanol and ethylene glycol (the 'toxic alcohols') — both are metabolised by ALCOHOL DEHYDROGENASE (ADH) to highly toxic organic acids → SEVERE HIGH ANION GAP METABOLIC ACIDOSIS + end-organ injury. Methanol (CH3OH) → formaldehyde → FORMIC ACID → inhibits mitochondrial cytochrome c oxidase → RETINAL/optic nerve toxicity → BLINDNESS + basal ganglia injury. Ethylene glycol (HOCH2CH2OH) → glycoaldehyde → GLYCOLIC ACID (main acidosis driver) → glyoxylic acid → OXALIC ACID → precipitates with calcium → CALCIUM OXALATE CRYSTALS in renal tubules → ACUTE KIDNEY INJURY + hypocalcaemia. Both cause CNS depression, nausea, abdominal pain. DIAGNOSTIC CLUE: HIGH anion gap metabolic acidosis + HIGH osmolar gap EARLY (parent alcohol present — small osmotically active molecules). The osmolar gap FALLS as the anion gap RISES (parent alcohol is metabolised into organic acids) — so a LATE presenter may have a NORMAL osmolar gap. Latent period 12–24 h (metabolism required) — patient looks 'drunk' then deteriorates. Management PILLARS: (1) FOMEPIZOLE 15 mg/kg IV LOAD (blocks ADH → stops toxic metabolite formation — PREFERRED over ethanol — far safer, no CNS depression/hypoglycaemia) then 10 mg/kg q12h; (2) HAEMODIALYSIS (removes parent alcohol + metabolites — indicated for severe acidosis pH <7.3, AKI, visual symptoms, high levels >50 mg/dL, deterioration); (3) COFACTORS — FOLINIC ACID (methanol — folate-dependent oxidation of formate → CO2 + H2O) + THIAMINE + PYRIDOXINE (ethylene glycol — shunt glyoxylate to non-toxic glycine, AWAY from oxalate); (4) sodium bicarbonate for acidosis (also ion-traps formate/glycolate → enhances elimination). Ethanol is the ALTERNATIVE ADH inhibitor if fomepizole unavailable (target 100–150 mg/dL). Activated charcoal is USELESS (alcohols are small, rapidly absorbed, poorly bound). Outbreaks from illicit/counterfeit alcohol common. Mortality methanol 10–40% (up to 50% in outbreaks); ethylene glycol ~1–2% with early fomepizole + dialysis.
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Red flags
- HIGH anion gap metabolic acidosis + HIGH osmolar gap = TOXIC ALCOHOL until proven otherwise — start fomepizole immediately; do NOT wait for methanol/ethylene glycol levels (often unavailable for hours)
- Visual symptoms (blurred vision, 'snowstorm' vision, photophobia, optic disc hyperaemia) = METHANOL → start fomepizole + folinic acid + arrange haemodialysis NOW — delay = permanent BLINDNESS
- A NORMAL osmolar gap does NOT exclude toxic alcohol — the parent alcohol is metabolised over 12–24 h, so a LATE presenter has a HIGH anion gap with a NORMAL osmolar gap (parent alcohol gone, organic acids remain)
- Ethylene glycol + hypocalcaemia + AKI + calcium oxalate crystalluria — give thiamine + pyridoxine (shunt glyoxylate to glycine, away from oxalate) + correct calcium cautiously + fomepizole + haemodialysis
- Do NOT give activated charcoal for toxic alcohol ingestion — alcohols are small molecules that bind charcoal poorly and are absorbed within 30–60 min; it is useless and delays antidote
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References16ShowHide
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