ClinCalc Pro
Menu
ToxicologyEmergency

Methanol / ethylene glycol poisoning

Recognition of toxic alcohol ingestion (osmolar gap, anion gap), fomepizole/ethanol blockade and dialysis.

Source: TOXBASE/NPIS; AACT/EAPCCT; EXTRIP; BNF

Step 1 of ~6
warning

Suspect toxic alcohol — early treatment is sight- and life-saving

Mechanism: parent compound is relatively non-toxic; toxicity from alcohol dehydrogenase (ADH) metabolism. • Methanol → formate (retinal injury, blindness, putaminal necrosis). • Ethylene glycol → glycolate, oxalate (AKI, hypocalcaemia, calcium-oxalate crystals in urine, cardiac/cranial nerve injury). Clues: ingestion of windscreen wash, antifreeze, denatured alcohol; "drunk without alcohol" or persistently obtunded after ethanol metabolised. ABCDE; bloods: VBG (HAGMA), U&E, creatinine, calcium (low in EG), lactate, ethanol, paracetamol/salicylate, osmolality (measured), serum methanol/ethylene glycol if available, urine for crystals + Wood's lamp fluorescence (EG containing fluorescein — unreliable). Calculate osmolar gap = measured − calculated osmolality (calculated = 2×Na + glucose + urea + ethanol/4.6, all mmol/L). Early high osmolar gap → consider toxic alcohol. Late: gap closes as parent metabolised, anion gap acidosis emerges.

Related

Curated clinical cross-links plus same-class fallbacks.

Decision support only. Always apply local guidelines and clinical judgement.