IM22.8 | Toxic Alcohol Poisoning — Summary & Reflection

KEY TAKEAWAYS

Methanol poisoning:
- Source: illicit hooch, industrial solvents, spirit varnish
- Toxic metabolite: formic acid (formate), formed by ADH → formaldehyde → formate
- Mechanism: formate inhibits cytochrome c oxidase → optic nerve and CNS damage
- Cardinal symptom: visual disturbance (blurring → blindness) — pathognomonic
- Metabolic pattern: high anion gap metabolic acidosis + early elevated osmolar gap (falls as methanol metabolised)
- Antidotes: fomepizole (preferred) OR ethanol (target 100–150 mg/dL) + folic acid IV + sodium bicarbonate
- Haemodialysis: pH < 7.2, visual disturbance, methanol > 50 mg/dL, renal failure

Ethylene glycol poisoning:
- Source: antifreeze, industrial fluids
- Toxic metabolites: glycolic acid + oxalic acid (calcium oxalate crystals)
- Mechanism: oxalate precipitates in renal tubules → AKI + hypocalcaemia
- Clinical: intoxication (Stage 1) → cardiopulmonary (Stage 2) → AKI + hypocalcaemia (Stage 3); NO visual symptoms
- Urine: calcium oxalate crystals; fluorescent (antifreeze dye) under Wood's lamp
- Antidotes: fomepizole OR ethanol + calcium gluconate (for hypocalcaemia) + pyridoxine + thiamine
- Haemodialysis: pH < 7.25, AKI, EG level > 50 mg/dL, refractory hypocalcaemia

Key principle for both: ADH inhibition prevents ALL metabolite formation — start it EARLY, maintain target ethanol level DURING dialysis

REFLECT

The five patients in the opening hook — from a single village celebration, all drinking the same hooch — illustrate why toxic alcohol poisoning is not just a clinical problem but a public health emergency. Think about the systemic changes that would prevent the next hooch tragedy: stronger enforcement of illicit alcohol regulations; public awareness that blindness from country liquor is not rare and is caused by methanol, not 'bad luck'; greater availability of fomepizole and dialysis at secondary care hospitals in alcohol-heavy agricultural districts; and training of primary care and district hospital physicians to recognise the osmolar gap as an early diagnostic tool. On a personal clinical level: the next time you see a patient presenting with visual symptoms after alcohol consumption — think methanol. The clinical instinct to categorise this as 'drunk' or 'withdrawal' can cost the patient their sight. Visual symptoms after alcohol are methanol until proven otherwise.