PH3.8 | PH3.8 | Alcohol Toxicity Management — SDL Guide — Summary & Reflection

KEY TAKEAWAYS

Methanol poisoning: methanol → formaldehyde → formic acid (toxic; metabolic acidosis + optic nerve damage). Treatment: fomepizole (ADH inhibitor, first-line) or ethanol (competitive ADH substrate) → stop formate formation; NaHCO₃ (correct acidosis); haemodialysis (severe); folinic acid. Chronic ethanol: GABA-A potentiation + NMDA inhibition → tolerance + dependence; withdrawal: seizures (6-48h), delirium tremens (48-96h) → IV diazepam/lorazepam; Wernicke's encephalopathy (thiamine deficiency) → IV thiamine BEFORE glucose (mandatory rule). Disulfiram = ALDH inhibitor → acetaldehyde accumulation → aversive deterrent reaction; warn about hidden alcohol. Naltrexone (opioid antagonist) and acamprosate (NMDA/GABA-B) reduce craving in alcohol use disorder.

REFLECT

You are the medical officer in a primary health centre when 8 villagers present within 2 hours of each other with nausea, vomiting, increasing confusion, and in two cases, complaints of visual blurring. Three were drinking at the same event. Your facility has no fomepizole. You have oral ethanol (commercially available alcohol), sodium bicarbonate for injection, and a dialysis centre 3 hours away. Walk through your pharmacological management plan step by step, including the rationale for each intervention and the criteria for urgent transfer for haemodialysis.