## Distinguishing Methanol from Ethanol Poisoning ### Key Pathophysiologic Difference **Key Point:** Visual disturbances and optic nerve damage are the hallmark and most specific discriminating feature of methanol poisoning, rarely seen in ethanol toxicity. Methanol is metabolized by alcohol dehydrogenase to formaldehyde, then aldehyde dehydrogenase to formic acid. Formic acid accumulates and causes: - Selective retinal toxicity → photophobia, blurred vision, scotomata - Optic nerve atrophy → permanent blindness if untreated - Formic acid crosses the blood–brain barrier more readily than ethanol metabolites ### Comparison Table | Feature | Methanol | Ethanol | |---------|----------|----------| | **Visual symptoms** | ✓ Characteristic (optic neuritis, blindness) | ✗ Absent | | **Metabolic acidosis** | ✓ Severe, anion gap | ✓ Can occur but milder | | **CNS depression** | ✓ Present | ✓ Prominent | | **Optic nerve damage** | ✓ Pathognomonic | ✗ Never | | **Formic acid accumulation** | ✓ Yes | ✗ No | ### Clinical Pearl **Clinical Pearl:** The triad of **methanol poisoning** is: 1. Visual disturbances (earliest sign) 2. Severe metabolic acidosis with anion gap 3. CNS depression with altered mental status Visual symptoms appearing *before* severe acidosis develops is a red flag for methanol. ### High-Yield Mechanism **High-Yield:** Ethanol is preferentially metabolized over methanol by alcohol dehydrogenase. This is why **ethanol is the antidote** for methanol poisoning — it competitively inhibits the formation of toxic formic acid, buying time for dialysis and folic acid supplementation. ### Management Difference - **Methanol:** Fomepizole (alcohol dehydrogenase inhibitor) + folic acid + dialysis - **Ethanol:** Supportive care; no specific antidote needed [cite:Park 26e Ch 24]
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