## Cyanide Poisoning: Antidotes and Mechanisms ### Mechanism of Cyanide Toxicity Cyanide irreversibly binds to the ferric iron (Fe³⁺) in cytochrome c oxidase, blocking the electron transport chain and causing cellular hypoxia despite normal oxygen availability. ### Antidotes and Their Mechanisms | Antidote | Mechanism | Onset | Efficacy | |----------|-----------|-------|----------| | **Hydroxocobalamin** | Direct binding; forms cyanocobalamin (excreted) | Rapid (minutes) | First-line; safest | | **Sodium thiosulfate** | Substrate for rhodanese; converts CN⁻ → SCN⁻ | Slower (hours) | Adjunctive; enhances elimination | | **Sodium nitrite** | Induces methemoglobinemia (Fe²⁺ → Fe³⁺); Hb-Fe³⁺ binds CN⁻ | Rapid | Effective but risk of methemoglobinemia | | **Activated charcoal** | Adsorbs toxins in GI tract | GI only | NOT effective for inhaled or IV cyanide | **Key Point:** Hydroxocobalamin is now the preferred first-line antidote for cyanide poisoning because it directly chelates cyanide without the risk of methemoglobinemia. It is the only antidote that works for both ingested and inhaled cyanide. **High-Yield:** The cyanide antidote kit traditionally contained sodium nitrite + sodium thiosulfate, but hydroxocobalamin has largely replaced this regimen due to superior safety and efficacy [cite:Harrison 21e Ch 473]. **Warning:** Activated charcoal is useful for ingested poisons that remain in the GI tract, but cyanide is rapidly absorbed and acts systemically. In this case (inhalation), charcoal is ineffective and delays definitive treatment. **Clinical Pearl:** Sodium nitrite carries risk of severe methemoglobinemia, especially in patients with pre-existing anemia or hemoglobinopathies. Hydroxocobalamin avoids this complication.
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