## Acute Cyanide Poisoning Management **Key Point:** Cyanide inhibits cytochrome c oxidase in the electron transport chain, causing histotoxic hypoxia (cells cannot use oxygen despite normal oxygen saturation). The antidotes work by binding cyanide or converting it to non-toxic forms — NOT by adsorption. ### Antidotes in Cyanide Poisoning | Antidote | Mechanism | Timing | Notes | | --- | --- | --- | --- | | **Sodium nitrite** | Induces methemoglobinemia; cyanide binds Hb-Fe³⁺ with higher affinity than cytochrome c oxidase | First (if available) | Risk: hypotension, methemoglobinemia toxicity | | **Sodium thiosulfate** | Substrate for rhodanese enzyme; converts CN⁻ → SCN⁻ (thiocyanate), which is renally excreted | Second; can be repeated | Slower acting; safe; enhances nitrite effect | | **Hydroxocobalamin** | Direct binding of CN⁻ → cyanocobalamin; excreted in urine | Preferred in modern protocols | Faster, safer; no methemoglobinemia risk; now first-line in many countries | | **Activated charcoal** | Adsorbs cyanide in GI tract | Oral/gastric only | **NOT a systemic antidote**; only useful if ingestion is recent and patient is conscious | **High-Yield:** The classic triad of cyanide antidotes is **"SNS"** — **S**odium nitrite, **N**a-thiosulfate, and **S**odium hydroxocobalamin (modern). Activated charcoal is NOT a systemic antidote — it works only in the GI tract and is irrelevant once cyanide is absorbed. **Clinical Pearl:** The "pink" appearance of cyanide poisoning (flushed skin, pink lips) is due to high venous oxygen saturation (cells cannot extract oxygen), not hypoxemia. This is histotoxic hypoxia, not hypoxic hypoxia. **Warning:** Activated charcoal does NOT reverse systemic cyanide toxicity. In an unconscious patient with cyanide poisoning, activated charcoal is contraindicated (aspiration risk) and ineffective (cyanide is already absorbed). The focus is on IV antidotes: hydroxocobalamin (preferred) or sodium nitrite + thiosulfate.
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