## Clinical Presentation & Pathophysiology This patient presents with acute cyanide poisoning manifesting as: - Metabolic acidosis (pH 7.28, low HCO₃⁻) with respiratory compensation (low PaCO₂) - Tachycardia and tachypnea indicating cellular hypoxia - Normal PaO₂ despite respiratory distress — the hallmark of cyanide toxicity (oxygen delivery failure, not oxygenation failure) **Key Point:** Cyanide binds to cytochrome c oxidase (Complex IV) in the electron transport chain, preventing aerobic metabolism. Tissues cannot utilize oxygen despite adequate PaO₂ — this is histotoxic hypoxia. ## Management Algorithm for Acute Cyanide Poisoning ```mermaid flowchart TD A[Suspected acute cyanide poisoning]:::outcome --> B{Symptomatic?}:::decision B -->|Yes| C[Immediate antidote]:::action B -->|No| D[Supportive care + observation] C --> E[Sodium nitrite 300 mg IV]:::action E --> F[Induces methemoglobinemia]:::outcome F --> G[Cyanide binds to MetHb]:::outcome G --> H[Sodium thiosulfate 12.5 g IV]:::action H --> I[Converts thiocyanate for renal excretion]:::outcome I --> J[Clinical improvement]:::outcome ``` ## Antidote Mechanism **Sodium nitrite** converts hemoglobin to methemoglobin (MetHb), which has a higher affinity for cyanide than cytochrome oxidase. Cyanide is sequestered as cyanmethemoglobin. **Sodium thiosulfate** provides sulfur donor for rhodanese enzyme, converting cyanide to thiocyanate (less toxic, renally excreted). **High-Yield:** The combination of nitrite + thiosulfate is synergistic — nitrite acts immediately (within seconds), thiosulfate acts over minutes to hours. ## Dosing in India (Standard Protocol) | Agent | Dose | Route | Timing | |-------|------|-------|--------| | Sodium nitrite | 300 mg (10 mL of 3% soln) | IV over 5–10 min | Immediately | | Sodium thiosulfate | 12.5 g (50 mL of 25% soln) | IV over 10–15 min | After nitrite | | Repeat doses | Half the original dose | IV | If symptoms recur after 30 min | **Clinical Pearl:** In severe cyanide poisoning with loss of consciousness, do NOT delay antidote administration for confirmatory tests. Treat empirically if clinical suspicion is high (history of exposure + metabolic acidosis + normal PaO₂). **Warning:** Excessive methemoglobin (>20%) causes its own hypoxia. Monitor MetHb levels if available; do not repeat nitrite if MetHb >20%. ## Why Oxygen Alone Is Insufficient Oxygen therapy supports aerobic metabolism in unaffected tissues and may help if cyanide levels are very low, but it does NOT displace cyanide from cytochrome oxidase. Antidote administration is mandatory in symptomatic cases. [cite:Park 26e Ch 12]
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