A 32-year-old male factory worker is brought to the emergency department unconscious after exposure to fumes in an industrial accident. On examination, he has a respiratory rate of 28/min, blood pressure 140/90 mmHg, and a peculiar finding of bright pink discoloration of the skin. His arterial blood gas shows PaO₂ 95 mmHg on room air, but venous oxygen saturation is 95% (unusually high). He has seizures and loss of consciousness. What is the most likely diagnosis and what is the mechanism of toxicity?

Explanation

## Diagnosis: Cyanide Poisoning **Key Point:** Cyanide poisoning causes **histotoxic hypoxia** — cells cannot utilize oxygen despite adequate arterial oxygenation. The hallmark finding is a **normal or elevated PaO₂ with elevated venous O₂ saturation** because tissues cannot extract oxygen. ### Mechanism of Toxicity **High-Yield:** Cyanide binds irreversibly to the **ferric iron (Fe³⁺) in cytochrome c oxidase** (Complex IV of the electron transport chain), blocking aerobic respiration. This forces cells into anaerobic metabolism, producing lactic acidosis. ### Clinical Features of Cyanide Poisoning | Feature | Explanation | |---------|-------------| | **Bright pink/cherry-red skin** | Due to elevated venous oxygen saturation (unused oxygen in blood) | | **Seizures & LOC** | Brain is highly metabolically active; affected early | | **Respiratory distress** | Reflex hyperventilation from lactic acidosis | | **Normal/high PaO₂** | Oxygen is present but cannot be used by cells | | **High venous O₂ sat** | Pathognomonic — tissues reject oxygen | | **Lactic acidosis** | Shift to anaerobic metabolism | ### Why NOT the Other Options - **Carbon monoxide:** Causes carboxyhemoglobinemia with LOW venous O₂ sat; skin is cherry-red but from carboxyhemoglobin, not unused oxygen. - **Hydrogen sulfide:** Causes direct myocardial depression and pulmonary edema; no characteristic high venous O₂ saturation. - **Methemoglobinemia:** Reduces oxygen-carrying capacity; PaO₂ may be normal but oxygen delivery is impaired; no high venous saturation. **Clinical Pearl:** The combination of **normal/high arterial PO₂ + high venous PO₂ + lactic acidosis + CNS symptoms** is virtually pathognomonic for cyanide poisoning. ### Management Priorities 1. **Immediate:** Remove from exposure, give 100% O₂ (supportive). 2. **Antidote:** Hydroxocobalamin (preferred in modern practice) or sodium thiosulfate + sodium nitrite (older regimen). 3. **Hydroxocobalamin mechanism:** Directly binds cyanide to form cyanocobalamin, which is excreted in urine. [cite:Parikh Forensic Medicine 3e Ch 18]