Sources of exposure
- Fires: Cyanide is released by various substances during combustion (e.g., plastics, upholstery, rubber).
- Long-term or high-dose treatment with sodium nitroprusside, especially in individuals with chronic renal failure
- Sodium nitroprusside releases cyanide ions.
- Industrial: metal industry, manufacture of nitrogen-containing materials and products (plastics and wool), electroplating
Pathophysiology
- Binds to the ferric ions in cytochrome oxidase IV within the mitochondria → Blocks the electron transport chain → ↓ oxidative phosphorylation → anaerobic metabolism, ↑ lactic acid, hypoxia
- Oxygen dissociation curve is usually normal (opposed to carbon monoxide poisoning)
Differential diagnostics
Cyanide poisoning vs CO poisoning
| Feature | Carbon Monoxide (CO) Poisoning | Cyanide (CN) Poisoning | Methemoglobinemia (MetHb) |
|---|---|---|---|
| Mechanism | Binds Hemoglobin (forms COHb) → ↓ O2 carrying & delivery. | Inhibits Cytochrome C Oxidase (Complex IV) → blocks ATP prod. | Iron in heme oxidized (Fe2+ → Fe3+) → cannot bind O2. |
| Source | Incomplete combustion (fires, car exhaust, faulty heaters). | Fires (plastics, wool), industrial, nitroprusside. | Oxidizing drugs (dapsone, nitrites, benzocaine), G6PD deficiency. |
| Presentation | Headache, dizziness, N/V. Cherry-red skin (late, unreliable). Normal SaO2 on pulse ox. | Rapid onset: confusion, seizures, coma. Cherry-red skin. Almond breath (unreliable). | Cyanosis (dusky/brown skin/blood) unresponsive to O2. Dyspnea. |
| Dx | ↑ COHb level (CO-oximetry). Pulse ox misleadingly normal. | ↑ Lactate. Clinical suspicion + history. High venous O2. | ↑ MetHb level (co-oximetry). “Saturation gap” (pulse ox ~85%). Chocolate-brown blood. |
| Tx | 100% O2. Hyperbaric O2 (HBO) if severe. | Hydroxycobalamin or Nitrites + Sodium Thiosulfate. | Methylene blue. O2. (Avoid MB in G6PD def.). |
| CT/MRI Brain | Bilateral globus pallidus lesions (hypodense CT, T2 hyper MRI). | Less specific; diffuse edema or basal ganglia lesions possible. | Non-specific hypoxic changes if severe. |
| O2-Myoglobin Curve | Shifts Left (impairs O2 release to muscle). | No direct significant effect. | No direct significant effect; O2-HGB curve shifts left for normal Hb. |
| Buzzwords | ”Faulty heater,” “car exhaust,” “globus pallidus lesions." | "Almond breath,” “plastic fire,” “nitroprusside." | "Dapsone,” “benzocaine,” “chocolate-brown blood,” “saturation gap.” |
Management
- Initial steps: Decontaminate the patient, secure the airway (ABCs), and administer 100% oxygen. While oxygen alone doesn’t reverse the enzyme inhibition, it aids in supportive care and treats potential concurrent CO poisoning.
- Antidotes: Do not delay antidote administration if suspicion is high.
- Hydroxocobalamin (first-line): Binds directly to cyanide to form cyanocobalamin (Vitamin B12), which is renally excreted. It is safe and the preferred agent, especially in smoke inhalation victims where inducing methemoglobinemia is contraindicated.
- Nitrites + Sodium Thiosulfate (traditional therapy):
- Amyl nitrite (inhaled) or Sodium nitrite (IV): Induces methemoglobinemia. Methemoglobin (Fe³⁺) has a high affinity for cyanide, pulling it off cytochrome oxidase to form cyanomethemoglobin. Use with caution due to hypotension and risk in CO poisoning.
- Sodium thiosulfate: Acts as a sulfur donor for the enzyme rhodanese, which converts cyanide to the less toxic, renally excreted thiocyanate.