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
| Carbon monoxide poisoning | Cyanide poisoning | |
|---|---|---|
| Etiology | House fires, wood-burning stoves/gas heaters, furnaces in enclosed and poorly ventilated spaces | Fires: combustion of certain substances (e.g., plastics, upholstery, rubber) |
| Motor vehicle exhaust fumes | Food containing cyanide or amygdalin (e.g., cassava, apricot seeds, bitter almonds) | |
| Can affect multiple individuals from the same location, especially during the winter (e.g., family members sharing a heating device) | Long-term or high-dose treatment with sodium nitroprusside | |
| Change in oxygen-myoglobin dissociation curve | Shift to the left | Usually normal |
| Clinical features | Headache, dizziness. fatigue, nausea/vomiting | Breath smells of bitter almonds |
| Altered mental status, seizures, loss of consciousness/coma | Confusion, agitation, vertigo, headache, seizures, coma | |
| Inhalation injury: associated with exposure to fire | Nausea, vomiting | |
| Postmortem: cherry-red skin with bullous skin lesions | Cardiac arrhythmia | |
| Dyspnea, respiratory failure | ||
| Flushing of the skin | ||
| Postmortem: bright red livor mortis (cherry red skin) | ||
| Laboratory measurements | An elevated COHb level falsely elevates the SaO2 measurements from pulse oximetry | PaO2: normal |
| PaO2: usually normal | High anion gap metabolic acidosis (↑ lactate) | |
| High anion-gap metabolic acidosis | ||
| CT/MRI brain | The globus pallidus is commonly affected. | The globus pallidus is rarely affected. |
| Management | Administration of 100% oxygen | Patient decontamination |
| Hyperbaric oxygen in severe cases | Administration of 100% oxygen | |
| Antidotes: hydroxycobalamin, sodium nitrite/amyl nitrite, or sodium thiosulfate |
Management
- Patient decontamination (e.g., remove clothes, wash skin)
- Administration of 100% oxygen regardless of saturation readings
- Supportive care
- Antidote
- Hydroxocobalamin (precursor of vitamin B12): binds cyanide directly and forms cyanocobalamin, which is excreted in urine (first-line antidote)
- Sodium nitrite, amyl nitrite, or 4-dimethylaminophenol (4-DMAP) to induce methemoglobinemia (via oxidation of Hb): Methemoglobin binds to cyanide to form cyanomethemoglobin, which diverts cyanide from cytochrome complex IV and increases oxidative phosphorylation.
- Sodium thiosulfate: supplies sulfur donors to the mitochondrial enzyme rhodanese. Rhodanese detoxifies cyanide into thiocyanate, which is excreted in urine (usually coadministered with hydroxocobalamin).