Toxicology – Cyanide Poisoning

Source

Cyanide exposure can occur during smoke inhalation from structural fires, especially when materials such as wool, silk, plastics, insulation, or rubber burn. It may also be encountered in certain industrial settings, some foods or plant products, and rarely from prolonged nitroprusside therapy.

Typical Presentation

A patient exposed to heavy smoke or an occupational cyanide source may rapidly develop confusion, shortness of breath, chest discomfort, seizures, or cardiovascular collapse. Cyanide toxicity should be considered in severe smoke inhalation with unexplained lactic acidosis or sudden hemodynamic deterioration.

Clinical Features

Possible findings include:

• Headache
• Nausea and vomiting
• Altered mental status
• Dilated pupils
• Rapid breathing
• Tachycardia
• Early hypertension
• Later hypotension and respiratory depression
• Chest pain
• Seizures
• Cardiovascular collapse

Laboratory abnormalities may show:

• Severe lactic acidosis
• High anion gap metabolic acidosis
• Unusually high venous oxygen content because tissues cannot effectively extract oxygen

Mechanism of Action

Cyanide inhibits cytochrome c oxidase in the mitochondrial electron transport chain. This blocks aerobic cellular respiration, preventing tissues from using oxygen despite adequate oxygen delivery and causing rapid anaerobic metabolism and lactate accumulation.

Management

Treatment requires immediate supportive care:

• High-flow oxygen and airway support
• Cardiac and hemodynamic monitoring
• Aggressive management of seizures and shock
• Hydroxocobalamin is a preferred antidotal therapy because it binds cyanide to form a less toxic compound that can be eliminated
• Sodium thiosulfate may also be used to enhance conversion of cyanide to thiocyanate

Nitrite-based antidotes induce methemoglobinemia and are generally less desirable when carbon monoxide exposure is also suspected, as commonly occurs in fire victims.

Key Points

• Think of cyanide toxicity in patients with severe smoke inhalation plus cardiovascular collapse or marked lactic acidosis.
• Cyanide prevents cells from using oxygen rather than preventing oxygen from reaching the blood.
• Hydroxocobalamin is a major antidote used in suspected cyanide poisoning.
• A markedly elevated lactate level can serve as an important indirect clue.