Epidemiology

Cyanide poisoning is uncommon. It is also potentially rapidly fatal. Cyanide is used in precious metal extraction, electroplating, metal hardening, photography, and various other industries. Cyanide has also been used as an agent of chemical warfare and in judicial executions.

Cyanide exists in several forms. The gaseous form is hydrogen cyanide (HCN); the salt forms are potassium cyanide and sodium cyanide. The inorganic salts release HCN gas when they are dissolved in water. Cyanogens are compounds that are metabolized to cyanide in vivo. The two clinically important cyanogens are amygdalin and acetonitrile. Amygdalin is a naturally occurring cyanogen found in the seeds of plants in the Prunus species and in the pits of other fruits (Box 153.1). Acetonitrile is found in some artificial nail removal products. Unlike other cyanide products, cyanogens may produce delayed cyanide toxicity because of the time required for their biotransformation. Cyanide gas is also released during combustion of certain natural and synthetic materials (Box 153.2). Consequently, cyanide poisoning can occur in victims of structure fires.

Pathophysiology

Cyanide is a potent cellular poison. The primary clinical effect occurs through the inhibition of oxidative phosphorylation. Cyanide binds to the ferric (Fe³⁺) moiety of cytochrome oxidase aa₃, the last enzyme of the electron transport chain.¹ The net effects of cyanide poisoning are reduced oxygen consumption and conversion of aerobic to anaerobic metabolism; these effects lead to profound metabolic acidosis and an elevated serum lactate concentration.

Presenting Signs and Symptoms

The clinical presentation of cyanide poisoning is protean and depends on the route of exposure and the cyanide compound involved. The early signs and symptoms are dyspnea, headache, weakness, nausea, vomiting, diaphoresis, hypotension, tachycardia, and altered mental status. The late signs and symptoms are bradycardia, atrioventricular heart block, ventricular dysrhythmias, asystole, seizures, and coma. Exposure to any form of cyanide can result in death.

Cyanide gas is a knockdown agent, causing those exposed to lose consciousness rapidly. Patients with exposure to 300 parts per million (ppm) of cyanide gas rapidly collapse and typically do not survive to admission to the emergency department. Exposure to 100 ppm for more than 30 minutes is considered life-threatening. An oral dose of 200 mg of potassium cyanide is considered a fatal ingestion. Features of cyanide poisoning typically develop 15 to 30 minutes after ingestion of cyanide salts. Exposure to cyanogens can result in delayed symptoms and signs because the parent compound must be metabolized before cyanide is produced.

Differential Diagnosis and Medical Decision Making

Without a history of cyanide exposure, the diagnosis is often difficult to make (Table 153.1). All medical causes of altered mental status, hypotension, and acidosis must be considered. The differential diagnosis of cyanide poisoning is listed in Box 153.3.

Whole-blood cyanide measurement is not readily available in the emergency department. The hallmark findings in cyanide poisoning are profound metabolic acidosis with a wide anion gap and an elevation of serum lactate.