Cyanide is a highly toxic chemical used widely in research and commercial laboratories and many industries. Its gaseous form, hydrogen cyanide, is an important component of smoke in fires. Cyanide-generating glycosides are also found in the pits of apricots and other related plants. Cyanide is generated by the breakdown of nitroprusside, and poisoning can result from rapid high-dose infusions. Cyanide is also formed by metabolism of acetonitrile, a solvent found in some over-the-counter fingernail glue removers. Cyanide is rapidly absorbed by inhalation, skin absorption, or ingestion. It disrupts cellular function by inhibiting cytochrome oxidase and preventing cellular oxygen utilization.
The onset of toxicity is nearly instantaneous after inhalation of hydrogen cyanide gas but may be delayed for minutes to hours after ingestion of cyanide salts or cyanogenic plants or chemicals. Effects include headache, dizziness, nausea, abdominal pain, and anxiety, followed by confusion, syncope, shock, seizures, coma, and death. The odor of “bitter almonds” may be detected on the victim’s breath or in vomitus, though this is not a reliable finding. The venous oxygen saturation may be elevated (greater than 90%) in severe poisonings because tissues have failed to take up arterial oxygen.
A. Emergency and Supportive Measures
Remove the victim from exposure, taking care to avoid exposure to rescuers. For suspected cyanide poisoning due to nitroprusside infusion, stop or slow the rate of infusion. (Metabolic acidosis and other signs of cyanide poisoning usually clear rapidly.)
For cyanide ingestion, administer activated charcoal. Although charcoal has a low affinity for cyanide, the usual doses of 60–100 g are adequate to bind typically ingested lethal doses (100–200 mg).
B. Specific Treatment
In the United States, there are two available cyanide antidote regimens. The conventional cyanide antidote package (Nithiodote) (see eTable 38–1) contains sodium nitrite (to induce methemoglobinemia, which binds free cyanide) and sodium thiosulfate (to promote conversion of cyanide to the less toxic thiocyanate). Administer 3% sodium nitrite solution, 10 mL intravenously, followed by 25% sodium thiosulfate solution, 50 mL intravenously (12.5 g). Caution: Nitrites may induce hypotension and dangerous levels of methemoglobin.
++ Table Graphic Jump Location eTable 38–1.Currently available cyanide (CN) antidote kits. ||Download (.pdf) eTable 38–1. Currently available cyanide (CN) antidote kits.
|Antidote ||Contents ||Action |
|Conventional cyanide antidote kit1 ||Administer 3% sodium nitrite solution, 10 mL intravenously followed by 25% sodium thiosulfate solution, 50 mL intravenously (12.5 g) ||Nitrites induce methemoglobinemia, which binds CN; thiosulfate hastens CN conversion to less toxic thiocyanate. |
|Cyanokit2 ||Hydroxocobalamin 5 g in two 2.5-g vials ||Converts CN to cyanocobalamin (vitamin B12). |
The other approved cyanide treatment in the United States is hydroxocobalamin (Cyanokit, EMD Pharmaceuticals), a newer and potentially ...