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Cyanide is a highly toxic chemical with a variety of uses, including chemical synthesis, laboratory analysis, and metal plating. Aliphatic nitriles (acrylonitrile and propionitrile) used in plastics manufacturing are metabolized to cyanide. The vasodilator drug nitroprusside releases cyanide upon exposure to light or through metabolism. Natural sources of cyanide (amygdalin and many other cyanogenic glycosides) are found in apricot pits, cassava, and many other plants and seeds, some of which may be important, depending on ethnobotanical practices. Acetonitrile, a solvent that was a component of some artificial nail glue removers, has caused several pediatric deaths.

Hydrogen cyanide is a gas easily generated by mixing acid with cyanide salts and also is a common combustion by-product of burning plastics, wool, and many other natural and synthetic products. Hydrogen cyanide poisoning is an important cause of death from structural fires, and deliberate cyanide exposure (through cyanide salts) remains an important instrument of homicide and suicide. Hydrogen cyanamide, an agricultural chemical used as a plant regulator, is a potent toxin that inhibits aldehyde dehydrogenase but does not act as a cyanide analog.

  1. Mechanism of toxicity. Cyanide is a chemical asphyxiant; binding to cellular cytochrome oxidase, it blocks the aerobic utilization of oxygen. Unbound cyanide is detoxified by metabolism to thiocyanate, a much less toxic compound that is excreted in the urine.

  2. Toxic dose

    1. Exposure to hydrogen cyanide gas (HCN), even at low levels (150–200 ppm), can be fatal. The air level considered immediately dangerous to life or health (IDLH) is 50 ppm. The Occupational Safety & Health Administration (OSHA) legal permissible exposure limit (PEL) for HCN is 10 ppm. The recommended workplace ceiling limit (ACGIH TLV-C) is 4.7 ppm (5 mg/m3 for cyanide salts). Cyanide in solution is well absorbed across the skin.

    2. Adult ingestion of as little as 200 mg of the sodium or potassium salt may be fatal. Solutions of cyanide salts can be absorbed through intact skin.

    3. Acute cyanide poisoning is relatively rare with nitroprusside infusion (at normal infusion rates) or after ingestion of amygdalin-containing seeds (unless they have been pulverized).

  3. Clinical presentation. Abrupt onset of profound toxic effects shortly after exposure is the hallmark of cyanide poisoning. Symptoms include headache, nausea, dyspnea, and confusion. Syncope, seizures, coma, agonal respirations, and cardiovascular collapse ensue rapidly after heavy exposure.

    1. A brief delay may occur if the cyanide is ingested as a salt, especially if it is in a capsule or if there is food in the stomach.

    2. Delayed onset (minutes to hours) also may occur after ingestion of nitriles and plant-derived cyanogenic glycosides because metabolism to cyanide is required.

    3. Chronic neurologic sequelae may follow severe cyanide poisoning, consistent with anoxic injury.

  4. Diagnosis is based on a history of exposure or the presence of rapidly progressive symptoms and signs. Severe lactic acidosis is usually present with significant exposure. The measured venous oxygen saturation may be elevated owing to blocked cellular oxygen consumption. The classic “bitter almond” odor of hydrogen cyanide may or ...

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