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  • Cyanide poisoning causes profound tissue hypoxia.
  • Poisoning causes rapid onset of central nervous system and cardiovascular toxicity.
  • Helpful laboratory clues include lactic acidosis and a diminished arterial–venous O2 difference.
  • Antidotal therapy with nitrites and sodium thiosulfate or with hydroxocobalamin needs to be considered early.

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Cyanide poisoning is unusual in the United States and very rare among children, although its contribution to toxicity and death may be underestimated in victims of smoke inhalation from building fires.1 Hydrogen cyanide gas is formed as a combustion product of wool, silk, synthetic fabrics, and building materials in fires and is now recognized as a major cause of toxicity among fire victims previously thought to be poisoned by carbon monoxide.2,3 Acetonitrile, or methyl cyanide, is found in agents used to remove sculpted nails and has caused cyanide poisoning in children.4 Pediatric cyanide poisoning has also occurred from ingestion of cyanide-containing metal cleaning solutions imported from Asia and cyanogenic glycosides, like amygdalin, found in the seeds and pits of certain plants such as apples, apricots, and peaches.5

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Hydrogen cyanide gas is rapidly absorbed in the lungs and may cause profound toxicity within seconds. Ingested cyanide salts, such as sodium cyanide and potassium cyanide, are also rapidly absorbed across the gastric mucosa and may result in toxicity within minutes. Acetonitrile appears to release cyanide through oxidative metabolism by the hepatic cytochrome P450 system, thus delaying clinical manifestations of toxicity for 2 to 6 hours from the time of ingestion. Ingestion of amygdalin and other cyanogenic glycosides requires hydrolysis to release cyanide, so toxicity may also be delayed up to several hours after ingestion.

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The endogenous enzyme rhodanase (sulfurtransferase) converts cyanide to nontoxic thiocyanate: this mechanism is augmented in the presence of thiosulfate. In the presence of hydroxocobalamin (vitamin B12a), cyanide is converted to cyanocobalamin (vitamin B12), which is also nontoxic.

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Cyanide primarily causes tissue hypoxia by binding with ferric iron (Fe3+) in cytochrome a-a3 of the mitochondrial cytochrome oxidase. Inhibition of cytochrome oxidase prevents efficient cellular oxygen use and disrupts ATP production, which results in anaerobic metabolism and severe lactic acidosis (Fig. 128–1). Cyanide also shifts the oxygen-hemoglobin dissociation curve to the left, further impairing oxygen delivery to the tissues. Cyanide inhibits a wide variety of other iron- and copper-containing enzymes, although their contribution to clinical toxicity is uncertain. The critical targets of cyanide are those organs most dependent on oxidative phosphorylation, namely, the brain and the heart.6

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Figure 128-1.
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Pathway of cyanide and hydrogen sulfide toxicity and detoxification.

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The clinical presentation depends on the route and dose of exposure. Inhalation of cyanide gas causes loss of consciousness within seconds, whereas symptoms from an oral exposure develop anywhere from 30 minutes to several hours. Initial symptoms ...

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