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Cyanide (hydrocyanic acid, prussic acid) is a rare but rapidly lethal poison for humans. The most common source of exposure in industrialized countries is combustion of household goods containing carbon and nitrogen. Occupational exposure can occur during elecroplating, plastic and rubber manufacturing and use of pesticides. Medical therapy with amygdalin (Laetrile) or nitroprusside can also cause cyanide toxicity.

Cyanide is rapidly absorbed through the respiratory tract and mucous membranes, but can also be absorbed through the gastrointestinal tract and skin.  Cyanide inhibits cellular respiration by tightly binding to ferric ion (Fe3+) in cytochrome oxidase a3, blocking electron transport and oxidative phosphorylation. Cells must then rely on anaerobic metabolism of glucose to generate ATP. Although cyanide has a primary affinity for ferric iron, a small amount may bind to ferrous (Fe2+) iron in hemoglobin, forming cyanohemoglobin and interfering with oxygen transport. This is an additional cause of tissue hypoxia

Cyanide blocks cellular respiration by binding to and inactivating hemoglobin and enzymes such as cytochrome oxidase having prosthetic groups containing ferric iron (Fe+++). Cyanide is metabolized rapidly by the liver where it is converted to thiocyanate.

Symptoms of cyanide poisoning include headache, anxiety, confusion, giddiness, seizures, coma; tachypnea followed by bradypnea; tachycardia and hypertension followed by bradycardia and hypotension; and cherry red skin color followed by cyanosis. Depending on cyanide concentration, death may occur within a few minutes to 3 hours. Cyanide toxicity can be reversed with hydroxocobalamin or a combination of sodium nitrite or sodium thiosulfate.

Cyanide poisoning produces severe metabolic acidosis with an increased anion gap. Blood lactate concentration is elevated due to tissue hypoxia. Because of decreased utilization of oxygen by tissues, venous oxyhemoglobin concentration remains high and there is a narrowing of the venous to arterial PO2 gradient.

Blood cyanide concentrations may be ordered for diagnostic confirmation, but results are usually not available in time to be clinically useful. Blood concentrations in the average population may as high as 0.2 ug/mL due to ingestion of vegetables such as brussel sprouts. Smokers have an average cyanide concentration of 0.4 ug/mL. After exposure, some patients may have cyanide concentrations as high as 2.0 ug/mL without exhibiting symptoms. Cyanide concentrations of 2.0 to 4.0 ug/mL are usually associated with symptoms. Cyanide concentrations greater than 5.0 ug/mL are potentially lethal.

Cyanide levels are not useful in monitoring toxicity from nitroprusside (Nipride) treatment of hypertensive crisis. Patients may have cyanide concentrations as high as 8.0 ug/mL without exhibiting symptoms of toxicity. Thiocyanate should be ordered to determine the potential for cyanide toxicity during nitroprusside therapy.

Specimen requirement is a lavendar top tube of blood. 

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