Cyanide is a rapidly acting substance that is traditionally known as a poison. Hydrogen cyanide was first isolated from Prussian blue dye in 1786 and cyanide first extracted from almonds around 1800. Cyanide can exist as a gas, hydrogen cyanide, a salt, potassium cyanide. Natural substances in some foods such as lima beans, almonds can release cyanide. Cyanide is also found in manufacturing and industrial sources such as insecticides, photographic solutions, plastics manufacturing, and jewelry cleaner. It has been used as a poison in mass homicides and suicides. This activity reviews the etiology, presentation, evaluation, and management/prevention of cyanide toxicity, and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition.Cyanide poisoning may result from a variety of exposures, including structural fires, industrial exposures, medical exposures such as sodium nitroprusside, and certain foods. In domestic countries, the most common cause of cyanide poisoning is domestic fires. Cyanide also is used in a number of industrial applications such as electroplating injury production, photography, plastics and rubber manufacturing, and pesticides. Sodium nitroprusside, a medication used to treat a hypertensive emergency, contains five cyanide groups per molecule. Toxic levels of cyanide may be present in patients who receive prolonged infusions of sodium nitroprusside.According to the Toxic Exposure Surveillance System, there were 3165 human exposures to cyanide from 1993 to 2002. Of that number, only 2.5% were fatal. Fire is the most common source of cyanide exposure in industrialized countries such as the United States. Approximately 35% of all fire victims will have toxic levels of cyanide in their blood on presentation for medical treatment. According to the National Poison Data System of a Poison Control Centers annual report, there were 247 reported cases of chemical exposures to cyanide in the United States in 2007, five of which were fatal.Intravenous and inhalation of cyanide produce a more rapid onset of signs and symptoms than exposure via the oral or transdermal route. This is due to the first two routes providing fast diffusion into the bloodstream. The toxicity of cyanide is linked mainly to the cessation of aerobic cell metabolism. Cyanide reversibly binds to the ferric ions cytochrome oxidase three within the mitochondria. This effectively halts cellular respiration by blocking the reduction of oxygen to water.Cyanide's main effect is that it inhibits oxidative phosphorylation, a process where oxygen is utilized for the production of essential cellular energy sources in the form of ATP. It does so by binding to the enzyme cytochrome C oxidase and blocks the mitochondrial transport chain. After that, cellular hypoxia and the depletion of ATP occur, leading to metabolic acidosis. The utilization of oxygen by the tissue occurs and is followed by the impairment of vital functions.Cyanide absorbs quickly through the respiratory tract and mucous membranes as well as the gastrointestinal tract and skin. Signs and symptoms begin at blood cyanide concentrations of approximately 40 mol/L. In vivo, cyanide metabolism and neutralization involve a number of mechanisms. The most important of these is the detoxification of cyanide via rhodanese, an enzyme found abundantly in many tissues but in the liver and muscle particularly. Thiosulfate serves as a sulfur donor in the reaction catalyzed by rhodanese that converts cyanide to thiocyanate, a water-soluble molecule excreted in the urine.

Submit manuscript at https://www.scholarscentral.org/submissions/toxicology-open-access.html or send as an e-mail attachment to the Editorial Office at toxicol@peerjournal.org

Kind regards

Managing editor 

Catherine

Toxicology: Open Access