Cyanide is a fast-acting substance traditionally known as a poison. Cyanide was first isolated from Prussian blue dye in 1786, and cyanide was first extracted from almonds around 1800. Cyanide can exist as gas, hydrogen cyanide, salt and potassium cyanide. Natural substances found in some foods such as lima beans and almonds can release cyanide. Cyanide is also found in manufacturing and industrial sources such as pesticides, photographic solutions, plastic manufacturing, and jewelry cleaners. It was used as a poison in mass murder and suicide. This activity reviews the etiology, symptoms, assessment, and treatment/prevention of cyanide toxicity, and the role of professional teams in evaluating, diagnosing, and treating the condition. Cyanide is a fast-acting substance traditionally known as a poison. Cyanide was first isolated from Prussian blue dye in 1786, and cyanide was first extracted from almonds around 1800. Cyanide can exist as gas, hydrogen cyanide, salt and potassium cyanide. Natural substances found in some foods such as lima beans and almonds can release cyanide. It was used as a poison in mass murder and suicide. During World War II, the Nazis used cyanide as a means of genocidal gas chambers. Cyanide poisoning can result from a variety of exposures, including structural fires, industrial exposures, medical exposures such as sodium nitroprusside, and certain foods. Domestically, house fires are the most common cause of cyanide poisoning. Cyanide is also used in many industrial applications. B. Electroplating damage production, photography, plastic and rubber manufacturing, and pesticides. Sodium nitroprusside, a drug used to treat hypertensive emergencies, contains five cyanide groups per molecule. Toxic levels of cyanide develop in patients receiving long-term infusions of sodium nitroprusside. There is likely to be. From 1993 to 2002, he had 3,165 exposures to cyanide, according to the Toxic Exposure Surveillance System. Only 2.5% of these were fatal. In developed countries such as the United States, fire is the most common source of cyanide exposure. About 35% of all fire victims have toxic levels of cyanide in their blood when they receive treatment. According to the Center for Poisons Control's National Poison Data System annual report, in 2007 there were 247 reported exposures to cyanide chemicals in the United States, five of which were fatal. Intravenous and inhaled cyanide hastens the onset of signs and symptoms more than oral or dermal routes of exposure. This is because the first two routes allow rapid diffusion into the bloodstream. This effectively stops cellular respiration by blocking the reduction of oxygen to water. The main effect of cyanide is to inhibit oxidative phosphorylation, the process that uses oxygen to generate an essential cellular energy source in the form of ATP. It binds to the enzyme cytochrome c oxidase and blocks the mitochondrial transport chain. Cellular hypoxia and ATP depletion then occur, leading to metabolic acidosis. Tissue utilization of oxygen occurs and impairment of vital functions continues. Cyanide absorbs fast via the breathing tract and mucous membranes in addition to the gastrointestinal tract and skin. Signs and signs start at blood cyanide concentrations of about forty mol/L. In vivo, cyanide metabolism and neutralization contain some of mechanisms. The maximum crucial of those is the detoxing of cyanide through rhodanese, an enzyme located abundantly in lots of tissues however with inside the liver and muscle particularly. Thiosulfate serves as a sulfur donor with inside the response catalyzed with the aid of using rhodanese that converts cyanide to thiocyanate, a water-soluble molecule excreted with inside the urine.