Hydrogen Cyanide Poisoning 

This article addresses the management of hydrogen cyanide (HCN) poisoning. HCN (North Atlantic Treaty Organization [NATO] designation AC) is 1 of 2 cyanide chemical warfare agents^{[1, 2, 3]} ; the other is cyanogen chloride (NATO designation CK).

Cyanide is a rapidly lethal agent when used in enclosed spaces where high concentrations can be achieved easily.^{[4, 5, 6, 7]} In addition, because of the extensive use of cyanide in industry in the United States, this agent presents a credible threat for terrorist use.^[2] Emergency physicians may also encounter cyanide casualties resulting from industrial accidents or fires.

Cyanide was first used as a chemical weapon in the form of gaseous HCN in World War I. Starting in 1915, the French military used approximately 4000 tons of cyanide, without notable success. The failure of this measure was probably attributable to the high volatility of cyanide and the inability of the 1- to 2-lb munitions used to deliver the amounts of chemical required for biologic effects.^{[2, 3]}

The introduction of cyanogen chloride by the French in 1916 made available a compound that, being both more toxic and less volatile, was a more effective chemical agent. Other alleged military uses of cyanide include Japanese attacks on China before and during World War II and Iraqi attacks on Kurds in the 1980s.

For related information, see the Disaster Preparedness and Aftermath Resource Center.^{[8, 9]}

Whereas liquid cyanide can be absorbed through the skin or eyes, the primary route of exposure is by inhalation or ingestion. Once absorbed, cyanide is distributed rapidly to all organs and tissues in the body. It inhibits multiple enzymes, most importantly cytochrome a3, a component of cytochrome oxidase in the electron transport chain of the mitochondria. This prevents intracellular oxygen use and the generation of cellular adenosine triphosphate (ATP), causing aerobic energy production to cease.

Hydrogen ions accumulate as they fail to combine with oxygen at the end of the electron transport chain, causing a metabolic acidosis. As anaerobic metabolism ensues, pyruvate accumulates and is converted to lactate, resulting in an elevated lactate concentration.^[10]

The LCt₅₀ (the concentration-time product capable of killing 50% of the exposed group) for HCN is 2500-5000 mg/min/m³. The lethal oral doses of HCN and cyanide salts are estimated to be 50 mg and 100-200 mg, respectively. The LD₅₀ (the dose capable of killing 50% of the exposed group) for skin exposures is estimated to be 100 mg/kg. Vapor exposures in high concentrations (at or above the LCt₅₀) typically can cause death in 6-8 minutes.^[11]

Causes of cyanide casualties include deliberate use as a chemical warfare agent, industrial exposures, and toxic byproducts of fires.^{[12, 11]} Emergency physicians are unlikely to encounter casualties from HCN used as a weapon except in the setting of a terrorist attack^[11] ; the other causes are more common.

Specific industrial processes involving cyanide include metal cleaning, reclaiming, or hardening; fumigation; electroplating; and photo processing.^[12] Other potential sources of cyanide are fires involving plastics or synthetics, acrylic nail removers containing acetonitrile or propionitrile, and nitroprusside infusions.^[12] Numerous plants (eg, apricots, apples, and bitter almonds) contain within their seeds and pits amygdalin, which can be hydrolyzed to HCN after the ingestion and may be poisonous in large quantities.^[12]

The prognosis is good for patients who have only minor symptoms that do not necessitate the administration of antidotes.

The prognosis is poor in patients with cyanide poisoning sufficiently severe to cause cardiovascular collapse. In a mass casualty setting, these victims would be classified as expectant.

The prognosis is fair for patients with seizures or recent-onset apnea if antidotes can be administered rapidly. In a mass casualty setting, these victims would be classified as immediate.

It is important that patients exposed to HCN be educated about potential neurologic sequelae and the importance of follow-up evaluation.

For patient education resources, see the Bioterrorism and Warfare Center and the Poisoning Center, as well as Chemical Warfare, Personal Protective Equipment, Cyanide Poisoning, and Carbon Monoxide Poisoning.