Background: Hydrogen cyanide (HCN; North Atlantic Treaty Organization [NATO] designation AC) is 1 of 2 cyanide chemical warfare agents. The other is cyanogen chloride (NATO designation CK). Cyanide first was used as a chemical weapon in World War I. The French used approximately 4000 tons without notable military success. This was most likely because of the high volatility of cyanide and the fact that the 1- to 2-lb munitions used could not deliver the amounts of chemical required for biological effects. Other alleged military employments of cyanide include Japanese attacks on China before and during World War II and Iraqi attacks on Kurds in the 1980s.
Cyanide is a rapidly lethal agent when used in enclosed spaces where high concentrations can be achieved easily. In addition, because of the extensive use of cyanide in industry in the US, this agent presents a credible threat for terrorist use. Emergency physicians also may encounter cyanide casualties resulting from industrial accidents. Specific industrial processes involving cyanide include fumigation; metal cleaning, reclaiming, and/or hardening; electroplating; or photoprocessing. Other potential sources of cyanide are fires involving plastics and/or synthetics, acrylic nail removers containing acetonitrile or propionitrile, or nitroprusside infusions. Numerous plants contain amygdalin, which can be hydrolyzed to AC following the ingestion of large quantities.
Pathophysiology: While liquid cyanide can be absorbed through the skin or eyes, the primary route of exposure is by inhalation or ingestion. Following absorption, cyanide is distributed rapidly to all organs and tissues in the body. Cyanide combines with ferric iron in cytochrome a3 (a component of the cytochrome oxidase complex in mitochondria) and inhibits this enzyme. This prevents intracellular oxygen use and results in imbalance between ATP hydrolysis and production. Metabolic acidosis is a hallmark of cyanide toxicity. It develops as cells are forced to use anaerobic metabolism and accumulate hydrogen ions and lactate.
Frequency:
In the US: Emergency physicians are unlikely to encounter casualties from AC used as a weapon except in the setting of a terrorist attack. Typical cyanide exposures are the result of liberation of the chemical during house and/or industrial fires or accidents.
Mortality/Morbidity: The LCt50 (concentration-time product capable of killing 50% of exposed group) for AC is 2500-5000 mg·min/m3. The lethal oral dose of AC and cyanide salts is estimated to be 50 mg and 100-200 mg, respectively. The LD50 (dose capable of killing 50% of exposed group) for skin exposures is estimated at 100 mg/kg. Vapor exposures in high concentrations (at or above the LCt50) typically can cause death in 6-8 minutes. CLINICAL Section 3 of 10
History: Key historic features for suspected AC casualties include the time and nature of exposure; route of exposure; presence of smoke; odors and colors of gas; onset, severity, and time course of symptoms; effects on surroundings (dead animals, other human casualties); and evidence of exposure to other chemicals or co-ingestants. As many as 50% of patients exposed to cyanide may describe an odor of bitter almonds.
Symptoms after high vapor exposure
Transient hyperpnea and hypertension 15 seconds after inhalation
Convulsions 15-30 seconds later
Respiratory arrest 2-3 minutes later
Bradycardia, hypotension, and cardiac arrest within 6-8 minutes of exposure
Symptoms after exposure to lower vapor concentrations or after ingestion and/or liquid exposure
May be several minutes before onset
Transient hyperpnea
Feelings of apprehension or anxiety
Vertigo
Feeling of weakness
Nausea with or without vomiting
Muscular trembling
Progression of symptoms to unconsciousness
Bradypnea followed by apnea
Convulsions
Cardiac dysrhythmias followed by cardiac arrest
Exposure to nitriles (acetonitrile and/or propionitrile) - May be associated with a significant delay in onset of symptoms
Physical: Physical findings are nonspecific and are similar to those of severe hypoxemia.
Severe respiratory distress in an acyanotic patient suggests possible cyanide toxicity.
When observed, "cherry-red" skin suggests concomitant carbon monoxide poisoning or high venous oxygen content from failure of tissues to extract oxygen. Arterialization of the venous blood also may be noted during phlebotomy or examination of the retinal veins.
Bright red skin and absence of cyanosis seldom are described in patients with cyanide poisoning, most likely because of concomitant cardiovascular collapse.
Patients may demonstrate diaphoresis with normal or dilated pupils.
Initial hypertension and compensatory bradycardia are followed by hypotension and tachycardia.
Terminal hypotension is accompanied by bradyarrhythmias prior to asystole.
Causes: Causes of cyanide casualties include deliberate use as a chemical warfare agent, industrial exposures, and toxic byproducts of fires. DIFFERENTIALS Section 4 of 10
CBRNE - Cyanides, Cyanogen Chloride
CBRNE - Nerve Agents, Binary: GB2, VX2
CBRNE - Nerve Agents, G-series: Tabun, Sarin, Soman
CBRNE - Nerve Agents, V-series: Ve, Vg, Vm, Vx
Shock, Septic
Toxicity, Carbon Monoxide
Toxicity, Ethylene Glycol
Toxicity, Hydrogen Sulfide
Toxicity, Isoniazid
Toxicity, Organophosphate and Carbamate
Other Problems to be Considered:
Consider the diagnosis of cyanide poisoning in patients with rapid collapse or seizures accompanied by metabolic acidosis and decreased oxygen consumption. Other agents that may have similar features in toxicity include the following:
Methemoglobin-inducing agents
Carbon monoxide
Inert gases (simple asphyxiants)
Hydrogen sulfide
Azides
Arsine
Phosphine
Monomethylhydrazine
Isoniazid
Water hemlock
Strychnine
Organophosphates
Metformin