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CBRNE - Cyanides, Cyanogen Chloride
Updated: Sep 5, 2008
Introduction
Background
Cyanogen chloride (North Atlantic Treaty Organization [NATO] designation CK) is one of two volatile cyanide military chemical warfare agents. The other similar agent is hydrogen cyanide, or AC (please see CBRNE - Cyanides, Hydrogen). These agents first were used in large quantities by the French and British during World War I. While the United States maintained 500-pound and 1000-pound CK bombs, these were not used during World War II. More recently, Iraq is suspected to have used a cyanide-like agent against the Kurds in the 1980s.
Although CK and AC are similar in their toxicity, a few important differences exist. Firstly, CK is less volatile than AC, making it more effective at low concentrations. Secondly, by nature of its chlorine moiety, CK causes irritation of the eyes and respiratory tract and potential delayed pulmonary toxicity similar to chlorine or phosgene gases. In high concentrations (eg, in enclosed spaces), CK is a rapidly acting lethal agent, causing death within 6-8 minutes if inhaled at doses at or above its LCt50 (lethal concentration that kills 50% of people; 11,000 mg·min/m3).
CK is synthesized in the United States for industry by Matheson Tri-Gas and is used as an organic precursor and in mining and metalworking. Therefore, an emergency physician may be more likely to encounter CK-exposed victims following an industrial accident rather than in a warfare or terrorism scenario.
Pathophysiology
In addition to CK's local irritant effects, systemic toxicity occurs through mechanisms similar to those seen with hydrogen cyanide exposure (see CBRNE - Cyanides, Hydrogen). CK liberates a cyanide molecule, which enters the blood stream and distributes to tissues. Once inside cells, CK binds to mitochondrial cytochrome aa3, interrupts electron transport, and creates imbalance between ATP synthesis and hydrolysis. Oxygen is unable to be used effectively as the terminal electron acceptor, which forces a shift to anaerobic metabolism. While all organ systems are impacted, the most oxygen-dependent ones are the most affected (ie, brain, heart).
Frequency
United States
The major source of cyanide poisoning in the United States does not come from CK but rather from smoke inhalation during house and/or industrial fires in which plastics (acrylonitriles, polyurethanes), wool, or silk are burned. Cyanide poisoning also is found in association with chemical synthesis, electroplating, mineral extraction, dyeing, photography, and agriculture.
Mortality/Morbidity
In high concentrations, which can be obtained in enclosed spaces, CK is a rapidly acting lethal agent causing death within 6-8 minutes.
Clinical
History
When taking a history from a patient with possible toxic gas exposure, ask about the smell and color of the gas, onset of symptoms, duration and severity of symptoms, and effect on surroundings (eg, dead animals, other people). CK is a colorless liquid or gas with a pungent biting odor, which may in fact go unnoticed because of discomfort. Symptoms that may be associated with CK exposure include the following:
- In low doses
- Bronchorrhea
- Lacrimation
- Rhinorrhea
- Moderate range doses
- Onset possibly takes several minutes, except for immediate irritant effects
- Transient hyperpnea
- Feelings of anxiety or apprehension
- Vertigo
- Nausea and/or vomiting
- Prolonged prodrome prior to loss of consciousness
- Seizures
- Bradypnea followed by apnea
- Cardiac arrest
- In high doses
- Transient hyperpnea
- Seizures 15-30 seconds later
- Apnea 2-3 minutes later
- Cardiac arrest 6-8 minutes postexposure
Physical
Patients may suffer from any of the above symptoms. Physical findings are generally nonspecific and similar to those of severe hypoxemia.
- Severe prolonged exposure culminates in respiratory distress, convulsions, and apnea.
- Patients may have cherry red or pink skin because of concomitant carbon monoxide poisoning or because of cyanide-induced lack of extraction of oxygen at the tissue level and vasodilation. Arterialization of the venous blood also may be noted at phlebotomy or upon examination of the retinal veins. However, note that bright red skin or absence of cyanosis rarely is described. Cyanosis may be observed and most likely stems from concomitant cardiovascular collapse, seizures, or apnea. Finally, many cyanide victims have normal-appearing skin.
- Patients initially are hypertensive, tachypneic, and bradycardic, but eventually they become hypotensive. They may experience a transient tachycardia before spiraling into bradydysrhythmia that deteriorates into asystole.
Causes
Other than acts of terrorism or war, a mass casualty may develop in an industrial accident in which CK comes in contact with water (eg, during a fire-fighting expedition). Containers of CK may rupture or explode if exposed to high heat or following prolonged storage.
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References
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Further Reading
Keywords
cyanide toxicity, cyanide poisoning, chlorine cyanide, chlorocyan, chlorocyanide, chlorocyanogen, cyanochloride, cyanide gas, ClCN, CK, chemical warfare agents, cyanogen chloride, cyanide exposure, cyanogen chloride exposure, cyanogen chloride inhalation, blood agents
Overview: CBRNE - Cyanides, Cyanogen Chloride