Practice Essentials
Phosgene oxime (CX) is an urticant or nettle agent that causes a corrosive type of skin and tissue injury and may produce systemic effects. [1, 2] Although CX is often grouped with the vesicant chemical warfare agents, it is not a true vesicant because it does not cause blisters. [3, 4, 5, 6] Both vapor and liquid CX cause immediate tissue damage on contact. CX in its pure form is a colorless, crystalline solid at temperatures below 95°F, but the vapor pressure of the solid is high enough to produce symptoms. As a munitions grade compound, CX is in liquid form with a yellowish brown appearance.
Although Germany and Russia both developed CX before World War II, no uses of the agent on the battlefield are known. [7] CX is of military interest because it penetrates garments and rubber much more quickly than other chemical agents and it produces a rapid onset of severe and prolonged effects. [6, 8, 9] For this reason, it could be produced as a weaponized mixture with other chemical warfare agents to enhance their deleterious effects. No antidotes against CX-induced injury are available; treatment is supportive. [10]
For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.
Pathophysiology
The mechanism of toxicity for CX is uncertain. [11] Possible mechanisms of toxicity include necrotizing effects of the chloride component or a direct effect of the oxime or carbonyl groups. It primarily affects the skin, eyes, respiratory system, and gastrointestinal tract. The agent seems to cause its greatest systemic effects in the first capillary bed encountered. For example, skin exposure or intravenous (IV) injection of CX causes pulmonary edema, while injection into the portal vein produces hepatic necrosis but not pulmonary edema. [11]
The acute effects of CX following its cutaneous exposure in SKH-1 hairless mice show that topical cutaneous exposure to CX vapor causes blanching of exposed skin with an erythematous ring, necrosis, edema, mild urticaria and erythema within minutes after exposure and up to 8 hours post-exposure. These clinical skin manifestations were accompanied with increases in skin thickness, apoptotic cell death, mast cell degranulation, myeloperoxidase activity indicating neutrophilinfiltration, p53 phosphorylation and accumulation, and an increase in COX-2 and TNFα levels. Topical CX-exposure also resulted in the dilatation of the peripheral vessels with a robust increase in red blood cells in vessels of the liver, spleen, kidney, lungs and heart tissues. These events could cause a drop in blood pressure leading to shock, hypoxia and death. [12]
Epidemiology
Exposures to CX result from its deliberate use as a chemical warfare agent. [3, 6, 9] Since this chemical has no useful industrial applications, accidental exposures are extremely unlikely.
Prognosis
Prognosis is generally good for minimal exposures. Severe and early respiratory distress portends a poor prognosis. Morbidity and mortality for exposures to CX are dose dependent. Concentrations below 8% cause no or inconsistent effects. [13] The estimated LCt50 (concentration-time product capable of killing 50% of exposures) for CX vapor is 1500-2000 mg·min/m3. The LD50 (lethal dose for 50% of exposures) for skin exposures is estimated at 25 mg/kg. Skin and mucous membrane irritation can begin within 12 seconds of a vapor exposure of 0.2 mg·min/m3. Unbearable pain and irritation occur within 1 minute of vapor exposure to 3 mg·min/m3.
Potential complications include the following:
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Scarring
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Wound infections
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Loss of vision
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Death from severe respiratory injury
Patient Education
Educate outpatients about the signs and symptoms of wound infection, for which they immediately should seek further medical care. For patient education information, see Chemical Warfare and Personal Protective Equipment. [3, 6]
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Anteroposterior portable chest radiograph in a male patient who developed phosgene-induced adult respiratory distress syndrome. Notice the bilateral infiltrates and ground glass appearance.
