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CBRNE - Urticants, Phosgene Oxime
Updated: Mar 11, 2008
Introduction
Background
Phosgene oxime (CX) is an urticant or nettle agent that causes a corrosive type of skin and tissue injury. Although CX is often grouped with the vesicant chemical warfare agents, it is not a true vesicant because it does not cause blisters. 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. 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.
For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.
Pathophysiology
The mechanism of toxicity for CX is uncertain. 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.
Mortality/Morbidity
Morbidity and mortality for exposures to CX are dose dependent. 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.
Clinical
History
- Important historic features of a potential toxic chemical exposure include the following:
- Estimated time of occurrence
- Duration and circumstances of exposure
- Onset and time course of symptoms
- Odor and/or color of gases or vapors
- Protective clothing worn (if any)
- Effects on surroundings (eg, other human or animal casualties)
- CX casualties typically report unbearable pain in exposed skin and eyes; difficulty with sight or blindness after ocular exposure; and sore throat, hoarseness, dyspnea, chest pain, and cough after respiratory exposure.
- Some casualties may experience a peppery or pungent odor during their initial CX vapor exposure, but this is typically lost quickly because of accommodation.
Physical
- Skin: A blanching, grayish skin lesion surrounded by an erythematous ring can be observed within 30 seconds of exposure. A wheal develops on exposed skin within 30 minutes. The original blanched area acquires a necrotic, brown pigmentation by 24 hours. An eschar forms in the pigmented area by 1 week and sloughs after approximately 3 weeks.
- Eyes: Eye examination typically demonstrates conjunctivitis, lacrimation, lid edema, and blepharospasm after even minute exposures. More severe exposures can result in keratitis, iritis, corneal perforation, and blindness.
- Respiratory: Irritation of the mucous membranes may be observed on examination of the oropharynx and nose. Evidence of pulmonary edema, including rales and wheezes, may be noted on auscultation. Necrotizing bronchiolitis and pulmonary venule thromboses are prominent features of severe CX exposure.
- Gastrointestinal: Some animal data suggest that CX may cause hemorrhagic inflammatory changes in the GI tract.
Causes
Exposures to CX result from its deliberate use as a chemical warfare agent. Since this chemical has no useful industrial applications, accidental exposures are extremely unlikely.
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References
ATSDR. Medical management guidelines for phosgene oxime. [Full Text].
Armstrong J. Chemical warfare. RN. Apr 2002;65(4):32-9. [Medline].
Dang C. Chemical warfare agents. Top Emerg Med. 2002;24(2):25-39.
Department of the Army. Phosgene oxime. In: Field Manual 8-285: Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. 1995:IV-17-22.
McAdams AJ Jr, Joffe MH. A Toxico-pathologic Study of Phosgene Oxime. 1955. Army Medical Laboratories Research Report 381.
McManus J, Huebner K. Vesicants. Crit Care Clin. Oct 2005;21(4):707-18, vi. [Medline].
Rosenbloom M, Leikin JB, Vogel SN, Chaudry ZA. Biological and chemical agents: a brief synopsis. Am J Ther. Jan-Feb 2002;9(1):5-14. [Medline].
USAMRICD. Phosgene oxime. In: Medical Management of Chemical Casualties Handbook. 3rd ed. 2000:96-101.
Zajtchuk R, Bellamy RF, eds. Phosgene oxime. In: Textbook of Military Medicine Part I: Medical Aspects of Chemical and Biological Warfare. 1997:220-222.
Russell D, Blain PG, Rice P. Clinical management of casualties exposed to lung damaging agents: a critical review. Emerg Med J. Jun 2006;23(6):421-4. [Medline].
Further Reading
Keywords
CX, dichloroformoxime, urticant, nettle agent, chemical warfare agent, chemical burn, chemical exposure, CX exposure, CX injury, urticants, phosgene oxime, vesicant chemical warfare agent, terrorism
