Phosgene Oxime Exposure
- Author: Erik D Schraga, MD; Chief Editor: Robert G Darling, MD, FACEP more...
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.[1, 2, 3, 4] 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.[4, 5, 6]
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Pathophysiology
The mechanism of toxicity for CX is uncertain.[7] 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.[7]
Epidemiology
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.
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.
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].
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.
Zajtchuk R, Bellamy RF, eds. Phosgene oxime. In: Textbook of Military Medicine Part I: Medical Aspects of Chemical and Biological Warfare. 1997:220-222.
McAdams AJ Jr, Joffe MH. A Toxico-pathologic Study of Phosgene Oxime. 1955. Army Medical Laboratories Research Report 381.
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].
ATSDR. Medical management guidelines for phosgene oxime. [Full Text].
USAMRICD. Phosgene oxime. In: Medical Management of Chemical Casualties Handbook. 3rd ed. 2000:96-101.
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