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Phosgene Oxime Exposure

  • Author: Erik D Schraga, MD; Chief Editor: Zygmunt F Dembek, PhD, MPH, MS, LHD  more...
 
Updated: Jun 24, 2016
 

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]

For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.

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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]

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Epidemiology

Mortality/Morbidity

Morbidity and mortality for exposures to CX are dose dependent. Concentrations below 8% cause no or inconsistent effects.[8] 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.

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Contributor Information and Disclosures
Author

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Coauthor(s)

Andre Pennardt, MD, FACEP, FAAEM, FAWM Professor and Vice Chairman for Operational Medicine, Department of Emergency Medicine and Hospitalist Services, Georgia Regents University

Andre Pennardt, MD, FACEP, FAAEM, FAWM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Florida Medical Association, National Association of EMS Physicians, Special Operations Medical Association, International Society for Mountain Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US, Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zygmunt F Dembek, PhD, MPH, MS, LHD Associate Professor, Department of Military and Emergency Medicine, Adjunct Assistant Professor, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Zygmunt F Dembek, PhD, MPH, MS, LHD is a member of the following medical societies: American Chemical Society, New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Fred Henretig, MD Director, Section of Clinical Toxicology, Professor, Medical Director, Delaware Valley Regional Poison Control Center, Departments of Emergency Medicine and Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital

Disclosure: Nothing to disclose.

References
  1. Armstrong J. Chemical warfare. RN. 2002 Apr. 65(4):32-9. [Medline].

  2. Dang C. Chemical warfare agents. Top Emerg Med. 2002. 24(2):25-39.

  3. McManus J, Huebner K. Vesicants. Crit Care Clin. 2005 Oct. 21(4):707-18, vi. [Medline].

  4. Rosenbloom M, Leikin JB, Vogel SN, Chaudry ZA. Biological and chemical agents: a brief synopsis. Am J Ther. 2002 Jan-Feb. 9(1):5-14. [Medline].

  5. Department of the Army. Phosgene oxime. Field Manual 8-285: Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. 1995. IV-17-22.

  6. Zajtchuk R, Bellamy RF, eds. Phosgene oxime. Textbook of Military Medicine Part I: Medical Aspects of Chemical and Biological Warfare. 1997. 220-222.

  7. McAdams AJ Jr, Joffe MH. A Toxico-pathologic Study of Phosgene Oxime. 1955.

  8. Hurst CG, Petrali JP, Barillo DJ, Graham JS, Smith WJ, Urbanetti JS, et al. Vesicants. Tuorinsky SD. Medical Aspects of Chemical Warfare. 1st. Washington, D.C.: Office of the Surgeon General, Textbook of Military Medicine; 2008. 259-310. [Full Text].

  9. Russell D, Blain PG, Rice P. Clinical management of casualties exposed to lung damaging agents: a critical review. Emerg Med J. 2006 Jun. 23(6):421-4. [Medline].

  10. ATSDR. Medical management guidelines for phosgene oxime. [Full Text].

  11. USAMRICD. Phosgene oxime. Medical Management of Chemical Casualties Handbook. 3rd ed. 2000. 96-101.

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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.
 
 
 
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