Phosgene Toxicity Follow-up

  • Author: Daniel Noltkamper, MD, FACEP; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Apr 19, 2011
 

Further Inpatient Care

  • Admit patient to an intensive care setting for continued monitoring and supportive care. Improvement typically occurs within 48-72 hours.[8]
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Further Outpatient Care

  • In a case of suspected exposure to phosgene, monitor the patient for a minimum of 8-12 hours because of the potential for delayed-onset pulmonary edema. (The patient must remain asymptomatic and have no chest x-ray changes or hypoxemia after observation to be released from the ED or inpatient ward.)
  • Instruct patients discharged from the hospital after recovery from pulmonary edema to avoid exertion and any pulmonary toxins that may precipitate a recurrence. Also, instruct patients to avoid circumstances similar to their exposure and to warn others of the same dangers.
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Transfer

  • Provide supplemental oxygen and/or bilevel positive airway pressure (BiPAP) and immediately transfer patients to an appropriate facility if they present to clinics or hospitals without endotracheal intubation capability, ventilator capability, or ICU monitoring.
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Deterrence/Prevention

  • A standard field protective mask or gas particulate filter provides adequate protection.
  • Personnel working with chlorinated hydrocarbon compounds should ensure adequate ventilation and avoid exposing the compounds and the vapors to heat or UV sources.[13]
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Complications

  • Recurrence of pulmonary edema because of exertion, re-exposure, or exposure to other pulmonary toxins
  • Pneumonia
  • Development of reactive airway dysfunction syndrome with bronchospasm and chronic airway inflammation
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Prognosis

  • The prognosis of acute phosgene exposure is good with early intervention. Few significant long-term sequelae occur after recovery.
  • Studies involving combat personnel and workers involved in the uranium enrichment process have shown increased morbidity and mortality with high level exposure because of the development of pneumonitis, chronic bronchitis, emphysema, and impaired pulmonary function.
  • The degree of the patient's cyanosis provides a rough estimate of survivability. Historically, patients with a mouse grey cyanosis have a worse prognosis than those with a plum blue cyanosis (quantitative assessment of hypoxemia was not routinely available at the time of these historical observations). To estimate the time until respiratory failure, double the length of time from exposure to the development of crackles.
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Patient Education

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Contributor Information and Disclosures
Author

Daniel Noltkamper, MD, FACEP  EMS Medical Director, Department of Emergency Medicine, Naval Hospital of Camp Lejeune

Daniel Noltkamper, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen W Burgher, MD, FACEP  Medical Director, Emegency Preparedness and Management, Department of Emergency Medicine, Baylor University Medical Center

Stephen W Burgher, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT  Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Clinical Toxicologists, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Fred Harchelroad, MD, FACMT, FAAEM, FACEP  Director of Medical Toxicology, Allegheny General Hospital

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References

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  10. Bardana EJ Jr. 8. Occupational asthma and allergies. J Allergy Clin Immunol. Feb 2003;111(2 Suppl):S530-9. [Medline].

  11. Ng TP, Tsin TW, O'Kelly FJ. An outbreak of illness after occupational exposure to ozone and acid chlorides. Br J Ind Med. Oct 1985;42(10):686-90. [Medline].

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  13. Parkhouse DA, Brown RF, Jugg BJ, Harban FM, Platt J, Kenward CE. Protective ventilation strategies in the management of phosgene-induced acute lung injury. Mil Med. Mar 2007;172(3):295-300. [Medline].

  14. Phosgene Medical Experts Group. Phosgene: Information on Options for First Aid and Medical Treatment. American Chemistry Council: Phosgene Panel. Available at http://www.americanchemistry.com/s_acc/bin.asp?CID=1175&DID=4396&DOC=FILE.PDF. Accessed 3/3/2008.

  15. British War Office. Medical Manual of Chemical Warfare. London: 1941:31-38.

  16. Sciuto AM, Stotts RR. Posttreatment with eicosatetraynoic acid decreases lung edema in guinea pigs exposed to phosgene: the role of leukotrienes. Exp Lung Res. May-Jun 1998;24(3):273-92. [Medline].

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British machine-gunners in anti-phosgene masks, Somme, 1915. (Photograph courtesy of the Imperial War Museum, London)
Phosgene structure.
The chest radiograph of a 42-year-old woman chemical worker 2 hours postexposure to phosgene. Dyspnea progressed rapidly over the second hour; PO2 was 40 mm Hg breathing room air. This radiograph shows bilateral perihilar, fluffy, and diffuse interstitial infiltrates. The patient died 6 hours postexposure. (Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine, 1997, p 258)
A lung section of the patient whose chest radiograph is presented above. This patient died 6 hours following exposure to phosgene; the biopsy section was taken during postmortem examination. The section shows nonhemorrhagic pulmonary edema with few scattered inflammatory cells. Hematoxylin and eosin stain; original magnification X 100. (Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine, 1997, p 258)
An anteroposterior (AP) portable chest radiograph of a male patient, who developed phosgene-induced adult respiratory distress syndrome. Notice the bilateral infiltrates and ground-glass appearance. (Image courtesy of Fred P. Harchelroad, MD, and Ferdinando L. Mirarchi, DO)
 
 
 
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