Phosgene Toxicity Clinical Presentation

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

History

Diagnosis of phosgene toxicity depends largely on history of exposure.[9] Consider phosgene toxicity in patients involved in the manufacture of dyes, resins, coal tar, and pesticides. Query patients regarding occupation and any exposure to chemicals, especially around sources of heat.[10] In the work setting and at home, phosgene can be produced by the combustion of methylene chloride (paint remover) or trichloroethylene (a degreasing solvent). Patients typically have an asymptomatic period of 30 minutes to 72 hours, but most significant exposures have a latent period less than 24 hours. The duration and concentration of exposure determine the time to symptom onset.

Pulmonary

  • Cough (initially nonproductive, later frothy white-to-yellow sputum) or hemoptysis
  • Dyspnea (exertional early on, subsequently becomes resting dyspnea)
  • Chest tightness or discomfort (may be pleuritic but frequently is described as retrosternal burning)

Head, ears, eyes, nose, and throat

  • Mucosal irritation - More common with intense exposure
  • Eye irritation and tearing
  • Nasal irritation (irritation and burning of the nasal passages) - Occurs with phosgene concentrations higher than 3 ppm, but, with lower respiratory tract disease, may occur at even lower concentrations
  • Throat irritation extending to the retrosternal area - Common with exposures more than 5 ppm and may be described as a burning sensation
  • Sudden death secondary to laryngospasm with large exposures

Cardiovascular (caused by volume depletion or hypoxemia)

  • Lightheadedness, palpitations
  • Angina

Other

  • Headache (thought to be secondary to the hypoxemia and the inflammatory response initiated in the pulmonary parenchyma)
  • Anorexia, nausea, and vomiting
  • Flat metallic taste when smoking cigarettes or overall altered taste sensation
  • Weakness
  • Anxiety and sense of impending doom (likely from the hypoxemia and tachycardia)
  • Skin burning if the patient has been sweating or if clothing is wet (caused by the breakdown to hydrochloric acid)
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Physical

Physical examination is useful with patients with active symptoms. Patients who relate a recent exposure may be in the latent phase and have no specific findings related to the exposure.

Pulmonary

  • Tachypnea and bronchorrhea
  • Wheezes, crackles, or rales on auscultation
  • Cyanosis
  • Apnea (late finding)

Head, ears, eyes, nose, and throat

Upper airway findings are not good prognostic indicators because significant injury may occur to the lower airways without upper airway involvement.

  • Conjunctival injection and lacrimation
  • Oropharyngeal hyperemia and salivation
  • Nasal mucosa hyperemia associated with rhinorrhea

Cardiovascular

  • Tachycardia
  • Hypotension

Skin

  • Cyanosis from pulmonary injury and resultant hypoxemia
  • Chemical burns from liquefied phosgene (Although it also is considered a frostbite hazard in the compressed liquid form)
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Causes

The major risks are occupational exposure and close proximity to an industrial incident.[11]

  • Present day exposures described in literature are caused by the combustion products from chlorinated chemicals (eg, methylene chloride, trichloroethylene).[1]
  • Welding metals recently treated with degreasers, such as trichloroethylene, may produce phosgene.[3, 4, 12] Solvents used for degreasing purposes should be stored more than 200 feet from a welding arc, as the exposure to UV light can create phosgene by photodegradation.
  • Use of methylene chloride, a commonly used chemical paint remover, near a heat source allows the release of phosgene.
  • Carbon monoxide is released in vivo as a metabolic product of methylene chloride.
  • Phosgene is a breakdown product of chloroform that is stored for more than 6 months, even if the chloroform is stabilized with amylene.
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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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  4. Sjogren B, Plato N, Alexandersson R, et al. Pulmonary reactions caused by welding-induced decomposed trichloroethylene. Chest. Jan 1991;99(1):237-8. [Medline].

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  9. Schelble DT. Phosgene and phosphine. In: Haddad LM, Shannon MW, Winchester J, eds. Clinical Management of Poisoning and Drug Overdose. 3rd ed. Philadelphia: WB Saunders; 1998:960-3.

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  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].

  12. Weiss SJ, Lesser SH. Hazards associated with metalworking by artists. South Med J. Jul 1997;90(7):665-71. [Medline].

  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.

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  19. Sciuto AM. Assessment of early acute lung injury in rodents exposed to phosgene. Arch Toxicol. Apr 1998;72(5):283-8. [Medline].

  20. Kennedy TP, Michael JR, Hoidal JR, et al. Dibutyryl cAMP, aminophylline, and beta-adrenergic agonists protect against pulmonary edema caused by phosgene. J Appl Physiol. Dec 1989;67(6):2542-52. [Medline].

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  24. Dombi A, Fekete ZA, Kiricsi I. In Situ Photocatalytic Reactor with FT-IR Analysis for Heterogeneous Catalytic Studies. Applied Catalysis. 2000;193:L5-L8.

  25. Grainge C, Rice P. Management of phosgene-induced acute lung injury. Clin Toxicol (Phila). Jul 2010;48(6):497-508. [Medline].

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  27. Warden CR. Respiratory agents: irritant gases, riot control agents, incapacitants, and caustics. Crit Care Clin. Oct 2005;21(4):719-37, vi. [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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