Quiz: phosgene exposure

November 21, 2013, 1:30 am




Phosgene Exposure: A Case of Accidental Industrial Exposure. Hardison LS et al. J Med Toxicol 2013 Jul 12 [Epub ahead of print[


This interesting case report describes a 58-year-old man who was exposed to a large dose of phosgene gas in an industrial accident. When he presented to hospital shortly after the incident he was complaining only of mild throat irritation, and had unremarkable vital signs and an oxygen saturation of 98% on room air.

However, over the next few hours he developed increasing respiratory distress, cough, rales, wheezing and hypoxia. Despite intensive treatment, he continued to deteriorate and died approximately 32 hours after exposure.

The authors’ presentation of this case  is somewhat vitiated by lengthy discussion of animal models and unproven treatments, causing a lack of focus and failure to emphasize the really important points about phosgene. I will attempt to highlight some of these crucial points in the following quiz. (Click on the question to reveal the answer.)

Delayed pulmonary edema.

There are two major mechanisms:

  1. Hydrolysis: COCl2 + H2) -> CO2 + HCl. This produces only small amounts of HCl and relatively little damage.
  2. Acylation: the -C=O (carbonyl) group attacks hydroxyl, thiol, and sulfhydryl groups, causing oxidative damage and depleting glutathione.

Phosgene has poor solubility, which explains why only small amounts of HCl are formed when it contacts moisture in the respiratory tract. This means that it has poor warning properties, as early symptoms can be limited mild throat irritation.

Delayed. Pulmonary. Edema. Because of the poor warning properties, phosgene gas can work its way down to the alveoli where the carbonyl group attacks the alveolar membrane, increasing permeability and causing noncardiogenic pulmonary edema. Severe signs and symptoms of respiratory distress can be delayed for up to 24 hours. (This article claims that the delay can be as great as 48 hours). Therefore, any patient who presents after phosgene exposure should be admitted for extended observation. Most experts also recommend that any physical exertion (such as walking to the bathroom) can increase manifestations of toxicity, and should be avoided.

  1. Observation and rest, as above.
  2. Good supportive care.
  3. The authors recommend delaying supplemental oxygen until signs of toxicity are seen, and restricting concentrations to < 40%.
  4. ARDSnet ventilation strategies if patient is intubated.
  5. The authors recommend various interventions such as early administration of corticosteroids, nebulized N-acetylcysteine, ibuprofen, and leukotriene antagonists; to my knowledge there’s not good data on any of these.
  6. Consider veno-venous lung protective ECMO if available.

Do not be fooled if a patient presents soon after exposure to phosgene and looks relatively well.  Do not send this patient home from the emergency department!


  1. milkshake Says:

    Some recommendations for managing the phosgene-induced lung edema:
    1. Diuretics are to be avoided; they are not effective against the lung edema and they actually worsen the hypovolemia problem (caused by massive alveolar leakage) 2. Albuterol and the like are useful for treating bronchospasm but corticosteroids are ineffective 3. The patients benefit from anti-anxiety agents; the extreme stress levels caused by the suffering worsen the lung edema

  2. Leon Says:


    Thanks for the comments. I generally agree, except it may be reasonable to try a course of steroids in case the exposure — in addition to causing direct damage — has triggered underlying bronchospastic disease. Of course, this is all empirical. It hasn’t been studied, and there’s no data to make an informed risk-benefit estimation regarding use of steroids in these cases.