Phosgene

BASIC Provider Course, January 2009, Hong Kong.
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Carolyne Chau

Phosgene was used during World War I by both sides and caused over 85% of all gas fatalities. Both acute and chronic exposure to phosgene causes toxic pulmonary oedema. Exposure causes instant upper respiratory tract irritation, but there is a latent period of 4 to 24 hours before the onset of toxic pulmonary oedema. This period is dose dependent: high dose: 1 to 4 hours; low doses 8 to 24 hours. Phosgene attacks primarily the lower airways and alveoli as a result of limited water solubility.

Management

There has been considerable debate about the rationale for the use of systemic and inhaled steroids in the treatment of toxic pulmonary oedema. Theoretically, there should be many advantages such as the inhibition of phospholipase A2 through induced lipomodulin and macrocortin, inhibition of macrophages, inhibition of production of prostanoids and leukotrienes, and stimulation of surfactant production in type II cells. However, its use is still unproven. Beneficial effects only follow early administration, whereas late administration may be deleterious.

Another tool to combat the development of toxic pulmonary oedema is the use of acetylcysteine. The rationale is to increase intracellular glutathione levels to prevent lipid peroxidation induced pulmonary oedema.

The timing and technique of intermittent positive pressure ventilation may have important consequences for the management of development of toxic pulmonary oedema. Inappropriate ventilation may provoke ARDS as e result of kinin release from repeated opening and closing of alveoli. This has lead to the “open lung” strategy of ventilation in which collapsed alveoli are opened and then kept open by PEEP and low tidal volumes. Patients who have been exposed t oedemagens but have not yet showed any signs or symptoms of developing pulmonary oedema should confine to bed and observed for at least 24 hours as exercise after exposure o phosgene increase likelihood of developing toxic pulmonary oedema after 24 hours.

©Charles Gomersall, November, 2008 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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