Approach Considerations
In patients who are asymptomatic despite recent phosgene exposure, no combinations of laboratory or radiographic studies have been shown to discriminate reliably between those who remain asymptomatic and those who are in the latent phase and will later develop life-threatening pulmonary edema. Initial findings on chest radiography may be normal, but radiographic findings may evolve rapidly over the first few hours after phosgene exposure. Pulse oximetry measurements remain normal during the latent phase, but it is useful for following progression over several hours of observation. Increase the triage priority and level of intervention if the oxygen saturation begins to decline, as hypoxemia heralds the onset of pulmonary edema.
Arterial blood gas measurements may be normal during the latent phase but are useful for following progression of manifest illness after the onset of pulmonary edema. In addition, arterial blood gas measurements may be useful for making adjustments in respiratory care therapy (ventilator settings). Acidosis typically occurs, initially as a respiratory acidosis, but later becoming a mixed acidosis due to anaerobic metabolism in the wake of profound tissue hypoxia.
In patients who develop hypoxemia, a partial pressure of oxygen (pO2) as low as 23 mm Hg on 8 L/min of oxygen by face mask has been reported. Typical presenting pO2 levels are 50-60 mm Hg while breathing room air. The carboxyhemoglobin level is important for cases involving exposure to methylene chloride or when carbon monoxide exposure is suspected. Methemoglobinemia may suggest other causes.
A complete blood cell count (CBC) may be obtained as a baseline level or if pneumonia is high on the differential diagnosis list. An elevated white blood cell count is not specific because it may result from hypoxemic stress or an infectious process. The CBC may reveal hemoconcentration late in the disease process, due to third-spacing of fluid into lungs once pulmonary edema has occurred, but this test is of little value prognostically.
A 2009 study noted that levels of secreted phospholipase A2 (sPLA-IIA) found on bronchial alveolar lavage increased markedly after phosgene exposure, peaking at 6 hours, and correlated well with severity of lung injury in the study population. While not specific for phosgene exposure, measurement of sPLA-IIA in bronchial lavage is a potential future measurement for the progression of lung injury from phosgene exposure. [19]
Electrolytes may be obtained as baseline studies because of the anticipated large fluid shifts that occur. Cardiac enzymes (eg, creatine kinase-MB [CK-MB], troponin T, troponin I) may be obtained if cardiogenic pulmonary edema is high on the differential.
Chest Radiography
Initial findings on chest radiography may be normal. Radiographic findings may evolve rapidly over the first few hours after phosgene exposure, however. Using a low-energy exposure technique (50-80 kV) may facilitate early identification of evolving pulmonary edema, while the patient is still asymptomatic (as early as halfway through the latent period).
Early changes include hyperinflation and hilar enlargement. Later changes are typical for noncardiogenic pulmonary edema: fluffy "batwing" perihilar interstitial infiltrates. See the images below.
British machine-gunners in anti-phosgene masks, Somme, 1915. Courtesy of the Imperial War Museum, London.
The chest radiograph of a 42-year-old woman chemical worker 2 hours after exposure 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.
In patients without preexisting cardiac disease, the heart silhouette should be normal. A chest radiograph may help exclude other possibilities in the differential diagnosis (pneumothorax, pneumonia, hemothorax, pleural effusion). Chest radiographs clear over several days as clinical improvement occurs.
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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 Image courtesy of Fred P. Harchelroad, MD, and Ferdinando L. Mirarchi, DO.
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British machine-gunners in anti-phosgene masks, Somme, 1915. Courtesy of the Imperial War Museum, London.
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Phosgene structure.
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The chest radiograph of a 42-year-old woman chemical worker 2 hours after exposure 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.
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A lung section of the patient who died 6 hours after 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.
