ABSTRACT
Acute eosinophilic pneumonia (AEP) has been described as an idiopathic febrile illness with a duration of less than seven days with severe hypoxemia, pulmonary infiltrates, and no history of asthma. It has been reported that AEP is associated with smoking. Although the pathogenesis of smoking induced AEP is being actively studied, there is no direct histological evidence that smoking actually induces AEP. Recently, we encountered a case of AEP that may have been caused by smoking. We performed a cigarette smoking challenge test to verify that smoking was indeed the cause of AEP in this patient. Smoking induced an increase the proportion of eosinophils in the bronchoalveolar lavage fluid without any respiratory symptoms or abnormal radiological findings. This result suggests that smoking was the cause of AEP in this patient.
Subject(s)
Humans , Hypoxia , Asthma , Bronchoalveolar Lavage Fluid , Eosinophils , Pulmonary Eosinophilia , Smoke , SmokingABSTRACT
PURPOSE: To evaluate the incidence and type of low attenuation seen on high resolution computed tomography (HRCT) performed after artificially induced pulmonary embolism. MATERIALS AND METHODS: Using permanent embolic materials, pulmonary embolism was induced in ten Yorkshire pigs. Pre- and postembolic pulmonary angiography was performed, and HRCT was performed immediately and 1, 3, and 6 weeks after embolization. The incidence and type of low attenuation of all segments, as seen on HRCT, was evaluated. Low attenuation was classified as mottled, lobular, segmental, or peripheral. The pigs were sacrified after 6 weeks and contact radiographs were obtained. RESULTS: Low attenuation developed in eight of ten pigs. Pulmonary angiography revealed arterial occlusion in 15 large and 19 small segmental arteries (34 of 45 segments). In the remaining 11 segments, follow-up HRCT demonstrated areas of low attenuation. This was present in 25 of 35 segments (71%) as seen on HRCT images obtained immediately; in 16 of 41 segments (39 %) on images obtained 1 week after embolization; in 17 of 41 segments (41 %) on those acquired at 3 weeks; and in 25 of 45 segments (56 %) on those acquired at 6 weeks. The overall incidence of low attenuation was 83/166 (50 %). The types of low attenuation were mottled in 32/83 cases, lobular in 13/83, segmental in 13/83, and peripheral in 25/83. In large segmental arterial occlusion, the incidence of low attenuation on HRCT was 100% immediately, 57% at 1 week, 60% at 3 weeks, and 80 % at 6 weeks. In small segmental arterial occlusion, the incidence was 47%, 25 %, 11 %, and 21 % respectively. The overall incidence of low attenuation was 40/55 (73 %) in large segmental arterial occlusion and 18/71 ( 25%) in small segmental arterial occlusion. CONCLUSION: Low attenuation on HRCT is a finding of pulmonary embolism and is more common on HRCT performed immediately after embolization (71%) and in large segmental arterial occlusion (73%). Low attenuation on HRCT is an ancillary finding and may be useful in the diagnosis of pulmonary embolism.