Correct!
2. Pulmonary venous infarction
The presence of left-sided pulmonary venous stenosis and occlusion provides the vascular etiology for pulmonary infarction, and the subpleural, non-segmental areas of ground-glass opacity and consideration are consistent with that process. While organizing pneumonia can present similarly, the data to date- including that lack of appropriate histopathology following lung biopsy, the lack of response to corticosteroid therapy, the presence of hemoptysis, and the presence of pleural effusion- do not support this diagnosis, and an alternative explanation- pulmonary venous infarction is evident. While elements of pulmonary hemorrhage are undoubtedly present, given the underlying pulmonary venous stenosis and occlusion with infarction, the hemorrhage is the result of pulmonary infarction, not capillaritis or other histopathologic derangements typically associated with diffuse alveolar hemorrhage. Recurrent aspiration is a consideration for recurrent and migratory pulmonary opacities, but no predisposing factors for aspiration have been noted in the patient’s clinical history and the CT abnormalities are entirely left-sided and non-segmental in appearance. While chronic eosinophilic pneumonia typically presents as peripheral, often frankly subpleural, non-segmental areas of ground-glass opacity and consolidation, typically pulmonary opacities are bilateral, not unilateral, and the patient’s complete blood count did not reveal peripheral eosinophilia. Furthermore, pulmonary tissue sampling did not reveal the presence of eosinophilia and the patient’s lung abnormalities did not respond to corticosteroid therapy.
The patient was referred to cardiology and transesophageal echocardiography was performed and showed left superior pulmonary venous occlusion and severe stenosis with slow flow in the left inferior pulmonary vein. The left atrium and left atrial appendage were patent and cardiac function was normal. The patient was referred for pulmonary venous stent placement (Figure 9) which was successful.
Figure 9. Catheter pulmonary venous angiography with angioplasty and stent placement shows the left inferior pulmonary vein crossed with a wire (A) and subsequently dilated with a balloon (B). A stent was subsequently placed into the left inferior pulmonary vein (C) and subsequently injected and shown to be patent (D).
The patient recovered uneventfully and repeat CT (Figure 10) showed a patent pulmonary venous stent with decreased, and eventual resolution of the previously noted left-sided pulmonary opacities and left pleural effusion.
Figure 10. Representative images from axial enhanced CT performed following the catheter pulmonary venous stent placement shows a patent left inferior pulmonary venous stent and decreased left pleural effusion. The left upper and lower lobe foci of consolidation and ground-glass opacity have regressed.
Diagnosis: Pulmonary venous infarction following pulmonary vein stenosis occlusion induced by radiofrequency ablation for atrial fibrillation
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