Chest
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A 57-year-old man with a history of polysubstance use presented with shortness of breath, wheezing, productive cough, subjective fever, and chills of 3-day duration. Additionally, he reported worsening shortness of breath for the last 3 months. ⋯ He was also diagnosed several years prior with adult-onset asthma due to intermittent wheezing and was prescribed an albuterol inhaler. The albuterol did not help relieve his wheezing, and he stopped refilling it.
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A 63-year-old, non-smoking Asian woman presented to our hospital due to abnormal findings on chest radiography. She had no history of dust exposure. Chest radiography and CT imaging showed patchy ground-glass attenuation (GGA) in the bilateral lower lung lobes, a ground-glass nodule in the right lower lung lobe (diameter, 9.8 mm), and some thin-walled cysts in both lungs (Fig 1). ⋯ Simultaneously, the lung background showed diffuse lymphocytic infiltration in the alveolar septum and peribronchovascular interstitium (Fig 2). There were no symptoms suggestive of autoimmune diseases such as dryness, arthralgia, skin rash, or fever. The patient was followed up without treatment for the interstitial lung disease.
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Research on COVID-19, the cause of a rapidly worsening pandemic, has led to the observation of laboratory derangements such as a propensity towards a hypercoagulable state. However, there are currently no reports on the incidence of pulmonary venous thrombosis in the setting of COVID-19. We report a case in which follow-up chest CT scans revealed an expansile filling defect in a branch of the right inferior pulmonary vein, which is consistent with pulmonary venous thrombosis. Our objective was to provide insight into an uncommon sequela of COVID-19 and consequently garner increased clinical suspicion for pulmonary VTE during hospitalization.
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Pleuroparenchymal fibroelastosis (PPFE) is a progressive and frequently fatal interstitial lung disease that involves the upper lobes. Although its cause remains unknown, the histopathologic evidence underlying PPFE bears striking resemblance to that of the pulmonary apical cap (PAC), a relatively common and benign entity. ⋯ Given the histologic similarity between these two conditions, we propose that these two entities underlie common biologic pathways of abnormal response to lung injury, with the presence of a PAC increasing susceptibility to the development of PPFE in the face of ongoing inflammatory insults. This case describes the histopathologic evolution of PAC to PPFE before and after an inciting injury.
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A 70-year-old man presented to the ED with sudden onset of left thigh pain followed by transient chest discomfort. His history included cerebrovascular disease, hypertension, and cocaine and methamphetamine use. ⋯ His cardiac examination revealed an irregular tachycardia at 129 beats/min and normal first and second heart sounds without murmurs, gallops, or rubs. The remainder of the examination was unremarkable.