Chest
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Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. ⋯ Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact. In this review, we discuss the clinical presentation, pathophysiology, and management of negative-pressure or postobstructive pulmonary edema.
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Cysts are commonly seen on CT scans of the lungs, and diagnosis can be challenging. Clinical and radiographic features combined with a multidisciplinary approach may help differentiate among various disease entities, allowing correct diagnosis. It is important to distinguish cysts from cavities because they each have distinct etiologies and associated clinical disorders. ⋯ Multifocal/diffuse cysts can occur with lymphoid interstitial pneumonia, Birt-Hogg-Dubé syndrome, tracheobronchial papillomatosis, or primary and metastatic cancers. Multifocal/diffuse cysts may be associated with nodules (lymphoid interstitial pneumonia, light-chain deposition disease, amyloidosis, and Langerhans cell histiocytosis) or with ground-glass opacities (Pneumocystis jirovecii pneumonia and desquamative interstitial pneumonia). Using the results of the high-resolution CT scans as a starting point, and incorporating the patient's clinical history, physical examination, and laboratory findings, is likely to narrow the differential diagnosis of cystic lesions considerably.
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A 43-year-old man was referred to our tertiary sleep center for the initiation of sleep apnea treatment. A prior diagnostic overnight polysomnography (Fig 1) had revealed an apnea-hypopnea index (AHI) of 22/h of sleep. The apneas were predominantly central (central AHI, 18.2/h; obstructive AHI, 3.8/h), more pronounced in the supine position (AHI supine, 36.6/h; AHI nonsupine, 11/h) and during non-rapid eye movement (non-REM) sleep (REM, 15.8/h; non-REM, 23.5/h). ⋯ He was not taking any medication but had noticed a slow decline in general physical performance in the last year, with dyspnea (New York Heart Association class I) after running distances of 1 to 2 km. He had never experienced syncope. His family history was unremarkable.