Chest
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Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulopathy, neuronal injury, and organ dysfunction. Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome. Further, patients who experience cardiac arrest are at risk for a number of other pulmonary complications. ⋯ Risk factors include aspiration, pulmonary contusions (from chest compressions), systemic inflammation, and reperfusion injury. Early evidence suggests that they may benefit from ventilation with low tidal volumes. Meticulous attention to mechanical ventilation, early assessment and optimization of respiratory gas exchange, and therapies targeted at potential pulmonary complications may improve outcomes after cardiac arrest.
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Thoracic sarcoidosis is the most common form of sarcoidosis, encompassing a heterogeneous group of patients with a wide range of clinical features and associated outcomes. The distinction between isolated thoracic lymphadenopathy and pulmonary involvement matters. Morbidity is often higher, and long-term outcomes are worse for the latter. ⋯ This review highlights recent advances in the pathogenesis of pulmonary sarcoidosis, including the nature of the sarcoidosis antigen, the role of serum amyloid A and other host factors that contribute to alterations in innate immunity, factors that shape adaptive T-cell profiles in the lung, and how these mechanisms influence the maintenance of granulomatous inflammation in sarcoidosis. We discuss questions raised by recent findings, including the role of innate immunity in the pathogenesis, the meaning of immune cell exhaustion, and mechanisms that may contribute to lung fibrosis in sarcoidosis. We conclude with a reflection on when and how immunosuppressive therapies may be helpful for pulmonary sarcoidosis, a consideration of nonpharmacologic management strategies, and a survey of potential novel therapeutic targets for this vexing disease.
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Detection of pleural abnormalities on CT scan is critical in diagnosis of pleural disease. CT scan detects minute parenchymal lung nodules, but often fails to detect similar-sized pleural nodularity. This is likely because the density of the visceral/parietal pleura and pleural fluid is similar. ⋯ However, pneumothorax (either ex vacuo or from a genuine air leak) after pleural fluid drainage permitted the visualization of small pleural abnormalities on CT scan, which would be amenable to imaging-guided biopsies. This case series provides proof-of-principle evidence that the sensitivity of CT scan detection of pleural abnormalities is dependent on adjacent tissue density and can be enhanced by intrapleural air. Future studies of the potential for artificial pneumothorax to improve the diagnosis of pleural disease are warranted.
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Misdiagnosis of COPD is common. The goal of this study was to quantify the health services burden of undiagnosed and overdiagnosed COPD in a real-world, North American population. ⋯ Undiagnosed and overdiagnosed COPD contribute to significant health care burden. Given that misdiagnosed COPD was fivefold more common than correctly diagnosed COPD, these findings point to a substantial misdiagnosis-associated burden of disease that might be prevented, at least in part, with a correct diagnosis.
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Case Reports
A 68-Year-Old Lung Transplant Recipient With Shortness of Breath, Weight Loss, and Abnormal Chest CT.
A 68-year-old man presented to our ED with shortness of breath, weakness, and a 25-lb unintentional weight loss. He had undergone bilateral lung transplantation (cytomegalovirus [CMV]: donor+, recipient+; Epstein-Barr virus: donor+; recipient+) for idiopathic pulmonary fibrosis (IPF) 18 months prior. His posttransplant course was fairly unremarkable until 1 month earlier, when he was admitted for breathlessness and weakness. ⋯ His cortisol level was undetectable; he was diagnosed with adrenal insufficiency and fludrocortisone was initiated. He was taking prednisone, tacrolimus, and everolimus for immunosuppression and valganciclovir, itraconazole, and trimethoprim-sulfamethoxazole for antimicrobial prophylaxis. His 25-lb weight loss occurred over the span of just one month.