Patients with both COPD and heart failure (HF) pose particularly high costs to the health-care system. These diseases arise from similar root causes, have overlapping symptoms, and share similar clinical courses. Because of these strong parallels, strategies to reduce readmissions in patients with both conditions share synergies. Here we present 10 practical tips to reduce readmissions in this challenging population: (1) diagnose the population accurately, (2) detect admissions for exacerbations early and consider risk stratification, (3) use specialist management in hospital, (4) modify the underlying disease substrate, (5) apply and intensify evidence-based therapies, (6) activate the patient and develop critical health behaviors, (7) setup feedback loops, (8) arrange an early follow-up appointment prior to discharge, (9) consider and address other comorbidities, and (10) consider ancillary support services at home. The multidisciplinary care teams needed to support these care models pose expense to the health-care system. Although these costs may more easily be recouped under financial models such as accountable care organizations and bundled payments, the opportunity cost of an admission for COPD or HF may represent an underrecognized financial lever.

COPD is associated with cardiovascular disease (CVD), and coronary artery calcification (CAC) provides additional prognostic information. With increasing use of nongated CT scans in clinical practice, this study hypothesized that the visual Weston CAC score would perform as well as the Agatston score in predicting prevalent and incident coronary artery disease (CAD) and CVD in COPD.

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. CT of the chest during that admission revealed mild intralobular and interlobular septal thickening. A bronchoscopy with BAL and transbronchial biopsies did not show acute cellular rejection, but the BAL fluid was positive for coronavirus. 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.

A 47-year-old man who was a redo double lung transplant recipient (cytomegalovirus [CMV] status: donor positive/recipient positive; Epstein-Barr virus status: donor positive/recipient positive) presented to the hospital with 1 week of generalized malaise, low-grade fevers, and dry cough. His redo lung transplantation was necessitated by bronchiolitis obliterans syndrome, and his previous lung transplantation 5 years earlier was for silicosis-related progressive massive fibrosis. He denied any difficulty breathing or chest pain. There was no history of GI or urinary symptoms, and the patient had no anorexia, weight loss, night sweats, sick contacts, or history of travel. He had a history of 1 earlier episode of CMV viremia that was treated with valganciclovir. His immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and prednisone, and his infection prophylaxis included trimethoprim-sulfamethoxazole, itraconazole, and valganciclovir. Results of a chest radiograph 8 weeks earlier were normal.

A 68-year-old man with a history of chronic lymphocytic leukemia well controlled on ibrutinib, hypertension, obesity, and a remote history of smoking (10 pack-years) presented with increasing dyspnea on exertion and cough. He had previously finished two courses of oral antibiotics for his symptoms without significant improvement. On presentation, he had no fevers or sputum production.

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. We hypothesize that an air-pleural interface enhances detection of pleural abnormalities. We describe six patients with pleural abnormalities that were not (or barely) detected on initial CT scan. 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.