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Background The concerns regarding air leak after lung surgery or spontaneous pneumothorax include detection and duration. Prior studies have suggested that digital drainage systems permit shorter chest tube duration and hospital length of stay (LOS) by earlier detection of air leak cessation. We conducted a systematic review to assess the impact of digital drainage on chest tube duration and hospital LOS after pulmonary surgery and spontaneous pneumothorax. Methods Ovid MEDLINE, PubMed, Embase, the Cochrane Library, Scopus, and Google Scholar were searched from inception through January 2019. We included randomized controlled trials, cohort studies, and case series of adult patients, using digital or traditional drainage devices for air leaks of either postsurgical or spontaneous pneumothorax origin. Results Of 1,272 references reviewed, 23 articles were included. Nineteen articles addressed postoperative air leak, and four articles pertained to air leak after spontaneous pneumothorax. Thirteen studies were randomized controlled trials. Digital drainage resulted in significantly shorter chest tube duration in eight of 18 studies and shorter hospital LOS in six of 14 studies for postoperative air leak. For postpneumothorax air leak, digital drainage resulted in significantly shorter chest tube duration in two of three studies and hospital LOS in one of two studies with an analog control group. Conclusions Most studies show no significant differences in chest tube duration and hospital LOS with digital vs analog drainage systems for patients with air leak after pulmonary resection. For post-spontaneous pneumothorax air leak, the limited published evidence suggests shorter chest tube duration and hospital LOS with digital drainage systems.

We report a rare case of a 70-year-old male with recurrent pneumothoraces within one year treated with intermittent insertion of chest tube on each occasion. Diagnostic testing was notable for a cystic lesion in the left lung that was initially interpreted as bulla on chest x-ray and chest computed tomographic scan. Due to thickening and nodularity changes of the thin wall of the cystic lesion, the patient underwent left upper lobectomy. Pathology showed poorly differentiated squamous cell carcinoma of the cystic lesion wall. This case emphasizes the importance of monitoring pulmonary cystic lesions especially in patients with a history of smoking and emphysema.

This study aims to compare the severity and outcomes of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) between Hispanics and Caucasians living in the same geographical area. All patients diagnosed with AAV at two academic institutions in Chicago from January 2006 to December 2012 were retrospectively and prospectively identified. Disease activity was measured with the Birmingham Vasculitis Activity Score (BVAS), and disease damage was measured with the Vasculitis Damage Index (VDI). Student's t test and chi-square tests were employed; p ≤ 0.05 was considered significant. Seventy patients with AAV were identified; 15 patients were excluded. Fifty-five patients were included in the study: 23 Hispanics and 32 Caucasians, 35 patients with granulomatosis with polyangiitis (Wegener's), 12 with microscopic polyangiitis, 7 with eosinophilic granulomatosis with polyangiitis, and 1 with renal-limited vasculitis. Compared to Caucasians, Hispanics had a higher BVAS at presentation (16.3 ± 7.6 versus 10.7 ± 7.5, p = 0.006), a higher VDI at presentation (2.90 ± 1.50 versus 2.06 ± 1.30, p = 0.030), and a cumulative VDI (3.90 ± 1.70 versus 2.50 ± 1.90, p = 0.010). Renal involvement was more common among Hispanics (85 % of Hispanics versus 48 % of Caucasians, p = 0.01). Seventy percent of Hispanics had acute renal failure (mean creatinine = 3.37 ± 4.4 mg/dl) of whom seven (50 %) required dialysis, versus 25 % of Caucasians (mean creatinine = 1.78 ± 1.57 mg/dl, p = 0.03) and only two requiring dialysis. Compared to Caucasians, Hispanics with AAV present with more severe disease and higher damage indices. Larger studies are required to confirm these findings and delineate the respective roles of environment and genetics in the pathogenesis of the disease.