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IntroductionProlonged air leak in secondary spontaneous pneumothorax (SSP) patients remains one of the biggest challenges for thoracic surgeons. This study investigates the feasibility, effectiveness, clinical outcomes, and economical benefits of the autologous blood patch pleurodesis method in SSP.Material and methodsFirst-episode SSP patients undergoing autologous blood patch pleurodesis for resistant air leak following underwater-seal thoracostomy, between January 2010 and June 2013 were taken into the study. Timing and success rate of pleurodesis, recurrence, additional intervention, hospital length of stay, and complications that occurred during follow-up were examined from medical records, retrospectively.ResultsThirty-one (27 male, 4 female) SSP patients with expanded lungs on chest X-ray and resistant air leak on the 3rd post-interventional day were enrolled. Mean age was 53.7 ± 18.9 years (range: 23-81). Twenty-four patients were treated with tube thoracostomy, 2 with pezzer drain, and 5 with 8 F pleural catheter. 96.8% success was achieved; air leak in 29 of 31 patients (93.5%) ceased within the first 24 hours. No procedure-related complication such as fever, pain or empyema was seen. Late pneumothorax recurrence occurred in 4 (12.9%) patients; 1 treated with talc pleurodesis where the other 3 necessitated surgical intervention.ConclusionsAutologous blood patch pleurodesis is a safe, effective, and easily performed procedure with no need of any additional equipment or extra cost. This method can be applied to all patients with radiologically expanded lungs and continuous air leak after 48 hours following water-seal drainage thoracostomy, to reduce hospital stay duration, unnecessary surgical interventions, and the expenses.

Although impaired LV diastolic function was detected using conventional parameters, only novel advanced echocardiographic modalities demonstrated impaired bi-ventricular and atrial mechanical functions in patients with sarcoidosis.

OBJECTIVES:The choice of treatment according to the inflammation type in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) has been of recent interest. This study investigated the role of novel biomarkers, hospital outcomes, and readmission rates in the first month in patients with eosinophilic or neutrophilic AECOPD. MATERIALS AND METHODS:We conducted a retrospective observational cohort study in a Chest Teaching Hospital with hospitalized AECOPD patients. Subjects' characteristics, hemogram results, C-reactive protein (CRP), neutrophil/lymphocyte ratio (NLR), platelet/ lymphocyte ratio (PLR), platelet/mean platelet volume (PLT/MPV), length of hospital stay, mortality, and steroid use were recorded. Eosinophilic AECOPD defined as peripheral blood eosinophilia (PBE) was >2% and neutrophilic AECOPD as PBE ≤2%. Readmission within 28 days of discharge was recorded. RESULTS:Of 2727(31.5% females) patients, eosinophilic AECOPD was found in 510 (18.7%) patients. Leucocytes, CRP, NLR, and PLR were significantly higher in neutrophilic AECOPD than in eosinophilic AECOPD (p<0.001). Steroid use and mortality rate were 45% and 0.6% in eosinophilic AECOPD and 71%, and 1.4% in neutrophilic AECOPD, respectively (p=0.001, p=0.19). Age >75 years, albumin <2.5 g/dL, CRP >50 mg/dL, and PLT/MPV <20×103 were found to be risks factors for hospital mortality (p<0.05 each). Readmission rates within 28 days of discharge were 5% (n=136), and this rate was higher in eosinophilic AECOPD patients not taking steroids (p<0.001).CONCLUSION: NLR, PLR, and CRP levels were higher in neutrophilic AECOPD compared with eosinophilic AECOPD. These markers decreased with treatment in neutrophilic AECOPD. A PLT/MPV ratio of <20×103 resulted in an increased mortality rate. Thus, appropriate steroid therapy may reduce readmission rates in the first 28 days after discharge in eosinophilic AECOPD.

PS patients demonstrate reduced cardiac contractility, independent of CMR-proven structural cardiac lesions, while patients with structural lesions have a more pronounced drop in strain parameters. Tn-C and Gl-3 are promising markers for the diagnosis of PS, but they are not specific for cardiac involvement.