Chest
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Pneumothorax following ultrasound-guided thoracentesis is rare. Our goal was to explain the mechanisms of pneumothorax following ultrasound-guided thoracentesis in a setting where pleural manometry is routinely used. ⋯ Unintentional pneumothoraces cannot be prevented by monitoring for symptoms or excessively negative pressure. These pneumothoraces were drainage related rather than due to penetrating lung trauma or external air introduction. We speculate that unintentional pneumothoraces are caused by transient, parenchymal-pleural fistulae caused by nonuniform stress distribution over the visceral pleura that develop during large-volume drainage if the lung cannot conform to the shape of the thoracic cavity in some patients with unexpandable lung. These fistulae appear to be pressure dependent, and the resulting pneumothoraces rarely require treatment. Drainage-related pneumothorax is an unavoidable complication of ultrasound-guided thoracentesis and appears to account for the vast majority of pneumothoraces occurring in a procedure service.
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Bronchiectasis and pulmonary infection with nontuberculous mycobacteria (NTM) may be associated with disease-causing mutations in the cystic fibrosis transmembrane regulator (CFTR). ⋯ Mutations in CFTR that alter RNA splicing and/or functional chloride conductance are common in this population, and are likely to contribute to the susceptibility and pathogenesis of adult bronchiectasis and pulmonary NTM infection. Careful clinical evaluation for disease cause should be undertaken in this clinical context.
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To determine the complication rate from supervised training bronchoscopy in a single pulmonary fellowship program, and to examine the effects of fellow and faculty experience on this complication rate. ⋯ Training bronchoscopy performed during a pulmonary fellowship is a safe procedure in a supervised setting. Patients undergoing bronchoscopy performed by novice bronchoscopists have an increased complication rate during the first trimester of bronchoscopist training.
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Hyperchloremic acidosis is common in the critically ill and is often iatrogenic. We have previously shown that hyperchloremic acidosis increases nuclear factor-kappaB DNA binding in lipopolysaccharide-stimulated RAW 264.7 cells. However, evidence that hyperchloremic acidosis leads to increased inflammation in vivo has been limited to nitric oxide. ⋯ Moderate (SBE, - 5 to - 10) and severe (SBE, - 10 to - 15) acidosis, induced by HCl infusion, increases circulating levels of IL-6, IL-10, and TNF in normotensive septic rats.