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© 2006 Elsevier Ltd. All rights reserved. Development of a sterile, exudative pleural effusion (simple parapneumonic effusion) is a common complication of bacterial pneumonia, and the majority of cases resolve with antibiotic treatment alone. A minority become secondarily infected (complex parapneumonic effusions), and require chest drainage for clinical resolution. Infected pleural fluid is characterized biochemically by a low pH and glucose, and an elevated lactate dehydrogenase. Pleural infection is associated with activation of the coagulation cascade, and the subsequent deposition of fibrin within the pleural space results in the formation of septations and impedes drainage. Ongoing infection leads to the accumulation of pus in the pleural cavity (empyema). Treatment of pleural infection comprises appropriate antibiotics, chest drainage, nutritional support, and in some cases surgery; intrapleural fibrinolytics are ineffective. Tuberculous pleural effusions develop as a result of a delayed hypersensitivity reaction to mycobacteria in the pleural space. Diagnosis is based on mycobacterial culture of pleural fluid or pleural tissue, or may be inferred from the finding of granulomas on pleural biopsy. Treatment of tuberculous pleurisy involves the same antimicrobial regimen as that used for pulmonary tuberculosis. The use of steroids to treat tuberculous pleurisy is controversial, although they may lead to symptomatic benefit by hastening pleural fluid absorption.

Background CPAP treatment for symptomatic OSA improves surrogate markers of cardiovascular risk, such as endothelial function and arterial stiffness, and may reduce actual cardiovascular events. Minimally symptomatic OSA is far more prevalent than symptomatic OSA but the effects of CPAP on endothelial function and arterial stiffness in minimally symptomatic patients are not known. Methods In two centres taking part in the MOSAIC trial (Oxford and Taunton), 253 patients with minimally symptomatic OSA (ODI>7.5 h) were randomised to either 6 months of CPAP or supportive care. 245 patients had measurements of arterial stiffness by pulse wave analysis at baseline (augmentation index, AIx) and in 64 patients endothelial function was assessed by brachial artery flow-mediated dilatation (FMD, expressed as % change from baseline arterial diameter) measurements by ultrasonography. Multivariable analyses adjusting for baseline FMD or AIx, ODI and Pocock vascular risk score (age, sex, systolic BP, smoking, diabetes, cholesterol, height, creatinine, LVH, previous MI or stroke) were performed to assess the effect of CPAP treatment on FMD and AIx. Results Of the 245 patients 8 withdrew or were lost to follow-up and in 8 patients pulse wave analysis was not possible at 6 months. All 64 patients who had FMD measurements at baseline attended follow-up measurements. Baseline characteristics of 229 patients with complete data on pulse wave analysis are shown in the table (values are mean (SD) were applicable). CPAP improved endothelial function (FMD at follow-up +1.97% with CPAP compared to control group, 95% CI +0.84 to +3.09%, p=0.001), but there was no evidence of an effect on arterial stiffness (AIx at follow-up −0.56% with CPAP compared to control group, 95% CI −2.87 to +1.75, p=0.64). CPAP improved daytime sleepiness as assessed by the Epworth sleepiness score (mean (SE) change −1.91 (0.30) with CPAP; control group +0.08 (0.26), mean difference −1.99, 95% CI −2.77 to −1.21, p t -test). Conclusions 6 months of CPAP is associated with improved endothelial function, but does not reduce arterial stiffness in minimally symptomatic OSA. Thus patients with minimally symptomatic OSA may benefit from CPAP therapy in terms of cardiovascular risk reduction.

Background The intercostal artery is thought to be shielded in the groove of the superior rib; however, the course and variability of the intercostal artery, and factors which may influence these, have not been described in vivo. Describing these variables in vivo has potentially important implications for avoiding complications during common pleural procedures. Methods Maximum intensity projection (MIP) reformats in the coronal plane were produced from CT pulmonary angiograms, to identify the posterolateral course of the contrast opacified intercostal artery. A novel semi-automated computer segmentation algorithm was used to identify and measure distances between the lower border of the superior rib, the upper border of the inferior rib and the position of the intercostal artery when exposed in the intercostal space, and manually verified by a radiologist. Position and variability of the artery were described and then analysed for association with clinical factors using a random effects regression model. Results 298 arteries were analysed from 48 patients (mean age 60 years). The mean lateral distance from the spine over which the artery was exposed within the intercostal space (‘unsafe artery length’) was 39 mm with wide variability (SD=10 mm, 10th to 90th centile 28 mm to 51 mm, Abstract P64 Figure 1A). At 3 cm lateral distance from the spine 16.6% of arteries were shielded by the superior rib, compared to 96.6% at 6 cm. Unsafe artery length was not associated with age, sex, rib space or side. Using regression modelling, variability of arterial position (as SD and coefficient of variation) was significantly associated with age (coeff 0.91, p Conclusions The intercostal artery is exposed within the intercostal space in the first 6 cm lateral to the spine; variability of its vertical position is greater in older patients and more cephalad rib spaces. This implies that pleural interventions within 6 cm lateral to the spine should be conducted with caution and that the risk of intercostal artery laceration is potentially higher in older patients and more cephalad rib spaces.