During certain activities, the FP device seems to be favorable, since it causes less discomfort than the CP.

Purpose: The aim of this study was to identify factors predisposing to lung infarction in patients with pulmonary embolism (PE). Materials and Methods: We performed a retrospective analysis on 154 patients with the final diagnosis of PE being examined between January 2009 and December 2012 by means of a Toshiba Aquilion 64 CT scanner. The severity of clinical symptoms was defined by means of a clinical index with 4 classes. The pulmonary clot load was quantified using a modified severity index of PE as proposed by Miller. We correlated several potential predictors of pulmonary infarction such as demographic data, pulmonary clot burden, distance of total vascular obstruction and pleura, the presence of cardiac congestion, signs of chronic bronchitis or emphysema with the occurrence of pulmonary infarction. Results: Computed tomography revealed 78 areas of pulmonary infarction in 45/154 (29.2?%) patients. The presence of infarction was significantly higher in the right lung than in the left lung (p?

Objectives: To evaluate the technical success, clinical outcome and safety of percutaneously placed totally implantable venous power ports (TIVPPs) approved for high-pressure injections, and to analyse their value for arterial phase CT scans. Methods: Retrospectively, we identified 204 patients who underwent TIVPP implantation in the forearm (n5152) or chest (n552) between November 2009 and May 2011. Implantation via an upper arm (forearm port, FP) or subclavian vein (chest port, CP) was performed under sonographic and fluoroscopic guidance. Complications were evaluated following the standards of the Society of Interventional Radiology. Power injections via TIVPPs were analysed, focusing on adequate functioning and catheter's tip location after injection. Feasibility of automatic bolus triggering, peak injection pressure and arterial phase aortic enhancement were evaluated and compared with 50 patients who had had power injections via classic peripheral cannulas. Results: Technical success was 100%. Procedure-related complications were not observed. Catheter-related thrombosis was diagnosed in 15 of 152 FPs (9.9%, 0.02/100 catheter days) and in 1 of 52 CPs (1.9%, 0.002/100 catheter days) (p,0.05). Infectious complications were diagnosed in 9 of 152 FPs (5.9%, 0.014/100 catheter days) and in 2 of 52 CPs (3.8%, 0.003/100 catheter days) (p.0.05). Arterial bolus triggering succeeded in all attempts; the mean injection pressure was 213.8 psi. Aortic enhancement did not significantly differ between injections via cannulas and TIVPPs (p.0.05). Conclusions: TIVPPs can be implanted with high technical success rates, and are associated with low rates of complications if implanted with sonographic and fluoroscopic guidance. Power injections via TIVPPs are safe and result in satisfying arterial contrast. Conventional ports should be replaced by TIVPPs.

The blood-spinal cord barrier (BSCB) prevents leakage of molecules, such as pronociceptive mediators, into the spinal cord, but its role in the pathophysiology of neuropathic pain is not completely understood. Rats with chronic constriction injury (CCI) develop mechanical allodynia, thermal hypersensitivity, and reduced motor performance (Rota-Rod test) compared with sham-injured mice-similar to mice with spared nerve injury (SNI). The BSCB becomes permeable for small and large tracers 1 day after nerve ligation. Messenger RNA (mRNA) expression of tight junction proteins (TJPs) occludin, claudin-1, claudin-5, claudin-19, tricellulin, and ZO-1 significantly declines 7-14 days after CCI or SNI. ZO-1 and occludin are reduced in the cell membrane. In capillaries isolated from the spinal cord, immunoreactivity of claudin-5 and ZO-1 is fainter. In parallel, the number of platelet-derived growth factor receptor β (PDGF-β) and CD13 pericytes in the spinal cord drops. Reduced levels of cytosolic transcription factors like β-catenin, but not SMAD4 and SLUG, could account for reduced TJP mRNA. In summary, neuropathy-induced allodynia/hypersensitivity is accompanied by a loss of pericytes in the spinal cord and a leaky BSCB. A better understanding of these pathways and mechanisms in neuropathic pain might foster the design of novel treatments to maintain spinal cord homeostasis.

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