Troubleshooting Paracentesis Using POCUS.

Paracentesis is a procedure routinely performed at the bedside in the evaluation and management of ascites. While point of care ultrasound (POCUS) assistance during paracentesis is known to reduce the risk of procedure-related complications, intraprocedural POCUS to overcome commonly occurring issues, such as obstructed flow through the centesis catheter, remain poorly described. In this report, we present two cases in which bowel adhered to the catheter during paracentesis. POCUS was used in an attempt to restore flow. Based on our literature review and procedural experience, we propose an algorithm to surmount this routinely encountered problem.

Incidence of Ventral Hernia Repair after Open Abdominal Aortic Aneurysm and Open Aortofemoral or Aortoiliac Bypass Surgery: An Analysis of 17,594 Patients in the State of New York.

The purpose of our study was to evaluate the rate of ventral hernia repair (VHR) after open abdominal aortic anneurysm in New York State compared with the rate of VHR after open abdominal aortic bypass procedures. The Statewide Planning and Research Cooperative System database was queried for all abdominal aortic aneurysm (AAA) and bypass procedures performed between 2000 and 2010. Social security death index was used to identify patients who died. The cause-specific Cox proportional hazard model was applied to compare the risk of having follow-up VHR between patients with AAA and bypass with death as a competing risk event. A multivariable model was used to explore independent relationship with the risk of having follow-up ventral hernia after adjusting for other factors. There were 9314 patients who underwent open AAA repair, 739 (7.93%) of which had subsequent VHR. Comparatively, 8280 patients underwent aortofemoral or aortoiliac bypass procedures, with 480 (5.8%) undergoing subsequent VHR. The observed one-year, five-year, and 10-year VHR rates for AAA versus bypass were 2.8 versus 1.8 per cent, 10.0 versus 8.0 per cent, 10.7 versus 9.38 per cent, respectively. After controlling for all other factors, patients undergoing AAA repair were more likely and elderly patients were less likely to undergo VHR (P < 0.0001). Patients with serious comorbid conditions such as valvular disease, diabetes mellitus, and neurologic disorders were less likely to undergo subsequent VHR controlling for other factors. VHR after AAA procedures is more common compared with bypass procedures for occlusive disease. Because this patient population has significant comorbidity, prophylactic mesh placement may play a role in preventing necessity for future procedures.

ZO-1 protein is required for hydrogen peroxide to increase MDCK cell paracellular permeability in an ERK 1/2-dependent manner.

Hydrogen peroxide (H2O2) increases paracellular permeability of Madin-Darby canine kidney (MDCK) cells, but the mechanism mediating this effect remains unclear. Treatment of MDCK cells with H2O2 activated ERK 1/2. Inhibition of ERK 1/2 activation blocked the ability of H2O2 to increase paracellular permeability. Knockdown of zonula occludens-1 (ZO-1) protein but not occludin eliminated the ability of H2O2 to increase paracellular permeability. H2O2 treatment did not, however, affect the total cell content or contents of the Triton X-100-soluble and -insoluble fractions for occludin, ZO-1, or ZO-2. H2O2 treatment decreased the number of F-actin stress fibers in the basal portion of the cells. Similar to wild-type MDCK cells, H2O2 increased ERK 1/2 activation in ZO-1 knockdown and occludin knockdown cells. Inhibition of ERK 1/2 activation blocked the increase in paracellular permeability in occludin knockdown cells. ZO-1 knockdown cell paracellular permeability was regulated by PP1, an src inhibitor, indicating that the loss of response to H2O2 was not a general loss of the ability to regulate the paracellular barrier. Inhibition of myosin ATPase activity with blebbistatin increased paracellular permeability in ZO-1 knockdown cells but not in wild-type MDCK cells. H2O2 treatment sensitized wild-type MDCK cells to inhibition of myosin ATPase. Knockdown of TOCA-1 protein, which promotes formation of local branched actin networks, reproduced the effects of ZO-1 protein knockdown. These results demonstrate that H2O2 increases MDCK cell paracellular permeability through activation of ERK 1/2. This H2O2 action requires ZO-1 protein and TOCA-1 protein, suggesting involvement of the actin cytoskeleton.