Patient Reported Injuries After Ventral Hernia Repair.

BACKGROUND AND AIMS:: The Swedish National Patient Insurance Company (LÖF) can compensate patients who believe they have been exposed to an avoidable injury or malpractice in healthcare. Its register covers 95% of Swedish healthcare providers. MATERIAL AND METHODS:: Data on patients operated for primary or incisional ventral hernia in Sweden between 2010 and 2015 and who had filed a claim, were retrieved from LÖF. A total of 290 cases were identified and included. Files include a copy of records, relevant imaging, and an expert advisor's opinion. RESULTS:: Inadvertent enterotomy occurred during 25 repairs and in these cases, laparoscopic repair was clearly overrepresented ( p < 0.001). Complications related to the surgical site (infection and ugly scar) were predominantly related to open repairs ( p < 0.001). Twenty percentage (57/290) of the claims were directly related to an anesthetic mishap. Univariate ordinal regression showed that the odds of receiving a high reimbursement was significantly increased if laparoscopic repair was performed p < 0.001 (odds ratio: 0.37; 95% confidence interval: 0.21-0.65). Sixty-three percentage of claims were filed by women. CONCLUSION:: Inadvertent enterotomy is overrepresented, and the probability that a claim filed for an avoidable injury leads to high reimbursement is greater if laparoscopic repair is performed rather than open ventral hernia repair. The high amount of injuries related to general anesthesia during umbilical hernia repair may be reduced with an increased proportion executed in local anesthesia.

Particles binding beta(2)-integrins mediate intracellular production of oxidative metabolites in human neutrophils independently of phagocytosis.

Complement-opsonised particles are readily ingested by human neutrophils through a complement receptor-mediated process leading to phagolysosome fusion and production of oxidative metabolites. To investigate the complement receptor 3 (CR3)-associated signal system involved, cells were challenged with protein A-positive, heat-killed Staphylococcus aureus to which antibodies with specificity for the subunits of the beta(2)-integrins, i.e. anti-CD11b (the alpha subunit of CR3) and anti-CD18 (the beta subunit of CR3), were bound through their Fc moiety. Despite not being ingested by the neutrophils, the surface associated anti-CD18- and anti-CD11b-coated particles were able to activate the neutrophil NADPH-oxidase. Also anti-CD11a- (the alpha subunit of LFA-1) and to a lesser extent anti-CD11c- (the alpha subunit of CR4) coated particles were able to trigger the NADPH-oxidase. The NADPH-oxidase was activated without extracellular release of reactive oxygen species. The activity was inhibited by cytochalasin B, suggesting a necessary role for the cytoskeleton in the signalling pathway that activates the oxidase. We show that particle-mediated cross-linking of beta(2)-integrins on the neutrophil surface initiates a signalling cascade, involving cytoskeletal rearrangements, leading to an activation of the NADPH-oxidase without phagosome formation or extracellular release of reactive oxygen species.

Gemfibrozil in familial combined hyperlipidaemia: effect of added low-dose cholestyramine on plasma and biliary lipids.

Gemfibrozil is frequently used for lipid-lowering in familial combined hyperlipidaemia (FCHL) and in other forms of combined hyperlipidaemia. This therapy increases biliary cholesterol saturation, enhancing the risk for gallstone formation. Furthermore, in hypertriglyceridaemia, LDL cholesterol levels often tend to rise. We have explored the possibility that addition of a low dose of cholestyramine to gemfibrozil therapy obliterates these phenomena. Eighteen gallstone-free patients with definite (n = 5) or probable (n = 10) FCHL, or combined hyperlipoproteinaemia (n = 3) were randomized to a 6 week treatment with gemfibrozil, 600 mg b.i.d., or gemfibrozil 600 mg b.i.d. plus 4 g cholestyramine o.d. After 6 weeks the patients were crossed over to the alternative treatment. Plasma lipoproteins and biliary lipids were determined at baseline and at the end of each period. Institution of gemfibrozil treatment resulted in a decrease in plasma cholesterol by 15% (P less than 0.05) and in plasma triglycerides by 47% (P less than 0.05); HDL cholesterol increased by 18% (P less than 0.05). Addition of cholestyramine further decreased plasma and LDL total cholesterol by 9% (P less than 0.05). Total triglycerides and HDL cholesterol did not change. Gemfibrozil treatment was associated with a rise in the relative biliary concentration of cholesterol from 5.6 +/- 0.4 to 6.9 +/- 0.5 molar percent (P less than 0.01), and a parallel decrease in the relative concentration of bile acids, resulting in an increased cholesterol saturation of the bile, from 77 +/- 5 to 90 +/- 6% (P less than 0.05). This change was not observed during the combined therapy (mean cholesterol saturation, 82 +/- 4%).(ABSTRACT TRUNCATED AT 250 WORDS)