OBJECTIVE:Laparoscopic cholecystectomy (LC) has become the gold standard for the surgical treatment of gallbladder disease, but conversion to open cholecystectomy is still inevitable in certain cases. Knowledge of the rate and impact of the underlying reasons for conversion could help surgeons during preoperative assessment and improve the informed consent of patients. We decided to review the rate and causes of conversion from laparoscopic to open cholecystectomy.METHOD:This study included all laparoscopic cholecystectomies due to gallstone disease undertaken from May 1999 to June 2010. The exclusion criteria were malignancy and/or existence of gallbladder polyps detected pathologically. Patient demographics, indications for cholecystectomy, concomitant diseases, and histories of previous abdominal surgery were collected. The rate of conversion to open cholecystectomy, the underlying reasons for conversion, and postoperative complications were also analyzed.RESULTS:Of 5382 patients for whom LC was attempted, 5164 were included this study. The overall rate of conversion to open cholecystectomy was 3.16% (163 patients). There were 84 male and 79 female patients; the mean age was 52.04 years (range: 26–85). The conversion rates in male and female patients were 5.6% and 2.2%, respectively (p<0.001). The most common reasons for conversion were severe adhesions caused by tissue inflammation (97 patients) and fibrosis of Calot's triangle (12 patients). The overall postoperative morbidity rate was found to be 16.3% in patients who were converted to open surgery.CONCLUSION:Male gender was found to be the only statistically significant risk factor for conversion in our series. LC can be safely performed with a conversion rate of less than 5% in all patient groups.

No abstract

This experimental study was designed to assess and to compare intra-abdominal adhesions following the use of five commercially available prosthetic mesh grafts in the repair if abdominal wall defects. Sixty Wistar albino rats were randomly divided into six groups (n = 10). A 2 x 1 cm defect at abdominal wall was created and defects were closed either primarily or with one of the following prosthetic mesh grafts: monofilament polypropylene, polytetrafluoroethylene, sodium hyaluronate/carboxymethylcellulose-coated polypropylene, polypropylene/polyglactin 910 composite, or resorbable hydrophilic collagen-coated multifiber polyester. The severity of adhesions was graded, tensile strengths of adhesions were measured, and histopathological grades of inflammation and fibrosis were evaluated. Polypropylene mesh resulted in more adhesion formation in comparison to primary repair and other grafts used in this study, except polypropylene/polyglactin 910 composite mesh. In addition, the highest tensile strength of omental adhesions was detected in the polypropylene group (chi2 = 26.249; p = .0001). Polyester composite mesh caused the least adhesion formation among the groups. Sodium hyaluronate/carboxymethylcellulose-coated polypropylene and polyester composite meshes revealed the highest fibrosis scores (chi2 = 50.776; p = .0001). The highest inflammatory activity was detected in the polytetrafluoroethylene mesh group (chi2 = 16.564; p = .005). Thus, sodium hyaluronate/carboxymethylcellulose-coated polypropylene and polytetrafluoroethylene meshes following polyester composite mesh were the minimal adhesion-forming grafts in this study. Disadvantages of the polytetrafluoroethylene mesh were lower fibrotic activity and higher inflammatory reaction to the graft.

No abstract

Previous studies showed that absence of chemokine receptor Cxcr3 or its blockade prolong mouse cardiac allograft survival. We evaluated the effect of the CXCR3 receptor antagonist MRL-957 on cardiac allograft survival, and also examined the impact of anti-CXCR3 mAb in human CXCR3 knock-in mice. We found only a moderate increase in graft survival (10.5 and 16.6 days, p < 0.05) using either the antagonist or the antibody, respectively, compared to control (8.7 days). We reevaluated cardiac allograft survival with two different lines of Cxcr3 −/− mice. Interestingly, in our hands, neither of the independently derived Cxcr3 −/− lines showed remarkable prolongation, with mean graft survival of 9.5 and 10.8 days, respectively. There was no difference in the number of infiltrating mononuclear cells, expansion of splenic T cells or IFN-c production of alloreactive T cells. Mechanistically, an increased other chemokine receptor fraction in the graft infiltrating CD8 T cells in Cxcr3 −/− recipients compared to wild-type recipients suggested compensatory T-cell trafficking in the absence of Cxcr3. We conclude Cxcr3 may contribute to, but does not govern, leukocyte trafficking in this transplant model.