The present study investigates a possible source of inflammatory mediators involved in the pathogenesis of bladder inflammation characteristics of interstitial cystitis disease. Our tested hypothesis is that in response to injury, tissues of the urinary bladder participate in the initiation of bladder inflammation by releasing inflammatory mediators such as neutrophil chemotactic factors. Bladders of anesthetized rabbits (n = 7) were instilled with an acidic solution (pH 4.5) for 15 minutes, then washed with saline and instilled with sterile phosphate buffered saline (PBS) (pH 7.2) for an additional 45 minutes prior to sacrificing the rabbits. Control rabbits (n = 7) were instilled with sterile PBS (pH 7.2) for 15 minutes, then 45 minutes. The levels of neutrophil chemotactic factors were measured using modified Boyden chambers and rabbit peritoneal neutrophils as indicator cells. Results indicated the release of high levels of neutrophil chemotactic factors (via a checkerboard analysis) from acid-treated bladders after 15 minutes (70 +/- 4% of standard) and 45 minutes (80 +/- 7%). Electron microscopy analysis of these acid-treated bladders revealed the infiltration of a large number of neutrophils, which correlates with the recovery of neutrophil chemotactic factors. Control rabbits, on the other hand, showed low levels of chemotactic activity (less than 10 percent) and exhibited normal bladder morphology with absence of neutrophils. The glycosaminoglycan (GAG) layer was intact in both acid-treated and control bladders. High levels of neutrophil chemotactic factors were also detected in urine samples from eleven patients with interstitial cystitis (113 +/- 25%) (not due to interleukin-1 or leukotriene B4) which were not detected in urine samples from healthy volunteers (n = 9) or from thirteen control patients with bladder diseases other than interstitial cystitis. These preliminary studies indicate the capability of injured bladder tissues to release neutrophil chemotactic factors which contribute to the initiation of bladder inflammation. The presence of neutrophil chemotactic factors in urine samples of interstitial cystitis patients suggests a possible role of these mediators in the pathogenesis of the disease.

Treatment of colonic injury has progressed since the recognition of the value of colostomy or bowel exteriorization during the second World War. The treatment guidelines take into consideration the time interval between perforation and treatment as well as the nature, the site, and the cause of perforation. Laparoscopic primary repair of relatively small colonic perforations without spillage of bowel content has been reported. Extensive large bowel injury with appreciable colonic spillage usually requires a laparotomy and diversion. We report a case of a 57-year-old woman who presented with extensive rectosigmoid injury and colonic spillage after colonoscopy and was treated using laparoscopic assistance.

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Several techniques have been described for the trocar placement in laparoscopic-assisted colectomy (LAC). They share the placement of four or five trocars in different areas of the abdomen. A specimen extraction incision in these techniques generally incorporates only one or two trocar sites, and combined length of these incisions approximates the length of a limited laparotomy incision for open colectomy. In addition, intracorporeal communication between the surgeon and the first assistant, who usually works "against" the camera, is challenging and may actually prolong the procedure. We describe here a three-trocar midline approach to laparoscopic-assisted colectomy that allows incorporation of these trocar sites into a midline laparotomy approximately 3 inches long for "open" bowel resection and anastomosis. As a result, the total length of the abdominal wall incision is smaller and cosmesis is superior, while the relative simplicity of the technique, in comparison to complete laparoscopic colectomy, is emphasized. In this technique, the surgeon is much less dependent on the assistant's laparoscopic skills, allowing the laparoscopic part of the procedure to be performed by one surgeon assisted only by a camera operator.

The inability to completely mobilize the redundant colon in perineal rectosigmoidectomy (Altemeier's procedure) for full-thickness rectal prolapse is a main contributor to the recurrence rate associated with the procedure. However, the presence of a redundant sigmoid after the Ripstein procedure or other rectal sling operations is the main cause of the high rate of postoperative constipation and stool impaction. Low anterior resection as the definitive treatment is associated with the higher morbidity of laparotomy and the risk of anastomotic leak. We describe a laparoscopic-assisted surgical approach which combines the benefits of completely resecting the redundant sigmoid colon as well as the performance of extraperitoneal anastomosis at the level of the anus.