Anastomotic leakage after laparoscopic single-port sigmoid resection: combined transanal and transabdominal minimal invasive management.

BACKGROUND: Laparoscopic colorectal surgery has become the gold standard in the therapy of benignant and malignant colorectal pathologies. Anastomotic leakage is still a reason for laparotomy; applying a diverting stoma or performing a Hartman's procedure is common [1, 2]. Laparoscopic treatment of an early-detected anastomotic leakage is suggested from other authors [3, 4]. In our video we demonstrate a combined minimal invasive transabdominal and transanal treatment concept in patients with early-detected anastomotic leakage. METHODS: Two consecutive patients developing an anastomotic leakage after single-port laparoscopic sigmoid resection for stage II/III diverticulitis (Hanson & Stock) were treated with a combined minimal invasive approach. Anastomotic leakage was diagnosed by triple contrast computed tomography on postoperative day 4 in patient one and on postoperative day 7 in patient two. Operative treatment was performed immediately on the same day without delay. RESULTS: In both patients a combined transanal and transabdominal approach was performed. First step was a diagnostic laparoscopy in order to exclude fecal peritonitis. Using a single-port device (SILS Port Covidien), transanal inspection of the anastomosis was also performed: In both patients anastomotic tissue margins were vital, and the leakage affected only a quarter of the anastomotic circumference. Transanal stitches were placed to close the anastomotic leakage. Laparoscopic transabdominal irrigation was performed, and two suction drainages were placed in the pelvis. Postoperative antibiotic treatment and a gradual return to slid food were carried out. Functional result at follow-up of 102 and 112 days (with rectoscopy) showed no residual leak and no stricture of the anastomosis, and both of patients had a normal rectal function.

Inhibition of NO biosynthesis, but not elevated blood pressure, reduces angiogenesis in rat models of secondary hypertension.

Arterial hypertension (AH) is characterized by reduced nitric oxide (NO) biosynthesis, vasoconstriction, and reduced microvascular density. In this study we asked whether AH also reduces the number of microvessels by impairing angiogenesis. AH was induced in Dahl salt-sensitive rats (DSS) with a salt diet and in Wistar-Kyoto rats by inhibiting NO formation with Nomega-nitro-L-arginine (NNA). Three weeks after induction of AH, two wound chambers containing collagen I (Vitrogen) were sutured into the mesenteric cavity of each animal. After additional 14 days, wound chamber neovascularization and the extent of vascularized connective tissue ingrowth were quantified. In NNA-induced AH, the number of newly formed vessels and the ingrowth of vascularized connective tissue into the wound chamber decreased as compared to controls. However, the number of newly formed vessels and the ingrowth of vascularized connective tissue did not change with increasing blood pressure in salt-fed DSS rats as compared to those fed a normal diet. Inhibition of NO biosynthesis, but not necessarily elevating blood pressure, reduces angiogenesis. Microvascular rarefaction in AH may be partially due to reduced angiogenesis because of impaired NO biosynthesis.