The role of tissue ischemia in the pathogenesis of anastomotic stricture.

In a chronic dog model, colocolostomies with intact blood supplies were constructed with the circular stapler. By means of "tight" stapling, an ischemic suture line was induced (suture line blood flow reduced to less than 10% of baseline mucosal blood flow). Under these conditions, only one of 20 anastomoses resulted in stenosis at 1 month. Correctly stapled colocolostomies were then performed in bowels rendered ischemic by removal of all mesenteric arcades for 4 to 6 cm. Mucosal blood flow in such ischemic bowels was reduced to 30% and 16% of control, respectively, and suture line blood flow was as low as that of the tightly stapled anastomoses. Significant stenosis (more than 68% reduction of the lumen) was observed in the group with 6 cm of mesenteric clearance. In no dogs did peritonitis or colonic gangrene develop. Gross and histologic revascularization was evident when dogs were killed at 6 weeks. These findings suggest that it is ischemia of the bowel, rather than ischemia at the suture line itself, that leads to anastomotic stricture. In view of the known susceptibility of the human intestine to ischemia, the model may have overstated the degree of ischemia necessary to produce strictures in clinical practice. Since the induced acute ischemia did not persist in the chronic state, we conclude that it is the adequacy of collateral development that determines the outcome in this model.