Even under the most expert care, a properly constructed intestinal anastomosis can fail to heal resulting in leakage of its contents, peritonitis and sepsis. The cause of anastomotic leak remains unknown and its incidence has not changed in decades. Here, we demonstrate that the commensal bacterium Enterococcus faecalis contributes to the pathogenesis of anastomotic leak through its capacity to degrade collagen and to activate tissue matrix metalloprotease-9 (MMP9) in host intestinal tissues. We demonstrate in rats that leaking anastomotic tissues were colonized by E. faecalis strains that showed an increased collagen-degrading activity and also an increased ability to activate host MMP9, both of which contributed to anastomotic leakage. We demonstrate that the E. faecalis genes gelE and sprE were required for E. faecalis-mediated MMP9 activation. Either elimination of E. faecalis strains through direct topical antibiotics applied to rat intestinal tissues or pharmacological suppression of intestinal MMP9 activation prevented anastomotic leak in rats. In contrast, the standard recommended intravenous antibiotics used in patients undergoing colorectal surgery did not eliminate E. faecalis at anastomotic tissues nor did they prevent leak in our rat model. Finally, we show in humans undergoing colon surgery and treated with the standard recommended intravenous antibiotics, that their anastomotic tissues still contained E. faecalis and other bacterial strains with collagen-degrading/MMP9 activity. We suggest that intestinal microbes with the capacity to produce collagenases and to activate host metalloproteinase MMP9 may break down collagen in the gut tissue contributing to anastomotic leak.

In this review, we examine the major known risk factors and technical considerations that have been implicated as factors in leakage. Although surgical technique has evolved over the past several decades with the advent of newer surgical staplers, laparoscopy, and robotics, we have not witnessed a decrease in the incidence of colorectal anastomotic leaks suggesting that the fundamental pathogenesis of anastomotic leak remains unknown. Among the factors contributing to anastomotic healing, intestinal bacteria remains largely overlooked even though compelling evidence exist that intraluminal microbes could play a major role in pathogenesis of anastomotic leak. Further investigation focusing on intestinal microbes could be one such avenue for uncovering the elusive cause of colorectal anastomotic leak.

In the present study, preoperative vedolizumab exposure did not affect the risk of 30-day postoperative complications in UC and CD. Further, larger studies are required to confirm our findings.

Robotic proctectomy is a safe and effective technique for patients with IBD. It is comparable to LP with regard to perioperative outcomes, complications, and short-term functional results.

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Infliximab is not associated with increased rates of postoperative complications after laparoscopic resection.

PVT is a potentially serious complication that is more likely to occur after TPC and in the presence of postoperative intraabdominal septic complications, particularly in patients with a coagulation disorder. Prompt diagnosis and treatment with oral anticoagulation are recommended to avoid long-term sequelae.

In the present retrospective cohort study of real-world experience, vedolizumab was shown to be commonly used as postoperative treatment for CD especially in high risk patients. Multivariate and propensity score-matched analyses showed that postoperative endoscopic recurrence in CD was higher with vedolizumab than with anti-TNF-α agents, but further investigation including controlled trials is required before determining the utility of vedolizumab in preventing postoperative recurrence of CD.