an intestinal anastomosis because it reduces collagen content at the level of the anastomosis. The combination of bacterial and neutrophil collagenases increases the collagen fibers breakdown. The collagen synthesis and deposition are reduced by the peritonitis (Ahrendt et al. 1996; Munireddy et al. 2010). The septic exudate present in the anastomosis prevents synthesis and deposition of collagen and angiogenesis (Thornton and Barbul 1997).
1.3.8 Medications
In an experiment in rats, it was shown that the administration of methylprednisolone did not affect the mechanical strength of colonic anastomosis (Mastboom et al. 1991a). However, the effect of steroids on the healing of the gastrointestinal tract is controversial (Thornton and Barbul 1997; Thompson et al. 2006).
The administration of NSAIDs after gastrointestinal surgery is also very controversial (Mastboom et al. 1991b; Gorissen et al. 2012; Bhangu et al. 2014; Collaborative 2014). The non‐selective cyclo‐oxygenase inhibitors seem to increase the risk of leakage after colorectal surgery (Gorissen et al. 2012). Two meta‐analyses in human patients reported opposite results (Bhangu et al. 2014; Collaborative 2014). However, both of those studies have focused on colorectal surgery, which is not performed frequently in small animal surgery. In one of the studies, animal experiments were reviewed and showed that NSAID administration in the post‐post‐operative period increased the risk of leakage (Bhangu et al. 2014). The NSAIDs affect production of VEGF and angiogenesis. They also interfere with collagen formation and cross‐linking (Inan et al. 2006; Gorissen et al. 2012). After administration of NSAIDs, hydroxyproline concentration was significantly reduced after resection and anastomosis of the ileum. This effect was mostly present three days after surgery. Seven days after surgery, the concentration of hydroxyproline had risen again (Mastboom et al. 1991b). In a study on rats, NSAIDs increased the morbidity and mortality rates without necessarily leading to an increased risk of leakage (Mastboom et al. 1991b).
The chemotherapy drugs because of their immunosuppressant effect can negatively affect the healing of the gastrointestinal tract (Thornton and Barbul 1997).
1.3.9 Disease
There is very little evidence that diabetes interferes with gastrointestinal healing. In a rat model of diabetes, collagen synthesis was not affected. However, the bursting pressure of the intestinal anastomosis was reduced on day 3 after surgery, but this effect did not persist past day 7 (Verhofstad and Hendriks 1994; Thornton and Barbul 1997). Icterus has been shown to interfere with tissue healing (Bayer and Ellis 1976; Muftuoglu et al. 2005).
1.3.10 Large Intestine
The colon is considered by most surgeons as a rather “unforgiving” structure when it is incised and repaired, largely because of its unique healing qualities, and when leakage occurs, the results are often devastating to the animal (Williams 2012). An understanding of colonic healing is important, and incorporation of all the principles of repair are critical to reduce life‐threatening anastomotic dehiscence. Healing of the colon undergoes similar phases of wound healing to those found in the skin and other tissue layers but with a number of important differences (Agren et al. 2006). During the inflammatory phase, a fibrin clot forms over the site and, although this clot has minimal strength, it is important to achieve an early “seal,” and it is vital that it remains to act as a scaffold for fibroblast migration during the early repair phase. For the first three to four days, nearly all support for the colonic repair comes from the suture or staple line. Angiogenesis and migration of fibroblasts occurs and eventually replaces the fibrin clot scaffold during days 3 and 4. It is during this stage of repair that breakdown is most likely to occur (Williams 2012).
Although a fragile mucosal bridge also occurs within the first three to four days, depending on the size of the defect, substantive wound strength occurs only when local recruited smooth muscle cells and fibroblasts from the colonic submucosa and muscularis bridge the incision and begin producing collagen. Appropriate‐sized tissue bites are particularly important when repairing the colon because a zone of active collagen lysis occurs in a 1–3 mm zone immediately adjacent to the incised colon edge. The activity of matrix metalloproteases that cause collagen degradation peaks during the debridement phase through day 3 (Agren et al. 2006). Provided there is ample vascular supply after this time, collagen synthesis is accelerated, coupled with a rapid gain in wound strength. Aggressive tissue handling and excess contamination of the colonic wound can greatly increase the debridement activity at the sutured wound edge and this increases the risk of early tissue disruption, leading to dehiscence and leakage (Williams 2012). Return of strength at the healing site reaches about 75% of normal strength at four months after surgery, which is considerably slower than in the small intestine (Thornton and Barbul 1997). Surgeons can influence uncomplicated colonic healing by ensuring adequate tissue perfusion, eliminating any tension on the repair, accurately apposing colonic edges without inducing excess trauma, containing contamination, and avoiding increased intraluminal pressures by eliminating any distal obstruction (Holt and Brockman 2003; Williams 2012). Omental pedicle wraps have been advocated to reinforce the gastrointestinal repairs and support the local healing environment. Omentum may stimulate and augment angiogenesis and may also help maintain the vital fibrin clot and seal during the early phases of wound healing. The benefit of omental wraps in colonic surgery have not been proven in recent human clinical studies of colonic resection and anastomosis. However, most surgeons still recommend covering colonic repairs with omentum (Hao et al. 2008).
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