Читать книгу Gastrointestinal Surgical Techniques in Small Animals - Группа авторов - Страница 16

As soon as the wall of the gastrointestinal tract is incised, hemorrhage occurs but it is rapidly controlled by an intense vasoconstriction. Following this initial phase, vasodilation occurs with migration of neutrophils, macrophages, platelets, and liberation of inflammatory mediators which characterizes the inflammatory phase. The platelets, by releasing diverse platelet‐derived growth factors (PDGF) and cytokines, contribute to hemostasis and cell recruitment like macrophages and fibroblasts. The neutrophils predominate during the first 24 hours but then macrophages become predominant past 48 hours following the initial injury. The macrophages play an important role in healing of the gastrointestinal tract by controlling local infection with phagocytosis, production of oxygen radicals, and nitric oxide. They also participate in debridement with phagocytosis and production of collagenase and elastase. The macrophages also regulate matrix synthesis and cell recruitment and activation. They release several growth factors (PDGF, transforming growth factor (TGFβ), fibroblast growth factor (FGF), IGF) and cytokines (TNFα, IL‐1) important for tissue healing. The macrophages recruit lymphocytes that liberate interleukin (IL‐6) and interferon (IFN) and promote angiogenesis with production of VEGF (Vasculogenic Endothelial Growth Factor). Finally, the capillary permeability is increased resulting in inflammation and edema on the edges of the incision that can persist for two weeks. Care should be taken initially when the sutures are placed to not induce tissue strangulation and necrosis. A fibrin seal develops over the serosa very quickly to provide a leakage protection of the surgical site (Pascoe and Peterson 1989; Thornton and Barbul 1997; Thompson et al. 2006).

Overlapping with the inflammatory phase is the debridement phase, with removal of injured tissue by macrophages. The debridement phase should not exceed 1–2 mm from the edges of the incision. During this process, collagen is resorbed by collagenase and synthesized by smooth muscle and fibroblast. The smooth muscles are the major contributor in collagen production within the gastrointestinal tract. The collagen degrade by the collagenase activity weakens the strength of the anastomosis. In the colon, the collagenase activity is increased over the entire length of the colon while in the small intestine, it is increased only at the site of the anastomosis (Hawley 1970; Jiborn et al. 1978a). The risk of dehiscence is high between 3 and 10 days after surgery. Usually, after 4 to 5 days, collagen synthesis is superior to lysis and the anastomosis regains strength. This collagenase activity can be increased by the amount of trauma induced by tissue manipulation at the time of surgery or the presence of a foreign body, and by the degree of contamination. The amount of collagen synthesized is affected by hypotension, hypovolemia, shock, and certain medications.

The granulation tissue appears at the beginning of the proliferative phase of intestinal healing. Fibroblast is the major cell type present past day 4 after surgery. The fibroblasts migrate under the control of PDGF, TGFβ and FGF. Fibroblast and smooth muscle lay down collagen fibers and new capillaries appear in the field.

After one to two weeks following the anastomosis, the epithelial layer is fully restored. The epithelialization of the anastomosis reduces the formation of excessive fibrosis tissue secondary to inflammation. The excessive fibrosis could lead to stricture formation. During the maturation phase, the collagen fibers are reorganized and the anastomosis is becoming thinner.

In summary, an intestinal anastomosis loses bursting strength during the first 3 to 5 days to finally regain 50–70% of the initial bursting strength in 2 to 3 weeks (Jiborn et al. 1978a, 1978b; Thompson et al. 2006; Munireddy et al. 2010).