ObjectiveTo investigate the pathophysiologic mechanisms that lead to ileus after abdominal surgery. Summary Background DataThe common supposition is that more invasive operations are associated with a more extensive ileus. The cellular mechanisms of postsurgical ileus remain elusive, and few studies have addressed the mechanisms. MethodsRats were subjected to incremental degrees of surgical manipulation: laparotomy, eventration, "running," and compression of the bowel. On postsurgical days 1 and 7, muscularis infiltrates were characterized immunohistochemically. Circular muscle activity was assessed using mechanical and intracellular recording techniques in vitro. ResultsSurgical manipulation caused an increase in resident phagocytes that stained for the activation marker lymphocyte function-associated antigen (LFA-1). Incremental degrees of manipulation also caused a progressive increase in neutrophil infiltration and a decrease in bethanechol-stimulated contractions. Compression also caused an increase in other leukocytes: macrophages, monocytes, dendritic cells, T cells, natural killer cells, and mast cells. ConclusionThe data support the hypothesis that the degree of gut paralysis to cholinergic stimulation is directly proportional to the degree of trauma, the activation of resident gut muscularis phagocytes, and the extent of cellular infiltration. Therefore, postsurgical ileus may be a result of an inflammatory response to minimal trauma in which the resident macrophages, activated by physical forces, set an inflammatory response into motion, leading to muscle dysfunction.Postsurgical ileus is a persistent feature of abdominal surgery that can lead to significant morbidity and mortality rates. 2 Ileus is generally accepted as a normal response to abdominal surgery. Besides causing significant patient discomfort (respiratory compromise, abdominal distention, nausea, emesis, and pain) and more serious problems (e.g., acute gastric dilatation, aspiration), ileus prolongs the hospital stay, delays early enteral nutrition, and increases medical costs. Despite the widespread presence of this problem, little is known about the underlying pathogenesis.

Postoperative ileus is an iatrogenic condition that follows abdominal surgery. Three main mechanisms are involved in its causation, namely neurogenic, inflammatory and pharmacological mechanisms. In the acute postoperative phase, mainly spinal and supraspinal adrenergic and non-adrenergic pathways are activated. Recent studies, however, show that the prolonged phase of postoperative ileus is caused by an enteric molecular inflammatory response and the subsequent recruitment of leucocytes into the muscularis of the intestinal segments manipulated during surgery. This inflammation impairs local neuromuscular function and activates neurogenic inhibitory pathways, inhibiting motility of the entire gastrointestinal tract. The mechanisms underlying the recruitment of the inflammatory cells, and their interaction with the intestinal afferent innervation, are discussed. Finally, opioids administered for postoperative pain control also contribute to a large extent to the reduction in propulsive gastrointestinal motility observed after abdominal surgery.

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