Postoperative paralytic ileus refers to obstipation and intolerance of oral intake due to nonmechanical factors that disrupt the normal coordinated propulsive motor activity of the gastrointestinal tract [1-3]. The word ileus is derived from the Greek word 'eileos,' which means twisting . There is general consensus among surgeons that some degree of postoperative ileus is a normal obligatory and physiologic response to abdominal and nonabdominal surgery [3,5,6].
Average postoperative gut dysmotility (ie, "normal" physiologic postoperative ileus) is widely reported as lasting 0 to 24 hours in the small intestine, 24 to 48 hours in the stomach, and 48 to 72 hours in the colon [2,7,8]. However, this belief has been challenged; the duration of postoperative gastrointestinal dysmotility appears to be shorter than previously thought [5,9-11]. Moreover, reported gastrointestinal recovery times, to a large extent, depend on the type of surgery and the wide variety of endpoints used to measure gut recovery (eg, radiographic emptying studies, passage of flatus, tolerance of solid food); there is no consensus as to which one is most clinically meaningful. Generally, it appears that gastric and small intestinal activity return within hours of surgery, and colonic activity returns a day or two thereafter [5,9-15]. Accordingly, the physiologic postoperative ileus that typically follows surgery has a benign and self-limited course.
When prolonged, however, postoperative ileus can increase patient pain and discomfort, decrease his/her mobility, and thereby increase his/her sense of dissatisfaction with the surgical outcome . Prolonged delays in oral feeding may compromise postoperative nutrition, which can lead to greater postoperative catabolism, poor wound healing, susceptibility to infection, and the need for nutritional support [17,18]. These problems contribute to prolonged hospitalizations and are a significant burden on the health system. In fact, it was estimated that in 2000 alone, postoperative ileus was responsible for more than one billion dollars in direct health care costs in the United States .
CONTROL OF GASTROINTESTINAL MOTILITY
Control of gastrointestinal function and motor activity is complex and based upon the interactions of various neural networks and neurohumoral peptides. Neurons located in the gut wall comprise the intrinsic neural network, which is called the enteric nervous system. The extrinsic network consists of visceral sensory afferents in the vagus, splanchnic, and pelvic nerves, and visceral motor efferents of the autonomic nervous system. These extrinsic neurons synapse with the enteric nervous system and connect it to the central nervous system (figure 1).
In general, vagal afferents are thought to be important in the coordinated integration of motility, secretion, and absorption while spinal afferents are thought to be responsible for the transmission of noxious stimuli and inflammation. Visceral motor efferent outflow consists of the sympathetic thoracolumbar and parasympathetic craniosacral arms of the autonomic nervous system. Sympathetic activity is generally inhibitory to smooth muscle activity, while parasympathetic input can be excitatory or inhibitory.