The gastrointestinal tract has an active motor function with spontaneous pacesetting activities in all areas. The spontaneous activity is influenced by nervous and humoral activities, which are both stimulating and inhibiting. The esophagus exhibits both peristaltic and non-peristaltic movements. Orderly peristalsis is dependent on intact innervation. With regard to motor function, the stomach can be divided into a proximal and a distal part. The former acts as a reservoir and the fundus has an active receptive relaxation which depends on intact vagal innervation. Gastric emptying depends on peristaltic movements which involve the entire stomach and bring small portions of the antral content through the relaxed pylorus. This function also depends on intact innervation. Retropulsion, caused by closure of the pylorus at the end of the antral contraction, generates mixing of the gastric contents. Increased intragastric volume increases the rate of gastric emptying. Gastric motility is stimulated by the amount and consistency of the intraluminal content. Fatty acids as well as acid in the duodenum are potent inhibitors of gastric emptying. Solids are retained by the antrum, and in normal states the majority of particles emptied through the pylorus have dimensions of less than 1 mm. After a meal fluids are emptied immediately while solids are retained in the fundus of the stomach to be reduced.
The small intestine has a basal electrical 'rhythm' (slow waves). The frequency of these slow waves is highest in the proximal part of the duodenum. These slow waves are the pacesetters, and some give rise to action potentials. Slow waves are propagated along the entire gut, and the mechanical activity is also propagated in this manner. During certain periods every slow wave gives rise to an action potential, and such complexes migrate along the entire small intestine. The electrical action also has a mechanical consequence. This activity has a periodicity of 60 to 90 cycles/min, so that when one cycle ends in the ileum a new one starts in the duodenum.
Colonic motility provides the prerequisite for a steady slow flow of the bowel content. This slow flow is interrupted periodically by mass contractions causing an urge to defecate.
Critical illness, intra-abdominal surgery, and intraperitoneal abscess usually cause paralytic ileus. This condition typically affects all levels of the gastrointestinal tract through one or more of the following mechanisms: increased activity of intrinsic or extrinsic inhibiting neurons, decreased activity of intrinsic or extrinsic stimulating neurons, or increased levels of inhibitory hormones. In peritonitis a complete cessation of motor function is likely; drainage and/or removal of the causative factor has to be performed before motor activity will recommence. Local paralysis affecting an intestinal loop close to a regional inflammatory process constitutes another possibility, for example duodenal paralysis in a patient with acute pancreatitis.
The influence of critical illness and intra-abdominal surgery on motility varies between levels of the gastrointestinal tract. The stomach, and particularly the colon, are characteristically slow in regaining adequate motor function, while the small intestine will usually have returned to adequate motor activity within hours. This is the background to early enteral feeding in critically ill and postoperative patients.
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