Ileus is defined as a reversible decrease in gut motility occurring secondary to a physiological derangement and resulting in functional obstruction to the passage of enteric contents. In the ICU patient, ileus is far more frequent than obstruction and has a typically multifactorial etiology ( Smith...,.etal 1977) (Table..,.!,). Metabolic and pharmacological causes predominate; therefore correction of electrolyte and acid-base abnormalities is the first step in treatment. Medications that can alter gut motility should be avoided, particularly drugs which exhibit adrenergic and cholinergic activity.

Ileus Suction Output
Table 1 Common causes of ileus

Many ICU patients will have a history of recent abdominal surgery. Postoperative ileus, which is believed to be due to a somatic inhibitory reflex, is common and prolonged if there has been intestinal manipulation. Following laparotomy, ileus resolves in a predictable sequence that begins with the small bowel (5-10 h), followed by the stomach (up to 3 days), and finally the colon (up to 5 days). It is important to appreciate that bowel sounds arise only in the presence of fluid, air, and peristalsis. Their presence or absence is largely non-specific and offers little aid in reliably distinguishing ileus from obstruction.

The length of surgery or degree of manipulation cannot predict the extent of ileus. While adrenergic stimulation impairs gut motility, circulating catecholamines play no significant role. Adrenalectomy, adrenergic blockade, or epidural anesthesia to block efferent sympathetic fibers have negligible protective effects against postoperative ileus.

While small bowel resection and re-anastomosis interrupts propagation of migrating motor complexes for 30 to 40 days, the distal small bowel will still maintain its own intrinsic pacesetter rhythm. The postprandial peristaltic response and absorptive capacity of the bowel are unaffected by resection. This phenomenon accounts for the success of early postoperative feeding. Early feeding also prevents villus atrophy and helps to maintain normal gut physiology.

The diagnosis of ileus requires that mechanical obstruction be excluded. Serial abdominal films showing non-specific intestinal distension, with or without scattered air-fluid levels on upright or decubitus films, are the best adjunct to repeated clinical evaluation ( Table.,.?).

Table 2 Plain radiograph features of ileus versus obstruction

After correction of metabolic abnormalities, medications should be reviewed and rationalized to reduce cumulative sympathomimetic effect. Opiates should be reduced, although not to the exclusion of adequate pain control as both pain and immobilization contribute to prolongation of ileus.

Treatment of ileus is expectant. Nasogastric decompression is not essential if there is no emesis. Intravenous hydration to provide adequate urine output is essential, and total parenteral nutrition should be initiated promptly if the conditions believed to be responsible for the ileus are unlikely to abate within 3 to 5 days. Parasympathomimetic agents (neostigmine, bethanechol) and sympatholytics have been used with some success. Prokinetic agents are frequently tried;

metaclopramide enhances gastric and small bowel motility but with no reproducible capacity to relieve ileus. Cisapride, by augmenting acetylcholine release in the myenteric plexus, is of some benefit in the treatment of postoperative ileus (V§r!ind§.D...®(J/ 198.7). Even in the face of moderate ileus, it is often possible to initiate enteral feeds at a slow infusion rate (20-40 ml/h) and increase as tolerated.

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