Pathophysiology

Physiologic bowel motility is a complex process that results from the interaction of various neural networks and neurohormonal mediators. During the fasting state, the coordinated contractions of the GI tract are referred to as migrating motor complexes (MMC). The contractions can be viewed as occurring in three phases: the resting phase, intermittent contractions of moderate amplitude, and high-pressure waves. When a food bolus is introduced into the intestine, the MMCs terminate, and the digested food, or chyme, is propelled through the GI tract via coordinated contractions of the smooth muscle in the intestinal wall, also referred to as peristalsis. This process is regulated primarily by the enteric nervous system (ENS), which is comprised of myenteric and submucosal sensory and motor nerve plexi and the interstitial cells of Cajal. The ENS transmits sensory information from the intestinal wall to the central nervous system (CNS) via a network of visceral sensory afferents in the vagus, splanchnic, and pelvic nerves. The ENS also connects the visceral motor efferents in these same nerves with the intestinal smooth muscle cells. The ENS and intestinal smooth muscle activity are inhibited by sympathetic signaling and stimulated by parasympathetic cholinergic signaling. Alternatively, the ENS can function independently of CNS control via the autonomic nervous system through secreted mediators that include substance P, vasoactive intestinal peptide, and nitric oxide.

Ileus can develop when physiologic neural signaling and neurohormonal networks are disrupted. Ileus can result from the presence of inhibitory neuroenteric signaling through increased sympathetic activity, inflammation of surrounding organs or the bowel wall itself, paracrine and endocrine activity of inhibitory gastrointestinal peptides or endogenous opioids, and the use of exogenous opioids for analgesia. The most common clinical situation associated with ileus is the immediate period following abdominal operations. In normal circumstances, physiologic small-bowel motility returns within the first 24 hours after the procedure, gastric motility returns within 24 to 48 hours, and colonic motility within 48 to 72 hours. If the return of normal GI function exceeds these time limits, or ileus develops that is independent of a recent operation, a cause for ileus should be sought.

Clinical Features and Diagnosis

Most patients with ileus exhibit abdominal distension, poorly localized bloating and pain, inability to tolerate oral intake, nausea and vomiting, and obstipation. The absence of bowel sounds on abdominal examination can help distinguish ileus from mechanical bowel obstruction; in the latter condition, high-pitched bowel sounds and/or borborygmi are often audible. Patients with severe and advanced cases of ileus can present with peritonitis due to intestinal ischemia or perforation from bowel dilatation, as well as abdominal compartment syndrome.

Radiographic studies are often obtained during the evaluation of patients with suspected ileus. Abdominal radiographs sometimes can be helpful for differentiating ileus from mechanical small bowel obstruction. The presence of gas in the stomach, small intestine, and colon (Figure 24-1) suggests ileus. In contrast, a paucity of gas within the abdomen, air/fluid levels within the small bowel, and absence of air within the colon suggest mechanical small bowel obstruction (Figure 24-2). A computed tomography (CT) scan with enteral contrast administration can better distinguish patients with ileus from those with mechanical bowel obstruction. Inspection of the abdominal CT scan often makes it possible to accurately localize a point of obstruction or a region of transition from dilated to decompressed bowel. If these findings are present, the diagnosis of mechanical bowel obstruction is established. Passage of oral contrast into the colon within 4 hours favors ileus over a bowel obstruction as the cause of intestinal dysmotility. The CT scan can also identify other intraabdominal inflammatory processes that can be the cause of ileus (e.g., appendicitis, pancreatitis, intraabdominal abscess).

Figure 24-1 Ileus.

Abdominal radiograph shows multiple air-filled dilated loops of small bowel as well as an air-filled colon and rectum.

Figure 24-2 Small Bowel Obstruction.

Abdominal radiograph shows dilated loops of small bowel and multiple air/fluid levels. Small bowel has a paucity of gas. No evidence of air within colon.

Treatment and Outcome

Treatment is largely supportive until motility returns. Patients should be made nil per os (NPO) and given adequate intravenous fluids to replace insensible losses and sequestration of fluid (“third spacing”) within the wall and lumen of the gut. Serum electrolyte levels should be measured and corrected as indicated. Electrolyte abnormalities, including hypokalemia, hyponatremia, hypo- and hypermagnesemia, and hypo- and hypercalcemia, can contribute to the development of ileus. Medications that can inhibit bowel motility—narcotics, phenothiazines, diltiazem, anticholinergics, and clozapine—should be discontinued if possible.

Nasogastric (NG) tube decompression is reserved for patients with abdominal distension, nausea, or vomiting. Several randomized clinical trials have shown that NG decompression does not shorten the duration of ileus in postoperative patients.² Moreover, presence of an NG tube can contribute to respiratory complications such as atelectasis and pneumonia.

Nonsteroidal antiinflammatory agents (NSAIDs) should be used for pain control where appropriate; NSAIDs have been shown to reduce postoperative nausea and vomiting as well as improve GI transit in several experimental and clinical studies.³ NSAIDs not only reduce the need for high doses of narcotics but also can decrease inflammation in the intestinal wall.

A midthoracic epidural catheter should be considered for patients who are undergoing abdominal procedures. The level of the epidural catheter is important because low thoracic and lumbar catheters are less effective. Epidural administration of local anesthetics can reduce the incidence and degree of ileus by blocking afferent as well as efferent inhibitory reflexes, including inhibitory sympathetic efferent signals.⁴ Total parenteral nutrition (TPN) should be considered when the duration of ileus exceeds 5 days, particularly for patients who are malnourished.

Most pharmacologic promotility agents that have been tested to hasten the resolution of ileus are ineffective. Metoclopramide hydrochloride (Reglan), the most frequently used prokinetic agent, is a cholinergic agonist and dopamine antagonist. A number of randomized trials of metoclopramide have failed to demonstrate significant reduction of the duration of postoperative ileus.⁵

More recently, the mu opioid receptor antagonists, alvimopan⁶ and methylnaltrexone,⁷ have been evaluated in phase III randomized, controlled clinical trials. Because these agents do not cross the blood-brain barrier, they do not interrupt the analgesic effects of narcotics. Unfortunately, results from studies of these newer agents have been mixed, and the trial designs used to evaluate them were less than optimal; neither are routinely used in clinical practice. Erythromycin is another prokinetic agent that binds to and stimulates the motilin receptor on small-intestinal smooth muscle cells. Two randomized trials examined the effects of erythromycin on the duration of postoperative ileus, and neither demonstrated a beneficial effect.⁸