Ileus and Mechanical Bowel Obstruction

Published on 26/03/2015 by admin

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106 Ileus and Mechanical Bowel Obstruction

Rajeev Dhupar, Juan B. Ochoa

Definition

Ileus is defined as the absence of physiologic motility of the bowel leading to a disturbance in the progression of bowel contents through the gastrointestinal (GI) tract. Ileus must be distinguished from mechanical bowel obstruction, which is defined as the presence of anatomic barriers, either extrinsic or intrinsic, that prevent the normal progression of bowel contents through the GI tract.

Pathophysiology

Normal Gastrointestinal Motility

Coordinated contraction of the GI tract can be measured by evaluating its electrical and motor activity. During fasting states, the coordinated contractions are called migrating motor complexes (MMC) and are divided into three phases: resting phase, intermittent contractions of moderate amplitude, and high-pressure waves.¹ When a food bolus is introduced into the intestine, the organized MMC disappear, and digested food (chyme) is propelled through the GI tract by spikes in the contraction of smooth muscle in the wall of the gut. Longitudinal progression of intestinal contents (made up by food and secretions) occurs through the coordinated response of several systems. These are:

1 Autonomic nervous system. Activation of the sympathetic nervous system decreases GI motility. Activation of the parasympathetic nervous system increases GI motility.²

2 Interstitial cells of Cajal (ICC). ICC are distributed throughout the tunica muscularis and are electrically coupled with one another. These cells, which are mesenchymal in origin, are responsible for the pacemaker activity of the GI tract.¹

3 Myenteric and submucosal nerve plexi. These plexi integrate with the autonomic nervous system. Nitric oxide produced by neuronal nitric oxide synthase (nNOS) induces smooth muscle relaxation.

4 Endocrine system. Multiple endocrine substances affect GI motility. Some of these substances, including motilin, gastrin, and cholecystokinin, increase GI motility. Other hormones such as somatostatin and glucagon decrease GI motility.

5 Smooth muscle. Although there are differences in the muscular layers of the stomach, small bowel, and colon, intestinal motility depends on the coordinated contraction of an outer longitudinal layer and an inner circular layer.

6 Immune system. Activation of the innate immune system can produce profound alterations in GI motility. This appears to be especially evident after surgical manipulation of the small bowel and colon. Inflammatory mediators such as nitric oxide, cytokines, prostaglandins, and oxygen free radicals have direct inhibitory effects on normal contractile activity and may play an important role in the development of ileus due to sepsis and/or after abdominal operations.^3,⁴

Integration of the aforementioned processes results in coordinated muscular contractions in the wall of the stomach and intestine that move fluids in the GI tract in an aboral direction. Additionally, this activity helps to ensure that food is adequately mixed with GI secretions and digested. When motility is normal, there is adequate contact time between the absorptive surfaces of the bowel and chyme to permit absorption. Normal motility ultimately leads to the evacuation of undigested food as fecal matter.

Clinical Consequences of Ileus

Ileus results in the inability to tolerate enteral feeding, nausea, vomiting, constipation, and obstipation. Accumulation of fluid and air in the bowel results in abdominal distention. Symptoms and consequences of ileus can range from minimal to life threatening. Serious consequences of ileus can include electrolyte abnormalities, intestinal ischemia, intestinal perforation, and abdominal compartment syndrome. Intolerance of enteral nutrition compromises the ability to provide adequate nutritional support to critically ill patients.

Diagnosis

Tools to aid clinicians in identifying and diagnosing GI dysfunction are poorly developed. Ileus is diagnosed by clinical evaluation of the following signs and symptoms:

1 Abdominal distention

2 Nausea, vomiting, or high output through a nasogastric (Salem sump) tube

3 Reflux of enteral tube feedings

4 Abdominal pain and discomfort (either spontaneous or elicited by palpation of the abdomen)

5 Decreased or absent bowel sounds

6 Constipation and obstipation

7 Suggestive radiologic patterns including increased air in the small intestine, bowel distention, and presence of air-fluid levels

There is no objective measure that defines abnormal abdominal distention or excessive nasogastric output. The true incidence of ileus in critical illness is therefore unknown.

Ileus is often diagnosed by challenging the patient with an enteral diet. Gastric ileus (i.e., absence of normal gastric emptying) is observed in as many as one third of all critically ill patients and is more common in hemodynamically unstable patients. Thus, clinicians often attempt to place feeding tubes into the small bowel, where success in achieving nutritional goals is more commonly achieved.

Three types of clinical ileus are observed: adynamic ileus, spastic ileus (observed rarely in diseases such as porphyria or lead poisoning), and ischemic ileus, identified in hemodynamically unstable patients with low-flow states and classified as nonocclusive mesenteric ischemia (NOMI).

Treatment

1 Adequate hemodynamic resuscitation. This helps to ensure adequate organ blood flow. It is especially important to minimize the infusion of exogenous catecholamines, since these agents can promote the development of ileus.

2 Judicious administration of intravenous fluids. Excessive fluid infusion can result in bowel edema, thereby decreasing intestinal blood flow and increasing intraabdominal pressure.

3 Maintaining electrolyte balance. The presence of hypokalemia prevents normal muscle contraction and nerve depolarization. It is also important to prevent or treat acidemia as well as maintain normal concentrations of other electrolytes (e.g., sodium ion, calcium ion, magnesium ion).

4 Avoid or minimize opioid use. Morphine and other opioids decrease coordinated contractions of the gut and forward propulsion of chyme. These effects may be a particularly prominent cause of ileus and intolerance to oral or enteral nutrition in postoperative or trauma patients.

5 Avoid prolonged starvation. Starvation and parenteral nutrition are associated with GI mucosal atrophy.⁵ Early use of the GI tract (within the first 24-48 hours of the onset of critical illness) is associated with better clinical outcomes.⁶ Early enteral nutrition is associated with earlier achievement of caloric goals, earlier time to bowel movements, shorter lengths of stay, and a trend toward lower mortality. The initial goal of early enteral nutrition is to prevent intestinal atrophy, and thus low infusion rates (e.g., 10-20 mL/h) have been advocated. The benefits, risks, and indications of so-called “trickle tube feeds” are still unclear.

6 Do not assume that a patient has ileus and should not be fed enterally. It is unnecessary to wait for the passage of flatus and/or the presence of bowel sounds before attempting to feed enterally.⁷ It also is untrue that the bowel “needs to rest” for adequate healing of intestinal anastomoses. On the contrary, provision of enteral nutrition is associated with more deposition of collagen and increased bursting strength in wounds.⁸ Virtually all hemodynamically stable postoperative patients should be fed enterally as soon as hemodynamic stability and adequate resuscitation are achieved.

7 Total parenteral nutrition (TPN) is not an ideal substitute for enteral nutrition. TPN rarely achieves adequate nitrogen retention in critical illness and is associated with increased incidence of complications including infections. There are no data to support indiscriminate use of TPN in patients with ileus.⁹

8 Use nonsteroidal antiinflammatory agents (NSAIDs). In surgical patients, the use of systemic NSAIDs such as ketorolac is associated with earlier bowel movements and tolerance to oral diet. This is thought to be due to a quelling of the inflammatory response, as well as a resultant decrease in narcotic use.¹⁰ In animals subjected to surgical manipulation of the GI tract, ketorolac is associated with faster gastric emptying and restoration of normal migrating motor complexes.¹¹

9 Promotility agents. Although use of promotility agents has not been routinely implicated, recent protocols advocate starting these early with the objective of achieving caloric goals. There is a paucity of evidence, however, to support the view that systemic promotility agents such as metoclopramide, erythromycin, or cholecystokinin affect overall outcome.¹² Newer agents are being tested for clinical use to aid in the prevention of or hasten the resolution of ileus. These agents include mu-opioid antagonists, motilin analogs, and intestinal chloride channel modifiers.¹³