Intestinal Obstruction and Malrotation

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109 Intestinal Obstruction and Malrotation

Andrew Chu

In its most simplistic conceptualization, the gastrointestinal (GI) tract is a long, flexible tube designed for active, unidirectional flow, with its only openings to the outside world being the mouth for input and the anus for output. Any impediment to the forward progress of ingested contents results in luminal distension proximal to the obstruction and eventual vomiting or perforation. A variety of congenital and acquired defects may cause throughput failure, with clinical presentations ranging from subtle findings that go undiagnosed for years to acute clinical deterioration. The clinician’s first responsibilities are to triage the severity of the obstruction and provide relief of the obstruction to prevent further complications, most notably intestinal perforation, peritonitis, sepsis, and death.

Etiology and Pathogenesis

The many etiologies that cause intestinal obstruction ultimately result in a final common pathophysiologic pathway (Figure 109-1). Anything that prevents forward progress of intestinal contents sets into motion this sequence of events, leading to worsening distension, vomiting, and systemic dysfunction. Not only do the resulting dehydration and electrolyte imbalances create significant complications, bacterial proliferation within the static intestinal contents and compromised mucosal integrity set the stage for bacterial translocation across the intestinal wall, with consequent bacteremia and sepsis.

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Figure 109-1 Intestinal obstruction, adynamic ileus.

Although many disorders may cause obstruction (Figure 109-2), they can be summarized by several pathophysiologic categories that aid in constructing a rational differential diagnosis.

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Figure 109-2 Alimentary tract obstruction.

Extrinsic Compression

Because the bowel is a flexible organ, anything that compresses it externally can decrease the intraluminal diameter and precipitate obstruction. For example, adhesions are fibrous bands of tissue that spontaneously arise within the peritoneum in reaction to insults, such as peritonitis or abdominal surgery, and can encircle and constrict loops of bowel. They are relatively common after surgery, with up to a 25% 5-year readmission rate caused by adhesions, depending on the type of operation.

Intraabdominal masses, such as Wilms’ tumor, can compress and obstruct bowel by their sheer size (“mass effect”). Annular pancreas is an anatomic variant in which a ring of pancreatic tissue encircles and can cause duodenal obstruction. Superior mesenteric artery (SMA) syndrome results from compression of the third duodenal segment by the artery against the aorta. It is sometimes seen in patients who have had precipitous weight loss with resultant loss of the mesenteric fat pad that protects the duodenum from compression; external body cast application; or after intestinal or orthopedic surgery that results in traction upon the SMA, pulling it down upon the duodenum. Another example is closed loop obstruction (internal hernia), in which a loop of bowel passes through a mesenteric defect or similar orifice (e.g., inguinal hernia) and becomes lodged within it, resulting in occlusion of both the proximal and distal ends of the loop.

Intrinsic Decrease in Lumen Caliber

Congenital Defects

Children can be born with an abnormally reduced lumen caliber that leads to obstruction. For example, atresias and webs represent a spectrum of disorders potentially affecting any region of the GI tract from the esophagus to the colon. In some cases, mucosal membranes within the lumen precipitate obstruction (web). In other instances, there is total or near-total discontinuity of a segment of bowel (atresia). Hirschsprung’s disease is a disorder of the rectum and colon in which absence of enteric neurons caused by defective migration during development leads to smooth muscle dysfunction in the affected regions and severe constipation.

Acquired Defects

Chronic bowel inflammation can, over time, lead to narrowing of the lumen. An important example is Crohn’s disease, in which there is discontinuous full-thickness bowel inflammation anywhere from the mouth to the anus (see Chapter 110). Over time, inflamed areas may stricture and obstruct. Another example of this is eosinophilic esophagitis, an entity that lies within the spectrum of food allergies and atopic disease. Because of persistent eosinophilic inflammation in the presence of the offending antigen, the esophagus can eventually stricture over time, leading to dysphagia and the need for esophageal dilatation to relieve the obstruction. Malignancy, although relatively uncommon in children compared with adults, is another important cause of decreased lumen caliber. For example, the GI tract is the most common extranodal site affected in non-Hodgkin’s lymphoma. Infiltration of the bowel wall by tumor leads to decreased effective luminal diameter and a higher risk of obstruction. Achalasia causes functional esophageal obstruction caused by aperistalsis and inadequate lower esophageal sphincter relaxation. An example of gastric outlet obstruction caused by decreased diameter is hypertrophic pyloric stenosis, a disease primarily affecting infants in the first few months of life in which smooth muscle hypertrophy leads to occlusion of the pylorus (Figure 109-3).

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Figure 109-3 Hypertrophic, pyloric stenosis.

Internal Blockage

A wide variety of etiologies may be associated with internal blockage of the GI tract. Areas that are inherently narrow relative to the rest of the GI tract (upper esophageal sphincter, esophagus adjacent to the carina, lower esophageal sphincter, pylorus, ileocecal valve) are at more risk of becoming obstructed by large foreign bodies. In a special example of this, bezoars are accumulations of indigestible material (e.g., hair, fiber from vegetables) that become trapped in the GI tract (typically the stomach) and can cause obstruction when they grow large enough. Injury to the wall of the small intestine from blunt abdominal trauma, as can occur when bicycle handlebars injure a child’s duodenum, may instigate a hematoma, which can obstruct the small intestine because of its small caliber.

In neonates, meconium ileus is a cause of distal GI obstruction shortly after birth. Meconium is a conglomeration of sloughed intestinal mucosa, bile salts, and other debris that accumulates during fetal development. It is normally passed within the first day of life, but when it is exceedingly inspissated, as occurs in cystic fibrosis, patients may be unable to expel it, leading to obstructive symptoms. In young children, intussusception is an example in which the bowel obstructs itself because of telescoping of one portion of bowel into the adjacent region of bowel.

Defects in Bowel Arrangement

Malrotation is an important entity that clinicians must be aware of when evaluating intestinal obstruction of unknown etiology. Malrotation is a congenital defect typically involving both the small and large intestines that occurs when the bowel assumes an abnormal spatial arrangement within the abdomen. Intestinal development is a complex, continuous process spanning the fourth fetal week to birth that takes the primitive gut, which begins as a short, straight tube, and transforms it into a long, highly specialized organ. As part of this process, the intestinal tract, after rotating 270 degrees, becomes fixed in a specific arrangement such that the duodenum ends at the ligament of Treitz in the left upper quadrant and the cecum is found in the right lower quadrant. When this final arrangement fails to take place properly, the bowel is malrotated. Although this may not result in any clinical symptoms in mild cases, the most feared complication is volvulus, a surgical emergency in which the bowel, as a result of its inappropriate positioning and lack of usual support, twists upon its mesenteric stalk, causing not only intestinal obstruction but also ischemia (Figure 109-4). Ladd’s bands, intraperitoneal fibrous bands that can encircle and obstruct the duodenum, are also associated with malrotation.

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Figure 109-4 Malrotation and volvulus.

Motility Failure

Even when there is not an occlusive obstruction of the intestine, failure of appropriate peristalsis can nonetheless create obstructive symptoms. A common example is postinfectious ileus, which is an interruption in normal intestinal motility and forward propulsion of contents without physical occlusion that most often occurs after viral gastroenteritis. It is usually mild and self-limited, but in rare instances, it can result in severe and prolonged gastroparesis, feeding intolerance, and the need for postpyloric nasogastric enteral feeding until it resolves. Intestinal surgery can cause postoperative ileus, a temporary disruption of normal motility, particularly when combined with narcotics, which have intrinsic antimotility effects.

Another important consideration is intestinal pseudoobstruction, which is a spectrum of congenital and acquired disorders involving the small or large bowel (or both) that ultimately results from failure of either the enteric nervous system or the intestinal smooth muscle to coordinate appropriate peristalsis. Examples of factors that can trigger pseudoobstruction are trauma, electrolyte abnormalities, sepsis, orthopedic and cardiovascular surgery, and pregnancy.

Clinical Presentation

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