The small intestine and the right side of the colon constitute the embryologic midgut, which, during the process of marked elongation in fetal development, herniates into the umbilical cord. Following a 270° counterclockwise rotation, the midgut returns to the peritoneal cavity. Errors during this complex series of events are common, resulting in varying degrees of malrotation with or without volvulus. This may result in bowel obstruction and ischemia, and may present in infancy or be delayed into adult life.

In the fetus, the omphalomesenteric or vitelline duct connects the distal small bowel with the yolk sac. In neonates, the vitelline duct normally atrophies and disappears; failure of involution results in a Meckel diverticulum, a blind outpouching from the distal ileum.

The jejunum begins at the duodenojejunal flexure, which is often acutely angulated, as it is suspended by the suspensory ligament of the duodenum (ligament of Treitz) and extension of the right crus of the diaphragm. The jejunum constitutes about 40% of the small bowel, and is about 2-3 meters long.

The jejunum normally lies primarily in the left upper quadrant, and is distinguished by having a thicker, more vascular wall than the ileum. Its circular folds (valvulae conniventes and folds of Kerckring) are taller and more closely spaced (4-7 per inch).

The ileum constitutes the distal 60% of the small intestine, though there is no clear line of delineation, and usually lies in the right side of the abdomen and pelvis. Relative to the jejunum, the wall of the ileum is thinner and less vascular, but has more prominent lymphoid follicles in the submucosal layer.

The small intestine is supplied entirely by the superior mesenteric artery and vein (SMA and SMV). Occlusion of the SMA by thrombus or embolus results in small bowel ischemia, but arterial occlusion may be difficult to diagnose on clinical or imaging evaluation until frank infarction with bowel wall pneumatosis develops. SMV occlusion results in more impressive edema of the bowel wall and mesentery. Various vasculitides affect long segments of the bowel and are manifested by impressive bowel wall edema and luminal dilation.

Lymphatic drainage begins at the level of the villi (tiny projections of the mucous membrane) with the lacteals, specialized lymphatic vessels that absorb fat from the gut lumen. The lacteals empty milky, lipid-rich chyle into the regional lymphatic plexus in the mesentery, and then progressively into the lymph nodes, intestinal lymphatic trunks, cisternal chyli, and thoracic duct. The thoracic duct transports dietary lipids directly into the bloodstream as it empties into the left subclavian vein. Intestinal lymphangiectasia results from a congenital abnormality of lymphatic development or from lymphatic obstruction in the small bowel wall or mesentery. The resulting interference with lipid absorption from the gut can result in malnutrition, chylous ascites, and other complications.

There are 5 layers of the small bowel wall. The innermost is the mucosa, an absorptive surface of the bowel. The jejunal mucosa is extensively plicated (folded) and these transverse (“circular”) folds lie perpendicular to the long axis of the bowel. The other layers are the submucosa, circular muscle, longitudinal muscle, and serosa. The serosa is the peritoneal lining of the bowel. The mucosal surface of the jejunum is increased by prominent villi, which are finger-like projections of mucosa. The submucosa has a network of capillaries, lymphatics, and a nerve plexus (of Meissner) within loose areolar tissue.

The ileum has the same 5 layers, but its wall is thinner and less vascular, with less prominent transverse folds and villi.

The small bowel follow through (SBFT), or SB series consists of “overhead” radiographs of the abdomen, supplemented by fluoroscopic spot films, with and without compression, as ingested barium traverses the length of the SB, culminating in opacification of the colon. The SBFT is relatively comfortable for the patient, although slow gastric emptying or SB transit may result in a very prolonged study. It offers an assessment of the length and function of the SB, both pertinent in patients with functional or anatomic deficiencies of the bowel, such as Crohn disease with prior resection and suspected recurrence. Dilution of barium by gastric contents and lack of complete distention are further limitations. Moreover, it is very difficult to distinguish among the many potential causes of an abnormal fold pattern suggested by the SBFT.

Enteroclysis entails nasojejunal intubation and pump infusion of contrast medium (barium for the fluoroscopic type and neutral contrast for CT enteroclysis). Advantages include shorter exam time and better distention of bowel lumen, resulting in greater accuracy for a range of SB pathology including strictures, adhesions, and intrinsic bowel disease (celiac-sprue disease or masses). Disadvantages include more time investment by the radiologist and more patient discomfort.

While enteroclysis is more accurate than CT in detection of mucosal lesions and sources of GI bleeding, both have been supplanted to a large degree by endoscopic techniques. Double-balloon enteroscopy and wireless capsule endoscopy both allow direct visualization of the SB mucosal surface.

CT remains the preferred method for evaluating the “acute abdomen” (abdominal pain and distention) and more accurately depicts extraluminal disease, such as abscess, fistula, large masses, and mesenteric and vascular disease.

Almost all acute bowel injuries result in thickening of the submucosal layer (“thickened folds”). The etiology of the injury may be suggested by the attenuation of the submucosal layer on CT evaluation.

Submucosal gas (pneumatosis) often indicates bowel infarction, but there are many other “benign” (nonischemic and less threatening) causes, including various medications and prior interventions such as surgery or endoscopy.

At the other extreme of attenuation, intramural hemorrhage may be detected as higher-than-soft tissue density within the bowel wall, and may result from trauma or coagulopathy.