The small bowel is the segment of the GI tract responsible for nutrient absorption. It receives its blood supply form the superior mesenteric artery, which distributes its branches along the mesentery. The small bowel mesentery originates to the left of L1–L2, at the level of the duodenojejunal junction. It travels diagonally towards the right sacroiliac joint, crossing anterior to the duodenum, pancreas, and great vessels.

There have been varied estimations of the length of the small bowel, with a 20–25 % elongation of the bowel reported in cadavers as compared to live subjects. Intraoperative measurements have shown an average length of 460 cm (15 ft), with a standard deviation of 78 cm (30 in.). No statistically significant differences in small bowel length on the basis of sex, height, age, and weight exist. Excluding the duodenum, the jejunum comprises approximately 30–40 % of the small bowel and the ileum 60–70 % [1].

Distinguishing the jejunum from the ileum may be difficult. Several criteria have been proposed, but none are completely reliable. It has been noted that the jejunum has thicker walls, a larger lumen, more prominent plicae circulares, and a single line of arterial arcades with longer vasa recta. All traits are related to the larger amount of nutrient it handles and its greater absorptive capacity. The jejunal mesenteric fat does not extend onto the bowel.

The ileum has more specialized absorptive functions, including the absorption of bile salts, fat-soluble vitamins, and vitamin B12. The ileum also possesses a greater concentration of lymphatic tissue (Peyer’s patches), which are involved both in the maintenance of immune tolerance to gut antigens and nutrients and in the defense against pathogens. This abundance of lymphoid tissue explains the greater frequency of infectious bowel perforations in the terminal ileum, as well as the predilection of autoimmune disease and lymphomas for this segment of the GI tract [2].

Classically, the rotation of the small bowel has been described as occurring in three steps [3]:

While herniation of the midgut has been explained by a disproportion in the size of the gut in comparison to the size of the abdomen, the driving force behind an en bloc midgut rotation has not been identified.

In complete malrotation there is less than 90° of rotation. The small bowel lies in the right abdomen, and the cecum is to the left, in the caudal portion of the abdomen. In incomplete malrotation there is near to 180° of rotation. Again, the small bowel lies in the right abdomen, with the cecum located cranially and to the left. In either case, the mesenteric attachment of the small bowel is narrow and prone to shortening. In addition, bands between the cecum and right body wall (Ladd’s bands) cross in front of the duodenum, potentially compressing it [4]. Ladd’s procedure addresses these defects as illustrated below (Fig. 13.1).

Embryologic studies in rat models suggest that there is no true midgut rotation; rather, the adult configuration of the midgut is the product of differential growth of segments of the small bowel. According to this model, the growth of the duodenojejunal region “pushes” the proximal jejunum behind the mesenteric vessels towards the left upper quadrant. The position of the cecum is attributed to the pattern of return of the bowel. Under this model, the anomalies termed “malrotation” are in reality a failure in the growth of the duodenojejunal junction that remains to the right of the midline [5].

What both models agree upon is that there is greater degree of growth in the segment proximal to the axis of the superior mesenteric artery than in the caudal part. This explains the proximity of Meckel’s diverticulum to the ileocecal valve.

Bilious vomiting in the neonatal period is suggestive of an obstruction distal to the ampulla of Vater, i.e., at the junction of the foregut and midgut. The three common anomalies affecting this area are duodenal atresia, midgut malrotation, and annular pancreas.

Duodenal atresia is the most common of the three, occurring in 1:10,000 live births. It is thought to be a result of failure in the recanalization of the small bowel at 8–10 weeks of gestation. It is commonly associated with annular pancreas, preduodenal portal vein, malrotation, biliary malformations, and esophageal atresia. The diagnosis is suggested by polyhydramnios and bile-stained amniotic fluid, reflecting the lack of passage into the more distal gastrointestinal tract. Although classically described in duodenal atresia, the double bubble sign can be seen in other forms of postampullary obstruction. Duodenal stenosis may have a more delayed and subtle presentation. Treatment consists of duodenoduodenostomy or resection of the duodenal web when present [6] (Fig. 13.2).

It is thought that intestinal atresia is the result of ischemia to the developing midgut. In fact, this condition has been experimentally reproduced by vascular ligation. Furthermore, intestinal atresia has been linked to maternal exposure to tobacco and other vasoconstricting agents. Patients with intestinal atresia present with obstruction during the first days of life. While failure to pass meconium is often quoted, atresias occurring later in fetal development may allow enough time for meconium to reach the bowel distal to the point of obstruction. Type 1 intestinal atresia (web) may be treated with web excision and stricturoplasty if needed. A search for further webs must be undertaken. Other types of atresia require re-anastomosis of the separated segments of the bowel. It is often necessary to resect segments of the bowel that have become excessively dilated [7].

Both the midgut and hindgut may give rise to duplicated segments of the intestine, being more common in the former, especially in the terminal ileum. They are typically located along the mesenteric border of the normal bowel, with which they have a shared blood supply. This feature dictates that they must be removed by segmental bowel resection and anastomosis. These structures have serosal, muscular, and mucosal layers. They often present by causing abdominal pain and obstruction or as an abdominal mass [8].

Duodenal diverticula are present in 5–22 % of the population. They are most often false diverticula located along the pancreatic border of the duodenum and may be in close proximity to the ampulla of Vater. While they are most often asymptomatic, they may give rise to inflammation, perforation, hemorrhage, and obstruction of the common bile duct and pancreatic duct [9].

Diverticula of the jejunum and ileum are much less frequent than those of the duodenum, affecting approximately 1 % of the population. 80 % are located in the jejunum, along the mesenteric border. Their incidence increases with age, a finding which is consistent with their occurrence through a pulsion mechanism generating false diverticula. Like duodenal diverticula, they are most often asymptomatic, but may give rise to inflammatory and hemorrhagic complications [10].

Meckel’s diverticulum is the most common of the omphalomesenteric duct (vitelline duct) abnormalities. During embryonic life, this structure allows the herniation of the midgut into the vitelline sac and subsequent return. The omphalomesenteric duct usually becomes obliterated by weeks 8–9 of gestation. Failure in this process may lead to persistence of the omphalomesenteric duct, formation of sinuses, cysts, or fibrous bands connecting the ileum with the umbilicus and its most common anomaly, the Meckel’s diverticulum [11, 12]. In addition to these anomalies, the urachus and umbilical veins may also give rise to pathology in this area (Fig. 13.3).

Meckel’s diverticulum is a true diverticulum located over the antimesenteric border of the ileum, usually within 2 ft of the ileocecal valve. It is present in up to 2 % of the population. While mostly asymptomatic, they usually present within the first 2 years of life [13].

The most common presentation is obstruction, in which the diverticulum acts as a lead point for intussusception. When attached to the umbilicus, it may also serve as an axis for torsion.

Bleeding is the next most common complication, and it is caused by the presence of ectopic gastric mucosa leading to ulceration. In this setting, the ectopic mucosa and the diverticulum harboring it may be detected through a technetium-99m pertechnetate scan (Meckel’s scan). Clinically, ectopic mucosa appears as a solid structure during the transillumination of the Meckel’s diverticulum (Fig. 13.4).

Inflammation is clinically undistinguishable from acute appendicitis and is a finding of up to 1 % of appendectomies. A rare complication of a large Meckel’s diverticulum is malabsorption and presence of multiple “Meckoliths.”

Treatment of the complications of Meckel’s diverticulum involves either wedge resection with transverse closure or segmental resection and anastomosis, depending upon the status of the adjacent bowel. The treatment of incidentally discovered Meckel’s diverticula is controversial [14] (Fig. 13.5).