An algorithmic approach for diagnosis of various small bowel diseases is suggested which include small bowel wall thickening (Algorithm 10.3), location of the thickening (Algorithm 10.4), length (Algorithm 10.5), pattern of enhancement (Algorithm 10.6), epicenter of the lesion in relation to the bowel (Algorithm 10.7), as well as extraluminal manifestations (Algorithm 10.8).

The normal small bowel diameter should be less than 3 cm. If the luminal diameter is greater than 3 cm with no transition point, a small bowel ileus may be present. If the small bowel lumen is greater than 3 cm in diameter, air fluid levels are present, and if there is a transition point (with decompressed distal small bowel loops) (Fig. 10.2 and Algorithm 10.9), small bowel obstruction from various etiologies must be considered (Algorithm 10.12). Small bowel obstruction can be termed as simple or closed loop obstruction and may be partial (low grade) or complete (high grade) (Algorithm 10.10). Small bowel obstruction with intact blood supply is termed simple (Algorithm 10.11). In partial obstruction, there is narrowed bowel lumen with conserved passage of gas and intestinal contents distally. In complete obstruction, there is total luminal occlusion with paucity of gas and fecal material in colon or decompressed distal small bowel. In closed loop obstruction, the bowel segments occluded at two points are usually adjacent to each other, and this type of bowel obstruction is more prone to ischemia potentially resulting in bowel necrosis, sepsis, peritonitis, and death. The involved small bowel loop in a closed loop obstruction is usually fluid filled and may assume a coffee bean (U shape) or C shape on CT imaging (Figs. 10.3 and 10.7). Moderate to severe small bowel obstruction may be confirmed by the presence of small bowel feces sign (Fig. 10.4); however, this is neither sensitive nor specific for the diagnosis. The small bowel feces sign is defined as the presence of gas and particulate material within a dilated small bowel loop that simulates the appearance of feces and is most likely caused by stasis within the obstructed loop, allowing more time for fluid absorption across the bowel wall and accumulation of undigested food particles. Strangulated obstruction involves small bowel obstruction with evidence of bowel ischemia. Strangulation may occur in a setting of closed loop obstruction, which on CECT may appear as thickened bowel wall, hemorrhage in the bowel wall and mesentery, non-enhancing bowel wall, engorged mesenteric vessels, and pneumatosis (Fig. 10.5). Occasionally, small bowel dilatation may result in a setting of a large bowel mass associated with a patulous ileocecal valve (Fig. 10.6).

Congenital rotation anomalies involving the midgut often present within the first month of life. However, few patients present during the later years or remain asymptomatic for life. Malrotation is defined as any deviation from the normal 270° counterclockwise rotation of the midgut during embryologic development [8]. These anomalies are classified as either incomplete rotation or nonrotation [9]. Malrotation results in malposition of the bowel and is often associated with mesenteric malfixation as noted by the presence of a narrow pedicle of attachment, which predisposes to midgut volvulus. Rotation anomalies may occur in combination with situs abnormalities in approximately 70 % of the cases [10].

On CECT, malrotation appears as an abnormal duodenojejunal junction that fails to cross the midline and lies below the level of the duodenal bulb and with malposition of the right colon (Fig. 10.8). However, in 20 % of patients, the cecum may be located in a normal location, and in such cases, a quiescent malrotation may be missed [9]. Deviation of the normal relationship between the SMA and SMV is a useful indicator of malrotation [11], with a vertical relation or left–right inversion seen in most cases [12]. Importantly, an abnormal SMA–SMV relationship in isolation is not entirely diagnostic of malrotation [12]. An additional finding seen in cases of malrotation is underdevelopment of the uncinate process of pancreas.

Malrotation may be complicated by midgut volvulus secondary to a narrow mesenteric attachment, which results in clockwise twisting of the bowel around the SMA axis. On CECT, features of volvulus include a corkscrew appearance of the proximal small bowel, duodenal obstruction, congestion of the mesenteric vasculature, and mesenteric ischemia. Another complication of malrotation is internal hernia, caused by abnormal peritoneal Ladd bands.

Enteric duplication cysts are an uncommon congenital abnormality, which typically occur on the mesenteric side of the gut. The small intestine is the most common site of involvement, with the ileum being the preferred site. Duplication cysts usually manifest in the first year of life, although late manifestation in older patients is reported [13]. Duplication cysts may be complicated by intussusception, bowel obstruction, volvulus, perforation, and malignancy. Duplication cysts may be associated with vertebral or urogenital malformations [14].

On USG, these cysts appear as fluid-filled sacs with an echogenic inner mucosal layer surrounded by a hypoechoic outer muscular layer of variable thickness, which is further surrounded by an outer echogenic serosa. On CECT, a duplication cyst appears as a non-enhancing cystic mass, which may be complicated by the presence of intracystic hemorrhage or proteinaceous material (Fig. 10.9) [15]. Occasionally gastric mucosa may be present in a duplication cyst, which may be identified using a technetium-99m sodium pertechnetate study.

Meckel’s diverticulum results from an incomplete involution of the omphalomesenteric duct [16] and represents the most common congenital anomaly of the gastrointestinal tract, with an approximate incidence of 2–3 % [17]. It is usually located within 2 ft from the ileocecal valve. This is a true diverticulum occurring along the antimesenteric border of the distal ileum (Fig. 10.10) and frequently contains heterotopic gastric or pancreatic mucosa. The diverticulum may connect with the umbilicus via a fibrous band.

On CECT, Meckel’s diverticulum appears as a saccular, blind-ending structure along the antimesenteric border of the distal ileum, with a triradiate fold pattern converging to the ileum. Complications associated with Meckel’s diverticulum include enteroliths, hemorrhage, inflammation (diverticulitis), obstruction, inversion that may produce obstruction or act as a lead point for intussusception, and rarely neoplasms.

Crohn’s disease typically involves the small bowel, with dominant involvement of the terminal ileum. The pattern of involvement is typically transmural with characteristic skip lesions and often penetrating disease in the form of enteric fistulae or abscesses [18]. Conventional oral and intravenous contrast-enhanced CT does not precisely identify inflammatory small bowel disease. In such a setting, CT enterography is an invaluable technique to diagnose inflammatory bowel disease as it exquisitely delineates the bowel wall and is useful in differentiating active inflammatory strictures from fibrotic strictures. This information is critical, as active inflammation is likely to be treated medically, whereas fibrotic strictures are likely to have a surgical outcome [19, 20]. Capsule endoscopy is another technique to evaluate the inflammatory small bowel disease; however, it is more useful in delineating mucosal-based pathologies rather than mural pathologies [21]. Capsule endoscopy is reserved for patients with a strong clinical suspicion for Crohn’s disease with negative CT enterography results. However, small bowel capsule endoscopy is contraindicated in the presence of inflamed or fibrotic strictures with a potential for impaction leading to bowel obstruction (Fig. 10.11).

Characteristic CT enterographic findings of active Crohn’s disease include bowel wall thickening, segmental mucosal hyperenhancement, mural stratification, perienteric mesenteric fat stranding, and engorged vasa recta [22, 23]. Bowel wall thickening is typically eccentric, with involvement of the mesenteric border, and occasionally associated with pseudosacculations, sinuses, fistulae, or intramural/extraenteric abscesses. Segmental mucosal hyperenhancement is the most sensitive feature of active disease [24] and typically refers to increased attenuation of inflamed mucosa relative to nearby normal-appearing loops. If the bowel loops are collapsed, secondary signs of mural inflammation need to be elicited prior to making the diagnosis. Mural stratification represents visualization of a trilaminar appearance of the bowel wall, with intense enhancement of the mucosa and serosal layers of the involved bowel, interspersed by a hypoattenuating edematous submucosal layer (Fig. 10.12). Skip lesions are pathognomonic of Crohn’s disease (Fig. 10.13). Absence of the trilaminar pattern but presence of a homogeneously enhancing wall suggests a fixed fibrotic stricture (Fig. 10.14). Engorged vasa recta, also called the comb sign (Fig. 10.15) [25, 26], appears as vessels penetrating the bowel wall perpendicularly and is a characteristic sign of active inflammation. Comb sign is known to correlate with the disease severity [27].

Magnetic resonance enterography is a noninvasive imaging technique increasingly being used in the assessment of complex or recurrent Crohn’s disease, allowing for the depiction of both intraenteric and extraenteric disease using multiplanar techniques without ionizing radiation. MR enteroclysis may hold a slight advantage over MR enterography in the detection of early disease. Due to the limited spatial resolution, the earliest changes of Crohn’s disease including mucosal nodularity, erythema, and superficial aphthous ulceration are not seen on cross-sectional imaging [28]. MR imaging findings in Crohn’s disease can predict the presence of active or long-standing disease (Algorithm 10.13). Findings are typically subdivided into intra- and extraenteric abnormalities.

Wall thickening in small bowel Crohn’s disease usually ranges between 5 and 10 mm [29] and is better assessed with a HASTE sequence due to the absence of a chemical shift artifact. Abnormal fold pattern is commonly recognized, with preferential involvement of the mesenteric border, which produces an asymmetric pattern of disease involvement. Three patterns have been described which include the following: picket fence, reduced or distorted folds due to ulceration, and cobblestone pattern. Ulceration is a common feature of the disease, with better depiction of moderate to deep ulcers on MR enterography, which show thin high-signal-intensity lines oriented longitudinally or transversely within the thickened bowel wall. Early or superficial ulceration may not be well demonstrated even with full luminal distention. Acute wall thickening represents disease activity. It may appear as a hyperintense stripe within the low T2 signal muscle on the fat-suppressed HASTE sequences and suggest the presence of mucosal or submucosal edema [30, 31] (Fig. 10.16). Small bowel strictures are well seen on MR enterography and appear as narrowed thick-walled segments of bowel with or without bowel obstruction. Fibrotic wall thickening appears as diffuse low to intermediate T2 signal within the muscle. Narrowed bowel segments may also be seen in adhesions, without wall thickening. Fatty infiltration of the bowel wall may occur in chronic IBD and can be differentiated from wall edema, with the use of fat saturation sequences or in-phase/opposed phase sequences which demonstrate chemical shift artifact (Fig. 10.17). Occasional fat within the bowel wall may occur in obese individuals [32]. Mural enhancement is a useful imaging feature to predict disease activity. The presence of layered [30, 33] or diffuse transmural enhancement usually suggests active disease, whereas the presence of reduced inhomogeneous enhancement suggests quiescent disease. The combination of bowel wall thickness greater than 4 mm and a ratio of greater than 1.3:1 between bowel wall enhancement and enhancement of normal bowel may be predictive of active disease [34]. Fibrotic strictures lead to apparent dilatation of the opposing bowel wall, especially along the antimesenteric border resulting in the formation of pseudosacculations, and dilatation of the bowel segment proximal to the fibrotic stricture.

Extraenteric disease includes the presence of mesenteric edema, vascular engorgement, fat proliferation, mesenteric nodes, fistulae and sinuses, abscesses, and coexistent colonic abnormalities. Mesenteric edema is present in some cases with advanced active disease and is usually associated with bowel wall hyperemia and enhancement. Mesenteric vascular engorgement is called the comb sign as described above, and it appears as low-signal-intensity parallel lines on gradient echo images or high-signal-intensity enhancing parallel lines on post-contrast T1-w fat-suppressed images, oriented perpendicular to the longitudinal axis of the affected bowel wall. Fat wrapping is a pathognomonic sign of long-standing quiescent Crohn’s disease and represents asymmetric increased fat proliferation along the mesenteric border causing mass effect. Enhancing nodes typically lie along the vascular supply of an affected disease. Deep transmural ulcers may lead to the formation of enterocutaneous (Fig. 10.18), entero-enteric (Fig. 10.19), or enterovesical (Fig. 10.20) fistulae, which appear as enhancing high-signal-intensity tracts. These fistulous or sinus tracts may be associated with abscesses (Fig. 10.21) or loculated peritoneal collections (Fig. 10.22). Lastly, coexistent colonic abnormalities may be seen, which tend to mimic the small bowel findings. Additional findings include sacroiliitis or renal calculi.

Note that though the contents of the collection demonstrate attenuation similar to enteric contrast, the lack of communication with bowel and caliber discrepancy confirms its extraluminal location.

Ulcerative colitis predominantly involves the large bowel leading to proctocolitis (Fig. 10.23); however, the terminal ileum may be involved, which is termed as backwash ileitis. The pattern of involvement is typically continuous without evidence of skip lesions (Algorithm 10.14). Mural thickening is the specific feature. Pneumatosis and perforation may occur. In addition, rectal strictures, presacral fat accumulation, and rectal carcinoma [35] may also be identified. Colonoscopy is the primary diagnostic method for investigating ulcerative colitis [36]. Capsule endoscopy is useful to evaluate mucosal abnormalities of the small bowel, including pseudopolyp formations. CT enterography is primarily used to exclude small bowel involvement. MR enterography may provide information in cases in which endoscopy is inadequate and may depict mucosal abnormalities, wall thickening, mural stratification, and strictures.

Celiac disease is an autoimmune disorder, which represents chronic intolerance to gluten. Celiac disease primarily affects the small bowel mucosa, resulting in progressive villus inflammation and destruction with induction of crypt hyperplasia. The definitive diagnosis of celiac disease requires both duodenal biopsies and a favorable response to gluten-free diet [37, 38]. CTE is useful in demonstrating features indicative or even specific of the diagnosis in patients with celiac disease [39–43]. The key imaging features of celiac disease are listed in Algorithm 10.15.

Common CT enterographic findings include characteristic features of malabsorption pattern involving the small and large bowel – duodenitis, dilution, small bowel dilatation, slow transit, flocculation, small bowel intussusception, villous atrophy, jejunization of the ileum (Fig. 10.24), colonic malabsorption pattern, hyposplenism, adenopathy, and celiac-associated T-cell lymphoma. The various causes of malabsorption are discusses in Algorithm 10.16.

Reversal of jejunoileal fold pattern is typical of celiac disease [39, 40, 44] and is characterized by paucity or loss of jejunal folds and greater number of ileal folds (ileal jejunization). Lymphadenopathy is most marked in the upper small bowel mesentery and is due to follicular hyperplasia caused by proliferation of reactive B and T lymphocytes. Cavitating and low-attenuation nodes with fat-fluid levels have been reported in the advanced stages of the disease [45, 46]. Nodal cavitation is probably due to mesenteric lymphoid depletion and antigenic material crossing abnormal intestinal mucosa [47, 48]. Other features include hypervascular small bowel mesentery, edematous mesentery, and intramural fat in the small and large bowel.

Another diagnostic consideration in patients with diffuse small bowel thickening is graft-versus-host disease. This occurs when the immunocompetent graft reacts to the immune-incompetent host. GVHD of the bowel is frequently seen after bone marrow transplantation. The acute form primarily affects the small bowel. The CT appearance is nonspecific with diffuse mucosal enhancement and bowel wall thickening (Fig. 10.25). Small bowel involvement is more frequent than large bowel involvement. Diffuse involvement of small bowel is more often seen than segmental involvement. Ascites is frequently present. Long-term sequelae include strictures [49].

Radiation enteritis occurs when radiation therapy exceeds 45 Gy with resultant obliterative vasculitis in the intestinal wall and mesentery. The ileum is predominantly affected with changes also in the colorectal bowel. Complications include fistulae and bowel obstruction. In early disease, affected bowel segments show homogeneous wall thickening with progressive luminal narrowing and irregular outer wall contours (Fig. 10.26). The circumferentially thickened hypoattenuating submucosal layer produces a target pattern in the bowel wall. Perirectal and mesenteric fibrotic strands with thickened fascial planes and peritoneal adhesions are seen. In late radiation enteritis, fibrosis leads to minimally enhancing narrowed bowel with varying degrees of proximal dilatation. Perirectal fat proliferation may be present. The affected bowel loops are those involved in the radiation port [50].

Eosinophilic enteritis is an uncommon inflammatory disease characterized by focal or diffuse eosinophilic infiltration of the GI tract, more commonly the stomach and esophagus. An allergic disorder and peripheral eosinophilia are present in most patients. The most common CT abnormality is bowel stenosis and fold thickening. Most patients respond well to steroid therapy. The CT appearance can mimic the inflammatory appearance of Crohn’s disease including bowel wall thickening, luminal narrowing without obstruction, mesenteric lymphadenopathy with peripheral rim-like enhancement and marked necrosis, and possible ascites. CT findings are more characteristic of an inflammatory disease rather than a tumor, and these findings are helpful for assessing the extent and location of the disease and guiding biopsy [51].

Gastrointestinal manifestations of scleroderma can occur in up to 90 % of patients with scleroderma with the commonest site of GI involvement being the esophagus. Smooth muscle atrophy and fibrosis is thought to be the chief underlying mechanism which leads to luminal dilatation, reduced motility, and reduced sphincter tone. Small bowel is affected in more than 60 % of scleroderma patients, the duodenum most frequently involved. Patients may be asymptomatic or may present with bloating or malabsorption due to bacterial overgrowth. The radiographic features include luminal dilatation (can be massive), hidebound bowel sign (crowding of valvulae conniventes – thought to be pathognomonic of scleroderma), accordion sign (well seen evenly spaced mucosal folds in duodenum), and sacculations (focal dilatations or pseudo-diverticula along the antimesenteric border). Differential diagnoses include sprue and small bowel obstruction.

Amyloidosis is defined as the extracellular deposition of protein fibers with a β-sheet fibrillary structure. The gastrointestinal tract is involved in 98 % of cases of systemic amyloidosis, with colonic involvement being most common. Small bowel involvement results in abdominal pain, malabsorption, hemorrhage, and perforation [52].

CT findings are nonspecific and tend to overlap with inflammatory bowel disease. Findings include focal or diffuse bowel wall thickening, thickened mucosal pattern, jejunization of ileum, intramural hemorrhage, bowel dilatation and obstruction, and rarely perforation. Other features include mesenteric infiltration and adenopathy. Occasionally nodular or diffuse omental [53] and peritoneal infiltration [53, 54] is seen, with the nodular deposits representing enlarged nodes and the diffuse form representing infiltration of the omental or retroperitoneal fat. Secondary calcification of the omental deposits is characteristic of amyloidosis [55]. Extraintestinal manifestations include splenomegaly and diffuse hepatic and gallbladder wall infiltration.

Brunner’s glands are mucosal and submucosal glands that secrete mucus, pepsinogen, and urogastrone into the crypts of Lieberkuhn. Majority of these glands are seen proximal to the ampulla of Vater, with gradual reduction in the distal duodenum and few located in the prepyloric region of the stomach. Pathologic changes involving Brunner’s gland range from hyperplasia, hamartoma, and adenoma, with the terms being used interchangeably. Lesions less than 5 mm in size are termed hyperplasia and those greater than 5 mm in size are termed hamartoma [56]. Brunner’s gland hyperplasia is an incidental finding on 2 % of gastroscopies [57]. Typically, these are considered benign entities; however, associated dysplasia or adenocarcinomas have been reported.

On US, Brunner’s glands reveal heterogeneous hyperechogenicity, with hamartomas appearing as heterogeneous lesions having an indistinct margin [58]. Endoscopic ultrasound is useful in detecting submucosal lesions and when biopsies need to be performed. On NECT, these lesions appear iso-attenuating relative to the pancreas. Following administration of contrast, the lesions appear hypoattenuating to the pancreas, surrounded by a peripheral enhancing rim, which represents the duodenal mucosa [59].

Nodular lymphoid hyperplasia is a rare disorder of the small bowel, often reported with immune deficiency disorders. NLH represents hyperplasia of the lymphoid follicles with large germinal centers located within the submucosa or lamina propria and may present either as a localized segmental or diffuse form. The disorder is characterized by the presence of numerous mucosal nodules, usually measuring less than 0.5 cm in diameter. NLH has a potential risk for developing both intestinal and extraintestinal lymphoma [60]. NLH may be associated with Giardia lamblia infection [61], common variable immunodeficiency [62], Familial Adenomatous Polyposis (FAP) [63], Gardner’s syndrome [63], and HIV [64]. CT imaging may show mural thickening, polypoid masses, nodular fold thickening, separated bowel loops, and enlarged retroperitoneal nodes [65].

Tuberculosis may involve any segment of the gastrointestinal tract, with preponderance for the terminal ileum, ileocecal valve, and cecum [66], primarily due to the abundance of lymphoid tissue in this region associated with relative stasis. Intestinal tuberculosis may produce small bowel obstruction [67]. In the early stages, bowel wall thickening with slight luminal narrowing and few regional adenopathy may only be identified. In later stages, the transmural wall thickening produces severe concentric luminal narrowing with or without proximal bowel dilatation, distortion of the ileocecal valve, and enlarged necrotic and non-necrotic locoregional nodal masses (Fig. 10.27). Associated findings include multifocal involvement of the small or large bowel, mesenteric haziness, omental and peritoneal nodules, and coexistent extra-abdominal lesions. In chronic cases or following antituberculous therapy, healing may be associated with the formation of fibrotic strictures and marked distortion of the cecal pole.

Gastrointestinal disorders are among the most frequent presenting complaints in patients with HIV. In HIV patients, multifocal abnormalities are a common occurrence, including the presence of multiple and widely disseminated opportunistic infections, multiple foci of Kaposi’s sarcoma, coexistence of opportunistic infections and tumor, or even multiple coexisting tumors such as lymphoma or Kaposi’s sarcoma. Various forms of small bowel involvement in HIV correlates with CD4 levels (algorithm 10.17).

Common opportunistic infections involving the small bowel include CMV, cryptosporidiosis, MAIC, tuberculosis, and bacillary angiomatosis (Algorithm 10.17).