24 Gastrointestinal Tract


24 Gastrointestinal Tract

Herzog\, Christopher

Together with abdominal magnetic resonance imaging (MRI), computed tomography (CT) has become the chief imaging modality for the assessment of abdominal pain. Whereas MRI has its strengths in organ-based diagnostics, CT is a superb modality for any kind of staging examination.

Multidetector CT scanners allow for subsecond image acquisition and overall scan times < 10 seconds, making motion and breathing artifacts a negligible issue in assessing parenchymatous abdominal organs on CT scans. However, instruction and preparation play an important role in properly displaying the intestine. The stomach and duodenum should therefore be assessed by a pplying the hydro-CT technique, the distal parts of the small intestine by proper a dministration of oral contrast material, and the colon by rectal filling with oral contrast. Optimal opacification of the stomach and small intestine is achieved by slowly and continuously drinking 1500 mL of either a 2% mixture of Gastrografin or a 1% mixture of barium sulfate suspension (contraindication is suspected perforation due to a high risk of barium-induced peritonitis) over a period of 60 minutes prior to the examination. Optimal colonicopacification is achieved by rectal instillation of 300 mL of 2% water-soluble contrast medium. Virtual colonography (see Figs. 24.36 [ p. 763 ] , 24.37 [ p. 763 ] , 24.40 [ p. 764 ]) requires bowel cleansing and stool tagging with oral contrast 24 hours prior to the examination, as well as transrectal insufflation of air or carbon dioxide—depending on availability—immediately prior to the examination. Although the method offers high diagnostic accuracy in experienced hands, its clinical relevance is usually still restricted to assessment of patients in whom conventional colonoscopy is either not possible (see Fig. 24.40 [ p. 764 ]) or not desired.

Intravenous (IV) contrast medium (≥ 300 mg I/mL administered with a flow rate of > 3.5 mL/s) is required for all abdominal scans. Usually scanning during the parenchymal phase (PP; ~70–80 seconds after starting contrast injection) suffices. However, when assessing arterial or portal venous abdominal vessels, higher flow rates (5 mL/s) and proper timing of contrast injection are critical; use of the bolus- triggering technique is therefore highly recommended. The bolus triggering scout may be placed in the aorta at the level of the celiac trunk, and scanning is started either immediately after a mean aortic density of 160 HU is reached (arterial phase [AP]) or with a delay of 10 seconds (portal venous phase [PVP]).

CT may be used to assess the stomach. However, in experienced hands, barium studies still have a higher diagnostic accuracy in identifying relevant pathology and may even be better than endoscopy in detecting scirrhous carcinoma. The thickness of the well-distended stomach wall ranges from 2 to 5 mm, as measured at the depth of a rugal fold. Any measurement > 1 cm is considered abnormal. Rugal thickness varies (Figs. 24.1 , 24.2). The gastroesophageal junction often appears as a focal thickening on CT and may be confused with a lesion, particularly if the stomach is not fully distended. Viscous stomach contents may simulate nonexistent wall thickening (Fig. 24.3). Because the diagnostic accuracy of CT in detecting abnormalities of the stomach is rather low, it may be better to use it for adjuvant abdominal staging and assessment of perigastric tissue.

The small bowel and its mesentery typically lie in the central abdominal cavity and may be found on CT scans between the level of the renal hilum and the aortic bifurcation. The wall of normally distended contrast-filled small bowel loops measures < 3 mm in thickness. Jejunal and ileal folds may be visible but usually measure at most 2 to 3 mm in thickness (Fig. 24.4). Healthy bowel loops usually show a well-defined, homogeneous, hyperattenuating wall on postcontrast scans and no visible locoregional lymph nodes or stranding of surrounding mesenteric fat. The latter is always suspicious of an inflammatory/infectious/neoplastic process. A general thickening of small bowel folds may be due to hypoproteinemia, radiation enteritis, ischemia, or an adjacent inflammatory process and thus be nonspecific. However, infectious diseases, such as tuberculosis, cryptosporidiosis, and cytomegalovirus infections, may also cause thickening of small intestine and colonic mucosa. These diseases particularly occur in immunocompromised patients.

The wall of normally distended colon measures < 3 mm in thickness (Fig. 24.5). Any wall thickness > 4 mm is considered suspicious. A wall thickness > 6 mm is definitely not normal. The colon is sharply outlined by surrounding pericolonic fat; thus, stranding of pericolonic fat is indicative of a pathologic process. Local mural thickening may be caused by surgical anastomosis, but apart from this is always highly suspicious of a malignancy.

Fig. 24.1 Rugal folds. Normal-sized rugal folds in the contrast-filled stomach (arrows) of a patient with a biliary obstruction.
Fig. 24.2 Rugal folds. Well-distended stomach with flattening of the rugal folds.
Fig. 24.3 Liver transplant patient with periportal edema. Viscous contents of the stomach create a false-positive thickened stomach wall (SW). Note the streaks of contrast media slowly penetrating into the viscous contents (arrow).

The jejunum, ileum, cecum, transverse colon, and sigmoid are intraperitoneal structures; the distal duodenum and ascending and descending colon lie in the retroperitoneal space (Fig. 24.5). The ascending colon is located in the far right lateral abdomen, reaching from the cecum up to the right hepatic flexure just below the liver. The descending colon lies in the far left lateral abdomen and stretches from the splenic flexure to the pelvic brim. It is usually collapsed. The position and length of the transverse colon and sigmoid vary, depending on the extent of the mesocolon and sigmoid mesentery, respectively. Thus, a diverticulitis in the presence of an elongated sigmoid may project the maximum pain into the right lower abdomen. Anterior and lateral surfaces of the proximal rectum are covered by peritoneum, whereas the distal rectum is completely extraperitoneal.

Fig. 24.4 Small bowel folds. Normal small bowel folds (arrows) as visualized after administration of water-soluble contrast material. Note the absence of folds in the colon (arrowhead).
Fig. 24.5 Topographic relations of the colon in the upper a bdomen. Contrast medium in the ascitic fluid eases the retroperitoneal location of the ascending (AC) and descending (DC) colon. The ascending colon is distended with gas, and its wall appears very thin. The descending colon is collapsed—which is common—and therefore has a thicker wall. The transverse colon (TC) floats behind the a nterior abdominal wall and contains gas.

Congenital malrotation of the bowel usually is an incidental finding and may include transposition of the superior mesenteric artery.

A malrotated distal duodenum is usually found in the right abdomen, with the cecum and large bowel lying in the left abdomen.

A retrogastric colon is observed in 0.2% of patients: in these patients, the transverse colon and splenic flexure are positioned posterior to the stomach (types I and II), and sometimes posterior to the spleen and anterior to the pancreas (type III). A lthough it is usually an isolated finding, this anomaly may be associated with small bowel malrotation.

Interposition of the colon between the right hemidiaphragm and the liver may take place anteriorly or posteriorly but is of no pathologic significance. Anterior colonic interposition is common in patients treated with neuroleptic medication and may be confused with pneumoperitoneum. Chilaiditi syndrome describes a symptomatic clinical presentation with abdominal pain that worsens during deep inspiration (Fig. 24.6). Posterior colonic interposition is usually associated with right renal agenesis, ectopia, or nephrectomy.

Fig. 24.6 Chilaiditi syndrome. Anterior interposition of the right transverse colon between the right hemidiaphragm and the liver in a patient with recurrent inspiratory pain (Chilaiditi syndrome).

Mobile portions of the bowel are more often injured than retroperitoneally located portions. CT is usually performed to assess the intra-abdominal extent of injury. Findings may include bowel wall hematoma, laceration, perforation, and herniation. Pneumoperitoneum, pneumoretroperitoneum, and pneumomediastinum may be concomitant after perforation of the colon. Small gas collections may be missed on soft tissue CT images; thus, additional provision of lung window CT images is highly recommended in patients with acute abdominal pain. Free intra- abdominal or intrapelvic fluid may be the only sign of bowel perforation. Hematoma and laceration of the bowel walls a ppear as focal mural thickening and edema. Rupture of the diaphragm may result in bowel herniation into the thoracic cavity. It is better seen on the left side, as the diaphragm is concealed by the liver on the right side.

Differential diagnoses of gastrointestinal abnormalities are discussed in Tables 24.1 , 24.2 , and 24.3 .

Table 24.1 Abnormal stomach


CT Findings



Gastric varices

Pathologic enlargement of intramural and/or submucous gastric veins.

Diagnostic pearls: Well-defined clusters of round or tubular structures running along the circumference of the gastric fundus/posteromedial gastric wall that enhance with contrast and are inseparable from the wall (see Fig. 16.4 , p. 594).

Reopening of venous collaterals typically in the wake of splenic vein thrombosis or portal hypertension. Retroperitoneal and umbilical varices are optimally visualized on CT scans.

Peripancreatic varices and cavernous transformation of the splenic vein are equally well visualized by angiography.



Multifactorial inflammation of the gastric mucosa.

Diagnostic pearls: Three-layered appearance of gastric wall—hyperattenuating mucosa and serosa, as well as hypoattenuating submucosa; also, partly thickened hyperdense gastric folds.

Atrophic gastritis: Tubular stomach with thin, smooth mucosa.

Erosive gastritis: Areas of edematous/ulcerated mucosa.

Multifactorial etiology: Drugs, radiation, stress, lymphoma, caustic ingestion, infectious (H elicobacter pylori, human immunodeficiency virus [HIV], tuberculosis [TB]; Crohn disease).

Emphysematous gastritis

Fig. 24.7

Gastritis with concomitant intramural gas collections.

Diagnostic pearls: Thickened gastric wall with streaklike or mottled intramural gas bubbles associated with large amounts of secretions and debris.

Particularly due to infections with Escherichia coli, Clostridium perfringens, and Staphylococcus aureus. Poor prognosis (up to 80% mortality).

Use water-soluble contrast media to avoid perforation-associated peritoneal complications.

Gastric ulcer

Craterlike mucosal lesion of the stomach.

Diagnostic pearls: Rarely visualized as irregularity or contrast medium collection protruding into the gastric wall.

Usually hyperattenuation of gastric wall.

CT helps to rule out perforation: Stranding of perigastric fat with or without free air in lesser sac/abdomen.

Difficult to distinguish malignant (more often on the greater curvature) from benign gastric ulcers (typically on lesser curvature and posterior wall). Use water-soluble contrast media (risk of perforation). Double-contrast barium fluoroscopy is imaging modality of choice. H. pylori irradiation and H2-receptor antagonists are therapies of choice. Consider surgery only in case of recurrence or complications.

Ménétrier disease

Fig. 24.8a, b

Hyperplastic gastropathy characterized by prominent rugae along the greater curvature and sparing of the antrum.

Scan recommendation:

Biphasic CT (nonenhanced CT, parenchymal phase [PP]).

Nonenhanced CT: Markedly thickened gastric folds.

PP: Three-layered appearance of stomach fold with submucous edema and high-attenuation mucosa and serosa.

Diagnostic pearls: Elongation and thickening of the rugal folds are seen in the presence of otherwise normal gastric wall.

Condition characterized by hyperrugosity, mucosal hypertrophy, and hyposecretion of acid. Rarely seen on CT scans. Fluoroscopy is imaging modality of choice.

Medical therapy (anticholinergic antibiotics) is preferable and thus done prior to surgery (gastrectomy with or without vagotomy).

CT is not an indication in this disease, but may still present with typical features.

Zollinger–Ellison syndrome

Severe peptic ulcer disease due to pancreatic gastrinoma.

Scan recommendation:

Triphasic CT (nonenhanced CT, arterial phase [AP], portal venous phase [PVP]).

Nonenhanced CT: Thickened gastric walls, hypodense (liver) metastases.

AP: Hyperattenuation of primary lesion with or without metastases.

PVP: Hyperattenuation of gastric folds (gastritis), vessel invasions, general overview of abdomen.

Diagnostic pearls: Thickened rugal folds, normal gastric wall thickness, multiple peptic ulcers, liver metastases, and hypervascular pancreatic mass.

Pancreatic gastrinomas are non-beta-cell islet cell tumors of the pancreas causing overproduction of gastric acid secretion and in the wake of it severe ulcerations in the upper gastrointestinal (GI) tract. CT is particularly helpful to detect perforation. Treatment of choice is medical therapy with H1/H2-receptor antagonist.

Surgery is useful to remove the primary tumor, as well as stomach or liver metastases.


Fig. 22.10 , p. 725

Thickening of the inferior gastric wall associated with signs of acute pancreatitis.

Common cause of gastric wall thickening. Rarely a ssociated with a pseudocyst of the gastric wall.


Gastric duplication

Rounded left upper quadrant cystic mass adjacent to the stomach.

Diagnostic pearls: Cystic lesions attached to the greater curvature but without communication to the stomach. May show calcifications.

Rare malformation of the GI tract, usually presenting as gastric outlet obstruction. Distinction from pancreatic, omental, splenic, or mesenteric cyst may not be possible.

Gastric diverticulum

A sac opening from the stomach.

Diagnostic pearls: A thin-walled, cystic-appearing mass lying adjacent to the fascia of Gerota and the left adrenal gland.

Typically congenital but may also be acquired. Can be confused with an adrenal mass, pancreatic cyst, renal cyst, duplication cyst, or bowel diverticulum. Rare complications are ulceration, malignant transformation, and bleeding. Usually no treatment is necessary.


Hiatal hernia

Fig. 24.9a–f

Protrusion of (part) of the stomach through the esophageal hiatus of the diaphragm.

Diagnostic pearls: Axial hernias often resemble esophageal masses. A second contrast-filled lumen lateral to the distal esophagus is always conspicuous for paraesophageal hernia. Best visualized on coronal reformations.

Rule out other cystic mediastinal masses.

Differentiation between axial (sliding) hernias and paraesophageal hernias. In axial hernias, the gastroesophageal (GE) junction and the cardia are displaced intrathoracically. In paraesophageal hernias, the fundus with or without the GE junction is displaced intrathoracically. A complete intrathoracic herniation of the entire stomach is called upside-down stomach.

Benign neoplasms

Eosinophilic granuloma

Gastric wall thickening in the wake of an eosinophilic gastritis, which can simulate malignancy.

Diagnostic pearls: Thickened gastric folds in the body of the stomach with antral rigidity and stenosis.

Local gastric wall thickening simulating malignancy may also be caused by syphilis, pseudolymphoma, TB, Crohn disease, and radiation.

In patients with acquired immunodeficiency syndrome (AIDS), similar changes may be caused by cytomegalovirus (CMV) or cryptosporidiosis infection.

Adenomatous polyp

Pedunculated mass projecting into the gastric lumen.

Diagnostic pearls: Oval or round mass protruding into the gastric lumen and thickening of the adjacent gastric wall.

The most common benign neoplasm of the stomach. Differential diagnoses include lipoma; leiomyoma; neurogenic, fibrous, vascular, glomus, or granular cell tumor; myoblastoma; and hemangiopericytoma.

Benign intramural gastric tumors

Fig. 24.10a, b

Homogeneous, well-defined submucosal masses with smooth surface.

Diagnostic pearls: Fatty tissue between tumor and adjacent organs is preserved.

Lipomas usually are hypoattenuating (−60 to −130 HU); leiomyomas are strong enhancing, may show intratumoral calcifications and ulcerations within the inner margin; neurofibromas and schwannomas typically occur as multilocular nodular lesions.

Benign gastric tumors of different histologic origin, usually leiomyomas, lipomas, neurofibromas, schwannomas, hemangiomas, or lymphangiomas. Typically located in the antrum and body of the stomach. Differentiation from malignant gastric tumors usually not possible on CT scans.

Barium contrast fluoroscopy is the imaging method of choice.

Ectopic pancreas

Diagnostic pearls: Smooth submucosal mass with central umbilication, most commonly on the greater curvature of the distal antrum close to the pylorus.

Central umbilication represents the orifice of the aberrant pancreatic duct rather than ulceration.

Malignant neoplasms

Gastric carcinoma

Fig. 24.11a–d

Mucosal tumor of the stomach, either locally infiltrating polypoid or diffuse infiltrating circumferential mass.

Diagnostic pearls: Focal mucosal thickening with or without ulceration. Stranding of perigastric fatty tissue is indicative of extragastric growth.

Scirrhous carcinomas typically induce distinct global thickening of the whole stomach.

Mucinous carcinomas appear hypoattenuating (mucin) as compared with normal gastric wall with presence of intratumoral calcifications.

Histologically, papillary, tubular, or mucinous a denocarcinoma, “signet ring” cell carcinoma. Carcinoma in situ without infiltration of the lamina propria; early carcinoma restricted to mucosa and submucosa; advanced carcinoma with infiltration of the muscularis propria and serosa.

CT staging:

Stage I: Intraluminal mass without gastric wall thickening

Stage II: Intraluminal mass with wall thickness > 10 mm

Stage III: Extension into adjacent organs and presence of perigastric lymph nodes

Stage IV: Distant metastases

CT less accurate in staging; tendency to under- rather than overstage.


Diagnostic pearls: Large, well-marginated intramural mass with one or more cystic components. Fat and calcification are common.

Rare tumor, mainly seen in children. Usually contains skin appendages, cartilage, bone, and adipose tissue.


Fig. 24.12

Involvement of stomach may be primary or secondary.

Diagnostic pearls: Typically manifests with > 1-cm thickening of a large area of the stomach, if not the entire stomach wall. Wall thickening may ≤ 3 cm. Outer contour of lymphoma usually smooth or lobulated. Surrounding fat planes are preserved. Gastric folds may be thickened but typically are sustained.

Up to 5% of all malignant gastric tumors are lymphomas, either secondary as part of generalized lymphoma or (in 10%) as isolated GI lymphomas. Primary lesions are either high-grade non–Hodgkin (B-cell) or low-grade mucosa-associated lymphoid tissue (MALT) lymphomas.

It is often difficult to distinguish gastric lymphomas from adenocarcinomas or severe peptic gastritis (Ménétrier disease).


Large (usually > 10 cm in diameter), mainly extraluminal mass.

Diagnostic pearls: Central necrosis and calcifications are common.

Early settlement of liver metastases (often with central necrosis).

Leiomyosarcomas make up only 0.5% of gastric neoplasms; 60% of GI leiomyosarcomas occur in the stomach.

Gastrointestinal stromal tumor (GIST)

Fig. 24.13a–c

Well-defined, exophytic gastric mass often with central ulceration.

Diagnostic pearls: May be hypo- or hyperattenuating on postcontrast scans. Calcified in 30% of cases. Metastases occur in the lung, peritoneal cavity, and liver.

Most common mesenchymal tumor of the GI tract; > 60% occur in stomach, followed by small bowel. Surgical resection is treatment of choice.

Chemotherapy (Gleevec) should be considered only in case of metastases.

Prognosis is dependent on completeness of surgical resection (5-y survival 15%–67%).


Most commonly hematogenous spread and direct invasion. Rarely lymphatic spread.

Diagnostic pearls: Hydro-CT is more sensitive for detecting intramural lesions.

Enhancement pattern is similar to primary tumor. Look out for metastases in surrounding organs. Metastases of malignant melanoma typically appear hypodense compared with gastric wall.

Malignant melanoma and lung and breast carcinoma are the most common primary tumors with a hematogenous spread to the stomach. Hepatocellular, pancreas, and colon carcinomas are the predominant primary neoplasms leading to direct invasion of metastases.

Lymphatic spread is mainly through colon and esophageal carcinoma.

It is often difficult to distinguish metastases from primary gastric tumors.

Fig. 24.7 Emphysematous gastritis. The thickened gastric wall is atonic and contains gas (arrows). (Reprinted from Krestin GB. Radiology of the Acute A bdomen. Stuttgart: Thieme; 1994, with permission.)
Fig. 24.8a, b Ménétrier disease. Markedly thickened gastric folds (a) with submucous edema and high-attenuation mucosa and serosa (b).
Fig. 24.9a–f Different types of hiatal hernias. Axial hernia (a) with intrathoracically displaced gastroesophageal (GE) junction and cardia (b). Paraesophageal hernia (c) with intrathoracically displaced fundus and GE junction (d), as well as upside-down stomach (e), with almost complete intrathoracic herniation of the entire stomach (f). Note the double lumen of the paraesophageal hernia as compared with the single lumen of the axial hernia on transverse CT scans.
Fig. 24.10a, b Submucosal gastric leiomyoma. Homogeneous, well-defined, strong enhancing submucosal mass with smooth surface.
Fig. 24.11a-d Adenocarcinoma of the stomach. Adenocarcinoma may present as a subtle intraluminal mass such as in the scan of the posterior wall (a) or as focal circular thickening in the gastric antrum (b). Distinct global thickening of the whole stomach is typical for scirrhous carcinomas (c,d). Note the increased perigastric lymph nodes (a,c).
Fig. 24.12 Primary gastric lymphoma. Smooth, marginated, large submucous lesion of the lesser curvature with central necrosis and marked bulging into the gastric lumen.
Fig. 24.13a–c Gastrointestinal stromal tumor (GIST). Hypodense intragastric mass (a) with metastases to the small intestine and liver (b), showing a hemangioma-like attenuation pattern of liver metastases (c).

Table 24.2 Abnormal small intestine


CT Findings




Fig. 24.14a, b

Insufficient blood supply due to arterial or venous occlusion (ischemic enteritis).

Diagnostic pearls: Lack of mucosal enhancement typical for superior mesenteric artery (SMA) occlusion (clots in SMA?) due to compromised arterial blood flow. “Target” sign appearance of bowel wall (low-attenuating edematous submucosa framed by hyperdense mucosa and serosa) typical for shock bowel (i.e., reperfusion following hypotension). Rarely pneumatosis intestinalis.

Arterial occlusion is predominant cause (90%); venous occlusion accounts for < 10%.

Clinical symptoms are sudden onset of abdominal pain, diarrhea, and vomiting.

Emergency surgery is usually the treatment of choice. Prognosis depends on the speed of treatment and the amount of small bowel affected.

If SMA clot is ruled out, check superior mesenteric vein (SMV) for occlusion (i.e., outflow obstruction), typically accompanied by mesenteric fat stranding.

Pneumatosis intestinalis

Fig. 24.15

Submucosal/subserosal gas collection.

Diagnostic pearls: Beadlike intramural gas with or without portal venous, mesenteric, and biliary gas collections.

May affect colon with or without small bowel. Intraluminal gas with increased intramural pressure or mucosal damage by enteric organism may result in gas permeation into the bowel wall. Etiologic agents are ischemia, bowel disruption, bacterial infection, and autoimmune diseases.


Fig. 24.14a, b

Concomitant inflammation of intramural blood vessels in the wake of systemic diseases.

Diagnostic pearls: Thickened hypoattenuating bowel wall with distinct stranding of mesenteric fat.

In an acute setting, vasculitis is indistinguishable from shock bowel.

Usually affects the entire small intestine. Multifactorial agents: autoimmune diseases, drug-related, infection-triggered, paraneoplastic, and arthritis induced.

Radiation vasculitis is typically confined to the treatment portal.

Usually indistinguishable from ischemic enteritis (check patient history).

Graft versus host reaction

Fig. 24.16

Rare concomitant bowel affliction in patients who have undergone bone marrow transplantation.

Diagnostic pearls: Diffuse, nonspecific mural thickening involving entire intestine from stomach to colon as well as stranding of mesenteric fat and lymphadenopathy.

The most common GI complication after bone marrow transplantation. Clinical symptoms are profuse secretory diarrhea, cramping, and malabsorption caused by immunocompetent T cells of the donor reacting against host tissues.


Crohn disease

Fig. 24.17a, b

Discontinuous, chronic, recurrent transmural inflammation.

Diagnostic pearls: Discontinuous segmental thickening and target appearance of bowel wall seen in the acute phase, with mesenteric stranding, fistulas, abscess formation, and lymphadenopathy.

Also characterized by long-segment narrowing with discontinuous segmental stenosis and homogeneous late enhancement of thickened bowel wall (transmural fibrosis) during delayed phase (DP) CT in chronic stage.

Histologically, lymphoid aggregates, coalescing into noncaseating granulomas.

Typically affects the distal ileum, but skip lesions may be found everywhere in the intestine.

Fistulas may be better seen on precontrast scans (hyperattenuating oral contrast material within the mesentery), but hydro-CT is better at identifying mural contrast attenuation.


Thickened bowel folds associated with distinct stranding of mesenteric fat and poor delineation of segmental mesenteric veins; relative sparing of retroperitoneal fat.

Hypoalbuminemia most often due to cirrhosis, nephrosis, intestinal lymphangiectasia, or SMV thrombosis.

Exclude wall edema due to focal lesions occluding mesenteric veins.

Whipple disease

Bacterial infection leading to malabsorption and chronic diarrhea.

Diagnostic pearls: Micronodular irregularities on thickened folds in the proximal small intestine, distinct submucosal edema, and near-fat-density mesenteric lymph nodes.

Rare disease. Caused by Tropheryma whippelii bacteria. Micronodular irregularities represent bacteria-laden macrophages within the lamina propria. Submucosal edema is due to malabsorption leading to hypoalbuminemia.

Sprue (nontropical or tropical)

Malabsorption due to an intolerance to gluten (nontropical) or observed in inhabitants of tropical countries.

Diagnostic pearls: Distended fluid-filled small bowel loops with prominent folds in the distal jejunum and ileum, as well as mesenteric lymph nodes.

Common cause of malabsorption. Typically diagnosed in children. Second peak between age 20 and 40 y. Fluoroscopy is imaging modality of choice.

CT findings often not typical.

Gluten-free diet (nontropic) and antibiotics are therapies of choice.



Insufficient or nonrotation of the small intestine during embryogenesis.

Diagnostic pearls: Colon located left and small bowel right in the abdominal cavity.

SMV on the left side of SMA.

Often hypoplasia of pancreas/aplasia of uncinate process is seen.

Three grades of malrotation: Reversed rotation, incomplete rotation, and nonrotation.

May cause a volvulus.

Usually diagnosed in children (80% < 1 y). Treatment of choice is surgical repair after Ladd.

Meckel diverticulum

Fig. 24.18a, b

Persistent congenital omphalomesenteric duct forming an ileal diverticulum.

Diagnostic pearls: Blind-ending saccular outpouching usually located 40 to 70 cm proximal of ileocecal valve.

Histologically, incomplete occlusion of ileal a nastomosis of vitelline duct during embryogenesis. Clinical symptoms (if symptomatic) are bleeding, perforation, inflammation, and abscess formation. May contain ectopic gastric or pancreatic tissue.

Duplication cyst

Bowel-like tubular structures that are not connected with the bowel lumen.

Diagnostic pearls: Cystic nonenhancing mass contiguous to a segment of normal small bowel.

Most common in the small bowel and esophagus. Spinal anomalies are often associated.

CT-guided aspiration biopsy and injection of contrast material into the cystic cavity are diagnostic.


Blunt trauma

Fig. 22.9a, b , p. 723

Typically due to seat-belt injuries, but any other abdominal trauma (e.g., falls and assaults) may be causative.

Diagnostic pearls: Extraluminal oral contrast specific for bowel perforation.

A dense mesenterial clot (sentinel clot) indicates a likely location of bleeding. Extraluminal/intra-abdominal gas not specific for bowel perforation (alternative causes may be barotraumas and mechanical ventilation).

Use lung and abdominal window/level settings for image assessment.

Due to its rather fixed position, the duodenum is the most frequently injured segment of small bowel. Retroperitoneal rupture of the duodenum is usually evident on CT but not on plain films.

Very often intramural hematoma is the cause of obstruction.

Gas and fluid in the anterior pararenal space indicate retroperitoneal duodenal rupture.


Fig. 24.19

Locoregional thickening of the small bowel wall and valvulae.

Diagnostic pearls: Hyperattenuating (52–80 HU) solid intramural mass is seen on noncontrast scans.

A partially cystic mass with fluid layers may be observed in cases of anticoagulation-induced bleeding.

Intramural hematoma of the small bowel is most commonly due to blunt abdominal trauma (50%), anticoagulation treatment (10%), pancreatic disease (10%), and collagenosis. Any isodense mural mass is unlikely to be a hematoma. Rule out tumors such as lymphoma, melanoma, or an inflammatory condition.


Tuberculosis (TB) (cytomegalovirus [CMV], cryptosporidiosis)

Thickened mucosal folds and wall particularly affecting the ileocecal region.

Stierlin sign: Narrowing of ileocecal area.

Fleisher sign: Hypertrophy of ileocecal valve.

Diagnostic pearls: Lymphadenopathy with hypoattenuating center (necrosis), nodular omental and mesenteric thickening (typically for miliary TB), high-attenuating ascites, nodules in the liver and spleen, and hepatosplenomegaly.

May result from a secondary reaction of pulmonary TB (miliary TB).

Often also a Mycobacterium avium intracellulare infection in patients with AIDS.

Differential diagnosis:

CMV: Often with severe ulcerations, causing mesenteric stranding.

Cryptosporidiosis: Mural thickening and usually nonnecrotic lymphadenopathy.

Benign neoplasms


Fig. 24.20

Smooth, round intramural lesion with intraluminal protrusion.

Diagnostic pearls: A large, homogeneous, intra- or extraluminal mass.

Low-attenuation center indicative for necrosis; may calcify.

The most common benign neoplasm of the small bowel; 50% > 5 cm in diameter.


Diagnostic pearls: Solitary small, fat-density-like mass located intramurally or intraluminally.

Characteristically changes shape when compressed.


Fig. 24.21a, b

Unopacified small bowel. May simulate a mass.

Diagnostic pearls: Use multiplanar reconstruction (MPR) for further assessment or rescan after additional oral contrast.

Loops of bowel that have altered motility (e.g., following a Whipple or Billroth II procedure) may mimic a pseudotumor of the small bowel. Also, unopacified small bowel diverticula or malrotation of the small bowel may simulate pancreatic, intra-abdominal, or even pelvic masses.

Polyp (adenomatous or hamartomatous)

May be hereditary or nonhereditary, with or without other associated lesions.

Diagnostic pearls: Small, often multiple, intraluminal filling defects. Polyps are more common in the colon. If multiple, polyps usually < 5 mm in diameter.

May be associated with polyposis syndromes including Peutz–Jeghers syndrome, Rendu–Osler–Weber syndrome, Cowden syndrome, Cronkhite-Canada syndrome, Gardner syndrome, and familial polyposis.

Malignant neoplasms


Rare primary neoplasm of the small intestine.

Diagnostic pearls: Annular solid enhancing mass of soft tissue density found on the bowel wall. May be ulcerated.

Often associated with small bowel obstruction or GI bleeding. Most common in the jejunum.


Large, well-defined, strongly enhancing inhomogeneous mass with or without necrosis and calcifications.

Diagnostic pearls: CT-based differentiation between leiomyoma and leiomyosarcoma is not possible (see Fig. 24.20 , p. 751).

Approximately 50% of small bowel smooth muscle tumors are malignant.

The remainder are benign leiomyomas.


Fig. 24.22a, b

Typically malignant neoplasm from B lymphocytes.

Diagnostic pearls: Either diffuse bowel wall thickening or segmental annular mass with ulcerations with or without mesenteric lymphadenopathy.

Most common manifestation of non–Hodgkin lymphoma. Intussusception is frequent.

Neurogenic tumor

Single or multiple, sessile or pedunculated masses of soft tissue density that enhance with contrast and may contain ulcerations.

Associated with neurofibromatosis.

Carcinoid tumor

Neuroendocrine active primary malignant neoplasm of small bowel.

Diagnostic pearls: Mesenteric mass of soft tissue density with spiculated margins; retraction of the bowel loops toward itself is characteristic.

Hepatic or lymph node metastases may be present. Tumors arise from enterochromaffin cells of Kulchitsky.

After liver metastasis, typical clinical signs include flush, diarrhea, and cardia-related symptoms.


Fig. 24.23

Spread may be contiguous, hematogenous, or intraperitoneal.

Diagnostic pearls: Heterogeneous appearance—soft tissue nodules, scirrhous lesions, intramural deposits, or polypoid intraluminal masses.

Greatest portion of metastatic deposits is usually located in the mesentery adjacent to the wall of the small bowel.

Most common primary tumors include carcinomas of the lung, breast, colon, pancreas, kidney, uterus, and skin.

Gastrointestinal stromal tumor (GIST)

Fig. 24.13 , p. 747

Well-defined, exophytic gastric mass often with central ulceration.

Diagnostic pearls: May be hypo- or hyperattenuating on postcontrast scans; calcified in 30% of cases. Metastasizes to the lung, peritoneal cavity, and liver.

Most common mesenchymal tumor of the GI tract; > 60% occur in stomach, followed by small bowel. Surgical resection is treatment of choice.

Consider chemotherapy (Gleevec) only in case of metastases.

Prognosis depends on the completeness of surgical resection (5-y survival 15%–67%).



Fig. 24.24a–c

Twisting of small bowel around its mesenteric axis.

Diagnostic pearls:

“Whirl” sign: Small bowel loops and their mesenteric attachment converge centrally at the point of torsion. Typically, SMV winds around SMA.

“Coffee bean” sign: U-shaped configuration of bowel loops.

Acute onset of abdominal pain. Markedly dilated bowel loops seen on plain abdominal radiographs. May lead to ischemia and necrosis of bowel due to vessel strangulation.

Treatment of choice usually is surgery.


Fig. 24.25a, b

Bowel trapped within bowel.

Diagnostic pearls:

Cockade sign: Three concentric layers forming a soft tissue mass (inner layer representing the lumen of the intussuscepted bowel; the middle layer, mesenteric fat; and the outer layer, the intussuscipiens).

May appear sausagelike if cut longitudinally (use MPR). Also seen: Proximal bowel distention and distal tiny, non-contrast-filled (i.e., “hungry”) bowel loops.

Typically painful, short-segment, palpable intra-abdominal mass; often transient. Equally affects men and women of all age groups.

A typical postoperative complication (disturbed bowel motility and adhesions).

Etiology is often obscure.

Always rule out inflammation, tumors (benign and malignant), and diverticula (Meckel diverticulum).

Gallstone ileus

Mechanical obstruction of the small bowel through intraintestinal impaction of gallstones.

Diagnostic pearls:

Rigler’s triad: Multiple dilated small bowel loops with fluid and gas, a calcified stone in the lower abdomen, and gas in the biliary tree or gallbladder.

Typical complication of chronic cholecystitis. Erosion of gallbladder wall and transmural passage into small intestine.

May also occur after repeated endoscopic retrograde cholangiography (ERCP) or sphincterectomy.

Small bowel obstruction

Fig. 24.26

Primary or secondary obstruction of the small intestine.

Diagnostic pearls:

Simple obstruction: Dilated fluid-filled, thin-walled loops of small intestine with or without air–fluid levels. Closed loop obstruction: Obstruction at two ends. One or several grossly distended, fluid-filled U-shaped loops with two adjacent limbs showing a zone of abrupt transition (i.e., incarceration).

Strangulating obstruction: Slight circumferential wall thickening and enhancement (target sign) and engorgement of mesenteric vessels indicate mild ischemia. Increased bowel wall attenuation, mesenteric hemorrhage, and pneumatosis indicate severe ischemia and infarction.

May be mechanical (i.e., intrinsic or extrinsic) or nonmechanical. Typical extrinsic causes are diverticulitis, appendicitis, hernias, adhesions, and peritoneal carcinomatosis.

Typical intrinsic causes are intraluminal lesions, neoplasms, inflammations (e.g., Crohn disease), and infections.

Nonmechanical bowel obstruction is mainly due to neuromuscular disturbances.

Diverticular disease

Fig. 24.27a, b

Antimesenteric outpouching of small intestine wall.

Diagnostic pearls: Small bowel diverticula, segmental mural thickening, and luminal narrowing in combination with mesenteric stranding are highly suspicious for small bowel diverticulitis.

Locoregional mesenteric gas is indicative of abscess formation.

Free intra-abdominal gas is indicative of free perforation.

Use lung and abdominal window/level settings for assessment.

Rare. May mimic Crohn disease and appendicitis.

Fig. 24.14a, b CT features of small bowel ischemia. Superior mesenteric artery (SMA) occlusion with a clearly visible clot, dilated small bowel loops in the left, and segmental wall thickening in the right a bdominal cavity (a). Wall edema of the small intestine in the ileocecal region with patchy “target sign” appearance. (b). The target appearance is also typical for patients with vasculitis.
Fig. 24.15 Pneumatosis intestinalis. Severe pneumatosis intestinalis presenting with beadlike intramural and biliary gas collections.
Fig. 24.16 Graft versus host reaction. Diffuse nonspecific mural thickening involving the entire intestine from the stomach to the colon. Stranding of mesenteric fat and lymphadenopathy can be seen in the mesenteric root.
Fig. 24.17a, b Crohn disease. Mesenteric stranding, local lymphadenopathy, discontinuous segmental thickening, and target appearance of terminal ileum during the acute phase (a). The cecum is also involved. Long-segment narrowing with discontinuous segmental stenosis in the chronic phase (b).
Fig. 24.18a, b Meckel diverticulum. Well-distended, blind-ending saccular outpouching in the lower right abdomen between the right acetabulum and bladder (arrows).
Fig. 24.19 Duodenal hematoma. Intramural hyperdensity causing widening of the circumference of the duodenum and effacement of the valvulae conniventes in a hemophiliac. (Reprinted from Krestin GB. Radiology of the Acute Abdomen. Stuttgart: Thieme; 1994, with permission.)
Fig. 24.20 Leiomyoma. A smooth, homogeneous, extraluminal mass adhering to the proximal jejunum. Note the homogeneous but discrete contrast enhancement and central necrosis. The leiomyoma is not distinguishable from a leiomyosarcoma.
Fig. 24.21a, b Pseudotumor of the duodenum. Lesion with central necrosis in the horizontal portion of the duodenum on axial scan (a), which proved to be a mucus-filled duodenal diverticulum on multiplanar reconstruction (MPR) (b).
Fig. 24.22a, b CT appearance of small bowel lymphoma. Segmental annular lesion at the level of the navel with mucosal ulceration (central hyperdensity) but without lymphadenopathy (a). Diffuse thickening of the horizontal portion of the duodenum associated with bulky mesenteric and retroperitoneal lymphadenopathy (b).
Fig. 24.23 Metastasis in the small bowel. Small bowel metastasis of pancreas carcinoma (hypodense mural nodule) infiltrating the horizontal portion of the duodenum. Ascites and mesenteric stranding are signs of peritoneal carcinosis.
Fig. 24.24a–c Small bowel dilation. Volvulus with “whirl” sign due to twisting of the small bowel around its mesenteric axis (a). MPR clearly reveals the point of twisting with dilated bowel loops proximally and nondilated bowel loops distally to it (arrow) (b). Another patient showing a typical “coffee bean” sign of dilated small bowel loops (c).
Fig. 24.25 a, b Intussusception of ileal bowel loops. Axial scan shows typical cockade sign in the right lower abdomen (arrow), as well as proximal bowel distention and distal “hungry” bowel loops (a). On MPR, the intussusception appears sausagelike (b). Note the normal-sized, well-opacified distal ileum and colon.
Fig. 24.26 Small bowel obstruction due to transmesenteric postoperative hernia. Dilated small bowel with no overlying omental fat displacing both hepatic flexures inferiorly and posteriorly and the main mesenteric trunk to the right. The right hepatic flexure is stool-filled; the left hepatic flexure contrast, media-filled.
Fig. 24.27a, b Duodenal diverticula in typical location. Antimesenteric outpouching with air/contrast level on axial scan (a) and coronal MPR (b).

Table 24.3 Abnormal colon


CT Findings




Fig. 24.28a–c

Insufficient blood supply due to arterial or venous occlusion.

Diagnostic pearls: Markedly dilated small bowel loops and segmental wall thickening; clots in internal mammary artery and vein; three-layered appearance of bowel on postcontrast scans (target sign): low-attenuating edematous submucosa framed by hyperdense mucosa and serosa (i.e., shock bowel); stranding of mesenteric fat.

Pneumatosis intestinalis and mesenteric or portal venous gas are usually visible earlier on CT than on plain films.

Typical symptoms are acute abdominal pain and rectal bleeding. Precipitating factors include bowel obstruction, vascular thrombosis, and recent surgery. Ischemic colitis is a predominantly left-sided, segmental, or diffuse disease and may mimic pseudomembranous colitis.

Arterial occlusion predominant cause (90%); venous occlusion accounts for < 10%. Prognosis depends on the speed of treatment and the amount of small bowel affected.

Epiploic appendagitis

Fig. 24.29

Acute infarction/inflammation of epiploic appendages.

Diagnostic pearls: Oval to round pericolonic fatty mass with hyperattenuating ring, surrounded by stranding of mesenteric fatty tissue.

Torsion of epiploic appendages leads to thrombosis and thus infarction of small veins.

Important differential diagnosis to diverticulitis and appendicitis. CT pattern is pathognomonic.

Treatment primarily with analgetics. Surgery only required in cases with larger infarctions.



Fig. 24.30a, b

Transmural inflammatory and sometimes necrotizing process.

Diagnostic pearls: Inhomogeneous wall thickening of the cecum and ascending colon; occasionally, spreading to the distal ileum and/or appendix. Pneumatosis and pericolic inflammatory changes are common. Perforation and pericolic abscess formation may occur.

Histologically, an inflammatory process of the mucosa with deep ulcerations and necrosis due to local ischemia. Particularly observed in neutropenic patients, including leukanemia, HIV, chemotherapy, aplastic anemia, bone/organ transplants, and lymphoma.

Treatment of choice is antibiotics/antiinflammatory drugs. In severe cases, surgical resection is needed.

Pseudomembranous colitis

Fig. 24.31a, b

Clostridium difficile–induced acute inflammation of the colonic mucosa with or without submucosa.

Diagnostic pearls: Pancolitis with nodular circumferential wall thickening (≤ 15 mm).

Oral contrast between the thickened folds may create an “accordion” sign. “Targetlike” appearance of colon wall: Hypodense (i.e., edematous) submucosa embedded between hyperintense mucosa and serosa.

Usually most prominent in the ascending and transverse colon.

Usually a complication of antibiotic therapy with copious nonbloody diarrhea, abdominal cramps, and tenderness. Secondary to cytotoxin produced by C. difficile. CMV colitis causes wall thickening of the right colon and the terminal ileum only, without lymphadenopathy, and is usually seen in patients with AIDS.

Infectious colitis

Diffuse or segmental wall thickening with or without mucosal ulcerations.

Diagnostic pearls:



Actinomycosis: Predominantly in the ileocecal and rectosigmoid colon. Cecum may appear shrunken (differential diagnosis: TB) but lack of mass or fistulous tracts.

Actinomycosis: Typically in the wake of appendicitis or after insertion of intrauterine device (IUD).


Amebiasis: Irregular thickening of the colonic wall sometimes masslike. Often skip lesions. Cecum is involved in 90% of cases. Ileum is spared. Campylobacter: Concomitant wall thickening of small intestine and colon.

Amebic colitis: Often cannot be morphologically differentiated from primary adenocarcinoma or paracolic mass in the wake of diverticulitis.


CMV: Nodular wall thickening involving cecum and proximal colon. May also affect the terminal ileum.

E. coli: May primarily affect the transverse colon but often the whole colon.

CMV: Without biopsy, difficult to differentiate from Crohn disease diagnosis.


Herpesvirus/chlamydia/gonorrhea: Typically found in the rectosigmoid colon.

Histoplasmosis: Usually affects ileocecal region.

Salmonellosis/yersiniosis: Predominantly ileum, but may also spread to cecum and right colon.

Schistosomiasis: Multiple polypoid filling defects in the sigmoid colon or rectum. Larger lesions may mimic carcinoma.

Shigellosis: Nodular mucosal thickening affecting mainly the left-sided colon.

Herpesvirus/chlamydia/gonorrhea: Usually sexually transmitted.

Histoplasmosis: May mimic appendicitis.

Salmonellosis/yersiniosis: Both always involve the ileum. Marked thickening of wall and folds.

Schistosomiasis: Filling defects (granulomas) are a late manifestation of heavy infestation and chronic exposure to Schistosoma.


TB: Thick-walled, shrunken cecum, narrowed terminal ileum, and thickened ileocecal valve (Fleischner sign). Worm infestation (Ascaris and Trichuris): Bolus of ascariasis may cause a solitary filling defect. Trichuriasis may induce excessive mucus production and numerous irregular filling defects.

TB: Colonic TB is almost exclusively limited to the cecum. May lead to neoplasmlike colonic stenoses. Worm infestation: Trichuris trichiura is a relatively common inhabitant in the cecum and appendix. Symptomatic infections occur commonly in the tropics and subtropics.


Fig. 24.32a–d

Inflammation and subsequent infection of the appendix due to an acute luminal obstruction.

Diagnostic pearls: Dilated appendix (> 6 mm), hyperattenuation and thickening of appendicular (and sometimes also cecal) wall, and periappendicular fat stranding. Calcification represents a fecalith.

An appendicular abscess appears as a well-demarcated fluid collection in the right lower quadrant of the pelvis.

High diagnostic accuracy (> 97%) for CT as compared with all other diagnostic methods.

Differential diagnoses: diverticulitis and epiploic appendagitis.


Small, flask-shaped, air-containing diverticula in the colonic wall. Usually incidental finding.

Occurs in 6% to 8% of the Western population, increasing with age. Highest incidence in the sigmoid.


Fig. 24.33a–c

Inflammation with or without perforation of saccular outpouchings in the antimesenteric colon wall.

Diagnostic pearls: Diverticula, segmental mural thickening, and luminal narrowing in combination with mesenteric fat stranding are highly suspicious for diverticulitis (stage I/IIA).

Locoregional mesenteric gas points to abscess formation (stage IIB).

Free intra-abdominal gas is indicative of free perforation (stage IIC).

Use lung and abdominal window/level settings for assessment.

Occurs in 10% to 25% of patients with diverticulosis due to obstruction of the diverticular neck and subsequent diverticular distention and perforation.

Staging and management per Hansen and Stock:

Stage 0: Asymptomatic diverticulosis

Stage I: Inflammation restricted to bowel wall (i.e., no wall thickening)

Stage IIA: Phlegmonous

Stage IIB: Abscess-forming

Stage IIC: Free perforated

Stage III: Chronically relapsing

Stages I and IIA are usually managed conservatively, stages IIB and III, surgically.



Fig. 24.34

Focal thickening of the bowel wall.

Diagnostic pearls: Hyperattenuating (52–80 HU) solid intramural mass on noncontrast scans.

A partially cystic mass with fluid layers may be observed in cases of anticoagulation-induced bleeding.

Intra-abdominal or retroperitoneal hemorrhage may be associated.


Pneumoperitoneum or pneumoretroperitoneum.

Diagnostic pearls: Extraluminal oral contrast specific for colon perforation.

Extraluminal/intra-abdominal gas not specific for colon perforation (alternative causes may be barotraumas and mechanical ventilation).

Use lung and abdominal window/level settings for image assessment.


Crohn colitis

Fig. 24.17 , p. 749

Discontinuous chronic recurrent transmural inflammation.

Diagnostic pearls: Thickening of the bowel wall and “sandwich” sign of bowel wall (edematous submucosa between hyperattenuating mucosa and serosa). Abscesses, fistulas, and regional adenopathy may be present.

Terminal ileum involved in 80%, ascending colon in 20% to 55%. Rectum and sigmoid are usually spared. Initial inflammation is confined to the mucosa; thus, barium study and endoscopy are more sensitive for detecting these changes.

Ulcerative colitis

Idiopathic chronic inflammation affecting primarily the colorectal mucosa and submucosa.

Diagnostic pearls: Pancolitis with thickened target-like colonic wall (< 10 mm), luminal narrowing, stranding of pericolonic fat, and fibrofatty perirectal proliferation (presacral space > 2 cm).

Changes may be only subtle and constricted to the rectum.

Extraluminal extension of the disease is uncommon, unlike in Crohn disease.

Chronic inflammation confined to the mucosa and exclusively progressing retrograde and continuous from the rectum to the cecum. Within the first 10 y, the risk of colonic cancer increases by 2% annually. Barium enema and colonoscopy are much more sensitive than CT in the diagnosis of initial inflammation.

Radiation enteritis

Iatrogenic-induced damage to the bowel wall due to therapeutic abdominal irradiation.

Diagnostic pearls:

Acute changes: Nonspecific wall thickening, target sign

Chronic changes: Bowel wall thickening, fibrosis, and luminal narrowing

Perirectal fat proliferation (> 10 mm) with accompanying pararectal fibrosis (halo sign).

Complication after radiation therapy with > 40 to 50 Gy.

Affects ~10% of treated patients.

Radiation enteritis may occur up to 20 y after treatment, radiation colitis within 2 y after radiation. Typically confined to the rectum (pelvic irradiation is very common).

Graft versus host reaction

Fig. 24.16 , p. 749

Rare concomitant bowel affection in patients who underwent bone marrow transplantation. Diagnostic pearls: Diffuse nonspecific mural thickening involving the entire intestine from the stomach to the colon, as well as stranding of mesenteric fat and lymphadenopathy.

The most common GI complication after bone marrow transplantation. Clinical symptoms are profuse secretory diarrhea, cramping, and malabsorption caused by immunocompetent T cells of the donor reacting against host tissues.

Colitis cystica profunda

Rectosigmoid wall thickening due to multiple submucosal cysts.

Diagnostic pearls: Multiple, up to 2-cm submucosal low-density cystic lesions in the rectum with or without sigmoid.

Unknown etiology (inflammatory or traumatic).

The cysts are filled with thick mucinous material and lined by a cuboidal flattened epithelium.

Presents clinically with bright rectal bleeding, mucus discharge, and diarrhea.

Commonly associated with solitary ulcer syndrome and rectal prolapse.


Submucosal deposition of fibrils of light-chain immunoglobulins.

Diagnostic pearls: Normal or thickened rectal wall with small hypoattenuating polypoid lesions.

On venous phase images, delayed contrast enhancement may be present.

May be primary or secondary.

Preferentially involves the rectal submucosa, which thus represents a preferred site for diagnostic biopsy (even in the absence of CT findings).

Pneumatosis cystoides coli

Fig. 24.35a, b

Cystic/linear gas collection in submucosal/subserosal layers of the GI tract.

Diagnostic pearls: Intramural gas collection within normal-sized colonic wall.

Findings may be completely missed on soft tissue CT images (lung window is the key).

May be idiopathic, associated with chronic obstructive pulmonary disease, or secondary to surgery or ischemia.

Lack of intravascular or biliary air (liver) indicates idiopathic origin.

Benign neoplasms


Diagnostic pearls: Submucosal mass with fatlike density and smooth margins.

The most common submucosal tumor in the colon. Typically occurs in the cecum and ascending colon.


Diagnostic pearls: Large, strongly enhancing soft tissue mass in the bowel wall that may contain necrosis and ulceration.

Rare in the colon, more common in the upper GI tract.


Diagnostic pearls: Multiple strongly attenuating tumors characteristically located on the mesenteric side of the colon. May show central necrosis.

Associated with neurofibromatosis type 1 (Recklinghausen disease).

Malignant neoplasms

Adenomatous polyp

Fig. 24.36a,b

Sessile or broad-based polypoid mass in the luminal side of the colonic wall.

Diagnostic pearls: Incidental finding on axial CT scans. Polyps usually enhance after contrast.

Apply CT virtual colonoscopy.

Use prone and supine scans (to differentiate from stool).

Adenomatous polyps account for > 50% of all polyps; > 2 cm considered malignant.

Multiple polyps may be associated with a polyposis syndrome.

CT colonoscopy allows detection of polyps ≥ 10 mm with > 95% accuracy.

CT colonoscopy requires adequate patient preparation (bowel cleansing, stool tagging, and CO2 insufflation).

Villous adenoma

Adenomatous polyp containing predominantly villous elements.

Diagnostic pearls: Low-attenuating (< 10 HU), irregular polypoid mass, usually located in the rectum or sigmoid colon. May occupy > 50% of the lumen.

Characteristic CT appearance of villous adenomas is based on high mucus content. When using CT to evaluate a suspected villous adenoma, oral and rectal contrast material should not be used.

Giant anorectal condyloma acuminatum

Sexually transmitted wart in the rectoanal region.

Diagnostic pearls: Attenuating infiltrating mass with a cauliflower-like surface appearance and subcutaneous tissue/perirectal fat infiltration.

Associated with human papillomavirus. Also called Buschke–Löwenstein tumor. May show different histologic patterns and even malignant transformation. CT cannot distinguish histologic subtypes.


Neuroendocrine tumors arising from endocrine cells.

Diagnostic pearls: Polypoid soft tissue mass is found in the appendix or right colon, less commonly in the rectum.

Strong enhancement is seen during the arterial phase.

Small appendicular carcinoids are usually benign. Large, broad-based intraluminal tumors in elderly patients suggest a less common malignant carcinoid. Flush symptom occurs after hepatic spread.


Fig. 24.37a–c

Fig. 24.38 , p. 764

Segmental wall thickening and luminal narrowing.

Diagnostic pearls: Intraluminal or intramural mass, often no or only distinct attenuation; extracolonic growth, necrosis, and perforation. Stranding of pericolonic fat indicates transmural growth. Low-attenuation and subtle calcifications are typical for mucinous adenocarcinoma.

Adenocarcinomas represent 95% of all colon cancers. Histologic subtypes are mucinous (signet ring cells), mucin-producing, and colloid.

Most common tumor of the GI tract.

Lymphatic spread and size of lymph nodes do not correlate.

Modified Dukes staging:

Stage A (T1N0M0): Restricted to (sub) mucosa

Stage B (T2or3N0M0): Limited to serosa/pericolonic tissue

Stage C (T2or3N1M0): Lymphatic spread

Stage D (any T, any N, M1): Distant metastases

Metastatic disease

Fig. 24.38 , p. 764

Segmental or multifocal wall thickening with or without luminal narrowing.

Diagnostic pearls: Features usually are indistinguishable from those of primary colonic cancer.

Primary tumors of the uterus, ovary, prostate, bladder, pancreas, kidney, and stomach may directly invade nearby colonic segments or induce distant seeding through ascites.


Fig. 24.39 , p. 764

Fig. 24.40a, b , p. 764

Segmental wall thickening with mucosal ulcerations.

Diagnostic pearls: Most common in the cecum. Associated with massive mesenteric/retroperitoneal lymphadenopathy.

Rare; represents only 1.5% of all abdominal lymphoma. Usually non–Hodgkin lymphoma.


Mechanical bowel obstruction

Primary or secondary obstruction of the small intestine.

Diagnostic pearls:

Simple obstruction: Dilated fluid-filled, thin-walled loops of small intestine with or without air–fluid levels.

Closed loop obstruction: Obstruction at two ends. One or several grossly distended fluid-filled U-shaped loops with two adjacent limbs showing a zone of abrupt transition (i.e., incarceration).

Strangulating obstruction: Slight circumferential wall thickening and enhancement (target sign), as well as engorgement of mesenteric vessels, indicate mild ischemia.

Causes may be intrinsic or extrinsic. Typical extrinsic causes are diverticulitis, appendicitis, hernias, adhesions, and peritoneal carcinomatosis.

Typical intrinsic causes are intraluminal lesions, neoplasms, inflammations, and infections.

Colonic pseudo-obstruction

Dilated colonic loops containing gas, stool, and possibly contrast medium.

Diagnostic pearls: Often concomitant dilation of small bowel loops.

CT findings in general are nonspecific.

Pseudo-obstruction may be induced by ischemia, inflammation (toxic megacolon), impaired neuromuscular function (diabetic neuropathy, uremia, and hypokalemia), postoperative paralytic ileus, and iatrogenic causes (vagotomy and irradiation).

Fig. 24.28a–c CT findings in ischemic colon. Dilation of the descending colon and segmental wall thickening with “target” sign (a). Restriction of changes to the left-sided colon is indicative of ischemic origin (b). Pneumatosis intestinalis (arrow) in another patient is particularly visible when using lung window CT scans (c).
Fig. 24.29 Epiploic appendagitis. Oval to round pericolonic fatty mass (arrow) in the left lower abdomen with hyperattenuating ring, surrounded by stranding of mesenteric fatty tissue.
Fig. 24.30a, b Typhlitis. Marked wall thickening of the cecum and ascending colon (a). Axial scan shows no involvement of descending and transverse colon (b).
Fig. 24.31a, b Pseudomembranous colitis. Pancolitis with nodular circumferential wall thickening (“accordion” sign) (a) and targetlike appearance of colonic wall (b).
Fig. 24.32a–d CT appearance of appendicitis. Simple appendicitis with discrete periappendicular fat stranding (a). Clearly visible fecalith within normal appendix (arrow) (b). Acute periappendicular inflammation and exudation (c). Appendicular abscess with central air bubble (arrow) (d).
Fig. 24.33a–c Equivalent CT findings to diverticulitis grading according to Hansen and Stock. Stage I usually not visible. Stage IIA, or phlegmonous (a). Stage IIB, or abscess-forming (b). Stage IIC, or free perforated with presence of free air within perisigmoid fat (c).
Fig. 24.34 Colonic wall hematoma. Colonic wall hematoma due to anticoagulation therapy appears as partially cystic submucous mass with fluid layers (arrow).
Fig. 24.35a, b Idiopathic pneumatosis cystoides coli. Soft tissue MPR shows normal-looking distended colon loops (a) and thus completely misses marked submucosal gas collection within the entire left colon (b).
Fig. 24.36a–c Adenomatous polyps. CT appearance of a sessile polyp (arrow) in the distal part of the descending colon (virtual colonography [a] and MPR [b]) as well as of a broad based polyp (arrow) in the ascending colon (virtual colonography [c]).
Fig. 24.37a–c Sigmoid adenocarcinoma. Luminal narrowing and wall thickening on MPR would correspond to Dukes A classification (a). However, perisigmoidal fat stranding on axial scan indicates stadium Dukes B (b), but local lymphadenopathy led to a final stage Dukes C. Note significant luminal narrowing in virtual colonography (c).
Fig. 24.38 Rectal adenocarcinoma. The tumor is limited to the serosa, and there is no evidence of local lymphadenopathy, thus corresponding to a stage Dukes B or T2N0M0.
Fig. 24.39 Metastatic disease. Segmental wall thickening and luminal narrowing in the descending colon due to a metastasis from adenocarcinoma of the pancreas head, which is also visible.
Fig. 24.40a, b Primary colonic lymphoma. Segmental wall thickening lateral in the ascending colon (a). Incidental finding during preoperative virtual colonography (b) in a patient with a nonpassable sigmoid cancer (same patient as in Fig. 24.37).

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Jul 6, 2020 | Posted by in GENERAL RADIOLOGY | Comments Off on 24 Gastrointestinal Tract

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