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.
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
CMV: Often with severe ulcerations, causing mesenteric stranding.
Cryptosporidiosis: Mural thickening and usually nonnecrotic lymphadenopathy.
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.
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.
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).
Mechanical obstruction of the small bowel through intraintestinal impaction of gallstones.
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.
Primary or secondary obstruction of the small intestine.
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.
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.
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.
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.
Diffuse or segmental wall thickening with or without mucosal ulcerations.
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.
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.
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.
Iatrogenic-induced damage to the bowel wall due to therapeutic abdominal irradiation.
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).
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
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.
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.
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).