Gastrointestinal System

Congenital Type

Congenital tracheoesophageal (TE) fistulas result from the failure of a satisfactory esophageal lumen to develop completely separate from the trachea. The lack of the development of the esophageal lumen resulting in a blind pouch describes congenital esophageal atresia. Esophageal atresia and TE fistulas are often associated with other congenital malformations involving the skeleton, cardiovascular system, and GI tract.

Acquired Type

About 50% of acquired fistulas between the trachea and esophagus are caused by malignancy in the mediastinum. Almost all the rest result from infectious processes or trauma.

Fistulization between the esophagus and the respiratory tract is a major late complication of esophageal carcinoma and is often a terminal event (Figure 5-6). A fistula can also be a complication of erosion into the esophagus either by carcinoma of the lung arising near or metastasizing to the middle mediastinum or by mediastinal metastases from other primary sites. Regardless of therapy, the overall prognosis of malignant TE fistulas is dismal, and more than 80% of patients with this complication die within 3 months from uncontrollable hemorrhage or from pulmonary infection caused by repeated episodes of aspiration pneumonia.

Fistulous communications between the esophagus and the tracheobronchial tree can be the result of esophageal instrumentation and perforation (Figure 5-7). It is most common after esophagoscopy but may also occur after instrumental dilation of strictures by bougienage, pneumatic dilation of the esophagus for the treatment of achalasia, or even the insertion of a nasogastric tube. Blunt or penetrating trauma to the chest, especially after crush injury, can result in esophageal perforation and fistulization.

Reflux (Gastroesophageal Reflux Disease)

Although the reflux of gastric acid contents is the most common cause of acute esophagitis, infectious and granulomatous disorders, physical injury (caustic agents, radiation injury), and medication may produce a similar

inflammatory response. Gastroesophageal reflux disease (GERD) describes any symptomatic condition or structural changes caused by reflux of the stomach contents into the esophagus. Alcohol, chocolate, caffeine, and fatty foods tend to decrease the pressure of the esophageal sphincter, allowing reflux to occur. Regardless of the cause, acute esophagitis produces burning chest pain that may simulate the pain of heart disease. Superficial ulcerations are most typical of reflux. The esophagus is often dilated, with a loss of effective peristalsis. Nonpropulsive peristaltic waves, ranging from mild tertiary contractions to severe segmental spasms, are an early finding.

Reflux esophagitis develops when the lower esophageal sphincter fails to act as an effective barrier to the entry of gastric acid contents into the distal esophagus. Although there is a higher-than-normal likelihood of gastroesophageal reflux in patients with sliding hiatal hernias, reflux esophagitis can be endoscopically demonstrated in only about one fourth of these patients. On the other hand, esophagitis is often encountered in patients in whom no hiatal hernia can be demonstrated.

Several radiographic approaches have been suggested for the demonstration of gastroesophageal reflux. One procedure is to increase intraabdominal pressure by straight-leg raising or manual pressure on the abdomen, often with Valsalva maneuver (forced expiration with the glottis closed). Having the patient turn from prone to supine or vice versa may demonstrate reflux of barium from the stomach into the esophagus. It must be remembered, however, that the failure to demonstrate reflux radiographically does not exclude the possibility that a patient’s esophagitis is related to reflux. As long as typical radiographic findings of reflux esophagitis are noted, there is little reason to persist in strenuous efforts to actually demonstrate retrograde flow of barium from the stomach into the esophagus.

Barrett’s Esophagus

Barrett’s esophagus is a condition related to severe reflux esophagitis in which the normal squamous lining of the lower esophagus is destroyed and replaced by columnar epithelium similar to that of the stomach. Ulceration in Barrett’s esophagus typically occurs at the squamocolumnar junction (Z-line). In addition to exhibiting postinflammatory stricture, Barrett’s esophagus has an unusually high propensity for development of malignancy in the columnar cell–lined portion. These tumors are almost always adenocarcinomas, which are otherwise very rare in the esophagus (accounting for about 5% of esophageal cancers).

Candida and Herpesvirus

Candida (fungal) and herpesvirus are the organisms most often responsible for infectious esophagitis, which usually occurs in patients with widespread malignancy who are receiving radiation therapy, chemotherapy, corticosteroids, or other immunosuppressive agents. It also can develop in patients with acquired immunodeficiency syndrome (AIDS) and even in otherwise healthy adults who have received antibiotics (especially tetracycline) for upper respiratory infection.

Treatment for Esophagitis

Modifications to lifestyle, including weight loss, changes in diet to prevent decreased esophageal sphincter control, and medications to reduce acidity, are the first line of treatment. One technique, called proton pump inhibitor therapy (using esomeprazole), can help control progression in reflux disease and Barrett’s esophagus. Other techniques used are photodynamic therapy and thermal ablation to destroy the Barrett’s tissue. If these therapies do not work, surgical fundoplication (tucks in the stomach fundus and distal esophagus) is an option. Infectious esophagitis caused by Candida or herpesvirus may require a regimen of antifungal or antiviral drugs to eradicate the cause.

Radiographic Appearance

The earliest radiographic evidence of infiltrating carcinoma of the esophagus appears on a double-contrast barium swallow image as a flat, plaquelike lesion, occasionally with central ulceration, that involves one wall of the esophagus (Figure 5-15). At this stage, there may be minimal reduction in the caliber of the lumen. Unless the patient is carefully examined in various positions, this earliest form of esophageal carcinoma can be missed. As the infiltrating cancer progresses, irregularity of the wall is seen, indicating mucosal destruction. Advanced lesions encircle the lumen completely, causing annular constrictions with overhanging margins and often some degree of obstruction. The lumen through the stenotic area is irregular, and mucosal folds are absent or severely ulcerated (Figure 5-16). Less commonly, carcinoma of the esophagus can appear as a localized polypoid mass, often with deep ulceration and a fungating appearance.

Luminal obstruction as a result of carcinoma causes proximal dilation of the esophagus and may result in aspiration pneumonia. Extension of the tumor to adjacent mediastinal structures may lead to fistula formation, especially between the esophagus and the respiratory tract (see Figure 5-20).

Wall thickening greater than 3 to 5 mm on a CT scan is suggestive of esophageal cancer. CT has become a major method of staging patients with esophageal carcinoma (with 90% accuracy), providing information on tumor size, extension, and resectability that was previously available only at thoracotomy (Figure 5-17). Evidence of tumor spread includes the obliteration of fat planes between the esophagus and adjacent structures (left atrium, aorta), the formation of a fistula to the tracheobronchial tree, and recognition of metastatic disease (e.g., low-density masses in the liver, enlargement of draining lymph nodes). Use of contrast enhancement improves the detail of tumor delineation.

Treatment

If the cancerous lesion has not extended into surrounding tissue, surgical resection may result in cure. When the cancerous lesion involves surrounding tissue, treatment becomes palliative surgery together with radiation therapy or chemotherapy. If the esophagus is severely narrowed, a technique known as bougienage can be employed; this is the introduction of a long instrument to dilate and help maintain an adequate lumen. Laser therapy aids in treating the dysphagia in patients with unresectable lesions. A newer technique, photodynamic therapy using laser-activated chemicals, is a method of destroying tumor tissue. The prognosis of the patient who is diagnosed in the late stages of esophageal cancer is extremely poor.

Radiographic Appearance

Zenker’s diverticula arise from the posterior wall of the upper (cervical) esophagus (Figure 5-18). Occasionally, they can become so large that they almost occlude the esophageal lumen. CT prominently demonstrates the cricopharyngeal muscle, which aids in locating the origin of Zenker’s diverticula at the pharyngoesophageal junction. Diverticula of the thoracic portion of the esophagus are primarily found opposite the bifurcation of the trachea, in the region of the hilum of the lung (Figure 5-19). These traction diverticula reflect motor function disturbance and develop in response to the pull of fibrous adhesions after infection of the mediastinal lymph nodes. Epiphrenic diverticula arise in the distal 10 cm of the esophagus (Figure 5-20). They are associated with incoordination of esophageal peristalsis and sphincter relaxation, which increases the intraluminal pressure in this segment.

Treatment

Diverticula do not require treatment unless they interfere with swallowing. In Zenker’s diverticulum, surgery consists of excision of the diverticulum and correction of any motility issues.

Radiographic Appearance

The characteristic radiographic appearance of esophageal varices is serpiginous (wavy border) thickening of folds, which appear as round or oval filling defects resembling the beads of a rosary (Figure 5-21). Precise technique is required to demonstrate esophageal varices. A double-contrast barium swallow study best demonstrates the serpiginous and wormlike filling defect. Complete filling of the esophagus with barium may obscure varices, and powerful contractions of the esophagus may squeeze blood out of the varices and make them impossible to detect. Upright and recumbent imaging may best demonstrate the varices dilated and empty, respectively.

Varices can be demonstrated with endoscopic ultrasound imaging (ultrasonography) as compressible hypoechoic or cystic masses in the GI tract from the outer to the submucosal layers.

The major complication of esophageal varices is bleeding. Their appearance in patients with cirrhotic liver disease implies significant portal venous hypertension and is an ominous sign, because up to 90% of the deaths from liver disease in patients with cirrhosis occur within 2 years of the diagnosis of varices.

Treatment

Vasoconstrictor drugs to constrict the dilated vessels are commonly used to treat esophageal varices. Active bleeding can be controlled by a technique called balloon tamponade, which creates pressure to stop the bleeding. If bleeding cannot be controlled, surgery is performed to tie off collateral vessels.

Radiographic Appearance

Although the diagnosis of hiatal hernia generally requires a barium study (Figure 5-22), at times a large hiatal hernia may appear on plain chest radiograph as a soft tissue mass in the posterior mediastinum, often containing a prominent air-fluid level (Figure 5-23). The esophagus and stomach are distinguished by their appearance; mucosal folds are linear and parallel in the esophagus, whereas in the stomach the folds appear numerous and thicker without a parallel orientation.

Treatment

In most cases, a hiatal hernia requires no treatment. If surgical intervention is necessary, the hiatus is tightened, and the stomach secured below the diaphragm.

Radiographic Appearance

On plain chest radiographs, the dilated, tortuous esophagus may produce a widened mediastinum (often with an air-fluid level) on the right side adjacent to the cardiac shadow (Figure 5-24). The hallmark of achalasia, seen on barium studies, is a gradually tapered, smooth, conical, 1- to 3-cm narrowing of the distal esophageal segment (rat-tail or beak appearance) (Figure 5-25). On sequential radiographs, especially with the patient upright, only small spurts of barium are seen to pass through the narrowed distal segment to enter the stomach.

Treatment

Medications are given before meals to assist in relaxing the esophageal sphincter. If these do not control the symptoms, endoscopic balloon dilation with a bougienage may be helpful. A last resort is surgery (Heller’s myotomy) to open the sphincter.

Radiographic Appearance

Nonopaque foreign bodies in the esophagus, especially pieces of poorly chewed meat (masticated food bolus), can be demonstrated only after the ingestion of barium (Figure 5-27). Such a foreign body usually becomes impacted in the distal esophagus just above the level of the diaphragm and is often associated with a distal stricture. The intraluminal filling defect usually has an irregular surface and may resemble a completely obstructing carcinoma.

Treatment

Medications are the first line of treatment to relax the esophagus and allow the foreign body to move naturally into the stomach. In some instances, especially for a sharper-pointed object, retrieval of the foreign body using endoscopy may be appropriate. Interventional approaches are attempted before the patient is taken to surgery to remove the obstruction. If the esophageal foreign body causes obstruction for more than 12 hours, there is an increased risk of perforation.

Radiographic Appearance

A perforation that extends throughout the entire esophageal wall can lead to free air in the mediastinum or periesophageal soft tissues. The administration of radiopaque contrast material may demonstrate extravasation through the perforation (Figure 5-28) or an intramural dissection channel separated by an intervening lucent line from the normal esophageal lumen. CT is the preferred modality to define the extent of the process.

Treatment

An expandable stent is placed and then the complications are treated (chest tube for pneumothorax; antibiotics to prevent infection). A surgical procedure (band ligation) can be performed to close the perforation.

Radiographic Appearance

Alcoholic gastritis may produce thickening of gastric folds (Figure 5-29), multiple superficial gastric erosions, or both. In corrosive gastritis, the acute inflammatory reaction heals by fibrosis and scarring, which result in severe narrowing of the antrum and may cause gastric outlet obstruction. In bacterial (phlegmonous) gastritis, inflammatory thickening of the gastric wall causes narrowing of the stomach that may mimic gastric cancer. The diagnosis of infectious gastritis can be made if there is evidence of gas bubbles (produced by the bacteria) in the stomach wall (Figure 5-30). These types of gastritis are known as erosive or acute gastritis.

Chronic atrophic gastritis (nonerosive) refers to severe mucosal atrophy (wasting) that causes thinning and a relative absence of mucosal folds, with the fundus or entire stomach having a bald appearance. This is a nonspecific radiographic pattern that can be related to such factors as age, malnutrition, medication, and complications of alcoholism. Chronic atrophic gastritis also occurs in patients with pernicious anemia, who cannot absorb vitamin B₁₂ because of an inability of the stomach to secrete intrinsic factor (or hydrochloric acid).

Treatment

The causative agent in erosive gastritis determines treatment. Eliminating the causative agent, such as alcohol, reduces the changes in the mucosal lining as well as the symptoms because production of the protecting mucus is not inhibited. If overproduction of stomach acid produces the changes, acid-reduction medications are used to help maintain the mucous defense barrier. Antibiotics are the appropriate medication for bacterial or infectious gastritis. Patients with H. pylori gastritis receive a regimen of multiple antibiotics because this infection may be antibiotic resistant. Use of a combination of antibiotics has resulted in an 80% to 90% cure rate.

Pyloric Stenosis

Pyloric stenosis, also known as infantile hypertrophic pyloric stenosis (IHPS), occurs when the two muscular layers of the pylorus become hyperplastic and hypertrophic. Environmental and hereditary factors are believed to cause this process in 2 to 4 per 1000 live births. The gastric antrum and the pyloric canal become lengthened, whereas the mucosa is usually edematous and thickened. This causes a complete or near-complete obstruction, preventing food from entering into the duodenum. The edematous and thickened pylorus may be palpated and is described as a mobile, hard “olive.”

Radiographic Appearance

In today’s imaging arena, ultrasound is the modality of choice due to its high sensitivity and specificity, an accuracy approaching 100%. Pyloric stenosis appears as a thickened pyloric muscle (width greater than 3 mm) and an elongated pyloric canal (greater than 1.2 cm) on the longitudinal sonogram (Figure 5-31). The palpable olive appears as a “doughnut” or “target” sign in the cross-sectional image. When ultrasonographic findings are inconclusive, an upper GI series may aid in confirming the diagnosis by demonstrating the shouldering caused by a filling defect at the antrum as a result of the hypertrophic pyloric sphincter and delayed gastric emptying.

Duodenal Ulcer

Duodenal ulcer is the most common manifestation of peptic ulcer disease. More than 95% of duodenal ulcers occur in the first portion of the duodenum (the duodenal bulb).

Gastric Ulcer

Gastric ulcers, another form of peptic ulcer disease, usually occur on the lesser curvature of the stomach. Unlike duodenal ulcers, which are virtually always benign, up to 5% of gastric ulcers are malignant.

Superficial Gastric Erosions

Superficial gastric erosions are ulcerations that are so small and shallow that they are rarely demonstrated on conventional single-contrast upper GI examinations. With the increasing use of double-contrast techniques, a superficial gastric erosion typically appears radiographically as a tiny fleck of barium, which represents the erosion, surrounded by a radiolucent halo, which represents a mound of edematous mucosa (Figure 5-39). Possible factors implicated in the production of superficial gastric erosions include alcohol, antiinflammatory drugs (aspirin, steroids), Crohn’s disease (see later discussion), and candidiasis (see earlier discussion “Candida and Herpesvirus”).

Treatment of Ulcers

Lifestyle modifications are the first line of treatment for ulcers. First, the patient should avoid foods that cause an increase in the acid secretions (i.e., alcohol and caffeine). Antacids aid in neutralizing stomach acid. If stress is the cause of the increase in acidic secretions, stress management is appropriate. When the ulceration is caused by an infection (H. pylori), antibiotics are given to kill the bacteria. If the acidic secretions cannot be controlled by these methods, histamine H₂ antagonists help in reducing stomach acids and protecting the stomach lining. When more aggressive treatment is required, proton pump inhibitors may be used. Surgical treatment for management of complications may be necessary when ulcers do not respond to other treatments.

Radiographic Appearance

Gastric carcinoma can have a broad spectrum of radiographic appearances. Tumor infiltration of the gastric wall may stimulate intense fibrosis, which produces diffuse thickening, narrowing, and fixation of the stomach wall (a linitis plastica pattern) (Figure 5-40). The stomach is contracted into a tubular structure without normal pliability. This fibrotic process usually begins near the pylorus and progresses slowly upward; the fundus is the area least involved.

Another major form of gastric carcinoma is a large irregular polypoid mass (about one third of cancers). Irregularity and ulceration within the mass are suggestive of malignancy, whereas the presence of a stalk and normal-appearing gastric folds extending to the tumor are sign of benignancy. Ulceration can develop in any gastric carcinoma and occurs in approximately one third. It varies from shallow erosions in relatively superficial mucosal lesions to huge excavations within fungating polypoid masses (Figure 5-41).

CT is of major value in the staging of gastric carcinoma, in planning its treatment, in assessing the response to therapy, and in detecting tumor recurrence (Figure 5-42). Carcinoma of the stomach may appear as thickening of the gastric wall or as an intraluminal mass. The earliest stage (stage I) demonstrates as an intraluminal mass without wall thickening. Stage II consists of wall thickening of greater than 1 cm without invasion of other tissue or organs. As the disease progresses, the stomach wall thickens and invades adjacent organs (stage III). Obliteration of the fat planes (the covering layers of fat) around the stomach is a reliable indicator of the extragastric spread of tumor (stage IV). CT can demonstrate direct tumor extension to intraabdominal organs and distant metastases, especially to the liver.

Gastric carcinoma may also be demonstrated using endoscopic ultrasound. The gastric mucosa produces an increased echogenicity and demonstrates vertical invasion through the gastric wall. If diagnosed at a late stage, the lesion may extend into the perigastric lymph nodes.

Treatment

In most cases, treatment of stomach cancer consists of surgical resection of all or part of the stomach.

Radiographic Appearance

In the small bowel, the earliest radiographic changes of Crohn’s disease include irregular thickening and distortion of mucosal folds caused by submucosal inflammation and edema. Transverse and longitudinal ulcerations can separate islands of thickened mucosa and submucosa, leading to a characteristic rough cobblestone appearance (Figure 5-43). Rigid thickening of the entire bowel wall produces pipelike narrowing. Continued inflammation and fibrosis can result in a severely narrowed, rigid segment of small bowel in which the mucosal pattern is lost (string sign) (Figure 5-44). When several areas of small bowel are diseased, involved segments of varying length are often sharply separated from radiographically normal segments (skip lesions). On CT images, there is thickening of the wall of the small bowel, and the mesentery has an appearance that is described as “dirty fat.” The new technology of CT enterography demonstrates subtle findings, such as mild wall thickening and mucosal vascular changes. CT is recommended for a patient with active Crohn’s disease to determine the nature of the mass (Figure 5-45).

Fistula formation, a hallmark of chronic Crohn’s disease, is found in at least half of all patients with this condition (Figure 5-46). The diffuse inflammation of the serosa and mesentery in Crohn’s disease causes involved loops of bowel to be firmly matted together by fibrous peritoneal and mesenteric bands. Fistulas apparently begin as ulcerations that burrow through the bowel wall into adjacent loops of small bowel and colon. In addition to fistulas between loops of bowel, a characteristic finding in Crohn’s disease is the appearance of fistulous tracts ending blindly in abscess cavities surrounded by dense inflammatory tissue. These abscess cavities can produce palpable masses, persistent fever, or pain. Although less common than bowel-to-bowel fistulas, internal fistulas extending from the bowel to the bladder or vagina can occur. A common complication is the development of external gastrointestinal fistulas, which usually extend to the perianal area and may be associated with fissures and perirectal abscesses.

Treatment

Whenever possible, Crohn’s disease is treated with medications, and surgery is performed only if complications require it. Surgical resection of an involved segment of small bowel is associated with a high incidence of recurrence of Crohn’s disease adjacent to the anastomosis.

Radiographic Appearance

Distended loops of small bowel containing gas and fluid can usually be recognized radiographically within 3 to 5 hours of the onset of complete obstruction. Almost all gas proximal to a small bowel obstruction represents swallowed air. On upright or lateral decubitus projections, the interface between gas and fluid forms a straight horizontal margin (Figure 5-47). Although the presence of gas-fluid levels at different heights in the same loop has traditionally been considered evidence for mechanical obstruction, an identical pattern can also be demonstrated in some patients with adynamic ileus (see later discussion). The air-filled bowel appears as a dilated proximal bowel and a collapsed distal bowel. On upright images, a string-of-beads sign appears. In adynamic ileus, the bowel has no caliber change.

As time passes, the small bowel may become so distended as to be almost indistinguishable from the colon. To make the critical differentiation between small and large bowel obstruction, it is essential to determine which loops of bowel contain abnormally large amounts of air. Small bowel loops generally occupy the more central portion of the abdomen, whereas colonic loops are positioned laterally around the periphery of the abdomen or inferiorly in the pelvis (Figure 5-48). Gas within the lumen of the small bowel outlines the thin valvulae conniventes, which completely encircle the bowel. In contrast, colonic haustral markings are thicker and farther apart and occupy only a portion of the transverse diameter of the bowel.

The site of obstruction can usually be predicted with considerable accuracy if the number and position of dilated bowel loops are analyzed. The presence of a few dilated loops of small bowel located high in the abdomen (in the center or slightly to the left) indicates an obstruction in the distal duodenum or jejunum. The involvement of additional small bowel loops is suggestive of a lower obstruction. As more loops are affected, they appear to be placed one above the other upward and to the left, producing a characteristic stepladder appearance (Figure 5-49). The point of obstruction is always distal to the lowest loop of dilated bowel.

Patients with complete mechanical small bowel obstruction demonstrate little or no gas in the colon. This is a valuable point in the differentiation between mechanical obstruction and adynamic ileus, in which gas is seen within distended loops throughout the bowel. Although a small amount of gas or fecal accumulation may be present at an early stage of a small bowel obstruction (see Figure 5-48), the detection of a large amount of gas in the colon effectively eliminates this diagnosis.

The bowel proximal to an obstruction may contain no gas but be completely filled with fluid. This may produce a confusing picture of a normal-appearing abdomen or a large soft tissue abdominal mass.

Plain abdominal radiographs are occasionally insufficient for a distinction to be made between small and large bowel obstructions. In these instances, a carefully performed barium enema examination can document or eliminate the possibility of large bowel obstruction. If it is necessary to determine the precise site of small bowel obstruction, barium can be administered in either a retrograde (by means of an enema) or an antegrade (by way of the mouth) manner. Orally administered barium (not water-soluble agents) is the most effective contrast material for demonstrating the site of small bowel obstruction (Figure 5-50). The large amount of fluid proximal to a small bowel obstruction prevents any trapped barium from hardening or increasing the degree of obstruction. The density of barium permits excellent visualization far into the intestine; water-soluble agents, however, are lost to sight because of dilution and absorption. It must be emphasized that if plain radiographs clearly demonstrate a mechanical small bowel obstruction, a contrast examination is unnecessary.

Strangulation of bowel caused by interference with the blood supply is a serious complication of small bowel obstruction. In a closed-loop obstruction (e.g., volvulus and incarcerated hernia) (Figure 5-51), the loops going both toward (afferent) and away from (efferent) the area of narrowing become obstructed. The involved segments usually fill with fluid and appear radiographically as a tumorlike soft tissue mass. A closed loop is a clinically dangerous form of obstruction, because the continuing outpouring of fluid into the enclosed space can raise intraluminal pressure and rapidly lead to occlusion of the blood supply to that segment of bowel. Because venous pressure is normally lower than arterial pressure, blockage of venous outflow from the strangulated segment occurs before obstruction of the mesenteric arterial supply. Ischemia can rapidly cause necrosis of the bowel with sepsis, peritonitis, and a potentially fatal outcome.

CT may aid in demonstrating small bowel obstruction when the plain abdominal radiographs are normal or nonspecific. In addition to showing the site, level, and cause of the obstruction, this modality may indicate whether there is strangulation of the involved loops of bowel. Specifically, herniation causes slight wall thickening that appears as a “target sign” as a result of engorgement of the superior and inferior mesenteric vessels. CT appears to be the most valuable modality for patients with a history of abdominal malignancy and for those who have signs of infection, bowel infarction, or a palpable abdominal mass (Figure 5-52).

Treatment

Surgery is usually required to decompress the bowel as soon as possible to prevent necrosis or bowel perforation from occurring.

Radiographic Appearance

The radiographic hallmark of adynamic ileus is the retention of large amounts of gas and fluid in dilated small and large bowel. The entire small and large bowel in adynamic ileus, unlike in mechanical small bowel obstruction, appears almost uniformly dilated with no demonstrable point of obstruction (Figure 5-53).

There are two major variants of adynamic ileus. Localized ileus refers to an isolated distended loop of small or large bowel (the sentinel loop), which is often associated with an adjacent acute inflammatory process. The portion of the involved bowel can offer a clue to the underlying disease. Localized segments of the jejunum or transverse colon are frequently dilated in patients with acute pancreatitis. Similarly the hepatic flexure of the colon can be distended in acute cholecystitis, the terminal ileum can be dilated in acute appendicitis, the descending colon can be distended in acute diverticulitis, and dilated loops can be seen along the course of the ureter in acute ureteral colic (Figure 5-54). Unfortunately, isolated segments of distended small bowel are commonly seen in patients with abdominal pain and thus the sentinel loop may be found “guarding” the wrong area.

Colonic ileus refers to selective or disproportionate gaseous distention of the large bowel without an obstruction (Figure 5-55). Massive distention of the cecum, which is often horizontally oriented, characteristically dominates the radiographic appearance. Colonic ileus usually accompanies or follows an acute abdominal inflammatory process or abdominal surgery. The clinical presentation and the findings on plain abdominal radiographs simulate those in mechanical obstruction of the colon. A barium enema examination is usually necessary to exclude an obstructing lesion.

Treatment

Adynamic ileus caused by surgery usually resolves itself spontaneously in 36 to 48 hours if no complications are involved. Treatment involves insertion of a nasogastric tube to aspirate the stomach, decompress the bowel, and allow the intestine to rest. Electrolyte and fluid imbalances are corrected by intravenous (IV) injection.

Radiographic Appearance

Radiographically, an intussusception produces the classic coiled-spring appearance of barium trapped between the intussusceptum and the surrounding portions of bowel (Figure 5-56A). Reduction of a colonic intussusception can sometimes be accomplished by a barium enema examination (Figure 5-56B and C), although great care must be exercised to prevent excessive intraluminal pressure, which may lead to perforation of the colon. On CT images, intussusception appears as three concentric circles forming a soft tissue mass.

Ultrasound, used especially in children, demonstrates the obstructive mass as a doughnut-shaped lesion on the transverse scan and as a “pseudokidney” on the longitudinal scan (Figure 5-57).

Treatment

Reduction of intussusceptions by rectal insufflation of air (instead of barium) has been reported to be an effective technique in children. In older children and adults, a second barium enema examination after reduction is necessary to determine whether an underlying polyp or a tumor caused the intussusception.

Radiographic Appearance

Many of the diseases that cause malabsorption produce radiographic abnormalities in the small bowel, although malabsorption can exist without any detectable small bowel changes. The two major radiographic appearances are (1) small bowel dilatation with normal folds (Figure 5-58) and (2) a pattern of generalized, irregular, distorted small bowel folds (Figure 5-59).

Treatment

Patients afflicted with malabsorption disorders take medications to assist in absorbing key nutrients to keep the body’s systems in good health. Probiotics are live microbial food supplements that aid in improving the intestinal microbial balance. These supplements enhance the bioavailability of nutrients to the body.

Radiographic Appearance

Plain abdominal radiographs demonstrate a round or oval, laminated calcified fecalith in the appendix (appendicolith) (Figure 5-60) in about one third of patients. Surgical experience indicatesthat the presence of an appendicolith in combination with symptoms of acute appendicitis usually implies that the appendix is gangrenous (necrotic) and likely to perforate. Most appendicoliths are located in the right lower quadrant overlying the iliac fossa. Depending on the length and position of the appendix, however, an appendicolith can also be seen in the pelvis or in the right upper quadrant (retrocecal appendix), where it can simulate a gallstone.

Because of the danger of perforation, barium enema examination is usually avoided in acute appendicitis. If it is performed, an irregular impression of the base of the cecum (caused by inflammatory edema), in association with failure of barium to enter the appendix, is a characteristic finding. Nevertheless, failure of barium to fill the appendix is not a reliable sign of appendicitis, because the normal appendix does not fill with barium in about 20% of cases. Partial filling of the appendix with distortion of its shape or caliber strongly suggests acute appendicitis (Figure 5-61), especially if there is a cecal impression. In contrast, a patent (open) appendiceal lumen effectively excludes the diagnosis of acute appendicitis, especially when barium extends to fill the rounded appendiceal tip.

When the clinical presentation is unclear, high-resolution ultrasound with graded compression is the imaging modality of choice for diagnosing acute appendicitis, especially when use of ionizing radiation is contraindicated in the patient. A noncompressible appendix measuring 7 mm or more in maximal outer diameter is considered virtually pathognomonic of acute appendicitis (Figure 5-62).

CT, the gold standard, shows an appendiceal abscess as a round or oval mass of soft tissue density that may contain gas. After administration of IV contrast material, the appendix appears as a dilated structure with a thickened, circumferentially enhancing wall (Figure 5-63). This modality provides a more precise evaluation of the nature, extent, and location of the pathologic process and can detect intraabdominal disease unrelated to appendicitis that may explain the patient’s clinical presentation.

Treatment

When a patient is diagnosed with appendicitis, an immediate appendectomy should be performed before perforation occurs to prevent complications (e.g., peritonitis, gangrene, and abscess formation). If perforation occurs, a regimen of antibiotics helps reduce the risk of peritonitis and sepsis.

Radiographic Appearance

Colonic diverticula appear radiographically as round or oval outpouchings of barium projecting beyond the confines of the lumen. They vary in size from barely visible dimples to saclike structures 2 cm or more in diameter. Giant sigmoid diverticula up to 25 cm in diameter, which probably represent slowly progressing chronic diverticular abscesses, may appear as large, well-circumscribed, lucent cystic structures in the lower abdomen.

Diverticula are usually multiple and tend to occur in clusters, although a solitary diverticulum is occasionally found. When diverticula are multiple, deep crisscrossing ridges of thickened circular muscle (saw-toothed configuration) can produce a characteristic series of sacculations (Figure 5-64).

Diverticula also commonly occur in the esophagus and duodenum and infrequently may develop in the jejunum and ileum.

Radiographic Appearance

The radiographic diagnosis of diverticulitis requires direct or indirect evidence of diverticular perforation. The most specific sign is extravasation, which can appear either as a tiny projection of contrast material from the tip of a diverticulum (Figure 5-65A) or as an obvious filling of a pericolic abscess (Figure 5-65B). A more common, although somewhat less specific, sign of diverticulitis is the demonstration of a pericolic soft tissue mass that is attributable to a localized abscess and represents a walled-off perforation. This extraluminal mass appears as a filling defect causing eccentric narrowing of the bowel lumen. The adjacent diverticula are spastic, irritable, and attenuated and frequently seem to drape over the mass. It is important to remember, however, that a peridiverticular abscess caused by diverticulitis can occur without radiographically detectable diverticula (Figure 5-66).

Severe spasm or fibrotic healing of diverticulitis can cause a rigidity and progressive narrowing of the colon that simulates annular carcinoma. Although radiographic distinction from carcinoma may be impossible, findings favoring the diagnosis of diverticulitis include the involvement of a relatively long segment, a gradual transition from diseased to normal colon, a relative preservation of mucosal detail, and fistulous tracts and intramural abscesses. At times, colonoscopy or surgery may be required to make a definitive diagnosis.

Acute diverticulitis on ultrasound appears as a hypoechoic projection that arises from the wall of the bowel and is surrounded by inflamed fat. CT demonstrates pericolic fluids or gas collections, usually with nonspecific colonic wall thickening that produces narrowing of the bowel lumen (Figure 5-67). Inflammatory stranding may appear in the adjacent fat.

Treatment of Diverticulosis and Diverticulitis

Noninvasive treatment is the first choice for diverticulosis, with use of dietary modifications (nothing with seeds, nuts, popcorn, etc.) and exercise (to increase peristalsis). If diverticulitis has developed, antibiotics and diet adjustments (liquids) are given until the bowel heals. Perforation requires surgical repair and a regimen of antibiotics.

Radiographic Appearance

In the radiographic evaluation of a patient with known or suspected ulcerative colitis, plain abdominal radiographs are essential. Large nodular protrusions of hyperplastic mucosa, deep ulcers outlined by intraluminal gas, or polypoid changes along with a loss of haustral markings (normal indentations in the wall of the colon) may indicate the diagnosis. Plain abdominal radiographs can also demonstrate evidence of toxic megacolon, a dramatic and ominous complication of ulcerative colitis that is characterized by extreme dilatation of a segment of colon (Figure 5-68), or evidence of an entire diseased colon, combined with systemic toxicity (abdominal pain and tenderness, tachycardia, fever, and leukocytosis). Toxic megacolon can lead to spontaneous perforation of the colon, which can be dramatic and sudden and can cause irreversible shock. Because there is such a high danger of spontaneous perforation, barium enema examination is absolutely contraindicated during a recognized attack of toxic megacolon.

Ulcerative colitis has a strong tendency to begin in the rectosigmoid area. Although by radiographic criteria alone the rectum appears normal in about 20% of patients with ulcerative colitis, true rectal sparing is infrequent, and there is usually evidence of disease on sigmoidoscopy or rectal biopsy. Isolated right colon disease with a normal left colon does not occur, and ulcerative colitis may spread to involve the entire colon (pancolitis). The disease is almost always continuous, without evidence of the skip areas seen in Crohn’s disease. Except for “backwash ileitis” (minimal inflammatory changes involving a short segment of terminal ileum), ulcerative colitis does not involve the small bowel, a feature distinguishing it from Crohn’s disease, which may involve both the large and the small intestines.

On double-contrast studies, the earliest detectable radiographic abnormality in ulcerative colitis is fine granularity of the mucosa corresponding to the hyperemia and edema seen endoscopically (Figure 5-69). Once superficial ulcers develop, small flecks of adherent barium produce a stippled mucosal pattern. As the disease progresses, the ulcerations become deeper. Extension into the submucosa may produce broad-based ulcers with a collar-button appearance (Figure 5-70). Perirectal inflammation can cause widening of the soft tissue space between the anterior sacrum and the posterior rectum (retrorectal space).

When the disease is chronic, fibrosis and muscular spasm cause progressive shortening and rigidity of the colon (Figure 5-71). The haustral pattern is absent, and the bowel contour is relatively smooth because of ulcer healing and subsequent reepithelization. Eventually, the colon may appear as a symmetric, rigid, tubular structure (lead-pipe colon).

Carcinoma of the colon is about 10 times more frequent in patients with ulcerative colitis than in the general population. During the first 10 years of disease, there is only a small risk of malignancy. Thereafter, it is estimated that there is a 20% chance per decade that carcinoma will develop in a patient with ulcerative colitis. Malignant lesions in patients with ulcerative colitis generally occur at a much younger age than they occur in the general population, and they tend to be extremely virulent. Carcinoma of the colon in patients with chronic ulcerative colitis often appears as a bizarre stricture rather than with the more characteristic polypoid or apple-core appearance of a primary colonic malignancy (Figure 5-72). The tumor typically produces a narrowed segment with an eccentric lumen, irregular contours, and margins that are rigid and tapered. Because it is frequently difficult to distinguish carcinoma from benign stricture in patients with ulcerative colitis, colonoscopy or surgery is often required for an unequivocal diagnosis.

Radiographic Appearance

The earliest radiographic findings in Crohn’s disease of the colon are seen on double-contrast examinations. Isolated tiny, discrete erosions (aphthous ulcers) appear as punctate collections of barium with a thin halo of edema around them (Figure 5-73). Aphthous ulcers in Crohn’s disease have a patchy distribution against a background of normal mucosa, unlike the blanket of abnormal granular mucosa seen in ulcerative colitis.

As Crohn’s colitis progresses, the ulcers become deeper and more irregular, with a great variation in size, shape, and overall appearance. Deep linear, transverse, and longitudinal ulcers often separate intervening mounds of edematous but nonulcerating mucosa, producing a characteristic cobblestone appearance (see Figure 5-43). If the penetrating ulcers extend beyond the contour of the bowel, they can coalesce (grow together) to form long tracts running parallel to the long axis of the colon (Figure 5-74). The penetration of ulcers into adjacent loops of bowel or into the bladder, vagina, or abdominal wall causes fistulas, which can often be demonstrated radiographically. Inflammatory and fibrotic thickening of the bowel wall leads to narrowing of the lumen and stricture formation. Occasionally an eccentric stricture with a suggestion of overhanging edges can be difficult to distinguish from annular carcinoma (Figure 5-75). In most instances, however, characteristic features of Crohn’s disease elsewhere in the colon (deepulcerations, pseudopolyps, skip lesions, sinus tracts, fistulas) clearly indicate the correct diagnosis.

CT demonstrates the mesenteric and extraintestinal extent of the disease, and any abscess formation or colonic wall thickening. Magnetic resonance (MR) spectroscopy is currently under investigation as a way to help distinguish ulcerative colitis from Crohn’s colitis. Preliminary results indicate that this technique is able to differentiate between the two inflammatory bowel diseases in more than 90% of cases.

Patients with Crohn’s colitis appear to have a higher incidence of developing colon cancer than the general population, although this association is less striking than that between colon cancer and ulcerative colitis. Carcinoma complicating Crohn’s colitis is most common in the proximal portion of the colon and usually appears radiographically as a fungating mass with typical malignant features, unlike the mildly irregular stricture

characteristic of colon cancer in patients with ulcerative colitis. A small bowel examination may be necessary to demonstrate the terminal ileum.

Treatment of Ulcerative Colitis and Crohn’s Colitis

The initial treatments for ulcerative colitis and Crohn’s disease are identical, as both are inflammatory bowel diseases. First, nutritional supplements and dietary modifications (decrease bulk to reduce stool frequency) begin to diminish the inflammatory process. A regimen of antiinflammatory drugs interrupts the inflammatory cycle. Stress-related conditions require psychological support to control episodes. For ulcerative colitis, surgical resection may be necessary to prevent the spread of the condition. With proper treatment or spontaneous remission, many of the radiographic changes in this disease are reversible. In Crohn’s colitis, surgery is usually ineffective because the area adjacent to the anastomosis becomes involved as a result of the resection. For severe cases of the disorder, parenteral (IV) nutrition allows the intestine time to heal.

Radiographic Appearance

The initial radiographic appearance of ischemic colitis is fine superficial ulceration caused by inflammatory edema of the mucosa. As the disease progresses, deep penetrating ulcers, pseudopolyps, and characteristic thumbprinting can be demonstrated. Thumbprinting refers to sharply defined, finger-like indentations along the margins of the colon wall (Figure 5-76). In most cases, the radiographic appearance of the colon returns to normal within 1 month if good collateral circulation is established. Extensive fibrosis during the healing phase can cause tubular narrowing and a smooth stricture. If blood flow is insufficient, acute bowel necrosis and perforation may result.

Treatment

In some cases, no intervention is needed, as the bowel heals itself. Patients taking vasoconstricting drugs are most susceptible, and when the diagnosis is ischemic colitis, these medications are discontinued and supportive care is given. Immediate surgical intervention is required for bowel infarctions and other complications.

Radiographic Appearance

Although there are no specific radiographic findings in irritable bowel syndrome, patients with this condition usually undergo a barium enema examination to exclude another chronic disorder as the cause of the symptoms. When the patient is symptomatic, a barium enema may demonstrate areas of irritability and spasticity and accentuated haustration, although similar radiographic findings may be observed in normal asymptomatic persons, especially those who have received laxatives and enemas.

Treatment

No cure exists for irritable bowel syndrome. Because the precise cause of this functional disorder has not been determined, symptomatic relief is provided. It is necessary to identify trigger foods so that they can be avoided, thus decreasing the spasms and pain. Alternative therapies, relaxation, meditation, and physical exercise have value if the patient can use them to help ease some of the spasms and pain.

Radiographic Appearance

Because cancer of the colon is curable if discovered early in its course, delay in diagnosis is the most significant factor in the poor prognosis. There is considerable evidence to indicate that many, if not most, carcinomas of the colon arise in preexisting polyps. Therefore, the early diagnosis of colonic cancer depends on polyp detection. Malignant polyps (Figure 5-77) tend to be sessile lesions (without stalks) with an irregular or lobulated surface, unlike benign polyps, which are usually smooth and often have a stalk (are pedunculated). Other radiographic criteria suggestive that a polyp is malignant include large size (especially if more than 2 cm in diameter), retraction or indentation (puckering) of the colon wall seen on profile view at the site of origin of a sessile polyp, and evidence of interval growth of a polyp on sequential examinations.

Annular carcinoma (described as apple-core or napkin-ring carcinoma) is one of the most typical forms of primary colonic malignancy (Figure 5-78). Annular carcinomas appear to arise from flat plaques of tumor (saddle lesions) that involve only a portion of the circumference of the colon wall. Unless meticulous care is taken to search for an area of minimal straightening or slight contour defects, the small and subtle, but lethal, saddle carcinoma can be easily overlooked. As the tumor grows, it characteristically infiltrates the bowel wall rather than forming a bulky intraluminal mass. This produces a classic bilateral contour defect with ulcerated mucosa, eccentric and irregular lumen, and overhanging margins. Progressive constriction of the bowel can cause complete colonic obstruction, most commonly in the sigmoid region.

Ulceration is common in carcinoma of the colon. It can vary from an excavation within a large fungating mass to mucosal destruction within an annular apple-core tumor.

A patient with carcinoma of the colon has a 1% risk of having multiple synchronous (occurring simultaneously) colon cancers. Therefore, it is essential to carefully examine the rest of the colon once an obviously malignant lesion has been detected. In addition, such a patient has a 3% risk of developing additional metachronous cancers later.

CT virtual colonoscopy has become more frequently used as a screening tool for colon cancer. Today, two- or three-dimensional CT colonoscopy can demonstrate lesions of 8 to 10 mm with an accuracy similar to that obtained with traditional colonoscopy. CT virtual colonoscopy is an alternative for incomplete or equivocal results of traditional colonoscopy. CT is also the modality of choice for staging carcinoma of the colon and for assessing tumor recurrence (Figure 5-79). Carcinoma causes asymmetrical or circumferential thickening of the bowel wall with narrowing and deformity of the lumen. CT can demonstrate local extension of tumor to the pelvic organs as well as lymphadenopathy and metastases to the adrenal glands or liver (Figure 5-80).

Transrectal ultrasound produces the most accurate images for staging of local rectal cancer by demonstrating the depth of invasion within the bowel wall. Ultrasound also may determine the presence of a tumor in adjacent, normal-size lymph nodes.

Positron emission tomography (PET) with fluorodeoxyglucose F 18 (FDG-PET), although less specific than CT and ultrasound, has a higher accuracy for detecting distant nodular metastases. Fusion imaging, which superimposes the functional (PET) and anatomic (CT) studies, provides more specific detail to localize and evaluate the severity of the disease process.

Treatment

Surgical resection is required to remove a solitary carcinoma. Postoperative treatment may involve chemotherapy or radiation therapy. Following resection, FDG-PET in combination with a CT scan helps rule out recurrence. FDG-PET images can differentiate recurrence of the tumor from adhesions or scar tissue resulting from the resection. The presence of multiple lesions requires irradiation and chemotherapy.

Radiographic Appearance

The radiographic appearance of colonic obstruction depends on the competency of the ileocecal valve. If the ileocecal valve is competent, obstruction causes a large, dilated colon with a greatly distended, thin-walled cecum and little small bowel gas (Figure 5-81). The colon distal to the obstruction is usually collapsed and free of gas. If the ileocecal valve is incompetent, there is distention of gas-filled loops of both colon and small bowel, which may simulate an adynamic ileus.

The major danger in colonic obstruction is perforation. If the ileocecal valve is competent, the colon behaves like a closed loop, and the increased pressure caused by the obstruction cannot be relieved. Because the cecum is spherical and has a large diameter, it is the most likely site for perforation. In acute colonic obstruction, perforation is very likely if the cecum distends to more than 10 cm; in intermittent or chronic obstruction, however, the cecal wall can become hypertrophied, and the diameter of the cecum can greatly exceed 10 cm without perforation (see Figure 5-81). In the patient with suspected large bowel obstruction, a low-pressure barium enema can be safely performed (Figure 5-82) and demonstrates the site and often the cause of the obstruction (Figure 5-83).

Some professionals recommend an abdominal/pelvic CT scan as an initial examination, especially for patients without a surgical history who have symptomatic signs suggesting infection, bowel infarction, or a palpable mass. CT can demonstrate causes of an obstruction, such as diverticulitis or appendicitis.

Cecal Volvulus

The ascending colon and the cecum may have a long mesentery as a fault of rotation and fixation during the embryonic development of the gut. This situation predisposes to volvulus, with the cecum twisting on its long axis. It should be stressed, however, that cecal volvulus develops in only a few patients with an extremely mobile cecum.

Sigmoid Volvulus

A long, redundant loop of sigmoid colon can undergo a twist on its mesenteric axis and form a closed-loop obstruction. In sigmoid volvulus, the greatly inflated sigmoid loop appears as an inverted U-shaped shadow that rises out of the pelvis in a vertical or oblique direction and can even reach the level of the diaphragm. The affected loop appears devoid of haustral markings and has a sausage or balloon shape.

Treatment for Large Bowel Obstruction or Volvulus

Surgical detorsion is usually required for large bowel obstruction or volvulus, although a water-soluble enema may be therapeutic and resolve the obstruction.

Radiographic Appearance

On barium enema examinations, hemorrhoids occasionally can produce single or multiple rectal filling defects that simulate polyps (Figure 5-86). The proper diagnosis can easily be made by inspection, digital examination, or direct vision through the anoscope.

Treatment

Hemorrhoids may be treated nonsurgically and surgically. The nonsurgical approach consists of rubber band ligation. The surgical intervention consists of circumferential mucosectomy, which is a stapled hemorrhoidectomy, a safe and effective procedure for advanced stages (third- and fourth-degree hemorrhoidal prolapse).

Radiographic Appearance

Because cholesterol is not radiopaque, most gallstones are radiolucent and visible only on contrast examinations or ultrasound. In up to 20% of patients, however, gallstones contain sufficient calcium to be detectable on plain abdominal radiographs (Figure 5-87). Gallstones can have a central nidus (or focus) of calcification, a laminated appearance (with alternating opaque and lucent rings), or calcification around the periphery. Occasionally, a nonopaque stone may contain gas-filled fissures that produce the Mercedes-Benz sign, a characteristic triradiate pattern similar to the German automobile trademark (Figure 5-88).

Oral cholecystography (OCG) was the traditional technique for the diagnosis of gallstones. It is rarely used today because it has been replaced in most institutions by ultrasound (see later). Gallstones appear as freely movable filling defects in the opacified gallbladder. They fall by gravity to the dependent portion of the gallbladder and frequently layer out at a level that depends on the relationship of the specific gravity of the stone to that of the surrounding bile (Figure 5-89). Solitary gallstones are usually rounded; multiple stones are generally faceted. Large numbers of stones can have a sandlike or gravel-like consistency and be visible only when they layer out on radiographs obtained using a horizontal beam and with the patient in an erect or lateral decubitus position. Infrequently a gallstone is coated with tenacious mucus and adheres to the gallbladder wall.

Malabsorption of the radiopaque contrast material, hepatocellular dysfunction (serum bilirubin value ≥ 2 mg/dL), and intrinsic disease of the gallbladder (cystic duct obstruction, chronic cholecystitis) can lead to nonvisualization of the gallbladder on OCG. If these causes can be excluded, failure of the gallbladder to opacify after the administration of two doses of orally administered cholecystographic contrast material is highly reliable evidence of gallbladder disease.

Ultrasound is now the imaging modality of choice for demonstrating gallstones. This noninvasive technique is as accurate as OCG, is independent of hepatic function, and does not rely on patient compliance in taking oral contrast agents. In addition to imaging the gallbladder, ultrasound can provide important additional information by effectively demonstrating the biliary tree and hepatic parenchyma. Gallstones appear on ultrasound as foci of high-amplitude echoes associated with posterior acoustic shadowing (Figure 5-90). The mobility of free-floating gallstones may be demonstrated by performing the examination with the patient in various positions.

Radiographic Appearance

Either ultrasound or radionuclide scanning can be used. The ultrasonographic diagnosis of acute cholecystitis requires the demonstration of a distended gallbladder containing gallstones. Important additional findings include edema of the gallbladder wall and focal tenderness elicited directly over the gallbladder. A normal gallbladder ultrasound image virtually excludes the diagnosis of acute cholecystitis. Because many disorders may mimic acute cholecystitis, ultrasound can also be used to evaluate the remainder of the right upper quadrant for any other acute abnormality.

When the results of a radionuclide cholescintigram are normal, they demonstrate the bile ducts, the gallbladder, and early excretion of radionuclide into the duodenum and proximal jejunum, within 30 minutes after the IV injection of the radionuclide (technetium Tc 99m) (Figure 5-91). Failure to accumulate radioactivity (after 4 hours) in the gallbladder is highly sensitive (98%) and specific for cystic duct obstruction. If associated with appropriate symptoms, this finding is virtually diagnostic of acute cholecystitis.

When ultrasound findings are inconclusive, MR cholangiopancreatography can demonstrate the cystic duct and any obstructing calculi located in the gallbladder neck. MR imaging (MRI) does not, however, evaluate the gallbladder wall thickness as well as ultrasound.

Radiographic Appearance

Plain abdominal radiographs demonstrate gas in the gallbladder lumen that dissects into the wall or pericholecystic tissues. This produces the pathognomonic appearance of a rim of lucent bubbles or streaks of gas outside of and roughly parallel to the gallbladder lumen (Figure 5-92).

Radiographic Appearance

The calcification in a porcelain gallbladder can appear as a broad continuous band in the muscular layers, or it may be multiple and punctate and occur in the glandular spaces of the mucosa.

The detection of extensive calcification in the wall of the gallbladder should indicate the possibility of carcinoma. Although a porcelain gallbladder is uncommon in cases of carcinoma of the gallbladder, there is a striking incidence of carcinoma in patients with porcelain gallbladder (up to 60% of the cases).

Treatment

Because of the high incidence of associated carcinoma, patients with porcelain gallbladder usually undergo prophylactic cholecystectomy even if they are asymptomatic.

Radiographic Appearance

Viral hepatitis in the earliest stages is not visible on diagnostic images. As the disease progesses, complications of cirrhosis or hepatocellular carcinoma can be demonstrated on ultrasound, CT, and MRI. On ultrasound, cirrhosis due to viral hepatitis usually manifests as macronodules (Figure 5-94), which may vary in size from 3 mm to 5 cm. The liver has an internal coarse texture with increased echogenicity, and the surface may have a nodular appearance representing fibrosis (Figure 5-95). Portal hypertension, due to enlargement or blockage of the portal system, can also be detected. CT demonstrates hepatocellular necrosis with scattered inflammatory cells and evidence of a fatty liver. Normally the density of the liver is similar to that of the spleen. In fatty liver, infiltrates of fat appear as discrete or diffuse areas of low density within the liver. Contrast-enhanced CT in the portal venous phase is best for demonstrating a lobulated liver. Due to atrophy, the intrahepatic fissures appear more prominent. T1-weighted contrast MR images show the liver to have irregular diffuse enhancement with ill-defined margins; there may be rim enhancement in the venous phase. T2-weighted fat-suppressed MR images demonstrate a heterogeneous mass appearance with moderate elevation of the signal intensity. MRI enhancement with gadolinium is superior to that produced by iodinated contrast agents on CT for distinguishing abnormalities.

Treatment

At this time, prevention is the best method to control hepatitis. Standard precautions for healthcare workers should include the use of personal protective equipment for all patients. Vaccines exist for HAV and HBV. For short-term immunization, immune globulin is used.

Radiographic Appearance

Cirrhosis causes many physiologic changes that can be detected clinically or radiographically. In alcoholic cirrhosis, a large amount of fat accumulates within the liver. This fatty infiltration is beautifully demonstrated on CT. In normal individuals, the liver always appears brighter than the spleen, whereas in patients with cirrhosis the liver is much darker because of the large amount of fat (Figure 5-96). The portal veins appear as high-density structures surrounded by a background of low density caused by hepatic fat; this is the opposite of the normal pattern of portal veins, which are low-density channels on noncontrast scans. Ultrasound images of the liver demonstrate coarse echogenicity, which results from diffuse liver disease. Multiple hyperechoic micronodules (0.1 to 1 cm) or macronodules (varying up to 5 cm) cause a nodular surface pattern.

Nodular regeneration of the liver combined with fibrosis causes obstruction of the portal vein, which drains blood from the gastrointestinal tract through the liver before emptying into the inferior vena cava near the heart. Increased pressure within this vessel causes pronounced enlargement of the spleen (splenomegaly). Because blood cannot flow through the obstructed portal vein, it must find an alternative route to bypass the liver. This leads to the development of collateral circulation, with large dilated veins becoming prominent on the abdominal wall in the area of the umbilicus. Another alternative route for blood to take in its return to the heart is the periesophageal veins, which dilate to become esophageal varices, which then can rupture and result in fatal hemorrhage (see Figure 5-21). Destruction of liver cells substantially decreases the ability of the organ to synthesize proteins, such as albumin, and several of the factors required for blood clotting. A deficiency of albumin (hypoalbuminemia) results in fluid leaking out of the circulation and the development of generalized edema, which is evidenced by swelling of the lower extremities. When edema involves the wall of the intestinal tract, it can produce regular, uniform thickening of small bowel folds.

One of the most characteristic symptoms of cirrhosis is the accumulation of fluid in the peritoneal cavity (ascites), which causes characteristic abdominal distention. The abdomen is tight and quite hard, and an increase in exposure factors is required if a large amount of fluid has accumulated. Ascites develops because of a combination of albumin deficiency and increased pressure within obstructed veins, which permits fluid to leak into the abdominal cavity. Large amounts of ascitic fluid are easily detectable on plain abdominal radiographs as a general abdominal haziness (ground-glass appearance) (Figure 5-97A). With the patient in a supine position, the peritoneal fluid tends to gravitate to dependent portions of the pelvis and accumulate within the pelvic peritoneal reflections, thus filling the recesses on both sides of the bladder and producing a symmetrical density resembling a dog’s ears. Smaller amounts of fluid (300 to 1000 mL) may widen the flank stripe and obliterate the right lateral inferior margin of the liver (the hepatic angle). Ascites is exquisitely shown on ultrasound as a mobile, echo-free fluid region shaped by adjacent structures (Figure 5-97 B) or on CT as an extravisceral collection of fluid with a low attenuation value (Figure 5-97C).

Cirrhosis may lead to the development of jaundice, either from destruction of liver cells or from obstruction of bile ducts. Because the liver cannot perform its usual task of inactivating the small amounts of female sex hormones secreted by the adrenal glands in both men and women, men with cirrhosis often have breast enlargement (gynecomastia). The inability of necrotic liver cells to detoxify harmful substances leads to an accumulation of ammonia and other poisonous material in the circulation. The patient becomes confused and disoriented, demonstrates a typical flapping tremor or shaking, becomes abnormally sleepy (exhibits somnolence), and may lapse into a potentially fatal hepatic coma. Ascites occurs in advance stages of cirrhosis; of those afflicted, only 20% survive 5 years.

Treatment

The damage caused by cirrhosis is irreversible and incurable except by liver transplantation. Most patients without a liver transplant die within 15 years of diagnosis. The patient may control the process by choosing a nutritional diet that decreases the metabolic load on the liver, stopping alcohol consumption, resting, and managing the complications of liver failure.

Radiographic Appearance

CT is the modality of choice in the diagnosis of hepatocellular carcinoma. The tumor appears as a large mass, with an attenuation value close to that of normal parenchyma, that tends to alter the contour of the liver by projecting beyond its outer margin (Figure 5-98). After the rapid administration of IV contrast material, there is usually dense, diffuse, and nonuniform enhancement of the tumor. Unlike metastases, hepatocellular carcinoma tends to be a solitary mass or to produce a small number of lesions (thus appearing multinodular). Hepatocellular carcinoma tends to invade the hepatic and portal venous systems, and tumor thrombi within these veins are well demonstrated on CT. Currently, a three-phase contrast helical CT study is performed to image the arterial phase, the portal circulation, and the contrast-staining tumor in the venous or excretory phase (Figure 5-99).

Ultrasonography is used to screen chronic hepatitis B virus carriers. With the use of microbubble contrast agents, Doppler ultrasound imaging demonstrates lesion vascularity through the use of phasing techniques similar to those used in CT. MRI may permit a specific diagnosis by demonstrating (during the arterial phase, after gadolinium injection) a characteristic capsule of compressed liver tissue, an accumulation of fat within the tumor, and the propensity of the tumor to spread into the hepatic and portal venous system.

Treatment

Although the overall prognosis for patients with hepatocellular carcinoma remains bleak, radiographic studies can determine whether the tumor can be successfully removed surgically. If the tumor is confined to one lobe of the liver and there is no evidence of metastases, arteriography is usually indicated to demonstrate the precise surgical anatomy and to detect small, staining tumor nodules that cannot be identified with noninvasive imaging techniques. Surgery and chemotherapy are the treatments of choice. Metastases occur late and are usually not the cause of death. A common cause of death is catastrophic bleeding into the peritoneal cavity from hepatic failure or esophageal varices.

Radiographic Appearance

CT and MRI are probably the most sensitive techniques for detecting hepatic metastases. On CT, most metastases are relatively well marginated and appear less dense than normal liver parenchyma (Figure 5-100A). Although frequently detectable on noncontrast scans, most metastatic lesions are best seen as areas of increased density adjacent to normally enhancing hepatic parenchyma after the administration of IV contrast material. CT-guided fine-needle aspiration biopsy can be used to obtain cells that can be studied for a definitive diagnosis. MRI demonstrates liver metastases as areas of low signal intensity on T1-weighted sequences and bright lesions on T2-weighted sequences. This modality is especially important for patients who cannot receive IV iodinated contrast agents.

Ultrasound (Figure 5-100B) and radionuclide scans can demonstrate hepatic metastases, but these modalities are slightly less sensitive than CT. CT has the additional advantage of being able to detect extrahepatic metastases, such as those to abdominal lymph nodes.

Treatment

Once diagnosed with hepatic metastases, most patients face imminent death (within months).

Radiographic Appearance

The findings on plain abdominal radiographs are often normal in the patient with acute pancreatitis; even when abnormal, they are usually nonspecific and consistent with any intraabdominal inflammatory disease. The most common abnormalities include a localized adynamic ileus, usually involving the jejunum (the “sentinel loop”); generalized ileus with diffuse gas-fluid levels; isolated distention of the duodenal sweep (C-loop); and localized distention of the transverse colon to the level of the left colonic flexure (the colon cutoff sign). Pancreatic calcifications indicate that the patient has chronic pancreatitis, and moreover they may indicate an exacerbation of the inflammatory disease.

Ultrasound and CT are the imaging modalities that most precisely define the degree of pancreatic inflammation and the pathways of its spread throughout the abdomen. They are also of great clinical importance in the early diagnosis of complications of acute pancreatitis, such as abscess, hemorrhage, and pseudocyst formation.

CT in acute pancreatitis demonstrates diffuse or focal enlargement of the gland. The margins of a normal pancreas are sharply delineated by surrounding peripancreatic fat. Spread of inflammation and edema beyond the confines of the pancreas obscures the peripancreatic soft tissues and often thickens the surrounding fascial planes (Figure 5-100), making CT superior to ultrasound.

Acute pancreatitis may alter both the size and the parenchymal echogenicity of the gland on ultrasound examination. Although the pancreas usually enlarges symmetrically and retains its initial shape, nonspecific enlargement of the pancreatic head or tail can simulate focal pancreatic carcinoma. Gallstones causing pancreatitis can be demonstrated. The accompanying interstitial inflammatory edema causes the pancreas to appear relatively sonolucent in comparison with the adjacent liver (Figure 5-102). One limitation of ultrasound in patients with acute pancreatitis is the frequent occurrence of adynamic ileus with excessive intestinal gas, which may prevent adequate visualization of the gland.

Radiographic Appearance

Pancreatic calcifications are a pathognomonic finding in chronic pancreatitis, developing in about one third of patients with this disease (Figure 5-103). The small, irregular calcifications are seen most frequently in the head of the pancreas and can extend upward and to the left to involve the body and tail of the organ.

On ultrasound examination, the major feature of chronic pancreatitis is an alteration of the intrinsic echo pattern caused by calcification and fibrosis (Figure 5-104). The pancreas may be atrophic as a result of fibrous scarring or may appear significantly enlarged during recurrences of acute inflammation. Dilatation of the pancreatic duct as a result of gland atrophy and obstruction can be seen, although a similar pattern can be produced by the ductal obstruction in pancreatic cancer. CT can also demonstrate ductal dilatation, calcification, and atrophy of the gland in patients with chronic pancreatitis. However, because similar information can be obtained less expensively and without ionizing radiation with the use of ultrasound, CT is usually reserved for patients with chronic pancreatitis in whom technical factors make ultrasound suboptimal.

Enlargement of the pancreatic head can cause widening and pressure changes on the inner aspect of the duodenal sweep on barium studies. These changes produce narrowing of the lumen (the double-contour effect) and spiny protrusions of mucosal folds (spiculation) that can be indistinguishable from those of pancreatic carcinoma.

Radiographic Appearance

On ultrasound examination, a pseudocyst typically appears as an echo-free cystic structure with a sharp posterior wall (Figure 5-106). Hemorrhage into the pseudocyst produces a complex fluid collection containing septations of echogenic areas. CT demonstrates pseudocysts as sharply marginated, fluid-filled collections that are often best delineated after the administration of IV contrast material (Figure 5-107).

Large pseudocysts are visible on plain radiographs of the abdomen when they displace the gas-filled stomach and bowel. Similarly, pseudocysts in the head of the pancreas can cause pressure defects and widening of the duodenal sweep, whereas those arising from the body or tail of the pancreas can displace and deform the stomach, proximal jejunum, or colon. However, because ultrasound is highly accurate in diagnosing pancreatic pseudocysts, it has completely replaced plain abdominal radiographs and barium studies, which display only indirect signs.

Treatment

Pseudocysts may undergo spontaneous resolution or persist as chronic collections that may require surgical intervention. Because ultrasound is relatively inexpensive and does not involve ionizing radiation, serial sonograms are usually used to monitor the progression of a pancreatic pseudocyst. Percutaneous drainage of a pseudocyst and endoscopic drainage of cysts extending into the stomach are interventional therapies used today.

Radiographic Appearance

Because it is noninvasive and relatively inexpensive, ultrasound is often the initial screening modality for a patient with suspected pancreatic carcinoma. Ultrasound can demonstrate most tumors more than 2 cm in diameter that lie in the head of the pancreas, but lesions in the body and tail of the pancreas are more difficult to detect. Pancreatic carcinoma typically causes the gland to have an irregular contour and a semisolid pattern of intrinsic echoes (Figure 5-108).

CT is the most effective modality for detecting pancreatic cancer in any portion of the gland and for defining its extent. CT can demonstrate the mass of the tumor, ductal dilatation, and invasion of neighboring structures. After the administration of IV contrast material, the relatively avascular tumor appears as an area of decreased attenuation in comparison with the normal pancreas (Figure 5-109). CT is the best procedure for staging pancreatic carcinoma and may prevent needless surgery in patients with nonresectable lesions. This technique may permit detection of hepatic metastases or involvement of regional vessels and adjacent retroperitoneal lymph nodes.

Cytologic examination of tissue obtained by percutaneous fine-needle aspiration under ultrasound or CT guidance can often provide the precise histologic diagnosis of a neoplastic mass, thus making surgical intervention unnecessary.

Carcinoma of the head of the pancreas often causes obstructive jaundice and the appearance of narrowing of the distal common bile duct on transhepatic cholangiography (Figure 5-110) or ERCP. Percutaneous biliary drainage may represent an alternative to surgical intervention for relieving biliary obstruction in patients with pancreatic carcinoma who cannot be cured. Although the transhepatic insertion of biliary drainage tubes does not alter the dismal prognosis, it can reduce patient morbidity and the need for hospitalization.

A barium upper GI series demonstrates distortion of the mucosal pattern and configuration of the duodenal sweep in about half of patients with carcinoma of the head of the pancreas. Early or small lesions, however, rarely produce detectable radiographic abnormalities; tumors of the body or tail of the pancreas must be quite large to be visible on barium examinations.

Treatment

Finding pancreatic cancer in the earliest stages can result in a cure (the 5-year survival rate is 2%). In most cases, the diagnosis of the disease occurs after metastasis, and most patients die within 12 to 24 months of diagnosis. Nevertheless, treatment can improve the quality of life. Surgical resection, radiation therapy, chemotherapy, and biologic therapy help alleviate the patient’s symptoms.

Surgical resection (total pancreatectomy) involves the removal of the entire pancreas, duodenum, common bile duct, gallbladder, spleen, and surrounding lymph nodes. The Whipple procedure consists of removing only the head of the pancreas, the duodenum, a portion of the stomach, and other nearby tissue. If a distal pancreatectomy is performed, only the body and tail of the pancreas are removed. In most cases, the purpose of the surgery is to alleviate biliary and small bowel obstruction. Surgery and chemotherapy are most effective for islet cell cancers.

Radiographic Appearance

The radiographic demonstration of free air in the peritoneal cavity is a valuable sign in the diagnosis of perforation of the gastrointestinal tract. As little as 1 mL of free intraperitoneal gas can be identified. Free air is best demonstrated by examination of the patient in the upright position with a horizontal beam (Figure 5-111). Because the gas rises to the highest point in the peritoneal cavity, it accumulates beneath the domes of the diaphragm. Free intraperitoneal gas appears as a sickle-shaped lucency that is easiest to recognize on the right side between the diaphragm and the homogeneous density of the liver. On the left side, the normal gas and fluid shadows present in the fundus of the stomach can be confusing. The free air is shown to best advantage if the patient remains in an upright (or lateral decubitus) position for 10 minutes before a radiograph is obtained.

If the patient is too ill to sit or stand, a lateral decubitus view (preferably with the patient on the left side) can be used. In this position, free air moves to the right side and collects between the lateral margin of the liver and the abdominal wall (Figure 5-112). Some gas also collects in the right iliac fossa and, when large amounts are involved, can be seen along the flank down to the pelvis.

When the patient is in the supine position, free intraperitoneal gas accumulates between the intestinal loops and is much more difficult to demonstrate. However, a large quantity of gas can be diagnosed indirectly because the outer margins of the intestinal wall can be visualized (Figure 5-113). The demonstration of distinct inner and outer contours of the bowel wall is often the only sign of pneumoperitoneum in patients who are in such poor condition that they cannot be turned on their side or be examined while upright.

In children, pneumoperitoneum can manifest as a generalized greater-than-normal lucency of the entire abdomen. An important sign of pneumoperitoneum on the supine radiograph is demonstration of the falciform ligament. This almost vertical, curvilinear, water-density shadow in the upper abdomen to the right of the spine is outlined only when there is gas on both sides of it, as in pneumoperitoneum (Figure 5-114).

The most common cause of pneumoperitoneum with associated inflammation is perforation of a peptic ulcer, either gastric or duodenal. Colonic perforations, especially those involving the cecum, give the most abundant quantities of free intraperitoneal gas. Septic infection of the peritoneal cavity by gas-forming organisms can result in the production of a substantial amount of gas and the radiographic appearance of pneumoperitoneum. Pneumoperitoneum can also develop after penetrating injuries of the abdominal wall and after blunt trauma causing rupture of a hollow viscus.

Iatrogenic pneumoperitoneum is generally asymptomatic and usually follows abdominal surgery. Postoperative pneumoperitoneum can be radiographically detectable for up to 3 weeks after surgery, but usually it can no longer be demonstrated after the first postoperative week. Rarely, free air in the peritoneal cavity may be the result of perforation during an endoscopic procedure.

Treatment

Immediate surgical repair of a perforation is required to reduce the risk of peritonitis and sepsis. IV antibiotics help control infection.

Radiographic Appearance

Plain abdominal radiographs can demonstrate the inferior border of the enlarged spleen well below the costal margin. An enlarged spleen can elevate the left hemidiaphragm, impress the greater curvature of the barium-filled stomach, and displace the entire stomach toward the midline. Splenomegaly can also cause downward displacement of the left kidney and the splenic flexure of the colon.

CT is of value when it is unclear whether a mass palpated in the left upper quadrant represents an enlarged spleen or a separate abdominal mass. When splenomegaly is present (Figure 5-115), CT findings may indicate the cause of the splenic enlargement by demonstrating a tumor (Figure 5-116), abscess, or cyst. Associated abdominal lymph node enlargement is suggestive of lymphoma; characteristic alterations in the size and shape of the liver and prominence of collateral venous structures in the splenic hilum indicate that splenomegaly may be a result of cirrhosis and portal hypertension.

Radiographic Appearance

CT is the best imaging procedure for screening patients with blunt abdominal trauma for the presence of splenic injury. Indeed, its almost 100% sensitivity in detecting splenic injury has substantially decreased the need for abdominal arteriography and exploratory surgery. Subcapsular hematomas appear on CT as crescentic collections of fluid that flatten or indent the lateral margin of the spleen (Figure 5-117). Splenic lacerations, which may occur with or without an accompanying subcapsular hematoma, produce a CT appearance of splenic enlargement, an irregular cleft or defect in the splenic border, and free blood in the peritoneal cavity.

Before the advent of CT, splenic arteriography was the procedure of choice for demonstrating splenic rupture. Major positive findings include extravasation of contrast material into the splenic parenchyma, obstruction of a major splenic artery, and—in an enlarged spleen—vascular defects that indicate sites of rupture and hematoma.