Gastrointestinal System

Chapter 5

Gastrointestinal System


As in other body systems, certain pathologic conditions in the gastrointestinal (GI) system require alterations in the technical factors chosen for imaging. In patients with ascites, a common complication of advanced cirrhosis, an increased kilovolt peak (kVp) is required to penetrate the additional fluid content of the abdomen. On the other hand, a decreased kVp is needed in patients with suspected large or small bowel obstruction because of the excessive amount of gas in the abdominal cavity. When using a computed radiography or a direct digital imaging system, the radiographer should still consider the pathology condition in relationship to its attenuation factor.

The radiographer is usually called on to assist the radiologist during fluoroscopic examinations of the GI tract. Indeed, it is generally the radiographer’s task to coerce the patient into drinking (and not vomiting) the rather unpleasant-tasting contrast material and to urge the patient to turn around several times to provide adequate mucosal coating for the double-contrast upper GI series. Similarly, the radiographer may have to persuade the patient to retain barium and air during the often uncomfortable barium enema examinations. It is frequently time well spent for the radiographer to explain fully to the patient both the mechanics of the procedure and the extreme importance of patient cooperation.

Radiographer Notes

Plain abdominal radiographs and contrast studies of the digestive tract remain the most common imaging examinations of the gastrointestinal system. Ultrasound and computed tomography (CT) are the major imaging modalities for the pancreas and biliary tract, and magnetic resonance imaging (MRI) is now being used in some institutions to screen for hepatic metastases.

Plain abdominal radiographs must illustrate an appropriate scale of contrast to demonstrate the many different tissue densities in the abdominal cavity. When using a screen-film combination, this goal requires the use of a middle to high kVp range (70 to 80 kVp). The use of digital imaging does allow for a slight increase in the kVp range as the contrast is controlled by the digital processing parameters. Bony structures, such as the lumbar spine and its transverse processes, must be well demonstrated along with soft tissue shadows of the liver, kidney, and psoas muscle. For barium studies of the gastrointestinal tract, adequate penetration of the dense barium solution requires a high kVp range (about 120 kVp). For double-contrast (air-barium) studies, a kVp range of 90 to 100 kVp is needed to allow penetration of the barium combined with excellent visualization of mucosal detail. Gallbladder studies require a shorter scale of contrast than other abdominal examinations and therefore are usually performed with a kVp in the low to middle range (about 70 kVp). Computed radiography and direct imaging systems utilize the computer algorithm to control the image contrast, so the use of slightly higher kVp ranges (approximately 10 kVp higher) to produce the same images as obtained on screen-film systems aids in reducing the patient radiation dose. The radiographer must select the proper algorithm (combination of procedure and position) to obtain an image with the proper contrast and density.

Physiology of the digestive system

The basic function of the digestive system is to alter the chemical and physical composition of food so that it can be absorbed and used by body cells. This process depends on secretions of the endocrine and exocrine glands and on the controlled movement of ingested food through the tract so that absorption can occur (Figure 5-1).

Digestion begins in the mouth with chewing (mastication), the mechanical breakdown of food. The secretion of saliva moistens the food in preparation for swallowing. Swallowing (deglutition) is a complex process that requires coordination of many muscles in the head and neck and the precise opening and closing of esophageal sphincters. Digestion continues in the stomach with the churning movement of gastric contents that have become mixed with hydrochloric acid and the proteolytic enzyme pepsin (Figure 5-2). The resulting milky white chyme is propelled through the pyloric sphincter into the duodenum by rhythmic smooth muscle contractions called peristalsis.


Figure 5-2 Stomach

The greatest amount of digestion occurs in the duodenum, the first part of the small bowel. In addition to intestinal secretions containing mucus and enzymes, secretions of the pancreas and liver enhance digestion in this region. The pancreas secretes enzymes for the digestion of proteins (trypsin and chymotrypsin), fat (lipase), and carbohydrates (amylase). It also secretes an alkaline solution to neutralize the acid carried into the small intestine from the stomach. Bile is secreted by the liver, is stored in the gallbladder, and enters the duodenum through the common bile duct. Bile is an emulsifier, a substance that acts like soap by dispersing the fat into very small droplets that permit it to mix with water.

When digestion is complete, the nutrients are absorbed through the intestinal mucosa into blood capillaries and lymph vessels of the wall of the small bowel. The inner surface area of the small bowel is increased by the formation of numerous finger-like projections (villi), which provide the largest amount of surface area possible for digestion and absorption.

Material that has not been digested passes into the colon, where water and minerals are absorbed, and the remaining matter is excreted as feces (Figure 5-3). If the contents of the lower colon and rectum move at a rate that is slower than normal, extra water is absorbed from the fecal mass to produce a hardened stool and constipation. Diarrhea results from increased motility of the small bowel, which floods the colon with an excessive amount of water that cannot be completely absorbed.

The vermiform (worm-shaped) appendix arises from the inferomedial aspect of the cecum about 3 cm below the ileocecal valve. Although the appendix has no functional importance in digestion, it is often classified as an accessory digestive organ merely because of its location.

The liver is the largest gland in the body and is responsible for several vital functions. Liver cells detoxify (make harmless) a variety of poisonous substances that enter the blood from the intestines. Toxic chemicals that are changed to nontoxic compounds in the liver include ammonia (converted to urea and excreted by the kidneys), alcohol, and barbiturates. Liver cells secrete about 1 pint of bile each day. As mentioned, bile is an emulsifier; it is essential for the digestion and absorption of dietary fat and the fat-soluble vitamins A, D, E, and K. Bile is a greenish liquid consisting of water, bile salts, cholesterol, and bilirubin (a breakdown product of hemoglobin).

Liver cells play a vital role in the metabolism of proteins, fats, and carbohydrates. The liver is the major site of synthesis of the enzymes necessary for various cellular activities throughout the body. Liver cells also synthesize blood proteins, such as albumin, which maintains the correct amount of fluid within blood vessels, and the essential proteins required for blood clotting (fibrinogen and prothrombin). Therefore, liver damage may result in edema (excess water in the soft tissues) and a serious bleeding tendency. The liver plays an important role in maintaining the proper level of glucose in the blood by taking up excess glucose absorbed by the small intestine and storing it as glycogen. When the level of circulating glucose falls below normal, the liver breaks down glycogen and releases glucose into the bloodstream. Liver cells also store iron and vitamins A, B12, and D.

The gallbladder is a pear-shaped sac that lies on the undersurface of the liver (Figure 5-4). Its function is to store bile that enters by way of the hepatic and cystic ducts and to concentrate the bile by absorbing water. In response to the presence of dietary fat in the small bowel, the gallbladder contracts and ejects the concentrated bile into the duodenum.

The pancreas controls the level of circulating blood glucose by secreting insulin and glucagon in the islets of Langerhans. An increased concentration of glucose in the blood stimulates the beta cells to increase secretion of insulin, which decreases the blood glucose level probably by accelerating the transport of glucose into cells. A blood glucose concentration less than normal triggers the alpha cells to secrete glucagon, which accelerates the breakdown of glycogen into glucose by the liver.

As discussed, pancreatic secretions are vital for digestion. Pancreatic enzymes that pass through the pancreatic duct into the duodenum are necessary for the breakdown of proteins, carbohydrates, and fats.


Tracheoesophageal Fistula

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.

Radiographic Appearance: In the second most common type of esophageal anomaly, type I, both the upper and lower segments of the esophagus are blind pouches. This anomaly can be differentiated from the type III lesion (the most common type) only by plain abdominal radiographs, which demonstrate the absence of air below the diaphragm in the type I lesion and the presence of air below the stomach in the type III lesion.

In the type II form of TE fistula, the upper esophageal segment communicates with the trachea, whereas the lower segment ends in a blind pouch. Because there is no connection between the trachea and the stomach, there is no radiographic evidence of gas within the abdomen. Oral administration of contrast material in this condition immediately outlines the tracheobronchial tree.

The type III TE fistula (seen in 85% to 90% of cases) consists of an upper segment that ends in a blind pouch at the level of the bifurcation of the trachea or slightly above it, and a lower segment attached to the trachea by a short fistulous tract. Radiographic demonstration of the looping of a small esophageal feeding tube indicates that the proximal esophagus ends in a blind pouch (Figure 5-5A). Plain radiographs of the abdomen demonstrate the presence of air in the bowel that has freely entered the stomach through the fistulous connection between the trachea and the distal esophagus.

There are two forms of type IV TE fistula. In one, the upper and lower esophageal segments end in blind pouches, both of which are connected to the tracheobronchial tree. In this form, gas is seen in the stomach, and oral contrast material outlines both fistulas and the bronchial tree. In the other form of type IV TE fistula (called an H fistula), both the trachea and the esophagus are intact. These two structures are connected by a single fistulous tract that can be found at any level from the cricoid cartilage of the trachea to the tracheal bifurcation (Figure 5-5B). Unlike the other forms of TE fistula, the H fistula may not be identified in infancy and, if it is small and only occasionally causes emptying of material into the lungs, can permit survival into adulthood.

Computed tomography (CT) esophagography without use of a contrast agent that is performed using a multidetector CT scanner with three-dimensional reconstructions demonstrates TE fistulas. CT is less invasive than contrast radiography and provides clinicians with critical surgical planning information.

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.

Radiographic Appearance: The earliest radiographic findings in reflux esophagitis are detectable on double-contrast studies. They consist of superficial ulcerations or erosions that appear as streaks or dots of barium superimposed on the flat mucosa of the distal esophagus. In single-contrast studies of patients with esophagitis, the outer borders of the barium-filled esophagus are not sharply seen but rather have a hazy, serrated appearance with shallow, irregular protrusions indicating erosions of varying length and depth. Widening and coarsening of edematous longitudinal folds can simulate filling defects. In addition to diffuse erosion, reflux esophagitis can result in large, discrete, penetrating ulcers in the distal esophagus (Figure 5-8) or in a hiatal hernia sac (Figure 5-9). Fibrotic healing of diffuse reflux esophagitis or a localized penetrating ulcer may cause narrowing of the distal esophagus. Strictures resulting from reflux esophagitis tend to be smooth and tapering with no demonstrable mucosal pattern (Figure 5-10).

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).

Radiographic Appearance: Although a hiatal hernia with gastroesophageal reflux is commonly demonstrated, Barrett’s ulcer is usually separated from the hiatal hernia by a variable length of normal-appearing esophagus (Figure 5-11), in contrast to reflux esophagitis, in which the distal esophagus is abnormal down to the level of the hernia. As in reflux esophagitis, fibrotic healing of the ulceration in Barrett’s esophagus often leads to a smooth, tapered stricture (Figure 5-12).

Because the distal esophagus consists of a gastric type of mucosa in Barrett’s esophagus, it actively takes up the intravenously injected radionuclide pertechnetate. The demonstration of a continuous concentration of the isotope from the stomach into the distal esophagus to a level that corresponds approximately to that of the ulcer or stricture is indicative of Barrett’s esophagus.

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.

Ingestion of Corrosive Agents

The ingestion of alkaline or acidic corrosive agents produces acute inflammatory changes in the esophagus. Superficial penetration of the toxic agent results in only minimal ulceration. Deeper penetration of the submucosa and muscular layers causes sloughing of destroyed tissue and deep ulceration. Ingestion of strong alkaline agents causes deeper lesions than ingestion of strong acids, and only half of those who ingest an acid suffer severe injury. Drug-induced esophagitis may occur in patients who have delayed esophageal transit time, which permits prolonged mucosal contact with the ingested substance. The most common drug causing esophageal ulceration is potassium chloride in tablet form. Other medications that can cause esophagitis are weak caustic agents that are harmless when they pass rapidly through the esophagus.

Esophageal Cancer

Progressive difficulty in swallowing (dysphagia) in a person older than 40 years must be assumed to be caused by cancer until proven otherwise. Because the symptoms of esophageal carcinoma tend to appear late in the course of the disease, and because the lack of a limiting outer layer (serosa) commonly permits direct extension of the tumor by the time of the initial diagnosis, carcinoma of the esophagus has a dismal prognosis. Most carcinomas of the esophagus are of the squamous cell type and they occur most often at the esophagogastric junction. The incidence of carcinoma of the esophagus is far higher in men than in women. There is a strong correlation between excessive alcohol intake, smoking, and esophageal carcinoma.

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.

Esophageal Diverticula

Esophageal diverticula (outpouchings) are common lesions that either contain all layers of the wall (traction or true diverticula) or are composed of only mucosa and submucosa herniating through the muscular layer (pulsion or false diverticula). Small diverticula do not retain food or secretions and are asymptomatic. When a diverticulum fills with food or secretions, aspiration pneumonia may result.

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.

Esophageal Varices

Esophageal varices are dilated veins in the wall of the esophagus that are most commonly the result of increased pressure in the portal venous system (portal hypertension), which is in turn usually a result of cirrhosis of the liver. In patients with portal hypertension, much of the portal blood cannot flow along its normal pathway through the liver to the inferior vena cava and then on to the heart. Instead, it must go by a circuitous collateral route, and increased blood flow through these dilated veins causes the development of esophageal (and gastric) varices. Esophageal varices are infrequently demonstrated in the absence of portal hypertension. “Downhill” varices are produced when venous blood from the head and neck cannot reach the heart because of an obstruction of the superior vena cava caused by tumors or inflammatory disease in the mediastinum. In this situation, blood flows “downhill” through the esophageal veins before eventually entering the portal vein, through which it flows to the inferior vena cava and the right atrium.

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.

Hiatal Hernia

Hiatal hernia is the most common abnormality (occurring in 50% of the population) detected on upper GI examination. Its broad radiographic spectrum ranges from large esophagogastric hernias, in which much of the stomach lies within the thoracic cavity and there is a predisposition to volvulus (twisting), to small hernias that emerge above the diaphragm only under certain circumstances (related to changes in intraabdominal or intrathoracic pressure) and easily slide back into the abdomen through the hiatus (sliding hiatal hernia). The symptoms associated with hiatal hernia and its complications (esophagitis, esophageal ulcer, esophageal stenosis) are related to the presence of esophageal reflux rather than to the hiatal hernia itself. Most hiatal hernias do not produce symptoms and are clinically of no importance.

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.


Achalasia is a functional obstruction of the distal section of the esophagus with proximal dilation caused by incomplete relaxation of the lower esophageal sphincter. It is related to a paucity or absence of ganglion cells in the myenteric neural plexuses of the distal esophageal wall.

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.

Foreign Bodies

A wide spectrum of foreign bodies can become impacted in the esophagus, usually in the cervical esophagus at or just above the level of the thoracic inlet (Figure 5-26). Symptomatically, the patient is unable to swallow without regurgitation. Most metallic objects, such as pins, coins, and small toys, are radiopaque and are easily visualized on radiographs or during fluoroscopy. Objects made of aluminum and some light alloys may be impossible to detect radiographically because the density of these metals is almost equal to that of soft tissue. It is essential that any suspected foreign body be evaluated on two projections to be certain that the object projected over the esophagus truly lies within it.

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.

Perforation of the Esophagus

Perforation of the esophagus may be a complication of esophagitis, peptic ulcer, neoplasm, external trauma, or instrumentation. At times, perforation of a previously healthy esophagus can result from severe vomiting (the most common cause) or coughing, often from dietary or alcoholic indiscretion. Complete rupture of the wall of the esophagus may cause the sudden development of severe upper gastric pain simulating that of myocardial infarction. In the Mallory-Weiss syndrome, an increase in intraluminal and intramural pressures associated with vomiting (severe retching) after an alcoholic bout causes superficial mucosal laceration or fissures near the esophagogastric junction that produce severe hemorrhage. Endoscopy is required to best demonstrate lacerations, especially those close to the sphincter.



Inflammation of the stomach can be the result of a variety of irritants including alcohol, corrosive agents, and infection. Gastritis changes the normal surface pattern of the gastric mucosa. Helicobacter pylori can cause chronic gastritis that may lead to peptic ulcer disease.

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).

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.

Peptic Ulcer Disease

Peptic ulcer disease is a group of inflammatory processes involving the stomach and duodenum. It is caused by the action of acid and the enzyme pepsin secreted by the stomach and occurs most frequently on the lesser curvature. The spectrum of peptic ulcer disease varies from small and shallow superficial erosions to huge ulcers that may perforate through the bowel wall.

The major complications of peptic ulcer disease are hemorrhage (20%), gastric outlet obstruction (5% to 10%), and perforation (less than 5%). Peptic ulcer disease is the most common cause of acute upper GI bleeding. Free perforation of a peptic ulcer located in the anterior wall of the stomach or duodenum is the most common cause of pneumoperitoneum with peritonitis (see later discussion “Pneumoperitoneum”). Narrowing of the lumen of the distal stomach or duodenal bulb caused by peptic ulcer disease is by far the most common cause of gastric outlet obstruction.

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).

Radiographic Appearance: An unequivocal diagnosis of active duodenal ulcer requires the demonstration of an ulcer crater, which appears in profile as a small collection of barium projecting from the lumen. When seen en face (face on), the ulcer niche appears as a rounded or linear collection of contrast material surrounded by lucent folds that often radiate toward the crater (Figure 5-32). Secondary signs of duodenal ulcer disease include thickening of the mucosal folds and a deformity of the duodenal bulb. Acute ulcers incite muscular spasm, leading to deformity of the margins of the duodenal bulb that may be inconsistent and varied during the examination. With chronic ulceration, fibrosis and scarring cause a fixed deformity that persists even though the ulcer heals. Symmetrical narrowing of the duodenal bulb in its midportion may produce the typical cloverleaf deformity of chronic duodenal ulcer disease (Figure 5-33). CT demonstrates an irregularity or collection of contrast material in the gastric wall; however, as with barium studies, this appearance may be difficult to differentiate from that of malignancy.

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.

Radiographic Appearance: Radiographic signs that indicate whether a gastric ulcer is more likely to be benign or malignant have been described. The classic sign of a benign gastric ulcer in profile is penetration, with clear projection of the ulcer outside the normal barium-filled gastric lumen because the ulcer represents an excavation in the wall of the stomach (Figure 5-34). A thin lucency at the base of the ulcer, reflecting mucosal edema caused by inflammatory exudate, is another sign of benignancy. When viewed en face, a gastric ulcer appears as a persistent collection of barium surrounded by a halo of edema (the ulcer collar) (Figure 5-35).

A hallmark of benign gastric ulcer is radiation of mucosal folds to the edge of the crater. However, because radiating folds can be identified in both malignant and benign ulcers, the character of the folds must be carefully assessed. If the folds are smooth and slender and appear to extend into the edge of the crater, the ulcer is most likely benign (Figure 5-36A). In contrast, irregular folds that merge into a mound of polypoid tissue around the crater are suggestive of malignancy (Figure 5-36B).

Although the size, shape, number, and location of gastric ulcers have been suggested as criteria for distinguishing between benign and malignant lesions, these findings are of little practical value. One exception is ulcers in the gastric fundus above the level of the esophagogastric junction—essentially all of which are malignant.

An abrupt transition between the normal mucosa and the abnormal tissues surrounding a gastric ulcer is characteristic of a malignant lesion (Figure 5-37), in contrast to the diffuse and almost imperceptible transition between the normal gastric mucosa and the mound of edema surrounding a benign ulcer. Neoplastic tissue surrounding a malignant ulcer is usually nodular, unlike the smooth contour of the edematous mound around a benign ulcer. A malignant ulcer does not penetrate beyond the normal gastric lumen but remains within it because the ulcer merely represents a necrotic area within an intramural or intraluminal mass.

Most benign gastric ulcers heal completely with medical therapy (see “Treatment of Ulcers”) (Figure 5-38). Complete healing does not necessarily mean that the stomach returns to an absolutely normal radiographic appearance; bizarre deformities can result from fibrotic retraction and stiffening of the stomach wall. Although many malignant ulcers show significant healing, there is almost never complete disappearance of the ulcer crater.

The role of endoscopy in evaluating patients with gastric ulcers is controversial. At present, endoscopy is indicated only when the radiographic findings are not typical for a benign ulcer, when healing of the ulcer does not progress at the expected rate, or when the mucosa surrounding a healed ulcer crater has a nodular surface or any other feature suggestive of an underlying early gastric cancer.

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”).

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Apr 10, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Gastrointestinal System

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