Chapter 5 After reading this chapter, the reader will be able to: 1 Classify the more common diseases in terms of their attenuation of x-rays 2 Explain the changes in technical factors required for obtaining optimal quality radiographs in patients with various underlying pathologic conditions 3 Define and describe all bold-faced terms in this chapter 4 Describe the physiology of the gastrointestinal system 5 Identify anatomic structures on both diagrams and radiographs of the gastrointestinal system 6 Differentiate the various pathologic conditions affecting the gastrointestinal system and their radiographic manifestations 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. 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. 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. 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. Radiographic Appearance: After traumatic perforation of the thoracic esophagus, chest radiographs may demonstrate air dissecting within the mediastinum and soft tissue, often with pleural effusion or hydropneumothorax. The introduction of an oral contrast agent may demonstrate the site of perforation and the extent of fistulization. Reflux (Gastroesophageal Reflux Disease) 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. 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). 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). Figure 5-11 Barrett’s esophagus. Ulcerations (arrow) have developed at a distance from esophagogastric junction. Figure 5-12 Barrett’s esophagus. Note the smooth, tapered stricture in the upper thoracic esophagus. Radiographic Appearance: The classic radiographic appearance of infectious esophagitis is an irregular cobblestone pattern with a shaggy marginal contour of the esophagus caused by deep ulcerations and sloughing of the mucosa (Figure 5-13). Candida infection manifests as plaques and nodules resulting from a superficial collection of fungi. Characteristics of herpetic esophagitis include small mucosal ulcers or plaques. Radiographic Appearance: Healing of the intense mucosal and intramural inflammation of acute esophagitis may lead to pronounced fibrosis and stricture formation. These benign strictures tend to be long lesions with tapered margins and relatively smooth mucosal surfaces (Figure 5-14), in contrast to the irregular narrowing, mucosal destruction, and overhanging margins that are generally associated with malignant processes. Treatment: The type of agent ingested determines the therapy. The local or state poison control service is usually called for specific treatments if the situation is not drug induced. Vomiting is generally not induced because this would cause a second exposure of the esophagus to the agent. Dilution by administration of milk or water is appropriate unless the corrosive agent is acidic (in this case, water should not be used as it would produce excessive heat). 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. 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. Figure 5-21 Esophageal varices. Note the diffuse round and oval filling defects, which resemble rosary beads. 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. 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. 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. 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, 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: 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. 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).
Gastrointestinal System
Physiology of the digestive system
Esophagus
Congenital Type
Acquired Type
Esophagitis
Barrett’s Esophagus
Candida and Herpesvirus
Ingestion of Corrosive Agents
Esophageal Cancer
Radiographic Appearance
Esophageal Diverticula
Radiographic Appearance
Esophageal Varices
Radiographic Appearance
Hiatal Hernia
Radiographic Appearance
Achalasia
Radiographic Appearance
Perforation of the Esophagus
Stomach
Radiographic Appearance
Pyloric Stenosis
Peptic Ulcer Disease
Duodenal Ulcer
Gastric Ulcer
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Gastrointestinal System
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