Diseases of the Stomach


Other Gastric Lesions

Menetrier’s Disease

Menetrier’s disease (giant hypertrophic gastritis) is an uncommon disorder of unknown cause that is charac¬terized by massive enlargement of rugal folds due to hyperplasia of the gastric glands. There is usually hy posecretion of acid and excessive secretion of gastric mucus. Loss of protein into the lumen of the stomach may result in hypoproteinemia and edema. The thick-ened gastric rugae become contorted and folded on each other in a convolutional pattern suggestive of the gyri and sulci of the brain. Enlarged rugal folds are particu¬larly prominent along the greater curvature. Although the disorder is classically described as a lesion of the fundus and body, involvement of the entire stomach can occur. The disease can be diffuse or localized, and the transition between normal and pathologic folds is usually abrupt.
Radiographically, affected rugal folds are thick, tor¬tuous, and angular with no uniformity in pattern or di¬rection. When seen on end, the folds may closely simulate polypoid filling defects. Lines of barium can be seen perpendicular to the stomach because of spicules of contrast material trapped by apposed giant rugal folds.

Menetrier’s disease must be differentiated from a malignant process, especially lymphoma. If the thickened rugal folds predominantly involve the fundus and spare the lesser curvature, if there is no ulceration or true rigidity, or if excess mucus can be demonstrated, Menetrier’s disease is the probable diagnosis. If the enlarged rugal folds predominantly involve the distal portion of the stomach and the lesser curvature, or if there’ is some loss of pliability of the gastric wall, lymphoma is more likely.

Gastric Mucosal Prolapse

Redundant mucosa of the gastric antrum can prolapse through the pylorus under the influence of active peristalsis, resulting in single or tabulated filling defects at the base of the duodenal bulb. Mucosal folds in the prepyloric area of the stomach can usually be traced through the pylorus to the base of the bulb, where they become continuous with the characteristic mushroom-, umbrella-, or cauliflower-shaped prolapsed mass. Under fluoroscopy, mucosal prolapse can be detected as a gastric peristaltic wave passes through the antrum. As the wave relaxes, the mucosal folds tend to return into the antrum, and the defect in the base of the bulb diminishes or completely disappears. Some degree of mucosal prolapse is frequently observed during gastrointestinal examinations. Antral prolapse is generally considered to be asymptomatic, though associated ulceration and bleeding have occasionally been reported.

Gastric Volvulus

Gastric volvulus is an uncommon acquired twist of the stomach upon itself that can lead to gastric outlet obstruction. It usually occurs in conjunction with a large paraesophageal hernia or eventration of the diaphragm that permits part or all of the stomach to assume an intrathoracic position. Organoaxial volvulus refers to rotation of the stomach upward along its long axis (a line connecting the cardia with the pylorus). In this condition, the antrum moves from an inferior to a superior position. In the mesenteroaxial type of gastric volvulus, the stomach rotates from right to left or left to right around the long axis of the gastrohepatic omentum (a line connecting the middle of the lesser curvature with the middle of the greater curvature).

Gastric volvulus can be asymptomatic if there is no outlet obstruction or vascular compromise. Acute volvulus associated with interference of the blood supply is a surgical emergency with a high mortality rate.

The radiographic signs of gastric volvulus are characteristic. They include a double air-fluid level on upright films, inversion of the stomach with the greater curvature above the level of the lesser curvature, positioning of the cardia and pylorus at the same level, and downward pointing of the pylorus and duodenum.

Foreign Bodies and Bezoars

Small blunt foreign bodies such as coins, marbles, or even closed safety pins usually pass through the stomach and bowel without difficulty. Elongated, sharp objects such as needles, toothpicks, or open safety pins may hold up at some point and cause obstruction, ulceration, bleeding, abscess, or peritonitis. Metallic foreign bodiesappear opaque on plain abdominal radiographs. Non-metallic foreign bodies appear as lucent filling defects within the barium-filled stomach.

A bezoar is an intragastric mass composed of accumulated ingested material. Phytobezoars, which are composed of undigested vegetable material, have classically been associated with the eating of unripe persimmons. This fruit contains substances that coagulate on contact with gastric acid to produce a sticky gelatinous material, which then traps seeds, skin, and other foodstuffs. Trichobezoars (hairballs) occur predominantly in females, especially those with schizophrenia or other mental disorders. Bezoars in the gastric remnant are a common complication following partial gastric resection with Billroth I or II anastomoses. The chief constituent of postgastrectomy bezoars is the fibrous, pithy component of fruits and vegetables, the consumption of which should be reduced as much as possible in postgastrectomy patients.

Symptoms of gastric bezoars result from the mechanical presence of the foreign body. They include cramplike epigastric pain and a sense of dragging, fullness, lump, or heaviness in the upper abdomen. The incidence of associated peptic ulcers is high, especially with the more abrasive phytobezoars. When bezoars are large, symptoms of pyloric obstruction can clinically simulate symptoms of a gastric carcinoma. Occasionally, bezoars can lodge in the jejunum or ileum and cause small bowel obstruction.

Plain abdominal radiograpl often show a bezoar as a soft tissue mass floating in the stomach at the air-fluid interface. On barium studies, contrast material coating the mass and infiltrating into the interstices results in a characteristic mottled or streaked appearance. The filling defect may oc sionally be completely smooth, simulating an enor.uous gas bubble that is freely movable within the stomach.

Atrophic Gastritis

In atrophic gastritis, severe mucosal atrophy may cause thinning and a relative absence of mucosal folds, with the fundus or the 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; it also occurs in patients with pernicious anemia. Although atrophic gastritis itself does not produce symptoms, the condition is associated with an increased incidence of gastric malignancy. Conversely, in the elderly an atrophic stomach may be hypotonic and show limited distensibility, simulating scirrhous carcinoma.

Eosinophilic Gastritis

Eosinophilic gastritis causes thickening of the muscular layer of the wall of the stomach due to edema and a diffuse infiltrate of predominantly mature eosinophils. It primarily involves the antrum and produces irregular narrowing and rigidity (linitis plastica pattern) that may simulate an infiltrating carcinoma. The disease is characterized by peripheral eosinophilia and the development of gastrointestinal symptoms and signs following the ingestion of specific foods. Although eosinophilic gastritis can simulate a more aggressive process, it is essentially a benign condition that is self-limited and often completely returns to normal after steroid therapy.

Corrosive Gastritis

The ingestion of corrosive agents results in a severe form of acute gastritis characterized by intense mucosal edema and inflammation. RadiographicaIly, thickened gastric folds are associated with mucosal ulcerations, atony, and rigidity. A fixed, open pylorus is usually seen, probably due to extensive damage to the muscular layer. The presence of gas in the wall of the stomach after the ingestion of corrosive agents is an ominous sign that may precede the development of free gastric perforation.

Corrosive gastritis predominantly involves the antrum, though the entire stomach may be involved. Ingested acids generally produce more severe gastric damage than ingested alkalies, in contrast to the effects of acids and alkalies on the esophagus.

The acute inflammatory reaction of corrosive gastritis heals by fibrosis and scarring, which results in stricturing of the antrum within several weeks of the initial injury. In patients who have rigidity and narrowing of the stomach without a history of corrosive ingestion, the clinical symptoms of weight loss and early satiety, combined with the radiographic pattern of narrowing of the stomach (linitis plastica), can be impossible to distinguish from gastric malignancy.

stomach cancer · esophagus surgeries · Bariatric surgery ·

Benign Tumors of The Stomach

Leiomyoma and Rare Benign Tumors

Spindle cell tumors constitute the overwhelming majority of benign submucosal gastric neoplasms. These lesions vary in size from tiny nodules, often discovered incidentally at laparotomy or autopsy, to bulky tumors with large intraluminal components, that can be associated with hemorrhage, obstruction, or perforation. Exo-gastric extension of these tumors can mimic extrinsic compression of the stomach by normal or enlarged liver, spleen, pancreas, or kidney. It may be extremely difficult to distinguish radiographically between benign spindle cell tumors and their malignant counterparts. Although large, markedly irregular filling defects with prominent ulcerations suggest malignancy, a radiographically benign tumor can be histologically malignant.

Leiomyoma is the most common spindle cell tumor of the stomach. Usually single rather than multiple, leiomyomas may present as small, rounded filling defects simulating sessile polyps or as large lesions predominantly located in intraluminal, intramural, or extramural locations. Because of their tendency toward central necrosis and ulceration, bleeding is common as the tumor grows.

Lipomas, fibromas, hemangiomas, leiomyoblastomas (granular cell tumors), and neurogenic tumors, all of which can be radiographically indistinguishable from leiomyomas, are far less common submucosal gastric neoplasms.

benign tumor in stomach · benign stomach tumor · benign tumors of the stomach ·

Malignant Tumors of the Stomach


Carcinoma of the stomach has a dismal prognosis because symptoms are rarely noted until the disease is far advanced. The incidence of gastric cancer varies widely throughout the world. It is very high in Japan, Chile, and parts of eastern Europe, while low in the United States, where for an unknown reason the incidence of the disease has been decreasing. Atrophic gastric mucosa, as in pernicious anemia, especially when associated with intestinal metaplasia, appears to be a predisposing factor. Adenomatous gastric polyps more than 2 cm in diameter frequently contain carcinoma, although it is un clear whether these uncommon large polyps are malignant from the outset or whether they were originally benign. There is also an increased risk of gastric cancer 10 to 20 years following a Billroth II partial gastrectomy for peptic ulcer disease.

Gastric carcinoma can present a broad spectrum of radiographic appearances. Tumor infiltration of the gastric wall may stimulate a desmoplastic response, which produces diffuse thickening, narrowing, and fixation of the stomach wall (linitis plastica pattern). The involved stomach is contracted into a tubular structure without normal pliability. This scirrhous process usually begins near the pylorus and progresses slowly upward, the fundus being the area least involved. Gastric carcinoma can also cause segmental narrowing of the stomach. At an early stage, this may appear as a plaquelike infiltrative lesion along one curvature that progresses to form a constricting lesion similar to that produced by annular carcinoma of the colon.

Polypoid masses larger than 2 cm, partic ularly sessile ones, are often malignant, though many are benign. Irregularity and ulceration suggest malignancy; a stalk, pliability of the wall of the stomach, normal-appearing gastric folds extending to the tumor, and unimpaired peristalsis are signs of benignancy. Mottled, granular calcific deposits in association with a gastric mass suggest mucinous adenocarcinoma of the stomach.

Ulceration can develop in any gastric carcinoma. The radiographic appearance of malignant ulceration runs the gamut from shallow erosions in relatively superficial mucosal lesions to huge excavations within fungating polypoid masses. Signs of malignant ulcer include a lac k of penetration beyond the normal gastric lumen; an abrupt transition between the nodular surrounding neoplastic tissue and the normal mucosa; and adjacent infiltration, rigidity, and mucosal destruction. Although many malignant ulcers show significant healing in response to therapy, there is almost never complete disappearance of the ulcer crater. Endoscopy is indicated if there are radiographic findings suspicious of malignancy or if the ulcer does not heal at the expected rate.

Gastric carcinoma infrequently presents a radiographic pattern of enlarged, tortuous, and coarse gastric folds simulating lymphoma. Unlike most cases of diffuse infiltrating adenocarcinoma, in this form of the disease the gastric volume, pliability, and peristaltic activity remain relatively normal.

In the fundus, carcinoma frequently extends proximally to involve the distal esophagus, producing a radiographic appearance that mimics achalasia.

Following surgery, recurrence of a gastric carcinoma can cause a defect in the gastric remnant, infiltration of the wall with straightening and loss of normal distensibility, or mucosal destruction with superficial ulceration. The major sign of recurrence at the anastomosis is symmetric or eccentric narrowing with local mucosal effacement.

Computed tomography is of major value in the staging and treatment planning of gastric carcinoma as well as in assessing the response to therapy and in detecting recurrence. Carcinoma of the stomach may appear as concentric or focal thickening of the gastric wall or as an intraluminal mass. Obliteration of the perigastric fat planes is a reliable indicator of the extragastric spread of tumor. Computed tomography can demonstrate direct tumor extension to intra-abdominal organs and distant metastases to the liver, ovary, adrenals, kidney, and peritoneum.


As elsewhere in the bowel, in the stomach lymphoma is a great imitator of both benign and malignant disease. One manifestation of lymphoma of the stomach is a large, bulky polypoid lesion, usually irregular and ulcerated, that can be difficult to differentiate from gastric carcinoma. These polyps can be combined with thickened folds (infiltrative form of lymphoma) or separated by a normal-appearing mucosal pattern, unlike the atrophic mucosal background that is seen with multiple carcinomatous polyps in patients with pernicious anemia. A multiplicity of ulcerated masses suggests lymphoma, as does relative flexibility of the gastric wall.

Thickening, distortion, and nodularity of gastric rugal folds simulating Menetrier’s disease is another pattern of lymphoma of the stomach. If the enlarged rugal folds predominantly involve the distal portion of the stomach and the lesser curvature, or if there is some loss of pliability of the gastric wall, lymphoma is more likely. However, if the process stops at the incisura and spares the lesser curvature, if there is no ulceration or true rigidity, or if excess mucus can be demonstrated, Menetrier’s disease is the probable diagnosis.

Invasion of the gastric wall by an infiltrative type of lymphoma can cause a severe desmoplastic reaction and a radiographic pattern that mimics the linitis plastica appearance of scirrhous carcinoma. Unlike the rigidity and fixation of scirrhous carcinoma, residual peristalsis and flexibility of the stomach wall are often preserved in lymphoma.

Enlargement of the spleen and an extrinsic impression on the stomach by retrogastric and other regional lymph nodes suggest lymphoma as the underlying disorder.

On CT, gastric lymphoma tends to produce bulky masses and a lobulated inner contour of the gastric wall representing thickened gastric rugae. However, gastric lymphoma may also produce smooth, concentric wall thickening or a focal mass simulating adenocarcinoma of the stomach. The demonstration of other signs of lymphoma (splenomegaly, diffuse retroperitoneal and mesenteric lymphadenopathy), when present, suggests the correct histologic diagnosis.


Gastric leiomyosarcomas are large, bulky tumors most often found in the body of the stomach. Although originally arising in an intramural location, leiomyosarcomas often present as intraluminal, occasionally pendunculated masses. They frequently undergo extensive central necrosis, causing ulceration and gastrointestinal bleeding. Extensive spread into the surrounding tissues is common (as are metastases to the liver, omentum, and retroperitoneum), and the resulting large exogastric component may suggest an extrinsic lesion. It is frequently impossible to radiographically differentiate a leiomyosarcoma from a benign leiomyoma, though the presence of a large exogastric mass suggests a malignancy.

Computed tomography may demonstrate either the primary intragastric lesion or the large extraluminal component of a leiomyosarcoma. Characteristic findings in tumors of this histologic type are small foci of calcification and well-defined, low-density areas within the mass representing either areas of necrosis and liquefaction or a cystic component to the tumor. Unlike gastric adenocarcinoma or lymphoma, gastric leiomyosarcoma commonly metastasizes to the liver and lung, while spread to regional lymph nodes is unusual.”

stomach · gastric cancer · tumor in stomach ·

Complications and Syndromes After Peptic Ulcer Surgery

Recurrent Ulceration

Recurrent (marginal) ulceration develops in about 5 percent of patients following surgery for peptic ulcer disease. Recurrence is much more common following vagotomy and pyloroplasty (6 to 8 percent) than after vagotomy and antrectomy (less than 2 percent). The marginal ulcer is really not a recurrent one, but rather represents a new ulceration due to the residual action of acid and pepsin on the sensitive intestinal mucosa. Thus it is usually situated in the jejunum within the first few centimeters of the anastomosis. Because marginal ulcers are rarely found on the gastric side of the anastomosis, development of postoperative ulceration at this site should suggest the possibility of gastric stump malignancy. In most cases, the site of the original ulcer for which surgery was performed is the duodenum; marginal ulcers are much less frequent following surgery for gastric ulcers.

Because up to half of marginal ulcers are too superficial or shallow to be detected radiographicaliy, endoscopy is often required for diagnosis. Overlapping jejunal mucosal folds or surgical deformity can hide an ulcer; conversely, barium trapped between converging gastric or jejunal folds about the distorted anastomotic site c an simulate an ulcer niche.

Marginal ulcers may appear radiographicaliy as small circumscribed collections of barium or huge contrast-filled masses that mimic postoperative pseudodiverticula. Secondary signs of marginal ulceration include edema of the duodenal or jejunal folds at the anastomotic site, flattening and rigidity of the jejunum adjacent to the ulcer, and wide separation of jejunal and gastric segments.

Afferent Loop Syndrome

Distension and poor drainage of the afferent intestinal loop of a Billroth II anastomosis may cause abdominal bloating and pain following eating, often associated with nausea and vomiting. Because of complete or partial obstruction, it may be difficult to demonstrate the afferent loop on upper gastrointestinal examination. Complete obstruction of the afferent loop at the anastomosis may be caused by retrograde jejunogastric intussusception, which appears radiographically as a clearly defined spherical or ovoid intraluminal filling defect in the gastric remnant. If the obstruction is proximal to the anastomosis, barium may fill a short segment of the afferent loop to the point of obstruction. If there is preferential filling of the afferent loop and no organic obstruction, barium examination will demonstrate a dilated afferent loop that fills rapidly and empties slowly and incompletely.

Bile Reflux Gastritis

Highly alkaline digestive secretions are normally prevented from entering the stomach by an intact pylorus. When the pyloric mechanism is destroyed or circumvented by partial gastric resection, free reflux can produce severe gastritis and ulceration. Bile reflux gastritis appears radiographically as thickened folds in the gastric remnant. The most severe changes tend to occur near the anastomosis. Ulcerations due to bile reflux gastritis occur on the gastric side of the remnant, unlike true marginal ulcerations, which occur on the jejunal side of the anastomosis.

Gastrojejunocolic Fistula

A fistulous communication between the stomach, jejunum, and colon (gastrojejunocolic fistula) or directly between the stomach and colon represents a grave complication of marginal ulceration after gastric surgery for peptic ulcer disease. Most patients with this condition (there is a heavy predominance in men) have diarrhea and weight loss; pain, vomiting, and bleeding are common. The fistulas are usually demonstrated during a barium enema examination in which contrast material is observed to extend directly from the transverse colon into the stomach. These postsurgical fistulas are associated with a high mortality rate, especially if recognized late.

Carcinoma after Partial Gastrectomy

The development of recurrent symptoms after 10 years or more of relatively good health following partial gastrectomy for ulcer disease should suggest the possibility of gastric stump carcinoma. The incidence of carcinoma in the gastric remnant is two to six times bigher than in the intact stomach. Gastric stump carcinoma may be difficult to demonstrate on barium examination. The tumor usually appears as an irregular polypoid mass at the anastomotic margin or in the gastric remnant. Decrease in the size of the gastric remnant can occur secondary to uniform infiltration by carcinoma. This sign of malignancy requires comparison with previous studies and is an excellent reason for obtaining a baseline upper gastrointestinal examination several months after partial gastrectomy.

Gastric stump malignancy can also appear as a marginal ulceration near the anastomosis. Patients with this type of carcinoma tend to have a long symptom-free period averaging in excess of 20 years, in contrast to patients with benign mucosal ulcerations, which usually occur within 2 years of surgery. Since benign marginal ulcerations usually occur on the jejunal side of the anastomosis, any ulcer on the gastric side should be considered malignant until proved otherwise.”

afferent loop syndrome · gastrojejunocolic fistula · billroth 2 ·

Complications of Peptic Ulcer Disease


Peptic ulcer disease is the most common cause of acute upper gastrointestinal bleeding. The proper diagnostic approach depends on the severity and activity of the hemorrhage. Patients with massive hemorrhage, whose vital signs cannot be maintained, require emergency surgery for both diagnostic and therapeutic purposes. In the patient with acute upper gastrointestinal hemorrhage who has relatively stable vital signs, endoscopy, not a barium study, is the initial diagnostic procedure of choice. The 95 percent accuracy of endoscopy is substantially higher than the accuracy of barium studies, even using double-contrast technique. Barium examinations may be technically difficult to perform in the patient with acute hemorrhage since the presence of fresh and clotted blood severely affects the quality of mucosal coating. Unlike barium studies, endoscopy allows the physician not only to visualize the abnormality but also to say with some certainty whether or not a specific lesion is the cause of the acute bleeding episode. This is important because a significant number of patients with acute upper gastrointestinal hemorrhage are found to have more than one lesion. If emergency endoscopy is not available, a double-contrast upper gastrointestinal series should be performed following vigorous lavage through a large-bore tube to remove clots that could simulate a gastric mass or obscure an acute ulcer crater.

In a patient with active bleeding at a rate of at least 0.5 to 1 ml/minute, selective celiac and superior mesenteric arteriography can often demonstrate extravasation of contrast material from the vascular tree and thus localize the site of bleeding. In addition to peptic ulcer disease, virtually all other causes of acute upper gastrointestinal hemorrhage (gastritis, varices, arteriovenous malformations, Mallory-Weiss tears) can be diagnosed and treated via the arteriographic catheter. The specific cause of the hemorrhage generally determines whether vasoconstrictive agents or embolization will be the most effective therapy. In patients with massive hemorrhage, arteriography and transcatheter therapeutic measures may allow time for vascular volume replacement and a more stable patient before surgical intervention.

Radionuclide scanning with Tc-labeled sulfur colloid or red blood cells can accurately localize gastrointestinal bleeding with minimal discomfort and risk. The addition of rapid sequential images (radionuclide angiogram) to the routine static scans increases the rate of lesion detection. Although more sensitive, radionuclide scanning is less specific than arteriography and offers no therapeutic value.


Perforation is an occasional complication of peptic disease, especially involving ulcers in the pyloroduodenal region. Free perforation of a peptic ulcer is the most frequent cause of pneumoperitoneum with peritonitis.

With the patient in an erect position, as little as 1 ml of air can be demonstrated as a sickle-shaped lucency beneath the domes of the diaphragm. Free intraperitoneal gas is easiest to recognize on the right side between the diaphragm and the homogeneous density of the liver. On the left, the normal gas and fluid shadows present in the fundus of the stomach can be confusing. Free air is shown to best advantage if the patient remains in an upright 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 his or her left side) can be used. In this position, free gas moves to the right and collects between the lateral margin of the liver and the abdominal wall. On supine views of the abdomen, free intraperitoneal air accumulates between intestinal loops and is much more difficult to demonstrate. However, a large quantity of air can be diagnosed indirectly because it permits visualization of the outer margins of the intestinal wall. The distinct demonstration of the inner and outer contours of the bowel wall is often the only sign of pneumoperitoneum in patients in such poor condition that they cannot be turned on their side or be examined upright.

It is important to remember that in about 30 percent of perforated peptic ulcers, no free intraperitoneal gas can be identified. Therefore, the failure to demonstrate a pneumoperitoneum is of no value in excluding the possibility of a perforated ulcer. In patients with suspected perforation and no pneumoperitoneum, extensive extravasation from the upper gastrointestinal tract can often be demonstrated following the oral administration of a small amount of water-soluble contrast material.

Ulcers of the posterior wall of the duodenum tend to penetrate into the pancreas and frequently result in increased levels of serum amylase. Less commonly, duodenal ulcers may penetrate into the liver, biliary tract, colon, or lesser sac, as well as dissecting along retroperitoneal fascial planes. Penetrating ulcers involving the pancreas can cause radiographic changes of pancreatitis such as serrations and spiculations of the mucosa of the descending duodenum, effacement of folds, and a mass effect.

Perforation of a peptic ulcer may become walled off and form an abscess cavity. A persistent connection to the lumen may result in an air-fluid level on upright abdominal radiographs and may permit barium to fill the abscess and sinus tract during a contrast examination. If the communication with the lumen has closed, the abscess may appear as a soft tissue density producing a mass effect on the stomach or duodenum.

Gastric Outlet Obstruction

This is discussed in the section “Gastric Outlet Obstruction” earlier in this chapter.


peptic ulcer disease · perforated peptic ulcer · peptic ulcer perforation ·

Peptic Ulcer Disease


Duodenal Ulcer

Duodenal ulcer is the most common manifestation of peptic disease. More than 95 percent of duodenal ulcers occur in the first portion of the duodenum (duodenal bulb). An unequivocal diagnosis of active duodenal ulcer requires demonstration of the ulcer crater, which can be seen using double-contrast techniques in about 90 percent of ulcers. When seen in profile, the ulcer crater is a small collection of barium projecting from the lumen. When seen en face, the ulcer niche appears as a rounded or linear collection of contrast material surrounded by lucent folds that often radiate toward the crater as they do with gastric ulcers. Secondary signs of duodenal ulcer disease are thickening of mucosal folds and deformity of the duodenal bulb. Acute ulcers incite muscular spasm leading to marginal deformity of the duodenal bulb that may be inconstant and vary during the examination. With chronic ulceration, fibrosis and scarring cause a fixed deformity that persists even though the ulcer heals.The degree of deformity is not directly related to ulcer size; small ulcers may produce large deformities, and huge ulcers may produce little alteration in bulb contour. Symmetric narrowing of the duodenal bulb in its mid-portion, associated with dilatation of the inferior and superior recesses at the base of the bulb (pseudodiver-ticula), may produce the typical cloverleaf deformity of chronic duodenal ulcer disease. An apparent eccentric position of the pyloric canal may be due to muscular spasm associated with an ulcer at the base of the bulb.

It must be emphasized that although secondary signs such as thickened folds, spasm, and deformity of the duodenal bulb are indications of peptic disease, demonstration of the crater itself is necessary for the diagnosis of an active duodenal ulcer. However, once the diagnosis of duodenal ulcer disease is clearly established radiographically or by endoscopy, there is usually no reason to repeat the upper gastrointestinal examination. The patient should be treated symptomatically rather than depending on radiographic confirmation of healing or recurrence of an active duodenal ulcer.

Although the vast majority of duodenal ulcers are small (less than 1 cm in diameter) and involve only a small portion of the duodenal bulb, some duodenal ulcers are extremely large (3 to 6 cm in diameter) and completely replace the bulb. Unlike the normal duodenal bulb or a duodenal diverticulum, these giant duodenal ulcers are rigid-walled cavities that lack a normal mucosal pattern and remain constant in size and shape throughout the gastrointestinal examination.

Postbulbar Ulcer

Ulceration in the postbulbar region represents only about 5 percent of duodenal ulcers secondary to benign peptic disease. Although postbulbar ulcerations are often difficult to detect radiographicaly, their identification is important because they so frequently are the cause of obstruction, pancreatitis, gastrointestinal bleeding, and atypical abdominal pain. Hyperactive peristalsis, mucosal edema, and poor barium coating can obscure the ulcer niche. Severe spasm of the duodenum in the area of ulceration can narrow and deform the lumen and prevent barium from filling the ulcer crater.

The classic radiographic appearance of a benign postbulbar ulcer is a shallow, flattened niche on the medial aspect (rarely the lateral) of the upper second portion of the duodenum or just past the apex of the duodenal bulb. Intense spasm often produces an incisura, an indentation defect on the opposite duodenal margin at the same level as the ulcer crater. This causes eccentric narrowing of the lumen that may persist if there is chronic ulceration or fibrotic scarring during the healing phase of the postbulbar ulcer.

Peptic ulcers arising distal to the mid-descending duodenum are rare. Single or multiple ulcers in this location strongly suggest the Zollinger-Ellison syndrome.

Gastric Ulcer

The detection of gastric ulcers and the decision whether these represent benign or malignant processes are major parts of the upper gastrointestinal examination. Up to 95 percent of gastric ulcers can be revealed using double-contrast techniques. Certain technical factors preclude demonstration of a small percentage of gastric ulcers. The ulcer can be shallow or be filled with residual blood, mucus, food, or necrotic tissue that prevents barium from filling it. Similarly, the margins of an ulcer can be so edematous that barium cannot enter it; a small ulcer can be obscured by large rugal folds. In contrast, a false-positive ulcerlike pattern can be caused by barium trapped between gastric folds.

The classic sign of a benign gastric ulcer on profile view is penetration—the clear projection of the ulcer outside the normal barium-filled gastric lumen because the ulcer represents an excavation in the wall of the stomach. Three other signs of benignancy on profile view are the Hampton line, the ulcer collar, and the ulcer mound, all of which are related to undermining of the mucosa (relatively resistant to peptic digestion), which appears to overhang the more rapidly destroyed submucosa. The amount of mucosal edema due to inflammatory exudate determines which of these three signs will be produced. When visualized en face, the ulcer appears as a persistent collection of barium surrounded by a halo of edema. A hallmark of benign gastric ulcer is radiation of mucosal folds to the edge of the crater.

However, since 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. In contrasts irregular folds that merge into a mound of polypoid tissue around the crater suggest malignancy. Although the size, shape, number, and location of gastric ulcers were formerly 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 cardia, essentially all of which are malignant. A lesser curvature ulcer may cause intense muscular spasm and an indentation on the opposite wall (incisura). The incisura may be mistaken for a gastric mass..nless the underlying lesser curvature ulcer is demonstrated.

At times, it may be difficult to decide whether a persistent collection of barium in the stomach or elsewhere in the gastrointestinal tract represents an acute ulceration or a nonulcerating deformity. If the barium collection has an elliptical configuration, the orientation of the long axis of the ellipse can be an indicator of the nature of the pathologic process (ellipse sign). If the long axis is parallel to the lumen, the collection represents an acute ulceration. If the long axis is perpendicular to the lumen, the collection represents a deformity without acute ulceration.

An abrupt transition between the normal mucosa and the abnormal tissue surrounding a gastric ulcer is characteristic of a malignant lesion, in contrast to the diffuse and almost imperceptible transition between the mound of edema surrounding a benign ulcer and the normal gastric mucosa. 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. Carman’s meniscus sign is diagnostic of a specific type of ulcerated neoplasm. When examined in profile with compression, this ulcer is seen to have a semicircular (meniscoid) configuration that is convex toward the lumen and surrounded by the lucent shadow of an elevated ridge of neoplastic tissue.

The vast majority of gastric ulcers (more than 95 percent) are benign and heal completely with medical therapy. Most benign ulcers diminish to one-half or less their original size within 3 weeks and show complete healing within 6 weeks. Complete healing does not necessarily mean that the stomach returns to an absolutely normal radiographic appearance; bizarre deformities can result due to fibrotic retraction and stiffening of the wall of the stomach. It is essential to remember that many malignant ulcers show significant healing, though 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 whenever the radiographic findings are not typical of a benign ulcer, if healing of the ulcer does not progress at the expected rate, or if 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 are defects in the epithelium of the stomach that do not penetrate beyond the muscularis mucosae. Because they are very small and shallow, superficial gastric erosions have rarely been demonstrated on conventional upper gastrointestinal examinations. With the increasing use of double-contrast techniques, however, more than half the superficial gastric erosions noted endoscopically can be demonstrated radiographically. The classic radiographic appearance of a superficial gastric erosion is a tiny fleck of barium, which represents the erosion, surrounded by a radiolu-cent halo, which represents a mound of edematous mucosa. Possible factors implicated in the production of superficial gastric erosions include alcohol, anti-inflammatory agents (e.g., aspirin, steroids), analgesics, Crohn’s disease, and candidiasis.


A variety of acute ulcerative lesions of the stomach and duodenum are clinically distinct from, though radio-graphically identical to, those arising from chronic peptic ulcer disease. “Stress” ulcers can develop rapidly in patients with shock, burns, sepsis, or severe trauma. They most commonly present with gastrointestinal hemorrhage, which may be substantial. Although gastric acid appears to be involved in the production of these acute stress ulcers, there is usually no evidence of acid hypersecretion. Often multiple, stress ulcers are frequently too superficial to be detected on barium examination and may only be identified by upper gastrointestinal endoscopy. Celiac or selective left gastric arteriography may be of value in localizing a site of hemorrhage, and intra-arterial infusion of vasopressin may decrease or stop the bleeding.

Anti-inflammatory agents such as aspirin, steroids, phenylbutazone, and indomethacin have been associated with an increased incidence of ulcer disease and upper gastrointestinal hemorrhage. Therefore, the use of these substances should be limited in patients with peptic ulcer disease. Radiographically, a superficial gastric erosion due to anti-inflammatory agents usually appears as a tiny fleck of barium surrounded by a radiolucent halo of edematous mucosa.


The Zollinger-Ellison syndrome is caused by a non-beta islet cell tumor of the pancreas that continually secretes gastrin. The persistently high blood level of this hormone results in a strong stimulus to the gastric parietal cells that causes voluminous gastric: hypersec retion and hy peracidity and a c linical picture of severe, often intractable, peptic ulcer disease. Although most ulcers in patients with Zollinger-Ellison syndrome occur in the stomach or duodenal bulb up to 25 percent may be in an atypical location in more distal portions of the duodenum and in the jejunum. The unusual location of the peptic ulcers seen distal to the duodenal bulb is due to the excessively large volume of highly acid gastric fluid that bathes the duodenum and proximal jejunum and overwhelms the alkaline biliary and pancreatic secretions. The resultant chemical enteritis produces severe ulceration and inflammatory fold thickening in the vulnerable distal duodenum and proximal jejunum, which are not normally exposed to such an acid environment. Because the normal succus entericus in the more distal portions of the small bowel dilutes the acid gastric contents and raises the pH, the mucosal pattern of the distal jejunum and the ileum is usually normal. Giant duodenal ulcers, though not pathognomonic, should suggest the possibility of the Zollinger-Ellison syndrome.

In the stomach, the Zollinger-Ellison syndrome is associated with diffuse thickening of gastric folds and excessive fasting gastric secretions without any demonstrable gastric outlet obstruction. The duodenal ulcers, though radiographically indistinguishable from those secondary to benign peptic disease, usually fail to respond to traditional medical and surgical therapy. The large amount of fluid entering the small intestine from the hypersecreting stomach leads to small bowel dilatation, thickening of duodenal and jejunal folds, and a considerable dilution of the barium, which appears to have a gray, watery appearance.

About 90 percent of gastrinomas are found within the pancreas. The remainder lie in ectopic locations such as the stomach, duodenum, or splenic hilum. Less than half of gastrinomas can be identified by contrast-enhanced computed tomography (CT) or pancreatic arteriography. Although most gastrinomas are very small, about 50 percent are malignant. Metastases (usually to regional lymph nodes or the liver) continue to secrete gastrin and stimulate the gastric parietal cell mass even after the primary tumor of the pancreas has been removed or a total pancreatectomy has been performed. Partial gastric resection or vagotomy with pyloroplasty is almost invariably followed by prompt and often fulminant ulcer recurrence. Therefore, the surgical procedure of choice is removal of the entire target organ (i.e., the parietal cell mass of the stomach) by total gastrectomy.

The Zollinger-Ellison syndrome frequently coexists with multiple endocrine adenomatosis. In addition to the pancreas, the most commonly involved endocrine glands are the adrenals, parathyroids, ad pituitary.”

carmans meniscus sign · Carman meniscus sign · duodenal bulb erosion ·

Abnormal Gastric Emptying


Gastric Outlet Obstruction

In adults, peptic ulcer desiase is by far the most common cause of gastric outlet obstruction.The obstructing lesion in peptic ulcer disease is usually in the duodenum, occasionally in the pyloric channel or prepyloric gastric antrum, and rarely in the body of the stomach.Narrowing of the lumen due to peptic ulcer disease can result from spasm, acute inflammation and edema, muscular hypertrophy, or contraction of scar tissue.

The second leading cause of gastric obstruction is an annular constricting lesion near the pylorus representing carcinoma of the antrum.Other infiltrative primary malignant tumors or metastatic lesions obliterating the lumen of the distal stomach and proximal duodenum can also produce the radiographic pattern of gastric outler obstruction.
Patients with gastric outlet obstruction caused by peptic disease typically have a long history of ulcer symptoms .About one-third of patients with obstruction due to malignancy have no pain; most of the rest have a history of the pain of less than 1 year’s duration.
Less common causes of gastric outlet obstruction include inflammatory diseases that produce infiltrative and spactic narrowing of the distal stomach and proximal duodenum (Croch’s disease, pancreatitis, cholecystitis, sarcoidosis, syphilis, tuberculosis), congenital disorders (hypertrophic, pyloric stenosis, antral mucosal diaphragm), gastric volvulus, prolapsed antral polyps, and massive bezoars.
Plain abdominal radiographs often demonstrate the shadowy outline of the distended stomach in patients with gastric outlet obstruction.On upright films, there is frequently a fuzzy air-fluid level distinct from the sharp, even air-fluid levels seen elsewhere in the bowel.On barium examination, a mottled density of nonopaque material represents excessive overnight gastric residual.At times the stomach may become huge and, with the patient in the upright position, hang down into the lower abdomen or pelvis.The critical differential diagnosis is between a benign (primarily peptic ulcer disease) and a malignant cause of gastric outler obstruction.The presence of a persistent fleck of barium in a narrowed pyloric channel suggests peptic disease.A discrete filling defect suggest malignancy, as does nodularity or irregularity of the mucosa proximal to the constricted area.It is essential that every effort be made to express barium into the duodenel bulb.The finding of distortion and scarring of the bulb with formation od pseudodiverticula makes peptic ulcer disease the most likely cause.Conversely, a radiographically normal, duodenal bulb increases the likelihood of underlying malignant disease.In many patients, unfortunately, it isimpossible to differentiate confidently on barium studies between a benign and a malignant cause of gastric outlet obstruction.In the cases, endoscopy or surgical exploration is required to exclude the possibility of a malignant lesion.


Gastric Dilatation Without Outlet Obstruction

Acute or chronic dilatation of the stomach with prolonged retention of food and barium can occur without any organic gastric obstruction. Gastric retention is defined as vomiting of food eaten more than 6 hours earlier or the presence of food in the stomach at the time of an upper gastrointestinal series (assuming that the patient has not eaten for 8 to 10 hours). It is critical to remember that gastric retention does not necessarily mean gastric outlet obstruction and that “corrective” surgery may be contraindicated.

On plain radiographs, the appearance of gastric dilatation without obstruction is indistinguishable from that of organic gastric outlet obstruction. Huge quantities of air and fluid fill a massively enlarged stomach that can extend even to the floor of the pelvis. The administration of barium demonstrates a large amount of solid gastric residue. Peristalsis is irregular, sluggish, and ineffectual. The failure of radiographic studies to demonstrate an organic cause for gastric outlet obstruction in patients with dilatation of the stomach does not imply at all that no abnormality exists. In addition, when retained food is seen in the stomach during a barium examination, the various nonobstructive causes of gastric retention must be excluded before the patient can be accused of disregarding instructions and eating just before the examination.

Acute gastric dilatation refers to sudden and excessive distension of the stomach by fluid and gas, usually accompanied by vomiting, dehydration, and peripheral vascular collapse. Within minutes or hours, a normal stomach can expand into a hyperemic, cyanotic, atonic sac that fills the abdomen. Most cases of acute gastric dilatation occur during the first several days after abdominal surgery. The incidence of this postoperative complication has dramatically decreased with the advent of nasogastric suction, improved anesthetics, close monitoring of acid-base and electrolyte balance, and meticulous care in the handling of tissues at surgery. Acute gastric dilatation can also be related to abdominal trauma, severe pain, peritonitis, electrolyte and acid-base imbalance, diabetic acidosis, the use of body casts, or large doses of anticholinergic drugs.

The danger of acute gastric dilatation lies in its potential for complications and death if the early signs are not appreciated and a nasogastric tube is not promptly inserted to decompress the stomach. Unfortunately, pain is seldom severe until gastric dilatation is pronounced. Distension can progress rapidly due to aerophagia, or air sucking. Sudden relaxation of the gastric cardia can lead to copious vomiting, aspiration, asphyxiation, and cardiac arrest. Acute gastric dilatation can cause gastric perforation with peritonitis or can result in severe fluid and electrolyte disturbances, dehydration, decreased urinary output, and shock.

The development of gastric dilatation can be indolent and essentially asymptomatic. Gastric motor abnormalities occur in 20 to 30 percent of diabetic patients, primarily those who have long-term disease under relatively inadequate control and evidence of peripheral neuropathy or other complications. Other causes of chronic gastric dilatation include neurologic abnormalities (brain tumor, bulbar poliomyelitis, tabes dorsalis), surgical or chemical vagotomy (atropine or drugs with an atropine-like action), scleroderma, trauma, and severe electrolyte or acid-base imbalances.

gastric emptying · gastric outlet obstruction in adults · gastric outlet obstruction ·