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Miscellaneous Abnormalities of the Stomach and Duodenum
Gastric Varices
Pathophysiology
Portal Hypertension
The gastric fundus is normally drained by numerous short gastric veins that anastomose distally with the splenic vein and proximally with the coronary vein and venous channels surrounding the distal esophagus. The short gastric veins normally empty via the splenic vein into the portal vein. In portal hypertension, however, increased pressure in the portal and splenic veins leads to reversal of flow from the splenic vein into the short gastric veins, producing fundal varices. As a result, gastric varices develop in 20% of patients with portal hypertension. Because elevated portal pressure also causes reversal of flow from the coronary vein into periesophageal veins, some patients with portal hypertension have combined gastric and esophageal varices, whereas others have isolated gastric varices and an even greater number have isolated esophageal varices.
The frequent absence of gastric varices in portal hypertension is most likely related to thicker connective tissue support for venous channels in the fundus than for the thin-walled, loosely supported veins in the distal esophagus. Even when present, gastric varices may be obscured on barium studies or endoscopy by overlying rugal folds.
Splenic Vein Obstruction
In splenic vein obstruction, increased pressure in the splenic vein proximal to the obstruction leads to reversal of flow through the short gastric veins, producing gastric varices. Because of normal portal pressure, however, these fundal varices drain via the coronary vein into the portal vein, so splenic vein obstruction is characterized by isolated fundal varices without esophageal varices.
Splenic vein obstruction most commonly results from extrinsic compression of the splenic vein by pancreatitis, pancreatic pseudocysts, pancreatic carcinoma, metastatic tumor, lymphoma, or retroperitoneal fibrosis. , Less frequently, splenic vein obstruction is caused by intrinsic thrombosis of the splenic vein secondary to polycythemia or other myeloproliferative disorders.
Clinical Findings
Gastric varices are important because of the risk of upper gastrointestinal (GI) bleeding, ranging from low-grade bleeding to massive hematemesis. When this complication occurs, gastric varices are associated with more severe bleeding and a higher mortality than esophageal varices. Patients with combined esophageal and gastric varices usually have other stigmata of portal hypertension, whereas patients with isolated gastric varices from splenic vein obstruction often present with abdominal pain and weight loss secondary to underlying pancreatitis or pancreatic carcinoma.
Radiographic Findings
Abdominal Radiographs
Large gastric varices are occasionally recognized on chest or abdominal radiographs as one or more lobulated soft tissue densities in the gas-filled fundus. Depending on the cause of the varices, abdominal radiographs may also reveal splenomegaly, pancreatic calcification, and ascites.
Barium Studies
Gastric varices are typically seen on barium studies as multiple rounded submucosal defects in the gastric fundus, resembling a bunch of grapes ( Fig. 22.1 ). , Occasionally, a conglomerate mass of fundal varices, also known as “tumorous” gastric varices, are manifested by a lobulated mass that could be mistaken for a polypoid carcinoma or even a gastrointestinal stromal tumor (GIST) on barium studies ( Fig. 22.2A ) or unenhanced computed tomography (CT) ( Fig. 22.2B ). , When viewed in profile, however, the diagnosis of tumorous varices is suggested by a confluent cluster of undulating submucosal lesions on the posteromedial wall of the fundus. Rarely, gastroepiploic varices are found in the gastric antrum or body.
Combined esophageal and gastric varices are almost always caused by portal hypertension, whereas isolated gastric varices sometimes result from splenic vein obstruction. , Nevertheless, portal hypertension is so much more common than splenic vein obstruction that most patients with isolated gastric varices are found to have portal hypertension as the underlying cause (see Fig. 22.2 ).
Computed Tomography
Gastric varices are usually recognized on CT as enhancing, well-defined, round or tubular densities on the posteromedial wall of the gastric fundus ( Fig. 22.3 ). CT is more sensitive than barium studies for detecting these lesions because it can delineate deep intramural and perigastric varices. Other CT findings include cirrhosis, splenomegaly, and ascites in portal hypertension (see Fig. 22.3 ) and splenomegaly and pancreatic disease in splenic vein obstruction.
Angiography
Angiography may be performed to confirm the presence of gastric varices and determine the underlying venous abnormality. With portal hypertension, reversal of flow through the coronary and short gastric veins produces esophageal and gastric varices. With splenic vein obstruction, however, delayed images reveal normal filling of a patent portal vein without evidence of esophageal varices, as blood is diverted from gastric fundal varices via the coronary vein into the portal vein, bypassing the obstructed splenic vein.
Differential Diagnosis
Gastric varices sometimes resemble thickened, nodular folds in gastritis (especially Helicobacter pylori gastritis), Ménétrier’s disease, and lymphoma, but the presence of esophageal varices should suggest the correct diagnosis. A conglomerate mass of fundal varices may occasionally resemble a malignant GIST or even a polypoid carcinoma (see Fig. 22.2 ), , but the vascular origin of these lesions is suggested by their smooth, undulating contour and typical location on the posteromedial wall of the gastric fundus. CT or angiography is sometimes required for a definitive diagnosis.
Treatment
When upper GI bleeding occurs in patients with splenic vein obstruction, affected individuals are almost always cured by simple splenectomy because portal pressure is normal. In contrast, a portosystemic shunt is sometimes required for gastric varices caused by portal hypertension, as splenectomy alone has no effect on portal pressure in this setting.
Portal Hypertensive Gastropathy
Portal hypertensive gastropathy is a distinct pathologic entity caused by portal hypertension. Chronic venous congestion in the stomach results in mucosal hyperemia, capillary ectasia, and increased submucosal arteriovenous communications with dilated arterioles, capillaries, and veins in the gastric wall. Portal hypertensive gastropathy causes acute and chronic upper GI bleeding, even in the absence of esophageal or gastric varices. In fact, nonvariceal bleeding from portal hypertensive gastropathy is responsible for 30% of upper GI bleeds in portal hypertension.
RADIOGRAPHIC FINDINGS
Portal hypertensive gastropathy predominantly involves the gastric fundus and is characterized on barium studies by thickened, undulating folds ( Fig. 22.4 ), most likely because of mucosal hyperemia and dilated submucosal vessels. Gastric varices may have a similar appearance but tend to have a more serpentine configuration and are often manifested by rounded submucosal masses (see Fig. 22.1 ). The differential diagnosis also includes gastritis (especially H. pylori gastritis), lymphoma, and, rarely, Ménétrier’s disease.
Diverticula
GASTRIC DIVERTICULA
Gastric diverticula almost always arise on a discrete neck from the posterior wall of the gastric fundus, so they are best seen in profile on lateral views ( Fig. 22.5 ). A fundal diverticulum rarely causes symptoms, but pooling of barium within the diverticulum can occasionally mimic an ulcer (see Fig. 22.5 ).
Intramural or partial gastric diverticulum is a rare anomaly of no clinical importance in which the mucosa invaginates into the muscular layer of the gastric wall on the greater curvature of the distal antrum. The diverticulum is recognized on barium studies by a tiny collection of barium extending outside the contour of the adjacent greater curvature ( Fig. 22.6 ). These structures can be mistaken for ulcers but have a changeable configuration at fluoroscopy, whereas true ulcers have a fixed appearance.
DUODENAL DIVERTICULA
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