Pathophysiology

Clinical Findings

Gastric varices are important because of the risk of gastrointestinal (GI) bleeding, which can range from low-grade, intermittent bleeding to massive hematemesis. Gastric varices are less likely to bleed than esophageal varices because of their subserosal location and the greater thickness of overlying gastric tissue. When gastric variceal bleeding occurs, however, it tends to be more severe than esophageal variceal bleeding and is associated with a higher mortality rate. When gastric varices are associated with esophageal varices, affected individuals usually have the stigmata of portal hypertension. In contrast, patients with isolated gastric varices caused by splenic vein obstruction may present with abdominal pain and weight loss from underlying pancreatitis or pancreatic carcinoma. Splenomegaly is also a frequent finding in splenic vein obstruction, but a normal-sized spleen does not exclude this condition.

Radiographic Findings

Barium Studies.

Conventional single-contrast barium studies are thought to be unreliable for detecting gastric varices. Double-contrast technique has therefore been advocated to improve visualization of these structures. Gastric varices may appear as thickened, tortuous folds or as round submucosal filling defects in the gastric fundus, resembling the appearance of a bunch of grapes ( Fig. 34-1 ). Less frequently, a conglomerate mass of fundal varices, also known as tumorous gastric varices, may be manifested by a large polypoid mass that can be mistaken on barium studies for a polypoid carcinoma or even a malignant gastrointestinal stromal tumor (GIST) ( Figs. 34-2 and 34-3 ). Tumorous varices have characteristic features, however, appearing in profile as smooth submucosal masses with an undulating contour and discrete borders on the posteromedial wall of the gastric fundus (see Figs. 34-2 and 34-3 ) and en face as thickened, tortuous folds that fade peripherally into the adjacent mucosa. These radiographic features should allow differentiation from polypoid gastric neoplasms in most cases. Rarely, dilated gastroepiploic veins may be manifested by varices in the antrum or body of the stomach ( Fig. 34-4 ).

Gastric varices.

Multiple rounded submucosal filling defects are seen in the gastric fundus, resembling the appearance of a bunch of grapes.

(From Levine MS, Kieu K, Rubesin SE, et al: Isolated gastric varices: Splenic vein obstruction or portal hypertension? Gastrointest Radiol 15:188–192, 1990.)

Conglomerate mass of gastric varices (also known as tumorous varices).

A. Barium study shows a large, lobulated submucosal mass ( arrows ) on the medial aspect of the gastric fundus. Although this lesion could be mistaken for a malignant GI stromal tumor or even a polypoid carcinoma, note its smooth undulating contour. B. Unenhanced CT scan shows a lobulated soft tissue mass ( arrows ) on the posteromedial wall of the fundus. C. Endoscopic photograph shows a conglomerate mass of varices ( arrows ) in the gastric fundus adjacent to the cardia. This patient had underlying portal hypertension.

( B and C from Levine MS, Kieu K, Rubesin SE, et al: Isolated gastric varices: Splenic vein obstruction or portal hypertension? Gastrointest Radiol 15:188–192, 1990.)

Conglomerate mass of isolated gastric varices caused by splenic vein obstruction.

A smooth, undulating mass ( arrows ) is seen on the posteromedial wall of the gastric fundus. Note the resemblance to the gastric varices in Figure 34-2 . This patient had underlying pancreatitis causing splenic vein obstruction.

(Courtesy William M. Thompson, MD, Minneapolis.)

Nonfundal gastric varices.

Thickened, tortuous folds are seen in the body of the stomach caused by markedly dilated gastroepiploic veins. This patient had severe portal hypertension.

(From Levine MS: Radiology of the Esophagus. Philadelphia, WB Saunders, 1989.)

When gastric varices are detected on barium studies, it is important to determine whether uphill esophageal varices are also present in these patients. The presence of combined esophageal and gastric varices almost always indicates portal hypertension as the underlying cause. In contrast, isolated gastric varices should raise the possibility of splenic vein obstruction with a patent portal vein (see Fig. 34-3 ). Nevertheless, portal hypertension is much more common than splenic vein obstruction, so most patients with gastric varices, even in the absence of esophageal varices, are found to have portal hypertension as the underlying cause (see Fig. 34-2 ). If necessary, CT or angiography may be performed to document the presence of varices and elucidate their pathophysiology.

Computed Tomography.

Gastric varices are usually recognized on CT as enhancing, well-defined, round or tubular densities on the posterior or posteromedial wall of the gastric fundus ( Fig. 34-5 ). CT is more sensitive than conventional radiologic examinations in detecting these lesions because barium studies can only demonstrate varices that protrude into the lumen, whereas CT can delineate deeper intramural and perigastric varices. CT may also reveal cirrhotic liver disease, splenomegaly, or ascites in patients with portal hypertension (see Fig. 34-5 ) and splenomegaly or pancreatic disease in patients with splenic vein obstruction.

Gastric varices on CT.

Enhancing collaterals are seen in the gastric wall ( arrowheads ), gastrohepatic ligament ( open arrows ), and left retroperitoneal space. This patient also has cirrhosis with splenomegaly and minimal ascites ( solid arrow ) caused by portal hypertension. S, stomach; SP, spleen.

(Courtesy Richard M. Gore, MD, Evanston, IL.)

Angiography.

Angiography may be performed to confirm the presence of gastric varices and determine the nature of the underlying venous abnormality. With portal hypertension, reversal of flow through the coronary and short gastric veins leads to the formation of esophageal and gastric varices, with absent visualization of the portal and splenic veins. 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 the fundal plexus of veins via the coronary vein to the portal venous system, bypassing the obstructed splenic vein ( Fig. 34-6 ). Thus, portal hypertension can usually be differentiated from splenic vein obstruction by angiography, so appropriate therapy can be instituted in these patients.

Angiographic demonstration of gastric varices due to splenic vein obstruction.

Image from the venous phase of a splenic arteriogram shows a densely opacified spleen with absent visualization of the splenic vein, extensive gastric varices (G), and a dilated coronary vein (cv) diverting blood from the fundal plexus of veins to the portal vein (pv). Note the presence of a dilated gastroepiploic vein (gev).

(Courtesy Dana R. Burke, MD, Bethesda, MD.)

Differential Diagnosis

When gastric varices are manifested on barium studies by thickened, nodular folds in the fundus, the differential diagnosis includes Helicobacter pylori gastritis, Ménétrier’s disease, Zollinger-Ellison syndrome, pancreatitis, and lymphoma. However, gastric varices tend to be more tortuous or lobulated than these other conditions and are often associated with esophageal varices. Occasionally, a conglomerate mass of fundal varices may resemble a polypoid carcinoma or even a malignant GIST (see Figs. 34-2 and 34-3 ). However, 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 may be required for a definitive diagnosis. It is particularly important to differentiate gastric varices from other lesions before performing endoscopic biopsy or surgery because inadvertent perforation of a varix may lead to catastrophic GI bleeding.

Treatment

Emergent treatment for bleeding gastric varices is rarely necessary. When major bleeding does occur in patients with splenic vein obstruction, the patients are almost always cured by simple splenectomy because portal venous pressure is normal in these individuals. In contrast, some form of portosystemic shunt may be required for gastric varices caused by portal hypertension, as splenectomy alone has no effect on portal venous pressure in these patients. Thus, the choice of treatment for gastric varices depends on the underlying cause.

True Diverticula

Duodenal diverticula are detected as incidental findings on upper GI barium studies in up to 15% of patients. The diverticula are acquired lesions, consisting of a sac of mucosal and submucosal layers herniating through a muscular defect. These diverticula often fill and empty by gravity as a result of pressure generated by duodenal peristalsis. Most duodenal diverticula are located on the medial border of the descending duodenum in the periampullary region ( Fig. 34-11 ), but they not infrequently are found in the third or fourth portion of the duodenum and can occasionally be located on the lateral border of the descending duodenum ( Fig. 34-12 ).

Duodenal diverticulum.

A typical diverticulum ( arrows ) is seen arising from the medial border of the descending duodenum.

(From Eisenberg RL: Gastrointestinal Radiology: A Pattern Approach, 3rd ed. Philadelphia, JB Lippincott, 1996.)

Lateral duodenal diverticulum.

A diverticulum ( long arrow ) is seen arising from the lateral border of the descending duodenum. Note how the diverticulum has a discrete neck ( short arrow ). Also note how the diverticulum is compressing the adjacent duodenum.

Duodenal diverticula typically appear on barium studies as smooth, round or ovoid outpouchings arising on a discrete neck from the medial border of the descending duodenum (see Fig. 34-11 ). They are often multiple and may change in size and shape at fluoroscopy. The lack of inflammatory reaction (spasm or edema) allows a duodenal diverticulum to be differentiated from a postbulbar ulcer. Bizarre multilobulated or giant diverticula are occasionally seen. Filling defects representing inspissated food particles or blood clots can sometimes be found within the diverticulum ( Fig. 34-13 ).

Duodenal diverticulum with a blood clot. This diverticulum contains a large, irregular filling defect representing a blood clot in a patient with recent upper GI bleeding.

(From Eisenberg RL: Gastrointestinal Radiology: A Pattern Approach, 3rd ed. Philadelphia, JB Lippincott, 1996.)

When duodenal diverticula contain gas or a combination of fluid and gas, they are readily visible on CT. However, a diverticulum that is predominantly fluid-filled can occasionally mimic the CT findings of a cystic neoplasm in the head of the pancreas ( Fig. 34-14A ). The correct diagnosis can still be established, however, if intradiverticular gas is identified ( Fig. 34-14B ).

Duodenal diverticulum mimicking a cystic pancreatic neoplasm on CT.

A. CT scan with oral and intravenous contrast material at the level of the pancreatic head shows a fluid-filled cystic lesion ( long arrow ) that was initially thought to represent a cystic pancreatic tumor. Note air and contrast material in the duodenum ( short arrow ). B. A follow-up CT scan at a similar level 6 months later shows filling of the diverticulum with gas ( arrow ), confirming the diagnosis of a duodenal diverticulum.

(From Macari M, Lazarus D, Israel G, et al: Duodenal diverticula mimicking cystic neoplasms of the pancreas: CT and MR imaging findings in seven patients. AJR 180:195–199, 2003.)

More than 90% of patients with duodenal diverticula are asymptomatic. Occasionally, however, these patients may develop serious complications such as duodenal diverticulitis, upper GI bleeding, gastric outlet obstruction, and pancreaticobiliary disease. Because duodenal diverticula are retroperitoneal structures, duodenal diverticulitis and perforation can occur without clinical signs of peritonitis or radiographic signs of free intraperitoneal air. Instead, abdominal radiographs may reveal localized retroperitoneal gas adjacent to the duodenum and upper pole of the right kidney. Studies with barium or water-soluble contrast agents may demonstrate localized extravasation of contrast material from the perforated diverticulum into a contained extraluminal collection or a deformed diverticulum secondary to a previous perforation that subsequently sealed off. CT is particularly helpful for showing a contained perforation or inflammatory changes involving adjacent structures.

Rarely, duodenal diverticula may cause massive upper GI bleeding. In such cases, scanning with ^99m Tc–labeled red blood cells or angiography may be required to localize the site of bleeding. Duodenal diverticula have also been described as a rare cause of duodenal or even biliary obstruction. Anomalous insertion of the common bile duct and pancreatic duct into a duodenal diverticulum can be demonstrated in about 3% of carefully performed T-tube cholangiograms. This anatomic variation can impair drainage of bile into the duodenum, predisposing these patients to biliary obstruction, bile duct stones, and pancreatitis.

Pseudodiverticula

Pseudodiverticula are exaggerated outpouchings or sacculations of the inferior and superior recesses of the duodenal bulb related to acute or chronic duodenal ulcer disease ( Fig. 34-15 ). The sacculations may be caused by edema and spasm associated with an active ulcer or by asymmetric fibrosis and retraction associated with scarring from a healed ulcer. However, the degree of deformity is not directly related to the size of the ulcer because some small duodenal ulcers may produce large sacculations, whereas other large ulcers may have little or no effect on the contour of the bulb.

Duodenal pseudodiverticula.

Two exaggerated outpouchings or pseudodiverticula ( arrows ) are seen at the base of the bulb caused by scarring from previous peptic ulcer disease.

Intraluminal Diverticula

An intraluminal duodenal diverticulum is a sac of duodenal mucosa originating from the second portion of the duodenum near the papilla of Vater. The term intraluminal diverticulum is actually a misnomer because this structure is not a diverticulum, but begins as a congenital duodenal web or diaphragm containing a small central aperture; the web gradually elongates over time because of forward pressure by food and duodenal peristalsis. As a result, the diverticulum usually extends antegrade into the distal descending duodenum or, occasionally, the third or fourth portion of the duodenum. When filled with barium, this structure has a characteristic radiographic appearance on barium studies and abdominal CT, with a finger-like intraluminal sac separated from barium in the adjacent lumen by a thin radiolucent stripe representing the elongated web, or “wall,” of the diverticulum ( Fig. 34-16 ). Because of the resemblance to a wind sock at small airports, this structure has also been called a “wind sock” diverticulum.

Intraluminal duodenal diverticulum.

A. The finger-like, barium-filled sac in the descending duodenum is separated from barium in the adjacent lumen by a radiolucent band ( arrows ) representing the wall of the diverticulum. B and C. Axial (B) and coronal (C) CT scans also show the barium-filled intraluminal sac separated from barium in the adjacent duodenal lumen by a thin lower density web ( arrows ).

Both an intraluminal duodenal diverticulum and congenital duodenal diaphragm can be associated with a variety of other anomalies, including annular pancreas, midgut volvulus, situs inversus, choledochocele, congenital heart disease, Down syndrome, imperforate anus, Hirschsprung’s disease, omphalocele, and exstrophy of the bladder.

Patients with an intraluminal duodenal diverticulum may present with nausea and vomiting from associated duodenal obstruction. The usual treatment is surgery, but some patients may benefit from endoscopic disruption of the underlying duodenal web responsible for their symptoms, avoiding the need for surgery.