Thursday, August 26, 2010

Portal Hypertensive Gastropathy

Portal hypertensive gastropathy (previously known as "hemorrhagic gastritis," "alcoholic gastritis," "congestive gastropathy," and "gastric mucosal hyperemia") refers to mucosal hyperemia and dilated submucosal vessels in the stomach of patients with chronic portal hypertension. Portal hypertensive gastropathy tends to occur more commonly in cirrhotic patients compared to patients with noncirrhotic causes of portal hypertension.

It is thought that chronic venous congestion and hyperdynamic flow in the splanchnic circulation causes mucosal hyperemia, capillary ectasia, and increased numbers of submucosal arteriovenous communications. This results in dilated intramural arterioles, capillaries, and veins.

It is estimated to cause up to 30% of upper gastrointestinal bleeding in patients with portal hypertension and can occur even in the absence of esophageal or gastric varices. It can also cause persistent bleeding needing medical or surgical treatment. In addition, the presence of portal hypertensive gastropathy may be a risk factor for variceal hemorrhage.

On fluoroscopy, there will be thickened nodular folds in the gastric fundus. Although varices or various forms of gastritis can also produce thickened gastric folds, portal hypertensive gastropathy should be suspected when this finding is detected in patients with known portal hypertension.

Dynamic (e.g., multi-phase liver) CT can also help. A transient gastric perfusion sign has been described as a fairly specific sign for portal hypertensive gastropathy. In normal subjects, the collapsed gastric wall demonstrates homogeneous enhancement during arterial, portal, and delayed CT images. In portal hypertensive gastropathy, on the other hand, there is transient, segmental or subsegmental low-attenuation mucosa in the fundus or body of the stomach on the arterial phase that returns to normal attenuation on portal venous or equilibrium-phase images (see image). This sign has a sensitivity of 75%, specificity of 89%, positive predictive value of 90% and negative predictive value 72%.

Differential considerations include the other causes of gastric wall thickening:
  • Gastritis: For example Helicobacter pylori. The thickened folds are not confined to the fundus. Other abnormalities, such as ulcers, erosions, nodules, or enlarged areae gastricae may also be seen.
  • Lymphoma: Usually much thicker and more lobulated folds.
  • Ménétrier disease: Usually much thicker and more lobulated folds.
  • Gastric varices: May mimic thickened folds on fluoroscopy, but the folds tend to have a serpentine configuration with discrete submucosal nodules (bunch of grapes)


  • Chang D, Levine MS, Ginsberg GG, Rubesin SE, Laufer I. Portal hypertensive gastropathy: radiographic findings in eight patients. AJR Am J Roentgenol. 2000 Dec;175(6):1609-12.
  • Kim TU, Kim S, Woo SK, Lee JW, Lee TH, Jeong YJ, Heo J. Dynamic CT of portal hypertensive gastropathy: significance of transient gastric perfusion defect sign. Clin Radiol. 2008 Jul;63(7):783-90.

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