Portal Hypertension

GENERAL PRINCIPLES

• Portal hypertension is the main complication of cirrhosis and is characterized by increased resistance to portal flow and increased portal venous inflow. Portal hypertension is established by measuring the pressure gradient between the hepatic vein and the portal vein (normal portosystemic pressure gradient is approximately lt;5 mm Hg).

• Direct and indirect clinical consequences of portal hypertension appear when the portosystemic pressure gradient exceeds 10 mm Hg.

• Causes of portal hypertension in patients without cirrhosis include idiopathic portal hypertension, schistosomiasis, congenital hepatic fibrosis, sarcoidosis, cystic fibrosis, arteriovenous fistulas, splenic and PVT, HVT (Budd-Chiari syndrome), myeloproliferative diseases, nodular regenerative hyperplasia, and focal nodular hyperplasia.

DIAGNOSIS

Portal hypertension frequently complicates cirrhosis and presents with ascites, splenomegaly, and GI bleeding from varices (esophageal or gastric), PHG, gastric antrum vascular ectasia (GAVE), or portal hypertensive colopathy.

• Ultrasonography, CT, and MRI showing cirrhosis, splenomegaly, collateral venous circulation, and ascites are suggestive of portal hypertension.

• Upper endoscopy may show varices (esophageal or gastric), PHG, or GAVE.

• Transjugular portal pressure measurements are uncommonly needed except when clinical diagnosis cannot be made.

TREATMENT

Treatment of GI bleeding because of portal hypertension is covered in Chapter 18, Gastrointestinal Diseases.