Portal hypertension is a frequent syndrome characterized by a chronic increase in portal venous pressure and by the formation of portal-systemic collaterals. Its main consequence is massive bleeding from ruptured esophageal and gastric varices. Bleeding is promoted by increased portal and variceal pressure, and is favored by dilatation of the varices. The evaluation of the portal hypertensive patient should include the assessment of portal vein patency by ultrasonography, endoscopic evaluation of the presence, size, and extent of esophageal varices, and hemodynamic studies with measurements of portal pressure and of portal-collateral blood flow. The preferred techniques are hepatic vein catheterization and measurement of azygos blood flow. Endoscopic measurements of variceal pressure and estimations of portal blood velocity by the Doppler technique have recently been introduced, but are still research procedures. Acute variceal hemorrhage should be treated under intensive care. Specific therapy to arrest variceal bleeding includes balloon tamponade, vasopressin, somatostatin, sclerotherapy, and emergency surgery. Treatment of portal hypertension is aimed at preventing variceal hemorrhage and bleeding-related deaths. Pharmacologic prophylaxis is based on the use of drugs that cause a sustained reduction in portal pressure; most studies have used propranolol. Surgery and endoscopic sclerotherapy can also be used to prevent rebleeding.