Portal hypertension is a major complication of cirrhosis characterized by a pathological hepatic venous pressure gradient (HVPG) ≥ 5 mmHg. The structural changes observed in the liver leading to intrahepatic vascular resistance and, consequently, portal hypertension appear in the early stages of cirrhosis. Clinically significant portal hypertension (HVPG ≥ 10 mmHg) is associated with several clinical consequences, such as ascites, hyponatremia, gastroesophageal variceal bleeding, hepatorenal syndrome, cardiopulmonary complications, adrenal insufficiency, and hepatic encephalopathy. The diagnosis and management of these complications depend on their early identification and treatment. Regarding ascites, diuretics are a useful treatment, although plasma sodium levels must be properly controlled to avoid hyponatremia. The management of hypovolemic hyponatremia usually consists in stopping diuretics and the administration of volume. On the contrary, hypervolemic hyponatremia is managed with fluid and sodium restriction. Transjugular intrahepatic portosystemic shunt (TIPS) should be considered in patients with refractory ascites. Primary prophylaxis of variceal bleeding should be based mainly on non-selective beta-blockers. Management of acute gastroesophageal variceal bleeding includes vasoactive drugs and endoscopic band ligation and, in patients at high risk of failure and rebleeding, preemptive use of TIPS. Secondary prophylaxis with a combination of non-selective beta-blockers and endoscopic band ligation is the treatment of choice. This article focuses on the management of ascites, hyponatremia, and gastroesophageal variceal bleeding.





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