Portal vein hypertension is a common and serious complication of cirrhotic liver disease. Because the blood flow entering the portal vein is being resisted by the inflamed, fibrostic and nodular liver tissue, the pressure in the portal vein is increased. Severe complications can occur as the result of this increased pressure and these include ascites(water retention), gastroesophageal varices and encephalopathy(mental disorientation).

In viral hepatitis B and C, portal vein hypertension mainly stems from hepatic damages, caused by chronic persistent inflammation and fibrosis in the liver. As the liver inflammation and fibrosis progresses, the pressure in the portal vein will continually rise. When this pressure becomes two times higher than the normal range, collateral complications will start to surface. Under this pressure level, the portal vein and systematic blood vessels form collaterals, which will cause the development of gastroesophageal varices. Varices are the main contributory factor in bleeding, which is the most serious complication in cirrhotic liver diseases. Another cause of this type of bleeding is the drop of platelet count and reduced production of blood clotting factors in the liver.

When a severe gastro esophageal bleeding occurs, the patient’s stool color will turn shiny black and blood pressure will drop sharply and may cause shock. If this happens, the patient should be rushed to the nearest emergency room immediately.

Another common complication related to the hypertension of portal vein is ascites. In this stage of the liver disease, the liver's ability to synthesize albumin is greatly deteriorated. The resulting low albumin level causes the osmotic pressure of the blood to decrease and the serum’s ability to hold fluid is compromised. Fluid then leaks into the stomach cavity and forms the ascites.

When ascites occurs, the patient should restrict salt intake (salt causes water retention). To treat ascites, the first measure is to improve the overall function of the liver and increase albumin production.