Portal hypertension is abnormally increased portal venous pressure – blood pressure in the portal vein and its branches, that drain from most of the intestine to the liver. Portal hypertension is defined as a hepatic venous pressure gradient greater than 5 mmHg. Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are therefore grouped as non-cirrhotic portal hypertension. When it becomes severe enough to cause symptoms or complications, treatment may be given to decrease portal hypertension itself or to manage its complications. Signs and symptoms
Signs and symptoms of portal hypertension include:

Ascites (free fluid in the peritoneal cavity),Abdominal pain or tenderness  (when bacteria infect the ascites, as in spontaneous bacterial peritonitis). Increased spleen size (splenomegaly), which may lead to lower platelet counts (thrombocytopenia)
Anorectal varices
Swollen veins on the anterior abdominal wall (sometimes referred to as caput medusae) In addition, a widened (dilated) portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff value of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well. Causes
The causes for portal hypertension are classified as originating in the portal venous system before it reaches the liver (prehepatic causes), within the liver (intrahepatic) or between the liver and the heart (post-hepatic). The most common cause is cirrhosis (chronic liver failure).
Prevention of bleeding
Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin such as terlipressin) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding.The management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide), endoscopic banding ligation, balloon tamponade and TIPS. Ascites
The management of ascites needs to be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, kidney failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, and transjugular intrahepatic portosystemic shunt (TIPS). Hepatic encephalopathy
A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated. References
Further reading


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