Portal hypertension is hypertension (high blood pressure) in the portal vein and its tributaries. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 10 mmHg or greater.

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Symptoms
Treatment Options

SYMPTOMS

Causes can be divided into prehepatic, intrahepatic, and posthepatic. Intrahepatic causes include liver cirrhosis, and hepatic fibrosis (e.g. due to Wilson's disease, hemochromatosis, or congenital fibrosis). Prehepatic causes include portal vein thrombosis or congenital atresia. Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.

Consequences of portal hypertension are caused by blood being forced down alternate channels by the increased resistance to flow through the systemic venous system rather than the portal system.

TREATMENT OPTIONS

Both pharmacological (B-blocker like Propranolol and isosorbide mononitrate) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is superior to either of them at reducing rate of rebleeding. Disadvantages of TIPS include high cost and increased risk of hepatic encephalopathy, and it does not improve the mortality rate.

Managment of active variceal bleeding: After resuscitation, the management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide or terlipressin), endoscopic banding ligation, balloon tamponade and TIPS.

Management of ascites: This should be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, renal failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, transjugular intrahepatic portosystemic shunt (TIPS) and peritoneovenous shunt.

Control of hepatic encephalopathy: This includes reduction of dietary protein, followed by lactulose and use of oral antibiotics.

Ascites (free fluid in the peritoneal cavity).
Hepatic encephalopathy.
Increased risk of spontaneous bacterial peritonitis.
Increased risk of hepatorenal syndrome.
Splenomegaly (enlargement of the spleen) with consequent sequestration therein of red blood cells, white blood cells, and platelets, together leading to mild pancytopenia.
Portacaval anastomoses: Esophageal varices, gastric varices, anorectal varices (not to be confused with hemorrhoids), and caput medusae. Esophageal and gastric varices pose an ongoing risk of life-threatening hemorrhage, with hematemesis or melena.