A portal hypertension is an increased pressure in the portal vein. It is usually the result of cirrhosis (in developed countries), a schistosomiasis (in endemic areas) or a change of liver vessels. The consequences of portal hypertension include esophageal varices and portosystemic encephalopathy. Diagnosis is based on clinical criteria, often associated with imaging and endoscopic procedures. Treatment includes prevention of gastrointestinal bleeding with the aid of endoscopy, with drugs or a combination of both, and the rare setting a portocaval shunts or a liver transplant.

A portal hypertension is an increased pressure in the portal vein. It is usually the result of cirrhosis (in developed countries), a schistosomiasis (in endemic areas) or a change of liver vessels. The consequences of portal hypertension include esophageal varices and portosystemic encephalopathy. Diagnosis is based on clinical criteria, often associated with imaging and endoscopic procedures. Treatment includes prevention of gastrointestinal bleeding with the aid of endoscopy, with drugs or a combination of both, and the rare setting a portocaval shunts or a liver transplant.

See also liver structure and function and evaluation of the patient with liver disease.) A portal hypertension is an increased pressure in the portal vein. It is usually the result of cirrhosis (in developed countries), a schistosomiasis (in endemic areas) or a change of liver vessels. The consequences of portal hypertension include esophageal varices and portosystemic encephalopathy. Diagnosis is based on clinical criteria, often associated with imaging and endoscopic procedures. Treatment includes prevention of gastrointestinal bleeding with the aid of endoscopy, with drugs or a combination of both, and the rare setting a portocaval shunts or a liver transplant. The portal vein, which is formed by the confluence of the superior mesenteric vein and splenic vein, blood passes from the gastrointestinal tract, from the spleen and from the pancreas into the liver. Within the sinusoids the blood from the portal circulation mixed with the arterial blood. From the sinusoids the blood via the hepatic veins into the inferior vena cava flows. The normal portal pressure is 5 to 10 mmHg (7-14 cm H2O), it exceeds the pressure in the inferior vena cava 4 to 5 mmHg (portalvenöser gradient). Higher values ??are defined as portal hypertension. Portal hypertension etiology resulted primarily from increased resistance in the blood flow in the portal vein. A common cause of this resistance is a disease of the liver; unusual causes a blockage of the spleen or portal vein and a disturbed venous outflow liver (see table: The most common cause is a portal hypertension). An increased flow volume is rarely the cause, although it may contribute to portal hypertension in cirrhotic and cause massive splenomegaly in hematologic diseases. The most common cause is a portal hypertension mechanism or location cause Prähepatisch closure portal or splenic vein thrombosis Increased portal flow (rare) arteriovenous fistula Massive splenomegaly caused by a primary hematologic disorder Hepatic Presinusoidal Idiopathic portal hypertension Other periportal disorders (eg. , Primary biliary cirrhosis, sarcoidosis, congenital hepatic fibrosis) Schistosomiasis Sinusoidal cirrhosis (all causes) Postsinusoidal Hepatic sinusoidal obstruction syndrome (hepatic veno-occlusive disease) posthepatic closure hepatic vein thrombosis (Budd-Chiari syndrome), obstruction of inferior vena cava resistance against right heart filling Constrictive pericardium itis Restrictive cardiomyopathy Pathophysiology of cirrhosis connective tissue changes and regeneration leading to an increased resistance in the sinusoids and in the terminal portal vessels. Other potentially reversible factors can contribute to portal hypertension; This information can include the contractility of Sinusoidalzellen, the production of vasoactive substances (eg. B. Endothelin, NO), various systemic mediators arteriolar resistance and may be a swelling of the hepatocytes. Over time, the portal hypertension leads to portosystemic venous collateral formation. You can decrease the portal vein pressure slightly, but can lead to complications. Advanced serpentine submucosal vessels (varices) in the distal esophagus and occasionally in gastric fundus can rupture and cause bleeding to a sudden life-threatening gastrointestinal. Bleeding are rare, unless the portal pressure gradient> 12 mmHg. Congestion in the gastric mucosa (portal hypertensive gastropathy) can cause acute or chronic bleeding regardless of varices. Visible collateral in the abdominal wall are common; venous vessels that go away from the umbilicus (caput medusae) are rare and point to a strong flow in the umbilical and periumbilical veins. Collateral around the rectum can cause Rektumvarizen that can bleed. Portosystemic collateral decrease blood flow in the liver. Therefore, the liver receives less blood when the portal flow increases (decreased hepatic reserve). In addition, toxic substances from the intestine directly into the systemic circulation and contribute to the formation of a portosystemic encephalopathy. The venous stasis in the visceral organs as a result of portal hypertension contributes about altered Starling forces ascites. Splenomegaly and hypersplenism often arise as a result of increased pressure in the splenic vein. Consecutive thrombocytopenia, leukopenia and less frequently haemolytic anemia can result. Portal hypertension and a hyperdynamic circulation are often associated with each other. The underlying mechanisms are complex and seem an altered sympathetic tone, production of nitric oxide and other endogenous vasodilators, and increased activity of humoral factors to bring (z. B. glucagon) with itself. Symptoms and complaints The portal hypertension is asymptomatic, symptoms and clinical signs based on their complications. The most dangerous is acute variceal bleeding. In the patients typically a sudden painless upper gastrointestinal bleeding occurs, which is often massive. Bleeding due to a portalhypertensiven gastropathy often run subacute or chronic. There may be ascites, splenomegaly and portosystemic encephalopathy. Usual diagnostic clinical evaluation A portal hypertension is considered in a patient with chronic liver disease when signs of collateralization, splenomegaly, ascites or portosystemic encephalopathy present. The detection requires the measurement of hepatic venous pressure gradient through a transjugular catheter. In order for the portal pressure can be estimated. However, this method is invasive and is not performed in the routine. Imaging techniques can be useful in cases of suspected cirrhosis diagnosis. An ultrasound or computed tomography often show dilated intra-abdominal collaterals, a Doppler ultrasound examination provides information on the continuity and flow in the portal vein. Oesophagogastric varices and gastropathy portalhypertensive be diagnosed by endoscopy, as well as the existence of a risk of bleeding from varices (z. B. reddened spots on the veins, so-called. Cherry spots). Prognosis The mortality in acute variceal bleeding is> 50%. The prognosis depends on the degree of hepatic reserve and the bleeding. In the survivors, there is a bleeding risk of recurrence within the next one to two years of 50 to 75%. A controlled permanent, endoscopic or drug treatment reduces the risk of bleeding, but affects the long-term mortality only marginally. Treatment of acute bleeding overview of gastrointestinal bleeding: treatment is in varices: discussed therapy. Ongoing therapy endoscopic therapy and monitoring Non-selective beta-blocker with or without isosorbide Sometimes portal vein shunts If possible, the underlying disease should be treated. The long-term treatment of esophageal varices that have bled, is the endoscopic banding to obliterate the remaining varices, then recurrent varices are monitored by regular endoscopy. The medical long-term treatment of varices that have bled, consists of the administration of beta-blockers; these drugs set the portal pressure v. a. reduced by reducing portal flow. Their effect can vary. These include propranolol (40-80 mg po 2 times a day), nadolol (40-160 mg po 1 times daily), timolol (10-20 mg po 2 times a day) and carvedilol (6.25 to 12.5 po mg 2 times daily) the dose is adjusted based on the decrease in heart rate of about 25%. Addition of isosorbide mononitrate 10-20 mg p.o. can 2 times a day reduce portal pressure in addition. The combination of langzeitendoskopischer and drug therapy appears to be more effective than therapy alone. In patients who do not respond adequately to the forms of therapy, a transjugular intrahepatic portosystemic shunt (TIPS) or, less frequently, a surgical shunt portocaval should be discussed. In a TIPS the shunt is formed by a stent between the portal and hepatic venous circulation is placed in the liver. (See also the American Association for Study of Liver Disease practice guideline The Role of transjugular Intrahepatic portosystemic shunt (TIPS) in the management of portal hypertension: Update 2009.) Although TIPS may lead to fewer deaths as a direct shunt operations, especially by acute bleeding, can the preservation of continuity require repeated because the stent can narrow or close over time operations. Long-term results are not known. A liver transplant may be indicated in certain patients. In patients where the veins have not bled, non-selective beta-blockers may reduce the risk of bleeding. Bleeding due to a portalhypertensiven gastropathy can be treated with portal antihypertensive drugs. If the drugs do not lead to success, a shunt may be considered, although the results are here less successful compared to oesophageal varices. A hypersplenism rarely leads to clinical problems, it usually requires no specific treatment. Splenectomies should be avoided. Conclusion The portal hypertension is usually the result of cirrhosis (in developed countries), a schistosomiasis (in endemic areas) or a change of liver vessels. Complications can acute variceal bleeding (with a high mortality), ascites, splenomegaly and portosystemic encephalopathy. The diagnosis of portal hypertension is based on clinical criteria. To acute variceal bleeding to prevent, to Initiate regular monitoring and endoscopic banding. To prevent bleeding, non-selective beta-blocker with or without isosorbide mononitrate, transjugular intrahepatic portosystemic shunt (TIPS), or both are used.

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