Prevention and treatment of variceal haemorrhage in 2017

Felix Brunner, Annalisa Berzigotti, Jaime Bosch
Liver International: Official Journal of the International Association for the Study of the Liver 2017, 37 Suppl 1: 104-115
Variceal haemorrhage is a major complication of portal hypertension that still causes high mortality in patients with cirrhosis. Improved knowledge of the pathophysiology of portal hypertension has recently led to a more comprehensive approach to prevent all the complications of this condition. Thus, optimal treatment of portal hypertension requires a strategy that takes into account the clinical stage of the disease and all the major variables that affect the risk of progression to the next stage and death. In patients with compensated liver disease, the correction of factors influencing the progression of fibrosis, in particular aetiologic factors, is now feasible in many cases and should be achieved to prevent the development or progression of gastroesophageal varices and hepatic decompensation. Once gastroesophageal varices have developed, non-selective beta-blockers remain the cornerstone of therapy. Carvedilol provides a greater decrease in portal pressure and is currently indicated as a first-choice therapy for primary prophylaxis. The treatment of acute variceal haemorrhage includes a combination of vasoactive drugs, antibiotics and endoscopic variceal band ligation. In high-risk patients, the early use of transjugular intrahepatic portosystemic shunt (TIPS) lowers the risk of re-bleeding and improves survival. Transjugular intrahepatic portosystemic shunt is the choice for uncontrolled variceal bleeding; a self-expandable metal stent or balloon tamponade can be used as a bridging measure. The combination of non-selective beta-blockers and endoscopic variceal band ligation reduces the risk of recurrent variceal bleeding and improves survival. In these cases, statins seem to further improve survival. Transjugular intrahepatic portosystemic shunt is indicated in patients who rebleed during secondary prophylaxis.

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