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Fig. 1: Pathophysiology of portal hypertension in cirrhosis. Portal hypertension results from increased intrahepatic vascular resistance and portal–splanchnic blood flow. In addition, cirrhosis is characterized by splanchnic and systemic arterial vasodilation. Splanchnic arterial vasodilation leads to increased portal blood flow and thus elevated portal hypertension. An increased hepatic venous pressure gradient leads to the formation of portosystemic venous collaterals. Esophagogastric varices represent the most clinically important collaterals given their associated high risk of bleeding. Treatment consists of pharmacologic therapy to decrease portal pressure, endoscopic treatment of varices (band ligation or sclerotherapy) to treat variceal bleeding, and creation of a transjugular intrahepatic portosystemic shunt (TIPS) to reduce portal pressure if drug therapy and endoscopic treatment fail. Photo by: Lianne Friesen and Nicholas Woolridge
Fig. 2: Algorithm for the treatment of variceal bleeding. TIPS = transjugular intrahepatic portosystemic shunt. *The therapeutic option depends on what was done in primary prophylaxis.
Fig. 3: Prophylaxis of variceal bleeding in cirrhosis. Preprimary prophylaxis is aimed at preventing esophagogastric varices (EV) from developing. The goal of primary prophylaxis is to prevent a first variceal bleeding episode once medium or large varices have formed. Secondary prophylaxis is used to prevent recurrent variceal bleeding. Photo by: Lianne Friesen and Nicholas Woolridge
Fig. 4: Algorithm for the primary prophylaxis of variceal bleeding in cirrhosis.
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