Primary prophylaxis of gastroesophageal variceal bleeding: consensus recommendations of the Asian Pacific Association for the Study of the Liver

Abstract

The Asian Pacific Association for the Study of the Liver (APASL) set up a Working Party on Portal Hypertension in 2002, with a mandate to develop consensus guidelines on various clinical aspects of portal hypertension relevant to disease patterns and clinical practice in the Asia-Pacific region. Variceal bleeding is a consequence of portal hypertension, which, in turn, is the major complication of liver cirrhosis. Primary prophylaxis to prevent the first bleed from varices is one of the most important strategies for reducing the mortality in cirrhotic patients. Experts predominantly from the Asia-Pacific region were requested to identify the different aspects of primary prophylaxis and develop the consensus guidelines. The APASL Working Party on Portal Hypertension evaluated the various therapies that have been used for the prevention of first variceal bleeding. A 2-day meeting was held on January 12 and 13, 2007, at New Delhi, India, to discuss and finalize the consensus statements. Only those statements that were unanimously approved by the experts were accepted. These statements were circulated to all the experts and were subsequently presented at the annual conference of the APASL at Kyoto, Japan, in March 2007.

Current Role of Surgery in Portal Hypertension

“…Traditionally, at the ultrastructural level, PHT has been classified into presinusoidal, sinusoidal, and postsinusoidal. It is for the sinusoidal and postsinusoidal blocks that there is an accurate but invasive way of monitoring the portal pressure by using the method to estimate the hepatic venous pressure gradient (HVPG) in the vascular/hemodynamic lab [1][2][3]. In cirrhotic patients, as about a third to half of them will actually have PHT; HVPG >5 mmHg indicates PHT.…”

“…In cirrhotic patients, as about a third to half of them will actually have PHT; HVPG >5 mmHg indicates PHT. PHT becomes clinically significant when the HVPG is ≥10 mmHg [1][2][3]. This is the pressure threshold when PHT leads to the formation of esophagogastric varices, retroperitoneal and periportal collaterals, hypersplenism, low serum albuminascitic albumin gradient ascites, spontaneous bacterial peritonitis, etc.…”

“…It has been shown that reduction of HVPG to 12 mmHg or less or 20% reduction from baseline reduces the risk of first bleed [1][2][3][4][5]. HVPG has been used to identify patients with high risk of variceal bleeding and nonresponders to pharmacotherapy in clinical trials [1][2][3][4][5].…”

“…It is generally believed that surgery and EST have no important role to play in the preprimary and primary prophylaxis of variceal bleeding in PHT due to cirrhosis [2,4,32,33]. By and large, β-blockers and EVL are preferred in this setting [2][3][4].…”

“…This is the pressure threshold when PHT leads to the formation of esophagogastric varices, retroperitoneal and periportal collaterals, hypersplenism, low serum albuminascitic albumin gradient ascites, spontaneous bacterial peritonitis, etc. Varices rupture and bleed only when the HVPG >12 mmHg [1][2][3]. …”