Management of Esophageal Variceal Bleeding
Variceal bleeding is a fatal complication of portal hypertension, which can be secondary to cirrhosis or various disorders that lead to increased portal pressures in a patient with preserved hepatic function. Current guideline recommendations base prophyl
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Management of Esophageal Variceal Bleeding Demetrios Tzimas, Juan Carlos Bucobo, and Dana Telem
Introduction Variceal bleeding is a devastating complication of portal hypertension, with a mortality rate of 20 % at 6 weeks after hemorrhage in cirrhotic patients with higher mortality rates in those with Child-Turcotte-Pugh (CTP) Class C disease [1]. Although treatments for variceal bleeding were classically surgical in order to divert blood flow from the portal system, there are various medical, endoscopic, and radiologic techniques that currently are pursued prior to any type of definitive surgical management. In 2007, the American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of Liver (EASL) held the 6th international single-topic consensus conference on varices and variceal hemorrhage, which helped to develop the most recent guidelines on the prevention and management of variceal bleeding [2].
Pathophysiology Clinically significant portal hypertension that leads to gastric and esophageal varices is most often associated with cirrhosis, although it can occur without any cirrhosis or liver dysfunction, termed as non-cirrhotic portal hypertension (NCPH)
D. Tzimas, M.D. (*) • J.C. Bucobo, M.D. Stony Brook University Hospital, 101 Nicolls Road, HSC Building, Room 17-060, Stony Brook, NY 11794-8173, USA e-mail: [email protected]; Juancarlos.bucobo@ stonybrookmedicine.edu D. Telem, M.D. Stony Brook University Hospital, 101 Nicolls Road, HSC T18-040, Stony Brook, NY 11794, USA e-mail: [email protected] © Springer International Publishing AG 2016 A.D. Pryor et al. (eds.), Gastrointestinal Bleeding, DOI 10.1007/978-3-319-40646-6_3
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[3]. In cirrhosis, there is both an increase in portal venous blood inflow from splanchnic vasodilation and hyperdynamic circulation, and an increased resistance to portal flow. Increased resistance to flow is secondary to intrahepatic vascular resistance from structural changes in the liver architecture, as well as dynamic factors such as an increased vascular tone in the microcirculation secondary to endothelial dysfunction, decreased vasodilators such as nitric oxide, increased vasoconstrictors such as thromboxane A2, increased recruitment of stellate cells in sinusoidal vessels, and irregular growth patterns secondary to angiogenesis [4, 5]. This increase in portal venous resistance leads to the development of porto-systemic collaterals via vascular endothelial growth factor (VEGF) and placental growth factor (P1GF), the most important of which are gastric and esophageal varices [5]. Splanchnic vasodilation and cardiac output both increase to compensate for this diversion of flow, leading to increased portal venous inflow in an already high-resistance portal venous system and therefore exacerbating portal hypertension [4, 5]. Portal hypertension in cirrhosis can be measured by the hepatic venous pressure gradient (HVPG), which is calculated as the difference between the wedged hepatic
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