Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis

Abstract

PREAMBLE These recommendations provide a data-supported approach to the management of patients with varices and variceal hemorrhage. They are based on the following: (1) formal review and analysis of the recently published world literature on the topic (Medline search); (2) several consensus conferences among experts; (3) the American College of Physicians' Manual for Assessing Health Practices and Designing Practice Guidelines (1); (4) guideline policies, including the American Association for the Study of Liver Diseases' Policy Statement on Development and Use of Practice Guidelines and the American Gastroenterological Association's Policy Statement on the Use of Medical Practice Guidelines (2); and (5) the authors' years of experience caring for patients with cirrhosis and varices. Intended for use by healthcare providers, these recommendations suggest preferred approaches to the diagnostic, therapeutic, and preventive aspects of care. As with other practice guidelines, this guideline is not intended to replace clinical judgment but rather to provide general guidelines applicable to the majority of patients. They are intended to be flexible, in contrast to standards of care, which are inflexible policies designed to be followed in every case. Specific recommendations are based on relevant published information. To more fully characterize the quality of evidence supporting recommendations, the Practice Guidelines Committee of the AASLD requires a class (reflecting benefit versus risk) and level (assessing strength or certainty) of evidence to be assigned and reported with each recommendation (Table 1, adapted from the American College of Cardiology and the American Heart Association Practice Guidelines (3, 4)).Table 1: Grading System for RecommendationsWhen little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Further controlled clinical studies are needed to clarify aspects of this statement, and revision may be necessary as new data appear. Clinical considerations may justify a course of action that differs from these recommendations. These recommendations are fully endorsed by the American Association for the Study of Liver Diseases and the American College of Gastroenterology. INTRODUCTION Portal hypertension is a progressive complication of cirrhosis. Therefore, the management of the patient with cirrhosis and portal hypertensive gastrointestinal bleeding depends on the phase of portal hypertension at which the patient is situated, from the patient with cirrhosis and portal hypertension who has not yet developed varices to the patient with acute variceal hemorrhage for whom the objective is to control the active episode and prevent rebleeding. Practice guidelines for the diagnosis and treatment of gastroesophageal variceal hemorrhage, endorsed by the American Association for the Study of Liver Diseases (AASLD), American College of Gastroenterology (ACG), American Gastroenterological Association (AGA), and American Society of Gastrointestinal Endoscopy (ASGE), were published in 1997 (5). Since then, a number of randomized controlled trials have advanced our approach to managing variceal hemorrhage. Three international consensus conferences have been held (Baveno III in 2000, Baveno IV in 2005, and an AASLD/EASL single topic conference in 2007) in which experts in the field have evaluated the changes that have occurred in our understanding of the pathophysiology and management of gastroesophageal hemorrhage (6, 7). In this updated practice guideline we have reviewed the randomized controlled trials and meta-analyses published in the last decade and have incorporated recommendations made by consensus. PATHOPHYSIOLOGY OF PORTAL HYPERTENSION IN CIRRHOSIS Cirrhosis, the end stage of any chronic liver disease, can lead to portal hypertension. Portal pressure increases initially as a consequence of an increased resistance to flow mostly due to an architectural distortion of the liver secondary to fibrous tissue and regenerative nodules. In addition to this structural resistance to blood flow, there is an active intrahepatic vasoconstriction that accounts for 20–30% of the increased intrahepatic resistance (8), and that is mostly due to a decrease in the endogenous production of nitric oxide (9, 10). Portal hypertension leads to the formation of porto-systemic collaterals. However, portal hypertension persists despite the development of these collaterals for 2 reasons: 1) an increase in portal venous inflow that results from splanchnic arteriolar vasodilatation occurring concomitant with the formation of collaterals (11); and 2) insufficient portal decompression through collaterals as these have a higher resistance than that of the normal liver (12). Therefore, an increased portal pressure gradient results from both an increase in resistance to portal flow (intrahepatic and collateral) and an increase in portal blood