The Banding of an Esophageal Varix

Abstract

The proportion of patients with upper gastrointestinal bleeding (UGI) from esophageal varices varies among centres; however, in approximately 10% of all emergency patients with UGI bleeding, the source is identified as esophageal varices (1). Centres that have a special interest in liver disease may have a higher proportion of patients presenting with this problem. The significance of these lesions is highlighted by the high morbidity and mortality rates associated with the presence of acutely bleeding varices. Although varices from portal hypertension may develop within the stomach (ie, fundal), small intestine (duodenal, jejunal or ileal) or colon (classically rectal), the most common site is within the esophagus. The etiology of the varices is usually cirrhosis; however, any cause of portal hypertension (ie, portal vein thrombosis) can theoretically result in a similar vascular outcome. Overall, approximately 60% of patients with cirrhosis develop esophageal varices and 60% of these have a bleeding episode (2). The natural history of esophageal varices is dramatic in that up to one-third of patients may rebleed over the subsequent six weeks if untreated. The significance of this problem has therefore spawned numerous studies, and the optimal management of bleeding esophageal varices has been determined. The first step in the management of any UGI bleeding patient is resuscitation. As endoscopic therapy has become more widely available, the urgent call for the endoscopist tends be rapidly transmitted with alarming speed from the emergency room when an unstable patient arrives with hematemesis and/or melena. It should be clearly recognized that in the ‘ABCs’ of resuscitation, the ‘E’ for endoscopy actually comes after airway, breathing and circulation have been adequately managed. Most patients with UGI bleeding (approximately 80%) stabilize with intravenous fluid resuscitation. Access with two large-bore intravenous lines is preferable so that pharmacological agents and blood transfusions may be simultaneously administered. In the setting of esophageal variceal hemorrhage, the use of ancillary medications to improve outcomes (primarily by decreasing portal pressures) has been advocated. For many years, vasopressin (with or without nitroglycerin) was used at a dose of 0.4 units/min. Morbidity from the vasopressin occurs in 20% of patients if it is used in isolation; therefore, the addition of nitroglycerin has been instituted to decrease this risk. Another approach to avoid complications from vasopressin is to alter its underlying structure, so that a ‘slow-release’ vasopressin analogue results (glypressin). Glypressin has been associated with fewer side effects, but without improved efficacy. Unlike vasopressin, octreotide has no effect on systemic arterial pressure, cardiac index or pulse rate. Somatostatin and its longer-acting analogue octreotide are presently the primary pharmacological modality of therapy for UGI bleeding from esophageal varices. Somatostatin has a half-life of 2 min to 3 min, with a pharmacological half-life of 90 min. A bolus of 75 µg to 100 µg decreases splanchic blood flow by 25%, total hepatic blood flow by 25%, wedged hepatic vein pressure by 10% and measured varix pressure by approximately 35% (3-5). Somatostatin has been compared with vaso