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Gastroesophageal varices are among the most dangerous complications associated with cirrhosis. They are present in 50% to 60% of cirrhotic patients.1 Approximately 30% of patients will experience an episode of variceal hemorrhage within 2 years of the diagnosis of varices.1 The major factors that determine the risk of bleeding are variceal size and the degree of liver dysfunction.1-3 Variceal bleeding stops spontaneously in 20% to 30% of cases.1-4 It recurs in 70% of patients within 1 year of the initial episode.1-4 Mortality is as high as 50% in the first year.5 Variceal bleeding accounts for almost one-third of deaths in cirrhotic patients. Variceal hemorrhage has a poor prognosis if it is associated with coexisting or subsequent complications (e.g., rebleeding, infection, hepatic dysfunction, and portal pressure ≥ 12 mmHg).6,7 Somatostatin and its analogues cause splanchnic vasoconstriction, leading to reduced portal pressure and portal blood flow, whereas venodilators reduce portal pressure by reducing resistance to portal flow.7,8
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Doctors Sengstaken and Blakemore developed the concept of balloon tamponade to control bleeding esophageal and gastric varices in 1950. They developed a triple-lumen and double-balloon system that bears their names. The Sengstaken-Blakemore (SB) tube is used as a temporizing measure to stop variceal bleeding until more definitive means are available (Figures 81-1 and 81-2). The SB tube was designed for the control of esophageal varices and as a diagnostic aid to determine the source of hemorrhage into the stomach. There are variants of the SB tube (e.g., the Minnesota tube and the Linton-Nachlas tube). The Minnesota tube is a quadruple-lumen, double-balloon system (Figure 81-3).9 The Linton-Nachlas tube was designed with only an esophageal balloon (Figure 81-4). It controls bleeding for esophageal varices. These tubes are rarely used today due to the significant complications and the widespread availability of endoscopy and its therapeutic interventions.
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