Gastroesophageal variceal bleeding

Abstract

Massive upper gastrointestinal bleeding from ruptured gastroesophageal varices is the main complication of portal hypertension and represents a frequent cause of death and of liver transplantation in cirrhotic patients. Formation of varices is an almost unavoidable complication in cirrhosis. Varices are already present in about 40% of compensated asymptomatic patients at diagnosis, and the incidence increases to 90% of patients during long-term follow up. Variceal bleeding is the last step in a chain of events that starts with portal hypertension, followed by the development and growth of the varices, until they eventually bleed. In the Hospital Nacional Edgardo Rebagliatis gastrointestinal bleeding unit, 18% of 8 365 admitted patients presented variceal rupture. The therapeutic options to stop the bleeding are divided into general and specific. The pharmacological therapy is addressed to reducing the increased intrahepatic resistance and blood flow. Terlipresin has demonstrated similar efficacy as endoscopic methods, and also as somastatin or octreotide. Sengstaken-Blackmore tubes are still helpful, mainly where no specialists are available. Sclerotherapy for esophageal varices, used since 1982 at our institution, is still the first line endoscopic therapy (96% of success in stopping bleeding). Esophageal varices Stents are the therapeutic option of choice to stop the bleeding, and they produce fewer complications than sclerotherapy. Success in treating bleeding esophageal varices will depend on the readiness of a specialized surgical-medical team that can take decisions in high alert situations.