Pathogenesis of Esophageal Varix Rupture

Abstract

An understanding of the pathogenesis of esophageal varix rupture is of more than academic importance, since upon such knowledge depends the development of a rational approach to the prophylaxis and therapy of this highly lethal disorder. Although much is known about the mechanisms responsible for the formation of esophageal varices, considerable controversy exists regarding the exact cause of varix rupture. Two major factors have been implicated in the pathogenesis, namely, erosion of the varix due to reflux acid-peptic esophagitis, and bursting of the varix due to increased hydrostatic pressure in the portal venous system. The treatment of bleeding esophageal varices has consisted, in large part, of measures directed at counteracting one or the other of these two factors. Much of the evidence cited to support the acid-peptic hypothesis has come from animal experiments of uncertain applicability to man,^1,2,15,16 from esophagoscopic examination of cirrhotic patients performed many days after bleeding