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Article
August 1963

Pathogenesis of Esophageal Varix RuptureA Study Based on Gross and Microscopic Examination of the Esophagus at the Time of Bleeding

Author Affiliations

TORRANCE, CALIF
Professor and Chief of Surgery and Markle Scholar in Medicine (Dr. Orloff); Resident in Surgery (Dr. Thomas).; From the Departments of Surgery, Harbor General Hospital and the University of California, Los Angeles School of Medicine.

Arch Surg. 1963;87(2):301-307. doi:10.1001/archsurg.1963.01310140109019
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

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