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October 1, 1955


JAMA. 1955;159(5):484. doi:10.1001/jama.1955.02960220074012

Esophageal varices develop secondarily to partial or complete obstruction of the portal blood flow at the junction of the esophagus and cardia of the stomach between the coronary vein, a branch of the portal circulation, and the esophageal veins, branches of the azygos vein, of the systemic circulation. Portal hypertension may be one of two types, intrahepatic or extrahepatic, or a combination of both. Apparently, the portacaval shunt created by the natural anastomosis of the two systems at the gastroesophageal junction is inadequate to prevent increased intraportal tension and the consequent development of esophageal varices.

Chiles and his co-workers1 at the Mayo Clinic found that, in a study of 80 cases of ruptured esophageal varices in which hemorrhage led to death, rupture was caused in 39% of the cases by the increased hydrostatic pressure within the varix and in 50% by ulceration of the varix. In the majority of

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