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March 11, 1961

Pathogenesis of Esophageal Varix Rupture

Author Affiliations

New York City

From the Department of Medicine, New York University School of Medicine, and Bellevue Hospital.

JAMA. 1961;175(10):874-879. doi:10.1001/jama.1961.03040100038010
Abstract

Clinical, pathological, and hemodynamic studies indicate that peak elevations in portal blood pressure, coupled with flooding of the cardioesophageal pathways by blood precipitously mobilized from the stagnant splanchnic basin, underlie the pathogenesis of varix rupture. Retching, vomiting, straining, coughing, etc., influence the magnitude and integrity of the varicosities and are often the mechanisms that trigger such vascular accidents. Several facts argue against the hypothesis of erosion by acid and pepsin, especially when the site of hemorrhage is located out of range of the corrosive gastric juice. Prophylactic and therapeutic considerations of the patient with esophageal varices must take into account all of the varied factors which determine blood flow in that region.

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