Pathology of fundic varices of the stomach and rupture

Gastric varices, the rupture of which can be a fatal complication of portal hypertension, have not been well documented histopathologically. While cardiac varices develop in continuity with esophageal varices, fundic varices develop independently, having characteristic pathophysiology. Elucidation of the angioarchitecture of fundic varices will facilitate future improvement of treatment.

Twelve stomachs with fundic varices, either resected or autopsied, were examined by injecting a barium-gelatin solution into the vein that was forming varices, soft X-rayed for the study of the vessel course, and then the stomach made into transparent preparations for stereoscopic study. Five fundic varices with a recognizable rupture site were studied histologically.

Fundic varices could be classified into two types: Type I, single vein forming the supplying vessel, varix and draining vessel without changing caliber (eight cases) or plural veins supplying the varix (one case) and; Type II, many branching vessels existing beside the main supplying and draining vessels (three cases). Fundic varices exist in the submucosa with no enlarged vein in the lamina propria, and rupture occurs through the portion of the varix that protrudes into the stomach lumen penetrating the muscularis mucosae and lamina propria.

Fundic varices form with the supplying vessel, mostly singular, and the draining vessel is frequently a gastrorenal collateral. Fundic varices form in the submucosa, unlike esophageal varices, and perforate through the overlying muscularis mucosae and lamina propria.