ABSTRACT
In this article, the gross pathology of varices and supplying veins are described comparing esophageal varices and varices of the cardia and fundus of the stomach. The angioarchitecture of the lower esophagus is such that normally very thin parallel veins in the lamina propria mucosae in the palisade zone become enlarged in portal hypertension and join the few larger submucosal veins to form esophageal varices. Enlarged parallel veins come to pile up and join the submucosal veins at an acute angle, rendering this area vulnerable to rupture. Most ruptures occur in this critical area. The basic differences between esophageal and gastric varices are the layers in which the varicose veins form: the lamina propria mucosae and submucosa in the esophageal varices and the submucosa in gastric varices. While cardiac veins and varices are continuous with esophageal varices, fundic varices develop independently as part of a splenogastrorenal shunt that runs through the stomach wall, having rare communications with other veins. The fundic varix is so large in caliber that when it ruptures, the muscularis mucosae and lamina propria are penetrated with massive bleeding. The treatment of varices calls for complete thrombosis of all varicose veins, and merits and demerits of available treatment modalities are discussed based on autopsies from the pathologic point of view. Because of the large size, the management of fundic varices is difficult, and the new technique called balloon-occluded retrograde transvenous obliteration for occluding fundic varices is discussed.
KEYWORD
Esophageal varices - cardiac varices - fundic varices - variceal rupture - palisade zone - parallel veins
