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