film Fig. 1. Preexplorotory of the showil “g dilatation hepati c ducts and flow of dye into th mesmall intestine.
serum bilirubin
urobilinogen phosphatase
from
2.2 mg/iOO
the
urine.
was 29 K.A.
units.
ml. c~,n-
S G0.T.
xnd
760
KERAMIDAS
ET Al
GASTRIC
HETEROTOPIA
Fig. 3. Microscopic appearance chief, and parietal cells ( x 160).
of the m~cosa of the ectopic gastric
tissue. There
are tnucus,
The patient was initially treated with parenteral antibiotics. in combination with antispasmodic+ and appropriate diet. He improved. but tenderness was still present on repeated examination. X-ray studies of the biliary tract revealed dilatation of the hepatic ducts. passage of dye into the small intestine, and no visuali/-atton of the gallbladder (Fig. I). At laparotomy the gallbladder was found distended with adhesions and thickening of the w..dl, particularly in the area of the neck. An intraoperative cholangiogram showed no obstruction. The cystic duct was ligated and the gallbladder removed. The excised gallbladder measured 7 x 5 cm. Bisection extending from the fundus up to the cystic duct disclosed two macroscopically different segments of mucosa. The cystic duct and the proximal area of the neck were of unusual appearance with coarse folds of whitish color. The wall of the gallbladder was increased to several times its normal thickness. No stones were found. Macroscopic examination disclosed gastric tissue in sections taken from the neck and the cysttc duct. The gastric tissue contained chief, mucus, and parietal cells and was composed of all layers including muscularis mucosae (Figs. 2. 3). The wall of the gallbladder showed typical chronic inflammation.
DISCUSSION Gastric and biliary tree primordia are closely associated in early gestational life. Heterotopia of gastric tissue in the gallbladder may result from a developmental accident or heterotopic ditferentiation. In the present case the ectopic gastric tissue in the cystic duct and neck caused some degree of obstruction leading to stasis. It seems that stasis and secretions of gastric mucoza in the gallbladder led to inflammation and adhesions between the gallbladder and the adjacent extrahepatic biliary tract. Hyperbilirubinemia was a complication of acute noncalculous cholecyctitis. This development may result from compression of the common duct by an acutely distended gallbladder from intrahepatic cholostasis or from alteration of impermeability of the gallbladder epithelium to conjugated bilirubin.’