ROBERT McKEE KISKADDON, M.D.
FREDERIC E. TEMPLETON, M.D.
R. JOHN F. RENSHAW, M.D.
The pathologic physiology in gastrocolic fistula has not been fully explored, and there are conflicting opinions as to the mechanism which produces the syndrome.1,2,3,4,5 Gastrocolic fistula does not occur frequently, but it is one of the most dreaded complications of surgical treatment for peptic ulcer. It may produce a devastating syndrome which includes diarrhea, weight loss, malnutrition, anemia, and steatorrhea.
Haller6 described the first case of gastrocolic fistula in 1755, and in 1903 Czerny7 made the first report of fistula following gastrojejunal ulcer. Voorhoeve8 collected 103 cases in the literature in 1912.
As the utilization of gastroenterostomy in the treatment of peptic ulcer increased the incidence of gastrojejunocolic fistula secondary to jejunal ulcer increased. Atwater, Butt, and Priestley9 reported that 11 o t 14 per cent of gastrojejunocolic ulcers finally develop into gastrojejunocolic fistulae. In their series of 42 cases, 40 were secondary to gastrojejunal ulcer following surgical treatment of peptic ulcer, and 2 were the result of carcinoma. There are other causes for gastrojejunocolic fistula, but they are rare. These include tuberculosis, syphilis, ulcerative colitis, peritoneal abscess, trauma, and congenital deformities.
Direction of the flow of aliment has been the subject of much discussion. Earlier workers8,10 accepted fecal vomiting as evidence of a flow of colonic contents into the stomach. Other authors indicate that the flow is largely from the stomach to the colon. They believe that the shunting of food through the fistula from the stomach into the colon is a major factor in the production of the. . .