Some Aspects of Vascular Disease of the Small Intestine

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Abstract
VASCULAR compromise of the intestine may produce a broad spectrum of pathologic change; corresponding roentgen patterns are not specific for a given disease but reflect the stage of compromise. These patterns have been the subject of a previous paper (30). Recognition of an increasing number of cases of noncatastrophic vascular involvement of the small bowel has focused attention on their importance. Our experience would indicate that such minor insults are far more frequent than superior mesenteric occlusion. Some clinical, pathologic, and experimental aspects of this problem are presented in this paper. Arterial or arteriolar insufficiency and venous obstruction, congestion, and resultant oxygen deprivation may vary in degree. Similarly, the segment of small bowel involved may vary in length. The end-result depends upon an interplay between these factors and the collateral blood supply. Of all the intestinal layers, the mucosa is most sensitive to ischemia; therefore the earliest and mildest changes resulting from reduction in blood flow are mucosal ulceration or atrophy of intestinal villi. Ulceration usually results from relatively acute episodes, while chronic ischemia is more apt to produce atrophic change. More severe degrees of insufficiency may damage the rest of the intestinal wall with deeper ulceration and perforation, with late stenosis, or with inflammatory changes resembling those of enteritis. The clinical manifestations of any given case depend upon the degree of intestinal damage. Thus, the many diseases responsible for intestinal ischemia can produce a gamut of symptoms varying from mild abdominal pain to the shock of frank necrosis. It is to be anticipated that eventually the entire range of pathologic change and corresponding symptomatology will be observed in all these entities. Some examples already reported are malabsorption following superior mesenteric artery embolectomy and atherosclerosis (32, 36), intestinal angina following stenosis of the superior mesenteric artery (23), perforation caused by necrotizing arteriolitis (12) and polyarteritis (26), ileitis secondary to trauma (20) and aortic surgery (38), and gross infarction with intimal hyperplasia and heart failure (1, 10). Ulceration and the attendant complications of hemorrhage and perforation are recognized sequelae of vascular compromise. Controversy exists as to the etiology of so-called nonspecific ulcer (34). It is our firm belief, based on clinical, experimental, and pathologic evidence, that this entity is also the result of vascular compromise and that it most frequently presents as an ulcer-stenosis-dilatation complex. Since becoming interested in this problem, we have collected 10 cases of smallbowel ulcer with stenosis at the ulcer site and dilatation proximal thereto (Table I). During the same period we have encountered no small-bowel ulcers presenting with hemorrhage and 2 presenting with perforation.