Colonic Endometriosis: Roentgenologic Aspects

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Abstract
Involvement of the colon by endometriosis is not an unusual occurrence. According to Cullen, about one-half of all extensive cases will show some form of intestinal involvement. Meigs pointed out, more than fifteen years ago, that endometriosis was definitely increasing in frequency; therefore, more pelvic complications were to be expected. It behooves the physician to bear in mind the possibility that a given colonic lesion may represent endometriosis. The radiologist should exert great caution in distinguishing between this condition and carcinoma or inflammatory disease, and should carefully correlate his findings with the clinical and laboratory evidence. Endometrial lesions may occur in the serosa of the appendix, cecum, sigmoid, rectum, mesentery, or epiploic appendages. It is believed to result from retrograde menstruation through the fimbriated end of the fallopian tube, with implantation of bits of endometrial tissue on adjacent structures such as the lateral surface of the ovary and the peritoneum in the posterior cul-de-sac. Thus the peritoneal surfaces of the uterus, tubes, and intestine become involved, and subsequently the rectovaginal septum. The implants become adherent and growth proceeds. The peritoneum resists invasion and reacts in an inflammatory-like manner, giving rise to typical “shotty” indurations which are palpable on pelvic examination. The implants never produce endometrial cysts of any size, such as are seen in the ovary. They do, however, rupture and spread the disease. In contradistinction to primary carcinoma, endometriosis grows from the outside in. Most often it occurs as a harmless plaque or implant. The bowel, however, may become adherent and then twist, with consequent stenosis or obstruction. Occasionally, invasion takes place to such an extent that the entire bowel wall is involved, including the mucosa, and varying degrees of obstruction may result. These endometrial lesions naturally display cyclical, features related to the menstrual cycle and regress at the menopause, leaving a puckered scar. Resection is rarely required. The sigmoid at the level of the cul-de-sac is most often involved. The appendix may be invaded but appendicitis never results. It is difficult to assess accurately the incidence of obstructing endometriosis of the colon. Many lesions undoubtedly involve the rectosigmoid without producing constriction, stenosis, or obstruction. Of Jenkinson and Brown's series of 47 patients with rectosigmoid involvement, 21 had symptoms of some degree of obstruction. It would thus appear that endometrial disease of the colon occurs more commonly than has been suspected. It is undoubtedly true that it is frequently overlooked because other symptoms and signs of pelvic endometriosis are more prominent and draw attention away from the possibility of bowel involvement. Many times the menopause automatically terminates the disease process, and it is never discovered.

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