Endometriosis and tuboperitoneal fistulas after tubal ligation.

I read with interest the report on endometriosis and the development of tubal peritoneal fistulas after tubal ligation. The authors stated that they had not seen recanalization of the oviducts. I call your attention to observations in the past. A review of these papers will provide evidence that recanalization does in fact occur. I have personally seen 2 such cases after Pomeroy procedures. Your observation that the changes which you describe as endometriosis occur only in the proximal stump may be critical. If this is true, it appears that you may be correct in saying that this is endometriosis and that the past assumption that the process was invasion of tissue by tubal epithelium was incorrect. On the other hand, you did not spell out exactly how many of your cases revealed epithelium-lined spaces which could be strictly classified as endometriosis. Certainly, at least some of them have stroma and epithelium which appeared to be that of endometriosis. Sampson stated that the misplaced tubal mucosa may assume the structure and function of uterine mucosa and he goes on to describe a patient, aged 37, whose tubes and ovaries were severed from the uterus. The uterus was then drawn through the abdominal incision and pulled into the subcutaneous part of the abdomen. Later, a firm mass was detected adherent to the cornua of the uterus. Endosalpingosis was present in both nodules which had invaded the adipose tissue of the abdominal wall. Microscopically, the tubal mucosa appeared to be invading the adipose tissue. Sampson regards the behavior of tubal epithelium in repair of salpingectomy wounds as a striking exception to the rule which covers the healing of operative wounds of hollow viscera. In the stumps of tubes, sprouts of its epithelium often invade the wall and grow beyond it. It may continue after healing is complete. This phenomenon was designated by Sampson as endosalpingosis, and he reported seeing it in 3 similar cases. In reviewing Sampson's observations, it does appear that this anatomical change does not occur in the distal stump, as he speaks only about the described. Why does tubal ligation incite this change? The question is whether it is really endometriosis or some type of transformation of the tubal mucosa? Why should there be more of a tendency for endometrium to implant on this tissue after ligation compared to prior ligation? Sampson seemed to be convinced that this was tubal epithelium. Only careful study of this by experienced pathologists may reveal the answers. Perhaps in some cases, this is tubal epithelium. The other possibilities include metaplasia into endometrial mucosa, as well as true dennovo implants of ectopic endometrium.