Advanced laparoscopic surgery for the removal of rectovaginal septum endometriotic or adenomyotic nodules.

In the pelvis, three different forms of endometriosis (Donnez et al, 1992) must be considered: (1) peritoneal, (2) ovarian, (3) rectovaginal septum. By evaluation of the mitotic activity and the stromal vascularization, we have recently suggested (Nisolle et al, 1993) that peritoneal red lesions were the most aggressive form of the disease and progress to the so-called typical or black lesion, which must be considered as an enclosed implant surrounded by fibrosis. This type of infiltration must be clearly differentiated from the rectovaginal endometriotic nodule. Koninckx (1993) recently described three types of deep-infiltrating endometriosis: deep-infiltrating endometriosis of type I is a rather large lesion in the peritoneal cavity, infiltrating conically with the deeper parts becoming progressively smaller. It has been suggested that this type of endometriosis is caused by infiltration. In type II lesions, the main feature is that bowel is retracted over the lesion which thus becomes deeply situated in the rectovaginal septum although not actually infiltrating it. Type III lesions are the deepest and most severe. They are spherically shaped, situated deep in the rectovaginal septum, often only visible as a small typical lesion at laparoscopy or often not visible at all. This lesion is often more palpable than visible and is acutely tender if the patient is examined at the time of menstruation, and gives rise to severe dyspareunia. In our experience there are two different types of 'deep-infiltrating endometriosis': 1. True deep-infiltrating endometriosis caused by the invasion of a very active peritoneal lesion deep in the retroperitoneal space. In cases of lateral peritoneal invasion, uterosacral ligaments can be involved as well as the anterior wall of the rectosigmoid bowel junction resulting in a retraction, adhesions and secondary obliteration of the cul-de-sac. 2. Pseudo deep-infiltrating endometriosis or adenomyosis of the rectovaginal septum. This lesion originates from the rectovaginal septum tissue and consists essentially of smooth muscle with active glandular epithelium and scanty stroma. In our study, the rectovaginal nodule was histologically similar to an adenomyoma (Zaloudek and Norris, 1987). It was a circumscribed, nodular aggregate of smooth muscle, endometrial glands and endometrial stroma. As in the 'adenomyoma', secretory changes were frequently absent in 'endometriotic' rectovaginal nodules. The invasion of the muscle by a very active glandular epithelium, without stroma, proved that the stroma is not necessary for invasion in this particular type of pathology called adenomyosis. In some instances, it can be seen that the vaginal pluristratified epithelium was replaced by a glandular epithelium. The fact that ciliated cells were present and the co-expression of both vimentin and cytokeratin (Donnez and Nisolle, personal communication) proved the Mullerian origin of the nodule, where certain histological characteristics are completely different to those observed in peritoneal lesions (Nisolle et al, 1990). In our series, deep fibrotic tissue assumed to contain endometriosis was excised or vaporized from the anterior rectum with the aid of multiple rectovaginal examinations. Cul-de-sac dissection was followed by excision of deep fibrotic endometriosis, without cul-de-sac reconstruction. In three cases, the bowel lumen was entered. A comprehensive laparoscopic procedure, while not eradicating all the endometriosis, may result in considerable pain relief or a desired pregnancy.