Endoscopic management of ovarian endometriosis and deep endometriotic lesions

Abstract

The pathogenesis of typical ovarian endometriosis is a source of controversy. The original paper of Sampson on this condition reported that perforation of the so-called chocolate cyst led to spillage of adhesions and the spread of peritoneal endometriosis. The findings of Hughesdon (1957) contradicted Sampson's (1922, 1927) hypothesis and suggested that adhesions are not the consequence but the cause of endometriomas. In 93% of typical endometriomas, the pseudocyst is formed by an accumulatation of menstrual debris from the shedding and bleeding of active implants located by ovarioscopy at the site of inversion, resulting in a progressive invagination of the oortex. Some other authors have suggested that large endometriomas may develop as a result of secondary involvement of functional ovarian cysts in the endometriotic process. According to our opinion, the haemorrhagic cysts are the consequence of metaplasia of epithelial inclusions in the ovary. Ovarian endometriosis > 3cm In our series of 2912 patients with endometriosis, ovarian endometriomas larger than 3cm in diameter were found in 481 patients. During diagnostic laparoscopy, the endometrial cyst was washed out with irrigation fluid (saline solution) . and a biopsy was taken. Then, gonadotropin releasing hormone (GnRH) agonist (Zoladex, ICI, UK) therapy was given for 12 weeks to decrease the cyst size. A decrease of 50% in cyst diameter was observed after drainage followed by a 12-week course of a GnRH agonist. Drainage alone (if not associated with GnRH agonist) was ineffective: indeed. 12 weeks after drainage, the ovarian cyst diameter was found to be unchanged when compared to the diameter observed before drainage. Thereafter, a second-look laparoscopy was carried out. If the diameter of the residual endometrial cyst was < 3cm after GnRH agonist therapy (n=233) , the interior wall of the cyst was vaporized as previously described. If the diameter of the residual cyst was > 3cm after GnRH agonist therapy, another technique was proposed. In this series. the range of the ovarian cyst sizes was 3-8cm. A portion of the ovarian cyst was first removed by making a circular cut over the protruded ovarian cyst portion. using the CO,, laser. Partial cystectomy was then carried out. Ovarian cystoscopy was performed for evaluation of the interior cyst wall. and a biopsy was taken. The residual endometrial cyst wall was then vaporized with the CO2 laser, equipped with the SurgiTouch. Pregnancy rates A pregnancy rate of more than 55% was achieved in moderate endometriousis and 44°o in severe endometriosis. The maiority of pregnancies occurred during the first 10 months after surgery. Is the adenomyotic nodule limited to the rectovaginal space? Mullerian rests are not only present in the rectovaginal space but also in the vesico-uterine space and in the cardinal ligaments. 1. Bladder andometriosis must also be considered as retroperioneal disease. Indeed, in one of our recent studies, 35% of bladder adenomyosis cases had no associated peritoneal andometriotic lesions, but they were associated with rectovagianl adenomyosis in 45% of cases. The theory that extraperitoneal endometriosis, such as bladder endometriosis, derives from endoperitoneal disease can therefore not be proposed to explain bladder endometriosis. Indeed. the bladder adenomyotic nodule is also a circumscribed nodular aggregate of smooth muscle and endometrial glands surrounded by scanty stroma. As in the « uterine adenomyoma » and in rectovaginal adenomyotic nodules, secretory changes are adsent in « adenomyotic » bladder nodules. Sometimes, we observed invasion of the muscle by very active glandular epithelium without stroma which proved that stroma is not mandatory for invasion in this particular type of pathology. Not only the frequent association with adenomyotic rectovaginal nodules, but also the similar histological findings observed in our study, have lead us to strongly suggest that bladder endometriosis is actually bladder adenomyosis and also the consequence of metaplasia of Mullerian remnants which can be found in the rectovaginal septum as well as the vesico-vaginal septum. One of the hypotheses advanced by Fedele et al claming that detrusor endometriosis could result from the extension of adenomyotiv lesions from the anterior uterine wall to the bladder is not supported by our study. Indeed. although the vesical adenomyotic nodule was systematically found to be adherent to the uterine wall, no adenomyotic nodules of the anterior uterine wall were found. These data, observed at surgery, were corroborated by the absence of uterine adenomyosis at vaginal echography and MRI. Moreover, on histological examination, we noted that there was no continuity between the endometrial glands and the mesothelium, proving that the bladder nodule constitutes retroperitoneal disease. A further argument to support this view is the intact vesical mucosa observed in 94% of cases. 2. Side-wall endometriosis and ureteral endometriosis are the consequences of retroperitoneal adenomyotic disease. The concept of adenomyosis of the retroperitoneal space should thus cover not only the rectovaginal space and the vesicovaginal space but also the area extending laterally in the direction of the cardinal ligaments. From our experience, we recommend clinically investigating the presence of a nodular adenomyotic lesion either in the posterior vaginal fornix or the anterior vaginal fornix in all patients suffering from chronic pelvic pain and/or severe dysmenorrhea or deep dyspareunia. In cases of rectovaginal adenomyotic nodules or nodules developed more extensively laterally, and in cases of large uterosacral endometriotic nodules (> 2.5cm) , patients should systematically undergo preoperative diagnosis of ureteral endometriosis. Lateral extension from the retovaginal space to the side-wall through the cardinal ligaments also happens in the retroperitoneal space, sometimes provoking ureteral stenosis. erroneously called ureteral endometriosis.