Endometriosis presenting with ascites is rare. Since the first case was reported in 1954, there are only 63 cases in total until 2011[4]. Bernstein et al. [5] firstly suggested that irritation of peritoneal cells by endometrial debris in peritoneal cavity eventually cause ascites. Ussia et al. [6] later promoted a concept by retrospective analysis that the source of massive ascites is the excessive ovarian transudation similar to a Meigs syndrome consisting of an ovarian fibroma, massive ascites, and hydrothorax. As the mechanism of endometriosis is under study, the pathophysiology of endometriosis-related ascites is similarly unclear. Patients most frequently complain of anorexia, abdominal distention and abdominal pain while typical symptoms of endometriosis such as dysmenorrhea are revealed by detailed history. Considering the similar symptoms, the existence of pelvic mass and the elevation of CA 125, ascites secondary to endometriosis is usually mistaken for ascites associated with ovarian malignancy. Although fine-needle cytology of ascites has been successfully applied to confirm endometriosis[7, 8], the overwhelming majority of patients are definitively diagnosed by postoperative histology or exclusion of other conditions causing ascites.
Maximum removal of the lesion is the key of treatment for endometriosis. Surgical approaches for bowel endometriosis are mainly divided into three categories: shaving excision, disc resection and segmental resection. Influence factors of the choice of surgery type includes location of the bowel lesion, depth of infiltration, number of nodules, and presence or absence of stricture. Generally speaking, bowel occlusion of > 50% or nodule larger than 2–3 cm indicates a need for elective bowel resection[9]. In this case, segmental bowel resection was performed to completely excise the mass and all scattered lesions were removed by shaving excision or bipolar coagulation. However, it’s reported that occult microscopic endometriosis exists in 15% specimens of resection margins even when radical segmental resection is performed[1], which makes appropriate postoperative medicine significant for inhibiting and removing residual microlesions. Nevertheless, there are no authoritative regiments at present. Several medication options can be used alone or in combination such as long-term oral contraceptive, progestins, GnRH-a and levonorgestrel-releasing intrauterine devices. Some studies have demonstrated that GnRH-a and non-oral contraceptive are more effective in DIE[9, 10]. Considering the large lesion load and deep infiltration, GnRH-a were applied immediately after optimal lesion excision to reach a maximum suppression of residual lesions and a total of 6 courses. Later two levonorgestrel-releasing intrauterine devices and subcutaneous implants keep the progestin level within an effective range for continuous inhibition locally and systematically. The patient presented with amenorrhea without any perimenopausal symptoms which indicated an appropriate estrogen level.
No lesions found in the bowel in the second surgery demonstrated our therapeutic strategies successfully prevented bowel recurrence. Interestingly, new lesions appeared on the ovaries even when the ovarian function is suppressed at a low level. Residual endometriotic lesions are commonly suggested to be the main origin of recurrence. That’s obviously not consistent with present situation. No disease reappeared in the bowel demonstrates radical removal of lesions and other source of ovary recurrence. Lymph node involvement and lymphatic vessel invasion which are frequently found in deep infiltrating rectosigmoid could also be responsible for recurrence, especially in DIE[11]. This indicates the value to detect lymph node involvement in DIE. However, postoperative histology of lymph node revealed no disease in our case. Development and implant in different position from primary disease of de novo lesions in retrograde bleeding may contribute to recurrence in new organs[12]. In addition, immunological factors might play an important role in this process. Massive ascites can be a sign of inflammatory sensitive status. A significant elevation of CD158α(+) NK cells (CD158α-expressing cells among CD16-expressing natural killer cells) in both ascites and peripheral blood can be observed in women with endometriosis. Besides, this increase of CD158α(+) NK cells in peripheral blood could not be diminished by surgery and GnRH-a treatment[13]. Which means CD158α(+) NK cells may be a potential biomarker for endometriosis. Furthermore, young age at primary surgery(≤ 35 years), high body mass index(≥ 23 Kg/m2), intraoperative finding of adhesion extension, the presence of adenomyosis, dysmenorrhea are reported to be risk factors of recurrence[2, 14, 15].
In conclusion, DIE should be considered as a differential diagnosis for ovarian cancer in the presence of massive ascites and pelvic mass. Endometriosis occurring in different organs may have different pathogenesis, which leads to different treatment focus. Physicians must take clinical symptoms, patients’ expectations, the range and depth of the lesions into consideration when make treatment plan. Application of high dose levonorgestrel-releasing systems after surgery and GnRH-a therapy improves the treatment effect of bowel endometriosis. The mechanism of recurrent endometriosis that occurs in different organs may relate to lymph node involvement and individual immune state.