Sampson gave the term “endometriosis” to a pathology primarily described in 1860 by Von Rokitansky. This pathology is a benign disease with high prevalence in women of reproductive age. Its etiology and pathogenesis are controversial but it is believed to involve multiple, genetic, environmental, immunological, angiogenic, endocrine, and even embryonic processes (1, 2). It is defined by the presence of endometrial and stromal glands out of the uterine cavity. It is estimated that 10–20% of women of childbearing age are affected (3), causing a variety of symptoms and diminishing their quality of life.

Vesico-sphincteral disorders such as voiding troubles are often masked by other symptoms of endometriosis such as pelvic pain (dysmenorrhea, dyspareunia, and chronic pelvic pain), menstrual cycle disturbances, and infertility.

The authors aim through this manuscript to update implications of endometriosis in vesico-sphincteral disorders.

Adenomyosis, previously called “internal endometriosis,” is distinguished from “external endometriosis,” actually simply called endometriosis. Adenomyosis is defined as the invasion of the myometrium by endometrial tissue (glands and stroma) (4). Endometriosis is defined as all other locations of endometrial tissue. Deep infiltrating endometriosis (DIE) is characterized by an infiltration of more than 5 mm of endometrial tissue into retroperitoneal space. Locations of DIE include the uterine torus, posterior fornix, uterosacral ligaments, rectum, vagina, and urinary tract (4).

The distribution of endometriotic lesions, regardless to their type (deep, superficial, or cyst-like), is heterogeneous, but the disease is most often pelvic-located (fallopian tubes, broad ligaments, ovaries, bladder and urethra, pelvic peritoneum including the Douglas’ pouch, utero-sacral ligaments, recto-vaginal septum, lower digestive system). Lesions are more likely situated in the posterior wall and on the left side of the pelvis (4). Ten percent of women with deep endometriosis show a gastrointestinal involvement. In those cases, involvement of the rectum and the recto-sigmoid portion occurs in 70–93% of the cases (4).

Involvement of the lower urinary tract is found in 0.2–2.5% of the cases (3, 5). Bladder and ureteral lesions occurred in, respectively, 25–85 and 15–75% of the cases, while renal and urethral involvement remains rare (5%) (3, 6).

Extra-pelvic endometriosis locations such as the perineum, laparotomy scars, trocar orifice, and spinal cord are reported in medical literature (3).

Two hypotheses about the etiology of endometriosis are still up to date and debated: –

The first one is the “implantation theory” (1), developed in 1927 by Sampson, suggesting that fragments of normal endometrium flow back into the peritoneal cavity during retrograde menstruations, passing through the tuba, then graft on different sites. Till nowadays, this hypothesis has found the largest approval. As a matter of fact, desquamated endometrial cells were found in the peritoneal cavity throughout the menstrual cycle. It seems rational to assume that these cells can implant on the peritoneum.

Lower urinary tract endometriosis can be explained through several physio-pathological theories (5, 7), among them:

The Sampson’s migratory theory, with implantation of endometrial cells in the vesico-uterine pouch.

It seems quite logical that a single theory can’t explain all clinical situations, but they are complementary.

Pelvis innervation and voiding function are two complex systems that associate an autonomous and a voluntary nervous system for bladder emptying.

Bladder innervation is composed of: –

A voiding control center located in the brainstem and the sacral segment of the spinal cord.

Vesico-sphincteral disorders observed in endometriosis (day-time and night-time pollakiuria or urge incontinence, spontaneous and stress incontinence, urinary urgency, cystalgia, dysuria, urinary retention, cramps or pain during or at the end of urination, decreased bladder sensitivity, macroscopic hematuria, lower back pain…) imply an infiltration of the hypogastric plexus by endometriosis lesions, in combination with inflammatory phenomena. The involvement of the bladder, the ureter, or the urethra by endometriotic lesions directly explains some of these urinary symptoms (5, 8). According to Anaf et al., these events would be related to an overexpression of neural growth factors (9).

Medullary invasion by endometriotic nodules is an exceptional situation of the association between lower urinary tract disorders and endometriosis. Only seven cases (of medullary invasion) have been reported in literature with various neurological manifestations (hypoesthesia, weakness, failure of motor function), as well as constipation and urinary retention (10).

In case of pelvic endometriosis surgery, especially if involving the Douglas’ pouch, the rectum, the recto-sigmoïd junction, and the parameters, the postoperative bladder and sphincter disturbances are due to damages caused to the inferior hypogastric plexus that passes the utero-sacral ligaments laterally close to the rectum and the vaginal fornix (4, 9).

Deep endometriosis surgery, involving the uterosacral ligaments, the rectum, and recto-vaginal septum, induces (as described above) de novo vesico-sphincteral disorders caused by per operative nerve damage of the pelvic plexus. To distinguish preexisting disorders from those appeared de novo, some authors such as Lapasse et al. (8) propose to systematically carry out a preoperative urodynamic investigation in case of deep endometriosis (Table 2). To our knowledge, no other study about urodynamic evaluation in case of deep endometriosis has been published.

The urinary flow study may reveal a multiphasic curve (related to urination with abdominal thrust), a decreased flow (<150 mL/s), and a significant post voiding residual (>10% of the urinated volume). Cystometric evaluation may show a hyper or hypo compliant bladder (hypo or hypersensitive bladder, flat curve, the first voiding-need may be delayed or absent), a detrusor hypocontractility with an increase in voiding duration, and/or a post-voiding residual. Urethral profilometry may be normal; however, a decreased urethral closure pressure is possible (in case of pudendal or vegetative nerve lesion) (18).

In most cases and regardless of the localization, the management of deep endometriosis lesions is surgical. The definitive diagnosis of endometriosis is histological, although a bundle of clinic-radiological findings guide toward the diagnosis (20). The surgical approach (conventional open surgery vs laparoscopy) depends on the team and surgeon’s expertise and skills. When comparing the delta values of urinary symptoms and quality of life using IPSS score, Ballester et al. (9) found no significant difference between laparoscopy and conventional open surgery. For voiding symptoms, ΔIPSS was 3.3 for laparoscopy and 1.3 for open surgery (p: 0.17), while for storage symptoms ΔIPSS was 1.2 for laparoscopy and −2.2 for open surgery (p: 0.16). Quality of life was comparable in both surgical routes (p: 0.45).

Different postoperative vesico-sphincteral manifestations (as mentioned above) as well as anatomical and physio-pathological data emphasize the need to develop a pelvic nerve-sparing surgery. Since the first publication of Possover et al. (21), several authors (11) have confirmed the feasibility of this surgical procedure (nerve-sparing surgery) with encouraging results. Indeed, Possover et al. (21) have developed the LANN technique, a technique of laparoscopic neuro-navigation to identify pelvic autonomic nerves. This reduces the incidence of postoperative bladder and sphincter disorders to <1%. Another method with encouraging results was proposed by the same team (22), by establishing a nerve stimulator on the hypogastric plexus to prevent bladder atony.

Regarding bladder lesions, the treatment of choice is partial cystectomy (full-thickness surgical excision of the bladder endometriosis lesion and its surrounding bladder wall), performed by classic laparoscopy or laparotomy (20, 23). Laparoscopic partial cystectomy offers the same results as laparotomy with several advantages such as less bleeding, shortened operative time, shortened hospital stay, quicker return to work, a major reduction in postoperative pain, and a major decreased risk of postoperative morbidity. To avoid recurrences and postoperative pain, the excision has to be as complete as possible. Concomitant cystoscopy can be useful for better defining the margins of the endometriotic lesion. Preventive catheterization of the ureters may be advisable, especially when the distance between the caudal border of the endometriotic lesion and the interureteric ridge is <2 cm (24). An accurate preoperative workup (anamnesis, clinical examination, and imaging information; cystoscopy) is essential for planning a correct laparoscopic approach. It is essential to ascertain the precise location of the vesical endometriotic nodule (the distance with the ureteral meatus and the lower endometriotic margins) (24).

Cystoscopy approach is not recommended and several arguments were against it. First, endometriotic bladder lesions develop inwards and complete resection involves accepting the risk of bladder perforation. Second, endometriosis being a disease of the peritoneal cavity, a complete assessment of the cavity is needed and cystoscopy does not allow this (20).

Ureteral lesions are treated by ureterolysis or resection/anastomosis based on intraoperative findings. When endometriotic lesions sheath the ureter, surgical procedure requires the placement of a stent before ureterolysis. Lateral involvement of the ureter usually requires resection/anastomosis (uretero-ureteral or uretero-vesical anastomosis) (20).

Robotic-assisted laparoscopy has the advantage of an improved level of freedom of instrumentation that allows more precise dissections, reduces nerve lesions (owing to 3D vision) and improves suturing techniques. However, the longer set-up time and greater expense limit its use for reference centers (24, 25).

Medical therapies for endometriosis may be used alone or as a complement to surgery. Prescribing medical treatment only implies certainty or at least a strong suspicion of the diagnosis. It is based on the sensitivity of the endometriotic tissue to hormones. The main treatments used are progestogens, local progestogens such as IUD with levonorgestrel, danazol, combined contraceptive pills, and GnRH analogs. Treatments success varies depending on the location of endometriosis lesions. Even when symptoms improve, it will tend to relapse when stopping treatment with a recurrence rate of 56% (24).

Aromatase inhibitors are approved adjuvants for the treatment of estrogen receptor-positive breast cancer. Molecular studies have revealed the presence of aromatase P450, the key enzyme in the biosynthesis of ovarian estradiol, inside the endometriotic tissue, indicating local synthesis of estradiol. Thereby, AIs represent an appealing medical option for the management of different aspects of this enigmatic disease, especially pelvic pain and infertility. Accordingly, this review aims to evaluate the potential role of AIs in the treatment of endometriosis-associated symptoms, mainly pain and infertility. Notably, several studies have demonstrated that the combination of AIs with conventional therapy as oral contraceptive pills, progestins, or gonadotropin-releasing hormone analogs can be used to control endometriosis-associated pain and pain recurrence in premenopausal women, particularly those with pain due to rectovaginal endometriosis refractory to other medical or surgical treatment. Some case reports have shown promising results in the treatment of postmenopausal endometriosis as first-line treatment, when surgery is contraindicated, or as second-line treatment in the case of postoperative recurrence (26).

In case of de Novo urinary disorders after surgery (urinary retention, dysuria, …), different drug treatments have been proposed, such as cholinergics or prokinetics (cisapride and bétanéchol), but their effectiveness has not been demonstrated yet. To date, standard treatment of urinary retention after surgery remains self-catheterization. Neuromodulation of the superior hypogastric plexus (inhibiting internal sphincter contraction and strengthening detrusor contraction) for treatment of refractory atonic bladder seems promising but should be confirmed by further studies. In terms of prevention, surgical nerve sparing techniques have been developed in order to minimize intraoperative injury of pelvic nerve plexus and reduce postoperative morbidity (18).

It appears that bladder and sphincter disorders exist among patients with deep endometriosis regardless of its location, and thus before any surgery. The absence of previous symptoms couldn’t exclude endometriotic lesions. A precise anamnesis is fundamental to detect symptoms. The use of specific validated questionnaires, such as IPSS and BFLUTS, improve screening. Although it seems obvious that the implementation of urodynamic evaluation before surgery for deep endometriosis could help to detect unsuspected abnormalities, no recommendations can be found in recent literature. Localization of endometriosis lesions, such as in the posterior recto-vaginal septum, in Douglas’pouch, in the rectum and recto-sigmoïd junction, appears to be associated with a higher incidence of bladder and sphincter disorders. Surgery for deep endometriosis, in particular when extensive tissue resection is needed, is also responsible for de novo bladder and sphincter disorders. Processes such as the neuro-navigator and the neuro-stimulator placed laparoscopically seem promising techniques. That being said, most publications lack of proof and therefore do not allow extrapolating conclusions or making recommendations about optimal management of deep pelvic endometriosis related and its implication in vesico-sphinteral disorders.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The Supplementary Material for this article can be found online at http://journal.frontiersin.org/article/10.3389/fsurg.2015.00023