Endometriosis of the urinary tract

Urol Clin N Am 29 (2002) 625–635

Endometriosis of the urinary tract Craig V. Comiter, MD University of Arizona College of Medicine, P.O. Box 245077, 1501 N. Campbell Avenue, Tucson, AZ 85724, USA

Endometriosis is the growth of endometrial tissue outside the normal confines of the myometrium or uterine cavity. There are two types of symptoms: those caused by pelvic endometriosis itself and those secondary to urinary involvement. Genitourinary involvement occurs in 1% to 2% of cases. The clinical diagnosis is made based on history, physical examination, laparoscopy, and biopsy of any suspicious lesions. Treatment depends on age, fertility desire, extent of bladder disease, severity of lower urinary tract symptoms, presence of other pelvic disease, and the degree of menstrual dysfunction. Both medical and surgical treatment play an important role in the management of endometriosis. Definition and prevalence Endometriosis is the growth of endometrial tissue outside the normal confines of the myometrium or uterine cavity. First described at autopsy by Von Rokintasky in 1860 [1], these ectopic lesions may consist of endometrial glands and/or stroma and may interfere with normal physiologic processes by their infiltrative nature or by the formation of adhesions [2]. Women are most often affected between the years of menarche and menopause, with an estimated prevalence of 10% to 20% for the general female population [3–8], but approaching 30% to 40% in infertile women [9]. It is estimated that 5 million women in the United States are affected by this condition. Endometriosis is the second most common pathologic condition in the female pelvis [10] and the most frequent gynecologic diagnosis responsible for hospitalization of women between the ages of

E-mail address: [email protected] (C.V. Comiter).

15 and 44 years [11]. The most common sites of involvement include the ovaries, uterosacral ligaments, cul-de-sac, pelvic peritoneum, oviducts, and cervix. Endometriosis outside the confines of the reproductive tract is less common. Genitourinary involvement (i.e., bladder, ureter, kidney, or urethra) occurs in 1% to 2% of cases [12–16]. Other sites of endometriosis include the gastrointestinal tract, lungs, pelvic lymph nodes, umbilicus, extremities, vulva, and episiotomy and laparotomy incisional scars [17–20]. Pathogenesis The pathogenesis of endometriosis has been an ongoing debate for more than a century. The main theories can be categorized as embryonic, migratory, and immunologic: Migratory Tubal regurgitation Direct extension Embolic Lymphatic metastases Hematogenous metastases Embryonic Celomic metaplasia Mullerian remnants Wolffian remnants Immunologic disorder Iatrogenic Postsurgical direct implantation Composite theory Migratory, embolic, embryonic Von Recklinghusen hypothesized that endometrial tissue could arise from ectopic embryonic rests derived from wolffian duct remnants [3,4]. Cullen [21] first theorized that mullerian duct remnants could give rise to ectopic endometrial tissue

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in the ovary. It was proposed that the ovary and mullerian ducts arise form a common celomic mesothelium, and therefore the germinal epithelium of the ovary may ‘‘recapitulate’’ the endometrium, which is derived from mullerian ducts. These mullerian rests explain the rare, but well-described occurrence of endometriosis in men on estrogen therapy for prostate cancer [22]. Furthermore, the peritoneal mesothelium (also derived from the celomic mesothelium) may undergo in situ metaplasia, thus explaining the development of peritoneal endometriosis [23]. Migratory theories of endometriosis are more widely accepted today than are embryonic mechanisms. Sampson [24] hypothesized that viable endometrial cells may transplant onto ectopic sites and grow into endometriomas. This ‘‘implantation’’ theory has significant supportive evidence. First, retrograde menstruation is a common physiologic event [25,26], and living endometrial cells harvested from both menstrual discharge and peritoneal fluid have been successfully tissue cultured [27]. Furthermore, endometrium has been experimentally implanted and grown in the peritoneal cavity [25,28]. Finally, factors that increase the amount of peritoneal menstrual debris, such as anatomic menstrual outflow obstruction [29,30], early menarche, short cycles with long flow periods [31], and delayed childbearing [32] are known to increase the risk of developing endometriosis. Another migratory route is lymphovascular metastasis [33,34]. Metastatic dissemination best explains the occurrence of endometriosis in distant sites, such as lung, pleura, nose, extremities, and pelvic and mediastinal lymph nodes. Disease so distant from the pelvis cannot otherwise be explained by retrograde menstruation, nor do these structures arise from celomic mesothelium (embryologic theory). In addition, iatrogenic endometrial implantation has been well described. Several cases of endometriosis in laparotomy scars from cesarean deliveries and other gynecologic procedures have been documented [12,35,36]. Endometriosis has also occurred in episiotomy scars after childbirth [17,18,37]. The immune system appears to factor in the pathogenesis of endometriosis. Normally, the immune system has a method of disposing of tissue fragments. Endometriosis may develop, however, if there is a deficient disposal system or if a normal system is overwhelmed by retrograde menstruation. Suboptimal immune surveillance can therefore result in ectopic endometrial implantation [38]. Changes seen in rhesus monkeys and humans

with endometriosis include decreased natural killer cell activity, decreased recognition of the autologous endometrial antigens, and diminished cytotoxic effects of peripheral blood lymphocytes against endometrial cells [39,40]. Other noted changes include increased titers of autoantibodies, augmented activation of peripheral macrophages, and increased concentrations of growth factors in the peritoneal fluid of patients with endometriosis [37,41]. The growth of endometriomas is estrogen dependent, and hormonal factors clearly influence the development of endometriosis. The disease never occurs before menarche, occurs seldom in postmenopausal women, and occurs only rarely in men. Most postmenopausal cases occur in women with high levels of estrogen (caused by obesity or estrogen replacement therapy), and all male cases occur in individuals on estrogen treatment for prostate cancer [42]. Beginning with Javert in 1949 [33] and continuing today, most gynecologists believe in a composite theory of endometrial migration, including retrograde menstruation, lymphovascular metastases, direct extension of the lesions, with the rare occurrence of metaplastic changes of wolffian, mullerian, and occasionally peritoneal (celomic-derived) structures. Pathophysiology and symptomatology Endometriosis is a benign disease; ectopic endometrial tissue is incapable of autonomous growth and is therefore not neoplastic. It can follow a malignant clinical course, however, metastasizing through lymphatic and vascular channels and invading nearby structures. Moreover, numerous case reports have documented the malignant transformation of endometriomas, and an association exists between endometriosis and endometrioid and clear-cell adenocarcinoma of the ovaries [43,44]. Common menstrual abnormalities include hypermenorrhea, metrorrhagia, and intermittent spotting. Ovulation may be affected by ovarian involvement, exacerbating the menstrual abnormalities. Infertility commonly affects 30% to 40% of patients with endometriosis versus only 15% to 20% of women without the disease [41]. In infertile women, up to 60% are diagnosed with endometriosis at laparoscopy [45]. In addition to ovulatory disorders, distortion of normal anatomic relationships because of fibrosis and adhesions and embryotoxic factors (e.g., prostaglandins, cytokines, and growth factors) [46], which are

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produced by the implants of ectopic endometrial tissue, contribute to infertility. Dyspareunia can result from disease involving the cul-de-sac, uterosacral ligaments, rectovaginal septum, upper vagina, or cervix. Pelvic pain is caused by inflammation, mechanical compression of cystic nodules, adhesions, direct nerve involvement, prostaglandin production, and even psychological factors [47]. Deeply infiltrating endometriosis (i.e., more than 5 mm depth of penetration) is the most severe form of the disease, often with the most debilitating pain. This phenomenon was first described in 1913 [48]. Deeply infiltrating disease occurs in the cul-de-sac (55%), uterosacral ligaments (35%), and uterovaginal fold (11%) [49]. Dyspareunia is invariably present with this type of disease, and pain may become chronic in nature and is likely caused by adhesions, fibrosis, and scarring. The clinical diagnosis is made based on history and physical examination and confirmed through laparoscopy and biopsy of any suspicious lesions. The ‘‘classic triad,’’ including infertility, dyspareunia, and dysmenorrhea, affects 40% of presenting patients. Also common are catamenial pelvic pain and dyschezia. Pain results from the cyclic growth of ectopic endometrial tissue followed by hemorrhagic necrosis and extravasation of blood and menstrual debris into the tissues surrounding the endometrioma. The location and degree of pain depends on the site and invasiveness of the ectopic endometrial implants and on the innervation of the tissue. Abnormal findings on physical examination vary with the location of disease. Tender nodularity is commonly appreciated in the cul-de-sac and uterosacral ligaments, and the uterus is often fixed and retroverted. Speculum examination may reveal vaginal or cervical lesions, which is visible as blue or powder burn-colored deposits [50]. Tenderness and bleeding (during menses) may be noted in any area of disease, including the umbilicus, episiotomy scars, and cesarean delivery incisions. Laparoscopy is a more reliable diagnostic method than is physical examination [51]. During laparoscopic examination, a systematic review of the pelvis is mandatory, including inspection of the peritoneal fluid, ovaries, tubes, anterior uterus, broad ligaments, and bladder—first on one side and then on the contralateral side. Thereafter, the posterior uterus, cul-de-sac, uterosacral ligaments, sigmoid colon, and ureters are inspected bilaterally [51]. Any abdominal viscus at risk for disease, such as the small intestine, appendix, liver,

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spleen, and diaphragm, should also be surveyed. The size and color of any lesions should be noted and may range from black to blue to red to white [52]. Biopsy is necessary because histologic diagnosis is more accurate than visual diagnosis [53]. With all this information, the extent of disease may be staged. The most widely accepted staging system is the Revised American Fertility Society (R-AFS) system, which utilizes a weighted value system to document certain organs involved and the depth of invasion [54]. Although the R-AFS has prognostic value for fertility, it does not include any weighting for genitourinary involvement. Further discussion on classification systems used by gynecologists is beyond the scope of this article. Radiographic imaging is typically used to evaluate a palpable mass and for preoperative planning, especially if genitourinary involvement is suspected. Sonography is usually the initial study used to evaluate a pelvic mass, and it can reliably distinguish between solid and cystic lesions. Computed tomography provides little information; however, magnetic resonance imaging (MRI) has proved quite useful in evaluating endometriosis [55–57]. It is better than ultrasound at differentiating among endometriosis, teratomas, hemorrhagic cysts, and cystadenomas [1]. Intravenous urography (IVU) is indicated in any patient with endometriosis in whom involvement of the urinary tract is suspected.

Treatment Treatment for endometriosis is based on the severity of symptoms, extent of disease, duration of infertility, patient age and desire for future fertility, and urinary symptoms [58]. A conservative approach is recommended for those with mild or no symptoms and with minimal pelvic findings. For those with more significant disease, therapeutic options include medical and surgical treatment. Nonsteroidal anti-inflammatory medications may often provide satisfactory pain relief in mild cases. Medical treatment Medical treatment is based on modifying the cyclical response of endometriosis to hormonal stimulation. This action may be accomplished by creating a pseudopregnancy with progestational agents or estrogen and progestins or by creating a pseudomenopause by inhibiting estrogen production, often through medical hypophysectomy with a gonadotropin-releasing hormone (GnRh)

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agonist. A state of pseudopregnancy causes hyperhormonal amenorrhea [59]. Progestational drugs cause decidualization with eventual atrophy of the ectopic endometrial tissue. The most commonly used progestational agent is medroxyprogesterone acetate 10 to 30 mg/d orally [41,60]. Side effects include breakthrough bleeding, nausea, breast tenderness, fluid retention, and depression [61]. Another medication commonly used to create a pseudopregnancy is the oral contraceptive pill (OCP), containing a progestin and estrogen. Taken daily, the OCP suppresses pituitary and ovarian function resulting in amenorrhea, thereby ameliorating the dysmenorrhea [62]. Side effects are common and include weight gain, bleeding, hypertension, and nausea [62]. All brands of OCP are equally efficacious for treating mild endometriosis [62]. A state of pseudomenopause can be achieved with danazol, an orally active synthetic derivative of 17-ethinyl testosterone. This medication, which is approved for endometriosis by the US Food and Drug Administration [63], acts on the hypothalamus, pituitary, ovary, and endometrial tissue [41]. Gonadotropin release is inhibited, and without the midcycle surge in luteinizing hormone (LH) and follicle-stimulating hormone (FSH), ovulation does not occur. Gonadal steroid production is also diminished, allowing regression of ectopic endometriomas [64–66]. At the standard dose of 400 to 800 mg/d, 85% of patients will suffer from side effects, such as weight gain, acne, hirsutism (reversible), voice changes, hot flashes, and atherosclerosis (not reversible) [59,67]; many of these side effects are caused by an increase in free testosterone levels [68]. Recently, GnRH agonists have been used to manage endometriosis. After a transient rise in FSH and LH (during which there may be a temporary increase in vascular congestion, edema, and decidual transformation), a state of hypogonadotropic hypogonadism is reached, and serum estrogen concentration falls to castrate levels. Necrosis and absorption of uterine and ectopic endometrium may then occur. Side effects of medical hypophysectomy include hot flashes, vaginal dryness, migraines, breast tenderness, insomnia, depression, irritability, fatigue, and osteoporosis [69,70]. Surgical treatment Surgical treatment of endometriosis ranges from diagnostic to conservative management to extirpative procedures in patients in whom future

fertility is no longer desired. With diagnostic laparoscopy, visual inspection and biopsy is performed for the purpose of staging. The goal of conservative therapy is to remove all apparent endometriotic implants, to restore normal anatomy, and to preserve the ovaries and uterus [63]. Although studies comparing open and laparoscopic conservative surgery have not shown any differences in efficacy, a shorter recovery time and cost savings are achieved with the laparoscopic approach [71–74]. Moreover, all methods of laparoscopic dissection and excision (e.g., scissors, cautery, laser vaporization, and hydrodissection) are equally efficacious [75]. Definitive surgery, on the other hand, is extirpative. All endometriosis is ablated, and abdominal hysterectomy and bilateral oophorectomy are performed. With ovarian preservation, the rate of reoperation is eight times higher than with oophorectomy [76]. Therefore, definitive surgery is preferred to a conservative approach in the woman who does not desire future fertility. Surgical interruption of neural pathways is a well-accepted treatment for debilitating pain associated with endometriosis. Laparoscopic uterosacral nerve resection destroys the uterine sensory fibers by interrupting the uterosacral ligament near its cervical insertion [77]. Presacral neurectomy (laparoscopic or open), which involves interruption of the sympathetic innervation of the uterus and central pelvis, is indicated for intractable midline pelvic pain. The superior retroperitoneal portion of the hypogastric plexus (located just below the aortic bifurcation) is excised. In summary, a clear role exists for both medical and surgical treatment of endometriosis; each approach having its own merits. Surgery is better than diagnostic laparoscopy for pain relief [78]. Surgery is obviously limited to visible and accessible lesions only, however, leaving microfoci of ectopic endometrium, which may recur. In addition, deep lesions and those in vital organs may not be easily resected, and postoperative adhesions can result in significant morbidity. Medical treatment on the other hand is cheap and easy to administer, is efficacious, manages both macroscopic and microscopic disease and deep lesions and those in vital organs. Pharmacotherapy does not require surgical or laparoscopic skill, does not permanently destroy ovarian tissue, and does not cause adhesions. By and large, all standard medical treatments have proved better than placebo for treating pain; however, no one treatment seems better than any other [62]. Medical treatment does

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not eradicate the disease, however, but simply modulates the hormonal environment to suppress cyclic ovarian estrogen and progesterone secretion. Lesions and pain may be slow to resolve, side effects are common, and the recurrence rate on cessation of treatment is high. Combinations of medical and surgical approaches would appear to be a reasonable option, with several randomized trials showing the efficacy of postoperative drug therapy with respect to pain and the rate of reoperation [79–81].

Genitourinary involvement The incidence of genitourinary involvement ranges from 1% to 3% [3,12–14,16,82] and most commonly affects women between the ages of 25 and 40 years [83]. Most instances of postmenopausal genitourinary endometriosis occur in women on estrogen replacement or in obese individuals with higher serum levels of estrogen. The bladder is most commonly involved, followed by the ureters and kidneys, occurring with a ratio of 40:5:1 (Fig. 1) [12,15]. In addition, several case reports have noted urethral and prostate involvement [22]. The urinary tract may also be indirectly affected by the treatment of endometriosis. The incidence of ureteral or bladder injury is 1% during the surgical treatment of endometriosis [12]. Therefore, the urologist is well served by a good working knowledge of the diagnosis and treatment of urinary tract involvement with endometriosis. Bladder Bladder disease can be intrinsic (i.e., involving the detrusor muscle) or extrinsic (i.e., involving the serosal or peritoneal surface). Retrograde menstruation is the most likely explanation for peritoneal and serosal lesions. Intrinsic lesions more likely occur from iatrogenic implantation. In 43% to 50% of cases, a history of pelvic surgery

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can be elicited [12,36,84–86]. A well-documented association has been noted between bladder endometriosis and cystitis cystica [15]. It is unclear if this is caused by a metaplastic change or simply an inflammatory response to repeated release of the products of menstruation is unclear. Symptoms depend on the size and location of disease [83]. Extrinsic disease is often asymptomatic, whereas 75% of patients with intrinsic lesions have irritative voiding symptoms and suprapubic pressure [83]. One third of patients with bladder involvement have a history of gross hematuria, usually occurring at the time of menses [86]. Other symptoms include frequency, urgency, and dysuria, which vary with the menstrual cycle in two thirds of patients [87,88]. Suprapubic pressure relieved by voiding is noted by 80% of patients [89], and nearly half will also complain of menstrual abnormalities [3,87] (Table 1). These symptoms may mimic those of interstitial cystitis [86,89,90]. Bladder endometriosis should be considered in any patient with significant urinary symptoms who is status posthysterectomy or other gynecologic surgery. Diagnosis is usually made only if there is a high index of suspicion based on symptoms. Physical examination reveals a tender anterior vaginal wall with a palpable pelvic mass in 50% of cases [3,12,15,83,87,89]. In 12% of women, the bladder lesion(s) may be the only site of disease [90]. Cystoscopy typically shows a bluish submucosal lesion (Fig. 2). Endoscopic visualization with biopsy is the best method to confirm the diagnosis [3], and 90% of patients with bladder involvement will have an abnormal cystoscopic examination. Radiographically, bladder lesions mimic cancer if they are large enough to be visualized [1]. Ultrasound shows a bladder mass, whereas IVU often shows a filling defect in the posterior wall and/or dome of the bladder [91]. MRI will show a high signal intensity on T1WSE and low signal on T2WTSE

Table 1 Symptoms of vesical endometriosis

Fig. 1. Organs most commonly affected by genitourinary endometriosis.

Symptom

Frequency (%)

Frequency Urgency Dysuria Suprapubic pain Nocturia Urge incontinence Hematuria Pelvic mass

41–71 41–78 14–21 38–78 50–75 21 19–30 50

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Fig. 2. Cystoscopic image of endometriosis involving the bladder.

[56]. If suspicion is high, consideration should be given to performing laparoscopy under the same anesthetic as cystoscopy. Treatment depends on age, fertility desire, extent of bladder disease, severity of lower urinary tract symptoms, presence of other pelvic disease, and the degree of menstrual dysfunction. In young women, treatment should attempt to relieve symptoms and to preserve reproductive function. Although some authors have reported reasonable symptomatic relief with medical treatment [86,92], most believe that hormonal management is palliative only [93,94]. For intrinsic disease, pharmacotherapy is usually suboptimal, as the desmoplastic reaction within the bladder wall from repetitive bleeding and resorption of menstrual debris is often unresponsive to hormonal manipulation [95]. Although biopsy is often indicated to differentiate between endometriosis and cancer, superficial cold-cup biopsy may only reveal normal or inflamed mucosa. Deep biopsy or transurethral resection (TUR) is often necessary for definitive diagnosis [3,15,96]. Because of the transmural nature of intrinsic disease, however, complete TUR may risk bladder perforation [88,90,94,97]. Furthermore, TUR rarely suffices as definitive treatment [86,98]. Successful management of the bladder lesion, including the inflammation and scar surrounding the intramural endometrioma, is best accomplished by partial cystectomy [15,19, 89,94]. This procedure may be accomplished using either an open approach or laparoscopic approach [99–101] and is equally effective when using laser, electrocautery, or sharp dissection [75]. It is prudent to arrange gynecologic assistance

if extravesical pelvic disease is present and/or if hysterectomy/oophorectomy is indicated. Intrinsic disease frequently recurs after medical therapy is discontinued, and continuous medical treatment, especially with danazol, can adversely alter the lipid profile, thereby increasing the risk of atherosclerotic heart disease. Therefore, medical management is often regarded as a suboptimal long-term treatment [102]. In a recent study comparing medical versus surgical treatment of vesical endometriosis, 14 of 16 cases treated hormonally recurred, whereas there were no recurrences in 21 cases treated surgically [91]. In addition, the wellknown phenomenon of malignant transformation of vesical endometriosis makes definitive surgical resection the procedure of choice [97]. Moreover, medical treatment was ineffective in all patients treated for endometriosis in a cesarean delivery scar [83,94,103,104]. Ureter Ureteral endometriosis was first described by Cullen in 1917 [16]. Like vesical endometriosis, ureteral disease is classified as intrinsic or extrinsic, occurring with a 1:4 ratio. With intrinsic disease, ectopic endometrial tissue directly infiltrates the muscularis, lamina propria, or ureteral lumen. Intrinsic ureteral endometriosis likely arises from lymphatic or venous metastases [105–108]. With extrinsic disease, endometrial tissue invades only the ureteral adventitia or surrounding connective tissue [15]. This extrinsic involvement may arise from adjacent disease of the ovary, broad ligaments, or uterosacral ligaments [109]. In addition,

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scar only without true endometriotic involvement of the ureter proper may also be classified as extrinsic disease. Unlike bladder endometriosis and cystitis cystica, no relationship exists between ureteral endometriosis and ureteritis cystica [15]. Endometriosis virtually always involves the ureter below the pelvic brim [110], with only one reported case affecting the extrapelvic ureter [111]. Most instances of ureteral disease occur in premenopausal women, with only occasional reports in postmenopausal women [112,113]. Symptoms are of two main varieties: those caused by pelvic endometriosis itself and those secondary to urinary involvement. The most common findings include menstrual symptoms, flank pain, gross hematuria, and pelvic mass (Table 2). The clinical presentation is usually obstruction. This obstruction may be asymptomatic [92] and may occur with extensive or with minimal disease [15,16,110] and has even occurred with a solitary intraluminal or periureteral lesion [110,114]. With extensive pelvic disease and extrinsic ureteral involvement, dysmenorrhea and dyspareunia may predominate, and the ureteral symptoms may be silent [115]. Differential diagnosis is that of any benign or malignant ureteral obstruction. Intravenous urography and retrograde pyelography are indicated if one suspects ureteral disease (Fig. 3) [4,116,117]. Unfortunately, the most common finding on IVU is nonvisualization of the renal unit [109], often in patients without urinary symptoms. In addition, ureteroscopy may help make the correct diagnosis [114,118]. As many as 25% to 50% of renal units are lost when ureteral endometriosis is present [12,87,92, 96,105,116,117,119]. This high rate of renal loss is caused by surgical removal (nephroureterectomy) when the patient is assumed to have a ureteral malignancy or an obstructive uropathy. Treatment options depend on the degree of obstruction, the nature of ureteral involvement (intrinsic vs extrinsic), age, menopausal status, and fertility desires. Table 2 Symptoms of ureteral endometriosis Symptom

Frequency (%)

Flank pain Abdominal pain Dysuria Gross hematuria Uremia Pelvic mass Asymptomatic

17–26 24–45 9–15 13–18 2–4 13–14 50

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Fig. 3. Retrograde pyelogram showing distal ureteral obstruction caused by ureteral endometriosis.

As with vesical disease, medical treatment tends to be palliative only. In the presence of normal renal function or minimal obstruction, however, hormonal therapy may be initiated, provided that close follow-up is possible to ensure preservation of renal function [19,117,120–122]. This followup may be accomplished by serial IVU and by measurement of serum blood urea nitrogen and creatinine concentration. Surgical management is preferred for definitive treatment, especially in patients older than 35 years [87,117]. The ureteral obstruction must be relieved by ureterolysis, ureteral resection, or nephrectomy. If resection is performed, the integrity of the ureter must be re-established, and the technique depends on the location and amount of resected ureter. Short distances may be managed by ureteroneocystostomy with or without psoas hitch, and larger defects may be bridged by Boari flap, ileal interposition, or autotransplantation. Laparoscopic ureteral resection and ureteroureterostomy can be performed by the experienced laparoscopic surgeon; however, this technique is associated with a 35% complication rate [123]. A recent report of permanent ureteral stenting for endometriosis has been described [124]; however, this is not currently a standard procedure. If parity is desired, surgical extirpation of the ureter may be performed, adjuvant hormonal treatment should be considered, and the patient

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must be followed closely with serial IVU and blood urea nitrogen and creatinine measurement. In the patient in whom parity is not desired, ovarian ablation is indicated, with or without hysterectomy [87]. With ovarian conservation, 27% need more surgery, whereas only 3% of patients undergoing hysterectomy and oophorectomy require reoperation [110]. With extensive disease, medical treatment alone is inadequate, with long-term relief of obstruction being the exception rather than the rule [115,125–127]. Incomplete surgery is also suboptimal, because endometrial remnants will regrow under persistent estrogenic influence [19,114]. A final argument in favor of medical therapy is the rare but well-known phenomenon of malignant transformation of ureteral endometriosis to adenosquamous carcinoma [43,44]. There have been less than 20 cases of renal endometriosis reported in the literature. This condition was first described by Marshall in 1943 [128]. Most cases were diagnosed at pathology in kidneys removed for presumed renal cell carcinoma [129, 130]. Although prostatic endometriosis in the male has been described [131], it occurs only in individuals receiving estrogen therapy for prostate cancer. The prevailing sentiment is that embryologic (mullerian) rests in the prostatic utricle are stimulated to undergo metaplastic change by the estrogenic hormonal environment [22]. Summary Genitourinary endometriosis is a rare manifestation of a common disease. Ectopic endometrial tissue may extrinsically involve or intrinsically invade the bladder or ureter, and, less commonly, the urethra or kidney. Bladder involvement usually presents with irritative symptoms, whereas ureteral disease may present with asymptomatic renal failure. Therefore, a high index of suspicion is necessary, and genitourinary endometriosis should be considered in all symptomatic women with a history of cesarean delivery of other gynecologic surgery. In women beyond reproductive age, definitive surgical treatment is preferred, with removal of the ectopic tissue, relief of obstruction, and castration with or without hysterectomy. In those who desire future fertility, conservative surgery and/or hormonal therapy is often recommended. References [1] Umaria N, Olliff JF. Imaging features of pelvic endometriosis. Br J Radiol 2001;74:556–62.

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