{"paper_id":"2c422977-7ba9-4994-bbcc-d9ab977200af","body_text":"Clin. Exp. Obstet. Gynecol. 2024; 51(8): 172\nhttps://doi.org/10.31083/j.ceog5108172\nCopyright: © 2024 The Author(s). Published by IMR Press.\nThis is an open access article under the CC BY 4.0 license .\nPublisher’s Note: IMR Press stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nReview\nUrinary Tract Endometriosis: A Review of Literature\nRalph Saadeh1,*, Elie Finianos 1, Houssein El Hajj 2\n1Obstetrics Gynecology Department, CHU Brugmann, 1020 Bruxelles, Belgium\n2Gynecological Surgery, Institut Curie, 75248 Paris, France\n*Correspondence: ralph.saadeh@chu-brugmann.be (Ralph Saadeh)\nAcademic Editor: V alerio Gaetano V ellone\nSubmitted: 9 April 2024 Revised: 8 May 2024 Accepted: 21 May 2024 Published: 5 August 2024\nAbstract\nObjective: Deep endometriosis (DE) is the most severe form of endometriosis. Bowel and urinary tract are the most common sites\nof intrapelvic DE. Urinary tract endometriosis (UTE) mainly involves the bladder and the ureters. The two mostly accepted theories\nexplaining the pathophysiology of UTE are the “Retrograde Menstruation Theory” and the “Müllerian Remnants Theory”. The purpose\nof this paper is to provide a review of literature on the UTE, a rare form, affecting only 1–6% of patients with endometriosis. Mechanism:\nA literature review was conducted using keywords specific to UTE and DE to identify peer-reviewed, original research articles published\nbetween 1996 and 2024. Findings in Brief : When the bladder is involved, the patient presents lower urinary tract symptoms. Ureteral\nendometriosis is usually asymptomatic, thus delaying early diagnosis and efficient treatment leading to cases of chronic ureteral stricture.\nClinical history and examination as well as questionnaires play an important role in guiding the clinician. Diagnostic modalities include\nconventional imaging such as ultrasonography and magnetic resonance imaging (MRI) as well as invasive techniques such as cystoscopy.\nAs for all endometriotic lesions, definitive diagnosis should be confirmed by histopathology. Treatment modalities include medical\nhormonal treatments or surgical treatment. There are a multitude of surgical techniques that are more or less invasive depending on the\nlocation and the extent of the lesion. Conclusions: UTE, is an underdiagnosed form of endometriosis, and specialists should be aware\nof this important entity, due to the serious health implications for women.\nKeywords: urinary endometriosis; deep infiltrating endometriosis; urinary symptoms; surgical treatment; medical treatment\n1. Introduction\nEndometriosis is a debilitating gynecological condi-\ntion characterized by the presence of endometrial-like tis-\nsue outside the uterus, leading to significant clinical chal-\nlenges. Although commonly found within the pelvic cavity,\nendometriosis can also manifest in extrapelvic sites such as\nthe diaphragm [ 1] and more rarely, the umbilical region,\ninguinal area, and around nerves and organs like the sciatic\nnerve, liver, and pancreas [2]. The condition can be catego-\nrized based on lesion localization and depth of infiltration\ninto three types: superficial, ovarian, and deep endometrio-\nsis (DE) [ 3]. DE, specifically, involves the endometrial-\nlike tissue on or under the peritoneal surface [ 4], with a\ncontentious definition that has been termed adenomyosis\nexterna by Gordts et al . [ 5], characterized by large, often\nsolitary lesions.\nUrinary tract endometriosis (UTE), a subtype of\nDE, includes bladder endometriosis (BE) and ureteral en-\ndometriosis (UE), both associated with severe pelvic pain\nand significantly impaired quality of life [ 6]. BE is defined\nby the infiltration of the bladder’s detrusor muscle by en-\ndometrial glands and stroma, typically multifocal and af-\nfecting the bladder’s trigone and dome [ 7]. UE involves\neither direct endometriotic invasion of the ureters or indi-\nrect compression by associated fibrosis, potentially leading\nto intrinsic or extrinsic ureteral obstruction [ 8].\nDiagnosing UTE poses significant difficulties due to\nits often-subtle symptoms and the complex nature of its\npresentation, which can mimic other urological conditions.\nStandard imaging techniques may fail to detect the extent of\nthe disease or differentiate it from other pelvic pathologies,\nnecessitating more invasive procedures like laparoscopy for\ndefinitive diagnosis. Treatment of UTE is equally challeng-\ning; it requires a multidisciplinary approach that balances\nsurgical intervention with the preservation of renal function\nand fertility. Surgical treatment, particularly for ureteral en-\ndometriosis, involves risks of significant complications and\nrecurrence of the disease.\nThis review will explore the diagnostic complexities\nand therapeutic challenges in managing UTE, emphasiz-\ning the need for improved diagnostic tools and more ef-\nfective, less invasive treatment options. It will examine\nthe latest advancements in imaging and surgical techniques,\nand discuss the emerging research on medical management\nstrategies that could offer alternatives to surgery. The re-\nview aims to highlight critical gaps in current knowledge\nand suggest directions for future research to enhance patient\noutcomes in UTE.\n2. Epidemiology\nWhile endometriosis affects almost one-fifth of repro-\nductive aged women, DE prevalence is 1% in reproductive\naged women, and 15 to 20% of patients with endometriosis\n[9]. UTE, a rare entity affecting only 0.3 to 12% of pa-\n\ntients with endometriosis [ 8], is more frequent among pa-\ntients with DE with an incidence of 16.4% to 52.6% [ 10].\nUTE mainly involves the bladder (70–85%), the ureters (9–\n23%), the kidneys (4%) and the urethra (2%) [11]. The peak\nage of incidence is 30–35 years.\nAs for all rare diseases, most of the studies consist\nof small retrospective cohorts and are performed in refer-\nral centers leading to a divergence between the published\nand the real occurrence. The lack of prospective trials and\nthe short term follow up prevent us from establishing stan-\ndardized diagnosis and therapeutic approaches.\nBE is usually associated with other forms of pelvic\nendometriosis (superficial peritoneal, ovarian endometri-\nomas, adhesions and extravesical DE). UE is rarely isolated;\nit is associated with ovarian endometriomas in half of the\npatients with a predilection to the left side [ 12].\nInversely, literature suggests that the presence of rec-\ntovaginal endometriosis multiplies the risk of developing\nUE by more than ten if the largest nodule is >3 cm [13].\n3. Methods\nA literature review was conducted using keywords\nspecific to UTE and DE to identify peer-reviewed, origi-\nnal research articles published in English between 1996 and\n2024.\n4. Pathophysiology\nWhen DE lesions invade the urinary tract (bladder,\nureters or kidneys), it results in UTE. Similarly, to DE, the\npathogenesis is still unclear. Non-UTE lesions can also\nremotely cause UTE like symptoms without an actual in-\nvolvement, this can be caused by an inflammation or an in-\nfiltration of the hypogastric plexus resulting in an involve-\nment of sympathetic and parasympathetic lesions [ 14].\nThe two mostly accepted theories are “Retrograde\nMenstruation Theory” and “Müllerian Remnants Theory”.\n“Retrograde Menstruation Theory” suggests a retro-\ngrade flow of endometriotic tissue through the fallopian\ntubes. The asymmetrical distribution of endometriotic le-\nsions is a major argument supporting this theory. The fact\nthat most of DE lesions are located in the declivous parts\nof the pelvis, particularly the involvement of the bladder\nin UTE, is explained by the gravitational effect on regurgi-\ntated endometrial tissue and the presence of the recto sig-\nmoid colon. This favors adhesion of sloughed endometrial\ndebris on the left pelvic wall and peritoneum followed by in-\nflammation and fibrotic nodules formation. Other anatomic\nobservations supporting this theory are the absence of BE\nin patients with retroverted uterus, and the mode of progres-\nsion of lesions from the bladder serosa inwards, sparing the\nmucosal layer most of the time [ 15].\n“Müllerian Remnants Theory” or the “Müllerianosis”\nhypothesis relies on the histology of DE and UTE lesions to\nhypothesize that DE lesions are in fact adenomyotic lesions\nsecondary to embryonic remnants of the Müllerian ducts\nand originating in the retroperitoneum. Thus, the presence\nof fibrotic tissue and smooth muscle cells surrounding the\nstrains of gland and stroma in these lesions [ 16].\nThis theory may explain the presence of DE without\nconcomitant peritoneal involvement which cannot be ex-\nplained by the Retrograde Menstruation Theory.\nNisolle and Donnez [ 3] in 1997 suggested that DE,\nperitoneal and ovarian endometriosis are separate entities\nwith different pathogenesis, with the DE presenting more\ninvasive mechanisms.\nOther theories include the “Hematogenic or Lym-\nphatic Spread” of specific cell-free endometrial products\ncapable of inducing the metaplasia of undifferentiated mes-\nenchyme into endometrial epithelium and glands [17]. This\ncan be responsible for distant implants and probably ex-\nplaining intrinsic UE or isolated DE. The “Iatrogenic The-\nory” states that history of pelvic surgery predisposes the\ndissemination of endometrial cells in the abdominal cavity\n[17]. “The forgotten menstruation”, according to Brosens\net al . [ 18], states that 5% of neonates have neonatal\nmenstruation during the first week after birth which can\nplay a role in the pathogenesis of endometriosis. “The\nmetaplasia theory” was suggested because some women\nwith Mayer–Rokitansky–Küster–Hauser syndrome devel-\noped endometriosis. “The genetic and epigenetic theory”\nsince endometriosis is a hereditary disease with the preva-\nlence increasing from 6 to 15% in first degree relative and\ndepending on the severity of the disease [ 5].\n5. Clinical Presentation\nIn reproductive age patients, the presence of dys-\nmenorrhea, dyspareunia and non-cyclic pelvic pain should\nevoke DE.\nEndometriosis rarely involves both the bladder and the\nureters. When the bladder is involved, the posterior wall\nis usually infiltrated [ 19] and the patient typically presents\nlower urinary tract symptoms (LUTS) such as frequency,\ndysuria, hematuria, urgency and bladder pain and it is fre-\nquently misdiagnosed for cystitis [19]. These symptoms are\ngenerally cyclic and worsen during menstruation but may\nas well be constant. As a matter of fact, hematuria is infre-\nquent because the lesions rarely infiltrate the mucosal layer.\nBladder involvement rarely results in severe sequelae espe-\ncially that this is a very symptomatic entity leading to in-\nvestigation and early treatment. Ureteral dilation and renal\nfailure could occur only if the ureteral tract is blocked by\nthe endometriotic lesion [ 20].\nUE, as well, is usually asymptomatic, thus delaying\nearly diagnosis and efficient treatment. This may lead, in\nrare cases, to chronic unnoticed ureteral stricture resulting\nin renal failure or silent kidney loss. When symptomatic,\nUE causes non-specific symptoms such as dysmenorrhea,\npelvic pain, flank pain, gross cyclical hematuria or pelvic\nmass [21].\n2\n\n\nFrequently, UTE is diagnosed incidentally during la-\nparoscopy for extensive endometriosis.\n6. Diagnosis\n6.1 Clinical History & Examination\nIn patients presenting possible deep endometriotic le-\nsions, physical examination should include pelvic, abdomi-\nnal, vaginal and rectal examination. V aginal examination is\nessential for evaluating patients with DE and especially for\ndetecting BE [ 22]. A palpable nodule or a thickened area\nalong the anterior vaginal wall may be felt and it is painful\nmost of the time. The combined rectovaginal examination\nhelps assessing the parametrial involvement and the palpa-\ntion of deep infiltrating nodules in the pouch of Douglas or\nin the uterosacral ligaments associated. Since physical ex-\namination in UTE is usually normal, this diagnosis should\nbe evoked if DE nodules are palpated on rectovaginal exam\n[23].\nDifferential diagnoses should be considered in pa-\ntients with suspected UTE. When patients present lower uri-\nnary tract symptoms, the physician should consider BE but\nshould also rule out infectious or interstitial cystitis, over-\nactive bladder, bladder carcinoma, bladder pain syndrome\nand chronic urethral syndrome [24]. When UE is suspected,\nthe physician should also consider other causes or intrin-\nsic or extrinsic ureteral stenosis such as stones, primary or\nmetastatic neoplastic lesions, retroperitoneal adenopathy,\nidiopathic retroperitoneal fibrosis and infection [21]. Imag-\ning techniques should be used to rule out these entities.\n6.2 Questionnaires\nThe modified American Urologic Association Symp-\ntom Index (AUASI) questionnaire is a 7-itemed question-\nnaire developed in 2007 to evaluate specific catamenial\nsymptoms, and was proven effective in identifying patient\nwith BE [25].\nThe Bristol Female LUTS is another questionnaire\nvalidated in assessing the variety of LUTS symptoms asso-\nciated with DE and UTE, as well as the follow up of patients\nafter treatment. It is made of 3 domains: symptoms, sexual\nfunction and quality of life questions [ 26].\n6.3 Imaging\n6.3.1 Ultrasonography\nUltrasonography, a non-invasive, cost effective and\nreproducible diagnostic tool is recommended for systematic\nuse in assessing women with DE [ 27]. In BE, it evaluates\nthe location and size of lesions and measures the distance\nbetween the lesion and the ureteral orifices. When the blad-\nder is full, endometriotic lesions appear as filling defects\nof the posterior wall with a variable protrusion into the lu-\nmen of the bladder. Bladder lesions are usually spherical,\nor comma shaped with regular contours. When contours\nare irregular, malignancy should be ruled out. Barra et al.\n[28], detected nodules with a mean diameter of 20 mm ±\n9.1 mm. On colored Doppler, bladder endometriotic lesions\npresent minimal to moderate internal blood flow. Abdom-\ninal ultrasonography does not visualize the entire ureteral\ncourse, making it impossible to directly detect ureteral en-\ndometriotic lesions, but it can evaluate the presence and the\nseverity of hydronephrosis thus indirectly diagnosing UE\nand obstruction [29].\nBoth abdominal and transvaginal ultrasound (TVUS)\nmay be used to detect vesical endometriotic lesions, with\nTVUS being the preferred method and should be used as\nfirst-line.\nDuring ureteral dilation assessment, the location of the\nstenosis and its distance from the bladder should be evalu-\nated as well as the ureteral diameter upstream and down-\nstream the obstruction [ 21]. A ureteral diameter of ≥6 mm\nwas associated with ureteral dilation [ 30].\nWith color Doppler, TVUS was found superior to cys-\ntoscopy in detecting BE nodules partially affecting the de-\ntrusor muscle [ 31] and at least as effective as the magnetic\nresonance imaging (MRI) in diagnosing and planning the\ntreatment of BE. It is suggested that it may improve the as-\nsessment of endometriotic nodules, their sizes, volume and\ninfiltration of the bladder wall [32]. Color Doppler can also\nhelp to evaluate Relative Jet Frequency which can be a good\nindicator of obstruction if reduced ( <25%) [33].\nIntraluminal ultrasonography is an invasive exam\ncurrently under evaluation, consisting of introducing a\ncatheter-based ultrasound probe in the ureters, to assess the\nureteral lumen, wall and peri-ureteral tissues [ 21].\n6.3.2 Magnetic Resonance Imaging\nMRI is the second-line imaging technique used for the\nevaluation of UTE. In BE assessment, it offers a higher res-\nolution, better delineation of the bladder wall layers, better\ntissue characterization and better multiplanar analysis when\ncompared to non-3D ultrasonography [ 34].\nIn MRI, BE lesions may manifest as localized or dif-\nfuse wall thickening associated with signal intensity abnor-\nmalities. Typical features are low signal on T2 weighted im-\nages with intermediated signal on T1 weighted images and\nspots of high signal on T1 and T2 weighted images repre-\nsenting hemorrhagic content. Systematic reviews showed\nno advantage for 3.0-T MRI or for Gadolinium-enhanced\nimaging. MRI reaches an 88% sensitivity and 99% speci-\nficity and 98% diagnostic accuracy for BE diagnosis [ 20].\nIt is the best imaging for UE assessment; lesions ap-\npear as solid nodules with spiculated margins surrounding\nthe ureter and showing low intensity signal on T1 and T2\nweighted images. Concurrent retractile adhesions appear\nas peri-ureteral hypo-intense linear foci with angular devia-\ntion. In cases of extrinsic endometriosis, the loss of fatty in-\nterface between the nodule and the ureter suggests ureteral\ninfiltration. MRI showed to be more sensitive but less spe-\ncific than laparoscopy in identifying intrinsic ureteral in-\nvolvement [35].\n3\n\nA new pre-operative (MRI, TVUS) classification,\n#ENZIAN, can be used to describe DE lesions including\nUE [36].\nSince MRI is more expensive but not superior to\nTVUS performed by experienced physicians, it should not\nbe used as a first line diagnostic tool [ 34].\n6.3.3 Other Imaging\nIntravenous and retrograde pyelography were tradi-\ntionally used to evaluate women with suspected UTE but\nhave been replaced with MRI [ 37].\nRenal scintigraphy should be performed in cases of se-\nvere hydronephrosis to assess the renal function and plan\nsurgical treatment in association to nephrectomy or kidney\npreservation. A kidney is considered salvageable if preop-\nerative glomerular filtration rate is more than 10%.\n6.3.4 Cystoscopy\nIt is commonly performed in the outpatient setting to\nassess the urethra, bladder inner wall and ureteral orifices.\nEven in the presence of BE, cystoscopy findings are usu-\nally normal due to the sparing of the mucosal layer [ 24].\nThe lesions may appear as adenomatous nodular masses\nwith varying shades of colors (red, blue, brown or black)\n[38]. Cystoscopy should be planned immediately before\nor during menstruation to best visualize the nodules when\nthey are enlarged and congested. It helps planning the\nsurgery by estimation of the distance between the nodules\nand the ureteral openings [ 7], especially when no feasible\nwith TVUS, should also be used to rule out malignancy\n[24].\n6.3.5 Urodynamics\nData in the literature evaluating the role of urodynam-\nics in assessing patients with UTE and DE is very scarce.\nPatients present typically higher bladder sensation, painful\nbladder filling, voiding symptoms, urgency, frequency and\nbladder pain. Its use is not recommended in clinical prac-\ntice and is currently limited to scientific research purposes\n[39].\n7. Histology\nAs for all endometriotic lesions, definitive diagnosis\nis confirmed by histopathology. In contrast with surgery,\nhistology can precisely assess the depth of invasion. The\ntwo main pathological subtypes are extrinsic and intrinsic\nendometriosis. Extrinsic endometriosis only invades the\nureteral adventitia or surrounding connective tissue, while\nintrinsic endometriosis directly infiltrates the muscularis,\nsubmucosa and rarely the mucosal layer. The two subtypes\ncan sometimes coexist [ 40].\nWhen evaluating UE, two patterns were described: an\nendometriotic pattern corresponding to endometrial glands\nor stromal cells seen in the wall of the ureters or in the peri-\nureteral space and a fibrotic pattern made of fibrotic tissue\nonly [41].\nThe endometriotic pattern is more prevalent and as-\nsociated with the presence of ureteral obstruction and hy-\ndronephrosis. The fibrotic pattern is associated with the\nrectovaginal nodules which might be related to the inflam-\nmatory process caused by a DE close to the ureters [ 3,41].\n8. Treatment\nDE involves mainly the posterior compartment of the\npelvis and is frequently associated to UTE and causes\nLUTS. Treatment modalities for DE/UTE include medical\nand surgical treatments. Medical treatment can be cho-\nsen for asymptomatic women without hydronephrosis. Per-\nsisting symptoms along with ureteral obstruction and hy-\ndronephrosis require surgery. Compared to minimally inva-\nsive surgery (MIS), laparotomy is associated with poorer vi-\nsualization of small infiltrating lesions resulting in larger in-\ncisions, increased blood loss, increased post-operative pain\nand recovery time. Laparoscopic management of severe ex-\ntra genital endometriosis was published in the 1980s. Sur-\ngical treatment of UTE is still not very common due to its\nunderdiagnoses and failure to identify endometriotic lesions\nby unexperienced surgeons. Furthermore, most of the gen-\neral, urology and gynecology surgeons are not trained to\ntreat DE.\n8.1 Medical/Hormonal Treatment\nCombined hormonal contraceptives and progestogens\nare the first line therapies for patients with DE and UTE\nand have proven efficacious in the treatment of different DE\nincluding UTE [42].\nRecent data suggest that symptoms and lesions may\nnot respond completely to medical therapies because of\nthe desmoplastic reaction within the tissues resulting from\nrepetitive bleeding and resorption of menstrual debris [ 43].\nGonadotropin-releasing hormone agonists (GnRH-\nas): leuprolide acetate and danazol are second line ther-\napy because of the hypoestrogenism related adverse effects\nranging from hot flashes, sleep disturbances, irregular vagi-\nnal bleeding, weight gain and vaginal dryness. Further-\nmore, once the treatment is discontinued, symptoms tend\nto recur [44].\nAromatase Inhibitors can be prescribed to patients re-\nfractory to conventional therapies in the setting of clinical\nresearch [45].\nWomen treated medically must undergo regular clini-\ncal examination, ultrasonography and laboratory testing to\nmonitor renal function, disease progression, and necessity\nfor surgery [24].\nMedical treatment is contraindicated in patients with\nureteral obstruction because of the risk of disease progres-\nsion and increased severity of ureteral stricture and hy-\ndronephrosis, thus surgery is the standard approach for mild\nto severe UE. However, post-operative medical treatment\nmay be useful in preventing recurrence of endometriosis\n4\n\n\n[21].\n8.2 Surgical Treatment\nThe aim of surgical treatment is to entirely resect the\nUTE lesions, relieve related symptoms, ureteral obstruc-\ntion, preserve renal function and avoid recurrence. The sur-\ngical approach should be tailored to the extent of the dis-\nease, the renal function and the surgeon’s skills, thus the\nmajor importance of preoperative accurate mapping of all\nlesions and their distance to the ureteral meatuses [ 46].\nMIS remains the recommended approach because la-\nparoscopy has demonstrated its superiority to laparotomy\nfor treating UE [ 21].\nDuring surgery for UTE, identification of the ureters is\nessential to avoid iatrogenic injury and to evaluate for pos-\nsible ureteral involvement [ 29]. Surgical options for BE\ninclude trans urethral resection (TUR) and partial cystec-\ntomy [ 24]. For UE, surgical options include conservative\nureterolysis and radical approaches such as ureterectomy\nwith an end-to-end anastomosis, ureteroneocystostomy or\nnephroureterectomy.\nConservative treatments like ureterolysis should be\nlimited to patients with minimal ureteral involvement.\nWhen ureteral endometriosis does not cause stenosis and\nhydronephrosis, ureterolysis with or without ureteral shav-\ning may be considered. The indication for ureteroneo-\ncystostomy should be the presence of moderate/severe hy-\ndronephrosis due to ureteral obstruction.\nThe risk of conservative treatment is mainly steno-\nsis with a risk up to 12 to 20% of patients who underwent\nureteroureterostomy and ureterolysis, respectively [ 12].\n8.2.1 TUR Surgery\nTUR is a proposed technique to treat BE without\nenough evidence supporting its efficacy or safety. Since\nBE develop from the bladder serosa inwards, complete ex-\ncision of endometriotic lesions is impossible by trans ure-\nthral resection without exposing the patient to increased risk\nof bladder perforation or short-term recurrence in case of\nincomplete resection [47].\n8.2.2 Segmental Bladder Resection\nPartial cystectomy is a bladder conserving option\nproven effective with excellent long-term results in control-\nling symptoms and lowering the risk of recurrence. It con-\nsists of partial bladder resection for detrusor endometriosis\nperformed via laparotomy or MIS with or without robotic\nassistance. Suturing the bladder defect can be performed in\n1 or 2 layers, continuous or interrupted sutures [ 19].\nUreter catheterization is not systematic and depends\non the distance between the caudal margin of the lesion and\nthe inter-ureteric ridge; if the distance is less than 2 cm,\ncatheterization is advisable. But in case of recurrent en-\ndometriosis, lesions tend to be closer to the ureteral mea-\ntuses, thus catheterization is mandatory.\nThis surgery is considered as simple and safe with fast\nhealing of bladder sutures and low risk of vesical fistula if\nprolonged drainage is performed [ 46].\nSome surgeons combine the TUR surgery with the\nsegmental bladder resection to overcome the limitations of\nboth techniques by allowing complete resection of the nod-\nule (contrary to the TUR) without any accidental excision\nof healthy tissue [ 48].\n8.2.3 Ureterolysis\nSafe and efficient, it aims to mobilize and free the\nureter from the surrounding endometriosis and fibrosis. It\nis indicated in patients presenting minimal extrinsic non-\nobstructive UE, but it is also performed in cases of mild to\nsevere obstruction in order to clearly visualize the stenotic\narea [13].\nIntra-urethral injection of near infra-red Indocyanine\nGreen improves the visualization of ureters, therefore pre-\nventing iatrogenic injuries [ 49]. Moreover, it helps assess\nureteral perfusion after conservative surgery.\n8.2.4 Endoscopic Excision\nRetrograde ureteroscopy is a minimally invasive pro-\ncedure allowing effective excision in cases of polypoid en-\ndometriotic lesions obstructing the ureteral lumen. It is not\nefficient for patients presenting deep ureteral wall fibrosis\nand periureteral connective tissue fibrosis [ 50].\n8.2.5 Ureteral Stenting\nLiterature shows that the risk of ureteral injury dur-\ning laparoscopic surgery is 1.5% for patients having UE\nversus 21% for patients presenting hydronephrosis [ 51].\nUreteral stenting serves mainly to release the obstruction,\nimprove renal function, facilitate ureteral identification,\nguide ureterolysis and prevent ureteral injury as well as pre-\nventing postoperative ureteral obstruction due to the local\ninflammation and edema.\n8.2.6 Partial Ureteral Wall Resection\nDescribed by Nezhat et al. [ 52] and Ghezzi et al. [ 53]\nin 1996 and 2007, respectively with no major complications\nreported. But this technique should undergo further evalu-\nation [52].\n8.2.7 Ureteral Resection with End to End Anastomosis\nThis technique allows complete excision of the in-\nvolved segment of the ureter and its surrounding fibrosis.\nAnastomotic breakdown or anastomotic stricture are the\nmost described complications. By preserving the distal part\nof the ureter and the vesico-ureteral junction, patients are at\na higher risk of recurrent endometriosis [ 54]. This tech-\nnique is indicated in patients presenting severe segmental\nureteral obstruction limited to the middle or upper parts of\nthe ureter.\n5\n\n8.2.8 Uretero-Neocystotomy\nThis technique is indicated for cases of extensive\nureteral involvement, lesions close to the bladder insertion\nand lesions extending over a long pelvic ureteral segment\nmaking ureterolysis and end to end anastomosis impossi-\nble. It consists of excision and reimplantation of the ureter\ninto the bladder, bypassing the endometriotic zone and its\nsurrounding fibrosis. Depending on the length of the re-\nsected area, a psoas bladder hitch or a Boari flap may be\nrequired to insure tension free anastomosis [ 14].\nLiterature shows a significant improvement of the\nsymptoms with this procedure, a low rate of recurrence at\n24 months (1.2%) and a low rate of major complications\n(4.4%) [21].\n8.2.9 Nephrectomy\nChronic gradual ureteral stenosis can ultimately lead\nto loss of renal function and eventually silent kidney loss\n(End Stage Renal Disease). This can be evaluated by kidney\nscintigraphy in patients presenting UE related hydronephro-\nsis [ 13]. Nephrectomy is indicated in patients with renal\nfunctions less than 15%, suffering from flank pain, kid-\nney stones, renovascular hypertension and recurrent urinary\ntract infection or pyelonephritis [ 55].\n9. Conclusions\nUTE is rare but frequently documented in the context\nof DE. Careful preoperative planning should be scheduled\nto diagnose an advanced-stage disease defining the depth,\nseverity and site of these lesions.\nMedical management could be proposed in a subset\nof patients, however, the minimally invasive surgical treat-\nment remains associated with a long-term optimal outcome.\nAuthor Contributions\nHEH: Data collection, manuscript writing. RS: Data\ncollection, manuscript editing. EF: Interpretation of Data,\nmanuscript editing. All authors read and approved the final\nmanuscript. All authors have participated sufficiently in the\nwork and agreed to be accountable for all aspects of the\nwork.\nEthics Approval and Consent to Participate\nNot applicable.\nAcknowledgment\nWe would like to express our gratitude to all those who\nhelped us during the writing of this manuscript. Thanks to\nall the peer reviewers for their opinions and suggestions.\nFunding\nThis research received no external funding.\nConflict of Interest\nThe authors declare no conflict of interest.\nReferences\n[1] Andres MP , Arcoverde FVL, Souza CCC, Fernandes LFC,\nAbrão MS, Kho RM. Extrapelvic Endometriosis: A Systematic\nReview. Journal of Minimally Invasive Gynecology. 2020; 27:\n373–389.\n[2] Fedele F, Di Fatta S, Busnelli A, Bulfoni A, Salvatore S, Candi-\nani M. Rare extragenital endometriosis: pathogenesis and ther-\napy. Clinical and Experimental Obstetrics & Gynecology. 2022;\n49: 43.\n[3] Nisolle M, Donnez J. Peritoneal endometriosis, ovarian en-\ndometriosis, and adenomyotic nodules of the rectovaginal sep-\ntum are three different entities. Fertility and Sterility. 1997; 68:\n585–596.\n[4] International working group of AAGL, ESGE, ESHRE and\nWES, Tomassetti C, Johnson NP , Petrozza J, Abrao MS, Einars-\nson JI, et al . An International Terminology for Endometriosis,\n2021. 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