Matches in SemOpenAlex for { <https://semopenalex.org/work/W2920686088> ?p ?o ?g. }
- W2920686088 endingPage "443" @default.
- W2920686088 startingPage "427" @default.
- W2920686088 abstract "Ejaculatory duct obstruction is an uncommon but surgically correctable cause of male infertility. With the advent and increased use of high-resolution transrectal ultrasonography, anomalies of the ejaculatory ducts related to infertility have been well documented. Although there are no pathognomonic findings associated with ejaculatory duct obstruction, the diagnosis should be suspected in an infertile male with oligospermia or azoospermia with low ejaculate volume, normal secondary sex characteristics, testes, and hormonal profile, and dilated seminal vesicles, midline cyst, or calcifications on transrectal ultrasound (TRUS). Although additional larger prospective and comparative studies are needed, it appears that TRUS with aspiration is the most effective method for diagnosis. While intrusive, it is less invasive than vasography. The most robust and published evidence for treatment involves transurethral resection of ejaculatory duct (TURED). More recent experience with antegrade endoscopic approaches are promising and may also be considered. An alternative to surgeries for reversal of obstruction is sperm retrieval for in vitro fertilization/intracytoplasmic sperm injection. A thorough discussion of all alternatives, including risks and benefits, should be held with couples facing this uncommon condition to allow them to make informed decisions regarding management. Ejaculatory duct obstruction is an uncommon but surgically correctable cause of male infertility. With the advent and increased use of high-resolution transrectal ultrasonography, anomalies of the ejaculatory ducts related to infertility have been well documented. Although there are no pathognomonic findings associated with ejaculatory duct obstruction, the diagnosis should be suspected in an infertile male with oligospermia or azoospermia with low ejaculate volume, normal secondary sex characteristics, testes, and hormonal profile, and dilated seminal vesicles, midline cyst, or calcifications on transrectal ultrasound (TRUS). Although additional larger prospective and comparative studies are needed, it appears that TRUS with aspiration is the most effective method for diagnosis. While intrusive, it is less invasive than vasography. The most robust and published evidence for treatment involves transurethral resection of ejaculatory duct (TURED). More recent experience with antegrade endoscopic approaches are promising and may also be considered. An alternative to surgeries for reversal of obstruction is sperm retrieval for in vitro fertilization/intracytoplasmic sperm injection. A thorough discussion of all alternatives, including risks and benefits, should be held with couples facing this uncommon condition to allow them to make informed decisions regarding management. Discuss: You can discuss this article with its authors and other readers at https://www.fertstertdialog.com/users/16110-fertility-and-sterility/posts/42580-27518 Discuss: You can discuss this article with its authors and other readers at https://www.fertstertdialog.com/users/16110-fertility-and-sterility/posts/42580-27518 A couple may be evaluated for infertility if they are unable to conceive after 12 months of unprotected intercourse. In ∼15% of these couples, the male partner has azoospermia, due to obstructive azoospermia in 40%, indicating that spermatogenesis is preserved but the sperm is unable to reach the ejaculate. Ejaculatory duct obstruction (EDO), a specific type of obstructive azoospermia, is present in 1%–5% of infertile men (1Modgil V. Rai S. Ralph D.J. Muneer A. An update on the diagnosis and management of ejaculatory duct obstruction.Nat Rev Urol. 2016; 13: 13-20Crossref PubMed Scopus (31) Google Scholar, 2Aggour A. Mostafa H. Maged W. Endoscopic management of ejaculatory duct obstruction.Int Urol Nephrol. 1998; 30: 481-485Crossref PubMed Scopus (8) Google Scholar). Classic bilateral complete EDO is characterized by low volume, low pH, and azoospermia without fructose in the ejaculate in the setting of normal hormonal values. In cases of incomplete or partial obstruction, the patient may have low-normal volume and low-normal pH oligoasthenospermia. Typically, spermatogenesis is preserved unless there exists simultaneous hypothalamic-pituitary-gonadal axis pathology (Table 1). In addition to infertility, other symptoms may include hematospermia andor pelvic or perineal pain exacerbated by ejaculation. Farley and Barnes are credited with the first documentation of defining stenosis of the ejaculatory duct (ED) and management with transurethral resection in 1973 (3Farley S. Barnes R. Stenosis of ejaculatory ducts treated by endoscopic resection.J Urol. 1973; 109: 664-666Crossref PubMed Scopus (71) Google Scholar). In the absence of anatomic obstruction, there may be functional obstruction indicating abnormal emptying of the ejaculatory apparatus without a physical obstruction (4Font M. Pastuszak A. Case J. Lipshultz L. An infertile male with dilated seminal vesicles due to functional obstruction.Asian J Androl. 2017; 19: 256-257Google Scholar).Table 1Characteristics of categories of ejaculatory duct obstruction.ParameterComplete obstructionIncomplete/partial obstructionFunctional obstructionsVolume of ejaculateLowLow-normalLowSperm countAbsentLow-normalAbsent–lowSperm motilityAbsentLowAbsent–lowFructose in ejaculateAbsentAbsent–lowAbsent–lowEjaculate pHLowLow–normalLow–normalHormonal evaluationNormalNormalNormalSeminal vesicle sizeNormal–enlargedNormal–enlargedNormal–enlargedTestis sizeNormalNormalNormal Open table in a new tab Table 2Brief description of reference studies, detailing study type, patient populations, diagnostic methods, intervention, and outcomes.ReferenceStudy designNo. of patientsPresenting diagnosisMethod of diagnosisaMost studies included initial workup of semen analysis, physical exam, hormone parameters, ± urine analysis for retrograde ejaculation, and ± testis biopsy. Additional unique diagnostic tools are listed.InterventionOutcome reportedSemen analysis (SA)PregnancySymptom assessmentComplications54retrospective5azoo± scrotal exploration± epididymo-vasostomy with interval TURED in 4 menSA3 men with postop SA: 1 at 12 mo several mil. sperm/mL, 5% motility, 1 azoo, 1 initial increase in vol. but returned to 0.5 mL at 6 monone reportedn/anot reported45retrospective21EDOTRUS20 transurethral seminal vesiculoscopy (TRU-SVS), 1 TURED (failed TRU-SVS)SA, pregnancy19/21 (90%) improved sperm count; by 3 mo postop average sperm count 6.6 mil. (preop 0.019 mil.)4/21 (19%) spontaneous pregnancyby 3 mo postop: resolution of 3/3 painful ejaculation, 5/7 hematoserpmia, and 7/7 perineal/testicular pain7 men with postop painful ejaculation or discomfort that resolved by 3 mo postop8retrospective87subfertile men: azoo (n = 67), severe oligo (n = 17), oligo (n = 1), normal sperm concentration (n = 2) in low-vol. ejac. with acidic pH and little or no fructose grouped by etiologyscrotal exploration and vasography43 men underwent TURED ± TUIED, ± epididymovasostomySA and pregnancy18/31 (58%) “patent” after surgeryspontaneous pregnancy by etiology: müllerian duct cyst 5/12 (41%), post-infectious causes 1/6 (16.6%)n/anot reported47case report1pelvic pain/hematospermiaTRUS, SV aspiration, and vesiculographyantegrade access/retrograde balloonsymptom assessmentn/an/aresolution of symptomsnone49case report1secondary infertilityTRUS, MRIattempted antegrade trans-rectal US guided ED balloon dilationunable to complete treatmentn/an/an/anone38case report1hematospermiaTRUS, MRI, vasographycold knife incision of cystresolution of hematospermian/an/aresolution of hematospermia up to 7 mo postopnone46retrospective22infertility (complete EDO in 6, partial EDO in 16)TRUS, vasographydilation of ED by seminal vesiculoscopy, 4 pts required TURED to see EDOSA, voiding cystourethrography, symptom assessment18/22 (81%) had improved SP; 13/22 (59%) had sperm present; 7/22 (31%) had normal SP6 pregnancy3/3 (100%) pain/hematospermia resolved1 with SV reflux after TURED37retrospective26subfertile men with azoo or severe oligovasographyendoscopic incision with urethrotome, ± redo incision, ± TUREDvisualization of methylene blue, SA10 persistent azoo or severe oligo (<1 mil. sperm/mL), 5 pts with 1-10 mil. sperm/mL, 9 pts with >11 mil. sperm/mL8 spontaneous pregnancy (31%)2 unsuccessful resectionnone52case report1complete EDO (azoo)TRUS, MRI, seminal vesiculography, midline prostatic cyst aspirationlaser incision to unroof cyst then TUREDSA2 mo follow-up: vol. 3 mL, 15.2 mil. sperm/mLn/an/anone50retrospective11infertility specifically with MPCTRUStransrectal ultrasonically-guided cyst aspirationSA, pregnancy1 mo postop: sig. reduction in MPC vol., improvement of semen vol. (10/11). total sperm count (11/11), and sperm motility/morphology; 3 mo postop: sig. increase in MPC vol., decrease in semen vol., sperm concentration, and total sperm count compared with 1 mo but still sig. improvement from baseline4/11 (36%) spontaneous pregnancy, 1 ICSI pregnancyn/anone48case report1pelvic painMRI, TRUS, SV aspirationtransrectal US–guided seminal vesiculography and wire access for canalization of ED; retrograde ED balloon dilation for EDOsymptom assessmentn/an/aresolution of painnone44retrospective72hematospermian/atransurethral seminal vesiculoscopy completed in 67/72symptom assessmentn/an/adefinite diagnosis in 67/72 (93.1%), hematospermia resolved in 70/72 (97.2%)none51case report1infertility, oligovasography, TRUSTRUS guided laser incision of cystvisualized release of seminal fluidimproved ejac. vol.not reportedn/anot reported40prospective analysis25men with EDO, 2/2 calculi, or ED disorders (excluded infertility)TRUS, TRUS SV aspiration, fluoroscopy-monitored seminal vesiculographytransurethral incision of ED with intraoperative TRUS and fluoroscopy and chromotubationsymptom assessment, SA at 1 moSA not reportedn/a96% symptom relief at 3 mo3 with epididymitis31retrospective23infertility (17 complete, 6 partial)TRUS ± MRITUREDsemen parametersstatistically sig. improvement in ejac. vol, sperm count, and motility in all pts treated; by subgroup, incomplete EDO (and not complete EDO) pts had statistically sig. increase in sperm count and motility13% (3/23) spontaneousn/a26% (2 epididymo-orchitis, 1 partial EDO with azoo, 3 watery ejaculate)26case report1infertility, azooMRI, cystoscopyTUREDvisualized release of seminal fluidn/an/an/anot reported24case report1infertility with partial EDOTRUSTUREDSA, pregnancyimproved vol. from 1.7 to 2.2 mL, sperm count from 12 mil. to 131 mil. sperm/mL, and motility from 23% to 34% within 1 y of surgerypregnancy with IUIn/apostoperative incontinence20case reports2partial EDOTRUS, intraoperative vasotomy with methylene blue in 1TUREDSA, pregnancynormalization of SA for 2 pts2 pregnancy (100%)n/anone27retrospective38partial/complete EDO for infertilityTRUS ± MRITUREDSAsig. improvement in mean ejac. vol., sperm concentration. and % motility; improvement in sperm variables observed in 59% (13/22) of pts with complete EDO and in 94% of pathologies (15/16) with partial EDO5 pregnancy (13%), 15 (40%) became candidates for IUIn/a5 (13%): AUR, UTI, epididymitis, oligo to azoo29retrospective24infertility (primary and secondary) azoo and oligointraoperative vasography ± TRUSTUREDSA, pregnancy12 (50%) improvement in sperm density and/or motility; 8 (33%) improved ejac. vol. only; 6 without improved SP7 (27%)n/a2 hematuria requiring catheterization22retrospective8infertility with complete azoo divided into cystic and noncystic causesTRUSTUREDSA, pregnancy, symptom assessment and postop TRUScystic: 3/3 (100%) increase in semen vol., pH, and sperm count; noncystic: 3/5 (60%) increase in semen vol., pH, and sperm count0% pregnancy reportedall symptoms resolved; no persistent dilated SV or ED evident after “successful” TURED by TRUS in 6/8 mennone21case reports21 primary, 1 secondary infertilitycase 1: TRUS, MRI; case 2: TRUS, intraoperative vasographyTUREDSA, pregnancy(6 mo postop) case 1: 1 mL, 10 mil. sperm/mL, 22% forward motility; case 2: 4 mL, 46 mil. sperm/mL, 40% forward motility1 (50%) spontaneous pregnancy by 12 mo, 1 pregnancy with IVFn/a1 (50%) case with increase in creatinine in seminal plasma suggesting reflux of urine32retrospective42infertility (38 azoo, 4 oligo)TRUS ± vasography, MRITUREDSA, pregnancy38/42 (90.5%) had increased semen vol. (avg. 3.68 mL); 23/38 (60.5%) with azoo had sperm postop; 4/4 oligo had increase in sperm counts (no numbers or avg. reported), 16/42 (38.1%) had normal semen parameters postopBy mean follow-up of 18 mo, 13/42 (31%) spontaneous pregnancyn/a2/42 (4.7%): 1 case of epididymitis and 1 case of watery ejaculate28retrospective46primary (80%) and secondary infertility, including azoo and oligoTRUSTUREDSA, pregnancyin total, 30/46 (65%) had improved semen quality (>50% increase in total motile sperm count); 13/22 (60%) of low-vol. azoo had increase in TMC, 3/22 (13%) of low-vol. azoo had increase in ejac. vol., 6/22 (27%) of low-vol. azoo had no change20% initiated a pregnancy avg. 6.1 mo after surgeryn/a10/46 (22%): watery high-vol. ejac. in 5; 1 GH requiring catheter, 1 UTI, 1 epididymitis, 1 post-void dribbling, 1 premature ejaculation; 1/24 (4%) of pts with sperm in ejac. preop became azoo postop24retrospective5azoo or severe oligo (<1 mil. sperm/mL)TRUS ± vasogramTUREDSA, pregnancy2 remained azoo (underwent VE without improvement), 3 men with increased vol., fructose, and sperm count (2 with normozoospermia)no pregnancy reportedn/anot reported42case report1secondary complete EDO after TURED for partial EDOTRUS, SV aspiration, chromotubationTUREDSAaverage of 3.8 mL, 12 mil. sperm/mL, and 30% motilityreferred for ARTn/anone10retrospective16low-vol. azoo or oligo (12 azoo, 4 oligo; 7 MPC, 9 noncystic EDO)TRUSTUREDSA, pregnancy, 15/16 with intraoperative patency8/16 (50%) with improved SA (including 6 with MPC)2 with MPC had spontaneous pregnancy (1 was azoo and 1 oligo pre-TURED)n/anot reported41retrospective43all with hematospermia >1 y, including 6 with infertilityTRUS ± MRI or CTTURED and vesiculoscopy, ± incision and dilation of proximal ED, ± incision of cyst, bx of SVSV biopsy − all inflammation; SA if presented with infertility; symptom assessmentSA at 1 and 3 mo postop: sperm densities 16.7 mil. and 43.9 6 mil./mL, motility rates 35.3% and 64.5%, 3 men initially azoo became normospermic2/6 (33%) men had children within a year42 hematospermia resolved; 1 man underwent repeated surgery and resolvednone2retrospective11azooTRUS, intraoperative vasographyTURED confirmed by intraoperative vasography for 11/11successful vasography in 10/117/11 (63%) patency rate by SA2/11 (18%)n/a3/10 (30%): 2 epididymitis, 1 AUR11prospective25clinical symptoms ± infertility: 18 infertile (72%), 2 painful ejac. (8%), 2 hematospermia and azoo (8%), 2 pain (8%), and 1 hematospermia (4%)TRUS, vesiculography, seminal vesicle aspiration and duct chromotubationTURED in 12 pts (including 8 for infertility)comparative analysis of diagnostic tools, SA6/8 (75%) men with infertility had improved semen quality: mean ejac. vol. from 0.89 to 3.4 mL, mean total number of ejaculated sperm from 3.5 mil. to 124 mil.2/8 (25%) spontaneous pregnancy2/2 (100%) had resolution of pain, 2 hematospermia resolved4/25 (16%; 3 after TURED): 1 epididymitis, 2 limited hematuria requiring urologic reevaluation, 1 with limited19prospective9suspected EDO (complete, partial, or functional) for infertility or symptomsTRUS, SV aspiration and chromotubation, manometryTURED in 6/9symptom assessment and SA4/5 with preop SA had increase in ejac. vol. and/or 100% increase in TMC (range 4–60 mil. sperm)not examined2/3 improved1 epididymitis30retrospective15symptomatic EDO in infertilityTRUSTURED with prostatic massageSA and symptom assessment after 2 moincrease in mean ejac. vol. to 2.3 mL and total motile sperm count to 38.1 mil.4/15 (26.6%)subjective improvement in 14/15 (93.3%)none39case report1prior fertility with reduced ejac vol., painTRUSTURED with prostatic massageSA and symptom assessmentvol. from 0.8 mL to 2.1 mL, sperm count of from 75.2 mil. to 27 mil. sperm/mL, morphology from 12% to 11%, and progressive motility from 52% to 50%n/asymptoms resolvednew “fluid” eja.c with findings of elevated creatinine in the ejac. consistent with urinary reflux35retrospective14partial EDO grouped into acquired vs. congenital etiologyTRUS, intraoperative vasographyTURED with prostatic massageSA, pregnancycongenital: 6/6 (100%) improved vol. and motility, 5/6 (83%) improved sperm count; acquired: 3/8 (37.5%) improved sperm quality, 2/8 (25%) with worse SPcongenital: 4/6 (66.6%) spontaneous pregnancy, 1/6 (16.6%) by stimulated cycle/IUI; acquired: 1/8 (12.5%) spontaneous pregnancyacquired: 1 spontaneous pregnancywatery high-vol. ejac., UTI, development of azoo34retrospective12infertility with complete EDO (all azoo)TRUSTURED with TRUS-guided chromotubationSA, pregnancy, symptom assessmentat 3 mo postop: 12/12 (100%) normal ejac. vol., 11/12 (92%) had sperm present, 5/12 (41.6%) had >20 mil. sperm/mL with >30% motile sperm, 3/12 (25%) 5–15 mil. sperm/mL, 3/12 (25%) had <5 mil. sperm/mL, 1 azoototal 5 pregnancy (41.6%): 3/12 (25%) spontaneous (all with sperm count >20 mil.), 1 (8.3%) by IUI, 1/12 (8.3%) vy IVF3/3 pain ejaculation resolved, 2/2 (100%) hematospermia resolved, 2/2 (100%) perineal/testicular pain resolvednot reported22retrospective85 with infertility, ± hematospermia, testicular/ejaculatory painvasography, ± TRUS, ± MRITURED, ± vasoepididymostomySA, pregnancy, symptom assessment5/6 (83%) men with semen vol. <1 mL and <10 mil. sperm/mL improved markedly in semen vol. and sperm concentration2/5 (40%) pregnancy (1 normal delivery, no pregnancy for man after VE)4/4 (100%) resolution of pain symptoms, 1/1 (100%) resolution of hematospermianot reportedNote: ART = assisted reproductive technology; AUR = acute urinary retention; azoo = azoospermia; CT = computerized tomography; ED = ejaculatory duct; EDO = ejaculatory duct obstruction; ejac. = ejaculate; ICSI = intracytoplasmic sperm injection; IUI = intrauterine insemination: IVF = in vitro fertilization; MPC = midline prostatic cyst; MRI = magnetic resonance imaging; oligo = oligospermia; pt/pts = patient/patients; sig. = significant; SP = sperm parameters; SV = seminal vesicle; TMC = total motile sperm count (volume × concentration × motile fraction); TRUS = transrectal ultrasonography; TRU-SVS = transurethral seminal vesiculoscopy; TURED = transurethral resection of ejaculatory duct; UTI = urinary tract infection; VE = vasoepididymostomy.a Most studies included initial workup of semen analysis, physical exam, hormone parameters, ± urine analysis for retrograde ejaculation, and ± testis biopsy. Additional unique diagnostic tools are listed. Open table in a new tab Note: ART = assisted reproductive technology; AUR = acute urinary retention; azoo = azoospermia; CT = computerized tomography; ED = ejaculatory duct; EDO = ejaculatory duct obstruction; ejac. = ejaculate; ICSI = intracytoplasmic sperm injection; IUI = intrauterine insemination: IVF = in vitro fertilization; MPC = midline prostatic cyst; MRI = magnetic resonance imaging; oligo = oligospermia; pt/pts = patient/patients; sig. = significant; SP = sperm parameters; SV = seminal vesicle; TMC = total motile sperm count (volume × concentration × motile fraction); TRUS = transrectal ultrasonography; TRU-SVS = transurethral seminal vesiculoscopy; TURED = transurethral resection of ejaculatory duct; UTI = urinary tract infection; VE = vasoepididymostomy. The purpose of the present review is to survey the existing data in support of treating EDO in an effort to improve male infertility and pregnancy outcomes. Whereas the prostate is derived from the endoderm, the EDs, in addition to the body and tail of the epididymis, vas deferens, and seminal vesicles (SV) are derived from the wolffian duct (mesonephric duct). The SVs typically are 4.5–5.5 cm in length and 2.2 cm in width (5Jurewicz M. Gilbert B.R. Imaging and angiography in male factor infertility.Fertil Steril. 2016; 105: 1432-1442Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar). The vas deferens course to the medial aspect of the SVs, where the ampulla of the vas deferens joins the ducts of the SV to form the ED. The paired EDs are direct continuations of the ducts of the SV and are similar histologically. There is an inner pseudostratified columnar epithelium, a middle collagenous layer that thins over the duct's course, and an outer longitudinal muscular layer that continues from the SV and attenuates over its course. The inner circular muscular layer of the SV does not continue around the EDs (Fig. 1). Within the prostate, the EDs gain a common sheath of connective tissue as they run parallel to each other (6Nguyen H.T. Etzell J. Turek P.J. Normal human ejaculatory duct anatomy: a study of cadaveric and surgical specimens.J Urol. 1996; 155: 1639-1642Crossref PubMed Scopus (48) Google Scholar). The EDs enter the posterior aspect of the prostate at an oblique angle and then run for ∼1–2 cm anteromedially through the prostate. Based on autopsy studies, the diameter of the ducts range from widest proximally at ∼1.31 mm and taper to ∼0.45 mm as they approach their opening at the prostatic urethra (7McMahon S. An anatomical study by injection technique of the ejaculatory ducts and their relations.J Anat. 1938; 72: 556-574Google Scholar). Another group found 1.7 mm luminal diameter at the proximal ED narrowing down to 0.3 mm distally (6Nguyen H.T. Etzell J. Turek P.J. Normal human ejaculatory duct anatomy: a study of cadaveric and surgical specimens.J Urol. 1996; 155: 1639-1642Crossref PubMed Scopus (48) Google Scholar). The ducts typically open separately at an acute angle into the prostatic urethra at the verumontanum, also known as seminal colliculus. The prostatic utricle, a remnant of the müllerian duct, lies between the paired EDs within the verumontanum. Rarely do the EDs unilaterally or bilaterally open into the utricle. Autopsy studies show that the openings of the EDs are typically anterolateral to the opening of the utricle, which is blind ending (6Nguyen H.T. Etzell J. Turek P.J. Normal human ejaculatory duct anatomy: a study of cadaveric and surgical specimens.J Urol. 1996; 155: 1639-1642Crossref PubMed Scopus (48) Google Scholar, 7McMahon S. An anatomical study by injection technique of the ejaculatory ducts and their relations.J Anat. 1938; 72: 556-574Google Scholar). EDO can be characterized as complete or incomplete, anatomic or functional, or congenital versus acquired. Whereas complete obstruction of both ducts and functional obstructions result in low volume ejaculate, partial or unilateral obstruction may be associated with normal or low seminal volumes. Although most patients with any type of EDO may present with postejaculatory pain or hematospermia, most are asymptomatic beyond infertility. Patients with unilateral or partial EDO may have severe oligoasthenospermia. Complete obstruction involves both EDs. Incomplete or partial obstruction involves only one ED or partial obstruction of one or both EDs. Congenital causes of EDO include congenital atresia or stenosis of ED, utricular cysts, müllerian duct cysts, and wolffian duct cysts. Acquired causes include iatrogenic trauma secondary to prolonged catheterization, pelvic or bladder outlet surgeries damaging the SVs, vas deferens, and EDs or pelvic trauma, infectious etiologies such as genital/urinary tuberculosis infections, stones and prostatic abscesses, and even prostate cancer, which all may lead to SV calculi, inflammation, and scarring (Fig. 2) (8Pryor J.P. Hendry W.F. Ejaculatory duct obstruction in subfertile males: analysis of 87 patients.Fertil Steril. 1991; 56: 725-730Abstract Full Text PDF PubMed Scopus (172) Google Scholar). Functional obstruction is failure of peristalsis of the SVs. This is primarily a diagnosis of exclusion, especially persistent low-volume ejaculate with azoospermia despite confirmed patency of bilateral EDs and normal spermatogenesis. Failure of emission may be observed secondary to spinal cord injury, multiple sclerosis, retroperitoneal lymph node dissection, and pelvic surgery (9Phillips E. Carpenter C. Oates R.D. Ejaculatory dysfunction.Urol Clin North Am. 2014; 41: 115-128Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar). In addition, patients with diabetes may experience neurogenic dysfunction. Medications can also alter ejaculation, including alpha-blockers, typical antipsychotics, and tricyclic antidepressants (4Font M. Pastuszak A. Case J. Lipshultz L. An infertile male with dilated seminal vesicles due to functional obstruction.Asian J Androl. 2017; 19: 256-257Google Scholar). Pryor and Hendry reviewed 87 of their subfertile patients diagnosed with EDO. Patients were evaluated by means of scrotal exploration, testicular biopsy, and vasography with methylene blue simultaneously with cystourethroscopy. Acknowledging that there may be some overlaps between etiologies, they found 41% to have a congenital malformation of the müllerian or wolffian duct, 17% to have a traumatic cause, 22% to have a post-infectious cause, 9% tuberculosis, 9% megavesicles, and 1% a neoplastic source. Congenital causes from müllerian duct include cysts at the prostatic utricle. It is thought that an azoospermic or oligospermic man with low-volume ejaculate and low pH with absent fructose with normal examination (palpable vas bilaterally) is pathognomonic for EDO. The epididymis may not show clearly dilated tubules, because the pressure at this distal obstruction may not translate to increased pressure in the epididymis (8Pryor J.P. Hendry W.F. Ejaculatory duct obstruction in subfertile males: analysis of 87 patients.Fertil Steril. 1991; 56: 725-730Abstract Full Text PDF PubMed Scopus (172) Google Scholar). Although the criterion standard for diagnosis has been open scrotal vasography under fluoroscopy or x-ray imaging, additional methods include transrectal ultrasonography (TRUS), magnetic resonance imaging (MRI) with an endorectal coil, SV aspiration, SV chromotubation, seminal vesiculography, and seminal vesiculoscopy. Imaging may identify midline cysts that may be müllerian or utricular cysts, ED or SV dilation, ED cysts, or diverticula. Scrotal vasography is a fluoroscopic study performed by injection of contrast into the vas deferens, usually with vasal access via an open hemivasotomy that should be microsurgically repaired. Obstruction is diagnosed if contrast does not pass into the urethra or bladder. Vasography, in addition to delineating the level of obstruction, offers the secondary benefit of examination of the vasal fluid for sperm and cryopreservation of sperm if found. The absence of sperm in the vasal fluid suggests epididymal or more proximal vasal obstruction which may exist in addition to a more distal EDO. Although vasography is considered to be the criterion-standard diagnostic method, it is invasive and time intensive and risks secondary iatrogenic vasal stricture or stenosis (10Schroeder-Printzen I. Ludwig M. Köhn F. Weidner W. Surgical therapy in infertile men with ejaculatory duct obstruction: technique and outcome of a standardized surgical approach.Hum Reprod. 2000; 15: 1364-1368Crossref PubMed Scopus (55) Google Scholar). It is mentioned primarily for historical purposes (Fig. 3). Although TRUS is most frequently used in urology for imaging the prostate for prostate biopsy, it is also a method for evaluating obstructive azoospermia. The SVs are identified at the posterior base of the prostate. The vas deferens may be found medial to the ipsilateral SV. The ED is a hypoechoic structure on transrectal ultrasound (TRUS) (5Jurewicz M. Gilbert B.R. Imaging and angiography in male factor infertility.Fertil Steril. 2016; 105: 1432-1442Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar). EDO should be suspected if TRUS shows SV width >1.5 cm or ED diameter >2.3 mm. The diagnosis is more likely if observed with a cyst or duct calcification (10Schroeder-Printzen I. Ludwig M. Köhn F. Weidner W. Surgical therapy in infertile men with ejaculatory duct obstruction: technique and outcome of a standardized surgical approach.Hum Reprod. 2000; 15: 1364-1368Crossref PubMed Scopus (55) Google Scholar). However, the specificity of positive findings is not great as not all men with dilated SVs have EDO and not all men with EDO have dilated SVs. A prospective study comparing TRUS with duct chromotubation, SV aspiration, and seminal vesiculography in men suspected of EDO, though including complete and likely partial obstruction, found that only 50% of men needed surgery based on TRUS findings. Of patients considered to have EDO according to TRUS, the authors diagnosed EDO in 48%, 36%, and 52% with the use of SV aspiration, chromotubation, and vesiculography. TRUS alone is a limited screening tool for EDO (11Purohit R.S. Wu D.S. Shinohara K. Turek P.J. A prospective comparison of 3 diagnostic methods to evaluate ejaculatory duct obstruction.J Urol. 2004; 171: 232-235Crossref PubMed Scopus (71) Google Scholar). Although its minimally invasive, TRUS is limited as a static anatomic study and by the skills of the operator. Guo et al. investigated the utility of MRI, either plain or with enhancement, in 18 patients with suspected complete and incomplete EDO. They recommended diagnosis of EDO if the diameter of the ED is >2 mm. The wall of the ejaculate duct may be thick and enhancing. The authors did not discuss the management or outcomes of their patients (12Guo Y. Liu G. Yang D. Sun X. Wang H. Deng C. Role of MRI in assessment of ejaculatory duct obstruction.J Xray Sci Technol. 2013; 21: 141-146Google Scholar)." @default.
- W2920686088 created "2019-03-11" @default.
- W2920686088 creator A5058645773 @default.
- W2920686088 creator A5059966737 @default.
- W2920686088 creator A5065842395 @default.
- W2920686088 creator A5087500960 @default.
- W2920686088 date "2019-03-01" @default.
- W2920686088 modified "2023-10-17" @default.
- W2920686088 title "Transurethral resection of the ejaculatory ducts: etiology of obstruction and surgical treatment options" @default.
- W2920686088 cites W1608659604 @default.
- W2920686088 cites W1699967432 @default.
- W2920686088 cites W1741749532 @default.
- W2920686088 cites W1963706070 @default.
- W2920686088 cites W1965655017 @default.
- W2920686088 cites W1969394304 @default.
- W2920686088 cites W1972546108 @default.
- W2920686088 cites W1983886436 @default.
- W2920686088 cites W2017577239 @default.
- W2920686088 cites W2018437068 @default.
- W2920686088 cites W2034130287 @default.
- W2920686088 cites W2035581007 @default.
- W2920686088 cites W2040032257 @default.
- W2920686088 cites W2042569311 @default.
- W2920686088 cites W2044276572 @default.
- W2920686088 cites W2050876316 @default.
- W2920686088 cites W2050877273 @default.
- W2920686088 cites W2074682756 @default.
- W2920686088 cites W2080042812 @default.
- W2920686088 cites W2086963014 @default.
- W2920686088 cites W2087978228 @default.
- W2920686088 cites W2088552264 @default.
- W2920686088 cites W2092593859 @default.
- W2920686088 cites W2094409560 @default.
- W2920686088 cites W2097028365 @default.
- W2920686088 cites W2110257169 @default.
- W2920686088 cites W2110960878 @default.
- W2920686088 cites W2111877228 @default.
- W2920686088 cites W2119384412 @default.
- W2920686088 cites W2123800247 @default.
- W2920686088 cites W2136415908 @default.
- W2920686088 cites W2136605478 @default.
- W2920686088 cites W2136903425 @default.
- W2920686088 cites W2141773200 @default.
- W2920686088 cites W2148079476 @default.
- W2920686088 cites W2148828758 @default.
- W2920686088 cites W2149266976 @default.
- W2920686088 cites W2158748842 @default.
- W2920686088 cites W2256625486 @default.
- W2920686088 cites W2269736687 @default.
- W2920686088 cites W2277957556 @default.
- W2920686088 cites W2291269997 @default.
- W2920686088 cites W2333362376 @default.
- W2920686088 cites W2342845489 @default.
- W2920686088 cites W2410904512 @default.
- W2920686088 cites W254604773 @default.
- W2920686088 cites W2895051810 @default.
- W2920686088 cites W4231141488 @default.
- W2920686088 cites W98269629 @default.
- W2920686088 doi "https://doi.org/10.1016/j.fertnstert.2019.01.001" @default.
- W2920686088 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30827517" @default.
- W2920686088 hasPublicationYear "2019" @default.
- W2920686088 type Work @default.
- W2920686088 sameAs 2920686088 @default.
- W2920686088 citedByCount "24" @default.
- W2920686088 countsByYear W29206860882019 @default.
- W2920686088 countsByYear W29206860882020 @default.
- W2920686088 countsByYear W29206860882021 @default.
- W2920686088 countsByYear W29206860882022 @default.
- W2920686088 countsByYear W29206860882023 @default.
- W2920686088 crossrefType "journal-article" @default.
- W2920686088 hasAuthorship W2920686088A5058645773 @default.
- W2920686088 hasAuthorship W2920686088A5059966737 @default.
- W2920686088 hasAuthorship W2920686088A5065842395 @default.
- W2920686088 hasAuthorship W2920686088A5087500960 @default.
- W2920686088 hasBestOaLocation W29206860881 @default.
- W2920686088 hasConcept C121608353 @default.
- W2920686088 hasConcept C126322002 @default.
- W2920686088 hasConcept C126894567 @default.
- W2920686088 hasConcept C137627325 @default.
- W2920686088 hasConcept C141071460 @default.
- W2920686088 hasConcept C159110652 @default.
- W2920686088 hasConcept C2776235491 @default.
- W2920686088 hasConcept C2777362289 @default.
- W2920686088 hasConcept C2781171107 @default.
- W2920686088 hasConcept C71924100 @default.
- W2920686088 hasConceptScore W2920686088C121608353 @default.
- W2920686088 hasConceptScore W2920686088C126322002 @default.
- W2920686088 hasConceptScore W2920686088C126894567 @default.
- W2920686088 hasConceptScore W2920686088C137627325 @default.
- W2920686088 hasConceptScore W2920686088C141071460 @default.
- W2920686088 hasConceptScore W2920686088C159110652 @default.
- W2920686088 hasConceptScore W2920686088C2776235491 @default.
- W2920686088 hasConceptScore W2920686088C2777362289 @default.
- W2920686088 hasConceptScore W2920686088C2781171107 @default.
- W2920686088 hasConceptScore W2920686088C71924100 @default.
- W2920686088 hasIssue "3" @default.
- W2920686088 hasLocation W29206860881 @default.
- W2920686088 hasLocation W29206860882 @default.