Ej
aculatory duct obstruction (EDO) remains a rare but surgically correctable cause of male sexual dysfunction and male infertility due to obstructive azoospermia, diagnosed in up to 5% of infertile men. EDO should, therefore, be considered within the list of differential diagnoses for men undergoing infertility investigations, with work up including clinical examination, transurethral ultrasonography, semen analysis, chromotubation, seminal vesiculography and seminal vesicle aspiration. Obstruction can be limited to the distal ends of the ducts or it can extend proximally to include the terminal portions of the vasa deferentia, with the site and length of the obstruction having implications for surgical intervention. Early endoscopic treatment can reverse symptoms and prevent the progression of partial obstruction to bilateral, complete obstruction, and transurethral resection of the ejaculatory duct remains the main treatment option for EDO. Alternative treatment options include endoscopic laser-assisted resection of the ducts, antegrade seminal-vesicle lavage to relieve EDO secondary to inspissated material or
calculi, or dilatation of the ejaculatory ducts using 9F seminal vesicoscopy or balloon
Azoospermia (the absence of sperm in the ejaculate) is found in 15% of infertile men; in 40% of these patients, obstructive azoospermia is the cause1. Obstruction, either at the level of the epididymis or more distally in the vas deferens, is amenable to surgical reconstruction and is, therefore, a surgically reversible cause of male infertility2. Obstructions more distal than the vas deferens are rare and seldom diagnosed, although these are still amenable to treatment using endoscopic surgical techniques3–10. Ejaculatory duct obstruction (EDO) is rare and is diagnosed in 1–5% of infertile men11. The availability of high-resolution transrectal ultrasonography (TRUS) has led to an increase in the diagnosis of this disorder in men who might or might not be symptomatic4,12–14. In the majority of men, EDO is treated using transurethral resection of the ejaculatory ducts (TURED), and several reports of successful pregnancies following surgery have been published3,5,6,11,15–17. EDO is one of the few surgically correctable causes of male infertility3,6,15 and clinicians should, therefore, consider it in the differential diagnosis of men presenting with nonspecific complaints related to sexual dysfunction such as periejaculatory pain, low-volume ejaculate and haematospermia, all of which can be associated with underlying EDO.
In this Review, we will provide an overview of EDO, its aetiology, presentation, and clinical assessment.
A description of current imaging and diagnostic techniques together with treatment options and outcomes is also considered
Anatomy and embryology
The ejaculatory ducts, seminal vesicles and vas deferens develop from the Wolffian duct system at 8–12 weeks of gestation, in line with the production of testosterone18. The ejaculatory ducts are paired, collagenous, tubular structures that form as a result of the confluence of the seminal vesicles and vas deferens19. They enter the prostate gland obliquely and posterior to the base, and then course medially and anteriorly through the prostatic glandular tissue, eventually opening into the prostatic urethra at the verumontanum as slit-like orifices. The duct is split into three regions: a proximal extraprostatic portion, a middle intraprostatic portion and a short distal segment within
the verumontanum near the urethra20. They are 1–2 cm in length and lined by cuboidal or pseudostratified epithelium; the epithelium of the proximal and distal portions resembles the lining of the seminal vesicles. The prostatic utricle — a remnant of the Müllerian duct — is found between the ostia at the verumontanum and is noncommunicating21. The existence of a valve or sphincter-like mechanism, ‘sphincter spermaticus’ has been postulated at the
junction of the ejaculatory ducts and the urethra, although it is now widely believed that the acute angle of duct insertion acts to preserve ejaculatory continence and prevent urinary reflux (FIG. 1).
Seminal vesicle function
The seminal vesicles are located posterior to the bladder and add an alkaline fluid rich in fructose to the ejaculate. They are approximately 13 cc in volume, 5–6 cm in length and 3–5 cm in width, although their size decreases with age22. Approximately 50–80% of the male ejaculate is produced in the seminal vesicles23.
The mechanism by which the ejaculatory duct is related to the seminal vesicle has been investigated in animal studies by Turek and colleagues24, showing it to be similar to the relationship between the bladder and urethra. More specifically the compliance and contractile properties of the seminal vesicles are akin to those of the bladder. Thus, just as in bladder outlet obstruction at the level of the prostate or urethra, EDO can occur anywhere along the ejaculatory ducts. Obstruction can be limited to the distal ends of the ducts or extend more proximally and include the terminal portions of the vasa deferentia. The site and length of the obstruction has implications with respect to potential options for surgical intervention. Functional or neurological dysfunction of the seminal vesicles can result in functional EDO, similar to voiding dysfunction caused by a
neurogenic bladder9,24
Pathophysiology of EDO
EDO is an uncommon condition that can be caused by congenital or acquired disorders (BOX 1). Acquired EDO is often secondary to seminal vesicle calculi, postinflammatory scar formation at the prostate level, a history of indwelling urethral catheter use, urethral trauma, and previous transurethral surgery, such as bladder-neck incision or transurethral resection of the prostate (TURP)11,25,26. Our clinical experience suggests that minimally invasive prostate cancer treatments using prostate cryotherapy and high-intensity focused ultrasonography (HIFU) are also linked to the development of EDO.
Congenital causes of EDO include congenital atresia or stenosis of the ejaculatory ducts and Müllerian duct (utricular) or Wolffian duct (diverticular) cysts. Prostatic cysts seem to be more common in infertile men than in the general population (FIG. 2); up to 17% of infertile men have been shown to have prostatic cysts, compared with a screening population, in which the prevalence was 5%27.
Midline cysts can be classified into two groups: cysts containing sperm and cysts that do not contain sperm (FIG. 3)16,28–30; however, differentiating these two groups from
each other is often difficult. Cysts that do not contain sperm are called utricle cysts or Müllerian duct cysts (FIG. 4)28,29,31. Utricle cysts are derived from the endoderm germ layer and tend to be found in the midline, close to the verumontanum32, whereas Müllerian duct cysts are mesodermal in origin and are located near the base of the prostate13,14,32. Both types of cyst can directly compress the ejaculatory ducts, resulting in EDO and either azoospermia or severe oligozoospermia, or, in some cases, the ejaculatory ducts open directly into the cyst whereby patients are generally azoospermic with a low volume ejaculate32. Sperm-containing cysts are known as Wolffian cysts, ejaculatory-duct cysts, or diverticula, and are less common than the Müllerian duct cysts13,28,29. These are paramedian cysts, located laterally, close to the midline, and posterior to the prostatic urethra33.
Patients with EDO often have no relevant antecedent history. Authors of several studies have reported that patients with congenital or noninfectious causes of EDO tend to have better outcomes compared with those who have EDO secondary to infection9–11,15,17, although others have refuted this finding34–36. Those patients presenting with idiopathic EDO have a 50% prevalence of cystic fibrosis gene (
CFTR) mutations and patients diagnosed with congenital blockage should be considered for genetic evaluation for
CFTR mutations37. The most frequent
CFTR mutation found in such patients is the
5T polymorphism38
Presentation and evaluation
The diagnosis of EDO requires a high index of suspicion, and early endoscopic treatment can reverse symptoms and also prevent the progression of partial obstruction to bilateral, complete obstruction7,11,39,40. A diagnosis might be established during the course of infertility investigations for azoospermia or severe oligospermia3, or patients might present with symptoms related to periejaculatory pain or a reduction in ejaculatory volume. Excluding ‘seminal vesicle dysfunction’ or functional obstruction — which occurs in patients taking certain pharmacotherapies (BOX 2) and in those with diabetes mellitus41, multiple sclerosis, or spinal cord injury — 42 is also important. Patient concerns that suggest a potential diagnosis of EDO often include infertility3,11, decreased force of ejaculation3,6,10, pain during or after ejaculation11,34, decreased ejaculatory volume34,35, haematospermia (persistent or recurrent)2, perineal or testicular pain related to ejaculation11,35, and/or a history of symptoms suggestive of prostatitis or epididymitis (BOX 3)40,43. Patients might also present with more generalized symptoms, such as lower back pain, dysuria, or chronic scrotal pain11,40,43.
In patients who are found to have partial EDO, the preceding symptoms are typically less pronounced or even absent.

However, partial obstruction can progress to complete obstruction5–7; thus, no single symptom or constellation of symptoms can specifically point to a diagnosis of EDO. Furthermore, patients with EDO can have normal examination findings in the genitalia and normal secondary sexual characteristics. Chronic obstruction is, however, associated with marked dilatation of the epididymal heads and dilatation of the vasa deferentia, which can also be unilateral. The seminal
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vesicles might be palpable on digital rectal examination, and prostatic or epididymal tenderness might be elicited, although these are not frequent findings3,6,34,35,44.

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Semen analysis
Often the semen analysis is the only test that produces abnormal results in patients with EDO. Semen analysis is primarily performed in patients presenting with infertility, although semen analysis should also be performed in men in whom a high index of clinical suspicion of EDO exists (TABLE 1): a low volume ejaculate of <1 ml (normal >1.5 ml), semen pH <7.2 and an absence of fructose in the seminal fluid should alert the clinician to a diagnosis of either EDO or congenital bilateral absence of vasa deferentia (CBAVD)45. Men with partial EDO can have severe oligospermia or azoospermia, decreased motility and decreased ejaculatory volume, whereas in men with unilateral or partial EDO, the semen analysis results can approach normal parameters or show variable sperm concentrations, although the sperm motility might
remain low5,7,35. Pryor and Hendry11 suggested that a small volume of acidic semen and absence of fructose in a patient with palpable vasa deferentia is pathognomonic for EDO, a hypothesis with which our clinical observations are in accordance. The presence of these semen analysis findings along with a positive clinical history warrants
further investigation for EDO.
Imaging in EDO
TRUS using a 7 MHz probe is often the only imaging modality required for an imaging-based diagnosis of EDO12. Historically, vasography was the gold standard for diagnosing proximal and distal EDO; however, the invasive nature and associated high risk of iatrogenic strictures and vasal occlusion has led to TRUS becoming the standard imaging modality12,46. TRUS findings in men with EDO include the presence of midline cysts, dilated seminal vesicles or ejaculatory ducts, hyperechoic regions suggestive of calculi, absence of the vas, intraprostatic Müllerian duct remnants, and cysts along the ducts themselves, each of which are highly suggestive of EDO in an infertile man with oligospermia or azoospermia and low semen volume47,48. TRUS is integral to diagnosing EDO — a seminal vesicle width >1.5 cm or ejaculatory duct >2.3 cm on TRUS, particularly in the presence of a cyst or calcification along the duct, helps confirm the diagnosis (FIG. 2)13.
However, the use of TRUS has several drawbacks. As a static study that provides only anatomical detail, TRUS is not, therefore, able to provide functional information relating to the emptying of the seminal vesicles49. Furthermore, some patients with EDO have normal TRUS findings13. Where TRUS findings have been equivocal, T2‑weighted MRI with an endorectal coil can enable excellent tissue resolution with multiplanar capabilities and the ability to detect small obstructing cysts50.
It should be noted that EDO is not always associated with seminal vesicle dilation: and, conversely, normally fertile men can at times have dilated seminal vesicles, depending
on the duration of sexual abstinence51. Thus, the observation of dilated seminal vesicles is a sensitive, but not specific, sign of EDO52. Neither MRI nor TRUS provide sufficient resolution to observe the status of the ejaculatory ducts directly, and both are unable to distinguish between functional and physical EDO. Making treatment decisions based solely on either the MRI or TRUS findings, could, therefore, lead to unnecessary surgical procedures. The use of TRUS alone leads to a false-positive diagnosis of EDO (with no clinical benefit) in up to 50% of patients, highlighting it as a sensitive imaging technique for EDO, but one which lacks specificity49. The clinician must be aware that anatomical imaging such as TRUS alone is unsatisfactory for diagnosing all the forms of EDO that might be presented.
Seminal vesicle aspiration
TRUS-guided seminal vesicle aspiration can be useful in diagnosing partial EDO, based on the presence of motile sperm in the aspirate53. The finding of >3 sperm per high-powered microscopic field (400×) in the aspirate is considered positive and suggestive of obstruction54. For accuracy, the procedure should be carried out within 24 h of ejaculation. Although the technique does not offer anatomical information regarding the site of the blockage, it confirms that spermatogenesis is ongoing54. Engin
et al.55 carried out a retrospective case controlled study that compared TRUS-guided seminal vesicle aspiration to TRUS alone in 70 patients in an attempt to diagnose EDO55. 78.6% of patients were found to have evidence of EDO on diagnostic TRUS; however, obstruction on TRUS was confirmed in just 49.1% of patients using seminal vesicle aspiration, leading the team to conclude that TRUS alone was not a reliable tool for diagnosing EDO55. TRUS-guided seminal vesicle aspiration can also be used to collect sperm for assisted reproduction techniques in men with EDO56.
Seminal vesiculography
Seminal vesiculography uses a combination of TRUS-guided injection of a nonionic contrast agent and fluoroscopy to provide detailed dynamic and anatomical information related to the ejaculatory ducts. Ejaculatory duct patency is confirmed by the presence of contrast within the urethra on fluoroscopy or visualization of methylene-blue-impregnated contrast in the urethra on cystoscopic examination. Seminal vesiculography also provides a retrograde vasogram in approximately two‑thirds of patients, confirming patency of the vas57.
Seminal vesicle chromotubation
Antegrade injection of indigo carmine or methylene blue into each seminal vesicle under TRUS guidance can confirm patency of the ejaculatory ducts. Cystourethroscopy concurrently with antegrade injection is then used to assess whether there is antegrade flow of methylene blue from the seminal vesicle into the prostatic urethra49.
Which is the optimal diagnostic test?
Although a number of investigations are available to evaluate EDO, the relative sensitivity of these diagnostic tests is unclear. A prospective study by Purohit
et al.49 evaluating all the techniques of TRUS, chromotubation, seminal vesiculography and seminal vesicle aspiration, used the measure of which investigation best predicts a successful outcome after ejaculatory duct resection as their definition of accuracy of the technique. The study included 25 patients with EDO, and men with suspected EDO based on clinical evaluation and TRUS findings underwent further evaluation with intraoperative duct chromotubation, seminal vesiculography, and seminal vesicle aspiration. Obstruction diagnosed using TRUS was confirmed in 52%, 36%, and 48% of chromotubation, vesiculography and aspiration studies, respectively, and the study authors concluded that patency on chromotubation — defined by the presence of dye egressing from the ejaculatory duct orifices after seminal vesicle injection — was the most accurate way to diagnose complete or partial EDO49.
Treatment of EDO
In recent years, TRUS has replaced vasography as the primary diagnostic investigation for suspected EDO, which has improved the ability of urologists to diagnose EDO and to commence therapy. Indications for beginning treatment of EDO include infertility owing to obstructive azoospermia or severe oligozoospermia, recurrent haematospermia, and/or periejaculatory pain. Discontinuation of any medications that could be causing physiological EDO (BOX 2) should occur before endoscopic resection is performed. The majority of patients with a diagnosis of EDO confirmed on seminal vesiculography or chromotubation can be considered for TURED. Alternative treatment options include endoscopic laser-assisted resection of the ducts58 or the use of antegrade seminal-vesicle lavage to relieve EDO secondary to inspissated material or calculi59. Dilatation of the ejaculatory ducts using 9F seminal vesicoscopy or balloon has also been described49,60.
TURED
TURED — initially described in 1973 by Farley and Barnes for the treatment of ejaculatory duct stenosis — remains the mainstay of treatment for EDO (FIG. 5)43. The procedure can be performed under general or regional anaesthesia, and the standard surgical setup is as for transurethral resection of the prostate (TURP), with the added use of an O’Conor drape to aid the palpation and expression of the seminal vesicles. TURED is performed using cystourethrosocopy to inspect the verumontanum, urethral sphincter, and the position of the bladder neck34. Careful inspection for midline cysts, splaying of the ejaculatory ducts, bulbous or bilobed verumontana, and inflammatory calcifications is conducted. Resection using either a paediatric resectoscope (which has a smaller resection loop) or conventional resectoscope near the verumontanum in the midline (for complete obstruction), or laterally (hemiTURED for unilateral obstruction) is carried out with pure cutting current in order to minimize further cauterisation of the
ejaculatory ducts which can cause restenosis (FIG. 2). The level of resection is guided by synchronous TRUS, particularly when the obstruction is in the proximal ducts, in order to avoid inadvertent injury to the rectum — the surgeon must always be vigilant of potential injuries to the rectum, bladder neck, and external urethral sphincter. HemiTURED can be used to spare resection of the entire verumontanum in patients with partial EDO. At the correct level of resection, cloudy, milky fluid is usually seen flowing from the opened ducts (FIG. 6).
Patients will typically require urinary catheterisation for 24 h postoperatively. After the TURED procedure, ejaculation can resume after 7–10 days. A formal semen analysis can be carried out as early as 2 weeks after TURED, and then repeated at regular intervals thereafter until the semen parameters stabilize61.
Outcomes following TURED. Patients reporting periejaculatory pain secondary to EDO often have relief of symptoms following the TURED procedure. Findings of a cohort study of patients with obstructive azoospermia carried out by Popken
et al.62 showed that TURED eliminated painful ejaculation and haematospermia associated with EDO in all patients. A similar study by Weintraub
et al.6 using TURED as the preferred treatment method for patients with radiologically proven EDO also demonstrated the resolution of periejaculatory pain as well as haematospermia and perineal and/or testicular pain in the majority of patients. Long-term relief of postcoital or perineal pain after TURED can be expected in 60% of patients43,49. Yurdakul
et al.63 showed a 100% response rate in achieving normal ejaculatory volumes following TURED in their retrospective review of 12 azoospermic men with complete EDO. Haematospermia has also been shown to be reduced, although the literature regarding this symptom remains wholly anecdotal. Smith
et al.50 showed in their decade-long series that men treated for low-volume azoospermia or low-volume oligoasthenospermia were equally likely (65–70%) to have improvements in semen quality after TURED.
One study has shown that the underlying aetiology of EDO is a significant factor in the likelihood of successful resolution of symptoms following TURED. The authors reported that patients with congenital EDO had superb treatment success rates, with 100% improvement in semen parameters (motility and volume), 83% improvement in sperm count and a 66% successful conception rate. By contrast, patients who had acquired EDO experienced only a 37.5% improvement in their semen parameters and only 12.5% of them were able to conceive64. In a smaller series of 16 patients, EDO due to cysts seemed to respond better to TURED than obstruction due to calcification17. The same study also highlighted that patients with partial EDO responded better to TURED (94% of patients demonstrated improvement) compared to men with complete EDO (59% of patients demonstrated improvement) on postoperative semen analysis17.
Complications. Complications after TURED occur in approximately 13–26% of patients (TABLE 2)11,17,65. In the immediate postoperative period, patients can develop acute epididymoorchitis65 or frank haematuria3. The incidence of these immediate complications tends to be low. In one study of 24 patients treated for EDO with TURED,
two patients developed frank haematuria required repeat catheterisation3. Another retrospective study of 23 patients described two patients who developed postoperative epididymoorchitis65. Early-to-late complications are less frequent. Acute urinary retention can occur after catheter removal, particularly in patients with prior voiding dysfunction. Catheter reinsertion for 24–48 h is often all that is required34. Urinary reflux into the vasa deferentia, seminal vesiculitis and urinary incontinence can result from resection too distally causing damage to the external sphincter44. Erectile dysfunction and rectal perforation are rare66,67. The treating clinician should be aware of the possibility of complications in the early postoperative period, but keep in mind that many can be self-limiting.
Patients should be counselled regarding the possible outcomes of TURED. Approximately 10–15% of patients undergoing TURED for low-volume azoospermia convert to normal-volume azoospermia60; this change is usually indicative of more proximal obstruction at the level of the epididymis, and might be amenable to treatment using epididymovasostomy50. Around 4% of patients treated with TURED for partial EDO become azoospermic, probably secondary to postoperative fibrosis of the ejaculatory ducts60. Thus, men who are oligozoospermic owing to partial EDO should, in our opinion, be offered preoperative sperm cryopreservation. We suggest that men who are not willing to accept the potential risks of the procedure, or those in whom TURED is not possible, should be considered for surgical sperm extraction in order to obtain sperm for assisted reproduction using intracytoplasmic sperm injection (ICSI).
Conclusions
EDO is a rare cause of infertility, although, as a surgically reversible cause of obstructive azoospermia, a correct diagnosis is important. EDO is responsible for azoospermia in a small percentage of infertile males, but can be associated with other symptomatology. Patients with EDO can present with sexual dysfunction resulting in functional, as well as physical, obstruction.
Detection of complete EDO requires correct interpretation of semen analysis and the use of high-resolution TRUS. However, in cases of partial obstruction or functional obstruction, the results of these investigations are rarely diagnostic. Although a valuable technique, TRUS is sensitive but not specific for EDO and should not be used in isolation. TRUS features such as dilated seminal vesicles, calcifications, or cysts along the ducts themselves are highly suggestive of EDO in an infertile man with oligospermia or azoospermia and low semen volume47,48. The use of additional diagnostic modalities such as chromotubation, seminal vesiculography, vasography and seminal-vesicle aspiration should all be considered, as they increase the specificity of the diagnosis and identify more accurately those patients benefiting from surgical treatment.
In selected patients, TURED can result in marked improvements in semen parameters and subsequent successful conception rates, and offers a safe and minimally invasive technique to resolve EDO. As with all surgical cases, careful patient selection, adequate patient counselling and the surgeon’s operative experience are essential for optimal results. Patients should be made aware of the extended follow-up periods required to assess the long-term effects of the procedure. In those patients with evidence of concomitant testicular dysfunction, chances of success are minimal; in these men, overall spontaneous conception rates are low (20–30%) and patients should be informed of the potential poor outcomes before the procedure, in order to ensure realistic patient expectations49. With this in mind clinicians should always keep a high index of suspicion for EDO when presented with patients suffering from male factor infertility.
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