Chapter 10:

Ejaculatory Duct Obstruction: Diagnosis and Treatment

Bruce R. Gilbert, M.D.,Ph.D.
Clinical Assistant Professor of Surgery (Urology)
edited by Marc Goldstein,M.D.

Until recently, relatively few surgical options have existed for the man with an impaired semen quality. Varicoceles have been and remain the most common surgically treatable condition associated with male subfertility. Technical advances have markedly improved the prognosis for men with obstructive azoospermia (1). Historically, men with azoospermia or severely oligospermia have been successfully treated with transurethral resection of a portion of the prostate. However, this has required a formal microsurgical vasotomy and vasogram to identify obstruction of the ejaculatory ducts (2)(3)(4)(5)(6)(7)(8)(9)(10)(11). In addition, men presenting with a severely impaired semen quality, a markedly decreased number of forwardly progressive spermatozoa, pyospermia or hematospermia have had only expectant therapy. With the widespread use of transrectal ultrasonography many cases of partial genital duct obstruction have been identified [Pryor, 1991 #16](12)(13). This has made the previously rare finding of obstruction of the ejaculatory duct a much more common and treatable cause of male factor subfertility. In addition, 'partial' ductal obstruction can be identified and treated.
This chapter will discuss the diagnosis and treatment of ejaculatory duct obstruction. A particular emphasis on the diagnostic modalities will be made since identification of the pathology is as important as the skill of the surgeon in its repair.

Diagnostic Techniques
Clinical History and Physical Examination

The history and physical examination of the infertile man should include factors associated with obstruction of the ejaculatory ducts. These include a decline in ejaculatory volume, a history of genitourinary tract infection or injury as well as perineal pain or discomfort. Use of a questionnaire facilitates the accumulation of necessary information in an expeditious manner. The questionnaire that we use has been previously published(14). The history should initially include classification of the prior fertility of the man. Has he previously contributed to a pregnancy in this partner or a previous partner? If this is true, then information regarding any infections or traumatic injuries should be obtained. After delineation of primary or secondary infertility for the man, a careful sexual history should be obtained. This not only directs the physical examination but also yields insight as to the couples timing of relations. The couple needs to have an understanding of the menstrual cycle and the importance of the appropriate frequency of intercourse, without use of anti-sperm agents such as lubricants and avoidance of douching after intercourse. Brief assessment of the infertility evaluation of the female partner should be obtained so that inappropriate intervention is not entertained for the man when fertility is not possible for the women (e.g., ovulatory failure).

A history directed toward the general physical health and hormonal status of the man should also be performed with specific attention to factors that impair male fertility potential. Childhood illnesses associated with infertility include cryptorchidism and postpubertal mumps orchitis. The timing of pubertal landmarks and characteristics of secondary sexual development should be noted (onset of axillary & pubic hair, start of shaving, density of beard relative to male siblings). Operative intervention on the bladder neck (including Y-V plasty for UTI or vesicoureteral reflux) may be associated with retrograde ejaculation. Retroperitoneal Iymph node dissection for testis tumor and other retroperitoneal surgery may disrupt sympathetic pathways necessary for emission and antegrade ejaculation.

Medical conditions such as diabetes or medications taken for diseases such as hypertension may affect ejaculation. The neuropathy associated with diabetes can affect bladder neck closure and antegrade ejaculation. Sympathomimetic drugs or electroejaculation may be used for treatment of these patients.

Prescription as well as "recreational" drugs may also impair ejaculatory function (15)(16) (TABLE 1). A detailed history of all medications is needed to assess their potential effect on ejaculatory function as well as fertility. Medications that interfere with preganglionic and postganglionic autonomic function have the potential to interfere with both emission and ejaculation. Male sexual function has been associated with almost every antihypertensive agent available. The alpha-adrenergic blocking agents phenoxybenzamine and phentolamine are common causes of ejaculatory inhibition (17),(15). This effect was found by Kedia and Persky (18) o be due to absent seminal emission and not retrograde ejaculation.

Use of many psychotropic agents, like the antihypertensives, have been reported to causes ejaculatory dysfunction. The major tranquilizers Thioridazine (Mellaril), Chlorpromazine (Thorazine) and Mesoridazine (Serentil) have all been reported to inhibit or reduce ejaculation. Thioridazine in particular inhibits ejaculation in up to 49% of men using this medication(18). This effect of Thioridazine is likely due to its significant peripheral alpha-adrenergic blocking action. The antidepressants (both tricyclic antidepressants and monamine oxidase inhibitors) have both peripheral and central effects (17). The minor tranquilizers (including the benzodiazepines) have been implicated in ejaculatory dysfunction (19) although the mechanism is not well defined (17).

Blood alcohol level is associated with a decreased arousal and an increased ejaculatory latency (20). Prolonged use of both cocaine and amphetamines has been reported to cause a decreased libido and ejaculatory difficulty(17). Androgenic drugs, such as anabolic steroids, can inhibit function of the hypothalamic-pituitary-testicular axis, leading to hypogonadism as well as possible alterations in seminal vesicle fluid volume.

The physical examination of the infertile man should be complete and thorough, since any significant medical condition may adversely affect testicular function. A warm room is critical to allow adequate relaxation of the scrotum to facilitate examination of the scrotal contents. A global assessment of androgen action should initially be performed. Temporal balding requires DHT action. Normal axillary and pubic hair distribution are related to androgen action. Gynecomastia results from excessive estrogen action or an imbalance between androgens and estrogens. The general appearance of men with recognized syndromes (e.g., Kallmann's syndrome: anosmia, lack of sexual secondary characteristics, long arms, short 4th metacarpals, etc.) should be considered, although a definitive diagnosis of idiopathic hypogonadotropic hypogonadism requires serum hormone evaluation.

Specific attention to the genitourinary examination is necessary. The penis should be evaluated for lesions, curvature and Peyronie's plaques. Location of the urethral meatus should be noted, and assessed relative to the ability of the patient to place the ejaculate deep within the vagina during intercourse for hypospadiac men. The abdomen should be palpated for abdominal masses and the inguinal regions closely inspected for scars.

The scrotal exam is most easily performed in a warm room. Scrotal evaluation should asses the spermatogenic potential of the testes and the presence of potentially obstructing lesions. Initially the patient is examined supine. The consistency of the testis can be best evaluated in this position, including the presence of any testicular masses. Testicular examination should carefully assess the volume and consistency of the testis which directly correlates to the spermatogenic potential of the testis. Induration of the epididymis may be associated with inflammation and epididymal obstruction. Post-epididymal obstruction of the reproductive tract may result in fullness" of the epididymis. If clinically indicated a scrotal ultrasound should be performed to define the intratesticular and peri-testicular structures.

The presence of vasa deferentia bilaterally should be confirmed by palpation. Vascular engorgement of the spermatic cords should be assessed and the size of varicoceles recorded. Large bilateral varicoceles or a varicocele that does not decompress with the patient supine may suggest a fixed obstruction in the retroperitoneum and should be further evaluated with ultrasonography and possibly computed tomography of the abdomen. Hernias in the inguinal region should also be assessed. Rectal examination should be performed to assess for prostatic irregularities, bogginess or tenderness. When indicated (see below) a transrectal ultrasound examination should be performed to evaluate the prostate, seminal vesicles and ejaculatory ducts. Routine digital rectal assessment for masses as well as guaiac testing of stool from the examining glove is also performed.

Laboratory Evaluation

Urinalysis can detect urinary tract infections, retrograde ejaculation and medical renal disease all of which can be related to an impaired ejaculatory or semen quality. The urinalysis should include a dip stick analysis of leukocytes, pH, protein, glucose, ketones, blood and hemoglobin. I routinely obtain a post ejaculate urine (PEU) after a semen specimen is given. The entire contents of the bladder should be evacuated, the volume measured and concentrated if too large a volume is obtained. The total number of sperm in the specimen is determined. The spun specimen should be evaluated microscopically (preferably by phase contrast microscopy) and the number of sperm, round cells, bacteria and crystals quantified. Chlamydia is a common pathogen that impairs both female and male fertility. Simplified kits for evaluation of Chlamydia in a voided urine specimen (Kodak SureCell) are readily available and easily incorporated into the routine evaluation.

Semen analysis

Semen analysis is usually the first test performed in male factor evaluation. There are many excellent reviews that detail the procedure(21),(22),(23). There are factors to consider in evaluation of partial or complete obstruction of the male genital ductal system. (1) Multiple analyses separated by 3-4 week intervals are needed to document volume and/or motility. (2) It is important to provide patients with clearly written instructions on how to produce a specimen and as to the type of container to use. Routinely we ask for 48-72 hours of abstinence. When the specimen is received in the laboratory it is placed in an incubator at 370C. We note the time of collection, the time that we evaluate it and whether it is a complete sample or whether some loss occurred during collection. We also ask for a post-ejaculate urine to be given at this time. In men with a low volume specimen a post-ejaculate urine is essential to eliminate retrograde ejaculation as the etiology. The physical characteristics such as liquefaction, viscosity, volume, color and pH are noted and recorded. A microscopic examination is then performed. The parameters recorded are concentration, total sperm count, motility and forward progression and morphology. If no sperm are seen, and/or the volume is less than 1.5 cc, a fructose test should be done to confirm the presence of seminal vesicle fluid, as well as a post ejaculate urine, to rule out retrograde ejaculation. If motility is less than 50% a viability stain is done using Eosin Y with Nigrosin as a counterstain. Greater then 50% of the sperm should be viable (i.e., non-stained). Morphology is the most subjective parameter measured in the semen analysis. The two standard atlases are the WHO laboratory manual (21) and the Atlas of Human Sperm Morphology (22).

Hormonal evaluation

An appropriate hormonal milieu must exist for the reproductive organs to produce, mature and transport the highly specialized male gamete to the ejaculatory duct. Our routine blood studies include testosterone, FSH, LH, prolactin and estradiol. FSH is usually elevated when seminiferous tubular function is impaired. However, the secretory functions of the prostate and seminal vesicles is regulated primarily by androgens (24). Testosterone production by the Leydig cell provides locally high intratesticular concentrations of this hormone that stimulates spermatogenesis. However, it is the circulating levels of androgens that are important in seminal vesicle and prostatic secretions. Testosterone concentrations in peripheral blood of men change dramatically during man's aging. Testosterone reaches a maximum concentration during the second or third decade of life, then reaches a plateau, and declines thereafter. Additionally, annual and daily rhythms in testosterone concentration occur, typically with a testosterone peak in the early morning. Other, irregular fluctuations in testosterone concentration may also be detectable in peripheral blood. Within 2 - 14 days following castration seminal plasma production ceases resulting from a de-activation of both RNA and protein synthesis (25). Therefore, LH, prolactin and estradiol, all of which might have an effect of androgen function need to be evaluated.

Transrectal Ultrasound Evaluation
The use of high resolution and high frequency (5-7 MHz) transducers has allowed superb imaging of the prostate, seminal vesicles and ejaculatory ducts. Vasography (chapter ) is presently the gold standard. However, vasography requires a microsurgical procedure and carries the risk of scarring of the vas deferens. Transrectal ultrasound (TRUS) on the other hand, is a relatively non invasive technique that offers superb resolution of the prostate seminal vesicles and ampulla of the vas deferens and is a technique well known to most Urologists. It is also less costly than either CT scan or MRI and therefore is more cost effective in following resolution of a pathologic lesion after medical or surgical intervention. In evaluating the subfertile male TRUS has become increasingly important (26),(27),(28),(29). Meacham et al (13) have used TRUS for evaluation of men with low ejaculate volumes (1.5 cc). reduced sperm density and/or motility with FSH levels that were not greater than three times normal. Indications for TRUS in evaluating the subfertile male include:
1) Azoospermia
2) Abnormal digital rectal examination
3) Retrograde ejaculation
4) Suspicion of partial obstruction

( volume 1.5cc, motility 20% or a forward progression 2)
5) Hematospermia or Pyospermia
6) History of rectal injury, pelvic fracture or genital trauma

In the azoospermic patient, seminal vesicle and ejaculatory duct obstruction can be documented. Formally, only vasography was able to delineate ductal obstruction. However, the advent of high resolution ultrasonography using transrectal solid state probes has made the TRUS exam one of the first tests to be done in the evaluation of the azoospermic male. The presence of seminal vesicle dilation (presently defined as a seminal vesicle cross-sectional width greater than 1.5cm (12), ejaculatory duct obstruction (defined as an internal ductal diameter of greater than 0.2mm) with or without a calcification is diagnostic. The echo texture of the seminal vesicles is also suggestive of altered function. When the normal homogenous appearance of the seminal vesicle is replaced by a heterogenous appearance with hypoechoic regions and dilation (Figure 1), careful inspection of the ejaculatory ducts and prostate might uncover an obstructive lesion (Figure 1). In addition, the diagnosis of agenesis of the distal portions of the vas deferens can be suspected by absence or atresia of the ampulla of the vas deferens. Agenesis of the vas deferens is often associated with abnormalities of the seminal vesicles.

An abnormal digital rectal examination in the subfertile man also needs to be examined by TRUS. Chronic prostatitis, utricular or ejaculatory duct cysts or other mass lesions can be suspected by palpation but can be identified by TRUS (Figure 1). The ability to confirm our suspicions by TRUS has allowed us to make a diagnosis and formulate a treatment plan. This has often eliminated the need to perform a formal microsurgical vasotomy and vasogram.

Occasionally , in patients with retrograde ejaculation anatomic abnormalities might exist. These often can be diagnosed by transrectal ultrasonography (Figure 2). In many of these anomalies the ejaculatory ducts and seminal vesicles can be found to enter intravesically or at the bladder neck . Thus treatment with sympathomimetics would not be expected to be effective.

In the patient with a low volume ejaculate ( 1.5cc), poor motility (20%) and/or poor forward progression (2) a partial obstruction of the ejaculatory duct is suspected. These are important indications for transrectal ultrasonography in the subfertile male. Prostatic calcifications (Figure 3), cystic masses (Figure 4) and inflammatory lesions all can obstruct the transit of seminal plasma and spermatozoa and can readily be identified by TRUS. Resolution of the lesion and the effectiveness of treatment can be evaluated post operatively.

The presence of hematospermia and/or pyospermia have long eluded diagnostic evaluation. In male factor subfertility, clinical and subclinical infections of the male genitourinary tract are routinely evaluated by seminal fluid and urine cultures when indicated. When pyospermia or hematospermia is found in evaluation of the subfertile male with an impaired semen profile, TRUS should performed to identify correctable lesions. These included obstruction of the ejaculatory duct or seminal vesicles as well as prostatic or ejaculatory duct calcifications (Figure 1) .

Medical Therapy

The diagnosis of an anatomic obstruction is paramount since surgical intervention is not initial therapy for functional obstructions (i.e., the absence of an anatomic obstruction) of the ejaculatory ducts. The most common functional obstructions seen in male factor subfertility are retrograde ejaculation and anejaculation either secondary to diabetes or surgical intervention (e.g., retroperitoneal lymph node dissection). Treatment of retrograde ejaculation usually begins with a trial of a medication containing alpha-sympathomimetic properties (Table 2)(30),(31),(32). If medical therapy fails to produce an antegrade ejaculate then retrieving sperm from the post ejaculate urine after systemic alkalinization, followed by sperm processing and intrauterine insemination(33)(34) ,has been used with good results . Electroejaculation is often successful in patients with anejaculation after retroperitoneal lymph node dissection(35),(36),(37). Surgical therapy for functional obstruction usually consists of aspiration of epididymal or vasal sperm with assisted reproductive technology incorporating microinsemination.

Surgical Therapy
The ejaculatory ducts are paired structures approximately 2 cm in length. They are formed by the union of the medially positioned ampulla of the vas deferens and the laterally placed duct of the seminal vesicle (Figure 5). These ducts extend from the base of the prostate and run within the central zone of the prostate(38),(39) in an antero-inferior direction (Color Plate). They terminate just within or lateral to the prostatic utricle. The thin wall of the ejaculatory duct is composed of three layers (40): (1) the outer fibrous layer disappears as the ejaculatory ducts enter the prostate, (2) an inner layer of muscular fibers consisting of a thin outer circular layer and an inner longitudinal layer and (3) a mucus membrane covered with columnar epithelium. The proximity of the ducts to each other together with their thin walls is the reason why bilateral obstruction might result from a single local lesion. The physiology of the ejaculatory ducts is not well defined. It is thought that the basal tones tends to keep the walls of the ejaculatory duct coapted. Thus imaging of the long axis of normal ejaculatory duct yields two slightly echogenic lines (representing the muscular layer) separated by no more than a 2 mm hypoechoic line (representing the epithelial layer) (Figure 6,7)(41).

The goal of surgical therapy is to eliminate the obstruction while minimizing complications
(e.g., ductal scarring, bladder neck injury, rectal injury). Classically, treatment of ejaculatory duct obstruction was only suspected prior to surgery. Therefore, the protocol that was followed in the operating room, was to first localize the obstruction by vasotomy and vasography. Cannulation of the of the distal (abdominal) end of the vas deferens together with vasal injection of a dye (indigo carmine or methylene blue) then allowed visual confirmation of patency of the ejaculatory duct during resection. Intraoperative vasography prior to resection documents the obstruction while intraoperative dye injection confirms patency. This approach often requires repositioning of the patient from a supine position needed for microsurgical vasotomy and cannulation of the ductus deferens to the dorsal lithotomy position necessary for transurethral resection.
Recently, the availability and experience with transrectal ultrasonography has changed this classic approach. With transrectal ultrasonography seminal vesicle obstruction or seminal vesicle cysts (Figure 8), ejaculatory duct obstruction, cysts or calculi (Figure 9) and utricular cysts (Figure 10) can be defined both preoperatively and intraoperatively. Intraoperative sonography allows confirmation as to the depth of the resection and elimination of the obstructing pathology. It does not however, document elimination of the obstruction as does visualization of dye emanating from the ejaculatory duct after resection of the obstruction. Operative vasography is still required when obstruction cannot be documented preoperatively by transrectal ultrasonography. In addition, failure of transurethral resection might be due to inadequate resection, a secondary epididymal obstruction, testicular failure or a functional obstruction. Therefore, in men with azoospermia and/or severe oligozoospermia a testicular biopsy is done to document spermatogenesis prior to transurethral resection. A 'wet prep' can be done at the time of transurethral resection to document the presence of mature spermatozoa. Several types of 'wet prep' have been described ((42),(43),(44),(45). My preference is that prescribed by Jow et al (42). In this technique after a portion of testicular parenchyma is sent in Bouins' solution for formal pathologic evaluation a second portion of testicular parenchyma is placed on a glass slide. A drop of lactated Ringers is placed on top together with a cover slip. The margins of the compressed tissue specimen is then viewed immediately under phase contrast microscopy. The presence of spermatozoa with tails confirms spermatogenesis. The presence of motile sperm suggests obstruction of the ductal system (42).

Operative Technique
Transurethral Incision (TUI) and transurethral resection (TUR) are the primary surgical techniques used to treat these obstructions. TUI is used primarily for incising short strictures of the ejaculatory ducts and for the initial opening (prior to TUR) of ejaculatory ducts visualized by a dye vasogram. For lesions easily visualized by TRUS, I routinely use intraoperative transrectal ultrasonography in lieu of a formal vasotomy and vasogram In addition, all cystoscopic procedures are performed under video guidance. If a biopsy had not been done previously a bilateral testicular biopsy is done and placed in Bouin's solution for formal sections.
With the patient in a dorsal lithotomy position cystourethroscopy is performed. Particular emphasis is given to the region just lateral to the verumontanum. It often is here that one can visualize the opening to at least one ejaculatory duct. Particularly in cases of secondary subfertility following a prostatic infection the ejaculatory duct will be blocked proximal to these openings. A resectoscope with a 24f loop is used. The lesion is localized by TRUS (Figure 11A) while the resectoscope is in place. This allows for measurement of the depth of resection necessary. By simultaneous observation of both the video monitor for cytoscopy and the TRUS monitor, the length, depth and location of the lesion is determined. Resection is then done with a pure cutting current (to prevent injury to the ejaculatory duct). The removal of the lesion (or opening of the cyst) is confirmed both by TRUS and by video documentation (Figure 11B). Resection usually involves removal of the verumontanum and occasionally requires relatively deep resection in a small gland (Figure 12). This is often unnerving to the most seasoned resectionist. Intraoperative TRUS is invaluable in making this a safe and effective procedure. In addition, external sphincter injury is avoided by keeping the tip of the resectoscope at the level of the external sphincter and advancing the resectoscope loop from this anchored position. Large bleeding vessels are fulgurated with great care being taken to identify the ejaculatory ducts (and to keep clear of them) during fulguration. The patient is discharged to home the day of the procedure usually with an indwelling catheter for 24 to 48 hours. He is placed on an oral quinolone antibiotic and begun on a non-steroidal anti-inflammatory agent 24 hours after the procedure.
Patients are followed with semen analyses monthly. Improvement in seminal fluid volume is seen by the first month. Oftentimes improvement in semen quality (count, motility and morphology) will require 3 to 6 months. As mentioned previously, failure of transurethral resection might be due to inadequate resection, a secondary epididymal obstruction, testicular failure or a functional obstruction. If the seminal fluid volume improves with little or no improvement in semen quality and the biopsy suggests good spermatogenesis (better than 20 mature spermatids per seminiferous tubule with a minimum of ten tubules counted per testis (46)) then a secondary obstruction probably at the level of the epididymis is likely and repair indicated.


The potential for complications exists with all transurethral procedures (47), (48). Injury can occur not only to the urinary tract but also to adjacent organ systems. Most often treatment of ejaculatory duct obstruction requires only limited resection. However, the small size of the glands in these young patients and/ or the need for deeper resection might predispose these men to complications.

Impairment of semen quality

Patients should always be informed that worsening of semen quality is possible after surgical resection. Scarring and possible recurrent obstruction of the ejaculatory ducts is possible post operatively. This can be minimized by limiting fulguration of bleeding sites near the ejaculatory ducts and ensuring a widely patent and obliquely transected duct prior to completion of the procedure. In addition, a secondary obstruction at the level of the epididymis is common. Bilateral testis biopsy either prior to, or at the time of resection, will help identify a secondary epididymal obstruction.

Retrograde ejaculation

Occasionally extensive resection is required to uncover ejaculatory ducts obstructed proximal to their course through the central zone (Color Plate). In these cases resection at the level of the bladder neck may be necessary, possibly resulting in retrograde ejaculation. Post operatively, if the post ejaculate urine has a significant amount of sperm, medical therapy may be attempted (see above). If retrograde ejaculation persists, then recovery of sperm from the post ejaculate urine after systemic alkalinization or instillation of a buffer is usually successful.

Anatomic Abnormalities

Phimosis, meatal stenosis and urethral stricture may be present prior to transurethral surgery or occur after the procedure. Dilation with urethral sounds prior to introduction of the resectoscope may not adequately dilate the urethral passage. In the case of phimosis a circumcision (or a limited dorsal slit) might be required. Urethral strictures might require an internal urethrotomy or urethrostomy to allow passage of the resectoscope. These anatomic abnormalities are usually known pre-operatively and planned for at the time of the procedure. Injury to the urethra might also occur as a result of the surgery. These complications are usually avoided by proper technique and use of the smallest size sheath possible (24 Fr).

Post operative bleeding
Bleeding in the post operative period can be minimized by meticulous intraoperative hemostasis. However, as mentioned above this is occasionally counterproductive and might result in re scarring of the ducts. An indwelling catheter left for one to two day postoperatively will usually limit this residual postoperative bleeding. The patient is usually discharged to home with the indwelling catheter and placed on an oral broad spectrum antibiotic.

Injury due to transurethral resection
Rectal injury, sphincteric injury resulting in incontinence, urethral injury, bladder neck contracture and erectile dysfunction including corporal fibrosis have all been described after transurethral resections (47), (48). The incidence of these complications after transurethral resection of ejaculatory duct obstruction will only be known after a large series of patients undergoing this procedure are evaluated. The limited resection necessary for correction of the obstructed ejaculatory duct together with the use of intraoperative transrectal ultrasound scanning for localization of the lesion and identification of the depth of the resection, likely limits the occurrence of these injuries. However, the patient should be informed pre operatively that these are possible complications of this surgery.


Interpretation of data from prior studies has been difficult due to the limited number of cases reported upon. In case reports limited to single case presentations (2)(3)(11) all have documented and improvement in semen quality and pregnancy. Two of these men had been treated by transurethral resection (2)(3) and one by urethrotome (11). While reports that have had series ranging from 2 to 9 patients (4)(5)(6)(49)(8)(9) , improvement in semen quality occurred in 41% of patients while pregnancy occurred in 21% of men treated for their partial obstruction with transurethral resection.

In the largest series to date, Meacham et al (13) recently reported on 22 subfertile male patients with various abnormalities noted on transrectal ultrasound (Table 3). Patients were treated with transurethral resection which unroofed the obstructed ejaculatory ducts (Figure) and placed in one of three groups dependent upon postoperative results. 55% of patients had an improvement in sperm density and/or sperm motility (Group I). 27% had improvement in ejaculate volume only (Group II) and 18% had no improvement in seminal parameters (Group III). Eleven of these patients had partial obstruction of the ejaculatory duct (not azoospermic) 9 of these 11 achieved an improvement in sperm density or motility postoperatively and 6 went on to achieve a pregnancy.

Ejaculatory duct obstruction is a much more common and treatable cause of male subfertility then previously described. This is due, in large part to the widespread use of transrectal ultrasound technology. The relatively non-invasive method of diagnosis and excellent results of therapy support the use of transrectal ultrasound examination as part of the initial evaluation in many men with male factor subfertility.


Pharmacologic Agents Associated with Impaired Ejaculation
(after Murphy et al,(16))


Guanethidine sulfate
Phenoxybenzamine hydrochloride
Prazosin hydrochloride

Antipsychotics (major tranquilizers)
Trifluoperazine hydrochloride

Antidepressants (tricyclic antidepressants and monoamine oxidase inhibitors)

lmipramine hydrochloride
Phenelzine sulfate


Epsilon aminocaproic acid


Treatment of Retrograde Ejaculation
(after Murphy et al, (16))

Alkalinization (monitor urine pH)

Sodium bicarbonate 650 mg q.i.d. 2 days before & day of collection

Sympathomimetic Agents (initially as a 2-week trial)

Pseudoephedrine hydrochloride 60 mg q.i.d.

Ephedrine sulfate 25-50 mg q.i.d.

Phenylpropanolamine hydrochloride 75 mg b.i.d.

Imipramine hydrochloride 25 mg b.i.d., 50 mg h.s.


Abnormalities Noted on Transrectal Ultrasonography Among Patients in Each Treatment Response Group (after Meacham et al, (13)

Group 1* Group 2** Group 3***

Ejaculatory duct cyst 4 3 1
Dilated seminal vesicle 4 2 1

Dilated vasal ampullae or
ejaculatory ducts 3 0 0

Calcification of ejaculatory
ducts 1 1 1

Non-diagnostic ultrasound 0 0 2~

Postoperative improvement in sperm density and/or motility.
**Improvement in ejaculate volume only.
***No postoperative improvement in semen parameters.
~Two patients did not Undergo preoperative ultrasonography.


Figure 1
Transrectal ultrasound image in a patient with secondary subfertility. Patient had a protracted course of prostatitis just after the birth of their first child. Top: transverse view of prostate demonstrating increased echogenicity in the region of the ejaculatory ducts bilaterally. Bottom: transverse image of dilated seminal vesicles which measure greater than 1.5 cm in anterior-posterior dimension and demonstrating a heterogenous echogenic pattern.

Figure 2 Transverse TRUS image (left) and axial view (right) of a 26 year old patient with retrograde ejaculation. Cystoscopy demonstrated a patulous bladder neck. Note the open bladder neck (large arrow) and seminal vesicle cyst (arrow head).

Figure 3 Transverse TRUS image (left) and axial view (right) of a patient with secondary subfertility and a fructose positive specimen with a volume of 0.2 cc, a total sperm count of 400,000 sperm, a 46% motility with a forward progression of 1-2. Note the calcification at the level of the verumontanum (large arrow) and the ejaculatory duct entering the calcification (arrowheads). Intraoperative TRUS at the time of resection is shown in Figure 11.

Figure 4 Transverse TRUS image near the apex (top image) and base (lower image) of the prostate in a patient with a large midline (utricular) cyst.

Figure 5 Schematic representation of the prostate, seminal vesicles and ampulla of the vas deferens. The ejaculator ducts usually enter the prostatic urethra just lateral and proximal to the prostatic verumontanum. However, variation is great and oftentimes the ejaculatory duct orifice cannot be visualized at the time of cystoscopy..(From Oates (50); copyright Medical Economics Publishing, Inc., used with permission)

Figure 6 A neurovascular fibrous stroma surrounds each ejaculatory duct. The wall of the ejaculatory duct consists of a layer of muscular fibers consisting of a thin outer circular layer and an inner longitudinal layer.(From Oates (50); copyright Medical Economics Publishing, Inc., used with permission)

Figure 7 The ejaculatory duct is shown in this axial view as two slightly echogenic lines.

Figure 8 Transverse and axial TRUS image of a seminal vesicle cyst (arrows).

Figure 9 Markedly dilated ejaculatory duct (arrows) is shown in these axial views.

Figure 10 A midline (utricular) cyst is shown in transverse projection at the level of the mid prostate (top) and verumontanum (lower left) and in axial projection (lower right).

Figure 11A Intraoperative transverse image of case presented in Figure 3. The location and depth of the calcification (arrows) from the resectoscope (arrowhead) is easily determined.

Figure 11B Intraoperative transverse image after resection. Note the calcification has been removed and a cystic region (arrows) identified. The resectoscope is in place (arrowheads).

Figure 12 Resection of the verumontanum is oftentimes all that is required for unroofing ejaculatory duct cysts or removing calcifications located at the distal end of the ejaculatory ducts. However, more proximal obstructions and/or cysts might require deeper and more lateral resection from the bladder neck to the verumontanum. Intraoperative transrectal ultrasound is particularly valuable in these cases. (From Meacham RB et al(13) Reproduced with permission of the publisher, The American Fertility Society)

Color Plate: Normal prostate gland based on McNeal's morphology provides the orientation for longitudinal ultrasound scanning. TZ=transition zone, CZ=central zone, PZ = peripheral zone, AFS = anterior fibromuscular stroma, PPS=pre prostatic sphincter, POPS=post prostatic sphincter, v=verumontanum, LSM=longitudinal smooth muscle, PUG=periurethral glands. (From Kaye, KW (51), copyright Medical Economics Publishing, Inc., used with permission)


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