Obstructive azoospermia accounts for 40% of azoospermia and results from obstruction of the excurrent ducts (due to many causes) at any location between the rete testis and the ejaculatory ducts. The diagnosis of obstructive azoospermia (OA) requires a stepwise approach to differentiate it from nonobstructive OA and to formulate management options. Localization of the site of obstruction relies on history, physical examination, and possibly laboratory, genetic, imaging tests, and intraoperative findings. The prospects for patients with OA are excellent given recent advances in microsurgical approaches and in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI). Successful outcomes are increasingly likely after microsurgical reconstruction techniques, permitting non-IVF pregnancies for many couples. When reconstruction is not an option, microsurgical sperm retrieval provides excellent outcomes for patients in conjunction with IVF and ICSI.
Key points
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Obstructive azoospermia accounts for 40% of azoospermia and results from obstruction of the excurrent ducts (due to many causes) at any location between the rete testis and the ejaculatory ducts.
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Physical examination, along with possible use of genetic/laboratory testing, ultrasonography, vasography, and/or testis biopsy as indicated helps to definitively diagnose obstructive azoospermia, determine the location of the obstruction, and select appropriate management.
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Treatment options include microsurgical reconstruction (possible in most cases) or sperm aspiration (ie, microsurgical epididymal sperm aspiration) without reconstruction.
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Surgical reconstruction relies on central microsurgical tenets including mucosa-to-mucosa approximation, cutting back to healthy tissue with good blood supply, and assuring a tension-free anastomosis.
Background
Azoospermia, the absence of sperm in the ejaculate (confirmed by 2 centrifuged semen specimens), is identified in 15% of infertile men and results from pretesticular, testicular, or posttesticular causes, and may be classified as obstructive azospermia (OA) or nonobstructive azoospermia (NOA). OA, which is caused by excurrent duct obstruction, comprises 40% of all azoospermia cases. Excurrent ductal obstruction, which can occur anywhere along the male reproductive tract (rete testis, efferent ducts, epididymis, vas deferens, and ejaculatory duct) is classically characterized by normal spermatogenesis. In most cases of OA, normal or near-normal sperm production continues in the testis. Microsurgical reconstruction, when possible, is a safe, efficacious treatment in most cases of vasal or epididymal obstruction by vasovasostomy (VV) or vasoepididymostomy (VE), respectively. Occasionally, transurethral resection of the ejaculatory ducts (TURED) is necessary for ejaculatory duct obstruction. In unreconstructable cases, viable sperm can almost always be retrieved for use with in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI).
Background
Azoospermia, the absence of sperm in the ejaculate (confirmed by 2 centrifuged semen specimens), is identified in 15% of infertile men and results from pretesticular, testicular, or posttesticular causes, and may be classified as obstructive azospermia (OA) or nonobstructive azoospermia (NOA). OA, which is caused by excurrent duct obstruction, comprises 40% of all azoospermia cases. Excurrent ductal obstruction, which can occur anywhere along the male reproductive tract (rete testis, efferent ducts, epididymis, vas deferens, and ejaculatory duct) is classically characterized by normal spermatogenesis. In most cases of OA, normal or near-normal sperm production continues in the testis. Microsurgical reconstruction, when possible, is a safe, efficacious treatment in most cases of vasal or epididymal obstruction by vasovasostomy (VV) or vasoepididymostomy (VE), respectively. Occasionally, transurethral resection of the ejaculatory ducts (TURED) is necessary for ejaculatory duct obstruction. In unreconstructable cases, viable sperm can almost always be retrieved for use with in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI).
Causes
The most frequent causes of vasal obstruction are vasectomy and iatrogenic vasal obstruction, which occurs most often after inguinal hernia repair (either pediatric or adult herniorrhaphy especially when mesh is used). Vasal obstruction may also be caused by previous vasography with improper technique or irritation from contrast medium. Epididymal obstruction may occur secondary to existing vasal obstruction (which exerts increased intraluminal pressure leading to microrupture and obstruction of the fragile epididymal tubules). Such epididymal obstruction secondary to previous vasal obstruction may occur in up to 60% of men 15 years after vasectomy. In other cases, epididymal obstruction may occur after trauma. Hydrocelectomy is commonly associated with iatrogenic epididymal injury because the epididymis may be difficult to identify especially in large chronic hydroceles. It is important to recognize that one stitch through an epididymal corpus or cauda tubule can result in complete obstruction of this side. Percutaneous epididymal sperm aspiration (PESA), or less frequently microsurgical epididymal sperm aspiration (MESA) or inadvertently performed epididymal incision or biopsies, may result in iatrogenic obstruction. Congenital abnormalities are a common cause of OA, usually congenital unilateral absence of the vas deferens (CUAVD), congenital bilateral absence of the vas deferens (CBAVD), and, less commonly, partial or complete absence of the epididymis, or idiopathic epididymal obstruction.
In addition to intentional and unintentional surgical obstruction or trauma of the vas or epididymis, genitourinary infection may also cause unilateral or bilateral obstruction. Severe acute or chronic epididymitis, and prostatic or seminal vesicle inflammation can lead to scar formation and eventual obstruction. Idiopathic cases of primary epididymal obstruction are often caused by lower genitourinary tract infection. In addition, Young syndrome, which includes sinobronchial disease and OA caused by thickened secretions and impaired ciliary and sperm tail function, is characterized by the absence of structural abnormalities, normal hormones, and normal testicular biopsy.
In addition to vasal and epididymal obstruction, ejaculatory duct obstruction (EDO) should also be considered in the differential for OA ( Box 1 ). EDO, present in less than 5% of azoospermic men, may result from trauma, previous surgery, infection, or congenital prostatic, seminal vesicle, or utricular cyst. In the case of cysts, external pressure from cysts can lead to EDO. EDO is classically defined by low semen volume, low semen pH, absent fructose in semen (basic, fructose-positive fluid is the normal contribution of seminal vesicles), and palpable vas deferens (obviously not found in CBAVD) on physical examination. If EDO is a consideration, improper semen collection (the most common cause of reduced ejaculate volume) and ejaculatory dysfunction (including retrograde ejaculation for which postejaculate urinalysis should be completed) must also be ruled out because the presentation could be similar. In addition, if none of the aforementioned apply, then cystic fibrosis transmembrane conductance regulator (CFTR) mutation may be the cause. Markers of an obstructed system include the absence of marker substances from the epididymis (α-glucosidase), seminal vesicle (fructose), and prostate (zinc) in the semen. However, if obstruction is unilateral or partial, these substances may be present.
Epididymis
Infection (acute/chronic epididymitis)
Previous iatrogenic epididymal incision for sperm aspiration/biopsy
Previous scrotal surgery (ie, hydrocelectomy)
Congenital (partial or complete absence of epididymis)
Young syndrome
Vas Deferens
Vasectomy
Iatrogenic: herniorrhaphy or other previous scrotal surgery with accidental vas deferens ligation
CUAVD, CBAVD
Vasotomy/vasography with improper technique
Ejaculatory Duct
Cysts (Mullerian utricular, prostastic, seminal vesicular)
Traumatic
Iatrogenic (postoperative)
Infection (ie, prostatic)
Diagnosis
OA is characterized by normal testicular volume (15–25 mL per testis), normal follicle-stimulating hormone (FSH) level, and azoospermia. History and physical examination are critical to identify predisposing factors for OA. To differentiate OA from nonobstructive azoospermia (NOA), patients should be specifically queried regarding OA and NOA risk factors. OA risk factors include previous vasectomy, other previous surgery (inguinal, scrotal, or genitourinary tract), genitourinary infection, chronic bronchopulmonary infection, or gastrointestinal (GI) abnormality associated with congenital absence of the vas deferens (CUAVD or CBAVD). Reproductive history with previous successful pregnancy and/or children suggests OA. NOA risk factors include delayed development, history of cryptorchidism, and previous gonadotoxic treatments including chemotherapy, radiation, environmental exposures, and treatment with exogenous testosterone.
Unlike NOA, the exocrine and endocrine capabilities of the testes remain functional in OA. Physical examination includes inspection for previous surgical scars in the pelvis or inguinal region, evaluation of the vasa to ensure that they are present, and palpation of the epididymides to identify fullness, induration, irregularity, partial absence, or complete absence. Epididymal obstruction is suspected with a full epididymis, the presence of the vas deferens, and normal testicular volume. Vasal gaps and length of the testicular remnant vasal end should be examined. The testicular vas length indicates whether vasectomy was performed in the convoluted vas (which may cause increased intraluminal pressure and possible epididymal injury) compared with a vasectomy higher in the scrotum which would theoretically decrease intraluminal pressure. The presence of sperm granuloma at the vasectomy site should also be assessed because granuloma relieves back pressure on the epididymis and is associated with decreased risk of epididymal obstruction, better quality intraoperative vasal fluid, and is considered to be a predictor of microsurgical vasectomy reversal outcome. Testicular volume and consistency must also be assessed because normal volume, firm testes are characteristic of OA, whereas small, soft testes more likely reflect NOA. If the vas is absent on one or both sides, then genetic testing for cystic fibrosis (CF) mutations is warranted as described later. Digital rectal examination may identify risk factors for EDO including midline prostatic cysts or seminal vesicle dilation.
Scrotal ultrasonographic imaging can be useful to confirm physical examination findings with direct imaging of testicular/paratesticular regions for abnormalities that may be associated with obstruction, including spermatocele, varicocele, vasal absence or dilation, epididymal absence or duct ectasia, masses, or cystic epididymal abnormalities in men with a normal FSH level. Particularly, ultrasonographic analysis of the caput epididymis may be useful to confirm OA. Transrectal ultrasonography is particularly helpful in the diagnosis of EDO, and can detect prostatic and seminal vesicle changes including infectious alterations and congenital or traumatic structural anomalies (midline Mullerian duct prostatic cysts, ejaculatory duct calcification, ejaculatory duct dilation, and seminal vesicle dilation >1.5 cm wide). In the case of EDO, seminal vesicles may be aspirated and can reveal high concentrations of sperm or EDO may be confirmed by vasography (discussed in EDO treatment). Transrectal and scrotal ultrasonography together can help to confirm the diagnosis of OA or NOA.
In terms of the initial laboratory tests, FSH (<7.6 IU/L) and testosterone levels should be checked and should be normal in OA, which reflects intact Sertoli and Leydig cell function, respectively. FSH, if increased, may suggest an increased requirement for assisted reproduction after vasectomy reversal. Inhibin B may also be checked and should be in the normal range, not decreased as it is in NOA. Despite variability in intralaboratory and interlaboratory testing, young healthy men should have an FSH level less than 7.6 IU/L and testosterone level greater than 300 ng/dL. By contrast, NOA includes both primary and secondary testicular failure and these can be differentiated by a serum panel of total testosterone, luteinizing hormone (LH), FSH (>7.6 IU/L), and prolactin. In NOA caused by secondary testicular failure (hypogonadotropic hypogonadism), testosterone is decreased secondary to decreased LH and FSH from hypothalamic or pituitary dysfunction. In primary testicular failure, LH and FSH are typically increased with poorly functioning testes producing lower levels of testosterone and inhibin B, which exert less negative feedback on pituitary gonadotropin secretion. In addition, a history of a positive serum antisperm antibody test indicates active spermatogenesis and can obviate the need for testicular biopsy before reconstruction.
Semen analysis is critical in the diagnosis of OA because bilateral obstruction results in azoospermia (no sperm in semen pellet after centrifugation on 2 separate tests), whereas unilateral obstruction and partial epididymal obstruction may be compensated for by the contralateral nonobstructed side. Unilateral and partial obstructions bilaterally can lead to severe oligospermia or asthenoteratospermia. Ejaculate volume remains within the normal range (>1.5 mL) if obstruction is located proximally to the ejaculatory ducts because most of the seminal fluid is derived from the prostate gland and seminal vesicles. Ejaculate volume is low by definition in the situation of EDO. With incomplete obstruction, occasionally rare sperm can be identified in the ejaculate, which may be adequate for successful ICSI. In addition, rare intact sperm in centrifuged pellets in semen are identified in approximately 10% of men seeking vasectomy reversal, and this finding indicates that sperm can be found in the testicular vasal lumen on at least 1 side, and is associated with favorable outcomes.
If testis volume is normal, vasa are present on physical examination, and there is strong suspicion for obstruction with serum FSH level less than 7.6 IU/L and normal semen volume, no genetic testing is indicated. Genetic testing is also not indicated in patients who have an established previous history of fertility or those patients with a sperm concentration greater than 5 million/mL. If CUAVD or CBAVD is suspected, then genetic testing is conducted for CFTR gene mutation as well as renal ultrasonography to rule out renal agenesis. Men with CBAVD carry 2 affected CFTR alleles with a 10% to 15% chance of additional abnormalities. If renal agenesis exists with CBAVD, however, this likely occurs secondary to non-CF mutation–mediated genetics caused by abnormal mesonephric duct development. In patients with CUAVD/CBAVD, semen volume is low, has low pH (<7) and is fructose negative, consistent with seminal vesicle atresia, which is common in these patients. If vasa are palpable but semen volume is low (<1.5 mL), genetic testing for CFTR mutation is indicated as well because seminal vesicle atresia/obstruction is a possible cause and could indicate normal scrotal vasa and absent retroperitoneal vasa (partial absence of the vas). In addition, many patients with CUAVD have contralateral obstruction of the seminal vesicle and commonly carry CF mutations. If there is suspected idiopathic epididymal obstruction, then some groups advocate checking CFTR mutations because up to 50% of these men may demonstrate mutations. Female partner testing (up to 5% may be heterozygotes among whites) and genetic counseling are critical before assisted reproductive technology (ART). If the woman is a CF heterozygote, selection of unaffected embryos with preimplantation genetic diagnosis may reduce the chances of having a child with clinical CF or infertility, but it will not eliminate the possibility.
CF, the most common autosomal recessive condition in the non-Hispanic white population, is a disease with a progressive clinical course affecting lung, pancreas, and GI systems. CF is caused by genetic abnormalities in the CFTR gene, which is involved in the regulation of exocrine epithelial cell secretion consistency and results in increased sweat chloride concentration (>60 mmol/L). More than 95% of males with CF demonstrate CBAVD. More than 1700 mutations and abnormalities have been discovered, with a spectrum of consequences (isolated CBAVD, cordlike vas without lumen, hypoplastic or absent epididymal corpus/cauda, CF) based on whether there is reduction or absence of CFTR protein product. Following the recommendations of 2 groups, the American College of Medical Genetics (ACMG) and the American College of Obstetricians and Gynecologists (ACOG), most CF screening panels include 30 to 50 mutations (commonly F508del and 5T,7T,9T variants), which occur most frequently in patients of Jewish and northern European origin who manifest clinical CF. Such mutations are not necessarily identified in patients with CBAVD. More complete CFTR gene screening can be conducted, but mutations may still not be identified in up to 25% of patients with CBAVD. In addition, complete analysis of the CFTR gene with DNA sequencing is generally used for patients with a history of CF or males with CBAVD. In cases of OA without the possibility of reconstruction (CBAVD), MESA is indicated with ART leading to excellent outcomes.
Open testis biopsy (optimally performed with the microscope) may be indicated to distinguish OA from NOA in azoospermic men with normal-sized testes, palpable vasa deferentia, normal FSH levels, and a negative serum antisperm antibody test. Testis biopsy specimens should always be placed in Bouin, Zenker, or collidine-buffered glutaraldehyde solutions, but never formaldehyde, which distorts testicular architecture. In men with CBAVD, testicular biopsy commonly demonstrates spermatogenesis and does not need to be performed before definitive aspiration for IVF/ICSI.
Treatment and outcomes
Options for men with OA are microsurgical reconstruction or sperm retrieval to be used for ART including IVF/ICSI. When reconstruction is feasible, the decision when to reconstruct or to retrieve is based on numerous factors including the number of children desired, previous surgical history, previous fertility as a couple, female partner age, female factor infertility, religious beliefs, possibility for natural conception, and financial situation. Of the 600,000 men undergoing vasectomy annually in the United States, up to 6% of men ultimately seek vasectomy reversal. Obstruction may occur at any location along the genital tract and this can be confirmed by vasography at the time of definitive reconstruction. Indications for vasectomy reversal include the desire to have more children, postvasectomy pain management, and treatment of iatrogenic (herniorrhaphy, orchidopexy, hydrocelectomy), traumatic or infectious causes of vasal or epididymal obstruction. For patients with infertility before vasectomy, preoperative evaluation and occasionally testicular biopsy may be performed either before or at the time of initiation of vasectomy reversal.
VV/VE Surgical Principles
Vasal obstruction is treated by microsurgical VV ( Fig. 1 , [CR] ) and epididymal obstruction is treated by microsurgical VE ( Fig. 2 , [CR] ). Microsurgical reconstruction is most often performed under general anesthesia in the supine position with all pressure points padded in standard fashion. Bilateral, high, vertical incisions are made, approximately 1 cm lateral to the base of the penis. This incision location facilitates testicular delivery and exposure of the vas (up to the inguinal canal) and epididymis as needed to ultimately facilitate tension-free anastomosis. Alternatively, an inguinal incision may be incorporated if the patient has a history of herniorrhaphy or orchidopexy with likely obstruction of the inguinal vas. Successful anastomosis relies on meticulous mobilization of the vas to increase vasal remnant length without stripping the vasal vessels. With a history of vasectomy, the vasectomy site is identified and the vas is transected on the testicular side of the vasectomy site. The vas is cut with an ultrasharp knife drawn through a slotted 2.0-mm or 2.5-mm diameter nerve holding clamp, which permits a perfect 90° cut. A healthy white mucosal ring of the vas should be identified. If the tissue is scarred or the mucosa is floppy and easily detaches from the underlying muscle, the vas should be recut until healthy bleeding with a crisp clean mucosal ring is noted. Vasal fluid is then examined using a bench microscope under 400× magnification ( Table 1 ). If there is no history of vasectomy and primary epididymal obstruction is suspected, the vas is hemitransected at the junction between straight and convoluted vas. If sperm are identified in vasal fluid, then the location of obstruction is identified by vasography toward the abdominal portion of the vas. If no sperm or sperm parts are identified in vasal fluid, then epididymal obstruction is confirmed and VE is completed.
| Vasal Fluid Quality | Microscopic Examination | Procedure Recommended |
|---|---|---|
| Clear, cloudy, creamy | Sperm heads alone | Vasovasostomy |
| Sperm heads with whole nonmotile sperm | ||
| Whole nonmotile sperm | ||
| Whole motile sperm | ||
| Clear copious | Sperm (whole, parts) absent | Vasovasostomy |
| Toothpastelike, creamy | Sperm (whole, parts) absent | Vasoepididymostomy |
| No fluid | Sperm (whole, parts) absent | Vasoepididymostomy |
Confirmation of abdominal end vasal patency is obtained using a 24-gauge angiocatheter to inject normal saline with a 1 mL syringe that does not encounter resistance. If patency is not certain, then 1 mL of indigo carmine (in a 1:1 ratio with lactated Ringer’s solution) may be injected in the abdominal end of the vas using a 24-gauge angiocatheter while a 16-Fr Foley catheter with a 5-mL balloon is placed on gentle traction against the bladder neck. Indigo carmine, rather than methylene blue, is used because of the known toxic effects of methylene blue on sperm. With a patent abdominal vas, the urine becomes blue. Furthermore, a 2-0 prolene suture may be passed into the abdominal end of the vas (with a clamp placed on the suture when it meets obstruction) to calculate the distance to the location of the distal obstruction. This is particularly useful when iatrogenic vasal obstruction from hernia repair is suspected. Vasography is relatively indicated in men with low semen volume and evidence of EDO. If vasal fluid contains no sperm, this indicates probable epididymal obstruction and vasography (indigo carmine or saline) confirms abdominal vas patency before VE. If vasal fluid is copious with many sperm, this indicates vasal obstruction or EDO, and formal contrast vasography pinpoints the precise site of obstruction. If vasal fluid is copious, toothpastelike, and without sperm in a dilated vas, this indicates secondary epididymal obstruction with possible simultaneous distal obstruction (of vas or the ejaculatory duct). Vasography must be performed precisely because improper technique can lead to stricture formation, sperm granuloma, or obstruction caused by vasal blood vessel injury at the vasography site. Proper vasography technique includes isolation of a clean vas segment and hemitransection with a 15° ophthalmic microknife. Extruded vasal fluid is examined microscopically to determine fluid quality, which indicates the location of the obstruction. If cryopreservation is desired, motile sperm samples should be obtained before the vasogram. Formal vasography is completed with a no. 3 whistle-tip ureteral catheter placed gently into the lumen of the abdominal end of the vas. A 16-Fr Foley catheter is placed into the bladder, the balloon is filled with 5 mL of air, and it is placed on mild traction. Subsequently, 0.5 mL of water-soluble radiographic contrast medium is injected to conduct the vasogram. If TURED is indicated, the vasography site is microsurgically closed after confirmation that the TURED was successful by verification with indigo carmine at the vasography site.
If VV is indicated, a tension-free, watertight, mucosa-to-mucosa approximation is of paramount importance to achieve successful outcomes. Such an anastomosis is facilitated using the microdot multilayer technique (first described in 1998) and the Goldstein microspike approximator clamp (ASSI Corp, New York, USA) both pioneered at Weill Cornell Medical College (see Fig. 1 ). The microdot technique, with marking pen delineation of needle exit sites, permits accurate realignment of the vasal ends, and is particularly useful when there is a significant difference in luminal diameter between the two vasal ends. The mucosal layer is completed with interrupted, double-armed, 10-0 monofilament sutures. The second deep muscularis layer is reapproximated using interrupted 9-0 monofilament sutures. The third adventitial layer is completed with interrupted 9-0 monofilament sutures. Reapproximation of the vasal sheath with 8-0 monofilament sutures minimizes tension on the anastomosis. The technique has been described in further detail previously. Anastomoses in the convoluted vas can be completed with similar outcomes. Large vasal gaps may be dealt with using crossed VV or testicular transposition. After vasectomy (with ligation of vasal vessels), the testicular end of the vas receives all the blood supply from the testicular artery/epididymal arteries, whereas the abdominal end of the vas receives blood supply from the deferential artery. Two simultaneous VVs cannot be performed in the same vas if the vasal vessels have been disrupted at both locations.
VE is the indicated for OA secondary to epididymal obstruction. After preliminary reports of VE in the early 1900s with low success rates, the introduction of the microsurgical approach in the late 1970s resulted in patency rates ranging from 50% with end-to-end single tubule anastomoses to 70% with end-to-side anastomoses. Introduction of intussusception end-to-side VE techniques, initially described by Berger using a 3-suture triangulation method, were subsequently modified to include longitudinal placement of sutures in the epididymal tubule known as longitudinal intussusception VE (LIVE), which has resulted in patency rates of 80% or greater in animal models and humans. The LIVE technique, our preferred approach, permits a larger diameter for flow from the epididymal tubule to the vas, with improved outcomes compared with perpendicular placement of 2 sutures in the epididymal tubule or the 3-suture triangulation technique. The LIVE technique permits accurate approximation of the 300- to 400-μm vasal lumen to the 150- to 250-μm epididymal tubule lumen with 90% patency and 40% pregnancy rates.
After appropriate mobilization of the abdominal vas to permit tension-free anastomosis to the epididymis, the tunica vaginalis is incised longitudinally, and the epididymis is examined at up 25× magnification to identify the eventual anastomotic site proximal (toward the caput) to the site of obstruction. Classically, a sperm granuloma is noted with dilated tubules proximally, whereas collapsed nondilated tubules are found distally. A straight tubule with larger diameter is selected and a 3- to 4-mm buttonhole opening is made into the epididymal tunic to match the outer diameter of the vas. If the level of obstruction is not readily apparent, then a 10-0 needle (70 μm tapered) is used to puncture an epididymal tubule starting distally and progressing proximally (toward the caput), checking for sperm presence in the fluid under the microscope after each puncture. The puncture hole from which sperm are identified is sealed with bipolar microforceps. A virgin tubule proximal to the punctured site is selected for anastomosis. VE anastomosis is completed using an epididymal tubule with abundant sperm regardless of motility. The quality of the epididymal fluid from the selected tubule is not known until after the sutures are placed using the LIVE technique. If sperm or abundant sperm parts are absent after incision of the epididymal tubule, then epididymal obstruction is located more proximally (closer to testicle) and the sutures must be removed and the anastomosis restarted using a more proximal tubule. Although successful VE may be performed using epididymal tubules or even efferent ductules, obstruction of the intratesticular rete testis is not amenable to microsurgical reconstruction.
With the VE anastomotic site selected, the vas is pulled through an opening made in the tunica vaginalis and is secured to the tunica vaginalis using polypropylene sutures (through the vasal adventitia and tunica vaginalis) so that the vasal lumen reaches the desired epididymal tubule without tension. The posterior edge of the vas (adventitia and muscularis) is secured to the posterior edge of the epididymal tunic with two 9-0 monofilament nylon sutures. With the LIVE technique, 4 microdots are placed on the vasal end (indicating the exit points of the 4 needles), and two 10-0 monofilament nylon double-armed sutures with 70-μm taper-point needles are placed longitudinally into the epididymal tubule under 25× to 40× magnification (see Fig. 2 ). An ophthalmic microknife (15°) is used to incise between the needles, which are not pulled through until after incision (because leakage occurs given the larger diameter of the needle than the suture). Epididymal tubule fluid is aspirated with 5-μL pipettes by capillary action. The fluid is examined under a light microscope for the presence of sperm. If abundant sperm with motility are identified, the fluid is aspirated into multiple micropipettes and flushed into human tubal fluid medium for cryopreservation. The anastomosis is then completed by placing the 4 needles from the 2 double-armed sutures inside-to-out through the vasal mucosa, exiting through each microdot on the vas. Double-armed sutures, as with VV, obviate the need to place outside-to-inside stitches (which can lead to back walling of the vasal lumen mucosa and obstruction). Before tying the two 10-0 sutures, a stay suture of 9-0 nylon is placed from the anterior vasal adventitia to the edge of the epididymal tunic and partially tied, bringing the vasal mucosa directly into the opening in the epididymal tubule. After tying the 10-0 sutures, the outer layer of the anastomosis is completed by using 8 to 12 interrupted 9-0 nylon sutures from the vasal sheath to the epididymal tunic taking care not to injure the nearby epididymal tubules. After meticulous hemostasis, the testis and epididymis are returned to the tunica vaginalis, which is closed using absorbable suture, the testis is replaced into the scrotum in anatomic position, and incisions are closed in the same manner as for VV.
Postoperatively, patients are advised to use an ice pack intermittently for 48 hours on the operative site, avoid ejaculating, strenuous activity, or heavy lifting for 3 weeks, and wear scrotal support for 6 weeks. Although complications are infrequent, the most common postoperative complication is scrotal hematoma (which may be obviated if scrotal drains are placed intraoperatively when extensive dissection is required). Additional possible complications include wound infection, scrotal edema, orchalgia, and, rarely, ischemic epididymal fibrosis or testicular atrophy. Secondary azoospermia or recurrent stricture is another possibility postoperatively, although this occurs rarely after VV in 0.5% to 6% of cases. After VE, the failure rate has been reduced to as low as 4% using the LIVE technique, whereas failure can occur in up to 37% using nonintussusception techniques. The increased failure rate of VE is related to the delicate anastomosis between the vas and epididymis compared with VV. Semen analyses are performed at 4 to 6 weeks postoperatively and subsequently every 2 to 3 months. Patients with motile sperm in the ejaculate postoperatively are encouraged to cryopreserve especially after VE or redo surgery.
Recent analyses indicate that microsurgical reconstruction in appropriately selected patients is the safest and most cost-effective method to manage men with vasal or epididymal obstruction. IVF/ICSI carries increased costs associated with multiple births. A recent large study reported in the New England Journal of Medicine also showed that IVF/ICSI is associated with a doubling in the incidence of birth defects in IVF/ICSI babies. Robotic VE using the LIVE technique has been described in animals and humans, but outcomes and cost-effectiveness of this technique require further study. Outcome after vasectomy reversal has been well predicted by our treatment nomogram based on vasal fluid quality from the testicular end of the vas at the time of surgery, the presence of sperm granuloma, microsurgeon experience, and the vasal obstructive interval. The need for VE is predicted by the time interval since vasectomy and the presence of sperm granuloma. The significance of increased obstructive interval results from time-dependent testicular and epididymal damage as well as secondary epididymal obstruction. Overall patency rates range from approximately 70% to 99.5% (VV) and 30% to 90% (VE) in the literature with pregnancy rates from 36% to 92% (after VV) and from 20% to 50% (after VE). In addition, return of sperm to the ejaculate depends on the procedure type, with intraoperative motile sperm, VV (rather than VE which can take up to 1 year), and obstructive interval (<8 years) demonstrating more rapid return of sperm to the ejaculate. After successful vasectomy reversal, the age of the female partner plays a significant role in pregnancy and live delivery rates. Outcomes after reconstruction for iatrogenic vasal injury leading to obstruction (longer vasal defects, decreased blood supply, and increased obstructive duration) are poorer than for patients with OA as a result of vasectomy. Intraoperative sperm retrieval should be offered to men undergoing VE or redo surgery for cryopreservation and future use for IVF/ICSI in the event of reconstruction failure. If spontaneous pregnancy does not occur after successful surgical reconstruction, ejaculated sperm may be used for ART. Additional long-term studies of VV and VE outcomes are needed in the future.
EDO
If EDO is identified, TURED is the treatment of choice. Alternatively, sperm retrieval techniques (discussed later) can be used. After TURED, a significant proportion of patients develop epididymitis from urine reflux in the efferent ductal system. If transurethral ultrasonography reveals dilated seminal vesicles or a midline cyst, transurethral ultrasound–guided aspiration of seminal vesicles (with examination for sperm) and injection of indigo carmine with radiographic contrast may be diagnostic. Sperm aspirate may be frozen for future IVF/ICSI attempts. Once the site of obstruction is confirmed, TURED is performed, which should result in blue dye effluxing from the ejaculatory ducts to confirm sufficient resection. If no sperm are identified in seminal vesicle aspirate, however, then secondary epididymal obstruction is most likely. Initial vasography (after sperm extraction at the vasotomy site for cryopreservation) may be performed. However, simultaneous transurethral resection with VE is usually unsuccessful. TURED results in improved semen parameters in most patients. However, if TURED is unsuccessful, then sperm aspiration (ie, MESA) is the next step in management.
Alternatives to Reconstruction, MESA
If patency is not desired or men are not candidates for reconstruction (ie, surgically unreconstructable OA including CBAVD), men with OA of all causes may select sperm retrieval techniques to be used with IVF/ICSI. Sperm retrieval is accomplished via percutaneous or microsurgical sperm retrieval from the epididymis (preferable) or testis and cryopreserved into multiple vials for future use in IVF/ICSI. In men with OA, cryopreservation is as good as fresh semen, so there is no need to synchronize sperm retrieval with egg retrieval. Sperm retrieval rates for men with OA using ICSI are excellent (96%–100%) regardless of the cause of the obstruction. Since the initial description of successful pairing of aspirated epididymal sperm with IVF, MESA has become the reference standard with excellent yield and minimal contamination ( Fig. 3 ). During MESA, the epididymis is surveyed at 10× to 15× magnification to select dilated tubules with semitranslucent fluid for aspiration. Tubules are exposed with accurate incision and hemostasis of the epididymal tunic. The selected tubule is then sharply punctured with an ophthalmic microknife (15°) to yield adequate fluid. Once adequate fluid is observed using a phase contrast microscope, 5-μL standard laboratory glass pipettes are used to collect fluid via capillary action with a total of 10 to 20 μL of epididymal fluid collected. If motile sperm are not identified, the surgeon moves toward the caput of the epididymis and, if needed, the efferent ducts with each puncture until sufficient sperm are obtained for both fresh and cryopreservation use. Improved motility will be identified moving toward the testis within the epididymal caput. As a last resort, testicular tissue can be retrieved, and in men with OA, this usually contains motile sperm.
