0022-5347 /85 /1346-1131$02,00 /0 THE JOURNAL OF UROL(JGY
December in US,A
Vol
Copyright© 1985 by The WiEiams & Wiikins Co,
TRANSSEPT AL CROSSED VASOV ASOSTOMY ELI F. LIZZA, JOEL L. MARMAR, STANWOOD S. SCHMIDT, JOSEPH A LANASA, JR., IRA D. SHARLIP, ANTHONY J. THOMAS, ARNOLD M. BELKER AND HARRIS M. NAGLER* From the Departments of Urology, Columbia-Presbyterian Medical Center, New York, New York, Cooper Hospital/University Medical Center, Rutgers Medical School, Camden, Massachusetts, University of California Medical Center, San Francisco, California, Louisiana State University Medical Center, New Orleans, Louisiana, Cleveland Clinic Foundation, Cleveland, Ohio, and University of Louisville School of Medicine, Louisville, Kentucky
ABSTRACT
We examined 11 patients with acquired obstructive azoospe:rmia resulting from irreparable obstruction of 1 vas deferens and severe damage to the contralateral testis. All of the patients underwent transseptal crossed vasovasostomy with no morbidity. Of 8 patients evaluated with postoperative semen analyses 4 (50 per cent) demonstrated total sperm counts of 29 to 205 million and 2 pregnancies (25 per cent) have been reported, with followup ranging from 5 months to 2 years. The etiologies of the vasal obstruction included previous inguinal surgery in 7 patients, vasectomy in 1, ejaculatory duct obstruction in l, ectopic ureter in 1 and vasal agenesis in l. Factors leading to loss of the contralateral testis were torsion in 5 patients, mumps orchitis in 2, varicocele in 1, pediatric inguinal hemiorrhaphy in l, epididymal blow out in 1 and unknown in 1. A representative case involving a unilateral ectopic ureter emptying into the seminal vesicle and subsequent contralateral testicular torsion is presented. The results indicate that a transseptal crossed vasovasostomy should be done in patients satisfying the criteria presented. The majority of the patients presenting with acquired obstructive azoospermia can be aided by vasovasostomy or vasoepididymostomy.1 However, a subset consists of men whose azoospermia results from multiple contributing factors and, therefore, is not amenable to standard surgical treatment. Patients with irreparable obstruction of a vas deferens plus severe damage to the contralateral testis resulting in unilateral loss of spermatogenesis represent a unique group. The result of this combination is a testis that produces sperm without an excurrent duct system and a nonfunctioning testicle with a normal ductal system. This condition presents a unique surgical opportunity to use the "spare part" of 1 side to reconstruct the contralateral mate. Eleven cases from the practices of 7 urologists performing reproductive microsurgery were accumulated. The etiologies of the irreparable unilateral vasal abnormalities and contralateral testicular abnormalities, as well as the surgical approach to this unusual clinical problem and the results obtained are presented. PATIENT POPULATION
TABLE 1.
PL No,-Age 1-36
Accepted for publication July 17, 1985. * Requests for reprints: Department of Urology, Columbia-Presbyterian Medical Center, 630 West 168th St., New York, New York 10032, 1131
Etiology of ContralaL Testicular Abnormality
2 previous inguinal explorations for obstruction Pediatric inguinal herniorrhaphy Pediatric inguinal herniorrhaphy Pediatric inguinal herniorrhaphy Vasectomy Ejaculatory duct obstruction Pediatric inguinal herniorrhaphy Nephroureterectomy and seminal vesiculectomy for ectopic ureter Pediatric inguinal herniorrhaphy Pediatric inguinal herniorrhaphy Agenesis of distal vas deferens
3-31 4-29 5-31 6-31
7-37 8-30
9-26
Appropriate cases were solicited from 7 urologists who are known to perform microsurgery for the correction of male infertility. A total of 11 patients fit the criteria outlined. All 11 patients had azoospermia that was documented on multiple semen analyses. Evaluation included testis biopsies and vasography. All of the patients had 1 testis with normal sperrnatogenesis and an obstruction of the ipsilateral vas deferens that could not be repaired surgically. Furthermore, in all but 1 case the contralateral testis demonstrated atrophy with loss of spermatogenesis in continuity with a normal vas deferens. The remaining patient demonstrated severe epididymal obstruction not amenable to surgical correction. Each patient underwent a transseptal crossed vasovasostomy by joining the ipsilateral normal testis to the contralateral
Details of patient population
Etiology of Vasa! Obstruction
10-25
11-33
Mumps orchitis
Varicocele Torsion Pediatric inguinal herniorrhaphy Mumps orchitis Unknown Torsion Torsion
Epididymal blow out* Torsion Torsion
* Irreparable obstruction high in epididymis,
TABLE 2,
PL No, 1 2 6 7 8 9
10 11
Results in patients treated with transseptal crossed vasovasostomy
Sperm Count (Xl06/sample)
Sperm Density (Xl06 /mL)
Duration of Followup
Pregnancy
0 205 0 32 72
0
1 yr, 6 mos, 1 yr, 5 mos, 13 mos, 20 mos, 2 yrs, 6mos,
No Yes No Yes No No No No
0 18 29
0
0
132 0
36 0
1132
LIZZA AND ASSOCIATES
A
C
Seminal Vesicle
II cjisA, initial pathological state demonstrates left ectopic ureter with renal loss. B, findings at presentation for evaluation of infertility. C, transseptal crossed vasovasostomy and removal of atrophic right testis.
patent vas deferens via a microscopic technique. To accomplish this the vas deferens was brought through a window created through the scrotal septum. Results are based upon patient followup, semen analyses and the occurrence of pregnancy. The causes of the irreparable unilateral vasal obstruction varied (table 1) but most patients (9 of 11) had undergone a previous operation, the most prevalent being pediatric inguinal herniorrhaphy (6). Similarly, contralateral testicular damage resulted from varied etiologies, with previous testicular torsion as the prominent cause (5 patients). RESULTS
Postoperative semen analyses were obtained from 8 of the 11 patients. The remaining 3 patients were lost to followup. Of the 8 patients 4 (50 per cent) demonstrated postoperative sperm counts from 29 to 205 million per ejaculate (table 2). Pregnancies have been reported in 2 of these patients (25 per cent), with followup from 5 months to 2 years (table 2). No complications were reported and convalescence was uneventful in all of the patients. One of the more unusual cases is presented. CASE REPORT
W. M., a 30-year-old man, presented for evaluation of primary infertility and azoospermia. History was significant for an episode of left epididymitis when he was 16 years old. Shortly thereafter left nephroureterectomy and seminal vesiculectomy were done for an ectopic ureter emptying into the left seminal vesicle (part A of figure). Several months postoperatively the patient presented with an episode of right scrotal swelling, which was believed to be owing to acute right epididymitis. Physical examination demonstrated normal male secondary sex characteristics and the phallus was without pathological conditions. Scrotal examination demonstrated the left testis and epididymis to be normal in size, shape and consistency. The right testis was an atrophic nubbin, presumably secondary to a missed torsion at the time of scrotal swelling (part B of figure). Semen analysis demonstrated azoospermia on 2 occasions. Post-ejaculatory urinalysis revealed no sperm. Testicular biopsy confirmed the absence of spermatogenesis on the right side and diminished but complete spermatogenesis on the left side. Upon bilateral scrotal exploration, vasography demonstrated obstruction of the left vas deferens at the level of the previous operation and patency of the right vas deferens into the bladder. Transseptal crossed vasovasostomy then was performed with a
microsurgical technique, connecting the testicular end of the left vas deferens to the abdominal end of the right vas deferens through a window created in the scrotal septum (part C of figure). Postoperative semen analysis demonstrated a total count of 29 million sperm at 5 months. DISCUSSION
The patient population for which a transseptal crossed vasovasostomy is indicated obviously is small. It includes patients with a testis with normal spermatogenesis and an associated ipsilateral vas deferens that is irreparably obstructed or absent, as well as a contralateral testis with absence of spermatogenesis but an associated patent vas deferens. The technique of using the contralateral vas deferens as a spare part to create a functional and anatomically complete reproductive unit has been described by Silber. 2 We examined a series of patients treated in this manner, categorized the etiological factors, and reported the results of transseptal vasovasostomy on sperm count and pregnancy rate. It is apparent that a previous inguinal operation, especially during childhood, is a strong predisposing factor for vasal damage. Furthermore, torsion was the cause of the majority of atrophic testes. Patients with azoospermia should be investigated for the coexistence of these factors. In the clinical situation outlined the minimal increase in operative time and greater technical difficulty appear to be justified by the rate of successful reanastomosis and lack of complications. Although the rate of return of acceptable sperm count (50 per cent) and subsequent pregnancy rate (25 per cent) are low compared to those reported for routine vasovasostomy, these values are encouraging in the complicated patient population studied. 1 •3 Indeed, comparison to patients undergoing vasovasostomy for reversal of elective vasectomy may not be valid because of the multiple abnormalities present in each of our patients and because each had only 1 functioning testicular unit. Because of these successes and the lack of associated morbidity transseptal crossed vasovasostomy should be performed in all patients who satisfy the aforementioned criteria. REFERENCES
1. Lipshultz, L. I. and Howards, S. S.: Surgical treatment of ·male
infertility. In: Infertility in the Male. New York: Churchill Livingstone, part Ill, chapt. 17, pp. 349-361, 1983. 2. Silber, S. J.: Microsurgery of the male ductal system. In: Reproductive Infertility Microsurgery in the Male and Female. Baltimore: The Williams & Wilkins Co., chapt. 3, pp. 154-156, 1984. 3. Schoysman, R. and Stewart, B. H.: Epididymal causes of male infertility. Monogr. Urol., 1: 1, 1980.