Obstructive azoospermia is azoospermia due to obstruction of the vas deferens that impairs the transport of sperm. The incidence of obstructive azoospermia in male infertility is about 1%. The percentage of obstructive causes is also higher in patients with azoospermia, ranging from 42.4% to 48%.
Etiology and classification
(A) Congenital vas deferens obstruction
Congenital obstruction of the vas deferens can occur in any part of the vas deferens tract, from the intra-testicular ductal system to the ejaculatory duct. Intratesticular obstruction has been reported to account for approximately 15% of obstructive azoospermia, often due to post-inflammatory disease resulting in testicular network obstruction. Epididymal obstruction is the most common cause of obstructive azoospermia. Young’s syndrome is characterized by proximal epididymal obstruction and chronic epididymal lumen infection, which is due to mechanical obstruction caused by inflammatory debris in the proximal epididymal duct.
The prevalence of congenital bilateral vas deferens (CBAVD) in men is approximately 1:1600. Approximately 85% of CBVAD patients have mutations in the cystic fibrosis gene. Therefore, CBVAD can be considered as a genital type of cystic fibrosis disease.
(ii) Acquired vas deferens obstruction
Among acquired epididymal obstruction, secondary obstruction due to acute epididymitis (e.g., Linococcus infection) and subclinical epididymitis (e.g., Chlamydia infection) is considered to be the most common. Bilateral epididymal cystectomy can often result in postoperative secondary azoospermia.
The most common cause of acquired vasectomy obstruction is vasectomy. Approximately 2-6% of men who undergo this sterilization require vasectomy reversal. In 5-10% of patients undergoing vasectomy, an epididymal vasectomy is necessary due to combined epididymal obstruction. Surgery in the inguinal region, such as hiatal hernia repair, varicocelectomy, cryptorchid fixation, and intra-scrotal surgery such as syringomyelia reversal, may damage the vas deferens or epididymis, or may be secondary to damage to their vessels, nerves, or post-surgical infection, and such surgical damage is difficult to repair by reoperation.
Ejaculatory duct obstruction accounts for about 1 to 3% of patients with obstructive azoospermia. This obstruction can be classified as cystic obstruction or post-inflammatory obstruction. Cystic obstruction is a congenital obstruction that manifests as a Mullerian duct cyst, urogenital sinus/ejaculatory duct cyst; the location of the cyst is usually between the prostate and the ejaculatory duct. In urogenital sinus anomalies, the ejaculatory duct can empty into the cystic lumen unilaterally or bilaterally, whereas in Mullerian duct anomalies, the ejaculatory duct is squeezed by the cystic lumen in an abnormal position outward. Post-inflammatory ejaculatory duct obstruction is usually a complication following urethro-prostatic inflammation.
Complete obstruction of the ejaculatory duct, either congenital or acquired, is characterized by decreased ejaculate volume, negative seminal plasma fructose, and an acidic pH. Transrectal ultrasonography often reveals dilated seminal vesicles (anterior and posterior diameters greater than 15 mm
).
The typical clinical picture of obstructive azoospermia is one of normal testicular volume (>15
The typical clinical signs of obstructive azoospermia are: normal testicular volume (greater than 15 ml), enlarged and hardened epididymis, nodules in the epididymis or vas deferens, clinical signs of urethritis or prostatitis, and abnormal rectal examination of the prostate. In patients with azoospermia or severe oligospermia with normal testicular volume and endocrinology, obstruction of the ejaculatory duct should be suspected.
Clinical manifestations
Obstructive azoospermia
First, radiation exposure.
The male body is in a radioactive irradiation environment for a long time, which can be very harmful to the movement of sperm in the body. If there are very powerful electromagnetic waves, or radiation in front of the body, often the strength of sperm activity will be greatly restricted, so it is very important to do a good job of prevention.
Secondly, anaplasmosis.
The testes are the only place for male sperm output, if there are no testes, the sperm in the body will not be able to produce, so there will be a great impact on the fertility of the next generation of men.
Third, damage to reproductive organs.
Men may suffer some external injuries in their life, which will produce some damage to the testicles or twist, sperm cord twist, and then there may be patients who have done some surgeries, some trauma to the reproductive organs will affect the normal function of the testicles, leading to sperm production dysfunction.
Fourth, bilateral cryptorchidism.
The most obvious symptom of azoospermia is cryptorchidism. The symptom of cryptorchidism is that the testicles do not descend into the scrotum, but stay in the abdominal cavity, and because the temperature of the abdominal cavity is higher than that of the scrotum, it will affect the normal output of sperm and prevent spermatogenesis, so azoospermia will also occur.
Fifth, the local temperature of the testicles is elevated.
The occurrence of azoospermia is mainly due to frequent scalding baths, saunas, or other temperature type work, all of which can affect the normal temperature of the testicles to occur elevated, resulting in sperm production disorders, leading to the phenomenon of dead sperm and weak sperm.
Diagnosis
1. Semen examination: At least 2 times with an interval of 2 to 3 months, semen is examined by centrifugation according to WHO standards. Those with semen volume less than 1.5 ml, acidic pH and fructose negative are the first to wonder if it is obstructive azoospermia. When the semen volume is low, post-ejaculatory urine examination is also performed to rule out retrograde ejaculation.
2, medical history: usually patients with inflammatory obstruction have a history of reproductive tract infections, such as orchitis, epididymitis, and for those with a history of tuberculosis, the chances of triggering obstructive azoospermia will be higher.
Physical examination: The testicular volume of patients with obstructive azoospermia is within the normal range. In patients with epididymal obstruction and vas deferens obstruction, epididymal or vas deferens nodules, or vas deferens defects or local atresia can be palpated.
4.Ultrasound examination: Scrotal ultrasound is useful for the detection of some obstruction signs, such as epididymal cysts and vas deferens, and can also discharge testicular dysplasia. Transrectal ultrasound is also useful to find out whether the three seminal vesicles are absent, ejaculatory duct obstruction, and dilated ejaculatory ducts.
To confirm the diagnosis of azoospermia, more than 3 consecutive accurate sperm retrievals must be performed and no sperm are detected by centrifugal sedimentation microscopy technique. After that, further tests must be done to accurately identify non-obstructive, or obstructive azoospermia, which will provide the key basis for treatment. Traditional testicular biopsy is a complicated procedure that can cause varying degrees of damage to the testicles and complications.
Treatment methods
There are many treatment methods for obstructive azoospermia. The common clinical treatment methods for azoospermia include vasectomy, ejaculatory duct dilatation and vasovaginal epididymal anastomosis, and these three surgical methods have significant efficacy in treating obstructive azoospermia and have been chosen by the majority of azoospermia patients.