When semen is not seen in three consecutive laboratory tests and centrifuged, we call it azoospermia. Azoospermia accounts for about 15-20% of male infertility patients and the causes can be divided into two main categories. One is the dysfunction of the testes themselves, called primary azoospermia. The second is normal testicular sperm production function, but due to the obstruction of the vas deferens, sperm can not be discharged out of the body, known as obstructive azoospermia. Consultation needs: medical history, physical examination: including secondary sexual characteristics, development of external genitalia, testicular size, epididymis size, vas deferens, spermatic cord, prostate, seminal vesicles, etc.; semen laboratory tests; sex hormones; chromosomes. Invasive tests: testicular biopsy: it is necessary to determine whether to do it according to testicular size, sex hormones, and chromosomes. In diagnosis, the first step is to distinguish between obstruction and non-obstruction. This can be done by history questioning, physical examination, semen, seminal plasma biochemistry, blood sex hormone testing, ultrasound, and chromosome testing to make a preliminary diagnosis. If there is a clear history of reproductive tract infection, nodules are palpated in the scrotal segment of the vas deferens or the caudal part of the epididymis on physical examination, and the seminal plasma a-neutral glycosidase is reduced, the initial diagnosis of obstructive azoospermia can be made; if the semen volume is low, the semen is not coagulated, and the pH value is lower than 7.0 combined with fructose negativity, the basic diagnosis of ejaculatory duct obstruction can be made; the genital system and transrectal ultrasound can clarify whether there are defects in the vas deferens and seminal vesicles; and semen exfoliative cell examination reveals The presence of spermatocytes can basically exclude obstructive factors. In addition, it is generally believed that unilateral testicular volume <12ml and abnormally elevated follicle-stimulating hormone are more likely to have low spermatogenic function, and vice versa, which is more likely to have obstruction. However, this is not sufficient to determine obstruction or non-obstruction. Except for cases with very poor testicular development (volume <5 ml) and markedly elevated follicle estrogen and chromosomal abnormalities, the final diagnosis needs to be confirmed by epididymal/testicular puncture and testicular biopsy pathology.