Major. M.P.Vora, M.B.B.S., D.V.D., I.M.S. (Rtd.)
Indian Medical Record
A monthly journal of Public Health, Tropical Medicine and Surgery etc .
Volume LXXXVII, Number-2 of February 1967
This article was solely contributed to Indian Medical Record
Discussion about the male sterility may seem strange at a time when the talk on the family planning is afloat. However, the subject has its own profound significance, when one is confronted with conjugal sterility and a fervent desire of the sterile couple to have children. The physician has no choice but to suggest a remedy to end the state of infertility. Being sterile in no way signifies absence of virility. A male may be perfectly potent and efficient and yet be sterile. To come across an individual who has excellent virility but suffers from sterility because of either azoospermia or necrospermia is not uncommon.
The number of involuntary sterile couples amounts to about ten percent and the responsibility for barren marriage is distributed between the marital partners. Since the substantial percentage of the husbands are responsible for the conjugal sterility, it is necessary to subject the husband to examination to ascertain his procreative ability. Human fertility is not so simple and emotions can at times play an important role. Its study is fascinating but its causes are still incompletely understood. The male infertility can be proved by (1) the female partner’s failure to conceive when she is found to be sound and normal on various tests and carries normal relations with her male partner over a period of 6 to 12 months and (2) a defect is found in the husband’s semen. If the quality of the husband’s semen could be improved and it is then followed by pregnancy, the initial fault lay obviously in the husband to label him sterile
The semen is collected by coitus interruptus or masturbation, the last method being condom. A rubber condom must not be used for its collection. The specimen must be kept at body temperature. If the husband is not co-operative, the post coital examination of the cervical mucus ca be undertaken to judge his capacity for fecundation. But if the female has her vaginal secretion very acidic which may be spermicidal, the result of the examination may turn out to be of no diagnostic value. However, such a test helps to decide the need for artificial homologous insemination, if the husband has active motile sperms in his ejaculate.
The examination of the semen must be done within two hours of its collection. The four principle parameters of semen quality are (1) ejaculate volume, (2) sperm count, (3) sperm motility and (4) morphology of the germ cells. The minimum standards to enable semen to be defined as fertile are:-
The volume of the ejaculate is of considerable importance. Sufficient quantity of semen to neutarlise the deleterious and spermicidal activity of the vaginal secretion is considered necessary. The mean ejaculate volume after three days of continence is about 3.5 ml with a range between 2 to 5 ml. Volume lower than 2 ml must be viewed with suspicion. If there is malposition of the uterus or the vaginal secretion is strongly acidic, the sperms may not gain access readily into the cervical canal. Under these circumstances, correction of the uterine position and institution of an alkalizing vaginal douche before coitus may prove helpful.
Number of spermatozoa
The average sperm count varies from about 60 to 185 million, lowest acceptable level being 50 million per ml. The number of spermatozoa necessary, although important their activity in terms of active forward progression and the structure of the cells are of immense importance from the point of conception. The chance of conception is related not so much to the count but to the percentage of active cells and to the quality of motility exhibited by these calls. Above the level of 20 million per ml the possibility of conception is related to the motility and not to the count. Even at a count level below 20 million per ml, the chance of conception is reasonably good, if the quality of motility is very good. Unfortunately, poor motility often accompanies lower count. Where the sperm count of the male after 3 days of continence is 20 million per ml, a higher frequency of intercourse can be safely suggested to him, without endangering his fertility potential. There is positive correlation between frequency of intercourse during the fertile period and the chances of conception; the quality of sperm motility is enhanced by frequency of ejaculation. Hence the advice often given to barren couples to refrain from intercourse for many weeks or days before the expected time of ovulation, in order to increase semen quality, is quite baseless and indeed may defeat the desired purpose. Greater importance has to be given to the number of active sperms than the total number of spermatozoa. If the sperm count is under 20 million/ml, the chances of conception are reduced, although the semen quality may be good. The minimum standards of fertility are the sperm count of 20 million/ml, and the ejaculate volume 2.5 ml, and at least 40 % of these cells should show vigorous forward aggressive progression and that at least 60% should show normal structure. Instances of pregnancy where the sperm count of the husband has repeatedly been under 20 million/ml have been reported. Though the lowest acceptable count level in the presence of good motility and morphology is stated 20 million/ml, normal fertilization of the human ovum can and does occur at much lower count level also. It will be wrong to suppose that the semen quality determined at one time represents that present at the time of conception. Some variations cannot be ruled out.
Motility of sperms should persist upto 9 to 18 hours at body temperature. The spermatozoa which fertilize the ovum must have the potential for aggressive forward motion. A husband with necrospermia whatever his sperm count may be, cannot initiate pregnancy. The chances of conception vary with the percentage of active spermatozoa in the ejaculate and the quality of motility shown by the germ cells. The most important single criterion of semen quality is the rate of forward aggressive movement, exhibited by the spermatozoa. Though good motility can compensate for low sperm count, it is equally true that the viga of spermatozoa can compensate in part for the low percentage of active cells. Although poor sperm motility usually accompanies oligospermia, it is often found in the presence of good sperm count and excellent morphology. A temporary low percentage of active cells (with high sperm count) may be present where the period of continence is long. In such cases, the number of active sperms may be markedly increased by increasing the frequency of intercourse. And this can improve the chances of conception. But when poor motility is chronic, inspite of adequate sperm count and good morphology, it is often due to failure of the epithelium of the epididymis and the vas deferens. Poorly functioning ductal epithelium may contribute to poor sperm motility in the ejaculate. It is not clearly known whether the ductal epithelium is under the influence of thyroid, androgenic steroids or vitamins such as vitamin A, E, and B complex; for these preparations are often prescribed in an attempt to correct this defect and some cases do seem to profit but there is no reliable evidence to support this hypothesis.
The study of morphology with meticulous care and in detail is essential. A spermatogram should be a part of routine examination for sterility. The degree of aberration in structure of sperms and their poorness of motility go hand in hand. Fair motility in the presence of a large number of abnormal spermatozoa is rare. Spermatozoa with gross deviation in structure such as giant or pin heads are capable of aggressive forward motion and do not possess the capacity for fertilization of the ovum. Abnormal forma do not survive in the cervical mucus, and hence cannot be demonstrated in the post coital examination. Sterility in the presence of a high degree of abnormality in spermatozoa is definitely related to the failure of these cells to reach the ovum. The gross aberration in sperm structure may be due to various causes such as ingestion of drugs, poor blood supply to the testicles, and toxins which are known to produce changes in human spermatogenesis. There is a definite suggestion that some part of the male infertility problem is environmental rather than congenital. The poor sperm morphology is related to poor testicular function. Abnormal morphology is rare with good motility and good sperm count. The testicular disturbance, poor sperm morphology and oligospermia usually co-exist. Treatment consists in finding out and eradicating the cause.
Causes of male sterility
Impotence either psychogenic, physical or organic in origin may be responsible in a small percentage of cases. Sexual anxiety disseminated multiple sclerosis, diabetic neuropathy and drugs taken to reduce blood pressure etc. can induce impotency. Treatment of these cases is often difficult.
Congenital anomalies such as an extreme degree of hypospadias and ejaculate antepartus, in which artificial insemination is the treatment of choice.
Plastic induration of the penis (peyronie’s disease) or thrombosis in the corpora cavernosum or badly performed circumcision can seriously hinder normal marital relations.
Urethral stricture or stenosis .
Testicular affections – orchitis, gumma, trauma, atrophy, undescended testicles etc. Timely prevention of damage to the testicles should be the objective. In cases of mumps, rest in bed, prescribing in time anti-viral drugs, and diethylstilbestrol 2 mg daily can save the testis from damage. Early surgical interference in cases of hydrocele, hernia and varicocele is indicated. Improvement of sperm count and motility is a dominant feature after operation. In cases of cryptorchidism, injections of chorionic gonadotropins at early stages and Torek operation at one or two years before puberty should be considered.
Endocrine disturbances – thyroid, pituitary or adrenal – On clinical examination, hypogonadism is obvious. Testicular biopsy is helpful in determining the measures to be employed.
Hydrocele, hernia and varicocele . Any of these conditions produce progressive pressure, promotes fibrosis, reduces size of testis and impairs testicular function. Early operation should be done. Results are excellent.
Azoospermia – Absence of spermatozoa in the semen. It is encountered in about 5% of sterile males. For confirmation, examination of the centrifuged semen is necessary. It may be occlusive or non-occlusive; congenital absence of vas deferens, complete atrophy of the testicles, x-ray exposures and long-standing hydrocele or hernia of large size can be responsible. Donor insemination is the only remedy.
Oligospermia – It is the most common cause of male infertility. The causes which lead to the reduction in the number of spermatozoa are: - undescended testicles, hypogonadism, viral orchitis, prolonged fever, toxaemia, irradiation, hydrocele, varicocele, inguinal hernia etc. It is of importance to determine whether oligospermia is due to the defect in spermatogenesis or due to post-inflammatory changes. It is also necessary to discriminate between the forms of oligospermia which will respond to treatment and those which will derive no benefit from it. From these points of view, careful examination of the patient, his genitals, secondary sexual characters, sperm count, spermatogram and biopsy are considered necessary. To find out the efficacy of therapy, repeated examinations of semen and biopsies have to be undertaken. In most cases of oligospermia, it is difficult to elevate the sperm count. There is no satisfactory adequate evidence at present, that hormone therapy in the form of gonadotropins, steroids or thyroid derivatives have any beneficial effect on the sperm count. Where the sperm count fluctuates between 3 and 30 million/ml response is very doubtful, while where it shows values between 25 to 70 million/ml, the response is likely to be satisfactory. New human gonadotropins may be effective in selected cases of azoospermia such as primary pituitary failure where the testicular biopsy reveals germinal cells at the primitive level. The combined gonadotropins therapy of HMG or HPG plus HCG (human menopausal or pituitary hormone and human chorionic gonadotropins) has been found to be effective in such cases. However, in cases of oligospermia in which maturation of spermatozoa is present, indicating normality of gonadotropins hormone, administration of gonadotropins will be superfluous and, indeed, of no value. Androgenic steroids which depress temporarily spermatogenesis are often prescribed in oligospermia to produce what is called ‘rebound phenomenon’; but the actual experience does not seem to prove its utility or help the cause.
Varicocele – may impair testicular function so as to produce human infertility. It elevates the temperature in the scrotum, produces increased pressure and inhibits spermatogenesis either by thermal or chemical action. In varicocele, retrograde blood flow from the renal vein down the left internal spermatic vein is common. Whatever may be the actual process, impaired fertility is often associated with varicocele; and removal of the varicocele or the conditions which gives rise to it, causes marked improvement in the semen quality leading to fertility. High ligation of the left internal spermatic vein invariably leads to total or partial recovery. Hence it is a fine tool in the male infertility. The high incidence of male infertility may be due to a deficient blood circulation of the testicles.
In treating oligospermia, following objectives should be kept in mind:-