AZOOSPERMIA AND ASPERMIA*
0 . J. POLLAK, M.D.
From the Wilmington General Hospital, Wilmington, Delaware
No matter what text book one consults, the chapter on semen examination
is rather brief and incomplete. Erroneous statements appear even in the latest
editions. Such terms as "azoospermia" and "aspermia" are usually confused
(Table 1) and are often misleadingly called "non-obstructive" and "obstructive
azoospsrmia". Azoospsrmia and aspsrmia are two distinct entities differentiated by cytodiagnosis5 of the ejaculate. Testicular biopsies aid in the differentiation of alterations in azoospermia and form the basis for treatment in
aspermia.
TABLE 1
DISTINCTION BETWEEN AZOOSPERMIA AND ASPERMIA
AZOOSPERMIA
No spermatozoa
CYTOSPERMIA
Testicular elements present in semen
Testicular biopsy always subnormal (hypoplasia or atrophy)
Misleadingly called "non-obstructive azoospermia"
ASPERMIA
No semen
No testicular cells, no spermatozoa
ACYTO-AZOOSPERMIA
No testicular elements in ejaculate
Testicular biopsy usually normal
Falsely called "obstructive azoospermia"
Azoospermia indicates that the semen lacks spermatozoa, but early cells of
the spermatogenic series are invariably present. Such cells usually are detected
in direct smears and always are found in stained films of centrifuged material.
The term "cytospermia" is appropriate for such semen. In aspermia, on the
other hand, the ejaculate is devoid of all testicular elements, consists of secretions of the accessory glands only and should not be called semen. The term
"acytoazoospermia" could be used for such an ejaculate.
In azoospermia, the microscopic picture of the semen (spermiocytogram)
reflects the quality of the germ tissue. The spermatocytes or the spermatogonia
present the end state of spermatogenesis. Azoospermia occurs with testicular
hypoplasia as in cryptorchidism or late descent of the testicle; atrophy as in
endocrinopathies, constitutional factors, circulatory disturbances, or mechanical
* Presented at the Twenty-Sixth Annual Meeting of the American Society of Clinical
Pathologists, in Chicago, October 28, 1947. Received for publication, October 28, 1947.
542
AZOOSPERMIA AND ASPERMIA
F I G . 1. Normal testicle. Testicles were of normal size. There was bilateral postgonorrhoic epididymal obstruction. Ejaculate showed aspermia. X 800.
F I G . 2. Testicular hypoplasia. T h e right testicle had not descended; the
left testicle was one-third normal size and had descended late. Ejaculate
showed azoospermia. X 800.
F I G . 3. Testicular atrophy, grade 1. T h e testicles were of normal size.
The cause of the a t r o p h y was undetermined. Ejaculate showed oligospermia. X 800.
F I G . 4. Testicular atrophy, grade 2, with m a t u r a t i o n arrest. T h e
testicles were two-thirds normal size. T h e autopsy revealed a neuroblastoma of the pituitary gland. Ejaculate showed azoospermia. X SOO.
543
544
POLLAK
FIG. 5. Testicular atrophy, grade 3, with interstitial edema. The
testicles were of normal size. A possible cause of the atrophy was chronic
osteomyelitis. Ejaculate showed asthenospermia. X 800.
FIG. 6. Testicular atrophy, grade 3, with peritubular fibrosis. The
testicles were of normal size. The cause of the atrophy was undetermined.
Ejaculate showed azoospermia. X 800.
FIG. 7. Testicular atrophy, grade 3, with hyperplasia of interstitial
cells. The testicles were slightly smaller than normal. The cause of the
atrophy was undetermined. Ejaculate showed azoospermia. X 830.
FIG. S. Testicular atrophy, grade 3, with sclerotization of interstitial
tissue. The cause of the atrophy was undetermined. (The patient was a
chronic alcoholic.) The testicles were of normal size. Ejaculate showed
asthenospermia. X 800.
AZOOSPERMIA AND ASl'EKMIA
545
interference with spermatogenesis; and degeneration.6 Testicular biopsies aid
in the differentiation of these changes. Hypoplasia is characterized by the
presence of separated, isolated tubules which show a maturation arrest resulting
from failure of development of the third zone of the germ tissue, less frequently
by central collections of Sertoli's cells. Atrophy is characterized by edema and
vacuolization of spermatids and even younger cells, and by decrease in the
height of the germ tissue layers. Accordingly, in the presence of a single layer
of cells, there are various degrees of depression of function up to cessation of
spermatogenesis. At the present time, differentiation of the many causes of
F I G . 9. Testicular degeneration with diffuse hyalinization. Testicles
were of normal size. T h e cause of the degeneration was a t t r i b u t a b l e to
pulmonary and bilateral epididymal tuberculosis. Ejaculate showed
aspermia. X 800.
F I G . 10. Testicular degeneration with hyalinization and diffuse fibrosis.
The testicles were about one-fourth the normal size. Cause of the degeneration was hypernephroma. Ejaculate showed azoospermia. X S00.
these alterations cannot be based on results of testicular biopsies. The concept that interstitial cell hyperplasia characterizes an endocrine disturbance
is not generally valid. Degeneration, that is, hyalinization of the tubules, is a
secondary process and follows complete atrophy. The term "degeneration"
is frequently used where "atrophy" is meant. In all these states there is shedding of germ cells.
I t is important to perform biopsies until sufficient knowledge is accumulated
to differentiate between testicular atrophy, based on certain endocrinopathies,
and atrophy clue to constitutional disorders, generalized infections or intoxications. Cryptorchidism can be repaired regardless of whether it is complete
or not. Treatment of testicular hypoplasia with androgens is successful only
546
POLLAK
when accompanied by external hypogenitalism.2 The treatment of other conditions causing azoospermia is not successful with the exception of those which
are caused by local circulatory disturbances or are due to local pressure.
Aspermia is due to bilateral absence of part or all of the internal sex organs,
or may be due to developmental or acquired obstruction of the seminal passages.
TABLE 2
DEVELOPMENTAL ANOMALIES WHICH HAVE A BEARING ON FERTILITY OF THE MALE
BILATERAL ANOMALIES
A. Testicular
Anorchidia
Cryptorchidism
total
partial
Late descensus
complete
incomplete
with epididymis
with head only
without epididymis
Hypoplasia
with rests of epididymis
without rests
FINDINGS I N EJACULATE
Aspermia
Azoospermia to normospermia*
Azoospermia to normospermia*
Azoospermia to normospermia*
Azoospermia to normospermia*
Azoospermia to normospermia*
Aspermiaft
Aspermiaf
Aspermia!
Aspermia
B. Epididymis
Anepididymis
Autonomous descensus
Aspermia
Aspermia!
C. Lower tract
Absence of ampulla
Absence of vas
Hypoplasia of vas
Aspermia
Aspermia
Aspermia to normospermia*
D. Combinations
Aspermia to normospermia*
* The findings depend on the age at descensus. The probability of events increases in
the following order: normospermia, oligospermia, hypospermia, asthenospermia and azoospermia.
f Developmental obstruction.
J Not certain.
Postgonorrhoic scars of the epididymis are the most common cause of aspermia
and a frequent cause of male sterility. Post-traumatic scars are less common
causes of aspermia while developmental anomalies are considered rare. With
the present progress of therapy, complications of gonorrhea should become less
and less frequent, and aspermia should become less common. Developmental
anomalies3 • 4 • 8 may acquire in' erest, since they are not as rare as is often believed (Table 2). The biopsy of the testicle in aspermia appears normal, unless
there is also one of the disorders leading to testicular alterations.
AZOOSPERMIA AND ASPEHMIA
547
In aspermia, thorough exploration of the anatomic causes is indicated. Where
aspennia is a symptom of developmental abnormalities, we have no treatment.
To ascertain the patency of seminal passages, irrigation 1 of the vas deferens
from the ampulla and probing7 of the ejaculatory ducts are attempted first. If
patency cannot be established by these procedures, one can perform epididymovasostomy. I t is imperative to ascertain the presence of normal spermatogenesis by testicular biopsies before attempting therapeutic procedures.
The occurrence of a combination of lesions should be kept in mind. Unilateral, late testicular descensus and contralateral obstruction may yield a
semen which shows azoospermia while on testicular biopsy, one of the gonads
may appear normal.
REFERENCES
1. CHAKNY, C. W.: Cited in reference 6.
2. J O E L , C. A . : D i e miinnliche Sterilitiit.
250,1945.
Monatschr. f. Geburtsh. u. Gyiu'ik., 120: 225-
3. L I C H T E N B E R G , A., V O E L C K E B , F . , AND W I N D B O L Z , H . : H a n d b u c h der Urologie.
4.
5.
6.
7.
8.
Spezielle
Urologie. Volume 3. Berlin: Julius Springer, 1928, 1095 p p .
Modern Urology. Edited by Hugh Cabot. Philadelphia: L e a and Febiger, 1918,
428 p p .
POLLAK, O. J . : Semen and seminal stains. Arch. P a t h . , 35: 140-196, 1943; p . 13 of extended reprint
POLLAK, 0 . J . : Theoretical and practical aspects of t h e problems of h u m a n sterility.
Delaware S t a t e M. J., 19: 157-162, 1947.
SIMMONS, F . A., AND S N I F F E N , R . : Testicular biopsy in the sterile male. T h e West. J .
of Surg., 55:503, 517, 1947.
T H O H E K , M A X : The H u m a n Testis. Philadelphia: J . JB. Lippincott Co., 1924, 548 p p .