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The testes are the primary reproductive organs or gonads in the male. They are ovoid, reproductive and endocrine organs responsible for sperm production and testosterone production. They are suspended in the scrotum by scrotal tissues including the dartos muscle and spermatic cords. Average testicular dimensions are 4–5 cm in length, 2.5 cm in breadth and 3 cm in anteroposterior diameter; their weight varies from 10.5–14 g. The left testis usually lies lower than the right testis. Each testis lies obliquely within the scrotum, the upper pole tilted anterolaterally and the lower posteromedially. The anterior aspect is convex, whereas the posterior aspect is nearly straight and has the spermatic cord attached to it. Anterior, medial and lateral surfaces and both poles are convex, smooth and covered by the visceral layer of the serosal tunica vaginalis, the parietal layer and the scrotal tissues, in that order from within outwards (Fig. 76.4). Each testis is separated from its fellow by a fibrous median raphe which is deficient superiorly. The posterior aspect of each testis is only partly covered by serosa; the epididymis adjoins its lateral part (see below). The testis is invested by three coats, which are, from outside inwards, the tunica vaginalis, tunica albuginea and tunica vasculosa (Fig. 76.4).


Fig. 76.4  The left testis, exposed by incising and laying open the cremasteric fascia and parietal layer of the tunica vaginalis on the lateral aspect of the testis.
(From Sobotta 2006.)

Tunica vaginalis

The tunica vaginalis is the lower end of the peritoneal processus vaginalis, whose formation precedes the descent of the fetal testis from the abdomen to the scrotum (see p. 1320). After this migration, the proximal part of the tunica, from the internal inguinal ring almost to the testis, contracts and is obliterated, leaving a closed distal sac into which the testis is invaginated. The tunica is reflected from the testis onto the internal surface of the scrotum, so forming the visceral and parietal layers of the tunica. The visceral layer covers all aspects of the testis except most of the posterior aspect. Posteromedially it is reflected forwards to the parietal layer. Posterolaterally it passes to the medial aspect of the epididymis and lines the epididymal sinus, and then passes laterally to its posterior border where it is reflected forwards to become continuous with the parietal layer. The visceral and parietal layers are continuous at both poles, but at the upper pole the visceral layer surmounts the head of the epididymis before reflexion. There is always a very fine film of fluid between the two layers of the tunica vaginalis. This fluid layer can increase in inflammatory and neoplastic conditions of the testis, leading to a hydrocele (see below).

The more extensive parietal layer reaches below the testis and ascends in front of and medial to the spermatic cord. The inner surface of the tunica vaginalis has a smooth, moist mesothelium: the potential space between its visceral and parietal layers is termed the cavity of the tunica vaginalis.

Tunica albuginea

The tunica albuginea is a dense, bluish-white covering for the testis, composed mainly of interlacing bundles of collagen fibres. It is covered externally by the visceral layer of the tunica vaginalis, except at the epididymal head and tail and the posterior aspect of the testis, where vessels and nerves enter (Fig. 76.5A,B). The tunica vaginalis covers the tunica vasculosa and, at the posterior border of the testis, projects into the testicular interior as a thick, incomplete fibrous septum, the mediastinum testis, which extends from the upper to the lower end of the testis. Testicular vessels run within the mediastinum testis.


Fig. 76.5  A, Vertical section through the testis and epididymis, showing the arrangement of the ducts of the testis and the mode of formation of the vas deferens (B).
(From Sobotta 2006.)

Tunica vasculosa

The tunica vasculosa contains a plexus of blood vessels and delicate loose connective tissue, and extends over the internal aspect of the tunica albuginea, covering the septa and therefore all the testicular lobules.

Vascular supply and lymphatic drainage

Testicular arteries

The testicular arteries are two long, slender vessels which arise anteriorly from the aorta a little inferior to the renal arteries. Each passes inferolaterally under the parietal peritoneum on psoas major. The right testicular artery lies anterior to the inferior vena cava and posterior to the horizontal part of the duodenum, right colic and ileocolic arteries, root of the mesentery and terminal ileum. The left testicular artery lies posterior to the inferior mesenteric vein, left colic artery and lower part of the descending colon. Each artery crosses anterior to the genitofemoral nerve, ureter and the lower part of the external iliac artery and passes to the deep inguinal ring to enter the spermatic cord and travel via the inguinal canal to enter the scrotum (Figs 76.3A, 76.6). At the posterosuperior aspect of the testis the testicular artery divides into two branches on its medial and lateral surfaces: these pass through the tunica albuginea and ramify in the tunica vasculosa. Terminal branches enter the testis over its surface. Some pass into the mediastinum testis and loop back before reaching their distribution. Capillaries lying next to seminiferous tubules penetrate the layers of interstitial tissue and may form part of the ‘blood–testis’ barrier. They run either parallel to the tubules or across them but do not enter their walls. They are separated from germinal and supporting cells by a basement membrane and variable amounts of fibrous tissue containing interstitial cells: selective exchange phenomena involving androgens and immune substances occur here.


Fig. 76.6  Arterial blood supply and venous drainage of the testis.
(From Sobotta 2006.)

In the abdomen the testicular artery supplies perirenal fat, the ureter and iliac lymph nodes, and in the inguinal canal it supplies cremaster. Sometimes the right testicular artery passes posterior to the inferior vena cava. The testicular arteries represent persistent lateral splanchnic aortic branches that enter the mesonephros and cross ventral to the supracardinal vein, but dorsal to the subcardinal vein. Normally the lateral splanchnic artery – which persists as the right testicular artery – passes caudal to the suprasubcardinal anastomosis, which forms part of the inferior vena cava. When it passes cranial to the anastomosis, the right testicular artery lies behind the inferior vena cava.

The testis also receives blood from the cremasteric branch of the inferior epigastric artery, and from the artery to the vas deferens (Fig. 76.6). Interference with the testicular artery high in the abdomen therefore usually leaves the testis unharmed, whereas interruption in the region of the spermatic cord may interfere with all of these vessels and lead to infarction. Ligating both the testicular artery and vein high up interrupts the venae comitantes of the artery which anastomose with the internal spermatic veins and can be responsible for recurrence of a varicocele (see below).

Testicular veins

The testicular veins emerge posteriorly from the testis, drain the epididymis and unite to form the pampiniform plexus, a major component of the spermatic cord that ascends anterior to the vas deferens (Fig. 76.7). In the inguinal canal the pampiniform plexus is drained by three or four veins which run into the abdomen through the deep inguinal ring. Within the abdomen these veins coalesce into two veins, which ascend on each side of the testicular artery, anterior to psoas major and the ureter, and behind the peritoneum. The left veins pass behind the lower descending colon and inferior margin of the pancreas and are crossed by the left colic vessels, and the right veins pass behind the terminal ileum and horizontal part of the duodenum and are crossed by the root of the mesentery, ileocolic and right colic vessels. The veins join to form single right or left testicular veins: the right testicular vein opens into the inferior vena cava at an acute angle just inferior to the level of the renal veins, and the left testicular vein opens into the left renal vein at a right angle (Fig. 76.7). The testicular veins contain valves.


Fig. 76.7  Multislice CT of the inferior vena cava showing the left testicular vein draining to the left renal vein and the right testicular vein draining directly to the inferior vena cava. 1. Right testicular vein. 2. Inferior vena cava. 3. Left renal vein. 4. Left testicular vein.

The testicular veins in the scrotum and inguinal canal may be varicose in up to 15% of the male population. In fact between 25–35% of men with fertility problems may also have a varicocele. Varicocele formation, which is almost always on the left, may be due to the orthogonal junction of the left testicular and renal veins. There is evidence that the presence of a varicocele raises testicular temperature and impairs spermatogenesis. Varicoceles may also cause testicular pain, which is often a dragging type of pain experienced towards the end of the day after long periods of standing. Varicoceles may be treated surgically for pain but the role of varicocele surgery for treating male infertility is controversial. Varicoceles can also be treated by radiological embolization of the left testicular vein via a right femoral vein approach. After ligation of a varicocele, venous return is by the small veins of the vas deferens, cremaster and scrotal tissues.

Lymphatic drainage

Testicular vessels start in a superficial plexus under the tunica vaginalis and a deep plexus in the substance of the testis and epididymis. Four to eight collecting trunks ascend in the spermatic cord and accompany the testicular vessels on psoas major, ending in the lateral aortic and pre-aortic nodes.


Testicular nerves accompany the testicular vessels and are derived from the tenth and eleventh thoracic spinal segments via the renal and aortic autonomic plexuses. Catecholaminergic nerve fibres form plexuses around smaller blood vessels and among the interstitial cells in the testis and epididymis.


The surface of the testis is covered closely by the visceral tunica vaginalis, a layer of flat mesothelial cells similar to, and continuous with, the peritoneal lining. The visceral layer is separated from the parietal tunica vaginalis (the outer layer of the double fold of peritoneum that accompanies the descending testis (see p. 1320)), by a potential space containing serous fluid, which acts as a lubricant and allows movement of the testis within the scrotum. The testicular capsule proper, the tunica albuginea, is tough and collagenous and thickened posteriorly as the mediastinum testis. Beneath the tunica albuginea is a thin layer of connective tissue containing the superficial blood vessels. Blood vessels, lymphatics and the genital ducts enter or leave the body of the testis at the mediastinum (Fig. 76.8).


Fig. 76.8  Colour Doppler scan of the scrotal contents showing normal flow. The linear echogenic band (arrow) seen centrally represents the mediastinum testis composed of fibrofatty material.

Septa from the mediastinum extend internally to partition the testis into approximately 250 lobules (Fig. 76.5A). These differ in size, and are largest and longest in the centre. Each lobule contains one to four convoluted seminiferous tubules, much-coiled loops whose free ends both open into channels (the rete testis) within the mediastinum. The loose connective tissue between seminiferous tubules contains several layers of contractile peritubular myoid cells and clusters of androgen-producing interstitial (Leydig) cells.

There are 400–600 seminiferous tubules in each testis, each 70–80 cm long and 0.12–0.3 mm. in diameter. They are pale in early life, but in old age they contain much fat and are deep yellow. Each tubule is surrounded by a basal lamina, on which rests a complex, stratified seminiferous epithelium containing spermatogenic cells and supportive Sertoli cells (Fig. 76.9A). When active, the spermatogenic cells include basally situated spermatogonia and their progeny in the adluminal compartment, spermatocytes, spermatids and mature spermatozoa. Among the spermatids may be residual bodies, spherical structures derived from surplus spermatid cytoplasm shed during maturation and phagocytosed by Sertoli cells.


Fig. 76.9  A, Seminiferous tubules (ST; cut in various planes of section), and the interstitial tissue (Leydig cells, L) of the testis. The seminiferous tubules are highly convoluted and lined by a stratified epithelium which consists of cells in various stages of spermatogenesis and spermiogenesis (collectively referred to as the spermatogenic series). Non-spermatogenic cells are the Sertoli cells. B, Human seminiferous tubule showing the differentiation sequence of spermatozoa from basally situated spermatogonia (SG). Large primary spermatocytes (SC) have characteristic threadlike chromatin in various stages of prophase of the first meiotic division. Smaller haploid spermatids (ST) have round nuclei initially, but mature to possess the dense, elongated nuclei and flagellae of spermatozoa (SZ). Sertoli cells (S) are identified from their oval or pear-shaped nuclei orientated perpendicular to the basal lamina, and prominent nucleoli. The tubule is surrounded by peritubular myoid cells (M). Clusters of large endocrine Leydig cells (L) are seen in the interstitial connective tissue.


Spermatogonia, the stem cells for all spermatozoa, are descended from primordial germ cells which migrate into the genital cords of the developing testis (Fig. 76.9B). In the fully differentiated testis they are located along the basal laminae of the seminiferous tubules. Several types of spermatogonia are recognized on the basis of cell and nuclear dimensions, distribution of nuclear chromatin (dark, condensed or pale, euchromatic) and histochemical and ultrastructural data. The three basic groups of spermatogonia are dark type A (Ad), pale type A (Ap), and type B. Ad cells divide mitotically to maintain the population of spermatogonia which, before puberty, is small but increases under androgenic stimulation. Some divisions give rise to Ap cells which also divide mitotically but remain linked in clusters by fine cytoplasmic bridges. These are the precursors of type B cells, which are committed to the spermatogenic sequence. At about the time that type B cells enter a final round of DNA synthesis, without undergoing cytokinesis, they leave the basal compartment and cross the blood–testis barrier to enter meiotic prophase as primary spermatocytes. These coordinated processes are under the control of Sertoli cells.

Primary and secondary spermatocytes

Primary spermatocytes have a diploid chromosome number but duplicated sister chromatids (DNA content is thus 4N, where N is the DNA content of haploid spermatozoa), and are all at some stage of a long meiotic prophase (p. 22) of approximately 3 weeks. Primary spermatocytes are large cells with large round nuclei in which the nuclear chromatin is condensed into dark, threadlike, coiled chromatids at different stages in the process of crossing over and genetic exchange between chromatids of maternal and paternal homologues. These cells give rise to secondary spermatocytes with a haploid chromosome complement (but 2N DNA content), the reduction division is designated as meiosis I. Few secondary spermatocytes are seen in tissue sections because they rapidly undergo the second meiotic (equatorial) division, where sister chromatids separate (DNA content now being N), to form haploid spermatids. Theoretically each primary spermatocyte produces four spermatids, but some degenerate during maturation so that the yield is lower.


Spermatids do not divide again but gradually mature into spermatozoa by a series of nuclear and cytoplasmic changes known as spermiogenesis. All of these maturational changes take place while the spermatids remain closely associated with Sertoli cells and linked by cytoplasmic bridges with each other. The first phase of spermiogenesis is the Golgi phase, when hydrolytic enzymes accumulate in Golgi vesicles that subsequently coalesce into a single large acrosomal vesicle close to the nucleus. The pair of centrioles migrates to the opposite posterior pole. The distal centriole begins to generate the axoneme, a circular arrangement of nine microtubule doublets surrounding a central pair. In the cap phase, the acrosomal vesicle flattens and envelops the anterior half of the nucleus to form an acrosomal cap which comes to occupy the presumptive anterior pole of the spermatozoon, furthest from the lumen of the tubule.

During the acrosome phase, nuclear chromatin condenses and the nucleus elongates into a spearhead shape. The anterior cytoplasmic volume is considerably reduced, so that the wall of the acrosomal vesicle is brought into contact with the plasma membrane. A perinuclear sheath of microtubules develops from the posterior edge of the acrosome to form the manchette, which extends towards the posterior pole. The axonemal complex continues to extend into the developing tail region, which now protrudes into the tubule lumen. The neck region forms at the posterior pole of the nucleus: it contains the centrioles. Mitochondria migrate through the neck region and along the axoneme into the developing middle piece. Here, they assemble into a helical sheath and surround a ring of nine coarse fibres forming along the length of the axonemal complex in the developing tail. In the final phase of maturation, excess cytoplasm is detached as a residual body that is phagocytosed and degraded by Sertoli cells. During the formation of residual bodies, spermatids lose their cytoplasmic bridges and separate from each other before being released into their tubule.


A spermatozoon that is released from the wall of the seminiferous tubule into the lumen is non-motile but structurally mature. Its expanded head contains little cytoplasm and is connected by a short constricted neck to the tail. The tail is a complex flagellum, divided into middle, principal and end pieces, that greatly exceeds the head region in volume. The head has a maximum length of approximately 4 μm and a maximum diameter of 3 μm. It contains an elongated, flattened nucleus with condensed, deeply staining chromatin, and is covered anteriorly by an acrosomal cap. The latter contains acid phosphatase, hyaluronidase, neuraminidase and proteases necessary for fertilization (see p. 168). The neck is approximately 0.3 μm long. In its centre is a well-formed centriole that corresponds to the proximal centriole of the spermatid from which it differentiated. The axonemal complex is derived from the distal centriole. A small amount of cytoplasm exists in the neck, covered by a plasma membrane continuous with that of the head and tail (Fig. 76.10).


Fig. 76.10  The main ultrastructural features of a mature spermatozoon.

The middle piece of the tail is a long cylinder, approximately 1 μm in diameter and 7 μm long. It consists of an axial bundle of microtubules, the axoneme, outside which is a cylinder of nine dense outer fibres surrounded by a helical mitochondrial sheath. At the caudal end of the middle piece is an electron-dense body, the anulus. The principal piece of the tail becomes the motile part of the cell. It is approximately 40 μm long and 0.5 μm in diameter and forms the majority of the spermatozoon. The axoneme and the surrounding dense fibres are continuous from the neck region through the whole length of the tail except for its terminal 5–7 μm, in which the axoneme alone persists. The tail therefore has the typical structure of a flagellum, with a simple nine plus two arrangement of microtubules, in the terminal portion of the end piece.

Sertoli cells

Sertoli cells form a major cellular component of the tubule before puberty, and in the elderly. They are the supporting, non-spermatogenic cells of the seminiferous tubules. Variable in overall cell shape, they all contact the basal lamina and their cytoplasm extends to the tubule lumen where their apical plasma membranes form complex recesses which envelop spermatids and spermatozoa until the latter are mature enough for release. Long cytoplasmic processes also extend between the spermatogonia in the basal compartment and spermatocytes in the adluminal compartment of the tubule. Adjacent Sertoli cell processes are joined at this level by tight junctions, creating a diffusion barrier between the extratubular and intratubular compartments. This is the blood–testis barrier which, if breached by traumatic or inflammatory events, can allow immune responses to develop against sperm antigens, resulting in subfertility.

The Sertoli cell nucleus is euchromatic and irregular or pear-shaped, contains one or two prominent nucleoli, and is usually aligned perpendicular to the basal lamina. The cytoplasm is rich in lysosomes, consistent with its phagocytic phenotype. Sertoli cells provide trophic support for the surrounding germ cells, secrete androgen-binding protein and play an important role in controlling spermatocyte and spermatid differentiation and maturation. The proteinaceous fluid they secrete into the tubule lumen provides nutrients and facilitates the transport of spermatozoa into the excurrent duct system. Sertoli cells change considerably during the spermatogenic cycle and respond to the hypophysial hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). They also produce a hormonal substance, inhibin B, which is thought to be involved in local paracrine functions.

Spermatogenic cycle

At any locus in a seminiferous tubule, generation of germ cells occurs in a cycle with a periodicity of approximately 16 days. Stages in the cycle are characterized by the presence of different combinations of cells within the spermatogenic sequence. The generation of a mature spermatozoon from a spermatogonium takes four such cycles, or approximately 64 days. In cross-section, the seminiferous tubule shows more than one phase of the cycle around its circumference, because waves of progression through a spermatogenic cycle occur in spirals down the length of the tubule.

Testicular interstitial tissue

The tissues between the seminiferous tubules include various connective tissue components, peritubular myoid cells, vessels and nerves. The myoid cells are contractile: their rhythmic activity may propel non-motile spermatozoa through the tubule towards the rete testis and excurrent ductal system. Clusters of Leydig cells lie between the tubules. These large, polyhedral cells have eccentric nuclei with one to three nucleoli and pale staining cytoplasm containing a considerable amount of smooth endoplasmic reticulum, lipid droplets and unique needle-shaped crystalloid inclusions up to 20 μm long (crystals of Reinke), of unknown function. Leydig cells synthesize and secrete androgens and are stimulated by LH and by prolactin, which induces expression of the LH receptor. Their activity varies with age: they are active in fetal life in the development of the genital tract, but decline in function postpartum until the onset of puberty.

Age-related changes in the testis

Functionally, the fetal testis is predominantly an endocrine gland that produces testosterone and the anti-Müllerian hormone, a specifically fetal gonadal hormone. These two hormones play crucial roles in the induction and regulation of male sexual differentiation. Postnatally the testis gradually changes its role, but retains the ability to manufacture testosterone and other regulatory materials, e.g. the peptide hormone oxytocin, that act in either an endocrine or a paracrine fashion.

The seminiferous tubules do not become canalized until approximately the seventh month of gestation, although this may occur later. At puberty, the testis becomes primarily a source of spermatozoa. The fetal Leydig cells, responsible for the androgen-induced differentiation of the male genitalia, degenerate after birth, and are replaced, during puberty, by an adult population of androgen-producing cells that persist throughout adult life. The testes grow slowly until the age of 10 or 11 years, at which time there is a marked acceleration of growth rate, and spermatogenesis begins.

There is no definite age for the onset of the progressive testicular involution associated with advancing age. Testicular size, sperm quality and quantity, and the numbers of Sertoli cells and Leydig cells, have all been reported to decrease in the elderly. Leydig cell activity is driven by LH. The decrease in Leydig cell function in the elderly, as part of what has been described as the normal ageing process, may be affected by changes in the secretion of LH, which is controlled by the hypothalamus. The volume occupied by the seminiferous tubules decreases, whereas that occupied by interstitial tissue remains approximately constant. The most frequently observed histological change in the ageing testis is variation in spermatogenesis in different seminiferous tubules: it is complete, though reduced, in some, but absent in others, when sclerosis may occur. In tubules where spermatogenesis is complete, morphological abnormalities, e.g. multinucleation, may be observed in the germ cells.

Germ cell loss generally begins with the spermatids, but progressively affects the earlier germ cell types, i.e. the spermatocytes and spermatogonia. Sertoli cells are also affected by ageing, and show a range of morphological changes including dedifferentiation, mitochondrial metaplasia and multinucleation. In the Leydig cells, the quantity of smooth endoplasmic reticulum and mitochondria decrease, and lipid droplets, crystalline inclusions and residual bodies increase; some cells become multinucleate. Tubules in which the entire epithelium has been lost have been observed in testes where other tubules appeared normal. The development of tubular involution with advancing age is similar to that observed after experimental ischaemia, suggesting that vascular lesions may be involved in age-related testicular atrophy. However, there is no abrupt change in testicular function equivalent to the female climacteric.

Undescended testis

In the early fetal period the testes are located posteriorly in the abdominal cavity. Their descent to the scrotum appears to be under hormonal control (gonadotropins and androgens) (see p. 1320). Testicular descent may be arrested at any point along its route into the scrotum: a clinically undescended testis may be in the abdomen, at the deep inguinal ring, in the inguinal canal, or between the superficial inguinal ring and the scrotum. Occasionally, the testis may lie outside its normal path of descent and is termed an ectopic testis.

A unilateral undescended testis is present in 3% of boys at birth and 1% of boys by 3 months of age. Bilateral maldescent is seen in just over 1% of male births. Undescended testes can be associated with a higher risk of infertility and testicular tumours. There is evidence that surgical correction of an undescended testis at any age may not improve its spermatogenesis. Impairment of fertility can be seen in men with both bilateral and unilateral undescended testis. Leydig cell function is not usually affected by maldescent, so androgen production usually remains within the normal range. Patients with an undescended testis are at increased risk of developing testicular tumours, particularly seminoma. The risk is highest in abdominal testes. Surgery may not reduce the risk of tumour development, but maximizes the chance of early detection of any tumour. An undescended testis can usually be found by ultrasonography if it is in or close to the inguinal canal. Laparoscopy is more reliable in the pelvis. Magnetic resonance imaging may help localizing testis not seen on ultrasound. Retention in the inguinal canal is often complicated by congenital hernia, because the processus vaginalis remains patent. The testis may traverse the canal but reach an abnormal site.

Obliterated part of the processus vaginalis

The obliterated part of the processus vaginalis is often seen as a fibrous thread in the anterior part of the spermatic cord, extending from the internal end of the inguinal canal – where it is connected to the peritoneum – as far as the tunica vaginalis. Sometimes it disappears within the cord. However, its proximal part may remain patent, so that the peritoneal cavity communicates with the tunica vaginalis, or the proximal processus may persist, although it may be shut off distally from the tunica. Occasionally its cavity may persist at an intermediate level as a cyst. When patent, its cavity may admit a loop of intestine, to form an indirect inguinal hernia. The processus is usually obliterated by 18 months of age.

Hydrocele, spermatocele, epididymal cyst

In congenital hydrocele the fluid is in the tunical sac, which communicates with the peritoneal cavity through a non-obliterated processus vaginalis. Infantile hydrocele occurs when the processus is obliterated only at or near the deep inguinal ring. It resembles vaginal hydrocele, but fluid extends up the cord into the inguinal canal. If the processus is obliterated at both the deep inguinal ring and above the epididymis, leaving a central open part, this may distend as an encysted hydrocele of the cord. A spermatocele is a cyst related to the caput epididymis: it may contain spermatozoa and it is probably a retention cyst of one of the seminiferous tubules. Removal is usually unnecessary and may result in epididymal obstruction. The same applies to a simple epididymal cyst, which may have a similar aetiology to a spermatocele but remains free of sperm.

Testicular and epididymal appendices

At the upper extremities of the testis and epididymis are two small, stalked bodies, the appendix testis and appendix epididymis (Fig. 76.5A,B). They are developmental remnants of the paramesonephric (Müllerian) duct and the mesonephros, respectively. They may undergo torsion and produce symptoms that are difficult to differentiate from testicular torsion.

Testicular torsion

The testis and epididymis are usually fixed to their surrounding tissues. In some patients this fixation may be insufficient, so that the structures are able to twist within the tunica vaginalis. This is termed testicular torsion and normally results in severe scrotal pain, which is a surgical emergency. Torsion produces an initial venous infarction followed by arterial occlusion: histopathological changes leading to gangrene occur in the testis if the twist is not reversed within 4–6 hours. Fertility may be affected by an episode of torsion. Other structures may also twist within the scrotum, e.g. the testicular appendix (otherwise termed the hydatid of Morgagni) and the appendix epididymis: torsion of these structures may also result in scrotal pain.

Male sub-fertility

Approximately one in seven couples will find difficulty in conceiving. In approximately 10% of couples the cause for their sub-fertility will be unknown: in 50% of couples, the reason will be due to male factors. A seminal analysis may demonstrate a spectrum of abnormalities from complete absence of sperm in the ejaculate (azoospermia) to too few sperm (oligozoospermia).

The causes of azoospermia are extensive but broadly can be classified into obstructive causes (rare) or testicular failure. Occasionally spermatogenesis may be arrested at a specific point in development, a condition known as maturation arrest.

Testicular failure is usually testicular in origin. It may have an underlying genetic aetiology, or may occur secondary to damage to the testis such as occurs following radiation therapy, torsion, trauma to the testis or undescended testis. Testicular failure resulting from these conditions may be associated with an increase in pituitary FSH and LH (hypergonadotrophic hypogonadism). Rarely, testicular failure may be the result of pituitary or hypothalamic damage leading to hypogonadotrophic hypogonadism. Histopathologically, testicular failure may be characterized by a spectrum of histopathological findings from Sertoli-cell-only syndrome (see Fig. 76.12) to varying degrees of hypospermatogenesis. Testicular sperm can be extracted from some men and injected into their partners’ eggs, a process known as intra-cytoplasmic sperm injection (ICSI).


Fig. 76.12  Testis biopsy from a patient with azoospermia demonstrating Sertoli-cell-only syndrome. Only the Sertoli cells are present: this condition may also be caused by a deletion on the Y chromosome.

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