Incomplete testicular descent affects 2–8 % of male newborns. Testicles located in the abdomen and inguinal canal are subject to a 2–3 °C temperature increase, which inhibits spermatogenesis and increases the risk of malignant transformation. Endocrine function, including testosterone production, is normal in undescended testicles. In cases of unilateral cryptorchidism, the contralateral testis has normal function and no increased risk of developing cancer. Approximately 20 % of undescended testicles are non-palpable. While ultrasound may be useful in identifying testicles in the inguinal canal, the gold standard for the diagnosis of intra-abdominal testicles is laparoscopy. In the past, it had been thought that intra-abdominal testicles carried a particularly elevated risk of malignant transformation when compared to more caudal locations; however, this has not been proven to be the case.

The testicles originate from the urogenital ridge. Initially, they are attached to the abdominal surface of the diaphragm by the cranio-suspensory ligament, which degenerates to allow testicular descent. Caudally, the testicles are attached to the gubernaculum testis, which guides the testicles into the scrotum. In the female, the cranio-suspensory ligament persists, forming the ovarian ligament, while the gubernaculum becomes the round ligament.

During testicular migration, the gubernaculum thickens considerably and widens the inguinal canal to allow testicular passage. The forces driving testicular descent appear to be an increase in intra-abdominal pressure as well as lengthening of the embryo while the gubernaculum remains with a fixed length. The idea that the gubernaculum “pulls” the testicle into the scrotum is no longer considered accurate. Testicular descent is an androgen-mediated process [1, 2].

Undescended testicles are at risk of malignant transformation, with a relative risk of 2.75–8 in relation to the normal population. Orchiopexy after puberty carries a two to sixfold risk of malignancy in comparison to prepubertal orchiopexy [3]. Surgically descended testicles have an increased risk of developing non-seminomatous tumors, while undescended testicles tend to develop seminomas [4]. Optimal treatment of cryptorchidism consists of orchiopexy, ideally between 6 and 12 months of age, and at worse before puberty in cases of delayed diagnosis. Cryptorchidism is always associated with a patent processus vaginalis that must be ligated at the time or orchiopexy. Undescended testicles diagnosed later in life should be removed. Occasionally observation may be acceptable in patients with high anesthesia risk or those older than 50 years [5, 6].

Treatment with human chorionic gonadotropin (hCG) has an efficacy of approximately 20 %, as compared to a 95 % success rate of surgery. In addition, there is evidence to suggest that hCG treatment may induce germinal cell apoptosis, leading to testicular atrophy and dysfunction later in life.

Another entity of interest is retractile testicle. They are defined as suprascrotal testis that can be easily manipulated into the scrotum and remain there without tension, until they ascend due to the cremasteric reflex. They carry no risk of infertility or malignancy. However, follow-up is recommended because up to one third of cases may become fixed in a suprascrotal position (acquired undescended testicles) [7].

As the testicles descend into the scrotum, they are preceded by the gubernaculums as well as by a fingerlike projection of peritoneum, which forms the processus vaginalis. The processus vaginalis normally becomes obliterated by the 36th–40th week of gestation (except for the portion that becomes the tunica vaginalis), thereby closing the internal inguinal ring. Frequently, the processus vaginalis is patent at birth and closes in early life. The left processus vaginalis becomes obliterated before the right, owing to the earlier descent of the left testicle [1].

Patency of the processus vaginalis is necessary for, but not synonymous with, the occurrence of indirect inguinal hernias and communicating hydroceles. It has been shown that inguinal hernias occur in only 8–12 % of patients with a patent processus vaginalis. Given the central role of patency of the processus vaginalis in pediatric inguinal hernias, treatment consists of high ligation of the hernial sac. In females, the processus vaginalis becomes the canal of Nuck, which normally becomes obliterated. However, the canal of Nuck may give rise to hydroceles, which manifest as inguinolabial masses [8–10].

In the adult, the tunica vaginalis is a two-layered mesothelial sac that envelops the testis almost completely, leaving the epididymal region uncovered (upper pole and posterior border).

The sensory innervation of the penis, scrotum, and pubic region is provided by multiple branches of the lumbar plexus. These nerves may be subject to injury during inguinal and pelvic surgery.

The ilioinguinal nerve supplies the base of the penis, upper scrotum, and medial thigh. It is readily identified in the inguinal canal where it courses anterior to the spermatic cord, just beneath the external oblique aponeurosis. The genital branch of the genitofemoral nerve accompanies the spermatic artery and vein along the dorsal aspect of the spermatic cord. Its motor branch is responsible for the innervations of the cremaster muscle. Its sensory branch supplies the scrotum. The iliohypogastric nerve runs along the lower edge of the internal oblique muscle and supplies the skin of the pubic region [11–13].

The sensory supply of the penis is provided by the pudendal nerves which originate in the sacral plexus and course along the ischiorectal fossa. The autonomic nerves supply of the penis is provided by the nervi erigentes, which course along the pelvic sidewalls (Fig. 21.1).

Microscopically, the testicles are divided into approximately 300 pyramidal lobules, which contain the convoluted seminiferous tubules, where spermatogenesis occurs. Posteriorly, the seminiferous tubules come together forming the rete testis that carries the sperm cells into the head of the epididymis. Testosterone is produced in the cells of Leydig, which occupy the spaces between the seminiferous tubules. Sertoli cells are modulated by testosterone and FSH, playing a key role in the maturation of sperm cells.

The epididymis is a very long and convoluted duct that lies along the posterior aspect of the testicle. Its function is to participate in the maturation and storage of sperm cells. It is divided into a head, body, and tail. The latter gives rise to the vas deferens, which forms part of the spermatic cord. Once in the pelvis, it reaches the prostate after fusing with the seminal vesicles to form the ejaculatory duct, which enters the prostate and empties into the urethra [14, 15].

Although their name may suggest otherwise, the seminal vesicles do not participate in the storage of the sperm cells. This function is carried out by the caudal aspect of the epididymis. Rather, the seminal vesicles are glands that produce a fructose- and a prostaglandin-rich fluid that makes up to 70 % of the ejaculate volume [16]. The ejaculatory ducts traverse the prostate to reach the prostatic urethra on either side of the verumontanum. The prostatic utricle is a small crypt in the central portion of the verumontanum and is thought to represent the remnants of the Müllerian system. Rarely, neoplasms similar to those found in the uterus can be found in this location. Cowper’s glands are located within the genitourinary diaphragm and empty into the bulbous urethra. They produce a fluid that precedes ejaculation. Its function is thought to be the alkalinization of the urethra [17] (Fig. 21.2).

During vasectomy, the vas deferens is divided and a portion is excised. Rarely, extravasation of sperm cells may lead to the formation of an inflammatory mass known as sperm granuloma [18].

The prostate had been classically divided into paired lobes. However, further anatomical studies allowed the division of the prostate into histologically and embryologically distinct zones [19].

The central zone of the prostate envelops the ejaculatory ducts and is of Wolffian origin. It comprises 25 % of the prostatic mass and is glandular in nature. The transition zone surrounds the urethra and is anterior to the central zone. It shares a common origin with the urethra. It constitutes 5 % of the prostatic mass and gives rise to benign prostatic hyperplasia (BPH). Its periurethral location explains the symptoms of urinary obstruction in BPH. The peripheral zone is the largest of the four and surrounds both the central and transitional zones posteriorly and laterally. It is also formed by glandular tissue that gives rise to prostatic carcinoma. Due to its peripheral location, masses in this zone seldom cause urinary obstruction. Finally, the anterior fibromuscular stroma contains no glands and lies anterior to the transition zone, and between the anterolateral projections of the peripheral zone [20, 21].

Prostatic venous drainage deserves special mention. It is formed by a valveless system of veins that communicates with the extradural venous plexus of Batson. This communication provides an anatomical basis for the propensity of prostate cancer to metastasize to the spine and skull [22] (Fig. 21.3).

The male urethra is divided into three segments: prostatic, membranous, and penile. The prostatic urethra is 1–1.5 cm in length. It receives the ejaculatory ducts and is marked by the urethral crest (a continuation of the bladder trigone), the verumontanum, and the prostatic utricle, as described previously. The membranous urethra crosses the urogenital diaphragm, which anchors it to the pelvis, making it vulnerable to shearing forces. The penile urethra starts distal to the urogenital diaphragm and ends in the urethral meatus.

Urethral injury occurs in up to 25 % of male patients with pelvic fractures. Among the fractures, the ones caused by a straddle mechanism causing sacroiliac diastasis have the highest risk. The main types of urethral injury occur above and below the urogenital diaphragm. In injuries above the urogenital diaphragm, the prostate may be displaced cephalad. Urine accumulates in the extraperitoneal pelvis, like with extraperitoneal bladder ruptures. In contrast, injury to the urethra distal to the urogenital diaphragm causes perineal infiltration with urine.

Blood at the urethral meatus, perineal ecchymoses, blood in the scrotum, inability to void, and a high riding prostate on rectal exam all suggest urethral injury. Management includes diagnosis of the injury via retrograde urethrogram. Principles of treatment include urinary diversion (usually by a suprapubic catheter) and delayed repair [22].

Testicular cancer is the most common tumor in males between the ages of 15 and 34. However, its overall incidence is low, affecting only 1 % of the male population. The main risk factor is a history of cryptorchidism. Testicular cancer can arise from the germ cells (seminoma and non-seminoma tumors) as well as from the stroma (Sertoli and Leydig cell tumors).

Seminomas are the most common type of testicular cancer. They typically do not produce any markers. In contrast, non-seminomas may produce β-HCG (choriocarcinoma) and α-fetoprotein (yolk sac tumor). Teratocarcinomas are a third type of non-seminomatous tumor; it does not produce any hormones. Stromal tumors may produce androgens.

Presentation usually consists of the self-diagnosis of a testicular mass. Testicular ultrasound is the imaging modality of choice. Additional studies include tumor markers, lactate dehydrogenase, and chest X-ray. Transinguinal orchiectomy is the treatment of choice and also allows pathologic confirmation. Trans-scrotal approaches are contraindicated because they disrupt lymphatic drainage patterns and violate the multiple testicular envelopes that limit the local extension of malignant processes. Nodal staging is done through CT scanning. Seminomas are very radiosensitive, and nodal control is achieved with radiation therapy. In contrast, non-seminomas have less sensitivity and may require nodal dissection [23–25].

Classic intravaginal testicular torsion consists of 540° (1½ turns) or greater rotation of the spermatic cord including the epididymis and testicle. This is the most common type of torsion, resulting in elevation of the testicle with the epididymis in an anterior location. Presentation is that of acute onset testicular pain often accompanied by nausea and vomiting. The cremasteric reflex is abolished. The diagnosis can be confirmed by duplex ultrasound.

Less commonly testicular torsion is the result of an anatomical abnormality in which the tunica vaginalis completely surrounds the testicle and distal spermatic cord, which are freely mobile within this investment (bell clapper deformity). In this setting, the testicle and spermatic cord rotate within the tunica vaginalis.

Treatment should be prompt, with restoration of blood flow within 6 h. While medial to lateral manual detorsion might be successful, definitive treatment is surgical and consist of a trans-scrotal approach, detorsion, and orchiopexy. Contralateral orchiopexy is mandatory. If the testicle is necrotic, orchiectomy is performed.

Extravaginal torsion occurs in approximately 5 % of cases. It is often a prenatal event which occurs before testicular fixation is complete. It presents as a firm scrotal mass in the neonatal period and is not associated with the bell clapper deformity (Fig. 21.4).

Torsion of the appendix testis is an important differential diagnosis. In this scenario, there is also sudden testicular pain. However, tenderness is focal, and the infracted appendage may be seen through the scrotum (blue dot sign). The most important differential diagnosis of testicular torsion is epididymo-orchitis, which often affects the same age group. A wrong diagnosis may be devastating, as epididymo-orchitis is treated medically. The two most important diagnostic tools are ultrasonography and nuclear scan, which must be done on emergency basis because of the time limit to correct testicular torsion [26, 27] (Fig. 21.5).