The cryptorchid testis may be of normal size early in life, but some degree of atrophy usually is evident by the onset of puberty. Microscopically, tubular atrophy begins to appear by 5 to 6 years of age, and is usually advanced by the time of puberty. Germ cell neoplasia in-situ (discussed later) may be present in cryptorchid testes and is a likely precursor of subsequent germ cell tumors. Atrophic changes similar to those in cryptorchid testes may be caused by other insults, including chronic ischemia, trauma, irradiation, and anti-neoplastic chemotherapy, as well as conditions associated with chronically elevated estrogen levels (e.g., cirrhosis).
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Cryptorchidism referstoincompletedescentofthetestisfromtheabdomentothescrotumandispresentinabout1%of1-year-oldmaleinfants.
Bilateralor,insomecases,evenunilateralcryptorchidismisassociatedwithtubularatrophyandsterility.
Thecryptorchidtestiscarriesa3-to5-foldhigherriskfortesticularcancer,whicharisesfromfociofgermcellneoplasiain-situwithintheatrophictubules.Earlyorchiopexyreducestheriskforsterilityandcancer.
Inflammatory lesions of the testis are more common in the epididymis than in the testis proper. Sexually transmitted infectious disorders are discussed later in the chapter. Other causes of testicular inflammation include nonspecific epididymitis and orchitis, mumps, and tuberculosis. Nonspecific epididymitis and orchitis usually begin as a primary urinary tract infection that spreads to the testis through the vas deferens or the lymphatics of the spermatic cord. The involved testis is swollen and tender, and histologic examination reveals numerous neutrophils. Mumps infection involving the testes is rare in male children but occurs in roughly 20% of infected adults. Affected testes are edematous and congested, and contain a lymphoplasmacytic inflammatory infiltrate. Severe mumps orchitis may lead to extensive necrosis, loss of seminiferous epithelium, tubular atrophy, fibrosis, and sterility. Several conditions, including infections and autoimmune injury, may elicit granulomatous inflammation in the testis. Of these, tuberculosis is the most common. Testicular tuberculosis generally begins as an epididymitis, with secondary involvement of the testis. Histologically, there is granulomatous inflammation and caseous necrosis identical to that seen in active tuberculosis in other sites.
Torsion, or twisting of the spermatic cord, typically results in obstruction of testicular venous drainage while leaving the thick-walled and more resilient arteries patent. This leads to intense vascular engorgement and infarction unless the torsion is relieved. There are two types of testicular torsion. Neonatal torsion occurs either in utero or shortly after birth. There is no associated anatomic defect to account for its occurrence. Adult torsion typically is seen in adolescence and manifests with the sudden onset of testicular pain. In contrast with neonatal torsion, adult torsion results from a bilateral congenital anomaly whereby the testis is abnormally anchored in the scrotal sac giving rise to increased mobility (bell clapper abnormality). It often occurs without any inciting injury; sudden pain heralding the torsion may even awaken the patient from sleep.
Torsion constitutes one of the few urologic emergencies. If the testis is explored surgically and the cord is manually untwisted within approximately 6 hours, the testis will likely remain viable. To prevent the catastrophic occurrence of torsion in the contralateral testis, the unaffected testis typically is surgically fixed within the scrotum (orchiopexy).