- Author: Oreoluwa I Ogunyemi, MD; Chief Editor: Edward David Kim, MD, FACS more...
Testicular torsion refers to the torsion of the spermatic cord structures and subsequent loss of the blood supply to the ipsilateral testicle. This is a urological emergency; early diagnosis and treatment are vital to saving the testicle and preserving future fertility.
Testicular torsion is primarily a disease of adolescents and neonates. It is the most common cause of testicular loss in these age groups. Surgical treatment may prevent further ischemic damage to the testis. Rarely, observation is appropriate, depending on the pathology. Diagnosis of testicular torsion is clinical, and diagnostic testing should not delay treatment.
Testicular torsion is caused by twisting of the spermatic cord and the blood supply to the testicle (see the image below). With mature attachments, the tunica vaginalis is attached securely to the posterior lateral aspect of the testicle, and, within it, the spermatic cord is not very mobile. If the attachment of the tunica vaginalis to the testicle is inappropriately high, the spermatic cord can rotate within it, which can lead to intravaginal torsion. This defect is referred to as the bell clapper deformity. This occurs in about 17% of males and is bilateral in 40%.
Intravaginal torsion most commonly occurs in adolescents. It is thought that the increased weight of the testicle after puberty, as well as sudden contraction of the cremasteric muscles (which inserts in a spiral fashion into the spermatic cord), is the impetus for acute torsion.
By contrast, neonates more often have extravaginal torsion. This occurs because the tunica vaginalis is not yet secured to the gubernaculum and, therefore, the spermatic cord, as well as the tunica vaginalis, undergo torsion as a unit. Extravaginal torsion is not associated with bell clapper deformity. This can occur up to months prior to birth and, therefore, is managed differently depending on presentation. Of course, neonates can have intravaginal torsion and this should be managed in the same manner as adolescents.
Testicular torsion is associated with testicular malignancy, especially in adults; one study found a 64% association of testicular torsion with testicular malignancy. This is thought to be secondary to a relative increase in the broadness of the testicle compared with its blood supply.
The testes are paired ovoid structures that are housed in the scrotum and positioned so that the long axis is vertical. The testicle is covered by the tunica vaginalis. Beneath the tunica vaginalis is the capsule of the testis, termed the tunica albuginea. See Male Reproductive Organ Anatomy.
The anterolateral two thirds of the organ is free of any scrotal attachment. There is a potential space here, between the tunica vaginalis and the tunica albuginea, where fluid from a variety of sources may accumulate. The tunica vaginalis attaches to the posterolateral surface of the testicle and allows for little mobility of the testicle within the scrotum.
The epididymis, connective tissue, and vasculature cover the posterolateral aspect of the organ.
The contents of the spermatic cord include the following:
Ductus deferens and associated vasculature and nerves
Pampiniform plexus, which ultimately forms the testicular vein
Genital branch of the genitofemoral nerve
For normal development and optimal sperm production, the testis must descend from its original position near the kidney into the scrotum. Researchers propose that various mechanisms, including gubernacular traction and intra-abdominal pressure, are responsible for testicular descent; however, endocrine factors of the hypothalamic-pituitary-testicular axis also play a major role in this process.
Around the 23rd week of gestation, the testis undergoes transabdominal migration to a location near the internal inguinal ring. The testis does not migrate transinguinally to its final position until after the 28th week of gestation, and this is usually complete between the 30th and 32nd week of gestation.
In neonates, the testicle frequently has not yet descended into the scrotum, where it becomes attached within the tunica vaginalis. This mobility of the testicle predisposes it to torsion (extravaginal testicular torsion). Inadequate fusion of the testicle to the scrotal wall typically is diagnosed within the first 7-10 days of life.
In males who have an inappropriately high attachment of the tunica vaginalis, as well as abnormal fixation to the muscle and fascial coverings of the spermatic cord, the testicle can rotate freely on the spermatic cord within the tunica vaginalis (intravaginal testicular torsion). This congenital anomaly, called the bell clapper deformity, can result in the long axis of the testicle being oriented transversely rather than cephalocaudal.
This congenital abnormality is present in approximately 12% of males and is bilateral in 40% of cases. The bell clapper deformity allows the testicle to twist spontaneously on the spermatic cord.
Torsion occurs as the testicle rotates between 90° and 180°, compromising blood flow to and from the testicle. Complete torsion usually occurs when the testicle twists 360° or more; incomplete or partial torsion occurs with lesser degrees of rotation. The degree of torsion may extend to 720°.
The twisting of the testicle causes venous occlusion and engorgement as well as arterial ischemia and infarction of the testicle. The degree of torsion the testicle endures may play a role in the viability of the testicle over time.
In addition to the extent of torsion, the duration of torsion prominently influences the rates of both immediate salvage and late testicular atrophy. Testicular salvage is most likely if the duration of torsion is less than 6-8 hours. If 24 hours or more elapse, testicular necrosis develops in most patients.
Extravaginal torsion occurs in the fetus or neonate, because the testes may freely rotate prior to the development of testicular fixation via the tunica vaginalis within the scrotum.
Normal testicular suspension ensures firm fixation of the epididymal-testicular complex posteriorly and effectively prevents twisting of the spermatic cord. In males with the bell-clapper deformity, torsion can occur because of a lack of fixation, resulting in the testis being freely suspended within the tunica vaginalis.
An abnormal mesentery between the testis and its blood supply can predispose it to torsion if the testicle is broader than the mesentery. Contraction of the spermatic muscles shortens the spermatic cord and may initiate testicular torsion.
Extravaginal torsion constitutes approximately 5% of all torsions. Of these cases of testicular torsion, 70% occur prenatally and 30% occur postnatally. The condition is associated with high birth weight. Bilateral perinatal torsion is thought to be rare, although an increase in the number of case reports has been observed. Currently, there are about 56 case reports in the literature.
Intravaginal torsion constitutes approximately 16% of cases in patients presenting to an emergency department with acute scrotum. This form of testicular torsion is most often observed in males younger than 30 years, with most aged 12-18 years. Peak incidence occurs at age 13-14 years. The left testis is more frequently involved. Bilateral cases account for 2% of all torsions.
The incidence of torsion in males younger than 25 years is approximately 1 in 4000. In an Israeli study of pediatric patients presenting to an ED with scrotal/testicular pain of less than 1 week duration, only 17 (3.3%) had testicular torsion.
Several case reports describe familial testicular torsion. In one study of 70 boys with testicular torsion, 11.4% had a positive history in a family member.
Success in the management of spermatic cord torsion is measured by immediate testicular salvage and the incidence of late testicular atrophy. A recent publication documented that approximately 32% of pediatric torsion cases resulted in the orchiectomy. Increased risk was associated with African American race, younger age, and lack of private insurance. The higher association with younger age may be secondary to delay in diagnosis in young children, who may not be able to communicate the symptoms to caregivers.
The time elapsed between onset of pain and performance of detorsion, and the corresponding salvage rate, is as follows[9, 10] :
<6 hours – 90-100% salvage rate
12-24 hours – 20-50%
>24 hours – 0-10%
Orchiopexy is not a guarantee against future torsion, though it does reduce the odds of a future torsion.
Consequences of testicular torsion may include the following:
Infarction of testicle
Loss of testicle
Infertility secondary to loss of testicle
Exocrine and endocrine function is substandard in men with a history of unilateral torsion. A correlation may exist between the duration of torsion and abnormal semen parameters. The following 3 theories explain the contralateral disease noted in torsion patients:
Unrecognized or unreported repeated injury to both testes
A preexisting pathologic condition predisposing to both abnormal spermatogenesis and torsion of the spermatic cord 
Induction of pathologic changes in the contralateral testis by retention of the injured testis
To explain the decreased fertility observed in unilateral torsion of the spermatic cord, several specialists suggest an autoimmune mechanism. This hypothesis is based upon knowledge of the blood-testis barrier, which isolates the luminal compartment of the seminiferous tubule; animal studies in which researchers induced experimental allergic orchitis; and comparison of contralateral testicular disease to sympathetic ophthalmia, a cell-mediated immune response.
In fact, clinical experience does not support either inherent bilateral testicular abnormalities or a humoral effect adversely affecting the contralateral testis in patients with unilateral torsion, since the fertility of adults with pre–pubertal testicular torsion does not appear to be reduced.
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