Testicular torsion: a surgical emergency

Author: John M. Prater, Bonnie S. Overdorf
Date: Sept, 1991

Anatomically, the normal testis is surrounded by the tunica vaginalis except posteriorly, where it attaches to the epididymis and scrotal wall [1] (Figure 1). In older boys and men with testicular torsion, the tunica vaginalis completely surrounds the testis and inserts higher up on the spermatic cord, thus preventing posterior fixation. This anomaly, or "bell-clapper" deformity, allows the testis to be freely movable within the the tunica vaginalis, predisposing it to intravaginal rotation [2] (Figure 1).

Extravaginal torsion (a rotational twisting of the testis and the tunica vaginalis) occurs in the newborn when the intrascrotal contents are not fixed and are free to move in and out of the scrotal sac [2] (Figure 1). Attachment occurs within the first seven to 10 days after birth. [3] Extravaginal torsion is less common than intravaginal torsion and presents clinically as a swollen, nontender, hard scrotal mass that does not transilluminate. [4]

The entire vascular supply of the testis passes through the spermatic cord, primarily via the testicular artery. An acute surgical emergency is created when the cord twists, resulting in impaired blood flow to the testis, with subsequent ischemic injury. The most important factor in testicular salvage and future viability of the testis is the interval between the onset of symptoms and operative or manipulative reduction of the torsion. [5] The rapidity of necrosis and the degrees of necrosis also depend on the number of twists in the spermatic cord and the degree of arterial compression. [1]

Based on several series, salvage rates have been reported as approximately 100 percent if correction occurs within three hours, 83 to 90 percent at five hours, 75 percent at eight hours, 50 to 70 percent at 10 hours, and only 10 to 20 percent at 10 to 24 hours; viability is rare if intervention is delayed for 24 hours or longer from onset of symptoms. [6]

Incidence

Torsion of the testis or its appendage is estimated to occur in as many as one in 160 men aged 25 years or younger. [5] The annual incidence is approximately one case per 4,000 males. [7] Although testicular torsion can occur at almost any age, two-thirds of cases occur in patients between 12 and 18 years of age. [5] The peak incidence is at age 14, [1] with a second, smaller peak occurring in the first year of life. [4] Bilateral torsion has been reported in up to 2 percent of cases. [1] Familial occurrence of testicular torsion has been recorded, but rarely. [8]

History

Patients with testicular torsion typically present with the acute onset of unilateral scrotal pain, often associated with nausea and vomiting. Coexisting urinary symptoms are rarely present. Lower abdominal or suprapubic pain occurs in nearly 40 percent of cases and sometimes predominates over the scrotal symptoms, [5] leading to erroneous diagnoses such as appendicitis, gastroenteritis, muscle spasm and constipation. [9] One-third to one-half of patients report having had similar episodes of testicular pain in the past, which presumably represented torsion with spontaneous resolution. [10]

Trauma, unusual body movements and vigorous exercise have been implicated as precipitators of torsion. However, the on-set of symptoms has also been reported to occur during sleep, demonstrating that a precipitating factor is not always obvious. [4,5]

Physical Examination

Physical examination is crucial in the diagnosis and assessment of testicular torsion. Soon after torsion has occurred, the involved testis is exquisitely tender and firm. Due to twisting of the spermatic cord, the testis is often located higher than usual in the scrotum. Careful palpation is necessary to determine the position of the epididymis. If it is not found in its typical posterolateral position, torsion should be suspected; however, if the epididymis is in its normal position, torsion cannot be excluded, since the testis may have rotated 360 or 720 degrees. [11] The cremasteric reflex--testicular retraction elicited by stroking the medial thigh--is usually absent in testicular torsion. [2]

As vascular compromise progresses, swelling and erythema of the scrotum occur, making further evaluation of the affected scrotal contents difficult. If the bell-clapper deformity is bilateral, the contralateral testis may be found in a horizontal position rather than the normal vertical lie. [1]

Prehn's sign (elevation of the scrotum without relief of pain is said to indicate testicular torsion; however, this finding is nonspecific and unreliable. [1,5,6] Fever is rarely present in testicular torsion.

Differential Diagnosis

Torsion of the testis or its appendage and acute epididymitis are the cause of acute scrotal pain in approximately 94 percent of cases. [9] Other possible etiologies include orchitis, idiopathic scrotal edema, incarcerated inguinal hernia, vasculitis, tumor and trauma. [11] Clinically, the major diagnostic difficulty involves the differentiation of testicular torsion from acute epididymitis.

Acute epididymitis is the most common cause of painful swelling of the testis in adulthood. [12] It is uncommon in adolescent boys in the absence of underlying urinary tract disease. [5] Unfortunately, it is the most frequent misdiagnosis in cases of testicular torsion, which often leads to testicular loss. Studies indicate that a patient with testicular torsion who consults a primary care physician has a nearly 25 percent chance of losing the involved testis because of the delay caused by misdiagnosis and subsequent treatment of presumed epididymitis. [1]

The pain in epididymitis is typically of gradual onset, and a history of previous episodes of scrotal pain is uncommon. About 50 percent of patients with epididymitis have fever, urethral discharge and urinary symptoms, but nausea and vomiting are rare. [11] Physical examination reveals pain and swelling of the epididymis and often of the testis. Urinalysis commonly shows pyuria.

Torsion of the testicular appendage usually occurs between the ages of seven and 14. [5] The appendix testis, a remnant of the mullerian duct, is located at the upper pole of the testis. The pain associated with torsion of the testicular appendage is either acute or gradual in onset, and is typically less severe than than of torsion of the entire testis. Pyuria is uncommon. The "blue-dot" sign at the superior aspect of the testis, caused by the cyanotic appendage beneath the scrotal skin, is diagnostic [11] (Figure 1).

Acute orchitis may be caused by an extending epididymitis or a variety of viral agents, most commonly the mumps virus. [13] Symptoms typically include testicular swelling and pain, with associated fever and vomiting.

Idiopathic scrotal edema appears to be an allergic phenomenon in the three-to-nine-year-old age group. [13] Erythema and swelling of the scrotum is usually bilateral and may extend to the penile shaft and perineum. Discomfort is confined to the scrotal skin, and the testis and cord are usually nontender and of normal size. [5]

Any vasculitic disease, such as HenochSch nlein syndrome or Kawasaki's disease, can cause acute scrotal pain, [9] usually in conjunction with other manifestations of the disease.

Diagnostic Tests

Prompt and accurate diagnosis of testicular torsion is essential so that treatment can be initiated in time to preserve testicular viability. Differentiating testicular torsion from other causes of scrotal pathology can be difficult based solely on the history and physical examination. Ancillary laboratory tests and noninvasive radiologic techniques can be helpful in determining the need for emergency surgical intervention.

Urinalysis is the most important laboratory test; it is normal in 90 percent of patients with testicular torsion. [6]

Radionuclide testicular scanning (Figure 2), using technetium pertechnetate, is performed to determine the presence or absence of testicular blood flow. In cases of testicular ischemia resulting from torsion, the scan demonstrates decreased flow; acute inflammatory states such as epididymitis reveal increased activity secondary to hyperemia. [14] False-positive results can be obtained when a hydrocele or hernia is overlying the testis. [1] Various studies show the diagnostic accuracy of testicular scanning to be 87 to 100 percent. [15] The primary disadvantage of testicular scanning is that it requires skilled personnel, making it sometimes difficult to perform in an emergency.

Doppler ultrasound examination is also used to evaluate testicular blood flow. This test is relatively simple to perform, but it must be done properly to ensure accuracy. The Doppler technique involves placing the probe at the lower end of the testis to check for arterial blood flow. Perfusion is decreased or absent in testicular torsion. If a pulse is found, testicular arterial flow and scrotal hyperemia can be distinguished by the funicular compression test, in which the examiner compresses the ipsilateral spermatic cord between the fingers. If the pulse disappears, it came from the testicular artery and, thus, torsion has not occurred. If the pulse persists, it probably originates in inflamed scrotal vessels, and the study is nondiagnostic. [1,11] The accuracy of Doppler ultrasound has been reported to be as high as 88 percent [1]; however, others have reported false-negative results in up to 31 percent of patients. [16] A direct comparison of the two techniques, correlated with surgical results, showed that the testicular scan is more reliable in the evaluation of the patient with possible testicular torsion. [17]

Treatment

Surgical intervention is inevitable in all patients with testicular torsion. However, some clinicians advocate the technique of manual detorsion for early relief of testicular ischemia. This procedure involves manipulative rotation of the testis in an attempt to restore normal anatomy and alleviate pain. [18] Unfortunately, relief of pain does not always indicate complete resolution of ischemia; therefore, prompt surgery is still indicated to confirm successful manual detorsion. [19]

At surgery, the involved testis is detorsed, and bilateral orchiopexy is performed to prevent future torsion (Figure 3). Since the use of absorbable suture has been associated with recurrent torsion, it is recommended that a nonabsorbable material, such as nylon or silk, be used for permanent testicular fixation. [7,20]

If the torsed testis is nonviable, orchiectomy is performed (Figure 4). It is important to inform the patient that a prosthesis is available for cosmetic and psychologic benefit. [9]

Prognosis

Spermatogenesis following unilateral testicular torsion may be impaired. Experimental studies in dogs reveal changes at the cellular level, with elimination of spermatogenic cells by six hours of testicular ischemia and elimination of Leydig cells by 10 hours. [21] Human studies show a close correlation between the duration of torsion and the degree of subsequent testicular atrophy. [22-24]

Unilateral torsion is commonly followed by abnormal findings on semen analysis, such as oligospermia or abnormalities of motility or morphology. [22-24] Several theories explain this exocrine dysfunction. In testes prone to torsion due to bilateral bell-clapper deformity, impaired spermatogenesis may result from cumulative testicular damage secondary to recurrent subclinical torsion [23-25] or preexisting congenital cellular dysplasia. [25] Alternatively, ischmic testicular injury may lead to the formation of autoantibodies, which subsequently attack the contralateral testis. [23]

Following testicular torsion, endocrine function, as determined by levels of luteinizing hormone, prolactin, testosterone and follicle-stimulating hormone, are generally normal, [23] as is libido and sexual potency. [22]

REFERENCES

[1] Haynes BE, Bessen HA, Haynes VE. The diagnosis of testicular torsion. JAMA 1983; 249: 2522-7.

[2] Son KA, Koff SA. Evaluation and management of the acute scrotum. Prim Care 1985; 12:637-46.

[3] Ryken TC, Turner JW, Haynes T. Bilateral testicular torsion in a pre-term neonate. J Urol 1990;143:102-3.

[4] Matthews PN. Spermatic cord torsion [Editorial]. Arch Dis Child 1986; 61: 426-7.

[5] Williamson RC. Torsion of the testis and allied conditions. Br J Surg 1976; 63:465-76.

[6] Sonda LP, Wang S. Evaluation of male external genital diseases in the emergency room setting. Emerg Med Clin North Am 1988;6: 473-86.

[7] Barada JH, Weingarten JL, Cromie WJ. Testicular salvage and age-related delay in the presentation of testicular torsion. J Urol 1989; 142:746-8.

[8] Collins K, Broecker BH. Familial torsion of the spermatic cord. J Urol 1989; 141: 128-9.

[9] Knight PJ, Vassy LE. The diagnosis and treatment of the acute scrotum in children and adolescents. Ann Surg 1984; 200:664-73.

[10] Cas AS. Elective orchiopexy for recurrent testicular torsion. J Urol 1982;127:253-4.

[11] O'Brien WM, Lynch JH. The acute scrotum. Am Fam Physician 1988;37(3):239-47.

[12] Witherington R, Jarrell TS. Torsion of the spermatic cord in adults. J Urol 1990; 143:62-3.

[13] Donohue RE, Utley WL. Torsion of spermatic cord. Urology 1978;11:33-6.

[14] May DC, Lesh P, Lewis S, Anderson RJ. Evaluation of acute scrotum pain with testicular scanning. Ann Emerg Med 1985;14:696-9.

[15] Stage KH, Schoenvogel R, Lewis S. Testicular scanning: clinical experience with 72 patients. J Urol 1981;125:334-7.

[16] Haynes BE. Doppler ultrasound failure in testicular torsion. Ann Emerg Med 1984; 13:1103-7.

[17] Rodriguez DD, Rodriguez WC, Rivera JJ, Rodriguez S, Otero AA. Doppler ultrasound versus testicular scanning in the evaluation of the acute scrotum. J Urol 1981;125:343-6.

[18] Cattolica EV. Preoperative manual detorsion of the torsed spermatic cord. J Urol 1985; 133: 803-5.

[19] Haynes BE, Haynes VE. Manipulative detorsion: beware the twist that does not turn. J Urol 1987;137:118-9.

[20] Kuntze JR, Lowe P, Ahlering TE. Testicular torsion after orchiopexy. J Urol 1985; 134: 1209-10.

[21] Smith GI. Cellular changes from graded testicular ischemia. J Urol 1955;73:355-62.

[22] Krarup T. The testes after torsion. Br J Urol 1978;50:43-6.

[23] Thomas WE, Cooper MJ, Crane GA, Lee G, Williamson RC. Testicular exocrine malfunction after torsion. Lancet 1984;2(8416):1357-60.

[24] Bartsch G, Frank S, Marberger H, Mikuz G. Testicular torsion: late results with special regard to fertility and endocrine function. J Urol 1980;124:375-8.

[25] Anderson JB, Williamson RC. The fate of the human testes following unilateral torsion of the spermatic cord. Br J Urol 1986;58698-704.

THE AUTHORS

JOHN M. PRATER, M.D. is in private practice in Wilkes-Barre, Pa. Dr. Prater is a graduate of Hahnemann University School of Medicine, Philadelphia, and completed a residency in family medicine at Wyoming Valley Family Practice, Kingston, Pa.

BONNIE S. OVERDORF, P.A.-C is currently attending the physician assistant surgical residency program at Yale University, New Have, Conn. She is a graduate of the physician assistant program at King's College, Wilkes-Barre.

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