Background

Torsion of the testis, or more correctly, torsion of the spermatic cord, is a surgical emergency because it causes strangulation of gonadal blood supply with subsequent testicular necrosis and atrophy. Acute scrotal swelling in children indicates torsion of the testis until proven otherwise. In approximately two thirds of patients, history and physical examination are sufficient to make an accurate diagnosis.

History of the Procedure

Patients often complain of acute-onset scrotal discomfort, which may occur at rest or may relate to sports or physical activities. They may describe similar previous episodes, which may suggest intermittent testicular torsion.[1] Patients deny voiding problems or painful urination but may describe nausea and vomiting.

Problem
Testicular torsion refers to twisting of the spermatic cord structures, either in the inguinal canal or just below the inguinal canal. The following are the 2 most common types of testicular torsion (see image below).

Testicular torsion: (A) extravaginal; (B) intravaginal.

Extravaginal torsion: This type manifests in the neonatal period and most commonly develops prenatally in the spermatic cord, proximal to the attachments of the tunica vaginalis. Intravaginal torsion: This type occurs within the tunica vaginalis, usually in older children. Intravaginal torsion is related to an anomalous testicular suspension that has been referred to as the bell-clapper anomaly. In many instances, this anomaly may be bilateral.

Epidemiology
Frequency

Extravaginal torsion comprises approximately 5% of all torsions. The condition is most often a prenatal (in utero) event and is associated with high birth weight. Up to 20% of cases are synchronous, and 3% are asynchronous bilateral. Intravaginal torsion comprises approximately 16% of patients with torsion presenting in emergency departments with acute scrotum. Peak incidence occurs in adolescents aged 13 years, and the left testis is more frequently involved. Bilateral cases account for 2% of all torsions.

Etiology

Extravaginal torsion: The testes may freely rotate prior to the development of testicular fixation via the tunica vaginalis within the scrotum. Intravaginal torsion: Normal testicular suspension ensures firm fixation of the epididymal-testicular complex posteriorly and effectively prevents twisting of the spermatic cord. In contrast, the bell-clapper deformity allows torsion to occur because of a lack of fixation, resulting in the testis being freely suspended within the tunica vaginalis. A large mesentery between the epididymis and the testis can also predispose itself to torsion, although this is rare. Contraction of the spermatic muscles shortens the spermatic cord and may initiate testicular torsion.

Pathophysiology
Torsion of the spermatic cord may interrupt blood flow to the testis and epididymis. The degree of torsion may vary from 180-720. Increasing testicular and epididymal congestion promotes progression of torsion. The extent and duration of torsion prominently influence both the immediate salvage rate and late testicular atrophy. Testicular salvage most likely occurs if the duration of torsion is less than 6-8 hours. If 24 hours or more elapse, testicular necrosis develops in most patients.

Presentation
Prenatal torsion manifests as a firm, hard, scrotal mass, which does not transilluminate in an otherwise asymptomatic newborn male. The scrotal skin characteristically fixes to the necrotic gonad. In older boys, the classic presentation of testicular torsion is the sudden onset of severe testicular pain followed by inguinal and/or scrotal swelling. Pain may lessen as the necrosis becomes more complete. Approximately one third of patients also have gastrointestinal upset with nausea and vomiting. In some patients, scrotal trauma or other scrotal disease (including torsion of appendix testis or epididymitis) may precede the occurrence of subsequent testicular torsion. A physical examination may reveal a swollen, tender, high-riding testis (see image below). The absence of the cremasteric reflex in a patient with acute scrotal pain supports the diagnosis of

torsion. In time, a reactive hydrocele, scrotal wall erythema, and ecchymosis become more striking.

A 17-year-old teenager with a 72-hour history of scrotal pain.

Differential diagnosis

Torsion of testicular or epididymal appendage o This condition usually occurs in children aged 7-12 years. o Systemic symptoms are rare. o Usually, localized tenderness occurs but only in the upper pole of the testis. o Occasionally, the blue dot sign is present in light-skinned boys. Epididymitis, orchitis, epididymo-orchitis o These conditions most commonly occur from the reflux of infected urine or from sexually acquired disease caused by gonococci and Chlamydia. o Patients occasionally develop these conditions following excessive straining or lifting and the reflux of urine (chemical epididymitis). o These conditions may be secondary to an underlying congenital, acquired, structural, or urologic abnormality and are often accompanied by systemic signs and symptoms associated with urinary tract infection. o Pyuria, bacteriuria, or leucocytosis is possible. o A complete urological evaluation (ie, renal sonography, urodynamic study) is necessary in prepubertal boys with acute epididymitis. Hydrocele (usually associated with patent processus vaginalis) o Painless swelling is usually present. o Scrotal contents can be visualized with transillumination. o Incarcerated hernia may be diagnosed by careful examination of the inguinal canal. Testis tumor o Scrotal enlargement occurs, only rarely accompanied by pain. o Presentation is rarely acute. Idiopathic scrotal edema o Scrotal skin is thickened, edematous, and often inflamed. o The testis is not tender and is of normal size and position.

Indications

If clinical evaluation reveals testicular torsion, transfer the patient to the operating room for urgent scrotal exploration, regardless of the number of hours since the onset of presenting symptoms.

Relevant Anatomy
For normal development and 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. Between the 12th and 17th 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 the seventh month of gestation. The testes are paired ovoid structures that are housed in the scrotum and positioned so that the long axis is vertical. The anterolateral two thirds of the organ is free of any scrotal attachment. The epididymis, connective tissue, and vasculature cover the posterolateral aspect of the organ. The capsule of the testis is termed the tunica albuginea.

Laboratory Studies

If the patient does not show clinical evidence of testicular torsion, a urinalysis and culture may help exclude urinary tract infection and epididymitis as the etiology of the scrotal complaints. If testicular torsion is clinically suggested, perform immediate surgical exploration, regardless of laboratory studies because a negative finding upon exploration of the scrotum is more acceptable than the loss of a salvageable testis.

Imaging Studies

The following diagnostic tests may be useful when a low suspicion of testicular torsion exists: o Scrotal color Doppler sonogram is usually diagnostic by verifying arterial flow. o Nuclear testicular scan can help differentiate torsion from acute epididymitis by demonstrating cold spot and ring signs.

Medical Therapy
Manual detorsion of the torsed testis may be attempted but is usually difficult because of acute pain during manipulation. This nonoperative detorsion is not a substitute for surgical exploration. If successful (ie, confirmed by color Doppler sonogram in a patient with complete resolution of symptoms), perform definitive surgical fixation of the testes before the patient leaves the hospital as an urgentrather than emergentprocedure.

A recent study has shown that the use of nicotinamide may successfully decrease ischemiareperfusion injury in early and late periods in both testicles.[2]

Surgical Therapy
Treatment of testicular torsion varies according to patient age.

Treat patients who are born with testicular torsion by performing early elective exploration and contralateral orchidopexy (anchoring) because bilateral (synchronous or asynchronous) neonatal testicular torsion is described. The potential for salvage of such a testis is nil, making the risk of immediate surgery before complete stabilization of the newborn unwarranted. In distinct contrast, a newborn with a normal testis at birth who subsequently undergoes torsion requires immediate exploration. Perform the operation through the midline scrotal raphe. Enter the ipsilateral scrotal compartment; then, deliver and untwist the testis. Evaluate the testis for viability. Remove the necrotic testis to avoid prolonged, debilitating pain and tenderness. Retention of a necrotic testis may exacerbate the potential for subfertility, presumably because of development of an autoimmune phenomenon. To prevent subsequent torsion, fix viable gonads to the scrotal wall with 3-4 nonabsorbable sutures. Perform both exploration and anchoring of the contralateral testis through the same incision.

Intraoperative Details
Signs of a viable testis after detorsion (see image below) include a return of color, return of Doppler flow, and arterial bleeding after incision of tunica albuginea.

Intraoperative findings in testicular torsion.

Postoperative Details

Testicular prosthesis placement o Patients requiring an orchiectomy because of a nonviable testis may benefit from the placement of a testicular prosthesis. o Delay this placement, usually for 6 months, until healing is complete and inflammatory changes resolve.

Perform the prosthetic placement through an inguinal incision.

Complications
Torsion of the spermatic cord continues to be one of the few emergencies in urologic practice. Delay of more than 6-8 hours between onset of symptoms and the time of surgical (or manual) detorsion reduces the salvage rate to 55-85%. A correlation may exist between the duration of torsion and abnormal semen parameters, and some authorities suggest that retention of an injured testis can induce pathologic changes to the contralateral testis.

Outcome and Prognosis

Success in the management of spermatic cord torsion is measured by immediate testicular salvage and incidence of late testicular atrophy, which are, in turn, directly related to the duration and degree of testicular torsion. Delaying surgical intervention worsens the intraoperative testicular salvage and incidence rate and the extent of subsequent testicular atrophy. The delay between the onset of symptoms and the time of surgical or manual detorsion is obviously of utmost importance in achieving a viable testis.

Future and Controversies

Recent studies show that exocrine and endocrine function is substandard in men with a history of unilateral torsion. The following 3 theories explain the contralateral disease noted in torsion:

Unrecognized or unreported repeated injury to both testes Preexisting pathologic condition predisposing to both abnormal spermatogenesis and torsion of the spermatic cord[3] 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 the following:

Knowledge of the blood-testis barrier, which isolates the luminal compartment of the seminiferous tubule Inducing experimental allergic orchitis Likening contralateral testicular disease to sympathetic ophthalmia, a cell-mediated immune response

Updated: Sep 24, 2010 Edward David Kim, MD, FACS

Testicular torsion: (A) extravaginal; (B) intravaginal.

1. Johnston BI, Wiener JS. Intermittent testicular torsion. BJU Int. May 2005;95(7):933-4. [Medline]. 2. Kar A, Ozden E, Yakupoglu YK, Kefeli M, Sarikaya S, Yilmaz AF. Experimental unilateral spermatic cord torsion: the effect of polypolymerase enzyme inhibitor on histopathological and biochemical changes in the early and late periods in the ipsilateral and contralateral testicles. Urology. Aug 2010;76(2):507.e1-5. [Medline]. 3. Sun J, Liu GH, Zhao HT, Shi CR. Long-term influence of prepubertal testicular torsion on spermatogenesis. Urol Int. 2006;77(3):275-8. [Medline]. 4. Barada JH, Weingarten JL, Cromie WJ. Testicular salvage and age-related delay in the presentation of testicular torsion. J Urol. Sep 1989;142(3):746-8. [Medline]. 5. Brandt MT, Sheldon CA, Wacksman J, Matthews P. Prenatal testicular torsion: principles of management. J Urol. Mar 1992;147(3):670-2. [Medline]. 6. Chan JL, Knoll JM, Depowski PL, Williams RA, Schober JM. Mesorchial testicular torsion: case report and a review of the literature. Urology. Jan 2009;73(1):83-6. [Medline]. 7. Kalfa N, Veyrac C, Lopez M, Lopez C, Maurel A, Kaselas C, et al. Multicenter assessment of ultrasound of the spermatic cord in children with acute scrotum. J Urol. Jan 2007;177(1):297-301; discussion 301. [Medline]. 8. Kapoor S. Testicular torsion: a race against time. Int J Clin Pract. May 2008;62(5):821-7. [Medline]. 9. Kyriazis ID, Dimopoulos J, Sakellaris G, Waldschmidt J, Charissis G. Extravaginal testicular torsion: a clinical entity with unspecified surgical anatomy. Int Braz J Urol. Sep-Oct 2008;34(5):617-23; discussion 623-6. [Medline]. 10. Lewis AG, Bukowski TP, Jarvis PD, et al. Evaluation of acute scrotum in the emergency department. J Pediatr Surg. Feb 1995;30(2):277-81; discussion 281-2. [Medline].

11. Mor Y, Pinthus JH, Nadu A, Raviv G, Golomb J, Winkler H, et al. Testicular fixation following torsion of the spermatic cord--does it guarantee prevention of recurrent torsion events?. J Urol. Jan 2006;175(1):171-3; discussion 173-4. [Medline]. 12. Rabinowitz R, Hulbert WC Jr. Acute scrotal swelling. Urol Clin North Am. Feb 1995;22(1):101-5. [Medline]. 13. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician. Nov 15 2006;74(10):173943. [Medline]. 14. Schmitz D, Safranek S. Clinical inquiries. How useful is a physical exam in diagnosing testicular torsion?. J Fam Pract. Aug 2009;58(8):433-4. [Medline]. 15. Smith-Harrison LI, Koontz WW. Torsion of the Testis: Changing Concepts. AUA Updates. 1990;32.

Testicular Torsion

Author: Oreoluwa I Ogunyemi, MD; Chief Editor: Edward David Kim, MD, FACS

Updated: Aug 25, 2011

Background
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[1] 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.[1] 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.[1] 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.[1]

Testicular torsion: (A) extravaginal; (B) intravaginal. For patient education information, see the Men's Health Center, as well as Testicular Pain. For additional information, see Testicular Torsion in Emergency Medicine and Pediatric Testicular Torsion .

Anatomy
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 Testicular artery Pampiniform plexus, which ultimately forms the testicular vein Genital branch of the genitofemoral nerve

Testicular descent

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.[1]

Pathophysiology
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.[2] 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.

Etiology

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.

Epidemiology
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.[3] 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.[4] 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.[5]

Prognosis
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.[6] 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[7, 8] :

< 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 Infection Infertility secondary to loss of testicle Cosmetic deformity

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[9] 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.[10]

History
Intravaginal testicular torsion produces a sudden onset of severe unilateral scrotal pain followed by inguinal and/or scrotal swelling. Pain may lessen as the necrosis becomes more complete. Gradual onset of pain is an uncommon presentation. Torsion can occur with sports or physical activity, can be related to trauma in 4-8% of cases,[8] or can develop spontaneously. Approximately one third of patients also have gastrointestinal upset with nausea and vomiting. In the pediatric population, nausea and vomiting has a positive predictive value of greater than 96%.[11] Duration of pain of less than 6 hours, fever, vomiting, history of trauma or activities, absence of cremasteric reflex, and abnormal testicle direction have all been determined to be significantly associated with a diagnosis of testicular torsion.[12] Patients rarely report voiding difficulties or painful urination.

In some patients, scrotal trauma or other scrotal disease (including torsion of appendix testis or epididymitis) may precede the occurrence of subsequent testicular torsion. Patients may describe previous episodes of recurrent acute scrotal pain that has resolved spontaneously.[13] This history is highly suggestive of intermittent torsion and detorsion of the testicle. Patients who complain of what sounds like torsion-detorsion should be referred promptly to a urologist, since patients with symptoms of intermittent torsion who electively have surgical exploration are less likely to develop subsequent torsion and loss of the testicle.[14] Creagh et al reported that acute torsion developed in 10% of patients with intermittent torsion while they waited for surgery.[15] In neonates, prenatal extravaginal torsion presents as a hard, nontender testis that is fixed to the overlying discolored scrotal skin. It is thought that unilateral absence of the testicle with blindending vessels is a manifestation of early in utero torsion as hemosiderin is often found in the distal section of the spermatic cord.[1] However, if acute scrotal swelling and tenderness are present without fixation to the scrotal wall, this may represent a postnatal torsion with some hope of subsequent testicular salvage with surgical management.

Physical Examination
The physical examination is useful, but imperfect, in diagnosing acute testicular torsion.[16] The physical examination, moreover, may be difficult to perform, as the testicle is typically very tender and patients are often in significant discomfort. Patients may also have a reactive hydrocele or massive scrotal edema, making testicular examination event more difficult. Prenatal torsion manifests as a firm, hard, scrotal mass, which does not transilluminate in an otherwise asymptomatic newborn male. The scrotal skin characteristically fixes to the necrotic gonad. In an older patient, a physical examination may reveal a swollen, tender, high-riding testis with abnormal transverse lie and loss of the cremasteric reflex (see the image below).

A 17-year-old adolescent boy with a 72-hour history of scrotal pain.

In the pediatric population, there is a higher likelihood for testicular torsion if the testis is high riding compared with the other side.[5] While abnormal lie can help diagnose testicular torsion, fewer than 50% of cases demonstrate true horizontal lie.[16] The cremasteric reflex is almost always absent or diminished on the affected side in patients with testicular torsion, and its presence may help to distinguish other causes of acute scrotal pain from testicular torsion. Case reports, however, have noted the opposite to be true.[16, 17, 18] Although a negative Prehn sign (relief of pain with elevation of the testicle) is classically thought to be a predictor of torsion, this is unreliable for diagnosis. Other symptoms may include the following:

Enlargement and edema of the testicle; edema involving the entire scrotum Scrotal erythema Fever (uncommon)

In one study of 523 patients presenting to the ED with acute scrotum, no single clinical finding had 100% sensitivity for the presence of testicular torsion, but all patients with testicular torsion had 1 or more of the following[5] :

Nausea or vomiting Pain duration of less than 24 hours High position of the testis Abnormal cremasteric reflex

Diagnostic Considerations
Problems to be considered in the differential diagnosis of testicular torsion include the following:

Torsion of testicular or epididymal appendage Epididymitis, orchitis, epididymo-orchitis Hydrocele Testis tumor Idiopathic scrotal edema Idiopathic testicular infarction Traumatic rupture Traumatic hematoma

Torsion of the testicular or epididymal appendage usually occurs in boys aged 7-12 years. Systemic symptoms are rare. Usually, localized tenderness occurs, but only in the upper pole of the testis. Occasionally, the blue dot sign (ie, a tender nodule with blue discoloration on the upper pole of the testis) is present in light-skinned boys. Epididymitis, orchitis, and epididymo-orchitis conditions most commonly occur from the reflux of infected urine or from sexually acquired disease caused by gonococci and Chlamydia. Patients

occasionally develop these conditions following excessive straining or lifting and the reflux of urine (chemical epididymitis). These conditions may be secondary to an underlying congenital, acquired, structural, or urologic abnormality and are often accompanied by systemic signs and symptoms associated with urinary tract infection. Pyuria, bacteriuria, or leukocytosis is possible. A complete urologic evaluation (ie, renal sonography, urodynamic study) is necessary in prepubertal boys with acute epididymitis. Hydrocele is usually associated with patent processus vaginalis. Painless swelling is usually present. Scrotal contents can be visualized with transillumination. Incarcerated hernia may be diagnosed by careful examination of the inguinal canal. Testis tumor produces scrotal enlargement, only rarely accompanied by pain. The presentation is rarely acute. In idiopathic scrotal edema, the scrotal skin is thickened, edematous, and often inflamed. The testis is not tender and is of normal size and position.

Differentials

Appendicitis Fournier Gangrene Henoch-Schonlein Purpura in Emergency Medicine Hernias Scrotal Trauma Spermatocele Testicular Choriocarcinoma Testicular Seminoma Testicular Trauma Varicocele

Approach Considerations
If testicular torsion is clinically suggested, perform immediate surgical exploration, regardless of laboratory studies because a negative finding upon exploration of the scrotum is more acceptable than the loss of a salvageable testis. Laboratory tests are unlikely to be of consequence, as no single test has high sensitivity or specificity in diagnosing testicular torsion. However, when there is a strong suspicion of an alternate diagnosis, laboratory tests may be of some use. Imaging studies usually are not necessary. Ordering them wastes valuable time when the definitive treatment is emergent urologic consultation for surgical management. However,

imaging studies (eg, ultrasonography, nuclear scans) may be useful when a low suspicion of testicular torsion exists.

Urinalysis
If the patient does not show clinical evidence of testicular torsion, a urinalysis and culture may help exclude urinary tract infection and epididymitis as the etiology of the scrotal complaints. Urinalysis results are usually normal in testicular torsion. The presence of white blood cells (WBCs) can be observed in as many as 30% of patients who have torsion; therefore, do not rely on the presence of WBCs to exclude the diagnosis.

Blood Studies
The complete blood count can be normal. However, the WBC count is elevated in as many as 60% of patients who have torsion. Elevation in acute-phase proteins (ie, C-reactive protein) has been postulated as a diagnostic aid in differentiating inflammatory causes of acute scrotal pain (eg, epididymitis) from noninflammatory causes (eg, testicular torsion).[19] However, sample sizes in these studies have been too small to support using CRP as a diagnostic adjunct to definitively rule out testicular torsion.

Ultrasonography
Testicular torsion is a clinical diagnosis. If the history and physical examination strongly suggest testicular torsion, the patient should go directly to surgery without delaying to perform imaging studies. When a low suspicion of testicular torsion exists, color Doppler and power Doppler ultrasonography can be used to demonstrate arterial blood flow to the testicle while providing information about scrotal anatomy and other testicular disorders. (For images, see Testicular Torsion Imaging.) Plain Doppler ultrasonography is less accurate than color Doppler in assessing testicular blood flow. In fact, early in the course of testicular torsion, gray-scale ultrasonographic examination may be absolutely normal. Ultrasonographic findings suggestive of acute testicular torsion include the following[20] :

Absent or decreased blood flow in the affected testicle Decreased flow velocity in the intratesticular arteries Increased resistive indices in the intratesticular arteries Hypervascularity with a low resistance flow pattern (after partial torsion-detorsion)

The sensitivity of color Doppler examination with newer ultrasonography equipment in detecting acute testicular torsion in children is 90-100%, with the specificity of technically adequate studies being essentially 100%.[11] Other studies have suggested that color Doppler ultrasonography was only 86% sensitive, 100% specific, and 97% accurate in the diagnosis of torsion and ischemia in the painful scrotum.[21] A 3-year study demonstrated that Doppler ultrasonography had 94% sensitivity, 96% specificity, 95.5% accuracy, 89.4% positive predictive value, and 98% negative predictive value.[22] The detection of a color or power Doppler signal in a patient presenting with the clinical findings suggestive of testicular torsion does not absolutely exclude torsion. Clinical correlation should be incorporated in the evaluation of acute scrotum because color Doppler ultrasonography is not 100% sensitive.[23] Spectral and color flow Doppler sonography has also been used to evaluate for partial testicular torsion. Variability of the Doppler waveform when compared with the contralateral testicle and reversal of diastolic blood flow are indirect clues that aid in the diagnosis of partial testicular torsion.[24] Some smaller studies have evaluated the accuracy of emergency medicine physicians in performing bedside ultrasonography to evaluate for testicular torsion. While these studies have had generally favorable outcomes, diagnostic accuracy is always operator and institution dependent.[25, 26] A study of the use of contrast-enhanced ultrasonography demonstrated no advantage of this modality over Doppler ultrasonography in the evaluation of the acute scrotum. Contrastenhanced ultrasonography can, however, be used as a supplement to traditional Doppler sonography when the diagnosis is uncertain and following appropriate clinical and radiographic evaluation.[27]

Magnetic Resonance Imaging

Small studies to date suggest that magnetic resonance imaging (MRI), particularly when performed with contrast enhancement, is highly accurate in the diagnosis of testicular torsion, particularly when torsion knot or whirlpool patterns are evident. Dynamic contrast-enhanced MRI has also demonstrated accuracy.[28] The clinical utility of these studies, however, remains to be elucidated.

Radionuclide Scans
If the diagnosis is equivocal, radionuclide scan of the testicles can be helpful to assess blood flow and to differentiate torsion from other conditions. (For images, see Testicular Torsion Imaging.) These studies should preferably be ordered once urologic consultation has been completed and only for equivocal presentations.

Scan results are abnormal in torsion when they demonstrate decreased uptake in the affected testicle, suggesting no blood flow to that side. Radionuclide scans have a sensitivity of 90-100% accuracy in detecting testicular blood flow.

Approach Considerations
Surgical detorsion is the definitive treatment for testicular torsion. Manual detorsion of the torsed testis may be attempted but is usually difficult because of acute pain during manipulation. Nonoperative detorsion is not a substitute for surgical exploration. If manual detorsion is successful (ie, confirmed by color Doppler sonogram in a patient with complete resolution of symptoms), the patient should undergo definitive surgical fixation of the testes before leaving the hospital, so that the operation can be performed as an urgentrather than emergentprocedure. A study in an animal model has shown that the use of nicotinamide may successfully decrease ischemia-reperfusion injury in early and late periods in both testicles.[4]

Historical perspective
Testicular torsion is treated with orchiopexy, in which the testis is anchored to the scrotal wall. The surgical procedure was initially developed as treatment for cryptorchidism, with the first successful orchiopexy performed in the 1870s by Annandale. The main technical improvements have been in how the testis is anchored to the scrotal wall. Anchoring mechanisms have ranged from using an external cage to fastening the testis to the fascia lata of the thigh or the contralateral testis for lengthening of the spermatic cord. The current method to attach the testis to the scrotal pouch was initially described the 1930s.[29] With testicular torsion, the testicles need only be secured in the correct orientation to the scrotal wall, as the spermatic cord does not need to be lengthened. In current practice, a bilateral scrotal orchiopexy is often recommended to treat the torsed testis and prevent torsion of the other testis.

Surgical Detorsion
Treatment of testicular torsion varies according to patient age. Neonatal torsion is treated with elective exploration and contralateral orchiopexy (anchoring) because bilateral (synchronous or asynchronous) neonatal testicular torsion, while rare, has been described. The potential for salvage of such a testis is exceptionally small, making the risk of immediate surgery before complete stabilization of the newborn unwarranted. In distinct contrast, a newborn with a normal testis at birth who subsequently undergoes torsion requires immediate exploration.

Similarly, if clinical evaluation reveals testicular torsion in an older patient, transfer the patient to the operating room for urgent scrotal exploration, regardless of the number of hours since the onset of presenting symptoms.

Intraoperative details
Either a midline raphe incision or bilateral transverse scrotal incisions can be made. Enter the ipsilateral scrotal compartment, incise the tunica vaginalis, and then deliver the testicle for examination. The spermatic cord is then untwisted. Evaluate the testis for viability. If viability is in question, place the testicle in warm sponges and reevaluate after several minutes. If the testis is necrotic, perform an orchiectomy to avoid prolonged, debilitating pain and tenderness. In addition, retention of a necrotic testis may exacerbate the potential for subfertility, presumably because of development of an autoimmune phenomenon. To prevent subsequent torsion, fix viable gonads to the scrotal wall with 3-4 nonabsorbable sutures. A dartos pouch can be made, into which the testicle is placed. Always perform contralateral orchiopexy when testicular torsion is confirmed intraoperatively, in order to prevent future torsion of that testicle. Signs of a viable testis after detorsion (see the image below) include a return of color, return of Doppler flow, and arterial bleeding after incision of the tunica albuginea.

Intraoperative findings in testicular torsion.

Testicular prosthesis placement

Patients requiring an orchiectomy because of a nonviable testis may benefit from the placement of a testicular prosthesis. Delay this placement, usually for 6 months, until healing is complete and inflammatory changes resolve. Perform the prosthetic placement through an inguinal incision

Medication Summary
Analgesic and antianxiety medications are valuable adjuncts in the treatment of testicular torsion. Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary

toilet, and enables physical therapy regimens. Antiemetics can be used to counter the nausea and vomiting that may accompany testicular torsion.

Analgesics
Class Summary
Most analgesics have sedating properties, which are beneficial for patients who have sustained painful trauma.
View full drug information

Morphine sulfate (Duramorph, Astramorph, MS Contin, Kadian)

Morphine is the drug of choice for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used; the dose is commonly titrated until the desired effect is obtained.

Antiemetics
Class Summary
These agents are used to prevent nausea and vomiting.
View full drug information

Prochlorperazine (Compro)

Prochlorperazine may relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through its anticholinergic effects and depressing the reticular activating system. In addition to its antiemetic effects, it has the advantage of augmenting hypoxic ventilatory response, acting as a respiratory stimulant at high altitude.
View full drug information

Metoclopramide (Reglan, Metozolv)

Metoclopramide blocks dopamine receptors in the chemoreceptor trigger zone of the central nervous system.
View full drug information

Ondansetron (Zofran)

Odansetron is a selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. It prevents nausea and vomiting, including that associated with emetogenic cancer chemotherapy (eg, high-dose cisplatin), and complete body radiotherapy.

Antianxiety Agents
Class Summary
These agents are used to reduce anxiety.
View full drug information

Diazepam (Diastat, Valium)

Diazepam modulates the postsynaptic effects of gamma-aminobutric acidA (GABA-A) transmission, resulting in an increase in presynaptic inhibition. It appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. It also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders. Diazepam rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, the serum concentration drops to 20% of maximum plasma concentration (Cmax). Individualize dosage and increase cautiously to avoid adverse effects References 1. Schneck FX, Bellinger ME. Abnormalities of the testis and scrotum and their surgical management. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell- Walsh Urology. 9th ed. Philadelphia, Pa: WB Saunders; 2007:Chapter 127. 2. Dogra V, Bhatt S. Acute painful scrotum. Radiol Clin North Am. Mar 2004;42(2):349-63. [Medline]. 3. Roth CC, Mingin GC, Ortenberg J. Salvage of bilateral asynchronous perinatal testicular torsion. J Urol. Jun 2011;185(6 Suppl):2464-8. [Medline].

4. Kar A, Ozden E, Yakupoglu YK, Kefeli M, Sarikaya S, Yilmaz AF. Experimental unilateral spermatic cord torsion: the effect of polypolymerase enzyme inhibitor on histopathological and biochemical changes in the early and late periods in the ipsilateral and contralateral testicles. Urology. Aug 2010;76(2):507.e1-5. [Medline]. 5. Beni-Israel T, Goldman M, Bar Chaim S, Kozer E. Clinical predictors for testicular torsion as seen in the pediatric ED. Am J Emerg Med. Sep 2010;28(7):786-9. [Medline]. 6. Cost NG, Bush NC, Barber TD, Huang R, Baker LA. Pediatric testicular torsion: demographics of national orchiopexy versus orchiectomy rates. J Urol. Jun 2011;185(6 Suppl):2459-63. [Medline]. 7. Cattolica EV, Karol JB, Rankin KN, Klein RS. High testicular salvage rate in torsion of the spermatic cord. J Urol. Jul 1982;128(1):66-8. [Medline]. 8. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician. Nov 15 2006;74(10):173943. [Medline]. 9. Sun J, Liu GH, Zhao HT, Shi CR. Long-term influence of prepubertal testicular torsion on spermatogenesis. Urol Int. 2006;77(3):275-8. [Medline]. 10. Puri P, Barton D, O'Donnell B. Prepubertal testicular torsion: subsequent fertility. J Pediatr Surg. Dec 1985;20(6):598-601. [Medline]. 11. Coley BD. The Acute Pediatric Scrotum. Ultrasound Clinics. 2006;1:485-96. [Full Text]. 12. Yang C Jr, Song B, Liu X, Wei GH, Lin T, He DW. Acute scrotum in children: an 18year retrospective study. Pediatr Emerg Care. Apr 2011;27(4):270-4. [Medline]. 13. Johnston BI, Wiener JS. Intermittent testicular torsion. BJU Int. May 2005;95(7):933-4. [Medline]. 14. Hayn MH, Herz DB, Bellinger MF, Schneck FX. Intermittent torsion of the spermatic cord portends an increased risk of acute testicular infarction. J Urol. Oct 2008;180(4 Suppl):1729-32. [Medline]. 15. Creagh TA, McDermott TE, McLean PA, Walsh A. Intermittent torsion of the testis. BMJ. Aug 20-27 1988;297(6647):525-6. [Medline]. [Full Text]. 16. Schmitz D, Safranek S. Clinical inquiries. How useful is a physical exam in diagnosing testicular torsion?. J Fam Pract. Aug 2009;58(8):433-4. [Medline]. 17. Brenner JS, Ojo A. Evaluation of scrotal pain or swelling in children and adolescents. UpToDate [serial online]. 2006;Accessed July 28, 2011. Available at http://www.uptodate.com/contents/evaluation-of-scrotal-pain-or-swelling-in-childrenand-adolescents?source=search_result&selectedTitle=2~13. 18. Eyre RC. Evaluation of the acute scrotum in adults. Accessed July 28, 2011. Available at http://www.uptodate.com/contents/evaluation-of-the-acute-scrotum-in-adultmen?source=search_result&selectedTitle=1~13. 19. Doehn C, Fornara P, Kausch I, Bttner H, Friedrich HJ, Jocham D. Value of acute-phase proteins in the differential diagnosis of acute scrotum. Eur Urol. Feb 2001;39(2):215-21. [Medline]. 20. Prando D. Torsion of the spermatic cord: the main gray-scale and doppler sonographic signs. Abdom Imaging. Sep-Oct 2009;34(5):648-61. [Medline]. 21. Dogra VS, Bhatt S, Rubens DJ. Sonographic Evaluation of Testicular Torsion. Ultrasound Clinics. 2006;1:55-66. 22. Yagil Y, Naroditsky I, Milhem J, Leiba R, Leiderman M, Badaan S, et al. Role of Doppler ultrasonography in the triage of acute scrotum in the emergency department. J Ultrasound Med. Jan 2010;29(1):11-21. [Medline].

23. Turgut AT, Bhatt S, Dogra VS. Acute Painful Scrotum. Ultrasound Clinics. 2008;3:93107. 24. Cassar S, Bhatt S, Paltiel HJ, Dogra VS. Role of spectral Doppler sonography in the evaluation of partial testicular torsion. J Ultrasound Med. Nov 2008;27(11):1629-38. [Medline]. 25. Blaivas M, Sierzenski P, Lambert M. Emergency evaluation of patients presenting with acute scrotum using bedside ultrasonography. Acad Emerg Med. Jan 2001;8(1):90-3. [Medline]. 26. Bomann JS, Moore C. Bedside ultrasound of a painful testicle: before and after manual detorsion by an emergency physician. Acad Emerg Med. Apr 2009;16(4):366. [Medline]. 27. Moschouris H, Stamatiou K, Lampropoulou E, Kalikis D, Matsaidonis D. Imaging of the acute scrotum: is there a place for contrast-enhanced ultrasonography?. Int Braz J Urol. Nov-Dec 2009;35(6):692-702; discussion 702-5. [Medline]. 28. Terai A, Yoshimura K, Ichioka K, Ueda N, Utsunomiya N, Kohei N, et al. Dynamic contrast-enhanced subtraction magnetic resonance imaging in diagnostics of testicular torsion. Urology. Jun 2006;67(6):1278-82. [Medline]. 29. Park K, Choi H. An evolution of orchiopexy: historical aspect. Korean J Urol. Mar 2010;51(3):155-60. [Medline]. [Full Text].

Pediatric Testicular Torsion

Author: Krishna Kumar Govindarajan, MBBS, DNB, MNAMS, MRCS, FAIS, FICS, FEBPS; Chief Editor: Marc Cendron, MD

Updated: May 22, 2009Background

Testicular torsion is an acute vascular event in which the spermatic cord becomes twisted on its axis, such that the blood flow to and/or from the testicle becomes impeded. This results in ischemic injury and infarction. The condition may result in loss of the testis. The photograph below depicts testicular torsion.

Torsion testis cord twist clearly demonstrated.

Testicular torsion is one of the more common acute pediatric surgical conditions, although few studies have documented the actual incidence. In 1976, a study from the United Kingdom reported the annual incidence of testicular torsion as 1 case per 4000 in males younger than 25 years.[1] Testicular torsion has a bimodal incidence; one group presents in the perinatal period (perinatal testicular torsion; depicted in the image below), and the other group presents in early puberty (although torsion can present at any age, well into adulthood [see Testicular Torsion]). Another condition that mimics testicular torsion in presentation is torsion of the appendix testis (appendix epididymis), which is most commonly seen in older prepubertal boys.

Perinatal torsion. Because testicular torsion is a potentially reversible condition when diagnosed and treated early, the emphasis should be on prompt evaluation of children who present with acute scrotum. General public awareness and awareness in referring pediatricians and general practitioners is key to improving outcomes in these boys.[2]

History of the Procedure

Testicular torsion was first described by Delasiauve in 1840. It was not widely regarded as a significant problem until 1907, when Rigby and Russell published their work on torsion of the testis in Lancet. The first description of neonatal torsion was by Taylor in 1897. Subsequently, Colt reported torsion of the appendage testis in 1922.[3, 4] The initial use of Doppler ultrasonography was reported in 1975; Nadel et al reported sodium pertechnetate testicular scintigraphy in 1973.[5]

Etiology
A rotational twisting of the spermatic cord is the basis of all torsion events. When the twist is sufficient to obstruct arterial inflow, testicular ischemia results. If the duration of ischemia is long enough, infarction results. Lesser degrees of cord twisting may result in obstruction of venous outflow, causing congestion and swelling of the testis without frank infarction. Unfortunately, no reliable indicator for risk of torsion has been identified. Numerous factors have been observed in association with torsion, but none can be used to predict torsion risk in a clinical setting.[6]

Bell clapper deformity: In this anatomic variant, the testis hangs freely within parietal tunica vaginalis secondary to an extension of the tunica high onto the spermatic cord. This extension allows the testis to rotate easily within the tunica because of the lack of normal fixation of the posterior testis to the scrotal tissues. The bell clapper deformity is often noted at the time of exploration in older children and adolescents with testicular torsion. The anomaly is seen in 12% of males in cadaveric studies and is often bilateral.[7] Pubertal changes: The observation that the risk of torsion is increased around the time of puberty has led to speculation regarding the role of pubertal changes in torsion risk. Increased testosterone levels at puberty result in an increased testicular volume and mass. These increases could predispose the testis to torsion because of increased movement around the axis of the cord. The cords torsional rigidity and other resistances, which tend to limit the angle of rotation, may increase less markedly with growth and development. Thus, normal physical activity may result in angular momentum sufficient to easily overcome the opposing resistances, allowing complete testicular torsion.[8] Anatomical abnormalities: Various anatomical abnormalities of the testis are associated with torsion. Most significant of these is cryptorchidism (see image below). Cryptorchid testes are at significantly higher risk of torsion than scrotal testes.[9] Other anatomic abnormalities that may predispose to torsion include a horizontal lie of the testes,

polyorchidism,[10] and epididymal anomalies.[11] Torsion of undescended testis. Physical activities: In some cases, specific physical activities, including sports, weight training, or trauma, appear to induce an episode of torsion, perhaps due to a sudden cremasteric reflex. Epidemiological studies have shown that testicular torsion is more common in winter months and in northern latitudes, prompting speculation that coldinduced cremasteric contraction may play a role in the development of torsion.[12] Tunica and scrotal tissue adhesion: In the newborn, the scrotal parietal tunica vaginalis has not yet fully adhered to the outer tissues of the scrotum. Thus, the entire testes, tunica vaginalis, and gubernaculum may twist together within the scrotum, resulting in an extravaginal torsion. This is the most common form of torsion in the perinatal period. Because the adhesion between the tunica and scrotal tissues is bilaterally deficient, these infants are at risk for bilateral torsion events (either synchronous or metachronous).[8, 13]

Pathophysiology
Testicular torsion can take place either inside (intravaginal) or outside (extravaginal) the tunica vaginalis. The distinction is important because these conditions are associated with different ages of presentation and etiologies; hence, they differ in management. Intravaginal testicular torsion, as depicted in the photograph below, is far more common and represents almost all torsion events in older boys, whereas extravaginal testicular torsion is commonly seen in perinatal torsion. The tunica vaginalis takes about 6 weeks after birth to adhere to the surrounding tissues,

possibly explaining the preponderance of the condition in neonates. Large birth weight, difficult labor, breech presentation, and overreactive cremasteric reflex have been proposed as possible causes for perinatal torsion.[8, 14]

Intravaginal torsion with ischemia in a adolescent boy. Testicular torsion is classically described as involving a medial rotation; however, in up to one third of cases, a lateral rotation has been described.[15, 16] When manual detorsion is contemplated, the testis is typically rotated laterally ("opening the book"); however, if the testis is already laterally rotated, this maneuver worsens the condition.

Presentation
Testicular torsion presents as an acute onset of severe scrotal pain, commonly with associated scrotal swelling and erythema. Nausea and vomiting are common, as are local scrotal redness and pain. Although the pain is usually severe, with a rapid onset, patients occasionally present with a history of pain lasting many hours or even days. Upon examination, the classic findings of testicular torsion include an exquisitely tender, highriding testis with an abnormal (transverse) orientation. Scrotal swelling and edema are common. The cremasteric reflex is generally absent in cases of testicular torsion. In one series, the absence of cremasteric reflex was 100% sensitive for testicular torsion but was only 66% specific (because many boys have absent or decreased cremasteric reflex at baseline).[17, 18] An intact cremasteric reflex in the setting of torsion has been reported; thus, the presence of the reflex should not be used to rule out torsion in a patient whose presentation is otherwise suspicious for torsion.[18] Torsion of the appendix testis may present similarly to testicular torsion. The age of the patient may be helpful, as torsion of the appendix testis is more common in prepubertal boys.[14] These boys are less likely to have nausea and vomiting than boys with testicular torsion. Upon examination, a classic "blue-dot sign" may be seen; this finding on the upper scrotum is a typical finding in torsion of the appendix testis, as depicted in the photograph below. However, in the acute setting, differentiating testicular torsion from torsion of the appendix is often impossible, and scrotal exploration should be performed whenever the diagnosis is uncertain.

Torsion of appendix testis. Intermittent torsion that persists with recurrent attacks of pain requires a careful examination to reveal subtle signs, such as excess testicular mobility and transverse testicular orientation. An elective scrotal exploration may be planned to look for a bell clapper deformity and to avoid a dead testicle. Torsion of the cryptorchid testis can be very challenging to diagnose. This condition may be mistaken for incarcerated hernia, appendicitis, or other causes of acute abdomen. Intraabdominal testicular torsion is often associated with malignant degeneration.[19] Testicular torsion can occur in boys who have undergone prior orchidopexy, although this is unusual. Hence, testicular torsion should be suspected and considered in the differential diagnoses of acute scrotum in this group.[12, 20]

Differential diagnoses

Torsion appendage testis Hydatid of Morgagni Idiopathic scrotal edema (dermatitis, insect bite) Trauma Epididymitis Orchitis Scrotal abscess/cellulitis Epididymal torsion Tumor Acute hydrocele Obstructed/incarcerated hernia Furuncle Hemangioma Varicocele Abdominal trauma with hemiscrotum Perforated appendicitis Splenogonadal fusion Adrenal neuroblastoma Adrenal hemorrhage Meconium peritonitis Antenatal Meckel diverticulum perforation Henoch-Schnlein purpura Hernial sac torsion

Pyocele Ventriculoperitoneal shunt migration

Indications
Neonate with acute scrotum at birth
Recommendations are controversial. Although most authorities recommend exploration of the ipsilateral side and fixation of the contralateral testis, some have suggested that observation is acceptable because of the negligible salvage rate of the ischemic testis and the low incidence of contralateral torsion. The risk of anesthesia in children younger than 1 year may also factor into decision-making process.

Neonate with acute scrotum a few days after birth

The recommendations are the same as those for the neonate with acute scrotum at birth.

Prepubertal boy with acute scrotum

Exploration with salvage of ipsilateral testis is recommended, if possible. If testicular torsion is confirmed, contralateral orchiopexy is recommended. Differential diagnoses to consider include torsed appendix epididymis ("blue-dot sign") and epididymitis. If a clear-cut "blue dot sign" is identified and confirmed with Doppler ultrasonography findings, a conservative approach is justified.

Adolescent with acute scrotum

Exploration with salvage of ipsilateral testis is recommended, if possible. If torsion is confirmed, contralateral orchiopexy is recommended. If the testis has not been salvaged, ipsilateral orchiectomy is usually performed.

Relevant Anatomy
The normal testis lies suspended in the scrotum, with the visceral tunica vaginalis wrapping the anterior, inferior, superior, and mediolateral margins, leaving the posterior surface adherent to the surrounding scrotal soft tissues. The testicular arteries arise from the abdominal aorta and pass inferolaterally through the retroperitoneum to the internal inguinal ring, where they meet the vasa deferentia and enter the inguinal canal. The spermatic cord (artery, vein, vas, and supporting structures) passes through the canal, out the external inguinal ring, over the pubic tubercle, and into the scrotum, where it meets the testis.

Laboratory Studies

Urinalysis may help to suggest an infectious etiology of scrotal pain when positive for pyuria and bacteriuria; however, urinalysis should not be allowed to delay treatment in cases suspicious for acute testicular torsion.

Imaging Studies
Although contemporary imaging techniques are generally able to correctly reveal testicular torsion in most cases, pediatric urologists have been hesitant to rely too heavily on these diagnostic tests. Concerns over false-negative findings and the lengthy wait necessary to complete studies at some centers (and the lack of availability of radiology services of any kind at certain hours) have led many urologists to rely on the clinical history and examination to guide the decision for surgery in most cases. According to this philosophy, a negative exploration finding is indeed a better outcome than a necrotic testis due to a missed diagnosis. Such practices are reinforced by medicolegal concerns, particularly given the well-documented incidence of false-negative results.[21, 22] Thus, at many centers, imaging studies are used primarily when the diagnosis is uncertain but the index of suspicion for testicular torsion is low. Clearly, many patients present with scrotal pain, but only a fraction of these have torsion.[23, 24]

Doppler scanning
The most widely used imaging modality for evaluation of testicular torsion is ultrasonography with Doppler scanning for blood flow. An absent Doppler signal in the testicular parenchyma is diagnostic of testicular torsion. Initial parenchymal echogenicity is decreased but may increase once infarction has ensued. However, as with any ultrasonographic modality, the study is highly operator-dependent. Important factors to consider include the presence or absence of blood flow in the central parts of the testis, taking into account the Doppler signals only from the centripetal branches of the testicular artery, minimizing motion artifact, and carefully comparing findings with the contralateral testis to make a confident decision.[21] A markedly enlarged, echogenic, and avascular/hypovascular epididymis is an ancillary ultrasonographic sign in testicular torsion. A hypervascular enlarged epididymis can occur in 5% of cases and should not be dismissed as epididymitis.[25] In old torsion, the testis size is small, appearing echo-poor, with a prominent, enlarged epididymis. In cases of intermittent and early testicular torsion, false-negative findings can be expected. Ultrasonography can be used to differentiate extratesticular pathology, including hydrocele, abscess, wall edema, and hematoma, from testicular etiologies such as tumor or torsion. Ultrasonography is often helpful in diagnosing epididymo-orchitis, characterized by increased blood flow to the testis and epididymis. In case of a torsed testicular appendage, an extra testicular hyperechogenic nodule can be identified between the head of the epididymis and the upper pole of the testis.[24] Overall, ultrasonography with Doppler has been reported to yield a sensitivity of 88% and specificity of 90% for identifying testicular torsion. However, the sensitivity and specificity of

this modality widely varies among institutions, depending on factors ranging from equipment to operator and radiologist experience. False-positive findings can be particularly troublesome in infants because of difficult flow detection in prepubescent testes.[26, 27]

High-resolution ultrasonography
Ultrasonography with a high-resolution probe (at least a 7.5-MHz transducer) is a recent addition to the armamentarium to detect testicular torsion. This study is used to examine the cord in its entirety, from the inguinal canal downward, to detect a spiral twist, yielding a sensitivity of 97.3% and a specificity of 99% in confirming torsion. High-resolution ultrasonography has been reported to be superior to Doppler ultrasonography alone. Again, the concern is that the findings are operator-dependent. This study is widely used in tertiary care centers but may not be available in many community or rural settings.[28]

Nuclear scanning
Radioisotope scanning has been reported to be highly accurate for diagnosis of testicular torsion. The ischemic area is seen as a photopenic zone in testicular ischemia. In cases of inflammation and infection, increased uptake is seen. Unfortunately, this modality is not widely available, and even centers with functioning nuclear medicine capabilities may not have these available at all hours. For this reason, ultrasonography imaging is more widely used in the United States in most settings. Radioisotope scanning involves a low dose of radiation (2 millisievert).[29]

Medical Therapy
In some cases of testicular torsion, manually untwisting the spermatic cord may allow reestablishment of vascular flow. The technique involves manipulating the involved testis so that the anterior surface rotates from medial to lateral. This is termed the "open book" method because the motion resembles opening the cover of a book (for a right testis). When successful, this maneuver almost immediately relieves pain in most patients. Manual detorsion is best performed with the intention of buying time before the surgical team is ready but not with the intention of altogether avoiding a surgical procedure.[30] Reports of this procedure have suggested that it is highly effective, in that it allows the acute emergency to be converted into an elective surgical procedure, with a quoted salvage rate of 100%.[15] Cornel et al report that no testicular atrophy was detected after performing a manual detorsion.[31] In actuality, manual detorsion is difficult and rarely used. Application of this maneuver in an emergency department setting in a child with a swollen painful scrotum can be difficult or impossible without anesthesia. Furthermore, the testis may not be fully detorsed or may retorse shortly after the patient leaves the hospital. In addition, knowing which way the testis is torsed a priori is impossible; thus, attempting detorsion may simply worsen the degree of torsion.

Surgical Therapy

Testicular torsion is a surgical emergency, and all efforts should be aimed at bringing the patient to the operating room as quickly as possible within the limits of surgical and anesthetic safety. Outcomes directly depend on the duration of ischemia; thus, time is of the essence.[4] Time wasted attempting to arrange for imaging studies, laboratory testing, or other diagnostic procedures results in lost testicular tissue. The goals of surgical exploration include (1) confirmation of the diagnosis of torsion, (2) detorsion of the involved testis, (3) assessment of the viability of the involved testis, (4) removal (if nonviable) or fixation (if viable) of the involved testis, and (5) fixation of the contralateral testis, when appropriate. Because of the concern regarding the possibility of asynchronous testicular torsion, contralateral exploration and fixation is widely performed.[32, 33] The argument against surgical exploration includes the low probability of salvage in the setting of old torsion (>24-48 h). However, proponents of surgery argue that, in view of medicolegal implications, exploration needs to be performed to prove the diagnosis, to salvage the testis (if possible), and to concurrently perform a contralateral orchidopexy. Indeed, surgeons rarely experience medicolegal consequences for a negative exploration finding in the setting of acute scrotum, whereas lawsuits for failure to explore are routine.[34]

Intraoperative Details
Exploration can involve paramedian scrotal incision, transverse incision, or single midline scrotal incision. Some surgeons prefer to explore the acute scrotum through an inguinal incision, based on the theory that this approach offers better control of the high spermatic cord if the exploration reveals an unexpected diagnosis (eg, testis tumor). It may be difficult to intraoperatively determine whether a testis of marginal viability should be retained or excised. Although retaining a marginal testis may appear to carry no negative consequences, long-term concerns about the immunological consequences of the infarcted testis have been raised. Testicular ischemia disrupts the blood-testis barrier, which may result in autoimmunization against spermatozoa and formation of antisperm antibodies; this may affect sperm produced by both testes. However, both spermatogenesis and the blood-testis barrier are established after age 10 years; thus, some surgeons always retain the doubtful testis in children younger than 10 years.[8] Arda et al recommend that the testis be incised at exploration to look for bleeding, which is graded as I (immediate bleeding), II (bleeding after 10 min), and III (no bleeding after 10 min).[35] Excision of the testis is recommended for grade III. Once the testis has been detorsed and the decision is made to preserve it, the tunica vaginalis is everted, as in a Jaboulay procedure; 2-3 sutures are passed through the dartos and tunica albuginea of the testicle. Some surgeons avoid placing sutures directly into the tunica albuginea out of concern for disrupting the blood-testis barrier; instead, they place the sutures into the visceral tunica vaginalis of the mesorchium.[36] Kuntze et al reported that absorbable sutures predispose to recurrent torsion after orchiopexy; thus, nonabsorbable sutures are recommended for securing the testis.[37]

A window orchidopexy has been performed to ensure better fixation of testis to avoid recurrent torsion, based on the principle that creating a window in the tunica vaginalis makes a broad area of dense adhesion during healing, resulting in better apposition.[38] Sutureless fixation in a dartos pouch has been reported for neonatal orchiopexy when performing a contralateral exploration.

Follow-up
Although long-term observation to monitor for testicular atrophy would be helpful in patients with testicular torsion, in actuality, many of these patients (particularly the adolescents) do not return for follow-up. Annual scrotal ultrasonography during the 2-3 years after surgery can be use to document testicular volume and growth. Recurrent torsion following an orchiopexy is possible (although rare) and may occur several years after the initial fixation of the testis. Thus, patients and parents should be forewarned about this risk and should promptly seek medical care if testicular pain occurs, even after an orchiopexy has been performed.[20]

Complications

Testicular atrophy Torsion recurrence Wound infection Subfertility,[39] possibly related to ischemia-reperfusion injury that damages the bloodtestis barrier, with resulting antisperm antibody production

Outcome and Prognosis

Successful salvage of the torsed testis is directly related to the time elapsed from the onset of ischemia. If exploration is performed within 4-6 hours of symptom onset, salvage rates may approach 90%; however, these rates dramatically drop to 50% at 12 hours after symptom onset and to almost 10% after 24 hours. In contrast, perinatal testicular torsion almost always results in loss of the involved testis (salvage rate < 5%).[40] In a survey by Bennett et al, 55% of boys with testicular torsion (aged 3 mo to 16 y) had infarction with testis loss at scrotal exploration.[41] The main reason for the testicular loss was excessive delay before seeking medical attention, usually attributed to the patient or his parents. Survey data have suggested that most boys do not think it necessary to seek medical advice for testicular swelling, and a large minority do not think it necessary to seek medical advice for testicular swelling with pain.[42] Overall, the causes for testicular loss can be summed up as lack of patient awareness or denial and subsequent delay in presentation (58%), misdiagnosis by physician resulting in missed torsion (29%), and delay in treatment (13%).[43] Tryfonas et al reported that the results of testicular atrophy correlated with duration of symptoms and operative findings.[44] In all cases of surgical detorsion in which torsion lasted longer than 24 hours and viability of the testis was questionable, subsequent atrophy occurred.

Puri et al reviewed 18 patients with prepubertal torsion who had undergone untwisting of the nonviable testis after a period of 7-23 years.[45] Fourteen of the patients had absent testis on the affected side, and 4 had severe atrophy (< 1 mL). The contralateral side appeared normal or hypertrophic, and autosensitization due to sperm autoantibodies was not observed in these patients. Fertility was preserved, based on the semen analysis in 13 patients, 10 of whom had normal counts. Sertoli cell function and spermatogenesis in humans are reflected by serum inhibin B levels, which function as a useful marker of testicular function. Inhibin B has been proposed as a more reliable measure of testicular function than histopathological examination, as biopsy findings may not be representative of the entire testis (and performing a biopsy is invasive). Serum levels of inhibin B have been shown to decrease following torsion, suggesting contralateral damage.[46]

Future and Controversies

The necessity of seeking immediate medical care in the setting of the acute scrotum cannot be sufficiently emphasized to the public and to clinicians. The risk of testicular loss and reduced fertility are possible consequences of testicular torsion.[43] Ongoing controversy surrounds the issue of exploration versus observation for perinatal torsion. This condition is uncommon enough that few centers see enough cases to merit any prospective studies, and medicolegal issues likely drive much of the decision-making in this area.[47, 48] Various experimental studies in animal models have investigated ways to minimize the testicular injury associated with ischemia and reperfusion injury. Agents as varied as superoxide dismutase, catalase, calcium channel blockers, oxypurinol, and allopurinol have been used. Other agents recently used include melatonin,[49] zinc aspartate,[50] and dehydroepiandrosterone.[51] Unfortunately, none of these models has yet generated adequate evidence to justify trials in human. References 1. Williamson RC. Torsion of the testis and allied conditions. Br J Surg. Jun 1976;63(6):465-76. [Medline]. 2. Gilchrist BF, Lobe TE. The acute groin in pediatrics. Clin Pediatr (Phila). Aug 1992;31(8):488-96. [Medline]. 3. Mac Nicol. Torsion of testis in childhood. Br J Surg. 1974;61:905-8. 4. Chapman RH, Walton AJ. Torsion of the testis and its appendages. Br Med J. Jan 15 1972;1(5793):164-6. [Medline]. 5. Nadel NS, Gitter MH, Hahn LC, Vernon AR. Preoperative diagnosis of testicular torsion. Urology. May 1973;1(5):478-9. [Medline]. 6. Mansbach JM, Forbes P, Peters C. Testicular torsion and risk factors for orchiectomy. Arch Pediatr Adolesc Med. Dec 2005;159(12):1167-71. [Medline]. 7. Caesar RE, Kaplan GW. Incidence of the bell-clapper deformity in an autopsy series. Urology. Jul 1994;44(1):114-6. [Medline].

8. Hutson J. Undescended testis, torsion, and varicocoele. In: Grosfeld JL, et al, eds. Pediatric Surgery. 2006:1193-214. 9. Cilento BG, Najjar SS, Atala A. Cryptorchidism and testicular torsion. Pediatr Clin North Am. Dec 1993;40(6):1133-49. [Medline]. 10. Ferro F, Iacobelli B. Polyorchidism and torsion. A lesson from 2 cases. J Pediatr Surg. Oct 2005;40(10):1662-4. [Medline]. 11. Favorito LA, Cavalcante AG, Costa WS. Anatomic aspects of epididymis and tunica vaginalis in patients with testicular torsion. Int Braz J Urol. Sep-Oct 2004;30(5):420-4. [Medline]. 12. Anderson JB, Williamson RC. Testicular torsion in Bristol: a 25-year review. Br J Surg. Oct 1988;75(10):988-92. [Medline]. 13. King P, Sripathi V. The acute scrotum. In: Ashcraft KW et al. Pediatric Surgery. 2005:717-22. 14. Gatti JM, Patrick Murphy J. Current management of the acute scrotum. Semin Pediatr Surg. Feb 2007;16(1):58-63. [Medline]. 15. Cattolica EV. Preoperative manual detorsion of the torsed spermatic cord. J Urol. May 1985;133(5):803-5. [Medline]. 16. Sessions AE, Rabinowitz R, Hulbert WC, Goldstein MM, Mevorach RA. Testicular torsion: direction, degree, duration and disinformation. J Urol. Feb 2003;169(2):663-5. [Medline]. 17. Rabinowitz R. The importance of the cremasteric reflex in acute scrotal swelling in children. J Urol. Jul 1984;132(1):89-90. [Medline]. 18. Nelson CP, Williams JF, Bloom DA. The cremasteric reflex: a useful but imperfect sign in testicular torsion. J Pediatr Surg. Aug 2003;38(8):1248-9. [Medline]. 19. Lewis RL, Roller MD, Parra BL, Cotlar AM. Torsion of an intra-abdominal testis. Curr Surg. Sep 1 2000;57(5):497-499. [Medline]. 20. Mor Y, Pinthus JH, Nadu A, Raviv G, Golomb J, Winkler H. Testicular fixation following torsion of the spermatic cord--does it guarantee prevention of recurrent torsion events?. J Urol. Jan 2006;175(1):171-3; discussion 173-4. [Medline]. 21. Steinhardt GF, Boyarsky S, Mackey R. Testicular torsion: pitfalls of color Doppler sonography. J Urol. Aug 1993;150(2 Pt 1):461-2. [Medline]. 22. Ingram S, Hollman AS, Azmy A. Testicular torsion: missed diagnosis on colour Doppler sonography. Pediatr Radiol. 1993;23(6):483-4. [Medline]. 23. Kalfa N, Veyrac C, Lopez M, et al. Multicenter assessment of ultrasound of the spermatic cord in children with acute scrotum. J Urol. Jan 2007;177(1):297-301; discussion 301. [Medline]. 24. Karmazyn B, Steinberg R, Livne P, et al. Duplex sonographic findings in children with torsion of the testicular appendages: overlap with epididymitis and epididymoorchitis. J Pediatr Surg. Mar 2006;41(3):500-4. [Medline]. 25. Nussbaum Blask AR, Rushton HG. Sonographic appearance of the epididymis in pediatric testicular torsion. AJR Am J Roentgenol. Dec 2006;187(6):1627-35. [Medline]. 26. Schalamon J, Ainoedhofer H, Schleef J, et al. Management of acute scrotum in children-the impact of Doppler ultrasound. J Pediatr Surg. Aug 2006;41(8):1377-80. [Medline]. 27. Kravchick S, Cytron S, Leibovici O, Linov L, London D, Altshuler A, et al. Color Doppler sonography: its real role in the evaluation of children with highly suspected testicular torsion. Eur Radiol. 2001;11(6):1000-5. [Medline].

28. Sidhu PS. Clinical and imaging features of testicular torsion: role of ultrasound. Clin Radiol. Jun 1999;54(6):343-52. [Medline]. 29. Luscombe CJ, Mountford PJ, Coppinger SM, Gadd R. Diagnosing testicular torsion. Isotope scanning is useful. BMJ. May 25 1996;312(7042):1358-9. [Medline]. 30. Garel L, Dubois J, Azzie G, Filiatrault D, Grignon A, Yazbeck S. Preoperative manual detorsion of the spermatic cord with Doppler ultrasound monitoring in patients with intravaginal acute testicular torsion. Pediatr Radiol. Jan 2000;30(1):41-4. [Medline]. 31. Cornel EB, Karthaus HF. Manual derotation of the twisted spermatic cord. BJU Int. Apr 1999;83(6):672-4. [Medline]. 32. Frank JD, O'Brien M. Fixation of the testis. BJU Int. Mar 2002;89(4):331-3. [Medline]. 33. Olguner M, Akgur FM, Aktug T, Derebek E. Bilateral asynchronous perinatal testicular torsion: a case report. J Pediatr Surg. Sep 2000;35(9):1348-9. [Medline]. 34. Kass EJ, Stone KT, Cacciarelli AA, Mitchell B. Do all children with an acute scrotum require exploration?. J Urol. Aug 1993;150(2 Pt 2):667-9. [Medline]. 35. Arda IS, Ozyaylali I. Testicular tissue bleeding as an indicator of gonadal salvageability in testicular torsion surgery. BJU Int. Jan 2001;87(1):89-92. [Medline]. 36. Steinbecker KM, Teague JL, Wiltfong DB, Wakefield MR. Testicular histology after transparenchymal fixation using polytetrefluoroethylene suture: an animal model. J Pediatr Surg. Dec 1999;34(12):1822-5. [Medline]. 37. Kuntze JR, Lowe P, Ahlering TE. Testicular torsion after orchiopexy. J Urol. Dec 1985;134(6):1209-10. [Medline]. 38. Morse TS, Hollabaugh RS. The "window" orchidopexy for prevention of testicular torsion. J Pediatr Surg. Apr 1977;12(2):237-40. [Medline]. 39. Scheiber K, Marberger H, Bartsch G. Exocrine and endocrine testicular function in patients with unilateral testicular disease. J R Soc Med. Aug 1983;76(8):649-51. [Medline]. 40. Davenport M. ABC of general surgery in children. Acute problems of the scrotum. BMJ. Feb 17 1996;312(7028):435-7. [Medline]. 41. Bennett S, Nicholson MS, Little TM. Torsion of the testis: why is the prognosis so poor?. Br Med J (Clin Res Ed). Mar 28 1987;294(6575):824. [Medline]. 42. Nasrallah P, Nair G, Congeni J, Bennett CL, McMahon D. Testicular health awareness in pubertal males. J Urol. Sep 2000;164(3 Pt 2):1115-7. [Medline]. 43. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician. Nov 15 2006;74(10):173943. [Medline]. 44. Tryfonas G, Violaki A, Tsikopoulos G, Avtzoglou P, Zioutis J, Limas C. Late postoperative results in males treated for testicular torsion during childhood. J Pediatr Surg. Apr 1994;29(4):553-6. [Medline]. 45. Puri P, Barton D, O'Donnell B. Prepubertal testicular torsion: subsequent fertility. J Pediatr Surg. Dec 1985;20(6):598-601. [Medline]. 46. Ozkan KU, Kucukaydin M, Muhtaroglu S, Kontas O. Evaluation of contralateral testicular damage after unilateral testicular torsion by serum inhibin B levels. J Pediatr Surg. Jul 2001;36(7):1050-3. [Medline]. 47. Cuervo JL, Grillo A, Vecchiarelli C, Osio C, Prudent L. Perinatal testicular torsion: a unique strategy. J Pediatr Surg. Apr 2007;42(4):699-703. [Medline]. 48. Lee SD, Cha CS. Asynchronous bilateral torsion of the spermatic cord in the newborn: a case report. J Korean Med Sci. Oct 2002;17(5):712-4. [Medline].

49. Abasiyanik A, Dagdonderen L. Beneficial effects of melatonin compared with allopurinol in experimental testicular torsion. J Pediatr Surg. Aug 2004;39(8):1238-41. [Medline]. 50. Ozkan KU, Boran C, Kilinc M, Garipardic M, Kurutas EB. The effect of zinc aspartate pretreatment on ischemia-reperfusion injury and early changes of blood and tissue antioxidant enzyme activities after unilateral testicular torsion-detorsion. J Pediatr Surg. Jan 2004;39(1):91-5. [Medline]. 51. Aksoy H, Yapanoglu T, Aksoy Y, Ozbey I, Turhan H, Gursan N. Dehydroepiandrosterone treatment attenuates reperfusion injury after testicular torsion and detorsion in rats. J Pediatr Surg. Oct 2007;42(10):1740-4. [Medline].

Korean J Urol. 2010 March; 51(3): 155160. PMCID: PMC2855448 Published online 2010 March 19. doi: 10.4111/kju.2010.51.3.155 Copyright The Korean Urological Association, 2010 An Evolution of Orchiopexy: Historical Aspect Kwanjin Park and Hwang Choi Department of Urology, College of Medicine, Seoul National University, Seoul, Korea. Corresponding author. Corresponding Author: Kwanjin Park. Department of Urology, College of Medicine, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul 110-744, Korea. TEL: +82-2-2072-0695, FAX: +82-2-742-4665, Email: urodori9@snu.ac.kr Received February 26, 2010; Accepted March 9, 2010. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY o ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE o ESTABLISHMENT OF CURRENT ORCHIOPEXY o CONCLUSIONS o References

Abstract The history of treatment for cryptorchidism dates back more than 200 years. This review is intended to highlight some historical aspect that led us to our current surgical treatment of this condition. The medical and historical surgical literatures pertaining to cryptorchidism were

reviewed. Data sources were PubMed, Embase, conference proceedings, and bibliographies. No language, date, or publication status restrictions were imposed. The study of cryptorchidism began with the anatomical descriptions of Baron Albrecht von Haller and John Hunter. Attempts at surgical correction of the undescended testis began in the early 1800s, culminating in the first successful orchiopexy by Thomas Annandale in 1877. Max Schller, Arthur Dean Bevan and Lattimer contributed to the establishment of current techniques for standard orchiopexy. Later, laparoscopy, high inguinal incision (Jones' approach) and scrotal approach were added to the list of current orchiopexy. Keywords: Cryptorchidism, Orchiopexy, History

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY o ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE o ESTABLISHMENT OF CURRENT ORCHIOPEXY o CONCLUSIONS o References

INTRODUCTION Cryptorchidism (from the Greek kryptos, meaning "hidden," and orchis, meaning "testis") refers to the absence of a testis from the scrotum. Isolated cryptorchidism is the most common congenital anomaly of the male genitalia, affecting almost 1% of full-term infants at the age of 1 year [1]. During embryonic life, the testes form beside the mesonephric kidneys and descend via the inguinal canal to the scrotum. If this process is faulty, a cryptorchid testis may halt along the normal path of descent (undescended or retractile testis), may travel off the normal path of decent (ectopic testis), or may die or never develop (absent testis). The history of the study of cryptorchidism and the first attempt to correct it began in the 18th century. Like other areas of medicine, which is a combined action of art and science, the progress of techniques in orchiopexy has been supported by an improved understanding of cryptorchidism. In this context, this review aimed to describe the historical landmarks in the progress of orchiopexy in parallel with the growing knowledge of cryptorchidism that had spurred the technical advances in orchiopexy.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM

o o o o o

ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE ESTABLISHMENT OF CURRENT ORCHIOPEXY CONCLUSIONS References

THE ERA OF PIONEERS The theoretical bases that justify orchiopexy in patients with cryptorchidism originated from some critical observations by two pioneers in the 18th century, Baron Albrecht von Haller and John Hunter. Over the ensuing years, theories on the mechanism of descent, and study of the histological and physiological alterations in the cryptorchid testis came out, aiding the development of orchiopexy. Baron Albrecht von Haller, who became the Chairman in Anatomy and Surgery at Gttenger University in the 1730s, described the abdominal position of the fetal testis in his famous work 'Opuscula Pathologica,' published in 1755. In the chapter regarding congenital hernia, he accurately indicated the presence of abdominal testis, though he did not know the exact timing of testicular descent. Also, his explanation of the phenomenon responsible for the descent of the testis was wrong. However, it was important that his description attracted the interest of John Hunter, who later made some great observations that still hold true today. John Hunter is known as one of the fathers of modern surgery and anatomy. He was born on a small farm near Glasgow, Scotland, in 1728, the youngest of 10 children. Among his 10 siblings, he and his older brother William made a significant contribution to medicine. They founded the first independent anatomical school in London. John Hunter was a brilliant anatomist with unending curiosity, a variety of interests, and a colorful character. Although William wanted his younger brother to be a classic gentleman, his character made him a house-surgeon and later a partner in the anatomy school. He was the leading expert in the study of comparative anatomy, infectious diseases, and gunshot wounds [2,3]. John Hunter began to study on the descent of fetal testis with an interest in Baron von Haller's observations. In 1762, Hunter confirmed the abdominal position of the fetal testes as well as the neurovascular supply and the cremaster or musculus testis (a more proper name, according to Hunter). Through postmortem dissection, he first observed that the testis descends generally around the eighth month. He also described the retractile testes, undescended testes, and testicular ectopia. He did not agree with the current suggestion that the testis was forced into the scrotum by the compressive force of respiration, or pulled by the cremaster muscle. Instead, he proposed the significance of gubernaculum as a helm or rudder for testicular descent [4]. Although the precise cause of failure to descend has not been clearly understood at this time, his association of cryptorchidism with faulty testis appears interesting, as he stated that: "when one or both testicles remain through life in the belly, I believe that they are exceedingly imperfect and probably incapable of performing their natural functions, and that this imperfection prevents the disposition for descent from taking place." He believed in the necessity of treatment of undescended testis after a period of patient observation. He wrote "As this progress is very slow, especially when the testicle is creeping through the ring, a doubt often arises whether it is better entirely to prevent its passage or to assist it by exercise or other means; and it would certainly be the best practice to assist it, if that could be done effectually and safely."

Hunter's accurate description of fetal testicular descent made great progress in the understanding of cryptorchidism. Although testicular decent and maldescent are now being explored on the molecular level, most of our knowledge on cryptorchidism is still based on his observations. Furthermore, even though many theories such as abdominal pressure, endocrine factors, cremasteric muscle contraction and gravity have been proposed to explain testicular descent, none is more important than the gubernaculum as Hunter claimed more than 2 centuries ago. After the great discovery of Hunter, the discussion of the nature of the gubernaculum, the role of the cremaster, and the process of descent continued. In 1866 Thomas B. Curling summarized what was known at that time regarding undescended testicles in his book, A Practical Treatise on the Diseases of the Testis [5]. Some of his observations hold true today, such as abnormal testicular function in undescended testis and proper evolutionary time limits to recovery of retained testicles. He also summarized the possible cause of the retained testicle: either the defective development of the cremasteric muscle, adhesions secondary to peritonitis, or a contracted external ring. Although he reported some misconceptions in current understandings, his observations surely gave a theoretical basis on which later doctors attempted the first orchiopexy.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY o ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE o ESTABLISHMENT OF CURRENT ORCHIOPEXY o CONCLUSIONS o References

UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM The structure of the gubernaculum, or genitoinguinal ligament, was first described and named by Hunter in 1762. Although most authors believe that it contributes significantly to testicular descent, there is little consensus on the mechanism involved. Controversies around gubernaculum were related to its tail structures and its role in the development of ectopic testis. In 1840, Curling noted the gubernaculum to be a soft, solid protruding body that varied in shape and size at different stages of testicular descent [6]. He also claimed that the gubernaculum terminated in three muscular processes, which he could trace before, during and after testicular descent. He listed these as (i) external - connected to Poupart's ligament; (ii) middle - through the external ring to the bottom of the scrotum; and (iii) internal - to the os pubis and the rectus muscle sheath. Since the gubernaculum contains muscle that is likely to contract, this led Lockwood to propose the 'traction theory' of testicular descent. Following the examination of eight fetuses (7 weeks' gestation to full term), he noted the change of distal gubernaculum from a soft, jelly-like mass into a leash of fibers that spread out to several areas and pulled the testis into the scrotum [7].

Sometime later, his description of the fibers became known as the 'tails of Lockwood' and the presumed cause of testicular ectopia (Fig. 1) [8]. Although Lockwood himself did not mention that abnormal development of the gubernacular tail could be the cause of testicular ectopia, some authors referred to Lockwood's work as an explanation for testicular ectopia [9-11]. FIG. 1 Theories of testicular ectopia [8]. (A) Old theory: Mythical 'tails of Lockwood' was used to explain the location of ectopic testis because the gubernaculum pulled the testis into position. (B) Current theory: The testis migrates to the scrotum (or elsewhere) (more ...) In the early 20th century, the concept of gubernacular tails as a cause of testicular maldescent prevailed. Coley found many similarities between Curling's and Lockwood's theories and tried to amalgamate both theories [12]. Some authors reported findings in conflict to the "tails of Lockwood." Sonneland could not find any corroborative evidence either embryological or anatomical for the existence of multiple processes [9]. Instead of multiple gubernacular tails, he claimed a singular gubernacular process and believed that the fibrous attachment of ectopic testis was just a result and not the cause of testicular maldescent. McGregor also failed to find any subdivision of the gubernaculum and concluded that Lockwood's theory was unproved and proposed the 'third inguinal ring' or congenital fascial packets or barriers as a cause of testicular ectopia [13,14]. Backhouse proposed his own theory regarding the gubernaculums [15]. He described the gubernaculum as consisting only of mesenchyme (not muscles and fibers, as previous believed), which formed a column in the abdomen at taching the testis to the inguinal region and then to the floor of the scrotum. His theory was that the gubernacular mesenchyme could be disrupted by surrounding fibrous tissues to cause undescended or maldescended testis. He proposed that 'a fibrous band is formed (a "tail of Lockwood") which anchors the gubernaculum and later the testicular apparatus to the surrounding tissues, and, by virtue of the processus vaginalis having being formed normally elsewhere, the descending testis is diverted from its course in the direction of the band. This then is the aetiology of an ectopic testis and also the formation of the tails of Lockwood, which are a pathological feature rather than a normal component of the gubernaculum.' According to his theory, the tail of Lockwood indicated either a gubernacular process or an abnormal fibrous attachment, causing great confusion [15,16]. By the mid 1980s most investigators completely rejected the theory of multiple gubernacular tails providing traction to cause testicular descent. In 1987, Heyns published a landmark paper describing testicular descent in 178 human fetuses, the largest number of fetuses examined at the time. What he found was no inclusion of muscle in the gubernaculum and singular rather than multiple processes of distal gubernaculum [17]. At present, many studies have now shown conclusively that multiple gubernacular processes (or tails) do not exist and that the distal gubernaculum is unattached to surrounding tissues during inguinoscrotal migration in both rodents and humans. Attachment to the scrotum (or elsewhere) occurs only after normal (or abnormal) testicular descent is complete. Although some recent papers still referred to tails of Lockwood as a cause of ectopic testis and even transverse testicular ectopia, it is certainly time to dispel the myth of the tails of Lockwood as a cause for ectopic testis.

Other Sections o Abstract

o o o o o o o o o

INTRODUCTION THE ERA OF PIONEERS UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE ESTABLISHMENT OF CURRENT ORCHIOPEXY CONCLUSIONS References

THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM Before the periods when orchiopexy was widely accepted, an inguinal ascended testis was managed primarily with the use of truss or castration. It was said the surgery for correction of undescended testis was attempted by several German doctors such as J.F. Rosenmerkel of Munich in 1820 and M.J. von Chelius in 1837 [4]. However, the first recorded attempt was performed by James Adams in the London Hospital in 1871 on an outpatient. His reason for correction was shown in the Lancet published at that time [18]. He proposed 3 reasons to operate on an undescended testis: poor scrotal development due to cryptorchidism, the risk of atrophy of the abdominal testis, and the likelihood of injury or pain associated with the abnormal location. He reported on one 11-week-old patient who was referred for an empty left scrotum, normal right testicle and an "oval swelling in the perineum, to the left of the middle line.. in front of the anus." Adams performed the orchiopexy with Curling through a 1.5 inch incision over the external ring. The spermatic cord and testicle were freed from attachments. The tunica vaginalis was uninjured and a catgut suture was used to affix the testicle into the scrotal pouch, after which the wound was closed. Owing to the high prevalence of erysipelas in the hospital, the operation was performed on an outpatient basis and the child was sent home. Nevertheless, the patient developed a wound infection on postoperative day 3 that progressed to fatal erysipelas. Adams personally performed the autopsy and concluded that "death was caused by peritonitis commencing in the tunica vaginalis and extending upwards." The importance of identifying and ligating a patent processus vaginalis during orchiopexy was not recognized at that time [18]. In the 1870s even minor surgical procedures carried a high risk of morbidity from infection. Adams concluded that "no operation should be undertaken in early life" because of the high likelihood of wound infection and subsequent peritonitis, unless the patient is "destined to become an equestrian." Because most orchiopexies at that time were conducted for a perineal ectopic testis, which could have caused significant discomfort to the horseman, he seemed to suggest orchiopexy limited to this kind of occupation.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM

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THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE ESTABLISHMENT OF CURRENT ORCHIOPEXY CONCLUSIONS References

ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY Thomas "Tommy" Annandale was born at Newcastle-on-Tyne on February 2, 1838. At the age of 15 years Tommy began work as an apprentice to his father, and at age 18 he matriculated at the University of Edinburgh, receiving a doctorate in medicine 4 years later in 1860. For his surgical training, He remained in Edinburgh under the tutelage of James Syme. Then he served as private assistant for 10 years until Syme's death in 1870. At that time, he became acquainted with Joseph Lister, who had already been the senior assistant under Syme. Besides, he also got the idea of antiseptics by using a carbolic acid wound dressing from Lister. The concept of an antiseptic wound dressing technique, first reported by Lister, was revolutionary at that time, significantly reducing the risk of wound infection. In 1877, he succeeded Joseph Lister as the regius professor (chair) of clinical surgery at the University of Edinburgh. He occupied the surgical chair at Edinburgh for 30 years, from 1877 to 1907, maintaining an active surgical practice in general surgery, orthopedics, otolaryngology, urology, and other subspecialties [19]. On June 1877, Annandale was referred a 3-year-old boy with pain in the perineum on walking and running. Annandale described the care of this patient in 'The British Medical Journal' in 1879, detailing the first recorded successful orchiopexy [20]. The patient had a right ectopic testis palpated on ipsilateral perineum. On July 5, 1877, he did orchiopexy after freeing the testicle and gubernaculum from its attachment. Annandale credited Curling, who had attempted to perform orchiopexy with Adams, with the idea of anchoring the testis to the bottom of the scrotum, and his patient further benefited from the application of Lister's antiseptic technique as a dressing of carbolic acid (phenyl alcohol) was applied to the wound. Unlike the cases of Adams, the postoperative course was "satisfactory in every way," possibly due to the proper use of antiseptic techniques as Annandale has written "the whole of the operation was performed antiseptically." Unquestionably, in the right place and at the right time, Annandale integrated the art and science of medicine. He recognized the importance of Lister's work and Curling's previous experiences, and fused their ideas into the first successful orchiopexy.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY

o o o o

ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE ESTABLISHMENT OF CURRENT ORCHIOPEXY CONCLUSIONS References

ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE Following the successful orchiopexy by Annandale, several authors refined the techniques, which helped to give birth to the current technique. Max Schller, in the 1881 Annals of Anatomy and Surgery, wrote an extensive treatise on undescended testis that included a description of the malignant potential of cryptorchidism [21]. In describing the surgical technique, he first advocated the division of the processus vaginalis to mobilize the spermatic cord in correction of the malpositioned testis. Additionally, he stressed the full division of cremaster upon the testicle and obstruction of the inguinal canal to reduce the re-ascent of testis. In contrast to Schller's technique, in 1893, Leonard Bidwell, assistant surgeon of the West London Hospital, described a technique for inverting the testis to gain approximately an inch and a half of length and anchoring the testis to an external wire cage to provide continuous traction [22]. Arthur Dean Bevan was Professor and Head of the Department of Surgery at Rush Medical College in Chicago and later President of the American Medical Association and the American Surgical Association. In 1899, He brought the Schller's concepts, such as division of the processus vaginalis, to the United States for the first time and took another step further, emphasizing the tension-free mobilization of the testis to the scrotum by releasing the spermatic vessels to the retroperitoneum and possible resection of them to gain further length [23]. He claimed that the need for spermatic vessel division would be lessened after increased study and experience. He also described sewing the deep layer of the superficial fascia to the aponeurosis of the external oblique to prevent retraction of the testis, using a purse-string technique. With these kinds of modifications, he reported his results in over 400 cases with an overall success rate of approximately 95% [24]. Bevan also recommended the early correction of undescended testis. His statement was further supported by Eisendrath, who showed a 90% occurrence of seminiferous tubule atrophy by 2 years of cryptorchidism [25]. This was followed by the landmark animal study by Carl Moore, who observed loss and recovery of testicular function after surgical cryptorchidism and orchiopexy, respectively [26]. From Bevan's work, three main issues concerning the surgical treatment of the undescended testis became apparent: the requirement for mobilization of the cord, the questionable necessity of division of the spermatic vessels to gain additional cord length, and the debate between traction and tension-free repositioning of the testis within the scrotum. In the beginning of the 20th century, several concepts concerning cryptorchidism that are currently useful for understanding the disease were accepted, such as the prevalence of hernias, the possibility of torsion, the malignant potential of the "arrested" testis, and functional limitations of cryptorchid testis, both in terms of spermatogenesis and hormone production. These were well summarized by Eccles in a lecture named "The Anatomy, Physiology, and Pathology of the Imperfectly Descended Testis" [27,28].

Some surgeons tried to overcome the problem of a short length of spermatic cord. They fixed the testis to another site, such as the fascia lata or contralateral testis, for the purpose of possible lengthening of the cord. Torek in Newyork and Keetley in England independently reported the technique of fixation in the fascia lata in a similar period [29,30]. The testis was recommended to be kept in situ for 3 to 6 months and then detached carefully and repositioned in the scrotum. Torek also reported 64 cases of successful staged operation, which did not need to divide the spermatic vessels [29]. The concepts of continuous traction were revisited by Cabot and Nesbit of Michigan University again with the use of a rubber band and wire cage for approximately 12 days [31]. Although there is enthusiasm for one stage repair of orchiopexy, some difficult cases with short testicular cord will benefit by the judicious use of staged operations with traction of the testicular cord for the time being. This concept is still valid and is applied to some staged operations. Robert J. Prentiss of San Diego County Hospital added additional technical insight with his detailed depiction of the surgical anatomy of the spermatic vessels and the anatomic proof that relative lengthening of the spermatic cord could be achieved by division of the inferior epigastric vessels and medial displacement of the spermatic vessels [32]. The current method of testicular fixation within the subdartos pouch was first described by Schoemaker [33] in 1932 but was popularized by John K. Lattimer [34], at Columbia University, in 1957. He also worked out a way to implement gentle traction via an elastic band anchored in the vicinity of the patient's knee for 10 days. With the inclusion of the subdartos pouch technique, the four key steps of standard orchiopexy were established just before the 1960s. The standard orchiopexy can be applied to almost all undescended testes with the exception of high undescended testes. The success rate ranges from 89% to 92%. Therefore, attention has turned to the treatment of high undescended testes which were not adequately treated by standard orchiopexy.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY o ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE o ESTABLISHMENT OF CURRENT ORCHIOPEXY o CONCLUSIONS o References

ESTABLISHMENT OF CURRENT ORCHIOPEXY In 1979, Jones and Bagley suggested a high inguinal incision as the open surgical alternative for high canalicular or intraabdominal testes [35]. A transverse incision is made medial to the anterior superior iliac spine and carried down to the external oblique fascia just superior to the internal ring. This incision made it possible to approach the peritoneal cavity easier than through a standard inguinal incision. The point is the preservation of the spermatic vessels, high

retroperitoneal mobilization of the spermatic vessels, and passage of the testis directly through the abdominal wall at the pubic tubercle (Prentiss maneuver). This procedure shares similar indications and surgical principles with laparoscopic orchiopexy and was the popular surgical approach before the advent of laparoscopic management of an intra-abdominal testis. In case of a high undescended testis, the testicular artery and veins often limit the distal mobility of these testes. As mentioned earlier, attempts to divide the testicular artery were made well before the 20th century. However, a high atrophy rate precluded wide application. In 1959, Fowler and Stephens [36] studied the vascular anatomy of the testis and devised a means to repair a high undescended testis and preserve its blood supply via collateral circulation. Children with a long, looping vas that extends down the inguinal canal are the ideal candidates for this surgery, but less than one third of the children with intraabdominal testes were found to have this condition. Originally, Fowler and Stephens orchiopexy was known as a staged technique but it was further modified into a 2-staged operation with a better success rate (77% vs. 67%). Prior to 1976, the non-palpable testis was only located by inguinal exploration. However Cortesi et al [37] first described the laparoscopy as a modality that could reveal the location of nonpalpable testis. With increased experience, its indication was further expanded to therapeutic purposes. Bloom in 1991 described a procedure for staged pelviscopic orchiopexy [38]. The pure one-stage laparoscopic orchiopexy was first reported by Jordan and Winslow [39]. Therapeutic laparoscopy has the advantage of 1) high magnification and improved visualization 2) capability of extensive vascular dissection up to the origin of gonadal vessels, 3) minimal morbidity, and 4) the ability of creating a new internal ring medial to inferior epigastric vessels to achieve the straight vascular course to the scrotum. Laparoscopic orchiopexy can be conducted as either one-stage orchiopexy with preservation of spermatic vessels or Fowler and Stephens orchiopexy. While current orchiopexy includes a variety of methods, all methods stem from the basic concepts of standard orchiopexy. CONCLUSIONS More than 200 years ago, the discussion of cryptorchidism began and the surgical techniques and philosophies have continued to evolve. The current technique of standard orchiopexy is the end result of evolved concepts. A study of the history of surgical management of the undescended testis sheds light on the rationale behind the current management. Footnotes The authors have nothing to disclose.

Other Sections o Abstract o INTRODUCTION o THE ERA OF PIONEERS o UNDERSTANDING AND CONTROVERSIES ABOUT GUBERNACULUM o THE FIRST ATTEMPT AT SURGICAL CORRECTION OF CRYPTORCHIDISM o ANNANDALE'S SUCCESS FOR 1st ORCHIOPEXY o ESTABLISHMENT OF MODERN STANDARD ORCHIOPEXY: INTEGRATING MORE KNOWLEDGE INTO PRACTICE o ESTABLISHMENT OF CURRENT ORCHIOPEXY o CONCLUSIONS o References

References 1. Berkowitz GS, Lapinski RH, Dolgin SE, Gazella JG, Bodian CA, Holzman IR. Prevalence and natural history of cryptorchidism. Pediatrics. 1993;92:4449. [PubMed] 2. Rutkow I. Surgery: an illustrated history. St. Louis: Mosby-Year Book; 1993. pp. 229233. 3. Palmer JF. The works of John Hunter, F.R.S. with notes. London: Longman, Rees, Orme, Green & Longman; 1835. pp. 1525. 4. Tackett LD, Patel SR, Caldamone AA. A history of cryptorchidism: Lessons from the eighteenth century. J Pediatr Urol. 2007;3:426432. [PubMed] 5. Curling TB. A practical treatise on the diseases of the testis. London: J. Churchill; 1866. pp. 1255. 6. Curling JB. Observations on the structure of the gubernaculum, and on the descent of the testis in the foetus. Lancet. 1840;2:70. 7. Lockwood CB. Development and transition of the testis, normal and abnormal. J Anat Physiol. 1888;22:505541. 8. Nightingale SS, Al Shareef YR, Hutson JM. Mythical 'Tails of Lockwood'. ANZ J Surg. 2008;78:9991005. [PubMed] 9. Sonneland SG. Undescended testicle. Surg Gynecol Obstet. 1925;40:535545. 10. Johnston JH. The undescended testis. Arch Dis Child. 1965;40:113122. [PMC free article] [PubMed] 11. Elder JS. The undescended testis. Hormonal and surgical management. Surg Clin North Am. 1988;68:9831005. [PubMed] 12. Coley WB. The treatment of the undescended or maldescended testis associated with inguinal hernia. Ann Surg. 1908;48:321350. [PMC free article] [PubMed] 13. McGregor AL. The third inguinal ring. Surg Gynecol Obstet. 1929;49:273307. 14. McGregor AL. Synopsis of surgical anatomy. Bristol: Wright; 1975. pp. 106135. 15. Backhouse KM. The gubernaculum testis hunteri: testicular descent and maldescent. Ann R Coll Surg Engl. 1964;35:1533. [PMC free article] [PubMed] 16. Backhouse KM. The natural history of testicular descent and maldescent. Proc R Soc Med. 1966;59:357360. [PMC free article] [PubMed] 17. Heyns CF. The gubernaculum during testicular descent in the human fetus. J Anat. 1987;153:93112. [PMC free article] [PubMed] 18. Adams JE. Remarks on a case of transition of the testicle into the perineum. Lancet. 1871;1:710. 19. Fischer MC, Milen MT, Bloom DA. Thomas Annandale and the first report of successful orchiopexy. J Urol. 2005;174:3739. [PubMed] 20. Annandale T. Case in which a testicle congenitally displaced into the perineum was successfully transferred to the scrotum. Br Med J. 1879;1:7. 21. Schller M. On inguinal testicle, and its operative treatment by transplantation into the scrotum. Ann Anat Surg. 1881;4:89. 22. Bidwell LA. Modified operation for the relief of undescended testis. Lancet. 1893;1:1439. 23. Bevan AD. Operation for undescended testicle and congenital inguinal hernia. JAMA. 1899;33:773. 24. Bevan AD. The surgical treatment of undescended testicle: a further contribution. JAMA. 1903;41:718. 25. Eisendrath DN. Undescended testis. Ann Surg. 1916;64:324328. [PMC free article] [PubMed]

26. Moore CR, Oslund R. Experiments on the sheep testis-cryptorchidism, vasectomy and scrotal insulation. Am J Physiol. 1924;67:595. 27. Eccles WM. The Hunterian lectures on the anatomy, physiology, and pathology of the imperfectly descended testis, lecture I. Br Med J. 1902;1:503. 28. Eccles WM. The Hunterian lectures on the anatomy, physiology, and pathology of the imperfectly descended testis, lectures II & III. Br Med J. 1902;1:570. 29. Torek F. The technique of orcheopexy. New York Med J. 1909;90:948. 30. Keetley CB. Two cases of retained testis presenting points of special interest. Trans Med Soc Lond. 1894;17:349. 31. Cabot H, Nesbit RM. Undescended testis. Arch Surg. 1931;22:850. 32. Prentiss RJ, Weickgenant CJ, Moses JJ, Frazier DB. Undescended testis: surgical anatomy of spermatic vessels, spermatic surgical triangles and lateral spermatic ligament. J Urol. 1960;83:686692. [PubMed] 33. Schoemaker J. Uber Kryptorchismus und seine behandlung. Chirurg. 1932;4:13. 34. Lattimer JK. Scrotal pouch technique for orchiopexy. J Urol. 1957;78:628632. [PubMed] 35. Jones PF, Bagley FH. An abdominal extraperitoneal approach for the difficult orchidopexy. Br J Surg. 1979;66:1418. [PubMed] 36. Fowler R, Stephens FD. The role of testicular vascular anatomy in the salvage of high undescended testes. Aust N Z J Surg. 1959;29:92106. [PubMed] 37. Cortesi N, Ferrari P, Zambarda E, Manenti A, Baldini A, Morano FP. Diagnosis of bilateral abdominal cryptorchidism by laparoscopy. Endoscopy. 1976;8:3334. [PubMed] 38. Bloom DA. Two-step orchiopexy with pelviscopic clip ligation of the spermatic vessels. J Urol. 1991;145:10301033. [PubMed] 39. Jordan GH, Winslow BH. Laparoscopic single stage and staged orchiopexy. J Urol. 1994;152:12491252. [PubMed

Testicular Torsion Imaging

Author: David Paushter, MD; Chief Editor: Eugene C Lin, MD

Updated: May 25, 2011

Overview
Testicular torsion, also termed torsion of the spermatic cord, is a relatively common and potentially devastating acute condition due to obstruction of the arterial blood supply to the testis.[1] Fortunately, this entity is relatively well known, and it usually occurs with enough discomfort to lead to its diagnosis and subsequent testicular salvage. However, atypical presentations of testicular torsion, delayed recognition of the condition, and its confusion with other causes of acute scrotum can potentially delay diagnosis and lead to testicular necrosis necessitating orchiectomy. Diagnostic imaging, particularly Doppler ultrasonography, plays an important role in the assessment of the patient with acute scrotal pain. (See the images below.)[2]

Normal testis. Transverse color Doppler image demonstrates uniform

echogenicity and flow throughout the testicle Normal testes. Transverse color Doppler images of both testes demonstrate symmetric echogenicity and flow.

Normal testis and epididymis. Longitudinal color Doppler image shows

diffuse, normal flow to the testis and epididymis. Testicular torsion. Longitudinal color Doppler image demonstrates no flow to the testicle and enlargement of the

epididymis and spermatic cord, which are avascular as well. torsion. Longitudinal color Doppler image of the left testicle without evident flow.

Testicular

Testicular torsion. Transverse color Doppler image of both testes demonstrates enlargement, slightly decreased echogenicity, and absent flow on the left side.

Preferred examination
In general, laboratory tests are not diagnostically useful in distinguishing torsion from other acute scrotal syndromes. Urinalysis results are negative in 98%, and a mild leukocytosis may occur in as many as 30% of patients. Within the past decade, ultrasonography with color and power Doppler imaging has emerged as the primary imaging modality for the diagnosis of testicular torsion.[3, 4, 5, 6, 7] It not only helps in corroborating the diagnosis by alteration of testicular echotexture but also provides valuable information on vascular perfusion of the testis. In addition, sonographic findings frequently allow other diagnoses to be made in those patients presenting with an acute scrotum who do not have torsion.[8] Prior to the development of high resolution, real-time ultrasonography coupled with sensitive color Doppler, nuclear scintigraphy was the mainstay of tests available to evaluate the acute scrotum. Given associated radiation, less widespread availability, limited ancillary information, and the accuracy of color Doppler imaging, scrotal scintigraphy is no longer used as frequently.[9, 10] In cases with a clinically ambiguous picture or with indeterminate sonographic findings, scintigraphy remains a viable imaging alternative.[11] Information about the role of MRI in the diagnosis of torsion is limited, although MRI is likely to be highly sensitive.[12, 13] However, with its limited availability, particularly at night, and its cost, MRI is unlikely to become a front-line examination for the patient presenting with acute scrotal pain.

Limitations of techniques
Color Doppler ultrasonography is highly operator dependent. In the diagnosis of testicular torsion, gray-scale findings are combined with dynamic flow information. Inaccurate results may be obtained in the prepubertal patient with small testicular volume or in cases with multiple imaging and Doppler artifacts. Such imaging artifacts may result from inappropriate gain settings and the non-use of slow-flow techniques.[14] Testicular scintigraphy is straightforward, although it requires intravenous access. An infiltrated radionuclide bolus prevents an adequate examination. False-negative results are unusual. Falsepositive results are more frequent because of the changing scintigraphic appearance of infarction over time and potential interpretation errors. For excellent patient education resources, visit eMedicine's Men's Health Center. Also, see eMedicine's patient education article Testicular Pain.

Magnetic Resonance Imaging

Limited information is available on the potential role of magnetic resonance imaging (MRI) in the diagnosis of acute testicular torsion. Findings from small studies to date suggest a high degree of accuracy with MRI, particularly when it is performed with contrast enhancement. These finding are corroborated by results of controlled animal models. In addition, phosphorus31 magnetic resonance spectroscopy can demonstrate rapidly decreasing levels of adenosine triphosphate (ATP) associated with ischemia.

Degree of confidence
To our knowledge, no adequate, controlled clinical trials have been performed to assess the degree of confidence with MRI as a diagnostic tool for testicular torsion. However, if the torsion knot or whirlpool patterns are recognized in conjunction with testicular enlargement and absent vascularity, the diagnosis is virtually certain.

Ultrasonography
On normal gray-scale and color Doppler images, the testes are homogeneous and symmetrical in echotexture, as shown on straddle views. The testes are relatively symmetrical in size, but the normal range varies widely. On color or power Doppler ultrasonogram, flow to the testes and epididymis should be symmetrical. However, flow may be difficult to visualize in young patients. In patients with torsion, gray-scale images may show testicular enlargement due to engorgement; uniformly hypoechoic testicle (early); heterogenous, hypoechoic texture, which indicates necrosis and nonviability; echogenic areas inside the infarcted testis, which may represent hemorrhage; twisting of swollen cord, which gives the appearance of a torsion knot (an echogenic or complex extratesticular mass); or in infarcted testis, tunica albuginea and mediastinum, which have

increased echogenicity (ie, target sign, which is more common in neonatal torsion). (See the images below.)

Testicular torsion. Transverse color Doppler image of the left groin

illustrates an undescended testicle without flow. Testicular torsion. Epididymitis. Longitudinal color Doppler image depicts normal vascularity of the right testicle, with

increased flow in the epididymal tail and a small hydrocele. Testicular torsion. Epididymo-orchitis. Longitudinal color Doppler image of the left testis shows diffuse, markedly

increased vascularity. Testicular torsion. Epididymo-orchitis. Transverse color Doppler image demonstrates increased epididymal flow and a hydrocele.

Testicular torsion. Scrotal hernia. Transverse color Doppler image of the left hemiscrotum shows heterogeneous mass superior to the testicle, with small vessels depicted.

Testicular torsion. Scrotal trauma. Transverse color Doppler image demonstrates an enlarged, non-hypervascular epididymis (EPID) adjacent to the upper testicle (TEST).

Testicular torsion. Testicular tumor. Transverse color Doppler image displays a hypervascular mass in the periphery of the testis.

Color and/or power Doppler imaging should be performed in all cases. Flow to the affected testicle is absent, although normal or increased flow may be seen with spontaneous detorsion. The symptomatic side should be compared with the asymptomatic side by using the straddle view obtained with optimal technical settings. Epididymitis is visualized as an enlarged, hyperemic epididymis, usually with a diffusely affected area.[15, 16] Involvement of the testis also produces enlargement and increased vascularity. A scrotal abscess, whether intratesticular or extratesticular, is typically seen as a complex fluid collection, often with a vascular capsule. Torsion of the epididymal appendage is easily recognized as a mass adjacent to the epididymal head without flow; this mass does not affect the testicular vasculature. Finally, an intratesticular hematoma may mimic a necrotic testis, but it typically has normal surrounding blood flow. An extratesticular hematoma appears as a complex, cystic collection clearly separate from but possibly displacing the testis.

Degree of confidence
An absence of flow in a symptomatic, enlarged testicle, with flow demonstrated in the contralateral testicle, is highly specific. Power Doppler and color Doppler imaging should be used together in prepubertal boys, but it demonstrates flow in only 79-90% of normal cases.[17, 18, 19] Color Doppler and power Doppler sonography both demonstrate flow in almost 100% of postpubertal patients.[20] Color Doppler and power Doppler imaging have similar sensitivities for demonstrating flow in small testes, although the combination of the 2 techniques has a sensitivity that exceeds the sensitivity of each alone. Overall, the specificity is 77-100%, and the sensitivity is 86-100%.

False positives/negatives
Posttorsion hyperemia may be confused with epididymo-orchitis, producing a false-negative finding. Capsular blood flow must be distinguished from intratesticular arterial flow; these observations may produce false-negative results. Although flow may be visible in one testis and is usually evident in the other, false-positive findings are possible in the young child. Technical factors (eg, erroneous flow settings, motion artifacts on power Doppler images) may produce false-positive or false-negative results. A scrotal abscess may cause a false-positive diagnosis of torsion because of the depiction of hyperemia surrounding a fluid core. Ultrasonography can be used to distinguish abscess from testicular torsion because of its combination of characteristic imaging and flow dynamics.[21]

Nuclear Imaging
Technetium-99m pertechnetate is the agent of choice, with an adult dose of 10-20 mCi and a pediatric dose of at least 5 mCi. Typically, immediate radionuclide angiograms are obtained, with subsequent static images as well. In the healthy patient, images show symmetric flow to the testes, and delayed images show uniformly symmetric activity. The appearance of testicular torsion on scintigraphy depends upon the chronicity. In acute torsion (usually < 7 h), blood flow may range from normal to absent on the involved side, and a nubbin sign may be visible. The nubbin sign is a focal medial projection from the iliac artery representing reactive increased flow in the spermatic cord vessels terminating at the site of torsion. (This sign can also be seen in later stages.) Static images demonstrate a photopenic area in the involved testis. In the subacute and late phases of torsion (missed torsion), there is often increased flow to the affected hemiscrotum via the pudendal artery with a photopenic testis and a rim of surrounding increased activity on static images. This has been called a rim, doughnut, or bull's-eye sign. Acute epididymitis generally appears as an area of focal or diffuse increased activity in the involved hemiscrotum. Testicular appendix torsion has a variable appearance: it may have a normal scan or a focal area of increased or decreased activity. An abscess, tumor, or hematoma may be indistinguishable from a torsed testicle, demonstrating a hyperemic rim surrounding an area of decreased activity.

Degree of confidence
Scintigraphy has a sensitivity of 90% and a specificity of 60% in the diagnosis of testicular torsion. Color Doppler ultrasonography has distinct advantages in diagnosing nonvascular causes of acute scrotum. Scintigraphy may be more sensitive in the neonatal period than at other times because of the difficulty in detecting flow by means of Doppler imaging. Scrotal scintigraphy may be more sensitive than color or power Doppler imaging to the presence or absence of flow in the prepubescent testicle.

Limitations of techniques
An abscess, tumor, or hematoma may produce false-positive findings (rim sign). A hyperemic epididymis may be misinterpreted as a halo, producing false-positive study. Most false-negative studies are due to technical reasons or interpretative errors. References 1. Lin EP, Bhatt S, Rubens DJ, Dogra VS. Testicular torsion: twists and turns. Semin Ultrasound CT MR. Aug 2007;28(4):317-28. [Medline]. 2. Watanabe Y, Nagayama M, Okumura A, Amoh Y, Suga T, Terai A. MR imaging of testicular torsion: features of testicular hemorrhagic necrosis and clinical outcomes. J Magn Reson Imaging. Jul 2007;26(1):100-8. [Medline]. 3. Pearl MS, Hill MC. Ultrasound of the scrotum. Semin Ultrasound CT MR. Aug 2007;28(4):225-48. [Medline]. 4. Barth RA, Shortliffe LD. Normal pediatric testis: comparison of power Doppler and color Doppler US in the detection of blood flow. Radiology. Aug 1997;204(2):389-93. [Medline]. 5. Albrecht T, Lotzof K, Hussain HK, et al. Power Doppler US of the normal prepubertal testis: does it live up to its promises?. Radiology. Apr 1997;203(1):227-31. [Medline]. 6. Lee FT Jr, Winter DB, Madsen FA, et al. Conventional color Doppler velocity sonography versus color Doppler energy sonography for the diagnosis of acute experimental torsion of the spermatic cord. AJR Am J Roentgenol. Sep 1996;167(3):78590. [Medline]. 7. Patriquin HB, Yazbeck S, Trinh B, et al. Testicular torsion in infants and children: diagnosis with Doppler sonography. Radiology. Sep 1993;188(3):781-5. [Medline]. 8. Coley BD, Frush DP, Babcock DS, et al. Acute testicular torsion: comparison of unenhanced and contrast- enhanced power Doppler US, color Doppler US, and radionuclide imaging. Radiology. May 1996;199(2):441-6. [Medline]. 9. Middleton WD, Siegel BA, Melson GL, et al. Acute scrotal disorders: prospective comparison of color Doppler US and testicular scintigraphy. Radiology. Oct 1990;177(1):177-81. [Medline]. 10. Yuan Z, Luo Q, Chen L, et al. Clinical study of scrotum scintigraphy in 49 patients with acute scrotal pain: a comparison with ultrasonography. Ann Nucl Med. Jun 2001;15(3):225-9. [Medline].

11. Paltiel HJ, Connolly LP, Atala A, et al. Acute scrotal symptoms in boys with an indeterminate clinical presentation: comparison of color Doppler sonography and scintigraphy. Radiology. Apr 1998;207(1):223-31. [Medline]. 12. Trambert MA, Mattrey RF, Levine D, Berthoty DP. Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology. Apr 1990;175(1):53-6. [Medline]. 13. Watanabe Y, Dohke M, Ohkubo K, et al. Scrotal disorders: evaluation of testicular enhancement patterns at dynamic contrast-enhanced subtraction MR imaging. Radiology. Oct 2000;217(1):219-27. [Medline]. 14. Lerner RM, Mevorach RA, Hulbert WC, Rabinowitz R. Color Doppler US in the evaluation of acute scrotal disease. Radiology. Aug 1990;176(2):355-8. [Medline]. 15. Gordon LM, Stein SM, Ralls PW. Traumatic epididymitis: evaluation with color Doppler sonography. AJR Am J Roentgenol. Jun 1996;166(6):1323-5. [Medline]. 16. Horstman WG, Middleton WD, Melson GL. Scrotal inflammatory disease: color Doppler US findings. Radiology. Apr 1991;179(1):55-9. [Medline]. 17. Bader TR, Kammerhuber F, Herneth AM. Testicular blood flow in boys as assessed at color Doppler and power Doppler sonography. Radiology. Feb 1997;202(2):559-64. [Medline]. 18. Atkinson GO Jr, Patrick LE, Ball TI Jr, et al. The normal and abnormal scrotum in children: evaluation with color Doppler sonography. AJR Am J Roentgenol. Mar 1992;158(3):613-7. [Medline]. 19. Luker GD, Siegel MJ. Color Doppler sonography of the scrotum in children. AJR Am J Roentgenol. Sep 1994;163(3):649-55. [Medline]. 20. Luker GD, Siegel MJ. Scrotal US in pediatric patients: comparison of power and standard color Doppler US. Radiology. Feb 1996;198(2):381-5. [Medline]. 21. Burks DD, Markey BJ, Burkhard TK, et al. Suspected testicular torsion and ischemia: evaluation with color Doppler sonography. Radiology. Jun 1990;175(3):815-21. [Medline].