Eugene Minevich, MD,
Assistant Professor, Department of Surgery,
Division of Pediatric Urology, University of
Cincinnati
Nothing to disclose.
Leslie Tackett McQuiston, MD, FAAP,
Assistant Professor of Surgery (Urology)
Dartmouth Medical School; Staff Pediatric Urologist,
Dartmouth-Hitchcock Hospital
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Specialty Editor(s)
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
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J Stuart Wolf Jr, MD, FACS,
The David A Bloom Professor of Urology,
Director, Division of Endourology and Stone Disease,
Department of Urology, University of Michigan Medical
School
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Raymond Rackley, MD,
Professor of Surgery, Cleveland Clinic Lerner
College of Medicine at Case Western Reserve University; Staff
Physician, Center for Pelvic Medicine and Pelvic
Reconstruction, Glickman Urological Institute, Cleveland
Clinic Foundation
Shlomo Raz, MD,
Professor, Department of Surgery, Division of
Urology, University of California at Los Angeles School of
Medicine
Nothing to disclose.
Chief Editor
Edward David Kim, MD, FACS,
Professor of Surgery, Division of Urology,
University of Tennessee Graduate School of Medicine;
Consulting Staff, University of Tennessee Medical
Center
Lilly Consulting
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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.
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.
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).
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.
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.
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.
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.
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.
View Image
A 17-year-old teenager with a 72-hour history of scrotal pain.
Differential diagnosis
Torsion of testicular or epididymal appendage
This condition usually occurs in children 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 is present in light-skinned boys.
Epididymitis, orchitis, epididymo-orchitis
These 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 leucocytosis is possible.
A complete urological evaluation (ie, renal sonography, urodynamic study) is necessary in prepubertal boys with acute epididymitis.
Hydrocele (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
Scrotal enlargement occurs, only rarely accompanied by pain.
Presentation is rarely acute.
Idiopathic scrotal edema
Scrotal skin is thickened, edematous, and often inflamed.
The testis is not tender and is of normal size and position.
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.
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.
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.
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 urgent—rather than emergent—procedure.
A recent study has shown that the use of nicotinamide may successfully decrease ischemia-reperfusion injury in early and late periods in both testicles.[2]
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.
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.
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.
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.
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
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