Testicular Torsion 

Updated: Oct 30, 2020
Author: Oreoluwa I Ogunyemi, MD; Chief Editor: Edward David Kim, MD, FACS 


Practice Essentials

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.[1, 2] The rate of testicular viability decreases significantly after 6 hours from onset of symptoms.[3]

Testicular torsion is primarily a disease of adolescents and neonates. It is the most common cause of testicular loss in these age groups. However, torsion may occasionally occur in men 40-50 years old.[4]

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. The TWIST (Testicular Workup for Ischemia and Suspected Torsion) score uses clinical features to assess the risk of testicular torsion (see Workup/Approach Considerations). Ultrasound evaluation is indicated for intermediate-risk patients; low-risk patients do not require ultrasound to rule out torsion, and patients at high risk can proceed directly to surgery, with more than 50% avoiding ultrasound.[5]

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[6] 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.[6]

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.[6] 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 affected testicle compared with its blood supply.[6]  However, in a review of 32 patients who had been diagnosed with testicular torsion, testicular cancer was found in 2 of the 20 patients who had undergone orchiectomy, a rate of 6.4%.[7]

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

For patient education information, see the Testicular Torsion.

For additional information, see Testicular Torsion in Emergency Medicine and Pediatric Testicular Torsion .


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.[6] A case report describes a necrotic testicle in a newborn that resulted from torsion at an estimated 20th week of gestation.[8]


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.[9] The bell clapper deformity allows the testicle to twist spontaneously on the spermatic cord.

Torsion occurs as the testicle rotates between 90° and 180°, compromising blood flow to and from the testicle. Complete torsion usually occurs when the testicle twists 360° or more; incomplete or partial torsion occurs with lesser degrees of rotation. The degree of torsion may extend to 720°.

The twisting of the testicle causes venous occlusion and engorgement as well as arterial ischemia and infarction of the testicle. The degree of torsion the testicle endures may play a role in the viability of the testicle over time.

In addition to the extent of torsion, the duration of torsion prominently influences the rates of both immediate salvage and late testicular atrophy. Testicular salvage is most likely if the duration of torsion is less than 6-8 hours. If 24 hours or more elapse, testicular necrosis develops in most patients.


Extravaginal torsion occurs in the fetus or neonate, because the testes may freely rotate prior to the development of testicular fixation via the tunica vaginalis within the scrotum.

Normal testicular suspension ensures firm fixation of the epididymal-testicular complex posteriorly and effectively prevents twisting of the spermatic cord. In males with the bell-clapper deformity, torsion can occur because of a lack of fixation, resulting in the testis being freely suspended within the tunica vaginalis.

An abnormal mesentery between the testis and its blood supply can predispose it to torsion if the testicle is broader than the mesentery. Contraction of the spermatic muscles shortens the spermatic cord and may initiate testicular torsion.


Extravaginal torsion constitutes approximately 5% of all torsions. Of these cases of testicular torsion, 70% occur prenatally and 30% occur postnatally. The condition is associated with high birth weight. Bilateral perinatal torsion is thought to be rare, although an increase in the number of case reports has been observed. Currently, there are about 56 case reports in the literature.[10]

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.[11] 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.[12]

Several case reports describe familial testicular torsion. In one study of 70 boys with testicular torsion, 11.4% had a positive history in a family member.[13]


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.[14] 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[15, 16] :

  • < 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[17]

  • 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.[18]




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,[16] 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%.[19] 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.[20]

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.[21] 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.[22] Creagh et al reported that acute torsion developed in 10% of patients with intermittent torsion while they waited for surgery.[23]

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 blind-ending vessels is a manifestation of early in utero torsion as hemosiderin is often found in the distal section of the spermatic cord.[6] 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.[24] 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 histor 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.[12] While abnormal lie can help diagnose testicular torsion, fewer than 50% of cases demonstrate true horizontal lie.[24]

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.[24]

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 one or more of the following[12] :

  • 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.

Differential Diagnoses



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.

The TWIST (Testicular Workup for Ischemia and Suspected Torsion) scoring system was developed for the purpose of determining the risk of testicular torsion on clinical grounds, thus decreasing the indication for ultrasound.[25] TWIST has been validated when scored by nonurological nonphysician providers as well as urologists.[5]  TWIST consists of the following urological history and physical examination parameters:

  • Testis swelling (2 points)
  • Hard testis (2)
  • Absent cremasteric reflex (1)
  • Nausea/vomiting (1)
  • High-riding testis (1)

Based on TWIST scores, patients are classified as being at low, intermediate, or high risk. TWIST has shown 100% negative predictive value when scored by a urologist, using a cutoff value of 2 to identify low-risk patients, and when scored by trained emergency medical technicians (EMTs) using a cutoff of 0 in children.[5, 25] Cutoff values of 5 (scored by a urologist) and 6 (EMTs) have been used to identify high-risk patients. Ultrasound evaluation is indicated for intermediate-risk patients; low-risk patients do not require ultrasound to rule out torsion, and patients at high risk can proceed directly to surgery, with more than 50% avoiding ultrasound.[5]


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.

Mean platelet volume (MPV) has been suggested as a source of diagnostic and prognostic information, with some small studies reporting a higher likelihood of testicular torsion and a greater risk of postoperative testicular atrophy in patients with higher MPVs.[26, 27] However, those studies have proposed different cut-off values for MPV, and other studies have reported conflicting information.[28]

Elevation in acute-phase proteins (ie, C-reactive protein [CRP]) has been postulated as a diagnostic aid in differentiating inflammatory causes of acute scrotal pain (eg, epididymitis) from noninflammatory causes (eg, testicular torsion).[29] However, sample sizes in these studies have been too small to support using CRP as a diagnostic adjunct to definitively rule out testicular torsion.


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[30] :

  • 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%.[19] 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.[31]

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.[32]

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.[33]

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.[34]

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.[35, 36]

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. Contrast-enhanced ultrasonography can, however, be used as a supplement to traditional Doppler sonography when the diagnosis is uncertain and following appropriate clinical and radiographic evaluation.[37]

In a study of 104 adolescent boys, Boettcher et al found that ultrasound predictors alone were not able to identify all cases of testicular torsion. However, clinical features (pain lasting less than 24 hours, nausea and/or vomiting, abnormal cremasteric reflex, and high position of the testis) were predictive with no false positives reported, thus reducing the negative exploration rate by over 55%. Because scrotal ultrasonography is unpleasant in these cases, Boettcher and colleagues recommend that the procedure be used for diagnosis only in patients who lack the clinical features of testicular torsion.[38]

In a study of 342 patients who presented to the emergency department with acute scrotum pain, Liang and colleagues reported no false-negative findings but a 2.6% false-positive rate on ultrasounds performed to assess for testicular torsion. High rates of the clinical features of sudden-onset scrotal pain (88%), abnormal position of testis (86%), and absent cremasteric reflex (91%) were also reported in the patients with testicular torsion. The investigators concluded that color Doppler ultrasound was accurate and sensitive for diagnosis of torsion.z[39]

Altinkilic et al provided further evidence that routine surgical exploration is unnecessary in patients with symptoms of testicular torsion and a normal color-coded duplex sonography. In their prospective study of 236 patients with clinical suspicion of testicular torsion, the sensitivity, specificity, and positive and negative predictive values of color coded duplex sonography were 100%, 75.2%, 80.4%, and 100%, respectively.[40]

In a review of 155 surgical explorations for acute scrotal pain, Nason el al reported rates of 96.9%, 88.9%, 96.9% and 89% for sensitivity, specificity, and positive predictive value and negative predictive value, respectively, for Doppler ultrasound used to assess testicular torsion.[41]

McDowall et al reported that the whirlpool sign—a spiral-like pattern seen on assessment of the spermatic cord, using standard high-resolution ultrasonography and/or color Doppler sonography—is a definitive sign for testicular torsion in pediatric and adult patients, but has a limited role in neonates. In their meta-analysis, the whirlpool sign had a pooled sensitivity and specificity of 0.73 (95% CI, 0.65-0.79) and 0.99 (95% CI, 0.92-0.99), respectively. Removal of neonates increased the pooled sensitivity to 0.92 (95% CI, 0.70-0.98) while the pooled specificity remained almost unchanged.[42]

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.[43] 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.

Near-Infrared Spectroscopy

Near-infrared spectroscopy (NIRS) is an emerging tool to assess testicular torsion. It can measure oxygen saturation 3-4 cm deep in the skin, is rapid (lasting 20 seconds), and is noninvasive. Aydogdu et al performed a small prospective study evaluating 16 adult patients with testicular torsion and found NIRS to be 100% sensitive and specific for torsion when compared with the contralateral testis. More studies are needed confirmation before this modality becomes available for clinical use.[44]



Approach Considerations

Immediate surgical exploration is indicated for patients with testicular torsion. For reliable salvage of the testicle, surgical repair must occur within 6 hours of symptom onset.[39, 45] If treatment is delayed, the patient may experience decreased fertility or may require orchiectomy.[46]

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, but it may improve rates of surgical salvage,[47] can protect testicular viability in cases of surgical delay, and also provides significant pain relief. Color Doppler ultrasonography can be used to determine the direction of testicular torsion and guide manual detorsion.[48]

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 urgent—rather than emergent—procedure.

In rat models of testicular torsion, various agents have successfully decreased ischemia-reperfusion injury. Benefit has been shown with nicotinamide, tadalafil and verapamil, and rapamycin and metformin.[11, 49, 50]

Historical perspective

Testicular torsion is treated with orchiopexy, in which the testis is anchored to the scrotal wall. This surgical procedure was initially developed as treatment for cryptorchidism, with the first successful orchiopexy performed in the 1870s by Annandale. Subsequently, 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 of attaching the testis to the scrotal pouch was initially described the 1930s.[51] 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 controversial, but is most often treated with elective exploration and contralateral orchiopexy (anchoring) because bilateral (synchronous or asynchronous) neonatal testicular torsion has been described.

The potential for salvage of a neonatally torsed testis is exceptionally small, making the risk of immediate surgery before complete stabilization of the newborn unwarranted. However, some controversy lies in the fact that there is a risk of synchronous or asynchronous testicular torsion in the neonate and therefore possible loss of both testes if surgery is not available immediately. In addition, neonatal anesthesia is becoming safer, especially in the hands of a pediatric anesthesiologist.[52] A newborn with a normal testis at birth who subsequently undergoes torsion, on the other hand, definitely 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. Contralateral orchiopexy is always performed 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. However, Lian et al reported that even when the testis was intraoperatively assessed as viable, half of their patients who underwent salvage therapy for testicular torsion developed testicular atrophy. Factors that predicted testicular atrophy were pain duration of longer than a day and heterogeneous echogenicity on sonographic examination.[53]

Intraoperative findings in testicular torsion. Intraoperative findings in testicular torsion.

Working on the assumption that invasion of the tunica albuginea has a negative impact on spermatogenesis, Kozminski et al employ orchiopexy without use of a fixation suture that pierces the tunica albuginea. These authors report a high rate of favorable outcomes in a study that included 155 procedures performed in 101 patients to remedy testicular torsion.[54]

Testicular prosthesis placement

Patients requiring an orchiectomy because of a nonviable testis may benefit from the placement of a testicular prosthesis.

The placement of a testicular prosthesis is usually delayed for 6 months, until healing is complete and inflammatory changes resolve. However, some early studies show that simultaneous testicular prosthesis placement is safe in postpubertal males who have reached full testicular size.[52]

The prosthetic placement should be performed 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.

Studies have looked at anti-inflammatory adjuncts to testicular torsion in the rat model. Phosphodiesterase type-5 inhibitors and statin medications have been shown to decrease inflammatory markers and to increase blood flow to the testicles. These adjuncts are still in the research stage and are not clinically available for this use.[52]


Class Summary

Most analgesics have sedating properties, which are beneficial for patients who have sustained painful trauma.

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.


Class Summary

These agents are used to prevent nausea and vomiting.

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.

Metoclopramide (Reglan, Metozolv)

Metoclopramide blocks dopamine receptors in the chemoreceptor trigger zone of the central nervous system.

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.

Diazepam (Diastat, Valium)

Diazepam modulates the postsynaptic effects of gamma-aminobutric acid–A (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.


Questions & Answers


What is testicular torsion?

Which age groups are at highest risk for testicular torsion?

What are the causes of testicular torsion?

How does testicular torsion occur in neonates?

What is the prevalence of testicular malignancy in patients with testicular torsion?

What is the anatomy of the testes?

What is the purpose of testicular descent, and how does the process happen?

What is the pathophysiology of testicular torsion in neonates?

What is bell clapper deformity, and how is it related to testicular torsion?

What is the progression of untreated testicular torsion?

What causes testicular torsion?

What is the prevalence of testicular torsion?

What is the prognosis of testicular torsion?

What are the salvage rates for testicular torsion?

What are the consequences of testicular torsion?

What causes contralateral disease in testicular torsion?

What causes a decrease in facility following testicular torsion?


Which history is characteristic of testicular torsion?

Which specialist should be consulted early in cases of suspected testicular torsion?

Which history is characteristic of testicular torsion among neonates?

What is the role of physical exam in the evaluation of testicular torsion?

Which physical findings are characteristic of testicular torsion?

Which physical finding indicates testicular torsion in the pediatric population?

What is the role of the cremasteric reflex and Prehn sign in the evaluation of testicular torsion?

What are symptoms of testicular torsion?

Which four symptoms indicate testicular torsion?


Which conditions should be included in the differential diagnoses of testicular torsion?

How is testicular torsion differentiated from epididymitis and orchitis?

How is testicular torsion differentiated from hydrocele, testis tumor or scrotal edema?

What are the differential diagnoses for Testicular Torsion?


When is surgical exploration indicated in the evaluation of testicular torsion?

What is the TWIST (Testicular Workup for Ischemia and Suspected Torsion) scoring system?

How is the Testicular Workup for Ischemia and Suspected Torsion (TWIST) scoring system used to determine risk for testicular torsion?

What is the role of urinalysis in the evaluation of testicular torsion?

What is the role of blood studies in the evaluation of testicular torsion?

What is the role of ultrasonography in the evaluation of testicular torsion patients?

Which ultrasonographic findings suggest testicular torsion?

How accurate is ultrasonography in the evaluation of testicular torsion?

What is the role of MRI in the diagnosis of testicular torsion?

What is the role of radionuclide scans in the diagnosis of testicular torsion?

What is the role of near-infrared spectroscopy (NIRS) in the diagnosis of testicular torsion?


What is the role of surgery in the treatment of testicular torsion?

What is the role of nicotinamide in the treatment of testicular torsion?

What is the role of orchiopexy in the treatment of testicular torsion?

What is the efficacy of surgical detorsion for the treatment of testicular torsion in neonates?

What is the efficacy of surgical detorsion in the treatment of testicular torsion in older patients?

How is surgical detorsion performed for testicular torsion?

What are the signs of a viable testis following detorsion?

When is a testicular prosthesis indicated in the treatment of testicular torsion?


Which medications are used in the treatment of testicular torsion?

Which medications in the drug class Antianxiety Agents are used in the treatment of Testicular Torsion?

Which medications in the drug class Antiemetics are used in the treatment of Testicular Torsion?

Which medications in the drug class Analgesics are used in the treatment of Testicular Torsion?