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Neonatal testicular torsion

Neonatal testicular torsion
Literature review current through: Jan 2024.
This topic last updated: May 16, 2023.

INTRODUCTION — Neonatal testicular torsion, defined as torsion occurring within the first 30 days of life, is a rare occurrence. However, it can result in vascular compromise, leading to testicular ischemia and injury and, if not corrected, necrosis and testicular loss. Nevertheless, the management of neonatal testicular torsion remains controversial as opinions differ on whether surgery can successfully salvage the torsed testis, which may have occurred in utero, and whether the contralateral side is at increased risk for torsion. However, when bilateral torsion does occur, the outcome can be devastating, as the child will be anorchic, rendering him infertile and committing him to hormone supplementation for life.

The clinical presentation and the controversies regarding management of neonatal testicular torsion will be reviewed here. Testicular torsion in children and adolescents is presented separately. (See "Causes of scrotal pain in children and adolescents", section on 'Testicular torsion'.)

DEFINITIONS

Neonatal testicular torsion is defined as torsion that occurs prenatally and up to 30 days after delivery [1].

Neonatal testicular torsion can be divided into two groups based upon the timing of torsion event, occurring before or after birth.

Prenatal (non-acute) event – Because prenatal testicular torsion is an in utero event, it is a non-acute event. The torsion can generally be detected in the immediate postpartum period (ie, at delivery or during the initial newborn examination). However, it may be misinterpreted as a nonpalpable, undescended testicle ("vanishing testis syndrome") if the torsion occurred early enough during the pregnancy for resolution of the inflammatory response and atrophy of the testicle. Rarely, antenatal torsion is identified on fetal ultrasound [2].

Postnatal (acute) event – Postnatal testicular torsion occurs after birth. It is detected as a change in the testicular examination in a testicle that was previously noted to be normal during the newborn examination. Postnatal torsion is considered an acute event because intervention may potentially salvage a functioning testis, if the torsion is detected in a timely manner.

The clinical presentation and management approaches differ based on whether the testicular torsion occurs prenatally or postnatally as an acute event. (See 'Clinical presentation' below and 'Management' below.)

Testicular torsion can also be divided by the following two underlying pathologic processes: extravaginal and intravaginal testicular torsion (figure 1). Both mechanisms result in vascular compromise to the testes. If blood flow is not restored in a timely fashion (approximately four to six hours [3]), testicular ischemia, infarction, and subsequent atrophy of the testicle will occur.

Extravaginal testicular torsion involves the entire testicle, including the tunica vaginalis covering of the testicle, as the tunica vaginalis (serous outpouching of the peritoneum, the processus vaginalis, which covers the testicle and sections of the body and tip of the epididymis) is not fixed to the scrotal wall in neonates [4,5]. Neonatal testicular torsion is most commonly an extravaginal process.

Intravaginal testicular torsion, which is typically seen in older patients, is caused by the testis and spermatic cord twisting within the tunica vaginalis. It is due to an anatomic defect affecting how the tunica vaginalis covers the testicle, such that the testicle is fixed in a higher, more cranial position, allowing it to twist within the tunica vaginalis cover (the "bell clapper defect") (figure 2).

EPIDEMIOLOGY — Neonatal testicular torsion accounts for 10 to 12 percent of all cases of pediatric testicular torsions [6,7]. The reported incidence from a study from Great Britain was 6.1 per 100,000 live births [8]. However, this may be an underestimation of the true denominator of neonatal testicular torsion events, as monorchidism (absence of one testicle) due to an atrophic testicle is most likely due to an undetected intrauterine torsion event, also referred to as the "vanishing testis syndrome." (See 'Monorchidism' below.)

In the majority of cases, torsion occurs in utero as demonstrated by case series reporting 70 to 80 percent of patients presenting with prenatal torsion, and the remaining presenting after the immediate postpartum period [1,6].

Bilateral involvement has been reported in approximately 5 to 20 percent of all neonatal torsion events [1,9-11]. However, the true rate of bilateral torsion remains uncertain, as there may be reporting bias of bilateral involvement, which skews the results to a higher incidence [1].

PATHOGENESIS — The exact mechanism of neonatal testicular torsion is unknown [12]. Neonatal testicular torsion is most commonly an extravaginal event involving the entire testicle including the tunica vaginalis investment (figure 1) [4,5]. It is thought that torsion occurs after the testicle descends into the scrotum, but prior to fixation in the scrotum [1,13]. The mobility of the fetal/neonatal tunica vaginalis within the scrotum appears to make the testicle more susceptible to twisting with rotation along the long axis of the spermatic cord resulting in extravaginal torsion [14]. The attachment of the tunica vaginalis appears to occur within the first few weeks of life [7,13]. However, if the securing of the tunica vaginalis was the only predisposing factor for torsion, one would expect torsion to be more frequent in preterm infants, contrary to what is observed [15-17]. Therefore, other factors must play a role in the pathogenesis of neonatal torsion.

It has been postulated that an increased intrauterine pressure during the third trimester of pregnancy and/or delivery results in a brisk cremaster response in the setting of loose tunic-scrotal attachment. This would predispose the testicle to twisting of the spermatic cord, and results in compromise of testicular blood flow [6,18]. Support for this mechanism is based upon the observation that neonatal torsion has been associated with complicated pregnancies, including breech presentation and preeclampsia, post-term births, difficult vaginal deliveries, and full-term infants who are above average birth weights [14-16,18].

In contrast, intravaginal torsion with twisting of the testicle and spermatic cord within the tunica vaginalis occurs in older patients and rarely in neonates [16]. (See "Causes of scrotal pain in children and adolescents", section on 'Testicular torsion'.)

CLINICAL PRESENTATION — The clinical presentation and course vary depending upon whether testicular torsion occurs in utero (prenatal or non-acute event) or after birth (postnatal or acute event).

Prenatal — Prenatal torsion is detected at or within 24 hours of delivery during the initial newborn examination. The neonate does not demonstrate any clinical signs of distress. The timing of the torsion in utero is estimated by the physical appearance of the testicle, which impacts the management approach (see 'Perinatal presentation' below):

Early prenatal torsion – If the torsion occurred early in utero, the neonate presents with a firm, small testicle or even with an absent, pea-sized and/or "nubbin" testicle ("vanishing testis syndrome"). In these cases, it is difficult to differentiate between a torsed testicle that has atrophied versus an undescended, abdominal testicle, which is nonpalpable. For this reason, we do not recommend intervening on the contralateral testicle, as testicular torsion cannot be confirmed.

Late prenatal torsion – Torsion occurring close to or during the time of delivery presents with an enlarged, firm testicle. The testicle can be tender or nontender, depending on proximity to delivery, with a typically discolored hemiscrotum (picture 1A) [4,6,14]. Often, there can be a reactive hydrocele and fluid around the contralateral, non-torsed testicle (picture 1B).

In infants with prenatal torsion, surgery generally fails to save the testis. Reported salvage rates range from 0 to 5 percent [6,10,13,18], although one study reported a higher salvageable rate of 27 percent (3 of 11 patients) [19]. Since it is extremely rare to preserve function in the prenatal or non-acute torsion event, management is focused on preserving the health of the contralateral testis and prevention of the rarely reported contralateral synchronous (concomitant) or asynchronous torsion that results in bilateral anorchia. (See 'Contralateral testicle' below.)

Postnatal — Postnatal torsion presents with acute tenderness, swelling, and overlying scrotal skin changes in a testicle that was previously noted to be normal on physical examination [20,21]. Surgical intervention has a reported salvage rate of 30 to 40 percent in postnatal torsion cases [6,21-23]. Neonatal torsion occurs in the first month of life, prior to fixation of the tunica vaginalis in the scrotum (extravaginal torsion). Infants older than one month typically present with intravaginal torsion, and there is up to a 50 percent association with undescended testicles [16].

Bilateral involvement — A minority of neonatal torsion events are bilateral, but it can be difficult to detect bilateral torsion if the two sides torse at different times. In a 2021 meta-analysis of nearly 1000 neonates, 15 percent of torsion events were bilateral [9]. Bilateral torsion can present in a synchronous (concomitant) fashion or an asynchronous (subsequent) fashion, with synchronous occurring slightly more often in the meta-analysis [9]. This distinction is important as it can impact the timing of intervention when surgical exploration is pursued. In patients with an asynchronous presentation, the median time to the second torsion was one day, with a range of one to eight days. In the asynchronous presentation, the infant will initially have a normal contralateral testicle [6]. The contralateral testicle will be detected either during surgical exploration or later clinically [24]. The asynchronous presentation may offer a higher potential for testicular salvage, as the torsion may be detected before significant testicular ischemia occurs if timely emergent intervention is provided. However, while neonatal torsion is defined as occurring within the first month of life, others argue that asynchronous torsion can present within the first six weeks of life and has been documented up to six months [25].

Therefore, in neonates presenting with apparent unilateral torsion, it is important to surgically explore both halves of the scrotum, because torsion of the contralateral testis may be difficult to detect with physical examination and radiography alone [24,26-29]. Timely emergent exploration may detect a contralateral torsion before significant testicular ischemia occurs (picture 2).

COMPLICATIONS

Testicular ischemia — Twisting of the spermatic cord (torsion) causes testicular vascular compromise, resulting in testicular ischemia and injury. The extent of the damage is mostly dependent upon the following factors [3]:

Duration of torsion – Testicular viability appears to become compromised if ischemia lasts beyond four to six hours. When testicular torsion is greater than four hours duration, some degree of testicular injury in anticipated [3]. In dogs, viability of spermatogenic and Sertoli cells is lost after six hours of ischemia, and viability of Leydig cells after 10 hours [30].

Increasing rotation of the spermatic cord – Increasing the degree of rotation of the spermatic cord may increase the potential for testicular damage and loss in both extravaginal and intravaginal testicular torsion. In some case series, if torsion is less than 360 degrees (partial torsion), there is a higher likelihood of testicular viability compared with torsion greater than 360 degrees (complete torsion) [3,31]; however, testicular infarction can still occur with 180 degrees of torsion [31]. In contrast, others have found no association between the degree of torsion and testicular viability [32].

However, it can be clinically challenging to distinguish between a complete 360-degree twist from a partial torsion. Because a partial torsion is associated with a greater time before nonviability, surgical exploration is still suggested in patients who are symptomatic for 24 hours or longer [3].

Monorchidism — Monorchidism refers to the absence of one testicle, which may be due to either a nonpalpable, undescended abdominal testicle or a testicle that has atrophied post-torsion. The atrophic testicle, also referred to as the "vanishing testis," is now commonly recognized as an intrauterine torsion event [33-35]. Thus, infants born with a nonpalpable testicle are often assumed to have an undescended, abdominal testicle. This is later recognized to be an in utero torsion event at the time of surgical intervention for the presumed abdominal testicle, performed around 6 to 12 months of age. This conclusion is supported by the presence of characteristic histopathologic findings for testicular atrophy secondary to ischemia (ie, presence of vas deferens, epididymis, calcification, or hemosiderin pigmentation in pathology specimens) in almost 90 percent of cases [34].

Further investigation is required to determine whether or not monorchidism due to prenatal torsion is associated with an increased risk of testicular torsion in the remaining solitary testicle. If monorchidism is associated with an increased risk of testicular torsion, then this strengthens the argument to perform contralateral orchiopexy in infants with history of testicular torsion. However, if there is no increased risk for contralateral testicular torsion, a nonoperative approach is acceptable [25]. (See 'Contralateral orchiopexy' below.)

Endocrine abnormalities — Infertility and long-term sequelae of sex steroid deficiencies are potential complications for patients with bilateral involvement. Patients with loss of function of both testicles should be referred to a pediatric endocrinologist to ensure proper sex steroid hormonal replacement therapy. Unilateral testicular torsion appears to have a low impact on subsequent fertility [36].

Contralateral testicle — It remains unknown whether individuals with an atrophic testicle are at increased risk for subsequent torsion of the remaining solitary testicle [37,38]. In a report of seven atrophic testicles, five of the six contralateral testicles that were explored had abnormal testicular fixation ("bell clapper defect") that is associated with an increased risk of testicular torsion beyond the neonatal period. Other case series have not demonstrated an increased likelihood of subsequent testicular torsion of the remaining testicle [39,40]. In one of these studies, the presence of the bell clapper anomaly was exceedingly small, arguing against the contralateral testicle being at increased risk for subsequent intravaginal torsion [39]. As a result, at the time of exploration for an undescended testicle and confirmation of antenatal torsion, many experts in the field do not perform contralateral orchiopexy, as the risk of subsequent contralateral torsion is too low to justify the procedure.

Limited data do suggest that the contralateral testicle sustains injury independent of concomitant torsion [41-45]. These findings have resulted in the recommendation by some experts in the field to remove the torsed testis because leaving the injured testis in situ may lead to potential risk to the contralateral testicle [44,45] (see 'Our approach' below). Conversely, in the case of bilateral torsion, an atrophic testicle may be left in place in the hopes of maintaining some future endocrine function [6,10].

DIAGNOSIS — The suspected diagnosis of neonatal testicular torsion is based upon the presence of characteristic physical findings of testicular torsion. In particular, a hardened, fixed, nontender scrotal mass with a discolored scrotum is almost pathognomonic for prenatal torsion [6]. Surgical exploration confirms the diagnosis.

Imaging — In cases where the diagnosis is uncertain, diagnostic imaging is often performed. However, the accuracy and value of diagnostic testing varies, as these are challenging studies to perform in the neonate. Diagnostic imaging should not delay emergent intervention that is deemed necessary based upon the clinical examination and presentation, particularly for patients with an acute presentation.

Diagnostic studies include the following:

Ultrasonography with Doppler color flow is the imaging modality of choice, including in our center, because of its general availability and noninvasive nature. With an experienced operator, it has a high sensitivity in detecting testicular torsion by the lack of detected blood flow to the affected testis (image 1) [46,47]. A heterogeneous parenchymal echogenicity suggests a torsion event and testicular nonviability [48-50], and subsequent examinations may demonstrate a decrease in testicular mass with ongoing testicular atrophy (image 1). In contrast, a homogeneous appearance indicates testicular viability [48]. Ultrasonography also detects other scrotal pathology both on the affected and contralateral side, such as testicular tumors, hernias, or hydroceles.

In older patients, high-resolution ultrasonography of the spermatic cord can also improve diagnosis as a visualized "twist" or "whirlpool sign" in the spermatic cord has high sensitivity (96 percent) and specificity (99 percent) in non-neonatal torsion [51,52]. It remains uncertain whether these findings are useful in the diagnosis of neonatal torsion [52]. High-frequency color Doppler ultrasound has had promising results in the differentiation between prenatal and postnatal testicular torsion based on testicular size and echogenicity [53]. However, performing an accurate Doppler evaluation in neonates is challenging [54]. It can be difficult to detect blood flow in normal neonates, which may lead to inaccurate diagnoses. In addition, there are case reports of asynchronous bilateral testicular torsion confirmed by surgical exploration, in which a preoperative ultrasound did not identify torsion or compromised blood flow to the contralateral testicle [10,19,26,28].

Radionuclide scintigraphy with 99m technetium-pertechnetate is a sensitive but less specific test in detecting testicular torsion. The study can be especially difficult to interpret in the neonatal period. The "bull's eye sign" (ie, hyperemic peritesticular rim) is predictive of late torsion [48]. However, the bull's eye sign indicating lack of blood flow does not differentiate torsion from other diagnoses, such as hematocele, hematoma, or necrotic neoplasm [55]. Radionuclide scintigraphy also does not provide any other additional anatomical information [55]. In addition, many institutions may not have the proper equipment and personnel to perform this study. Radionuclide scintigraphy is rarely performed in practice, including in our institution.

Magnetic resonance imaging (MRI) offers excellent anatomic detail and has been used to differentiate subacute torsion from epididymitis in the adolescent population [56]. However, it is costly and logistically difficult to obtain in an emergency setting, which may delay organ preserving surgery. In addition, these infants will generally require anesthesia and/or sedation to undergo MRI. As a result, MRI is not routinely used in the management/diagnosis of neonatal torsion.

Prenatal diagnosis — Prenatal torsion is being identified on fetal sonography with increasing frequency [2,54,57,58]. A hydrocele detected prenatally also may be a sign of testicular torsion [58,59]. However, the accuracy of prenatal diagnosis is unknown, and postnatal imaging should be performed to confirm the diagnosis [54]. When testicular torsion is confirmed to be an in utero event, testicular salvage by surgical correction is not possible, and thus, induced delivery and emergent surgery are not recommended [2].

DIFFERENTIAL DIAGNOSIS — When an infant presents with an abnormal scrotal examination, one must consider other causes of scrotal swelling in the differential diagnosis, such as hematocele, hydrocele, incarcerated hernia, epididymoorchitis, torsion of the appendix testis or appendix epididymis, meconium peritonitis, and testicular tumor. In most cases, ultrasonography with Doppler color flow is able to differentiate these diagnoses from testicular torsion.

For patients with nonpalpable testes, the differential diagnosis includes antenatal torsion, cryptorchidism, and disorders of sexual development (DSD) (eg, gonadal dysgenesis). However, a diagnosis of DSD is unlikely in a patient with unilateral testicular involvement and normal-appearing penis (absence of hypospadias) and in this clinical setting, evaluation for DSD is not necessary. However, male infants with bilateral nonpalpable testicles should be evaluated for a DSD, especially if circumcision is being considered. (See "Undescended testes (cryptorchidism) in children: Clinical features and evaluation" and "Evaluation of the infant with atypical genital appearance (difference of sex development)" and "Causes of differences of sex development", section on 'Global defects in testicular function'.)

MANAGEMENT

Overview — The management of neonatal testicular torsion is a complicated and controversial subject. Opinions differ and data are lacking on whether surgery can successfully salvage the prenatally diagnosed torsed testis, and whether the contralateral side is at increased risk for concomitant or subsequent torsion. A meta-analysis of 197 neonates with testicular torsion demonstrated that bilateral scrotal exploration can salvage 7 percent of torsed testicles and prevent asynchronous torsion in 4 percent of neonates and concluded that approximately 10 percent of neonates presenting with neonatal torsion would benefit from bilateral exploration with orchiopexy of the contralateral testicle [60]. However, in a subsequent metanalysis of 974 infants, one testicle could be salvaged in 2.5 percent of synchronous bilateral torsion events, while a testicle could be salvaged in 48.5 percent on asynchronous bilateral torsion events [9]. The authors calculated that the number to treat (ie, explore) to avoid loss of both testes was 1.6 [9].

Our approach — In our center, the management of neonatal testicular torsion is based on the following different clinical presentations (algorithm 1):

Early prenatal event typically presents as an absent testicle or a very small, pea-sized nubbin. In this setting, observation is suggested as antenatal torsion cannot be confirmed and there is potential for an undescended, abdominal testicle.

Late prenatal event occurring within 10 days of delivery presents generally as a painless scrotal mass. In this setting, our management approach includes either nonemergent surgical exploration or continued observation based on informed discussion with parents/caregivers to review risks of asynchronous torsion versus risks of surgical or anesthetic complications. If surgery is performed, we proceed urgently (within days), once clinical stability is confirmed. Bilateral scrotal exploration with removal of the atrophic testicle and contralateral orchiopexy would also be performed.

Bilateral involvement, regardless of whether the event is pre- or postnatal, requires immediate surgical exploration. Whenever possible, detorsion and fixation of the injured testes are performed. (See 'Orchiectomy or leave testicle in situ?' below.)

Postnatal acute event requires immediate surgical exploration and contralateral orchiopexy (fixation to the scrotum) to prevent unrecognized synchronous or future, asynchronous torsion. (See 'Contralateral orchiopexy' below.)

Perinatal presentation — A reasonable approach to perinatal torsion or a non-acute event is that treatment should focus on the healthy testis. In the neonate, the decision to perform orchiopexy of the noninvolved testis needs to consider the risk of anesthesia, complexity of the surgery (associated hydrocele and hernia in the normal testis), and comfort level of the health care team and facility with operative management of neonates. Access to pediatric specialists, including anesthesiologists as well as pediatric urologists and/or pediatric surgeons is also a key consideration. While most studies from tertiary sites with access to pediatric specialists report a low complication rate, other case series report up to an 18 percent complication rate associated with surgery [11].

Several treatment choices must be made:

When and if to perform surgical exploration. Options include:

Emergent (early) surgical exploration as soon as possible, preferably within six hours based upon animal data. (See 'Testicular ischemia' above.)

Delayed surgical exploration until the neonate is clinically stable. In our tertiary center, we prefer that urgent surgery be performed (within the first few days of life) once the infant is clinically stable in order to preserve the contralateral testicle and prevent asynchronous testicular torsion [9]. Others suggest postponing surgery to one month of age, when anesthetic risks have decreased [6].

Observation with deferred exploration [6].

Observation with no further plans for intervention.

If surgical exploration is performed, whether to remove (orchiectomy) or leave in place a nonviable or questionably viable testicle.

If surgical exploration is performed, whether to explore the contralateral normal testicle and perform an orchiopexy. The risk of potential testicular injury when operating on an otherwise healthy testicle must be weighed against the risk of potential missed or asynchronous torsion to the contralateral testicle. (See 'Contralateral testicle' above and 'Contralateral orchiopexy' below.)

Type of anesthesia (general versus spinal). In the neonate, the risk of anesthesia complications is higher because of changes in metabolism and organ function that occur in the first weeks of life. The use of spinal anesthesia mitigates concerns about the neurotoxic effects of anesthetic agents and avoids the need for intubation [61]. We prefer to perform the surgery under spinal anesthesia, when possible.

When and if to perform surgery — The only option for potentially salvaging the affected testis is surgical intervention with detorsion of the vessels. However, the poor salvage rates, especially in patients with prenatal torsion or non-acute events, the high risk of surgical and anesthetic complications in the neonate, and the relatively low rate of bilateral involvement have led to a debate on when and if surgery should be performed for patients with prenatal torsion.

The following factors should be considered regarding the decision of whether or not to perform surgical exploration [25]:

Prenatal torsion almost always occurs so far ahead of clinical presentation that salvage of a testis is exceedingly rare.

Although bilateral torsion is rare, surgical intervention is suggested for even a small possibility of successful salvage of either testis.

There are several case reports of incidentally identified contralateral testicular torsion during exploration for presumed unilateral torsion. Salvage rates for the contralateral testicles in these instances are higher [24].

An acute torsion event is painful.

Asynchronous torsion generally occurs in infants up to four to six weeks of age; however, there are case reports of it occurring at three to six months of age.

A tense hydrocele in the contralateral, non-torsed testicle can make testicular examinations difficult, making it more complicated to recognize an asynchronous torsion event.

Timing of surgery — The uncertainty of the optimal timing of surgery for prenatal torsion was illustrated in a survey of pediatric urologists (primarily in the United States) that reported a varied response to the management of antenatal exploration as follows [62]:

Immediate exploration – 34 percent

Urgent exploration – 26 percent

Elective exploration – 28 percent

No exploration – 12 percent

There is also global variation in clinical practice [63]. In the above survey primarily from the United States, 88 percent of urologists would perform surgical exploration for prenatal torsion, whereas lower rates were noted for clinicians in Great Britain (75 percent exploration for nonspecified neonatal testicular torsion) and in Canada (67 percent exploration for prenatal torsion).

Postnatal testicular torsion — Patients with postnatal torsion have more favorable salvage rates of 30 to 40 percent and should undergo emergent surgical intervention regardless of whether there is unilateral or bilateral involvement [6,21-23]. In these cases, we believe the salvage rate justifies the potential surgical and anesthetic risks [62].

Surgery versus observation — As noted above, some experts in the field advocate emergent surgical exploration in all patients with neonatal testicular torsion [9,10,15,18,24,64]. These proponents perform expectant surgery even in cases of prenatal torsion with negligible salvage rates because of the possibility of undetected and potential asynchronous (subsequent) torsion of the contralateral testis [9,10,24,60]. Others in the field advocate nonsurgical management of neonatal torsion because of the overall poor salvage rates, their perspective that there is little benefit of removing the torsed testicle, and the potential risks of surgery and anesthesia [10,11,20,65,66]. In the United States, medical legal factors have also influenced the management of neonatal testicular torsion, often prompting early intervention [36].

Some experts in the field, including the author, have adopted a stratified approach based upon the clinical presentation (algorithm 1):

Non-acute event (prenatal presentation) – In patients with prenatal torsion, surgery generally fails to save the testis, with salvage rates ranging from 0 to 5 percent [6,10,13,18]. Thus, in cases of unilateral involvement with a palpable hard or atrophic testicle, our approach is to delay surgery until the neonate is stable enough to undergo anesthesia [1]. In this author's practice where there is access to appropriate expertise in pediatric anesthesia, if surgery is the management choice, we typically perform the operation urgently within the first few hours to days of life based on data suggesting that the median time to asynchronous torsion is one day [9].

Others have advocated waiting until one month of age when there is a decrease in both surgical and anesthetic risks [6,67]. The risk of asynchronous torsion persists during the first month of life [60]. Until the time of surgery, parents/caregivers are instructed to perform serial examinations of the contralateral testis with each diaper change. An acute change is an indication for emergent evaluation and possible surgical intervention. One potential risk is missing the diagnosis of an unrecognized, contralateral testicular torsion during the one-month delay before surgical exploration, however this may be an uncommon complication. A contralateral hydrocele can make examination difficult and thus mask an asynchronous torsion event. (See 'Contralateral testicle' above.)

In contrast, emergent surgery is indicated in patients with bilateral involvement with the hope of averting anorchia and the long-term complications of infertility and sex steroid deficiencies [10,15,26]. In this situation, recommendations are to leave the testicles in place, as Leydig cells are more resistant to ischemia, and there is potential for preservation of testosterone production.

Acute event (postnatal presentation) – Surgery is performed for patients with evidence of acute testicular torsion (unilateral and bilateral involvement) as there is a more favorable salvage rates of 30 to 40 percent [6,21-23]. In these neonatal cases, the salvage rate justifies the potential surgical and anesthetic risks.

Surgery — Surgery should be performed in centers with pediatric surgeons/urologists and anesthesiologists who have clinical expertise and experience with neonatal patients.

Surgical exploration includes either an inguinal or scrotal approach. An inguinal approach should be considered if an ultrasound has not been performed, because of the possibility that the scrotal mass may be due to a malignancy and, if so, the need to adhere to principles of oncologic surgery of local tumor control. In addition, hydroceles are commonly observed in the torsed and the contralateral testicle, and some surgeons prefer an inguinal incision, which would facilitate closing off a hernia sac if identified at the time of the surgery. However, a scrotal approach appears to be safe as the majority of contralateral hydroceles are noncommunicating and there is little risk of developing a postsurgical hernia or recurring hydrocele [68]. Ultimately, the surgical approach will be determined by the comfort level of the surgeon, as avoiding complications is a high priority when performing surgery in a neonate to salvage a torsed testicle or prevent potential contralateral torsion.

Orchiectomy or leave testicle in situ? — If surgical exploration is performed, most experts in the field perform orchiectomy in patients with unilateral torsion. This approach is based upon the poor salvage rates, and, as previously discussed, limited data that suggest leaving the injured testicle in situ results in injury to the contralateral side. (See 'Contralateral testicle' above.)

In cases with bilateral involvement, when feasible, surgeons should detorse and fix the testicles rather than perform orchiectomy, since the attenuated testes may retain some residual Leydig cell function [6,10].

Contralateral orchiopexy — One must weigh the risk of injuring a healthy, uninvolved contralateral testicle when proceeding with a prophylactic maneuver to prevent potential future torsion. However, as discussed above, individuals with unilateral neonatal testicular torsion may be at increased risk for torsion of the remaining solitary testicle, especially during the neonatal window [29,37,38,60].

The decision for contralateral orchiopexy also varies globally [63]. In the United States, almost all pediatric urologists (approximately 96 percent [62]) would perform contralateral orchiopexy, whereas 22 percent of British surgeons would not perform this surgical procedure because of concerns of injuring the uninvolved testis. The authors agree with recommendations to explore the contralateral testicle once the decision has been made to proceed with surgery. This alleviates concerns for missed contralateral torsion and prevents potential asynchronous torsion.

Observation — There are others in the field who propose nonsurgical management of neonatal torsion because of the overall poor salvage rates, and their perspective that there is little benefit of removing the torsed testicle [20,65,66]. In this approach, parents are instructed to perform serial examinations of the contralateral testicle with each diaper change. An acute change is an indication for emergent evaluation and possible surgical exploration. Ultrasound evaluation may be helpful to confirm nonviable appearance of the torsed testicle and assess the contralateral testicle. Asynchronous contralateral involvement is uncommon and the reported incidence may be inflated because of biased publication of its devastating outcome. Nevertheless, if there is concern for contralateral involvement, emergent surgical exploration is warranted.

Concerns about this approach include the presence of other scrotal conditions (eg, hydrocele) that hinder an adequate assessment, and a possible long delay in obtaining care when an acute change is noted, especially if there is significant distance between the family's home and a tertiary care center with the appropriate resources and personnel. Also, as noted above, contralateral, asynchronous torsion can be missed on physical examination and radiologic findings [24,26].

SUMMARY AND RECOMMENDATIONS

Definition – Neonatal testicular torsion is defined as torsion diagnosed within the first 30 days of life. It accounts for 10 to 12 percent of all pediatric testicular torsions with a reported incidence of 6.1 per 100,000 live births. (See 'Epidemiology' above.)

Pathogenesis – Neonatal testicular torsion is typically an extravaginal process that involves twisting of the testicle, the spermatic cord above the testicle and its tunica vaginalis investments. It is distinct from testicular torsion in the older infant (>1 month of age), child, and adolescent, which is an intravaginal process (figure 1). (See 'Pathogenesis' above and "Causes of scrotal pain in children and adolescents", section on 'Testicular torsion'.)

Clinical presentation – Neonatal testicular torsion is divided into prenatal and postnatal torsion, and presents in the following scenarios (see 'Definitions' above and 'Clinical presentation' above):

Prenatal torsion is detected in the immediate postpartum period and is an intrauterine event. The neonate typically does not demonstrate any clinical signs of distress:

-Prenatal torsion that occurs early in gestation presents as a nonpalpable testicle or an atrophic, nontender nubbin. The affected testis is generally not salvageable regardless of the timing of surgery.

-Late prenatal torsion that occurs closer to the time of delivery presents with enlarged, firm, and nontender testicle with a discolored hemiscrotum (picture 1A-B). It remains uncertain what the salvageable rate is for late prenatal torsion

Postnatal torsion presents with acute tenderness and swelling in a testicle that was previously noted to be normal during the birth hospitalization. The surgical salvageable rate may be as high as 30 to 40 percent.

Complications – The major complication of neonatal torsion is vascular compromise, resulting in testicular ischemia and injury, and if not corrected, necrosis and testicular nonviability. Infertility and long-term sequelae of androgen deficiencies are potential complications for patients with bilateral involvement. (See 'Complications' above.)

Diagnosis – The diagnosis of neonatal torsion is based upon the presence of characteristic physical findings. In cases where the diagnosis is uncertain, ultrasonography is the preferred initial imaging modality. (See 'Diagnosis' above.)

Management –Management of neonatal testicular torsion is controversial because of the lack of data regarding the true incidence of salvageable testis and contralateral involvement, which can be synchronous (concomitant) or asynchronous (subsequent) torsion. Treatment options include emergent or delayed surgery, or observation. (See 'Management' above.)

Surgery – Surgical exploration for all cases of neonatal testicular torsion is an acceptable approach.

Observation – An alternative approach is to observe and perform surgery only when an acute postnatal torsional event occurs. In patients with a prenatal torsion who are managed nonsurgically, parents are taught to perform scrotal examinations of the contralateral side at each diaper change and to inform care providers of any change in the examination. (See 'When and if to perform surgery' above.)

Our approach – In our center based on our clinical experience and review of the literature, we use a stratified approach based on clinical presentation (algorithm 1):

Emergent surgery is reserved for patients with bilateral involvement or unilateral postnatal (acute) torsion.

For patients with a prenatal non-acute event, the families are counseled about nonemergency surgery (when neonate is stable for surgical intervention) regarding the choice between contralateral orchiopexy versus observation of the contralateral testicle (picture 1A). However, others advocate emergent surgery for all cases of neonatal torsion. (See 'Timing of surgery' above and 'Our approach' above.)

At the time of surgery, in patients with unilateral involvement, we perform orchiectomy of the affected testis, and perform orchiopexy of the contralateral testis (fixation to the scrotum) to prevent potential future torsion. In patients with bilateral involvement, detorsion and orchiopexy of both testicles are performed, whenever possible. (See 'Orchiectomy or leave testicle in situ?' above and 'Contralateral orchiopexy' above.)

  1. Das S, Singer A. Controversies of perinatal torsion of the spermatic cord: a review, survey and recommendations. J Urol 1990; 143:231.
  2. Melcer Y, Mendlovic S, Klin B, et al. Fetal diagnosis of testicular torsion: what shall we tell the parents? Prenat Diagn 2015; 35:167.
  3. Visser AJ, Heyns CF. Testicular function after torsion of the spermatic cord. BJU Int 2003; 92:200.
  4. Gillenwater JY, Burros HM. Torsion of the spermatic cord in utero. JAMA 1966; 198:1123.
  5. McFarland JB. Testicular strangulation in children. Br J Surg 1966; 53:110.
  6. Kaye JD, Levitt SB, Friedman SC, et al. Neonatal torsion: a 14-year experience and proposed algorithm for management. J Urol 2008; 179:2377.
  7. Driver CP, Losty PD. Neonatal testicular torsion. Br J Urol 1998; 82:855.
  8. John CM, Kooner G, Mathew DE, et al. Neonatal testicular torsion--a lost cause? Acta Paediatr 2008; 97:502.
  9. O'Kelly F, Chua M, Erlich T, et al. Delaying Urgent Exploration in Neonatal Testicular Torsion May Have Significant Consequences for the Contralateral Testis: A Critical Literature Review. Urology 2021; 153:277.
  10. Yerkes EB, Robertson FM, Gitlin J, et al. Management of perinatal torsion: today, tomorrow or never? J Urol 2005; 174:1579.
  11. Djahangirian O, Ouimet A, Saint-Vil D. Timing and surgical management of neonatal testicular torsions. J Pediatr Surg 2010; 45:1012.
  12. Kyriazis ID, Dimopoulos J, Sakellaris G, et al. Extravaginal testicular torsion: a clinical entity with unspecified surgical anatomy. Int Braz J Urol 2008; 34:617.
  13. Kaplan GW, Silber I. Neonatal torsion- to pex or not?. In: Urologic Surgery in Neonates and Young Infants, WB Saunders, Philadelphia 1988. p.386.
  14. Burge DM. Neonatal testicular torsion and infarction: aetiology and management. Br J Urol 1987; 59:70.
  15. Baglaj M, Carachi R. Neonatal bilateral testicular torsion: a plea for emergency exploration. J Urol 2007; 177:2296.
  16. Mano R, Livne PM, Nevo A, et al. Testicular torsion in the first year of life--characteristics and treatment outcome. Urology 2013; 82:1132.
  17. Callewaert PR, Van Kerrebroeck P. New insights into perinatal testicular torsion. Eur J Pediatr 2010; 169:705.
  18. Brandt MT, Sheldon CA, Wacksman J, Matthews P. Prenatal testicular torsion: principles of management. J Urol 1992; 147:670.
  19. Al-Salem AH. Intrauterine testicular torsion: a surgical emergency. J Pediatr Surg 2007; 42:1887.
  20. Kaplan GW, Retik A, Snyder HM III, et al. Neonatal Torsion: Immediate Surgical Exploration versus Conservative Mangagement. Dialogues in Pediatric Urology 2004; 26:2.
  21. Sorensen MD, Galansky SH, Striegl AM, et al. Perinatal extravaginal torsion of the testis in the first month of life is a salvageable event. Urology 2003; 62:132.
  22. Stone KT, Kass EJ, Cacciarelli AA, Gibson DP. Management of suspected antenatal torsion: what is the best strategy? J Urol 1995; 153:782.
  23. Pinto KJ, Noe HN, Jerkins GR. Management of neonatal testicular torsion. J Urol 1997; 158:1196.
  24. Roth CC, Mingin GC, Ortenberg J. Salvage of bilateral asynchronous perinatal testicular torsion. J Urol 2011; 185:2464.
  25. Snyder HM, Diamond DA. In utero/neonatal torsion: observation versus prompt exploration. J Urol 2010; 183:1675.
  26. Ahmed SJ, Kaplan GW, DeCambre ME. Perinatal testicular torsion: preoperative radiological findings and the argument for urgent surgical exploration. J Pediatr Surg 2008; 43:1563.
  27. Abraham MB, Charles A, Gera P, Srinivasjois R. Surgically managed perinatal testicular torsion: a single centre experience. J Matern Fetal Neonatal Med 2016; 29:1265.
  28. Abbas TO, Ali M. Bilateral Neonatal Testicular Torsion; Hidden Surgical Nightmare. Front Pediatr 2018; 6:318.
  29. Erlich T, Ghazzaoui AE, Pokarowski M, et al. Perinatal testicular torsion: The clear cut, the controversial, and the "quiet" scenarios. J Pediatr Surg 2022; 57:288.
  30. SMITH GI. Cellular changes from graded testicular ischemia. J Urol 1955; 73:355.
  31. Sessions AE, Rabinowitz R, Hulbert WC, et al. Testicular torsion: direction, degree, duration and disinformation. J Urol 2003; 169:663.
  32. Cimador M, DiPace MR, Castagnetti M, DeGrazia E. Predictors of testicular viability in testicular torsion. J Pediatr Urol 2007; 3:387.
  33. Abeyaratne MR, Aherne WA, Scott JE. The vanishing testis. Lancet 1969; 2:822.
  34. Lamesch AJ. Monorchidism or unilateral anorchidism. Langenbecks Arch Chir 1994; 379:105.
  35. Belman AB, Rushton HG. Is an empty left hemiscrotum and hypertrophied right descended testis predictive of perinatal torsion? J Urol 2003; 170:1674.
  36. DaJusta DG, Granberg CF, Villanueva C, Baker LA. Contemporary review of testicular torsion: new concepts, emerging technologies and potential therapeutics. J Pediatr Urol 2013; 9:723.
  37. Harris BH, Webb HW, Wilkinson AH Jr, Stevens PS. Protection of the solitary testis. J Pediatr Surg 1982; 17:950.
  38. Bellinger MF. The blind-ending vas: the fate of the contralateral testis. J Urol 1985; 133:644.
  39. Martin AD, Rushton HG. The prevalence of bell clapper anomaly in the solitary testis in cases of prior perinatal torsion. J Urol 2014; 191:1573.
  40. Kehoe JE, Christman MS. To 'Pex or Not to 'Pex: What to Do for the Contralateral Testis When a Nubbin Is Discovered. Curr Urol Rep 2017; 18:9.
  41. Cosentino MJ, Nishida M, Rabinowitz R, Cockett AT. Histological changes occurring in the contralateral testes of prepubertal rats subjected to various durations of unilateral spermatic cord torsion. J Urol 1985; 133:906.
  42. Tanyel FC, Büyükpamukçu N, Hiçsönmez A. Contralateral testicular blood flow during unilateral testicular torsion. Br J Urol 1989; 63:522.
  43. Madarikan BA. Testicular salvage following spermatic cord torsion. J Pediatr Surg 1987; 22:231.
  44. Nagler HM, White RD. The effect of testicular torsion on the contralateral testis. J Urol 1982; 128:1343.
  45. Barkley C, York JP, Badalament RA, et al. Testicular torsion and its effects on contralateral testicle. Urology 1993; 41:192.
  46. Arena F, Nicòtina PA, Romeo C, et al. Prenatal testicular torsion: ultrasonographic features, management and histopathological findings. Int J Urol 2006; 13:135.
  47. van der Sluijs JW, den Hollander JC, Lequin MH, et al. Prenatal testicular torsion: diagnosis and natural course. An ultrasonographic study. Eur Radiol 2004; 14:250.
  48. Kaye JD, Shapiro EY, Levitt SB, et al. Parenchymal echo texture predicts testicular salvage after torsion: potential impact on the need for emergent exploration. J Urol 2008; 180:1733.
  49. Brown SM, Casillas VJ, Montalvo BM, Albores-Saavedra J. Intrauterine spermatic cord torsion in the newborn: sonographic and pathologic correlation. Radiology 1990; 177:755.
  50. Traubici J, Daneman A, Navarro O, et al. Original report. Testicular torsion in neonates and infants: sonographic features in 30 patients. AJR Am J Roentgenol 2003; 180:1143.
  51. Kalfa N, Veyrac C, Lopez M, et al. Multicenter assessment of ultrasound of the spermatic cord in children with acute scrotum. J Urol 2007; 177:297.
  52. McDowall J, Adam A, Gerber L, et al. The ultrasonographic "whirlpool sign" in testicular torsion: valuable tool or waste of valuable time? A systematic review and meta-analysis. Emerg Radiol 2018; 25:281.
  53. Xiao H, Gao Y, Li Y, et al. Ultrasound assessment of perinatal testicular torsion. Br J Radiol 2016; :20151077.
  54. Ricci P, Cantisani V, Drudi FM, et al. Prenatal testicular torsion: sonographic appearance in the newborn infant. Eur Radiol 2001; 11:2589.
  55. Vieras F, Kuhn CR. Nonspecificity of the "rim sign" in the scintigraphic diagnosis of missed testicular torsion. Radiology 1983; 146:519.
  56. Trambert MA, Mattrey RF, Levine D, Berthoty DP. Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology 1990; 175:53.
  57. Arena F, Nicòtina PA, Scalfari G, et al. A case of bilateral prenatal testicular torsion: Ultrasonographic features, histopathological findings and management. J Pediatr Urol 2005; 1:369.
  58. Tripp BM, Homsy YL. Prenatal diagnosis of bilateral neonatal torsion: a case report. J Urol 1995; 153:1990.
  59. Hubbard AE, Ayers AB, MacDonald LM, James CE. In utero torsion of the testis: antenatal and postnatal ultrasonic appearances. Br J Radiol 1984; 57:644.
  60. Monteilh C, Calixte R, Burjonrappa S. Controversies in the management of neonatal testicular torsion: A meta-analysis. J Pediatr Surg 2019; 54:815.
  61. Ebert KM, Jayanthi VR, Alpert SA, et al. Benefits of spinal anesthesia for urologic surgery in the youngest of patients. J Pediatr Urol 2019; 15:49.e1.
  62. Broderick KM, Martin BG, Herndon CD, et al. The current state of surgical practice for neonatal torsion: a survey of pediatric urologists. J Pediatr Urol 2013; 9:542.
  63. Friedman AA, Elder JS. Words of wisdom: Re: The current state of surgical practice for neonatal torsion: a survey of pediatric urologists. Eur Urol 2013; 64:513.
  64. Cuervo JL, Grillo A, Vecchiarelli C, et al. Perinatal testicular torsion: a unique strategy. J Pediatr Surg 2007; 42:699.
  65. Duckett JW. Routine Contralateral Explorationand Fixation Is Unjustified. Dialogues in Pediatric Urology 1991; 14:5.
  66. Huff DS, Wu HY, Snyder HM 3rd, et al. Evidence in favor of the mechanical (intrauterine torsion) theory over the endocrinopathy (cryptorchidism) theory in the pathogenesis of testicular agenesis. J Urol 1991; 146:630.
  67. Cohen MM, Cameron CB, Duncan PG. Pediatric anesthesia morbidity and mortality in the perioperative period. Anesth Analg 1990; 70:160.
  68. Kaefer M, Agarwal D, Misseri R, et al. Treatment of contralateral hydrocele in neonatal testicular torsion: Is less more? J Pediatr Urol 2016; 12:306.e1.
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