1436864372905.847 Pediatric Testicular Torsion: Background, Anatomy, Pathophysiology

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Pediatric Testicular TorsionAuthor: Krishna Kumar Govindarajan, MBBS, MS, DNB, MRCS, MCh; Chief Editor: Marc Cendron, MD more...

Updated: Mar 30, 2015

BackgroundPediatric testicular torsion is an acute vascular event in which the spermatic cord becomes twisted on its axis (seethe image below), so that the blood flow to or from the testicle becomes impeded. This results in ischemic injuryand infarction. The condition may result in loss of the testis.[1]

Testicular torsion has a bimodal incidence: one group presents in the perinatal period (perinatal testicular torsion),and the other group presents in early puberty (though torsion can present at any age, well into adulthood [seeTesticular Torsion]). Another condition that mimics testicular torsion in presentation is torsion of the appendix testisor appendix epididymis, which is most commonly seen in older prepubertal boys.

Testicular torsion presents as acuteonset severe scrotal pain, commonly with associated scrotal swelling anderythema. Nausea and vomiting are common, as are local scrotal redness and pain (see Clinical).

Testicular torsion is a surgical emergency, and all efforts should be aimed at bringing the patient to the operatingroom as quickly as possible within the limits of surgical and anesthetic safety. Outcomes directly depend on theduration of ischemia; thus, time is of the essence.[2] Time wasted attempting to arrange for imaging studies,laboratory testing, or other diagnostic procedures results in the loss of testicular tissue. (See Treatment.)

Because testicular torsion is a potentially reversible condition when diagnosed and treated early, the emphasisshould be on prompt evaluation of children who present with acute scrotum. General public awareness andawareness in referring pediatricians and general practitioners is key to improving outcomes in these boys.[3] Thenecessity of seeking immediate medical care in the setting of the acute scrotum cannot be sufficiently emphasizedto the public and to clinicians.

Historical background

Testicular torsion was first described by Delasiauve in 1840. It was not widely regarded as a significant problem until1907, when Rigby and Russell published their work on torsion of the testis in Lancet. The first description ofneonatal torsion was by Taylor in 1897. Subsequently, Colt reported torsion of the appendix testis in 1922.[4, 2]

The initial use of Doppler ultrasonography was reported in 1975; Nadel et al reported sodium pertechnetatetesticular scintigraphy in 1973.[5]

AnatomyThe normal testis lies suspended in the scrotum, with the visceral tunica vaginalis wrapping the anterior, inferior,superior, and mediolateral margins, leaving the posterior surface adherent to the surrounding scrotal soft tissues.The testicular arteries arise from the abdominal aorta and pass inferolaterally through the retroperitoneum to theinternal inguinal ring, where they meet the vasa deferentia and enter the inguinal canal.

The spermatic cord (artery, vein, vas, and supporting structures) passes through the canal, out the external inguinalring, over the pubic tubercle, and into the scrotum, where it meets the testis.

PathophysiologyTesticular torsion can take place either inside the tunica vaginalis (intravaginal) or outside it (extravaginal). Thedistinction is important because the two forms of torsion are associated with different ages of presentation andetiologies. Intravaginal testicular torsion (see the image below) is far more common and represents almost alltorsion events in older boys. In a minority, a predisposing factor such as horizontal lie/bell clapper deformity makesthe opposite testis prone to torsion.

Intravaginal testicular torsion with ischemia in adolescent boy.

Extravaginal testicular torsion is commonly seen in perinatal cases. Hence, the diagnosis is often made late, longafter the torsion event has taken place. The tunica vaginalis takes about 6 weeks after birth to adhere to thesurrounding tissues, possibly explaining the preponderance of the condition in neonates. Large birth weight, difficultlabor, breech presentation, and overreactive cremasteric reflex have been proposed as possible causes for perinataltorsion.[6, 7]

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Testicular torsion is classically described as involving a medial rotation; however, in as many as one third of cases, alateral rotation has been described.[8, 9] When manual detorsion is contemplated, the testis is typically rotatedlaterally ("opening the book"); however, if the testis is already laterally rotated, this maneuver worsens the condition.For this reason, manual detorsion is not a commonly performed procedure.

EtiologyA rotational twisting of the spermatic cord is the basis of all torsion events. When the twist is sufficient to obstructarterial inflow, testicular ischemia results. If the duration of ischemia is long enough, infarction results. Lesserdegrees of cord twisting may result in obstruction of venous outflow, causing congestion and swelling of the testiswithout frank infarction.

Unfortunately, no reliable indicator for risk of torsion has been identified. Numerous factors have been observed inassociation with torsion, but none can be used to predict torsion risk in a clinical setting.[10]

Bell clapper deformity

In this anatomic variant, the testis hangs freely within parietal tunica vaginalis secondary to an extension of thetunica high onto the spermatic cord. This extension allows the testis to rotate easily within the tunica because of thelack of normal fixation of the posterior testis to the scrotal tissues.

The bell clapper deformity is often noted at the time of exploration in older children and adolescents with testiculartorsion. The anomaly is seen in 12% of males in cadaveric studies and is often bilateral, being the reason behindthe surgical fixation of the uninvolved testis in a proven case of torsion testis.[11]

Pubertal changes

The increased incidence in torsion around the time of puberty has led to speculation regarding the role of pubertalchanges in torsion risk. Increased testosterone levels at puberty result in an increased testicular volume and mass.These increases could predispose the testis to torsion because of increased movement around the axis of the cord.

The cord’s torsional rigidity and other resistances, which tend to limit the angle of rotation, may increase lessmarkedly with growth and development. Thus, normal physical activity may result in angular momentum sufficient toeasily overcome the opposing resistances, allowing complete testicular torsion.[6]

Anatomic abnormalities

Various anatomic abnormalities of the testis are associated with torsion. The most significant of these iscryptorchidism (see the image below). Cryptorchid testes are at significantly higher risk of torsion than scrotal testes.[12] Other anatomic abnormalities that may predispose to torsion include a horizontal lie of the testes, polyorchidism,[13] and epididymal anomalies.[14]

Torsion of undescended testis.

Physical activities

In some cases, specific physical activities (eg, sports, weight training and trauma) appear to induce an episode oftorsion, perhaps by way of a sudden cremasteric reflex. Epidemiologic studies have shown that testicular torsion ismore common in winter months and in northern latitudes, prompting speculation that coldinduced cremastericcontraction may play a role in the development of torsion.[15]

Tunica and scrotal tissue adhesion

In the newborn, the scrotal parietal tunica vaginalis has not yet fully adhered to the outer tissues of the scrotum.Thus, the entire testes, tunica vaginalis, and gubernaculum may twist together within the scrotum, resulting in anextravaginal torsion. This is the most common form of torsion in the perinatal period. (See the image below.)Because the adhesion between the tunica and scrotal tissues is bilaterally deficient, these infants are at risk forbilateral torsion events (either synchronous or metachronous).[6, 16]

Perinatal testicular torsion.

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EpidemiologyTesticular torsion is one of the more common acute pediatric surgical conditions, although few studies havedocumented the precise incidence. In 1976, a study from the United Kingdom reported the annual incidence oftesticular torsion as 1 case per 4000 in males younger than 25 years.[17]

Extravaginal torsion constitutes approximately 5% of all torsions. Of these cases of testicular torsion, 70% occurprenatally and 30% occur postnatally. The peak incidence of intravaginal torsion occurs at age 1314 years. The lefttestis is more frequently involved. Bilateral cases account for 2% of all torsions.

Prognosis

Successful salvage of the torsed testis is directly related to the time elapsed from the onset of ischemia.[18] Ifexploration is performed within 46 hours of symptom onset, salvage rates may approach 90%; with delayedintervention, however, these rates drop dramatically—to 50% at 12 hours after symptom onset and to almost 10%after 24 hours. In contrast, perinatal testicular torsion almost always results in loss of the involved testis (salvagerate < 5%).[19]

In a survey by Bennett et al, 55% of boys with testicular torsion (age range, 3 months to 16 years) had infarctionwith testis loss at scrotal exploration.[20] The main reason for the testicular loss was excessive delay before seekingmedical attention, usually attributed to the patient or his parents. Survey data have suggested that most boys donot think it is necessary to seek medical advice for testicular swelling, and a large minority do not think it isnecessary to seek medical advice for testicular swelling with pain.[21]

Overall, the causes for testicular loss can be summed up as follows[1] :

Lack of patient awareness or denial and subsequent delay in presentation (58%)Misdiagnosis by physician resulting in missed torsion (29%)Delay in treatment (13%)

Tryfonas et al reported that the results of testicular atrophy correlated with duration of symptoms and operativefindings.[22] In all cases of surgical detorsion in which torsion lasted longer than 24 hours and viability of the testiswas questionable, subsequent atrophy occurred.

Reduced fertility is a possible longterm complication of testicular torsion.[23] It may be related to ischemiareperfusion injury that damages the bloodtestis barrier, with resulting antisperm antibody production. A study in therat model by Ozkan et al found that serum inhibin B levels decrease after unilateral testicular torsion, suggestingcontralateral testicular damage.[24] In humans, serum inhibin B levels function as a useful marker of testicularfunction, as they reflect Sertoli cell function and spermatogenesis.

A study by Puri et al in 18 men who had undergone testicular torsion 723 years previously found the following[25] :

Five patients had fathered one or more childrenTen patients had normal results on seminal analysisTwo patients had low sperm density but normal semen volume and motilityOne patient had pathologic semen analysis results

All 18 patients had experienced prolonged unilateral testicular torsion before puberty and had undergone surgicaluntwisting with replacement of the nonviable testis in the scrotum. Fourteen of the patients had an absent testis onthe affected side, and four had severe atrophy (< 1 mL). The contralateral side appeared normal or hypertrophic.Autosensitization due to sperm autoantibodies was not observed in these patients.

Contributor Information and DisclosuresAuthorKrishna Kumar Govindarajan, MBBS, MS, DNB, MRCS, MCh MNAMS, FAIS, FICS, FACS, FEBPS,Assistant Professor and Consultant Pediatric Surgeon, Jawaharlal Institute of Postgraduate Medical Educationand Research, India

Krishna Kumar Govindarajan, MBBS, MS, DNB, MRCS, MCh is a member of the following medical societies:American College of Surgeons, International College of Surgeons, British Association of Paediatric Surgeons,Association of Surgeons of India, Indian Association of Pediatric Surgeons, Association of Colon and RectalSurgeons of India, Association of Minimal Access Surgeons of India, National Academy of Medical Sciences(India)

Disclosure: Nothing to disclose.

Coauthor(s)Caleb P Nelson, MD, MPH Assistant Professor of Surgery (Urology), Department of Urology, Harvard MedicalSchool; Consulting Staff, Department of Urology, Children's Hospital Boston

Caleb P Nelson, MD, MPH is a member of the following medical societies: American Urological Association,Endourological Society, Phi Beta Kappa, Society for Pediatric Urology, Society for Fetal Urology

Disclosure: Nothing to disclose.

Specialty Editor BoardMary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College ofPharmacy; EditorinChief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief EditorMarc Cendron, MD Associate Professor of Surgery, Harvard School of Medicine; Consulting Staff, Departmentof Urological Surgery, Children's Hospital Boston

Marc Cendron, MD is a member of the following medical societies: American Academy of Pediatrics, AmericanUrological Association, New Hampshire Medical Society, Society for Pediatric Urology, Society for Fetal Urology,Johns Hopkins Medical and Surgical Association, European Society for Paediatric Urology

Disclosure: Nothing to disclose.

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