Pediatric Testicular Torsion

Pediatric Testicular Torsion

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Pediatric testicular torsion is an acute vascular event in which the spermatic cord becomes twisted on its axis, so that the blood flow to or from the testicle becomes impeded. [1] This results in ischemic injury and infarction. The condition may result in loss of the testis. [2]

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 [see Testicular Torsion]). Another condition that mimics testicular torsion in presentation is torsion of the appendix testis or appendix epididymis, which is most commonly seen in older prepubertal boys.

Testicular torsion presents as acute-onset severe scrotal pain, commonly with associated scrotal swelling and erythema. Nausea and vomiting are common, as are local scrotal redness and pain (see Presentation).

Testicular torsion is a surgical emergency, and all efforts should be aimed at bringing the patient to the operating room as quickly as possible within the limits of surgical and anesthetic safety. Outcomes directly depend on the duration of ischemia; thus, time is of the essence. [3] 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 emphasis should be on prompt evaluation of children who present with acute scrotum. General public awareness and awareness in referring pediatricians and general practitioners is key to improving outcomes in these boys. [4] The necessity of seeking immediate medical care in the setting of the acute scrotum cannot be sufficiently emphasized to the public and to clinicians.

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

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

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

Extravaginal testicular torsion is commonly seen in perinatal cases. Hence, the diagnosis is often made late, long after the torsion event has taken place. The tunica vaginalis takes about 6 weeks after birth to adhere to the surrounding tissues, possibly explaining the preponderance of the condition in neonates. Large birth weight, difficult labor, breech presentation, and overreactive cremasteric reflex have been proposed as possible causes for perinatal torsion. [5, 6]

Testicular torsion is classically described as involving a medial rotation; however, in as many as one third of cases, a lateral rotation has been described. [7, 8] When manual detorsion is contemplated, the testis is typically rotated laterally (“opening the book”); however, if the testis is already laterally rotated, this maneuver worsens the condition. For this reason, manual detorsion is not a commonly performed procedure.

A rotational twisting of the spermatic cord is the basis of all torsion events. When the twist is sufficient to obstruct arterial inflow, testicular ischemia results. If the duration of ischemia is long enough, infarction results. Lesser degrees of cord twisting may result in obstruction of venous outflow, causing congestion and swelling of the testis without frank infarction.

Unfortunately, no reliable indicator for risk of torsion has been identified. Numerous factors have been observed in association with torsion, but none can be used to predict torsion risk in a clinical setting. [9]

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

The bell clapper deformity is often noted at the time of exploration in older children and adolescents with testicular torsion. The anomaly is seen in 12% of males in cadaveric studies and is often bilateral, being the reason behind the surgical fixation of the uninvolved testis in a proven case of torsion testis. [10]

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

The cord’s torsional rigidity and other resistances, which tend to limit the angle of rotation, may increase less markedly with growth and development. Thus, normal physical activity may result in angular momentum sufficient to easily overcome the opposing resistances, allowing complete testicular torsion. [5]

Various anatomic abnormalities of the testis are associated with torsion. The most significant of these is cryptorchidism (see the image below). Cryptorchid testes are at significantly higher risk for torsion than scrotal testes are. [11] Other anatomic abnormalities that may predispose to torsion include a horizontal lie of the testes, polyorchidism, [12] and epididymal anomalies. [13]

In some cases, specific physical activities or events (eg, sports, weight training, and trauma) appear to induce an episode of torsion, perhaps by way of a sudden cremasteric reflex. Epidemiologic studies have shown that testicular torsion is more common in winter months and in northern latitudes, prompting speculation that cold-induced cremasteric contraction may play a role in the development of torsion. [14]

In the newborn, the scrotal parietal tunica vaginalis has not yet fully adhered to the outer tissues of the scrotum. Thus, the entire testes, tunica vaginalis, and gubernaculum may twist together within the scrotum, resulting in an extravaginal torsion. This is the most common form of torsion in the perinatal period. (See the image below.) Because the adhesion between the tunica and scrotal tissues is bilaterally deficient, these infants are at risk for bilateral torsion events (either synchronous or metachronous). [5, 15]

Testicular torsion is one of the more common acute pediatric surgical conditions, though few studies have documented the precise incidence. In 1976, a study from the United Kingdom reported the annual incidence of testicular torsion as 1 case per 4000 in males younger than 25 years. [16]

Extravaginal torsion constitutes approximately 5% of all torsions. Of these cases of testicular torsion, 70% occur prenatally and 30% occur postnatally. The peak incidence of intravaginal torsion occurs at age 13-14 years. The left testis is more frequently involved. Bilateral cases account for 2% of all torsions.

Successful salvage of the torsed testis is directly related to the time elapsed from the onset of ischemia. [17] If exploration is performed within 4-6 hours of symptom onset, salvage rates may approach 90%; with delayed intervention, 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 (salvage rate, <5%).<ref>18</ref>

In a survey by Bennett et al, 55% of boys with testicular torsion (age range, 3 months to 16 years) had infarction with testis loss at scrotal exploration. [19] The main reason for the testicular loss was excessive delay before seeking medical attention, which was usually attributed to the patient or his parents. Survey data have suggested that most boys do not think it is necessary to seek medical advice for testicular swelling, and a large minority do not think it is necessary to seek medical advice for testicular swelling with pain. [20]

Overall, the causes for testicular loss can be summed up as follows [2] :

Tryfonas et al reported that the results of testicular atrophy correlated with duration of symptoms and operative findings. [21] In all cases of surgical detorsion where torsion lasted longer than 24 hours and the viability of the testis was questionable, subsequent atrophy occurred.

Reduced fertility is a possible long-term complication of testicular torsion. [22] It may be related to ischemia-reperfusion injury that damages the blood-testis barrier, with resulting antisperm antibody production. A study in the rat model by Ozkan et al found that serum inhibin B levels decrease after unilateral testicular torsion, suggesting contralateral testicular damage. [23] In humans, serum inhibin B levels function as a useful marker of testicular function, in that they reflect Sertoli cell function and spermatogenesis.

A study by Puri et al in 18 men who had undergone testicular torsion 7-23 years previously found the following [24] :

All 18 patients had experienced prolonged unilateral testicular torsion before puberty and had undergone surgical untwisting with replacement of the nonviable testis in the scrotum. Fourteen of the patients had an absent testis on the 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.

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Krishna Kumar Govindarajan, MBBS, MS, MCh, MRCS, DNB Associate Professor and Consultant Pediatric Surgeon, Jawaharlal Institute of Postgraduate Medical Education and Research, India

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

Disclosure: Nothing to disclose.

Caleb P Nelson, MD, MPH Assistant Professor of Surgery (Urology), Department of Urology, Harvard Medical School; 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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Marc Cendron, MD Associate Professor of Surgery, Harvard School of Medicine; Consulting Staff, Department of Urological Surgery, Children’s Hospital Boston

Marc Cendron, MD is a member of the following medical societies: American Academy of Pediatrics, American Urological 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.

Pediatric Testicular Torsion

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