Cryptorhidism Means

Testicular torsion or spermatic cord torsion is the most common genitourinary tract emergency of childhood and probably the second most common surgical emergency in the adolescent age group after acute appendicitis [1-3] . This clinical entity is commonly referred to as "the acute scrotum." Of the diseases that cause an acute scrotum, spermatic cord torsion is undoubtedly the most important. Misdiagnosis and inappropriate treatment lead to male factor infertility. Thus, a child presenting with an acute scrotum is clinically one of the most difficult situation for pediatricians, pediatric surgeons, and pediatric radiologist [3, 4].

Tissue ischemia is a major cause of morbidity and mortality. Cell death following ischemic injury is a clinically important process involved in a number of human diseases, including stroke, heart disease, renal failure, and cancer. The primary pathophysiologic event in testicular torsion is ischemia followed by reperfusion; thus, testicular torsion/detorsion is an ischemia/reperfusion (I/R) injury to the testis. The torsion must be treated promptly to avoid loss of function of ipsilateral and contralateral testis. This syndrome often leads to subfertility or infertility of the ipsilateral (torted) and contralateral (not torted) testis, but the mechanisms of cellular injury remain incompletely understood [5].

Mammalian testes are highly sensitive to oxidative stress and particularly to lipid peroxidation due to their high concentration of polyunsaturated fatty acids in the plasma membrane. The fatty acids are an essential requirement for the male germ cell to maintain sperm functions. Some detrimental factors such as I/R injury in testicular torsion may cause deoxyribonucleic acid (DNA) damage, inhibition of protein synthesis, and corruption of the sperm formation cycle, inducing in abnormal spermatogenesis [6]. On the other hand, unilateral testicular torsion reduces contralateral testicular blood flow, which gradually increases after the detorsion procedure. Ischemic damage leads to breakdown of the blood-testis barrier [7, 8]. I/R injury is also associated with activation of neutrophils, inflammatory cytokines, and adhesion molecules with increased thrombogenicity, release of massive intracellular calcium, and overgeneration of reactive oxygen species (ROS) and reactive nitrogen species (RNS). They damage several cellular components by peroxidation of cell membrane lipids [9,10]. In addition, experimental studies have suggested that unilateral testicu-lar torsion results in increase in lipid peroxidation products in the contralateral untwisted testis. Several studies have shown that applying substances to prevent the formation of oxygen free radicals or scavenging them before testicular detorsion significantly reduces damage in the ipsilateral and/or contralateral testis [11-14],

Testicular damage after testicular torsion is related to the duration of ischemia and to the severity of the torsion [1, 3, 15, 16]. Early diagnosis and definitive management are important to avoid testicular loss [17]. Anamnesis, physical examination, scrotal Doppler ultrasonography, and testicular scintigraphy are the main diagnostic methods. The diagnosis is particularly clinical and the management is emergency surgical untwisting and bilateral fixation.

To date, a number of chemicals, drugs, and physical methods such as intratesticu-lar testosterone, melatonin, carnitine, ibuprofen, rosiglitazon, immunosuppression with cyclosporine and prednisone, pentoxifylline, vasoactive intestinal polypeptide (VIP), zinc aspartate, biocompatible surfactant (tetronic 1107), hyperbaric oxygen therapy, and chemical sympathectomy have been used to prevent I/R injury in testicular torsion and detorsion. They were found to be effective in preventing testicular damage, but none have been implemented in clinical practice. In addition, none have been tested in clinical trials and they cannot be applied in patients because of severe adverse effects [18, 19], apart from cooling the scrotum [20, 21] . It is very crucial that long-term effects of testicular torsion and its treatment should be observed in adulthood in terms of reduced fertility and impairment of spermatogenesis.

17.2 Testicular Torsion 17.2.1 Definition

Torsion of the testis was first described by Delasiauve [22]. The condition was first reported in the newborn in 1897 by Taylor [ 23 ] . In 1893, Nash first described manipulative detorsion of the testis in 1893 [24] . Testicular torsion is a medical urologic syndrome mainly caused by torsion of the spermatic cord that constitutes a surgical emergence.

17.2.2 Incidence

The annual incidence of testicular torsion is between one in 4,000 males and one in 158 males younger than 25 years [25, 26].

17.2.3 Laterality

Torsion is usually unilateral. Bilateral torsion occurs with only 2% of the patients and is an extremely tragic condition especially in neonates [27]. For instance, Bagci et al. recently reported the case of a patient with bilateral perinatal testicular torsion [28]. The left side is more commonly affected [1].

17.2.4 Age

Testicular torsion can occur at any age, but there are two peaks in incidence, the largest around puberty (accounting for 65% of all torsions) with another much smaller peak in the first year of life [1, 29]. Testicular torsion can also be present in adult man, the oldest age at which torsion has been reported is 69 years [30], but testicular torsion is rare in the adults [31, 32].

17.2.5 Etiology

The risk factors for acute testicular torsion are poorly understood. Torsion usually occurs in the absence of any precipitating event [16]. Environmental factors have been implicated by some authors and discredited by others. Srinivasan et al. [33] speculated that an increased incidence of testicular torsion is seen with decreasing atmospheric temperature humidity. Some reports demonstrated that no statistically significant differences were seen with regard to the seasonal or monthly occurrence of testicular torsion [34-36]. However, there is a cold weather seasonal trend for the torsion [37], and higher incidence rates of torsion have been reported during the colder months, especially December [36]. It has been reported that 40 of 46 cases of testicular torsion occurred when the ambient temperature was less than 2°C (35.6°F) and the torsion occurred from a cold-induced contraction of the cremasteric muscles [38, 39],

The child's age is the first clue to the etiology of the testicular torsion, since spermatic cord torsion is more common in adolescents and newborns, whereas torsion of the appendix testes/epididymis more commonly presents in prepubertal boys [40]. Marulaiah et al. [41] analyzed retrospectively the pathology results of all testicular and paratesticular 502 specimens (474 patients) between August 1995 to September 2007, and testicular torsion was found in 11.2%, with bimodal peak ages of <1 year and 13-14 years; the mean age was 9.4 years. Interestingly, it occurred more on the left side testis. Similar results are reported in other studies [42, 43]. Other predisposing factors are an increase in testicular volume (often associated with puberty), testicular trauma, tumor, testicles with horizontal lie, a history of cryptorhidism, and a spermatic cord with a long intrascrotal portion [16].

Familiar testicular torsion has been infrequently reported in the literature. Only a few cases have been reported so far. Shteynshlyuger and Freyle [44] have identified 11 families with familial testicular torsion, with 30 probands and 37 testicular torsions among them. They reported the largest number of first-degree relatives affected by testicular torsion in three consecutive generations of one family. Okeke and Ikuerowo [45] reported a familial series of a man and his three children all suffering from left testicular torsion. Family history in first-degree relatives may be helpful in the evaluation of a patient with testicular torsion. There is a strong predisposition in familial testicular torsion history.

Based on anatomy and age, testicular torsion is divided into two types: extravaginal and intravaginal torsion.

17.2.6.1 Intravaginal Torsion

This is the most common type of testicular torsion. Normally, tunica vaginalis invests the epididymis and posterior surface of the testicle, which fixes it to the scrotum and prevents it from twisting. If the tunica vaginalis attaches in a more proximal position on the spermatic cord, the testicle and epididymis hang free in the scrotum and can twist around the longitudinal axis of the spermatic cord within the tunica vaginalis. The testis usually undergoes torsion on the last few centimeters of the spermatic cord. The predisposing anatomical factors are the spiral arrangement and low insertion of the fibers of the cremasteric muscle, the tunica vaginalis, which extends proximally around the spermatic cord (the bell-clapper deformity), and the abnormality of the junction of the epididymis with the testis, forming a mesor-chium. Bell-clapper deformity is the most common type, found 12% in cadaveric studies and often bilateral. The intravaginal spermatic cord may rotate and cause infarction of the testis and epididymis in the bell-clapper deformity.

Intravaginal testicular torsion is commonly seen in adolescents and older males; the peak incidence is 13 years and the left testis is more frequently involved. This type commonly occurs during sleep. It is possibly the result of a strong cremasteric reflex and spasm associated with nocturnal erections [1, 54]. The other initiating forces may be trauma, cold weather, or vigorous exercise such as cycling, ice-skating, swimming, parachuting, football, and rugby. Hormonal causes, rapid growth, and the increase of the size and vascularity of the testis during puberty may also be precursors to intravaginal torsion. Furthermore, testicular torsion is ten times more likely in undescended testes [1, 16, 29, 36].

17.2.6.2 Extravaginal Torsion

This type of testicular torsion includes approximately 5% of all torsions. Up to 20% of cases are synchronous, and 3% are asynchronous bilateral. Extravaginal torsion is usually seen in the prenatal or postnatal (neonatal) period. Prenatal torsion usually occurs in utero around 32 weeks and is present at birth. The pathogenesis is unknown and there isn't generally any anatomic defect. The other is postnatal testicular torsion occurring within the first 30 days of life. High birth weight and trauma during difficult delivery or breech presentation are important for torsion. The difference is important since the postnatal torsion requires emergent exploration and treatment with detorsion and fixation.

17.2.7 Pathogenesis

Torsion results from twisting of the spermatic cord, which causes ischemic changes depending on the degree and duration of twisting. Torsional twisting usually occurs away from the midline, probably secondary to the direction of the cremasteric muscle fibers. The degree of the torsion varies from 180° to more than 1,440°. This variation in torsion contributes to the variant presentations of acute torsion from severe to subacute and chronic torsion. Torsion blocks both arterial supply and venous drainage. This contributes to edema, congestion, swelling, hemorrhage, ecchymosis, and cellulitis. The edema further results in altered blood flow dynamics to the testis and accentuates arterial blockage, hypoxia, degeneration, infarction, necrosis, apoptosis, and gangrene of the testis [1, 15, 55, 56]. Ischemia may cause ultrastructural changes in the contralateral testis [13] and induce antitesticular or antisperm antibody production [57-60].

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