SEARCH

SEARCH BY CITATION

Keywords:

  • spermatic cord;
  • spermatogenesis;
  • testicular function;
  • testis;
  • torsion

INTRODUCTION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Torsion of the spermatic cord is a surgical emergency, as ischaemic injury of > 4 h seriously threatens the continued viability of the ipsilateral testis. However, the function of the contralateral testis may also be damaged by unilateral torsion. In this review we focus on the prognosis for testicular function after torsion, and the possible mechanisms responsible for testicular damage.

TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Experimental studies in dogs show the elimination of all spermatogenic and Sertoli cells by 6 h of testicular ischaemia, and the elimination of Leydig cells by 10 h of ischaemia [1]. When the duration of torsion is > 4 h some degree of testicular atrophy is almost inevitable. Infarction is possible as early as 4 h if the cord has twisted through several revolutions. Beyond 10 h of torsion most patients will have significant atrophy, unless spontaneous reduction had occurred or the torsion was limited to 180–360°[2]. With torsion of > 360° lasting > 24 h all patients will have complete or severe atrophy [3]. However, several reports have appeared of testes salvaged after 3–5 days of torsion. The salvage rates in undescended testes undergoing torsion are poorer than in descended testes, with an orchidectomy rate of 60–71%[4].

The two most important factors determining testicular damage are the time from the onset of symptoms to the reduction of torsion, and the degree of twisting in the cord. Manual detorsion is successful in > 80% of attempts, usually when the duration was < 12 h, and in such cases > 90% of the testes are salvaged [5].

Urgent surgical exploration is mandatory in all cases of testicular torsion of < 24 h duration, in those with symptoms lasting up to 48 h but with no induration, when torsion may have been incomplete or intermittent, and when the diagnosis is in doubt. In those with a history of continuous pain for > 24 h, semi-elective exploration is necessary with a view to contralateral orchidopexy [6,7].

We calculated the early salvage rate (testis viable at exploration) and late atrophy rate in two meta-analyses of 1140 patients in 22 series and 535 patients in eight series, respectively (Fig. 1). In one report the immediate orchidectomy rate before 1960 was 80%, from 1960 to 1984 it was 38%, and in the later part of this period (1980–84) testicular loss was 33%[4]. To salvage the testis three factors are needed: prompt presentation, prompt diagnosis and referral, and immediate surgery. According to one study the cause of testicular loss is a delay in seeking medical attention in 58% of cases, a wrong initial diagnosis by the GP in 29%, and delayed treatment at the referral hospital in 13%[8]. Earlier diagnosis and treatment can be achieved by educating medical students and physicians, but earlier presentation also requires educating the general population.

image

Figure 1. Immediate (early) surgical salvage after torsion (a) and subsequent atrophy (b) of surgically salvaged testes after torsion of various time intervals.

Download figure to PowerPoint

TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Prenatal torsion probably occurs at ≈ 32 weeks of gestation, is almost exclusively extravaginal and presents at birth with a hard, swollen, non-tender testis. Postnatal torsion presents within the first 30 days of life, with symptomatic scrotal swelling and a documented normal scrotum at birth. Of the reported neonatal cases, 60% required orchidectomy and 34% of testes were left in place, while only 5% of all cases were not atrophied at follow-up. Despite an aggressive surgical approach in neonatal torsion, the long-term salvage rates are none and 7% in the two largest reported series [9,10].

EFFECT ON TESTICULAR FUNCTION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Unilateral testicular torsion seriously interferes with subsequent spermiogenesis in about half the patients and produces borderline impairment in another 20%[11]. Subfertility (sperm count < 20 million/mL) is found in 36–39% of patients after torsion [2,12]. In a long-term follow-up the semen analysis may be normal in only 5–50%[12,13]. The sperm count and the degree of atrophy both correlate closely with the duration of torsion [2]. Patients who have atrophy or who have undergone orchidectomy have a significantly lower sperm count than those without atrophy [14]. There is controversy as to whether prepubertal testes are more resistant to the effects of torsion.

Contralateral testicular biopsies are abnormal in 57–88% of cases at the time of torsion, and therefore some abnormalities must be present before the onset of torsion [11,15]. Abnormalities noted in the contralateral testis include extensive apoptosis in the germinal epithelium, atrophic Leydig cells, malformation of the late spermatids, fewer late spermatids, and pathological changes in Sertoli cells. Trauma to the blood–testis barrier initiated by torsion may induce the release of apoptotic-activating factors (cytokines) which damage the contralateral germinal epithelium [16]. Some studies suggest that leaving a nonviable or severely damaged testis in situ instead of removing it causes more damage to the contralateral testis [13].

Sperm antibodies occur in 0–11% of patients at the time of torsion or at a later follow-up [15,17]. Although torsion is a common event, it is not a significant contributor to adult male infertility, because < 1% of males with infertility have a history of torsion [18]. Hormonal function is relatively well preserved, with elevated levels of LH and FSH only in patients with torsion of > 8 h or testicular atrophy [14].

There may be a 3.2-fold increased risk of developing a testis tumour 6–13 years after torsion. However, two of nine reported cases had torsion of a tumour-bearing testis and four had tumour contralateral to the torsion, indicating that torsion is unlikely to be important in the cause of the tumour [19].

MECHANISM OF INJURY

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

The injury to the affected testis is caused by a combination of ischaemia and reperfusion injury by reactive oxygen species, which arise from the activation of the xanthine oxidase system in parenchymal cells or from leukocytes that adhere to the re-perfusing venule walls before undergoing diapedesis into the interstitial tissue.

The contralateral testis also deteriorates if an ipsilateral testis is damaged for various reasons, including torsion, incarcerated inguinal hernia, undescended testis, varicocele, vas deferens obstruction and tumour. There are several theories to explain bilateral exocrine failure after unilateral torsion, including an immunological mechanism, previous episodes of silent intermittent torsion, congenital dysplasia, and reflex vasoconstriction.

IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

The testis is an immunologically privileged site and ischaemic damage may lead to breakdown of the blood–testis barrier. Antigenic material from the dying testis would be exposed to the immune system, and the resultant auto-antibodies may then attack the unaffected testis. A wealth of experimental data supports this theory, but direct evidence in man is lacking.

In rats, experimentally induced torsion of 720° causes damage to the contralateral testis. Detorsion after 24 h offers no protection, but both orchidectomy after 24 h and treating the animals with perioperative antilymphocyte globulin and splenectomy on day 3 prevents contralateral testicular damage. This indicates that contralateral damage is mediated by immunological events, because immunosuppression and removal of the antigenic stimulus provide protection [20]. Ischaemic rat testes release into the bloodstream a heat-soluble factor that is cytotoxic to spermatozoa, and contralateral testicular damage can be prevented by splenectomy and by administering immunosuppressants such as steroids, azathioprine or cyclosporin [21].

Agglutinating antitestis antibodies have been found in 20% of patients after torsion, but they were not correlated with infertility, and neither were immunofluorescent antibodies. However, immobilising antibodies were significantly correlated with infertility [22]. Anti-testis auto-antibodies may be present in 13% of patients, but there appears to be no correlation with exocrine or endocrine dysfunction [23]. However, some studies found little evidence of antisperm or antitestis antibody formation after unilateral testicular torsion [11].

INTERMITTENT SILENT TORSION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Oligospermia after unilateral testicular torsion may be a result of an underlying defect in both testes. Biopsies of the contralateral testis, taken at the time of exploration for torsion, show evidence of pathology in 57–88% of cases, consisting of maturation arrest, germ cell degeneration, tubular hyalinization, immature tubules and focal thickening of basement membranes. These abnormalities are present in patients with torsion of < 24 h, suggesting that they are pre-existing rather than a result of the acute torsion. The changes in both testes may result from episodes of asymptomatic intermittent torsion [11,15].

CONGENITAL DYSPLASIA

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Pre-existing congenital testicular dysplasia may also explain the disturbance of spermiogenesis in the contralateral testis. The anatomical abnormality predisposing to torsion may be associated with defective spermiogenesis, such as is also found in unilateral cryptorchids, who are often infertile, often have histological abnormalities in the normally descended testis, and may have up to a 10-fold increased risk of torsion [24].

However, there is a clear correlation between the duration of torsion and total sperm count, and this is not explained by the theory of pre-existing dysplasia, unless the damage is compounded by another mechanism [2].

Surgical exploration and fixation is unlikely to be responsible for the damage to the contralateral testis. In experimental studies orchidopexy alone does not impair spermiogenesis [20]. In humans, histopathological damage is already present at exploration, and seminal abnormalities occur in patients with and with no contralateral fixation [12].

REFLEX VASOCONSTRICTION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

The most recent theory suggests that the spermatic cord under distress induces sympathetically mediated reflex vasoconstriction of the contralateral spermatic vessels, with resultant ischaemic damage. In rabbits, experimental torsion caused an immediate and progressive decrease in contralateral testicular blood flow, with a gradual increase after detorsion [25]. In rats there is a significant increase in indicators of tissue ischaemia in both the twisted testis and the contralateral untwisted testis, indicating that there is a decrease in perfusion of the contralateral testis. After 2 h of experimental torsion in the rat, blood flow in the ipsilateral spermatic artery decreased by 73%, and in the contralateral artery by 43%. A significant increase in the amplitude of vasomotion in the contralateral testicular microcirculation may be an attempt at compensation by reducing the vascular resistance. The hypoxia resulting from decreased blood flow may cause the contralateral testicular damage [26].

In domestic piglets there was a bilateral decrease in spermatic blood flow after unilateral torsion, and after detorsion there was a bilateral increase in blood flow. Contralateral testicular damage occurred only in the group that was untwisted, suggesting that damage is caused by the increased perfusion after detorsion and not by the initially decreased blood flow [27].

As contralateral testicular hypoxia is caused by torsion of the spermatic cord only, the testis and epididymis do not seem to be necessary for this, and the testicular artery under distress appears to be the important structure, resulting in contralateral testicular hypoxia [28]. Contralateral testicular injury after unilateral torsion is most probably caused by pre-existing damage combined with hypoxia resulting from sympathetic reflex-mediated vasospasm.

LIMITING TESTICULAR DAMAGE

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

Many experimental treatments to prevent or decrease bilateral testicular damage after torsion have been studied, with varying success. These experiments include cooling the testis, limiting reperfusion injury, suppressing immune-mediated damage, and chemical sympathectomy to prevent contralateral vasoconstriction.

In animal experiments external cooling delays the effect of ischaemia for a few hours. Treatments aimed at decreasing reperfusion injury include verapamil, surfactant, allopurinol, platelet-activating factor inhibitors and hyperbaric oxygen. Immunosuppression has been used in the form of dexamethasone, hydrocortisone, cyclosporin and azathioprine [21].

Chemical sympathectomy probably works by inhibiting the afferent impulses from the ipsilateral testis under stress, thus preventing contralateral vasospasm and hypoxia. Drugs used for this purpose include capsaicin, 6-hydroxy dopamine hydrobromide, guanethidine monosulphate and nitric oxide. However, apart from cooling the scrotum, none of these methods has thus far been implemented in humans.

CONCLUSION

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES

The two most important factors determining testicular salvage after torsion are the duration and the degree of testicular rotation. Saving the ipsilateral testis requires prompt presentation by the patient, prompt diagnosis and immediate surgery. Earlier diagnosis and treatment can be achieved by educating medical students and physicians, whereas improving earlier presentation requires educating the general population. Contralateral testicular damage, although well documented, is perhaps not regarded seriously enough as yet, and experimentally tested methods of prevention still await clinical application.

REFERENCES

  1. Top of page
  2. INTRODUCTION
  3. TESTICULAR SALVAGE AFTER INTRAVAGINAL TORSION
  4. TESTICULAR SALVAGE AFTER EXTRAVAGINAL TORSION
  5. EFFECT ON TESTICULAR FUNCTION
  6. MECHANISM OF INJURY
  7. IMMUNOLOGICAL/SYMPATHETIC ORCHIDOPATHY
  8. INTERMITTENT SILENT TORSION
  9. CONGENITAL DYSPLASIA
  10. REFLEX VASOCONSTRICTION
  11. LIMITING TESTICULAR DAMAGE
  12. CONCLUSION
  13. REFERENCES