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Spermatic cord torsion happens rather frequently in young men. It must be discovered early on, to allow for the possibility of removal by surgery. It appears from recently written medical articles that the endocrine function of the testis is protected following several hours of torsion and the risk of immunological damage to the contralateral testis is subsequently reduced.
Experimental unilateral spermatic cord torsion has been shown to induce both ipsilateral and contralateral intratesticular biochemical changes indicative of hypoxia. An experimental study was conducted to see whether the presence of the ipsilateral testicular tissue is necessary for the occurrence of the biochemical changes in the contralateral testis. Male, adult, albino rats were divided into four groups each containing 10 rats. One group served to determine basal values of biochemical parameters indicative of tissue hypoxia, another group was subjected to unilateral spermatic cord torsion in the presence of ipsilateral testis; a further group was subjected to unilateral spermatic cord torsion after ipsilateral subepididymal orchiectomy, and the last group underwent unilateral subepididymal orchiectomy alone as control. Lactic acid, hypoxanthine and lipid peroxidation product levels which are biochemical indicators of tissue hypoxia were determined in testicular tissues and kidneys. All three parameters increased significantly in contralateral testes but not in kidneys after unilateral spermatic cord torsion both when the ipsilateral testis was present and absent (p < 0.05). It is concluded that the ipsilateral testis does not play a role in transmitting these contralateral changes after unilateral spermatic cord torsion. Impulse-triggering contralateral changes may arise from spermatic vessels or nerves.
Presentation of the finding of the echographic image of a torsion knot as a pathognomonic sign of spermatic cord torsion. Discussion of this finding as well as aspects related to imaging diagnosis of cord's torsion.
OBJECTIVE: To distinguish spermatic cord torsion from acute orchitis by color Doppler flow imaging (CDFI). METHODS: Thirteen patients with acute orchialgia were examined by CDFI. The clinical data of diagnosis and treatment were reviewed and analyzed. RESULTS: The findings of CDFI showed lower or even no blood flow in the testes in 8 cases, which were diagnosed as spermatic cord torsion. Among them, 1 received manual detorsion and 7 were proved by operations. The other 5 showed abundant blood flow signal in the testes and were diagnosed as acute orchitis or epididymo-orchitis. After the use of antibiotics, their symptoms were relieved and the blood flow of the testes reduced upon reexamination. CONCLUSIONS: CDFI plays an important role in the diagnosis and differential diagnosis of spermatic cord torsion, and could be regarded as a detecting method of first choice for patients of acute orchialgia.
Although deteriorating effects of unilateral spermatic cord torsion are generally accepted, the mechanism remains controversial. An experimental study was performed to evaluate the necessity of testicular and spermatogenetic material for contralateral testicular deterioration following unilateral spermatic cord torsion in rats. The animals were allocated to four groups: control, spermatic cord torsion, subepididymal orchiectomy, and spermatic cord torsion 14 days after subepididymal orchiectomy. The testes were removed on the 14th days and mean seminiferous tubular diameters and mean testicular biopsy scores were determined. Although contralateral testicular deterioration was more pronounced in the presence of testicular tissue, the absence of testicular tissue and/or spermatogenetic material did not prevent its occurrence. This is highly suggestive that autoimmune mechanism does not play a role in contralateral testicular damage following unilateral spermatic cord torsion.
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Torsion of the spermatic cord is not uncommon among young men. Various abnormalities in the histology of the contralateral testis have been reported due to unilateral torsion of the spermatic cord. We quantitatively estimated the germ cells from three groups of men: normal individual (Group I), men with unilateral torsion of short duration (Group II), and men with unilateral torsion of long duration or some other condition such as varicocele or intermittent torsion to the contralateral testis (Group III). No significant difference in the number of spermatogonia, spermatocytes, and spermatids of Groups I and II patients was observed. This observation indicates that there was no pre-existing morphophysiologic defect in the testis of Group II patients. Severe damage in the contralateral testis was noted in Group III patients. This indicates that if a damaged testis is retained in the body for a long time, the contralateral testis may be affected. Contralateral testis may also be affected by intermittent torsion or varicocele.
To distinguish spermatic cord torsion from other intrascrotal pathology, scrotal ultrasound and radionuclide scanning have been highly recommended on the basis of both clinical and experimental studies. We review the data from six patients in whom ultrasound or nuclear medicine examination was misleading. We emphasize that history, physical examination, and urinalysis remain the cornerstones of the diagnosis of spermatic cord torsion. Scrotal ultrasound and nuclear medicine scans are useful adjuncts and are reassuring when in agreement with the clinical picture. However, they are not 100% sensitive or specific, and a negative study should not prevent emergency operative exploration of a clinically suspicious lesion.
Unilateral spermatic cord torsion has been shown to cause damage to the contralateral testis in humans and animal models. In an attempt to explain conflicts among various laboratories concerning the extent of this contralateral effect and to determine the importance of the extent of torsion, prepubertal rats (35 to 40 days) were subjected to unilateral spermatic cord torsion of various degrees (zero to 1440 degrees). Sham surgeries were performed and served as controls (0 degrees of torsion). The animals were allowed to recover from the surgeries and to attain puberty before a period of fertility testing. Fertility, fecundity, organ weight and testicular histological data were obtained after the breeding period. Our data indicate that animals undergoing 360 degrees of torsion exhibited no changes in the parameters studied. However, if 720 degrees, 1080 degrees or 1440 degrees of torsion was induced, a significantly lower percentage of fertile males and pregnant females resulted for each of these experimental groups when compared to those values for the 0 degrees controls. These data indicate that the extent of contralateral testicular degeneration is dependent upon the degree of spermatic cord torsion to which the ipsilateral testis is subjected. The induction of unilateral spermatic cord torsion at 720 degrees or more causes a significant reduction of subsequent fertility while torsion of a lesser degree has little or no effect in the development of this phenomenon.
We studied 25 patients with spermatic cord torsion occurring after puberty. The elapsed time between the onset of symptoms and observation varied from 6 months to 7 years. We evaluated the semen of these patients and found that the number of spermatozoa was lower in patients with an atrophic testis (13 patients) than in those with a normal testis or, in those with torsion treated by orchidectomy. Moreover, the number of spermatozoa was lower in patients who had torsion for more than 2 years before being checked (12 patients) than in patients who had a more recent torsion (13 patients). Agglutinating antibodies were present in 20% of the patients but, they are not correlated fertility or sterility. Immunofluorescent antibodies also were not correlated with the changes found by semen analysis. They are not present in patients with a normal testis at the time of observation. On the other hand, immobilizing antibodies were significantly correlated with sterility and, particularly with changes of motility. These data suggest that sterility after spermatic cord torsion is correlated with an autoimmune mechanism. It may occur particularly in those patients with atrophic testes and has a slow onset taking more than 2 years to evolve completely.
Infertility is frequent in patients after spermatic cord torsion usually when the twisted testis is not removed and becomes atrophic. The mechanism seems to be autoimmune. To see if the atrophic testis may be the source of antigens we carefully examined the histology of atrophic testis of 6 patients. The two patients that had spermatic cord torsion more than 3 years before surgical removal did not show recognizable testicular structures while the other patients that had spermatic cord torsion less than 1 year still showed some spermatogonia in the tubules and some spermatozoa in the epididymis. We think that the surgical removal of the atrophic testis after more than 1 year from the acute episode is of doubtful utility for preventing or blocking the autoimmune phenomenon because testicular antigens are absent and the autoimmune mechanism is able to maintain itself.
Torsion of the spermatic cord constitutes a surgical emergency. Morphologically and functionally, the fate of the compromised testis largely depends on the time elapsed between the acute episode and surgical intervention. Patients who had been treated for testicular torsion by our group from 1976 to 1989 were requested to return for outpatient evaluation. These patient were divided into two groups according to the time elapsed between the diagnosis and surgical intervention. We observed that surgical correction within 12 hours following presentation permitted testicular salvage. Testicular volume was generally preserved and remained normal or slightly diminished. However, when the time elapsed was over 12 hours, testicular atrophy was observed in 46% of the patients. We can conclude, therefore, that detorsion must be performed as soon as possible. Vaginalis testis eversion will generally achieve stable and lasting fixation.
Semen quality and endocrine parameters after spermatic cord torsion were investigated. Of 24 patients evaluated following spermatic cord torsion 12 were treated with bilateral orchiopexy (orchiopexy group), and 12 were treated with ipsilateral orchiectomy and contralateral orchiopexy (orchiectomy group). The average sperm density and the average total sperm count in the orchiectomy group were significantly lower than those in the orchiopexy group (p < 0.05, p < 0.05, respectively). The mean serum follicle stimulating hormone level in the orchiectomy group was significantly higher than that in the orchiopexy group (p < 0.05). These findings suggest a significant decrease in testicular function in the orchiectomy group. All the patients in the orchiopexy group demonstrated a normal semen quality and endocrine parameters during followup. Four of the 8 patients in the orchiectomy group whose duration of followup was more than two years still demonstrated oligozoospermia (< 20 x 10(6)/ml, one of 4 was azoospermia). The average age at operation of these four patients with abnormal semen quality was significantly higher than that of the other 4 patients with normal semen quality (p < 0.05), whereas no significant difference in duration of torsion preceding surgical therapy was observed between these two groups. These findings suggest that subsequent semen quality is likely to remain within normal limits with early surgical treatment by bilateral orchiopexy. Ipsilateral orchiectomy in the younger generation seems to result in less damage of the contralateral testis than in the older generation.
Prepubertal rats were exposed to unilateral spermatic cord torsion for 0, 1, 3, 5, 9 or 12 hours duration. At the end of this time the damaged testes were either removed or untwisted and pexed into place. The animals were then allowed to mature to 77 days of age at which time the contralateral testes were examined for 12 histological parameters and scored according to the degree of pathology noted in each. Pathological changes in the contralateral testes were found to be dependent on the duration of spermatic cord torsion but were less severe in the orchiectomized group. Thus, removal of the damaged organ minimized the long-term damage to the contralateral testes. We also noted that specific histological parameters of the contralateral testes correlated well with fertility and that specific changes in the ipsilateral testes predicted contralateral pathology.
Delay in the diagnosis of spermatic cord torsion (SCT) is still a significant cause of testicular loss in children. The aim of this experimental study was to assess the diagnostic value of serum creatine kinase (CK) in the early period following SCT. Forty male rats were assigned randomly into five similar groups: group A, control; group B, sham, right testis exposed, manipulated, and blood sampling at 6th h; group C, right SCT, blood sampling at 2nd h; group D, right SCT, blood sampling at 4th h; and group E, right SCT, blood sampling at 6th h. Ck and its isoenzymes were measured in the sera of all animals. All testes were removed and examined histopathologically. Significant increases in serum CK levels compared to control and sham groups were observed at 4 and 6 h following SCT. The major increase in CK was observed in the CK-MM isoenzyme fraction. Histologic pictures showed varying degrees of edema, vascular congestion, and hemorrhage in the testicular tissue, but no necrosis in any of the study groups. These results showed that serum CK levels in rats in the early period following SCT increase significantly before necrosis of testicular tissue. This may be of value as a diagnostic test, to corroborate findings from clinical studies.
Sixty prepubertal rats were subjected to unilateral spermatic cord torsion for a duration of 0, 1, 3, 5, 9 or 12 hours. At the end of this period, the ipsilateral testes either were removed for immediate processing or subjected to detorsion and orchiopexy, followed by a six-week recovery period prior to histologic study. Twelve histologic parameters were each scored according to the degree of pathologic findings, thus allowing for a quantitative assessment of testicular damage. The sequence of specific histologic degeneration that occurred with spermatic cord torsion is described. These changes were found to be dependent on the duration of torsion, with the greatest damage occurring after three hours or more. In the animals undergoing detorsion followed by a six-week recovery period, severe degeneration was noted for all durations of torsion studied. The extent of this degeneration was significantly correlated with a reduction in fertility.
Unilateral spermatic cord torsion causes damage to the contralateral testis in humans and animals models. It is now known, however, at what age an animal's reproductive capacity is most susceptible to this type of trauma. To determine if the animal's age is a factor in its susceptibility to reproductive damage, rats at 30 to 70 days of age were subjected to unilateral spermatic cord torsion. Rats of the same ages underwent sham surgery and served as controls. The animals were allowed to recover from the surgery and to attain puberty before a period of fertility testing. Fertility, serum testosterone, organ weight, and testicular histologic data were obtained after the breeding period. Our data indicate that animals undergoing torsion at the youngest (30 days) and oldest (70 days) ages exhibited no change in the parameters studied. Animals between the ages of 35 and 50 days are highly susceptible to reproductive damage due to unilateral spermatic cord torsion, and the 35-day-old animals exhibit the most susceptibility. The stages of testicular development occurring during this period are such that damage to one testicle will result in degeneration of both organs. However, once the animal is older than 50 days, its reproductive capacity is not affected by spermatic cord torsion. The specific period of susceptibility in the development of human testes is yet to be defined.
Three cases of spermatic cord torsion in neonates are presented. Support is given to the nonoperative management of both the unaffected contralateral testis and late presentation cases.