Testicular hemorrhage, necrosis, and vasculopathy: likely manifestations of intermittent torsion that clinically mimic a neoplasm.
Academic Article
Overview
abstract
We report 30 cases of testicular hemorrhage and/or necrosis with associated vascular damage that caused clinical concern for a neoplasm and that raised the question of a vasculitis syndrome on pathologic examination. The patients were 12 to 66 years old (median, 33 y) and presented with pain (n=15), mass (n=12), or both (n=2); 1 case had no available clinical information. Ultrasonographic interpretations included a neoplasm in the differential diagnoses in 14 of 18 cases in which this information was available, and most (n=24) had orchiectomy because of this possibility. Only 4 were clinically suspected to represent testicular infarction. Circumscribed, hemorrhagic lesions occurred in 10 cases, less demarcated hemorrhagic foci in 5, and discrete nodules or ill-defined foci of varying color and consistency in the remainder. No clear testicular lesion was described in 2, with 1 of these having a "dusky" appearance. On microscopic examination all but 1 case showed damaged blood vessels (vasculopathy), with either associated hemorrhage/hematoma (n=24) and/or areas of parenchymal necrosis (n=21). One case showed only segmental tubular atrophy with interstitial inflammation and vasculopathy; no infarct or hemorrhage was identified. A variety of vascular changes was identified, including prominent intimal thickening in arteries (n=22) and fibrinoid change in both arteries (n=5) and vessels of indeterminate type (n=8). Medial fibrosis was present in veins (n=12) and vessels of indeterminate type (n=4), whereas thrombi (remote, recanalized, and/or recent) occurred in arteries (n =7), veins (n=9), and vessels of indeterminate type (n=11). Dilated, blood-filled vessels were present in the testis and/or paratestis in 15 cases. In addition, 7 cases showed arteriolar hyalinization, and 19 had inflammation of blood vessels. The latter was lymphohistiocytic and mostly light but occasionally prominent (n=5). Interstitial inflammation was seen adjacent to damaged testicular parenchyma in all 30 cases. Clinical follow-up in 20 patients (4 to 131 mo, mean 38 mo) showed no evidence of recurrence in the contralateral testis or later development of systemic vasculitis. The histologic findings were compared with those in 11 orchiectomies resected for clinical acute torsion. All clinical acute torsion cases showed both parenchymal and fibrinoid vascular necrosis, and 10 had hemorrhage/hematoma; they lacked vasculitis, interstitial inflammation, and chronic vascular changes. Testicular vasculopathy, characterized by acute and chronic vascular injury, commonly occurs in testes with parenchymal hemorrhage and necrosis that clinically mimic a tumor. It shares the acute features of recent torsion but also has findings indicative of chronic injury. Testicular vasculopathy is most likely a result of chronic intermittent torsion that leads to localized hemorrhage/necrosis and should be distinguished from cases of systemic vasculitis given the significantly different clinical implications.
