Prompt recognition of BCG epididymitis, along with the early institution of appropriate antituberculous therapy, may abort the progression to end-stage tissue destruction and abscess formation. Because the interval between treatment with BCG and the onset of related sequelae can sometimes be quite long, the physician may understandably be slow to recognize the causal relationship. Indeed, latent BCG epididymitis has been mistaken for testis tumor, with consequent radical orchiectomy.
Our experience suggests that patients who have undergone resection of the prostate (whether transurethrally or by a simple open prostatectomy) may be at higher risk for this complication, because resection of the ejaculatory ducts might allow reflux of BCG-containing urine into the vasa. Theoretically, by evacuating the instilled BCG solution via catheter rather than by voiding, one might reduce this risk. On the other hand, there may be a therapeutic advantage to emptying the bladder by voiding, in that the BCG-containing urine, by washing through the urethra, may reduce the risk of transitional cell cancer migrating into the urethra. Moreover, one might well question whether subjecting every BCG-treatment patient who has undergone prostate resection to double catheterizations is justified to achieve an unproven advantage in reducing the risk of subsequent epididymitis, which is already less than 1 in 500.
The finding of an epididymal inflammation or mass in any man who has previously undergone BCG instillation therapy (and especially if he had undergone prostatic resection before those instillations) should trigger suspicion for the possibility of a BCG tuberculous cause. A heightened index of suspicion, which leads to timely diagnosis and prompt initiation of appropriate antituberculous therapy, is of key importance.