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.
