In October 2007, an 82 year-old male presented for investigation of painless macroscopic hematuria on a background of BPH and emphysema. Initial investigations included urine cytology, urine culture, TRUS and CT of the abdomen and pelvis. Laboratory investigations were unremarkable, while imaging results demonstrated an enlarged prostate measuring 130 cc. Diagnostic cystoscopy conducted in the same month demonstrated a lesion on the right bladder wall that was resected. Histology showed a high-grade papillary bladder cancer. His repeat cystoscopy 6 weeks later was clear.
On surveillance cystoscopy 6 months later, an area of erythema suggestive of carcinoma-in-situ (CIS) near the right ureteric orifice was noted and resected; this was confirmed on histology. Given his tumor profile, the patient was commenced on a 6-weeks course of induction BCG therapy in March 2008. The patient completed six rounds of induction intravesical BCG therapy that was well tolerated. No maintenance therapy was given.
The patient underwent TURP in July 2008, following an episode of urinary retention in conjunction with a history of obstructive voiding symptoms. At the time of the TURP, the bladder looked macroscopically normal with a good capacity and no sign of contractions. The histology of the prostate specimen showed nodular hyperplasia of the prostate in addition to granulomatous inflammation indicative of the BCG effect. Serial surveillance cystoscopies and urine cytology were clear.
By late 2010, almost 3 years following BCG therapy, the patient began experiencing issues with nocturnal frequency and incontinence. Urine cultures taken were positive for mycobacteria. A repeat cystoscopy showed marked inflammatory changes within the bladder, with associated thickened bladder mucosa; biopsies taken at the time confirmed BCG cystitis. The patient was commenced on a course of oral Rifampicin, Isoniazid and Pyridoxinein in standard doses for a total of 9 months for reactivation of BCG.
Ongoing daytime frequency and urge incontinence prompted repeat urine cultures that grew Klebsiella oxytoca and was appropriately treated based on sensitivities. In spite of appropriate antibiotic treatment, the patient's symptoms persisted. Further investigation with a CT abdomen and pelvis in September 2011 demonstrated marked mural thickening of the bladder with bilateral hydro-ureter and hydronephrosis. Check cystoscopy in the same month showed significant improvement in the inflammation, however, some areas of bullous edema persisted. Biopsies taken at the time revealed congestion and inflammatory cell infiltrate, but no evidence of malignancy. Additionally, repeat urine cultures were negative for Mycobacterium bovis BCG but did show a small number of atypical cells that were considered to be reactive in nature. The patient was advised to undertake bladder training, wear a urodome and was commenced on solifenacin succinate.
Repeat urine cultures following the completion of tuberculosis treatment were all negative for M. bovis, suggesting successful treatment of his BCG reactivation. However, his symptoms of frequency and urge incontinence persisted despite medication and behavioral therapy. Subsequent surveillance cystoscopy showed no cancer recurrence, but did demonstrate bladder irregularity with multiple septae, diverticuli and evidence of contractures.
Over the next 2 years continued surveillance did not identify a recurrence of bladder cancer, though the bladder remained fibrotic and poorly contractile. The patient was not a candidate for surgery due to his anesthetic risk, thus his ongoing incontinence was managed with incontinence pads and urodomes indefinitely (Figure 1, Figure 2).