Augmentation for Neuropathic Bladder Dysfunction—A Thing of the Past?

Augmentation for Neuropathic Bladder Dysfunction—A Thing of the Past? PRESERVE renal function. Achieve urinary and fecal continence. Create patient independence in managing bowel and bladder dysfunction. These have been the mantras and expectations that the urological reconstructive surgeon and patient/family have adopted during the last 3 or more decades. The learning curve has been steep with advances in intermittent catheterization, bladder outlet surgery to increase outlet resistance, and bladder augmentation to increase compliance and capacity. Most recently there has been inclusion of the Mitrofanoff principle to create catheterizable channels for bowel and bladder. As we aggressively pursued urinary continence, it become clear that none of these procedures are without complications, such as the risk of infection with intermittent catheterization or the need for revisionary surgery with outlet surgery and catheterizable channels. Bladder augmentation, specifically enterocystoplasty, has created new and sometimes long-term additional risks. These include metabolic/absorption issues and mucus production with inherent problems of infection and stones. However, the most problematic issues are lifelong and potentially life threatening. These include bladder perforation and bladder cancer. The complications of enterocystoplasty clearly fall into 2 distinct categories, including problems that can be potentially eliminated or significantly reduced, and problems that might be unavoidable and require long-term surveillance. An example of a potentially avoidable complication is bladder stones. Once this association with bladder augmentation was recognized, reports appeared with occurrence rates as high as 50%.1 With time the association of bladder mucus and stone formation was recognized and the simple addition of daily bladder irrigation has clearly lowered but not eliminated the rate of bladder stones. This is evident in a recent review of 500 patients with bladder augmentation from our institution in which we reported a stone risk of 15%.2 Rupture of the augmented bladder can occur as either an early or late complication and is thought to be secondary to chronic over distention of the bladder with weakening of the anastomotic junction be0022-5347/10/1836-2124/0 THE JOURNAL OF UROLOGY® © 2010 by AMERICAN UROLOGICAL ASSOCIATION EDUCATION

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tween the bladder and the intestinal segment. Not surprisingly, this occurs most frequently in patients during the teenage years, when compliance with the catheterization schedule may become less regimented, and in patients with higher outlet resistance.3 Presentation may vary from florid urosepsis and an acute abdomen to otherwise clinically silent fluid accumulation in the abdomen. There has been a great deal of interest and concern regarding the risks of cancer in the augmented bladder since the concept was reintroduced in the early 1990s.4 Most series present a small number of cancers at a single institution but it has become clear that these tumors tend to be histologically aggressive and frequently present with metastasis. In our review of 4 patients with transitional cell carcinoma developing after intestinocystoplasty all of the patients had high grade invasive tumors with metastatic disease at diagnosis and died.5 Recent reports have provided further proof that patients with neuropathic bladder with or without bladder augmentation are at increased risk for cancer6 and high grade aggressive tumors are common even without augmentation. One of the frustrating problems is an inadequate surveillance technique to identify early and alter the outcome of these more aggressive tumors. Husmann and Rathbun reviewed the Mayo Clinic experience with malignancy following enteric augmentation and were able to stratify risk based on underlying bladder pathology.7 It is clear from this report that coexisting cancer risk factors, such as immunosuppression or tobacco exposure, markedly increase the risk of cancer, as does underlying bladder pathology, such as bladder exstrophy. Clearly neuropathic bladder and chronic inflammation independently increase the risk of malignancy, which is magnified by placing a bowel segment in the urinary tract. Given these significant risks of enterocystoplasty, there has been ongoing and renewed interest in other options for bladder augmentation. Seromuscular colocystoplasty, ureterocystoplasty and detrusorectomy/autoaugmentation have all been described and in properly selected patients have led to outVol. 183, 2124-2125, June 2010 Printed in U.S.A. DOI:10.1016/j.juro.2010.03.067

AUGMENTATION FOR NEUROPATHIC BLADDER DYSFUNCTION

comes similar to those of bowel augmentation with regards to improving bladder compliance and/or capacity.7–10 One could still argue that the need to perform any of these procedures represents a failure in medical treatment of the children early in the course of the disease/disability with the intent of preventing the end stage histological and functional changes in the bladder. The concepts of early bladder cycling, and earlier institution of intermittent catheterization and anticholinergic therapy are directed toward minimizing the terminal changes in the bladder. It has now been several decades since the introduction of these concepts and we are likely just now seeing the benefits of more aggressive early medical therapy. To date this has not eliminated the need for bladder augmentation in all patients. The article by Snodgrass et al (page 2361) in this issue of The Journal is an extension of the above concepts that bladder augmentation can and should be avoided in patients who do not require bladder enlargement to become socially dry and independent. Historically it has been difficult to determine which patients might require bladder augmentation simultaneous with procedures that increase outlet resistance but many of these patients in the past did not benefit from earlier aggressive bladder management. Despite the commitment in our practice to avoid unnecessary enterocystoplasty, we found it interesting that the week that we were asked to write this editorial questioning the future of enteric bladder augmentation we performed an ileal augmentation in a teenage patient and counseled another who may need an augmentation. Mitrofanoff channels and bladder neck slings were performed almost 10 years ago in both patients. Both had achieved complete

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dryness and both later developed tethered spinal cord, moderate hydronephrosis and reflux between annual visits. Both patients were ideal examples of why short followup may not reflect long-term outcomes and risks, especially in pediatric patients. As Dr. David Bloom once wisely counseled, “You really need to show me data on 100 patients with 10-year followup to make a convincing argument.” So where are we today with respect to bladder augmentation in children? Clearly this is an area of intense research, and there are promising technologies in the area of tissue engineering and neuromodulation therapy that bypass the neurological problem in patients with spina bifida.11 Currently many of these therapies are under investigation or are being studied in the laboratory only but there is optimism that they may provide an alternative or further decrease the need for enterocystoplasty in this patient group. Our current clinical goals should be to minimize the need for enteric bladder augmentation by maximizing early and aggressive medical management. Despite the best management, there still are patients who develop a small capacity, poorly compliant bladder and in this scenario we would still recommend enterocystoplasty as the gold standard. No matter whether a bladder outlet procedure is performed in isolation or combined with bladder augmentation, both family and surgeon should commit to long-term careful followup. Mark P. Cain and Richard C. Rink Department of Urology Indiana University School of Medicine Riley Hospital for Children Indianapolis, Indiana

REFERENCES 1. Palmer LS, Franco I, Kogan SJ et al: Urolithiasis in children following augmentation cystoplasty. J Urol 1993; 150: 726. 2. Metcalfe PD, Cain MP, Gilley DA et al: What is the need for additional bladder surgery after bladder augmentation in childhood? J Urol 2006; 176: 1801. 3. Metcalfe PD, Casale AJ, Kaefer MA et al: Spontaneous bladder perforations: a report of 500 augmentations in children and analysis of risk. J Urol 2006; 175: 1466. 4. Filmer RB and Spencer JR: Malignancies in bladder augmentations and intestinal conduits. J Urol 1990; 143: 671.

5. Sung M, Zhang S, Wang M et al: Urothelial carcinoma following augmentation cystoplasty: an aggressive variant of urothelial carcinoma with distinct clinicopathological characteristics and molecular genetic alterations. Histopathology 2009; 55: 161. 6. Austin JC, Elliott S and Cooper CS: Patients with spina bifida and bladder cancer: atypical presentation, advanced stage and poor survival. J Urol 2007; 178: 798. 7. Husmann DA and Rathbun SR: Long-term follow up of enteric bladder augmentations: the risk for malignancy. J Pediatr Urol 2008; 4: 381. 8. Gurocak S, DeGier RPE and Feitz W: Bladder augmentation without integration of intact bowel seg-

ments: critical review and future perspectives. J Urol 2007; 177: 839. 9. Gonzalez R, Ludwikowski B and Horst M: Determinants of success and failure of seromuscular colocystoplasty lined with urothelium. J Urol 2009; 182: 1781. 10. Johal NS, Hamid R, Aslam Z et al: Ureterocystoplasty: long-term functional results. J Urol 2008; 179: 2373. 11. Lewis JM and Cheng EY: Non-traditional management of the neurogenic bladder: tissue engineering and neuromodulation. Sci World J 2007; 7: 1230.