- Email: [email protected]
Re: Management of Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia With Open Prostatectomy: Results of a Contemporary Series
2398
LETTERS TO THE EDITOR
retroperitoneal organs. Indeed, prospective comparative studies for other laparoscopic retroperitoneal surgeries have not revealed profound advantages of either method, and small time differences are related to experience.1–3 Based on these series, we suspect that when the prospective laparoscopic pyeloplasty study is completed a similar conclusion will be reached. The “old-school” dogma must give way to tailored approaches based on individual patients and physicians. 1. Rubinstein M, Gill IS, Aron M, Kilciler M, Meraney AM, Finelli A et al: Prospective, randomized comparison of transperitoneal versus retroperitoneal laparoscopic adrenalectomy. J Urol 2005; 174: 442. 2. Desai MM, Strzempkowski B, Matin SF, Steinberg AP, Ng C, Meraney AM et al: Prospective randomized comparison of transperitoneal versus retroperitoneal laparoscopic radical nephrectomy. J Urol 2005; 173: 38. 3. Nadler RB, Loeb S, Clemens JQ, Batler RA, Gonzalez CM and Vardi IY: A prospective study of laparoscopic radical nephrectomy for T1 tumors—is transperitoneal, retroperitoneal or hand assisted the best approach? J Urol 2006; 175: 1230.
Re: Renal and Bladder Functional Status at Diagnosis as Predictive Factors for the Outcome of Primary Vesicoureteral Reflux in Children C. K. Yeung, B. Sreedhar, J. D. Sihoe and F. K. Sit J Urol 2006; 176: 1152–1157. To the Editor. In this interesting study of children with high grade primary vesicoureteral reflux (VUR) Yeung et al report that lower urinary tract dysfunction detected by urodynamic testing and renal scars are predictive of low spontaneous resolution of reflux, urinary tract infection and the appearance of new renal scars. After reading this study 2 questions arise. First, is what the authors describe as abnormal bladder function really a true dysfunction of the bladder, or is it simply an effect of severe reflux in the bladder? Also, is urodynamic study a necessary step in VUR investigation? Unfortunately, no answers emerge from the data presented. It is not clear if the groups of patients with and without abnormal bladder function are comparable. We do not know if the patients were selected consecutively and if there was a significant difference in the average age and in followup between the groups. Also, the VUR grade distribution does not seem to be comparable between the groups. There was an 85% rate of grades IV and V reflux in patients with abnormal kidney and bladder function, while grade III reflux was predominant (56%) in patients with normal kidney and bladder function. In fact, no grade IV reflux was seen in the group with normal function. Because the worst VUR was present in the so-called abnormal bladder function group, the outcome (lower rate of spontaneous VUR resolution, higher rate of urinary tract infection and higher rate of new renal scars) should also probably be the worst. However, the authors found a higher incidence of dysfunctional voiding in patients without renal
scars. This finding is unusual because vesicoperineal incoordination is a risk factor for renal lesion. Two conclusions can be drawn regarding this finding. Either the renal scars preceded the presence of dysfunctional voiding, or there was an inaccuracy in the dysfunctional voiding evaluation, which is understandable in children. There was no comment on how the bladder-sphincter incoordination was evaluated. The authors considered the presence of hypercontractility and impaired emptying as bladder decompensation. However, this classification does not seem correct. A pattern of bladder decompensation should be that in which there is an association between hypocontractility and high post-void residual volume. The high post-void residual finding in some patients may be a result of post-void ureteral drainage in severe VUR. The hypercontractility is justified by the highest detrusor effort to empty a high capacity bladder, which is commonly found in these patients. According to the data presented by the authors, we cannot verify that the bladder functioned abnormally and that abnormal bladder function resulted in the worst outcome. Instead, the urodynamic findings seem to be related to more severe reflux and a more incompetent vesicoureteral junction. In this instance work on bladder function would not improve the spontaneous resolution of VUR and, in turn, would make urodynamics unnecessary. I acknowledge the attempt by the authors to reach a better understanding of the relationship between VUR and bladder function by performing urodynamic testing in asymptomatic children. However, I encourage those who intend to perform a similar study to use less invasive methods, such as ultrasound, post-void residual measurement and uroflowmetry, and to focus primarily on treatment. Respectfully, Ubirajara Barroso, Jr. Federal University of Bahia and Baiana School of Medicine and Public Health Bahia, Brazil
Re: Management of Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia With Open Prostatectomy: Results of a Contemporary Series B. Helfand, S. Mouli, R. Dedhia and K. T. McVary J Urol 2006; 176: 2557–2561. To the Editor. The authors confirm, “To our knowledge long-term detailed outcomes using these clinical tools [prostate specific antigen (PSA)] have never been determined for open prostatectomy . . . ” and “ . . . this is the first study to indicate that following open prostatectomy PSA decreases to less than 1.0 ng/ml by 1 month and it is maintained at this level for up to 52 months postoperatively.” I would like to clarify that in my own prospective study (possibly the first published study) involving 180 patients PSA was determined before and at intervals after open prostatectomy, ie
LETTERS TO THE EDITOR transvesical removal of the adenoma (group 1, 65 patients) between January 1991 and December 1995 at a single intitution.1 Additional treatment groups either underwent transurethral prostatectomy (group 2, 51 patients) or received drug therapy (doxazosin, group 3, 64 patients). After all modes of treatment the decrease in PSA value was largest in group 1 (mean value decreased from 7.9 to 0.79 ng/ml). I have also detailed the long-term outcome in 45 patients using serum PSA for open prostatectomy at intervals up to 5 years postoperatively.2 Respectfully, Slawomir A. Dutkiewicz Department of Urology ATTIS Center Central Teaching Hospital of Ministry of Internal Affairs and Administration Warsaw, Poland 1.
Dutkiewicz S and Stepien K: Serum PSA levels at 6 month after surgery, TURP or doxazosin therapy for BPH. Mater Med Pol 1996; 28: 69. 2. Dutkiewicz S: Benign prostatic hyperplasia. What are the factors which determine pharmacologic versus surgical approach? Research thesis, Legraf, Warsaw, Poland, 1997.
Reply by Authors. We appreciate the opportunity to reply to the letter by Dutkiewicz concerning our article. He is correct in saying that we were not aware of his previously published article in the journal Materia Medica Polona from 1996. This article still does not appear when performing Internet based search methods using PSA as a proxy for prostate tissue resected in surgery for benign disease. We suppose that this circumstance may be the main reason this contribution was omitted in our review of the topic. Since the article by Dutkiewicz is not yet available for our review, our comments are gleaned from a careful reading of the abstract. Those excuses made, our statements concerning the longterm use of PSA as a clinical tool in determining the completeness of open prostatectomy still stand, given that our study follows patients from 1 through 52 months postoperatively, whereas the report by Dutkiewicz (in abstract form anyway) details PSA followup for only 6 months. What is important for the reader to appreciate is that PSA can be a proxy for completeness of resection in the short and long term. The brief medical communication by Dutkiewicz detailing PSA in the short term and our more recent publication concerning long-term followup are consistent with each other. Unfortunately, the thesis cited by Dutkiewicz is not actually a publication, and, therefore, qualifies as a personal communication only.
We have performed 89 pyeloplasties during the last 9 years under the care of a senior surgeon. We preferentially use a 4Fr Pippi Salle stent over a 0.889 mm guidewire placed antegrade without intraoperative screening to protect the anastomosis and to allow ipsilateral renal and bladder drainage. Before passage of the stent we routinely gently pass a 4Fr feeding tube via the ureterovesical junction (UVJ), and only pass the Pippi Salle stent through the UVJ if the feeding tube passes easily and drains urine. If the feeding tube does not enter the bladder, the distal end of the Pippi Salle stent is trimmed to rest in the upper ureter, and an antegrade nephrostogram is performed before removal of the stent. To date, we have not had a case of iatrogenic UVJ obstruction secondary to antegrade stent placement. We believe that there is insufficient evidence in the study reviewed1 and in the article referenced2 to reach the conclusion that antegrade stenting in this situation is potentially dangerous. The study reviewed contains small numbers of patients and does not attempt to use any statistical analysis to test the hypothesis that retrograde stenting is superior to antegrade stenting to protect a pyeloplasty postoperatively. In fact, in the methodology for his study Chandrasekharam explains that antegrade stenting was initially his preferred method of stenting. It was only after he experienced some failures that he resorted to a retrograde technique, which poses a further bias. The article referenced by Canning is a retrospective study of 3 patients among a series of 32 diagnosed with UVJ obstruction after pyeloplasty.2 One of the cases presented may even have involved the rare combination of congenital ureteropelvic junction obstruction and UVJ obstruction, since a 6Ch probe could not be passed at surgery. The editorial comment published is, at best, level 5 evidence and contrary to our retrospective experience. Therefore, we will continue to use antegrade stent placement during fashioning of the ureteropelvic anastomosis as our procedure of choice to protect the anastomosis in the postoperative period. Respectfully, Stephen J. Griffin and Henrik A. Steinbrecher Department of Paediatric Urology Southampton General Hospital Tremona Rd. Southampton SO16 6YD United Kingdom e-mail: [email protected] 1.
2.
Re: Editorial Comment D. A. Canning J Urol 2006; 176: 2242. To the Editor. We read with interest the editorial comment by Canning regarding the study by Chandrasekharam.1 We do not concur with the conclusion that antegrade stenting is suboptimal and, at worst, potentially dangerous.
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Chandrasekharam VV: Is retrograde stenting more reliable than antegrade stenting for pyeloplasty in infants and children? Urology 2005; 66: 1301. Cserni T, Jozsa T, Csizy I, Carr MC, Canning DA and Rushton HG: The danger of intraoperative antegrade cannulation of the ureter in infancy and early childhood. J Urol 2005; 173: 967.
Reply by Authors. I thank Griffin and Steinbrecher for their comments. Each surgeon has his or her recipe for successful repair. I agree with them that my comments are biased. The bias is based on my own surgical experience and that of others who have observed complications following blind antegrade stenting in newborns and infants.
LETTERS TO THE EDITOR
retroperitoneal organs. Indeed, prospective comparative studies for other laparoscopic retroperitoneal surgeries have not revealed profound advantages of either method, and small time differences are related to experience.1–3 Based on these series, we suspect that when the prospective laparoscopic pyeloplasty study is completed a similar conclusion will be reached. The “old-school” dogma must give way to tailored approaches based on individual patients and physicians. 1. Rubinstein M, Gill IS, Aron M, Kilciler M, Meraney AM, Finelli A et al: Prospective, randomized comparison of transperitoneal versus retroperitoneal laparoscopic adrenalectomy. J Urol 2005; 174: 442. 2. Desai MM, Strzempkowski B, Matin SF, Steinberg AP, Ng C, Meraney AM et al: Prospective randomized comparison of transperitoneal versus retroperitoneal laparoscopic radical nephrectomy. J Urol 2005; 173: 38. 3. Nadler RB, Loeb S, Clemens JQ, Batler RA, Gonzalez CM and Vardi IY: A prospective study of laparoscopic radical nephrectomy for T1 tumors—is transperitoneal, retroperitoneal or hand assisted the best approach? J Urol 2006; 175: 1230.
Re: Renal and Bladder Functional Status at Diagnosis as Predictive Factors for the Outcome of Primary Vesicoureteral Reflux in Children C. K. Yeung, B. Sreedhar, J. D. Sihoe and F. K. Sit J Urol 2006; 176: 1152–1157. To the Editor. In this interesting study of children with high grade primary vesicoureteral reflux (VUR) Yeung et al report that lower urinary tract dysfunction detected by urodynamic testing and renal scars are predictive of low spontaneous resolution of reflux, urinary tract infection and the appearance of new renal scars. After reading this study 2 questions arise. First, is what the authors describe as abnormal bladder function really a true dysfunction of the bladder, or is it simply an effect of severe reflux in the bladder? Also, is urodynamic study a necessary step in VUR investigation? Unfortunately, no answers emerge from the data presented. It is not clear if the groups of patients with and without abnormal bladder function are comparable. We do not know if the patients were selected consecutively and if there was a significant difference in the average age and in followup between the groups. Also, the VUR grade distribution does not seem to be comparable between the groups. There was an 85% rate of grades IV and V reflux in patients with abnormal kidney and bladder function, while grade III reflux was predominant (56%) in patients with normal kidney and bladder function. In fact, no grade IV reflux was seen in the group with normal function. Because the worst VUR was present in the so-called abnormal bladder function group, the outcome (lower rate of spontaneous VUR resolution, higher rate of urinary tract infection and higher rate of new renal scars) should also probably be the worst. However, the authors found a higher incidence of dysfunctional voiding in patients without renal
scars. This finding is unusual because vesicoperineal incoordination is a risk factor for renal lesion. Two conclusions can be drawn regarding this finding. Either the renal scars preceded the presence of dysfunctional voiding, or there was an inaccuracy in the dysfunctional voiding evaluation, which is understandable in children. There was no comment on how the bladder-sphincter incoordination was evaluated. The authors considered the presence of hypercontractility and impaired emptying as bladder decompensation. However, this classification does not seem correct. A pattern of bladder decompensation should be that in which there is an association between hypocontractility and high post-void residual volume. The high post-void residual finding in some patients may be a result of post-void ureteral drainage in severe VUR. The hypercontractility is justified by the highest detrusor effort to empty a high capacity bladder, which is commonly found in these patients. According to the data presented by the authors, we cannot verify that the bladder functioned abnormally and that abnormal bladder function resulted in the worst outcome. Instead, the urodynamic findings seem to be related to more severe reflux and a more incompetent vesicoureteral junction. In this instance work on bladder function would not improve the spontaneous resolution of VUR and, in turn, would make urodynamics unnecessary. I acknowledge the attempt by the authors to reach a better understanding of the relationship between VUR and bladder function by performing urodynamic testing in asymptomatic children. However, I encourage those who intend to perform a similar study to use less invasive methods, such as ultrasound, post-void residual measurement and uroflowmetry, and to focus primarily on treatment. Respectfully, Ubirajara Barroso, Jr. Federal University of Bahia and Baiana School of Medicine and Public Health Bahia, Brazil
Re: Management of Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia With Open Prostatectomy: Results of a Contemporary Series B. Helfand, S. Mouli, R. Dedhia and K. T. McVary J Urol 2006; 176: 2557–2561. To the Editor. The authors confirm, “To our knowledge long-term detailed outcomes using these clinical tools [prostate specific antigen (PSA)] have never been determined for open prostatectomy . . . ” and “ . . . this is the first study to indicate that following open prostatectomy PSA decreases to less than 1.0 ng/ml by 1 month and it is maintained at this level for up to 52 months postoperatively.” I would like to clarify that in my own prospective study (possibly the first published study) involving 180 patients PSA was determined before and at intervals after open prostatectomy, ie
LETTERS TO THE EDITOR transvesical removal of the adenoma (group 1, 65 patients) between January 1991 and December 1995 at a single intitution.1 Additional treatment groups either underwent transurethral prostatectomy (group 2, 51 patients) or received drug therapy (doxazosin, group 3, 64 patients). After all modes of treatment the decrease in PSA value was largest in group 1 (mean value decreased from 7.9 to 0.79 ng/ml). I have also detailed the long-term outcome in 45 patients using serum PSA for open prostatectomy at intervals up to 5 years postoperatively.2 Respectfully, Slawomir A. Dutkiewicz Department of Urology ATTIS Center Central Teaching Hospital of Ministry of Internal Affairs and Administration Warsaw, Poland 1.
Dutkiewicz S and Stepien K: Serum PSA levels at 6 month after surgery, TURP or doxazosin therapy for BPH. Mater Med Pol 1996; 28: 69. 2. Dutkiewicz S: Benign prostatic hyperplasia. What are the factors which determine pharmacologic versus surgical approach? Research thesis, Legraf, Warsaw, Poland, 1997.
Reply by Authors. We appreciate the opportunity to reply to the letter by Dutkiewicz concerning our article. He is correct in saying that we were not aware of his previously published article in the journal Materia Medica Polona from 1996. This article still does not appear when performing Internet based search methods using PSA as a proxy for prostate tissue resected in surgery for benign disease. We suppose that this circumstance may be the main reason this contribution was omitted in our review of the topic. Since the article by Dutkiewicz is not yet available for our review, our comments are gleaned from a careful reading of the abstract. Those excuses made, our statements concerning the longterm use of PSA as a clinical tool in determining the completeness of open prostatectomy still stand, given that our study follows patients from 1 through 52 months postoperatively, whereas the report by Dutkiewicz (in abstract form anyway) details PSA followup for only 6 months. What is important for the reader to appreciate is that PSA can be a proxy for completeness of resection in the short and long term. The brief medical communication by Dutkiewicz detailing PSA in the short term and our more recent publication concerning long-term followup are consistent with each other. Unfortunately, the thesis cited by Dutkiewicz is not actually a publication, and, therefore, qualifies as a personal communication only.
We have performed 89 pyeloplasties during the last 9 years under the care of a senior surgeon. We preferentially use a 4Fr Pippi Salle stent over a 0.889 mm guidewire placed antegrade without intraoperative screening to protect the anastomosis and to allow ipsilateral renal and bladder drainage. Before passage of the stent we routinely gently pass a 4Fr feeding tube via the ureterovesical junction (UVJ), and only pass the Pippi Salle stent through the UVJ if the feeding tube passes easily and drains urine. If the feeding tube does not enter the bladder, the distal end of the Pippi Salle stent is trimmed to rest in the upper ureter, and an antegrade nephrostogram is performed before removal of the stent. To date, we have not had a case of iatrogenic UVJ obstruction secondary to antegrade stent placement. We believe that there is insufficient evidence in the study reviewed1 and in the article referenced2 to reach the conclusion that antegrade stenting in this situation is potentially dangerous. The study reviewed contains small numbers of patients and does not attempt to use any statistical analysis to test the hypothesis that retrograde stenting is superior to antegrade stenting to protect a pyeloplasty postoperatively. In fact, in the methodology for his study Chandrasekharam explains that antegrade stenting was initially his preferred method of stenting. It was only after he experienced some failures that he resorted to a retrograde technique, which poses a further bias. The article referenced by Canning is a retrospective study of 3 patients among a series of 32 diagnosed with UVJ obstruction after pyeloplasty.2 One of the cases presented may even have involved the rare combination of congenital ureteropelvic junction obstruction and UVJ obstruction, since a 6Ch probe could not be passed at surgery. The editorial comment published is, at best, level 5 evidence and contrary to our retrospective experience. Therefore, we will continue to use antegrade stent placement during fashioning of the ureteropelvic anastomosis as our procedure of choice to protect the anastomosis in the postoperative period. Respectfully, Stephen J. Griffin and Henrik A. Steinbrecher Department of Paediatric Urology Southampton General Hospital Tremona Rd. Southampton SO16 6YD United Kingdom e-mail: [email protected] 1.
2.
Re: Editorial Comment D. A. Canning J Urol 2006; 176: 2242. To the Editor. We read with interest the editorial comment by Canning regarding the study by Chandrasekharam.1 We do not concur with the conclusion that antegrade stenting is suboptimal and, at worst, potentially dangerous.
2399
Chandrasekharam VV: Is retrograde stenting more reliable than antegrade stenting for pyeloplasty in infants and children? Urology 2005; 66: 1301. Cserni T, Jozsa T, Csizy I, Carr MC, Canning DA and Rushton HG: The danger of intraoperative antegrade cannulation of the ureter in infancy and early childhood. J Urol 2005; 173: 967.
Reply by Authors. I thank Griffin and Steinbrecher for their comments. Each surgeon has his or her recipe for successful repair. I agree with them that my comments are biased. The bias is based on my own surgical experience and that of others who have observed complications following blind antegrade stenting in newborns and infants.