- Email: [email protected]
Post-Prostatectomy Incontinence: The Influence of Bladder Dysfunction
0022-534 7/87 /1383-057 4$02.00/0 Vol. 138, September
THE JOURNAL OF UROLOGY
Copyright © 1987 by The Williams & Wilkins Co.
Printed in U.S.A.
POST-PROSTATECTOMY INCONTINENCE: THE INFLUENCE OF BLADDER DYSFUNCTION GARY E. LEACH, CHI-MING YIP
AND
BRENDA J. DONOVAN
From the Department of Urology, Kaiser Permanente Medical Center, Los Angeles, California
ABSTRACT
The urodynamic studies of 38 patients referred for evaluation of incontinence after prostatectomy were reviewed. Only 15 patients (39.5 per cent) had pure sphincteric insufficiency as the sole cause of the incontinence. Of the 38 patients 16 (42 per cent) had sphincteric insufficiency combined with a significant component of bladder dysfunction (detrusor instability and/or low bladder wall compliance) as the cause of the incontinence. A total of 7 patients (18.5 per cent) had no evidence of sphincteric insufficiency but they had post-prostatectomy incontinence solely caused by detrusor instability and/or low bladder wall compliance. Of the patients referred for post-prostatectomy incontinence 60.5 per cent had bladder dysfunction as a major factor in the incontinence, which emphasizes the need for comprehensive urodynamic evaluation before treatment is recommended. Of 26 patients whose treatment was based on urodynamic findings and who were available for followup 23 (88 per cent) were adequately continent after treatment, with 35 per cent responding to pharmacological treatment alone and 54 per cent requiring placement of an artificial urinary sphincter with or without associated pharmacological therapy. The potential role of bladder dysfunction as a causative factor in post-prostatectomy incontinence must be considered to optimize the results of treatment and to avoid an unnecessary operation. (J. Ural., 138: 574-578, 1987) The reported incidence of incontinence after prostatectomy has ranged from 2 to 87 per cent. 1- 3 Although incontinence after prostatectomy frequently is caused by damage to the distal sphincteric mechanism,4 the role of bladder dysfunction in postprostatectomy incontinence must be considered. We examine the causes of post-prostatectomy incontinence in 38 patients and evaluate the success of treatment in 26. Special emphasis is placed on the importance of comprehensive evaluation and appropriate treatment based on this evaluation.
Warm water was instilled through a 12F straight red Robinson catheter. Bladder pressure, intra-abdominal pressure·and electronically determined true detrusor pressure were recorded. Urodynamic testing was performed with the aid of a 6-channel Dantech 2100 urodynamic system. During the filling phase of cystometry, stress incontinence, detrusor instability and/or low bladder wall compliance was noted during provocative maneuvers with the patient in multiple positions. After bladder filling an 8F urethral catheter was used to monitor intravesical pressure during the pressure flow study. Cystourethroscopy was performed after the urodynamic studies were completed. The response to treatment based on the urodynamic evaluation was graded according to the subjective improvement stated by the patient and the number of pads required for protection. Repeat urodynamic studies were performed to document the response to pharmacological therapy before surgical intervention.
METHODS AND MATERIALS
During the last 3 years 38 patients between 55 and 82 years old (mean 68 years) were evaluated for post-prostatectomy incontinence. The operations performed were suprapubic prostatectomy in 5 patients, transurethral resection of the prostate in 8, radical retropubic prostatectomy in 24 and radical perinea! prostatectomy in 1. The interval between the operation and the urodynamic evaluation ranged from 6 months to 30 years, with 17 of the 38 patients being evaluated between 6 and 12 months postoperatively. Of 26 patients who were followed for more than 6 months 14 were followed for more than 1 year (maximum followup was 3 years). The treatment results were analyzed and correlated with the urodynamic results. All terminology corresponded to the guidelines of the International Continence Society. 5 Although preoperative symptoms of urgency, frequency and incontinence were elicited, most of the recollections understandably were vague. All patients had been performing perinea! strengthening exercises without improvement in incontinence. Postoperative symptoms of urgency, stress incontinence or spontaneous loss of urine were noted. Physical examination was performed in all patients, with special attention to the neurological examination (lower extremity reflexes, perinea! sensation, anal sphincter tone and bulbocavernosus reflex). A noninvasive free flow was obtained with measurement of the post-void residual urine volume. Multi-positional water cystometry was performed with bladder filling at 100 cc per minute. Accepted for publication March 11, 1987.
RESULTS
The patients were divided into 2 · main groups: those with cancer who underwent radical prostatectomy and those with benign disease who underwent transurethral resection of the prostate or suprapubic prostatectomy. Before prostatectomy 13 patients had symptoms of urgency and/or urgency incontinence. However, 3 of the 13 patients had no urodynamic evidence of bladder dysfunction (low bladder wall compliance and/or detrusor instability) postoperatively (table 1). After prostatectomy 22 patients noticed symptoms of stress urinary incontinence only. However, the urodynamic evaluation demonstrated pure sphincteric insufficiency in only 10 of these 22 patients (table 2). A major component of bladder dysfunction with or without sphincteric insufficiency was noted in 12 of the 22 patients. A total of 14 patients complained of urgency incontinence or spontaneous loss of urine with stress urinary incontinence postoperatively. Despite these symptoms water cystometry showed that 5 of these patients had sphincteric insufficiency only. Two patients who complained of spontaneous loss of urine with equivocal symptoms of stress urinary incontinence had findings of low bladder
574
POST-PRl)STATECTOlvIY Ii¾If:ONTI1\TENCE
wall with or without detrusor instability but no sphincteric insufficiency. The preoperative and postoperative symptoms were unreliable in defining the true cause of the incontinence as demonstrated on urodynamic evaluation. The free flow and pressure flow studies were normal in all except 1 patient who had outflow obstruction secondary to a urethral stricture. No patient had any demonstrable neurological abnormality. Cystometric findings are presented in table 3. Only 32 per cent of the cancer group and 54 per cent of the benign disease group had sphincteric insufficiency as the sole cause of the post-prostatectomy incontinence (fig. 1). Detrusor instability and low bladder wall compliance were major factors causing the incontinence in 68 per cent of the cancer patients, and they were the sole causes for the incontinence in 7 patients (18.5 per cent) (fig. 2). Cystourethroscopy revealed no evidence of outflow obstruction except in 1 patient with a urethral stricture. The presence of bladder wall trabeculation did not correlate with the urodynamic demonstration of detrusor instability or low compliance.
575
V~~,OH<~H'O,V
Postoperative urodynamic findings in 13 patients with a preoperative history of urgency with or without urge incontinence
Bladder Pressure
Abdomim1I Pressure
Detrusor Prsssyre
TABLE 1.
Genuine stress urinary incontinence plus bladder dysfunction Bladder dysfunction only Genuine stress urinary incontinence only
TABLE 2.
Total No. Pts.
12
12
10
2
Ca No. Pts.
Benign Disease No. Pts.
4
3
2
1 2
1
Postoperative symptoms related to urodynamic findings Postop. Symptoms
U rodynamic Findings (No. pts.)
Ca group Genuine stress urinary incontiStress urinary incontinence (4), genuine stress urinence only nary incontinence plus bladder dysfunction (5). bladder dysfunction (3) Genuine stress urinary incontiUrge, stress urinary nence (4), genuine stress uriincontinence nary incontinence plus bladder dysfunction (7), bladder dysfunction (1) Bladder dysfunction only Urge, ? stress urinary incontinence Benign disease group Genuine stress urinary incontiStress urinary incontinence (6), genuine stress urinence only nary incontinence plus bladder dysfunction (4) Genuine stress urinary incontiUrge, stress urinary nence (1), bladder dysfuncincontinence tion (1) Bladder dysfunction only Urge, ? stress urinary incontinence
TABLE 3.
Cystometric findings in 38 patients Ca Pts. No.(%)
Genuine stress urinary incontinence: Alone Plus low compliance Plus detrusor instability Plus detrusor instability and low compliance Low compliance plus detrusor instability Low compliance only Detrusor instability only Totals
Benign Disease No.(%) (54)
:1 ::: 25
(100)
il
13
(46)
(100)
Umflow
FIG. 1. Urodynamic demonstration of genuine stress urinary incontinence with cough. Note lack of any increase in detrusor pressure coincident with leakage.
The urodynamic findings of the 26 patients who were treated and followed for 6 months to 3 years are noted in table 4. The results and treatment in these 26 patients were divided into 3 main grnups (table 5). Group 1 included 9 patients (6 in the cancer and 3 in the benign disease group) who underwent implantation of an artificial urinary sphincter only, with subsequent minimal incontinence not requiring pads for protection. Patients with bladder dysfunction in addition to stress urinary incontinence (group 2) were treated with anticholinergic therapy (oxybutynin hydrochloride, propantheline bromide or imipramine hydrochloride) before the insertion of an artificial urinary sphincter. Group 2A consisted of 6 patients with stress minary incontinence and low compliance. Of these patients 2 of 5 with cancer and 1 with benign disease had persistent severe stress incontinence after bladder pressures were normalized with anticholinergic therapy. These 3 patients experienced almost complete resolution of the incontinence with continued pharmacological therapy and artificial urinary sphincter insertion. One of the cancer patients in group 2A with severe stress incontinence and low bladder wall compliance only at large bladder volumes became totally continent after implantation of an artificial sphincter combined with fluid restriction and timed voiding. The remaining 2 patients continued to have extremely poor bladder wall compliance despite aggressive combination anticholinergic therapy. Owing to the inability to provide an adequate intravesical storage capacity at normal pressures implantation of an artificial urinary sphincter was deferred and augmentation cystoplasty was recommended. These patients elected to defer further intervention. Group 2B included 2 cancer patients and 2 with benign disease who suffered stress incontinence plus detrusor instability. The incontinence improved with anticholinergic therapy alone in all 3 patients such that they required only 1 to 2 pads per day for protection. These 3 men refused implantation of an artificial urinary sphincter, since the residual stress urinary
576
LEACH, YIP AND DONOVAN
B A
i 11 •·
I
CMG
1 1 ,,
I
Detrusor Pressure H.O
1I 10cm
,,.
CMG
FIG. 2. A, cystometry in patient incontinent after prostatectomy owing to detrusor instability. Arrowheads indicate uninhibited detrusor contractions. B, ascending type of cystometric curve in patient with incontinence related to low bladder wall compliance.
TABLE
4. Cystometric findings in 26 patients who were treated and available for followup Cystometric Findings
Ca Pts. No.
Benign Disease No.
Genuine stress urinary incontinence
6
3
Genuine stress urinary incontinence and low compliance Genuine stress urinary incontinence and detrusor instability Genuine stress urinary incontinence, low compliance and detrusor instability
5
1
2
1
1
0
Detrusor instability and low compliance Detrusor instability only Low compliance only
1
0
1 3
0 2
Group 1
only 2A 2B 2C
3A 3B 3C
TABLE 5.
Group*
Treatment results with regard to incontinence
No. Pts.
1
6
2A
2
2B
1 2 2
2C
1
3
4
1
Treatment
Results
Radical prostatectomy (19 pts.) Artificial urinary sphincter Minimal incontinence, no pads required Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required Artificial urinary sphincter Completely continent Anticholinergics Severe incontinence Anticholinergics Incontinence, requires 1-2 pads per day Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required Anticholinergics Incontinence, requires 0-2 pads per day Anticholinergics Severe incontinence
Transurethral or suprapubic prostatectomy for benign disease (7 pts.) 1 3 Artificial urinary sphincter Minimal incontinence, no pads required 2A 1 Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required 2B 1 Anticholinergics Minimal incontinence, no pads required Anticholinergics 3 2 Minimal incontinence, no pads required * Group 1-genuine stress urinary incontinence only. Group 2A-genuine stress urinary incontinence plus low compliance. Group 2B-genuine stress urinary incontinence plus detrusor instability. Group 2C-genuine stress urinary incontinence, detrusor instability and low compliance. Group 3-bladder dysfunction only.
incontinence was a minimal problem after the detrusor instability was controlled. Group 2C consisted of 1 cancer patient who had minimal incontinence not requiring pads for protection subsequent to implantation of an artificial urinary sphincter after intravesical pressures were normalized with anticholinergic medication. Group 3 included 1 cancer patient with detrusor instability and low compliance (group 3A), 1 cancer patient with detrusor instability only (group 3B), and 3 cancer and 2 benign disease patients with low compliance only (group 3C). Of these patients 4 with cancer and both with benign disease (incontinence owing to bladder dysfunction alone) responded well to anticholinergic therapy alone with significant improvement in the incontinence. One patient could not tolerate pharmacological therapy and he refused further treatment. Over-all, 23 of the 26 patients (88 per cent) achieved a socially acceptable level of continence as a result of the treatment directed by the urodynamic testing. An artificial urinary sphincter was required in only 14 patients (54 per cent) with excellent results. Patients with elevated intravesical pressures and genuine stress urinary incontinence achieved adequate low pressure storage capacity with the aid of pharmacological therapy as documented on followup urodynamic testing before implantation of an artificial urinary sphincter. Nine patients (35 per cent) were adequately continent on anticholinergic therapy alone. DISCUSSION
Fitzpatrick and associates suggested that postoperative symptoms correlated poorly with the urodynamic findings. 6 Our results support this conclusion, since 12 of 22 patients with symptoms of stress urinary incontinence only had urodynamic findings of bladder dysfunction and 5 of 14 with symptoms of urgency incontinence or spontaneous loss of urine with stress urinary incontinence had urodynamic findings of genuine stress urinary incontinence only. It should be noted that a minority of the patients (15 of 38) had sphincteric insufficiency only. Although this select group did well after implantation of an artificial urinary sphincter alone, if an artificial urinary sphincter were placed as a "kneejerk" reflex in all patients who are incontinent after prostatectomy the majority would receive inappropriate treatment. The incidence of bladder dysfunction in the patient who is incontinent after prostatectomy has been reported by others.
577
POST-PROSTATECTOMY INCONTINENCE
Mayo and Ansell reported detrusor hyperreflexia in 8 of 15 patients studied for incontinence after prostatectomy. 7 Abrams noted that 12 of 30 post-prostatectomy incontinent patients had unstable bladders. 8 Reid and associates reported that 66 per cent of 77 patients had unstable bladders, while 74 per cent had sphincteric damage. Of the patients who were treated pharmacologically and surgically 53 and 65 per cent, respectively, were improved. 9 The role of pharmacological therapy in patients who were treated surgically was not addressed. Y alla and associates reported a 38 per cent incidence of instability in 21 post-prostatectomy incontinent patients. 10 Detrusor instability has been found in 50 per cent of the patients with obstructive prostatism. 11 Approximately a quarter of these patients will have persistent detrusor instability after prostatectomy. Price and associates reported that no patient with preoperative detrusor instability reverted to stable bladder function after 6 months postoperatively. 12 Abrams reported an increasing incidence of detrusor instability with age, regardless of the presence or absence of outflow obstruction.11 The incidence of detrusor instability increased from less than 35 per cent in patients between 40 and 50 years old to greater than 65 per cent in patients more than 70 years old. While the cause of detrusor instability in the elderly or in patients with bladder outflow obstruction is unknown, these factors may be related to the finding of detrusor instability and/or low bladder wall compliance in 60.5 per cent of the patients who are incontinent after prostatectomy. Interestingly, the incidence of postoperative bladder dysfunction was much higher (68 per cent) in the radical surgery group compared to the benign disease group (46 per cent). This higher incidence of bladder dysfunction may be related to some functional change in the bladder induced by the radical prostatectomy itself. Recognition of this abnormal bladder function is of the utmost importance in the management of these patients. When minimal or no sphincteric insufficiency is demonstrable satisfactory continence may be obtained with pharmacological therapy alone. Bladder dysfunction (detrusor instability or low compliance) associated with significant stress incontinence must be corrected before an artificial urinary sphincter is implanted. If an artificial sphincter is inserted before normalization of bladder
pressures by either pharmacological therapy, augmentation cystoplasty, electrical stimulation or some other form of therapy, then hydroureteronephrosis, vesicoureteral reflux, persistent incontinence or periurethral cuff erosion may develop. Since this situation existed potentially in 16 of 38 patients studied this principle cannot be overemphasized. Also, the presence of incontinence after prostatectomy should not be considered as being synonymous with stress incontinence owing to sphincteric damage. Of 38 patients 7 had no evidence of sphincteric insufficiency and they were incontinent only because of high intravesical pressures. This bladder dysfunction may be related to pre-existing outflow obstruction before prostatectomy, it may be secondary to age-related changes in bladder function or it may be precipitated by the operation itself. In any case, 6 of these 7 patients became satisfactorily continent with pharmacological therapy alone. If followup urodynamic studies demonstrate persistent incontinence related to high intravesical pressure while on maximal pharmacological treatment, augmentation cystoplasty should be considered. 13 In summary, our results underscore the importance of urodynamic evaluation with special attention to bladder function in the management ofpost-prostatectomy incontinence (fig. 3). Urinary symptoms in the patient who is incontinent after prostatectomy correlate poorly with the urodynamic findings and the true cause of the incontinence. Treatment based on the urodynamic findings resulted in 88 per cent of the patients becoming adequately continent. To achieve this success rate 54 per cent of the patients required placement of an artificial urinary sphincter with or without pharmacological therapy to normalize bladder pressures, while 35 per cent were satisfactorily continent on anticholinergic therapy alone. The significant incidence of bladder dysfunction in this study group raises some interesting questions. Was the dysfunction present preoperatively and was it related to outflow obstruction? Did the bladder dysfunction develop postoperatively and might it change with time? In an attempt to answer these questions, we currently are performing a prospective study to evaluate lower urinary tract function before and after radical prostatectomy.
Postprostatectomy Incontinence
Urodynamic Evaluation
Significant Sphincteric Insufficiency Only
Sphincteric Insufficiency & Bladder Dysfunction
Artificial Urinary Sphincter
Pharmacologic Therapy
Bladder Dysfunction Controlled Yes
No
Bladder Dysfunction Only
Controlled
i
Continent
Uncontrolled
i Augmentation Cystoplasty/ Other Options
Augmentation Cystoplasty/ Other Options Minimal
i
No Surgery
Significant
Artificial Urinary Sphincter
Fm. 3. Suggested algorithm for management of post-prostatectomy incontinence. Other options include behavior modification, electrical stimulation, biofeedback, cystolysis and urinary diversion.
578
LEACH, YIP AND DONOVAN REFERENCES
1. Walsh, P. C.: Radical prostatectomy for the treatment oflocalized prostatic carcinoma. Urol. Clin. N. Amer., 7: 583, 1980. 2. Lindner, A., deKernion, J.B., Smith, R. B. and Katske, F. A.: Risk of urinary incontinence following radical prostatectomy. J. Urol., 129: 1007, 1983. 3. Rudy, D. C., Woodside, J. R. and Crawford, E. D.: Urodynamic evaluation of incontinence in patients undergoing modified Campbell radical retropubic prostatectomy: a prospective study. J. Urol., 132: 708, 1984. 4. Raz, S. and Kaufmann, J. J.: Editorial. Urodynamics of postprostatectomy incontinence. Urol. Res., 4: 447, 1976. 5. International Continence Society: Fourth report on the standardisation of terminology of lower urinary tract function. Brit. J. Urol., 53: 333, 1981. 6. Fitzpatrick, J. M., Gardiner, R. A. and Worth, P. H. L.: The evaluation of 68 patients with post-prostatectomy incontinence.
Brit. J. Urol., 51: 552, 1979. 7. Mayo, M. E. and Ansell, J. S.: Urodynamic assessment of incontinence after prostatectomy. J. Urol., 122: 60, 1979. 8. Abrams, P.H.: Investigation ofpostprostatectomyproblems. Urology, 15: 209, 1980. 9. Reid, G. F., Fitzpatrick, J.M. and Worth, P.H. L.: The treatment of patients with urinary incontinence after prostatectomy. Brit. J. Urol., 52: 532, 1980. 10. Yalla, S. V., Karsh, L., Kearney, G., Fraser, L., Finn, D., DeFelippo, N. and Dyro, F. M.: Postprostatectomy urinary incontinence: urodynamic assessment. Neurourol. Urodynam., 1: 77, 1982. 11. Abrams, P.: Detrusor instability and bladder outlet obstruction. Neurourol. Urodynam., 4: 317, 1985. 12. Price, D. A., Ramsden, P. D. and Stobbart, D.: The unstable bladder and prostatectomy. Brit. J. Urol., 52: 529, 1980. 13. Lindner, A., Leach, G. E. and Raz, S.: Augmentation cystoplasty in the treatment of neurogenic bladder dysfunction. J. Urol., 129: 491, 1983.
THE JOURNAL OF UROLOGY
Copyright © 1987 by The Williams & Wilkins Co.
Printed in U.S.A.
POST-PROSTATECTOMY INCONTINENCE: THE INFLUENCE OF BLADDER DYSFUNCTION GARY E. LEACH, CHI-MING YIP
AND
BRENDA J. DONOVAN
From the Department of Urology, Kaiser Permanente Medical Center, Los Angeles, California
ABSTRACT
The urodynamic studies of 38 patients referred for evaluation of incontinence after prostatectomy were reviewed. Only 15 patients (39.5 per cent) had pure sphincteric insufficiency as the sole cause of the incontinence. Of the 38 patients 16 (42 per cent) had sphincteric insufficiency combined with a significant component of bladder dysfunction (detrusor instability and/or low bladder wall compliance) as the cause of the incontinence. A total of 7 patients (18.5 per cent) had no evidence of sphincteric insufficiency but they had post-prostatectomy incontinence solely caused by detrusor instability and/or low bladder wall compliance. Of the patients referred for post-prostatectomy incontinence 60.5 per cent had bladder dysfunction as a major factor in the incontinence, which emphasizes the need for comprehensive urodynamic evaluation before treatment is recommended. Of 26 patients whose treatment was based on urodynamic findings and who were available for followup 23 (88 per cent) were adequately continent after treatment, with 35 per cent responding to pharmacological treatment alone and 54 per cent requiring placement of an artificial urinary sphincter with or without associated pharmacological therapy. The potential role of bladder dysfunction as a causative factor in post-prostatectomy incontinence must be considered to optimize the results of treatment and to avoid an unnecessary operation. (J. Ural., 138: 574-578, 1987) The reported incidence of incontinence after prostatectomy has ranged from 2 to 87 per cent. 1- 3 Although incontinence after prostatectomy frequently is caused by damage to the distal sphincteric mechanism,4 the role of bladder dysfunction in postprostatectomy incontinence must be considered. We examine the causes of post-prostatectomy incontinence in 38 patients and evaluate the success of treatment in 26. Special emphasis is placed on the importance of comprehensive evaluation and appropriate treatment based on this evaluation.
Warm water was instilled through a 12F straight red Robinson catheter. Bladder pressure, intra-abdominal pressure·and electronically determined true detrusor pressure were recorded. Urodynamic testing was performed with the aid of a 6-channel Dantech 2100 urodynamic system. During the filling phase of cystometry, stress incontinence, detrusor instability and/or low bladder wall compliance was noted during provocative maneuvers with the patient in multiple positions. After bladder filling an 8F urethral catheter was used to monitor intravesical pressure during the pressure flow study. Cystourethroscopy was performed after the urodynamic studies were completed. The response to treatment based on the urodynamic evaluation was graded according to the subjective improvement stated by the patient and the number of pads required for protection. Repeat urodynamic studies were performed to document the response to pharmacological therapy before surgical intervention.
METHODS AND MATERIALS
During the last 3 years 38 patients between 55 and 82 years old (mean 68 years) were evaluated for post-prostatectomy incontinence. The operations performed were suprapubic prostatectomy in 5 patients, transurethral resection of the prostate in 8, radical retropubic prostatectomy in 24 and radical perinea! prostatectomy in 1. The interval between the operation and the urodynamic evaluation ranged from 6 months to 30 years, with 17 of the 38 patients being evaluated between 6 and 12 months postoperatively. Of 26 patients who were followed for more than 6 months 14 were followed for more than 1 year (maximum followup was 3 years). The treatment results were analyzed and correlated with the urodynamic results. All terminology corresponded to the guidelines of the International Continence Society. 5 Although preoperative symptoms of urgency, frequency and incontinence were elicited, most of the recollections understandably were vague. All patients had been performing perinea! strengthening exercises without improvement in incontinence. Postoperative symptoms of urgency, stress incontinence or spontaneous loss of urine were noted. Physical examination was performed in all patients, with special attention to the neurological examination (lower extremity reflexes, perinea! sensation, anal sphincter tone and bulbocavernosus reflex). A noninvasive free flow was obtained with measurement of the post-void residual urine volume. Multi-positional water cystometry was performed with bladder filling at 100 cc per minute. Accepted for publication March 11, 1987.
RESULTS
The patients were divided into 2 · main groups: those with cancer who underwent radical prostatectomy and those with benign disease who underwent transurethral resection of the prostate or suprapubic prostatectomy. Before prostatectomy 13 patients had symptoms of urgency and/or urgency incontinence. However, 3 of the 13 patients had no urodynamic evidence of bladder dysfunction (low bladder wall compliance and/or detrusor instability) postoperatively (table 1). After prostatectomy 22 patients noticed symptoms of stress urinary incontinence only. However, the urodynamic evaluation demonstrated pure sphincteric insufficiency in only 10 of these 22 patients (table 2). A major component of bladder dysfunction with or without sphincteric insufficiency was noted in 12 of the 22 patients. A total of 14 patients complained of urgency incontinence or spontaneous loss of urine with stress urinary incontinence postoperatively. Despite these symptoms water cystometry showed that 5 of these patients had sphincteric insufficiency only. Two patients who complained of spontaneous loss of urine with equivocal symptoms of stress urinary incontinence had findings of low bladder
574
POST-PRl)STATECTOlvIY Ii¾If:ONTI1\TENCE
wall with or without detrusor instability but no sphincteric insufficiency. The preoperative and postoperative symptoms were unreliable in defining the true cause of the incontinence as demonstrated on urodynamic evaluation. The free flow and pressure flow studies were normal in all except 1 patient who had outflow obstruction secondary to a urethral stricture. No patient had any demonstrable neurological abnormality. Cystometric findings are presented in table 3. Only 32 per cent of the cancer group and 54 per cent of the benign disease group had sphincteric insufficiency as the sole cause of the post-prostatectomy incontinence (fig. 1). Detrusor instability and low bladder wall compliance were major factors causing the incontinence in 68 per cent of the cancer patients, and they were the sole causes for the incontinence in 7 patients (18.5 per cent) (fig. 2). Cystourethroscopy revealed no evidence of outflow obstruction except in 1 patient with a urethral stricture. The presence of bladder wall trabeculation did not correlate with the urodynamic demonstration of detrusor instability or low compliance.
575
V~~,OH<~H'O,V
Postoperative urodynamic findings in 13 patients with a preoperative history of urgency with or without urge incontinence
Bladder Pressure
Abdomim1I Pressure
Detrusor Prsssyre
TABLE 1.
Genuine stress urinary incontinence plus bladder dysfunction Bladder dysfunction only Genuine stress urinary incontinence only
TABLE 2.
Total No. Pts.
12
12
10
2
Ca No. Pts.
Benign Disease No. Pts.
4
3
2
1 2
1
Postoperative symptoms related to urodynamic findings Postop. Symptoms
U rodynamic Findings (No. pts.)
Ca group Genuine stress urinary incontiStress urinary incontinence (4), genuine stress urinence only nary incontinence plus bladder dysfunction (5). bladder dysfunction (3) Genuine stress urinary incontiUrge, stress urinary nence (4), genuine stress uriincontinence nary incontinence plus bladder dysfunction (7), bladder dysfunction (1) Bladder dysfunction only Urge, ? stress urinary incontinence Benign disease group Genuine stress urinary incontiStress urinary incontinence (6), genuine stress urinence only nary incontinence plus bladder dysfunction (4) Genuine stress urinary incontiUrge, stress urinary nence (1), bladder dysfuncincontinence tion (1) Bladder dysfunction only Urge, ? stress urinary incontinence
TABLE 3.
Cystometric findings in 38 patients Ca Pts. No.(%)
Genuine stress urinary incontinence: Alone Plus low compliance Plus detrusor instability Plus detrusor instability and low compliance Low compliance plus detrusor instability Low compliance only Detrusor instability only Totals
Benign Disease No.(%) (54)
:1 ::: 25
(100)
il
13
(46)
(100)
Umflow
FIG. 1. Urodynamic demonstration of genuine stress urinary incontinence with cough. Note lack of any increase in detrusor pressure coincident with leakage.
The urodynamic findings of the 26 patients who were treated and followed for 6 months to 3 years are noted in table 4. The results and treatment in these 26 patients were divided into 3 main grnups (table 5). Group 1 included 9 patients (6 in the cancer and 3 in the benign disease group) who underwent implantation of an artificial urinary sphincter only, with subsequent minimal incontinence not requiring pads for protection. Patients with bladder dysfunction in addition to stress urinary incontinence (group 2) were treated with anticholinergic therapy (oxybutynin hydrochloride, propantheline bromide or imipramine hydrochloride) before the insertion of an artificial urinary sphincter. Group 2A consisted of 6 patients with stress minary incontinence and low compliance. Of these patients 2 of 5 with cancer and 1 with benign disease had persistent severe stress incontinence after bladder pressures were normalized with anticholinergic therapy. These 3 patients experienced almost complete resolution of the incontinence with continued pharmacological therapy and artificial urinary sphincter insertion. One of the cancer patients in group 2A with severe stress incontinence and low bladder wall compliance only at large bladder volumes became totally continent after implantation of an artificial sphincter combined with fluid restriction and timed voiding. The remaining 2 patients continued to have extremely poor bladder wall compliance despite aggressive combination anticholinergic therapy. Owing to the inability to provide an adequate intravesical storage capacity at normal pressures implantation of an artificial urinary sphincter was deferred and augmentation cystoplasty was recommended. These patients elected to defer further intervention. Group 2B included 2 cancer patients and 2 with benign disease who suffered stress incontinence plus detrusor instability. The incontinence improved with anticholinergic therapy alone in all 3 patients such that they required only 1 to 2 pads per day for protection. These 3 men refused implantation of an artificial urinary sphincter, since the residual stress urinary
576
LEACH, YIP AND DONOVAN
B A
i 11 •·
I
CMG
1 1 ,,
I
Detrusor Pressure H.O
1I 10cm
,,.
CMG
FIG. 2. A, cystometry in patient incontinent after prostatectomy owing to detrusor instability. Arrowheads indicate uninhibited detrusor contractions. B, ascending type of cystometric curve in patient with incontinence related to low bladder wall compliance.
TABLE
4. Cystometric findings in 26 patients who were treated and available for followup Cystometric Findings
Ca Pts. No.
Benign Disease No.
Genuine stress urinary incontinence
6
3
Genuine stress urinary incontinence and low compliance Genuine stress urinary incontinence and detrusor instability Genuine stress urinary incontinence, low compliance and detrusor instability
5
1
2
1
1
0
Detrusor instability and low compliance Detrusor instability only Low compliance only
1
0
1 3
0 2
Group 1
only 2A 2B 2C
3A 3B 3C
TABLE 5.
Group*
Treatment results with regard to incontinence
No. Pts.
1
6
2A
2
2B
1 2 2
2C
1
3
4
1
Treatment
Results
Radical prostatectomy (19 pts.) Artificial urinary sphincter Minimal incontinence, no pads required Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required Artificial urinary sphincter Completely continent Anticholinergics Severe incontinence Anticholinergics Incontinence, requires 1-2 pads per day Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required Anticholinergics Incontinence, requires 0-2 pads per day Anticholinergics Severe incontinence
Transurethral or suprapubic prostatectomy for benign disease (7 pts.) 1 3 Artificial urinary sphincter Minimal incontinence, no pads required 2A 1 Artificial urinary sphincter Minimal incontinence, plus anticholinergics no pads required 2B 1 Anticholinergics Minimal incontinence, no pads required Anticholinergics 3 2 Minimal incontinence, no pads required * Group 1-genuine stress urinary incontinence only. Group 2A-genuine stress urinary incontinence plus low compliance. Group 2B-genuine stress urinary incontinence plus detrusor instability. Group 2C-genuine stress urinary incontinence, detrusor instability and low compliance. Group 3-bladder dysfunction only.
incontinence was a minimal problem after the detrusor instability was controlled. Group 2C consisted of 1 cancer patient who had minimal incontinence not requiring pads for protection subsequent to implantation of an artificial urinary sphincter after intravesical pressures were normalized with anticholinergic medication. Group 3 included 1 cancer patient with detrusor instability and low compliance (group 3A), 1 cancer patient with detrusor instability only (group 3B), and 3 cancer and 2 benign disease patients with low compliance only (group 3C). Of these patients 4 with cancer and both with benign disease (incontinence owing to bladder dysfunction alone) responded well to anticholinergic therapy alone with significant improvement in the incontinence. One patient could not tolerate pharmacological therapy and he refused further treatment. Over-all, 23 of the 26 patients (88 per cent) achieved a socially acceptable level of continence as a result of the treatment directed by the urodynamic testing. An artificial urinary sphincter was required in only 14 patients (54 per cent) with excellent results. Patients with elevated intravesical pressures and genuine stress urinary incontinence achieved adequate low pressure storage capacity with the aid of pharmacological therapy as documented on followup urodynamic testing before implantation of an artificial urinary sphincter. Nine patients (35 per cent) were adequately continent on anticholinergic therapy alone. DISCUSSION
Fitzpatrick and associates suggested that postoperative symptoms correlated poorly with the urodynamic findings. 6 Our results support this conclusion, since 12 of 22 patients with symptoms of stress urinary incontinence only had urodynamic findings of bladder dysfunction and 5 of 14 with symptoms of urgency incontinence or spontaneous loss of urine with stress urinary incontinence had urodynamic findings of genuine stress urinary incontinence only. It should be noted that a minority of the patients (15 of 38) had sphincteric insufficiency only. Although this select group did well after implantation of an artificial urinary sphincter alone, if an artificial urinary sphincter were placed as a "kneejerk" reflex in all patients who are incontinent after prostatectomy the majority would receive inappropriate treatment. The incidence of bladder dysfunction in the patient who is incontinent after prostatectomy has been reported by others.
577
POST-PROSTATECTOMY INCONTINENCE
Mayo and Ansell reported detrusor hyperreflexia in 8 of 15 patients studied for incontinence after prostatectomy. 7 Abrams noted that 12 of 30 post-prostatectomy incontinent patients had unstable bladders. 8 Reid and associates reported that 66 per cent of 77 patients had unstable bladders, while 74 per cent had sphincteric damage. Of the patients who were treated pharmacologically and surgically 53 and 65 per cent, respectively, were improved. 9 The role of pharmacological therapy in patients who were treated surgically was not addressed. Y alla and associates reported a 38 per cent incidence of instability in 21 post-prostatectomy incontinent patients. 10 Detrusor instability has been found in 50 per cent of the patients with obstructive prostatism. 11 Approximately a quarter of these patients will have persistent detrusor instability after prostatectomy. Price and associates reported that no patient with preoperative detrusor instability reverted to stable bladder function after 6 months postoperatively. 12 Abrams reported an increasing incidence of detrusor instability with age, regardless of the presence or absence of outflow obstruction.11 The incidence of detrusor instability increased from less than 35 per cent in patients between 40 and 50 years old to greater than 65 per cent in patients more than 70 years old. While the cause of detrusor instability in the elderly or in patients with bladder outflow obstruction is unknown, these factors may be related to the finding of detrusor instability and/or low bladder wall compliance in 60.5 per cent of the patients who are incontinent after prostatectomy. Interestingly, the incidence of postoperative bladder dysfunction was much higher (68 per cent) in the radical surgery group compared to the benign disease group (46 per cent). This higher incidence of bladder dysfunction may be related to some functional change in the bladder induced by the radical prostatectomy itself. Recognition of this abnormal bladder function is of the utmost importance in the management of these patients. When minimal or no sphincteric insufficiency is demonstrable satisfactory continence may be obtained with pharmacological therapy alone. Bladder dysfunction (detrusor instability or low compliance) associated with significant stress incontinence must be corrected before an artificial urinary sphincter is implanted. If an artificial sphincter is inserted before normalization of bladder
pressures by either pharmacological therapy, augmentation cystoplasty, electrical stimulation or some other form of therapy, then hydroureteronephrosis, vesicoureteral reflux, persistent incontinence or periurethral cuff erosion may develop. Since this situation existed potentially in 16 of 38 patients studied this principle cannot be overemphasized. Also, the presence of incontinence after prostatectomy should not be considered as being synonymous with stress incontinence owing to sphincteric damage. Of 38 patients 7 had no evidence of sphincteric insufficiency and they were incontinent only because of high intravesical pressures. This bladder dysfunction may be related to pre-existing outflow obstruction before prostatectomy, it may be secondary to age-related changes in bladder function or it may be precipitated by the operation itself. In any case, 6 of these 7 patients became satisfactorily continent with pharmacological therapy alone. If followup urodynamic studies demonstrate persistent incontinence related to high intravesical pressure while on maximal pharmacological treatment, augmentation cystoplasty should be considered. 13 In summary, our results underscore the importance of urodynamic evaluation with special attention to bladder function in the management ofpost-prostatectomy incontinence (fig. 3). Urinary symptoms in the patient who is incontinent after prostatectomy correlate poorly with the urodynamic findings and the true cause of the incontinence. Treatment based on the urodynamic findings resulted in 88 per cent of the patients becoming adequately continent. To achieve this success rate 54 per cent of the patients required placement of an artificial urinary sphincter with or without pharmacological therapy to normalize bladder pressures, while 35 per cent were satisfactorily continent on anticholinergic therapy alone. The significant incidence of bladder dysfunction in this study group raises some interesting questions. Was the dysfunction present preoperatively and was it related to outflow obstruction? Did the bladder dysfunction develop postoperatively and might it change with time? In an attempt to answer these questions, we currently are performing a prospective study to evaluate lower urinary tract function before and after radical prostatectomy.
Postprostatectomy Incontinence
Urodynamic Evaluation
Significant Sphincteric Insufficiency Only
Sphincteric Insufficiency & Bladder Dysfunction
Artificial Urinary Sphincter
Pharmacologic Therapy
Bladder Dysfunction Controlled Yes
No
Bladder Dysfunction Only
Controlled
i
Continent
Uncontrolled
i Augmentation Cystoplasty/ Other Options
Augmentation Cystoplasty/ Other Options Minimal
i
No Surgery
Significant
Artificial Urinary Sphincter
Fm. 3. Suggested algorithm for management of post-prostatectomy incontinence. Other options include behavior modification, electrical stimulation, biofeedback, cystolysis and urinary diversion.
578
LEACH, YIP AND DONOVAN REFERENCES
1. Walsh, P. C.: Radical prostatectomy for the treatment oflocalized prostatic carcinoma. Urol. Clin. N. Amer., 7: 583, 1980. 2. Lindner, A., deKernion, J.B., Smith, R. B. and Katske, F. A.: Risk of urinary incontinence following radical prostatectomy. J. Urol., 129: 1007, 1983. 3. Rudy, D. C., Woodside, J. R. and Crawford, E. D.: Urodynamic evaluation of incontinence in patients undergoing modified Campbell radical retropubic prostatectomy: a prospective study. J. Urol., 132: 708, 1984. 4. Raz, S. and Kaufmann, J. J.: Editorial. Urodynamics of postprostatectomy incontinence. Urol. Res., 4: 447, 1976. 5. International Continence Society: Fourth report on the standardisation of terminology of lower urinary tract function. Brit. J. Urol., 53: 333, 1981. 6. Fitzpatrick, J. M., Gardiner, R. A. and Worth, P. H. L.: The evaluation of 68 patients with post-prostatectomy incontinence.
Brit. J. Urol., 51: 552, 1979. 7. Mayo, M. E. and Ansell, J. S.: Urodynamic assessment of incontinence after prostatectomy. J. Urol., 122: 60, 1979. 8. Abrams, P.H.: Investigation ofpostprostatectomyproblems. Urology, 15: 209, 1980. 9. Reid, G. F., Fitzpatrick, J.M. and Worth, P.H. L.: The treatment of patients with urinary incontinence after prostatectomy. Brit. J. Urol., 52: 532, 1980. 10. Yalla, S. V., Karsh, L., Kearney, G., Fraser, L., Finn, D., DeFelippo, N. and Dyro, F. M.: Postprostatectomy urinary incontinence: urodynamic assessment. Neurourol. Urodynam., 1: 77, 1982. 11. Abrams, P.: Detrusor instability and bladder outlet obstruction. Neurourol. Urodynam., 4: 317, 1985. 12. Price, D. A., Ramsden, P. D. and Stobbart, D.: The unstable bladder and prostatectomy. Brit. J. Urol., 52: 529, 1980. 13. Lindner, A., Leach, G. E. and Raz, S.: Augmentation cystoplasty in the treatment of neurogenic bladder dysfunction. J. Urol., 129: 491, 1983.