Neurourology and Urodynamics 1:77-87 (1982)

Postprostatectomy Urinary Incontinence: Urodynamic Assessment Subbarao V. Yalla, Lawrence Karsh, Gary Kearney, Lionel Fraser, Daniel Finn, Noel DeFelippo, and Frances M. Dyro

Department of Urology, Surgical Service (S. V. Y.) and Rehabilitation Medicine (F. M. D.), West Roxbury Veterans Administration Medical Center, and the Harvard Medical Program in Urology (Longwood Area)@. V. Y., L. K., G. K., L.F., D.F., N. D.), Boston

This communication deals with our urodynamic observations in 21 incontinent postprostatectomy patients. The factors causing incontinence were I ) persistent detrusor hyperactivity, 2) sphincter failure causing passive incontinence, and 3) a combination of the above two factors. None of the 21 subjects had any evidence of residual outlet obstruction.

Ke) words: postprostatectomj , urinar? incontinence, passive incontinence, radical prostatectomj fluid bridge test, micturitional static urethral pressure

INTRODUCTION

Urinary continence has both an active and passive component. The active con- tinence is of short duration and can only be intermittent [ 11. It is achieved by voluntary (skeletal), periurethral, and pelvic muscle contractions, whereas passive continence may be achieved by many factors such as the resting tonus of the somatic innervated periurethral voluntary muscle [2], alpha-adrenergic innervated smooth muscle [3], elastin, and collagen. In the male, continence mechanisms of the bladder outlet can be subdivided anatomically and physiologically into proximal and distal sphincter mechanisms [ I ] . The former is composed of smooth muscle in the vicinity of the bladder neck and proximal prostatic urethra, whereas the distal mechanism has two components: a) an intrinsic continence mechanism made up of the involuntary (smooth) muscle, collagen, and elastin, and b) an extrinsic mechanism made up of the voluntary (skeletal) periurethral musculature.

Several factors have been postulated to be responsible for postprostatectomy incontinence, including high-pressure detrusor contractions, residual outflow obstruc- tion, weak distal sphincter mechanism, and persistent sensory urgency [4]. However,

Address reprint requests to Dr. Subbarao V. Yalla, Department of Urology, Surgical Service and Re- habilitation Medicine, West Roxbury Veterans Administration Medical Center, Boston, M A 02 132.

0733-2467/82/0101-0077$03.50 0 1982 Alan R. Liss. Inc.

78 Yalla et al

in patients with radical prostatectomy , the incontinence usually results from inefficient sphincter mechanisms, which could either be preexistent or iatrogenic [2,5].

MATERIALS AND METHODS

Detailed urodynamic evaluation was performed in patients with intractable uri- nary incontinence developing immediately after prostatectomy . However, excluded from this study were those who were already incontinent preoperatively and those with clinically significant neurologic disorders such as spinal cord injury and multiple sclerosis. Several of these patients were operated on elsewhere and were referred to our center after unsuccessful pharmacologic and/or surgical therapy.

Urodynamic Technique Our evaluation consisted of a detailed physical examination with special em-

phasis on the neurologic assessment. The components of the actual urodynamic study were a) urethral closure pressure profiles in standing and supine positions, b) striated sphincter dynamics (21, c) outlet competence tests (fluid bridge test) [6], d) cysto- metry, and e) uroflowmetry. The entire evaluation was done with fluoroscopic mon- itoring. Electrophysiologic evaluation (electromyography and sacral evoked poten- tials) and pharmacologic testing were performed whenever necessary. Micturitional vesicourethral static pressure profiles [7] were obtained in patients who needed uro- dynamic confirmation of outlet obstruction and in those with suspect or borderline outlet obstructions. The details of the urodynamic instrumentation and technique have been described elsewhere [2,7].

RESULTS

Twenty-one incontinent postprostatectomy patients were urodynamically eval- uated and the results analyzed.

Five of the 21 patients had radical prostatectomy and 16 had transurethral resection of the prostate. Eight patients had a moderate to severe degree of detrusor hyperactivity. The latter was characterized by low cystometric bladder capacity and/ or involuntary detrusor contractions. Two of these eight subjects symptomatically improved 6 months after surgery, but still have some urge incontinence.

Thirteen of 21 patients demonstrated passive urinary incontinence. This type of incontinence was characterized by various degrees of stress incontinence. The most severe degree of incontinence has been termed “gravitational incontinence” since urine passively dribbled out in standing position, without coexistent detrusor contractile activity. The incontinence was more obvious with cough and Valsalva maneuvers that led to marked spurts of dribbling. Three patients of this passive incontinence group (V.M., V.P., A.G.) had “gravitational incontinence.”

Two of the 21 patients had a combination of detrusor hyperactivity and faulty distal sphincter mechanisms (A.G. and E.G.). One of them (E.G.) had normal per- iurethral musculature as suggested by electromyography and sacral evoked potentials.

None of these 21 patients showed either residual obstruction or high-pressure detrusor contractions.

Urodynamic Assessment of Postprostatectomy Incontinence 79

Fig. 1. V.M. Voiding cystourethrogram (VCUG) shows unobstructed outlet.

CASE SUMMARIES Case 1

This patient (V.M.) a 67-year-old male, underwent a TURP (transurethral resection of prostate) in 1979 that was complicated by postoperative urinary incontinence. He re- quired several pads daily and he leaked more while in the standing position. Cystogram and urodynamic studies were consistent with stress and gravitational incontinence (Fjgs. 1-3). These studies indicated that the patient had a severe degree of stress incontinence without any coexistent detrusor hyperactivity. The detrusor contractions were of nor- mal amplitude. He also showed periurethral muscular denervation, as suggested by the electrophysiologic studies. The pre-Kaufman device urodynamic evaluation with mod- erate perineal compression suggested that he would benefit from perineal compression prosthesis without developing outlet obstruction. Studies following insertion of the device, including voiding cystourethrogram, showed that ideal perineal compression was achieved without creating undue obstruction, thus significantly minimizing the stress

9 c

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Urodynamic Assessment of Postprostateetomy Incontinence 81

82 Yalla et a1

Fig. 4. to the prosthesis. During voiding, no obstruction occurred.

V.M. VCUG after Kaufman prosthesis implantation shows deviation of the bulbous urethra due

incontinence. The patient voided freely and demonstrated no leaking in the erect position or upon coughing, straining, or sneezing. Urodynamic studies repeated 1 week after surgery showed excellent results (Figs. 4-6).

The patient has been followed regularly in clinic and has no further incontinence at this time.

Case 2 This patient (A.G.), a 6 1 -year-old male, developed severe urinary incontinence

following a TURP 20 years ago. He later had another unsuccessful resection for what was presumed to be residual obstruction. His incontinence became worse and at the time of our evaluation it was “gravitational.” He constantly dribbled urine in a standing position and was losing large amounts during efforts that involved abdominal straining (cough, sneeze, and laughter). Cystoscopy was said to reveal apical prostatic tissue. He was then referred to our center for urodynamic evaluation to rule out residual obstruction as the cause of persistent incontinence.

Initial uroflowmetry showed no evidence of obstruction (peak flow 25 mUsec; volume 250 ml; flow time 20 sec). Urethral closure pressure profile demonstrated a closure pressure in the vicinity of the membranous urethra, encompassing 2.0 cm. length. The maximum closure pressure was 80 cm H20. The patient could not generate any voluntary periurethral striated sphincter contractions. The fluid bridge test was negative in the supine position, across the membranous and bulbous urethral regions. The test was positive, however, in a standing position (Fig. 7). The micturitional vesicourethral static pressure profile showed no evidence of outlet obstruction. The detrusor contraction pressure was 60 cm H20 and the detrusor activity could not be

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84 Yalla et al

Fig. 6. Postoperative micturitional study, recording the static pressure profile with a 5F single lumen urethral catheter. The top tracing shows the vesicourethral static pressure configuration during voiding. Two separate pressure drops can be seen in the regions of urogenital diaphragm (UGD) and the area of bulbous urethra where prosthetic compression was created (KP). R, Rectum, B, bladder; SPR, suprapubic route.

Fig. 7. A.G. Patient with severe degree of postprostatectomy incontinence has no evidence of outlet obstruction. Fluid bridge test in supine position was negative. In standing position, it was positive at membranous and bulbous urethral regions, suggesting inefficiency of distal sphincter mechanisms. The fluid bridge test [6] consists of recording urethral closure pressure at a urethral test point (membranous or bulbous urethral regions in these patients) by means of a fluid-filled urethral pressure catheter with and without fluid infusion. The competence of the sphincter regions is assessed during cough and/or Valsalva efforts. The objective of this test is to recognize whether or not a bridge of fluid bolus is established between the bladder and the urethral test point. The test is considered positive (incompetent sphincter) if a bolus of fluid reaches the urethral test point and synchronously registers a pressure elevation response via the noninfused urethral pressure catheter (dry catheter). Such synchronous elevation of urethral pressure with cough will not be seen if the proximal urethral region is competent and prevents escape of fluid from the bladder through its outlet. In this patient, during cough efforts (C), registration of bulbous urethral pressure elevations occurred only in standing position, although no infusion was allowed through the pressure recording catheter.

86 Yalla et al

suppressed in a standing position. Also, the patient could void with Valsalva, without a coexistent detrusor contraction. He was treated with a Kaufman’s prosthesis with excellent results.

This case represents the participation of minimal detrusor hyperactivity and inefficiency of the distal sphincter mechanisms as the causative factors of postpros- tatectomy incontinence.

Case 3 This patient (E.G.), a 58-year-old male with a history of severe urgency, fre-

quency, and nocturia, was treated by with TURP. He developed severe postoperative incontinence that was erroneously considered to be secondary to residual prostatic obstruction. Further resection of the apical prostatic tissue aggravated his incontinence to “gravitational incontinence .” Urodynamic study revealed detrusor hyperactivity and impairment of the sphincter mechanisms. However, the periurethral striated musculature was normal as evidenced by sacral evoked potentials and electromyog- raphy . The patient improved with parasympatholytic agents and with some recovery of the intrinsic component of the distal sphincter mechanims. He continues to have mild urgency and has no incontinence.

This patient’s problem thus represented temporary impairment of the intrinsic distal sphincter mechanism and long-standing detrusor hyperactivity.

DISCUSSION

Although factors responsible for the onset of postprostatectomy incontinence have been described, the precise factor(s) responsible in an individual patient cannot be determined without an adequate urodynamic evaluation. These physiologic eval- uations will not only determine the diagnosis, but in addition they may help the urologist to formulate an appropriate plan for treatment. In our present analysis, the factors responsible for postprostatectomy incontinence have been 1) detrusor hyper- activity without residual obstruction, 2) inefficient distal sphincter mechanisms, and 3) a combination of both. Although it is popularly believed that residual prostatic obstruction (usually apical tissue) and high-pressure detrusor contractions could lead to postprostatectomy incontinence, these detailed studies did not support such views. We therefore suggest that any repeat prostatic surgery for patients with postoperative urinary incontinence is not justified unless residual obstruction is established uro- dynamically.

Several patients in this series had subclinical neurologic deficits involving the periurethral and pelvic floor musculature and these deficits could be recognized only with detailed urodynamic evaluation that included electrophysiologic testing. Some patients, indeed, had clinicaily significant peripheral neuropathies (diabetes-and ethanol- related) that were not given enough attention before prostatic surgery was undertaken. It is our belief that patients with inefficient periurethral musculature resulting from such neuropathies, are prone to varying degrees of postoperative passive incontinence. In these situations, the intrinsic mechanisms are not effectively supported (or rein- forced) by the periurethral or pelvic musculature. Consequently, depending upon the degree of bladder neck and prostatic resection and the degree of periurethral muscular hypofunction, different degrees of incontinence might result. We always stress, there- fore, the importance of evaluating the conus reflex activity of the patient before

Urodynamic Assessment of Postprostatectomy Incontinence 87

undertaking extensive prostatic resection. Patients with neuropathies who exhibit poor voluntary periurethral musculature are warned of the probability of incontinence and we avoid aggressive prostatic resection in the vicinity of verumontanum in such patients.

Eight of the 21 patients with postprostatectomy incontinence had detrusor hy- peractivity that had probably been present preoperatively . We have been unable to attribute this hyperactivity to any significant neurologic disorder. None of these patients revealed any evidence of upper motor neuron disease. In the absence of an overt neurologic lesion they are categorized as having an unstable detrusor [8]. However, neurologic followup must be frequently performed since detrusor hyper- activity may be an early manifestation of a neurologic disorder [9].

REFERENCES 1. Turner-Warwick RT: Clinical problems associated with urodynamic abnormalities with special ref-

erence to the value of synchronous cine/pressure/flow cystography and the clinical importance of detrusor function studies. In Lutzeyer W, Melchior H (eds): “Urodynamics-Upper and Lower Urinary Tract.” New York: Spring-Verlag, 1973, p 237.

2. Yalla SV, DiBenedetto M, Fam BA, Blunt KJ, Constantinople N, Gabilondo FB: Striated sphincter participation in distal passive urinary continence mechanisms. Studies in male subjects deprived of proximal sphincter mechanism. J Urol 122:655, 1979.

3. Donker PJ, Ivanovici F, Noach EL: Analysis of the urethral pressure profile by means of electro- myography and the administration of drugs. Br J Urol 44:180, 1972.

4. Worth P Urinary incontinence in the male. Urol Clin North Am 6199, 1979. 5 . Hauri D: Urinary continence after radical prostatectomy. The urodynamic proof of an anatomical

hypothesis. Urol Int 32:149, 1977. 6. Brown M, Sutherst JR: A test for bladder neck competence: The fluid bridge test. Urol Int Br J Urol

34:403, 1979. 7. Yalla SV, Sharma GVRK, Barsamian E: Micturitional static urethral pressure profile: A method of

recording urethral pressure profile during voiding and the implications. J Urol 124549, 1980. 8. International Continence Society. Fourth report on the standardization of terminology of lower urinary

tract function-Terminology related to neuromuscular dysfunction of the lower urinary tract. Br J Urol 53:333, 1981.

9. Hebjorn S, Andersen JT, Walter S , Mouritzen Dam A: Detrusor hyperreflexia: A survey on its etiology and treatment. Scand J Urol Nephrol 10:103, 1976.