Does Uroflow Predict ISD?

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1 Neurourology and Urodynamics 27:40 44 (2008) Does Uroflow Predict ISD? Phillip P. Smith* and Rodney A. Appell Scott Department of Urology, Baylor College of Medicine, Houston, Texas Aim: The term superflow has been given to abnormally high flow rates in women, and has been thought to be indicative of intrinsic sphincteric deficiency (ISD), as ISD is associated with low urethral pressure. Pelvic organ prolapse (POP) damages the sphincteric mechanism extrinsic to the urethra. The aim of this study was to determine if ISD can be predicted from voiding flow rates in women with symptomatic POP. Methods: The charts of 82 patients who had undergone surgery for repair of symptomatic vaginal prolapse were reviewed. Uroflow and urodynamic endpoints were compared between dry and stress incontinent patients, and correlations between abdominal leak point pressures (LPP) and pressure/flow data evaluated. Results: Average maximum flow (Q max ) at uroflow was greater than at urodynamics with no significant difference in voided volumes. Twenty eight patients were found to have urodynamic stress incontinence (SUI), and an additional 19 to have occult stress incontinence. Patients with SUI had higher flow rates at urodynamics than continent patients. Voiding detrusor pressures and flow rates were not different when categorized by LPP cutoffs of 100 and 60 cm/w. Abdominal leak point pressure did not significantly correlate with any uroflow or urodynamic pressure/flow parameter. Conclusions: Flow rates, whether determined by uroflow testing or at urodynamics, are not predictive of ISD as defined by a low abdominal leak point pressure, in patients with symptomatic POP. Either the effect of ISD on flow rates is a non-linear complex relationship or LPP does not adequately define ISD. Neurourol. Urodynam. 27:40 44, ß 2007 Wiley-Liss, Inc. Key words: urinary incontinence; urodynamics (G ); stress (C ; C ) INTRODUCTION The stress urinary continence mechanism has been considered to have two fundamental components, an extrinsic anatomic system, and an intrinsic sphincteric mechanism. 1 The normal urethra offers some impedence to voiding flow. Women with an impaired intrinsic urethral sphincteric function have been thought to have decreased outflow resistance to flow, resulting in abnormally high voiding urine flow rates, termed superflow. 2,3 The finding of superflow is thus thought to denote the low pressure urethra of intrinsic sphincteric deficiency (ISD). As defined by severe SUI in the absence of urethral hypermobility, ISD is associated with increasing age, menopausal status, previous surgery, a positive supine empty stress test, leakage during cystometry and shorter functional urethral length. 4 Leak point pressures (LPP) have been advocated as a defining feature of ISD, based upon the finding that SUI resulting from increased abdominal pressure (or detrusor pressure in the neurologically impaired patient) bears little relationship to maximal urethral pressures. 5 Anterior vaginal laxity and urethral hypermobility compromise the sphincteric mechanism extrinsic to the urethra Patients with stress incontinence can therefore be classified according to LPP and urethral mobility, although these categories are not mutually exclusive. 11 Urethral hypermobility is not predictive of stress urinary incontinence, 12 implying that intrinsic urethral sphincteric function is able to compensate for the defective extrinsic mechanisms in many women. Anterior prolapse correlates well with urethral hypermobility, and virtually all patients with POP-Q Stage II (within 1 cm of the introitus) anterior prolapse or greater demonstrate urethral hypermobility. 13 Therefore, by compromising the external sphincteric function, anterior vaginal prolapse should result in a greater dependence upon intrinsic urethral sphincteric function for stress urinary continence. We hypothesized that if elevated flow rates are due to impaired urethral outflow resistance, LPPs should be inversely related to voiding urine flow rates and thus confirm the principle of superflow. Any correlation should be enhanced in women with anterior prolapse due to their increased reliance upon the intrinsic urethral sphincteric mechanism. We therefore conducted a review of pre-operative urodynamic studies in women undergoing surgery for symptomatic vaginal prolapse. MATERIALS AND METHODS The charts of all patients who underwent surgery for vaginal prolapse in our practice between July 2004 and December 2005 were reviewed. Charts were excluded from review if the patient underwent urethrolysis, fistula repair, complex surgery, or did not have a urodynamic study performed. Data extracted included age and parity, history of symptoms of irritative, obstructive or urinary incontinence symptoms, history of prior prolapse or incontinence surgery, initial POP- Q stage for anterior, apical and posterior compartments, urethral mobility (fixed, normal, or strain angle >30 degrees), and post void residual. Uroflow and videourodynamic parameters, procedure(s) performed, and postoperative No conflict of interest report by the author(s). Dirk De Ridder led the review process. Abbreviations: Q ave, average flow rate; Q max, maximum flow rate; P detmax, maximum voiding detrusor pressure; P detqmax, detrusor pressure at maximum flow; LPP, abdominal leak point pressure; SUI, (urodynamic) stress incontinence; ISD, intrinsic sphincteric deficiency; POP, pelvic organ prolapse. *Correspondence to: Phillip P. Smith, MD, Division of Voiding Dysfunction and Female Urology, Scott Department of Urology, Suite 2100, Scurlock Tower, 6560 Fannin Ave., Houston, TX ppsmith@bcm.tmc.edu Received 12 March 2007; Accepted 19 April 2007 Published online 26 June 2007 in Wiley InterScience ( DOI /nau ß 2007 Wiley-Liss, Inc.

2 Uroflow, LPP, and ISD 41 obstructive, irritative, and urinary incontinence symptoms were recorded. Obstructive symptoms included hesitation, poor stream, incomplete emptying, retention, dribbling. Irritative symptoms included urgency, frequency, nocturia. Incontinence symptoms included both urge and stress incontinence symptoms. Urodynamic Evaluation All patients in the reviewed charts underwent uroflow and videourodynamic study prior to surgery, utilizing Laborie Aquarius TT hardware and software (Laborie Medical Technologies, Williston, VT). Studies were conducted by an experienced Fellow and a technician according to ICS recommendations, 14 with the following exceptions. Videofluoroscopy was utilized in all studies to aid in the evaluation of prolapse and voiding function. During the time period of this study, a change was made from fluid-filled to microtip catheters. All catheters were 7 Fr. The rectal and bladder catheters were zeroed to static rectal/bladder pressures prior to infusion. The initial infusion rate was 60 ml/min, and slowed to ml/ min if detrusor overactivity was provoked by the faster rate. Patients were in a sitting position for the study. Valsalva and cough abdominal leak point pressures were determined at 150, 200, and ml. The lowest abdominal pressure producing observed leakage at any of these points was recorded as the abdominal leak point pressure (LPP). In patients with vaginal prolapse in which the leading part was past the introitus, reduction testing was performed if no stress incontinence was observed without reduction. Manual reduction or vaginal packing was used at the preference of the physician. Voided volume and maximum flow rates were obtained at unistrumented uroflow study. Voided volume, maximum and average flow rates, maximum voiding detrusor pressure, detrusor pressure at maximum flow, and post-void residual volumes during urodynamic voiding study were recorded. Statistics The data was sorted according to urodynamic continence status into three groups, no stress incontinence (dry), stress incontinent (SUI), and stress incontinent only with prolapse reduction (occult SUI). The latter two groups together constitute the wet group. Parametric data were compared between groups using Student t-test or ANOVA as appropriate. Categorical data were compared using Fischer exact test or chi-square for trend. A correlation matrix of LPP and voiding urodynamic parameters was constructed, and relationships demonstrating r 2 > 0.25 tested further, in addition to the planned correlation calculations with LPP. Pearson correlation and multiple regression analysis was performed to assess relationships between leak point pressures and flow rates, volume voided and detrusor pressures, as well as between flow rates and voided volume and detrusor pressures. Due to the small sample size, no tests for normality were made. For correlations not including leak point pressures, regressions were calculated for the full group of patients, as well as in stress-incontinent patients only. RESULTS The charts of 111 patients were reviewed, The records of 29 patients were excluded, due to urethrolysis (8), vesicovaginal fistula repair (1), revision of prior sacrocolpopexy (1), or radical cystectomy (1), and no urodynamic studies (17), leaving 82 charts for data extraction. Average age, gravity and parity were 62.2 years, 3.0 and 2.8, respectively. At the initial office visit, 59 (72%) of patients complained of incontinence, 51 (62%) of irritative symptoms, and 44 (54%) of obstructive symptoms. Twenty three (28%) had undergone at least one prior operation for prolapse, and 25 (56%) had undergone at least one prior operation for incontinence. At urodynamics, 29 patients had SUI without reduction of their prolapse, and an additional 19 had SUI upon prolapse reduction, for a total of 48 wet patients. Thirty-four patients had no demonstrable stress incontinence and were considered dry. Table I presents the mean values of historical and clinical examination findings in the three groups. Three stress-incontinent patients had a non-hypermobile (>30 degrees change with strain) urethra. The three groups did not differ with respect to gravidity, parity, history of prior incontinence or prolapse surgery, posterior and apical prolapse, presence of urethral hypermobility, and uroflow parameters. Patients with occult incontinence were older than patients with SUI. All patients with SUI had stress incontinence symptoms, unlike the other two groups. Patients with SUI had an average anterior POP-Q stage of 1.9, significantly less than dry or occult incontinent patients. Dry patients had a larger PVR than stress incontinent patients. At urodynamics, dry patients voided less volume than those with occult incontinence. Patients with SUI had a faster maximum flow rate (Q max ) than did dry or occult incontinent patients. No other statistically significant differences between these groups were found at urodynamics. Combining all three groups, average maximum flow rate at unistrumented uroflow (16.5þ/ 11 ml/sec) was significantly greater than at urodynamics (12.4þ/ 6.1 ml/sec) (P ¼ 0.02). Average voided volumes were not significantly different between uroflow and urodynamics. Q max at uroflow was correlated with the volume voided (r 2 ¼ 0.25, P ¼ ). Q max at urodynamics was also significantly correlated with volume voided (r 2 ¼ 0.22, P ¼ ), however Q ave demonstrated no significant correlation with voided volume. Pressure/flow data were categorized according to LPPs of 100 cm/w (CMS/Medicare cutoff value for ISD) and 60 cm/w. 5 Using these cutoff points, no significant differences between high and low LPP groups for any flow parameter were observed. These data are presented in Table II. Of the 28 patients with urodynamic SUI without reduction, LPPs were determined in 23 patients. No significant correlation was found between uroflow rate and LPP using Pearson correlation calculations. An additional 8 LPPs were determined in those patients stress incontinent only after reduction of POP. There was no significant correlation between uroflow rate and LPP in the total group of wet patients. A plot of LPP as a function of Q max at uroflow is presented in Figure 1. There were no significant correlations of voided volume, flow rates, or pressures with LPP at urodynamic voiding study in SUI or all wet patients. Elimination of two patients with exceptionally high flow rates (50 cm/sec) did not alter these results. Multiple regression analysis testing for the relationship of LPP to pressure and flow parameters at urodynamics demonstrated a significant correlation (r 2 ¼ 0.53, P ¼ 0.044) with the urodynamic parameters Q max (b ¼ 6.6, P ¼ 0.013), Q ave (b ¼ 11.1, P ¼ 0.031) and P detqmax (b ¼ 0.98, P ¼ 0.009). Testing for multicollinearity in this model revealed none. DISCUSSION Normal voiding flow rates in unobstructed, uninstrumented women have been reported to average ml/sec, with peak flows of ml/sec Flow rates increase with

3 42 Smith and Appell TABLE I. Patient Data Categorized and Compared According to Stress Continence Status SUI Dry Occult SUI n Mean s.e.m. Mean s.e.m. Mean s.e.m. ANOVA Age (years) SUK < occult, P < 0.05 g n.s. P n.s. SUI symptoms P Surgical history Incontinence n.s. Prolapse n.s. POPO stage Anterior SUI < dry, occult, P < 0.01 Posterior n.s. Apical n.s. Hypermobile n.s. PVR (ml) SUK < dry, P < 0.05 Uroflow Volume voided ml n.s. Q max (ml/w) n.s. Urodynamics Volume voided ml dry < occult, P < 0.01 Q max (ml/w) SUI > dry, occult, P < 0.05 Q ave (ml/w) n.s. P detmax (cm/w) n.s. P detqmax (cm/w) n.s. SUI, stress urinary incontinence; dry, absence of stress incontinence and occult stress incontinence; occult SUI, stress incontinence only with reduction of vaginal prolapse; Q max,maximumflowrate;q ave, average flow rate; P detmax, maximum voiding detrusor pressure; P detqmax, detrusor pressure at maximum flow; statistical comparisons by ANOVA for continuous data, and chi-square test for categorical data, P < 0.05 significant. voided volume and decrease with age, 15 thus making a precise definition of normal flow rate difficult. Light arbitrarily defined super flow as flow rates in excess of 50 ml/sec, 3 and felt this represented particularly severe stress urinary incontinence. The term superflow in the context of voiding does not otherwise appear in the primary literature. A low pressure urethra offers less impedence to urine flow during sudden increases in intra-abdominal pressure, and thus may result in higher voiding flow rates. Consequently, abnormally high flow rates have been thought to be indicative of the low pressure urethra of ISD. The primary finding of this study is that flow rates obtained from an uninstrumented void are not correlated with abdominal leak point pressures at urodynamics in women with symptomatic prolapse and stress urinary incontinence. If some cutoff value for abdominal leak point pressure (LPP) is considered as the definition of ISD, then isolated flow rates obtained at uroflow or urodynamics cannot be used to predict ISD. Superflow may therefore be a flawed concept insofar as LPPs cannot be predicted from flow rates. Whether or not superflow (or uroflow rates) can be utilized as a measure of incontinence severity, a decision point for treatment, or a predictor of treatment outcomes, was not tested by this study. The definition, identification, and meaning of ISD are problematic, and this fact contributes to the interpretation of our findings. The concept of an impaired sphincteric action inherent to the urethra, distinct from sphincteric failure due to bladder neck or proximal urethral mobility, was initially as a fixed urethra with poor urethral closing function. 19 This was termed low pressure urethra, to be distinguished from genuine stress urinary incontinence due to urethral hypermobility. The components of the intrinsic urethral sphincteric mechanism include factors such as mucosal adhesion, the urethral vascular plexes, the urethral connective tissue (both collagen and elastin), and the smooth muscle of the urethra. 20 These provide a urethral closure function intrinsic to the urethra TABLE II. Uroflow and Voiding Pressure/Flow Data Categorized and Compared According to Leak Point Pressure Cutoff Values of 100 cm/w and 60 cm/w Uroflow Q max (ml/sec) Urodynamic Q max (ml/sec) Urodynamic Q ave (ml/sec) P detmax (cm/w) P detmax (cm/w) LPP n Mean s.e.m. Mean s.e.m. Mean s.e.m. Mean s.e.m. Mean s.e.m. <100 cm/w >100 cm/w P n.s. n.s. n.s. n.s. n.s. <60 cm/w >60 cm/w P n.s. n.s. n.s. n.s. n.s. Q max,maximumflowrate;q ave, average flow rate; P detmax, maximum voiding detrusor pressure; P detqmax, detrusor pressure at maximum flow; statistical comparison using student t-test, P < 0.05 significant.

4 Uroflow, LPP, and ISD 43 Fig. 1. Plot of leak point pressure as a function of maximum flow rate at uninstrumented void. No statistically significant correlation by Pearson r, with and without the exclusion of the two 50 ml/sec flow rates. itself, and failure of this mechanism is usually due to prior surgery and, less often, neurologic disease. 21 The specific terminology intrinsic sphincter deficiency (ISD) is more recent, first appearing in the literature in the early 1990s in relationship to incontinent women who were felt to be good candidates for prosthetic sphincters 22 or men who were rendered incontinent following TURP. 23 The categorization of the cause of stress urinary incontinence as ISD or hypermobility was formalized by the Agency for Health Care Policy and Research, who defined ISD as A cause of stress urinary incontinence in which the urethral sphincter is unable to contract and generate sufficient resistance in the bladder, especially during stress maneuvers. 24,25 The identification of ISD has been variously made by history and clinical examination, with or without radiologic investigation of the bladder neck, 4,19,26,27 by leak point pressures which in principle address the relationship of the expulsive force of the bladder to the resistive effort of the urethral tube, and by urethral pressures which are meant to quantitate the resistance of the urethra to opening Complicating the debate about the identification of ISD 34,35 is a lack of clarity about the meaning of ISD. Intrinsic sphincteric deficiency may be considered as a statement about the pathogenesis of SUI, 1,11,36 an indicator of the severity of incontinence, 37 or as a prognostic construct regarding treatment outcomes These groupings may not be mutually exclusive. The potential sphincteric components extrinsic to the urethra include the integrated striated muscle contiguous with the pubococcygeus, the fascial attachments to the ATFP, and the anterior vaginal wall (which may include a suburethral fascia) normally attached to the ATFP. 20 Several mechanisms have been proposed by which these tissues external to the urethra provide a stress continence mechanism, including a suburethral hammock against which the urethra can be compressed, 41 urethral stretching between the mid-urethral attachments to the pubis and levator complex, 8 and prevention of differential wall motion due to mid-urethral anchoring. 7 In fact, the full functions of these extrinsic mechanisms are probably redundant and interrelated as demonstrated by the success of the mid-urethral tension-free sling despite its inconsistent effect on urethral hypermobility. 9,42,43 Anterior vaginal prolapse and urethral hypermobility compromise these mechanisms 10,33,44 and thus result in a greater dependence upon closure mechanisms intrinsic to the urethra. We therefore examined the relationship of LPP to flow rate in a group of women with POP in order to minimize any contribution of extrinsic sphincter mechanisms on flow rate. Our primary findings contrast with previous work demonstrating higher flow rates and lower detrusor pressures in women with ISD defined by LPP or closure pressures. 45,46 However, these studies evaluated women having surgery for SUI, both with and without vaginal prolapse. More advanced prolapse has been associated with lower flow rates. 47 Obstructed voiding in women with advanced prolapse is relieved with pessary reduction, 48 suggesting the lower flow rates are due to urethral kinking rather than an intrinsic urethral effect. Patients with SUI in our study had significantly less anterior prolapse than did dry and occult incontinent patients, which is consistent with our finding of higher flow rates in patients with SUI. Additionally, the average urodynamic pressure/flow data in our SUI patients does not suggest obstructed voiding. We interpret these findings to mean that any modifying or obstructive effect of the sphincter function external to the urethra were minimized in our SUI cohort, and thus any association between LPP and flow rates in this study are indeed representative of intrinsic sphincter function. The dependence of flow rate on urethral and anterior vaginal support also casts further doubt on the ability of flow rates to predict intrinsic urethral sphincter function. We identified a significant complex correlation of LPP with a combination of maximum and average flow rates and voiding detrusor pressure at maximum flow, signifying that leak point pressures are in fact a function of intrinsic urethral characteristics. McGuire argued that once flow begins, the pressure required to flow urine is a function not of abdominal pressure, but of urethral characteristics. 30 Thus, LPP may represent a combined effect of intrinsic and extrinsic sphincteric/urethral function, whereas voiding flow rates in the absence of obstructive prolapse more accurately reflect the instrinsic characteristics of the urethra. Alternatively, since our analysis evaluated the possibility of a linear relationship between LPP and flow rate and found none, the complex correlation we found with pressure/flow parameters could mean that a non-linear relationship between LPP and uroflow exists. Our secondary findings that flow rates in a catheterized void are less than in an uninstrumented void, and are dependent upon voided volume, are consistent with previous studies. 16,47,49,50 In the case of our urodynamic pressure/flow findings, the increased flow observed to accompany higher voided volumes may be due to a degree of voiding obstruction in the dry patients, as suggested by the higher voiding pressures and greater post-void residual volume in the dry group. CONCLUSIONS Voiding flow rates do not predict low leak point pressures, therefore superflow is not a valid concept in stress incontinent women with prolapse. Intrinsic sphincteric deficiency is an imprecise term, needing clarification regarding its definition, identification, and meaning. Pressure/flow studies might identify women with impaired intrinsic sphincter mechanisms in the absence of obstructive prolapse. Further study is required to determine the prognostic value of these parameters in the treatment of SUI. 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