Abstract
Introduction and hypothesis
The aim of this study was to assess whether prolapse repair affects voiding and whether this results in the resolution of overactive bladder syndrome (OAB).
Methods
Forty women with OAB and detrusor overactivity together with anterior wall prolapse who underwent a repair between 2003 and 2007 were studied. Each woman was assessed pre-operatively and post-operatively with a clinical assessment and cystometry. Patients were divided into those who experienced resolution of their OAB symptoms and those with persistent OAB symptoms. Wilcoxon matched pairs signed rank test was used to assess any change in flow rates between these groups.
Results
Resolution of OAB was associated with a significant increase (p = 0.049) in the maximum flow rate.
Conclusion
Improvement in voiding function may be important in symptom resolution in women with OAB and prolapse.
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Introduction
Urinary incontinence is a prevalent and distressing health problem which has been reported to affect 35% of adult women [1]. The International Continence Society defines overactive bladder syndrome (OAB) as urinary urgency with or without urge incontinence usually with frequency and nocturia, if there is no infection or proven pathology [2]. Of women with urinary incontinence, many will have OAB and 50% will have objective evidence of detrusor overactivity (DO) on cystometry [3, 4]. Uterovaginal prolapse affects 50% of parous women with 20% of these being symptomatic [5]. Eleven percent of women will have had an operation for prolapse by the age of 70 [6]. The anterior vaginal wall is the most common compartment to prolapse [7]. The socioeconomic, psychological and physical impacts of urinary incontinence and prolapse are considerable [8, 9].
Despite the association of urinary symptoms with prolapse there has been little research to identify how the conditions are linked and if there is any link to be found [10]. Previous work has suggested that there is an association between voiding and the presence of OAB and DO [11].
It may be expected that an anterior repair operation would improve voiding by relieving anatomical distortion of the urethra. The association between prolapse and OAB symptoms may be due to functional obstruction caused by the urethral distortion. We postulate that the bladder may become overactive due to hypercontractility in order to overcome the obstructive element. If this is the case, relief of the obstruction by restoring the anatomy of the anterior compartment may be expected to improve bladder emptying and lead to resolution of OAB symptoms and objective resolution of DO. The aims of our study were to evaluate whether the anterior repair operation affects voiding and whether this relieves the symptoms of OAB and DO.
Methods
This was a retrospective observational cohort study. Inclusion criteria were symptomatic anterior wall prolapse (grade II or above), either in isolation or in combination with posterior/apical compartment prolapse, with confirmed DO on cystometry. All patients complained of a lump in the vagina and/or “something coming down” and were undergoing surgery primarily for these symptoms but were found to have DO when cystometry was performed. Only women with lower urinary tract symptoms (LUTS) are routinely offered cystometry prior to surgery. Exclusion criteria included women with prolapse but the absence of DO on cystometry and women with coexistent urodynamic stress incontinence (USI). Women with USI were treated with a concurrent suburethral sling and as this may alter voiding they were excluded. Women with neurological disorders or bladder pathology identified at cystoscopy were also excluded. The study was restricted to patients undergoing a repair incorporating the anterior compartment as this was felt to be more likely to be associated with changing in voiding. All cystometry studies were performed when the patient was not taking anticholinergics.
All the women in the study group had been assessed pre-operatively with a detailed urogynaecological history and examination. Urogenital prolapse was examined for with the patient in the left lateral position and graded as 0-IV, according to the Baden–Walker Halfway system [12]. Women with LUTS underwent twin-channel subtraction normal saline cystometry, at a filling rate of 50 ml/s whilst supine and standing. Ultrasonographic measurement of bladder residual was performed prior to filling. Filling and voiding were carried out without the use of a ring pessary. Patients were asked to cough with the prolapse manually reduced to check for USI. The bladder was filled to 500 ml or until the patient requested termination of the filling phase, or experienced pain or severe urgency. A 7F double lumen catheter was used for all measurements. A voiding pressure-flow study was assessed with women sitting on a uroflow chair, at cystometric capacity. The finding of DO at this point prompted inclusion into the study. Prior to the prolapse repair, women were offered anticholinergics for their urgency symptoms. Women were not treated with vaginal oestrogens prior to surgery.
All women underwent a standard fascial anterior repair; this was performed in combination with repair of other compartments if indicated. Clamps were placed beneath the external urethral meatus and at the innermost point of the prolapse to mark out the extent of the repair. A longitudinal incision was made in the vaginal mucosa between the clamps. Forceps were placed along the incised vaginal skin edges and the pubocervical fascia was carefully dissected away from the vaginal epithelium. Two or more buttress sutures were placed laterally into the fascia and then tied in the midline using No. 1 vicryl. The redundant vaginal tissue was excised and the vaginal edges opposed using No 1 vicryl continuous locking sutures. A cystoscopy was performed in all women.
A size 14F Foley catheter was left in situ to drain the bladder and was removed on day 2 and a vaginal pack was removed on day 1. Each patient had a single dose of prophylactic antibiotic (Co-amoxiclav or cefuroxime) intra-operatively.
Post-operative assessment was undertaken at 2–3 months and then at a later date in a research clinic. Patients were assessed using a King’s Health questionnaire [13], Patient Global Impression of Improvement, clinical examination and repeat filling and voiding cystometry. A patient was considered cured of her DO if she did not show abnormal detrusor activity during the filling phase of cystometry. A patient was considered to be cured of her OAB if she did not document urgency in the symptom domain of the Kings quality of life questionnaire and denied overactive symptoms on direct questioning (denied frequency, nocturia, urgency and urge incontinence). Rises in detrusor pressure during filling, evidence of urodynamic stress incontinence (USI), cystometric capacity, maximum flow rate, volume voided, detrusor pressure at maximum flow and post-void residual volume were recorded for each patient.
The data was entered into a Microsoft Excel database, and separated into those who experienced resolution of OAB, as reflected in the relevant domains of the King’s Health Questionnaire and the PGI-I (group 1) and those who had worsening or no change in OAB symptoms (group 2). A Wilcoxon-matched pairs signed rank test was used to look for a significant change in flow rates following the anterior repair, and a student’s t-test was used to elicit any difference in maximum flow rate at baseline and post-operatively. A Fisher’s exact test was used for discrete data. A p-value of less than 0.05 was considered significant. Ethical approval was obtained from West Kent Research Ethics Committee and each patient was asked to provide informed consent.
Results
A total of 67 women were identified and invited to enter the study. Forty-nine women were successfully contacted and agreed to attend for follow-up and 40 agreed to a repeat urodynamic evaluation. Patient demographics and the surgical procedure performed are described at Table 1. DO was not observed in 24% of participants (10/40 women) who underwent repeat urodynamics, 76% of participants (30/40 women) had persistent DO. Fifty-three percent were subjectively cured of OAB (22/40 women). Thirteen women had DO on cystometry, but did not document OAB symptoms in the King’s Health Questionnaire and denied symptoms on direct questioning. There was a significant association between persistent OAB symptoms and persistent DO (17 of 18 patients with persisting symptoms had DO on cystometry, p = 0.0003). The changes in flow rate are described at Table 2.
Two of the 49 women (4%) women had symptomatic recurrent grade 2 cystoceles and were offered surgical management. These women were both in group 1. Two women in group 1 developed USI. Each was offered a TVT after conservative measures had failed to control their symptoms. Nine patients declined urodynamics and supplied qualitative data only. Of these, five had overactive bladder symptoms and one had stress incontinence symptoms, as indicated by the relevant domains of the King’s Health Questionnaire.
Eighteen patients did not respond to the invitation to take part in the study. On review of their notes, nine of these patients had no urinary symptoms at 2–3 months post-operatively. The other nine had persistent overactive bladder symptoms. Twelve of these patients were able to be contacted by telephone, and were asked about any urinary symptoms. Five of the nine patients who had been asymptomatic post-operatively were contacted and denied any recurrent urinary symptoms. Seven of the nine patients who had had persistent overactive symptoms were contacted. Of these patients, five remained on anticholinergic medications and two described very mild symptoms which did not require treatment. There was no significant difference in the presence or absence of symptoms at the time of the study between those who consented to undergoing urodynamics and those who did not (p = 0.67).
The pre- and post-operative values for voided volume and detrusor pressure at maximum flow are detailed in Table 3. The mean values for post-void residual for groups 1 and 2 were similar (16.3 vs. 18.0 ml, p = 0.72) and did not change significantly following surgery.
Discussion
The results have shown that 53% of women having prolapse surgery experience resolution of their OAB. Women in whom OAB symptoms resolve demonstrate a significant increase in maximum flow rate after the repair. In women who did not show an improvement in OAB symptoms, the maximum flow rate fell. This finding suggests that changes in flow rates may be important in the aetiology of OAB and raises the issue that impairment of flow may be important in the aetiology of OAB.
There is limited information regarding the co-existence of urinary symptoms and prolapse. One study reported that 68% of women with prolapse also complain of urgency, with 50% suffering from urge incontinence [9]. Forty-one percent of a cohort of women with severe prolapse was reported to have DO [14]. Other studies have found there to be no association between anterior wall prolapse and OAB symptoms or even voiding dysfunction [15]. A recent Cochrane review of the surgical management of pelvic organ prolapse noted that level Ia evidence concerning anterior repair and urinary symptoms is limited and inconclusive [16].
There have been several studies examining the effect of a prolapse repair on OAB which show resolution of urgency symptoms in a high proportion of patients [17–19]. There is also evidence that nonsurgical correction of prolapse may lead to similar beneficial effects on OAB symptoms. Fernando et al. reported a significant decrease in urinary urge and urge incontinence after 4 months usage of a vaginal pessary [20].
OAB and prolapse may be linked due to vaginal prolapse causing dysfunctional voiding. Impaired opening of the bladder outflow tract due to anatomical distortion leads to functional voiding impairment in these women. Previous work has implied a place for dysfunctional voiding in the pathophysiology of DO in women [10]. Women who were less obstructed after a TVT procedure were more likely to experience resolution of OAB symptoms and objective resolution of DO on cystometry. An increase in detrusor wall thickness in women with DO may be the result of obstruction causing hypertrophy of the detrusor muscle (Figs. 1 and 2) [21]. Dietz has described an anatomical basis for dysfunctional voiding in women with prolapse using ultrasound [22]. Women who had voiding dysfunction on cystometry were more likely to have ultrasound evidence of a cystocele with an intact retrovesical angle. Interestingly, the women with voiding dysfunction were also more likely to have enteroceles on ultrasound; hence, repair of the posterior vaginal wall may also have an impact on the resolution of voiding dysfunction and OAB symptoms. Further evidence to link OAB with voiding dysfunction is seen in women with prolapse and OAB treated with anticholinergics. Women with anterior wall prolapse are less likely to improve with anticholinergics. Possibly, the physical distortion caused by the prolapse results in an anatomical basis for the OAB which is less likely to be overcome with conventional drug therapy [23].
A similar obstructive mechanism (prostatic) for DO with OAB symptoms has been postulated in men. Cucchi et al. have shown that men with prostatic obstruction have a DO-related facilitation of bladder contractility [24]. A more recent study showed an increased prevalence of DO amongst men with untreated bladder outlet obstruction over a 10-year period [25]. However, there is ongoing debate regarding the relationship between obstruction and DO in men [26].
There are certain limitations relating to the above study. This is a very select population and it is possible that the results are not generalisable to all women with OAB and DO. The retrospective nature of the study may lead to bias although the proportion of women with OAB symptoms at 8-week follow-up amongst the women who did not come back for review was similar to the proportion seen in the study group. There was also no difference between those women who underwent post-operative cystometry and those who did not. The strength of the study is the use of pressure-flow data after prolapse repair, which, to the best of our knowledge, has not been previously documented. Our study is limited by the fact that anterior repair was carried out in conjunction with other prolapse procedures; this may be a potential source of bias. In practical terms, the majority of women undergoing prolapse surgery will have multi-compartmental prolapse requiring repair of more than one compartment. It would therefore be difficult and impractical to identify a population undergoing anterior repair alone. However, voiding dysfunction is not only related to anterior compartment prolapse and therefore including repairs of other compartments may be an advantage and result in a higher resolution of voiding dysfunction [22]. The time to follow-up varied between patients, although none had undergone subsequent continence or prolapse procedures in the interval between the anterior repair and follow-up. A validated instrument was not routinely used pre-operatively to assess LUTS; this does have an impact on the comparability of the study, and has been incorporated into the protocol for a larger prospective study.
It may be argued that one cannot use the term OAB in this study since the definition precludes proven pathology [2], and some may consider anterior compartment prolapse as pathology. However, there is no consensus in the literature as to whether prolapse is a true causative factor in OAB. There is a known association between the two, as has already been discussed, but no firm causative relationship. Taking individual symptoms separately, e.g. frequency and urgency, might help in deciding which symptoms of OAB are likely to improve. However, previous papers published in this area have referred to OAB, rather than taking each symptom separately [18, 19].
The group with persistent OAB symptoms had a significant fall in maximum flow rate following repair. The significance of this fall in flow rate in group 2 should be treated with caution since this is accompanied by a significant fall in volume voided. Flow rate is related to voided volume. Hence, the lower voided volume may be responsible for the lower flow rate. These finding may be consistent with worsening OAB symptoms and DO although we did not use a scale to assess symptom severity pre- and post-operatively to assess this factor. There was an increase in voided volume post-operatively in group 1, which did not reach statistical significance. It may be argued that the increase in flow rates in this group is simply a reflection of this factor. It should be noted, however, that the change in flow rates was significant, whilst the change in volume was not. Liverpool nomograms are not entirely appropriate to this situation since they relate to non-intubated flow studies; however, if the changes in volume are plotted using the Liverpool nomograms [27], they indicate an expected increase in flow of only 2 ml/s, which is less than 50% of the actual change that we found. We therefore suggest that the change in flow rates in this group reflects a true change in voiding function.
The results for detrusor pressure at maximum flow indicated that there was no change in this parameter post-operatively regardless of changes in flow rates or symptoms. We would suggest that this supports the idea that the improvement in voiding was purely due to opening up of the bladder outflow and relief of the urethral kinking caused by a cystocele. It may be commented that the PdetQmax in these patients was higher than usual pre-operatively (again, perhaps to overcome anatomical distortion caused by anterior wall prolapse) and in fact remained high, despite the improvement in flow rates and symptoms. This in itself is a factor which merits further investigation.
Despite an extensive literature search, we have been unable to find any other papers documenting an association between changes in flow rates and outcome in women with OAB and prolapse. Our findings suggest that improvement in urinary flow rates caused by prolapse repair is of importance in symptom resolution in these women. This study has raised a number of questions which need to be addressed by further research and a larger prospective study is underway. Further research will also concentrate on whether the anterior repair operation results in an anatomical change in the posterior urethrovesical angle. Possibly, failure to correct this deficit will result in persistent voiding dysfunction and OAB. The challenge for future research may be to identify how to improve flow rates consistently after the anterior repair and to elucidate the possible impact of alterations in surgical technique on this outcome.
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Acknowledgements
We would like to thank Maria Eaton, Nurse Practitioner in urogynaecology.
Ethical approval
Obtained from the West Kent Research Ethics Committee in a letter dated 22 February 2007. REC reference 06/Q1801/100.
Funding
Study funded by a grant from the UK Continence Society.
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Basu, M., Duckett, J. Effect of prolapse repair on voiding and the relationship to overactive bladder and detrusor overactivity. Int Urogynecol J 20, 499–504 (2009). https://doi.org/10.1007/s00192-009-0807-z
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DOI: https://doi.org/10.1007/s00192-009-0807-z