UvA-DARE (Digital Academic Repository) Voiding dysfunction ... · Prevention and treatment:...

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UvA-DARE is a service provided by the library of the University of Amsterdam (http://dare.uva.nl) UvA-DARE (Digital Academic Repository) Voiding dysfunction after vaginal prolapse surgery: etiology, prevention and treatment Hakvoort, R.A. Link to publication Citation for published version (APA): Hakvoort, R. A. (2012). Voiding dysfunction after vaginal prolapse surgery: etiology, prevention and treatment. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Download date: 08 Mar 2021

Transcript of UvA-DARE (Digital Academic Repository) Voiding dysfunction ... · Prevention and treatment:...

Page 1: UvA-DARE (Digital Academic Repository) Voiding dysfunction ... · Prevention and treatment: Standard prolonged catheterisation and catheterisation when indicated For decades gynaecologists

UvA-DARE is a service provided by the library of the University of Amsterdam (http://dare.uva.nl)

UvA-DARE (Digital Academic Repository)

Voiding dysfunction after vaginal prolapse surgery: etiology, prevention and treatment

Hakvoort, R.A.

Link to publication

Citation for published version (APA):Hakvoort, R. A. (2012). Voiding dysfunction after vaginal prolapse surgery: etiology, prevention and treatment.

General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s),other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons).

Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, statingyour reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Askthe Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam,The Netherlands. You will be contacted as soon as possible.

Download date: 08 Mar 2021

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Chapter

Introduction and outline of the thesis

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Clinical problem of incomplete voidingPelvic organ prolapse (POP) is a common disease 1-3 for which a significant number of patients will require and demand surgical correction in order to correct anatomical abnormalities and to restore normal pelvic floor function. 4 After this type of surgery sometimes a total inability to void develops (urinary retention) and more frequently the problem of incomplete bladder emptying occurs resulting in an abnormal postvoid residual volume (PVR). With a prevalence of 1 to 22% the occurrence of this incomplete voiding is one of the most frequent complications directly related to vaginal prolapse surgery.5-7 When incomplete voiding is left untreated, the bladder can be stretched beyond its physical limits which can decrease achievable detrusor pressure and change elasticity. 8-10 This can lead to impairment of bladder function in the long term. 8,9

To prevent such sequelea, bladder drainage through catheterisation is applied. However, often the initiation and continuation of catheterisation in hospitalised patients is poorly indicated.10-13 Reported reasons for prolongation of catheterisation are negligence (i.e. forgetting the presence of a catheter) and convenience for nursing staff.11, 14 Also a large practice variation exists in type and duration of catheterisation. Presumably, a lack of evidence can be held accountable for this practice variation. To improve awareness and recognition, to develop optimal preventive measures and to optimise treatment more evidence is needed that evaluates common practice and to optimise this practice.

Prevention and treatment: Standard prolonged catheterisation and catheterisation when indicatedFor decades gynaecologists routinely applied bladder catheterisation for several days after vaginal prolapse surgery.12 This postoperative standard insertion of a catheter may initially be prompted by the presence of a vaginal gauze, by inhibition of bladder sensibility and contractility through the action of anaesthetics and by impaired mobility of the patient post-operatively. It can also be considered necessary to prolong catheterisation as postoperative pain15, urethral elevation16 and peri-urethral oedema and/or innervation trauma17 may hamper optimal emptying of the bladder. Although such prolonged catheterisation appears relatively safe and straightforward, it proved to be unnecessary after vaginal hysterectomy.18 Furthermore, catheterisation inevitably increases the risk of urinary tract infections and results in longer hospital stay, more discomfort and higher disappointment for patients about the treatment they received.19,20 As the majority of patients does not encounter the problem of incomplete voiding the standard postoperative insertion of catheters for longer durations implies that a majority of patients receives suboptimal treatment. Therefore it could be rational to restrict standard catheterisation to the period of impaired

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mobility and the possible negative influence of anesthetics on bladder function has not worn out yet. After this period of standard catheterisation a proportion of patients will require additional treatment because of the occurrence of abnormal post void residual volume. When this complication has been diagnosed, again a great variation seems to exist between departments regarding the choice for type of catheterisation and the continuation of catheterisation. Most likely this results from the absence of studies and guidelines regarding this matter.

EtiologySome risk factors have been identified for incomplete voiding after vaginal prolapse surgery. Identification of such risk factors is relevant as it could be used to adjust preventive strategies and treatment regimens. Contrary to vaginal prolapse surgery, more risk factors are known for development of incomplete voiding after incontinence surgery. Some of the identified mechanisms for the development of abnormal post void residual volume after this type of surgery may also account for prolapse surgery. We will explore the aetiology of incomplete voiding after vaginal prolapse surgery by identifying more risk factors for incomplete voiding after vaginal prolapse surgery.

Detrusor underactivityDetrusor underactivity has been defined by the international continence society as a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span. 20 It can be influenced by the following factors.

AgeIn clinical studies of patients undergoing incontinence surgery a negative effect of age on voiding postoperatively was demonstrated.10, 21-25 In other studies age was related to detrusor underactivity and a reduced sensation to bladder filling. 26, 27 On a morphological level these phenomena can be explained by a reduction in axonal content 27 and changes in neurotransmission. 28

Influence of anestheticsAnaesthetic agents used in general anaesthesia can reduce bladder function by suppression of the pontine micturition center (animal studies). 29,30

Intrathecally administered local anesthetics block neurons of the sacral spinal cord (S2–S4). The action is by blocking the transmission of the afferent and efferent information of nervous fibers from and to the bladder.31 The block as a rule wears off within 7-8 hours. To prolong the duration of sensory block with spinal anesthesia

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intrathecal opoids can be administered. These agents inhibit bladder contractility and can increase bladder capacity. The duration of this effect on the bladder is dependent on the type of opoid used and the administered dose but will last maximally 24 hours. 32, 33 For the purpose of analgesia in vaginal prolapse surgery, which are in general relatively short lasting operations, intrathecal opoids are seldomly administered. In the clinical studies in this thesis analgesia was mostly reached using a spinal block without addition of opoids. Therefore, on the role of anesthetics in postoperative incomplete voiding will not be focused in this thesis.

Surgical damage to innervation of the bladderIt has been well established that innervation trauma of the bladder can be a consequence of major pelvic and colorectal surgery. 34, 35, 36 Although it is likely that dissection and suturing part of the bladder wall in the case of anterior repairs can also result in innervation trauma, it has not been proved. Indirect evidence comes from one study in which a higher stage preoperative anterior wall prolapse was found to be a predictor for the occurrence of abnormal post void residual volumes postoperatively. 17 This can be explained by a more extensive dissection with higher stage prolapse surgery and innervation damage of the bladder as a consequence. 17

AnxietyWe hypothesise that anxiety can be of influence in the development of incomplete voiding after vaginal prolapse surgery. Anxiety is likely to obstruct bladder outflow through an alfa adrenergic stimulation of the bladder outlet 8, 26, 37 and also by pelvic floor contraction. 38 The idea that, pre- and postoperatively, anxiety levels rise while patients are faced with hospitalisation, loss of autonomy and (an unusual) request for efficient micturition is supported in literature. 39-41 The negative effect of posing such conditions to patients was illustrated by the observation in another study that a request for micturition in a hospitalised environment led to an absolute inability to void in 8 of 18 (44%) otherwise healthy non surgical subjects. 41

PainPain is an inevitable consequence of surgery. It is known that it can negatively influence bladder function through central inhibition and is likely to cause bladder outflow obstruction through a disturbed relaxation of the pelvic floor. This has been mentioned as a possible cause of voiding impairment postoperatively. 8,19, 26, 37 Support for this hypothesis comes from studies in patients undergoing proctological and posterior compartment surgery. Although there is no direct anatomical relationship

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between the surgical site and the bladder in such patients, they are however still at risk of developing incomplete voiding. 15,17

ObstructionThe assumption that postoperative edema, haematoma formation and/or urethral elevation can contribute to a bladder outlet obstruction (BOO) leading to voiding disorder is widespread. 6, 42-44 However, no evidence exists to support this hypothesis. There are no urodynamic studies combining flow parameters with detrusor pressure available to establish the cause of incomplete voiding following vaginal prolapse surgery. A few studies have investigated mixed populations of incontinence and prolapse surgery. In these studies vaginal prolapse surgery shows an increase of incomplete voiding in the first few days which wears off in the longer run while incontinence procedures tend to result in incomplete voiding for longer periods. Therefore, the observed voiding disorder seems to be dominated by direct postoperative effects of the surgery 24,45 and for longer term voiding disorders incontinence surgery plays a more important role. An explanation could be a more obstructive nature of stress-incontinence surgery. 16,23, 46 This is supported by the finding that the degree to which the bladder neck is elevated and the type of bladder neck suspension are both predictive for incomplete voiding after incontinence surgery. 16,23

At the time the studies in this thesis were designed it was common practice to routinely prolong indwelling catheterisation for several days after vaginal prolapse surgery. 12,13

Further, these catheterisation protocols varied to a great extent which implied suboptimal treatment for many patients. Further, no evidence existed concerning the optimal technique and duration of treatment of incomplete voiding after surgery. Nor was there any insight in patient preferences for treating incomplete voiding and finally, the etiology of incomplete voiding after vaginal prolapse surgery was unknown. This all is important as it could give direction to new preventive strategies.

Objectives of this thesisThe following objectives were identified: 1. To determine the preferred practice and practice variation in Dutch hospitals

concerning bladder care management after vaginal prolapse surgery. 2. To optimise postoperative bladder care. The first aim is to optimise the duration

of the commonly applied standard bladder catheterisation after vaginal prolapse surgery. The second aim is to optimise the actual treatment of an established abnormal PVR and further insight will be provided in the preferences of patients.

3. To understand the underlying mechanisms of abnormal PVR.

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(2009). Symptomatic pelvic organ prolapse and possible risk factors in a general population. Am J Obstet Gynecol 200(2),184.

2. Tegerstedt G, Maehle-Schmidt M, Nyrén O, Hammarström M (2005). Prevalence of symptomatic pelvic organ prolapse in a Swedish population. Int Urogynecol J Pelvic Floor Dysfunct 16(6),497-503.

3. MacLennan AH, Taylor AW, Wilson DH, Wilson D (2000). The prevalence of pelvic floor disorders and their relationship to gender, age, parity and mode of delivery. BJOG 107(12):1460-70.

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9. Carpenter FG (1983). Impairment and restoration of rat urinary bladder responsiveness following distension. Am J Physiol (Regulatory Integrative Comp Physiol (13) 244: R106-Rl13

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12. Hilton P (1988). Bladder drainage: a survey of practices among gynaecologists in the British Isles. BJOG 95,1178-89.

13. Ottesen M, Møller C, Kehlet H, Ottesen B (2001). Substantial variability in postoperative treatment, and convalescence recommendations following vaginal repair. A nationwide questionnaire study. Acta Obstet Gynecol Scand 80(11), 1062-8.

14. Saint S, Wiese J, Amory JK, Bernstein ML, Patel UD, Zemencuk JK et al. (2000). Are physicians aware of which of their patients have indwelling urinary catheters? Am J Med 109:476-80.

15. Kleeman S, Goldwasser S, Vassallo B, Karram M (2002). Predicting postoperative voiding efficiency after operation for incontinence and prolapse. Am J Obstet Gynecol 187(1), 49-52.

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16. Bombieri L, Freeman RM, Perkins EP, Williams MP, Shaw SR (2002). Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? BJOG 109, 402-412.

17. Steinberg BJ, Finamore PS, Sastry DN, Holzberg AS, Caraballo R, Echols KT (2010). Postoperative urinary retention following vaginal mesh procedures for the treatment of pelvic organ prolapse. Int Urogynecol J Pelvic Floor Dysfunct. 2010 Dec;21(12):1491-8.

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20. Elkadry EA, Kenton KS, FitzGerald MP, Shott S, Brubaker L (2003). Patient-selected goals: a new perspective on surgical outcome. Am J Obstet Gynecol 189(6), 1551-7

21. Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, van Kerrebroeck P, Victor A, Wein A; Standardisation Sub-committee of the International Continence Society (2002). The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 21(2), 167-78.

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23. Kobak WH, Walters MD, Piedmonte MR (2001). Determinants of voiding after three types of incontinence surgery: a multivariable analysis. Obstet Gynecol 97(1), 86-91

24. Sokol AI, Jelovsek JE, Walters MD, Paraiso MF, Barber MD (2005). Incidence and predictors of prolonged urinary retention after TVT with and without concurrent prolapse surgery. Am J Obstet Gynecol 192(5), 1537-43.

25. Haylen BT, Lee J, Logan V, Husselbee S, Zhou J, Law M (2008). Immediate postvoid residual volumes in women with symptoms of pelvic floor dysfunction. Obstet Gynecol 111(6), 1305-12.

26. De Groat WC, Downie JW, Levin RM, Lin ATL, Morrison JFB, Nishizawa O, WD Steers, Thor KB (1999). Basic neurophysiology and neuropharmacology. In: Abrams P, Khoury S, Wein A, eds. Incontinence . Plymouth, UK: Health publication Ltd, 107-154.

27. Gilpin SA, Gilpin CJ, Dixon JS, Gosling JA, Kirby RS (1986). The effect of age on the autonomic innervation of the urinary bladder. Br J Urol 58(4), 378-81.

28. Yoshida M, Homma Y, Inadome A, Yono M, Seshita H, Miyamoto Y, Murakami S, Kawabe K, Ueda S (2001). Age-related changes in cholinergic and purinergic neurotransmission in human isolated bladder smooth muscles. Exp Gerontol 36(1):99-109.

29. Matsuura S, Downie JW (2000). Effect of anesthetics on reflex micturition in the chronic cannula-implanted rat. Neurourol Urodyn 19(1), 87-99.

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30. Combrisson H, Robain G, Cotard JP (1993). Comparative effects of xylazine and propofol on the urethral pressure profile of healthy dogs. Am J Vet Res 54(12):1986-9.

31. Kamphuis ET, Ionescu TI, Kuipers PW, de Gier J, van Venrooij GE, Boon TA (1998). Recovery of storage and emptying functions of the urinary bladder after spinal anesthesia with lidocaine and with bupivacaine in men. Anesthesiology 88(2), 310-6.

32. Kuipers PW, Kamphuis ET, van Venrooij GE, van Roy JP, Ionescu TI, Knape JT, Kalkman CJ (2004). Intrathecal opioids and lower urinary tract function: a urodynamic evaluation.Anesthesiology 100(6), 1497-503.

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34. Lupton EW (1986). Management of urinary outflow obstruction after pelvic surgery: a review. J R Soc Med 79(12), 734-7.

35. Mundy AR (1982). An anatomical explanation for bladder dysfunction following rectal and uterine surgery. Br J Urol 54(5):501-4.

36. Schönberger B (2003). [Bladder dysfunction and surgery in the small pelvis. Therapeutic possibilities]. Urologe A 42(12), 1569-75.

37. Morrison JF (1995). The excitability of the micturition reflex. Scand J Urol Nephrol Suppl 175, 21-5.

38. Van der Velde J, Laan E, Everaerd W (2001). Vaginismus, a component of a general defensive reaction. An investigation of pelvic floor muscle activity during exposure to emotion-inducing film excerpts in women with and without vaginismus. Int Urogynecol J Pelvic Floor Dysfunct 12(5), 328-31.

39. Hoff SD, Bailey HR, Butts DR, Max E, Smith KW, Zamora LF, Skakun GB (1994). Ambulatory surgical hemorrhoidectomy--a solution to postoperative urinary retention? Dis Colon Rectum 37(12), 1242-4.

40. Renzi C, Peticca L, Pescatori M (2000). The use of relaxation techniques in the perioperative management of proctological patients: preliminary results. Int J Colorectal Dis 15(5-6), 313-6.

41. Blok BF, Sturms LM, Holstege G (1998). Brain activation during micturition in women. Brain 121 (11), 2033-42.

42. Wiser WL, Morrison JC, Loveday GL, McIntosh RE, Kennedy BS, Shaw BH, Fish SA (1974). Management of bladder drainage following vaginal plastic repairs. Obstet Gynecol 44(1):65-71.

43. Jannelli ML, Wu JM, Plunkett LW, Williams KS, Visco AG (2007). A randomized controlled trial of clean intermittent self-catheterization versus suprapubic catheterization after urogynecologic surgery. Am J Obstet Gynecol 197(1), 72.

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45. Partoll LM (2002). Efficacy of tension-free vaginal tape with other pelvic reconstructive surgery. Am J Obstet Gynecol 186(6),1292-5

46. Komesu YM, Rogers RG, Kammerer-Doak DN, Olsen AL, Thompson PK, Walters MD (2007. Clinical predictors of urinary retention after pelvic reconstructive and stress urinary incontinence surgery. J Reprod Med 52(7), 611-5.

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