Libro Incont Orina P Abrams

UNDERSTANDING STRESS URINARY INCONTINENCE
Paul Abrams Walter Artibani
This booklet is published by Ismar Healthcare. Its publication was supported by an educational grant from Lilly and Boehringer Ingelheim. Prof. P. Abrams (Bristol, UK) and Prof. W. Artibani (Verona, Italy) reviewed the content of this booklet. Although all reasonable care has been taken to supply complete and accurate information, Ismar Healthcare does not assume liability for any errors or omissions. The views and opinions expressed do not necessarily represent the views of the publisher, the reviewers or the sponsors. Please direct all correspondence to Ismar Healthcare, Berlarij 104, 2500 Lier, Belgium Eli Lilly and Company and Boehringer Ingelheim 2004 All rights reserved.
Foreword
Stress urinary incontinence is a frequent and bothersome condition in many women and has a significant impact on their and their partners quality of life. Still many of these women suffer in silence and do not seek medical advice or delay a consultation until symptoms become very severe. This is due to the fact that patients are not only embarrassed to admit that they are incontinent, but also because they are not very well informed about this condition. Many women still believe that incontinence is a natural part of aging and they are afraid that surgery is the only treatment option available. Educating women suffering from stress urinary incontinence, therefore, seems to be essential in order to optimise the management of this disease. This booklet is intended for healthcare professionals involved in the management of women with stress urinary incontinence. The reader will receive a short overview and the latest status on several topics related to urinary incontinence in general and stress urinary incontinence in particular. The topics included range from the anatomy, physiology and innervation of the lower urinary tract in females to the epidemiology, aetiology, diagnosis and treatment of stress urinary incontinence. The current unmet needs in the management of this condition and questions which are frequently raised by patients suffering from the condition are also discussed. These may be of help in improving the education of women with stress urinary incontinence and eventually to the improved management of these patients. We are grateful to Eli Lilly and Boehringer Ingelheim for sponsoring the publication of this booklet.
Paul Abrams
Walter Artibani
List of abbreviations
ACE ACh AR CNS DO GAX ICI ICS IDC ISD LUT LUTD LUTS MUI NA NSAID PFM PFMT PMC POP PPA PVR QoL RCT SUI TCA TVT UDS UI USI UTI UUI Angiotensin converting enzyme Acetylcholine Adrenoceptor Central nervous system Detrusor overactivity Gluteraldehyde cross-linked bovine International Consultation on Incontinence International Continence Society Involuntary detrusor contraction Intrinsic sphincter deficiency Lower urinary tract Lower urinary tract dysfunction Lower urinary tract symptoms Mixed urinary incontinence Noradrenaline Nonsteroidal anti-inflammatory drug Pelvic floor muscles Pelvic floor muscle training Pontine micturition centre Pelvic organ prolapse Phenylpropanolamine Post-void residual Quality of life Randomised controlled trial Stress urinary incontinence Tricyclic antidepressant Tension-free vaginal tape Urodynamic studies Urinary incontinence Urodynamic stress incontinence Urinary tract infection Urge urinary incontinence
Table of Contents
1 1.1 1.2 1.2.1 1.2.2 1.2.3 1.3 1.3.1 1.3.2 Female lower urinary tract anatomy, physiology and neural control ............................ 9 Basic anatomy of the female lower urinary tract ....................................................................11 Lower urinary tract innervation and the normal micturition cycle .................................12 Storage phase (bladder filling).........................................................................................................13 Conscious inhibition of the micturition reflex............................................................................13 Voiding phase (bladder emptying)................................................................................................14 Neurotransmitters.................................................................................................................................14 Role of serotonin and noradrenaline ............................................................................................14 Role of glutamate...................................................................................................................................15 Summary ...................................................................................................................................................16 2 2.1 2.2 2.2.1 2.2.2 2.2.3 2.2.4 2.3 Definitions, classification and types of urinary incontinence ...........................................17 Definitions of urinary incontinence................................................................................................19 Classification of urinary incontinence..........................................................................................19 Symptoms.................................................................................................................................................19 Signs ............................................................................................................................................................19 Urodynamic observations ...............................................................................................................20 Conditions ................................................................................................................................................20 Types of urinary incontinence ........................................................................................................20 Summary ...................................................................................................................................................21 3 3.1 3.2 3.3 3.4 4 4.1 4.1.1 4.1.2 4.1.3 4.2 4.2.1 4.2.2 4.3 Stress urinary incontinence: symptom, sign, urodynamic observation and condition ...............................................................................................................23 The symptom of stress urinary incontinence.........................................................................25 The sign of stress urinary incontinence ....................................................................................25 The urodynamic observation of stress urinary incontinence ........................................25 The condition of stress urinary incontinence .........................................................................25 Epidemiology of stress urinary incontinence .........................................................................27 Prevalence of urinary incontinence in women ......................................................................29 Overview of prevalence of urinary incontinence..................................................................29 Reasons for variation in prevalence of urinary incontinence......................................... 30 Prevalence of urinary incontinence by age..............................................................................31 Prevalence of different types of urinary incontinence in women..................................31 Overall prevalence of the most common types of urinary incontinence ..................31 Prevalence of the most common types of urinary incontinence by age .................33 Racial differences in prevalence of stress urinary incontinence ..................................34 Summary ..................................................................................................................................................34 5 5.1 5.1.1 5.1.2 5.1.3 5.1.4 5.2 Aetiology of stress urinary incontinence...................................................................................35 Main risk factors associated with urinary incontinence....................................................37 Predisposing factors ...........................................................................................................................37 Inciting factors ....................................................................................................................................... 38 Promoting factors.................................................................................................................................39 Decompensating factors ..................................................................................................................41 Pelvic floor disorders............................................................................................................................41 Summary ..................................................................................................................................................42
6 6.1 6.2 6.3
Impact of stress urinary incontinence on the patients quality of life ...........................43 Bother associated with stress urinary incontinence ..........................................................45 Stress urinary incontinence and quality of life ........................................................................45 Stress urinary incontinence and healthcare seeking behaviour .................................45 Summary ..................................................................................................................................................46
7 7.1 7.2 7.3
Pathophysiology of stress urinary incontinence................................................................... 47 Stress continence versus stress incontinence.....................................................................49 Urethral hypermobility ........................................................................................................................49 Intrinsic sphincter deficiency...........................................................................................................50 Summary ..................................................................................................................................................50
8 8.1 8.1.1 8.1.2 8.1.3 8.1.4 8.1.5 8.2 8.3
Diagnosis of stress urinary incontinence ..................................................................................51 Initial evaluation of women complaining of stress urinary incontinence...................53 History and general assessment .................................................................................................53 Symptom assessment ......................................................................................................................53 Physical examination ..........................................................................................................................54 Baseline tests..........................................................................................................................................54 Office-based tests of urinary function .......................................................................................54 Specialised management................................................................................................................55 Symptoms suggestive of a diagnosis of stress urinary incontinence .......................56 Summary ..................................................................................................................................................57
9 9.1 9.1.1 9.1.2 9.2 9.2.1 9.2.2 9.2.3 9.3 9.3.1 9.3.2 9.3.3 9.3.4 9.3.5
Treatment of stress urinary incontinence.................................................................................59 Conservative treatment .....................................................................................................................61 Lifestyle interventions ..........................................................................................................................61 Pelvic floor muscle training ...............................................................................................................61 Pharmacological treatment .............................................................................................................61 1-Adrenoceptor agonists................................................................................................................62 Tricyclic antidepressants ..................................................................................................................62 Oestrogens..............................................................................................................................................62 Surgical treatment................................................................................................................................63 Urethral bulking agents......................................................................................................................63 Sub-urethral sling procedures.......................................................................................................64 Colposuspensions...............................................................................................................................66 Artificial sphincter..................................................................................................................................67 Summary of surgical treatments ..................................................................................................67 Summary ..................................................................................................................................................68
10 10.1
Costs associated with stress urinary incontinence ............................................................69 Economic burden of stress urinary incontinence.................................................................71 Summary ..................................................................................................................................................72
11 11.1 11.2
Unmet needs in managing stress urinary incontinence...................................................73 Awareness ............................................................................................................................................... 75 Treatment modalities .......................................................................................................................... 75 Summary ..................................................................................................................................................76
12 13 14 15
Frequently asked questions by patients on stress urinary incontinence ................. 77 Summary ..................................................................................................................................................83 Current guidelines in urinary incontinence ..............................................................................87 References ...............................................................................................................................................91
1
Female lower urinary tract anatomy, physiology and neural control
1.1
Basic anatomy of the female lower urinary tract

The lower urinary tract (LUT) comprises the bladder and urethra in a functional unit serving the two purposes of storage and voiding during the micturition cycle (Figure 1-1) [1-3]. The bladder neck area becomes funnel-like at the start of micturition to facilitate urine flow into the proximal part of the urethra.
1
Figure 1-1:
The female LUT. (Reproduced with permission of Elsevier [3].)
The urinary bladder is a hollow, muscular organ which acts as a compliant reservoir for urine. It comprises the bladder body, in which urine collects, and the bladder wall. The bladder wall is composed of several layers, including the smooth muscle of the detrusor which allows the bladder to expand without pressure rise during bladder filling, and which is responsible for bladder contraction during voiding. The trigone is a small muscular triangular area, lying at the posterior wall of the bladder, next to the bladder neck which, among other functions, prevents reflux of urine to the upper urinary tract during voiding. At the uppermost angles of the trigone the 2 ureters enter the bladder; at the lowermost apex of the trigone is the opening of the bladder through the bladder neck into the urethra. The female urethra is a fibro-muscular tube of approximately 3.5 cm long. Its wall consists of an inner layer of smooth muscle fibres, an outer layer of striated muscle fibres, and non-muscular elements including the mucosa, sub-mucosal vessels and connective tissue (Figure 1-2).
Figure 1-2 :
Urethral sphincteric mechanisms (cross - section). Structures of the sphincteric mechanism are shown in bold face. The smooth muscle consists of an inner circular sheet and outer longitudinal sheet. (Reproduced with permission of Lippincott Williams & Wilkins [4].)
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Two urethral sphincteric mechanisms are involved in controlling urine flow in women: the bladder neck smooth muscle sphincter and the striated muscle sphincter, also called the rhabdosphincter. The smooth muscle sphincter at the bladder neck begins at the junction of the bladder and the urethra and extends down most of the length of the urethra. This sphincter is under involuntary control to keep the bladder and the upper urethra closed during the storage phase. This is less well developed in women and often becomes incompetent in later life, even though the woman is continent. The rhabdosphincter is composed of striated muscle fibres which are under voluntary control. It is thickest in the anterior middle 2-thirds of the urethra, while proximally and distally it is horseshoe-shaped and intermingled posterior with connective tissue in the anterior wall of the vagina. In addition to the structures in the LUT, the pelvic floor is critical for urinary continence (Figure 1-3). The pelvic floor muscles (PFM or levator ani muscles) support and maintain the position of the bladder neck and urethra, and allow compression of the urethra against the anterior vaginal wall. This is important, particularly when physical activities produce a sudden increase in abdominal pressure and the bladder neck tends to thrust downward.
Figure 1- 3 :
Female urethra and surrounding structures (cross - section). (Adapted with permission of Elsevier [5].)
1.2
Lower urinary tract innervation and the normal micturition cycle

The normal micturition cycle with its alternating urinary storage and voiding phases requires an adequate interplay between the reservoir and outlet functions of the LUT structures, including the detrusor muscle, the urethral smooth muscle, the rhabdosphincter and the PFM [1]. The control of these functions is complex and involves the central nervous system (CNS) and the afferent sensory and efferent somatic and autonomic divisions of the peripheral nervous system. At each level of neural control, different pathways and neurotransmitters are involved [6]. The peripheral motor innervation of the LUT involves parasympathetic, sympathetic, and somatic efferent nerves [1], as illustrated in Figure 1-4.
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1
Figure 1- 4 :
Neural pathways involved in bladder filling and voiding. (Reproduced with permission of Elsevier [3].)
The parasympathetic nerves emanate from the sacral spinal cord and traverse the pelvic nerve. The sympathetic nerves originate in the thoracic-lumbar spinal cord and travel through the hypogastric nerve. The somatic motor innervation to the striated rhabdosphincter originates in a circumscribed region of the sacral spinal cord, Onufs nucleus, and traverses the pudendal nerve. Direct sacral fibres innervate the levator ani [3]. Afferent sensory nerve fibres coursing along the same routes, conduct sensory signals from the bladder wall and the urethra to the spinal cord. The pontine micturition centre (PMC), located in the brain stem, coordinates the contraction of the detrusor smooth muscle and relaxation of the bladder neck and the rhabdosphincter during voiding. It is under conscious control of the cerebral cortex.
1.2.1 Storage phase (bladder filling)

When urine starts to accumulate during bladder filling, distension of the bladder activates stretch receptors in the bladder wall and generates afferent sensory signals that are transmitted to the CNS. These impulses cause reflex activation of the sympathetic nucleus in the thoraco-lumbar spinal cord which activates the efferent sympathetic fibres of the hypogastric nerve to release noradrenaline (NA) peripherally. At the neuroeffector junctions in the detrusor and urethral smooth muscles, NA mediates urine storage respectively through activation of 3 -adrenergic receptors to relax the detrusor smooth muscle and stimulation of 1A-adrenergic receptors to induce contraction of the urethral smooth muscle. During filling, the efferent somatic fibres of the pudendal nerve are also activated and release acetylcholine (ACh) peripherally which stimulates nicotinic receptors in the striated rhabdosphincter inducing its contraction. Because the bladder is relaxed and the sphincters are contracted, the pressure in the urethra overcomes that of the bladder and urine loss is prevented.
1.2.2 Conscious inhibition of the micturition reflex

When the bladder reaches its threshold capacity, stimuli from the bladder are transmitted to the PMC in the brainstem in order to initiate voiding. However, the cerebral cortex can consciously facilitate or inhibit this micturition reflex. If it 13
is decided to postpone micturition until a convenient time to urinate occurs, the cerebral cortex suppresses the parasympathetic impulses from the PMC (which induce detrusor smooth muscle contraction: see 1.2.3) and sends signals to the LUT to contract the rhabdosphincter and the levator ani.
1.2.3 Voiding phase (bladder emptying)

If the desire/need to urinate becomes strong enough, the PMC stimulates output from the parasympathetic nucleus in the spinal cord causing release of ACh from the pelvic parasympathetic efferent fibres. ACh acts on muscarinic (M3) receptors of the detrusor smooth muscle to induce bladder contraction. Simultaneously the PMC sends impulses to the pudendal motor nucleus, which inhibits the activity of the pudendal nerve, allowing the rhabdosphincter to relax. These coordinated effects of detrusor contraction, relaxation of the urethral smooth muscle and rhabdosphincter and relaxation of the levator ani results in increased detrusor pressure and reduced urethral pressure and permits the bladder to empty.
1.3
Neurotransmitters
Ongoing animal and early human studies have attributed a key role to the monoamine neurotransmitters, serotonin (5-hydroxytryptamine) and NA, in the central control of the LUT. Most studies have indicated that central serotonergic activation inhibits bladder sensory mechanisms, inhibits bladder parasympathetic excitatory efferent pathways, augments the sympathetic activity to the bladder and urethra and enhances the somatic motor input to the rhabdosphincter [7-12]. NA variably affects the LUT, depending on the receptor subtype with which it interacts [13-18]. At Onufs nucleus in the sacral spinal cord, terminals of nerve tracts from higher centres in the CNS (the medulla and locus ceruleus) synapse with the pudendal motor neurons (Figure 1-5). Animal studies have shown that the neurotransmitters, serotonin and NA, are involved at this level of interaction [12,19-21] and facilitate from Onufs nucleus the impulses that travel along the pudendal motor fibres to release ACh at the rhabdosphincter neuroeffector junction inducing its contraction.
1.3.1 Role of serotonin and noradrenaline
Figure 1- 5 :
Dense populations of noradrenergic and serotonergic motor neuron terminals were demonstrated in a discrete area of the ventral horns of the spinal cord, known as Onufs nucleus. No other motoric area in the spinal cord is currently known to have similar high concentrations of serotonin and NA. (Reproduced with permission of Wiley- Liss Inc., a subsidiar y of John Wiley & Sons, Inc. [19].)
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1.3.2 Role of glutamate

Glutamate plays an important role as a neurotransmitter in both supraspinal efferent tracts and in the afferent limb of the micturition reflex [1]. Though the exact function of glutamate has not been definitely established, it is believed that glutamate functions as the obligatory on switch to initiate rhabdosphincter contraction and that removal of glutamatergic synaptic input is the signal for sphincter relaxation during voiding. Based on pharmacological studies of facial motor neurons it would be predicted that serotonin and NA only amplify the excitatory effect of glutamate on the rhabdosphincter motor neurons [22]. Therefore, it is likely that prolonging the effect of endogenous serotonin and NA results in contraction of the rhabdosphincter during bladder filling but not during voiding (Figure 1-6).
Storage
Glutamate
Serotonin
NA
1
Sacral Spinal Cord DC DH LF
Bladder
VH
5HT-2-R
1-R
Pudendal nerve
Nic-R
Onuf's nucleus Lateral motor nucleus
ACh rhabdosphincter
Voiding
Glutamate
Sacral Spinal Cord DC DH LF VH
Serotonin
NA
Bladder
5HT-2-R
1-R
Pudendal nerve
Nic-R
Onuf's nucleus Lateral motor nucleus

Figure 1- 6 :
ACh
rhabdosphincter
Suggested roles of glutamate, serotonin and NA in the storage and voiding phase of the micturition cycle. During the storage phase, serotonin and NA facilitate the ef fects of glutamate in Onufs nucleus to stimulate ACh release from the pudendal ner ve which acts on nicotinic receptors to contract the rhabdosphincter. During the voiding phase, glutamate signal is inactive, and hence serotonin and NA also lack ef fect, resulting in rela xation of the rhabdosphincter. Black = inactive. (Reproduced with permission of Blackwell Publishing [23].)
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Summary
Several pathways and neurotransmitters are involved in the neural control of the LUT. The sympathetic hypogastric nerve and its neurotransmitter NA are involved in muscle and
3 -adrenoceptor (AR) mediated relaxation of detrusor smooth 1A-AR mediated contraction of urethral smooth muscles
thus promoting bladder storage. Bladder storage is also promoted by the somatic pudendal nerve and its neurotransmitter ACh inducing nicotinic receptor mediated contraction of the striated rhabdosphincter. The activity of the pudendal nerve is controlled by glutamate whose action is facilitated by the neurotransmitters serotonin and NA in Onufs nucleus in the lower spinal cord. Voiding is initiated by removal of glutamate, the inhibition of the sympathetic and somatic nervous system and the activation of the parasympathetic nervous system which releases ACh inducing M3 receptor mediated detrusor smooth muscle contraction. The processes of urine storage and voiding are under CNS control in the pontine micturition centre.
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2
Definitions, classification and types of urinary incontinence
2.1
Definitions of urinary incontinence

Over the last decades, the definitions of urinary incontinence (UI) have varied widely. In 1979, Bates and colleagues defined UI as an involuntary loss of urine, which is objectively demonstrable and causes a social or hygienic problem (previous International Continence Society (ICS) definition) [24]. Diokno et al, in 1986, described UI as loss of urine of any volume beyond voluntary control [25]. Variation in definitions makes it extremely difficult to compare results from different studies and undermines progress in the research of UI. Therefore, in 2002 the ICS updated the standardisation of terminology and definitions in LUT function. This was in order to agree on and subsequently consistently use the same uniform terms and definitions of conditions associated with LUT dysfunction (LUTD) such as UI [26].
2
2.2
Classification of urinary incontinence

The ICS has defined 4 levels at which LUTD such as UI can be described: as a symptom, sign, urodynamic observation or condition as a whole.
2.2.1 Symptoms
Symptoms are the subjective indicator of a disease or change in condition as perceived by the patient, caregiver or partner and may lead him/her to seek help from healthcare professionals. Symptoms may either be volunteered or described during the patients interview and are usually qualitative. However, LUT symptoms (LUTS) cannot be used to make a definite diagnosis [26]. According to the ICS, the symptom of UI is the complaint of any involuntary leakage of urine. UI occurs during the storage phase and should be further described by type, frequency, severity (= frequency x amount), precipitating factors and quality of life (QoL), the measures used to contain the leakage and whether or not the individual seeks or desires help. Validated symptoms and QoL questionnaires are instruments to describe the symptoms of UI.
2.2.2 Signs
Signs are observed by the physician during further examination including the use of simple means to verify symptoms and quantify them. The sign of UI is described as urine leakage seen during examination by the physician and this may be urethral or extra-urethral. Extra-urethral incontinence is defined as the observation of urine leakage through channels other than the urethra.
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2.2.3 Urodynamic observations

Urodynamic observations are observations made during urodynamic studies (UDS). These urodynamic observations may have a number of possible underlying causes and do not necessarily represent a definite diagnosis of a disease or disorder. Different symptoms and signs can accompany the urodynamic observations. There are 2 principal methods of urodynamic investigations used to measure intra-vesical pressure within the bladder and abdominal pressure surrounding the bladder. The detrusor pressure representing passive and active forces in the bladder wall is estimated by subtracting the abdominal pressure from the intra-vesical pressure (Pdet=P ves - Pabd). Conventional UDS normally take place in the urodynamic laboratory and usually involve artificial bladder filling via a catheter with a specified liquid at a specified rate. Ambulatory UDS are more physiological tests of the LUT, utilising natural filling with urine, and allows the patient to reproduce every day activities. Bladder and urethral function need to be assessed during filling and voiding. Detrusor overactivity (DO) is the urodynamic observation of involuntary detrusor contractions (IDCs) during bladder filling and can result in UI. An incompetent urethral closure mechanism will allow leakage of urine in the absence of detrusor contractions, e.g. during increases in abdominal pressure due to effort or exertion, coughing or sneezing (USI, urodynamic stress incontinence). Urethral relaxation incontinence is leakage due to urethral relaxation in the absence of raised abdominal pressure or DO.
2.2.4 Conditions
The condition of UI is defined by the presence of urodynamic observations associated with characteristic symptoms or signs and/or non-urodynamic evidence of relevant pathological processes.
2.3
Types of urinary incontinence

The 3 most common types of UI are stress urinary incontinence (SUI), urge urinary incontinence (UUI) or a combination of stress and urge UI called mixed urinary incontinence (MUI). Based on the symptoms, signs or urodynamic observations, these types of UI can be described as outlined in Table 2-1.
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Table 2-1:
The 3 most common types of UI described as a symptom, sign or urodynamic obser vation [26].
Type of UI Stress Urinary Incontinence
Symptom The complaint of involuntary leakage on effort or exertion, or on sneezing or coughing
Sign The observation of involuntary leakage from the urethra, synchronous with exertion/effort, or sneezing or coughing
Urodynamic observation Urodynamic stress incontinence is the involuntary leakage of urine during increased abdominal pressure in the absence a detrusor contraction Urgency is the sudden compelling desire to void during filling cystometry DO incontinence is due to IDCs during filling cystometry
Urge Urinary Incontinence
Mixed Urinary Incontinence
The complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing
Not defined by the ICS
The urodynamic observation of both USI and DO incontinence during the same test is MUI.
Summary
In the past, various definitions to study LUTD such as UI made it very difficult to compare results of different studies. In 2002, the ICS has updated the terminology and definitions of LUTD such as UI. LUTD can be classified at 4 different levels: as symptoms, signs, urodynamic observations or as the condition as a whole. The symptoms are the patients complaints taken from medical history when the patient visits a physician. The signs are the objective observations made by the physician during further examination. Urodynamic studies such as filling cystometry and pressure flow studies can give further insight in the cause of the condition. The symptom of UI is the complaint of any involuntary leakage of urine which can be differentiated in 3 major types: SUI, UUI and MUI. The symptom of SUI is the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing. The symptom of UUI is the complaint of involuntary leakage accompanied by or immediately preceded by urgency. The symptom of MUI is the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing.
The complaint of involuntary leakage accompanied by or immediately preceded by urgency. Urgency is the complaint of a sudden compelling desire to pass urine, which may be difficult to defer
Not defined by the ICS
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3
Stress urinary incontinence: symptom, sign, urodynamic observation and condition
As discussed in Chapter 2, according to the ICS, SUI can be defined at 4 levels: as a symptom, a sign, a urodynamic observation or a condition (Table 2-1) [26]. For more information on the diagnosis of SUI, it is also referred to Chapter 8.
3.1
The symptom of stress urinary incontinence

The symptom of SUI is the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing.
3.2
The sign of stress urinary incontinence

In the physicians office, SUI can be observed as the involuntary leakage of urine from the urethra, synchronous with exertion or effort, or sneezing or coughing. The physician may perform a cough stress test by asking the patient to cough with a full bladder and then objectively assess the leakage of urine.
3
Stress urinary incontinence: symptom, sign, urodynamic observation and condition
3.3
The urodynamic observation of stress urinary incontinence

Urodynamic stress incontinence (USI) is noted during filling cystometry and is defined as the involuntary leakage of urine during increased abdominal pressure (due to e.g. physical effort or exertion, sneezing or coughing), in the absence of IDCs. Coughing may induce a detrusor contraction, hence the sign of SUI is only a reliable indication of urodynamic SUI when leakage occurs synchronously with the first proper cough and stops at the end of that cough. Stress leakage is presumed to be due to raised abdominal pressure, resulting in raised bladder pressure, with the urethra being unable to resist this pressure increase. USI is now the preferred term of the ICS for what was formerly know as genuine stress incontinence.
3.4
The condition of stress urinary incontinence

The ICS has not specifically classified SUI as a condition. It is, however, clear that this is a combination of the symptoms, signs and/or urodynamic observations of USI.
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4
Epidemiology of stress urinary incontinence
4.1
Prevalence of urinary incontinence in women

UI is a distressing disorder which has a major impact on the QoL of incontinent patients. Although it is very common in the female population, it is believed to be considerably underreported. The prevalence of UI is the probability of being incontinent within a defined population and at a defined point in time, estimated as the ratio of the number of incontinent respondents identified in a cross-section survey to the number of all respondents in the survey [27].
4.1.1 Overview of prevalence of urinary incontinence

Over the past decades, various studies were carried out to assess the prevalence of UI in the general population. These studies differ in definitions of UI (e.g. frequency of UI episodes, severity, degree of bother), types of UI, population studied (e.g. age, ethnicity, institutionalisation or community-dwelling) as well as the study design and the means of assessment/data collection (e.g. postal questionnaire or personal interview, self-reporting or clinical assessment). Therefore, a wide variety of prevalence rates have been reported. Most studies performed are epidemiological studies using questionnaires to assess the prevalence of UI, based on self-reported symptoms. An overview of several studies sheds light on the prevalence of UI in the female population (Table 4-1). Overall, the prevalence of UI ranged from 11% to 72%. In the EPINCONT study, which included the largest number of patients and where the definition of UI as any involuntary loss of urine was used, 25% of the 27,936 women living in a county in Norway from 1995-1997 reported having UI [28]. A recent literature review including many world-wide studies also showed that the prevalence of UI in women was 27.6% (range 4.8-58.4%) [29].
4
29
Table 4 -1:
Over view of dif ferent studies assessing the prevalence of UI in women.
Reference Yarnell [30] Diokno [25] Sandvik [31] Samuelsson [32] Hgglund [33] Simeonova [34] Samuelsson [35] Ueda [36] Bortolotti [37] Moller [38] Temml [39] Sampselle [40] Burgio [41] Hannestad [28] Minassian [29] Hampel [42]
(3) (2)
N of women in study population 1,000 434 1,820 491 3,076 2,176 491 968 2,767 2,860 1,262 3,258 523 27,936 -
Age (years) 17 60 20 20-59 18-70 20 20-59 40-80 40 40-60 20-96 42-52 14-42 20 30 30-60 >60
Prevalence of UI (%) 45 (1) 37.7 29.4 27.7 26 14 27.9 53.7 11 72 26.3 56.9 11.3 25 27.6 51 24.5 23.5
(1) At least one episode of UI during the previous year. (2) Meta-analysis of 35 epidemiological surveys. 21 studies investigated women only; in 14 studies both males and females were assessed. (3) Meta-analysis of 48 epidemiological studies. Reported figures are based on the analysis per age group.
4.1.2 Reasons for variation in prevalence of urinary incontinence

The design of most epidemiological studies assessing UI in the general population is very straight forward. Percentages of UI are reported without control for confounding factors, stratification or multivariate analysis. However, assessing the prevalence of UI in a larger population should involve stratification for differences in the population studied and differences in study design. Various differences in the study population can contribute to inconsistent results. For example, the prevalence of UI varies with age and in institutions more UI will be reported (not only because institutionalised women are older). Moreover, the availability and efficacy of healthcare around the world may influence the prevalence of UI reported and so regional and cultural differences are important factors. Variations in study design (e.g. definitions for UI, the type of questions in the questionnaires etc.) further lead to differences in study results. Most studies done in the past used different definitions for UI and this might contribute to the wide variety of prevalence rates reported. The lack of one good definition leads to problems when assessing sensitivity and specificity of the epidemiological findings in these surveys. Different severity levels based on time and/or amount of urine leakage are used to classify UI. To further complicate the matter, UI is a chronic and dynamic condition that often starts slowly and comes and goes for a considerable time period before it becomes fully established. If people get used to their UI or notice it less, it can interfere with the assessments. Furthermore, the format of the questions about UI 30
can influence the outcome because of skewed answers based on social and perceived differences, personal hygiene and coping ability. Low response rates may further bias the prevalence estimates and the major problem is the unknown difference between responders and non-responders. Incontinent women may not answer because of embarrassment or, on the contrary, will respond to a greater extent because they are interested in the matter [27].
4.1.3 Prevalence of urinary incontinence by age

The EPINCONT study also reported on the prevalence of UI by age. In women, the prevalence of UI augmented with increasing age and produced an early prevalence peak in midlife and a steady increase from 60 years onwards (Figure 4-1).
45 40 35 Percentage of women 30 25 20 15 10 5 0 Total 25-29 35-39 45-49 55-59 65-69 75-79 85-89 Age
4
Figure 4 -1:
The prevalence of UI in women by age. (Reproduced with permission of Health Publication Ltd [28].)
The recent extensive literature review by Minassian et al [29] confirmed the relationship between prevalence of UI and age. The median prevalence of any UI had 2 peaks, one at the 5th decade (45-54 years) and another at the 8th decade (75-84 years) of life.
4.2
Prevalence of different types of urinary incontinence in women

Most epidemiological studies assess the prevalence of the different types of UI based on symptoms with different questions in the survey. Although prevalence of SUI, UUI and MUI, like the prevalence of UI in general, varied widely amongst the various populations studied because of different reasons as described above, almost all surveys concluded that SUI is the most common type of UI in women (Table 4-2). In the large EPINCONT study, 50% of the incontinent women had SUI, 36% MUI and 11% UUI [28]. This indicates that the majority of incontinent women have at least stress symptoms. The recent literature review by Minassian reported similar prevalence rates for the different types of UI [29] (Figure 4-2). The survey carried out by Diokno et al [25] differs from the other studies as only an elderly population was assessed. In this subgroup, the symptoms of MUI were most frequently reported. 31
4.2.1 Overall prevalence of the most common types of urinary incontinence
Table 4 -2 :
Prevalence of the most common types of UI in women as the percentage of the incontinent population.
Reference
N of women in study group with UI 670 445

(1)
Prevalence of SUI (%) 42.7 49.0 26.7 50 55 50
Prevalence of UUI (%) 6.1 20.7 9.0 11 12 12
Prevalence of MUI (%) 39.3 30.3 55.5 36 24 38
Elving [43] Yarnell [30] Diokno [25]
434 6,876 316 541
Hannestad [28] Bortolotti [37] (2) Burgio [41]
(1) Survey in 1,955 non-institutionalised elderly over 60 years of age, 1,150 were women. (2) Case-control survey in Italy in men and women. The female subjects assessed were 40 years or older.
4%
SUI UUI MUI Other
32%
50%
14%
Figure 4 -2 :
Prevalence of UI by type [28].
Yet, if assessed clinically by means of urodynamics, one study in 863 women proved that the majority of the subjects with symptoms of MUI were diagnosed to have pure SUI (42%) during UDS [44]. Another study in 950 women gave similar results [45]. Based on symptomatology, 33% of the women included in the analysis presented with SUI alone, 12% had UUI and 51% had MUI (Figure 4-3). The final urodynamic diagnosis was 62% for SUI, 13% for UUI and only 12% for MUI. However, these results may be a selection bias when referring women to urodynamic investigation. Sandvik et al conducted a study in 250 women referred from primary healthcare because of UI to calculate sensitivity and specificity of diagnostic questions and to use this as corrective measures for epidemiological surveys [46]. Their main finding was also that the majority of women who reported MUI would probably be given a diagnosis of SUI when examined more closely with UDS. Whereas 51% and 39% had SUI and MUI according to a symptom-based diagnosis, this was 77% and 11% during UDS. The reason for this is the low specificity or high number of false positives of the diagnostic questions for MUI.
32
Therefore, even though MUI is reported in high numbers when assessed in epidemiological surveys, the majority of these subjects would eventually be diagnosed with SUI. This reinforces that SUI is the major type of UI in women.
100% 80% % of incontinent women 60% 40% 20% 0%

Figure 4 - 3 :
Symptoms UDS
SUI
MUI
UUI
Other
Percentage of incontinent women with SUI, MUI or UUI based on symptoms or UDS [45].
4
4.2.2 Prevalence of the most common types of urinary incontinence by age

As the prevalence of UI in general depends highly on age, obviously the most common types of UI will also be influenced by age. The EPINCONT study showed that the prevalence of SUI was highest amongst women between 25 and 49 years of age and that there was a relative decrease with increasing age (Figure 4-4) [28]. In older women, MUI becomes the most prevalent type of UI. This is mainly due to an increase in urge symptoms with age.
SUI
70 60 Percentage of women 50 40 30 20 10 0
Figure 4 - 4 :
UUI MUI
20-24
30-34
40-44
50-54
60-64
70-74
80-84
90+
Prevalence of the 3 most common types of UI by age. (Reproduced with permission of Health Publication Ltd [28].)
Again, by pooling data of 14 epidemiological studies including the EPINCONT study, similar findings could be concluded. The prevalence of SUI was highest in the younger subgroup (<55 years) with a peak in the 4th decade (35-44 years). UUI as well as MUI peaked in the group of women older than 75 [29]. 33
4.3
Racial differences in prevalence of stress urinary incontinence

Most prevalence studies were performed on Caucasian women and only few studies have been done to assess the racial differences in prevalence of UI. In the few studies performed, a significantly larger percentage of Caucasian women reported UI compared to African-American or Hispanic females (Table 4-3). Urodynamic diagnosis confirmed that SUI is more reported in Caucasian women compared to African-Americans. However, it is not known if this lower prevalence of UI in Hispanic and black women is due to genetic predisposition, anatomic differences or other factors (e.g. reporting bias due to cultural differences) [47]. More research with regard to racial differences in the prevalence of UI and SUI in particular is required.
Table 4 - 3 :
Racial dif ferences in prevalence of SUI as percentage of the subpopulation.
Reference Sze [48] Graham [47]
Hispanic N = 639 24% -
Caucasian N = 932+132 39% 46%
African-American N = 799+183 27% 22%
Summary
The prevalence of UI as reported in epidemiological surveys varies largely. This is mainly due to differences in definitions, populations and data collection methods used in these surveys. Overall, approximately 1 out of 4 women have UI. SUI is the most common type of UI in females. About half of all incontinent women have complaints of SUI. Because about one third have MUI, the majority of incontinent women have SUI with or without additional urge symptoms. The prevalence of UI increases with age. SUI is the most prevalent type of UI in younger and middle-aged women. MUI becomes the most prevalent type of UI in older women.
34
5
Aetiology of stress urinary incontinence
Few studies have explored the cause and natural history of SUI. Most epidemiological studies in volunteers and clinical patients revealed a number of variables related to SUI including risk factors and contributing variables. However, only age, parity and obesity seem to be investigated most rigorously.
5.1
Main risk factors associated with urinary incontinence

Four major classes of risk factors associated with SUI can be identified [27,49-51]: 1. Predisposing factors increase the risk of having SUI when other inciting and/or promoting factors are present. Sometimes, predisposing factors alone are significant enough to cause SUI. 2. Inciting factors could cause SUI, mostly because of significant damage to the continence mechanism. 3. Promoting factors contribute to the development of SUI, usually after a longer period of time, by continuously deteriorating the continence mechanism. 4. Decompensating factors could cause SUI for a period of time or even permanently, sometimes without any weakening of the continence mechanism.
Familiar predisposition Genetic factors may play a role in the development of UI and SUI. A subgroup analysis of the EPINCONT study found evidence of the impact of hereditary factors. Women, whose mother and/or older sisters are incontinent, have an increased risk for developing SUI and MUI, and more severe symptoms. If the woman has an incontinent mother and grandmother, the risk is even increased further [52]. Gender Gender is the most understood predisposing factor. The prevalence of UI and especially SUI is higher in women. Women over 60 years of age are 1.5 to 2 times more likely to have UI compared to men and in the younger age group this is even 3 to 7 times more [51]. Race Most epidemiological studies of UI have been conducted in Caucasian women. Few studies investigated the racial differences of prevalence and conflicting results were obtained because of poor study design. However, 2 recent American studies suggested that Caucasian women are more susceptible to SUI than African-American women [47,48]. See also Chapter 4. Anatomic, neurological and muscular abnormalities Various abnormalities of the LUT and pelvic floor can exist. Congenital defects of the ureters or urethra or urinary fistulae can cause UI. Several neurological problems, of congenital nature (e.g. spina bifida) or injuries of the spinal cord or brain (because of accidents, haemorrhages or infarcts) are likely to increase the prevalence of UI [38].
5.1.1 Predisposing factors
37
5.1.2 Inciting factors

Pregnancy/Childbirth/Parity SUI is proven to be more common in pregnant women. The prevalence of SUI reported in different studies varies from 8% to 85% during pregnancy. However, in a significant proportion of these women, the SUI will resolve after delivery. This suggests that the size of the uterus may play a role. Nevertheless, it is speculated that women who developed SUI during pregnancy are more likely to be incontinent later in life. A study in 278 women showed that 30% of them suffered from SUI 5 years after delivery [53]. In the group of women without any symptoms of SUI during pregnancy or after delivery, the incidence of SUI 5 years after delivery was only 19%. Of the women who developed SUI during their first pregnancy or puerperium and in whom the symptoms resolved 3 months after delivery, 42% had recurrent SUI 5 years later. Of those in whom the SUI symptoms did not resolve 3 months after delivery, 5 years later the symptoms were still there in 92% (Figure 5-1).
100 80 % of women with SUI 60 42 40 20 0 19
92
No incontinence before or 3 months after 1st delivery
Onset of incontinence during 1st pregnancy or puerperium, but remission 3 months after delivery
Onset of incontinence during 1st pregnancy or puerperium, but no remission 3 months after delivery
Figure 5 -1:
Percentage of women with SUI 5 years af ter childbir th [53].
Childbirth may weaken or damage the pelvic floor structures and innervation to the urethral sphincter mechanism and several studies have evidently proven the correlation of childbirth and UI, mainly SUI. SUI has been reported in 6% to 73% of the women during puerperium. Episiotomy and delivery with instruments (mainly vacuum extraction) may increase the risk. Caesarean sections were believed to have a protective effect on the pelvic floor but probably only for the first delivery and less for multiple births. However, a subgroup analysis of the recent EPINCONT study found that the prevalence of SUI was higher in women who delivered their baby with a caesarean section compared to nulliparous women, and even higher amongst those who had had vaginal delivery and who suffered the more severe SUI. In the older age group, the prevalence of SUI was similar both for women with caesarean section and vaginal delivery [54]. Parity has been found to be a risk factor for SUI, but the impact of subsequent deliveries seems to be less important for the development of long-lasting SUI than does the first delivery [50]. Since age is an effect-modifier it may be difficult to prove the impact of previous pregnancy and delivery for UI in elder women [55]. 38
Side ef fects of Pelvic Surgery and Radio Therapy The impact of pelvic floor surgery on LUT damage and hence the development of potential UI is debatable. Hysterectomy, for example, can cause vesical denervation, but it remains controversial whether it increases the risk of developing UI. Other types of pelvic surgery have been implicated as contributing to pelvic floor dysfunction (e.g. uterosacral transection for dysmenorrhea, radical hysterectomy, rectal surgery and vaginal surgery with extensive pelvic dissection). Also other procedures like radiation can lead to nerve and muscle damage of the LUT [51]. Yet, no data show profound evidence that there is a direct link with UI.
5.1.3 Promoting factors

Promoting factors increase a womans risk of experiencing UI. These include areas of womens everyday lives that increase their potential to suffer from UI. Many of these factors put increased pressure on the LUT and pelvic floor or interfere with these structures ability to withstand increased pressure. Treatment or modification of these factors may aid in the management of UI.
Constipation Severe constipation can affect the continence mechanism in several ways. Faeces in the rectum can form a physical outflow obstruction resulting even in urinary retention and subsequent overflow. But also impaction stretches the pelvic floor inhibiting pelvic floor contractions and thus causing SUI [56].
Chronic constipation with repeated and prolonged straining efforts can cause pudendal nerve damage and eventually will lead to neuropathy and dysfunction, thus causing incontinence [51]. Older women with UI have been shown to be significantly more likely to have both constipation and faecal incontinence than women without UI, lending further evidence to the association [51].
Lung disease and smoking Diseases or situations that irreversibly increase abdominal pressure like chronic bronchitis or emphysema can increase the risk of UI.
Based on clinical studies of patients with UI, there appears to be a link between smoking and UI. One study demonstrated that women who smoked were 2 to 3 times more likely to have UI than non-smokers [57]. The precise mechanism for this relationship is not known, but smokers were shown to generate greater increases in bladder pressure during coughing. Furthermore, smoking is the primary risk factor for lung disease and has an anti-oestrogen effect.
Urinary tract infection One study suggested that acute urinary tract infection (UTI) is associated with acute
39
Obesity Obesity is an established risk factor for the development of UI and, in particular SUI [38]. The added weight in obese patients will increase abdominal and intra-vesical pressure and bear down on the pelvic tissues causing straining, stretching and weakening of the muscles, nerves and connective tissues of the pelvic floor. The prevalence of UI, especially SUI, is known to be higher in patients with higher body mass index and greater weight [49]. Obese women are 4.2 times more likely to develop SUI and 2.2 times more likely to develop UUI [38].
SUI and UUI in about 25% of infected women. When asymptomatic bacteruria was treated, normalisation of urodynamic observations was seen in women with known SUI [51]. Nevertheless, the impact of UTI on SUI later in life remains controversial [50].
Neurological diseases UI can be seen in association with neurological diseases like stroke, Parkinsons disease, depression, multiple sclerosis etc [50]. Occupational and recreational stresses Intuitively, it would be obvious that occupational and recreational activities that cause an increase in abdominal pressure will lead to UI. However, it is not clear from studies whether this is effectively the case and the evidence is limited and when not doing the exercise, the risk of UI may be insignificant to zero.
Some studies demonstrate that UI is not uncommon in young nulliparous athletes and more common in women who exercise than in those who are more sedentary. There is also an increase of prevalence and severity with higher impact activities [51].
Menopause The atrophic changes occurring in the transitioning from the pre- to the post-menopausal state increase the susceptibility to UTIs and can cause storage symptoms, dysuria, vaginal dryness and dyspareunia. Furthermore, LUT tissue is oestrogen sensitive but the exact role of oestrogen in the continence mechanism is not yet clear. No sound evidence can be found that menopause is an independent risk factor for UI, also because it is difficult to separate from the effect of age. Likewise, oestrogen replacement as a therapy for UI remains controversial [49]. See also Chapter 9. Drugs/Medication Many frequently used drugs cause side effects that can directly or indirectly influence the continence mechanism [Table 5-1]. -AR antagonists may cause urethral incompetence and therefore SUI. Diuretics may cause nocturia or provoke UI when patients have IDCs. Alcohol has a sedative and diuretic effect and will impair mobility. Angiotensin converting enzyme (ACE) inhibitors can induce chronic cough with the consequence of increased abdominal pressure. Psychotropic drugs and narcotic analgesia can lead to urine retention and sedation. Various other chemicals like, for example, nonsteroidal anti-inflammatory drugs (NSAIDs) can cause constipation which can have a direct effect on UI [51].
Table 5 -1:
Medications and substances that can af fect LUT function.
Medication Alcohol -AR antagonists Anticholinergic agents Diuretics ACE inhibitors NSAIDs, antacids, calcium, iron
Indications and uses
Possible direct/indirect effects on LUT Sedation, impaired mobility, diuresis
Hypertension UUI Hypertension, heart failure Hypertension, heart failure Various
SUI Urinary retention, overflow incontinence Increased urinary volume, frequency and urgency Chronic cough that may increase abdominal pressure and can lead to SUI Constipation, which can contribute to UI
40
5.1.4 Decompensating factors

Decompensating factors can temporarily (e.g. certain medication) or permanently (e.g. dementia) disrupt the bodys ability to maintain continence. Decompensating factors are not sufficient on their own to cause incontinence, but in a patient with inciting factors, promoting factors and predisposing factors, the presence of a decompensating factor may be enough to tip the balance towards UI.
Age Most studies indicate that UI is correlated with age, although UI is not part of the natural aging process (see also Chapter 4). With aging, changes in the bladder (decreased capacity) and the pelvic floor structures occur that can be factors involved in UI. Furthermore, several other conditions associated with old age, like dementia or diabetes mellitus, are also known to play a role in the progress of UI. Dementia and debility Studies in nursing homes and in other institutionalised patients have proven that dementia and cognitive impairment in general are correlated with UI. Dementia may interfere with the patients ability to consciously control micturition. Physical debility may interfere with the patients ability to get to a toilet in time. Drugs/Medication Several drugs (see Table 5-1) can be a decompensating factor in patients with other risk factors for UI. Co - morbidities and changes in environment Co-morbid diseases like diabetes, vascular insufficiency or congestive heart failure may devastate fragile continence reserves with UI as a result. Also, decreased mobility or dexterity may prevent the individual from getting to the toilet in time. Likewise, changes in the environment such as design of furniture, location and accessibility of toilets can contribute to UI [58].
5
5.2
Pelvic floor disorders

Several pelvic floor disorders can also contribute to the development of UI. Pelvic organ prolapse (POP) strongly correlates with UI. Vaginal prolapse is the loss of position or support from the anterior or posterior vaginal walls. Women with anterior vaginal wall support defects often have bladder neck hypermobility with SUI [59]. Uterine prolapse is the descent from the uterus from its anatomical position into the vagina. It is a common indication for hysterectomy.
41
Summary
The aetiology of UI and SUI in particular is still poorly understood Four groups of risk factors for UI can be identified: familiar predisposition gender Predisposing factors race anatomic, neurological and muscular abnormalities Inciting factors pregnancy/childbirth/parity obesity constipation Promoting factors lung disease and smoking (chronic cough) neurological diseases drugs / medication age Decompensating factors dementia and debility co-morbidities and changes in environment The most studied and proven risk factors are age, obesity and parity
42
6
Impact of stress urinary incontinence on the patients quality of life
6.1
Bother associated with stress urinary incontinence

Although limited studies are available about the impact of SUI, it goes without saying that SUI can be bothersome and seriously impair a womans well-being. The majority of women affected by SUI consider it a problem. Approximately half of the women with SUI are slightly bothered and one third of them are moderately to extremely bothered by their symptoms [28,60].
6.2
Stress urinary incontinence and quality of life

SUI can have a major impact on all aspects of well-being. This impact can be assessed by using validated condition-specific QoL instruments. The I-QOL, for example, asks about avoidance and limiting behaviour, psychosocial impact and social embarrassment associated with UI [61]. Since SUI is mainly prevalent in young and middle-aged women who still have an active professional and/or social life, this may have even greater impact. They may experience limitations in terms of physical (e.g. lifting heavy objects, playing sports, etc.), occupational and social activities because of fear of leakage of urine and related consequences (e.g. smell of urine, wetness, visibility of pads) [62]. A UK study of women with SUI found that as a result of their symptoms, 28% reported that their sex life was spoiled, 50% reported interference with their social activity and 31% reported interference with their social relationships [63]. The presence of SUI may, therefore, affect confidence and self-perception of women.
6
Impact of stress urinary incontinence on the patients quality of life
6.3
Stress urinary incontinence and healthcare seeking behaviour

Despite the high degree of bother associated with SUI and its impact on QoL, many women with SUI do not consult a physician but instead suffer in silence. It seems that only about 25-33% of women with UI look for medical help [29,36,60,64]. This percentage increases to 54% in cases of severe UI [64]. Many women feel ashamed about their condition and are embarrassed to talk about their problem [65]. Social embarrassment also seems to be the strongest predictor of bother [60]. They also hesitate to seek help because they have little hope for treatment, fear surgery or believe that their condition is a normal consequence of aging or childbearing [29,66,67]. Only when symptoms worsen and the patient becomes considerably bothered, patients consult a physician. This leads to considerable delays in seeking medical advice [64,66]. In one study, 58% of patients waited for longer than 1 year and 27% for at least 5 years before consulting a physician [66].
45
Although SUI is not life-threatening, it certainly threatens the QoL of its sufferers. Therefore they do deserve understanding and interest and must be stimulated to talk about their urinary problem. In this regard, as it happens with other conditions or diseases where the feeling of shame is present, an open and proactive attitude from healthcare providers and physicians can help patients to talk about the problem. It would be helpful if primary care physicians would raise the subject of UI during routine visits.
Summary
SUI is associated with significant bother. Approximately half of women with SUI are slightly bothered and approximately one third moderatelyto-severely bothered. SUI results in a restricted lifestyle, impacts confidence and selfperception and interferes with social relationships. Therefore, SUI has a considerable impact on the patients QoL. Many women with SUI, however, suffer in silence. Only 25-33% consult a physician and usually there is a considerable delay in healthcare seeking. This is because they are embarrassed by their condition, regard this as a natural part of aging and/or have limited expectations from treatment and fear surgery. Patients with SUI should, therefore, be educated on these aspects.
46
7
Pathophysiology of stress urinary incontinence
7.1
Stress continence versus stress incontinence

Continence is maintained, provided the maximum pressure inside the urethra is greater than the pressure inside the bladder (intra-vesical pressure). Activities such as exercising, coughing, sneezing or laughing induce a temporary increase in abdominal pressure. This temporary increase is evenly distributed to the bladder body and bladder neck/proximal urethra and the pressure gradient is maintained. In patients with SUI, the temporary increase in abdominal pressure is transmitted to the bladder but incompletely transmitted to the bladder neck/urethra. Consequently, the bladder pressure inside the bladder temporarily overrides urethral pressure, which results in leakage of urine. This pressure difference is called the pressure transmission deficit (Figure 7-1).
Figure 7-1:
Stress continence versus stress incontinence.
7.2
Urethral hypermobility
Urethral hypermobility is caused by weakening of the extrinsic support of the proximal urethra by the endopelvic fascia and pelvic floor muscles. As a result, the bladder neck and/or proximal urethra are incompetent and descend during stress. This descent prevents compression of the urethra during stress and results in an incomplete distribution of abdominal pressure to the urethra. Bladder pressure exceeds urethral pressure and urine leakage occurs (Figure 7-2). Urethral hypermobility can be caused by childbirth, aging or surgical procedures.
Figure 7-2 :
Urethral hypermobility may be due to loss of ex trinsic suppor t of the urethra. The proximal urethra descends and can no longer receive transmitted abdominal pressure during stress. This induces a pressure transmission deficit which results in urine leakage.
Pathophysiology of stress urinary incontinence
At present, there are 2 known causes of SUI. SUI can be caused by anatomical defects due to bladder neck/urethral hypermobility and/or neuromuscular defects resulting in intrinsic sphincter deficiency (ISD) [68].
49
7.3
Intrinsic sphincter deficiency

SUI can also be caused by ISD. This is often the result of damage to the intrinsic urethral sphincter mechanism and its nerve supply due to prior events such as neurological disease or surgery. The sphincteric mechanisms of the urethra fail to maintain adequate intrinsic tone to keep the urethra closed, especially during stressful activities (Figure 7-3). Women who demonstrate urine leakage when lying supine with a relatively empty bladder are likely to have ISD, rather than hypermobility as the cause of their incontinence.
Figure 7- 3 :
Patients with SUI caused by ISD fail to maintain suf ficient urethral closure pressure.
Summary
SUI is caused when a sudden increase in bladder pressure due to stress (exertion, effort, sneezing or coughing) exceeds intra-urethral pressure. There are currently 2 patho-anatomical explanations for SUI: bladder neck/urethral hypermobility and/or ISD. (The ICI will probably change this terminology this summer) Bladder neck/urethral hypermobility results in descend of the bladder neck and/or proximal urethra during stress and prevents the urethra from being compressed so that intra-urethral pressure fails to sufficiently increase in response to the increase in abdominal pressure to overcome the increase in bladder pressure. ISD results in insufficient contraction of the rhabdosphincter and prevents a sufficient increase in intra-urethral pressure to compensate for the increase in abdominal pressure.
50
8
Diagnosis of stress urinary incontinence
8.1
Initial evaluation of women complaining of stress urinary incontinence

The International Consultation on Incontinence (ICI) recommends that the initial evaluation of every woman complaining of UI should include a history and general assessment, a symptom assessment, a physical examination and baseline tests [69].
8.1.1 History and general assessment

A history and general assessment is helpful for healthcare professionals to see the sufferer as a whole individual. Many factors may influence the sufferers symptoms and affect the outcomes of treatment. Therefore, the following aspects should be discussed during the patients visit. The nature and duration of LUTS. This includes description of leakage or urine loss, including frequency, activity at the time of urine loss, sensations of urge to urinate, approximate volume of urine loss and onset and cessation of the problem. It is also helpful to assess which symptoms are most bothersome. Previous surgical procedures with dates, especially those that affect the genitourinary tract, e.g. abdominal and pelvic surgery, possible nerve damage following spinal surgery, etc. Living environment, e.g. social and cultural environment. Patient mobility, since patients with compromised mobility require adapted management. Mental status, to assess whether the woman is able to understand the proposed management strategy and to check whether the patient will be able to go into discussion with the healthcare professional when a variety of treatment options are available. Disease status, since co-existing diseases may have a profound effect on UI, e.g. a patient with coexisting asthma and SUI will leak urine during attacks. Some diseases can precipitate UI. Patient medication, to see if any medication may cause or worsen the patients condition, e.g. 1-AR antagonists may impair urethral closure pressure and cause SUI. See also Chapter 5, Table 5-1. Sexual function, if appropriate. Bowel function, because constipation can contribute to UI. Obstetric history, information about pregnancies and deliveries (e.g. mode of delivery, length of labour). Patients goals and expectations of treatment should also be assessed. Patients general condition for possible surgical procedures should also be assessed.
8
8.1.2 Symptom assessment

The frequency of UI, the perceived quantity of leakage, the perceived impact of leakage on every day life and symptoms of POP should be assessed. The frequency of micturition, the voided volumes, the episodes of UI and the use of UI pads should be documented by means of a simple frequency/volume chart (voiding or bladder diary) (Figure 8-1). The frequency/volume chart records fluid intake and urine output within 24-hour period. The chart gives objective information on the number of micturitions, each voided volume and the distribution of voiding between daytime and night time.
53
Time 6:50 am
Amount Voided 425 ml
Activity Getting up/ Breakfast Leaving for work At work Cough Working, lunch Bending Leaving work Dinner Getting ready for bed
Leakage* (1-3 Scale ) 0
Urge Present Yes
Fluid Amount/Type 200 ml coffee 90 ml orange juice 50 ml coffee 100 ml water 50 ml water 50 ml wine, 100 ml water
7:45 8:20 9:10 12:25 pm 2:45 5:30 7:45 10:00
150 ml 250 ml 275 ml 400 ml 250 ml 250 ml
0 0 2 0 1 0 0 0
No Yes No No No No No No
*Leakage: 1=drops; 2=wet underwear or light pad; 3=soaked pad or clothing

Figure 8 -1:
Example of a bladder diar y [69].
8.1.3 Physical examination

The physical examination of patients with UI is needed to check for reversible conditions that may contribute to UI. Certain aspects of the physical examination need to be more detailed, when indicated. Abdominal examination after voiding includes bimanual palpation and intends to rule out diastasis recti, masses, ascites, organomegaly and other conditions that can influence abdominal pressure, such as obesity. Rectal examination to assess anal tone, pelvic floor function and the consistency of stool. External genitalia, including skin condition, to exclude irritative or inflammatory conditions. Vaginal examination to assess POP and, with the patient bearing down, pelvic floor muscle function and oestrogen status. Pelvic floor muscle function should be assessed for resting tone, and the patients ability to perform a pelvic floor contraction. Neurological examination, concentrating on the sacral segments S2-4 (the nerve supply of bladder and urethra, rectum and anal canal), to exclude a neurological cause of the UI. This includes testing of the lower extremities movements and innervation and perineal sensation.
8.1.4 Baseline tests

A standard urinalysis and urine culture is recommended, to exclude UTIs or conditions that may cause symptoms associated with UI (e.g. diabetes mellitus, malignancy). Standard biochemical tests for renal function are recommended in patients with UI and a high probability of renal impairment, or prior to surgery.
8.1.5 Of fice - based tests of urinary function

A number of tests can be performed in the physicians office. Cough stress test for SUI: patients with suspected SUI should be asked to cough repeatedly and strain with a full bladder in order to objectively demonstrate urine loss. A pad test for urine leakage is not highly recommended by the ICI, but is considered 54
an optional test for the routine evaluation of UI. Either a short test (1 hr) or a 24 hr test is suggested. The pad test is a method of quantification of urine loss based on the measurement of weight gain of absorbent pads during a test period under standardised conditions. A pre-weighed sanitary towel is placed in the patients underwear. A series of manoeuvres (walking, stair climbing, coughing, etc) are carried out by the patient over a 1 hr period, following which the pad is removed and re-weighed. Weight gain in excess of 1g is considered to be a positive 1 hr test. It is recommended that the patient drinks 500 ml volume of fluid 15 minutes prior to the test. Variations to the test include different test times and instilling a standard volume of urine into the bladder prior to testing. A 24 hr test with home-pads may result in more representative data. A pad weight gain 4 g is considered to be a positive 24 hr test. A 24 hr pad test is more reliable than the short test but may not discriminate so well between UUI and SUI. A cotton swab (Q-tip) test measures the degree of urethral movement that occurs when a patient is asked to cough or strain with a small cotton-tipped applicator inserted into the urethra. If the angle circumscribed by the distal end of the swab relatively to the horizontal, with the patient lying, is higher than 30 degrees, urethral hypermobility is present (Figure 8-2). Post-void residual (PVR) can be assessed via ultrasound or catheterisation. It is considered significant if the amount of urine remaining in the bladder after voiding exceeds 30% of the total bladder capacity (usually > 50 to 100 ml).
8
Figure 8 -2 :
Q -tip test; if the angle is greater than 30 this indicates bladder neck /urethral hypermobility.
8.2
Specialised management
In women with SUI, urodynamic evaluation is recommended when conservative and pharmacological therapy has failed and/or when surgery is planned. It is recommended that routine urodynamic evaluation consists of filling and voiding cystometry. Filling cystometry measures the pressure/volume relationship of the bladder during bladder filling and may help to distinguish between SUI and UUI. Severe urgency at less than 300-400 ml bladder volume or the observation of IDCs is suggestive of UUI. USI is noted during filling cystometry when involuntary leakage of urine occurs during increased abdominal pressure (e.g. provoked by means of a forceful cough in the supine, sitting or standing position) in the absence of IDCs (Figure 8-3). 55
Advanced multichannel urodynamics are reserved for complicated cases, which require a more detailed estimate of urethral function. This includes resting Kegel, Valsalva and dynamic urethral pressure profilometry with pressure transmission ratio determination, abdominal leak point pressures, and eventually videourodynamics and electromyography. Ambulatory urodynamics or repeated provocative routine urodynamics are optional tests when initial urodynamics failed to demonstrate the cause for the patients UI.
Detrusor pressure Flow rate
100 (cm H2O) (ml/s)
50
50 40 30 20 10 0
Time cough Leakage with no detrusor contraction Instruction to void Bladder contracts & empties
Start fill Detrusor activity Min. pressure rise throughout fill
Figure 8 - 3 :
Typical cystometrogram from a patient with SUI.
8.3
Symptoms suggestive of a diagnosis of stress urinary incontinence

SUI might be present when the history/symptom assessment reveals a predominant complaint of urine leakage during physical activities, or on sneezing or coughing without a predominant complaint of urge symptoms (i.e. normal daytime and nocturnal frequency, no urgency during provocative manoeuvres, e.g. hand washing or key in the door). A positive cough and/or pad stress test, together with a PVR < 100 ml in the absence of demonstrable SUI (after normal voiding) and a negative urinalysis suggest the presence of SUI (Figure 8-4).
Evidence of urine leakage during effort or exertion, or on sneezing or coughing Positive cough and/or pad stress test Negative urinalysis PVR < 100 ml (after normal voiding) Urodynamic testing Involuntary leakage of urine during increased abdominal pressure, in the absence of IDCs during bladder filling
Figure 8 - 4 :
Findings suggestive of SUI [69].
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Summary
The initial evaluation of every woman complaining of UI should include a history and general assessment and a symptom assessment. A physical examination and baseline tests are needed to exclude other reasons for UI. Evidence of urine leakage during effort or exertion, or on sneezing or coughing, together with a positive cough and/or pad stress test are indications of SUI. Based on this diagnosis, conservative, including pharmacological, treatment can be initiated. Urodynamic testing is highly recommended after treatment failure and/or before surgery. USI can be diagnosed during bladder filling when involuntary urine leakage occurs during increased abdominal pressure in the absence of IDCs.
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9
Treatment of stress urinary incontinence
There are 3 types of treatment options available for women with SUI: conservative, pharmacological and surgical treatment
9.1
Conservative treatment
Conservative treatment options include lifestyle interventions, pelvic floor muscle training (PFMT) and other treatments which are used to improve the function of the PFM. Conservative therapy is considered the first-line treatment for SUI, unless the patients condition is very severe (in which case, referral to a specialist is suggested). Only limited data are available that adequately studied the outcomes of conservative treatments in a large number of women. Data comparison is difficult due to the lack of consistency in the selection and reporting of outcome measures.
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9.1.1 Lifestyle interventions

Lifestyle interventions such as weight loss, stopping smoking and fluid management (including caffeine) are often recommended as supportive measures, in order to prevent further aggravation of SUI. Many women with SUI already modify their lifestyle themselves, to better cope with their condition. Most studies that assessed the effect of these lifestyle changes on SUI did not actually studied the effect of applying or removing the behaviour in question, but did only report associations [70].
9.1.2 Pelvic floor muscle training

PFMT is the most commonly recommended conservative therapy for women with SUI. PFMT increases the ability to produce an increase in urethral resistance, in case the patient is able to perform a correct voluntary PFM contraction. PFMT includes long, slow contractions at regular intervals and short, sharp pull-ups. A patientspecific regimen should be established, depending on the status of the muscles. The major drawback of this type of treatment is compliance, which decreases over time. There also seems to be no consistency in PFMT programs used in clinical practice. Combined therapy of PFMT and adjuncts like vaginal cones, biofeedback and electrical stimulation seems to have no additional benefit compared to PFMT alone, but might be useful for some women to learn how to perform a correct PFM contraction [70]. Treatments such as electromagnetic stimulation and weighted vaginal cones can also be used individually to improve the function of the PFM [70]. Compliance seems to be low and adverse effects such as bleeding and discomfort have been reported [71].
9.2
Pharmacological treatment
At present, there is no globally developed or widely approved pharmacological treatment available to treat SUI in women. Various drugs have been used off-label; a few of these are approved in some countries (Table 9-1). There is, however, limited or no evidence on the efficacy of these drugs and some are associated with significant side effects.
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Table 9 -1 :
Pharmacological agents used for SUI and its side ef fects.
Off-label used Oestrogens Tricyclic antidepressants imipramine
On-label used in some countries
Side effects increased risk cardiovascular disease and breast/endometrial cancer dry mouth, constipation, retention, orthostatic hypotension, falls
2-adrenoceptor agonists clenbuterol: Japan 1-adrenoceptor agonists phenylpropanolamine*: Finland midodrine hydrochloride: Portugal
tremor, tachycardia, headache elevated blood pressure, palpitations, abnormal cardiac rhythm *removed from US market due to risk of hemorrhagic stroke
9.2.1 1 -Adrenoceptor agonists
The 1A-subtype is involved in urethral smooth muscle contraction. It is hypothesised that 1-AR agonists stimulate 1A-ARs located in the bladder neck and in the urethral smooth muscle, which induces contraction of the smooth muscle, both during bladder filling and voiding. This action increases urethral closure pressure and prevents urine loss [72]. Outcomes of a recent Cochrane review suggest there is only weak evidence that the use of 1-AR agonists is better than placebo in the treatment of SUI [73]. Side effects such as headache and cold extremities have been reported. Non-selective -AR agonists, such as phenylpropanolamine (PPA), lack selectivity for urethral 1-ARs and may increase blood pressure. This may also cause sleep disturbances, headache, tremor and palpitations. Rare but serious side effects such as cardiac arrhythmias, hypertension and deaths have also been reported. The Food and Drug Administration recently removed the over-the-counter form of PPA from the market due to the risk of haemorrhage stroke [74,75].
9.2.2 Tricyclic antidepressants

Tricyclic antidepressants (TCAs; e.g. imipramine) are sometimes used for the treatment of SUI. Imipramine inhibits the re-uptake of NA and serotonin in adrenergic nerve endings, which might enhance the contractile effects of NA on urethral smooth muscle. However, no randomised controlled trials (RCTs) of good quality are available. TCAs are associated with dry mouth, constipation, retention, orthostatic hypotension and falls [72,76].
9.2.3 Oestrogens
The role of oestrogens in the treatment of SUI is controversial. Oestrogen and progesterone receptors are present in the vagina, urethra, bladder and pelvic floor. During the menstrual cycle and in pregnancy the circulating level of oestrogens and progesterone fluctuate, which can influence the prevalence of urinary symptoms. Furthermore, the menopause and subsequent oestrogen deficiency might be an aetiological factor in the development of UI [77]. Some RCTs show that oestrogens can induce a subjective symptom improvement, but this might be due to the fact that oestrogens improve feelings of well-being. However, results of the Heart and Estrogen/Progestin Replacement study (HERS) demonstrate that daily oral estrogen plus progestin therapy induced a worsening of UI in postmenopausal women with weekly incontinence [78]. Long-term treatment with parenteral estrogens should be avoided, because of an increased risk of cardiovascular disease and breast/endometrial cancer [76,79]. Recently, the Food and 62
Drug Administration has announced that drugs that contain estrogen (either alone or combination therapy) for the treatment of symptoms associated with menopause (vaginal discomfort, UTIs and LUTS) must include a warning on the labels, which states that estrogens may increase the risk of heart attacks, strokes, blood clots and breast cancer. See also Chapter 5.
9.3
Surgical treatment
If conservative or pharmacological treatments are not successful, or when women suffer from severe SUI, a surgical procedure is likely to be considered. A wide variety of surgical procedures have been described in literature, which can be divided into 3 basic types: urethral bulking agents (injectables), sub-urethral sling procedures and colposuspensions. The choice of the surgical procedure depends on the cause of SUI.
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9.3.1 Urethral bulking agents

Injection of urethral bulking agents is the least invasive surgical procedure. It can be performed under local anaesthesia. This procedure might be acceptable for women who wish to avoid the complications associated with more invasive surgery. Main indication. The procedure is most suitable for patients with SUI due to ISD, although it might also be effective in patients with urethral hypermobility. Bulking materials. Various bulking agents are available, such as autologous fat, gluteraldehyde cross-linked bovine (GAX)-collagen, silicone micro-implants and carbon beads. Silicone micro-balloons and dextranomer/hyaluronic acid copolymer have recently been introduced. The majority of published data on injectables describe the use of GAX-collagen. Technique. The bulking agent is injected transurethrally or periurethrally into the periurethral tissue around the bladder neck, proximal or mid-urethra to increase outlet resistance (Figure 9-1). The means of injecting and positioning differs between the various agents. The stability of the agents also differs: organic substances may be reabsorbed, while synthetic, biocompatible products seem to have better stability [80]. Outcomes. Short-term cure rates (defined as complete dryness) range between 30-78%. Success rates (defined as leakage < 1 pad/day) range between 40-86% [80,81]. Long-term results (up to 2 years) show a continuous decline in success rates [81]. Complications. Urgency, UTIs and urinary retention occur to a minimal extent. Drawbacks. Repeat injections are often required to maintain efficacy, which also affects the costs of this procedure. In addition, the surgeon is unable to determine the quantity of material needed for an individual patient and the occurrence of side effects when using non-autologous injection materials (e.g. migration, foreign body reaction and immunological effects) [82]. More short-term and long-term RCTs taking into account efficacy, safety and cost-effectiveness are required [83].
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Bladder neck
Urethroscope
Injection needle
Figure 9 -1:
The bulking agent is injected at the bladder neck at 2 opposing lateral planes.
9.3.2 Sub - urethral sling procedures

Sling procedures can be divided into the classic sling procedure and the low tension tape procedures.
Classic sling procedure Main indication. The classic sling procedure is indicated for patients with ISD. It is often used for women who failed previous UI surgery, but some consider it also appropriate as a first-line surgical treatment option. Sling materials. Both autologous (e.g. rectus fascia, fascia lata) and synthetic materials (e.g. Mersilene, Gore-Tex) are available. Synthetic slings have the advantage that they are directly available and do not require harvesting from a second operative site. This decreases operation time, discomfort and potential postoperative complications. Technique. A sling is passed completely beneath the urethra or bladder neck, and is anchored anteriorly to some point on the abdominal wall or pelvic structures to stabilise the urethra [84]. Outcomes. Cure rates (defined as complete continence) vary between 73-95% and success rates (defined as continent or improved) between 64-100% [81,85]. Outcomes might be better in women undergoing primary surgery than repeat surgery. Few long-term follow-up data are available. Usually, failure of a sling procedure becomes apparent within the first 6 months, because of degeneration of fascia or failure of anchoring sutures. In general, autologous material seems to be associated with a higher cure rate and fewer complications than synthetic material [86]. However, more data are needed to assess whether the choice of material influences treatment outcome. Complications. Voiding dysfunction with retention (in 1-4% of patients), de novo DO (in 6-14% of patients) and erosion of the sling in the bladder, urethra and vagina (when permanent materials are used) are the most frequent complications [81,87-90]. Misplacement of the suburethral sling can also be a problem.
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Low tension tape procedures Main indication. One of these techniques, the tension-free vaginal tape (TVT) has become very popular and is mainly performed in women with urethral hypermobility. TVT and other similar techniques are less invasive than the traditional sling procedures (and colposuspension). Technique. The concept behind these procedures is that SUI results from inadequate urethral support due to deficient pubourethral ligaments in the mid-urethra and sub-urethral vaginal walls. The tape aims to reinforce the poorly functioning pubourethral ligaments and secure proper fi xation of the mid-urethra to the pubic bone to maintain continence. A polypropylene tape is inserted via a small vaginal/abdominal incision (Figure 9-2). The procedure can be carried out under local or regional anaesthesia, because the surgeon can check intra-operatively if continence has been obtained. The patient is asked to perform a series of coughs in order to adjust the position of the tape. The aim is to have the tape lying free at rest whilst exerting sufficient pressure on the urethra during a cough to prevent urine leakage [90]. Outcomes. Cure rates (defined as complete dryness or dryness with stress) range between 66-91% [91-94]. One open study in an unselected patient population reported that 94% of women were either continent (defined among others as continent during post-operative urodynamics, negative stress test and no leakage on pad test) or significantly improved (defined among others as negative stress test and 75% improvement on visual analogue scale) [93]. Efficacy is sustained up to 36 months [95]. A patient satisfaction of 85% has been reported [92]. Complications. Bladder perforation is the most frequent intra-operative complication, occurring in around 1 in 25 procedures [92,93,96]. Voiding difficulties (in 3-5% of patients), UTIs (in 6-22% of patients) and de novo DO (in 3-9% of patients) can occur post-operatively [88,90,92,93,97]. In 0-5% of cases, a retropubic haematoma can occur [97]. In the long-term, complications related to the use of the tape, particularly erosion into the vagina or urinary tract, may rarely occur [96].
A new group of tape procedures has been introduced in the last year, the transobturator vaginal tape procedures, in which a tape is placed percutaneously and lies horizontally without tension beneath the urethra [98].
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Figure 9 -2 :
The tension -free vaginal tape. The tape is placed around the mid - urethra in a U - shape.
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9.3.3 Colposuspensions
Colposuspension is used in patients with SUI caused by urethral hypermobility alone. It is still considered the gold standard surgical procedure to correct SUI. Two types of colposuspensions are used: retropubic (open) and laparoscopic colposuspensions.
Retropubic colposuspensions Technique. Retropubic colposuspensions are performed through a low abdominal incision (i.e. retropubic approach). The urethra is stabilised by lifting the tissues near the bladder neck and proximal urethra in the area of the pelvis behind the anterior pubic bones. Various structures are used to achieve the elevations. The MarshallMarchetti-Krantz procedure approximates the periurethral tissue to the symphysis pubis. The Burch colposuspension lifts the tissues near the bladder neck and proximal urethra in the area behind the anterior pubic bones (Coopers ligament) to correct deficient urethral closure [99] (Figure 9-3). The Burch colposuspension has been studied most extensively. Outcomes. Short-term cure rates (defined as complete continence) vary between 73 and 92%. Success (defined as cured or improved) is obtained in 81-96% of women [100]. Efficacy is sustained in the long-term. After 5-10 years, approximately 70% of patients were still continent. Results from a recent Cochrane review indicate that open colposuspension is the most effective treatment modality for SUI, especially with regard to long-term outcomes. Patient satisfaction is high (82%) [92]. Complications. Voiding dysfunction (in 2-27% of patients) and de novo DO (in 8-27% of patients) are the most frequent complications [81,92,101].
ileo-pectineal ligament (pubic bone)
urethra
vaginal wall
Figure 9 - 3 :
Burch colposuspension. Stabilisation of the urethra by lif ting the vaginal wall lateral to the urethra and bladder neck towards the pubic bone.
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9.3.4 Artificial sphincter

This device will not be discussed in detail here. The technique of implantation is difficult and mechanical failure is common, even with todays sophisticated devices. Moreover, the devices are very expensive [99].
9.3.5 Summary of surgical treatments

Table 9-2 summarizes the expected outcomes for the various types of surgery. However, it should be realized that it is difficult to compare studies that included various patient populations and used different outcome measures and time of follow-up.
Table 9 -2 :
Summar y of expected outcomes of the 3 types of surger y [80,81,92,93,97].
Outcomes
Injectables TVT
Sling procedures Classic sling 73-95% 64-100%
Colposuspension (Burch)
Cure rate*: % of patients Success rate # : % of patients Post-operative complications: % of patients Voiding dysfunction De novo DO
30-78% 40-86%
66-91% 94%
73-92% 81-96%
3-5% 3-9%
1-4% 6-14%
2-27% 8-27%
*Complete continence (objective and/or subjective); #leakage < 1 pad/day (mostly for injectables) or objective/subjective cure and improvement. These definitions were used in most of the studies that are discussed.
Laparoscopic colposuspensions Technique. Laparoscopic techniques require several small incisions, with the aim of minimising peri-operative morbidity. Outcomes. A recent systematic review [102] evaluated the effectiveness of laparoscopic colposuspension and compared it with open colposuspension. The objective cure rate (assessed as leakage on clinical stress test and urodynamically) was lower for laparoscopic compared to open colposuspension. Women who underwent laparoscopic colposuspension had a 8% higher risk of leakage on a stress test at follow up than those who received an open colposuspension. Subjective cure rates were comparable (85-100%) at 6-18 months follow-up. Complications. Post-operative complications (e.g. urgency, voiding dysfunction and de novo DO) were comparable between both procedures. The intra-operative blood loss was less and the hospital stay and time to return to normal function was shorter with the laparoscopic technique compared to the open colposuspension. The limited data currently available indicates no difference in cure rates between laparoscopic and open colposuspension. More well designed RCTs with adequate sample sizes and long-term follow-up are needed to assess the effectiveness of laparascopic colposuspensions.
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Summary
Women with SUI have the choice between conservative and surgical treatment options. Conservative treatment (especially PFMT) is the first-line treatment for SUI. PFMT is non-invasive, but requires the patient to accept gradient improvement rather than immediate cure. Compliance decreases over time. Surgery can be performed in case conservative treatment fails or in patients with severe SUI. Surgical procedures usually give fast results, but carry the risk of complications. More scientific data with validated outcome measures, which take into account patient satisfaction, are needed to evaluate the various surgical procedures. The fact that there is no globally developed and widely approved pharmacological treatment available for SUI represents a treatment gap in the management of SUI. There is a need for an effective and safe pharmacological treatment.
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Costs associated with stress urinary incontinence
10.1
Economic burden of stress urinary incontinence

From an economical point of view, UI imposes a significant financial burden on sufferers, their families, healthcare organisations and the government. The costs of UI include both the direct use of resources for care or treatment of UI, and indirect economic effects that may result from UI, e.g. productivity loss due to morbidity or disability (Table 10-1) [103]. Most studies focus on the direct costs of UI.
Table 10 -1:
Direct and indirect costs associated with UI [103].
Direct costs of UI Diagnosis and evaluation Laboratory tests Physical examination Physician consultation Urodynamic evaluation Conservative therapies (e.g. devices) Medication Surgery Complications of treatment Pads Supplies (laundry, hygiene products)
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Costs associated with stress urinary incontinence
Treatment
Routine care Indirect costs
Lost productivity due to early retirement, inability to work, hospitalisation, recovery from surgery Informal community care giving
In the US, the annual societal cost of UI is estimated between $16-26 billion [104,105]. Costs for community-dwelling women are greater than for institutionalised women (69% versus 31%, respectively). Routine care comprises 70% of total costs (Figure 10-1). Unlike the costs of diagnosis and treatment, this type of cost is usually not reimbursed by third party payers and is often paid by sufferers themselves. This can lead to a considerable financial burden for the sufferers. Approximately 9% of the direct costs are related to treatment. SUI accounts for 82% of this type of costs [104]. This is not surprising, since SUI is the most prevalent type, and among the treatment options are costly surgical procedures. A recent systematic review estimated the total costs (including theatre costs, inpatient and outpatient costs) of various surgical procedures for SUI. A Markov model was developed comparing TVT with its comparators (retropubic colposuspension, classic sling and injectables), based on the results of the review of effectiveness, data on resource use and costs from previously conducted studies. The estimated total costs of the procedures ranged between 1114 (TVT) and 1340 (classic sling) and increased to 1494-1559 (TVT) and 1626-1908 (classic sling) after 5 years of follow-up. The economic model suggested that TVT was more likely to be considered cost-effective compared with the other surgical procedures [96].
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routine care nursing home admissions treatments complications diagnosis
14% 70% 9% 6% 1%
Figure 10 -1:
Percentage of annual direct cost of UI in the US [104,105].
Cost of illness analysis describes the economic impact of a disease. The US National Institutes of Health (NIH) published disease-specific estimates of costs of illness of various diseases, including UI. The annual direct cost of UI in all ages was approximately $17.5 billion (in 1995 dollars). This cost estimate was quite comparable to the direct costs of other common diseases in women, such as osteoporosis and breast cancer (Figure 10-2) [106].
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Estimated costs of illness (billion dollars)
20
17.5 13.8 11.1
10
UI
Gynecological/Breast cancer
Osteoporosis
Figure 10 -2 :
Comparison of annual direct costs of women diseases in the US [106].
Summary
The annual direct cost of UI in the US is estimated at $16-26 billion. These costs are mainly related to routine care. SUI accounts for 82% of total treatment costs of UI. Total cost expenditures are comparable to other chronic diseases in women.
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11
Unmet needs in managing stress urinary incontinence
11.1
Awareness
As discussed in Chapter 6.3, many women with SUI are reluctant to seek medical advice. A recent study [60] illustrated that even among those women with moderate to extreme bother, less than one half had ever sought medical advice for these symptoms. How can these findings be explained? Uncontrolled micturition is considered normal in the newborn and is accepted in extreme old age. However, uncontrolled micturition is unacceptable between those extremes of life. Shame, the conviction that there is no solution and social isolation often mean that women with incontinence do not talk about their problem, even with their physician [107]. These issues clearly illustrate the need for increasing the awareness on SUI among women. The working committee Promotion, Education and Organisation for Continence Care from the 2nd ICI developed recommendations on how to deal with education issues in the broad sense [108]. They recommend that public awareness campaigns are essential in order to educate the public, break down taboos and to empower health-seeking behaviour. They also indicate that the management of UI should be a compulsory subject for all healthcare professional curricula, as many healthcare professionals lack training on this subject. Obviously healthcare professionals can play a prominent role in this process by proactively facilitating women to speak about their incontinence and educating them on all relevant aspects of their problem. Only through appropriate guidance and knowledge of the different available treatment options, will women be able to make informed choices on coping strategies [65]. Although progress has been made in the promotion and education over the past few years, many new initiatives will be needed to reach the millions of women suffering from SUI.
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Unmet needs in managing stress urinary incontinence
11.2
New treatment modalities

There is no widely approved or globally developed pharmacological treatment available for the early treatment of women with SUI. While several drugs have been used off-label, there is limited or no evidence on the efficacy of these drugs and some are associated with significant side effects (see Chapter 9). A wide variety of surgical procedures for SUI is used as second line treatment. It is very difficult to compare the available data on surgical procedures, because patient populations and treatment outcomes are not consistently defined (e.g. various definitions of cure). The patients assessment is an important measure of success of the intervention, but is often not taken into account [109,110]. In this regard, it is also important to assess the patients expectations of a treatment, in order to create reasonable expectations of intervention success [111]. There is a need for more adequately blinded, randomised and powered RCTs with a well-defined patient population of sufficient (e.g., long-term) follow-up performed according to good clinical practice (e.g., patient informed consent). These RCTs should also use 75
validated and standardised outcome measures for efficacy, and complications should be analysed according to the intention-to-treat principle. The unavailability of a pharmacological treatment represents a major unmet need in the treatment of SUI. Emerging science suggest that the neurotransmitters serotonin and NA play a prominent role in controlling the micturition process and are likely to enhance rhabdosphincter contraction during bladder filling. A new potent and balanced dual serotonin and NA reuptake inhibitor is in final stage of development for treating women with SUI. This compound is likely to be the first globally approved pharmacological treatment, and its potential role in the early treatment of SUI should be defined. There will also be the need for clinical studies evaluating the effects of combining conservative treatment (lifestyle interventions and PFMT) and pharmacological treatment in SUI.
Summary
Awareness on SUI should be improved in order to break down taboos and to empower health-seeking behaviour. Improvement of standardisation and consistent use of efficacy and safety definitions is needed in clinical research for SUI in order to compare different treatment modalities, and to identify the most appropriate treatment for different patient groups. There is a high need for a globally developed, widely approved, effective and safe pharmacological treatment in SUI.
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Frequently asked questions by patients on stress urinary incontinence
Is stress urinary incontinence a normal part of aging?

Involuntary loss of urine is never normal. There are several risk factors associated with SUI and thorough epidemiological research has shown that middle-aged women have the highest risk for SUI with an increase from young age. SUI is reported by about 20% of the women around 50 years of age. However, MUI becomes the most common type of UI in older women and, therefore, women of all ages may suffer from urinary symptoms related to stress situations with or without additional urinary symptoms related to urge. Symptoms may wax and wane over time, but if they persist, underlying abnormalities of the LUT should be investigated and properly treated.
Will my stress urinary incontinence aggravate with aging?

With increasing age, changes in the bladder and the pelvic floor structures that occur can contribute to worsening of SUI. Furthermore, menopause and oestrogen deficiency and other medical problems in the elderly, like diabetes or dementia can make SUI worse.
What is the cause of stress urinary incontinence?

SUI is the complaint of involuntary loss of leakage on effort or exertion, or on sneezing or coughing. Continence is maintained providing the pressure inside the urethra is greater than the pressure in the bladder. For example with exercising or coughing, the pressure in the abdomen rises and this pressure should be equally transmitted to the bladder and the bladder neck/urethra so the urethral pressure rises to maintain continence. However, if the pressure in the bladder exceeds the pressure in the urethra, urine will leak from the urethra. The underlying cause can be hypermobility of the bladder neck and urethra because there is a lack of extrinsic support (the vagina and pelvic floor). SUI can be also due to ISD, a problem with the intrinsic sphincter mechanism of the urethra because of neuromuscular defects.
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Should I lose weight to overcome my stress urinary incontinence?

Several studies have proven that greater weight and higher body mass index are correlated with SUI. The added weight of the obese patient will bear down on the pelvic floor structures causing stretching and weakening of the muscles and connective tissues. This can lead to a hypermobile bladder neck and/or urethra causing urine leakage on effort. Some studies have shown evidence that weight loss will reduce the severity and may even lead to resolution of the SUI symptoms.
Will a special diet be helpful to overcome my stress urinary incontinence?

It is very important to manage the fluid and food intake carefully. Excessive drinking should be avoided because this will only worsen the symptoms. However, drastic reduction of fluid intake must be avoided because the bladder will become sensitive to low volumes. It is recommended to drink 1.5-2 litres per day. Constipation is a predisposing factor for SUI and should therefore be avoided. Good diet and sometimes the intake of laxative drugs, can help overcome constipation.
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Should I restrict physical activities?

The prevalence of SUI is higher in young female athletes and women who exercise. Higher impact activities cause more severe SUI. Physical activities that cause the abdominal pressure to rise can trigger episodes of SUI. However, some physical activity is important for general health purposes and, therefore, SUI should not restrict all physical activities.
Should I stop smoking?

The direct correlation between smoking and UI has not been clearly proven. However, smoking is the primary risk for lung diseases. Diseases like chronic bronchitis or emphysema will irreversibly increase the abdominal pressure and, therefore, the risk for SUI symptoms is high. Chronic cough will increase the severity of SUI. Therefore, stopping smoking will reduce the risk factors for SUI.
Does stress urinary incontinence run in the family?

Most of the underlying conditions that give rise to SUI are not genetically predisposed, apart from muscular dystrophy, which is rare. However, some of the predisposing, promoting factors and decompensating factors (e.g. obesity, diabetes mellitus, dementia) can be family related and, therefore, different members of the same family can suffer from SUI. Recently, is has been shown that women, whose mothers and older sisters are incontinent, have a higher risk for SUI and MUI, and more severe symptoms. The risk is even increased when both the mother and grandmother suffer from UI.
Why did my stress urinary incontinence start af ter I had a baby?

SUI is very common in pregnant women and this is likely to be caused by the growth and the size of the uterus putting pressure on the bladder. SUI usually resolves after pregnancy but can persist after delivery and later on in life. Furthermore, labour puts high stress on the pelvic floor and the LUT and damage to the pelvic floor and LUT structures can cause SUI. Episiotomy and delivery with forceps or vacuum extraction increase the risk for developing SUI.
What is the outcome of pelvic floor muscle training?

PFMT will strengthen the muscles of the pelvic floor, increasing the support of the urethra and bladder and this may help to overcome SUI. In most cases, a degree of symptomatic relief will be experienced with PFMT. However, there is no real evidence that these exercises after childbirth will protect against developing SUI.
Should I continue with pelvic floor muscle training now that my stress urinary incontinence is improved?
A patient-specific regimen of PFMT should be established, based on the status of the patients muscles. The major drawback is the compliance that is high in the beginning but decreases over time. PFMT should therefore be maintained for life on a continued regimen.
Is surgery the only treatment option for stress urinary incontinence?

First of all, the underlying condition of SUI should be investigated. Urodynamic testing should definitely be performed before undertaking surgery. In many cases, conservative measurements can be taken to treat SUI before surgery has to be considered. Conservative treatment includes lifestyle changes such as 80
weight loss, stopping smoking, managing fluid intake and PFMT to strengthen the muscles of the pelvic floor with or without the aid of electromagnetic stimulation or weighed vaginal cones. In addition, pharmacological therapy can be tried before proceeding to surgery. A new pharmacological treatment enhancing sphincter contractility during bladder filling is in final stage of development for treating women with SUI and will be available soon.
Can stress urinary incontinence be treated by pills?

At present, no globally developed or widely approved pharmacological treatment is available to treat SUI in women. Although various drugs have been used offlabel, efficacy of these drugs has not been proven in RCTs and considerable side effects were noted. A new potent and balanced dual serotonin and NA reuptake inhibitor enhancing sphincter contractility during bladder filling is in final stage of development for treating women with SUI and will be available soon.
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Summary
Summary
Continence is maintained when the intra-urethral pressure is greater than the intra-vesical pressure. Patients with symptoms of SUI complain of involuntary leakage on effort or exertion, or on sneezing or coughing. These activities induce a temporary increase in abdominal pressure which overrides the intra-urethral pressure with subsequent loss of urine. SUI can be due to bladder neck/urethral hypermobility and/or to ISD. In patients with hypermobility, the bladder neck and/or urethra descend outside the abdominal cavity during stress, thereby preventing urethral compression and thus preventing an increase in intra-urethral pressure. In patients with ISD, the intrinsic urethral sphincter mechanism is damaged and therefore cannot sufficiently maintain urethral tone during stressful activities. Approximately 1 in every 4 women has UI. SUI is the most common type of incontinence: about half of all incontinent women suffer from pure SUI symptoms. Moreover, since around one third of all incontinent women have MUI symptoms, it seems that the majority of women with incontinence leak urine during stress activities. Whereas pure SUI is most prevalent in younger and middle-aged women, MUI becomes the most prevalent type of incontinence in older women. The aetiology of SUI is still poorly understood but age, pregnancy/ childbirth/parity and obesity are significant risk factors. There is still a lot of uncertainty whether other factors such as smoking, constipation and the menopause/oestrogen deficiency also increase the risk of developing SUI. Further research in these areas is necessary. SUI can be very bothersome for the women affected. Approximately half of all women with SUI are slightly bothered and one third are moderately to severely bothered. This is not surprising as these women experience limitations in performing daily activities which may lead to incontinence, such as lifting heavy objects and playing sports. This can be in particular disturbing for young and middle-aged women who still have an active lifestyle. Because of the fear of urine leakage and odour, they limit or avoid social and/or sexual relationships. It is without doubt that this significantly reduces the overall QoL of these women. Despite this, many women with SUI suffer in silence. It seems that only 25-33% of women with SUI symptoms consult a physician with their problem. In addition, women with (S)UI who visit a physician, very often wait one or more years. This is because women with SUI feel ashamed and embarrassed about their condition. Many also believe that SUI is a natural part of aging and that there are no effective and/or safe treatments available except surgery of which they are afraid. Therefore, women should be educated in all aspects of SUI in order to motivate them to consult a physician once incontinence affects their QoL. In the diagnostic work-up of women presenting with complaints of UI, it is important to differentiate stress from urge symptoms. This can be done by questioning the patient related to the type of complaints. If incontinence occurs during exercising such as walking up the stairs, sneezing, coughing and/or laughing, it is more likely that the patient has SUI. If leakage is predominantly related to urgency (e.g. with hand washing or key in the
13
Summary
85
door), the patient probably suffers from UUI. Office-based tests such as the cough and/or pad stress test can be used to provide further evidence in favour of the diagnosis of SUI and/or to quantify the amount and, therefore, the severity of leakage. Once it is suspected that the patient has SUI based on these assessments, non-invasive conservative and/or pharmacological treatment is usually initiated. Any conservative treatment should start with advice on lifestyle such as fluid management, weight loss (in heavy patients) and stopping smoking. The most frequently administered conservative treatment is PFMT. The major drawback is the fact that it takes some time before patients experience the benefit of these exercises and that compliance with performing them decreases over time. So far there are unfortunately no globally developed and/or widely approved pharmacological treatments available. Although some drugs are used off-label (e.g. 1-AR agonists, TCAs and oestrogens), there is no or limited evidence from RCTs showing their efficacy in SUI and they can sometimes be associated with considerable side effects (such as increased risk of cardiovascular disease, and breast or endometrial cancer with oestrogens, and increased risk of haemorrhagic stroke with PPA). Patients who fail conservative and/or pharmacological therapy or who have severe SUI, should receive specialised diagnostic work-up before surgery is performed. Filling cystometry can be used to distinguish between SUI and UUI. If a patient experiences involuntary leakage of urine during e.g. cough-induced increased abdominal pressure in the absence of IDCs, there is urodynamic evidence for SUI (i.e. USI). If IDCs occur during bladder filling, a diagnosis of UUI is most likely. Only patients with SUI should undergo surgery. The Q-tip test can be used to assess urethral hypermobility. This is needed because some surgical interventions provide better outcomes in hypermobility while others are preferred for ISD. There are 3 types of surgical interventions available with increasing rates of invasiveness, efficacy and complications (such as de novo DO, voiding dysfunction): 1. urethral bulking agents or injectables (most suitable for patients with ISD) of which the GAX-collagen has been most intensively studied, 2. sub-urethral sling procedures (of which the classical slings are indicated for patients with ISD whereas newer low tension tapes such as TVT are mainly used in hypermobility), and 3. colposuspension (still considered to be the gold standard surgical intervention in hypermobility). It is obvious that, due to the lack of globally developed or widely approved, effective and safe pharmacological therapies, there is currently a treatment gap between conservative treatment on one hand and surgical interventions on the other. If such a pharmacological treatment was available, this might reduce the threshold at which women suffering from SUI seek medical advice. In this regard, it is promising that a new pharmacological therapy for SUI will become available in the near future. This drug is a potent and balanced dual serotonin and NA reuptake inhibitor which enhances urethral rhabdosphincter muscle contraction and as such may help to resist sudden increases in abdominal pressure during stress activities.
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Current guidelines in urinary incontinence
Agence Nationale dAccrditation et dEvaluation en Sant

http://www.anaes.fr/ANAES/anaesparametrage.nsf/Page?ReadForm&Section=/ anaes/SiteWeb.nsf/wRubriquesID/APEH-3YTFUH?OpenDocument&Defaut=y& http://www.anaes.fr/anaes/Publications.nsf/nPDFFile/GU_LILF-5LLGWD/$File/ urinary_incontinence.pdf?OpenElement
American Academy of Family Physicians

http://www.aafp.org/afp/20001201/2433.html http://www.aafp.org/PreBuilt/videocme/urinary_mono.pdf
American Urological Association

http://www.incontinet.com/aua2hcfa.htm http://shop.auanet.org/timssnet/products/clinical_guidelines/FSUIptguide.pdf
British Medical Journal

http://bmj.bmjjournals.com/cgi/content/full/321/7272/1326
Canadian Continence Foundation

http://www.continence-fdn.ca/consensus/intro.htm
European Association of Urology

http://www.uroweb.org/files/uploaded_files/incontinence.pdf
http://www.continet.org/documents/ici_pdfs/MENUS/RECOMM.PDF http://www.tenamagazine.com/artiklar/reom.1.pdf http://www.continet.org/documents/StandardisationReports.asp
National Guidelines Clearinghouse

http://www.guideline.gov/guidelines/ftngc-2453.pdf http://www.guideline.gov/summary/summary.aspx?doc_id=1812 http://www.guideline.gov/summary/summary.aspx?doc_id=3400 http://www.guideline.gov/summary/summary.aspx?doc_id=2925 http://www.guideline.gov/summary/summary.aspx?doc_id=3227 http://www.guideline.gov/summary/summary.aspx?doc_id=1724
National Institute for Clinical Excellence

http://www.nice.org.uk/pdf/56_TVT_full_guidance.pdf
Royal College of Obstetricians and Gynecologists

http://www.rcog.org.uk/resources/Public/Urodynamic_stress_incontinence_ No35.pdf
University of California, San Diego Medical Group

http://health.ucsd.edu/ClinicalResources/incont101.pdf
Current guidelines in urinary incontinence
International Continence Society World Health Organization / International Consultation on Incontinence
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UNDERSTANDING STRESS URINARY INCONTINENCE

Paul Abrams Walter Artibani

UNDERSTANDING STRESS URINARY INCONTINENCE

6 6.1 6.2 6.3

7 7.1 7.2 7.3

8 8.1 8.1.1 8.1.2 8.1.3 8.1.4 8.1.5 8.2 8.3

Basic anatomy of the female lower urinary tract

The female LUT. (Reproduced with permission of Elsevier [3].)

Female lower urinary tract anatomy, physiology and neural control

UNDERSTANDING STRESS URINARY INCONTINENCE

Lower urinary tract innervation and the normal micturition cycle

1.2.1 Storage phase (bladder filling)

1.2.2 Conscious inhibition of the micturition reflex

Female lower urinary tract anatomy, physiology and neural control

UNDERSTANDING STRESS URINARY INCONTINENCE

1.2.3 Voiding phase (bladder emptying)

1.3.1 Role of serotonin and noradrenaline

1.3.2 Role of glutamate

Sacral Spinal Cord DC DH LF

Onuf's nucleus Lateral motor nucleus

Onuf's nucleus Lateral motor nucleus

UNDERSTANDING STRESS URINARY INCONTINENCE

Definitions of urinary incontinence

Classification of urinary incontinence

UNDERSTANDING STRESS URINARY INCONTINENCE

2.2.3 Urodynamic observations

Types of urinary incontinence

Type of UI Stress Urinary Incontinence

Symptom The complaint of involuntary leakage on effort or exertion, or on sneezing or coughing

Urge Urinary Incontinence

Mixed Urinary Incontinence

Not defined by the ICS

Definitions, classification and types of urinary incontinence

Not defined by the ICS

The symptom of stress urinary incontinence

The sign of stress urinary incontinence

The urodynamic observation of stress urinary incontinence

The condition of stress urinary incontinence

Prevalence of urinary incontinence in women

4.1.1 Overview of prevalence of urinary incontinence

UNDERSTANDING STRESS URINARY INCONTINENCE

Over view of dif ferent studies assessing the prevalence of UI in women.

4.1.2 Reasons for variation in prevalence of urinary incontinence

4.1.3 Prevalence of urinary incontinence by age

Prevalence of different types of urinary incontinence in women

4.2.1 Overall prevalence of the most common types of urinary incontinence

UNDERSTANDING STRESS URINARY INCONTINENCE

N of women in study group with UI 670 445

Prevalence of SUI (%) 42.7 49.0 26.7 50 55 50

Prevalence of UUI (%) 6.1 20.7 9.0 11 12 12

Prevalence of MUI (%) 39.3 30.3 55.5 36 24 38

Elving [43] Yarnell [30] Diokno [25]

434 6,876 316 541

Hannestad [28] Bortolotti [37] (2) Burgio [41]

Prevalence of UI by type [28].

100% 80% % of incontinent women 60% 40% 20% 0%

4.2.2 Prevalence of the most common types of urinary incontinence by age

UNDERSTANDING STRESS URINARY INCONTINENCE

Racial differences in prevalence of stress urinary incontinence

Racial dif ferences in prevalence of SUI as percentage of the subpopulation.

Reference Sze [48] Graham [47]

Hispanic N = 639 24% -

Caucasian N = 932+132 39% 46%

African-American N = 799+183 27% 22%