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Managing Incontinence in General Practice

Clinical Practice Guidelines

Prepared by the WA Research Unit of the RACGP with the assistance of the National Continence Management Strategy, Commonwealth Department of Health and Ageing.

MANAGING INCONTINENCE IN GENERAL PRACTICE CLINICAL PRACTICE GUIDELINES 1ST EDITION, 2002
Prepared by the WA Research Unit of the Royal Australian College of General Practitioners.

COPYRIGHT STATEMENT
Apart from any fair dealing for the purposes of study, research, criticism or review, as permitted under the Copyright Act, no part of this work may be reproduced by any process without written permission. Enquiries should be made to The Royal Australian College of General Practitioners or Commonwealth Department of Health and Ageing.

DISCLAIMER
The information presented in these guidelines is intended to guide general practice only and does not necessarily reflect the position or opinions of The Royal Australian College of General Practitioners. Every care has been taken to summarise the relevant scientific literature and clinical opinion as accurately as possible but the publisher takes no responsibility for errors, omissions or inaccuracies contained herein, or for the consequences of any action taken by any person as a result of anything contained in the publication.

ACKNOWLEDGMENT
The publisher gratefully acknowledges the financial assistance of the Commonwealth Department of Health and Ageing through the National Continence Management Strategy. The Royal Australian College of General Practitioners College House 1 Palmerston Crescent South Melbourne Victoria Australia www.racgp.org.au

Contents
SECTION
1 2 3 4 5 6

TITLE
Foreword Introduction Research Methodology Definitions Prevalence - General Population Urinary Incontinence 6.1 Presentation 6.2 Clinical Assessment 6.3 Management

PAGES
3 5 7 9 11 13 13 14 17 19 19 21 22 25 26 35 40 47 52 59 75 79 83 87
1

Faecal Incontinence 7.1 Presentation 7.2 Clinical Assessment 7.3 Management

High-Risk Populations 8.1 Women of child-bearing age 8.2 Menopause 8.3 Men 8.4 Children 8.5 Elderly 8.6 Other medical conditions

Appendix 1 Appendix 2 Appendix 3 Appendix 4

Bladder diary Bowel diary Female urinary incontinence score questionnaire Public toilet mapping information

NB - PLEASE SEE MANAGING INCONTINENCE IN GENERAL PRACTICE PACKAGE FOR FURTHER RESOURCES

1 Foreword
This publication has been designed for the purpose of assisting GPs in recognising and managing patients who suffer from urinary and/or faecal incontinence. Research for this publication was conducted by the WA Research Unit of The Royal Australian College of General Practitioners, with funding provided by the Department of Health and Ageing (DHA) through the National Continence Management Strategy (NCMS). The provision of these guidelines nationally follows the successful implementation of a demonstration project within the Perth metropolitan region, also funded by DHA through the NCMS. As part of the Governments Staying at Home package, the Commonwealth Department of Health and Aged Care also funded two other demonstration projects: the Hunter Continence Awareness Project, and the Ovens and King Continence Care and Resource Model Demonstration Project. All three demonstration projects were evaluated by the University of Newcastle and informed these guidelines. Authors and members of the RACGP steering committee included: Dr Farida Tilbury Dr Clare Matthews Mr Lee Barclay Ms Jan Taylor Dr Douglas Cordell Ms Linda Bailey Ms Marissa Williams Dr Jane Talbot Project Manager Consultant GP Research Officer Research Officer, Nurse Research Officer, Consultant GP Research Officer Media Officer Consultant GP
3

Additional support and advice were provided by Dr Sally Roach and Rita Colliander of the RACGP (WA). We also acknowledge the invaluable advice of the reviewers of these guidelines, who were: Glenice Wilson Continence Nurse Consultant Dr Helen OConnell Urological Surgeon Dr Rachel Horncastle Consultant GP Janet Chase Continence Physiotherapist Kay Josephs Continence Advisor, Clinical Nurse Specialist Deane Dight Pharmacist, Australian College of Pharmacy Practice Prof David Fonda Expert Advisory Committee, NCMS Prof Charles Bridges-Webb Director, RACGP Research Unit (NSW) Gavin Anderson Consultant - Public Toilet Mapping Project Dr Chris Hogan Director, RACGP Research & Health Promotion Unit (VIC) Hugh Carter National Caucus of Disability Consumer Organisations Dr Lloyd Singam Geriatrician Dr Annabel Shannon Consultant GP Dr Janet Zint Consultant GP Dr NickTsokos Urogynaecologist Centre for Health Outcomes and Innovations Research Additional copies of these guidelines may be requested from The Royal Australian College of General Practitioners.

2 Introduction
Incontinence is largely a hidden condition. Patients do not readily admit to symptoms, and many doctors are unaware of their prevalence. Within the general population, up to 19% of children (1) and at least 20% of women and 10% of men (2) may be affected by some form of urinary incontinence. Rates of faecal incontinence in the adult population are also thought to be high, with recent Australian statistics highlighting a 12-month incidence of 11.2% (3). These largely under-reported conditions often have a significant negative influence on quality of life and mental health (4, 5) and are usually a major influence on decisions to place an elderly person in long-term institutionalisation (6). A large proportion of incontinence can be cured or improved, often through simple pelvic floor exercises and other behavioural strategies such as bladder training (7). General Practitioners are ideally placed within the Australian Health System to provide and coordinate care for persons affected by incontinence. GPs are the leading providers of health-care to the Australian community, averaging 6000 consultations each per year (8). Up to 90% of Australians visit a GP each year (8). The cost of incontinence to patients and the wider community is difficult to estimate due to its lack of visibility. An Australian study estimated that the median personal cost per week is A$5.61 and the total annual treatment cost of medical treatments is A$462 on average. Total direct cost (median) was found to be A$12.89 per week (9). Financial cost is more than matched by the social cost of the condition. Incontinence may be described as a social death, due to its debilitating effect on the ability of sufferers to travel and interact with other community members. It is clear that a large amount of incontinence remains unmanaged. A major barrier to patients help-seeking behaviour is certainly embarrassment. Many patients, however, simply lack knowledge of their condition and of the available treatments (10, 11). Others believe that incontinence is a normal part of ageing or childbirth or that it is not a "medical" condition (10-12). A growing body of research and clinical opinion suggests that incontinence should not be considered either normal or untreatable. These guidelines provide sufficient information to enable GPs to feel confident in their ability to identify and manage incontinence within their own practices. Effective treatment may take time, however, and management can often be optimised by appropriate referral to other health providers such as nurse continence advisors, physiotherapists, occupational therapists, pharmacists, and specialists. Links to such professionals are provided in the package that accompanies these guidelines. These guidelines represent a summary of the strongest available data and management recommendations for urinary and faecal incontinence, contextualised to the particular needs of Australian General Practice. Information is presented in three levels, providing detailed background, summarised guidelines, and an assessment and management algorithm that provides a convenient visual representation of the major decision points and preferred management pathways. A number of resources are also present on CD-ROM. We encourage GPs to use these resources and are confident that their use will assist in uncovering and managing a substantial amount of previously unreported incontinence. Other practical guides that may be useful for patients and GPs include: Womens Waterworks by Pauline Chiarelli (13) Bladder care by Prem Rashid and Vicky Hibbard (14) Simply Busting edited by C. B. Pinnock (15) The Voice, a free magazine produced by the Continence Foundation of Australia

References: 1. Bower, W. F., Moore, K. H., Shephard, R., et al. (1996). The epidemiology of childhood enuresis in Australia. British Journal of Urology, 78: 602-606. 2. Hunskaar, S., Arnold, E. P., Burgio, K., et al. (1999). Epidemiology and natural history of urinary incontinence (UI), in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publication Ltd. p. 197-226. 3. Kalantar, J. S., Howell, S., & Talley, N. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 4. Ashworth, D. & Hagan, M., (1993). The meaning of incontinence: A qualitative study of non-geriatric urinary incontinence sufferers. Journal of Advanced Nursing, 18: 1415-1423. 5. Payne, C. (1998). Epidemiology, pathophysiology, and evaluation of urinary incontinence and overactive bladder. Urology, 51 (2a): 3-10. 6. Pranikoff, K. (1996). Urologic care in long-term facilities. Urologic Clinics of North America, 23 (1): 137-146. 7. Roe, B., Williams, K., & Palmer, M. (2001). Bladder training for urinary incontinence in adults (Cochrane Review), in The Cochrane Library, 4, Update Software: Oxford. 8. Commonwealth Department of Health and Aged Care. (2000). General practice in Australia: 2000. Canberra: Commonwealth of Australia. 9. Dowell, C. J., Bryant, C., Moore, K. H., & Simons, A. M. (1999). Calculating the direct cost of urinary incontinence: A new test instrument. British Journal of Urology, 83: 596-606. 10. Goldstein, M., Hawthorne, M. E., Engeberg, S., et al. (1992). Urinary incontinence: Why people do not seek help. Journal of Gerontological Nursing, 18 (4): 15-20. 11. Shaw, C., Tansey, R., Jackson, C., et al. (2001). Barriers to help seeking in people with urinary symptoms. Family Practice, 18 (1): 48-52. 12. Umlauf, M. G., Goode, P. S., & Burgio, K. L. (1996). Psychosocial issues in geriatric urology: Problems in treatment and treatment seeking. Urologic Clinics of North America, 23 (1): 127-135. 13. Chiarelli, P. (2002). Womens waterworks: Curing incontinence. New South Wales: George Parry. 14. Rashid, P. & Hibbard, V. (2002). Bladder care: Your self-help guide. New South Wales: Uronorth Group. 15. Pinnock, C. B. (1993). Simply busting: A guide to bladder and bowel control. South Australia: Wakefield Press.

3 Research Methodology
LITERATURE SEARCH
Literature was obtained through searches in PubMed, Medline, and Cochrane databases, and by further manual scanning of the reference lists of relevant journals. The only limit applied to these searches was that articles be in English. The literature searches concentrated on the period 1990 to 2001, however, articles published prior to 1990 were included if they offered useful data or clinical perspectives. The final literature search was conducted in February, 2002.

LEVELS OF EVIDENCE AND RECOMMENDATION


Research into incontinence is a relatively recent and growing area and controlled trials are so far uncommon. For these reasons, we are, at the time of publication, unable to make a large number of strong recommendations. We encourage GPs to base their clinical decisions not only on these guidelines, but on the constantly updating body of worldwide research that will continue to follow them. The levels of evidence that are presented in these guidelines are adapted from those published by the National Health and Medical Research Council. Recommendations are based upon those used by the RACGP.

Levels of Evidence (adapted from NH&MRC) Level


I II III IV O

Interpretation
Evidence obtained from a systematic review of all relevant randomised controlled trials. Evidence obtained from at least one properly designed randomised controlled trial. Evidence obtained from controlled trials without randomisation, cohort or case control analytic studies, preferably from more than one centre or research group. Evidence obtained from case-series, either post-test or pre-test and post-test. Opinions of respected authorities based on clinical expertise, descriptive studies, or reports of expert committees.

Strength of Recommendations (RACGP) Level


A B C D E

Interpretation
There is good evidence to support the recommendation. There is fair evidence to support the recommendation. There is insufficient evidence to recommend for or against, but recommendation may be made on other grounds. There is fair evidence to exclude the intervention There is good evidence to exclude the intervention

4 Definitions
URINARY INCONTINENCE
The definitions associated with urinary incontinence presented here (see Table 1, below) are those arising from the combined work of the International Continence Society and a large number of experts worldwide (1). The terms are used throughout these guidelines and are useful as guides to assessment. Clinical observation of these signs and symptoms, however, does not provide a definite diagnosis. The causes of incontinence can only be absolutely determined by urodynamic studies (2).

TABLE 1: TERMINOLOGY Term

ASSOCIATED WITH URINARY INCONTINENCE

Definition

Urinary incontinence/enuresis The complaint of any involuntary leakage of urine. Nocturnal enuresis Any involuntary loss of urine during sleep. Urgency The complaint of a sudden, compelling desire to pass urine, which is difficult to defer. Urge urinary incontinence The complaint of involuntary leakage accompanied by or immediately preceded by urgency. Stress urinary incontinence The complaint of involuntary leakage on effort or exertion, or on sneezing or coughing. Mixed urinary incontinence The complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing. Overflow incontinence The involuntary loss of urine associated with over-distension of the (now referred to as chronic bladder, or associated with poor bladder emptying. retention of urine) Chronic retention of urine A non-painful bladder, which remains palpable or percussable after the (see also overflow patient has passed urine. Such patients may be incontinent. incontinence) Nocturia The complaint that the individual has to wake at night one or more times to void. Increased daytime frequency The complaint by the patient who considers that he/she voids too often by day. Detrusor overactivity A urodynamic observation characterised by involuntary detrusor contractions during the filing phase which may be spontaneous or provoked. Detrusor underactivity A contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span. Post void residual (PVR) The volume of urine left in the bladder at the end of micturition. Bladder compliance The relationship between change in bladder volume and change in detrusor pressure. Bladder outlet obstruction Obstruction during voiding characterised by increased detrusor pressure and reduced urine flow rate. Dysfunctional voiding An intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the peri-urethral striated muscle during voiding, in neurologically normal individuals. Continuous urinary The complaint of continuous leakage. incontinence Terminal dribble The term used when an individual describes a prolonged final part of micturition, when the flow has slowed to a trickle/dribble. Post micturition dribble The term used when an individual describes the involuntary loss of urine immediately after he or she has finished passing urine, usually after leaving the toilet in men, or after rising from the toilet in women. Detrusor sphincter dyssynergia A detrusor contraction concurrent with an involuntary contraction of the urethral and/or periurethral striated muscle. Occasionally, flow may be prevented altogether.

FAECAL INCONTINENCE
Research surrounding faecal incontinence has been hampered by the widespread use of a variety of definitions. It is suggested that a useful definition of faecal incontinence is as follows: An involuntary loss of anal sphincteric control leading to unwanted release of liquid or solid faeces (not flatus) at an inappropriate time or in an inappropriate place (2). It remains to be seen whether this definition will continue to be used in future research. Its face validity appears good in that it defines the problem of clinically significant faecal incontinence well. It does not overestimate serious incontinence by including involuntary loss of flatus.
References: 1. Abrams, P., Cardozo, L., Fall, M., et al. (2002). The standardisation of terminology of lower urinary tract function: Report from the standardisation sub-committee of the International Continence Society. Neurourology and Urodynamics, 21 (2): 167-178. 2. Abrams, P., Wein, A., Schussler, B., et al. (1999). 1st International Consultation on Incontinence: Recommendations of the International Scientific Committee: The evaluation and treatment of urinary incontinence, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publications Ltd. p. 945-975. 3. Kalantar, J. S., Howell, S., & Talley, N. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57.

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5 Prevalence - General Population


ADVANCED SUMMARY
Research has demonstrated that up to 40% of a GP waiting room population may suffer from some form of incontinence. Urinary incontinence is thought to be present in at least 1 in 10 of the general population. The 12-month incidence of faecal incontinence (not due to acute diarrhoea) in the wider Australian community has been reported at 11.2%. Incontinence has been consistently identified as a major factor influencing placement of a patient in long-term-care. Incontinence is not limited to the elderly it can affect children, adults, sports-people, post-partum and post-menopausal women, and patients with other serious medical conditions.

There are few studies of the prevalence of urinary incontinence that have included all age-groups, however the available estimates suggest that symptoms are present in just below 10% of the general population (eg. 1, 2). It is thought that only 30% of sufferers seek health-care for urinary incontinence (3). The prevalence of faecal incontinence is also likely to be both high and under-reported. A recent Australian study was able to demonstrate that during a 12-month period, 11.2% of the surveyed population experienced involuntary loss of anal sphincteric control that led to unwanted release of liquid or solid faeces (not flatus) at an inappropriate time or in an inappropriate place (4). Instances of acute diarrhoea were not included in this analysis. This study also highlighted that only 27% of those with faecal incontinence sought health-care for the condition and that doctor-initiated discussion was reported by 14.6% of patients in whom the condition was present (4). Population statistics suggest that, within a General Practice population of 1000 patients, at least 100 patients may currently experience some form of urinary incontinence. A potentially distinct 100 patients may suffer from faecal incontinence during any 12-month period. Given the unique characteristics of a waiting room population however, the actual prevalence in the GP setting may be much higher. Preliminary research suggests that up to 40% of an average waiting room population may suffer from some form of incontinence (7). While incontinence is found throughout the general population, rates are often much higher in certain patient groups. It is unusual, for example, for studies to report urinary incontinence in less than 20% of women and most reports indicate that at least 40% have experienced symptoms (5). Rates also clearly increase with age (5). At the extreme, incontinence is usually a major factor in the prediction of institutionalisation of the elderly (6). Information related to high-risk groups for incontinence can be found in Section 8 of these guidelines. Specialist guidelines are available for children, post-partum and post-menopausal women, men, the elderly, and those with serious medical conditions. Reports of the prevalence of incontinence in these groups can be several times higher than that of the general population. High rates of incontinence in the general population, combined with low rates of doctor-patient communication, suggest that screening for incontinence in General Practice should be increased. Sensitive questioning of patients during routine examination is likely to uncover previously unreported and unmanaged incontinence.

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The figure below presents the prevalence of incontinence in the UK as compared to several other common conditions (8):

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IT IS RECOMMENDED THAT DUE TO THE POTENTIALLY LARGE NUMBER OF UNTREATED PATIENTS, SCREENING FOR INCONTINENCE SHOULD BE INCREASED IN GENERAL PRACTICE (O/A).

References: 1. Thomas, T. M., Plymat, K. R., Blannin, J., et al. (1980). Prevalence of urinary incontinence. British Medical Journal, 281: 12431245. 2. Roe, B. & Doll, H. (2000). Prevalence of urinary incontinence and its relationship with health status. Journal of Clinical Nursing, 9 (2): 178-187. 3. Versi, E., Defever, M., Hu, T. W., et al. (1999). Socio-economic consideration, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publication Ltd. p. 869-892. 4. Kalantar, J. S., Howell, S., & Talley, N. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 5. Hunskaar, S., Arnold, E. P., Burgio, K., et al. (1999). Epidemiology and natural history of urinary incontinence (UI), in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publication Ltd. p. 197-226. 6. Ouslander, J. G., Kane, R. L., & Abrass, I. B. (1982). Urinary incontinence in elderly nursing home patients. Journal of the American Medical Association, 248: 1194-1198. 7. Tilbury, F., Jayasuriya, P., Taylor, J., Williams, L. (2001). Continence care in the community: Final Report, August 2001. Western Australia: The Royal Australian College of General Practitioners, WA Research Unit. 8. The Continence Foundation (2000). Making the case for an integrated continence service. UK: The Continence Foundation.

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6 Urinary Incontinence
6.1 PRESENTATION
In order to determine the most appropriate management strategy, it is useful to categorise incontinence according to its various clinical characteristics. Urinary incontinence can be divided into five major groups (stress, urge, mixed, overflow*, and functional). The aetiology and clinical features are briefly summarised in Table 1 (below). All information presented in this section comes from the work of the RACGP Continence Care in the Community Project (1), and the work done by Millard (2).

TABLE 1: TYPES Type


Stress

OF

URINARY INCONTINENCE Features


Involuntary loss of urine associated with increased intra-abdominal pressure, such as: Coughing Sneezing/laughing Lifting Exercise

Aetiology
a. Intrinsic sphincter deficiency (ISD) b. Hyper mobility of bladder neck, weakened pelvic muscles, caused by: Childbirth Menopause Trauma/surgery a. Associated with detrusor instability that causes uninhibited bladder contractions. Causes can be: CVA Demyelinating diseases Local irritating symptoms (UTI or bladder tumours) b. Underactive, low tone bladder, due to: Drugs Neuropathy Spinal Cord Injury Pelvic surgery/trauma Combination of urge and stress incontinence

Urge

Involuntary loss of urine at unexpected times, associated with a strong desire to void (urgency).

13

Mixed

Common in women. One symptom may be more bothersome than another. Involuntary loss of small amounts of urine from a full bladder. Patients may have a variety of symptoms including constant or frequent dribbling, or urge or stress incontinence symptoms. Urine loss associated with difficulty reaching a toilet when needed.

Overflow *

Factors that inhibit bladder contraction: Bladder failure Factors that obstruct outflow: Tumours Benign strictures Prostatic hypertrophy Relatively normal micturition but other chronic impairment of physical or cognitive functioning. Causes include: Dementia CVA Decreased dexterity (eg. arthritis)

Functional

(*) Now referred to as chronic retention of urine see Section 4: Definitions.

6.2 CLINICAL ASSESSMENT HISTORY


A basic assessment of any patient who presents with urinary incontinence should include a detailed history such as that shown in Table 2 (below). Using sensitive questioning that utilises the patients own words for their condition is more likely to place them at ease and allow more accurate information to be collected. It may be appropriate to ask patients about incontinence during routine pap smear and prostate examinations. The question may be framed as an enquiry about a surprisingly common and perhaps embarrassing condition, to allay patient concerns.

TABLE 2: KEY Assessment

ASPECTS OF THE MEDICAL HISTORY

Content
General Health Co-morbidity (eg. locomotor problems) Previous surgery/trauma

General medical and genitourinary review

Characteristics of the presenting incontinence

Duration Frequency - bladder diary Amount - bladder diary Precipitants (eg, stress, urgency) Impact on quality of life

Other related symptoms

Haematuria Nocturia Pain (eg. dysuria, burning, stinging) Hesitancy or abnormal stream Constipation or faecal impaction

14

Fluid intake Medication use (see Table 3) Environmental factors

Caffeine, alcohol & fizzy drinks Include over-the-counter drugs Access to toilet Is toilet clearly identified? (esp. in dementia) Presence of carer support

Cognitive status

Dementia Depression

Expectations of treatment

Goals and motivation for treatment

A key aspect to history-taking in patients who suffer from incontinence is medication-use. It is important to collate an exhaustive list of medications, including those available over-the-counter. As shown by Table 3 (below), there are a large number of medications that may potentially influence continence in a variety of ways. GPs should also be careful to consult the product information for each drug to establish whether drug interactions are likely.

TABLE 3: DRUGS Agent


Alpha blockers Prazosin Doxazocin Phenoxybenzamine Terazosin Bladder relaxants Anticholinergics

THAT MAY CAUSE OR AGGRAVATE URINARY INCONTINENCE

Mechanism of action Type of incontinence


Decreased sphincter resistance Stress

Urinary retention and/or chronic constipation

Overflow

Tricyclic antidepressants Bladder stimulants Cholinergic agents Anticholinesterase agents Caffeine Acidifiers SSRIs Sedatives Early antihistamines Tricyclic antidepressants Antipsychotics Tranquillisers Hypnotics Miscellaneous Alcohol Loop diuretics Lithium ACE inhibitors Narcotic analgesics Alpha agonists Beta agonists Calcium channel blockers
(*) Table compiled from 1-3

Increased detrusor hypersensitivity

Increased urgency and frequency

Clouding of consciousness less awareness of bladder sensation Anticholinergic sideeffects.

Overflow and/or especially poor warning urge

15 Lowers central inhibition Increases rate of bladder filling Polydipsia May induce chronic cough Urethral relaxation Retention Retention Retention Urge, frequency Urge, frequency Urge Stress Stress Stress/overflow Stress/overflow Stress/overflow

NB - ANY DRUG THAT CAUSES CONSTIPATION CAN PRECIPITATE BLADDER DYSFUNCTION.

PHYSICAL EXAMINATION
Together with the history presented in Tables 2 and 3 (above), a basic assessment of a patient with urinary incontinence should include a physical examination. The suggested elements to such examination are presented in Table 4 (below). Those patients who belong to any of the high-risk populations covered by these guidelines will benefit from the more detailed and specific assessment suggestions presented in Section 8 of these guidelines.

TABLE 4: SUGGESTED
Physical Examination CNS

PHYSICAL EXAMINATION AND INVESTIGATIONS Long tracts Saddle anaesthesia Anal tonus Parkinsons disease Dementia

Abdomen

Palpable bladder Pelvic masses Constipation or faecal impaction Organ enlargement/tenderness

Genitourinary

Atrophic changes Cystocele, urethrocele, prolapse Leakage from other than urethra fistula or ectopia Obvious stress incontinence on coughing Tenderness of urethra/bladder

Perineal 16

Strength of pelvic floor contraction Prostate size and consistency Determine sensation Bulbocavernous reflex

Other Investigations

Post-void residual urine volume Bladder diary Urine culture

Check by ultrasound. Repeat if high (>100ml)

Time and volume charted (see Appendix 1) Send MSU Nitrate test not reliable Dipstick for glucose, blood and protein

Specialist referral: Urologist IVP Geriatrician Cystometry, cystoscopy Urodynamics Urogynaecologist

6.3 MANAGEMENT
Much urinary incontinence can be managed successfully and relatively easily within a General Practice setting. Where GPs have limited time resources, initiation of a Care-Plan should be considered. Professionals recommended to be included in a Care-Plan include nurse continence advisors and physiotherapists specialising in incontinence. Occupational therapists may also be consulted, particularly if the incontinence is functional. It is worthwhile exhausting all non-surgical options before specialist referral is considered. Specialists may include urologists, urogynaecologists and geriatricians. Table 5 (below) presents potential management strategies for each type of urinary incontinence. Again, those patients who belong to any of the high-risk populations covered by these guidelines will benefit from the more detailed and specific suggestions presented in Section 8 of these guidelines.

TABLE 5: MANAGEMENT Type


Stress

OF URINARY INCONTINENCE

Management strategies
Weight reduction Pelvic floor muscle exercises Treat constipation or faecal impaction Treat chronic cough Pelvic floor electrostimulation, biofeedback Review patients medications (see table 3) Remove alpha-adrenergic blockers Trial alpha-adrenergic agonists

Relevant Health Services


Dietician Physiotherapist Nurse Continence Advisor Pharmacist Specialist

Urge

Exclude urinary tract infection Treat constipation or faecal impaction Reduce caffeine and alcohol, polydipsia/polyuria Bladder training Biofeedback Review patients medications (see table 3) Trial anticholinergic, or: Trial tricyclic antidepressant

As above 17

Overflow

Consider whether retention due to: bladder outlet obstruction, or detrusor contractile dysfunction/bladder failure, faecal impaction, spinal pathology Confirm diagnosis by urodynamics Remove any outlet obstruction (referral for surgery) Review patients medications Discourage excessive abdominal straining Clean intermittent self-catheterisation

As above

Mixed Functional

Treat presenting symptoms as above Exclude UTI and constipation/faecal impaction Improve access to toilet Manage immobility Manage dexterity, modify clothing (ie, velcro not buttons) Consider bedside commode or urinal Organise assistance, educate family members Arrange chairs/beds that are easy to get out of In cognitively impaired; Prompted or timed voiding Clearly identify toilet

As above As above, plus: Independent Living Centres

All types

Review regularly and titrate any medications Referral to specialist if unsuccessful

References: 1. Tilbury, F., Jayasuriya, P., Taylor, J., Williams, L. (2001). Continence care in the community: Final Report, August 2001. Western Australia: The Royal Australian College of General Practitioners, WA Research Unit. 2. Millard, R. J. (2001). Tackling Incontinence in the community. New South Wales: The Hunter Continence Awareness Project. 3. Pharmaceutical Society of Australia. (2002). Medicines and urinary incontinence, in Australian Pharmaceutical Formulary and Handbook. Canberra: Pharmaceutical Society of Australia. p. 222-225.

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7 Faecal Incontinence
7.1 PRESENTATION
The ability to remain continent .is fundamental to our functioning as socially capable individuals (1). Faecal incontinence, defined as the involuntary loss of anal sphincter control leading to unwanted release of liquid or solid faeces (not flatus) at an inappropriate time or in an inappropriate place, is a major cause of physical, psychological and social disability (2). Moreover, many suffering from faecal incontinence often fail to report it to their family doctors (2) and therefore suffer in silence. Faecal incontinence affects all ages of adult life and in one US study was estimated to cost the community $400,000,000 for pad-style management alone (3).

Physiology
Continence of faeces is maintained by the internal anal sphincter (IAS), the external anal sphincter (EAS) and a number of other inter-related factors including rectal compliance, rectal sensation and an intact anorectal inhibitory reflex. The IAS, which is responsible for 50% to 80% of anal sphincter resting tone, develops spontaneous tone due to its own myogenic activity and extensive adrenergic properties. The EAS, puborectalis and levator ani muscles form a skeletal muscle complex (innervated by the pudendal and inferior rectal nerves) which contributes to the remainder of anal tone. This remaining resting tone results from a reflex arc involving stretch receptors in the levator ani, the anal sphincters and afferent and efferent nerves to the cauda equina (4).

Aetiology
Faecal incontinence can be classified into two broad groups, those with and without structural damage to the sphincter mechanism.
19

TABLE 1: AETIOLOGY
Structural

OF FAECAL INCONTINENCE

Non-Structural

Obstetric-related Damage due to surgery Congenital anorectal abnormalities Smooth muscle degeneration with age Neurological disease (eg. MS, cauda equina lesions) Inflammatory bowel disease Connective tissue disorders Diabetes mellitus Faecal impaction

Structural Damage
Obstetric-related Recent research by Sultan and colleagues (5) has demonstrated that up to one-third of women undergoing their first vaginal delivery show ultrasound evidence of sphincter damage that persists to six months post partum. Thirteen percent of these primigravida women developed symptoms of flatal incontinence or urgency post delivery and in all of these, structural defects were demonstrated (5). In contrast, only 4% of multiparous women developed new sonographic defects although 40% demonstrated pre-delivery sphincter damage. The same study showed anal sphincter defects in 81% of forceps deliveries compared with 24% of vacuum extractions and 36% of unassisted births. These associations of type of delivery and sphincter damage are in the absence of overt third degree tears. A number of large studies have measured the incidence of third degree tears in vaginal deliveries to be between 0.5%-1% (6-8). Risk factors for a woman sustaining a third degree tear include forceps, primiparous delivery, birth weight greater than 4kgs, occipito-posterior position and prolonged second stage of labour. The presence of a third degree tear increases the incidence of faecal incontinence from .074% to 7%.

Damage arising from surgery This is the second most common cause of structural sphincter damage, due primarily to the unavoidable consequences of necessary anal surgery or through outdated therapies such as anal dilatation for anal fissure. Congenital anorectal abnormalities Despite corrective surgery in children with disorders such as ectopic and imperforate ani, incontinence of faeces can persist into adult life indicating ongoing deficiencies in sphincter mechanisms that failed to be corrected during initial surgery (9).

Non Structural Sphincter smooth muscle degeneration associated with advancing age appears to be the most common nonstructural cause of faecal incontinence (10). Other causes include neurological disease eg multiple sclerosis and cauda equina lesions, inflammatory bowel disease, connective tissue disorders, diabetes mellitus and importantly, faecal impaction.

Prevalence
Accurate estimates of the prevalence of faecal incontinence are hampered by differences in the definition of incontinence and specific target populations chosen in community surveys. Ten community-based studies completed around the world since 1984 have been reviewed by Kallantar and his colleagues in a recent Victorian study (2). Where respondents in these studies were limited to 50 years of age or older, the prevalence of incontinence ranged from 3.1% to 15% with a mean of 6.5%. Two studies, one from Germany (11), the other from Australia (12), questioned adults over the age of 18 years and recorded prevalences of 18% and 15% respectively. Kallantar's study, the most recent estimate of faecal incontinence prevalence in Australia in adults over 18 years, recorded an overall prevalence of 11.2%. This study also observed increasing prevalence with age and confirmed earlier research cited above of a prevalence in the 60 years and older age group of approximately 17%. Fifty five percent of those affected in this study were women. In many instances patients with faecal incontinence may not report their condition to their GP. In Kallantars study only 9 out of 33 (27.3%) respondents reported their faecal incontinence to their doctor and only 7 out of 48 sufferers (14.6%) reported being asked about faecal incontinence by their medical practitioner. Patients with incontinence may report loss of either liquid or solid faeces. The incontinence may be passive in nature, where a loss of faeces occurs without the patient being aware. This is often associated with dysfunction of the IAS. In contrast, urge incontinence, where the patient is unable to suppress defecation, is suggestive of EAS damage. Often, faecal incontinence co-exists with urinary stress incontinence.

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7.2 CLINICAL ASSESSMENT History and Physical Examination


Patients should be assessed in regard to type of incontinence (solid, liquid or gas), frequency and impact on lifestyle, including employment and social activities away from home, sport, sexual activity and the requirement to change underwear, shower or use pads. A history of those conditions associated with faecal incontinence (see Table 1) should be sought. Physical examination should be guided by the likely aetiology. Neurological examination should be performed if neurological disease or diabetes is suspected.

TABLE 2: KEY Assessment

ASPECTS OF THE HISTORY AND PHYSICAL EXAMINATION

Content
General Health Co-morbidity (eg. locomotor problems) Previous surgery Presence of conditions presented in Table 1 (above) Inspect anal region for surgical scars, fistulae, patulours anus and the degree to descent on straining (normally less than 1cm) Digital rectal examination to test resting and squeeze pressures Duration Frequency Amount Precipitants (eg. Laxative use) Consistency (gas, solid, liquid) Level of awareness of leakage Psychosocial impact Pain Hesitancy or straining Constipation or faecal impaction Fluid, fibre Include over-the-counter drugs Access to toilet Is toilet clearly identified? (esp. in demented patients) Presence of carer support Dementia Depression Goals and motivation for treatment

General medical and gastrointestinal review

Characteristics of the presenting incontinence

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Other related symptoms

Diet Medication-use Environmental factors

Cognitive status Expectations of treatment

7.3 MANAGEMENT
Management of faecal incontinence will depend on the likely aetiology and the severity. In women of child bearing age the cause may be obstetric-related (damage to the sphincter). Such women will need further investigation that is best undertaken at specialist centres or by individual colorectal surgeons specialising in incontinence. In patients where the incontinence is not severe, conservative management may be undertaken by the GP. Strategies which have been shown to be beneficial include: Altering stool consistency by decreasing the fibre in the diet The use of loperamide which increases EAS tone Encouraging patients to try to keep the rectum empty Referring patients to experienced physiotherapists or continence advisers to learn to perform pelvic floor exercises. Patients not responding to conservative management or those with more serious degrees of incontinence are best referred for specialist management.

TABLE 3: MANAGEMENT
CONDITIONS

OF FAECAL INCONTINENCE AND ASSOCIATED

Conservative strategies for Manipulating stool hardness faecal incontinence Manipulating dietary fibre Loperamide to increase EAS tone Encourage patients to keep rectum empty Pelvic floor exercises Referral to Physio, Nurse continence advisor Faecal impaction
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Evacuation with enemas if extended high Bowel regimen including dietary fibre, fluids, stool softeners and motility agents Full gastroenterological investigation Ensure not caused by laxative misuse Use antidiarrhoeal agents with caution Surgery for anal sphincter weakness Direct sphincter repair Post-anal repair Gracilis muscle transposition with functional electrostimulation Artificial sphincter or colostomy (as last resort) Correction of rectal prolapse Abdominal or perineal rectopexy Procedures for slow transit Caecostomy or appendicostomy and irrigation, constipation or partial colectomy

Chronic Diarrhoea

Specialist Procedures

(*) Please also see the constipation management pamphlet provided in the larger Managing Incontinence in General Practice package.

Specialist investigations
Endorectal ultrasound has enabled damage to the internal and external sphincter mechanisms to be clearly visualised. Anal manometry is used to quantify anal canal pressure and nerve conduction studies to assess pudendal nerve function.

Therapy
Biofeedback techniques have been found to assist approximately two thirds of patients including those with structural sphincter defects (6). Biofeedback and sphincter rehabilitation can assist the majority of patients. Surgical repair is required in a small proportion of patients, especially younger women who are incontinent due to obstetric related damage. Current surgical techniques include direct repair of the external sphincter, replacement of the sphincter with muscle (dynamic graciloplasty) or the use of a prosthesis - the artificial bowel sphincter. Direct anterior repair of the external sphincter has delivered substantial and durable improvement in 70-80% of patients (13). Experience with the artificial bowel sphincter is more limited but a small series currently being evaluated at the Alfred Hospital and the Monash University Department of Surgery suggests promising results, with a reduction of 89% in incontinence following surgery.
References: 1 Kalantar, J. S., Howell, S., & Tally, M. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 2 Kamm, M. A. (2002). Faecal incontinence: Common and treatable. Medical Journal of Australia, 176: 47-8. 3 Johannsen, J. S., & Lafferty, J. (1996). Epidemiology of faecal incontinence: The silent affliction. American Journal of Gastroenterology, 91: 31-36. 4 Cook, T. A. & Mortensen, N. J. (1998). Management of faecal incontinence following obstetric injury. British Journal of Surgery, 85: 293-299. 5 Sultan, A. H, Kamm, M. A., Hudson, C. N., Thomas, J. M., Bartram, C. I. (1993). Anal sphincter disruption during vaginal delivery. New England Journal of Medicine, 329: 1905-11. 6 Buckens, T., Latasse, R., Dramaix, N., Wollast, E. (1985). Episiotomy and third degree tears. British Journal of Obstetrics and Gynaecology, 92: 820-3. 7 Sultan, A. H., Kamm, M. A., Hudson, C. N., Bartram, C. I. (1994). Third degree obstetric anal sphincter tears: Risk factors and outcome of primary repair. British Medical Journal, 308: 887-91. 8 Walsh, C. J., Moody, E. S., Upton, G. J., Motsen, R. W. (1996). Incidence of third degree perineal tears in labour and outcome after primary repair. British Journal of Surgery, 83: 218-21. 9 Hintale, R., Lindahl, H., Marltinen, E., Sariola, H. (1993). Constipation is a major functional complication after an internal sphincter saving posterior sagital anorectoplasty for high and intermediate anorectal malformations. Journal of Pediatric Surgery, 28: 1054-58. 10 Vaizey, C. J., Bartram, C. I., Kamm, M. A. (1997). Primary Degeneration of the Internal Anal Sphincter as a Cause of Passive Faecal Incontinence. Lancet, 349: 612-15. 11 Giebel, G. D., Lefering, R., Troidl, H., Blochl, H. (1998). Prevalence of faecal incontinence: What can be expected? International Journal of Colorectal Disease, 13: 73-77. 12 Lamb, L., Kennedy, M., Chen, S. et al. (1999). Prevalence of faecal incontinence: Obstetric and constipation risk factors: A population based study. Colorectal Disease, 1: 197-203. 13 OBrien, P. (2000). Faecal incontinence: Options for control. Current Therapeutics, 2000: 49-53.

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8 High-Risk Populations
This section presents more detailed information related to incontinence in several high-risk populations. While incontinence is present in all strata of the general population, it is the populations presented in this section that may be most likely to suffer from it. The patient groups covered include: Women of child-bearing age Post-Menopausal women Men Children Elderly Those with serious medical conditions, including: Cancer Dementia Diabetes mellitus Intrinsic bladder disease Intrinsic bowel disease Multiple sclerosis Parkinsons disease Spina bifida/myelomeningocele Spinal cord injury Stroke

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8.1 INCONTINENCE IN WOMEN OF A CHILD BEARING AGE BACKGROUND


Urinary incontinence is common in women of child-bearing age where childbirth is a major risk factor. That is, the prevalence of incontinence is much lower in nulliparous women. The most common form is stress incontinence with urge incontinence having a much lower prevalence and mixed incontinence being quite uncommon.

Maintenance of Continence
For continence to be maintained, intra-urethral pressure must be greater than intra-vesical pressure both at rest and during activity. To achieve this, urine is prevented from leaking during bladder filling by a number of factors acting in concert on the bladder and the urethra. During bladder filling, reflex inhibition of the detrusor muscle maintains a low constant pressure within the bladder. This pressure is exceeded by the intra-urethral pressure, which ensures that no urine escapes until voluntary voiding (1). During micturition, detrusor contraction results in funnelling which opens the bladder neck. This, in conjunction with shortening of the urethral smooth muscle which assists funnelling, and the reflex inhibition of the external urethral sphincter (rhabdosphincter), enables the passage of urine. Following micturition, closure results from elastic recoil of the connective tissue and contraction of bladder neck smooth muscle.

How is Intra-Urethral Pressure Maintained between Voiding?


A number of complex and inter-related factors act to maintain intra-urethral closure pressure in excess of intravesical pressure: 1.
26

2.

3. 4.

5.

The bladder (in its normal anatomical position) is suspended by the pubo-urethral ligament and the levator ani muscle fascia. In this position it is ideally placed to receive transmitted abdominal pressure to the external urethral sphincter which increases in tone during coughing and straining etc (2). The external urethral sphincter (rhabdosphincter), which extends from the bladder neck to the urogenital diaphragm, maintains constant tone for long periods. It is also capable of reflexly increasing tone, and therefore pressure, during sudden increases in abdominal pressure during coughing, laughing etc. It is innervated by the pudendal and pelvic splanchnic nerves. Smooth muscle within the urethra (longitudinal and circular) also contributes to urethral closure. Pelvic floor factors have been postulated by Petros and Ulmsten (3) which comprise three distinct closure mechanisms: The contraction of the anterior pubococcygeus which closes the urethra The bladder neck closure mechanism in which the bladder neck is closed off by elongation backwards and downwards against an immobilised proximal urethra A voluntary group of pelvic floor muscles which are normally not involved in bladder neck closure but can be trained by pelvic floor exercises. The urethral mucosa is richly folded and thus juxtaposes both sides to help form a urethral seal (4).

Urinary Incontinence and Childbirth


Although the incidence of urinary incontinence increases with age, pregnancy and childbirth are important factors in women of child-bearing age (5, 6). Electromyographic studies performed during pregnancy and the puerperium have demonstrated varying degrees of pudendal nerve denervation in primiparous women (5, 7, 8). Labour itself is believed to damage branches of the pudendal nerve by direct pressure of the foetal head on the pelvic floor. The longer the active part of the second stage of labour and the heavier the baby the more likelihood of nerve damage (5). Other research has also identified instrumental delivery and caesarean section during labour, but not prior to labour, as risk factors (7, 8). How long pregnancy related pudendal nerve damage persists is unclear as few women have been followed up for extended periods. However, EMG verifiable pudendal neuropathy in women up to five years following childbirth has been identified (9) and another five year follow up study of women delivering at a Birmingham hospital found persistence of birth onset stress incontinence in 75% of affected women for greater than one year following childbirth (10). Direct injury to anatomical supports structures (muscle ligaments and fascia) during childbirth is also thought to weaken the pelvic floor and predispose women to stress incontinence (6). It has been observed that scar tissue that forms as a result of tissue damage is never as strong as the original tissue and this has been attributed to a reduction in the ratio of collagen type II to type III fibres (11). Thus, childbirth and chronic straining can lead to overstretching of pelvic tissue with faulty tissue deposition and scar formation (12). Abnormal collagen (reduction of type II and III ratio) has also been reported in women with prolapse and nulliparous women with stress urinary incontinence (13). The consequence of tissue collagen damage and varying degrees of muscle enervation is to weaken and loosen the attachments of striated smooth muscle involved in the support of the pelvic floor and in particular the closure mechanism of the urethra. Consequently, the pressure transmission mechanism that closes the urethral sphincter during sudden increases in intra abdominal pressure fails and stress incontinence occurs (3).

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Pathogenesis of Incontinence
Stress Incontinence Genuine stress incontinence may be defined as the involuntary loss of urine occurring when, in the absence of a detrusor contraction, the intravesical pressure exceeds the maximum urethral pressure (14). This definition is derived from urodynamic studies.
Women experience this as the involuntary loss of urine during physical activity which increases intra-abdominal pressure, eg coughing, sneezing, lifting, jumping etc. It is invariably a failure of the sphincter mechanism to maintain closure pressure, most commonly due to a factor or factors acting in concert, eg muscle and or nerve damage, age related denervation of muscle, changes in collagen and elastin as a result of birth related damage or genetic factors, and declining hormonal status.

Urge Incontinence During normal bladder filling the detrusor muscle does not voluntarily contract despite provocation (14). Under certain circumstances the detrusor may become unstable where it contracts either spontaneously or on provocation. This instability is thought to be due to age-related detrusal changes or urinary tract infection where inflammatory changes increase afferent fibre output with a corresponding increase in efferent activity and hence detrusor contraction (2).
Alternatively, it may be considered to be hyper-reflexic where its overactivity has a neurological cause, eg CNS tumours, cerebrovascular disease, dementia or peripheral causes such as multiple sclerosis, cauda equina injury and peripheral neuropathy. Whichever type, the common feature is a degree of denervation resulting in increased excitability of muscle with resulting abnormal detrusor contractions. For the woman, this results in involuntary loss of urine associated with a strong desire to void (urgency).

PREVALENCE
Prevalence studies for urinary incontinence have been carried out using cross-sectional studies since the early 1980s. These community-based studies have used various questions to measure incontinence in different age groups and in specific sub-groups such as pregnant women. Therefore, estimates have often varied considerably. When self-reported symptoms of incontinence are verified by urodynamic studies it would appear that stress incontinence is under reported in community surveys and mixed incontinence over-represented. Sandvick and colleagues (15) validated prevalence estimates in a study of Swedish women by subsequent urodynamic testing. They observed the prevalence of stress incontinence to increase from 51% on questionnaire to 77% following urodynamic testing. Mixed incontinence, which was reported by 39% of women, was found to exist in only 11% with confirmatory studies and urge incontinence essentially remained unchanged. Acknowledging this possible under diagnosis from answers gleaned from community surveys, the prevalence in four major studies in which women of child-bearing age were included yielded estimates from 14% to 29% with a mean of 21% (16-19). The three main types of incontinence have been investigated by a number of researchers across a wide range of age groups. These are listed in Table 1 (below):

TABLE 1: RELATIVE
Author Iosif Hrding Elving Sommer Harrison Yarnell Diokno Holst Burgio Lara Sandvik Mean (range)

PROPORTIONS OF DIFFERENT TYPES OF

UI

IN THE GENERAL

FEMALE POPULATION.

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Age (years) 61 45 30-59 20-79 20+ 18+ 60+ 18+ 42-50 18+ 20+

N 902 515 2 631 414 314 1 000 1 955 851 541 556 1 820

Stress (%) 40 75 48 38 48 50 29 52 50 48 51 48 (29-75)

Urge (%) 27 11 7 33 9 19 10 25 12 27 10 17 (7-33)

Mixed (%) 33 14 45 29 44 31 61 23 38 21 39 34 (14-61)

(*) Adapted from 20. Diagnoses other than stress, urge and mixed are excluded.

The above estimates give a mean prevalence of approximately 48% for any kind of incontinence and 41%, 17% and 34% for stress, urge and mixed incontinence respectively. This overall prevalence is somewhat higher than the 35.3% reported in a large cross sectional study of 1,541 women in South Australia (21).

Severity
When severity is explored, the variation in reported prevalence diminishes. Although various methods are used to measure severe incontinence, when moderate or severe incontinence is combined with the degree of bother (ie only those women bothered by their leakage), about 20% of incontinent women or 6% of all women appear to suffer incontinence severe enough to seek help.

Incontinence in Pregnancy
As the measurement of prevalence in the population of pregnant women has involved different study designs (cross-sectional, prospective, retrospective), definitions and types of incontinence, wide estimates of prevalence ranging from between 20-60% have resulted. Because of this three of the larger studies are reported here: A survey of 1,505 women at 3 months post partum in Christchurch, New Zealand (22) recorded a prevalence of 34.3%. Of these, 29.9% suffered stress incontinence while 14.8% were classified as having urge incontinence. Daily pad usage was required by 1.1% and used sometimes by 7.4%. Forty-three percent of primigravidas were

incontinent prior to three months post partum. Of these 43%, 19.4% suffered incontinence prior to pregnancy, 62.6% developed incontinence during the pregnancy while 17.6% of incontinent primigravidas first developed incontinence following childbirth. In a large retrospective study of 11,701 Birmingham women, (10) 15.2% reported stress incontinence starting for the first time within three months of birth and lasting for longer than six weeks. Another 5.4% reported a similar duration but had experienced it previously either during pregnancy or before. Of the 15.2% who experienced stress incontinence for the first time in the post partum period, 75% continued to suffer from it for at least one year and 70% were afflicted for between one and nine years following childbirth. Another large cross sectional study of women in Dublin in 1987 (23), consisting of interviews of 7,771 women on the second or third day of the puerperium, 61% were incontinent, however the type of incontinence was not specified. Of the primigravida subgroup 55% were incontinent, 5% reporting incontinence before the pregnancy and 50% during pregnancy. With increasing parity, more women reported incontinence before pregnancy and less developed it during pregnancy although the net prevalence in multiparous women was higher than primigravida, being 68.3% versus 55%.

PRESENTATION Help Seeking Behaviour


It would seem the majority of incontinent women do not report their condition. For many women with mild incontinence, non-disclosure may be appropriate. For those with more severe symptoms, cultural, religious and other factors have been identified to influence help seeking behaviour. For those who do seek help increasing age, duration of symptoms, severity and urge and mixed types are more predictive of seeking help.
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Stress Incontinence
As mentioned previously, many women with minor degrees of incontinence may not seek medical assistance. Those with more severe symptoms may report loss of urine during physical exertion, coughing, laughing, sneezing or lifting where intra-abdominal pressure is increased. Women may report restrictions to social and sporting activities, the need to change underwear frequently or having to wear pads.

Urge Incontinence
Unlike stress incontinence where urinary symptoms are more characteristic, women with detrusor instability often report more varied symptoms however, the hallmark of this type of incontinence is an uncontrollable urge to pass urine which cannot be controlled and which leads to loss of urine. It is often associated with urinary frequency during the day and may be associated with a degree of nocturia.

Gastrointestinal symptoms
As noted in Section 7, faecal incontinence is often the result of structural damage suffered while giving birth, particularly on first vaginal delivery (38). Where faecal incontinence is obstetric-related resulting in damage to the sphincter, further investigation undertaken at specialist centres or by individual colorectal surgeons is recommended.

CLINICAL ASSESSMENT History

Assessment of women requires the dual task of clarifying the type of incontinence (stress, urge or mixed) and attempting to find a cause. It is not always easy to be confident from the history as to which type of incontinence the patient has or, if mixed incontinence is suspected, which component is dominant. Ishiko and colleagues (24) have devised a urinary incontinence questionnaire containing 15 questions which can be scored to produce aggregate stress and urge scores (see Appendix 3). Women with high stress scores and low urge scores (stress 7-26, urge 0-6) have high predictability of stress incontinence, those with high urge scores and low stress scores (urge 7-26, stress 0-6) are likely to have urge incontinence. Mixed incontinence is likely when both stress and urge scores are in the range of 7-18. Scores attained from this instrument are also sensitive to therapy, making the questionnaire useful for monitoring progress following treatment. In addition to classifying the type of incontinence, doctors need to assess the severity of symptoms by asking about quality of life issues and the womans desire for treatment. Questions should be directed to the following (see Table 2, below):

TABLE 2: KEY
* * * * * * *

ASPECTS OF HISTORY-TAKING

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Degree of recurrence Presence of pain Presence of haematuria History of recurrent UTI Voiding symptoms Past pelvic irradiation or surgery Obstetric history, especially parity, birth weights, prolonged second stage of labour, instrumental delivery * History of neurological disease or trauma

This section focuses on urinary incontinence. For assessment of faecal incontinence refer to Section 7.2

Physical Examination
Table 3 (below) presents a suggested examination of an incontinent woman (25).

TABLE 3: SUGGESTED PHYSICAL EXAMINATION


Physical Examination Examine the perineum. Observe the laxity of the anterior and posterior pelvic walls. Normally these do not cross the longitudinal midline of the vaginal axis. Assess the degree of cervical or vaginal apex (in hysterectomised women) descent during valsalva manoeuvre. Note presence of perineal scarring and oestrogen status of the vaginal epithelium. Assess sacral neurological status (anal reflex- S2-S5) of the perineum and lower limbs (where indicated). Conduct digital rectal examination to test for passive and active anal tone and to exclude impacted faeces. The patient should be asked to cough or strain (stress test), noticing any leakage of urine. This can be done in the lateral or standing position. Test the urine with a dipstick for bacteriuria and send suspected samples for microscopy and culture. Voiding diary - Although there is no consensus over how long to record symptoms, a period of between 3 and 7 days would seem reasonable. The amount of urine passed is recorded along with the time and amount of drinks and episodes of urgency or leakage (26) (see Appendix 1). Post Void Urine - Incontinent women with complex symptoms, with a history of previous pelvic surgery or irradiation, require evaluation of post-void urine using ultrasound.

Special tests

31

MANAGEMENT
The management of stress, urge and mixed incontinence, where no significant organ prolapse is evident and when symptoms are not severe, may be competently undertaken in general practice in the first instance with lifestyle interventions, pelvic floor muscle training, antimuscarinic medication and bladder retraining techniques where appropriate (27). Patients with overflow incontinence (post void residual greater than 200mls) are best referred for specialist management to exclude bladder outlet obstruction or detrusor under activity (27). Where there is evidence of urinary infection, antibiotics should be prescribed as 60% of women with stable bladders will develop detrusor overactivity with urinary infection. If oestrogen deficiency is suspected local or systemic hormonal therapy should be considered, although this is most effective for urinary tract symptoms rather than incontinence itself (27).

Lifestyle interventions
Evidence suggests that only women who are morbidly obese are likely to benefit from weight loss for obvious reasons all women who are overweight or obese should be encouraged to lose weight.
(28)

. However,

Caffeine and fluid intake appear to have a minor role, if any, in the pathogenesis of incontinence. Restrictions on these are not necessarily supported by evidence and decisions should be based on the individual patients circumstances (28).

Pelvic Floor Muscle Training (pelvic floor exercises)


There is level 1B evidence that Pelvic floor muscle training (PFMT) is better than no treatment for a range of incontinence symptoms (stress, urge, mixed). In the short term cure/improvement rates can be expected in about 65-74% of women. Improvement is generally more common than cure (28). For women with only stress incontinence PFMT should be offered through experienced physiotherapists or nurse continence advisers. In women with urge incontinence or mixed symptoms PFMT should also be offered on its own or in conjunction with a bladder retraining program. Bo (29) has suggested the following regimen for PFMT: 3 sets of 8-12 slow maximum contractions lasting 6-8 seconds performed 3-4 times per week for a duration of 15-20 weeks. Please see the file accompanying these guidelines for Continence Foundation of Australia pamphlets, including patient information of pelvic floor training. Patients may benefit from referral to physiotherapists and nurse continence advisers for PFMT.

Bladder Retraining
Level 1B evidence exists that bladder retraining is effective for urge, stress and mixed incontinence (28). Bladder retraining programs can be of various types but generally have the following features: Scheduled voiding regimen with increasing intervals Urgency control strategies ie relaxation techniques, distraction and PFMT Self-monitoring of voiding behaviour Women must be cognitively intact and motivated to undergo bladder retraining.
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Please see the file accompanying these guidelines for Continence Foundation of Australia pamphlets, including patient information of bladder retraining. Patients may benefit from referral to nurse continence advisers for bladder retraining.

Pharmacotherapy
Where urge incontinence is presumed, anticholinergic drug treatment may be tried in conjunction with the above methods. Drugs which have been shown to be efficacious and recommended by the Pharmacological Treatment of the Urinary Incontinence Committee of the First International Consultation on Incontinence (30) are; Propantheline Emepronium Trospium Tolterodine Oxybutynin Propiverine.

Doctors need to be cognisant of the anticholinergic side effects on other organs when contemplating prescribing these medications and should weigh the benefits against potential side effects.

Specialist Management
Patients not responding to initial empirical therapy in general practice or those with severe symptoms or evidence of pelvic organ prolapse are best referred for specialist management. In particular, genuine stress incontinence, which does not respond to initial empiric therapy, may benefit from surgery. Some authorities argue that research evidence demonstrates the superiority of surgical intervention over physiotherapy and recommend patients be given the choice of surgery initially instead of physiotherapy (31). In all cases where surgery is contemplated, the International Continence Society recommends that prior urodynamic studies should be undertaken.

The following procedures are often used: 1. Colposuspension - This operation is considered the gold standard for stress incontinence. The prevalence of continence at five to ten years in five follow up studies following colposuspension was approximately 75% (31). 2. Suburethral sling operation - These elevate the bladder neck and are popular in the USA. Although the success rate equals colposuspension, voiding difficulties and detrusor instability are three times greater than with colposuspension (31). 3. Tension free vaginal tape - Prolene mesh is taped under the distal urethra and tensioned to produce elevation. This technique is quick to perform, has short hospitalisation and similar success and complication rates in the short term as colposuspension (31). 4. Laparoscopic colposuspension - This method produces similar short-term success rates as open colposuspension with less intraoperative trauma and blood loss. It is still too early to tell whether this technique should be first choice in surgical procedures (31). 5. Transurethral Injections - Fat, collagen and silicone may be injected around the proximal urethra for women who are either too unfit for surgery, or following surgery for intrinsic sphincter deficiency where it augments closure pressure (31). 6. Artificial Sphincters - In some patients who have undergone recurrent surgery for stress incontinence success rates of 92% can be obtained with artificial sphincters (32). However, follow up revision surgery is common for a proportion of patients undergoing this procedure.

Faecal Incontinence

Faecal incontinence can be addressed conservatively with dietary modification such as increasing fluids and manipulating stool consistency. Pads may be used to manage symptoms initially. Pelvic floor exercises may be useful, and biofeedback has been found to assist a majority of patients with structural sphincter damage (33, 34). Medication such as Loperamide can be used to increase resting anal pressure of the internal sphincter although further studies are required.
(35, 36)

33

For those with mechanical disruption of sphincter, surgical repair may be required. Techniques include direct repair of the external sphincter, artificial sphincter implant or graciloplasty (35, 36, 37).
References 1. De Groat, W. C., Downie, J. W., Levin, R. M. (1999). Basic neurophysiology and pharmacology, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 105-154. 2. DeLancey, J. O., Foeler, C. J., Keane, K. et al (1999). Pathophysiology, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 227-294. 3. Petros, P. E., & Ulmsten, U. I. (1990). An integral theory of female urinary incontinence: Experimental and clinical considerations. Acta Obstetricia et Gynecologica Scandinavica,153: 7-31. 4. Zinner, N. R., Sterling, A. M., & Ritter, R. C. (1980). Role of inner urethral softness in urinary incontinence. Urology, 16: 115-117. 5. Allen, R. E., Hosker, G. L., Smith, A. R., & Warrell, D. W. (1990). Pelvic floor damage and childbirth: A neurophysiological study. British Journal of Obstetrics and Gynaecology, 97: 770-779. 6. Handa, V. L., Toni, A., Harris, M. D. et al (1996). Protecting the pelvic floor: Obstetric management to prevent incontinence and pelvic organ prolapse. Obstetrics and Gynecology, 88 (3): 470-478. 7. Snooks, S. J., Setchell, M., Swash, M., et al (1984). Injury to innervation of pelvic floor sphincter musculature in children. Lancet, 2(8402): 546-550. 8. Snooks, S. J., Swash, M., Henry, M. M., et al (1985). Risk factors in childbirth causing damage to pelvic floor innervation. British Journal of Surgery, 72: S15-S17. 9. Snooks, S. J., Swash, M., Mathers, S. E., Henry, M. (1990). Effect of vaginal delivery on the vaginal floor: A 5-year follow-up. British Journal of Surgery, 77 (12): 1358-1360. 10. MacArthur, C., Lewis, M., Rick, D. (1993). Stress incontinence after childbirth. British Journal of Midwifery, 1 (5): 98-103. 11. Norton, P., Boyd, C., Deak, S. (1992). Abnormal collagen ratios in women with genitourianry prolapse. Neurourology and Urodynamics, 11: 2-4. 12. Benson, J. T. (1992). Female pelvic floor disorders: Investigation and management. New York: WW Norton & Company. 13. Jackson, S., Avery, N., Eckfoed, S., et al (1995). Connective tissue analysis in genitourinary prolapse. Neurourology and Urodynamics, 14: 412-414. 14. Abrams, P., Blaivas, J. G., Stanton, S. L., & Andersen, J. T. (1988). The standardisation of terminology of lower urinary tract function. Scandinavian Journal of Urology and Nephrology Suppl, 114: 5-19. 15. Sandvik, H., Hunskaar, S., Vanvik, A. et al (1995). Diagnostic classification of female urinary incontinence: An epidemiologic survey corrected for validity. Journal of Clinical Epidemiology, 48: 339-343. 16. Yarnell, J. W., Voyle, G. J., Richards, C. J. & Stephenson, T. P. (1981). The prevalence and severity of urinary incontinence in women. Journal of Epidemiology and Community Health, 35: 71-74.

2 Refer also to section 7.3 for general guidelines on management of faecal incontinence.

34

17. Holst, K., & Wilson, P. D. (1988). The prevalence of female urinary incontinence and reasons for not seeking treatment. New Zealand Medical Journal, 101: 756-758. 18. Mkinen, J., Gronroos, M., Kilholma, P., et al (1992). Incidence of urinary incontinence in adult Finnish women. Duodecim, 108: 481-485. 19. Sandvik, H., Hunskaar, S., Seim, A., et al (1993). Validation of a severity index in female urinary incontinence and its implementation in an epidemiological survey. Journal of Epidemiology and Community Health, 47: 497-499. 20. Hunskarr, S., Arnold, E. P., Burgio, K. et al (1999). Epidemiology and natural history of urinary incontinence, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 197-226. 21. MacLennan, A. W, Taylor, A. W., Wilson, D. H. et al (2000). The prevalence of pelvic floor disorders and their relationship to gender, age, parity and mode of delivery. British Journal of Obstetrics and Gynaecology, 107: 1460-1470. 22. Wilson, R. D., Herbisole, R. M., & Herbisole, G. P. (1996). Obstetric practice and the prevalence of urinary incontinence three months after delivery. British Journal of Obstetrics and Gynaecology, 103: 154-161. 23. Marshall, K., Thompson, K. A., Walsh D. M., et al (1998). Evidence of urinary incontinence and constipation during pregnancy and post partum: Survey of current findings at the Rotunda Lying in Hospital. British Journal of Obstetrics and Gynaecology, 105: 400-402. 24. Ishiko, O., Hirai, K., Sumi, T. et al (2000). The urinary incontinence score in the diagnosis of female urinary incontinence. International Journal of Gynaecology and Obstetrics, 68: 131-137. 25. Shull, B. L., Hurt, G., Halaska, M. et al (1999). Physical examination, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 333-350. 26. Donovan, J., Naughton, M., & Gotoh, M. (1999). Symptom and quality of life assessment, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 295-332. 27. Thuroff, J. W., Abrams, P., & Artinbani, W. (1999). Clinical guidelines for the management of incontinence, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 931-944. 28. Wilson, R. D., Bo, K., Boudier, R., et al (1999). Conservative management in women, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 579-636. 29. Bo, K. (1995). Pelvic floor muscle exercise for the treatment of stress urinary incontinence: An exercise physiology perspective. International Urogynecology Journal, 6: 282-291. 30. Anderson, K., Appell, R., Cardozo, L. et al (1999). Pharmacological treatment of urinary incontinence, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 447-486. 31. Jarvis, G. J., Bent, H., Cortesse, A. et al (1999). Surgical treatment incontinence in adult women: Surgery of female lower genito-urinary fistulae, in Incontinence, P. Abrams, S. Khoury, A. Wein, (Eds). London, UK: Health Publications Ltd. p. 637668. 32. Webster, S. D., Perez, L. M., Khoury, J. M. et al (1992). Management of stress urinary incontinence using artificial urinary sphincter. Urology, 39: 499-503. 33. Buckens, T., Latasse, R., Dramaix, N., Wollast, E. (1985). Episiotomy and third degree tears. British Journal of Obstetrics and Gynaecology, 92: 820-3. 34. Cook, T. A. & Mortensen, N. J. (1998). Management of faecal incontinence following obstetric injury. British Journal of Surgery, 85: 293-299. 35. Cheetham, M. J., Kamm, M. A., & Phillips, R. K. S. (2001). Topical phenylephrine increases anal canal resting pressure in patients with faecal incontinence. Gut, 48: 356-359. 36. Nagle, D., (1999). Rectal prolapse and fecal incontinence. Primary Care, 26 (1): 101-111. 37. OBrien, P. (2000). Faecal incontinence: Options for control. Current Therapeutics, 2000: 49-53. 38. Sultan, A. H, Kamm, M. A., Hudson, C. N., Thomas, J. M., Bartram, C. I. (1993). Anal sphincter disruption during vaginal delivery. New England Journal of Medicine, 329: 1905-11.

8.2 INCONTINENCE AND THE MENOPAUSE BACKGROUND


The mean age at which the menopause occurs is 51 years (1). Most women therefore live up to half of their lives in a state of oestrogen depletion. A number of urogenital and gastrointestinal changes occur in these older women, however there is debate as to whether incontinence is actually related to menopause itself, or is simply a product of ageing (2, 3, 4). Oestrogen has been employed in the management of urinary incontinence for over 50 years (5), and there does appear to be good theoretical indication for such treatment. Oestrogen receptors have been identified in the urethra, vagina, bladder, and pelvic floor (3, 4, 6, 7, 8). Receptors have also been located in areas of the brain concerned with urine storage and release (2, 3). The role of oestrogen in incontinence is strengthened by reports of variation of urinary symptoms with oestrogen levels across the menstrual cycle (2, 4). It has been argued that declining oestrogen leads to the atrophy of oestrogen dependent cells, predisposing to problems with continence control (9). In practice, however, while hormone replacement therapy (HRT) may relieve some urogenital symptoms it in fact does very little to reverse incontinence in postmenopausal women. Rates of incontinence in women taking HRT are often higher than in those who take no such therapy (8, 10, 11). This section aims to describe the various factors influencing the presentation and management of incontinence in postmenopausal women. While information specifically related to the effects of the menopause is presented, it is suggested that management of incontinence in postmenopausal women is essentially the same as for any older adult.

PRESENTATION Urinary symptoms


Postmenopausal women typically present with a range of significant urogenital changes. The vaginal epithelium usually atrophies without oestrogen and can become inflamed, contributing to a range of irritative symptoms (see Table 1) (12). The female urethra is also highly receptive to oestrogen and menopause may predispose to stress incontinence through an inability of the urethra to maintain normal pressure (3, 12). Indeed, proximal urethral pressure has been observed to be lower after menopause and this appears to be independent of age (13, 14). Prolonged oestrogen deficiency is thought to be associated with urinary frequency, nocturia, incontinence, and urgency (3, 4). Urinary incontinence in postmenopausal women is also associated with urinary tract infection (UTI) (3, 4, 15). Postmenopausal women with recurrent UTI are also more likely than case-controlled women with no UTI to have clinically significant post-voiding residual urine volumes and cystocele (15). Women who have undergone hysterectomy may be more likely to develop incontinence (16). Such surgicallyinduced menopause not only decreases oestrogen but may cause damage to the supportive structures of the urethra or bladder, or to the pelvic plexus (17). It appears, though, that the risk of urinary incontinence after hysterectomy is not immediate but increases many years post-surgery (8). Similarly, there is no evidence to suggest that there is a large increase in the prevalence of incontinence at the time of natural menopause (16) and severe symptoms may only occur many years later. In fact, levels of oestrogen are in decline for many years following the last menstrual period, and some women may maintain reasonably high levels for some time (16). Symptoms may therefore not be reported by patients when presenting around the time of menopause.

35

Gastrointestinal symptoms
Older women are reluctant to volunteer a history of faecal incontinence during consultation about the menopause although, of the normal general population, faecal incontinence is most prevalent in postmenopausal women (18, 19) . It is thought that the decline of oestrogen may have an effect on the integrity of pelvic floor connective tissues, and that a lack of oestrogen may allow the effects of previous obstetric injury to become more noticeable (18). Most gastrointestinal changes, such as reduced anal sphincter pressure, are linear with age and are not thought to be related to the menopause (20). However, a decrease in the electrosensitivity of the anal mucosa has been found to be associated with menopause (21), and may mean that menopausal women have a reduced anal sensation. Constipation is a commonly reported symptom of menopause, and may be particularly associated with hysterectomy, although results are inconsistent (21). Table 1 (below) lists a range of physiological factors found in post-menopausal women that may be influential in incontinence.

TABLE 1: PHYSIOLOGICAL

36

CHANGES FOUND IN POST-MENOPAUSAL WOMEN*

Reduced urinary flow rate Increased post-void residual volume Stronger first desire to void Increased bladder capacity Decreased detrusor pressure during voiding Increased fibrosis of the bladder neck Increased collagen content in the bladder Decrease in the number and diameter of muscle fibres in pelvic floor Increase in night-time urine output Vaginal atrophy symptoms Dryness Itching Burning Dyspareunia Higher rate of recurrent urinary tract infection
(*) Adapted from 3

PREVALENCE
Clinically significant urogenital symptoms are usually found to be present in around 50% of post-menopausal women (22). Actual urinary incontinence is typically reported in over 30% of postmenopausal women (23), however rates may be far higher. A study that compared subjective and objective urinary incontinence in postmenopausal women found that, on average, self-reported continent women had a similar amount of leakage on pad weight test as self-reported incontinent women (23). Rates have in fact been as high as 57% for urge incontinence in women during early menopause, and this was found to be unrelated to hormonal levels or use of HRT (24). Indeed, urge incontinence is thought to rise in post-menopausal women, while stress incontinence seems to fall (3). In 1084 71-year-old women and 611 81-year-old women, urinary incontinence (stress, urge, or mixed) was present in 46% and 45% of women respectively. The symptoms were moderate, severe or unbearable in 48% and 59% respectively (11). Of note, in this study and in a review (8) women on current oestrogen replacement therapy had a higher prevalence of symptoms. The reason for this is unclear, however, it may reflect the severity of pretreatment symptoms and the lack of success of the therapy. An Australian study found a 7-year incidence of 35% for incontinence in women between 45 and 55 years of age (25) . Most likely to be affected were women who were overweight, who had previous gynaecological surgery, history of UTI, diarrhoea or constipation, or three or more children (25). Others agree that prevalence is likely to be higher following surgical rather than natural menopause (26). In summary, the prevalence of urinary incontinence in post-menopausal women is probably between 30% and 50% for any incontinence and between 6% and 14% for daily incontinence (8). As with older men, rates of reporting of incontinence are not ideal in postmenopausal women. One study found

that only 26% of incontinent postmenopausal women had ever seen their doctor about urinary incontinence (26). Even in socially progressive countries such as Sweden, up to 40% of women do not seek medical advice for moderate-to-unbearable incontinence (11).

ASSESSMENT
Assessment of a post-menopausal woman with incontinence should not assume that a lack of oestrogen alone is the cause. A detailed examination such as that presented in Section 8.5 (Elderly) of these guidelines should be performed to rule out all possible causes. Table 2 (below) adds to the information presented in that section by more specifically detailing a suggested gynaecological examination. TABLE 2: GYNAECOLOGICAL
EXAMINATION FOR POSTMENOPAUSAL WOMEN*

Inspect peri-vaginal skin for signs of irritation caused by urine Examine vulva for signs of dystrophy or lesion Inspect labia minora for signs of irritation Examine for prolapse Examine cervix (in women with uterus) Examine vaginal epithelium for atrophy, inflammation Investigate presence of masses Measure vaginal pH Oestrogen level

(*) Based on 12

MANAGEMENT
Management of incontinence in older women should essentially follow the guidelines presented more broadly for elderly patients (see section 8.5). Oestrogen has been used for the treatment of urinary symptoms for many years, however there are few randomised, placebo-controlled, double-blind trials to support its efficacy in treating incontinence (2). Two meta-analyses have failed to find that oestrogen is beneficial in objectively treating urinary incontinence, however subjective improvement may be found (8), especially with symptoms of urgency and frequency (27, 28). Overall, however, oestrogen does not appear useful in managing incontinence (29, 12, 8). Similarly, oestrogen-progestin combination therapy has not been shown as successful in treating urinary incontinence and a recent study has shown the reverse trend (10). Oral oestrogen may be more helpful in irritative symptoms associated with vaginal atrophy (2, 4), however most controlled studies appear to have found little benefit over that of placebo (2). Oestrogen, when applied intravaginally, may be more useful in treating urinary tract infection (UTI). A doubleblind, placebo-controlled study demonstrated a reduction in the incidence of recurrent UTI in postmenopausal women (30). It is thought that topical oestrogen may alleviate symptoms of urgency, frequency, nocturia, and dysuria and atrophic vaginitis (31, 2), however no non-oral treatment has been shown to be superior to others (12). Treatment of faecal incontinence in post-menopausal women is under-researched. One study trialed HRT in 20 post-menopausal women with faecal incontinence for six months. A quarter of these women was asymptomatic after six months and a further 65% had improved flatus control, reduced urgency and reduced faecal staining (18). The treatment of faecal incontinence with HRT requires further research. Observations of no or very little objective improvement in urinary incontinence when oestrogen is used alone have led a number of researchers to trial alpha-adrenergic agonists in combination with HRT. This approach has been shown to be more successful than either drug alone (32, 33). Decisions regarding commencement of hormone replacement therapy (HRT) are likely to be influenced by a variety of factors. Levels of oestrogen in post-menopausal women are highly variable, even many years postmenopause and therefore there is not always an urgent need for its replacement (34). Patients views on the risks and benefits of HRT are influenced by their own and members of their familys medical history (35). Older breast cancer survivors are more reluctant to take HRT (35).
37

Management of incontinence in postmenopausal women may include any of the treatments found in Section 8.5 of these guidelines (Elderly). Table 3 (below) adds to that information by presenting specifically oestrogen-based therapies for urogenital symptoms not including incontinence. Oestrogen alone is not recommended as a treatment for urinary incontinence and there is currently insufficient evidence to support its use in the treatment of faecal incontinence.

Table 3: Oestrogen-based treatments for urinary symptoms in post-menopausal women*


Vaginal cream Slow-release oestrogen-releasing vaginal ring Vaginal oestrogen tablets Skin patches Oral oestrogen Oral oestrogen-progestin combination

(*) Adapted from 12

Oestrogen alone is not recommended as a treatment for urinary incontinence in postmenopausal women and there currently insufficient evidence to support its use in the treatment of faecal incontinence (II/B)

38

References: 1. McKinley, S. M., Brambilla, D. J., & Posner, J. G. (1992). The normal menopause transition. Maturitas, 14: 103-105. 2. Hextall, A. (2000). Oestrogens and lower urinary tract function. Maturitas, 36: 83-92. 3. Hextall, A. & Cardozo, L. D. (1998). The effect of estrogen deficiency on the bladder, in The Management of the Menopause: Annual review 1998, J. Studd (Ed). London, England: The Parthenon Publishing Group. p. 39-47. 4. Hextall, A. & Cardozo, L. (2001). The role of estrogen supplementation in lower urinary tract dysfunction. International Urogynecologic Journal of Pelvic Floor Dysfunction, 12 (4): 258-261. 5. Salmon, U. L., Walter, R. I., & Gast, S. H. (1941). The use of estrogen in the treatment of dysuria and incontinence in postmenopausal women. American Journal of Obstetrics and Gynecology, 14: 23-31. 6. Ingelman-Sundberg, A., Rosen, J., Gustafson, S. A., et al. (1981). Cystosol estrogen receptors in urogenital tissues in stressincontinent women. Acta Obstetricia et Gynecologica Scandinavica, 60: 585-586. 7. Smith, P., Heimer, G., Noegren, A., et al. (1990). Steroid hormone receptors in pelvic muscles and ligaments in women. Gynecology and Obstetrics Investigations, 30: 27-30. 8. Thom, D. H. & Brown, J. S. (1998). Reproductive and hormonal risk factors for urinary incontinence in later life: A review of the clinical and epidemiologic literature. Journal of the American Geriatrics Society, 46: 1411-1417. 9. Ouslander, J. G. (1997). Aging and the lower urinary tract. American Journal of Medical Science, 314 (4): 214-218. 10. Grady, G., Brown, J., Vittinghoff, E., et al. (2001). Postmenopausal hormones and incontinence: The heart and estrogen/progestin replacement study. Obstetrics and Gynecology, 97: 116-120. 11. Stenberg, A., Heimer, G., Holmberg, L., et al. (1999). Prevalence of postmenopausal symptoms in two age groups of elderly women in relation to oestrogen replacement therapy. Maturitas, 33: 229-237. 12. Pandit, L. & Ouslander, J. G. (1997). Postmenopausal vaginal atrophy and atrophic vaginitis. American Journal of Medical Science, 314 (4): 228-231. 13. Falconer, C., Ekman-Orderberg, G., Blomgren, B., et al. (1998). Paraurethral connective tissue in stress-incontinent women after menopause. Acta Obstetricia et Gynecologica Scandinavica, 77: 95-100. 14. Versi, E. (1990). Incontinence in the climacteric. Clinical Obstetrics and Gynecology, 33: 392-398. 15. Raz, R., Gennesin, Y., Wasser, J., et al. (2000). Recurrent urinary tract infections in postmenopausal women. Clinical Infectious Diseases, 30: 152-156. 16. Milsom, I., Ekelund, P., Molander, U., et al. (1993). The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. The Journal of Urology, 149: 1459-1462. 17. Taylor, T., Smith, A., & Fulton, M. (1990). Effects of hysterectomy on bowel and bladder function. International Journal of Colorectal Disease, 5: 228-231. 18. Donnelly, V., O'Connell, P. R., & O'Herlihy, C. (1997). The influence of oestrogen replacement on faecal incontinence in postmenopausal women. British Journal of Obstetrics and Gynaecology, 104: 311-315. 19. Kalantar, J. S., Howell, S., & Talley, N. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 20. Ryhammer, A. M., Laurberg, S., & Sorensen, F. H. (1997). Effects of age on anal function in normal women. International Journal of Colorectal Disease, 12 (4): 225-229. 21. Ryhammer, A. M., Laurberg, S., & Bek, K. M. (1997). Age and anorectal sensibility in normal women. Scandinavian Journal of Gastroenterology, 32: 278-284. 22. Milsom, I. (1996). Rational prescribing for postmenopausal urogenital complaints. Drugs and Aging, 9 (2): 78-86. 23. Ryhammer, A. M., Laurberg, S., Djurhuus, J. C., et al. (1998). No relationship between subjective assessment of urinary incontinence and pad test weight gain in a random population sample of menopausal women. The Journal of Urology, 159: 800803. 24. Larson, B., Collins, A., & Landgren, B. M. (1997). Urogenital and vasomotor symptoms in relation to menopausal status and the use of hormone replacement therapy (HRT) in healthy women during transition to menopause. Maturitas, 28 (2): 99-105. 25. Sherburn, M., Guthrie, J. R., Dudley, E. C., et al. (2001). Is incontinence associated with menopause? Obstetrics and Gynecology, 98 (4): 628-633. 26. Rekers, H., Drogendijk, A. C., Valkenburg, H. A., et al. (1992). The menopause, urinary incontinence and other symptoms of the genito-urinary tract. Maturitas, 15 (2): 101-111. 27. Fantl, J. A., Cardozo, L. D., McClish, D. K., et al. (1994). Estrogen therapy in the management of urinary incontinence in postmenopausal women: A meta-analysis. First report of the Hormones and Urogenital Therapy Committee. Obstetrics and Gynecology, 83: 12-18. 28. Sultana, C. J. & Walters, M. D. (1990). Estrogen and urinary incontinence in women. Maturitas, 20: 129-138. 29. Fantl, J. A., Bump, R. C., Robinson, D., et al. (1996). Efficacy of estrogen supplementation in the treatment of urinary incontinence. Obstetrics and Gynecology, 88 (5): 745-749. 30. Raz, R., & Stamm, W. (1993). A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections. New England Journal of Medicine, 329: 753-756. 31. Cardozo, L. D. & Kelleher, C. J. (1995). Sex hormones, the menopause and urinary problems. Gynecology and Endocrinology, 9 (1): 75-84. 32. Beisland, H. O., Fossberg, E., Moer, A., et al. (1984). Urethral insufficiency in postmenopausal females: Treatment with phenylpropanolamine and estriol separately and in combination. Urology International, 39: 211-216. 33. Hilton, P., Tweddel, A. L., & Mayne, C. (1990). Oral and intravaginal estrogens alone and in combination with alpha adrenergic stimulation in genuine stress incontinence. International Urogynecology, 12: 80-86. 34. Kuchel, G. A., Tannenbaum, C., Greenspan, S. L., et al. (2001). Can variability in the hormonal status of elderly women assist in the decision to administer estrogens? Journal of Womens Health and Gender Based Medicine, 10 (2): 109-116. 35. Ghali, W. A., Freund, K. M., Boss, R. D., et al. (1997). Menopausal hormone therapy: Physician awareness of patient attitudes. American Journal of Medicine, 103: 3-10.

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8.3 INCONTINENCE IN MEN BACKGROUND


Urinary incontinence (UI) is sometimes thought to be a consequence of ageing. Continence requires integrated functioning of multiple body systems and although impaired physical functional accompanies older age, incontinence can be found throughout the lifespan. Indeed, the psychological implications of incontinence are more significant for those with severe incontinence, and for younger rather than older men (1). Only a quarter of men with urinary incontinence find it a negligible problem (2). The differences between men and women are not just seen in the prevalence of incontinence. Men may be more likely to limit their fluids and less likely to see their physician than are women (1). The association between UI and increased mortality is stronger for men than it is for women, even after adjustment for illness and functioning (1). Due to gender differences in anatomy, the pathophysiology of urinary incontinence (UI) differs between men and women. In men, overflow incontinence and urge incontinence are more common (1). Stress incontinence is usually only found following pelvic or prostate surgery which has caused sphincter damage.

URINARY SYMPTOMS Anatomy & Physiology


The prevalence of UI is lower for older men than for older women, with detrusor instability increasing with age (1, 3) . The growth of the prostate is positively associated with increasing age. The pathophysiology of each type of incontinence is outlined below:

Overflow incontinence Overflow incontinence can be due to:


40

blockage of the bladder outlet, often owing to BPH, prostate cancer or urethral stricture, kidney stones or renal calculi the inability of the detrusor to generate adequate pressure use of agonists or anticholinergic medications in men with subclinical bladder outlet obstruction

Urge incontinence (detrusor instability) Urge incontinence can be due to:


local factors such as lower genitourinary tract infections, faecal impaction and pelvic irradiation idiopathic detrusor instability bladder outlet obstruction There are two types of symptoms (6, 7):

Storage (or filling) symptoms urinary frequency urgency urge incontinence nocturia Emptying (or voiding) symptoms hesitancy straining to void diminishing or intermittent stream feeling of incomplete bladder emptying urinary retention terminal dribble

Inappropriate bladder contractions that overcome bladder outlet resistance usually cause almost complete emptying of the bladder. Patients often present with frequent urination, nocturia and involuntary urine loss of greater than 100ml. The volume loss varies and is not related to bladder volume (1). Symptoms of urge incontinence are not sensitive or specific for objective diagnosis of detrusor instability, with up to 20% of those with proven detrusor instability not complaining of irresistible urge to urinate.

Stress Incontinence Patients with stress incontinence will complain of small amounts of urine loss with coughing, lifting, straining or changing posture, although these may also induce involuntary bladder contractions. This can occur in men with sphincter or nerve trauma during prostatectomy.
Incontinence after transurethral resection is most likely to be due to poor compliance or detrusor instability, rather than direct sphincter injury (4). After radical prostatectomy, de novo instability and intrinstic sphincter deficiency are cited as the most significant in persistent incontinence (4). There is also some debate regarding whether detrusor instability is a primary or secondary factor to UI. Incontinence after radical prostatectomy is a complex and multifactoral problem (4). As the amount of striated muscle in the rhabdosphincter decreases with age, this has been suggested as one of the reasons for a greater incidence in UI in older men following radical prostatectomy.

PREVALENCE
Urinary incontinence is lower for men than it is for women, with 7% to 15% of older men complaining of involuntary urine loss (1). Prevalence varies in the literature depending on the definition of incontinence used, who is identifying it (physician or patient) and how it is quantified. An Australian community-based questionnaire survey identified urge urinary incontinence in 12% and stress urinary incontinence in 4% of men (5). Lower urinary tract symptoms (LUTS) also include other urinary-related symptoms such as nocturia, frequency and urgency. The prevalence of moderate to severe LUTS in men older than 50 is as high as 25%-30%, and also increases with age (6). Of those presenting with LUTS, approximately two thirds can be attributed to a bladder outlet obstruction (BOO) (7, 8, 9, 10) . Of those two thirds who have a BOO, at least two thirds will have a concomitant diagnosis (8, 9). In a study involving 160 men with storage symptoms suggestive of detrusor instability, 17% had urge incontinence, 36% frequency and urgency, 19% nocturia and 28% difficulty voiding (10). Detrusor instability strongly correlated with UI, although other LUTS did not correlate well with urodynamic findings. These studies, along with several others (3, 11) demonstrate that symptoms do not have sufficient specificity and sensitivity to determine the cause of urinary incontinence in men.
41

Post surgical UI
The prevalence of urinary incontinence following surgical treatment for prostate cancer varies between 0-88%, depending on the type of surgery, the definition and quantification of incontinence, and who evaluates the presence or absence of incontinence (physician or patient) (4). After transurethral resection, UI is rare, but after radical prostatectomy the problem is significant. Donnellan et al. (12) report that 6% were mildly incontinent, 6% moderately incontinent and 4% were severely incontinent one year after surgery. These figures are in line with an Australian study that highlighted that newer methods of radical surgery result in an average of 93% continence achieved at an average of 68 days post-operation (13). Rates of incontinence following treatment of prostate cancer with radiotherapy may be comparable to surgical techniques, with reports of between 34% and 44% experiencing urinary symptoms (14). In contrast, following highintensity, localised ultrasound treatment of prostate cancer, a recent study reported that none of 184 patients experienced severe incontinence (15), a rate only slightly increased in Brachytherapy (6%-7%) (16). Risk factors which have been identified for post radical prostatectomy UI are abnormalities of detrusor contractility and age (4). Other related factors include preoperative radiotherapy, trauma, spinal cord lesion, new obstruction, bladder neck contracture, or urethral stricture, Parkinson's disease, dementia, medications and surgical expertise (4).

GASTROINTESTINAL SYMPTOMS Anatomy and Physiology


Faecal incontinence (FI) has been found to be associated with increased age, perineal surgery and injury, faecal impaction and overflow incontinence (17). Its association with constipation is possibly due to related nerve damage (17) . Passive FI is due to degenerative disorder of the internal anal sphincter, which becomes fibrotic and weak leading to reduced maximum anal canal resting pressure (18).

Prevalence
The reported prevalence of faecal incontinence (FI) in men varies depending on the definition of incontinence used and the way in which it was identified. The definition of FI used may include or exclude inability to control flatus. Lam et al (5) stated that men may be more likely to admit FI anonymously rather than in a face to face interview. Several studies involving postal questionnaires do demonstrate a higher prevalence than those that were interview based. This has implications for GP interactions with patients during consultations. Only 27.3% of men with FI reported seeking medical attention and 14.6% reported being asked about it by the medical practitioner (17). Two large Australian community based studies found that the prevalence of faecal incontinence in men is between 10.8% (17) and 20% (5) (this higher figure includes uncontrolled flatus). The presence of liquid FI was 9.4% compared to 3.1% with solid FI (17).

Clinical Assessment
Symptoms alone are not a reliable means of diagnosing the cause of urinary incontinence in men (3, 9, 11). The bladder has been found to be an unreliable witness, with LUTS having varied pathophysiology. It is important to identify the underlying pathology to prevent unnecessary medical and surgical treatments.
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In taking a detailed medical history, the following conditions and factors may be identified as possible causes of incontinence (see Table 1, below).

TABLE 1: CONDITIONS

RELATED TO INCONTINENCE*

Neurological disorders (e.g. history of stroke, Parkinsonism, Multiple Sclerosis, dementia, spinal cord injury) Previous urinary or pelvic surgery Medications Acute UTI Neoplasm of the urogenital system CHF Diabetes (neuropathy related to) Alcohol abuse (neuropathy related to) Physical mobility Glaucoma and visual problems Chronic constipation Bladder outlet obstruction
(*) Adapted from 1, 3, 8, 9.

Table 2 (below) presents the key aspects of clinical assessment of the male with incontinence:

TABLE 2: KEY ASPECTS TO THE CLINICAL ASSESSMENT OF A MALE PATIENT WITH


INCONTINENCE

History

Nature and duration of symptoms Onset Amount of urine lost Associated factors at time of urine loss Other LUT symptoms Irritative - frequency, urgency, nocturia Obstructive - intermittent stream, weak stream, incomplete emptying, hesitancy Other - kidney stones, haematuria General history Review of active medical conditions History of pelvic or prostate surgery Medications that may cause polyuria or impaired bladder contractility - diuretics, anticholinergics, a-agonists, psychotropics, alcohol Neurological symptoms - lower extremity weakness, spasticity, reflex changes, psychological Bowel function (consistency and frequency, and duration of symptoms for FI) Sexual function Effect on quality of life and desire for treatment. Abdominal and genital Rectal Faecal impaction, prostate enlargement and abnormalities Resting tone and voluntary contraction with FI Mobility Mental status/cognition Neurological for patients with symptoms Sensory Motor function Reflex integrity Bladder diary Cough test Urinalysis Post-void residual Urodynamic investigation
43

Physical Examination

Other investigations

Referral to specialist if

Recurrent incontinence Incontinence associated with: Pain Haematuria Recurrent infection Voiding symptoms Prostate enlargement, mass or irradiation Radical pelvic surgery Significant PVR

MANAGEMENT Urinary incontinence


Management approaches to urinary incontinence in men are represented in Table 3 (below). It is important to determine the cause of the incontinence in order to use the most appropriate management approach. Those with urge symptoms and who stop flow and abort involuntary detrusor contractions should benefit from pelvic floor exercises, bladder retraining and behaviour modification only. Those who are unable to abort involuntary detrusor contractions may require anticholinergics (10). For those with stress symptoms presenting post prostatectomy, a Cochrane review (4) found that the value of the various approaches to conservative management remains uncertain. All trials showed improvement in the period 0-3 months after surgery, then continued improvement 6-12 months post surgery. In the immediate post-operative period, the most important aspect of management may be support, reassurance and education. Given that most men's symptoms improve, particularly in the first three months after surgery, referral to a nurse continence advisor for advice regarding padding and other forms of protection may be a good interim measure before more aggressive strategies are trialed. Iselin et al (19) found that periurethral collagen injections have shown improvements in 58-85% of patients during short term follow up (7-10 months). This is lower (35-65%) over longer follow up (15-29 months) and has a cure rate of 6-24%. Time related decrease in success is due to the progressive reabsorption of collagen. It is also important to note that 15-20% still underwent artificial urethral sphincter placement after treatment. Prognostic factors for success for collagen injections are having not undergone adjuvant radiotherapy, low incontinence magnitude, no detrusor instability, no contracture of the bladder neck and a Valsalva leak point pressure of 60cmH20 (19). If tissue superior to external sphincter is identifiable on video study then collagen injections are a viable treatment option (20).
44

The surgical option for sphincter damage in those who have leakage driven by abdominal pressure on videourodynamics is an artificial sphincter implantation around the prostatic urethra (20). This review found that sling procedures remained investigational at this time (20).

TABLE 3: AVAILABLE Treatment type


Behavioural

TREATMENTS FOR URINARY INCONTINENCE IN MEN

Treatment
Prompted/timed voiding Fluid intake Pelvic floor physiotherapy Biofeedback Electrical stimulation

Relevant conditions
Functional incontinence Urge incontinence(21) Stress incontinence - not total incontinence (post prostatectomy) (22)(23)

Stress incontinence - (post prostatectomy) (23) Overflow incontinence (24, 25, 26) (Should not be used with urinary retention.) Urge incontinence (27, 28) Overflow incontinence

Pharmacological -blockers (terazosin) Anticholinergics (oxybutynin, tolterodine) Discontinuation of medication causing urinary retention Appliances

Intermittent catheterisation Overflow incontinence (for those with poor contractility) Pads Functional incontinence Stress incontinence Relief of obstruction (TURP) Collagen injections Artificial sphincter Overflow incontinence with BPH (29, 30) (in those who are bothered by symptoms and who have coexisting causes of UI ruled out) Stress incontinence (19, 31) Stress incontinence (20, 31)
45

Surgical

Faecal Incontinence
Faecal incontinence can be addressed conservatively with dietary modification such as determination of lactose intolerance, increasing fluids and using fibre for bulking. Behaviourally, bowel movements should be scheduled daily (32). Pads or anal plugs can be used to manage symptoms initially (18). Medication such as Loperamide can be used to increase resting anal pressure of the internal sphincter although further studies are required.
(18, 32)

For those with mechanical disruption of sphincter, major reconstructive surgery such as artificial sphincter implant or graciloplasty can be used although this is still in development (18, 32).

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References: 1. Johnson, T. M., & Ouslander, J. G. (1999). Urinary incontinence in the older man. Medical Clinics of North America, 83 (5): 1247-1266. 2. Hunskaar, S., & Sandvik, H. (1993). One hundred and fifty men with urinary incontinence: III. Psychosocial consequences. Scandinavian Journal of Primary Health Care, 11: 193-196. 3. Ameda, K., Sullivan, M. P., Bae, R. J., et al. (1999). Urodynamic characterization of nonobstructive voiding dysfunction in symptomatic elderly men. The Journal of Urology, 162: 142-146. 4. Moore, K. N., Cody, D. J., & Glazener, C. M. A. (2001). Conservative management for post prostatectomy urinary incontinence (Cochrane Review). The Cochrane Library, (3). 5. Lam, L., Kennedy, M., & Chen, F. (1999). Prevalence of faecal incontinence and constipation risk factors: a population based study. Colorectal Disease, 1: 197-203. 6. Dorey, G. (2000). Male symptoms with lower urinary tract symptoms 1: Assessment. British Journal of Nursing, 9 (8): 497-501. 7. Chaikin, D. C., & Blaivas, J. G. (2001). Voiding dysfunction: definitions. Current Opinion in Urology, 11: 396-398. 8. Fusco, F., Groutz, A., Blaivas, J. G., et al. (2001). Videourodynamic studies in men with lower urinary tract symptoms: A comparison of community based versus referral urological practices. The Journal of Urology, 166: 910-913. 9. Kuo, H. C. (2000). Pathophysiology of lower urinary tract symptoms in aged men without bladder outlet obstruction. Urologica Internationalis, 64: 86-92. 10. Hyman, M. J., Groutz, A., & Blaivas, J. G., (2001). Detrusor instability in men: correlation of lower urinary tract symptoms with urodynamic findings. The Journal of Urology, 166: 550-553. 11. Ding, Y. Y., Liey, P. K., & Choo, P. W. J. (1997). Is the bladder "an unreliable witness" in elderly males with persistent lower urinary tract symptoms? Geriatric Nephrology and Urology, 7: 17-21. 12. Donnellan, S. M., Duncan, H. J., MacGregor, R. J., et al. (1997). Prospective assessment of incontinence after radical retropubic prostatectomy: Objective and subjective analysis. Urology, 49 (2): 225-230. 13. Kaye, K. W., Creed, K. E., Wilson, G. J., et al. (1997). Urinary continence after radical retropubic prostatectomy: Analysis and synthesis of contributing factors. A unified concept. British Journal of Urology, 80: 444-451. 14. Hanlon, A. L., Watkins-Bruner, D., Peter, R., et al. (2001). Quality of life study in prostate cancer patients treated with threedimensional conformal radiation therapy: Comparing late bowel and bladder quality of life symptoms to that of the normal population. International Journal of Oncology, Biology and Physiology, 49 (1): 51-59. 15. Chaussy, C. & Thuroff, S. (2001). Results and side effects of high-intensity focused ultrasound in localized prostate cancer. Journal of Endourology, 15 (4): 437-440. 16. Benoit, R. M., Naslund, M. J., & Cohen, J. K. (2000). A comparison of complications between ultrasound-guided prostate brachtherapy and open prostate brachtherapy. International Journal of Oncology, Biology and Physiology, 47 (4): 909-913. 17. Kalantar, J. S., Howell, S., & Talley, N. J., (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 18. Cheetham, M. J., Kamm, M. A., & Phillips, R. K. S. (2001). Topical phenylephrine increases anal canal resting pressure in patients with faecal incontinence. Gut, 48: 356-359. 19. Iselin, C. E. (1999). Periurethral collagen injections for incontinence following radical prostatectomy: does the patient benefit? Current Opinion in Urology, 9: 209-212. 20. Leng, W. W., & McGuire, E. J. (1999). Reconstructive surgery for urinary incontinence. Urologic Clinics of North America, 26 (1): 61-80. 21. Griffiths, D. J., McCracken, P. N., Harrison, G. M., et al. (1996). Urge incontinence in elderly people: Factors predicting the severity of urine loss before and after pharmacological treatment. Neurourology and Urodynamics, 15 (1): 53-57. 22. Moore, K. N., Griffiths, D. J., & Hughton, A., (1999). Urinary incontinence after radical prostatectomy: A randomized controlled trial comparing pelvic muscle exercises with or without electrical stimulation. British Journal of Urology International, 83: 57-65. 23. Van Kampen, M., De Weerdt, W., Van Poppel, H., et al. (2000). Effect of pelvic-floor re-education on duration and degree of incontinence after radical prostatectomy: A randomised controlled trial. The Lancet, 355: 98-102. 24. Lepor, H., Williford, W. O., Barry, M. J., et al. (1996). The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia: Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group. New England Journal of Medicine, 335 (8): 533-539. 25. Lepor, H., Williford, W. O., Barry, M. J., et al. (1998). The impact of medical therapy on bother due to symptoms, quality of life and global outcome, and factors predicting response. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group. Journal Urology, 160 (4): 1358-1367. 26. Brawer, MK, Adams, G, & Epstein, H. (1993). Terazosin in the treatment of benign prostatic hyperplasia: Terazosin Benign Prostatic Hyperplasia Study Group. Archives of Family Medicine, 2 (9): 929-935. 27. Drutz, H. P., Appell, R. A., Gleason, D., et al. (1999). Clinical efficacy and safety of tolterodine compared to oxybutynin and placebo in patients with overactive bladder. International Urogynecologic Journal of Pelvic Floor Dysfunction, 10 (5): 283-289. 28. Appell, R. A., Sand, P., Dmochowski, R., et al. (2001). Prospective randomized controlled trial of extended-release oxybutynin chloride and tolterodine tartrate in the treatment of overactive bladder: results of the OBJECT Study. Mayo Clinical Procedings, 76 (4): 358-363. 29. Wasson, J. H., Reda, D. J., Bruskewitz, R. C., et al. (1995). A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. New England Journal of Medicine, 332 (2): 75-79. 30. Flanigan, R. C., Reda, D. J., Wasson, J. H., et al. (1999). 5-year outcome of surgical resection and watchful waiting for men with moderately symptomatic benign prostatic hyperplasia: A Department of Veterans Affairs cooperative study. Journal of Urology, 160 (1): discussion 16-17. 31. Fantl, J., Newman, D., Colling, J., et al. (1996). Urinary incontinence in adults: acute and chronic management. Rockville, Maryland: Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research. 32. Nagle, D., (1999). Rectal prolapse and fecal incontinence. Primary Care, 26 (1): 101-111.

8.4 CHILDHOOD INCONTINENCE BACKGROUND


Continence problems often present in the course of childhood. Symptoms may be extremely varied and provide a challenge to the general practitioner. Contrary to popular belief, there is no basis for ignoring a chronic problem by expecting that children will grow out of problems with continence (1). The development of normal continence requires both social learning and maturation of the nervous system. Unless physiological abnormalities are present, children are normally physically and socially continent by between four and six years of age (2). Only around one in eight four and a half-year olds are wet at night. Childhood urinary incontinence is defined as the loss of urine in a socially inappropriate setting by a child old enough to have gained control. The term enuresis is often used interchangeably with incontinence although it refers to non-structural forms of incontinence and is usually associated with full rather than partial bladder emptying (3). All very young children are faecally incontinent. Some children never gain continence because of anorectal malformations or medical conditions such as spina bifida. Information on this and other medical conditions is found in Section 8.6 of these guidelines. Faecal incontinence in otherwise normal children is usually due to behavioural problems or poor bowel habits resulting in stool retention and overflow (1).

URINARY INCONTINENCE Presentation


Development of continence in the child is dependant upon three independent factors maturing concomitantly (4): Development of normal bladder capacity Maturation of normal urethral sphincter function Development of neural/volitional control over bladder-sphincter function
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According to Abrams et al (5), urinary symptoms in children can be grouped into three categories: nocturnal enuresis, day-time symptoms, and complicated incontinence. These categories and the presentations within them are presented in Table 1 (below).

TABLE 1: TYPES
Symptom category Nocturnal enuresis

OF URINARY INCONTINENCE IN CHILDREN

Presentations Primary nocturnal enuresis Secondary nocturnal enuresis Day wetting Giggle incontinence Urge incontinence (examine for vesicoureteral reflux) Dysfunctional voiding Lazy bladder

Day-time incontinence (with or without nocturnal enuresis)

Complicated incontinence

Structural incontinence Neurogenic lesions Urinary tract infection (examine for vesicoureteral reflux) Pelvic surgery Hinmans syndrome

Nocturnal Enuresis
The most common form of incontinence is nocturnal enuresis. This category is applied to children who wet their bed during the night and experience no daytime leakage. The condition has a clear familial tendency (1). From early infancy, there is usually a gradual evolution to continence and rarely is occasional nocturnal enuresis unacceptable in children under the age of 5 years (4). Nocturnal enuresis can be divided in primary and secondary types. Primary Nocturnal Enuresis (PNE) is defined as night-time bed-wetting after daytime continence has been achieved (5). To achieve a diagnosis of PNE, the individual should not have been continually dry at night during the previous six months (6). Various factors contribute to the development of nocturnal enuresis, most notably genetic factors and stressful early life events (2, 8). Primary nocturnal enuresis is potentially caused by abnormalities in nocturnal circadian rhythms and a deficiency of inhibitory signal processing in the brain stem (2). Secondary Nocturnal Enuresis is defined as bed-wetting in children who have been previously dry at night for an uninterrupted period of six months (9). Urinary tract infection, neurological abnormality, diabetes, stressful life events, constipation or renal disease are more likely to be causes of secondary than primary nocturnal enuresis (9).

Day-time Incontinence
Day wetting is an uncommon condition where, usually, bladder and urethra function is normal (10). It presents with highly variable frequency of leakage and is often associated with attention deficit disorders or stressful lifeevents (10). Usually patients show either extreme urinary frequency with infrequent leaking or bladder instability. Giggle incontinence is a form of incontinence induced by laughter. It is more common in young females than in males (11). Leakage is due to bladder contraction combined with relaxation of the urethral sphincter and may result in complete bladder emptying (11). Giggle incontinence is distinct from genuine stress incontinence in which there is no bladder contraction (11). A family history of similar incontinence is common and symptoms usually present after normal bladder control has been achieved (11). Urge incontinence in children presents much as it does in adults. Leakage is associated with frequent sensations of urgency. Episodes increase with tiredness and may be more common in the afternoon (12). Clinical signs are those suggesting obvious discomfort, such as pressing the legs together or contracting the pelvic floor muscles (12) . Urge incontinence is often associated with perigenital dermatitis, urinary tract infections, soiling and nocturnal wetting (12). Constipation is also very common and essential to treat. Dysfunctional Voiding refers to the abnormal urine stream associated with overactivity of the pelvic floor muscles and uncoordinated detrusor and urethral sphincter (2). Children with dysfunctional voiding may also present with detrusor instability and incomplete bladder emptying (2). Residual urine increases the risk of urinary tract infection and may increase the risk of vesicoureteral reflux in children (10). Dysfunctional voiding requires specialist referral and voiding retraining with a paediatric continence physiotherapist or nurse continence advisor. Lazy bladder is a problem more prevalent in female children (13). Due to poor bladder sensation and minimal frequency, incontinence can result from overflow. Children with this condition typically pass urine only twice each day (13). Voiding is usually achieved by straining as the bladder is under-active and typically does not empty completely (10,13). Infections often develop due to urine stasis, and constipation and/or soiling may accompany the urinary symptoms (10).

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Complicated Incontinence
Complicated incontinence generally classifies structural and neurogenic forms of incontinence. Structural Incontinence is far less common than non-structural forms of incontinence and can be primary (i.e, the lesion directly results in incontinence) or secondary (i.e, the lesion results in incontinence by influencing other factors). Primary structural incontinence may include exstophy, epispadias, and ectopic ureter (3). Secondary structural incontinence is mostly due to obstruction and incontinence results from overflow or bladder instability (3). Trauma can also be a causal factor (3). Neurogenic incontinence is usually found in children suffering from serious neurological conditions or spinal cord injury. More detailed information on these types of incontinence is located in Section 8 of these guidelines. Urinary tract infection is common and often recurrent in childhood. It requires prompt treatment. Urinary tract infections, particularly those located in the upper urinary tract and those related to vesicoureteral reflux, can lead to scarring and damaged kidneys (13). Presenting signs may include: dysuria, frequency, dribbling/hesitancy, incontinence, malodourous urine, haematuria, squatting and abdominal/suprapubic pain, fever, vomiting, diarrhoea, and flank/back pain (14). Hinmans Syndrome is a collection of urinary symptoms, constipation, and faecal incontinence, and is often associated with psychiatric illness or psychological stress (3). It is not, however, believed that the condition is caused by psychological factors (3, 10). Significant renal damage is common, together with hypertrophied, elongated, hypertonic bladder, poor bladder emptying, and a variable incidence of hydronephrosis (with or without UTI) or vesicoureteral reflux (3).

Vesicoureteral Reflux
Vesicoureteral reflux occurs when the peristaltic activity of the ureter is poor or when the ureteric tunnel in the bladder wall is short (6). Bladder pressure is then able to cause urine to move back up the ureter toward the kidney. Vesicoureteral reflux exerts pressure on the renal parenchyma and moves bacteria from the bladder. Even when asymptomatic, vesicoureteral reflux can cause renal scarring and upper urinary tract deterioration, especially in younger children (6). In all male children and female children under 5, urinary tract infections should prompt the GP to further investigate the possibility of vesicoureteral reflux. Micturating cystourethrogram (MCU) and USS may be indicated. Some children may require sedation or GA.
49

PREVALENCE
An Australian epidemiological study of 2392 five- to twelve-year olds found a prevalence of 18.9% for nocturnal enuresis and 5.5% for any urinary incontinence. Nocturnal enuresis and day-time wetting occurred at least weekly in 5.1% and 1.4% of children respectively (15). Another Australian study has highlighted that the prevalence of day-time wetting is highest in younger children, with 19% of those starting school suffering this condition (16). It has been argued that children with ADHD are 4.5 times more likely to wet by day than age-matched controls (17).

ASSESSMENT History
Detailed assessment of children requires the assistance of parents or carers. Informed consent for particular assessments is an issue of which GPs must be keenly aware. Gaining the trust and cooperation of both patient and their parents should be a primary aim of GPs. Clinical assessment of children with incontinence should consist of a detailed and structured history, a bladder diary, and a physical examination. Leakage should if possible be clarified objectively, noting time and amount of leakage (18). A questionnaire, completed by the parents, may also be useful (10). Information should be sought regarding neurological and congenital abnormalities, and previous urinary infections and surgery (7). Bowel function should also be examined, as symptoms such as constipation often coexist with urinary incontinence (7). As with all patients, medications with potential effects on continence should be noted.

Physical Examination
A suitable physical examination for children is presented in Table 2 (below). The GP should always offer the child the opportunity of having parents or carers present during a physical examination although it may be the childs decision to be unaccompanied. GPs should consider having a practice nurse present if the child is unaccompanied by parents or carers.

TABLE 2: SUGGESTED

PHYSICAL EXAMINATION OF AN INCONTINENT CHILD

Growth, using a growth chart and previous and current growth values Blood pressure, using norms for age and height A palpable bladder, suggesting inefficient or incomplete emptying or, in the male, possibly posterior urethral valves Abnormalities of the external genitalia Presence of a full sigmoid colon or descending colon Anal tone, which may be decreased if sacral innervation is abnormal; Urinalysis and urine culture to rule out infection Perineal sensation Constipation and faecal impaction

MANAGEMENT Conservative
Conservative management of occasional childhood incontinence is usually not commenced before 5 years of age, as such wetting may be considered a relatively normal maturational delay (9). While active treatment is usually not indicated in children under 5, screening for infection, liberalising fluids and managing constipation are important considerations. Investigation and treatment should be considered when the incontinence either becomes chronic, is a social problem, or is causing the child emotional upset. Enuresis alarms have been used for some time. This technique involves the use of a urine sensor and alarm apparatus that wakes the child when wet. The child gradually learns to associate waking with a sensation of bladder fullness and so eventually uses the toilet instead of being incontinent during sleep (6). A Cochrane review highlights that children treated with alarm interventions are significantly more likely to become dry than untreated controls (20). While complete cures are attained slowly, the success rate is higher than other modes of therapy alone (19). Positive reinforcement has been proposed as a method of both involving the child in their treatment and conditioning success. In particular, there should be no punitive action for incontinence (19). A chart that records dry nights may be useful. A frequent waking program involves a parent waking the child several times during the night to go to the toilet until the child requires no prompting to remain dry during the night (6). Such programs are not used widely and are not recommended. Waking regularly throughout the night to urinate does not actively combat the problem of incontinence at its source and will affect the childs concentration during the day.

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Pharmacological
Drug-based treatment of childhood incontinence is recommended only in children over the age of six who are refractory to behavioural management. In all cases, such prescription should come only after all conservative efforts have failed and the patient has been assessed by a specialist. Residual volumes should be checked 2 to 3 weeks following commencement. Medication choice is determined by whether symptoms are nocturnal or diurnal.

Nocturnal enuresis Desmopressin acetate may be employed in a nasal spray form. Currently this medication is available in Australia only on authority script for children over six years-of-age who are refractory to enuresis alarm intervention. The initial dose is 20mcg at bed-time (2 squirts of nasal spray) which may be titrated to response. An oral form of this drug has been developed.

Day-time incontinence Incontinence during the day is usually due to unstable bladder or, less frequently, psychological stress. If due to unstable bladder (confirmed by specialist assessment), the following medications may be trialed:
1 Oxybutinin hydrochloride (ditropan) 0.1mg/kg t.d.s. The tablets are 5mg, or the pharmacy may make up a syrup at 1mg/ml. Oxybutynin is used for one month and its effect assessed. If there has been a UTI, then it may take one month for oxybutynin to be effective. With frequent UTIs, antibiotic prophylaxis should be considered.

If side effects or no response to oxybutinin hydrochloride: 2 Dicyclomine hydrochloride (merbentyl) may be trialed. This medication is available in syrup form and the dose for 4 8 year olds is 5mg t.d.s. (1mg/ml syrup). The dose for 8-12 year-olds is 10mg t.d.s. If no response to 1 or 2, then specialist review and urodynamics are indicated, and: 3 Propantheline bromide (pro-banthine) may be trialed 7.5 to 15 mg t.d.s.

IMIPRAMINE HAS BEEN PREVIOUSLY USED FOR CHILDHOOD INCONTINENCE BUT IT IS NOW NOT RECOMMENDED DUE TO THE RISK OF CARDIOTOXICITY. Specialist referral
Specialist referral is indicated in cases of recurrent infection or dysfunctional voiding, and where conservative treatments for other symptoms have been unsuccessful.
References: 1. Discipio, W. (2001). Enuresis and Encopresis, in Primary Care Paediatrics, C. Green-Hernandez, J. Singleton, and D. Aronson (Eds). Lipincott Williams and Wilkins. p. 809. 2. Nijman, R. (2000). Paediatric voiding dysfunction and enuresis. Current Opinion in Urology, 10: 365-370. 3. Wojcik, L. & Kaplan, G. (1998). The Wet Child. Urologic Clinics of North America, 25 (4): 735. 4. Van Gool, J. D., Bloom, D. A., Butler, R. J., et al. (1999). Conservative Management in Children, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publication Ltd. p. 487-550. 5. Abrams, P., Wein, A., Schussler, B., et al. (1999). 1st International Consultation on Incontinence: Recommendations of the International Scientific Committee: The evaluation and treatment of urinary incontinence, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). UK: Health Publications Ltd. p. 945-975. 6. Guillot, A., & McNamara, I. (2001). Chronic Urinary Problems, in Primary Care Paediatrics, C. Green-Hernandez, J. Singleton, and D. Aronzon, (Eds). Lippincott Williams and Wilkins. 7. Norgaard, J., van Gool, J., Hjalmas, K., et al. (1998). Standardization of definitions in lower urinary tract dysfunction in children. British Journal of Urology, 81 (3): 1-16. 8. Evans, J. (2001). Nocturnal Enuresis. Western Journal of Medicine, 175: 108-111. 9. Oates, K., Currow, K., & Hu, W. (2001). Child health: A practical manual for General Practice. Sydney: MacLennan and Petty Pty Ltd. 10. Van Gool, J. D., Bloom, D. A., Butler, R. J., et al. (1999). Conservative Management in Children, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds), UK: Health Publication Ltd. p. 487-550. 11. Bloom, D. A., Faerber, G., & Bomalaski, M. (1995). Urinary Incontinence in Girls. Urologic Clinics of North America, 22 (3): 521-537. 12. von Gontard, A. (1998). Annotation: Day and Night Wetting in Children- A Paediatric and Child Psychiatric Perspective. Journal of Child Psychiatry, 39 (4): 439-451. 13. Casale, A. (1993). Functional Voiding Disorders of Childhood. Journal of the Kentucky Medical Association, 91: 185-191. 14. Ahmed, S. M. & Swedlund, M., (1998). Evaluation and Treatment of Urinary Tract Infections in Children. American Family Physician, (April 1998). 15. Bower, K., Moore, K., Adams, R., et al. (1997). Frequency-volume chart data from incontinent children. British Journal of Urology, 80: 658-662. 16. Sureshkumar, P., Craig, J., Roy, L. P., et al. (2000). Daytime urinary incontinence in primary school children: A population based survey. Journal of Pediatrics, 137: 814-818. 17. Robson, W. L. M, Jackson, H. P., Blackhurst, D., et al. (1997). Enuresis in children with attention deficit hyperactivity disorder. Southern Medical Journal, 90: 503-505. 18. Norgaard, J., van Gool, J., Hjalmas, K., et al. (1998). Standardization of definitions in lower urinary tract dysfunction in children. British Journal of Urology, 81 (3): 1-16. 19. Shefler, A. G. (1992), The Hospital for Sick Children Handbook of Paediatrics 8th edition. Toronto, Canada: The Hospital for Sick Children. 20. Glazener, C. M. A., & Evans, J. H. C., (2002). Alarm interventions for nocturnal enuresis in children (Cochrane Review). In: The Cochrane Library, 1, 2002. Oxford: Update Software.

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8.5 INCONTINENCE IN THE ELDERLY BACKGROUND


Due predominantly to age-related physiological changes and the presence of high rates of serious medical conditions and polypharmacy, the elderly population is disproportionately affected by incontinence (1-3). It appears that elderly patients are also particularly unlikely to seek medical help, or may substantially delay seeking help for incontinence (4). As with all age-groups, a range of cultural and social factors act to minimise reporting. The elderly are particularly likely to misattribute incontinence to just being old, and attempt to adapt to the condition, often normalising it (4). Many will self-manage with pads, which are expensive and do not treat the underlying cause of the condition. Regardless of these concealing and coping mechanisms, incontinence in older adults is likely to be associated with extreme embarrassment, reduced social relationships and activities, psychological distress, avoidance of sexual activity, and poor quality of life (4, 5). Persistent incontinence is also a major factor influencing the placement of an elderly person in institutionalised care (6). Increasing the number of older people who are able to maintain a comfortable and healthy existence in the community has enormous benefits to the patient and to the wider community. Much incontinence in elderly people can be successfully treated, however careful assessment is paramount. Clinical presentation of symptoms can be more complex than in younger patients. The GP must also be aware of the patients cognitive status, mobility, and of a potentially large number of transient causes of incontinence. Individualised management may make an enormous impact on quality of life of the elderly.

PRESENTATION Age-related physiological changes


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With age comes a range of physiological changes highly relevant to the maintenance of continence control. At a cellular level, actual cell-function and levels of neurotransmitters and hormones can alter (2). Of note, noradrenaline has an overall contracting effect on the older patients bladder, in contrast to the relaxing effect observed in younger bladders (7). Altered immune function can result in an increased risk of bacteriuria and symptomatic urinary tract infection (2). Degeneration of detrusor muscle can also be a part of the normal process of ageing. The bladder muscle produces less energy and fatigues faster (7). Other changes include decreased bladder capacity and contractility, increased post-void residual urine volume, increased frequency of uninhibited bladder contractions and lower urethral pressure (2). A reduced sensitivity of pelvic nerve afferents has also been noted and an accompanying reduction in bladder sensation may result in incomplete emptying. In females in particular, there is a decreased innervation of the pelvic floor and urinary sphincter (7). The effects of prostate enlargement and estrogen depletion are covered respectively in the Male and Menopausal sections of this guideline.

Associated medical conditions


Whether living in the community or within long-term care, the elderly often present with multiple and chronic medical conditions (1). A number of these conditions have a potential influence on continence and are listed in the section of this guideline entitled Incontinence in Other Medical Conditions. Of particular relevance to the elderly are neurologic, cerebrovascular and cardiovascular diseases and diabetes, although other conditions such as vitamin B12 deficiency, pulmonary disease, tuberculosis, herpes zoster, spinal spondylosis/stenosis, neurosyphilis and musculoskeletal disease can play a role in incontinence (1).

Medication-use
Numerous individual drugs are known to have effects on continence, however due to the increased rate of chronic medical conditions in the elderly, many patients present with polypharmacy. Incontinence, multiple drug-use, and delirium are in fact well-linked phenomena in the elderly (8). Medication is also often a primary cause of constipation (9). Table 1 (below) presents some of the drugs known to be associated with continence problems in the elderly. The elderly are also, of course, prone to the effects of those drugs listed more generally within Table 3 of Section 6 of these guidelines, that referring to urinary incontinence more generally.

TABLE 1: COMMON ELDERLY*

MEDICATIONS THAT MAY AFFECT CONTINENCE IN THE

Medication Type Sedatives/hypnotics Alcohol Anticholinergics impaction Narcotic analgesics -adrenergic antagonists -adrenergic agonists Calcium channel blockers Potent diuretics Angiotensin converting enzyme inhibitors Vincristine Caffeine
(*) Adapted from 10 & 11.

Potential Effects on Continence Sedation, delirium, immobility Polyuria, frequency, urgency, sedation, delirium, immobility Urinary retention, overflow incontinence, delirium, faecal Urinary retention, faecal impaction, sedation, delirium Urethral relaxation may lead to stress urinary incontinence Urinary retention in men Urinary retention, nocturnal diuresis owning to fluid retention Polyuria, frequency, urgency Drug induced cough can lead to stress urinary incontinence Urinary retention Aggravation of existing symptoms

Urinary symptoms
The main urinary symptom in the elderly appears to be detrusor instability or overactivity (3, 12, 13). Consequently, the most common complaint in both males and females is urgency with urge incontinence (13). Many elderly, however, complain that they feel no warning of an impending episode of incontinence. A large post-void residual volume is also reasonably common, and in hospitalised patients is associated with poor prognosis (14). In women, the second most common complaint is stress incontinence and in men it is outlet obstruction (13). The remainder of older patients usually present with mixed symptoms (3). Urinary incontinence is also often associated with skin problems in the elderly, particularly in institutionalised persons. Pressure sores, rashes, and ulcers can be a significant problem where incontinence is poorly managed (15).
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Gastrointestinal symptoms
Constipation is common in the elderly although bowel transit time and frequency of bowel movements do not necessarily change with age. It seems that many elderly people perceive constipation as straining and a sensation of incomplete emptying (9), rather than as the historical medical definition of <3 bowel movements per week (16). Medications are often a common cause of constipation in the elderly, however diet, dehydration and immobility may also play a substantial role (9). As discussed in other sections of these guidelines, constipation can lead to faecal impaction, faecal incontinence, urinary frequency and urinary incontinence. Faecal incontinence in the elderly is often associated with other medical conditions such as stroke, dementia, depression and diarrhoea, although it can also be a long-term result of various surgical procedures. Reduced pelvic floor innervation (7) with age may lead to poor rectal sensation and patients may not sense the need to defecate or may be unable to distinguish between solid, liquid and gaseous bowel contents (16). Incontinence may commonly be due to urgency of defecation combined with mobility problems, or to faecal impaction and overflow (16).

PREVALENCE Community-dwelling elderly


Urinary incontinence is present in up to 30% of elderly persons residing in the community and up to one third of those report that episodes occur at least weekly (5, 11, 17, 18). It appears that urinary incontinence is at least twice as common in elderly women as compared to elderly men (17, 18). However, many elderly community-dwelling men will experience frequency, urgency, and flow problems due to prostatism. In a relatively large study, Diokno et al (17) highlighted what might be considered normal urination in the elderly. Between 75% and 82% of asymptomatic men and women urinated between four and eight times during a 24-hour period. Three-quarters of asymptomatic men and women urinated either not at all or once during the night. Constipation is also reasonably common. In a population study of people over 65 years of age, 26% of men and 34% of women reported constipation (19). Overall, 30% to 50% of the elderly use laxatives (16). Faecal incontinence in the general population has been recently shown to be around 11% during any 12-month period. Faecal incontinence is significantly associated with age and is particularly likely to be found in those elderly who report that their overall health is fair to poor (20).

Institutionalised elderly
Urinary incontinence is widely accepted to be present in around 50% of institutionalised older people (18, 11, 6), and can be much higher in the hospitalised elderly (16). In institutionalised or hospitalised elderly persons, episodes of urinary incontinence can often be a daily occurrence (6). Constipation has been reported in 41% of those elderly in acute geriatric wards and in over 80% of those residing in longterm care(9). Faecal incontinence is thought to be present in around 10% of those residing in nursing homes and in 30% of hospitalised patients(9).

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CLINICAL ASSESSMENT History


Key aspects of the medical history for elderly persons presenting with incontinence are highlighted in Table 2 (below). Medical history of elderly patients is likely to be complicated and a primary aim should be to rule out any transient causal factors (6). Assessment of the patients mobility, medication-use, and environment should be an early consideration. Simple aids to improve mobility, environmental changes to aid toileting, or medication changes may reduce the need for additional pharmacological treatment (21, 12).

TABLE 2: KEY

ASPECTS OF THE MEDICAL HISTORY*

General medical, neurologic, genitourinary, gastroenterological review Characteristics of the presenting incontinence Duration Frequency Amount (and with faeces, consistency) Impact on quality of life Precipitants Other related symptoms (eg. Nocturia, dysuria, hesitancy, pain, constipation) Fluid (including alcohol and caffeine) and fibre intake Laxative-use Previous treatments Expectations of treatment
(*) Adapted from 11 & 22

A useful aid to guide the initial search for transient causes of incontinence is the mnemonic DIAPPERS, presented in Table 3 (below).

TABLE 3: DIAPPERS,
D I A P P E R S

POTENTIAL CAUSES OF TRANSIENT INCONTINENCE*

Delirium Infection Atrophic vaginitis, vaginitis Pharmaceuticals Psychological, especially severe depression Excess urine output (eg. due to CHF or hyperglycaemia, or fast acting diuretics) Restricted mobility Stool impaction

(*) Adapted from 23 & 13

PHYSICAL EXAMINATION
Following a detailed history, confirmed if necessary by the primary carer, physical examination should focus on the following, presented in Table 4 (below):

TABLE 4: KEY

ASPECTS OF THE PHYSICAL EXAMINATION*

Oedema Neurologic examination Mobility and dexterity Cognition (capacity to accurately report symptoms and engage in treatment) Abdominal examination Organomegaly, masses, peritoneal fluid Rectal examination Perineal sensation, sphincter tone (resting and active), faecal impaction, rectal mass, prostate, puborectalis muscle, wink reflex Genital examination Foreskin abnormalities, glans penis, perineal skin, vaginal atrophy Pelvic examination Perineal skin, genital atrophy, pelvic organ prolapse, pelvic mass, paravaginal muscle tone Bladder function and direct observation of urine loss Cough stress test Urinary flow rate Residual urinary volume

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(*) Adapted from 11 , 22, & 9 In well-functioning patients, additional referred assessments may include anorectal manometry and defaecography, electromyography to eliminate muscular disease, pudendal nerve studies to investigate latency from nerve stimulation to muscle contraction, endoanal ultrasound, anoscopy, sigmoidoscopy, cystometry, and urethral function (leak-point pressure test or pressure profile) (9).

MANAGEMENT
Management of incontinence in the elderly will be largely dictated by the patients mental and physical status (21, 12) . In most cases, management will follow the guidelines suggested for younger adults.

Conservative treatments
The most simple management option of padding should not be the first choice. Long-term use of pads is expensive for the community-dwelling elderly and is arguably a deterrent to functional continence, doing nothing to treat the underlying cause. In long-term care, the cost of pads forms around half of the direct costs associated with incontinence (6). Similarly, penile sheaths and other external collection devices do not assist functional continence and should not be a first step. If indicated by assessment, early management strategies should include optimising toilet access and reviewing current drug-use (24). Many patients may also benefit from physiotherapy to reduce the risk of falls that may occur during night-time trips to the toilet. In suitable (mobile but less-cognitively-aware) patients, prompted voiding can be highly effective in reducing the frequency of incontinence, although it will not cure it. Behavioural treatments such as pelvic floor exercises, biofeedback and bladder training may be useful in mobile and cognitively-aware elderly patients (25, 6, 24).

TABLE 5: MANAGEMENT

OF URINARY INCONTINENCE IN THE ELDERLY

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Improve mobility and/or toilet access Treat any medical causes eg. Atrophic vaginitis Modify fluid intake and, if appropriate, medication-use Trial behavioural techniques; Prompted voiding Bladder training Biofeedback Pelvic Floor exercises Trial pharmacological agents appropriate to symptoms Detrusor overactivity/instability anticholinergics Stress incontinence -adrenergic agonists Refer to specialist if unsuccessful Conservative management of constipation should begin with a one-off dose of laxative and a trial of additional dietary fibre. Patients should also be encouraged to become more active if possible and limit any constipating drugs (9). Laxatives may be required. Suppositories and tap-water enemas may also be useful but should not be considered as a long-term treatment plan (9).

TABLE 6: MANAGEMENT

OF CONSTIPATION IN THE ELDERLY*

Review diet and fluid intake Review medication Remove any faecal impaction Refer for colonoscopy if associated with weight loss, anemia, heme-positive stool, abdominal distention or mass, family history of colon cancer, or recent change in bowel habits Educate patient as to normal bowel habits Encourage increased fibre intake Encourage fluid intake Encourage physical activity

(*) Adapted from 16.

Management of faecal incontinence should also begin conservatively. Dietary changes should be trialed with the aim of stool-bulking and eliminating foods or medications that cause diarrhoea (9). Faecal impaction can have potentially serious complications and should be removed manually and any inflammation should be treated. A trial of biofeedback in patients with intact rectal sensation may be useful (9).

TABLE 7: MANAGEMENT

OF FAECAL INCONTINENCE IN THE ELDERLY*

Manipulate stool consistency Review diet and drug-use Trial low-dose bulking agents (with caution) Trial antidiarrhoeal agents Avoid large meals Improve mobility and/or toilet access Tap-water enemas For solid stools; Scheduled toileting Glycerin suppositories Offer biofeedback therapy If no response, proceed with specialist referral (*) Adapted from 16.

Pharmacological treatment
Medication should be contemplated only when behavioural therapy and environmental modifications have proved fruitless. Anticholinergic drugs have been variously reported as successful in managing urinary incontinence in the general population, however this is not entirely supported by a number of controlled clinical trials in nursing homes (6). In genuine stress urinary incontinence, -adrenergic agonists may be helpful. Cholinergic agonists may be useful for poorly-contractable bladders (26). There is some suggestion that nocturnal polyuria in older people may be treated by restoring night-time vasopressin levels (27), however this is currently under-researched. For constipation, if conservative efforts fail, prokinetic agents, stool softeners, stimulant laxatives, saline laxatives, and osmotic agents may be useful (9). Antidiarrhoeal agents and low-dose bulking agents may be helpful in managing faecal incontinence, as may regular glycerine suppositories (16).

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Surgical treatment
Surgery for incontinence in the elderly has a very limited role and should be reserved for conditions that have not been treated successfully by other means, including pessary and TVT. Due to the complexity of presentation in the elderly, it is essential that significant urodynamic and/or gastroenterological testing be performed to confirm that surgery is in fact necessary (28). For urinary incontinence in men, transurethral resection of the prostate is a common procedure with minimal side-effects and in women with stress incontinence, intraurethral injection of collagentype substances may be useful. Both may be added-to with pharmacological treatment (21, 12). More aggressive surgeries are not recommended in the elderly unless substantial improvement in quality of life is expected. Surgical treatment of faecal incontinence may include sphincter repair, postanal repair, colostomy, and artificial sphincter, however careful risk-outcome decisions related to such surgery are imperative.

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References: 1. DuBeau, C. E. (1996). Interpreting the effect of common medical conditions on voiding dysfunction in the elderly. Urologic Clinics of North America, 23 (1): 11-18. 2. Ouslander, J. G. (1997). Aging and the lower urinary tract. American Journal of Medical Science, 314 (4): 214-218. 3. Payne, C. K. (1998). Epidemiology, pathophysiology, and evaluation of urinary incontinence and overactive bladder. Urology, 51 (Suppl 2A): 3-10. 4. Umlauf, M. G., Goode, P. S., & Burgio, K. L. (1996). Psychological issues in geriatric urology. Urologic Clinics of North America, 23 (1): 127-135. 5. Naughton, M. J. & Wyman, J. F. (1997). Quality of life in geriatric patients with lower urinary tract dysfunction. American Journal of Medical Science, 314 (4): 219-227. 6. Pranikoff, K. (1996). Urologic care in long-term facilities. Urologic Clinics of North America, 23 (1): 137-146. 7. Downie, J. W., Levin, R. M., Lin, A. T. L., et al. (1999). Basic neurophysiology and neuropharmacology, in Incontinence, P. Abrams, S. Khoury, and A. Wein (Eds). Monaco: 1st International Consultation on Incontinence. p. 105-154. 8. Hogan, D. B. (1997). Revisiting the O complex: Urinary incontinence, delirium and polypharmacy in elderly patients. Canadian Medical Assocaition Journal, 157: 1071-1077. 9. De Lillo, A. R. & Rose, S. (2000). Functional bowel disorders in the geriatric patient: Constipation, fecal impaction, and fecal incontinence. The American Journal of Gastroenterology, 95 (4): 901-905. 10. Resnick, N. M. (1994). Geriatric medicine, in Harrison's principles of internal medicine, K.J. Isselbacher, E. Braunwald, and J.D. Wilson, (Eds). New York: McGraw-Hill. p. 34. 11. Johnson, T. M. & Busby-Whitehead, J. (1997). Diagnostic assessment of geriatric urinary incontinence. American Journal of Medical Science, 314 (4): 250-256. 12. O'Donnell, P. D. (1998). Special considerations in elderly individuals with urinary incontinence. Urology, 51 (Suppl 2A): 2023. 13. Resnick, N. M. (1996). Geriatric Incontinence. Urologic Clinics of North America, 23 (1): 55-73. 14. Grosshans, C., Passadori, Y., & Peter, B. (1993). Urinary retention in the elderly: A study of 100 hospitalized patients. Journal of the American Geriatric Society, 41 (6): 633-638. 15. Jeter, K. F. & Lutz, J. B. (1996). Skin care in the frail, elderly, dependent, incontinent person. Advances in Wound Care, 9 (1): 29-34. 16. Romero, Y., Evans, J. M., Fleming, K. C., et al. (1996). Constipation and fecal incontinence in the elderly population. Mayo Clinical Procedings, 71: 81-92. 17. Diokno, A. C., Brock, B. M., Brown, M. B., et al. (1986). Prevalence of urinary incontinence and other urological symptoms in the noninstitutionalized elderly. Journal of Urology, 136: 1022-1025. 18. Fultz, N. H. & Herzog, A. R. (1996). Epidemiology of urinary symptoms in the geriatric population. Urologic Clinics of North America, 23 (1): 1-10. 19. Hale, W. E., Perkins, L. L., May, F. E., et al. (1986). Symptom prevalence in the elderly: An evaluation of age, sex, disease, and medication use. Journal of the American Geriatrics Society, 34: 333-340. 20. Kalantar, J. S., Howell, S., & Talley, N. J. (2002). Prevalence of faecal incontinence and associated risk factors: An underdiagnosed problem in the Australian community? Medical Journal of Australia, 176: 54-57. 21. O'Donnell, P. D. (1998). Behavioral modification for institutionalized individuals with urinary incontinence. Urology, 51 (Suppl 2A): 40-42. 22. Pushpangadan, M. & Burns, E. (1996). Caring for older people: Community services: Health. British Medical Journal, 313: 805808. 23. Resnick, N. M. (1984). Urinary incontinence in the elderly. Medical Grand Rounds, 3: 281-290. 24. Whishaw, M. (1998). Urinary incontinence in the elderly: Managing for maximum outcomes. Australian Family Physician, 27 (12): 1091-1094. 25. Burgio, K. L. & Goode, P. S. (1997). Behavioral interventions for incontinence in ambulatory patients. American Journal of Medical Science, 314 (4): 257-261. 26. Goode, P. S. & Burgio, K. L. (1997). Pharmacologic treatment of lower urinary tract dysfunction in geriatric patients. American Journal of Medical Science, 314 (4): 262-267. 27. Donahue, J. L. & Lowenthal, D. T. (1997). Nocturnal polyuria in the elderly person. American Journal of Medical Science, 314 (4): 232-238. 28. Galloway, N. T. M. (1997). Surgical treatment of urinary incontinence in geriatric women. American Journal of Medical Science, 314 (4): 268-272.

8.6 INCONTINENCE ASSOCIATED WITH OTHER MEDICAL CONDITIONS


(CNS DISEASE OR INJURY, DIABETES, CANCER & INTRINSIC BLADDER & BOWEL DISEASE)

BACKGROUND
In comparison to the general population, urinary and faecal incontinence are often highly prevalent in patients who already suffer from a medical condition. In many cases, these symptoms can be viewed as fundamental components of the predominant condition. Incontinence may also be seen as secondary to such general factors as immobility, poor diet, or laxative misuse (1). Much incontinence associated with a predominant medical condition can be managed conservatively within the General Practice setting. Management of incontinence in these populations within a familiar, non-hospital setting has the potential to make the predominant condition far more bearable for both the patient and carer. By treating incontinence in medical populations, GPs can certainly also contribute to improving patients social mobility and quality of life (2). Table 1 (below) highlights a number of medical conditions in which incontinence and/or constipation have been reported in the scientific literature. Constipation has been included because of its strong relationship with faecal, and in some cases urinary incontinence (3).

TABLE 1: MEDICAL
CONSTIPATION

CONDITIONS ASSOCIATED WITH INCONTINENCE OR

Condition Cancer Dementia Diabetes Mellitus Intrinsic Bladder Disease Intrinsic Bowel Disease Multiple Sclerosis Parkinsons Disease Spina Bifida/Myelomeningocele Spinal Cord Injury Stroke

Urinary Incontinence

Faecal Incontinence

Constipation

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In addition to the conditions highlighted in Table 1, incontinence has been reported in several conditions that may be considerably more rare in General Practice. These conditions, which are not covered in this section, include: anorectal atresia, Behects syndrome, chronic alcoholism, cirrhosis, collagen diseases, Hirschprung disease, inflammatory diseases such as Guilain-Barre syndrome, multiple system atrophy, schizophrenia, and spinocerebellar degeneration (4, 5, 6, 7, 8). The large number of conditions that have been reported to present with bladder and bowel problems is a product of the complexity of moderating and mediating areas for urination and defecation within the central nervous system. There are a large number of distinct sites in which pathology may affect normal function.

PRESENTATION AND PREVALENCE CANCER Urinary symptoms


Anatomy & Physiology: Urgency, frequency and interrupted flow of urine caused by either malignant tumour or enlargement of the prostate are perhaps the most widely known urinary effects of cancer. There is growing awareness that urinary incontinence may be a side-effect of radical prostatectomy or radiation treatment, however newer treatments are lessening the risks. Urinary incontinence, however, may occur with many other types of cancer and their associated therapies (9) and its effect on quality of life and self-esteem is often apparently overlooked within a broader focus on survival. Malignancies located in the bladder (10), cervix (11), and those that are most likely to spread to the autonomic system, such as lung and breast cancer (12), are likely to cause urinary problems. In particular, treatment by means of radical resection or radiotherapy in crucial areas such as the bladder will have serious long-term effects (10). Analgesics (13) and chemotherapy (14) are also acknowledged to have a wide range of effects on micturition that can include incontinence. Prevalence: The rate of urinary incontinence in cancer depends largely on the location of tumour and type of treatment. Following radical prostatectomy, incontinence has been variously reported at between 0 and 57% and it seems that much of this may be small-volume stress incontinence (15). Rates of incontinence following treatment of prostate cancer with radiotherapy may be similar, with reports of between 34% and 44% experiencing urinary symptoms (16). In contrast, following high-intensity, localised ultrasound treatment of prostate cancer, a recent study reported that none of 184 patients experienced severe incontinence (17), a rate only slightly increased in Brachytherapy (6%-7%) (18). Of women with cervical cancer, only 17% have normal pre-treatment urodynamic presentation and up to half may present with urinary incontinence (51%) (11). Rates of incontinence may decrease following radical hysterectomy, however, with 48%, 29.6% and 31.2% of women remaining incontinent at 6 weeks, 3 months and 12 months respectively (19).
In rectal cancer, a recent study reported that 34% of male and 45% of female patients treated surgically were incontinent of urine at five-year follow-up (20).

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Gastrointestinal symptoms
Anatomy & Physiology: Malignancies present in the colon, or close to the sphincter in the lower rectum may cause gastrointestinal symptoms including incontinence, particularly when treated either with radiotherapy or radical resection (21). Gastrointestinal symptoms may also be associated with tumours in the brain stem and oesophagus (22), the latter of which probably has much to do with altered diet. In general, cancers that are more likely to invade the autonomic nervous system, or directly affect the bowel and sphincters themselves, are most likely to present with gastrointestinal symptoms that are typically aggravated by treatment. Analgesics may also have many influential effects, including constipation (13), which may be exacerbated by a lack of activity and presence of depression. Prevalence: Faecal incontinence - In men treated with radiotherapy for prostate cancer, between 22% and 40% experienced faecal urgency at follow-up, however actual incontinence was present in only 10% and only in those with the more severe pre-treatment tumours (16). Treatment of rectal cancer is usually associated with worse outcome, particularly if resection or radiotherapy is performed close to the sphincter, however recent surgical developments potentially reduce the requirement for permanent colostomy in these patients (21). Constipation has been a reported symptom of cancer in between 23% (13) and 33% of patients (23). However, rates may be more than double that in advanced cancer with up to 71% of patients experiencing constipation during the course of treatment (23). This may be highly related to opiate analgesic prescription (23).

DEMENTIA Urinary symptoms


Anatomy & Physiology Much incontinence in dementia may be the result of neural pathology within areas of the brain specifically devoted to urination, or in areas more concerned with adherence to social norms concerning toileting. However, incontinence may also be secondary to a variety of other factors, including sedation, lack of mobility, dietary changes, difficulty communicating (ie. letting someone know the need to go to the toilet), transient confusion due to delirium, or urinary tract infection (24). Prevalence A review of urinary incontinence in dementia has highlighted that, depending on definitions, anywhere between 11% and 90% of persons with dementia experience urinary incontinence (24). Of those with incontinence, up to two-thirds will experience it at least once a week (24). It has also been reported that urinary incontinence may appear earlier in both vascular dementia and dementia with Lewy bodies than in Alzheimers disease, in which it is more associated with actual cognitive decline (25). Silverman et al (26) highlighted that much incontinence in dementia might go untreated, with 24% of their retrospective survey of records indicating no management recommendations.

Gastrointestinal symptoms
Anatomy & Physiology Overflow-type faecal incontinence may be present in dementia and may be associated with impaction or constipation, perhaps reflecting side-effects of drug treatment and lack of activity rather than sphincter dysfunction (27). Diarrhoea and or/constipation are noted symptoms of drug treatment for Alzhemiers disease, such as tacrine and donepezil (28, 29). Diarrhoea, in particular, has been identified as a significant predictor of patients withdrawal of such treatment (28). Other important considerations, as with urinary incontinence, include sedation, dietary changes, inactivity, and communication problems. Prevalence Faecal incontinence in dementia has to date been reported predominantly in studies that have investigated predictors of incontinence in nursing home populations (eg 27). Within one study population, 46% of residents were incontinent of faeces, a group in which a diagnosis of dementia was highly prevalent (30). Incontinence is in fact one of the best predictors of institutionalisation among older adults (31), suggesting that it is perhaps less-prevalent in stable, community-dwelling patients. More likely to be incontinent are male patients, and those with associated diarrhoea and restricted mobility (30).
Constipation in dementia is thought to be more prevalent in those patients who are inactive, whose diet is poor, and who are on multiple medications (27). There does not appear to be any conclusive naturalistic data indicating the prevalence of constipation in unmedicated persons with dementia. Of note, discomfort and pain associated with constipation may not be communicated particularly well by patients and may in fact be the cause of much behavioural disturbance. Depression is present in between 13% and 31% of patients and may also be influential in constipation (32).

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DIABETES MELLITUS (DM) Urinary symptoms


Anatomy & Physiology Urinary symptoms in diabetes are thought to be associated with the autonomic neuropathy of the disease process. Many GPs may be most aware that diabetes is associated with frequent urination and urine that is abnormally high in albumin (33). Other symptoms may include decreased bladder sensation, detrusor areflexia, and a large posturination residual volume (12). Retention, a major problem in itself, can also result in incontinence due to overflow (12). Urinary tract infection is also more common in diabetics than in the general population, as are the complications of such infection (34). Urinary symptoms may worsen considerably in long-term diabetes, as the disease is now recognised as the leading cause of end-stage renal-failure in Western countries (33, 35). Prevalence The prevalence of actual incontinence in diabetes is probably low and associated with the autonomic neuropathy found in between 5% and 7% of diabetics (36). Of those with autonomic neuropathy, urinary incontinence has been observed in less than 1% of patients, while incomplete emptying and decreased frequency were noted in 6% and 8% respectively (37). Rates may be higher in those patients requiring admission to hospital a large review of discharge notes characterised 26% of diabetics as having neurogenic bladder (38).

Gastrointestinal symptoms
Anatomy & Physiology Faecal incontinence in diabetes can result from dysfunction of the anorectal sphincter, abnormal rectal sensation, bacterial overgrowth, or rapid transit caused by uncoordinated small bowel motor activity (22). Incontinence is highly related to diarrhoea, a link which is thought to be explained by a common autonomic neuropathy affecting both the gastrointestinal tract (reducing fluid absorption), and internal sphincter (39). It has been suggested that diabetics may have abnormal autonomic innervation of the internal anal sphincter or defects in the smooth muscle itself (39). Interestingly, one study found that diabetics with faecal incontinence had thresholds for rectal sensation and phasic external sphincter control within a similar range to that found in Multiple Sclerosis (40). There is typically reduced resting and maximal voluntary anal sphincter pressures (40), and delayed gastric emptying (39) . Hyperglycaemia may directly inhibit intestinal transit but autonomic neuropathy is thought to be the primary cause of constipation (41). Prevalence It has been noted that between 68% (42) and 76% (43) of diabetics experience gastrointestinal symptoms.
Constipation is the most common symptom and becomes more frequent with increasing symptoms of autonomic neuropathy, such as esophageal dysmotility (39). In a survey of 136 patients, 60 were identified as constipated (43). In a much larger population sample, a lesser number of 27.1% of diabetics reported being constipated some of the time, as compared to 17% of the non-diabetic population (44). Laxative-use during the past month was reported by 22.7% of diabetics compared to 9.9% of non-diabetics (44). Faecal incontinence prevalence rates are difficult to estimate due to research definitions that include diarrhoea. Diarrhoea is considered common in diabetes and has been reported as a reasonably regular occurrence in about 20% of patients (43). Faecal incontinence is likely to be more related to autonomic neuropathy and considerably more rare. Rates from one study documented faecal incontinence in less than 1% of patients (45). Where poor rectal sensation and abnormal sphincter function are observed in association with naturally-occurring or laxativeinduced diarrhoea, incontinence is more likely to be a problem.

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INTRINSIC BLADDER/BOWEL DISEASE Urinary symptoms


Anatomy & Physiology Infection by pathogens such as E. coli may be a major cause of urinary symptoms in intrinsic bladder and urinary tract conditions, however autoimmune processes may also be implicated (46). Most intrinsic bladder diseases, such as Interstital Cystitis (47), are not well understood. It is known, however, that collagen is important in the structure and tensile strength of the bladder, and diseases in which it is affected may be likely to present with urinary symptoms (12). A further poorly-understood cause of urinary symptoms such as hyper-reflexia may be an increased hypersensitivity of the bladder afferents (48). Prevalence Little is known of the prevalence of non-carcinoma type intrinsic bladder disease such as interstital cystitis. It is a major cause of morbidity, though most patients seem to suffer from urgency, frequency and pain, rather than incontinence.
Urinary tract infection, however, is common, especially in patients with indwelling catheters (49). This management technique is becoming more rare and is likely to be seen in older patients with conditions such as SCI or spina bifida. Intermittent self-catheterisation, popular as a replacement strategy for indwelling catheter and diversion, also carries the risk of infection. E. coli has been reported as being the predominant cause of urinary tract infection, found in up to 54.7% of cases (50).

Gastrointestinal symptoms
Anatomy & Physiology Gastrointestinal symptoms may appear as part of a variety of diseases of the gastrointestinal system. Ulcerative colitis, characterised by diffuse inflammation of the colon and rectum, and Crohns disease, which involves a similar but wider-spread pathology, can both be associated with urgent diarrhoea (51). Related scarring and intestinal lumen narrowing may be precursors to problems with constipation. In Coeliac disease, gluten, probably via immune responses, is responsible for damage to the mucosa of the small intestine leading to malabsorption (51) and diarrhoea. For most of these conditions, an auto-immune cause is suspected (51). Other diseases associated with symptoms include scleroderma, Whipples disease, acute intermittent porphyria (51), and irritable bowel syndrome (52). Viruses, parasites, and bacteria are all also capable of causing urgent diarrhoea that, at inopportune moments, may lead to transient incontinence. Prevalence Serious diseases of the gastrointestinal system are reasonably rare. Whipples disease and Coeliac disease, for example, are most likely to be found in European populations (51). It has been noted, though that there has been a steady rise over the past few decades in Crohns disease but not of ulcerative colitis (51). Irritable bowel syndrome may be more common and can be associated with incontinence (52).

63

MULTIPLE SCLEROSIS (MS) Urinary symptoms


Anatomy & Physiology In the first major survey of bladder symptoms in MS, Miller et al (53) noted a variety of influential physiological changes. These include hyper-reflexia of the bladder, increased urethral sphincter resistance, and complete or partial urinary retention. While the major symptom appears to be urgency, more serious urge incontinence may result simply because the patient lacks the mobility to reach a toilet in sufficient time (54). Prevalence Most studies indicate that between 55% (3) and 60% (55) of patients report some kind of bladder dysfunction, however an older (but larger) study suggested a much higher prevalence of 78% (53). These symptoms do not appear to differ between the sexes, but have been observed to be worse in later-onset and more severe MS, and with longer duration of the disease (53, 55). Typically, patients will present with a mixture of symptoms, with the most common being urgency (53). Frequency, urge incontinence, hesitancy, unconscious incontinence, and retention have been reported to be the next most common symptoms, in that order (53).

Gastrointestinal symptoms
Anatomy & Physiology Reports of the bowel function of MS patients indicate that there is commonly poor rectal sensation, and both poor coordination and minimised strength of the pelvic floor muscles (54, 40, 1). Also observable is an increased threshold of phasic contraction of the external anal sphincter in response to rectal distension (40), and a reduced contractile strength of external anal sphincter (40, 1). More hypothetically, a further physiological result of MS lesions may be removed cortical inhibition of colonic motor activity (3). As with urinary incontinence, difficulty in accessing the toilet may certainly contribute (54). Reduced fluid intake, poor mobility and anticholinergic drugs may contribute to constipation (1). Prevalence Between 41% (55) and 68% (3) of MS patients experience some form of bowel dysfunction, of which a combination of constipation and incontinence is common (1). Interestingly, a close relationship (r = .74) has also been observed between bowel and bladder dysfunction (55).
Faecal incontinence has been an acknowledged symptom of MS for some time. In one reported series, 51% of patients had experienced soiling at least once in the past 3 months (3). This symptom appears to have no relationship with gender, but is related to age, and both disease duration and severity (3). Of note, it has been reported that 59% of patients with faecal incontinence had never informed their physicians (3). Constipation has been suggested to be present in around 40% of patients (39% (53); 43% (3), and becomes both more prevalent and severe as the disease progresses. In those patients with constipation, the symptom may precede the onset of the disease in close to half (45%) (3), and may therefore be, as in Parkinsons disease, an early marker for the disease itself. Patients tend to self-medicate with laxatives, a strategy which has been reported at rates of more than one dose per week in about 1 in 5 patients (18%) (3). Laxative use, however, may simply exacerbate incontinence.

64

PARKINSONS DISEASE Urinary symptoms


Anatomy & Physiology Parkinsons disease commonly presents with detrusor hyper-reflexia and a reduced bladder capacity (56), which may result in day and night-time frequency, urgency, and urge incontinence (57, 58). Symptoms such as hesitancy and weak-flow may be less common and might be due to anticholinergic drug treatment, or obstructive neuropathy (58). In a small SPECT study, urinary incontinence was found to be related to degeneration of the nigrostriatal dopaminergic cells of the brain (57). Muscle monitoring during voiding has highlighted a delayed relaxation of sphincter and pelvic muscles (58). Urinary symptoms (and constipation) may be some of the very early manifestations of PD (59). Prevalence Detrusor hyper-reflexia has been observed in 92.8% of women with Parkinsons disease (56), and in between 67% (60) and 81% of combined-sex samples (57). Detrusor-sphincter dysynergia, however, is apparently not commonly observed during actual voiding (57, 60). In 33%, of patients the urethral sphincter may involuntarily relax, releasing urine (57). Weak detrusor-strength was found in 66% of women and 40% of men with PD (57), while hypo- or areflexia were present in 16% (60). Urinary incontinence increases with disease severity (60).

Gastrointestinal symptoms
Anatomy & Physiology Consistent with the depletion of dopamine characteristic of PD, patients typically demonstrate impaired coordination of pelvic and sphincter muscles and slow colon transit (61, 62), for which the degeneration of the colonic myenteric plexus, in particular, has been implicated (61). Difficulty in defecating, or more severe constipation, are common complaints (63). Patients typically show a decreased anal tone and an abnormal straining pattern including paradoxic muscle contractions or lack of inhibition (64). Prevalence Constipation has been proposed as the predominant gastrointestinal symptom in PD. Up to 50% of patients experience constipation (61), which usually accompanies considerable muscle straining during defecation and a sensation of incomplete evacuation (63). Of particular note, constipation may precede the diagnosis of Parkinsons disease by a number of years (61). Most patients pass faeces on less than 3 occasions per week (64).
Faecal incontinence is an acknowledged symptom of PD (64) but, as in the general population, it is underresearched. It is likely to be present either in later stages of the disease when muscle control is most severely affected, and in particular association with laxative-use. As with urinary incontinence, a potentially large proportion of faecal incontinence may be explained by a lack of sufficient mobility to reach a toilet.

65

SPINA BIFIDA MYELOMENINGOCELE Urinary Symptoms


Anatomy & Physiology Patients with Spina Bifida commonly have minimised bladder sensation, areflexic bladder, and a nonfunctional urethral sphincter (65). Detrusor hyperflexia and/or urethral sphincter dyssynergia may also be symptoms (66), and are in common with traumatic spinal cord injury. Bladder capacity is often minimised and when urination occurs there is typically incomplete emptying (66). In terms of long-term observation, high bladder pressure due to retention can cause considerable urethral sphincter damage (65). Prevalence It is difficult to estimate the naturally-occurring prevalence of incontinence in spina bifida as in the majority of patients this is managed at a very early stage. Given the severity of the disease, however, it may be reasonable to suggest that most, if not all unmanaged patients will be incontinent of urine at some stage (65). Even in those patients where surgical management of urinary incontinence has been initiated, rates of incontinence have been demonstrated to remain at around 30% (67).

Gastrointestinal Symptoms
Anatomy & Physiology The most common gastrointestinal symptoms of spina bifida are a lack of rectal sensation and a lack of external anal sphincter control (68, 69). Pelvic floor muscles may also suffer a type of disuse atrophy (70). Constipation can occur very quickly due to poor peristalsis (71), poor diet, and lack of exercise, and if untreated can lead to toxic megacolon (65). The bowel is also slow to develop in spina bifida and patients may be 8 or 9 years of age before it is mature and incontinence lessens (65).
66

Prevalence
Faecal incontinence has been reported in up to 90% of patients (72), and even at long-term follow-up of managed patients, rates can be as high as 53% (67). Those with incomplete, less-severe spinal cord lesions, however, seem to fare much better, experiencing constipation but rarely incontinence (66). Faecal incontinence is a major factor limiting the social adjustment of spina bifida patients (71) and may be a particular problem during times of physical activity (65). Constipation has been reported in up to 78% of patients (71). In one study, 37% regularly took oral laxatives, 31% took rectal laxatives, and 44% used manual evacuation methods for combating constipation (72).

SPINAL CORD INJURY (SCI) Urinary Symptoms


Anatomy and Physiology During the immediate post-injury period, it is common to observe urinary retention in patients with SCI. Following a period of between days-to-weeks of the occurrence of the injury, however, spontaneous reflex voiding develops. It has been suggested that this change might be mediated by a reorganisation of neural connections (73). Furthermore, it has been suggested that increased sensitivity of bladder afferents might ultimately lead the brain to receive information that the bladder is more full than is in fact the case (73). A SCI patient may present with any or all of the following symptoms: urinary retention, detrusor hyper-reflexia, detrusor/sphincter dyssynergia, lack of bladder sensation, large post-urination residual volume, and bladder stones (74). Prevalence Naturalistic data is apparently sparse, presumably because urinary incontinence is both prevalent and managed early. However, even in managed patients, urinary incontinence may be as high as 54% (75). Death in SCI due to diseases of the urinary system is higher than in the general population (76) and is greater in the first few decades post-injury than in later decades (77).

Gastrointestinal symptoms
Anatomy and Physiology Typically, patients with SCI have a slower colon transit-time in comparison to normal populations, especially in the left colon and rectum (2). While there is often an almost normal basal anal pressure due to maintenance of internal anal sphincter function, voluntary control of the external anal sphincter is often minimised or absent (2). The reflex which causes relaxation of the internal anal sphincter as the rectum fills is usually normal or increased and this factor, combined with reduced rectal sensation and external sphincter control, can lead to faecal incontinence (2). Prevalence In one study, 50% of SCI patients had at some time received medical attention for gastrointestinal problems (78). It is likely, however, that the number of patients requiring such attention is much higher than reported due the potentially large number of patients attempting to manage with minimal or no professional assistance in their own home (79). The presence of gastrointestinal symptoms is generally not influenced by age, gender, or level of lesion, but is instead associated with severity (or completeness) of lesion and time since the lesion (2).
Constipation is the most prevalent gastrointestinal symptom of SCI. It has been suggested that up to 95% of patients are required to employ at least one initiating-method for defecation, which can include manual stimulation or laxative-use (78). Indeed, in 65% of one series of patients, the predominant method was found to be digital evacuation or other manual stimulation (2). Almost half of patients may take more than 15 minutes to complete evacuation (2), a factor that has been demonstrated to influence quality of life (78). Faecal incontinence may be present in up to 75% of patients, however studies highlight that this is mostly occasional only a very small number experience leakage every day or every week (2). Incontinence is usually caused by a combination of a lack of rectal sensation (in up to 81% of patients) (2), loss of external anal sphincter control, and use of laxatives to treat constipation (78). Along with time taken to defecate, frequency of faecal incontinence has been identified as a factor influencing the quality of life of those with SCI (78). Most spinal cord injured patients require a management plan to prevent faecal impaction and its consequences.

67

STROKE Urinary symptoms


Anatomy & Physiology As in dementia, urinary incontinence may in some cases be due to pathology in areas of the brain with particular control over urination, however other causal factors may include immobility, confusion, and difficulty with communicating the desire to pass urine (80, 81). Common in stroke, incontinence may also be associated with apraxia and aphasia (80). Depression has also been suggested to play a potential role in the voiding behaviour of stroke patients (80). The most common problem observed is usually detrusor instability. Prevalence A large survey of stroke patients demonstrated that roughly half present with urinary incontinence at admission (82). A review of 9 studies widens this percentage to between 32% and 79% of patients (80). At discharge, however, the rate of urinary incontinence has typically dropped to around a quarter of patients (80). Further reports confirm the transitory nature of this symptom. In up to 41% of patients, incontinence may clear within 2 weeks (81), and it has been reported that only 20% (81, 82) and 15% (81) of patients remained incontinent at 6 and 12 months respectively. Perhaps the most notable statistic, however, is that of stroke patients with urinary incontinence at admission, 52% are dead within 6 months, indicating that these patients may require more aggressive rehabilitation (82). There is suggestion, also, that a significant number of stroke patients may already have been incontinent (80).

Gastrointestinal symptoms
Anatomy & Physiology It has been suggested that stroke-induced lesions in the pontine defecatory centre of the brain may be related to constipation or impaction, and that lesions in pre-frontal areas may be more related to faecal incontinence (83). Inactivity, medication, and dehydration caused by dysphagia may also contribute to constipation (83). General symptoms such as confusion, and reduced adherence to social conventions concerning timing and location of toileting may also contribute to incontinence (83), as may apraxia and aphasia (80). Prevalence Faecal incontinence in stroke is generally a little less prevalent than urinary incontinence. In one study, of those with urinary incontinence, 84% also had faecal incontinence (82). Overall, between 31 and 40% of stoke patients present with faecal incontinence at admission, and figures tend to drop over the following months (80). Only 7.6% of one series of patients were still incontinent of faeces after 12 months (81). In those that are incontinent within nursing home populations, stroke is common (84). As with urinary incontinence, the death rate of those that present with faecal incontinence is very high (59%) (82).
Constipation is acknowledged as a common symptom of stroke (83), however sound prevalence data is limited. It may be that the diet of many stroke inpatients is provided with constipation in mind and this decreases its observation in clinical populations. It likely that constipation will be most prevalent in those stroke patients who are community-dwelling, on multiple medications, inactive or immobile, or in whom diet has been significantly altered.

68

ASSESSMENT/MANAGEMENT
It is likely that, if presenting to a GP, many patients with a serious medical condition of which incontinence is a symptom will have a pre-existing treatment regime that may require either maintenance or alteration. In less serious conditions, where incontinence has perhaps not been investigated or addressed by a specialist, treatment may need to be initiated. In all cases, management decisions should be made in close consultation with the patient and specialist and, if possible, the patients carer. Management strategies will often fail without the support and time of a carer (85), particularly in immobile patients. The general algorithms included in this package may be useful in planning your consultation with the patient. Initially, a clear history of symptoms should be gained through interview and physical examination. Bowel and bladder diaries (examples of which found are found as appendices) may be extremely helpful in supplementing and verifying patient report, which may not always be accurate, particularly where neural pathology is present (eg. 61). Important first steps in the consultation are presented in Table 2 (below).

TABLE 2: FIRST

STEPS IN THE CONSULTATION

Symptoms of uremia due to retention or renal failure (requires immediate ED referral) * Symptoms of autonomic dysreflexia due to faecal impaction or urinary retention (requires immediate ED referral) *. Catheterisation may need to be performed by the GP Presence, type and frequency of urinary or faecal incontinence Whether incontinence is due to faulty device or complication with surgery Presence of constipation and use of laxatives Concomitant medications Fluid and dietary fibre intake Any current or past management strategies and their success Patient goals for treatment (*) Please see file for pamphlet on autonomic dysreflexia. See also below.
69

Symptoms of uremia:
Nausea Vomiting Headache Dizziness Dimness of vision Perspiration Raised blood pressure Hard rapid pulse

Symptoms of autonomic dysreflexia


Sudden hypertension Bradycardia Perspiration Severe headache Gooseflesh

NEXT STEPS/MANAGEMENT
While the actual number of treatment options available to these patients is reasonably large, data on their efficacy are sparse. Most reports are of surgical procedures and those that discuss conservative options most often provide only anecdotal evidence, or base recommendations on reports of treatment efficacy in normal populations. Largesampled, randomised, double-blind, placebo-controlled trials of therapeutic approaches are notably absent in the available literature. At present, we find no reason to disagree with the conclusions of Wiesel, Norton, & Brazzelli, who conducted the 2001 Cochrane review of the management of faecal incontinence and constipation in medical populations (86), nor do we fault the arguments presented by the International Consultation on Incontinence who met in Monaco in 1999 (87). There is currently insufficient evidence to draw conclusions for practice from the available literature. In this light, we recommend that a patient-centered approach to management be taken. That is, when initiating new treatment, GPs should trial the most conservative treatment available for that particular patient. Initiation of surgical management should remain a final option as much gastrointestinal or genitourinary surgery, if it fails, may seriously complicate treatment from that point on.

Table 3 (below) presents the treatment options that have been highlighted in the literature as potentially useful for urinary incontinence in medical populations, and the associated level and strength of evidence for their use. Using the same format, Table 4 (also below) presents similar information related to faecal incontinence sufficient data does not exist to include constipation. It must be stressed that these tables do not present all of the available treatments for medical populations. Many treatments and many individual studies have been omitted because they either a) did not adequately describe the patient population, b) were of extremely small sample size, or c) did not show any observable success. Furthermore, for many treatments no trials exist.

TABLE 3: AVAILABLE
POPULATIONS Treatment type

TREATMENTS FOR URINARY INCONTINENCE IN MEDICAL Conditions reported potentially useful in Dementia (88) Dementia (89, 90) MS (91), prostatectomy, (92) cervical cancer surgery (11) MS (93) MS (94) Spina bifida (SB) (95) SCI (96) SB
(70)

Treatment

Level of Evidence

Strength of Recommendation B/C B/C

Behavioural

Daily exercise Prompted/timed voiding Pelvic floor physiotherapy Biofeedback

IV III/IV

IV IV III IV V IV IV/V V

B/C C B C C B C C B/C C B/C V B/C B/C B/C C B

70 Pharmacological

Aerobic training Desmospressin Anticholinergics Miscellaneous Transcutaneous electrical stimulation Intermittent catheterisation Padding Surgical Electrical stimulation of sacral spinal nerves Botulinum toxin injection into bladder or sphincter Polydimethylsiloxane injection Indewelling catheter Collagen injection Fascial sling Cystostomy/diversion Double dynamic graciloplasty Artificial urinary sphincter

SCI (75; 97, 98) SCI (98) SCI


(99, 100)

, MS

(101, 102)

IV/V IV/V IV V IV IV IV/V V IV

SCI (103) SB (104, 105) SCI (98) SB (106) SB (107, 108) SB


(109, 110)

SB (111) SB (112, 113)

TABLE 4: AVAILABLE
POPULATIONS Treatment type

TREATMENTS FOR FAECAL INCONTINENCE IN MEDICAL

Treatment

Conditions reported potentially useful in

Level of Evidence

Strength of Recommendation

Behavioural Pharmacological

Biofeedback Laxatives/ suppositories Enema

SB (69), MS (54) Cancer (114) SCI (115)

III, IV IV

B/C C

SB (72) SCI (116), Stroke (116), SB (117) Spina bifida (68)

IV IV IV

C B/C B/C

Miscellaneous

Anal plug Transrectal electrical stimulation

Surgical

Electrical stimulation of sacral spinal nerves Antegrade colonic enema Double dynamic graciloplasty

SCI (99; 118, 119)

IV

Spina Bifida (120-122)

IV

SB (111)

71

72

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SPECT imaging of the dopamine transporter with [(123)I]-beta-CIT reveals marked decline of nigrostriatal dopaminergic function in Parkinson's disease with urinary dysfunction. Journal of Neurological Science, 187 (1-2): 55-59. 58. Singer, C. (1998). Urinary dysfunction in Parkinson's disease. Clinical Neuroscience, 5 (2): 78-86. 59. Chaudhuri, K. R. (2001). Autonomic dysfunction in movement disorders. Current Opinion in Neurology, 14 (4): 505-511. 60. Araki, I., Kitahara, M., Oida, T., et al. (2000). Voiding dysfunction and Parkinson's disease: Urodynamic abnormalities and urinary symptoms. Journal of Urology, 164 (5): 1640-1643. 61. Ashraf, W, Pfeiffer, R.F., Park, F, et al. (1997). Constipation in Parkinson's disease: Objective Assessment and response to Psyllium. Movement Disorders, 12 (6): 946-951. 62. Pfeiffer, R. F. (1998). Gastrointestinal dysfunction in Parkinson's disease. Clinical Neuroscience, 5 (2): 136-146. 63. Quigley, E.M.M. (1996). Gastrointestinal dysfunction in Parkinson's disease. Seminars in Neurology, 16 (3): 245-250. 64. Stocchi, F., Badiali, D., Vacca, L., et al. (2000). Anorectal function in multiple system atrophy and Parkinson's disease. Movement Disorders, 15 (1): 71-76. 65. Spina Bifida Foundation of Victoria. (2001). Taking control: Effective continence management in spina bifida. Australian Family Physician, 30 (Suppl 2): 1-47. 66. Keshtgar, A.S. & Rickwood, A.M.K. (1998). Urological consequences of incomplete cord lesions in patients with myelomeningocele. British Journal of Urology, 82: 258-260. 67. Malone, P.S., Wheeler, R.A., & Williams, J.E. (1994). Continence in patients with spina bifida: Long-term results. Archives of Disease in Childhood, 70: 107-110. 68. Palmer, L.S., Richards, I, & Kaplan, W.E. (1997). Transrectal electrostimulation therapy for neuropathic bowel dysfunction in children with myelomeningocele. The Journal of Urology, 157: 1449-1452. 69. Loening-Baucke, V, Desch, L, & Wolraich, M. (1988). Biofeedback training for patients with myelomeningocele and fecal incontinence. Developmental Medicine and Child Neurology, 30: 781-790. 70. Balcom, A.H., Wiatrak, M, Biefeld, T, et al. (1997). Initial experience with home therapeutic electrical stimulation for continence in the myelomeningocele population. The Journal of Urology, 158: 1272-1276. 71. Ponticelli, A, Iacobelli, B.D., Silveri, M, et al. (1998). Colorectal dysfunction and faecal incontinence in children with spina bifida. British Journal of Urology, 81 (Suppl 3): 117-119. 72. Scholler-Gyure, M., Nesselaar, C., van Wieringen, H., et al. (1996). Treatment of defecation disorders by colonic enemas in children with spina bifida. European Journal of Pediatric Surgery, 6 (Suppl 1): 32-34. 73. Downie, J.W., Levin, R.M., Lin, A.T.L., et al. (1999). Basic neurophysiology and neuropharmacology, in Incontinence, P. Abrams, S. Khoury, and A. Wein, (Eds). Monaco: 1st International Consultation on Incontinence. p. 105-154. 74. Chen, Y., DeVivo, M. J., & Lloyd, L. K. (2001). Bladder stone incidence in persons with spinal cord injury: Determinants and trends. Urology, 58 (5): 665-670. 75. Gray, M., Rayome, R., & Anson, C. (1995). Incontinence and clean intermittent catheterization following spinal cord injury. Clinical Nursing Reseach, 4 (1): 6-18. 76. Soden, R. J., Walsh, J., Middleton, J. W., et al. (2000). Causes of death after spinal cord injury. Spinal Cord, 38 (10): 604-610. 77. Frankl, H. L., Coll, J. R., Charlifue, S. W., et al. (1998). Long-term survival in spinal cord injury: A fifty year investigation. Spinal Cord, 36 (4): 266-274. 78. Glickman, S & Kamm, M.A. (1996). Bowel dysfunction in spinal-cord-injury patients. The Lancet, 347: 1651-1653. 79. Vaidyananthan, S., Soni, B. M., Brown, E., et al. (1998). Effect of intermittent urethral catheterization and oxybutynin bladder instillation on urinary continence status and quality of life in a selected group of spinal cord injury patients with neuropathic bladder dysfunction. Spinal Cord, 36 (6): 409-414. 80. Brittain, K.R., Peet, S.M., & Castleden, C.M. (1998). Stroke and incontinence. Stroke, 29: 524-528. 81. Brocklehurst, J.C., Andrews, K, Richards, B, et al. (1985). Incidence and correlates of incontinence in stroke patients. Journal of the American Geriatrics Society, 33: 540-542. 82. Nakayama, H, Jorgensen, H.S., Pederson, P.M., et al. (1997). Prevalence and risk factors of incontinence after stroke. Stroke, 28: 58-62. 83. Ullman, T & Reding, M. (1996). Gastrointestinal dysfunction in stroke. Seminars in Neurology, 16 (3): 269-275. 84. Chiang, L., Ouslander, J., Schnelle, J., et al. (2000). Dually incontinent nursing home residents: Clinical characteristics and

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treatment differences. Journal of the American Geriatrics Society, 48 (6): 673-676. 85. Jirovec, M. M. & Templin, T. (2001). Predicting success using individualized scheduled toileting for memory-impaired elders at home. Research in Nursing and Health, 24 (1): 1-8. 86. Wiesel, P.H., Norton, C, & Brazzelli, M. (2001). Management of faecal incontinence and constipation in adults with central neurological diseases (Cochrane Review). In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software. 87. Abrams, P, Khoury, S, & Wein, A, (Eds). Incontinence. 1999, Health Publication Ltd: UK. 88. Jirovec, M. M. (1991). The impact of daily exercise on the mobility, balance, and urine control of cognitively impaired nursing home residents. International journal of Nursing Studies, 28: 145-151. 89. Flint, A.J. & Skelly, J. (1994). The management of urinary incontinence in dementia. International Journal of Geriatric Psychiatry, 9: 245-246. 90. Schnelle, J. F. (1990). Treatment of urinary incontinence in nursing home patients by prompted voiding. Journal of the American Geriatrics Society, 38: 356-360. 91. De Ridder, D., Vermeulen, C., Ketelaer, P., et al. (1999). Pelvic floor rehabilitation in multiple sclerosis. Acta Neurologica Belgica, 99 (1): 61-64. 92. Mathewson-Chapman, M. (1997). Pelvic muscle exercise/biofeedback for urinary incontinence after prostatectomy: An education program. Journal of Cancer Education, 12 (4): 218-223. 93. Klarskov, P, Heely, E, Nyholdt, I, et al. (1994). Biofeedback treatment of bladder dysfunction in multiple sclerosis. A Randomized trial. Scandinavian Journal of Urology and Nephrology, 157 (Suppl): 61-65. 94. Petajan, J.H., Gappmaier, E, White, A.T., et al. (1996). Impact of aerobic training on fitness and quality of life in multiple sclerosis. Annals of Neurology, 39: 432-441. 95. Horowitz, M, Combs, A.J., & Gerdes, D. (1997). Desmopressin for nocturnal incontinence in the spina bifida population. The Journal of Neurology, 158: 2267-2268. 96. Stohrer, M., Madersbacher, H., Richter, R., et al. (1999). Efficacy and safety of propiverine in SCI-patients suffering from detrusor hyperreflexia: A double-blind, placebo-controlled clinical trial. Spinal Cord, 37 (3): 196-200. 97. Waller, L., Jonsson, O., Norlen, L., et al. (1995). Clean intermittent catheterization in spinal cord injury patients: Long-term follow-up of a hydrphillic low-friction technique. Journal of Urology, 153 (2): 345-348. 98. Bennett, C. J., Young, M. N., Adkins, R. H., et al. (1995). Comparison of bladder management complication outcomes in female spinal cord injury patients. Journal of Urology, 153 (5): 1458-1460. 99. Ganio, E., Masin, A., Ratto, C., et al. (2001). Short-term sacral root stimulation for function anorectal and urinary disturbances: Results from 40 patients: Evaluation of a new option for anorectal function disorders. Diseases of the Colon and Rectum, 44 (9): 1261-1267. 100.Varma, J.S., Binnie, N, Smith, A.N., et al. (1986). Differential effects of sacral anterior root stimulation on anal sphincter and colorectal motility in spinally injured man. British Journal of Surgery, 73: 478-482. 101.Chartier-Castler, E. J., Ruud Bosch, J. L., Perrigot, M., et al. (2000). Long-term results of sacral nerve stimulation (S3) for the treatment of neurogenic refractory urge incontinence related to detrusor hyperreflexia. Journal of Urology, 164 (5): 1476-1480. 102.Ruud Bosch, J.L.H & Groen, J. (1996). Treatment of refractory urge incontinence with sacral spinal nerve stimulation in multiple sclerosis patients. Lancet, 348: 717-719. 103.Schurch, B, Schmid, D.M., & Stohrer, M. (2000). Treatment of neurogenic incontinence with botulinum Toxin A. The New England Journal of Medicine, 342 (9): 665. 104.Guys, J.M., Fakhro, A, Louis-Borrione, C, et al. (2001). Endoscopic treatment of urinary incontinence: Long-term evaluation of the results. The Journal of Urology, 165: 2389-2391. 105.Guys, J.M., Simeoni-Alias, J, Fakhro, A, et al. (1999). Use of polydimethylsiloxane for endoscopic treatment of neurogenic urinary incontinence in children. The Journal of Urology, 162 (2133-2135). 106.Silveri, M, Capitanucci, M.L., Mosiello, G, et al. (1998). Endoscopic treatment for urinary incontinence in children with a congenital neuropathic bladder. British Journal of Urology, 82: 694-697. 107.Austin, P.F., Westney, O.L., Leng, W.W., et al. (2001). Advantages of rectus fascial slings for urinary incontinence in children with neuropathic bladders. The Journal of Urology, 165 (6): 2369-2372. 108.Barthold, J.S., Rodriguez, E, Freedman, A.L., et al. (1999). Results of the rectus fascial sling and wrap procedures for the treatment of neurogenic sphincteric incontinence. The Journal of Urology, 161: 272-274. 109.Liard, A, Seguier-Lipszyc, E, Mathiot, A, et al. (2001). The Mitrofanoff procedure: 20 years later. The Journal of Urology, 165: 2394-2398. 110.Stein, R, Fisch, M, Ermert, A, et al. (2000). Urinary diversion and orthotopic bladder substitution in children and young adults with neurogenic bladder: A safe option for treatment? The Journal of Urology, 163: 568-573. 111.Geerdes, B.P., Heesakkers, J.P.F.A., Heineman, E, et al. (1997). Simultaneous treatment of faecal and urinary incontinence in children with spina bifida using double dynamic graciloplasty. British Journal of Surgery, 84: 1002-1003. 112.Castera, R, Podesta, M.L., Ruarte, A, et al. (2001). 10-year experience with artificial urinary sphincter in children and adolescents. The Journal of Urology, 165: 2373-2376. 113.Simeoni, J, Guys, J.M., Mollard, P, et al. (1996). Artificial urinary sphincter implantation for neurogenic bladder: A multiinstitutional study in 107 children. British Journal of Urology, 78: 287-293. 114.Beddar, S. A., Holden-Bennett, L., & McCormick, A. M. (1997). Development and evaluation of a protocol to manage fecal incontinence in the patient with cancer. Journal of Palliative Care, 13 (2): 27-38. 115.House, J. G. & Stiens, S. A. (1997). Pharmacologically initiated defecation for persons with spinal cord injury: Effectiveness of three agents. Archives of Physical and Medical Rehabilitation, 78 (10): 1062-1065. 116.Kim, J., Shim, M. C., Choi, B. Y., et al. (2001). Clinical application of continent anal plug in bedridden patients with intractable diarrhea. Diseases of the Colon and Rectum, 44 (8): 1162-1167. 117.Mortensen, N & Humphreys, M.S. (1991). The anal continence plug: A disposable device for patients with anorectal incontinence. The Lancet, 337: 295-297. 118.Chia, Y.W., Lee, T.K.Y., Kour, N.W., et al. (1996). Microchip implants on the anterior sacral roots in patients with spinal trauma: Does it improve bowel function? Diseases of the Colon and Rectum, 39: 690-694. 119.MacDonagh, R.P., Sun, W.M., Smallwood, R, et al. (1990). 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Appendix 1

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BLADDER DIARY
Patient Name : Please record the amount of fluid intake (mls) at the time you drink. Also record the time and amount of urine (mls) you pass on each visit to the toilet (use a measuring jug) and any accidental passing of urine (if accidental, just estimate the amount leaked). Day 1 __/__/__ Output (urine mls) Accidental (Y/N) TIME Input (mls) Day 2 __/__/__ Output (urine mls) Accidental (Y/N) Day 3 __/__/__ Output (urine mls) Accidental (Y/N)

Input (mls)

1:00 2:00 3:00 4:00 5:00 6:00 7:00 8:00 9:00 10:00 11:00 MD 1:00 2:00 3:00 4:00 5:00 6:00 7:00 8:00 9:00 10:00 11:00 MN Please record any other observations (eg. Pain, blood in urine etc.)
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Input (mls)

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Appendix 2

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BOWEL DIARY
Patient Name : Please record the time of your bowel motions (with a tick) and their consistency (solid/liquid). Also record next to the episode whether it was an accident (yes or no). Day 1 __/__/__ Accidental (Y/N) TIME Time of motion Consistency Time of motion Day 2 __/__/__ Accidental (Y/N) Time of motion Day 3 __/__/__ Accidental (Y/N)

Consistency

1:00 2:00 3:00 4:00 5:00 6:00 7:00 8:00 9:00 10:00 11:00 MD 1:00 2:00 3:00 4:00 5:00 6:00 7:00 8:00 9:00 10:00 11:00 MN Please record any other observations (eg. Pain, blood in urine etc.)
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Consistency

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Appendix 3

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FEMALE URINARY INCONTINENCE SCORE QUESTIONNAIRE

Stress-score Urge-score
1 1 1 1 1 1 1 1

How often do you experience urine leakage? 1: Rarely 2: Sometimes 3: Every day, many times a day 4: Constantly On what occasions have you experienced urine leakage? 1: When coughing or sneezing 2: When sitting or lying down How much urine leaked? 1: Only a few drops to a small amount 2: A considerable amount

At what intervals do you go to the toilet to pass urine every day? 1: At 3-6 h intervals 3 2: At 1-2 h intervals Do you go to the toilet to pass urine after falling asleep at night? 1: Never, or once a night 3 2: More than once a night or many times a night Do you ever experience urine leakage when sleeping at night? 1: Never 2: Often When you feel urinary urgency, can you control it? 1: Yes, I can 2: Unless I go to the toilet soon (in 10-20 min), I leak urine 3: I cannot control it, and I leak urine Do you ever leak urine on the way to the toilet? 1: Never, or rarely 2: Almost always Do you ever leak urine because you feel sudden and strong urinary urgency and cannot control it? 1: Never 2: Sometimes, or often Can you stop and start voiding in the middle of urination? 1: Yes, I can 2: No, I cannot After urinating, do you have a feeling of residual urine ( a feeling that there is urine left in the bladder)? 1: No, I do not not 2: Yes, I do Do you often feel such urinary urgency that you want to go to the toilet immediately? 1: No, never 2: Yes, I do 3: Yes, very often Have you ever experienced childbirth? 1: Yes, I have 2: No, I have not 1

1 3 2 3 3 3
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3 3 1 2

10

11

1 1

12

3 3 2 1 1

13

14

How do you feel about your urine leakage? 1: It sometimes troubles me, or it does not bother me very much 1 2: It troubles me very much How much do you weigh? 1: I weigh less than 65kg 2: I weigh 65kg or more

1 1

15

O. Ishiko et al. / International Journal of Gynecology & Obstetrics 69 (2000) 255-260

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Appendix 4

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WHAT IS THE NATIONAL PUBLIC TOILET MAP?


On 19 September 2001 the Federal Minister for Aged Care the Honourable Bronwyn Bishop MP launched the National Public Toilet Map. The National Public Toilet Map identifies the location of more than 13000 public toilet facilities in Australian towns and cities, including rural areas, and along major travel routes. Useful information is provided about each toilet, such as opening hours and access for people with a disability. Making the Map accessible to the public through the World Wide Web enables simple and easy access to public toilet information. Maps of specific locations can be downloaded and printed from the Website for later use. The development of the Map and Website was funded by the Commonwealth Government under the National Continence Management Strategy. Although the Map will be of use to all persons requiring information about public toilets, the Government recognises that incontinence can be an isolating condition which makes travel difficult. For this reason, the Map was designed specifically to assist persons experiencing incontinence with travel and daily living arrangements. NGIS (National Geographic Information Systems) undertook the development of the database and the interactive map server for the Website. The site is hosted and supported by GISCA (Centre for Social Applications of GIS).

WHY WILL THE MAP BE USEFUL?


The Public Toilet Website will be useful for a range of reasons. Members of the general public and tourists wishing to identify the nearest public toilet locations should find the Map and Website useful. People living with incontinence or their carers can plan toilet locations for short or long trips and people with disabilities can identify toilets with disability access. People who do not have access to a computer will be able to request maps from councils, and potentially other outlets such as motor vehicle associations, tourist information centres and support services.
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HOW CAN THE MAP ASSIST?


The Public Toilet Map can assist with: Finding toilets in a locality Identifying toilets with disability access Finding the opening hours of toilets Planning a trip or holiday by identifying suitable locations for a break Planning a trip around town for social or business purposes Improving the independence and quality of life for persons experiencing incontinence

See www.toiletmap.gov.au

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