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Definition, classification and triage of female UI
Francesco Cappellano, MD, FEBU Head of Urology and Neurourology Clinic Pelvic Care Centre Harley Street Hospital – Abu Dhabi ( UAE)
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Definition Urinary incontinence is defined by the International Continence Society as “ the involuntary loss of urine that represents a hygienic or social problem to the individual “ It can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder.
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Background Urinary incontinence should not be thought of as a disease, because no specific etiology exists… most individual cases are likely multifactorial in nature. It is an underdiagnosed and underreported problem that increases with age (affecting 50-84% of the elderly in long-term care facilities ) and at any age is more than twice as common in females than in males.
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Types of urinary incontinence
Four types of urinary incontinence are defined in the Clinical Practice Guideline Functional incontinence is the inability to hold urine due to reasons other than neuro-urologic and lower urinary tract dysfunction: Enuresis - Involuntary loss of urine Nocturnal enuresis - Loss of urine occurring during sleep Continuous urinary incontinence - Continuous leakage
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Historical context Urinary incontinence in women is not a recent medical and social phenomenon They are more willing to talk openly about this disorder as urinary incontinence is a treatable condition With ageing incontinence becomes a more frequent concern
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Facts An estimated 50-70% of women with urinary incontinence fail to seek medical evaluation and treatment because of social stigma Only 5% of individuals who are incontinent and 2% of nursing home residents who are incontinent receive appropriate medical evaluation and treatment Patients who are incontinent often cope with this condition for 6-9 years before seeking medical therapy
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Facts In a 1997 survey of primary care physicians, about 40% reported that they sometimes, rarely, or never ask patients about incontinence. McFall, J Family Med, 1997 More than 40% of internists and family practitioners routinely recommended absorbent pads to their patients as a solution to incontinence disorders A 2009 survey of women in a managed care population found that the prevalence of undiagnosed urinary incontinence was 53% in the preceding year (Wallner, Am J Med) 2009
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Facts Some individuals pay out of pocket for adult incontinence undergarments, absorbable pads, skin care products, deodorants, and increased laundry expenses. The psychosocial costs and morbidities are even more difficult to quantify. Embarrassment and depression are common Several questionnaires are available for urge incontinence, stress incontinence, and quality of life.
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Questionnaires Urinary Distress Inventory (UDI)–6,
Incontinence Quality of Life (IQoL) Questionnaire, Incontinence Impact Questionnaire (IIQ)–7, UDI Overactive Bladder Symptom and Health-Related Questionnaire (OAB-Q), King’s Health Questionnaire (KHQ)
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Physiology of micturition
As the bladder fills, sympathetic tone contributes to closure of the bladder neck and relaxation of the dome of the bladder and inhibits parasympathetic tone The cerebral cortex exerts a predominantly inhibitory influence, whereas the brainstem facilitates urination by coordinating urethral sphincter relaxation and detrusor muscle contraction
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Physiology of micturition
When urination occurs, sympathetic and somatic tones in the bladder and periurethral muscles diminish, resulting in decreased urethral resistance. Cholinergic parasympathetic tone increases, resulting in bladder contraction Normal bladder capacity is mL, and the first urge to void generally occurs between bladder volumes of 150 and 300 mL.
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Stress incontinence During episodes of stress incontinence, an increase in intra-abdominal pressure raises pressure within the bladder to the point where it exceeds the urethra’s resistance to urinary flow The major cause of stress incontinence is urethral hypermobility due to impaired support from pelvic floor. A less common cause is an intrinsic sphincter deficiency, usually secondary to pelvic surgeries
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Urethral hypermobility
Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. When this occurs, the proximal urethra and the bladder neck descend to rotate away and out of the pelvis at times of increased intra-abdominal pressure Because the bladder neck and proximal urethra move out of the pelvis, more pressure is transmitted to the bladder
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In women without urethral hypermobility, the urethra is stabilized during stress by three interrelated mechanisms. One mechanism is reflex, or voluntary, closure of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra, bladder neck and the perineal body, which may serve as a urethral backstop.
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The second mechanism involves intact connective tissue support to the bladder neck and urethra.
The pubocervicovesical or connective tissue, the arcus tendineus fascia pelvis, and the perineal membrane. The pubourethral ligaments also suspend the middle portion of the urethra to the back of the pubic bone
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The third mechanism involves 2 bundles of striated muscle,
the urethro-vaginal sphincter and the compressor urethrae, found at the distal aspect of the striated urethral sphincter. These muscles may aid in compressing the urethra shut during stress maneuvers and lie along the lateral and ventral aspects
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Childbirth and incontinence
Damage to the nerves, muscle, and connective tissue of the pelvic floor Injury during childbirth probably is the most important mechanism. Aging, hypoestrogenism, chronic connective tissue strain due to primary loss of muscular support, activities or medical conditions resulting in long-term repetitive increases in intra-abdominal pressure, and other factors can contribute
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During childbirth, 3 types of lesions can occur:
levator ani muscle tears, connective tissue breaks pudendal/pelvic nerve denervation. Any of these injuries can occur in isolation but 2 or more in combination are more likely to occur. The long-term result may be the loss of active and passive urethral support and loss of intrinsic urethral tone Impairment of urethral closure mechanisms during times of increased intra-abdominal pressure
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The hammock theory The mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey The urethra lies on a supportive layer This layer gains structural stability through its lateral attachment to the arcus tendineus fascia pelvis and levator ani muscle. Pressure from above compresses the urethra against this hammock-like supportive layer, compressing its lumen closed
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An alternative theory stems from ultrasound visualization of the bladder neck and proximal urethra during stress maneuvers. 93% of patients with stress incontinence displayed funneling of the proximal urethra with straining, and half of those individuals also showed funneling at rest Dietz 1998 During stress maneuvers, the urethra did not rotate and descend as a single unit
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Intrinsic sphincter deficiency
Urethral sphincter is unable to coapt and generate enough resting urethral closing pressure Devascularization and/or denervation of the bladder neck and proximal urethra. After pelvic surgery because of nearby nerve damage or excessive scarring of the urethra and surrounding tissues. Additional causes include pelvic radiation or neurologic injury, including myelomeningocele.
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Estrogens Female urethral function is influenced by estrogen.
The lack of estrogen at menopause leads to atrophy and replacement of submucosa by fibrous tissue. When estrogen is administered the mucosa regains its turgor, with simultaneous up-regulation of alpha-receptors and angiogenesis of vascular plexus
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Occult stress incontinence
Stress incontinence on prolapse reduction is a term used to describe stress incontinence observed only after reduction of pelvic prolapse Kinking of the urethra caused by the prolapse itself provides for at least part of the continence mechanism. These patients may have a history of stress incontinence that improved and finally resolved as their prolapse worsened.
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The diagnosis can be made by stress testing with the prolapse reduced or by pessary placement and pad testing. No particular method of prolapse reduction has been proved superior. In a study of continent women with severe pelvic organ prolapse, reduction of the prolapse with a pessary revealed occult incontinence in 58% of cases. Chaichin, 2000
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Urge incontinence Urge incontinence is involuntary urine loss associated with a feeling of urgency. The corresponding urodynamic term is detrusor overactivity, involuntary detrusor contractions during filling cystometry Wein,2006 Urge incontinence may be a result of detrusor myopathy, neuropathy, or a combination of both.
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The term overactive bladder describes a syndrome of urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection or other obvious pathology. Is a disorder of unclear etiology and incompletely understood pathophysiology Some researchers believe that detrusor overactivity represents the premature initiation of a normal micturition reflex
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A relative cholinergic denervation may explain some of these findings.
Cases of “de novo” detrusor overactivity, which follow hysterectomy or other pelvic surgery. The mechanism of denervation in idiopathic detrusor overactivity is less certain. Subtle obstruction and the effects of aging on smooth muscle and the autonomic nervous system are 2 possible contributors.
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In bladder muscle specimens from patients with detrusor overactivity there is local loss of inhibitory neurologic activity. VIP, a smooth muscle relaxant, is decreased markedly in the bladders of patients with detrusor overactivity. In addition, deficiency in smooth muscle–relaxing prostaglandins is evident
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Mixed incontinence
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Reflex incontinence Is due to neurologic impairment of the central nervous system. Common neurologic disorders associated with reflex incontinence include stroke, Parkinson disease, and brain tumors. Reflex incontinence also occurs in patients with spinal cord injuries and multiple sclerosis. When patients with suprapontine or suprasacral spinal cord lesions present with symptoms of urge incontinence, this is known as detrusor hyperreflexia.
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Overflow incontinence
The major contributing factor to overflow incontinence is incomplete bladder emptying secondary to impaired detrusor contractility or bladder outlet obstruction Impaired detrusor contractility is typically neurogenic in nature; causes include diabetes mellitus, lumbosacral nerve disease from tumors, meningomyelocele, MS, prolapsed intravertebral disks, and high spinal cord injuries In most cases, both sensory and motor neuropathies are present
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The maximal storage capacity of the bladder is reached, oftentimes without the individual realizing that this has occurred. Incontinence occurs off the top of a chronically over-filled bladder In women, urethral obstruction after anti-incontinence surgery such as a sling or bladder neck suspension can result in iatrogenically induced overflow incontinence.
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Functional incontinence
Patients with normal voiding systems but who have difficulty reaching the toilet because of physical or psychological impediments or concomitant conditions DIAPPERS D - Delirium I - Infection, urinary A - Atrophic urethritis or vaginitis P - Pharmacologic agents P - Psychiatric illness E - Endocrine disorders R - Reduced mobility or dexterity S - Stool impaction
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Continuous incontinence
Constant or near constant leakage with no symptoms other than wetness. Significant breech in the storage capabilities of the bladder or urethra. Urogenital fistulas are a classic example. Scarring and fibrosis from previous surgery, partial urethral resection for vulvar cancer, pelvic irradiation may not only cause urogenital fistula but also bladder noncompliance that results in continuous incontinence
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