Confronting the challenges of postmenopausal urogenital health

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Confronting the challenges of postmenopausal urogenital health Miranda A Farage†1, Kenneth W Miller1 & William Ledger2 The global population is aging, especially in Western industrialized nations. In the USA, 38% of adults are over the age of 45 and 13% of adults are over the age of 65 years. Moreover, postmenopausal women now comprise 60% of adults aged over 65 years of age, a proportion that will rise as the population ages. This article reviews some of the more common urogenital health issues among older women. Changes to urogenital morphology and physiology are discussed, highlighting the impact on tissue atrophy, sexuality, prevalence of certain vulvar dermatoses, susceptibility to infection and urinary continence. We review treatment approaches, challenge some of the current paradigms and discuss the need for future research.

We are in an era of global population aging. By 2030, one in every eight people worldwide will be aged over 65 years and this age group will outnumber children below the age of 5 years for the first time in history [201] . For example, 38% of the US population is over the age of 45 years, and only 24.5% is under the age of 18 years [1] . A total of 13% of Americans are over 65 years of age [1] ; moreover, because women generally live longer than men, in time a substantial proportion of older people will be women. This population will have more medical problems, straining the capacity of the medical care system. Improved care will begin with a better understanding of the changes associated with menopause. As menarche represents the beginning of womanhood, the menopause is a seminal transition for the older woman. This article reviews some of the more common urogenital health issues and challenges that lie ahead to promote the wellbeing of older women in Western industrialized countries. Postmenopausal changes to urogenital morphology and physiology are discussed, highlighting the impact on tissue atrophy, sexuality, susceptibility to urogenital infection, the prevalence of vulvar dermatoses and urinary continence. We challenge some of the current paradigms and highlight the need for future research. Neoplastic changes are beyond the scope of this article.

Feminine & Adult Care, The Procter & Gamble Company, Cincinnati, OH, USA The New York Presbyterian Hospital, Weill Medical College of Cornell University, NY, USA † Author for correspondence: Tel.: +1 513 634 5594 Fax: +1 866 622 0465 [email protected]

Menopause occurs when ovarian function ceases and ovarian estradiol production decreases to miniscule levels. Some residual peripheral estrogen is produced by adrenal androgen conversion; however, overall circulating levels decline dramatically from greater than 120 pg/ml to

approximately 18 pg/ml during the menopausal transition [2] . The classic definition of menopause is reached when a woman has not menstruated for a year, but women are often symptomatic and will consult their physician for care prior to this time. The median age of menopause in a multiethnic sample of women in the USA was 51.4 years [3] . Menstruation after the age of 60 years is rare [4] . Urethral and vulvovaginal tissues have high levels of estrogen receptors that mediate tissue structure and function [5–7] . Urinary symptoms often precede menopause and many women view increased frequency, urgency and nocturia as early signs of an age-related decline in function. These will be addressed in more detail in a later section. Along with the cessation of menstruation, vulvovaginal atrophy is a hallmark of the menopausal transition [8,9] . The vagina becomes shorter and narrower and loses its typical folds or rugae. The loss of vasculature in the lamina propria decreases blood flow and vaginal lubrication declines. The vaginal epithelium is more friable and prone to friction-induced bleeding. Loss of a glycogen-rich environment disfavors colonization by vaginal microbes that produce lactic acid [10] and reduces hydrogen ion production by vaginal epithelial cells [11,12] ; this causes the vaginal pH to rise above 4.5 and thus increases the susceptibility to vaginal infection. On the vulva, the labia majora lose fat and elasticity, the labia minora shrink and become thin, the introitus narrows, the clitoral hood may become phimotic and the exposed glans clitoris may fibrose. Cohort studies suggest that an estimated 10–50% of postmenopausal women have symptoms and signs of urogenital atrophy (Box 1) [13–15] . Some women may perceive growing urinary

10.2217/AHE.10.44 © 2010 Future Medicine Ltd

Aging Health (2010) 6(5), 611–626

ISSN 1745-509X

Postmenopausal hypoestrogenism & urogenital atrophy

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Keywords • antimuscarinic drugs • dehydroepiandrosterone • DHEA • erosive lichen planus • hormone therapy • intravaginal estrogen • lichen sclerosus • menopause • postmenopausal • testosterone • tibolone • urinary incontinence • urogenital infections • vaginal atrophy

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review – Farage, Miller & Ledger and genital discomfort to be connected to the menopausal transition [16] . Genital symptoms of atrophic changes are decreased vaginal secretions, vaginal burning or irritation, vulvar pruritus, dyspareunia and postcoital bleeding [8] . Urinary symptoms include urethral discomfort, frequency and dysuria [8] . As noted earlier, hypoestrogenism alters the ecological balance of the vaginal and urethral microbiota and therefore increases the risk of infection. Consequently, malodorous vaginal discharge, vulvovaginal inflammation or recurrent urinary tract infection (UTI) may accompany atrophic changes. Signs of vaginal atrophy are introital narrowing (which, if not discerned, may make insertion of the speculum difficult and painful); Box 1. Symptoms and signs of urogenital atrophy. Symptoms • Genital –– Vaginal dryness –– Itching, burning –– Vulvar pruritus –– Dyspareunia –– Malodorous discharge –– Leukorrhea (when desquamative inflammatory vaginitis is present) • Urinary –– Urinary frequency –– Dysuria –– Nocturia –– Urinary tract infection Signs • Genital –– Vaginal epithelium is smooth, pale and friable –– Limited vaginal secretions –– Vaginal pH >4.5 –– Sparse pubic hair –– Shrunken labia –– Inelastic labial skin –– Labial fusion –– Introital narrowing or stenosis –– Phimotic clitoral hood –– Fibrosed glans clitoris –– Genital organ prolapse –– Higher proportion of immature basal cells on Pap smear • Urethral –– Eversion of urethral mucosa –– Ecchymoses –– Peri-introital lacerations Adapted from [9].

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decreased vaginal depth; vaginal epithelial pallor and loss or rugae; and increased friability and sparse secretions [8,9] . Externally, pubic hair is sparser, and the labia are thinner with diminished turgor and elasticity [8,9] . Coitus may induce minor lacerations of the anterior and posterior fourchette. In advanced cases or when vulvar dermatoses coexist, labial adhesions may be present. In patients free of infection, a vaginal pH of greater than 5 is a sign of hypo estrogenism [10,17] . A Papanicolaou smear of the upper third of the vagina will reveal a higher proportion of parabasal cells and lower levels of superficial squamous cells [17–19] . Women differ in the degree to which such changes affect quality of life. For many women, urinary symptoms disturb sleep; stress or urge incontinence may eventually become significant enough to impair social freedom, as severe incontinence generates a profound sense of shame and loss. In the frail older woman, incontinence dermatitis may be a significant source of morbidity. Dyspareunia secondary to vaginal atrophy is often cited as a significant cause of intercourse avoidance, which can diminish sexual satisfaction and impair spousal or partner relationships; however, as will be discussed later, the significance of these physical changes may be overemphasized, as several other factors may affect sexual health and satisfaction at midlife. The degree to which a woman is troubled by vulvovaginal changes alone depends upon her individual life circumstances. For those women who are bothered by vaginal symptoms, hormone therapy (HT) is effective in relieving moderate-to-severe vaginal dryness, atrophic vaginitis and dyspareunia [20] . Vasomotor symptoms (e.g., hot flashes and night sweats) are the primary indication for systemic HT; in North America, HT is approved for treating vaginal symptoms and for preventing (but not treating) osteoporosis. Over the past years, the benefits and risks of HT have been re-evaluated in light of increased breast cancer and cardiovascular risks identified in older postmenopausal women who participated in the Women’s Health Initiative (WHI) trial [21–24] . The study has been subjected to considerable analysis and critique: its implications have been reassessed based on the characteristics of the participants (women who initiated HT approximately 10 years after menopause and who generally lacked symptoms) and by comparison to observational studies and other trials. Cardiovascular risk may not be as pertinent to younger women who start therapy early after the future science group

Confronting the challenges of postmenopausal urogenital health –

cessation of menstruation [23] ; breast cancer incidence appears to have fallen in concert with the decline in HT use in the population (although surveillance methods also changed) [25] , and the risk declined in WHI participants after treatment discontinuation [22] . The risks and benefits of HT must be evaluated in terms of each patient’s severity of symptoms, the impact on quality of life and the individual risk profile. The 2010 position statement of the North American Menopause Society (NAMS) concludes that the benefit:risk ratio is favorable for women who initiate HT close to menopause but decreases in older women and with time since menopause in previously untreated women [20] . Low-dose, intravaginal estrogen therapy (ET) is the conservative and recommended choice when HT is considered solely for the relief of symptomatic vaginal atrophy [20] . Local therapy avoids the first pass through the liver, thereby minimizing systemic side effects such as breast tenderness and uterine bleeding. Some systemic absorption occurs initially; however, an adverse impact on the endometrium or breast is very rare. The usual regimen includes daily applications for several days followed by less frequent application, depending on the patient’s symptomology. Absorption will likely lessen as the vaginal skin barrier function improves following initial treatment. If individual risk from absorption is a concern, or if potentially elevated absorption is suspected because of heightened tissue atrophy (e.g., owing to treatment with aromatase inhibitors), blood estradiol and follicle-stimulating hormone levels can be monitored prior to and a few weeks after local treatment commences; if there is no significant change in these parameters, concern regarding possible systemic effects diminishes. In North America, local ET is available as intravaginal tablets, creams or an impregnated slow-release intravaginal ring. A Cochrane review evaluated the existing clinical data on efficacy (clinical signs, patient symptoms, and objective cytological and vaginal pH measurements), safety (endometrial stimulation, breast symptoms and clinical adverse events) and patient acceptability (acceptability, adherence to treatment and study withdrawals) for treatment durations of at least 3 months [26] . All forms relieved symptoms relative to placebo, but they were not completely free of side effects. Patients preferred the intravaginal ring, which is inserted once at the beginning of the 3 month treatment period as opposed to daily or several times per week. The sustained-release vaginal estradiol ring (which future science group

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releases 5–10 µg per day) reduced vaginal pallor, dryness, friability, burning and itching, and dyspareunia, relative to placebo and was not significantly different in efficacy from the cream. The tablets (17b-estradiol, 25 µg every 3 days) were more effective for dryness, urinary frequency, burning and itching, and dyspareunia, when compared with the ring and placebo. The cream (conjugated equine estrogen, 0.625-mg/g cream or approximately 0.3 mg per dose, every evening for 2 weeks, then three-times a week for 6 months) was the only treatment associated with statistically significant adverse effects (uterine bleeding, breast pain and perineal pain), based on the results of two trials. Regardless of form, all treatment groups had a low frequency (4.5) +

Mucopurulent Variable –

Grayish green, frothy, purulent

–

Increased leukocytes; intracellular bodies (chlamydia); Gram-negative diplococci (gonorrhea)

Motile protozoans

Increased leukocytes; immature epithelial cells

Increased leukocytes and epithelial cells; high concentration of invading microbes

Amine Microscopy test

Discharge

Elevated – (>5)

Yellow or gray Normal

Greenish or yellow

Appearance pH and odor

Table 1. Characteristics of vulvovaginitis with discharge in the older female patient.

Vulvitis is not a primary feature

Vulvitis is not a primary feature; vestibular erythema may be present

Erosions (with Wickham’s striae); nonerosive white plaques on nonkeratinized tissue (inner labia minora, vestibule); vulvar skin unaffected

Glazed erythema

None

Extra-genital effects

Cervicitis

Abdominal pain may signal pelvic inflammatory disease

None Vaginal erythema; ‘strawberry cervix’

Oral papules or Friable ulcers with vaginal epithelium; Wickham’s striae erythema in fornices

Glazed erythema

Vagina or cervix

Mucocutaneous changes Vulva

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subject that may be facilitated by using patient education pamphlets in conjunction with the physical examination. Urinary tract infections

As circulating estrogen declines, cell densities of lactic-acid-producing microbes in the vagina fall and the incidence of vaginal colonization with E. coli rises [68] ; vaginal E. coli are a reservoir for urethral colonization with this pathogen, which causes UTIs. Systemic HT (combined equine estrogen with progesterone) normalizes the vaginal microbiota [69,70] , but studies of the impact of systemic therapy on the risk of UTIs are conflicting: several studies show no reduction in risk [71–73] . Local HT may be more efficacious for this indication. A Cochrane review [74] concluded that two small randomized trials support a reduced risk of recurrent UTIs with intravaginal HT [75,76] , and a meta-analysis of available studies found the strongest evidence for a benefit with this route of administration [77] . Whether the clinical efficacy of local HT translates into realworld effectiveness remains to be determined: a prospective study that followed 1017 generally healthy, postmenopausal women with and without diabetes for 2 years found neither vaginal nor oral estrogen to be protective against UTIs [78] . Clinical practice guidelines issued by the Society of Obstetricians and Gynecologists of Canada recommend that intravaginal ET be offered to menopausal women with recurrent UTIs who have no contraindications [79,80] . However, no HT product has regulatory approval for a urinary health indication. Desquamative inflammatory vaginitis

Perimenopausal women aged over 40 years are more likely to suffer from a bothersome and persistent inflammatory vaginal infection known as desquamative inflammatory vaginitis [81] . These patients experience discharge, soreness and painful intercourse. The condition produces a copious, purulent discharge and the vulva and vaginal vault exhibit a glazed erythema owing to epithelial sloughing (Table 2) . Vaginal pH is greater than 4.5 and the whiff test is negative (no fishy odor when a drop of vaginal secretion is added to 10% aqueous potassium hydroxide). Microscopy reveals a marked outpouring of inflammatory white cells (a hallmark sign) with a paucity of lactobacilli, large numbers of other bacterial forms and many immature, squamous vaginal epithelial cells. Typical treatment is a 2-week course of future science group

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clindamycin. Some clinicians prescribe treatment with both the topical antibiotic as well as a steroid cream. The differential diagnosis includes erosive lichen planus (discussed later), STIs and mucous membrane pemphigoid, a very rare, autoimmune disease (for a comprehensive review of conditions that produce vulvovaginal symptoms, see [40]). Vulvar dermatoses

Erosive lichen planus is a rare chronic disorder that affects the mucosa of the vagina and vulvar vestibule, but not vulvar skin. Peak incidence is between the ages of 30 and 70 years [82] . Signs and symptoms mimic those of desquamative inflammatory vaginitis. Patients present with intense vulvar itch and pain, dyspareunia, postcoital bleeding and discharge. The discharge results from erosive shedding and the vaginal epithelium may bleed upon speculum insertion. Distinguishing features (Table 1) include the presence of white, lacy plaques on the vulvar vestibule and inner aspects of the labia minora and the possible presence of white plaques on the buccal mucosa, gingiva, palate or tongue, a common extragenital manifestation. Erosive lichen planus may be recalcitrant to standard anti-inflammatory therapy: options to manage the disease are potent topical steroids (e.g., clobetasol propionate) or topical macrolides (tacrolimus). Oral corticosteroids (e.g., prednisone) are a second-line treatment if topical medication fails. A more common disease, lichen sclerosus, affects both the mucosa and the skin of the anogenital region (Table 2) . Incidence peaks bimodally in adolescents and peri- or post-menopausal women. Patients present with intense vulvar itch, soreness, pain and dyspareunia, but rarely discharge. White polygonal plaques with a wrinkled appearance emerge bilaterally on the vulva and perineum. The introitus, vestibule, labia and perineum can also be affected. A classic presentation of advanced disease is the ‘keyhole’ or ‘figure-eight’ configuration of sclerotic tissue surrounding the introitus and anus. Potent topical corticosteroids or macrolides are options for managing symptoms and disease progression. Urinary incontinence

Urinary incontinence is a large, under-reported and growing medical condition. Incidence begins to rise prior to menopause. Reported prevalence rates vary widely depending on the type (stress, urge or mixed) and demographic variables such as age, race, parity and Aging Health (2010) 6(5)

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Vagina, cervix and urethra are also affected

Extragenital flu-like symptoms in primary outbreak; oral mucosa may have eruptions

Not typical, but can appear at sites of friction or trauma (Koebner phenomenon; e.g., inner thigh, neck, wrists and submammary areas)

Vesicles that rupture to form ulcers; ulcers crust over and heal without scars

Data taken from [41].

Herpes vulvovaginitis

All ages and races affected: bimodal peak incidence in white prepubertal girls and peri- or postmenopausal women

Genetic predisposition; postulated hormonal link

New or multiple sexual partners; Genito–oral, genital–genital contact

Mild to intense

May be Burning, present soreness; dysuria; dyspareunia

Burning; soreness; dyspareunia

Vulva Pain Itch Lichen sclerosus

Sexually active women

Vagina or cervix

Bilateral, wrinkled, white, polygonal papules Not affected and plaques; sclerosis of introitus and perianal area in ‘keyhole’ or ‘figure-of-eight’ configuration; loss of vulvar architecture in advanced disease

Extragenital lesions Mucocutaneous changes Symptoms Risk factors Patient characteristics

Table 2. Characteristics of lichen sclerosus and herpes vulvovaginitis. 618

BMI, among others [83] . Prevalence ranges from 10 to almost 40% among subgroups of community-dwelling individuals [84,85] and 43 to 77% among nursing home residents [86] . Women can experience stress incontinence, urge incontinence or a combination of the two. Stress and urge incontinence have different symptoms, risk factors and underlying patho logy (Table 3) . With stress incontinence, uncontrolled urine loss occurs when sudden force is applied to the abdomen (e.g., a cough, sneeze or during intercourse). Athletic women may experience symptoms when engaged in sports. Stress symptoms are caused by a weakened sphincter at the junction of the bladder and urethra and typically first develop in younger women aged 30–50 years; incidence peaks between the ages of 45 and 49 years [85] . Both childbirth and obesity are risk factors: notably, obese women (BMI ≥30) have twice the risk independent of age and parity. A recent review of the epidemiological data on obesity and incontinence concluded that each five-unit increase in BMI is associated with 20–70% increase in urinary incontinence risk [87] . Urogenital prolapse sometimes coexists with stress incontinence. Prolapse is the downward descent of the internal urogenital organs toward the vagina owing to weakened support; in severe cases, the organs may physically protrude from the vagina. Risk factors are the relaxation of the musculature of the vaginal vault and weakening of the pelvic muscles caused by childbirth. The condition may manifest as or exacerbate stress incontinence; however, severe prolapse can inhibit urination until the organs are physically manipulated to relieve the obstruction. In its early stages, stress incontinence is episodic and involves small volumes of urine. Mild stress incontinence is manageable with strengthening pelvic muscle training (Kegel exercises), limiting fluid intake, more frequent voiding and feminine pads. The pelvic floor muscle exercises reduce stress incontinence episodes to a greater degree in younger than older women [88] , although both groups benefit. Weight loss may alleviate symptoms in women who are overweight. A 6-month weight loss program in 338 overweight and obese women (mean age 53 ± 11 years) that included diet, exercise and behavior modification reduced the frequency of self-reported stress (yet not urge) incontinence episodes [89] . Bariatric surgery patients also experienced a reduction in incontinence episodes [90,91] . Weight loss is a first-line intervention in overweight or obese women with stress urinary incontinence [92] .

Menstruation, stress, trauma and intercourse may trigger outbreaks

Affects both keratinized and nonkeratinized vulvar epithelia; remits and relapses; statistically associated with vulvar carcinoma

Other characteristics

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Devices for stress incontinence include pessaries and urethral orifice plugs. Some pessaries are designed to relieve prolapse; those designed to support the urethrovesical junction relieve stress incontinence symptoms. However, it can be difficult to convince North American women to try them. Discharge and odor may become a problem if they are left in place too long, and irritation of the atrophied vagina may be an issue in postmenopausal women. Consequently, a pessary may be reserved for times when the woman is most active. Many patients are reluctant to accept intraurethral devices that act as plugs. Duloxetine, a serotonin and nora drenaline reuptake inhibitor prescribed in the USA for mood disorders, reduces the frequency of stress incontinence in randomized controlled trials [93] . It has regulatory approval for this indication in Europe but not in the USA. For severe cases of stress incontinence, surgery is the least conservative but possibly most effective option. The traditional Burch colposuspension developed in 1961 has a success rate of 82% at 5 years and 69% at 10 years [94,95] . The current trend is to use minimally invasive procedures. The retropubic, midurethral

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synthetic slings (tension free vaginal tape) based on monofilament polypropylene mesh are thought to reduce the risk of vaginal erosions that has been observed with other materials. The newer, transobturator approach avoids anchoring the sling in the retropubic space and is thought to minimize the risk of complications [96] . Surgery has its drawbacks: although a majority of women report satisfaction, its success is not easily predicted. In some instances, surgery triggers de novo urge symptoms, voiding dysfunction and the increased risk of UTI. The impact on sexual function is variable [97] . Long-term data are not yet available on the most recent procedures, and a paucity of data exists on the effectiveness of surgery in the older postmenopausal patient. Urge incontinence is characterized by a strong urge to urinate and the inability to voluntarily control urine loss. An abnormality in the sensory reflex mechanism causes heightened contractions (spasms) in the bladder wall, exerting pressure on the bladder neck and creating a feeling of urgency at lower urine volumes than is typical. The patient may be unable to voluntarily contract the external sphincter enough to

Table 3. Major types of urinary incontinence in adult women†. Characteristic

Stress

Urge

Patient population

Women aged 30–50 years, especially those who have given birth

Older, usually postmenopausal women (aged >50 years)

Symptoms

Uncontrolled urine loss when sudden pressure is applied to the bladder (e.g., sneezing, coughing, lifting heavy objects, intercourse)

Increased frequency and urgency that cannot be suppressed with uncontrolled urine loss

Causes

Weakness of the sphincter muscle Overactive bladder muscle (i.e., stronger, at the junction of the bladder neck more frequent bladder contractions at lower urine volumes); weakened outlet and the urethra

Risk factors

Childbirth; obesity; genital prolapse; Caucasian race

Childbirth may contribute to the problem in younger women by weakening the outlet; the risk after age 50–60 years is independent of childbearing history and probably reflects age-related changes

Mechanism

Possible nerve damage, sphincter muscle damage, or damage to the connective tissue supporting the bladder neck

Childbirth may weaken the outlet, making the impact of bladder contractions more apparent; age-related changes include impaired nerve–brain reflexes regulating bladder wall contractions; shortening and thinning of the urethra after menopause; slower and less efficient voiding (retention)

Most common efficacious treatment

Pelvic floor muscle training (Kegel exercises); weight loss in overweight or obese patients; surgery

Pharmacology: drugs for overactive bladder

Mixed stress–urge occurs in about a third of cases.

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review – Farage, Miller & Ledger prevent urine release. Childbirth may contribute to sphincter weakness, so that the impact of bladder contractions is more apparent. Urge incontinence can be more distressing as it is unpredictable and sometimes involves larger urine loss. Fortunately, several efficacious antimuscarinic drugs (e.g., Oxybutynin and Tolterodine) are available. These block cholinergic muscarinic receptors associated with uncontrolled bladder contractions. Side effects of this class of drugs are dry mouth and constipation. Anticholinergic drugs are contraindicated in patients with documented untreated narrow-angle glaucoma. Behavioral modifications for urge incon tinence include moderating f luid intake (although low intakes may increase bladder contractions at lower urine volumes); bladder retraining through scheduled voids and conscious urge suppression; limiting intake of caffeine, alcohol and diuretics; and adding fiber or probiotics to the patient’s dietary intake to avoid constipation. Kegel exercises may alleviate the contribution of a weakened sphincter; however, they will not affect bladder contractions. Sacral nerve stimulation through surgical implants and intravesical botulinum toxin injections are being investigated for the most refractory cases [98] . Hormone therapy does not alleviate urinary incontinence. The WHI trial found that women receiving oral estrogen or estrogen with progesterone developed incontinence at higher rates than women receiving placebo; incontinence in the treatment groups also worsened compared with the placebo group [99] . Similarly, in a study on postmenopausal women who had undergone hysterectomy, those taking oral estrogen developed incontinence at a higher rate than those on Raloxifene® or placebo [100] . Based on a comprehensive review of the currently available data, HT is not indicated for incontinence treatment [101] . Incontinence management in the nursing home setting requires special consideration, as the patient may have comorbidities that may contribute to their condition. These comorbidities have been summarized in the mnemonic: delirium, infection, atrophic vaginitis, pharmaceuticals, psychological factors, excess urine output, restricted mobility and stool (DIAPPERS) impaction [102] . These comorbidities must first be addressed. In nursing homes, behavioral interventions such as prompted voiding and timed voiding are used to a limited degree, and antimuscarinics are only an adjunct treatment. Incontinence products and catheterization aim 620


to achieve urine containment. Prompted voiding involves caregivers checking and querying patients, giving toileting prompts and reinforcing initiative on the part of the patient. Timed voiding is bringing the patient to the toilet at fixed intervals regardless of whether the patient requests it or has voided during the previous interval. In randomized trials, prompted voiding over the course of 3 months was associated with small improvements in daytime incontinence in nursing homes where the population had substantial cognitive and mobility limitations [103] . In a review of treatment trials [104] , no clear evidence was found for a benefit of prompted voiding with strength and endurance exercise versus prompted voiding alone. Nursing home trials with antimuscarinic agents are mixed [104] , despite evidence for improvements in urinary symptoms relative to placebo in older community-dwelling individuals [93,105] . Consistent with the implications of the WHI trial, adding oral estrogen and progesterone provided no benefit to nursing home patients with urinary incontinence relative to prompted voiding alone [72] . The key barriers to helping women with urinary incontinence are awareness, education and cost. Many women view their experience as an inevitable consequence of aging [106] , something to be endured. The self-treatment option for the community-dwelling older woman is feminine protection; a woman will search for other options only when the use of a pad becomes burdensome or inadequate, when symptoms interfere significantly with her quality of life or when she fears her symptoms indicate more serious problems, such as cancer. When a woman does raise the issue, she may be reluctant to reveal her most embarrassing symptoms, such as urine loss during intercourse or loss of voluntary control. Urinary incontinence causes shame, lack of confidence and increased social isolation. In North America, menstruation, prostate problems and erectile dysfunction are ‘out of the closet’: female urinary incontinence, however, is one of the last taboos. In Europe, the subject is first broached during postpartum care, and awareness is greater. No concerted education or public awareness effort exists in North America to help a woman recognize that she should seek medical help for her symptoms and that options exist to manage the condition. Consequently, it is up to the clinician to broach the subject sensitively as part of the medical history: simple algorithms (such as the Three Incontinence Questions questionnaire [107]) can future science group


be offered to assist the patient in defining the nature and cause of her symptoms (stress, urge or mixed incontinence). The economic burden of urinary incon tinence is substantial and growing: an estimated $16 billion annually is spent in the USA on urinary incontinence management [108] ; in nursing homes, an hour per day is spent on dealing with incontinence at a total cost per incontinent patient of approximately $10,000 per year [109] . Despite clinical evidence for a benefit from behavioral interventions in nursing homes, these interventions are costly and labor intensive and implementation is limited. Staff attitudes, training and compliance are also barriers to implementation. Conclusion

We need to view menopause and the conditions that accompany it as a life transition rather than as a series of distinct medical conditions. Vasomotor symptoms and the cessation of menstruation are visible signals of what was once termed ‘the change of life’, yet women’s urinary problems, vaginal discomfort and sexual health remain covert subjects when compared with the cultural emphasis on prostate disease and virility in men. Clinicians can help their patients by exploring these concerns holistically in conjunction with the medical history and physical examination. Several validated tools are available to broach these subjects when taking the medical history; for example, the menopause-specific quality of life questionnaire examines vasomotor symptoms, sleep disorders, urinary incontinence, mood and sexual function [42] . The patient should be asked if she has any urinary problems that she finds troublesome or that interfere with sleep, daytime or sexual activity. A simple algorithm, such as the Three Incontinence Questions questionnaire [107] , is a simple way to discern the nature of the symptoms, helps the patient understand the different diagnoses and discusses possible interventions. If the patient has signs and symptoms of vaginal atrophy, she can be asked whether these are bothersome, and whether they interfere in any way with sexual activity. If she experiences pain, the characteristics of the pain in terms of onset, intensity, duration and localization may offer clues regarding the possible causes, including vulvodynia unrelated to hypoestrogenism. If atrophic vaginitis is a contributing factor to discomfort, this can lead to a discussion regarding conservative nonhormonal lubricants as well as the range of hormonal therapies that are now future science group

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available to the patient, along with their benefits and risks in light of other symptoms the patient may be experiencing and their particular medical history. If the patient is sexually active, she could be asked if her male partner is being treated for erectile dysfunction and whether they were both counseled when treatment was prescribed. A reminder is warranted that STIs continue to be a risk with new sexual partners and that condoms offer some protection. A simple pamphlet could be offered to explain the rising incidence of STIs in elders and what symptoms she should discuss with her doctor. Despite the advances that have been made in the treatment of postmenopausal gynecological problems, areas of uncertainty remain: • How does the benefit:risk ratio of HT change with long-term use? Vasomotor symptoms often recur and the risk of bone loss rises when HT is discontinued; however, the effect of prolonged use on cardiovascular disease and breast cancer risks is still being defined. Moreover, evidence is growing that each type of estrogen, progestogen, route of administration and timing of initiation may have a distinct benefit:risk profile. • Have we found the optimum dose, frequency and duration of local ET to maximize benefits for vaginal atrophy while minimizing risks and side effects from systemic absorption? • How effective are local ET regimens for reducing the risk of UTI in older patients? • Is there a defined range of circulating testosterone that supports cardiovascular health and also provides sexual health benefits to the older women? • What are the optimum dose levels, treatment durations and long-term effects of intravaginally administered DHEA? • To what extent does vulvodynia contribute to dyspareunia in postmenopausal women? • How can we increase public awareness of the rising incidence of STIs in older adults? • How do we increase public awareness of urinary incontinence as a treatable medical condition? • What are the long-term cure rates and side effects of the newer synthetic slings and minimally invasive surgical procedures for stress incontinence? • Would a combination of measures (e.g., behavioral interventions and high-performing absorptive products) provide incontinence relief in nursing home patients at an affordable cost? Aging Health (2010) 6(5)

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review – Farage, Miller & Ledger These are some of the areas that will continue to be explored in order to adequately care for and treat the growing number of older women in Western developed countries with post-menopausal urogenital health problems.

Future perspective

Two major changes in the care of postmenopausal women are anticipated in the next decade. New pharmacological products will be introduced to increase skin, bone, CNS and cardiovascular health

Executive summary Postmenopausal hypoestrogenism & urogenital atrophy • Along with the cessation of menstruation, vulvovaginal atrophy secondary to hypoestrogenism is a hallmark of the menopausal transition. • An estimated 10–50% of postmenopausal women may have symptoms and signs of urogenital atrophy. • Genital symptoms are decreased vaginal secretions, vaginal burning or irritation, vulvar pruritus, dyspareunia and postcoital bleeding. • Urinary symptoms include urethral discomfort, frequency and dysuria. • Low-dose, intravaginal estrogen therapy (ET) is an option to relieve vaginal atrophy symptoms. • Intravaginal administration of the sex steroid precursor, dehydroepiandrosterone, is under investigation as an alternative treatment for vaginal atrophy that avoids systemic effects of sex-steroid supplementation. Sexual health • Women in the peri- and post-menopausal years may experience a declining libido, discomfort during intercourse and diminished sexual satisfaction. • Women are unlikely to broach the subject with a healthcare provider. The clinician may need to sensitively initiate a conversation about sexual health. • Psychosocial stressors, prescription medications and atrophic vaginitis contribute to diminished sexual health. Provoked vestibulodynia (vulvar vestibulitis syndrome) may be underestimated as a cause of dyspareunia in older women. • Testosterone increases libido and sexual satisfaction in women who have undergone surgically induced and natural menopause. However, it does not have regulatory approval for this use in North America. • Effects of testosterone on breast and cardiovascular health are under investigation. • Intravaginal dehydroepiandrosterone demonstrates some promise in treating vaginal atrophy symptoms that affect sexual health. Urogenital infections • Newly acquired, sexually transmitted infections, including HIV and AIDS, are on the rise among older adults. Older women must be reminded that condoms reduce the risk of acquiring sexually transmitted infection. • Local ET may reduce risk of urinary tract infections in older women by normalizing vaginal pH and microbiota, but the research shows conflicting results. • The Society of Obstetricians and Gynecologists of Canada has concluded that intravaginal ET may be offered to menopausal women with recurrent urinary tract infections who have no contraindications. • Desquamative inflammatory vaginitis is a persistent inflammatory vaginal infection with increased incidence in older women. Erosive lichen planus is a rare vulvar dermatosis with similar clinical signs and symptoms. Vulvar dermatoses • Lichen sclerosus affects vulvar and perineal skin as well as the vulvovaginal mucosa. It is characterized by white, wrinkled polygonal plaques that may become sclerotic. A classic presentation of advanced disease is the ‘keyhole’ or ‘figure-eight’ configuration of sclerotic skin around the introitus and anus. Potent topical corticosteroids are used to slow disease progression. Urinary incontinence • Urinary incontinence is prevalent in community-dwelling women aged over 30 years and in older, nursing home residents. • Public education is needed to help women recognize that urinary incontinence is treatable. • Stress and urge incontinence have different symptoms, risk factors and pathology. • Childbirth and obesity are risk factors for stress incontinence. Mild stress incontinence is managed with pelvic muscle exercises, limiting intake of fluids and use of feminine pads. Pessaries are an option for women willing to try them. Surgery is the least conservative option, reserved for severe cases. • Weight loss is a first-line treatment to alleviate symptoms in overweight and obese women. • Urge incontinence is managed by moderating fluid intake, bladder retraining through schedule voiding, limiting caffeine and alcohol intake, and with the use of antimuscarinic drugs. • Hormone therapy does not alleviate urinary incontinence and may worsen it. • Incontinence management is in the institutional setting is focused on urine containment. Costly and labor intensive interventions, such as prompted voiding, are limited.

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with few concerns about breast and uterine neoplasia. Specific genetic testing will become clinically available to identify individuals at risk with some standards of care and also to identify those who will need individualized care to prevent or treat medical problems. Acknowledgements The authors acknowledge D Hutchins of Hutchins & Associates, LLC (Cincinnati, OH, USA) for the literature search and technical writing assistance.

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Simple questionnaire to help distinguish between stress and urge incontinence symptoms.

