Keywords

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

1 Introduction

Menopause occurs when ovarian function ceases and estradiol production decreases to miniscule levels. Although peripheral androgen conversion by the adrenals continues to produce a low level of estrogen after menopause, overall circulating levels decline dramatically from greater than 120 pg/mL to about 18 pg/mL [1]. The perimenopausal transition begins sometime after the age of 45 and lasts about 4 years. A constellation of symptoms emerges as follicular function declines. The most notable is menstrual cycle irregularity, reflecting an increase in the number anovulatory cycles and cycles with a prolonged follicular phase. Other symptoms can include cramps, bloating or breast tenderness, vasomotor symptoms (“hot flashes”), migraine headaches, and vaginal dryness. Menopause has transpired when a woman has not menstruated for a year [2]. Median age of menopause in a multiethnic sample of American women was 51.4 years [3].

Vulvovaginal and urethral epithelia have high levels of estrogen receptors that mediate hormonal action on the tissue. Consequently, the dramatic drop in circulating estrogen that accompanies menopause profoundly affects urogenital tissue structure and function. This chapter discusses postmenopausal vulvovaginal changes, with an emphasis on alterations in vulvar skin physiology, tissue atrophy, urinary changes, and susceptibility to infection. Vulvar dermatoses that are more common in older women are also discussed.

2 Vulvar Skin Physiology

Skin hydration, coefficient of friction, and permeability of vulvar skin differ from that of exposed skin (reviewed in [4, 5]). Although menopause affects these parameters on exposed skin, age-related effects on vulvar skin appear negligible (Table 27.1). In brief, keratinized skin of the labia majora is more hydrated than forearm skin as measured by trans-epidermal water loss [6], and its coefficient of friction is higher [7]. Following menopause, small differences in these parameters have been measured on exposed skin, but changes in the water barrier function and friction coefficient of vulvar skin are insignificant [7].

Table 27.1 Comparative skin physiology and menopausal status
Full size table

Skin penetration of hydrocortisone and testosterone also has been compared on the forearm and on the vulva. (For perspective, penetration of testosterone but not hydrocortisone is mediated by androgen receptors.) In young women, vulvar skin is more permeable to hydrocortisone than forearm skin; however, following menopause, skin penetration of this steroid drops on the forearm but not on the vulva. By contrast, comparable testosterone penetration rates were measured at both sites in younger women, and menopause had no impact on testosterone penetration at either site [8].

Studies with the model irritant, sodium lauryl sulfate, revealed differences in susceptibility to skin irritation between exposed skin and vulvar skin. Forearm skin was far more susceptible to the model irritant, aqueous sodium lauryl sulfate (1 % w/v): this agent caused intense erythema on the forearms of premenopausal women but no visually discernible response on the vulva in either pre- or postmenopausal women [10].

3 Vulvovaginal Atrophy

Vulvovaginal atrophy often develops as hormonal stimulation declines through the menopausal transition (reviewed in [11, 12]). Reportedly, 10–50 % of postmenopausal women exhibit clinical signs and symptoms (Table 27.2) [14–16]. Pubic hair becomes sparse, the labia majora lose subcutaneous fat, and the labia minora and vestibule atrophy [17, 18]. In addition, the introitus narrows, the clitoral hood may become phimotic, and the exposed glans clitoris may fibrose. At the cytological level, estrogen-induced parakeratosis of vulvar stratum corneum, which is highest in the third decade of life, is rarely observed by the eighth decade [19].

Table 27.2 Signs and symptoms of urogenital atrophy
Full size table

Vaginal changes also ensue. The vaginal vault becomes shorter and narrower, losing its typical folds (rugae). Blood flow decreases and vaginal lubrication declines. As the epithelium thins, it becomes susceptible to friction-induced bleeding. Moreover, the loss of a glycogen-rich environment both disfavors colonization by lactic acid-producing microbes [20] and reduces hydrogen ion production by vaginal epithelial cells [21, 22]. Consequently, vaginal pH rises above 4.5, which heightens susceptibility to vaginal infection. A Papanicolaou smear of the upper third of the vagina reveals a higher proportion of parabasal cells and lower levels of superficial squamous cells [23–25].

Genital symptoms include decreased vaginal secretions, vaginal irritation, vulvar pruritus, dyspareunia, and postcoital bleeding [12]. Urinary symptoms include urethral discomfort, increased frequency, and dysuria [12]. If the vulvovaginal microbiota becomes disturbed, malodorous vaginal discharge, vulvovaginal inflammation, or recurrent urinary tract infection may accompany atrophic changes. In the patient free of infection, a vaginal pH of greater than 5 is a sign of hypoestrogenism [20, 23].

Only about 25 % of women who experience symptoms mention them to their health-care provider, as many consider their discomfort to be an inevitable consequence of aging. However, urinary pain, vulvovaginal irritation, or dyspareunia secondary to vaginal atrophy may prompt a woman to seek treatment. Low-dose, intravaginal estrogen therapy ameliorates vulvovaginal atrophy without significant systemic side effects and is the conservative and recommended choice when hormone supplementation is considered solely for the relief of this condition [26, 27]. Randomized trials of an ultralow-dose, 10-μg estradiol tablet demonstrated efficacy in normalizing vaginal pH and vaginal cytology and in reducing the most bothersome symptoms of atrophy [28, 29]. This dose exhibited low overall systemic absorption and was associated with no significant evidence of endometrial hyperplasia [28]. The North American Menopause Society concludes that opposing progestogen is generally not indicated at the low estrogen doses administered locally for vaginal atrophy [26, 27].

Intravaginal administration of dehydroepiandrosterone (DHEA), an androgenic sex steroid precursor, has been proposed as an alternative approach to treating postmenopausal vaginal atrophy and associated sexual dysfunction [30, 31]. Locally applied DHEA is converted by vaginal cells to estrogens and androgens without affecting serum concentrations of estradiol or testosterone, thereby avoiding effects on other organs [32]. In randomized trials, treatment improved clinical signs of atrophy (pH, cytology, vaginal secretions, and epithelial thickness) and measures of sexual health [30, 31]. However, in contrast to intravaginal estradiol therapy, which requires application of a tablet two to three times a week, DHEA requires daily dosing of a cream preparation, a regimen that women may find more onerous [33]. The North American Menopause Society (NAMS) Web site (menopause.org) is a good source of information on treatment options for health conditions associated with menopause.

4 Urogenital Infections

4.1 Urinary Tract Infections

Escherichia coli is the primary organism involved in urinary tract infections (UTIs), and the vagina is a reservoir for urethral colonization [34–36]. As circulating estrogen declines, cell densities of lactic acid-producing microbes fall, and the incidence of vaginal colonization with E. coli rises [37]. This elevates the risk of UTIs. Insulin-dependent diabetes and a prior history of recurrent UTIs are associated with higher risk of UTIs after menopause [38]. Although the number of studies is limited [39, 40], a meta-analysis found evidence that intravaginal estradiol therapy may reduce the risk of urinary tract infection [41]. However, the therapy does not have regulatory approval in the USA for this indication.

4.2 Sexually Transmitted Infections

Many people remain sexually active in old age and can be at risk of acquiring sexually transmitted infection. Transmission of genital herpes simplex remains pertinent, and both women with an intact cervix and women who have undergone a hysterectomy can acquire trichomonadal, gonorrheal, or chlamydial infection. With advent of modern treatment, HIV/AIDS is now a chronic illness in the developed world; infected people can now live into their 70s or longer and may transmit the disease. The use of condoms should be encouraged. Sexually transmitted infection among older adults is a sensitive subject that may be facilitated in the clinical setting with a nonthreatening conversation and by using patient education pamphlets.

4.3 Desquamative Inflammatory Vaginitis (DIV)

Women over age 40 can suffer from desquamative inflammatory vaginitis, a rare inflammatory vaginal infection that occurs primarily in white women [42, 43]. It produces a copious, purulent discharge, and the vulva and vaginal vault appear glazed due to epithelial sloughing. Vaginal pH is greater than 4.5, but the “whiff test” is negative (no fishy odor when a drop of vaginal secretion is added to 10 % aqueous potassium hydroxide). Microscopy reveals an outpouring of inflammatory white cells (a hallmark sign), a paucity of lactobacilli, large numbers of other bacteria, and a preponderance of immature, squamous vaginal epithelial cells. Typical treatment is a 2-week course of clindamycin. Prognosis is good if there is a favorable initial response, but in some cases, long-term maintenance therapy is required.

5 Urinary Incontinence

Urinary incontinence is underreported condition. It may emerge prior to menopause, but incidence increases with age. Reported prevalence rates vary depending on the condition (stress, urge, or mixed incontinence) and demographic variables (age, race, parity, body mass index, etc.) [44]. Reported rates range from 10 to 40 % among subgroups of community-dwelling individuals [45, 46] and from 43 to 77 % among nursing home residents [47].

Stress and urge incontinence have different symptoms and underlying pathology (Table 27.3). Stress incontinence involves the uncontrolled loss of urine induced by sudden pressure on the abdominal organs (such as a cough, a sneeze, heavy lifting, exercise, or coital penetration). It stems from a weakened sphincter at the junction of the bladder and urethra. Stress incontinence may be first experienced by younger women aged 30–50 when the bladder sphincter is weakened by childbirth. However, its incidence peaks during the perimenopausal period (between the ages 45 and 49) [46], possibly because aging manifests the underlying weakness. Another important factor is obesity, which places additional stress on the bladder. Obese women (BMI ≥30) have twice the risk of developing stress incontinence independent of age and parity. Epidemiological data indicate that each 5-unit increase in BMI is associated with 20–70 % increase in urinary incontinence risk [48].

Table 27.3 Types of urinary incontinence in adult womena
Full size table

Urogenital prolapse, the downward descent of the internal urogenital organs toward the vagina due to weakened support, can coexist with stress incontinence. Relaxation of the musculature of the vaginal vault and weakening of the pelvic muscles due to childbirth contributes to urogenital prolapse.

Mild stress incontinence is manageable with pelvic muscle training (Kegel exercises), by limiting fluid intake, by more frequent voiding, and with the use of feminine pads. Pelvic floor muscle exercises are more effective in younger than older women [49]. Devices for stress incontinence include pessaries and urethral orifice plugs, but most women are disinclined to use them. Duloxetine, a serotonin and noradrenaline reuptake inhibitor used to treat mood disorder, reduces the frequency of stress incontinence in randomized controlled trials in younger and postmenopausal women [9, 50, 51]. It is approved for this indication in Europe but not in the USA. In overweight or obese women, weight loss is a first-line intervention for stress urinary incontinence. For severe cases of stress incontinence, surgery is the least conservative remaining option for therapy; however, a paucity of data exists on the effectiveness of surgery in the older postmenopausal patient.

Urge incontinence involves the strong urge to urinate and inability to voluntarily control urine loss. Urge incontinence is unpredictable and more distressing when involving large urine losses. 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. Childbirth may contribute to sphincter weakness, so that the impact of bladder contractions is more apparent.

Several therapeutic approaches exist for this condition. Efficacious antimuscarinic drugs (e.g., oxybutynin, Tolterodine) block cholinergic muscarinic receptors associated with uncontrolled bladder contractions [52]. Common side effects are dry mouth and constipation. Anticholinergic drugs are contraindicated in patients with documented untreated narrow-angle glaucoma. Behavioral interventions include moderating fluid intake (although low intakes may increase contractions at lower urine volumes); bladder retraining through scheduled voids and conscious urge suppression; limiting caffeine, alcohol, and diuretics; and adding dietary fiber or probiotics to avoid constipation. Kegel exercises may alleviate the contribution of a weakened sphincter but will not affect bladder contractions.

Interstitial cystitis is a poorly understood condition with symptoms that may contribute to urinary frequency and urge incontinence (reviewed in [53, 54]). One prevailing theory is that compromise of the protective mucus layer of bladder mucosa (possibly from prior injury, subclinical infection, or autoimmune destruction) is a precipitating event. Potassium ions, present at high concentration in urine, cross this “leaky” epithelium, triggering chronic inflammation, injury, and neuronal damage to the bladder interstitium. Interstitial cystitis manifests as symptoms of urgency, frequency, burning pain associated with bladder filling, and dysuria. Patients with interstitial cystitis but not those with healthy bladders are sensitive to instilled potassium (potassium sensitivity test), which elicits reduced bladder capacity and pain. In the early stages of the condition, the patient may not recognize the increased voiding as dysfunctional; however, pain and greater frequency develop as the disease progresses. Most patients with this condition also experience dyspareunia. Interstitial cystitis often coexists with vulvodynia [55–57] and that both conditions may have a neurogenic component [58]. Because interstitial cystitis is associated with bladder pain, dysuria, high voiding frequency, low void volumes, and nocturia, it shares the symptomatic characteristics of overactive bladder syndrome or urge incontinence.

For the active, community-dwelling older woman with urinary incontinence [59], feminine protection is the self-treatment option of choice. She will search for other options only when symptoms become too difficult to manage or when she fears her symptoms signal pathology. 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 [3IQ] questionnaire [60]) can be offered to assist the patient in defining the nature and cause of her symptoms (stress, urge, or mixed incontinence).

For the older woman unable to maintain adequate perineal hygiene independently, incontinence dermatitis can become a significant problem. Several factors contribute to its development [59] (see Chap. 17 in this book) (Fig. 27.1). First, chronic exposure to urinary moisture makes the skin more susceptible to friction damage; in the older adult, excess skin hydration is dissipated more slowly than in younger people [61]. Bacterial action on the urine generates urinary ammonia, which elevates the local pH; this alters skin barrier function and activates fecal enzymes, which further compromise skin integrity and increase skin susceptibility to microbial infection [62–65]. Atrophied genital tissue is especially susceptible to pH changes and to enzymatic action. Moreover, in the incapacitated patient, reduced mobility creates higher shear forces on the tissue, a trigger for the development of decubitus ulcers (pressure sores). Lastly, those with impaired cognition may be unable to alert caregivers to incontinent episodes. These factors underscore the need for vigilant hygiene and physical assistance for the older adult with incontinence.

Fig. 27.1
figure 1

Risk factors for incontinence dermatitis in the older person

Full size image

In community-dwelling individuals receiving home care, helpful interventions include prompted or timed toileting, use of incontinence garments, use of antimuscarinic drugs where appropriate [66, 67], and assistance with perineal care. In nursing homes, urine containment with incontinence products is a first-line intervention. Catheterization is sometimes used but carries the risk of infection. Behavioral interventions such as prompted voiding and timed voiding are used to a limited degree, and antimuscarinics are only an adjunct treatment [68]. Prompted voiding involves caregivers checking and querying patients, giving toileting prompts, and reinforcing initiative on the part of the patient. 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 [69]. Timed voiding is bringing the patient to the toilet at fixed intervals regardless of whether she requests it or has voided during the previous interval.

In the USA, an estimated 16 billion dollars annually is spent on urinary incontinence management [70]; 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 [37]. By 2030, it is estimated that one in eight people worldwide will be over the age of 65, and the economic impact of incontinence management will become even more significant [71].

6 Vulvar Dermatoses

Lichen sclerosus affects the skin and the vulvovaginal mucosa (reviewed in [72]). Incidence peaks bimodally, rising in adolescents and in peri- or postmenopausal women. Symptoms are intense vulvar itch, soreness, pain, and dyspareunia, but there is no abnormal vaginal discharge. White polygonal plaques with a wrinkled appearance appear bilaterally on the vulva; the labia, vestibule, and introitus as well as the perineum can be affected. Advanced disease is typified by a “keyhole” or “figure-eight” configuration of sclerotic tissue surrounding the introitus and anus. Potent topical corticosteroids or macrolides are used to manage symptoms and retard disease progression.

Erosive lichen planus is a rare, chronic disorder that affects only the mucosa of the vagina and vulvar vestibule; vulvar skin is unaffected [72]. Peak incidence is between the ages of 30 and 70. Signs and symptoms include intense vulvar itch and pain, dyspareunia, excessive discharge, and postcoital bleeding. Discharge is due to erosive shedding, and the vaginal epithelium may bleed upon speculum insertion. These signs and symptoms mimic those of desquamative inflammatory vaginitis, but the distinguishing features of erosive lichen planus are the absence of infection and the presence of white, lacy plaques on the vulvar vestibule and inner aspects of the labia minora. White plaques on the oral mucosa (buccal mucosa, gingiva, palate, or tongue) are a common extragenital manifestation. Erosive lichen planus requires the use of potent topical steroids (e.g., clobetasol propionate) or topical macrolides (tacrolimus). Oral corticosteroids (e.g., prednisone) are a second-line treatment for more recalcitrant cases.

7 Summary

Vulvovaginal atrophy secondary to hypoestrogenism affects 10–50 % of postmenopausal women. Genital symptoms include vulvar irritation and pruritus, decreased vaginal secretions, vaginal burning, dyspareunia, and postcoital bleeding; urinary symptoms include urethral discomfort, frequency, and dysuria. Low-dose, intravaginal estrogen therapy is an option to relieve symptoms of vulvovaginal atrophy and improve quality of life. Although the risk factors and precipitating events vary, postmenopausal women are also more likely to experience stress or urge incontinence. Stress incontinence, linked to childbirth or obesity, is uncontrolled urine loss provoked by abdominal pressure on a weakened bladder sphincter. Urge incontinence is the inability to suppress voiding and is likely due to age-related changes in the nervous system that cause abnormal bladder spasms; however, interstitial cystitis, thought to result from a disrupted bladder mucosal barrier, mimics some of the symptoms of urge incontinence. Women are unlikely to seek treatment until their symptoms become highly disruptive: health-care providers can assist by sensitively broaching the subject and by providing literature that describes these conditions and available treatment options. Vigilant perineal hygiene in the older person who is unable to care for herself is critical to avoiding incontinence dermatitis. Lastly, certain rare infections and vulvar dermatoses are more prevalent in postmenopausal women. Desquamative inflammatory vaginitis is a persistent inflammatory vaginal infection that erodes the vaginal mucosa and requires aggressive antibiotic treatment. Lichen sclerosus is a vulvar dermatosis of the skin as well as the mucosa. White, wrinkled polygonal plaques manifest bilaterally and may become sclerotic. Erosive lichen planus affects only the mucosa and causes discharge with shedding of the vaginal epithelium. Although its signs and symptoms mimic those of desquamative inflammatory vaginitis, its distinguishing features are the absence of infection and the presence of white, lacy plaques on the vulvar vestibule and inner aspects of the labia minora. Potent topical corticosteroids are used in treatment of both these dermatoses.