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].

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.

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].

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.