Abstract
The term vulvo-vaginal atrophy (VVA) defines the anatomic and physiological changes in the vulvo-vaginal tissues, which are directly related to reduced circulating estrogen levels, associated with menopause and aging. Atrophic vaginitis connotes a state of inflammation or infection that may be present in some women with VVA.
The term vulvo-vaginal atrophy (VVA) defines the anatomic and physiological changes in the vulvo-vaginal tissues, which are directly related to reduced circulating estrogen levels, associated with menopause and aging. Atrophic vaginitis connotes a state of inflammation or infection that may be present in some women with VVA.
VVA or atrophic vaginitis is a medical challenge because it is under-reported by women, under-recognized by health care providers (HCPs) and, therefore, under-treated. The most common symptoms associated with VVA are dryness, itching, irritation, burning and dyspareunia. These may negatively influence well-being and relationships. Urinary symptoms are also associated with VVA, and include increased frequency, urgency, dysuria, and recurrent urinary tract infections (rUTIs), as well as urinary incontinence resulting mainly from pelvic floor problems [1]. More recently, VVA has been renamed genitourinary syndrome of menopause (GSM), to highlight the many genital, sexual and urinary symptoms associated with atrophic changes of vulvo-vaginal and urological tissues, in association with estrogen deficiency, occurring at midlife and beyond. Of note, the new definition GSM includes signs and symptoms that cannot be all reversed by evidence-based endocrine therapies and may require different strategies according to their true etiology [2]. Recent surveys indicate that around 50 per cent of postmenopausal women experience vaginal discomfort attributable to VVA and symptoms are already evident during the perimenopause/early postmenopause. Longitudinal data showed that the prevalence of vaginal dryness, the most common symptom associated with VVA, ranged from about 3 per cent at premenopause to 47 per cent at 3 years postmenopause. Epidemiological findings are influenced by a range of factors, including women’s age, time since menopause, frequency of sexual activity, general health, partner’s availability, socio-cultural background. In addition, most of the data rely on self-reported symptoms and the severity of symptoms (from mild to severe) is rather subjective. Indeed, objective signs of VVA may be present, but women may not report symptoms because they are self-treating, feel the symptoms are not important enough, abstain from sexual activity because of no partner/a partner with health/sexual problems or are embarrassed to discuss such an intimate topic.
HCPs should be proactive in order to help their patients to disclose symptoms related to VVA and to seek adequate treatment when vaginal discomfort is clinically relevant. Women are not aware that VVA is a chronic condition with a significant impact on sexual health and quality of life and that effective and safe treatments may be available. VVA can lead to symptoms not only in response to sexual activity (reduced lubrication, pain, low desire and arousal, impaired sexual pleasure and orgasm), but also during simple activities such as walking or exercising (itching, burning, discharge, malodour, discomfort). Dyspareunia may be accompanied by postcoital bleeding and secondary vaginismus triggered by avoidance, anxiety and loss of sexual desire due to the anticipation of coital pain. A woman with VVA may also experience bleeding with minimal trauma, such as during a medical examination or whilst undertaking physical activities. That being so, it is very important to include VVA in the menopause agenda, by encouraging an open conversation on the topic of urogenital health and performing a gynaecological examination, if indicated. According to very recent guidelines on appropriate management of VVA in clinical practice, it is essential to overcome the vaginal ‘taboo’ in order to optimize affected women’s health care [1].
VVA as a Chronic Condition
In European countries natural menopause occurs between 51 and 52 years of age and increased life expectancy means that most women will spend at least one-third of their life in the postmenopausal hypoestrogenic state. Menopause is a multidimensional phenomenon in which biological variables are modulated by intrapersonal and interpersonal factors, varying according to the socio-cultural environment and the health care system.
VVA is one of the many changes occurring at the time of the menopause transition, as a consequence of reduction of estrogen production by aging ovaries. It may occur as a consequence of other hypoestrogenic states, but this is less common. Unlike hot flushes, which usually resolve over time, VVA has a chronic/progressive course throughout the menopause transition and beyond. The areas of a woman’s life most likely to be negatively impacted by VVA are sexual intimacy (64 per cent), having a loving relationship with a partner (32 per cent), overall quality of life (32 per cent), feeling healthy (21 per cent) and feeling attractive (21 per cent). The presence and severity of symptoms are variable, from mild discomfort to significant impairment, depending on age, time and type of menopause, parity and vaginal delivery, frequency of coital activity, cigarette smoking and certain medical conditions/medications. Breast cancer survivors are a special group of women that may suffer from VVA and require individualized care.
Estrogen is vital to maintain normal structure and function of the vagina and surrounding urogenital tissues. However, the science of intracrinology points to the age-related decline of circulating DHEA as an additional cause of both estrogen’s and androgen’s local intracellular deficiency. Estrogen receptors (both α and β), which are widely present in the vagina, vulva, muscles of the pelvic floor, endopelvic fascia, urethra and bladder trigone during reproductive life, decline with menopause and may be restored by estrogen treatment. Androgen receptors (ARs) are also well expressed at multiple levels (mucosa, submucosa, stroma, smooth muscle and vascular endothelium) and cross-talk with ERs, influencing neurovascular and neuromuscular function.
Early data show that untreated postmenopausal women with less than 50 pmol/l of estradiol suffer more from symptoms associated with VVA. The absence of estrogen stimulation contributes to the loss of mucosal elasticity by inducing fusion and hyalinization of collagen fibres and fragmentation of elastin fibres. Mucosal hydration is reduced in the dermal layer with a reduction of intracellular mucopolysaccharide and hyaluronic acid. The vagina loses its rugae, the epithelial folds that allow for dispensability, and there is a shortening and narrowing of the vaginal canal. The mucosa of the vagina, introitus, the labia minora become thin and pale and the significant reduction of vascular support induces a decrease of the volume of vaginal transudate and of other secretions. Over time, there is a progressive dominance of parabasal cells with fewer intermediate and superficial cells. This is a marker of estrogen deprivation in the vaginal squamous epithelium, which becomes friable with petechiae, ulceration and eventually bleeding after minimal trauma. With thinning of the vaginal epithelium there is a significant reduction in glycogen, which affects the population of lactobacilli and increases vaginal pH (between 5.0 and 7.5). A decrease of vaginal hydrogen peroxide supports the growth of pathogenic bacteria, including staphylococci, group B streptococci and coliforms. Similar anatomical and functional changes in the vulva as well as in the pelvic floor and within the urinary tract occur, resulting in an impairment of the pelvic floor efficiency. In particular, the vulvar introitus retracts, and hymeneal carunculae involute and lose elasticity, leading to significant entry dyspareunia. The urethral meatus appears prominent relative to the introitus and thinning of the urinary epithelium and weakening of the surrounding tissue may promote reduced urethral closure pressure, reduced sensory threshold in the bladder, and in some cases, increased risk of rUTIs [6].
In summary, VVA is a chronic condition during the postmenopausal years and it cannot regress unless adequately treated.
How to Recognize Symptoms and Signs of VVA
During menopausal consultation, women are often uncomfortable to report intimate symptoms spontaneously and they assume that problems associated with VVA are a natural part of aging. However, postmenopausal women like to be asked and very simple questions may help HCPs to ‘break the ice’ in order to discuss vaginal and sexual health. Unfortunately, HCPs tend not to take a proactive approach to urogenital health management in the middle- and later-life age groups, mainly because of inadequate training, constraints of time and personal attitudes and beliefs that sex is not a priority for older patients [4]. Whenever postmenopausal women report urogenital symptoms in clinical practice, an accurate pelvic examination should be performed to look for signs of VVA (Table 11.1). Dyspareunia is generally less reported later in life mainly because older women are less likely to still have a spousal or other intimate relationship and sexually related personal distress declines with age. Tissues may be easily traumatized and irritated and a gentle approach is mandatory in the most severe cases. It has been comprehensively described that the inspection should include the tissues of the vulva, vestibule, vagina and urethra, and clinical scales may be used in the attempt to quantify VVA. Organ prolapse and the muscle tone of the pelvic floor should be also noted, as well as other disorders that can cause symptoms similar to those of VVA. Although VVA is typically a clinical diagnosis, other laboratory tests may be used to support the diagnosis, such as an evaluation of vaginal pH and the vaginal maturation index (VMI), which describes the relative proportion of parabasal, intermediate and superficial vaginal epithelial cells. A more alkaline pH (>5) leads to a shift in the vaginal flora towards more coliforms and, together with the other atrophic changes, is responsible for increased susceptibility to and frequency of infections and odour, as well as traumatic bleeding associated with sexual intercourse or secondary to speculum insertion during routine gynaecological examination. Dominance of parabasal cells, calculated on specimens obtained directly from the lateral upper vaginal walls, indicates hypoestrogenism and atrophy. Thus, the shift to a higher number of superficial cells is a primary end point of any treatment prescribed to relieve symptoms of VVA [1].
Table 11.1 Symptoms and signs associated with VVA in menopause.
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