Ridley's The Vulva

The clitorourethrovaginal complex is a term used to describe the interplay between the three structures and their role in the sexual response [36]. There is a long‐standing debate about the existence of an erogenous zone in the anterior vagina (G‐spot), but there is no evidence for any distinct structure.

The sexual response is a sequence of events involving initial stimulation of the sensory receptors and nerves of the clitoris, mainly via the sensory function of the epithelium, which stimulates the release of neurotransmitters [37]. Afferent fibres then transmit to the spinal cord roots at S2‐4, leading to activation of the parasympathetic system leading to vasodilatation in the erectile tissue. Genital arousal in females involves an increase in blood flow, clitoral engorgement and erection, and swelling of the labia minora, which is sufficient to induce some traction on the clitoris. The suspensory ligament in the female can restrict movement of the clitoris so that it can move up with arousal but it does not straighten [38]. If the threshold for orgasm is reached, there is then a central component which activates skeletal and autonomic smooth muscle contraction [39].

There is conflicting evidence about sexual desire and arousal in relation to the menstrual cycle, but it is generally accepted that sexual desire does peak mid‐cycle and in the pre‐menstrual phase. Hypoactive sexual desire disorder can be related to numerous physical, endocrine, and psychosocial factors [ 40], and it is helpful to screen patients and then refer appropriately.

Several changes occur during pregnancy, mainly related to increased production of hormones via the placenta. There are changes in blood flow, pigmentation, and in the immune response (see above). A fivefold increase in blood flow through the pelvic circulation occurs during the first two months of pregnancy, and this doubles again during the third month. Progesterone causes increased venous distension, which predisposes to vulval varicosities (see Chapter 34). There is increased blood flow in the vulva which can give a bluish appearance. One case of a spontaneous vulval haematoma is described in pregnancy [41]. Isolated vulval oedema can occur in hypoalbuminaemic patients [42].

Figure 3.1 Central loss of hair on mons pubis post menopause.

The rise in oestrogen stimulates increased melanogenesis, particularly in the areolae, nipples, and vulva. Pigmentation of the labia majora, rims of the labia minora, and the perineum can be marked. There may also be facial melasma and linear pigmentation of the anterior abdominal wall, termed linea nigra.

There is an increased incidence of candidiasis during pregnancy, probably as a result of increased glycogenation of the vaginal epithelium and a reduction in cell‐mediated immunity [43]. Candida colonisation of the vagina may be a risk factor for pre‐term birth and treating asymptomatic patients may reduce this, but larger trials are needed to confirm this [44].

Menopause is defined as the permanent cessation of menstruation resulting from the loss of follicular activity. There is a period of about four years termed perimenopause when the first menopausal symptoms, such as irregular menstrual cycles, commence. Menopause is established one year after the final menstrual period with an average age of 50 in Western societies, but can be earlier in other parts of the world. Thereafter, oestrogen and progesterone levels remain low while gonadotrophin levels increase and may remain elevated for perhaps 20–30 years. There are several symptoms, including flushing, insomnia, and headaches. There are also effects on the cardiovascular system and bone metabolism [45].

The post‐menopausal changes in the genital and urinary tracts are a result of the fall in oestrogen levels. The constellation of genital, urinary, and sexual symptoms has been re‐named as the genitourinary syndrome of menopause (GSM) [46]. However, it is very important to remember that several inflammatory dermatoses common in this age group and other more serious pathology can present with similar symptoms and must always be included in the differential diagnosis [47].

The vagina becomes less rugose, narrower, and drier and the epithelium more fragile and easily damaged. The epithelium is thinner and glycogen levels reduce, making the environment more alkaline. The number of lactobacilli is also reduced. The mucosa can look pale, and there is increased fragility. Similar changes occur in the vulval vestibule, transitional epithelium of the urethra, and bladder, with the consequent increased risk of recurrent urinary tract infections. Although the vasomotor effects of menopause tend to improve with time, the vulval and vaginal symptoms remain and may worsen.

The symptoms of GSM are common and can have an impact on quality of life. In a study of 913 post‐menopausal women, 79% of women described these symptoms at some point [48]. Vaginal dryness was reported in 100% of the women with dyspareunia and burning commonly described as well. The urinary symptoms are frequency, nocturia, stress and urge incontinence, and urinary tract infections.

Changes in the vulva after menopause include loss of hair on the labia majora and central part of the mons pubis due to a reduction in the number of hair follicles ( Figure 3.1). The labia majora become less prominent and slack due to loss of the subcutaneous fat, and the introitus may become patulous. Loss of muscle tone contributes to vaginal and uterine prolapse. Urinary incontinence is present in more than 40% of women over the age of 70 [49], and this will have significant clinical effects on the anogenital skin. There is no major difference in hydration, permeability, and irritancy of the vulval skin between pre‐ and post‐menopausal women [ 1, 16]. However, irritant dermatitis secondary to urinary incontinence is very common in this age group, and other factors such as occlusion and difficulty with good hygiene may also play a part.

Sexual desire and arousal are also reduced [50]. While many women report a reduced sexual desire, this does not fulfil criteria for a diagnosis of hypoactive sexual desire disorder [51].

Similar symptoms to those seen at the menopause also occur in women with premature ovarian insufficiency. This can be caused by genetic defects, autoimmune disorders, or following treatment for malignancy. However, in many cases, no specific cause is found. Aromatase inhibitors used in the treatment of breast cancer can cause extreme oestrogen deficiency and marked vulval and vaginal symptoms. These patients should be referred for expert advice as hormone replacement therapy may be contraindicated [52].

The symptoms of menopause and ovarian insufficiency can be modified by lubricants, hormone replacement therapy (HRT) which is taken by many women, and non‐hormonal treatment modalities. Lubricants that are hyperosmolar can cause irritancy and ideally should be kept as physiologically similar to normal levels of osmolality and acidity [53]. Many types of HRT exist, and although these can help to improve vaginal and introital symptoms, it will have no effect on the keratinised vulval skin [ 54].

Guidelines

British Menopause Society www.thebms.org.uk

Royal College of Obstetricians and Gynaecologists www.rcog.org.uk

Menopause Matters www.menopausematters.co.uk

Menopause Support www.menopausesupport.co.uk