Vulvovaginal atrophy

Most common in postmenopausal women, but can occur at anytime.

Affects more than 50% of midlife an older women.

It is recognized that the loss of estrogen resulting from the cessation of ovarian function may also promote vulvovaginal atrophy symptoms and also produce urinary frequency and urgency.

Decreased estrogen levels after menopause lead to the genitourinary syndrome of menopause (GSM), previously known as vulvovaginal atrophy. 

The term genitourinary syndrome of menopause now includes vulvovaginal atrophy.

Decreased estrogen levels after menopause lead to the genitourinary syndrome of menopause  previously known as vulvovaginal atrophy. 

Symptoms associated with decreased estrogenization of the vulvovaginal tissues.

Vaginal atrophy, atrophic vaginitis, and urogenital atrophy alternative names for the process.

Symptoms include: vaginal dryness, vaginal irritation, postcoital bleeding, and soreness.

Vaginal discharge and dyspareunia may occur.

The genitourinary syndrome of menopause affects the quality of life and causes pain during sex, loss of libido, avoidance of intimacy, urinary urgency, dysuria, and recurrent symptomatic urinary tract infections.

Unmanaged genitourinary syndrome can progress and debilitate with severe symptoms and anatomic changes sometimes requiring pelvic floor physical therapy and vaginal dilator therapy.

Vaginal spotting may occur due to the thinning of vaginal epithelium and secondary tears.

Some patients have thin yellow or gray watery discharge related to increased pH.

Microscopic hematuria may a company urgency, frequency, nocturia and urge incontinence.

Recurrent UTIs may occur.

Lack of lubrication during intercourse is often the initial symptom.

Patients may experience urinary frequency, urgency, and urge incontinence.

Caused by hypoestrogenism.

VVA is related to reduced serum estrogen levels and aging.

The vagina, vestibule, and bladder trigone contain high levels of estrogen receptors.

Serum estrogen level reductions result in thinning of the vaginal epithelium, healing and retraction of the labia minors, reduction in lubrication, decreased vaginal elasticity, and increased friability all leading to dyspareunia.

The vaginal epithelium is squamous in nature, and until menopause is moist and thick with rugae.

At menopause, the vaginal epithelium thins from declining levels of estrogen.

With menopause, fewer epithelial cells exfoliate into the vagina.

Exfoliated epithelial cells die and release glycogen, which is hydrolyzed to glucose, and in turn glucose is broken down into lactic acid by Lactobacillus, a normal vaginal organism.

If the above process doesn’t occur the pH of the vagina will rise with the loss of lactobacilli andovergrowth of other bacteria, including group B. Streptococcus, staphylococci, coliforms, and diptheroids (Roy S).

Overgrowth of these other bacteria can cause vaginal infections and inflammation.

Progesterone creates thick mucus and epithelium proliferation with infiltration of leukocytes.

Following menopause elasticity of the vagina is reduced and connective tissues increase, vaginal blood flow is decreased, as is vaginal lubrication.

Most common cause of hypoestrogenism is postmenopausal state but lactation and medications for breast cancer can be responsible.

Prevalence 4% percent in early premenopausal females and 47% in late postmenopausal women.

Prevalence in breast cancer survivors is much higher and as high as 23.4% in premenopausal and 61.5% in postmenopausal patients (Crandall C).

Clinical findings include atrophy of the labia majora and vaginal introitus and receding of the labia minora.

The vaginal mucosa may be dry, and pale, although if inflammation is present it may appear erythematous and contain petechiae.

Vaginal rugae may disappear, the vagina may shorten and narrow

Vaginal discharge may be present.

A urethral change with a smooth friable erythematous outgrowth at the edge of the urethra may develop, known as a urethral caruncle.

Diagnosis is a clinical one, but vaginal pH and vaginal maturation index can support the evaluation.

A pH of the vaginal secretion of 4.6 or greater supports the diagnosis, in the absence of bacterial vaginosis.

Premenopausal women have a vaginal wall pH of 4.5 or less.

Vaginal maturation index assesses the relative proportion of parabasal, intermediate and superficial vaginal epithelial cells: premenopausal women have greater than 15% of superficial cells, and post menopausal women with vulvovaginal atrophy have typically less than 5% of superficial cells.

Differential diagnoses include: vaginal infections, irritants, and dermatoses.

Treatment includes vaginal moisturizers and lubricants that are water based liquids, gels, or ovules for dysparenuia.

Treatments include vaginal estrogens, ospemifene oral tablets, prasterone vaginal inserts.

If patients do not have in concomitant menopausal hot flashes or night sweats, local vaginal administration is the preferred estrogen delivery management.

Vaginal lubricants are shorter acting than moisturizers and need to be applied at the time of sexual activity.

Vaginal estrogen is effective treatment in all forms-cream, ring or tablet in reducing symptoms.

Ospemifene (Osphena) a estrogen agonist/antagonist effectively treats vulvovaginal atrophy.

Vaginal estrogen relieves symptoms more effectively than non hormonal treatments.

Low doses vaginal therapies are recommended for vulvovaginal symptoms that include dryness, itching, recurrent vaginitis, dyspareunia, and urinary symptoms of frequency, urgency and recurrent urinary tract infections not relieved by lubricants and vaginal moisturizers.
Vaginal preparations with creams, tablets, suppositories, and low-dose rings can restore vaginal epithelium, flora, moisture, secretions, and increase the number of superficial cells, and normalize acidic vaginal pH.

Various vulvovaginal treatments have similar efficacy for relieving symptoms and treatment is selected based on a shared decision between the physician and patient based on preference, cost and adverse effect profile.

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