Vaginal Atrophy

The urethral and vaginal mucosas are rich in estrogen receptors and share a common embryologic origin from the urogenital sinus. As such, these tissues are exquisitely sensitive to estrogen deprivation, and symptoms may appear promptly as soon as estrogen levels begin to decline. Vaginal atrophy will present with a variety of symptoms along a continuum of severity. Symptoms are typically vaginal dryness and associated dyspareunia, which may be initially presented as vaginal irritation. This will progress to loss of vaginal rugation and development of a progressively pale, hypovascular mucosa. Eventually, a thin inflammatory exudate can develop, sometimes in large quantities. This may result in a watery vaginal discharge that on microscopic examination is replete with inflammatory and basal squamous epithelial cells, but with no evidence of bacterial infection. As with other more obvious mucosal hypoestrogenic states, a chronic watery vaginal discharge without an infectious cause in a postmenopausal woman warrants a course of local estrogen therapy. Up to this stage of atrophy progression, resultant changes are readily reversible with local estrogen administration. Left untreated, chronic vaginal atrophy will progress to loss of vaginal caliber and length, changes that are not reversible with estrogen therapy alone. Progressive coalescence of the apical vaginal mucosa will result in vaginal foreshortening. Lack of sexual activity exacerbates the progression of urogenital atrophy.

Because the progression of urogenital atrophy is in large part attributed to a devascularization of the mucosal tissues, systemic hormone replacement may not be sufficient to alleviate symptoms of vaginal atrophy. Sys-temically administered estrogen will not reach a devascu-larized mucosa. As such, many women receiving low-dose systemic replacement therapy will still have urogenital atrophy and will require concomitant local hormonal replacement therapy.

Upon initiation of local hormone replacement therapy, there is a prompt revascularization of the vaginal and ure-thral mucosa. This can be clinically detected within 6 weeks of initiation of local estrogen therapy. As might be expected, vaginal irritative symptoms (i.e., tingling, itching) may occur during the initiation of the neovascularization process. These symptoms are typically short-lived.

Table 11-1.1. Signs and symptoms of urogenital atrophy

Vaginal Dryness Pallor

Decreased rugation Mucosal thinning

Inflammation with/without discharge Decreased caliber and depth Increased pH


Thinned skin Loss of hair volume Labial fusion

Decreased introital diameter Urethral

Decreased alpha receptors Decreased vascularity Decreased epithelial thickness Formation of caruncle Bladder

Increased bladder wall collagen Decreased bladder epithelial thickness Increased parasympathetic sensitivity Decreased beta sympathetic activity

Vaginal atrophy can be easily detected on vaginal examination with identification of a thin, pale, and dry vaginal mucosa. In addition, vaginal pH will increase to greater than 5.0. This can be assessed during a pelvic examination, using pH paper. To quantify the degree of vaginal atrophy, a maturation index is most useful. This is a cytologic evaluation of the vaginal mucosa determining the percentage of basal, parabasal, and superficial squamous cells identified on a smear of the vaginal epithelium, much like a pap smear. A ratio distribution of cell types can be determined (% superficial/% parabasal/% basal). Women who are well-estrogenized will have a predominance of superficial cells, whereas atrophic women will have greater than 50% of the cells being basal or parabasal, with few superficial cells. A change in maturation index can be documented during treatment with local estrogen therapy, as the percentage of superficial cells increases. This is typically an inexpensive test, with which most pathologists are familiar.

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