Vaginal atrophy develops in all women when estrogen depletion occurs at menopause. However, not all women with vaginal atrophy develop atrophic vaginitis. The estrogen concentration in perimenopausal women is approximately 120 ng/ml and after menopause begins its concentration decreases to approximately 19 ng/ ml. The predominant hormone produced by the postmenopausal ovary is androstenedione and this hormone is converted in the peripheral fatty tissue to estrogen. Testosterone is also produced in the ovary and most of this is converted into estradiol in the ovaries. Thus there is an endogenous supply of estrogen as long as the postmenopausal ovaries continue to function. However, the decrease in estrogen is significant and the vaginal epithelial surface loses its folds, or rugae, and thickness, then becomes thin and pale. The vaginal tissue loses its elasticity and its ability to distend, thus it becomes shorter and narrower. These changes result in the patient experiencing dyspareunia and avoiding sexual intercourse.
There are noticeable changes in the appearance of vaginal squamous epithelial cells in the absence of sufficient estrogen. There is also a lack of mature or naviculated squamous epithelial cells and a significant increase in intermediate and parabasal cells. Physiological changes within the vaginal ecosystem also occur. The most noticeable change is a decrease in the available glycogen, creating an insufficient supply of carbohydrate, which results in a decrease in Lactobacillus growth. The decrease in Lactobacillus growth results in a decrease in acid production and, in turn, the vaginal pH rises above 5 allowing the non-lactobacilli to grow. Once non-lactobacilli gain dominance, the vaginal discharge can change from white to dirty gray or purulent, depending upon the number of white blood cells (WBC) present. Once this condition is established, the patient’s status changes from vaginal atrophy to atrophic vaginitis. It also appears that women who smoke enhance the development of atrophic vaginitis. Those women whose ovaries produce testosterone and androstenedione, and continue to be sexually active appear to experience less severe atrophic changes. Women whose ovaries have become completely non-functioning are more likely to develop vaginal atrophy.
Patients often develop vaginal atrophy without knowing the process occurs. Individuals who have infrequent sexual intercourse will note tightness in their vagina during intercourse. Because of the lack of lubrication, as well as shortness and narrowing of the vagina, these patients eventually complain of pain and discomfort. These individuals will often refuse to have sexual intercourse. At this point, the patient may come to the physician if their husband or sexual partner encourages them to do so. The development of vaginal spotting, profuse discharge, or vaginal burning is the most likely reason patients seek a physician’s assistance.
The most frequently reported symptoms are:
(1) vaginal narrowing and shortness;
(2) vaginal spotting or bleeding, especially during or after intercourse;
(3) development of a urethral carbuncle;
(5) vulvar burning;
(6) vulvar pruritus;
(7) dyspareunia; and
(8) watery discharge that is dirty gray to purulent.
Pelvic examination reveals:
(1) vaginal epithelium is pale, may observe petechial hemorrhages;
(2) severe thinning of the vaginal epithelium results in a deep erythema of the vagina;
(3) vaginal walls have lost their rugae and are smooth;
(4) fissures are commonly observed on the medial aspect of the labia minora, posterior fourchette, and vestibule; and
(5) synechiae can develop between opposing vaginal walls that have become denuded.
Patients with vaginal atrophy sometimes develop urinary tract infections (UTI) as well as urinary in continence. The postmenopausal woman with urinary incontinence should not be subjected to a comprehensive evaluation of the urinary tract as the initial step in the work-up. The evaluation should begin by obtaining a clean catch urine specimen. If the patient has a copious discharge an evaluation of the vagina should be performed, i.e. physician inspection, determination of the vaginal pH, and microscopic examination of the vaginal discharge. Following completion of the pelvic examination, a lubricated tampon (place estrogen cream on the surface of the tampon) should be inserted into the vagina and the patient asked to provide a clean catch urine specimen. If the patient has atrophic vaginitis, and has copious discharge, the urine specimen will be contaminated by a variety of bacteria from the vagina. Once the specimen has been obtained the tampon should be removed. When evaluating the patient with urinary incontinence the presence of a UTI should be ruled out. If the patient exhibits signs of vaginal atrophy and vaginitis, a trial of estrogen therapy should be administered. If the patient continues to complain of urinary incontinence once the vagina has been restored to a healthy state, a comprehensive evaluation of the lower urinary tract should be conducted.
Treatment of Atrophic Vaginitis
The treatment for vaginal atrophy and atrophic vaginitis is estrogen replacement, administered either orally or intravaginally. Estrogen administered in the form of an intravaginal cream results in plasma concentrations of estrone and estradiol similar that obtained with orally administered estrogen. For this reason, oncologists do not want patients with breast cancer to use estrogen cream administered intravaginally. Initially, the absorption of estrogen from the vagina is low because of the decreased vascularity; however, with continued treatment both the vascularity of the vagina and estrogen absorption increase. Various forms of estrogen that are used for the treatment of vaginal atrophy and atrophic vaginitis (Table Estrogen replacement therapy for treatment of vaginal atrophy and atrophic vaginitis).
Table Estrogen replacement therapy for treatment of vaginal atrophy and atrophic vaginitis
|1. Rings that release 0.2 and 0.5 mg of 17p-estradiol at a constant rate are effective in correcting|
|vaginal atrophy, atrophic vaginitis, and urogenital atrophy|
|2. Estrogen vaginal suppositories, 25 mg|
|3. Estradiol vaginal tablets, 10 and 25 mg|
|4. Transdermal estrogen patch, 12.5 µg per 24 h|
|5. Estrogen secreted from vaginal pessaries, 25 µg|
Selections from the book: “Vaginitis: Differential Diagnosis and Management” (2003).