With the cessation of ovarian follicular activity at the menopause, blood estrogen levels become much lower than during normal reproductive life. This decrease has just as an important effect upon the vulvar and vaginal tissues as upon the uterine lining. This is a normal physiologic process and, in the early stages, may give rise to no subjective manifestations, although it can usually be observed clinically as a general shrinking in the caliber of the vaginal canal, with shortening of the fornices. The rugae become less prominent, and the epithelium is of a pale rather than a rosy hue and is increasingly friable. Cracking, vulvar itching, dyspareunia, and postcoital bleeding may be early signs of estro- gen loss. Because the vagina normally harbors many different pathogenic bacteria in a quiescent state, as the result of estrogen deﬁciency the progressive decrease in the resistance of the vaginal epithelium often leads to inﬂammation and an increased risk of infection. There is a change in vaginal pH toward the alkaline as the normal vaginal ﬂora are lost.
The histology of the vagina after the menopause is characterized by a thin superﬁcial epithelium. In the subepithelium is found a diffuse inﬁltration of both polymorphonuclear leukocytes and lymphocytes. The stroma is edematous. Correspondingly, the smear from the postmenopausal vagina shows cells typical of complete atrophy, with a heavy inﬂux of polymorphonu-clear leukocytes.
The clinical picture of atrophic vaginitis is quite characteristic. The vagina is narrowed, especially near the apex, making visualization of the cervix difﬁcult. The thin epithelium is covered with numerous small petechial hemorrhages; in some areas, these have coalesced with breakdown of the superﬁcial epithelium and the formation of small ulcerations. The epithelium around the hemorrhages and denuded areas exhibits marked pallor and almost complete absence of rugae. A thin, pale, malodorous, and irritating discharge is usually present. Clinically, the condition may be con- fused with a Trichomonas infection, and infestation with
T. vaginalis is not infrequently superimposed upon senile vaginitis. Almost any type of bacterial organism may be involved, and the infection is usually mixed.
As the condition advances, attempts at regeneration and repair lead to the formation of adhesions, which at ﬁrst are ﬁlmy and friable but which eventually become ﬁrm and ﬁbrous and may occlude a part or the entire vagina. A speculum view of this type of case is seen in the middle of the plate, with trabecular adhesions running across the upper vagina, like stalactites, completely obliterating the canal and obscuring the cervix. Signiﬁcant atrophic vaginitis, both in the early and in the late stage, may lead to postmenopausal bleeding and is one of the commonest causes of this symptom.
In the milder forms, a pinkish discharge may result from chaﬁng of denuded areas, whereas in the advanced stage, rupture of one of the adhesions as a result of trauma may result in profuse hemorrhage. The latter is to be particularly avoided during pelvic examinations on elderly women or in the course of a vaginal prepara- tion for an operative procedure. A tear of one of these adhesions may extend upward into the broad ligament and cause direct injury to the uterine vessels.
Therapy consists of estrogen replacement, either topically or systemically. Care must be exercised with topical therapy in these patients, for up to 25% of estrogen placed in the vagina may be absorbed into the circulation. This amount may be even greater for patients with atrophic changes. Continuous estrogen exposure without periodic or concomitant progestins increases the risk of endometrial carcinoma six- to eightfold when the uterus is present.