Atrophic vaginitis is defined as inflammation of the vaginal epithelium due to atrophy secondary to decreased levels of circulating estrogen. The features of this disease are estimated to be seen in 15% of premenopausal and 50% menopausal women. Patients present with the symptoms of vaginal dryness, itching, irritation, and dyspareunia. Diagnosis of atrophic vaginitis requires subjective assessment of the severity of symptoms to be correlated with the physical examination findings. The prominent physical examination findings include atrophic vaginal or vulvar tissue, pale, smooth and shiny vaginal epithelium with increased friability and inflammation with patchy erythema. The characteristic findings to confirm the diagnosis are: a left shift of the vaginal maturation index on a vaginal smear and a alkaline pH of the vagina. However, other secondary causes such as lichen sclerosus and lichen planus must be ruled before the confirmation of the diagnosis. The therapeutic management is based on the severity of the symptoms: lubricants are the first line of therapy for mild symptoms, in patients unresponsive to lubricants and with moderate to severe symptoms topical or oral estrogen therapy is effective for the management of patients . Majority of the patients have resolution of symptoms but due to the chronic nature of the condition it requires continuous treatment.
In 1898, Charles B. Penrose described vaginitis in elderly women as senile Vaginitis. The areas of patchy inflammation were treated with 5% silver nitrate solution.[1]
In 1940, Jacob described the use of vaginalpH in determination of hypoestrogenic state.[2]
In 1947, Racoff gave a description the efficacy and safety of a synthetic estrogen, dienestrol for the treatment of menopausal syndrome and atrophic vaginitis is described.[3]
In 1963, topical Dinesterol vaginal cream was used for the treatment of senile vaginitis.[4]
In 1967, the relationship between the vaginal maturation index and estrogen therapy was described.[5]
In 2013, vulvovaginal atrophy is renamed as genitourinary syndrome of menopause.[6]
Cytology of the vaginal cells show an increase in the parabasal cells and decreased superficial cells. In situations of low estrogen levels the vaginal epithelium ceases to produce superficial and intermediate squamous cells, leaving only the parabasal and basal cells lining the vaginal wall.[12]
Atrophic vaginitis is characterized with pale dry vaginal epithelium and increased pH. This predisposes the patients to recurrent vaginal infections with common pathogens such as candida, gardnerella vaginalis and trichomonas, therefore it is essential to rule out these infections.
Atrophic vaginitis is caused by any condition that may lead to decreased circulating estrogen levels. A hypoestrogenic state may be due to ovarian failure or other causes:[8]
Atrophic vaginitis is often an underdiagnosed condition and exact prevalence estimation is difficult because of the following reasons:
Majority of women are embarrassed to discuss their symptoms with doctors and few others think the symptoms associated with atrophic vaginitis as a process of natural aging.[14]
Only 25% of patients with symptoms seek medical care.[15]
The features of atrophic vaginitis are estimated to be seen in 15% of premenopausal women and 40-54% of post-menopausal women.[17]
Based on self-reported symptoms of vaginal dryness, the prevalence of atrophic vaginitis ranged from 4% to 47%, depending on the stage of menopause (early or late menopause).[9]
The risk factors associated with vaginal atrophy are related to decreased estrogen levels, which can be due to menopause (most common cause) or other causes that may lead to hypoestrogenism or vaginal atrophy. These include:[8]
There are no screening recommendations for atrophic vaginitis.[18]
Differentiating atrophic vaginitis from other diseases[edit | edit source]
Atrophic vaginitis must be differentiated from other disease processes that may present with similar symptoms. These can be divided into 4 categories:[9][8]
Presents with purulent, malodorous, thin discharge associated with burning, pruritus, and dysuria, with the signs of vaginal inflammation and elevated vaginal pH (>4.5)
Atrophic vaginitis is a chronic progressive medical problem affecting postmenopausal women and in younger women with low estrogen levels. Women present with vaginal dryness, pruritus, urinary disturbances and dyspareunia.[34]
Atrophic vagnitis is a chronic disease and requires continuous treatment with estrogen or other alternatives. Majority of the patients have significant resolution of the symptoms with treatment, however the symptoms recur once the treatment is stopped.[35]
Physical examination in women with atrophic vaginitis includes a general inspection of the external genitalia, a speculum examination.[10][21]
Physical examination in women with atrophic vaginitis begins with inspection of the external genitalia. Findings include sparsity of pubic hair, dryness of the labia and/or fusion of the labia minora.
Gynecologic examination is carried using a small speculum to avoid damage to the atrophic vaginal or vulvar tissue. Vaginal epithelium may be atrophic and appear pale, smooth and shiny. Other findings include increased friability, inflamed epithelium with patchy erythema and petechiae.
Vaginal Cytology: It demonstrates a decrease in the superficial squamous cells and an increased parabasal cells.[12]
Vaginal Maturation Index(VMI): It represents the percentage of the parabasal, intermediate and superficial squamous cells. It read from left to right as follows, for example if its represented as 0/35/65-it means the smear has 0% parabasal cells, 35% intermediate cells and 65% superficial cells. A shift to the left indicates vaginal atrophy.[38]
Vaginal Maturation Value (VMV): It is calculated using a formula: 0 * %parabasal cells + 0.5 * %intermediate cells + 1.0 * superficial cells divided by 2.
A lower VMV indicates a low number of superficial cells indicating hypoestrogenic state.[39]
Vaginal pH : Normal vaginal pH is acidic and is maintained by the lactobacillus flora by the breakdown of glucose (from the vaginal epithelial cell glycogen-the level of which is based on the estrogen) to lactic acid.
In lower estrogen states, the vaginal pH is typically greater then 5; higher than normal due to lower levels of glycogen in the epithelial cells. It is a useful and inexpensive test in the absence of bacterial vaginosis to indicate vaginal atrophy.[40]
FSH Level: Estimation of FSH is not neccessary for the diagnosis of hypoestrogenic state as alkaline pH of vaginal secretions is equally sensitive.[41]
Atrophic vaginitis is a chronic condition requiring continuous treatment. The choice of therapy is based on the severity of the symptoms and associated factors such as history of hormone dependent cancer. [42][43]
In patients with mild symptoms, the vaginal lubricants are the first line therapeutic choice to relieve symptoms.[44]
In patients with moderate to severe symptoms unresponsive to lubricants, the topical estrogen or oral estrogen therapy is preferred. In patients with menopause, the topical agents are preferred over systemic therapy.
In patients with the history of harmone dependent cancer, discuss the risks and benefits with the patient and the oncologist before initiation of therapy.
Progesterone is not indicated in patients with topical low dose estrogen therapy, however endometrial safety studies are lacking in this group who receive treatment greater than a year.
The following behavioral changes are advised to slow down the progression of atrophic vaginitis, and also help in maintenance of normal vaginal tissue:[66]
Encouraging sexual activity helps in the maintenance of vaginal elasticity and lubrication in response to sexual stimulation.
Stress reduction therapy is helpful in patients with non-organic causes of vaginal dryness.
↑Beilly, Jacob S. (1940). "DETERMINATION OF PH OF VAGINAL SECRETION AS AN INDEX OF OVARIAN ACTIVITY IN HYPOOVARIAN STATES". Endocrinology. 26 (6): 959–964. doi:10.1210/endo-26-6-959. ISSN0013-7227.
↑Rakoff, A. E.; Paschkis, K. E.; Cantarow, A. (1947). "A CLINICAL EVALUATION OF DIENESTROL, A SYNTHETIC ESTROGEN1". The Journal of Clinical Endocrinology & Metabolism. 7 (10): 688–700. doi:10.1210/jcem-7-10-688. ISSN0021-972X.
↑Falk, Henry C.; Hassid, Roger (1963). "ATROPHIC OR SENILE VAGINITIS: TREATMENT WITH DIENESTROL CREAM". Journal of the American Geriatrics Society. 11 (12): 1152–1157. doi:10.1111/j.1532-5415.1963.tb02686.x. ISSN0002-8614.
↑ 8.08.18.28.38.48.58.68.78.8Gandhi J, Chen A, Dagur G, Suh Y, Smith N, Cali B, Khan SA (2016). "Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management". Am. J. Obstet. Gynecol. doi:10.1016/j.ajog.2016.07.045. PMID27472999.
↑Lewis, F. M. (2015). "Vulval symptoms after the menopause - Not all atrophy!". Post Reproductive Health. 21 (4): 146–150. doi:10.1177/2053369115608019. ISSN2053-3691.
↑ 17.017.1DiBonaventura, Marco; Luo, Xuemei; Moffatt, Margaret; Bushmakin, Andrew G.; Kumar, Maya; Bobula, Joel (2015). "The Association Between Vulvovaginal Atrophy Symptoms and Quality of Life Among Postmenopausal Women in the United States and Western Europe". Journal of Women'sHealth. 24 (9): 713–722. doi:10.1089/jwh.2014.5177. ISSN1540-9996.
↑ Centers for Disease Control and Prevention. 2015 Sexually Transmitted Diseases Treatment Guidelines. Bacterial Vaginosis. http://www.cdc.gov/std/tg2015/bv.htm Accessed on October 13, 2016
↑van der Linden, M.; Meeuwis, K.A.P.; Bulten, J.; Bosse, T.; van Poelgeest, M.I.E.; de Hullu, J.A. (2016). "Paget disease of the vulva". Critical Reviews in Oncology/Hematology. 101: 60–74. doi:10.1016/j.critrevonc.2016.03.008. ISSN1040-8428.
↑"Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN1072-3714.
↑"Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN1072-3714.
↑Woods NF, Mitchell ES (2005). "Symptoms during the perimenopause: prevalence, severity, trajectory, and significance in women's lives". Am. J. Med. 118 Suppl 12B: 14–24. doi:10.1016/j.amjmed.2005.09.031. PMID16414323.
↑Simon, James A.; Kokot-Kierepa, Marta; Goldstein, Jeffrey; Nappi, Rossella E. (2013). "Vaginal health in the United States". Menopause. 20 (10): 1043–1048. doi:10.1097/GME.0b013e318287342d. ISSN1072-3714.
↑Weber, M. A.; Limpens, J.; Roovers, J. P. W. R. (2014). "Assessment of vaginal atrophy: a review". International Urogynecology Journal. 26 (1): 15–28. doi:10.1007/s00192-014-2464-0. ISSN0937-3462.
↑"Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN1072-3714.
↑Holmgren PA, Lindskog M, von Schoultz B (1989). "Vaginal rings for continuous low-dose release of oestradiol in the treatment of urogenital atrophy". Maturitas. 11 (1): 55–63. PMID2498619.
↑Palacios, Santiago; CasteloBranco, Camil; Currie, Heather; Mijatovic, Velja; Nappi, Rossella E.; Simon, James; Rees, Margaret (2015). "Update on management of genitourinary syndrome of menopause: A practical guide". Maturitas. 82 (3): 308–313. doi:10.1016/j.maturitas.2015.07.020. ISSN0378-5122.
↑Willhite, Laurie A.; O'Connell, Mary Beth (2001). "Urogenital Atrophy: Prevention and Treatment". Pharmacotherapy: Official Journal of the American College of Clinical Pharmacy. 21 (4): 464–480. doi:10.1592/phco.21.5.464.34486. ISSN0277-0008.
↑"Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN1072-3714.