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Review

Management of Vulvovaginal Disorders in Older Women

April 2021

Abstract

Due to hormonal changes in older women during menopause, the epithelium gets thinned out and causes much vulvar discomfort, which effects their sexual and psychological function. Trained nurses need to be assigned to this population when they are in nursing homes for regular inspection of vaginal area, which can significantly improve quality of life. The objective of this paper is to emphasize the common vulvovaginal problems, other than infections, in older women and their management.

Citation: Ann Longterm Care. 2021;29(2):13-17.
doi: 10.25270/altc.2020.4.00001
Received August 12, 2019; accepted December 5, 2019.
Published online April 13, 2020.

Introduction

Vulvar skin is more sensitive to irritants than other skin sites, a sensitivity enhanced in postmenopausal women through the combination of age and estrogen deficiency. Aging and estrogen deficiency cause epithelial thinning, which results in loss of the skin’s acid mantle. This increases pH and decreases the antimicrobial action of the skin. A decrease in lactobacilli and cell-mediated immunity also occurs, which increases risk of infection. A decrease in lipid production slows healing from injury.1 What is more, because it is close to the rectum and its pathogens, the vulva is prone to infections. In instances of urinary incontinence, the vulva is exposed to ammonia. Clothing and pantyliners can also cause abrasions.

All of these changes in the skin, combined with the anatomical position of vulva, point to the importance of taking care of vulvovaginal symptoms. Yet, too often they are ignored by patients and physicians. Many women would prefer not to discuss vulvovaginal problems with their primary care provider because of embarrassment, and many providers are unfamiliar with appropriate diagnosis and management. 

For most of the vulvar disorders included in this article, symptoms will usually not improve unless addressed. In some cases, symptoms may indicate an increased risk of cancer. Not adequately identifying and treating vulvovaginal symptoms can decrease quality of life, especially in older women residing in nursing care facilities. Vulvar discomfort, especially in women unable to communicate due to dementia, a cerebrovascular event, or another condition, could go undetected for years.

This article reviews and discusses vulvovaginal pathology other than infections and vulvovaginal cancers, providing practical guidance for health care professionals.

Guidance for Diagnosis, Management

Atrophic changes occur in the vulvar region due to aging and can worsen with increased sensitivity to heat, friction, and occlusion. This can lead to multiple symptoms such as dryness, itching, soreness, burning, lesions, and ulceration.

Common symptoms of vulvovaginal disorders are often chronic, and they can significantly interfere with women’s sexual function and well-being (Table 1). Despite the high prevalence and significantly negative impact of vulvar conditions in postmenopausal women, several barriers hinder diagnosis and effective treatment. Older women in nursing homes are at increased risk of vulvovaginitis due to immobilization, estrogen deficiency, and urinary incontinence.2,3 Unfortunately, many of these women cannot report their symptoms effectively for several reasons, including cognitive impairment and an inability to pinpoint the cause of their discomfort. Because of the high prevalence of vulvovaginal infections in this population, a trained nurse should perform vulvar examinations. Unfortunately, there are no guidelines to determine how often vulvar examination should be done. Clinicians should use their discretion to determine how often each individual patient should be examined.4 Though a thorough history and focused examination will provide most of the information needed for diagnosis, clinicians should not hesitate to refer women to vulvar specialists.

Article continues after Table 1

Table 1

The history should explore systemic pathology at other skin areas, along with history of urinary and fecal incontinence, personal or family history of autoimmune or atopic conditions, and drug history, including anticholinergics and recent antibiotics. The workup should include testing for thyroid disease, diabetes, or autoimmune-associated conditions if suspected. Swabs for infection should be considered when symptoms warrant. Visual inspection following acetic acid application can be used. Biopsy is not mandated for every lesion; most are diagnosed clinically. However, if vulvar lesions do not respond to initial treatment or present suspicious pathology, colposcopy-guided biopsy or punch biopsy under anesthesia using a 4-mm Stifel disposable punch should be performed to assist diagnosis and subsequent management.5 

A wide variety of lesions can occur on the vulva, but lesions common in older adults include lichen planus (LP), dermatitis, genitourinary syndrome (vulvovaginal atrophy), and premalignant conditions like lichen sclerosis (LS) and vulvar intraepithelial neoplasia (VIN). 

Lichen Sclerosis

LS is a common vulval condition in postmenopausal woman, affecting one-fourth of women presenting to vulvar clinics.6 LS is an inflammatory dermatosis, involves vulval and perianal skin, and is commonly associated with autoimmune disorders such as hypothyroidism, alopecia, and vitiligo.

Women with LS commonly report intense itching, soreness, and burning. However, women can also be asymptomatic. Clinical signs of LS include porcelain-white plaques and parchment paper-like skin lesions in a figure-of-8 distribution around the vulva and perineum but not extending to the vagina. Erosion, fissures, ecchymoses, and hyperkeratosis appear in active LS. Chronic LS results in loss of architecture that includes loss of labia minora, fusion of the clitoral hood, and introital narrowing, all of which can lead to urethral obstruction. Intense pruritis and characteristic distribution of lesions helps in diagnosing the lesions. In early presentations, biopsy is advised because clinical signs and symptoms change over time.

Topical application of ultrapotent steroids such as clobetasol or halobetasol is used to control inflammation. Topical steroids are typically used once a day for 1 month, on alternate days the next month, and twice a week for the third month. A 30-g tube lasts 3 months to 6 months. If symptoms flare up during the regimen, patients should return to the most effective frequency of application. 

Lesions relapse in 84% of women within 4 years. Once stabilized, vulvar examination is advised every 6 months to 12 months. Biopsy should be considered in nonhealing or nonresponding lesions because there is 4% to 5% increased risk for malignant transformation.7 Calcineurin inhibitors like tacrolimus are second-line treatment, but cancers and lymphomas have been reported in patients using these preparations. Surgery may be considered for complications such as urethral strictures and labial adhesions. Women not responding to primary therapy should receive care from a specialist.

Genitourinary Syndrome 

Genitourinary syndrome of menopause (GSM) was previously known as vulvovaginal atrophy or atrophic vaginitis. It is a chronic, progressive, hypoestrogenic condition with external genital, urological, and sexual implications that affect more than 50% of menopausal women with the condition.8  

Clinical features of GSM are categorized into external genital and urological. Most postmenopausal women report vaginal dryness, but women can also have dyspareunia due to lack of lubrication and vaginal itching, discharge, and pain.9,10 Urologic symptoms include frequency, urgency, dysuria, postvoid dribbling, nocturia, and recurrent urinary tract infections. Clinical features include scant pubic hair, loss of labial fat pad, thinning and resorption of labia minora, and narrowing of the introitus on external examination. Vaginal examination shows pale mucosa with loss of rugae, cervical flush with the vaginal vault, increased pH, and only basal epithelial cells on vaginal cytology. Ultrasound and hysteroscopy assist with diagnosis.8-10

Management of GSM depends on its severity. For mild symptoms and women at risk of estrogen-dependent neoplasia, nonhormonal therapies such as lubricants and vaginal moisturizers are recommended. Water-, oil-, and silicon-based lubricants are available over-the-counter.

Local estrogen therapy (ET) is the preferred treatment when only genitourinary symptoms are present and are unresponsive to nonprescription therapies. Though local ET does not reduce the risk of osteoporosis or manage vasomotor symptoms, up to 90% of women who use it report improvement in symptoms.11 Vaginal tablets, creams, and rings are equally effective, according to the 2006 Cochrane database of systematic reviews.12 Systemic ET is preferred when vasomotor symptoms are also present. Common side effects of systemic ET are breast tenderness, breast enlargement, and vaginal bleeding. Contraindications to ET include known or suspected breast cancer, estrogen-dependent cancers, undiagnosed vaginal bleeding, history of thromboembolism, endometrial hyperplasia, hypertension, hypersensitivity lung disease, and liver disease.

Selective estrogen receptor modulators (SERMs) are synthetic nonsteroidal agents that exert variable mixed estrogen agonist and antagonist effects on target tissues. Ospemifene is the only SERM approved by the Food and Drug Administration (FDA) for the treatment of moderate to severe dyspareunia caused by GSM in menopausal women. Ospemifene can be used by patients with contraindications to ET. When given orally at a dose of 60-mg daily, ospemifene exerts estrogenic effects on vulvovaginal tissues and results in acidic vaginal pH and improvements in the vaginal maturation index and dyspareunia. It increases the risk of thromboembolism similar to ET.

Vaginal dehydroepiandrosterone (DHEA), a steroid prohormone in the biosynthetic pathway of testosterone and estradiol, improves GSM symptoms. It is a safer alternative to vaginal ET in patients with contraindications to estrogen use (eg, breast cancer). Due to the lack of the aromatase enzyme in the endometrium, vaginal DHEA is not converted to estradiol in the endometrium and does not exert any endometrial proliferative effects. Prasterone (Intrarosa) 6.5-mg insert was recently approved by the FDA for the treatment of GSM.

The FDA approved the use of fractional microablative laser therapy for genitourinary surgery. The microablative carbon dioxide laser used for vaginal epithelial resurfacing activates heat shock proteins that, in turn, activate growth factors, resulting in an increase in vascularity, collagen, extracellular matrix production, and thickness of vaginal epithelium. The laser has been shown efficacious and is an alternative to hormone replacement therapy for GSM. The Erbium YAG laser has improved symptoms of GSM with minimal adverse effects, and, compared with estriol, the benefits were more pronounced and longer lasting More research is necessary, however, to further determine safety and long-term outcomes of therapy.13 

Contact Dermatitis

Contact dermatitis can be irritant or allergic in nature and is most commonly seen in women with overwashing, urinary incontinenice, and fecal incontinence. Commonly involved irritants include soaps, antiseptics, disinfectants, and tea tree oil.14,15 Patients typically present with itching, soreness, and burning. Clinical features of contact dermatitis include localized erythema, edema, and erosions. 

The first-line treatment is to remove all irritants and potential allergens. Educate patients about generalized treatment measures, such as using petroleum jelly or other emollients, and avoiding overwashing. Because aqueous creams act like emollient for vulvar skin, they should be replaced with soap.15 Mild to moderate topical steroid ointments are used to reduce inflammation.15 

Lichen Simplex Chronicus 

Intractable itching and scratching during sleep is a typical presentation of lichen simplex chronicus. Due to long-standing nature of the condition, thickening and whitening of the skin occurs. A history of eczema, atopy, and dermatitis assist in diagnosis. 

Educate the patient on generalized vulvar care measures, which include avoiding topical perfumes and preservatives and not overcleaning vulvar skin. Potent steroids are used for the initial 7 to 10 days, then 1% hydrocortisone is used for maintenance therapy for 2 to 3 months.16,17 Sedating antihistamines like hydroxyzine at night help ease itching and stopping the itch-scratch cycle.

Lichen Planus

LP is an inflammatory condition that affects hair, nails, and mucus membranes. LP is much less common than LS and affects both the vulva and vagina, unlike LS, which is confined to the vulva. Three clinical variants of LP can affect the vulva: erosive, papulosquamous, and hypertrophic. Presenting symptoms include soreness, burning, dyspareunia, and increased vaginal discharge. Vulvar LP presents as red, raw, nonspecific erosions involving the mucous membrane of the vestibule and vagina.18 Advanced lesions present with adhesions, synechiae, introital narrowing and scarring overlapping with LS, and severe atrophic vulvovaginitis. LP should be considered in patients who fail to respond to topical steroids for a clinical diagnosis of LS.

Topical potent or ultrapotent steroids are first-line treatment for LP. They are applied daily for 3 months, then tapered. Topical local anesthetic gel can help with discomfort. Due to high chances of scarring, hydrocortisone suppositories with vaginal dilators is recommended. Psychosexual counselling plays a role too, because of LP’s chronic relapsing-remitting nature. Surgery in the absence of active disease is an option for younger or sexually active women who seek to reverse severe scarring. LS and LP are thought to be present simultaneously in some patients with more resistant disease. Topical tacrolimus and oral systemic steroids are common second-line treatments for resistant disease.19,20 There is rare risk of malignant transformation, so follow-up is advised.18 

Vulvar Intraepithelial Neoplasia

VIN encompasses all high-grade squamous lesions. Based on histopathologic features, VIN is classified as usual type or differentiated type.

Usual type VIN is further categorized as basaloid, warty, or mixed type. Usual type VIN is associated with human papillomavirus (HPV), and both smoking and immunosuppression increase the persistence of HPV.19 Incidence of usual type VIN is increasing in younger women due to increased prevalence in HPV. Differentiated type VIN is associated with LS, not HPV. Clinical features of both usual type and differentiated type include unifocal lesions in the form of a plaque or ulcer; sometimes lesions may be flat. Biopsy is required for histopathology.

Treatment is recommended for all women with vulvar high-grade squamous lesions. Wide local excision is preferred; 0.5- to 1-cm margins should be excised. It is difficult if the lesion is in critical areas because excision of the lesion can cause significant psychosexual dysfunction. Women with clear margins have a low recurrence compared with women with positive margins.21

Skinning vulvectomy should be performed only in cases of multifocal lesions. Laser ablation is an option when cancer is not suspected. It can be used for single, multifocal, or confluent lesions, although the risk of recurrence may be higher with laser ablation than with excision.22,23 Topical 5% imiquimod demonstrated effectiveness for the treatment of VIN in some studies but is not yet approved by the FDA.24,25 Topical cidofovir and fluorouracil 5% creams haven been tested with varying results.26,27 Women with complete response to treatment and no new lesions should be assessed at 6 months, and 12 months after initial treatment, with annual visual inspections afterward.

Paget Disease of the Vulva

Paget disease of the vulva is a rare intraepithelial neoplasm of apocrine-bearing skin, with peak incidence at age 65 years. Between 10% and 20% of women with this condition have underlying adenocarcinoma.28 The most common early symptom is pruritus. Clinical features include moderately well-demarcated erythematous patches with white hyperkeratotic areas; in advanced disease, the lesions become plaque-like and desquamative. Distinctive histopathologic features include Paget cells, which are pluripotent epithelial cells. Though invasive disease is rare, there is association with underlying internal malignancies like breast, genito-urinary, and intestinal tract that needs to be excluded.29 

The main mode of treatment is surgical excision, but it is difficult to get clear margins due to multicentric foci in a macroscopically normal epithelium. Laser therapy, radiotherapy, photodynamic therapy, and fluorouracil 5% cream can be used in cases of recurrence if there is no invading disease.30,31 

Vulvodynia

Vulvar discomfort longer than 3 months in absence of any external visible findings or clinically identified neurologic disorder is termed vulvodynia. Clinical diagnosis of vulvodynia is a diagnosis of exclusion. It is classified as provoked or unprovoked, and localized or generalized.

Pain that occurs with light touch at the vaginal vestibule is termed localized vulvodynia, which was previously known as vestibulitis. Unlike localized, which is provoked by touch, generalized vulvodynia is a more constant type of neuropathic pain with an unclear etiology. Treating generalized vulvodynia is difficult. Patients should be educated about the condition and understand that the condition is real despite a lack of physical findings. Treatment should begin with generalized vulvar care, local anesthetics, and low-strength topical steroids, which are generally useful in provoked vulvodynia. Afterward, the patient moves on to systemic treatment. Therapies for neuropathic pain, such as amitriptyline, nortriptyline, gabapentin, or pregabalin, can be used.32,33 The most common therapy is amitriptyline started at 10-mg daily and increased to between 60 and 150-mg daily as side effects permit. Cognitive behavioral therapy and biofeedback to the pelvic floor have had limited success.32,34 

Conclusion

Timely detection and appropriate therapy can prevent progress of vulvovaginal disorders and significantly improve women’s quality of life. Therefore, it is vital for physicians to manage vulvar conditions proactively. Again, clinicians should not hesitate to refer women to vulvar specialists when warranted. 

Affiliations, Disclosures, & Correspondence

Authors: Rohani Manda, MD1 • Nader Tavakoli, MD, CMD, FAAFP1 • Richard Stefanacci, DO, MGH, MBA, AGSF, CMD2 • Nkenna Odom, MD1 • Stacy Ross, MD1 • Tiffany Mapp, MD1

Affiliations: 
1Department of Family Medicine, University of Maryland-Prince George’s Hospital, Cheverly, MD
2EVERSANA ENGAGE™

Disclosures: 
The authors report no relevant financial relationships.

Correspondence:
Nader Tavakoli, MD, CMD, FAAFP
Chair, Dept of Family Medicine
University of Maryland-Capital Region Health
3001 Hospital Dr
Cheverly, MD 20785
Phone: (301) 352-7118
Fax: (301) 352-7779

References

  1. Summers P, Hunn J. Unique dermatologic aspects of the postmenopausal vulva. Clin Obstet Gynaecol. 2007;50:745-751. doi:10.1097/GRF.0b013e3180db96ae
  2. Barber H. Perimenopausal and Geriatric Gynecology. New York, NY: Macmillan Publishing Company; 1988.
  3. Clark A. Gynecological disorders. In: Yoshikawa T, Lipton-Cobb E, Brummel-Smith K, eds. Ambulatory Geriatric Care. St Louis, MO: Mosby;1993:239-248.
  4. Ruiz BA, Tabloski PA, Frazier SM. The role of gerontological advanced practice nurses in geriatric care. J Am Geriatr Soc. 1995;43(9):1061-1064. doi:10.1111/j.1532-5415.1995.tb05576.x
  5. McCullough AM, Seywright M, Roberts DT, Maclean AB. Outpatient biopsy of the vulva. J Obstet Gynaecol. 1987;8(2):166-169. doi:10.3109/01443618709008790
  6. Olsson A, Selva-Nayagam P, Oehler MK. Postmenopausal vulval disease. Menopause Int.  2008;14(4):169-172. doi:10.1258/mi.2008.008030
  7. Smith YR, Haefner HK. Vulvar lichen sclerosus: pathophysiology and treatment. Am J Clin Dermatol. 2004;5(2):105-125. doi:10.2165/00128071-200405020-00005
  8. Gandhi J, Chen A, Dagur G, et al. Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management. Am J Obstet Gynecol. 2016;215(6):704-711. doi:10.1016/j.ajog.2016.07.045
  9. Wines N, Willsteed E. Menopause and the skin. Australasian J Dermatol. 2001;42(3):149-60. doi:10.1046/j.1440-0960.2001.00524.x 
  10. North American Menopause Society. The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of The North AmericanMenopause Society. Menopause. 2007;14(3 Pt 1):355-369; quiz 370-371. doi:10.1097/gme.0b013e31805170eb
  11. Cardozo L, Bachmann G, McClish D, Fonda D, Birgerson L. Meta-analysis of estrogen therapy in the management of urogenital atrophy in postmenopausal women: second report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol. 1998;92(4 Pt 2):722-727. doi:10.1016/s0029-7844(98)00175-6
  12. Lethaby A, Ayeleke RO, Roberts H. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2016;(8):CD001500. doi:10.1002/14651858.CD001500.pub3
  13. Rabley A, O’Shea T, Terry R, Byun S, Louis Moy M. Laser therapy for genitourinary syndrome of menopause. Curr Urol Rep. 2018;19(10):83. doi:10.1007/s11934-018-0831-y
  14. Ball SB, Wojnarowska F. Vulvar dermatoses: lichen sclerosus, lichen planus, and vulval dermatitis/lichen simplex chronicus. Semin Cutan Med Surg. 1998;17(3):182-188. doi:10.1016/s1085-5629(98)80012-6
  15. Margesson LJ. Contact dermatitis of the vulva. Dermatol Ther. 2004;17(1):20-27. doi:10.1111/j.1396-0296.2004.04003.x 
  16. Welsh B, Howard A, Cook K. Vulval itch. Aust Fam Physician. 2004 ;33(7):505-510. 
  17. Welsh BM, Berzins KN, Cook KA, Fairley CK. Management of common vulval conditions. Med J Australia. 2019;178(8):391-395. 
  18. Moyal-Barracco M, Edwards L. Diagnosis and therapy of anogenital lichen planus. Dermatol Ther. 2004;17(1):38-46. doi:10.1111/j.1396-0296.2004.04005.x 
  19. Kirtschig G, Van Der Meulen AJ, Ion Lipan JW, Stoof TJ. Successful treatment of erosive vulvovaginal lichen planus with topical tacrolimus. Br J Dermatol. 2002;147(3):625-626. doi:10.1046/j.1365-2133.2002.488713.x 
  20. Lonsdale-Eccles AA, Velangi S. Topical pimecrolimus in the treatment of genital lichen planus: a prospective case series. Br J Dermatol. 2005;153(2):390-394. doi:10.1111/j.1365-2133.2005.06544.x 
  21. Modesitt SC, Waters AB, Walton L, Fowler WC Jr, Van Le L. Vulvar intraepithelial neoplasia III: occult cancer and the impact of margin status on recurrence. Obstet Gynecol. 1998;92(6):962-966. doi:10.1016/s0029-7844(98)00350-0 
  22. Sideri M, Spinaci L, Spolti N, Schettino F. Evaluation of CO2 laser excision or vaporization for the treatment of vulvar intraepithelial neoplasia. Gynecol Oncol. 1999;75(2):277-281. doi:10.1006/gyno.1999.5584 
  23. Reid R. Superficial laser vulvectomy. III. A new surgical technique for appendage-conserving ablation of refractory condylomas and vulvar intraepithelial neoplasia. Am J Obstet Gynecol. 1985;152(5):504-509. doi:10.1016/0002-9378(85)90616-7
  24. van Seters M, van Beurden M, ten Kate FJ, et al. Treatment of vulvar intraepithelial neoplasia with topical imiquimod. N Engl J Med. 2008;358(14):1465-1473. doi:10.1056/NEJMoa072685
  25. Mathiesen O, Buus SK, Cramers M. Topical imiquimod can reverse vulvar intraepithelial neoplasia: a randomised, double-blinded study. Gynecol Oncol. 2007;107(2):219-222. doi:10.1016/j.ygyno.2007.06.003 
  26. Sillman FH, Sedlis A, Boyce JG. A review of lower genital intraepithelial neoplasia and the use of topical 5-fluorouracil. Obstet Gynecol. Surv. 1985;40(4):190-220. doi:10.1097/00006254-198504000-00002
  27. Tristam A, Fiander A. Clinical responses to Cidofovir applied topically to women with high grade vulval intraepithelial neoplasia. Gynecol Oncol. 2005;99(3):652-655. doi:10.1016/j.ygyno.2005.07.127
  28. Fanning J, Lambert HCL, Hale TM, Morris PC, Schuerch C. Paget’s disease of the vulva: prevalence of associated vulvar adenocarcinoma, invasive Paget’s disease, and recurrence after surgical excision. Am J Obstet Gynecol. 1999;180(1):24-27. doi:10.1016/s0002-9378(99)70143-2 
  29. ACOG Practice Bulletin No. 93: Diagnosis and management of vulvar skin disorders. Obstet Gynecol. 2008;111(5):1243-1254. 
  30. Moreno-Arias GA, Conill C, Castells-Mas A, Arenas M, Grimalt R. Radiotherapy for genital extramammary Paget’s disease in situ. Dermatol Surg. 2001;27(6):587-590. doi:10.1046/j.1524-4725.2001.00304.x
  31. Shieh S, Dee AS, Cheney RT, Frawley NP, Zeitouni NC, Oseroff AR. Photodynamic therapy for the treatment of extramammary Paget’s disease. Br J Dermatol. 2002;146(6):1000-1005. doi:10.1046/j.1365-2133.2002.04801.x
  32. Haefner HK, Collins ME, Davis FD, et al. The vulvodynia guideline. J Low Genit Tract Dis. 2005;9(1):40-51. doi:10.1097/00128360-200501000-00009
  33. Reed BD. Vulvodynia: diagnosis and management. Am Fam Physician. 2006;73(7):1231-1238. 
  34. Gunter J. Vulvodynia: new thoughts on a devastating condition. Obstet Gynecol Surv. 2007;62(12):812-819. doi:10.1097/01.ogx.0000290350.14036.d6

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