Current Geriatrics Reports

https://doi.org/10.1007/s13670-020-00332-8

INVITED COMMENTARY

Geriatric Vulvar Dermatology

Nga Nguyen 1 & Sarah Corley 2

Accepted: 26 October 2020

# Springer Science+Business Media, LLC, part of Springer Nature 2020

Abstract
Purpose of Review The purpose of this review is to provide the diagnosis and management of inflammatory vulvar dermatoses in
the geriatric population. The increasing geriatric population in the USA necessitates informing a broad base of healthcare
providers on this topic.
Recent Findings In the elderly, there are increasing case reports of contact dermatitis due to sanitary napkins, incontinence pads,
and over the counter medications. Superimposed vulvovaginal candidiasis and lichen simplex chronicus can occur simultaneous-
ly with the primary vulvar disease. The limited research specific to geriatric populations confirms the current state of vulvar
dermatosis underdiagnosis.
Summary In order to close the gaps in diagnosis and treatment of vulvar dermatoses, providers should carefully review the
patient’s medical history and complete a physical examination of the genitoanal area for asymptomatic and symptomatic elderly
women. Prompt, consistent treatment can vastly improve the patient’s quality of life and is critical to preventing the advancement
of lesions to squamous cell carcinoma in conditions that incur this increased risk such as lichen sclerosus and lichen planus.

Keywords Geriatric . Vulvar dermatoses . Contact dermatitis . Lichen planus . Lichen sclerosus . Vulvovaginal candidiasis

Introduction Negative stigmatization of sexual activity may foster feelings

In this review, we will outline the critical components of di-
agnosis and management of common inflammatory vulvar
dermatoses in the geriatric population. This group is generally
defined as individuals greater than the age of 65 years old. The
geriatric population is expected to comprise 20% of the total
US population by 2030 [1]. Primary care providers, gynecol-
ogists, and dermatologists are the main interfaces for geriatric
patients to seek care for vulvar complaints [2].
Despite the number of providers that can assist with vulvar
dermatoses, there is still underdiagnosis or misdiagnosis of the
vulvar condition. Patients can be reluctant to share their con-
cern with providers due to anxiety and embarrassment [3].
This article is part of the Topical Collection on Dermatology and Wound
Care
* Sarah Corley
sarah_corley@med.unc.edu
1
University of North Carolina at Chapel Hill School of Medicine,
Chapel Hill, USA
2
University of North Carolina at Chapel Hill Department of
Dermatology, 410 Market Street, Suite 400, Chapel Hill, NC 27516,
USA
of “guilt” and “shame” that prevent patient’s from seeking the
necessary medical treatment for dysfunction [4]. Cervical can-
cer screening allows us to systematically screen for
vulvovaginal conditions without requiring the patient to ver-
bally express their discomfort, but this process is recommend-
ed to end at the age of 65 [5]. The US Preventive Service Task
Force determined cervical cancer screening for women past
the age of 65 did not provide a positive net benefit if they
received appropriate prior screenings [5]. The cervical screen-
ing process may be stopped even earlier in patients who have
received a total hysterectomy [5].
Pruritus is a common symptom across many vulvar dis-
eases that is often misdiagnosed as vulvovaginal candidiasis
[2]. Providers treat the symptom with antifungals without di-
rectly examining the vulva [2]. In approaching a patient with a
vulvar complaint, it is crucial to conduct a full physical exam
[3, 6]. The disease can have manifestations in areas of the
body other than the anogenital areas and identifying these
specific involvements can lead to earlier diagnosis. No single
medication can serve as a treatment plan for all patients. The
treatment plan must follow a phased approach with continu-
ous assessment of the patient’s clinical progress or symptom
relief. Expeditious treatment is important for improving the
quality of life in patients with vulvar dermatoses and

decreasing the risk of squamous cell carcinoma in lichen
sclerosus and lichen planus.
Vulvar Anatomy
The vulva is the external layer of the female genitalia [6]. The
border of the vulva extends anteriorly from the mons pubis to
the posterior commissure or fourchette posteriorly [6]. The
lateral borders are from the genitocrural folds to the hymenal
ring medially [6]. The vulva comprises major structures in-
cluding the clitoral hood, clitoris, outer labia, inner labia, and
vestibule (introitus) [6]. Hart’s line is an anatomic marker that
separates the medial aspect of the labia minora and the mucous
membranes of the vestibule [6]. Figure 1 details the normal
external female genitalia. Normal variations of the vulva in-
clude differences in size, shape, pigmentation, and symmetry.
These changes are dependent on age, hormonal status, and
ethnicity. Special consideration should be given when exam-
ining patients with darker complexion as it may disguise ery-
thema commonly seen in inflammatory skin conditions [7].
From childhood to adulthood, the normal vulvar changes
expected during pubertal development include fat deposition
of the mons pubis and labia majora, prominence of the clitoris,
thickening of the epithelium, and pubertal hair growth.
Reversal of these features can be observed during the meno-
pausal period. The decrease in estrogen leads to vaginal atro-
phy, graying of pubic hairs, and decrease in vaginal secretions
[8]. Genitourinary syndrome of menopause (GSM) consists of
a constellation of symptoms secondary to postmenopausal
changes from low estrogen levels [9]. This condition is prev-
alent in 40–54% of postmenopausal women [9]. Treatment for
GSM is estrogen therapy and can restore the vaginal epitheli-
um and secretions reducing symptoms related to sexual dis-
comfort, urological complications, and external genital
Fig. 1 Normal female external
genitalia (Printed with copyright
permission from John Wiley &
Sons – Books) [6]
Curr Geri Rep
changes [9]. Treatment with estrogen therapy should be con-
sidered in postmenopausal women with genitoanal skin dis-
ease as GSM often co-exists with the inflammatory vulvar
diseases discussed herein. Without treatment of GSM, the
patient may still experience bothersome symptoms that are
falsely attributed to ineffective treatment of the dermatologic
condition. Not all vulvar conditions can be attributed to attri-
tion and diagnosis requires a thorough clinical exam, pertinent
history gathering, and further diagnostic tests including saline
microscopy of vaginal secretions to evaluate the maturity of
the vaginal epithelium.
Lichen Planus
Lichen planus is a chronic inflammatory condition of undeter-
mined etiology that can affect the skin, oral mucosa, and
anogenital area [10, 11, 12•, 13, 14]. Approximately 1% of
the population has oral lichen planus and 10 to 51% of women
who are diagnosed with oral lichen planus may also present
with vulvovaginal disease [11, 13, 15]. The wide range in
incidence may be due to differences in provider awareness
of this skin disease. The average age of onset is within the
4th and 5th decades of life [16].
Lichen planus can have more than one subtype present with
the most common being classic cutaneous lichen planus, hy-
pertrophic, and erosive [16]. The most common subtype in
anogenital lichen planus is the erosive subtype. Erosive lichen
planus presents as erythema and erosions that can extend into
the vagina and perianal regions [10, 13]. The classic purple
papules of lichen planus are seen on the hair-bearing portion
of the vulva in only 3–5% of vulvovaginal lichen planus cases
[10, 17–19]. Up to two-thirds of patients with erosive lichen
planus can have oral involvement; therefore, clinical diagnosis
can be facilitated by examining the oral mucosa for lichen
Curr Geri Rep
planus involvement evidenced by white, reticulate, lacy,
plaques on the buccal mucosa or gingiva [10, 13].
The erosive lesions can lead to symptoms including
pain, burning, irritation, and sensation of rawness [10].
Without treatment, these lesions can transition to areas
of scarring and over time cause agglutination of the labia,
burying of the clitoral hood, and narrowing of the
introitus [10]. This can lead to dyspareunia, anxiety, ex-
ercise limitations, clothing irritation, and difficulty with
urinary outflow obstruction due to stenosis. Treatment is
focused on controlling the disease and symptoms as there
is no cure. Erosive lichen planus is difficult to treat and
therapy often requires trial and error [10]. First-line ther-
apy for erosive lichen planus is a potent or ultra-potent
corticosteroid [10]. Ointments are recommended for the
genital area to reduce the risk of burning and irritation
upon placement [10]. Initial therapy with systemic ste-
roids followed by transition to topical corticosteroids can
be used for patients with severe disease [10]. The topical
calcineurin inhibitors, tacrolimus and pimecrolimus, are
considered second line of therapies. [20]. In a case series
of 16 patients who failed other therapy regimens for the
treatment of lichen planus, 94% of patients showed symp-
tomatic improvement within 3 months after use of tacro-
limus ointment [20]. Otherwise, systemic immunomodu-
latory therapy should be offered after failing topical treat-
ments with corticosteroids and calcineurin inhibitors.
Lichen Sclerosus
Lichen sclerosus is an inflammatory skin disease of un-
known etiology [21]. One study reported 10% of patients
having family members with the same condition, reveal-
ing the potential for a genetic component to the disease
[11]. While it does have a bimodal distribution with the
first peak in childhood, it is most often diagnosed in
older, postmenopausal women with an onset in the mid
to late 50s [11, 13, 21, 22]. The estimated prevalence of
lichen sclerosus in women over the age of 80 years old is
3% [11]. Lichen sclerosus often affects the vulva, perine-
um, and perianal skin in a classic figure eight distribution,
though other areas of the body can be affected as well
[13, 21]. Figure 2 is an image of the classic presentation
of lichen sclerosus.
Patients with lichen sclerosus present most commonly with
pruritus that may be severely life disrupting [21, 22]. Vulvar
examination shows a well-defined, porcelain white plaque
with an atrophic wrinkled appearance similar to “cigarette
paper” [21, 22]. Lichen simplex chronicus can be
superimposed on the lesion due to continuous scratching to
relieve pruritus. Thus, as with many of vulvar cases, there may
be two co-existing diagnoses. In the advanced stages, scarring
Fig. 2 Image of vulvar manifestation of lichen sclerosus. Appearance of
white atrophic plaques with mild peripheral erythema extending from the
labia majora to the medical buttocks. (Courtesy of Dr. Sarah Corley,
Chapel Hill, NC)
leads to vulvar anatomy distortion with labia minora resorp-
tion, clitoral phimosis, and introital stenosis [11, 21]. It is
important to note that patients may be asymptomatic and li-
chen sclerosus can be an incidental finding found on routine
exams [21, 22]. Appearance is not correlated with symptom
severity [21, 22]. Patients should be educated regarding a 2 to
6% risk in progression to squamous cell carcinoma requiring
long-term follow-up to monitor disease progression even if
they are asymptomatic and have normal vulvar architecture
[21, 22]. Treatment for lichen sclerosus begins with an induc-
tion phase that can last up to a year followed by lifelong
maintenance treatment [21, 22]. The mainstay of treatment
for remission of lichen sclerosus is ultrapotent topical cortico-
steroids [21, 22]. Consistent use of a topical corticosteroid
individualized to the patient following remission can preserve
normal skin color and texture in addition to relief of pruritus
[21, 22]. Additional control of pruritus and reduction in
scratching of the area can be achieved with a sedating hista-
mine at night. Providers should emphasize the importance of
treatment adherence to achieve optimal resolution of symp-
toms [23••].
Lichen planus and lichen sclerosus can be diagnosed in
a patient simultaneously. They can have similar clinical
appearances depending on subtype and may require biop-
sy to differentiate. Lichen sclerosus biopsies should be
taken from the mostly dense white area [21, 22]. Lichen
planus biopsies should be taken from the edge of an ero-
sion [10]. The increased scarring in each disease process
leads to vulvar architectural changes and an increased risk
in development of skin cancer. Prompt treatment and
long-term follow-up are necessary to minimize the risk
of squamous cell carcinoma and architectural changes of
the vulva in both conditions.
 Curr Geri Rep

Allergic Contact Dermatitis
The vulva is particularly prone to allergic contact dermatitis
(ACD) due the nature of the location. Barrier dysfunction
allows exposures to potential allergens. Additionally, many
women are embarrassed to seek medical help and thus per-
form self-treatments with over the counter or at home reme-
dies. Allergic contact dermatitis is a delayed hypersensitivity
reaction. On the first contact, the sensitization occurs, and on
subsequent contacts, the hypersensitivity reaction takes place.
While the exact incidence is unknown, several studies have
shown a high rate of allergic contact dermatitis in patient with
dermatitis of the vulva. A review of patients presenting with
vulvar symptoms at the Mayo Clinic showed that of 90 pa-
tients, 39% experienced positive patch tests which were
deemed relevant [24]. The Oxford vulva clinic in the UK
found 43% of patients with vulvar dermatitis had positive
patch test results for allergens [25]. In older patients, greater
than the age of 70, this prevalence of positive patch testing
increases to 62% compared to 32% in patients younger than
the age of 70 [25]. Disruptions in barrier function due to in-
creased urinary incontinence and decreased estrogen in post-
menopausal women reduces the protection from potential
allergens or irritant [25]. The most common allergens impli-
cated in allergic contact dermatitis of the vulva are listed in
Table 1.
The most common allergens are associated with medica-
tions, fragrances, and preservatives [25]. Convenient access
and self-treatment with over the counter medications increase
exposure to products associated as an allergen including ben-
zocaine, corticosteroids, and antibiotics [7, 25]. Vagisil and
sometimes antihemorrhoidal creams contain benzocaine [7].
Among patients diagnosed with anogenital ACD, 12.5% of
patients had reactions to benzocaine [25]. Benzocaine also
cross-reacts with specific dyes or sulfa drugs [7]. Verifying
the patient’s history for allergies to hair dyes or sulfa can
support clinical suspicion for ACD to benzocaine [7, 25].
Corticosteroids are another class of topical medications that
is a potential anogenital allergen [25]. The sensitization rate
ranges from 1.1 to 3.3% and develops over time due to long-
term use for treatment of other genital conditions [25]. If treat-
ment with corticosteroids worsens the condition, ACD due to
steroid use may be considered [25].
In elderly patients, use of absorbent disposable underwear
for incontinence and wipes are two major sources of ACD.
Fragrance Mix I and Balsam of Peru are two fragrances that

Table 1 Common vulvar allergens [2, 24, 26–32]

Topical Local anesthetics Benzocaine, dibucaine, tetracaine, lidocaine

medications

Corticosteroids
Antibiotics Neomycin, bacitracin, clindamycin
Antifungals Terconazole
Vehicle components Propylene glycol, lanolin
Fragrance Cosmetics Fragrance I/II, Balsam of Peru, cinnamic alcohol, tolu balsam, hydroxyisohexyl
Perfumes/sprays 3-cyclohexane carboxaldehyde, hydroxycitronellal, eugenol
Toilet paper
Wipes
Shave cream
Sanitary pads/incontinence pads
Lubricants
Preservatives Cosmetics Methylisothiazolinone, methylchloroisothiazolinone, formaldehyde,
Lotions/creams quaternium-15, DMDM hydantoin, thimerosal, benzalkonium chloride, methyl
Soaps/shampoos dibromo glutaronitrile, benzoic acid, butylhydroyanisole, parabens, bronopol,
ethylenediamine, chlorocresol
Wipes
Sanitary pads/incontinence pads
Medications
Adhesives/resin Sanitary pads/incontinence pads Acrylates, colophony
Rubber Condoms Tetramethylthiuram disulfide, mercaptobenzothiazole, diphenylguanidine, thiuram
accelerators Catheters mix, latex
Pessaries
Textiles Undergarments and clothing Disperse blue, disperse orange 3, paraphenylenediamine, PABA
Spices and Personal care products, food products with hand Primin, peppermint oil, nutmeg, coriander, curry powder, onion powder,
herbs to genital contact or excretion in feces chamomile, arnica, propolis, jojoba oil, jasmine
Curr Geri Rep
can be found in incontinence pads and are responsible for
genital ACD in up to 20% of patients [25]. Dryness of the
vaginal area may lead to increased frequency of wipes for
comfort as compared to toilet paper. Increasing case reports
of allergic contact dermatitis to wipes or moist toilet paper are
published in the literature. Within a 6-month period, one in-
stitution found 4 adult patients with allergic contact dermatitis
caused by methylchloroisothialzolione/methylisothialozlione
(MCI/MI) [33]. All four cases reported seeing numerous pro-
viders and misdiagnosis including psoriasis and pityriasis
rubra pilaris prior to seeing a dermatologist who recommend-
ed patch testing [33]. This theme is challenging for patients
and can lead to a decrease in quality of life as treatments fail to
improve their persistent symptoms.
Patients with ACD often present with a chief complaint of
pruritus [7]. The exam may demonstrate erythema, edema,
vesicles, or bullae with weeping in the acute and subacute
stages. These lesions are present in the vulva and can extend
into the perianal area [33]. Over time, they can develop into
scaling plaques with erythema, hyperpigmentation, and
lichenification as seen in cases of more chronic ACD [7,
25]. The first step to diagnosis includes a discussion of the
patient and their partner’s personal product use. To increase
the sensitivity of patch testing results, selection of patch-
testing options should be guided by the discussed history.
Products to specifically inquire about include cosmetics, over
the counter products, prescribed medications, foreign prod-
ucts, spices, alternative medicine preparations, sanitary/
incontinence pads, hygiene wipes, cleansers, lubricants, and
undergarment materials [25]. Treatment requires avoidance of
suspected allergens and those confirmed through patch test-
ing. Prior to patch testing results, discontinuation of any elec-
tive topical products and conversion to products with less dye
and free of fragrance should be recommended. Patch testing
can also inform which topical treatments are appropriate for
treatment of ACD [25].
Irritant Contact Dermatitis
Of all cases of contact dermatitis, the majority is due to irritant
contact dermatitis (ICD). Although ICD is a common disease,
the exact incidence of vulvar involvement in the geriatric pop-
ulation is unknown [34]. Similar to allergic contact dermatitis,
barrier dysfunction is a mechanism that allows the vulva to be
more prone to irritants leading to acute or chronic ICD [35].
Unlike allergic contact dermatitis, ICD results from direct cy-
totoxic damage without prior sensitization [34]. Acute ICD is
caused by exposure to a strong irritant through avenues such
as contamination of skin and clothes or direct application [35].
Chronic exposure to irritants occurs more frequently and
symptoms tend to develop after skin damage has exceeded
an individualized threshold [35]. This threshold is lowered
in incontinent women due to increased skin moisture resulting
in increased penetration of irritants into the skin [34, 36].
Other threshold lowering factors include friction and obesity
[34].
External factors for irritant contact dermatitis include over
the counter products ranging from cosmetics to medications.
Common vulvar irritants include skin care products, personal
cleanliness products, and deodorants [34]. Excessive washing
practices by patients to reduce odor and infection fall under
the category of physical vulvar irritants and is worsened with
use of caustic chemicals such as bleach or alcohol [27].
Common vulvar irritants are listed in Table 2.
In particular for the older population, possible irritants in-
clude incontinence pads or briefs, feminine wipes, and topical
medications [36]. Incontinence-associated dermatitis (IAD)
was found in 5.7% of older individuals in long-term care fa-
cilities [38]. The risk of IAD increases with immobility and
the use of absorptive products saturated with urine or fecal
matter [38]. Urine disrupts the vulvar skin barrier by increas-
ing moisture and acts as an irritant [35]. Sanitary napkins can
also cause ICD through a different mechanism. A prior case
series describes 28 women who experienced ICD due to re-
peated episodes of vulvar itching and burning after use of
Always sanitary napkins [39]. The condition was resolved
after discontinuation and switching to another brand of sani-
tary napkins [39]. In a subset of the women, there was recur-
rence of ICD after resuming use of Always sanitary napkins
[39]. A potential cause for this irritation or chafing is the Dry
Weave plastic that is a component of the “wings” portion of
sanitary napkin preferred by the women [39].
Patients with ICD may present with a chief complaint of
pain in addition to itching and burning [18, 19]. In acute ICD,
the examination demonstrates vesicles, erosions, and edema
[18, 19]. In chronic ICD, the examination shows a different
appearance with deeper red tones of erythema, absence of
vesicles, and increased lichenification [18, 19]. Similar to
ACD, treatment requires discontinuation of suspected inciting
products or habits [34]. Patient should be counseled regarding
cleansing practices with hands and water only in the area no
more than twice daily [34]. The vulvar area should not be in
contact with soap, cleanser, or detergent [34]. For relief of
symptoms, patients are recommended a Sitz bath for approx-
imately 5–10 min twice daily [34]. For barrier protection, a
moisturizing emollient such as plain white petrolatum should
be applied [34, 38]. An appropriate strength corticosteroid
corresponding to severity of the vulvar eruption should be
applied twice daily until resolved [34].
Other considerations in diagnosing contact dermatitis in-
clude performing a skin biopsy, patch testing, and consider-
ation of other superimposed skin conditions [31, 34]. Skin
biopsies can confirm the presence of contact dermatitis, but
further investigation into the patient’s history and examination
are required to differentiate between ACD or ICD [34].
 Curr Geri Rep

Table 2 Common Vulvar Irritants [27–30, 32, 34, 35, 37] 41]. In patients with recurrent vulvar dermatitis, attention to
Topical vehicle Propylene glycol timing may be helpful in determining an allergen or irritant
preparations Hexylene glycol [39].
Lanolin
Ethanol/Alcohol based creams and gels
Physical Overcleaning
Vulvovaginal Candidiasis
Sanitary/incontinence pads
Vulvovaginal candidiasis (VVC) or vaginal yeast infection is
Clothing
a common problem, but its prevalence in postmenopausal
Sponges
women is approximately 5 to 6% with decreasing odds of
Towels
detection with each increasing year of age [42]. Candidal
Hairdryer
growth is not favored in postmenopausal women due to the
Prolonged sexual intercourse
vaginal environment with pH level greater than 5.0 and low
Endogenous Urine
glycogen concentrations from decreased hormonal circulation
Feces
[42]. Patients may be at increased risk for candida vulvovag-
Perspiration
initis if they are receiving estrogen hormone replacement ther-
Vaginal secretions
apy, antibiotics, or steroids [42]. Other conditions that results
Obesity ➔ increased skin moisture and
in increased risk include immunosuppression and diabetes
friction
[42]. Patients may present with symptoms of itching, burning,
Saliva (frequent oro-genital contact)
and vaginal discharge [42]. These symptoms overlap with a
Semen
wide array of vulvovaginal inflammatory conditions; there-
Personal care products Wipes
fore, key physical exam findings or KOH microscopy results
Bubble baths/soap/shower gels/cleansers
are important in distinguishing the diagnosis. The exam may
Powders
demonstrate bright erythematous patches, thin plaques, or fis-
Douches
sures with satellite papules [18, 19]. Pustules or collarettes of
Deodorants
scale from dissolved pustules can also be present [18, 19].
Sprays/perfumes
VVC is the number one cause of fissures on the interlabial
Depilatories
creases of the vulva [18, 19]. For KOH microscopy, the pres-
Lotions/creams
ence of pseudohyphae and yeast buds confirms the diagnosis
Caustic irritants Bleach
of VVC [18, 19]. This test sensitivity is approximately 40%
Lye
and may require further testing with a fungal culture if there is
Isopropyl alcohol clinical suspicion for VVC in spite of a negative KOH micros-
Topical medications Tea tree oil copy result [18, 19]. Treatment of choice is an azole antifungal
5-Fluorouracil cream or a one-time dose of fluconazole 150 mg for an un-
Imiquimod complicated infection with Candida albicans [18, 19].
Phenol
Podophyllin
Trichloroacetic acid Lichen Simplex Chronicus
Sexual support Lubricants
Condoms with lubricant or spermicide Lichen simplex chronicus (LSC) is a condition defined as the
chronic scratching and rubbing of the skin [2]. LSC can be
primary with no identified cause or secondary to underlying
Biopsy is crucial when there is a concern for malignancy and inflammatory vulvovaginal diseases described in this article
the biopsy should be taken from an active lesion [3]. A neg- [2]. Heightened sensation of itch is a result of increased stim-
ative patch test may guide diagnosis towards ICD over ACD, ulation from scratching or rubbing behavior that leads to the
but patch testing of the upper limb or back may not be repre- prominent “itch-scratch cycle” in LSC [2]. Affected individ-
sentative of the vulvar skin reaction towards an allergen [40]. uals tend to struggle with controlling their scratching behavior
ACD should be considered in recurrent vulvar dermatitis even during the night time [43]. Common triggers for itching in-
in the case of a negative patch test. Candidal vulvovaginitis clude heat, sweating, rubbing of thighs, and mental stress [43].
and lichen simplex chronicus are both conditions that can be This may be due to factors such as tight-fitting clothing, use of
superimposed or occur simultaneously with contact dermati- over the counter medications, use of incontinence or sanitary
tis. Lesions may resolve with antifungal creams or corticoste- pads, or obesity [2]. Psychological factors have been de-
roids in parallel to discontinuation of allergens or irritants [39, scribed in literature as a risk factor for developing LSC. One
Curr Geri Rep
study found individuals with anxiety had a 41-fold greater risk
of developing LSC compared with individuals in the cohort
matched for age, sex, and index date of anxiety [44]. The labia
majora is the most commonly affected location. The exam
demonstrates lichenified, erythematous, or hyperpigmented
plaques [2, 43]. In chronic LSC, the involved skin can cause
hyperpigmentation or hypopigmentation [2, 43]. LSC is a di-
agnosis that requires physical examination and potentially bi-
opsy to rule out other conditions that may be instigating the
pruritic sensation [2].
Autoimmune Blistering Disorders
Autoimmune blistering disorders are differentiated based on
specific targets of autoantibodies in the skin and mucosa. The
most common subsets that affect middle-aged or elderly indi-
viduals in order of incidence include bullous pemphigoid,
mucous membrane pemphigoid (cicatricial pemphigoid), and
pemphigus vulgaris [45]. Patients typically present with pru-
ritus and tense bullae with bullous pemphigoid. With pemphi-
gus vulgaris, flaccid bullae and painful erosions of the skin
and oral mucosa are seen. One study reviewed clinical data
from 1988 to June 2005 in a tertiary dermatology referral
center and identified 34 patients with genital involvement of
pemphigus vulgaris [46]. Physical examination that shows
erosions of the genital mucosa should prompt further inspec-
tion of the oral mucosa for lesions since this is a prominent site
for involvement [17–19]. The presence of lesions in the
vulvovaginal area alone without oral mucosal involvement is
rare [47]. Diagnosis can be confirmed with a biopsy for H&E
stain and direct immunofluorescence as well as serum for
indirect immunofluorescence to identify target location of
the antibodies [47]. First-line treatment of pemphigus vulgaris
is systemic corticosteroids and rituximab [48, 49]. Oral corti-
costeroids in combination with immunosuppressive drugs
such as methotrexate, azathioprine, mycophenolate mofetil,
dapsone, or cyclophosphamide are also possible treatment
regimens [50].
Psoriasis
Psoriasis is a chronic inflammatory condition that affects
2 to 3.2% of adults in the USA [51, 52]. The estimated
prevalence of genital involvement in patients with psori-
asis ranges from 29 to 46% [53]. Genital psoriasis is more
common than realized previously since there is a lack of
examination of the genital area for chronic psoriatic pa-
tients, which accounts for the variable range of prevalence
[53]. This condition may have a negative effect on quality
of life or sexual health by interfering with patients’ activ-
ities of daily living, social life, and self-esteem [52, 53].
Patients can present on opposite ends of the spectrum,
from no symptoms to extreme pruritus with pain and
burning [18, 19, 53]. Physical exam may demonstrate
well-demarcated plaques which may lack characteristic
thick scale in the intertriginous areas due to occlusive
nature of the site [18, 19, 31]. Clinical suspicion of gen-
ital psoriasis can be further evaluated with inspection of
the nails for onycholysis or pitting [18, 19]. Characteristic
psoriatic plaques can also be demonstrated in other areas
of the body [18, 19]. Topical therapy with corticosteroids,
calcineurin inhibitors, and/or calcipotriene is the first-line
therapy for mild to moderate psoriasis in elderly patients
[18, 19, 54]. Advancement of treatment with combina-
tions of phototherapy or immunomodulators requires con-
sideration for the balance of side effects with therapy
benefits [54••].
Conclusion
Vulvar inflammatory dermatoses continue to be
underreported, misdiagnosed, and undertreated in the elderly
population. Key themes for provider improvement include
careful review of the patient’s medical history and physical
examination of the genitoanal area for asymptomatic and
symptomatic elderly women. Overlapping symptoms of pru-
ritus or pain and disease processes including genitourinary
syndrome of menopause, vulvovaginal candidiasis, or lichen
simplex chronicus can often complicate the diagnosis of the
primary vulvar dermatosis. Vulvar dermatoses which cannot
be controlled require altering the treatment plan to the next
tier for the condition or reinvestigating potential causes.
Prompt, consistent treatment can vastly improve the patient’s
quality of life and is critical to minimizing the risk of devel-
oping squamous cell carcinoma in conditions predisposed to
this risk such as lichen sclerosus and lichen planus. When
treatment requires advancing to systemic immunosuppres-
sive therapy or oral corticosteroids, there should be a discus-
sion regarding risk versus benefits of treatment with patients
due to the increased vulnerability of geriatric patients to side
effects. Further research should be aimed at developing tools
for communicating with patients regarding this topic, identi-
fying modifiable risk factors, and determining optimal
therapy.
Compliance with Ethical Standards
Conflict of Interest The authors declare that there is no conflict of
interest.
Human and Animal Rights and Informed Consent This article does not
contain any studies with human or animal subjects performed by any of
the authors.

References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major importance
1. Hamidi M, Joseph B. Changing epidemiology of the american pop-
ulation. Clin Geriatr Med. 2019;35:1–12.
2. Savas JA, Pichardo RO. Female genital itch. Dermatol Clin.
2018;36:225–43.
3. Mauskar MM, Marathe K, Venkatesan A, Schlosser BJ, Edwards
L. Vulvar diseases: Approach to the patient. J Am Acad Dermatol.
2020;82:1277–84.
4. Dhingra I, De Sousa A, Sonavane S. Sexuality in older adults:
clinical and psychosocial dilemmas. J Geriatr Ment Health.
2016;3:131.
5. USPSTF, Curry SJ, Krist AH, Owens DK, Barry MJ, Caughey AB,
et al. Screening for cervical cancer: US preventive services task
force recommendation statement. JAMA. 2018;320:674–86.
6. Schlosser BJ, Mirowski GW. Approach to the patient with
vulvovaginal complaints. Dermatol Ther. 2010;23:438–48.
7. Connor CJ, Eppsteiner EE. Vulvar contact dermatitis. Proc Obstet
Gynecol. 2014;4:1–14.
8. Farage M, Maibach H. Lifetime changes in the vulva and vagina.
Arch Gynecol Obstet. 2006;273:195–202.
9. Gandhi J, Chen A, Dagur G, Suh Y, Smith N, Cali B, et al.
Genitourinary syndrome of menopause: an overview of clinical
manifestations, pathophysiology, etiology, evaluation, and man-
agement. Am J Obstet Gynecol. 2016;215:704–11.
10. Moyal-Barracco M, Edwards L. Diagnosis and therapy of
anogenital lichen planus. Dermatol Ther. 2004;17:38–46.
11. Kirtschig G. Lichen sclerosus-presentation, diagnosis and manage-
ment Dtsch Arztebl Int 2016;113:337–343.
12.• Melnick LE, Steuer AB, Bieber AK, Wong PW, Pomeranz MK.
Lichen sclerosus among women in the United States. Int J Womens
Dermatol. 2020;6(4):260-262. Published 2020 May 8. https://doi.
org/10.1016/j.ijwd.2020.05.001
13. Day T, Moore S, Bohl TG, Scurry J. Comorbid vulvar lichen planus
and lichen sclerosus. J Low Genit Tract Dis. 2017;21:204–8.
14. Dubey R, Fischer G. Vulvo-vaginal lichen planus: a focussed re-
view for the clinician. Australas J Dermatol. 2019;60:7–11.
15. Lewis FM. Vulval symptoms after the menopause - not all atrophy!
Post Reprod Health. 2015;21:146–50.
16. Schwager Z, Stern M, Cohen J, Femia A. Clinical epidemiology
and treatment of lichen planus: a retrospective review of 2 tertiary
care centers. J Am Acad Dermatol. 2019;81:1397–9.
17. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. Elsevier Health
Sciences; 2012.
18. Md LE. Genital dermatology atlas. 2nd ed. Philadelphia: Lww;
2010. p. 384.
19. Black M, Ambros-Rudolph, Christina M, Edwards L. Obstetric and
gynecologic dermatology. 3rd ed. Edinburgh: Mosby; 2008. p. 424.
20. Byrd JA, Davis MDP, Rogers RS. Recalcitrant symptomatic vulvar
lichen planus: response to topical tacrolimus. Arch Dermatol.
2004;140:715–20.
21. Lee A, Fischer G. Diagnosis and treatment of vulvar lichen
sclerosus: an update for dermatologists. Am J Clin Dermatol.
2018;19:695–706.
22. Lee A, Bradford J, Fischer G. Long-term management of adult
vulvar lichen sclerosus: a prospective cohort study of 507 women.
JAMA Dermatol. 2015;151:1061–7.
23.•• Kohn JR, Connors TM, Chan W, Liang CS, Dao H, Vyas A (2020)
Clinical outcomes and adherence to topical corticosteroid therapy in
Curr Geri Rep
women with vulvar lichen sclerosus: A retrospective cohort study. J
Am Acad Dermatol. https://doi.org/10.1016/j.jaad.2020.05.006
24. O’Gorman SM, Torgerson RR. Allergic contact dermatitis of the
vulva. Dermatitis. 2013;24:64–72.
25. Yale K, Awosika O, Rengifo-Pardo M, Ehrlich A. Genital allergic
contact dermatitis. Dermatitis. 2018;29:112–9.
26. Woodruff CM, Trivedi MK, Botto N, Kornik R. Allergic contact
dermatitis of the vulva. Dermatitis. 2018;29:233–43.
27. Sand FL, Thomsen SF. Skin diseases of the vulva: eczematous
diseases and contact urticaria. J Obstet Gynaecol. 2018;38:295–
300.
28. Margesson LJ. Vulvar disease pearls. Dermatol Clin. 2006;24:
145–55 v.
29. Margesson LJ. Practice gaps: practice gaps “down there”: failures
in education, physical examination, recognition, diagnosis, therapy,
follow-up care, and cancer surveillance in lichen sclerosus. JAMA
Dermatol. 2013;149:1203.
30. Schlosser BJ. Practice gaps. Missing genital lichen sclerosus in
patients with morphea: don’t ask? Don’t tell?: comment on “High
frequency of genital lichen sclerosus in a prospective series of 76
patients with morphea”. Arch. Dermatol. 2012;148:28–9.
31. Hoang MP, Reutter J, Papalas JA, Edwards L, Selim MA. Vulvar
inflammatory dermatoses: an update and review. Am J
Dermatopathol. 2014;36:689–704.
32. Pichardo-Geisinger R. Atopic and contact dermatitis of the vulva.
Obstet Gynecol Clin N Am. 2017;44:371–8.
33. Gardner KH, Davis MDP, Richardson DM, Pittelkow MR. The
hazards of moist toilet paper: allergy to the preservative
methylchloroisothiazolinone/methylisothiazolinone. Arch
Dermatol. 2010;146:886–90.
34. Schlosser BJ. Contact dermatitis of the vulva. Dermatol Clin.
2010;28:697–706.
35. Bauer A, Rodiger C, Greif C, Kaatz M, Elsner P. Vulvar
dermatoses–irritant and allergic contact dermatitis of the vulva.
Dermatology (Basel). 2005;210:143–9.
36. Farage MA, Miller KW, Berardesca E, Maibach HI. Incontinence
in the aged: contact dermatitis and other cutaneous consequences.
Contact Derm. 2007;57:211–7.
37. ACOG Practice Bulletin No. 93: diagnosis and management of
vulvar skin disorders. Obstet Gynecol. 2008 May;111(5):1243–
53. https://doi.org/10.1097/AOG.0b013e31817578ba
38. Incontinence associated dermatitis in the elderly patient: assess-
ment, prevention and management* – Aging Life Care
AssociationTM [Internet]. [cited 2020 May 28]. Available from:
https://www.aginglifecarejournal.org/incontinence-associated-
dermatitis-in-the-elderly-patient-assessment-prevention-and-
management/. Accessed 28 May 2020.
39. Eason EL, Feldman P. Contact dermatitis associated with the use of
Always sanitary napkins. Can Med Assoc J. 1996;154:1173–6.
40. Wakashin K. Sanitary napkin contact dermatitis of the vulva:
location-dependent differences in skin surface conditions may play
a role in negative patch test results. J Dermatol. 2007;34:834–7.
41. Schlosser BJ, Mirowski GW. Introduction: the diagnosis and
treatment of vulvar and vaginal disorders. Dermatol Ther.
2010;23:435–7.
42. Hoffmann JN, You HM, Hedberg EC, Jordan JA, McClintock MK.
Prevalence of bacterial vaginosis and Candida among postmeno-
pausal women in the United States. J. Gerontol. B, Psychol. Sci.
Soc. Sci. 2014;69 Suppl 2:S205–14.
43. Rajalakshmi R, Thappa DM, Jaisankar TJ, Nath AK. Lichen sim-
plex chronicus of anogenital region: a clinico-etiological study.
Indian J Dermatol Venereol Leprol. 2011;77:28–36.
44. Liao YH, Lin CC, Tsai PP, Shen WC, Sung FC, Kao CH. Increased
risk of lichen simplex chronicus in people with anxiety disorder: a
nationwide population-based retrospective cohort study. Br J
Dermatol. 2014;170:890–4.
Curr Geri Rep
45. Bertram F, Bröcker E-B, Zillikens D, Schmidt E. Prospective anal-
ysis of the incidence of autoimmune bullous disorders in Lower
Franconia, Germany. J Dtsch Dermatol Ges. 2009;7:434–40.
46. Malik M, Ahmed AR. Involvement of the female genital tract in
pemphigus vulgaris. Obstet Gynecol. 2005;106:1005–12.
47. Davis SA, Davis LS. Pemphigus vulgaris presenting as chronic
vulvovaginal erosions: the importance of autoantibody testing: a
case report. J Reprod Med. 2016;61:589–91.
48. Murrell DF, Peña S, Joly P, Marinovic B, Hashimoto T, Diaz LA,
et al. Diagnosis and management of pemphigus: recommendations
of an international panel of experts. J. Am. Acad. Dermatol.
2020;82:575–585.e1.
49. Joly P, Maho-Vaillant M, Prost-Squarcioni C, Hebert V, Houivet E,
Calbo S, et al. First-line rituximab combined with short-term pred-
nisone versus prednisone alone for the treatment of pemphigus
(Ritux 3): a prospective, multicentre, parallel-group, open-label
randomised trial. Lancet. 2017;389:2031–40.
50. Schmidt E, Zillikens D. The diagnosis and treatment of autoim-
mune blistering skin diseases. Dtsch Arztebl Int. 2011;108:399–
405 I.
51. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis preva-
lence among adults in the United States. J Am Acad Dermatol.
2014;70:512–6.
52. Weigle N, Mcbane R. Psoriasis. Am Fam Physician. 2013 May
1;87(9):626–633. https://www.aafp.org/afp/2013/0501/
afp20130501p626.pdf
53. Meeuwis KAP, Potts Bleakman A, van de Kerkhof PCM, Dutronc
Y, Henneges C, Kornberg LJ, et al. Prevalence of genital psoriasis
in patients with psoriasis. J Dermatolog Treat. 2018;29:754–60.
54.•• Kamel JG,Yamauchi PS.Managing mild-to-moderate psoriasis in
elderly patients: Role of topical treatments. Drugs Aging.
2007;34:583–8. https://doi.org/10.1007/s40266-017-0480-8
Publisher’s Note Springer Nature remains neutral with regard to jurisdic-
tional claims in published maps and institutional affiliations.