INTRODUCTION — Vulvar dermatitis is the most common type of vulvar dermatosis. One-third to one-half of vulvar complaints stem from this problem [1-4]. It can develop in isolation or may occur as part of dermatitis in other areas of the body. Women with vulvar dermatitis often experience chronic irritation or pruritus, which cause them to persistently rub and scratch the vulva. These activities lead to histologic changes in the dermis, termed lichen simplex chronicus .
This topic will discuss the clinical manifestations, diagnosis, and management of vulvar dermatitis. Other vulvar dermatoses and vulvar lesions are discussed separately.
●(See "Vulvar lichen sclerosus".)
●(See "Vulvar lichen planus".)
ENDOGENOUS VERSUS EXOGENOUS DERMATITIS — Vulvar dermatitis has been traditionally divided into two subtypes, endogenous and exogenous. However, these categories are not mutually exclusive, and it is possible for both to exist concomitantly in an individual patient:
●Endogenous vulvar dermatitis (eczema) is the term used to describe atopic dermatitis of the vulva. Atopic dermatitis has a familial predisposition, often begins in childhood, and is characterized by pruritus. Although some experts feel that vulvar involvement is unusual, even when there is severe and widespread atopic dermatitis elsewhere, others believe it is more prevalent than previously acknowledged [6,7]. In women with atopic dermatitis at nongenital sites, the occurrence of erythema in the labial folds, the perianal region, and in the skin between the buttocks probably represents endogenous vulvar dermatitis. However, in such cases, it is important to rule out allergic contact dermatitis as a complicating factor or as the causal diagnosis . (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)
●Exogenous vulvar dermatitis results from external factors and is also called contact dermatitis (picture 1A-B). In allergic contact dermatitis, the trigger (allergen) induces an immune response, while in irritant contact dermatitis, the trigger (irritant) itself directly damages the skin. Although exposure to irritants may have been the initial cause of dermatitis, secondary sensitization to allergens can also occur.
The most common agents that cause irritant or allergic contact dermatitis of the vulva are listed in the table (table 1). Active and inert constituents of topical medications are a very common etiology of allergic dermatitis of the vulva in women with persistent vulvar symptoms . Sensitivity to latex or proteins in seminal plasma are infrequent etiologies [10,11]. (See "Irritant contact dermatitis in adults" and "Clinical features and diagnosis of allergic contact dermatitis" and "Allergic reactions to seminal plasma".)
PATHOPHYSIOLOGY — Vulvar tissue is more permeable than exposed skin due to differences in structure, occlusion, hydration, and susceptibility to friction [11,12]. The vulvar skin is particularly vulnerable to irritants. Compared with other body regions, the stratum corneum overlying the vulva appears to function less efficiently as a barrier, thereby permitting increased susceptibility to irritants . As an example, preservatives such as benzalkonium chloride and maleic acid induce a greater response after application to normal vulvar skin than when applied to the skin of the forearm .
The vulvar skin is also sensitive to allergens. New exposure to an allergen is most likely to induce a reaction, although patients may also react to products that they have used for months or years. A delayed hypersensitivity (type IV) reaction takes from 12 to 72 hours to develop, is usually pruritic, and often lasts for several weeks. In acute cases, an exposure occurring up to two weeks prior to the dermatitis can often be identified. In chronic cases, the dermatitis may have been present for months or years; identifying the offending trigger in these patients can be difficult.
CLINICAL MANIFESTATIONS — In acute vulvar dermatitis, the skin displays mild to severe erythema of varying extent with some scaling in dry areas (picture 1B). Fissures may be present along the labial folds. Excoriations from scratching are common and can be complicated by secondary infection with yeast or bacteria (eg, Staphylococcus aureus, Streptococcus pyogenes, or Escherichia coli). Although crusts and scales are commonly observed with dermatitis elsewhere on the body, these signs are often not present in the moist areas of the vulva.
In chronic cases, the vulvar mucosa is erythematous and may display papillae, a sign of chronic inflammation (picture 2). The origin of vulvar papillomatosis is uncertain; the papillae can be normal anatomic variants of the vestibular mucosa or a postinflammatory change [15,16]. Papillomatosis is not a cause of vulvar pain.
The most common symptom of vulvar dermatitis is pruritus, which can be intense and nocturnal. Other symptoms include burning, stinging, or rawness. Symptoms may be exacerbated by heat, sweat, stress, or menstruation. Self-medication and excessive washing of the vulva by women fearful of a lack of cleanliness often aggravate the dermatitis.
In response to the epithelial irritation and persistent pruritus, the patient may chronically rub and scratch her skin. Repeated cycles of intense itching and scratching result in the thickening of the vulvar skin and accentuation of the normal skin markings (lichenification), a condition called lichen simplex chronicus (picture 3) [4,17]. Labial skin folds appear greatly exaggerated, often edematous, and pubic hair can be broken or sparse (picture 4A-B) [9,18]. Other changes include hypopigmentation or hyperpigmentation and hyperkeratosis (picture 5). Due to local moisture, scale is usually absent and the skin surface appears soft and whitened. (See "Vulvar lesions: Differential diagnosis of red lesions", section on 'Lichen simplex chronicus'.)
DIAGNOSIS — The diagnosis of vulvar dermatitis is in most cases clinical, based on the clinical presentation, a personal or family history of atopy, or a personal history of vulvar exposure to medications, perfumes, or other chemicals causing persistent irritation. One should have a high index of suspicion of contact allergy in any chronic vulvar dermatitis, and patients should be referred for patch testing. The frequency of clinically relevant patch test results in patients with vulvar complaints is high, ranging from 16 to 54 percent [8,9,19-23]. A skin biopsy is not routinely performed in women with vulvar dermatitis; however, histopathologic examination may be necessary if the diagnosis is uncertain or there is a suspicion of neoplasia. (See 'Differential diagnosis' below.)
History — Women with vulvar complaints should be questioned regarding a personal or family history of atopy (eg, atopic dermatitis, asthma, rhinitis, conjunctivitis) or autoimmune diseases. Chronic pruritus should be ascertained. Specific areas to address in the history include:
●What are her major complaints? Pruritus can vary from mild to intolerable, sometimes interfering with sleep or other activities. When the dermatitis involves mucosal areas, burning, rawness, and stinging are more common than pruritus and the symptoms are often exacerbated during menstruation and with coitus.
●What are her hygienic practices (eg, daily use of panty liners, feminine products, baby wipes)? Women often erroneously regard their personal practices as safe since they have engaged in them for a long time.
●Does she wear occlusive clothing, such as tight Lycra garments, confining undergarments, noncotton underwear, or thongs? These types of garments trap sweat, promote candidiasis, chafe the skin, and facilitate allergen penetration in sensitized individuals. Allergy to textile dyes and textile formaldehyde resins may be an additional cause of vaginal pruritus .
●Does she apply any medications (eg, topical antifungals) or other agents (eg, lubricants, spermicides, perfumed or deodorant soaps) to the vulva? Women seldom reveal this information unless asked directly. Patients with vulvar dermatitis have often been treated with multiple antifungal agents without success. A report that these creams never helped their symptoms is significant information, indicating that Candida is probably not the source of the complaints.
●Does she have fecal or urinary incontinence? Both feces and urine are skin irritants.
The answers to these questions help to differentiate an endogenous process (eg, atopy) from that induced by an exogenous agent. Conscientious analysis of the woman's personal practices is the best way to detect potential irritants and allergens in her environment (table 1) as well as habits unhealthy for the vulvar skin. In a study of 530 women attending a specialty clinic for vulvar diseases, over 60 percent of patients described adverse personal hygiene or self-treatment practices when specifically questioned .
Physical examination — Physical examination should include:
●Careful visual inspection of the vulva – Assess for signs of inflammation (erythema, edema, excoriations, fissures, scaling), changes in vulvar architecture (loss/distal flattening of labia minora, adhesions of clitoral prepuce to glans, narrowing of introitus) (picture 9B), and signs of atrophy, which indicate long-standing inflammation or inflammatory vulvar dermatosis, such as lichen sclerosus (picture 6) or inverse psoriasis (picture 7). (See 'Inflammatory vulvar dermatoses' below.)
●Vaginal examination – Assess for signs of inflammation (erythema, edema erosions, lesions) or atrophy; perform evaluation of vaginal discharge, including pH, odor, and saline and potassium hydroxide microscopy to rule out acute vaginitis or desquamative inflammatory vaginitis. Vaginal discharge is usually unremarkable in women with vulvar dermatitis. If Candida is suspected by exam findings, a vaginal culture should be obtained even if microscopy is negative. (See "Vaginal discharge (vaginitis): Initial evaluation".)
●Complete skin examination – Examine mouth, nail beds, flexor and extensor surfaces, and scalp for evidence of nongenital dermatitis. Look for scaly scalp plaques or nail pitting that suggest psoriasis. Also look for desquamative gingivitis or buccal Wickham striae suggesting lichen planus.
Patch testing — Patch testing is recommended to rule out allergic contact dermatitis and may be helpful to distinguish between atopic and allergic contact dermatitis. Patch testing should be performed by a specialist (ie, dermatologist or allergist with access to the appropriate testing panels). In addition to standard series of allergens, the patient's own topical medications, popular remedies, or other suspected products should also be tested . (See "Patch testing".)
Positive patch tests for relevant substances occur in 25 to 60 percent of women with vulvar pruritus; fragrances, medications, and preservatives are most frequently implicated [9,19,27-31]. In a study including 282 women with vulvar symptoms undergoing patch testing with a European standard series and a gynecologic series, 54 percent reacted to one or more allergens . Nickel was the most commonly found allergen, although the authors felt it was not clinically relevant. In contrast, positive reactions to fragrances, topical antibiotics or anesthetics, and patients' own products were almost always relevant (table 2).
Contact allergy to topical corticosteroids is an important cause of vulvar dermatitis that should not be overlooked [9,10,19]. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)
A less common but described cause of genital rash is systemic contact dermatitis [20,32]. Patients sensitized to a topical allergen can develop contact dermatitis if exposed to that allergen systemically (eg, by ingestion, parenteral administration, or inhalation). Four main groups of allergens are generally responsible: metals (eg, nickel, cobalt, and chromium); medications (eg, hydroxyzine, an ethylenediamine-derived antihistamine, or oral medications that contain propylene glycol); plant and herbal products, fragrances, and flavorings (eg, citrus, wine, beer, cinnamon, cola, curry, vanilla, or other flavorings); and preservatives (eg, formaldehyde in aspartame). (See "Common allergens in allergic contact dermatitis".)
Biopsy — Biopsy is not routinely performed in patients with vulvar dermatitis. However, a biopsy may be necessary if the diagnosis cannot be made on clinical grounds or there is suspicion of neoplasia. Histopathologically, vulvar dermatitis is characterized by spongiosis (epidermal edema) and a dermal infiltrate of lymphocytes with occasional eosinophils . Chronic lesions may show changes of lichen simplex chronicus, consisting of elongation, widening of the rete ridges and irregular thickening of the Malpighian layer of rete ridges (acanthosis), hyperkeratosis, and parakeratosis with a modest mid-dermal inflammatory infiltrate . Periodic acid-Schiff stain for yeasts may be helpful if chronic candidal vulvovaginitis is suspected in patients with negative microscopy and culture of vaginal discharge.
DIFFERENTIAL DIAGNOSIS — Inflammatory vulvar dermatoses (eg, lichen sclerosus, lichen planus, psoriasis, seborrheic dermatitis), infections (eg, human papillomavirus [HPV], herpes simplex, Candida), neoplasia, and vulvar pain syndromes are all sources of vulvar complaints (table 3). These conditions should be ruled out by laboratory tests and skin biopsy, if necessary. (See "Vulvar lesions: Diagnostic evaluation" and "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers" and "Vulvar pain of unknown cause (vulvodynia): Clinical manifestations and diagnosis".)
Inflammatory vulvar dermatoses — Common inflammatory dermatoses involving the vulva include:
●Lichen sclerosus – Lichen sclerosus is a chronic, progressive, inflammatory mucocutaneous disease of the vulva that occurs in women of all ages, with a peak incidence in prepubertal girls and perimenopausal or postmenopausal women. Pruritus, irritation, and discomfort are the predominant symptoms, although women can be totally asymptomatic even in the presence of active disease. Lichen sclerosus is characterized by "parchment-like" or "cigarette paper" skin, although thickened, hyperplastic, or lichenified areas are not uncommon (picture 8A-B). Fissures and telangiectasia are common. Untreated disease leads to loss of the normal architecture of the external genitalia and constriction of the vaginal orifice (picture 9A-B). The diagnosis can be confirmed by histologic examination of biopsy specimens if either clinical doubt exists about the diagnosis or if there is concern about possible neoplasia . Patients with lichen sclerosus may also develop lichen simplex chronicus from chronic scratching, and more than one biopsy may be necessary for the correct diagnosis. (See "Vulvar lichen sclerosus".)
●Lichen planus – Vulvar lichen planus may present with erosive, papulosquamous, or hypertrophic lesions. Erosive lichen planus is the most common type and typically involves the inner aspects of the vulva and vagina (picture 10). In longstanding disease, loss of the labia minora and narrowing of the introitus may be seen (picture 11). A skin biopsy for routine histopathologic examination can confirm the diagnosis. Immunofluorescence studies are useful to differentiate erosive lichen planus from autoimmune blistering diseases (eg, mucous membrane pemphigoid and pemphigus). (See "Vulvar lichen planus".)
●Vulvovaginal-gingival syndrome – Vulvovaginal-gingival syndrome is a variant of erosive lichen planus that can affect the vagina, vulva, and oral cavity (picture 12) either concurrently or individually . Vulvar lesions are painful, glassy erosions, while those in the vagina are erythematous and friable. Synechiae can develop in the vagina, which may become obliterated with severe disease. Patients typically have irritation, pain, rawness, and soreness and may have a serosanguinous discharge from vaginal involvement. (See "Vulvar lichen planus", section on 'Clinical manifestations'.)
●Psoriasis – Psoriasis appears as bright red, sharply demarcated lesions that are raised above the surrounding normal skin (picture 7). Silver scales, commonly observed in psoriasis, may be seen on the mons but are not found elsewhere on the vulva. The presence of typical psoriatic lesions on other body areas suggests the diagnosis. A skin biopsy can be performed for confirmation. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Inverse (intertriginous) psoriasis'.)
●Seborrheic dermatitis – Seborrheic dermatitis is a chronic inflammatory disorder typically involving areas of the body that are rich in sebaceous glands, such as the scalp, face, axilla, groin, and upper trunk. Involvement of the vulva is uncommon. The lesions are erythematous, poorly defined, and scaling. (See "Seborrheic dermatitis in adolescents and adults".)
Infection — Candida vulvovaginitis causes pruritus, irritation, burning, and soreness of the vulva. Cutaneous findings of lichen simplex chronicus often accompany Candida infection. Candida is less common in postmenopausal women but can occur in those on estrogen replacement or using potent topical corticosteroids (eg, for treatment of lichen sclerosis). Candida infection should be excluded by culture. (See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)
If there is a malodorous vulvar exudate, bacterial cultures of the vulva should be obtained to aid in the diagnosis of secondary bacterial infection. Bacterial cultures of the vagina are not recommended, as the results are usually nonspecific.
Testing for herpes simplex virus is recommended when recurrent ulcerations are noted, as these may be a sign of genital herpes. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection", section on 'Diagnosis'.)
Vulvar intraepithelial neoplasia — Vulvar intraepithelial neoplasia related to HPV infection, or non-HPV related, may cause irritation and pruritus of the vulva or raised (picture 13) or macular (picture 14) lesions. Vulvar biopsy is required for the diagnosis. Appropriate sites for biopsy are identified by physical examination and colposcopy.
The diagnostic evaluation and management of vulvar intraepithelial neoplasia are discussed in detail elsewhere. (See "Vulvar squamous intraepithelial lesions (vulvar intraepithelial neoplasia)".)
Vulvar cancer — Most patients with vulvar cancer present with a unifocal vulvar plaque, ulcer, or mass (fleshy, nodular, or warty) on the labia majora (picture 15), whereas the labia minora, perineum, clitoris, and mons are less frequently involved. Pruritus is the most common complaint, especially if there is an underlying inflammatory vulvar dermatoses (eg, lichen sclerosus or lichen simplex chronicus). Bleeding, discharge, or an enlarged inguinal lymph node may also be present, but patients can be asymptomatic as well. Vulvar biopsy is required for diagnosis. (See "Vulvar cancer: Epidemiology, diagnosis, histopathology, and treatment".)
Paget disease (extramammary) — Vulvar Paget disease typically has an eczematous appearance and may occur anywhere on the vulva. It is well demarcated, with slightly raised edges and a red background (picture 16). Pruritus is the most common symptom. Diagnosis is based upon characteristic histopathology. Vulvar biopsy should be performed in patients with suspicious lesions, including those with persistent pruritic eczematous lesions that fail to resolve within six weeks of appropriate therapy. Invasive adenocarcinomas may be present within or beneath the surface lesion or at distant noncontiguous sites, and a work-up for underlying malignancy should be considered [36,37]. (See "Vulvar cancer: Epidemiology, diagnosis, histopathology, and treatment".)
Vulvar pain syndromes — Vulvar pain may be related to a specific disorder (infectious, inflammatory, neoplastic, or neurologic). Vulvodynia refers to vulvar discomfort of unknown etiology, usually described as burning pain accompanied with allodynia on vestibular/vulvar Q-tip examination. Pruritus is uncommon; nevertheless, persistent pruritus and erythema with a negative yeast culture, nonspecific vulvar biopsy, and failure to respond to standard treatment raises the possibility of vulvodynia. Vulvodynia is a diagnosis of exclusion after specific, relevant disorders have been ruled out. (See "Vulvar pain of unknown cause (vulvodynia): Clinical manifestations and diagnosis".)
Vulvovaginal atrophy — Vulvovaginal atrophy is characterized by dryness, inflammation, and thinning of the epithelial lining of the vagina and lower urinary tract due to loss of estrogen. Symptoms include vaginal dryness, burning, pruritus, discharge, bleeding, and dyspareunia. Urinary tract symptoms (eg, frequency, recurrent infection) may also occur. The diagnosis is clinical, based upon the typical finding of pale, dry, thin vaginal epithelium that is smooth and shiny with loss of most rugation. Office analysis reveals basic vaginal pH in the absence of other causes (eg, infection, blood, or semen) and parabasal cells on microscopy. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)
MANAGEMENT — The treatment of vulvar dermatitis requires a multimodal approach involving habit modification, appropriate skin care and hygiene practices (table 4), treatment of coexistent infection, control of pruritus, and topical or systemic medication. Various popular soaps marketed as "fragrance free" or "sensitive skin" contain flower extracts or fragrances/flavorings and should be avoided. As an example, Dove Sensitive Skin unscented bar soap contains maltol, a fragrance/flavoring, and Basis Sensitive Skin bar soap contains the fragrance chemical cyclopentadecanolide. An explanation of the condition, emphasizing the need for long-term treatment with maintenance regimens, and vigilance to prevent and diagnose recurrent yeast infections are important factors for success . Therapy that fails to interrupt the itch-scratch cycle will not lead to consistent, prolonged clinical improvement. For persistent cases, a multidisciplinary approach involving gynecologists, dermatologists, and allergists may be necessary.
In the absence of data from large, randomized trials, we suggest the regimens discussed below based upon our clinical experience and results from small, observational studies.
General measures — Behavior modification and adoption of appropriate personal care practices are important components of the management of vulvar dermatitis:
●If the patient has clothing or hygiene habits that facilitate dermatitis, these habits must be modified. Key elements of healthy vulvar hygiene are listed in the table (table 4).
●Patients should be reassured that skin issues are not the result of a lack of cleanliness and that excessive washing can worsen dermatitis.
●Known or suspected allergens and irritants in the environment should be eliminated.
●Gentle skin care should be encouraged. Soaking in warm water, without additives, for five minutes in the morning and night hydrates the skin and relieves vulvar discomfort and pruritus. If the patient does not have access to a bathtub or a sitz bath placed under a toilet seat, a hand-held shower device can be used for hydration. Moisture is then sealed into the skin with the application of a nonallergenic emollient (eg, petroleum jelly) or a topical corticosteroid ointment ("soak and seal").
●The patient's personal care practices should be reviewed at each visit to ensure ongoing good practices are being followed.
Diagnosis and treatment of coexistent infection — Diagnosis of coexistent infections is essential. If a vaginal or vulvar exudate is present, a vulvar bacterial culture, saline and potassium hydroxide (KOH) preparation, and yeast culture should be obtained. If herpes simplex infection is suspected, a viral culture, direct fluorescent antibody (DFA) test, or polymerase chain reaction (PCR) should be performed (see "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection"):
●Candidiasis – Candidiasis may be present in the absence of the usual vaginal symptoms and may be the cause of recurrent vulvar fissures. Candidiasis should be excluded in all patients by yeast culture if the organism is not present on wet mount with 10 percent KOH, which is only 50 percent sensitive. It is important to repeat the search for Candida with wet mount and cultures at each follow-up visit, since a previous negative culture does not rule out Candida infection. (See "Candida vulvovaginitis: Clinical manifestations and diagnosis", section on 'Diagnostic approach'.)
Candidiasis should be treated with oral fluconazole, assuming the patient is not allergic to this. Oral therapy is preferred to topical therapy because women with infection superimposed on vulvar dermatitis are at increased risk for worsening dermatitis from the irritant effects of topical drugs . For uncomplicated Candida infection, fluconazole 150 mg is given as a one-time dose. Complicated or recurrent infections may require longer courses of therapy or long-term suppression. Nonalbicans yeast do not usually respond to fluconazole and will require alternative treatment. (See "Candida vulvovaginitis: Treatment", section on 'Recurrent treatment'.)
●Bacterial infection – Vaginal bacterial cultures are not generally useful because many types of bacteria normally colonize the vagina. Heavy growth of Staphylococcus or Streptococcus should be treated . We use cephalexin (500 mg orally three times per day) or cefadroxil (500 mg orally twice daily) for five to seven days, if appropriate by sensitivity testing. For women allergic to penicillin, we prescribe azithromycin (250 mg as a single oral dose daily for six days).
●Genital herpes simplex infection – If herpes simplex virus is detected, appropriate antiviral therapy can be considered in the individual patient based upon the type of infection (primary or recurrent) and severity of symptoms. (See "Treatment of genital herpes simplex virus infection".)
Control of pruritus — Oral sedating antipruritic agents such as hydroxyzine (a first-generation H1 antihistamine) or doxepin (a tricyclic antidepressant with antihistamine properties) given in the evening may be helpful to control nighttime itching and scratching. Nonsedating antihistamines are of little benefit for vulvar pruritus. (See "Pruritus: Therapies for localized pruritus".)
Doxepin is also available as a cream formulation; however, it is a known contact sensitizer and should not be used on inflamed vulvar skin . Additionally, it produced drowsiness in 25 percent of users due to systemic absorption, which is another limitation to its usefulness .
Patients with mild symptoms — Mild vulvar dermatitis usually responds to low- to medium-potency topical corticosteroid ointments (groups 4 to 7 (table 5)) such as hydrocortisone 1% or 2.5%, desonide 0.05%, or triamcinolone 0.1%. Topical corticosteroids can be used one or more times daily, for two to four weeks, although a clear benefit has not been demonstrated with more than once daily application [42-44]. Therapy is continued indefinitely at the minimum frequency necessary to control pruritus with a goal of less than 14 days per month.
Patients with moderate to severe symptoms — For patients with moderate to severe vulvar dermatitis, a high-potency topical corticosteroid in ointment formulation is generally required (groups 1 to 3 (table 5)). We prescribe clobetasol propionate or augmented betamethasone dipropionate 0.05% ointment at night daily for 30 days and then reevaluate.
Ointments are preferred to creams because creams contain more preservatives than ointments. Additionally, some high-potency topical corticosteroid creams contain moderate sensitizers, such as formaldehyde-releasing preservatives or methylisothiazolinone. Potent topical steroids have been used for up to 12 weeks on the vulva without adverse effects [45,46].
Another acceptable regimen is to give one of these steroids twice daily for two weeks, then daily for two weeks, then on Monday and Wednesday and Friday for two weeks, and then reevaluate. If there is a partial response, we either continue corticosteroids for another two weeks or else switch to intralesional injections or topical calcineurin inhibitors.
Corticosteroid-dependent vulvar dermatitis — In some patients, corticosteroid-dependent vulvar dermatitis (ie, dermatitis that relapses rapidly after stopping or tapering topical corticosteroids) can be controlled with the use of the calcineurin inhibitors tacrolimus 0.03% ointment or pimecrolimus 1% cream [47,48]. The ointment or cream is applied sparingly twice daily for 14 to 30 days, followed by maintenance therapy twice per week. Intermittent prolonged treatment may be necessary because the dermatitis in many cases recurs upon discontinuation. Some patients cannot tolerate tacrolimus because of burning or stinging. These side effects may be minimized by applying a film of petroleum jelly before applying the ointment. Calcineurin inhibitors can also be used in conjunction with steroids to allow for a more sparing use of steroids.
The US Food and Drug Administration (FDA) has issued a public health advisory regarding a potential cancer risk (lymphoma, skin cancer) from use of topical calcineurin inhibitors . Despite the FDA's boxed warning, no clear evidence has been found linking the topical calcineurin inhibitors to an increased incidence of malignancy in either children or adults [50-52].
Patients with severe refractory disease — For patients with localized areas of involvement that do not respond to topical therapies, we suggest intralesional corticosteroids. A total of 0.1 to 2 mL of triamcinolone acetonide 3.3 to 10 mg/mL is given by injecting small amounts to include the entire lesion or plaque (table 6). If helpful, the injection can be repeated at monthly intervals for up to four times a year. Prior application of a small amount of a topical anesthetic, such as EMLA, facilitates injection. Symptomatic localized areas that do not respond to intralesional corticosteroids should be biopsied to exclude malignancy.
Patients with severe, persistent symptoms may require systemic immunosuppressive therapy. These patients should be managed in conjunction with appropriate specialists including gynecologists, dermatologists, and allergists.
Oral or intramuscular (IM) corticosteroids can be used for patients experiencing a severe flare such that they cannot tolerate topical application or for patients who require a short-term bridge to other systemic steroid-sparing therapy . The authors prefer the use of oral corticosteroids, so that any adverse side effects can be minimized by titration of dose, which is not possible after IM administration. Oral prednisone is given at a dose of 0.5 to 1 mg/kg per day (maximum daily dose 60 mg) for three to seven days and then tapered by 10 to 20 mg every three to seven days. More gradual tapering of treatment can be required for severe disease, and regimens are often customized based on the clinical picture.
The short- and long-term side effects of systemic steroid therapy are well documented and include hypertension, hyperglycemia (diabetics may require more frequent blood glucose monitoring), weight gain, sleep or mood disturbance, gastritis, and adrenal suppression. (See "Major side effects of systemic glucocorticoids".)
A number of other systemic immunosuppressants, including methotrexate, mycophenolate mofetil, azathioprine, and cyclosporine, are variably effective in the management of atopic dermatitis, psoriasis, lichen sclerosus, and lichen planus. All require ongoing monitoring and should be administered by a clinician experienced in their usage.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Vulvar dermatitis".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Vulvar itching (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Vulvar dermatitis is the most common cause of vulvar complaints in women. Vulvar dermatitis has been traditionally divided into two subtypes, endogenous (atopic) and exogenous (irritant or allergic). However, these categories are not mutually exclusive, and it is possible for both to exist concomitantly in an individual patient. (See 'Introduction' above and 'Endogenous versus exogenous dermatitis' above.)
●The most common symptom of vulvar dermatitis is pruritus, which can be intense and nocturnal. Other symptoms include burning, rawness, or stinging. Physical signs depend upon the chronicity of disease and include erythema (picture 1B), papillomatosis (picture 2), and lichenification (picture 3). (See 'Clinical manifestations' above.)
●The diagnosis of endogenous or exogenous vulvar dermatitis can usually be made clinically, based upon characteristic symptoms, a personal or family history of atopy, or personal history of vulvar exposure to medications, perfumes, or other chemicals. Patch testing is helpful to distinguish between atopic and allergic contact dermatitis. (See 'Diagnosis' above.)
●Infection should be excluded by vulvar cultures for candidiasis, herpes simplex virus (if ulcers are noted), and potential bacterial pathogens. In uncertain cases and those not responding to standard treatment, a biopsy may be necessary to identify an underlying inflammatory dermatosis or neoplasia. (See 'Differential diagnosis' above.)
●The treatment of vulvar dermatitis requires a multimodal approach involving behavior modifications, appropriate skin care and hygiene practices (table 4), treatment of coexistent infections, control of pruritus, and topical or systemic medication. An explanation of the condition, emphasizing the need for long-term treatment with maintenance regimens, and vigilance to prevent and diagnose recurrent infections are important factors for success. (See 'Management' above.)
●Soaking in warm water temporarily relieves vulvar discomfort. Sealing in the moisture with medication prescribed or emollient (eg, plain petroleum jelly) is also a mainstay of therapy. A sedating antihistamine such as hydroxyzine given in the evening helps to control nighttime itching and scratching. (See 'General measures' above and 'Control of pruritus' above.)
●For women with mild symptoms, we suggest low- to medium-potency topical corticosteroids (Grade 2C). Hydrocortisone 1% or 2.5%, desonide 0.05%, or triamcinolone 0.1% ointment is applied daily for two to four weeks. Therapy is continued indefinitely, at the minimum frequency necessary to control pruritus, with a goal of less than 14 days per month. (See 'Patients with mild symptoms' above.)
●For women with moderate to severe symptoms, we suggest high-potency topical corticosteroids, such as clobetasol propionate 0.05% or betamethasone dipropionate 0.05% (groups 1 to 3 (table 5)) (Grade 2C). Topical corticosteroids are applied at bedtime daily for 30 days. Ointments are preferred to creams, as they contain fewer preservatives. (See 'Patients with moderate to severe symptoms' above.)
●For patients with localized severe vulvar dermatitis that does not respond to high-potency topical corticosteroids, we suggest intralesional corticosteroids (Grade 2C). A total of 1 to 2 mL of triamcinolone acetonide 3.3 to 10 mg/mL is given by injecting small amounts to include the entire involved area. Localized disease that does not respond to intralesional corticosteroids should be biopsied to exclude malignancy. Patients with severe, persistent symptoms may require systemic immunosuppressive therapy. (See 'Patients with severe refractory disease' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Elizabeth Gunther Stewart, MD, who contributed to earlier versions of this topic review.