Vulvitis: Predisposing Factors, Clinical Manifestations, Diagnosis, and Treatment

Vulvitis is an inflammation of the vulvar tissues that generally occurs secondary to various vulvar conditions. The disease tends to affect the labia minora and majora, clitoris, mons pubis, and vestibule of the vagina.

Vulvitis is common among premenarchal girls and postmenopausal women. Both groups have low estrogen levels that may cause the vulvar tissues to become thin and dry. Thin vulvar tissues, in turn, are more prone to injuries and infections.

Note that generally, inflammation is not limited to the vulva but spreads further to the vagina; such cases are described as vulvovaginitis.

Besides an infectious nature, vulvitis may develop as an idiopathic condition. For instance, one of the forms is granulomatous vulvitis, which manifests as chronic, painless edema of the genitalia and shows histological signs of granulomatous inflammation.

One more distinct category among vulvar conditions is vulvar dermatoses:

• Vulvar lichen sclerosus;
• Vulvar lichen planus;
• Lichen simplex chronicus;
• Vulvar eczema;
• Vulvar psoriasis;
• Vulvar intraepithelial neoplasia;
• Genital ulcer of the vulva;
• Lipschütz ulcer of the vulva.

In vulvitis, infectious agents typically belong to the opportunistic pathogenic microflora. In approximately 90% of cases, vulvitis is associated with Candida albicans. The remaining reports indicate involvement of E. coli, Staphylococcus epidermidis, group B Streptococcus, Enterobacterales, etc. The list of bacterial pathogens is not limited to the species mentioned above and may also include Neisseria gonorrhoeae, Trichomonas vaginalis, and Chlamydia trachomatis.

The most common viral agent is the herpes simplex virus.

Occasionally, vulvitis may develop due to bacteria causing tuberculosis and diphtheria. However, such instances are rare.

Note that infections only develop when vulvar tissues are injured by a specific factor.

Predisposing Factors of Vulvitis

Vulvitis may develop due to certain conditions when the integrity of the skin and mucosa of the external genitalia is compromised. These include:

• Vulvovaginal atrophy;
• Urinary incontinence, either as a standalone factor or in combination with a prolonged use of incontinence pads;
• Endocrine and metabolic disorders (e.g., diabetes mellitus, obesity);
• Synthetic or tight underwear that causes the mucosal microinjuries;
• Allergies to dyed or scented toilet paper, sanitary pads, or tampons; soap, vaginal sprays, and shower products that contain harsh ingredients; laundry detergents and rinse aids;
• A wet bathing suit or underwear if worn over a long period, leading to skin macerations;
• Trauma caused by physical activities such as cycling or horse riding;
• Spermicides that cause allergic reactions;
• Vulvar scratching due to scabies or pubic lice infestation;
• Radiotherapy.

Clinical manifestations of vulvitis

Patients may not have any specific complaints but experience:

• Pruritus;
• Burning sensations;
• Hyperemia and edema;
• Fissures and scratch marks (excoriations);
• Rashes in the form of macules, patches, papules, plaques, nodules, vesicles, bullae, or pustules.

These lesions may be of normal skin color or develop reddish, whitish, brownish, or black shades.

In cases of vulvovaginitis, patients may also observe an abnormal foul-smelling discharge.

Chronic inflammation in the vulvar region may induce the following:

• Swelling, induration, and deformation of the external genitalia;
• Younger females may develop synechiae.

In such instances, patients report persistent dyspareunia (painful sexual intercourse) and dysuria (painful or uncomfortable urination).

Differential diagnosis

Vulvar lichen sclerosus

Vulvar lichen sclerosus mainly affects the labia minora and majora, prepuce of the clitoris (clitoral hood), and perianal region. Generally, the vagina remains intact. Around 10% of patients experience extragenital lesions.

Upon examination, the tissues look pale and often atrophic. Atypical variations may present with hyperkeratosis.

As a pathognomonic symptom, purpura (or bruising, ecchymosis) is also observed. Compromised morphology of the external genitalia leads to resorption of the labia minora and/or midline fusion. Furthermore, the clitoral hood may become fused with an otherwise unaffected clitoris. Erosions are common; lichenification and hyperkeratosis may be occasionally observed. Note that these signs are not typical for vulvitis and may be indicative of vulvar intraepithelial neoplasia.

The changes may either be localized (generally on the clitoral hood) or include the perianal region and resemble a figure of 8.

Vulvar lichen planus

Depending on clinical manifestations, vulvar lichen planus may be classified as follows:

• Classic: the keratinized anogenital skin bears typical papules, with or without stretch marks on the internal surface of the vulva. Upon healing, papules leave hyperpigmentation patches, especially in women with a darker skin type. One of the features of this condition is that it may be absolutely asymptomatic.
• Hypertrophic: this type of the disease is relatively uncommon and is difficult to diagnose. In general, the perineum and perianal region are affected. The skin is covered with thickened warty eruptions or plaques that may become ulcerated, infected, and painful but do not spread to the vagina. Such lesions may be confused with signs of malignant neoplasms.
• Erosive: this is the most common form of vulvar lichen planus. Erosions are detected on the mucosa. The erosions are contoured by a pale purple, lacelike net (Wickham striae). If left untreated, the erosions may heal on their own, leading to scars, synechiae, and complete vaginal stenosis. The lesions may look like loose telangiectasias with focal erythema, responsible for general symptoms such as postcoital bleeding, dyspareunia, and variable serohemorrhagic discharge.

Lichen simplex chronicus vulvar

Lichen simplex chronicus vulvar is frequently associated with atopic eczema or psoriasis. Continuous scratching leads to lichenification, meaning thickened, slightly scaly skin that has a pale or earthy tint. Clinically, it appears as erythematous inflammation with poorly defined edges; it might present with fissures. The skin appears very dry (xerosis), slightly scaly, and becomes thickened and lichenified due to chronic scratching.

Irritant contact dermatitis

Irritant contact dermatitis typically appears as coalesced lesions and is limited to the area that has been in direct contact with the irritant.

Allergic contact dermatitis

Unlike the irritant form, the skin affected by allergic contact dermatitis may present with macular lesions; the lesion edges are less defined and cover a larger surface than the contact area with the suspected allergen. Signs and symptoms of allergic contact dermatitis typically show 48-72 hours after the allergen contacts the previously sensitized skin. In severe cases, the skin of the genitalia becomes extremely inflamed and edematous; sometimes weeping, blisters, and erosions may develop.

Seborrheic dermatitis

Seborrheic dermatitis typically manifests as slightly pink, shiny, poorly outlined patches with a thin whitish scale. Skin alterations may affect the pubic region, inguinal grooves, anal region, and vulva. Lichenification is also typical for the condition. The affected areas often bear excoriations, and pubic hair loss may be observed.

Vulvar psoriasis

Vulvar psoriasis generates clearly defined, brightly colored erythematous plaques that appear symmetrical and are found on the labia majora. The lesions may spread to the inguinal grooves and perianal skin. Fissures may be observed, whereas scaling is rare. Other body regions, such as the scalp, umbilicus, or nails, also tend to be involved.

Squamous intraepithelial lesion

Clinical manifestations of a squamous intraepithelial lesion (earlier referred to as vulvar intraepithelial neoplasia) may vary. The condition may generate white or erythematous, pigmented, often wart-like plaques. Multifocal lesions are often nonresponsive to treatment. Lesions may be hyperkeratotic, erosive, or ulcerated. They are commonly found around the clitoris, labia minora, and vaginal introitus, as well as the internal surface of the labia majora. The perianal area and perineum are rarely affected.

Diagnosis of vulvitis

1. Detailed medical history and gynecological examination.
2. Highly sensitive techniques: DNA testing of a smear from the affected site. The method helps determine the following pathogens:
   • Candida;
   • Trichomonas vaginalis;
   • Chlamydia;
   • Neisseria gonorrhoeae;
   • As well as E. coli, Streptococcus spp.;
   • Staphylococcus spp. and others.
3. Vulvoscopy;
4. Biopsy as needed when:
   • The diagnosis is complicated;
   • The course of the diseases is atypical;
   • An intraepithelial lesion or malignancy is suspected;
   • No response to first-line treatment has been achieved;
   • Atypical pigmented patches are observed.
5. Patch testing (performed when secondary allergies or contact dermatitis is suspected).

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Treatment of vulvitis

1. Antibiotic therapy. Vulvitis complicated by a bacterial infection requires local broad-spectrum antibiotics. If Trichomonas vaginalis, Сhlamydia trachomatis, or Neisseria gonorrhoeae is identified, specific antibiotics are prescribed.
2. Antifungal agents are used to treat candidal vulvitis. Azole antifungal agents relieve symptoms in 80–90% of patients. The most commonly used drugs are:
   • Clotrimazole;
   • Miconazole;
   • Tioconazole;
   • Butoconazole;
   • Terconazole.
3. Antiviral therapy is aimed at treating herpes infections. The following medications are recommended:
   • Acyclovir;
   • Famciclovir;
   • Valacyclovir.

Vulvar dermatosis is treated locally with glucocorticosteroids.