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Vulvitis

Vulvitis is an of the , the external folds of surrounding the vaginal opening in females, often presenting as a symptom of underlying irritants, , or dermatological conditions rather than a standalone . It commonly affects individuals across all ages, including prepubertal girls and postmenopausal women, and is characterized by localized discomfort that can significantly impact daily activities and . The primary causes of vulvitis encompass a range of non-infectious and infectious factors. Non-infectious triggers include exposure to irritants such as perfumed soaps, shampoos, detergents, synthetic underwear, or activities like prolonged contact with wet swimsuits and bicycle seats, which can provoke an allergic or response. Infectious etiologies involve yeast infections (), bacterial overgrowth, sexually transmitted infections like , or parasites such as pubic lice and . Hormonal imbalances, particularly low levels during , can thin vulvar tissues and increase susceptibility to inflammation, while chronic dermatoses like , , or contribute to persistent cases. Symptoms typically include intense itching (pruritus), redness, swelling, and burning sensations, which may worsen with touch or during and ; additional manifestations can involve blisters, open sores, scaly or thickened patches, and cracks in the . Diagnosis generally relies on a thorough , of the , and targeted tests such as swabs for , pH measurements, or biopsies to rule out precancerous changes in presentations. Treatment strategies are tailored to the underlying cause and severity, emphasizing symptomatic relief and prevention of recurrence. Avoiding known irritants, wearing breathable underwear, and practicing gentle with plain water or unscented products form the foundation of management. For inflammatory responses, topical corticosteroids or creams are commonly prescribed, while infections require , , or medications; severe or refractory cases may necessitate systemic therapies like oral steroids or referral to a dermatologist. Early intervention is crucial to alleviate discomfort and prevent complications such as scarring or secondary infections.

Overview

Definition

Vulvitis is defined as an of the , the external portion of the female genitalia. The encompasses the , , , and vaginal vestibule, which is the area surrounding the vaginal opening. This condition primarily affects the soft, sensitive skin and mucous membranes in this region, leading to localized inflammatory changes. Vulvitis must be distinguished from related conditions such as vaginitis, which involves inflammation of the internal vaginal lining rather than the external structures. Unlike vulvodynia, a chronic pain syndrome in the vulvar area without evidence of inflammation or infection, vulvitis specifically denotes an inflammatory process. The term "vulvitis" derives from the Latin word vulva, meaning "wrapper" or "covering," combined with the suffix -itis indicating inflammation; it entered medical usage in the mid-19th century to describe inflammatory responses in vulvar tissues. Early descriptions in medical literature from the 1800s recognized it as a distinct entity involving irritation and swelling of the external genitalia, often linked to various irritants or infections.

Epidemiology

Vulvitis affects a significant portion of women worldwide, with estimates indicating that up to 75% experience at least one episode during their lifetime, often linked to common causes such as . The condition is prevalent across all age groups but is particularly common in reproductive-aged women, where 8-18% of reproductive-aged women report annual symptomatic episodes. Demographically, vulvitis is exclusive to individuals with vulvar anatomy, predominantly females, with higher incidence in specific subgroups due to hormonal influences. Prepubertal girls face elevated risk owing to low levels, which result in thinner vulvar tissues more susceptible to and . Postmenopausal women also exhibit increased rates, attributed to estrogen decline leading to atrophic changes in vulvar , exacerbating vulnerability to . Key risk factors include diabetes mellitus, which elevates glucose levels in vulvovaginal secretions and promotes opportunistic infections like . Obesity contributes by altering local microenvironment and , while —such as from or use—impairs defenses against pathogens. Poor practices and frequent exposure to irritants, including scented soaps, products, and tight clothing, further heighten susceptibility by disrupting the vulvar barrier. Globally, vulvitis prevalence varies, with higher rates reported in developing regions; for instance, studies in show an overall vulvovaginitis prevalence of 50% among women attending clinics, often tied to limited access to hygiene resources and elevated burdens. In contrast, developed countries report lower symptomatic rates, though lifetime exposure remains high due to similar infectious .

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Causes

Vulvitis, the of the , arises from a variety of etiologic factors that can be broadly classified as infectious or noninfectious. Infectious causes are among the most common triggers, often resulting from microbial overgrowth or direct invasion. Bacterial infections may involve pathogens such as group B or species, which can lead to acute , particularly in children or immunocompromised individuals. Fungal infections, primarily caused by , are frequent in adults and manifest as yeast infections that extend to the . Viral agents like can produce recurrent ulcerative lesions contributing to vulvar . Parasitic infestations, including or pubic lice, may also provoke intense itching and secondary irritation in the vulvar area. Noninfectious causes encompass irritants, allergens, hormonal imbalances, dermatologic conditions, and physical trauma. Contact irritants such as soaps, detergents, synthetic underwear, or chlorinated water can disrupt the vulvar skin barrier, leading to dermatitis-like . Allergens including , spermicides, or perfumed may elicit hypersensitivity reactions in susceptible individuals. Hormonal factors, particularly low levels during , contribute to atrophic changes that predispose the to and . Autoimmune or skin disorders like and can chronically affect the vulvar , causing persistent inflammatory changes. from activities such as cycling or procedures like may induce mechanical injury and subsequent . Vulvitis often exhibits a multifactorial , where an initial irritant may predispose the area to secondary bacterial or , amplifying the inflammatory response.

Pathophysiology

Vulvitis involves an inflammatory cascade initiated by triggers such as irritants, pathogens, or allergens that disrupt the vulvar epithelial barrier, prompting the release of pro-inflammatory mediators like (e.g., IL-1β, IL-6, and [TSLP]) and from local immune cells. This activation stimulates sensory nerves via protease-activated receptor-2 (PAR-2) and promotes a Th2-biased , leading to , increased , , and infiltration of leukocytes such as neutrophils and lymphocytes into the affected tissues. In infectious cases, such as those driven by species, the pathogen's hyphal forms invade superficial epithelial layers, amplifying production and sustaining the inflammatory milieu without eliciting a fully protective adaptive response. Tissue changes in vulvitis arise from this cascade, with initial epithelial disruption increasing permeability and , which heightens susceptibility to secondary infections and perpetuates . In acute phases, hyperemia and predominate, while chronic inflammation can induce through sustained signaling and remodeling, or via repeated barrier compromise. For instance, in conditions like contributing to vulvitis, dermal hyalinization and homogenization occur alongside epidermal thinning, reflecting progressive fibrotic changes. Hormonal influences, particularly deficiency as seen in postmenopausal women, exacerbate vulvitis by thinning the vulvar , reducing content, and elevating , thereby diminishing defenses and increasing vulnerability to irritants and microbial overgrowth. This hypoestrogenic state, characteristic of genitourinary syndrome of , impairs epithelial integrity and promotes a pro-inflammatory environment conducive to persistent inflammation. Histological features of vulvitis vary by etiology but commonly include , hyperemia, and inflammatory infiltrates in the . Lymphocytic infiltrates predominate in autoimmune or allergic forms, such as , forming a band-like pattern beneath the , while -rich infiltrates—often exceeding 50% of the cellular component—characterize entities like Zoon vulvitis or vulvitis, accompanied by , vascular proliferation, and deposits from chronic hemorrhage. In infectious vulvitis, predominance may be evident alongside epithelial invasion.

Clinical Features

Symptoms

The primary symptoms of vulvitis include intense itching (pruritus) and a burning sensation in the vulvar area, which can be severe and persistent. Patients often report soreness or pain, particularly during urination () or (), which may exacerbate the discomfort. Associated symptoms may include when vulvitis occurs concurrently with , and a foul odor in cases involving bacterial or parasitic infections. General discomfort can affect daily activities, such as walking or sitting, leading to significant interference with . Symptoms vary by severity and duration; acute episodes typically present with sudden onset of intense irritation, while chronic vulvitis involves persistent low-level itching and burning that may wax and wane over time. These subjective experiences are often accompanied by visible changes in the vulvar tissue, as described in the signs section.

Signs

Vulvitis presents with various objective physical findings observable during clinical examination, primarily affecting the vulvar and mucosa. The most common local signs include , manifesting as localized or diffuse redness of the vulvar tissues, and , which appears as swelling particularly around the and minora. Excoriations, often linear abrasions from scratching, and fissures or cracks in the are also frequent, especially in cases of or . Lesion types vary depending on the underlying but are key objective features. Vesicles or clear fluid-filled blisters may be present, particularly in infectious or allergic contexts, while white plaques or scaly patches are characteristic of fungal infections or lichenoid conditions. Erosions, representing superficial loss of the epithelial layer, and ulcers, deeper defects, can occur in more severe or erosive presentations. The extent of these signs can range from localized involvement of the to diffuse changes encompassing the and . In chronic or severe cases, secondary lichenification—thickening and of the skin—may develop due to repeated rubbing or scratching.

Diagnosis

Clinical Evaluation

The clinical evaluation of vulvitis begins with a detailed history-taking to identify potential triggers and contextualize the patient's presentation. Key components include assessing the onset and duration of symptoms, such as acute versus chronic irritation, to differentiate infectious from noninfectious etiologies. Aggravating factors should be explored, including exposure to irritants like soaps, detergents, or hygiene products, as well as sexual activity that may exacerbate or introduce pathogens. Associated symptoms, such as , , or fever, are inquired about to gauge severity and possible systemic involvement, while relevant encompasses conditions like , which predisposes to recurrent infections, and menopausal status, which can contribute to atrophic changes. The focuses on gentle, non-invasive techniques to minimize discomfort and accurately assess vulvar involvement. Under adequate lighting, the is inspected for , , fissures, or excoriations, often without a speculum if internal is not indicated, to avoid further . Tenderness is evaluated through light or by using a for pinpoint testing of specific areas, such as the , to identify localized . This approach helps elicit signs like tenderness or while considering the patient's comfort. Differential diagnosis is informed by targeted questioning during history-taking to rule out mimics of vulvitis. For instance, inquiries into recent product use or allergies help distinguish , while details on sexual history and multiple partners aid in excluding sexually transmitted infections like or . Such considerations ensure a focused evaluation tailored to common noninfectious and infectious confounders.

Diagnostic Tests

Diagnostic tests for vulvitis aim to identify infectious, inflammatory, or neoplastic causes through laboratory and procedural methods, often guided by clinical findings. Vaginal and vulvar swabs are commonly collected to detect bacterial, fungal, or viral pathogens. These include , cultures, and amplification tests (NAATs) such as for organisms like species, , or bacterial vaginosis-associated . For suspected candidal vulvitis, a wet mount preparation of the swab may reveal pseudohyphae or budding yeast under microscopy, while cultures confirm non-albicans if needed. Bacterial cultures or NAATs target pathogens like in cases of acute infectious vulvitis. is indicated for chronic, persistent, or suspicious vulvar lesions to exclude , , or infiltrates as in Zoon vulvitis. A punch or shave provides histopathological confirmation, revealing features such as acanthosis, parakeratosis, or dense infiltration. Additional tests include pH measurement of , where a pH greater than 4.5 suggests or contributing to vulvitis. analysis screens for urinary tract infections that may coexist or mimic symptoms, while blood glucose testing evaluates for underlying diabetes mellitus, a for recurrent candidal vulvitis due to glucosuria. Comprehensive STI screening via NAATs on swabs or detects , , or , which can cause or exacerbate vulvitis. Imaging such as is rarely required but may be used for detailed visualization of the if precancerous changes are suspected, allowing directed .

Management

Treatment

Treatment of vulvitis focuses on addressing the underlying while providing symptomatic relief through general supportive measures and targeted therapies. Initial often includes non-pharmacologic interventions such as sitz baths in warm water to soothe and promote hygiene, application of emollients like to protect the skin barrier and reduce dryness, and avoidance of potential irritants including scented soaps, tight clothing, and synthetic underwear. For acute , short-term use of low-potency topical corticosteroids, such as 1% cream applied twice daily for 1-2 weeks, can effectively reduce and pruritus without significant risk of when limited in duration. Cause-specific treatments are selected based on identified pathogens or contributing factors. For infectious vulvitis due to candidal overgrowth, topical antifungals like miconazole 2% cream applied twice daily for 7 days or oral 150 mg as a single dose provide high cure rates of 80-90%. Bacterial causes, such as those associated with or secondary infections, are managed with antibiotics including 500 mg orally twice daily for 7 days or topical clindamycin cream. Viral etiologies like require antivirals such as acyclovir 400 mg orally three times daily for 7-10 days to shorten outbreak duration and alleviate symptoms. In cases of atrophic vulvitis related to deficiency, topical creams (e.g., 0.01%) applied intravaginally or externally daily for 2 weeks followed by twice-weekly maintenance restore mucosal integrity and relieve . For steroid-resistant or refractory vulvitis, particularly in inflammatory conditions like or plasma cell vulvitis, topical calcineurin inhibitors such as 0.1% ointment applied twice daily for 4-6 weeks offer an alternative by modulating and reducing symptoms without side effects. Surgical excision may be considered for persistent lesions unresponsive to medical therapy, such as in provoked vestibulodynia or chronic fissuring, with achieving 60-80% symptom resolution in select cases. Multidisciplinary referral to or is recommended for suspected autoimmune associations to optimize long-term control. Ongoing monitoring involves clinical follow-up within 1-4 weeks to evaluate response, adjust , and detect recurrence, with periodic assessments every 6 months for conditions to prevent complications like scarring or .

Prevention

Maintaining proper is essential for preventing vulvitis, as irritants and moisture can disrupt the vulvar skin barrier. Women should clean the gently with warm water or mild, unscented soap, avoiding vigorous scrubbing, and pat the area dry afterward to minimize moisture retention. Douching, , and the use of scented products, sprays, or powders should be avoided, as these can alter the natural and flora, increasing irritation risk. Additionally, wiping from front to back after using the toilet helps prevent bacterial transfer from the to the . Lifestyle modifications further reduce vulvitis risk by promoting a dry, breathable environment and addressing underlying factors. Wearing loose-fitting clothing and breathable cotton underwear—while avoiding synthetic fabrics, tight pants, pantyhose without cotton crotches, or underwear at night—helps prevent moisture buildup and friction. Promptly changing out of wet swimsuits, sweaty clothes, or after exercise is recommended to avoid prolonged dampness. For infection-related causes, practicing safe sex with condom use and limiting sexual partners can prevent sexually transmitted vulvitis, while maintaining glycemic control in diabetes reduces recurrent infections. Avoiding hot tubs, baths, or whirlpool spas also minimizes exposure to irritants and pathogens. In at-risk groups, targeted strategies can mitigate vulvitis development. Postmenopausal women, who face increased risk due to decline leading to , may benefit from low-dose vaginal therapy under medical supervision to restore tissue health and prevent irritation. Individuals with conditions or should perform regular vulvar checks and adhere to disease management to avoid exacerbations. plays a key role, emphasizing recognition of early irritants like new soaps or fabrics and prompt discontinuation to prevent escalation, with consultation for persistent issues.

Special Populations

Vulvitis in Children

Vulvovaginitis, which often presents as vulvitis in children, is a common gynecologic concern in prepubertal girls, accounting for approximately 62% of pediatric visits for such issues. It is particularly prevalent in girls aged 1 to 10 years, with peak incidence often noted between 2 and 6 years due to the prepubertal state of low levels, which results in thin, fragile vaginal and vulvar that is more susceptible to irritation and infection. The majority of cases (70% to 80%) are nonspecific, arising from poor practices, such as inadequate wiping after or hand-to-genital contact, which allows fecal to enter the area. Common irritants include soaps, bubble baths, scented wipes, and tight synthetic clothing that traps moisture, exacerbating inflammation in the sensitive tissues. Infectious causes account for about 25% of cases and include like Escherichia coli from the , β-hemolytic streptococci, or from respiratory sources; additionally, pinworms (Enterobius vermicularis) can cause perianal itching leading to secondary vulvar irritation. Symptoms in children typically manifest as mild to moderate vulvar redness, itching (pruritus), and soreness, often accompanied by scant that may be clear, white, or yellow without a foul odor in nonspecific cases. (burning during urination) can occur if affects the urethral opening, and children may report discomfort while sitting or walking. In infectious cases, discharge may become more profuse or malodorous, prompting earlier parental concern. Management focuses on and supportive care, beginning with counseling for parents and children, including wiping front to back, daily warm water rinses or baths (optionally with 1-2 tablespoons of baking soda or per bath to soothe), and avoiding irritants like bubble baths or perfumed products. Emollients such as or zinc oxide ointment are recommended to protect the skin and reduce . For confirmed bacterial infections, a short course of oral or topical antibiotics (e.g., amoxicillin for streptococcal causes) is prescribed, while pinworm infections are treated with . Topical steroids are generally avoided unless there is severe or chronic inflammation, such as in associated , to prevent skin thinning; instead, parental reassurance is emphasized to alleviate anxiety. Complications like scarring are rare with prompt management, but untreated chronic cases may lead to labial adhesions.

Zoon Vulvitis

Zoon vulvitis, also known as plasma cell vulvitis or vulvitis chronica plasmacellularis, is a rare, benign, inflammatory dermatosis of the vulvar mucosa characterized by a predominant infiltrate in the . It represents an idiopathic condition, though potential triggers include local irritants, , or , with no definitive established. The condition primarily affects women between 26 and 70 years of age, with a mean age of 55.3 years and a noted predominance in postmenopausal individuals; it is underrecognized, with a mean diagnostic delay of approximately 4.7 years (or a of 12 months in some reports). Clinically, it presents as well-demarcated, orange-yellow to erythematous plaques on the vulvar mucosa, often featuring a glistening surface and characteristic "" spots due to dotted vascular ; erosions may occur, and lesions are typically bilateral and symmetrical, most commonly involving the and introitus. Symptoms are often mild and include (reported in 44% of cases), , burning or stinging (52%), and pruritus (41%), though some patients remain . Diagnosis relies on clinical suspicion in persistent vulvar lesions unresponsive to initial therapies, confirmed by vulvar revealing a dense lichenoid infiltrate composed of more than 50% plasma cells, along with deposits, vascular proliferation, and erythrocyte extravasation; epidermal atrophy and mixed inflammatory cells may also be present. Treatment typically involves first-line topical high-potency corticosteroids, such as 0.05% ointment, or calcineurin inhibitors like 0.1%, which achieve symptomatic improvement in approximately 88% of cases, though recurrence is common. Alternative options include laser therapy, , or surgical excision for refractory lesions. The is favorable, with no reported malignant potential, but long-term monitoring is recommended to detect any rare associated .

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