Vulvar Dermatoses, Bartholin Disease & Vulvar Cancer
White, thick, or ulcerated—know when to treat and when to biopsy
Vulvar dermatoses
Lichen sclerosus. A chronic, autoimmune-type inflammatory dermatosis with two peaks: prepubertal girls and postmenopausal women. Intense, often nocturnal pruritus is typical, with dyspareunia, dysuria, or painful defecation (constipation in children). The skin becomes thin, white, and crinkled like cigarette paper in a figure-of-eight around the vulva and anus, with fissures and purpura; over time the labia minora resorb, the clitoral hood fuses (phimosis), and the introitus narrows. The vagina is spared. In girls, purpura and fissures can be mistaken for sexual abuse.
Treatment of lichen sclerosus. Biopsy confirms the diagnosis in adults and is required for any thickened, ulcerated, or nonhealing area. Clobetasol 0.05% ointment nightly, tapered to maintenance 1–3 times weekly, relieves symptoms and limits scarring; topical testosterone is obsolete. Because a few percent of patients develop squamous cell carcinoma, examine every 6–12 months for life.
Lichen simplex chronicus. Chronic rubbing and scratching—triggered by atopy, irritants, or candidiasis—thicken the skin into leathery, lichenified plaques with exaggerated markings, usually on the labia majora. Treatment breaks the itch-scratch cycle: remove irritants, apply a mid- to high-potency topical steroid, give a sedating antihistamine (hydroxyzine) at night, and treat the trigger.
Erosive lichen planus. A T-cell–mediated disease producing glazed red erosions with white lacy (Wickham) borders on the vulva and vagina, often with oral lesions. Burning, dyspareunia, and discharge are common, and vaginal adhesions can obliterate the canal. Treat with ultrapotent topical steroids (including intravaginal preparations) and vaginal dilators.
| Feature | Lichen sclerosus | Lichen simplex chronicus | Erosive lichen planus |
|---|---|---|---|
| Skin | Thin, white, wrinkled | Thick, leathery | Red erosions, lacy white border |
| Vagina | Spared | Spared | Involved; synechiae |
| Architecture | Labia minora resorb, clitoral phimosis | Preserved | Scarring, narrowing |
| Treatment | Clobetasol, lifelong follow-up | Steroid, nighttime antihistamine, remove trigger | Ultrapotent steroid, dilators |
Bartholin duct cysts and abscesses
The Bartholin glands open into the posterolateral vestibule at about 4 and 8 o'clock. Duct obstruction produces a painless cyst; infection produces a tender, fluctuant abscess, usually polymicrobial and occasionally gonococcal or chlamydial.
- Asymptomatic cyst, under 40observe; sitz baths for mild symptoms
- Abscess or symptomatic cystincision and drainage with a Word catheter left 4–6 weeks so a new duct epithelializes; antibiotics if cellulitis or STI risk
- Recurrencemarsupialization; gland excision is a last resort
- Over 40 or solid or persistent massbiopsy or excise to exclude Bartholin gland carcinoma
Needle aspiration or simple incision without a catheter tends to recur.
Vulvar intraepithelial neoplasia
Vulvar HSIL (usual-type VIN). Driven by HPV 16 and seen in younger women who smoke or are immunosuppressed (HIV). Lesions are often multifocal raised white, red, or pigmented plaques and may itch. Biopsy is required, and the cervix, vagina, and anus are examined because HPV neoplasia is often multicentric. Options are wide local excision (when invasion cannot be excluded), laser ablation, or topical imiquimod; recurrence is common. Vulvar LSIL is flat condyloma (HPV effect), not a precancer.
Differentiated VIN. An HPV-independent, TP53-mutated lesion in older women with lichen sclerosus or lichen planus. It is subtle and usually unifocal but progresses faster to keratinizing squamous cell carcinoma, so it is excised.
Vulvar malignancies
Squamous cell carcinoma. About 90% of vulvar cancers, typically in women around 70, arising through either the HPV/HSIL pathway or the lichen sclerosus/differentiated VIN pathway. Long-standing pruritus is the usual complaint, followed by a mass, ulcer, or bleeding, most often on the labia majora. Diagnosis is frequently delayed by months of empiric creams—punch-biopsy any vulvar lesion that persists or fails treatment. Spread is local and lymphatic: superficial inguinal, then deep femoral, then pelvic nodes.
Treatment. Radical local excision with 1–2 cm margins plus inguinofemoral node evaluation. Sentinel node biopsy is used for unifocal tumors <4 cm with clinically negative groins; otherwise lymphadenectomy, with both groins assessed for midline lesions. Tumors with stromal invasion ≤1 mm do not need node assessment. Groin dissection causes wound breakdown, lymphocysts, and chronic leg lymphedema. Locally advanced disease is treated with cisplatin-based chemoradiation.
Melanoma. The second most common vulvar cancer, presenting as a pigmented (or amelanotic) lesion, often on the clitoris or labia minora of older women. Prognosis tracks depth of invasion. Biopsy any new or changing pigmented vulvar lesion; treat with wide excision ± sentinel node biopsy.
Extramammary Paget disease. An intraepithelial adenocarcinoma in postmenopausal women: a pruritic, sharply bordered, red velvety eczematous plaque with white islands that fails steroid therapy. Biopsy shows large, pale, mucin-rich Paget cells. Evaluate for an underlying adnexal adenocarcinoma and for breast, colorectal, and urinary tract cancers. Wide local excision is standard but recurrence is common; imiquimod is an alternative.