Vulval lichen sclerosus

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Lichen sclerosus is a chronic inflammatory disorder with a strong predilection for anogenital skin. It occurs at any age, including before puberty, and is common after menopause. Ask about itch, soreness, tearing, dyspareunia, dysuria, urinary spraying, constipation, bleeding and previous treatments. Explore autoimmune history and irritant products, but make no assumption that symptoms are sexual. Explain the purpose of examination, obtain consent, offer a chaperone and allow the patient to stop. Children should receive age-appropriate explanation and assent, with a caregiver present unless a safe alternative is clinically appropriate.

Examine the complete vulva and perianal skin under good illumination. Active disease may be porcelain white, pale, ivory, pink-white or less conspicuously pale against richly pigmented skin; texture, fissures, fragility, purpura and loss of architecture are often more reliable than colour. Record clitoral hood, labia minora, introitus and perineum on a diagram. The classic figure-of-eight distribution can include perianal fissuring and painful defaecation. Vaginal mucosal involvement is unusual and should prompt reconsideration of lichen planus, mucous-membrane pemphigoid or another diagnosis.

Treatment has three aims: suppress symptoms and inflammation, prevent additional scarring and reduce cancer risk through control and surveillance. Teach the exact fingertip amount and site using a mirror or diagram, provide an induction and maintenance plan in writing and continue a bland emollient barrier and soap avoidance. Scheduled review is part of treatment, not an optional extra. A patient whose symptoms settle can still have active hyperkeratosis or architectural progression, while persistent burning may reflect infection, contact allergy, neuropathic pain or genitourinary syndrome rather than steroid failure.

Key points

Vulval lichen sclerosus causes itch, soreness, fissuring and fragile white or pale atrophic plaques, often in a figure-of-eight pattern around vulva and anus.
Ecchymosis, purpura and erosions reflect fragility and scratching; in a child they require careful assessment but do not by themselves prove sexual abuse.
The vagina and cervix are usually spared, which helps distinguish lichen sclerosus from erosive lichen planus and some inflammatory vaginitides.
Chronic inflammation can resorb labia minora, bury the clitoris and narrow the introitus; early control aims to prevent further scarring but may not reverse established architecture.
Diagnosis is often clinical, but biopsy is needed for diagnostic uncertainty, non-response or any persistent ulcer, induration, hyperkeratosis, new lump or suspected neoplasia.
First-line induction is clobetasol propionate 0.05% ointment: once nightly for four weeks, alternate nights for four weeks, then twice weekly for four weeks, with review and technique check.
A 30 g tube is usually sufficient for the 12-week adult induction when applied correctly; excess or very low use should trigger review of technique and disease extent.
Many patients need individualised maintenance, often twice weekly, to prevent relapse and scarring; controlled use is safer than leaving active disease untreated.
Offer a mirror-based monthly self-check where appropriate and at least annual clinical review, with earlier assessment for any focal change because vulval squamous-cell carcinoma risk is increased.
Use trauma-informed language, explicit consent, offered chaperone and the minimum necessary exposure; discuss sexual, urinary and bowel effects without assumptions about gender, partners or practices.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Immune susceptibility

Autoimmune association and familial clustering support an immune-mediated predisposition, although no single antibody or inherited variant establishes the diagnosis.

Hormonal and age influence

Incidence peaks before puberty and after menopause, but disease occurs at every age and is not explained by oestrogen deficiency alone.

Local trauma and occlusion

Friction, urine, scratching and occlusion can accentuate disease at vulnerable sites through an isomorphic response without being its sole cause.

Inflammatory field change

Persistent vulval inflammation creates a tissue environment associated with differentiated intraepithelial neoplasia and squamous-cell carcinoma in a minority.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Interface inflammation
Immune injury near the epidermal junction damages basal keratinocytes and produces fragile epithelium, pallor, erosion and easy bleeding.
2
Dermal sclerosis
Collagen homogenisation and remodelling beneath the epidermis create crinkled white texture, reduced elasticity and progressive fusion or narrowing.
3
Itch and mechanical injury
Inflammatory itch drives scratching, which produces fissures, purpura and further barrier disruption, particularly around urine and stool exposure.
4
Scarring remodels anatomy
Repeated active inflammation resorbs labia minora, fixes the clitoral hood and constricts the introitus, impairing urinary and sexual function.
5
Chronic carcinogenic pressure
Long-standing inflammatory and molecular change can select atypical keratinocyte clones, explaining the need for lifelong focal-lesion surveillance.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Figure-of-eight inflammation

Pale atrophic plaques, fissures and purpura encircle vulval and perianal skin while vaginal mucosa is generally spared.

Fragility and symptom pattern

Intense itch, soreness, splitting with wiping or intercourse, dysuria and painful defaecation arise from inflamed fragile skin and perianal fissures.

Architectural change

Labia minora flatten or fuse, the clitoral hood scars and the introitus narrows; compare with prior diagrams because progression may be gradual.

Childhood presentation

Prepubertal disease may cause vulval itch, bruised-looking purpura, dysuria, constipation and stool withholding and can be mistaken for infection or trauma.

Extragenital disease

Pale crinkled or sclerotic plaques can occur on upper trunk, flexures or thighs and support the diagnosis but do not replace genital examination when symptoms localise there.

Cancer-warning focusRed flag

A persistent hard lump, ulcer, warty or thick keratotic area, focal erosion or bleeding that differs from surrounding disease requires urgent biopsy.

Red flags requiring action

A new persistent lump, thickened or warty focus, induration, ulcer, unexplained bleeding, treatment-resistant erosion, enlarged groin node, urinary obstruction, severe pain or a diagnosis that remains uncertain requires prompt vulval specialist review and usually biopsy of the suspicious focus.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Consent-led vulval and perianal examinationFirst step
Why
Confirm morphology, distribution and architectural change and locate any neoplastic focus.
Interpretation and limitations
Document pallor, texture, purpura, fissures, fusion, clitoral hood and introitus on a body diagram; examine oral and extragenital sites when the differential requires it.
02
Clinical photography
Why
Support comparison of architecture or a focal lesion over time.
Interpretation and limitations
Take only when it will change care, with specific consent, chaperone and secure storage; a patient may decline without losing access to treatment.
03
Skin biopsy
Why
Resolve uncertain diagnosis, explain non-response or exclude differentiated VIN and squamous-cell carcinoma.
Interpretation and limitations
Biopsy an active sclerotic edge or the focal ulcerated, indurated or hyperkeratotic abnormality rather than an excoriated non-representative centre; tell pathology the site and treatment history.
04
Infection testing
Why
Identify Candida, HSV or bacterial infection when discharge, vesicles, purulence or disproportionate pain is present.
Interpretation and limitations
Use a targeted swab or PCR and interpret colonisation in context; do not delay cancer assessment or assume infection explains a persistent lesion.
05
Autoimmune assessment
Why
Investigate symptoms suggesting associated thyroid, coeliac, pernicious-anaemia or other autoimmune disease.
Interpretation and limitations
Order targeted tests from history and examination rather than a universal panel; fatigue, weight change, bowel symptoms and family history guide selection.
06
Treatment-use audit
Why
Distinguish active resistant disease from underuse, wrong site, excessive use or an alternative pain syndrome.
Interpretation and limitations
Review the actual tube, grams used, frequency and application map; approximately 30 g over a standard adult 12-week induction is a practical technique check, not a rigid dose for every body.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Erosive lichen planus

Glazed painful erosions, white lacy edge, vaginal or oral mucosal involvement and scarring suggest lichen planus.

Genitourinary syndrome of menopause

Diffuse dryness, dyspareunia and vaginal mucosal atrophy can coexist but lack the classic sclerotic figure-of-eight skin pattern.

Candida or contact dermatitis

Discharge, satellites or exposure-linked erythema may identify infection or allergy, although either can complicate lichen sclerosus.

Vitiligo

Depigmented skin retains normal texture and architecture and does not ordinarily cause itch, fissures, purpura, scarring or sclerosis.

Differentiated VIN or carcinoma

A persistent focal thick, warty, ulcerated or indurated lesion requires biopsy because morphology can be subtle within inflamed skin.

Additional chapter-specific clues

Alternative mucosal pattern

Vaginal discharge, bright glazed erosions, white lacy border, oral erosions or gingivitis supports lichen planus or immunobullous disease rather than uncomplicated lichen sclerosus.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line inductionSuppress active inflammation with clobetasolFirst stepFirst lineClinical or biopsy-confirmed active vulval lichen sclerosus has no untreated infection or suspicious cancer focus requiring simultaneous assessment.

1Demonstrate a thin layer of clobetasol propionate 0.05% ointment to affected skin once nightly for four weeks, using a mirror or diagram and recording the treated boundary.
2Reduce to alternate nights for four weeks, then twice weekly for four weeks, while continuing bland emollient protection and avoiding soap, wipes, fragrance and friction.
3Review around 12 weeks for symptom, texture, fissure and architecture response, check the tube and technique and biopsy any focal lesion that persists despite correct therapy.

02MaintenancePrevent relapse and further scarringInduction has controlled activity or symptoms recur between courses.

1Agree an individual lowest effective schedule, commonly clobetasol 0.05% twice weekly to previously active skin, rather than waiting for severe relapse.
2Treat a documented flare by returning temporarily to the last effective frequency and arrange review if control is not regained promptly.
3Assess for atrophy, infection and contact allergy but distinguish steroid toxicity from atrophy caused by uncontrolled lichen sclerosus.

03Cancer-surveillance routeFind focal change earlyA new lump, induration, ulcer, hyperkeratosis, warty area, persistent erosion or bleeding appears.

1Arrange urgent vulval specialist or suspected-cancer assessment and mark the exact focus on a diagram or consented photograph.
2Obtain representative biopsy and clinicopathological review; do not repeatedly increase steroid potency without tissue diagnosis.
3Continue control of surrounding lichen sclerosus and maintain long-term self-check and clinical surveillance after any benign or neoplastic result.

04Child and safeguarding routeTreat disease and assess context proportionatelyA child has vulval itch, purpura, fissures, dysuria, constipation or a concerning history or associated injury.

1Use age-appropriate consent and assent, avoid repeated intimate examinations, document the child's words and examine only what is clinically necessary with an appropriate chaperone.
2Recognise that lichen sclerosus itself causes bruised-looking purpura and fissuring and is not evidence of abuse; treat constipation, dysuria and skin inflammation promptly.
3Seek paediatric safeguarding advice when the complete history, development, behaviour or other findings raise concern, without asking leading questions or delaying medical treatment.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

First-line ultrapotent topical anti-inflammatory treatment that controls symptoms, heals fissuring and helps prevent further scarring and malignant evolution.

Clobetasol propionate 0.05% ointment

For a typical adult induction, apply a thin layer to affected vulval and perianal skin once nightly for 4 weeks, on alternate nights for 4 weeks, then twice weekly for 4 weeks; about 30 g usually covers 12 weeks. Individualise paediatric and maintenance schedules through the specialist plan.

Demonstrate the exact site and amount, avoid vagina and unaffected skin, treat infection when present and review non-response. Long-term controlled intermittent use is often necessary; monitor local adverse effects while avoiding harmful undertreatment due to steroid fear.

Reduces friction, urine sting and irritant exposure and supports barrier comfort alongside anti-inflammatory treatment.

Bland emollient ointment

Apply a fragrance-free ointment barrier as often as required, including before urine, after gentle washing and at a separate time from clobetasol if mixing would dilute the medicated layer.

Avoid perfumed emollients, wipes and botanical sensitising products. Ointment contamination and slippage matter, and residue on fabrics increases fire intensity, so keep away from flames and smoking.

A second-line anti-inflammatory option for selected patients, not a superior substitute for correctly used clobetasol induction.

Topical calcineurin inhibitor

Use only on specialist advice at the product-licensed age and frequency when corticosteroid is unsuitable or an adjunct is justified; apply thinly and review response rather than continuing indefinitely without examination.

Burning can be prominent on fissured skin, long-term cancer-protection evidence is less established than for ultrapotent corticosteroid, and a persistent focal lesion still requires biopsy.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Architectural scarring

Labial resorption, clitoral burial and introital narrowing can impair hygiene, urination, examination, tampon use and sexual function.

Vulval squamous-cell carcinoma

A minority develop malignancy, particularly with uncontrolled disease, making prompt biopsy of focal change and long-term surveillance essential.

Pain and sexual dysfunction

Fissures, narrowing, pelvic-floor guarding and fear can perpetuate dyspareunia and sexual distress even after cutaneous inflammation improves.

Urinary and bowel difficulty

Periurethral inflammation, altered anatomy and perianal fissures can cause spraying, dysuria, painful defaecation, constipation and stool withholding.

Psychological harm

Delayed diagnosis, repeated intimate examination, cancer anxiety, altered appearance and unsupported safeguarding interpretation can cause lasting distress.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review after the 12-week induction to compare symptoms, pallor, fissures, hyperkeratosis and architecture and to inspect how much clobetasol remains.
Arrange another review after maintenance is established, then at least annually in stable disease, with shorter intervals for previous neoplasia, uncertain control or limited self-examination.
Teach a monthly mirror check where appropriate for a new lump, hard or thick area, ulcer, warty focus, bleeding or persistent erosion and provide a rapid-access route.
Track urinary stream, sexual pain, introital narrowing, clitoral hood mobility, bowel symptoms and quality of life; refer for pelvic-floor, psychosexual, paediatric or surgical support as needed.
In children review constipation, dysuria, sleep, school and adherence, involve them progressively in care and maintain a low threshold for paediatric vulval expertise when diagnosis or response is uncertain.
After biopsy, reconcile pathology with the exact sampled site and clinical picture; re-biopsy or seek specialist pathology review when a concerning lesion persists despite a non-diagnostic sample.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Symptoms can improve before signs

Less itch does not guarantee that hyperkeratosis and architectural inflammation are controlled, so visual and tactile review remains necessary.

Thirty grams is a technique clue

A typical adult 12-week induction uses roughly one 30 g tube; a nearly full or repeatedly replaced tube can reveal underuse, overuse or an incorrectly mapped area.

White is not the only colour

In richly pigmented vulval skin, fissure, purpura, crinkled texture and architecture may show disease more reliably than striking porcelain pallor.

The vagina redirects the differential

Substantial vaginal mucosal inflammation is atypical for lichen sclerosus and supports lichen planus, immunobullous disease or infection.

Control and surveillance are linked

Suppressing chronic inflammation and detecting a focal lesion early are complementary strategies; neither replaces the other.

Purpura is not a verdict

Fragile inflamed childhood skin can bleed with scratching, so safeguarding decisions require the full account and developmental context.

11Common pitfallsFrequent interpretation and management errors.

01
Prescribing clobetasol without showing the patient exactly where, how much and for how long to apply it.
02
Stopping all anti-inflammatory therapy after induction despite recurrent active disease.
03
Reassuring a persistent indurated ulcer because background lichen sclerosus is already diagnosed.
04
Assuming bruised-looking purpura or fissures in a child prove abuse, or ignoring broader safeguarding concern because lichen sclerosus is present.
05
Ending follow-up when symptoms improve and omitting lifelong focal-change surveillance.