Clinical overview
Contact dermatitis is one of the commonest reasons for vulval itch, soreness, and erythema, and one of the most chronically mismanaged. It is split into two pathological types — irritant (most common; non-immunological injury) and allergic (immune-mediated, delayed hypersensitivity). The vulval skin is uniquely vulnerable: thinner stratum corneum, occluded environment, exposure to urine, faeces, menses, perspiration, and a long list of cosmetic and hygiene products. The registrar must know how each type presents, what to ask in history, how to confirm allergic contact dermatitis (patch testing), and how to manage the often months-long process of identifying and removing triggers.
Core knowledge
Irritant contact dermatitis (ICD)
Irritants directly damage the thin vulval skin barrier, producing spongiosis, erythema and fissuring at the contact site.
Pathology:
- Non-immunological direct cytotoxic injury to keratinocytes.
- Occurs in any individual with sufficient exposure to an irritant.
- Disruption of skin barrier (loss of ceramides, increased trans-epidermal water loss).
- Epidermal spongiosis (oedema between keratinocytes) on histology in acute disease.
- Chronic: lichenification (thickened skin with accentuated skin markings) from repeated scratching, hyperkeratosis, mild lymphocytic dermal infiltrate.
Clinical correlate:
- Burning, stinging more than itch.
- Erythema, oedema, fissuring, sometimes vesiculation.
- Sharply demarcated to area of contact.
- Improves on irritant removal.
- Common irritants: urine (especially incontinence — see urinary-incontinence), faecal contamination, soaps, body washes, wipes, panty liners, lubricants, spermicides, chemotherapy agents excreted in urine.
Allergic contact dermatitis (ACD)

Pathology:
- Type IV (delayed) hypersensitivity reaction.
- Two phases:
- Sensitisation: hapten penetrates skin, binds protein, presented by Langerhans cells to T-cells in regional lymph nodes; T-cell clonal expansion (10–14 days).
- Elicitation: re-exposure produces inflammatory response 24–72 hours later.
- Histology: spongiosis, lymphocytic infiltrate, eosinophils sometimes.
- Confirmed by patch testing.
Clinical correlate:
- Itch dominant.
- Erythema, vesiculation, papules; can extend beyond exact area of contact.
- Develops 1–3 days after exposure.
- Common vulval allergens: fragrances (in soaps, wipes, sanitary products), preservatives (parabens, methylisothiazolinone), latex (condoms, gloves), lanolin, dyes, topical antibiotics (neomycin, bacitracin), nickel (jewellery, fastenings), benzocaine (in topical anaesthetic preparations).
- Recurrence common until allergen identified.
Atopic dermatitis (eczema) of vulva
- Type IV reaction with strong familial atopy.
- Often coexists with atopic dermatitis elsewhere (flexures, face).
- Predisposing to ICD and ACD due to barrier defect.
Lichen simplex chronicus
- Chronic scratch-itch cycle leads to lichenification (thickened, leathery skin).
- May start from any trigger (irritant, allergic, infectious, dermatosis) but becomes self-perpetuating.
- Treatment: break the cycle with potent topical steroid + antihistamine for sleep + barrier protection.
Assessment
History
- Itch, burning, soreness — relative dominance.
- Duration, time course.
- Hygiene practices: soaps, body washes, douching, wipes, deodorants, perfumes.
- Sanitary products: pads, tampons, liners, brand changes.
- Lubricants, spermicides, condom use (latex or non-latex).
- Topical medications (including over-the-counter remedies — neomycin, hydrocortisone, anaesthetic creams).
- Underclothing: fabric type, washing detergents, fabric softeners.
- Incontinence (urinary or faecal).
- Sexual practices, partner products.
- Occupation if exposure-relevant.
- Atopic history (eczema, asthma, hay fever).
- Previous treatments — including unsuccessful — and what was applied (may itself contain allergens).
Examination
- Distribution: sharply demarcated → ICD/ACD; ill-defined and lichenified → atopic / chronic scratching.
- Vesicles, weeping, fissures.
- Coexisting dermatosis (LS, lichen planus, psoriasis).
- Documentation with diagram.
Investigations

- Patch testing — gold standard for ACD. Refer to dermatology; standard battery plus vulval-specific allergens (fragrances, preservatives, latex). Read at 48 and 96 hours.
- Biopsy — usually not needed; consider if diagnostic uncertainty or persistent disease, to exclude other dermatoses (lichen-sclerosus, lichen planus, VIN).
- Microbiology: culture if suspected secondary candida/bacterial infection.
Management
Stepwise approach
- Identify and remove triggers (history-driven; supported by patch testing for ACD).
- Restore barrier: emollients (paraffin-based, fragrance-free, preservative-free), liberal application, also use as soap substitute.
- Control inflammation:
- Acute flare: topical steroid — moderate (e.g., betamethasone valerate 0.1%) to potent (clobetasol propionate 0.05%) for 2–4 weeks short course.
- Maintenance / chronic: lower-potency steroid intermittently, or steroid-sparing topical calcineurin inhibitor (tacrolimus 0.1% ointment).
- Treat secondary infection if present.
- Address scratching: nocturnal antihistamine (sedating); short nails; soft cotton gloves at night for severe cases.
- Education — clear written guidance about what to avoid; specific brands; reassurance about expected course.
Counselling
- Recovery takes weeks; lichenified disease may take months.
- Avoid the temptation of new topical products applied to "fix" the problem.
- Importance of plain emollient as cornerstone.
- Discuss allergen-free alternatives (e.g., fragrance-free organic cotton pads).
Pregnancy and lactation
- Topical steroids generally safe.
- Most emollients safe.
- Avoid sensitisers; minimise topical exposures.
Postmenopausal
- Coexisting atrophic vaginitis common.
- Topical oestrogen alongside steroid.
Red flags / pitfalls
- Iterative empirical topical treatments worsening the picture (e.g., neomycin allergy from "antibiotic cream").
- Missing coexistent LS / lichen planus — biopsy if persistent.
- Failing to identify the trigger — methodical product elimination.
- Discharging without education — relapse certain if hygiene practices unchanged.
- Overlooking faecal/urine contamination in incontinent or immobile patients.
- Long-term potent steroid use without review — atrophy of vulval skin.
- Treating "candida" repeatedly when problem is contact dermatitis.
Evidence anchors
- British Association of Dermatologists (BAD) — Patient Information on Contact Dermatitis.
- BSSVD (British Society for the Study of Vulval Disease) — Clinical Guidance.
- European Society of Contact Dermatitis (ESCD) — Patch Testing Guidelines.
- ISSVD 2015 Terminology and Classification of Vulval Dermatoses.
- NICE Clinical Knowledge Summaries — Dermatitis - Contact.
- Margesson LJ. Contact dermatitis of the vulva. Dermatol Ther 2004 — foundational vulval-specific review.
- South African Dermatological Society — patch testing services and standard tray.
