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)
