Clinical recognition

Usually affects older adults with chronically sun-damaged, atrophic scalp skin; the vertex scalp is a common site.
Crusted erosions, shallow ulcers, sterile pustules, yellow-brown scale/crust and areas of scarring alopecia are typical.
Onset or flare may follow skin surgery, grafting, cryotherapy, radiotherapy, topical field therapy, trauma, herpes zoster, burns or photodynamic therapy.
Symptoms range from mild tenderness or itch to pain and bleeding from adherent crusts.
The disorder is chronic and relapsing; apparent “non-healing wound” behaviour is common.

Skin-oncology pitfalls

Erosive pustular dermatosis can closely mimic actinic keratosis, SCC in situ, invasive cSCC, BCC, pyoderma gangrenosum and chronic infection.
A background history of actinic keratoses, previous cSCC or previous scalp surgery increases the chance that inflammatory change and neoplasia coexist.
Biopsy is required for any focal thickening, nodularity, rolled edge, persistent bleeding, increasing pain, rapid enlargement or treatment-resistant area.
Avoid assuming that all crusting on an EPDS scalp is inflammatory; map and sample the most clinically suspicious focus.
Culture is useful when infection is plausible, but sterile or mixed colonising flora does not exclude malignancy.

Diagnosis is clinicopathological and usually one of exclusion: infection, autoimmune blistering disease, vasculitis, pyoderma gangrenosum and malignancy must be considered.
Swabs or scrapings may help exclude bacterial, fungal or herpetic infection when pustules, pain or acute deterioration are present.
Histology is often non-specific, showing epidermal atrophy/erosion, mixed inflammation, pustulation or granulation tissue rather than a pathognomonic pattern.
Take a deep enough biopsy from the edge or thickest area if invasive SCC is in the differential.
Document baseline photographs when monitoring a large field, because subtle enlarging malignant foci can otherwise be missed.

Potent or superpotent topical corticosteroid is the usual first-line anti-inflammatory treatment, used as a finite course and then stepped down or repeated for flares.
Topical calcineurin inhibitors can be useful as steroid-sparing maintenance in recurrent disease, particularly on thin atrophic skin.
Gentle debridement/soaking, non-adherent dressings, emollient wound care and avoidance of further trauma are central practical measures.
Treat secondary bacterial infection only when clinically present; chronic colonisation alone should not drive prolonged antibiotics.
Refractory, extensive or diagnostically uncertain cases are best managed jointly with dermatology, dermatopathology and the skin-cancer team.

Follow-up should be individualised around cancer risk, treatment response and the number of actinic keratoses or previous keratinocyte cancers.
Review early after starting topical steroid to ensure the inflammatory component is improving and to identify any persistent suspicious focus.
Long-term surveillance is often required because relapse and new actinic keratoses/cSCCs may arise in the same field.
Escalate rather than simply repeating topical therapy if the clinical pattern changes or a focal lesion emerges.
Patient education should emphasise returning for new pain, bleeding, thickening, rapid growth or a non-healing focal ulcer.