EROSIVE PUSTULAR DERMATOSIS
Synonym: Erosive pustular dermatosis of the scalp
Key features
Sterile pustules plus erosions and superficial ulcerations with keratotic crusts Most commonly develops within photodamaged atrophic skin of the midline scalp Can occur in other locations where the skin is atrophic or fragile, including sites of injury
History
In 1979, Pye et al. described six elderly women with pustular and crusted lesions of the scalp that improved with potent topical corticosteroids.
Epidemiology
Erosive pustular dermatosis (EPD) occurs most commonly on the scalp of older adults with photodamaged skin. It has also been observed on the lower legs of individuals with venous insufficiency and at sites of injury, including in neonates.
Pathogenesis
It is unknown. The causes of erosive pustular dermatosis are not only limited to traumatic injuries but also include medications, comorbid conditions, and several dermatological procedures.
Significant cumulative photodamage in the setting of androgenetic alopecia and local mechanical trauma are risk factors, but how this leads to pustules and erosions is not known. Additional types of trauma include previous herpes zoster and thermal burns. There is a possible association with autoimmune disorders such as autoimmune thyroiditis.
EPD is characterized by pustules, along with erosions and keratotic crusting, within atrophic or fragile skin. Tenderness is a common symptom and there may be associated pain or pruritus as well as drainage. The most common site of involvement is the photodamaged skin of the midline scalp in an elderly adult. Additional locations include the lower extremities in the setting of venous hypertension and at sites of injury, e.g. from thermal burns, surgical procedures, and skin graft placement. There have been a few reports of EPD in neonates following scalp injuries.
EPD can slowly progress and may eventually lead to scarring alopecia. Occasionally, there is secondary infection.
The histopathologic findings are nonspecific. Regenerating epidermis in sun-damaged skin may show enlarged keratinocytes and should not be misinterpreted as actinic keratosis. Intraepidermal or subcorneal pustulation is usually observed.
The differential diagnosis for scalp lesions includes primarily hypertrophic actinic keratoses and squamous cell carcinomas. Additional entities to consider include folliculitis, pyoderma, cicatricial pemphigoid, EFGR inhibitor-induced pustular dermatosis and also, if at other sites, pustular psoriasis.
In case series or case reports, topical therapies – corticosteroids (initially potent), calcineurin inhibitors, vitamin D analogues, dapsone – have been reported as successful treatments. Silicone gels or sheeting as well as photodynamic therapy (PDT) are additional therapeutic options. Topical and systemic antibiotics, including mupirocin and doxycycline, respectively, can also led to improvement. Severe EPD may benefit from oral retinoids, dapsone, or zinc sulfate. Supplementing medical therapy with mild debridement of the crusted areas via curettage may accelerate the response.
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