Autoeczematisation

Autoeczematisation (autosensitisation dermatitis) is an acute, widespread eczematous eruption that follows a localised eczema or inflamed skin lesion. It appears days to weeks after the primary site flares, and settles when the primary site is controlled.

It is most often seen with stasis dermatitis, nummular dermatitis, allergic contact dermatitis, and infected or weeping eczema. It occurs mostly in adults, is more frequent in older people with leg disease, and is probably under recognised.

Triggers include bacterial infection of the primary site, topical sensitisers applied to damaged skin, and vigorous treatment with irritants. The primary site is itself an eczema, which separates it from a distant reaction to a fungal infection.

Pathophysiology.

Antigens released from the inflamed focus, or sensitisation to epidermal or bacterial antigens, are thought to activate circulating T cells that then react in distant skin. Barrier dysfunction and contact sensitisation to topical products at the primary site contribute.

• Primary focus: a weeping or infected eczema, often on the lower legs.
• Sudden symmetrical eruption of itchy papules, vesicles and eczematous plaques on the forearms, thighs and trunk, sometimes spreading to the face.
• Intense itch, sleep disruption, and weeping with crusting.
• Possible progression to erythroderma with malaise, fever and fluid loss.

Red flags.

• Erythroderma, fever, hypotension or dehydration.
• Spreading painful erythema or purulence, suggesting superimposed cellulitis.
• Failure to improve with treatment, suggesting an alternative diagnosis such as cutaneous T-cell lymphoma.

• Clinical, based on the sequence of events and the primary focus.
• Swab of the primary site for bacteria, and fungal scraping to exclude tinea with an id reaction.
• Patch testing to topical agents used at the primary site, after the acute phase.
• Review of drugs and scabies exclusion when the picture is unclear.
• Skin biopsy for non-responding or atypical cases. Check electrolytes, renal function and albumin in widespread disease.

Differential diagnosis. Id reaction, drug eruption, scabies, atopic dermatitis, generalised contact dermatitis, erythrodermic psoriasis and cutaneous T-cell lymphoma.

• Treat the primary focus: compression and leg elevation for stasis dermatitis (when the ankle brachial pressure index is over 0.8), removal of the contact allergen, and treatment of infection with flucloxacillin 500 mg four times daily for 7 days, or clarithromycin 500 mg twice daily if penicillin allergic.
• Emollients and potassium permanganate 1 in 10 000 soaks for weeping skin.
• Potent topical corticosteroid (betamethasone valerate 0.1%) once daily for 1 to 2 weeks on the trunk and limbs, and moderate potency (clobetasone butyrate 0.05%) on the face.
• Sedating antihistamine such as chlorphenamine 4 mg at night for itch.
• Severe disease: prednisolone 0.5 mg/kg/day (usually 30 to 40 mg) for 5 to 7 days, tapering over 2 to 3 weeks if symptoms recur on stopping.
• Resistant disease: narrowband ultraviolet B two to three times weekly, ciclosporin 2.5 to 5 mg/kg/day in two divided doses, or methotrexate 7.5 to 15 mg once weekly with folic acid 5 mg weekly.
• Admit for erythroderma, with fluid balance, temperature control and nutrition.

Monitoring. Review at 1 to 2 weeks. Monitor electrolytes and renal function in extensive disease.

Referral and escalation. Refer for dermatology review if the eruption fails to settle within 2 weeks, or urgently for erythroderma.