Autoeczematization or id reaction is described as a disseminated eczematous reaction triggered by a release of antigen(s) following exposure to a primary stimulus, additionally; eczema develops at a site different from the original one. T lymphocytes and keratinocytes may be involved in the pathogenesis of these reactions. This phenomenon is true for stasis dermatitis or tineapedis along with many others. 

Clinically, AE may initiate vesicular dissemination that unites to make papules or nummular patches. Legs, feet, arms, and/or trunk are frequently involved. 

Primary dermatitis appears as a small crusted vesicle with erythema, which may be extremely pruritic, interrupting daily activities or inability to fall asleep.

Id reactions commonly occur due to stasis dermatitis or tineapedis etc. Evaluation of the primary site will help identify the infectious or parasitic agent. 

These etiological agents cause localized dermatitis followed by the immunological response that induces a secondary reaction at a distant site.

Differential diagnoses of the Id reactions include varieties of eczema and some vesicular eruptions. Distinguishing AE from other causes of widespread eczematous dissemination is challenging. Vesicular eruptions like herpetic infections, insect bite reactions, and drug eruptions doubt the diagnosis.

The treatment should include managing the underlying condition to mitigate the inflammatory response causing the id reaction. An antifungal, antibacterial, antiviral, or antiparasitic should be given if AE is infectious. 

In cases of stasis dermatitis as an etiology to id reaction, compression stockings and leg elevation are indicated. The acute id reaction is treated with systemic or topical corticosteroids and wet compresses, which reduces patient discomfort caused by inflammation and pruritus.

Source: Bertoli MJ, Schwartz RA, Janniger CK. Autoeczematization: A Strange Id Reaction of the Skin. Cutis. 2021 September;108(03):163-166. doi:10.12788/cutis.0342