2.1.3 Eczema Herpeticum
Grading & Level of Importance: C
Disseminated virus infection, Kaposi varicelliform eruption.
Severe cutaneous infection mostly with herpes simplex virus Type I (HSV- 1). Infections with HSV-2, varicella zoster virus, or vaccinia adverse event have also been described.
Aetiology & Pathogenesis
Due to local and systemic immune dysfunction and impaired skin barrier function, patients with atopic dermatitis are at highest risk to develop eczema herpeticum. Infection occurs either by auto-inoculation (e.g. herpes labialis) or through contact with infected individuals.
Signs & Symptoms
Eruption of vesicles primarily in areas of severe dermatitis (face, neck, flexures), later developing into pustules, erosions and crusts. Generalised symptoms including high fever, marked pruritus, sometimes pain and lymphadenopathy.
Usually face, neck and flexures. Rapid spreading all over the body.
Laboratory & other workups
Non-specific, depending on the underlying disease, PCR confirmation.
Intraepidermal vesicles containing acantholytic cells, involvement of sebaceous glands, moderate dermal lymphocytic infiltration and edema.
Massive eruption of vesicles and high fever in the beginning. Later vesicles become pustular and erosive. After 4-5 days general symptoms improve, scarring is possible.
Ocular involvement, secondary bacterial infections, pneumonia, herpetic encephalitis, viral sepsis.
History of atopic dermatitis, identification of the virus by PCR.
Bacterial infection, pre-existing bullous disease, other viral exanthems (e.g. Coxsackie), drug eruptions.
Prevention & Therapy
Limited disease can be treated with oral aciclovir, famciclovir or valaciclovir. Disseminated disease requires I.V. aciclovir. Secondary infections should be treated with culture-directed antibiotic therapy. Topical therapy includes wet dressings and antiseptics.
Further Images / DOIA
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