Eczema Herpeticum in a 4-Year-Old Girl

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A 4-year-old girl with a past medical history of asthma and atopic dermatitis presented with 4 days of pruritus and worsening erythema, swelling, and erosions on her right knee.

Key point: The patient presents with erythematous papules around a large eroded plaque, seemingly consisting of individual round erosions. The erosions are clean-based, with sharp borders. While the patient has a history of atopic dermatitis and has increased itching, self-induced erosions should not be so well-formed and perfectly round. One may also be concerned about impetiginization; however, there is no honey-colored crust, no purulent drainage, and no significant erythema around the affected area.

The clinical findings, along with the classic “punched-out” appearance of many of the erosions, led to the diagnosis of eczema herpeticum. This diagnosis, also known as Kaposi varicelliform eruption, is often seen in patients with a defect in their primary cutaneous barrier, such as atopic dermatitis (most commonly), or other conditions, including Darier disease, a defect of keratinocyte adhesion. Eczema herpeticum is caused by herpes simplex virus (HSV), usually type 1, which proliferates in this environment of a disrupted skin barrier. The diagnosis can be confirmed by a Tzanck preparation where a swab from the lesion is spread on a slide, stained, and examined for the presence of multinucleated giant cells; or by direct fluorescent antibody (DFA) testing or viral culture. Of these, the Tzanck preparation is the fastest, followed by a DFA test and then viral culture. Timing is critical because this condition can rapidly progress and may involve other organs and structures such as the eyes (herpes keratitis, which can lead to blindness), especially if lesions are located on the face. This diagnosis is a relative dermatologic emergency and presumptive treatment with antivirals should be at least considered in a case in which the clinical diagnosis is even suspected.

Treatment: In this case, the patient was already admitted to the inpatient unit and treatment was initiated with IV acyclovir. Topical mupirocin was also applied to the affected area twice daily. Once the erosions started healing, a topical corticosteroid regimen was started to treat the underlying eczema, with marked improvement over the next several days.

Note: While our case demonstrated clean, punched-out erosions, the primary lesion in eczema herpeticum is a vesicle, which may form hemorrhagic crusts and lead to the aforementioned punched-out erosions. In severe cases, there may also be fever and malaise. Therapy is most often initiated with IV acyclovir in an inpatient setting. In some cases in which the lesions are limited and in non-critical areas, one may consider oral treatment with antiviral agents, such as valacyclovir, which is preferred over acyclovir because of its better bioavailability. Extended courses of therapy may be necessary, for 2 weeks or until all of the lesions have healed. It is also important to examine the patient for possible superinfection with bacteria such as Staphylococcus aureus. Antibiotic treatment may be necessary if there is any sign of bacterial superinfection, or prophylactic topical treatment may also be warranted, as it was in our case.

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