Diagnosis: Eczema herpeticum
The boy had eczema herpeticum, a serious complication of atopic dermatitis, or atopic eczema, in which a herpes simplex virus (HSV) infection is superimposed on already altered skin. Eczema-induced barrier dysfunction is thought to result in greater susceptibility to secondary infection.
Eczema herpeticum, which is also known as Kaposi varicelliform eruption, should always be suspected in patients who present with worsening eczema, pain, and fever. The secondary HSV infection will present as clusters of small vesicles on eczematous skin. However, due to excoriation, the vesicles are unlikely to be intact. Therefore, the hallmark is often circular, punched-out, shallow erosions. Clustered vesicles may coalesce to form larger erosions. With continued itching and subsequent spreading of the virus, additional isolated vesicles or erosions are frequently noted. Impetiginization or signs of a co-existing bacterial infection are not uncommon.
Eczema herpeticum is mainly a clinical diagnosis. Lab studies, such as Tzanck smear, viral culture, and HSV serology, are only supportive. Polymerase chain reaction of blister fluid that is positive for HSV is confirmatory.1 Western blot testing, which is both 99% sensitive and specific for HSV antibodies, is the gold standard of serologic diagnosis.
Eczema herpeticum is also seen in keratosis follicularis (Darier disease), pemphigus foliaceus, mycosis fungoides, ichthyosis vulgaris, bullous pemphigoid, familial benign pemphigus (Hailey-Hailey disease), staphylococcal scalded skin syndrome, multiple myeloma, erythroderma following ste-roid withdrawal, and transient acantholytic dermatosis (Grover disease).2 Dermabrasion, burns, and skin grafts also carry a risk of eczema herpeticum, which is more common on steroid-treated skin and in immunosuppressed patients.
To prevent dissemination, therapy should be started as soon as a secondary HSV infection is suspected. Oral or IV antiviral agents are the mainstay of treatment. Discontinue topical steroids on affected skin. Petroleum jelly can be used as an emollient. Antihistamines, antipyretics, and analgesics should be utilized as needed. Concomitant bacterial infection is not uncommon, so gram-positive antibiotic coverage should be provided until skin and blood cultures are negative for bacteria.
Our patient’s IV acyclovir was switched to oral acyclovir on discharge after four days, for a total of seven days of antiviral therapy. Cultures grew methicillin-sensitive Staphylococcus aureus, so inpatient IV vancomycin was started and changed to oral clindamycin on discharge. We treated the boy’s skin with topical petrolatum. He improved significantly over the next week, with eradication of the secondary HSV infection and significant decrease in pain and itch.
Dr. Harting is assistant professor of dermatology at the University of Michigan Medical School in Ann Arbor.
1. Rao G, Chalam KV, Prasad GP, et al. Mini outbreak of Kaposi’s varicelliform eruption in skin ward: a study of five cases. Indian J Dermatol Venereol Leprol. 2007;73:33-35.
2. Doherty SD, Giancola A, Nash J, et al. Papulo-vesicular eruption. Dermatol Online J. 2007;13(2):24.