Diagnosis: Eczema herpeticum
Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.
EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.1 EH occurs more often in infants and children than in adults,2 and is a potentially life-threatening dermatologic emergency.
Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.1 In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.1 (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.2
Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.2 The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.3 Fever, malaise, and lymphadenopathy may also be present.2,3
4 factors differentiate EH from other conditions
The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.1,4
EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.3
Perform a Tzanck smear to diagnose the underlying infection
If EH is suspected, treatment must be initiated immediately.3 (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)
Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.
If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.2 A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.