A 16-year-old-boy with a past medical history significant for atopic dermatitis presented to the Emergency Department with a 1-day history of sudden onset of tender blistering lesions on the face and neck associated with a burning sensation. Associated symptoms included lethargy, headache, and four episodes of vomiting since onset of symptoms. On exam, the boy was noted to be ill-appearing, moderately dehydrated, and febrile to 39°C. He was tachycardic but normotensive, warm, and well perfused. The skin exam revealed pustules, vesicles and crusts over his face, neck, elbows, both hands and both knees (Figure 132-1). He was admitted and treated with intravenous (IV) fluids, IV antibiotics, and IV acyclovir. Viral culture taken from an unroofed vesicular lesion revealed herpes simplex virus type 1. Bacterial cultures taken from the impetiginized lesions grew Staphylococcus aureus.

Eczema herpeticum is an acutely disseminated herpes simplex virus (HSV) infection associated with systemic symptoms that develops in the setting of underlying skin conditions or epidermal barrier disruption, such as atopic dermatitis. HSV type 1 is most commonly involved, but cases of HSV type 2 infection and other viruses have rarely been implicated.

Kaposi varicelliform eruption.

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  Infants and children with atopic dermatitis are at highest risk.¹

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  Diverse immune mechanisms have been proposed to explain the development of eczema herpeticum in patients with atopic dermatitis:

  
  
  
  
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    A disruption of the immune response against herpes simplex mediated by T cells.

    
    
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    A defect in antibody production against the virus.

    
    
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    A decrease in natural killer cells and IL-2 receptors.

    
    
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    Inhibition of TH-1 response due to increase in IL-4.

    
    
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    Decrease in dendritic cells that produce IL-1.²

  
  
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  Another possibility is that viral dissemination is directly favored by the disruption of the skin barrier that exists in atopic dermatitis.³

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  Early onset of atopic dermatitis and high levels of IgE in atopic patients, based on a retrospective study involving 100 patients with eczema herpeticum.⁴

  
  
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  The use of topical corticosteroids is not a predisposing factor.

  
  
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  Patients with chronic skin pathology like Darier disease, cutaneous T cell lymphoma, pityriasis rubra pilaris, benign familial pemphigus, seborrheic dermatitis, Wiskott-Aldrich syndrome, psoriasis, and systemic lupus erythematosis are susceptible to eczema herpeticum. Severe infections may develop even when the dermatitis is inactive.²

  
  
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  Other risk factors include conditions where the epidermal barrier has been disrupted, like burns, contact dermatitis, skin grafts, and dermabrasion.

Clinical Features

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  The diagnosis is primarily clinical, supported by isolation of HSV in culture.

  
  
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  Eczema herpeticum is characterized by cutaneous pain and multiple clusters of monomorphic papules, vesicles, pustules and crusts in areas of preexisting atopic dermatitis (Figure 132-2).

  
  
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  These lesions can spread rapidly leading to severe morbidity and mortality.⁵

  
  
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  The eruption of eczema herpeticum may sometimes be difficult to distinguish from the patient’s baseline eczema if the latter is poorly controlled.

  
  
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  Impetigo secondary to bacterial infection can be difficult to differentiate from eczema herpeticum, and can complicate the diagnosis.

  
  
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  The lesions can appear pustular or hemorrhagic (Figure 132-3) and can be associated with systemic symptoms like fever and general malaise. Such a presentation is also consistent with bacterial superinfection, which is one of the key considerations in the differential diagnosis.

  
  
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  Erythema and swelling of the periorbital area may be marked and may represent the primary process or a secondary bacterial cellulitis (Figure 132-4).

  
  
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  Duration of illness is 16 days on average, but ranges from 2 to 6 weeks. About 13 to 16 percent of patients can develop recurrent episodes, which tend to be milder, with limited skin involvement and are less commonly associated with systemic symptoms.²

  
  
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  The most common complication is secondary bacterial infection of the skin; S aureus is the most common pathogen isolated.

  
  
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  Rarely, eczema herpeticum may present as a fulminating disease with widespread lesions, multiorgan involvement, bone marrow suppression, and disseminated intravascular coagulation.