Spreading eczema and areas of raw, oozing skin

Eczema herpeticum (EH), also known as varicelliform eruption, pustulosis varioliformis acuta, and Kaposi-Juliusberg dermatitis, is a herpetic superinfection of inflamed skin. Although mild disease may be self-limited in healthy individuals,1 early diagnosis and treatment is critical to prevent systemic spread...

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Eczema herpeticum (EH), also known as varicelliform eruption, pustulosis varioliformis acuta, and Kaposi-Juliusberg dermatitis, is a herpetic superinfection of inflamed skin. Although mild disease may be self-limited in healthy individuals,¹ early diagnosis and treatment is critical to prevent systemic spread of the infection, particularly in higher-risk patients, such as infants, the elderly, and immunocompromised individuals.

Classic EH appears as clusters of monomorphic, dome-shaped, or umbilicated vesicles on an area of inflamed skin; it is often accompanied by abrupt onset of fever, malaise, and lymphadenopathy. As the disease progresses, vesicles may coalesce and transform to punched-out ulcerations, erosive pits, and crusts. Frequently affected areas are the head, neck, upper trunk,² and extremities.

EH commonly occurs in the setting of eczematous skin disease, but can also occur with Darier disease, allergic or irritant contact dermatitis,³ Hailey-Hailey disease, cutaneous T-cell lymphoma, and other dermatoses. Wolf et al⁴ described EH in the setting of sunburn. The underlying pathology among these conditions is an impaired stratum corneum and compromised skin integrity, which allows for viral invasion.

Most cases of eczema herpeticum are caused by herpes simplex virus I or II. It can result from either primary infection of the virus or from reactivation or reinfection.² Occasionally, it can be caused by coxsackievirus A16, or vaccinia virus. In addition, EH may become secondarily infected with Staphylococcus aureus, β-hemolytic streptococci, and Pseudomonas aeruginosa.⁵

Wollenberg et al² found that early onset of atopic disease, severe untreated lesions, and high levels of total serum immunoglobulin E were risk factors for EH. Conversely, secondary diagnoses, family history of atopy, and corticosteroid treatment were not found to be risk factors.

Although EH is typically a clinical diagnosis, laboratory testing can help confirm the diagnosis. Polymerase chain reaction, immunofluorescence, and electron microscopy are useful in detecting the herpes virus. The Tzanck test reveals multinucleated giant cells confirming viral infection, whereas viral culture and serologic testing are less useful.

The differential diagnosis of EH includes various disseminated infections, including impetigo, varicella zoster virus infection, and animal pox infection. In addition, bullous contact dermatitis and autoimmune bullous diseases should be considered.

Antiviral therapy should be initiated as soon as possible, with a 5 to 10 day treatment duration. Oral acyclovir or equivalent dosage of another anti-herpetic medication may be used.⁶ More severe cases may require intravenous administration in the hospital setting. In addition, oral antibiotics may be considered if there is a concern of bacterial superinfection. Pain should be assessed and adequately managed. Patients should remain adequately hydrated while on acyclovir; patients should also be instructed to apply bland emollients to the skin, reserving topical corticosteroids for when the EH resolves.⁷

Because the risk of virus reactivation is high, patients with severely compromised immune systems should be considered for prophylactic systemic antiviral agents.¹

For the patient in our case, the mother was educated regarding the serious nature of the infection and the need to be aware of signs of worsening infection. Treatment was initiated with acyclovir suspension, 250 mg, 4 times daily, for 5 days. At a follow-up appointment 3 days later, the patient was noted to have marked improvement of the eczema overall, as well as minimal remaining ulcerations.

Esther Stern, NP, is a family nurse practitioner at Advanced Dermatology & Skin Surgery, P.C., in Lakewood, N.J.

References

1. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Saunders-Elsevier; 2011.
2. Wollenberg A, Zoch C, Wetzel S, Plewig G, Przybilla B. Predisposing factors and clinical features of eczema herpeticum: a retrospective analysis of 100 cases. J Am Acad Dermatol. 2003;49:198-205.
3. Vanchinathan V, Christopher B, Sklar L. A case of vulvar eczema herpeticum. J Am Acad Dermatol. 2013;68(4 suppl 1):AB132.
4. Wolf R, Tamir A, Weinberg M, Mitrani-Rosenbaum S, Brenner S. Eczema herpeticum induced by sun exposure. Int J Dermatol. 1992;31:298-299.
5. Brook I, Frazier EH, Yeager JK. Microbiology of infected eczema herpeticum. J Am Acad Dermatol. 1998;38:627-629.
6. Lebwohl MG, Heymann WR, Berth-Jones J, Coulson I. Treatment of Skin Disease. 3rd ed. Philadelphia, PA: Saunders-Elsevier; 2009.
   
7. Paller AS, Mancini AJ. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. 5th ed. Toronto, Canada: Elsevier; 2016.