Eczema herpeticum
Immediate attention can prevent death from this infection
by John Kraft, MD and Charles Lynde, MD
Vol.19, No.02, March 2011

Eczema herpeticum (EH), also known as Kaposi’s varicelliform eruption, is a relatively common infection. EH mainly occurs in the presence of skin diseases with defective barrier function, usually atopic dermatitis, by herpes simplex viruses. EH is a true dermatological emergency that requires urgent assessment and treatment. Complications are often serious and it can be fatal.

Pathogenesis

Patients susceptible to developing EH have an underlying skin disease that affects the barrier function of the skin. This abnormality in the stratum corneum and epidermis facilitates entry of herpes simplex viruses that cause EH. Patients may also have decreased immune function, allowing the virus to replicate more easily. In atopic dermatitis, cytotoxic T-cell immunity is weaker and there’s decreased secretion of antimicrobial peptides.

Herpes simplex virus 1 — which usually causes herpes labialis or “cold sores,” and herpes simplex virus 2 — which usually causes genital herpes, can be transferred to the skin by direct contact from the patient or from another infected individual. Rarely, other viruses can cause EH and include vaccinia virus and Coxsackie A16 virus.

Although atopic dermatitis is the most common skin disease underlying EH, many other barrier defects can predispose to viral penetration (see Table 1).

Clinical features

EH is an acute painful eruption lasting for 7-10 days that usually starts on skin affected by the conditions discussed above. The head and neck are common sites. Lesions are initially erythematous papules that quickly evolve into vesicles. They tend to be grouped and monotonous. The vesicles often rupture, leaving punched out erosions and hemorrhagic crusts. As lesions coalesce, larger erosions form that can be an entry for additional infection. In extensive cases, accompanying symptoms include fever, lymphadenopathy and malaise.

Differential diagnosis

EH can resemble impetigo, and this is complicated as both may occur simultaneously in the same area. Clues that favour impetigo would be a honey-coloured crust, slower evolution and fewer constitutional symptoms. The monomorphic, punched-out erosions of EH are classic. Also consider other herpesvirus infections — e.g. varicella zoster — and non-infectious causes such as autoimmune blistering diseases.

Investigations

Investigations will help to confirm a viral infection, rule out other infections, and monitor for complications. A Tzank smear can be done by scraping the base of an erosion — ideally a de-roofed vesicle — fixing the debris to a slide, staining with Giemsa, and looking under a microscope for the presence of multi-nucleated giant cells. This test is fairly sensitive, but not specific for HSV, as many viral infections can induce similar changes.

Direct immunofluorescence is more sensitive and specific, fairly quick, and must be done in a specialized lab. Antibodies are used to probe for epitopes unique to HSV and varicella. Viral culture is the best test but takes several days. For patients who are unwell, additional investigations may be needed such as a complete blood count, liver function tests and blood cultures.

These patients may require careful monitoring for complications. Ophthalmology should be involved to rule out eye involvement. Herpes keratitis can lead to blindness. There may also be conjunctivitis, blepharitis and iritis. In disseminated infection, there can be herpes hepatitis, as well as brain, gastrointestinal, lung and adrenal involvement. Patients are also at risk of bacterial sepsis — Staphylococcus aureus, Pseudomonas aeruginosa — disseminated intravascular coagulation and death.

Treatment

EH is a dermatologic emergency and may require hospital admission for treatment and preventing complications. With treatment, the prognosis is excellent. Without treatment, the mortality rate can be as high as 50%.

EH requires urgent administration of antiviral therapy, with or with antibiotics to cover co-existent bacterial superinfection. For unwell patients, or immunocompromised patients, IV acyclovir is required. It’s often dosed at 15-30 mg/kg IV divided q8h. The duration of IV therapy depends on the response to treatment. Patients on IV acyclovir require adequate fluid intake and monitoring to prevent acute renal failure due to crystalline nephropathy. Usually 5 days of IV therapy is needed with transition to oral therapy. Foscarnet is used if there’s viral resistance to acyclovir.

When patients are well, early administration of oral antivirals can prevent complications and hasten resolution. Acyclovir in adults can be dosed at 400 mg po 5x/day for 5-10 days. Valacyclovir and famciclovir have better oral bioavailability.

Patients with recurrent HSV and EH can be offered daily antiviral prophylactic therapy. Examples for adults include acyclovir 400 mg po bid and valacyclovir 500 mg to 1g po daily.

John N. Kraft, MD, is a fifth year Dermatology Resident at the University of Toronto.
Charles Lynde, MD, FRCP(C) is an assistant professor of dermatology at the University of Toronto.

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