You came back! You walk into your Paeds ED shift, ready for the usual falls, scraps, and one or two snotty noses. However, your first patient is a 2-year-old baby with eczema that’s proving tricky to manage, and he is not feeling well. You start thinking about all the dermatology you learnt in med school. If the rash is wet, you dry it, and if it is dry, you wet it, right?
Baby G is not your typical atopic eczema exacerbation. He spiked a fever yesterday and now has painful blisters on his face. He’s miserable, febrile, and you notice clusters of punched-out erosions around his cheeks and eyelids.
You don’t think this is a simple give emollients case, so you ask your registrar to come and see him, and they say, “Let’s cannulate and admit under paeds”
Why? What are we dealing with?
What is eczema herpeticum?
Eczema herpeticum (EH) is one of those conditions every paediatrician, GP, and ED clinician needs to have on their radar. It’s uncommon, but when it appears, it can spiral quickly into something life-threatening.
Eczema herpeticum (EH) is a disseminated cutaneous infection with herpes simplex virus (HSV), most often HSV-1, occurring in the context of pre-existing dermatoses, particularly atopic dermatitis (also known as atopic eczema). EH represents a dermatological emergency due to its potential for rapid progression and severe complications, including bacterial superinfection, keratitis, encephalitis, and death.
Pathophysiology of atopic dermatitis and risk factors for eczema herpeticum
The pathogenesis of atopic dermatitis (AD )involves a combination of barrier dysfunction, immune dysregulation, genetic predisposition, and microbial interactions.
1. Compromised Skin Barrier
AD is characterised by a defective epidermal barrier caused by mutations or reduced expression of structural proteins such as filaggrin, loricrin, claudin-1, and E-cadherin. This dysfunction results in increased permeability and facilitates HSV entry into keratinocytes. Additionally, disruption of junctional proteins like nectin-1, an HSV receptor, provides further viral access.
2. Dysregulated Innate Immunity
Patients with AD have impaired innate antiviral responses, including reduced levels of antimicrobial peptides (e.g., cathelicidin LL-37, β-defensins) and diminished plasmacytoid dendritic cell function, leading to decreased type I interferon production. A Th2-skewed immune environment (IL-4, IL-13, TSLP, IL-25, IL-33) further suppresses antiviral defences.
3. Altered Innate Immune Cells
Natural killer (NK) cells in AD show impaired cytotoxic function despite increased TNF-α production. Altered expression of junctional proteins, including Necl-5 and E-cadherin, may also disrupt NK cell regulation, further weakening antiviral clearance.
4. Genetic Susceptibility
Although only a subset of AD patients develops EH, genetic studies suggest variants affecting barrier integrity, immune regulation, and hydration pathways predispose certain individuals to severe HSV infections.
5. Microbiome Dysbiosis
Colonisation with Staphylococcus aureus and its exotoxins, such as α-toxin, enhances susceptibility by exacerbating barrier dysfunction and potentially promoting HSV replication.
6. Risk Factors for Eczema Herpeticum
EH is more common in patients with early-onset AD, facial or neck involvement, and high IgE levels. EH arises in the first episode of a herpes simplex infection, hence it is more common in infants and younger children. Viral spread can be facilitated by scratching or contact with contaminated objects.
Histopathology
Histological findings include ballooning degeneration, multinucleated keratinocytes with Cowdry type A inclusions, intraepidermal vesiculation, spongiosis, and acantholysis. Dermal perivascular lymphocytic infiltrates are often observed.
Who gets it? Which children are most at risk?
Eczema herpeticum occurs most often in infants and young children, although it can also affect adults with eczema or those who are immunosuppressed.
Most cases arise in children with atopic dermatitis (AD). On first contact with the herpes simplex virus, the risk is higher in those with early-onset disease, more severe or uncontrolled eczema, or lesions involving the head and neck, where viral shedding from the lips and mouth is more likely.
Other predisposing skin conditions include psoriasis, seborrhoeic dermatitis, burns, and Darier disease. Children who are immunocompromised, whether due to systemic steroids, other immunosuppressive therapies, HIV, or congenital immune deficiencies, are also at increased risk.
Diagnosis:
Clinical presentation
The Skin Lesions
The skin lesions in this condition are characterised by monomorphic vesicles, meaning all the vesicles look the same and are in the same stage of development. These vesicles eventually rupture, leaving punched-out erosions covered with crusts. Unlike eczema or chickenpox, the lesions are typically painful rather than itchy. They often appear in clusters on the face, neck, and upper trunk but can spread to any part of the body. In some cases, lesions may start at the site of a cold sore and then disseminate across the body.
Systemic Features
Affected individuals may also show systemic symptoms, including fever, malaise, and irritability. Cervical lymphadenopathy is common, and infants may exhibit poor feeding.
Red Flags
Certain features require urgent attention. Periorbital involvement is particularly concerning due to the risk of herpetic keratitis and potential permanent vision loss. A child who appears toxic or septic, or those with rapidly progressive widespread disease, also warrant immediate evaluation.
Ocular Involvement
Periorbital lesions in eczema herpeticum (EH) demand prompt assessment. In the emergency department, it is crucial to carefully examine the eyes, checking for vesicles or punched-out erosions on the eyelids and looking for conjunctival injection. Always ask about photophobia and visual disturbances, and ensure visual acuity is assessed.
The eyes are a major concern because, if the condition progresses without intervention, herpetic keratitis may develop. This can result in corneal scarring and permanent visual loss. If corneal lesions are suspected, topical acyclovir should be started (check local guidelines for dosing). An urgent ophthalmology review is required for any child with ocular involvement.
Differential diagnosis:
The most common differential diagnoses are impetigo and chickenpox.
Chickenpox: Both cause blisters on red skin. In chickenpox, the spots vary in size and stage (some red, some blistered, some crusted) and are more spread out on the body. In eczema herpeticum, the blisters are all similar (monomorphic), close together, and often form punched-out ulcers.
Impetigo: Usually caused by Staphylococcus aureus. It often affects the face, appearing as yellow, honey-coloured crusts. Children with impetigo usually feel well. In eczema herpeticum, the child is often unwell with fever, and the blisters look different from impetigo crusts.
Eczema coxsackium: is an atypical form of hand-foot-and-mouth disease, usually caused by coxsackievirus A6, that tends to appear in areas of active eczema or skin barrier disruption. Lesions are vesiculobullous or papulovesicular and may look dramatic, but unlike eczema herpeticum, they are typically less painful, children are less systemically unwell, and the rash resolves spontaneously within 1–2 weeks.
Diagnosis is clinical, sometimes supported by enterovirus PCR, and the main pitfall is mistaking EC for EH. Importantly, EC is managed supportively (emollients, antipyretics, hydration), and antivirals are not indicated since the cause is enterovirus rather than HSV.
Eczema Herpeticum
Eczema Coxsackium
Impetigo
Why is early diagnosis important?
If untreated, it can spread widely and lead to serious complications such as bacterial superinfection, septicemia, herpetic keratitis, and even death. Missing the diagnosis delays acyclovir treatment and increases risk of blindness or mortality.
How do you make the diagnosis?
Diagnosis is clinical — don’t wait for lab results before treating*.
- Confirmatory tests (if needed or atypical presentation):
- HSV PCR (most sensitive)
- Viral culture.
- Direct fluorescent antibody (DFA).
- Tzanck smear (historical, rarely used).
2. Bacterial swabs if superinfection suspected.
3. Bloods (FBC, CRP, U&E) if unwell or admitted.
*The cases of EH I have managed have always been treated before any results are available. Generally, in kids, we would send blood tests routinely if doing a cannula for treatment, so familiarising yourself with the clinical presentation would be the most important step in diagnosing and managing EH.
Complications:
- Bacterial superinfection → cellulitis, sepsis.
- Herpetic keratitis → corneal scarring, blindness.
- HSV encephalitis (rare but devastating).
- Disseminated HSV infection in neonates or immunocompromised hosts.
Treatment:
1. Recognition and Referral
- Children with sudden-onset painful eczema, clusters of vesicles, or “punched-out” erosions, especially with fever or lethargy, should be suspected of EH.
- NICE guidance recommends that any child with suspected EH should:
– Receive immediate systemic antiviral treatment, and
– Be referred the same day for specialist dermatology assessment. - If periocular or ocular involvement is present, an urgent ophthalmology referral is required.
2. Antiviral Therapy
- First-line treatment is oral acyclovir, with the dose and duration determined by your local protocols. Treatment can last up to 14 days, but others suggest stopping it once the patient is fully healed.
- Valaciclovir is sometimes used in older children/adolescents where available.
- Intravenous (IV) acyclovir is indicated if:
– The child is systemically unwell, oral absorption is compromised (e.g., vomiting), or
– Severe or disseminated disease is suspected.
3. Secondary Bacterial Infection
- Bacterial superinfection (e.g., with Staphylococcus aureus) is common.
- If there is evidence of superinfection (weeping, honey-coloured crusts, worsening systemic illness), systemic antibiotics should be added in line with local antimicrobial guidelines, in addition to antivirals.
4. Supportive Care
- Hospital admission is often required in children with:
– Extensive skin involvement, dehydration risk, systemic symptoms (fever, malaise), or
– Infants or immunocompromised children. - Supportive measures include pain relief, hydration, and emollients.
5. What about steroids?
This is one of the trickiest debates in managing eczema herpeticum. The traditional teaching has been to stop topical corticosteroids as soon as eczema herpeticum is suspected, on the basis that steroids might fuel viral replication. However, the supporting evidence is quite limited. Retrospective series and reviews have not shown clear harm from continuing steroids. In fact, some dermatologists argue the opposite: stopping steroids completely risks a rebound eczema flare, further barrier breakdown, and potentially recurrent infection.
A pragmatic compromise suggested in some guidelines is to pause steroids for the first 48 hours of antiviral therapy, then restart once the child is improving. In a large multicentre cohort of over 1,300 hospitalised children, use of topical corticosteroids on day one was not associated with longer length of stay. What was strongly linked to worse outcomes was the delayed initiation of acyclovir.
What we can say is this: early antivirals save lives, and steroids should never delay or replace them. Beyond that, the decision to hold or continue steroids should be individualised, balancing control of eczema with concerns about viral replication.
Prognosis
With early recognition and prompt antiviral treatment, the prognosis of eczema herpeticum is generally favourable. Before the introduction of acyclovir, mortality rates were reported at 10–50%, but they have now fallen to less than 1% in immunocompetent children. Recurrence is uncommon, though possible, and long-term morbidity may include scarring or, in cases of ocular involvement, permanent vision loss.
Take Homes
Think EH in a child with eczema who suddenly develops painful vesicles + fever.
Monomorphic vesicles → punched-out ulcers are the clue.
Start acyclovir early — don’t wait for swabs, blood tests, or dermatology input (as sometimes these presentations are out of hours).
Always check around the eyes — and call ophthalmology (We also love our ophthalmologist friends in paeds <3) if involved.
Don’t confuse with impetigo or chickenpox.
References
Leung, A. K. C., Barankin, B., & Hon, K. L. (2012). Eczema herpeticum: Recognition and management. Drugs in Context. https://pmc.ncbi.nlm.nih.gov/articles/PMC3520662/ PMC
British Association of Dermatologists. (n.d.). Eczema herpeticum. Patient Information Leaflet. Retrieved August 27, 2025, from https://www.bad.org.uk/pils/eczema-herpeticum
DermNet NZ. (2023). Eczema herpeticum. https://dermnetnz.org/topics/eczema-herpeticum
National Institute for Health and Care Excellence (NICE). (2018). Atopic eczema in under 12s: Diagnosis and management (CG57). https://www.nice.org.uk/guidance/cg57/chapter/Recommendations
National Institute for Health and Care Excellence (NICE). (2013). Atopic eczema in children: Quality standard [QS44]. https://www.nice.org.uk/guidance/qs44/chapter/Quality-statement-7-Treatment-of-eczema-herpeticum
NHS Kingston & Richmond. (2023). Paediatric referrals: Eczema. https://www.kingstonandrichmond.nhs.uk/services/healthcare-professionals/how-refer/paediatric-referrals/eczema
Chovatiya, R., & Silverberg, J. I. (2020). Pathophysiology of atopic dermatitis and eczema herpeticum. Journal of Allergy and Clinical Immunology, 145(6), 1649–1660. https://pubmed.ncbi.nlm.nih.gov/31836943/
Fleming, P., & Wasserman, D. (2020). Eczema herpeticum. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK560781/
DermNet NZ. (2023). Eczema coxsackium. DermNet New Zealand. https://dermnetnz.org/topics/eczema-coxsackium
Wollenberg A, Zoch C, Wetzel S, Plewig G, Przybilla B. Predisposing factors and clinical features of eczema herpeticum: a retrospective analysis of 100 cases. Journal of the American Academy of Dermatology. 2003 Aug 1;49(2):198-205.
Seegräber M, Worm M, Werfel T, Svensson A, Novak N, Simon D, Darsow U, Augustin M, Wollenberg A. Recurrent eczema herpeticum–a retrospective European multicenter study evaluating the clinical characteristics of eczema herpeticum cases in atopic dermatitis patients. Journal of the European Academy of Dermatology and Venereology. 2020 May;34(5):1074-9.
Khan A, Shaw L, Bernatoniene J. Fifteen-minute consultation: eczema herpeticum in a child. Archives of Disease in Childhood-Education and Practice. 2014 Nov 18.
