Paediatric Vesiculobullous Rash

Questions to ask yourself?

• Are there any blisters?
  • Narrows the potential differential
• Is the rash red?
  • Redness is from Hb. Most red rashes blanch, if not, the Hb is outside the blood vessels i.e. purpura
• Is the rash scaly?
  • Is so, epidermis is involved. May be broken causing weeping, crusting or fissues (eczematous) or intact (red scaly rash)

Level of intercellular split

• Subcorneal
  • Thin roof, easily broken e.g. impetigo, SSSS
• Intraepithelial
  • Thin roof, easy to break e.g. varicella, HSV, eczema, pemphigus
• Subepidermal
  • Roof intact e.g. bullous pemphigoid, erythema multiforme, SJS/TEN

Differential

• Vesicles
  • Infections
    • HSV, VZV, Enterovirus, tinea, scabies, impetigo
  • Contact dermatitis
  • Drug reactions
  • Erythema multiforme
  • Photosensitivity
• Vesicular disease may present with multiple shallow erosions and bullous disease may present with large shallow erosion

• Larger blisters
  • Staphylococcal infection
  • SJS
  • Immune conditions
  • Arthropod bites
  • Fixed and bullous drug reactions
  • Mastocytosis
  • Burns 
  • Trauma

Varicella (Chicken pox)

• Usually children <15
• Incubation 2-3 weeks
• Contagious from 2 days before rash and continues until crusted lesions
• Rash arises over 3-5 days
• Erythematous macules become small vesicles that then crust within 10 days
• Face and trunk spreading to extremities
• Vaccination may allow for attenuated disease and no constitutional symptoms

• Complications
  • Secondary strep/staphy infection: Look for bullous, indurated, spreading or cellulitic lesions
  • CNS dysfunction: Encephalitis, meningitis, transverse myelitis, GBS, Reye’s syndrome
  • Pneumonia
  • Cerebellar ataxia as rash clears and usually resolves within weeks
  • More common in infants, people over 15 and immunocompromised

• Management
  • Bland emollients, oral antihistamine
  • Avoid aspirin (Reye’s)
  • If immunocompromised or premature neonate – IV Aciclovir
  • Term neonates should be admitted and treated with IV aciclovir if severe disease
  • Zoster immunoglobulin to immunocompromised children, newborns of mothers who have varicella any time from 5 days before to 2 days after delivery)
  • Exclude from school until all lesions crusted or at least one week since eruption first appeared
  • Offer VZV immunisation to non-immune contacts (prevents or attenuates infection if given within 5 days of exposure

Zoster

• Uncommon in childhood but may cover more than one dermatome
• Radicular pain may be first symptom but often not as severe as in adults
• Lesions resolve over 2 weeks
• Post-herpetic neuralgia is very uncommon in children

• Complications
  • Generalised dissemination during first week (pulmonary and/or brain involvement can occur)
  • Aseptic meningitis if on head (resolves fully without treatment)
  • Tip of nose (Hutchinson’s sign) suggests nasociliary branch of ophthalmic nerve involvement and may indicate keratitis/conjunctivitis
  • Facial nerve palsy and ear involvement (Ramsay Hunt syndrome)

Management

• IV or oral antivirals if immunocompromised or chronically unwell
• Oral antivirals in older adolescents may reduce pain and risk of post-herpetic neuralgia but in younger children these are so rare that benefits of treatment are not clear

Hand, foot and mouth

• Coxsackie A16 virus (one presentation of enteroviral infection) 
  • Or Enterovirus 71
• Mild prodrome of sore throat, malaise and fever
• Discrete 6mm vesicles on erythematous base in mouth (sparing lips gingiva usually)
• 1-2 days later: 3-7mm vesiculopustules on erythematous base on palms, soles and around fingers/toes and buttocks
• Resolution within a week
• Incubation period of about 5 days
• Virus is excreted for weeks in faeces and exclusion is not recommended
• Just need supportive care to ensure comfortable and feeding
• DDx:
  • Erythema multiforme, pustular psoriasis and EBV

Herpes simplex infection

• Mostly HSV 1 in children
• May be history of family member with cold sore (but often not)
• Painful grouped vesicles on erythematous base at any site
• Multiple lesions rupture, crust and coalesce into larger erosions with scalloped edges
• May be associated fever, malaise and lymphadenopathy

Management

• Supportive care
• Bathing of crusts
• Analgesia
• Aciclovir if underlying illness/immunocompromise
• Recurrent episodes are usually less severe but can lead to significant time off school
• Antiviral prophylaxis can be considered if debilitating
• Can involve fingers (herpetic whitlow) but thick skin does not rupture leading to pustular coalesced collections mistaken for bacterial abscesses

Eczema herpeticum

• Disseminated HSV-1 in atopic eczema
• Can occur with any severity of eczema
• Often misdiagnosed or missed
• Usually shallow 2-4mm monomorphic erosions on inflamed base
  • May have grouped vesicles, but more commonly just rudimentary or absent
  • Atypical appearance of herpetic lesions leads to misdiagnosis
• Need high index of suspicion in any eczematous child with areas of crusts/erosions not responding to standard therapy
• Resolution occurs in 1-4 weeks even without therapy
• Dissemination can occur though, with bacterial superinfection
• Recurrences can be frequent and severe but usually reduce in intensity over 1-2 years

Treatment

• Investigation and empiric treatment for both bacterial and herpetic infection
• Local stable disease does not need treatment
• Milder cases with progression or facial involvement can have oral aciclovir 20mg/kg QID
• If fever, multiple sites, widespread eczema, eye involvement, immunosuppression or <6mo = IV aciclovir 500mg/m2 up to 12yo or 10mg/kg TDS if >12yo
• Soak crusts
• Monitor for eye involvement, especially scleral redness
• Underlying eczema treatment with moisturiser and/or wet dressings until scabs removed and then topical cortisone re-started

Impetigo

• Staph or Group A Strep
• Non-bullous impetigo
  • Small erythematous vesicles that rapidly rupture to form yellow crusted lesions
  • Common on face and hands
• Bullous impetigo
  • S. aureus
  • Flaccid blisters on normal skin
  • Blisters rupture to form shallow moist erosions
  • Often loose epithelium and/or brown crusting peripherally with some central healing
  • May appear annular in chronic cases
• Often secondary to itching skin disorders (scabies, atopic eczema and head lice)

Management

• Need to consider post-strep GN and acute rheumatic fever in certain populations
• Swab if diagnosis unclear
• Bathe off crusts
• Topical bactroban 2% ointment q8h or oral cephalexin 33mg/kg (500mg) q8h if extensive
• Isolate for other children or sick adults unless all lesions covered or antibiotic treatment commenced
• Treat underlying itching disorder e.g. scabies
• If new blisters form after 2-3 days of antibiotic therapy, consider MRSA or other blistering disorder

Staphylococcal scalded skin syndrome

• Usually younger children or those with renal impairment
• Epidermolytic toxin from staphylococcal focus e.g. eyes/nose
• Fever and tender erythematous skin
• Exudation and crusting, especially around mouth
• Wrinkling, flaccid bullae and exfoliation of skin is extensive
• Nikolsky sign (‘normal’ skin separates if rubbed)
• Blisters are superficial and heal without scarring

• Management
  • Admit
  • Treat as burn if extensive
  • Consider SJS, TEN (skin biopsy can confirm diagnosis)
  • IV Flucloxacillin if evidence of sepsis or systemic involvement
  • Look for focus of infection and drain any collection
  • Emollient and careful handling

Erythema multiforme

• Hypersensitivity syndrome at any age
• Infectious triggers – HSV, Mycoplasma, Varicella, Adenovirus, Hepatitis virus, HIV, CMV, dermatophyte infections
• Drugs – Barbiturates, NSAID’s, penicillins, sulphonamides, phenothiazines and anticonvulsants
• Most diagnoses are wrong and child actually has urticaria with annular lesions
• Primary lesions are red papules, symmetrical involving forearms/palms/feet/face/neck/trunk
• Some will form classic ‘target lesions’
  • Inner zone of epidermal injury i.e. purpura, necrosis or vesicle
  • Outer zone of erythema
  • Middle zone of pale oedema

• Not migratory
• Involvement of mucous membranes is uncommon, but is isolated to specific patches (vs. SJS) and if severe = erythema multiforme major
• – In Mycoplasma, may get isolated mucositis (? Limited form of EM)
• Drugs are an uncommon cause
• Does not evolve into SJS

Management

• Fluid maintenance
• Analgesia
• Emollient to lips if involved
• If recurrent, likely HSV recurrence coincident – can consider antiviral prophylaxis
• Prednisolone alleviates symptoms but may prolong the duration and may cause recurrence of HSV

Stevens-Johnson syndrome/
Toxic epidermal necrolysis

• Variants of the same condition
• Mostly triggered by antibiotics (sulfonamides/penicillins), anticonvulsants (lamotrigine) and NSAID’s
• Mycoplasma or other infections may be implicated
• Prodromal fever, headache, myalgia, arthralgia with sudden widespread blisters on erythematous or purpuric macular background with mucous membrane haemorrhagic crusting
• Usually face and trunk or generalised vs. acral
• Target lesions not seen
• May be tender erythematous regions with positive Nikolsky sign
• Mucous membrane involvement can be extensive, severe and painful
• Conjunctivitis, corneal ulceration and blindness can occur
• Anogenital lesions can cause urinary retention and constipation

Management

• Treat as skin failure i.e. as a burn
• Admit with multidisciplinary team involvement including ophthalmology
• Emolient to mucous membranes
• Regular eye examination
• IVIG and commence ciclosporin
• Maintain good nutrition (as in burn)
• Intubation if severe oropharyngeal involvement

Dermatitis herpetiformis

• Autoimmune blistering disease presenting at any age as itchy papules or vesicles
• Rapid excoriation prevents blisters from being seen
• Mostly extensor surfaces of trunk and limbs
• Most patients have coeliac disease (but may be asymptomatic)
• Management
  • Biopsy peri-lesional skin to demonstrate granular IgA deposition
  • Investigate for Coeliac disease
  • Anaemia secondary to malabsorption should be identified
  • Dapsone therapy (limited by haemolysis side effect profile)
  • Gluten free diet leads to clearing of skin lesions

Sunburn and photosensitivity

• Any child presenting to ED with sunburn may have underlying photosensitivity
• Consider:
  • Primary photosensitivity disorders
  • Inherited disorders including porphyrias
  • Systemic disease e.g. SLE, dermatomyositis
  • Exogenous photosensitivity from drugs/plants
• Need high index of suspicion

• Any child with symptoms within half an hour of sun exposure should be assumed to have an underlying condition
• Consider suboptimal parental supervision (although usually accidental)
• Topical potent steroids can reduce severity and duration of symptoms if given within first few hours of exposure
• Cool compresses and wet dressings are appropriate
• Educate re: prevention

Primary photosensitivity disorders

• Polymorphous light eruption (PLE)
  • Presents in spring or early summer as skin-coloured or erythematous itchy papules or vesicles on exposed areas
  • Recurrent
• Juvenile spring eruption
  • Variant of PMLE in 4-12 yo boys. Recurrent blistering of ears each spring
• Hydroa vacciniforme
  • Sun-induced vesicular eruption on cheeks during spring and summer
  • Recurrent for many years
• Solar urticaria
  • Urticaria within minutes to hours of exposure. Settles within 24 hours
  • Sharp margins seen at edge of clothing
  • Chronically exposed skin is often spared

Porphyrias

• Inherited enzymatic defects in haem synthesis leading to increased levels of porphyrins and subsequent photosensitivity
• Erythropoietic porphyria
  • The most common childhood porphyria
  • Acute discomfort, burning sensation, itching, erythema, oedema, urticaria and vesicles on face and dorsum of hands after brief sun exposure
  • Recurrent and skin appears prematurely aged with repeated episodes
  • Raised erythrocyte protoporphyrin levels
• Congenital erythropoietic porphyria
  • Rare extreme photosensitivity with painful blisters filled with red fluid on face and dorsum of hands
• Familial porphyria cutanea tarda
  • Chronic blistering of hands, arms and face leading to poorly healing ulcers, atrophic scarring and mottled hypo- and hyper-pigmentation

Drug reactions causing photosensitivity

• Doxycycline, tetracyclines, griseofulvin, isotretinoin, NSAID’s, sulfonamides, fluoroquinolones and diuretics all implicated
• Tars, perfumes, cosmetics, sunscreens, artificial sweeteners and dyes
• Rash can arise rapidly or days after sun exposure
• Photosensitivity can persist for up to 3mo after drug exposure
• Prominent hyperpigmentation can persist
• Fixed drug eruptions
  • Usually due to paracetamol, NSAID’s and sulfonamides
  • Quite common and present as single or multiple circular red patches that may blister
  • Post-inflammatory hyperpigmentation is common

• Management
  • Recognise and stop causative agent
  • Strict sun protection measures for up to 3 months
  • Reduce dosage if drug must be continued

Photosensitivity to plants

• Furocoumarins are naturally occuring psoralens
• UVA light induces covalent bonding of psoralen into DNA, leading to cell death
• Typically, child playing outside in sun comes into close contact with psoralen-containing species (e.g. celery, parsley, parsnip, fig, hogweed, limes and citrus)
• Several hours later erythema, oedema and blistering develop
• Painful, limited to sun exposed areas and heal to leave striking hyperpigmentation that can persist for months to years
• Treat as for sunburn
• Sunscreen will prevent phytophotodermatitis

Contact dermatitis – plants

• Contact dermatitis to things other than plants usually do not blister in children
• Rhus and Grevilea species implicated
• Some only cause reactions at certain times of year
• Typically 1-3 days after exposure, get linear erythema, oedema and vesiculation
• Periorbital erythema and vesiculation often misdiagnosed as periorbital cellulitis
• Pruritis is the main symptom, pain and tenderness are much less severe than would be expected for cellulitis, fever is absent and outline is irregular corresponding to topical contact site
• Treatment
  • Oral prednisolone, topical potent steroid, cool compress
  • Does not induce long-term hyperpigmentation

Id reaction

• Repeat exposure to an allergen can cause papulovesicular eruption at site distant from contact secondary to systematised contact sensitisation
• May be local or generalised
• E.g. non-infective blisters on hands of child with chronic tinea of feet

Isolated blisters

• Mastocytoma
  • Usually infant with recurrent blistering at site of brownish macule, often thought to be localised impetigo
  • Insect bite
  • Irritant contact dermatitis
  • Spider bite
  • Scalds or burns
  • Fixed drug eruption
  • Friction
  • Artefactual by carer
  • Bullous Sweet syndrome
  • Pyoderma gangrenosum

Chronic erosions or ulcers

• Scabies
• Papular urticaria
• Immunodeficiencies i.e. recurrent boils
• Skin fragility syndromes
• Porphyria
• Pyoderma gangrenosum
• Mycobacterium ulcerans

Neonatal vesicles

• Consider HSV, VZV, Staph aureus
• Empiric IV aciclovir is crucial until herpes infection xcluded
• DDx
  • Epidermolysis bullosa
  • Miliaria (hot or occluded areas)
  • Ichthyosis
  • Langerhans cell histiocytosis
  • Incontinentia pigmenti
  • Mastocytosis

Mastocytosis

• Accumulation of mast cells in organs e.g. skin
• Positive Darier sign (wheal with stroking of skin) in all types
• May be solitary or widespread
• Solitary mastocytoma
• – Infant itchy yellow-brown thickened patch of skin. Resolves with time
• Maculopapular cutaneous mastocytosis
• – Most common. Widespread urticarial type rash which fails to resolve with time
• Usually conservatively managed

Last Updated on November 22, 2021 by Andrew Crofton