Atopic eczema is the most common inflammatory skin disorder in the UK and occurs in 20-30% of children. The condition is multifactorial in aetiology, with environmental, stress, genetic, skin barrier and immunological factors all contributing.
Diagnosis and management
The UK Working Party on Atopic Dermatitis criteria help to distinguish atopic eczema from other rashes (see box 1).1
A variety of skin changes may be seen in atopic eczema, including erythema, vesiculation, weeping, papules, xerosis, lichenification, excoriations and changes in pigmentation.
Atopic eczema typically presents in the first few months of life. In children aged under 18 months, it affects the extensor surfaces and cheeks, rather than the typical flexural distribution.
Children of African-Caribbean origin commonly have the extensor surfaces affected with a discoid or follicular pattern.
NICE recommends a step-wise treatment plan, depending on the site and severity of the eczema.2 Trigger factors should be avoided, and food and inhaled allergens considered. A written treatment plan is helpful. Emollients, together with parental and child education, are the mainstay of treatment.
Soaps, bubble baths and leave-on emollients containing sodium lauryl sulfate should be avoided. Ointments are generally preferred to creams because they contain fewer preservatives, but they can be less acceptable to patients.
At least 250g per week of emollient should be prescribed, with considerably more for severe cases and older children.
Mild potency topical steroids (for example, 1% hydrocortisone) are used initially, with more potent steroids on the limbs and trunk in children aged over two years if the eczema does not respond, or for short-term use (one to two weeks) in flare-ups.
Calcineurin inhibitors (pimecrolimus and tacrolimus) are used in children aged over two years for moderate to severe eczema not controlled by topical corticosteroids. Other therapies include bandages, UVB light and systemic immunosuppressants.
Referral to secondary care is recommended if the diagnosis is uncertain, if the eczema is severe with no response in a week, or for longer-term eczema that is not improving.
|BOX 1: DIAGNOSTIC CRITERIA AND DIFFERENTIAL DIAGNOSES|
UK Working Party criteria on diagnosis of atopic dermatitis
Differential diagnoses of atopic eczema
Atopic eczema typically has a relapsing course. Children may also develop other atopic conditions, including asthma, hay fever and food allergy. Up to 60% of atopic eczema remits by 10 years of age. Complications include secondary bacterial infections (Staphylococcus aureus and/or Streptococcus pyogenes) and viral infections, especially HSV (eczema herpeticum).
Impetigo is a contagious superficial bacterial skin infection, found most often in young children, with an annual incidence of about 2.8% in those aged up to four years and 1.6% in those aged five to 15 years. It is due to Staph aureus and Strep pyogenes. Two-thirds of cases are non-bullous, the remainder bullous, each with distinct characteristics (see box 2).
|BOX 2: NON-BULLOUS AND BULLOUS IMPETIGO|
|Type of lesion||Progresses from small red macule to vesicle/pustule to superficial erosion with crust||Large bullae/blisters, rupture less readily|
|Site||Face, nose, mouth, extremities||Face, buttocks, trunk, perineum|
|Systemic symptoms||Usually absent||May be present, especially in neonates, for example, pyrexia,
Diagnosis and management
A honey-coloured crust is the hallmark of impetigo. It may be a primary infection or secondary to underlying dermatoses, such as eczema and scabies. Minor skin trauma, such as an insect bite or scratch, often precedes clinical infection.
Differential diagnoses for impetigo include:
- Herpes zoster infection
- HSV infection
- Tinea corporis
- Discoid eczema
- Insect bites
- Thermal burns
- Blistering disorders, for example, bullous pemphigoid (rare)
- Stevens-Johnson syndrome
Treatment aims to resolve the soreness caused by lesions and the unsightly appearance (especially on the face), and to prevent recurrence and spread to others.
Hygiene measures should be stressed, such as washing the affected areas with soapy water, soaking off crusts, thorough handwashing and cutting nails short. Towels, flannels, bed sheets and bath water should not be shared with other household members until the infection has resolved.
Localised disease is treated with seven days of topical antibiotic. Mupirocin and fusidic acid are thought to be most effective. A seven-day course of systemic antibiotics (penicillin, flucloxacillin, or erythromycin if penicillin-allergic) should be given for more widespread lesions.
Bacterial resistance can develop in patients with impetigo, as can allergic contact dermatitis from a constituent of the topical antibiotic.
It is rare for a child with non-bullous impetigo to develop complications and in these cases, the lesions typically heal without scarring. Local and systemic spread of infection can occur, however, which may result in cellulitis, lymphangitis or septicaemia.
Non-infectious complications, which may occur one to three weeks after infection with Strep pyogenes, include guttate psoriasis and glomerulonephritis.
Toxin-mediated syndromes, including toxic shock syndrome, staphylococcal scalded skin syndrome and scarlet fever, are very rare complications.
Osteomyelitis, arthritis and pneumonia can occur, but tend to be in children with underlying immunodeficiency.
Hand, foot and mouth disease
HFMD is due to enteroviral infection, most commonly Coxsackie A16, but also several other Coxsackie viruses and enterovirus E71. This latter infection causes more severe disease. Infection is person-to-person or through direct contact with nasal discharge, saliva, blister fluid or stool from an infected person.
Diagnosis and management
HFMD typically affects children aged under 10 years. The first symptom is usually a low-grade fever, followed by scattered papules that develop into vesicles affecting the hands, feet and mouth, where they progress to shallow ulcers. Lesions may also be present on the buttocks in young children and infants.
The diagnosis is relatively easy when all sites are affected, but in some cases, only one site is affected. The lesions resolve in seven to 10 days and children tend to be constitutionally well during this time.
Although the signs and symptoms are usually enough to make a diagnosis of HFMD, it can be confirmed if needed by throat swab for viral PCR. Box 3 lists differentials.
|BOX 3: DIFFERENTIAL DIAGNOSES FOR HFMD|
Children who have atopic eczema and other dermatoses may develop a vesiculobullous eruption on the limbs and trunk with HFMD, termed eczema coxsackium.
Symptomatic treatment is required, ensuring enough fluid is drunk and soft foods are offered. Pain relief for mouth ulcers includes paracetamol, ibuprofen and analgesic mouth sprays or gels.
Good hygiene is required to prevent spread of this condition. In keeping with eczema herpeticum, it is prudent to stop topical corticosteroids in eczema coxsackium because they are thought to contribute to viral spread.
HFMD is usually a mild, self-limiting condition and full recovery is expected. Children with eczema coxsackium will require review of their eczema once the condition has resolved.
Measles and morbilliform rashes
Measles is a highly contagious paramyxovirus infection with respiratory droplet and occasionally, conjunctival spread. The incubation period is 10-14 days.
It has become relatively rare in the UK owing to herd immunity resulting from MMR vaccination. In 2011, 258,000 measles deaths were recorded worldwide. Measles vaccination has resulted in a 71% reduction in deaths from 2000 to 2011.
Diagnosis and management
Vaccination status should be checked, because the classical presentation is unlikely in those who have been vaccinated.
Prodromal symptoms include the three Cs: cough, coryza and non-purulent conjunctivitis, which occur two to four days before the rash develops.
Koplik spots are highly suggestive of measles. These are white/grey spots with an erythematous halo on the buccal mucosa opposite the molars, often described as looking like grains of salt.
There is a short period of overlap with the exanthem occurring 24-48 hours beforehand and lasting two to three days. The exanthem, which consists of red maculopapular lesions, some of which may be confluent (morbilliform rash), starts on the face and neck and spreads downwards. Fine desquamation may occur as the rash resolves.
Most children with clinically diagnosed measles will have other viral infections, not measles. Laboratory confirmed evidence is important and a throat swab should be taken for viral PCR. Serology (IgM) is only informative if performed a week after rash onset. Causes of a morbilliform rash include:
- Scarlet fever
- Graft versus host disease
- Viral exanthema, including German measles, adenovirus, roseola infantum, echovirus, Epstein-Barr virus (especially after ampicillin) and many more
- Drug hypersensitivity, including antiretrovirals
- Early meningococcal disease before purpuric patches occur
- Kawasaki disease
- Toxic shock syndrome
Measles is a notifiable disease and the local health protection unit should be informed. Treatment is symptomatic, giving paracetamol or ibuprofen for temperature control.
Vaccination with MMR should still go ahead, because valuable protection is offered against mumps and rubella.
Human immunoglobulin should be given to contacts of laboratory-proven measles who are immunosuppressed, or non-immune pregnant women.
Measles is usually self-limiting, resolving after seven to 10 days. A number of complications may occur, including pneumonia (superadded bacterial infection), otitis media, bronchitis, encephalitis, myocarditis and pericarditis. Before MMR vaccination, measles had up to a 30% mortality in developing countries, exacerbated by malnutrition.
- Dr Helen Goodyear is a consultant paediatrician with a special interest in paediatric dermatology at Heart of England NHS Foundation Trust, West Midlands
- Williams HC, Burney PGJ, Hay RJ et al. The UK Working Party’s Diagnostic Criteria for Atopic Dermatitis. I. Derivation of a minimum set of discriminators for atopic dermatitis. Br J Dermatol 1994; 131: 383-96.
- NICE. Atopic eczema in under 12s: diagnosis and management. CG57. London, NICE, December 2007.