1. Epidemiology, aetiology and diagnosis
Atopic eczema is predominantly a genetic disorder and is classified as one of the endogenous eczemas. Although it is not caused by external contact factors, they may play a role in exacerbating it; for example, clothes containing wool, soaps, detergents or extreme temperatures.
Incidence and prevalence
Atopic eczema is the most frequent dermatological consultation that patients make in primary care. It usually affects 5–15 per cent of school children and 2–10 per cent of adults.
The prevalence of eczema in children is increasing in Western countries and adult prevalence is, obviously, related to childhood prevalence two or three decades previously. The prevalence of eczema in children of up to four years of age is now around 20–25 per cent in the UK. It is estimated that approximately 30–40 per cent of children who have eczema will have eczema in adult life.
Diagnosis of atopic eczema
The key diagnostic features of atopic eczema are an itchy skin (or scratching or rubbing in a child); typical clinical pattern for eczema. This includes, a history of itchiness in skin creases, for example, folds of the elbows, behind the knees, fronts of ankles or around the neck. In children under four years it may involve the face (the cheeks especially).
There may be links to a family or personal history of the other atopic diseases such as asthma and hay fever.
The whole skin tends to be rough and dry and there is often localised thickening (lichenification), especially in areas subject to repeated scratching, typically the wrists, hands and feet.
The diagnosis of infected eczema
Eczematous skin is abnormally susceptible to infection. The most common colonising and infecting organism is Staphylococcus aureus. There is mounting evidence that staphylococcal superantigens play a role in the pathological process of atopic eczema.
Superantigens appear to perpetuate the inflammatory process already present in atopic eczema and may even initiate the appearance of lesions.
While bacterial infection is the most common infection, viral infection may also occur. Two common viruses are particularly troublesome: herpes simplex, in which infections may be widespread and severe, and molluscum contagiosum.
There is no clear quantitative laboratory method for assessing infection in eczema. Diagnosis of active Staph aureus infection is largely through clinical judgment on the appearance of the lesions. Excoriations and fissures are both common features of atopic eczema and may act as portals for entry of Staph aureus under the skin.
Bacterial infection is suggested by golden crusts, oozing, pustulation and/or surrounding cellulitis with erythema of otherwise normal-looking skin (pictured left).
In herpes simplex infected eczema there may be vesicles and/or erosions that can be, but are not always, grouped.
Bacterial swabs are not strictly necessary, but are helpful to identify antibiotic resistant strains if the patient does not respond to treatment. If herpes simplex infection is suspected swabs should be taken and screened for the presence of the virus.
Prevention of infection depends upon the sound and prompt management of the eczema. Crucial to the prevention of infection is to encourage the patient to carry out the simple management tasks properly to keep the eczema under firm control.
2. Management of atopic eczema
Mild to moderate atopic eczema can be managed with emollients and by intervening with topical steroids when there is a flare up of the condition.
Obvious aggravating factors should be avoided. For example, bath water should be relatively cool and irritants should be avoided as far as possible.
Pets may aggravate the skin. If the child has a strong history of food allergy, food exclusion can be considered under the supervision of a paediatric dermatologist or paediatric allergist in collaboration with a dietician.
Skin should be kept moisturised at all times. Use emollients liberally, particularly around bath time.
Use topical steroids to suppress itch and inflammation. Use the weakest amount of the weakest agent that is effective at controlling the condition.
There are grades of topical steroids appropriate to children of different ages, disease severity, and for different parts of the body. It is often worth using more powerful agents in short bursts rather than constant application of weaker steroids that are ineffective. Studies have shown that by using emollients and a potent topical steroid for two weeks you can achieve control, and retain that control when the topical steroid is reduced to twice weekly.
A major problem of topical steroids has been their under-use rather than their over-use. Education of patients to be confident about the use of intermittent steroids is a valuable part of controlling the disease. Instructions on steroid use can seem vague to parents and patients. The finger tip unit is a useful visual measure to show patients the appropriate amount of cream for different parts of the body and gives them confidence in applying the cream.
There are three specific techniques to be used in younger children. First, use tepid bath water, with plenty of bath oil in the water. Pat the skin dry and apply lots of emollient both before and after the bath. Next use wet wrapping using emollients and mild topical steroids — the bandages are soaked with fluid, saline or cream. This helps moisturise and humidify the skin. Medicated bandages containing calamine or tar can reduce puritus.
When steroid therapy alone is not effective in long-term maintenance alternatives can be used. The topical calcineurin inhibitors tacrolimus and pimecrolimus, in appropriate situations, are effective in either replacing or augmenting steroid therapy. They are used with increasing frequency in secondary care and, to some extent, in primary care.
In older children with more severe disease a course of UV therapy and immunosuppressive drugs in short courses might also be recommended.
3. Treating infection
Bacterial skin infection is a common exacerbation of atopic eczema. Early use of topical or systemic antibiotics may prevent a major flare up. The associated eczema is treated at the same time, usually with a topical steroid of moderate or high potency.
Antiseptic shampoos and products that combine an antiseptic with an emollient, or with a bath emollient, are available. These may reduce the bacterial population colonising the lesional and non-lesional skin.
For relatively limited clinical infection topical antibiotics such as fusidic acid or mupirocin cream are effective (see box). Fusidic acid should be used in short courses of no more than one to two weeks. This is to reduce the risk of drug resistance or skin sensitisation.
However a small study has shown no evidence to support the hypothesis that short-term treatment of atopic eczema with fusidic acid/ steroid combination increases fusidic acid resistant Staph aureus during a two-week period.
Fusidic acid is available in combination with either a low-potency topical steroid and a potent steroid. These are suitable to treat infected or potentially infected eczematous lesions.
If the infection goes beyond a modest level in extent and severity, then a topical antibiotic should be combined with a short course (14 days) of systemic antibiotic, notably erythromycin or flucloxacillin. Flucloxacillin orally is usually most appropriate for Staph aureus. Erthyromycin or one of the new macrolides can be used if there is a penicillin allergy or resistance. Penicillin should be given if beta-haemolytic streptococci are isolated.
In recurrent infected eczema, the staphylococcal carrier sites — the axillae, nose and perineum — can be treated prophylactically with topical antibiotics. Widespread herpes simplex infections should be treated with a systemic antiviral agent, such as acyclovir, early in the course of infection.
A version of this article appeared in MIMS Dermatology, June issue. If you have an interest in dermatology, you can register to receive free copies of MIMS Dermatology at www.hayreg.com/specials