Atopic eczema (AE) is a very common, chronic relapsing inflammatory skin disorder. It has a prevalence of 30% in developed countries and a worldwide cumulative prevalence of 15-20%. This disorder begins in youth, with 50% of cases occurring before the age of one year, and the remainder typically developing by the age of five years.
The incidence of AE decreases with age and it is unusual to develop it after the age of 30 years.1
Severe or inadequately managed AE can lead to significant detrimental effects on the wellbeing of affected children and their parents or carers, underscoring the importance of diagnosis and appropriate management.
Atopy is defined as a heritable tendency to become sensitised and initiate an IgE response to ordinary exposure to commonly occurring antigens in the environment.2 The atopic triad comprises atopic eczema, asthma and allergic rhinitis.
Patients with AE have a combination of atopy with heritable epidermal barrier dysfunction, leading to increasing penetrance of allergens and subsequent sensitisation.3
AE is mediated by cytokines (IL-4, IL-5 and IL-13), leading to reactions starting two to six hours after exposure, in contrast to histaminergic reactions, which occur within minutes.
The NICE guidelines for the diagnosis of AE in children are outlined in box 1.4
|Box 1: Diagnosing paediatric atopic eczema|
NICE guidelines4 for the diagnosis of paediatric AE specify children with an itchy skin rash and three of the following:
The history taken from patients with suspected paediatric AE should encompass the clinical details of the disease and its impact on the child and their parents or carers.
Distribution, time of onset and description of symptoms can help to quantify the severity of the disease. Pruritus is the predominant symptom and can sometimes precede the appearance of the rash.
Questions on exposure to dietary/inhaled allergens or contact irritants can sometimes point to specific trigger factors.
A full drug history is essential, specifically to determine what treatments – prescribed and OTC – have been tried. Children may also have undergone parents’ or carers’ attempts to manage their condition by adapting their diet or environment, and these should also be sought out.
There is a strong genetic component to AE and atopy, and a positive family history would be highly suggestive.
As with any paediatric history, the growth and development of the child should be assessed.
On clinical examination, assess the distribution and appearance of the rash. The appearance of the eczema varies with time of onset, severity and the patient’s age.
In the early stage, eczema starts as erythematous patches, which gradually become infiltrated plaques that subsequently lichenify. Excoriations are often present and will correlate with symptom severity.
In infantile AE (age less than two years), the disease manifests as papules and papulovesicles on the cheeks. With increasing age from childhood to adolescence, this develops into plaques within the antecubital and popliteal fossae, the creases of the wrist, neck, face and eyelids, with scattered, excoriated papules located elsewhere on the body.1
Head and neck involvement is present in 90% of these patients.3 Excoriation can lead to further changes in the rash, resulting in chronic lichenified lesions.
Eczematous skin can be colonised by Staphylococcus aureus, with actual bacterial infection manifesting as honey-coloured crusting, pyoderma and folliculitis.
There is no diagnostic investigation for eczema, except skin biopsy, and the diagnosis is made clinically. Bacterial or viral swabs are useful if an infection is suspected. Allergy testing through serum IgE (RAST) or skin prick testing has high specificity but low sensitivity,1 and is not recommended unless the history is suggestive of an allergic trigger or the disease fails to respond to conventional topical therapy.
Eczema herpeticum, which results from disseminated herpes simplex virus type 1 or type 2 infection, presents with a combination of systemic upset, pyrexia and the appearance of monomorphic painful/pruritic pustules in the areas of eczema. These burst to leave behind punched-out erosions which will eventually crust over.
This is a dermatological emergency and warrants immediate referral to dermatologists for assessment and oral antivirals.
Management in primary care
There are numerous treatment options for patients with eczema, allowing great flexibility when tailoring therapy to the individual, with the counterpoint being that there is no single reliable regimen for the entire spectrum of disease.
Common causes of a lack of response to therapy, particularly in primary care, include inadequate use of topical treatments, topical steroids of insufficient potency and confusion over the treatment regimen.
Exclusion diets for eczema in the absence of any other symptoms (anaphylaxis, urticaria) should only be carried out under the supervision of a dietitian and on the recommendation of a specialist. The NICE guidance contains a useful summary of treatment recommendations.4
Patients and their parents or carers should be educated about the flare and remit nature of the disease, and how to titrate their topical treatments accordingly.
There is some evidence that psychological and educational interventions in a multidisciplinary setting improve quality of life for patients with eczema, but there is a lack of any formalised intervention framework.5 In secondary care, this would be carried out by an eczema specialist nurse. For clinicians, the emphasis should be on ensuring compliance with the prescribed treatment regimen (see box 2).
|Box 2: Ensuring patient compliance|
Restoring the lipid barrier of the skin forms a cornerstone of AE treatment. This is basically achieved through avoidance of soap (which strips the lipids from the skin) and the use of emollients to restore moisture and repair the lipid barrier. There are many emollients available, on and off prescription.
The emollient ladder describes the greasiness of each preparation. As a general rule, the greasier the preparation, the more effective it is. However, this can come at the cost of compliance, particularly in older children and adolescents, who will be concerned about the poor cosmetic effect.
Any emollient is worthless if left in the tub, so the aim is to negotiate a compromise with the patient. One exception is if the eczema is wet and weeping, in which case, paraffin-based emollients will not adhere, and in this event, a lighter preparation with a higher water content should be used instead.
Emollients should be continued regardless of eczema activity, but when the skin is asymptomatic, lighter preparations can be used. Lighter emollients (creams and lotions) and OTC preparations often contain more excipients, which have the potential to irritate the skin. Aqueous cream, for example, contains sodium lauryl sulphate, a common irritant.
Topical corticosteroids, potent anti-inflammatory agents, are used as first line in treating AE. The selection of appropriate steroid therapy depends on the patient’s age, the site to be treated, the severity of the disease and the patient’s response to previous treatment.
Younger patients, milder disease and facial or flexural sites mandate the use of milder steroids. Older patients, those with more severe disease and the involvement of the palms and soles would suggest a need for more potent preparations. Treatment courses should last between one and two weeks.
If there are recurrent flares of eczema, consider continuous treatment of troublesome areas twice weekly, even when asymptomatic, with a six-monthly review of effectiveness. It would be appropriate to use a short course of potent steroids (two to three days) even in a younger child, before switching to a mild or moderate agent for the remaining treatment course.
Review the choice of steroid and the diagnosis if no response is observed. If the patient has not responded in the first one to two weeks, they are unlikely to respond at all and escalation of steroid potency would be warranted.
Prolonged courses of low-potency steroids may lead to a greater cumulative dose than a short burst of potent treatment. NICE guidance states that in children aged under 12 months potent topical steroids should only be used under specialist supervision.
Topical antibiotics and combined preparations with corticosteroids (for example, betamethasone/fusidic acid) should only be used if an infection is suspected and should not be used as a long-term management option. If recurrent infections are a concern, a soap substitute with chlorhexidine can be used regularly to reduce the bacterial load.
The potential side-effects of topical corticosteroids are often a cause for concern for patients and their carers. There are well-documented cutaneous side-effects (skin atrophy, striae, purpura, telangiectasia), but these are typically associated with continuous, prolonged use of potent/ultrapotent steroids.
An isolated two-week course, even with a potent steroid, is unlikely to cause significant harm, unless in the context of a neonatal patient. This is further balanced by the harm that could be incurred by leaving severe AE untreated.
If patients require recurrent courses (more than two or three per year) of potent topical steroids to maintain disease control, this would be an indication to refer for a specialist opinion. There are potential risks of systemic absorption and adrenal suppression, but these come with the use of very significant quantities of topical steroid.
Similarly to topical steroids, systemic corticosteroids have an anti-inflammatory and immunosuppressive effect. Although very effective in treating AE, they are not recommended because this can result in a rebound once treatment is stopped, and may lead to more rapid induction of systemic side-effects.
If a patient’s AE remains resistant to therapy, consider increasing the potency of topical steroid treatment and referring for a specialist opinion.
Systemic corticosteroids are sometimes used in secondary care for patients in crisis, particularly when bridging on to phototherapy or systemic therapy.
Some patients find benefit in the use of occlusive treatments, although they are not universally tolerated. Their effect is twofold, preventing excoriation of the affected areas of skin and increasing the potency of topical corticosteroids and emollients.
Occlusive treatments can take the form of garments (vests, trousers, gloves) or bandages. Soaking the garment or bandage in water before application (wet wraps) can have a cooling effect, reducing the sensation of pruritus. Infected eczema, however, should not be occluded.
Antihistamines may alleviate the pruritus experienced in eczema, but will not treat the underlying disease process. They should be used as symptomatic relief only. Some patients (aged >6 months) may find a short trial of sedating antihistamine at night helpful while other treatments take effect on their skin.
Other treatments in secondary care
Coal tar has long been used in the treatment of skin disease, particularly eczema and psoriasis.6 Although it is not on the list of NICE recommendations, recent in-vitro studies have demonstrated coal tar’s activity in restoring skin barrier proteins (specifically filaggrin, which is deficient in those with AE), in addition to inhibiting the Th2 cytokine pathway that is activated in AE.7
There have been concerns about carcinogenesis in animal studies, but this has not been demonstrated in human studies.8
UV phototherapy is a suitable treatment regimen for patients with particularly widespread eczema which is insufficiently severe for systemic therapy, or in which it is contraindicated or undesirable.
Narrowband UVB is typically available, and prospective patients undergo screening and assessment in secondary care before receiving this therapy.
The potential drawbacks of phototherapy are a risk of sunburn, accelerated photoageing, formation of cataracts and carcinogenesis secondary to UV exposure.
Systemic therapy is the last line of treatment in patients with severe, refractory AE. Treatment with immunosuppressive agents (azathioprine, mycophenolate mofetil, methotrexate and ciclosporin) is conducted in secondary care and continued for a number of years after remission is achieved.
Biological therapy is predicted to be the next development in the management of AE. In contrast to psoriasis, where biological therapy is mature, with multiple agents available on the NHS, the use of biologics in AE remains experimental. Agents currently under study include omalizumab (anti-IgE), licensed for use in asthma, and dupilumab, an IL-4 receptor blocker.
- Dr Andre Khoo is clinical fellow in dermatology, Norfolk & Norwich Hospital, Professor Viktor Gladko is head of the dermatology department and the postgraduate medical school, Moscow State University of Food Production, and Dr Ekaterina Burova is consultant dermatologist, Bedford Hospital Trust
- James WD, Berger T, Elston D. Andrews’ Diseases of the Skin (11th edition). Philadelphia, Elsevier, 2011.
- World Allergy Organization. WAO/EAACI Allergy Definitions.
- Bolognia JL, Jorizzo JL, Schaffer JV et al (eds). Dermatology (third edition). Philadelphia, Elsevier, 2012.
- NICE. Atopic eczema in children: management of atopic eczema in children from birth up to the age of 12 years. CG57. London, NICE, December 2007.
- Ersser SJ, Cowdell F, Latter S et al. Psychological and educational interventions for atopic eczema in children. Cochrane Database Syst Rev 2014; 1: CD004054
- McLean WHI, Irvine AD. Old King Coal — molecular mechanisms underlying an ancient treatment for atopic eczema. J Clin Invest 2013; 123: 551-3.
- Van den Bogaard EH, Bergboer JGM, Vonk-Bergers M et al. Coal tar induces AHR-dependent skin barrier repair in atopic dermatitis. J Clin Invest 2013; 123: 917-27.
- Roelofzen JHJ, Aben KKH, Oldenhof UTH et al. No increased risk of cancer after coal tar treatment in patients with psoriasis or eczema. J Invest Dermatol 2010; 130: 953-61.