Atopic eczema (atopic dermatitis) is a common inflammatory skin condition that typically presents early in life.
Atopic eczema normally presents in the first few years of life and normally follows a relapsing-remitting course. It is characterised by a dry, cracked and itchy rash that may follow a number of patterns of distribution. Episodic flares are followed by periods of remission, though the interval and length of episodes vary widely and some patients develop chronic disease without remission.
Management tends to follow a stepped approach that involves emollients and additional agents such as topical steroids, antihistamines and oral steroids where needed. Complications include secondary infection and the impact of the condition on patients quality of life and mental wellbeing.
Atopic eczema is thought to affect 10-30% of children and 2-10% of adults.
The majority of cases present early in life with an estimated 45% of cases developing before 6 months of age, and 70-90% by the age of 5.
The condition appears more common in those in higher socioeconomic classes and with smaller families. It occurs in all ethnic groups and does not show any significant gender imbalance.
Figures from NICE CKS.
Atopy refers to a predisposition to an abnormally exaggerated IgE response to allergen exposure.
Atopy involves the sensitisation to allergens/antigens that are detected by CD4+ type 2 helper (Th2) lymphocytes causing their differentiation and resulting in an exaggerated IgE response. This leads to increased risk of hypersensitivity reactions.
Atopic individuals are classically said to be at risk of developing a triad of conditions; atopic eczema, allergic rhinitis and asthma. Other conditions include food allergies and allergic conjunctivitis. The term ‘atopic march’ refers to the progressive development of atopic disease, often with atopic eczema presenting as an infant followed by asthma and/or allergic rhinitis early in childhood.
The aetiology of atopic eczema is complex and incompletely understood. It involves environmental, hereditary, and immunological factors.
A family history of atopic disease increases the risk of developing atopic eczema (as well as other atopic conditions). It is estimated that 70% of those with atopic eczema will have a family history of atopic disease. Twin studies have shown a concordance of 77-85% in monozygotic twins and 15-21% in dizygotic twins.
A mutation in the FLG gene has been implicated in up to 50% of cases. FLG encodes filaggrin, a protein required for skin to perform its role as an effective barrier. Deficiency is thought to allow access of antigens through the skin where they initiate an immune and inflammatory response.
The onset, appearance and distribution varies between individuals.
It often presents with scaly, itchy and erythematous patches commonly affecting the flexures (elbow, knees, wrists). Infants often present with rash affecting the cheeks.
Those of black ethnicity may demonstrate a different distribution with rashes affecting the extensor surfaces. Affected skin can develop patches of both hypo and hyperpigmentation.
Itchiness leading to scratching can be evidenced by excoriations and with time lichenification (thickening) of the skin develops.
There are a number of other dermatological conditions that should be considered.
Alternative diagnosis should be considered and when necessary excluded. These include:
NICE have published diagnostic criteria for eczema in children under 12.
NICE CG 57 (2021 update) describe a set of features diagnostic of atopic eczema for children under the age of 12:
Atopic eczema should be diagnosed when a child has an itchy skin condition plus 3 or more of the following:
Healthcare professionals should be aware that in Asian, black Caribbean and black African children, atopic eczema can affect the extensor surfaces rather than the flexures, and discoid (circular) or follicular (around hair follicles) patterns may be more common.
The medical management of atopic eczema consists of a stepped approach with emollients forming the base of treatment.
Many individuals will have specific triggers that appear to cause flares of disease. This can include perfumes, detergents, soaps, clothes, hormones, foods and hormones.
Diaries may be of use to demonstrate temporal relationships between triggers and flares - in particular food diaries. Food allergies are more commonly seen in atopic individuals.
Generally speaking a stepped approach to management is used. Emollients sit at the base of this approach with other agents added when indicated.
Emollients are moisturising agents that comes in the form of ointments, creams, sprays, lotions and soap substitutes. Regular and liberal use is advised even between flares of disease.
They help to soothe, smooth and hydrate skin in patients with both dry or scaling disorders. Their effects are short-lived and therefore regular application is critical.
There are many emollients and the choice depends on the severity, location and patient preference. The formulation of an emollient is often referred to as a 'vehicle'. For example, in topical hydrocortisone cream, hydrocortisone is the drug and the vehicle is the cream that helps it be applied. Emollients used alone do not have a drug (vehicle-only). A variety of vehicles may be used:
Emollients may also be used as soap substitutes or added to baths/showers. Ordinary wash products can have the potential to irritate and damage skin.
Soap substitues can be used for hand washing, showering and bathing. Products may be prescribed that are specificaly designed for this use or usual emollients can be used. Bath and shower oil products may be bought over the counter. These can be added to baths or used directly during a shower. They likely provide limited benefit to usual emollient treatment.
Topical steroids are frequently used. These are categorised by their potency:
The use of more potent options is typically controlled by specialists. Patients requiring this level of treatment will normally meet the requirements of specialist referral. Local side effects are common and may include a burning sensation, thinning of skin, contact dermatitis, acne and depigmentation. Doses vary depending on location of the rash and patients/family should be given clear instructions.
Topical calcineurin inhibitors (tacrolimus and pimecrolimus) may be used in moderate to severe disease with appropriate specialist input, typically when topical corticosteroids have failed. As the name suggests they inhibit calcineurin inhibitors, a chemical that normally activates T-lymphocytes.
NICE CG 57 (2021 update) describes the following stepped apprach to management:
Specialist referral should be made where disease is not well controlled, severe, affecting the face or where the diagnosis is uncertain. Patients affected by complications - infections or disease impacting quality of life - should also be referred.
The impact of atopic eczema on an individuals emotional wellbeing varies. At each assessment the impact of their disease on their mental health and quality of life should be assessed.
Where necessary further support, treatment, referral and review should be offered.
Complications of eczema include secondary infection and a negative impact on an individuals quality of life.
Breakdown in the skins normal barrier predisposes patients to infection. They are most commonly bacterial or viral in nature:
As discussed in the management section above it is important to be aware of, and assess for, the psychological effects eczema may be having.
Young children with eczema have been shown to have more behavioural difficulties and dependency on their parents. Support to both patients and their family should be given.
Atopic eczema has a tendency to improve as children grow older and transition into adolescence and adulthood.
As described above the development of atopic eczema as an infant increases the chance of developing other atopic conditions in childhood such as asthma and allergic rhinitis.
Atopic eczema normally improves as children grow up. It tends to follow a natural history of gradual resolution with the condition clearing in around 74% by the age of 16. Unfortunately some individuals will be affected well into adulthood and disease may even worsen.
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