Clinical features and epidemiology

Atopic eczema, or atopic dermatitis, is an itchy inflammatory skin disease, which usually involves the skin creases (Williams et al., 1995). The diagnostic criteria for atopic eczema are classified by the following clinical picture (Williams et al., 1995) an itchy skin condition, plus three or more of:

• Past involvement of the skin creases, such as bends of the elbows or behind the knees,
• A personal or immediate family history of asthma or hay fever,
• A tendency towards generally dry skin,
• Onset under the age of 2 year and
• Visible flexural dermatitis, as defined by photographic protocol.

The risk factors for children developing atopic eczemas include familial factors including genetics (atopy), family size and sibling order; social class (eczema has a higher incidence in more affluent social classes) and concurrent illness/ disruption to family life including teething, psychological stress and lack of sleep (National Institute for Health and Clinical Excellence [NICE], 2007).

Clinical signs
Atopic eczema is characterised by inflammation (redness), swelling, crusting, scaling of the skin; intensified by scratching in response to intense itch. It may be acute with oozing and vesicles or it may be chronic with lichenification, altered pigmentation and exaggerated surface markings. Itching is a predominant symptom that can lead to a cycle of scratching, leading to skin damage and in turn more itching (the itch–scratch cycle). A stubborn reverse pattern may occur when the extensor areas (a straight part of the body) as well as the flexural areas (a body part that flexes or bends) are affected, for example, around the elbow (see Figure 9.7).

Atopic eczema is now the commonest inflammatory skin disease of childhood, affecting around 15–20% of school children in the UK (Herd, 2000). Although only 1–2% of adults are affected by atopic eczema, their disease is often more chronic and severe (Herd et al., 1996). Atopic eczema is more frequent in childhood, especially in the first 5 years of life (Thomas et al., 2008). Young children represent the largest group of individuals with atopic eczema seen by dermatologists, GPs, primary care nurses and nurse specialists. Atopic eczema is the commonest of childhood dermatoses, accounting for 20% of all dermatology referrals (Lewis-Jones et al., 2001). There is reasonable evidence to suggest that the prevalence of atopic eczema has increased two to three-fold over the last 30 years, for reasons which are unclear but possibly due to environmental and lifestyle changes, (Williams, 1992) and in many countries this continues to rise (Asher et al., 2006).

Studies with twins demonstrate that genetic factors are important in atopic eczema but other evidence strongly suggests that environmental factors are critical in disease expression (Williams, 1995). Allergic factors such as exposure to house dust mites may be accountable, but non-allergic factors such as exposure to irritants and infectious agents may also be important. Atopic eczema may be further categorised into extrinsic and intrinsic forms, as highlighted earlier in the section. The former denotes individuals with evidence of raised circulating antibodies to common allergens, whereas the latter does not. It is also established that psychological factors, such as stress, play a vital role in the course of atopic eczema as a trigger or precipitating factor (Buske-Kirschbaum et al., 2001, 2002). Frequent exposure to infections may protect children from expressing atopy; this observation is based on an inverse relationship between prevalence of eczema and family size, leading to the ‘hygiene hypothesis’ (Strachan, 1989). As referred to in the section on the biology of eczema, atopic eczema is a multifactorial condition that is influenced by the interplay between genetics and the environment; this interplay and its relationship to the skin barrier is discussed in Cork et al. (2006). Some of the environmental trigger factors are now discussed.

Trigger factors
Trigger factors need to be identified and managed following clinical assessment; potential factors include (NICE, 2007):

• irritants (e.g. soaps and detergents)
• skin infections
• allergens
  • contact
  • food
  • inhalant
  
  

Atopic eczema assessment should consider all the identified trigger factors listed in Table 9.1.

Table 9.1 Trigger factors for atopic eczema.   Potential trigger factor Source of trigger factor   Irritants Wool and synthetic clothing, soaps, detergents, disinfectants and chemicals   Contact allergens Preservations in topical products, perfumes, metals and latex   Food/dietary factors Cow’s milk, eggs, peanuts, wheat   Inhalant allergens House dust mite, animal dander, tree/grass pollens and mould   Microbial colonisation/infection Staphylococcus aureus, Streptococcus species, Candida albicans, Pityrosporum yeasts and herpes simplex   Climate Extremes of temperature and humidity and seasonal variation   Environmental factors Hard water, proximity to traffic, cooking with gas and tobacco smoke     Source: Adapted from NICE (2007).

NICE (2007) provides guidance based on a synthesis of evidence, proposing the following considerations. Inhalation allergy may be seen in children with seasonal flares, and those whose eczema is associated with asthma and allergic rhinitis. Allergic contact dermatitis may be seen in children with exacerbations of previously controlled atopic eczema or reactions to topical preparations. Allergy testing on the high street or via the internet should be avoided since there is no evidence of their value. The role of factors such as stress, humidity or temperature extremes have in leading to flares is not known and as such these factors should be avoided where practical.

Health care professionals should consider a diagnosis of food allergy in children with atopic eczema who have previously reacted to food with immediate symptoms. This also applies to infants and young children with moderate to severe eczema that has not been controlled by optimum management, particularly if associated with gut dysmobility (including colic, vomiting and altered bowel habit) or failure to thrive (NICE, 2007).

In general there is little evidence to support a diet free of eggs, and milk in unselected patients with atopic eczema nor the use of a few-foods diet. There is, however, some evidence to support the use of an egg-free diet in infants with suspect egg allergy who have positive specific antibodies (IgE) to eggs (Williams et al., 2008). With exclusion, diet consideration also needs to be given to the risks of impaired growth and development in the child. It is not known whether altering a breast feeding mother’s diet is effective in reducing the severity of eczema (NICE, 2007). Evidence is currently not available to suggest the optimal feeding regimen in the first year of life for children with established atopic eczema.

Evidence to support the implication of environmental factors increasing the prevalence of atopic eczema in developed countries is outlined by a study showing associations between atopic eczema symptoms and the home environment (McNally et al., 2001). This highlights factors such as dampness in the home environment, the use of radiators in bedrooms (causing nocturnal overheating) and upholstered furniture, bedding and carpets; all these factors encourage house dust mites to thrive. The study concluded that there was an improvement in atopic eczema symptoms by controlling mite allergens through mattress covers and frequent vacuuming. Control of house dust mite by vacuuming is therefore advocated, based on this evidence; a similar principle will apply to damp dusting.