The terms ‘eczema’ and ‘dermatitis’ are synonymous.
Eczema can be acute or chronic and there are several
causes. Acutely, epidermal oedema (spongiosis) and
intra-epidermal vesiculation (producing multilocular
blisters) predominate, whereas with chronicity there is
more epidermal thickening (acanthosis). Vasodilatation
and T-cell lymphocytic infiltration of the upper dermis
There are several patterns of eczema (Box ) and
environmental causes may be identifiable. The clinical
features are similar, irrespective of the cause (Box).
Generalised, prolonged hypersensitivity to common
environmental antigens, such as pollen and house dust
mite, is the hallmark of atopy, in which there is a genetic
predisposition to produce excess IgE. Atopic individuals
manifest one or more of a group of diseases that includes
asthma, hay fever, food and other allergies, and atopic
eczema. There are strong familial associations with
atopic diseases. The diagnosis of atopic eczema is made
using clinical criteria (Box ). Its prevalence has
increased 2–5-fold since the early 1980s, and the disease
now affects 1 in 10 schoolchildren.
Genetic factors are important. Epidermal barrier impairment
is a major, and perhaps primary, factor in this form
of eczema. Mutations in the filaggrin gene have been
identified as important in some. Environmental factors,
such as exposure to allergens in utero or during childhood,
may also have an aetiological role and 60–80% of
individuals are genetically susceptible to the induction
of IgE-mediated sensitisation to environmental allergens
such as food and animal hair. Decreased skin barrier
function may also allow greater penetration of allergens
through the epidermis, and thus cause immune stimulation
and subsequent inflammation.
Atopic eczema. A This patient had life-long chronic atopic
eczema and experienced a generalised flare of disease triggered by
infection. B Lichenification of chronic flexural eczema secondary to
rubbing and scratching.
Atopic eczema is extremely itchy and scratching accounts
for many of the signs (Fig. ). Widespread cutaneous
dryness (roughness) is another feature. The distribution
and character of the rash vary with age (Box ).
Complications are listed in Box .
This is an erythematous scaly rash affecting the scalp
(dandruff), central face, nasolabial folds, eyebrows,
central chest and upper back. It is associated with, and
may be due to, overgrowth of Pityrosporum yeasts. When
severe, it may resemble psoriasis. Severe or recalcitrant
seborrhoeic eczema can be a marker of immunodeficiency,
including HIV infection .
This is common and characteristically consists of discrete
coin-shaped eczematous lesions, which are often
impetiginised and most commonly occur on the limbs
of men. It is an eczema type that can be due to any
chronic itchy condition, whether primarily of skin (e.g.
atopic eczema) or another system (e.g. renal failure).
Detergents, alkalis, acids, solvents and abrasives are
common irritants. Strong irritants have acute effects,
whereas weaker irritants commonly cause chronic
eczema, especially of the hands, after prolonged exposure.
Individual susceptibility varies and the elderly,
atopic and fair-skinned are predisposed. Irritant eczema
accounts for most occupational cases of eczema and is a
significant cause of time off work.
Allergic contact eczema
This occurs due to a delayed hypersensitivity reaction
following contact with antigens or haptens. Previous
allergen exposure is required for sensitisation and the
reaction is specific to the allergen or closely related
chemicals. Common allergens are listed in Box 28.26.
Allergy persists indefinitely and eczema occurs at
sites of allergen contact and can secondarily spread
Lichenification of eczema occurs secondary to chronic
rubbing and scratching, and lichen simplex is a localised
form. Common sites include the neck, lower legs and the
Intensely itchy vesicles and bullae occur on the palms,
palmar surface and sides of the fingers and soles. Pompholyx
may have several causes, which include atopic
eczema, irritant and contact allergic dermatitis and
Investigation of eczema
Patch tests are performed if contact allergic dermatitis is
suspected (see Box ). IgE and specific IgE tests are
not routinely undertaken in atopic eczema and, similarly,
prick tests are not usually helpful. Bacterial and
viral swabs for microscopy and culture are useful in
suspected secondary infection. Individuals with atopic
eczema have an increased susceptibility to herpes
simplex virus (HSV), and are at risk of developing a
widespread infection, eczema herpeticum. The presence
of small, punched-out lesions on a background of worsening
eczema suggests the possibility of secondary HSV
infection. Skin scrapings to rule out secondary fungal
infection should be considered. Skin biopsy is not
usually required unless there is diagnostic doubt, e.g. of
a drug adverse effect or cutaneous lymphoma.