Eczema is a common inflammatory skin disease presenting clinically with red papules or plaques containing small vesicles, which may itch, ooze and crust. There are several clinical subtypes. The characteristic histological feature is intercellular oedema in the epidermis (spongiosis), which separates the keratinocytes and can cause vesicle formation. Chronic inflammation with lymphocytic infiltration of the epidermis and dermis is often seen. Pathogenesis is variable and includes:

Psoriasis is a common chronic relapsing dermatitis that classically manifests as circumscribed red skin plaques often several centimetres in diameter, with silvery surface scale. Extensor surfaces of knees and elbows, the sacral region and the scalp are common sites. Nail changes are common and arthritis develops in a small percentage of patients. Onset is usually in early adult life. The pathogenesis is unclear but there is hyperproliferation of keratinocytes, with the epidermal turnover time reduced from the normal 13days to 3–4days. The histological features of classical psoriasis are:

• regular epidermal hyperplasia (thickening)

• parakeratosis (retained nuclei within the surface keratin layer)

• thinning of the granular layer

• neutrophil microabscesses

• increased mitotic activity (cell turnover).

Lichen planus presents clinically as multiple small itchy violet papules, around the wrist and elbows. Oral and genital lesions also occur. Skin lesions often resolve after several months or years. Histological features include:

Erythema multiforme (EM) is an uncommon but potentially serious hypersensitivity response to certain infections (herpes simplex and Mycoplasma) and drugs (including sulphonamides, penicillin and aspirin). Clinical lesions include red macules, papules and vesicles. The characteristic ‘target’ lesion has a pale, raised or eroded centre and erythematous (red) rim. Symmetrical involvement of the limbs is most commonly seen. Stevens–Johnson syndrome is severe erythema multiforme with oral mucosal lesions. Toxic epidermal necrosis is the most serious manifestation of EM, with a high risk of systemic sepsis and fluid imbalance due to extensive loss of skin and mucosal epithelium; mortality is 35%. Histological examination shows a lichenoid inflammatory infiltrate with epidermal cell apoptosis.

Vesico-bullous diseases are classified according to the site of the vesicle formation, which may be within the epidermis or at the dermo-epidermal junction. The pathogenesis in many cases involves immune complex formation with autoantibodies. Examples are shown in Table 61. Many of these diseases are described further below.

Burns can be caused by hot liquids (scalds), gases or solids, as well as fire. Burn injuries are classified as:

In first degree burns there is endothelial injury and leakage of intravascular fluid into the surrounding tissue. There is vascular congestion with pain and erythema, but no skin necrosis. Second degree burns show epidermal necrosis with blistering as the epidermis separates from the dermis. Regeneration of the skin surface cells can occur from adjacent viable epidermis or from surviving skin adnexal structures. More severe damage occurs in third degree burns, with necrosis of the epidermis and dermis. As the extent of severe burn injuries increases, so does the risk of serious or fatal complications, including:

Skin grafting is often required for healing of third degree burns.

Skin infections are common, with a wide variety of potential pathogens, including:

Lichenoid inflammatory pattern skin lesions may be part of systemic lupus erythematosus or more commonly isolated cutaneous disease, called discoid lupus erythematosus. Immunoglobulins and complement are deposited along the dermo-epidermal junction.

Recipients of immunocompetent bone marrow transplants often develop lesions in the skin, gastrointestinal tract and liver, when grafted lymphocytes attack host tissue. Cutaneous graft-versus-host disease has a lichenoid pattern.

Bullous pemphigoid is a blistering skin disease that occurs in the elderly. Up to 90% have IgG autoantibodies against the bullous pemphigoid major antigen located in the epidermal basement membrane. The vesicles and bullae usually contain eosinophils.

Pemphigus is an intraepidermal blistering disease with autoantibodies to various structural proteins involved in intercellular adhesion.

Dermatitis herpetiformis is a subepidermal blistering disease characterised by IgA antibody deposition, although the exact pathogenesis is unclear. There is a strong association with coeliac disease.