The Many Manifestations of Eczema

Eczema is a reaction pattern caused by inflammation of the epidermis that typically manifests as scaling or crusting of the skin. It may be acute, subacute, or chronic depending on the historical and physical characteristics. The list of potential etiologies is extensive and includes allergic, autoimmune, idiopathic, and inflammatory mechanisms. Although eczema is often used interchangeably with atopic dermatitis (shown), there are many different causes of eczematous dermatitis, including allergic contact dermatitis, seborrheic dermatitis, irritant contact dermatitis, nummular eczema, dyshidrotic eczema, asteatotic eczema, venous stasis dermatitis, and lichen simplex chronicus (neurodermatitis).

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Skin is made of up of 2 primary layers: the epidermis and dermis. The epidermis contains keratinocytes, melanocytes, Langerhans cells, and Merkel cells, and is responsible for waterproofing, temperature regulation, and serving as a barrier to infection. It contains no blood vessels, but is nourished via diffusion. The dermis contains connective tissues, hair follicles, sweat glands, sebaceous glands, lymphatic vessels, and blood vessels. The hypodermis lies underneath the skin connecting it to the underlying muscles and bones. Eczema is caused by damage to the epidermis, which can result in dryness, flaking, erythema, infection, blistering, and cracking.

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Atopic dermatitis is a pruritic disease of unknown etiology that typically starts in infancy. It is characterized by pruritus, eczematous lesions, xerosis, and lichenification. It may be associated with other atopic disorders, including asthma, allergic rhinitis, or urticaria. The major etiologic hypotheses are immune dysfunction leading to immunoglobulin (Ig)E sensitization and defective epithelial cells, both of which cause disruption of the skin's epithelial barrier. The prevalence is 10%-12% in children and 0.9% in adults, with a higher prevalence among blacks and Asians. The eczematous changes and morphology are seen in different locations depending on the age of the patient. In infancy, this dermatitis usually occurs first typically with erythema and exudation in the flexor creases and then the cheeks, forehead, and scalp. Lesions are usually ill-defined, erythematous, scaly, and crusted patches or plaques.

In childhood, lichenification is the most prominent manifestation due to repeated rubbing of the skin over bony protuberances. Lesions are eczematous and exudative, with excoriations and crusting common. In adulthood, lesions become more diffuse with an underlying background of erythema. A brown macular ring around the neck, due to localized amyloid deposition, may be found (shown). Lesions are typically very itchy for all age groups. Treatment typically involves maintenance therapy with moisturizers and topical steroids for flares. Immunomodulators, ultraviolet therapy, and chemotherapeutics are second-line agents recommended on a case-by-case basis. Patients should be instructed to avoid known environmental or dietary triggers. The majority of patients affected are children; this eruption will often resolve by adulthood.

Dyshidrotic eczema is a chronic relapsing form of vesicular palmoplantar dermatitis of unknown etiology. Although the etiology is unclear, there is a strong association with atopy. Fifty percent of patients with dyshidrotic eczema will also have atopic dermatitis. Exogenous factors, especially metals (such as nickel), may trigger episodes. Patients typically report pruritus of the hands and feet with a sudden onset of vesicles. On examination, patients will have symmetric crops of clear vesicles and/or bullae on the palms as well as lateral aspects of the fingers and toes, feet, and soles (shown). The distribution of lesions is 80% hands only, 10% feet only, and 10% feet and hands.

Vesicles are deep seated with surrounding erythema, which may enlarge to form confluent bullae. Bullae may rupture easily, especially on the feet (shown). With long-standing disease, fingernails may become dystrophic. Diagnosis is typically clinical, but a punch biopsy may be used for confirmation. Patients with mild symptoms will typically resolve in 2-3 weeks. Bullae may be drained without unroofing or treated with Burrow's solution compresses. Other therapies include topical or systemic corticosteroids, topical calcineurin inhibitors, UV-A therapy, or chemotherapeutics. Patients are advised to avoid known contact irritants or allergens, use regular emollients, and follow a hand care regimen. Secondary bacterial infections may easily occur if proper hygiene is not maintained.

Asteatotic dermatitis is characterized by pruritic, dry, cracked, and polygonally fissured skin with irregular scaling. Asteatotic dermatitis develops when excess water is lost from the epidermis, causing dehydration of the stratum corneum. Elderly persons are at increased risk because they have reduced sebaceous and sweat gland activity. On examination, lesions will appear as slightly scaly, inflamed, curvilinearly cracked and/or fissured skin. Lesions are most commonly found on the pretibial areas, but may also be present on the thighs, hands, and trunk. Treatment typically involves limiting warm water soaking, reducing soap usage, avoiding hard skin cleansers, applying petrolatum-based emollients, and applying topical steroid ointments. Most cases respond well to therapy.

Nummular, meaning "coin-shaped," dermatitis is characterized by round-to-oval erythematous plaques, commonly on the arms and legs. The exact pathophysiology is unknown, but it is considered a form of adult-onset atopic dermatitis. Patients typically report a history of days to months of a pruritic eruption, which may also burn or sting. Lesions are most commonly located on the extremities, but they may be found anywhere except the face and scalp. Lesions typically begin as erythematous papules or vesicles that coalesce to form confluent plaques (shown). The plaques become dry, scaly, and more violaceous before flattening to macules with a brown postinflammatory hyperpigmentation that gradually lightens. Secondary bacterial infection is common. Treatment is aimed at skin rehydration with topical moisturizers, reduction of inflammation with steroids, and treatment of any subsequent infection.

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. It is associated with an abnormal immune response to the fungus Malassezia, but Malassezia organisms are probably a cofactor rather than a cause. Dandruff is the mildest manifestation, but patients may report periods of intense burning, itching, and scaling. It may be aggravated during winter and early spring, excoriation, or emotional stress. On examination, patients may have mild, patchy scaling (shown) up to widespread, thick, adherent crusts. It typically begins on the scalp and then spreads to the forehead, posterior part of the neck, and postauricular skin. Hypopigmentation may be seen in dark-skinned individuals. Generalized distribution is typically present only in immunocompromised individuals. Dandruff usually responds to more frequent shampooing or a longer period of lathering. Early treatment of flares with topical antifungals or weak corticosteroids is typically effective, but thick plaques may require overnight occlusion with tar, bath oil, or Baker's P&S® solution (Baker Cummins; Miami, Florida).

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Allergic contact dermatitis is inflammation of the skin caused by contact with a specific allergen in a sensitized patient. It is a type IV delayed hypersensitivity reaction in which antigens are carried by Langerhans cells to regional lymph nodes where they are presented to T lymphocytes, which clonally reproduce, a process that takes 10-14 days. Subsequent allergen exposure will then produce a more rapid immunologic response, within hours to days of exposure. A detailed patient history is crucial in determining the etiologic agent for allergic contact dermatitis. Although poison ivy is the classic example, nickel is the leading cause worldwide typically because earrings and necklaces (shown) contain nickel and are in constant contact with the skin.

The site of the rash may also provide important clues to the etiologic agent, as in the patient shown who developed a reaction after hair dying. In some cases, patch testing may be needed to confirm suspected etiologic agents. On examination, patients with acute allergic contact dermatitis will have pruritic papules and vesicles on an erythematous base, whereas those with chronic exposure may have lichenified pruritic plaques. Symptomatic treatment is typically achieved with cool saline or aluminum acetate compresses, oatmeal baths, or oral antihistamines. For more serious cases, topical corticosteroids, topical immunomodulators, psoralen plus UV-A, or rarely immunosuppressive agents may be used.

Lichen simplex chronicus is a thickening of the skin with variable scaling that arises secondary to repetitive scratching or rubbing. It is not a primary process, but develops when patients sense pruritus, repetitively excoriate the area, and develop lichenification. The etiology of the pruritus may be due to any underlying pathology, or none at all. Patients typically report stable pruritic plaques, most commonly on the scalp, nape of the neck, extensor forearms, elbows, vulva, scrotum, upper medial thighs, knees, lower legs, and ankles. Erythema is found in early lesions. The plaques are typically well demarcated, lichenified, firm, and rough with exaggerated skin lines. Hyperpigmentation may be present. Treatment is aimed at reducing pruritus with topical corticosteroids or oral antihistamines. In some patients, antianxiety medications are required.

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Stasis dermatitis is an inflammatory condition that occurs in the lower extremities of patients with chronic venous insufficiency and venous hypertension. It usually affects middle-aged and elderly patients, unless there is an underlying process inducing earlier venous stasis, such as trauma. Stasis dermatitis develops as a direct consequence of venous insufficiency. Increased venous hydrostatic pressure causes increased permeability of the dermal capillaries and subsequent dermal fibrosis from the release of inflammatory mediators. Patients may report pruritus and skin discoloration, typically first experienced on the medial ankle. On examination, patients may have erythematous, scaling, eczematous patches (shown).

There may be exudative, weeping patches and plaques in severe, acute cases. In long-standing lesions, lichenification and hyperpigmentation may develop from chronic scratching and rubbing. Some patients may eventually develop ulceration (shown) and lipodermatosclerosis. Treatment is typically through compression therapy with stockings, topical therapy with moist gauze dressing and corticosteroids, good skin hygiene, and as-needed topical antibiotics for the management of infections. Chronic use of topical emollients can help maximize epidermal moisture, but places patients at risk for the development of subsequent allergic contact dermatitis.

Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage. It is the clinical result of inflammation arising from the release of proinflammatory cytokines from skin cells, principally keratinocytes. The major pathophysiologic changes are skin-barrier disruption, epidermal cellular changes, and cytokine release. Although a wide range of chemicals may be responsible, the most common causes are repeated exposure to low-grade irritants, such as soaps and detergents. Acute irritant contact dermatitis may develop within minutes to hours of exposure, whereas the cumulative form may be delayed by weeks. On examination, patients may exhibit macular erythema, hyperkeratosis, or fissuring over vesiculation with a scalded appearance of the epidermis (shown). Healing typically beings promptly after removal of the offending agent, although creams containing ceramides or dimethicone may be useful to help restore the epidermal barrier.