Internal Medicine/Eczema and Dermatitis

Eczema and Dermatitis
Eczema is a term that is often used interchangeably with dermatitis. It represents a complex reaction pattern in the skin characterized by variable clinical findings and a common histologic finding known as spongiosis. Spongiosis refers to intercellular edema of the epidermis, a hallmark of eczema. Eczema serves as the final common expression for a variety of skin disorders, including those discussed in the following sections.

Primary Lesions in Eczema: In eczema, primary lesions may include erythematous macules (flat red spots), papules (small raised bumps), and vesicles (fluid-filled sacs). These primary lesions can coalesce to form patches (larger flat areas) and plaques (raised, flat-topped areas). In severe cases of eczema, secondary lesions stemming from infection or excoriation may predominate. These secondary lesions are often marked by weeping and crusting. In chronic eczematous conditions, lichenification occurs, which involves cutaneous hypertrophy and accentuation of normal skin markings, ultimately altering the characteristic appearance of eczema.

Atopic Dermatitis (AD)
Atopic dermatitis (AD) is considered the cutaneous expression of the atopic state, which is characterized by a family history of conditions such as asthma, allergic rhinitis, or eczema. Several defining features help identify AD:


 * 1) Pruritus and Scratching: AD is notorious for causing intense itching (pruritus), leading to frequent scratching, which further exacerbates the condition.
 * 2) Exacerbations and Remissions: The clinical course of AD is marked by periods of exacerbations, where symptoms worsen, followed by remissions, where symptoms improve.
 * 3) Typical Lesions: AD presents with lesions typical of eczematous dermatitis, including erythematous (red) and edematous (swollen) skin.
 * 4) Atopic History: Many AD patients have a personal or family history of atopy, which includes asthma, allergic rhinitis, food allergies, or other forms of eczema.
 * 5) Duration: AD typically persists for more than 6 weeks, distinguishing it from acute conditions.
 * 6) Lichenification: Chronic AD often leads to lichenification, which is the thickening and accentuation of skin markings.
 * 7) Dry Skin: Dry skin is a common characteristic, and patients often experience worsening pruritus in response to dryness.

Clinical Presentation by Age: The clinical presentation of AD can vary depending on age. Approximately half of AD patients present within the first year of life, and around 80% present by the age of 5. Infants with AD often display weeping inflammatory patches and crusted plaques on the face, neck, and extensor surfaces. In contrast, older children and adolescents typically manifest dermatitis on flexural skin, particularly in the antecubital and popliteal fossae.

Persistence into Adulthood: AD may resolve spontaneously in some cases, but approximately 40% of individuals affected as children will continue to experience dermatitis in adulthood. Regardless of age, pruritus remains a prominent characteristic of AD and is exacerbated by dry skin. Many cutaneous findings in affected patients, such as lichenification, result from persistent rubbing and scratching.

Treatment of AD
Effective treatment for AD involves a multifaceted approach:


 * Avoidance of Cutaneous Irritants: Patients are often advised to bathe no more frequently than once a day, using warm or cool water, and to use only mild bath soap.
 * Adequate Moisturization: Following a bath, a topical anti-inflammatory agent in a cream or ointment base should be applied to areas of dermatitis, while all other skin areas should be moisturized.
 * Use of Topical Anti-Inflammatory Agents: Low- to mid-potency topical glucocorticoids are frequently employed in the treatment of AD. However, choosing the right glucocorticoid and its potency should take into consideration factors like the location of application to minimize the risk of skin atrophy, especially on the face and in intertriginous areas.
 * Alternative Anti-Inflammatory Agents: Non-glucocorticoid anti-inflammatory agents, including tacrolimus ointment, pimecrolimus cream, and crisaborole ointment, have gained approval for topical use in AD. These agents do not cause skin atrophy and do not suppress the hypothalamic-pituitary-adrenal axis.

This multifaceted approach aims to control inflammation, alleviate pruritus, and prevent further exacerbations of AD.

Lichen Simplex Chronicus and Contact Dermatitis
Lichen Simplex Chronicus (LSC)

Lichen simplex chronicus often represents the end stage of various pruritic and eczematous disorders, including AD. It manifests as circumscribed plaques or lichenified skin due to chronic scratching or rubbing. Commonly involved areas include the posterior nuchal region, dorsum of the feet, and ankles. Treatment focuses on breaking the cycle of chronic itching and scratching, often involving high-potency topical glucocorticoids.

Contact Dermatitis

Contact dermatitis results from skin exposure to exogenous agents that directly or indirectly injure the skin. Irritant contact dermatitis (ICD) occurs due to an inherent characteristic of a compound, such as a concentrated acid or base, and can develop rapidly without prior exposure to the irritant. Allergic contact dermatitis (ACD) results from an antigen-specific immune response and requires prior exposure to the offending agent, often taking hours to days to develop. Common allergens causing ACD include poison ivy, poison oak, and poison sumac, typically manifesting as erythema, vesiculation, and severe pruritus.

Treatment for Contact Dermatitis

The treatment approach for contact dermatitis depends on whether it is irritant or allergic in nature. Removing the offending agent leads to resolution in most cases. High-potency topical glucocorticoids can help alleviate symptoms while the dermatitis runs its course. In severe cases, systemic glucocorticoids may be considered.

Hand Eczema and Nummular Eczema
Hand Eczema

Hand eczema is a common, chronic skin disorder influenced by both exogenous and endogenous factors. It is often associated with other cutaneous disorders like AD. Chronic exposure to water, detergents, harsh chemicals, or allergens can initiate or exacerbate this condition. It may present with dryness, skin cracking, erythema, and edema, often starting beneath rings where irritants are trapped.

Evaluation of Hand Eczema: Assessing potential occupation-associated exposures is crucial when evaluating hand eczema. The patient's history should aim to identify possible irritants or allergen exposures.

Treatment for Hand Eczema: Therapy involves avoiding irritants, identifying possible contact allergens, treating coexisting infections, and using topical glucocorticoids. Protecting the hands with gloves is advisable, preferably vinyl gloves to avoid potential hypersensitivity reactions associated with latex gloves.

Nummular Eczema

Nummular eczema is characterized by circular or oval "coinlike" lesions. It begins as small, edematous papules that become crusted and scaly. While its exact cause remains unknown, dry skin is a contributing factor. Common locations include the trunk and the extensor surfaces of the extremities, particularly the pretibial areas or dorsum of the hands. It is more common in men and often occurs in middle age. Treatment approaches for nummular eczema are similar to those for AD.

Asteatotic Eczema and Stasis Dermatitis/ulceration
Asteatotic Eczema

Asteatotic eczema, also known as xerotic eczema or "winter itch," is a mildly inflammatory dermatitis that develops in areas of extremely dry skin, especially during dry winter months. Clinically, it may overlap with nummular eczema. It presents with fine cracks, scale, erythema, and pruritus, typically on the anterior surfaces of the lower extremities in elderly patients. Asteatotic eczema responds well to topical moisturizers and the avoidance of cutaneous irritants. Overbathing and the use of harsh soaps can exacerbate this condition.

Stasis Dermatitis and Stasis Ulceration

Stasis dermatitis develops on the lower extremities due to venous incompetence and chronic edema. It may be associated with a history of deep venous thrombosis or varicose veins. The initial signs include mild erythema and scaling with pruritus. Stasis dermatitis can become acutely inflamed, mimicking cellulitis, especially if it occurs bilaterally. Chronic stasis dermatitis often results in dermal fibrosis, clinically seen as brawny edema, and pigmentation changes due to chronic erythrocyte extravasation and hemosiderin deposition. Severe stasis dermatitis may lead to the development of stasis ulcers.

Treatment for Stasis Dermatitis and Stasis Ulceration

Patients with stasis dermatitis and stasis ulceration benefit from leg elevation and the use of compression stockings with a gradient of at least 30–40 mmHg. Emollients and mid-potency topical glucocorticoids can be used to manage symptoms. Protection of the legs from injury, including scratching, is crucial to prevent ulcers. Diuretics may be necessary to control chronic edema. Stasis ulcers require elevation, gentle debridement, semipermeable dressing, and compression. Superficial bacterial cultures of chronic stasis ulcers may yield polymicrobial colonizers.

Seborrheic Dermatitis
Seborrheic dermatitis is a common, chronic condition characterized by greasy scales overlying erythematous patches or plaques. It is frequently observed as severe dandruff on the scalp and can affect various facial areas, external auditory canals, and postauricular regions. It may also develop in the central chest, axilla, groin, submammary folds, and gluteal cleft. Severe cases can lead to generalized dermatitis. Pruritus varies in intensity.

Seborrheic dermatitis can appear in infancy (often as cradle cap) and reappear during adolescence and adulthood. While it is associated with conditions like Parkinson's disease, cerebrovascular accidents, and HIV infection, most individuals with seborrheic dermatitis have no underlying disorder.

Treatment of Seborrheic Dermatitis: Treatment often involves low-potency topical glucocorticoids, topical antifungal agents (like ketoconazole or ciclopirox), and antidandruff shampoos for scalp involvement. High-potency topical glucocorticoid solutions are effective for severe scalp cases but should not be used on the face to avoid complications like steroid-induced rosacea or atrophy.