BASIC SCIENCE

The structure and the function of skin change with age. In aging skin, the epidermis becomes thinner and loses its undulating rete pattern; the stratum corneum loses its ability to retain water, and cell replacement, barrier function, and wound healing decrease; the dermis becomes thinner and loses its elasticity, partly because of a decrease in the number of fibroblasts; the eccrine sweat glands shrink and secrete less sweat; and Langerhans cells decrease in number, affecting immune responsiveness.² All of these changes contribute to many of the skin conditions of the elderly.

DIAGNOSIS, EVALUATION, AND TREATMENT

Intrinsic factors (e.g., genetics) and extrinsic factors (e.g., ultraviolet [UV] exposure) affect the rate at which the skin ages. Excessive UV exposure produces structural changes (photo damage) in all layers of the skin: Collagen and elastic fibers in the dermis become frayed (solar elastosis); elastic tissue loses its integrity and sags or droops, clinically appearing as wrinkles; and connective tissue weakens and predisposes to traumatic solar purpura.

The stigmata of aging skin include wrinkles (rhytides), furrows, sagging, and sunken cheekbones (Fig. 1). Treatment is not necessary, but therapeutic options include topical retinoids (e.g., tretinoin to soften fine wrinkles); chemical peels using salicylic acid or glycolic acid for exfoliation; microdermabrasion; laser therapy (e.g., carbon dioxide for resurfacing); fillers such as botulinum toxin, hyaluronic acid, and collagen, to enhance volume; and plastic surgery.

Figure 1 Solar lentigines.

Solar lentigines often manifest as brown patches on sun-exposed areas.

Photo (sun) damage is the most common and most pervasive change of aging (white) skin, commonly identified as solar lentigines and actinic keratoses (see Fig. 1). Solar lentigines are benign growths—tan or brown macules or patches on sun-exposed areas (head, hands, forearms)—representing epidermal hyperplasia and proliferation of melanocytes. Their presence reflects appreciable sun exposure and can portend an increased risk of sun-induced skin cancer. Treatment is not necessary, except for cosmetic reasons. In contrast, actinic keratoses—rough, reddened, ill-defined plaques on sun-exposed areas—are precancerous growths. Malignant potential is extremely low, but left untreated, approximately 5% to 20% of actinic keratoses deteriorate to invasive squamous cell carcinoma within 10 to 25 years.³ Actinic keratoses deserve treatment to forestall progression into squamous cell carcinoma. Options include local destruction with either cryotherapy (liquid nitrogen) or curettage and the topical application of 5-fluorouracil (Efudex, Fluoroplex, Carac), imiquimod (Aldara), or diclofenac (Solaraze) for more extensive disease. Obviously, sun avoidance and the use of sunscreens help to minimize photo damage, solar lentigines, and actinic keratoses.

Solar or traumatic purpura (also known as senile purpura) is a common and benign condition of extravasated blood in the dermis characterized by ecchymotic, purpuric patches on the forearms, arms, or legs of older persons. The condition usually follows minor trauma and commonly affects those who take aspirin or other blood thinners (Fig. 2). Treatment is unnecessary and the extravasated blood is eventually reabsorbed.

Figure 2 Solar purpura.

Solar purpura often manifests as purpuric patches on the forearms.

Seborrheic keratoses are probably the most common benign growths on adult skin. Typically, they are greasy brown hyperkeratotic plaques that appear stuck to the skin surface; they can appear anywhere, except for palms and soles, and tend to congregate on the trunk. Their cause is unknown, but a genetic predisposition might exist in some families. Therapy is usually not necessary unless they are pruritic, irritated, or inflamed. Angiomas are benign vascular growths that commonly occur in adults as red macules and papules on the trunk and proximal extremities. Similar to seborrheic keratoses, therapy for angiomas is usually not necessary unless they are pruritic, irritated, or inflamed. Laser treatment is a successful method of destruction.

Pruritus (itching) is a common condition of advanced age, affecting nearly one half of older adults (older than 60 years) at some time, usually without a rash. Patients with chronic renal or hepatic insufficiency, anemia, thyroid disease, diabetes mellitus, drug allergy, or underlying malignancy might have itch with or without a rash. For patients without a rash, treatment is symptomatic (e.g., lubrication with emollients, and perhaps an antihistamine, coupled with treatment of any underlying problem). For patients with a rash, the treatment is the same, plus treatment of the skin disease (usually a secondary eczema) with topical or systemic corticosteroids.

Dermatitis (eczema) is a common cause of pruritus regardless of age. In older persons the most common cause of dermatitis is xerosis (asteatosis, i.e., dry skin), followed by seborrheic dermatitis, stasis dermatitis, and contact dermatitis. Asteatotic eczema, or winter itch, often affects aging skin, usually as itchy, scaly, cracked, red plaques on the extremities, most commonly the legs. Seasonal changes (e.g., low humidity and cold temperatures) aggravate the disease, which tends to occur more often in winter, especially in northern climates. The mainstay of treatment is dry skin care (minimizing bathing and hot water; avoiding harsh soap; pat drying afterwards) and hydration (liberal and frequent use of emollients, especially after bathing) and topical corticosteroids (e.g., triamcinolone or fluocinolone twice daily as needed) for the eczema.

Seborrheic dermatitis is a common type of eczema characterized by scaly, red plaques on the scalp, face, and central chest. The prevalence and severity are higher in patients with neurologic disease (e.g. Parkinson’s disease). Treatment includes shampoo for the scalp, such as those containing zinc pyrithione, selenium sulfide, or ketoconazole, and a mild topical corticosteroid.

Stasis dermatitis, also known as gravitational eczema, affects approximately 7% of older adults, usually the obese.⁴ Patients initially experience heaviness and swelling in their feet, which worsens with standing and progresses through the day, followed by the dermatitis—scaly, red, edematous plaques on the feet, ankles, calves, and shins, all as a result of vascular insufficiency or venous hypertension (Fig. 3). Secondary ulceration, cellulitis, and later postinflammatory hyperpigmentation can follow. If venous or stasis ulcers develop, they are typically shallow and irregularly shaped and usually occur just above the medial malleolus. Treatment involves compression, leg elevation, and often débridement, sometimes followed by skin grafting. Aspirin or pentoxifylline is a helpful adjunctive treatment to improve peripheral blood flow, allowing ulcers to heal more rapidly.