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.
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.
Solar lentigines
Figure 1: Click to Enlarge
Solar purpura
Figure 2: Click to Enlarge
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.
Stasis dermatitis.Stasis dermatitis typically occurs on the lateral aspects of the shins.
Figure 3: Click to Enlarge
Other causes of leg ulcers in the elderly are neuropathy, trauma, neoplasia, infection, panniculitis, and pyoderma gangrenosum. Vascular disease is the most common cause of leg ulcers in the elderly, and venous insufficiency is the most common etiology, accounting for approximately 60% to 70% of all leg ulcers.5
Vascular insufficiency can represent venous insufficiency or perhaps even venous thrombosis, valvular incompetence, or arterial insufficiency. Treatment should include weight reduction when warranted, compression stockings to reduce edema, leg elevation as much as possible, and reduction of prolonged standing. Affected areas require regular lubrication with emollients and topical corticosteroids if eczema occurs. Patients with stasis dermatitis and chronic leg ulcers have an increased risk for contact dermatitis, based on the likely use of multiple topical medications. When contact dermatitis is suspected, patch testing can help to resolve the issue and determine the likely allergen; its yield in elderly patients with stasis dermatitis is 60%.6 Contact dermatitis in older people is often persistent and recalcitrant to standard treatment (i.e., topical and oral corticosteroids as well as antihistamines).
Varicosities (varicose veins) occur commonly with venous insufficiency, characteristically as tortuous vascular channels on calves, thighs, and popliteal fossa. Sclerotherapy or laser treatment can minimize the appearance. Lipodermatosclerosis is an uncommon sequela of chronic venous insufficiency and is characterized by subcutaneous fibrosis with firm, indurated plaques on the legs. Treatment is analogous to the measures outlined for venous insufficiency.
Decubitus ulcers (bed sores, pressure sores or ulcers) can be an unfortunate occurrence in debilitated elderly patients, especially for hospitalized or bedridden patients, where 40% of all nursing care is devoted to skin care and decubital care.5 Such ulcers follow friction, pressure, or shearing forces over bony prominences, and affect underlying skin, muscle, connective tissue, cartilage, or bone; common sites are the sacrum, ischial tuberosities, and heels. Risk factors include immobility, fecal or urinary incontinence, diabetes, glucocorticoid use, and poor nutrition. Treatment includes surgical débridement if warranted; positional rotation every 2 hours to distribute the compressive forces and to minimize further injury; elevation of the head of the bed to increase upper body pressure; and cleansing the affected area in incontinent patients. All patients need an adequate diet, with vitamin supplementation, and treatment of any underlying conditions. A variety of dressings is available to improve wound or ulcer repair (e.g., transparent films, hydrogels, hydrocolloids, polysaccharides, alginates, foam, and laminates). Selection depends on the state of the ulcer (infected, soupy, or clean), the amount of exudate, ulcer depth, and patient compliance. Absorbent wound dressings (alginates) are useful for moist wounds; films for wounds without drainage; and hydrocolloids for ease of use and expense, which enhance patient compliance.