Elderly Adults and Skin Disorders

Common Problems for Nondermatologists

Chang R. Na, MD; Steven Wang, MD; Robert S. Kirsner, MD, PhD; Daniel G. Federman, MD

Disclosures

South Med J. 2012;105(11):600-606. 

In This Article

Senescent Changes in the Skin

Aging affects all organ systems, including the skin. As skin ages, it becomes wrinkled, lax, and easier to tear.[2,3] Histologically, the rete pegs, which help to hold the epidermis to the dermis, are retracted.[4] Cellular turnover slows, with progressive loss of cells in the dermis and epidermis, and concomitant loss of the extracellular matrix.[5,6] The epidermis at some body sites thins with age.[4] Reduced stratum corneum lipid biosynthesis impairs permeability barrier function.[7] There is a decrease of cutaneous blood flow, as well as of maintenance and remodeling of microvasculature.[8,9] Along with a decreased number of sweat glands and diminished subcutaneous fat, thermoregulation capability is weakened.[2]

Photoaging, the cumulative damage of the skin caused by ultraviolet (UV) radiation, appears to exploit similar cellular mechanisms as chronological aging. UV radiation activates signaling pathways that induce metalloproteinases, which degrade the extracellular matrix.[10] Chronic UV exposure also leads to progressive loss of cutaneous vasculature.[11]

A heterogeneous group of nonenzymatic metabolites known as advanced glycation end products (AGE) has been implicated in aging of the skin and a number of other conditions such as atherosclerosis and Alzheimer disease.[12,13] Hemoglobin A1c, now measured routinely to assess glycemic control in people with diabetes, is probably the most widely known AGE precursor.[14] AGEs accumulates over time, although more quickly with higher glucose levels, in various tissues. AGE has been shown to induce fibroblast apoptosis and degradation of the extracellular matrix.[15] Moreover, the presence of AGE appears to amplify the damaging effects of UV radiation.[15]

Hormone therapy (HT) with estrogen has shown to ameliorate aging of the skin and wrinkling by restoring skin collagen, thickness, and moisture content, as well as accelerating wound healing.[16] HT also increases bone density and reduces the risk of osteoporotic fracture; however, HT has been demonstrated to increase the risk of coronary heart disease, stroke, thromboembolic events, and breast cancer.[17]

Pruritus

Pruritus is one of the most common skin complaints in the geriatric population.[18] The causes of pruritus are numerous. A thorough skin examination and medical history may reveal an underlying skin disease, such as xerosis, seborrheic dermatitis, bullous pemphigoid, or herpes zoster.[19] Repeated scratching can result in lichenification, excoriation, infection, and traumatic purpura.[20] Drug-induced pruritus, although uncommon, also should be considered, given the prevalence of polypharmacy in elderly people.[21] Pruritus without a rash may be caused by such disparate underlying systemic diseases such lymphoma, iron deficiency, polycythemia vera, thyroid abnormalities, liver dysfunction, renal insufficiency, and human immunodeficiency virus infection.[22] A thorough medical workup should be undertaken for pruritus of unknown etiology (Table). The physical examination should include a search for any other skin or nail manifestations, and care should be taken to palpate for thyroid, liver, or lymph node abnormalities.

Often, pruritus is related to xerosis, or dryness of the skin.[22] Topical moisturizers are the preferred treatment modality and are typically a combination of agents that hydrate and hold water in the skin.[23] Several formulations may need to be used before the optimal one for a patient is mutually agreed upon. In addition, the use of lipid-lowering agents has been associated with xerosis.

Other treatments that may be considered include those that substitute a different sensation, such as heating or cooling the skin. Topical agents such as menthol, camphor, or phenol also may be used to induce the sensation of cooling.[24] Other agents such as lidocaine, a local anesthetic, or capsaicin, a substance P depleter, also have been used with some success.[23]

Asteatotic Eczema

Xerosis may present as asteatotic eczema, plaques that may be scaly and erythematous with interconnected fissures. The rash classically involves the lower leg but may also involve the upper arms, anterior thighs, and lower back.[25] The development of generalized disease in an adult should raise the suspicion of an internal malignancy.[26] A special type of asteatotic eczema on the lower extremities with an appearance similar to cracked porcelain is known as eczema craquelé.[27]

Xerosis being the underlying cause of asteatotic eczema, conditions, or environments that dry out the skin worsens the disease. Xerosis also is known as winter eczema because cold weather with a lower ambient humidity or extremely cold air conditioning will aggravate it.[28] Frequent bathing with soap and hot water also dries out the skin.[29] Treatment also is directed at avoiding these provocative factors and correcting the underlying xerosis, such as with topical moisturizers.

Seborrheic Keratosis

Seborrheic keratosis is a common benign epidermal neoplasm with multiple clinical appearances. The typical lesion appears on hair-bearing surfaces such as the head, neck, and trunk; classically demonstrates a verrucous surface with a "stuck on" appearance; and is tan to dark brown in color (Fig. 1).[30] There are multiple variants with different distributions and appearances. For example, dermatosis papulosa nigra is a form of seborrheic keratosis that occurs in darker pigmented individuals and presents as small hyperpigmented papules.[30] Stucco keratosis appears as rough, "stuck on" papules that are easily scraped off with minimal bleeding, and is found more frequently on the lower extremities.[30]

Figure 1.

Seborrheic keratosis.

It is unclear whether sun exposure is an independent risk factor for the development of seborrheic keratosis or if there is conclusive evidence associating it with skin malignancies;[30,31] however, there is still some overlap in the clinical appearance of skin malignancies and seborrheic keratosis.[32] In general, any lesion that is atypical in appearance or has undergone recent inflammatory changes should be examined histologically to rule out malignancy. Finally, the sudden appearance of multiple seborrheic keratoses may be the paraneoplastic manifestation of an internal malignancy, also known as Leser-Trelat syndrome.[33] As seborrheic keratosis accumulates pigment over time, this eruption may be suspected when many light-colored lesions are present.

Seborrheic keratoses are commonly removed for cosmetic reasons, although other reasons such as bleeding, itching, pain, or obstruction of vision are considered medically necessary.[34] Typically, removal is through operative means, although ablative laser and cryotherapy techniques also are available.[31] These alternative techniques do not allow specimen collection for definitive diagnosis and should not be used if there is any doubt that the lesions are benign.

Herpes Zoster

Commonly known as shingles, herpes zoster is a painful, blistering skin rash caused by the varicella-zoster virus, which also causes chickenpox. Among adults, shingles is more common in elderly people because of a decline in cell-mediated immunity.[35] The rash is typically unilateral, erythematous, with papules or painful vesicles, and confined to a dermatomal distribution. In 10% to 15% of patients, the virus involves the ophthalmic division of the trigeminal nerve, and the resulting damage to the cornea and uvea can cause blindness.[36] Definitive diagnosis, particularly useful in differentiating herpes zoster from herpes simplex virus, may be obtained with viral culture, immunoassays for viral antigen, or polymerase chain reaction.[36] The rash can persist for up to 2 weeks and eventually crusts over.[37] Even after the skin rash resolves, the patient can continue to experience pain and allodynia at the site, a condition known as postherpetic neuralgia, which at times can be debilitating.

Systemic antiviral treatment with valcyclovir, famcyclovir, or acyclovir is indicated for patients who present within 72 hours of the onset of rash. Antiviral treatment at presentation reduces pain and reduces the duration of subsequent postherpetic neuralgia.[38] Postherpetic neuralgia is challenging to treat, but various agents have proven useful, including tricyclic antidepressants, gabapentin, opioids, topical lidocaine, and capsaicin.[38] Patients older than 50 years should be offered the shingles vaccine Zostavax, which has been shown to reduce the incidence of herpes zoster disease and postherpetic neuralgia.[39–41]

Contact Dermatitis

Contact dermatitis remains a prevalent condition in the elderly population. There are two types of contact dermatitis: irritant, which is nonimmunologically mediated, and allergic, which is immunologically mediated. Early disease may be differentiated by symptoms and histology, in which irritant reactions are more likely to present with burning and stinging sensations and necrosis of epidermal keratinocytes, and allergic reactions are more likely to present with pruritus. Late in the course of the disease, however, it can be difficult to differentiate the two types. Not surprisingly, data using cytokine expression profiles suggest that the underlying inflammatory pathways are similar.[42]

Decreased immune response associated with aging helps with allergic-type contact dermatitis, but elderly adults also have had more cumulative exposures to develop contact sensitization. Overall, the incidence of allergic-type contact dermatitis decreases with age, but some allergens such as fragrance demonstrate increased sensitization rates with advancing age.[43] The presence of inflamed or ulcerated skin also increases sensitization rates, for example, in patients with chronic leg ulcers.[44]

Finding and avoiding the offending agent is the best form of treatment. Nickel and fragrance are common culprits. Ingredients such as balsam of Peru also should not be overlooked.[45] Patch testing to determine sensitivity should include an additional reading at days 5 to 7 because of possible delayed immune reactions associated with aging.[46] Patients should be advised that it can take up to 3 months of careful avoidance of the offending agent to see clinical improvement.[47]

Bullous Pemphigoid

Bullous pemphigoid is an autoimmune blistering disorder commonly found in older adults, which is characterized by tense blisters on normal or inflamed skin (Fig. 2). The disease is chronic and generalized, with a tendency to prefer the limb creases.[48] Definitive diagnosis is made through immunofluorescent staining of biopsy specimens demonstrating linear pattern deposition of immunoglobulin G and/or C3 along the epidermal basement membrane.[49] Oral corticosteroids are the mainstay of treatment, but adverse effects such as weight gain, hyperglycemia, hypertension, and decreased bone density can limit their use.[48] Topical corticosteroids may be used in cases of localized disease.[48] Otherwise, steroid-sparing agents such as methotrexate and azathioprine can be used in conjunction with corticosteroids.[48,50] Bullous pemphigoid has presented as a paraneoplastic syndrome, and patients should be evaluated for internal malignancy, particularly if their disease is refractory to treatment.[51,52] Drug-induced forms of bullous pemphigoid also have been described, incited by such drugs as furosemide, phenacetin, enalapril, ibuprofen, and influenza vaccine.[53] Bullous pemphigoid is thought to be otherwise benign, and it remains controversial whether significantly increased mortality exists in patients with bullous pemphigoid.[54]

Figure 2.

Bullous pemphigoid.

Venous Insufficiency

Chronic venous insufficiency, defined as impaired calf muscle pump function and venous return in the lower extremity, is a common affliction with significant morbidity. Edema caused by venous insufficiency is in itself an inflammatory agent, and the resulting dermatitis is prone to ulceration. The resulting ulcer heals poorly and is difficult to treat. For this reason, preventive measures are of paramount importance. For example, deep venous thrombosis can cause postthrombotic syndrome, essentially an acquired venous insufficiency, which may be prevented with the use of compression stockings.[55] In some cases in which the thrombus is large and proximal, some clinicians go as far as to advocate the use of chemical lysis or thrombectomy, although this is not yet standard practice.[56]

Venous dermatitis most commonly manifests at the medial perimalleolar area and is characterized by poorly demarcated erythema, pruritus, and sometimes pain. Chronic inflammation can lead to fibrosis, a condition known as lipodermatosclerosis (LDS).[57] An acute painful form, often without fibrosis, can mimic cellulitis. Well-demarcated, indurated, exquisitely tender lesions in the lower extremities in the setting of venous insufficiency should raise suspicions for LDS.[58] Chronic LDS develops as a hyperpigmented contraction of skin forming a characteristic "inverted champagne bottle" appearance of the lower extremities.[58] One should try to make a diagnosis of LDS by physical findings and a classic history because skin biopsies of these patients tend to heal poorly.[57]

The mainstay of the treatment for venous insufficiency and its sequelae is compression stockings or bandages and elevation of the affected extremity.[57,59] Topical steroids also are often prescribed to treat the dermatitis. Ulcers that are superinfected can be treated with antibiotics; however, ulcers that are refractory to treatment should raise suspicions for underlying squamous cell carcinoma.[60]

Peripheral arterial disease can lead to ischemic ulcers or gangrene.[61] In patients with leg ulcers, it is important not to overlook peripheral arterial disease as a potential cause because compression therapy with elastic bandages is contraindicated.[62] An ankle-brachial index in each lower extremity for people with leg ulcers should be checked before initiating compression therapy.

Precancerous and Malignant Skin Neoplasia

The common skin cancers are nonmelanoma skin cancers: basal cell carcinoma, squamous cell carcinoma, and keratoacanthomas. The incidence of nonmelanoma skin cancers greatly outnumbers that of melanoma, but they also carry a much lower mortality rate.[63] All of these skin cancers are related at least in part because of prior UV light exposure and resultant DNA damage.[64–66]

The classic appearance of basal cell carcinoma is that of a raised flesh to pink-red, pearly papule or nodule and associated telangiectasia, sometimes with central ulceration (Fig. 3). There are, however, several variants, such as morpheaform, superficial, and pigmented types, as well as scabs that fail to heal.[67] The typical appearance of squamous cell carcinoma is an enlarging papule or plaque that may ulcerate (Fig. 4).[68] Actinic keratosis is a squamous cell carcinoma precursor that appears clinically similar to squamous cell carcinoma (Fig. 5). In fact, some dermatopathologists consider actinic keratosis to be an intraepidermal form of squamous cell carcinoma.[69] It is said that "melanoma writes its message on the skin with its own ink, and it is there for all to see."[70] Early clinical detection is particularly important for melanoma because mortality is directly related to the depth of invasion. The 5-year survival rate for patients with lesions <1-mm thick is >95%, whereas those with >4-mm lesions have a 30% to 50% survival rate.[64] No particular clinical characteristic is diagnostic and clinicians often use the mnemonic ABCDE (asymmetry, irregular border, color variation, diameter >6 mm, evolving) to help determine which lesions warrant biopsy (Fig. 6). Use of dermoscopy, which provides magnification and lighting, can aid clinicians in determining which lesions warrant biopsying.

Figure 3.

Basal cell carcinoma with central ulceration.

Figure 4.

Squamous cell carcinoma.

Figure 5.

Actinic keratosis.

Figure 6.

Melanoma.

Although sun exposure in early childhood is more predictive of future skin cancer, recent data have shown that exposure at any period of life leads to an increased risk of cancer.[71] Therefore, prevention with sunscreen and protective clothing continues to be advised, even in elderly adults.

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