54 Upon completion of this chapter, the reader will be able to: • Describe lesions and rashes using a four-point process to facilitate differential diagnosis formulation, triage, and communication of dermatologic problems. • Diagnose and manage common, benign neoplastic skin growths in older patients. • Diagnose and discuss evidence-based management options for actinic keratosis (AK) and common skin cancers in the geriatric population. • Discuss the differential diagnoses and approach to older patients presenting with itch but without intact primary lesions. • Diagnose and manage common causes of eczematous skin disorders (dermatitis) in older individuals, including how to estimate appropriate potency and quantity of topical steroids. • Discuss the diagnosis and management of inflammatory conditions associated with aging. • Discuss evidence-based prevention and treatment of acute herpes zoster and management options for postherpetic neuralgia. CASE 1 Cándido Aguado (Part 1) You are in the middle of a busy clinic, and the next patient is an 84-year-old otherwise healthy Hispanic man, Cándido Aguado, who is in for an annual physical. He immediately hands you a meticulously written list of medical questions. He shakes his head as he explains his friend had a fourth skin cancer removed. The patient has two changing spots (Plates 2 and 3) and a request for a general skin check. Because your clinic is running a little behind, you have only 20 minutes to do his usual health care maintenance and also answer his questions. Health care reforms might lead to even greater pressure on primary providers to manage skin problems, thus making skin examination a common and important part of primary care. More than one third of patients presenting to primary care providers often have at least one skin complaint.1 Ironically, a recent study showed that the elderly, ethnic minorities, and patients with lower education tend to underestimate their risk of skin cancer. Because skin cancers are the most common malignancy,2 the primary care provider can make a significant impact in filling patient education and skin cancer screening. Recent data strongly suggest total body skin cancer screening might decrease melanoma mortality.3 One study showed cost effectiveness of skin cancer screening at least once in individuals over 50 years of age.4 Many challenges exist in the dermatology examination for the nondermatologist. First, many of us had very limited exposures during medical school or residency training.5 This barrier creates difficulty in approaching the skin from a systematic approach in and recognizing dermatologic conditions.6 Second, many primary care providers have time constraints and medically complex patients with a multitude of nondermatologic comorbidities.7 Third, there might be access limitations to dermatologic specialists, depending on geographic practice and patient demographic. Triaging patients with skin problems and communicating the urgency to the specialist can seem daunting. The purpose of this section is to facilitate the dermatologic examination and to address these barriers. Proposed approaches to general skin cancer screening will be outlined first, followed by heuristics for describing skin findings. The remainder of the chapter will focus on common dermatologic problems in primary care of geriatrics rather than providing an exhaustive litany of diagnoses. The primary care provider will be empowered to describe lesions and rashes to a dermatologist or to use clinical decision making tools (see Web Resources section) to facilitate referral, when needed. The total body skin examination (TBSE) is important for identifying premalignant and malignant skin disorders as part of the routine complete physical, but also should be considered for new rashes or to look for cutaneous clues of underlying systemic diseases.8 It should be especially encouraged in patients with a personal history of skin cancers or precancers, history of transplantation or immunosuppressant use, chronic anti–tumor necrosis factor use, exposure to known cutaneous carcinogens (e.g., tanning, arsenic), multiple moles (more than a dozen), or family history of skin cancer.9,10 Although fair-skinned patients are known to be at highest risk for skin cancer, a recent study highlighted the increasing incidence of melanoma among Hispanics and suggested a potential practice gap in preventive education and screening for minority ethnic groups.11 Several practical considerations can improve the efficiency and thoroughness of TBSE. During the routine primary care exam that includes palpation and auscultation, the overlying skin can be visually inspected. The patient should ideally disrobe and all accessories (e.g., watches, glasses, hearing aids, toupees, bracelets) that might obscure skin findings should be removed and all makeup should be removed.8,12 The mucous membranes, anogenital regions, interdigital spaces of fingers and toes, scalp and hair, nails, and posterior auricular neck should be inspected. Adequate lighting is required to visualize the skin, especially for subtle lesions or areas that cast shadows. Natural sunlight is ideal, otherwise bright lamps can be used with the patient positioned underneath.8 A portable light such as penlight or otoscope held in front of or tangentially to lesions can be helpful to detect subtle changes such as wrinkling, fluid within lesions, and sometimes lesion margins.8 The ABCDE (Asymmetry, irregular Border, Color variation, Diameter over 6 mm, Evolving characteristic over months) rule is a simple and popular screening method for melanoma (Plate 1).13,14 However, by itself, there are limitations in missing the rare amelanotic variant of melanoma or misdiagnosing seborrheic keratosis (Plate 3) as melanoma.10 For routine skin cancer screening, especially in patients with many skin lesions, a practical, rapid, gestalt approach is the “ugly duckling” detection method.15 A lesion that does not resemble the overall color, shape, texture of other pigmented lesions is considered suspect. Dermoscopy (using a special magnifying lens with polarized light) can be a helpful extension of the unaided eye, but is operator dependent and requires training.16 Several promising and noninvasive tools might facilitate the skin examination in the future, including a Food and Drug Administration (FDA)–approved spectroscopic device (MelaFind) and emerging confocal microscopy technology.17 Practical considerations of cost and technologic limitations are current barriers to routine implementation of such equipment. In patients with a specific lesion or rash complaint, the most succinct approach is a systematic four-point method that describes (1) anatomic distribution, (2) lesion configuration, (3) primary lesion and color, and (4) secondary change, if present.8 History is occasionally helpful, but these four descriptors are quintessential for efficiently framing the skin examination to use a dermatologic atlas or algorithm to narrow the differential diagnosis. No singular component of this four-point system is necessarily weighted more than the others. Several sophisticated Internet and handheld device clinical decision making aids are also available.18 In cases requiring dermatologic referral, skin findings can be efficiently communicated via these tools. Anatomic location of the dermatologic finding, and sometimes the areas that are relatively spared, can provide rapid clues for the pathogenesis of a rash. Configuration (Table 54-1) refers to how the lesion or rash is patterned. The primary lesion (Table 54-2) refers to an intact, unmanipulated representation of the process and includes description of color. Sometimes it can be difficult to identify a primary lesion if the patient has already self-medicated or excoriated their lesions; or if the lesion is short-lived (e.g., urticaria) or friable. Generally, if there is not an intact primary lesion, biopsy tends to be of low diagnostic value. Lastly, secondary change (Table 54-3) refers to the findings caused either by the evolution of a primary lesion or an external factor modifying the lesion. TABLE 54-1 Data from Bolognia J, Jorizzo JL, Rapini RP. Dermatology. 2nd ed. St. Louis, Mo.: Mosby/Elsevier; 2008. TABLE 54-2 Data from Bolognia J, Jorizzo JL, Rapini RP. Dermatology. 2nd ed. St. Louis, Mo.: Mosby/Elsevier; 2008. TABLE 54-3 Data from Bolognia J, Jorizzo JL, Rapini RP. Dermatology. 2nd ed. St. Louis, Mo.: Mosby/Elsevier; 2008. CASE 1 Cándido Aguado (Part 2) You successfully incorporate a general skin examination of Mr. Aguado while you do your usual health care maintenance examination, which is otherwise unremarkable. Plate 3 is a brown, stuck-on, waxy plaque that he admits to picking. You reassure the patient it is an irritated seborrheic keratosis. The lesion in Plate 2 concerns you, and the patient relays change over a few months following trauma. It is tender and frequently bleeds. You call a dermatologist: “On the left thumb is a solitary red, bleeding, tender nodule that is eroded, rapidly growing, and painful.” Eczema (dermatitis) is a common clinical sign that refers to a group of conditions that share histologic features but have differing etiologies and clinical appearances. Dermatitis is a misnomer, because the inflammation and edema (spongiosis) is at the level of the epidermis, not the dermis. In the acute phase it is often confused as being infected because of the oozing papulovesicles (Plate 8) or pustular appearance on acral surfaces. Chronic eczema appears as dry, scaly patches (Plate 22) or sometimes lichenified plaques with cracks.9 Several etiologies can lead to the final common pathway of eczema.9 Stasis dermatitis, caused by underlying venous insufficiency, is commonplace in older patients from acquired venous incompetence, saphenous vein grafting, or prior thromboembolism. The patient is often misdiagnosed as having bilateral leg cellulitis and has partial or no response to antibiotic therapy, which leads to unnecessary cost, hospitalization, and interventions (Plate 22).19 Nummular (discoid) eczema is an idiopathic variant of solitary or multiple coin-shaped plaques, typically on the extremities (Plate 13). It is often mistaken for “refractory” tinea corporis, though a skin scraping mounted in potassium hydroxide (KOH) can easily differentiate the two.9 Contact dermatitis is another common cause of eczema. It is typically well-demarcated and geometrically or linearly configured (Plate 8). It can be caused by a nonimmunologic response to a chemical irritant, such as soap residue.20 Allergic sensitization (i.e., type IV delayed hypersensitivity with cell-mediated immune reaction), which is exemplified by poison ivy or nickel allergy, is probably as common in older patients as irritant dermatitis.20,21 Ask about all personal products and topical medicaments, because geriatric patients and those with stasis dermatitis who are self-medicating have a high prevalence of allergic contact dermatitis, particularly to neomycin and fragrance mixes.20,22 Periocular and eyelid dermatitis can result from eyedrops or from nail cosmetic products.23 Airborne allergens (e.g., pollens) can mimic photodistributed rashes on exposed areas. Autoeczematization (“Id” reaction, autosensitization) is a symmetric eruption of eczematous papules that occurs distant to the primary sites of chronic skin inflammation. The classic example is chronic tinea pedis with symmetrically distributed eczematous papules on the upper extremities or torso.9 It can also be seen with severe contact or stasis dermatitis.24 The presumed pathophysiology is lymphocytes at the site of chronic inflammation circulate into the periphery and deposit at other anatomic sites.25 The differential diagnosis of eczema includes cutaneous T-cell lymphoma, scabies, syphilis, squamous cell carcinoma in situ (Bowen’s disease), drug eruptions, mammary or extramammary Paget’s disease, and dermatophytosis (tinea corporis).20 Consider skin biopsy or skin scraping if lesions are not responding or worsening with topical corticosteroids. Treatment regimens generally include dry skin care instructions (Box 54-1), brief courses of topical corticosteroids (Level of Evidence D) or calcineurin inhibitors (e.g., tacrolimus or pimecrolimus) (Level of Evidence D) for symptomatic relief.9 Tips for how to choose the steroid molecule potency, vehicle, and dispensed quantity are described in Boxes 54-2 and 54-3. When dermatitis is severe and widespread, systemic steroids (0.5-1 mg/kg per day for 3 to 4 weeks) can be considered (Level of Evidence D).9 A protracted course is required to prevent rebound flares of contact dermatitis. Allergic or irritant contactants should be avoided completely. Dietary restrictions (except in cases of test-proven allergens or additives) and water softeners are of uncertain value9,26,27. Seborrheic keratoses (SKs) are ubiquitous, benign epidermal hyperplasia (Plate 3). Mutations in fibroblast growth factor receptor 3 (FGFR3) might be involved.31 A distinctive variant consisting of smaller papules that are reminiscent of flat warts on the bilateral cheeks of ethnic skin is known as dermatosis papulosa nigra. The sign of Lesar-Trelat, or eruptive appearance of multiple SKs as a paraneoplastic phenomenon, is a rare and controversial entity.32 Three case-controlled studies33–35 suggest most eruptive SKs are not associated with underlying malignancy and probably do not justify expensive, invasive testing in the absence of other concerning review of systems. SKs can become symptomatic when they become irritated such as catching on clothing, though sometimes they spontaneously become inflamed. Anecdotally, many patients report the lesions disappearing (probably excoriated or coincidentally traumatized) but only to return. The differential diagnosis can sometimes include melanoma, verruca, or lentigines (sun spots).9 There are unfortunately no preventive measures. Reassurance is all that is generally required. Sebaceous hyperplasias (Plate 23) are benign overgrowths of normal sebaceous oil glands that are usually found on the face. They can be seen commonly on the vermilion lips and buccal mucosa (Fordyce spots), eyelids (meibomian glands), areola (Montgomery tubercles), and glans penis or clitoris (Tyson’s glands). There is a yellow to flesh-colored appearance and often associated central umbilication. The condition is usually idiopathic, though cyclosporine has been reported to cause diffuse lesions.36 The major differentials include nonmelanoma skin cancer, fibrous papules, xanthomas, sebaceous adenoma or carcinoma, syringoma, and milia. Treatment is usually not required, but cosmetic removal options can include electrodesiccation, or topical or systemic retinoids (Level of Evidence C).36,37 Dermatofibromas (benign fibrohistiocytomas) often appear on the lower extremities (or sometimes on the torso or upper extremities) as pink-brown dome-shaped firm papules. There will often be a characteristic dimple sign when squeezed (Plate 24). The lesions are usually asymptomatic, though sometimes can be pruritic or painful. They are thought to be caused by trauma, because the histologic appearance is similar to scar. The primary differential includes irritated nevus (when more brown in color or raised), melanoma, or dermatofibromosarcoma protuberans. When symptomatic, they can be excised or treated with intralesional triamcinolone acetate or topical ultrapotent steroids (Level of Evidence D). Recurrences can occur, because the process can often spread laterally and into the deep dermis.
Skin problems
Dermatologic examination: Challenges and practical approaches
Total body skin examination
Four-point dermatologic description
Description
Example
Annular
Ringlike
Tinea corporis (ringworm), granuloma annulare (Plate 4), porokeratosis (Plate 5)
Dermatomal (zosteriform)
Confined to a dermatome and abruptly stops at midline
Herpes zoster (Plate 6)
Grouped (herpetiform)
Clustered lesions
Herpes simplex (Plate 7)
Linear
Lesions arranged in a line, suggestive of an external cause
Contact dermatitis (Plate 8), scabies burrows
Reticular (retiform)
Netlike or meshlike, suggesting a process affecting the cutaneous vascular network
Livedo reticularis (Plate 9), erythema ab igne (red-brown patch in area of heating pad use)
Description
Example
Macule or patch
Flat without induration or significant elevation
Idiopathic guttate hypomelanosis (Plate 10), lentigo
Nodule/tumor
Deep-seated, indurated lesion, often fixed
Squamous cell carcinoma, basal cell carcinoma (Plate 11)
Papule or plaque
Elevated lesion confined to upper dermis or epidermis
Nevus (mole), seborrheic keratosis (Plate 3), lichen planus (Plate 12), eczema (Plate 13), psoriasis, cutaneous T-cell lymphoma (Plate 14)
Purpura or petechiae or ecchymosis
Nonblanching dark red-purple lesion, suggesting extravasated erythrocytes in skin (in contrast, “violaceous” means color partially blanches)
Vasculitis (inflammation and destruction of vascular walls), Bateman’s (solar) purpura from chronic sun damage, hypercoaguable state (Plate 9)
Pustules
Yellow, pus-filled
Folliculitis, rosacea (Plate 15)
Telangiectasia
Prominent blood vessel, blanches easily
Spider telangiectasia, rosacea (Plate 15), basal cell carcinoma (Plate 11)
Vesicle/bulla
Blister filled with nonpurulent material (e.g., serum, blood). If deeply seated in dermis, it is a cyst (e.g., sebaceous cyst).
Bullous pemphigoid (Plate 16), bullous tinea pedis, acute allergic contact dermatitis (Plate 8), insect bite, herpes (Plate 7)
Wheal/urticaria
Pink-white, blanchable, edematous hives
Hives, serum sickness (Plate 17)
Description
Example
Atrophy
Thinning of skin. When epidermis is involved, fine wrinkling, transparency of skin, stretch marks, or visualization of underlying dermal vessels might be present. When dermis or fat is involved, there is often skin depression.
Lichen sclerosus, steroid-induced atrophy (Plate 18)
Crust
Dried blood, pus, or serum
Impetigo (Plate 19), scab (Plate 20)
Erosion or avulsion
Partial thickness epidermal loss. In contrast, ulceration means full thickness loss of epidermis with exposure of at least dermis.
Excoriated skin (Plate 6)
Necrosis
Dead cutaneous tissue
Eschar (Plate 21), wet gangrene
Scale
Desiccated, flaky keratinocytes
Psoriasis, eczema, porokeratosis (Plate 5)
Eczematous dermatoses
Benign cutaneous processes
Precancerous and malignant cutaneous diseases
Skin problems
