Chapter 59 Geriatric dermatology
1. How common are skin disorders in the elderly population?
Survey studies have demonstrated that skin diseases are more common in the geriatric population than in the general population. One study revealed that 40% of Americans between the ages of 65 and 74 years had a cutaneous disease significant enough to warrant treatment by a physician. Patients older than 74 years are even more likely to develop significant skin diseases.
2. What is intrinsic aging of the skin?
Aging of the skin may be divided into that due to intrinsic aging and that secondary to extrinsic aging (Table 59-1). Intrinsic aging includes those changes that are due to normal maturity and senescence and thus occurs in all individuals. Classically, intrinsic aging has not been considered to be preventable, but there is renewed interest in the role of antioxidants, such as vitamins C and E, in preventing intrinsic aging. Despite numerous articles in the lay literature, there is no proof that these treatments are effective.
3. What is extrinsic aging of the skin?
Extrinsic aging of the skin consists of those changes produced by external agents. The most important extrinsic factor is cumulative ultraviolet (UV) light exposure. The cutaneous changes produced by sunlight are collectively referred to as dermatoheliosis. Most of the changes associated with aging of the skin, such as wrinkles, yellow leathery skin, thin skin, hyperpigmentation, hypopigmentation, lentigo senilis (liver spots), telangiectasias, and senile (solar) purpura, are all secondary to damage from the sun or other UV light sources such as tanning booths. Less important extrinsic agents that accelerate aging of the skin include smoking and possibly environmental pollutants.
| INTRINSIC AGING | EXTRINSIC AGING (PRIMARILY UV LIGHT) |
|---|---|
4. How does intrinsically aging human skin vary from young skin under the microscope?
Microscopically, the epidermis in aged skin demonstrates flattening of the dermoepidermal junction with loss of the normal rete ridge pattern (see Fig. 59-2A) with fewer melanocytes and Langerhans cells. The dermis demonstrates atrophy with fewer fibroblasts, mast cells, and blood vessels associated with depigmentation of hair, loss of hair follicles, and fewer sweat glands. The amount of collagen, elastin, and ground substance also decreases.
5. Why does skin wrinkle as we age?
The answer is complicated, because some authorities recognize as many as five different subtypes of wrinkles. The most common type of wrinkles on non–sun-exposed skin are fine wrinkles (glyphic wrinkles) that represent accentuation of normal skin markings. Microscopically, this is due to focal thinning and decreased numbers of keratinocytes. This appears to be intrinsic to aging (Fig. 59-1). The deeper wrinkles in photodamaged skin demonstrate a groove in the epidermis associated with solar elastosis that protrudes on both sides of the groove. These deeper wrinkles are due to extrinsic aging, primarily resulting from ultraviolet light.
6. Does smoking cigarettes accelerate skin aging?
Yes. Epidemiologic studies clearly indicate that smoking is an important extrinsic factor in accelerating aging of the skin. This is also support by animal studies and in vitro studies that have demonstrated that smoking increases the production of tropoelastin and matrix metalloproteinases, resulting in increased degradation of matrix proteins (e.g., collagen, elastic fibers) and abnormal production of abnormal elastotic material. Just another reason not to smoke!
Morita A: Tobacco smoke causes premature skin aging, J Dermatol Sci 48:169–175, 2007.
7. What is solar elastosis?
Solar (actinic) elastosis refers to the changes due to abnormal elastotic fibers (Fig. 59-2A) produced by fibroblasts in the papillary and superficial reticular dermis in response to UV light exposure. These abnormal elastotic fibers stain with elastic tissue stains; electron microscopy demonstrates that these fibers are similar, but not identical, to normal elastic fibers. Recent research suggests that they are the result of UVA damage to fibroblasts that results in the over-production and accumulation of elafin, which binds to elastic fibers making them resistant to normal degradation by elastase. Large aggregates of these fibers impart a yellowish color and account for the yellow leathery appearance of sun-exposed skin in geriatric individuals. Solar elastosis is often most easily appreciated in the posterior neck, where it is termed cutis rhomboidalis nuchae (Fig. 59-2B).
8. What is nodular elastosis with cysts and comedones?
Nodular elastosis with cysts and comedones, also known as Favre-Racouchot syndrome, is characterized by the presence of marked solar elastosis and comedones on the lateral and inferior periorbital areas (Fig. 59-3). Severe cases may demonstrate cysts. The reason for this regional presentation is not understood, but it has been suggested that the fibroblasts around the hair follicles are damaged by UV light and no longer produce normal elastic tissue. This predisposes to dilatation of the hair follicles, resulting in comedones and cysts. Most cases can be successfully treated with topical tretinoin cream and comedonal extraction.
Patterson WM, Fox MD, Schwartz RA: Favre-Racouchot disease, Int J Dermatol 43:167–169, 2004.
9. How do liver spots, solar lentigo, and lentigo senilis differ?
Liver spots, age spots, and the more proper dermatologic terms solar lentigo and lentigo senilis all refer to the same entity. More than one half of all patients over age 64 will have at least one solar lentigo, and most patients have more than one. Clinically, they are flat to slightly raised, tan to brown lesions on sun-exposed skin, most commonly on the dorsum of the hands, forearms, and face, where they are the result of excessive cumulative UV light exposure. Microscopically, solar lentigos demonstrate elongation of the rete ridges (lentiginous hyperplasia) and increased numbers of melanocytes that produce more than the normal amount of melanin. They may be removed with a light freeze of liquid nitrogen, various types of chemical peels, 2% mequinol/0.01% tretinoin, or special lasers. They may also be temporarily bleached with over-the-counter (1% to 2% concentration) or prescription (3% to 4% concentration) hydroquinone creams.
Farris PK: Combination therapy for solar lentigines, J Drugs Dermatol 3:S23–S26, 2004.
10. Why do elderly patients frequently develop bleeding into the skin on the dorsum of their hands and arms?
These lesions, referred to as senile purpura (solar purpura, Bateman’s purpura, purpura senilis), are common. One study of patients over age 64 years found them in 9% of those examined. The lesions are characterized by sharply demarcated areas of purpura that typically measure 1 to 5 cm (Fig. 59-4). The associated skin is atrophic and inelastic. Patients typically report that these lesions are brought on by minor trauma. It is believed that they are secondary to UV damage to the fibroblasts surrounding the blood vessels, which results in the loss of normal supporting collagen. The role of solar damage is supported by case reports of lateralization of solar purpura to one arm that receives more sunlight (e.g., left arm of a taxicab driver).
11. Advertisements in newspapers and magazines frequently tout products that “rejuvenate” the skin or make the skin younger. Is there truth to these claims?
No. There are no known therapies or products that rejuvenate the skin or make it younger. There are therapies that make the skin appear less wrinkled and thus appear younger. Topical applications of isotretinoin cream and α-hydroxy acids, such as lactic acid-containing moisturizers, both have been shown in controlled scientific studies to thicken the skin and make wrinkles less noticeable, but the results of these topical treatments vary from almost imperceptible to, at most, moderate. More dramatic results can be achieved by chemical facial peels, laser therapy (laser skin resurfacing), injection of bovine collagen into wrinkles, and facelifts. The best treatment for extrinsic aging of the skin is prevention, by minimizing sun exposure with avoidance, appropriate clothing, and sunscreens. Abstinence from the use of tobacco products also helps.
12. What is the difference between superficial, medium, and deep chemical peels?
As the names imply, it is related to the depth of injury produced. There are many variations and different techniques, but the most commonly used peels and their depth of injury are listed below:
Superficial peel (stratum granulosum to superficial papillary dermis)
15. Why are elderly patients prone to develop xerosis?
Xerosis (dry skin, asteatosis, dermatitis hiemalis) is the most common geriatric dermatosis and the most frequent cause of pruritus. Xerosis is believed to be more common in the elderly because of abnormal maturation and adhesion of keratinocytes, which results in rough skin characterized by fine white scale. Diminished eccrine function and sebaceous gland lipids may also play a role but do not represent the primary defect. Asteatosis, which means “without oil,” is really a misnomer because this is not the primary cause of dry skin.
16. What is the best way to treat xerosis?
Xerosis is aggravated by low ambient humidity, especially in dry climates and heated homes, and irritants such as soaps. Xerosis can be improved by increasing the ambient humidity (with a humidifier) and by using soaps that are mild, such as Dove or Oil of Olay. Most patients also require treatment with an emollient. The most effective emollients contain lactic acid or a lactate salt, but these are expensive, and the best ones require a prescription. The effectiveness of all emollients is improved by applying them immediately to the skin after bathing, when the skin is hydrated.
17. How common is chronic venous insufficiency in the geriatric population?
Epidemiologic studies show an incidence in the geriatric population that approaches 6%. The economic impact of this condition is enormous; the estimated total cost in the United States for the treatment of venous ulcers is more than 1 billion dollars per year in the United States and between 400 and 600 million pounds in the United Kingdom.
18. Explain the pathogenesis of chronic venous insufficiency.
Chronic venous insufficiency is due to venous hypertension secondary to valvular incompetence in the superficial, perforator, or deep veins, with many patients having defects in two or more valve systems. The most severe disease is produced by deep valvular insufficiency. Valvular insufficiency may be the consequence of hereditary factors (absent or congenitally incompetent valves), prolonged standing, and venous thrombosis that may damage valves. Chronic venous hypertension, depending on the degree of severity, may manifest as edema, varicosities, brown pigmentation secondary to hemosiderin, superficial neovascularization, dermatitis, and venous ulcers (Fig. 59-5). Studies have also shown that obesity is a separate risk factor for the development of chronic venous insufficiency.
19. How should you manage chronic venous insufficiency?
Treatment is directed primarily toward reducing venous pressure. This end can be achieved with elevation of the legs, active exercise, supportive stockings, sclerotherapy of selected perforator veins, or surgical treatment. Surgical options are dependent on the site involved but include ligation and stripping of the saphenous vein, ligation of incompetent perforators, or valve replacement. Dermatitis (stasis dermatitis), if present, may be treated with mild to moderate corticosteroids, and oral antibiotics may be used if secondary infection is present. Venous ulcers are treated with these options but also require wound management.
20. What is rosacea? How does it present?
Rosacea, or acne rosacea, is a common skin condition that may affect up to 12% of the geriatric population. The pathogenesis is not understood, but it is known that patients with rosacea have increased blood flow to the skin and are more likely to demonstrate infestation with Demodex folliculorum, the human hair follicle mite (although its relevance to the pathogenesis of rosacea is unclear). Rosacea primarily affects the forehead, cheeks, nose, and chin. The three primary lesions are telangiectasis, sebaceous gland hyperplasia, and acneiform papules and pustules (see Chapter 21). One or more of these primary lesions may predominate in a particular patient.
Key Points: Geriatric Dermatology
1. Forty percent of Americans between the ages of 65 and 74 years have had a cutaneous disease significant enough to warrant treatment by a physician.
21. Is rhinophyma related to alcohol abuse?
Rhinophyma is a clinical variant of rosacea that presents as severe sebaceous gland hyperplasia of the nose, which may distort its contour. The most famous example of rhinophyma is the actor W.C. Fields. The lay public often assumes that people with rhinophyma are alcohol abusers. Studies have not been able to demonstrate increased alcohol use in patients with rhinophyma. Patients with rosacea and rhinophyma demonstrate prominent flushing following the consumption of alcohol. This flushing has been incorrectly perceived as being the cause of rhinophyma.
Curnier A, Choudhary S: Rhinophyma: dispelling the myths, Plast Reconstr Surg 114:351–354, 2004.
22. Name the most common types of skin tumors seen in the elderly.
23. What are seborrheic keratoses?
Seborrheic keratoses are common, benign epidermal growths of the skin. In patients over age 64 years, the incidence of these growths is 88%. The pathogenesis is uncertain, but the most recent evidence suggests that they are derived from keratinocytes of the most superficial part of the hair follicle and are not derived from the epidermis, as previously thought. They typically begin appearing during middle age or later. They may be located on any cutaneous surface other than the palms and soles but are most commonly found on the face and trunk. Clinically, they present as tan, brown, gray, or black, sharply demarcated, exophytic papules that appear to be “stuck on” the skin. The surface often has an irregular contour or pebbly surface but may be verrucous or smooth (Fig. 59-6).
25. What is sebaceous hyperplasia?
Sebaceous hyperplasia is the most common benign sebaceous neoplasm. The lesions present in middle age and increase in number in the elderly. They present as asymptomatic, solitary or multiple yellow or yellowish-white papules that frequently demonstrate a central dell (Fig. 59-8). Increased numbers of lesions are seen in patients with Muir-Torre syndrome (sebaceous gland tumors associated with internal malignancy) and in transplant patients. Treatment options include no treatment, intralesional electrodesiccation, pulse dye laser, and shave removal.
Figure 59-7. Typical stucco keratosis manifesting as small white or white-gray scaly papules with “stuck-on” appearance.
26. A 70-year-old man presents to your clinic with the sudden onset of hundreds of seborrheic keratoses. Is there any reason for concern?
Yes. This patient may have the sign of Leser-Trélat, which is characterized by the sudden appearance of numerous seborrheic keratoses associated with an underlying malignancy. About one third of patients with this sign may also present with acanthosis nigricans, another potential cutaneous marker of internal malignancy. The most common associated malignancy is an abdominal adenocarcinoma.
Ceylan C, Alper S, Kiline I: Leser-Trélat sign, Int J Dermatol 41:687–688, 2002.
27. Describe the methods for treating seborrheic keratoses.
First of all, not all seborrheic keratoses need to be treated, and many health plans do not pay for their treatment because they are benign lesions. Patients frequently want them removed for cosmetic reasons or because they are pruritic. The most common treatment is cryotherapy with liquid nitrogen, because it is quick and effective. Seborrheic keratoses can also be removed by curetting or shave biopsy. Shave biopsies are usually done when the lesion has an atypical clinical appearance and a malignancy, such as squamous cell or basal cell carcinoma, is in the differential diagnosis. Seborrheic keratoses can also be treated with the topical application of α-hydroxy acids.
28. An elderly man presents with a soft blue papule on the helix of his cheek and is concerned about malignant melanoma. What is the most likely diagnosis?
The differential diagnosis includes a blue nevus, malignant melanoma, tattoo, and venous lake. In this case, the diagnosis of a venous lake can be established by compression of the papule, which will cause collapse of the lesion (Fig. 59-9). Venous lakes, like hemorrhoids, are dilated veins that have lost elasticity of their walls. They are usually 1 to 5 mm in diameter and are typically located on sun-exposed surfaces, such as the lips, ears, and face of the elderly. They are very common, with one epidemiologic study of elderly patients finding venous lakes in 12% of those examined. They are of no clinical significance, except that they may mimic malignant melanoma and occasionally become painful or thrombosed. They can be treated by excision, carbon dioxide laser, infrared coagulation, or by the injection of sclerosing agents such as polidocanol.
29. Is there a future in geriatric dermatology?
One hundred years ago, only 2% of the U.S. population was over 65 years old. By 1980, this percentage was 11%, and, by the year 2030, it will be 20%. Given the high incidence of significant dermatologic diseases in the elderly, it is clear that all health care providers need to familiarize themselves with the diagnosis, prevention, and treatment of skin diseases seen in this population.
