Photodamage, Photodermatoses, and Aging Skin
Kara Addison
Karrie Fairbrother
OBJECTIVES
After studying this chapter, the reader will be able to:
Define and list the etiology of photodamage and aging skin.
Discuss the etiology, pathophysiology, and various treatments of photodermatoses including actinic keratosis, lentigines, polymorphous light eruption, sunburn, porphyria cutanea tarda, and solar urticaria.
List and promote the widely available methods of protecting the skin from damage by the sun.
KEY POINTS
Photodamage is a cumulative damage to the skin caused by ultraviolet radiation, which can start as early as childhood and continues through one’s entire lifespan.
Phototoxic and photoallergic reactions occur in the presence of an exogenous agent, which absorbs the ultraviolet radiation. Phototoxicity is more common than photoallergic reaction.
Sunburn is caused by excessive ultraviolet radiation, which can present with many symptoms including pain, pruritus, edema, vesicles, or bulla.
Clinical knowledge on the various degrees of risk that accompany many common skin diseases, their behavioral, genetics, environmental causes, and effective treatments needs to be communicated to patients and families.
Patients require prospective education about skin changes and skin disorders caused by ultraviolet radiation in order to be ready to seek appropriate dermatology care when indicated.
Nurses are in the best position to educate communities, families, and individuals on the importance of ultraviolet protection.
The best sunscreens are those that block both ultraviolet A and ultraviolet B rays (broad spectrum). Sunscreen should be used continually throughout a patient’s life. No one is too old to slow down skin damage from ultraviolet exposure.
PHOTODAMAGE
I. OVERVIEW
Photodamage is exposure of the skin to ultraviolet (UV) radiation, which causes cumulative damage to all skin types starting in childhood through adult years. Variations in susceptibility, damage classification, presentation, and pathologies can be traced to climate conditions, genetic inheritance, and personal behavior patterns. Systematic treatment options include surgery, a wide variety of chemical applications and injections, cosmetic and laser therapies, and patient education to change the choices that induce preventable damage (Figure 15-1).
A. Definition: a term describing the skin of individuals who have been chronically exposed to UV radiation. The condition is identified by clinical and histologic findings.
B. Etiology (Figure 15-2).
1. Damage caused by UV exposure starts in early childhood.
2. The promotion of sun protection is a relatively recent campaign. Many older individuals were unprotected and vulnerable to sunburn in the past.
3. Both ultraviolet A (UVA) and ultraviolet B (UVB) rays play a significant role in damaging the skin.
4. Other influences on photodamage include: wind, chemical exposure, and the mechanics of smoking and tobacco smoke.
C. Pathophysiology.
1. Melanin is the basic physiologic sunscreen in humans. Individuals with less melanin, people with types I, II, and III skin, are more susceptible to burns and damage from the UV radiation. Individuals with more melanin, types IV, V, and VI skin, can also be damaged by UV rays (Table 15-1).
2. Changes that occur because of sunburn and tanning include:
a. Impaired immune response secondary to epidermal cell necrosis
b. Skin pigment darkening; quickly with UVB rays, delayed with UVA rays
 FIGURE 15-1. Solar radiation spectrum. (Copyright 2015 by the American Academy of Dermatology. All rights reserved.) |
c. Erythema caused by release of inflammatory mediators, such as cytokines and prostaglandins
d. Genetic changes in the cellular makeup due to UV radiation, increasing the risk of skin cancer
3. Between the ages of 0 and 28 years, the skin absorbs UV radiation while individuals participate in outdoor activities, tan on the beach, or are otherwise exposed. The sunburns and tans are only temporary, but the damage remains.
 FIGURE 15-2. Induction of a biologic response to solar radiation. (Copyright 2015 by the American Academy of Dermatology. All rights reserved.) |
TABLE 15-1 Fitzpatrick Sun-Reactive Skin Types | |||||||||||||||||||||
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4. As we approach the late 40s to early 50s, unprotected skin becomes leathery, dry, and nodular. Genetic changes caused by the UV radiation exposure begin to evolve.
5. Histologically, the UV-damaged epidermis is generally thicker than unexposed skin and shows some cellular atypia and damage.
6. There is a marked elastosis with a decrease in collagen fibers and bundles in the dermis causing thinned and increasing fragile skin.
7. Telangiectasia and solar lentigines develop with prolonged exposure in sun-damaged skin.
D. Treatment modalities.
1. Surgical treatment.
a. Dermabrasion is a standard method that has been successfully used for many years.
(1) It can be used for the total face or smaller local areas where other methods have not been effective.
(2) Some practitioner believe that elderly skin tends not to heal as well, causing greater incidence of hypertrophic scarring when dermabrasion is utilized.
(3) The older person tends to heal more slowly, leaving the skin open to a greater chance of infection.
b. Aluminum oxide crystal microdermabrasion is a relatively new and popular treatment for facial rejuvenation for damage caused by UV light.
(1) It is a simple, noninvasive procedure that can be repeated as often as every week for 4 to 12 weeks.
(2) The aluminum oxide crystals are used to abrade the skin.
(3) Following the procedure, a mild, transient erythema may occur.
c. Chemical peels.
(1) Phenol or various formulations containing phenol is a method of deeper peel for photodamaged skin.
(a) Side effects: there is a risk of renal toxicity and cardiac arrhythmias from phenol.
(b) Good results have been obtained from monitored use by well-trained practitioner.
(2) TCA is a medium-depth peel. TCA is used in various concentrations, 20% to 50%, to obtain good results in photodamaged skin.
(a) It is sometimes used with other agents such as Jessner solution.
(b) Side effects: hypo- or hyperpigmentation, scarring, and infection. Erythema may be persistent.
(c) Because of potential side effects, physicians may use a decreased concentration or a series of peels.
(3) Alpha hydroxy acids (the most common being glycolic acid) are found in natural sources.
(a) Lactic acid is found in sour milk, tartaric acid in grapes, and glycolic acid in sugar cane. Cosmetic manufacturers primarily use a synthetic glycolic acid.
(b) The smaller the molecular structure of the acid, the more it can penetrate the skin. With its two-carbon structure, glycolic acid is the smallest, followed by lactic acid and tartaric acid with three and four carbon atoms, respectively.
(c) Glycolic acid comes in concentrations of 5% to 99%; 50% to 70% solutions are most commonly used in the physician’s office, and 10% to 20% solutions can be found in over-the-counter applications.
(d) Best results of glycolic peels are seen months after a higher concentration peel.
(e) Glycolic acid is less sun sensitizing, but a patient should use a good sunscreen when receiving these peels.
d. Collagen injections may be used on the expressive lines and fine-line wrinkles caused by photoaging (Table 15-2).
TABLE 15-2 Glogau Photoaging Classification | ||||||||||||||||||||||||||||
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(1) The patient must have a skin test prior to starting the injections to check for any allergic reactions.
(2) The effects of the collagen injections are not permanent and must be repeated every 6 to 18 months for sustained results.
e. Lipotransfer is the transfer of the patient’s own fat from the buttocks or abdomen and injection into the facial expression lines.
(1) It is a relatively simple procedure done under local anesthesia.
(2) No skin tests are needed.
(3) The most commonly injected area is the nasolabial fold.
(4) Like collagen, it lasts only 6 to 18 months.
(5) An advantage is that extra fat may be withdrawn and frozen for injection several months later.
2. Topical treatment (retinoids).
a. Tretinoin, a retinoid, applied topically helps to even skin coloring, soften fine wrinkle lines, and increase the formation of blood vessels.
(1) Tretinoin acts by gently peeling the skin and also by normalizing the epidermal turnover.
(2) The patient may experience some skin irritation or dryness at first, but this usually subsides.
(3) When a patient is using a tretinoin, a sunscreen with SPF of 30 or more must be used, as this medication makes the skin very sun sensitive. A cream or lotion is preferred, since gels contain alcohol.
(4) Before applying tretinoin, the skin should be gently cleansed with warm water and patted dry. Wait 20 to 30 minutes before applying a thin layer to the skin, as skin irritation can occur when applied to damp skin.
(5) Because of increased sun sensitivity, tretinoin should be applied at night, and a 30 SPF broadspectrum sunscreen should be applied in the morning.
(6) Women who are pregnant, or may be pregnant, should not use tretinoin.
3. Cosmetic treatment.
a. Hylan B gels are derived from hyaluronan, a component of all connective tissues.
(1) Because they are biocompatible, there is no need for skin tests.
(2) Hylan B gels are water insoluble, they resist degradation, and they are unlikely to migrate.
(3) There are three hylan B gels with increasingly greater viscosities, so that each is suitable for a different contour, from fine wrinkles to common wrinkles to deep folds.
b. Many over-the-counter products exist that contain alpha hydroxy acids, vitamin C, and niacinamide; however, the skin is unable to absorb these molecules into the collagen layer.
 FIGURE 15-3. Solar lentigo. (From Goodheart, H. P. (2010). Goodheart’s same-site differential diagnosis: A rapid method of diagnosing and treating common skin disorders. Philadelphia, PA: Wolters Kluwer.) |
4. Laser therapy can be utilized for a variety of skinrelated complications (refer to Chapter 3 for further inquiry).
a. Telangiectasias on the face, a result of photodamaged skin, may be treated with vascular lesion lasers, such as the pulsed dye, copper bromide, and krypton laser.
b. Brown macular lesions (solar lentigines; Figure 15-3) may be treated with excellent results with several lasers, one of which is the Q-switched ruby laser.
c. Rhytides, fine lines around the eyes or upper lip, and scarring may be treated with BBL.
PATIENT EDUCATIONSunscreens
Broad-spectrum designation. Sunscreens that pass the FDA’s broad-spectrum test procedure, which measures a product’s ultraviolet A (UVA) protection relative to its ultraviolet B (UVB) protection, may be labeled as “broad-spectrum SPF [value]” on the front label. For broad-spectrum sunscreens, SPF values also indicate the amount or magnitude of overall protection. Broad-spectrum SPF products with SPF values higher than 15 provide greater protection and may claim additional uses, as described in the next bullet.
Use claims. Only broad-spectrum sunscreens with an SPF value of 15 or higher can claim to reduce the risk of skin cancer and early skin aging if used as directed with other sun protection measures. Non-broadspectrum sunscreens and broad-spectrum sunscreens with an SPF value between 2 and 14 can only claim to help prevent sunburn.
“Waterproof,” “sweatproof,” or “sunblock” claims. Manufacturers cannot label sunscreens as “waterproof” or “sweatproof” or identify their products as “sunblocks,” because these claims overstate their effectiveness. Sunscreens also cannot claim to provide sun protection for more than 2 hours without reapplication or to provide protection immediately after application (e.g., “instant protection”) without submitting data to support these claims and obtaining FDA approval.
Water resistance claims. Water resistance claims on the front label must indicate whether the sunscreen remains effective for 40 minutes or 80 minutes while swimming or sweating, based on standard testing. Sunscreens that are not water resistant must include a direction instructing consumers to use a waterresistant sunscreen if swimming or sweating.
Drug facts. All sunscreens must include standard “drug facts” information on the back and/or side of the container.
Application. Never spray sunscreen into the face (may be sprayed on the hand and then used on the face), and never spray with someone beneath you “catching” the spray. Adequate spray must be used to make the skin appear uniformly wet.
Do not rub off sunscreen. Inhalation of sunscreen and absorption into the eye membranes is a concern.
Don’t forget to apply an even layer of sunscreen. A patient’s handful is usually the correct amount for the body. Put sunscreen on the back of arms and legs, ears, nose, and lips!
PHOTODERMATOSES
I. ACTINIC KERATOSES
A. Definition: Actinic keratoses (AKs) or solar keratosis lesions caused by sun damage are commonly found in elderly patients with skin types I, II, and III. They comprise aggregates of anaplastic keratinocytes confined to the epidermis (Figures 15-4, 15-5, 15-6 and 15-7).
B. Etiology.
1. Sun exposure begins at a very early age, but AKs are not commonly seen in children or teenagers, except in patients with albinism.
2. AKs are found more in men than women and greatly increase in number with age.
3. Although they can appear on any sun-exposed area, AKs are most frequently seen in the face, scalp, ears, and arms.
4. People with blue eyes, fair skin, and albinos are at higher risk to develop AKs. AKs are rarely seen in people with darker skin; types IV, V, and VI.
5. If left untreated, 10% to 20% of AKs grow through the basement membranes of the epidermal-dermal junction and become squamous cell carcinomas.
6. Almost 60% of squamous cell carcinomas arise from AKs.
C. Assessment.
1. Clinically, AKs measure from 2 to 3 mm to 1 to 2 cm. An individual patient may have 1 to more than 100
lesions on their body. This generally depends on the type of skin and the amount of sun exposure.
lesions on their body. This generally depends on the type of skin and the amount of sun exposure.
 FIGURE 15-4. Diagram illustrating the pathophysiology of actinic keratosis. AKs are aggregates of anaplastic keratinocytes confined to the epidermis. (Provided by Anatomical Chart Co.) |
 FIGURE 15-5. Multiple actinic keratoses on the cheek and brow with signs of chronic sun damage. (Courtesy of Jurij Bilyk, MD.) |
 FIGURE 15-6. Bowenoid actinic keratosis. A crusted lesion on the ear helix. (From Elder, D. E. (2014). Lever’s histopathology of the skin. Philadelphia, PA: Wolters Kluwer.) |
 FIGURE 15-7. Actinic cheilitis results from excessive exposure to sunlight and affects primarily the lower lip. Fair-skinned men who work outdoors are most often affected. The lip loses its normal redness and may become scaly, somewhat thickened, and slightly everted. Because solar damage also predisposes to carcinoma of the lip, be alert to this possibility. (From Langlais, R. P., & Miller, C. S. (1992). Color atlas of common oral diseases. Philadelphia, PA: Lea & Febiger, used with permission.) |
a. AKs can vary in color from skin colored to a tan or reddish tone.
b. If they appear the same color as the skin, they must be palpated.
c. AKs appear are as individual papules that are scaly and rough on the epidermis.
2. A rare variation of the AK is the spreading pigmented AK.
a. These lesions are usually large in size, over 1 cm.
b. They may be smooth, slightly scaly, or warty in texture. They are variable in color.
c. There is a tendency for centrifugal spread.
d. The spreading pigmented AK is found mostly on the face and can mimic the lentigo maligna in appearance.
3. The lichenoid keratosis resembles a solitary lesion of lichen planus. There is learned discussion whether this is a totally benign lesion or an inflamed AK.
a. It begins small but can increase in size to 3 to 4 cm and has uneven borders.
b. The color tends toward red, and it is scaly in texture.
4. Histologically, AKs are well-defined aggregates of abnormal keratinocytes. The epidermis is generally hyperkeratotic.
a. The nucleus of the keratinocyte is enlarged, hyperchromatic, and irregular in shape. The keratinocyte may be multinucleated.
b. Cells of the sweat gland ducts and hair follicles tend to be normal.
c. Changes of solar elastosis often appear in the underlying dermis.
D. Treatment modalities.
1. Several methods for treating AKs are cryosurgery, electrodessication, and chemical peels, using TCA or glycolic acid.
a. These methods have cure rates of up to 95%.
b. They are excellent methods for discrete lesions and less diffuse actinically damaged skin.
c. Cryosurgery and electrodessication are more commonly used for all areas of the body.
d. Complications of these treatments are hypopigmentation, scarring, infection, and recurrence.
2. Medical treatment.
a. 5-Fluorouracil (5-FU) 1% to 5% cream or solution and imiquimod 5% are effective for patients with moderate to extensive actinic damage.
(1) 5-FU is applied one to two times a day for an average of 2 to 4 weeks, followed by 2 weeks of application of a gentle cortisone cream.
b. Imiquimod 5% is applied three times weekly for 16 weeks. The application of imiquimod results in an 86% reduction of actinic damage.
c. The skin may become very red and irritated. Therefore, in cases with severe actinic damage, the 5-FU or imiquimod is applied in sections, such as the forehead or left cheek.
d. Complications of 5-FU and imiquimod treatment include scarring, infection, loss of pigmentation, and recurrence. Also a color difference remains between the normal skin and the actinic-damaged skin after treatment.
e. Retreatment with 5-FU or imiquimod may be necessary every 3 to 5 years for patients with severe damage, as the AKs will continue to develop.
3. CO2 dermabrasion is another very effective method of removing multiple AKs.
a. The patient is generally not incapacitated as long as with the use of 5-FU.
b. Dermabrasion removes the skin uniformly; therefore, the skin heals uniformly, and the results are cosmetically appealing.
c. Complications are hypertrophic scarring, hypopigmentation, and infection.
4. Tretinoin has been used in several studies to eradicate AKs from the face and upper extremities.
a. It has some benefit on early facial AKs, but little effect on extremities.
b. There is little response by advanced lesions, even after twice a day application of 0.1% tretinoin.
c. Although there may be some local irritation at the time of treatment, there are no serious or permanent side effects.
5. Photodynamic therapy (PDT) is the newest treatment available.
a. It is useful for treating multiple lesions.
b. PDT requires two visits to the dermatologist’s office.
(1) A topical medicine, aminolevulinic acid (ALA), is applied to the AK lesions on the first visit.
(2) The second visit should be 14 to 18 hours after the application of ALA, when the lesions are exposed to a special blue light for less than 20 minutes.
(3) The blue light activates the ALA, causing a chemical reaction in the skin that kills the AK cells.
(4) In between visits, it is important to avoid all sun and UV light exposure.
PATIENT EDUCATIONPhotodermatoses
Any patient who has sun-damaged skin or has a history of AK should see a dermatology provider every 6 to 12 months for a full-body exam or sooner if changes are observed.
Identification of precancerous lesions (Figure 15-8) is critical to prevent the onset of squamous cell carcinoma.
 FIGURE 15-8. ABDCE’s of melanoma. (Artwork by Elissa Fairbrother, Smack-A-Mole Game.) |
II. LENTIGINES
A. Definition: generally pigmented macules that measure 1 to 5 mm. They are rarely seen larger than 1 cm. They are found on normal skin.
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