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.)
PATIENT EDUCATION
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–broad-spectrum 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 water-resistant 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 through 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.
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.
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.)