Stanger, Carolyn B. APRN-BC, MSN
Skin cancer is the most common form of cancer in the United States, affecting more than 1 million Americans annually—and its incidence is increasing.1 The most common skin cancers are basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and malignant melanoma (MM). BCC comprises the majority of new cases, followed by SCC. MM is responsible for the majority of deaths from skin cancer, while BCC and SCC have up to a 95% cure rate if detected and treated early.2
There are warning signs that indicate whether treatment or tracking is necessary to either diagnose cancer early or help prevent it from occurring. Actinic keratosis (AK) is a precancerous skin growth found on sun-exposed areas such as the face, scalp, forearms, and hands. It is caused by chronic UV light irradiation of the skin and generally recognizable on physical exam. AK lesions present as rough, scaly, thin papules or plaques, and approximately 10% of AKs will progress to SCC.3
NPs can incorporate a skin exam during routine visits and the annual physical exam. AK is characterized by abnormal proliferation of keratinocytes. Those at risk include whites with fair skin that burns easily, males, the elderly, and those experiencing immunosupression from organ transplants.
Patients may have a skin malignancy or premalignancy for some time before medical attention is sought or noted by a primary care provider, as is often found in the elderly who present with severe dermatoheliosis. Dermatoheliosis is skin damage from chronic sun exposure and aging that results in AK, loss of collagen, solar lentigos, freckling, and wrinkling. Many elderly patients are unaware of changes in skin lesions or may view AK as bouts of dry skin, persistent “pimples,” or part of the aging process.
Many skin conditions and lesions can be easily identified by inspection (bright lighting and magnification aid in the identification of skin lesions). Palpation of the affected area can also facilitate the identification of lesions by feeling surface changes or stretching the skin, which can reveal the indurated border of a BCC. AK is easily identified during physical exam, but may need skin biopsy to be distinguished from SCC.
When describing skin lesions, standard nomenclature should be used to identify the lesion's morphologic characteristics. Lesions are categorized as primary and secondary. Most skin diseases manifest as a primary lesion, but may present as a secondary lesion that develops as the skin disease evolves. Primary skin lesions include papules, plaques, macules, patches, nodules, pustules, vesicles, and bullae. Secondary lesions include scales, crusts, erosions, ulcers, and scars. Identification of skin lesions is aided by noting the color, shape, distribution, and location (see Primary skin lesions and Secondary skin lesions).
AKs are found in the epidermis and appear as scaly, thin, pinkish-white papules. Assessment should include light palpation of the skin, as touch may facilitate diagnosis. AKs are thin, gritty papules that can feel like sandpaper. Many times they are hyperkeratotic with a thick, yellow scale. They are usually at least 3 mm in diameter, but can exceed 1 cm, and are often grouped together and found on the face, scalp, forearms, and dorsal hands (see Actinic keratosis).
Counting the number of lesions is currently the only method of determining the severity of AK. Biopsy is indicated if a lesion resembles SCC. Controversy exists whether AKs are actually squamous cell carcinoma in situ.4 AKs can take approximately 2 years to progress to SCC.4
SCC stems from epidermal keratinocytes and are usually found on the head, neck, and dorsa of the hands, often on a background of AK. SCC will present as a defined papule or plaque that increases in width and depth, and becomes nodular, ulcerated, and weeping (see Squamous cell carcinoma). There is a wide range of metastatic potential depending on the location and aggressiveness of the tumor, which can be seen on histology. Lesions with a greater chance of metastasis are those found on the lip or ear, greater than 2 cm in diameter, often reoccur and are poorly differentiated, or have perineural invasion.3 The overall risk for metastasis is 2% to 6%; however, for certain high-risk tumors, such as those with perineural involvement, it can be as high as 47%. These require extensive surgical resection, radiation, and chemotherapy.5
Table. Primary skin ...Image Tools
Table. Secondary ski...Image Tools
BCC is the most common nonmelanoma skin cancer. BCCs are slow growing and rarely metastasize, but can cause significant morbidity and disfigurement. BCC appears as a pearly, pink translucent papule or nodule with telangiectasias on the surface. The borders of the nodule may appear indurated and can be defined by stretching, squeezing, and palpating the skin. Lesions are frequently found on the face, neck, and upper trunk (see Basal cell carcinoma).
Treatment should be pursued aggressively to prevent SCC. A biopsy should be performed if lesions resemble SCC or if they fail to resolve following treatment.
When deciding on a course of treatment, the NP should consider efficacy, convenience, tolerability, cosmetic outcome, and cost. Physical treatments include cryotherapy, curettage, dermabrasion, chemical peel, and laser resurfacing. Topical treatments include topical fluorouracil (Efudex, Carac, and Fluoroplex) and imiquimod (Aldara), as well as diclofenac sodium (Solaraze). Photodynamic therapy (PDT) with aminolevulinic acid (Levulan Kerastick) is rapidly becoming the gold standard for treatment.6 There are few studies comparing the treatment methods available, but cryotherapy, fluorouracil, imiquimod, and PDT have shown to be effective.7,8
Cryotherapy is ideal for individual lesions, especially when they number less than 10. Liquid nitrogen is applied to lesions with a cryogen spray unit, creating a freeze-thaw cycle on the lesion. Lesions will crust over and flake off in 7 to 10 days. Formation of a blister indicates the freeze was too deep, reaching into the dermis. Mild discomfort is expected, and hypopigmentation can occur.9 Daily posttreatment care includes cleansing with mild soap and water, and the application of petroleum jelly twice daily until healed.
Standard topical treatments include fluorouracil and imiquimod. Fluorouracil is an antineoplastic that inhibits DNA synthesis in hyperproliferative keratinocytes. Imiquimod is an immune-response modifier and stimulates interferon, tumor necrosis factor, and interleukin-12 to elicit a cytotoxic response in abnormal skin cells. Both result in sustained clearance of AK and are used to treat one area at a time, such as the forehead, scalp, or forearm.
PDT involves a two-step process to treat AK found on the face or scalp. First, the practitioner uses alcohol and acetone to degrease the skin allowing the aminolevulinic acid to absorb into the affected area. This acid makes the area more sensitive to light. After a waiting period, a blue light is focused on the treated area for 16 minutes and 40 seconds.
Patients can expect a burning and tingling sensation during treatment, followed by erythema, crusting, and peeling that should resolve in 1 to 4 weeks.10 Patients should avoid sun exposure for 48 hours after PDT, cleanse the treated area twice with a gentle cleanser, and apply petroleum jelly until peeling stops. Treatment can be repeated if necessary.
Figure. Actinic kera...Image Tools
Figure. Squamous cel...Image Tools
Figure. Basal cell c...Image Tools
It has been well established that sun exposure leads to the development of AK and skin cancer, as well as photoaging of the skin. The effect of chronic UV irradiation is photocarcinogenesis causing DNA damage in skin cells leading to skin cancer.11
Photoprotection with the use of sunscreens, as well as sun avoidance should be encouraged early in life and after the development of AK. The FDA has identified at least 23 sunscreen ingredients that are effective and tolerable. The American Academy of Dermatology recommends broad-spectrum coverage against UVB and UVA with a minimum SPF of 15 or higher. Higher SPF contained in new sunscreens may soon prove more effective. Sunscreen should be applied 20 minutes before exposure to allow adequate absorption. A liberal amount should be used and reapplied every 2 hours. Additionally, minimizing sun exposure between 11 a.m. and 3 p.m. and wearing protective clothing including long-sleeved shirts, wide-brimmed hats, and sunglasses is recommended.12
2. Rigel DS, Friedman RJ, Dzubow LM, et al. Cancer of the Skin. 2nd ed. Philadelphia, PA: Elsevier Saunders; 2005:47–58.
3. Fuchs A, Marmur E. The kinetics of skin cancer: progression of actinic keratosis to squamous cell carcinoma. Dermatol Surg. 2007;33(9):1099–1101.
4. Roewert-Huber J, Stockflesh E, Keri H. Pathology and pathobiology of actinic (solar) keratosis—an update. Br J Dermatol. 2007;157(Suppl 2):18–20.
5. Rigel DS, Friedman RJ, Dzubow LM, et al. Cancer of the Skin. 2nd ed. Elsevier Saunders: Philadelphia, PA;2005:133–149.
6. Gold MH, Nestor M. Current treatment of actinic keratosis. J Drugs Dermatol. 2006;5( Suppl 2):17–25.
7. Krawtchenko N, Roewert-Huber J, Ulrich M, et al. A randomized study of topical 5% imiquimod vs. topical 5-flourouracil vs. cryosurgery in immunocompetent patients with actinic keratoses: a comparison of clinical and histological outcomes including 1-year follow-up. Br J Dermatol. 2007;157(Suppl 2):34–40.
8. Touma D, Yaar M, Whitehead S, et al. A trial of short incubation, broad-area photodynamic therapy for facial actinic keratosis and diffuse photodamage. Arch Dermatol. 2004;140(1):33–40.
9. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Treatment. 3rd ed. St. Louis, MO: Mosby; 1996:819.
10. Jeffes E, Tang E. Actinic keratosis: current treatment options. Am J Clin Dermatol. 2000;1(30):167–179.
11. Maier T, Korting HC. Sunscreens—which and what for? Skin Pharmacol Physiol. 2005;18(6):253–262.
12. Moloney FJ, Collins S, Murphy GM. Sunscreens: safety, efficacy and appropriate use. Am J Clin Dermatol. 2002;3(3):185–191.
© 2009 Lippincott Williams & Wilkins, Inc.