Years of exposure to the sun are cumulative and damaging. The ultraviolet (UV) rays of the sun cause degenerative changes in the dermis, resulting in premature aging (e.g., loss of elasticity, thinning, wrinkling, drying of the skin). Prolonged and repeated sun exposure is a major factor in precancerous and cancerous lesions. Actinic keratosis, basal cell carcinoma, squamous cell carcinoma, and malignant melanoma are dermatologic problems that are associated with direct or indirect sun exposure.

Safe sun practices are important for you to emphasize to the patient. Specific wavelengths of the sun (Table 24-1) have different effects on the skin. Sunlight is composed of visible light and UV light. There are two types of UV light: UVA and UVB. UVA light is responsible for tanning and UVB for sunburn. Both types can damage the skin and increase the risk of skin cancer. Both UVA and UVB can cause collagen damage and accelerate the aging of skin. Tanning is the skin’s response to injury and is caused by the increased production of melanin. When sun exposure is excessive, the turnover time of the skin becomes shortened, which can result in peeling. Fair-skinned persons should be especially cautious about excessive sun exposure because they have less melanin and thus less natural protection.

Patients should recognize that sun safety guidelines include sun avoidance (especially during the midday hours), protective clothing, and sunscreen. Advise the patient on ways to avoid the damaging effects of the sun, such as wearing a large-brimmed hat, sunglasses, and a long-sleeved shirt of a lightly woven fabric or carrying an umbrella. Patients need to know that the rays of the sun are most dangerous between 10:00 am and 2:00 pm standard time or 11:00 am and 3:00 pm daylight saving time, regardless of the latitude. Even on overcast days, serious sunburn can occur because up to 80% of the sun’s UV rays can penetrate the clouds.

Other factors that increase the possibility of sunburn include being at high altitude, being in snow (reflects 80% of the sun’s rays), or being in or near water. Warn people of the dangers of tanning booths and sun lamps, which are UVA. Tanning booths increase the risk of sunburn and contribute to the development of skin cancer.¹

Sunscreens can filter both UVA and UVB wavelengths. The two types of topical sunscreens are chemical and physical. Chemical sunscreens are light creams or lotions designed to absorb or filter UV light, resulting in diminished UV light penetration. Physical sunscreens are thick, opaque, heavy creams that reflect UV radiation.

The U.S. Food and Drug Administration (FDA) rates sunscreen products on their sun protection factor (SPF). The SPF measures the effectiveness of a sunscreen in filtering and absorbing UV radiation. All sunscreen labels in the United States must state which rays they protect against. Products labeled with “broad protection” block both UVA and UVB.² Sunscreen broad protection labeling is allowed only if the product has an SPF of at least 15. Sunscreen should no longer be labeled as “waterproof” and “sweat proof.” The product should only state if it is “water resistant.”

Consumers need to select the sunscreen most appropriate for their needs. Para-aminobenzoic acid (PABA) and PABA esters, cinnamates, salicylates, and methyl anthranilate block UVB rays. PABA has been removed from many sunscreen products because it stains clothing and can cause allergic reactions, including contact dermatitis. Avobenzone (Parsol) blocks UVA rays and has been added to some sunscreens. The benzophenones block both UVA and UVB rays.

The general recommendation is that everyone should use a sunscreen with a minimum SPF of 15 daily. Teach patients to look for the term broad spectrum on sunscreen packaging. Sunscreens with an SPF of 15 or more filter 92% of the UVB rays that are responsible for erythema, and make sunburn unlikely when applied appropriately. Patients who have a history of skin cancer or problems with sun sensitivity should use a product with an SPF of at least 30. Sunscreens should be applied 20 to 30 minutes before going outdoors, even in cloudy weather. The SPF value of all sunscreens decreases with time after application, and therefore sunscreen should be reapplied every 2 hours in a sufficient amount. One ounce per total body application is recommended. The ears, toes, and lips also need sunscreen. Sunscreens are not “waterproof” and should be reapplied immediately after swimming. Regular sunscreen use decreases the rate of developing melanoma.³

Certain topical and systemic medications potentiate the effect of the sun, even with brief exposure. Categories of drug therapy that may contain common photosensitizing medications are listed in Table 24-2. Be aware that many drugs are included in these categories. Examine the photosensitivity of each individual drug. The chemicals in these medications absorb light when exposed to natural sunlight and release energy that harms cells and tissues. The clinical manifestations of drug-induced photosensitivity (Fig. 24-1) are similar to those of exaggerated sunburn. These include swelling; erythema; vesicles; and papular, plaquelike lesions. Skin that is at risk for photosensitivity reactions can be protected by the use of sunscreen products. Teach patients who are taking these drugs about their photosensitizing effect.

Rest and Sleep

Sleep is restorative to the skin, as well as to the rest of the body. Pruritic skin diseases often interfere with sleep. Therefore helping patients obtain high-quality sleep is an important health-promotion consideration. Adequate rest increases the patient’s ability to tolerate itching, thereby decreasing skin damage from the resultant scratching.

Exercise

Exercise increases circulation and dilates the blood vessels. In addition to the healthy glow produced by exercise, the psychologic effects can also improve one’s appearance and mental outlook. However, caution must be used to prevent overexposure to heat, cold, and sun during outdoor exercise.

Hygiene

Hygienic practices are influenced by the patient’s skin type, lifestyle, culture, age, and gender. The normal acidity of the skin and perspiration protect against bacterial overgrowth. Most soaps are alkaline and neutralize the skin surface, leading to a loss of protection. The use of mild, moisturizing soaps (e.g., Ivory) and lipid-free cleansers, plus avoidance of hot water and vigorous scrubbing, can noticeably decrease local skin irritation and inflammation. Skin piercings where jewelry has been inserted can be cared for with antibacterial soaps that do not contain sulfites.

In general, the skin and hair should be washed often enough to remove excess oil and excretions and to prevent odor. Older persons should avoid harsh soaps and shampoos and frequent bathing because of the dryness of their skin and scalp. Moisturizers should be used immediately after a bath or shower while the skin is still damp to seal in this moisture.

Nutrition

A well-balanced diet adequate in all food groups can produce healthy skin, hair, and nails. Important elements of skin nutrition include the following:

A deficiency of biotin, a water-soluble B-complex vitamin, may result in rashes and alopecia. The effectiveness of biotin supplements has not been proven. Foods high in biotin include liver, cauliflower, salmon, carrots, bananas, soy flour, cereals, and yeast.

Obesity has adverse effects on the skin. The increase in subcutaneous fat can lead to stretching and overheating (see Chapter 41). Overheating secondary to the greater insulation provided by fat causes increased sweating, which inflames and dries the skin. Obesity is also a risk factor for poor wound healing. Obesity can be associated with the development of type 2 diabetes mellitus, which may cause skin symptoms such as velvety dark skin of neck and body folds (acanthosis nigricans), rash in intertriginous sites (intertrigo), skin tags (acrochordons), and impaired arterial and venous flow (see Chapter 49).

Self-Treatment

Determine if the patient is aware of the dangers of self-diagnosis and treatment. The increasing variety of OTC skin preparations can be confusing.

In your general instructions to the patient, stress the duration of the treatment and the need to closely follow package directions. Skin problems may be slow to produce symptoms and slow to resolve. If the package insert of an OTC drug says its use should not exceed 7 days, patients should heed this warning. Tell the patient to always follow package directions for use of OTC drugs. If any systemic signs of inflammation or extensions of the skin problem (e.g., an increased number of lesions or increased erythema or swelling) develop, the patient should stop self-care and seek the help of a health care provider.

Nonmelanoma Skin Cancers

Nonmelanoma skin cancers, either basal cell or squamous cell carcinoma, are the most common forms of skin cancer.⁷ More than 2.2 million new cases are diagnosed every year. Nonmelanoma skin cancers develop in the epidermis. They do not develop from melanocytes, the skin cells that make melanin, as melanoma skin cancers do. The most common sites for the development of nonmelanoma skin cancer are in sun-exposed areas, such as the face, head, neck, back of the hands, and arms.

Although relatively few deaths are attributable to nonmelanoma skin cancer, the tumors have an inherent potential for severe local destruction, permanent disfigurement, and disability. The most common etiologic factor is sun exposure. Avoidance of exposure to the midday sun and the use of protective clothing and sunscreens beginning early in life can prevent the formation of skin malignancies later in life.

Actinic Keratosis

Actinic keratosis, also known as solar keratosis, consists of hyperkeratotic papules and plaques on sun-exposed areas. Actinic keratoses are premalignant skin lesions that affect nearly all of the older white population. These are the most common of all precancerous skin lesions. The clinical appearance of actinic keratoses can be highly varied. The typical lesion is an irregularly shaped, flat, slightly erythematous papule with indistinct borders and an overlying hard keratotic scale or horn (Table 24-3).

TABLE 24-3

PREMALIGNANT AND MALIGNANT CONDITIONS OF THE SKIN

Etiology and Pathophysiology	Clinical Manifestations	Treatment and Prognosis
Actinic Keratosis
Actinic (sun) damage. Premalignant skin lesions. Common in older whites.	Flat or elevated, dry, hyperkeratotic scaly papule. Possibly flat, rough, or verrucous (wartlike). Adherent scale, which returns when removed. Often multiple. Rough scale on red base. Often on erythematous sun-exposed area. Increase in number with age.	Cryosurgery, chemical peels, laser resurfacing, topical application of 5-FU over entire area for 14-28 days or topical application of imiquimod (Aldara) for 16 wk, photodynamic therapy followed by light irradiation. Recurrence possible even with adequate treatment.
Atypical or Dysplastic Nevi
Morphologically between common acquired nevi and melanoma. May be precursor of malignant melanoma.	Often >5 mm. Irregular border, possibly notched. Variegated color of tan, brown, black, red, or pink within single mole. Presence of at least one flat portion, often at edge of mole. Frequently multiple. Most common site on back, but possible in uncommon mole sites such as scalp or buttocks (Fig. 24-3).	Increased risk for melanoma. Careful monitoring of persons suspected of familial tendency to melanoma or dysplastic nevi. Excisional biopsy for suspicious lesions.
Basal Cell Carcinoma
Change in basal cells. No maturation or normal keratinization. Continuing division of basal cells and formation of enlarging mass. Related to excessive sun exposure, genetic skin type, x-ray radiation, scars, and some types of nevi.	Nodular and ulcerative: Small, slowly enlarging papule. Borders semitranslucent or “pearly,” with overlying telangiectasia. Erosion, ulceration, and depression of center. Normal skin markings lost (see Fig. 24-2). Superficial: Erythematous, pearly, sharply defined, barely elevated plaques.	Surgical excision, chemosurgery, electrosurgery, chemotherapy, cryosurgery. 90% cure rate. Slow-growing tumor that invades local tissue. Metastasis rare. 5-FU and imiquimod for superficial lesions, photodynamic therapy for small lesions, vismodegib (Erivedge) for metastatic or recurrent locally invasive lesions.
Squamous Cell Carcinoma
Frequent occurrence on previously damaged skin (e.g., from sun, radiation, scar). Malignant tumor of squamous cell of epidermis. Invasion of dermis, surrounding skin.	Superficial: Thin, scaly erythematous plaque without invasion into the dermis. Early: Firm nodules with indistinct borders, scaling and ulceration (see eFig. 24-1). Late: Covering of lesion with scale or horn from keratinization, ulceration. Most common on sun-exposed areas such as face and hands.	Surgical excision, cryosurgery, radiation therapy, chemotherapy, electrodesiccation and curettage. Untreated lesion may metastasize to regional lymph nodes and distant organs. High cure rate with early detection and treatment.
Malignant Melanoma
Neoplastic growth of melanocytes anywhere on skin, eyes, or mucous membranes. Classification according to major histologic mode of spread. Potential invasion and widespread metastases.	Irregular color, surface, and border. Variegated color, including red, white, blue, black, gray, brown. Flat or elevated. Eroded or ulcerated. Often <1 cm in size. Most common sites in males are back, then chest. In females are legs, then back (see Fig. 24-2).	Surgical excision and possible sentinel lymph node evaluation depending on the depth. Correlation of survival rate with depth of invasion. Poor prognosis unless diagnosed and treated early. Spreading by local extension, regional lymphatic vessels, and bloodstream. Possible use of adjuvant therapy after surgery if lesion >1.5 mm in depth.
Cutaneous T-Cell Lymphoma
Origination in skin. Localized chronic, slowly progressing disease. Possibly related to environmental toxins and chemical exposure. Mycosis fungoides (MF) is most common form. Sézary syndrome is an advanced form of MF. Prevalence twice as high in men as in women in United States.	Classic presentation involves three stages—patch (early), plaque, and tumor (advanced). History of persistent macular eruption followed by gradual appearance of indurated erythematous plaques on the trunk that appear similar to psoriasis. Pruritus, lymphadenopathy.	Treatment usually controls symptoms, not curative. UVB, PUVA, corticosteroids, topical nitrogen mustard, radiation therapy in patch and plaque stage disease. Interferon, systemic chemotherapy, extracorporeal photopheresis, romidepsin (Istodax) for progressive disease. Bexarotene (Targretin), denileukin diftitox (Ontak), and vorinostat (Zolinza) for advanced disease. Disease course is unpredictable, 10% will have progressive disease.

5-FU, Fluorouracil; PUVA, psoralen ultraviolet A; UVB, ultraviolet B.

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4. Nursing Management: Musculoskeletal Problems

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