As a person gets older, changes occur that can be classified as resulting from aging itself (“normal aging”) and those that result from diseases. In normal aging, many physiological functions are altered, but many not progress to disease. For instance, some degree of glucose intolerance is thought to be a part of normal aging, but diabetes, though very common, is considered a disease.
Age related skin changes are the result of both intrinsic factors, or genetically programmed changes, and extrinsic influence which includes the environmental wear and tear on the skin. Both factors result in changes to the skin structure and function with extrinsic factors causing the more pronounced changes. Some estimates state that from 80-99% of what we see on our skin as adults is the result of these environmental influences, in particular exposure to the sun.
Lines and wrinkles, thicker nails, and graying hair are constant reminders of the aging process. These result from common aging changes to the integumentary system that include flattening of the dermal-epidermal junction, reduced thickness and vascularity of the dermis, degeneration of elastic fibers, increased coarseness of collagen, loss of pigment cells that gives hair its color, atrophy of hair bulbs, and decline in rate of hair growth. The dermis thins by approximately 20%, and this is probably the biggest contributing factor to the paper-thin appearance of the skin in an older adult. Decreases in dermal cells, blood vessels, nerve endings, and collagen lead to altered sensation, thermoregulation, rigidity, and moisture retention. There is a loss of subcutaneous tissue (primarily adipose), which results in a loss of mechanical protection and insulation. This loss, in addition to the decrease in pain sensation due to alterations in nerve endings, may make the older adult far more vulnerable to traumatic injury. The increased fragility of the skin poses challenges to older adults and their caregivers in that there are heightened risks for skin tears, bruising, ulcer formation, and skin infections. In addition, the effects of this system’s aging on appearance are highly visible signs of the aging process, potentially affecting body image, self-concepts, reactions from others, socialization, and other psychosocial factors.
Extrinsically aged skin shows characteristic traits that include wrinkles, a sallow skin color, pigmented lesions such as freckles and lentigines, areas of hyper- and hypopigmentation. This is often accompanied by a loss of tone and elasticity, increased fragility, areas of purpura caused by blood vessel weakness and benign lesions such as keratoses, telangiectasias and skin tags. Under the microscope discreet changes are evident in the collagen and elastin structure and organization. Collagen becomes more fragmented and with thicker fibers while elastin fibers fragment and show signs of cross-linking and calcification.
Skin changes associated with aging occur in the third decade. With aging, the outer skin layer (epidermis) thins even though the number of cell layers remains unchanged. The rete ridges flatten out – epidermis not as effectively “fastened” to the dermis. This can result in skin tears. A skin tear is a traumatic wound resulting from separation of the epidermis from the dermis. Skin tears occur most frequently in persons 65 years of age or older. The number of pigment-containing cells (melanocytes) decreases, but the remaining melanocytes increase in size. Aging skin thus appears thinner, more translucent. Age spots or liver spots may appear in sun-exposed areas. Changes in the connective tissue reduce the skin's strength and elasticity. This is known as elastosis and is especially pronounced in sun-exposed areas. Thinning of the outer layer -1% decrease in collagen per year. Since collagen gives skin tensile strength, loss of it leads to wrinkling. Slowing of cell replacement causes a decrease turnover rate of the epidermis by 50%, which slows the healing process Liver spots or age spots are a type of skin change that are associated with aging. The increased pigmentation may be brought on by exposure to sun, or other forms of ultraviolet light, or other unknown causes.
As our skin ages, it loses much of the underlying tissue that made it so soft and supple as a child. Over time, collagen (the “glue” that holds elastin together) is depleted from the dermis. Collagen depletion makes our skin thinner and less supple and causes skin to sag and lose its resiliency. In addition, as we age, decreased blood flow to our skin results in slower healing. Finally, for post menopausal women, skin produces less protective oils so our skin dries out more easily. Decreased elasticity as elastin fibres significantly decrease in size and number. Since elastin maintains the skin’s elasticity and recoil…loss leads to wrinkling. Decreased sensation to pressure and light touch and increased threshold for pain, leading to a type of neuropathy Studies of aged skin tissue indicate the majority of age-dependent changes take place in the dermis. These changes include a loss of the vascular system accompanied by a loss of cell structure and form. The dermis as a whole can lose from 20-80% of its thickness while aging. Fibroblasts, the cells responsible for collagen, elastin and hyaluronic acid biosynthesis, degenerate slowing down production of new protein which may account for the overall dermal atrophy in aged skin and its inability to repair itself as quickly. The overall collagen content per unit area of skin surface decreases approximately 1% per year after we reach 30 years. Despite the loss of collagen as we age, the network appears more dense due its haphazard organization.
Turgor is the rigidity of cells due to the presence of water. It is demonstrated by the ability of the skin to return to normal shape after deformation, the elasticity of the skin. Skin turgor is generally tested by pinching up the skin and observing how fast it takes to return to normal. Decreased skin turgor is a normal finding in elderly patients, making it an unreliable indicator of dehydration. To accurately assess skin turgor in an elderly patient, try squeezing the skin of the sternum or forehead instead of the forearm. Skin turgor—the skin’s elasticity—is determined by observing the time required for the skin to return to its normal position after being stretched or pinched. With decreased turgor, pinched skin “holds” for up to 30 seconds, then slowly returns to its normal contour.
Atrophy of subcutaneous fat on hands, face, shins, waist in men and thighs in women…loss leads to sagging and folds.
The eccrine and apocrine glands decrease in size, number, and function as a person ages. Increased dryness as the eccrine glands decrease in number and decrease sweat gland production Changes in the sebaceous glands are associated with cracked, dry skin.
Decreased subcutaneous fat, muscle laxity, elastic fibers, collagen (stiffening), decreased skin thickness (paper-thin, transparent skin with an increased susceptibility to trauma). Increased transparency and fragility: increased susceptibility to injury. The thinning skin with a decreased attachment between the dermis and the epidermis is at an increased risk for injury in response to even minimal trauma or shearing events. Decreased tone and elasticity: wrinkles, sagging breasts and abdomen, redundant flesh around eyes, slowness of skin to flatten when pinched together (tenting). Decreased blood flow and wound healing.
The combination of normal aging and photoaging results in an altered process of wound healing in the older adult. There is a progressive loss of skin function, increased vulnerability to the environment, and decreased homeostatic ability. The healing function in older adults is delayed but ultimately is as effective as that of younger adults.
Decreased sebum and sweat: dry skin; decreased ability for thermoregulation (more susceptible to extremes of temperature, hot and cold). Dry skin with minimal to no perspiration. Degeneration of nerve endings: decreased sensory perception. Degeneration of melanocytes: actinic lentigo on face and back of hands (age or liver spots). As skin ages there is also an increase in solar lentigos. As the name suggests, these are the result of sun exposure and often occur after the age of fifty, hence they are also referred to as senile lentigos . They are characterized by an increased number of melanocytes with increased melanin pigmentation, as well as, clubbed or elongated rete ridges that are infiltrated with an excess of melanin at the epidermal-dermal junction. Interestingly, they do not occur on sun protected areas of the skin.
UV rays bring about a premature ageing of the skin, known as photoageing or solar elastosis. Repeated exposure to ultraviolet light is known to cause solar elastosis, the “old age” type of skin wrinkling that results from the replacement of collagen by elastin. The damage caused to the skin resulting from this sun-induced ageing are different from and added to those of natural aging . They involve changes in the skin clinically characterized by wrinkles, roughness, a lack of elasticity, depigmentation or hyperpigmentation marks and a variety of benign or malignant tumors. Skin aging is a complex process that involves intrinsic and exogenous causes. Although intrinsic skin aging is associated with other physiological processes and is inevitable, exogenous aging is caused by extrinsic harmful environments and can be prevented. UV is one of the most noxious factors among the harmful environments. UV irradiation induces inflammatory processes in the skin, and the irradiated skin becomes metabolically hyperactive associated with epidermal hyperproliferation and accelerated collagen fiber breakdown. In contrast, physiologically aged skin is usually characterized by a slow decline in many of these processes. The UV-irradiated skin is characterized by fine and coarse wrinkling, roughness, dryness, laxity, and pigmentation changes.
Increased transparency and fragility: increased susceptibility to injury.
Seborrheic keratosis - Benign proliferation of keratinocytes in the epidermis associated with ageing and chronic sun exposure. Actinic keratosis is associated with cumulative skin damage, caused by repeated exposure to the ultraviolet light found in sunshine. Over the years, the genetic material of cells becomes irreparably damaged and produces lesions similar to the ones in this photograph. The lesions may later become cancerous (pre-cancerous). Acrochordons (also called skin tags) are small benign tumors that form primarily in areas where the skin forms creases, such as the neck, armpits, and groin. They also occur on the face, usually on the eyelids. They range in size from two to five millimeters, although larger ones have been seen. The surface of acrochordons may be smooth or irregular in appearance. Often, they are raised from the surface of the skin on a fleshy stalk called a "peduncle." It is estimated that by age 70, up to 59 percent of people have them. A genetic component (causation) is thought to exist. Skin tags are harmless, but they may be an indication of, or result from, carbohydrate sensitivity or carbohydrate-related, metabolic disorders.
Seborrheic keratoses are dark, wartlike projections on the skin. Older adults commonly have these lesions on various parts of their bodies. The lesions may be as small as a pinhead or as large as a quarter. They tend to increase in size and number with age. In the sebaceous areas of the trunk, face, and neck and in persons with oily skin, these lesions appear dark and oily; in less sebaceous areas, they are dry in appearance and of a light color. Normally, seborrheic keratoses will not have swelling or redness around their base. Sometimes abrasive activity with a gauze pad containing oil will remove small seborrheic keratoses. Larger, raised lesions can be removed by freezing agents or by a curettage and cauterization procedure. Although these lesions are benign, medical evaluation is important to differentiate them from precancerous lesions. In addition, the cosmetic benefit of removal should not be overlooked for the older patient.
Changes to the hair are caused by altered melanocytes and declining hormones. Gray hair is one of the most familiar signs of aging. The age when greying starts depends on one's genetic inheritance. But in half of all Caucasoid people, half the hairs on the scalp are grey by the age of 50. The loss of hair color is due to a gradual fall in melanin production in the hair bulb. If you look at the hairs on a greying head you find a full range of color, from the normal shade through to white along each hair, and also from one hair to another. Usually people notice their first gray hairs near their temples. Then the grayness spreads to the crown, and later to the back of the head. Hirsutism as a result of aging: Male facial distribution of hair in women. Normal for very elderly women who are many years (usually decades) past menopause. Not normal for younger, pre-menopausal women. In younger women, it is one manifestation of hormonal imbalance, such as occurs with Cushing’s syndrome or ovarian dysfunction. You would want to assess for additional associated changes in fat distribution and capillary fragility, and deepening of the voice.
The nails of the older person become dull, and yellow or gray in color. Nail growth slows, which results in thicker nails that are likely to split. Longitudinal striations (or ridges) also appear due to damage at the nail matrix.
Emollients agents are bland oily substances which sooth & soften skin. They form an occlusive flim over the skin, preventing evaporation, thus restoring elasticity of cracked and dry skin. They are also used as vehicle for topically applied medicaments.
As a patient ages, the skin undergoes many changes that can increase the risks of wounds. Subcutaneous tissue decreases in older adults Skin turgor may not be a reliable sign of hydration Attention to skin status is essential to prevent complications
There are three major nursing diagnoses for problems of the integument Risk for impaired skin integrity Impaired tissue integrity Damage to integument, cornea, or mucous membranes Impaired skin integrity Damage to epidermal or dermal tissue Impaired skin integrity related to lesions and inflammatory response Risk for impaired skin integrity related to physical immobility Risk for impaired skin integrity related to decrease skin turgor
Dry skin (xerosis) accompanied by pruritus is the most common dermatologic problem of older adults. It causes itching, burning, stinging, and a feeling of tightness that may affect quality of life. Occurs in 59-85% of elderly people. Stimulation of itch receptors at dermal-epidermal junction. Subjective sensation, worse at night. Dryness results when water content in the stratum corneum is reduced to less than 10%. Xerosis has an age-component, a genetic component, and an environmental component (exacerbated by cold or dry climates and the use of soaps and harsh cleansers). Occurs primarily in the extremities, especially the legs, but can affect the face and trunk as well. Older skin less efficient at holding moisture. The thinner epidermis allows more moisture to escape from the skin. Diminished amounts of available sebum lessen the availability of the protective lipid film that retards the evaporation of water from the skin.
The cause of the itch must be found out in order effectively manage the problem. Treatment should be directed to the underlying cause of the itch. The first step to treating pruritus is determining whether the older adult is itchy with a rash or itchy without a rash. In patients who are just itchy, scratch marks and lesions will only occur in areas where the patient can reach, such as the upper back but not on the shoulder blades. Patients with a rash are more likely to have a primary skin disease, such as candida infection or parasites, that results in pruritus. Careful assessment also is required to assure conditions, such as scabies, that demand special precautions are not present. Patients who itch without a rash tend to have a systemic cause to their pruritus. The most common cause of itch in older adults is xerosis (dry skin). A typical history is one of aggravation of pruritus in the winter and alleviation of itch with the use of moisturizers. The approach to treating the itch is similar to the approach to pain, in that a systemic approach determining severity, temporal relationship, and exacerbating/ alleviating factors is required. Obtaining a detailed history and performing careful physical examination as well as other appropriate investigations are necessary to determine the etiology. Pruritus, like pain, is subjective and can be influenced by comorbid illnesses, medications, and emotional and environmental factors. Pruritus can be precipitated by any circumstance that dries the person’s skin, such as excessive bathing and dry heat. Persons who are cared for in institutions (hospitals, nursing homes) are at greater risk for dry skin through routine bathing, use of drying soap, prolonged bed rest, and the action of bed linen on the patient’s skin. Repeated wetting and drying of the skin layer causes subsequent tissue drying. Persons in institutions at greater risk: routine bathing, harsh soaps, bed rest, linens against skin, inadequate fluid intake Worse in dry climates. Wind, cold, and sunlight contribute to the problem. Exposure to environmental elements, such as artificial heat in cold areas (Called a “winter itch”), decreased humidity, use of harsh soaps, frequent hot baths, nutritional deficiencies, and smoking contribute to skin dryness. If not corrected, the itching may cause traumatizing scratching, leading to breakage and infection of the skin. Prompt recognition of this problem and implementation of corrective measures are, therefore, essential. If possible, the underlying cause should be corrected. Must do complete health history and labs to rule out systemic diseases, such as chronic renal disease, liver disease, poorly-controlled diabetes, and medication side effects. Inadequate fluid intake has a systemic effect – it pulls moisture form the skin to assist in overall hydration of the body.
Avoid activities and environments that increase perspiration. Sweating is diminished in late life. Overheating and heat intolerance are important problems. Also avoid intense cold and wind, if possible. Encourage elders to wear hat in sun and light; loose-fitting, cotton clothing; drink sufficient amounts of fluid Use tepid water -- never hot water -- to bathe. The water should be at or just below body temperature. Daily partial sponge baths or shower every other day Dirty areas: around neck, under armpits, groin, perineal area. Complete bath or shower every 3 rd or 4 th day. Frequent bathing has the tendency to dry out the skin.
Minimize use of soaps or soap products. Avoid products with alcohol, hexachlorophene, or perfume additives. Avoid harsh deodorant soaps. Use a superfatted soap (soap with added palm oil, coconut oil, olive oil, or lanolin – Basis, Dove, Tone, and Caress) to prevent drying of skin and to encourage moisture retention. Rinse off soap thoroughly with water. Then, immediately apply skin lotion/cream/ointments (while the skin is still damp) to trap moisture into the skin and reduce water loss (within 2-3 minutes after bathing). Pat dry – don’t rub. Avoid pouring bath oil or emollient preparations into the bathtub – very slippery and potential for falls. Don’t use anything that will coat the bathtub and make it slippery. It is safer and more effective to apply the moisturizing agent directly to the moist skin as above. It is best to always use a bath mat and grab rails to reduce the risk of slipping. Use a moisturizer. Moisturizers are designed to replace natural skin oils that normally form a barrier to prevent water evaporation from the skin. Apply soothing creams or emollients several times daily, especially on hands, feet, and face. A recent study demonstrated that petroleum jelly is the most effective moisturizer. Unfortunately, it tends to be sticky, greasy, and staining. Light mineral oil or vegetable oil are effective and more economical than commercial brands. Eucerin cream is often a good option. Avoid steroid ointments. Topical steroids (such as hydrocortisone cream) should only be used if the skin becomes inflamed or eczematous. Use only low-potency topical steroids (1% hydrocortisone ointment). Vitamin supplements and a high-quality, vitamin-rich diet may be recommended. Provide a cool environment, cool mist humidifier, and cool soaks or wet dressings to promote vasoconstriction.
Topical application of zinc oxide is effective in controlling itching in some individuals. AVOID antihistamines (Benadryl, Atarax) - sudden, severe, dangerous side effects. AVOID topical and/or systemic corticosteroids – unpredictable absorption, complications. Provide diversional activities to distract patient from discomfort or pruritus.
Skin cancer is the most common of all cancers. Between 40 to 50% of all cancer cases diagnosed every year are skin cancer. Estimates vary, but 500,000 to 1 million new SCCs are diagnosed every year in the U.S. According to the American Cancer Society, 40% to 50% of Americans who live to age 65 will develop skin cancer. People with fair skin that freckles easily, light-colored eyes, and red or blond hair are at greater risk. There are two broad categories of skin cancer: malignant melanoma and nonmelanoma skin cancer. There are three major skin cancers that are common in late life: basal cell carcinoma, squamous cell carcinoma, and melanoma. Because sun damage is an age-related skin finding, screening for suspicious lesions is an integral part of routine physical assessment of the older adult. Chronic sun exposure also causes premature wrinkling and aging of the skin, skin cancer, and cataracts.
Actinic or solar keratoses are small, light-colored lesions, usually gray or brown, on exposed areas of the skin. Small sandpaper-like growths on a red base. Yellow or brown scale. Actinic keratoses are most likely to form on areas of skin that are frequently exposed to direct sunlight, such as arms, face, ears or bald areas of the scalp. First appearing as small tan, brown, or reddish-brown patches, actinic keratoses can range from a few millimeters to a few centimeters in diameter. These lesions may be flat or raised, and generally have ill-defined borders. Typically, actinic keratoses will have a white scaly top and will be rough and gritty to the touch. Some may form a hard, depressed scar-like mass. Highest risk for actinic keratoses: Usually found on the skin surface of fair-skinned individuals who are 50 years of age or older. Chronically sun-damaged skin (yellow, wrinkled, weatherbeaten skin). Pre-malignant: If left untreated, approximately 1 percent of these lesions will progress to squamous cell carcinoma. Close nursing observation for changes in keratotic lesions is vital because they are precancerous.
Skin biopsy: punch, shave, excisional biopsy of suspicious lesions. The doctor will take a sample of skin from the suspicious area for examination under a microscope. Freezing agents and acids can be used to destroy the keratotic lesions, but electrodessication or surgical excision ensures a more thorough removal.
Basal cell carcinoma (BCC) is the most common type of skin cancer in Caucasians. About 80% of skin cancers arise from this layer in skin. It is usually found on the sun-exposed areas of the body, such as the neck and head. It occurs more often in men than in women. Basal cell carcinoma (BCC) is the most common form of skin cancer in white people. Basal cell carcinoma is the most common cancer in humans worldwide. In the US, it accounts for more than 80 percent of nonmelanoma skin cancers. The majority of basal cell carcinomas are easily and successfully treated. Basal cell carcinomas arise in the lowest layer of the epidermis, the basal cell layer. Under the squamous cells, in the lower epidermis, are round cells known as the basal keratinocytes. Basal cell carcinomas are most often found on the face, neck, hands, or other parts of the body that have been exposed to the sun. This type of cancer often appears as a small, pink pearly bump or a smooth growth with a dent in the center. Often these dome-shaped elevations are covered by small blood vessels. Advanced basal cell carcinomas appear as an open sore that bleeds or oozes. Basal cell carcinomas grow slowly and rarely spread throughout the body (metastasize) and deaths from them are very rare. However, because they often occur on the face, their locally destructive effects can result in serious cosmetic deformity if not diagnosed and treated early. Risk factors include advanced age, cumulative lifetime exposure to the sun, and ultraviolet radiation. Middle-aged and elderly persons, especially those with fair complexions and frequent sun exposure, are most likely to be affected. Overexposure to UV radiation is the major cause of skin cancer. Sources of UV radiation include the sun and artiﬁcial sources such as sunlamps or tanning booths. Many people aren’t aware that UV radiation is present outdoors on cold and even cloudy days.
Invasion and erosion of adjoining tissue – tissue destruction; oozing, crusty areas. Usually does not go deep enough to metastasize. Very disfiguring.
The only way to diagnose basal cell carcinoma is to biopsy suspicious looking lesions. The preferred type of biopsy is called a shave biopsy in which the lesion is shaved off with a flexible razor. Treatment options depend on information gleaned from the biopsy: Cryotherapy/ Cryosurgery - This procedure involves destroying the tissue by freezing it with liquid nitrogen. This may be effective for small, well-defined superficial tumors. This procedure is inexpensive and time-efficient but can only be used in a small number of cases. Normally after cryosurgery, the area will be red with a blister in the center. This should heal without incidence. Electrodessication and curettage - This procedure involves destroying the tumor with an electrocautery device then scraping the area with a curet. Many times the diseased tissue can be differentiated from the normal tissue by the texture felt while scraping. T his process is repeated several times to ensure complete removal of the tumor. This procedure is useful for small tumors (6 mm), but it tends to leave a scar. • Topical chemotherapy, such as ﬂuorouracil (5-FU), is used on BCCs and SCCs located in the epidermis.The beneﬁt of 5-FU is that scarring after healing is minimal. • Photodynamic therapy requires injecting a chemical into the body then activating it with a beam of light to destroy the cancer cells. This method is useful for BCC and SCC located only at the surface of the skin. Simple excision - This procedure involves surgical excision of the lesion including a margin of normal skin. This method is preferred for larger lesions (>2cm) on the cheek, forehead, trunk, and legs. The advantage of this treatment is that it is quick and inexpensive. However, the difference between normal and cancerous tissue must be judged with the naked eye. Mohs' micrographic surgery - This procedure is must be performed by an experienced Mohs' surgeon. It involves excision of the tumor and immediate examination of the tissue under the microscope to determine margins. If any residual tumor is left, it can be mapped out and excised immediately. The process of excision and examination of margins may have to be repeated several times. The advantage of this technique is that it is usually definitive and has been reported to have a lower recurrence rate than other treatment options. The disadvantage is the time and expense involved. After treatment, basal cell carcinoma may grow again on the same spot or appear elsewhere on the skin. Between 35 to 50% of people who develop one basal cell carcinoma will grow a new skin cancer within five years of diagnosis.
Squamous cell carcinoma (SCC) is the second most common form of skin cancer in white people but the most common in persons with dark skin. It occurs more often in men than in women. The top layer of the epidermis is mostly made up of flat, scale-like cells called squamous cells. Squamous cell carcinoma arises in the squamous cells that are on the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Approximately 16% of skin cancers begin in this layer. Squamous cell carcinomas may develop from a flat area showing only slight changes from normal skin. A new growth, a spot or bump that gets larger over months or years, or a sore that doesn't heal are warning signs. A squamous cell lesion typically appears as a firm, skin-colored or red nodule. It often has a crusty surface that doesn't clear up. It may develop into a firm, growing lump that may ulcerate (become an open sore). The most common areas squamous cell carcinoma is found are in sun-exposed areas such as the back of the hand, scalp, lip, and upper portion of the ear. Squamous cell carcinomas often start as flat red or brown splotches that become rough, dry and scaly. Most often looks like a scab. There may be a crusted or scaly area of the skin, with a red, inflamed base. Normally a scab will heal within 2 weeks. However, squamous cell carcinoma does not heal and may intermittently bleed. As it spreads into the dermis, this skin cancer can appear like an ulcer with hard, raised edges. Squamous cell carcinoma can develop in scar tissue and also is associated with suppression of the immune system. If it is not treated, it may eventually grow large enough to spread to nearby internal organs (metastasis) and be fatal. The lower lip is a common site of metastasis.
Squamous cell carcinoma is more aggressive than basal cell carcinoma, and grows quicker, is more aggressive, and is more likely to metastasize than basal cell carcinoma. If treated in a timely manner, however, it is uncommon for skin squamous cell carcinoma to spread to other areas of the body. Squamous cell carcinoma usually arises from sun exposure, but can appear on skin that has been burned, damaged by chemicals, or exposed to x-rays. Sun exposure is the most prevalent factor contributing to the development of this cancer, although some less common factors (e.g., exposure to chemicals, arsenic, radiation) can facilitate its growth.
Chemotherapy - used for advanced stages of squamous cell carcinoma. Primary prevention: avoid sun. Secondary prevention: have suspicious lesions checked out - If you have a question, get it checked out. Treating premalignant lesions prevents their transformation to potentially metastatic skin cancer. • Topical chemotherapy, such as ﬂuorouracil (5-FU), is used on BCCs and SCCs located in the epidermis.The beneﬁt of 5-FU is that scarring after healing is minimal. • Photodynamic therapy requires injecting a chemical into the body then activating it with a beam of light to destroy the cancer cells. This method is useful for BCC and SCC located only at the surface of the skin.
Melanoma is the least common type of skin cancer. But it is also the most dangerous and deadly type. Melanoma accounts for only 4% of all skin cancer cases, but accounts for 79% of all skin cancer-related deaths. The incidence of melanomas has been rising in the United States, probably due to sun exposure. Melanoma tends to metastasize, or spread to lymph nodes and other parts of the body, more easily than the other forms of skin cancer, making it more deadly if not caught early. Fair-skinned individuals are at higher risk for melanomas than the general population, and the incidence increases with age. Melanoma is the most common cancer in people ages 25-29. It is second only to breast cancer in women ages 30-35.
Melanoma arises in the melanocytes , which are the pigment-producing cells in the deep epidermis. Possible lesions involved include moles, lentigo, freckles, and birthmarks. Moles are most often involved, and most malignant melanomas begin on or near a mole. Can occur anywhere on body, especially where there are nevi ; commonly found on trunk and lower legs Unlike other skin cancers, melanoma may appear on skin that is not exposed to the sun. The melanocytes become malignant , which means they are abnormal and grow uncontrollably. Melanoma can be a little black or discolored mole that is ignored and by the time it is noticed, the patient has disease that has spread throughout his system. Typically appears on the torso of males and lower legs of females. Dark-skinned individuals can develop melanoma on the palms, soles, and under the nails. Most significant: a CHANGE in the color or size of a mole. It typically becomes irregularly-shaped, with uneven colors: red, white, and blue tones. Suspicious: any spots, sores, lumps, blemishes or markings on the skin that change in shape, size or color. A new growth. A sore that does heal. Scaliness, oozing, bleeding.
Risk factors: Light-skin complexion: fair skin that burns and freckles easily; red or blond hair. Excessive sun/ UV light exposure. One blistering sun burn more than doubles the risk. Usually occurs at least once during childhood. Many moles (more than 50); irregular or large moles. Sometimes these moles should be removed before possible malignant changes can take place. The incidence increases with age. Mean age for lentigo malignant melanoma is 67. Incidence for superficial spreading melanoma (most common type) peaks in middle age and continues to be high through the eighth decade. Majority of cases: men ages 25 to 55.
Irregularly-shaped, pigmented papule or plaque Recognizing Suspicious Moles The common rule of thumb is to apply the ABCD's. Asymmetry - Draw a line through the middle of the mole. If the halves don't match, the mole is asymmetric and more likely to be abnormal. Border - The borders of atypical moles are not well defined or can look scalloped with notches between the scallops. Color – Variation of colors within a mole, or an uneven color throughout the mole is a sign of abnormality. Especially involving red, white, or bluish tones. Diameter - Most melanomas spread horizontally before they start to spread vertically. Therefore look for moles that are enlarging in diameter greater than 5 mm or 1/4 inch. This is about the size of a pencil eraser. Hallmark Sign: Variation of colors within one lesion: red, white, and blue tones
Two growth phases: radial and vertical. The lesion will spread out superficially, then descend down into the dermis. During the radial growth phase, the lesion will spread out superficially in a radial fashion in the epidermis. With time, most melanomas progress to the vertical growth phase, when the malignant cells invade the dermis and develop the ability to metastasize. This can happen at only 1.5 mm deep! Some forms of melanoma are extremely aggressive, with RAPID progression from the radial to the vertical growth phase.
It is very important to know the color, size, and location of the moles on your body, so you’ll recognize any changes that might take place. Simple monthly skin self-examination (use mirrors). Takes only 10 minutes a month, and may save your life. You need to be unclothed when performing a skin self-exam and need a large wall mirror, preferably full-length, and a hand mirror with long handle in a well-lighted room. The best time to perform the exam at home is after showering and drying. You will need to bend your elbows and look closely at your forearms, upper underarms, and palms. Stand up and examine the back of your neck and scalp with the wall mirror and hand mirror. Part your hair with a brush or blow dryer, or ask a family member to check your scalp. Check your back and buttocks with the hand mirror or using a combination of the wall mirror and hand mirror. Sit down and look at the backs of your legs and feet, including the soles and spaces between toes using the hand mirror. Looking for CHANGES in the color or size of a mole. Identify moles that demonstrate changes in pigmentation or size, and seek immediate evaluation of suspicious lesions. Early detection significantly improves the prognosis!
Prognosis is most dependent on the thickness of the lesion. 1.5mm or greater—chance of metastasis. If melanoma is diagnosed early and removed before it begins to spread it is 100% curable by simple, painless removal in a doctor’s office without any need for radiation or chemotherapy. Once the melanoma has metastasized, the prognosis is grim . Median survival: six to nine months. Melanomas can spread so quickly that a patient can have large masses of metastasized cancer in the lymph nodes, lungs, brain, GI tract, or liver while the original skin melanoma is still small. Melanoma that has spread to other parts of the body may not be detectable until long after the original melanoma was removed from the skin.
Treatment: Excisional biopsy of the lesion. R emoves the possible melanoma and a ring of tissue around it (to make sure no cancer cells were missed). If the lesion turns out to be malignant melanoma, the stage of the cancer is determined by how many millimeters thick the cancerous tissue is. The doctor may also examine lymph nodes in the groin, underarm, or neck areas near the abnormal area of skin. Enlarged lymph nodes suggest the melanoma has spread. If so, lymph nodes in the area are removed and examined to see if they contain cancerous cells. To make sure the cancer hasn't spread to other areas of the body, a chest x-ray is taken and a lab test checking the liver is also done. Metastasis: Chemotherapy - to kill cancer cells that have spread throughout the body. Immunotherapy - interferon-alfa and interleukin-2 may be given to help the body's immune system prevent a recurrence of the melanoma. Radiation therapy - to kill cancer cells that may have spread beyond the tumor.
A. Basal cell carcinoma Basal cell carcinoma is the most common form of skin cancer and it grows slowly and rarely metastasizes. The growths tend to be small, dome-shaped elevations covered by small blood vessels that often resemble benign, flesh-colored moles with a “pearly” surface.
Pressure ulcers (PUs) , also termed decubitis ulcers or bed sores, are lesions that usually develop where tissues are compressed between bony prominences and hard surfaces, causing damage to underlying tissue. The damage consists of areas of tissue ischemia, necrosis and ulceration The incidence and prevalence of pressure ulcers is sufficiently high to warrant a great deal of concern based upon the morbidity of the problem and the high cost to the health care system Incidence: > 1 million people each year; nearly 60,000 deaths annually. The majority of pressure ulcers occur on persons over 70 years of age. Pressure ulcers are a common and expensive problem in acute care, nursing home, and home care populations. Prevalence acute care setting (3.5-29.5%) long-term facilities (24%) community (17%) Older adults are at high risk for pressure ulcers because they: Costs: $5 - $8.5 billion each year Pressure ulcers are among the most prevalent, costly and dangerous conditions a patient can acquire in the hospital or long-term care facility. In addition to interfering with recovery, lengthening hospital stays and causing extreme pain and discomfort, pressure ulcers can increase the risk of infection and untimely death. Pressure ulcers are one of the most common bases for elder abuse lawsuits. In addition to developing more easily in older persons, pressure ulcers require a longer period to heal than in younger people. The Centers for Medicare and Medicaid Services recently that it will no longer reimburse hospitals for treating ten "reasonably preventable" conditions. Among these conditions: Stage III & Stage IV pressure ulcers that were acquired during the hospital stay. In addition to pressure ulcers, the preventable conditions for which Medicare will no longer reimburse hospitals include injuries from patient falls, urinary-tract infections, vascular-catheter-associated infections and mediastinitis, an infection following heart surgery. Also included are so-called never events, meaning they never should happen: objects left in the body during surgery, air embolisms and blood incompatibility. Therefore, the most important nursing measure is to prevent their formation.
Stage I: Observable pressure related alteration Skin is intact There is a persistent patch of red skin that does not blanch (turn white) when pressed with a finger (Non blanchable erythema) Darker pigmented skin may not have visible blanching, but the color may be different than the surrounding area The affected skin may also be tender or itchy, and it may feel warm and firm to the touch. Changes in one or more of: Skin temperature Tissue consistency (firm or boggy) Sensation (pain or itching) Stage II There is blistering or an ulcer (open sore) that does not extend through the full thickness of the skin. There may also be a surrounding area of redness or purple discoloration, mild superficial swelling and some oozing. Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough Presents as a shiny or dry shallow ulcer without slough or bruising May also present as an intact or open/ruptured serum-filled blister. Stage III: The ulcer has become a crater and invades subcutaneous tissues (soft tissues just below the skin surface). Full-thickness skin loss Deep crater involving damage or necrosis of subcutaneous tissue Stage IV: The crater has eroded into a muscle, bone, tendon or joint. Extensive destruction, tissue necrosis or damage to muscle, bone, or supporting structures
Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding skin. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissues. Category/ Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk).
Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising*. This Category/ Stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation. *Bruising indicates suspected deep tissue injury.
Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a Category/ Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and Category/ Stage III ulcers can be shallow. In contrast, areas of significant adiposity (fat) can develop extremely deep Category/ Stage III pressure ulcers. Bone/ tendon is not visible or directly palpable.
Full thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often includes undermining and tunneling. The depth of a Category/ Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and these ulcers can be shallow. Category/ Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone/ tendon is visible and directly palpable.
Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Presentation may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Progression may be rapid exposing additional layers of tissue even with optimal treatment.
Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore Category/ Stage cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as the body’s natural (biological ) cover and should not be removed.
Any part of the body can develop a pressure ulcer, but the most common sites are the sacrum, greater trochanter, and ischial tuberosities. They can also develop behind the ears when nasal cannulas are used for prolonged periods and in the corners of the mouth in patients needing nasogastric or endotracheal tubes. Do not massage bony prominences, as this can actually cause deep tissue damage in frail older adults with compromised skin.
The major factors contributing to PU development include pressure, friction, and shearing forces and moisture. Pressure: Pressure describes a force over an area. Persistent, unrelieved pressure on the skin is the most important reason for the development of bedsores. This occurs when soft tissues are compressed between bony prominences and contact surfaces for prolonged periods. Pressure ulcers result from pressure on skin, soft tissue, muscle, and bone that exceeds capillary-filling pressure for an extended period of time. This pressure temporarily cuts off the blood supply to the skin (tissue anoxia and ischemia), which leads to the injury and death of skin cells (necrosis, sloughing, and ulcerations of tissue). Unless pressure is relieved and normal circulation resumes, the affected skin soon begins to show signs of injury. Friction is the force that resists relative motion in a parallel direction between 2 surfaces that are in contact with each other. Socks and long sleeves are very helpful in preventing friction. Elbows and heels should be covered to avoid rubbing on the bed. Be careful not to drag the skin across the sheet when moving or turning a patient as this creates friction and shearing. Use a lift sheet instead. Make sure all underlying sheets are wrinkle-free. Shear is the force per unit area exerted parallel to the plane of interest. Shear occurs when 2 surfaces move in opposite directions. Shearing forces result from forces that tend to cause 2 opposing surfaces to slide and displace against each other. Unlike pressure, which is a perpendicular force, shearing forces act parallel to the tissue surface. Shearing forces occur when the skin is fixed; the consequent sliding pressure is transmitted to deeper tissues with angulation, often causing thrombosis of blood vessels. Use a lift sheet when pulling a patient up in the bed. An example of this is when the upper body of a supine patient is raised to an angle >= 30° and is in contact with the mattress or other firm surface. Moisture – Wetness from perspiration, urine or feces can increase the skin's vulnerability to damage from pressure. For this reason, patients who suffer from incontinence are at particularly high risk for bedsores. Urine and feces can macerate and irritate the skin, predisposing to breakdown. Patients who are wet with incontinence need to be promptly cleaned up.
Shearing, the sliding of parallel surfaces, causes stretching and occlusion of arterial supply, which is usually of the fascia and muscle. Sharing forces can decrease blood supply, leading to tissue ischemia and necrosis. The most common position for shearing is when the head of the bed is elevated, causing the body to slide downward. This puts undue pressure on the tail bone. Resistance keeps the skin in place while gravity pulls the body toward the foot of the bed. Shearing forces cause as many as 40% of pressure ulcers. Shearing occurs when the body shifts and slides downward. Most shearing injuries can be eliminated with proper placement. For example, not elevating the head of the bed greater than 30 degrees and elevating the knees slightly when the head is elevated prevent slipping down in bed. When the client is sitting in a chair, placing the feet on a stool prevents sliding downward.
Age: Elderly individuals have an increased risk of bedsores because the skin usually becomes thinner with age and there is also a decrease in skin perfusion. Also, superficial fat (subcutaneous fat) tends to shift away from the body surface (where it acts as a cushion) to be deposited in deeper areas of the body. They often have skin that is fragile and damages easily. There is often a decreased muscle mass with bony prominences. Poor nutrition: If a patient is poorly nourished, the vulnerability to bedsores increases. Specifically, studies show that bedsores are more likely to develop in patients who have an inadequate daily intake of protein, vitamin C, vitamin E, calcium or zinc. Decreased sensation: Bedsores are common in persons who have spinal cord injuries or other neurological problems that decrease the capacity to feel pain or discomfort. Without normal sensation, the patient cannot feel the effects of prolonged pressure on the skin and may not ask for assistance in shifting pressure away from the affected area. These wounds occur in individuals that are unable to sense the pressure or are unable to change their body position to relieve the pressure. Decreased movement: Patients who can move without assistance have a lower risk of bedsores because they are capable of periodically shifting their weight away from vulnerable areas of skin. Bedsores are also common in patients who are immobilized because of any of the following problems: severe arthritis, prolonged recuperation from surgery, extended treatment in an intensive care unit or incapacitating neurological problems (stroke, spinal cord injury, multiple sclerosis).
Prevention: The most important nursing measure is to prevent the formation of pressure ulcers in the first place. To do this, it is essential to avoid unrelieved pressure. Mobility and activity considerations are a major aspect for the modification of risk factors, prevention, and healing of pressure ulcers. Encouraging activity or turning the patient who cannot move independently is necessary. When sitting in a char, patients should be urged to move and should be assisted with shifting their weight at certain intervals. Assessment: Skin should be assessed on admission or first contact. Afterwards, the skin should be inspected at least once every shift. Bath time affords an excellent opportunity for head-to-toe skin assessment. The Braden Scale is an excellent tool to determine pressure ulcer risk. Infection: Because the broken skin of a bedsore is a prime target for bacteria, bedsores are extremely vulnerable to infections. This is especially true if the sore is frequently contaminated by the urine or feces of a patient who has incontinence. Signs of infection in a bedsore include: Pus draining from the sore A foul-smelling odor Tenderness, heat and increased redness in the surrounding skin Fever (sometimes). Reducing pressure, friction, and shearing forces: Reducing tissue pressure is a critical component of both treatment and prevention and is accomplished with repositioning, using protective devices, and modifying support surfaces.
The Braden Scale was developed in 1987 and comprises six subscales that reflect degrees of sensory perception, moisture, activity, mobility, nutrition, friction, and shear. Each subscale is rated on a scale according to risk and the scores are then totaled. Higher scores indicate higher risk for pressure ulcer development. The Braden Scale has been tested extensively in acute and long-term settings. It is, therefore, one risk assessment tool that can be utilized with confidence. The Braden scale helps predict risk of pressure sores for All bed- or chair-bound patients, or reposition impairment All at-risk patients on admission to health care facilities and regular intervals All older patients with decreased mental status, incontinence, and nutritional deficits The lower the score, the greater the risk. Very high risk: score of 9 or below Same as above, but use a pressure relieving surface. Manage moisture, nutrition, and friction/shear. High risk: score of 10 to 12 Same as above, but add the following: Increase the turning frequency. Do small shifts of position. Moderate risk: score of 13 to 14 Same as above but provide foam wedges for 30-degree lateral position. At-risk: score of 15 to 18 Frequent turning; consider every 2 hour schedule; use a written schedule. Maximize patient's mobility. Protect patient's heels. Use a pressure-reducing support surface if patient is bed- or chair-bound.
Reducing pressure, friction, and shearing forces: Reducing tissue pressure is a critical component of both treatment and prevention and is accomplished with repositioning, using protective devices, and modifying support surfaces. Repositioning of immobilized patients should occur on a schedule, with frequency based on patient risk of developing additional PUs and tissue response to pressure. A written repositioning schedule is most effective, although some patients can be taught to shift their position regularly. Usually, immobilized, bedbound patients must be turned at least every 2 h to the right or left 30° oblique position to relieve pressure on major pressure points; patients should not be placed on their sides (90° lateral position) because this position puts intense pressure on the greater trochanter and lateral malleolus. Patients who already have skin breakdown should not be positioned on the PU unless there is no alternative. Shearing forces that cause two layers of tissue to move across each other should be prevented by not elevating the head of the bed more than 30 (except when patient is eating), not allowing patients to slide in bed, and lifting instead of pulling patients when moving them. A lift sheet should be used to move patients, never pull a patient up in the bed without one.
Moisture reduction: Moisture reduction requires gentle washing and drying. Incontinence must be managed, usually using diapers or pads, and assessed frequently; occasionally, bladder catheterization or rectal tubes may be temporarily helpful. The person who is incontinent should be thoroughly cleansed with soap and water and dried after each episode to avoid skin breakdown from irritating excretia. Protective devices include pillows or foam wedges placed between knees, ankles, and heels when a patient is in a lateral or decubitus position; pillows, foam, or sheepskin heel protectors when supine; and high-density foam, plastic cushions, or silicone gel pads when seated. Rubber rings (donuts) should not be placed on chairs because they may exacerbate soft-tissue compression and decrease blood flow to tissues near the center of the donut ring. A bed trapeze may help patients with upper motor strength to shift their weight or otherwise reposition themselves while in bed. Nutritional support: Patients with or at risk of developing PUs should be screened for nutritional deficiencies. Markers include albumin < 3.5 mg/dL, BMI < 18 in patients, and unintentional weight loss > 15% of baseline. A high-protein, vitamin-rich diet to maintain and improve tissue health is also essential to avoid formation of pressure ulcers. Studies show that bedsores are more likely to develop in patients who have an inadequate daily intake of protein, vitamin C, vitamin E, calcium or zinc. Caloric intake of at least 30 cal/kg/day and protein intake of 1.25 to 1.5 g/kg/day are desirable for optimal healing; oral or parenteral supplementation may be needed. Good skin care: Skin should be kept clean and dry; blotting the patient dry will avoid irritation from rubbing the skin with a towel. Lotions used prophylactically help keep the skin soft and intact.
Braden Scale Risk of pressure ulcer formation is high among older adults so gerontological nurses need to assess patients’ risk for pressure ulcers. The Braden Scale can assist in the objective assessment of pressure ulcer risk. The Pressure Sore Status Tool is an instrument to assess and monitor existing pressure ulcers.
Once evidence of an ulcer is noted, aggressive intervention is necessary to avid the multiple risks associated with this impairment of skin integrity. Treatment measures depend on the state/ stage of the pressure ulcer.
1Care of Aging SkinCare of Aging SkinNURS 4100 Care of the Older AdultFall 2013Joy A. Shepard, PhD(c), MSN, RN, CNE
2ObjectivesObjectives Summarize the effects of aging on the skin Distinguish skin changes due to aging from thosethat result from diseases or injury List practices that promote good skin health inolder adults Describe signs of and nursing care for xerosis,pruritus, actinic keratosis, seborrheic keratosis,skin cancer, and pressure ulcers in older adults
3Key TermsKey Terms Acrochordon – A small, soft penduous growth on the skin, especiallyaround the eyes or on the neck, armpits, or groin Actinic damage – Exposure & damage by the sun Actinic (solar) keratotic lesions - Red-tan scaly plaques occurring on sunexposed surfaces; increase in size, become raised with rough surface.Precancerous Friction - Occurs with the lateral movement of pulling sheet or clothingfrom under a persons bodyweight Keratosis - Raised, thickened, areas of pigmentation which look crusty,scaly and warty Lentigo – A brownish spot (of the pigment melanin) on the skin Melanocytes - Produce melanin, give the skin its color and shield thebody from the harmful effects of the sun
4Key TermsKey Terms Premalignancy – Any abnormal tissue, which is not cancerous, butwhich could become cancerous (if left untreated) Pruritus – Intense itching sensation Seborrheic keratosis – Superficial benign skin growth on face, trunk, orextremities. Yellow, light tan, brown or black; round or oval. Is flat orslightly elevated with a scaly surface Sebum - Oily substance that keeps hair supple and lubricates the skin Senile purpura - Bruised and discolored areas caused by damage to thecapillaries Shearing Force - Occurs when tissue layers move on each other,causing blood vessels to stretch as they pass through subcutaneoustissue Xerosis – Abnormal dryness of the skin
6Effects of Aging: IntegumentEffects of Aging: Integument Flattening of dermal-epidermal junction Reduced thickness of dermis– Degeneration of elastic fibers– Increased coarseness of collagen Atrophy of hair bulbs/ decline in hair growth Decrease in pain sensation Decreased sweat and sebum Loss of subcutaneous adipose tissue Increased fragility of skin
7Normal Changes of Aging in theNormal Changes of Aging in theIntegumentary SystemIntegumentary System
10Skin Turgor: LooseSkin Turgor: LooseForehead, collarbone, or sternumForehead, collarbone, or sternum(center of chest)(center of chest)Not on back of hand orNot on back of hand orforearm for an elder clientforearm for an elder client
11Aging: SubcutaneousAging: Subcutaneous(Hypodermis)(Hypodermis) Loss of SubQ tissue &thinning of dermis Atrophy thinningfeatures, hands andlower legs Hypertrophy increase inproportional body fat
12Aging: GlandsAging: Glands Eccrine & apocrineglands– Decrease in size– Decrease in number– Decrease in function Sebaceous glands– Increased size +decreased sebum water evaporation cracked, dry skin
13Aging: Skin and GlandsAging: Skin and Glands Decreasedsubcutaneous fat,elastic fibers, collagen(stiffening), skinthickness: wrinklesand sagging Decreased blood flow:delayed woundhealing
14Changes in Wound Healing WithChanges in Wound Healing WithIncreased Age: DelayedIncreased Age: Delayed
15Aging: Skin and GlandsAging: Skin and Glands Degeneration ofnerve endings Degeneration ofmelanocytes:Lentigo (“liverspots”)
16Solar ElastosisSolar Elastosis: UV Radiation: UV Radiation Leathery skin/Roughness Inelastic Deep wrinkles Yellowish Depigmentation/hyperpigmentationPhotoagingPhotoaging superimposed on normal agingsuperimposed on normal aging
17Aging: Skin and GlandsAging: Skin and Glands Decreased sebum:dry skin (xerosis) Decreased sweat:impairedthermoregulation Increasedtransparency andfragility Risk for Injury
18Skin Changes in Older AdultSkin Changes in Older Adult Seborrheic keratosis– Dark raised lesions Actinic keratosis– Reddish raisedplaques on areas ofhigh sun exposure canbecome malignant Acrochordon– Skin tags
19Seborrheic Keratosis (benign)Seborrheic Keratosis (benign) Description Increase in size and number with age Areas of the body affected Treatment Need to be evaluated to differentiate themfrom a precancerous lesion
20Aging: HairAging: Hair Altered melanocytes nonpigmented (gray) hairfollicles Declining hormones graying, thinning, baldness– Pubic + axillary hair loss– Facial hair in women(hirsuitism)– Thicker hair in ears +nose– Balding in men by 50 yrs
21Aging: NailsAging: Nails Decreased blood flow,rate of growththicker nails Longitudinal(striations) nail ridges Thick, brittle nails Dull, yellow, or graycoloration
22Integumentary HealthIntegumentary HealthPromotionPromotion Avoid irritating agents Promote activity Adequate fluid intake Use emollients, topicalcreams, lotions, &moisturizers No bath oils Avoid excessive bathing Avoid exposure to UVrays
28Xerosis/ PruritusXerosis/ Pruritus Most common dermatologic problem– Very high incidence over age 70– Can be very severe in the elderly Thinner epidermis, less sebum, easilyirritated– Increase water loss/ decrease water content– Exacerbated by cold air/ dry air
29Xerosis/ PruritusXerosis/ Pruritus Pruritus – find out cause– Rash or no rash?– Xerosis – most common cause Heat, temperature changes, perspiration, contact withclothing, emotional stress Persons in institutions at greater risk Risk for skin breakdown/ infection– Scratching: excoriation, lichenification Assess underlying cause– Dehydration, renal failure, liver dz, peripheral vascular dz
30TreatmentTreatment Avoid perspiration Soft, absorbent clothing, such as cotton Tepid water to bathe or shower (90-105º)– At or just below body temperature Less soap– Mild soap only– Avoid soaps with fragrance Complete bath or shower every other day Daily partial sponge baths– Dirty areas: neck, underarms, groin, perineum
31TreatmentTreatment Superfatted soap (Basis, Dove, Tone, Caress) Avoid: harsh soaps, rubbing alcohol, drying agents Use emollients, topical creams, lotions, &moisturizers (i.e., Vaseline petroleum jelly, Eucerin)– While skin is moist (immediately after bath)– At least 2-3 times daily Pat dry No bath oil (slippery!) Cool environment, cool mist humidifier
39Basal Cell CarcinomaBasal Cell Carcinoma Most common skin cancer in Caucasions 80% of nonmelanoma cancers Arises in the basal cells (lower epidermis) Pearly papule with central crater; rolled, waxy borders Grows slowly and rarely metastasizes Advanced: oozing, crusty areas Sun-exposed areas (head, neck, nose, ears) Risk factors:– Chronic sun/ UV light exposure– Light-skin complexion
40Basal Cell Carcinoma:Basal Cell Carcinoma:AdvancedAdvanced Invasion anderosion of adjoiningtissue withoutmetastasis Oozing, crustyareas Very disfiguring
41Basal Cell Carcinoma: TxBasal Cell Carcinoma: Tx Biopsy (shave preferred): diagnosis Cryotherapy – area will be red with a blisterin the center Electrodessiccation and curettage Topical chemotherapy (5-FU) Photodynamic therapy Surgical excision– Mohs’ micrographic surgery Recurrence common
43Squamous Cell CarcinomaSquamous Cell Carcinoma Second most common skin cancer in Caucasions;most common in dark-skinned persons Squamous cells (top layer of epidermis) Sun-exposed areas (head, upper ear, lower lip,neck) Starts as dry scaly patch Firm, skin-colored or red nodule with scab or crust orcentral area of ulceration Advanced: ulcer with hard, raised edges Metastasis
44Squamous Cell Carcinoma: RiskSquamous Cell Carcinoma: RiskFactorsFactorsChronic skin irritation or injurySun/ UV light exposureBurnsDamage by chemicalsX-ray exposure
47MelanomaMelanomaLeast common, but most dangerousform of skin cancer–Spreads earlier than other skin cancers–Metastasize quickly–Invasive malignant disease–Potential for fatal outcome–Rising incidence
48MelanomaMelanoma Melanocytes (pigment-producing cells) Moles, lentigo, freckles, birthmarks Irregularly-shaped, pigmented lesion Most begin on or near a mole Commonly found on trunk and lower legs Variation of colors: red, white, blue tones Most significant: change in color or size of amole (nevus)
49Melanoma: Risk FactorsMelanoma: Risk FactorsLight-skin complexionExcessive sun/ UV light exposure–One blistering sunburn doubles riskMany moles, irregular or largemolesIncidence increases with age
50ABCD’s of Melanoma: RecognizeABCD’s of Melanoma: RecognizeSuspicious MolesSuspicious Moles Asymmetry: halves don’tmatch Border: indistinct orirregular border Color: variation of colorwithin one lesion Diameter: greater than 5mm (pencil eraser)
52Melanoma: PathophysiologyMelanoma: Pathophysiology Two growth phases:radial and vertical Spreads outsuperficially, thendescends Prognosis mostdependent on depth oflesion 1.5mm or greater:possibility of metastasishttp://matrix.ucdavis.edu/atlas/melanoma-ssmm-III-.72mm-aro.gif
55Note this suspicious mole has severalNote this suspicious mole has severaldifferent shades of color presentdifferent shades of color present
56Melanoma: PrognosisMelanoma: Prognosis Thickness of lesion Early diagnosis(before metastasis):– 100% curable Once melanomahas metastasized,prognosis is grim:– Six to nine monthshttp://www.columbia.edu/itc/hs/nursing/m8786/Skin-John.html
57Melanoma: TreatmentMelanoma: Treatment Excisional biopsy (removes lesion with at least 1cm border of healthy tissue; lymph nodes) Staging of the CA Prognosis: most dependent on the thickness ofthe lesion (≥ 1.5 mm) Check for metastasis: chest x-ray, liver profile,lymph nodes Metastasis: chemotherapy, immunotherapy,radiation
58QuestionQuestion Which of the following types of skin cancersgrows slowly and rarely metastasizes andincludes small, dome-shaped elevationscovered by small blood vessels?– A. Basal cell carcinoma– B. Squamous cell carcinoma– C. Melanoma– D. Lymphoma
59Skin Cancer PreventionSkin Cancer Prevention
60Skin Cancer PreventionSkin Cancer Prevention Sunscreen (SPF of 30or greater) whenexposed to sun Avoid sun during peakhours (10AM-2PM) Long sleeve cottonshirts, long pants, sunhats, & sunglasseswhen outdoors No tanning beds
64Pressure Ulcer Stage I:Pressure Ulcer Stage I:Nonblanchable erythema ofNonblanchable erythema oflocalized area of skinlocalized area of skin
65Pressure Ulcer Stage II: PartialPressure Ulcer Stage II: PartialThickness Skin LossThickness Skin LossPartial-thickness loss of the epidermis and somePartial-thickness loss of the epidermis and someof the dermisof the dermis
66Pressure Ulcer Stage III: FullPressure Ulcer Stage III: FullThickness Skin LossThickness Skin LossFull thickness loss of the skin and necrosisFull thickness loss of the skin and necrosis(death) of subcutaneous tissue(death) of subcutaneous tissue
67Pressure Ulcer Stage IV: FullPressure Ulcer Stage IV: FullThickness Tissue LossThickness Tissue LossFull thickness loss of the skin/ underlying tissue includingFull thickness loss of the skin/ underlying tissue includingthe epidermis, dermis, and subcutaneous tissue (extendsthe epidermis, dermis, and subcutaneous tissue (extendsto muscle and/or bone)to muscle and/or bone)
68Suspected Deep Tissue Injury:Suspected Deep Tissue Injury:Depth UnknownDepth UnknownLocalized area of discolored skin that isLocalized area of discolored skin that ispurple or maroon in colorpurple or maroon in color
69Unstageable: Depth UnknownUnstageable: Depth UnknownFull thickness tissue loss covered by eitherFull thickness tissue loss covered by eitheran eschar or extensive necrotic tissuean eschar or extensive necrotic tissue
70QuestionQuestionA client presents on admission withpressure ulcers extending into thebone. The nurse documents this ulcerat what stage?– A. I– B. II– C. III– D. IV
71QuestionQuestionA serum-filled blister is an exampleof which stage pressure ulcer?–A. I–B. II–C. III–D. IV
Modifiable Risks Contributing to PUDevelopment in Nursing Homes
79PU: Priority InterventionsPU: Priority Interventions Repositioning of immobilized patients: written schedule– Turn every 2 hr (right or left) 30° oblique position– Do not place on sides (90° lateral position)– Do not position on existing PU unless no alternative– HOB not elevated > 30° (except when eating)– Wrinkle-free pull sheet to move patients– Do NOT massage the skin near or on the ulcer. It can causemore skin damage.– Do NOT massage bony prominences.– Use pressure-relieving cushion in chairs, but do NOT use adonut-shaped or ring-shaped cushions. They interfere withblood flow to that area and cause complications.
80PU: Priority InterventionsPU: Priority Interventions Correct transfer techniques– Use lift sheet– Do not drag across linens Moisture reduction– Clean incontinence promptly– Barrier creams Protective devices Nutritional Support– Protein, vitamin C, vitamin E, calcium or zinc Good skin care
81QuestionQuestionWhich of the following assessmenttools is used to determine risk ofpressure ulcers?– A. Folstein Scale– B. Braden Scale– C. Geriatric Skin Scale– D. Pressure Sore Status Tool
82Pressure Ulcer CarePressure Ulcer Care Cleanse the wound with a noncytotoxic cleanser (saline)during each dressing change If necrotic tissue or slough is present, consider the use ofhigh-pressure irrigation Debride necrotic tissue Do not debride dry, black eschar on heels Perform wound care using topical dressings determinedby wound and availability Choose dressings that provide a moist woundenvironment, keep the skin surrounding the ulcer dry,control exudates, and eliminate dead space
83Pressure Ulcer Care (cont’d)Pressure Ulcer Care (cont’d) Reassess the wound with each dressing changeto determine whether treatment planmodifications are needed Identify and manage wound infections Clients with Stage III and IV ulcers that do notrespond to conservative therapy may requiresurgical intervention Note: Adapted from National Guidelines ClearingHouse Guideline for Prevention and Managementof Pressure Ulcers (http://www.guideline.gov)
84Nursing Diagnoses for PUsNursing Diagnoses for PUsRisk for Impaired Skin Integrity relatedto the effects of pressure, friction, orshearRisk for Impaired Tissue Integrityrelated to decreased circulationRisk for Infection related to pressureulcer