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SKIN CARE: Keeping the outside healthy


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UNLIKE OTHER ORGANS, OUR SKIN SURROUNDS AND PROtects us. And when something goes wrong, the results are readily apparent.

A self-repairing organ, the skin is constantly affected by both internal body conditions and the environment. Aging and disease can cause various signs and symptoms, including pain, swelling, eruptions, and dryness. External factors can create immediate reactions (such as a cut or skin tear) or cause more gradual signs of injury from friction, shear, or pressure.

In this handbook, you'll learn how to assess your patient's skin, identify risk factors, and prevent injury. First, let's review the skin's structure and function.

Under the skin

Made up of two layers—the epidermis and dermis—and supported by subcutaneous tissue, the skin (also called the integument) accounts for 15% to 20% of a person's total body weight. The epidermis, the outermost layer, can vary in thickness from 0.1 mm on the eyelids to more than 1 mm on the palms of the hands and soles of the feet. The dermis lies beneath the epidermis and varies in thickness from 0.5 mm to over4 mm. The subcutaneous layer varies in thickness depending on the amount of adipose tissue. (See Anatomy of the Skin.)

  • Epidermis. The epidermis is an avascular layer of skin composed of three cell types. Keratinocytes make up 90% of this outer layer and contain keratin, a fibrous protein. Melanocytes, pigment-producing cells, compose approximately 5% of the epidermal layer. Langerhans cells, which make up the rest, function with helper T cells to trigger immune responses.
  • The epidermis consists of five layers: the stratum corneum, the stratum lucidum, the stratum granulosum, the stratum spinosum, and the stratum basale. The most superficial layer of the epidermis, the stratum corneum, is continuously shed or worn away; new keratinocytes migrate upward to replenish the skin's surface.
  • Dermis. The dermis contains muscle and nerve fibers, blood and lymph vessels, hair follicles, and sweat and sebaceous glands. Composed of two layers, the papillary dermis and the reticular dermis, it's sometimes called the true skin.
  • The papillary dermis forms wavelike projections that contour to the epidermis. This layer contains the dermal side of the epidermal-dermal junction and is composed of connective tissue, collagen, and elastic fibers. The reticular dermis is a dense network of collagen and elastin fibers and provides the point of attachment for muscle fibers.

Composed of adipose tissue, nerves, and blood vessels, the subcutaneous tissue insulates underlying tissue, absorbs shock, and houses fat, which can be used for energy in times of nutritional deprivation.

From protection to regulation

The skin performs diverse functions: It provides protection, delivers information through sensations, permits movement and growth, conducts chemical synthesis, and aids in excretion, immunity, and thermoregulation.

  • Protection. Elastic and pliable, the skin buffers people from trauma. The outermost layer of skin, the stratum corneum, is an acid-mantle composed of sebum and dead skin cells. This creates a thin surface film that provides lubrication and hydration. It also retards bacterial and fungal growth and provides a barrier to prevent fluid and electrolyte loss. Melanin produced in the epidermis helps to protect it from ultraviolet radiation.
  • Sensation. The skin transmits sensations through neurotransmitters (somatic sensory receptors) that provide information from the environment. This includes pain, temperature, pressure, and touch.
  • Movement and growth. The skin's elasticity and ability to recoil allow it to accommodate muscle movement and growth without injury or tearing. It allows for motion and interaction with the environment.
  • Chemical synthesis. When exposed to sunlight, chemicals in the skin are converted to cholecalciferol. The body converts this into vitamin D, which is needed for mineralization of bones and teeth, regulation of calcium and phosphorus levels, and synthesis of blood from the hematopoietic cells.
  • Excretion. The skin regulates the volume and chemical content of perspiration. It also influences the total fluid volume and amount of waste products excreted. Skin excretes water to aid in thermoregulation. It can also excrete urea, ammonia, and uric acid in certain pathologic conditions, as well as pheromones, which play a role in sexual and social behavior.
  • Immunity. Langerhans cells identify antigens and function with helper T cells to trigger immune responses. Phagocytic cells within the skin then destroy the microorganisms and remove debris.
  • Thermoregulation. The internal body temperature generally varies very little. The skin helps to balance heat produced with heat lost by regulating blood flow to the skin through vasoconstriction and dilation and by the evaporation of sweat.

Step-by-step assessment

To assess your patient's skin, start by taking a complete health history. Assess his medical history, his current health status, and his lifestyle habits, including smoking, medications, and nutrition. Also consider occupational and environmental exposures to such substances as paint, aerosol sprays, weed killers, cleaning solvents, and dyes.

Focus on factors affecting the skin, such as sun exposure, dryness, rashes, or open wounds. If your patient has a skin disorder, ask what topical creams, lotions, ointments, or cleansers he uses. Be sure to ask when the problem first started.

While you're obtaining your patient's history, observe posture, clothing (check for tight fit, which can cause irritation, and also for evidence of latex allergies), hair distribution, and condition of nails. Look for signs of disease.

Also consider developmental changes. At birth, skin is pliable. A newborn's skin and nails are thinner than an adult's and will thicken as he ages. In adolescence, hormones stimulate hair growth and sebaceous gland activity.

In adulthood, the dermis begins to thin and epidermal cells reproduce less rapidly. By age 35, replenishing epidermal cells may take twice as long as during adolescence. This prolonged turnover affects the skin's barrier functions and increases the risk of skin cancer and infection.

In older adults, even more significant skin changes occur. The number of Langerhans cells decreases, which diminishes inflammatory responses. Decreased epidermal regeneration and vascular supply alter allergic reactions and delay wound healing.

What's more, an elderly patient may sweat less because he has fewer sweat glands. This can be dangerous because an elderly person who doesn't feel hot may not use a fan or air conditioner to cool himself during a heat wave.

An elderly patient also has less subcutaneous fat and less skin sensation, and his capillaries will be more fragile. Less collagen and elastin are produced, causing the skin to become thinner and less elastic. Skin tears and epidermal stripping can occur easily in the elderly, especially if the skin is dry.

Physical examination

Before starting your physical assessment, be sure the room is well lit and the temperature is comfortable. Remember, ethnic differences may affect skin and mucous membrane coloring as well as hair texture and distribution. For example, erythema and macular rashes may not be readily apparent in dark-skinned persons, and you can't check skin for blanching (except for palms and feet). Expose areas sequentially and use appropriate draping for your patient's privacy.

You should both inspect and palpate the skin.

  • Inspection. Begin at your patient's head and work downward, observing for skin color and surface changes. Look for symmetry in color, texture, and contour on both sides of his body. Assess vascular supply of extremities by checking capillary refill time and noting hair distribution, especially on his legs. Sparse or no hair on lower extremities may indicate peripheral vascular disease. Note odors as well as skin abnormalities.
  • Identify and describe any abnormal skin variations. Describe abrasions, lacerations, and nonpressure ulcers as either partial- or full-thickness injuries. Don't stage these wounds; reserve that for pressure ulcers, which we'll discuss in a minute.
  • You can classify most abnormalities as either primary or secondary lesions. Primary lesions occur in response to an injury or irritation or result from a disease. Secondary lesions evolve from primary lesions. (See Identifying Primary Lesions and Identifying Secondary Lesions.)
  • Palpation. Use palpation to assess skin texture, consistency, moisture, and turgor. Wear gloves to examine moist body areas and lesions. Note the skin's general texture and any rough or indurated areas. Assess temperature bilaterally by palpating similar areas at the same time. If you note a temperature difference, check the area with the back of your other hand, which is more sensitive than the front of the hand. If you feel a change in one area with both hands, you've found a change in your patient's skin and not a variation of your own body temperature.
  • Palpate for edema over areas that appear enlarged, taut, or shiny. Palpate gently to assess consistency, temperature, pain or tenderness, and mobility. Assess for pitting edema by pressing a fingertip firmly into the edematous area for 5 seconds. Your patient has pitting edema if your fingertip leaves a residual indentation caused by fluid displacement. Measure the pitting depth in millimeters or centimeters, which is more accurate than rating it on a scale of 1 to 4.
  • Assess skin turgor by gently pulling up and releasing a skin fold, preferably on your patient's forearm, not his hand. Normal skin should resume a flat shape immediately. Skin that remains elevated for 3 seconds or more has decreased turgor.

Assessing for pressure ulcers

Pressure ulcers are among the most serious skin injuries. Recognizing the magnitude of this problem, the Agency for Health Care Policy and Research (AHCPR) has developed a clinical practice guideline for pressure ulcer prediction and prevention. This guideline recommends identification of at-risk adults and defines interventions for pressure ulcer prevention. (See Pressure Ulcers: Who's at Risk.)

Pressure ulcers can be caused by various factors:

  • intensity of pressure. Intense pressure over a bony prominence even for a short time can result in a pressure ulcer.
  • duration of pressure. Less intense pressures over a long time also can cause a pressure ulcer.
  • decreased tissue tolerance. Previous injuries resulting in scar tissue, poor perfusion, and thin, dry skin decrease tolerance to pressure, friction, and shear.
  • friction. This occurs when two forces move against one another. When skin is pulled or dragged over bed linen, the friction of the skin against the linen can cause tissue injury. Abrasions or epidermal stripping from friction can develop in patients who are pulled up in bed, who are in traction, or who wear braces, splints, orthotics, or poorly sized footwear.
  • shear. Deeper than a friction injury, this occurs when skin and tissues over a bony prominence slide over a hard surface. The skin and subcutaneous structures remain in one position because pressure keeps the skin stuck to an outside surface (bed linen, for example). The shearing tears at the skin, subcutaneous layer, and even muscle. Deep tissue and blood vessel damage can occur. Friction and shear forces usually occur together.
  • moisture. Prolonged moisture on the skin alters pH and decreases skin resiliency.

Transient pressure against the skin causes pallor where blood flow has stopped to a specific area. When the area has been without blood flow more than1 minute, the area will blanch. When the pressure is relieved, the area becomes reddened or hyperemic as blood flows back and revitalizes the area. This rush of blood back into the area is called reactive hyperemia, the earliest sign of tissue compromise and pressure-related ischemia.

If the pressure is prolonged, reactive hyperemia isn't sufficient to revitalize ischemic tissue. In healthy tissue, the skin will blanch if you apply pressure to a hyperemic area as blood is pushed away from the area. It then becomes erythemic again as blood rushes back to the area. But in compromised tissue, you won't be able to make the hyperemic area blanch. Nonblanching erythema is a serious sign that tissues aren't receiving adequate oxygen and nutrients.

Be especially attentive to assessing reactive hyperemia in dark-skinned patients. Look for increased darkening of the skin over bony prominences and palpate the area for warmth, edema, induration, or hardness.

The keys to preventing pressure ulcers are routine assessment of skin integrity and aggressive interventions. You can use assessment scales to identify and score key items that contribute to ulcer formation. Categories usually include friction/shear, continence, nutrition, mobility/activity, and sensory perception.

Commonly used assessment tools include the Norton and Braden scales. Regardless of the scale you use, perform the assessment at regular intervals. (See Braden Scale for Predicting Pressure Ulcer Risk and Norton Scale.)

Staged according to the AHCPR guideline, pressure ulcers may be either small or large wounds, usually with irregular edges. Remember that even in a wound that appears small, the underlying tissue damage may be extensive. You can't stage areas covered with necrotic tissue until the tissue has been removed and you can assess the injury's depth. (See Staging Pressure Ulcers.)

Risk factors for skin breakdown

Various factors can complicate an injury and promote skin breakdown. These include dry skin, incontinence, diseases, medications, malnutrition, environmental forces, and infection.

  • Dry skin. Frequent bathing with alkaline soaps, exposure to cold, and humidity less than 40% can lead to dry, cracked skin. Adequate skin hydration is essential to protect against injuries. Loss of surface moisture can lead to dry, flaky, scaling skin, as well as cracking and fissuring of the skin surface. Severely dry skin is more susceptible to breakdown from pressure and takes longer to recover from injury.
  • Incontinence/moisture. On the other hand, prolonged or repeated exposure to moisture also makes the skin more susceptible to injury. Severe epidermal-dermal breakdown, bacterial or fungal infections, and pressure ulcers can occur in wet, eroded skin. This is especially true in the perineal area, which may be exposed to prolonged moisture from incontinence, perspiration, or wound drainage. Urine and feces can accelerate skin breakdown if left in contact with the skin for long periods. Wound drainage containing enzymes and bacteria also can erode skin.
  • Disease/disorders. Arterial insufficiency, venous hypertension, and diabetes are the most common causes of lower-extremity ulcers. Many patients with arterial insufficiency have peripheral ischemia: Typically, their feet and legs appear thin and hairless with a dry epidermis, and they usually have no edema. Peripheral venous hypertension, also known as venous insufficiency, can cause edema, thickening of the dermis, pigment changes, and dry, scaly skin. Severe edema can make the skin split open and weep.
  • Diabetic patients can experience neuropathy from ischemic injury to the nerves and prolonged hyperglycemia. Neuropathy can cause decreased sensation and muscle atrophy in the feet. Distal anhidrosis (the inability to sweat in the lower extremities) can cause dry, cracked skin. These conditions can lead to lower-extremity ulcers in diabetic patients.
  • Obesity can decrease mobility and contribute to pressure ulcers, especially in bedridden patients. Additionally, moist body folds can become excoriated and provide a favorable environment for bacterial and fungal infections.
  • Medications. Many medications affect the skin. Glucocorticoids, for example, interfere with epidermal regeneration and collagen synthesis. Prolonged steroid therapy can thin the skin and impair healing. Some antibiotics can cause photosensitivity or phototoxicity. Antihistamines, nonsteroidal anti-inflammatory drugs, and some analgesics can alter the skin's inflammatory response.
  • Malnutritio/dehydration. Malnutrition associated with weight loss and decreased protein levels make tissues more susceptible to breakdown and impairs wound healing. Patients who don't consume enough calories lose adipose tissue and lean body mass. Monitor for an unintentional weight loss of 1% to 2% in a week or 5% in a month. The inability to feed oneself, a declining appetite, and low dietary protein intake can all place a person at higher risk for pressure ulcer development and skin breakdown. Dehydration, which often accompanies malnutrition, also is a risk factor because reduced blood volume interferes with peripheral circulation and nutrient and oxygen supply to tissues.
  • Chronic illness can lead to depletion of essential vitamins, minerals, and proteins. Adequate protein; vitamins such as A, C, and E; and minerals such as zinc are essential to promote skin integrity.
  • Environmental factors. One major external factor that can lead to skin breakdown is the use of soap. Although soap removes soil and bacteria, it also emulsifies and removes the skin's sebum coating, which can lead to severe drying of the skin. Soap also thins the stratum corneum. This can lead to severe dryness and skin compromise.
  • What's more, alkaline soaps and cleansers can alter the skin's pH, disrupting the acid-mantle and interfering with the skin's ability to retain moisture and possibly decreasing bacterial resistance. Recovering the skin's normal pH after using an alkaline soap can take more than 18 hours, depending on the length of exposure to the soap.
  • Another factor, ultraviolet radiation, accelerates aging. Skin damaged by ultraviolet radiation is called photodamaged or photoaging. Signs and symptoms include dry, tight skin (in milder cases), a tough leathery appearance, wrinkling, and irregular skin pigmentation. Excessive sun exposure also increases the risk of basal or squamous cell carcinoma and malignant melanoma. Cold can cause the same kind of injuries as the sun, resulting in dry, chapped skin that can crack and split open.
  • Finally, toxic agents such as dyes, bleach, and chemicals all can injure the skin.
  • Infection. Fever, debilitation, stress, and poor nutrition may all accompany systemic infections. These factors can impair the immune response and limit the body's ability to resist environmental injuries. Local infections, such as wounds or fungal rashes, can damage surrounding skin and tissues.

Skin care techniques

With these dangers in mind, you can understand the importance of comprehensive skin care. Protecting your patient involves cleaning and moisturizing his skin, managing incontinence, preventing pressure ulcers, and ensuring good nutrition and hydration.

  • Skin cleaning. Although we associate daily bathing with good hygiene, many patients, especially the elderly, don't need a full bath daily. In fact, daily bathing can lead to dryness and skin breakdown.
  • Traditionally, nurses have used washbasins for daily bed baths. But basins that haven't been thoroughly cleaned and dried can become contaminated with bacteria. Oils or lotions placed in the bathwater coat the basin and create an ideal medium for bacterial growth.
  • For these reasons, many facilities have switched to basinless systems; mild, nonalkaline soaps; and soap-free cleaning agents for routine bathing. Mild, nonalkaline cleansers prevent dryness and preserve the skin's natural pH.
  • Moisturizing. Commonly used ingredients to soften, lubricate, and protect the skin include lactic acid, glycolic acid, mineral oil, glycerin, and petrolatum. Creams are thicker and generally more lubricating than lotions.
  • Apply moisturizing agents as often as necessary to keep skin supple. Before applying any agent, determine if your patient has any allergies or has had adverse reactions to skin care products.
  • Moisturizing agents, except for greasy lubricants, are most effective when applied during or immediately after bathing. This is because the cells of the stratum corneum become hydrated in the presence of water. Moisturizing agents can trap this water on the skin.
  • Incontinence management. Incontinence increases the risk of perineal dermatitis and pressure ulcers because of tissue maceration and chemical irritation to the skin. Fecal incontinence is more significant than urinary incontinence in pressure ulcer development. That's because fecal material contains increased acid, bacteria, and irritants, and these patients tend to be debilitated and functionally limited.
  • To manage incontinence, aim interventions at the cause, not just the effect. For example, fecal impaction may cause fecal incontinence. Removing the impaction and promoting regular bowel evacuation can correct this problem.
  • Urine incontinence may be caused by a weak urethral sphincter. You can use behavioral techniques, medications, and pelvic muscle exercises to manage this type of incontinence.
  • When incontinence occurs, clean your patient's skin as soon as possible. This will help to prevent the chemical irritation that could lead to skin breakdown. A mild, pH-balanced, no-rinse cleanser or basinless bathing system can be used to avoid stripping the skin of its natural oils, which would make the skin even more susceptible to irritation from urine and feces. If water is used, it should be only slightly warm, not hot. Also, use minimal force and friction while cleaning the skin to prevent mechanical trauma. A moisturizer can be used after the skin is cleaned to soothe and rehydrate the skin. To protect skin from being damaged by future incontinent episodes, consider using a barrier product to repel excess moisture and condition the skin.
  • Preventing pressure ulcers. Follow these AHCPR recommendations:
    • Use a validated risk assessment tool at regular intervals and document the assessment.
    • Perform a systematic skin assessment daily on all patients at risk for pressure ulcers.
    • Clean the skin at time of soiling and at routine intervals to minimize skin exposure to moisture and irritants.
    • Use warm, not hot, water.
    • Use a mild cleansing agent.
    • Minimize factors leading to dry skin, such as low humidity (less than 40%) and exposure to cold.
    • Moisturize dry skin.
    • Don't massage bony prominences. This may lead to deep tissue trauma.
    • Turn and reposition your patient every 2 hours. Post a turning schedule at the bedside.
    • Use a lift sheet or pad when moving the patient to avoid friction and shear.
    • Don't use doughnut-type devices to relieve pressure. They can cause venous congestion and pressure ulcers.
    • Use pillows or pads to separate skin surfaces and support limbs.
    • Position the patient 30 degrees on his side, not directly on the trochanter.
    • Keep the bed positioned at a 30-degree angle or less to reduce friction and shear (unless contraindicated).
    • When your patient sits, remind him to shift his weight every 15 minutes, or reposition him in the chair every hour.
    • Elevate heels off the bed, but don't use doughnut devices. Instead, use pillows, pads, or other protective devices.
    • Ensure adequate intake of protein and calories and fluids.
    • Improve or maintain activity level, mobility, and range of motion if possible.
    • Use pressure-reducing devices on the bed or chair for at-risk patients. On a bed, the device can be used on top of a standard mattress, can be a mattress replacement system, can be placed on a bed frame, or can be a pressure-reducing bed.
    • Provide structured and comprehensive education for health care providers, patients, and family or caregivers.
  • Nutrition and hydration. Assess and document your patient's nutritional status, including food and fluid intake. Take a calorie count, and use lab data such as albumin, transferrin, and prealbumin levels to determine his protein status. Obtain a consult from a dietitian as needed.
  • Encourage your patient to eat a well-balanced diet, including foods high in protein. Give liquid nutritional supplements, as ordered.

Preventing the worst

Preventing skin care problems is easier than treating them. Unfortunately, many people realize the need for careful skin care only after an injury.

You can help prevent debilitating, dangerous skin injuries by careful skin care and solid patient education. And if the worst happens and your patient suffers a skin injury, your management and effective nursing care can help the healing begin.




Stratum corneum. Also called the horny layer, this is the most superficial layer of the epidermis. It's composed of sebum and thin, dead, platelike cells that are continuously shed and replaced. An acid-mantle that retards bacterial and fungal growth, this layer also functions as a barrier to prevent water loss and external injury.

Stratum lucidum. Also called the clear layer, this layer is absent in areas of thin skin, such as the eyelids, but is very apparent in thicker skin areas, such as the palms of the hands and soles of the feet. The stratum lucidum contains eleidin, a gellike substance that is rich in protein-bound lipids and blocks water loss or penetration.

Stratum granulosum. Also called the granular layer, this is the layer where cells are filled with keratin and moved to the skin's surface—a process called keratinization. Langerhans cells are found here. These cells identify antigens and initiate immune responses.

Stratum spinosum. Also called the spiny layer, this layer has prominent intercellular bridges that join adjacent cells and create a spiny appearance. These cells have high levels of ribonucleic acid, which is needed for protein synthesis and keratin production. Langerhans cells also are found here.

Stratum basale. Only in this layer (also called the base layer) does mitosis occur. In this layer, new epithelial cells are created and eventually migrate up through the layers of the epidermis. This layer also contains the melanocytes responsible for skin pigmentation. This layer forms downward protrusions, called rete ridges, that provide a sculptured surface for the epidermal-dermal junction.






  • Patients with spinal cord injuries have absent or diminished sensations. If they try to reposition themselves, they may experience friction and shear injuries.
  • Diabetic patients on bed rest are at risk for pressure ulcers. Pay special attention to the lower extremities, especially the heels, because diabetic neuropathy can diminish or destroy foot sensation.
  • Patients who've had orthopedic surgery, especially those with total hip replacement or femoral fractures, are at high risk. Pressure ulcers have been reported in more than 60% of patients admitted with femoral fractures.
  • ICU patients with hypotension, especially those with systolic BPs of 60 mm Hg or less, even for a short time, can experience tissue breakdown because of decreased perfusion pressures.
  • Elderly patients and those with multiple diseases (such as dementia, diabetes mellitus, arteriosclerosis, diseases that require steroid use, or infection) can experience impaired skin integrity and delayed healing.
  • Patients with a history of previous pressure ulcers are especially at risk. Healed full-thickness wounds have only 80% of the tensile strength of noninjured skin. Areas of scar tissue are more likely to break down than intact skin.
  • Patients with low ejection fractions have significantly reduced peripheral perfusion and very low capillary closing pressures. Less pressure over a shorter time will produce an injury.
  • Malnutrition is a significant factor in the development of pressure ulcers. Patients with serum albumin levels less than 3.5 grams/dl are protein deficient. The more severe the deficiency, the greater the risk.
  • Incontinence increases risk by causing chemical irritation and by creating an excessively moist environment. Excoriation and maceration can occur even after a brief episode of incontinence. Patients with fecal incontinence have more than 20 times the risk of pressure ulcers than continent patients.


Assess the patient for each category, assign a score of 1 to 4, and then calculate the total score. If the patient's score is 18 or less, consider him at high risk for pressure ulcer development.



Stage I—An observable pressure-related alteration of intact skin whose indicators, as compared to the adjacent or opposite area on the body, may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), and/or sensation (pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or purple hues.

Stage II—partial-thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater.

Stage III—full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.

Stage IV—full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (for example, a tendon or joint capsule). Undermining and sinus tracts also may be associated with Stage IV ulcers.


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