Pathophysiology

Dry skin (xerosis) is a common problem, especially in older patients. It is seen as a fine flaking of the stratum corneum (outermost skin layer). The problem is usually worse on the lower legs where blood flow is poorer. Generalized pruritus (itching) often occurs with dry skin. In patients with chronic skin conditions, unrelieved itching causes the patient to scratch and rub the skin in an attempt to relieve the intense itching. These actions may result in secondary skin lesions, excoriations, lichenification (thickening), and infection.

Xerosis is worse in areas with dry climates and higher altitudes, such as in the southwestern part of the United States. Central heating and air-conditioning reduce the humidity in the air and increase skin dryness. Wind, cold, and sunlight also worsen the problem. Frequent bathing with harsh soap and hot water further dries the skin, especially if moisturizers are not applied immediately after bathing when skin is damp.

Patient-Centered Collaborative Care

Nursing interventions focus on teaching the patient and family how to maintain healthy skin, rehydrate the outer skin layers, and relieve itching. Chart 27-1 lists practical ways to avoid overdrying the skin. Remind the patient that bathing with moisturizing soaps, oils, and lotions may reduce dryness. Some soaps and body washes, especially those described as “antimicrobial” and those with perfumes and other scents, may make dry skin worse. Limiting the use of soap to soiled or skinfold areas can also reduce dryness. A 20-minute soak in a warm bath, followed by application of an emollient cream or lotion, will help rehydrate the skin and reduce itching. If the patient cannot take a tub bath, teach him or her to wrap the trunk and extremities in warm, moist towels covered by plastic sheeting or a clean garbage bag for 15 to 20 minutes before applying moisturizers. Skin creams or lotions are more effective when applied to slightly damp skin within 2 to 3 minutes after bathing.

Inform patients that, contrary to popular belief, the cream or lotion is not what makes the skin soft and supple. Water is the agent that softens the outer skin layers. Lubricating creams and lotions seal in the moisture provided by water, promoting suppleness and preventing flaking. Some skin lotions are hydrophilic (water seeking) and actually draw moisture from the skin, making the dryness worse if they are not applied directly to damp skin.

Pathophysiology

Pruritus (itching) is a distressing symptom that may or may not occur with skin disease. It is caused by stimulation of itch-specific nerve fibers at the dermal-epidermal junction. Physical or chemical agents either act directly on these nerve fibers or activate chemical mediators, such as histamine, which then act on the itch receptors.

Itching is a subjective symptom similar to pain. Thus the sensation varies among patients in location and severity. Regardless of the underlying cause, patients usually report that itching is worse at night when there are fewer distractions. Other conditions that make itching worse include poor skin hydration, increased skin temperature, perspiration, and emotional stress.

Patient-Centered Collaborative Care

The priority nursing interventions focus on increasing patient comfort and preventing skin injury. Patients usually try to relieve itching by scratching or rubbing the skin, a response that further stimulates the itch receptors and causes a pattern referred to as the “itch-scratch-itch” cycle. When itching occurs as a symptom of skin lesions, relief can usually be obtained by treatment of the underlying skin disorder with topical or systemic drugs. Systemic diseases, such as liver and venous disorders, can also cause itching without skin lesions. Liver disease often increases the buildup of bilirubin in the skin, which stimulates itch receptors. Pruritus can also be associated with too little or too much blood flow to an area (especially the feet and legs).

Plan care to promote comfort and prevent disruption of skin integrity that can result from vigorous scratching. Because dry skin worsens itching, emphasize proper bathing and skin moisturizing techniques (see Chart 27-1). Encourage patients to keep the fingernails trimmed short, with rough edges filed to reduce skin damage from scratching and to prevent secondary infection. Tell patients that wearing mittens or splints at night can help prevent inadvertent scratching during sleep. If the patient cannot perform self-care, teach the family (for home care) and unlicensed assistive personnel (UAP) to trim the patient’s fingernails and apply mittens or gloves. As always, be sure to stress the importance of not breaking the skin or digging into nail corners when trimming the nails of patients with diabetes.

A cool sleeping environment along with comfort measures such as a cool shower and application of moisturizers may help promote sleep. Additional measures such as using sleep-promoting herbal teas or sedating antihistamines at bedtime (when the side effect of drowsiness is welcome) may provide an uninterrupted night’s sleep. Therapeutic baths with colloidal oatmeal preparations or tar extracts may also provide temporary relief.

If antihistamines are prescribed, closely monitor the patient’s response to therapy so that the dosage can be adjusted as needed. The anti-inflammatory properties of topical steroid preparations and other topical agents are increased if the drug is applied to slightly damp skin.

Using topical drugs under an occlusive dressing increases the dose of anti-inflammatory being delivered. Avoid occluding treated areas unless specifically ordered by the health care provider.

Pathophysiology

Skin trauma can vary from an aseptic surgical incision to a grossly infected, draining pressure ulcer with deep tissue destruction. Injury to the skin starts a series of actions to repair the skin and re-establish this protective barrier.

Phases of Wound Healing

Wound healing occurs in three phases: the inflammatory (lag) phase, the proliferative (connective tissue repair) phase, and the maturation (remodeling) phase. Table 27-1 lists the key events of normal wound healing. The length of each phase depends on the type of injury, the patient’s overall health status, and whether the wound is healing by first, second, or third intention (Fig. 27-1).

TABLE 27-1 NORMAL WOUND HEALING

Inflammatory Phase

• Begins at the time of injury or cell death and lasts 3 to 5 days. • Immediate responses are vasoconstriction and clot formation. • After 10 minutes, vasodilation with increased capillary permeability and leakage of plasma (and plasma proteins) into the surrounding tissue. • Migration of white blood cells (especially macrophages) into the wound. • Clinical manifestations of local edema, pain, erythema, and warmth.

Proliferative Phase

• Begins about the fourth day after injury and lasts 2 to 4 weeks. • Fibrin strands form a scaffold or framework. • Mitotic fibroblast cells migrate into the wound, attach to the framework, divide, and stimulate the secretion of collagen. • Collagen, together with ground substance, builds tough and inflexible scar tissue. • Capillaries in areas surrounding the wound form “buds” that grow into new blood vessels. • Capillary buds and collagen deposits form the “granulation” tissue in the wound, and the wound contracts. • Epithelial cells grow over the granulation tissue bed.

Maturation Phase

• Begins as early as 3 weeks after injury and may continue for a year. • Collagen is reorganized to provide greater tensile strength. • Scar tissue gradually becomes thinner and paler in color. • The mature scar is firm and inelastic when palpated.

FIG. 27-1 The process of wound healing.

A wound without tissue loss, such as a clean laceration or a surgical incision, can be closed with sutures or staples. The wound edges are brought together with the skin layers lined up in correct anatomic position (approximated) and held in place until healing is complete. This type of wound heals by first intention because closing the wound eliminates dead space, thereby shortening the three phases of tissue repair. Inflammation resolves quickly, and connective tissue repair is minimal, resulting in less remodeling and a thin scar.

Deeper tissue injuries or wounds with tissue loss, such as a chronic pressure ulcer or venous stasis ulcer, result in a cavity-like defect that requires gradual filling in of the dead space with connective tissue. This healing occurs by second intention and prolongs the repair process.

Wounds at high risk for infection, such as surgical incisions that enter a nonsterile body cavity or traumatic wounds that occur under unclean conditions, may be intentionally left open for several days. After debris (dead cells and tissues) and exudate have been removed (débrided) and inflammation has subsided, the wound is closed by first intention. This type of healing involves delayed primary closure (third intention) and results in a scar similar to that found in wounds that heal by first intention. Healing can be impaired by many factors (Table 27-2).

TABLE 27-2 CAUSES OF IMPAIRED WOUND HEALING

CAUSE	MECHANISM
Altered Inflammatory Response
Local
Arteriosclerosis Diabetes Vasculitis Thrombosis Venous insufficiency Lymphedema Pharmacologic vasoconstriction Irradiated tissue Crush injuries Primary closure under tension	Reduced local tissue circulation, resulting in ischemia, impaired leukocytic response to wounding, and increased probability of wound infection
Systemic
Leukemia Prolonged administration of high-dose anti-inflammatory drugs: • Corticosteroids • Aspirin	Systemic inhibition of leukocytic response, resulting in impaired host resistance to infection
Impaired Cellular Proliferation
Local
Wound infection Foreign body Necrotic tissue Repeated injury or irritation Movement of wound (e.g., across a joint) Wound desiccation or maceration	Prolonged inflammatory response, which can result in low tissue oxygen tension and further tissue destruction
Systemic
Aging Chronic stress Nutritional deficiencies: • Calories • Protein • Vitamins • Minerals • Water Impaired oxygenation: • Pulmonary insufficiency • Heart failure • Hypovolemia Cirrhosis Uremia Prolonged hypothermia Coagulation disorders Cytotoxic drugs	Impaired cellular proliferation and collagen synthesis Decreased wound contraction

Mechanisms of Wound Healing

When injury occurs, the body restores skin integrity through three processes: re-epithelialization, granulation, and wound contraction. The depth of injury and extent of tissue loss determine how and to what degree each of these processes contributes to wound healing.

Partial-Thickness Wounds

Partial-thickness wounds are more superficial, involving damage to the epidermis and upper layers of the dermis. These wounds heal by re-epithelialization, the production of new skin cells by undamaged epidermal cells in the basal layer of the dermis, which also lines the hair follicles and sweat glands (Fig. 27-2). Skin injury is followed immediately by local inflammation. The inflammatory response causes the formation of a fibrin clot and the release of growth factors that stimulate epidermal cell division (mitosis). New skin cells move into open spaces on the wound surface, where the fibrin clot acts as a frame or scaffold to guide cell movement. Regrowth across the open area (resurfacing) is only one cell layer thick at first. As healing continues, the cell layer thickens and stratifies (forms layers) to resemble normal skin. A healed wound re-establishes the protective barrier properties of the skin with keratin production.

FIG. 27-2 Re-epithelialization.

In a healthy patient, healing of a partial-thickness wound by re-epithelialization takes about 5 to 7 days. This process occurs more rapidly in tissue that is hydrated, oxygenated, and has few microorganisms present.

Full-Thickness Wounds

In deep partial-thickness wounds and full-thickness wounds, damage extends into the lower layers of the dermis and underlying subcutaneous tissue. As a result, most of the epithelial cells at the base of the wound have been destroyed. Thus re-epithelialization is not the major healing process for this type of wound. Removal of the damaged tissue results in a defect that must be filled with scar tissue (granulation) for healing to occur. During the proliferative phase of healing, new blood vessels form at the base of the wound and fibroblastic cells begin moving into the wound space. Fibroblasts deposit new collagen to replace the damaged tissue.

Some of these fibroblasts act like smooth muscle cells and begin to pull the wound edges inward along the path of least resistance (contraction) (see Fig. 27-1). This causes the wound to decrease in size at a uniform rate of about 0.6 to 0.75 mm/day. Complete closure of a wound by contraction depends on the mobility of the surrounding skin as tension is applied to it. If tension in the surrounding skin exceeds the counterforce of wound contraction, healing will be delayed until undamaged epidermal cells at the wound edges can bridge the defect. Unlike re-epithelialization in partial-thickness wounds, which results in the return of a near-normal epithelial barrier, the bridging of epithelial cells across a large area of granulation tissue results in an unstable barrier. A venous leg ulcer is one example of a skin defect that heals poorly by contraction. Re-epithelialization of these chronic wounds often results in a thin epidermal barrier that is easily re-injured.

Re-epithelialization, granulation, and contraction do not continue indefinitely. Natural healing processes can slow down and even stop in the presence of infection, unrelieved pressure, or mechanical obstacles. For example, dead tissue not only supports the overgrowth of organisms but also obstructs collagen deposition and wound contraction. Therefore thorough wound débridement is necessary for healing to occur. In the case of chronic wounds, healing may cease spontaneously and without an obvious cause. In addition, infection in chronic wounds may not show the expected manifestations. Often the only manifestation is an increase in wound size or failure of the wound to decrease in size (Broderick, 2009).

Considerations for Older Adults

As skin ages, the process of wound healing becomes less efficient. Both re-epithelialization and wound contraction slow, and replacement of connective tissue is reduced. Thus the strength of a healed wound in an older adult is reduced and the area is at greater risk for re-injury. When aging skin is further hindered from healing by inadequate nutrition, incontinence, or immobility, any wound in an older adult has a high risk for becoming a chronic wound. Although prevention strategies provide the best outcome, aggressive treatment of any degree of loss of skin integrity, no matter how small, should be started as soon as it is discovered in an older adult (Bianchi & Cameron, 2008; Touhy & Jett, 2010).

Patient-Centered Collaborative Care

Management of skin trauma varies with the depth and type of injury. The collaborative management for any type of skin trauma focuses on enhancing wound healing, preventing infection, and restoring function to the area. Effective management of pressure ulcers or of burns includes interventions that support a healing environment (see Chapter 28).

Pathophysiology

A pressure ulcer is tissue damage caused when the skin and underlying soft tissue are compressed between a bony prominence and an external surface for an extended period. Although they commonly occur over the sacrum, hips, and ankles, pressure ulcers can occur on any body surface. For example, nasal cannula tubing that is too tight can cause pressure ulcers behind the ears or in the nares.

Tissue compression from pressure restricts blood flow to the skin, resulting in reduced tissue perfusion and oxygenation and, eventually, leading to cell death. Ulcers occur most often in people with limited mobility because they cannot change their position to relieve pressure. Sensory impairment is also a contributing factor. Patients who cannot feel or communicate the pain that occurs with unrelieved pressure are more likely to develop pressure ulcers. Once formed, these chronic wounds are slow to heal, resulting in increased morbidity and health care costs. Complications associated with chronic pressure ulcers include sepsis, kidney failure, infectious arthritis, and osteomyelitis.

Other factors increase the risk for pressure ulcer formation. Friction and shear are mechanical forces that impair skin integrity and set the stage for skin breakdown. Excessive skin moisture, such as urinary or fecal incontinence, increases the risk for skin damage when external mechanical forces are applied. Nutritional status is also an important concern. Protein malnutrition not only makes normal tissue more prone to breakdown but also delays healing (Slachta, 2008).

Mechanical Forces

Pressure occurs as a result of gravity. Dependent tissues in contact with a fixed surface experience varying degrees of pressure. Pressure is determined by the amount of weight exerted at the point of contact, the distribution of weight at the point of contact, and the density of the contacting surface. Excessive or prolonged pressure can compress blood vessels at the point of contact, such as over bony prominences. Unrelieved pressure leads to ischemia, inflammation, and tissue necrosis. Pressure occurs when the patient is positioned on a hard surface that does not diffuse his or her weight or when he or she remains in the same position too long.

Friction occurs when surfaces rub the skin and irritate or directly pull off epithelial tissue. Such forces are generated when the patient is dragged or pulled across bed linen.

Shear or shearing forces are generated when the skin itself is stationary and the tissues below the skin (e.g., fat, muscle) shift or move (Fig. 27-3). The movement of the deeper tissue layers reduces the blood supply to the skin, leading to skin hypoxia, anoxia, ischemia, inflammation, and necrosis.

FIG. 27-3 Shearing forces pulling skin layers away from deeper tissue. The skin is “bunched up” against the back of the mattress while the rest of the bone and muscle in the area presses downward on the lower part of the mattress. Blood vessels become kinked, obstructing circulation and leading to tissue death.

Gravity plays a role in the development of shearing forces. A shear injury usually occurs when a patient is in bed in a semi-sitting position and gradually slides downward. Often the skin over the sacrum does not slide down at the same pace as the deeper tissues; thus the skin is mechanically “sheared,” causing blood vessels to stretch and break. Shearing leads to soft-tissue ischemia and deep tissue injury, even though no external break in skin integrity is observed.

Considerations for Older Adults

Older adults are at particular risk for skin tears and pressure ulcers because of the presence of age-related skin changes. Progressive flattening of cells at the dermal-epidermal junction predisposes older people to skin tears from mechanical shearing forces, such as the removal of tape and friction from tightly applied restraints. In addition, skin moisture and irritation from incontinence combined with friction over bony prominences can lead to partial-thickness skin destruction and pressure ulcer formation. Patients with cognitive impairments may not readily report discomfort from inadequate pressure relief. If pressure is unrelieved, tissue destruction progresses to full-thickness injury.

Health Promotion and Maintenance

Pressure ulcers can be prevented if the risk is recognized and intervention begins early (Chart 27-2) (Ackerman, 2011). Key health care team members for pressure ulcer prevention and management are the certified wound care specialist and the dietitian.

A pressure ulcer prevention program consists of two steps: (1) early identification of high-risk patients, and (2) implementation of aggressive intervention for prevention with the use of pressure-relief or pressure-reduction devices. Pressure mapping is a method for identifying specific anatomic areas at risk for breakdown and planning interventions for patients who are bedridden or wheelchair bound. The process of pressure mapping involves the use of a computerized tool that measures pressure distribution for a person sitting in a chair or lying on a mattress (Hanson et al., 2007). The map is displayed as colored areas on the computer screen based on temperature differences. Shades of red indicate areas of greater heat production and are associated with increased pressure loads. Shades of blue indicate cooler areas under lower pressure. When used in combination with more traditional risk assessment tools, pressure mapping appears to help identify problem areas before visual changes occur and allows for more targeted prevention strategies.

Effective risk identification and prevention measures include education of the patient and the caregiver. Documentation of risk assessment, implementation of prevention measures, and education of all people involved in the care of the patient at risk for pressure ulcer formation are key to the plan’s success (Dunleavy, 2008). Periodic re-assessment of risk and continuing evaluation are critical, especially when the patient’s condition changes.

Identification of High-Risk Patients

As suggested by The Joint Commission’s National Patient Safety Goals (NPSGs), all patients admitted to a health care facility or home care agency should be assessed for pressure ulcer risk. The use of a risk assessment tool increases the chances of identifying those patients at greater risk for skin breakdown. The Braden Scale (Fig. 27-4) is the most commonly used skin risk assessment tool. This validated tool helps the nurse assess and document the various risk categories for pressure ulcer formation including mental status, activity and mobility, nutritional status, and incontinence.

FIG. 27-4 The Braden Scale for predicting pressure ulcer risk. IV, Intravenous; NPO, nothing by mouth.

Mental status changes and decreased sensory perception determine whether the patient is a partner in the prevention of pressure ulcers. When the patient understands that turning and shifting of weight prevent tissue damage, the risk for pressure ulcers decreases. Stroke, head injury, organic brain disease, Alzheimer’s disease, or other problems with cognition increase the risk for pressure ulcer formation.

Independent mobility is a direct factor in the risk for pressure ulcer formation. Patients who have unimpaired mobility and can respond to pain are at low risk for pressure ulcer formation. Regardless of age, any patient who requires assistance with turning and positioning or who is unable to verbalize discomfort is at higher risk for pressure ulcer formation. Anyone who is confined to bed or a chair also is at higher risk than a patient who requires assistance only with ambulation.

Nutritional status is a critical risk factor for pressure ulcer development and for successful healing (Slachta, 2008). Intact skin and wound healing depend on a positive nitrogen balance and adequate serum protein levels. The patient in negative nitrogen balance not only heals more slowly but also is at greater risk for accelerated tissue destruction. Draining wounds contribute to protein loss and require more aggressive intervention.

Nutritional status assessment includes laboratory studies; evaluation of weight and recent weight change; ability of the patient to consume an adequate diet; and the need for vitamin, mineral, or protein supplementation. Serum albumin and prealbumin levels are often used to monitor nutritional status. Prealbumin is a more sensitive marker because it has a shorter half-life. Nutrition is considered inadequate when the serum albumin level is less than 3.5 g/dL, the prealbumin level is less than 19.5 mg/dL, or the lymphocyte count is less than 1800/mm³. However, serum protein levels are affected by a number of other factors including level of hydration, metabolic stress, and infection. Therefore laboratory values are valuable only when supported by additional assessment information. Other indicators of inadequate nutrition include poor daily intake of food and fluids with a weight loss greater than 5% change in 30 days or greater than 10% change in 180 days (Dorner et al., 2009).

A positive nitrogen balance requires an intake of 30 to 35 calories per kilogram of body weight daily with a protein intake of 1.25 to 1.5 g/kg/day. Up to 2 g/kg/day of protein may be needed when nutritional deficits are severe or protein loss is ongoing. Vitamin and mineral supplementations are based on the patient’s nutritional status.

Incontinence results in prolonged contact of the skin with such substances as urea, bacteria, yeast, and enzymes carried in urine and feces. These substances are irritants that destroy the integrity of the skin’s barrier, predisposing that patient to skin breakdown. Excessive moisture macerates intact skin, further increasing the risk for breakdown. Daily inspection of the skin for any areas of redness, maceration, or skin breakdown is a major part of pressure ulcer prevention. Maintenance of clean, dry, intact skin also assists in the prevention process. The skin should be washed with a pH-balanced soap to maintain the normal acid level. Creams or lotions are used to lubricate and moisturize the skin. Barrier ointments protect intact skin from urine and feces when incontinence is present. Absorbent pads or garments must be changed immediately with each incontinence episode to avoid prolonged skin contact with urine or feces.

 Nursing Safety Priority

Action Alert

Teach all nursing care personnel and family members not to massage reddened areas directly because this action can damage capillary beds and increase tissue necrosis.

 Nclex Examination Challenge

Safe and Effective Care Environment

The newly admitted client has all of the following laboratory test values. Which value suggests to the nurse that the client may be at an increased risk for pressure ulcer formation?

A. International normalized ratio (INR) of 1.5

B. White blood cell (WBC) count of 5200/mm³

C. Serum sodium concentration of 134 mEq/L

D. Serum prealbumin concentration of 15.2 mg/dL

Assessment

Wound Assessment

The appearance of pressure ulcers changes with the depth of the injury. Chart 27-3 lists the features of the six categories or stages of pressure ulceration, and Fig. 27-5 shows examples.

Chart 27-3

Key Features

Pressure Ulcers

Suspected Deep Tissue Injury

• The intact skin area appears purple or maroon.

• Blood-filled blisters may be present.

• Before the above-listed changes appeared, the tissue in this area may first have been painful.

• Other changes that may have preceded the discoloration include that the area may have felt more firm, boggy, mushy, warmer, or cooler than the surrounding tissue.

Stage 1

• Skin is intact.

• Area, usually over a bony prominence, is red and does not blanch with external pressure.

• For patients with darker skin that does not blanch:

• Observable pressure-related alteration of intact skin; changes are compared with an adjacent or opposite area and include one or more of these:

Skin color (darker or lighted than the comparison area)

Skin temperature (warmth or coolness)

Tissue consistency (firm or boggy)

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 2

• Skin is not intact.

• There is partial-thickness skin loss of the epidermis or dermis.

• Ulcer is superficial and may be characterized as an abrasion, a blister (open or fluid-filled), or a shallow crater.

• Bruising is not present.

Stage 3

• Skin loss is full thickness.

• Subcutaneous tissues may be damaged or necrotic.

• Damage extends down to but not through the underlying fascia; bone, tendon, and muscle are not exposed.

• The depth can vary with anatomic location; areas of thin skin (e.g., the bridge of the nose) may show only a shallow crater, whereas thicker tissue areas with larger amounts of subcutaneous fat may show a deep, crater-like appearance.

• Undermining and tunneling may or may not be present.

Stage 4

• Skin loss is full thickness with exposed or palpable muscle, tendon, or bone.

• Often includes undermining and tunneling.

• Sinus tracts may develop.

• Slough and eschar are often present on at least part of the wound.

Unstageable

• Skin loss is full thickness, and the base is completely covered with slough or eschar, obscuring the true depth of the wound.

Data from National Pressure Ulcer Advisory Panel (NPUAP). (2010, January). Updated staging system. Retrieved October 2010, from www.npuap.org.

FIG. 27-5 Various stages of pressure ulcers. A, Stage 1 pressure ulcer. B, Stage 2 pressure ulcer. C, Stage 3 pressure ulcer. D, Stage 4 pressure ulcer. E, Unstageable ulcer. F, Suspected deep tissue injury.

Assess wounds for location, size, color, extent of tissue involvement, cell types in the wound base and margins, exudate, condition of surrounding tissue, and presence of foreign bodies. Document this initial assessment to serve as a starting point for determining the intervention plan and its effectiveness. How often a wound is assessed is determined by the written policies and procedures at the facility or agency. Weekly documented assessment is the standard in many long-term care facilities; however, daily assessment is needed when the patient is in an acute care setting. Also assess the wound at each dressing change, comparing the existing wound features with those documented previously to determine the current state of healing or deterioration.

For intact areas that are red (in lighter-skinned patients), press firmly with fingers at the center of the area and assess whether the area blanches (lightens) with pressure. An area that blanches with pressure and then returns to normal when pressure is removed indicates color changes related to blood vessel dilation rather than tissue damage or inflammation. When blanching does not occur with pressure, the redness is more likely to be a manifestation of skin injury. Document whether the reddened area blanches with pressure.

Record the location and size of the wound first. Wounds are sized by length, width, and depth using millimeters or centimeters. In standardizing wound size for documentation and communication purposes, assess the wound as a clock face with the 12 o’clock position in the direction of the patient’s head and the 6 o’clock position in the direction of the patient’s feet. Always measure the length from the 12 o’clock position to the 6 o’clock position and the width between the 9 o’clock position and the 3 o’clock position. Measure depth as the distance from the deepest portion of the wound base to the skin level. Use disposable paper tape measures to obtain the length and width of a wound. Touch the bottom of the wound with a cotton-tipped applicator or swab and mark the place on the swab that is level with the skin surface to obtain wound depth. Then measure the area of the swab between the tip and the mark. When all caregivers use this format, measurement is accurate and wound progress can be determined (Hanson et al., 2007).

Inspect the wound margins for cellulitis (inflammation of the skin cells) extending beyond the area of injury. Progressive tissue destruction, seen as an increase in the size or depth of the ulcer and increased wound drainage, usually indicates impairment in the patient’s ability to resist infection if proper measures have been taken to relieve pressure.

Inspect the wound for the presence or absence of necrotic tissue. Because of the depth of tissue destruction, a full-thickness pressure ulcer is often covered by a layer of black, gray, or brown nonviable, denatured collagen called wound eschar.

In the early stages of wound healing, the eschar is dry, leathery, and firmly attached to the wound surface. As the inflammatory phase of wound healing begins and removal of wound debris progresses, the eschar starts to lift and separate from the tissue beneath. This nonliving eschar is a good breeding ground for bacteria normally found on the skin surface, as well as those introduced by incontinence or other means. As bacteria increase, they release enzymes that soften necrotic tissue. This tissue becomes softer and more yellow. In the presence of bacterial colonization, wound exudate increases substantially; the color and odor of wound exudate indicate the major organism present. The features of wound exudate are listed in Table 27-3.

TABLE 27-3 TYPES OF WOUND EXUDATE

CHARACTERISTICS	SIGNIFICANCE
Serosanguineous Exudate
Blood-tinged amber fluid consisting of serum and red blood cells	Normal for first 48 hr after injury Sudden increase in amount precedes wound dehiscence in wounds closed by first intention
Purulent Exudate
Creamy yellow pus	Colonization with Staphylococcus
Greenish blue pus causing staining of dressings and accompanied by a “fruity” odor	Colonization with Pseudomonas
Beige pus with a “fishy” odor	Colonization with Proteus
Brownish pus with a “fecal” odor	Colonization with aerobic coliform and Bacteroides (usually occurs after intestinal surgery)

Beneath the separating dead tissue, granulation tissue appears. Early granulation is pale pink, progressing to a beefy red color as it grows and fills the wound. Palpate the wound to determine the texture of the granulations. Healthy granulation tissue is moist and has a slightly spongy texture. Wounds with poor local arterial blood supply or that have stopped healing appear dry with granulation tissue that is hard (fibrotic) when palpated. Venous obstruction causes an excessively moist ulcer surface with a deep reddish purple color (reflective of the deoxygenated blood beneath the ulcer surface).

Pressure ulcers may involve more extensive tissue destruction than is first seen on inspection. Separation of the skin layers at the wound margins from the underlying granulation tissue is known as undermining. Inspect undermined areas for gradual filling with healthy granulations and for wound-healing progress. Palpate the bony prominences for deep hardening of the surrounding soft tissue, which often occurs with deep tissue ischemia.

After ischemia has occurred, continued pressure over the area increases tissue destruction from the deep tissue layers toward the surface, resulting in the formation of tunnels. This “hidden” wound may first have a small opening in the skin with purulent drainage. If such an opening is observed, use a cotton-tipped applicator to probe gently for a much larger tunnel or pocket of necrotic tissue beneath the opening. Additional tunnels may also occur along the main wound. Check all wounds for tunneling and, if present, document the location and length of each tunnel.

Managing Wounds

Planning: Expected Outcomes

The patient with a pressure ulcer is expected to demonstrate progress to complete wound healing and not develop new pressure ulcers. Indicators include:

• Presence of granulation, re-epithelialization, and scar tissue formation

• Decreased wound size

• Absence of new pressure ulcers

Interventions

Wound care techniques for pressure ulcers vary according to each patient’s needs and the health care provider’s preferences. Surgery with aggressive removal of necrotic tissue may be indicated for some patients, whereas a nonsurgical approach to ulcer débridement is preferred for an older patient who has adequate defenses but is too ill or debilitated for surgery.

Nonsurgical Management

General interventions for pressure ulcer care are listed in Chart 27-4. Nonsurgical intervention of pressure ulcers is often left to the discretion of the nurse, who coordinates with the health care provider and certified wound care specialist (if available) to select a method of wound dressing on the basis of the identified goal of wound management. Many agencies have guidelines or protocols for wound dressings based, for example, on wound size and depth and presence of drainage.

Chart 27-4 Best Practice for Patient Safety & Quality Care

Wound Management of Pressure Ulcers

• If ulcer is covered, remove old dressings/coverings daily (unless the dressing type is to remain in place until it loosens naturally).

• Measure wound size at greatest length and width using a disposable paper tape measure or, for asymmetric ulcers, by tracing the wound onto a piece of plastic film of sheeting (plastic template) at least daily.

• Compare all subsequent measurements against the initial measurement.

• Assess the ulcer for presence of necrotic tissue and amount of exudates.

• Assess and document the condition of the skin surrounding the pressure ulcer in terms of color, temperature, texture, moisture, and appearance.

• Remove or trim loose bits of tissue (may be done by a certified wound care specialist, physical therapist, advanced practice nurse, or other as specified by the agency and the state’s nurse practice act).

• Cleanse the ulcer with saline or a prescribed solution (after diluting it as per manufacturer’s directions or prescriber’s instructions).

• Rinse and dry the ulcer surface.

• In collaboration with the certified wound care specialist, select and apply the dressing materials most appropriate for the volume of wound drainage.

• If possible, avoid positioning the patient on the pressure ulcer.

• Re-position at least every 1 to 2 hours to prevent ulcer extension or generation of additional pressure ulcers.

• Use prescribed pressure-relieving and pressure-reducing devices and techniques as described in Chart 27-2.

Dressings

A properly designed dressing can speed healing by removing unwanted debris from the ulcer surface, protecting exposed healthy tissues, and creating a barrier between the body and the environment until the ulcer is closed. For a patient with a draining, necrotic ulcer, the dressing must also remove excessive exudate and loose debris without damaging epithelial cells or newly formed granulation tissue. If necrosis is extensive and the eschar is thick, dead tissue must be surgically or chemically removed before further débridement with dressings can be effective. Depending on the dressing material used, dressings help remove debris either through mechanical débridement (mechanical entrapment and detachment of dead tissue), topical chemical débridement (enzyme preparations applied topically to loosen necrotic tissue), or by natural chemical débridement (creating an environment that promotes self-digestion of dead tissues by naturally-occurring bacterial enzymes [autolysis]) (Table 27-4).

TABLE 27-4 COMMON DRESSING TECHNIQUES FOR WOUND DÉBRIDEMENT

TECHNIQUE	MECHANISM OF ACTION
Wet-to-damp saline-moistened gauze	As with the wet-to-dry technique, necrotic debris is mechanically removed but with less trauma to healing tissue.
Continuous wet gauze	The wound surface is continually bathed with a wetting agent of choice, promoting dilution of viscous exudate and softening of dry eschar.
Topical enzyme preparations	Proteolytic action on thick, adherent eschar causes breakdown of denatured protein and more rapid separation of necrotic tissue.
Moisture-retentive dressing	Spontaneous separation of necrotic tissue is promoted by autolysis.

After all the dead tissue has been removed, protection of any exposed tendons, bone, and newly formed collagen is critical to pressure ulcer care. The ideal environment for healing is a clean, slightly moist ulcer surface with minimal bacterial colonization. Heavy moisture from an excessively draining ulcer or a dressing that is too wet interferes with healing by promoting the growth of organisms and causing maceration (mushiness) of healthy tissue. Likewise, if a clean ulcer surface is exposed to air or if highly absorbent dressing materials are used for prolonged periods, the drying effect can dehydrate surface cells, form scabs, and convert the wound to a deeper injury.

Assess the ulcer for necrotic tissue and the quantity of exudate. Coordinate with a wound care specialist to select a dressing material with properties that promote an optimal environment for healing. For example, a material that does not stick to the wound surface and does not remove fragile epithelial cells when it is changed is the dressing of choice for protecting new tissue. Depending on the amount of drainage, select either a hydrophobic or a hydrophilic material:

• A hydrophobic (nonabsorbent, waterproof) material is useful when the wound is relatively free of drainage and the purpose is to protect the ulcer from external contamination.

• A hydrophilic (absorbent) material draws excessive drainage away from the ulcer surface, preventing maceration.

A variety of synthetic materials with different absorbent properties are available (Table 27-5). Unlike cotton gauze dressings, these may be left intact for extended periods. Biologic and synthetic skin substitutes are available that can also prevent tissue dehydration and promote healing (see Chapter 28). However, the use of these products for chronic wounds is often cost prohibitive.

TABLE 27-5 COMMONLY USED DRESSING MATERIALS

The frequency of dressing changes depends on the amount of necrotic material or exudate. Dry gauze dressings are changed when “strike through” occurs or when the outer layer of the dressing first becomes saturated with exudate. Gauze dressings used for débridement, such as those placed on a wound wet, allowed to become damp, and then removed, are changed often enough to take off any loose debris or exudate, usually every 4 to 6 hours.

 Nursing Safety Priority

Action Alert

Change synthetic dressings when exudate causes the adhesive seal to break and leakage to occur.

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