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NURSING PROCESS: THE PATIENT WITH IMPAIRED SKIN INTEGRITY
An estimated 1.5 to 3 million patients develop pressure ulcers an-nually (Mayo Clinic Rochester, 2001). Both prevention and treat-ment of pressure ulcers are costly in terms of health care dollars and quality of life for patients at risk. Because the cost in terms of pain and suffering for a person with a pressure ulcer cannot be quanti-fied, all possible efforts should be made to prevent skin breakdown.
Patients confined to bed for long periods, patients with motor or sensory dysfunction, and patients who experience muscular at-rophy and reduction of padding between the overlying skin and the underlying bone are prone to pressure ulcers. Pressure ulcers are localized areas of infarcted soft tissue that occur when pressure applied to the skin over time is greater than normal capillary clo-sure pressure, which is about 32 mm Hg. Critically ill patients have a lower capillary closure pressure and are at greater risk for pressure ulcers. The initial sign of pressure is erythema (redness of the skin) caused by reactive hyperemia, which normally resolves in less than 1 hour. Unrelieved pressure results in tissue ischemia or anoxia. The cutaneous tissues become broken or destroyed, leading to progressive destruction and necrosis of underlying soft tissue, and the resulting pressure ulcer is painful and slow to heal.
Immobility, impaired sensory perception or cognition, decreased tissue perfusion, decreased nutritional status, friction and shear forces, increased moisture, and age-related skin changes all con-tribute to the development of pressure ulcers.
When a person is immobile and inactive, pressure is exerted on the skin and subcutaneous tissue by objects on which the person rests, such as a mattress, chair seat, or cast. The development of pressure ulcers is directly related to the duration of immobility: if pressure continues long enough, small vessel thrombosis and tis-sue necrosis occur, and a pressure ulcer results. Weight-bearing bony prominences are most susceptible to pressure ulcer devel-opment because they are covered only by skin and small amounts of subcutaneous tissue. Susceptible areas include the sacrum and coccygeal areas, ischial tuberosities (especially in people who sit for prolonged periods), greater trochanter, heel, knee, malleolus, medial condyle of the tibia, fibular head, scapula, and elbow (Fig. 11-3).
Patients with sensory loss, impaired level of consciousness, or paralysis may not be aware of the discomfort associated with pro-longed pressure on the skin and, therefore, may not change their position themselves to relieve the pressure. This prolonged pres-sure impedes blood flow, reducing nourishment of the skin and underlying tissues. A pressure ulcer may develop in a short period.
Any condition that reduces the circulation and nourishment of the skin and subcutaneous tissue (altered peripheral tissue perfu-sion) increases the risk of pressure ulcer development. Patients with diabetes mellitus experience an alteration in microcircula-tion. Similarly, patients with edema have impaired circulation and poor nourishment of the skin tissue. Obese patients have large amounts of poorly vascularized adipose tissue, which is sus-ceptible to breakdown.
Nutritional deficiencies, anemias, and metabolic disorders also contribute to pressure ulcer development. Anemia, regardless of its cause, decreases the blood’s oxygen-carrying ability and pre-disposes a patient to pressure ulcer formation. Patients who have low protein levels or who are in a negative nitrogen balance ex-perience tissue wasting and inhibited tissue repair. Serum albu-min is a sensitive indicator of protein deficiency; serum albumin levels of less than 3 g/mL are associated with hypoalbuminemic tissue edema and increased risk of pressure ulcers. Specific nutri-ents, such as vitamin C and trace minerals, are needed for tissue maintenance and repair.
Mechanical forces also contribute to the development of pres-sure ulcers. Friction is the resistance to movement that occurs when two surfaces are moved across each other. Shear is created by the interplay of gravitational forces (forces that push the body down) and friction. When shear occurs, tissue layers slide over one another, blood vessels stretch and twist, and the microcir-culation of the skin and subcutaneous tissue is disrupted. Evi-dence of deep tissue damage may be slow to develop and maypresent through the development of a draining tract. The sacrum and heels are most susceptible to the effects of shear. Pressure ul-cers from friction and shear occur when the patient slides down in bed (Fig. 11-4) or when the patient is moved or positioned improperly (eg, dragged up in bed). Spastic muscles and paraly-sis increase the patient’s vulnerability to pressure ulcers related to friction and shear.
Prolonged contact with moisture from perspiration, urine, feces, or drainage produces maceration (softening) of the skin. The skin reacts to the caustic substances in the excreta or drainage and be-comes irritated. Moist, irritated skin is more vulnerable to pres-sure breakdown. Once the skin breaks, the area is invaded by microorganisms (eg, streptococci, staphylococci, Pseudomonasaeruginosa, Escherichia coli), and infection occurs. Foul-smellinginfectious drainage is present. The lesion may enlarge and allow a continuous loss of serum, which may further deplete the body of essential protein needed for tissue repair and maintenance. The lesion may continue to enlarge and extend deep into the fascia, muscle, and bone, with multiple sinus tracts radiating from the pressure ulcer. With extensive pressure ulcers, systemic infections may develop, frequently from gram-negative organisms.
In older adults, the skin has diminished epidermal thickness, der-mal collagen, and tissue elasticity. The skin is drier as a result of diminished sebaceous and sweat gland activity. Cardiovascular changes result in decreased tissue perfusion. Muscles atrophy, and bone structures become prominent. Diminished sensory percep-tion and reduced ability to reposition oneself contribute to pro-longed pressure on the skin. Therefore, the older adult is more susceptible to pressure ulcers, which cause pain and suffering and reduce quality of life (Agency for Health Care Policy and Research [AHCPR], 1994).
In assessing the patient for potential risk for pressure ulcer devel-opment, the nurse assesses the patient’s mobility, sensory per-ception, cognitive abilities, tissue perfusion, nutritional status, friction and shear forces, sources of moisture on the skin, and age. The nurse
• Assesses total skin condition at least twice a day
• Inspects each pressure site for erythema
• Assesses areas of erythema for blanching response
• Palpates the skin for increased warmth
• Inspects for dry skin, moist skin, breaks in skin
• Notes drainage and odor
• Evaluates level of mobility
• Notes restrictive devices (eg, restraints, splints)
• Evaluates circulatory status (eg, peripheral pulses, edema)
• Assesses neurovascular status
• Determines presence of incontinence
• Evaluates nutritional and hydration status
• Reviews the patient’s record for laboratory studies, includ-ing hematocrit, hemoglobin, electrolytes, albumin, trans-ferrin, and creatinine
• Notes present health problems
• Reviews current medications
Scales such as the Braden or Norton scale may be used to fa-cilitate systematic assessment and quantification of a patient’s risk for pressure ulcer, although the nurse needs to recognize that the reliability of these scales is not well established. They tend to over-estimate those at risk and may promote unwarranted use of costly preventive equipment. See Chart 11-8 for a list of risk factors for development of pressure ulcers.
If a pressure area is noted, the nurse notes its size and location and may use a grading system to describe its severity (see Chart 11-9). Generally, a stage I pressure ulcer is an area of nonblanch-able erythema, tissue swelling, and congestion, and the patient complains of discomfort. The skin temperature is elevated be-cause of the increased vasodilation. The redness progresses to a dusky, cyanotic blue-gray appearance, which is the result of skin capillary occlusion and subcutaneous weakening.
A stage II pressure ulcer exhibits a break in the skin through the epidermis or the dermis. An abrasion, blister, or shallow crater may be seen. Necrosis occurs along with venous sludging and throm-bosis and edema with cellular extravasation and infiltration.
A stage III pressure ulcer extends into the subcutaneous tissues. Clinically, a deep crater with or without undermining of adjacent tissues is noted.
A stage IV pressure ulcer extends into the underlying structures, including the muscle and, possibly, the bone. The skin lesion may appear insignificant when in reality, beneath the small surface ulcer is a large undermined area of necrotic tissue.
The appearance of purulent drainage or foul odor suggests an infection. With an extensive pressure ulcer, deep pockets of infec-tion are often present. Drying and crusting of exudate may be present. Infection of a pressure ulcer may advance to osteomyelitis, pyarthrosis (pus formation within a joint cavity), sepsis, and septic shock.
Based on the assessment data, the nursing diagnoses may include the following:
· Risk for impaired skin integrity
· Impaired skin integrity (related to immobility, decreased sensory perception, decreased tissue perfusion, decreased nutritional status, friction and shear forces, increased mois-ture, or advanced age)
The major goals for the patient may include relief of pressure, improved mobility, improved sensory perception, improved tis-sue perfusion, improved nutritional status, minimized friction and shear forces, dry surfaces in contact with skin, and healing of pressure ulcer, if present.
Frequent changes of position are needed to relieve and redistrib-ute the pressure on the patient’s skin and to prevent prolonged reduced blood flow to the skin and subcutaneous tissues. This can be accomplished by teaching the patient to change position or by turning and repositioning the patient. The patient’s family mem-bers should be taught how to position and turn the patient at home to prevent pressure ulcers. Shifting weight allows the blood to flow into the ischemic areas and helps the tissues recover from the effects of pressure. Thus, the patient should be cared for as follows:
• Turned and repositioned at 1-hour to 2-hour intervals
• Encouraged to shift weight actively every 15 minutes
The patient should be positioned laterally, prone, and dorsally in sequence unless a position is not tolerated or is contraindicated. The recumbent position is preferred to the semi-Fowler’s posi-tion because of increased supporting body surface area in this po-sition. In addition to regular turning, there should be small shifts of body weight, such as repositioning of an ankle, elbow, or shoulder. The skin is inspected at each position change and as-sessed for temperature elevation. If redness or heat is noted or if the patient complains of discomfort, pressure on the area must be relieved.
Another way to relieve pressure over bony prominences is the bridging technique, accomplished through the correct position-ing of pillows. Just as a bridge is supported on pillars to allow traf-fic to move underneath, so can the body be supported by pillows to allow for space between bony prominences and the mattress. A pillow or commercial heel protector may be used to support the heels off the bed when the patient is supine. Placing pillows su-perior and inferior to the sacrum relieves sacral pressure. Sup-porting the patient in a 30-degree side-lying position avoids pressure on the trochanter. In the aging patient, frequent small shifts of body weight may be effective. Placing a small rolled towel or sheepskin under a shoulder or hip will allow a return of blood flow to the skin in the area on which the patient is sitting or lying. The towel or sheepskin is moved around the patient’s pressure points in a clockwise fashion.
At times, special equipment and beds may be needed to help re-lieve the pressure on the skin. These are designed to provide sup-port for specific body areas or to distribute pressure evenly.
Patients sitting in wheelchairs for prolonged periods should have wheelchair cushions fitted and adjusted on an individualized basis, using pressure measurement techniques as a guide to selec-tion and fitting. The aim is to redistribute pressure away from areas at risk for ulcers, but no cushion is able to eliminate exces-sive pressure completely. The patient should be reminded to shift weight frequently and to rise for a few seconds every 15 minutes while sitting in a chair (Fig. 11-5).
Static support devices (such as high-density foam, air, or liq-uid mattress overlays) distribute pressure evenly by bringing more of the patient’s body surface into contact with the supporting sur-face. Gel-type flotation pads and air-fluidized beds reduce pres-sure. The weight of a body floating on a fluid system is evenly distributed over the entire supporting surface (according to Pas-cal’s law). Therefore, as the patient’s body sinks into the fluid, additional surface becomes available for weight bearing, body weight per unit area is decreased, and there is less pressure on the body parts.
Soft, moisture-absorbing padding is also useful because the softness and resilience of padding provides for more even distrib-ution of pressure and the dissipation and absorption of moisture, along with freedom from wrinkles and friction. Bony promi-nences may be protected by gel pads, sheepskin padding, or soft foam rubber beneath the sacrum, the trochanters, heels, elbows, scapulae, and back of the head when there is pressure on the sites.
Specialized beds have been designed to prevent pressure on the skin. Air-fluidized beds float the patient. Dynamic support sur-faces, such as low air-loss pockets, alternately inflate and deflate sections to change support pressure for very high-risk patients who are critically ill and debilitated and cannot be repositioned to relieve pressure. Oscillating or kinetic beds change pressure by means of rocking movements of the bed that redistribute the pa-tient’s weight and stimulate circulation. These beds are frequently used with patients who have injuries due to multiple trauma.
The patient is encouraged to remain active and is ambulated whenever possible. When sitting, the patient is reminded to change positions frequently to redistribute weight. Active and passive exercises increase muscular, skin, and vascular tone. Ac-tivity stimulates circulation, which relieves tissue ischemia, the forerunner of pressure ulcers. For the patient at risk for pressure ulcers, turning and exercise schedules are essential: repositioning must occur around the clock.
The nurse helps the patient recognize and compensate for altered sensory perception. Depending on the origin of the alteration (eg, decreased level of consciousness, spinal cord lesion), specific interventions are selected. Strategies to improve cognition and sensory perception may include stimulating the patient to in-crease awareness of self in the environment, encouraging the pa-tient to participate in self-care, or supporting the patient’s efforts toward active compensation for loss of sensation (eg, a paraplegic patient lifting up from the sitting position every 15 minutes). When decreased sensory perception exists, the patient and care-giver are taught to inspect potential pressure areas visually every morning and evening, using a mirror if necessary, for evidence of pressure ulcer development.
Exercise and repositioning improve tissue perfusion. Massage of erythematous areas is avoided because damage to the capillaries and deep tissue may occur.
In patients who have evidence of compromised peripheral cir-culation (eg, edema), positioning and elevation of the edematous body part to promote venous return and diminish congestion im-prove tissue perfusion. In addition, the nurse or family must be alert to environmental factors (eg, wrinkles in sheets, pressure of tubes) that may contribute to pressure on the skin and dimin-ished circulation and remove the source of pressure.
The patient’s nutritional status must be adequate, and a positive nitrogen balance must be maintained, because pressure ulcers de-velop more quickly and are more resistant to treatment in patients with nutritional disorders. A high-protein diet with protein sup-plements may be helpful. Iron preparations may be necessary to raise the hemoglobin concentration so that tissue oxygen levels can be maintained within acceptable limits. Ascorbic acid (vitamin C) is necessary for tissue healing. Other nutrients associated with healthy skin include vitamin A, B vitamins, zinc, and sulfur. With balanced nutrition and hydration, the skin is able to remain healthy, and damaged tissues can be repaired (Table 11-2).To assess nutritional status response to therapeutic strategies, the nurse monitors the patient’s hemoglobin, albumin, and body weight weekly.
Shear occurs when the patient is pulled, is allowed to slump, or moves by digging heels or elbows into the mattress. Raising the head of the bed by even a few centimeters increases the shearing force over the sacral area; therefore, the semireclining position is avoided in patients at risk. Proper positioning with adequate sup-port is also important when a patient is sitting in a chair. Poly-ester sheepskin pads are thought to reduce shear and friction and may be used with at-risk patients.
Continuous moisture on the skin must be prevented by meticu-lous hygienic measures. Perspiration, urine, stool, and drainage must be removed from the skin promptly. The soiled skin should be washed immediately with mild soap and water and blotted dry with a soft towel. The skin may be lubricated with a bland lotion to keep it soft and pliable. Drying agents and powders are avoided. Topical barrier ointments (eg, petroleum jelly) may be helpful in protecting the skin of patients who are incontinent.
Absorbent pads that wick moisture away from the body should be used to absorb drainage. Patients who are incontinent need to be checked regularly and have their wet incontinence pads and linens changed promptly. Their skin needs to be cleansed and dried promptly.
Regardless of the stage of the pressure ulcer, the pressure on the area must be eliminated, because the ulcer will not heal until all pressure is removed. The patient must not lie or sit on the pressure ulcer, even for a few minutes. Individualized positioning and turning schedules must be written in the plan of nursing care and followed meticulously.
In addition, inadequate nutritional status and fluid and elec-trolyte abnormalities must be corrected to promote healing. Wounds that drain body fluids and protein place the patient in a catabolic state and predispose to hypoproteinemia and serious secondary infections. Protein deficiency must be corrected to heal the pressure ulcer. Carbohydrates are necessary to “spare” the protein and to provide an energy source. Vitamin C and trace el-ements, especially zinc, are necessary for collagen formation and wound healing.
To permit healing of stage I pressure ulcers, the pressure is re-moved to allow increased tissue perfusion, nutritional and fluid and electrolyte balance are maintained, friction and shear are re-duced, and moisture to the skin is avoided.
Stage II pressure ulcers have broken skin. In addition to measures listed for stage I pressure ulcers, a moist environment, in which migration of epidermal cells over the ulcer surface occurs more rapidly, should be provided to aid wound healing. The ulcer is gently cleansed with sterile saline solution. Use of a heat lamp to dry the open wound is avoided, as is use of antiseptic solutions that damage healthy tissues and delay wound healing. Semipermeable occlusive dressing, hydrocolloid wafers, or wet saline dressings are helpful in providing a moist environment for healing and in min-imizing the loss of fluids and proteins from the body.
Stage III and IV pressure ulcers are characterized by extensive tissue damage. In addition to measures listed for stage I, these advanced draining, necrotic pressure ulcers must be cleaned (débrided) to create an area that will heal. Necrotic, devitalized tissue favors bacterial growth, delays granulation, and inhibits healing. Wound cleaning and dressing are uncomfortable; there-fore, the nurse must prepare the patient for the procedure by ex-plaining what will occur and administering prescribed analgesia.
Débridement may be accomplished by wet-to-damp dressing changes, mechanical flushing of necrotic and infective exudate, application of prescribed enzyme preparations that dissolve necrotic tissue, or surgical dissection. If an eschar covers the ulcer, it is re-moved surgically to ensure a clean, vitalized wound. Exudate may be absorbed by dressings or special hydrophilic powders, beads, or gels. Cultures of infected pressure ulcers are obtained to guide selection of antibiotic therapy.
After the pressure ulcer is clean, a topical treatment is pre-scribed to promote granulation. New granulation tissue must be protected from reinfection, drying, and damage, and care should be taken to prevent pressure and further trauma to the area. Dress-ings, solutions, and ointments applied to the ulcer should not dis-rupt the healing process. Multiple agents and protocols are used to treat pressure ulcers, but consistency is an important key to success. Objective evaluation of the pressure ulcer (eg, measure-ment of the pressure ulcer, inspection for granulation tissue) for response to the treatment protocol must be made every 4 to 6 days. Taking photographs at weekly intervals is a reliable strat-egy for monitoring the healing process, which may take weeks to months to complete.
Surgical intervention is necessary when the ulcer is extensive, when potential complications (eg, fistula) exist, and when the ulcer does not respond to treatment. Surgical procedures in-clude débridement, incision and drainage, bone resection, and skin grafting.
Recurrence of pressure ulcers should be anticipated; therefore, ac-tive, preventive intervention and frequent continuing assessments are essential. The patient’s tolerance for sitting or lying on the healed pressure area is increased gradually by increasing the time that pressure is allowed on the area in 5- to 15-minute incre-ments. The patient is taught to increase mobility and to follow a regimen of turning, weight shifting, and repositioning. The pa-tient teaching plan includes instruction on strategies to reduce the risk for development of pressure ulcers and methods to detect, in-spect, and minimize pressure areas. Early recognition and inter-vention are keys to long-term management of potential impaired skin integrity.
Expected patient outcomes may include:
Maintains intact skin
a) Exhibits no areas of nonblanchable erythema at bony prominences
b) Avoids massage of bony prominences
c) Exhibits no breaks in skin
Limits pressure on bony prominences
a) Changes position every 1 to 2 hours
b) Uses bridging techniques to reduce pressure
c) Uses special equipment as appropriate
d) Raises self from seat of wheelchair every 15 minutes
a) Performs range-of-motion exercises
b) Adheres to turning schedule
c) Advances sitting time as tolerated
Sensory and cognitive ability improved
a) Demonstrates improved level of consciousness
b) Remembers to inspect potential pressure ulcer areas every morning and evening
Demonstrates improved tissue perfusion
a) Exercises to increase circulation
b) Elevates body parts susceptible to edema
Attains and maintains adequate nutritional status
a) Verbalizes the importance of protein and vitamin C in diet
b) Eats diet high in protein and vitamin C
c) Maintains hemoglobin, electrolyte, albumin, transfer-rin, and creatinine levels at acceptable levels
Avoids friction and shear
a) Avoids semireclining position
b) Uses sheepskin pad and heel protectors when appropriate
c) Lifts body instead of sliding across surfaces
Maintains clean, dry skin
a) Avoids prolonged contact with wet or soiled surfaces
b) Keeps skin clean and dry
c) Uses lotion to keep skin lubricated
Experiences healing of pressure ulcer
a) Avoids pressure on area
b) Improves nutritional status
c) Participates in therapeutic regimen
d) Demonstrates behaviors to prevent new pressure ulcers
e) States early indicators of pressure ulcer development
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