Normal Aging

With increasing age, several changes occur throughout the skin, resulting in increased risk of pressure ulcer development. Epidermal turnover rates decrease by 30% to 50% by the age of 70, resulting in rougher skin with decreased barrier function.¹² Theoretically, this change plays a role in decreased healing of epidermal wounds. The dermal-epidermal junction flattens, resulting in decreased contact between the two layers. As a result, the two layers may separate easily, making older skin more likely to tear and blister.

The dermis provides the basic structure of the skin between the epidermis and the deeper structures (muscle and bone). The dermis is a complex connective tissue matrix consisting of collagenous, elastic, and reticular fibers, which provide strength and elasticity. The blood vessels, lymphatics, nerves, and deeper portions of the hair follicles are located in the dermis. Normal aging changes the structure and function of the dermis. Basal and peak levels of cutaneous blood flow are reduced by about 60%, resulting in compromised vascular responsiveness during injury or infection.¹² This change may be mediated by endothelial dysfunction.¹³ With age, collagen synthesis decreases and degradation increases, resulting in a loss of the connective tissue matrix and impaired wound healing.¹² Elastic fibers decrease in number and size, resulting in decreased skin elasticity. Photo aging may worsen these normal changes.

Subcutaneous fat decreases with age, decreasing its ability to protect deeper structures from injury. Distribution of subcutaneous fat changes (decreasing in face and hands, increasing in thighs and abdomen), which decreases pressure diffusion over bony prominences.

Pathophysiology of Pressure Ulcers

Pressure that disrupts normal circulation to the skin and deep structures is the primary factor in the development of pressure ulcers. A complex vascular system, consisting of large vessels and a network of capillaries, courses through the dermis to supply the skin with oxygen and nutrition and remove waste. Motor nerves monitor arterioles and excretion production.¹⁴ Blood flow through the macrocirculatory system is controlled by the microcirculatory system. Small conductance vessels in between these two systems conduct blood and resist flow.^15,16 Dermis capillary blood flow pressures range from 11 mm Hg at the venule side to 32 mm Hg on the arterial side. If capillary pressures rises above 32 mm Hg, blood flow will be disrupted, causing ischemia within hours.^17,18 An older adult patient, supine on a bed, generates pressure between 50 and 90 mm Hg at the location of the heel and greater trochanter, well above the capillary filling pressure. Animal skin studies suggest damage can begin in 2 hours in the presence of only 100 mm Hg pressure.¹⁹

In addition to pressure, friction and shear also are extrinsic factors contributing to ulcer development. Friction causes epidermal injury, which can increase damage already present by pressure. This often occurs when objects such as bed linen or clothes are allowed to rub on the skin, removing the epidermis. The age-associated decrease in epidermal turnover rate may delay repair. Moisturizer use can decrease effects of friction.

Shear is the internal force that is generated when a body shifts or moves in a direction parallel to the plane of contact.²⁰ As an older person slides down in the bed, the skin adheres to the bed surface but the underlying structures move with the body. This causes tearing of capillaries and disruption in blood flow. Now less pressure is needed to occlude blood flow. These phenomena may be worsened by the loss of subcutaneous fat seen with normal aging. Using a draw sheet and keeping a low head of bed elevation can minimize shear.

The final extrinsic factor contributing to pressure ulcer development is excessive moisture. Moisture from urinary or fecal incontinence or profuse sweating can lead to skin maceration and perhaps increased friction and sheer forces when left the skin is left sticky and wet. Absorbent pads can improve moisture.

Aside from extrinsic forces, several intrinsic forces also impact the development of pressure ulcers. These factors include immobility, poor nutrition, decreased sensory perception, and low body mass.¹⁸ Older adults are at increased risk for immobility because of increased rates of cerebral vascular disease, hip fracture, and increased recovery time from acute illness or surgery. If these comorbidities are present, physical therapy and occupational therapy consults may minimize the effects of immobility. Decreased sensory perception may be the result of diabetic neuropathy or cerebral vascular disease, which may prevent an older adult from feeling the pain associated with damage from extrinsic forces. Inadequate nutrition increases risk for ulcer development and impairs healing.²¹ Large wounds may require twice the normal protein intake to heal.²² Tube feeding has not been asso­ciated with preventing or healing pressure ulcers in advanced dementia.²³

Although the extrinsic and intrinsic factors previously discussed may initiate pressure ulcer formation, cell death results from ischemia-reperfusion injury.²⁰ The initial ischemic injury occurs when blood flow ceases. Deeper structures such as skeletal muscle can tolerate only short periods of ischemia, compared to the epidermis, which can tolerate longer periods. Initially, the microcirculation dilates and releases histamine (blanchable erythema). Next, the capillaries and venules engorge with red blood cells and then hemorrhage (nonblanchable erythema). Necrosis of all skin structures is seen by stage III.²⁴ Reperfusion begins with removal of pressure. Damage seen with blanchable and nonblanchable erythema may be reversible. Nitrous oxide production decreases during ischemic periods, causing blood vessel constriction. During reperfusion, blood vessels dilate as nitrous oxide production increases. If damage is extensive, the reperfusion spreads toxic metabolites and oxygen free radicals, destroying surrounding tissue.²⁰

Risk Assessment

Prevention remains the mainstay of pressure ulcer treatment. The health care provider should carefully examine high-risk areas for pressure ulcer development, such as the occiput, spine, sacrum, ischium, heels, trochanter, knee, and ankle. Several scales, including the Norton, Braden, and Waterlow scales, exist to assess patients at risk for pressure ulcer development. The Norton scale assesses five areas on a 4-point scale; these areas are physical condition, mental condition, activity, mobility, and incontinence. A modified scale deducts 1 point for each of the following: comorbidities (diabetes, hypertension), low hemoglobin, low hematocrit, low albumin (<3.3 mg/dL), fever higher than 99.6° F, polypharmacy, and mental status changes/lethargy in the past 24 hours. A score of 10 is high risk.²⁵ The Braden scale is used in both research and clinical settings. This 3-point scale assesses risks in six categories: sensory perception, activity, mobility, nutrition, moisture level, and friction/shear. The maximum score is 23. A score of 18 indicates increased risk for older patients.^26,27 The Waterlow scale is a modification of the Norton scale and assesses eight factors: build, sex, age, continence, mobility, appetite, medication, and special risk factors.²⁸ The higher the score on this complex scale indicates an increased risk. A 2007 review and study using the three scales in an inpatient geriatric setting showed that sensitivity and specificity of all scales depended on selected cutoff points sample changes.²⁹ The positive predictive value of the Braden and Norton scales is approximately 37%.³⁰ As a result, it is recommended that the scales be used in conjugation with a good physical examination by a nurse or physician.^7,29 In a 2014 update, the Cochrane Database of Systemic Reviews found two studies (one randomized controlled) that showed no statistical significance between assessment and pressure ulcer incidence; the authors concluded assessment does not reduce pressure ulcer development.³¹

Pressure Ulcer Classification

The National Pressure Ulcer Advisory Panel (NPUAP) defines a pressure ulcer as localized injury to the skin and/or underlying tissue usually over a bony prominence as a result of pressure or pressure in combination with shear and/or friction. Blanchable erythema or reactive hyperemia often precede pressure ulcer development and can resolve in 24 hours if treatment starts. However, once the skin changes go beyond the initial stage, pressure ulcer formation has started. The NPUAP uses a four-stage system of pressure ulcer classification.³² In 2007, two new stages were added: suspected deep tissue injury and unstageable.³³

Suspected deep tissue injury is a purple or maroon localized area of discolored intact skin or blood-filled blister caused by damage of underlying soft tissue. The skin may be painful and may be a different temperature compared with surrounding skin. Deep tissue injury may progress rapidly to a pressure ulcer, despite treatment. Stage I is intact skin with nonblanchable erythema of a localized area usually over a bony prominence. The skin may be painful and may be a different temperature compared with surrounding skin. This indicates that there is inadequate perfusion to the cutaneous microcirculation. Stage II is a partial thickness loss of dermis presenting as a shallow open ulcer with a red-pink wound bed, without slough or bruising. An open or ruptured blister may also be present. At this stage, tissue anoxia has progressed to such an extent that the epidermis starts to necrose. Stage III is full-thickness tissue loss associated with undermining and tunneling. Subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Ulcers on areas with no subcutaneous tissue (nose, ear, malleolus) may be very shallow compared with areas with significant subcutaneous tissue such as the sacrum. Stage IV is full thickness tissue loss with exposed bone, tendon, or muscle. It is often associated with slough or eschar, undermining and tunneling, and osteomyelitis. An unstageable ulcer is full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. The slough and/or eschar must be removed before the true stage can be determined. However, an eschar on the heels is considered stable if it is dry, adherent, and intact without erythema and should not be removed.

Once staging of the ulcer is completed, ulcer progression must be documented. One method of documenting a wound is as follows³⁴: (1) stage the ulcer, time present, setting where occurred; (2) describe the location anatomically; (3) measure ulcer in centimeters (length × width × base); (4) describe percentage of ulcer covered by granulation tissue versus yellow slough versus necrotic tissue/eschar; (5) note any odor; (6) describe the surrounding tissue; and (7) document undermining or tunneling (use clock as reference point).