|WOUND WATCH: Assessing pressure ulcers
Volume 5 Number 1
Pages 20 - 23
OVER THE CENTURIES, pressure ulcers have been referred to as decubitus ulcers, bedsores, and pressure sores. The term pressure ulcer has become the preferred name of choice because it most closely describes the etiology and resultant ulcer. The National Pressure Ulcer Advisory Panel (NPUAP) revised its definition of pressure ulcers at its 2007 consensus conference to read: “localized injury to the skin and/or underlying tissue over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.”
Pressure ulcers are usually located over bony prominences, such as the sacrum, coccyx, hips, and heels, and are staged according to the extent of observable tissue damage. Pressure ulcers can occur even with the best preventive measures. Effective treatment depends on a thorough assessment of the developing wound. Meaningful ulcer assessment requires a systematic and objective approach. Clinical assessment should include:
* ulcer history, including etiology, duration, and prior treatment
* anatomic location
* size (length, width, depth in centimeters)
* sinus tracts, undermining, and tunneling
* necrotic tissue (slough and eschar)
* granulation tissue (newly formed tissue within a healing wound)
* epithelialization (regenerated tissue within a healing wound).
On the border
Pressure ulcer borders can provide clues to healing potential. Assess skin around the ulcer for redness, warmth, induration or hardness, swelling, and signs of infection. Before you examine the ulcer, assess the patient's pain. In most cases, pressure ulcers cause some degree of pain; in some cases, pain is severe. Have the patient rate his pain on a visual analog scale of 0 to 10, with 0 representing no pain and 10 representing severe pain. Similarly, ask the patient whether the pain interferes with his ability to function normally and, if so, to what degree.
Rubbing you the wrong way
Pressure ulcers usually develop over bony prominences, such as the sacrum or heels, where excessive pressure damages underlying tissue, eventually resulting in tissue ulceration. Ulcers are more common on the lower half of the body because it has more major bony prominences and more body weight than the upper half of the body. Two-thirds of pressure ulcers occur within the pelvic girdle (the area between and including the hips). Areas where pressure ulcers may be overlooked include the occiput or head (especially in infants and toddlers), ears (especially in patients using nasal oxygen cannulas), and the great toe region.
Body tissues differ in their ability to tolerate pressure. The blood supply to the skin originates in the underlying muscle. Muscle is more sensitive to pressure damage than skin. Tissue tolerance is further compromised by extrinsic and intrinsic factors. Examples of extrinsic factors are moisture, friction, and irritants. Intrinsic factors that affect the ability of the skin and supporting structures to respond to pressure and shear forces are numerous. They include age, spinal cord injury, nutrition, and steroid administration that are believed to affect collagen synthesis (a process involving collagen [a protein] that helps form healthy tissue) and degradation. Other intrinsic factors that affect tissue perfusion are systemic BP, blood circulation (vascular disease), serum protein, smoking, hemoglobin and hematocrit, diabetes mellitus, vasoactive drugs, and increase in body temperature.
Friction (when two surfaces move across one another) and shear (a mechanical force that acts on an area of skin in a direction parallel to the body's surface) contribute to pressure ulcer formation. The tissue injury resulting from these forces may look like a superficial skin injury. Shear and friction are two separate forces that often work together to create tissue ischemia and ulcer development.
Usually, reactive hyperemia is the first visible sign of ischemia. When the pressure causing ischemia is released, skin flushes red as blood rushes back into the tissue. This reddening is called reactive hyperemia, and it's due to a protective mechanism in the body that dilates vessels in the effected area to increase blood flow and speed oxygen to starved tissues. Reactive hyperemia first appears as a bright flush that lasts about one-half or three-quarters as long as the ischemic period. If the applied pressure is too high for too long, reactive hyperemia fails to meet the demand for blood and tissue damage occurs.
Blanchable erythema can signal imminent tissue damage. Erythema results from capillary dilation near the skin's surface. In the patient with pressure ulcers, the redness results from the release of ischemia-causing pressure. Blanchable erythema is red when it blanches, turns white when pressed with a fingertip, and then immediately turns red again when pressure is removed. Tissue exhibiting blanchable erythema usually resumes its normal color within 24 hours and suffers no long-term damage. However, the longer it takes for tissue to recover from finger pressure, the higher the patient's risk for developing pressure ulcers.
In dark-skinned patients, erythema is hard to discern. Use bright light and look for taut, shiny patches of skin with a purplish tinge. Also, assess carefully for localized heat, induration, or edema, which can be better indicators of ischemia than erythema.
Nonblanchable erythema can be the first sign of tissue destruction. In high-risk patients, nonblanchable tissue can develop in as little as 2 hours. The redness associated with nonblanchable erythema is more intense and doesn't change when compressed with a finger. If recognized and treated early, nonblanchable erythema is reversible.
In many cases, the full extent of ulceration can't be determined by visual inspection because there may be extensive undermining along fascial planes (the area that connects skin to the underlying tissues). For example, tunneling can connect ulcers over the sacrum to ulcers over the trochanter of the femur or the ischial tuberosities. These cavities can contain extensive necrotic tissue.
Document the location of the pressure ulcer, for example, right greater trochanter rather than right hip. Include a drawing of the human body (some preprinted skin assessment forms will have a body drawing on them), with the pressure ulcer's location noted on the drawing, in your assessment record to provide complete admission documentation. If there are two or more ulcers near one another, label and number them so you can accurately refer to them in your assessment.
Using a disposable measuring tape measure wound length (in centimeters) as the longest dimension of the wound and width as the longest distance perpendicular to the length. Alternatively, carefully trace the wound margins on a piece of paper (your facility may use wound photography instead). Measure the ulcer's depth at its deepest point by inserting a gloved finger or cotton-tipped swab. If you're using a probe other than your finger, be very careful; it's easy to cause further damage. Note any visible tunnels or undermining. If possible, use a gloved finger to gauge the extent.
Wound color is a good indication of wound status. Record wound color using the red-yellow-black classification system. If more than one color is evident, classify the wound using the least healthy color.
The type of tissue in the ulcer base determines the potential for healing and the type of treatment. Know how to identify necrotic tissue, granulation tissue, and epithelial tissue.
* Necrotic tissue. Necrotic tissue may appear as a moist yellow or gray area of the tissue that's separating from viable tissue. When dry, necrotic tissue appears as thick, hard, and leathery black eschar. Areas of necrotic or devitalized tissue may mask the underlying abscesses and collections of fluid. Before the ulcer can begin to heal, necrotic tissue, drainage, and metabolic wastes must be removed from the wound.
* Granulation tissue. Granulation tissue appears as beefy red, bumpy, shiny tissue at the base of the ulcer. As it heals, a full-thickness ulcer develops more and more granulation tissue. Such factors as tissue oxygenation, tissue hydration, and nutrition can alter the color and quality of granulation tissue.
* Epithelial tissue. Epithelialization is the regeneration of epidermis across the ulcer surface. It appears as pale or dark pink skin, first becoming evident at ulcer borders in full-thickness wounds and as islands around hair follicles in partial-thickness wounds. Wound healing can be assessed and quantified by the percentage of surface covered by new epithelium.
Ulcers with drainage, or exudate, take longer to heal. Drainage characteristics include amount, color, consistency, and odor. Record the amount as scant, moderate, large, or copious. Describe the color and consistency together with clear, descriptive terms, such as serous (clear, watery); serosanguinous (clear red or reddish brown); purulent (thick, yellow, cloudy).
Odor is a subjective observation —one that can suggest infection. It's important to clean the wound thoroughly before assessing the color and odor of the drainage. Otherwise, perceived drainage may be, in actuality, a combination of dressing residue and dead cells —a combination that always produces a noxious odor. However, putrid odor that remains after wound cleaning may indicate anaerobic infection.
Pressure ulcer edges, or margins, have distinct characteristics including color, thickness, and degree of attachment to the wound base. Assess epithelial rim as an integral part of the wound base. Ideally, there should be a free border of epithelial cells. These are the cells that proliferate and migrate across the wound bed during healing. When epidermis at the ulcer edges thickens and rolls under, it impairs migration of epithelial cells. In epiboly, the wound edges thicken and the pressure ulcer becomes chronic, with little or no evidence of new tissue growth.
In undermining, which occurs when necrosis of subcutaneous fat or muscle occurs, a pocket extends beneath the skin at the ulcer's edge. Tunneling differs from undermining in that both ends of a tunnel emerge through the skin's surface. In many cases, a tunnel connects two otherwise distinct pressure ulcers and it may be necessary to open the tunnel before the ulcer can heal.
Sometimes full-thickness pressure ulcers form tracts along fascial planes and extensive, external palpation is the only way to determine the direction and length of the tracts. If this is necessary, use a felt-tipped pen to outline the tract on the skin and measure the resulting image.
Assess intact surrounding skin for redness, warmth, induration (hardness), swelling, and signs of infection. Palpate for heat, pain, and edema. The ulcer bed should be moist, but the surrounding skin should be dry. The skin should be adequately moisturized but neither macerated nor eroded. Macerated skin appears waterlogged and may turn white at the wound's edges.
A saline-soaked dressing can cause maceration of the surrounding skin, unless the skin is protected. Other common causes of maceration include wound drainage and urine or feces contamination. Irritation or stripping may be the result of poor technique during dressing changes.
Appearing on stage
Pressure ulcer staging reflects the depth and extent of tissue involvement. The classification system developed by NPUAP is the most widely used system for staging pressure ulcers. The NPUAP recently redefined its pressure ulcer stages by adding two new stages for deep tissue injury and unstageable ulcers.
Stage I ulcers are characterized by intact skin with nonblanchable redness of a localized area, usually over a bony prominence (see Stage I). Darkly pigmented skin may not have visible blanching, but its color may differ from the surrounding area.
|Figure. Stage I
To identify a stage I pressure ulcer, compare the suspected area to an adjacent area or to the same region on the other side of the body. Indications of a stage I pressure ulcer include differences in skin temperature (warmth or coolness), tissue consistency (firm), and sensation (pain).
Stage II ulcers are characterized by partial-thickness loss of the dermis, presenting as a shallow, open ulcer with a red-pink wound bed without slough (see Stage II). It may also present as an intact or open serum-filled blister.
|Figure. Stage II
Stage III ulcers are characterized by full-thickness tissue loss (see Stage III). Subcutaneous fat may be visible, but bone, tendon, and muscle aren't exposed. Slough may be present but doesn't obscure the depth of tissue loss. Undermining and tunneling may be present. The depth of a stage III ulcer varies by anatomical location.
|Figure. Stage III
Stage IV ulcers involve full-thickness tissue loss with exposed bone, tendon, or muscle (see Stage IV). Slough or eschar may be present on some parts of the wound bed. Undermining and tunneling are also common. The depth of a stage IV ulcer varies by anatomical location.
|Figure. Stage IV
Unstageable ulcers are characterized by full-thickness tissue loss in which the base of the ulcer in the wound bed is covered by slough (yellow, tan, gray, green, or brown), eschar (tan, brown, or black), or both. Until enough slough or eschar is removed to expose the base of the wound, the true depth, and therefore stage, can't be determined.
Once a thorough assessment of the pressure ulcer is completed, the healthcare provider can put together a treatment plan.
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