Pressure ulcers will remain enshrouded in controversy and litigation until caregivers recognize the skin’s vulnerability and develop proactive strategies.

W

ith all the recent discussion on Federal Tag 314 (Tag F314) and the guidance to surveyors now celebrating its first birthday, I thought it appropriate to review one of the largest dilemmas facing us as long-term care providers: pressure ulcers. Pressure ulcer prevalence is estimated to be around 15% in acute care, up to 28% in long-term care, and up to 29% in home care.¹ The term “pressure ulcer” is somewhat of a misnomer, since pressure is only part of the problem. Other terms, such as bedsore, pressure sore, or decubitus ulcer, are often used interchangeably in the medical community. Decubitus comes from the Latin decumbere, meaning “to lie down.” Hence, “decubitus” does not adequately describe the breakdown or ulceration that can occur from other positions (eg, sitting), which can cause ischial tuberosity ulcers. According to the National Pressure Ulcer Advisory Panel (NPUAP), pressure ulcers are any lesions caused by unrelieved pressure resulting in damage of underlying tissue.
       It is thought that pressure ulcers are caused by localized pressure or shear forces that lead to ischemia and cell death, thus causing skin and tissue breakdown. Pressure is equal to force divided by area. So the greater the surface area of the load, the less pressure exerted. For instance, a sitting individual is at a higher risk of developing a pressure ulcer than a person in the supine position. Tissue compression and ischemia can lead to tissue destruction and pressure ulcer formation, and the amount of pressure and the duration of the pressure are inversely proportional.² For instance, low amounts of pressure over longer periods of time can be just as detrimental as high pressure for shorter times.

Pathophysiology

       Many factors contribute to the development of pressure ulcers, but pressure leading to ischemia and necrosis is the final shared path. Pressure is exerted on the skin, soft tissue, muscle, underlying tissue, and bone by the weight of an individual against the contacting surface. These pressures are often in excess of capillary filling pressure, thought to be approximately 32mm Hg.³ Tissues are capable of withstanding enormous pressures when brief in duration, but prolonged exposure to pressures just slightly above capillary-filling pressure initiates a series of events that can lead to tissue necrosis and ulceration. The provocative event is compression or deformation of the tissues (due to shear forces) against external objects, such as a mattress, shoe, wheelchair, or bed rail. Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. Many sores that we consider pressure ulcers are actually shear-induced ulcers. In addition, maceration may occur in the incontinent patient, predisposing the skin to injury by decreasing its tensile strength. Pressure, shear, and friction cause microcirculatory occlusion, resulting in ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia can then lead to cell death, necrosis, and ulceration. Irreversible changes may occur in as few as 2 hours of uninterrupted pressure, depending on individual risk factors and comorbidities.⁴
       Healthy individuals with normal sensation, mobility, and mental faculty usually do not succumb to pressure ulcers. Feedback, both conscious and unconscious, from the areas of compression leads us to change our position. We constantly make micro-movements to compensate. They shift the pressure from one area to another prior to any irreversible ischemic damage to the tissues. Weight shifting for insensate individuals or those with poor mobility should take place every 15 minutes in the seated person and at least every 2 hours in the recumbent individual.⁵
       Individuals with decreased mobility and those who are unable to avoid long periods of uninterrupted pressure are at increased risk for developing necrosis and ulceration. This group of patients typically includes the elderly, the neurologically impaired, and patients hospitalized or institutionalized with acute or chronic illness.

Causes

       Although prolonged, uninterrupted pressure is the main cause of pressure ulcers, impaired mobility is probably the most common reason patients are exposed to unrelieved pressure. This is common in those who are neurologically impaired, heavily sedated or anesthetized, restrained, demented, or suffering from a traumatic injury (eg, a pelvic or femur fracture). These patients are incapable of assuming the responsibility of altering their position to relieve pressure. Moreover, this immobility, if prolonged, leads to muscle and soft tissue atrophy, decreasing the bulk over which bony prominences are supported—further increasing the risk of developing a pressure ulcer.

Table 1

       When initially evaluating a patient with pressure ulceration, it is important to note the following information from the history:
• Overall physical and mental health (ie, concurrent diseases and/or disabilities)
• Prior hospitalizations, operations, or wounds
• Diet (ie, recent weight changes, food avoidances)
• Bowel and bladder continence
• Presence of spasticity or flexion contractures
• Medications and allergies
• Tobacco, alcohol, and recreational drug use
• Place of residence
• Any paralysis or breeches in sensation
• Support surface used in bed or while sitting
• Level of independence, mobility, and ability to comprehend and cooperate with care
• Underlying social and financial support structure
• Presence of specific cultural, religious, or ethnic issues
• Presence of advanced directives, power of attorney, or specific preferences regarding care
• Presence of signs or symptoms related to the current ulceration (ie, pain, fever, exudate, odor)
• History of the present ulcer (ie, length of time the ulcer has been present, treatments attempted in the past).

Where Pressure Ulcers Occur

       Generally, pressure ulcers occur over bony prominences, such as the heels, sacrum, ischial tuberosities (“sitting” bones), or greater trochanters (hip bones). Many are concentrated in and around the pelvis due to its bony structure and posture issues related to both sitting and reclining. Heels present a big challenge since pressure, coupled with other comorbidbid states like arterial disease, can further complicate treatment and increase risk.

Risk Assessment

       A risk assessment tool is helpful to identify risk factors and alert the clinical team of increased pressure ulcer risk. The Braden Scale for Predicting Pressure Ulcer Risk (see Table 2) and the Norton Scale are 2 of the most common risk assessment tools.⁶ Both scales are valid and reliable.

Table 2

       Using the Braden Scale, healthcare professionals can assess 6 broad categories, including sensory perception, moisture, activity, mobility, nutrition, friction, and shear. A score of 18 or below indicates a risk for developing a pressure ulcer. The Braden Q is a modified Braden Risk Assessment Tool specifically useful with pediatric patients. As an alternative, the Norton Scale assesses physical condition, mental state, activity, mobility, and incontinence. A score of 16 or below indicates risk for ulceration. It is generally accepted that risk for pressure ulcer formation is both intrinsic and extrinsic. The intrinsic factors include age, nutrition, disease process, drug therapy, lack of sensation, immobility, bed rest, smoking, radiation, obesity, infection, low blood pressure, incontinence, dehydration, and edema. Extrinsic risk factors include pressure, shear, friction, moisture, and heat.

Assessment

       Assessment includes all of the same criteria that we equate with any and all chronic wounds. When evaluating pressure ulcers, however, it is important to determine the greatest or lowest level of tissue destruction or the ulcer’s stage. A number of systems have been developed over the years for classification or “staging” of wounds involving the skin and underlying structures. The staging system currently recommended by Agency for Healthcare Policy and Research (AHCPR) and Wound, Ostomy and Continence Nursing (WOCN) Society—and accepted by Medicare and the Centers for Medicare & Medicaid Services—is a 4-stage system based on the tissue layers involved. The system is derived from previous staging systems proposed by Shea,⁷ the International Association for Enterostomal Therapy (IAET), and the National Pressure Ulcer Advisory Panel (NPUAP).

Pressure Ulcer Stages

       A stage 1 pressure ulcer involves only the epidermis or outermost, avascular layer of skin. A stage 1 pressure ulcer involves intact skin that is nonblanchable in pale skin tones and can appear as an observable, pressure-related alternation of intact skin. (The blanching test is performed by pushing on the discolored area of skin for a second or two and then releasing the pressure to evaluate return of blood flow; if there is no change in color from pale to more pink—or darker in people of color—then the tissue is damaged and considered a stage 1 pressure ulcer.) The indicators, as compared to an adjacent or opposite area on the body, may include changes in one or more of the following: skin temperature (ie, warmth or coolness), tissue consistency (ie, firm or boggy feel), and/or skin sensation (ie, pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin. In darker skin tones, however, the ulcer may appear with persistent red, blue, or purple hues.
       One caveat in assessing a stage 1 pressure ulcer is to consider that the wound will potentially progress to a higher-stage pressure ulcer. This sign could be the “tip of the iceberg,” so to speak. Do not confuse deep purple areas or dark necrotic tissue to be a stage 1 pressure ulcer. These areas are usually indicative of deeper, full-thickness damage to underlying tissue and not the superficial damage associated with a stage 1 pressure ulcer. The thought is that deep tissue injury (DTI) occurs near the bone (or from the outside in). Later, damage is seen superficially when tissue dies or undergoes necrosis, reaches the outer layers of skin, and opens the skin.⁸
       The NPUAP’s proposed definition of DTI is, “a pressure-related injury to subcutaneous tissue under intact skin. Initially, these lesions have the appearance of a deep bruise. These lesions may herald the subsequent development of a [stage 3 to stage 4] pressure ulcer, even with optimal treatment.”⁸ They are unique forms of dangerous pressure ulcers that should be differentiated from superficial stage 1 damage, since they can deteriorate quickly. They should not be confused with a bruise, contusion, hematoma, or gangrene. In addition, dermatologic manifestations (eg, incontinent perineal dermatitis, candidiasis or tinea, maceration, or denudation) should not be classified as a pressure ulcer. Describe skin conditions as what you see. These are not pressure-related assaults.
       A stage 2 pressure ulcer involves the epidermis and the dermis and usually appears clinically as an abrasion, blister, or shallow crater.
       A stage 3 pressure ulcer involves 3 layers of damage, extending to the subcutaneous tissue and presenting clinically as a deep crater. Stage 1 and 2 pressure ulcers are considered partial-thickness tissue loss and heal by regeneration of the epithelium via the hair follicles.
       A stage 4 pressure ulcer (see Figure 1) involves extensive destruction to muscle, bone, or supporting structure.

Figure 1

       An unstageable pressure ulcer is a wound that is covered with devitalized material, making it impossible to visualize the wound bed. Granted, this is probably a full-thickness wound, but technically clinicians cannot stage a wound until they can see the lowest anatomical structural damage.
       Assessment of all wounds, no matter their etiology, should include information on the location; size (ie, length, width, and depth); wound bed (ie, color and type of tissue); any devitalized material; the peri-wound or surrounding skin; exudate or drainage type; amount, color, consistency, and odor; wound margins and any turning under of the wound’s edge (ie, undermining); and assessment of pain and possible causes. The comprehensive assessment should be documented on the medical record and be reevaluated periodically. As the wound changes, so too should the plan of care.
       The National Pressure Ulcer Advisory Panel (NPUAP) is attempting to reach consensus on staging and deep tissue injury. At its February meeting, presentations and discussions reflected shortcomings inherent in the present staging definitions of stage 1 and 2 pressure ulcers and how they do not capture deep tissue injury.8 The European Pressure Ulcer Advisory Panel (EPUAP) recently published the Statement on Pressure Ulcer Classification, coinciding with similar issues brought forth by the NPUAP.^10,11 Its new classification includes 4 grades of pressure ulcers.

Caveats

       Keep in mind that only a full-thickness wound (stage 3 and 4 pressure ulcers) can develop devitalized material, such as slough and/or eschar. These wounds heal by granulation, contraction, and, finally, epithelialization. Since the various strata (ie, muscle, fascia, subcutaneous) are not replaced, a wound does not reverse stages as it heals or closes.¹¹ For example, a stage 3 pressure ulcer is always a stage 3 pressure ulcer, even as it granulates, contracts, and epithelializes to closure. A stage 3 does not become a stage 2 or stage 1, for instance. It could be described in terms of percentage of healing as the size of the wound decreases. (A helpful way to quantify healing is the Pressure Ulcer Scale for Healing (PUSH) tool available at http://www.npuap.org.)
       Even after a wound has granulated and epithelialized to closure, the tissue continues to “remodel” and gain strength for up to 2 years. Furthermore, the healed tissue will never regain all of the tensile strength it once had. At best, it will regain 70% to 80% of its original strength.¹²

Skin Tears

       Although skin tears (see Figure 2) are not considered pressure ulcers, it is important to mention these traumatic sores because they tend to occur to some of the same individuals who experience pressure ulcers. As the skin ages, the basement membrane (ie, the junction between the epidermis and the dermis) flattens, making it loose and more prone to traumatic injury and unintentional separation—in essence, a skin tear.

Figure 2

The anatomy of aging skin makes skin tears nearly inevitable in the elderly. In addition, harsh soaps, surfactant cleansers, and nonnutritional moisturizers and protectants containing hydrocarbons (eg, petroleum and mineral oil, which do not contribute to lipid replacement), further add to the skin’s vulnerability. Choosing a skin care regime that replaces soap and harsh surfactant cleansers with pH-balanced, mild cleansers and phospholipids cleansers can decrease the incidence of skin tears and spur overall cost savings and comfort.¹³

Heel Pressure Ulcers

       The heel presents a problematic source of pressure due to its bony prominence, especially in the recumbent individual. Care should be taken to mobilize the immobile, provide good skin care, and off-load the vulnerable heel area with pressure relief equipment. Unlike pressure ulcers on other areas of the body, if the heel ulcer (see Figure 3) is dry, black, and intact, it should be left alone without debridement.

Figure 3

This is considered best practice if there is a chance of compromised blood flow and if there is no edema, redness, or drainage—in other words, a “stable” heel eschar.¹⁴

Healing

       Pressure ulcers do not heal by regeneration; rather, granulation tissue fills in the tissue void, the wound surface contracts, and the wound seals off by epithelization. Muscle, fascia, subcutaneous, and underlying tissue that is destroyed will be replaced by scar tissue. Therefore, the patient is at a higher risk for developing another pressure ulcer in the same area. Prevention measures should commence immediately after healing takes place to reduce the chance of reoccurrence. Simple strategies (eg, continuing the use of a prevention support surface and/or pressure relieving cushion or device, providing good skin care, off-loading problem areas, mobilizing the immobile, and utilizing preventative dressings) can avert future pressure ulcers.
       Treatment of pressure ulcers includes supporting the host medically, surgically, and nutritionally if necessary; mobilizing the immobile; relieving pressure; preparing the wound bed (ie, cleaning, debriding, management of any bioburden, and moisturizing); and trying adjunctive therapies.

Prevention Basics

       Pressure ulcer prevention encompasses alleviating the possible causative factors. If we consider that the lack of viable blood flow to the tissue is the main cause of pressure ulcers, we can further classify that damage into pressure, shear, friction, moisture, and heat and therefore better support the patient. We can also prevent pressure ulcers by managing various negative effects (see Table 2). (These prevention recommendations are adapted from WOCN’s 2003 Guidelines for Prevention and Management of Pressure Ulcers, which is available at http://www.wocn.org, and guidelines from the US Department of Health and Human Services Agency for Health Care Policy and Research.¹⁵)

Current Controversy

       The latest debate with pressure ulcers is whether they are unavoidable. Are they secondary only to poor care, or are some ulcers simply inescapable? According to CMS (whose guidance is available at http://www.cms.hhs.gov/manuals/pm_trans/R4SOM.pdf), an avoidable pressure ulcer is one that the resident developed while under a facility’s care when the facility did not do one of the following:
• Evaluate the resident’s clinical condition and pressure ulcer risk assessment
• Define and implement interventions that are consistent with resident needs and goals and recognized standards of practice
• Monitor and evaluate the impact of the interventions or revise them as appropriate.
Unavoidable pressure ulcers, according to CMS, are those that the resident develops even though the facility:
• Evaluated the resident’s clinical condition and pressure ulcer risk factors
• Defined and implemented interventions that are consistent with resident needs and goals and recognized standards of practice
• Monitored and evaluated the impact of the interventions
• Revised the approaches as appropriate.
       Keep in mind that it is imperative that we document any and all nonmodifiable risk factors (eg, refusal or inability to eat in addition to the refusal of a feeding tube) that a resident may have and why they may lead to the development of a pressure ulcer. Pressure ulcers will continue to be surrounded by controversy and litigation until we as healthcare providers recognize that the body’s largest organ, the skin, can and will fail just as easily as any other major organ.