48: Pressure Ulcers

Causes

Pressure ulcers are the visible evidence of pathologic changes in the blood supply to dermal tissues. The chief cause is attributed to pressure, or force per unit area, applied to susceptible tissues. However, external pressure or shear force is increasingly viewed as a necessary but insufficient cause for pressure ulcers. In patients exposed to the same pressure load and duration of surgery, individual intrinsic factors appear to play a larger role in development of a pressure ulcer than the tissue interface pressure. Intrinsic factors leading to derangement in tissue perfusion may account for the development of a pressure ulcer, despite the provision of common prevention measures that include pressure reduction. These factors are beginning to be identified but more research is needed.

Management

Therapy for pressure ulcers is generally empiric, based on anecdotal experience, or borrowed from the treatment of patients with acute wounds. It is problematic because of multiple comorbidities, chronic duration of pressure ulcers, and, frequently, the physician's relative unfamiliarity with options.

Recognition of risk, relief of pressure, and optimizing nutritional status are components of both prevention and management guidelines. For persons with identified pressure ulcers, assessing the wound and implementing strategies for local wound care are paramount.

Incidence

The primary source of pressure ulcers appears to be the acute hospital. Among patients who experience pressure ulcers, 57% to 60% do so in the acute hospital. Incidence in hospitalized patients ranges from 3% to 30%; common estimates range from 9% to 13%. A randomized national sample of Medicare beneficiaries estimated a 4.5% incidence of a new hospital-acquired pressure ulcer from 2006 thru 2007. The incidence differs by hospital location; ICU patients and orthopedic patients are at greatest risk. In patients with a hip fracture, 15% develop a pressure ulcer during hospital admission, and one-third develop a pressure ulcer in 1 month. Pressure ulcers develop early in the course of hospitalization, usually within the first week. The incidence of pressure ulcers in nursing homes is difficult to quantitate.

After discharge from the hospital, pressure ulcers remain a major problem in community care settings. Characteristics associated with pressure ulcers include recent institutional discharge, functional impairment, incontinence, and having had a previous ulcer.

Risk Assessment & Risk Factors

In theory, persons who are at high risk for pressure ulcers can be identified, and an increased effort can be directed to preventing ulcers. The classical risk assessment scale is the Norton Score, developed in 1962 and still widely used. Patients are classified using 5 risk factors graded from 1–4. Scores range from 5–20; higher scores indicate lower risk. The generally accepted at-risk score is ≤14; patients with scores <12 are at particularly high risk.

A commonly used risk assessment instrument in the United States is the Braden Scale. This instrument assesses 6 items: sensory perception, moisture exposure, physical activity, mobility, nutrition, and friction/shear force. Each item is ranked from 1 (least favorable) to 3 or 4 (most favorable), with a maximal total score of 23. A score of ≤16 indicates a high risk.

Both the Norton Score and the Braden Scale have good sensitivity (73% to 92% and 83% to 100%, respectively) and specificity (61% to 94% and 64% to 77%, respectively), but poor positive predictive value (approximately 37% at a pressure ulcer incidence of 20%). In populations with a lower incidence of pressure ulcers, such as those in nursing homes, the same sensitivity and specificity produce a positive predictive value of 2%. The net effect of poor positive predictive value means that many patients who will not develop pressure ulcers will receive expensive and unnecessary treatment.

In clinical practice, risk assessment is problematic. A systematic review of 33 clinical trials of risk assessment found no decrease in pressure ulcer incidence that could be attributed to the use of an assessment scale. In long-term care settings, a Braden score had no predictive value for the development of a pressure ulcer.

Because most pressure ulcers develop in the acute hospital, risk assessment in this setting is particularly important. In an ICU, 5 factors contribute to the risk of pressure ulcer after adjusting for 18 univariately significant risk factors: norepinephrine infusion, Acute Physiology and Chronic Health Evaluation (APACHE) II score, fecal incontinence, anemia, and length of stay in the ICU. Independent risk factors for the development of a pressure ulcer after admission to a surgical service include emergency admission (which increased the risk 36-fold), age, days in bed, and days without nutrition.

Risk factors for the prevalence of pressure ulcers at admission include the presence of a fracture (increasing the risk 5-fold), fecal incontinence (increasing the risk 3-fold), and decreased serum albumin level (increasing the risk 3-fold). Applied prospectively to at-risk patients without pressure ulcers, these factors were associated with development of a pressure ulcer.

In functionally limited (bed- or chair-confined) hospitalized patients, 9 factors were associated with the development of pressure ulcers, including nonblanchable erythema (increasing the risk 7-fold), lymphopenia (increasing the risk almost 5-fold), and immobility, dry skin, and decreased body weight (each of which increase the risk 2-fold).

Not surprisingly, risk factors in long-term care populations differ. In this population, the factors associated with development of pressure ulcers are facility dependent. In low-risk nursing homes, difficulty in ambulation, difficulty feeding oneself, and male gender were associated with a 2- to 4-fold risk of pressure ulcer. In high-risk nursing homes, difficulty with ambulation, fecal incontinence, difficulty feeding oneself, and diabetes mellitus predicted pressure ulcer development.

The risk of pressure ulcer may include a history of cerebrovascular accident (5-fold increase), bed or chair confinement (3.8-fold increase), and impaired nutritional intake (2.8-fold increase). In data derived from the Minimal Data Set, logistic regression analysis determined that dependence in transfer or mobility, confinement to bed, history of diabetes mellitus, and a history of pressure ulcer were significantly associated with an existing stages II–IV pressure ulcer.

In community-dwelling persons age 55–75 years, the presence of a pressure ulcer was predicted by self-assessed poor health, current smoking, dry or scaly skin on examination, and decreased activity level.

The importance of these epidemiologic risk predictors lies in understanding which factors are amenable to correction. Risk factor predictors from various sites suggest that immobility, dry skin, and nutritional factors are potentially modifiable. Efforts have centered on correction of these problems.

Quality of Care

Pressure ulcers are increasingly used as indicators of quality of care. Whether or not pressure ulcers are preventable remains controversial. When aggressive measures for prevention of pressure ulcers have been applied, a “floor effect” for incidence has been noted. Pressure ulcers often occur in terminally ill patients, for whom the goals of care may not include prevention of pressure ulcers. Pressure ulcers also occur in severely ill patients, such as orthopedic patients or ICU patients, for whom the necessity for immobilization may preclude turning or the use of pressure-relieving devices.

Systematic efforts at education, heightened awareness, and specific interventions by interdisciplinary wound teams suggest that a high incidence of pressure ulcers can be reduced. Over time, reductions of 25% to 30% have been reported. The reduction may be transient, unstable over time, vary with changes in personnel, or occur as a result of random variation. Development of pressure ulcers can be, but is not always, a measure of quality of care.

Pressure Relief

The first efforts toward prevention should be to improve mobility and reduce the effects of pressure, friction, and shear forces. The theoretical goal is to reduce tissue pressure below capillary closing pressure of 32 mm Hg. If the target pressure reduction is unachievable, then pressure must be intermittently relieved to allow time for tissue recovery.

The most expedient method for reducing pressure is frequent turning and positioning. A 2-hour turning schedule for spinal injury patients was deduced empirically in 1946. However, turning the patient to relieve pressure may be difficult to achieve despite best nursing efforts and is very costly in terms of staffing. The exact interval for optimal turning in prevention is unknown. The interval may be shortened or lengthened by host factors. Despite commonsense approaches to turning, positioning, and improving passive activity, no published data support the view that pressure ulcers can be prevented by passive positioning.

Because of the limitations and cost of turning schedules, a number of devices have been developed to prevent pressure injury. Devices can be defined as pressure relieving (consistently reducing interface pressure <32 mm Hg) or pressure reducing (less than standard support surfaces but not <32 mm Hg). The majority of devices are pressure reducing. Pressure-reducing devices can be further classified as static or dynamic. Static surfaces attempt to distribute local pressure over a larger body surface. Examples include foam mattresses and devices filled with water, gel, or air. Dynamic devices use a power source to alternate air currents and promote uniform pressure distribution over body surfaces. Examples include alternating pressure pads, air suspension devices, and air–fluid surfaces.

Some pressure-reducing devices have been proven more effective than “standard” hospital foam mattresses in moderate- to high-risk patients. Pressure-relieving mattresses in the operating theater have reduced the incidence of pressure sores postoperatively. Limited evidence suggests that low-air-loss beds reduce the incidence of pressure sores in ICUs. The differences among devices are unclear and do not demonstrate a superior device compared with other devices. There is some evidence that air–fluid beds and low-air-loss beds improve healing rates.

Nutritional Interventions

One of the most important reversible factors contributing to wound healing is nutritional status. Of newly hospitalized patients with stage III or stage IV pressure ulcers, most were below their usual body weight, had a low prealbumin level, and were not taking in enough nutrition to meet their needs.

The results of trials to increase improve pressure ulcer healing have been disappointing. Only 1 of 5 trials has shown a small effect of nutritional supplements on prevention of pressure ulcers. In addition, overnight supplemental enteral feeding has not been shown to affect development of pressure ulcers and severity.

Basal metabolic rate appears to be similar or slightly increased in persons with a pressure ulcer. Clinical judgement and prediction equations suggest an caloric intake of 30 kcal/kg per day. An optimum dietary protein intake in patients with pressure ulcers is unknown but may be much higher than current adult recommendations of 0.8 g/kg per day. Half of chronically ill older persons are unable to maintain nitrogen balance at this level. Increasing protein intake beyond 1.5 g/kg per day may not increase protein synthesis and may cause dehydration. A reasonable protein requirement is, therefore, between 1.2–1.5 g/kg per day.

The deficiency of several vitamins has significant effects on wound healing. However, supplementation of vitamins to accelerate wound healing is controversial. There is no substantial evidence to support use of a daily vitamin C supplement for healing pressure sores.

Zinc supplementation has not been shown to accelerate healing except in zinc-deficient patients. High serum zinc levels interfere with healing, and supplementation >150 mg/day may interfere with copper metabolism.

Immune function declines with age, which increases risk for infection, and is thought to delay wound healing. Specific amino acids such as arginine and branched-chain amino acids have not demonstrated an effect on pressure ulcer healing.

Several differing scales have been proposed for assessing the severity of pressure ulcers. The most common staging, recommended by the National Pressure Ulcer Task Force, is derived from a modification of the Shea Scale. Under this schematic, pressure ulcers are divided into 6 clinical stages.

The first response of the epidermis to pressure is hyperemia. Blanchable erythema occurs when capillary refilling occurs after gentle pressure is applied to the area. Nonblanchable erythema exists when pressure of a finger in the reddened area does not produce a blanching or capillary refilling. A stage I pressure ulcer is defined by nonblanchable erythema of intact skin. Nonblanchable erythema is believed to indicate extravasation of blood from the capillaries. A stage I pressure ulcer always understates the underlying damage because the epidermis is the last tissue to show ischemic injury. Diagnosing stage I pressure ulcers in darkly pigmented skin is problematic.

Stage II ulcers extend through the epidermis or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater. With stage III pressure ulcers, there is full-thickness skin loss involving damage or necroses of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.

Stage IV pressure ulcers are full-thickness wounds with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures. Undermining and sinus tracts are frequently associated with stage IV pressure ulcers. Stage I pressure ulcers occur most frequently, accounting for 47% of pressure ulcers, followed by stage II ulcers (33%). Stages III and IV ulcers comprise the remaining 20%.

This staging system for pressure ulcers has several limitations. The primary difficulty lies in the inability to distinguish progression between stages. Pressure ulcers do not progress absolutely through stage I to stage IV, but may appear to develop from the inside out as a result of the initial injury. Healing from stage IV does not progress through stage III to stage I; rather, the ulcer heals by contraction and scar tissue formation. Second, clinical staging is inaccurate unless all eschar is removed, because the staging system reflects only depth of the ulcer.

Because the staging system is based only on the depth of an ulcer, an ulcer that is covered by eschar, or when the depth is unable to be assessed, is designated as “unstageable.”

Muscle tissue, subcutaneous fat, and dermal tissue are differentially susceptible to injury, in that order. The differential effect of pressure on the tissue layers suggests that injury occurs first in muscle tissue before changes are observed in the skin. This is the basis for the so-called deep tissue injury. In many cases, the changes visible at the surface of the tissue are minor compared to the damage seen at the deepest layers of tissue. The surface discoloration is often classified as a stage I pressure ulcer, which rapidly evolves into a deep stage IV ulcer. This differential tissue susceptibility suggests that a number of factors are involved in the development of pressure ulcers, including the type of pressure load and biochemical changes in the tissue because of reperfusion injury or tissue compression.

Because pressure ulcers heal by contraction and scar formation, reverse staging is inaccurate in assessing healing. No single measure of wound characteristics has been useful in measuring healing. Several indexes of ulcer healing have been proposed but lack validation studies. The Pressure Ulcer Status for Healing (PUSH) tool (Figure 48–1) was developed and validated by the National Pressure Ulcer Advisory Panel to measure healing of pressure ulcers. The tool measures 3 components—size, exudate amount, and tissue type—to arrive at a numerical score for ulcer status. The PUSH tool adequately assesses ulcer status and is sensitive to change over time.

Acute wounds proceed through an orderly and well-described process to produce healing with structural and functional integrity. Chronic wounds fail to proceed through this process and result in poorly healing wounds of long duration. There are 4 types of chronic wounds: peripheral arterial ulcers, diabetic ulcers, venous stasis ulcers, and pressure ulcers. Each of these wounds differ in their underlying pathophysiology, and, more importantly, differ with respect to local wound treatment.

Arterial ulcers tend to occur over the distal part of the leg, especially the lateral malleoli, dorsum of the feet, and the toes. The clinical appearance is that of gangrene, which can be wet or dry. Arterial ulcers tend to be painful, and pain control features prominently in their management. Peripheral arterial disease results from atherosclerosis of aorta, iliac and lower extremity arteries. Ischemic vascular ulcers are difficult to heal, and therapy is aimed at improving blood flow. A careful examination for arterial pulses may be useful, but is dependent on the examiner's skill and may be misleading. An ankle-brachial pressure index is an inexpensive and accurate diagnostic test for peripheral arterial disease.

The etiology of diabetic ulcers is multifactorial. Among these, the presence of neuropathy is the most important factor in the development of a diabetic ulcer, while inadequate vascular supply is the most important factor in healing. Diabetic ulcers typically occur in areas of repetitive trauma, producing a callus formation. Microvascular changes in blood flow lead to a deep crater-like appearance, especially in areas of foot deformity.

The underlying pathophysiology of venous leg ulcers includes reflux, obstruction, or insufficiency of the calf muscle pump, involving the superficial venous system (greater and smaller saphenous vein), the deep venous system, or the veins that perforate between those systems. The etiology of chronic deep venous disease results from primary (often idiopathic) or secondary causes (postthrombotic obstruction), but most commonly represents a combination of both. The skin in chronic venous stasis disease demonstrates hyper- or hypopigmentation, lipodermatosclerosis, weeping of the skin, and ulceration. Edema is often present but not necessary for the diagnosis. A venous leg ulcer is irregularly shaped and shallow, but with well-defined borders. Location is usually from the malleolar area upwards to the knee (the “gaiter” area, so-called because this area is covered by leggings known as gaiters). The ulcer bed is often exudative, and bacterial and fungal overgrowth on the wound and surrounding skin surface is common.

Pressure ulcers are the visible evidence of pathologic changes in the blood supply to dermal tissues. Pressure ulcers usually occur over bony prominences, when the tissue is compressed to pressures above capillary closing pressure. However, patient-specific intrinsic factors may lessen the time or pressure amounts required to produce tissue damage. The most common site for the development of a pressure ulcers is the sacrococcygeal area, followed by the heels.

All of the 4 types of chronic wounds have in common some relationship to pressure. However, the classification of these wounds should be related to the underlying pathophysiology in respect to treatment.

Colonization of chronic wounds with bacteria is common and unavoidable. All chronic wounds become colonized, usually with skin organisms followed in 48 hours by Gram-negative bacteria. The presence of microorganisms alone (colonization) does not indicate an infection in pressure ulcers. The primary source of bacterial infections in chronic wounds appears to be the result of suprainfection resulting from contamination. Therefore, protection of the wound from secondary contamination is an important goal of treatment.

Evidence suggests that occlusive dressings protect against clinical infection, although the wound may be colonized with bacteria. Occlusive dressings very rarely cause a clinical infection.

It is often difficult to determine the presence of an infection in chronic pressure ulcers. The diagnosis of infection in chronic wounds must be based on clinical signs: advancing erythema, edema, odor, fever, or purulent exudate. When there is evidence of clinical infection, topical or systemic antimicrobials are required. Topical treatment may be useful when the wound is failing to progress toward healing. Systemic antibiotics are indicated when the clinical condition suggests spread of the infection to the bloodstream or bone.

Wounds with extensive undermining create pockets for infection with an increased likelihood for infection with anaerobic organisms. Obliteration of dead space reduces the possibility of infection.

Maintaining a moist wound environment increases the rate of healing. Moist wound healing allows experimentally induced wounds to resurface up to 40% faster than air-exposed wounds. Any therapy that dehydrates the wound such as dry gauze, heat lamps, air exposure, or liquid antacids is detrimental to chronic wound healing.

Dressings allow moisture to escape from the wound at a fixed rate measured by the moisture vapor transmission rate (MVTR). An MVTR of <35 g of water vapor/m²/h is required to maintain a moist wound environment. Woven gauze has an MVTR of 68 g/m²/h, and impregnated gauze has an MVTR of 57 g/m²/h. In comparison, hydrocolloid dressings have an MVTR of 8 g/m²/h.

Dressings that maintain a moist wound environment are occlusive, describing the propensity of a dressing to transmit moisture vapor from the wound to the external atmosphere. The available dressings differ in their properties of permeability to water vapor and in wound protection.

Topical Dressings

Occlusive dressings can be divided into broad categories of polymer films, polymer foams, hydrogels, hydrocolloids, alginates, and biomembranes. Each has several advantages and disadvantages. The choice of a particular agent depends on the clinical circumstances. The agents differ in the ease of application. This difference is important in pressure ulcers in unusual locations or when considering their use for home care. Dressings should be left in place until wound fluid is leaking from the sides, a period of days to 3 weeks.

Polymer films—

Polymer films are impermeable to liquid but permeable to both gas and moisture vapor. Because of low permeability to water vapor, these dressings are not dehydrating to the wound. Nonpermeable polymers such as polyvinylidene and polyethylene can be macerating to normal skin. Polymer films are not absorptive and may leak, particularly when the wound is highly exudative. Most films have an adhesive backing that may remove epithelial cells when the dressing is changed. Polymer films do not eliminate dead space and do not absorb exudate.

Hydrogels—

Hydrogels are 3-layer hydrophilic polymers that are insoluble in water but absorb aqueous solutions. They are poor bacterial barriers and do not adhere to the wound. Because of their high specific heat, these dressings are cooling to the skin, aiding in pain control and reducing inflammation. Most of these dressings require a secondary dressing to secure them to the wound.

Hydrocolloid dressings—

Hydrocolloid dressings are complex dressings similar to ostomy barrier products. They are impermeable to moisture vapor and gases (their impermeability to oxygen is theoretically a disadvantage) and are highly adherent to the skin. In addition, they offer bacterial resistance. Their adhesiveness to surrounding skin is higher than some surgical tapes, but they do not adhere to wound tissue and do not damage epithelialization of the wound. The adhesive barrier is frequently overcome in highly exudative wounds. Hydrocolloid dressings cannot be used over tendons or on wounds with eschar formation. Several of these dressings include a foam padding layer that may reduce pressure to the wound.

Alginates—

Alginates are complex polysaccharide dressings that are highly absorbent in exudative wounds. This high absorbency is particularly suited to exudative wounds. Alginates do not adhere to the wound; however, if the wound is allowed to dry, damage to the epithelial tissue may occur with removal.

Biomembranes—

Biomembranes offer bacterial resistance but are very expensive and not readily available. These dressings could be problematic in wounds contaminated by anaerobes, but this effect has not been demonstrated clinically.

Saline-soaked gauze—

Saline-soaked gauze that is not allowed to dry is an effective wound dressing. Moist saline gauze and occlusive-type dressings have similar pressure ulcer-healing abilities. The use of occlusive-type dressings has been shown to be more cost-effective than traditional dressings primarily because of a decrease in nursing time for dressing changes. Table 48–1 provides a comparison of dressing types. Table 48–2 presents general guidelines.

Growth Factors

Acute wound healing proceeds in a carefully regulated fashion that is reproducible from wound to wound. A number of growth factors have been demonstrated to mediate the healing process, including transforming growth factor-α and -β, epidermal growth factor, platelet-derived growth factor, fibroblast growth factor, interleukin-1 and -2, and tumor necrosis factor-α. Accelerating healing in chronic wounds using these acute wound factors is attractive. Several of these factors have been favorable in animal models; however, they have not been as successful in human trials.

In pressure ulcers, recombinant platelet-derived growth factor (rhPDGF-BB) failed to improve the rate of complete healing, although a 15% difference in percentage of initial volume of ulcers has been shown with PDGF-BB. One report showed that more subjects had >70% wound closure with basic fibroblast growth factor. Sequential application of growth factors to mimic wound-healing progression has not been effective in pressure ulcers.

Adjunctive Therapies

Alternative or adjunctive therapies include electrical therapy, electromagnetic therapy, ultrasound therapy, low-level light therapy/laser therapy, and vacuum-assisted closure. None of these interventions has been clearly proven effective despite widespread clinical use.

Debridement

Necrotic debris increases the possibility of bacterial infection and delays wound healing. The preferred method of debriding pressure ulcers remains controversial. Options include mechanical debridement with dry gauze dressings, autolytic debridement with occlusive dressings, application of exogenous enzymes, or sharp surgical debridement.

Surgical sharp debridement produces the most rapid removal of necrotic debris and is required in the presence of infection. Mechanical debridement can be easily accomplished by allowing a saline gauze dressing to dry before removal. Remoistening of gauze dressings in an attempt to reduce pain can defeat the debridement effect.

Both surgical and mechanical debridement can damage healthy tissue or fail to clean the wound completely. Debridement with a dry gauze should be stopped as soon as a clean wound bed is obtained because dry dressings have been associated with delayed healing.

Thin portions of eschar can be removed by occlusion under a semipermeable dressing. Both autolytic and enzymatic debridement require periods of several days to several weeks to achieve results. Enzymatic debridement can dissolve necrotic debris, but whether it harms healthy tissue is debated. Penetration of enzymatic agents is limited in eschar and requires either softening by autolysis or cross-hatching by sharp incision before application.

Only 1 enzyme preparation is available in the United States for débridement. Topical collagenase reduced necrosis, pus, and odor compared with inactivated control ointment and produced debridement in 82% of pressure ulcers at 4 weeks compared with petrolatum. Papain produced measurable debridement in 4 days compared with a control ointment. The issues of when to debride and which method to use remain controversial. Whether debridement improves the rate of healing remains undetermined.

A total of 5 trials have not shown that the use of enzymatic agents increased the rate of complete healing in chronic wounds compared with control treatment.

Surgical Therapy

Surgical closure of pressure ulcers results in a more rapid resolution of the wound. The chief problems are frequent recurrence of ulcers and inability of frail patients to tolerate the procedure.

The efficacy of surgical repair of pressure ulcers is high in the short-term; however, its long-term efficacy has been questioned. Problems with surgical repair include suture line dehiscence, nonhealing, and recurrence.

The proportion of pressure ulcers suitable for operation depends on the patient population, but normally only a low percentage are candidates for surgery. However, among selected groups of patients, such as those with spinal cord injury and deep stage III or IV pressure ulcers, surgery may be indicated for the majority. If the factors contributing to the development of the pressure ulcer cannot be corrected, the chance of recurrence after surgery is very high.

Pressure ulcers have been associated with increased mortality rates in both acute and long-term care settings. Death has been reported during acute hospitalization in 67% of patients who develop a pressure ulcer compared with 15% of at-risk patients without pressure ulcers. Patients who develop a new hospital-acquired pressure ulcer are 2.8 times as likely to die in the hospital compared to persons without a pressure ulcer. The odds ratio for mortality in 30 days is 1.7 times as high, and readmission within 30 days is 1.3 times as high. In long-term care settings, development of a pressure ulcer within 3 months among newly admitted patients was associated with a 92% mortality rate compared with 4% among residents who did not subsequently develop a pressure ulcer. Residents in a skilled nursing facility who had pressure ulcers experienced a 6-month mortality rate of 77.3% compared with 18.3% in those without pressure ulcers. Patients whose pressure ulcers healed within 6 months had a significantly lower mortality rate (11% vs. 64%) than those whose pressure ulcers did not heal.

Despite this association with death rates, it is not clear how pressure ulcers contribute to increased mortality. Patients with stage II pressure ulcers have been equally as likely to die as those with stage IV pressure ulcers. In the absence of complications, it is difficult to imagine how stage I or II pressure ulcers contribute to death. Pressure ulcers may be associated with mortality because of their occurrence in otherwise frail, sick patients.