David R. Thomas MD, FAGS, FACP
ESSENTIALS OF DIAGNOSIS
Pressure ulcers are the visible evidence of pathological changes in the blood supply to dermal tissues. The chief cause is pressure, or force per unit area, applied to susceptible tissues. Comorbid conditions, especially those resulting in immobility or reducing tissue perfusion, greatly increase the risk of pressure ulcers.
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.
Thomas DR: Issues and dilemmas in the prevention and treatment of pressure ulcers: a review. J Gerontol Biol Sci Med Sci 2001;56:M328. [PMID: 11382790]
Thomas DR: Prevention and treatment of pressure ulcers: what works? What doesn't? Cleve Clin J Med 2001;68:704. [PMID: 11510528]
Thomas DR, Kamel HK: Wound management in postacute care. Clin Geriatr Med 2000;16:783. [PMID: 10984756]
The primary source of pressure ulcers appears to be the acute hospital. Among patients who experience pressure ulcers, 57–60% do so in the acute hospital. Incidence in hospitalized patients ranges from 3–30%; common estimates range from 9–13%. The incidence differs by hospital location; intensive care unit (ICU) patients and orthopedic patients are at greatest risk. Up to 66% of orthopedic patients have pressure ulcers of varying severity. 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. Pressure-relieving devices and other wound care strategies appeared to be underused and often indiscriminately applied.
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 (73–92% and 83–100%, respectively) and specificity (61–94% and 64–77%, respectively) but poor positive predictive value (~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 has been problematic for 2 reasons. First, risk assessment is not universally applied. Less than 50% of the high-risk elderly persons admitted to acute care with a hip fracture had any sort of risk assessment performed. It is possible that resistance to implementing risk assessment models is due to recognition by clinicians that the instruments are inadequate. Second, no risk assessment study has demonstrated that persons identified at risk or who have a plan of care based on risk assessment are less likely to develop 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, 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 stage II–IV pressure ulcer.
In community-dwelling persons aged 55–75, 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 epidemiological 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.
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 25–30% 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.
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 32mm 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-h turning schedule for spinal injury patients was deducted 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. Seat cushions and simple, constant-low-pressure devices have not been adequately evaluated. There is good evidence that air-fluid beds and low-air-loss beds improve healing rates.
Clark M: Repositioning to prevent pressure sores what is the evidence? Nurs Standard 1998;13:56. [PMID: 9847811]
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 nutrient intake have been disappointing. It has been suggested that nutritional supplements have no effect on prevention of pressure ulcers. In addition, overnight supplemental enteral feeding has not been shown to affect development of pressure ulcers and severity.
Dietary intake, especially of protein, is important in healing pressure ulcers. An optimum dietary protein intake in patients with pressure ulcers is unknown but may beM much higher than current adult recommendations of 0.8 g/kg/day. Half of chronically ill elderly persons are unable to maintain nitrogen balance at this level. Increasing protein intake beyond 1.5 g/kg/day may not increase protein synthesis and may cause dehydration. A reasonable protein requirement is, therefore, between 1.2–1.5 g/kg/day.
The deficiency of several vitamins has significant effects on wound healing. However, supplementation of vitamins to accelerate wound healing is controversial. There is insubstantial 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. Arginine supplementation has not been shown to enhance the proliferative response or pressure ulcer outcome.
Houston S et al: Adverse effects of large-dose zinc supplementation in an institutionalized older population with pressure ulcers. JAm Geriatr Soc 2001;9:1130. [PMID: 11555083]
Thomas DR: Improving outcome of pressure ulcers with nutritional interventions: a review of the evidence. Nutrition 2001;17:121. [PMID: 11240340]
Thomas DR: The role of nutrition in prevention and healing of pressure ulcers. Clin Geriatr Med 1997;13:497. [PMID: 9227941]
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 4 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%). Stage 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 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 28-1) 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.
Stotts NA et al: An instrument to measure healing in pressure ulcers: development and validation of the pressure ulcer scale for healing (PUSH). J Gerontol Biol Sci Med Sci 2001;56:M795. [PMID: 11723157]
Colonization of chronic wounds with bacteria is common and unavoidable. All chronic wounds become colonized, usually with skin organisms followed in 48 h by gram-negative bacteria. The presence of micro-organisms 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.
Figure 28-1. PUSH tool version 3.0
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.
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 interleukin-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.
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.
Necrotic debris increases the possibility of bacterial infection and delays wound healing. The preferred method of débriding pressure ulcers remains controversial. Options include mechanical débridement with dry gauze dressings, autolytic débridement with occlusive dressings, application of exogenous enzymes, or sharp surgical débridement. Surgical sharp débridement produces the most rapid removal of necrotic debris and is required in the presence of infection. Mechanical débridement 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 débridement effect. Both surgical and mechanical débridement can damage healthy tissue or fail to clean the wound completely. Débridement 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 débridement require periods of several days to several weeks to achieve results. Enzymatic débridement 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.
Three enzyme preparations are currently marketed in the United States for débridement: collagenase, papain/urea, and a papain/urea-chlorophyll combination. Collagenase reduced necrosis, pus, and odor compared with inactivated control ointment and produced
débridement in 82% of pressure ulcers at 4 weeks compared with petrolatum. Papain produced measurable débridement in 4 days compared with a control ointment. The issues of when to débride and which method to use remain controversial. Whether débridement improves the rate of healing remains undetermined.
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. It has been shown, however, that growth factor treatment may improve the outcome of surgical repair.
Bradley M et al: Systematic reviews of wound care management: dressings and topical agents used in the healing of chronic wounds. Health Tech Assess 1999;3:1. [PMID: 10683589]
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 pressure ulcer within 6 weeks after hospitalization are 3 times as likely to die as those who do not develop a pressure ulcer. In long-term care settings, development of a pressure ulcer within 3 mo 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-mo mortality rate of 77.3% compared with 18.3% in those without pressure ulcers. Patients whose pressure ulcers healed within 6 mo had a significantly lower mortality rate (11% vs. 64%) than those whose pressure ulcers did not heal.
Table 28-1. Comparison of occlusive wound dressings.
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.
Thomas DR: Are all pressure ulcers avoidable? J Am Med Direct Assoc 2001;2:297.
effective in improving the healing rate of pressure ulcers. However, it is difficult to distinguish among various devices.
Table 28-2. Therapeutic recommendations for treatment of pressure ulcers.