Pressure Ulcers and Wound Care 

Pressure ulcers, or PRUs, have affected humans for ages, and addressing the overall management of pressure ulcers is now a prominent national healthcare issue. Despite current interest and advances in medicine, surgery, nursing care, and self-care education, pressure ulcers remain a major cause of morbidity and mortality. This is particularly true for persons with impaired sensation, prolonged immobility, or advanced age.^[1] See the image below.

Research in the area of pressure ulcers, specifically in characterization, prevention, and treatment of pressure ulcers, is important in preventing secondary complications in persons with disabilities. As the standards of acute, posttraumatic, and rehabilitation care improve, the population of persons with lifelong functional impairments continues to grow. Consequently, the prevention of secondary complications has become an increasingly prominent concern.

Definitions

Webster's New Riverside University Dictionary defines an ulcer as "an inflammatory, often suppurating lesion on the skin or an internal mucosal surface of the body, as in the duodenum, resulting in necrosis of the tissue." Dorland's Medical Dictionary describes an ulcer (Latin, ulcus; Greek, heliosis) as "a local defect or excavation on the surface of an organ or tissue which is produced by sloughing of inflammatory necrotic tissue."

The National Pressure Ulcer Advisory Panel (NPUAP) is an independent nonprofit organization formed in 1987 and dedicated to the prevention, management, treatment, and research of pressure ulcers. The NPUAP defines a pressure ulcer as an area of unrelieved pressure over a defined area, usually over a bony prominence, resulting in ischemia, cell death, and tissue necrosis.^[2]

Description

The taxonomic description of pressure ulcers lacks general consistency.^{[1, 3, 4]} Textbooks refer to these lesions in various ways, usually in regard to the depth of the lesion based on macroscopic and morphologic criteria.^[2] The ulcers are often referred to as pressure sores, bedsores, or decubitus ulcers (from the Latin word decumbere, which means "to lie on one's side"). Because persons at risk can develop lesions in various positions (eg, sitting), the term pressure ulcers is used in this article.

Measurement

Standardized measuring techniques are necessary to provide quantitative information on wound healing and to validate research.

The most common method of monitoring the healing of pressure ulcers utilizes photography and diagrams.^[4] The Vista MED wound measurement system, manufactured by Verg, Inc (Manitoba, Winnipeg, Canada), uses color-balanced and light-balanced computerized photographic images to help clinicians obtain precise objective information about the size, shape, outline, area, and color of the wound. It also provides objective information regarding the changes of surrounding tissue.

In addition, digital subpixel techniques are available to measure clinician-defined image areas, such as wound edges, eschar, necrotic tissue, or granulation formation. Concise documented measurement contributes to efficient wound treatment, management, and progress review.

Numerous other devices have been used to measure the volume (volumetrics) and the dimensions of the pressure ulcer wound. One simple method is to use a measured amount of saline to infer the volume of the wound. More sophisticated radiographic techniques, such as sinus radiographs, CT scans, and MRIs, are available but too expensive for routine use.^[4]

Common sites of involvement

Several studies reveal varying sites of occurrence with different diagnoses.^{[1, 2, 3, 5, 6, 7]} These sites of occurrence include the ischium (28%), the sacrum (17-27%), the trochanter (12-19%), and the heel (9-18%). See the image below.

Pressure ulcers commonly develop on the occiput of geriatric and pediatric patients who spend extended amounts of time lying supine. Patients with the secondary manifestations of osteoporosis and associated thoracic kyphosis can develop pressure ulcers over the spinous processes. Elderly patients and patients with diabetes often have pressure ulcers on the heel.

Epidemiology

According to Gosnell and VanEtten, approximately 1 million pressure ulcers occur in the United States; however, definitive information on the epidemiology and natural history of this condition is still limited. Unfortunately, studies to date have been encumbered by methodologic issues and variability in describing the lesions.^{[2, 8]}

The incidence in hospitalized patients ranges from 2.7%^[9] to 29%, and the prevalence in hospitalized patients is 3.5%^[10] to 69%.^[11] Patients in critical care units have an increased risk of pressure ulcers, as evidenced by a 33% incidence^[12] and 41% prevalence.^[13] Elderly patients admitted to acute care hospitals for nonelective orthopedic procedures, such as hip replacement and treatment of long bone fractures, are at even greater risk, with a 66% incidence.^{[14, 15]}

In the nursing home environment, the prevalence of pressure ulcers is in the range of 2.6-24%.^{[8, 16]} The incidence is 25% in residents admitted from an acute care hospital.^[16] Patients with preexisting pressure ulcers demonstrate a 26% incidence of additional pressure ulcer formation over a 6-month period. The incidence in chronic care hospitals is reported to be 10.8%,^[17] whereas 33% of those admitted to a chronic care hospital have pressure ulcers.^[18] Long-term follow-up demonstrates that most ulcers healed within a year.^{[8, 18]}

Persons with spinal cord injury (SCI) and associated comorbidity are also at increased risk.^{[19, 20]} The incidence of pressure ulcers in this population is in the range of 25-66%.^{[6, 21]}

One study of the prevalence of pressure ulcers in community residents with SCI demonstrated that those with higher-level SCI lesions carry a greater risk of developing pressure ulcers than those with lower-level lesions. Of 100 patients with pressure ulcers, 33 had ulcers that were classified as stage 2 or greater. Blacks (n =13) had more severe ulcers than other racial groups in the study.^[6] Some authors speculate that detecting erythema can be more difficult with skin that has darker pigmentation.^[22] This difficulty can result in undetected grade I pressure ulcers, as prolonged nonblanching erythema is typically an early warning sign of pressure ulcer risk and development.

Economic impact

In 1991, a market study was performed to estimate the treatment costs and the costs of hospitals stays for patients who developed ulcers during hospitalization. These costs were estimated to be as much as $6 billion a year. In elderly populations and in those who are institutionalized, pressure ulcers are one of the most costly diseases to treat.

These ulcers add an estimated burden of over $1 billion of expenditures and an additional 2.2 million Medicare hospital days to the United States healthcare system.^[23] The cost of treatment is $2000-$40,000 per pressure ulcer,^{[2, 24, 25]} depending on the stage of development.^{[26, 27]}

For reconstructive surgery, costs are estimated at $25,000 per patient.^[2] These costs alone, without the cost of human suffering, demonstrate the importance of preventing pressure ulcers and of cost-effective treatment practices.

A 2011 cost-effective analysis study by Pham et al determined that both clinical and economic evidence maintains that pressure redistribution mattresses should be used to prevent pressure ulcers in long-term care patients. In addition, the study found that perineal foam cleansers and dry skin emollients are also economical ways to stop pressure ulcers from developing.^[28] Pham et al also concluded in a separate study that pressure redistribution foam mattresses should also be used to help improve elderly patients' health and save hospital expenses in the emergency department.^[29]

Morbidity and mortality

Patients predisposed to pressure ulcers are at higher risk of morbidity and mortality. Infection is the most common major complication of pressure ulcers. The offending pathologic organisms in pressure ulcers can be anaerobic or aerobic. Aerobic pathogens commonly are present in all pressure ulcers,^[30] whereas anaerobes tend to be present more often in larger wounds (65% in grade III and above).^[31]

The most common organisms isolated from pressure ulcers are Proteus mirabilis, group D streptococci, Escherichia coli, Staphylococcus species, Pseudomonas species, and Corynebacterium organisms. Patients with bacteremia are more likely to have Bacteroides species in their pressure ulcers.^[31] These wounds do not need to be cultured routinely unless systemic signs of infection are present (eg, malodorous drainage, leukocytosis, fever, hypotension, increased heart rate, changes in mental status).

Clinical alertness is needed because the signs commonly associated with impeding or fulminating infection are frequently absent in elderly patients or in patients who are immunocompromised. In geriatric patients with pressure ulcers, bacteremia is reported to occur at the rate of 3.5 per 10,000 hospital discharges.^[23] Because the mortality rate in this population approaches 50%,^[32] antibiotic treatment for wound infection or secondary bacteremia provides the appropriate spectrum of coverage specific to the offending organisms. Because indiscriminate use of antibiotics leads to resistant organisms and because the specific drugs of choice and antimicrobial agents change rapidly, physiatrists typically need to consult an infectious disease specialist to facilitate the management of these complex problems.

Sepsis also can occur secondary to osteomyelitis, which has been reported to occur in 26% of nonhealing ulcers.^[23] A prospective study demonstrated that osteomyelitis was associated with nonhealing grade IV pressure ulcers in 86% of the study population.^{[33, 34]} This study utilized 3-phase technetium methyl diphosphate radionuclide flow to detect early osteomyelitis.

Various tests can be used to diagnose osteomyelitis in patients with pressure ulcers. Plain radiographs have a sensitivity of 78% and a specificity of 50%, but radiographic findings often are not present in the early stages of infection. Bone scans are more sensitive, but they have low specificity (50%). Bone biopsy has the highest specificity (96%) and sensitivity (73%).^{[33, 34]}

A combination of diagnostic tests, such as a determination of the leukocyte count and erythrocyte sedimentation rate (ESR) with plain radiography provides a sensitivity of 89% and a specificity of 88%. If all 3 test results are positive, the positive predictive value of this combination is 69%. If all 3 test results are negative, the negative predictive value is 96%.^{[33, 34]}

Osteomyelitis should be considered whenever an ulcer does not heal, especially if the ulcer is over a bony prominence. Clinicians also should rule out other conditions associated with nonhealing ulcers, such as heterotopic calcification or ossification. Most findings indicate that antibiotic treatment for osteomyelitis should last 6-8 weeks. Surgery is needed for some cases of chronic osteomyelitis.^[19]

Systemic amyloidosis can result from chronic suppurative pressure ulcers. Additional complications of pressure ulcers include spreading cellulitis, a sinus tract abscess, septic arthritis, squamous cell carcinoma in the ulcer, a periurethral fistula, and heterotopic ossification. Because some of the secondary complications of pressure ulcers can preclude wound healing, they should be aggressively prevented and treated.^[4] Complications may include infection, pain, depression, and even death.

Approximately 60,000 people die each year from complications of pressure ulcers.^[3] Development of pressure ulcers has been associated with a 4.5-times greater risk of death than that for persons with the risk factors but without pressure ulcers.^[23] A secondary complication, wound-related bacteremia, can increase the risk of mortality to 55%.^{[3, 5, 32, 35]}

For patient education resources, see the Skin, Hair, and Nails Center and Diabetes Center, as well as Wound Care and Diabetic Foot Care.

Overview

Numerous diverse etiopathologic factors interact to cause pressure ulcers. These factors can be classified as pathomechanical or pathophysiologic.^{[3, 36, 37]}

Pathomechanical Factors (Extrinsic or Primary)

Prolonged pressure

The most important factor in the development of pressure ulcers is unrelieved pressure.^{[38, 39]} Pressure ulcers arise from prolonged tissue ischemia caused by pressure that exceeds the tissue capillary pressure. Prolonged pressure deprives tissues of oxygen and essential nutrients, owing to ischemia and hypoxia, which then causes the necrosis and ulceration.^[39]

Several critical questions at the heart of pressure ulcer research still remain unanswered: How much pressure is required to produce predictable ulceration? How long must pressure be sustained to produce predictable ulceration? Which tissues are at greatest risk of ulceration?

In 1930, Landis used a microinjection method to cannulate the arteriolar limb of capillaries in human fingernail beds to study capillary blood pressure.^[40] He reported an average pressure of 32 mm Hg in the arteriolar limb, 22 mm Hg in the midcapillary bed, and 12 mm Hg on the venous side. Decades later, these findings were reproduced by utilizing laser Doppler methods in an animal model in which the mean capillary pressure, at 45 mm Hg, approximated human capillary pressure. This finding is useful for future studies of this component of the pressure ulcer cascade.^{[41, 42, 43]}

Interface pressure

Interface pressure remains an ambiguous factor in the development of pressure ulcers. Defined as "perpendicular force per unit area between the body and support surface" by the NPUAP, it is commonly believed that interface pressure is affected by the stiffness and composition of the body tissue and by the geometric shape of the body being supported. While interface pressures less than 32 mm Hg are assumed by many clinicians to be safe, pressures in excess of 32 mm Hg are thought to lead to closure of capillary beds and tissue ischemia. However, these perceptions remain to be challenged.

Products aimed at reducing or relieving pressure have tended to use interface pressure as the standard for judging product efficacy.^{[41, 44]} Further investigation of the application of the criterion standard of 32 mm Hg that resulted from Landis' work to pressure ulcer pathology is needed, particularly since the transmission of load on tissue and muscle can decrease or increase based on characteristics of the tissue at different sites.^[45] Tissue can be more or less able to withstand pressure, depending on other patient characteristics.

The area of pressure as the primary factor in the development of pressure ulcers also requires more thorough study. For example, what helps persons with able bodies to withstand extreme tissue loads in areas at risk and avoid developing pressure ulcers? Why are persons with certain types of disease processes typically free from these ulcers? A few articles have noted that persons with amyotrophic lateral sclerosis are at relatively low risk for developing pressure ulcers because of the dermal thickening and increased collagen secondary to the increased density of the collagen fibrils associated with amyotrophic lateral sclerosis.^[46]

One hypothesis asserts that pressure overcoming capillary closing pressure leads to ischemia and reperfusion injury, notably in the muscle, which develops the lesion and eventually ulcerates. This ischemia-reperfusion mechanism ultimately leads to neutrophil-mediated inflammatory tissue destruction, most likely a free radical injury, that eventually causes pressure ulceration.^{[41, 42, 43]}

Shear

Shear is mechanical stress directed parallel to the plane of interest. Shearing forces have been implicated as pathomechanical contributors in the development of pressure ulcers, especially those on the sacrum. Though scientific evidence is lacking, it is logical to conclude that the angular and vertical force that occurs downward when patients are in the semi-upright position in bed tends to distort the tissues and blood vessels near the sacrum, placing this region at risk for tissue breakdown.^{[37, 47]} Furthermore, in a research project focused on assessing the pressure-reducing effects of operating-table mattresses, Defloor et al concluded that elevation of the top end of the operating table at 30° might cause high pressure and shearing force on the sacrum during head and neck surgery.^[48] The synergy of shear and pressure leads to the formation of pressure ulcers.

Friction

Friction is the force of 2 surfaces moving across one another.^[32] Friction and the increased drag coefficient that occurs when moving patients across bedsheets and other support surfaces can cause microscopic or macroscopic tissue trauma. Moisture, maceration, and tissue breakdown increase the surface tension of the skin and the support surface. Moisture from sensible fluid loss or incontinence leads to maceration of tissues, which in turn makes the tissues more susceptible to pressure, shear, and friction damage.

Immobility

Immobility is a major extrinsic factor associated with the risk and formation of pressure ulcers. Immobility in bed tends to cause pressure ulcers on the occiput, sacrum, heels, malleoli, and trochanteric regions, whereas patients who use wheelchairs for mobility tend to develop pressure ulcers over the ischial tuberosity.^[49]

In patients who are paralyzed or who are neurologically compromised or who underwent prolonged periods of sedation or anesthesia, the afferent nerves are unable to engage the sensorimotor feedback system. As a result, early warnings of prolonged ischemia, such as discomfort, do not produce the normal adjustments in body position that intermittently relieve pressure on areas at risk.^[32] Such adjustments occur instinctively in persons who are neurologically intact, even during sleep. While asleep, healthy subjects show some movement and change of position every 15 minutes.^[50] Making fewer than 20 movements per night increases the risk of developing a pressure ulcer.^[51]

In a study of 40 elderly patients, nocturnal movements associated with sleep tended to decrease as the length of the hospital stay increased.^{[17, 51]} Analysis of periodic movements in persons at risk for pressure ulcers clearly suggests a relationship between spontaneous body movement and the development of pressure ulcers.^[50]

In surgical patients, the duration of the immobility is even longer than the duration of the surgery because patients are already immobile during the preoperative period and remain so until arrival in the recovery room. Research has shown that the chance of developing pressure ulcers at least doubles in operations lasting longer than 4 hours.^{[52, 53, 54]}

Studies using diverse measurement techniques have documented pressures at specific anatomic sites that are at risk for pressure ulcers.^[55] In 1991, Schubert et al utilized a laser Doppler technique to measure local blood flow in geriatric patients at risk for pressure ulcers.^[56] Their study demonstrated that geriatric patients have a delayed hyperemic response to increased regional blood flow as a result of pressure applied to areas at risk. Tissue at risk and ulcerous tissue were slower to exhibit increased blood flow as a result of a controlled local hyperthermic stimulation.^[56]

Pathophysiologic Factors (Intrinsic or Secondary)

Pathophysiologic factors underlying pressure ulcers include fever, anemia, infection, ischemia, hypoxemia, hypotension, malnutrition, SCI, neurologic disease, decreased lean body mass, and increased metabolic demands. Nutrition and anemia are important factors in the healing and prevention of pressure ulcers.

Individuals with pressure ulcers should have adequate nutrition, especially good protein intake and stores. Decreased lean body mass is a particular risk factor. Clinical parameters indicating good nutrition and immunocompetence are adequate calorie intake and maintenance of ideal body weight. The indirect measurements of these parameters are total lymphocyte count, transferrin level, and total albumin and protein.^{[8, 57, 58, 59, 60, 61, 62, 63, 64]} Anemia is not an intrinsic risk factor; in addition, patients whose hemoglobin value is below 10 g/dL have difficulty healing.^{[65, 66]}

Hypotension is an additional intrinsic risk factor for the formation of pressure ulcers.^{[24, 67]} Treating the medical condition that predisposes a patient to these ulcers is imperative. If possible, the pathophysiologic factors should be controlled in conjunction with eliminating the pathomechanical factors. If any problem is treated in isolation, the multifactorial problem is not resolved.

Summary of Contributing Factors

Factors contributing to pressure ulcers are summarized below.

Pathomechanical factors (extrinsic or primary) include the following:

• Compression
• Maceration
• Immobility
• Pressure
• Friction
• Shear

Pathophysiologic factors (intrinsic or secondary) include the following:

• Fever
• Anemia
• Infection
• Ischemia
• Hypoxemia
• Malnutrition
• Spinal cord injury^[20]
• Neurologic disease
• Decreased lean body mass
• Increased metabolic demands

Brief Review of Pressure Ulcer Research

A monograph prepared by the Research Committee of the NPUAP suggests several research priorities for pressure ulcers: (1) outcome-focused research, (2) intervention and product efficacy studies, (3) basic research related to staging of ulcers, (4) refinement of risk assessment methods, and (5) risk-based, multi-interventional trials. Additional issues requiring investigation include cost issues, ethical decision making, guideline dissemination, public policy, and national outcome evaluations. Methodologic issues, such as research design, study population, and control group use, also need further investigation.^[2]

Early investigators tended to focus on pressure as the primary cause of pressure ulcers.^{[39, 68]} Groth, Kosiak, and Dinsdale were among the first investigators to explore pressure and tissue injury relationships.

Groth found that pressure ulcers similar to those of humans could be produced experimentally in animals.^[69] His experiments showed that larger muscle masses withstood pressure better. He noted that effective pressure force increases toward the smaller surface. This accounts for the greater destruction of tissue at the base of the inverted cone, typified by the small area of skin redness or destruction overlying a bony prominence. This condition is frequently observed in ischial ulcers, trochanteric ulcers, and (to a lesser degree) ulcers over the sacrum.

Groth also noted that generalized sepsis can result in local infection at the site of pressure, with abscess formation, extension of inflammation, thrombosis of the larger vessels, and, consequently, a larger area of tissue necrosis. He concluded that large-vessel thrombosis is not typically a cause of ulceration because of the extensive collateral circulation usually present in the skin.

In a classic experiment, Kosiak, a physiatrist, subjected dogs to accurately controlled pressures ranging from 100-550 mm Hg for 1-12 hours. Microscopic examination of tissue obtained 24 hours after the application of 60 mm Hg of pressure for only 1 hour showed cellular infiltration, extravasation, and hyaline degeneration. Tissues subjected to higher pressures for longer periods also showed muscle degeneration and venous thrombosis. Kosiak concluded that intense pressure of short duration was as injurious to tissues as lower pressure applied for longer periods of time. In both cases, tissue ischemia led to irreversible cellular changes and, ultimately, to necrosis and ulceration. He also concluded that prolonged pressure was the direct and primary cause of pressure ulcers.

Kosiak disagreed with Groth about the location and severity of skin damage, stating that it extended equally to the area under pressure instead of being most severe at the deepest part overlying the bony prominence. Kosiak concluded that skin and subcutaneous tissue provide a sling or suspension effect that allows only a fraction of the applied pressure to be transmitted to the deep tissues.

Husain reported microscopic changes in rat muscle subjected to a pressure of 100 mm Hg for as little as 1 hour.^[70] His microscopic findings were similar to those of Groth and Kosiak. Keane observed that muscle is more susceptible to pressure injury than skin. Keane also noted that the body weight is borne on superficial, weight-bearing, bony prominences that are covered only with skin and superficial fascia.^[71] Nola and Vistnes supported Keane's ideas by documenting significant areas of muscle necrosis on histological examination of rats when pressure was applied to a transposed muscle flap over a bone.^[72] In cadaver dissections, Daniel and coworkers found that muscle is seldom interposed between bone and skin over bony prominences in normal human weight-bearing positions.^[73]

Dinsdale analyzed the role of pressure and friction in the production of pressure ulcers in healthy and paralyzed pigs.^[74] Pressures of 160-1120 mm Hg were mechanically applied with friction and without friction for 3 hours. The ulcerations that were produced extended into the dermis and persisted after 24 hours. Dinsdale concluded that friction is a factor in the pathogenesis of decubitus ulcers since it applies mechanical force in the epidermis. He also concluded that a constant pressure of 70 mm Hg applied for longer than 2 hours produced irreversible tissue damage. However, he did caution against blindly accepting the pressure ischemia relationship as the only cause for ulceration. Dinsdale also found that minimal changes occurred with intermittent pressure relief, even at pressures of 240 mm Hg.

In a later animal model experiment, involving anesthetized rats, Salcido and colleagues confirmed that muscle is more sensitive to pressure-induced ischemia than skin is.^[43] They also noted that the association between ischemia reperfusion injury and experimentally derived pressure ulcers is evidenced by oxygen-free radical-mediated tissue destruction (as studied in biopsy specimens from animal lesions).

Clinical studies of pressure ulcers are difficult to assess because they are often qualitatively based on random observation and uncontrolled studies. More fundamental approaches must be considered with respect to these ulcers to arrive at more reliable conclusions. For example, what are the basic histologic, pathologic, and biochemical markers in an evolving pressure ulcer? Is it ethical to take a biopsy specimen of a human pressure ulcer for purposes of research? What are the multiple variables in the formation of pressure ulcers in the human environment?

Histology

A paucity of literature on the histopathologic nature of decubitus ulcers exists, particularly literature relating to ulcers in humans. Witkowski and Parish were among the first to publish on the histology of decubitus ulcers in human skin; however, their findings, which included vascular infiltrates, thrombosis, and edema, were not intended to represent a histopathologic continuum of the evolving pressure ulcer. Husain's experiments utilized hairy rats to analyze the histologic changes (primarily in the muscle) resulting from the application of pressure, and Kosiak's classic work on dogs focused primarily on the epidermis. Dinsdale showed that a combination of friction and pressure produced lesions in the epidermis of swine.

Salcido's research team has developed an analog system to study pressure ulcers in an animal model in which computer-controlled pressure was applied for 6 hours to the skin over the hip of anesthetized fuzzy rats.^[43] Interval histopathologic changes seen in experimentally derived pressure ulcers have been characterized. Histologic findings included a scattering of neutrophils in the dermis and subcutaneum along the line of necrosis and patchy necrosis to the muscularis in the subdermal region. Foci of damage appeared to be associated with high concentrations of neutrophils, and lesions appeared to develop first in the muscle rather than in the dermis or epidermis.

Evidence indicates that the erosion typical of pressure ulcers is mediated via a neutrophil, an eosinophil, or a macrophage-induced exacerbation. Vascular damage is also apparent when these ulcers are present. Recurrent pressure results in increasingly severe damage to the vascular system and parenchyma consistent with an ischemia-reperfusion insult initiated through a free radical mechanism, which has implications for preventing and treating pressure ulcers.

Agency for Healthcare Research and Quality, formerly Agency for Health Care Policy and Research

National consensus indicates a need for guidelines that can help providers standardize the treatment of pressure ulcers. These guidelines should improve the quality of care and help control the cost of treating pressure ulcers.^{[25, 75]}

In response to this need, the Agency for Health Care Policy and Research (AHCPR), which is now known as the agency for Healthcare Research and Quality (AHRQ), selected pressure ulcers as one of the major areas in which to develop clinical practice guidelines for prevention and treatment. The AHCPR guidelines were developed for the management of some other diseases and reflect a national trend toward standardization of care.^{[25, 75]}

The AHCPR was established in December 1989 under the Omnibus Reconciliation Act. This agency was charged with the task of establishing science-based guidelines for patient care whenever a problem is common and treatment is highly variable and costly. After convening a multidisciplinary panel of experts, AHCPR released guidelines for the prediction and prevention of pressure ulcers in May 1992. Despite the fact that pressure ulcers are preventable and should not occur, they continue to be one of the most pervasive and perplexing problems in treating persons who are ill, recovering from illness, or functionally impaired.

Effective prevention and treatment measures depend on a comprehensive care plan that includes scheduled turning and body repositioning.^[76] Uncertainties about the level of pressure at which cell damage occurs still remain. In fact, there is evidence that the frequency and intervals between turnings may be more critical than pressure in the production of pressure ulcers. Reswick and Rogers suggested the practice of turning patients every 2 hours, and this procedure remains the mainstay of prevention strategies. Various other factors clearly contribute to the development of pressure ulcers. However, the best advice still is to establish a regimen in which pressure is completely relieved on all areas of the body at regular intervals.^{[39, 76]}

Providers working with persons at risk need to be able to recognize skin changes that might indicate an impending breakdown. This is particularly true in elderly patients or in patients who are immunocompromised because the signs of impending or fulminating infection are frequently absent in these patients. Systemic signs of infection that mark the need to culture wounds include malodorous drainage, leukocytosis, fever, hypotension, increased heart rate, and changes in mental status. The earliest clinical evidence of damage to the skin is inflammation of the skin that blanches on application of digital pressure. This process originally presents like a hyperemic response; however, unlike hyperemia, the inflammation persists longer, usually 30 minutes.^[24] Prevention of progression to more serious damage requires immediate, complete elimination of pressure to the involved area.

If the proposition that pressure in excess of capillary pressure is the chief cause of pressure ulcers is accepted, then the primary prevention efforts have to be directed toward reducing or eliminating pressure over susceptible areas. The intensity and duration of external pressure and shearing forces necessary for pressure ulcers to occur depend on an individual's susceptibility, which could be summarized as the tissue tolerance. Nursing strategies include prevention of prolonged pressure, elimination of shearing forces and friction, and removal of skin secretions and excretions.

In a prospective follow-up study, 21.2% of patients who underwent surgery for more than 4 hours developed 70 pressure ulcers in the first 2 days following surgery. Twenty-one pressure ulcers deteriorated in the days following surgery. More than half (52.9%) of the lesions developed on the heels, and 15.7% developed in the sacral area.^[53]

Additional interventions that may be indicated for patients most at risk for pressure ulcers include avoiding hot water; using a mild cleansing agent that does not irritate or dry the skin; using moisturizers; using topical agents such as moisture barriers; keeping the sheets dry and wrinkle free; providing adequate intake of protein and calories; and maintaining current levels of activity, mobility, and range of motion.

Massaging body prominences should also be avoided since this practice has been associated with increased tissue breakdown and risk for the formation of pressure ulcers.^{[24, 25, 77]} Positioning devices such as pillows or foam wedges should be used to prevent direct contact between bony prominences (eg, knees, ankles). Donut-type devices should not be used because they are known to cause venous congestion and edema.^[78]

Other recommendations are to avoid positioning patients directly on the trochanter, to maintain the head of the bed as low as possible, to utilize pressure-reducing devices on the bed (eg, various mattresses) and in the wheelchair (eg, cushions), and to use lifting devices such as a trapeze rather than dragging the patient. Of paramount importance is to use pressure-relieving surfaces during the first couple of days following surgery and to restrict continuous sitting in a chair to less than 2 hours until the patient is able to mobilize independently.

Interventions should be monitored and documented. Specific details that are required include who should provide the care, how often it should be provided, and the supplies and equipment needed. How the care is to be undertaken should be individualized, written down, and readily available. Results of the interventions and the care being rendered should be documented. To ensure continuity, documentation of the plan of care should be clear, concise, and accessible to every caregiver. Patient education is of utmost importance. Patients and everyone involved in their care should have the knowledge necessary to prevent the formation of pressure ulcers.^[24]

Milne et al reported the results of a long-term acute care hospital's program to reduce the occurrence of pressure ulcers. The facility used a failure mode and effects analysis to determine where improvements in care were most needed.^[79] The hospital found that its ulcer prevalence rates, which were believed to be above average, could be traced to such problems as "a lack of 1) wound care professionals, 2) methods to consistently document prevention and wound data, and 3) an interdisciplinary wound care team approach." Addressing these issues, the hospital reduced the prevalence of facility-acquired pressure ulcers from 41% (the baseline figure) to an average of 4.2%, over a 12-month period.

Outline of AHCPR prevention guidelines

Risk assessment includes the following:

• Complete medical history taking
• Determination of Norton (or Braden) score (see Table 1, below).
• Skin examination
• Identification of previous pressure ulcer sites

Prime candidates for pressure ulcers includes the following:

• Elderly persons
• Persons who are chronically ill (eg, those with cancer, stroke, or diabetes)
• Persons who are immobile (eg, due to fracture, arthritis, or pain)
• Persons who are weak or debilitated
• Patients with altered mental status (ie, under the effects of narcotics, anesthesia, or coma)
• Persons with decreased sensation and/or paralysis

Secondary factors include the following:

• Illness or debilitation increases pressure ulcer formation
• Fever increases metabolic demands
• Predisposing ischemia
• Diaphoresis promotes skin maceration
• Incontinence causes skin irritation and contamination
• Other factors, such as edema, jaundice, pruritus, and xerosis (dry skin)

Rationale for strategies to prevent pressure ulcers

Skin care is paramount and must be carried out in conjunction with the following principles:

Pressure relief is important. Patients should be shifted or turned in position every 2 hours. Support surfaces and specialty beds require criteria for use.

Patients can benefit from lying prone.

Minimize shearing forces by keeping the head of the bed lower than 45°.

Use an air-fluidized bed.

Persons who use a wheelchair should be taught to perform pushup exercises and to lean side to side for pressure relief.

Use of pressure-relieving cushions of air, foam, gel, or a combination can help relieve pressure.

Frictional relief is also important.

Nutritional support involves several steps, as follows:

• Obtain the patient's nutritional history.
• Perform physical examination.
• Obtain anthropometric measurements.
• Order laboratory studies (eg, albumin, total lymphocyte count, transferrin level).
• Provide enteral or parenteral support.
• Provide vitamin therapy.

Muscle spasms should be controlled. Involuntary muscle contractions can lead to abrasions. The use of oral antispasticity agents is the simplest method of controlling spasticity. Pressure ulcers occur more frequently in patients with flaccid paralysis than in those with spasticity.

Prevention of contractures is another strategy. Uncontrolled spasticity or lack of movement causes shortening of the muscles, usually the hip, knee, elbow, and ankle plantar flexors. Contractures can limit the patient to only a few positions. Contractures can be prevented in patients who have some mobility by encouraging ambulation and range-of-motion exercises twice daily.

Evaluation tools

Various investigators have sought to establish the reliability and predictive validity of instruments, such as the Braden scale. Prospective studies of these instruments and other risk assessment tools, combined with a study of additional risk factors, are needed to refine the instrumentation, thereby permitting improvement in prediction technologies and the targeting of specific preventive interventions.

Numerous approaches and techniques have been tested to identify persons at risk for the formation of pressure ulcers. A person who uses a wheelchair, is in bed for most of the day, or has impaired ability to reposition the body should be assessed for additional factors that increase risk of pressure ulcers Research has shown that a person's general physical and mental condition, nutritional status, activity level, mobility, and degree of bowel and bladder control all affect this risk.^{[24, 32, 57, 80, 81]} Patients should be assessed when they are admitted to a unit or a facility and periodically thereafter or when they begin home care.

A simple clinical prediction rule based on 5 patient characteristics may help identify patients at increased risk for pressure ulcer development and in need of preventive measures. Detection of a pressure ulcer grade 2 or worse during admission to the hospital is directly related to the following independent predictors of pressure ulcers:^[82]

• Age
• Weight at admission
• Abnormal appearance of the skin
• Friction and shear
• Planned surgery in the coming week

A systematic risk assessment can be accomplished by using a validation risk assessment tool such as the Braden scale or the Norton scale (see Table 1, below). Both of these instruments provide a means of predicting persons at risk for the development of pressure ulcers. No information is currently available to suggest that adaptations of these risk assessment tools or the assessment of any single risk factor or a combination of risk factors predicts risk as well as the overall scores obtained with these tools.^{[54, 83]}

Table 1. Norton and Braden Scales (Open Table in a new window)

This section is based in part on the AHCPR guidelines for the treatment of pressure ulcers.^[25] Once a pressure ulcer has developed, immediate treatment is required. Commonly used treatments over the years have included innovative mattresses, ointments, creams, solutions, dressings, ultrasound, ultraviolet heat lamps, sugar, and surgery. In choosing a treatment strategy, consideration should be given to the stage of the wound and the purpose of the treatment (eg, protection, moisture, removing necrotic tissue). An algorithm for assessment and treatment is available.^{[35, 84, 85]}

Steps in wound assessment and treatment are as follows:

• Wound care may be divided into nonoperative and operative methods.
• Wound care is usually nonoperative for stage I and II pressure ulcers.
• Stage III and IV lesions may require surgical intervention.
• Approximately 70%-90% of pressure ulcers are superficial and heal by second intention.

Solutions for wound cleansing

The major purpose of cleansing the wound is to decrease its bioburden and facilitate healing.^{[84, 86]} Normal saline is used when no germicidal action is required. Saline solution should also be used as a rinse after other solutions are used to irrigate the wound and minimize fluid shifts within newly forming tissue. Normal saline solution also reduces the drying effects that some irrigants may have on tissue.^{[84, 87]}

Povidone-iodine is useful against bacteria, spores, fungi, and viruses. Dilution is recommended, and this treatment should be discontinued when granulation occurs.^[84] Laboratory data demonstrate that povidone-iodine is toxic to fibroblasts in vitro, a finding that has theoretical implications for wound healing. Because povidone-iodine can affect thyroid function, it could be contraindicated for some patients.^[87]

Acetic acid (0.5%) is specifically effective against Pseudomonas aeruginosa, a particularly difficult and common organism in fungating lesions. Acetic acid can change the color of tissue and can mask potential superinfection. Rinsing with normal saline also is recommended.^[87]

Sodium hypochlorite (2.5%) is another oxidizing agent available for cleansing. Although it has some germicidal activity, it is used primarily to debride necrotic tissue. Before using it, zinc oxide should be placed around the edges of the wound to reduce the amount of irritation.^[84] Normal saline should be used as a rinse after sodium hypochlorite is used.^[87] A multitude of cleansing agents are on the market, but none has been shown to be more efficacious than the others, and expert opinion still favors normal saline.^[25]

Debridement and debriding agents

The purpose of wound debridement is to remove all materials that promote infection, delay granulation, and impede healing, including necrotic tissue, eschar, and slough (ie, the stringy yellow, green, or gray nonviable debris in an ulcer). Accurate ulcer staging cannot be made until necrotic tissue is removed.^[88] Three debridement procedures are commonly used: enzymatic debridement, mechanical nonselective debridement, and sharp debridement.

Enzymatic debridement uses various chemical agents (proteolytic enzymes) that act by attacking collagen and liquefying necrotic wound debris without damaging granulation tissue.^{[25, 84]} Proteolytic enzymes are used to chemically debride wounds. The action of these enzymes is aimed specifically at necrotic tissue.

Mechanical nonselective debridement, in which necrotic tissue is loosened and removed, is generally accomplished by whirlpool treatments, forceful irrigation, or use of wet-to-dry dressings. Wet-to-dry dressings involve placing wet gauze into the lesion and allowing it to dry. A few hours later, when the dressing is removed, the necrotic debris that has adhered to the dressing is also removed. Solutions commonly used for wet-to-dry dressings include normal saline and 0.25% acetic acid solution.

Povidone-iodine solution can be used to debride infected ulcers. Although the effervescent action of hydrogen peroxide results in wound debridement, it is not recommended for frequent use in pressure ulcers, because it indiscriminately removes necrotic material and fragile granulation tissue.^[25]

The widespread practice of using hydrogen peroxide continues, but it is not recommended for long-term use because it and other cleansing agents have been found to be toxic to fibroblasts.^{[86, 89]}

Once debridement has been completed and clean granulation tissue has been established, the use of debridement agents should be discontinued and the site should be kept clean and moist.^[89]

Sharp debridement is surgical removal of the eschar and any devitalized tissue within it. Although sharp debridement is the most effective method of removing necrotic tissue, it is contraindicated in certain patients, particularly those who cannot withstand the loss of blood that may occur during the procedure. Moist devitalized tissue supports the proliferation and growth of pathogens. The removal of this devitalized tissue is a prerequisite to new tissue growth.

Sharp debridement is indiscriminate in the removal of vital and devitalized tissue. A great deal of clinical skill and judgment are needed in surgically debriding a wound.^{[80, 90]}

Elderly patients and those with diabetes often have pressure ulcers of the heel that look black and have eschar. Conventional wisdom encourages physicians to debride the eschar, but it is usually protective and should be left to autodebride unless an active infection dictates more aggressive measures.

Surgical debridement is well established as an approach to pressure ulcer care, but more research is needed.

Dressings for pressure ulcers

Transparent adhesive dressings are semipermeable and occlusive. They allow gaseous exchange and transfer of water vapor from the skin, and they prevent maceration of the healthy skin around the wound. In addition, these dressings are not absorptive, they reduce the incidence of secondary infection, and they eliminate the risk of traumatic removal. However, transparent adhesive dressings do not function well on patients who are diaphoretic or on patients with wounds that have significant exudate.^[35]

Hydrocolloid wafer dressings contain hydroactive particles that interact with wound exudate to form a gel. These dressings provide absorption of minimal to moderate amounts of exudate and keep the wound surface moist. This gel can have fibrillolytic properties that enhance wound healing, protect against secondary infection, and insulate the wound from contaminants.^{[35, 91]}

Gel dressings are available in sheet form, in granules, and as liquid gel. All forms of gel dressings keep the wound surface moist as long as they are not allowed to dehydrate. Some gel dressings provide limited to moderate absorption, some provide insulation, and some provide protection against bacterial invasion. All gel dressings provide atraumatic removal(see Table 2, below).^{[25, 35, 92]}

Calcium alginate dressings (eg, Sorbsan) are semiocclusive, highly absorbent, and easy to use.^{[93, 94]} They are natural, sterile, nonwoven dressings derived from brown seaweed. Calcium alginate dressings are extremely effective in treating wet (exudative) wounds and can be used on wounds that are contaminated or infected.^[93]

Treatment strategies for topical therapy

Assessment for appropriate topical therapy includes the following:

• The nature of the wound surface and depth of the lesion must be evaluated.
• Is the skin intact or covered by eschar?
• If the epidermis is denuded, does the ulcer have a clean granulating surface or a necrotic base?
• Is the ulcer nondraining or draining?
• If the wound is draining, what is the amount, color, and odor of the exudate?

Categories of topical products and dressings include the following:

• Antimicrobials
• Moisturizers
• Emollients
• Topical circulatory stimulants
• Semipermeable dressings
• Calcium alginate dressings
• Hydrocolloid and hydrogel dressings
• Exudate absorbers
• Wet-to-dry dressings
• Moist-to-dry dressings
• Enzymes and liquid or gel film formers

Table 2. Eight Major Dressing Types and Their Key Performance Characteristics (Open Table in a new window)

A wide variety of additional therapeutic methods are being evaluated for the treatment of chronic wounds, specifically for pressure ulcer management.^[95] These include electrotherapy,^[96] the application of growth factors,^{[97, 98]} and negative pressure wound therapy using vacuum-assisted closure.^{[99, 100, 101]} Negative pressure therapy enhances wound healing by reducing edema, increasing the rate of granulation tissue formation, and stimulating circulation. Increased blood flow translates into a reduction in the bacterial load (removal of interstitial tissue) and delivery of infection-fighting leukocytes.^[102]

The following are general indications for negative pressure wound therapy^[103] :

• Chronic wounds
• Acute wounds
• Traumatic wounds
• Partial-thickness wounds
• Dehisced wounds
• Diabetic ulcers
• Pressure ulcers
• Flaps
• Grafts

The following are general contraindications for negative pressure wound therapy^[103] :

• Malignancy of the wound
• Untreated osteomyelitis
• Nonenteric or unexplored fistulas
• Known allergies or sensitivity to acrylic adhesives
• Placement of negative pressure dressings directly in contact with exposed blood vessels, organs, or nerves

Antimicrobials and antibiotics

Silver sulfadiazine has an excellent antimicrobial spectrum of activity, low toxicity, ease of application, and minimal pain. Silver sulfadiazine inhibits DNA replication and modification of the cell membrane of Staphylococcus aureus; Escherichia coli; Candida albicans; Klebsiella, Pseudomonas, and Proteus species; and Enterobacteriaceae. It may cause a transient leukopenia (5-15% incidence) for large burn wounds.

With antibiotics and antisepsis, an algorithmic approach is important when one evaluates a patient with an infected wound. First, the practitioner must decide whether the patient has a local or a systemic infection. Local signs of infection in a wound include rubor, dolor, and calor; systemic signs of infection include fever, tachycardia, hypotension, delirium, and alterations in mental status in older patients.

Then, the practitioner must decide which antibiotic is most appropriate for the patient. Systemic antibiotics administered to combat wound infection can be divided into 5 main groups: penicillins, cephalosporins, aminoglycosides, fluoroquinolones, and sulfonamides. Other antibiotics include clindamycin, metronidazole, and trimethoprim.

When one is considering antibiotic therapy for a patient with a wound, most practitioners make their selection on the basis of the spectrum of coverage the antibiotic provides. Before a final selection is made, however, practitioners should consider parameters beyond the wound and targeted pathogen. Many important questions must be answered before prescribing an antibiotic to a patient with a wound, including the following:

• Does the patient have known allergies?
• Does the patient have any metabolic impairments that would alter the pharmacokinetics or the pharmacodynamics of the drug (eg, impaired renal or liver function)?
• What are the effects of the drug on the hemopoietic system?
• What attributes does the drug possess for effective tissue penetration (eg, how much of the drug actually ends up in the tissue of interest)? (This is especially important in patients with osteomyelitis.)
• How is the drug metabolized?
• What are the patient's total weight and lean body and fat mass? (These compartmentalized components of body mass affect the delivery of antibiotic to the targeted site.

The adverse effects of antibiotics are well known and those that impede wound healing should be considered and counteracted. By their very nature, antibiotics eliminate normal flora (especially in the gastrointestinal tract), predisposing a patient to Clostridium difficile infection and diarrhea. This scenario makes a pelvic wound hard to keep dry and predisposes a patient to dehydration.

Antibiotic resistance is a major concern, specifically that involving methicillin-resistant S aureus (MRSA), penicillin-resistant Streptococcus pneumoniae, vancomycin-resistant Enterococcus species, and multidrug-resistant Gram-negative bacilli. Therefore, when antibiotic therapy is ordered, the wound care specialist must be alert to detect signs of antibiotic resistance, and he or she must be attentive to the results of the laboratory data, especially culture and sensitivity results. Consider establishing a relationship with an infectious disease specialist who can participate as an active member of the wound care team.

Patients who are immunocompromised or have impaired chemotaxis resulting in bacterial overgrowth or candidiasis need concomitant treatment with selected antimycotic or antifungal agents.

Other considerations in prescribing an antibiotic include the patient's length of hospital stay, the availability of home health services and infusion services, the influence of the pharmacy and therapeutics committee, the hospital's formulary, and the influence of the payer's approval of prescription benefits.

Overview

When the tissues are compromised by pressure ulcer formation, a vascular and cellular response to injury occurs. This inflammatory response serves to destroy, dilute, or sequester injurious agents and is the precursor to wound healing and repair. Local signs of this inflammatory reactive hyperemia (or nonblanching erythema) include redness, swelling, heat, and pain. The systemic indicators of infection or inflammation include elevated temperature and leukocytosis.

Healing by Primary and Secondary Union

Primary union

Wounds that are clean or surgically controlled can close by primary intention. Healing of this type of wound only requires reepithelialization. This type of wound heals by first intention.

Secondary union

Wounds that have some complicating factor that precludes immediate closure, such as infection or contamination, are allowed to form granulation tissue to fill the crater or gap. Such wounds are typically pressure ulcers, abscesses, or large-surface wounds. Large tissue defects fill by granulation followed by epithelialization. Wound closure occurs via wound contracture.

Wound healing by secondary intention or delayed closure differs from primary closure: (1) The inflammatory response is more intense, (2) greater amounts of granulation tissue are formed when larger wounds heal, and (3) wound contraction of large-surface wounds produces a scar that is considerably smaller than the initial dimensions of the wound.

Another problem encountered in wound healing is exuberant granulation (ie, proud flesh). This tissue protrudes above the margins of the wound and the closing defect, which precludes epithelialization. Some persons tend to form keloids, which are large, bulging, tumorous scars caused by abnormal amounts of collagen in connective tissues.

Several options are available for surgical management of pressure ulcers, including direct closure, skin grafting, skin flaps, and musculocutaneous flaps. See the images below.

Surgical management of pressure ulcers can provide skin coverage as well as soft tissue coverage. Flaps containing muscle provide a physiologic barrier to infection, eliminate dead space in the wound, and improve vascularity. Improved vascularity enhances local oxygen tension, provides extended soft tissue penetration for antibiotics, and improves total lymphocyte function.^{[36, 104, 105]}

When operative repair is considered, many other factors should be considered as well. These factors are perhaps best addressed by the entire team caring for the patient.

The patient should be medically stable and able to benefit from the procedure. The patient should also participate in the decision. Operative procedures often result in blood loss and prolonged exposure to general anesthesia. The nutritional status of the patient must be considered because good nutritional parameters are required for good wound healing and immune function.

Tobacco use and smoking are associated with intrinsic factors that compromise wound healing.^[106] For example, carbon monoxide and nicotinic acid are potent vasoconstrictors that increase blood viscosity.^[107] These factors predispose tissue to excessive oxidase activity and free radical injury. Under normal conditions, the body is able to handle normal oxidative stress. However, with excessive stress comes increased risk for development of pressure ulcers and impaired wound healing. A neutrophil-mediated free radical injury results in excessive oxidase activity, which can cause vascular damage and thrombosis leading to cell death and tissue destruction.^{[41, 42, 43]}

Factors associated with impaired healing should be corrected preoperatively. Several procedures are commonly utilized and discussed next.

Direct closure

Although direct closure is the simplest procedure, pressure ulcers considered for surgery are usually too large to be closed by direct primary closure. Because these wounds are tense as a result of large soft-tissue defects, direct closure can lead to wound defects, excessive wound tension, and a paucity of soft tissue coverage. Tissue expanders have been used to provide more skin surface and to facilitate closure.^[37]

Skin grafts

Split-thickness skin grafts can be used to repair shallow defects and pressure ulcers, but skin grafts provide only a skin barrier. When applied directly to granulating bone, skin grafts quickly erode, thus precluding healing. They also cause scars in the area from which the skin is harvested, and the transplanted skin is never as tough as the original skin.

Skin flaps

Before the 1970s, repair using local full-thickness skin flaps was the standard surgical treatment for ulcers; today, they are typically used as alternatives to secondary repair.^[108] Local skin flaps have a random vascular supply, and the tissue repair is essentially a redistribution of inadequately perfused tissue rather than a planned revascularization by using specific blood vessels. See the images below.

Musculocutaneous flaps

Musculocutaneous flaps are usually the best choice for patients with SCIs and for those who have a loss of muscle function that does not contribute to a comorbidity. For patients who are ambulatory, the choice is less clear since the improved blood supply and reliability of the muscle flap must be balanced against the need to sacrifice functional muscle units.^{[109, 110, 111]} Musculocutaneous flaps can help heal osteomyelitis and limit the damage caused by shearing, friction, and pressure.^{[73, 112, 113]} They bring muscle and skin to the area of the defect and are probably as resistant to future pressure ulcers as the original skin.

Free flaps

Free flaps are muscle-type flaps in which the vein and artery are disconnected at the donor site and are reconnected to the vessels at the recipient site with the aid of a microscope. This is the most complex method of wound closure and has not yet been described in the literature addressing pressure ulcers.

Support surfaces have become an important and widely used modality in the treatment and prevention of pressure ulcers. Numerous products that claim to reduce the occurrence of pressure ulcers are on the market; however, few clinical trials have been performed to evaluate the effectiveness of these products. These claims are based on studies evaluating tissue interface pressures, which have become standards in distinguishing pressure relief from pressure reduction.^{[114, 115, 116, 117, 118, 119, 120]} These concepts as well as device types have been used to develop a convenient classification to help select the appropriate products for pressure ulcer treatment and prevention.^{[44, 121]}

Selection of a product must be based on the patient's management plan and the evaluation of an individual's risk factors for developing a pressure ulcer.^{[116, 122]} These risk factors must be monitored, and the modalities must be reevaluated as the patient's condition improves or worsens. Finally, cost and service support must be evaluated.

An important focus in pressure ulcer prevention and treatment is reducing pressure over the bony prominences to below capillary closing pressure (ie, 32 mm Hg), which has become the standard threshold value for evaluating support surfaces.^{[114, 115, 117, 123, 124]} Since capillary closing pressure cannot be measured under clinical conditions, tissue interface pressure has been used to evaluate and compare products. Tissue interface pressure, an approximation of capillary closing pressure, is the force per unit area that acts perpendicularly between the body and the support surface.^[121] Tissue interface pressure is measured using a pressure sensor placed between the patient and the support surface.

Much of the research comparing the tissue interface pressures of various surfaces involves case studies on healthy human adults.^{[32, 114, 115, 119, 123]} These experiments use various sensors, making comparisons of the findings difficult, and they do not address other etiologic factors.^[55]

Newer technologies, including transcutaneous oxygen tension and laser Doppler blood flow, are currently being evaluated.^{[55, 124]} The force sensing array (FSA) pressure measurement assessment system uses a thin, flexible mat to determine interface pressures in a clinically effective method. The Windows-based computer software visually demonstrates the pressure map in a way that is easy for the clinician, patient, and support staff to understand. This software is useful in patient teaching, wheelchair or cushion selection, bed positioning, and documentation because it enables the clinician to track the pressure-relieving strategies chosen for each patient. Currently, no clear evidence supports the adequacy of these instruments, and further studies must be undertaken.

Classification

In 1992, Bryant developed a convenient classification system of support surfaces and special beds. The Bryant classification system distinguishes 3 types of devices: mattress overlays, mattress replacements, and specialty beds. Each device has specific characteristics as well as advantages and disadvantages (see Table 3, below). The mattress overlay is designed to be effective when applied directly over a mattress. Mattress replacement systems are designed for use on an existing hospital bed frame without an underlying mattress. Finally, specialty beds are entire units used in place of hospital beds.

Table 3. Advantages and Disadvantages of Support Surfaces (Open Table in a new window)

Each type of device may be subdivided into dynamic systems, which require an energy source to alternate pressure points, and static systems, which rely on redistribution of pressure over a large surface area and do not require an energy source. Each device may be further described as a pressure-reducing or pressure-relieving device.

Pressure-relieving devices are those that consistently reduce pressure below capillary closing pressure. Pressure-reducing devices keep pressures lower than with the standard hospital bed but not consistently below capillary closing pressure. Mediums used in mattress overlays and replacements include water, gel, foam, air, and composite products.

Air mattresses and overlays may be static or dynamic. Static devices work by redistributing local pressure over a wider tissue area. Dynamic devices use a power source to alternate air currents in order to redistribute the pressure against the human body. Most overlays and replacement mattresses are considered pressure-reducing devices. Specialty beds include low-air loss beds and air-fluidized beds. Low-air loss beds use separate air-filled cushions that are individually monitored to reduce pressures below capillary closing pressures. Air-fluidized therapy uses warm air forced through silicone beads to simulate a fluid environment in reducing pressures. The specialty beds are considered pressure-relieving devices.

Clinical trials for prevention and treatment of pressure ulcers have been performed on air-fluidized and low-air loss beds (see Table 4, below).^{[5, 125, 126, 127]}

Although there is evidence that these surfaces can provide an environment in which ulcers can be prevented or improved, no evidence suggests that one support surface consistently performs better than all others in all circumstances.^{[5, 126, 128, 129, 130, 131]} Therefore, patients should be actively treated on an individual basis to reduce specific risk factors. Selection of a support surface is an adjunct to other therapy.

A systematic review published in the Cochrane Database of Systematic Review concluded that special foam mattresses designed to prevent pressure ulcers are generally more effective than standard mattresses in patients at risk. Organizations might consider the use of pressure-relief devices for high-risk patients in the operating room because this is associated with a reduction in the postoperative incidence of pressure ulcers.^[132] An updated systematic study not only confirmed the benefit of higher-specification foam mattresses but also suggested that sheepskin overlays are also beneficial. One of the trials included in this analysis determined that alternating-pressure mattresses may be more cost effective than alternating-pressure overlays. Additional research on support surfaces for prevention of pressure ulcers was recommended.^[133]

Several studies found only limited evidence when comparing higher-technology products.^{[134, 132]}

General measures, such as the introduction of adequate mattresses and guidelines for prevention and treatment, are promising tools. In a study from the Netherlands, the authors saw a significant decrease in hospital-acquired pressure ulcer frequency from 18% to 13% (P = .003) after 4 months and 11% (P < .001) after 11 months when adequate mattresses were used along with guidelines for prevention and treatment.^[135]

Selection of a support surface

Selecting a support surface is futile unless the product's appropriateness can be assessed adequately beforehand. In addition to frequent written risk assessments, a dynamic management plan for each individual should include discontinuing the use of a support surface when it is determined that the patient is no longer at risk for developing pressure ulcers.^{[5, 128, 129, 136, 137]}

Any individual thought to be at risk for developing pressure ulcers should be placed on a pressure-reducing device (eg, foam, static air, alternating air, gel, water) when lying in bed to relieve pressure on the heels.^{[78, 136, 138, 139, 140, 141]}

For persons who use a wheelchair, pressure-reducing devices of foam, gel, air, or a combination of these materials should be used.^{[77, 118, 142, 143, 144]}

Pressure-reducing devices should be used in addition to standard nursing care.^{[1, 81, 145]}

Guidelines developed by the AHCPR Pressure Ulcer Panel for managing existing pressure ulcers include the following:

• Use positioning devices to raise a pressure ulcer off the support surface. If the patient is no longer at risk for developing pressure ulcers, these devices may reduce the need for pressure-reducing overlays, mattresses, and beds. Avoid using donut-type devices.^[78]
• Assess all patients with existing pressure ulcers to determine their risk for developing additional pressure ulcers. If the patient remains at risk, use a pressure-reducing surface.^{[12, 68, 146, 147]}
• If patients can assume a variety of positions without bearing weight on the lesion and without "bottoming out," a static support surface should be used.^{[126, 128, 131, 148]}
• If the patient cannot assume a variety of positions without bearing weight on the ulcer, if the patient fully compresses the static support surface, or if the pressure ulcer does not show evidence of healing, a dynamic surface should be used.^[126]
• Finally, if the patient has large stage III or stage IV pressure ulcers on multiple turning surfaces, a pressure-relieving product is warranted.^{[2, 5, 126, 131, 148, 149]}

Currently, no perfect product exists; therefore, it is important to tailor product selection to the patient's needs. Add to this the considerations of variation in cost and customer services associated with each product, and the choices become even more difficult. Each institution needs a written policy and procedure guidelines addressing the variables associated with product selection. Additional randomized clinical trials to distinguish efficacy are needed. Further, research that addresses the accuracy of tissue interface pressures in determining prevention of pressure ulcers and in advancing new technologies relating to capillary closing pressure must be continued.

Table 4. Clinical Trials of Pressure-Relief Surfaces (Open Table in a new window)

Discharge planning

Discharge planning begins early during hospitalization and requires an interdisciplinary approach. Knowledge of available resources facilitates smooth transitions through all levels of the continuum of care. With more care conducted in the home environment, education of the patient and caregiver in the prevention and treatment of pressure ulcers becomes increasingly important. A variety of methods can be employed to facilitate this educational process, including charts, diagrams, photographs, and videos. This comprehensive approach can positively influence the overall patient outcome.^[85]

Future trends in management

While physicians continue to strive for the ultimate treatment for pressure ulcers, the role of newer therapies such as cytokine growth factors (eg, recombinant platelet-derived growth factors and basic fibroblast growth factors and skin equivalents) must be considered.^{[4, 150]} An increasing amount of evidence indicates that electrical stimulation may enhance the rate of wound healing in pressure ulcers.^[151] Other exciting possibilities include free radical scavengers and special drug delivery systems used in a preventive way for areas at risk for pressure ulcers.^{[41, 42, 43]} More research is needed, and a multitude of opportunities exist in this rapidly developing field. The gaps between basic, applied, and clinical outcomes research must be closed.

Summary

Many factors influence the development and healing of pressure ulcers. Nursing plays a pivotal role in this challenging and complex process, using a multifaceted approach involving skin care, pressure relief, and nutritional support. Prevention is the key to managing pressure ulcers, and it begins with a complete medical and nursing history, a risk assessment, and skin examination when the patient is admitted.^{[24, 25, 75]}

Pathomechanical and pathophysiologic factors that subject the tissue at risk to potential skin breakdown should receive particular attention. Patients should be kept clean and dry and should be repositioned frequently. For patients at risk, adequate pressure relief must be provided, along with adequate nutritional support.

For patients who develop pressure ulcers, these preventive measures must be used with the techniques of general wound care. Nonoperative wound care may involve simple topical therapy, as for pressure ulcers with unbroken skin or superficial lesions with nondraining, noninfected granulation tissue. For draining necrotic or infected lesions, treatment also may include absorption agents, calcium alginate dressings, wound coverings, debridement, and antimicrobial therapy. Other therapeutic modalities, such as whirlpool, physical therapy, and specialty beds, may also be added to the treatment regimen.

Other resources

Agency for Healthcare Research and Quality

(Formerly the Agency for Health Care Policy and Research)

540 Gaither Road

Rockville, MD 20850

Telephone: (301) 427-1364

E-mail: info@ahrq.gov

National Pressure Ulcer Advisory Panel

Robin M. Turner, Executive Director

12100 Sunset Hills Road, Suite 130

Reston, VA 20190

Phone: (703) 464-4849

Fax: (703) 435-4390

E-mail: rturner@drohanmgmt.com