Chapter 100. Decubitus (Pressure) Ulcers

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PRESSURE ULCERS AT A GLANCE

Commonly known as decubitus ulcers, pressure sores, and bedsores.
Affect approximately 0.5% to 2.2% of the population.
Tend to occur over bony prominences, more common from the waist down.
Etiologic factors include pressure, shearing, frictional forces, and moisture.
Related risk factors are prolonged immobilization, sensory deficit, impaired consciousness, circulatory disturbance, poor nutrition, and chronic diseases.
Staged according to the degree of tissue damage observed (I to IV); pathologic findings depend on the stage of evolution.
No specific laboratory findings. The diagnosis is made clinically.

See references 1 and 2.

Epidemiology

Estimates are that between 1.5 and 3 million people in the United States have pressure ulcers. Hospital stays with pressure ulcers listed as a diagnosis increased by nearly 80% in the United States between 1993 and 2006. These chronic wounds cost approximately $5 billion annually to treat, and Center for Medicaid and Medicare Services (CMS) no longer reimburses for additional costs arising from nosocomial stage III or IV pressure ulcers.1–6

The prevalence and incidence of pressure ulcers varies with the clinical setting. In acute care, the incidence ranges from 0.4% to 38%; in long-term care, from 2.2% to 23.9%; and in home care, from 0% to 17%. Most pressure ulcers develop during the first few weeks of hospitalization. The prevalence of pressure ulcers in acute care settings is approximately 15%, in long-term care settings from 2.3% to 28%, and in home care from 0% to 29%.1–4

Pressure ulcers are more common in the elderly, especially those over the age of 70, in patients who have had surgery for hip fracture, and in patients with spinal cord injury. A multicenter study of 3,233 elderly admitted from the emergency demonstrated a pressure-ulcer incidence (mostly stage II) of 6.2% on hospital day 3, with significant associations to advanced age, male gender, dry skin, urinary and fecal incontinence, difficulty turning in bed, and poor nutritional status.7

The majority of pressure ulcers occur on the lower part of the body, 65% in the pelvic area and 30% on the lower limbs, though other locations include the scalp in infants with neurological injury or the face from endotracheal tubes during long surgeries or intensive care unit (ICU) stays.1–4

Etiology and Pathogenesis

The main etiologic factors contributing to pressure ulcer development include pressure, shearing forces, friction, and moisture.

Pressure or force per unit area is considered to be the most important factor in pressure ulcer formation. Normal tissue pressure is between 12 and 32 mm Hg. Pressures higher than this upper limit can compromise tissue circulation and oxygenation. When a patient lies immobile on a hospital bed, pressures as high as 150 mm Hg can be generated, especially over bony prominences. At pressures of 70 mm Hg or more, there is an inverse time–pressure curve with rapid pressure ulcer formation.2 Sitting positions can also generate elevated pressure over precise body surfaces. The duration as well as degree of pressure is important. If pressure is relieved regularly, tissue recovery can occur, whereas constant pressure can lead to tissue death (Fig. 100-1). Often, damage occurs deep at the bone–muscle interface, in which the limited cutaneous injuries may be only the “tip of the iceberg” of deeper, more extensive damage (eFig. 100-1.1). Patients who are immobile should therefore be turned regularly to prevent pressure ulceration. The pathophysiology of pressure ulcer formation is summarized in eFigure 100-1.2, and common sites of pressure ulcers are shown in Figure 100-2.

Figure 100-1

Pressure ulcer, stage IV. (From Wolff K and Johnson RA. Fitzpatrick's Color Atlas, 2009.)

eFigure 100-1.1

Tissue under pressure. (From Preventing Pressure Ulcers: Clinical Practice Guideline. Washington, DC, US Department of Health and Human Services, AHCPR publication 92–0047 May 1992.)

eFigure 100-1.2

Pathophysiology of pressure ulceration. (From Grey JE, Harding KG, Enoch S: Pressure ulcers. BMJ 332:472, 2006, with permission of Blackwell Publishing.)

Figure 100-2

Common sites of pressure ulcer development. (From Preventing Pressure Ulcers: A Patient's Guide. Washington, DC, US Department of Health and Human Services, USGPO 617-025/68298, 1992.)

Shear force results from the motion of bone and subcutaneous tissues relative to the skin when the skin is fixed (e.g., when the upper body of a supine patient is raised to an angle above 30° and the skin remains in contact with the bed). Shearing forces are parallel to the tissue surface, and the subsequent sliding pressure is transmitted to deeper tissues, which can become angulated and occlude the blood vessels (Fig. 100-3A). Spinal cord injury patients develop such shearing forces with muscle spasms, which may be controlled with muscle relaxants.8

Figure 100-3

Shear force generated when a patient slides down a bed, for example, in the sacral region (A) or on the heels (B). (From Grey JE, Harding KG, Enoch S: Pressure ulcers. BMJ 332:472, 2006, with permission of Blackwell Publishing.)

Friction is the force that resists the relative motion between two surfaces that are in contact. This causes damage to the superficial layers of the skin (e.g., when a patient is dragged across the bedsheets) (Fig. 100-3B).

A moist environment from urinary or fecal incontinence, perspiration, or excessive wound drainage can cause maceration of the skin, which increases the risk of pressure ulcer formation fivefold (Fig. 100-4). Other risk factors for pressure ulcer development include prolonged immobilization, sensory deficit, circulatory disturbances, poor nutrition, acute illness, advanced age, and a previous history of pressure ulcers as well as fecal and urinary incontinence, hip fractures, smoking, and dry skin. Concomitant use of medications such as corticosteroids, which can impair healing; sedatives and analgesics, which can impair consciousness; and drugs that can cause alterations in cutaneous blood flow, such as antihypertensive medications, can also increase pressure ulcer risk, and such drugs should be used with care (Table 100-1).

Figure 100-4

Pressure ulcer, stage III, complicated by fecal incontinence.

Table 100-1 Major Risk Factors for Developing Pressure Ulcers

Table 100-1 Major Risk Factors for Developing Pressure Ulcers

Alteration in sensation or response to discomfort

Degenerative neurologic disease
Cerebrovascular disease
Central nervous system injury
Depression
Drugs that adversely affect alertness

Alteration in mobility

Neurologic disease or injury
Fractures
Pain
Use of restraints

Significant changes in weight (≥5% in 30 days or ≥10% in previous 180 days)

Protein–calorie undernutrition
Edema

Incontinence

Bowel and bladder

Excerpted from American Medical Directors Association: Clinical Practice Guideline: Pressure Ulcers. Columbia, MD, American Medical Directors Association, 2008. © 2008 American Medical Directors Association.

Clinical Findings

(See eFig. 100-4.1)

eFigure 100-4.1

Algorithm for the approach to a patient with pressure ulcer.

History

History taking and physical examination for pressure ulcer patients should incorporate a risk assessment scale. A number of risk assessment tools have been devised in an attempt to identify persons at risk for pressure ulcers. The Braden, Waterlow, and Norton scales have been extensively tested for reliability and validity and have been recommended by the Agency for Healthcare Research and Quality for predicting the risk of developing pressure sores. Currently, best practices in acute care, long-term care, and home-health care dictate that such risk assessments be performed initially at admission and at subsequent precise intervals. Components of these scales assess the following risk factors: mobility, activity level, nutritional status, mental status, incontinence/moisture conditions, general physical condition, skin appearance, medication use, friction and shear, weight, age, predisposing diseases, and prolonged pressure (eTable 100-1.1).

eTable 100-1.1 Components of Three Risk Assessment Scales for Pressure Ulcers

eTable 100-1.1 Components of Three Risk Assessment Scales for Pressure Ulcers

Risk Factor

Norton

Waterlow

Braden

Mobility

Yes

Activity level

Yes

Nutritional status

Yes

Mental status

Yes

Incontinence/moisture conditions

Yes

General physical condition

Yes

Skin appearance

Yes

Medication

Yes

Friction and shear

Yes

Weight

Yes

Age

Yes

Specific predisposing diseases

Yes

Prolonged pressure

Yes

Data from Grey JE, Enoch S, Harding KG: Pressure ulcers. BMJ 332;472, 2006.

Cutaneous Lesions

Staging is an assessment system that classifies pressure ulcers based on anatomic depth of soft-tissue damage. Pressure ulcers often progress from lower to higher stages, and any small pressure ulcer should be considered as the possible “tip of an iceberg.” Table 100-2 shows the clinical appearance of pressure lesions and ulcers and their histopathologic correlates as defined by the National Pressure Ulcer Advisory Panel (NPUAP). Palpation is important to assist visual evaluation. Ulcers that initially appear superficial can end up being classified as stage III or IV after débridement reveals their true depth. The epidermis may be hypertrophic at the ulcer margin with varying degrees of pigmentation.10

Table 100-2 Comparison of Clinical and Histologic Findings by Ulcer Stage

Table 100-2 Comparison of Clinical and Histologic Findings by Ulcer Stage

Classification/Stage9

Clinical Findings

Histopathologic Description

Stage I

Nonblanchable erythema of intact skin

Epidermis appears normal.

Striking red blood cell engorgement of capillaries and venules, mainly in papillary dermis with platelet thrombi and hemorrhage. Degeneration of sweat glands and subcutaneous fat is often seen.

Stage II

Partial-thickness skin loss involving epidermis, dermis, or both

Epidermis is lost.

Dermal papillae are often identifiable. Acute inflammation of papillary and reticular dermis is found. In addition to a perivascular lymphocytic infiltrate, neutrophils are seen.

Necrotic changes in the appendages and fat are more pronounced.

Stage III

Full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.

Hemorrhagic crust containing acute inflammatory cells or a thin zone of coagulation necrosis on the surface.

Diffusely fibrotic dermis.

Loss of appendageal structures.

Stage IV

Full-thickness skin loss with extensive necrosis of or damage to muscle, bone, or supporting structures.

Full-thickness destruction of skin.

The tissue appears basophilic with obliteration of cellular detail, although the general dermal architecture is preserved.

Inflammatory infiltrate is often not seen.

NPUAP = National Pressure Ulcer Advisory Panel.

There are several staging systems for classifying pressure ulcers. The most commonly used include the NPUAP, Shea, and Yarkony et al systems. In February 2007, the NPUAP redefined the stages of pressure ulcers established in 1989 by preserving the four original stages and adding two new stages of deep tissue injury and unstageable pressure ulcers. The unstageable category was created to avoid unnecessary removal of slough or eschar simply for the purpose of staging, which might hinder ulcer healing (Fig. 100-5). eTable 100-2.1 compares these four classification systems.2,10–13

eTable 100-2.1 Staging Systems for Classifying Pressure Ulcers

eTable 100-2.1 Staging Systems for Classifying Pressure Ulcers

Classification

Shea (1975)9

NPUAP (1989)

Yarkony and Kirk (1990)7

NPUAP (2007)

Suspected deep tissue injury

Purple/maroon “bruise” or blood-filled blister

Stage I

Limited to epidermis, exposing dermis

Nonblanchable erythema of intact skin

Red area

A. Present >30 minutes but <24 hours

B. Present longer than 24 hours

Nonblanchable erythema of intact skin

Stage II

Full thickness of dermis to junction of subcutaneous fat

Partial-thickness skin loss involving epidermis, dermis, or both

Epidermis and/or dermis ulcerated with no subcutaneous fat observed

Partial-thickness skin loss involving epidermis, dermis, or both

Stage III

Fat obliterated, limited by deep fascia undermining of skin

Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, underlying fascia

Subcutaneous fat observed, no muscles observed

Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, underlying fascia

Stage IV

Bone at the base of ulceration

Full-thickness skin loss with extensive necrosis of or damage to muscle, bone, or supporting structures

Muscles observed, but no bone observed

Full-thickness skin loss with extensive necrosis of or damage to muscle, bone, or supporting structures

Stage V

Close large cavity through a small sinus (closed pressure ulcer)

—

Bone observed but no involvement of joint space

Stage VI

In joint spaces

Unstageable

—

Full-thickness skin loss obscured by slough or eschar over the base of the wound

NPUAP = National Pressure Ulcer Advisory Panel.

Figure 100-5

Unstageable pressure ulcer covered with slough. (Used with permission from Mary Gloeckner, RN, MS, CWOCN.)

Related Physical Findings

All pressure ulcer patients should undergo a full physical examination to identify systemic disease contributing to wound development, such as anemia, chronic cardiac or respiratory disease, and neurologic disorders.

Tenderness, erythema, edema and warmth of surrounding skin, exudate, and foul odor are symptoms and signs of infection. Fever and declining mental or physical status should raise suspicion of bacteremia or osteomyelitis.

Spasticity secondary to inflammation and infection may trigger muscle contractures and joint deformity that can limit motion, which complicates positioning. Weakness and signs of anemia and dehydration can be found secondary to profound loss of fluid and protein from these open, draining wounds.

Laboratory Tests

The diagnosis is made clinically. However, anemia, leukocytosis, hypoproteinemia, hypoalbuminemia, elevated ESR, or reduced serum iron levels may be present. It is important to exclude other diseases that can cause skin ulcers, including calciphylaxis, vasculitis, and connective tissue diseases.

Special Tests

Biopsy

Histologic analysis may be helpful to diagnose the pressure ulcer stage when clinical findings are insufficient to determine depth and exclude other diseases that can present with skin ulcers such as collagen vascular diseases. In long-standing pressure ulcers, squamous cell carcinoma can develop (Marjolin's ulcer). Histologic findings in pressure ulcers are described in Table 100-2.

Imaging Studies

Radiology is most useful to identify complications, particularly of deep pressure sores. Plain radiographs can identify ectopic bone, air in the ulcer cavity, and sclerotic or destructive changes in the underlying bony prominence. Ectopic bone can cause a pressure sore by altering the patient's posture and locally increasing pressure over soft tissue.14 When there is clinical uncertainty about the size or extent of a pressure ulcer, sinography can be performed. Direct magnification radiography of sacral areas is useful when plain radiographs leave doubt about the condition of the bony cortex adjacent to a pressure sore. If the cortex is intact, osteomyelitis is unlikely.

Computed tomographic scanning is useful to determine the extent of a pressure ulcer and its anatomic relation to surrounding structures. It is helpful in assessing large, complicated lesions with associated sinus tracts or extensive undermined margins. Computed tomography is the only radiographic modality that can define the external margin of the lesion.

Magnetic resonance imaging (MRI) is helpful in determining the depth and extent of soft-tissue involvement underlying decubitus ulcers. It can also be a useful tool for identifying osteomyelitis, fluid collections, abscesses, and sinus tracts.15,16 The gold standard for the diagnosis of osteomyelitis is histologic/microbiologic analysis of surgical biopsy specimens, but MRI is accurate in the diagnosis of osteomyelitis (sensitivity, 98%; specificity 89%) and associated soft-tissue abnormalities. It also can delineate the extent of infection to assist in guiding limited surgical resection and preserving viable tissue.14

Complications

(See Table 100-3)

Table 100-3 Complications of Pressure Ulcers

Table 100-3 Complications of Pressure Ulcers

Local infections
Bacteremia
Osteomyelitis
Sinus tracts
Malignancies
Necrotizing fasciitis
Myonecrosis
Metabolic alterations
- Hypercalcemia
- Hypoproteinemia
- Anemia
Postsurgical complications
- Hematoma
- Seroma
- Wound dehiscence
- Abscess
Amyloidosis and others
Death

Local Infection/Bacteremia

It is important to distinguish between bacterial colonization (the harmless presence of bacteria on the wound) and infection (bacterial invasion into tissue). Most chronic wounds are colonized by bacteria.2 Common bacterial strains isolated from chronic wounds include Staphylococcus aureus (the most prevalent), Pseudomonas aeruginosa, Escherichia coli, Proteus mirabilis, Enterobacter cloacae, Serratia marcescens, Streptococcus group G, S. epidermidis, β-hemolytic Streptococcus group A, Enterococcus and Acinetobacter sp., and other organisms.15 Anaerobic bacteria may also be present.

Results of superficial swab culture generally reflect colonization rather than infection, and ideally tissue samples should be obtained by needle aspiration, biopsy, or curettage.2

Wounds with fewer than 106 bacteria per gram of tissue may improve without systemic antibiotic therapy, whereas clinical signs and symptoms such as erythema, warmth, local pain or tenderness, purulent discharge, and the presence of a foul odor may indicate infection into soft tissue with more than 106 bacteria per gram of tissue. In patients with associated comorbidities and advanced age, however, systemic signs of infection such as fever and leukocytosis may not be obvious, and delayed wound healing may be the only sign of infection.15

Pressure ulcers can cause bacteremia and may be complicated by osteomyelitis, endocarditis, sepsis, and death. Bacteremia is caused predominantly by hospital-associated organisms and occurs mainly in diabetic, malnourished, or immunosuppressed patients. This complication is associated with a mortality rate of 50% to 70%.

Osteomyelitis

Long-standing, deep decubitus ulcers (i.e., stage III or IV) are often complicated by osteomyelitis. This can occur through direct extension or blood dissemination. If bone is visible in a long-standing deep pressure ulcer, osteomyelitis is highly likely. Common organisms causing osteomyelitis include S. aureus, Bacteroides fragilis, P. mirabilis, E. coli, Klebsiella sp., Pseudomonas sp., streptococci, and enterococci.16 Osteomyelitis should be considered whenever a pressure sore does not heal.

Fistulas/Sinus Tracts

Sinus tracts are drainage pathways from a deep focus of acute infection through tissue and/or bone to an opening on the skin surface. A sinogram is useful in determining the extent of the sinus tract or fistula. These can extend deep enough to reach the joint space or even deep viscera and cause osteomyelitis. Large sinus tracts can be demonstrated by MRI.

Malignancies (Marjolin's Ulcers)

The term Marjolin's ulcer is often used to describe neoplastic transformation in chronic ulcers. Squamous cell carcinoma has an estimated incidence of 0.5% of pressure ulcers and usually behaves aggressively, with a metastatic rate of 61%.2 This makes early diagnosis and treatment imperative.17 The possibility of malignant transformation should be considered in pressure ulcers that are unresponsive to treatment or show morphologic changes indicative of malignancy.

Metabolic Alterations

Patients with pressure sores can demonstrate typical features seen in patients with chronic inflammatory disorders, including normocytic, normochromic anemia with reduced serum iron levels and reduced transferrin levels and transferrin saturation, but elevated ferritin levels. Hypoproteinemia with hypoalbuminemia, inverse albumin–globulin ratio, increased level of globulins, high erythrocyte sedimentation rate, and high C-reactive protein level and white cell counts may also be seen. These abnormalities return slowly to normal levels after healing of pressure sores. Bone reabsorption can lead to hypercalcemia, hypercalciuria, ectopic calcification, renal calculi, and bladder stasis.

Necrotizing Fasciitis/Myonecrosis

Necrotizing fasciitis is an aggressive soft-tissue infection that requires rapid diagnosis, early surgical intervention, frequent operative débridements, and soft-tissue reconstruction. It is rare but has a very aggressive course (see Chapter 179).

Myonecrosis and rhabdomyolysis have been described after prolonged surgery. Initially, the disorder presents with an area of buttock skin breakdown, diagnosed as a simple decubitus ulcer, but it then develops into extensive myonecrosis leading to renal failure that necessitates dialysis.

Other Complications

Among elderly bedridden patients who have surgery for pressure ulcers, the mortality rate is high (68% in one series).18 Other postsurgical complications include hematoma, seroma, wound dehiscence, abscess formation, sepsis, and death. Death has been reported to occur during acute hospitalization in 67% of patients who develop a pressure ulcer compared with 15% of at-risk patients without pressure ulcers. The risk does not appear to correlate with the severity of the pressure ulcer.

Other less commonly reported complications of pressure ulcers include amyloidosis, endocarditis, meningitis, septic arthritis, myiasis, pseudoaneurysm formation, heterotopic bone formation, and gangrene.

A recently published systematic review investigated the quality-of-life concerns associated with pressure ulcer diagnoses, demonstrating that pressure ulcer patients may have concerns about pain control, social constraints, and changes to body image.19

Prognosis

The prognosis of pressure ulcers depends on the cause. In paraplegic patients 50% to 70% of pressure ulcers heal with nonsurgical intervention, though pressure ulcer recurrence can be a concern. A study of spinal cord injury patients demonstrated recurrent pressure ulcers in 38% of patients, usually at the same anatomical site and within 4 months.20 In the long-term care setting in which patients may have multiple medical problems, the prognosis is worse, and complications such as sepsis, osteomyelitis, amyloidosis, anemia, and malignancy can develop.21

The age-adjusted mortality rate for pressure ulcers has been calculated as 3.79 deaths per 100,000 population. The majority of pressure ulcer–associated deaths occur in people at least 75 years of age. Septicemia was present in 40% of patients whose deaths were associated with pressure ulcers. Incapacitating chronic and neurodegenerative conditions were common comorbidities, and mortality rates in blacks were higher than those in other racial or ethnic groups.

Interestingly, although stage II pressure sores were found to be more likely to heal than pressure ulcers of stage III or IV, the depth of the pressure ulcer did not correlate with mortality. Patients with a stage II pressure ulcer on admission to care were as likely to die as patients with a stage III or IV ulcer.22

Treatment

Therapy should be individualized for each patient and involves more than simple wound management. Pressure ulcers are frequently a clinical sign of underlying medical conditions which should be treated to facilitate healing. Treatment takes great coordination by inpatient facilities such as nursing homes, where caretakers often use the NPUAP-designed PUSH (Pressure Ulcer Scale for Healing) tool or the Bates–Jensen Wound Assessment Tool (BWAT) to document wound healing.23,24 Photography can also be an important means of documenting improvement and should include dimensions, date, and wound location.25 Few controlled trials have evaluated specific treatment modalities for pressure ulcers, but reasonable interventions include use of basic support surfaces, repositioning the patient, optimizing nutritional status, and moisturizing sacral skin with expectations of some improvement within 2 weeks.26 The general principles of therapy for pressure ulcers are as follows.

Relief of Pressure, Shear, and Frictional Forces

Positioning

Positioning techniques are critical in the management of tissue loads.

While in bed, patients should be positioned to avoid pressure over existing ulcers or over bony prominences, especially the trochanter. Pillows or foam wedges can be used to raise a pressure ulcer off its support surface or to prevent direct contact between bony prominences, such as knees or ankles. It is important to limit the amount of time the head of the bed is elevated and to maintain the head of the bed at the lowest possible level of elevation tolerable to reduce shearing forces at sacral tissues. Immobilized patients are usually placed in a 30° oblique position to the left or right, which should be alternated every 2 hours at a minimum. International best practices have validated this approach though controlled studies are still needed.

The patient and caregivers must learn appropriate transfer or mobilization techniques to avoid friction. The patient should be lifted rather than dragged across the bedsheets, using lifting devices such as a trapeze or bed linen.27 Repositioning should be done as frequently as warranted by the patient's condition.

Moisture from urinary or fecal incontinence, perspiration, or wound drainage should be minimized, and the skin should be kept clean. Absorbing underpads or briefs, diapers, and occasionally urinary catheters or rectal tubes may be required to help manage incontinence. Skin barrier creams can help protect the skin from maceration.

Patients, who are sitting, may select a pressure-relieving cushion based on specific needs. Donut-type devices should be avoided because they result in venous congestion and may worsen ulcers. Patients should be encouraged to reposition themselves frequently.

Support Surfaces

Support surfaces can be used on top of or instead of standard mattresses. They distribute pressure over a large surface area, and the type of support surface used will depend on the patient's needs and abilities. Support surfaces are typically divided into static and dynamic, the latter powered by electricity (eTable 100-3.1).

eTable 100-3.1 Special Support Surfaces for Patients with Pressure Ulcers

eTable 100-3.1 Special Support Surfaces for Patients with Pressure Ulcers

Support Surface

Description

Advantages

Disadvantages

Indications

Thick foam mattress

Thick foam mattress overlay

Inexpensive, portable

Difficult to clean, not reusable for other patients

Prevention or treatment of solitary ulcers

Air mattress

Inflatable, waffle-shaped plastic or nylon mattress overlay

Inexpensive, very portable, usable on transport carts, easy to store, reusable

—

Prevention or treatment of solitary ulcers

Water mattress

Water-filled mattress overlay

—

Difficult to maintain

Prevention or treatment of solitary ulcers

Air-fluidized bed

A box containing glass beads and covered with a polyester sheet; the beads are fluidized by a flow of warm, pressurized air, which floats the polyester cover

Feces and body fluids flow through the sheet, frequent turning of patient unnecessary

Very expensive and heavy, generates heat, causes insensible water loss, reduces access to patient, noisy

Treatment of ulcers in functionally dependent patients with large, deep, or multiple ulcers; preferred for patients with incontinence or nonhealing wounds, or patients who are not surgical candidates

Low-air-loss bed

Multiple inflated fabric pillows attached to a modified hospital bed frame

Lightweight, similar to a hospital bed

Expensive

Treatment of ulcers in functionally dependent patients with large, deep, or multiple ulcers; prevention of ulcers in patients in intensive care unit

From Evans JM et al: Pressure ulcers: prevention and management. Mayo Clin Proc 70:789, 1995, with permission.

Static support surfaces are recommended for patients who can assume several positions without bearing weight on an ulcer. These include specialized foam mattresses and mattresses with various fillings. They may also be overlays used atop of a base mattress.

“Low-tech” foam mattresses are the most commonly used material for pressure reduction, given their ease of use, affordability, and evidence base. A Cochrane Systematic Review examined five trials comparing foam alternatives with standard hospital mattresses, demonstrating a relative risk reduction of 60% in pressure ulcer incidence with the use of foam mattresses.28 Foam slabs should be 3–4 inches thick to effectively reduce pressure. A trial with 70 intensive care unit patients in France showed 85% risk reduction in heel ulcers in patients using a total foam body support system compared to control groups receiving standard pressure ulcer protocol including a water mattress.29

Other “low-tech” pressure supports include static supports filled with air, water, gel, silicone, polyvinyl, heel elevators, and sheepskins. Most of them permit a high degree of immersion, allowing the body to sink into the surface as it conforms to the bony prominences. This increases the surface pressure distribution area and lowers the interface pressure by transferring the pressure to adjacent areas. Unfortunately, many of the water-filled and bead-filled mattresses that demonstrated success in clinical trials are no longer available. A Cochrane Systematic Review of two trials examining the effects of sheepskins showed relative risk of 0.42 for pressure ulcer development compared to standard low-tech support surfaces.28

Patients who cannot tolerate frequent turning, immobile patients, those with large or multiple ulcers, and patients with unresponsive ulcers may require dynamic support surfaces, which are electrically powered. These provide cyclical, alternating pressure relief, and include air-fluidized, low-air-loss, and/or alternating-air beds.

Air-fluidized beds contain microspheric silicon-coated beads encased in an air-permeable fabric (polyester or Gore-Tex). The beads are suspended by pressurized streams of warmed air, which allows patients to “float” and decreases pressure through the principle of immersion while simultaneously reducing shear. Feces and body fluids flow freely through the sheet; thus, the skin is kept dry.

Low-air-loss systems use a series of connected, air-filled cushions that are inflated to specific pressures. Some have alternating and pulsating pressure features. A prospective, randomized trial demonstrated that the use of low-air-loss beds resulted in threefold faster wound healing than use of a foam mattress.30 Unlike with air-fluidized beds, urine and feces do not pass through the fabric of low-air-loss beds.

Alternating-pressure systems distribute pressure by shifting the body weight to different surface contact areas. The air is pumped into the chambers at periodic intervals to inflate and deflate them in opposite phases, which thereby changes the location of contact pressure. Though alternating-pressure systems have not been proven more efficacious than low-tech supports, a cost effectiveness analysis by the UK National Health Service associated them with 80% probability of being cost saving due to shorter hospital stays and delay in ulceration.28,31

Other pressure supports that may be of modest benefit include kinetic turning beds, operating table overlays, and seat cushions. Kinetic turning beds are primary used in ICU settings for pulmonary concerns. Operating table overlays may decrease postoperative pressure ulcer incidence and should be employed with high-risk patients undergoing long procedures.

Wound Management

Cleansing

Cleansing should be performed gently to minimize mechanical and chemical trauma to healing tissues. Normal saline is preferred because it is most physiologic in relation to the wound. Safe and effective irrigation pressures for ulcers range from 4 to 15 psi; higher pressures than this may cause trauma and drive bacteria into the wound tissue. Certain skin cleansers and antiseptics such as povidone iodine, sodium hypochlorite solution, hydrogen peroxide, acetic acid, and liquid detergents should be avoided, because these agents are cytotoxic and may retard epithelialization.

DéBridement

Ulcers with devitalized, necrotic tissue should be débrided, because necrotic tissue supports the growth of pathogenic organisms. Mechanical débridement techniques include application of moistened saline or wet-to-moist dressings, hydrotherapy (whirlpool), wound irrigation, and application of dextranomers. Wet-to-dry dressings changed every 4 to 6 hours are painful and are nonselective for necrotic tissue. Whirlpool devices can be considered for pressure ulcers with thick exudate, slough, or necrotic tissue. For wound irrigation, a large 35-mL syringe and 19-gauge angiocatheter can be used to provide adequate pressure.1

Sharp débridement involves the use of a scalpel, scissors, or other sharp instrument to remove devitalized tissue and is generally indicated in cases in which there is eschar. For smaller ulcers, local anesthesia can be used, whereas larger stage III or IV ulcers may require extensive surgical débridement under general anesthesia. Enzymatic débridement can be used in patients who cannot tolerate surgery. Topical agents such as sutilains, collagenase, fibrinolysin, and deoxyribonuclease can be used. Papain was removed from the market due to hypersensitivity reactions.32 Dressings should be changed once to several times daily. Contact dermatitis can sometimes occur, and these agents should not be used if tendon is exposed.2

Autolytic débridement involves the use of synthetic dressings to cover the wound, which allows digestion of necrotic tissue by enzymes normally present in wound fluids.

In addition to traditional débridement methods, the use of sterile fly larvae (maggots) to clean necrotic tissue is gaining popularity and appears to be safe and effective.

Dressing Products

Dressings can help protect the wound from the environment, reduce or prevent wound infection, stimulate autolytic débridement, reduce wound pain, and stimulate the development of granulation tissue. It has been demonstrated experimentally that wounds maintained in a moist environment heal 40% faster than air-exposed wounds. Control of moisture and drainage from the wound helps provide an optimum wound environment for healing. There are several types of dressings, each one of which has specific properties, advantages, and disadvantages (eTable 100-3.2). Higher stage ulcers usually require more absorptive dressings to maintain a moist environment. A variety of specialized dressings may be helpful for pressure ulcer management, including a bilayer matrix wound dressing, pig-derived acellular small intestine submucosa, and natural latex biomembrane. Both the NPUAP and the EPUAP (European Pressure Ulcer Advisory Panel) state in their international pressure ulcer guidelines that gauze dressings should be avoided in clean, open pressure ulcers since they may stick to wounds, causing pain with dressing changes.24 In fact, a systematic review of 29 studies demonstrated hydrocolloid dressings to be superior to gauze in terms of pressure ulcer healing, pain associated with dressing change, absorption capacity, side effects, and cost.33

eTable 100-3.2 Summary of Wound Care Products Available for the Treatment of Pressure Ulcers

eTable 100-3.2 Summary of Wound Care Products Available for the Treatment of Pressure Ulcers

Bacterial Colonization and Infection Management

Ulcer cleansing and débridement are important to control microbial burden in pressure sores. Systemic antibiotic therapy is not recommended for contamination or minor localized infections but is indicated when bacteremia, cellulitis, or osteomyelitis is present.

Topical antibiotics are used to prevent or treat wound infection, reduce bacterial load, or reduce odor and signs of inflammation. Topical antibiotics such as neomycin and bacitracin are common allergens and can cause contact dermatitis and, rarely, anaphylaxis. Topical formulations of antibiotics that are used systemically (e.g., gentamicin) should be avoided because bacterial resistance may develop. However, the Agency for Healthcare Research and Quality guideline recommends a short 2-week course of topical antibiotics for a clean ulcer that is not healing or that is producing a moderate amount of exudate despite appropriate care.35 The use of topical metronidazole 1% solution or 0.75% or 0.80% gel has gained popularity in reduction of wound odor, though randomized controlled trials are still needed to prove efficacy.36

Pain Management

Pain management requires a combination of conservative measures, medications, and appropriate wound care. Muscle relaxants and physical and occupational therapy may be helpful to decrease muscle spasm in the area of ulceration. Transcutaneous electrical nerve stimulation may help relieve acute and chronic pain. The use of topical anesthetics such as lidocaine-prilocaine cream on wounds 30 minutes before débridement significantly reduces pain associated with wound care procedures. An opiate diamorphine gel was also shown to significantly reduce pain with dressing changes in a small randomized controlled trial of patients with stage II and III ulcers.37

Nonopioid analgesics (aspirin, other nonsteroidal anti-inflammatory drugs) are first-line systemic therapy, followed by stronger medications such as opioids. Adjuvant medications such as tricyclic antidepressants can be used to enhance analgesia.37 They can also improve depression in some chronic pain states and have sedative, sleep-enhancing qualities.

Nutritional Management

Screening for nutritional deficiencies is an important part of assessment and management of pressure ulcers. Adequate patient dietary intake of protein is important in healing pressure ulcers.38 A reasonable protein amount is between 1.2 and 1.5 g/kg/day, and caloric intake should be between 30 and 35 kcal/kg/day. Vitamin C or zinc deficiency can have negative effects on wound healing, but supplementation is useful only when deficiency is confirmed or suspected. If dietary intake continues to be inadequate, oral or parenteral nutritional supplementation may be required. A study of 672 critically ill patients showed that oral supplementation of 400 kcal/day resulted in 17% risk reduction for the development of pressure ulcers.39 Markers of nutritional deficiency include a serum albumin level of less than 3.5 mg/dL and unintentional weight loss of more than 15% of baseline. Patients should be kept adequately hydrated.

Surgery

The long-term efficacy of surgical repair of pressure ulcers, especially in older patients, has been questioned because of high recurrence rates and mortality. The decision to undertake surgical repair should be made with full knowledge of the risks and benefits, surgical and nonsurgical alternatives, and complications associated with each procedure. Surgical techniques include skin grafting; creation of cutaneous, muscle, and fasciocutaneous flaps or pedicled flaps; microvascular free tissue transfer reconstruction; and simple direct suture, depending on the site, number, and grade of lesions, and the patient's clinical condition. In general, surgery is often required for stage IV ulcers, whereas more superficial ulcers may heal with conservative therapy.

Adjunctive Therapies

Adjunctive therapies have been used in case studies, but more data are needed to determine the effectiveness of these therapies, which include ultrasound, electromagnetic therapy, electrical stimulation, negative pressure (vacuum-assisted closure), monochromatic phototherapy, and honey.40

Whenever possible, others factors that impair healing such as smoking; hypovolemia; cold; chronic diseases including diabetes mellitus, systemic arterial hypertension, anemia, and vascular alterations; and the use of medications such as corticosteroids should be limited or controlled.

Prevention

Preventive actions can decrease the patient's risk of developing pressure ulcers. These steps can also keep pressure ulcers from getting worse. Preventive measures are listed in Table 100-4.

Table 100-4 Preventive Measures

Table 100-4 Preventive Measures

Maintain personal hygiene. Consider topical lotions containing fatty acids.

Try to assure adequate nutrition and hydration.

Evaluate and manage urinary and fecal incontinence.

Position to alleviate pressure over bony prominences and shearing forces over heels and elbows, base of head, and ears.

Try to reposition every 2 h when in bed and every hour when in a chair; if alert and capable, the patient should be taught to shift his or her weight every 15 min while in a chair.

Use appropriate positioning devices and foam padding; do not use donut-shaped devices. Consider dynamic supports in high-risk patients.

Try to avoid placing the patient on his or her trochanters or directly on the wound.

Maintain the lowest head elevation possible (no greater than 30°)

Use lifting devices such as draw sheets or a trapeze.

Try to prevent contractures.

Do not massage reddened areas over bony prominences.

Modified from American Medical Directors Association: Clinical Practice Guideline: Pressure Ulcers. Columbia, MD, American Medical Directors Association, 2008. © 2008 American Medical Directors Association.

References