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The National Pressure Ulcer Advisory Panel has classified pressure ulcers according to 4 stages (NPUAP, 1989) :
Stage I: Non-blanchable erythema of intact skin.
Stage II: Partial-thickness skin loss involving the epidermis or dermis; lesions may present as an abrasion, blister, or superficial ulcer.
Stage III: Full-thickness skin loss that may extend to, but not through, the fascia; the ulcer may be undermined.
Stage IV: Full-thickness skin loss involving deeper structures, such as muscle, bone, or joint structures.
Most pressure ulcers arise in hospital, where the prevalence among inpatients is 3%-14%, although it can be as high as 70% in elderly inpatients with orthopaedic problems.
The incidence of pressure ulcers in hospitals is 1%-5%.
In patients who are confined to bed or to a chair for more than one week, the incidence rises to almost 8%.
In long term healthcare facilities up to 25% of patients develop pressure ulcers.
Almost a fifth of pressure ulcers develop at home and a further fifth in nursing homes.
The prevalence of pressure ulcers in nursing homes is not much higher than in hospitals. Pressure ulceration in elderly patients is associated with a fivefold increase in mortality, and in-hospital mortality in this group is 25%-33%
Risk factors for the development of pressure ulcers are either intrinsic or extrinsic. Limited mobility and poor nutrition are the strongest intrinsic predictors of pressure ulcer formation.
Incontinence, increased age, diabetes mellitus, stroke, white race, skin abnormalities, and male sex have also been implicated by multivariate analysis in some studies (Allman RM, 1997).
Extrinsic factors include pressure, friction, shear stress, and moisture; of these, the most important is pressure.
A patient lying on a hospital mattress can generate pressures of 45–75 mm Hg over such bony prominences as the sacrum, greater trochanters, and heels, where pressure ulcers commonly form.
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If this pressure is sustained for 3–4 h, capillary perfusion pressure within the deep tissues (estimated to be 20–30 mm Hg) is exceeded, and pressure ulcers may result (Woolsey RM, 1991).
It is important to recognize that pressure is highest at the muscle/bone interface, and that fat and muscle are more susceptible to pressure-related damage than is skin. Thus, the appearance of the visible skin lesion often results in an underestimation of the degree of deep-tissue involvement.
Friction and shear stress can occur when a patient is dragged across a surface or is positioned with the head of the bed in a raised position.
Friction can damage superficial skin, and shear stress can crimp the deeper vessels, leading to increased ischemia.
Ulcers produced by shear stress can have extensive deep-tissue necrosis and can be much worse than external inspection may suggest.
Moisture, such as that resulting from incontinence, can increase the risk of a pressure ulcer developing by 5-fold. It can also serve as a source of bacterial contamination.
The challenge of microbiological evaluation is to distinguish between bacterial invasion and colonization.
Blood cultures or cultures of deep-tissue biopsy specimens generally are more clinically significant than are cultures of superficial swab specimens or aspiration of the pressure ulcer (Rudensky B, 1992).
However, aspirated samples of clinically non-infected ulcers have also been shown to contain bacteria in 30% of cases (Nicolle LE, 1994).
Guidelines for microbiological evakluation are :
On the basis of the aforementioned information, it can be concluded that
(1) superficial swab cultures generally reflect colonization rather than infection and are not useful clinically,
(2) needle aspirations are difficult to interpret and either should not be used or should be interpreted with caution, and
(3) culture results by themselves, even results of bone culture or culture of other deep-tissue biopsy specimens, should not be used as the sole criterion for infection without clinical or histo-pathological evidence of infection.
Imaging studies are useful in the evaluation of pressure ulcers for determination of the presence of osteomyelitis and for delineation of the extent of deep-tissue involvement.
Plain radiographs have a limited role in the evaluation of pressure ulcers.
Bony changes, such as periosteal reactive changes and heterotopic new bone formation usually associated with osteomyelitis, can also be present in non-infected pressure ulcers.
Furthermore, lytic bony lesions rarely are seen in cases of osteomyelitis associated with pressure ulcers (Darouiche RO, 1994).
Sinograms can be useful to define the extent of the ulcer, but their value probably has diminished with the availability of CT and MRI.
CT and MRI.
CT may be more useful for definition of the extent of deep soft-tissue damage associated with pressure ulcers.
Although highly specific, CT has a relatively low sensitivity for the diagnosis of associated osteomyelitis (11%) (Lewis VL, 1988).
MRI is more useful for the detection of osteomyelitis associated with pressure ulcers.
Although 3-phase technetium-99m diphosphate bone scans and gallium scintigraphy are very useful in the diagnosis of hematogenous osteomyelitis, they have been shown to lack specificity for the detection of osteomyelitis caused by pressure ulcers (Bergstrom N, 1994).
The goals of treatment of infected pressure ulcers are to resolve the infection and to aid in wound healing. Implementation of the appropriate therapy requires an understanding of the risk factors and pathophysiology that lead to pressure ulcer formation.
Treatment to aid in wound healing.
Attention should be given to promoting healing of the pressure ulcer itself, in addition to treating infection.
This requires ameliorating both intrinsic and extrinsic risk factors and providing meticulous local wound care.
Although many intrinsic risk factors for the development of pressure ulcers are not amenable to intervention, some comorbid conditions associated with delayed wound healing, such as poor nutritional status, congestive heart failure, and diabetes mellitus, can be optimally controlled (Herman LE, 1989).
Dressings that maintain a moist wound environment facilitate healing and can be used for autolytic debride-ment (Kerstein MD, 2001).
Synthetic dressings reduce caregiver time, cause less discomfort, and potentially provide more consistent moisture (Hess CT, 2002).
These dressings include transparent films, hydrogels, alginates, foams, and hydrocolloids.
Transparent films effectively retain moisture, and may be used alone for partial-thickness ulcers or combined with hydrogels or hydrocolloids for full-thickness wounds. hydrogels can be used for deep wounds with light exudate. Alginates and foams are highly absorbent and are useful for wounds with moderate to heavy exudate. hydrocol-loids retain moisture and are useful for promoting auto-lytic debridement.
Dressing selection is dictated by clinical judgment and wound characteristics; no moist dressing (including saline-moistened gauze) is superior (Bouza C, 2005).
There is evidence that patients who have a high protein intake may experience improved wound healing, compared with patients who have an inadequate caloric intake of protein.
Supplementation with enteral feeding, however, has not been demonstrated to improve wound healing or prevent pressure ulcers (Thomas DR, 1997).
Reduction of extrinsic factors (in particular, pressure relief) is a cornerstone of therapy.
There is no evidence to determine an optimal patient repositioning schedule, and schedules may need to be determined empirically (Whitney J, 2006).
According to recommendations from the Agency for Health Care Policy and Research, patients who are bedridden should be repositioned every two hours (AHCPR, 2007).
To minimize shear, the head of the bed should not be elevated more than 30 degrees and should be maintained at the lowest degree of elevation needed to prevent other medical complications, such as aspiration and worsening congestive heart failure symptoms.
Mechanical devices to lower pressure can be classified as either static or dynamic. Static devices, such as foam- or fluid-filled mattresses or supports, maintain constant pressure when the patient is not moving, but they disperse pressure over a greater area than do standard bed mattresses.
These devices are appropriate for patients who can assume different positions without bearing weight on the ulcer and without compressing the support material (Bergstrom N, 1994).
For patients who cannot avoid bearing weight on the ulcer or who are not healing as expected, a dynamic pressure-relieving device, such as an air-fluid bed, may be a better choice.
These devices change their support by alternating currents of air to redistribute pressure against the body, and they can achieve a greater degree of pressure reduction than can static devices.
Thus, most authorities recommend the use of dynamic beds for the management of persons with stage III to stage IV pressure ulcers and for those that do not respond to standard therapy (Bergstrom N, 1994).
Local wound care is another fundamental component of pressure ulcer therapy. Debridement of necrotic tissue, appropriate dressing selection, and surgical repair are all important aspects of wound care, and these have been extensively reviewed elsewhere (Goode PS, 1997).
Sharp debridement is needed if infection occurs or to remove thick and extensive eschar. Healing after sharp debridement requires adequate vascularization; thus, vascular assessment for lower extremity ulcers is recommended (RNAO, 2007).
Enzymatic debridement is useful in the long-term care of patients who cannot tolerate sharp debridement; however, it takes longer to be effective and should not be used when infection is present (Püllen R, 2002).
Treatment of infection.
A combination of surgical and medical interventions may be required.
Surgical debridement is necessary to remove necrotic tissue and drain abscesses. Systemic antimicrobial therapy should be used for patients with serious pressure ulcer infections, including those with spreading cellulitis, osteomyelitis, or bacteremia.
Because of the high associated mortality, empiric antibiotics are appropriate if bacteremia or sepsis is suspected. Administration of topical antibiotics is not indicated.
The choice of antibiotics is based on the current understanding of the microbiology of infected pressure ulcers. Because such infections usually are polymicrobial, therapeutic regimens should be directed against both gram-positive and gram-negative facultative organisms as well as anaerobic organisms
Because of poor tissue perfusion in infected pressure ulcers, antibiotic therapy initially should be administered intravenously to patients with signs of systemic infection.
Infection Control Measures
Infection-control recommendations from the Agency for Healthcare Research and Quality (formerly known as the Agency for Health Care Policy and Research) for residents of long-term care facilities who have pressure ulcers (Bergstrom N, 1994).
Clinical assessment of pressure ulcers begins with identification of patients considered to be at risk and examination for early signs of pressure sore formation at the anatomical sites where such sores are most commonly encountered.
A thorough clinical examination is critical to the identification of pressure ulcers that may serve as an occult focus for infection.
It is helpful to recognize the typical signs of soft-tissue involvement, such as warmth, erythema, local tenderness, purulent discharge, and presence of foul odor. However, because of associated comorbidities and advanced age, systemic signs, such as fever and leukocytosis, may be minimal or absent, and even local signs of inflammation may not be obvious (Parish LC, 1989).
However, the manifestations of infection in pressure ulcers can be extremely variable. Delayed wound healing may be the only sign of infection.
More serious manifestations of infection are osteomyelitis and bacteremia.
Osteomyelitis can present as a poorly healing wound with or without systemic manifestations, such as fever, leukocytosis, and other signs of sepsis.
In contrast, bacteremia due to infected pressure ulcers usually presents with signs of a systemic inflammatory response, including fever, chills, confusion, and hypotension,
and the mortality rate among patients with bacteremia due to infected pressure ulcers approaches 50% (Galpin JE, 1976).