Pressure Injuries (Pressure Ulcers) and Wound Care

Practice Essentials

Although the terms decubitus ulcer, pressure sore, and pressure ulcer have often been used interchangeably, the National Pressure Injury Advisory Panel (NPIAP; formerly the National Pressure Ulcer Advisory Panel [NPUAP]) currently considers pressure injury the best term to use, given that open ulceration does not always occur.^[1]According to the NPIAP, a pressure injury is localized damage to the skin and underlying soft tissue, usually over a bony prominence or related to a medical or other device. It can present as intact skin or an open ulcer and may be painful. It occurs as a result of intense or prolonged pressure or pressure in combination with shear.

See the image below.

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Advanced sacral pressure ulcer shows effects of pressure, shearing, and moisture.

Signs and symptoms

The following important information should be obtained from the history:

Overall physical and mental health, including life expectancy
Previous hospitalizations, operations, or ulcerations
Diet and recent weight changes
Bowel habits and continence status
Presence of spasticity or flexion contractures
Medications and allergies to medications
Tobacco, alcohol, and recreational drug use
Place of residence and the support surface used in bed or while sitting
level of independence, mobility, and ability to comprehend and cooperate with care
Underlying social and financial support structure
Presence of specific cultural, religious, or ethnic issues
Presence of advanced directives, power of attorney, or specific preferences regarding care
Information related to the current ulceration - Pain, foul odor or discharge, natural history of the present ulcer, and associated medical cause of the ulcer

A thorough physical examination is necessary to evaluate the patient’s overall state of health, comorbidities, nutritional status, and mental status. After the general physical examination, attention should be turned to the wound.

For the purposes of workup and treatment, it is helpful to stage the pressure injury according to the system promulgated by the NPUAP,^[2]as follows:

Stage 1 pressure injury - Nonblanchable erythema of intact skin
Stage 2 pressure injury - Partial-thickness skin loss with exposed dermis
Stage 3 pressure injury - Full-thickness skin loss
Stage 4 pressure injury - Full-thickness skin and tissue loss
Unstageable pressure injury - Obscured full-thickness skin and tissue loss
Deep pressure injury - Persistent nonblanchable deep red, maroon or purple discoloration

Complications of ulceration include the following:

Malignant transformation
Autonomic dysreflexia
Osteomyelitis
Pyarthrosis
Sepsis
Urethral fistula
Amyloidosis
Anemia

See Presentation for more detail.

Diagnosis

Laboratory studies that may be helpful include the following:

Complete blood count (CBC) with differential
Erythrocyte sedimentation rate (ESR)
Albumin and prealbumin
Transferrin
Serum protein

When indicated by the specific clinical situation, the following should be obtained:

Urinalysis and culture in the presence of urinary incontinence
Stool examination for fecal WBCs and Clostridium difficile toxin when pseudomembranous colitis may be the cause of fecal incontinence
Blood cultures if bacteremia or sepsis is suggested

Additional studies that may be considered include the following:

Plain radiography
Bone scan
Magnetic resonance imaging
Tissue or bone biopsy

See Workup for more detail.

Management

General principles of wound assessment and treatment are as follows:

Wound care may be broadly divided into nonoperative and operative methods
For stage 1 and 2 pressure injuries, wound care is usually conservative (ie, nonoperative)
For stage 3 and 4 lesions, surgical intervention (eg, flap reconstruction) may be required, though some of these lesions must be treated conservatively because of coexisting medical problems^[3]
Approximately 70%-90% of pressure injuries are superficial and heal by second intention

Successful medical management of pressure injuries relies on the following key principles:

Reduction of pressure
Adequate débridement of necrotic and devitalized tissue
Control of infection
Meticulous wound care

If surgical reconstruction of a pressure injury is indicated, medical status must be optimized before reconstruction is attempted. General measures for optimizing medical status include the following:

Control of spasticity
Nutritional support as appropriate
Cessation of smoking
Adequate pain control
Maintenance of adequate blood volume
Correction of anemia
Maintenance of the cleanliness of the wound and surrounding intact skin
Management of urinary or fecal incontinence as appropriate
Management of bacterial contamination or infection

Additional nonsurgical treatment measures include the following:

Pressure reduction - Repositioning and use of support surfaces
Wound management - Débridement, cleansing agents, dressings, and antimicrobials
Newer approaches still being studied - Growth factors (eg, becaplermin), negative-pressure wound therapy, and electrotherapy

Surgical interventions that may be warranted include the following:

Surgical débridement
Diversion of the urinary or fecal stream
Release of flexion contractures
Wound closure
Amputation

Options available for surgical management of pressure injuries are as follows:

Direct closure (rarely usable for pressure injuries being considered for surgical treatment)
Skin grafts
Skin flaps
Myocutaneous (musculocutaneous) flaps
Free flaps

The choice of reconstruction approach depends on the location of the pressure injury (eg, ischial, sacral, or trochanteric).

Prevention, if achievable, is optimal. Prevention of pressure injuries has two main components:

Identification of patients at risk
Interventions designed to reduce the risk

See Treatment and Medication for more detail.

References

Background

The terms decubitus ulcer (from Latin decumbere, “to lie down”), pressure sore, and pressure ulcer have often been used interchangeably in the medical community. However, as the name suggests, decubitus ulcer occurs at sites overlying bony structures that are prominent when a person is recumbent. Hence, it is not an accurate term for ulcers occurring in other positions, such as prolonged sitting (eg, ischial tuberosity ulcer). Because the common denominator of all such ulcerations is pressure, pressure ulcer came to be considered the best term to use.

The National Pressure Ulcer Advisory Panel (NPUAP) was an independent nonprofit organization formed in 1987 and dedicated to the prevention, management, treatment, and research of pressure ulcers. In April 2016, the NPUAP announced that it was changing its preferred terminology from pressure ulcer to pressure injury, on the grounds that the latter term better described this injury process in both intact and ulcerated skin.^[1] In November 2019, the NPUAP changed its name to the National Pressure Injury Advisory Panel (NPIAP).

Currently, the NPIAP defines a pressure injury as localized damage to the skin and underlying soft tissue, usually over a bony prominence or related to a medical or other device.^[1]Such injury can present either as intact skin or an open ulcer and may be painful. It results from intense or prolonged pressure or pressure combined with shear. The NPIAP also notes that the tolerance of soft tissue for pressure and shear may be affected by microclimate, nutrition, perfusion, comorbid conditions, and the condition of the soft tissue.

Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual against a surface beneath. These pressures often exceed capillary filling pressure (~32 mm Hg). In patients with normal sensitivity, mobility, and mental faculty, pressure injuries do not occur. Feedback, conscious and unconscious, from the areas of compression leads them to change their body position, and these changes shift the pressure before any irreversible tissue damage develops. (See Pathophysiology and Etiology.)

Those who cannot avoid long-term uninterrupted pressure over bony prominences (eg, persons who are elderly, have neurologic impairment, or are undergoing acute hospitalization^[4]) are at increased risk for pressure injuries. They cannot protect themselves from the pressure unless they consciously change position or are helped to do so. Even a highly conscientious patient with an extensive support group and unlimited financial resources may develop such injuries as a result of a brief lapse in avoidance of the ill effects of pressure.^{[5, 6]}

Addressing the overall management of pressure injuries is now a prominent national healthcare issue. Despite current interest and advances in medicine, surgery, nursing care, and self-care education, pressure injuries remain a major cause of morbidity and mortality, and patients with pressure injuries are important users of medical resources.^{[7, 8, 9, 10, 11, 12, 13, 14]}

Many factors are involved in the management of pressure injuries. Nursing plays a pivotal role in this challenging and complex process, using a multifaceted approach that includes skin care, pressure relief, and nutritional support. Prevention is the key to managing pressure injuries, and it begins with a complete medical and nursing history, a risk assessment, and skin examination when the patient is admitted.^{[9, 10, 15]}(See Treatment.)

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 injuries, these preventive measures must be used in conjunction with the techniques of general wound care. Nonoperative wound care may involve simple topical therapy, as for pressure injuries 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.

Research in the area of pressure injuries—specifically, in the characterization, prevention, and treatment of these lesions—is important for 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.

To date, clinical studies of pressure injuries have been difficult to assess because they have often been qualitatively based on random observation and uncontrolled studies. To arrive at more reliable conclusions, more fundamental approaches to these injuries must be considered. Questions that might be asked include the following:

What are the basic histologic, pathologic, and biochemical markers in an evolving pressure injury?
Is it ethical to take a biopsy specimen of a human pressure injury for purposes of research?
What are the multiple variables in the formation of pressure injuries in the human environment?

A monograph prepared by the Research Committee of the NPUAP (now the NPIAP) suggested the following research priorities^[7]:

Outcome-focused research
Intervention and product efficacy studies
Basic research related to staging of ulcers
Refinement of risk assessment methods
Risk-based, multi-interventional trials

Additional issues requiring investigation included 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 were considered to warrant further investigation.

References

Etiology

Impaired mobility is probably the most common reason why patients are exposed to the prolonged uninterrupted pressure that causes pressure injuries. This situation may be present in patients who are neurologically impaired, heavily sedated or anesthetized, restrained, demented, or recovering from a traumatic injury. These patients cannot alter their position far enough or often enough to relieve the pressure. Prolonged immobility may lead to muscle and soft tissue atrophy, decreasing the bulk over which bony prominences are supported.

Contractures and spasticity often contribute to ulcer formation by repeatedly exposing tissues to trauma through flexion of a joint. Contractures rigidly hold a joint in flexion, whereas spasticity subjects tissues to repeated friction and shear forces. Skin breakdown and pressure injuries may frequently be found under and between toes and on the palm of the hand.

Inability to perceive pain, whether from neurologic impairment or from medication, contributes to pressure injuries by removing one of the most important stimuli for repositioning and pressure relief. Conversely, pain from surgical incisions, fracture sites, or other sources may make the patient unwilling or unable to change position.

The quality of the skin also influences whether pressure leads to ulceration. Paralysis, insensibility, and aging lead to atrophy of the skin with thinning of this protective barrier. A decrease in epidermal turnover, a flattening of the dermal-epidermal junction, and a loss of vascularity occur with advanced age.

In addition, the skin becomes more susceptible to minor traumatic forces, such as the friction and shear forces typically exerted during the moving of a patient. Trauma that causes deepithelialization or skin tears removes the barrier to bacterial contamination and leads to transdermal water loss, creating maceration and causing the skin to adhere to clothing and bedding.

Incontinence or the presence of a fistula contributes to ulceration in several ways. These conditions cause the skin to be continually moist, thus leading to maceration. In addition, frequent soiling has the effect of regularly introducing bacteria into an open wound.

Bacterial contamination, though not truly an etiologic factor, must be considered in the treatment of pressure injuries, in that it can delay or prevent wound healing. These lesions are warm, moist reservoirs for bacterial overgrowth, where antibiotic resistance may develop. A pressure injury may progress from simple contamination (as in any open wound) to gross infection (indicating bacterial tissue invasion). This may lead to uncommon but life-threatening complications (eg, bacteremia, sepsis, myonecrosis, gangrene, or necrotizing fasciitis).

Malnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute to tissue vulnerability to trauma as well as cause delayed wound healing. Poor nutritional status certainly contributes to the chronicity often seen in these lesions and inhibits the ability of the immune system to prevent infections. Anemia indicates poor oxygen-carrying capacity of the blood. Vascular disease and hypovolemia also may impair blood flow to the region of ulceration.

In patients with normal sensitivity, mobility, and mental faculty, pressure injuries are unlikely. Conscious or unconscious feedback from the areas of compression leads them to change position, thereby shifting the pressure from one area to another long before any irreversible ischemic damage occurs. In individuals who cannot avoid long periods of uninterrupted pressure, the risk of necrosis and ulceration is increased. These individuals cannot protect themselves from the pressure unless they consciously change position or are helped to do so.

References

Epidemiology

United States statistics

Pressure injuries are common among patients hospitalized in acute- and chronic-care facilities. It has been estimated that about 1 million pressure injuries 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.^{[7, 25]}

Reported incidences of pressure injuries in hospitalized patients range from 2.7% to 29%, and reported prevalences in hospitalized patients range from 3.5% to 69%.^{[26, 27, 28, 29, 30]}Patients in critical care units have an increased risk of pressure injuries, as evidenced by a 33% incidence and a 41% prevalence.^{[31, 32]}

The fifth National Pressure Ulcer Prevalence Survey, conducted in 1999 among patients in acute care hospitals, showed an overall prevalence of 14.8%, with 7.1% of ulcers having occurred during that hospital visit.^[33]Of the various hospital settings, intensive care units (ICUs) had the highest prevalence, at 21.5%. The largest single age group of patients with pressure injuries consisted of patients aged 71-80 years (29%).

Elderly patients admitted to acute care hospitals for nonelective orthopedic procedures are at even greater risk for pressure injuries than other hospitalized patients are, with a 66% incidence.^{[34, 35]}In a study of 658 patients aged 65 years or older who underwent surgery for hip fracture, Baumgarten et al found that 36.1% developed an acquired pressure injury within 32 days after hospital admission.^[36]

In nursing homes, the prevalence of pressure injuries is 2.6-24%.^{[25, 37]}; the incidence is 25% in residents admitted from an acute care hospital.^[37]Patients with preexisting pressure injuries show a 26% incidence of additional pressure injury formation over a 6-month period. The incidence in chronic care hospitals is reported to be 10.8%,^[38]whereas 33% of those admitted to a chronic care hospital have pressure injuries.^[39]Long-term follow-up demonstrates that most ulcers heal within 1 year.^{[25, 40]}

Among patients with neurologic impairments, pressure injuries occur with an incidence of 7-8% annually,^[41]with a lifetime risk estimated to be 25-85%.^[42]Moreover, pressure injuries are listed as the direct cause of death in 7-8% of all individuals with paraplegia; these individuals also have the highest recurrence rate (80%).^[43]In persons with spinal cord injury (SCI) and associated comorbidity, the incidence of pressure injuries is in the range of 25-66%.^{[44, 45, 46, 47]}

A study of the prevalence of pressure injuries in community residents with SCI demonstrated that those with higher-level SCI lesions carry a greater risk of developing pressure injuries than those with lower-level lesions do.^[44]Of 100 patients with pressure injuries, 33 had injuries that were classified as stage 2 or greater. Black patients had more severe injuries than other racial groups did.

Some authors speculate that detecting erythema can be more difficult with skin that has darker pigmentation.^[48]Because prolonged nonblanching erythema is typically an early warning sign of pressure injury risk and development, difficulty in detecting erythema can result in failure to recognize grade I pressure injuries.

International statistics

In a study from Germany that reviewed the prevalence of pressure injuries in more than 18,000 patients residing in long-term care facilities, the prevalence was found to have decreased from 12.5% in 2002 to 5% in 2008.^[49]This decrease is thought to be due to more effective management strategies and better prevention.

Age-related demographics

The prevalence of pressure injuries appears to have a bimodal age distribution. A small peak occurs during the third decade of life, reflecting ulceration in those with traumatic neurologic injury. Immobility and lack of sensation make these patients susceptible to developing pressure injuries. Treatment of these lesions in this patient population represents a financial challenge, with one hospital reporting an average cost of $78,000 for each admission of a patient with a pressure injury.

As patients move from the age category of 40-58 years to the age category of 75 years or older, a larger increase in the incidence of pressure injuries occurs.^[50]Two thirds of pressure injuries occur in patients older than 70 years.^[38]As elderly individuals become the fastest-growing segment of the population, with an estimated 1.5 million people living in extended-care facilities, the problem of pressure injuries will have an even more profound influence on the American economy.^[51]

Sex-related demographics

Most younger individuals suffering from pressure injuries are males. The higher incidence in males reflects the greater number of men suffering traumatic SCIs. In the older population, most patients with pressure injuries are women, as a consequence of their survival advantage over men.

Race-related demographics

A study by Howard and Taylor found the incidence of pressure injuries in nursing home residents in the southeastern United States to be higher in black patients than in white ones.^[52]The authors examined data from 113,869 nursing home residents, none of whom had pressure injuries at nursing home admission. They determined that 4.7% of black residents developed postadmission ulcerations, compared with 3.4% of white residents.

In addition, the racial differences in pressure injury incidence displayed a sex predilection based on patient characteristics.^[52]The variation in incidence between black and white males was noted in residents who were dependent in mobility, whereas the difference in incidence between black and white females was noted in residents who were bedfast and living in nursing homes with fewer than 200 beds.

References

Prognosis

Pressure injuries are listed as the direct cause of death in 7-8% of all patients with paraplegia.^{[53, 41]}As many as one third of hospitalized patients with pressure injuries die during their hospitalization. More than half of those who develop a pressure injury in the hospital will die within the next 12 months. As a rule, these patients die of their primary disease process rather than of pressure ulceration, but the pressure injury may be a contributing factor in some instances.

Each year, approximately 60,000 people die of complications of pressure injuries.^[54]Individuals with pressure ulcers have a 4.5-times greater risk of death than persons with the same risk factors but without pressure injuries.^[8]A secondary complication, wound-related bacteremia, can increase the risk of mortality to 55%.^{[54, 55, 56, 57]}

The most common causes of fatality for patients with chronic pressure injuries are renal failure and amyloidosis. In general, mortality is higher for patients who develop a new pressure injury and in whom the injury fails to heal.

Infection is the most common major complication of pressure injuries. The offending pathologic organisms can be either anaerobic or aerobic. Aerobic pathogens commonly are present in all pressure injuries,^[58]whereas anaerobes tend to be present more often in larger wounds (65% in grade 3 and above).^[59]

The organisms most commonly isolated from pressure ulcers are as follows:

Proteus mirabilis
Group D streptococci
Escherichia coli
Staphylococcus
Pseudomonas
Corynebacterium

Patients with bacteremia are more likely to have Bacteroides species in their pressure injuries.^[59]These wounds need not 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 vital because the signs commonly associated with impeding or fulminating infection are frequently absent in elderly or immunocompromised patients. In geriatric patients with pressure injuries, bacteremia is reported to occur at a rate of 3.5 per 10,000 hospital discharges.^[8]

In view of the high mortality in this population (nearly 50%),^[56]it is important that antibiotic treatment of wound infection or secondary bacteremia provide 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, management of these complex problems may be facilitated by consulting an infectious disease specialist.

Sepsis also can occur secondary to osteomyelitis, which has been reported to occur in 26% of nonhealing ulcers.^[8]A prospective study demonstrated that osteomyelitis was associated with nonhealing grade 4 pressure injuries in 86% of the study population.^{[60, 61]}This study utilized three-phase technetium methyl diphosphate radionuclide flow to detect early osteomyelitis.

Various tests can be used to diagnose osteomyelitis in patients with pressure injuries. 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 their specificity is low (50%). Bone biopsy has the highest specificity (96%) and sensitivity (73%).^{[60, 61]}

A combination of diagnostic tests (eg, white blood cell [WBC] count, erythrocyte sedimentation rate [ESR], and plain radiography) provides a sensitivity of 89% and a specificity of 88%. If all three test results are positive, the positive predictive value of this combination is 69%. If all three test results are negative, the negative predictive value is 96%.^{[60, 61]}

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.^[45]

Systemic amyloidosis can result from chronic suppurative pressure injuries. Additional complications of pressure injuries 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 injuries can preclude wound healing, they should be aggressively prevented and treated.^[62]Complications may include infection, pain, depression, and even death.

References

Physical Examination

A thorough physical examination is necessary to evaluate the patient’s overall state of health, comorbidities, nutritional status, and mental status. The patient’s level of comprehension and extent of cooperation dictate the intensity of nursing care that will be required. The presence of contractures or spasticity is important to note and may help identify additional areas at risk for pressure ulceration.

After the general physical examination, attention should be turned to the pressure injury. Adequate examination of the wound may necessitate the administration of intravenous (IV) or oral pain medications to ensure patient comfort. Chronic pain may be present among these patients and may be exacerbated by examination ulcer.

Many classification schemes have been developed to define the severity of pressure ulcers.^[64] For a considerable period, the most widely accepted approach was that of Shea, which was modified and subsequently refined by the National Pressure Ulcer Advisory Panel (NPUAP).^[65] In April 2016, the NPUAP (now known as the National Pressure Injury Advisory Panel [NPIAP] since November 2019) announced an updated version of its staging system, along with a change in preferred terminology from pressure ulcer to pressure injury.^{[1, 2]}

The NPIAP system consists of four main stages of pressure injury but is not intended to imply that all pressure injuries follow a standard progression from stage 1 to stage 4 or that healing pressure injuries follow a standard regression from stage 4 to stage 1 to a healed wound. Rather, the system is designed to describe the degree of tissue damage observed at a specific time of examination and is meant to facilitate communication among the various disciplines involved in the study and care of patients with these lesions.

The categories specified in the current NPIAP staging system are as follows^[2]:

Stage 1 pressure injury - Intact skin with a localized area of nonblanchable erythema, which may appear differently in darkly pigmented skin; presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes; color changes do not include purple or maroon discoloration, which may indicate deep tissue pressure injury
Stage 2 pressure injury - Partial-thickness skin loss with exposed dermis; the wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister; adipose (fat) and deeper tissues are not visible, and granulation tissue, slough and eschar are not present; these injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel
Stage 3 pressure injury - Full-thickness skin loss, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present; slough or eschar may be visible; the depth of tissue damage varies by anatomic location; areas of significant adiposity can develop deep wounds; undermining and tunneling may occur; fascia, muscle, tendon, ligament, cartilage, and bone are not exposed
Stage 4 pressure injury - Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer; slough or eschar may be visible; epibole (rolled edges), undermining, and tunneling often occur; depth varies by anatomic location
Unstageable pressure injury - Full-thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar; if slough or eschar is removed, a stage 3 or 4 pressure injury will be revealed
Deep tissue pressure injury - Intact or nonintact skin with localized area of persistent nonblanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister; pain and temperature change often precede skin color changes; discoloration may appear differently in darkly pigmented skin; the injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface

Such staging is only a small part of the initial assessment. The injury location, the size of the skin opening (if present), and the presence of any surrounding maceration or induration must be accurately recorded. The presence of multiple pressure injuries prompts a search for interconnecting tracts with overlying skin bridging that may not be readily apparent. The presence or absence of foul odors, wound drainage, and soiling from urinary or fecal incontinence provides information about bacterial contamination and the need for debridement or diversionary procedures.

References

Complications

Complications fall into one of two categories: complications of chronic pressure injury (see below) and complications of reconstruction (see Treatment).

Complications of chronic injury include the following:

Malignant transformation
Autonomic dysreflexia
Osteomyelitis
Pyarthrosis
Sepsis
Urethral fistula
Amyloidosis
Anemia

Malignant transformation

The most serious complication of chronic ulceration is malignant transformation or degeneration (see the images below), also referred to as Marjolin ulceration. Although Marjolin initially described malignant transformation of a chronic scar from a burn wound, the term Marjolin ulcer has been commonly applied to the malignant transformation of any chronic wound, including pressure injuries, osteomyelitis, venous stasis ulcers, urethral fistulas, anal fistulas, and other traumatic wounds.^[66]

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Heaps of verrucous white tissue around the ulcer suggest malignant transformation, as observed with Marjolin ulcers.

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Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation (as observed with....

Histologically, this malignant transformation is a well-differentiated squamous cell carcinoma^[67]; however, its behavior is very aggressive in pressure injuries, considerably more so than in burns or osteomyelitis.^{[68, 66]}There is a high likelihood of nodal metastasis at the time of diagnosis. Any long-standing, nonhealing wound should alert the examiner to the need for biopsy.

Marjolin ulcers arising from burns or osteomyelitis have been treated with wide local excision, amputation, and lymph node dissection. Because pressure injury carcinoma is substantially more aggressive, more radical treatment (eg, hemicorporectomy and regional node dissection) is required if a cure is to be effected.^{[68, 66]}

The actual rate for malignant transformation of a pressure injury is not known but can be assumed to be low, in that only 18 cases have been described in the literature to date. Although apparently rare, pressure ulcer carcinoma is highly lethal: 12 of the 18 known patients died within 2 years.

Autonomic dysreflexia

Autonomic dysreflexia is a disordered autonomic response to specific stimuli. It includes sweating and flushing proximal to the injury, nasal congestion, headache, intermittent hypertension, piloerection, and bradytachycardia. Patients with midthoracic spinal cord lesions are most prone to this response. When autonomic dysreflexia is suggested, the patient is first positioned with the head up and monitored for changes in heart rate and blood pressure. Then, the precipitating stimulus must be removed.

The most common precipitating cause of autonomic dysreflexia is bladder distention, which is treated by inserting a Foley catheter or irrigating an already placed Foley catheter to remove blockage. Rectal examination to evaluate for fecal impaction should be considered. Nifedipine, hydralazine, or topical nitroglycerin may be administered to stabilize blood pressure. If autonomic dysreflexia does not respond to these measures, spinal anesthesia may be required.

Osteomyelitis

Foremost in the treatment of osteomyelitis is the removal of all nonviable bone, down to bone that bleeds bright red.^[69]In the reconstruction of reconstructing pressure injuries associated with osteomyelitis, it is important to use bone that is in the base flaps and has a muscle component. The muscle is placed over this bone after appropriate bone debridement. The flap reconstruction can be performed at the same time as the bone debridement. A 6-week course of IV antibiotics is then administered.

Pyarthrosis

Pyarthrosis of the hip joint can occur with communication of ischial or trochanteric ulcers. Often, the femoral head contains osteomyelitis, which necessitates its removal. The Girdlestone arthroplasty procedure has been employed in this situation (ie, hip pyarthrosis), including removal of the femoral head and reconstruction of this space with the vastus lateralis muscle flap (see the image below).^[70]

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Illustrated is Girdlestone arthroplasty for femoral head osteomyelitis pyarthrosis of hip joint. Femoral head is removed, and hip joint space is recon....

Sepsis

Pressure injuries do not cause sepsis. In patients who present with sepsis and pressure injuries, the sepsis is usually caused by a urinary tract infection. These wounds are almost always open to drain and therefore do not constitute debridement emergencies. Only on rare occasions are these injuries entirely occluded by a thick leathery eschar that prevents open drainage. In these cases, debridement is required to facilitate drainage and prevent systemic infection. In general, patients do not die of pressure injuries, but they can die with them.

Urethral fistula

Pressure injuries can also erode into the urethra (see the images below). Treatment of this complication (ie, urethral fistula) involves urinary diversion. Pressure injury reconstruction can be considered once the fistula has healed.

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Patient has urethral fistula within his pressure ulcer. When he performs Valsalva maneuver, urine leaks through this opening.

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Close-up view in patient who has urethral fistula within his pressure ulcer. When he performs Valsalva maneuver, urine leaks through this opening.

References

Approach Considerations

Once a pressure injury (pressure ulcer) has developed, immediate treatment is required.^[10]Commonly used treatments over the years have included innovative mattresses, ointments, creams, solutions, dressings, ultrasonography, 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, or removal of necrotic tissue). An algorithm for assessment and treatment is available.^{[57, 76, 77]}

General principles of wound assessment and treatment are as follows:

Wound care may be broadly divided into nonoperative and operative methods
For stage 1 and 2 pressure injuries, wound care is usually conservative (ie, nonoperative)
For stage 3 and 4 lesions, surgical intervention (eg, flap reconstruction) may be required, though some of these lesions must be treated conservatively because of coexisting medical problems^[3]
Approximately 70-90% of pressure injuries are superficial and heal by second intention

With thorough and comprehensive medical management, many pressure injuries may heal completely without the need for surgical intervention. Successful medical management of pressure ulcers relies on the following key principles:

Reduction of pressure
Adequate débridement of necrotic and devitalized tissue
Control of infection
Meticulous wound care

If surgical reconstruction of a pressure injury is indicated, it cannot be emphasized too strongly that medical management must be optimized before reconstruction is attempted; otherwise, reconstruction is doomed to failure. That is, spasticity must be controlled, nutritional status must be optimized, and the wound must be clean and free of infection. If there is significant fecal soiling into the injury, diverting colostomy should be considered before reconstruction. If there is a urethral fistula, it should be diverted and healed before reconstruction.

Wound reconstruction can be considered once the bacterial load has been sufficiently minimized to reduce the risk of infectious complications. Furthermore, the patient’s social situation and nutritional status must be optimized (albumin level >3.5 g/mL) to reduce the risk of an adverse outcome.

Because the complication rate after pressure injury reconstruction can be extremely high, patients who are poor surgical candidates in general should not undergo this procedure. Those who do not have a proper support network and a pressure-release bed at home also are not good candidates for pressure injury reconstruction, because of the risk of recurrence or other complications. Patients who do not comply with nonoperative measures used to promote healing by secondary intention are poor reconstruction candidates as well.

Treatment options of unproven efficacy that are currently being studied include hyperbaric oxygen therapy, electrotherapy, growth factors, and negative-pressure wound therapy (NPWT). Initial studies of electrotherapy seem promising, and topical application of the recombinant human growth factor becaplermin has been approved for use in patients with diabetic neuropathic ulcers of the lower extremity. However, not enough evidence is available to permit these treatments to be recommended for the treatment of pressure injuries.

Discharge planning begins early in the hospital stay and requires an interdisciplinary approach. Knowledge of available resources facilitates smooth transitions through all levels of care. With more care being conducted in the home environment, education of the patient and caregiver in preventing and treating pressure injuries becomes increasingly important. Various methods can be used to facilitate the educational process, including charts, diagrams, photographs, and videos. This comprehensive approach can positively influence outcome.^[77]

As a final note, some consideration should be given to the ethics of treating pressure injuries. For some individuals with pressure injuries, such as acutely hospitalized patients with a recoverable illness, aggressive treatment, as outlined in this article, is certainly indicated.

For other persons, however, such as chronically or terminally ill patients with long-standing or recurrent ulceration, aggressive treatment may not be in their best interests. In such instances, the wishes of the patient or the patient’s family should be weighed carefully. It may prove to be the case that the patient’s interests are better served by providing medical care and maintaining patient comfort than by instituting major invasive procedures.

In March 2015, the American College of Physicians (ACP) published clinical practice guidelines for risk assessment, prevention, and treatment of pressure ulcers (see Guidelines).^{[78, 79]}

References

General Measures for Optimizing Medical Status

Spasticity should be controlled pharmacologically with medications such as diazepam, baclofen, or dantrolene sodium. Patients with spasticity refractory to medication may be candidates for neurosurgical ablation. Flexion contractures may also be relieved surgically.

Nutritional status should be evaluated and optimized to ensure adequate intake of calories, proteins, and vitamins.^[80]Malnutrition is one of the few reversible contributing factors for pressure injuries, and establishing adequate caloric intake has been shown to improve healing of these lesions.

In a review of six clinical studies aimed at examining the effect of oral nutritional supplementation (ONS) enriched with arginine, vitamin C, and zinc in pressure ulcer care, ONS was found to have positive effects on pressure injury healing and potentially to reduce the risk of developing these injuries.^{[39, 81]}

Implementation of more invasive methods of nutrient delivery becomes an ethical issue and must be weighed against the complications of such delivery. Goals of nutritional support should include adequate protein intake and the establishment of a positive nitrogen balance, with 1.0-2.0 g/kg/day being recommended for patients with pressure injuries.

Other important considerations include cessation of smoking, adequate pain control, maintenance of adequate blood volume, and correction of anemia, the primary aims of which are to prevent vasoconstriction in the wound and to optimizing the oxygen-carrying capacity of the blood.

The wound and surrounding intact skin must be kept clean and free of urine and feces through frequent inspection and cleansing. Appropriate evaluation of urinary or fecal incontinence is complex but must be performed thoroughly. Potentially reversible causes should be identified and treated. Urinary incontinence secondary to urinary tract infection (UTI) should be treated with antibiotics. Fecal incontinence secondary to diarrhea may be related to an infectious cause (eg Clostridium difficile pseudomembranous colitis) that resolves with appropriate antibiotics.

Manual disimpaction and the addition of stool bulking agents to the diet may relieve overflow fecal incontinence. Urinary or fecal incontinence with no treatable cause may be minimized by establishing a bowel and bladder regimen. Constipating agents and a low residue diet also may be helpful.

Diapers and incontinence pads may be useful absorbing moisture away from the surface of the skin, provided that they are checked regularly and changed when soiled. If used inappropriately, these products may actually aggravate maceration and result in dermatitis. A bladder catheter or (in males) a condom catheter may be used to control urinary incontinence. In very severe cases involving chronic stool contamination, surgical diversion should be considered.

Bacterial contamination must be assessed and treated appropriately. Differentiation of infection from simple contamination through tissue biopsy (see Workup) helps ensure that antibiotics are used judiciously (ie, only in cases of actual infection) and, ideally, helps minimize the development of resistant species. Antibiotics also are indicated when accompanying osteomyelitis, cellulitis, bacteremia, or sepsis is present.

A system of assessing wound healing must be in place to facilitate continuity of care among the various health care providers involved in the care of the patient. This often includes serial photography, detailed descriptions of the wound, and measurement of wound dimensions.

References

Pressure Reduction

The first step in healing a pressure injury is determination of the cause (ie, pressure, friction, or shear).^{[5, 82, 83]}Turning and repositioning the patient remains the cornerstone of prevention and treatment through pressure relief. Patients who are capable of shifting their weight every 10 minutes should be encouraged to do so. Repositioning should be performed every 2 hours, even in the presence of a specialty surface or bed.

Patients who are bedbound should be positioned at a 30° angle when lying on their side to minimize pressure over the ischial tuberosity and greater trochanter. Efforts should be made to avoid sliding the patient over a surface to prevent shear forces and friction. Patients who develop a pressure injury while sitting should be placed on bed rest with frequent repositioning.

Pressure reduction may be achieved through the use of specialized support surfaces for bedding and wheelchairs that can keep tissue pressures below 32 mm Hg (the standard threshold value for evaluating support surfaces).^{[84, 85, 86, 87, 88]}In theory, reduction of tissue pressures below capillary filling pressures should allow adequate tissue perfusion. Various different types of specialized support surfaces are available (see Table 1 below).

Table 1. Advantages and Disadvantages of Specialized Support Surfaces

View Table

See Table

These support surfaces may be divided 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 either pressure-reducing or pressure-relieving. Pressure-relieving devices consistently reduce pressure below capillary closing pressure; pressure-reducing devices keep pressures lower than standard hospital beds but not consistently below capillary closing pressure.

These pressure-relief surfaces are often heavy, expensive, and difficult to clean, and they require ongoing maintenance to ensure proper function. In addition, they must be used properly to be effective. The patient’s head and shoulders should be only minimally elevated on one pillow or a foam wedge to reduce shear forces and prevent the patient from “bottoming out” or having the sacrum or ischial tuberosities resting on the bed frame.

In a comparative study, two different cushions to prevent heel pressure injuries were investigated: a wedge-shaped, bed-wide, viscoelastic foam cushion and an ordinary pillow.^[89]The patients using the wedge-shaped cushion had a decreased incidence of heel pressure injuries, and the probability of remain free of pressure injuries remained higher.

To date, relatively few clinical trials have been performed to evaluate the effectiveness of specialized support surfaces. Those that have been published have mostly been based on evaluation of tissue interface pressure, which is the force per unit area that acts perpendicularly between the body and the support surface and serves as an approximation of capillary closing pressure.^{[84, 85, 90, 86, 91, 92, 93, 94, 87, 88, 56]}

Clinical trials for prevention and treatment of pressure injuries have been performed on air-fluidized and low-air loss beds.^{[55, 95, 96, 97]}Although there is evidence that all of these surfaces can help prevent or treat pressure injuries can be prevented or improved, no data suggest that one support surface consistently performs better than all others in all circumstances.^{[55, 96, 98, 99, 100, 101]}Therefore, patients should be actively treated on an individual basis to reduce specific risk factors.

A systematic review concluded that special foam mattresses designed to prevent pressure injuries were generally more effective than standard mattresses in patients at risk.^[102]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 injuries.

An updated systematic study not only confirmed the benefit of higher-specification foam mattresses but also suggested that sheepskin overlays were beneficial as well.^[103]One of the trials included in this analysis determined that alternating-pressure mattresses may be more cost effective than alternating-pressure overlays. Several studies found only limited evidence when higher-technology products were compared.^{[104, 102]}

Selection of a support surface should be based on the patient’s management plan, his or her risk factors for developing pressure injuries, and the cost of obtaining and servicing the device.^{[90, 105]}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 injuries.^{[55, 98, 99, 106, 107]}

Any individual thought to be at risk for developing pressure injuriesshould be placed on a pressure-reducing device (eg, foam, static air, alternating air, gel, or water) when lying in bed to relieve pressure on the heels.^{[108, 106, 109, 110, 111, 112]}For persons who use a wheelchair, pressure-reducing devices of foam, gel, air, or a combination of these materials should be used.^{[113, 91, 114, 115, 116]}Pressure-reducing devices should be used in addition to standard nursing care.^{[4, 117, 118]}

The Agency for Healthcare Policy and Research (AHCPR) Pressure Ulcer Panel has developed guidelines for managing existing pressure ulcers (see Guidelines).^{[108, 31, 119, 120, 121, 96, 98, 101, 122, 7, 55, 122, 123]}

References

Wound Management

Débridement and debriding agents

The purpose of wound débridement 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 injury staging cannot be accomplished until necrotic tissue is removed.^[124]The following three débridement procedures are commonly used:

Enzymatic débridement - This uses various chemical agents (proteolytic enzymes) that act by attacking collagen and liquefying necrotic wound debris without damaging granulation tissue^{[10, 76]}
Mechanical nonselective débridement - In this approach, necrotic tissue is loosened and removed is accomplished by means of whirlpool treatments, forceful irrigation, or the use of wet-to-dry dressings
Sharp débridement - This consists of surgical removal of the eschar and any devitalized tissue within it (see Surgical Debridement); it is indiscriminate in the removal of vital and devitalized tissue and thus requires a great deal of clinical skill and judgment^{[125, 126]}

Povidone-iodine solution can be used to debride infected wounds. Although the effervescent action of hydrogen peroxide results in wound débridement, it is not recommended for frequent or long-term use in pressure injuries, because it indiscriminately removes necrotic material and fragile granulation tissue and because it and other cleansing agents have been found to be toxic to fibroblasts.^{[127, 128, 10]}

Once débridement has been completed and clean granulation tissue has been established, the use of debriding agents should be discontinued, and the site should be kept clean and moist.^[128]

Solutions for wound cleansing

The major purpose of cleansing the wound is to decrease its bioburden and facilitate healing.^{[76, 127]}When no germicidal action is required, normal saline is used. 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 can reduce the drying effects that some irrigants may have on tissue.^{[76, 129]}

Povidone-iodine is useful against bacteria, spores, fungi, and viruses. Dilution is recommended, and this agent should be discontinued when granulation occurs.^[76]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.^[129]

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.^[129]

Sodium hypochlorite (2.5%) has some germicidal activity but is primarily used to debride necrotic tissue. Before it is used, zinc oxide should be placed around the edges of the wound to reduce the amount of irritation.^[76]After cleansing with sodium hypochlorite, normal saline should be used as a rinse.^[129]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.^[10]

Wound dressings

The choice of wound dressings varies with the state of the wound, the goal being to achieve a clean, healing wound with granulation tissue. A stage 1 pressure injury may not require any dressing. For more advanced injuries, various dressing options are available (see Table 2 below).

Table 2. Key Performance Characteristics of Major Wound Dressing Types

View Table

See Table

Hydrocolloid dressings form an occlusive barrier over the wound while maintaining a moist wound environment and preventing bacterial contamination. A gel is formed when wound exudate comes in contact with the dressing. This gel can have fibrillolytic properties that enhance wound healing, protect against secondary infection, and insulate the wound from contaminants.^{[57, 130]}Hydrocolloids help prevent friction and shear and may be used in stage 1, 2, 3, and some stage 4 pressure injuries with minimal exudate and no necrotic tissue.

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 allow atraumatic removal.^{[10, 57, 131]}

Transparent adhesive dressings are semipermeable and occlusive. They allow gaseous exchange and transfer of water vapor from the skin and prevent maceration of healthy skin around the wound. In addition, they are nonabsorptive, reduce secondary infection, and allow atraumatic removal. These dressings minimize friction and shear and may be used in shallow stage 1, 2, and 3 pressure injuries with minimal exudate and no necrotic tissue; however, they do not work well on patients who are diaphoretic or have wounds with significant exudation.^[57]

Alginate dressings are semiocclusive, highly absorbent, and easy to use.^{[132, 133]}They are natural, sterile, nonwoven dressings derived from brown seaweed. Alginate forms a gel when it comes into contact with wound drainage, and may be used in light to heavily draining stage 2, 3, and 4 injuries. It may be used in both infected and noninfected wounds^[132]; however, it should not be applied to dry or minimally draining wounds, as it can cause dehydration and delay wound healing.

Wounds with surface debris or fibrinous exudate may be mechanically debrided with wet-to-dry dressings incorporating normal saline or enzymatically debrided with collagenase. Wounds with a high level of bacterial contamination may benefit from wound irrigation. It has been shown that irrigation by low-pressure pulsatile lavage therapy with saline is more effective than continuous saline irrigation in decreasing bacterial loads within wounds.^[134]

Vacuum-assisted closure (VAC) sponges conform to the wound surface by suction and stimulate wound contracture while removing exudate and edema. Daily whirlpool therapy or pulse lavage therapy may be used to irrigate and mechanically debride the wound.

The choice of dressings is not as important as their appropriate application. The following points should be kept in mind:

These dressings are not a substitute for sharp débridement in the presence of eschar or other necrotic material
Dressings should be applied by trained individuals
Care should be taken to keep the wound dressing within the boundaries of the wound to prevent maceration of the surrounding skin
A hydrocolloid pad or skin sealant can be used to protect the surrounding skin and serve as a surface to which tape may be applied to hold dressings in place; tubular mesh gauze is an alternative for holding dressings in place in patients with extremely fragile skin

Antimicrobials and antibiotics

Antibiotic creams such as silver sulfadiazine may be applied to wounds to decrease bacterial load. Silver sulfadiazine has an excellent antimicrobial spectrum of activity, low toxicity, ease of application, and minimal pain. It inhibits DNA replication and modification of the cell membrane of Staphylococcus aureus; Escherichia coli; Candida albicans; Klebsiella, Pseudomonas, and Proteus species; and Enterobacteriaceae.

Mafenide, an antimicrobial agent that is bacteriostatic to many gram-positive and gram-negative organisms, including Pseudomonas aeruginosa, can penetrate an eschar and promote autolytic softening of the eschar prior to débridement.

Evaluation of a patient with an infected wound should follow an algorithmic approach. The following questions should be asked:

Is the infection local (rubor, dolor, calor) or systemic (fever, tachycardia, hypotension, delirium, altered mental status)?
Which antibiotic is most appropriate for the patient?
Does the patient have any known allergies?
Does the patient have any metabolic impairments that would alter the pharmacokinetics or pharmacodynamics of the drug?
What are the effects of the drug on the hematopoietic system?
What attributes does the drug possess for effective tissue penetration (ie, how much of the drug actually ends up in the tissue of interest)?
How is the drug metabolized?
What are the patient’s total weight and lean body and fat mass?

The adverse effects of antibiotics are well known, and those that impede wound healing should be considered and counteracted. Antibiotic resistance is a major concern. 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.

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.

Other wound treatments

A wide variety of additional therapeutic methods are being evaluated for the treatment of chronic wounds, specifically for pressure injury management.^[135]These include electrotherapy,^{[136, 137]}application of growth factors,^{[138, 139, 140, 62]}and preventive use of free radical scavengers and special drug delivery systems.^{[141, 142, 143]}

The recombinant human platelet-derived growth factor becaplermin has been approved by the US Food and Drug Administration (FDA) for the treatment of lower-extremity diabetic neuropathic ulcers that extend into the subcutaneous tissue or beyond. Studies are underway to explore the possibility of expanding its approved indications to include other wounds. Other growth factors also are being evaluated for use in human clinical settings.

Another potentially promising treatment option is NPWT using VAC.^{[144, 145, 146]}NPWT 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.^[147]

The following are general indications for NPWT^[148]:

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

The following are general contraindications for NPWT^[148]:

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

References

Options for Wound Closure

Several options are available for surgical management of pressure injuries, including direct closure, skin grafting, skin flaps, and musculocutaneous flaps. Such management 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.^{[149, 150, 151]}

The patient should be medically stable and able to benefit from the procedure. The patient should also participate in the decision. The nutritional status of the patient must be considered because good nutritional parameters are required for good wound healing and immune function. Involuntary muscle spasms should be controlled preoperatively with baclofen or diazepam.

Factors associated with impaired healing should be corrected preoperatively. Tobacco use and smoking are associated with intrinsic factors that compromise wound healing.^[152]For example, carbon monoxide and nicotinic acid are potent vasoconstrictors that increase blood viscosity.^[153]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 injuries 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.^{[141, 142, 143]}

Patient positioning is dictated by the location of the ulcer and the planned reconstruction. Many pressure ulcers occur in the gluteal region and require prone positioning. Most anesthesiologists choose to use general endotracheal anesthesia, particularly if the patient is prone, but ulcer closure may be performed under regional or local anesthesia if necessary. Significant blood loss is possible; accordingly, 2 units of type-specific packed red blood cells should be available during the operation.

Arrangements should be made to have a pressure-reducing mattress available for the postoperative period to reduce the risk of immediate recurrence or dehiscence. If urinalysis and urinary culture findings (ie, nitrites, leukocyte esterase) confirm the presence of a urinary tract infection (UTI), appropriate treatment should be provided.

Direct closure

Although direct closure is the simplest approach, pressure injuries considered for surgical treatment are usually too large to be amenable to 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.^[154]

Skin grafts

Split-thickness skin grafts can be used to repair shallow defects and pressure injuries, but their main disadvantage is that they 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 pressure injuries; today, it is typically employed as an alternative to secondary repair.^[155]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 that makes use specific blood vessels.

Myocutaneous flaps

Myocutaneous (musculocutaneous) flaps are usually the best choice for patients with spinal cord injuries (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, in that the improved blood supply and reliability of the muscle flap must be balanced against the need to sacrifice functional muscle units.^{[156, 157, 158]}

Myocutaneous flaps can help heal osteomyelitis and limit the damage caused by shearing, friction, and pressure.^{[159, 160, 161]}They bring muscle and skin to the area of the defect and are probably as resistant to future pressure injuries 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 subsequently reconnected to the vessels at the recipient site with the aid of a microscope. This is the most complex method of wound closure and would be considered only after all other options for reconstruction have been exhausted. In paraplegic patients dependent on their upper body for mobility, the latissimus dorsi would typically be an unacceptable donor for free tissue transfer; however, a portion of the muscle may be used with limited donor site morbidity. A protocol for postoperative care must be followed strictly for free flap survival.^[162]

References

Surgical Management of Specific Pressure Injury Types

The choice of reconstruction approach depends on the location of the pressure injury.

Ischial pressure injury

The ischial location is the most common site of pressure injury in individuals with paraplegia. In the course of excisional débridement in preparation for flap repair of an ischial wound, aggressive resection of the ischial tuberosity may raise the risk of a contralateral ischial pressure injury from increased contralateral pressure. Bilateral ischiectomy increases pressure on the perineum and thus increases the risk of perineal pressure injury.

Recurrence of the pressure injury is common in the ischial location.^[163]Therefore, the first option for reconstruction of ischial wounds is the gluteal thigh rotation flap, which does not preclude the future use of the inferior portion of the gluteus maximus muscle.^{[164, 165]}

The gluteal thigh rotation flap is an axial flap based on the inferior gluteal artery. Both the biceps femoris flap and the hamstring myocutaneous flap transect the inferior gluteal artery. With the gluteal thigh flap, a superiorly based flap is elevated, with its axis being the inferior gluteal artery located between the greater trochanter and the ischial tuberosity (see the image below).

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With gluteal thigh flap, superiorly based flap is elevated, with inferior gluteal artery located between greater trochanter and ischial tuberosity as ....

The gluteal thigh rotation flap is raised as a fasciocutaneous flap superiorly to the gluteal crease (see the image below).

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Gluteal thigh rotation flap is raised as fasciocutaneous flap superiorly to gluteal crease.

The gluteal thigh flap may be raised to include the inferior portion of the gluteus maximus. This increases the arc of rotation and allows the flap to be used to reconstruct sacral defects (see the image below).^[164]

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Gluteal thigh flap may be raised to include inferior portion of gluteus maximus, which increases arc of rotation to allow flap also to be used to reco....

Another popular option for ischial reconstruction, the inferior gluteus maximus myocutaneous flap, limits options for reconstruction of sacral wounds. Bilateral V-Y advancement flaps, inferiorly based random flaps, and superior gluteal myocutaneous flaps are not options for sacral reconstruction if an inferior gluteal myocutaneous flap has been used.

Additional options described for ischial reconstruction include the hamstring myocutaneous flap, the biceps femoris myocutaneous flap, the tensor fasciae latae (TFL) flap, the gracilis myocutaneous flap,^[163]and the medially based posterior thigh skin flap with or without the biceps femoris.

Sacral pressure injury

Sacral pressure injuries (see the image below) are common in patients who have been on prolonged bed rest. Treatment involves complete excision, including the entire bursa, and conservative ostectomy.

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Sacral pressure ulcer before and after flap closure.

Small sacral pressure injuries can be reconstructed with an inferiorly based skin rotation flap, with or without a superior gluteus maximus myocutaneous flap (see the images below). The use of the random skin rotation flap does not preclude later use of the gluteus maximus. When a random skin rotation flap is used, it is essential to design a large and wide flap with an axis of rotation that permits tension-free closure.

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Small sacral pressure sores can be reconstructed with the inferior-based skin rotation flap, with or without the superior gluteus maximus myocutaneous....

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Small sacral pressure ulcer reconstructed with inferiorly based skin rotation flap.

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Small sacral pressure ulcer reconstructed with inferiorly based skin rotation flap.

With a superior gluteal myocutaneous flap, a wide skin rotation flap is elevated with the superior portion of the gluteus maximus. Landmarks for the superior gluteal artery on which this flap is based include the posterior superior iliac spine (PSIS) and the ischial tuberosity (see the image below).

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Landmarks for superior gluteal artery, on which superior gluteus maximus muscle flap is based, include posterior superior iliac spine and ischial tube....

The superior and inferior gluteal arteries branch from the internal iliac artery superior and inferior to the piriformis approximately 5 cm from the medial edge of the origin of the gluteus maximus from the sacrococcygeal line (from PSIS to coccyx; see the image below).

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Superior and inferior gluteal arteries branch from internal iliac superior and inferior arteries to piriformis approximately 5 cm from medial edge of ....

When the superior portion of the gluteus maximus muscle is used as a flap, it is elevated in a lateral-to-medial direction to keep from injuring the superior gluteal artery, which can be difficult to identify from the medial direction because of the inflammation and scarring associated with the sacral pressure injury. The insertion of the superior portion of the gluteus maximus is the iliotibial tract; this insertion is released.

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When superior portion of gluteus maximus is used as flap, it is elevated in lateral-to-medial direction to avoid injury to superior gluteal artery. In....

The superior gluteal artery is only 4 cm long, which limits the rotation of the muscle. Thus, harvesting the entire length of the muscle may be necessary to allow for rotation or turnover into the defect without tension.

Larger sacral pressure injuries require the use of bilateral flaps such as bilateral V-Y myocutaneous advancement flaps (see the first image below). V-Y flaps can be based on the superior, inferior, or entire gluteus maximus, depending on the location of the pressure injury (see the second image below).

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Larger sacral ulcers require use of bilateral flaps, such as bilateral V-Y advancement flaps.

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V-Y flaps can be based superiorly or inferiorly or on entire gluteus maximus.

The V should be fashioned wide enough and long enough to permit closure as a Y without tension. The medial edge of the origin of the gluteus maximus is elevated in a medial-to-lateral direction for approximately 4 cm because the superior and inferior gluteal arteries enter the gluteus maximus 5 cm from its origin.

Release of the gluteal muscle insertion laterally is important for medial advancement and tension-free approximation of the muscles medially. Inflamed fibrous tissue along the medial muscle edge can be preserved and used to hold sutures for midline muscle approximation. Another option for sacral reconstruction is the transverse lumbosacral flap.^[166]

Trochanteric pressure injury

Trochanteric pressure injuries are less common and are typically associated with minimal skin loss. Excisional debridement of these injuries in preparation for flap repair involves resection of the entire bursa and greater trochanter of the femur. The first option for reconstruction of trochanteric pressure injuries is the TFL flap, a myocutaneous flap based on the lateral femoral circumflex artery.^[167]The TFL is 13 cm long, 3 cm wide, and 2 cm thick, and it originates from the anterior superior iliac spine (ASIS) and the iliac crest and inserts into the iliotibial tract.

The skin paddle is harvested in a width of 10 cm and designed over the muscle along an axis from the ASIS to the lateral tibial condyle (see the image below).

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Skin paddle is harvested 10 cm in width and designed over muscle along axis from anterior superior iliac spine to lateral tibial condyle.

The inferior limit of the cutaneous territory can be extended to 6 cm above the knee and 25-35 cm in length (see the image below). The lateral femoral circumflex artery can be found approximately 6-8 cm inferior to the ASIS. In patients with lumbar lesions, a sensate TFL flap can be designed to include the T12 dermatome by fashioning the flap to include the area 6 cm posterior to the ASIS.

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Inferior limit of cutaneous territory can be extended to 6 cm above knee and 25-35 cm in length. Lateral femoral circumflex artery can be found approx....

Other described modifications of the TFL flap include the retroposition V-Y flap and the bipedicled TFL flap. Other options for trochanteric pressure injury reconstruction include the vastus lateralis myocutaneous flap, the gluteal thigh flap, and the anterior thigh flap.

Multiple pressure injuries

Multiple pressure injuries may be observed in the same patient. Reconstruction of multiple injuries may require the use of a total thigh flap (see the image below). The total thigh flap is a long and formidable operation that typically involves the transfusion of 6-20 units of blood. It should be reserved for use as a salvage procedure when other attempts have been unsuccessful. Patients who have undergone a unilateral total thigh flap can sit a wheelchair (see image below).

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Patient required reconstruction of extremely large pressure ulcer with fillet total thigh flap procedure.

References

Prevention

Although in principle, pressure injuries are preventable and should not occur, they continue to be among the most pervasive and perplexing problems encountered in the treatment of persons who are ill, recovering from illness, or functionally impaired.

In 2016, the Wound, Ostomy and Continence Nurses Society (WOCN) issued guidelines for the prevention and management of pressure ulcers (injuries).^[168](See Guidelines.)

In 2017, the WOCN Society issued an updated position statement on the topic of avoidable and unavoidable pressure ulcers (injuries).^[169] This statement defined unavoidable pressure ulcers as those that develop even though the patient's clinical condition and pressure ulcer risk factors were properly evaluated and interventions consistent with patient needs, management goals, and standards of practice were implemented, monitored, and revised as appropriate.

To the extent that prevention is achievable, it is the optimal form of treatment. Prevention of pressure ulcers has two main components: identification of patients at risk and interventions designed to reduce the risk.

Identification of patients at risk

Various approaches to the identification of persons at risk for the formation of pressure injuries have been tested. 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 injuries. General physical and mental condition, nutritional status, activity level, mobility, and degree of bowel and bladder control are all known to affect this risk.^{[9, 56, 170, 125, 117]}

A simple clinical prediction rule based on five patient characteristics may help identify patients who are at increased risk for pressure injury development and thus in need of preventive measures. Detection of a stage 2 or worse pressure injury during admission to the hospital is directly related to the following independent predictors of pressure injuries^[171]:

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

A systematic assessment of pressure injury risk can be accomplished by using a assessment tool such as the Braden scale or the Norton scale (see Table 3 below). 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.^{[172, 173]}

Table 3. Norton and Braden Scales for Assessing Pressure Ulcer Risk

View Table

See Table

In 1992, the Agency for Health Care Policy and Research (AHCPR), now known as the Agency for Healthcare Research and Quality (AHRQ), developed guidelines for the prediction and prevention of pressure ulcers in adults.^[15]In 1994, these guidelines were followed by guidelines for the treatment of these lesions.^[10]

According to the AHPCR prevention guidelines, risk assessment should include the following^[15]:

Complete medical history taking
Determination of Norton (or Braden) score (see above)
Skin examination
Identification of previous pressure ulcer sites

Prime candidates for pressure ulcers include the following^[15]:

Elderly persons
Persons who are chronically ill (eg, those with cancer, stroke, or diabetes)
Persons who are immobile (eg, as a consequence of fracture, arthritis, or pain)
Persons who are weak or debilitated
Patients with altered mental status (eg, from the effects of narcotics, anesthesia, or coma)
Persons with decreased sensation or paralysis

Secondary factors include the following^[15]:

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)

The WOCN Society has also issued guidelines on preventing pressure injuries (see Guidelines).^[168]

Interventions for minimizing risk

Effective prevention of pressure injuries depends on a comprehensive care plan that includes strategies and practices aimed at reducing or eliminating the risk of these injuries. Elements of such a plan may include the following:

Scheduled turning and body repositioning - Although numerous factors are known to contribute to the development of pressure injuries, it remains essential to establish a regimen in which pressure is completely relieved on all areas of the body at regular intervals^{[174, 175]}
Appropriate bed positioning - Patients can benefit from lying prone; shearing forces can be minimized by keeping the head of the bed lower than 45°
Protection of vulnerable bony prominences - Positioning devices such as pillows or foam wedges (not donut-type devices^[108]) should be used to prevent direct contact between bony prominences (eg, knees and ankles); massage of body prominences should be avoided^{[9, 10, 113]}
Skin care - Removal of skin secretions and excretions; avoidance of hot water; use of nonirritating, nondrying skin-cleansing agents; use of moisturizers; use of topical agents such as moisture barriers; use of dry, wrinkle-free sheets
Alertness for skin changes that might indicate an impending breakdown (eg, inflammation of the skin that blanches on application of digital pressure^[9]), particularly in elderly or immunocompromised patients
Control of spasticity and prevention of contractures
Use of support surfaces and specialty beds (see Pressure Reduction)
Nutritional support as required - This may involve enteral or parenteral nutrition or vitamin therapy
Maintenance of current levels of activity, mobility, and range of motion; persons who use a wheelchair should be taught to perform pushup exercises and to lean side to side for pressure relief

All 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 also essential.^[9]

In a study assessing the results of a long-term acute care hospital’s program to reduce the occurrence of pressure injuries, the hospital traced its apparently above-average ulcer prevalence rates to the lack of wound care professionals, methods for consistently documenting prevention and wound data, and an interdisciplinary wound care team approach.^[176]By addressing these issues, the hospital was able to reduce the prevalence of facility-acquired pressure injuries from 41% to an average of 4.2% over a 12-month period.

References

WOCN Guidelines

In 2016, the Wound, Ostomy and Continence Nurses Society (WOCN) issued guidelines on the prevention and management of pressure ulcers (injuries).^[168]Recommendations for prevention included the following:

Implement measures to reduce the risk of developing pressure ulcers: minimize/eliminate pressure, friction, and shear.
Minimize/eliminate pressure from medical devices such as oxygen tubing, catheters, cervical collars, casts, and restraints.
Maintain the head-of-bed elevation at/or below 30°, or at the lowest degree of elevation consistent with the patient's medical condition to prevent shear-related injury, and use a 30° side-lying position.
Schedule regular repositioning and turning for bedbound and chairbound individuals, taking into consideration the condition of the patient and the pressure redistribution support surface in determining the repositioning strategy.
Position sitting patients with special attention to the individual's anatomy, postural alignment, distribution of weight, and support of the feet.
Consider prophylactic dressings to prevent sacral and heel ulcers in at-risk patients.
Use heel suspension devices for patients who are at risk for pressure ulcers that elevate (float) and offload the heel completely, and redistribute the weight of the leg along the calf without putting pressure on the Achilles tendon.
Utilize support surfaces (on beds and chairs) to redistribute pressure. Pressure redistribution devices should serve as adjuncts and not replacements for repositioning protocols.
Place individuals who are at risk for pressure ulcers on a pressure redistribution surface.
Consider using the WOCN Evidence- and Consensus-Based Support Surface Algorithm (http://algorithm.wocn.org) to identify the appropriate support surface (overlay, mattress, or integrated bed system) for adults (≥16 years) and bariatric patients in care settings where the length of stay is 24 hours or more.
Use a high-specification reactive or alternating pressure support surface in the operating room for individuals at high risk for developing pressure ulcers.
Avoid foam rings, foam cut-outs, or donut-type devices for pressure redistribution because they concentrate pressure on the surrounding tissue.
Use incontinence skin barriers such as creams, ointments, pastes, and film-forming skin protectants as needed to protect and maintain intact skin in individuals who are incontinent and at risk for pressure ulcers.
Offer individuals with nutritional and pressure ulcer risks a minimum of 30-35 kcal/kg body weight per day, 1.25-1.5 g of protein/kg body weight per day, and 1 ml of fluid intake/kcal per day.
Educate the patient/caregiver(s) about the causes and risk factors for developing pressure ulcers and ways to minimize the risk.

Recommendations for management included the following:

Float/elevate the heel(s) completely off the surface with a pillow or heel suspension device for stage 1 and 2 pressure ulcers or a heel suspension device for stage 3 and 4 heel pressure ulcers.
Turn and reposition the patient regularly and frequently.
Utilize support surfaces for patients with pressure ulcers (i.e., mattresses, mattress overlays, integrated bed systems, seat cushions or seat cushion overlays) that meet the individual's needs, and are compatible with the care setting.
Consider using the WOCN Society's Evidence-and Consensus-Based Support Surface Algorithm (http://algorithm.wocn.org) to identify the appropriate support surface for adults (≥16 years) and bariatric patients in care settings where the length of stay is 24 hours or more.
Utilize seating redistribution support surfaces that meet the needs of sitting individuals who have a pressure ulcer.
Establish an individualized bowel/bladder management program for the patient with incontinence.
Screen for nutritional deficiencies at the patient's admission to the care setting, when their condition changes, and/or if the pressure ulcer is not healing.
Provide daily calorie and protein intake for adult patients with pressure ulcers: 30-35 kcal/kg and protein 1.25-1.5 g/kg.
Consider evaluation of laboratory tests such as albumin and prealbumin as only one part of the ongoing assessment of nutritional status.
Cleanse the wound and periwound at each dressing change, minimizing trauma to the wound.
Choose appropriate solutions for cleaning pressure ulcers, which may include potable tap water, distilled water, cooled boiled water, or saline/salt water.
Determine the bacterial bioburden by tissue biopsy or Levine quantitative swab technique.
Consider a 2-week course of topical antibiotics for nonhealing, clean pressure ulcers.
Consider use of antiseptics for "maintenance wounds," which are defined as wounds that are not expected to heal, or for wounds that are critically colonized.
Use systemic antibiotics in the presence of bacteremia, sepsis, advancing cellulitis, or osteomyelitis.
Debride the pressure ulcer of devitalized tissue, or when there is a high index of suspicion that biofilm is present (i.e., wound fails to heal despite proper wound care and antimicrobial therapy), and when consistent with the patient's condition and goals of therapy.
Modify the type of dressing as appropriate due to changes in the wound during healing or if the pressure ulcer deteriorates. Monitor and assess the wound on a regular basis and at every dressing change to determine if the type of dressing is appropriate or should be modified.
Consider adjunctive therapies as indicated: platelet-derived growth factor (PDGF); electrical stimulation; negative-pressure wound therapy (NPWT).
Evaluate the need for operative repair for patients with stage 3 and 4 ulcers that do not respond to conservative medical therapy.
Implement measures to eliminate or control the source of pressure ulcer pain.
Implement appropriate treatment of pressure ulcers to optimize healing, recognizing that complete healing may be unrealistic in some patients.
Educate the patient/caregiver(s) about strategies to prevent pressure ulcers, promote healing, and prevent recurrences of ulcers; and emphasize these are lifelong interventions.

References

What are pressure injuries (pressure ulcers)?What is the focus of history for pressure injuries (pressure ulcers)?Why is a general physical exam needed in the evaluation of suspected pressure injuries (pressure ulcers)?How are pressure injuries (pressure ulcers) staged?What are possible complications of ulcerated pressure injuries (pressure ulcers)?What is the role of lab studies in the diagnosis of pressure injuries (pressure ulcers)?When are lab studies indicated in the workup of pressure injuries (pressure ulcers)?Which imaging studies and procedures may be helpful in the diagnosis of pressure injuries (pressure ulcers)?What are the general principles of wound assessment and treatment for pressure injuries (pressure ulcers)?How are pressure injuries (pressure ulcers) treated?How is medical status optimized prior to surgery for the treatment of pressure injuries (pressure ulcers)?What are nonsurgical options in the treatment of pressure injuries (pressure ulcers)?What surgical options for the treatment of pressure injuries (pressure ulcers)?What are the options for surgical closure of pressure injuries (pressure ulcers)?How is a reconstruction approach selected for pressure injuries (pressure ulcers)?How are pressure injuries (pressure ulcers) prevented?What are other names used for pressure injuries (pressure ulcers)?What are the National Pressure Ulcer Advisory Panel (NPUAP) and the National Pressure Injury Advisory Panel (NPIAP)?How are pressure injuries (pressure ulcers) defined?How do pressure injuries (pressure ulcers) develop?What are risk factors for pressure injuries (pressure ulcers)?Why are pressure injuries (pressure ulcers) a national healthcare issue?What is involved in the management of pressure injuries (pressure ulcers)?How are pressure injuries (pressure ulcers) prevented?What are therapeutic modalities used in the treatment of pressure injuries (pressure ulcers)?Why is research in the area of secondary prevention of pressure injuries (pressure ulcers) needed?Which research questions need to be addressed regarding pressure injuries (pressure ulcers)?What are the National Pressure Ulcer Advisory Panel (NPUAP) recommended research priorities for pressure injuries (pressure ulcers)?Which methodologic and policy issues associated with pressure injuries (pressure ulcers) require investigation?Where are pressure injuries (pressure ulcers) most likely to occur on the body?What tissue levels are involved in pressure injuries (pressure ulcers)?What is the pathogenesis of pressure injuries (pressure ulcers)?How do pressure injuries (pressure ulcers) become ulcerated?What are the ranges of pressure that can cause pressure injuries (pressure ulcers)?What are important components of the mechanism of injury by pressure injuries (pressure ulcers)?What is the order of tissue damage in pressure injuries (pressure ulcers)?What is the role of reperfusion in pressure injuries (pressure ulcers)?What is the most common cause of pressure injuries (pressure ulcers)?What is the role of contractures and spasticity in the etiology of pressure injuries (pressure ulcers)?What role of pain in the etiology of pressure injuries (pressure ulcers)?What is the role of skin quality in the etiology of pressure injuries (pressure ulcers)?What is the role of incontinence in the etiology of pressure injuries (pressure ulcers)?Which factor increases the mortality risk of pressure injuries (pressure ulcers)?Which factors inhibit healing of pressure injuries (pressure ulcers)?Which patient groups are at increased ricks for pressure injuries (pressure ulcers)?What is the incidence of pressure injuries (pressure ulcers) in the US?What is the overall prevalence of pressure injuries (pressure ulcers) in hospital settings in the US?What is the incidence of pressure injuries (pressure ulcers) among elderly persons in the US?What is the prevalence of pressure injuries (pressure ulcers) in nursing homes in the US?What is the incidence and mortality rate of pressure injuries (pressure ulcers) in patients with spinal cord injury (SCI)?Why are patients with spinal cord injury (SCI) at increased risk of pressure injuries (pressure ulcers)?Why are blacks with SCI at increased risk for pressure injuries (pressure ulcers)?What is the global prevalence of pressure injuries (pressure ulcers)?How does the prevalence of pressure injuries (pressure ulcers) vary by age?How does the incidence of pressure injuries (pressure ulcers) vary by sex?What are the racial predilections of pressure injuries (pressure ulcers)?What is the mortality rate for pressure injuries (pressure ulcers)?What are the common causes of fatality from chronic pressure injuries (pressure ulcers)?What is the most common complication of pressure injuries (pressure ulcers)?Which infectious agents are commonly isolated in pressure injuries (pressure ulcers)?How is bacteremia managed in patients with pressure injuries (pressure ulcers)?What is the incidence of bacteremia in elderly patients with pressure injuries (pressure ulcers)?When is consultation with an infectious disease specialist indicated in the treatment of pressure injuries (pressure ulcers)?What is the role of osteomyelitis in the progression of pressure injuries (pressure ulcers)?How is osteomyelitis diagnosed in patients with pressure injuries (pressure ulcers)?How is osteomyelitis managed in patients with pressure injuries (pressure ulcers)?What are possible complications of pressure injuries (pressure ulcers)?What information about pressure injuries (pressure ulcers) should patients and caregivers receive?What are the signs and symptoms of pressure injuries (pressure ulcers)?What should be the focus of history in the evaluation of pressure injuries (pressure ulcers)?What should be the focus of history of a current pressure injury (pressure ulcers)?What systematic symptoms should be reviewed during the evaluation of pressure injuries (pressure ulcers)?Why is a thorough physical exam necessary for patients with pressure injuries (pressure ulcers)?How should the wound be examined in patients with pressure injuries (pressure ulcers)?What is the severity of a pressure injury (pressure ulcers) defined?What is the National Pressure Injury Advisory Panel (NPIAP) staging system for pressure injuries (pressure ulcers)?What should be assessed in the physical exam of pressure injuries (pressure ulcers)?How are complications of pressure injuries (pressure ulcers) categorized?What are the complications of chronic pressure injuries (pressure ulcers)?What is the most serious complication of chronic pressure injuries (pressure ulcers)?What are the histological findings indicative of malignant transformation of pressure injuries (pressure ulcers)?How are Marjolin ulcers due to pressure injuries (pressure ulcers) treated?What is the prevalence of malignant transformation of pressure injuries (pressure ulcers)?What are the signs and symptoms of autonomic dysreflexia due to pressure injuries (pressure ulcers)?What is the most common precipitating cause of autonomic dysreflexia in pressure injuries (pressure ulcers)?What is the treatment for osteomyelitis due to pressure injuries (pressure ulcers)?What is the treatment for pyarthrosis due to pressure injuries (pressure ulcers)?What is the treatment of sepsis in patients with pressure injuries (pressure ulcers)?What is the treatment for urethral fistula due to pressure injuries (pressure ulcers)?How is a complete blood count (CBC) used for the diagnosis of pressure injuries (pressure ulcers)?Which lab tests are useful in the evaluation of pressure injuries (pressure ulcers)?Which lab studies are performed in diagnosis of pressure injuries (pressure ulcers) based on a specific clinical situation?What is the role of imaging studies in the diagnosis of pressure injuries (pressure ulcers)?What is the role of tissue biopsy in the diagnosis of pressure injuries (pressure ulcers)?What is the role of tissue biopsy in the management of chronic pressure injuries (pressure ulcers)?What is the role of bone biopsy in the diagnosis of pressure injuries (pressure ulcers)?Which histologic findings are characteristic of pressure injuries (pressure ulcers)?What are treatment options for pressure injuries (pressure ulcers)?What are the general principles of assessment and treatment of pressure injuries (pressure ulcers)?What are the goals of medical management of pressure injuries (pressure ulcers)?What medical treatment must be completed prior to surgical reconstruction for pressure injuries (pressure ulcers)?When is wound reconstruction considered as a treatment for pressure injuries (pressure ulcers)?Which patient groups are not good candidates for surgical reconstruction of pressure injuries (pressure ulcers)?Which promising treatment options are being studied for pressure injuries (pressure ulcers)?What is included in the discharge planning of patients with pressure injuries (pressure ulcers)?When should less aggressive treatment for pressure injuries (pressure ulcers) be considered?How is spasticity in pressure injuries (pressure ulcers) controlled?Why is it important to optimize nutritional status in patients with pressure injuries (pressure ulcers)?What are the goals of nutritional support in patients with pressure injuries (pressure ulcers)?What steps should be taken to prevent vasoconstriction in pressure injuries (pressure ulcers)?How should urinary and fecal incontinence be managed in patients with pressure injuries (pressure ulcers)?How is bacterial infection managed in pressure injuries (pressure ulcers)?How should wound healing be assessed in patients with pressure injuries (pressure ulcers)?What is the role of pressure reduction in the management of pressure injuries (pressure ulcers)?How are bedbound patients monitored to reduce the development of pressure injuries (pressure ulcers)?How is pressure reduction achieved in the treatment of pressure injuries (pressure ulcers)?What are the support surfaces used for pressure reduction in patients with pressure injuries (pressure ulcers)?What special cushions may be used in the prevention of pressure injuries (pressure ulcers)?Which clinical trials have been performed to evaluate the effectiveness of specialized support surfaces for prevention of pressure injuries (pressure ulcers)?Which support surface is most effective in the prevention of pressure injuries (pressure ulcers)?What is the efficacy of foam mattresses for the prevention of pressure injuries (pressure ulcers)?What is the basis for selection of support surfaces for prevention of pressure injuries (pressure ulcers)?When are pressure-reducing devices indicated for the prevention of pressure injuries (pressure ulcers)?What guidelines are available for the management of existing pressure injuries (pressure ulcers)?What care is given following débridement of pressure injuries (pressure ulcers)?What are the débridement procedures used in the treatment of pressure injuries (pressure ulcers)?What is the role of povidone-iodine solution in the treatment of pressure injuries (pressure ulcers)?What is the goal of wound cleansing in patients with pressure injuries (pressure ulcers)?How is povidone-iodine used in the treatment of pressure injuries (pressure ulcers)?What is the role of acetic acid in the treatment of pressure injuries (pressure ulcers)?What is the role of sodium hypochlorite in the treatment of pressure injuries (pressure ulcers)?What are the wound dressing options for the treatment of pressure injuries (pressure ulcers)?How are hydrocolloid dressings used in the treatment of pressure injuries (pressure ulcers)?How are gel dressings used in the treatment of pressure injuries (pressure ulcers)?How are transparent adhesive dressings used in the treatment of pressure injuries (pressure ulcers)?How are alginate dressings used in the treatment of pressure injuries (pressure ulcers)?How are wet-to-dry dressings used in the treatment of pressure injuries (pressure ulcers)?How are vacuum-assisted closure (VAC) sponges used in the treatment of pressure injuries (pressure ulcers)?How should wound dressings be applied in the treatment of pressure injuries (pressure ulcers)?What is the role of topical antibiotics in the treatment of pressure injuries (pressure ulcers)?What is the role of mafenide in the treatment of pressure injuries (pressure ulcers)?What is an algorithmic approach to evaluation of pressure injuries (pressure ulcers)?What are the limitations of antibiotics in the treatment of pressure injuries (pressure ulcers)?How are immunocompromised patients with pressure injuries (pressure ulcers) managed?Which factors should be considered prior to initiating antibiotics to treat pressure injuries (pressure ulcers)?Which therapeutic methods are being evaluated for the treatment of chronic pressure injuries (pressure ulcers)?What is the role of becaplermin in the treatment of pressure injuries (pressure ulcers)?What is the role of negative-pressure wound therapy (NPWT) in the treatment of pressure injuries (pressure ulcers)?What are the indications for negative-pressure wound therapy (NPWT) in the treatment of pressure injuries (pressure ulcers)?What are the contraindications for negative-pressure wound therapy (NPWT) in the treatment of pressure injuries (pressure ulcers)?What are the goals of débridement in the treatment of pressure injuries (pressure ulcers)?When is surgery indicated for pressure injuries (pressure ulcers)?When is urinary or fecal diversion indicated in the treatment of pressure injuries (pressure ulcers)?How are flexion contractures managed in patients with pressure injuries (pressure ulcers)?What are the goals of reconstruction in patients with pressure injuries (pressure ulcers)?How is reconstruction performed for pressure injuries (pressure ulcers)?What is the process of surgical débridement for the treatment of pressure injuries (pressure ulcers)?What are the options for wound closure in patients with pressure injuries (pressure ulcers)?What preoperative care is needed to ensure successful surgical management of pressure injuries (pressure ulcers)?What is the role of oxidative stress in the etiology of pressure injuries (pressure ulcers)?What is the importance of patient positioning in the surgical management of pressure injuries (pressure ulcers)?What should be included in postoperative care of pressure injuries (pressure ulcers)?What are the disadvantages of direct wound closure of pressure injuries (pressure ulcers)?What are the disadvantages of skin grafts for pressure injuries (pressure ulcers)?How are skin flaps used in the treatment of pressure injuries (pressure ulcers)?How are myocutaneous flaps used in the treatment of pressure injuries (pressure ulcers)?How are free flaps used in the treatment of pressure injuries (pressure ulcers)?How are trochanteric pressure injuries (pressure ulcers) repaired?How are muscle pressure injuries (pressure ulcers) repaired?How is the reconstruction approach selected for pressure injuries (pressure ulcers)?What is the most common site of pressure injuries (pressure ulcers) in individuals with paraplegia?What are the limitations to an inferior gluteal myocutaneous flap for the treatment of pressure injuries (pressure ulcers)?What options for ischial reconstruction of pressure injuries (pressure ulcers)?How are sacral pressure injuries (pressure ulcers) managed?How are sacral pressure injuries (pressure ulcers) reconstructed?What is a superior gluteal myocutaneous flap for sacral pressure injuries (pressure ulcers)?What anatomy is involved in repair of sacral pressure injuries (pressure ulcers)?How is the superior portion of the gluteus maximus used in the reconstruction of sacral pressure injuries (pressure ulcers)?What are the reconstruction limitations of sacral pressure injuries (pressure ulcers)?What is required for the reconstruction of larger sacral pressure injuries (pressure ulcers)?Why is release of the gluteal muscle important in the reconstruction of sacral pressure injuries (pressure ulcers)?What are the goals of postoperative care following reconstruction of pressure injuries (pressure ulcers)?What is included in initial postoperative care following reconstruction of pressure injuries (pressure ulcers)?What is included in postoperative care 6 weeks after surgery for pressure injuries (pressure ulcers)?What skin care is needed following surgery for pressure injuries (pressure ulcers)?What is the benefit of transfer to a subacute or rehabilitation facility following surgery for pressure injuries (pressure ulcers)?What are the possible complications reconstructive surgery for pressure injuries (pressure ulcers)?What measures should be taken to minimize the risk of adverse outcomes of the reconstruction of pressure injuries (pressure ulcers)?What is the likelihood of recurrence of pressure injuries (pressure ulcers)?What are the activity modifications following surgery for pressure injuries (pressure ulcers)?What are the activity modifications following surgery for ischial tuberosity pressure injuries (pressure ulcers)?How success is prevention of pressure injuries (pressure ulcers)?What is the Wound, Ostomy, and Continence Nurses Society (WOCN) definition of unavoidable pressure injuries (pressure ulcers)?What are the components of prevention of pressure injuries (pressure ulcers)?What are the risk factors for the formation of pressure injuries (pressure ulcers)?What are the predictive factors of pressure injuries (pressure ulcers)?Which assessment tools are used to assess risk for pressure injuries (pressure ulcers)?What are the Agency for Health Care Policy and Research (AHCPR) guidelines for risk assessment of pressure injuries (pressure ulcers)?Which patient groups are at highest risk of developing pressure injuries (pressure ulcers)?What are secondary risk factors for pressure injuries (pressure ulcers)?Which organization has issued guidelines on preventing pressure injuries (pressure ulcers)?What are the elements of a comprehensive care plan for effective prevention or pressure injuries (pressure ulcers)?What are the specific details that should be included in an intervention to prevent pressure injuries (pressure ulcers)?What institutional steps can be taken to reduce the prevalence of pressure injury (pressure ulcer)?Which specialist consultations are needed for management of pressure injuries (pressure ulcers)?How often should follow-up be performed after treatment of pressure injuries (pressure ulcers)?How is the healing of pressure injuries (pressure ulcers) monitored?How is wound healing promoted in an outpatient setting in patients with pressure injuries (pressure ulcers)?What is the role of home healthcare in the treatment of pressure injuries (pressure ulcers)?What are the ACP guidelines for prevention, and treatment of pressure injuries (pressure ulcers)?What are the AHCPR guidelines for managing existing pressure injuries (pressure ulcers)?What are WOCN guidelines for the prevention of pressure injuries (pressure ulcers)?What are the WOCN treatment guidelines for pressure injuries (pressure ulcers)?What is the role of medications in the treatment of pressure injuries (pressure ulcers)?Which medications in the drug class Antibiotics are used in the treatment of Pressure Injuries (Pressure Ulcers) and Wound Care?Which medications in the drug class Skeletal Muscle Relaxants (Direct Acting) are used in the treatment of Pressure Injuries (Pressure Ulcers) and Wound Care?Which medications in the drug class Skeletal Muscle Relaxants (Centrally Acting) are used in the treatment of Pressure Injuries (Pressure Ulcers) and Wound Care?

References

Author

Christian N Kirman, MD, Clinical Instructor, Department of Surgery, Division of Plastic Surgery, University of California, San Francisco, School of Medicine