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Pressure Ulcers and Wound Care

  • Author: Christian N Kirman, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
Updated: Jun 20, 2016

Practice Essentials

Although the terms decubitus ulcer, pressure sore, and pressure ulcer often are used interchangeably, pressure ulcer is the best term to use. The National Pressure Ulcer Advisory Panel (NPUAP) defines a pressure ulcer as an area of unrelieved pressure over a defined area, usually over a bony prominence, resulting in ischemia, cell death, and tissue necrosis. See the image below.

Advanced sacral pressure ulcer shows effects of pr 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 ulcer according to the system promulgated by the National Pressure Ulcer Advisory Panel (NPUAP), as follows:

  • (Suspected) deep tissue injury - A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure or shear
  • Stage I - Intact skin with signs of impending ulceration, initially presenting blanchable erythema indicating reactive hyperemia
  • Stage II - A partial-thickness loss of skin involving epidermis and dermis
  • Stage III - A full-thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia
  • Stage IV - A full-thickness tissue loss with extension into muscle, bone, tendon, or joint capsule
  • Unstageable - A full-thickness tissue loss in which the base of the ulcer is covered by slough or eschar to such an extent that the full depth of the wound cannot be appreciated

Complications of ulceration include the following:

  • Malignant transformation
  • Autonomic dysreflexia
  • Osteomyelitis
  • Pyarthrosis
  • Sepsis
  • Urethral fistula
  • Amyloidosis

See Presentation for more detail.


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.


General principles of wound assessment and treatment are as follows:

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

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 ulcer 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 ulcers are as follows:

  • Direct closure (rarely usable for pressure ulcers 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 ulcer (eg, ischial, sacral, or trochanteric).

Prevention, if achievable, is optimal. Prevention of pressure ulcers has 2 main components:

  • Identification of patients at risk
  • Interventions designed to reduce the risk

See Treatmen t and Medication for more detail.



The terms decubitus ulcer (from Latin decumbere, “to lie down”), pressure sore, and pressure ulcer often are 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 is the best term to use.

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

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 ulcers 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[3] ) are at increased risk for pressure ulcers. 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 ulceration resulting from a brief lapse in avoidance of the ill effects of pressure.[4, 5]

Addressing the overall management of pressure ulcers is now a prominent national healthcare issue. Despite current interest and advances in medicine, surgery, nursing care, and self-care education, pressure ulcers remain a major cause of morbidity and mortality, and patients with pressure ulcers are important users of medical resources.[2, 6, 7, 8, 9, 10, 11, 12]

Many factors are involved in the management of pressure ulcers. 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 ulcers, and it begins with a complete medical and nursing history, a risk assessment, and skin examination when the patient is admitted.[7, 8, 13] (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 ulcers, 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 ulcers with unbroken skin or superficial lesions with nondraining, noninfected granulation tissue. For draining necrotic or infected lesions, treatment also may include absorption agents, calcium alginate dressings, wound coverings, debridement, and antimicrobial therapy.

Other therapeutic modalities, such as whirlpool, physical therapy, and specialty beds, may also be added to the treatment regimen.

Research in the area of pressure ulcers—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 ulcers 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 ulcers must be considered. Questions that might be asked include the following:

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

A monograph prepared by the Research Committee of the NPUAP suggested the following research priorities with respect to pressure ulcers[2] :

  • 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.



Pressure ulcers are typically described in terms of location and depth of involvement. The hip and buttock regions account for up to 70% of all pressure ulcers, with ischial tuberosity, trochanteric, and sacral locations being most common.[14] The lower extremities account for an additional 15-25% of all pressure ulcers, with malleolar, heel, patellar, and pretibial locations being most common (see the images below).

Pressure ulcers of lateral aspect of right foot. Pressure ulcers of lateral aspect of right foot.
Heel pressure ulcer. Heel pressure ulcer.

The remaining small percentage of pressure ulcers may occur in any location that experiences long periods of uninterrupted pressure.[14] The nose, chin, forehead, occiput, chest, back, and elbow are among the more common of the infrequent sites for pressure ulceration. No surface of the body can be considered immune to the effects of pressure.

Pressure ulcers can involve different levels of tissue. Muscle has been proved to be most susceptible to pressure. However, Daniel and Faibisoff found that muscle rarely was interposed between bone and skin in normal weight-bearing positions in cadaver and clinical dissections.[15]



In 1873, Sir James Paget described the production of pressure ulcers remarkably well, and his description is still quite accurate today.[16] Many factors contribute to the development of pressure ulcers, but pressure leading to ischemia and necrosis is the final common pathway.

In this view, pressure ulcers result from constant pressure sufficient to impair local blood flow to soft tissue for an extended period. This external pressure must be greater than the arterial capillary pressure (32 mm Hg) to impair inflow and greater than the venous capillary closing pressure (8-12 mm Hg) to impede the return of flow for an extended time.

Tissues are capable withstanding enormous pressures for brief periods, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a downward spiral toward tissue necrosis and ulceration.[17, 18] The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface.

Lindan et al documented ranges of pressure applied to various anatomic points in certain positions.[19] The points of highest pressure with the patient supine included the sacrum, heel, and occiput (40-60 mm Hg). With the patient prone, the chest and knees absorbed the highest pressure (50 mm Hg). When the patient is sitting, the ischial tuberosities were under the most pressure (100 mm Hg). Obviously, these pressures are greater than the end capillary pressure, which is why these are the areas where pressure ulcers are most common.

Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury (see the image below).[20] Maceration may occur in a patient who has incontinence, predisposing the skin to injury. Pressure, shear forces, and friction cause microcirculatory occlusion and consequent ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration.

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

Of the various tissues at risk for death due to pressure, muscle tissue is damaged first, before skin and subcutaneous tissue, probably because of its increased need for oxygen and higher metabolic requirements.[21, 22] Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. Skin can withstand ischemia from direct pressure for up to 12 hours. By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone.

Reperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing an ulcer to enlarge or become more chronic—as, for example, when a paraplegic or quadriplegic patient is turned from one side to the other in an attempt to combat prolonged pressure on a given side. The exact mechanism of ischemia-reperfusion injury is yet to be fully understood. Continued production of inflammatory mediators and reactive oxygen species during ischemia-reperfusion may contribute to the chronicity of pressure ulcers.



Impaired mobility is probably the most common reason why patients are exposed to the prolonged uninterrupted pressure that causes pressure ulcers. 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 ulcers 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 ulceration 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 de-epithelialization 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 ulcers, in that it can delay or prevent wound healing. These ulcers are warm, moist reservoirs for bacterial overgrowth, where antibiotic resistance may develop. A pressure ulcer 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 ulcers 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.



United States statistics

Pressure ulcers are common among patients hospitalized in acute- and chronic-care facilities. It has been estimated that about 1 million pressure ulcers occur in the United States; however, definitive information on the epidemiology and natural history of this condition is still limited. Unfortunately, studies to date have been encumbered by methodologic issues and variability in describing the lesions.[2, 23]

Reported incidences of pressure ulcer in hospitalized patients range from 2.7% to 29%, and reported prevalences in hospitalized patients range from 3.5% to 69%.[24, 25, 26, 27, 28] Patients in critical care units have an increased risk of pressure ulcers, as evidenced by a 33% incidence and a 41% prevalence.[29, 30]

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.[31] 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 ulcers 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 ulcer than other hospitalized patients are, with a 66% incidence.[32, 33] 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 ulcer within 32 days after hospital admission.[34]

In nursing homes, the prevalence of pressure ulcers is 2.6-24%.[23, 35] ; the incidence is 25% in residents admitted from an acute care hospital.[35] Patients with preexisting pressure ulcers show a 26% incidence of additional pressure ulcer formation over a 6-month period. The incidence in chronic care hospitals is reported to be 10.8%,[36] whereas 33% of those admitted to a chronic care hospital have pressure ulcers.[37] Long-term follow-up demonstrates that most ulcers heal within 1 year.[23, 38]

Among patients with neurologic impairments, pressure ulcers occur with an incidence of 7-8% annually,[39] with a lifetime risk estimated to be 25-85%.[40] Moreover, pressure ulcers 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%).[41] In persons with spinal cord injury (SCI) and associated comorbidity, the incidence of pressure ulcer is in the range of 25-66%.[42, 43, 44, 45]

A study of the prevalence of pressure ulcers in community residents with SCI demonstrated that those with higher-level SCI lesions carry a greater risk of developing pressure ulcers than those with lower-level lesions do.[42] Of 100 patients with pressure ulcers, 33 had ulcers that were classified as stage 2 or greater. Black patients had more severe ulcers than other racial groups did.

Some authors speculate that detecting erythema can be more difficult with skin that has darker pigmentation.[46] Because prolonged nonblanching erythema is typically an early warning sign of pressure ulcer risk and development, difficulty in detecting erythema can result in failure to recognize grade I pressure ulcers.

International statistics

In a study from Germany that reviewed the prevalence of pressure ulcer 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.[47] This decrease is thought to be due to more effective management strategies and better prevention.

Age-related demographics

The prevalence of pressure ulcer 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 ulcers. 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 ulcer.

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 ulcers occurs.[48] Two thirds of pressure ulcers occur in patients older than 70 years.[36] 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 ulcers will have an even more profound influence on the American economy.[49]

Sex-related demographics

Most younger individuals suffering from pressure ulceration are males. The higher incidence in males reflects the greater number of men suffering traumatic SCIs. In the older population, most patients with pressure ulcers 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 ulceration in nursing home residents in the southeastern United States to be higher in black patients than in white ones.[50] The authors examined data from 113,869 nursing home residents, none of whom had pressure ulcers 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 ulcer incidence displayed a sex predilection based on patient characteristics.[50] 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.



Pressure ulcers are listed as the direct cause of death in 7-8% of all patients with paraplegia.[51, 39] As many as one third of hospitalized patients with pressure ulcers die during their hospitalization. More than half of those who develop a pressure ulcer 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 ulcer may be a contributing factor in some instances.

Each year, approximately 60,000 people die of complications of pressure ulcers.[52] Individuals with pressure ulcers have a 4.5-times greater risk of death than persons with the same risk factors but without pressure ulcers.[6] A secondary complication, wound-related bacteremia, can increase the risk of mortality to 55%.[52, 53, 54, 55]

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

Infection is the most common major complication of pressure ulcers. The offending pathologic organisms can be either anaerobic or aerobic. Aerobic pathogens commonly are present in all pressure ulcers,[56] whereas anaerobes tend to be present more often in larger wounds (65% in grade III and above).[57]

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 ulcers.[57] 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 ulcers, bacteremia is reported to occur at a rate of 3.5 per 10,000 hospital discharges.[6]

In view of the high mortality in this population (nearly 50%),[54] 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.[6] A prospective study demonstrated that osteomyelitis was associated with nonhealing grade IV pressure ulcers in 86% of the study population.[58, 59] This study utilized 3-phase technetium methyl diphosphate radionuclide flow to detect early osteomyelitis.

Various tests can be used to diagnose osteomyelitis in patients with pressure ulcers. Plain radiographs have a sensitivity of 78% and a specificity of 50%, but radiographic findings often are not present in the early stages of infection. Bone scans are more sensitive, but their specificity is low (50%). Bone biopsy has the highest specificity (96%) and sensitivity (73%).[58, 59]

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 3 test results are positive, the positive predictive value of this combination is 69%. If all 3 test results are negative, the negative predictive value is 96%.[58, 59]

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.[43]

Systemic amyloidosis can result from chronic suppurative pressure ulcers. Additional complications of pressure ulcers include spreading cellulitis, a sinus tract abscess, septic arthritis, squamous cell carcinoma in the ulcer, a periurethral fistula, and heterotopic ossification. Because some of the secondary complications of pressure ulcers can preclude wound healing, they should be aggressively prevented and treated.[60] Complications may include infection, pain, depression, and even death.


Patient Education

Patients and their support system must realize that it is their responsibility to avoid recurrent and new ulceration and that this is a lifelong process.[61] Education on the proper avoidance of pressure should begin in the hospital and continue into the home.

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

Contributor Information and Disclosures

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

Christian N Kirman, MD is a member of the following medical societies: Alpha Omega Alpha, American Society of Plastic Surgeons, American Society for Reconstructive Microsurgery

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.


Kat Kolaski, MD Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Consuelo T Lorenzo, MD Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Joseph A Molnar, MD, PhD, FACS Director, Wound Care Center, Associate Director of Burn Unit, Associate Professor, Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine

Joseph A Molnar, MD, PhD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, American Society of Plastic Surgeons, North Carolina Medical Society, Peripheral Nerve Society, Undersea and Hyperbaric Medical Society, and Wound Healing Society

Disclosure: Abbott Laboratories Honoraria Speaking and teaching; Clincal Cell Culture Grant/research funds Co-investigator; KCI, Inc Wake Forest University receives royalties Other

Michael Neumeister, MD, FRCSC, FRCSC, FACS Chairman, Professor, Division of Plastic Surgery, Director of Hand/Microsurgery Fellowship Program, Chief of Microsurgery and Research, Institute of Plastic and Reconstructive Surgery, Southern Illinois University School of Medicine

Michael Neumeister, MD, FRCSC, FRCSC, FACS is a member of the following medical societies: American Association for Hand Surgery, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Association of Academic Chairmen of Plastic Surgery, CanadianSocietyofPlastic Surgeons, Illinois State Medical Society, Illinois State Medical Society, Ontario Medical Association, Plastic Surgery Research Council, Royal College of Physicians and Surgeons of Canada, and Society of University Surgeons

Disclosure: Nothing to disclose.

Adrian Popescu, MD Research Fellow, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Patrick J Potter, MD, FRCP(C) Associate Professor, Department of Physical Medicine and Rehabilitation, University of Western Ontario School of Medicine; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre

Patrick J Potter, MD, FRCP(C) is a member of the following medical societies: American Paraplegia Society, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Don R Revis Jr, MD Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine

Don R Revis Jr, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons

Disclosure: Nothing to disclose.

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Wayne Karl Stadelmann, MD Stadelmann Plastic Surgery, PC

Wayne Karl Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society of Plastic Surgeons, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Bradon J Wilhelmi, MD Professor and Endowed Leonard J Weiner, MD, Chair of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine

Bradon J Wilhelmi, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Hand Surgery, American Association of Clinical Anatomists, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons,Association for Surgical Education, Plastic Surgery Research Council, and Wound Healing Society

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of Steve Jenkins in the Department of Physical Medicine and Rehabilitation at the University of Kentucky for his significant editorial assistance in preparing this article.

Dr Richard Salcido acknowledges that his studies cited in this article are supported by the National Heart, Lung and Blood Institute, the National Institutes of Health grant P01HL36552-07, the National Center for Medical Rehabilitation Research grant R01HD31426-01, the Paralyzed

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Advanced sacral pressure ulcer shows effects of pressure, shearing, and moisture.
Heel pressure ulcer.
Small sacral pressure sores can be reconstructed with the inferior-based skin rotation flap, with or without the superior gluteus maximus myocutaneous flap.
Sacral pressure ulcer before and after flap closure.
Heaps of verrucous white tissue around the ulcer suggest malignant transformation, as observed with Marjolin ulcers.
Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation (as observed with Marjolin ulcers).
Pressure ulcers of lateral aspect of right foot.
Radical bursectomy is performed by placing methylene blue–moistened sponge in bursa and excising pressure ulcer circumferentially, removing all granulation tissue, even from wound base.
With gluteal thigh flap, superiorly based flap is elevated, with inferior gluteal artery located between greater trochanter and ischial tuberosity as its axis.
Gluteal thigh rotation flap is raised as fasciocutaneous flap superiorly to gluteal crease.
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 reconstruct sacral defects.
Small sacral pressure ulcer reconstructed with inferiorly based skin rotation flap.
Small sacral pressure ulcer reconstructed with inferiorly based skin rotation flap.
Landmarks for superior gluteal artery, on which superior gluteus maximus muscle flap is based, include posterior superior iliac spine and ischial tuberosity.
Superior and inferior gluteal arteries branch from internal iliac superior and inferior arteries to piriformis approximately 5 cm from medial edge of origin of gluteus maximus from sacrococcygeal line.
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. Insertion of superior portion of gluteus maximus into iliotibial tract is released. Harvesting entire length of muscle may be necessary to allow rotation or turnover into defect without tension.
V-Y flaps can be based superiorly or inferiorly or on entire gluteus maximus.
Larger sacral ulcers require use of bilateral flaps, such as bilateral V-Y advancement flaps.
Skin paddle is harvested 10 cm in width and designed over muscle along axis from anterior superior iliac spine to lateral tibial condyle.
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 approximately 6-8 cm inferior to anterior superior iliac spine.
Patient required reconstruction of extremely large pressure ulcer with fillet total thigh flap procedure.
Illustrated is Girdlestone arthroplasty for femoral head osteomyelitis pyarthrosis of hip joint. Femoral head is removed, and hip joint space is reconstructed with vastus lateralis muscle flap.
Patient has urethral fistula within his pressure ulcer. When he performs Valsalva maneuver, urine leaks through this opening.
Close-up view in patient who has urethral fistula within his pressure ulcer. When he performs Valsalva maneuver, urine leaks through this opening.
Table 1. Advantages and Disadvantages of Specialized Support Surfaces
Surface Advantages Disadvantages
Air Low maintenance; inexpensive; multipatient use; durable Can be punctured; requires proper inflation
Gel Low maintenance; easy to clean; multipatient use; resists puncture Heavy; expensive; little research
Foam Lightweight; resists puncture; no maintenance Retains heat and moisture; limited life
Water Readily available in community; easy to clean Requires heater; transfers are difficult; can leak; heavy; difficult to maintain; procedures difficult
Dynamic overlays Easy to clean; moisture control; deflates for transfers; reusable pump Noisy; can be damaged by sharp objects; requires assembly; requires power
Replacement mattresses Reduced staff time; multipatient use; easy to clean; low maintenance High initial cost’ may not control moisture; loses effectiveness
Low air loss Head and foot of bed can be raised; less frequent turning required; relieves pressure; reduces shear and friction; moisture control Noisy; expensive; transfers are difficult; requires energy source; restricts mobility; requires skilled setup; rental charge
Air fluidized Reduces shear and friction; lowest interface pressure; low moisture; less frequent turning required Expensive; noisy; heavy; dehydration and electrolyte imbalances can occur; may cause disorientation; transfers are difficult; hot
Table 2. Key Performance Characteristics of Major Wound Dressing Types
Major Dressing Type Key Performance Characteristics
Alginates (sheets and fillers) Exudate absorption; obliteration of dead space; autolytic débridement
Foams (sheets and fillers) Obliteration of dead space; retention of moisture; exudate absorption; mechanical débridement
Gauzes (woven and nonwoven) Obliteration of dead space; retention of moisture; exudate absorption; mechanical débridement
Hydrocolloids (wafers and fillers) Occlusion; retention of moisture; obliteration of dead space; autolytic débridement
Hydrogels (sheets and fillers) Retention of moisture; autolytic débridement
Transparent films Occlusion; retention of moisture; autolytic débridement
Wound fillers Obliteration of dead space; exudate absorption; retention of moisture; autolytic débridement
Wound pouches Exudate control
Table 3. Norton and Braden Scales for Assessing Pressure Ulcer Risk
Area of Comparison Norton Scale Braden Scale
Assessment criteria Physical condition; mental condition; activity; mobility; incontinence (score ≥12 is at risk) Activity; mobility; sensory perception; moisture; nutrition; friction; shear
Attributes Tested on elderly persons in hospital settings Evaluated in diverse sites (eg, medical-surgical, intensive care units, nursing homes)
Replications Tested extensively Tested extensively
Reliability Not available Good interrater reliability
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