4885: Pressure Ulcers: Pathogenesis and Management

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Pressure ulcers are a considerable complication of poor circulation and chronic immobilization. The prevalence rate in long term nursing facilities has been estimated to be approximately 20% to 25%. In patients who are neurologically compromised, pressure ulcers appear with a yearly incidence of about 6% and a lifetime risk assessed to be anywhere from 25% to 75%. Pressure ulcers have been linked to the direct cause of death in roughly 7% to 8% of all paraplegics. Also known as pressure sores or ulcers, the prevalence of pressure ulcers has decreased over the years among bed-ridden patients, mostly because of the thorough use of pressure-reducing methods and increased mobilization. Nevertheless, not all pressure ulcers can be classified as preventable or potentially curable, due to impaired blood circulation, sensory loss, and immobility--causing some patients to become more vulnerable to them. Several dynamics give rise to the occurrence of pressure ulcers, but compression leading to ischemia is the ultimate communal culprit. Furthermore, cognitive impairment of some patients has made some preventive measures extremely challenging to employ. This course will outline the etiology, pathogenesis, identification, prevention, and treatment of pressure ulcers in any practice setting.

Education Category: Infection Control / Internal Medicine

Release Date: 05/01/2013

Expiration Date: 04/30/2016


This course is designed for physicians, primary care providers, and physician assistants involved in the care of patients at risk for pressure ulcer development.

Accreditations & Approvals

NetCE is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. NetCE has been accredited as an Authorized Provider by the International Association for Continuing Education and Training (IACET), 1760 Old Meadow Road, Suite 500, McLean, VA 22102. In obtaining this approval, NetCE has demonstrated that it complies with the ANSI/IACET Standard which is widely recognized as the Standard of good practice internationally. As a result of their Authorized Provider accreditation status, NetCE is authorized to offer IACET CEUs for its programs that qualify under the ANSI/IACET 1-2013 Standard.

Designations of Credit

NetCE designates this enduring material for a maximum of 10 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to 10 MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit. Completion of this course constitutes permission to share the completion data with ACCME. NetCE is authorized by IACET to offer 1 CEU(s) for this program.

Special Approvals

This activity is designed to comply with the requirements of California Assembly Bill 1195, Cultural and Linguistic Competency.

Course Objective

Without proper care and treatment, superficial ulcers can evolve into more serious and severe ulcers and life-threatening complications may result. The purpose of this course is to provide physicians, physician assistants, and nurse practitioners with the information necessary to prevent pressure ulcers, when possible, and to properly care for patients with pressure wounds.

Learning Objectives

Upon completion of this course, you should be able to:

  1. Discuss the epidemiology, etiology, and pathogenesis of pressure ulcers.
  2. Identify patients at risk based on extrinsic and intrinsic factors important to pathogenesis.
  3. Define the severity and progression of pressure ulcers by stage.
  4. Analyze techniques available for the diagnosis of pressure ulcers.
  5. Develop an effective strategy for prevention of pressure ulcers.
  6. Choose appropriate options for wound cleansing, debridement, and dressing based on wound types.
  7. Manage other aspects of the care of patients with pressure ulcers, including pain management and nutritional support.
  8. Create individual treatment plans based on patient characteristics and pressure ulcer stage.
  9. Identify the qualities of a pressure ulcer that should be monitored.
  10. Outline possible complications and comorbidities of pressure ulcers and their treatment.
  11. Describe the medico-legal aspects of pressure ulcers and the significance of correct documentation and patient education.


Jassin Jouria Jr., MD, graduated from Ross University School of Medicine, passed all USMLE medical board exams, and has held academic appointments. He has developed curricula and authored continuing education activities covering a variety of clinical topics.

Faculty Disclosure

Contributing faculty, Jassin Jouria Jr., MD, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planners

John M. Leonard, MD

Ronald Runciman, MD

Division Planners Disclosure

The division planners have disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

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4885: Pressure Ulcers: Pathogenesis and Management


A pressure ulcer is a localized skin erosion and subcutaneous crater, usually over a bony prominence, caused by the mechanical effect of unrelenting pressure [1,2]. The skin and soft tissues become vulnerable when extrinsic factors, such as prolonged pressure, shearing forces, friction, and moisture, coincide with intrinsic (host) factors, such as immobility, poor nutritional state, and incontinence. The most common areas where pressure ulcers occur include the sacrum, coccyx or tailbone, hips, heels, and elbows. These ulcers can range from superficial to deep and may even penetrate through deep muscle layers to bone.

In 400 B.C.E., Hippocrates was the first physician to document a pressure ulcer, but it is assumed they have existed for all of human history. The problem is commonly associated with the frail elderly, those with neurologic injury or disease, and with prolonged hospitalization and nursing home care. In fact, anyone with limited mobility, confined to bed or chair, and unable to shift position frequently is at risk.


The annual rate of pressure ulcers in persons with neurologic impairment, such as spinal cord injury, stroke, and dementia, is estimated to be 5% to 8%, and the lifetime risk is 25% to 85%. Pressure ulcers are listed as a primary cause of death in 7% to 8% of patients with spinal cord injury [63]. The rate of acquired pressure ulcer in patients hospitalized for acute illness is estimated to be 3% to 11%.

Pressure ulcers are among the most common conditions encountered in patients who are acutely hospitalized or require long-term institutional care, though prevalence varies widely by clinical setting [3,4,5]. In the United States, the incidence of ulcers in acute care is 0.4% to 38%; in long-term care, it is 2.2% to 23.9%, and in home care, it is 0.1% to 17%. Around 8% to 40% of intensive care unit (ICU) patients develop pressure ulcers [2]. Unfortunately, with all the achievements made by modern medicine, patients with resolved wounds still have recurrence rates of around 90% [63].

Every year, acute care facilities treat 2.5 million patients with pressure ulcers [4,5]. At present, the United States spends between $9.1 billion and $11.6 billion annually in the treatment of these ulcers [7].


In susceptible patients, the combination of immobility and extended periods of pressure or friction over bony prominences leads to reduced capillary blood flow, tissue hypoxia, and ischemic tissue injury. This in turn evokes an inflammatory response and localized edema that further impairs perfusion and augments soft tissue and skin injury. Current understanding favors a "bottom-up" model of tissue damage beginning deep in the muscle layer [85]. Muscle is more sensitive to pressure injury than skin because it is the more metabolically active layer and thus more susceptible to ischemic injury.

The age and health of overlying skin determine the ease with which ulceration of the superficial layers occurs. In the elderly, skin and subcutaneous tissue gradually lose regenerative, protective, and sensory functions. Chronic conditions or intercurrent illness such as diabetes, arthritis, incontinence, neurologic impairment, cigarette use, and hypotension are all associated with increased susceptibility and prevalence of pressure ulcers [63]. According to one national study, the most common sites for ulcer development are the sacrum and coccyx, accounting for 26% and 31%, respectively [6].


Unrelieved pressure is the most important factor in the development of pressure ulcers [10,11]. As indicated, risk factors for pressure ulcers may be categorized as extrinsic or intrinsic. Extrinsic risk factors are external factors in the immediate environment that make an individual prone to developing ulcers (e.g., moisture). Intrinsic risk factors are internal factors, like age or smoking, that make an individual prone to developing pressure ulcers.


Pressure and Shear

Pressure that results in the development of ulcers is defined as compression of soft tissues between two rigid surfaces. For example, blood vessels, muscle, subcutaneous fat, or skin may be compressed between a bone and an external surface, such as a bed or chair. All the tissues between the two points of pressure are affected, but the tissue closest to the bony prominence suffers the greatest damage. It is important to note that low-intensity pressure over a long period of time can create tissue damage, just as high-intensity pressure over a short period of time can result in damage [85].

The capillary level is the end point of circulation. From the capillaries, oxygen and nutrients diffuse into the tissues, and carbon dioxide and waste products are removed. A collapsed capillary bed is nonfunctioning and useless to the tissues. The minimal amount of pressure required to collapse a capillary is referred to as the capillary closing pressure [83]. Studies have shown that an average of 32 mm Hg will collapse the arterial side of the capillary circulation, and 18 mm Hg of pressure will collapse the venous end. However, these values cannot be accepted as universal; capillary pressures vary among persons, sites, and times [85]. Furthermore, the studies that elicited these values were done on healthy adult males, not debilitated or elderly patients. Other studies have shown that the functional capillary pressure in the peripheral tissues is around 17 mm Hg [122]. Extended pressure resulting in capillary collapse will cause tissue damage.

Shear is the result of gravity pushing down on the body and resistance (friction) between the patient and a surface, such as the bed or the chair, holding the skin in place [85]. For example, when the head of the bed is raised (e.g., high Fowler's position), gravity pulls the body down toward the foot of the bed. The skin on the patient's back resists the motion and is held in place by the bed's surface while the bones and tissues connected to the area actually slide within the skin, resulting in skin puckering in the gluteal area. This causes damage at the deeper fascia level, with stretching and angulation of the blood vessels and dissection of the tissues, which results in undermining. When the head of the bed is elevated more than 30 degrees, shear force occurs in the sacrum and coccyx. Shear injury is not usually visible at the skin level, but shear is responsible for much of the damage associated with pressure ulcers [82]. It is characterized by irregular deep lesions, undermining, and tunneling.


As noted, friction occurs when one surface moves across another surface, such as when a patient's skin slides across a bed sheet. This can result in the "sanding away" of the epidermal layer and upper part of the dermis, causing abrasions [85]. Friction injuries often present as erythema and tenderness followed by skin loss and usually appear under restraints, braces, and on the elbows, or with repetitive rubbing or repetitive cleansing. Patients with uncontrollable movements or spasticity are also at high risk for friction injury, often referred to as "sheet burn." Friction injury occurs more frequently when the skin is fragile or macerated, and tissues subjected to friction are more susceptible to pressure ulcer damage [82].


Moisture weakens the resilience of the epidermis to external forces. Maceration causes softening of the connective tissue, and a macerated epidermis erodes more easily, as overhydrated skin has decreased tensile strength. Skin can appear "water-logged," with areas of denuded skin and fissure formation. Shear and friction damage is increased when there is a moderate amount of moisture present, but it has been reported that shear and friction decrease in the presence of high levels of moisture. The role moisture plays in pressure ulcer development is an area of on-going research [86].

Major sources of moisture are incontinence, wound drainage, tube leakage, and sweating. Urinary and fecal incontinence expose the skin to excessive amounts of moisture and chemical irritation. There is a higher risk for skin breakdown and infection with fecal incontinence than urinary incontinence because of the pathogens in stool.



Patients older than 65 years of age experience pressure ulcers most frequently [83]. With aging, the skin becomes more fragile; the skin layers adhere less securely to each other and can appear paper thin and almost transparent. There is also evidence of increased dryness, decreased vascularization, and increased vascular fragility.

In elderly individuals, there is a decrease in surface barrier function. The ability of the soft tissue to evenly distribute the mechanical load without compromising blood flow is impaired. There is less subcutaneous tissue to cushion boney prominences. This, in addition to decreased sensory perception, makes elderly skin more vulnerable to pressure, shear, and friction [85]. Research has shown that, in the geriatric population, blood flow in the area of the ischial tuberosity while sitting on an unpadded surface is lower than in younger adults [82].

Although much less common, children can also develop pressure ulcers. These ulcers usually develop in the occipital region in infants and toddlers and on the sacrum in young children [83].


Immobile individuals carry the greatest risk of developing pressure ulcers. While sleeping, a healthy individual changes body position approximately once every 10 to 12 minutes. This constant change of position maintains healthy blood circulation, stimulates body organs, and ensures movement of body fluids. However, when an individual is immobile, decreased vascularization and prolonged pressure pair with possible loss of sensation to make the patient extremely vulnerable to ulcers. Immobility may be the result of multiple traumas or injuries, spinal cord injuries, stroke, prolonged hospitalization, coma, recovery after surgery, or cognitive deficits [82].


Comorbid conditions often precipitate pressure ulcers and can prolong their healing. Diseases characterized by muscle spasms or involuntary muscle movement cause frequent friction or shearing. Conditions that cause changes in perfusion, sensation, cognition, and/or posture can predispose a patient to the development and/or recurrence of ulcers. Common medical conditions associated with ulcer formation include:

  • Diabetes

  • End-stage renal disease (ESRD)

  • Thyroid disease

  • Congestive heart failure

  • Peripheral vascular disease

  • Collagen vascular disorders and vasculitis

  • Immune deficiency states

  • Malignancies

  • Chronic obstructive pulmonary disease

  • Depression and psychosis

  • Drugs that delay healing

  • Joint contractures

Sensory Loss

Patients with spinal cord injury, neurological disease, or even advanced diabetes carry an increased risk of developing pressure ulcers as a result of loss of protective sensation. Patients with sensory loss may not feel discomfort or the need to be repositioned.

Poor Nutrition and/or Dehydration

Poor nutrition and dehydration lead to unhealthy skin and impaired healing, which in turn increases the risk of developing pressure ulcers. Low body weight is also a concern. Weight less than 119 pounds or a body mass index (BMI) less than 20 indicates increased risk for pressure ulcer development [80].

Recent weight loss, decreased nutritional intake, lower dietary protein intake, and impaired ability to feed oneself have been identified as risk factors for pressure ulcer development. An estimated 50% of elderly patients admitted to hospitals have decreased protein nutrition [80]. Severe protein deficiency makes soft tissues more vulnerable to breakdown when exposed to pressure. Low protein levels also result in decreased resistance to infection. In addition, older adults have increased incidence of low calorie intake and low levels of zinc and vitamin B12.

Vitamin A, C, and E deficiencies have been associated with pressure ulcer formation. Vitamin A works in the body to maintain epithelial integrity and is involved in collagen synthesis. It also plays a role in protection against infection. A deficiency of vitamin A can inhibit collagen synthesis, delay re-epithelialization, and decrease cellular cohesion. Vitamin C is also involved in collagen synthesis, immune function, and wound repair. A deficiency of vitamin C can result in capillary fragility. Vitamin E deficiency often decreases the immune function of the skin.


Both urinary incontinence and bowel incontinence can result in excessive moisture on the skin, which decreases the tensile strength and increases skin breakdown. In addition, infection may occur more frequently.

Severe Mental Health Conditions

People with severe mental health conditions, such as uncontrolled schizophrenia or severe depression, have an increased risk of pressure ulcers. This is thought to be related to these patients having little interest in self care and nutrition. In addition, patients may have comorbid health conditions, such as diabetes or incontinence, that compound the risk of ulcer development.

Perfusion Status

Adequate circulation is needed to maintain tissue health by delivering oxygen and nutrients to the cells and removing waste products. Edema reduces tissue perfusion by increasing the distance between the cells and the capillary network. Normal, healthy tissue (in a person with normal sensation and movement) can tolerate short periods of ischemia because tissues require intermittent rather than continuous blood flow. However, extended periods of ischemia can result in tissue damage and can lead to pressure ulcers.


Nicotine impedes blood flow to the tissues in two ways: it is a potent vasoconstrictor, and it increases the adhesiveness of platelets, resulting in clot formation. Carbon monoxide contained in cigarette smoke prevents oxygen from attaching to the hemoglobin molecule. This significantly reduces the amount of oxygen circulating in the blood stream. The same reaction occurs to some extent in people exposed to secondhand smoke. Studies have shown that cigarette smoking is associated with a higher incidence of pressure ulcer development, and patients who smoke also have a higher rate of recurrence of pressure ulcers [81,82].


Low arterial blood pressure (systolic blood pressure less than 100 mm Hg and diastolic pressure less than 60 mm Hg) has been linked to increased risk for pressure ulcer development. A hypotensive body redirects the available blood supply to the vital internal organs to maintain their health at the expense of the peripheral vascular system, which serves the skin. As the perfusion level drops, so does the skin's ability to sustain external pressure. Capillaries subsequently close at lower levels of interface pressure, and there is an increased risk of damage due to ischemia [83].


Stress is a primitive response to injury or anticipated injury. Research has shown that during periods of stress, blood vessels in the peripheral tissues constrict. In a study designed to mimic the body's response to stress, healthy subjects were given an infusion of exogenous epinephrine [83]. The increased levels of epinephrine decreased the levels of subcutaneous tissue oxygen by 45%. Other studies have shown that psychological stress has a negative impact on healing [83].


In the United States, 60 million people are obese and 10 million are morbidly obese [80]. Obesity is defined as a BMI of 30 or greater; morbid obesity is defined as a BMI greater than 40. Factors that contribute to pressure ulcer development in obese individuals include decreased blood supply in adipose tissue, difficulty in turning and repositioning, moisture within skin folds, incontinence, skin-to-skin friction, immobility, and poor nutrition. Obese patients are particularly at risk for "unusual" pressure ulcers resulting from pressure within skin folds. Obese patients may have large panniculi ("aprons") weighing up to 50 pounds, and the abdominal panniculus must be regularly repositioned in order to prevent pressure injury. This may be accomplished by placing the patient in the side-lying position and lifting the panniculus away from the underlying skin surface, which allows air to the area and simultaneously relieves pressure.

Tubes or catheters can also cause pressure by burrowing into skin folds. Poorly fitting bed, chairs, or wheelchairs may also be a source of pressure [84].


No step is more important in preventing pressure ulcers than understanding a patient's risk. Risk assessment is used to identify:

  • Populations at risk

  • Level of risk

  • Type of risk

An informal risk assessment cannot take the place of a formal risk assessment, such as the one conducted using the Braden Scale. Research shows that without formal risk assessment, clinicians tend to intervene consistently only at the highest levels of risk [87]. In some studies, repositioning or turning, an important part of pressure ulcer prevention, was prescribed for fewer than 50% of the patients at mild-to-moderate risk for pressure ulcer development [82]. Although several scales/tools have been developed to assess pressure ulcer risk, the Braden Scale is probably the most widely used.

The Braden Scale

The Braden Scale was developed in 1987 by Barbara Braden and Nancy Bergstrom [87]. Since then, it has undergone testing in several clinical settings, and its validity has been established by expert opinion. It is considered one of the most reliable tools for identifying patients at risk for pressure ulcer development. The Braden Scale scores factors that contribute to prolonged pressure and factors that result in diminished tissue tolerance for pressure (Table 1) [87]. There are six items scored in the assessment [87]:

  • Sensory perception

  • Moisture

  • Activity

  • Mobility

  • Nutrition

  • Friction and shear


Sensory perception: The ability to respond meaningfully to pressure-related discomfortCompletely limited: Unresponsive (does not moan, flinch, or grasp) to painful stimuli due to diminished level of consciousness or sedation OR limited ability to feel pain over most of body surface.Very limited: Responds only to painful stimuli and cannot communicate discomfort except by moaning or restlessness OR has a sensory impairment that limits the ability to feel pain or discomfort over half of body.Slightly limited: Responds to verbal commands, but cannot always communicate discomfort or need to be turned OR has some sensory impairment that limits ability to feel pain or discomfort in 1 or 2 extremities.No impairment: Responds to verbal commands and has no sensory deficit that would limit ability to feel or voice pain or discomfort.
Moisture: Degree to which skin is exposed to moistureConstantly moist: Skin is kept moist almost constantly by perspiration, urine, etc. Dampness is detected every time patient is moved or turned.Very moist: Skin is often, but not always, moist. Linen must be changed at least once a shift.Occasionally moist: Skin is occasionally moist, requiring an extra linen change approximately once a day.Rarely moist: Skin is usually dry. Linen only requires changing at routine intervals.
Activity: Degree of physical activityBedfast: Confined to bedChairfast: Ability to walk severely limited or non-existent. Cannot bear own weight and/or must be assisted into chair or wheelchair.Walks occasionally: Walks occasionally during day, but for very short distances, with or without assistance. Spends majority of each shift in bed or chair.Walks frequently: Walks outside the room at least twice a day and inside the room every 2 hours during waking hours.
Mobility: Ability to change and control body positionCompletely immobile: Does not make even slight changes in body or extremity position without assistance.Very limited: Makes occasional slight changes in body or extremity position but unable to make frequent or significant changes independently.Slightly limited: Makes frequent though slight changes in body or extremity position independently.No limitations: Makes major and frequent changes in position without assistance.
Nutrition: Usual food intake patternVery poor: Never eats a complete meal. Rarely eats more than one-third of any food offered. Eats two servings or less of protein per day. Takes fluids poorly. Does not take a liquid dietary supplement. OR is nothing by mouth and/or maintained on clear liquids or intravenous for more than 5 days.Probably inadequate: Rarely eats a complete meal and generally eats only about half of any food offered. Protein intake includes only three servings of meat or dairy products per day. Occasionally will take a dietary supplement. OR receives less than optimum amount of liquid diet or tube feeding.Adequate: Eats more than half of most meals. Eats a total of four servings of protein each day. Occasionally will refuse a meal, but will usually take a supplement if offered. OR is on a tube feeding or total parental nutrition regimen that probably meets most of nutritional needs.Excellent: Eats most of every meal. Never refuses a meal. Usually eats a total of four or more servings of protein. Occasionally eats between meals. Does not require supplementation.
Friction and shearProblem: Requires moderate-to-maximum assistance in moving.Potential problem: Moves feebly or requires minimum assistance. During a move, skin probably slides to some extent against sheets, chair restraints, or other devices. Maintains relatively good position in chair or bed most of the time, but occasionally slides down.No apparent problem: Moves in bed and in chair independently and has sufficient muscle strength to lift up completely during move. Maintains good position in bed or chair at all times.
aA lower Braden Scale Score indicates a lower level of functioning and, therefore, a higher level of risk for pressure ulcer development. Risk levels assigned to each score range: ≤9 is very high risk, 10–12 is high risk, 13–14 is moderate risk, and 15–18 is mild risk. Scores of 19 or greater are considered very low or no risk.

Each item is scored on a scale between 1 and 4, with the exception of friction and shear, which is scored between 1 and 3. The lower the score, the more severe the impairment or problem in that area. Therefore, the lower the overall score, the higher the patient's risk for pressure ulcer development. Various studies have shown cut-off scores from 15 to 18 as being at risk [85]. Although cut-off scores vary, usually a score of 13–14 is considered moderate risk, 10–12 indicates high risk, and 9 or less is very high risk.

The Braden Scale should be used for assessment on admission to a care facility or after return from a hospital. Research shows that a repeat assessment done 48 hours to 72 hours after admission further defines pressure ulcer risk. In nursing home populations, the majority of pressure ulcers develop during the first 2 weeks following admission [83]. Most facilities set their own policies regarding reassessment frequency (e.g., quarterly). However, it is important to note that any change in a patient's condition warrants reassessment.

Braden Scale assessment is completed by licensed personnel familiar with the patient and is shared with all staff caring for the patient; good communication is essential to ensure a meaningful assessment [82]. Licensed and unlicensed staff must have a basic knowledge of Braden scores and how it directs patient care. Accuracy of scoring is very important to determining the appropriate intervention.


Pressure ulcers are classified into six stages by the National Pressure Ulcer Advisory Panel (NPUAP) [98]. In 2007, two stages, suspected deep tissue injury and unstageable, were added to the original four. Prolonged healing times are observed in higher stages. As noted, 75% of stage II ulcers heal within 8 weeks, whereas only 62% of stage IV ulcers ever heal, with only 48% healing within one year [9,44].


Suspected deep tissue injury is described as a purple or maroon localized area of discolored, intact skin or a blood-filled blister caused by damage of underlying soft tissue from pressure and/or shear (Image 1). The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue.


Deep tissue injury may be difficult to detect in individuals with dark skin tones. The injury may also present as a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment.


Stage I is characterized by intact skin with nonblanchable redness of a localized area, usually over a bony prominence (Image 2). Darkly pigmented skin may not have visible blanching, making detection difficult, but its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue.


Stage I lesions may indicate "at risk" persons (a heralding sign of risk). No tissue destruction occurs, and it is a reversible condition.


Partial thickness loss involves a shallow, open ulcer with a red-pink wound bed, without slough (Image 3). This stage of ulcer may also present as an intact or open/ruptured, serum-filled or serosanguineous-filled blister.


Stage II ulcers present as shiny or dry, shallow ulcers without slough or bruising; bruising indicates suspected deep tissue injury. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. Patients with stage II ulcers now have an entry point for pathogens; therefore, cleaning the wound and providing some type of dressing is of utmost importance.


In the stage III ulcer, subcutaneous fat may be visible, but bone, tendon, and muscle are not exposed or directly palpable (Image 4). Slough may be present but does not obscure the depth of tissue loss. These wounds may include undermining and tunneling. The depth of a stage III ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and stage III ulcers in these areas can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III ulcers. Because infection is a very strong risk at this stage, irrigation of the wound is done each time the dressing is changed. Wound debridement may be necessary for healing.



In stage IV ulcers, slough or eschar may be present on some parts of the wound bed (Image 5). Undermining and tunneling are often present. The depth of a stage IV ulcer varies by anatomical location. As with stage III ulcers, wounds on the bridge of the nose, ear, occiput, and malleolus may be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule), making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable. At this stage, the pressure ulcer is often extensively infected, with deep ulceration and tissue loss; therefore, the patient may need repair with myocutaneous flaps to close the defect.



Unstageable ulcers are defined as full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black), obscuring the wound bed (Image 6). Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined.



There are three phases of wound healing: inflammation, proliferation, and maturation. Wounds heal by two possible mechanisms: regeneration or scar tissue formation. The depth of the wound (i.e., the number of tissue layers involved) will determine the mechanism by which the wound will heal. Partial thickness wounds and stage I and II ulcers usually heal by tissue regeneration. Stage III and IV ulcers and full thickness wounds heal by scar formation and contraction. In one study, a 20% shrinkage in wound size in a period of two weeks was a reliable predictive indicator of healing [42].

Pressure ulcers are notoriously difficult to heal. Only 75% of stage II ulcers and 17% of stage III or IV ulcers heal in 8 weeks [43]. Up to 23% of stage II pressure ulcers and 48% of stage IV ulcers remain unhealed after 1 year [44].


The standard signs and symptoms of inflammation are erythema, swelling, increased temperature, and pain. In normal healing, these signs are only minimally noticeable, and during the inflammatory phase of wound healing, they are considered a normal response [88]. In general, this phase occurs in the first 0 to 3 days after ulcer development, but may last longer if healing is impaired.

The first part of inflammation is hemostasis, which begins soon after the wound develops. During the inflammatory phase, vasoconstriction results in platelets adhering to damaged endothelium, causing clumping of the thrombocytes and stopping bleeding. Polymorphonuclear leukocytes engorge the wound and clear the debris. Macrophages continue the cleansing process and stimulate growth factors, including cytokines, interleukin-1 (IL-1), tumor growth factor, tumor necrosis factor, and platelet-derived growth factor.


The proliferation phase lasts approximately 3 to 12 days. During this phase, angiogenesis results in a new network of blood vessels in the wound. Production of epithelial cells starts. Collagen synthesis and improved vascularity ensure healthy granulation tissue. Wounds in the proliferation phase are usually pink in color and do not bleed easily.

In full thickness wounds, the process of re-epithelialization occurs only from the wound edges [85]. Margin basal cells attached to the dermis eventually loosen and start migrating across the wound. The horizontal movement comes to a halt when the cells meet, which is referred to as contact inhibition. Wound contraction is the final part of the proliferative phase. Fibers in the wound contract to bring the wound edges closer together.


Maturation and remodeling of the wound involves rearranging collagen fibers from type III to type I and increasing the tensile strength of scar tissue. The number of blood vessels in the wound regresses and cellular activity is reduced. Scar tissue regains about 80% of normal tissue strength within three months, but it never achieves the full strength of the original tissue [85]. Therefore, the healed site of an old wound is vulnerable to further breakdown.


Diagnosis of pressure ulcers involves careful assessment of symptoms, medical history, physical examination, and certain medical tests. Usually, individuals will have a history of decreased mobility. Patients may complain about the appearance of a wound that may or may not be painful. In cases of infected wounds, fever may be present.

Careful examination in patients with pressure ulcers reveals skin ulceration surrounded by erythema. The size and depth of the ulcer should be determined and documented at this point. Bleeding, malodor, and fluids or debris in the wound indicate severe infection.

Blood tests may be ordered to assess nutritional status and overall health status. No laboratory study of nutritional status can absolutely predict pressure ulcers; however, monitoring a patient's protein status is of value. There are many serological markers used to asses a patient's nutritional status; prealbumin level is one of the most sensitive. Prealbumin is a protein with a much shorter half-life than the other serological markers; therefore, its level gives a more accurate picture of current conditions.

If infection is suspected, culture of the decubitus ulcer is important to determine the pathogen. In some cases, a wound biopsy is performed to rule out vasculitis and skin cancers. An x-ray is done if bone infection is suspected and to rule out osteomyelitis. A bone scan is carried out when x-ray findings are equivocal.


The principles and management strategies discussed in this section are applicable to prevention, control of early stage injury, and treatment of pressure ulcers.

The primary objectives are:

  • Pressure reduction and minimizing or eliminating friction and shear forces

  • Exudate management

  • Prevention of wound infection

  • Managing moist wound environments

  • Decreasing the frequency of dressing changes

The general treatment of established ulcers involves:

  • Pressure-relieving strategies

  • Intense ulcer care

  • Pain management

  • Prevention/eradication of infection

  • Adequate nutrition

  • Adjunctive treatment or surgery

The actual treatment plan is individualized based on the ulcer stage, patient health, and short- and long-term goals.


Pressure-relieving strategies are the cardinal approach for the prevention and treatment of pressure ulcers [14]. It involves the three-pronged approach of:

  • Careful patient positioning

  • Use of protective devices

  • Judicious use of support surfaces


Bedbound Patients

Bedbound patients should be properly positioned and frequently repositioned, at least every two hours. When in lateral decubitus position, patients' heads should be maintained at an angle of 30 degrees in order to mitigate pressure in the trochanteric region. Pillows or foam wedges should be placed between the legs, at the knees and ankles, to prevent pressure at these sites when patients have little or no ability to move legs and feet.

To the extent the patient is able, one should encourage activity. Even a few steps done frequently will help to maintain current activity level, mobility, and range of motion. Lifting devices, such as an overhead trapeze or bed linen, are helpful when moving patients. It is important to minimize dragging during transfers and position changes. Minimize environmental factors leading to skin drying, such as low humidity (less than 40%) and exposure to cold [82]. Posting an individualized turning schedule in patient rooms can be helpful to healthcare professionals and patients.

The heels are particularly vulnerable, and pressure ulcers at this location are very painful, and difficult to heal, and prone to infection with easy access to adjacent bone. Heel pressure ulcers can develop infection, and advanced cases may lead to amputation of the foot. To protect the heels, place a pillow under the calf to float the heels off the bed. There are also devices available that eliminate pressure on heels and prevent foot drop (e.g., suspension boots). Current guidelines state that heels are to be kept off the bed [85].

Chairbound Patients

Chairbound patients require special attention to positioning as well. The risk of pressure ulcers from prolonged sitting is greater than that from reclining in bed, as sitting puts the patient's weight on the relatively small surface areas of the buttocks, thighs, and soles of the feet. Much of this weight is centered over the small area of tissue covering the ischial tuberosities. It is important for patients who sit in a chair to regularly change position. A dependent patient must have his/her position changed in a chair at least every hour. Patients who are able to move themselves should shift their weight (even slightly) every 15 minutes.

A patient should be properly positioned in a chair for postural alignment, distribution of weight, balance, and stability. Patients should sit with their back erect and against the back of the chair, thighs parallel to the floor, knees comfortably parted, and arms horizontal and supported by the arms of the chair. This position distributes weight evenly over the available body surface area. Slouching can cause shearing and friction and places undue pressure on the sacrum and coccyx. Feet should be kept flat on the floor to protect the heels from pressure and distribute the weight of the legs over the largest available surface area. The thighs and arms should remain parallel to ensure that weight is evenly distributed instead of being focused on the ischial tuberosities and elbows. Parting the knees will prevent the knees and ankles from rubbing together. If a patient uses a footstool, it is vital that his or her knees are not above hip level, because this shifts the weight from the back of the thighs to the ischial tuberosities. This same problem can occur if the chair is too short for the patient.

Protective Devices

Protective padding and pillows should be utilized for pressure reduction whenever possible. Heel protectors, foam, and pillows can be helpful for patients in supine positions. Cutting a window through the cast can greatly reduce pressure at certain sites in patients immobilized by fractures. Patient should be provided soft seat cushions when sitting in a chair. Sheepskin and donut-shaped devices should not be used for treating pressure ulcers; ring cushions can reduce blood flow to an even wider area of tissue.

Support Surfaces

Support surfaces are indicated when patients are not able to reposition themselves or when periodic repositioning care is not available. In a comprehensive literature review researchers founds good evidence that specially designed support surfaces effectively prevent pressure ulcers [15].

An ideal support surface will manage microclimate, tissue loads, and other curative functions. Seat cushions, overlays, mattresses, and integrated bed systems are commonly used to prevent pressure ulcers. The type of device or surface selected is based on level of risk as well as degree of assistance necessary for repositioning or mobility (Table 2).


 Validated Risk Assessment Category or Pressure Ulcer Description

At risk


Redness present that fades quickly when pressure is removed

Moderate risk


One pressure ulcer (excluding the heels) where the patient can be positioned off the ulcer

High risk


One pressure ulcer (excluding the heels) and redness over another area

Very high risk


Multiple pressure ulcers (excluding the heels) or the patient cannot be positioned off of an ulcerated area

Ability to change position in bed (e.g., bed mobility)Total assist to change position in bed.Reactive support surface (non-powered) (e.g., air/gel/foam overlay)Reactive support surface (non-powered) (e.g., air/gel/foam overlay)
Active support surface:
Multi-zoned surface (e.g., alternating pressure mattress, rotational surface), or powered reactive support surface (e.g., low air loss)
Active support surface:
Multi-zoned surface (e.g., alternating pressure mattress, rotational surface) or powered reactive support surface (e.g., low air loss)
Moderate assistance with bed mobility required.Reactive support surface (non-powered) (e.g., air/gel/foam overlay or high-density foam mattress)Reactive support surface (non-powered) (e.g., foam overlay with air section inset in the area of the wound)Reactive support surface (non-powered) (e.g., foam overlay with air section inset in the area of the wound)
Active support surface:
Multi-zoned surface (e.g., alternating pressure mattress, rotational surface) or powered reactive support surface (e.g., low air loss)
Patient independent with or without a device with bed positioning. (Light assist may be required.)Reactive support surface (non-powered) (e.g., high-density foam mattress)Reactive support surface (non-powered) (e.g., foam overlay with air section insert)Reactive support surface (non-powered) (e.g., air/gel/foam overlay)Reactive support surface (powered if the control is within the patient's reach)
Instructions for use of this clinical tool: Determine the patient's level of risk and level of mobility in bed and follow the column-and-row intersection to determine the appropriate reactive or active support system.

Types of Support Surfaces

Overlays are filled with water, air, gel, or foam (or a combination of these products) and are applied to the top of a mattress. Foam overlays should be a minimum of 3 inches thick. If a patient's weight completely compresses an overlay, it is not effective.

Pressure relief mattresses are made of a combination of foam, water, or gel or layers of varying foam densities. They are usually indicated in place of standard mattresses used in hospitals and at home. Studies have shown that people at high risk of developing pressure ulcers should use higher-specification foam mattresses instead of standard hospital foam mattresses [16].

Air-fluidized beds are embedded with tiny, silicone-coated beads suspended by pressurized, temperature-controlled air. They are recommended for immobile patients who carry higher risk for posterior pressure ulcers. These beds reduce pressure against the patient's skin surface, resulting in increased capillary blood flow to the skin. This greatly increases granulation and healing of ulcers. These beds are beneficial in patients with multiple large ulcers; however, they are unsuitable for patients who are ambulatory, have pulmonary disease, or have spinal instability. They are usually used as an adjunct to comprehensive care.

Low-air-loss beds are made of numerous interconnected air-filled pillows designed to lose air through the cushions at a controlled rate. These beds distribute the patient's weight evenly, which in turn reduces friction, provides pressure relief, and increases capillary blood flow. They are indicated in patients with stage III or IV ulcers or stage I ulcers with hyperemia.

Combination air-fluidized/low-air-loss beds combine the benefits of both types of beds. The low-air-loss component is placed on the upper half of the bed, while the air-fluidized component is placed on the lower half of the bed.

The most important consideration when choosing a support surface is ease of use. Patient goals and overall care plan are also considerations when selecting a support surface. Pressure ulcer risk, bed mobility, transfer, posture and positioning, financial resources, and advantages and disadvantages of the support surfaces should all be taken into account prior to coming to a decision.


Regular wound cleansing is necessary to remove contaminants, bacteria, and remnants of previous dressings from the wound surface and adjacent area, usually with the help of fluids (irrigation). This process helps accelerate the healing process and decreases the likelihood of infection [17]. One must remember that cleansing is "clearing" a wound, not sterilizing it. Minimal mechanical force is used while cleansing the wound in order to minimize trauma to the wound bed and surrounding healthy tissue. Irrigation at a pressure in the 4 to 5 pounds per square inch range should be used.

The ulcer and surrounding skin should be cleansed at least daily. If the dressing is being changed more than once daily, wound cleansing should be done during each dressing change.

Generally, normal saline is used for cleansing pressure ulcers. In ulcers with necrotic tissue, debris, or confirmed or suspected infection, antimicrobials or surfactants should be considered. For infected wounds, diluted povidone-iodine may be used as the irrigation fluid. However, it should not be used during the granulation phase of healing. Acetic acid (0.5%) is highly effective in fungating lesions, especially against Pseudomonas aeruginosa. There are various cleansing agents available in the market, but normal saline is usually the best option. [18].


Debridement has been shown to accelerate the healing process in some patients with advanced ulcers. In addition to helping move the wound through the stages of healing, debridement is often necessary to visualize the wound bed and to stage the wound; a wound covered with necrotic tissue cannot be staged [82]. An exception is eschar on the heels, which acts as a natural biological cover and should not be removed unless infection is present.

The method of debridement used depends on the amount of necrotic tissue present, the location of the wound, and the patient's overall condition [88]. Patients with stage III or IV pressure ulcers who have undermining and/or tunneling or extensive necrotic tissue should have a surgical evaluation for possible surgical debridement of the wound, if this is consistent with their condition and goals of care [89]. Infected wounds may require systemic antibiotic treatment and immediate surgical debridement [82]. Maintenance debridement should be continued until there is a covering of granulation tissue in the wound bed and the wound is free of necrotic tissue [89]. Debridement is contraindicated if there is inadequate blood supply to support wound healing.

Autolytic Debridement

Autolytic debridement uses the body's own enzymes and moisture to heal the ulcer. To be successful, there must be sufficient white blood cells available to the wound and a moist environment [83]. A layer of wound exudate should be kept in contact with the surface of the wound, usually using a moisture-retaining dressing [82,85,88]. This allows fluid to accumulate in the wound, rehydrating necrotic tissue and making it possible for enzymes in the wound to digest the dead tissue [88]. For a wound covered with dry eschar, it is appropriate to crosshatch the eschar, as this allows a faster build-up of moisture in the wound [88]. In their clinical practice guidelines for pressure ulcer treatment, the Agency for Healthcare Research and Quality recommends autolytic and enzymatic debridement as the preferred approach for patients in long-term care and home care and for patients who cannot tolerate other methods of debridement [88,90]. In general, this type of debridement is ideal for patients with stage III or IV ulcers with light-to-moderate exudates.

Autolytic debridement is highly selective; healthy tissue is spared and only necrotic tissue is liquefied. It is considered very safe, as it uses patient's own immune system to promote healing and clean the wound of necrotic tissue. Autolytic debridement is easy to perform, very effective, and can be combined with other approaches. It is almost painless for the patient, making it a very attractive option.

However, there are disadvantages as well. It is comparatively slow in efficacy compared to surgical debridement, with progress usually seen in about one week [88]. Close monitoring of the ulcer is necessary to detect signs of infection. There is a risk of anaerobic growth when an occlusive hydrocolloid dressing is used, and this approach should not be used in infected ulcers.

Mechanical and Surgical Debridement

Mechanical or surgical debridement is one of the oldest forms of debridement. It is indicated for wounds with thick exudate and necrotic tissue. Approaches include hydrotherapy, laser, medical maggots, ultrasound, wound irrigation, whirlpool, dextranomer, or excision (with a scalpel or scissors). Extensive or deep ulcers should be debrided in operating rooms, although a moderate amount of necrotic tissue can be debrided at the bedside.

Because mechanical debridement is nonselective, it can be traumatic to healthy or healing tissue and is therefore not indicated for clean wounds. Although it is a low-cost procedure, mechanical debridement is time consuming and can be painful. Newer approaches, such as laser debridement, limit collateral damage, but these approaches can be prohibitively expensive [112].

Hydrotherapy can result in tissue maceration, and there is a risk of infection. Therefore, it is considered a less attractive option.

The use of ultrasound waves to debride wounds has also been explored. With this technique, low-frequency ultrasound creates small bubbles in the wound that implode, causing the necrotic tissue to liquefy [92]. This method is generally less painful and less traumatic than traditional methods, with faster healing rates compared to other mechanical debridements [93]. However, further comparative evidence is necessary before it can be recommended as a replacement for established treatment modalities [94].

Maggot Therapy

Maggot therapy, an approach popular at the early 20th century, is finding a new place in wound care debridement [82]. Much of this interest is centered on the ability of maggots to ingest and destroy micro-organisms without inducing resistance [83]. It is believed that the larvae secrete enzymes, including collagenase, that break down the necrotic tissue; they also ingest and destroy micro-organisms [83]. Maggots have the ability to access moist tissue throughout the wound bed and clean small areas without harming healthy tissue [91]. The process involves the application of sterilized larvae from the green-bottle fly maggots to the wound bed every 2 to 3 days [82]. The maggots can be applied to the wound directly or in a containment pouch [82]. The most appropriate dressing for wounds treated with maggots is one that keeps the larvae in place, allows for a flow of oxygen, and is suitable for the characteristics of the wound [88].

Wound debridement using maggot therapy is indicated for pressure ulcers with necrotic tissue with or without infection [91]. Maggots work well in wounds in which moisture and oxygen are readily available and the pH is fairly stable [88]. The therapy is considered mainly for the treatment of wounds for which other forms of treatment are either not appropriate or not successful, and it is contraindicated in patients who have bleeding abnormalities or deep tunneled wounds [82,85].

Precautions should be taken to prevent the larvae from coming in contact with healthy skin, as there is a possibility of enzymatic damage [83]. Otherwise, there are no reported side effects from maggot therapy [83]. However, some patients complain of a crawling or tingling feeling [83]. Maggot therapy may also cause psychological distress for many patients, and its use should be discussed thoroughly with the patient and/or family prior to commencing therapy [82]. This therapy should only be used with appropriately informed consent.

Enzymatic Debridement

Enzymatic debridement is used either alone or in combination with other techniques to remove necrotic tissue and promote wound healing [19,20]. It is also indicated when surgical debridement is not possible. Concentrated enzymes, such as collagenase, papain, becaplermin, or trypsin, are applied to help loosen the necrotic tissue, which is then manually removed. Usually, stage III or IV ulcers are considered candidates for enzymatic debridement. Application of the enzyme should be discontinued when the wound is free of necrotic tissue. If eschar is present, it should be crosshatched prior to introduction of the enzyme to improve efficacy, as enzymes are not active on a dry surface.

Enzymatic debridement is relatively fast acting, with progress evident in 48 to 72 hours. However, complete debridement may be a long process, so other methods (e.g., surgical removal of loosely adherent necrotic tissue) are often used in conjunction.

Enzymes should be applied only to necrotic tissue; if applied correctly, healthy tissues should be spared. It can be expensive and time consuming, with a high number of dressing changes necessary. Inflammation, pain, and discomfort may occur.


Wound dressings are a cardinal component in the treatment of pressure ulcers. There is a variety of available dressings, each with its own benefits and drawbacks (Table 3) [97]. The selection of dressing for an ulcer is determined by several parameters. These include:

  • Condition of the ulcer and wound bed

    • Size and depth

    • Necrosis/slough

    • Dry/exudating

    • Epithelializing

    • Presence of tunneling

    • Infection

    • Over-granulating

    • Malodorous

    • Malignant

    • Pain

  • Aim of treatment

    • Facilitate healing

    • Promote debridement

    • Combat infection

    • Relieve pain

    • Absorb exudates or add moisture

    • Prevent or treat scarring

    • Combat odor

    • Cosmetic/provide concealment

  • Condition of surrounding skin

    • Fragile

    • Macerated

  • Anatomical location

    • Difficult to dress

    • Dressing affects use of normal clothing or shoes

  • Etiology

    • External compression

    • Prospect of healing

    • Palliation

    • Indication of specific topical therapies (e.g., enzymatic debridement, antibiotics)

  • Economics

    • Cost

    • Availability (reimbursement issues)

One of the most important factors in the selection of a dressing is moisture maintenance in and around the ulcer. A dressing that absorbs but does not dry out the wound is needed for ulcers with excessive exudates. For ulcers with minimal drainage, a dressing that restores moisture and prevents drying is needed. Frequency of dressing change also depends on the quantity of drainage.


Dressing TypeDescriptionIndicationAdvantagesDisadvantages
Transparent filmAdhesive, semipermeable, polyurethane membrane that allows water to vaporize and cross the barrierManagement of stage I and II pressure ulcers with light or no exudates; may be used with hydrogel or hydrocolloid dressings for full-thickness wounds
Retains moisture
Impermeable to bacteria and other contaminants
Facilitates autolytic debridement
Allows for wound observation
Does not require secondary dressing (e.g., tape, wrap)
Not recommended for infected wounds or wounds with drainage
Requires border of intact skin for adhesion
May dislodge in high- friction areas
Not recommended on fragile skin
HydrogelWater- or glycerin-based amorphous gels, impregnated gauze, or sheet dressings; amorphous and impregnated gauze fill the dead tissue space and can be used for deep woundsManagement of stage II, III, and IV ulcers; deep wounds; and wounds with necrosis or slough
Soothing, reduces pain
Rehydrates wound bed
Facilitates autolytic debridement
Fills dead tissue space
Easy to apply and remove
Can be used in infected wounds or to pack deep wounds
Not recommended for wounds with heavy exudate
Dehydrates easily if not covered
Difficult to secure (amorphous and impregnated gauze need secondary dressing)
May cause maceration
AlginateDerived from brown seaweed; composed of soft, nonwoven fibers shaped into ropes or padsMay be used as primary dressing for stages III and IV ulcers, wounds with moderate-to-heavy exudate or tunneling, and infected or noninfected wounds
Absorbs up to 20 times its weight
Forms a gel within the wound
Conforms to the shape of the wound
Facilitates autolytic debridement
Fills in dead tissue space
Easy to apply and remove
Not recommended with light exudate or dry scarring or for superficial wounds
May dehydrate the wound bed
Requires secondary dressing
FoamProvides a moist environment and thermal insulation; available as pads, sheets, and pillow dressingsMay be used as primary dressing (to provide absorption and insulation) or as secondary dressing (for wounds with packing) for stage II to IV ulcers with variable drainage
Nonadherent, although some have adherent borders
Repels contaminants
Easy to apply and remove
Absorbs light-to-heavy exudate
May be used under compression
Recommended for fragile skin
Not effective for wounds with dry eschar
May require a secondary dressing
HydrocolloidOcclusive or semiocclusive dressings composed of materials such as gelatin and pectin; available in various forms (e.g., wafers, pastes, powders)May be used as primary or secondary dressing for stage II to IV ulcers, wounds with slough and necrosis, or wounds with light to moderate exudates; some may be used for stage I ulcers
Impermeable to bacteria and other contaminants
Facilitates autolytic debridement
Self-adherent, molds well
Allows observation, if transparent
May be used under compression products (compression stockings, wraps, Unna boot)
May be applied over alginate dressing to control drainage
Not recommended for wounds with heavy exudate, sinus tracts, or infection
May curl at edges
May injure fragile skin upon removal
Contraindicated for wounds with packing
Moistened gauze2×2- or 4×4-inch square of gauze soaked in saline for packingMay be used for stage III and IV ulcers and for deep wounds, especially those with tunneling or underminingAccessible
Must be remoistened often
Time-consuming to apply

Transparent Films

For ulcers with limited exudates, transparent films should be used; however, their use over cavities is contraindicated. These dressings should be changed every 3 to 7 days, and application of triple antibiotic ointment is also recommended by some experts [97].


Hydrogels are indicated for patients with very shallow wounds. These gels, sheets, sprays, or ribbons of cross-linked polymers require a secondary dressing to affix them to the patient. Hydrogels not only rehydrate the wound bed but also aid autolytic debridement and reduce pain. These dressings can be used in infected ulcers and are easily applied and removed from the wound. However, they are not recommended for pressure ulcers with heavy exudation. They also dehydrate easily and can cause maceration.


Hydrocolloids are indicated for wounds with light-to-moderate exudate. They are available as pastes, powders, or wafers composed of gelatin, pectin, and carboxymethylcellulose. These dressings promote angiogenesis, autolysis, and granulation. Some hydrocolloids are self-adhering, but secondary dressings are required when powders and pastes are used. These dressings are especially beneficial on heels and sacral ulcers that require contouring. They are recommended for partial and full thickness ulcers with or without necrotic tissue.

Hydrocolloid dressings can produce an odor upon removal [82]. In the absence of other signs of clinical infection, this is not an abnormal finding and should be explained to concerned patients and staff [82]. Hydrocolloids may also leave a residue in the wound bed, which should be gently irrigated out at dressing change [83]. These dressings lose their effectiveness if they are changed too frequently and should not be used for wounds that must be monitored daily [83].

Calcium Alginates

Calcium alginate dressings, or alginates, are polysaccharide seaweed derivatives containing alginic acid. Alginate dressings either form a moist gel when they come in contact with exudates or retain their original shape while absorbing exudates. They are hemostatic and may reduce risk of infection and of maceration of surrounding skin from excess fluid. These dressings are available in the form of ribbons, pads, and ropes.

Alginates are indicated for wounds with extensive exudates. They may also be used to control bleeding after surgical debridement. A secondary dressing is necessary to secure these dressings, and they should be changed every 12 hours to 4 days. Wounds treated with alginate dressings may smell fishy or like "low tide" [82].

Foam Dressings

Foam dressings are absorbent and non-linting; they are also permeable to gas and provide thermal insulation. Foam dressings accelerate healing of pressure ulcers by providing a moist environment. These dressings are a good choice for stage II and shallow stage III ulcers with drainage and for painful ulcers.

In patients with incontinence, waterproof versions of foam dressings are prescribed in order to protect the skin. They can also be used under compression to prevent damage from shear. However, foam dressings are not effective in removing necrotic tissue. If they become saturated, maceration of periwound skin can take place. Therefore, they should be paired with alginates if used for wounds with a high level of exudates.

Silver-Impregnated Dressings

Silver-impregnated dressings are a treatment option for infected or heavily colonized wounds or wounds that are at increased risk for infection [89]. Silver has an antimicrobial effect on a broad spectrum of organisms and has been shown to reduce the bacterial count in wounds [83]. Sustained-release sliver dressings are toxic to bacteria and fungi but do not adversely affect healthy wound tissue [85]. However, silver-resistant organisms do exist, and the judicious use of sliver is advised, similar to the approach adopted with antibiotics [83]. It is recommended that the use of silver dressings be limited to a 2- to 4-week period [83].

Cadexomer Iodine Dressings

Cadexomer iodine dressings are used for wounds with moderate-to-high amounts of drainage. They should not be used for patients who are sensitive to iodine or individuals with thyroid disease [89]. Cadexomer iodine dressings are antimicrobial and maintain a moist environment for wound healing [82]. Although these dressings are capable of reducing bacteria counts in wounds, they do not replace the need for systemic antibiotic therapy and are regarded as an adjunct in the treatment of wound infections [82].


Gauze packing was used frequently in the past, but it is now regarded as less effective in coping with wound drainage than calcium alginate or hydrocolloid fiber dressings [85]. Gauze dressings do not provide a barrier against bacteria, lower wound temperature, and can pull healthy granulating tissue out of the wound on removal [85]. Gauze dressings are also labor intensive, requiring several dressing changes daily, which adds to the cost of the overall care [82].

Composite Dressings

Composite dressings are a combination of more than one material used to fulfill several important functions in the wound [82]. They provide an effective barrier to bacterial contamination of the wound and include an absorptive layer and either foam, hydrocolloid, or hydrogel [82]. Composite dressings can have either a semi-adherent or non-adherent surface placed in contact with the wound bed [82]. Composite dressings are comfortable and are available in various shapes and sizes [83]. These dressings should not be cut, as this compromises the structure of the dressing [82].

Collagen Dressings

Some dressings incorporate collagen, which is an important protein involved in wound healing and repair [83]. The dressings can be 100% collagen or combined with other products, such as alginates [82]. They provide a high level of absorption while keeping the wound bed moist and are easily removed [82]. For wounds with very little drainage, collagen gel can be applied in a layer one-quarter inch thick [83]. Collagen used in most wound dressings is derived from cowhide [82]. Therefore, it should not be used in patients who are allergic to bovine products [82].


A research study concluded that severity of pain was correlated to pressure ulcer stage, and patients with later staged pressure ulcers may experience excruciating pain [21].The goal of pain management in the pressure ulcer patient is to eliminate the cause of pain and to provide analgesia. There are several interventions and practice modifications that can prevent or manage wound-associated pain.

Skin care and assessments should be performed at a time of day when the patient is less fatigued [2]. All procedures should be thoroughly explained before they are performed. If a patient has questions, this should be addressed, and healthcare professionals should be encouraging and provide positive reinforcement. It is important to avoid trauma (shearing and tear injuries) to fragile skin during transferring, positioning, or holding a patient. If necessary, adjunctive medications may be administered to improve sleep and reduce anxiety, which can contribute to experiences of pain.

Dressing changes are often very painful. An analgesic may be administered 30 minutes before dressing changes, and if possible, the number of daily changes should be kept to a minimum. Tape should always be avoided on fragile skin. If patients are able, they should be allowed to remove their own dressings or set the pace of dressing changes. All patients should be assessed for pain before, during, and after dressing changes, and these findings must be documented [2].

Physical therapy and occupational therapy may be helpful to decrease contractures and muscle spasm. Of course, ensuring proper seating and positioning can improve pain scores and decrease the risk for further pressure injuries.

For mild-to-moderate pain, nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen may be used. Opioids should be avoided as much as possible, as the sedative effects boost immobility; however, they may be necessary during dressing changes and/or debridement.


Surgical closure is required for large defects, particularly when musculoskeletal structures are exposed. In case of large but shallow defects, skin grafts may be beneficial. The most widely used reconstructions performed for pressure ulcers are local flaps. In this reconstruction, well-vascularized skin is transferred with underlying structures (such as subcutaneous tissue, fascia, and muscle) to the wound area. These procedures are classified as [40]:

  • Simple cutaneous: Includes skin and subcutaneous tissue only

  • Fasciocutaneous: Includes skin, subcutaneous tissue, and fascia

  • Myocutaneous: Includes all soft tissue layers from skin to muscle

There are benefits of surgical closure of pressure ulcers, including more rapid healing of the wound and short-term resolution of complications [113]. Surgery may be difficult for some patients, however, particularly elderly and frail persons. In addition, ulcers frequently recur, even in younger patients.


Continuous assessment of pressure ulcers for infection is vital. Signs of infection include erythema, fever, increased drainage, and increased leukocyte count, and these parameters should be monitored periodically. Topical treatment with silver sulfadiazine, triple antibiotic, or metronidazole is recommended for patients with infected ulcers or who are at risk for infection. In general, noninfected wounds produce little or no odor. A fruity odor is suggestive of staphylococcal infection; foul (fecal-like) odor is characteristic of mixed gram-negative and anaerobic bacteria [94].

Systemic antibiotic therapy is indicated when there are signs of cellulitis, purulent wound drainage, fever, or osteomyelitis. The choice of systemic agent should be supported by clinical assessment, imaging studies, and deep tissue culture.

Prophylaxis of infection is also important, as infected wounds are associated with pain, longer healing times, and greater impairments in patient functioning. Topical application of sulfa silver diazine and oral antibiotics are effective in infection prevention in pressure ulcers [22,23].


Malnutrition makes an individual prone to non-healing pressure ulcers. Individuals who are undernourished or dehydrated have an increased risk of ulcer development and delayed healing. Providing additional nutrition and dietary supplements, including protein, zinc, and vitamin C, can help in the wound repair process. Optimal healing of pressure ulcers requires a protein intake of 1.25 to 1.5 g/kg/day. Researchers have found that patients who received a 24% increase in protein intake had significant improvements in ulcer healing and prevention of new injuries compared to those receiving a 14% increase [24]. Zinc supplementation at a dose of 50 mg three times daily also promotes wound healing, and supplemental vitamin C is recommended. For adequate hydration, patients should be provided a drink of water at each repositioning.

Nutritional support is indicated when behavioral measures are not productive. Albumin of less than 3.5 mg/dL or weight less than 80% of ideal indicates malnutrition. Other signs of malnutrition include:

  • Loss of subcutaneous tissue

  • Muscle wasting

  • Generalized edema

  • Dry, pluckable hair

  • Dry, flaky, itchy skin

  • Cracks in the mucous membranes

  • Delayed wound healing/failure to granulate

Interventions to Promote Nutrition

For patients with inadequate nutrition, strategies must be employed to increase oral intake. The preferred route of nutritional support is oral; whenever possible, the gastrointestinal tract should be used for feeding. It is the easiest and most comfortable way to provide supplementation, and it is also the least expensive and most convenient way. Patients should have diets prescribed with protein and caloric content sufficient to meet metabolic needs, with consideration of the patient's preferences and special needs (e.g., mechanical soft diets) [82]. Daily multivitamin supplementation may be implemented. Mouth care should be performed prior to eating. Additionally, toileting and hand washing should be offered prior to meals.

Provide an environment conducive to eating. Position the patient properly; an upright position is preferred. Make sure the food is at the right temperature for the patient. Do not rush eating, particularly if the patient is elderly and requires more time to be oriented. Many patients benefit from the inclusion of snacks high in calories and protein in the diet (e.g., a peanut butter sandwich with milk). Consider adding powdered milk to yogurt and pudding to maximize caloric intake and protein levels. Commercial nutritional supplements, such as breakfast shakes, are also a common adjunct.

It is vital to maintain patient control as far as medically feasible. Some patients may not like ice in their water; others may prefer soup lukewarm. Patient preferences should be accommodated as much as possible.

Remind the patient to chew food thoroughly. If necessary, liquids may be offered between bites; some patients require this to help swallow their food.

Keeping patients hydrated is vitally important, and healthcare professionals should take all available opportunities to improve patients' hydration if it is medically indicated. Patients at risk of becoming dehydrated should be listed on assignment/report sheets as a reminder to monitor these patients. Fluids should be scheduled between meals at least 3 times a day. Patient preferences for fluids (e.g., straws, temperature, ice, etc.) should be observed and noted. Refill water pitchers frequently and keep them within reach of patients, especially those with restricted mobility. Patients should be offered something to drink at every interaction. Ambulatory patients should be provided with a water bottle. As with nutrition and positioning, it is necessary to educate patients/families about the importance of hydration. When, despite these measures, patients are unable to consume adequate levels of water or nutrients, tube feeding or parenteral feeding should be considered. Patient and family preferences and the overall goals of treatment guide these decisions [80].


There are many adjunctive treatments used in wound management. They include electrical stimulation, growth factors, hyperbaric oxygen, normothermic infrared and temperature therapy, and vacuum-assisted closure (VAC).

Electrical Stimulation

Electrical stimulation is effective in increasing the healing rate of chronic pressure ulcers [114]. It is generally indicated for persons with spinal cord instability and difficult-to-heal ulcers. In one study of individuals with spinal cord injury and pressure ulcers, low-frequency pulsed current (i.e., alternating current) was compared to direct current and control groups [25,26]. Researchers found that ulcers treated with electrical stimulation healed faster compared to controls and to standard treatment.

This therapy consists of the placement of a high-voltage, pulsed electrical current onto the wound bed (direct) or near the wound (induced), usually once daily for several weeks. The electrical settings (e.g., the polarity, amplitude and voltage, amperage) are established according to wound and patient characteristics. The Institute for Clinical Systems Improvement recommends considering the use of direct contact electrical stimulation in the management of recalcitrant stage II as well as stage III and IV pressure ulcers to facilitate wound healing [114].

Growth Factors

Fluids taken from chronic pressure ulcers have a significant degradation of growth factor activity compared to acute wounds [27,28]. The application of topical gels containing platelet-derived growth factor can increase fibroblast activity and accelerate healing for chronic wounds [28,30]. The application of 100 mcg/g becaplermin gel once daily has been found to increase the incidence of complete healing compared to placebo [117].

Hyperbaric Oxygen

The use of hyperbaric oxygen in the treatment of pressure ulcers is controversial. Hyperbaric oxygen therapy consists of 100% oxygen administered at a pressure of 2 to 3 atmosphere for a duration of 1 to 2 hours daily. This results in hemoglobin becoming saturated and oxygen spilling into the blood plasma. The vasoconstrictive effects result in reduction of edema in compromised flaps, pressure ulcers, burns, and crush injuries. Improved oxygenation causes increased fibroblast activity and antimicrobial activity, with the stimulation of the phagocytic activity of the white blood cells [31]. It has been hypothesized that hyperbaric oxygen therapy could promote healing of pressure ulcers; however, more research is necessary to evaluate the risks, benefits, and associated costs [118].

Normothermic Infrared and Temperature Therapy

Studies have shown that pressure ulcers treated with radiant heat heal faster and result in shrinking of the ulcer [32]. Because this requires special equipment and trained clinicians, however, it is not yet widely used.

Therapeutic Ultrasound

Theoretically, therapeutic ultrasound can be beneficial in healing pressure ulcers based on both thermal and non-thermal effects (Table 4). The NPUAP recommends that high-frequency ultrasound be considered as an adjunct for the treatment of infected pressure ulcers. However, a meta-analysis of available data on the efficacy of ultrasound in the treatment of pressure ulcers was inconclusive [115].


Increased collagen elasticity
Decreased muscle and joint stiffness
Decreased pain
Decreased muscle spasm
Increased oxygen transport
Speeds up inflammatory process
Increases release of growth factors
Fibroblast and endothelial cell proliferation
Increased collagen production
Accelerated angiogenesis
Better organization of collagen matrix

Pulsed Electromagnetic Field Energy

Pulsed electromagnetic field therapy can be an alternative treatment when pressure ulcers are resistant to conventional therapies. This technique has been found to increase synthesis of DNA, improve revascularization, reduce bacterial growth, and increase neurotransmitter receptor and hormone receptor activity [33,34,35]. Researchers have demonstrated complete healing within a few weeks of initiating this treatment in patients with stage III and IV ulcers [36,37,38,39].

Vacuum-Assisted Closure

Refractory wounds may be treated with VAC. In general, VAC consists of a foam sponge placed into the ulcer and connected to a drainage tube; a pump then exerts negative pressure on the wound bed. This therapy can reduce edema and bacterial load and promote angiogenesis. Treatment with VAC is especially beneficial in stage III and IV ulcers.

VAC decreases nursing time, as frequency of the dressing changes is most often three times a week rather than multiple times per day. As a result, patients experience less pain associated with manipulation of the wound. However, VAC should not be used in ulcers with necrotic tissue or malignancy in the margins.


The treatment plan for patients with pressure ulcers depends on the stage of the ulcer, the patient's physical and psychosocial status, and whether infection is present (Figure 1) [121]. The following sections outline the general goals of treatment based on the stage of the wound, but it is important to individualize treatment as well.


Suspected Deep Tissue Injury

At this stage, injuries often heal with proper care and treatment, but some will deteriorate further. The aim is to quantify the extent of the wound, increase blood circulation, and prevent further breakdown of skin. Treatment should focus on:

  • Pressure redistribution

  • Prevention of shear and friction

  • Moisture maintenance

  • Periodic assessment of the patient

  • Pain management

  • Prevention and treatment of infection

Stage I

The aim for patients with stage I ulcers is to prevent further deterioration of the ulcer and improve circulation. The same treatment plan implemented for suspected deep tissue injury should be the starting point. Skin should be cleansed and lightly moisturized. Massage on the affected area is contraindicated as it can to lead to further tissue injury. If indicated, hydrocolloid dressings and transparent film dressings should be used. Surgical treatment and debridement are not indicated.

Stage II

Promoting healing is the main goal for stage II ulcers, with a focus on prevention of advancement to full-thickness injury. Beginning with the same treatment plan implemented for previous stages, steps should be added to protect against infection. An appropriate dressing should be applied to promote healing and keep the wound bed clean. The skin is fragile at this stage, so adhesives should be avoided. Nutritional status should be re-evaluated, and supplements added, if necessary. Surgical treatment is not indicated, and debridement is rarely necessary.

Stage III

Maintenance of a clean, moist wound bed to prevent infection is the prime goal in the treatment of stage III ulcers. Promoting granulation and addressing local or systemic infection are also important.

Along with the measures described for the previous stages, debridement should be carried out if indicated. Autolytic or enzymatic debridement is recommended for stage III ulcers with light-to-moderate exudate; surgical debridement is necessary if there is necrotic tissue and infection [121].

Wound gels may be used if the ulcer is partially or completely covered with necrotic tissue. Foam dressings and cavity fillers are indicated if the ulcer bed is free of necrotic tissue and debris. Alginate dressings can also be applied if the wound has excessive exudates.

Stage III ulcers usually heal spontaneously with appropriate cleaning and dressing. However, when treated conservatively, they have a recurrence rate of between 32% and 77% [41]. Surgical management can reduce the rate of recurrence in some patients [41].

Stage IV

For patients with stage IV ulcers, the focus of treatment is to provide an environment for new tissue growth. This can also involve removal of necrotic tissue and drainage reduction.

First, the ulcer should be assessed for bone involvement and signs of infection. If indicated, antibiotics should be started. Surgical management is often indicated in stage IV ulcers to address or prevent complications due to the large size of the wound. Debridement is often necessary to remove necrotic tissue.


When treating patients with unstageable ulcers, practitioners should focus on providing a moist environment and preventing further deterioration. Ulcer stage should be reassessed when the base is visible and the treatment plan adjusted accordingly. The wound should be assessed for signs of infection, and antibiotics may be indicated. As with all stages, pain management and patient comfort should be ensured.

The wound should be debrided of nonviable tissue in the wound bed. One exception is the eschar on the heels, which should never be debrided unless infected.


During the treatment of pressure ulcers, routine evaluation of improvement or wound progression is essential and wounds should be assessed at each dressing change. In addition, a holistic patient assessment is indicated, which encompasses systemic factors, psychosocial factors, and local factors. Systemic factors include assessment of etiology, duration, and blood flow to the ulcer; infection; medications; and comorbidities. Determination of the patient's knowledge, beliefs, social support, and financial health (psychosocial factors) is also important. Finally, factors specific to the wound itself, such as amount of exudate, recurrent injury, and tissue necrosis, must be evaluated and documented.


When evaluating the wound, the most important factor to consider is whether the wound is progressing toward the goals established at the onset of treatment [83]. Clinical signs of improvement are expected to appear within 2 to 4 weeks [85]. If the wound is not progressing, further assessment and adjustment of the treatment approach are warranted [83].

For nonhealing wounds, the first factor to evaluate is the quality of wound care. This includes determining if dressing changes are being carried out at the recommended intervals, if the dressings are applied appropriately, and if the manufacturer's instructions for product use are being followed [83]. Factors affecting the patient's condition should be taken into consideration and addressed appropriately [85]. Failure of a wound to improve is often due to systemic factors, such as ischemia, infection, or malnutrition, or continuation of the causative factors [85]. These issues must be addressed first to achieve optimum wound healing. A change in the dressing treatment is indicated if any of the following problems occur [85]:

  • Maceration of the surrounding skin

  • Inadequate control of wound drainage

  • A change in the amount of drainage or the depth of the wound

Reverse staging of pressure ulcers is not an acceptable approach to gauging the level of wound healing. Healed pressure ulcers do not replace lost muscle, subcutaneous fat, or dermis [89]. Tools that appropriately measure degrees of healing include the Bates-Jensen Wound Assessment Tool and the Pressure Ulcer Scale for Healing (PUSH) tool [82,95]. The Bates-Jensen Wound Assessment Tool has thirteen variables that provide a composite picture of the status of the wound [82]. The PUSH tool uses scores in three domains (i.e., size, exudate amount, and tissue type) to indicate improvement or deterioration of the ulcer (Table 5) [103]. When using this tool, surface area is calculated by multiplying the greatest length (head to toe) by the greatest width (side to side) in centimeters. After removal of the dressing and before applying any topical agent to the ulcer, the amount of exudate is estimated as none, light, moderate, or heavy. Finally, the type(s) of tissue present in the wound bed is evaluated (i.e., necrotic, slough, granulation, epithelial, or closed). A score of 0 on the PUSH tool indicates the wound has healed, whereas the highest score of 17 indicates wound degeneration [82]. Results of the assessment should be recorded; a decrease in score over time indicates improvement.


Size (surface area)
0 cm20
<0.3 cm2 (but more than 0 cm2)1
0.3–0.6 cm22
0.7–1.0 cm23
1.1–2.0 cm24
2.1–3.0 cm25
3.1–4.0 cm26
4.1–8.0 cm27
8.1–12.0 cm28
12.1–24.0 cm29
>24.0 cm210
Exudate amount
Tissue in wound bed
Closed wound0
Epithelial tissue1
Granulation tissue2
Necrotic tissue4

Wound assessment also includes wound location, size and depth, signs of infection, and exudates. The wound is examined for presence of tissue debris, base tissues, quality and amount of exudate, odor, and pain.


Documentation of location is paramount for proper monitoring of pressure ulcers. Placement can affect healing and treatment decisions. Wounds that may be exposed to urine or feces should be provided special attention and care, and peripheral wounds may require more time to resolve.

The location of the wound should be stated in a manner that is clearly understood, such as the sacrum or right or left ischium [92]. Anatomical markings should be used when possible.

Size and Depth

Accurate measurement of the wound is probably the most important feature of wound assessment [88]. It provides information on the initial size and progression or non-progression of healing, allowing for valuable feedback on the effectiveness of clinical interventions [82]. Decreasing wound size is generally regarded as a sign of wound healing, but an increase in wound area is not necessarily indicative of deterioration [82].

Wounds should always be measured in centimeters, using a plastic or paper ruler. Wound length is measured from head to toe; width is measured from hip to hip [83]. The depth of the wound can be obtained by gently inserting a sterile cotton-tipped applicator into the wound bed and marking it at skin level. The applicator is then measured using a metric ruler [83].


Sinus tracts and undermining impair healing, and it is important to immediately identify their presence. A sinus tract is a tunnel that extends from any part of the wound and can bore through subcutaneous tissue and muscle. This tunnel creates dead space, which can result in abscess formation and further impede the healing process. A sinus tract can be measured using a sterile cotton swab.

Undermining is defined as destruction of the tissue under the skin around the edges of the wound. This frequently occurs in pressure ulcers that have been subjected to shear force as well as pressure. It is important to document the location and extent of undermining.

The easiest way to measure and describe undermining is by using the face of the clock [82]. With the patient's head representing 12 o'clock, sweep the area of undermining or probe the tunneling to ascertain the depth. For example, undermining along the right border would be recorded as extending from 1 o'clock to 5 o'clock with a depth of 4 cm. It is important to check around the entire perimeter of the wound, as undermining can occur in more than one location.

Wound Bed

It is also vital to assess and document the appearance of the wound bed (Table 6). If the wound bed has a mixture of tissue in it, this should be documented by an approximate percentage (e.g., 75% granulation tissue and 25% slough). Granulation results in "beefy" red tissue consisting of new capillaries, fibroblasts, and collagen fibers with a shiny, moist granular appearance. Grey or purple granulation is a sign of poor vascularization. Granulation present in the wound denotes healing.


ColorDescription and Clinical Implications
Clean and uniformly pink to red in color.
Usually heals by secondary intention.
Dressings need to be changed less often, but the wound should be moist at all times.
Varies from ivory to canary yellow or even green in color, depending on whether or not infection is present.
Caution: Tendon may appear as yellow or white
The goal of care is to manage exudate and remove slough through surgical, sharp, mechanical, enzymatic, or autolytic debridement.
Not all yellow is detrimental to healing; granulation grows through yellow fibrin.
Black or brown
Ranges in color from dark brown and gray to black.
The goal for most individuals is to remove the necrotic tissue by surgical, sharp, enzymatic, or autolytic debridement.
Where there is no drainage or there is boggy surrounding tissue, leave the hard, dry eschar or black scab intact on the lower legs, feet, or heels of individuals whose healing potential is compromised by inadequate circulation. It provides a protective covering for the wound.

Necrosis is gray, brown, or black unviable tissue that usually must be removed in order for healing to take place. Eschars are typically gray to black and dry or leathery in appearance. Slough tissue is yellow/white to gray in color. It may be stringy or thick and appear as a layer over the wound bed. Epithelial tissue will often begin to grow in from the edges over the wound surface. This tissue is generally pink and shiny. As a quick reference color guide, red is associated with normal healing, yellow indicates slough or dead tissue, and black is necrosis.


Exudates are an indication of inflammation in the wound. The presence of large amount of exudate can delay healing and increase the risk of infection. As such, this factor has a significant impact on treatment decisions, particularly dressing type. The amount and quality of any exudates should be noted. Amount may be denoted as:

  • Large/copious: Extends beyond dressing

  • Moderate: Contained within the dressing

  • Small/slight: Small amount of exudate in the center of dressing

  • None: Absence of exudate

The quality of the exudates may be described as [96]:

  • Purulent: Thick exudate that may be malodorous and tan, yellow, green, or opaque in appearance. Denotes presence of infection.

  • Serosanguineous: Thin and pink or light red in color.

  • Serous: Thin/watery and clear or straw colored, with no blood or debris.

  • Hemorrhagic: Red and thick, consisting mainly of blood.

  • Fibrinous: Cloudy and thin with strands of fibrin.


Malodor with purulent exudates suggests mixed infection often combined with ischemic necrosis. However, the majority of wounds (even those free of infection) do have some odor. As previously discussed, gram-negative and gram-positive infections have distinct odors. If present, an ulcer's odor (quality and strength) should be documented.


Wound edges are open and closed. Healthy wound edges are open and allow cell migration. Closed wound edges prevent cell migration and may delay healing. These edges may be described as calloused, approximated, or rolled. The presence or absence of erosion, papules, excoriation, denudement, pustules, or other lesions should be noted.

The condition of the surrounding skin surface up to 4 cm from the edge of the wound circumferentially must also be assessed and documented. Its characteristics should be noted, particularly color and integrity [85]. Maceration from excessive drainage may indicate that the dressing used is not appropriate and a different product is needed. Circumferential erythema and/or induration up to 2 cm from the wound are indicative of cellulitis.


Pressure ulcers cause considerable pain and suffering, ranging from sore to excruciating [98]. In one study, 75% of patients rated their pain as mild, discomforting, or distressing; 18% rated their pain as horrible or excruciating [99]. Pain and odor control are a major concern for patients, and studies have shown that patients rank pain control as more important than healing [82]. The level of pressure ulcer pain depends both on the stage of the ulcer and on manipulation of the area (e.g., if a dressing change is done at the time of assessment), although the majority of patients report pressure ulcer pain at rest as well as with dressing changes. Pressure ulcer pain may be due to tissue trauma, inflammation, damaged nerve endings, infection, and procedures such as debridement and dressing changes [100].

The gold standard for assessing pain intensity is self report using standard pain intensity instruments. Two of the most widely used pain assessment scales are the numeric pain intensity scale and the Wong-Baker Faces Pain Rating Scale [101]. The numeric pain intensity scale consists of ratings from 0 (no pain) to 10 (worst possible pain). This scale can be used for pain assessment with adults and children older than 7 years of age [102]. Visual presentation of the numeric pain intensity scale is helpful with hearing impaired patients, and the scale has been translated into many languages.

The Wong-Baker Faces Pain Rating Scale consists of six faces ranging from a happy smiling face (no pain), to a crying, frowning face (worst pain). The patient is asked to choose the face that best reflects his or her pain. The Faces Pain Rating Scale is the preferred scale for use with children and may also be used with the geriatric population, cognitively impaired patients, and those for whom English is a second language.

After the initial pain assessment has been completed, reassessment should be done at regular intervals. As noted, pain intensity should be rated by the patient, not a healthcare professional. The following questions may be used to help determine patients' pain levels:

  • What kind of pain are you experiencing?

  • What word(s) would you use to best describe it (e.g., burning, aching, shooting)?

  • What makes the pain better?

  • What makes it worse?

  • Where is the pain located?

  • Does the pain radiate?

  • Would you describe your pain as none, mild, moderate, severe, or excruciating?

  • How would you rate your pain on a scale of 0 to 10, with 0 representing no pain and 10 being the worst imaginable pain?

  • What is the pain intensity at its worst, best, and now?

  • Is the pain better or worse at any particular time of the day or night?

  • When does it start and when does it stop?


Infections remain a significant cause of both pain and poor outcomes in patients with pressure ulcers. At each wound assessment, the patient should be evaluated for signs of local or systemic infection. Common signs and symptoms include:

  • Systemic signs (e.g., fever, chills, sweats)

  • Local signs (e.g., rubor, calor, color of adjacent tissues)

  • Unusual odor

  • Friable or dysmorphic granulation

  • Purulent exudates

If any of these are present, infection should be suspected and treated. Culturing the wound may also be helpful, particularly for patients with refractive or recurring wound infections. Obtaining a good culture requires that a semi-quantitative swab collection also be taken. The gold standard is quantitative biopsy, but this procedure is invasive and expensive.


The prevention of complications in pressure ulcers begins with injury recognition. As soon as an ulcer is diagnosed, pressure relief and prevention and control of infection begin. Without proper care and treatment, a superficial stage I or II ulcer can evolve to a more serious and severe stage III or IV ulcer. The complications of more severe ulcers, including sepsis, cellulitis, and malignancies, can become life-threatening even with the best possible treatment and care.


Sepsis is one of the most serious complications of pressure ulcers. When bacteria present in the wound enter the bloodstream, systemic inflammatory response syndrome (SIRS), septic shock, and multi-organ failure can result [45,46]. This cascade of events can ultimately lead to death.

Diagnosis of SIRS is made by the presence of two or more of the following clinical findings:

  • Fever or hypothermia: Body temperature less than 36°C (96.8°F) or greater than 38°C (100.4°F)

  • Increased heart rate: Greater than 90 beats per minute

  • Hyperventilation: Respiratory rate greater than 20 breaths per minute or a partial pressure of carbon dioxide less than 32 mm Hg (4.3 kPa)

  • Abnormal white blood cell count: Less than 4,000 cells/mm3 (leukopenia) or greater than 12,000 cells/mm3 (leukocytosis) or greater than 10% band forms (bandemia)

Infection can also be detected by culture, stain, or polymerase chain reaction.

Treatment of sepsis involves administration of antibiotics, collection of infectious fluids by surgical drainage, and adequate replacement of fluids. Vasopressors and inotropic therapy may be necessary to restore adequate blood pressure and perfusion. Proper support for organ failure is indicated for patients with severe sepsis, and sedation, mechanical ventilation, and analgesia are often required in late-stage disease. Adequate nutrition (usually administered parenterally) and glucose control are necessary. The patient should be stabilized prior to restarting ulcer treatments.


Cellulitis can occur when infection spreads from the site of the ulcer to a deeper layer of skin, causing acute infection of connective tissue and possibly leading to sepsis. In rare cases of pressure ulcers involving the spine, coccyx, or lower back, cellulitis can progress to meningitis. Staphylococci and streptococci are the most common causative agents of cellulitis.

Physical exam may reveal signs of infection, including erythema, edema, warmth, and possibly increased drainage. Lymphadenopathy may be present near the area of cellulitis. Diagnosis may be confirmed by blood culture, complete blood count (CBC), or fluid or exudate culture from the affected area.

Treatment usually involves a course of antibiotics. Analgesics may be necessary if the area is painful.


When the infection from a full tissue ulcer, generally stage IV, spreads to bone and joints, periosteitis, septic or infectious arthritis, or osteomyelitis can result. Physical examination shows bone tenderness and possibly swelling and redness. Diagnosis is based on CBC, erythrocyte sedimentation rate, C-reactive protein, imaging studies, blood culture, bone biopsy, and needle aspiration.

X-ray studies are the most widely used imaging study; however, they may give false-positive or false-negative results in many bone infection cases. Computed tomography scans are helpful in demonstrating fluid collections, bony erosion, and joint involvement. Radionuclide bone scanning (with technetium methylene-99m diphosphate) can be beneficial, but it only has a moderate degree of sensitivity and specificity.

Bone biopsy is the definitive diagnostic test. Bone biopsy with histologic examination verifies bone involvement. Microscopic criteria are also used to confirm the diagnosis of osteomyelitis.


The goals in the treatment of bone or joint infections are to eradicate infection and reduce damage to the bone and adjacent tissues. Antibiotics are prescribed, often intravenously. In order to select a proper antibiotic, laboratory confirmation of the pathogen and its sensitivities is required. Surgical removal of bone necrosis may be indicated.

Ablative surgery of stage IV ulcers involves bone resection from the base of the ulcer. If this method is used, Gram staining and culture and sensitivity studies should be completed on resected bone specimens. Bone biopsy should also be carried out following a partial ostectomy. This helps in the decision of whether to embark on a 6-week postoperative course of antibiotics. Usually, osteomyelitis is cured by the partial ostectomy.


Long-standing pressure ulcers can develop into malignant tumors called Marjolin's ulcers. These tumors were named for surgeon Jean-Nicolas Marjolin, who first described the condition in 1820 [47]. They are very aggressive ulcerating squamous cell carcinoma found in the area of ulcers and other long-standing indolent wounds. It can develop many years after the initial trauma.

The first sign of Marjolin's ulcer is a change in the character of the wound. Drainage increases, and the odor of the drainage becomes putrid. In some cases, there is frank bleeding. Diagnosis is made after histologic examination of a specimen removed from the ulcer, usually at the time of a flap closure. Confirmation of the diagnosis requires a preoperative tissue biopsy; wedge biopsy is the method of choice.

Excision of the lesion with 1-cm margin is required. Oncologic assistance is also necessary in the management of this condition, and extensive treatment is often necessary.


Gas gangrene is a rare but serious form of Clostridium perfringens infection. These obligate anaerobes release gas and harmful toxins that can result in gas gangrene, sepsis, and septic shock. The most common symptoms are severe pain and rapid swelling of the skin around or near the ulcer.

Surgical debridement is usually necessary. In very serious cases, excision with amputation is required to prevent spread of the infection. Penicillin is administered as adjuvant therapy. Hyperbaric oxygen therapy is effective in growth inhibition and killing C. perfringens [48,49].


People with stage III and IV ulcers are at a risk for contracting the rapidly progressive infection necrotizing fasciitis. Necrotizing fasciitis is defined as a group A streptococcal infection of the fascia with accompanying necrosis of the subcutaneous tissues. It is an uncommon consequence of pressure ulceration [50,51].

Initial signs of this condition are fever, pain, and massive swelling. Visual and microscopic evaluation of the tissues confirms the diagnosis. Emergency treatment is required, and aggressive surgical debridement is vital to prevent spreading.

As soon as necrotizing fasciitis is suspected, antibiotics should be started. A combination of intravenous antibiotics, usually clindamycin, vancomycin, and penicillin, is administered. Hyperbaric oxygen therapy can also be effective.


Recurrence of a pressure ulcer is a common complication of treatment. As noted, as many as 90% of patients with a healed wound will experience a recurrence [7,63]. Compared to normal tissue, scar tissue has lower tensile strength, poor blood supply, and poor ability to withstand trauma, making it vulnerable to recurrent episodes. If an ulcer recurs at the same site within 4 months of the initial injury, it is likely due to incomplete healing rather than a true recurrence [104]. Risk factors for recurrence include male sex, younger age, African American race, lower socioeconomic status, nursing home residence, and previous pressure ulcer surgery [104].


Comorbid conditions both increase susceptibility to pressure ulcers and impair the healing process. Therefore, comorbid conditions should be addressed as part of the overall treatment plan. Common comorbid conditions in patients with pressure ulcers include:

  • Diabetes

  • Incontinence

  • Peripheral vascular disease (PVD)

  • Hypotension and hypoxia

  • Dehydration, poor nutritional status, or malnutrition

  • Cancers

  • ESRD

  • Depression and cognitive impairment

Even with the best medical care and preventive measures, pressure ulcers can occur [52]. It is unclear which combination of comorbid conditions can lead to ulcer formation, but changes in skin with comorbidities is believed to result in ulcers. Recent acute illnesses or acute exacerbation of comorbid conditions may cause lethargy and reduced mobility, increasing the risk of pressure ulcers. In patients with comorbid conditions, special attention to the drugs being used is necessary. Chemotherapeutic agents, systemic corticosteroids, and NSAIDs can impair healing.


In patients with long-standing diabetes, both macro- and microvasculature can be severely damaged, particularly if the disease is poorly controlled. Diabetes also causes neuropathy, and the resultant loss of sensation and protective reflexes is a risk factor for ulcer progression. Patients with diabetes have elevated glucose levels that result in rigid blood cell walls and decreased blood flow through microvasculature. The disease also impairs oxygen release by the hemoglobin, resulting in hypoxia. Leukocytes have less effective chemotaxis and phagocytosis, which makes the patient susceptible to infection. Diabetics are prone to fungal rashes that can result in perineal irritation and skin breakdown. Impaired granulocyte function inhibits wound healing. All of these factors contribute to the increased risk of pressure ulcer development in a patient with diabetes.

The aim of diabetes management is to keep blood glucose levels close to normal (i.e., glycosylated hemoglobin less than 7%). Usually, pharmacotherapy and/or insulin therapy is necessary for optimum disease control. In addition, eating habits should be modified and physical activity should be increased.


According to the National Association for Continence, approximately 25 million Americans have transient or chronic urinary incontinence [105]. It is also estimated that 50% to 70% of patients with urinary incontinence fail to seek medical intervention or treatment. The high prevalence of incontinence among certain populations (e.g., nursing home residents) makes this an important factor in pressure ulcer development and healing.

Extended exposure of skin to urine and feces can result in breakdown, making the patient more susceptible to ulcers [53]. Urinary incontinence results in maceration, which causes increased skin irritation and fragility. Coliform bacteria and C. difficile contamination of existing wounds can lead to severe infections.

The treatment of these patients is dependent on the determining the incontinence etiology. General approaches include regular assessment of skin; hydration and infection should not be ignored. Patients should be checked for incontinence every 2 hours. For patients who are cooperative and aware of bladder filling, a toilet program should be instituted, including planned voiding every 2 hours. For patients who are uncooperative or unaware of bladder filling, consider the use of absorptive products or condom catheters for men. It is important to use diapers and underpads that wick moisture away from patients' skin. Incontinent patients should be cleaned as soon as possible after soiling using specialized incontinence skin cleansers or soaps.

For patients with severe diarrhea, all potential causative factors should be explored and addressed. A rectal pouch may be useful for these patients. In cases of chronic incontinence, an every other day suppository or enema may be considered. In addition, barrier ointments help protect the skin from incontinent episodes. If used, apply a thick coat of ointment, wipe off the soiled top layer, and apply another layer. Do not clean off the paste to skin level when bathing or cleaning.


PVD is an important contributory factor in the development of vascular ulcers, particularly diabetic foot ulcerations (as the cause of 10% to 30% of all cases) [106]. The wounds of patients with severe PVD heal poorly as a result of inadequate blood supply, and minor trauma or pressure often leads to ulceration.

When conducting a thorough physical examination, signs and symptoms consistent with PVD should be documented and ankle-brachial index or pulse volume recordings should be recorded. The ankle-brachial index is not specific in patients with advanced calcific atherosclerotic disease, and for patients with this condition, photoplethysmography or magnetic resonance angiogram is more accurate [54].

Treatment of PVD first relies on assessment and management of modifiable risk factors (e.g., smoking, physical activity). Pharmacologic management with antiplatelets is the gold standard for patients whose disease is not well controlled with lifestyle changes [116]. In addition, comorbidities should be treated aggressively.


Prolonged hypotension and hypoxia can cause tissue hypoperfusion, especially in anatomical locations already at risk for developing ulcers. Patients with septic shock have microvascular endothelial dysfunction, which results in tissue hypoxia despite adequate oxygenation [55,56]. Tissue hypoxia and hypoperfusion may also be caused by hemorrhagic shock. Anemia and low cardiac output limit the blood's oxygen-carrying capacity and perpetuate tissue hypoperfusion. It is necessary to check vital signs, CBC, blood gas, and echocardiogram and manage accordingly.


Patients with poor nutritional status are more susceptible to pressure ulcer formation and have poor healing ability [58,59]. Therefore, assessment of nutritional status along with laboratory tests for albumin and prealbumin is important. The goal of the assessment is to identify the patient's current nutritional status, any changes that have occurred in recent months or weeks, and impact on the patient's overall level of functioning. Hydration status should also be included in the assessment; dehydration impairs wound healing by decreasing the blood volume available to transport oxygen and nutrients to healing wounds [88].

Patients with gastrointestinal disease usually have poor nutritional status, which makes complete ulcer resolution difficult. Patients with bowel resections and fecal diversion also have impaired absorption of moisture and nutrients. Conditions like celiac disease, Crohn's disease, and gastrointestinal malignancy can result in malabsorption and micronutrient deficiencies. C. difficile colitis can cause severe diarrhea and hypoalbuminemia, making patients nutritionally and hemodynamically compromised.

The primary cause of malnutrition should be treated along with managing the disease and any fecal incontinence. After the patient's nutritional needs have been identified, the plan of care will include interventions to increase nutritional intake, keeping in mind that the patient's and family's preferences play an important role in establishing a diet plan.


Malignancies can result in cachexia syndrome, which is characterized by weight loss, malnutrition, weakness, and anemia. However, there is limited research exploring the link between pressure ulcers and cancer [119]. Radiation therapy can cause dermatitis and desquamation and increase the risk for skin breakdown. Both the malignancy and associated treatments can cause immunosuppression and increase the likelihood and severity of infections.

Patients with cancer who are also experiencing skin breakdown should be assessed for nutritional status, and medications may be prescribed to combat the anorexia associated with chemotherapy. Optimum skin care, particularly in areas affected by radiation therapy, is a necessity.


Severe uremia associated with ESRD necessitates the use of dialysis to remove uremic toxins and prevent or control complications, and pruritus and xerosis are common in these patients. Malnutrition and dehydration are also risks. Dietary management of patients with ESRD should be aimed at control of electrolytes (including calcium, phosphorus, and potassium), prevention of malnutrition, and maintenance of acceptable fluid volume status.


The National Institute of Mental Health estimates that 6.7% of adults in the United States are suffering from depression, and major depression is the leading cause of disability worldwide [107]. Depressed patients have little interest in self care and nutrition, both of which may predispose an individual to pressure ulcers [82]. Pressure ulcers have also been found to contribute to depressive symptoms [120]. Patients should be regularly assessed for depression or other psychological illnesses and referred to mental health care.


Loss of cognition is associated with increased risk for pressure ulcers, and impaired mental status leads to a lack of awareness of discomfort or pressure and may be associated with incontinence. The ability to respond appropriately or to inform others of the need for assistance may be lost completely. As such, these patients often require intensive care.


Research and technical innovations are producing sophisticated technology and analytic devices to diagnose, prevent, and treat pressure ulcers. These new innovations are changing the way ulcers are cared for and prevented in a variety of settings.


Studies have shown that patients with less nocturnal periodic movements are at risk for pressure ulcers, but sleeping patients may be unaware of their lack of movement [61]. Alert systems have been implemented to remind staff to reposition the patient every two hours. Because repositioning is one of the basic hallmarks of pressure ulcer prevention, alerts may help address this risk factor better.


Early detection is of utmost importance in pressure ulcer management. Advanced technology and devices can be used to achieve better sensitivity and specificity in the diagnosis of ulcers. These techniques include laser Doppler, visible and near-infrared spectroscopy, ultrasound, and pulse oximetry [62]. Each of these approaches ascertains clinical parameters associated with blood flow and hemoglobin concentration, and combining such measures with clinical information allows for a high degree of sensitivity and specificity in identifying impending chronic wounds in patients with any skin color [62].


New methodologies for documenting and measuring wounds can help both with monitoring treatment and preventing legal complications. Highly advanced computerized documentation is being used by many organizations. Techniques are now available to thoroughly assess the geometric, physiological (i.e., pressure and degree of wound perfusion), and biochemical (i.e., concentrations of various enzymes involved in tissue degradation and healing) aspects of the wound.

Electronic records and images are preferred by many institutions. The role of wound photography is growing and is a vital aspect of monitoring response to treatment and in defending against possible future litigation. Approximately 75% of home health agencies in the United States now include wound photography as part of the patient's medical record [88].


Ultrasound has been explored as a diagnostic and monitoring tool. High-frequency ultrasound provides greater resolution than other ultrasound techniques, but the depth of penetration of the sound waves is less. Therefore, it is ideal for imaging near-surface pathology. High-resolution ultrasound can easily detect the fluid content of tissue and measure skin thickness. More research is necessary to determine the efficacy and cost effectiveness of ultrasound for the routine care of pressure ulcers.


Although the available skin substitutes are not perfect, they do offer benefits when treating ulcers, particularly those resistant to healing. Research in the field of skin tissue engineering focuses on improving the skin barrier properties and the structural interaction of the epidermal and dermal equivalent of composite grafts. There are two types of bioengineered skin replacements available: biosynthetic skin substitutes and skin grafts.

Biosynthetic skin substitutes are developed without allogenic cells and consist of a mesh coated with a dermal analogue (bilayer) or an acellular dressing (monolayer). They act as starting points to promote ingrowth of tissue in the wound. The bilayer options also include a removable silicone layer that functions as a protective dressing.

Skin grafts may be categorized as xenografts, autografts, or allografts. A xenograft is derived from a non-human source, usually porcine skin. An autograft is a graft taken from the patient, while an allograft is transplanted from a genetically non-identical individual, often from a cadaver donor. Grafts may be further identified as dermal or epithelial/epidermal (or both) and as cultured or processed. Within these categories, there are several specific options, each with their own benefits and drawbacks [108]. It has been suggested that the properties inherent to skin grafts, such as the presence of hair follicles, may make them a good option to accelerate wound healing [64]. Selection of the best option is dependent on the features of the wound, the goals of treatment, and patient preferences.


Gene therapy has a tremendous potential, but use of the technology in the treatment of pressure ulcers is still in its infancy. Gene therapy has been proposed to accelerate wound healing and also to reduce healing complications such as keloid formation or chronic ulceration.

Genetically modified skin grafts have a potential use for treatment of large wounds. Smaller wounds may be amenable to in vivo delivery of genetic material using a variety of approaches including gene injection, gene gun, microseeding, and liposomal gene delivery. The preclinical studies of genetically modified skin grafts are promising, but more tests are necessary to determine the effectiveness of this treatment option [123,124].


Negative pressure wound devices provide an environment that resolves edema and hematoma and results in increased local perfusion. Newer negative pressure wound devices are smaller and more portable than earlier devices, and some deliver continuous subatmospheric pressure to the wound bed to promote healing. It should be noted that these devices have been associated with extensive bleeding, particularly in patients with blood vessel grafts in the leg, with breastbone or groin wounds, or who are receiving anticoagulant therapy [109]. Hemorrhage may also occur when dressings attached to the tissues are removed.


Biologic wound products accelerate healing by augmentation or modulation of inflammatory mediators. Growth factors that hold great promise in wound healing include eicosanoids, prostaglandin E1, cytokines, and interleukin-1.


Lasers may also accelerate the process of tissue repairing [65]. The lasers appear to simulate fibroblastic activity, although the mechanism is not yet fully understood.

Nanoparticles containing chitosan have been shown to have effective antimicrobial activity against Staphylococcus saprophyticusandEscherichia coli [65]. These materials could be used to prevent infection and facilitate wound healing.

Researchers have shown that a novel peptide (UN3) created by the combination of two naturally occurring peptides found in platelet-rich plasma stimulates wound vascularization and promotes epithelial proliferation. This could lead to new treatments for pressure ulcers [66].

Electrical stimulation may also accelerate healing in pressure ulcers [67]. Free radical scavengers and special drug delivery systems can also be effective in prevention of ulcers [68,69,70].


Pressure ulcers are the most common wounds of medico-legal importance. There is an increasing number of litigations related to ulcer prevention, with patients/caregivers winning 87% of cases [72]. Residents of long-term care facilities and families of those who developed pressure ulcers in a facility's care were awarded an average of $3.5 million per lawsuit, with the greatest settlement reaching $312 million [73,74].

As litigation is becoming more common, adherence to established standards of care is very important and has legal implications [75]. Some experts have suggested that if institutional neglect is responsible for development of pressure ulcers, caregivers could be liable to criminal prosecution.


Federal law establishes standards for long-term care facilities [110].

Based on the comprehensive assessment of a resident, the facility must ensure that 1) a resident who enters the facility without pressure sores does not develop pressure sores unless the individual's clinical condition demonstrates that they were unavoidable; and 2) a resident having pressure sores receives necessary treatment and services to promote healing, prevent infection, and prevent new sores from developing.

As noted, despite best patient care and treatment, not all pressure ulcers are avoidable [76]. In long-term care, the NPUAP defines an unavoidable ulcer as one that occurs even though "the facility had evaluated the individual's clinical condition and pressure ulcer risk factors; defined and implemented interventions that are consistent with individual needs, goals, and recognized standards of practice; monitored and evaluated the impact of the interventions; and revised the approaches as appropriate" [111]. However, most pressure ulcers are avoidable, and in acute care, an ulcer is considered a never event. The decision of whether an ulcer is avoidable or not is made on the basis of an assessment of care and patient characteristics; it may not be made prior to ulcer development [111].

Facilities should institute adequate measures to prevent wounds, and in the case an ulcer develops, staff should respond appropriately to prevent worsening of the wound. Wounds detected in the early stages have a greater chance of cure than later stage wounds that are infected or necrotic. Therefore, regular assessment and early intervention are required for all ulcers, avoidable or not. The presence of risk factors, including comorbidities, inability to maintain adequate nutrition and hydration status (e.g., if an advance directive prohibits artificial feeding), certain drugs, and immobility, is an indicator of avoidability. After assessment of risk factors, the next step is to ascertain if the response was timely according to documentation of all interventions. If any skin ulceration develops in spite of timely, appropriate interventions, the ulcer may be considered unavoidable.


Suspicion that improper medical care resulting in the development and/or worsening of an ulcer requires a full, document-intensive investigation. Because many factors can be indicative of medical neglect, each domain of care should be assessed (Table 7). Furthermore, the best defense against a claim of neglect is complete documentation of appropriate care.


Inadequate prevention
Poor documentation
Inadequate nutrition
Inadequate medical care
No family notification
Poor care planning
Wound severity and outcome

New or worsening pressure ulcers are generally due to poor administrative organization, understaffing, and poor training. The medico-legal implications of proper care cannot be overlooked, as those injuries are responsible for a significant proportion of healthcare litigation.

Medical Record

The medical chart should be examined to determine the level of care planning, assessment, and interventions. Wound neglect is usually associated with improper treatment, inadequate nutrition, and/or poor survey results.

Family diaries, stage surveys, in-service records, complaint files, minutes of quality assurance meetings, and photographs can also be helpful for identification of deviations from standard ulcer care.

Wound Documentation

Documentation of pressure ulcer care must be timely and detailed. Regular and consistent descriptions of the ulcer should be documented, as should responses to treatment. Improper, irregular, or "late entries" are absolutely impermissible and unacceptable.

In patients with multiple ulcers, progression of each wound should be documented and tracked. With the growing awareness of the possibility of litigation in wound care, many facilities have instigated a policy of photo documentation. Wounds present on admission are photographed, and some facilities require serial photographs to track wound progress and status at the time of discharge. Signed consent is required before wound photographs can be taken, and in most instances, the photographs become a permanent part of the patient's medical record.

Nutritional Assessments

It has been found that 30% to 85% of nursing home residents are malnourished and 30% to 50% are considered underweight [54]. Pressure ulcer treatment requires proper nutritional assessment and intervention during every stage. Weight loss, lab results, protein consumption, and vitamin levels should be documented, as should attempts to address abnormalities. If tube feeding is indicated, it should be discussed with the family prior to initiation.

Treatment Records

Treatment administration records should be examined to ensure that treatments were carried out per orders. Documentation should also include staffing records and time-sheets. Dates and times should always be included.

Minimum Data Sets and Care Plans

Minimum data sets are required for all residents of skilled nursing facilities. Improper and inaccurate entries in the minimum data sets indicate a facility with under-staffing and disorganized structure providing poor treatment to the resident. Scrutiny of this document can lead to litigation.


A vital component of any pressure ulcer program is patient/family education, with an overall goal of decreasing the incidence of ulcer development or recurrence. If possible, pressure ulcer prevention should not be a passive process for the patient and his/her family members. Rather, it should be a dialogue in which the patient and family feel comfortable asking questions and discussing problems. Patients should have as much control as possible in the plan of care. Empowerment is very important in maintaining the patient's physical and emotional well-being, and the plan of care should be explained thoroughly to cognitively aware patients and/or their family. It is important for everyone involved to appreciate that the prevention of ulcer formation is a lifelong process [79].

At the same time, it is necessary to evaluate the patient's/family's existing knowledge regarding pressure and pressure ulcers. Healthcare professionals should show patients what they can do to facilitate pressure relief (e.g., how to make small position changes while in the chair). If possible, teach patients how to do simple range-of-motion exercises. Take time to train the patient as often as is appropriate; not everyone will absorb the information the first time they hear it [4]. It is important not to let noncompliance or a bad attitude from the patient or family discourage the teaching process. The subject should be approached as often as is reasonable. Include the family members and caregivers in the instructions; as well as assisting with care, they can encourage compliance. All efforts at patient and family/caregiver education should be documented, along with the patient's response (both verbal and behavioral).

Different methods of teaching, such as photographs, videos, charts, diagrams, and written materials in the patient's native language, should be used. Education should be reinforced regularly and consistently [78]. The information provided to patients and/or their families should be specific to the individual treatment plan and goals.

Patient education programs should include all of the following areas:

  • Etiology of pressure ulcers

  • Reduction of risk

  • Reduction of friction and shear

  • Skin protection and inspection

  • Importance of nutrition

  • Proper and safe cleansing procedures and agents

  • Procedure for recurrence(s)

  • Management approaches

  • Proper dressing change procedure


Patients should be provided information about factors involved in pressure ulcer development. The role of pressure, friction, shear, and moisture in the development of ulcers should be explained. Other conditions that can impact ulcer development should be outlined, including:

  • Immobility (partial or total)

  • Excessive moisture and/or incontinence

  • Poor local or systemic circulation

  • Uncontrolled diabetes

  • Severe trauma

  • Dehydration

  • Hypoxia

  • Malnutrition

  • Sepsis

  • Previous history of pressure ulcer


Pressure reduction techniques should be thoroughly explained. Proper use of mattresses, cushions, and overlays and the placement of pillows, heel protectors, and wedges are essential. The role of repositioning and turning of the patient should be stressed. If the patient will be sitting in a chair for a long period of time, pressure release tactics should be included. Repositioning should be done every 1 to 2 hours, depending on the patient's condition [92].


Patients and/or caregivers should have a clear understanding of measures to decrease friction and shear. Education should include the proper body alignments that should be maintained when sitting in a chair or lying on a bed. The importance of using lifting devices for repositioning or transferring should be stressed.


Careful skin inspection is paramount in the care of pressure ulcers. The patient or caregiver should carefully inspect the skin for new openings or breaks in the skin at every repositioning. Any discoloration or redness of the skin that does not resolve within 30 minutes after changing position should be reported.

Maintaining skin cleanliness and moisturizing frequently can protect skin integrity. The skin should be cleaned with water and a gentle soap, preferably a pH-balanced cleanser. Alkaline products remove skin lipids, which increases water loss and weakens the barrier function of the skin [2]. Avoid hot water for bathing and scrubbing or using harsh cleaning agents. A soft cloth should be used to pat rather than rub the skin dry. Thromboembolic deterrent hose should be removed when bathing, and the nurse or physician should be notified of any redness, discoloration, or skin breakdown.

It is important to individualize the frequency of skin cleansing based on the patient's age, skin texture, and dryness or excessive oiliness of the skin. A daily bath may not be needed for all patients.

The epidermis is about 30% water, but through a process called trans-epidermal water loss, skin can lose its natural moisture. Without sufficient moisture, skin can become dry, brittle, and vulnerable to breakdown [85]. Therefore, products should be used to keep the skin supple. Emollients, such as mineral oil, petrolatum, and lanolin, penetrate into the stratum corneum to increase the lipid component and add softness to the skin. The oil film on the skin surface also prevents water loss and helps to rehydrate the stratum corneum [85]. Moisture barriers such as dimethicone can prevent water loss and help to retain lipids and water within the skin cells [85].

Humectants, such as glycerin, urea, and lactic acid, increase the water content of the stratum corneum by pulling water from the environment. All moisturizers should be applied to clean, slightly moist skin. Special attention should be paid to bony prominences, heels, ears, and the back of the head.


Adequate nutrition is an essential area of patient education, as malnutrition makes individuals susceptible to the development of pressure ulcers and at increased risk for infections, including sepsis, necrotizing fasciitis, and gangrene. Patients must also understand that adequate hydration is essential to improve tissue perfusion and excreting waste products. Patients/caregivers should make sure they comply with dietitian recommendations for diet, adequate fluid intake, and nutritional supplements.


Patients should be advised to take the following actions should a pressure ulcer develop:

  • Increase the frequency of repositioning and turning.

  • Note the size, location, odor, color, and drainage of the wound and adjacent tissue.

  • Notify the physician immediately about this new development.

  • If the patient is receiving home care services, the home health nurse should be notified immediately.


After a treatment plan is set, all aspects should be explained to the patient or caregiver again. Key education points include:

  • Products being used for wound prevention or healing

  • Where to procure dressings and pressure redistribution surfaces

  • Signs and symptoms of pressure ulcer deterioration

  • The importance of compliance to the established plan

Patients should be advised to look for new necrotic tissue in the wound bed, wound drainage with odor, and erythema and induration around the ulcer. If a clean wound enlarges or becomes deeper, the patient should be instructed to contact his or her physician immediately.


Proper dressing change technique should be demonstrated. The patient/caregiver should be able to change the dressing without any assistance from the supporting staff, and clean technique should be used. Hand washing, use of gloves, and infection prevention should all be a part of basic patient education.


Pressure ulcers are a common but preventable condition frequently seen in elderly individuals and those with comorbid conditions. In the United States, the incidence of pressure ulcers ranges from 0% to 40%, depending on the site of care [2].

Pressure ulcers are a major psychological, physical, and social burden to patients and often result in significantly decreased quality of life. In addition, they are a major source of healthcare expenditures. Costs related to the care of patients with ulcers total more than of $11 billion annually in the United States [7].

Evolution of pressure ulcers is multifactorial, and individuals with specific risk factors are more susceptible to ulcer development. Without proper care and treatment, superficial ulcers can evolve into more serious and severe ulcers and life-threatening complications may result, even with the best possible treatment and care. Therefore, the best way to treat a pressure ulcer is to prevent its occurrence. An interdisciplinary approach of creating a care plan that includes steps for the prevention of ulcers is the best practice.

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Works Cited

1. Thomas DR. The new F-tag 314: prevention and management of pressure ulcers. J Am Med Dir Assoc. 2006;7(8):523-531.

2. The National Pressure Ulcer Advisory Panel. Pressure ulcers prevalence, cost and risk assessment: consensus development conference statement. Decubitus. 1989;2(2):24-28.

3. The National Pressure Ulcer Advisory Panel. Pressure ulcers in America: prevalence, incidence, and implications for the future. An executive summary of the National Pressure Ulcer Advisory Panel monograph. Adv Skin Wound Care. 2001;14(4):208-215.

4. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006;296(8):974-984.

5. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223-226.

6. Whittington K, Patrick M, Roberts JL. A national study of pressure ulcer prevalence and incidence in acute care hospitals.J Wound Ostomy Continence Nurs. 2000;27(4):209-215.

7. Agency for Healthcare Research and Quality. Preventing Pressure Ulcers in Hospitals: A Toolkit for Improving Quality of Care. Available at http://www.ahrq.gov/research/ltc/pressureulcertoolkit/putool1.htm. Last accessed January 14, 2013.

8. Pieper B. Mechanical forces: pressure, shear, and friction. In: Bryant RA (ed). Acute and Chronic Wounds: Nursing Management. St. Louis, MO: Mosby, Inc.; 2000: 221-264.

9. Thomas DR, Diebold MR, Eggemeyer LM. A controlled, randomized, comparative study of a radiant heat bandage on the healing of stage 3-4 pressure ulcers: a pilot study. J Am Med Dir. 2005;6(1):46-49.

10. Kosiak M. Etiology and pathology of ischemic ulcers. Arch Phys Med Rehabil. 1959;40(2):62-69.

11. Kosiak M. Prevention and rehabilitation of pressure ulcers. Decubitus. 1991;4(2):60-62, 64, 66.

12. Jiricka MK, Ryan P, Carvalho MA, Bukvich J. Pressure ulcer risk factors in an ICU population. Am J Crit Care. 1995;4(5):361-367.

13. Folkedahl BA, Frantz R. Treatment of Pressure Ulcers. Iowa City, IA: University of Iowa Gerontological Nursing Interventions Research Center; 2002.

14. Remsburg RE, Bennett RG. Pressure-relieving strategies for preventing and treating pressure sores. Clin Geriatr Med. 1997;13(3):513-541.

15. Agostini JV, Baker DI, Bogardus ST. Prevention of Pressure Ulcers in Older Patients. Available at http://www.ahrq.gov/legacy/clinic/ptsafety/chap27.htm. Last accessed March 26, 2013.

16. McInnes E, Jammali-Blasi A, Bell-Syer SE, Dumville JC, Cullum N. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev. 2011;13(4):CD001735.

17. Rodeheaver GT, Kurtz L, Kircher BJ, Edlich RF. Pluronic F-68: a promising new skin wound cleanser. Ann Emerg Med. 1980;9(11):572-576.

18. Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of Pressure Ulcers Guideline Panel. Rockville, MD: U.S. Department of Health and Human Services; 1994.

19. Kirshen C, Woo K, Ayella EA, Sibbald RG. Debridement: a vital component of wound bed preparation. Adv Skin Wound Care. 2006;19(9):506-517.

20. Ayello EA, Cuddigan JE. Debridement: controlling the necrotic/cellular burden. Adv Skin Wound Care. 2004;17(2):66-75.

21. Roth RS, Lowery J, Hamill J. Assessing persistent pain and its relation to affective distress, depressive symptoms and pain catastrophizing in patients with chronic wounds: a pilot study. Am J Phys Med Rehabil. 2004;83:827-834.

22. Romanelli M, Magliaro A, Mastronicola D, Siani S. Systemic antimicrobial therapies for pressure ulcers. Ostomy Wound Manage. 2003;49(5A Suppl):25-29.

23. Meaume S, Vallet D, Morere MN, Téot L. Evaluation of a silver-releasing hydroalginate dressing in chronic wounds with signs of local infection. J Wound Care. 2005;14:411-419.

24. Breslow RA, Hallfrisch J, Guy DG, Crawley B, Goldberg AP. The importance of dietary protein in healing pressure ulcers.J Am Geriatr Soc. 1993;41(4):357-362.

25. Stefanovska A, Vodovnik L, Benko H, Turk R. Treatment of chronic wounds by means of electric and electromagnetic fields. Part 2: value of FES parameters for pressure sore treatment. Med Biol Eng Comput. 1993;313:213-220.

26. Baker L, Rubayi S, Villar F, Demuth SK. Effect of electrical stimulation waveform on healing of ulcers in human beings with spinal cord injury. Wound Rep Regen. 1996;4(1):21-28.

27. Trengove NJ, Stacey MC, MacAuley S, et al. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Rep Regen. 1999;7(6):442-452.

28. Pierce GF, Tarpley JE, Tseng J, et al. Detection of platelet-derived growth factor PDGF-AA in actively healing wounds treated with recombinant PDGF-BB and absence of PDGF in chronic nonhealing wounds. J Clin Invest. 1995;96(3):1336-1350.

29. Pierce GF, Tarpley JE, Allman RM, et al. Tissue repair processes in healing chronic pressure ulcers treated with recombinant platelet-derived growth factor BB. Am J Pathol. 1994;145(6):1399-1410.

30. Mast BA, Schultz G. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Rep Regen. 1996;4(4):411-420.

31. Bryant RA. Acute and Chronic Wounds. St. Louis, MO: Mosby Year Book; 1992.

32. Kloth LC, Berman JE, Dumit-Minkel S, Sutton CH, Papanek PE, Wurzel J. Effects of a normothermic dressing on pressure ulcer healing. Adv Skin Wound Care. 2000;13(2):69-74.

33. Pezzetti F, DeMattei M, Caruso A, et al. Effects of pulsed electromagnetic fields on human chondrocytes: an in vitro study.Calcif Tissue Int. 1999;65(5):396-401.

34. Garland DE, Adkins RH, Matsuno NN, Stewart CA. The effect of pulsed electromagnetic fields on osteoporosis at the knee in individuals with spinal cord injury. J Spinal Cord Med. 1999;22(4):239-245.

35. Roland D, Ferder M, Kothuru R, Faierman T, Strauch B. Effects of pulsed magnetic energy on a microsurgically transferred vessel. Plast Reconstr Surg. 2000;105(4):1371-1374.

36. Griffin JW, Tooms RE, Mendius RA, Clifft JK, Vander ZR, el Zeky F. Efficacy of high voltage pulsed current for healing of pressure ulcers in patients with spinal cord injury. Phys Ther. 1991;71(6):433-442.

37. Salzberg CA, Cooper-Vastola SA, Perez F, Viehbeck MG, Byrne DW. The effects of non-thermal pulsed electromagnetic energy on wound healing of pressure ulcers in spinal cord-injured patients: a randomized, double-blind study. Ostomy Wound Manage. 1995;41(3):42-44, 46, 48.

38. Wagner DR, Jeter KF, Tintle T, Martin MS, Long JM. Bioelectrical impedance as a discriminator of pressure ulcer risk. Adv Wound Care. 1996;9(2):30-37.

39. Wood JM, Evans P, Schalheuter K, et al. A multicenter study on the use of pulsed low-intensity direct current for healing chronic stage II and stage III decubitus ulcers. Arch Dermatol. 1993;129(8):999-1009.

40. Burns A, Orenstein H. Pressure sores. Plastic Surg. 1990;5(39).

41. Conway H, Griffith B. Plastic surgery for closure of decubitus ulcers in patients with paraplegia, based on experience with 1000 cases. Am J Surg. 1956;91(6):946-975.

42. Flanagan M. Improving accuracy of wound measurement in clinical practice. Ostomy Wound Manage. 2003;49(10):28-40.

43. Ferrell BA, Osterweil D, Christenson P. A randomized trial of low-air-loss beds for treatment of pressure ulcers. JAMA. 1993;269(4):494-497.

44. Brandeis GH, Morris JN, Nash DJ, Lipsitz LA. The epidemiology and natural history of pressure ulcers in elderly nursing home residents. JAMA. 1990;264(22):2905-2909.

45. Bone RC. Systemic inflammatory response syndrome: a unifying concept of systemic inflammation. In: Fein AM, Abraham EM, Balk RA, Bernard GR, Bone RC, Dantzker DR, Fink MP (eds). Sepsis and Multiorgan Failure. Baltimore, MD: Williams & Wilkins; 1997: 3-10.

46. Wheeler AP, Bernard GR. Current concepts: treating patients with severe sepsis. N Engl J Med. 1999;340:207-214.

47. Marjolin JN. Ulcere. In: Dictionnaire de Medecine. 1820.

48. Hart GB, Strauss MB. Gas gangrene—clostridial myonecrosis: a review. J Hyperbaric Med. 1990;5(2):125-144.

49. Zamboni WA, Riseman JA, Kucan JO. Management of Fournier's gangrene and the role of hyperbaric oxygen. J Hyperbaric Med. 1990;5(3):177-186.

50. Sugarman B, Hawes S, Musher DM, Klima M, Young EJ, Pircher F. Osteomyelitis beneath pressure sores. Arch Intern Med. 1983;143(4):683-688.

51. Kaplan LJ, Pameijer C, Blank-Reid C, Granick MS. Adv Wound Care. 1998;11(4):185-189.

52. Lyder CH, Preston J, Grady JN, et al. Quality of care for hospitalized Medicare patients at risk for pressure ulcers. Arch Intern Med. 2001;161(12):1549-1554.

53. Levine JM. Historical perspective: the neurotrophic theory of skin ulceration. J Am Geriatr Soc. 1992;40(12):1281-1283.

54. Allen J. Photoplethysmography and its application in clinical physiological measurement. Physiol Meas. 2007;28:R1-R39.

55. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care. 2004;8(5):373-381.

56. Ellis CG, Jagger J, Sharpe M. The microcirculation as a functional system. Crit Care. 2005;9(Suppl 4):S3-S8.

57. Thomas DR. The role of nutrition in prevention and healing of pressure ulcers. Clin Geriatr Med. 1997;13(3):497-511.

58. Thomas DR, Goode PS, Tarquine PH, Allman RM. Hospital-acquired pressure ulcers and risk of death. J Am Geriatr Soc. 1996;44(12):1435-1440.

59. Thomas DR. Prevention and treatment of pressure ulcers. J Am Med Dir Assoc. 2006;7:46-59.

60. Berlowitz DR, Wilking SVB. Risk factors for pressure sores: a comparison of cross-sectional and cohort-derived data. J Am Geriatr Soc. 1989;37(111):1043-1050.

61. Barbenel JC, Ferguson-Pell MW, Kennedy R. Mobility of elderly patients in bed: measurement and association with patient condition. J Am Geriatr Soc. 1986;34(9):633-636.

62. Salcido RS. Finding a window into the skin. Adv Skin Wound Care. 2002;15(3):100.

63. Tauqir SF, Mirza S, Gul S, Ghaffar H, Zafar A. Complications in patients with spinal cord injuries sustained in an earthquake in northern Pakistan. J Spinal Cord Med. 2007;30(4):373-377.

64. Han I, Shim KJ, Kim JY, et al. Effect of poly (3-hydroxybutyrate-co-3-hydroxyvalerate) nanofiber matrices cocultured with hair follicular epithelial and dermal cells for biological wound dressing. Artif Organs. 2007;31(11):801-808.

65. Leonida MD, Banjade S, Vo T, Anderle G, Haas GJ, Philips N. Nanocomposite materials with antimicrobial activity based on chitosan. Int J Nano Biomater. 2011;3(4):310-334.

66. Demidova-Rice TN, Wolf L, Deckenback J, Hambli MR, Herman IM. Human platelet-rich plasma- and extracellular matrix-derived peptides promote impaired cutaneous wound healing in vivo. PLoS ONE. 2012;7(2):e32146.

67. Levine SP, Kett RL, Gross MD. Blood flow in the gluteus maximus of seated individuals during electrical muscle stimulation.Arch Phys Med Rehabil. 1990;71(9):682-686.

68. Salcido R, Carney J, Fisher S, et al. A reliable animal model of pressure sore development: the role of free radicals. J Am Paraplegia Soc. 1993;16:61.

69. Salcido R, Donofrio JC, Fisher SB, et al. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care. 1994;7(5):23-24, 26, 28.

70. Salcido R, Fisher SB, Donofrio JC, et al. An animal model and computer-controlled surface pressure delivery system for the production of pressure ulcers. J Rehabil Res Dev. 1995;32(2):149-161.

71. The Joint Commission. Strategies for preventing pressure ulcers. Joint Commission Perspectives on Patient Safety. 2008;8(1):5-7.

72. Voss AC, Bender SA, Ferguson ML, Sauer AC, Bennett RG, Hahn PW. Long-term care liability for pressure ulcers. J Am Geriatr Soc. 2005;53(9):1587-1592.

73. Lyder C, Shannon R, Emple-Grazier O, McGeHee D, White C. A comprehensive program to prevent pressure ulcers in LTC: exploring costs and outcomes. Ostomy Wound Manage. 2002;48(4):52-62.

74. Dorner B, Posthauer ME, Thomas D. The role of nutrition in pressure ulcer prevention and treatment: National Pressure Ulcer Advisory Panel white paper. Adv Skin Wound Care. 2009;22(5):212-221.

75. Tingle J. Legal implications of standard setting in nursing. Br J Nurs. 1992:1(14):728-731.

76. Burger SG, Kayser-Jones J, Prince Bell J. Malnutrition and Dehydration in Nursing Home Residents: Key Issues in Prevention and Treatment. Available at http://www.commonwealthfund.org/usr_doc/burger_mal_386.pdf. Last accessed January 14, 2013.

77. Gorecki C, Nixon J, Madill A, Firth J, Brown JM. What influences the impact of pressure ulcers on health-related quality of life? A qualitative patient-focused exploration of contributory factors. J Tissue Viability. 2011;20(1):3-12.

78. Oot-Giromini B, Bidwell FC, Heller NB, Parks ML, Wicks P, Williams PM. Evolution of skin care: pressure ulcer prevalence rates pre/post intervention. Decubitus. 1989;2(2):54-55.

79. Relander M, Palmer B. Recurrence of surgically treated pressure sores. Scand J Plast Reconstr Surg Hand Surg. 1988;22(1):89-92.

80. Stasik L. Hospital-Acquired Pressure Ulcers: Making the Nutrition Connection. Columbus, OH: Abbott Nutrition; 2008.

81. Smith BM, Guihan M, LaVela SL, Garber SL. Factors predicting pressure ulcers in veterans with spinal cord injuries. Am J Phys Med Rehabil. 2008;87(9):750-757.

82. Baranoski S, Ayello EA. Wound Care Essentials: Practice Principles. 2nd ed. Ambler, PA: Lippincott Williams & Wilkins; 2007.

83. Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby; 2007.

84. Gallagher S. The Challenges of Caring for the Obese Patient. Edgemont, PA: Matrix Medical Communications; 2005.

85. Emory University School of Medicine Wound, Ostomy and Continence Nursing Education Center. Skin and Wound Module. 6th ed. Atlanta, GA: Emory University WOCNEC; 2006.

86. Dolynchuk K, Keast D, Campbell K, et al. Best practices for the prevention and treatment of pressure ulcers. Ostomy Wound Manage. 2000;46(11):38-52.

87. Bergstrom N, Braden BJ, Laguzza A, Holman V. The Braden Scale for Predicting Pressure Sore Risk. Nurs Res. 1987;36:205-210.

88. Sussman C, Bates-Jensen BM. Wound Care: A Collaborative Practice Manual for Health Professionals. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.

89. European Pressure Ulcer Advisory Panel, National Pressure Ulcer Advisory Panel. Pressure Ulcer Treatment: Quick Reference Guide. Available at http://www.epuap.org/guidelines/Final_Quick_Treatment.pdf. Last accessed March 26, 2013.

90. AHRQ Panel for the Prediction and Prevention of Pressure Ulcers in Adults. Pressure Ulcers in Adults: Prediction and Prevention. Clinical Practice Guideline Number 3. Rockville, MD: Agency for Healthcare Research and Quality; 1992.

91. Pearson C. Something old is new again: debriding and reducing local wound infection with maggots. Wound Care Canada. 2007;5(2):22-26.

92. Medline Industries, Inc. The Wound Care Handbook. Mundelein, IL: Medline; 2007.

93. Butcher G. Low frequency ultrasonic debridement: a new tool in our armoury? J Foot Ankle Res. 2011;4(Suppl 1):P7.

94. Freedline A, Fishman TD. Wound Documentation Tips. Available at http://www.woundconsultant.com/files/Wound_Documentation_Tips_6.07.pdf. Last accessed January 14, 2013.

95. Harris C, Bates-Jensen B, Parslow N, Raizman R, Singh M, Ketchen R. Bates-Jensen wound assessment tool: pictorial guide validation project. J Wound Ostomy Continence Nurs. 2010;37(3):253-259.

96. Ratliff CR. Wound exudate: an influential factor in healing. Adv Nurse Pract. 2008;16(7):32-35.

97. Bluestein D, Javaheri A. Pressure ulcers: prevention, evaluation, and management. Am Fam Physician. 2008;78(10):1186-1194.

98. National Pressure Ulcer Advisory Panel. Pressure Ulcer Stages Revised by NPUAP. Available at http://www.npuap.org/pr2.htm. Last accessed April 4, 2013.

99. Szor JK, Bourguignon C. Description of pressure ulcer pain at rest and at dressing change. J WOCN. 1999;26(3):115-120.

100. Günes UY. A descriptive study of pressure ulcer pain. Ostomy Wound Manage. 2008;54(2):56-61.

101. Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P. Wong's Essentials of Pediatric Nursing: Wong-Baker Faces Pain Rating Scale. 6th ed. St. Louis, MO: Mosby; 2001.

102. Bergstrom N, Allman R, Alvaraz O, et al. Treatment of Pressure Ulcers: Clinical Guideline Number 15. Publication No. 95-0652. Washington, DC: Agency for Healthcare Policy and Research; 1994.

103. National Pressure Ulcer Advisory Panel. PUSH Tool 3.0. Available at http://www.npuap.org/resources/educational-and-clinical-resources/push-tool/push-tool. Last accessed March 26, 2013.

104. Bates-Jensen BM, Guihan M, Garber SL, Chin AS, Burns SP. Characteristics of recurrent pressure ulcers in veterans with spinal cord injury. J Spinal Cord Med. 2009;32(1):34-42.

105. National Association for Continence. Facts and Statistics. Available at http://www.nafc.org/media/media-kit/facts-statistics. Last accessed March 26, 2013.

106. Mills JI. Evaluation and management of peripheral arterial disease. In: Armstrong DG, Lavery LA. Clinical Care of the Diabetic Foot. Alexandria, VA: American Diabetes Association; 2005: 45-51.

107. National Institute of Mental Health. The Numbers Count: Mental Disorders in America. Available at http://www.nimh.nih.gov/health/publications/the-numbers-count-mental-disorders-in-america/index.shtml. Last accessed March 26, 2013.

108. Shores JT, Gabriel A, Gupta S. Skin substitutes and alternatives: a review. Adv Skin Wound Care. 2007;20(9 Pt 1):493-508.

109. U.S. Food and Drug Administration. Negative Pressure Wound Devices Draw FDA Notice, Advice. Available at http://www.fda.gov/forconsumers/consumerupdates/ucm193277.htm. Last accessed March 26, 2013.

110. U.S. Government Printing Office. 42 CFR 483.25: Quality of Care. Available at http://www.gpo.gov/fdsys/granule/CFR-2011-title42-vol5/CFR-2011-title42-vol5-sec483-25/content-detail.html. Last accessed March 26, 2013.

111. Black JM, Edsberg LE, Baharestani MM, et al. Pressure ulcers: avoidable or unavoidable? Results of the National Pressure Ulcer Advisory Panel Consensus Conference. Ostomy Wound Manage. 2011;57(2):24-37.

112. Wynne JJ, Felsenstein JM, Trzcinski R, Zupanski-Nielsen D, Connors DP. Collateral damage-free debridement using 193nm ArF laser. Proc SPIE 7883. Paper presented at: Photonic Therapeutics and Diagnostics VII; February 17, 2011; San Francisco, CA.

113. Thomas DR. Prevention and treatment of pressure ulcers: what works? What doesn't? Cleve Clin J Med. 2001;68(8):704-722.

114. Institute for Clinical Systems Improvement. Pressure Ulcer Prevention and Treatment Protocol. Bloomington, MN: Institute for Clinical Systems Improvement; 2012.

115. Baba-Akbari Sari A, Flemming K, Cullum NA, Wollina U. Therapeutic ultrasound for pressure ulcers. Cochrane Database Syst Rev. 2006;(3):CD001275.

116. Sontheimer DL. Peripheral vascular disease: diagnosis and treatment. Am Fam Physician. 2006;73(11):1971-1976.

117. Papanas N, Maltezos E. Becaplermin gel in the treatment of diabetic neuropathic foot ulcers. Clin Interv Aging. 2008;3(2):233-240.

118. Kranke P, Bennett MH, Martyn-St. James M, Schnabel A, Debus SE. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2012;4:CD004123.

119. Masaki F, Riko K, Seiji H, Shuhei Y, Aya Y. Evaluation of pressure ulcers in 202 patients with cancer. Wounds. 2007;19(1):13-19.

120. Galhardo VAC, Magalhães MG, Blanes L, Juliano Y, Ferreira LM. Health-related quality of life and depression in older patients with pressure ulcers. Wounds. 2010;22(1):20-26.

121. Hess CT. Clinical Guide to Skin and Wound Care. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2008.

122. Hall JE (ed). Guyton and Hall Textbook of Medical Physiology. 12th ed. Philadelphia, PA: Saunders Elsevier; 2011.

123. Jones JE, Nelson EA, Al-Hity A. Skin grafting for venous leg ulcers. Cochrane Database Syst Rev. 2013;1:CD001737.

124. Koyama T, Hackl F, Aflaki P, et al. A new technique of ex vivo gene delivery of VEGF to wounds using genetically modified skin particles promotes wound angiogenesis. J Am Coll Surg. 2011;212(3):340-348.

Evidence-Based Practice Recommendations Citations

1. Association for the Advancement of Wound Care. Association for the Advancement of Wound Care Guideline of Pressure Ulcer Guidelines. Malvern, PA: Association for the Advancement of Wound Care; 2010. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=24361. Last accessed March 27, 2013.

2. Institute for Clinical Systems Improvement. Pressure Ulcer Prevention and Treatment Protocol. Bloomington, MN: Institute for Clinical Systems Improvement; 2012. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=36059. Last accessed March 27, 2013.

3. National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel. Pressure ulcer treatment recommendations. In: Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline. Washington, DC: National Pressure Ulcer Advisory Panel; 2009. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=25139. Last accessed March 27, 2013.

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