eMedicine Specialties > Plastic Surgery > Pressure Ulcers

Pressure Ulcers, Nonsurgical Treatment and Principles

Author: Christian N Kirman, MD, Staff Physician, Department of Plastic and Reconstructive Surgery, Wake Forest University Baptist Medical Center
Coauthor(s): Joseph A Molnar, MD, PhD, FACS, Associate Professor of Plastic and Reconstructive Surgery, Associate Director, Burn Unit, Wake Forest University School of Medicine
Contributor Information and Disclosures

Updated: Jul 8, 2008

Introduction

Background

Although they are technically separate entities, the terms decubitus ulcer, bedsore, and pressure sore are often used interchangeably in the medical community. Decubitus, from the Latin decumbere, means "to lie down." Decubitus ulcers, therefore, occur at sites overlying bony structures that are prominent when the person is lying in a recumbent position. Decubitus ulcers may occur on the scalp, back, tailbone, hip, heel, or any other area to which pressure is applied while a person is lying down. Therefore, decubitus ulcer does not adequately describe ulceration that occurs while in other positions such as prolonged sitting. The pressure from prolonged sitting may cause an ischial tuberosity ulcer, which is commonly seen in persons confined to the sitting position. Because the common denominator of all such ulcerations is pressure, the term that best describes this condition is pressure sore.

Pressure sores have likely existed since the dawn of our infirm species. J. Thompson Rowling described pressure sores in unearthed Egyptian mummies in 1961, and scientific writings have addressed them since the early 1800s. Pressure sores continue to be an ever-present problem within our society. The prevalence of pressure sores in hospitalized patients has been reported to be from 14-21% over the last decade. The cost to heal a single full-thickness pressure sore may be as high as 70,000 dollars.¹ The overall annual cost has recently been estimated to be between 5 billion and 8.5 billion dollars,² with the cost of hospital-acquired pressure ulcers between 2.2 and 3.6 billion dollars.³

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Pathophysiology

In 1873, Sir James Paget described remarkably well the production of the pressure sore, and his description is still quite accurate today.⁴ Many factors contribute to the development of pressure sores, but pressure leading to ischemia and necrosis is the final common pathway. Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual against the surface beneath. These pressures are often in excess of capillary filling pressure (approximately 32 mm Hg). Tissues are capable of briefly withstanding enormous pressures, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a series of events that potentially leads to tissue necrosis and ulceration. The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface.

Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury.⁵ Maceration may occur in a patient who has incontinence, predisposing the skin to injury. Pressure, shear forces, and friction cause microcirculatory occlusion resulting in ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration.

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

Restoration of blood flow to an ischemic area of tissue, or reperfusion, has recently been suggested as a cause of more damage to that area, causing a pressure sore to enlarge or become more chronic. This occurs, for example, when a paraplegic or quadriplegic patient is turned from one side to the other, in a well-intentioned attempt to combat prolonged pressure on a given side. The exact mechanism of the ischemia-reperfusion cycle of injury has yet to be fully understood. Continued production of inflammatory mediators and reactive oxygen species during ischemia reperfusion may contribute to the chronicity of pressure sores. 

In patients with normal sensitivity, mobility, and mental faculty, pressure sores are unlikely to occur. Feedback, both conscious and unconscious, from the areas of compression leads one to change position. This shifts the pressure from one area to another long before any irreversible ischemic damage to the tissues occurs.

Individuals who are unable to avoid long periods of uninterrupted pressure are at increased risk for developing necrosis and ulceration. This group of patients typically includes people who are elderly, neurologically impaired, or hospitalized with acute illness. These individuals cannot protect themselves from the pressure exerted on their bodies unless they consciously change position or have assistance in doing so. Even the most conscientious patient with an extensive support group and financial resources may suffer from ulceration as the result of a brief lapse in avoidance of the detrimental effects of pressure.

Frequency

United States

The fifth National Pressure Ulcer Prevalence Survey, conducted in 1999 among patients in acute care hospitals, showed an overall prevalence rate of 14.8%, with 7.1% having occurred during that hospital visit.⁶ Intensive care units had the highest prevalence rates among different hospital settings, at 21.5%.⁶  The predominant age group of patients with pressure ulcers was the patients aged 71-80 years (29%).⁶

Pressure ulcer prevalence in long-term care facilities is an estimated from 11-30%. Among patients with neurological impairments, pressure sores occur with an incidence of 7-8% annually,⁷ with a lifetime risk estimated to be 25-85%.⁸

Anatomically, the buttock region is by far the most common area for pressure sores to develop. These account for over 70% of all occurrences, with sacral (46%) and ischial (26%) locations being most common.⁹ The lower extremities account for an additional 15% of all pressure sores, with malleolar, patellar, pretibial, and especially heel locations being most common.⁹ The remaining approximately 15% of pressure sores may occur in any location that experiences long periods of uninterrupted pressure.⁹ Nose, chin, forehead, occiput, chest, back, and elbow are among the infrequent sites for pressure ulceration. No surface of the body is immune to the ischemic effects of unrelieved pressure, but ulcers most often occur over a bony prominence. 

Mortality/Morbidity

Pressure sores are listed as the direct cause of death in 7-8% of all patients with paraplegia.^10,7 Evaluation of large groups of patients has revealed that one third of hospitalized patients with pressure sores die during their hospitalization. More than half of patients who develop a pressure sore in the hospital will die within the next 12 months. In general, these patients die of their primary disease process, but the pressure sore may be a contributing factor in some instances.

Sex

Most younger individuals suffering from pressure ulceration are males. This reflects the greater number of men suffering traumatic spinal cord injuries. In the older population, most patients are women because of their survival advantage over men.

Age

The prevalence of pressure sores appears to have a bimodal age distribution. A small peak occurs during the third decade of life, reflecting ulceration in those with traumatic neurologic injury. As patients move from the age category of 40–58 years to the age category of 75 years or older, a larger increase in the incidence of pressure ulcers occurs.²  Two thirds of pressure sores occur in patients older than 70 years.¹¹

Clinical

History

When initially evaluating a patient with pressure ulceration, note the following important information from the history:

• Overall physical and mental health, including life expectancy
• Prior hospitalizations, operations, or ulcerations
• Diet and recent weight changes
• Bowel habits and continence status
• Presence of spasticity or flexion contractures
• Medications and allergies to medications
• Tobacco, alcohol, and recreational drug use
• Place of residence and the support surface used in bed or while sitting
• Level of independence, mobility, and ability to comprehend and cooperate with care
• Underlying social and financial support structure
• Presence of specific cultural, religious, or ethnic issues
• Presence of advanced directives, power of attorney, or specific preferences regarding care
• Presence of signs or symptoms related to the current ulceration  
• Pain may be present at the ulcer site. However, it is more commonly absent because of paraplegia or the patient being in critical condition and unable to acknowledge pain.
• A foul odor or discharge could be a sign of a more serious infection at the ulcer site.
• Natural history of the present ulcer  
• Length of time the ulcer has been present
• Circumstances under which the ulcer has developed
• Local treatments currently and previously employed

Physical

A thorough physical examination is necessary to evaluate the overall state of health, comorbidities, nutritional status, and mental status of the patient. The level of comprehension and cooperation of the patient dictates the intensity of nursing care that is required. The presence of contractures or spasticity is important to note and may help identify additional areas at risk for pressure ulceration. Following the general physical examination, attention should be turned to the wound. Adequate examination of the wound may require the administration of intravenous or oral pain medications to ensure patient comfort. Chronic pain may be present among these patients and may be exacerbated by ulcer examination.

Clinical assessment and description of pressure sores can be quite difficult for the inexperienced observer; therefore, many classification schemes have been developed to define the severity of pressure ulcers. The National Pressure Ulcer Advisory Panel has recently updated its classification scheme for pressure ulcers.¹² The goal of the revision was to clarify each stage and reduce the number of incorrectly staged ulcers or other types of wounds and skin lesions. This system consists of 4 stages of ulceration but is not intended to imply that all pressure sores follow a standard progression from stage I to stage IV or that healing pressure sores follow a standard regression from stage IV to stage I to a healed wound. Rather, the system is designed to describe the degree of tissue damage observed at the specific time of examination and is meant to facilitate communication among the various disciplines involved in the study and care of these patients.

• (Suspected) Deep Tissue Injury: This is the most recent addition to the staging system. This stage is described as a “purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear.”¹² This stage may be difficult to detect in individuals with dark skin.
• Stage I: This classification represents intact skin with signs of impending ulceration. Initially, this presents as blanchable erythema indicating reactive hyperemia. When tissue becomes temporarily ischemic, relief of pressure causes hyperemia, which is probably a protective mechanism of increased blood flow designed to oxygenate the tissues and remove potentially harmful products of metabolism. Reactive hyperemia should resolve within 24 hours of the relief of pressure. Warmth and induration also may be present. Continued pressure creates erythema that does not blanch with pressure and may well represent the first outward sign of tissue destruction. Finally, the skin may appear white from ischemia.
• Stage II: This classification represents a partial-thickness loss of skin involving epidermis and dermis that appears as an open shallow ulcer with a pink wound bed.
• Stage III: This classification represents a full-thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia. This lesion presents as an ulcer that may include undermining and tunneling of adjacent tissue. Bone, tendon, and fascia are not exposed.
• Stage IV: This classification represents full-thickness tissue loss with extension into muscle, bone, tendon, or joint capsule. Slough or eschar may be present in the wound. Osteomyelitis with bone destruction and dislocations or pathologic fractures may be present. Sinus tracts and severe undermining are commonly present.
• Unstageable: An unstageable ulcer is defined as full-thickness tissue loss in which the base of the ulcer is covered by slough or eschar such that the full depth of the wound cannot be appreciated. Only when the slough or eschar is removed can the depth of the ulcer be evaluated and correctly staged.

Staging of wound depth is only a small part of the initial assessment. Ulcer location, size of the skin opening, and presence of any surrounding maceration or induration must be accurately recorded. The presence of multiple pressure ulcers prompts the search for interconnecting tracts with overlying skin bridging that may not be readily apparent. Also note the presence or absence of foul odors, wound drainage, and soilage from urinary or fecal incontinence. This provides information regarding the level of bacterial contamination and the need for debridement or diversionary procedures. Click here to complete a Medscape CME activity on fecal and urinary incontinence in adults.

Causes

Although prolonged uninterrupted pressure is the cause of pressure sores, impaired mobility is probably the most common reason patients are exposed to uninterrupted pressure. This situation may be present in patients who are neurologically impaired, heavily sedated or anesthetized, restrained, demented, or recovering from a traumatic injury such as a pelvic or femur fracture. These patients cannot adequately alter their position with enough frequency to relieve pressure. Moreover, this immobility, if prolonged, may lead to muscle and soft tissue atrophy, decreasing the bulk over which bony prominences are supported.

• Contractures and spasticity often contribute to ulcer formation by repeatedly exposing tissues to trauma through flexion of a joint. Contractures rigidly hold a joint in flexion, while spasticity subjects tissues to repeated friction and shear forces. Skin breakdown and pressure ulcers may frequently be found under and between toes and on the palm of the hand.
• The inability to perceive pain, from neurologic impairment or medication, contributes to pressure ulceration by removing one of the most important stimuli for repositioning and pressure relief. Conversely, pain from surgical incisions, fracture sites, or other sources may make the patient unwilling or unable to change position.
• Skin quality also affects whether pressure leads to ulceration. Paralysis, insensibility, and aging lead to atrophy of the skin with thinning of this protective barrier. A decrease in epidermal turnover, flattening of the dermal-epidermal junction, and loss of vascularity occur with advanced age. The skin becomes more susceptible to minor traumatic forces, such as friction and shear forces typically exerted during the moving of a patient. Trauma that causes de-epithelialization or skin tears removes the barrier to bacterial contamination and leads to transdermal water loss, creating maceration and adherence of the skin to clothing and bedding.
• Incontinence or presence of a fistula contributes to ulceration in several ways. These conditions cause the skin to be continually moist, leading to maceration. In addition, frequent soiling has the effect of regularly introducing bacteria to an open wound.
• Bacterial contamination from improper skin care or urinary or fecal incontinence, while not truly an etiologic factor, is an important element to consider in the treatment of pressure sores and can delay or prevent wound healing. These wounds serve as warm, moist reservoirs for bacterial overgrowth where antibiotic resistance may develop over time. Pressure sores may progress from being simply contaminated, as all open wounds are, to being grossly infected, which indicates tissue invasion by bacteria. This may lead to uncommon but life-threatening complications such as bacteremia, sepsis, myonecrosis, gangrene, or necrotizing fasciitis.
• Malnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute to tissue vulnerability to trauma as well as cause delayed wound healing. Poor nutritional status certainly contributes to the chronicity often seen in these lesions and inhibits the ability of the immune system to prevent infections. Anemia indicates poor oxygen carrying capacity of the blood. Vascular disease and hypovolemia also may impair blood flow to the region of ulceration. (Click here to complete a Medscape CME activity about a recently FDA-approved treatment for hypovolemia and other conditions.)

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