The terms decubitus ulcer and pressure sore often are used interchangeably in the medical community. Decubitus, from the Latin decumbere, means “to lie down.” Decubitus ulcer, therefore, does not adequately describe ulceration that occurs in other positions, such as prolonged sitting (eg, the commonly encountered ischial tuberosity ulcer). Because the common denominator of all such ulcerations is pressure, pressure sore is the better term to describe this condition.
A study by Howard and Taylor found the incidence of pressure sores in nursing home residents in the southeastern United States to be higher in black patients than in white ones. The authors examined data from 113,869 nursing home residents, none of whom had pressure sores at nursing home admission. They determined that 4.7% of black residents developed postadmission ulcerations, compared with 3.4% of white residents. In addition, the racial differences in pressure sore incidence displayed a sex predilection based on patient characteristics. The variation in incidence between black and white males occurred in residents who were dependent in mobility, while in females, such variation occurred in black and white residents who were bedfast and living in nursing homes with fewer than 200 beds.
History of the Procedure
Pressure sores have probably existed since the dawn of our infirm species. They have been noted in unearthed Egyptian mummies and addressed in scientific writings since the early 1800s. Presently, treatment of pressure sores in the United States is estimated to cost in excess of $1 billion annually.
Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual against a surface beneath. These pressures are often in excess of capillary filling pressure, approximately 32 mm Hg. In patients with normal sensitivity, mobility, and mental faculty, pressure sores do not occur. Feedback, conscious and unconscious, from the areas of compression leads individuals to change body position. These changes shift the pressure prior to any irreversible tissue damage.
Individuals who are unable to avoid long periods of uninterrupted pressure over bony prominences–a group of patients that typically includes elderly individuals, persons who are neurologically impaired, and patients who are acutely hospitalized–are at increased risk for the development of necrosis and ulceration. These individuals cannot protect themselves from the pressure exerted on their body unless they consciously change position or have assistance in doing so. Even the most conscientious patient with an extensive support group and unlimited financial resources may develop ulceration resulting from a brief lapse in avoidance of the ill effects of pressure.
Two thirds of pressure sores occur in patients older than 70 years. The prevalence rate in nursing homes is estimated to be 17-28%.
Among patients who are neurologically impaired, pressure sores occur with an annual incidence of 5-8%, with lifetime risk estimated to be 25-85%. Moreover, pressure sores are listed as the direct cause of death in 7-8% of all paraplegics.
Patients hospitalized with acute illness have a pressure sore incidence rate of 3-11%. In a study of 658 patients aged 65 years or older who underwent surgery for hip fracture, Baumgarten et al found that 36.1% developed an acquired pressure sore within 32 days after hospital admission.5 (The authors defined an acquired pressure sore as one that arose after hospital admission and had reached stage II or higher.) Although the 32-day period included time spent by patients in rehabilitation facilities and nursing homes, the highest incidence rate for pressure sores occurred during the patients’ acute hospital stays.
Disturbingly, even with current medical and surgical therapies, patients who achieve a healed wound have recurrence rates of as high as 90%.
Many factors contribute to the development of pressure sores, but pressure leading to ischemia is the final common pathway. Tissues are capable of withstanding enormous pressures when brief in duration, but prolonged exposure to pressures slightly above capillary filling pressure initiates a downward spiral towards ulceration.
Impaired mobility is an important contributing factor. Patients who are neurologically impaired, heavily sedated, restrained, or demented are incapable of assuming the responsibility of altering their position to relieve pressure. Moreover, this paralysis leads to muscle and soft-tissue atrophy, decreasing the bulk over which these bony prominences are supported.
Contractures and spasticity often contribute by repeatedly exposing tissues to pressure through flexion of a joint. Contractures rigidly hold a joint in flexion, while spasticity subjects tissues to considerable repeated friction and shear forces.
Sensory loss also contributes to ulceration, by removing one of the most important warning signals, pain.
Paralysis and insensibility also lead to atrophy of the skin with thinning of this protective barrier. The skin becomes more susceptible to minor traumatic forces, such as friction and shear forces, exerted during the moving of a patient. Trauma causing deepithelialization leads to transdermal water loss, creating maceration and adherence of the skin to clothing and bedding, which raises the coefficient of friction for further insult.
Malnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute to vulnerability of tissue and delays in wound healing. Poor nutritional status certainly contributes to the chronicity often observed with these lesions. Anemia indicates poor oxygen-carrying capacity of the blood. Vascular disease also may impair blood flow to the region of ulceration.
Bacterial contamination from improper skin care or urinary or fecal incontinence, while not truly an etiological factor, is an important factor to consider in the treatment of pressure sores and can delay wound healing.
The inciting event for a pressure sore is compression of the tissues by an external force, such as a mattress, wheelchair pad, or bed rail. Other traumatic forces that may be present include shear forces and friction. These forces cause microcirculatory occlusion as pressures rise above capillary filling pressure, resulting in ischemia. Ischemia leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration.
Irreversible changes may occur after as little as 2 hours of uninterrupted pressure.
Clinical presentation of pressure sores can be quite deceiving to the inexperienced observer. Soft tissues, muscle, and skin have a differential resistance to the effects of pressure. Generally, muscle is the least resistant and will necrose prior to skin breakdown. Also, pressure is not equally distributed from the bony surface to the overlying skin. Pressure is greatest at the bony prominence, decreasing gradually towards the periphery. Once a small area of skin breakdown has occurred, one may be viewing only the tip of the iceberg, with a large cavity and extensive undermining of the skin edges.
Many classification systems for staging pressure ulcers have been presented in the literature. The most widely accepted system is that of Shea, which has been modified to represent the present National Pressure Ulcer Advisory Panel classification system. 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. Nor does it imply that healing pressure sores follow a standard regression from stage IV, to stage I, to healed wound. Rather, it is a system designed to describe the depth of a pressure sore at the specific time of examination, in order to facilitate communication among the various disciplines involved in the study and care of such patients.
Stage I represents intact skin with signs of impending ulceration. Initially this would consist of blanchable erythema from reactive hyperemia that 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. This may be the first outward sign of tissue destruction. Finally, the skin may appear white from ischemia.
Stage II represents a partial-thickness loss of skin involving epidermis and possibly dermis. This lesion may present as an abrasion, blister, or superficial ulceration.
Stage III represents a full-thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia. This lesion presents as a crater with or without undermining of adjacent tissue.
Stage IV represents full-thickness loss of skin and subcutaneous tissue and extension into muscle, bone, tendon, or joint capsule. Osteomyelitis with bone destruction, dislocations, or pathologic fractures may be present. Sinus tracts and severe undermining commonly are present.
Other important characteristics of the wound should be noted in addition to depth. One should note the presence or absence of foul odors, wound drainage, eschar, necrotic material, and soilage from urinary or fecal incontinence. This provides information regarding the level of bacterial contamination and the need for dÃ©bridement or diversionary procedures.
The overall state of health, comorbidities, nutritional status, mental status, and smoking history also should be noted. Presence or absence of contractures and spasticity also are important in the formulation of a treatment plan. One should note where the patient normally resides and the extent of his or her support structure. Examining the support surfaces present on the patient’s bed or wheelchair also is important.
The hip and buttock regions account for 67% of all pressure sores, with ischial tuberosity, trochanteric, and sacral locations being most common. The lower extremities account for an additional 25% of all pressure sores, with malleolar, heel, patellar, and pretibial locations being most common.
The remaining 10% or so of pressure sores may occur in any location that experiences long periods of uninterrupted pressure. Nose, chin, forehead, occiput, chest, back, and elbow are among the more common of the infrequent sites for pressure ulceration. No surface of the body can be considered immune to the effects of pressure.
About the Author
Attorney Steven Peck has been practicing law since 1981. A former successful business owner, Mr. Peck initially focused his legal career on business law. Within the first three years, after some colleagues and friend’s parents endured nursing home neglect and elder abuse, he continued his education to begin practicing elder law and nursing home abuse law.