Management of Pressure Ulcers

Cancer can be a devastating illness causing severe debilitation and prolonged confinement to bed. It is, therefore, not unexpected that oncologists would be required to manage pressure ulcers as part of the comprehensive care of their cancer patients. The consequences of these lesions can be devastating, even fatal. Thus, the common bedsore should not be overlooked as an important clinical problem.

Other names assigned to these lesions include decubitus ulcer, skin breakdown, and pressure sore. Recent literature uses the term "pressure ulcer," which clearly indicates the etiology of the lesion. The Agency for Health Care Research and Quality (formerly, the Agency for Healthcare Policy and Research) conducted the most recent comprehensive review of the topic.[1] It defines a pressure ulcer as "any lesion caused by unrelieved pressure resulting in damage of underlying tissue." This usually occurs when tissue is compressed between a bony prominence and an external surface resulting in tissue necrosis.

Assistance with management may be obtained by consulting with colleagues knowledgeable in the field. But finding such physicians may be challenging because interest in this topic is underrepresented and spread across many disciplines, such as rehabilitation medicine, plastic surgery, critical care, family medicine, geriatrics, and palliative care. The field of nursing, however, has been very active in this area of research, and nurse specialists such as enterostomal therapists, who frequently are exposed to these problems, may be better able to provide assistance. Health-care workers in the fields of physiotherapy, occupational therapy, and nutrition science may also be helpful in developing a management plan.

Epidemiology

An estimated 1.5 to 3 million people in the United States suffer from pressure ulcers.[2] Approximately 100,000 of these people are nursing home residents.[3] Among these residents, incidence studies have shown that the longer the patient stays in the nursing home, the greater the likelihood of ulcer development.[4] One study indicated that 13.2% of residents developed an ulcer within 1 year and 21.6% developed an ulcer within 2 years.[3] Prevalence rates in long-term care facilities ranged from 2.4%[5] to 23%.[2,6] Statistics from acute-care facilities are remarkably similar, with incidence rates ranging from 2.7%[7] to 29.5%[8] and prevalence rates from 3.5%[9] to 29.5%.[10]

Individuals at particularly high risk of developing these lesions include elderly patients with femoral fractures (66% incidence)[11] and hospitalized quadriplegic patients (60% prevalence).[12] Among patients in the intensive care units, incidence rates average 33%,[13] and prevalence rates, 21%.[14] The majority of all pressure ulcers (50% to 70%) develop in patients older than age 70 years, thus highlighting the importance of age as a risk factor.[15]

Terminally ill cancer patients are also known to be at risk for this problem. A report from St. Christopher’s Hospice revealed a prevalence of 19% among 7,000 terminally ill patients.[16] Kaasa et al[17] found a higher incidence (33%) on reviewing consecutive patients in a palliative care unit. However, this rate was reduced to 7% after an interdisciplinary wound management committee was created.

Pressure ulcers may lead to lengthy periods of hospitalization.[18] Estimates of the total costs associated with treatment vary greatly. Within the United States, published estimates have ranged from $1.3 billion[19] to an excess of $5 billion[20-22] annually.

Etiology

Central to the development of pressure ulcers is the loss of an essential protective mechanism—that of spontaneous movement. Everyday life requires that we alter our position, shifting our weight while standing or sitting or adjusting our position while lying down, to alleviate the effects of pressure. This occurs consciously and subconsciously in response to the noxious stimulus of unrelieved pressure. (Think of how you squirm in your seat during a long lecture.) When this protective mechanism is impaired through neurologic injury or debility, the damage caused by unrelieved pressure becomes evident.[23] Factors such as pain, spinal cord compression, brain metastases, massive ascites or edema, pathologic fractures, asthenia, and coma may impair this protective mechanism in cancer patients.

The Development of Necrosis

Tissue that becomes trapped between the support surface and a bony prominence may sustain pressure that exceeds normal capillary filling pressure. Once this happens, capillary collapse occurs with the cessation of perfusion.[18,23-25] Normal tissue can tolerate this condition for brief periods, but ischemic damage occurs if pressure is not soon relieved. This process involves tissue hypoxia, acidosis, vessel leakage, hemorrhage, and accumulation of toxic cellular waste.[26] The resulting tissue necrosis can become the focus of a further complicating process, infection. It is often not appreciated that pressure within the tissue is greatest closest to the bony prominence, and this is where necrosis begins. The tissue damage, therefore, occurs first deep in muscle and subcutaneous tissue and then extends outward to the skin, resulting in a cone of tissue destruction that is largest adjacent to the bone (Figure 1).[23,24]

The recently employed term, "skin breakdown," is therefore a misnomer because it may imply that the damage begins at the skin. In reality, skin damage is only the tip of the iceberg,[24] indicating a much larger area of tissue necrosis with extensive undermining below what appear to be normal skin margins. Lesions of this type occur predominantly in the pelvic region related to the bony prominence of the sacrum (23% of ulcers), ischium (24% of ulcers), and greater trochanters (15% of ulcers).[23] Other areas that should be observed for the development of pressure ulcers include the heels, malleoli, fibular heads, knees, elbows, spinous processes, and scapulae.

Extrinsic and Intrinsic Factors

Extrinsic factors that may predispose tissue to injury include friction, maceration, and shear.[2,15] Friction may occur when the patient is accidentally dragged across the bedsheets while being positioned. Shearing occurs by elevating the head of the bed, thus causing the patient to slide downward while the surface of the skin remains in a relatively fixed position.[25] This deforms the vessels in the tissue and impedes profusion. Maceration caused by profuse sweating or urinary and fecal incontinence weakens the skin’s surface. Although these extrinsic factors may occur, it is important to note that unrelieved pressure is the prime contributing factor in the development of significant pressure ulcers.[1,23,24,26]

There are also intrinsic factors that increase the patient’s risk of developing pressure ulcers. These most importantly include conditions that limit spontaneous movement, as previously mentioned, and medical conditions that reduce tissue oxygenation such as peripheral vascular disease, diabetes, anemia, smoking, and dehydration. With age, the skin becomes more susceptible to damage and has a decreased rate of healing. The skin of the elderly has fewer elastic fibers and dermal blood vessels, and a reduced epidermal proliferation rate.[2,27] Poor nutrition is a known intrinsic factor in the development of pressure ulcers.[21,28,29]

Diagnosis of a pressure ulcer is usually uncomplicated. The ulcer develops in a patient who has suffered some loss of the protective mechanism of spontaneous movement and is usually situated over a dependent bony prominence. Differential diagnoses that should be considered include venous, arterial, neuropathic, and neoplastic ulcers as well as radiation injury.