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. 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.
An estimated 1.5 to 3 million people in the United States suffer
from pressure ulcers. Approximately 100,000 of these people are nursing home
residents. Among these residents, incidence studies have shown that the
longer the patient stays in the nursing home, the greater the likelihood of
ulcer development. One study indicated that 13.2% of residents developed an
ulcer within 1 year and 21.6% developed an ulcer within 2 years. Prevalence
rates in long-term care facilities ranged from 2.4% to 23%.[2,6] Statistics
from acute-care facilities are remarkably similar, with incidence rates ranging
from 2.7% to 29.5% and prevalence rates from 3.5% to 29.5%.
Individuals at particularly high risk of developing these
lesions include elderly patients with femoral fractures (66% incidence) and
hospitalized quadriplegic patients (60% prevalence). Among patients in the
intensive care units, incidence rates average 33%, and prevalence rates,
21%. 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
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. Kaasa et al 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. Estimates of the total costs associated with treatment vary
greatly. Within the United States, published estimates have ranged from $1.3
billion to an excess of $5 billion[20-22] annually.
Central to the development of pressure ulcers is the loss of an
essential protective mechanismthat 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. 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. 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, 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). 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. 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
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.
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