Pressure ulcers are the visible evidence of pathologic changes in the blood supply to dermal tissues. The chief cause is attributed to pressure, or force per unit area, applied to susceptible tissues. However, external pressure or shear force is increasingly viewed as a necessary but insufficient cause for pressure ulcers. In patients exposed to the same pressure load and duration of surgery, individual intrinsic factors appear to play a larger role in development of a pressure ulcer than the tissue interface pressure. Intrinsic factors leading to derangement in tissue perfusion may account for the development of a pressure ulcer, despite the provision of common prevention measures that include pressure reduction. These factors are beginning to be identified but more research is needed.
DR. Does pressure cause pressure ulcers? An inquiry into the etiology of pressure ulcers. J Am Med Dir Assoc
Therapy for pressure ulcers is generally empiric, based on anecdotal experience, or borrowed from the treatment of patients with acute wounds. It is problematic because of multiple comorbidities, chronic duration of pressure ulcers, and, frequently, the physician's relative unfamiliarity with options.
Recognition of risk, relief of pressure, and optimizing nutritional status are components of both prevention and management guidelines. For persons with identified pressure ulcers, assessing the wound and implementing strategies for local wound care are paramount.
DR. Issues and dilemmas in the prevention and treatment of pressure ulcers: a review. J Gerontol A Biol Sci Med Sci
DR. Prevention and management of pressure ulcers. Rev Clin Gerontol. 2008;17:1-–17.
DR. Prevention and treatment of pressure ulcers: what works? What doesn't? Cleve Clin J Med
. 2001;68(8):704-–707, 710-–714, 717-–722.CrossRef
The primary source of pressure ulcers appears to be the acute hospital. Among patients who experience pressure ulcers, 57% to 60% do so in the acute hospital. Incidence in hospitalized patients ranges from 3% to 30%; common estimates range from 9% to 13%. A randomized national sample of Medicare beneficiaries estimated a 4.5% incidence of a new hospital-acquired pressure ulcer from 2006 thru 2007. The incidence differs by hospital location; ICU patients and orthopedic patients are at greatest risk. In patients with a hip fracture, 15% develop a pressure ulcer during hospital admission, and one-third develop a pressure ulcer in 1 month. Pressure ulcers develop early in the course of hospitalization, usually within the first week. The incidence of pressure ulcers in nursing homes is difficult to quantitate.
After discharge from the hospital, pressure ulcers remain a major problem in community care settings. Characteristics associated with pressure ulcers include recent institutional discharge, functional impairment, incontinence, and having had a previous ulcer.
Risk Assessment & Risk Factors
In theory, persons who are at high risk for pressure ulcers can be identified, and an increased effort can be directed to preventing ulcers. The classical risk assessment scale is the Norton Score, developed in 1962 and still widely used. Patients are classified using 5 risk factors graded from 1–4. Scores range from 5–20; higher scores indicate lower risk. The generally accepted at-risk score is ≤14; patients with scores <12 are at particularly high risk.
A commonly used risk assessment instrument in the United States is the Braden Scale. This instrument assesses 6 items: sensory perception, moisture exposure, physical activity, mobility, nutrition, and friction/shear force. Each item is ranked from 1 (least favorable) to 3 or 4 (most favorable), with a maximal total score of 23. A score of ≤16 indicates a high risk.
Both the Norton Score and the Braden Scale have good sensitivity (73% to 92% and 83% to 100%, respectively) and specificity (61% to 94% and 64% to 77%, respectively), but poor positive predictive value (approximately 37% at a pressure ulcer incidence of 20%). In populations with a lower incidence of pressure ulcers, such as those in nursing homes, the same sensitivity and specificity produce a positive predictive value of 2%. The net effect of poor positive predictive value means that many patients who will not develop pressure ulcers will receive expensive and unnecessary treatment.
In clinical practice, risk assessment is problematic. A systematic review of 33 clinical trials of risk assessment found no decrease in pressure ulcer incidence that could be attributed to the use of an assessment scale. In long-term care settings, a Braden score had no predictive value for the development of a pressure ulcer.
Because most pressure ulcers develop in the acute hospital, risk assessment in this setting is particularly important. In an ICU, 5 factors contribute to the risk of pressure ulcer after adjusting for 18 univariately significant risk factors: norepinephrine infusion, Acute Physiology and Chronic Health Evaluation (APACHE) II score, fecal incontinence, anemia, and length of stay in the ICU. Independent risk factors for the development of a pressure ulcer after admission to a surgical service include emergency admission (which increased the risk 36-fold), age, days in bed, and days without nutrition.
Risk factors for the prevalence of pressure ulcers at admission include the presence of a fracture (increasing the risk 5-fold), fecal incontinence (increasing the risk 3-fold), and decreased serum albumin level (increasing the risk 3-fold). Applied prospectively to at-risk patients without pressure ulcers, these factors were associated with development of a pressure ulcer.
In functionally limited (bed- or chair-confined) hospitalized patients, 9 factors were associated with the development of pressure ulcers, including nonblanchable erythema (increasing the risk 7-fold), lymphopenia (increasing the risk almost 5-fold), and immobility, dry skin, and decreased body weight (each of which increase the risk 2-fold).
Not surprisingly, risk factors in long-term care populations differ. In this population, the factors associated with development of pressure ulcers are facility dependent. In low-risk nursing homes, difficulty in ambulation, difficulty feeding oneself, and male gender were associated with a 2- to 4-fold risk of pressure ulcer. In high-risk nursing homes, difficulty with ambulation, fecal incontinence, difficulty feeding oneself, and diabetes mellitus predicted pressure ulcer development.
The risk of pressure ulcer may include a history of cerebrovascular accident (5-fold increase), bed or chair confinement (3.8-fold increase), and impaired nutritional intake (2.8-fold increase). In data derived from the Minimal Data Set, logistic regression analysis determined that dependence in transfer or mobility, confinement to bed, history of diabetes mellitus, and a history of pressure ulcer were significantly associated with an existing stages II–IV pressure ulcer.
In community-dwelling persons age 55–75 years, the presence of a pressure ulcer was predicted by self-assessed poor health, current smoking, dry or scaly skin on examination, and decreased activity level.
The importance of these epidemiologic risk predictors lies in understanding which factors are amenable to correction. Risk factor predictors from various sites suggest that immobility, dry skin, and nutritional factors are potentially modifiable. Efforts have centered on correction of these problems.