prevolence, incidence, and precl ct on of

Prevolence, Incidence, and Precl ct on Pressure Ulcers on a Rehab itation Un t

of

Richard M. Schue, RN, MS, and Diane K. Langemo, PhD, RN

Objective; This retrospective chart review study was conduc ted to determine the prevalence and incidence of pressure ulcers, and the contribution of known risk factors toward the predicted occurrence of pressure ulcers in a long-term rehabilitation setting, Subjects and Setting: A continuous series of 170 adult men with a mean age of 69.2 years were studied during a 1-year period. Methods; Patient charts were reviewed retrospectively for risk factors and documenta- tion of pressure ulcer development by 1 researcher on a data recording form. Results; The pressure ulcer prevalence was 12% and the incidence over the 1-year observation period 6%. Using the odds ratio test, significant risk factors in the sample were identified as hypoalbuminemia (odds ratio = 11:1), low diastolic blood pressure (odds ratio = 4,6:1), stool and urine incontinence (odds ratio = 1.5:1), and peripheral edema (odds ratio = 3,5:1). Conclusion: Specific characteristics in this sample of patients in a long-term rehabilitation center contributed to the increased risk for pressure ulcer development. Risk assessment based on knowledge of specific risk factors, prevention, and eady intervention is crucial to lowering the prevalence and incidence of pressure ulcers in this setting. (J WOCN 1999;26:121-9)

p ressure ulcers (PUs) are a pervas ive p rob lem in heal th care inst i tut ions,

part icularly for older patients and patients who have exper ienced a stroke, spinal cord injury, or other condit ion causing a deficit in mobility. Both the PU incidence and prevalence are expected to rise as the popu la t i on of frail older, immobi le pat ients increases3 Conservat ively, PUs annual ly affect more than 1 million acute care and home pat ients . 2 The economic impac t of pressure ulcers is significant. When PU was the p r i m a r y diagnosis , Miller and Delozier 3 est imated the cost of care at $21,675. When PU was the secondary diagnosis, such as in a patient with a hip fracture, the cost of care was an additional $10,986.

The PU prevalence rate (the number of patients in a given popula t ion with a PU at any given time) has been repor ted between 20% and 80%. 4-6

RELATED LITERATURE The term pressure ulcer has been defined by the Nat ional Pressure Ulcer Adv i so ry

Panel in 1989 as a "localized area of tissue necrosis that tends to develop when soft t issue is compressed be tween a bony prominence and an external surface for a prolonged period of time. ,,2 This definition was endorsed and used by the Agency for Health Care Policy and Research (AHCPR) in their 1992 guidelines. 7

In 1940, Munro concluded that spinal injuries caused autonomic dysref lexia resul t ing in a d is turbance of cutaneous blood flow and increased vulnerabil i ty to skin ulceration. 8 Today most PUs are v i ewed by skil led pract i t ioners as pre- ventable sequelae ins tead of a tolerable complication of a disease or t rauma causing acute immobi l i ty such as a spinal injury. 9 On the basis of this observation, Fields and Hoshiko 9 reported that nursing care has shif ted from an or ientat ion of treatment to one of prevention, identifica- tion of risk factors, and implementat ion of t imely and appropria te interventions. It is genera l ly agreed that p revent ion is the preferred management strategy,7,1°-13 and in fact can "pay for itself. 'm The effectiveness of a prevention program depends on

Richard M, Schue, RN, MS, is Unit Manager, Restorative Care, Veterans Administration Hospital, Fargo, North Dakota.

Diane K. Langemo, PhD, RN, is Professor of Nursing, University of North Dakota, Grand Forks, North Dakota.

Supported in part by the Fargo, North Dakota, Veterans Administration Hospital.

Reprint requests: Richard Schue, RN, MS, 2313 341/2 Ave S, Fargo, hid 58104.

21/I /97577

121

122 Schue and Langemo JWOCN

May 1999

whether contributing factors are identified and eliminated, reduced, or counteracted. Adherence by hea l th care p rov iders to clinical guidel ines an d p rograms for the prevent ion and t rea tment of pat ients at risk for a PU contribute to consistent qual- i ty care. 14 The purpose of this s tudy was to determine the contribution of known risk

factors toward the predicted occurrence of PUs in a rehabilitation setting.

Risk Assessment In an effort to decrease PU incidence,

heal th care facilities have begun us ing tools to assess patient risk for developing pressure ulcers. Clinical guidel ines from

JWOCN Volume 26, Number 3 Schue and Langemo 123

the AHCPR on PU prevention recommend the use of a validated risk assessment tool. 7 These instruments typically include subscales that are based on specific risk factors known to contribute to PU development. Specific instruments recommend- ed for use by the AHCPR panel include the Braden and Norton scales.15,16 In con- junction with these scales, the AHCPR panel strongly advocated preventive strategies and early intervention as essential components of a comprehensive prevention program.

According to Braden and Bergstrom, 15 factors that predispose persons to prolonged and intense pressure have been identified as diminished activity, mobility, and sensory perception. These conditions, when combined with factors that affect tissue tolerance, predispose the individual to PU development. Extrinsic factors that affect tissue tolerance to prolonged exposure to pressure include insults to outer skin layers, such as those caused by exces- sive moisture, friction, and shear. Intrinsic factors that affect tissue tolerance to pressure influence the integrity and load- absorbing capacity of the skin's supporting structures. They include compromised nutrition, advanced age, and low arterio- lar blood pressure. 14,15

PU prevention requires skilled nursing assessment of the skin's integrity and knowledge of risk factors that predispose patients to formation of PU. 17 Norton 16 and Cooney and Reuler 18 have suggested that shearing forces, friction, and moisture, when combined with decreased mobility and incontinence, are the primary risk factors for pressure ulceration. Although a variety of additional variables may contribute to the occurrence of a PU, the magnitude of their contribution is postulated to be smaller than these primary factors.

Pressure The critical determinants of pressure

ulceration are the intensity and duration of pressure and the tolerance of the skin and supporting structures for this condition. 15 PUs arise from prolonged tissue ischemia that occurs when extrinsic forces exceed the tissue capillary pressure necessary to ensure local tissue needs. 19 Landis 2° reported that when extrinsic pressures exceed 32 mm Hg, local capillaries are closed and ischemia occurs. In contrast, Holstein and colleagues 21 reported that skin blood flow did not cease until extrinsic forces acting on the capillaries

exceeded diastolic blood pressure. Later work by Daniel and colleagues 22 on ani- mal models demonstrated that pressures greater than 200 mm Hg applied for longer than 15 hours produced skin breakdown, and pressures of 100 mm Hg for 10 hours caused muscle damage. However, this study involved only a one-time appli- cation of pressure. In contrast, PU may occur after a single episode of prolonged pressure exposure such as that observed during prolonged surgical procedures, but ulceration also may occur after repeated periods of pressure applied over bony prominences. Because normal cellular metabolism depends on an ongoing sup- ply of nutrients and elimination of metabo- lites, any condition that interferes with this exchange will affect the cellular fiznction. A prolonged compromise of capillary blood perfusion, even if it is not sufficient to completely prevent circulation, may lead to cell death and pressure ulceration. 8

Immobility Compromised mobility is i of the oldest

identified risk factors with regard to PU risk. 23-25 In addition to increasing the risk of pressure ulceration, immobility has been associated with a risk of developing larger ulcers. 26 A number of studies have confirmed that chairbound and bedbound individuals are at a significantly greater risk for PU developmentF, 27-29 as are patients with a paralysis. 3°

Sensory Perception A negative relationship exists between

the number of spontaneous movements bedfast and older individuals make and the incidence of PU. 24 The sensation of pressure cues a person to move or to seek assistance to shift the body's position. The inability to feel or recognize discomfort associated with prolonged exposure to pressure increases the risk for PU development. 27

Nutrition Inadequate nutrition is also a factor of

major consequence in PU development. In a study of 634 hospitalized patients, Allman and colleagues 31 found that body weight and serum albumin levels of patients with a PU were significantly lower than in patients without a PU. Two other studies reported nutrition to be the most significant factor in the development of a PU. 29,32 Recent studies have examined the role of nutrition during the acute

1 2 4 S c h u e a n d L a n g e m o

J W O C N M a y 1 9 9 9

C o d e # Age _ _ Adm. Date

Adm, Dx: Co-exist ing Dx.

(2)

1. Ht: Wt: Ideal Wt:

2, BP (diastol ic < 60)

3. Albumin (<3.5)

4, Incont inence: Urine

Edema p l e u r a l

5. Oral steroid the rapy

6, Adm. Braden Score (BS): __ A. Sensory percep t ion _ _

B. Moisture _ _ C. Act iv i ty _ _ D. Mobi l i ty _ _

E. Nutrition _ _ E Friction & s h e a r _ _

7. PU+ _ _ Date occur red _ _ Locat ion Stage _ _

BS A B C D E

Hgb:

_ _ Feces _ _ Peripheral edema: _ _

Current smoker _ _ Smoking Hx: _ _

Date healed: BS A B C D E F

8. PU+ _ _ Da te occur red _ _ Locat ion _ _ Stage _ _

BS A B C D E F Date healed: BS A

Figure I . D a t a r e c o r d i n g f o r m .

B C D E F

and convalescent phases of illness. 19,33 Pinchofsky-Devin and Kaminski 34 showed that well-nourished patients in nursing homes did not develop PU. In a later study, 35 they also noted a strong correlation between the severity of malnutrition and the severity of PU. Supplementing the intake of protein, calories, vitamin C, and zinc has been advocated for the prevention and management of PU. 35-37

Excess Skin Moisture]Incontinence

Conflicting data exist concerning the magni tude of risk when the skin is exposed to moisture in the form of perspi- ration, urine, or feces. The Braden Scale, for example, requires the assessment of the degree to which skin is exposed to moisture based on the hypothesis that maceration increases the risk of pressure ulceration. 27 In addition, Norton, 16 Blom, 38 and Towey and Erland 39 also report that incontinence of urine or feces is a significant risk factor in PU development. In contrast, others have suggested that fecal incontinence is a major risk factor for pressure ulceration, but urinary incontinence is not. 29,31 Shannon 40 has postulated that both shearing force and friction are increased in the presence of moisture, and this may lead to an increased risk of ulceration.

Friction and Shear Friction and shear are mechanical forces

that, when combined, may contribute to PU formation. Shear refers to a mechanical force that acts on an area of skin in a direc-

tion parallel to the surface of the body. 7 Friction is the mechanical force that occurs when skin is dragged across a coarse surface such as bed linen. 7 The Braden Scale refers to this in terms of the patient's abil- ity to assist with movement or be moved in such a way that the skin is free of con- tact with the surface of the linen or bed- ding during movement. 27 The importance of shearing force as a factor in the development of PU has been suppor ted by Bennett and Lee, 41 who found that when a high level of shear is present, the pressure necessary to produce vascular occlusion falls to half the amount needed when shear is not present. Friction or epidermal stripping and shearing or stretching of blood vessels compound the ischemic changes produced by external pressure, thereby increasing tissue breakdown3 9

Secondary Risk Factors Braden and Bergstrom 14 addressed

aging as a factor in pressure ulcer risk. Age influences the integrity and load- absorbing capacity of the skin and sub- cutaneous support ing structures. Age- related in tegumentary changes include thinning of the dermis, flattening of the dermal-epidermal junction, atrophy of skeletal muscle and sweat glands, decreased tissue water content, and a reduc- tion in epidermal cell growth and divi- sion. 42 Edema also acts as a secondary risk factor because it increases the distance from the capillary to the cell and thereby reduces the rate of diffusion of oxygen and nutrients to local tissues. 19,43

A low diastolic blood pressure (<60 m m Hg) also may increase the risk of pressure ulceration. 44 Bergstrom and colleagues 27 reported a significant association between diastolic blood pressure and PU development, a l though another s tudy found no significant difference when comparing admission diastolic and systolic blood pressures among patients with and without PU. 30 Additional secondary risk factors include cigarette smoking45, 46 and the administration of exogenous steroids. 47

METHODS

Sample and Setting This retrospective study was conducted

at a 174-bed Veterans Administrat ion Hospital in the north central part of the United States. The agency had implement- ed a standard procedure for assessment of

JWOCN Vo lume 26, N u m b e r 3

all patients within 24 hours of admission for PU p re sence / absence and PU risk assessment us ing the Braden Scale. The research popula t ion comprised a consecu- tive series of adul t males who were hospitalized on a 50-bed chronic rehabili tation unit dur ing a 1-year period. One hundred ninety patients were admit ted dur ing the s tudy period, and 170 (89%) charts were reviewed and included in the study. The other 20 charts were unavailable because of t ransfers to other facilities. Subjects ranged in age from 35 to 99 years (mean = 69.2 years, SD = 10.9). The pr imary admit- t ing d iagnoses inc luded cancer (41%), cerebrovascular accident (CVA, 40%), pe r iphe ra l vascular d isease (17%), and bone fractures (13%).

Instruments Pat ient charts were ob ta ined by our

Medical Records Depa r tmen t and were reviewed by i researcher using a data col- lection form des igned for this s tudy (Figure 1). Demographic data were collect- ed, as well as data related to known PU risk factors, which were rout inely documented on admiss ion and weekly there- after until the patient was discharged. The data recording form was reviewed by an expert panel for face and content validity. This panel compr i sed a WOC nurse, a nurse researcher with expertise in w o u n d care, and a unit registered nurse. It was pilot-tested on 5 charts and revisions were completed as indicated. Approva l for the conduct of this research was obta ined from our institutional review board.

RESULTS Descr ipt ive statist ics and odds rat ios

were used to determine the contr ibution of specific risk factors in the predict ion of pressure u lcera t ion wi th in this sample populat ion. Table 1 depicts the stages of PU that developed by body site. The most common PU stage was II, which account- ed for 57% of the ulcers. Another 24% were stage I ulcers, 15% were stage III, and 4% were stage IV. Nine ty percent of PU were located on 2 body sites, the sacral area (46%) and heel (44%). Near ly all of these wounds were stage I or II PUs. The pr imary admit t ing diagnoses for PU-negative subjects were CVA (27%), cancer (15%), and bone fracture (13%). For the subjects wi th a PU, the admi t t ing diagnoses were cancer (26%), per iphera l vascular disease (17%), and CVA (13%). Data

Schue and L a n g e m o 125

I 6 4 0 1 11 24 II 11 12 2 1 26 57

III 3 3 0 1 7 15

IV 1 1 0 0 2 4

Site n = 21 n = 20 n = 2 n = 3 n = 46 100

to ta l

% o f site 46 44 4 6

were not available for location of PU on body by diagnosis. In addit ion, 4% of the PUs were located on the elbow (all were stage II) and 6% were observed on the hip area (varying from stages I to III). To ana- lyze risk factors for pressure ulcerations, all pressure ulcers were combined.

Primary Risk Factors Using mul t ip le regression analysis

inclusive of all 170 cases in this study, risk factors included in the Braden Scale (activity, mobility, sensory perception, moisture, nutrition, fr ict ion/shear) with a P value > .05 were el iminated 1 at a time. Activi ty was el iminated initially (r = 0.11, P = .75); followed by sensory perception (r = 0.29, P = .48) and mobi l i ty (r = -0.45, P = .22). However , mois ture (r = 0.64, P = .028), nut r i t ion (r = -0.63, P = .01), and fric- t ion /shear (r = -1.54, P = .001) emerged as significant predictors of PU development in this sample.

Odds Ratios for Secondary Pressure Ulcer Risk Factors

Aging. Within our sample, the subjects' ages ranged from 35 to 99 years (mean = 69.2 years, SD = 10.9). The mean age for subjects wi th a pressure ulcer was 71.3 years (SD = 9.2), whereas those without a pressure ulcer averaged 69.1 years (SD -- 11.5). There were no significant differences with respect to age when comparing subjects wi th and without a PU.

Edema. The diagnosis of edema was based on documenta t ion of edema on chart during hospitalization. Chart review revealed that 6% (n = 10) had pu lmonary edema, representing 3% (n = 4) of the PU- negative subjects (mean = 0.03, SD = 0.17), and 13% (n = 6) of the PU-positive cases (M = 0.13, SD = .34). Odds ratio analysis revealed that pat ients wi th p u l m o n a r y edema were 4.5 times more likely to experience a PU than were those without this condit ion (Table 2).

Table 1. S t a g e o f PU r e l a t e d t o si te o f d e v e l o p m e n t a n d h e a l i n g t i m e

Sacral Heel S tage % of Stage a r e a a r e a Elbow Hip total Stage


May 1999

Table 2. Risk factors of PU-negat ive a n d PU-positive cases

PU- negative

PU- positive

Factor Value n % n %

95% CI

Odds Lower Upper ratio limit limit

Albumin (n = 136) ->3,5 62

<3.5 33 Diastolic blood pressure (n = 170) ->60 105

<60 19

Tobacco use (n = 149) Yes 38 No 70

Tobacco history (n = 123) Yes 76 Never 12

Steroids (n = 169) Yes 13

No 110

Incontinent urine (n = 170) Yes 31

No 93

Incontinent stool (n = 170) Yes 19

No 105

Peripheral edema (n = 170) Yes 21 No 103

Pulmonary edema (n = 170) Yes 4 No 120

<IBW by 10+ Ib (n = 168) Yes 39 No 85

>IBW by 10+ Ib (n = 168) Yes 49

No 75

65 6 15 10.96 4.18 28,42

35 35 85

85 25 54 4.64 2,15 9.82 15 21 46

35 10 24 0,59 0,26 1.33 65 31 76

86 28 80 0,62 0.22 1.73

14 7 20

11 4 9 0.80 0.25 2,59

89 42 91

25 15 33 1.45 0.67 2.93

75 31 67

15 10 22 1,53 0,64 3.52

85 36 78

17 19 41 3.45 1,60 7,20 83 27 59

3 6 13 4.50 1.21 16,76 97 40 87

32 21 48 1,98 0.94 3,83

68 23 52

40 16 36 0,87 2.11 8,75

60 28 64

Peripheral edema was present in 24% of subjects (n = 40), representing 17% (n = 21) of PU-negative subjects and 41% (n = 19) of the PU-positive subjects. Odds ratio analysis revealed that subjects with peripheral edema were 3.4 times more likely to experience a PU when compared

w i t h persons without this condition. H y p o t e n s i o n (diastol ic b lood pres-

sure). The documented diastolic blood pressures from the 170 subjects in this s tudy ranged from 40 to 112 m m Hg (mean = 70 m m Hg, SD = 12). Subjects were categorized as having low diastolic blood pressure if any of their charted values were <60 m m Hg during their hospital course. The diastolic blood pressure remained > 60 m m Hg in 130 subjects (76.5%), and values < 60 m m Hg were noted in 40 subjects (23.5%). Diastolic blood pressure readings for the 124 PU- negative subjects ranged from 40 to 112 m m Hg (mean = 72.2 m m Hg, SD = 11.3), of which 85% (n = 105) were >60 m m Hg and 15% (n = 19) were <60 m m Hg. Diastolic readings for the 46 PU-positive subjects ranged from 40 to 92 m m Hg (mean = 64.8 m m Hg, SD = 12.6), of which 54% (n = 25) were ->60 m m Hg and 46% (n

= 21) were <60 m m Hg. Analysis using the odds ratio test revealed that persons with a diastolic blood pressure <60 m m Hg were 4.6 times more likely to experience a PU compared with those with values con- sistently greater than 60 m m Hg (Table 2).

Tobacco use. Data concerning smoking could be obtained from 149 subject records. Within this group, 32% were described as active smokers, and 68% were described as nonsmokers. Smokers represented 35% (n = 38) of the cases in the PU-negative group, and 24% (n -- 10) of the PU-positive group. Information concerning smoking history was available from 123 records. Among this group, 85% (n = 104) had smoked but quit smoking before admission and 15% (n = 19) had never smoked. Ex-smokers represented 86% of the PU-negative cases and 80% (n = 28) of the PU-positive cases. Analysis using the odds ratio test demonstrated that being an active smoker or having a history of smoking did not increase the likelihood of experiencing a PU.

Steroid use. Data from 169 subjects documented that 10% (n = 17) were given oral steroidal agents during their hospital course. Steroid use was documented in

JWOCN Volume 26, Number 3 Schue and Langemo 127

11% of PU-negative cases, and 9% (n = 4) of PU-positive cases. The odds ratio was 0.80, or less than equal for a steroid user to experience a PU compared with patients who were not given steroids during their hospital course (Table 2).

Nutr i t ion. The Hamwi method was used to judge ideal body weight (IBW). 46 Thirty-six percent of subjects (n = 60) were more than 10 pounds below their IBW and 39% (n = 65) were more than 10 pounds above their IBW. The group without a PU had recorded weights ranging from 88 to 517 pounds (mean = 171.8 pounds, SD = 47.6) and the group with a PU from 105 to 296 pounds (mean = 167, SD -- 45.7).

In the less than IBW group, 32% (n = 39) did not have a PU, and 48% (n = 21) had a PU. It was 1.9 times more likely that a patient who was less than IBW would experience a PU than all other patients. Of those subjects with greater than IBW, 40% (n = 49) had no PU and 36% (n = 16) had a PU. Obesity did not increase the likelihood of experiencing a PU during the observation period.

In addition to evaluating body weight, nutrition was assessed by calculating the mean of all recorded serum albumin levels for each subject. Serum albumin levels were available for 136 subjects. These values ranged from 1.7 to 4.5 g / d L including 50% (n = 68) whose mean value was < 3.5 g /dL.

The mean albumin levels for the 95 subjects without a PU ranged from 2.5 to 4.5 g /dL; 65% (n = 62) were > 3.5 g / d L and 35% (n = 33) were < 3.5 g /dL. Albumin levels for the 41 subjects with a PU ranged from 1.7 to 4.4 g /dL; 15% (n = 6) were >_ 3.5 g / d L and 85% (n -- 35) were < 3.5 g /dL. Thus subjects with a low serum albumin were 10.9 times more likely to experience a PU compared with those with a higher mean albumin level (Table 2).

Incontinence. Subjects were considered incontinent if urine or fecal leakage was documented on their charts at any point during their hospital course. Data from 170 records revealed urinary incontinence in 46 subjects (27%). Twenty-five percent of subjects wi thout a PU had urinary incontinence (n = 31), and 33% (n = 15) of those with a PU had incontinence. Urinary incontinence increased the likelihood of pressure ulceration by a ratio of 1.4:1 compared with subjects who were continent of urine. Fecal incontinence occurred in 29 subjects (17%), representing 15% (n = 19) of subjects without a PU and 22% (n = 10)

of those with a PU. Subjects with fecal incontinence were approximately 1.5 times more likely to experience a PU compared with subjects who maintained bowel continence.

DISCUSSION The 12% prevalence rate for PU on this

rehabilitation unit falls within the range of other skilled care settings that reported prevalence ranges varying from 2.4% to 23% 49 and prevalence rates in hospital that vary from 3.5% to 29.5%. 49,50 The 6% incidence also falls within the ranges reported in other skilled care settings that vary from 2.4% to 23% 1 and that reported by hospitals varying from 2.7% to 29.5%.2, 51 The low incidence could be attributed to the interdisciplinary team approach of early and frequent assessment and intervention, as well as prevention practices. The unit used a preventive and practice approach to PU management , and any patient considered at risk for ulceration was placed on a pressure-reducing mat- tress. Distribution of the 46 PU according to stage and site were similar to Meehan's 1994 national PU prevalence survey. 52 The sacral and heel areas dominated, equaling 90% of total PU.

Although some relationships between commonly identified risk factors for PU development were observed in this study, other factors were not found to carry the same risk in this rehabilitation setting when compared with those reported in other settings. Activity, mobility, and sensory perception were not found to predict PU development, and this observation is consistent with the findings of Salzberg and associates. 30 In addition, a smoking history, administration of steroids, and body weight greater than 10 pounds over IBW failed to reach statistical significance when patients with and without pressure ulcerations during the 1-year observation period were compared. However, our findings do suggest that hypoalbuminemia, low diastolic blood pressure, incontinence of urine and stool, pulmonary and peripheral edema, and total body weight more than 10 pounds below IBW may help to identify patients at greatest risk for PU development in the rehabilitation setting. In addition, al though fecal and urinary incontinence is frequently associated with PU development,38, 40 only a minor effect was demonstrated in this setting. The rel- atively small magnitude of this effect may be attributable to attentive nursing care


May 1999

and the use of containment devices that minimized exposure to stool and urine.

The findings of this study suggest that certain characteristics can be identified which, in combination, allow identifica- tion of patients at significant risk for PU when cared for in a rehabilitation setting. This patient would be aged 70 years or older, and have multiple medical problems, especially cancer, peripheral vascular disease, or CVA. This person's nutritional level would be compromised, as reflected by an albumin level < 3.5 g /dL and a total body weight at least 10 pounds below IBW. The at-risk patient is also likely to experience a diastolic BP less than 60 mm Hg, as well as problems with peripheral or pulmonary edema. This individual is also likely to experience incontinence of stool sometime during this admission. Considered collectively, the data generat- ed from this study indicate that, along with the Braden Scale, other risk factors must be considered when assessing PU risk in the rehabilitation setting.

Recommendations This study was limited by an all-male

sample, incomplete data for some risk factors, and by its reliance on retrospective chart review. Although much has been accomplished, additional research is needed to better understand the complex processes that underlie PU development, and how to best assess this risk and prevent the occurrence of PU. Studies reported to date have some consistencies that can help to guide clinical practice, assess a risk factor's contribution, and determine the Braden Scale's usefulness in varying clinical settings.

PU risk assessment and prevention interventions are effective. Preventive measures must include the patient, family, and the interdisciplinary team responsible for the care.7, 53 All team members must be kept aware and informed regarding both documented and hypothesized risk factors that may predispose a patient to a PU. In addition, all caregivers must be taught to recognize early skin changes indicative of breakdown and prevention measures that can be instituted to prevent ulceration. Because of the critical time-pressure relationship associated with pressure ulceration, it is essential that assessment of PU risk be completed at the time of admission and whenever changes in a patient's status justify reevaluation. However, it is also important to acknowledge that any

PU risk assessment and prediction instru- ment may not adapt readily to all clinical settings. This limitation may be attributed to variability in underlying diseases, rou- tine activity schedules in a specific setting, medications, and other treatment variables. Norton 16 acknowledges this limitation when she states that "No scale, however sophisticated, can be more than an indicator of risk." Therefore further research is needed to refine PU risk instruments, making them more applicable to patients cared for in various settings.

Because this study was conducted in a rehabilitation setting of a Veterans Ad- ministration Hospital in an all-male popu- lation, only limited generalizations to other health care facilities can be made. Future research should be directed toward replication of this study in a variety of other settings. Extending the study in a Veterans Administration setting would also provide for a larger sample, as well as a longitudinal approach for identifying contributing variables that lead to development of a PU. The contribution of PU prevention and early intervention to con- taining costs and reducing human suffer- ing is also of paramount importance.

REFERENCES 1. Langemo DK, OIson B, Hunter S, Hanson D, Burd C, Cathcart-Silberberg T. Incidence and prediction of pressure ulcers in five patient care seflings. Decubitus 1991 ;3:25-6. 2. National Pressure Ulcer Advisory Panel. Pressure ulcer prevalence, cost and risk assessment: Consensus Development Conference statement. Decubitus 1989;2:24-8. 3. Miller H, Delozier J. Cost implications of the pressure ulcer treatment guideline. Columbia (MD): Center for Health Policy Studies (Contract No. 282- 91-0070); 1994. 4. Hunter S, Cathcart-Silberberg T, Langemo DK, Olson B, Hanson D, Burd C, et al. Pressure ulcer prevalence and incidence in a rehabilitation hospital. J Rehabil Nurs 1992;5:239-42. 5. Richardson RR, Meyer PR. Prevalence and incidence of pressure sores in acute spinal cord injuries. Paraplegia 1981 ;4;235-247. 6. Young JS, Burns PE, Bowen AM, McCutchen R. Spinal cord injury statistics: experience of the regional spinal cord injury system. Phoenix (AZ): Good Samaritan Medical Center; 1982. 7. Agency for Health Care Policy and Research. Pressure ulcers in adults: prediction and prevention (Clinical Practice Guideline No. 3, AHCPR Pub. No. 92-0047). Rockville (MD): US Department of Health and Human Services; 1992. 8. Torrance C. The aetiology, prevention and treatment of pressure sores. Edinburgh: Croom Helm; 1984.

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9. Fields LD, Hoshiko RR. Clinical validation of Braden and Bergstrom's conceptual schema of pressure sore risk factors. Rehabil Nurs 1989; 14:257-60. 10. Linder RM, Upton J. The prevention of pressure sores. Surgical Rounds 1983;6:42-55. 11. Xakellis GC, Frantz RA, Lewis A, Harvey R Cost- effectiveness of an intensive pressure ulcer prevention protocol in long-term care. Adv Wnd Care; 1998; 11:22-9. 12. Baldwin KM, Ziegler SM. Pressure ulcer risk fol- lowing critical traumatic injury. Adv Wnd Care 1998; 11 : 168-73. 13. Hibbs P. The economics of pressure ulcer prevention. Decubitus 1988; 1:32-8. 14. Braden B, Bergstrom N. Clinical utility of the Braden Scale for predicting pressure sore risk. Decubitus 1989;2:44-51. 15. Braden B, Bergstrom N. A conceptual schema for the study of the et iology of pressure sores. Rehabil Nurs 1987;12:8-12, 16. 16. Norton D. Calculating the risk: reflections on the Norton Scale. Decubitus 1989;2:24-31. 17. Gosnell DJ. Assessment and evaluation of pressure sores. Nurs Clin North Am 1987;22: 399-415. 18. Cooney TG, Reuler JB. Pressure sores. West J Med 1984;140:622-4. 19. Kosiak M. Prevention and rehabil itation of pressure ulcers. Decubitus 1991;4:60-68. 20. Landis K. Studies of capil lary blood pressure in the human skin. Heart 1930;15:209-28. 21. Holstein P, Nielsen PE, Barras J. Blood flow cessation at external pressure in skin of normal human limbs: photoelectr ic recordings compared to isotope washout and to local intraarter- ial blood pressure. Microvasc Res 1979;17:71-9. 22. Daniel K, Priest DL, Wheatley DC. Etiologic factors in pressure sores: an experimental model. Arch Phys Med Rehabi11981;62:492-8. 23. Clay E. Operation pressure sore. Nursing Times 1968;68:393-4. 24. Exton-Smith AN, Sherwin MA. The prevention of pressure sores: a signif icance of spontaneous bodily movements. Lancet 1961 ;2:1124-6. 25. Rudd TN. Pathogenesis of decubitus ulcers. J Am Geriatr Soc 1962; 10:48-53, 26. Abildgaard AU, Daugaard K. Pressure sores: a study on prevalence. Ugeskr Laeger 1979;141: 3147-51. 27. Bergstrom N, Braden B, Laguzza A, Holman V. The Braden Scale for predicting pressure sore risk. Nurs Res 1987;36:205-10. 28. Berlowitz DR, Wilking SV. Risk factors for pressure sores: a comparison of cross-sectional and cohort-derived data. J Am Geriatr Soc 1989;37: 1043-50. 29. Maklebust J, Bruckhorst L, Cracehiolo- Caraway A, DuCharme MA, Dundon R, Panfilli R, et al. Pressure ulcer incidence in high risk patients managed on a special three-layered air cushion. Decubitus 1988; 1:20-30. 30. Salzberg CA, Byrne DW, Cayten CG, Kabir R, van Niewerburgh P, Viehbeck M, et al. Predicting and preventing pressure ulcers in adults with paralysis. Adv Wnd Care 1998; 11:237-46. 31. AIIman RM, Laprade CA, Noel LB, Walker JM,

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