The link between tissue oxygen and hydration in nursing home residents with pressure ulcers: Preliminary data

WOUND CARE SECTION EDITOR: Barbara Pieper, PhD, RN, CS, CWOCN, FAAN

The Link Between Tissue Oxygen and Hydration in Nursing Home Residents With Pressure Ulcers: Preliminary Data Nancy A. Stotts, RN, EdD, FAAN, and Harriet W. Hopf, MD

Pressure ulcers are prevalent in nursing home residents. They heal slowly and result in pain and impaired quality of life. Strategies to enhance healing of pressure ulcers are critical to the treatment regime in nursing homes. This article explores the possibility that nursing home residents with pressure ulcers may experience low tissue oxygen and impaired hydration. Pilot data are presented suggesting that some proportion of nursing home residents with pressure ulcers experience low subcutaneous oxygen and that fluid administration increases the low tissue oxygen. Further research in this area is warranted. (J WOCN 2003;30:184-190.)

S Nancy A. Stotts, RN, EdD, FAAN, is Professor of Nursing and John A Hartford 2002-2004 Scholar, Department of Physiological Nursing, University of California–San Francisco. Harriet W. Hopf, MD, is Associate Adjunct Professor and Associate Director of the UCSF Wound Healing Laboratory, Departments of Anesthesia and Perioperative Care, University of California– San Francisco. Reprint requests: Nancy A. Stotts, RN, EdD, FAAN, University of California– San Francisco, School of Nursing, 2 Koret Way, #631, San Francisco, CA 94143-0610. Copyright © 2003 by the Wound, Ostomy and Continence Nurses Society. 1071-5754/2003/ $30.00 + 0 doi:10.1067/mjw.2003. 132

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low healing and significant morbidities are associated with pressure ulcers in nursing home residents.1 Patients with unhealed pressure ulcers experience pain,2 impaired quality of life,3 and in some cases, life-threatening infection.4 These ulcers also are expensive to treat.5 The prevalence of pressure ulcers in residents of nursing homes ranges between 13% and 24%.6,7 This means that at least 1 in 8 nursing home residents, and in some settings 1 in 5 nursing home residents, have a pressure ulcer. Given that there are 1.78 million nursing home beds in the United States today8 and that the number of elderly patients who will require nursing home care is increasing, it is imperative to find costeffective nursing interventions to improve the healing of pressure ulcers. Whereas prevention strategies may mitigate the problem of pressure ulcer development in nursing home residents, many residents are admitted to nursing homes with pressure ulcers, and thus strategies to enhance healing of ulcers are critical to the treatment regime of this population.9 The issue of healing pressure ulcers in this population is not simple. Nursing home residents often have multiple medical problems that complicate the management of their pressure ulcers. In addition, a large percentage of nursing home residents (63% to 78%) have some degree of cognitive impairment.10,11 Approaches to enhance healing need to make use of easyto-use, low-cost interventions that are effective in augmenting healing. Perfusion, long accepted as pivotal to the healing of pressure ulcers, has been accomplished in nursing home residents primarily through removal of external pressure over bony prominences with frequent turning and with the use of special beds.12 It is possible

that we have ignored or undervalued the importance of fluid intake in providing adequate perfusion to pressure ulcers in nursing home residents. Inadequate hydration is a significant clinical issue in nursing home residents.13 In fact, dehydration has been identified as the most frequently occurring fluid and electrolyte problem in nursing home residents.14 Inconsistency in the prescribed daily volume of fluid for residents10,13,14 and a variety of physical and environmental factors contribute to inadequate oral intake.13,15 From a theoretic perspective, a logical link exists between hydration and pressure ulcer healing; that is, those who are underhydrated are underperfused, and healing is impaired in the face of decreased tissue perfusion. A possible mechanism of impaired healing is that nutrients and endogenous growth factors are not able to get to the site of injury to participate in healing and healing is delayed. This article will explore the theoretic basis for the link between hydration and impaired tissue perfusion in nursing home residents with pressure ulcers. Preliminary data linking hydration and tissue perfusion in this population will be presented.

TISSUE PERFUSION AND HEALING OF PRESSURE ULCERS Pressure ulcers are areas of tissue damage that result from unrelieved pressure, usually located over bony prominences.1 Common sites of pressure ulcer formation are the sacrum, heels, ischea, and trochanters. Pressure ulcers occur because externally applied pressure exceeds capillary pressure, producing ischemia and, eventually, cell death.16,17 Data also suggest that reperfusion injury may be implicated in ulcer formation.18 There is agreement that high pres-

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sure over a short period or low pressure over a long period can both result in pressure ulcer formation.15,19 Whereas the rate of healing of pressure ulcers is quite variable, deeper ulcers take longer to heal than do shallow ulcers, and larger ulcers take longer to heal than do smaller ones.20 However, because the ischemia that leads to ulcer formation is initially created primarily by external pressure,17 the focus of pressure ulcer treatment in the past has been on reduction of external pressure, primarily between the bed or wheelchair surface and the tissue over bony prominences.12 Little attention has been paid to internal factors that affect the provision of perfusion to the site of injury, including transport of oxygen, blood volume, and fluid intake. Although external pressure produces tissue damage, even more important factors are internal. Tissue injured by unrelieved pressure is poorly perfused and hypoxic. The wound space lacks blood vessels and the tissue partial pressure of oxygen (pO2) falls as one moves from healthy tissue and perfused capillaries into the largely avascular wound space.1,21 When perfusion is restored either by angiogenesis or relief of vasoconstriction, oxygenation increases. Oxygen is required for critical events in healing, including the capillary endothelial response to angiogenic factors,18 collagen deposition,22 and protection against infection.23 These oxygendependent events are the primary activities that lay down new tissue and lead to the healing of the pressure ulcer. Oxygen and perfusion are intricately linked in the literature, and oxygen often is used as a proxy measure for perfusion. Healing of pressure ulcers requires the development of a new capillary bed, the laying down of collagen in the tissue bed, and ultimately the closure of the skin by contracture and epithelialization.24 When wounds heal, scar tissue fills the tissue defect and collagen is the principal component of scar tissue. Collagen is a group of glycoproteins characterized by 3 peptide chains composed of about equal amounts of glycine, proline, and hydroxyproline. Hydroxylation of proline and glycine requires oxygen and without hydroxylation of proline and glycine to make hydroxyproline, collagen formation ceases and wound healing cannot occur.24 Tissue oxygen begins its journey to injured tissue when oxygen diffuses across the alveoli into the bloodstream. Most of the oxygen attaches to hemoglobin, although a small proportion is dissolved in the blood. Blood flow transports both the bound and dissolved oxygen to the capillary bed. The dissolved oxygen diffuses across the capillary bed into the ulcer site. As the tissues utilize dissolved oxygen, additional oxygen is unloaded from hemoglobin until P50 is reached. At low flow, all possible oxygen is unloaded until tissue oxygen

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is quite low and the hemoglobin reservoir is depleted of oxygen.25 With inadequate hydration, there may be sufficient arterial oxygen but insufficient blood flow to get the oxygen to the site of injury for repair.

HYDRATION/DEHYDRATION IN NURSING HOME RESIDENTS Total body water (TBW) is the volume of fluid within a person. Total body water is the sum of extracellular water (ECW) and intracellular water (ICW).26 ECW includes water in the blood vessels (that is not in cells) and water in the interstitium. ECW is important in the transport of substrates to and from cells. ICW, located within cells, is important in intracellular processes. Overall body composition is important when thinking of fluid balance. It is known that as people age, their fat free mass (FFM) decreases. With the reduction in FFM, there is a proportional increase in ECW and a decrease in ICW.26-29 Some data suggest that a chronic cellular dehydration is present in aged persons and can be explained by the decrease in FFM.28,30 Dehydration results in disruption of intracellular processes. Dehydration can be either extracellular or intracellular. Each is regulated by a separate mechanism, but there are redundant backups in humans that allow for some overlap in function. Extracellular hydration is regulated primarily by blood volume. Changes in blood volume status are sensed by baroreceptors located in the aortic arch. When intravascular volume decreases, there is a sympathetic response that results in vasoconstriction in the subcutaneous bed, the gut, and the renal vasculature. In contrast, intracellular hydration is regulated primarily by changes in osmolality and is sensed centrally by osmoreceptors in the hypothalamus.15 Homeostatic responses of thirst and alterations in salt appetite are associated with both types of dehydration.29 These homeostatic mechanisms and the associated intake of fluids of varying tonicity are modulated by psychological factors and environmental factors.13 In elderly persons, normal compensatory mechanisms, such as thirst, are blunted. Nursing home residents often do not have fluids within reach or lack the ability to independently pick up or hold fluid containers.13 In addition, dehydration often is subtle in this population until it is far advanced, and usual procedures used to diagnose dehydration, for example, orthostatic hypotension, cannot be performed in a considerable proportion of nursing home residents because they lack the ability to stand to have their blood pressure taken.

THE LINK BETWEEN HYDRATION, TISSUE PERFUSION, AND HEALING Data from a series of studies22,31,32 showed that some persons with wounds are underhydrated.

Slow healing and significant morbidities are associated with pressure ulcers in nursing home residents.

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KEY POINTS • Some nursing home residents with pressure ulcers experience low subcutaneous tissue oxygen and underhydration. • The underhydration of some nursing home residents with pressure ulcers is subclinical. • Preliminary data suggest that supplemental fluid will increase tissue oxygen and mitigate underhydration in patients with low subcutaneous tissue oxygen. • Additional attention needs to be given to systemic factors that affect healing of pressure ulcers in nursing home residents. • Timing of fluid administration in underhydrated nursing home residents needs to be researched further.

Nursing home residents often do not have fluids within reach or lack the ability to independently pick up or hold fluid containers.

Early work by Chang and colleagues33 showed that there was a group of postoperative patients whose tissue oxygenation did not rise as expected when they were given supplemental oxygen at increased concentrations (fraction of inspired oxygen [FiO2] 0.5 and 0.7). When intravenous fluid was administered and FiO2 again was increased, tissue oxygenation rose to the expected levels. Of significance is the fact that these patients had no clinical signs of underhydration (i.e., decreased blood pressure, tachycardia, moist skin, and decreased urine output). Chang and colleagues termed this condition “subclinical hypovolemia” and hypothesized that this condition might contribute to the unexplained impaired healing seen in this population. Subsequent work by Jonsson and associates31 examined tissue oxygenation in surgical patients (n = 44) as a measure of the frequency with which surgeons encountered depressed peripheral tissue perfusion postoperatively in the presence of adequate urine output, a classic measure of systemic underperfusion. Perfusion was measured with subcutaneous oxygen levels. Of 30 patients with major abdominal surgeries, 12 were found to be suboptimally perfused; these patients were managed based on clinical criteria. Of those who had peripheral surgery (n = 14), 2 were underperfused. These data indicate that more than 30% of surgical patients in this series were underperfused and that urine output, an often-cited sign of hypovolemia, was not sensitive enough to detect the underperfusion. Jonsson and associates32 went on to examine the relationship between perfusion and collagen deposition in postoperative surgical patients. They examined the relationship between perfusion and collagen deposition on postoperative days 5 and 7. The level of collagen deposition was obtained with ePTFE tubes. They found that collagen deposition was significantly related to perfusion, and no significant correlations were found between collagen deposition and other factors commonly thought to

affect healing including hematocrit, estimated blood loss, length of surgery, smoking, age, weight, gender, or urine output. Building on this work, Hartmann and colleagues22 compared collagen deposition in patients whose postoperative fluid administration was based on tissue oxygenation and a standardcare control group. They found that in both groups a portion of patients were underhydrated postoperatively based on their tissue oxygenation (11/14 in the experimental group; 11/15 in the control group). Supplemental fluid was administered to the experimental group with low subcutaneous tissue oxygenation. Of these 11, 10 responded with increased tissue oxygenation. The next day, only 5 required supplemental fluid. On the third day, only 3 required supplemental fluid. Although fluid administered decreased over time (mean 1.1 L on day 1, 0.7 L on day 2, and 0.3 L on day 3), what is important is that the total volume of fluid was greater, the subcutaneous oxygen was higher, and the collagen deposition was significantly higher on day 7 in the treated group when compared with the control group. Heiner and associates34 used a randomized, 2group, repeated measures study to determine if a modified postoperative fluid replacement protocol in cardiothoracic surgery patients (n = 166) would result in improved tissue oxygen, blood flow, and healing. The treatment group received fluid augmentation during the first 36 postoperative hours while the control group received standard postoperative replacement fluids. Subcutaneous oxygen and temperature were measured at 8, 18, and 36 hours using a tonometer/oxygen electrode system. Hydroxyproline accumulation was evaluated from tissue obtained from subcutaneous expanded polytetrafluoroethylene tubes. Data showed that the treatment groups received a mean of less than 250 mL more fluid than did the control group over the study period. Collagen formation and tissue oxygenation was not different between the 2

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Figure 1. Mean subcutaneous oxygen of subjects who received supplemental fluid on days 1 and 3.

groups. There was a significant negative correlation (P = .01) between higher tissue oxygen values and lower (better) ASEPSIS leg wound scores (measure of risk of infection). More than 80% of the sample had subcutaneous tissue oxygen (PsqO2) values of ≤50 mmHg at each time of measure. Many subjects fell in the range of 30 to 40 mmHg, below what is ideal for control of bacteria and healing. Although the additional fluid in the experimental group did not significantly increase tissue oxygen, data showed that the majority of the sample experienced low tissue oxygenation in the immediate postoperative period. These studies show that a proportion of persons with surgical wounds are underperfused when measured by subcutaneous tissue oxygenation. Provision of fluid modulates tissue oxygenation and collagen formation in some situations. To date, these relationships have not been examined in nursing home residents with chronic wounds such as pressure ulcers.

PRELIMINARY RESEARCH DATA A pilot study was undertaken to determine whether (1) persons with pressure ulcers had low subcutaneous tissue oxygenation and (2) whether low tissue oxygenation could be enhanced with supplemental fluids administered on days 1 and 3.

Methods Sample. The sample was composed of nursing home residents with stage II to IV pressure ulcers with a white blood cell count of at least 2000/mm3 and whose physician believed that the resident’s medical condition would permit the administration of the supplemental fluid. Excluded were res-

idents with carbon dioxide–retaining chronic obstructive pulmonary disease, heart failure, kidney failure, and/or immunosuppressive therapy. Variables and measures. The dependent variable for this study was subcutaneous tissue oxygen. PsqO2 was defined as the amount of oxygen measured within a Silicon catheter implanted subcutaneously. The catheter was inserted in the upper arm using local anesthesia so that 6 cm of the catheter was under the skin. The catheter was filled with hypoxic saline solution, and the PsqO2 equilibrates with the surrounding tissue. A Licox polarographic oxygen probe (GMS, Germany) was inserted within the catheter and used to measure continuously. Temperature also was measured with a probe at the same site in the subcutaneous bed. The Licox probe was calibrated with room air. Accuracy has been documented as within 5% to 10% (P < .001).22 Calibration was rechecked on room air at the end of the measurement. If drift was >10%, findings were considered invalid and not included in the study data. In this study, low tissue oxygen was defined as PsqO2 ≤45 mmHg or <20% rise in PsqO2 to an oxygen challenge with 40% to 60% oxygen by face mask. The independent variable in this study is supplemental fluid. It was defined as 750 mL of fluid provided orally or through an existing nasogastric tube. Procedure. After the study was explained to the resident or legal guardian, written consent was obtained. The upper arm was cleansed with an antiseptic and local anesthetic (1% Lidocaine) was injected. After the local anesthetic was effective, the catheter was inserted subcutaneously under sterile conditions. The catheter was covered with a transparent dressing.

These studies show that a proportion of persons with surgical wounds are underperfused when measured by subcutaneous tissue oxygenation.

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Ultimately it needs to be determined whether supplemental fluid administered reaches the pressure ulcer site and what effect it has on healing.

Figure 2. Subcutaneous oxygen data of individual subjects with low baseline subcutaneous oxygen who received supplemental fluid on days 1 and 3.

Baseline PsqO2 was measured. An oxygen challenge (40% to 60% oxygen by face mask) was performed over a 20-minute period during which oxygen saturation and PsqO2 were monitored. Subjects who had low subcutaneous oxygen were given 750 mL of fluid during a 4-hour period. Lung sounds, heart rate, and blood pressure were monitored during fluid administration. Subjects with low PsqO2 had their PsqO2 measured again 24 hours after the catheter was inserted. Those with normal PsqO2 (>45 mmHg or who had >20% rise in PsqO2 to the oxygen challenge) had the catheter removed immediately after the oxygen challenge. On day 3, 750 mL of fluid was again administered during a 4-hour period to those who with low PsqO2 at baseline. The lungs, heart rate, and blood pressure were monitored. PsqO2 was measured after 24 hours. Throughout the study period, usual nursing care such as turning, intake of the usual diet, and pain control was provided by the facility’s nursing staff to these subjects.

Findings A sample of 8 residents was recruited for this exploratory study. Their mean age was 66.1 years (± 12.6). Three were men and 5 were women. Four were white, 2 were black, 1 was Asian, and 1 was Hispanic. The sample had a total of 15 stage II to IV pressure ulcers. The pressure ulcer distribution in the sample was as follows: 2 residents had 2 stage II ulcers; 1 resident had 1 stage III ulcer; 1 resident had 1 stage III and 1 stage IV ulcer; 1 resident had 2 stage III ulcers; 2 residents had 2 stage III ulcers; and 1 resident had 2 stage IV ulcers. At baseline, 6 of 8 (75%) of the residents had low tissue oxygen (mean 28.3 mmHg ± 8.13). On day 1,

750 mL of fluids were administered to subjects with low tissue oxygen and mean tissue oxygenation rose to 43.8 mmHg ± 28.13. On day 2, no fluids were given. On day 3, mean subcutaneous tissue oxygen was 36.1 ± 16.29. Fluids were given on day 3. Mean subcutaneous tissue oxygen on day 4 was 33.9 mmHg (± 20.14) (Figures 1 and 2). Baseline laboratory work from the low tissue oxygen group showed normal mean red blood cell count (4.3 million/mm3), hemoglobin level (12.28 g/dL), white blood cell count (7250/mm3), and serum osmolality (295 mOm/kg H20). The mean serum albumin was below normal in this sample (2.8 g/dL). None of these residents displayed clinical signs of dehydration, that is, increased heart rate, decreased blood pressure, decreased urinary output, or moist, cool skin.

DISCUSSION Findings show that 6 of 8 subjects in this pilot study had low tissue oxygen at baseline. Fluid was administered to subjects with low tissue oxygen at baseline and resulted in increased tissue oxygen in 5 of 6 subjects. There was a decrease in tissue oxygen in 1 of 6 subjects. No fluid was given on day 2. Tissue oxygen decreased on day 3 in 5 of 6 subjects, and it increased in 1 of 6 subjects. Fluid was given on day 3. On day 4, tissue oxygen decreased in the remaining 4 subjects. Mean data show that tissue oxygen was low at baseline, rose in response to the initial fluid administration, and then gradually decreased—however, never reaching the low mean value seen at baseline. It is clear from these data that a proportion of nursing home residents with pressure ulcers experience tissue hypoxia. Subcutaneous tissue oxygen is a systemic phenomenon. The fact that the oxy-

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gen level rose in response to fluid administration suggests that the problem is a decreased fluid volume or impairment of hydration. These findings are consistent with those of Chang and associates,33 Jonsson and associates,31,32 and Hartmann and associates.22 The decrease in tissue oxygen on day 3 was expected because no supplemental fluid was administered on day 2. However, there was not the increase in tissue oxygen that was anticipated on day 4 to fluids administered on day 3. It is not known whether these findings are a result of changes in the resident’s intake of their usual fluids to compensate for the supervised supplemental fluid, impairment of diffusion capacity of the catheter because of biofilm, or whether fluids changed compartments to compensate for intracellular dehydration.

CONCLUSION Although the sample was small, it appears that the problem of low tissue oxygen is significant in that it was present in 6 of 8 nursing home residents with pressure ulcers enrolled in this pilot study. Tissue oxygen increased in the majority of the subjects given supplemental fluid when measurement was performed 24 hours after the fluid was administered. Administration of fluid on day 3 did not result in enhanced tissue oxygen. These findings raise the question of what the effect would be of daily administration of fluid. Of interest is whether subcutaneous oxygenation could be raised and maintained at normal levels with supplemental fluid. Ultimately it needs to be determined whether supplemental fluid administered reaches the pressure ulcer site and what effect it has on healing. Further study is warranted. REFERENCES 1. National Pressure Ulcer Advisory Panel. Cuddigan J, Ayello EA, Sussman C, editors. Pressure ulcers in America: prevalence, incidence, and implications for the future. Reston (VA): the Panel; 2001. 2. Baharestani MM. The lived experience of wives caring for their frail homebound, elderly husbands with pressure ulcers. Adv Wound Care 1994;7:40-2, 44-6, 50. 3. Franks PJ, Winterberg H, Moffatt CJ. Health-related quality of life and pressure ulceration assessment in patients treated in the community. Wound Repair Regen 2002;10:133-40. 4. Aquilani R, Boschi F, Contardi A, Pistarini C,Achilli MP, Fizzotti G, et al. Energy expenditure and nutritional adequacy of rehabilitation paraplegics with asymptomatic bacteriuria and pressure sores. Spinal Cord 2001;39:437-41. 5. Lyder CH, Shannon R, Empleo-Frazier O, McGeHee D, White C. A comprehensive program to prevent pressure ulcers in long-term care: exploring costs and outcomes. Ostomy Wound Manage 2002;48: 52-62. 6. Bergstrom N, Braden B, Kemp M, Champaign M,

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Ruby E. Predicting pressure ulcer risk: a multisite study of the predictive validity of the Braden scale. Nurs Res 1998;47:261-9. 7. Brandeis GH, Ooi WL, Hossain M, Morris JN, Lipsitz LA. A longitudinal study of risk factors associated with the formation of pressure ulcers in nursing homes. J Am Geriatr Soc 1994;42:388-93. 8. American Association of Retired Persons. Across the states 1998: profiles of long-term care systems (2000 Nov 8). 3rd ed. Available from: URL: www.research.aarp.org 9. Brandeis GH, Morris JN, Nash DJ, Lipsitz LA. The epidemiology and natural history of pressure ulcers in elderly nursing home residents. JAMA 1990;264: 2905-9. 10. Chidester JC, Spangler AA. Fluid intake in the institutionalized elderly. J Am Dietetic Assoc 1997;97:238. 11. Holben DH, Hassell JT, Williams JL, Helle B. Fluid intake compared with established standards and symptoms of dehydration among elderly residents of a long-term-care facility. J Am Dietetic Assoc 1999;99:1447-50. 12. Defloor T. The effect of position and mattress on interface pressure. Appl Nurs Res 2000;13:2-11. 13. Kayser-Jones J, Schell ES, Porter C, Barbaccia JC, Shaw H. Factors contributing to dehydration in nursing homes: inadequate staffing and lack of professional supervision. J Am Geriatr Soc 1999; 47:1187-94. 14. Lavizzo-Mourey R, Johnson J, Stolley P. Risk factors for dehydration among elderly nursing home residents. J Am Geriatr Soc 1988;36:213-8. 15. Kenney WL, Chiu P. Influence of age on thirst and fluid intake. Med Sci Sports Exerc 2001;33:1524-32. 16. Daniel RK, Priest DL, Wheatley DC. Etiologic factors in pressure sores: an experimental model. Arch Phys Med Rehabil 1981;62:492-8. 17. Kosiak M. Etiology and pathology of ischemic ulcers. Arch Phys Med Rehabil 1959;40:62-9. 18. Kourembanas S, Hannon RL, Faller DV. Oxygen tension regulates the expression of platelet-derived growth factor-B chain gene in human endothelial cells. J Clin Invest 1990;86:670-4. 19. Dinsdale SM. Decubitus ulcers in swine: light and electron microscopy study of pathogenesis. Arch Phys Med Rehabil 1973;54:51-6. 20. Bates-Jensen BM. The Pressure Sore Status Tool a few thousand assessments later. Adv Wound Care 1997;10:65-73. 21. Niinikoski J. Effect of oxygen supply on wound healing and formation of experimental granulation tissue. Acta Physiol Scand 1969;334(suppl):1-72. 22. Hartmann M, Jonsson K, Zederfeldt B. Effect of tissue perfusion and oxygenation on accumulation of collagen in healing wounds: randomized study in patients after major abdominal operations. Eur J Surg 1992;158:521-6. 23. Hopf HW, Hunt TK,West JM, Blomquist P, Goodson EH III, Jensen JA, et al. Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg 1997;132:997-1004. 24. Hunt TK, Hopf HW. Wound healing and wound infection: what surgeons and anesthesiologists can do. Surg Clin North Am 1997;77:587-606. 25. Krogh A.The numbers and distribution of capillaries

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KEY POINTS 1) Evidence based practice is the use of current, best evidence when making decisions about the care of individual patients. 2) Identification of current, best evidence is determined by systematic review of all research within a specified time frame; this review focuses on identifying the safety and efficacy of specific interventions or care strategies. 3) Randomized, controlled clinical trials provide the strongest evidence; Quasi-experimental studies or non-experimental studies provide weaker evidence. 4) Expert opinion provides the weakest evidence of safety and efficacy; the process of content validation may be used to ensure that best practice statements truly reflect a consensus of best practice recommendations. 5) The WOCN has adopted a 5 level classification system for evaluating the strength of evidence based on systematic review: Level 1 recommendation is supported by positive results from more than one randomized controlled trial Level 2 recommendation reflects mixed evidence from multiple randomized controlled trials Level 3 is supported by the results of quasi-experimental studies Level 4 indicates the potential for safety and efficacy based on results of case studies or clinical series, and Level 5 is a Best Practice document that has undergone content validation.