Contribution of Skin Temperature Regularity to the Risk of Developing Pressure Ulcers in Nursing Facility Residents Mary Pat Rapp, PhD, RN; Nancy Bergstrom, PhD, RN, FAAN; and Nikhil S. Padhye, PhD INTRODUCTION Pressure ulcers (PrUs) are caused primarily by exposure to pres- sure and modified by tissue tolerance to pressure. 1,2 Intensity and duration 2 of external pressure applied to tissue increase the risk of PrUs by interrupting blood flow, which in turn causes tissue damage. 3–6 Inactivity while out of bed and immobility in bed are the primary sources of external exposure to pressure in nursing facility (NF) residents. 2 A conceptual schema for PrU etiology 2 expanded Kosiak’s pressure, time, and intensity model 4 to include tissue tolerance to pressure. Tissue tolerance, which is closely related to blood flow, is the ability of the tissue to withstand pressure. In the Braden and Bergstrom 1 schema, tissue tolerance to pressure is affected by both extrinsic and intrinsic factors. Extrinsic factors include moisture, friction, and shear. Intrinsic factors include undernutrition, advanced age, decreased arteriolar pressure, and other hypothetical factors, including interstitial fluid flow, emotional stress, smoking, and skin temperature. 2 The Braden Scale for Pressure Sore Risk operationalizes the Braden and Bergstrom 1 schema by assigning a score (from 6 to 23) and level of risk to a set of risk factors potentially amenable to nursing interventions, including sensory perception, mobil- ity, activity, nutrition, moisture, and friction/shear. 7 Following adequate initial training, the Braden Scale presents minimal burden for nurses as it takes approximately 1 to 2 minutes to perform and has no known risks for patients. The purpose of the study was to determine whether charac- terizing skin temperature regulation as a functional property of the skin as it relates to tissue tolerance improves the clinician’s understanding of PrU risk prediction. In PrU research, skin tem- perature has been used as a dichotomous variable (high or low) to predict or measure peripheral vascular integrity and to observe tissue tolerance to pressure. Quantifying skin temperature using a continuous variable may advance the clinician’s knowledge of PrU risk by further defining tissue tolerance to pressure. Such knowledge may be particularly beneficial in determining skin failure and whether a PrU is avoidable or unavoidable. BACKGROUND Skin Temperature and Skin Integrity Risks Changes in skin temperature are used in laboratory and clinical settings as a proxy measure of tissue perfusion at the depth of the papillary dermis 8 – 10 for the purpose of determining risk for lower- extremity vascular ulcers. Elevated skin temperature is thought to ADVANCES IN SKIN & WOUND CARE & VOL. 22 NO. 11 506 WWW.WOUNDCAREJOURNAL.COM ORIGINAL INVESTIGATION Mary Pat Rapp, PhD, RN, is an Associate Professor of Clinical Nursing; Nancy Bergstrom, PhD, RN, FAAN, is the Theodore J. and Mary E. Trumble Professor in Aging Research and the Director of the Center on Aging; and Nikhil S. Padhye, PhD, is an Associate Professor of Nursing-Research, University of Texas Health Science Center Houston School of Nursing, Houston, Texas. Acknowledgments: Authors involved in this research study had no financial arrangements with any company or product associated with the instruments or software used in the study. Mary Pat Rapp, PhD, RN, is a 2004 – 2006 recipient of a John A. Hartford Building Academic Geriatric Nursing Capacity Pre-Doctoral Scholarship. Submitted March 25, 2008; accepted in revised form January 26, 2009. ABSTRACT OBJECTIVES: The purpose of the study was to determine whether characterizing skin temperature regulation as a functional property of the skin as it relates to tissue tolerance improves the clinician’s understanding of pressure ulcer risk prediction. DESIGN: A 2-group time-series design was used to observe skin temperature regularity (entropy) and self-similarity (spectral exponent). METHODS: Twenty nursing facility residents wore skin temperature monitors continuously for 5 days. One bathing episode was observed because bathing is a commonly occurring care procedure. PRIMARY OUTCOME MEASURE: Difference in skin temperature multiscale entropy and spectral exponent by risk category and pressure ulcer outcome. RESULTS: Multiscale entropy (MSE) for skin temperature was lowest in those who developed pressure ulcers, F 1,18 = 35.14, P G .001. Skin temperature mean MSE, F 1,17 = 5.55, P = .031 and the skin temperature spectral exponent, F 1,17 = 6.19, P = .023 differentiated the risk groups. The change in skin temperature entropy during bathing was significant, t (16) = 2.55, P = .021. CONCLUSIONS: Skin temperature MSE and the spectral exponent were significantly different between low-risk and higher risk residents and residents who did and did not develop pressure ulcers. The study supports measurement of skin temperature regulation as a component of tissue tolerance to pressure. ADV SKIN WOUND CARE 2009;22:506 – 13 9 Copyright @ 200 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.