The relative contributions of interface pressure, shear stress, and temperature on tissue ischemia: a cross-sectional pilot study.

Tissue ischemia is thought to play a major role in the development of pressure ulcers. Pressure, shear, and temperature are acknowledged contributors, but the relative magnitude of each factor is largely unknown. A cross-sectional pilot study was conducted on the sacrums of four healthy volunteers to estimate the relative contributions of each variable by systematically varying and assessing the resulting level of ischemia in the skin tissue. Using a repeated measures design, 21 combinations of temperature (28˚C, 32˚C, and 36˚C); pressure (0 kPa, 8.0 kPa, and 13.3 kPa), corresponding to 0 mm Hg, 60 mm Hg, and 100 mm Hg; and shear stress (0 kPa, 6.7 kPa, and 14.0 kPa), corresponding to 0 mm Hg, 50 mm Hg, and 100 mm Hg (practical testing values), were tested twice, for a total of 168 trials. Using laser Doppler flowmetry, the magnitude of post-load reactive hyperemia was used as an index of ischemia. Fixed Effects and Ranks linear regression models were developed to predict three different indices of reactive hyperemic magnitude with pressure, shear stress, and temperature as the variables. Pressure and temperature were always highly significant predictors of the extent of reactive hyperemia (P <0.0001 for Perfusion Area, peak minus baseline blood flow, and Normalized Peak blood flow), and the contributions of shear stress were insignificant (P = 0.5351 for Perfusion Area, P = 0.6403 for Peak minus Baseline blood flow, and P = 0.8941 for Normalized Peak blood flow). Depending upon the model, comparison of coefficients suggested that an increase of 1.0˚C contributes as much to reactive hyperemia in the skin as 12 mm Hg to 15 mm Hg of interface pressure (coefficient ratios of temperature/pressure are 14.33 for Perfusion Area, 11.77 for Peak minus Baseline, and 12.97 for Normalized Peak, respectively). The findings also indicate that post-load metabolic repayment varied with temperature only at higher pressures, suggesting protective vasodilation was able to keep pace with mild compression. If confirmed in subsequent studies, the results suggest that managing both skin pressure and temperature may reduce the risk of ischemia.