Temperature effects on surface pressure-induced changes in rat skin perfusion: implications in pressure ulcer development.

The effect of varying local skin temperature on surface pressure-induced changes in skin perfusion and deformation was determined in hairless fuzzy rats (13.5+/-3 mo, 474+/-25 g). Skin surface pressure was applied by a computer-controlled plunger with corresponding skin deformation measured by a linear variable differential transformer while a laser Doppler flowmeter measured skin perfusion. In Protocol I, skin surface perfusion was measured without heating (control, T=28 degrees C), with heating (T=36 degrees C), for control (probe just touching skin, 3.7 mmHg), and at two different skin surface pressures, 18 mmHg and 73 mmHg. Heating caused perfusion to increase at control and 18 mmHg pressure, but not at 73 mmHg. In Protocol II, skin perfusion was measured with and without heating as in Protocol I, but this time skin surface pressure was increased from 3.7 to 62 mmHg in increments of 3.7 mmHg. For unheated skin, perfusion increased as skin surface pressure increased from 3.7 to 18 mmHg. Further increases in surface pressure caused a decrease in perfusion until zero perfusion was reached for pressures over 55 mmHg. Heating increased skin perfusion for surface pressures from 3.7 to 18 mmHg, but not for pressures greater than 18 mmHg. After the release of surface pressure, the reactive hyperemia peak of perfusion increased with heating. In Protocol III, where skin deformation (creep and relaxation) was measured during the application of 3.7 and 18 mmHg, heating caused the tissue to be stiffer, allowing less deformation. It was found that for surface pressures below 18 mmHg, increasing skin temperature significantly increased skin perfusion and tissue stiffness. The clinical significance of these findings may have relevance in evaluating temperature and pressure effects on skin blood flow and deformation as well as the efficacy of using temperature as a therapeutic modality in the treatment of pressure ulcers.

Skin perfusion responses to surface pressure-induced ischemia: implication for the developing pressure ulcer.

This study describes alterations in skin perfusion in response to step increases in surface pressure, before and after long-term (5 hr) exposure to pressure-induced ischemia. A provocative test was developed in which surface pressure was increased in increments of 3.7 mmHg until perfusion reached an apparent minimum by a computer-controlled plunger that included a force cell, a laser Doppler flowmeter to determine perfusion, and a thermistor to monitor skin temperature. Force was applied to the greater trochanters of adult male fuzzy rats. Skin perfusion (n=7) initially increased with low levels of surface pressure (up to 13.9+/-1.9 mmHg) and then decreased with further increases in pressure, reaching minimum (zero) perfusion at 58.2+/-3.64 mmHg. After pressure release, reactive hyperemia (3 x normal) was observed, with levels returning to normal within 15-30 min. The provocative test was then applied after a 5-hr ischemic episode (produced by 92 mmHg) and 3 hr of recovery. A comparison of responses between stressed and unstressed skin revealed: elevated (63%) control perfusion levels; loss of the initial increase in perfusion with low levels of increasing pressure; a depression (45%) in the hyperemic response with delayed recovery time; and a decrease (54%) in amplitude of low frequency (<1 Hz) rhythms in skin perfusion. Skin surface temperature gradually increased both during the control period and the period of incremental increases in surface pressure (total DT=3.3 degrees C). The results suggest a compromised vasodilator mechanism(s). The provocative test developed in this study may have clinical potential for assessing tissue viability in early pressure ulcer development.