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.

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