OBJECTIVE: To characterize PIV and RH at different sacral tissue depths in different populations under clinically relevant pressure exposure. METHODS: Forty-two subjects (<65 years), 38 subjects (≥65 years), and 35 patients (≥65 years) participated. Interface pressure, skin temperature, and blood flow at tissue depths of 1, 2, and 10 mm (using LDF and PPG) were measured in the sacral tissue before, during, and after load in a supine position. RESULTS: Pressure-induced vasodilation and RH were observed at three tissue depths. At 10 mm depth, the proportion of subjects with a lack of PIV was higher compared to superficial depths. The patients had higher interface pressure during load than the healthy individuals, but there were no significant differences in blood flow. Twenty-nine subjects in all three study groups were identified with a lack of PIV and RH. CONCLUSIONS: Pressure-induced vasodilation and RH can be observed at different tissue depths. A lack of these responses was found in healthy individuals as well as in patients indicating an innate susceptibility in some individuals, and are potential important factors to evaluate in order to better understand the etiology of pressure ulcers.
OBJECTIVE: To characterize PIV and RH at different sacral tissue depths in different populations under clinically relevant pressure exposure. METHODS: Forty-two subjects (<65 years), 38 subjects (≥65 years), and 35 patients (≥65 years) participated. Interface pressure, skin temperature, and blood flow at tissue depths of 1, 2, and 10 mm (using LDF and PPG) were measured in the sacral tissue before, during, and after load in a supine position. RESULTS: Pressure-induced vasodilation and RH were observed at three tissue depths. At 10 mm depth, the proportion of subjects with a lack of PIV was higher compared to superficial depths. The patients had higher interface pressure during load than the healthy individuals, but there were no significant differences in blood flow. Twenty-nine subjects in all three study groups were identified with a lack of PIV and RH. CONCLUSIONS: Pressure-induced vasodilation and RH can be observed at different tissue depths. A lack of these responses was found in healthy individuals as well as in patients indicating an innate susceptibility in some individuals, and are potential important factors to evaluate in order to better understand the etiology of pressure ulcers.