Decubitus ulcer development: pressure alone increases tissue temperature

Decubitus ulcer development: pressure alone increases tissue temperature Pressure ulcers of the buttocks in persons confined to wheel-chairs can be a serious problem. The reduction in blood flow to the tissues caused by the pressure from the ischial tuberosities is a key factor in pressure ulcer development of the buttocks. Also, increase in tissue temperature due to surface insulation, or systemic temperature increase, are risk factors in pressure ulcer development. The aim of this study was to investigate the effect on skin temperature of pressure alone, regardless of surface insulation. Able-bodied, healthy individuals ( n = 12) were subjected to an increase in pressure of the tissues overlaying the left ischial tuberosity up to 320 mmHg. The skin temperature was measured on the loaded left buttock half and on the unloaded right buttock half for control. The skin temperature increased significantly 2.7 (0.4)°C (men) and 2.7 (0.6)°C (women) on the loaded left side ( p < 0.001 for both groups). When pressure was relieved, a period of hyperemia followed, this increased the temperature further significantly (2.0 (1.0)°C (men, p < 0.01) and 1.3 (0.6)°C (women, p < 0.05)). During hyperemia, maximum temperature was reached after 366 (257) s (women) and 266 (88) s (men). In conclusion, the increase in temperature is most likely to be caused by facilitated heat conduction from the body core caused by compression of the tissues. An increase in temperature as a result of loading may make the tissues even more vulnerable to pressure-induced ischemia due to an increase in metabolic demand. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Plastic Surgery Springer Journals

Decubitus ulcer development: pressure alone increases tissue temperature

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Publisher
Springer-Verlag
Copyright
Copyright © 2009 by Springer-Verlag
Subject
Medicine & Public Health; Plastic Surgery
ISSN
0930-343X
eISSN
1435-0130
D.O.I.
10.1007/s00238-009-0351-6
Publisher site
See Article on Publisher Site

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