Etiologic factors in pressure sores: an experimental model.

The primary etiologic factor in the production of pressure sores is considered to be pressure-induced ischemia with the threshold being 35mmHg for 2 hours. However, clinical evidence indicates that skin can withstand normothermic ischemia of 8 to 12 hours without necrosis. A detailed review of the literature indicates that previous experimental models are few in number and limited in clinical relevance. Therefore, a continuously monitored computer-controlled electromechanical pressure applicator was designed to produce pressure sores over the greater femoral trochanter of normal and paraplegic swine. Examination of the pressure site at 1 week revealed 3 groups of lesions: 1) muscle damage only, 2) muscle and deep dermis damage, and 3) full-thickness damage extending from bone to skin. A critical pressure-duration curve for the production of pressure sores is presented for normal swine. Muscle damage occurred at high pressure-short duration (500mmHg, 4 hours), whereas skin destruction required high pressure-long duration (800mmHg, 8 hours). On analysis, muscle is more sensitive than skin to the effects of pressure, and the initial pathologic changes occur in muscle. Skin breakdown did not occur with a pressure of 200mmHg for 15 hours, thus contradicting previous statements that pressure exceeding 35mmHg for 2 hours would cause ischemia with subsequent tissue necrosis resulting in a pressure sore. We hypothesis that normal tissue is far more resistant to pressure-induced ischemia that previously considered, and that the pressure-duration threshold for the production of pressure sores is lowered dramatically following changes in the soft tissue coverage due to paraplegia, infection, or repeated trauma.