ETIOLOGIC FACTORS IN PRESSURE SORES - AN EXPERIMENTAL-MODEL

  • 1 January 1981
    • journal article
    • research article
    • Vol. 62  (10) , 492-498
Abstract
The primary etiologic factor in the production of pressure sores is considered to be pressure-induced ischemia with the threshold being 35 mm Hg for 2 h. Clinical evidence indicates that skin can withstand normothermic ischemia of 8-12 h without necrosis. A detailed review of the literature indicates that previous experimental models are few in number and limited in clinical relevance. 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 wk revealed 3 groups of lesions: muscle damage only, muscle and deep dermis damage, and 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 (500 mm Hg, 4 h), whereas skin destruction required high pressure-long duration (800 mm Hg, 8 h). 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 200 mm Hg for 15 h, contradicting previous statements that pressure exceeding 35 mm Hg for 2 h would cause ischemia with subsequent tissue necrosis resulting in a pressure sore. Apparently, normal tissue is far more resistant to pressure-induced ischemia than previously considered, and 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.