Pressure Sores Classification and Management

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Abstract
Of all the problems lacing the physician responsible for the care of severely injured or disabled patients, one of the most frustrating is the prevention and management of skin breakdown known as pressure sores. In the past they have been called decubitus ulcers, bed sores, and ischemic ulcers. The problem is no less disconcerting today than it was four hundred years ago when Fabricus10 suggested that a “pneuma” resulting from nerve severance, plus loss of blood supply, caused skin ulceration. Charcot,7 in 1879, also believed that nerve injury released a neurotrophic factor that led to tissue necrosis. Nerve injury was also implicated by Munro.16 who felt that the autonomie reflex are controlling skin circulation was interrupted. In guinea pigs with sectioned spinal cords, Brown-Sequard4 treated ulcers by keeping the area clean and free of pressure, thus associating pressure and moisture as contributing factors. No specific neurotrophic factor has been satisfactorily demonstrated. However, several other conditions have been suggested as being primary causes including a deficient blood supply, absent sensation and reflexes with incontinence, muscle wasting and atony, bacterial infection, anemia, and malnutrition. Recommendations for treatment have been no less confusing than theories of etiology. Almost any concoction imaginable has been placed in these ulcers with the intention of promoting wound healing. A partial list includes poultices of carrots and turnips, bread and charcoal, Dakin's solution, antibiotics, enzymes, vitamins, cod liver oil, dried blood plasma, gold, aluminum and silver, chlorophyll, sugar and brine baths.1–3, 11–13, 17, 19 Several physical and mechanical modalities have also been devised for preventing and treating skin breakdown, including electric lamps, ultraviolet light, hyperbaric oxygen, rubber rings, and donuts, water beds, sawdust beds, and a variety of pressure beds and paddings.-2, 3, 11, 12, 19 Since 1945, the literature has delined with increasing boldness the indications, techniques, and principles of surgical closure of pressure sores. 2, 6, 8, 13, 18 A critical review of this vast literature is difficult because a clear definition of the lesion or lesions being treated is lacking. Proper evaluation of a therapeutic technique necessitates a clear understanding of the disease process under treatment. As with all disease processes, pressure sores do not appear de vovo but develop in an orderly pathophysiologic manner which is influenced by a variety of local and systemic factors. The mechanism of etiology as outlined in this report, considers these various elements and suggests an orderly evolution and classification which serves as a guide for both treatment and prognosis.

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