Etiology and Pathology of Pressure Ulcers

Abstract

It has been observed that the application of constant pressure of 70 mmHg for more than 2 h produced irreversible tissue damage [1]. Minimal tissue damage was observed when the pressure exceeded 240 mmHg, providing there was intermittent pressure relief [2]. Histopathological changes secondary to pressure on the tissues include occluding of the blood flow to the tissues. If occluding occurs for short periods of time, the result is anoxia of the cells. If the pressure continues for longer periods of time, complete occlusion of the blood flow results in ischemia of the cells and then necrosis and, consequently, irreversible tissue damage. Muscle fibers are more sensitive to the ischemia effect of prolonged pressure than the skin [3, 4]. Shear forces are an etiologic factor in development of pressure, and ulcers [5, 6] are caused by movement of boney prominence against the subcutaneous tissues. This occurs when the position of the patient, for example, in bed, is shifted in a way that the skin remains stationary in relation to the support of the body and, as a result of the movement, the subepidermal vessels are bent at a right angle. Shear alone does not cause tissue necrosis; however, it is a predisposing factor in causing pressure ulcers. Shear forces are seen more frequently in clinical practice when a patient loses weight and tissue sliding can occur over the boney prominences. Friction forces relate to rubbing of the skin against linen or clothing, or even when lifting a patient on a sling. Most abrasion injuries are caused by friction, although friction does not lead to all pressure ulcers; it can damage the epidermis and make the skin susceptible to pressure ulcers [1].