Biochemical status of soft tissues subjected to sustained pressure

Abstract

The breakdown of soft tissue leading to the development of pressure ulcers has implications in terms of both the overall health of an individual and the overall resources required for health care. Although the cause of the condition is multifactorial [ii, it is well established that prolonged pressure ischaemia will affect the viability of soft tissues, leading to their eventual breakdown (see Chap. 1). There are a host of external factors, generally physical, biochemical and clinical in nature, which contribute to the development of tissue breakdown and the formation of pressure ulcers [21. However, the presence of pressures applied normally at the interface between the soft tissues and the patient support must be considered as an initiating factor. When prolonged pressure is applied to the skin, the underlying blood vessels may be partially or totally occluded, creating an anoxic environment, and oxygen and other nutrients are not delivered at a rate sufficient to satisfy the metabolic demands of the tissue. The lymphatic and venous drainage will also be impaired and thus the breakdown products of metabolism accumulate within both the interstitial spaces and the cells [3j. As energy stores diminish there is an increasing possibility of failure of some of the cellular processes and dissipation of ionic gradients across cellular membranes, resulting in cell damage [4j. In the able-bodied subject regular movement relieves these pressures at local tissue areas and there follows a period of increased blood flow after vascular occlusion, termed reactive hyperaemia. However, many immobile and disabled subjects are less able to relieve pressures, and their tissues, particularly adjacent to bony prominences such as the sacrum, are often compromised. This makes them a prime group for the development of pressure ulcers.