Pressure ulcers develop when persistent pressure on a bony site obstructs healthy capillary flow leading to tissue necrosis. This typically occurs over a bony prominence but can occur in any situation where blood flow to the skin is impeded. The aetiology of pressure ulcers is multi-factorial, with pressure, friction, sheer, moisture, and temperature being the main extrinsic factors, more than 100 extrinsic and intrinsic risk factors have been identified in the literature that reduce tissue tolerance and increase patient susceptibility.
The body has evolved to tolerate short periods of high pressure or longer periods of low pressure; this is characteristic of everyday life. However when independent mobility and tissue tolerance is affected by illness or infirmity the risk of pressure ulceration increases. Prolonged compression and/or distortion of subcutaneous tissue can reduce the supply of essential oxygen and nutrients to the tissue resulting in a buildup of toxic metabolites.
Pressure on the skin as low as 6 mmHg can occlude capillary blood flow and with a wide individual variation, it is impossible to say what a ‘safe’ level is for each individual.
Normal Physiological Response To Pressure
Healthy individuals make subconscious movement every few minutes in order to avoid prolonged pressure, even during sleep. This movement off-loads the tissue and re-perfusion occurs through a process of ‘reactive hyperemia’ which is a ‘flush’ of blood to the tissue. This normal physiological response replenishes the tissue with oxygen and nutrients and removes toxic waste: this may be visible on the skin surface as a reddened area (erythema) which blanches (whitens) under light finger pressure.
Note: This phenomenon should not be confused with redness that persists and does not blanch (grade 1 pressure ulcer) or with the re-perfusion that occurs after prolonged ischemia and is associated with re-perfusion injury.
Preventative And Therapeutic Strategies
Alternating pressure-redistributing support surfaces mimic spontaneous body movement by repeatedly and automatically, off-loading the tissue by means of inflating and deflating sections of the mattress or cushion. The effect can be measured in the laboratory using Interface Pressure (IP) and Doppler perfusion studies, and the rationale behind the development of these devices is explored in much more detail in The Principles of Alternating Pressure brochure, available from ArjoHuntleigh.
Alternating pressure unlike other modalities were designed purely for pressure ulcer management and as such, is supported by the widest range of clinical evidence from extensive all-comer clinical outcome studies to specialist care such as intensive care, burns, spinal injury and reconstructive surgery.