Aetiology
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Recommandations nationales pour la prévention des escarres de décubitusPublished by: KCELast published: 2013Een nationale richtlijn voor decubituspreventiePublished by: KCELast published: 2013Een nationale richtlijn voor de behandeling van decubitusPublished by: KCELast published: 2013Rol van de verpleegkundige bij de preventie van decubitusPublished by: FOD VolksgezondheidLast published: 2016Recommandations nationales pour le traitement des escarres de décubitusPublished by: KCELast published: 2013Rôle infirmier dans la prévention des escarres à domicilePublished by: SPF Santé publiqueLast published: 2016Pressure ulcers develop through the interplay of 4 main factors: pressure, shear, friction, and moisture. Pressure is clearly the most important factor and both the duration and intensity of pressure are important. Irreversible tissue damage may occur as a result of relatively short exposures to high levels of pressure or longer exposure to lower levels of pressure.
Pressure forces are distributed throughout the soft tissue, the extent depending on the mechanical properties of both the soft tissues and any external devices.[11] Shear forces, typically generated when patients slide down in bed, may cause stretching and tearing of small blood vessels and contribute to pressure-induced damage.
Friction and moisture can cause superficial injuries including skin tears and moisture-associated dermatitis. These superficial injuries should never be labelled as pressure ulcers but could facilitate the transmission of pressure to the deeper tissues. Additionally, moisture decreases the stiffness of the stratum corneum and increases the coefficient of friction so that skin is more adherent to the contact surface. This results in greater shear forces being transmitted to deeper tissues.[12]
The role of circulation and tissue perfusion in the development of pressure ulcers is being increasingly recognised.[13] Inadequate blood flow to the skin and soft tissues (as occurs in the setting of sepsis, hypotension, heart failure, or peripheral vascular disease) almost certainly contributes to tissue ischaemia and pressure ulceration. Physiological changes occurring at life’s end, including decreased perfusion, have been used to describe the concept of 'skin failure' and the high incidence of pressure ulcers with terminal disease.[14]
Pressure ulcers occur most commonly over bony prominences and are caused principally by unrelieved interfacial pressure. The risk factors for the development of pressure damage include: increased age, reduced mobility, neurological impairment resulting in loss of sensation or paralysis, and other conditions that prevent normal self-repositioning.[6] Relatively short exposure to high levels of pressure can cause serious damage.[15] Pressures generated between the body and a hard surface may be transmitted through underlying tissue to a point well away from the original area of contact. Shearing and frictional forces may facilitate tissue damage and deformation; these forces may stretch, distort, and ultimately damage or occlude small blood and lymph vessels, contributing to localised ischaemia, reperfusion injury, and tissue death.[15]
Hundreds of patient characteristics have been suggested as being risk factors for pressure ulcer development. In most cases, these risk factors are associated with aetiological factors such as pressure , moisture, or impaired circulation. However, for other proposed risk factors, the causal pathway may not be clear and further research is indicated. How these different risk factors impact on individual susceptibility is currently being researched.[16]
Pathophysiology
The mechanism by which pressure induces tissue death is not fully understood.
Direct deformation of cells from pressure and shear forces disrupts cell structures and results in cell death. Ischaemia also causes cell death through capillary occlusion. The blockage of lymphatic flow may lead to the accumulation of toxic waste products. Reperfusion injury with the accompanying free radical development may damage cells. Finally, an inflammatory response with increased interstitial oedema may result in further cellular deformation.[17]
Highest pressures are seen in the deep tissues, especially along bony prominences. These deep tissues appear to be most susceptible to pressure damage. Consequently, pressure often causes extensive deep tissue injury with little apparent damage initially in the more superficial tissues.These deep tissue injuries may present as an area of dark purple discoloration with intact overlying skin. This lesion may then evolve over the course of several days or weeks to a large necrotic ulcer with extensive undermining of the wound edges.
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