Bedsore pathophysiology
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Overview
Pathophysiology
Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area, which eventually turns purple. Left untreated, the skin may break open and become infected. Moist skin is more sensitive to tissue ischemia and necrosis and is also more likely to get infected.
Bedsores are accepted to be caused by three different tissue forces:
- Pressure, or the compression of tissues. In most cases, this compression is caused by the force of bone against a surface. After an extended amount of time with decreased tissue perfusion, ischemia occurs and can lead to tissue necrosis if left untreated in an immunocompromised patient.
- Shear force, or a force created when the skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity. This can also cause the pinching off of blood vessels which may lead to ischemia and tissue necrosis.
- Friction, or a force resisting the shearing of skin. This may cause excess shedding through layers of epidermis.
Aggravating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudate. Over time, this excess moisture may cause the bonds between epithelial cells to weaken thus resulting in the maceration of the epidermis. Other factors in the development of bedsores include age, nutrition, vascular disease, diabetes mellitus, and smoking, amongst others.
There are currently two major theories about the development of pressure ulcers. The first and most accepted is the deep tissue injury theory which claims that the ulcers begin at the deepest level, around the bone, and move outward until they reach the epidermis. The second, less popular theory is the top-to-bottom model which says that skin first begins to deteriorate at the surface and then proceeds inward.[1]
References
- ↑ Niezgoda, Jeffrey A. and Susan Mendez-Eastman. The Effective Management of Pressure Ulcers. Advances in Skin & Wound Care: The Journal for Prevention and Healing, Volume 19, Number 1 - Supplement (2006): 3-15.