Pressure Ulcers

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External Factors
External factors that lead to the development of pressure ulcers include pressure, shearing forces, friction, and moisture.
Pressure applied to the skin in excess of the arteriolar pressure (32 mm Hg) prevents the delivery of oxygen and nutrients to tissues, resulting in the accumulation of metabolic waste products. Pressures are greatest over bony prominences where weight-bearing points come in contact with external surfaces. A patient lying on a standard hospital mattress may generate pressures of 150 mmHg; sitting produces pressures as high as 300 mmHg over the ischial tuberosities. Pressure in excess of 70 mmHg for two hours results in irreversible tissue damage in animal models.

Ulcer formation occurs more rapidly with higher pressures, and intermittent relief of pressure prevents tissue damage. Pressure over a bony prominence tends to result in a cone-shaped distribution with the most affected tissues located deep, adjacent
to the bone-muscle interface. Tissues vary in their susceptibility to pressure-induced injury; muscle is the most susceptible, followed by subcutaneous fat and then dermis. Thus, extensive deep tissue damage may occur with little or no evidence of superficial
tissue injury.
Shearing forces
Shearing forces occur when patients are placed on an incline. Deeper tissues, including muscle and subcutaneous fat, are pulled downwards by gravity, while the superficial epidermis and dermis remain fixed through contact with the external surface. The result is stretching and angulation of local blood vessels and lymphatics. Shear forces alone may not cause ulceration, but appear to have an additive effect so that in the presence of pressure, more severe tissue damage will occur.
Friction occurs when patients are dragged across an external surface. This results in an abrasion with damage to the most superficial layer of skin.
Exposure to moisture in the form of perspiration, feces, or urine may lead to skin maceration and predispose to superficial ulceration.

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