Restoration of blood flow to an ischemic area of tissue, or reperfusion, has recently been suggested as a cause of more damage to the injured area, causing a pressure ulcer to enlarge or fail to heal. One mechanism of harm to tissue may be from reduction in capillary density from repeated loading and unloading along with ischemic insult [10]. The time to develop necrosis is reduced in patients with impaired circulation, such as those with peripheral vascular disease or hypotension.

Shear is also a cause of pressure ulcers and undermining in existing ulcers. Shear is a tangential (angular) force associated with movement, for example, sliding down in bed or being pulled over to the side of the bed. Shear forces distort blood vessels in the skin, making the effect of pressure more deleterious because the tissue is already hypoxic. Research has shown that positioning a patient at 45° head of bed elevation leads to the most detrimental combination of pressure and shear on the sacrum, because the shear stresses combined with pressure cause greater obstruction and distortion of capillaries in skeletal muscle around bony prominences than does pressure alone [11].

Microclimate, the moisture and heat of the skin, increases the risk for pressure ulcers because the moisture macerates the skin. The boggy skin does not glide against bed sheets and leads to superficial tissue injury. Skin exposure to urine or stool also injures the skin and increases risk of tissue damage from pressure and shear. Gefen [12] has provided a recent theoretical explanation of the ways in which a changing microclimate may influence the development of superficial pressure ulcers. From a mathematical model, Gefen postulated that four microclimate changes may influence pressure ulcer development – increases in skin temperature, increasing ambient temperature, increasing relative humidity, and decreasing the permeability of sheets or clothing.