Pressure Ulcer Treatment

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Pressure Ulcer Treatment

Pressure Ulcer Treatment


A monograph prepared by the Research Committee of the NPUAP suggests several research priorities for pressure ulcers: (1) outcome-focused research, (2) intervention and product efficacy studies, (3) basic research related to staging of ulcers, (4) refinement of risk assessment methods, and (5) risk-based, multi-interventional trials. Additional issues requiring investigation include cost issues, ethical decision making, guideline dissemination, public policy, and national outcome evaluations. Methodologic issues, such as research design, study population, and control group use, also need further investigation (Goode, 2006).

Early investigators tended to focus on pressure as the primary cause of pressure ulcers.37,66 Groth, Kosiak, and Dinsdale were among the first investigators to explore pressure and tissue injury relationships.

(Bradley, 2006) found that pressure ulcers similar to those of humans could be produced experimentally in animals.67 His experiments showed that larger muscle masses withstood pressure better. He noted that effective pressure force increases toward the smaller surface. This accounts for the greater destruction of tissue at the base of the inverted cone, typified by the small area of skin redness or destruction overlying a bony prominence. This condition is frequently observed in ischial ulcers, trochanteric ulcers, and (to a lesser degree) ulcers over the sacrum (Cullum, 2007).

Groth also noted that generalized sepsis can result in local infection at the site of pressure, with abscess formation, extension of inflammation, thrombosis of the larger vessels, and, consequently, a larger area of tissue necrosis. He concluded that large-vessel thrombosis is not typically a cause of ulceration because of the extensive collateral circulation usually present in the skin (Bradley, 2006).

In a classic experiment, (Palfreyman 2006), a physiatrist, subjected dogs to accurately controlled pressures ranging from 100-550 mm Hg for 1-12 hours. Microscopic examination of tissue obtained 24 hours after the application of 60 mm Hg of pressure for only 1 hour showed cellular infiltration, extravasation, and hyaline degeneration. Tissues subjected to higher pressures for longer periods also showed muscle degeneration and venous thrombosis. Kosiak concluded that intense pressure of short duration was as injurious to tissues as lower pressure applied for longer periods of time. In both cases, tissue ischemia led to irreversible cellular changes and, ultimately, to necrosis and ulceration. He also concluded that prolonged pressure was the direct and primary cause of pressure ulcers (Vermeulen, 2008).

(Palfreyman 2006) disagreed with Groth about the location and severity of skin damage, stating that it extended equally to the area under pressure instead of being most severe at the deepest part overlying the bony prominence. Kosiak concluded that skin and subcutaneous tissue provide a sling or suspension effect that allows only a fraction of the applied pressure to be transmitted to the deep tissues.

(Cullum, 2007) reported microscopic changes in rat muscle subjected to a pressure of 100 mm Hg for as little as 1 hour.68 His microscopic findings were similar to those of Groth and Kosiak. Keane observed that muscle is more susceptible to pressure injury than skin. Keane also noted that the body weight is borne on superficial, ...
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