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Diabetic Foot Ulcer

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Diabetic ulcers result from injury predisposed by underlying neuropathy and/or ischaemia. Prevention of ulceration or recurrence is improved by educating patients and their families about their role in the early identification and reduction of risk factors.

The risk factors that results in most diabetic ulcers are neuropathy and/or peripheral vascular disease with frequent complications of infection. It has previously been estimated that ulcer aetiology was primarily due to peripheral neuropathy in 60 to 70 percent of cases and peripheral vascular disease in 15 to 20 percent. However, in recent literature more diabetic patients now seem to be presenting with a combination of both conditions and are exhibiting more neuroischaemic wounds.
Neuropathic ulcers are most likely to occur on the plantar, medial or lateral surfaces of the feet. Ischaemic ulcers are more likely to begin as distal gangrenous lesions on the toe. Determination of the underlying ulcer aetiology, especially whether vascular flow will adequately support healing, is essential for effective treatment decisions and optimal outcomes.

Maintenance of an appropriate healing environment is essential during the management of diabetic foot ulcers. The choice of dressing is dependent on many factors including presence of infection, amount of exudate and the required frequency of wound bed inspection. Polyurethane foam dressings such as 3M™ Tegaderm™ Foam Dressing have proven to be very popular in caring for this patient group. Alginate dressings such as 3M™ Tegaderm™ Alginate Dressing can be used when there is medium to high exudate levels, while hydrocolloid dressings such as 3M™: Tegaderm™ Hydrocolloid Dressing and 3M™ Tegaderm™ Hydrocolloid Thin Dressing can be used. However, if frequent inspection of the wound is required or there is the presence of infection then these dressings would not be indicated. The use of a non-adherent wound contact layer such as 3M™ Tegaderm™ Contact Dressing may also be appropriate to prevent unnecessary damage to the wound bed during absorbent secondary dressing changes.

Information provided with support from the Wound Healing Research Unit, Cardiff.

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