Standard, Appropriate, and Advanced Care and Medical-Legal Considerations: Part One -- Diabetic Foot Ulcerations

Gerit Mulder, DPM, MS, David Armstrong, DPM, Susie Seaman, MSN, NP, CETN


Wounds. 2003;15(4) 

In This Article


Debridement may be considered one of the most important aspects of diabetic foot ulcer care, along with offloading and infection control. ADA guidelines recommend debridement of abscessed tissue along with incision and drainage.[2]

Debridement is the removal of necrotic tissue to decrease the risk of infection and to promote wound closure. Debridement should remove all necrotic tissue, callus, and foreign bodies down to the level of viable bleeding tissue. Wounds should be thoroughly flushed with sterile saline or a noncytotoxic cleanser following debridement. Hydrotherapy is not recommended for diabetic patients.[2,29,34,35] Debridement is essential for the removal of nonviable cells and for healing.[36] Periwound callus must also be removed, as it may contribute to periwound pressure and incomplete wound contraction. Ulcers may also be obscured by the presence of callus.

Vascular status must always be determined prior to sharp surgical debridement. This may be accomplished through techniques described earlier in this manuscript. Determining local perfusion is of particular importance when debriding ulcers on the distal aspect of the foot.

Debridement is contraindicated in patients with significant vascular compromise, without healing potential, or when they are placed at greater risk. Debridement of dry eschar in the compromised patient may not be necessary.[37] Special considerations include inadequate blood flow, immunosuppressive therapies, poor nutrition, inadequate diabetes control, and high levels of anticoagulants. Consideration of risk versus benefit must be made in cases where deeper structures, such as tendon, bone, or capsule, may be exposed as a result of debridement. Clean, granulating wounds should not be debrided.

Enzymatic debridement may be considered when sharp surgical intervention is not an option. Enzymatic debridement may be slow and ineffective where thick dry eschar is present. Enzymes will not debride the periwound callus. Autolytic debridement through accumulation of exudate under occlusion is not recommended in diabetic patients as the pooling of fluid promotes bacterial proliferation, which may place the diabetic patient at increased risk for infection. In this same population, one may also consider larval (maggot) therapy, although this is not a popular method in the US.[38]

In the absence of diabetes, an individual cellular immune response results in prolonged macrophage activity in a moist environment.[39] Increased moisture may promote autolysis without increasing the risk of infection. In persons with diabetes and other individuals with a compromised cellular immune response, pooling of fluid may promote colonization leading to infection.


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