Diabetic Foot

A diabetic foot ulcer usually develops when three problems converge: neuropathy removes the warning signal of pain, deformity or limited joint mobility concentrates pressure, and peripheral arterial disease limits the tissue’s ability to repair itself. A pebble in a shoe, a cracked heel, or a blister can therefore become an ulcer without the person noticing it. Loss of protective sensation is not simply numbness. It means the patient may continue walking on tissue that is being injured with every step. Repetitive pressure causes callus; callus increases focal pressure further; skin breaks down beneath or beside it. A plantar ulcer hidden under a thick callus may be deeper than it first appears. Hyperglycemia compounds the problem. It impairs leukocyte function, promotes neuropathy and microvascular injury, and slows collagen formation. Glycemic targets must be individualized, but an A1C below 7% is often appropriate when it can be achieved safely. An A1C above 9% is associated with substantially greater ulcer and amputation risk. [1]