| 5.) What is the pathophysiology in diabetic foot infections?
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The distribution of the atherosclerotic lesions in diabetic patients is different from non-diabetic patients. In diabetics, the distal profunda femoris, the distal popliteal, and the tibial vessels are more commonly involved. In addition there is a microangiopathy at arteriolar and capillary level with thickening of the intima and basement membrane which impairs oxygen delivery to tissue. The media of arteries is more often calcified.
Diabetic neuropathy is caused by segmental demyelination of both sensory and motor nerves resulting in atrophy of intrinsic muscles of the foot and deformity associated with sensory loss and the inability to detect minor injury, skin necrosis, or early infection. This neuropathy develops slowly and insidiously.
Uncontrolled hyperglycemia interferes with bactericidal activity of leukocytes and also increases collagenase activity which decreases collagen formation and slows wound healing. When infections occur, they are aggressive, rapidly extending into the musculofascial planes, tendon sheaths, and muscles of the foot and leg.
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