Pathophysiology

The pathogenesis of diabetic foot infection stems from three key factors: neuropathy, angiopathy, and immunopathy.35 6 Neuropathy, the most prominent risk factor for diabetic foot ulcers, develops when continuously high blood glucose levels damage motor, autonomic, and sensory nerves. Damage to motor neurons that supply the small intrinsic muscles of the foot causes deformation, resulting in altered muscular balance, abnormal areas of pressure on tissues and bone, and repetitive injuries. Damage to autonomic neurons results in the shunting of blood through direct arteriole-venous communications, thereby decreasing capillary flow. The secretion of sweat and oil is also diminished, producing dry, cracked skin that is more prone to infection. Finally, damage to sensory neurons produces a loss of protective sensation so that the patient becomes unaware of injury or ulceration.35,36

Angiopathy of large (macroangiopathy) and small (microangiopathy) vessels is also the result of high blood glucose concentrations. Angiopathy results in ischemia and skin breakdown.35,36

Finally, persons with diabetes have altered immune function that predisposes them to infection. Although their humoral immune responses remain intact, leukocyte function and cell-mediated immunity are compromised in poorly-controlled disease. Achieving and maintaining tightly controlled blood glucose levels can wholly or partially reverse diabetic immunopathy35,36

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