Physiopathology of the diabetic foot

Diabetic foot ulcerations result from different physiopathological mechanisms; a clear understanding of them is crucial to reduce their incidence, provide early care, and finally delay the amputation risk. The three main diabetes complications involved in foot ulcerations are neuropathy, peripheral arterial disease, and infection. The most common pathway to ulceration is peripheral sensorimotor and autonomic neuropathy, leading to loss of sensitivity, foot deformities, high foot pressure, and dry skin. Peripheral arterial disease is more frequent and more serious in the diabetic population. It delays cicatrization and causes gangrene and finally amputation. Infection is also a major complication of ulceration because of its risk of spreading into deep tissue and bone, which increases the risk of amputation. Infection may also generalize and become life-threatening. These complications preferentially affect the foot because it is exposed to hyper pressure, neuropathy, and peripheral arterial disease, which cause distal lesions, and the foot is exposed to a closed atmosphere, a source of soaking and skin frailty. Diabetes itself may enhance the risk of complications stemming from the disease's long-term progression and poor glucose control, thereby affecting ocular and renal functions. Finally, some psychosocial situations such as depression syndrome or poor hygiene possibly enhance diabetic foot occurrence.