2.24
A diabetic foot ulcer is a chronic foot wound that develops in diabetic people. It most often develops on weight-bearing areas such as the heel and the plantar surface of the metatarsal heads.
Its development involves four key mechanisms: neuropathy, hypoperfusion, infection, and impaired healing.
Neuropathy plays a central role. Loss of protective sensation prevents injury awareness.
Motor neuropathy leads to muscle imbalance and structural deformities. Autonomic dysfunction reduces sweating, leaving the skin dry and fissured.
Hypoperfusion, caused by peripheral artery disease and microvascular dysfunction, restricts blood flow.
Combined with impaired oxygen release from glycosylated hemoglobin, this leads to hypoxia, suppressing angiogenesis and cellular repair.
Disrupted skin barrier function, poor perfusion, and impaired immune function allow infection to develop easily and spread rapidly.
Hyperglycemia worsens healing by weakening neutrophils, prolonging macrophage activity, and reducing fibroblast and keratinocyte function.
These disturbances keep the ulcer in a chronic, non-healing state.
Definition
A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.
Pathophysiology
• The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing.
• Neuropathy is the most common factor. Sensory neuropathy reduces pain perception, so minor trauma often goes unnoticed. Motor neuropathy alters foot structure, leading to deformities that concentrate pressure at specific sites. Autonomic neuropathy decreases sweat production, causing dry, cracked skin that is more prone to breakdown.
• Ischemia, associated with peripheral arterial disease and microvascular dysfunction, restricts blood supply to the lower extremities. In addition, glycosylated hemoglobin reduces oxygen release. The resulting hypoxia suppresses angiogenesis and cellular repair, prolonging wound persistence.
• Infection occurs readily once the skin barrier is breached. Poor circulation limits the delivery of immune cells, while bacteria thrive in ischemic tissue. Persistent infection accelerates tissue destruction and increases the risk of deeper complications, such as osteomyelitis.
• Impaired wound healing reflects the systemic effects of hyperglycemia. Neutrophils show reduced chemotaxis and phagocytosis. Macrophages remain in a prolonged inflammatory state. Fibroblasts synthesize less collagen, and keratinocyte migration is impaired. These defects prevent wounds from progressing through the normal healing cascade.
• Together, these mechanisms keep the ulcer in a chronic inflammatory state, making it difficult to heal and prone to recurrence and severe complications.
A diabetic foot ulcer is a chronic foot wound that develops in diabetic people. It most often develops on weight-bearing areas such as the heel and the plantar surface of the metatarsal heads.
Its development involves four key mechanisms: neuropathy, hypoperfusion, infection, and impaired healing.
Neuropathy plays a central role. Loss of protective sensation prevents injury awareness.
Motor neuropathy leads to muscle imbalance and structural deformities. Autonomic dysfunction reduces sweating, leaving the skin dry and fissured.
Hypoperfusion, caused by peripheral artery disease and microvascular dysfunction, restricts blood flow.
Combined with impaired oxygen release from glycosylated hemoglobin, this leads to hypoxia, suppressing angiogenesis and cellular repair.
Disrupted skin barrier function, poor perfusion, and impaired immune function allow infection to develop easily and spread rapidly.
Hyperglycemia worsens healing by weakening neutrophils, prolonging macrophage activity, and reducing fibroblast and keratinocyte function.
These disturbances keep the ulcer in a chronic, non-healing state.
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