Investigating Diabetic Foot Pathophysiology and Amputation Prevention Strategies through Behavioral Modification

Abstract

Diabetic foot complications stem from intricate interactions between macrovascular and microvascular changes, neuropathy, inflammation, immune responses, hyperglycemia, oxidative stress, and infection susceptibility. Macrovascular factors like atherosclerosis lead to tissue ischemia, while microvascular dysfunction worsens perfusion deficits. Neuropathy contributes significantly to such complications, causing sensory loss, motor problems, and autonomic dysfunction. This results in unnoticed injuries, muscle atrophy, deformities, and dry skin, elevating the risk of non-healing wounds and infections. Inflammation and immune responses amplify tissue damage and hinder healing. Chronic hyperglycemia generates advanced glycation end products, stiffening tissues, while oxidative stress exacerbates damage. Mitochondrial dysfunction further compromises cellular energy production, worsening tissue repair challenges. These multifaceted factors collectively contribute to diabetic foot complications. The impact of modifiable behavior factors such as smoking, heavy alcohol consumption, and exercise on the risk of lower extremity amputation (LEA) in diabetic patients is also not to be ignored. Substantial data had identified increased LEA risk from smoking and heavy alcohol intake and reduced risk from regular exercise. The cumulative impact of these behaviors underscores the significance of behavior modification in preventing LEA and enhancing the well-being of diabetic patients. Understanding these mechanisms is vital for developing effective preventive strategies, diagnostics, and treatments, addressing the impact of diabetic foot complications on individuals and healthcare systems.