Clinical meaning
Diabetic foot complications result from the triad of peripheral neuropathy, peripheral arterial disease (PAD), and immune dysfunction. Sensory neuropathy eliminates protective pain sensation, allowing repetitive trauma from ill-fitting shoes and foreign objects to go undetected. Motor neuropathy causes intrinsic foot muscle atrophy leading to claw toe and hammer toe deformities that create abnormal pressure points. Autonomic neuropathy reduces sweating and sebaceous gland function, causing dry, cracked skin susceptible to fissure formation and bacterial entry. PAD reduces arterial blood flow, impairing wound healing and oxygen delivery. Hyperglycemia impairs neutrophil function, reducing phagocytosis and bacterial killing. Diabetic foot ulcers precede approximately 85% of diabetes-related amputations. The Wagner classification grades ulcers from Grade 0 (pre-ulcerative or healed ulcer) to Grade 5 (extensive gangrene requiring amputation). Comprehensive foot assessment, patient education, and early intervention are the keys to limb preservation.
Exam relevance
Risk factors: - Peripheral neuropathy with loss of protective sensation - Peripheral arterial disease with diminished pedal pulses - History of prior foot ulcer or amputation - Structural foot deformities (Charcot foot, bunions, hammer toes) - Poor glycemic control with HbA1c > 8%