diabetic foot

**Pathophysiology (3 interacting drivers):** 1. **Neuropathy (most important)** - Sensory: loss of protective sensation (stocking-glove distribution), so patients don't feel repetitive trauma, pressure, or ill-fitting shoes. Result is painless ulcers. - Motor: intrinsic foot muscle atrophy causes claw/hammer toes, prominent metatarsal heads, and abnormal pressure points. - Autonomic: anhidrosis causes dry, cracked skin that lets bacteria in, and arteriovenous shunting causes a warm foot with bounding pulses. - Mechanism: chronic hyperglycemia leads to polyol pathway (sorbitol accumulation via aldose reductase), AGEs, oxidative stress, and vasa nervorum ischemia. 2. **Peripheral arterial disease**: atherosclerosis of tibial and peroneal vessels (infrapopliteal) causes impaired wound healing and ischemic ulcers. Medial calcification (Mönckeberg sclerosis) makes vessels noncompressible, so ABI can be falsely elevated (>1.3). Use toe-brachial index (TBI) or toe pressures instead. 3. **Infection/immune dysfunction**: hyperglycemia impairs neutrophil chemotaxis and phagocytosis.

**Clinical presentations:** - **Neuropathic ulcer**: painless, at pressure points (plantar metatarsal heads, heel), surrounded by callus, with a warm foot and palpable pulses. - **Ischemic (arterial) ulcer**: painful, at the toe tips/lateral malleolus/between toes, pale base with no granulation, cool foot, absent pulses, hair loss, and pallor on elevation. - **Neuroischemic**: mixed features, which is common. - **Charcot neuroarthropathy**: a neuropathic joint that is warm, swollen, and erythematous but relatively painless, usually with a recent minor trauma history. It causes midfoot collapse (**rocker-bottom foot**). Differentiate from infection with imaging (MRI) and by the fact that it improves with elevation. Treat with immobilization and total contact casting. - **Infection**: mild cases are usually Staph aureus and Strep. Chronic or severe infections are polymicrobial (Gram-negatives, anaerobes, Pseudomonas). Complications include cellulitis, abscess, necrotizing fasciitis, and osteomyelitis.

**Diagnosis/workup:** - 10-g **Semmes-Weinstein monofilament** testing plus vibration (128-Hz tuning fork) for neuropathy screening. - **Probe-to-bone test**: positive suggests osteomyelitis. - Osteomyelitis workup: X-ray first (often negative early), then **MRI** (best test). **Bone biopsy/culture** is the gold standard. ESR >70 mm/h is suggestive. - Vascular: ABI/TBI, duplex ultrasound, and angiography if revascularization is planned.

**Management:** - Glycemic control. - **Offloading** (total contact cast is the gold standard for plantar neuropathic ulcers). - Sharp debridement and moist wound care. - Antibiotics for infection (cover MRSA, Gram-negatives, and anaerobes if severe). - Revascularization for PAD. - Surgical debridement or amputation for abscess, necrotizing infection, or refractory osteomyelitis. - Smoking cessation, statins, and antiplatelets.

**Prevention (high-yield):** - Annual comprehensive foot exam for all diabetics (at diagnosis in type 2 DM, and 5 years after diagnosis in type 1 DM). - Daily self-inspection, proper footwear, never walking barefoot, and podiatry referral for high-risk feet.

**Board pearls:** - Painless foot ulcer at a metatarsal head in a diabetic means neuropathic ulcer. - Rocker-bottom deformity in a diabetic means Charcot foot. - Falsely normal or high ABI in a diabetic means medial calcific sclerosis. - Probe-to-bone positive means likely osteomyelitis, so get MRI and bone biopsy. - Diabetic foot ulcers are the leading cause of non-traumatic amputation.