diabetic foot ulcer

**Pathophysiology (triad: neuropathy + ischemia + trauma/infection)** - Sensory neuropathy: chronic hyperglycemia leads to polyol pathway (aldose reductase converts glucose to sorbitol), AGE accumulation, oxidative stress, and vasa nervorum damage. This causes loss of protective sensation, so patients do not feel repetitive pressure, shoes that fit poorly, or foreign bodies. - Motor neuropathy: atrophy of intrinsic foot muscles causes claw/hammer toes, prominent metatarsal heads, and abnormal pressure points. Charcot neuro-arthropathy (midfoot collapse, "rocker-bottom" foot) is a related complication. - Autonomic neuropathy: decreased sweating causes dry, cracked skin that allows bacterial entry, and AV shunting. - Peripheral arterial disease (macrovascular atherosclerosis of tibial/infrapopliteal vessels, plus medial calcification) impairs healing. Microvascular dysfunction and impaired neutrophil function and wound healing add to this.

**Clinical features** - Neuropathic ulcer: painless, punched-out, with a callus rim, on pressure points (plantar metatarsal heads, heel, great toe). The foot is warm with palpable pulses and dry skin. - Ischemic (arterial) ulcer: painful, on the toe tips or lateral foot, with a pale or necrotic base. The foot is cool with diminished pulses, hair loss, and delayed capillary refill. - Neuroischemic ulcers combine features of both. - Exam: monofilament (10 g Semmes-Weinstein) testing, vibration (128 Hz tuning fork), ankle reflexes, pulses, and ABI. ABI may be falsely elevated (>1.3) from calcified, noncompressible vessels, so use toe-brachial index or toe pressures.

**Infection and osteomyelitis** - Common pathogens: *S. aureus* (including MRSA) and beta-hemolytic streptococci in mild infections. Chronic or severe infections are polymicrobial (gram-negatives, anaerobes). - Probe-to-bone test positive suggests osteomyelitis. Ulcer area >2 cm², ESR >70, and exposed bone are also suggestive. - Imaging: plain X-ray first, but it lags by 2-3 weeks. MRI is the most sensitive and specific imaging test. Bone biopsy/culture is the gold standard. - Treatment: antibiotics (the choice depends on severity, and MRSA coverage if risk factors are present), debridement, and possibly amputation.

**Classification** - Wagner: grade 0 (intact skin at risk) through grade 5 (gangrene of the entire foot). Grade 3 = deep ulcer with abscess or osteomyelitis. - Also: University of Texas and IDSA/IWGDF infection classification.

**Management** 1. Offloading: total contact cast is the gold standard for neuropathic plantar ulcers. Removable walkers and special footwear are alternatives. 2. Sharp debridement of necrotic tissue and callus. 3. Infection control with cultures from deep tissue (not superficial swabs) and appropriate antibiotics. 4. Vascular assessment and revascularization (angioplasty or bypass) for ischemia. 5. Glycemic control, moist wound dressings, and adjuncts (negative-pressure therapy, becaplermin [PDGF], skin substitutes, hyperbaric oxygen in selected cases). 6. Amputation for non-salvageable infection or gangrene.

**Prevention (high-yield for Step 2)** - Annual comprehensive foot exam for all diabetics (more frequent if high risk). - Daily foot inspection, proper footwear, avoid walking barefoot, podiatry referral, smoking cessation, and tight glycemic control.

**Boards pearls** - Painless plantar ulcer at the metatarsal head in a diabetic means neuropathic ulcer. - Painful toe ulcer with absent pulses means arterial insufficiency. - Painful, shallow, irregular ulcer on the medial malleolus with edema and hemosiderin deposition means venous stasis ulcer (a different entity). - Nonhealing ulcer + positive probe-to-bone: get MRI/bone biopsy for osteomyelitis. - Diabetic foot infections are a major cause of hospitalization and amputation in diabetics.