Key Facts

Diabetic foot disease is largely preventable with screening, education, and prompt management. The diabetic foot MDT approach has significantly reduced amputation rates. Charcot foot requires early recognition to prevent deformity.

Epidemiology

Lifetime risk of foot ulceration ~25% in diabetes. ~7,000 amputations/year in UK. 5-year mortality after major amputation ~50% (comparable to many cancers). PAD present in ~50% of diabetic foot ulcers.

Aetiology

Triad: neuropathy (sensorimotor — loss of protective sensation; autonomic — dry cracked skin, altered blood flow) + PAD (atherosclerosis) + biomechanical factors (deformity, callus, altered pressure distribution). Minor trauma (ill-fitting shoes, nail cutting) in insensate foot → unrecognised injury → ulceration → infection.

Pathophysiology

Neuropathy: loss of pain sensation → unrecognised repetitive trauma → ulceration; motor neuropathy → muscle wasting → foot deformity (claw toes, prominent metatarsal heads) → abnormal pressure distribution; autonomic → dry skin, loss of sweating → skin cracking → entry point for infection. PAD: impaired blood supply → ischaemic ulceration, poor healing, gangrene. Charcot neuroarthropathy: repetitive unrecognised trauma to insensate foot → inflammation → bone resorption and fractures → joint destruction → deformity ('rocker-bottom' foot).

Diabetic Foot Ulcer Types

Neuropathic (60%): painless, punched-out margins, plantar surface (metatarsal heads, heel), warm foot, bounding pulses, callus surrounding, often infected silently Ischaemic (10%): painful, irregular margins, toes/lateral border, cold foot, absent pulses, pale/mottled, may have gangrene Neuroischaemic (30%): features of both; commonest in clinical practice

Charcot Foot

• Acute: hot, red, swollen foot; often unilateral; easily mistaken for cellulitis, DVT, or gout
• Temperature difference >2°C between feet
• X-ray: may be normal initially; later: fractures, joint destruction, subluxation
• MRI: bone marrow oedema (earliest detectable change)
• Chronic: rocker-bottom deformity, midfoot collapse

Infection

• Cellulitis, deep soft tissue infection, osteomyelitis
• Often polymicrobial: S. aureus, streptococci, anaerobes, Gram-negatives
• Systemic sepsis: fever, tachycardia, raised WCC/CRP
• Probe-to-bone test: if probe reaches bone → osteomyelitis likely

Red Flags

• Spreading cellulitis, systemic sepsis, gas gangrene → emergency
• Charcot: acute hot swollen foot in diabetic → immobilise immediately
• Critical limb ischaemia: rest pain, tissue loss, ABPI <0.5

Foot Assessment (NICE NG19)

• 10g monofilament: loss of sensation at ≥1 site = at-risk
• Pulse palpation: dorsalis pedis, posterior tibial
• ABPI: <0.9 suggests PAD; >1.3 suggests calcified arteries (unreliable — use toe pressures instead)
• Risk stratification: low (no risk factors) → annual; moderate (1 risk factor) → 3-6 monthly; high (previous ulcer, neuropathy + deformity/PAD) → 1-3 monthly

Ulcer Assessment

• Size, depth, location, base (granulating, sloughy, necrotic)
• Probe-to-bone test: if bone palpable → osteomyelitis (sensitivity ~90%)
• Wound swab/deep tissue culture: for infected ulcers

Imaging

• X-ray foot: osteomyelitis (periosteal reaction, bone destruction — may take 2 weeks to appear), Charcot changes
• MRI foot: gold standard for osteomyelitis and Charcot (bone marrow oedema)

Vascular

• Duplex USS: PAD assessment
• CT/MR angiography: if revascularisation considered

Bloods

• FBC, CRP, ESR: infection markers
• HbA1c: glycaemic control
• Blood cultures: if systemic sepsis

Prevention (NICE NG19)

• Annual foot screening and risk stratification
• Patient education: daily foot inspection, appropriate footwear, avoid walking barefoot, prompt reporting of injury
• Podiatry: regular nail care, callus management
• Customised footwear/orthotics for high-risk feet

Ulcer Management (MDT — Diabetic Foot Team)

• Offloading: non-removable total contact cast or irremovable walker boot (NICE NG19 — reduces healing time)
• Wound care: debridement (sharp, autolytic), appropriate dressings, negative pressure wound therapy (complex wounds)
• Infection: mild — oral flucloxacillin 500mg QDS + amoxicillin-clavulanate 625mg TDS; moderate-severe — IV antibiotics (piperacillin-tazobactam, or co-amoxiclav + metronidazole); osteomyelitis — prolonged IV antibiotics (6 weeks) ± surgical debridement
• Vascular assessment: all ulcers; revascularisation (angioplasty/bypass) if significant PAD
• Glycaemic optimisation: insulin if needed for acute management

Charcot Foot

• Immediate immobilisation: total contact cast (TCC) or aircast boot; non-weight-bearing initially
• Continue immobilisation until temperature difference between feet <2°C and inflammatory markers normalised (may take 6-12 months)
• Bisphosphonates: limited evidence (not routine)
• Surgical reconstruction: for severe deformity causing ulceration

Surgical

• Revascularisation: angioplasty or bypass for PAD-related ischaemia
• Amputation: if life-threatening infection, non-reconstructable PAD, extensive necrosis; aim for most distal level possible

Referral Criteria

• Diabetic foot team: ALL active foot problems (ulcer, infection, Charcot) — seen within 24 hours (NICE NG19)
• Vascular surgery: PAD, critical limb ischaemia
• Orthopaedics: Charcot deformity requiring surgery

Diabetic foot ulcers: ~60% heal with appropriate management within 6 months; ~10-15% require amputation. 5-year mortality after major amputation ~50%. Charcot foot: if recognised and treated early, deformity can be minimised; late diagnosis leads to rocker-bottom deformity and recurrent ulceration. Recurrence rate for foot ulcers: ~40% at 1 year, ~60% at 3 years. MDT care has reduced amputation rates by ~40%.

Neuropathic vs Ischaemic Foot Ulcer

Diabetic Foot Risk Classification (NICE NG19)