DIABETIC FOOT

ETIOPATHOGENESIS

1. Peripheral Neuropathy

2. Peripheral Vascular Disease (Macrovascular + Microvascular)

3. Impaired Wound Healing

• Hyperglycemia reduces the function of neutrophils, macrophages, and fibroblasts
• Epigenetic modifications to wound macrophages maintain a persistent pro-inflammatory state, preventing transition to the proliferation/remodeling phase
• Glycation end-products impair chemotaxis of polymorphonuclear cells
• The net result is a chronic non-healing ulcer

4. Immune Dysfunction

5. Mechanical / Biomechanical Factors

CLINICAL FEATURES (C/F)

History

• Long-standing diabetes mellitus (often Type 2)
• Patient may not recall the specific injury - sensory neuropathy blunts pain
• Prior episodes of ulceration, prior amputations
• Symptoms of peripheral neuropathy: numbness, paresthesias, burning pain (feet and lower legs)
• Claudication or rest pain (if significant PAD)
• Visual impairment (retinopathy) - impairs daily foot inspection

General Examination

• Evidence of poor glycemic control
• Peripheral edema, hypertension

Local Foot Examination

• Dry, scaly skin; fissuring (autonomic dysfunction)
• Shiny, taut, hairless skin (PAD)
• Callus formation overlying pressure points
• Plantar ulcers - typically painless, pink/punched-out edges, surrounded by callus, located at metatarsal heads, heel, or inter-digital spaces (neuropathic ulcers)
• Ischemic ulcers may appear at toe tips with pale, pale wound beds

Classic neuropathic ulcers at the metatarsal heads (Fischer's Mastery of Surgery, 8e)

• Claw toes, hammer toes, pes cavus (motor neuropathy)
• Charcot neuroarthropathy: acute erythema + warmth + swelling of the foot, often mimicking infection; the "rocker bottom" deformity in late stages; distinguishes from infection by subsiding with elevation

• Absent or diminished dorsalis pedis and posterior tibial pulses
• Prolonged capillary refill time
• Dependent rubor, pallor on elevation

• Reduced or absent vibration sense (128 Hz tuning fork)
• Loss of proprioception
• Inability to feel 5.07 Semmes-Weinstein monofilament (10 g) - most predictive risk factor for foot morbidity
• Absent ankle reflexes

• Cellulitis, erythema, warmth, induration
• Purulent discharge from ulcer
• Crepitus (gas-forming organisms)
• Spreading lymphangitis
• Systemic signs: fever, tachycardia, hypotension, altered mental status (pedal sepsis = surgical emergency)

Severe diabetic foot infection with necrosis and hindfoot deformity (Bailey & Love, 28e)

ULCER CLASSIFICATION

Wagner Classification (most widely used)

Brodsky Depth-Ischemia Classification

Key point: Ulcers that are both infected and ischemic are 90 times more likely to require amputation. An infected ulcer alone carries a 40-55% chance of some form of amputation. - Campbell's Operative Orthopaedics, 15e

INVESTIGATIONS

Bedside / Clinical Tests

• Semmes-Weinstein 5.07 (10-g) monofilament - gold standard for screening protective sensation loss; 10 sites tested on the foot
• 128 Hz tuning fork - vibration sense assessment
• Probe-to-bone test - positive (bone felt on probing) has 57% PPV for osteomyelitis, 96% NPV; combined with raised inflammatory markers and abnormal X-ray, confirms the diagnosis

Laboratory Investigations

Vascular Investigations

Imaging

• First-line, widely available
• Findings: demineralisation, loss of trabecular pattern, periosteal reaction, joint destruction, soft-tissue gas (gas-producing organisms), foreign bodies
• Limitation: early osteomyelitis is NOT visible on X-ray - takes weeks to months before changes appear

• Most sensitive and specific imaging modality for osteomyelitis
• Distinguishes soft tissue infection from bone involvement and Charcot neuroarthropathy
• T1 shows bone marrow replacement; STIR shows oedema
• Preferred when clinically suspected osteomyelitis with normal/equivocal X-rays
• Limitations: scheduling delays, cost, metal implants

• Useful for bone architecture detail in multiple planes
• Detects subtle cortical disruptions, sequestra, involucrum
• Good for assessing aorta/iliac/femoral vessels in PAD evaluation

• High sensitivity but low specificity (positive in any cause of increased bone turnover)
• Useful when MRI is unavailable

• More specific for osteomyelitis than bone scan
• Helps differentiate Charcot from infection when MRI is equivocal

• Detects soft tissue collections, abscesses, and fluid
• Guides aspiration

MANAGEMENT

A. Glycaemic Control

• Target HbA1c <7%
• Tight glucose control halts progression of neuropathy; prolonged good control can partially reverse it
• Pre-operative glucose <200 mg/dL to minimise surgical complications
• ACE inhibitor for hypertension; statin for dyslipidaemia; aspirin for PAD

B. Prevention (Cornerstone of Treatment)

• Routine foot examination at every clinic visit; daily self-inspection for cuts, fissures, ulcers, callus
• Never walk barefoot; wear well-cushioned protective footwear (avoid sandals)
• Avoid heating pads/hot water bottles on feet (thermal burns)
• Professional toenail trimming
• Callus reduction by podiatrist to unroof occult ulcers
• Regular moisturising of dry skin
• Tobacco cessation

C. Wound Care & Off-loading

• Total contact cast (TCC) - gold standard for off-loading; extends above ankle, reduces plantar pressure by up to 60%; non-removable so patient compliance guaranteed
• Fixed ankle walking boot / Removable walker boot - alternative when frequent dressing changes are needed
• Custom orthotics / therapeutic footwear once healed

• Moist wound environment is the goal (saline- or Vaseline-impregnated gauze changed daily or twice daily)
• Silver-impregnated dressings for infection control
• Foam/cushioning dressings for pressure protection
• Wet-to-dry dressings: classic non-surgical debridement method

• Required when proteinaceous eschar or necrotic tissue inhibits healing
• Methods: wet-to-dry dressings, topical enzymatic debridement, surgical debridement
• Negative pressure wound therapy (VAC therapy): sponge applied to wound and placed on vacuum suction, changed 2-3x/week; promotes angiogenesis, accelerates granulation tissue, decreases healing time; infusion-VAC can deliver local antibiotics
• Medical maggot therapy: selective debridement of non-viable tissue; effective but limited by patient/provider acceptance
• Platelet-derived growth factor (PDGF): topical application for wounds failing other therapies - data supports use

• Increases tissue oxygenation by delivering oxygen-rich plasma
• Promotes angiogenesis within the wound bed
• Best candidates: good perfusion (palpable pulses, normal TBI)
• Multiple treatment sessions required (weeks of therapy)

D. Antibiotic Therapy

• Surface wound swabs are not reliable - they do not reflect deep infection organisms
• Bone biopsy culture is the gold standard and guides targeted therapy
• MRSA cover (vancomycin/linezolid) should be included in severe infections

E. Surgical Management

• Required for collections, necrotic areas, or osteomyelitis
• All non-viable tissue debrided at initial operation
• Wounds generally left open to drain and heal by secondary intention

• For deep-space abscess; explore for extensions and bony involvement

• Metatarsal head resection - reduces abnormal pressure and ulcer recurrence
• Achilles tendon lengthening - reduces forefoot pressure
• Arthroplasty/osteotomy - correction of structural deformity

• Superficial osteitis (periosteal only) may not require bone resection
• True osteomyelitis with cortical involvement requires resection of affected bone
• In good perfusion with limited disease: prolonged IV antibiotics may be considered
• Extensive osteomyelitis may require amputation

F. Revascularisation

• Mandatory assessment with ABI/TBI in all patients with poor pulses or non-healing wounds
• ABI >1.3 → non-compressible → use TBI instead
• ABI <0.5 or toe pressure <40 mmHg → refer to vascular surgery
• Revascularisation should precede debridement/amputation when not in septic emergency, to limit resection of ischaemic but potentially viable tissue
• Methods: angioplasty (endovascular, preferred), femoral-popliteal or tibial bypass (open)
• In distal tissue loss, pulsatile in-line flow to the foot must be restored
• Digital subtraction angiography remains the gold standard for infrageniculate assessment

G. Amputation

• Last resort, but often necessary
• Minor amputations: toe, ray (toe + metatarsal) resection
• Major amputations: below-knee (BKA) - preferred for maximal rehabilitation; above-knee (AKA) - reserved for extensive disease
• Wound healing after amputation is unreliable due to neuropathy and vascular compromise
• SVS WIfI classification (Wound, Ischemia, Foot Infection) is used to estimate benefit of revascularisation and risk of amputation
• Excess bone resected to allow tension-free skin closure; consider BKA over ray amputation if extensive peripheral neuropathy is present

H. Treatment of Charcot Neuroarthropathy

• Total contact casting in acute phase
• Elevation (distinguishes from infection - Charcot subsides with elevation)
• No weight bearing until acute inflammation resolves
• Surgical reconstruction for severe deformity causing recurrent ulceration

PROGNOSIS

• 5-year mortality of diabetic foot complications is comparable to many cancers (30.5% for DFU)
• Ulcers <1 cm² - 96% eventually heal without amputation
• Ulcers >3 cm² - only 72% heal without amputation
• Infected + ischaemic ulcers: 90x more likely to require amputation
• Up to one-third of patients with deep infections eventually undergo amputation

Sources: Fischer's Mastery of Surgery (8e), Campbell's Operative Orthopaedics (15e 2026), Bailey & Love's Short Practice of Surgery (28e), Goldman-Cecil Medicine, Rosen's Emergency Medicine.

Recent evidence note: A 2024 systematic review (PMID 39241769) confirms negative pressure wound therapy (NPWT/VAC) significantly improves healing rates in DFUs compared to standard care (RCT-level evidence). Smart wearable technology for pressure monitoring shows promise for prevention (PMID 40682082, 2025 systematic review).