Diabetic Foot

Epidemiology

Pathophysiology

1. Peripheral Neuropathy (most important)

• Glycosylation of hemoglobin, proteins, and arterial walls
• Thickening of basement membranes and reduced endothelial nitric oxide activity
• Epineural vessel atherosclerosis and multifocal ischemic proximal nerve lesions
• Metabolic effects: sorbitol accumulation, enzyme deficiencies, increased oxygen-free radical activity

• Sensory: Loss of protective sensation - the inability to feel a 10g Semmes-Weinstein monofilament is one of the most predictive risk factors for foot morbidity
• Motor: Muscle imbalance with weak intrinsic muscles overpowered by stronger extrinsic muscles → hammer toes, claw toes, distal migration of the fat pad; gastrosoleus contracture increases forefoot force loads
• Autonomic: Loss of skin oils → fissuring and skin breakdown; increased susceptibility to trauma

2. Peripheral Arterial Disease (ischemia)

• Diabetics are twice as likely to develop peripheral arterial disease
• Diabetics with PAD are nine times more likely to develop a foot ulcer
• Glycosylated end products deposit in arteriolar walls, impairing perfusion
• Results in ischemic ulcers and severely impairs healing

3. Immune Dysfunction

• Altered chemotaxis of polymorphonuclear cells
• Cell wall abnormalities increase susceptibility to infection
• Hyperglycemia impairs the normal immune response

Clinical Features

Severe diabetic foot infection with necrosis - Bailey & Love's Surgery 28e

Fixed flexion deformities from motor neuropathy - Campbell's Operative Orthopaedics 15e

• Plantar ulceration (typically under metatarsal heads) often surrounded by callus
• Ulceration of the calcaneum and forefoot bones
• Hammer/claw toes, skin fissuring
• Cellulitis, pus, crepitation (gas-producing organisms)
• Charcot foot (neuroarthropathy): repeated undetected fractures destroy normal foot architecture, causing the classic "rocker bottom" deformity

Ulcer Classification

Wagner Classification (most widely used)

Diagnosis and Investigations

Neurological Assessment

• Semmes-Weinstein 5.07 monofilament (10g): inability to feel this is a major risk factor
• Equivalent results can be obtained using a 4.5g monofilament under both first metatarsal heads

Vascular Assessment

• Ankle-Brachial Index (ABI): Normal 0.9-1.2; >1.3 suggests non-compressible calcified vessels; <0.5 indicates ulcer unlikely to heal without vascular intervention
• Ankle systolic pressure >60-90 mmHg is required for healing
• Toe pressures are more reliable when vessels are non-compressible (distal vessels often spared); absolute toe pressure >40 mmHg associated with wound healing; normal toe/brachial index >0.7

Lab Tests

• Blood tests are often unhelpful - inflammatory markers may be normal or only mildly raised
• CBC, ESR, CRP - useful for baseline in suspected infection
• HbA1c - higher levels are an independent risk factor for ulcer development; HbA1c >7% associated with higher surgical complications
• Blood glucose >200 mg/dL preoperatively increases risk of nonunion, infection, wound healing problems

Microbiology

• Superficial swabs from ulcers/sinus tracts are not reliable for identifying deep infection organisms
• Bone biopsy for culture should be considered in extensive or complex infection
• The "probe-to-bone" test combined with elevated inflammatory markers and abnormal plain radiographs confirms osteomyelitis

Imaging

Microbiology of Diabetic Foot Infections

• Mild infections: Gram-positive cocci predominate - S. aureus (including MRSA) and β-hemolytic streptococci
• Severe/deep infections: Polymicrobial - aerobic gram-positive cocci + gram-negative bacilli + anaerobes
• Pseudomonas is over-represented; empirical therapy for severe infections should cover it
• Anaerobes: consider adding metronidazole, particularly for abscesses and devitalized tissue

Management

General Principles

1. Tight glycemic control (HbA1c <7%)
2. Strict non-weight-bearing regimen
3. Meticulous wound care
4. Pressure off-loading

Wound Management

• Debridement of necrotic tissue is mandatory
• Pressure off-loading: special shoes, orthotics, or total-contact casting
• Wound size at 4 weeks is predictive: ≥50% reduction in 4 weeks = significantly higher healing at 12 weeks
• Ulcers <1 cm² heal without amputation in 96% of cases; ulcers >3 cm² only in 72%

Antibiotics

Vascular Intervention

• Full vascular assessment is mandatory in those with poor peripheral pulses
• Proximal angioplasty or bypass surgery to improve distal vascularity may be needed before wound surgery
• ABI <0.5 generally requires revascularization before ulcer management

Additional Treatments

• Negative-pressure wound therapy (NPWT): evidence supports use in diabetic foot ulcers (2024 meta-analysis, PMID: 39241769)
• Advanced wound dressings: a 2024 Italian guidelines meta-analysis evaluated various dressings vs. standard of care (PMID: 38864979)
• Bioengineered skin substitutes, autologous leukocyte/platelet preparations
• Hyperbaric oxygen: some efficacy in complicated infections, especially with anaerobic organisms
• Smart wearable technology for pressure monitoring is an emerging area (PMID: 40682082)

Surgical Management

• Debridement/drainage of collections, necrotic areas, or extensive osteomyelitis
• Distinguish superficial osteitis (loss of soft tissue cover) from deep osteomyelitis - in the former, antibiotics and biopsy may be less important than glycemic control + vascular supply + pressure relief
• Amputation: up to one-third of patients with deep infections eventually require amputation
  • Excision must be adequate to remove all infected material
  • Excess bone resection may be needed to allow tension-free closure
  • If extensive peripheral neuropathy, below-knee amputation in a sensate zone may be more appropriate than foot surgery with poor wound healing

Charcot Neuroarthropathy

• Results from repeated undetected micro-fractures in the insensate foot
• Destroys normal foot architecture → classic "rocker bottom" or Charcot deformity
• X-ray is the imaging modality of choice to stage progression
• Midfoot joint pressures are 46% higher in diabetic cadaver feet during simulated walking
• Treatment: off-loading, total-contact casting, surgical stabilization in select cases

Prevention

• Routine foot examination at every medical visit for those with sensory loss
• Daily self-inspection for cracks, fissures, ulcers, or inflammation
• Avoid walking barefoot (even at home); wear protective footwear (avoid sandals)
• Avoid heating pads or hot-water bottles on the feet (thermal injury risk)
• Referral to foot care specialist for sensory loss, foot deformity, extensive callus, or nonhealing ulcers
• Maintain HbA1c <7% to reduce neuropathy progression

• Bailey & Love's Short Practice of Surgery 28e, pp.628-629
• Campbell's Operative Orthopaedics 15e, pp.5054-5059
• Goldman-Cecil Medicine International Edition, p. (Diabetic Foot chapter)
• Rosen's Emergency Medicine 9e, pp.2540-2541