Diabetic Foot

Two Main Problems

1. Ulceration & Infection
   
2. Charcot Arthropathy

Pathophysiology

• Diabetes causes polyneuropathy, affecting sensory, autonomic, and motor nerves
  
• Sensory neuropathy predominates
  • Glove and stocking distribution, progressing from distal to proximal
    
  • Hyperglycemia and micro-vessel disease alter axoplasmic blood flow
    
  • Abnormal collagen cross-linking leads to stiffer tendons
    • Contributes to Achilles contracture
      
• Autonomic neuropathy reduces sympathetic activity
  • Warm, pink, and dry skin due to altered sweating
    
• Motor neuropathy is less dominant
  • Primarily affects tibialis anterior and intrinsics
    
  • Leads to equinus contracture and claw toes
    • Deformity increases cutaneous foot pressures

Susceptibility to Infection

• Main issue is decreased ability to combat infection
  
• Infections are invariably contiguous through skin breaks, rarely haematogenous

Risk Factors for Skin Breaks

• Dry skin susceptible to cracking
  
• Areas of high pressure – MT heads & equinus contracture
  
• Ulcers form due to impaired healing of fissures
  • Neutrophil function impaired
    
  • Microvascular blood flow decreased
    
• Osteomyelitis results from contiguous deep spread of infection
  • 67% (2/3) of ulcers probed to bone will have osteomyelitis

Pathophysiology of Charcot

• Exact cause unknown, but related to neuropathy
  
• Three theories:
  • Neurotraumatic theory
    • Loss of protective sensation and proprioception
      
    • Repetitive microtrauma leads to uncontrolled deformity
      
  • Neurovascular theory
    • Autonomic neuropathy causes hyperaemia
      
    • Hyperdynamic circulation alters bone resorption and synthesis balance
      
  • Inflammatory theory (favored)
    • Injury triggers an inflammatory cascade in susceptible patients
      
    • Osteoclast activation leads to abnormal bone resorption and remodeling
      
    • Loss of protective sensation allows deformity to progress
      
• Most commonly seen in diabetics but also found in:
  • Syphilis (historically, more common in knee)
    
  • Alcoholic neuropathy
    
  • CVA
    
  • Spina bifida
    
• Trauma is often the inciting event
  • May be remembered or subclinical
    
• Overactivity of osteoclasts and fracture healing cascade activation
  
• Deformity and arthrosis progress unchecked due to loss of neurologic protection
  • Predominantly affects midfoot but can occur anywhere

Classification

Wagner Classification of Diabetic Foot Ulcers

• Grade 0: No ulcer but foot deformity at risk of ulceration
  
• Grade 1: Superficial ulcer
  
• Grade 2: Deep ulcer with visible bone or tendon
  
• Grade 3: Deep ulcer with abscess or osteomyelitis
  
• Grade 4: Ulcer with gangrene limited to the forefoot
  
• Grade 5: Ulcer with gangrene of the whole foot

At each grade, management is influenced by:
- Vascularity of the foot
- Presence of infection

Eichenholz Classification of Charcot Foot

• Stage 0 (Pre-fragmentation): Acutely inflamed, painful foot with regional bone demineralization
  
• Stage 1 (Fragmentation): Painful, peri-articular fragmentation and joint dislocation, demineralization
  
• Stage 2 (Coalescence): Less painful, sclerosis, and bone resorption
  
• Stage 3 (Remodeling): Pain-free, malunited, ankylosed joints

Clinical Evaluation

History

• Ulcer-related factors: Pain, discharge, chronicity, treatments, previous ulcers
  
• Foot-related factors: Pain, swelling, functional impairment
  
• Diabetes-related factors: Type, control, complications (renal, eye, CV)
  
• PMH: Especially vascular disease

Examination

General Foot Appearance

• Charcot foot: dry, warm, swollen, bounding pulses
  • May resemble infection
    
• General motor exam for large muscle groups

Deformities

• Claw toes – fixed or flexible
  
• Plantar callus formation
  
• Silverskiöld test for Achilles contracture
  • Increases plantar forefoot pressures
    
  • May require release for treatment
    
• Other deformities – hallux valgus, etc.

Establishing Peripheral Neuropathy

• Semmes-Weinstein testing
  • Monofilament testing at multiple locations
    
  • 10g filament commonly used
    
  • Absence of response to 5.07 filament indicates neuropathy
    
• Two-point discrimination & vibration testing
  
• Light and sharp touch testing

Ulcer Examination

• Clear surrounding callus to expose ulcer
  
• Assess discharge – pus, blood, etc.
  
• Probe with sterile instrument – if down to bone, 67% chance of osteomyelitis

Vascular Examination

• Pulses
  • May be bounding due to calcified arteries & sympathetic neuropathy
    
  • Absence is a poor indicator – use Doppler
    
• ABPI

  • 0.8 is normal

  • 0.45 required for wound healing

• Transcutaneous oxygen saturation
  • 40 is normal, <25 indicates high breakdown risk

Investigations

Blood Tests

• FBC, CRP, U&E, HbA1c
  • CRP, ESR, and WCC may be elevated in infection or Charcot
    
  • Poor differentiators individually
    
  • Trends useful in established infection
    
• HbA1c
  • Indicates glucose control over past 3 months
    
  • Normal upper limit ~6.5%

Imaging

• X-rays (standing AP, lateral, oblique)
  • Established osteomyelitis visible
    
  • Charcot stages 1-3 clearly apparent
    
• MRI
  • Useful for early osteomyelitis but high false positive rate
    
  • Good for abscess detection
    
• Bone scan
  • Increased uptake in early Charcot before X-ray findings
    
  • Poor specificity for infection vs. Charcot vs. osteomyelitis
    
• WBC-labeled scan
  • More specific for osteomyelitis
    
• PET scan
  • Sensitive but expensive and not widely available

Diagnosing Infection

• Exposed bone through an ulcer is likely osteomyelitis until proven otherwise
  
• Superficial cultures are unreliable due to polymicrobial contamination
  
• Bone biopsy is the gold standard

Differentiating Between Infection and Charcot

• Main differentiator: presence of an ulcer
  
• If no ulcer, infection is highly unlikely
  
• Infection in diabetics is contiguous, not haematogenous
  
• PET, MRI, or WBC-labeled scan may help
  
• Bone biopsy is the gold standard

Management

Prevention

• Education, accommodative footwear, padding for high-risk feet, good diabetic control

Simple Non-Infected Ulcers

• Optimize diabetic control
  
• Optimize vascular perfusion
  
• Offload the ulcer
  
• Reduce mechanical risk factors
  
• Total Contact Cast (TCC) is ideal for offloading
  
• Consider Achilles lengthening or claw toe correction if contributing

Risk Factors for Treatment Failure:
- Large ulcers (>2 cm)
- Wagner Grade 3 ulcers (deep with abscess/osteomyelitis)
- Ulcer duration >2 months
- Mechanical risk factors (clawing, equinus contracture)

Infected Ulcers

• Optimize diabetic control & vascular flow before surgery
  
• Treatment ladder:
  1. Broad-spectrum antibiotics
     
  2. Debridement and abscess drainage
     
  3. Debridement of osteomyelitis
     
  4. Ray amputations
     
  5. Lisfranc amputation
     
  6. Chopart amputation (if performed, dorsiflexors must be reattached)
     
  7. Below-knee amputation (BKA)

Charcot Management

Early Disease

• Goal: minimize deformity progression
  
• Diabetic control slows progression
  
• Total contact casting to limit deformities
  
• Consider surgical fusion if early instability
  
• Hindfoot nail fusion for hindfoot and ankle involvement

Chronic Charcot

• Non-operative preferred
  • Good diabetic control, education, accommodative footwear
    
• Surgical indications:
  1. Recurrent ulceration
     
  2. Instability
     
  3. Pain
     
  4. Dysfunction due to deformity
     
• Surgical options:
  • Exostectomy
    
  • Corrective osteotomy
    
  • Fusion with osteotomy
    
  • Amputation proximal to Charcot disease