Diabetic foot

Incidence

25% of diabetics during lifetime

Pathophysiology

Risk factors

Poorly controlled diabetes
Vascular insufficiency
- Involved in 50% of diabetic foot ulcers and 70% of the mortality from ulcers
- Infra-popliteal occlusive disease with heavy calcification is the classic picture
- Higher risk of digital artery disease - can get digital ulceration even with palpable pedal pulses
- Also, femoral artery disease occurs in an equal incidence with the non-diabetic population
- Tibial revascularisation, in the angiosome in which the ulceration is located, is possible in the vast majority of diabetic patients to overcome foot ischaemia
Peripheral neuropathy
- Glycation-induced metabolic and vascular changes of nerve fibres
- Somatic
  - Unperceived foot trauma
    - Small-fibre neuropathy - burning, tingling, radiating electrical shock. Unable to perceive temperature differences.
    - Large-fibre neuropathy - numbness, tingling, formication. This is the one that leads to 'loss of protective sensation' and gradual injury. Assess with tuning fork, monofilament, or Achilles deep tendon reflexes.
    - Sensory impairment begins distally and progresses back from toes to ankle and legs.
  - Motor impairments expose patients to pressure injury
    - Unbalanced muscle pairs in foot
    - Contributes to hammer toe, hallux abductovalgus
  - Seen in combination with neuropathy - patchy hypoaesthesia, diminution of positional sense, two-point discrimination and vibratory perception
- Autonomic
  - Caused by increase in sympathetic tone.
  - Dysregulation leads to A-V shunting, small vessel ischaemia, and changes in soft tissue turgor (that leads to xerosis and fissuring, with subsequent ulcer formation).
  - Reduced sweating accompanied by dry, fragile skin
  - Charcot neuroarthropathy is a complication of autonomic neuropathy.
  - Need to treat this with frequent moisturising and compression stockings.
Impaired immune function
Soft tissue infection
- PEDIS (perfusion, extent, depth, infection and sensation)
Biomechanical abnormalities
- Check reducibility of any biomechanical deformity. Typically there is a progression from reducibility to non-reducibility.
- Reducible or semi-reducible deformities can be treated with soft tissue corrections such as tendon lengthening and rerouting. For example, achilles tendon lengthening reduces plantar forefoot pressures.
- Non-reducible deformities will require skeletal reconstruction
- Charcot neuroarthropathy
  - Complication of the diabetic foot process with devastating consequences
  - Pathophysiology
    - Initial resorptive phase
      - Peripheral neuropathy - loss of proprioception, autonomic neuropathy
      - Joint damage which induces pro-inflammatory cytokines and enhanced osteoclastic activity.
    - Hypertrophic repair phase - damaged joint replaced by abnormal bone and cartilage. Altered anatomy predisposes to additional damage.
  - Classification - Eichenholz:
    - Stage 0: Early/inflammatory. Warm, swollen, often painful foot
    - Stage 1: Development. Fragmentation/destruction, bony cysts, erosions
    - Stage 2: Coalescence. Joint subluxations
    - Stage 3: Remodelling. Arch collapse and coalescence
  - Presentation
    - Acute Charcot foot (acute diabetic neuroarthropathy/stage 0): classic presentation is oedema, erythema and heat with fractures and dislocations across joints of the foot or ankle. Often no wound or ulcer to explain the findings. WCC and CRP are typically normal.
    - Chronic Charcot foot: deformities, joint damage, ulceration from weightbearing on ill-suited parts of the foot.
  - Needs to be recognised early for immobilisation and NWB

Peripheral oedema
Plantar callus formation
Nephropathy
Age and longer duration of diabetes

Microbiology

Acute, superficial infections in antibiotic naïve patients
- Staph aureus
- Beta haemolytic strep
Chronic wounds
- Aerobic gram negative
- Anaerobic
- MRSA

Presentation

Severe/necrotising infections: cutaneous blistering, gas formation, skin discolouration, malodourous discharge
Charcot's arthropathy
- Unilateral, hot, swollen foot should be considered Charcot's foot until proven otherwise
- 'Rocker bottom foot' - severe midfoot plantar pressures
- Needs early offloading and immobilisation
Neuropathic ulcers
- Painless ulcer over pressure points/calluses (plantar surface of 5th MTPJ, base of distal phalanx of the great toe, dorsum of interphalangeal joints of toes with flexion contractures, or callused posterior rim of the heel pad)
- Completely painless
- Bleed with manipulation
- Can be surrounded by chronic inflammatory reaction

History:

Full diabetes history
History of ulcer, including trauma and new footwear
Recent travel
Previous vascular, orthopaedic interventions

Examination:

Ankle should be able to dorsiflex past neutral

Investigation

Start off with x-ray
If high index of suspicion for OM and not seen on x-ray, next step is MRI
PET and labelled white cell scans have the highest diagnostic accuracy for OM

Diagnosis

If no purulence/erythema, and no systemic features of infection, wound is uninfected.

Local extent: Irrigate copiously, and all necrotic tissue and foreign bodies should be removed. Probe wound base for sinus tracts/exposed bone.
- Consider OM if wound greater than 2 square cm, or 3mm deep; presence of 'sausage toe'; ESR > 70; non-healing ulcer after appropriate conservative management; radiographic evidence of bony destruction below ulcer. If bone is grossly exposed, there's little benefit to imaging.
- Most of the time when you can probe to bone, OM is present
Microbiology: Superficial cultures are only useful if probability of infection is high. It will most likely grow bacteria at any time, but it will only be a useful bacteria if you get the right one. Cultures from wound base after curette are more likely to be helpful.
Patient risk factors: Baseline vascular disease - thorough pulse examination, ABI (if >1.3, probably need to do pulse volume recordings, toe-brachial index, toe pressure)

General principles of management (in order)

Deal with urgent wound debridement (urgent OT for tracking abscesses, wet gangrene, gas in the tissue). If no urgent indication for debridement (no significant infection), optimise other factors first.
Evaluate need for revascularisation. The axiom is, restore pulsatile flow to the foot.
Manage wound and comorbidities
Discharge with plan to prevent recurrence

Inpatient treatment

Indications for admission
- Sepsis
- Severely infected wounds - tracking abscesses, wet gangrene, gas in the tissue
  - Note that dry gangrene with a bit of tracking cellulitis would not NECESSARILY need same-day debridement/amputation
- Suspected manifestation of CLTI needing inpatient evaluation and management
Wound debridement
- The aim is to convert a stagnant wound into an acute healing wound
- Remove abnormal tissue (hyperkeratotic epidermis, necrotic dermal tissue, foreign debris, bacteria) to promote a moist and healthy wound bed
- Sharp, surgical, enzymatic, autolytic, mechanical, ultrasonic, hydrosurgical
- Indications for debridement in theatre:
  - Anxious patient
  - Extensive debridement required
  - Unclear extent of infection
- Dressings:
  - Nonadherent occlusive dressings and melolite in between toes
  - VAC dressings are effective
  - Generally want something that will donate moisture to the wound bed, because neuropathic ulcers produce little exudate. Hydrogels like sorbact gel are good.
Vasculopathy
- Indications for treating PAD in diabetics:
  - Lifestyle limiting claudication
  - Rest pain
  - Tissue loss
- Investigation:
  - If no pedal pulses, get toe pressures (still useful in diabetics, as microvascular circulation less affected; whereas the ABI is not very useful). TBI >0.6 is predictive of disease healing.
  - CT is often difficult to interpret because the below-knee arteries are most affected
- Definitive management:
  - >2 square cm of tissue loss is likely to need a bypass as opposed to endovascular procedure, as per Rutherford's
  - BASIL trial suggested that angioplasty should be used first for patients with life expectancy <2 years, and that bypass is preferred when a vein conduit is available
  - Bypass used is often pop to distal artery such as medial and lateral plantar branches, since tibial arteries are so commonly involved. Autogenous vein is preferred.
Medical issues
- Antibiotics
- Address comorbidities
- Vitamin D supplementation may help for 12 weeks - data to support it
Allied health
- Offloading (single most important step in treatment)
  - Minimises pressure on the wound and prevents ulcers recurring
  - Ideal shoe is a multi-density accommodative insert, seamless inner, extra-depth, rocker-bottom shoe
  - 'Total contact cast' can also be used to treat an active plantar forefoot ulcer
  - Decubitus ulcers of the posterior heel should be offloaded while the patient is supine too
- Diabetes educator
- Podiatry
- Physiotherapy

Outpatient treatment

Indications:
- Stable chronic issues
Wound management
Comorbidities
Allied health
- Offloading
- Podiatry