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Diabetic foot

Section: Skin and soft tissue Sub-section: Skin infections and breakdown Curriculum: Curriculum, page 54

Definition

  • Diabetic foot infection is infection of a foot wound located below the malleoli
    • As defined by the International Working Group on the Diabetic Foot

May manifest as

  • Skin and soft tissue infection +/- ulcer +/- osteomyelitis.
  • Osteomyelitis under an ulcer +/- skin and soft tissue infection.

Pathogenesis

  • Affects distal large vessels – Spares Aorta & Iliacs
  • Hyperglycaemia causes endothelial damage
  • Microvascular Disease Mechanisms
    • Hyperglycaemia → Vasoconstriction, Inflammation & Thrombosis
    • ↓ Endothelial NO (NO causes vasodilation & protects against platelet/leukocyte interaction, hence atherosclerosis)
    • ↑ Release of ROS
    • Advanced Glycation End Products → Impair protein function
    • Calcification of the media – incompressible vessels
    • Thickening of basement membrane of capillaries
  • Macrovascular Disease
    • In TP trunk; cf more proximal disease in non-DM pts
  • Neuropathy
    • Peripheral Neuropathy leads to poor biomechanics & inability to respond to pain
    • Sensory - disease of vasa nervorum
    • Major cause in 90% of diabetic foot problems
    • Often asymptomatic and unnoticed
    • Glove & stocking distribution
    • Can be hyperaesthesia – burning/allodynia or numb/dull sensation
    • Trauma/ necrosis/ ulcers un-noticed
  • Autonomic Dysfunction
    • Reduced sweating therefore dry/cracked foot
    • Open arteriovenous shunts – warm foot with bounding pulses
    • Impaired vasodilation in response to injury / infection
  • Motor
    • Atrophy of small intrinsic muscles → Claw toes (smaller muscles overpowered by stronger ones) → Change of weight distribution → Dislocation of MTP joints → Prominent metatarsal heads
    • New pressure points (plantar aspect of 1st MTP (ball of foot), tips of toes, midfoot from flat feet)
    • Wasting (guttering) between metatarsals
  • Infection
    • Bacteria flourish in excess glucose → Polymicrobial infection
      • Staph & strep 80%
      • Proteus 50%
      • Mirabilis, gram negative
      • Cause of UTI & wound infection
      • Ampicillin/ cephalosporin
      • Bacteroides 50%
      • Gram –ve anaerobe
      • GIT
      • Enterococci
      • Pseudomonas
      • Peptococci
  • Visual impairment ± CVD
    • Contributes to trauma / onset of ulceration
    • ± other medical conditions CVA / IHD with ↓ ability to care for self

Predisposing factos

  • Sensory neuropathy
  • Peripheral neuropathy leading to changes in the foot - Charcot foot etc.
  • PVD
  • Hyperglycaemia - impairs host defenses and neutrophil function

Microbiology

  • Superficial infections - staph aureus, strep agalactiae, GAS
  • Deep infections - more likely to have polymicrobial infection which include enterobacter’s, pseudomonas aeruginosa and other anaerobes.
  • Wound with extensive necrosis - Bacteroides and Clostridium.

Clinical manifestations

  • Usually with pain and erythema.
  • With severe PVD - warmth may be absent
  • With severe neuropathy - pain may be absent.

Evaluating a diabetic foot

History

  • Duration of diabetes, overall glycaemia control, presence of micro/macrovascular disease
  • History of foot injury
  • Claudication symptoms
    • Seldom get claudication as disease mostly infragenicular
  • Smoking
  • History consistent with foot neuropathy - burning pain in feet, wakes at night, worst at night, relived by walking around.

Examination

  • Inspect
    • Lesions between toes, bunions, macerated areas.
    • Claw-foot deformity
    • Look for signs of infection
    • Assess gait
  • Feel
    • Evaluation of pedal pulses
    • Test sensation - Semmes-Weinstein monofilament - 12 sites of the foot. Test vibration at dorsum of first toe just proximal to nail bed.
  • ABPI - normal is 0.9-1.3
    • < 0.9 = PVD
    • < 0.4 = 0.4 critical limb ischaemia
  • PVD examination
  • Ulcer
    • Neuropathic ulcers: occur @ MTP heads or dorsum of toe, foot is typically warm with bounding pulses and distended veins
  • Neuro-ischaemic: occur @ tip of toes, heel and medial aspect of 1st metatarsal
    • No overlying callus, rim of ischaemic tissue around and often necrosis
  • Pain will depend on underlying neuropathy
  • Gangrene – dry (not infected) can be left and will autoamputate eventually
  • Wet gangrene (infected) will require debridement and often amputation
  • Infection: Cellulitis &/or osteomyelitis
  • Systemic signs of infection may be absent
  • Probe to bone – if +ve – PPV for osteomyelitis 50-65%

Prevention/patient education after assessment

  • Stop smoking
  • Avoid going barefoot
  • Test water temperature before stepping into bath.
  • Cut toenails.
  • Wash in lukewarm water.
  • Shoes should be snug.

Diagnosis of osteomyelitis

Features which make osteomyelitis highly likely

  • Visible bone
  • Positive “probe to bone test” (basically means you can stick an instrument straight onto bone through a wound)
  • Presence of a sinus tract.

Tests

  • Xray - cortical erosion, periosteal rection, mixed lucency, sclerosis
  • MRI - don’t need to perform if Xray already shows OM - features are cortical destruction, bone marrow oedema, soft tissue inflammation.
  • High inflammatory markers
  • Bone biopsy - this is the definitive way to diagnose osteomyelitis - also allows cultures to be obtained.

Reasons to get bone biopsy

  • Diagnostic uncertainty
  • Failure of empiric antibiotics - thus concern for antibiotic resistant bugs.
  • Mid or hindfoot lesions that could lead to high-level amputations if treatment fails.

Management of Ulcers

  • MDT
    • Physician, diabetic nurse specialist, physiotherapist, podiatrist, orthopaedic surgeon, vascular surgeon
  • Prevention better than cure
    • Identify ‘at risk foot’ (Neuropathy or absent pulses)
    • Refer to specialized diabetic foot clinic for r/v every 3-6 months
    • Education on foot care and footwear
      • Washing, callus care, foot wear, inspection, toenail cutting by podiatrist
      • Inspect feet
      • Antifungal powder daily
      • No hot water bottles
      • Better foot care → ↓ Amputations
  • Glycaemic control
  • Stop smoking
  • Control other risk factors: HT, Cholesterol

Ulcer classification

University of Texas System - looks at Grade and Stage

Grade

  • Grade 0 - pre-ulcer
  • Grade 1 - full thickness ulcer - not involving tendon, capsule, or bone.
  • Grade 2 - Tendon of capsular involvement without palpable bone.
  • Grade 3 - Probes to bone.

Stage

  • A - non-infected
  • B - infected
  • C - ischemic
  • D - infected and ischaemic

Management by ulcer stage

A - non-infected

  • Debrided at the bedside
  • Wound care
  • Mechanical offloading

B - infected

  • Antimicrobial therapy and surgical debridement
  • Should be managed by a surgeon if infection extends beyond the dermis.
  • Mechanical offloading

C - ischaemic

  • Wound care.
  • Revascularization - either endovascular or open.
  • Mechanical offloading

D - Infected and ischaemic

  • Require Vascular surgical management for treatment of infection and re-vascularization.
  • Mechanical offloading

Adjunctive treatments

  • Negative pressure therapy
  • Skin Grafts
  • Hyperbaric oxygen therapy - indications and efficacy of this treatment is not clear.
  • Topical oxygen therapy
  • Shock wave therapy

Mechanical offloading

  • Total contact cast - padded fibreglass or plaster shell designed to take pressure off the heel and average it across the whole sole of the foot.
  • Orthotic inserts.
  • Knee walker

Management of osteomyelitis

Indication for surgery

  • Many patients require surgery based on the degree of surrounding soft tissue infection - if OM is found the bone should be debrided
  • If there is not clear indication for soft tissue debridement - decision is more nuanced
  • If surgery is performed - important to re-vascularise first (if this is required)

Surgery can be avoided for patients with osteomyelitis who meet the following criteria:

  • Infection confined to forefoot (metatarsals or phalanges)
  • Soft tissue doesn’t require debriding
  • No exposed bone

Extent of surgery

  • Surgery involves either bone debridement, bone resection, or amputation.
  • Need to way up loss of foot function vs leaving behind infected bone.
  • Bone cultures should be obtained.

Antibiotics

  • Typically 6 weeks - often IV - depends on amount of residual bone is left and how infected it is.
  • In the setting of amputation - you don’t need any futher abx.

Charcot foot

  • 10% of pts with neuropathy and up to 20% with neuropathic ulceration
  • Destruction of weight-bearing joint – MTP, TMT, Ankle
  • Due to inflammatory arthropathy triggered by recurrent trauma
    • Sprain/fracture-dislocation of foot & ankle in pts with neuropathy often after unrecognized trauma
  • Acute phase: red, hot, swollen, oedematous, painful foot
    • Confused with infection but NO wound
    • Midfoot usually involved
    • May last for months-years
    • Result in ↑ bone formation, sclerosis & arthrodesis
    • Rx: Off-loading pressure area, prevent further trauma and protect skin
    • Best healing with total cast immobilization (> 6/12)
    • Some benefit with Pamidronate
  • Quiescent phase:
    • Rx: Custom-made footwear ± orthopaedic surgery
  • Treatment is based on
    1. Offloading ALL mechanical pressure off the foot
    2. Minimising the inflammatory cascade (NSAIDS)
    3. Minimising osteoclastic activity (Pamidronate)

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