Diabetic Foot

 

 

UlcerDiabetic Heel Abscess Xray

 

Diabetic Foot Complications

 

Diabetic foot infections

Diabetic foot ulcers

Charcot arthropathy

 

Epidemiology

 

5 year mortality

- diabetic foot ulcer 30%

- diabetic amputation 70%

 

20% of patients with diabetic foot ulcer will undergo an amputation

 

Pathophysiology 

 

1. Neuropathy

2. Peripheral vascular disease

3. Immunopathy

 

Neuropathy 

 

Most important factor in foot disease caused by

- glycosylation of nerves

- ischaemia

 

Sensory Autonomic Motor
Stocking distribution

20 – 40% of Diabetics

Loss of intrinsic muscle balance

Semmes Weinstein 5.07 monofilament

- applies 10gm of force

- tip pressed against skin until starts to bend

- patient asked if they can feel it

- 90% of patients who are able to feel won’t ulcerate

Skin dry / scaly / cracked  

Easier access for bacteria

Claw and hammer toes

Increased risk of plantar ulcers

 

Peripheral vascular disease

 

50% of diabetic foot ulcers have peripheral vascular disease

 

Large Vessel Disease Small vessel disease

Different to non diabetic population

- younger age

- at or below knee

- diffuse and longer occlusions

Microangiopathy

 

Vascular claudication

Hindfoot ulcers

Delayed ulcer healing

 

Immunopathy

 

Good blood sugar control and nutrition improves healing 

- HbA1C

- total protein > 6 g/dl or 60 g/L

- albumin > 3.5 g/dL or 35 g/L

- lymphocyte count > 1500 /mm3

- transferrin < 200mg/dl

 

Management

 

Multidisciplinary approach

 

Endocrinologist +/- diabetic nurse - glycemic control crucial

Podiatrist - non-surgical debridement / orthoses

Plaster technicians - total contact cast

Vascular surgeon

Orthopedic surgeon - total contact cast / surgical debridement / foot reconstruction / amputation

Infectious disease consultant - infections / non healing ulcers

 

Diabetic Foot Care

 

Daily foot hygiene

No walking barefoot

Immediate attention to blisters / ulcers

Custom shoes / orthoses

 

Infections

 

Microbiology Antibiotics

Acute mild infections

- usually mono microbial

- commonly S Aureus, Strep

Combination oral antibiotics

- Augmentin Duo Forte

- Cephalexin plus Metronidazole 

- Ciprofloxacin plus Clindamycin (Penicillin Allergy)

Chronic infections / ulcers

- polymicrobial

- gram positive cocci (Staph; Group B Strep)

- gram negative (E Coli; Pseudomonas)

- Anaerobes (ischaemic limbs, Bacteriodes fragilis)

Severe infections

- intravenous antibiotics

- Timentin / Pip-Taz

- Ciprofloxacin

- Clindamycin

 

Diabetic foot ulcers

 

Wagner Classification

Grade 0 Grade I Grade II
Pressure area Superficial ulceration

Deep ulceration

Probes to tendon / capsule

Footwear modification

Local treatment

Footwear modification

Total contact cast
Ulcer Ulcer Ulcer

 

Grade III Grade IV Grade V

Deep ulceration +

Secondary infection

Partial foot gangrene Whole foot gangrene
 

Amputation

Hyperbaric oxygen

Amputation
Ulcer Gangrene Gangrene

 

University of Texas Classification

 

Grade Stage

1 Preulcerative

2 Superficial Wound

3 Deep wound penetrating to capsule or tendon

4 Deep penetrating to bone or joint

A Clean

B Non ischemic Infected

C Ischemic Noninfected

D Ischemic Infected

 

Perfusion

 

Ankle Brachial Index (ABI) Transcutaneous O2 Measurement  (TcPO2) Toe Blood Pressure Angiogram

ABI: Ankle / Brachial

Systolic BP at ankle and arm

Normal 0.9 - 1.3

Electrode placed on warmed foot

Affected by edema/ infection / neuropathy

Plethysmography  

<0.9 suggests PVD

May be falsely elevated by calcified vessels

<25 mmHg = unlikely to heal >30 mmHg = good wound healing potential  

 

Wang et al J Vasc Surg 2016

- systematic review

- transcutaneous oxygen measurement predicts wound healing and amputation

- ABI predictive of amputation but not wound healing

 

Infection / osteomyelitis

 

Xray / MRI / probe to bone / ESR > 70

 

Diabetic Heel Abscess XrayDiabetic Heel Abscess MRIDiabetic Heel Abscess MRI 2

Calcaneal osteotomyelitis

 

UlcerdiabetesDiabetes

Diabetic foot ulcer with evidence of underlying osteomyelitis

 

Charcot arthropathy

 

Charcotcharcot

Midfoot ulcer with evidence of underlying Charcot arthropathy and midfoot collapse

 

www.boneschool.com/charcot-foot

 

Nonoperative management 

 

Options

 

Treat infection

Wound dressing and ulcer debridement

Offload foot - orthotics / total contact casts / CROW walkers

Hyperbaric oxygen

 

Infection

 

Microbiology Antibiotics

Acute mild infections

- usually mono microbial

- commonly S Aureus, Strep

Combination oral antibiotics

- Augmentin Duo Forte

- Cephalexin plus Metronidazole 

- Ciprofloxacin plus Clindamycin (Penicillin Allergy)

Chronic infections / ulcers

- polymicrobial

- gram positive cocci (Staph; Group B Strep)

- gram negative (E Coli; Pseudomonas)

- Anaerobes (ischaemic limbs, Bacteriodes fragilis)

Severe infections

- intravenous antibiotics

- Timentin / Pip-Taz

- Ciprofloxacin

- Clindamycin

 

Wound care and Ulcer debridement

 

Debridement

 

Wilcox et al JAMA Dermatol 2013

- 150,000 wound debridements

- increased healing with weekly (55%) versus less frequent debridement (28%)

 

Negative pressure therapy

 

 

 

Offload ulcers

 

Options

 

Total contact cast / Non removable walkers / removable walkers

- spread out force over a larger areag

- can reduce pressure by as much as 80 - 90%

 

Total Contact Cast 1CROW

 

Results

 

Lazzarini et al Diabetes Metabol Res 2024

- systematic review of 194 studies

- increased wound healing with non removable devices (82 v 66%)

- likely due to compliance

 

Operative management

 

Options

 

Surgical debridement

Soft tissue releases - tendoachilles lengthening, toe flexor tenotomy

Bony realignment www.boneschool.com/charcot-foot

Amputations  www.boneschool.com/diabetic-amputations

 

Fractures in Neuropathic / Diabetic feet

 

Principles

 

1.  Augment ankle ORIF

2.  Double time for sutures

3.  Double immobilization period

4.  Brace for 1 year after surgery

- to prevent late Charcot arthropathy

- assume Charcot joint will develop