Diabetic Foot

Overview

Diabetic foot disease represents one of the most devastating complications of diabetes mellitus, encompassing a spectrum of pathological conditions including neuropathy, peripheral arterial disease, ulceration, infection, and Charcot neuroarthropathy. [1] The condition affects approximately 19-34% of people with diabetes during their lifetime and remains the leading cause of non-traumatic lower extremity amputation worldwide. [2]

The pathogenesis involves a complex interplay between diabetic peripheral neuropathy, peripheral arterial disease (PAD), and immunopathy, creating a "perfect storm" for tissue breakdown and impaired healing. [3] Prevention through risk stratification, regular screening, and patient education remains the cornerstone of management, while multidisciplinary team (MDT) care is essential for limb salvage in established disease.

Understanding diabetic foot disease is critical for all clinicians, as early recognition and appropriate referral can prevent the catastrophic consequences of delayed treatment. The 5-year mortality following major amputation approaches 50-70%, exceeding that of many common malignancies. [4]

---

Epidemiology

Global Burden

The International Diabetes Federation estimates that 537 million adults have diabetes worldwide, with diabetic foot complications affecting a substantial proportion. [5]

Risk Factors for Ulceration

Non-modifiable Risk Factors:

• Previous ulcer (strongest predictor)
• Previous amputation
• Duration of diabetes > 10 years
• Male sex
• Age > 60 years

Modifiable Risk Factors:

• Peripheral neuropathy (loss of protective sensation)
• Peripheral arterial disease
• Foot deformity (hammer toes, bunions, Charcot)
• Poor glycaemic control (HbA1c > 8%)
• Visual impairment
• Chronic kidney disease
• Inappropriate footwear
• Tobacco smoking

IWGDF Risk Stratification System

The International Working Group on the Diabetic Foot (IWGDF) 2023 guidelines recommend stratified screening based on risk category. [10]

LOPS = Loss of Protective Sensation; PAD = Peripheral Arterial Disease

---

Pathophysiology

The Pathogenic Triad

Diabetic foot disease results from the convergence of three key pathological processes. [3,11]

1. Diabetic Peripheral Neuropathy (Most Common - 60-70%)

Diabetic peripheral neuropathy (DPN) affects sensory, motor, and autonomic nerve fibres through multiple mechanisms.

Metabolic Mechanisms:

• Polyol pathway activation: Hyperglycaemia leads to aldose reductase-mediated conversion of glucose to sorbitol, causing osmotic stress and NADPH depletion
• Advanced glycation end-products (AGEs): Non-enzymatic glycation of proteins leads to structural and functional nerve damage
• Protein kinase C activation: Altered vascular permeability and basement membrane thickening
• Oxidative stress: Mitochondrial dysfunction and reactive oxygen species accumulation
• Hexosamine pathway: Altered gene expression affecting nerve function

Clinical Manifestations by Fibre Type:

Diagnostic Criteria for DPN (Toronto Consensus):

• Possible DPN: Symptoms OR signs
• Probable DPN: Symptoms AND signs
• Confirmed DPN: Abnormal nerve conduction studies + symptoms or signs
• Subclinical DPN: Abnormal nerve conduction studies alone

2. Peripheral Arterial Disease (Present in 50% of DFU)

PAD in diabetes has distinctive characteristics compared to non-diabetic atherosclerosis. [12]

Distinguishing Features of Diabetic PAD:

• Predominantly affects infrapopliteal (tibial) vessels
• More diffuse, multisegment involvement
• Heavy arterial calcification (Monckeberg's sclerosis)
• Falsely elevated ankle-brachial index due to incompressible vessels
• Collateral vessel development often impaired
• Microangiopathy contributing to impaired perfusion

Pathophysiological Mechanisms:

• Endothelial dysfunction with reduced nitric oxide bioavailability
• Platelet hyperreactivity and procoagulant state
• Increased inflammatory mediators (IL-6, TNF-alpha)
• Accelerated atherosclerosis
• Impaired angiogenesis and collateral formation

3. Immunopathy and Impaired Wound Healing

Diabetes impairs multiple components of the immune response and wound healing cascade. [13]

Immune Dysfunction:

• Impaired neutrophil chemotaxis, phagocytosis, and bactericidal activity
• Reduced lymphocyte proliferation
• Impaired cytokine production
• Complement dysfunction
• Biofilm formation facilitation

Wound Healing Impairment:

• Reduced growth factor expression (VEGF, PDGF)
• Impaired keratinocyte and fibroblast migration
• Abnormal extracellular matrix deposition
• Prolonged inflammatory phase
• Impaired angiogenesis
• Chronic wound environment with elevated matrix metalloproteinases

Pathway to Ulceration

NEUROPATHY                           PERIPHERAL ARTERIAL DISEASE
    ↓                                           ↓
Sensory loss → Unnoticed trauma          Tissue ischaemia
Motor loss → Foot deformity              Impaired oxygen delivery
Autonomic loss → Dry skin/fissures       Reduced nutrient supply
    ↓                                           ↓
            MECHANICAL STRESS
         (abnormal pressure points)
                    ↓
              TISSUE BREAKDOWN
                    ↓
              ULCER FORMATION
                    ↓
    IMMUNOPATHY + HYPERGLYCAEMIA
                    ↓
    Impaired healing + Infection susceptibility
                    ↓
    DEEP TISSUE INFECTION / OSTEOMYELITIS
                    ↓
              GANGRENE / AMPUTATION

Ulcer Phenotypes

Understanding ulcer aetiology guides management. [14]

Clinical Pearl: Key Clinical Point: Most diabetic foot ulcers are neuroischaemic rather than purely neuropathic. Always assess vascular status even in the presence of neuropathy.

---

Clinical Assessment

History

Essential History Components:

1. Diabetes History

   • Type and duration of diabetes
   • Glycaemic control (recent HbA1c)
   • Other microvascular complications (nephropathy, retinopathy)
   • Current medications (especially insulin, SGLT2 inhibitors)

2. Foot History

   • Previous ulcers (number, location, healing time)
   • Previous amputations (level, year)
   • Previous revascularisation procedures
   • Current symptoms (pain, numbness, tingling)

3. Current Problem

   • Duration of ulcer
   • Precipitating event (trauma, new footwear)
   • Progression of symptoms
   • Systemic symptoms (fever, rigors, confusion)

4. Vascular Symptoms

   • Intermittent claudication (walking distance)
   • Rest pain (nocturnal, relieved by dependency)
   • Previous vascular intervention

5. Social Factors

   • Smoking history
   • Alcohol use
   • Living situation and support
   • Ability to inspect feet/perform self-care
   • Footwear practices

Physical Examination

General Inspection

• General health status
• Signs of systemic infection (fever, tachycardia, hypotension)
• Nutritional status
• Cognitive function (affects self-care ability)

Foot Inspection

• Skin condition (dry, cracked, macerated)
• Callus formation and location
• Nail abnormalities (onychomycosis, ingrown nails)
• Foot deformities (claw toes, hammer toes, bunions, Charcot)
• Interdigital spaces (fungal infection, maceration)
• Signs of ischaemia (dependent rubor, elevation pallor)
• Previous amputation sites

Wound Assessment

Systematic wound documentation using the following parameters:

Neurological Assessment

10-Gram Monofilament Testing [15]

• Standard screening tool for loss of protective sensation (LOPS)
• Test sites: plantar 1st, 3rd, and 5th metatarsal heads; great toe pulp; heel
• Technique: Apply perpendicular force until filament bends (10g), hold 1 second
• Positive result: Loss of sensation at ≥1 site indicates LOPS
• Sensitivity 66-91%, Specificity 34-86% for predicting ulceration

Ipswich Touch Test

• Simple alternative: Lightly touch tips of 1st, 3rd, and 5th toes for 1-2 seconds
• Sensitivity 77%, Specificity 90% compared to monofilament

128 Hz Tuning Fork

• Assesses large fibre (vibration sense) function
• Apply to bony prominence (1st MTP joint, medial malleolus)
• Patient indicates when vibration stops; compare to examiner's perception

Ankle Reflexes

• Absent ankle jerks indicate neuropathy (but can be normal age-related finding)

Semmes-Weinstein Monofilament Sites:

        (1)         (3)         (5)
         ○           ○           ○
    1st MTP     3rd MTP     5th MTP
         
              (Toe)
                ○
           Great toe
           
              (Heel)
                ○
              Heel

Vascular Assessment

Pulse Palpation

• Femoral, popliteal, posterior tibial, dorsalis pedis
• Document as present, diminished, or absent
• Absent pedal pulses: ~10% of normal population; higher significance in diabetics

Ankle-Brachial Index (ABI)

Exam Detail: ABI Limitations in Diabetes:

• Medial arterial calcification causes falsely elevated ABI in 30% of diabetics
• Cannot compress calcified vessels → ABI > 1.40 or "incompressible"
• Use alternative methods: toe-brachial index (TBI), transcutaneous oxygen (TcPO2), or skin perfusion pressure (SPP)

Toe-Brachial Index (TBI)

• More reliable in calcified vessels (digital arteries rarely calcified)
• Normal: ≥0.70
• Suggestive of PAD: less than 0.70
• Critical ischaemia: less than 0.25

Transcutaneous Oxygen Pressure (TcPO2)

• Measures tissue oxygenation at forefoot
• Normal: > 60 mmHg
• Impaired healing: less than 40 mmHg
• Critical ischaemia: less than 25 mmHg
• Predicts wound healing potential

Skin Perfusion Pressure (SPP)

• Normal: > 40 mmHg
• High amputation risk: less than 30 mmHg

---

Classification Systems

Wagner Classification (1981)

The Wagner classification grades ulcers by depth and infection. [16]

Limitations of Wagner:

• Does not account for ischaemia
• Does not quantify infection severity
• Limited prognostic value

University of Texas Classification (UT)

More comprehensive than Wagner, incorporating ischaemia and infection. [17]

Prognostic Value:

• Stage A: 90% heal without amputation
• Stage D: Only 40% heal without amputation
• Each stage progression increases amputation risk 2-fold

SINBAD Classification

Simple scoring system for audit and research. [18]

Interpretation: Score 0-6; higher scores indicate poorer prognosis

PEDIS Classification (IWGDF)

Developed by IWGDF for research purposes but useful clinically. [19]

IDSA/IWGDF Infection Classification

Standard for diabetic foot infection (DFI) severity grading. [8,20]

SIRS Criteria (≥2 required):

• Temperature > 38°C or less than 36°C
• Heart rate > 90 bpm
• Respiratory rate > 20/min or PaCO2 less than 32 mmHg
• WBC > 12,000 or less than 4,000 or > 10% bands

---

Investigations

Laboratory Studies

Clinical Pearl: ESR in Osteomyelitis: An ESR > 70 mm/hr has a sensitivity of 83% and specificity of 77% for osteomyelitis. Combined with positive probe-to-bone test, this combination has > 90% positive predictive value. [21]

Wound Culture

Principles:

• Superficial swabs reflect colonisation, not true pathogens
• Deep tissue cultures (curettage, biopsy) are gold standard
• Obtain BEFORE starting antibiotics when possible
• Send for aerobic and anaerobic culture

Technique:

1. Cleanse wound with saline (not antiseptic)
2. Debride necrotic tissue
3. Obtain sample from base of wound by curettage or deep tissue biopsy
4. Transport in appropriate medium (anaerobic if needed)

Imaging

Plain Radiography (First-Line)

Sensitivity for Osteomyelitis: 54% (poor for early disease) Specificity for Osteomyelitis: 68%

MRI (Gold Standard for Osteomyelitis)

• Sensitivity: 90-93%
• Specificity: 75-83%
• Can detect osteomyelitis within days of onset

MRI Findings in Osteomyelitis:

• T1-weighted: Decreased marrow signal (fat replaced by infection)
• T2/STIR: Increased signal (oedema)
• Post-gadolinium: Enhancement of infected bone and soft tissues

MRI Findings in Charcot:

• Subchondral bone oedema
• Joint effusion
• Bone fragmentation
• Can be difficult to distinguish from osteomyelitis (see below)

Differentiating Osteomyelitis from Charcot on MRI

Nuclear Medicine Studies

Three-Phase Bone Scan:

• Sensitive but not specific (cannot differentiate Charcot from osteomyelitis)
• Useful when MRI contraindicated

Labelled White Blood Cell Scan (In-111 or Tc-99m HMPAO):

• More specific for infection than bone scan
• Sensitivity: 72-100%, Specificity: 67-98%
• Useful for distinguishing Charcot from osteomyelitis

PET/CT (FDG):

• Increasing role in complex cases
• Can identify occult infection
• Useful for monitoring treatment response

Vascular Imaging (When PAD Present)

Probe-to-Bone Test

Simple bedside test for osteomyelitis. [22]

Technique:

1. Use sterile blunt metal probe
2. Insert gently into wound base
3. Positive: Hard, gritty sensation of bone felt

Diagnostic Value:

• Sensitivity: 66-87%
• Specificity: 85-91%
• Positive predictive value: 53-89% (depends on prevalence)
• Negative predictive value: 56-98%

Clinical Application:

• High pre-test probability: Positive PTB confirms osteomyelitis
• Low pre-test probability: Negative PTB reasonably excludes osteomyelitis
• Intermediate probability: Requires MRI for confirmation

---

Diabetic Foot Infection

Microbiology

Understanding typical pathogens guides empirical antibiotic selection. [8,20]

Mild/Superficial Infections (Usually Monomicrobial):

• Staphylococcus aureus (including MRSA)
• Streptococcus spp (Group A, B, and other beta-haemolytic)

Moderate-Severe/Chronic/Previously Treated (Polymicrobial):

Risk Factors for MRSA:

• Previous MRSA colonisation/infection
• Recent hospitalisation
• Chronic wounds
• Haemodialysis
• High local MRSA prevalence (> 10-15%)

Risk Factors for Pseudomonas:

• Water exposure/soaking feet
• Chronic wound
• Previous antibiotic therapy
• Tropical climate

Antibiotic Therapy

Empirical antibiotic selection based on infection severity. [8,20]

Mild Infection (Oral, Outpatient)

Moderate Infection (IV Initially, Step Down to Oral)

Severe Infection (IV, ICU May Be Required)

Antibiotic Duration

Exam Detail: De-escalation Principle:

• Begin with broad-spectrum coverage
• Narrow based on culture results
• Monitor response clinically (wound appearance, inflammatory markers)
• Switch IV to oral when infection controlled, patient stable, GI function adequate

Osteomyelitis Management

Diabetic foot osteomyelitis (DFO) management is complex and often requires combined medical-surgical approach. [21]

Diagnosis Confirmation:

• Clinical suspicion (PTB positive, ESR > 70)
• Imaging (MRI preferred)
• Bone biopsy for culture (gold standard for pathogen identification)

Treatment Approaches:

Bone Biopsy Technique:

• Through intact skin (not through ulcer) to avoid contamination
• Percutaneous or open surgical
• Send for histology AND culture
• Withhold antibiotics 2 weeks prior if clinical condition allows

---

Charcot Neuroarthropathy

Overview

Charcot neuroarthropathy (CN) is a progressive, destructive condition affecting the bones and joints of the foot in patients with neuropathy. [23]

Prevalence: 0.1-0.5% of diabetic patients (likely underdiagnosed)

Key Risk Factors:

• Peripheral neuropathy (essential)
• Diabetes > 10 years duration
• Good vascular supply (required for inflammatory response)
• Previous contralateral Charcot
• Renal transplant recipients
• Obesity

Pathophysiology

Two main theories explain Charcot development:

1. Neurotraumatic Theory:

• Neuropathy → Loss of protective sensation
• Repetitive microtrauma unnoticed
• Cumulative damage to bones and joints
• Progressive destruction

2. Neurovascular Theory:

• Autonomic neuropathy → Increased blood flow
• Bone resorption through osteoclast activation
• Osteopenia → Fractures and joint destruction

Current Understanding (RANKL Pathway):

• Trauma in neuropathic foot triggers inflammatory cascade
• Increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6)
• RANKL upregulation → Osteoclast activation
• Osteoprotegerin (OPG) downregulation
• Unopposed bone resorption
• Progressive destruction

Anatomical Classification (Sanders & Frykberg)

Clinical Stages (Eichenholtz)

Diagnosis

Clinical Features (Acute Charcot):

• Unilateral hot, swollen, erythematous foot
• Temperature difference > 2°C compared to contralateral foot
• Often minimal or no pain (neuropathy)
• May follow minor trauma
• Preserved pulses

Clinical Pearl: Acute Charcot vs Cellulitis/Osteomyelitis: This is a critical differential diagnosis. Misdiagnosis leads to inappropriate treatment.

Investigation:

• Plain radiographs: May be normal in Stage 0; fragmentation/destruction in Stage I
• MRI: Bone oedema, joint effusion; helps differentiate from osteomyelitis
• Bone scan: Increased uptake in all phases
• Labelled WBC scan: Cold or minimally increased (osteomyelitis shows increased)

Management of Charcot Neuroarthropathy

Acute Phase (Stage 0-I):

Bisphosphonates:

• Theoretical benefit (inhibit osteoclast activity)
• Limited evidence; small RCTs show conflicting results
• Not routinely recommended by IWGDF 2023
• Consider in refractory cases

RANKL Inhibitors (Denosumab):

• Emerging therapy
• Case reports and small series show benefit
• Not standard of care

Chronic Phase (Stage II-III):

• Gradual return to weight-bearing
• Custom footwear and orthotics
• Lifelong monitoring
• Address residual deformity

Surgical Management:

• Indications: Unstable deformity, recurrent ulceration despite offloading, severe malalignment
• Procedures: Exostectomy, osteotomy, arthrodesis
• Timing: Ideally in consolidation phase (Stage III)
• High complication rates (infection, non-union, recurrence)

---

Multidisciplinary Management

MDT Composition

Effective diabetic foot management requires a coordinated multidisciplinary team. [10,24]

Offloading

Pressure redistribution is fundamental to ulcer healing. [25]

Offloading Hierarchy (Most to Least Effective):

Exam Detail: Total Contact Cast Technique:

• Cast from toes to tibial tuberosity
• Minimal padding (hence "total contact")
• Distributes pressure across entire plantar surface
• Reduces shear forces
• Change weekly or when loose
• Contraindicated in: severe ischaemia, active infection with systemic signs, excessive exudate

Wound Debridement

Sharp Debridement Principles:

• Remove all callus (reduces pressure by ~30%)
• Debride to healthy bleeding tissue (if vascular supply adequate)
• Create a saucerised wound bed
• Obtain deep tissue for culture
• Caution in ischaemic wounds (may extend necrosis)

Wound Dressings

No single dressing is superior for diabetic foot ulcers. Selection based on wound characteristics. [26]

Negative Pressure Wound Therapy (NPWT):

• Creates subatmospheric pressure over wound
• Promotes granulation, removes exudate, reduces oedema
• Consider for large wounds, post-surgical wounds
• Evidence for faster healing rates

Revascularisation

Essential in ischaemic and neuroischaemic ulcers. [27]

Indications for Revascularisation:

• Non-healing ulcer with significant PAD
• Rest pain
• Gangrene (limited)
• TBI less than 0.70 or TcPO2 less than 40 mmHg

Revascularisation Options:

Angiosome Concept:

• Foot supplied by 3 angiosomes (posterior tibial, anterior tibial/dorsalis pedis, peroneal)
• "Direct" revascularisation targets artery supplying ulcer location
• Some evidence for improved healing with direct revascularisation

Advanced Therapies

For ulcers failing standard care (> 4 weeks without improvement):

---

Amputation

Prevention Strategies

Amputation prevention is the primary goal of diabetic foot care. [28]

Key Amputation Prevention Strategies:

1. Screening and risk stratification
2. Patient education
3. Glycaemic control
4. Smoking cessation
5. Prompt treatment of ulcers
6. Multidisciplinary team care
7. Appropriate offloading
8. Revascularisation when indicated
9. Infection control

Amputation Levels

Factors Determining Amputation Level:

• Vascular supply (healing potential)
• Extent of infection/gangrene
• Ambulatory potential
• Patient preference
• Prosthetic considerations

Post-Amputation Care

• Wound management and monitoring
• Prosthetic fitting (BKA typically 6-8 weeks post-op)
• Physiotherapy and rehabilitation
• Contralateral limb protection (50% develop contralateral ulcer/amputation within 5 years)
• Psychological support
• Cardiovascular risk management

---

Prevention and Screening

Primary Prevention

Patient Education Topics:

• Daily foot inspection
• Proper footwear selection
• Avoiding barefoot walking
• Not self-treating calluses/corns
• Recognising warning signs
• Smoking cessation
• Glycaemic control

Healthcare Provider Responsibilities:

• Annual foot examination for all diabetics
• Risk stratification using IWGDF system
• Referral to podiatry for high-risk patients
• Prescription of appropriate footwear

Secondary Prevention (Ulcer Recurrence)

Following ulcer healing, recurrence rates are extremely high. [7]

Prevention Strategies:

• Lifelong custom therapeutic footwear
• Regular podiatry review
• Home temperature monitoring
• Continued offloading of at-risk areas
• Treatment of pre-ulcerative lesions

Evidence for Prevention:

---

Special Considerations

Diabetic Foot in Dialysis Patients

• Significantly higher ulcer and amputation rates
• Accelerated arterial calcification
• Impaired wound healing
• Antibiotic dosing adjustments required
• Consider calciphylaxis in differential

Pregnancy and Diabetes

• Foot screening should continue
• Avoid certain antibiotics (fluoroquinolones, tetracyclines)
• Glycaemic targets are stricter
• Coordinate with obstetric team

Acute Diabetic Emergencies

• DKA/HHS may precipitate or complicate foot infection
• Severe foot infection may trigger DKA
• Manage both simultaneously

---

Prognosis

Healing Outcomes

Amputation and Mortality

Clinical Pearl: Mortality Context: The 5-year mortality after major amputation (50-70%) exceeds that of breast, colon, and prostate cancer. This underscores the critical importance of prevention and limb salvage. [4]

---

Viva Scenarios

Scenario 1: Acute Presentation

Q: A 62-year-old man with type 2 diabetes presents with a 3-day history of a painful, swollen right foot. Temperature is 38.2°C. Describe your approach.

Model Answer: "This is a diabetic foot emergency requiring urgent assessment. My immediate concerns are severe diabetic foot infection, necrotising fasciitis, or gas gangrene.

My initial approach would be:

1. Assess severity: Check vital signs for sepsis (temperature already elevated), assess mental status, obtain IV access
2. Examine the foot: Look for crepitus (gas gangrene), rapidly spreading cellulitis, fluctuance (abscess), exposed bone
3. Order urgent investigations: Plain X-ray to exclude gas, bloods including WBC, CRP, lactate, glucose, blood cultures
4. Initiate treatment: If severe infection, I would start empirical broad-spectrum IV antibiotics (vancomycin + piperacillin-tazobactam), fluid resuscitation, and request urgent surgical review

If gas or necrotising infection is confirmed, this requires emergent surgical debridement. I would involve the MDT including surgical team, infectious disease, and ICU if septic."

Scenario 2: Chronic Non-Healing Ulcer

Q: A patient with a plantar metatarsal head ulcer has failed to heal after 8 weeks of standard care. What is your approach?

Model Answer: "A non-healing ulcer at 8 weeks requires systematic reassessment of the key factors affecting healing:

1. Vascular status: Has adequate perfusion been confirmed? I would check toe pressures and TcPO2. If TBI less than 0.70 or TcPO2 less than 40 mmHg, revascularisation should be considered.

2. Offloading: Is the patient compliant with offloading device? A non-removable cast walker or TCC may be needed if adherence is the issue.

3. Infection: Is there occult osteomyelitis? I would perform probe-to-bone test, check ESR (> 70 suggests osteomyelitis), and consider MRI.

4. Wound bed: Is there adequate debridement? Slough and callus should be removed.

5. Systemic factors: Glycaemic control, nutritional status, smoking cessation.

If these are optimised and healing still fails, I would consider advanced therapies such as NPWT, bioengineered skin substitutes, or hyperbaric oxygen (if ischaemic component)."

Scenario 3: Charcot vs Osteomyelitis

Q: How do you differentiate acute Charcot from osteomyelitis clinically?

Model Answer: "This is a critical differential as management differs significantly.

Key differentiating features:

1. Ulcer presence: Osteomyelitis typically has an overlying ulcer with exposed or near-exposed bone; acute Charcot often presents without ulcer
2. Systemic features: Fever and raised WBC suggest infection; Charcot typically has normal WBC
3. Inflammatory markers: Both elevate CRP, but osteomyelitis typically more markedly
4. Elevation test: In Charcot, elevating the limb reduces temperature and swelling; in osteomyelitis, inflammation persists
5. Probe-to-bone: Positive in osteomyelitis with ulcer; cannot perform if no ulcer (Charcot)
6. Response to antibiotics: Charcot shows no improvement; osteomyelitis improves

If uncertain, MRI is the investigation of choice. Labelled WBC scan can also differentiate, showing increased uptake in osteomyelitis but cold/minimal uptake in Charcot."

---

Key Clinical Pearls

1. Most diabetic foot ulcers are neuroischaemic - always assess vascular status
2. Absence of pain does not exclude severe infection - neuropathy masks symptoms
3. ABI may be falsely elevated in diabetics - use TBI or TcPO2 for reliable assessment
4. Probe-to-bone positive + ESR > 70 - strongly suggests osteomyelitis
5. MRI is gold standard for osteomyelitis diagnosis
6. Total contact cast is gold standard for offloading plantar ulcers
7. Revascularisation is often limb-saving in neuroischaemic ulcers
8. 5-year mortality post-major amputation exceeds many cancers - prevention is critical
9. Acute Charcot is a diagnosis of exclusion - always rule out infection
10. MDT care reduces amputation rates by 40-85% - refer early

---

Common Exam Questions

1. What are the components of the pathogenic triad in diabetic foot disease?
2. Describe the IWGDF risk stratification system and screening intervals.
3. How do you differentiate neuropathic, ischaemic, and neuroischaemic ulcers?
4. What is the sensitivity and specificity of probe-to-bone test for osteomyelitis?
5. Compare the Wagner and University of Texas classification systems.
6. Describe the IDSA/IWGDF infection severity classification.
7. What are the MRI features of osteomyelitis?
8. How do you differentiate acute Charcot from osteomyelitis?
9. Describe the management of acute Charcot neuroarthropathy.
10. What is the evidence for total contact casting in diabetic foot ulcers?

---

References

1. Boulton AJM, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet. 2005;366(9498):1719-1724. doi:10.1016/S0140-6736(05)67698-2

2. Armstrong DG, Boulton AJM, Bus SA. Diabetic foot ulcers and their recurrence. N Engl J Med. 2017;376(24):2367-2375. doi:10.1056/NEJMra1615439

3. Edmonds M, Manu C, Vas P. The current burden of diabetic foot disease. J Clin Orthop Trauma. 2021;17:88-93. doi:10.1016/j.jcot.2021.01.017

4. Hoffstad O, Mitra N, Walsh J, Margolis DJ. Diabetes, lower-extremity amputation, and death. Diabetes Care. 2015;38(10):1852-1857. doi:10.2337/dc15-0536

5. International Diabetes Federation. IDF Diabetes Atlas, 10th edn. Brussels, Belgium: 2021. https://www.diabetesatlas.org

6. Zhang P, Lu J, Jing Y, Tang S, Zhu D, Bi Y. Global epidemiology of diabetic foot ulceration: a systematic review and meta-analysis. Ann Med. 2017;49(2):106-116. doi:10.1080/07853890.2016.1231932

7. Armstrong DG, Lavery LA, Harkless LB. Validation of a diabetic wound classification system. The contribution of depth, infection, and ischemia to risk of amputation. Diabetes Care. 1998;21(5):855-859. doi:10.2337/diacare.21.5.855

8. Lipsky BA, Senneville E, Abbas ZG, et al. IWGDF/IDSA Guidelines on the diagnosis and treatment of diabetes-related foot infections (IWGDF/IDSA 2023). Clin Infect Dis. 2024;78(2):e72-e117. doi:10.1093/cid/ciad527

9. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for prevention. Diabetes Care. 1990;13(5):513-521. doi:10.2337/diacare.13.5.513

10. Schaper NC, van Netten JJ, Apelqvist J, Bus SA, Fitridge R, Game F, et al. Practical guidelines on the prevention and management of diabetes-related foot disease (IWGDF 2023 update). Diabetes Metab Res Rev. 2024;40(3):e3657. doi:10.1002/dmrr.3657

11. Pop-Busui R, Boulton AJM, Feldman EL, et al. Diabetic neuropathy: a position statement by the American Diabetes Association. Diabetes Care. 2017;40(1):136-154. doi:10.2337/dc16-2042

12. Prompers L, Huijberts M, Apelqvist J, et al. High prevalence of ischaemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia. 2007;50(1):18-25. doi:10.1007/s00125-006-0491-1

13. Everett E, Mathioudakis N. Update on management of diabetic foot ulcers. Ann N Y Acad Sci. 2018;1411(1):153-165. doi:10.1111/nyas.13569

14. Edmonds ME. The diabetic foot: pathophysiology and treatment. Clin Endocrinol Metab. 1986;15(4):889-916. doi:10.1016/S0300-595X(86)80080-5

15. Feng Y, Schlösser FJ, Sumpio BE. The Semmes Weinstein monofilament examination as a screening tool for diabetic peripheral neuropathy. J Vasc Surg. 2009;50(3):675-682. doi:10.1016/j.jvs.2009.05.017

16. Wagner FW Jr. The dysvascular foot: a system for diagnosis and treatment. Foot Ankle. 1981;2(2):64-122. doi:10.1177/107110078100200202

17. Lavery LA, Armstrong DG, Harkless LB. Classification of diabetic foot wounds. J Foot Ankle Surg. 1996;35(6):528-531. doi:10.1016/S1067-2516(96)80125-6

18. Ince P, Abbas ZG, Lutale JK, et al. Use of the SINBAD classification system and score in comparing outcome of foot ulcer management on three continents. Diabetes Care. 2008;31(5):964-967. doi:10.2337/dc07-2367

19. Schaper NC. Diabetic foot ulcer classification system for research purposes: a progress report on criteria for including patients in research studies. Diabetes Metab Res Rev. 2004;20(Suppl 1):S90-S95. doi:10.1002/dmrr.464

20. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012;54(12):e132-e173. doi:10.1093/cid/cis346

21. Lázaro-Martínez JL, Aragón-Sánchez J, García-Morales E. Antibiotics versus conservative surgery for treating diabetic foot osteomyelitis: a randomized comparative trial. Diabetes Care. 2014;37(3):789-795. doi:10.2337/dc13-1526

22. Lavery LA, Armstrong DG, Peters EJ, Lipsky BA. Probe-to-bone test for diagnosing diabetic foot osteomyelitis: reliable or relic? Diabetes Care. 2007;30(2):270-274. doi:10.2337/dc06-1572

23. Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. Diabetes Care. 2011;34(9):2123-2129. doi:10.2337/dc11-0844

24. Turns M. Diabetic foot ulcer management: the podiatrist's perspective. Br J Community Nurs. 2013;Suppl:S14-S19. doi:10.12968/bjcn.2013.18.Sup3.S14

25. Bus SA, Valk GD, van Deursen RW, et al. The effectiveness of footwear and offloading interventions to prevent and heal foot ulcers and reduce plantar pressure in diabetes: a systematic review. Diabetes Metab Res Rev. 2016;32(Suppl 1):99-118. doi:10.1002/dmrr.2702

26. Wu L, Norman G, Dumville JC, O'Meara S, Bell-Syer SE. Dressings for treating foot ulcers in people with diabetes: an overview of systematic reviews. Cochrane Database Syst Rev. 2015;(7):CD010471. doi:10.1002/14651858.CD010471.pub2

27. Fitridge R, Chuter V, Mills J, et al. The intersocietal IWGDF, ESVS, SVS guidelines on peripheral artery disease in people with diabetes and a foot ulcer. Diabetes Metab Res Rev. 2024;40(3):e3686. doi:10.1002/dmrr.3686

28. Krishnan S, Nash F, Baker N, Fowler D, Rayman G. Reduction in diabetic amputations over 11 years in a defined U.K. population: benefits of multidisciplinary team work and continuous prospective audit. Diabetes Care. 2008;31(1):99-101. doi:10.2337/dc07-1178

---

Version History