DIABETIC FOOT ULCERS
Neuropathy + Vasculopathy + Immunopathy | Wagner and Texas Classifications | Offloading is Key
WAGNER CLASSIFICATION (0-5)
Critical Must-Knows
- Pathophysiology triad: sensory neuropathy (loss of protective sensation), peripheral vascular disease, and impaired immunity lead to ulcer formation
- Wagner classification: depth-based (0-5); Texas classification: adds ischemia and infection to depth grading (4x4 grid)
- Offloading is THE critical treatment - total contact casting reduces plantar pressure by 80-90% and is gold standard
- Probe-to-bone test: positive likelihood ratio 6.4 for osteomyelitis - if metal probe reaches bone, assume bone infection
- IDSA guidelines: treat infection (purulence OR 2+ inflammatory signs), NOT colonization - tissue cultures after debridement only
Examiner's Pearls
- "Monofilament testing: 10g (5.07 Semmes-Weinstein) = loss of protective sensation threshold
- "ABI less than 0.9 indicates PAD; less than 0.5 critical ischemia; greater than 1.3 falsely elevated (calcified vessels)
- "TCC (total contact cast) is gold standard offloading but instant total contact walker is alternative
- "Major amputation 5-year mortality is 50% - worse than most cancers
Clinical Imaging
Imaging Gallery



Clinical Imaging
Imaging Gallery
Critical Diabetic Foot Ulcer Exam Points
Pathophysiology Triad
Three pathological processes drive ulcer formation: (1) Sensory neuropathy leads to loss of protective sensation and unrecognized trauma, (2) Motor neuropathy causes intrinsic muscle atrophy, clawing, and abnormal pressure points, (3) Peripheral arterial disease impairs healing. Add immunopathy (WBC dysfunction) and you have the perfect storm.
Classification Systems
Wagner (0-5) is most commonly used and grades by depth only. University of Texas adds ischemia and infection to create a 4x4 grid (depth A-D, grade 0-3). PEDIS system (Perfusion, Extent, Depth, Infection, Sensation) is IWGDF standard. Know all three and when each is used.
Offloading Principles
No offloading = no healing. Total contact casting (TCC) is gold standard - reduces plantar pressure by 80-90%, healing rate 85-95% at 12 weeks. Alternative: instant total contact walker (iTCC). Removable devices fail due to non-compliance. Offloading is treatment, NOT adjunct.
Infection Diagnosis
IDSA criteria for infection: purulence OR 2 or more inflammatory signs (warmth, erythema greater than 2cm, lymphangitis, edema, pain/tenderness). Swab cultures are meaningless - colonization only. Deep tissue cultures AFTER debridement. MRI for osteomyelitis if probe-to-bone negative but high suspicion.
ULCER - Diabetic Foot Ulcer Pathophysiology
Memory Hook:ULCER reminds you of the five pathological processes that create diabetic foot ulcers
PEDIS - IWGDF Classification System
Memory Hook:PEDIS is the comprehensive assessment framework recommended by International Working Group on Diabetic Foot
OFFLOAD - Principles of Pressure Relief
Memory Hook:OFFLOAD summarizes the critical principles of mechanical pressure reduction in diabetic foot ulcer treatment
The 3 P's of Diabetic Foot Assessment
Memory Hook:The 3 P's are the essential bedside tests every diabetic foot needs
Overview and Epidemiology
Diabetic foot ulcers (DFUs) are chronic wounds occurring in individuals with diabetes mellitus, resulting from the interaction of neuropathy, peripheral arterial disease, and repetitive trauma. They represent the most common and costly complication of diabetes, with devastating consequences for patients and healthcare systems.
Epidemiology and Burden
Global Impact:
- Approximately 15% of individuals with diabetes will develop a foot ulcer during their lifetime
- Annual incidence: 2-4% among diabetic patients
- Prevalence in diabetic population: 4-10%
- 85% of diabetes-related amputations are preceded by foot ulcers
Outcomes and Prognosis:
- 5-24% of diabetic foot ulcers progress to amputation
- 50% of DFUs recur within 3 years despite initial healing
- 40% recur within 1 year
- 50% mortality at 5 years following major amputation (worse than most cancers)
- 30% mortality at 1 year following major amputation
Risk Factors
Major Risk Factors (evidence-based):
- Previous foot ulceration: strongest predictor (relative risk 12-36)
- Peripheral neuropathy: loss of protective sensation (10g monofilament)
- Peripheral arterial disease: ABI less than 0.9
- Foot deformity: claw toes, Charcot foot, hallux valgus
- High plantar pressure: greater than 600 kPa at forefoot
- Poor glycemic control: HbA1c greater than 8%
- Duration of diabetes: greater than 10 years
- Vision impairment: inability to self-inspect
Additional Risk Factors:
- Chronic kidney disease (dialysis patients 2-3x higher risk)
- Smoking (impairs wound healing)
- Limited joint mobility (especially ankle)
- Inappropriate footwear
- Male gender (1.6x higher risk)
- Low socioeconomic status
Exam High-Yield: Risk Stratification
IWGDF Risk Stratification System (0-3):
- Category 0: No neuropathy - annual screening
- Category 1: Neuropathy alone - screen every 6-12 months
- Category 2: Neuropathy + PAD or deformity - screen every 3-6 months
- Category 3: Previous ulcer or amputation - screen every 1-3 months
This guides surveillance frequency and prevention intensity.
Pathophysiology
The Pathophysiological Triad
Diabetic foot ulcers result from the interaction of three primary pathological processes: neuropathy, vascular disease, and trauma. When combined with immunopathy, these create the conditions for chronic non-healing wounds.
1. Neuropathy (85% of DFUs)
Sensory Neuropathy:
- Loss of protective sensation to 10g monofilament (5.07 Semmes-Weinstein)
- Unable to perceive minor trauma (foreign body, friction, thermal injury)
- Reduced pain perception delays recognition of injury
- Distal, symmetric, "stocking-glove" distribution
- Mechanism: sorbitol accumulation, advanced glycation end-products (AGEs), oxidative stress
Motor Neuropathy:
- Intrinsic muscle atrophy (lumbricals, interossei)
- Claw toe deformity develops from imbalance
- Met heads become more prominent
- Abnormal pressure distribution: peak pressures at met 2-3 heads
- Loss of dynamic shock absorption
Autonomic Neuropathy:
- Decreased sweating (anhidrosis) leads to dry, cracked skin
- Arteriovenous shunting in foot (bounding pulses despite poor perfusion)
- Warm, dry foot with dilated veins
- Impaired thermoregulation
2. Peripheral Arterial Disease (PAD)
Vascular Changes in Diabetes:
- Tibial and peroneal artery disease (below-knee)
- Spares foot vessels (pedal arch often patent)
- Medial arterial calcification (Mönckeberg sclerosis) - falsely elevated ABI
- Microvascular disease: capillary basement membrane thickening
Hemodynamic Consequences:
- Reduced tissue perfusion delays healing
- Critical ischemia: ABI less than 0.5, TcPO2 less than 30 mmHg
- Tissue hypoxia impairs fibroblast function, collagen synthesis
- Impaired angiogenesis in diabetic patients
3. Immunopathy
White Blood Cell Dysfunction:
- Neutrophil impairment: reduced chemotaxis, phagocytosis, bacterial killing
- Macrophage dysfunction: delayed wound debridement
- Lymphocyte abnormalities: impaired cellular immunity
- Mechanism: hyperglycemia interferes with WBC function at multiple steps
Clinical Consequences:
- Increased infection susceptibility
- Rapid progression of soft tissue infections
- Blunted inflammatory response - may have minimal systemic signs despite severe infection
- Osteomyelitis risk: 10-15% of infected DFUs
4. Repetitive Trauma (Mechanical)
Biomechanical Factors:
- High plantar pressure: normal walking = 300-500 kPa; DFU patients often greater than 600 kPa
- Shear stress: friction during gait cycle
- Repetitive microtrauma: 5,000-10,000 steps per day on insensate foot
- Callus formation: further elevates peak pressure by 30-50%
Pathway to Ulceration:
- High pressure point (e.g., prominent met head)
- Repetitive loading without pain feedback
- Subcutaneous hemorrhage and tissue breakdown
- Callus forms over area
- Pressure increases further under callus
- Autolysis creates fluid-filled space
- Skin ruptures → ulcer formation
Why Neuropathic Ulcers Don't Hurt
Patients often present late because neuropathic ulcers are painless. The same neuropathy that allows ulcer formation also prevents pain sensation. In contrast, ischemic ulcers ARE painful (rest pain). This clinical distinction helps differentiate neuropathic from neuroischemic ulcers at bedside.
Impaired Wound Healing in Diabetes
Cellular and Molecular Abnormalities:
- Prolonged inflammatory phase: persistent neutrophil infiltration
- Impaired proliferation: reduced fibroblast migration and proliferation
- Reduced growth factors: decreased PDGF, VEGF, EGF
- Extracellular matrix abnormalities: excess MMPs (matrix metalloproteinases)
- Senescent cells: cells in wound bed stop dividing
- Biofilm formation: 60-80% of chronic wounds have bacterial biofilms
Classification Systems
Wagner Classification (Most Widely Used)
The Wagner-Meggitt classification is the most commonly used system, grading ulcers by depth and presence of infection or gangrene (0-5).
Wagner Classification System
| Grade | Description | Treatment | Healing Rate |
|---|---|---|---|
| Grade 0 | Intact skin, pre-ulcerative (callus, bony deformity, erythema) | Prevention: orthotics, education, callus debridement | Not applicable |
| Grade 1 | Superficial ulcer, partial/full-thickness, no deeper structures | Offloading (TCC), sharp debridement, moist wound care | 85-95% at 12 weeks with proper offloading |
| Grade 2 | Deep ulcer to tendon, bone, or joint capsule (no abscess/OM) | Surgical debridement, antibiotics if infected, offloading | 70-80% at 12-16 weeks |
| Grade 3 | Deep ulcer with abscess, osteomyelitis, or septic arthritis | Surgical debridement, IV antibiotics, possible amputation | 50-60% limb salvage with aggressive treatment |
| Grade 4 | Localized gangrene (forefoot or heel) | Partial amputation (toe, ray, transmetatarsal) | 80-90% healing of amputation site |
| Grade 5 | Extensive gangrene of entire foot | Major amputation (below-knee or above-knee) | 80-90% BKA healing; 50-60% AKA healing |
Advantages of Wagner:
- Simple and easy to remember
- Widely used in clinical practice and research
- Good inter-observer reliability
- Guides treatment escalation
Limitations of Wagner:
- Does not separately grade ischemia and infection
- Limited prognostic value for healing
- Does not account for location
This completes the Wagner classification overview.
Clinical Assessment
History
Key Questions:
- Duration of diabetes and glycemic control (HbA1c)
- Previous ulcers or amputations (strongest risk factor)
- Claudication, rest pain (vascular symptoms)
- Sensory symptoms: numbness, tingling, burning (neuropathy)
- Trauma or precipitating event (often forgotten by patient due to neuropathy)
- Footwear: what do they wear at home? (many patients wear inappropriate slippers)
- Self-care ability: can they see their feet? Can they reach to inspect?
Physical Examination
Vascular Assessment (The 5 P's):
- Pulses: dorsalis pedis, posterior tibial (compare sides)
- Pallor: elevation pallor test (Buerger test)
- Perfusion: capillary refill time (normal less than 3 seconds)
- Paresthesias: neuropathic symptoms
- Pain: rest pain suggests critical ischemia
Neurological Assessment:
- 10g monofilament testing: 9 sites on plantar foot (hallux, met 1-5, mid-arch, heel)
- Loss of sensation at ANY site = loss of protective sensation
- Sensitivity 90%, specificity 80% for ulcer risk
- Vibration perception: 128 Hz tuning fork at hallux IPJ
- Ankle reflexes: absent in peripheral neuropathy
- Pinprick: assesses small fiber function
Musculoskeletal Assessment:
- Foot deformities: claw toes, hallux valgus, Charcot neuroarthropathy
- Ankle range of motion: equinus (less than 10° dorsiflexion) increases forefoot pressure
- Muscle strength: intrinsic atrophy, inability to spread toes
- Gait analysis: observe pressure pattern
Ulcer Assessment:
- Location: plantar (neuropathic), margins/dorsum (ischemic), interdigital (mixed)
- Size: measure in cm² (length × width)
- Depth: probe to bone test
- Base: granulation tissue (red = healthy), slough (yellow), eschar (black)
- Edges: callused, undermined, macerated
- Surrounding skin: erythema (measure distance), warmth, edema
- Exudate: amount, color, odor
Probe-to-Bone Test:
- Sterile metal probe inserted into debrided ulcer
- Positive: hard, gritty resistance = bone felt
- Sensitivity 87%, specificity 83% for osteomyelitis
- Positive likelihood ratio 6.4 - if positive, assume osteomyelitis
- Negative likelihood ratio 0.15 - if negative, osteomyelitis unlikely (unless high clinical suspicion)
Red Flags Requiring Urgent Action:
- Systemic signs: fever, tachycardia, hypotension (sepsis)
- Gas in tissues: crepitus on exam or air on X-ray (gas gangrene)
- Rapidly spreading erythema: necrotizing fasciitis
- Bullae or skin necrosis: limb-threatening infection
- Foul odor: anaerobic infection
- Critical ischemia: rest pain, ABI less than 0.5, tissue loss
These indicate limb- or life-threatening infection requiring same-day surgical consultation.
Investigations
Laboratory Tests
Baseline Blood Tests:
- HbA1c: glycemic control over 3 months (target less than 7%)
- Inflammatory markers: CRP, ESR (elevated in osteomyelitis, may be normal in acute infection)
- WBC: may be normal despite infection (blunted response)
- Renal function: many diabetics have CKD
- Blood cultures: if systemic signs
Vascular Assessment
Ankle-Brachial Index (ABI):
- Normal: 0.9-1.3
- PAD: less than 0.9
- Critical ischemia: less than 0.5
- Falsely elevated (calcified vessels): greater than 1.3 (use toe pressures instead)
Toe-Brachial Index (TBI): less affected by calcification
- Normal: greater than 0.7
- Critical ischemia: less than 0.5
Transcutaneous oxygen pressure (TcPO2):
- Greater than 40 mmHg: good healing potential
- 30-40 mmHg: borderline
- Less than 30 mmHg: poor healing, revascularization needed
Duplex ultrasound: if ABI abnormal, map disease for revascularization
CT angiography or MR angiography: if revascularization planned
Imaging for Osteomyelitis
Imaging Modalities for Osteomyelitis
| Modality | Sensitivity | Specificity | Advantages | Disadvantages |
|---|---|---|---|---|
| Plain X-ray | 54-68% | 68-75% | Cheap, widely available, detects gas | Insensitive early (2-3 weeks delay), cannot assess soft tissue |
| MRI | 90-95% | 70-85% | Best for bone marrow edema, soft tissue abscess | Expensive, cannot if metal implants, lower specificity |
| Nuclear (WBC scan) | 74-100% | 68-90% | Functional imaging, specific for infection | Time-consuming, radiation, may miss chronic OM |
| Bone biopsy | Gold standard | Gold standard | Histology + culture, definitive diagnosis | Invasive, may seed infection, patient refusal |
MRI Findings in Osteomyelitis:
- Bone marrow edema (low T1, high T2/STIR signal)
- Cortical destruction
- Soft tissue abscess or sinus tract
- Contrast enhancement
Plain X-ray Findings:
- Periosteal reaction
- Cortical erosion
- Bone destruction
- Soft tissue gas (indicates gas-forming organisms)
Microbiology
Specimen Collection:
- Do NOT swab superficial wound - this only cultures colonizers
- Deep tissue culture AFTER debridement:
- Curette or bone biopsy for best yield
- Send for aerobic, anaerobic, and fungal cultures
- Specify "diabetic foot infection" to lab (alerts to polymicrobial nature)
Common Organisms:
- Uninfected/mild: Staphylococcus aureus, Streptococci (monomicrobial)
- Moderate/severe: polymicrobial
- Gram-positives: S. aureus (including MRSA), Streptococci, Enterococci
- Gram-negatives: E. coli, Proteus, Klebsiella, Pseudomonas
- Anaerobes: Bacteroides, Peptostreptococcus (foul odor, necrosis)
Management Algorithm

Multidisciplinary Team Approach
Evidence: Multidisciplinary foot care teams reduce amputation rates by 49-85% compared to standard care.
Essential Team Members:
- Diabetologist or endocrinologist (glycemic control)
- Podiatrist (wound care, debridement, orthotics)
- Vascular surgeon (revascularization)
- Orthopaedic or plastic surgeon (reconstruction, amputation)
- Infectious disease specialist (complex infections, osteomyelitis)
- Orthotist (custom footwear, AFOs)
- Diabetes nurse educator (self-care, prevention)
The 5 Pillars of DFU Management
1. Offloading (CRITICAL) 2. Debridement 3. Infection Control 4. Vascular Assessment and Revascularization 5. Metabolic and Wound Environment Optimization
Offloading (Pillar 1)
Offloading is THE critical treatment for plantar neuropathic DFUs. No amount of antibiotics, dressings, or growth factors will heal an ulcer if repetitive pressure continues. In comparative studies, offloading alone heals 85-95% of superficial neuropathic ulcers within 12 weeks.
Total Contact Casting (Gold Standard)
Mechanism of Action:
- Redistributes pressure from ulcer site to entire plantar surface and lower leg
- Reduces peak plantar pressure by 80-90% at ulcer site
- Immobilizes ankle (reduces shear stress)
- Non-removable - ensures compliance (patients cannot cheat)
Technique:
- Apply minimal padding over ulcer and bony prominences
- Mold cast intimately to foot and leg (total contact)
- Extend to just below fibular head
- Heel rocker on bottom for gait
- Change weekly initially (edema reduction), then every 2 weeks
Outcomes:
- Healing rate: 85-95% at 12 weeks for Wagner 1-2 ulcers
- Healing time: 6-8 weeks average (vs 12-16 weeks in removable devices)
- Recurrence rate: 30-50% at 2 years (need long-term footwear)
Contraindications to TCC:
- Active infection (moderate or severe)
- Critical ischemia (ABI less than 0.5)
- Excessive edema (unstable limb volume)
- Non-compliant patient (fall risk)
- Suspected Charcot neuroarthropathy (acute phase)
Instant Total Contact Cast (iTCC Walker)
Alternative to TCC:
- Removable cam walker rendered non-removable with cohesive bandage or fiberglass
- Prefabricated device with custom foam padding
- Similar efficacy to TCC (75-90% healing) IF rendered non-removable
- Allows wound inspection without cast removal
Advantage: Can be temporarily removed for wound care by healthcare provider Disadvantage: If patient can remove it (non-compliance), efficacy drops to 30-50%
Other Offloading Devices
Offloading Modalities Comparison
| Device | Healing Rate | Compliance | Indications | Cost |
|---|---|---|---|---|
| Total Contact Cast | 85-95% | 100% (non-removable) | Gold standard for plantar neuropathic ulcers | $$ |
| iTCC Walker (non-removable) | 75-90% | 95% (cohesive wrap) | Alternative if TCC unavailable or infection present | $$$ |
| Removable Cast Walker | 30-50% | 20-30% (poor) | Non-compliant patients, acute Charcot | $$ |
| Half Shoe (wedge) | 30-40% | 40-60% | Post-op amputation, forefoot offloading | $ |
| Felted Foam | 40-60% | 70-80% | Temporary measure, outpatient debridement | $ |
| Custom Orthotics | Prevention | 80% | Healed ulcers, prevention, redistribution | $$$ |
Key Principle: Non-removable greater than removable. Studies show patients wear removable devices only 20-30% of the time when alone at home, despite reporting "full compliance."
Why Patients Don't Wear Their Walker
The same neuropathy that caused the ulcer also removes the pain signal that would remind patients to protect the foot. They genuinely forget because it doesn't hurt. This is why non-removable devices are essential - they provide external memory.
Surgical Offloading
Achilles Tendon Lengthening (ATL):
- Indication: Equinus contracture (ankle dorsiflexion less than 10°)
- Mechanism: reduces forefoot pressure by 25-30%
- Technique: percutaneous triple hemisection
- Outcomes: 60-80% reduction in recurrence vs standard care
- Risks: overlengthening → calcaneal ulcers
Metatarsal Head Resection:
- Indication: recurrent plantar ulcer under prominent met head
- Single met resection (usually met 2 or 3)
- Avoid multiple adjacent mets (transfer lesions)
Joint Arthroplasty (Met Head Resection with K-wire Fixation):
- Shortens metatarsal, elevates met head
- Healing rate: 80-90%
Debridement and Wound Care (Pillar 2)
Sharp Debridement (Essential)
Rationale:
- Removes necrotic tissue, callus, and biofilm
- Converts chronic wound to acute wound (restarts healing cascade)
- Reduces bacterial burden by 90-99%
- Exposes healthy bleeding tissue
Technique:
- Weekly debridement until healed (at minimum)
- Use scalpel to remove all hyperkeratosis (callus) around wound edges
- Debride to healthy, bleeding tissue (Spongey-bleeding base indicates dermis)
- Saucerize edges (bevel wound edges to prevent undermining)
- Send tissue for culture (NOT swab)
Evidence: Weekly sharp debridement associated with 2-3x higher healing rates vs episodic debridement.
Wound Dressing Principles
Goal: Maintain moist wound environment (improves epithelialization by 50% vs dry wounds)
Dressing Selection by Wound Characteristics:
| Wound Type | Exudate | Dressing | Mechanism |
|---|---|---|---|
| Necrotic | Minimal | Hydrogel | Autolytic debridement |
| Sloughy | Moderate | Hydrocolloid or foam | Absorb exudate, protect |
| Granulating | Light | Hydrocolloid, alginate | Maintain moisture |
| Epithelializing | Minimal | Film or hydrocolloid | Non-adherent, protect |
| Infected | Heavy | Antimicrobial (silver, iodine) + foam | Infection control + absorption |
Dressing Change Frequency:
- Infected wounds: daily
- Clean granulating: every 3-7 days
- Goal: minimize wound disruption
Advanced Wound Therapies
Negative Pressure Wound Therapy (NPWT):
- Indications: post-surgical wounds, deep wounds after debridement
- Mechanism: removes exudate, reduces edema, promotes granulation
- Evidence: 30-50% faster healing vs standard dressings in diabetic wounds
- Contraindications: untreated osteomyelitis, exposed vessels, malignancy
Biological Agents:
- Platelet-derived growth factor (becaplermin): 50% increase in healing vs placebo (NNT = 7)
- Apply daily after debridement
- FDA-approved for diabetic neuropathic ulcers
- Living cell therapy: human fibroblast/keratinocyte sheets (Apligraf, Dermagraft)
- Healing: 56% vs 38% with standard care at 12 weeks
- Expensive (USD 1000-2500 per application)
Hyperbaric Oxygen Therapy (HBOT):
- Controversial evidence: some RCTs show benefit, others don't
- Mechanism: increases tissue oxygenation, enhances WBC function, angiogenesis
- Indications (if available): Wagner 3-4 with failed standard care
- Regimen: 90-120 minutes at 2.0-2.5 ATA, 30-40 sessions
- Cochrane review: insufficient evidence to recommend routinely
Infection Control (Pillar 3)
IDSA/IWGDF Infection Criteria
Diagnosis of Infection (NOT just colonization):
- Purulence (pus), OR
- 2 or more inflammatory signs:
- Local warmth
- Erythema (greater than 2 cm from wound edge = moderate infection)
- Lymphangitis
- Edema
- Pain or tenderness (unusual in neuropathic patients - ominous if present)
Severity Grading:
IDSA Diabetic Foot Infection Severity
| Severity | Clinical Features | Treatment | Setting |
|---|---|---|---|
| Uninfected | No signs of infection | No antibiotics - wound care and offloading only | Outpatient |
| Mild | Erythema less than 2cm, superficial, no systemic signs | Oral antibiotics, outpatient debridement | Outpatient |
| Moderate | Erythema greater than 2cm OR deep tissue involved, no systemic signs | IV or oral antibiotics, surgical debridement often needed | Inpatient or close outpatient |
| Severe | SIRS present OR limb-threatening (necrotizing infection, gangrene) | IV broad-spectrum antibiotics, urgent surgery, ICU if septic | Inpatient (ICU if unstable) |
Antibiotic Therapy
Principles:
- Treat infection, NOT colonization - all chronic wounds are colonized
- Empiric therapy based on severity and previous cultures
- Narrow to culture results after 48-72 hours
- Duration: 1-2 weeks for soft tissue; 4-6 weeks for osteomyelitis
Empiric Regimens (IDSA Guidelines):
Mild Infection (outpatient, oral):
- Cephalexin 500mg QID, OR
- Amoxicillin-clavulanate 875mg BID, OR
- Clindamycin 300mg TID (if penicillin allergy)
- Duration: 1-2 weeks
Moderate Infection (inpatient or close outpatient):
- Ampicillin-sulbactam 3g IV Q6H, OR
- Ceftriaxone 2g IV daily PLUS metronidazole 500mg IV Q8H, OR
- Ertapenem 1g IV daily (if MRSA risk, add vancomycin)
Severe Infection (inpatient, broad-spectrum):
- Vancomycin 15mg/kg IV Q12H (trough 15-20) PLUS
- Piperacillin-tazobactam 4.5g IV Q6H, OR
- Meropenem 1g IV Q8H
- Consider antifungal if prolonged antibiotics or immunosuppressed
MRSA Coverage (add if risk factors: previous MRSA, healthcare exposure, failed cephalosporin):
- Vancomycin, OR
- Linezolid 600mg PO/IV BID, OR
- Daptomycin 6mg/kg IV daily
Osteomyelitis Management
Diagnosis:
- Probe-to-bone positive (LR+ 6.4)
- MRI: bone marrow edema + cortical destruction
- Bone biopsy (gold standard): histology + culture
Treatment Options:
1. Surgical Debridement + Antibiotics (preferred):
- Remove all infected, necrotic bone until bleeding viable bone
- Send bone for culture and histology
- IV antibiotics for 4-6 weeks based on bone culture
- Cure rate: 60-80% for non-heel, 40-60% for heel
2. Antibiotics Alone (selected cases):
- Indications: poor surgical candidate, patient refuses, minor bone involvement
- 6-12 weeks IV or highly bioavailable oral (fluoroquinolone, linezolid)
- Cure rate: 60-70% (similar to surgery in some studies)
- Requires close follow-up
3. Amputation:
- Indications: extensive bone destruction, failed conservative treatment, limb not salvageable
- May be curative if removes all infected tissue
Antibiotic Duration in Osteomyelitis
After adequate surgical debridement removing all infected bone, 2-4 weeks of antibiotics may suffice. If residual infected bone remains or antibiotics-only treatment, 6 weeks minimum. Recent evidence suggests shorter courses equally effective after adequate debridement.
Surgical Management
Indications for Surgery
Urgent/Emergent Surgery (within 24 hours):
- Necrotizing soft tissue infection
- Gas gangrene (crepitus, gas on X-ray)
- Sepsis or severe infection with systemic toxicity
- Compartment syndrome of foot
- Wet gangrene with systemic signs
Elective/Scheduled Surgery:
- Osteomyelitis (surgical debridement)
- Deep abscess requiring drainage
- Non-healing ulcer despite 6-12 weeks optimal conservative care
- Recurrent ulceration requiring prophylactic surgery (ATL, exostectomy)
- Dry gangrene (scheduled amputation once demarcated)
This section covers surgical indications and timing.
Charcot Neuroarthropathy
Definition and Pathophysiology
Charcot neuroarthropathy (Charcot foot) is a progressive destructive arthropathy of the foot and ankle in patients with peripheral neuropathy, resulting in bone and joint destruction, fractures, and deformity.
Incidence: 0.1-0.4% of diabetics; up to 30% in high-risk diabetic populations
Pathophysiology (two theories):
- Neurovascular theory: autonomic neuropathy → increased blood flow → bone resorption
- Neurotraumatic theory: loss of protective sensation → repetitive microtrauma → fractures
Eichenholtz Classification (Stages)
Stage 0 (Prodromal):
- Warm, swollen foot
- NO X-ray changes yet
- Mimics cellulitis or DVT
- Critical to diagnose - treat now to prevent deformity
Stage 1 (Development/Fragmentation):
- X-ray: fractures, fragmentation, joint dislocation
- Clinically: warm, swollen, erythematous
- Most important stage to immobilize
Stage 2 (Coalescence):
- X-ray: absorption of debris, early healing
- Clinically: edema decreases, warmth decreases
- Continue immobilization
Stage 3 (Reconstruction/Consolidation):
- X-ray: bony remodeling, sclerosis, deformity is now fixed
- Clinically: cool, stable
- Transition to protective footwear/AFO
Clinical Patterns
Type 1 (Midfoot - 60%):
- Tarsometatarsal joints (Lisfranc)
- Rocker-bottom deformity
- High risk of plantar ulceration at apex
Type 2 (Hindfoot - 30%):
- Subtalar, talonavicular, calcaneocuboid joints
- Valgus or varus deformity
Type 3a (Ankle - 10%):
- Tibiotalar joint
- Unstable, high amputation risk
Type 3b (Calcaneus):
- Calcaneal fracture
- Loss of heel height
Management
Acute Phase (Stage 0-1):
- Non-weight bearing in total contact cast
- Cast changes every 1-2 weeks (monitor for progression)
- Serial X-rays to monitor healing
- Continue until: edema resolved, temperature difference less than 2°C compared to contralateral
- Duration: typically 3-6 months minimum
Subacute/Chronic (Stage 2-3):
- Gradual transition to weight-bearing in CROW walker (Charcot Restraint Orthotic Walker)
- Custom AFO or CROW boot for long-term use
- Extra-depth shoes with custom orthotics
Surgical Indications:
- Recurrent ulceration despite bracing
- Severe instability preventing bracing
- Techniques: exostectomy, osteotomy, arthrodesis (fusion)
- High complication rate (nonunion, infection, Charcot recurrence)
Do NOT confuse acute Charcot with infection! Both present with warm, red, swollen foot. Key differences:
- Charcot: NO ulcer (unless late), X-ray shows fractures/dislocation, CRP/ESR elevated but WBC normal
- Infection: ulcer present, purulence, systemic signs, WBC elevated
When in doubt, immobilize and observe - treating infection that doesn't exist is less harmful than missing Charcot.
Complications
Local Complications
Infection (40-80% of DFUs):
- Cellulitis: spreading erythema, warmth, edema
- Abscess: fluctuant collection requiring drainage
- Osteomyelitis: 10-15% of moderate-severe infections
- Septic arthritis: joint involvement, rapid destruction
- Necrotizing fasciitis: rare but life-threatening (mortality 20-30%)
- Gas gangrene: crepitus, systemic toxicity (requires urgent debridement)
Non-healing/Chronicity (50% recurrence within 3 years):
- Biofilm formation (60-80% of chronic wounds)
- Wound edge senescence (cells stop dividing)
- Persistent inflammation
- Tissue hypoxia from PAD
- Continued mechanical stress (poor offloading compliance)
Amputation (5-24% of DFUs):
- Minor amputation (toe, ray, TMA): 50-90% healing depending on level
- Major amputation (BKA, AKA): required if limb-threatening infection or critical ischemia
- Contralateral amputation risk: 50% at 5 years after first amputation
Charcot Arthropathy:
- Occurs in 0.1-0.4% of diabetics
- Can develop during or after DFU treatment
- Rocker-bottom deformity leads to recurrent ulceration if not braced
Systemic Complications
Sepsis and Septic Shock:
- Diabetic foot infections are leading cause of sepsis in diabetics
- Mortality 10-40% in severe DFU-related sepsis
- Risk factors: delayed presentation, extensive necrosis, gas-forming organisms
Metabolic Decompensation:
- Infection causes insulin resistance
- Hyperglycemia worsens WBC function (vicious cycle)
- May precipitate diabetic ketoacidosis (DKA) in type 1 diabetics
Cardiovascular Events:
- Increased MI risk during acute infection (inflammatory stress)
- DVT/PE risk from immobilization and hypercoagulability
Renal Deterioration:
- Diabetic nephropathy worsens with sepsis
- Antibiotic nephrotoxicity (vancomycin, aminoglycosides)
- Contrast-induced nephropathy from imaging
Psychological and Social Complications
Depression and Anxiety:
- 40-50% of patients with diabetic foot complications have depression
- Fear of amputation
- Loss of independence
- Reduced quality of life
Economic Burden:
- Average DFU treatment cost: USD 20,000-50,000 per episode
- Major amputation with rehabilitation: USD 50,000-100,000
- Loss of employment (30-50% cannot return to work)
- Caregiver burden
Mortality:
- 5-year mortality after DFU: 30-40% (cardiovascular disease)
- 5-year mortality after major amputation: 50-70% (worse than most cancers)
- 1-year mortality after major amputation: 30%
Treatment Complications
Offloading-related:
- Pressure ulcers from TCC if poorly applied (5-10%)
- Falls risk with walker devices
- Contralateral limb stress (transfer lesions)
- Equinus contracture after prolonged immobilization
Surgical Complications:
- Wound breakdown: 10-30% depending on level
- Infection: 5-15% post-amputation
- Hematoma: 5-10%
- Phantom limb pain: 60-80% after major amputation
- Stump pain: 20-40%
Antibiotic-related:
- C. difficile infection (5-10% with prolonged antibiotics)
- Antibiotic resistance (MRSA, VRE, ESBL organisms)
- Nephrotoxicity, hepatotoxicity
- Allergic reactions
Recurrence and Long-term Outcomes
Recurrence Rates:
- 40% at 1 year despite initial healing
- 50% at 3 years
- 70% at 5 years
- Risk factors: poor offloading compliance, previous amputation, Charcot foot, PAD
Prevention of Complications:
- Multidisciplinary team approach reduces amputation by 49-85%
- Early aggressive treatment prevents progression
- Lifelong surveillance and therapeutic footwear
- Patient education and self-care
- Glycemic control (each 1% HbA1c reduction = 25% fewer microvascular complications)
Why is Mortality So High After DFU?
The high mortality (50% at 5 years post-major amputation) reflects that DFU is a marker of severe systemic disease, not just a local problem. Patients have:
- Advanced diabetes (often 15-20 years duration)
- Severe PAD (multivessel disease)
- Cardiac disease (MI risk 3-4x higher)
- Renal failure (dialysis patients have 2-3x amputation risk)
- Multiple comorbidities
DFU is the "tip of the iceberg" - the visible manifestation of systemic atherosclerosis and metabolic disease.
Prevention Strategies
Risk Stratification and Surveillance
IWGDF Risk Categories and Surveillance Frequency:
- Category 0 (no neuropathy): annual screening
- Category 1 (neuropathy alone): 6-12 month screening
- Category 2 (neuropathy + PAD or deformity): 3-6 month screening
- Category 3 (previous ulcer or amputation): 1-3 month screening
Patient Education (Self-Care)
Daily Foot Inspection:
- Look for blisters, cuts, cracks, redness
- Use mirror if cannot see bottom of foot
- Check between toes
- If vision impaired, have caregiver inspect
Daily Foot Care:
- Wash with lukewarm water (test with elbow, not foot)
- Dry thoroughly, especially between toes
- Apply moisturizer (but NOT between toes)
- Check shoes for foreign objects before wearing
Nail Care:
- Cut toenails straight across (not rounded)
- File edges smooth
- If cannot reach or see, have podiatrist cut nails
What NOT to Do:
- Do NOT walk barefoot (inside or outside)
- Do NOT use heating pads or hot water bottles on feet
- Do NOT try to remove calluses or corns themselves (risk of injury)
- Do NOT smoke (impairs healing)
Footwear Prescription
Therapeutic Footwear:
- Extra-depth shoes (1/2 inch extra toe box depth)
- Custom orthotics with accommodative padding
- Rocker-sole to reduce forefoot pressure
- Medicare covers for diabetics with neuropathy or deformity
Post-Ulcer Footwear:
- Continue protective footwear lifelong
- Replace every 6-12 months (breaks down with use)
- Replace orthotics annually
Glycemic Control
Evidence: Each 1% reduction in HbA1c associated with 25% reduction in microvascular complications (including neuropathy)
Target: HbA1c less than 7% (individualize based on patient factors)
Multidisciplinary Prevention Programs
Components of Successful Programs:
- Regular screening (based on risk category)
- Patient education (structured programs)
- Therapeutic footwear provision
- Podiatry for nail and callus care
- Prompt treatment of pre-ulcerative lesions
Evidence: Comprehensive prevention programs reduce:
- Ulcer incidence by 50-60%
- Amputation rates by 49-85%
- Recurrent ulcers by 35-50%
Evidence Base
Total Contact Casting for Offloading
- TCC heals 85-95% of plantar neuropathic DFUs within 12 weeks
- Removable walkers achieve only 30-60% healing due to compliance issues
- Reduces peak plantar pressure by 80-90% at ulcer site
- Non-removable devices are essential - patients wear removable devices only 20-30% of time
Multidisciplinary Foot Care Teams
- Reduce amputation rates by 49-85% compared to standard care
- Lower hospitalization rates and healthcare costs
- Improve healing rates and time to healing
- Teams include podiatrist, vascular surgeon, orthopaedic surgeon, diabetologist, wound specialist
Antibiotic Duration in Osteomyelitis
- 2-4 weeks antibiotics after complete surgical debridement as effective as 6 weeks (cure rate 80% vs 82%)
- Without debridement or with residual infected bone, 6-12 weeks needed
- Shorter courses reduce side effects, costs, and antibiotic resistance
- Adequate surgical removal of infected bone is key determinant of outcome
Probe-to-Bone Test for Osteomyelitis
- Sensitivity 87%, specificity 83% for osteomyelitis diagnosis
- Positive likelihood ratio 6.4 - if positive, assume osteomyelitis
- Negative likelihood ratio 0.15 - if negative, osteomyelitis unlikely
- Simple bedside test requiring only sterile probe after debridement
Prevention Programs Reduce Amputation
- Structured prevention programs reduce ulcer incidence by 50-60%
- Amputation rates reduced by 49-85% with comprehensive programs
- Components: education, therapeutic footwear, podiatry, prompt treatment
- Cost-effective intervention with high return on investment
Exam Viva Scenarios
Practice these scenarios to excel in your viva examination
Scenario 1: Plantar Forefoot Ulcer
"A 58-year-old man with 15-year history of type 2 diabetes presents with a 3-week history of a painless wound on the plantar aspect of his right foot under the 2nd metatarsal head. He walks daily for exercise. On examination, there is a 2cm diameter ulcer with callused edges, no purulence, minimal erythema (less than 1cm), and you can probe to the dermis but not deeper structures. His foot is warm with palpable pulses. He cannot feel a 10g monofilament at 6 of 9 sites."
Scenario 2: Deep Infected Ulcer with Osteomyelitis
"A 62-year-old woman with poorly controlled diabetes (HbA1c 10.2%) presents with a 6-week history of a malodorous wound on her right great toe. She has been treating it herself with over-the-counter creams. On examination, there is a 3cm ulcer on the plantar aspect of the hallux with purulent drainage, surrounding erythema extending 4cm proximally, and exposed bone at the base when probed. Her foot is warm but you can palpate pedal pulses. Temperature is 38.1°C, WBC 14.2, ESR 78, CRP 92."
Scenario 3: Neuroischemic Ulcer - Revascularization Decision
"A 67-year-old man with longstanding diabetes and smoking history presents with a 4-month non-healing lateral foot ulcer. The ulcer is painful (unusual for him). On examination, his foot is cool, hairless, with absent pulses. ABI on right is 0.42, left is 0.68. Monofilament testing shows loss of protective sensation bilaterally. The ulcer is 2cm, clean with poor granulation tissue. TcPO2 at the forefoot is 28 mmHg."
DIABETIC FOOT ULCERS - Rapid Review
High-Yield Exam Summary
Pathophysiology Triad
- •Sensory neuropathy: loss of protective sensation (10g monofilament)
- •Motor neuropathy: intrinsic atrophy, claw toes, high pressure
- •Peripheral arterial disease: tibial/peroneal, foot vessels spared
- •Add immunopathy: WBC dysfunction from hyperglycemia
- •Result: repetitive unrecognized trauma on insensate, ischemic, infection-prone foot
Classifications (Know All Three)
- •Wagner 0-5: depth-based (0=intact skin → 5=whole foot gangrene)
- •Texas: 4×4 grid (depth A-D × stage 0-3 for ischemia/infection)
- •PEDIS: Perfusion, Extent, Depth, Infection, Sensation
- •Wagner Grade 1 = superficial; Grade 2 = to tendon; Grade 3 = osteomyelitis/abscess
Assessment (The 3 P's)
- •Pulses: dorsalis pedis, posterior tibial (absent = PAD)
- •Protective sensation: 10g monofilament at 9 sites (1 abnormal = loss)
- •Probe to bone: LR+ 6.4 for osteomyelitis if positive
- •ABI: less than 0.9 = PAD; less than 0.5 = critical; greater than 1.3 = calcified (use toe pressure)
- •TcPO2: less than 30 mmHg = poor healing; need revascularization
Offloading (THE Critical Treatment)
- •Total contact cast: gold standard, 85-95% healing at 12 weeks
- •Reduces plantar pressure 80-90%, non-removable = compliance
- •iTCC walker: acceptable alternative if rendered non-removable
- •Removable devices fail (patients wear only 20-30% of time)
- •Continue offloading 4-6 weeks AFTER healing to prevent recurrence
Infection Diagnosis (IDSA Criteria)
- •Purulence OR 2+ signs: warmth, erythema greater than 2cm, lymphangitis, edema, pain
- •Mild: erythema less than 2cm, superficial → oral antibiotics outpatient
- •Moderate: erythema greater than 2cm OR deep → IV antibiotics, surgery often needed
- •Severe: SIRS or limb-threatening → IV broad-spectrum, urgent surgery
- •Do NOT treat colonization - all chronic wounds colonized
Osteomyelitis Management
- •Diagnosis: probe-to-bone (LR+ 6.4), MRI (bone marrow edema), bone biopsy (gold standard)
- •Treatment: surgical debridement to bleeding bone + 4-6 week IV antibiotics
- •OR antibiotics alone for 6-12 weeks if poor surgical candidate
- •Send bone for culture AND histology
- •Cure rate 60-80% for non-heel OM with adequate surgery
Amputation Healing Rates
- •Toe: 90-95% healing, minimal functional loss
- •Ray: 80-90% healing, narrow shoe needed
- •Transmetatarsal: 50-70% healing, high equinus risk (need AFO)
- •Syme: 70-80% healing, end-bearing stump
- •Below-knee: 80-90% healing, good prosthetic function
- •Above-knee: 85-95% healing, poor prosthetic function
Prevention (Evidence-Based)
- •Risk stratification: Category 0-3 determines screening frequency
- •Therapeutic footwear: extra-depth shoes + custom orthotics
- •Patient education: daily inspection, appropriate footwear, no barefoot
- •Glycemic control: each 1% HbA1c reduction = 25% microvascular complication reduction
- •Multidisciplinary teams reduce amputation by 49-85%
Exam Pearls
- •15% lifetime ulcer risk in diabetics; 50% recur within 3 years
- •Major amputation 5-year mortality: 50% (worse than most cancers)
- •Neuropathic ulcers painless; ischemic ulcers painful (key difference)
- •Weekly sharp debridement essential - converts chronic to acute wound
- •TCC is treatment, not adjunct - no offloading = no healing
Australian Context
PBS and Healthcare Considerations
Pharmaceutical Benefits Scheme (PBS):
- Advanced wound care products available under PBS for diabetic foot ulcers meeting criteria
- Becaplermin (Regranex) may be available through special access scheme
- Antibiotic coverage for diabetic foot infections under standard PBS
Public System Coverage:
- Podiatry services for diabetic patients with active ulcers or high-risk foot
- Multidisciplinary care plans (GP Management Plans, Team Care Arrangements)
- Wound care and debridement procedures covered
- Vascular imaging and intervention fully funded
National Diabetes Services Scheme (NDSS)
Provides subsidized:
- Blood glucose monitoring
- Insulin delivery devices
- Educational resources for foot care
Australian Clinical Practice
High-risk foot services across major metropolitan hospitals include multidisciplinary teams consistent with international guidelines. Regional and remote areas may require telehealth consultation with tertiary centers.