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Diabetic Foot Ulcers

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Contents
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Diabetic Foot Ulcers

Comprehensive guide to diabetic foot ulcer pathophysiology, Wagner and University of Texas classifications, assessment, offloading, wound care, surgical management, and prevention strategies

complete
Updated: 2025-12-25
High Yield Overview

DIABETIC FOOT ULCERS

Neuropathy + Vasculopathy + Immunopathy | Wagner and Texas Classifications | Offloading is Key

15%Lifetime risk in diabetics
85%Preceded by neuropathy
50%Recurrence within 3 years
5-24%Progress to amputation

WAGNER CLASSIFICATION (0-5)

Grade 0
PatternPre-ulcerative (callus, deformity)
TreatmentPrevention, orthotics
Grade 1
PatternSuperficial ulcer
TreatmentOffloading, debridement
Grade 2
PatternDeep ulcer (tendon/joint/bone)
TreatmentSurgical debridement
Grade 3
PatternDeep with osteomyelitis/abscess
TreatmentAntibiotics, surgery
Grade 4
PatternForefoot gangrene
TreatmentPartial amputation
Grade 5
PatternWhole foot gangrene
TreatmentMajor amputation

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

Three classes of chronic wound on a diabetic patient’s foot. This image shows a diabetic individual with three classes of chronic wound on the same foot: an ischemic third toe, a neuropathic/infected
Click to expand
Three classes of chronic wound on a diabetic patient’s foot. This image shows a diabetic individual with three classes of chronic wound on the same foCredit: Nunan R et al. via Dis Model Mech via Open-i (NIH) (Open Access (CC BY))
(a) A 51-year-old lady with underlying long-standing diabetes mellitus presented with large diabetic foot ulcer over her right foot dorsum, exposing extensor tendons and covered with slough tissue. (b
Click to expand
(a) A 51-year-old lady with underlying long-standing diabetes mellitus presented with large diabetic foot ulcer over her right foot dorsum, exposing eCredit: Mat Saad AZ et al. via ISRN Endocrinol via Open-i (NIH) (Open Access (CC BY))
The ulcer of case 9 in group A. The lesion was localized to the plantar surface of the 3rd intermetatarsal space and was 175 mm2 before ESWT.
Click to expand
The ulcer of case 9 in group A. The lesion was localized to the plantar surface of the 3rd intermetatarsal space and was 175 mm2 before ESWT.Credit: Moretti B et al. via BMC Musculoskelet Disord via Open-i (NIH) (Open Access (CC BY))

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.

Mnemonic

ULCER - Diabetic Foot Ulcer Pathophysiology

U
Unprotected sensation
Sensory neuropathy - cannot feel minor trauma
L
Loss of muscle function
Motor neuropathy - intrinsic atrophy, claw toes, high pressure
C
Circulation impaired
Peripheral arterial disease - ischemia prevents healing
E
Elevated glucose
Hyperglycemia impairs WBC function, delays healing
R
Repetitive trauma
Unrecognized pressure from walking on insensate foot

Memory Hook:ULCER reminds you of the five pathological processes that create diabetic foot ulcers

Mnemonic

PEDIS - IWGDF Classification System

P
Perfusion
Assess vascular status - ABI, pulses, TcPO2
E
Extent
Size and number of ulcers (cm²)
D
Depth
Superficial, to tendon, to bone
I
Infection
None, local, systemic
S
Sensation
Monofilament testing - protective sensation present or absent

Memory Hook:PEDIS is the comprehensive assessment framework recommended by International Working Group on Diabetic Foot

Mnemonic

OFFLOAD - Principles of Pressure Relief

O
Off-weight bearing
Total contact cast or walker to redistribute pressure
F
Footwear modification
Custom orthotics with accommodative padding
F
Forefoot rocker sole
Reduces pressure at met heads during gait
L
Limit ambulation
Activity modification - reduce steps per day
O
Observe for new areas
Monitor for pressure redistribution ulcers
A
Adherence essential
Non-removable devices have better compliance
D
Duration until healed
Continue offloading 4-6 weeks after closure

Memory Hook:OFFLOAD summarizes the critical principles of mechanical pressure reduction in diabetic foot ulcer treatment

Mnemonic

The 3 P's of Diabetic Foot Assessment

P
Pulses
Dorsalis pedis, posterior tibial - feel and compare
P
Protective sensation
10g monofilament at 9 sites on plantar foot
P
Probe to bone
Sterile probe in ulcer - if touches bone, osteomyelitis likely

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:

  1. High pressure point (e.g., prominent met head)
  2. Repetitive loading without pain feedback
  3. Subcutaneous hemorrhage and tissue breakdown
  4. Callus forms over area
  5. Pressure increases further under callus
  6. Autolysis creates fluid-filled space
  7. 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

GradeDescriptionTreatmentHealing Rate
Grade 0Intact skin, pre-ulcerative (callus, bony deformity, erythema)Prevention: orthotics, education, callus debridementNot applicable
Grade 1Superficial ulcer, partial/full-thickness, no deeper structuresOffloading (TCC), sharp debridement, moist wound care85-95% at 12 weeks with proper offloading
Grade 2Deep ulcer to tendon, bone, or joint capsule (no abscess/OM)Surgical debridement, antibiotics if infected, offloading70-80% at 12-16 weeks
Grade 3Deep ulcer with abscess, osteomyelitis, or septic arthritisSurgical debridement, IV antibiotics, possible amputation50-60% limb salvage with aggressive treatment
Grade 4Localized gangrene (forefoot or heel)Partial amputation (toe, ray, transmetatarsal)80-90% healing of amputation site
Grade 5Extensive gangrene of entire footMajor 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.

University of Texas Classification

The UT-San Antonio system adds ischemia and infection to depth grading, creating a 4x4 grid (16 categories).

Depth Grades (A-D):

  • Grade A: Superficial (epidermis/dermis only)
  • Grade B: To tendon or capsule
  • Grade C: To bone or joint
  • Grade D: Necrotizing infection or gangrene

Stages (0-3):

  • Stage 0: Pre- or post-ulcerative lesion (healed)
  • Stage 1: Clean wound (no infection or ischemia)
  • Stage 2: Infected wound
  • Stage 3: Ischemic wound (with or without infection)

Example: A ulcer to bone with infection = Stage 2, Grade C or C2

Advantages of UT:

  • Better prognostic value than Wagner
  • Separately identifies infection and ischemia
  • Validated for amputation risk prediction
  • Stage 3 wounds (ischemic) have 90% amputation rate vs 10% for Stage 1

This completes the University of Texas classification.

PEDIS System (IWGDF Standard)

The International Working Group on Diabetic Foot (IWGDF) uses the PEDIS system for comprehensive assessment.

ParameterAssessmentGrading
PerfusionABI, pulses, TcPO21 = No PAD; 2 = PAD without CLI; 3 = CLI
ExtentSize in cm²Measure length × width
DepthTissue layers involved1 = Superficial; 2 = To fascia/muscle/tendon; 3 = To bone/joint
InfectionIDSA criteria1 = None; 2 = Local; 3 = SIRS/sepsis
SensationMonofilament testing1 = Intact; 2 = Loss of protective sensation

Infection Grades (IDSA/IWGDF):

  • Grade 1 (uninfected): No signs of infection
  • Grade 2 (mild): Local infection, erythema less than 2cm, superficial
  • Grade 3 (moderate): Erythema greater than 2cm OR deeper structures involved
  • Grade 4 (severe): SIRS present (2 or more: temp greater than 38°C or less than 36°C, HR greater than 90, RR greater than 20, WBC greater than 12 or less than 4)

Which Classification to Use in Exams?

Use Wagner for initial communication (examiner will immediately understand Grade 1 vs 3). Then add UT or PEDIS details: "This is a Wagner Grade 2 ulcer, but using the Texas system it's a B2 - deep to tendon with infection, requiring surgical debridement and antibiotics." This shows comprehensive knowledge.

This completes the PEDIS classification system.

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

ModalitySensitivitySpecificityAdvantagesDisadvantages
Plain X-ray54-68%68-75%Cheap, widely available, detects gasInsensitive early (2-3 weeks delay), cannot assess soft tissue
MRI90-95%70-85%Best for bone marrow edema, soft tissue abscessExpensive, cannot if metal implants, lower specificity
Nuclear (WBC scan)74-100%68-90%Functional imaging, specific for infectionTime-consuming, radiation, may miss chronic OM
Bone biopsyGold standardGold standardHistology + culture, definitive diagnosisInvasive, 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

📊 Management Algorithm
diabetic foot ulcers management algorithm
Click to expand
Management algorithm for diabetic foot ulcersCredit: OrthoVellum

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

DeviceHealing RateComplianceIndicationsCost
Total Contact Cast85-95%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 Walker30-50%20-30% (poor)Non-compliant patients, acute Charcot$$
Half Shoe (wedge)30-40%40-60%Post-op amputation, forefoot offloading$
Felted Foam40-60%70-80%Temporary measure, outpatient debridement$
Custom OrthoticsPrevention80%Healed ulcers, prevention, redistribution$$$

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 TypeExudateDressingMechanism
NecroticMinimalHydrogelAutolytic debridement
SloughyModerateHydrocolloid or foamAbsorb exudate, protect
GranulatingLightHydrocolloid, alginateMaintain moisture
EpithelializingMinimalFilm or hydrocolloidNon-adherent, protect
InfectedHeavyAntimicrobial (silver, iodine) + foamInfection 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

SeverityClinical FeaturesTreatmentSetting
UninfectedNo signs of infectionNo antibiotics - wound care and offloading onlyOutpatient
MildErythema less than 2cm, superficial, no systemic signsOral antibiotics, outpatient debridementOutpatient
ModerateErythema greater than 2cm OR deep tissue involved, no systemic signsIV or oral antibiotics, surgical debridement often neededInpatient or close outpatient
SevereSIRS present OR limb-threatening (necrotizing infection, gangrene)IV broad-spectrum antibiotics, urgent surgery, ICU if septicInpatient (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.

Surgical Debridement Technique

Principles:

  • Remove ALL necrotic, infected, and devitalized tissue
  • Debride to healthy, bleeding tissue (red muscle, bleeding bone)
  • Open up all pockets and undermined areas
  • Do NOT close infected wounds primarily (leave open)

Steps:

  1. Incise along ulcer margins or make separate incision for better exposure
  2. Excise wound edges back to healthy dermis
  3. Explore all deeper planes - find and drain all pockets
  4. Remove necrotic fascia, tendon, muscle
  5. Debride bone until punctate bleeding (remove cortical and medullary infection)
  6. Irrigate copiously (3-9L pulsed lavage)
  7. Pack wound open with saline gauze
  8. Plan return to OR in 48-72h for reassessment (may need multiple debridements)

Specimens to Send:

  • Deep tissue for culture (aerobic, anaerobic, fungal)
  • Bone for culture AND histology (if osteomyelitis suspected)

Negative Pressure Wound Therapy Post-Debridement

After adequate debridement, consider NPWT:

  • Apply after 1-2 trips to OR when wound is clean
  • Use until granulation fills defect
  • May allow delayed primary closure or skin graft

This completes the debridement technique discussion.

Amputation Levels and Healing Rates

Principles:

  • Most distal level that will heal and preserve function
  • Adequate debridement of all infected tissue
  • Preserve length when possible (lever arm for ambulation)
  • Guillotine amputation if septic (revise later)

Amputation Levels (distal to proximal):

Amputation Healing Rates

LevelHealing RateFunctional OutcomeEnergy Cost
Toe amputation90-95%Excellent (minimal gait change)Baseline
Ray amputation80-90%Very good (narrow shoe)Baseline to +5%
Transmetatarsal (TMA)50-70%Good with AFO, risk of equinus+10-15%
Syme (ankle disarticulation)70-80%End-bearing prosthesis+20-30%
Below-knee (transtibial)80-90%Prosthesis, good ambulation+40-60%
Above-knee (transfemoral)85-95%Prosthesis, limited walking+100-120%

Specific Amputation Techniques

Toe Amputation:

  • Racquet incision (plantar longer than dorsal)
  • Disarticulate at MTP joint OR transect proximal phalanx
  • Preserve plantar pad if possible
  • Leave open if infected; primary closure if clean

Ray Amputation (metatarsal + toe):

  • Resect metatarsal to base (preserve base if rays 1 or 5 for stability)
  • Close primarily if non-infected
  • Central rays (2-4) tolerated well; 1st or 5th ray loss alters biomechanics

Transmetatarsal Amputation (TMA):

  • Long plantar flap, short dorsal flap
  • Transect mets at mid-shaft level
  • Bevel bone edges
  • Drain and close over drain
  • Post-op: high risk of equinus contracture (Achilles overpowers dorsiflexors)
    • Consider prophylactic Achilles lengthening
    • AFO (ankle-foot orthosis) for 6-12 months

Syme Amputation:

  • Ankle disarticulation preserving heel pad
  • Remove malleoli flush with tibial plafond
  • End-bearing stump (can walk short distances without prosthesis)
  • Good option for patients who may not tolerate BKA prosthesis

Below-Knee Amputation (BKA):

  • Level: 12-15cm below knee joint (preserves knee function)
  • Technique: long posterior flap, short anterior flap
  • Myodesis (suture muscle to bone) for better stump control
  • Healing: 80-90% (higher is better)
  • Prosthesis allows good ambulation (60-80% become community ambulators)

Guillotine Amputation:

  • Emergency procedure for septic patient
  • Open amputation through infected area
  • No flaps, no closure - pack open
  • Allows source control
  • Plan definitive revision in 3-7 days once sepsis controlled

This completes the amputation section.

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

Level I (RCTs)
Armstrong et al. (1997, 2005) • Diabetes Care
Key Findings:
  • 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
Clinical Implication: This evidence guides current practice.

Multidisciplinary Foot Care Teams

Level I (Systematic Reviews)
Krishnan et al. (2008), Canavan et al. (2008) • Cochrane Database Syst Rev, Diabetes Care
Key Findings:
  • 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
Clinical Implication: This evidence guides current practice.

Antibiotic Duration in Osteomyelitis

Level II (Prospective Cohorts)
Lázaro-Martínez et al. (2014), Senneville et al. (2020) • Diabetes Care, Clinical Infectious Diseases
Key Findings:
  • 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
Clinical Implication: This evidence guides current practice.

Probe-to-Bone Test for Osteomyelitis

Level II (Diagnostic Studies)
Grayson et al. (1995), Aragón-Sánchez et al. (2010) • JAMA, Diabetes Care
Key Findings:
  • 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
Clinical Implication: This evidence guides current practice.

Prevention Programs Reduce Amputation

Level I (RCTs and Systematic Reviews)
Lavery et al. (2005), Policarpo et al. (2014) • Diabetes Care, Cochrane Database
Key Findings:
  • 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
Clinical Implication: This evidence guides current practice.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Plantar Forefoot Ulcer

EXAMINER

"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."

EXCEPTIONAL ANSWER
This patient presents with a Wagner Grade 1 (or University of Texas Grade A1) plantar neuropathic ulcer under the 2nd metatarsal head. He has clear evidence of peripheral neuropathy (loss of protective sensation) but intact vascular supply (palpable pulses, warm foot). My systematic approach would be: **Assessment**: I would confirm this is an uninfected, superficial, non-ischemic ulcer. I would perform monofilament testing bilaterally, check ankle-brachial indices, and probe the wound after debridement. Blood tests would include HbA1c to assess glycemic control. **Classification**: This is Wagner Grade 1, University of Texas A1 (superficial, non-infected, non-ischemic). **Management priorities**: 1. **Offloading** - This is THE critical treatment. I would recommend total contact casting as gold standard, which reduces plantar pressure by 80-90% and achieves 85-95% healing at 12 weeks. If TCC not available, instant total contact walker rendered non-removable. 2. **Sharp debridement** - Weekly debridement of all callus and non-viable tissue to healthy bleeding base. This removes biofilm and converts chronic to acute wound. 3. **Wound care** - Moist wound environment with simple non-adherent dressing, changed after each debridement. 4. **Glycemic optimization** - Target HbA1c less than 7%. 5. **Education** - Explain that the ulcer is painless due to neuropathy, but continued walking on it prevents healing. **Follow-up**: Weekly initially for debridement and cast changes. Expect healing in 6-12 weeks with proper offloading. Once healed, transition to therapeutic footwear with custom orthotics to prevent recurrence. **Long-term**: This patient needs lifelong protective footwear, regular podiatry, and is now IWGDF Risk Category 3 (previous ulcer) requiring 1-3 monthly surveillance.
KEY POINTS TO SCORE
Emphasize offloading as THE critical treatment - not adjunct therapy
Wagner Grade 1 = superficial; Texas adds ischemia/infection status
TCC is gold standard with 85-95% healing rate
Weekly sharp debridement essential
Mention lifelong prevention after healing
COMMON TRAPS
✗Don't jump to antibiotics - this is uninfected (no purulence, minimal erythema)
✗Don't forget to classify using both Wagner AND Texas systems
✗Don't recommend removable walker without making it non-removable (compliance issue)
✗Don't ignore education about continued risk after healing
LIKELY FOLLOW-UPS
"What if this ulcer doesn't heal after 12 weeks of appropriate offloading? (Reassess: infection, osteomyelitis, ischemia, non-compliance; consider advanced therapies like NPWT, becaplermin, or surgical offloading)"
"How would you assess for osteomyelitis? (Probe-to-bone test, plain X-rays, elevated ESR/CRP, MRI if high suspicion, bone biopsy for gold standard)"
"What if he refuses TCC because he wants to shower daily? (Explain non-removable is essential for compliance; offer iTCC walker as alternative; explain that removable devices fail 70% of time; discuss temporary lifestyle modifications for limb salvage)"
VIVA SCENARIOChallenging

Scenario 2: Deep Infected Ulcer with Osteomyelitis

EXAMINER

"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."

EXCEPTIONAL ANSWER
This is a Wagner Grade 3 (or Texas C2-3) diabetic foot ulcer with moderate-to-severe infection and osteomyelitis requiring urgent surgical intervention. **Assessment**: This patient has: - **Deep ulcer** (probe-to-bone positive - osteomyelitis until proven otherwise) - **Moderate infection** by IDSA criteria (purulence, erythema greater than 2cm, systemic signs) - **Positive probe-to-bone** (LR+ 6.4 for osteomyelitis) - **Poor glycemic control** (HbA1c 10.2% - impairs WBC function and wound healing) - **Adequate perfusion** (palpable pulses) **Immediate management** (same-day admission): 1. **IV antibiotics** - Broad-spectrum empiric coverage for moderate diabetic foot infection: - Vancomycin 15mg/kg IV Q12H (cover MRSA) PLUS - Piperacillin-tazobactam 4.5g IV Q6H (cover gram-negatives and anaerobes) - Adjust based on cultures at 48-72 hours 2. **Blood cultures** - given fever 3. **Imaging**: - Plain X-rays (may show bone destruction if chronic) - MRI foot (gold standard for osteomyelitis diagnosis - bone marrow edema, cortical destruction) 4. **Surgical debridement** within 24 hours: - Remove all purulent material, necrotic tissue - Debride infected bone to healthy bleeding cortex - Send bone for culture AND histology - Leave wound open, pack with saline gauze - May need serial debridements **Definitive management**: After adequate debridement, two options: - **Toe amputation** (curative if removes all infected bone, 90-95% healing rate) - **Hallux salvage** with extensive bone debridement + 4-6 weeks IV antibiotics Decision depends on: extent of bone involvement on MRI, patient preference, functional impact. **Post-operative**: - Non-weight bearing until infection cleared - Transition to oral antibiotics once afebrile, WBC normalizing, wound improving - Total duration 4-6 weeks if residual bone, 2-4 weeks if complete debridement - Aggressive glycemic control (insulin if needed to achieve HbA1c less than 7%) **Long-term**: - Therapeutic footwear if hallux preserved - Toe filler orthotic if amputated - Lifelong foot surveillance (Category 3 risk)
KEY POINTS TO SCORE
Recognize moderate-to-severe infection requiring admission and IV antibiotics
Probe-to-bone positive = assume osteomyelitis, plan accordingly
Surgical debridement is priority (antibiotics alone insufficient for extensive bone infection)
Send bone for BOTH culture and histology
Address poor glycemic control as contributor to infection and poor healing
COMMON TRAPS
✗Don't treat as outpatient with oral antibiotics - this is moderate-severe infection
✗Don't forget anaerobic coverage (foul odor suggests anaerobes)
✗Don't close wound primarily - infected wounds must heal by secondary intention
✗Don't delay surgery - infected bone needs debridement urgently
✗Don't forget that fever in diabetic foot infection is ominous (often have blunted response)
LIKELY FOLLOW-UPS
"She declines toe amputation and wants to save the hallux. What do you counsel? (Explain risks: prolonged antibiotics with side effects, risk of treatment failure requiring later amputation anyway, functional outcomes similar if proper footwear used; if patient adamant, require strict compliance with antibiotics, offloading, follow-up)"
"What if pedal pulses were absent? (Check ABI; if less than 0.5 or non-compressible, vascular surgery consult for revascularization before/concurrent with debridement; ischemia dramatically worsens infection prognosis)"
"How do you decide between 4-week vs 6-week antibiotic course? (If post-debridement MRI shows residual bone marrow edema or clinical improvement slow, 6 weeks; if complete debridement confirmed and rapid improvement, 4 weeks sufficient; some evidence suggests shorter courses equally effective after adequate surgery)"
VIVA SCENARIOChallenging

Scenario 3: Neuroischemic Ulcer - Revascularization Decision

EXAMINER

"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."

EXCEPTIONAL ANSWER
This patient has a **neuroischemic diabetic foot ulcer** with critical limb ischemia requiring urgent vascular assessment for revascularization. **Key features**: - **Critical ischemia**: ABI 0.42 (less than 0.5), absent pulses, cool foot, TcPO2 28 mmHg (less than 30 indicates poor healing potential) - **Neuropathy**: loss of protective sensation, but ulcer is painful (ischemic pain component) - **Non-healing ulcer** despite 4 months (ischemia prevents healing) - **Modifiable risk factor**: active smoking **Assessment priorities**: 1. **Vascular workup**: - Duplex ultrasound arterial mapping (identify level and extent of disease) - CT angiography or MR angiography (plan revascularization) - Pedal arch assessment (important for foot salvage) 2. **Ulcer assessment**: - Wagner grade, infection status - Probe to bone (osteomyelitis) - Wound culture if signs of infection 3. **Medical optimization**: - **Smoking cessation** (critical - continued smoking associated with 2-3x higher revascularization failure) - Antiplatelet therapy (aspirin or clopidogrel) - Statin therapy - Glycemic control **Management plan**: 1. **Urgent vascular surgery referral** for revascularization: - **Endovascular** (angioplasty ± stenting) preferred first-line for infrapopliteal disease - **Bypass** if endovascular fails or anatomy unsuitable (vein bypass to tibial/pedal vessels) - Goal: restore inline flow to foot (at least one tibial vessel patent to ankle) 2. **Wound care** during revascularization planning: - Moist dressings - Offloading (but less critical than for neuropathic ulcers - ischemia is limiting factor) - Treat infection if present - Pain management (often significant rest pain) 3. **Post-revascularization**: - Re-assess healing potential (repeat ABI, TcPO2) - Target TcPO2 greater than 40 mmHg for reliable healing - If improves, proceed with standard ulcer care (offloading, debridement, wound care) - If no improvement or short-segment disease, consider **hyperbaric oxygen** as adjunct 4. **If revascularization not possible**: - Palliate symptoms - Discuss amputation (BKA vs AKA based on healing potential) - BKA may fail if proximal disease extensive (need popliteal patency for BKA healing) **Prognosis**: - With successful revascularization: 60-80% limb salvage at 1 year - Without revascularization: amputation likely (greater than 90% within 1 year) - Critical ischemia + diabetes has 50% major amputation or death at 5 years **Counseling**: Explain that **smoking cessation is mandatory** for limb salvage. Continued smoking doubles the risk of revascularization failure and amputation.
KEY POINTS TO SCORE
Recognize critical ischemia: ABI less than 0.5, TcPO2 less than 30 - needs revascularization
Neuroischemic ulcers are painful (unlike pure neuropathic) - key clinical clue
Urgent vascular surgery referral is priority - wound care alone will fail
Smoking cessation is mandatory, not optional
Know healing thresholds: ABI greater than 0.5, TcPO2 greater than 40 needed for reliable healing
COMMON TRAPS
✗Don't focus only on wound care - ischemia is the limiting factor here
✗Don't miss critical ischemia diagnosis (ABI less than 0.5 is urgent)
✗Don't forget that ABI can be falsely elevated in diabetics (if greater than 1.3, use toe pressures or TcPO2)
✗Don't offer TCC for neuroischemic ulcer - may worsen ischemia by compression
✗Don't underestimate importance of smoking cessation - must counsel aggressively
LIKELY FOLLOW-UPS
"What if ABI is 1.5 on the right? (Falsely elevated due to medial arterial calcification - non-compressible vessels. Use toe-brachial index or TcPO2 instead. TBI less than 0.5 indicates ischemia.)"
"Patient says he's tried to quit smoking many times but failed. How do you approach this? (Empathetic but firm: explain this is life/limb threatening; offer all resources: nicotine replacement, varenicline, bupropion, counseling; consider not offering revascularization if continues smoking due to futility; document counseling and patient decision)"
"After successful revascularization, ABI improves to 0.78 but ulcer still not healing after 8 weeks. What next? (Re-assess: infection? Osteomyelitis? Offloading adequate? Glycemic control? Consider advanced therapies: NPWT, growth factors, skin substitutes; consider hyperbaric oxygen; if all fails and infection develops, may still need amputation despite revascularization)"

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.

Quick Stats
Reading Time155 min
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