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DIABETIC FOOT
MS Orthopaedics - 20 Marks Answer
DEFINITION / INTRODUCTION
Diabetic foot refers to the spectrum of pathological conditions affecting the foot in a patient with diabetes mellitus, arising from the triad of peripheral neuropathy, peripheral vascular disease, and impaired immunity. It is the leading cause of non-traumatic lower extremity amputation worldwide. A diabetic patient has a lifetime risk of 15% for developing a foot ulcer, with an annual incidence of 2%. Foot ulcers result in the highest rate of hospital admissions and lower extremity amputations among diabetics.
PATHOPHYSIOLOGY / ETIOPATHOGENESIS
The pathology is multifactorial. Six distinct mechanisms operate simultaneously:
1. Peripheral Neuropathy (MOST IMPORTANT)
High blood glucose causes glycosylation of proteins and haemoglobin, forming advanced glycation end-products that precipitate in walls of small peripheral vessels and nerve tissue. This leads to:
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Sensory neuropathy: Polyneuropathic loss of sensation in a "stocking distribution," progressing proximally. Loss of protective sensation is the most common cause of plantar foot ulcers. Diagnosed by inability to perceive the 5.07 Semmes-Weinstein monofilament (10 g pressure). Patients with this finding have a 30% risk of developing a foot ulcer.
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Autonomic neuropathy: Abnormal sweating mechanism leads to a dry foot. This creates fissuring cracks, which become portals for infection.
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Motor neuropathy: Most commonly involves the common peroneal nerve, causing foot drop and loss of tibialis anterior function. Small intrinsic muscles are also affected, resulting in claw toes with toe-tip ulcerations due to excessive pressure.
2. Hypomobility Syndrome
Excessive glycosylation of soft tissues causes decreased joint range of motion, altered foot biomechanics, and increased plantar pressures (midfoot pressures are 46% higher in diabetic cadaver feet during simulated walking).
3. Peripheral Vascular Disease
Occurs in 60-70% of patients with diabetes for >10 years. Involves both large vessels (atherosclerosis) and small vessels (basement membrane thickening, reduced endothelial nitric oxide). Diabetic patients are twice as likely to develop peripheral arterial disease; with PVD present, they are nine times more likely to develop a foot ulcer.
4. Immune System Impairment
Hyperglycemia causes abnormal phagocytosis, altered chemotaxis of WBCs, and a poor cytotoxic environment - making it difficult to fight off infection once established.
5. Metabolic Deficiency
Reduced total protein (<6.0 g/dL), albumin (<2.5 g/dL), and WBC (<1500/mm³) result in poor wound healing potential.
6. Structural/Biomechanical Factors
Equinus contracture (Achilles tightening) transfers excessive load to the forefoot. Charcot joint further deforms foot architecture.
CLINICAL FEATURES
History
- Long-standing diabetes (usually >10 years)
- Peripheral neuropathy symptoms: numbness, tingling, paresthesias
- Claudication (suggests PVD)
- Prior ulcers, amputations, vision problems, renal disease
- Patients frequently deny trauma due to sensory loss
Physical Examination
Inspection:
- Shiny, hairless, taut skin - suggests peripheral arterial disease
- Dry, scaly, fissured skin - suggests autonomic neuropathy
- Erythema, swelling, warmth - may indicate infection or Charcot neuroarthropathy (distinguish by elevation: Charcot subsides; infection does not)
- Claw toes, hammer toes, midfoot collapse ("rocker bottom" deformity)
Ulcers: Note size (length × width), depth, wound bed quality (granulation vs. fibrous vs. necrotic), probe-to-bone test
Probe-to-bone test: 57% positive predictive value and 96% negative predictive value for osteomyelitis (Campbell's Operative Orthopaedics 15e)
Vascular examination:
- Palpate dorsalis pedis and posterior tibial pulses
- Doppler examination if pulses absent
- Ankle-Brachial Index (ABI): Normal = 1.0; Minimum for healing = 0.45; Value >1.3 indicates vessel calcification (non-compressible)
- Absolute toe pressures: Minimum for healing = 40 mmHg; TcPO₂ >40 mmHg predictive of healing
Neurological examination:
- 10-g monofilament testing at 10 sites on foot
- Vibration sense (128 Hz tuning fork), proprioception
- Silfverskiöld test: assesses gastrocnemius vs. Achilles contracture
Gait assessment for balance and safe mobilization
CLASSIFICATION OF DIABETIC FOOT ULCERS
Wagner-Meggitt Classification (Most Widely Used)
| Grade | Description |
|---|
| 0 | Intact skin; bony deformity only - "at risk foot" |
| 1 | Superficial ulcer - skin/subcutaneous only |
| 2 | Deep ulcer - involves tendon, capsule, or bone |
| 3 | Deep ulcer + osteomyelitis or abscess |
| 4 | Partial gangrene (forefoot) |
| 5 | Whole foot gangrene |
University of Texas (Depth-Ischemia) Classification (Modification)
Grades ulcers on Depth (0-3) × Ischemia (A-D):
| A (No ischemia) | B (Ischemia, no gangrene) | C (Partial gangrene) | D (Whole foot gangrene) |
|---|
| 0 | Skin intact; at risk | | | |
| 1 | Superficial ulcer | | | |
| 2 | Tendon/capsule exposed | | | |
| 3 | Bone/osteomyelitis exposed | | | |
INVESTIGATIONS
| Investigation | Purpose |
|---|
| Blood glucose, HbA1c | Assess glycemic control (HbA1c reflects past 3 months) |
| CBC, ESR, CRP | Inflammatory markers (may be normal even with infection) |
| Serum albumin, total protein | Healing potential |
| Renal function (BUN, Cr) | Frequent diabetic complication |
| Plain X-ray foot | Osteomyelitis (may be normal early), gas in soft tissues, Charcot changes |
| MRI foot | Gold standard for osteomyelitis - most sensitive modality for bone involvement |
| Doppler/ABI | Vascular assessment |
| Wound culture/bone biopsy | Guide antibiotic therapy; superficial swabs are unreliable for deep infection |
| Angiography | If revascularization considered |
MICROBIOLOGY
- Superficial/mild infections: Gram-positive cocci - S. aureus (including MRSA), Streptococci
- Severe/deep infections: Polymicrobial - aerobic Gram-negatives, Pseudomonas (over-represented), Anaerobes
- Empirical therapy for severe infections must cover Pseudomonas; add metronidazole for abscess/devitalised tissue
- Superficial swabs are unreliable for determining deep infection organisms - bone biopsy is preferred
CHARCOT NEUROARTHROPATHY (Charcot Joint)
A chronic, progressive, destructive process affecting bone architecture and joint alignment in patients lacking protective sensation.
- Occurs in 1-1.5% of diabetics; 7.5% of diabetic patients with neuropathy
- Two pathophysiologic theories: neurotraumatic (repeated microtrauma with no pain response) and neurovascular (autonomic dysfunction causes hyperemia and bone resorption)
- Presents as swollen, warm, erythematous foot - often confused with infection or gout
- Classic radiographic appearance: "bag of bones" pattern - fragmentation, dislocation, dense new bone
- Most commonly affects tarsometatarsal joints (Lisfranc) → "rocker bottom" deformity
Stages (Eichenholtz):
- Stage 0 (Prodromal): Warmth, swelling, normal X-ray
- Stage I (Fragmentation/Development): Bone fragmentation, joint dislocation
- Stage II (Coalescence): New bone formation, fusion begins
- Stage III (Reconstruction): Consolidation, deformity fixed
MANAGEMENT
Principles: Multidisciplinary Team
Endocrinology, Orthopaedics, Vascular Surgery, Infectious Disease, Podiatry, Nutrition
A. Medical / Conservative Management
- Glycemic control - HbA1c optimization (cornerstone of all treatment)
- Nutritional optimization - Delay surgery if albumin <2.5 g/dL or total protein <6 g/dL
- Antibiotics:
- Mild-moderate infection: Oral agent active against Gram-positive cocci (MRSA-active if risk factors)
- Severe infection: IV broad-spectrum (cover Gram-negatives, Pseudomonas, anaerobes)
- Duration guided by tissue vs. bone involvement (soft tissue: 2 weeks; osteomyelitis: 4-6 weeks)
- Wound care:
- Regular debridement of callus and necrotic tissue
- Moist wound dressings
- Negative-pressure wound therapy (NPWT/VAC dressing) for large wounds
- Biological dressings (collagen, growth factor-containing)
- Offloading (MOST IMPORTANT for ulcer healing):
- Total Contact Cast (TCC): Gold standard for plantar neuropathic ulcers - distributes pressure over entire plantar surface
- Removable cast walkers (RCW) / Scotchcast boots
- Extra-depth therapeutic shoes with custom insoles (Plastazote - closed-cell cross-linked polyethylene)
- Crutches/wheelchair
B. Vascular Intervention
- Full vascular assessment mandatory in patients with poor pulses
- Percutaneous transluminal angioplasty (PTA) for suitable lesions
- Bypass surgery (femoropopliteal/tibial) for long occlusions
- Improving vascularity is essential before foot salvage surgery
C. Surgical Management
1. Wound debridement:
- All necrotic tissue, slough, and infected bone must be removed
- Leave wound open; secondary closure or skin grafting once healthy granulation bed established
2. Procedures for specific deformities:
- Claw toes / dorsal toe ulcers: Flexor tenotomy or proximal interphalangeal joint resection
- Plantar hallux IP joint ulcers: Keller arthroplasty (if TCC failed)
- Achilles lengthening: For recurrent forefoot/midfoot ulcers with equinus contracture - offloads forefoot pressure
- Midfoot collapse (Charcot): Osteotomy of bony prominence (if stable deformity) OR midfoot fusion (if instability present)
- Charcot active phase: Total Contact Cast immobilization until Stage III; surgical reconstruction (superconstructs) for unstable deformity
3. Amputation:
Indication: Gangrene, severe uncontrolled infection, non-healing ulcer with no vascular inflow.
| Level | Indication |
|---|
| Ray amputation | Single metatarsal + toe |
| Transmetatarsal amputation (TMA) | Multiple forefoot involvement |
| Lisfranc/Chopart | Midfoot salvage |
| Syme's amputation | Ankle disarticulation; preserves heel pad |
| Below-knee (BKA) | Forefoot gangrene failing revascularization |
| Above-knee (AKA) | Unsalvageable limb / BKA non-healing |
In extensive peripheral neuropathy, a below-knee amputation in a zone with better sensation may be more appropriate than a foot-level procedure (Bailey & Love 28e).
Skin closure must be tension-free; excess bone may need resection to allow this.
PREVENTION (Highly Examinable)
- Optimal glycemic control - target HbA1c <7%
- Daily foot inspection (use mirror if needed; arrange assistance if retinopathy)
- Proper footwear - well-fitting shoes; avoid walking barefoot
- Regular chiropody/podiatry review
- Monofilament screening at every diabetes clinic visit
- Patient education on foot hygiene, nail care, avoidance of extremes of temperature
- Smoking cessation - worsens peripheral vascular disease
- Diabetic therapeutic shoe bill (USA) allows for extra-depth shoes + 3 custom insoles/year for at-risk patients
PROGNOSIS
- Infected diabetic foot ulcer must be regarded with urgency - can quickly progress to render the limb non-salvageable
- Five-year mortality of diabetic foot complications (30.5%) is comparable to that of many cancers
- Major amputation 5-year mortality: ~50-70%
- Goal of treatment: Ulcer-free, functional, plantigrade foot that fits within a brace or shoe
SUMMARY BOX (Bailey & Love 28e Key Points)
- Most important risk factor for osteomyelitis is presence of a foot ulcer
- Superficial swabs are unreliable for identifying deep pathogens
- In severe disease, surgical debridement is mandatory followed by culture-guided antibiotics
- Probe-to-bone test + elevated CRP + abnormal plain X-ray = confirmed osteomyelitis
- Full vascular assessment is mandatory in all diabetic foot infections
- Amputation wound healing is problematic; always plan for tension-free closure
Sources: Campbell's Operative Orthopaedics 15th Ed 2026 (Ch. 91); Miller's Review of Orthopaedics 9th Ed; Bailey & Love's Short Practice of Surgery 28th Ed (Ch. 43)