Charcot foot

General overview. Good starting point.

1. Charcot Foot Miss Sheweidin Aziz – ST3 T&O Boston Pilgrim Hospital June 2016

2. HISTORY In 1703 William Musgrave first described a neuropathic joint as an arthralgia caused by venereal disease In 1868 Jean-Martin Charcot gave the first detailed description of the neuropathic aspect. He noted this disease process as a complication of syphilis (most common cause until 1936 when Jordan linked it to Diabetes)

3. DEFINITION Neuropathic (Charcot) osteoarthropathy is a non infective, destructive, lesion of a bone and joint resulting from a fracture or dislocation or both in a patient who has peripheral neuropathy

4. A chronic and progressive joint disease following loss of protective sensation and leads to destruction of joints and surrounding bony structures. May lead to amputation if left untreated

5. RISK FACTORS Diabetic neuropathy Alcoholism Leprosy Meningomyelocele Tabes dorsalis /syphilis Syringomyelia Any condition that causes sensory or autonomic neuropathy

6. EPIDEMIOLOGY In diabetic patients: 0.1-1.4% In diabetics with neuropathy 7.5% Bilateral disease occurs in <10% Type 1 DM: 20-25 years post diagnosis Type 2 DM: 5-10 years post diagnosis Gender ?Male predominance

7. PATHOPHYSIOLOGY Neurotraumatic theory: German theory 1946 Peripheral neuropathy  loss of protective sensation  increase susceptibility to injuries (repeated minor or acute)  progressive destruction and damage to bone and joints

8. PATHOPHYSIOLOGY Neurovascular theory: French theory 1868 Spinal cord lesion  autonomic neuropathy  AV shunting  increased blood flow (warm foot and dilated veins)  Increased osteoclast activity  bone resorption and mechanical weakening  fractures and deformity

9. PATHOPHYSIOLOGY Molecular biology Inflammatory cytokines may cause destruction IL-1 and TNF – alpha  increased production of transcription factor - kB

10. CLINICAL PRESENTATION Symptoms Swelling foot and ankle Pain 50% Loss of function

11. CLINICAL PRESENTATION Acute Charcot Swelling Warmth (3.3° warmer) Erythema (will decrease with Charcot but not with infection on elevation)

12. CLINICAL PRESENTATION Chronic Charcot Structurally deformed foot Rocker bottom deformity Collapsed medial arch

13. CLASSIFICATION

14. Stage 0: Joint oedema. Negative radiographs.

15. Stage 1 : Fragmentation . Joint oedema. Bone resorption. Dislocations. Fractures

16. Stage 2: Coalescence. Decreased local oedema. Sclerosis. Fracture healing. Debris resorption. Decreased joint mobility.

17. Stage 3: Reconstruction . No joint oedema. Consolidation and remodelling of fracture fragments. Ulcers may develop.

18. INVESTIGATION Inflammatory markers: Elevated in Osteomyelitis and Charcot Bone scan: useful in presence of superimposed osteomyelitis Technetium bone scan: maybe positive in infection or Charcot Indium WBC scan: Negative in Charcot. Positive in osteomyelitis

19. MRI: differentiate between abscess and soft tissue swelling Biopsy: to guide antibiotic therapy Histology: Synovial hypertrophy and detritic synovitis

20. MANAGEMENT Non-operative Total contact casting every 2-4 weeks for 2-4 months Orthotics – Charcot restraint orthotics walker (CROW) boot can be used after TCC Shoe modifications to reduce ulcerations

21. Operative Resection of bony prominences ( exostectomy ) and Achilles Tendon lengthening Braceable foot with equinus deformity and focal bony prominence causing skin breakdown Aim to achieve plantigrade foot that allows ambulation without skin compromise

22. Deformity correction, arthrodesis +/- osteotomy Severe deformity that is not braceable High complication rate up to 70% Amputation Failed surgery. Unstable arthrodesis. Recurrent infection Aim is for partial or limited amputation if vascularity allows

23. Sohn et al performed a retrospective study to compare the risks of lower-extremity amputation Charcot patients had a 4.1 amputations per 100 person-years vs ulcer patients 4.7 In patients under 65 years amputation risk 7x in ulcer only vs. 12x for Charcot and ulcer

24. THANK YOU