Charcot FootMiss Sheweidin Aziz – ST3 T&O

Boston Pilgrim Hospital June 2016

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)

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

• 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

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

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

PATHOPHYSIOLOGYNeurotraumatic 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

PATHOPHYSIOLOGYNeurovascular 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

PATHOPHYSIOLOGYMolecular biology• Inflammatory cytokines may cause destruction IL-1 and TNF

– alpha increased production of transcription factor - kB

CLINICAL PRESENTATION• Symptoms

• Swelling foot and ankle • Pain 50% • Loss of function

CLINICAL PRESENTATION• Acute Charcot

• Swelling•Warmth (3.3° warmer)• Erythema (will decrease with Charcot but not with

infection on elevation)

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

CLASSIFICATION

Stage 0: Joint oedema. Negative radiographs.

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

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

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

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

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

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

•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

• 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

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

THANK YOU