Charcot joint

Charcot joint

• 1.
  CHARCOT JOINT (NEUROPATHIC ARTHROPATHY)
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  • Non-infectious, destructiveprocess causing eventual dislocation and peri-articular fracture • a destructive joint disorder initiated by trauma to a neuropathic extremity
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  Causes: • Diabetic Neuropathy(most common) • Spinal Cord Injury • Meningomyelocele • Syringomyelia • Leprosy • Chronic alcohol abuse • poliomyelitis • syphilis
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  Epidemiology • Charcot affectsbetween 0.1% to 0.9% of people with diabetes. • estimated 63% of patients with Charcot neuropathic osteoarthropathy will develop a foot ulceration.
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  Pathophysiology • Neurovascular theory– nerve damage results in increased local vascularity which precipitates osteoclastic activation • Neurotraumatic theory – microtrauma in insensate joints causes progressive bony destruction secondary to activation of pro- inflammatory cytokines
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  • Differential diagnosis:Sepsis, Gout, Cellulitis • initially misdiagnosed as a deep venous thrombosis or cellulitis. • Charcot can also be confused with osteomyelitis due to the similar clinical appearance of a red, hot swollen foot with skeletal lysis on radiographs and often unilateral presentation. • Charcot should be suspected to be active if temperature difference between both limbs is > 2o C (usually measured by infra-red thermometer)
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  History and Physical •High suspicion for Charcot needs to be present to diagnose the condition accurately. • erythematous foot with edema and calor. • Often, it is unilateral with a sudden onset of symptoms that may be precipitated by macro-trauma (ankle sprain) or repetitive micro- trauma (walking). • History of surgery to ankle & foot, infection or multiple micro/macro- traumas.
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  X-rays (depending onstage): • Bone fragmentation • Loss of bony architecture • Coalescence of bone fragment • Joint subluxation • Sclerosis
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  How to differentiatefrom septic joint? • Clinically: Elevate the affected extremity for 5 – 10 minutes. Oedema will decrease with elevation in Charcot neuroarthropathy while an infectious process is less likely to decrease. • Lab: inflammatory markers slight increase in Charcot compare to be higher in infection • MRI: collection of pus in sepsis • Bone scan: WBC labelled will be positive in infection • Bone Biopsy
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  Brodsky Classification
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  Eichenholtz classification
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  Management: Goals: • Stop inflammation •Preserve architecture of the foot • Relieve pain • Reverse bone demineralization
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  The main treatmentis immobilization until the acute phase/ulceration settles down Total contact cast • -Maintain foot architecture until consolidation • -Helps distribute weight bearing forces evenly & reduces pressure • -Changed weekly to avoid pistoning as oedema resolves • Custom made boot for rigid deformities
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  • Bisphosphonate infusionover 12 months may improve pain and bone turnover (NICE DO NOT recommend Bisphosphonates to treat acute Charcot arthropathy ) • Alternative agents include pamidronate or zoledronic acid
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  • The mainrationale behind Charcot reconstruction is surgical off- loading to prevent ulceration and deformity progression • Excision of bony prominences (exostosis) in stage 3 if causing ulcers • Arthrodesis in functional position • Poor quality of bone & soft tissue may lead to loosening & infection • Amputation for recurrent/persistent infection