Charcot joint

Neuropathic arthropathy - Charcot joint

1. CHARCOT JOINT ( NEUROPATHIC ARTHROPATHY)

2. Non-infectious, destructive process causing eventual dislocation and peri -articular fracture a destructive joint disorder initiated by trauma to a neuropathic extremity

3. Causes: Diabetic Neuropathy (most common) Spinal Cord Injury Meningomyelocele Syringomyelia Leprosy Chronic alcohol abuse poliomyelitis syphilis

4. Diabetes, neuropathy, trauma, and metabolic abnormalities of the bone result in an acute localized inflammatory condition. The inflammatory response can permanently disrupt the bony architecture of the foot resulting in abnormal plantar pressures that are at risk for ulceration, osteomyelitis, and amputation.

5. Epidemiology Charcot affects between 0.1% to 0.9% of people with diabetes .  estimated 63% of patients with Charcot neuropathic osteoarthropathy will develop a foot ulceration.

6. 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

7. Pathophysiologically , key inflammatory markers have been identified that contribute to the development of an acute Charcot foot. Calcitonin gene-related peptide (CGRP) acts typically at the nerve terminal to antagonist the synthesis of nuclear factor- kB ligand (RANKL), a cytokine involved in the inflammatory process. However , in the neuropathic foot, the CGRP is not functioning, and therefore RANKL is synthesized without inhibition. RANKL is a very important marker in the development of Charcot as it is responsible for the proliferation of osteoclastogenesis . The RANKL osteoclastic relationship is normally moderated by osteoprotegerin (OPG) by acting as a decoy receptor to RANKL binding . In the Charcot foot, this relationship between RANKL and OPG is disrupted. The unregulated synthesis of RANKL accounts for the excessive bony turnover and accumulation that is seen in the Charcot limb. Additionally , CGRP may have a further role in Charcot in that it is involved in upholding the integrity of the joint capsule.  Therefore , in its absence, it is presumed to lead to joint destruction and dislocation that is characteristic of the Charcot foot.

8. 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)

9. 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.

10. X-rays (depending on stage): Bone fragmentation Loss of bony architecture Coalescence of bone fragment Joint subluxation Sclerosis

11. How to differentiate from 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

12. Brodsky Classification

13. Eichenholtz classification

14. Management: Goals : Stop inflammation Preserve architecture of the foot Relieve pain Reverse bone demineralization

15. The main treatment is 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