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Lecture 30 parekh charcot
Charcot foot and ankle, also known as neuropathic arthropathy, is a progressive destructive disease affecting bones and joints in people with sensory neuropathy. It is most commonly seen in the foot and ankle. The main causes are diabetes, alcoholism, syphilis, leprosy, spinal cord injury, and renal dialysis. It results from repetitive mechanical trauma to an insensate foot. Treatment involves immobilization with a total contact cast to stabilize the foot during healing, which can take many months or years. Surgery may be needed for severe deformity or non-healing ulcers.
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Lecture 30 parekh charcot
- 1. Charcot Foot andAnkle Selene G. Parekh, MD, MBA Associate Professor of Surgery Partner, North Carolina Orthopaedic Clinic Department of Orthopaedic Surgery Adjunct Faculty Fuqua Business School Duke University Durham, NC 919.471.9622 http://seleneparekhmd.com Twitter: @seleneparekhmd
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- 3. Jean Martin Charcot(1825-1893) • Not 1st to describe neuropathic arthropathy (1703 by William Musgrave) • Syphilis • 1936-1st described in diabetes
- 4. Charcot Joints • Whatis it? Progressive, noninfectious, destructive disease of the bones and joints in persons with sensory neuropathy
- 5. Charcot Joints •“Neuroarthropathy” •Etiology (partiallist) •Diabetes •Alcoholism •Syphilis •Leprosy (Hansen’s disease) •Meningomyelocele •Spinal cord injury •Syringomyelia •Renal dialysis
- 6. Charcot Joints • Epidemiology •Foot and ankle most commonly • Incidence: 0.1% - 0.12% of diabetics • Radiographic incidence: 1.4%
- 7. Charcot Joints • Twotheories • Neurotraumatic • Cumulative mechanical trauma • Insensate joint • Neurovascular (autonomic neuropathy) • Neurally stimulated vascular reflex • Bone resorption, ligament weakening
- 8. Pathophysiology • NOT understoodwell • Neurotraumatic • Minor repetitive • Major • Neurovascular • Autonomic dysfunction increased blood flow via arteriovenous shunting • Recent theories • TNF α, IL-1 NTF- қβ osteoclast
- 9. Clinical Presentation • Assocw/ advance sequelae of diabetes • Nephropathy • Retinopathy • Obesity • Assoc w/ recipients of solid organ transplantation • Type 1 Db • 5th decade of life (20-40yrs) • Type 2 Db • 6th decade of life (6-9yrs)
- 10. Clinical Presentation • Differentialdiagnosis • Cellulitis • Elevation-dependent rubor resolves • Abscess • CT/MRI • Acute Charcot • Red • Hot • >3.3o C • Swollen • 50% pain
- 11. Clinical Presentation • Sub-acute& chronic Charcot • Deformity w/ bony prominences • Rocker-bottom • Loss of calcaneal pitch w/ relative PF
- 12. Clinical Presentation • Ulceration •Painless swelling • Neuropathic pain unrelated
- 13. Imaging • X-rays • Fractures,dislocations • Bone compression, disintigration • Fluffy new bone formation • Deformity
- 14. • Osteomyelitis • MRI •Most helpful in distinguishing an abscess from Charcot • Combination technetium-99m sulfur colloid marrow & indium- 111-labeled bone scans • May have improved specificity • Charcot Imaging
- 15. • Osteomyelitis • Charcot •May be difficult to distinguish from osteomyelitis • No surrounding osteopenia in Charcot • Hematogenous osteomyelitis in adults rare • Ulcer free extremity unlikely to have osteomyelitis Imaging
- 16. Eichenholtz Stages O: Normalradiographs I: Dissolution/Fragmentation • Xray – osteopenia, periarticular fragmentation, & subluxation or frank dislocation
- 17. Eichenholtz Stages II: Coalescence/Earlyhealing phase • Edema and warmth decrease • Xray – Absorption of debris, fusion of bony fragments, and early sclerosis of bone III: Consolidation/Reconstruction • Absence of inflammation • Xray – osteophytes and subchondral sclerosis are often present, along with narrowing of joint spaces
- 18. Eichenholtz Stage Clinical Radiography IDevelopment- fragmentation Erythema Warmth Swelling Bony debris Fragmentation Subluxation Dislocation II Coalescence Decreased erythema, warmth, swelling Absorption debris New bone Coalescence/sclerosi s III Consolidation Resolution of edema Residual deformity Remodeling, rounding of bone Decreased sclerosis
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- 21. Anatomic Classification • I:Midfoot 60% • II: Hindfoot 10% • IIIA: Ankle 20% • IIIB: Calcaneal Tubercle
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- 23. Type 1 • Midfoot •Require shorter immobilization • Rocker-bottom • Severe midfoot valgus • Most likely to develop ulcers
- 24. Type 2 • Hindfoot •“Bag of bones” • Persistent instability • Less likely to ulcerate (1/3) • Longer periods of immobilization (avg. ~2 yrs)
- 25. Type 3A • Ankle •Trauma • Similar to Type 2 • Instability & swelling leads to avg. immobilization >1 yr • Serious varus or valgus (ulceration @ malleoli)
- 26. Type 3B • Oscalcis • Pathologic fracture of tubercle • Leads to 2° collapse of foot
- 27. Conservative Treatment • Recommendations •Based on level IV evidence • Goals • Achieve 3rd stage of bony healing • Avoid & treat ulcers • Keep patient as ambulatory as possible during treatment
- 28. Conservative Treatment • MostCharcot treated nonoperatively • Can take several months to years
- 29. Conservative Treatment • TotalContact Cast • Rest & elevation decrease swelling • First cast change @ 1 week • Dramatic initial reduction in swelling • Cast loosens leading to blisters & new ulcers • Reduces load to about 1/3 of the normal foot • Do not overpad • Use felt or foam to pad bony prominences
- 30. Conservative Treatment • Prefabricatedbraces • Not customized (often will not accommodate bony prominences) • Do not control edema like TCC • Can be removed by patient
- 31. Eichenholtz Stage •I: TCC •II:Molded total contact AFO, custom fabricated lined w/ plastizote or CROW (Charcot Restraint Orthotic Walker) •III: Custom-molded insole w/ appropriate footwear
- 32. Weightbearing Status • NWBpreferred? • May not be possible • Wheelchairs • Limited WB/Protected WB
- 33. Complications • Ulceration • Deepinfection/osteomyelitis • Severe, uncontrollable deformity • Amputation
- 34. Surgical Treatment • Exostectomy •Medial or lateral incision • Excise bony prominence of tarsal bones • Flatten surfaces w/ osteotomes or saw • Smooth w/ rasps (leave no edges or ridges)
- 35. Surgical Treatment • Arthrodesis •Salvage procedure • Realign foot to relieve pressure/correct deformity • Stabilization of instability/dislocation • Enable brace or custom footwear w/o ulceration
- 36. Surgical Treatment • Arthrodesis •Timing • Avoid during Stage I • Leads to infection & loss of fixation • Goal: Stable aligned foot • Fibrous ankylosis may be positive result
- 37. Fixation Methods • Dorsalplating - compression
- 38. Fixation Methods • Plantarplating - tension
- 39. Fixation Methods • Medialplating
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- 43. Fixation Methods • IMfixation • Hindfoot
- 44. Fixation Methods • IMfixation • Midfoot
- 45. Fixation Methods • Timeto fusion w/ internal fixation • 11-22 weeks • High complication rate up to 69% • Infection, both superficial and deep • Post-op amputation rate 0-10% • Hardware malposition requiring removal • Recurrent ulceration • Fracture
- 46. Fixation Methods • ExternalFixation • Indications • Ulcers with underlying osteomyelitis • Poor soft-tissue envelope • Poor bone quality • Morbid obesity • Advantages • Singlestage treatment in the presence of osteomyelitis or ulceration • Easy monitoring of soft-tissue healing • Protect somewhat against noncompliance with postoperative non–weight-bearing instruction • Can adjust in office
- 47. Fixation Methods • ExternalFixation • Limb salvage rates were >90% • New or recurrent ulceration rare • Pin-tract infection - most common complication
- 48. Amputation • Indications • Failedsurgeries • Osteomyelitis • Unstable arthrodesis
- 49. Pharmacologic • Bisphosphonates • Promisingshort-term results in preventing bone resorption • Mechanism based on the promotion of osteoclast apoptosis and the inhibition of osteoclast activity
- 50. Pharmacologic • Bisphosphonates • Judeet al • 6 wks: significant reduction in bone turnover markers (bone specific alkaline phosphate, deoxypyridinoline • > 3 months differences not significant • ? Interval doses may be necessary • Pitocco et al • Improvement in bone turnover markers, BMD, and pain
- 51. Pharmacologic • Calcitonin • Judeet al • Daily dose of 200 IU intranasal calcitonin • 3 months of treatment • Decreased bone turnover markers • 6 months • No difference
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