In the Name of ALLAH, Ever Beneficent, Infinitely Merciful

1. In the Name of ALLAH, Ever Beneficent, Infinitely Merciful

2. Charcot Foot and Treatment Dr. Asim Bin Zafar M.C.P.S., M.D Consultant Physician & Senior Registrar Baqai Institute of Diabetology & Endocrinology Baqai Medical University Medical Unit –IV Karachi. Charcot Neuroarthropathy

3. Charcot Neuroarthropathy Background • originally described in 1868 by Jean Martin Charcot • patients with tabes dorsalis • massive joint destruction, subluxation and dislocation was seen Charcot Neuroarthropathy

4. Charcot - Background • Cause: Today, most common in diabetics, commonly in the lower extremity Charcot Neuroarthropathy

5. Charcot and Diabetes Mellitus • Average disease history of 10-12 years or more • Generally poor glycemic control • Reported incidence varies widely in literature, from 0.08-0.5% up to 16% of diabetics Charcot Neuroarthropathy

6. Pathogenesis • Three theories… • Neurotraumatic • Neurovascular • Inflammatory theory Charcot Neuroarthropathy

7. Pathogenesis Neuro traumatic Theory • proposes that Charcot arthropathy results from repetitive mechanical trauma from weight bearing on insensate extremity • this trauma can lead to intra capsular effusions, ligamentous laxity and joint instability Charcot Neuroarthropathy

8. Pathogenesis-Neurovascular Theory • proposes that Charcot is a sequelae of increased peripheral blood flow resulting from autonomic sympathectomy • autonomic sympathectomy produces a failure of the normal regulatory mechanisms that control blood flow Charcot Neuroarthropathy

9. Pathogenesis-Neurovascular Theory • autonomic dysfunction causes arteriovenous shunting and vasodilitation • increases rate of blood flow to extremity • correlated with increased osteoclastic activity Charcot Neuroarthropathy

10. Pathogenesis-Inflammatory Theory • It has been suggested that acute CN may be triggered in a susceptible individual by any event that leads to localized inflammation in the affected foot. William J. Jeffcoate; 2 January 2008 G. Mabilleau,1 N. L. Petrova,2 M. E. Edmonds, 2 and A. SabokbarDiabetologia. 2008June; 51(6): 1035–10401 Charcot Neuroarthropathy

11. Eichenholtz Classification Stage I - Developmental (acute) Hyperemia due to autonomic neuropathy weakens bone and ligaments Diffuse swelling, joint laxity, subluxation, frank dislocation, fine periarticular fragmentation, debris formation Charcot Neuroarthropathy

12. Clinical Presentation

14. Acute presentation Charcot Neuroarthropathy

16. Chronic presentation

18. Rocker bottom foot Charcot Neuroarthropathy

19. Rocker bottom foot Charcot Neuroarthropathy

20. Anatomic Classification(Sanders and Frykberg, 1991) • I - forefoot, 10-30% • II - Lisfranc’s joint, most common • III - midtarsal joint, often including naviculocuneiform joint • IV - ankle and subtalar joints, 8-10% • V - (“posterior pillar”) fractures of calcaneus, 2% Charcot Neuroarthropathy

21. Radiographic Staging(Eichenholtz, 1966) • I Developmental (acute) stage • II Coalescence (quiescent) stage • III Consolidation (resolution) stage Charcot Neuroarthropathy

24. Bone Scan

26. Radiographs • Stage I Charcot Neuroarthropathy

27. Stage I Charcot Neuroarthropathy

28. Eichenholtz Classification • Stage II - Coalescence (quiescent) • Absorption of osseous debris, fusion of larger fragments • Dramatic sclerosis • Joints become less mobile and more stable • the “hypertrophic”, or “subacute” phase of Charcot Charcot Neuroarthropathy

29. Stage II Charcot Neuroarthropathy

30. Stage II Charcot Neuroarthropathy

31. Eichenholtz Classification • Stage III - Consolidation (resolution) • Osseous remodeling • for clinical purposes, stage I is regarded as the acute phase, while stages II and III are regarded as the chronic or quiescent phase Charcot Neuroarthropathy

32. Stage III

33. Mimics • Osteomyelitis • DVT • Acute Gout

34. Treatment • Primary goals • Stability, plantigrade foot, and to keep the foot free of ulceration • Selection of treatment plan • Phase dependent, location, severity, and the +/- of ulceration • Conservative vs. Surgical Charcot Neuroarthropathy

37. Treatment • Initially consists of immobilization during acute phase to prevent disease progression • Generally via total contact casting • Some disagreement in the literature as to whether or not to permit any weight bearing during this time • Others: Unna boot, Pneumatic Walker brace, etc. Charcot Neuroarthropathy

38. Total Contact Cast • Permits ambulation while uniformly distributing weight bearing pressures over the entire foot surface Charcot Neuroarthropathy

40. Treatment • After acute phase has passed, long-term or permanent bracing is often needed • Gradual return to protected weight bearing • Examples: Charcot Restraint Orthotic Walker (CROW), patellar tendon-bearing braces, custom-molded shoes, etc. Charcot Neuroarthropathy

41. Patellar Tendon-Bearing Brace • Used to transfer weight bearing forces from the orthosis through the patellar tendon, thereby decreasing weight bearing forces through the foot and ankle Charcot Neuroarthropathy

42. Treatment • ONLY considered after all conservative measures exhausted • Surgical intervention is necessary in some cases of continued ulceration, gross instability, presence of infection, limb shortening and difficulty in shoe gear. Charcot Neuroarthropathy

43. Treatment • Rx is largely patient dependent • Ostectomy, arthrodesis, mid tarsus closing wedge osteotomy, external fixation Charcot Neuroarthropathy

44. Treatment • Bone mineral density alterations have been documented in Charcot patients • Example: localized osteopenic changes • Increasing interest in the use of bisphosphonates Charcot Neuroarthropathy

45. Conclusions • Charcot a potentially devastating sequela of diabetes mellitus • Treatment requires careful initial management and long-term follow-up • Conservative, surgical treatment options can be augmented with the pharmacologic use of bisphosphonates Charcot Neuroarthropathy

46. Thank You