charcot joint. Arthropathy. pptx

Charcot

1. Neuropathic Arthropathy Charcot joint

2. Jean- Martin Charcot Jean- Martin Charcot 29 November 1825 – 16 August 1893) was a French neurologist and professor of anatomical pathology. He is known as "the founder of modern neurology"

3. Definition Neuropathic arthropathy , neuropathic osteoarthropathy , Charcot joint refers to noninfectious progressive condition of the musculoskeletal system that is characterized by joint dislocations , pathologic fractures , and debilitating deformities.

4. History The first description of neuropathic arthropathy was by Musgrave in 1703, in his book De Arthritide Symptomatica.He described a neuropathic joint as an athralgia. 1868 Jean- Martin Charcot gave the first detailed description of this disease. In 1892, Sokoloff -- upper extremity with syringomyelia.

5. In 1927 Leriche stated that a lesion of sympathetic led to Hyperaemia and bone resorption. In 1936, Jordan - diabetes mellitus - - -neuropathic changes in the foot and ankle. Associated with intra- articular corticosteroid injections by Chandler and Wright in 1958. A.C Brower— Neurovascular theory

6. Etiology Any condition that causes sensory or autonomic neuropathy Diabetes mellitus neuropathy Multiple Sclerosis Alcoholic Neuropathy Syringomyelia Cerebral palsy Leprosy

7. Tabes Dorsalis Spinal cord injury Myelomeningocele Intra- articular steroid injections Congenital insensitivity to pain Familial interstial Polyneuropathy Amyloidosis Pernicious Anemia

8. Vitamin B12 Deficiency Phenylbutazone ,Indomethacin Ethyl Alcohol.

9. Diabetes mellitus is currently the most common cause of neuropathic arthropathy. Neuropathic joint destruction develops in approximately 0.1% of patients with diabetes and 5% of those with peripheral neuropathy

10. Neuroarthropathy among all pts with tabes dorsalis ranges b/w 5 to 10% 75% of this 5- 10% involve lower extremities and 25% upper extremities.

11. Pathophysiology Major theories Neurotraumatic theory Neurovascular theory Most probably both

12. Neurotraumatic Theory Loss of peripheral sensation and proprioception leads to repetitive micro trauma to the joint in question This damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. Poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.

13. More recent theories implicate the role of inflammatory cytokines such as TNF- α and IL- 1 in the pathogenesis of Charcot neuroarthropathy. On the molecular level, these factors lead to increased expression of nuclear transcription factor- κB, which in turn stimulates osteoclast formation.

14. Joint destruction in the neuropathic joint is probably brought on by a combination of factors that include damage to the nociceptors of the joint and the periarticular tissues.

15. The activity of peptides such as substance P, calcium gene related peptide, and vasoactive intestinal peptide (VIP) could result in increased vascularity and inflammation , contributing to further joint destruction. Substance P can enhance the cellular synthesis of collagenase and prostaglandin- E; activate T lymphocytes, monocytes, and neutrophils; and take an active part in inflammation

16. The initial pathologic changes occur in the underlying bone and cartilage. Recurrent effusions occur due to hyperplasia of the synovium. The articular cartilage is slowly destroyed by a pannus, which helps distinguish Charcot's joints from other forms of osteoarthritis.

17. Neurovascular theory Neuropathic patients have dysregulated autonomic nervous system reflexes, and de- sensitized joi nts receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads to bony destruction.

18. Clinical History A careful history may reveal an unrecognized traumatic event. Charcot neuroarthropathy most frequently presents in the fifth decade, after an average duration of diabetes of 20 to 24 years ; in those with type 2 diabetes.

19. Presentation DEPENDS OF DURATION OF DISEASE Mild swelling w/o deformity - Moderate deformity with extreme swelling. Signs of i nflammation . Profound unilateral swelling. WBC and ESR may be normal

20. Deformity - a) rocker bottom deformity 🞭 🞭 🞭 🞭 🞭 medial tarsal subluxation digital subluxation rearfoot equinovarus rearfoot subluxation hypermobility 🞭 cutaneous - a) neuropathic ulcer 🞭 🞭 hyperkeratosis infection

21. Increase in localized temp Erythema, Joint effusion. 75% pt. have pain. The deep tendon reflexes at the knee are absent in a majority of patients.

22. Marked Irregularities identified as bony projections. Bone formation in soft tissues. Bag of Bones: Joint can be passively and painlessly moved in all Directions

23. Acute Charcot neuropathy

24. Diagnosis

25. IMAGING

26. Early Changes similar to OA Nontraumatic dislocations may be an early sign. Later  Radiographic evidence of joint distention caused by fluid, hypertrophic synovitis, osteophytes, and subluxation.

27. Atrophic Stage: Rapid joint destruction Loose bodies Subchondral bone erosions Subluxation Pathological#

28. Hypertrophic Stage Reduced jt space. Subchondral bone sclerosis Pathological # healing with callus Multiple osteophyte formation with exoxtosis formation. Dislocations of joints

29. Radiographic features 6D’s Yochum and Rowe Dense bones (subchondral sclerosis) Degeneration Destruction of articular cartilage Deformity (pencil- point deformity of metatarsal heads) Debris (loose bodies) Dislocation

30. Commonly Affected Joints Foot Involvment Knee involvement Hip involvement Shoulder Elbow

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

32. Classification ( Brodsky and Rouse) Type 1 Midfoot Type 2 Hindfoot Type 3a Ankle 3b Calcis tubercle Type4 Combination Type 5 Forefoot

33. Neuropathic Joints Hy pe r r t t oph i c i c or Pr o du c t i v i v e MIXED Atrophic or Resorptive

34. Radiographic Staging (Eichenholtz, 1966 ) I Developmental (acute) stage II Coalescence (quiescent) stage III Consolidation (resolution) stage

35. Modified Eichenholtz Classification for the Progression of Charcot Neuroarthropathy

36. Stage 0(Shibata and Schon) Swelling and erythema No Radiographic Changes

37. 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

38. Radiographs Stage I

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

40. Radiographs Stage II

41. Radiographs Stage II

42. 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

43. Radiographs Stage III

44. Charcot Arthropathy

45. Rocker bottom deformity

46. HIP Charcot neuroarthropathy in the hip is rare. Try conservative management - total hip replacement. 50% of fractures of the femoral neck in diabetics developed Charcot's joints . Late manifestation of tabes dorsalis

47. KNEE Most Commonly secondary to Syphilis. Results in Gross Instability Total knee arthroplasty

48. Shoulder

49. Treatment

50. MEDICAL MANAGEMENT 🞭 Control of sugar in diabetic patient 🞭 Management of infection with antibiotics 🞭 In the setting of altered bone mineral density (BMD) in patients with diabetes, bisphosphonates can be use to prevent further osteoporosis in charcot arthropathy.

51. Treatment Primarily nonoperative. Consists of Acute and Postacute phases. – – Acute (unloading) Casting along with crutches and walkers. – – Postacute Include bracing, ankle- foot orthotics(AFO), specialized shoes.

52. OFF- LOADING OR IMMOBILIZATION DEVICES USED IN THE MANAGEMENT OF CHARCOT FEET. 🞭 - wheelchai r 🞭 - crutches 🞭 - walker 🞭 - Elastic bandage or jones dressing 🞭 - total contact cast 🞭 - fixed ankle walking brace 🞭 - Posterior splint 🞭 - patellar tendon- bearing brace 🞭 - charcot restraint orthotic walker (CROW )

53. Treatment Casting - changed every 1- 2weeks, if ulcerations are present changed every week for wound care, duration from 3- 6 months. Shoes, bracing, and orthotics- duration from 6- 24 months. Typical total healing time 1- 2 years. When the patient enters quiescence phase, management is directed at a gradual resumption of weight bearing with prolonged bracing.

54. Early stage (unloading) Total Contact cast.

55. CROW boots

56. Surgical options Arthrodesis Exostosectomy of bony prominences Osteotomies Reconstructive Surgeries Autologous bone Grafting Amputations

57. Complication Ulcers Osteomyelitis Gross Deformity of the foot Gangrene.

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