Osteoarthritis of The Hip how to diagnose.pptx

Osteoarthritis of The Hip how to diagnose

1. Osteoarthritis of The Hip Ahmadin Yusuf Rizal Susatyo

2. Definition a non-inflammatory degenerative joint disease characterised by : 1. progressive loss of articular cartilage 2. new bone formation 3. capsular fibrosis

3. Introduction Chronic joint disorder Degenerative end result > 80% in > 65yo Progressive erosion, fibrillation and cracking of articular cartilage forms loose bodies Subarticular cyst formation in bone Hardened articular bone Mild inflammation but painfulà morning stiffness Limited ROM Abnormal loading à frictional wear Often asymmetrically distributed

4. Osteoarthritis Primary à generalized factors Secondary (follows demonstrable abnormality & occurs following certain predisposing factors) à ­Trauma ­congenital deformity ­Infection ­metabolic disorder Degenerative Joint Disease Hyperthrophic Arthritis Degenerative Disc Disease Generelized Osteoarthritis (Kellgren’s syndrome)

5. Anatomy of HIP

6. The Neck shaft angle mostly is 125 degrees à varies (90-35 degrees) The angle of anteversion is approx 12 degrees in adults KINEMATICS à Motion Average range ­ Flexion 115 ­ Extension 30 ­ Abduction 50 ­ Adduction 30 ­ Internal rotation 45 ­ External rotation 45

7. Vascularization of the Hip Blood supply of the femoral head : ­ Medial circumflex femoral artery (a branch of the profunda femoris artery) à most important supply ­ Lateral circumflex artery (a branch of the profunda femoris artery) à supplies the inferior portion ­ Artery of the ligamentum teres ( a posterior branch of the obtuator artery) à minor blood supply in the adult,

8. Biomechanics of the Hip The Neck shaft angle mostly is 125 degrees à varies (90-35 degrees) The angle of anteversion is approx 12 degrees in adults KINEMATICS à Motion Average range ­ Flexion 115 ­ Extension 30 ­ Abduction 50 ­ Adduction 30 ­ Internal rotation 45 ­ External rotation 45

9. Pathophysiology Theory I : ­ The initiating event is fatigue of the collagen meshwork à increase hydration of the articular cartilage and loss of proteoglycans from the matrix into the synovial fluid ­ increased collagenolytic activity à collagen loss may also be due to mechanical causes

10. Pathophysiology Theory II : ­ The initial lesions are microfractures of the subchondral bone following repetitive loading ­ Healing of these microfractures à subchondral bone à osteophyte formation à fibrillation of the cartilage à reduplication and proliferation of chondrocytes

11. Pathogenesis Staging Initial stages ­ ↑ water content & failure of internal collagen network ­ ↑ Cell enzymes & DNA à proliferasi, mitosis, ↑ chondrocyt activity Early stages ­ Protease enzymes ↑ ­ 1 st damage to chondrocytes à irreguler surface

12. Pathogenesis Staging Intermediate stage ­ loss of proteoglycans & defects appear in cartilage → stiff ­ fibrilating (vertical splitting) ­ Tinning of cartilage surface ­ 2 nd damage to chondrocytes → release cell enzymes & matrix breakdown

13. Pathogenesis Staging Terminal Stage ­ Cartilage deformation → stress on collagen network → changes in a cycle → tissue breakdown ­ Artic cart → distributing & dissipating forces of joint loading ­ Integrity loses → ↑ concent in subchondral bone → focal trabecular deg & cyst formation ­ ↑ vascularity & reactive sclerosis in zone of max loading

14. Pathogenesis Osteophyte production occurs around the circumference of the joint margin Bits of bone or cartilage may break off and float into the joint space

15. Pathogenesis The hip → the commonest sites of OA

16. Molecular Changes Increased water content à weakening of type 2 collagen network, shorter chains and shifts in the concentration of proteoglycans ( chondroitin/keratin ratio is increased ) increase in collagenase and proteoglycan-degrading enzyme (stromelysin & plasmin) concentration

17. Pathology Cardinal features : 1. Progressive cart destruction 2. Subarticular cyst formation 3. Sclerosis of surrounding bone 4. Osteophytes formation 5. Capsular fibrosis

18. Etiology Trauma Obesity Overuse Aging (degenerative) Work/Car Accidents Repeated episodes of gout or another form of arthritis

19. Etiology Abnormal stresses on a weakened joint Genetic Susceptibility ­ gen defect type II colagen Microbial inciting agent ­ Epstein-Barr virus, Borrelia & Mycoplasma Autoimmunity ­ IGM anti IgG – RA Factor. ­ Helper T cell (CD4) against type II collagen & cartilage glycoprotein-39

20. GRADE of OA AHLBACK : ­ 1. narrowing of the joint surface ­ 2. narrowing of the joint surface + osteofit ­ 3. narrowing of the joint surface + osteofit + kissing of femoral condyle and prox. Tibia ­ 4. very narrowing of the joint surface + osteofit + subchondral cyst + varus/valgus

21. GRADE of OA Kellgreen & Lawrence : ­0. normal ­1. osteophyt minimally ­2. osteophyt in 2 point, subchondral sclerotic, subchondral cyst minimally, narrowing (-) ­3. osteophyt (+), deformity at the edge of the bone, narrowing (+) ­4. osteophyt (++), deformity at the edge of the bone (+), joint space was dissapeared, subchondral sclerotic (+) and cyst (+)

22. Risk Factors Joint dysplasia ­ Perthes’ disease ­ Hurry prophylactic surgery in child Trauma ­ # involving artic surf ­ Malunion long-bone # ­ repetitive stress in athletes Bone density Obesity Family history

23. Clinical Findings Osteophytes - “Bone Spurs” Loss of Joint Space Increased Density of Bone in Joint Lines Increased Synovial Fluid

24. Clinical Classification Monoarthritis ­ Acute: Bacterial, Trauma, Crystal, Reactive ­ Chronic : Tuberculosis, Lyme, Fungal, Trauma, Tumors Polyarthritis ­ Autoimmune : Rheumatoid, Ankylosing spondylitis, Reiter syndrome ­ Degenerative : Osteroarthritis ­ Crystal Deposition : ­ Gout à Monosodium urate ­ CPPD à Pseudo Gout Infective ­ Septic , TBC

25. Radiology Findings Narrowing of the joint space Sclerosis Osteophyte

26. Imaging X-rays → 4 cardinal signs Radionuclide scanning ­ 99mTc-HDP à activity in subchondral regions ­ ↑ vasc & new bone formation Arthroscopy → show cartilage damage

27. Differential Diagnosis Avascular necrosis Osteonecrosis Inflammatory arthropathies Diffuse idiopathic skeletal hyperostosis Multiple diagnosis OA

28. Differential Diagnosis

29. Management 3 observation : ­ symptoms characteristically wax & wane, & pain subside spontaneously for long periods ­ some less painful w/ passage of time & no more than pain killer ­ extreme, recognize by x-ray → rapidly progressive type of OA → reconstructive surgery before bone lose

30. Early Treatment Principles : 1. Maintain movement & muscle strength 2. Protect the joint from ‘overload’ 3. Relieve pain 4. Modified daily activity

31. Early Treatment Education Weight Reduction ­ wearing shock absorbing shoes ­ avoiding activities like climbing stairs Sport activity Diet Daily Activity à Biomechanics Pain Relief ­ vascular decompression of subchondral bone ­ redistribution of loading forces Physical therapy

32. Early Treatment Pharmaceuticals ­ Acetaminophen ­ NSAIDs ­ COX-2 inhibitors

33. Physical Therapy Problems of the Hip

34. Physical Therapy Interventions Patient education on joint care Increase strength Increase aerobic capacity Warm water swimming

35. Physical Therapy Interventions Application of heat or cold packs Exercise and stretching Walking aids Support pillows

36. Intermediate Treatment Surgical : ­ Arthroscopy ­ Diagnostic ­ Treatment ­ Realignment osteotomy ­ If the joint still stable & mobile ­ x-ray show major part of art surface is preserved ­ Lavage à Joint debridement, Localized cart defects

37. Arthroscopy Position : ­ Straight-Leg position ­ Flexed-Knee Position Port d’entre : 1. ANTERIOR 2. LATERAL 3. MEDIAL 4. POSTERIOR 5. IN BETWEEN

38. Straight-Leg Position Simple Side Position Varus-Valgus Control

39. Leg Holder

40. Late treatment Reconstructive surgery à Progressive joint destruction, w/ ↑ pain, instability & deformity Arthrodesis Arthroplasty → noticed timing Total joint replacement

41. Arthrodesis ­ Practical solution for younger adults w/ marked destruction of a single joint ­ Advanced reconstructive surgery → less ideal ­ Outcome : ­ Freedom from pain ­ Permanent stability ­ Disadvantages : ­ Restrictive mobility ­ Backache ­ Deformity & discomfort in other nearby joint

42. Hip Arthrodesis Indications : ­ relief of pain & instability ­ desire to return to near-normal physical activity with manual labor ­ relatively young age were working & satisfied w/ their results Position of hip fusion : ­ neutral abduction ­ external rotation of 0-30 deg ­ flexion 20-25 deg

43. Hip Arthrodesis Fixation : ­ AO Cobra Plate ­ Trans-articular sliding hip screw Osteotomy ­ supra-acetabular osteotomy ­ subtrochanteric osteotomy Contra-lateral epiphysiodesis ­ To equalize LLD

44. Knee Arthrodesis Indications : ­ relief of pain & instability ­ failed knee replacement ­ severe articular & ligamentous damage ­ Neuropatic joint dissease Optimal position : ­ slight valgus ­ 10-15 deg of external rotation ­ 0-7 degrees valgus ­ 0-20 deg of flexion (to previous arthroplasty should be fused in full extension) Techniques : ­ Ext Fix, IM Nail or Plate Fix

45. Arthroplasty Restore motion: joint Restore function: ­ Muscles ­ Ligaments ­ Other soft tissue structures Replace one side (hemiarthroplasty) Metal endoprostheses: the implants of choice ­ Hip: Moore & Thompson ­ Knee: MacIntosh & McKeever Improvement in function & ¯ pain Long-term pain relief ¯

46. Total Joint Replacement Goals: ­ Relieve pain ­ Provide motion w/ stability ­ Correct deformity Problems: ­ Optimal implant mechanical design ­ Materials w/ better wear resistance & bone compatibility ­ Fixation techniques ­ Improved instrumentation for ease of revision

47. COMPLICATIONS ­ Deformities ­ Subluxation ­ Capsular Herniation ­ Loose bodies

48. Thanks