Avascular Necrosis

1. Avascular Necrosis Presenter: Dr. J. W. Kinyanjui Moderator: Prof. Mulimba J. A. O. 22nd July 2013

2. Outline • Definition • Pathophysiology • Aetiology • Presentation • Imaging • Staging • Management

3. Definition • Cellular death of bone components secondary to interruption of blood supply • Consequent collapse of bone components • Pain, loss of function of joints • Proximal epiphysis of femur most commonly affected

4. Pathophysiology • Interruption of blood flow to bone • Affect bones with single terminal blood supply: • Talus • Carpals, tarsals • Proximal humerus • Proximal femur • Femoral condyles • Bone marrow, medullary bone and cortical bone necrosis results • Final pathway from multiple causes

5. Predisposing factors • Distance from vascular territory of bone • Enclosed by cartilage limiting vascularity • Endarterioles supply trabelcular bones

6. Pathways to necrosis • Vascular occlusion – direct trauma, stress fracture, SCD, venous stasis • Intravascular coagulation – hypercoaguable states • Primary cell death – alcohol, steroids, transplant patients

7. Bone necrosis after 12 – 48 hrs of anoxia • Reactive new bone formation around necrotic bone • Granulation tissue over necrosed bone – sclerosis • Structural failure – subchondral fracture 1st • Segmental collapse dependant on stress and area of necrosis

8. Aetiology • Trauma • Steroids • Alcohol abuse • CT diseases eg SLE • Hematologic (sickle cell disease, hemoglobinopathies, thrombophilia) • Metabolic (hyperlipidemia, gout, renal failure) • Orthopedic disorders (slipped capital femoral epiphysis, developmental dysplasia of the hip, Legg-Calve-Perthes disease) • Infection (osteomyelitis, HIV]) • Renal transplantation • Radiation therapy • Gaucher disease • Malignancy (marrow infiltration, malignant fibrous histiocytoma) • Caisson disease • Pregnancy • Bisphosphonate use

9. Trauma • Severance of blood supply – displaced femoral neck fractures • Scaphoid and talus – proximal osteonecrosis due to distal origin of vessels • Osteoarticular impact – localised osteonecrosis in convex surfaces (osteochondroses)

10. Non traumatic osteonecrosis

11. Presentation - History • Trauma • Corticosteroid use • Alcohol intake • Medical conditions – malignancy, thrombophilia, SLE, SCD • Pain – progressive, severity correlates with size of infarct • Deformity and stiffness – later stages

12. Presentation - examination • Limp • Antalgic gait • Restricted ROM • Tenderness around bone • Joint deformity • Muscle wasting

13. Imaging: X ray • Initially normal upto 3 months • Sclerosis • Flattening • Subchondral radiolucent lines (cresent sign) • Collapse of cortex • OA

16. Imaging: CT scan • Used to assess extent of disease and calcification • Clearly shows articular deformity • Calcification and bone collapse • Central sclerosis in femoral head produces asterix sign

18. Imaging: MRI • 90% sensitive • Reduced subchondral intensity on T1 representing boundary between necrotic and reactive bone • Low signal on T1 and high signal on T2 – reactive zone (diagnostic) • Changes detected early

20. Radionuclide scan • Donut sign – central reduced uptake with surrounding rim of increased uptake • More sensitive than plain films in early AVN • Less sensitive than MRI • Necrotic zone surrounded by reactive new bone formation

21. Histology • Definitive diagnosis • Usually retrospective/confirmatory during surgery for treatment • Occasionally biopsy of sclerotic lesion • Necrosis of cortical bone is followed by a regenerative process in surrounding tissues. • Increased osteoclastic activity to remove necrotic bone and increased osteoblastic activity as a reparative process

22. Intramedullary pressures • Cannula into metaphysis • Measure at rest and after saline injection • Femoral head: • 10 – 20 mmHg, increasing by 15 mmHg after saline • Markedly increased values in AVN (3 to 4 fold) • Less marked increase in OA

23. ARCO Staging

24. Management principles • Early stages (I & II): • Bisphosphonates prevent collapse • Unloading osteotomies • Medullary decompression + bone grafting • Intermediate stage (III & IV): • Realignment osteototmies, decompression • Arthrodesis • Late stage (V & VI): • Analgesia, activity modification • Arthrodesis • Arthroplasties

25. Management - conservative • Offloading affected joints with use of crutches • Immobilisation • Analgesia • Bisphosphonates to delay femoral head collapse • Statins in patients on high dose corticosteroids – reduced lipid deposition

26. Core decompression • Indicated in ARCO I and II • 8 – 10 mm anterolateral core of bone • Filled with bone graft (vascularised/non vascularised) • Decompresses medullary cavity, reduces pain • Cortical (osteoconductive) or cancellous(osteoinductive) bone graft • Vascularised graft may reverse necrosis

28. Realignment osteotomy • Indicated in ARCO III & IV • Used to relocate necrotic area from weight bearing portion of femoral head • Angular osteotomies more common • Multiple techniques for holding the fixation • Sugano intertrochanteric rotational osteotomy technically demanding but higher success rate

30. Arthroplasty • Indicated in ARCO IV onwards • Main aim is pain reduction • Young patients will need revision • Higher failure rates than in OA • Hemi arthroplasty an option

31. Eponymous syndromes • Kienbock’s disease – idiopathic avascular necrosis of the lunate bone that leads to collapse and progressive carpal arthritis. PRC as treatment • Legg-Calve-Perthes’s – idiopathic osteonecrosis of femoral capital epiphysis in children. Treated with orthotics, traction, surgery to rotate the femoral head • Preiser's disease – idiopathic osteonecrosis of scaphoid. Collapse with progressive arthritis. PRC, Excision and fusion,

32. THANK YOU