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Avascular necrosis ug class

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AVN

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Avascular necrosis ug class

  1. 1. Avascular Necrosis
  2. 2. Definition AVN OF BONE/OSTEONECROSIS means “BONE DEATH” Sudden Obstruction in arterial blood supply to a part of bone O S T E O N E C R O S I S
  3. 3. Causes Traumatic: Fracture -Femur Neck, Talus, Scaphoid. Dislocations – hip Non-Traumatic : Caisson Disease Sickle Cell Disease Gaucher’s Disease Coagulation Disorders Cortisone Administration Organ /Bone transplantation Metal corrosion Alcoholism Exposure to xrays and radioactive substances
  4. 4. Common sites of predilection -Femoral head -Scaphoid(Preiser’s Disease) -Talus -Segmental fracture -Others – capitellum , radial head , lateral femoral condyle
  5. 5. Pathogenesis BONE ISCHAEMIA is due to - Interruption of arterial inflow - Occlusion of Venous Outflow - Intravascular Blockage of arterioles & capillaries - Increase in marrow pressure
  6. 6. Repair process in a cancellous bone • Proliferating capillaries and fibrous stroma penetrate marrow space of dead bone • Phagocytes remove the marrow debris • Osteoblasts lay down immature woven bone • All these process further increases the radiodensity of necrotic bone
  7. 7. • Later osteoclastic resorption removes the woven bone as well as the old trabaeculae • This is replaced by well organised lamellar bone • This process of apposition of new bone on some surface and osteoclastic resorption on other surface is called CREEPING SUBSTITUTION
  8. 8. Repair process in cortical bone • Excavation of haversian canal by osteoclastic resorption proceeds • This enlarges the canal which multiple in number and uniform in size • Later osteoblasts lay down concentric rings of new bone
  9. 9. Pathology • Microscopically 4 stages are recognised -Stage of marrow necrosis and cell death. -Reactive vascularisation and infiltration. -Distortion of shape by collapse and compression of trabeculae -Subchondral collapse Deformation of articular cartilage
  10. 10. Dysbaric osteonecrosis  Caisson disease /Decompressionsickness/ Aeroembolism.  Seen in deep sea divers , tunnel workers, working in unpressurized aircrafts.  Nitrogen gas bubbles liberated in a concentration that cannot be readily absorbed by blood stream or excreted by lungs.  As a result gas bubbles accumulate in tissues causing local ischemia or intravascular occlusion
  11. 11. Corticosteroid induced AVN 1. Fat embolism theory : • Fat accumulates in liver in patients treated with steroid , and serum lipid concentration also increases • It gives rise to fat embolism and AVN 2. Subchondral osteoporotic fracture : Steroids induce protein catabolism Resulting in generalised osteoporosis Produces subchondral fractures and aseptic necrosis
  12. 12. Clinical Features Early stages: Pain-near joint Later stages: Stiffness, Limitation of movements Advanced stage: Fixed Deformities
  13. 13. Radiological features • Initially necrotic bone appears radiodense • Surrounding vascular bone shows relative osteoporosis • In Early stages- Articular cartilage is not affected - so joint space is normal • In later stages -Partial collapse,flattening of head,joint space narrowing,osteoarthotic changes
  14. 14. AVN of femoral head • Occurs mainly due to femur neck fracture and hip dislocation • Due to disruption of vascular channel in femoral neck
  15. 15. Vascular supply around femoral neck
  16. 16. Vascular disruption following #
  17. 17. Radiography of femur head - AVN
  18. 18. Treatment Core Decompression. Vasularised Fibular Graft. Hemiarthroplasty . Total hip arthroplasty.
  19. 19. Legg-calve perthe’s disease AVN of ossification centre of capital epiphysis of femoral head. 3-12 age group. c/f: Limp, antalgic gait, limited motion HIP DEFORMITY xray: Early findings include Medial joint space widening irregularity of femoral head ossification cresent sign (represents a subchondral fracture)
  20. 20. Treatment: Aim- preserve the femoral head, acetabular congruity, eliminate or reduce weight bearing. Nonoperative -observation, activity restriction, partial weight bearing, traction, and physical therapy. .Ambulation-Abduction Brace Operative- children > 8 years of age. -Femoral Osteotomy proximal femoral varus osteotomy -Pelvic Osteotomy.
  21. 21. AVN of scaphoid
  22. 22. Vascular supply of scaphoid
  23. 23. Vascular disruption in # scaphoid
  24. 24. Radiography of scaphoid # AVN
  25. 25. AVN of talus
  26. 26. Vascular supply of talus
  27. 27. Radiography showing AVN
  28. 28. Other bones susceptible for AVN Lateral femoral condyle Capitellum
  29. 29. The goal in treating avascular necrosis Is to improve the patient's use of the affected joint, Stop further damage to the bone and Ensure bone and joint survival.
  30. 30. • Various methods for delaying disease progression • Non surgical – • Bisphosphonate • Anticoagulants • Vasodilators • Biophysical modalities • Surgical – • Core decompression • Vascularised bone graft/muscle pedicle graft Usually arthroplasty is awaited without any big surgical intervention

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