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Avascular necrosis

  1. Osteonecrosis Under the guidance of Dr. Sanjay singh sir Dr. C.D. Sahu sir Dr. Amit Kumar sir Presented by RAVISH KUMAR
  2. Avascular necrosis  Also known as osteonecrosis ,aseptic necrosis, bone infarction  Implies that a segment has lost its blood supply so that cellular elements within it die.
  3. Anatomic predisposition for osteonecrosis Femoral head, Humeral head, Distal femur
  4. Clinical presentation Usually non-specific and depend on the cause and location. Early phase symptoms are variable and often absent or relatively minor. This clinical latent period may range from a few weeks up to 1 year in duration Evident, particularly when the articular surface collapses, altering joint function.. As progressive collapse of the joint surface occurs, greater pain and debility are to be expected. localized and referred pain, antalgia, reduced and painful ranges of motion,and adjacent muscle atrophy. Metaphyseal and diaphyseal infarcts -completely asymptomatic to acutely symptomatic.
  5. Etiology  Unilateral Bilateral Common  Spontaneous (idiopathic) Alcoholism  Surgery Corticosteroid therapy  Trauma (fracture, dislocation) Spontaneous (idiopathic) Uncommon  Gout Arteriosclerosis  Hemophilia Caisson’s disease  Infection Cushing’s disease Gaucher’s disease Hemoglobinopathy Lupus erythematosus Pancreatitis
  6. pathology  Ischemia results to death of all component of bone cell  Revascularization is seen at the live marrow and dead marrow interface.  Necrotic zone is invade by capillaries , fibroblasts and macrophages  Fibrous tissue replace dead marrow and may calcify.  New osteoblast lay down fresh woven bone on devitalise trabeculae  Neovascularisation and ossification-creeping substitution(Phemister)  Bone ends and cartilage recieves nutrition from synovial fluid.
  7. Osteonecrosis- femoral head VASCULAR SUPPLY: FEMORAL HEAD. There are two sources of blood supply: profunda femoris (1)and ligamentum teres (2). From the profunda femoris the circumflex vessels (3 and 4) provide the medial and lateral epiphyseal arteries (5 and 6). It is probable that the site of precipitating occlusion is at the lateral epiphyseal vessels.
  8. Radiological features  Anterosuperior location  Cortical collapse (step defect)  Cystic radiolucencies  Degenerative joint disease  Fragmentation  Periosteal bone apposition  Sclerosis (snowcap sign)  Subchondral fracture (crescent, rim sign)  Trabecular alteration  Wedged or semilunar shape (bite sign)
  9. EPIPHYSEAL INFARCTION: GENERAL FEATURES. F A. Collapsed Articular Cortex. Observe the sharp, angular deformity (arrow) in the weight-bearing cortex (step defect). Sclerosis of the femoral head is also evident. B. Epiphyseal Fragmentation. Note that multiple cystic and linear lucencies produce a mottled, fragmented appearance to the femoral head. This is owing to a combination of fractures, subchondral cysts, and localized repair response. C. Subchondral Fracture. Note the thin curvilinear radiolucency (arrow) just beneath the weight-bearing articular cortex (crescent sign).
  10. HIP AVASCULAR NECROSIS: PROGRESSIVE ARTICULAR COLLAPSE . A. Initial Film. Note the two sharp, angular deformities (step defects) at the weight- bearing superior articular cortex (arrows). A slight increase in density is visible in the femoral head. B. 12-Month Follow-Up. Note that greater collapse is evident.Degenerative changes have also intervened, with loss of joint space and osteophyte formation. C. 18-MonthFollow-Up. Note that severe collapse and fragmentation have occurred, with considerable lateral displacement of the femur.
  11. Pathologic-Radiologic Correlation in Epiphyseal Ischemic Necrosis  Pathologic Feature Radiologic Feature  Avascular Phase  Loss of blood supply Small epiphysis  Bone death Normal bone density  Cartilage growth Increased joint space  Low-grade synovitis Increased joint space Capsular swelling  Disuse, hyperemia Metaphyseal osteoporosis  Widened growth plate
  12.  Revascularization Phase  Neovascularization  Periphery Peripheral sclerotic rim  Center Homogeneous sclerosis (snowcap)  Subchondral fracture Crescent sign  Fibrous and granulation tissue Clefts and fragmentation  Woven bone Flattening of surface  Altered biomechanical stress Widened metaphysis
  13.  Repair  Bone deposition- Reconstitution of epiphysis  Regression of osteoclasis - Disappearance of clefts  Deformity  bone - Deformed, articular surface
  14. Metaphyseal diphyseal infarction  Cortical or medullary  Distal femur, proximal tibia and proximal humerus Cortical  The periosteum is often activated to produce a fine layer of new bone  Localise rarefaction Medullary  Central location Metaphyseal-diaphyseal location  Elongated lesion Sclerotic, serpiginous contour  Focal internal calcification Unaffected adjacent
  15. METAPHYSEAL-DIAPHYSEAL INFARCTS Observe the characteristic central location, undulating serpiginous contour, and dense calcific margin.
  16. METAPHYSEAL-DIAPHYSEAL INFARCTS. Plain Film. Note that two mature infarcts are present, one within the metaphysis (arrow), the other within the proximal humeral diaphysis (arrowheads).
  17. Ficat staging  Stage 1- No changes visible  Stage 2-Disuse osteoporosis except devitalise avascular bone which appears sclerosed.  Stage 3-subcortical zone of transradiancy and trabecular loss beneath thin sclerotic cortex leading to microfractures followed by collapse and trabecular compression.  Stage 4-flattened articular surface with increase subarticular density  Stage 5- Osteoarthritis with joint space narrowing
  18. MRI features of osteonecrosis  Highly sensitive and specific for AVN  Useful in equivocal radigraphs and contralateral normal hip on radiographs  Assist for decision to perform operative procedures  T1W characteristic serpiginous area of altered signal intensity of anterosuperior part of femoral head.  T2WI double line sign(pathognomonic) Outer low intensity rim and inner high intensity band bright band sign
  19. T1 images
  20. T2 images
  21. Mitchell classification  Based on appearace of center region signal,bounded by low signal rim on T1 and T2W images  Class A –fat like signal characteristic early stages of disease Class B-subacute blood like high signal on both T1 and T2 Class C-Fluid like signal intensity Class D- fibrous tissue like changes
  22. Mitchell class images A and B: Mitchell class A and D AVN: T1W coronal (A), STIR coronal image of both hips (B)—shows area of altered signal in both femoral heads with fat intensity signal on T1W and STIR on the right side-class A and hypointense signal on the left side-class D
  23. Mitchell class C and D AVN. T1W coronal image (A), T2W fat suppressed coronal image of both hips (B), shows bilateral areas of altered signal in femoral head showing hypointensity on T1W and mixed hypo- and hyperintensity on T2WI
  24. Secondary findings-  fatty marrow of intertrochantric region  Increase amount of synovial fluid  Bone marrow oedema
  25. Secondary findings AVN Fatty marrow infilteration T1W coronal (A) and STIR coronal images of both hips (B), showing increase in intertrochanteric fatty marrow on the right side with marrow edema on the left side with bilateral AVN
  26. STIR coronal image of both hips showing joint effusion on the left side with bilateral AVN
  27. Gadolinium enhanced imaging Bilateral AVN. T1W coronal (A) and T1W axial (B) fat suppressed, postgadolinium image of both hips showing necrotic nonenhancing areas with enhancing viable interface and viable fragments
  28. Dynamic contrast study detect early femoral ischemia delayed peak enhancement is noted ADC value are higher in hip AVN ,but staging is not possible MR spectroscopy can detect early changes in lipid/water spectra
  29. Prognostic indicators on MRI  Percentage of weight bearing surface that is involved by AVN lesion is most reliable factor.  In coronal image if less than 25%femoral head is involved ,there is less likelihood of lesion to develop collapse  If more than 2/3rd weight bearing surface is involved - 74%chance of collapse of head  On saggital if reactive interface cross the 12 oclock- 82% chance of collapse  High risk marker early conversion from hematopoietic to fatty marrow and dense intact physeal scar
  30. Pitfalls in Diagnosis  Fatty conversion does not occur occasionally  Synovial herniation pit  Subchondral bone cysts  Fovea centralis
  31. Pitfall images A and B: X-ray pelvis and both hips—AP view (A) shows decreased joint space on the left with subchondral cystic changes and osteophytes and T1W coronal image of both hips (B) depicting subchondral cyst with osteophytes—degenerative changes
  32. Study choice and workup  Radiograph-AP and Frog leg lateral projection  Radionuclide imaging- Tc 99MDP or Tc99S In early phase-cold photopenic zone pathognomonic for AVN Late stage reactive hyperemia and reparative response may result in doughnut sign  CT scan- adjunctive role, in pt. with MR contraindication
  33. prognosis  Rate of progression is unpredictable  If disease dicovered prior to articular collapse-core decompression and rotational osteotomy  Hip arthroplasty done in patients with interactable pain and femoral head collapse

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