Avascular Necrosis (AVN)
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This document discusses avascular necrosis (also known as osteonecrosis), which is the death of bone tissue due to a lack of blood supply. It begins by defining the condition and listing common sites of involvement. It then covers epidemiology, causes, pathogenesis, clinical features, investigations, treatment options and complications. Key points include that the femoral head is the most common site, risk factors include trauma, steroid use and sickle cell disease, and treatment ranges from non-operative options like core decompression to joint replacement surgeries depending on the stage of necrosis.
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Avascular Necrosis (AVN)
- 1. By Dr Salihi Abdulmalik National Orthopaedic Hospital Dala-Kano 2nd March, 2021
- 2. Introduction Epidemiology Aetiology Pathogenesis Sites Clinical features Investigations Treatment Complications Conclusion
- 3. Avascular necrosis is death of bone from deficient blood supply Aseptic necrosis=osteonecrosis=ischemic necrosis Bone death is irreversible
- 4. Femoral head Scaphoid Talus Humeral head Radial head Humeral capitellum Medial femoral condyle Lunate (Kienbock’s disease) Navicula (Kohler’s disease)
- 5. Head of femur ◦ 30-50 years ◦ M>F ◦ SCD M:F 1 ◦ 10-18% of THR ◦ 50-80% of cases is bilateral ◦ 3% of patients have multifocal
- 6. Idiopathic Traumatic ◦ Scaphoid ◦ Talus ◦ Femoral head Non traumatic ◦ Extraosseous ◦ intraosseous
- 8. Hip dislocation ◦ 2-40% ◦ 2-10% if reduced witihin 6 hours Femoral head # (75-100%) #NOF ◦ Basicervical (50%) ◦ Cervicotrochanteric (25%) Acetabular # SUFE
- 9. Extraosseous ◦ Intravascular ◦ extravascular Intraosseous ◦ Intravascular ◦ Extravascular
- 10. Extravascular ◦ Trauma intravascular ◦ Caisson’s disease ◦ Vasculitis (Raynauds disease ◦
- 11. Extravascular ◦ Steroid ◦ Alcohol ◦ Compartment syndrome ◦ Gauchers disease Intravascular ◦ SCD ◦ Steroid ◦ Caisson’s disease ◦ Fat emboli (hyperlipidemia – alcohol)
- 12. Infection Ionising radiation Perthes disease SLE
- 13. No advantitia layer in the vascular sinusoid Close compartment ◦ Venous stasis/retrograde arteriolar stoppage ◦ Intravascular thrombosis ◦ Sinusoid compression from marrow swelling
- 14. Asymptomatic Pain Click in the joint limp Stiffness Deformity
- 15. Features of possible aetiology Antalgic gait Positive trendelenburg sign LLD Decrease ROM Sectoral sign
- 16. Plain radiograph ◦ Seldom seen before 3 months after onset of necrosis ◦ Demineralization – osteopenia ◦ Reactive new bone formation – sclerosis ◦ Crescent sign – subchondral # ◦ Irregularity on the head/flattenning/collapse ◦ ?Joint space
- 18. MRI ◦ Most sensitive ◦ Focal lesion in anteriorsuperior portion of the femoral head, well demarcated
- 21. CT scan Bone scan Haemodynamic fucntion ◦ Intraosseous pressure ◦ Canular in metaphysis ◦ Measure at rest and after rapid ingestion of saline ◦ Normal 10-20mmhg at rest Raise by 15mmhg ◦ AVN Both can be increased by 3-4 fold
- 22. Hb genotype FBC ESR
- 23. Ficat and Arlet ARCO Shimuzu University of Pennsylvania Ohzono classification
- 24. Stage 1 (pre radiographic) ◦ Normal x ray ◦ MRI ◦ Intraosseous pressure ◦ Histology Stage 2 (pre collapse) ◦ Subchondral sclerosis/cysts ◦ Diffuse osteopenia
- 25. Stage 3 (early collapse) ◦ Crescent sign ◦ Irregularity of femoral head Stage 4 (OA) ◦ Flattened/collapse head ◦ Joint space affectation
- 27. Based on MRI images Defines the extent, location and intensity of the abnormal segment Findings suggested that extent of ischemic segment is determined at the outset and does not progress
- 29. Shimuzu Extent of femoral head affectation Weight bearing area affected Probability of head collapse within 3 years Likely Rx Grade I < ¼ Medial 1/3 Rarely Symptomati c Rx, monitor Grade II Upto 1/2 1/3 to 2/3 30% 1. Core decompress ion 2. Decompress ion and bone grafting Grade III >1/2 >2/3 70% Osteotomy Hemiarthro plasty
- 30. Prompt reduction of dislocations/#s Use of steroids when necessary and adequtely Prevent crisis in SCD Prompt and adequate treatment of bone/joint infections Gradual decompression of divers
- 31. Determinant factors ◦ Involved bone ◦ Part of the involved bone ◦ Extent of necrotic segment ◦ Patient’s age ◦ Aetiological agent persistent? ◦ General medical background
- 32. Non operative ◦ Waiting policy Non weight bearing areas Pain control Modification of activities ◦ Bisphosphonate
- 33. Operative ◦ Joint preserving surgery Core decompression Bone grafting Osteotomies ◦ Joint replacing surgery Hemiarthroplasty THR ◦ Others Resection arthroplasty Arthrodesis
- 34. Effective symptomatic release in all stages Reduces intramedullary pressure Removal of necrotic bone Aid revascularization Prevent additional ischemic events
- 35. Ficat and Arlet I and II 8 to 10mm diameter core track is created through lateral cortical window Protect weight bearing for 6 weeks
- 36. For Ficat and Arlet I and II Removal of the diseased femoral head segment and its replacement with bone graft
- 37. Redirectional Valgus or varus osteotomies combined with flexion or extension
- 39. Salvage procedure Failed non operative treatment with contraindication for arthroplasty Relieves pain Position ◦ Adduction 0-5 ◦ Flexion 25-30 ◦ External rotation 0 -15
- 40. AVN affects both children and adult Pain and subsequent joint collapse Treatment ranges from non operative to arthroplasty
- 41. Thank you for listening