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

Outline Definition Pathophysiology Aetiology Presentation Imaging Staging Management

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

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

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

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

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

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

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)

Non traumatic osteonecrosis

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

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

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

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

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

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

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

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

ARCO Staging StageClinical and radiological findings 0Asymptomatic, radiology normal, histological diagnosis I+-symptoms, normal CT and X ray, early changes on MRI IISymptomatic, bone density changes on X ray, diagnostic MRI findings IIICresent sign. IIIa - 30% IVCollapse of head IVa - 30% VOA – narrowed joint space, acetabular sclerosis, marginal osteophytes VIExtensive destruction of joint and involved bone

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

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

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

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

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

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,

THANK YOU