presenter: dr. j. w. kinyanjui moderator: prof. mulimba j. a. o. 22 nd july 2013
TRANSCRIPT
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Presenter: Dr. J. W. KinyanjuiModerator: Prof. Mulimba J. A. O.
22nd July 2013
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OutlineDefinitionPathophysiologyAetiologyPresentationImagingStagingManagement
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DefinitionCellular 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
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PathophysiologyInterruption of blood flow to boneAffect bones with single terminal blood
supply:TalusCarpals, tarsalsProximal humerusProximal femurFemoral condyles
Bone marrow, medullary bone and cortical bone necrosis results
Final pathway from multiple causes
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Predisposing factors
Distance from vascular territory of bone
Enclosed by cartilage limiting vascularity
Endarterioles supply trabelcular bones
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Pathways to necrosis
Vascular occlusion – direct trauma, stress fracture, SCD, venous stasis
Intravascular coagulation – hypercoaguable states
Primary cell death – alcohol, steroids, transplant patients
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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
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AetiologyTraumaSteroidsAlcohol abuseCT diseases eg SLEHematologic (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 transplantationRadiation therapyGaucher diseaseMalignancy (marrow
infiltration, malignant fibrous histiocytoma)
Caisson diseasePregnancyBisphosphonate use
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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)
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Non traumatic osteonecrosis
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Presentation - HistoryTrauma
Corticosteroid use
Alcohol intake
Medical conditions – malignancy, thrombophilia, SLE, SCD
Pain – progressive, severity correlates with size of infarct
Deformity and stiffness – later stages
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Presentation - examinationLimp
Antalgic gait
Restricted ROM
Tenderness around bone
Joint deformity
Muscle wasting
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Imaging: X rayInitially normal upto 3 months
Sclerosis
Flattening
Subchondral radiolucent lines (cresent sign)
Collapse of cortex
OA
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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
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Imaging: MRI90% 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
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Radionuclide scanDonut 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
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HistologyDefinitive diagnosisUsually retrospective/confirmatory during
surgery for treatmentOccasionally biopsy of sclerotic lesionNecrosis 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
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Intramedullary pressuresCannula 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
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ARCO StagingStage Clinical and radiological findings
0 Asymptomatic, radiology normal, histological diagnosis
I +-symptoms, normal CT and X ray, early changes on MRI
II Symptomatic, bone density changes on X ray, diagnostic MRI findings
III Cresent sign. IIIa - <15% articular surface, IIIb 15 – 30%, IIIc >30%
IV Collapse of head IVa - <15% surface collapsed, IVb 15 – 30%. IVc >30%
V OA – narrowed joint space, acetabular sclerosis, marginal osteophytes
VI Extensive destruction of joint and involved bone
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Management principlesEarly stages (I & II):
Bisphosphonates prevent collapseUnloading osteotomiesMedullary decompression + bone grafting
Intermediate stage (III & IV):Realignment osteototmies, decompressionArthrodesis
Late stage (V & VI):Analgesia, activity modificationArthrodesisArthroplasties
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Management - conservativeOffloading affected joints with use of
crutchesImmobilisationAnalgesiaBisphosphonates to delay femoral head
collapseStatins in patients on high dose
corticosteroids – reduced lipid deposition
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Core decompressionIndicated 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
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Realignment osteotomyIndicated 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
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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
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Eponymous syndromesKienbock’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,
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