Avascular Necrosis (AVN)

1,406 views 41 slides Jun 15, 2021
Slide 1
Slide 1 of 41
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41

About This Presentation

AVN


Slide Content

Avascular Necrosis By Dr Salihi Abdulmalik National Orthopaedic Hospital Dala-Kano 2 nd March, 2021

Introduction Epidemiology Aetiology Pathogenesis Sites Clinical features Investigations Treatment Complications Conclusion Outline

Avascular necrosis is death of bone from deficient blood supply Aseptic necrosis= osteonecrosis =ischemic necrosis Bone death is irreversible Introduction

Femoral head Scaphoid Talus Humeral head Radial head Humeral capitellum Medial femoral condyle Lunate ( Kienbock’s disease) Navicula (Kohler’s disease) Bones commonly affected

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 Epidemiology

Idiopathic Traumatic Scaphoid Talus Femoral head Non traumatic Extraosseous intraosseous Aetiopathogenesis

Blood supply to femoral head

Hip dislocation 2-40% 2-10% if reduced witihin 6 hours Femoral head # (75-100%) #NOF Basicervical (50%) Cervicotrochanteric (25%) Acetabular # SUFE Traumatic

Extraosseous Intravascular extravascular Intraosseous Intravascular Extravascular Non traumatic

Extravascular Trauma intravascular Caisson’s disease Vasculitis ( Raynauds disease Extraosseous

Extravascular Steroid Alcohol Compartment syndrome Gauchers disease Intravascular SCD Steroid Caisson’s disease Fat emboli ( hyperlipidemia – alcohol) Intraosseous

Infection Ionising radiation Perthes disease SLE Others

No advantitia layer in the vascular sinusoid Close compartment Venous stasis/retrograde arteriolar stoppage Intravascular thrombosis Sinusoid compression from marrow swelling Non traumatic

Asymptomatic Pain Click in the joint limp Stiffness Deformity Clinical features

Features of possible aetiology Antalgic gait Positive trendelenburg sign LLD Decrease ROM Sectoral sign Clinical features

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 Investigations

Radiographs

MRI Most sensitive Focal lesion in anteriorsuperior portion of the femoral head, well demarcated Investigations

MRI

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 Investigations

Hb genotype FBC ESR Investigations

Ficat and Arlet ARCO Shimuzu University of Pennsylvania Ohzono classification Staging

Stage 1 (pre radiographic) Normal x ray MRI Intraosseous pressure Histology Stage 2 (pre collapse) Subchondral sclerosis/cysts Diffuse osteopenia Ficat and Arlet staging

Stage 3 (early collapse) Crescent sign Irregularity of femoral head Stage 4 (OA) Flattened/collapse head Joint space affectation Ficat and Arlet staging

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 Shimuzu classification

Shimuzu

Shimuzu Extent of f emoral head affectation Weight bearing area affected Probability of head collapse within 3 years Likely Rx Grade I < ¼ Medial 1/3 Rarely Symptomatic Rx, monitor Grade II Upto 1/2 1/3 to 2/3 30% 1. Core decompression 2. Decompression and bone grafting Grade III >1/2 >2/3 70% Osteotomy Hemiarthroplasty THR

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 Prevention

Determinant factors Involved bone Part of the involved bone Extent of necrotic segment Patient’s age Aetiological agent persistent? General medical background Treatment

Non operative Waiting policy Non weight bearing areas Pain control Modification of activities Bisphosphonate Treatment

Operative Joint preserving surgery Core decompression Bone grafting Osteotomies Joint replacing surgery Hemiarthroplasty THR Others Resection arthroplasty Arthrodesis Treatment

Effective symptomatic release in all stages Reduces intramedullary pressure Removal of necrotic bone Aid revascularization Prevent additional ischemic events Core decompression

Ficat and Arlet I and II 8 to 10mm diameter core track is created through lateral cortical window Protect weight bearing for 6 weeks Core decompression

For Ficat and Arlet I and II Removal of the diseased femoral head segment and its replacement with bone graft Bone grafting

Redirectional Valgus or varus osteotomies combined with flexion or extension Osteotomies

Hemiarthroplasty THR Arthroplasty

Salvage procedure Failed non operative treatment with contraindication for arthroplasty Relieves pain Position Adduction 0-5 Flexion 25-30 External rotation 0 -15 Arthrodesis

AVN affects both children and adult Pain and subsequent joint collapse Treatment ranges from non operative to arthroplasty Conclusion

Thank you for listening
Tags