AVN

Osteonecrosis (AVN)

Definition

  • In situ death of a segment of bone due to ischaemia

Locations

  • Femoral Head
  • Femoral Condyles
  • Humeral Head
  • Capitellum
  • Lunate
  • Scaphoid
  • Talus
  • ie. Convex bones or small cuboidal bones
  • Following surgery
    • eg. Head of first metatarsal

Aetiology

  • Trauma
  • Fractures
  • Dislocations
  • Non-Traumatic
  • Alcohol abuse
  • Corticosteroid usage
  • Caissons Disease
  • Sickle cell disease
  • Thalassaemia
  • Gauchers disease
  • Infection
  • Congenital
    • medial (multiple epiphyseal dysplasia)
  • Developmental
    • Perthes disease
    • SUFCE
  • Idiopathic (most common)

Pathogenesis

  • Due to ischaemia of bone
  • Numerous theories
  • Four mechanisms that are mutual rather than exclusive
  • Interruption arterial supply
    • Capillary occlusion
    • Intraosseous capillary tamponade
    • Injury to vessel wall
  • 1. Arterial insufficiency
    • Fractures & dislocations most often seen
    • SUFCE & Perthes related
    • NOF
      • poor associated collateral blood supply
    • DDH
      • following treatment
  • 2. Intravascular Capillary Occlusion
    • Due to vascular sludging
    • Caissons Disease
      • nitrogen bubbles
    • Corticosteroids
      • fat emboli
    • Alcohol
      • fat emboli
    • Sickle Cell disease » abnormal RBC
  • 3. Intraosseous Capillary Tamponade (intraosseous HTN)
    • Osteonecrosis as a compartment syndrome
    • Commonest cause of AVN
    • Corticosteroids
      • enlarged marrow fat cells
    • Alcohol
      • enlarged marrow fat cells
    • Post-infection
      • inflammatory response
      • also related to activation of intravascular DIC
    • Gauchers Disease
      • glycocerebroside in bloated macrophages
  • 4. Vessel Wall Damage
    • DXRT
      • radiation-induced vessel disease
    • SLE
      • vasculitis
  • Can also add…
    • Venous Occlusion (Chandler’s disease)
    • Venular pressure > Arteriolar pressure
    • Must be very extensive to produce vascular stasis
    • Capsular tamponade from effusion, trauma etc
    • Perthes disease
    • Infection

Path>Pathogenesis

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  • Stages of disease process
  • 1. Death
    • Ischaemic event
    • Segmental bone death
      • opaque yellow marrow
    • Marrow cells die in 6-12 hours
    • Osteocytes die in 24-48 hours
  • 2. Inflammation/ Revascularisation
    • Capillaries & mesenchymal cells advance from adjacent live marrow
    • Grow into dead marrow spaces
    • Cuff of vascular granulation tissue
    • Mesenchymal cells differentiate
    • Pluripotential cells within femoral head
  • 3. Repair
    • Macrophages remove the dead fat & cellular debris
    • Dead bone resorbed by the osteoclasts
    • Creeping Substitution
    • New bone laid down on the dead trabeculae by osteoblasts
    • Sclerosis on XR
    • If healing incomplete
    • Dead bone replaced by fibrous tissue & granulation tissue
    • Cystic areas appear within lesion due to osteoclastic resorption
    • Surrounding bone becomes sclerotic
    • At this stage fracture/ collapse can occur due to
    • Stress fracture of dead bone
    • Stress riser at edge of creeping substitution
    • Weakness of repair front trabeculae due osteoclastic activity
    • Dead bone may fracture without superior articular surface collapse
    • Due to strength of the subchondral bone
  • 4. Remodelling
    • Dead trabeculae removed
    • Woven bone turned into lamella
  • 5. Osteoarthritis
    • Secondary to collapse
    • Altered force transmission due to subchondral collapse

    • Trau>Traumatic AVN

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  • Overlying superficial cartilage to tideline that receives nutrition from joint fluid not involved
  • Cartilage below tideline dies due to disruption of blood supply
  • The bone below this area also necrotic
  • Influx of inflammatory cells & macrophages to remove infarcted marrow
  • Then see ingrowth of fibrovascular tissue that differentiates into osteoblasts & deposits new bone on dead trabeculae
  • Then replacement of the central necrotic bone – Creeping substitution
  • If fibrovascular tissue fails to reach infarct then necrotic marrow undergoes ectopic calcification – MUCH more common in non-traumatic infarcts

    • Atra>Atraumatic AVN

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  • The differences are related to the fact that the original fibrovascular tissue from first infarct prevents further new ingrowth of mesenchymal tissue after this & so it becomes calcified with repeated infarction
  • The area of subchondral bone beneath viable cartilage resorbed & so stress fracture common in this area
  • Interior of infarct remains unrepaired
  • Subchondral/ Juxta-articular AVN
  • Most commonly affects
  • Anterosuperolateral portion of femoral head
  • Central dome of humeral head
  • Infarction of medullary bone & cortex
  • Loss of medullary & cortical architecture
  • Painful & progressive
  • If subchondral collapse
  • Crescent Sign
  • Secondary Osteoarthritis
  • Wrinkle appears at dead margin
  • Then fissures appear
  • Escape of bony detritus through crack into joint leads to synovitis
  • Cartilage may lift off
  • Fibrocartilage may form on sequestrum
  • Stage 1
  • Joint unaltered & external examination of joint shows no abnormalities
  • Cut section of necrotic zone shows wedge shaped region with dull-yellow & chalky marrow in subarticular area
  • Surrounding marrow separated by thin red hyperaemic border
  • Microscopically the articular cartilage is viable down to calcified zone (tidemark)
  • The subchondral bone has replaced marrow elements with eosinophilic granular material containing ghosts of fat cells
  • Extensive calcification maybe present due to repeated AVN episodes
  • At margin of infarct is proliferation of osteoblasts & fibroblasts/ capillaries moving into medullary space
  • Radiologically not detectable
  • Stage 2
  • The overall shape of bone intact & articular surface radiologically intact
  • However see Sclerotic Rim at the boundary between necrotic zone & unaffected marrow
  • Central region of necrosis unchanged but the hyperaemic zone thicker
  • Microscopically advancing front of granulation tissue, lipid laden macrophages, fibroblasts & capillaries at periphery & extending into necrotic zone
  • A second front at a distance has dead bone being resorbed by osteoclasts – Creeping Substitution (Phemister) » removal of necrotic tissue whilst maintaining structural integrity
  • Accounts for ↑ uptake on radionuclide scanning
  • Stage 3
  • Alteration in bone shape becomes radiologically identifiable
  • Collapse in necrotic area occurs
  • On gross inspection the trabecular bone is fractured below the bony end plate
  • Subchondral fracture follows – Crescent Sign » the cartilage above springs back & lucent line produced
  • Trabecular fracture due to
  • – Cumulation of fatigue-induced microfractures
  • – Weakness of trabecular bone in reparative front due to osteoclastic
  • activity
  • – Stress risers at the junction of necrotic bone & the reparative front
  • Microscopically appears as bony & cartilaginous debris
  • Overlying cartilage may still look viable
  • Appearance of unstable non-united fractures elsewhere
  • Deep trabecular fracture may produce no overlying changes although can see articular depression
  • Stage 4
  • Morphological changes of degenerative arthritis
  • Medullary Osteonecrosis
  • Infarction of medullary bone
  • Usually caused by medical conditions
  • Dysbarism
  • Haemoglobinopathies
  • Gauchers disese
  • Most commonly affects
    • Lower femur
    • Upper tibia
    • Upper humerus
  • Variable extent
  • Asymptomatic usually
  • Silent & non-progressive
  • Similar pathology
  • Collagen Calcium
  • “Coil of Smoke” sign
  • Pathology
  • Dead marrow yellow & opaque
  • Surrounded by dense collagen layer that maybe calcified
  • Cortical width ↑ if close

    • Radiology

    • Main change is calcification
    • Wavy line of ↑ density – Coil of Smoke Sign
    • Endosteal cortex thickened
    • Difficult to distinguish from
    • Bone island
    • Calcified enchondroma
    • Investigations
    • Blood Tests
    • Resistance to activated protein C
    • Lipoprotein Lp(a)
    • Protein C & S
    • Tissue plasminogen activator & inhibitor
    • Antiphospholipid antibodies
    • Plain radiographs
    • Mottling
    • Sclerotic line at junction of dead bone
    • Later
    • Crescent sign with joint collapse (best seen in frog leg lateral of femoral head)
    • Segmental collapse
    • End-stage changes of Osteoarthritis
    • Until Osteoarthritis joint space is maintained
    • Dead bone appears dense due to
    • Compression of dead trabeculae
    • Subchondral fracture
    • Calcium of dead marrow (saponification)
    • Onlay of new bone on dead trabeculae
    • Relative osteosclerosis with surrounding osteopenia
    • Bone Scan
    • Initially ↓ uptake
    • Doesn’t absolutely predict AVN as revascularization may occur without necrosis
    • Later ↑ uptake due to repair
    • Hot later doesn’t necessarily predict good outcome as revascularization may be inadequate
    • Non-specific
    • Cold areas may be metastases
    • Hot areas may have numerous causes
    • Most useful to detect avascularity
    • After acute femoral neck fracture or hip dislocation
    • CT Scan
    • Not useful in early stages
    • Best to differentiate precollapse stage 2 from structural collapse of stage 3
    • Good to detect
    • Extent of subchondral fracture
    • Flattening & collapse of articular surface
    • MRI
    • Gold standard in early detection
    • Most sensitive & specific
    • Femoral head most extensively studied
    • Normal marrow rich in fat » High signal intensity on T1
    • Dead marrow » Decrease in signal intensity on T1
    • T1 see low signal line
    • Earliest
    • Avascular-Vascular bone interface
    • T2 see double-line
    • Outer low signal line is thickened trabeculae
    • Inner high signal line is granulation tissue
    • Advantages are
    • Early detection » pre-radiological
    • Accurate localisation & extent of area involved
    • Change in signal early related to ↑ water content
    • Functional Exploration
    • 3-phase invasive investigations – Ficat
    • Intraosseous pressure
    • Abnormal > 30mmHg
    • Intramedullary Venogram
    • Biopsy
    • No longer used
    • Non-Traumatic Osteonecrosis of Femoral Head
    • Epidemiology
    • Most common in middle aged men
    • M:F is 4:1
    • Peak incidence is 30-60 years
    • Bilateral in 50% of idiopathic & 80% of the corticosteroid-related
    • Aetiology
    • Exposure to alcohol & steroids make up 90% of cases where aetiology established
    • Alcohol
    • Most common presentation
    • 15-75% of patients
    • 5-30% of alcoholics develop AVN
    • 50% bilateral
    • Studies suggest as little as 400ml/ week is enough
    • Most idiopathics likely to be alcohol-related
    • Steroids
    • Risk related to the length of treatment & size of dose
    • Overall risk is 3-25%
    • Interval from use to time of onset varies from 6 months to 3 years
    • Often multiple sites involved
    • Often bilateral (80%)
    • Usually progresses to joint failure
    • Conditions
    • Post-Transplantation
    • 20% initially
    • Now 2% due to use of Cyclosporin instead
    • Usually onset within 1 year but can be up to 6 years
    • Involves the
    • Femoral head
    • Humeral head
    • Femoral condyle
    • In decreasing order of frequency
    • Leukaemia/ Lymphoma
    • Rheumatoid
    • Asthma
    • Differences from traumatic AVN are
    • Anterolateral position of lesion in femoral head
    • Repetitive nature of lesions compared with single event in traumatic form
    • Clinical Features
    • Aching pain in groin & thigh
    • Radiates to knee & buttocks
    • Gradual onset
    • Occasionally sudden
    • Initially mechanical
    • ROM reduced due to pain particularly Internal rotation & Abduction
    • Click
    • Staging
    • Ficat & Arlet (1980)
    • Stage 1
    • Onset of ischaemia
    • Clinically evident
    • XR normal
    • MRI ± bone scan changes only
    • Stage 2
    • Pain
    • Early XR changes
    • Cystic/ Sclerotic areas appear
    • Stage 3
    • Structural changes
    • Classical XR changes
    • See Crescent Sign & Flattening
    • Stage 4
    • Degenerative changes
    • Modifications
    • Hungerford & Lennox
    • Added Stage 0 to Ficat & Arlet
    • Preclinical
    • XR normal
    • Bone scan cold
    • MRI double line on T2
    • Steinberg – Stages 0-6
    • Stage 3 divided into those with & those without collapse
    • Also quantified the extent of subchondral fracture
    • A – Mild < 15%
    • B – Moderate 15-30%
    • C – Severe > 30%
    • Japanese Investigation Committee
    • Radiographic location
    • Medial – A
    • Central – B
    • Lateral – C
    • Florida Classification – Enneking
    • Treatment
    • NON-Operative
    • Observation & Protected Weight-Bearing
    • Stage 1 & 2 left untreated will collapse in 85% at 2 years
    • Metanalysis of 21 studies & 819 hips at 3 years
    • – 74% had radiological progression
    • – 76% required arthroplasty
    • – The incidence of radiological progression was related to stage
    • time to failure was not related to degree of NWB
    • The very small lesions < 15% may heal & not progress with non op treatment
    • OPERATIVE
    • Core Decompression (Forage)
    • Ficat & Arlet 1964
    • Rationale
    • – Reduction of Intramedullary pressure
    • – Stimulate angiogenic & osteoblastic responses (enhances creeping substitution)
    • – Pain relief
    • – Tissue for diagnosis
    • Procedure
    • – Fracture table & II
    • – Lateral trochanteric approach
    • – Hollow biopsy trephine – 8-10mm
    • – The anterolateral part of head within 5mm of the articular surface
    • – 3mm drill used to penetrate the necrotic segment to subchondral bone
    • Results
    • Divergence of opinion
    • Metanalysis of 24 studies involving 1206 hips at 3 years
    • 37% did not progress radiologically
    • 33% required arthroplasty
    • Success related to stage
    • – Stage 1 – 84%
    • – Stage 2 – 65%
    • – Stage 3 – 47%
    • Two studies compared core decompression with non-op treatment
    • No collapse in 61% vs 39%
    • No arthroplasty in 75% vs 29%
    • Complications
    • Uncommon
    • Include
    • – Subtrochanteric fracture
    • – Infection
    • Indications
    • Stage 1 & 2 disease
    • Stage 3 where not suitable for more extensive procedure
    • Non Vascularised Bone Grafting
    • Cortical bone graft into defect produced with core decompression
    • Rationale
    • Provides mechanical support for articular surface during healing
    • Procedure
    • Cortical strut graft from the
    • – Ilium
    • – Fibula
    • – Tibia
    • Inserted into core track
    • Protected weight bearing for 3-6 months until radiographic evidence of healing
    • Results
    • Conflicting reports
    • Success rates of 60-80% with short term follow up
    • Some long term reports have 30% successful outcome
    • Disadvantages
    • Prolonged restricted weight bearing
    • Indications
    • Early stage 3 lesions ?
    • Unsuccessful core decompression
    • Vascularised Bone Grafting (Urbaniak 1987)
    • Rationale
    • To enhance revascularisation so that progression of necrosis altered
    • Vascularised grafts undergo more rapid & complete incorporation
    • Procedure
    • Considerable variability
    • Donor site
    • – Ilium
    • – Fibula
    • – GT
    • Muscle pedicle artery & vein used
    • – Inferior gluteal
    • – Profunda femoris
    • – Circumflex
    • Results
    • Most studies have short term follow up in small numbers
    • Most comprehensive is Yoo – 81 hips at 5 years
    • Vascularised fibula to profunda femoris
    • 91% of Stage 2 & 3 had Good-Excellent results
    • 89% had no radiological progression
    • However the rate of conversion to THR is identical to core decompression at 20%
    • Indications
    • Stage 2 or early Stage 3 lesion
    • Young patient
    • Large lesion
    • Osteotomy
    • Rationale
    • Transfer load from necrotic area to undamaged part
    • Transection of bone may afford decompression
    • Procedure
    • Maybe flexion/ extension/ valgus/ varus or rotational
    • If superolateral then need
    • Flexion
    • Valgus
    • If central then
    • Varus
    • Flexion
    • Sugioka
    • Transtrochanteric rotational osteotomy
    • Technically demanding
    • Can rotate through 90°
    • Poor results if not intertrochanteric with damage to blood supply of the head
    • Results
    • Sugioka osteotomy in 52 hips Stage 3
    • 56-69% at average of 5 years successful
    • If > 50% involved then results poor
    • Deterioration with time – only 40% of hips surviving 7-10 years
    • Cumulative necrotic sector angle (Kerboul)
    • Angle from centre of femoral head to edges of necrotic sector measured on AP & lateral films & added together – if < 200° then a favorable outcome after femoral osteotomy may be expected
    • Disadvantages
    • Make subsequent THR difficult
    • Indications
    • Stage 3 disease
    • Small lesion
    • No ongoing cause for AVN
    • Hemiarthroplasty
    • Poor results – 50% revision rate
    • Loosening & Protrusio biggest problem
    • Study showed almost universal acetabular cartilage disease at time of arthroplasty
    • Total Hip Replacement
    • Better results – preferred treatment?
    • Failure rate higher than for other diagnoses
    • Related to poorer bone stock
    • 30-50% revision rates at 10 years
    • In < 50 yo with AVN cemented THR (metal on poly) has 50% failure rates at 10 years (Dorr) – apparently no other study gives better results than this
    • Arthrodesis
    • Usually contraindicated
    • As the disease is bilateral in 50-80%
    • Reasonable option in young, active, heavy man with unilateral disease
    • Electrical Stimulation
    • Not proven technique
    • May be adjunct to other surgery
    • AVN of Humeral Head
    • 2nd most common site
    • Smoking ↑ risk 4x
    • Primary vascular supply
    • Anterior circumflex humeral artery
    • Arcuate artery once in bone
    • 26-75% rate AVN after 4-part fracture
    • Avoid activities above shoulder height
    • » Greatest joint reaction force
    • Benefit of core decompression ambiguous
    • 94% relief of pain with prosthesis