Consise and crisp explanation of Femur head Osteonecrosis.

1. AVASCULAR NECROSIS OF
FEMUR HEAD
By Dr.Swatantra Aurobind Mohanty
PGT, Dept. of Orthopaedics
KIMS & PBM Hospital, Bhubaneswar

2.  Avascular necrosis of femur head is death of bone tissue of
femoral head due to interruption in blood supply.
 Also called: Osteonecrosis/ Osteochondritis Dissecans/
Chandler’s disease.
 First described by Munro(1738)
 First described with femoral head morphological changes
secondary to blood flow interruption by Curveilhier(1835)
INTRODUCTION

5. EPIDEMIOLOGY
 Men:Women = 4:1
 Most common age group=30-50yrs
 In 10% of undisplaced and 15-50% of displaced femoral neck
fractures.
 In 10-25% of traumatic hip dislocations with risk increasing
with duration.
 Atraumatic AVN is B/L in 30-70% cases but typically
asymmetrical.

6. PATHOPHYSIOLOGY
 Compromise of the already tenuous bloody supply.
 Traumatic injuries causing mechanical obstruction to blood
supply:
◦ Proximal femur fractures
◦ Hip dislocations
◦ Iatrogenic(nailing)
 Atraumatic causes include blood supply compromise, direct
toxic effect on cells and impaired remodelling potential of
subchondral bone:
◦ Steroids(fat cell hypertrophy)
◦ Alcohol(toxic to osteogenic cells)
◦ Smoking
◦ Infections
◦ Radiation
o Chemotherapy
o Hyperlipidaemia
o Gout, SLE
o Haemoglobinopathies

7.  Intravascular factors:
◦ Extraosseous- Arterial(Most important)
◦ Intraosseous- Arterial and Venous
 Extravascular factors:
◦ Intraosseous
◦ Capsular

8.  Femoral head has an end-organ system of blood supply with
poor collaterals.
 Lateral Retinacular Vessels(main blood supply of femoral
head and neck) are disrupted commonly by microemboli.
 Enlargement of intramedullary fat cells cause obstruction of
venous drainage and stasis.
 Increased intra capsular pressure due to effusions may also
tamponade the vessels causing AVN.

9. CLINICAL FEATURES
 Non specific signs and symptoms
 Early stages: Painless
 Ultimate presentation: Pain and limitation of motion
Mostly localised to groin.
May manifest in I/L buttock, knee, GT.
 Passive ROM limited and painful.
 Pain on SLR.
 Flexion contractures in chronic cases.

10. INVESTIGATIONS
 X Rays:
◦ AP, Frog leg lateral views
◦ Early changes not visible but a predictable pattern of changes
over time
◦ Radiolucency: Bone resorption and new formation
◦ Crescent sign: Progressive microfractures, subchondral collapse
◦ Arthritic changes: Degenerative joint disease
◦ Necrotic angle of Kerboul: significant if >200deg

11. Angle formed by lines joining edges of lesion to centre of femur
head on coronal and sagital planes to be added.

14.  MRI:
◦ Most accurate
◦ Indispensable for AVN staging
◦ Size, Gross staging, Revascularisation, Response to treatment
◦ T1: Subchondral changes in antero-superior quadrant with single
line density demarcating normal from ischaemic bone
◦ T2: High signal line inside a low signal line

15. T1
T2

16. STAGING
 In 1960, Arlet and Ficat described a 3 part staging system
which was changed in 1970s to a 4 part system.
O/B of radiological features
 Disadvantages:
◦ Solely on radiographs that are unrevealing early on
◦ No lesion size significance

18.  University of Pennsylvania staging:
Stage Features
0 Normal
I
(Normal
Xray)
A <15% head affected in bone scan/MRI
B 15-30% head affected in bone scan/MRI
C >30% head affected in bone scan/MRI
II
(Lucent
changes in
Xray)
A <15% head affected
B 15-30% head affected
C >30% head affected
III
(Crescent
sign/
Collapse)
A <15% head affected
B 15-30% head affected
C >30% head affected
IV
(Flattening)
A <15% head affected
B 15-30% head affected
C >30% head affected
V(Joint
narrow with
acetabular
changes
A Mild
B Moderate
C Severe
VI Advanced degenerative changes

19.  CT Scan:
◦ Useful only in segregating late pre collapse from early collapse
stage.
 Bone Scan:
◦ Technetium 99m diphosphonate imaging

21. MANAGEMENT
 Aim: To preserve rather than replace femoral head
& cartilage as far as possible.
 Non operative management:
◦ Cane or crutch ambulation with restriced weight bearing
◦ Lipid lowering agents
◦ Iloprost(Prostacyclin derivatives)
◦ Enoxaparin in thrombophilic/hypofibrinolytic disorders
◦ Pulsed Electromagnetic Field Stimulation has a role in
potentiating healing and new bone formation.
◦ Extracorporeal Shockwave Therapy

22. ◦ Extracorporeal Shockwave Therapy
◦ Hyperbaric oxygen to improve oxygenation, reduce edema,
induce angiogenesis and hence reducing intraosseous
pressure.
◦ However, dosage, duration of treatment and long term
effects of drugs on normal bones make it a difficult mode of
management.

23.  Operative Management:
1. Core decompression
2. Bone grafting(Vascularised and Non Vascularised)
3. Osteotomy procedures
4. Hip resurfacing procedures
5. Total hip arthroplasties

24. Core decompression
 Reduction in intramedullary pressure to increase femoral head
blood flow.
 Relieves pain and allows creeping substitution to necrotic area
by bringing blood supply through drill channel.
 8-10mm Trephine/Cannula inserted under Fluoroscopy to
penetrate the lesion. Multiple drills = more delayed collapse but
hampers bone integrity.
 Preferred in Ficat stage I & 2, small central lesions in young non-
obese patients not on steroids.

26.  Osteoinductive substances may be used along with core
decompression:
Bone morphogenetic Protein
Bone marrow mesenchymal stem cell grafting combat
assoc.decrease in progenitor cells(2x10^6 stem cells in non
traumatic pre collapse stage)
Bone grafting
 Removing diseased bone and replacing with 1 or more variety
of bone graft
 Treating Stage I & II diseases.
 Techniques:- Lateral core track, Femoral neck window, Articular
surface window.
 May be Vascularized or Non vascularized

27. Lateral Core track technique

28. Femoral neck window
(Light bulb)

29. Articular surface window(Trapdoor)

31. Insertion of a porous Tantalum Rod functions
analogous to a cortical stud graft allowing structural and
osteoconductive properties.

32. Osteotomies
 To rotate necrotic segment away from weight bearing zone.
 Reduces venous hypertension and intramedullary pressure.
 2 types:
 Trans trochanteric rotational osteotomy
 Intertrochanteric varus/valgus osteotomy(usually with flexion/extension)
 Ideal patient: No steroids, Minimal arthritis, Small combined
necrotic angle.
 Technically demanding and subsequent THR difficult.

34. Varus Osteotomy
Valgus Osteotomy

35. Hip Resurfacing
 Since THR has a high failure rate in these patients(due to
relative youth & physical activity limitation).
 Temporizing procedures:
1. Resurfacing Hemi arthroplasty
2. Total resurfacing arthroplasty
 Have shown clinical promise but outcomes variable.
Total Hip Arthrolpasty
o Treatment of choice for advanced osteonecrosis.
o Excellent functional improvements but long term outcomes
variable.

37. STAGE TREATMENT MODALITY
I & II [asymptomatic] 1.Observation+/- Pharmacologic
2.Possible Core Decompression
I(A,B,C), II(A,B,C) [symptomatic] 1.Core decompression +/- bone
grafting(vascularised)
IC, IIC, III(A,B,C), IVA
[symptomatic]
1.Bone grafting(vascularised/non
vascularised)
2.Osteotomy
3.Limited femoral head resurfacing
4.THR
IVB, IVC [symptomatic] 1.Limited femoral head resurfacing
2.THR
V, VI [symptomatic] 1.THR
Treatment AlgorithmO/BofUniversity ofPennsylvania
system ofClassification andStaging

38. THANK YOU!