AVASCULAR NECROSIS

OF FEMUR HEAD
Dr. Mohammed Akbar Khan
Postgraduate in Orthopaedics

DEFINITION
Death of Osteocytes - Femoral head collapse &
Secondary hip joint osteoarthritis

Osteonecrosis, Aseptic necrosis or Ischemic bone

necrosis

Temporary or permanent loss of the blood supply Ischemia - Death and collapse of the Bone tissue &
Joint surface.

Affect several different bone.

HISTORICAL REVIEW

1888 - Konig - Osteochondritis dessicans of

femoral head
1925 - Haenish - first case - Idiopathic ischemic
necrosis of femoral head in an adult
1935 - Chandler - Coronary artery disease of the hip
1940 - Arterial occlusion was postulated as Etiology
1949 - Phemister - Femoral head drilling & Tibial bone
grafting
1957 - Pietrograndi - First case(AVN)-Steroid Therapy

TERMINOLOGY

1948 - Coronary artery disease of hip

Aseptic necrosis
Avascular necrosis or Ischemic necrosis Osteonecrosis (Term of choice)
More neutral in its presumption of causation.

Describes main features of this condition i.e.

bone death

INTRODUCTION

Ischemic death of the cellular constituents - Bone &

marrow
2/3 of heads removed at autopsy

Commonest site is Antero-superolateral Subchondral

50% of necrotic heads -wedge of viable area at fovea

Dead Bone

Foveal Live Bone

Dead Bone

INCIDENCE

Age: 3rd 5th decade

Very rare in extremes of age

Mean age of onset is 5th decade

Male : female = 4:1

Bilateral in 50 % of cases

COMMENEST SITES

Femoral Head

Femoral Condyles

Head of Humerus

Capitulum

Scaphoid

Lunate

Talus

CLASSIFICATION
Primary (idiopathic)
Secondary to:
Trauma Fracture of the femoral neck
Slipped capital femoral epiphysis
Proximal femoral epiphysiolysis
Dislocation of the femoral head
Epiphyseal compression
Vascular trauma
Burns
Radiation exposure
Hemoglobinopathies
Sickle cell disease
Hemoglobin S or hemoglobin C
Polycythemia

Caisson disease Dysbaric osteonecrosis

Local infiltrative disease
Gaucher disease
Infection
Neoplasms
Hypercortisolism
Corticosteroid medications
Cushing disease
Chronic renal failure
Cigarette smoking
Collagen vascular diseases
Congenital and developmental
Congenital dislocation of the hip
Ehlers-Danlos syndrome
Heredity dysostosis
Legg-Calv-Perthes disease

Fabry disease
Giant cell arteritis
Gout and hyperuricemia
Hemodialysis
Hypercholesterolemia
Hypercoagulable states
Hyperlipidemia
Hemophilia
Hyperparathyroidism
Intravascular coagulation
Organ transplantation
Alcohol consumption
Pancreatitis
Pregnancy
Systemic lupus erythematosus
Thrombophlebitis

BLOOD SUPPLY OF FEMORAL HEAD

ANATOMICAL RISK FACTORS

Subchondral part of bone - distance from the main

vascular territory

Subchondral trabaculae supplied by endarterioles.

Vascular sinusoids of marrow No adventitial layer compressed by marrow edema.

ETIOLOGICAL FACTORS

Interruption of arterial flow

Intravascular blockade of arterioles and capillaries

Expansion of marrow components and capillary

compression

Occlusion of venous outflow

ARTERIAL INTERRUPTION

Fracture Neck of Femur

Dislocation

SUFE

Infections

Frog leg Immmobilisation

ARTERIOLAR OCCLUSION

Sickle cell disease

Vasculitis - SLE

Caissons disease

Hemostatic disorders

Gout

CAPILLARY COMPRESSION

Gauchers disease

Fatty Infiltration
Corticosteroids
Alcohol abuse
Familial hyperlipidemia
Renal transplant

Hyperbaric conditions

MISCELLANEOUS

Hemarthrosis

Perthes disease

Pregnancy

Ionising radiation

Iatrogenic

Sickle cell
disease
Dysbaric
ischemia
Thrombocytop
enia
Fat embolism

Arteriolar occlusion

Marrow edema

Vicious cycle

Vascular stasis

Sinusoidal compression
Gauchers
Tuberculosis
Cortisone
Alchohol
Dysbaric ischemia

IDIOPATHIC AVN

Diagnosis of exclusion

Constitutes 25% cases

Thrombosis of vascular supply of femoral head unknown etiology

Diffuse osteoporosis with loss of trabeculae

surrounded by sclerosis

FEMORAL HEAD
DISLOCATION

Injury to the ligementum Teres

Disrupts the blood supply

Superior retinacular arteries may be injured

Reduction returns the bone to its normal stress bearing state

FEMORAL NECK FRACTURE

Extensive interruption of blood flow

Sinusoidal vascular bed interrupted

Subsynovial retinacular vessels disrupted

Only supply from Ligamentum teres

Valgus reduction helps in union but blood supply

STEROIDS
Pathogenesis of AVN in hypercortisolism is unknown.
1. Fat embolization from the liver, Bone marrow fat cells,
or destabilization and coalescence of plasma
lipoproteins.
2. Corticosteroids along insulin resistance hypertension
& arteriosclerosis - Coronary disease of the hip
3. Corticosteroid
Osteoporosis
Microfractures
AVN
4. Peak doses of steroid are significant than duration of
treatment

RENAL FAILURE

Congenital anomalies and Acquired renal disease

Complication of treatment with recombinant growth

hormone in children with Renal disease.

COLLAGEN VASCULAR DISEASE

Thickening & Necrosis of vessel basement membrane occlusion of vessels.

Rheumatoid arthritis

Scleroderma

SLE

Dermatomyositis

Corticosteroids used for treatment.

ALCHOHOL

Fatty Liver - Fat embolism.

Ac. or Ch. Pancreatitis - Circulating lipases - Fat

necrosis in bone

SICKLE CELL DISEASE

Sluggish blood flow - sickle shaped cells diminished blood supply - infarction of
epiphyseal & metadiaphyseal bone -AVN

Bone within bone appearance in x-ray Infarction of inner 1/3 of cortex

ENDOSTEAL SCLEROSIS

BONE WITHIN BONE APPEARANCE

LIGHT NECROTIC AREAS

DEMARCATED FROM VIABLE BONE

AREAS OF MOTTLING AND SCLEROSIS

SEQUESTRUM FORMATION
(BONE WITHIN A BONE)

IRRADIATION

Direct cell damage

Damage to cells in the walls of blood vessels

with obliteration of vessels

Highest risk seen in patients with Hodgkin's and

NHL receiving RT,CT and Steroids

DYSBARIC DISORDERS
Directly related to
Depth of dive
Number of dives
Uncontrolled decompression
Low oxygen saturation
Accumulation of undissolved nitrogen bubbles in
vascular & interstitial spaces

DYSBARIC OSTEONECROSIS

GAUCHERS DISEASE

Marrow sinusoids packed with glucocerebrocide filled

histiocytes (gaucher cells) - Increased pressure

Direct affection of femoral head

Liver disease
Fat embolism
AVN

PREGNANCY

Last trimester
Venous stasis with increased marrow pressure

PATHOGENESIS
Four phases
1) Avascular phase,

2) Revascularization phase,
3) Repair phase,
4) Deformity phase.

AVASCULAR PHASE

Infarction within fatty marrow adjacent to subchondral

cortex of the bone necrotic - overlying cartilage
hypertrophies (attempt to convert itself to bone).

Radiographic appearance - Minimal osteopenia or

subtle soft tissue changes.

Increase in the medial joint space between Kohler's

tear drop and the femoral head - 2 mm difference (Waldenstrom's sign)

WALDENSTORMS SIGN

Increase Medial Joint Space

Kohlers tear drop

Femoral Head

REVASULARIZATION PHASE

Osteoclastic & osteoblastic activity.

Mixed areas of luceny & sclerosis.

Cell death - beneath articular surface bone fragmentation and collapse of the overlying cortex
indication of collapse - Crescent sign.

Further collapse - Step sign

Snow Cap Sign - Diffuse sclerosis - Repair is sufficient

in revascularization phase.

CRESCENT SIGN & STEP SIGN

Thin curvilinear lucency in immediate subchondral bone &
located on the weight bearing portion. Further collapse
may result in a "step sign" in which cortical offset is
actually noted on the film

SNOW CAP SIGN

Diffuse sclerosis of femoral head

CRESCENT SIGN

SNOW CAP SIGN

REPAIR PHASE

Begins with revascularization.

Variable degree of reconstitution and healing

-Degree of blood loss and cell death - initial insult
-Patient's immune system and healing response
-Joint is weight-bearing vs. non-weight bearing

DEFORMITY PHASE

Highly variable - severity of other phases

- site specific & stresses in the area
(weight-bearing areas - increase in deformities)

Early and severe degenerative joint disease incongruent joint surfaces early hip replacement

Cell death - process will cascade - severe &

debilitating degenerative joint disease.

Fortunate aspect - Treatable if discovered early.

SEQUENCE OF REPAIR
8 PHASES
Phase 1

< 24 hours loss of cell viability

2-4 days Pyknosis and karyolysis
Phase 2
Invasion of marrow vascular spaces by
capillaries, primitive mesenchymal cells and
inflammatory cells
Occurs in adjacent live bone

SEQUENCE OF REPAIR
Phase 3
Invasion of capillaries and cells in dead bone
Phase 4
Synthesis of new bone
Mesenchymal cells differentiate into osteoblasts
Phase 5
Early internal remodelling

Phase 6
Late internal remodelling

SEQUENCE OF REPAIR
Phase 7
Resorption of subchondral bone
Bone resorption > bone formation

Phase 8
Pannus formation over articular cartilage
Fibrillation and destruction of cartilage
Osteoarthritic changes

ZONES IN AVN
Four zones

A - Central zone of cell death

B - Zone of ischemic injury

C - Active hyperemia

D - Normal tissue

AVN- 4 zones

A
B
C

FISSURING

BREAKING UP

DESTROYED JOINT SURFACE

HISTOPATHOLOGY

Wedge shaped area of necrosis - subchondral

portion of the head of femur at anterosuperolateral
part - weight bearing portion of the femoral head

Invasion of the vascularised cellular tissue from

surrounding living marrow into the necrotic segment

Necrotic trabeculae are ensheathed by the newly

deposited bone through reparative process

Increased radiological density

STAGING

FICAT & ARLET

SHIMIZU et al

RATLIFFE

MARCUS et al

HUNGERFORD & ZIZIC

AAOS

STEINBERG et al

ARCO

FICAT AND ARLET CLASSIFICATION

Sta symp

X-ray

B-scan

0 None

Normal

?Uptake

1 None/
mild

Normal

Cold
spot

2-A mild
2-B
3 mod

patho

Biopsy

Infarction Dead
marrow

Sclerosis Uptake
flattening

Repair

Collapse

Uptake

Subcho# Dead
bone

Uptake

OA
Deg.
changes change

4 severe Joint
space

New
bone

FICAT AND ARLET CLASSIFICATION

STAGE II

STAGE III

STAGE IV

SHIMIZU et al

Grade 1
Restricted to medial part

Grade 2
Occupy upto of head & bet. 1/3 to 2/3 of wt.
bearing surface

Grade 3
Occupy large part of head & more than 2/3 of
wt. bearing surface

RATLIFFE CLASSIFICATION

# NOF IN CHILDREN

MARCUS et al (1973)
STAGE

I
II
III
IV
V
VI

CLINICAL

RADIOGRAPH

Asymptomatic
Mottled densities
Asymptomatic Infarcted demarcated by density
Pain-mild & intermittent
Crescent sign
Pain with activity
Depression of infarct
Pain with activity
Flattening & compression
Pain at rest
Degenerative arthritis

HUNGERFORD & ZIZIC (1978)

1. Normal x-ray

May / may not be painful

2. X-ray show dense line but intact femoral head
3. Subchondral fracture sequestration of cartilage
4. OA with joint Space narrowing

AAOS
Stage

2
3
4

Description

X-ray

fat embolism
Normal
intraosseous, inflammatory
focal iv coagulation
Osteonecrosis
normal patchy
small areas of
density
Revascularisation
roundhead sclerotic
area near art. sur
Collapse & deformity
crescent sign
collapse ,seque.flat
Degenerative changes
Findings of OA

STEINBERG et al
Stage
Criteria
0 Normal or nondiagnostic x rays, bone scan & MRI
I Normal x rays, abnormal bone scan, and/or MRI
II Abnormal x rays (cystic, sclerotic without collapse)
III Subchondral collapse
IV Flattening of the femoral head without joint space
narrowing or acetabular involvement.
V Joint narrowing and/or acetabular involvement
VI Advanced degenerative changes
Staging - extent of lesion (A, B & C) - size by MRI /x-ray.

STEINBERG

MRI CLASSIFICATION
TAKORI
Group 1 - Type A
Fat intensity area confined to med anterosuperior fem. Head but not extend across head
Group 2 - Type B
Beyond the zenith to posterior part of head
Group 2 - Type C
occupy the posterior Half
Group 2 - Type D
Larger than Type C
Useful in pts at risk of AVN

OHZONO PROGNOSTIC

Sakamoto et al

- extent of lesion on MRI

ARCO

Ficat Arlet staging system

Hungerford-Lennox modification (Steinberg)
concept of prognosis based on location (Ohzono)

ARCO
ARCO

CLINICAL FEATURES

Asymptomatic - Discovered on radiography

Onset insidious and chronic

Pain is throbbing, deep & intermittent at groin

radiating to thigh or buttock exacerbated by
weight bearing and coughing

Initially mild but progressively worsens over time

and with use - present at rest and may present
or worsen at night

Antalgic gait

SIGNS

Initial findings are unrevealing.

Latter stages - Joint function deteriorates

Limp
Loss of range of motion( active and passive)
- Flexion, abduction, & internal rotation,
- Femoral head collapse
Tenderness around the affected area.

Neurological deficit.

SIGNS
Trendelenburg sign - Positive.
Click - patient rises from a chair or after external
rotation of the abducted hip.
Advanced disease - Joint deformity & muscle wasting

X-RAY

Evident only after 2-3 months

Sclerosis & cyst

Subchondral Fractures

Crescent sign

Collapse

Joint space narrowing & osteophytes

Acetabular changes

SCLEROSIS

CRESCENT SIGN

CRESCENT SIGN

SUBCONDRAL SCLEROSIS

SNOW CAP LESION

CT SCAN

Extent of involvement,

- Subchondral lucency & sclerosis Reparative stage

(before the collapse of the femoral head)

Detecting femoral head collapse

Early degenerative joint disease

Presence of loose bodies -Multiplanar reconstruction

MRI

Sensitive method for earliest diagnosis

Sensitivity 97% specificity 98%

Low intensity signal in T1 weighted image

High intensity signal in STIR image

Double line appearance on T2 weighted - Reactive

interface between ischemic & non-ischemic bone.

Accurate staging
- clearly depicting the size of the lesion
- multiplanar imaging
- excellent soft tissue resolution

Prognosis - Osteonecrotic femoral head - Operative

DOUBLE LINE SIGN

DOUBLE LINE SIGN

INCREASED SIGNAL INTENSITY

SPECT

Alternative - MRI cannot be performed

- MRI results are indeterminate.

Difficult to use - Requires remaining still for long

periods of time.

Bladder artifacts - Frequent problem

BONE SCAN

Early diagnosis next to MRI

99mTc-sulfur colloid

Early stages - Cold spot

Late stages - Hot spot

Scintigraphic imaging
Central area of decreased uptake,
surrounded by area of increased uptake
-Doughnut sign or cold in hot sign

OTHER IMAGING STUDIES

Radionuclide scintigraphy Sr 87m and Tc 99m

MDP scan
Tc isotope pickup
Radioisotope clearance of Na 24
Radio phosphorous pickup
Arteriography

BIOPSY

Usually done with core decompression

Empty lacunae in trabecular bone
Common finding is old & new hemorrhage in bone
marrow

FUNCTIONAL INVESTIGATION
(intra osseous pressure measurement)
Normal baseline IO pressure
10 - 20 mm Hg

AVNFH
> 30 mm Hg

Stress test - transient mild

Pressure elevation

> 10mm Hg for > 5mts

io venogram - Contrast
cleared within 5 Mts

venous stasis

TREATEMENT

Goal keep joints from breaking down - severe pain

and limitation in movement.

Arrest progression & prevent late collapse & AVN

Before collapse no treatment - Arresting progression

Age of the patient, stage of the disease, location &

amount of bone affected and underlying cause

SURGICAL

NONSURGICAL

NON SURGICAL

Bed rest

Statin therapy, Bisphosphonates or NSAIDS

Continuous traction

Non weight bearing - No effect on final outcome

OPERATIVE
SALVAGE PROCEDURE
Core decompression
Core decompression & Bone grafting
Transtrochanteric rotational Osteotomy

Intertrochanteric osteotomy
Hip arthrodesis
Trap door procedure

Resurfacing arthroplasty
RECONSTRUCTION
Total hip replacement

BONE GRAFTING
TYPES
Cancellous iliac graft
Phemister Free fibular graft
Muscle pedicle graft - Tensor fascia lata
- Quadratus femoris graft(meyers)
- Sartorius
Vascular pedicle graft Iliac crest

OSTEOTOMY

Flexion

Varus

Sugiokas ventral rotation

CORE DECOMPRESSION

Stage 1, 2A lesions

Small central lesion in young non-obese

Relieve pain in 75%

Not useful Post-traumatic cases

Decompression of rigid interosseous chamber

Improvement of vascularity

Prevention of additional ischemic episode

CORE DECOMPRESSION

Hungerford

Supine - Fracture table or lateral decubitus

2 3 cm longitudinal incision centered over

subtrochanteric region.

3.2mm threaded guide pin - lateral cortex of inferior

portion of greater trochanter & distal portion of lesser
trochanter.

Direct tip of guide pin - Center of diseased bone

Overream the guide pin 8 mm reamer.

Histology - Core reamer

AFTER TREATMENT

Partial weight bearing (50%) on crutches is

continued for at least 6 weeks

Patients with advanced disease, protected

weight bearing is prolonged

ELECTRICAL STIMULATION

Core decompression + CBG + Electrical

stimulation- More beneficial

Core decompression + non-vascularised fibular

graft for stage 1 & 2

OTHER GRAFTING METHODS

Gangji - Injection of autologous bone marrow
aspirate at cored femoral head
Lieberman & Urist Human BMP

Useful in 2A stage
93% success

NON VASCULARISED GRAFT

PHEMISTER

For stages 1 & 2

Not proved of much value

Combined with core decompression

VASCULARISED FIBULAR
GRAFT

Decompression of femoral head

Excision of sequestrum

Filling of defect with osteoinductive graft

Protection of graft by a period of limited weight

bearing

MUSCLE PEDICLE BONE GRAFT

MEYERS

Uses quadratus femoris

Posterior approach

For stages 1 & 2

BAKSI

Uses Tensor fascia lata

Usually anterior approach

For stages 1 & 2

OSTEOTOMIES

Transtrochanteric Rotational Osteotomy

SUGIOKA 1978

Age < 55 yrs

< 30% head involvement

In idiopathic and post traumatic

For stage 1 & 2

Reposition of necrotic anterosuperior part to non wt.

bearing locale

Prevents progressive collapse

Improve the congruity

ROTATIONAL OSTEOTOMY

Developed by sugioka

Allows greater movement of diseased portion of

femoral head

Capsule is incised circumferentially to allow

adequate rotation

Supplemented by mild varus with Retroversion of

neck

ROTATIONAL OSTEOTOMY

Capsule incised circumferentially

Near the acetabular rim

Trans trochanteric osteotomy-10mm distal to inter

trochanteric crest at 90* to the long axis of neck

Near the base of inter trochanteric osteotomy line

be 90* cephalad

ROTATIONAL OSTEOTOMY

ROTATIONAL OSTEOTOMY
GRADE

SUCCES RATE

88%

83%

74%

70%

OTHER OSTEOTOMIES

Intertrochanteric
Flexion
Extension

Varus or
Valgus

Stage 2 and 3 AVN with < 30% head

involvement

Scher and jakim - valgus extension IT osteotomy

TRAP DOOR PROCEDURE

Introduced in 1998

Necrotic area is exactly located

Cartilage overlying is opened like a door

Necrotic bone curetted out and filled with

cancellous bone, door is closed.

Good results in stage 3

STAGE 3 & 4 CASES

TOTAL HIP REPLACEMENT ARTHROPLASTY

ARTHROPLASTY - TYPES

Resurfacing hemiarthroplasty

Total resurfacing arthroplasty (Birmingham)

Unipolar and bipolar hemiarthroplasty

THR

RESURFACING ARTHROPLASTY

Excellent interim procedure that allows revision to

THR in young patients.

High failure rate

Total articular resurfacing arthroplasty [TARA]

Part of AVN head is removed, metal component
is attached through neck and trochanter and is
uncemented

Acetebular component is poly ethylene & fixed with

cement

RESURFACING
ARTHROPLASTY

Advantage:
Preservation of normal anatomy for later THR
with little FB implanted

Disadvantage:
Acetabular bone stock compromised by
osteolysis
Not useful in B/L AVN

THR

Usually done more than 50 yrs

Many AVN are in 25-45 yrs

Uncemented THR in these group is not satisfactory

Recurrent dislocation , infection and osteolysis are

common complications.

Use of cementless THR under evaluation.

Why separate treatment?

Features
Age
Revascularisa
tion and
repair
Problem
Biological
plasticity and
remodelling
Aim of
treatment

Perthes
4-8 yrs
Possible
Growth
arrest,
deformity
and loss of
containment
Present
Head
containment

AVN
Adult
Impossible
Joint
destruction

Absent
Head
preservation

THE JOURNAL OF BONE AND JOINT SURGERY

OSTEONECROSIS OF THE FEMORAL HEAD:

CURRENT CONCEPTS AND CONTROVERSIES
- Brian D. Mulliken, M.D.
Further research is needed to assess the
natural history of early AVN and evaluate the
role of surgery in preventing progression

Osteonecrosis of the Femoral

Head
Carlos J. Lavernia, Rafael J. Sierra, , and
Francisco R. Grieco,
J Am Acad Orthop Surg 1999;7:250-261

Carry home message

MC Cause - Idiopathic

Steroids - peak doses more significant

# NOF - displaced # and malreduced #

Once necrosis - Irreversible

MRI - Earliest to diagnose

No role of conservative treatment to preserve

head

Early diagnosis & joint preserving measures Better

BIBILOGRAPHY

Campbell operative Orthopaedics

Turek Orthopaedics

Apleys Orthopaedics

THANK YOU