Osteonecrosis of

Femoral Head

Scope

Definition
Etiology
Pathogenesis
Diagnosis
Treatment

Definition

Disease of impaired osseous blood flow

in which a circumscribed area of bone
becomes necrosis

Metatarsal head
navicular

Freibergs Disease
Kohler's Disease

lunate

Kienbock Disease

calcaneum
Tibial tuberosity

Severs Disease
Osgood-Schlatter's
disease

Etiology ("PLASTIC RAGS"):

Pancreatitis, Perthes
Lupus
Alcohol
Steroids
Trauma, Transplant
Idiopathic, Infection
C aisson disease,
Collagen vascular disease

Radiation,
Rheumatoid arthritis
Amyloid
Gaucher disease
Sickle cell disease

Etiology

Traumatic
Non-traumatic

Sickle cell disease

Caisson disease
Thrombocytopenia
Fat embolism

Gauchers disease
Tuberculosis
Cortisone/alcohol
Dysbaric ischemia(caisson)

Pathogenesis
Up to 4 month, the femoral head is supplied by
(1) metaphyseal vessel penetrate growth disc (2)
lateral epiphyseal vessel- run in retinaculum
(3)
vessel in ligamentum teres
The metephyseal supply gradually declines until, by the
age of 4 yrs, it has disappeared
By age of 7, vessel in ligamentum teres have developed.
Between 4-7 yrs, femoral head blood supply entirely on
LEV.

Effusion cause stretching & pressure to

LEV.
No enough pressure to block arterial flow
but cause venous stasis resulting raise in
intraosseous pressure and subsequent
ischemia. (Lin & Ho 1991)

(1)metaphyseal vessel penetrate growth disc

(2) lateral epiphyseal vessel- run in retinaculum
(3) vessel in ligamentum teres

#NOF
Dislocation

Incidence of osteonecrosis is 11% in undisplace #

15-50% in displaced #
Prevalence after dislocation: 10-15%
If reduction is delayed by more than few hours the
figure rise to 40%

Corticosteriods

20mg/day is associated with increased risk

Relative risk goes up 4-6 fold for every 10 mg/day
increase

Alcohol

>400ml/week increase the relative risk 8-9 fold

Sickle cell
disease

: the prevalence of osteonecrosis is

4-2%.
Age- dependent :33-50% of patients by age 35

SLE

incidence :15-44%:high dose (>30mg/d) AVN 44%

develops very early after starting high dose
corticosteroid treatment. Annals of Rheumatic
Diseases.2001;60(12):1145-8.

Etiology

Steroid usage
- 6-8 years (range 1-19)
- Kidney transplant AVN 4.5%
- 80% Bilateral

Steroid usage

Pathophysiology:
1)Direct cellular toxicity
2)Abnormal fat metabolism
-Adipocyte hypertrophy
-Fat embolism

Etiology

Marston SB, et al

Solid organ transplant (kidney+liver)

52 pt.
AVN femoral head 11% (20%)
AVN in 10 months
MRI screening in the first year

Etiology

Ferrari P, et al.

Homozygous 4G/4G PAI-1 genotype.

Ries MD.

HIV infection (risk factor of AVN)

Association between human immunodeficiency virus and

osteonecrosis of the femoral head. J Arthroplasty 2002 Feb:
17(2):135-9

Pathogenesis

Infarction theory
Fat embolism theory
Accumulative cell stress theory
Progressive ischemia theory
Immunologic reaction

Pathophysiology of sickle
cell disease
6 Glu

Val

Deoxy Hb S polymer forms with low

O2, depends on Hgb S concentration,
low pH, high temperature, high 2,3DPG
Under a variety of circumstances,
different organs are susceptible:
spleen, renal medulla (papillary
necrosis), & many other complications

Gaucher's disease

hereditary deficiency of the enzyme

glucocerebrosidase (also k/s acid glucosidase).
glucocerebroside accumulates in the spleen,
liver, kidneys, lungs, brain and bone
marrow.

HAEMODYNAMIC PRINCIPLE IN AVN

(1) arterial insufficiency

e.g. FON#, dislocation,

sufe

(2) venous occlusion

(3) intravascular capillary occlusion

e.g.venous drainage of the

femoral head is also reduced in Perthes disease .(Green & Griffin)
e.g. sickle
cell disease clumping of abnormal red cell lead to decreased
capillary perfusion. (Rickles & OLeary1974)
e.g. caission
disease : rapid atm decompression cause release of N 2
bubbles.
e.g. alcohol & steriod cause intraosseous fat
embolism due to hyperlipidaemia.

(4) intraosseous capillary tamponade

e.g. bone infection
e.g. Gauchers disease
-autosomal recessive trait
-lack of enzyme -glycosidase
-osteonecrosis is due to compression of the
marrow capillaries & sinusoids by mass of large macrophages
stuffed with glycocerebroside. (Jaffe, 1972)
e.g. alcohol & steriod: marrow fat cell is
significantly increased.
(Solomon)
e.g. Cushing syndrome &
familial hyperlipidaemia
e.g. cassion
disease: fat cell swelling contribute to the ischemic changes.
(Pooley & Walder)

Diagnosis

History
Physical examination
Laboratory test
CBC, ESR R/O infection
Cortisol level
No specific biochemical marker for high alcohol intake
( Whitehead, Clarke and Whitefield)

Elevation of four of the following is highly suggestive

transaminase
-glutamyl transpeptidase
serum urate
serum triglyceride

Radiological examination

aspartate

History

A high index of suspicious is essential

An associated risk factor
The most common presenting symptom is a
deep pain in the groin
Exacerbated by activity

Physical examination

Pain on internal rotation

Decrease ROM
Hip abductor weakness (G. medius)
Shortening of limb

Plain film X-ray

AP pelvis, frog leg

Crescent sign
Secondary OA
change

Conventional radiograph of the right femur in the frog-leg

position obtained with the patients thigh abducted and flexed
shows subchondral area of hyperlucency (arrows) in the
anterolateral aspect of the proximal femoral head.

Specimen radiograph of a coronally sectioned femoral head segment

reveals a subchondral fracture (arrows), which manifests as the
crescent sign.
Note the fragmentation and compaction
of the subchondral cancellous trabeculae, which weakens the
articulating surface.

Anteroposterior radiograph of the left humeral head

in a patient being treated with high-dose
corticosteroids shows multiple subchondral areas of
hyperlucency (arrowheads) that are indicative of
stage III AVN.

Technetium bone scan (Tc

99)
Preradiographic phase AVN
Decrease uptake
Sensitivity and specificity <
MRI
SPECT
(Single-photon emission
computed tomography)
sensitivity 100% in renal
transplant pt.

BONE SPECT

32 AVN of femoral head

SPECT detect 32/32 -> 100% sensitivity

MRI
detect 21/32 -> 66% sensitivity

(The Journal of Nuclear Medicine. 2002;43(8):1006-1011)

MRI

Investigation of choice
Decrease signal
Screening T1 coronal scan

CT scan
Arthroscopic examination

Ficats staging
Clinical

Plain film

MRI

Stage O

No pain

normal

abnormal

Stage I

pain

normal

Stage II

crescentsign

Stage III

Collapsed
femoral
head

Stage IV

Narrow joint
space+aceta
bulum

normal

sclerotic

Crescent sign

Collapse

Acetabular
involvement

Severe joint
destruction

Treatment

Conservative

Temporally non-weight
bearing
Electrical stimuli

Surgery
Joint preserving procedure
prosthetic replacement

Treatment

Conservative treatment

stage I-II
NWB with crutches (6 wks)
analgesic+exercise
F/U 2 years 80% poor result

Musso, et al. Result of conservative management of osteonecrosis

of the femoral head. A retrospective review. Clin Orthop 1986 June; 207:
209-215

Treatment Options
AVN, Hip

Non-weight bearing
Core decompression
Core decompression + vascularized fibular
graft
Core decomp + non-vascularized fibular graft
Core decomp+ autologous bone marrow cells
Osteotomy
Resurfacing arthroplasty
Bipolar arthroplasty
Total hip arthroplasty

Result of nonoperative Rx

55 AVN / nonoperative Rx

92% radiographic progression

84% arthroplasty, Av. Time 21 months
(Steinberg. Clin Orthop;1989)

15 AVN / nonoperative Rx

100% collapse, Av. Time 23 months

(Bradway and Morrey. J Arthroplasty;1993)

Joint preserving procedure

Core decompression
Osteotomy
Free vascularized fibular/ iliac
graft
Arthrodesis
Arthroscopic debridement
(+core)

Treatment

Core Decompression

Decrease BMP (bone marrow pressure)

Increase venous drainage
Promote vascular ingrowth
Bone graft, autologous bone marrow
Treatment of choice stage I-II

Core Decompression

Result of core
decompression

133 AVN, stage I+II, F/U 9.5 years

90% successful clinical result
79% no radiographic progression
(Ficat. JBJS;67B:3-9:1985)

204 AVN, F/U 3 years

no additional operative Rx was necessary
96% stage I
77% stage II
60% stage III
(Zizic and Hungerford. Textbook of Rheumatology

Ed 2, Vol.2:1689-1710)

Electrical stimulation

Goal: Enhance bone formation and fracture

healing

Alone or as an adjunct to other surgical

procedure
PEMF (pulsing electromagnetic fields)
-more effective than symptomatic Rx in
precollapse and minimally collapse
-as effective as core decompression in
precollapse
-more effective as core decompression in
minimally collapse

Osteotomy

Shift the necrotic segment out of

the region of major weight bearing
and replace it with normal bone
and cartilage
Early to intermediate stage that
acetabular cartilage is unaffected

Femoral Osteotomy

Candidate
< 40 years old
Small lesion (< 200 degrees)
Mobile hip
No longer taking steroid
Difficulty for THR
Removal of implants after
union

Result of Ostetomy

Sugioka Y (CORR.
1984)
1984

158 hip (success rate

86-95 %
(1992 , 295 pts,
79%, avn F/U 11 yrs)

Treatment

Vascularized bone graft

- fibular, iliac crest
- revascularized

Vascularized bone graft

Goal:

Decompress the femoral head

Remove necrotic bone
Fill necrotic defect with osteoinductive
cancellous bone graft
Support subchondral bone with strut
graft

Enhance revascularized process

Vascularized bone graft

Disadvantage:
Technical demand
A few centers have significant
experience with this technique
Well-trained microvascular surgeon
More complication

Vascularized bone graft

Advantage: The result is better than

core
decompression in stage II,
III
(Ficat classification)

Result of Vascularized bone

graft

Urbaniak JR (JBJS. 77-A.1995)

mean survival rate= 88%

Patients. stage I , II
Judet H (CORR.2001) FU 18 Year
Found that 80% of patients 60.
stage I,II It works well.

Prosthetic replacement
surgery

Limited resurfacing
arthroplasty
Resurfacing arthroplasty
Hemiarthroplasty
Total hip replacement

Limited Resurfacing
Arthroplasty

Hemisurface arthroplasty

Hemisurface or partial
resurfacing arthroplasty

Time-buying procedure for young and

active patient

Adequated bone quality and relative normal

articular cartilage
Bone stock preservation and intact
intramedllary canal
Survivorship 81% at 5.1 years
Survivorship 61% at 10 years

(Amstutz HC. Semin Arthroplasty ;9:261,1998)

Hemiarthroplas
ty

Treatment

Total hip arthroplasty

- femoral head + acetabulum
- stage IV
- survivorship in young patient is
less than in older patient

Total Hip Arthroplasty

Total Hip Arthroplasty

Ficat Stage I

Rx. 1. Conservative
2. Core deco

Ficat stage II

Rx. 1. Conservative
2. Core decom
3. Others

Ficat stage
III

Rx. 1. Conservative
2. Hemiarthro
3. Others

Ficat stage
IV

Rx. 1.
Conservative
2.
THR
3.
Arthrodesis

Thank You