Avascular Necrosis of Femoral Head

Dr Zameer Ali
 St Stephen’s hospital

1
 Definition
 Osteonecrosis of femoral head refers to the death
of osteocytes with subsequent structural changes
leading to femoral head collapse and secondary
osteoarthritis of hip joint

2
 Definition.

Osteonecrosis is
defined as an ―end
stage‖ condition of the
femoral head in which
there is necrosis of
the bone, secondary
to disruption of the
blood supply and
causes which are still
unknown.
3
 The death of cell components of bone & bone
marrow from repeated interruptions or a single
massive interruption of the blood supply to the
bone.

4
  AVN may involve all or part of head

5
6
The Problem.
 Commonly affects
young patients.
 Need to alter the life
style and leisure
activity.
 Accounts for 18 % of
all total hip
replacements.

7
  75% of cases are between 30 to 70 years of age
 Male: female ratio 4:1
 Bilateral involvement is seen in 50 % of cases

8
 History
1. Freund in 1926 gave detailed description of
Osteonecrosis
2. Chandler in 1948 termed disorder as "coronary
disease of hip‖ which accounts for eponym
Chandlers disease

9
 .
1) Chandler in 1948 referred this condition as
coronary artery disease of hip which even after
50 years correctly describes this condition
2) Aseptic necrosis was initially used to
distinguish this condition from infections

10
  3)Glimser and Kenzora in 1979 analyzed the
radiographic changes which accompany AVN

 Ficat in 1985 states that this condition resulted

from blockage of the osseus microcirculation with
intramedullary stasis and increased pressure .

11
 Anatomy
 Head of femur forms
about 2/3rd of sphere
and articulates with
acetabulum of hip
joint
 Connecting two
trochanters anteriorly
forms intertrochanteric
line and connecting
two trochanters
posteriorly forms
intertrochanteric crest.
12
 • Socket

• Ball

• Femoral neck

• Smooth weight-
bearing surfaces

• Smooth cartilage

• Femur

13
 Vascular supply of femoral head
 profunda femoris artery
 Artery to ligamentum teres
 Medial circumflex femoral artery
 Lateral circumflex femoral artery
 Lateral epiphyseal group

14
 Blood supply of the Head.

 3 main sources.

Ascending
cervical branches

Metaphyseal
blood vessels

Artery of
ligamentum teres.

15
 Vascular supply of femoral head
 Crook described Extra capsular arterial ring
located at base of femoral neck
 Ascending cervical branches or retinacular
arteries run on surface of femoral neck
 Arteries of round ligament or ligament teres.

16
17
  The proximity of
retinacular arteries to
bone put them at risk
of injury in any
fracture of femoral
neck.
 The ascending
cervical arteries puts
them at risk for injury
in any fracture of
femoral neck
18
  4 groups of ascending cervical arteries
 1. Anterior
 2. Posterior
 3. Medial
 4. Lateral
 Of these lateral group provides most of blood
supply to femoral head and neck

19
  The adult pattern of femoral head vascularity
usually becomes established with closure of
growth plate at approximately 18 years of age

20
 In neonate
 Three groups of vessels are identified
1. superior retinacular group or lateral epiphyseal
group
2. inferior metaphyseal group
3. foveal or medial epiphyseal group
4. All 3 groups anastomose with each other

21
 Between 4 years to 7 years
 The importance of lateral epiphyseal is
established as metaphyseal and foveal vessels
decrease in extent

22
 After 8 years of age
 Open growth plate represents an effective barrier
preventing anastomoses between vessels of
head and neck.
 An increased contribution of foveal vessels

23
  During adolescence
increased number of
inferior metaphyseal
vessel is recognized
 As the growth plate
closes the adult
pattern appears with
anastomosis between
3 arterial systems

24
 Causes.

 Traumatic causes

 Non Traumatic causes

25
 Traumatic

 Fractures of femoral neck. 15% - 50%

 Dislocation of the hip. 10% - 25%

26
  Currently accepted
term is Osteonecrosis
which describes main
common feature of
this condition THE
BONE DEATH

27
 Non Traumatic
 Idiopathic.
 Chronic alcoholism.
 Steroid intake.
 Sickle cell disease.
 Gauchers disease.
 Caissons disease.
 Malignancies.
 Drug induced

28
 Risk factors
 Gauchers disease
 Radiation induced
 Liver disease abnormal coagulation factor
synthesis

29
 Risk factors
 Traumatic Osteonecrosis usually involves
dislocation of hip or fracture femoral neck .
 52% of hips unreduced for more than 12 hours
developed AVN
 22 % of hips developed AVN if reduced within 12
hours
 Femoral neck fractures associated with 15 – 50
% incidence of AVN

30
 Risk factors
 Alcoholism: Accounts for 10 – 40 % of incidence
of AVN. Risk of development of AVN is increased
with cumulative doses of alcohol
 Drug induced: the association between
corticosteroid therapy,cushings syndrome, and
Osteonecrosis is well established

31
 Risk factors
 Collagen diseases rheumatoid arthritis,SLE have
been associated with AVN
 Radiation causes obliterative endarteritis and
cellular death.
 Gout sodium urate crystals enhance clotting by
activating haegmen factor in intrinsic coagulation
system

32
 Pathogenesis.
 Other than traumatic causes, the mechanism of
necrosis is still ―obscure‖.
 Coaugulation defect.
 Genetic predisposition.
 Emboli formation.
 ― IDIOPATHIC ‖

33
 Pathogenesis
 The bony compartment function essentially as
closed compartment within which one element
can expand only at expense of others
 A unifying concept of pathogenesis of AVN
emphasizes the central role of vascular occlusion
and ischaemia leading to osteocyte necrosis

34
  Pathogenesis of steroid or alcohol induced AVN is
not well understood ,but it is suggested that
embolic fat and attendant thrombi occlude
microcirculation.
 Lipocyte hypertrophy and subchondral lipid
accumulation may cause extra vascular
intraosseus compression.

35
  It matters little whether the initiating factor was
capillary occlusion (as in sickle cell disease)
venous occlusion (as suggested for perthes
disease) or intramedullary tamponade in
Gauchers disease, the end result is diffuse
ischaemia involving all the elements

36
 Biological sequence of repair

37
 Biological sequence of repair
1. loss of cell viability (cell necrosis)
2. Invasion of marrow spaces of dead bone by
proliferating capillaries and cells
3. Differentiation of mesenchymal cells to
osteoblast synthesis of new bone.
4. Early remodelling of repaired cancellous bone

38
 Biological sequence of repair
1. Late internal remodeling
2. Resorption of subchondral bone and invasion of
articular cartilage

39
 Biological sequence of repair
 To conclude this reparative process is self limiting
and incompletely replaces dead bone with living
bone.
 In subchondral bone ,bone formation occurs at
slower rate than does resorption resulting in net
removal of bone,
 loss of structural integerity, subchondral fractures
and collapse

40
Clinical features.
 Pain.
- Dull boring .
- Progressive.
- Worse at night
-Limp while walking.
- Restricted hip
motion.
- Unable to sit cross
legged.

41
 symptoms
 Clinical manifestation of bone ischaemia and
infarction are minimal and non specific and
depend on etiology.

42
 symptoms
 Initially vague and non specific.
 Localized or referred pain in buttocks,thighor
knee
 Gradual increase in intensity of pain and
decreased motion especially rotation and
abduction
 Over several years results in limping gait

43
 symptoms
 Initial pain is commonly misinterpreted as
radiating pain from lumbar spine.

44
 Diagnosis
 Asymptomatic during the early stages.

 Become symptomatic when significant collapse of

the head has occurred.

45
 Management protocol
 Early diagnosis
 Radiological evaluation
 Rule out other causes
 MRI
 Quantification
 Treatment algorithm

46
 Diagnosis
 Imaging
 Routine radiographs
 Scintigraphy
 CT scan.
 MRI.
 LASER Doppler flometry.

47
 Early Diagnosis – suspicion ?

 High degree of suspicion in a patient C/o anterior

HIP pain, Especially with:-
H/o Cortisone – Skin, Eye, Liver, Asthma,
RA, Weight gain
H/o Alcohol abuse
Traumatic - # N/F, D/ of F, # Acetabulum
Hemoglobinopathy – Sickle / Myelo-infiltrating

48
 Other causes
 Pregnancy
 Renal Diseases
 Radiation
 Gout / Collagen disorder
 Gaucher’disease
 Dysbarism
 Idiopathic

49
 Imaging
 Routine radiographs are usually first step in trying
to make diagnosis.
 High quality films taken at least two views 90
degree apart are critical to initial evaluation

50
 Radiology- sequential
Changes
 Crescent Sign
 Osteoporosis
 Sclerosis
 Cystic changes
 Loss of spherical bearing dome
 Partial collapse of head
 Secondary Osteoarthritis

51
 Xrays.
B/l involvement of femoral head with cystic
 Xray changes/sclerosis
changes are ―stageseen dependent‖
 Early stages : normal film.
 Subsequently there occurs increased ―
DENSITY ― of the femoral head.
 Crescent sign.
 Femoral head collapse.
 Osteoarthritis of the hip.

52
 X RAY changes
 Sclerosis
/subchondral cysts

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 X RAY changes
 Crescent changes
 Flattening of head of
femur

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 Bilateral Cystic changes
With patchy sclerosis

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 Scintigraphy
 Radionuclide scintigraphy is more sensitive for
osteonecrosis than standard radiographs and will
reveal changes when standardd radiographs are
normal

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 scintigram
 The hall mark of vascularity is photopenic effect
on scintigram
 RESULTS
1. Decreased uptake by necrotic bone
2. Increased uptake by remodeling bone
3. Normal uptake by normal bone

57
Bone scan.
 Technetium 99 bone scan
reveals decreased uptake.
 It is effective only if done
in early stages.
 During late phase there
are very variable resuts.
 No relationship b/w scan
appearance and the
function of the hip.

58
 MRI
 MRI is most sensitive technique for early
diagnosis in Osteonecrosis
 Can diagnose AVN as early as 48 hours
 The classical finding of AVN is decrease in the
normally high intensity signal of marrow of
femoral head

59
 MRI.
 Can detect early stages.

 Allows to determine exact stage of disease.

 Tells exactly the extent of damage.

 Useful in determining the efficacy of treatment.

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MRI

 Geographical area of
decreased marrow
signal. Necrotic area

 Surrounded by zone
of ―low signal‖ band.
Ischaemic bone.

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 MRI Findings.

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63
 MRI - Findings
 Bone Marrow edema
 Double Line – Head in Head sign
 Crescent sign
 Collapse
 Joint effusion
 Involvement of actabulum
 Status of other hip
 Marrow infiltrating disease

64
 LASER Doppler Flometry
 Laser Doppler flometry is technique at measuring
blood cell influx in a capillary bed
 The magnitude and frequency of Doppler shift is
proportionate to the velocity and concentration of
red cells under probe head

65
 Sequence of radiological events in
AVN
 Fragmentation : radiolucent clefts may be seen
due to necrosis of involved bone
 The entire epiphysis may be absent

 Mottled trabecular : pattern: scrutiny of

trabecular traversing the ischaemic bone
demonstrates thickened irregular pattern

66
  Sclerosis : with revascularisation new bone is
deposited around dead bone resulting in
increased bone density

 Subchondral cysts : patchy well circumscribed

rarefactions immediately beneath the articular
cortex are frequent
67
  These cysts are usually seen in region of greatest
articular stress and are identical to those found in
degenerative joint disease

 Collapse of articular cortex this generally

occurs at the region of maximal stress of involved
cortex and represents a localised impaction
fracture of weakened bone
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 Fragmentation

 Radiolucent clefts
seen traversing bone

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 Sclerosis/subchondral cysts
 Sclerosis

 subchondral cysts

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 Collapse of articular surface

Collapse of articular surface

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72
 Staging
 Several staging systems have been described.
 The staging system reported by sternbergs and
colleagues is similar to that outlined by
Marcus,Ficat and Arlet
 Sternbergs classification allows physician to
quantify extent of involvement of femoral head in
both early and late stages

73
 Staging / Grading --- too many
 Ficat Radiological
 Steinberg Quantification
 Enneking's Stages of Osteonecrosis
 Marcus and Enneking System
 Japanese criteria Location
 Sugioka Radiological
 University Of Pennsylvania System
 Association Research Classification Osseous Committee
(ARCO)-- Combination

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 Ficats radiological staging of
osteonecrosis of femoral head
Fi Stages of Bone Necrosis

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 Ficat Stages of Bone Necrosis

Stage Clinical Features Radiographs

 0 Preclinical 0 0
 1 Preradiographic +
 2 mild density changes in femoral
head
 2a Precollapse mild Diffuse
Porosis, Sclerosis,or
cyst
 2bTransition: Flattening, Crescent Sign

 3 Collapse mild/moder Broken Contour of

Head Certain
Sequestrum, Joint Space
Normal
76
 Stage 1

 Symptoms – none / mild

 Xrays are normal.

 Bone scan reveals a ―cold spot‖.

77
Stage 2
 2A
 Symptoms are mild.
 Xray shows increased
density.
subchondral cysts
joint line maintained.
normal head contour.

Bone scan reveals

increased uptake.

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2B

 Crescent sign.

 Flattening of the head.

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 Crescent sign.

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Stage 3
 Moderate symptoms.

 Loss of shape

 Subchondral collapse

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Stage 4
 Severe symptoms.

 Joint space narrowing.

 OA changes in
acetabulum.

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 Marcus radiological staging of
AVN
 Stage I normal or equivocal radiograph
 Stage II sclerotic or cystic lesion
 Stage III crescent sign
 Stage IV step off in outline of bone
 Stage V narrowing of joint space with
degenerative changes

83
 Shimizu’s classification.
1995.
Grade 1 lesion.

 A lesion involving medial 1/3 rd of weight bearing

surface of the head.
 In coronal plane ,these lesions occupy < 1/3 of
the head.
 These lesions rarely go into collapse.

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 Grade 2.

 Lesions involve 1/3 – 2/3 of the weight bearing

surface of the head.

 Involve ½ of the head in coronal plane.

 Such lesions collapse in 30% of patients.

85
 Grade 3.

 Lesions involving 2/3 of the weight bearing

surface of the femoral head.

 Such lesions collapse in 70% of patients in

around 3 years.

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 Treatment
1. Conservative /non surgical treatment
2. Core decompression
3. Bone grafting
 Cancellous autogenic/allogenic bone graft
 Osteochondral graft
 Muscle pedicle bone graft
 Free vascularized graft

87
 Treatment
1. Electric stimulation
2. Osteotomy
3. Joint reconstruction
 Cup arthoplasty
 Surface arthoplasty
 Hemiarthoplasty
 Total joint arthoplasty

88
  The natural history of osteonecrosis in its early
stage, before subchondral collapse, is still
unclear, but evidence suggests that the rate of
progression is high, especially in symptomatic
patients.

89
  Once subchondral
collapse occurs and
joint space is
lost, progressive
osteoarthritis
generally is
considered inevitable.

90
  Many studies have reported an extremely poor
prognosis, with a rate of femoral head collapse of
more than 85% at 2 years in symptomatic
patients (stage I or II disease)

91
  No treatment method has proved to be
completely effective in arresting the disease
process before subchondral collapse or in
slowing the progression of femoral head
destruction and osteoarthritis after subchondral
collapse

92
 The rate and course of progression of the
disease are unpredictable, and the radiographic
picture may not correlate with the clinical
symptoms; some patients maintain tolerable
function for an extended period after femoral
head collapse.

93
  Conservative treatment, such as crutch
ambulation or bed rest, generally is ineffective.
However, symptomatic patients that may benefit
from a head-preserving technique should be
placed on crutches until surgical treatment is
carried out to prevent collapse in the interim

94
 Management.
 Grade 1 lesions
- Continuous supervision to detect any
changes.

- Symptomatic treatment of pain.

95
 Grade 1 lesions
 Conservative treatment such as observation ,
 Analgesics
 Limited weight bearing may be successful in
minimal affected cases

96
 Core decompression Grade 2
lesions
 Ficart and Hungerford have popularized the
technique of core decompression of femoral head
 Rationale is that removing necrotic bone
decompresses the rigid osseous chamber,
thereby improving blood flow and preventing
additional ischaemic events

97
  The theoretical advantage of core decompression
is based on the belief that the procedure relieves
intraosseous pressure caused by venous
congestion, thereby allowing improved vascularity
and possibly slowing the progression of the
disease

98
 several authors noted
that the results of core
decompression are
better than those of
nonoperative
treatment.

99
  Several reports noted that the earlier the stage of
the disease, the better the results with core
decompression.
 . For more advanced Ficat stages (IIB or III) the
results of core decompression are much less
predictable, so alternative treatment methods
should be explored.

100
  Review of the literature currently supports the use
of core decompression for the treatment of Ficat
stages I and IIA small central lesions in young,
nonobese patients who are not taking steroids.
This surgery is relatively simple to perform and
has a very low complication rate

101
  The surgical field for
subsequent total hip
arthroplasty, if
needed, is not
substantially altered

102
 Bone grafting
 Phemister introduced concept of using cortical
strut graft in core decompression channel
 The accurate placement of graft within lesion and
under subchondral bone is important

103
  Structural bone
grafting techniques
after core
decompression have
been described using
cortical
bone, cancellous
bone, vascularized
bone graft, and
debridement of
necrotic bone from the
femoral head.
104
  Insertion of cancellous
bone into channel
speeds up
reossification by
osteoinductive and
osteoconductive
properties of bone
graft.
 Meyers procedure
used muscle pedicle
bone graft based on
quardratus femoris
105
muscle with
  Baksi employed multiple drilling and muscle
pedicle grafting using tensor fascia lata muscle
anteriorly

106
  Advances in
microsurgical
techniques made it
possible to preserve
the intrinsic
vascularity of bone
graft, several authors
independently
proposed implanting a
vascularised bone
graft into the core of
the femoral head.
107
 Vascular fibular strut grafting

108
  The rationale for vascularized bone grafting is
based on four aspects of the operation and
postoperative care: (1) decompression of the
femoral head, which may interrupt the cycle of
ischemia and intraosseous hypertension that is
believed to contribute to the disease;
 (2) excision of the sequestrum, which might inhibit
revascularization of the femoral head

109
  (3) filling of the defect that is created with
osteoinductive cancellous graft and a viable
cortical strut to support the subchondral surface
and to enhance the revascularization process
 (4) protection of the healing construct by a period
of limited weight-bearing.

110
 Advantages
 Advantages of free vascularized fibular grafting
compared with total hip arthroplasty:
 (1) the presence of a healed femoral head may
allow more activity,
 (2) there is no increased risk associated with the
presence of a foreign body,

111
  (3) if performed before the development of a
subchondral fracture, the procedure offers the
possibility of survival of a viable femoral head for
the life of the patient, and
 (4) if total hip arthroplasty is ultimately needed, it
is much simpler to perform than is a revision
arthroplasty after a failed total hip arthroplasty.

112
 Disadvantages
 Disadvantages include a longer recovery period
and less uniform and less complete relief of pain
than after total hip arthroplasty.

113
 Strut Fibular Grafting

• Decompression of Femoral Head

• Removal of Necrotic Bone
• Grafting of defect with cancellous graft
• Viable cortical Bone strut to support subchondral bone.
• Age 20 – 50, stage 2

114
 Summaries of cases with head
preservation by free fibula grafting

115
Grade 2.
 If detected before the
collapse

Core decompression
and fibular grafting.

Realignment
osteotomies.

116
 Fibular strut grafting

117
118
 Pre OP

Post OP

119
 Electrical stimulation
 Electrical stimulation has been advocated for AVN
because its histological appearance is similar to
that of non union
 Currently used in combination with head salvage
procedures

120
 osteotomies
 Various proximal femoral osteotomies have been
developed for the treatment of osteonecrosis with
the intent to move the involved necrotic segment
of the femoral head from the principal weight-
bearing area.
 These procedures have achieved best results for
small- or medium-sized lesions (less than 30%
femoral head involvement) in young patients in
whom it is optimal to delay a total hip arthroplasty.

121
 osteotomies
 Various osteotomies have been described
 Varus osteotomy
 Valgus derotation osteotomy
 Rotation osteotomy aid the loss of structural
integrity and collapse by redirecting the forces on
femoral head

122
  Intertrochanteric osteotomy may be considered
for the treatment of stage II or III osteonecrosis of
the femoral head in which less than 30% of the
femoral head is involved.
 Plain films and MRI can establish the extent of
femoral head involvement and can determine if a
satisfactory area of live bone is present under
unaffected cartilage in the femoral head and
whether this area can be rotated into a position of
weight-bearing.

123
  Valgus flexion osteotomy is described by wagner
when lesion is anterolateral and total angle of
necrosis is 200 degree and patient is young and
active
 If necrotic lesion is central varus extension
osteotomy is recommended

124
 Transtrochanteric Rotational
Osteotomy
 In 1978 Sugioka described a transtrochanteric
rotational osteotomy of the femoral head for
idiopathic osteonecrosis

125
  The rationale of the procedure is to reposition the
necrotic anterosuperior part of the femoral head
to a non-weight-bearing locale.
 The femoral head and neck segment is rotated
anteriorly around its longitudinal axis so that the
weight-bearing force is transmitted to what was
previously the posterior articular surface of the
femoral head, which is not involved in the
ischemic process

126
  Sugioka emphasized
the need for a
preoperative lateral
roentgenogram of the
femoral head while the
patient is supine and
the hip is flexed exactly
90 degrees, abducted
45 degrees, and in
neutral rotation. The
intact area of the
posterior part of the
femoral head on this
lateral view should be
greater than one third of
the total articular
127
surface of the head to
ensure the best result
 Post op regimen
 Skin traction of 2 kg is applied continuously for
the first week and for an additional 2 weeks at
night only. As soon as pain tolerance allows,
quadriceps setting is begun. Active range-of-
motion exercises of the hip are begun at 10 to 14
days.

128
  Walking exercises in a pool generally are allowed
at 5 to 6 weeks.
 Partial weight-bearing with crutches is begun at 8
weeks, and the use of crutches is recommended
for 6 months after surgery.
 If the necrotic area of the femoral head is
extensive or if involvement is bilateral, crutch use
is encouraged for up to 1 year postoperatively.

129
 Replacement - options
 Hemiarthroplasty
 Bipolar arthroplasty
 Surface replacement arthroplasty.
 Newer material for THR ceramic on ceramic
 Non cemented / cemented THR

130
 Birmingham Surface
replacement
 Surface replacement
has some advantages
over THR because it
preserves femoral
head and neck and
allows future THR if
necessary
 Effective in cases
when femoral head is
not involved entirely

131
 The BHR* System

Healthy hip Cuts Implant components Implanted

Overview
 Named for Birmingham,
England, where the
device’s creators practice
medicine
 Used globally since 1997;
More than 65,000
implanted
 In an international study
of 1,626 hips, 99.5% of
patients were ―Pleased‖
or ―Extremely Pleased‖
with the results of
the BIRMINGHAM HIP
Resurfacing (BHR)
System.
  Many failures of resurfacing hemiarthroplasty
have been attributed to acetabular cartilage wear.
Attention should be given to the quality of the
acetabular cartilage on preoperative
roentgenographic studies.
 Intraoperative assessment of the acetabular
cartilage is mandatory before implanting a
resurfacing hemiarthroplasty prosthesis. If the
quality of the acetabular cartilage is in question, a
total hip arthroplasty should be performed.

134
  Resurfacing hemiarthroplasty is an attractive
alternative for young patients with advanced
osteonecrosis because very little bone is
sacrificed. Should failure occur, conversion to
total joint arthroplasty is nearly as simple as
primary total hip surgery.
 Clearly, the results of primary total hip
arthroplasty for osteonecrosis are better than
resurfacing hemiarthroplasty. However, this
procedure can delay total joint arthroplasty and
buy valuable time in a young patient.
135
Head size
 Closely matches the size
of natural femoral head
 Larger than the head of Total
BHR
Healthy
hip
head
head
head
a total hip replacement
 Larger head means a
reduced chance of
dislocation after surgery—
a leading cause of revision
surgery
 1-3% of total hips
dislocate over the
lifetime of the implant
 0.3% of BHR* implants
dislocated in the first
5 years after surgery
(in a study of 2,385
hips)
Who is the typical candidate
for BHR* System?
 Adults under age 60 for
whom total hip
replacement may not be
appropriate due to an
increased level of physical
activity
 Active adults over age
60 may be
candidates, depending on
their
bone quality
 Conventional hip replacement

Healthy hip Cuts Implant components Implanted

The key benefits
 Head size
 Advanced bearing surface
 Bone conservation
Bone conservation
 Preserves your
natural femoral neck
Bone
Hip
Bone with
cuts
cuts for
for
 Neck length and angle osteoarthritis
a
BHR
traditional
System
determine accurate hip replacement
leg length
 With the BHR* System,
you retain original
equipment; with a total
hip, your femoral neck
is replaced by the
implant
―Minimally Invasive.‖
 Soft Tissue
 No. Incision length
of 6 to 8 inches
 Bone Conserved bone
 Yes. Preserves your
body’s natural bone
structure; It resurfaces
rather than replaces
 Conventional vs. the BHR*
System

Total hip cuts BHR System cuts

Bone conservation (cont.)
 Revises to a primary
 If you need ―revision‖
surgery, you don’t get
a revision implant
 The follow-up procedure
would be the same total
hip replacement you
would otherwise have
received
 Total Hip Arthroplasty and Bipolar
Hemiarthroplasty.
 Most series that have
examined both
unipolar and bipolar
hemiarthroplasty for
the treatment of
osteonecrosis have
reported uniformly
poor results.

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 THR
 Patient aged 50 & more
 Advance osteoarthritis and reduction of joint
space.
 Radiation necrosis
 Result less than Ideal. – necrotic bone
 Poor in Sickle cell disease.
 Cementless are superior over cemented THR

145
  With new bearing surfaces becoming
available, such as ceramic on ceramic, metal on
metal, and highly cross-linked
polyethylene, results may improve even more.
The results of primary total joint replacement for
osteonecrosis are now approaching those
reported for osteoarthritis in aged-matched
patients.


146
 Malakar post alcohol AVN Bil THR 1991

147
 THR
 At the end stage of
osteonecrosis, when
severe arthritic
changes are noted on
both sides of the hip
joint, total hip
arthroplasty is one of
the only viable
operative options
available

148
  Given the young age
of most patients
affected with this
disease, if total joint
replacement is
elected, the patient
should be well
informed of the almost
certain need for one
or more revision hip
replacements later in
life.
149

 Girdle stone arthoplasty
 Used as salvage procedure in special
circumstances like painful hip with superimposed
sepsis, failed THR with sepsis
 Femur without good bone stock
 Conversion to THR can be taken at later stage

150
 Hip fusion
 Not frequently recommended because of high
failure rates

151
 ….Thank you…

152