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 Avascular Necrosis (AVN) of the femoral head
is a pathological process that results from
interruption of the blood supply to the bone.
 Also known as Osteonecrosis/
Osteochondritis Dissecans/ Chandler’s
Disease
1.Extra Capsular Arterial Ring
-Formed posteriorly by MFCA.
-Formed anteriorly by LFCA.
2. Artery of Ligamentum Teres
3.Epiphyseal blood supply
4.Metaphyseal blood supply
Traumatic
Fracture neck
of Femur
femoral head
dislocation
Nontraumatic
Steroid use
Excess Alcohol intake
Sickle cell disease
Intravascular coagulation
Other blood cell disorders
Deep sea divers and
miners
 extraosseous arterial factors are the most
important. The femoral head is at increased
risk because the blood supply is an end-
organ system with poor collateral
development.
 Blood supply can be interrupted by trauma,
vasculitis (Raynaud disease), or vasospasm
(decompression sickness).
 Intraosseous arterial factors may block the
microcirculation of the femoral head through
circulating microemboli.
 These can occur in sickle cell disease (SCD),
fat embolization or air embolization from
dysbaric phenomena .
 Intraosseous venous factors affect the
femoral head by reducing venous blood flow
and causing stasis.
 These factors may accompany conditions
such as Caisson disease, SCD or enlargement
of intramedullary fat cells.
 Intraosseous extravascular factors affect the hip by the
increasing the pressure, resulting in a femoral head
compartment syndrome (2).
 For example:
 – Fat cells hypertrophy after steroid administration or abnormal
cells, such as Gaucher and inflammatory cells, can encroach on
intraosseous capillaries, reducing intramedullary circulation and
contributing to compartment syndrome.
 – Repeated microfractures in the weightbearing segment of the
femur may cause multiple vascular lesions resulting in ischemia
within fragile and poorly repaired bone.
 – Cytotoxic factors, such as alcoholism and steroid use, have a
direct toxic metabolic effect on osteogenic cells .
 – Decreased concentrations of 1,25 dihydroxyvitamin D3 can
cause a quantitative or qualitative deficiency in the bone
architecture, causing the bone to deform under pressure
 Extraosseus extravascular (capsular) factors
involve the tamponade of the lateral
epiphyseal vessels located within the synovial
membrane, through increased intracapsular
pressure.
 This occurs after as trauma, infection, and
arthritis, causing effusion that may affect the
blood supply to the epiphysis .
 Pain.
- Dull .
- Progressive.
- Worse at night
-Limp while
walking.
- Restricted hip
motion.
-Unable to sit
cross legged.
12
Pain:groin,buttocks,
Front of thigh
Stiffness Limp
14
 Imaging
 Routine radiographs
 Scintigraphy
 MRI.
 LASER Doppler flometry.
AVN femoral head
X-Rays
16
 Crescent changes
 Flattening of head
of femur
17
 Xray changes are “stage dependent”
 Early stages : normal film.
 Subsequently there occurs increased “
DENSITY “ of the femoral head.
 Crescent sign.
 Femoral head collapse.
 Osteoarthritis of the hip.
B/l involvement of femoral head with cystic
changes/sclerosis seen
18
 Radiolucent clefts
seen traversing
bone
19
Collapse of articular surface
20
22
 Radionuclide scintigraphy is more sensitive
for osteonecrosis than standard radiographs
and will reveal changes when standardd
radiographs are normal
23
24
 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
TREATMENT
Once AVN started : treatment
depends on
Stage of Disease and
symptoms/Age/general health of
patient
AVN is irreversible: no drugs can
restore blood supply to femoral
head
MEDICAL MANAGEMENT
Keeping weight of affected hip
Crutch walking
Anti inflammatory medications initially
• Simple analgesics for pain
Bisphosphnates :Reduces risk of femoral head
collapse
Blood thinning drugs
with a hope of maintaining precarious blood supply
SURGERY
AVN femoral head
• No Collapse  operations to increase blood
supply
• Core Decompression with or with out bone
graft
AVN Femoral Head : Advanced
stage
• Arthritic Hip
• Total Hip Replacement
DECOMPRESSION OF FEMORALHEAD
Drilling one or several holes through the
neck of femur into areas of head where there
is lack of blood supply
Principle:
1. It decreases the pressure inside the
femoral head
2. It helps to stimulate budding of new blood
vessels in affected areas
Reliving pressure helps in reduction of pain.
It does not cure the disease but can help to delay the
progression ofAVN
DECOMPRESSION OF FEMORAL
HEAD+ BONE GRAFTING
Decompression of femoral head
Inserting freeze dried allograft into the
decompressed canal
Pain relief due to decompression
• Graft acts as structural support preventing further
collapse.
DECOMPRESSION OF FEMORAL HEAD+
VASCULARISED FIBULAR GRAFT
Decompression of femoral head is done by making a
hole into femoral head.
A fibular graft along with its blood vessels is removed
from the leg and inserts into the hole created in femoral
neck and head. Surgeon then connects the blood vessels
of the fibula to the blood vessels around the hip.
It can help to restore the blood supply .
Fibular graft act as strut and help in preventing collapse
of femoral head
TOTAL HIPREPLACEMENT
Advanced Stage of AVN: Femoral head collapse
Secondary osteoarthritis of Hip joint
Total Hip Replacement
TOTAL HIPREPLACEMENT
Different designs & materials in Hip replacement
• Consists 2 basic components Ball & Socket
components
Ball component
• Highly polished Metal
• Ceramic material
Socket component
. Plastic (High molecular weight polyethylene)
. Ceramic
. Metal
CHOICE OF MATERIAL
Total hip replacement could be CEMENTED and CEMENTLESS.
Decision is based on number of factors like age, quality & strength
of bone and cost factor in some instances.
Surgeon can decide and choose that meets patients needs.
POSTOPERATIVE MANAGEMENT
After decompression it weakens
the femoral neck & head
Protected weight bearing with aid
of crutches and walker for 6
weeks
Weight bearing after 6 weeks and
return to regular activities.
Avascular necrosis of femur

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Avascular necrosis of femur

  • 1.
  • 2.  Avascular Necrosis (AVN) of the femoral head is a pathological process that results from interruption of the blood supply to the bone.  Also known as Osteonecrosis/ Osteochondritis Dissecans/ Chandler’s Disease
  • 3. 1.Extra Capsular Arterial Ring -Formed posteriorly by MFCA. -Formed anteriorly by LFCA. 2. Artery of Ligamentum Teres 3.Epiphyseal blood supply 4.Metaphyseal blood supply
  • 4. Traumatic Fracture neck of Femur femoral head dislocation Nontraumatic Steroid use Excess Alcohol intake Sickle cell disease Intravascular coagulation Other blood cell disorders Deep sea divers and miners
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  • 6.  extraosseous arterial factors are the most important. The femoral head is at increased risk because the blood supply is an end- organ system with poor collateral development.  Blood supply can be interrupted by trauma, vasculitis (Raynaud disease), or vasospasm (decompression sickness).
  • 7.  Intraosseous arterial factors may block the microcirculation of the femoral head through circulating microemboli.  These can occur in sickle cell disease (SCD), fat embolization or air embolization from dysbaric phenomena .
  • 8.  Intraosseous venous factors affect the femoral head by reducing venous blood flow and causing stasis.  These factors may accompany conditions such as Caisson disease, SCD or enlargement of intramedullary fat cells.
  • 9.  Intraosseous extravascular factors affect the hip by the increasing the pressure, resulting in a femoral head compartment syndrome (2).  For example:  – Fat cells hypertrophy after steroid administration or abnormal cells, such as Gaucher and inflammatory cells, can encroach on intraosseous capillaries, reducing intramedullary circulation and contributing to compartment syndrome.  – Repeated microfractures in the weightbearing segment of the femur may cause multiple vascular lesions resulting in ischemia within fragile and poorly repaired bone.  – Cytotoxic factors, such as alcoholism and steroid use, have a direct toxic metabolic effect on osteogenic cells .  – Decreased concentrations of 1,25 dihydroxyvitamin D3 can cause a quantitative or qualitative deficiency in the bone architecture, causing the bone to deform under pressure
  • 10.  Extraosseus extravascular (capsular) factors involve the tamponade of the lateral epiphyseal vessels located within the synovial membrane, through increased intracapsular pressure.  This occurs after as trauma, infection, and arthritis, causing effusion that may affect the blood supply to the epiphysis .
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  • 12.  Pain. - Dull . - Progressive. - Worse at night -Limp while walking. - Restricted hip motion. -Unable to sit cross legged. 12
  • 14. 14  Imaging  Routine radiographs  Scintigraphy  MRI.  LASER Doppler flometry.
  • 16. 16  Crescent changes  Flattening of head of femur
  • 17. 17  Xray changes are “stage dependent”  Early stages : normal film.  Subsequently there occurs increased “ DENSITY “ of the femoral head.  Crescent sign.  Femoral head collapse.  Osteoarthritis of the hip. B/l involvement of femoral head with cystic changes/sclerosis seen
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  • 22. 22  Radionuclide scintigraphy is more sensitive for osteonecrosis than standard radiographs and will reveal changes when standardd radiographs are normal
  • 23. 23
  • 24. 24  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
  • 25. TREATMENT Once AVN started : treatment depends on Stage of Disease and symptoms/Age/general health of patient AVN is irreversible: no drugs can restore blood supply to femoral head
  • 26. MEDICAL MANAGEMENT Keeping weight of affected hip Crutch walking Anti inflammatory medications initially • Simple analgesics for pain Bisphosphnates :Reduces risk of femoral head collapse Blood thinning drugs with a hope of maintaining precarious blood supply
  • 27. SURGERY AVN femoral head • No Collapse  operations to increase blood supply • Core Decompression with or with out bone graft AVN Femoral Head : Advanced stage • Arthritic Hip • Total Hip Replacement
  • 28. DECOMPRESSION OF FEMORALHEAD Drilling one or several holes through the neck of femur into areas of head where there is lack of blood supply Principle: 1. It decreases the pressure inside the femoral head 2. It helps to stimulate budding of new blood vessels in affected areas Reliving pressure helps in reduction of pain. It does not cure the disease but can help to delay the progression ofAVN
  • 29. DECOMPRESSION OF FEMORAL HEAD+ BONE GRAFTING Decompression of femoral head Inserting freeze dried allograft into the decompressed canal Pain relief due to decompression • Graft acts as structural support preventing further collapse.
  • 30. DECOMPRESSION OF FEMORAL HEAD+ VASCULARISED FIBULAR GRAFT Decompression of femoral head is done by making a hole into femoral head. A fibular graft along with its blood vessels is removed from the leg and inserts into the hole created in femoral neck and head. Surgeon then connects the blood vessels of the fibula to the blood vessels around the hip. It can help to restore the blood supply . Fibular graft act as strut and help in preventing collapse of femoral head
  • 31. TOTAL HIPREPLACEMENT Advanced Stage of AVN: Femoral head collapse Secondary osteoarthritis of Hip joint Total Hip Replacement
  • 32. TOTAL HIPREPLACEMENT Different designs & materials in Hip replacement • Consists 2 basic components Ball & Socket components Ball component • Highly polished Metal • Ceramic material Socket component . Plastic (High molecular weight polyethylene) . Ceramic . Metal
  • 33. CHOICE OF MATERIAL Total hip replacement could be CEMENTED and CEMENTLESS. Decision is based on number of factors like age, quality & strength of bone and cost factor in some instances. Surgeon can decide and choose that meets patients needs.
  • 34. POSTOPERATIVE MANAGEMENT After decompression it weakens the femoral neck & head Protected weight bearing with aid of crutches and walker for 6 weeks Weight bearing after 6 weeks and return to regular activities.