This document discusses avascular necrosis (AVN), also called osteonecrosis. It defines AVN as bone death caused by sudden obstruction of blood supply to bone. Common causes include trauma, corticosteroid use, and decompression sickness. Sites often affected are the femoral head, scaphoid, and talus. The goal of treatment is to improve joint function, stop further bone damage, and preserve the bone and joint. Methods include nonsurgical options to delay progression and surgical interventions like core decompression or grafts, with joint replacement usually performed later.

1. Avascular Necrosis

2. Definition
AVN OF BONE/OSTEONECROSIS means “BONE DEATH”
Sudden Obstruction in arterial blood supply to a part of bone
O S T E O N E C R O S I S

3. Causes
Traumatic: Fracture -Femur Neck, Talus, Scaphoid.
Dislocations – hip
Non-Traumatic :
Caisson Disease
Sickle Cell Disease
Gaucher’s Disease
Coagulation Disorders
Cortisone Administration
Organ /Bone transplantation
Metal corrosion
Alcoholism
Exposure to xrays and radioactive substances

4. Common sites of predilection
-Femoral head
-Scaphoid(Preiser’s Disease)
-Talus
-Segmental fracture
-Others – capitellum , radial head , lateral femoral
condyle

5. Pathogenesis
BONE ISCHAEMIA is due to
- Interruption of arterial inflow
- Occlusion of Venous Outflow
- Intravascular Blockage of arterioles & capillaries
- Increase in marrow pressure

6. Repair process in a cancellous bone
• Proliferating capillaries and fibrous stroma
penetrate marrow space of dead bone
• Phagocytes remove the marrow debris
• Osteoblasts lay down immature woven bone
• All these process further increases the
radiodensity of necrotic bone

7. • Later osteoclastic resorption removes the woven
bone as well as the old trabaeculae
• This is replaced by well organised lamellar bone
• This process of apposition of new bone on some
surface and osteoclastic resorption on other
surface is called CREEPING SUBSTITUTION

8. Repair process in cortical bone
• Excavation of haversian canal by osteoclastic
resorption proceeds
• This enlarges the canal which multiple in
number and uniform in size
• Later osteoblasts lay down concentric rings of
new bone

9. Pathology
• Microscopically 4 stages are recognised
-Stage of marrow necrosis and cell death.
-Reactive vascularisation and infiltration.
-Distortion of shape by collapse and compression of trabeculae
-Subchondral collapse
Deformation of articular cartilage

10. Dysbaric osteonecrosis
 Caisson disease /Decompressionsickness/
Aeroembolism.
 Seen in deep sea divers , tunnel workers,
working in unpressurized aircrafts.
 Nitrogen gas bubbles liberated in a
concentration that cannot be readily
absorbed by blood stream or excreted by
lungs.
 As a result gas bubbles accumulate in tissues
causing local ischemia or intravascular
occlusion

11. Corticosteroid induced AVN
1. Fat embolism theory :
• Fat accumulates in liver in patients treated with steroid , and serum lipid
concentration also increases
• It gives rise to fat embolism and AVN
2. Subchondral osteoporotic fracture :
Steroids induce protein catabolism
Resulting in generalised osteoporosis
Produces subchondral fractures and aseptic necrosis

12. Clinical Features
Early stages: Pain-near joint
Later stages: Stiffness, Limitation of movements
Advanced stage: Fixed Deformities

13. Radiological features
• Initially necrotic bone appears radiodense
• Surrounding vascular bone shows relative osteoporosis
• In Early stages- Articular cartilage is not affected - so
joint space is normal
• In later stages -Partial collapse,flattening of head,joint
space narrowing,osteoarthotic changes

14. AVN of femoral head
• Occurs mainly due to femur neck fracture and
hip dislocation
• Due to disruption of vascular channel in
femoral neck

15. Vascular supply around femoral neck

16. Vascular disruption following #

17. Radiography of femur head - AVN

18. Treatment
Core Decompression.
Vasularised Fibular Graft.
Hemiarthroplasty .
Total hip arthroplasty.

19. Legg-calve perthe’s disease
AVN of ossification centre of capital epiphysis of femoral
head.
3-12 age group.
c/f: Limp, antalgic gait, limited motion
HIP DEFORMITY
xray: Early findings include Medial joint space widening
irregularity of femoral head ossification
cresent sign (represents a subchondral fracture)

20. Treatment:
Aim- preserve the femoral head, acetabular
congruity, eliminate or reduce weight bearing.
Nonoperative -observation, activity restriction, partial
weight bearing, traction, and physical therapy.
.Ambulation-Abduction Brace
Operative-
children > 8 years of age.
-Femoral Osteotomy
proximal femoral varus osteotomy
-Pelvic Osteotomy.

21. AVN of scaphoid

22. Vascular supply of scaphoid

23. Vascular disruption in # scaphoid

24. Radiography of scaphoid # AVN

25. AVN of talus

26. Vascular supply of talus

27. Radiography showing AVN

28. Other bones susceptible for AVN
Lateral femoral condyle Capitellum

29. The goal in treating avascular
necrosis
Is to improve the patient's use of the
affected joint,
Stop further damage to the bone
and
Ensure bone and joint survival.

30. • Various methods for delaying disease progression
• Non surgical –
• Bisphosphonate
• Anticoagulants
• Vasodilators
• Biophysical modalities
• Surgical –
• Core decompression
• Vascularised bone graft/muscle pedicle graft
Usually arthroplasty is awaited without any big
surgical intervention