This document discusses avascular necrosis (AVN), also known as osteonecrosis. It begins by defining AVN as the death of bone components due to interrupted blood supply. Key areas that are commonly affected are described. The document then covers the pathophysiology, various causes (traumatic, non-traumatic), clinical presentation, imaging techniques, staging classifications, and management strategies for AVN. Treatment approaches include conservative options, decompression procedures, realignment osteotomies, arthrodesis, and arthroplasty.

1. Sonal
BPT 3rd year

3. Outline
 Definition
 Pathophysiology
 Aetiology
 Presentation
 Imaging
 Staging
 Management

4. Definition
 Cellular death of bone components secondary to interr
uption of blood supply
 Consequent collapse of bone components
 Pain, loss of function of joints

5. Areas commonly affected
• Femoral head
• Femoral condyles
• Head of humerus
• Capitulum of humerus
• Proximal part of scaphoid and talus

6. Predisposing factors
• Distance from vascular territory of bone
• Enclosed by cartilage limiting vascularity.
• Vascular sinusoids (type of capillaries which has open
pores which increases their permeability, and seen in b
one marrow, liver etc).
Are compressed by increased pressure and volume of
marrow tissue.

7. Pathophysiology
 Interruption of blood flow to bone
 Affect bones with single terminal blood supply:
 Talus
 Carpals, tarsals
 Proximal humerus
 Head of femur
 Femoral condyles
 Results in necrosis of Bone marrow, medullary cavity (
place where bone marrow resides) and cortical bone( t
ype of lamellar bone, with densely packed lamellae)
 Final pathway from multiple causes

8. Pathways to necrosis
 Bone necrosis after 12 – 48 hrs of anoxia
 Reactive new bone formation around necrotic bone
 Granulation tissue over necrosed bone – sclerosis
 Structural failure in heavily stressed part of the necroti
c segment – linear fractures

9.  Crack may break through the articular cartilage and at su
rgery necrotic part lifts off like cracked shell of hard boile
d egg.
 Articular cartilage retains it's thickness but in final stages
deformity and destruction of joint surface is seen.

11.  The medullary cavity is the central cavity of bone shafts
where red bone marrow and/or yellow bone marrow
(adipose tissue) is stored. It has walls composed of
spongy bone (cancellous bone) and is lined with a thin,
vascular membrane (endosteum).

12. Traumatic causes
 In fractures and dislocations of hip the retinacular vessels
supplying the femoral head are torn. If in addition, there is
damage to or thrombosis of the ligamentum Teres, osteone
crosis is inevitable.
 In fractures of scaphoid, proximal part is more prone to n
ecrosis

13. • Fracture of talus, avascular necrosis is commonly seen. It is
because the anastomotic ring of blood vessels run postero-
laterally. Therefore blood supply is often cut off during neck
fractures.

15. Non-Traumatic causes
• Intravascular thrombosis
• High dose of corticosteroids and alcohol abuse leads to
hyperlipidemia and fatty degeneration of liver.
• Hypercoaguable states- thrombophilia
• Systemic lupus erythrematosis - deficiency of anti-
phospholipid.
• Hematologic disorder- sickle cell anemia ( enhanced
coagulability)

17. Extravascular marrow swelling
• High dosage of alcohol and corticosteroids leads to fat cell
swelling in the marrow.
• This leads to intra-osseous pressure increase and compression
of sinusoids as in femoral head.
Caisson disease and Dysbaric osteonecrosis
• Decompression disease seen in deep - sea divers and
compress air workers.
• Under increased pressure, the blood and other tissues (fat)
becomes super saturated with nitrogen.

18. • These gas bubbles leads to tissue damage and prolonged tissue
damage leads to swelling of marrow fat cells and decrease
blood supply due to toxicity.
Gaucher's disease
• Lack of enzyme glucocerebrocide in the macrophages of the
reticuloendothelial system.
• Affects spleen and bone marrow.
• Leads to sinusoidal compression in hip.

19. Radiation therapy
• Prolonged exposure to radiations leads to bone death.
• This is due to combined effects of damage to small blood
vessel, marrow cells and bone cells
Malignancy
• Corticosteroids
• Bisphosphonates (long term IV use leads to osteonecrosis of
jaw)
• Certain types of chemotherapy
• Radiotherapy

20. • Patients who are being treated for acute myeloid
leukaemia, acute lymphoblastic leukaemia, lymphomas,
testicular cancer, ovarian cancer, breast cancer, and
multiple myeloma have an increased risk of developing
AVN regardless of the treatment they receive
• Bone Marrow or Stem Cell Transplantation

21. Presentation - History
 Trauma
 Corticosteroid use
 Alcohol intake
 Medical conditions – malignancy, thrombophilia, SLE, SCD

22. Presentation - examination
 Groin pain
 Antalgic gait
 Restricted ROM
 Tenderness around bone
 Muscle wasting
 'Click' sound in the joints
 Joint deformity

23. Imaging: X ray
 Initially normal upto 3 months
 Sclerosis
 Flattening
 Subchondral radiolucent lines (lines only seen in x-ray in b
one below the articular cartilage) (cresent sign)
 Collapse of cortex
 OA

25. Imaging: CT scan
 Used to assess extent of disease and calcification
 Clearly shows articular deformity
 Calcification and bone collapse
 Central sclerosis in femoral head produces star shaped
structure (asterisk sign)

27. Imaging: MRI
 90% sensitive
 Changes detected early

29. Radionuclide scan
 Donut sign – central reduced uptake with surrounding
rim of increased uptake
 More sensitive than plain films in early AVN
 Less sensitive than MRI
 Necrotic zone surrounded by reactive new bone forma
tion

31. Histology
 Definitive diagnosis
 Usually a confirmatory during surgery for treatment
 Occasionally biopsy of sclerotic lesion
 Necrosis of cortical bone is followed by a regenerative
process in surrounding tissues.

32. Intramedullary pressures
 Cannula into metaphysis
 Measure at rest and after saline injection
 Femoral head:
 10 – 20 mmHg, increasing by 15 mmHg after saline
 Markedly increased values in AVN (3 to 4 fold)
 Less marked increase in OA

33. Ficat and the Steinberg Classification
Stage 1 • X-ray - no changes
• Diagnosis will be based on
intra-osseous pressure and
bone biopsy
Stage 2 Femoral head contour was
still normal but there were
early signs of Reactive
changes in the subchondral
bone

34. Stage 3 Clear evidence of
osteonecrosis and
structural damage and
distortion of bone
outline.
Stage 4 Collapse of articular
surface and signs of OA.

36. Management principles
 Early stages (I & II):
 Bisphosphonates prevent collapse
 Unloading osteotomies
 Medullary decompression + bone grafting
 Intermediate stage (III):
 Realignment osteototmies, Decompression, Curettage
 Arthrodesis
 Late stage (IV):
 Analgesia, activity modification
 Arthrodesis
 Total joint replacement

37. Management - conservative
 Offloading affected joints with use of crutches
 Immobilisation
 Analgesia
 Bisphosphonates delays bone break down in femur
 Statins in patients on high dose corticosteroids – reduc
ed lipid deposition

38. Core decompression
 8 – 10 mm anterolateral core of bone
 Filled with bone graft (vascularised/non vascularised)
 Decompresses medullary cavity, reduces pain
 Vascularised graft may reverse necrosis

40. Realignment osteotomy
 Used to relocate necrotic area from weight bearing portion
of femoral head
 Angular osteotomies more common
 Multiple techniques for holding the fixation

42. Arthroplasty
 Main aim is pain reduction
 Young patients will need revision
 Higher failure rates than in OA
 Hemi arthroplasty an option