Avascular Necrosis

• = AVN = OSTEONECROSIS = ASEPTIC NECROSIS

• = consequence of interrupted blood supply to bone with death of
cellular elements

Terminology (now often used interchangeably):

• Osteonecrosis = ischemic bone death due to sepsis

• Avascular necrosis = avascular and aseptic bone necrosis
• Ischemic necrosis = necrosis of epiphyseal + subarticular bone
• Bone infarction = necrosis of metaphyseal + diaphyseal bone

Histo:

• cellular ischemia leading to death of hematopoietic cells (in 6-12

hours), osteocytes (in 12-48 hours) and lipocytes (in 2-5 days)
• necrotic debris in intertrabecular spaces + proliferation and infiltration
by mesenchymal cells + capillaries
• mesenchymal cells differentiate to osteoblasts on the surface of dead
trabeculae synthesizing new bone layers + resulting in trabecular thickening

Cause:

- NO predisposing factors in 25%!

- Traumatic interruption of arteries

o @ femoral head:
 Femoral neck fracture (60-75%)
 Dislocation of hip joint (25%)
 Slipped capital femoral epiphysis (15–40%)
o @ carpal scaphoid:
 4-6 months after fracture (
Site proximal fragment (most common)
:
o @ humeral head (infrequent)
o @ talus (after talar neck fracture)
• Embolization of arteries
o Hemoglobinopathy: sickle-cell disease
o Nitrogen bubbles: Caisson disease
o Fat: ethanol abuse with pancreatitis
• Vasculitis
o Collagen-vascular disease: SLE
o Radiation exposure
• Abnormal accumulation of cells
o Lipid-containing histiocytes: Gaucher disease
o Fat cells: steroid therapy
 • Idiopathic
•

Location femoral head (most common), humeral head, femoral condyles

:
Radiography:

• dense osteonecrotic bone (due to lack of resorption relative to healthy

osteopenic bone + new bone laid down over necrotic trabeculae)
• radiolucent rim around area of osteonecrosis (due to absorption around
necrotic bone)

Avascular Necrosis of Hip

• Involvement of one hip increases risk to contralateral hip to 70%!

Age 20-50 years

:
Plain film (positive only several months after symptoms):

• subtle relative sclerosis of femoral head secondary to resorption of

surrounding vascularized bone (earliest sign)
• radiolucent crescent parallel to articular surface in weight-bearing
portion secondary to subchondral structural collapse of necrotic segment

Site anterosuperior portion of femoral head (best seen on frog leg view)
:

- preservation of joint space (DDx: arthritis)

- flattening of articular surface

- increasedensity of femoral head (compression of bony trabeculae following

microfracture of nonviable bone, calcification of dendritic marrow, creeping
substitution = deposition of new bone)

NUC (80-5% sensitivity):

• More sensitive than plain films in early AVN (evidence of ischemia

seen as much as 1 year earlier)
• Less sensitive than MR

CT (utilized for staging of known disease):

• staging upgrades in 30% compared with plain films

MR (90-100% sensitive, 85% specific for symptomatic disease):

Prevalence of clinically occult 6%
disease:

• MR imaging changes reflect the death of marrow fat cells (not death of
osteocytes with empty lacunae)!
• Sagittal images particularly useful!

- EARLY AVN:

o decreased Gd-enhancement on short-inversion-recovery (STIR)

images (very early)
o low-signal intensity band with sharp inner interface + blurred
outer margin on T1WI within 12-48 hours (= mesenchymal + fibrous
repair tissue, amorphous cellular debris, thickened trabecular bone)
seen as
 band extending to subchondral bone plate
 complete ring (less frequent)

-double-line signal on T2WI (in 80%) [MORE SPECIFIC] = juxtaposition of inner

hyperintense band (granulation tissue) + outer hypointense band (chemical shift
artifact / fibrosis + sclerosis)

- ADVANCED AVN:

- pseudohomogeneous edema pattern= inhomogeneous large areas of mostly

decreased signal intensity on T1WI

- hypo- to hyperintense lesion on T2WI

- contrast-enhancement of interface + surrounding marrow + within lesion

• EPIPHYSEAL COLLAPSE:
o focal depression of subchondral bone