Radiology cases on avascular necrosis

1. CASE HISTORY

2. 41-year-old male presented with
PAIN
 Site: right sided low back, hip and knee pain
 Onset: from past six months. Fell from two meter high roof land on
his feet
 Intensity: worsening pain with time
 Pattern: antalgic limp and walked with the help of a cane.
 Radiation: into his right groin and anteromedial thigh region.
 Aggravating factors: walking and stair climbing.
 Relieving factors: sitting and resting.
 NO ASSOCIATED SYMPTOMS

3. PAST HISTORY
 Flu vaccine 14 months prior to injury.
 He subsequently developed an allergic reaction and was
diagnosed with leukocytoclastic vasculitis skin eruptions.
 Treated with four months of oral corticosteroid therapy with
doses up to 50 mg per day. The skin lesions resolved with
treatment.
 However he developed corticosteroid-induced glucose
intolerance subsequent to treatment.
 Past history also revealed a nasal fracture six years ago which
required two surgical interventions.
 No other significant point.

4. PHYSICAL EXAMINATION
 Severe pain and restricted movement across hip joint.
 Right hip region extreme tenderness
 Muscle atrophy noted in the right region
 Posterior joint provocation tests were painful for L4, L5.
 SI testing was painful for the right sacroiliac joint.

5. ON X-RAY
Irregularity to the right
femoral head
Sclerosis
Subchondral lucency
Mild collapse

6. DIAGNOSIS
AVASCULAR NECROSIS
(AVN)

7. DEFINITION
Cellular death of bone components due to
interruption of the blood supply;
the bone structures then collapse, resulting
in
bone destruction
pain
loss of joint function.

8. ETIOLOGY
 TOXIC (alter lipid metabolism)
 STEROID NOT LESS THAN TWO YEAR INTAKE
 ALCOHOL
 DRUD IMMUNOSUPPRESSIVE ANTI-INFLAMMMATORY
 TRAUMATIC (vascular occlusion)
 IDIOPATHIC
 FRACTURES
 RADIOTHERAPY
 INFLAMMMATORY
 SLE
 INFECTION
 RHEUMATOID ARTHRITIS
 HEMOPOIETIC DISORDERS (intravascular coagulation)
 SICKLE CELL ANEMIA
 HAEMOPHILIA
 MISCELLANEOUS

9. PATHOPHSIOLOGY

10. PATHOPHYSIOLOGY
 Interruption of the blood supply to the bone
 Effected bone have single terminal blood supply such as femoral head
and condyles, epiphysis of long bone carpals, talus, humerus,
 These bone have limited collateral blood supply
 Interruption of the vascular supply result in necrosis of
 bone marrow (2-5 days)
 Hemopoietic tissues (6-12 hours)
 Osteoblast, osteoclast, osteocystes (12-48 hours)

11. EPIDEMIOLOGY
 RACE:-
 Associated with sickle cell anemia, hemoglobin S and SC
 SEX:-
 More common in men. Male to female ratio 8:1
 AGE:-
 Middle age fourth or fifth decade of life

12. FICAT classification (5 stages) most commonly used
MITCHELL classification (4 types)
Steinburg classification (7 stages)
Radiologically
AVN Staging System:

13.  No changes are visible.
 Plain film:
 normal
 MRI:
 normal
 Clinical symptoms:
 nil
STAGE I

14. STAGE II
 plain film:
 Normal or minor osteopenia
 Avascular areas are of increased
density (ostesclerosis)
 MRI:
 Edema
 bone scan:
 Increased uptake
 clinical symptoms:
 Pain typically in the groin

15. STAGE III
 Plain film:
Mixed osteopenia
Sclerosis
 Subchondral cysts
without any subchondral
lucency
 MRI:
Geographic defect
 Bone scan:
Increased uptake
 Clinical symptoms:
 Pain and stiffness

16. STAGE IV
 Plain film:
 Crescent sign and cortical collapse
 MRI:
 Same as plain film
 Clinical symptoms:
 Pain and stiffness+/- radiation to knee and limp
 Sub classification depends on the extent of crescent, as follows:
 Stage a: Crescent is less than 15% of the articular surface.
 Stage b: Crescent is 15-30% of the articular surface.
 Stage c: Crescent is more than 30% of the articular surface.

17. STAGE V
 plain film:
 End stage with evidence of secondary
degenerative change (joint space narrowing)
 Collapsed
 MRI:
 Same as plain film
 clinical symptoms:
 Pain and limp
 Sub classification on the extent of collapsed surfaces:
 Stage a: Less than 15% of surface is collapsed.
 Stage b: Approximately 15-30% of surface is
collapsed.
 Stage c: More than 30% of surface is collapsed.

18. MRI staging of AVN
CLASS TI WEIGHT IMAGE T2 WEIGHT IMAGE Grading lesion
acuity
A BRIGHT INTERMEDIATE FAT SIGNAL
B BRIGHT BRIGHT BLOOD SIGNAL
C INTERMEDIATE BRIGHT FLUID/ EDEMA
SIGNAL
D DARK DARK FIBROSIS SIGNAL

19. MODALITY OF CHOICE
 X-RAY
 CT
 MRI
 RADIONUCLIDE BONE SCAN

20. X-RAY
 Mild-to-moderate AVN
Sclerosis (arrows)
Changes in bone density (asterisk).

21. X- RAY
Advanced disease
Bone deformities
Flattening
Subchondral radiolucent
lines (crescent sign)
Collapse of the femoral head

22. Computed Tomography
 To assess
 the extent of the disease
 Calcification
 Less sensitive then MRI

23. Computed Tomography
Sclerosis in the central part of
femoral head asterisk sign
(arrow head)
Low-density region (arrow)

24. Radionuclide Bone Scan
 In early AVN
 Less sensitive than MRI
 Findings are nonspecific
 Unilateral disease,
 Healthy side can be used for comparison
 Bilateral disease:
 difficult to interpret

25. Early AVN
 Sensitivity of radionuclide bone scan is better than plain films .
 Central area of decreased uptake is surrounded by an area of increased uptake.
 Doughnut sign (arrow):
 The reactive zone surrounding the necrotic area.

26. Magnetic Resonance Imaging
 Most sensitive (~95%) modality
 Demonstrates changes well before plain film changes are visible.
 The progression is:
 Diffuse oedema
 Focal serpentine low signal line with fatty center (most common appearance)
 Double line sign on T2WI is diagnostic
 Osteochondral fragmentation: rim sign
 Secondary degenerative change

27. Magnetic Resonance Imaging
 Decreased signal intensity in the subchondral region on both T1- and T2-
weighted images, suggesting edema (water signal) in early disease.

28. Magnetic Resonance Imaging
 The next stage is characterized by a reparative process (reactive zone) and shows
 Low signal intensity on T1-weighted scans ( band like area)
 High signal intensity on T2-weighted scans. (double line sign)

29. Advanced AVN
 Deformity of the articular surface
 Calcification

30. TREATMENT
 Medical management:
 Conservative measures
 Limit weight bearing
 Pain medications.
 Immobilization
 Bisphosphonates
 Delay collapse of the femoral head
 Delay the need for surgical intervention.
 Statin therapy
 Prevents corticosteroid-induced
 Surgical Management:
 In early stages:
 Core decompression with or without bone graft
 In late stages:
 Total hip arthroplasty is the most appropriate treatment

31. COMPLICATIONS:
 Total destruction of the joint may occur.
 Nonunion of fracture
 Secondary muscle wasting.

32. PROGNOSIS
 Depends on the disease stage at the time of diagnosis
 More than 50% of patients with AVN require surgical treatment within 3 years of
diagnosis.
 Half of patients with subchondral collapse of the femoral head develop AVN in
the contralateral hip.
 Poor prognostic factors:
 Age older than 50 years
 Advanced disease (stage 3 or worse) at the time of diagnosis
 Non-modifiable risk factors such as cumulative dose of corticosteroids (corticosteroid-
induced AVN)