MRI

Avascular Necrosis of the Hip

Edward C. Fritsch, D.C.

 Overview
Avascular necrosis (AVN) is cellular death of the components
of bone, including bone marrow, due to impaired blood supply.
AVN occurs in a number of conditions.
AVN usually involves the epiphysis of long bones.
Called bone infarct if in diaphysis or metaphysis
AVN of the hip is the most common encountered in clinical
practice.
Early diagnosis and appropriate intervention can delay the need
for joint replacement.
Patients on corticosteroids and organ transplant recipients are
particularly at risk of developing AVN.
 Pathophysiology:
AVN is due to blood supply disruption, and it
affects bones with single terminal blood supply.
Mechanical interruption of blood supply.
Thrombotic or embolic occlusion of blood vessel.
Injury to vessel wall
Pressure on vessel wall
Mechanism unknown (eg, high dose corticosteroids,
alcoholism, primary AVN)
 Etiology
SLE
Rheumatoid arthritis
Pancreatitis
Fracture / dislocation Gaucher's disease
Steroid use Polycythemia vera
Pregnancy
Alcoholism Septic emboli
Sickle cell disease Fadiation
Idiopathic Dysbarism (caisson disease):
scuba diver surfacing too fast
Thermal trauma (burns,
frostbite)
Cushing's disease
 Frequency
Frequency depends on the site involved.
The most common site is the hip, and other locations
include the carpals, talus, and humerus.
US approximately 15,000 new cases are reported each
year.
AVN accounts for >10% of total hip replacement
surgeries performed in the United States.
 Patient Profile
Sex: Depends on the underlying cause, the overall male-
to-female ratio is 8:1.
Age: Age at onset depends on the underlying cause.
Primary AVN most often occurs during the forth or fifth
decade, and it is bilateral in 40-80% of cases. On average,
women present almost 10 years later than men.
Race: No racial predilection exists except for AVN
associated with sickle cell disease and hemoglobin S and
SC disease, which predominantly occur in people of
African and Mediterranean descent.
 Methods of Imaging
Imaging Findings Time to Comments
Method Diagnosis

X-Ray Osteopenia Months Sensitivity poor

Reactive sclerosis Specificity good
Subchondral Collapse (late)
CT Reactive sclerosis Weeks to Sensitivity poor
Subchondral collapse Months Specificity OK
Bone Scan Decreased uptake early Weeks Sensitivity good
Increased uptake late Specificity poor
MRI Change of signal in Days Sensitivity excellent
marrow pattern Specificity good
 MRI Diagnosis of AVN
MRI is the most sensitive
noninvasive method for
diagnosis of AVN.
Diagnosis involves detection
of marrow foci of decreased
signal on T1-weighted images
and the characteristic double
line sign on T2-weighted
images.
(only condition that will do
the double line)
 MRI Diagnosis of AVN - T1

AVN is diagnosed when a

peripheral band of low
signal intensity is present
on all imaging sequences,
typically in the superior
portion of the femoral
head, outlining a central
area of marrow.
This peripheral band is
most apparent on T1-
weighted sequences.
 MRI Diagnosis of AVN - T2
On conventional T2
sequences, the inner
border of the peripheral
band shows high signal in
80% of cases.
This is called the "double
- line" sign of avascular
necrosis, and is considered
to be pathognomonic.
 MRI Findings
T2 with Fat Supression

Fat suppression is current

state of the art.
Dark, peripheral band of
AVN that is not seen in
contrast to the inner high
signal band of AVN.
Early edema of marrow
allowed MR to surpass
bone scans in early
diagnosis.
 MRI Findings Joint Effusions

Increased joint fluid is

commonly associated with
AVN, and its presence does
not indicate a septic joint
effusion.
The frequent presence of
joint effusions has led to
the hypothesis that patients
are presenting with pain
due to their effusion, rather
than the long-standing
process of AVN.
 Staging AVN
Ficat and Arlet Staging of AVN: (Radiographic staging)

Stage X-Ray MRI Bone Scan

0 Negative Marrow edema Maybe positive

Accidental finding
1 Osteopenia (hindsight) + bone necrosis Positive
Missed here and #2 s picture
perfect technique
2 Diffuses osteoporosis and sclerosis + joint edema Positive
on plain films. A reactive shell of
bone delimits the infarct. Spherical
femoral head.
3 Crescent sign (radiolucency) under + articular Positive
the subchondral bone representing cartilage
a fracture. Joint space preserved involvement
4 Femoral head collapse. Joint space + specificity of Positive
narrowing OA joint
NEED SURGERY HERE AND 3 destruction
Stage 0
Stage 1
Stage 2
Stage 3 (crescent sign in frogleg)
Stage 4
 Last Case

45 year old male

Chronic LBP & hip
pain
No response to
conservative care after
two weeks.
MRI recommended
patient wanted to
wait
The End