Imaging in Avascular Necrosis of The Femoral Head

3/12/2021 https://emedicine.medscape.
com/article/386808-print
emedicine.medscape.com
Imaging in Avascular Necrosis of

the Femoral Head
Updated: Nov 11, 2017
Author: Michael R Aiello, MD; Chief Editor: Felix S Chew, MD, MBA, MEd
Overview
Practice Essentials
Avascular necrosis (AVN) of the femoral head is an increasingly common cause of musculoskeletal disability, and it poses a
major diagnostic and therapeutic challenge. Although patients are initially asymptomatic, avascular necrosis of the femoral head
usually progresses to joint destruction, requiring total hip replacement (THR), usually before the fifth decade (see the images
below). In fact, 50% of patients with avascular necrosis experience severe joint destruction as a result of deterioration and
undergo a major surgical procedure for treatment within 3 years of diagnosis. Femoral head collapse usually occurs within 2
years after development of hip pain.[1, 2, 3, 4, 5, 6, 7]
(See the images of vascular necrosis below.)
Axial computed tomography scan in a patient without avascular necrosis of the femoral head shows prominent and thickened
but normal trabeculae (arrow) within the femoral head. Note the delicate, sclerotic, raylike branchings emanating in a radial
fashion from the central dense band. This is the asterisk sign. See also the next image.
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Avascular necrosis of the femoral head. Illustration of the normal circulation of the femoral head, viewed from the posterior
approach. The posterior-superior retinacular arteries provide the major blood supply to the epiphysis. They traverse the
femoral neck and are contained within the joint capsule and give rise to the lateral epiphyseal vessels at the junction of the
femoral head and neck. From there, they penetrate the femur and supply the femoral epiphysis. A. = artery.
Avascular necrosis of the femoral head. Illustration demonstrating that the blood supply to the femoral head is compromised
by subcapital femoral fractures or slipped capital femoral epiphysis. As the epiphysis or femoral neck separates from the
femoral head, the femoral metaphysis displaces superolaterally and the femur rotates externally. This causes the distal
posterior-superior retinacular arteries and proximal lateral epiphyseal vessels to kink or rotate, compromising the blood flow to
the epiphysis. If this condition were to persist, the femoral head would be at high risk for developing avascular necrosis.
Frogleg lateral view of the right hip in a patient with avascular necrosis shows the crescent sign, indicating subchondral
fracture. Therapeutic interventions are less likely to halt progression of the disease once this sign appears. The frogleg lateral
view is better than anteroposterior (AP) projection for demonstrating this sign, because the anterior and posterior margins of
the acetabulum on the AP projection are superimposed over the superior portion of the femoral head, the usual location of the
sign.
The incidence of avascular necrosis (AVN) has been increasing. The causes include greater use of exogenous steroids and an
increase in trauma. In 54-80% of renal transplant recipients in whom AVN is detected with plain radiographs, the disease is
bilateral. It is estimated that almost 10% of the nearly 500,000 THRs performed each year in the United States are intended to
treat AVN; at a cost of more than $1 billion, THRs performed to treat avascular necrosis of the femoral head constitute
approximately 25% of the total national costs for THR. Trauma is the most common cause of avascular necrosis; however,
nontraumatic AVN is commonly bilateral and occurs in younger persons. In addition, nontraumatic bilateral AVN usually occurs
at different times and progresses at different rates in different hips.
Treatment of AVN has been facilitated by the adoption of an international classification system, by effective early diagnosis using
magnetic resonance imaging (MRI), and by more aggressive surgical management; nevertheless; no universally satisfactory
therapy has been developed, even for early disease.
Because measures to preserve the joint are associated with better prognoses when the diagnosis of avascular necrosis (AVN) is
made early in the course of the disease and because the results of joint replacement therapy are poorer in younger age groups
than in older patients, it is critical to diagnose this condition as early as possible to prevent or delay progression of the disease.
Avascular necrosis is characterized by areas of dead trabecular bone and marrow extending to involve the subchondral plate.
The anterolateral aspect of the femoral head, the principal weightbearing region, is typically involved, but any region of the
femoral head may be involved. In the adult, the involved segment usually never fully revascularizes, and collapse of the femoral
head usually occurs sometime after AVN is detected radiographically.
The femoral head is the most vulnerable site for the development of avascular necrosis. The site of necrosis is usually
immediately below the weightbearing articular surface of the bone (ie, the anterolateral aspect of the femoral head). This is the
site of greatest mechanical stress.
Elderly persons are at decreased risk for developing avascular necrosis. Fat cells become smaller in elderly persons. The space
between fat cells fills with a loose reticulum and mucoid fluid, which are resistant to AVN. This condition is termed gelatinous
marrow. Even in the presence of increased intramedullary pressure, interstitial fluid is able to escape into the blood vessels,
leaving the spaces free to absorb additional fluid.
Anatomy
To understand the changes of avascular necrosis on radiologic studies such as computed tomography (CT) scanning and MRI,
it is necessary to understand the anatomy of the hip and to understand the vascular anatomy of the hip in children.
Gross anatomy
The hip is a ball-and-socket joint. The acetabulum, which provides bony coverage of 40% of the femoral head, has a horseshoe-
shaped lunate surface. The femoral head is round and smooth in all imaging planes. The fovea capitis, a small depression on
the medial femoral head, is the site of attachment of the ligamentum teres (see the image below).
Coronal T1 MRI of the pelvis and hips in a patient without avascular necrosis of the femoral head. A thin low-signal line,
representing the long cortex, surrounds the femur and iliac lines. The fovea is a small indentation along the medial aspect of
the femoral head and is the site of penetration of the artery of the ligamentum teres into the femur. High signal is present
within the medullary space of the proximal femur, representing normal fatty marrow. The physis is a thin line of low signal
extending from the lateral to the medial aspect of the femoral head.
The principal sources of blood flow to the femoral head are the lateral epiphyseal vessels (LEVs). LEVs are branches of the
posterior superior retinacular vessels (PSVs), which are themselves branches of the medial femoral circumflex artery; the
medial femoral circumflex artery is a branch of the profunda femoris artery (see the following 2 images). The PSVs run along the
posterior-superior aspect of the femoral neck under the synovial membrane. They are extraosseous in location and give rise to
the LEV.[8]
The LEV enters the femoral head within a 1-cm-wide zone between the cartilage of the femoral head and the cortical bone of
the femoral neck. They supply the lateral and central thirds of the femoral head. When patent, the artery of the ligamentum teres
(ALT) supplies the medial third of the femoral head.
Avascular necrosis of the femoral head. Illustration of the normal circulation of the femoral head, viewed from the posterior
approach. The posterior-superior retinacular arteries provide the major blood supply to the epiphysis. They traverse the
femoral neck and are contained within the joint capsule and give rise to the lateral epiphyseal vessels at the junction of the
femoral head and neck. From there, they penetrate the femur and supply the femoral epiphysis. A. = artery.
Avascular necrosis of the femoral head. Illustration demonstrating that the blood supply to the femoral head is compromised
by subcapital femoral fractures or slipped capital femoral epiphysis. As the epiphysis or femoral neck separates from the
femoral head, the femoral metaphysis displaces superolaterally and the femur rotates externally. This causes the distal
posterior-superior retinacular arteries and proximal lateral epiphyseal vessels to kink or rotate, compromising the blood flow to
the epiphysis. If this condition were to persist, the femoral head would be at high risk for developing avascular necrosis.
Branches of the LEVs and the ALT anastomose in the junction of the central and medial third of the femoral head. The thickest
part of the articular cartilage of the femoral head is located along the posterior-superior aspect and measures 3 mm in diameter.
It thins to 0.5 mm along the peripheral and inferior margins.
Blood supply in children
In children 4-7 years of age, the vascular anatomy of the proximal femur is in a transitional stage of development. The ALT does
not penetrate the epiphysis of the femoral head until age 9 or 10 years. The medial circumflex artery, a branch of the profunda
femoris artery, penetrates into the femoral proximal metaphysis but is prevented from passing into the femoral epiphysis by the
growth plate. The blood supply to the femoral head is especially vulnerable during this time.
Anatomy on CT scans
Physiologic thickening of bone trabeculae in the center of the femoral head is present and appears similar to a star, which is
termed the asterisk sign (see the image below). The configuration is related to the stress of weightbearing.
Sclerotic raylike branches of the star usually extend to the upper surface of the femoral head (see the image below). A dense
line, extending from the lateral to the medial portion of the mid femoral head, represents the fused epiphysis.
Anatomy on MRI
Fatty marrow is present in the femoral capital epiphysis and the greater trochanter of all individuals older than 2 years. Fatty
marrow has high signal intensity on T1-weighted images (T1WIs) and T2-weighted images (T2WIs) (see the images below).
Hematopoietic marrow, when present, is found in the femoral neck, the intertrochanteric region, and the acetabulum. It has low
signal intensity on T1WIs and high signal intensity on T2WIs (see the images below).
Avascular necrosis of the femoral head. Coronal T1-weighted magnetic resonance image in a patient showing hypointense
signal within the proximal femoral neck and intertrochanteric regions (arrows) representing hematopoietic marrow. Increased
signal is present within the greater trochanters and femoral capital epiphysis representing normal fatty marrow. See also the
next image.
Avascular necrosis of the femoral head. Coronal T2-weighted magnetic resonance image in a patient showing hypointense
signal within the proximal femoral neck and intertrochanteric regions, representing hematopoietic marrow. Increased signal is
present within the greater trochanters (single arrowhead) and femoral capital epiphysis (stars), representing normal fatty
marrow. The normal hip joints (double arrowheads) contain a small amount of fluid.
The medullary cavity contains prominent vertically oriented linear striations of low signal on all imaging sequences extending
from the inferolateral aspect to the superomedial aspect of the femoral head. These represent the weight-bearing trabeculae
and are analogous to the asterisk sign seen on CT scans. The medullary cavity is surrounded by a sharply marginated line of
low signal intensity, which represents the cortex of the bone. Cortex and trabeculae have weak MRI signal intensity because of a
low concentration and decreased mobility of hydrogen ions (see the 2 images above).
A thin line of high signal intensity, which represents the articular cartilage, surrounds the outer margin of the femoral head. A
curvilinear low-signal line, representing the physis, crosses the marrow of the femoral neck laterally to medially. The medullary
cavity of the iliac bone, adjacent to the acetabulum, is of slightly lower and less homogeneous signal intensity than the femoral
head (see the 2 images above).
Sequelae of avascular necrosis
Avascular necrosis progresses from minimal to more severe disease to mechanical failure.
Minimal avascular necrosis
If the vascular area is small and is not adjacent to an articular surface, the patient may be asymptomatic; healing may occur
spontaneously, or the disease may remain undetected or be discovered incidentally during workup for other conditions.
More severe avascular necrosis
Once AVN develops, repair begins at the interface between viable bone and necrotic bone. Ineffective resorption of dead bone
within the necrotic focus is the rule. Dead bone is reabsorbed only partially. Reactive and reparative bone is laid down on dead
trabeculae, resulting in a sclerotic margin of thickened trabeculae within an advancing front of hyperemia, inflammation, bone
resorption, and fibrosis. The incomplete resorption of dead bone has a mixed sclerotic and cystic appearance on radiographs.
Necrosis and repair are ongoing in various stages of evolution within a single lesion.
Mechanical failure
Mechanical failure of trabecular bone at the interface between dead and viable bone may exacerbate avascular necrosis. In the
subchondral region, such microfractures do not heal because they occur within an area of dead bone. Progression of the
microfractures results in a diffuse subchondral fracture, seen radiographically as the crescent sign (see the first image below).
Following subchondral fracture and progressive weightbearing, collapse of the articular cartilage occurs (see the second through
fifth images below). Continued fracture, necrosis, and further weightbearing may progress to degenerative joint disease (DJD)
and joint dissolution (see the second image and last 2 images below).
sign.
Avascular necrosis of the femoral head. Anteroposterior view of the pelvis shows flattening of the outer portion of the right
femoral head from avascular necrosis (arrow), with adjacent joint-space narrowing, juxta-articular sclerosis, and osteophytes
representing degenerative joint disease. See also the next image.
Anteroposterior view of the left hip in a patient with avascular necrosis obtained 6 months after presentation shows that the
patient has undergone core decompression but has developed mild flattening of the femoral head, indicating progression of
disease despite treatment.
Plain film finding in a patient with bilateral avascular necrosis of the femoral head 6 months after presentation demonstrates
that subtle flattening of the left femoral head (open arrow) has occurred. This indicates progression of disease from stage 2 to
stage 3 despite conservative treatment. The patient underwent bilateral core decompression and bone grafting. The defects
within the proximal femurs represent removal of the dead bone, and the tubular densities within each femur represent bone
grafts in an attempt to revascularize the region of avascular necrosis.
Plain film findings in a patient with bilateral avascular necrosis of the femoral head who underwent bilateral core
decompression and bone grafting. Despite treatment, an anteroposterior plain film of the pelvis obtained 6 months later shows
further flattening of the right femoral head (black arrows). Note the progressive increase in the size of the lucency within the
right femoral head, which resulted in further weakening of the femoral head. This lucency represents removal of dead bone.
Once fracture of the femoral head occurs, operative attempts to stabilize the femur usually fail. Disease usually progresses
rapidly, requiring total joint replacement.
Axial computed tomography scan in a patient with avascular necrosis. This image shows joint space narrowing, juxta-articular
sclerosis, and osteophyte formation (degenerative joint disease) around the anteromedial and posterolateral aspects of the
right hip.
Anteroposterior plain film of the pelvis in a patient with avascular necrosis of the femoral head shows asymmetric joint-space
narrowing (arrow), juxta-articular sclerosis, and subchondral cyst formation around the right hip secondary to degenerative
joint disease. This may be confused with avascular necrosis, but the intimate localization of all of the bindings and the
absence of femoral head collapse makes a diagnosis of avascular necrosis highly unlikely.
Preferred examination
This section will discuss various imaging modalities. For more detailed information, please see their respective sections in this
article.
MRI
MRI is the most sensitive means of diagnosing avascular necrosis. This imaging modality provides the criterion standard of
noninvasive diagnostic evaluation and is more sensitive than CT scanning or planar scintigraphy. In addition, MRI is much more
sensitive than plain film radiography for detecting avascular necrosis (AVN). However, low-field magnets (0.1 Tesla [T]) are not
as sensitive for diagnosing AVN.
7-T hip MRI showed comparable results in hip joint imaging compared with 3 T, with slight advantages in contrast detail
(cartilage defects) and fluid detection at 7 T when accepting image degradation medially. Image homogeneity of 7 T compared
with 3 T (3.9-4.0 for all sequences) was degraded, especially in TSE sequences at 7 T through signal variations (7 T: 2.1-2.9).[9]
MRI is indispensable for the accurate staging of avascular necrosis, because images clearly depict the size of the lesion, and
gross estimates of the stage of disease can be made. MRI allows sequential evaluation of asymptomatic lesions that are
undetectable on plain radiographs.[1] MRI facilitates better response to treatment because, with the use of MRI, AVN is
diagnosed at an earlier stage, and therapeutic measures are more successful the earlier they are begun.
MRI does not employ ionizing radiation—a factor that is especially important in the growing skeleton—and it is accepted widely
and is easy to perform. MRI is also capable of imaging in multiple planes (ie, axial, sagittal, coronal, or any variation thereof),
demonstrates superior soft-tissue resolution, and has high spatial and contrast resolution, allowing evaluation of morphologic
features.
MRI may help guide interventional procedures such as core decompression, may demonstrate response of the femoral head to
treatment, and may detect the joint effusions and bone edema that often accompany avascular necrosis. MRI is a noninvasive
means of evaluating articular cartilage congruity, and it allows sequential evaluation of asymptomatic lesions that are
undetectable on plain radiographs.[10, 11]
Early MRI detection and closed bone graft epiphysiodesis (CBGE) may mitigate the effects of AVN after slipped capital femoral
epiphysis (SCFE). In one study, 17 patients (17 hips) had a scheduled MRI between 1 and 6 months from initial surgery. Six hips
diagnosed by MRI received surgical intervention (4 CBGE, 1 free vascularized fibula graft, and 1 repinning due to screw cutout)
at a mean of 4.1 months (range, 1.3 to 7.2 mo) postoperatively. None of the 4 patients treated with CBGE within 2 months
postoperatively progressed to stage IVC AVN.[12]
Similar sensitivity and specificity were found between low-field MRI and planar radionuclide bone scanning. At high magnetic
field strength, MRI has a higher sensitivity than radionuclide scanning. Using a 1.5-T magnet, Beltran et al reported 88%
sensitivity, 100% specificity, and 94% accuracy with MRI and 78% sensitivity, 75% specificity, and 76% accuracy with bone
scintigraphy.[13] The high sensitivity of MRI has been confirmed by others.
In another study, MRI performed at 0.6 T and single-photon emission CT (SPECT) bone imaging using technetium-99m (99mTc)
methylene diphosphonate (MDP) were similarly effective in diagnosing avascular necrosis.[14] MRI had a sensitivity of 87% and
a specificity of 83%; whereas SPECT scanning had a sensitivity of 91% and a specificity of 78%. Both were more effective than
planar bone scintigraphy, which had a sensitivity of 83% and a specificity of 83%. MRI was also more effective than SPECT for
diagnosing cases of avascular necrosis (AVN) of the hip in which pain was absent. MRI detected avascular necrosis (AVN) in 10
of 15 patients, but SPECT scanning detected AVN in only 5 of 15 patients. Using receiver operating characteristic (ROC) curves,
MRI was better than CT scanning by more than 2 standard errors and better than radionuclide scanning by more than 3
standard errors in helping diagnose early AVN.
Magnetic resonance perfusion imaging has been able to identify significant differences between avascular necrosis, bone
marrow edema, and subchondral insufficiency fractures of the proximal femur, particularly regarding maximum enhancement
values (Emax), slope (Eslope) and time to peak (TTP). Diffusion weighted imaging of bone marrow of the proximal femur did not
show significant differences in the same study.[15]
Gadolinium-enhanced perfusion MRI (pMRI) after closed reduction/spica casting for developmental dysplasia of the hip (DDH)
has been suggested as a potential means to identify and avoid avascular necrosis (AVN) by helping the surgeon evaluate
femoral head vascularity.[16]
Single-photon emission CT scanning
SPECT scanning provides images of the radioactivity within the target organ in 3 dimensions. With this modality, overlying and
underlying areas of radioactivity may be separated into sequential tomographic planes, thus providing increased image contrast
and improved lesion detection and localization, as compared with planar scintigraphy. SPECT scanning eliminates radioactivity
resulting from hyperemia about the hip joint and from the underlying acetabulum and adjacent bladder. SPECT scanning is used
as an alternative to MRI when MRI cannot be performed or when the results of MRI are indeterminate.[17]
Initially, SPECT images reflect vascular integrity; early in the disease, SPECT scans may demonstrate an avascular focus; such
findings are missed with MRI unless contrast is used. Collier et al found a sensitivity of 85% for SPECT scanning.[18] With
triple-head high-resolution SPECT scanning, Lee et al reported a sensitivity of 97%.[19]
Nuclear imaging
Planar radionuclide imaging, bone scintigraphy using pinhole collimation, and planar scintigraphic imaging using quantitative
bone scanning are briefly discussed below.[14, 17, 20, 21, 22, 23]
Collier reported a sensitivity of 55% with planar radionuclide imaging for AVN.[18] However, bone scintigraphy equipped with a
pinhole collimator has greater sensitivity for diagnosing AVN than bone scintigraphy using a high-resolution parallel-hole
collimator.
The pinhole collimator is a conical collimator with a small circular aperture (3-5 mm) that produces an inverted image of the
object in a manner analogous to photographic cameras. The image obtained is magnified, allowing better visualization of small
structures and improving detection of scintigraphic abnormalities. The pinhole collimator optimizes resolution in the evaluation of
circumscribed areas, and the acquisition time is only 15 minutes, compared to up to 45 minutes for SPECT scanning. The
technique is an alternative to MRI when MRI cannot be performed or when MRI results are not clear-cut.
Planar scintigraphic imaging using quantitative bone scanning provides physiologic data that cannot be obtained with other
modalities, including MRI; for example, this technique allows quantification of uptake in the perfusion and static phases.
However, correct computer programming is required.[24, 25]
In one study, F-18 fluoride PET/CT showed good agreement with MRI in the initial diagnosis of AVN and was better than MRI in
detecting early disease. MRI was 96.5% sensitive, 100% specific, and 98.03% accurate, while PET/CT was 100% sensitive,
100% specific, and 100% accurate in diagnosing AVN.[20]
In a comparative study of technetium-99m-methylene diphosphonate (99mTc-MDP) SPECT/CT versus planar bone scintigraphy
(BS) for diagnosis of AVN, SPECT/CT was found to be superior to planar BS and SPECT alone. The diagnostic accuracy of
planar BS, SPECT, and SPECT/CT was 67%, 78%, and 95%, respectively. Planar BS was found to have the lowest sensitivity
(75%) and specificity (40%), whereas SPECT/CT had the highest sensitivity (98%) and specificity (87%).[21]
CT scanning
The high spatial resolution and contrast resolution of CT scanning allow analysis of morphologic features (see the images
below), and the sensitivity of CT scanning in detecting early avascular necrosis is 55%, which is similar to the sensitivity of
planar nuclear medicine imaging. Thus, CT scanning is more appropriate in evaluating the extent of involvement, such as
subchondral lucencies and sclerosis during the reparative stage, before the onset of femoral head collapse and superimposed
degenerative disease.
Coronal multiplanar reconstructed computed tomography image in a patient without avascular necrosis of the femoral head.
Thickened trabeculae are seen at the medial aspect of the junction of the femoral head and neck and extend to the
subchondral region. The physis (arrowhead) is a transverse white line located between the lateral and medial aspect of the
femoral head.
Axial computed tomographh scan of a patient with avascular necrosis of the femoral head shows clumping and distortion of
the central trabeculae representing the asterisk sign (arrowhead) and an adjacent low-density region (arrow) representing the
reparative zone. See also the next image.
Axial computed tomography (CT) scan of a patient with avascular necrosis of the femoral head shows a fracture to the
anterior aspect of the femoral head. This finding was demonstrated on an axial fat-saturated T2-weighted magnetic
resonance image, but it is delineated more clearly using CT scanning because of the superior resolution of CT scanning. See
also the next image.
Axial computed tomography scan in a patient with avascular necrosis. This image shows joint space narrowing, juxta-articular
sclerosis, and osteophyte formation (degenerative joint disease) around the anteromedial and posterolateral aspects of the
right hip.
CT scanning is better able to help define the extent of disease at stages II and higher than MRI and plain film radiography. CT
scanning enables detection of subchondral or cancellous fractures and collapse, especially when multiplanar reconstruction is
used. This information is essential for planning treatment (see the third and fourth images above).
Plain film radiography
Although unable to detect disease of stage 0 or 1, plain film radiography may be helpful in assessing flattening of the femoral
head and associated degenerative changes (see the images below).
sign.
Anteroposterior view of the left hip in a patient with avascular necrosis obtained 6 months after presentation shows that the
patient has undergone core decompression but has developed mild flattening of the femoral head, indicating progression of
disease despite treatment.
Anteroposterior view of the pelvis in a patient with bilateral avascular necrosis of the femoral head. Mild flattening to the
superior aspect of the right femoral head (open arrow) indicates stage 3 disease. The left femoral head has a normal contour,
indicating stage 2 disease. The black arrows indicate the margins of the reparative zone, representing new bone formation on
dead trabeculae. When avascular necrosis is bilateral, it usually occurs in each hip at different times, and the staging of
disease in each hip can be, and often is, at different stages. See also the next image.
Plain film finding in a patient with bilateral avascular necrosis of the femoral head 6 months after presentation demonstrates
that subtle flattening of the left femoral head (open arrow) has occurred. This indicates progression of disease from stage 2 to
stage 3 despite conservative treatment. The patient underwent bilateral core decompression and bone grafting. The defects
within the proximal femurs represent removal of the dead bone, and the tubular densities within each femur represent bone
grafts in an attempt to revascularize the region of avascular necrosis.
Limitations of techniques
MRI
Bone biopsy analysis has been rarely reported to be positive when MRI findings are normal. MRI cannot be performed in
patients who have cardiac pacemakers or when intracranial clips are present, nor can MRI be performed in patients who have
claustrophobia. In addition, problems related to malpositioning may lead to misrepresentation. In children, slight pelvic obliquity
may cause the normal dark-appearing growth plate to appear in the same axial cut as the contralateral bright-appearing
epiphysis; in such cases, the normal growth plate may appear to be abnormal on MRI.
Children may require sedation as a result of the long imaging times that MRI requires. It may be difficult to detect AVN after
surgery to repair a hip fracture because of the presence of orthopedic hardware, which creates significant image distortion.
Marrow cells are more resistant to ischemia than hematopoietic cells or osteocytes. Because MRI images reflect changes within
marrow fat signal intensity, MRI findings of avascular necrosis may not be seen for up to 5 days after the ischemic event, until
the marrow fat cells have died. In this situation, contrast-enhanced MRI is needed.
SPECT scanning
SPECT scanning demonstrates poor spatial resolution. Artifacts from the bladder are frequently encountered; these artifacts
may obscure the photon-deficient region of the femoral head. A number of techniques, such as the use of multihead cameras
with shorter acquisition times that improve resolution and increase sensitivity, have been advocated, but none has gained
universal acceptance.
SPECT imaging requires a cooperative patient who must remain immobile for up to 45 minutes of acquisition time; thus, this
modality is difficult to use in children because of the necessity to remain motionless for long periods of time. Children may
require sedation. In addition, diagnosing Legg-Calve-Perthes (LCP) in small children may be difficult because of the small size
of the femoral epiphysis and associated bladder artifacts.
Planar scintigraphy
Planar scintigraphy demonstrates poor spatial resolution (see the following images). The ring of increased activity reflecting
hyperemia in the early stages and bone healing later obscures the photon-deficient necrotic center within the femoral head,
which is indicative of avascular necrosis. The site may show a uniform high level of activity, making it impossible to distinguish
AVN from other causes of increased activity, such as osteoarthritis, fracture, and inflammatory arthritis. A cold spot in the
femoral head is highly specific but not sensitive for diagnosing AVN.[6]
Bone scan of a patient with avascular necrosis of the femoral head shows increased uptake in the superolateral aspect of the
right femoral head, indicative of avascular necrosis but providing little information concerning the structural integrity of the hip.
Planar bone scan of the pelvis in a patient with bilateral avascular necrosis of the femoral head shows marked increased
uptake of radiopharmaceutical agent in both hips.
Artifacts from radioactivity in the bladder are frequently encountered, obscuring the photon-deficient region. Entities causing
increased uptake about the hip joint, such as arthritis and inflammatory disease, may obscure the photopenic necrotic focus
within the femoral head. Results can be judged only by comparison with the other hip and may be of little use in the presence of
bilateral involvement.
CT scanning
Although CT scanning may delineate subtle alterations of bone density when plain radiograph findings are normal, MRI and
SPECT scintigraphy are much more sensitive for evaluating early manifestations of the disease, such as bone marrow edema.
CT scans are insensitive for detecting stage 0 and 1 avascular necrosis, but they are excellent for detecting femoral head
collapse, early degenerative joint disease (DJD), and the presence of loose bodies.
CT scanning may improve the accuracy of radiographic staging using thin-slice thicknesses of 1 mm or less and by
incorporating multiplanar reconstruction. In one study, 30% of hips with stage 2 (precollapse) AVN, evaluated with plain film
radiography, had stage 3 disease when evaluated with CT scans.
Plain film radiography
Using plain film radiography, the sensitivity for detecting early stages of the disease is as low as 41%. Plain film does not detect
stage 0 and 1 avascular necrosis. A delay of 1-5 years may occur between the onset of symptoms and the appearance of
radiographic abnormalities. Normal radiographic findings do not necessarily mean that disease is not present.
Demineralization of the femur may be detected, and the disease may be suggested only after bone resorption has occurred. If
early diagnosis is needed for the prompt initiation of therapy, more sensitive imaging methods (ie, MRI) must be used, especially
in patients who are at increased risk for AVN.
Differential diagnosis and other problems to be considered

Bone metastases should be considered in the differential diagnosis as well as transient osteoporosis.[7] Other problems to be
considered when viewing findings on plain film radiographs, bone scintigraphs, CT scans, and MRIs are as follows:
Plain film radiograph
Malignancy
Osteomyelitis
Transient osteoporosis of the hip
Bone sarcoma
Advanced DJD (see the following image)
fracture. Therapeutic interventions are less likely to halt progression of the disease once this sign appears. The frogleg
lateral view is better than anteroposterior (AP) projection for demonstrating this sign, because the anterior and
posterior margins of the acetabulum on the AP projection are superimposed over the superior portion of the femoral
head, the usual location of the sign.
Insufficiency fractures
Epiphyseal dysplasia
Bone metastases
Bone scintigram
Infection
Plasma cell myeloma
Skeletal metastasis
Hemangioma
Radiation therapy
Arthritis
Sympathetic dystrophy
Bone marrow edema syndrome
Bone metastases
CT scan
Degenerative disease
Insufficiency fracture
Malignancy
Infection
Plasma cell myeloma
Bone metastases
MRI
Transient osteoporosis of the hip
Transient bone marrow syndrome
Bone bruise
Epiphyseal stress fracture
Infection
Infiltrative neoplasm
Insufficiency fracture
Bone metastases
Special concerns
Failure to diagnose such a potentially devastating condition as avascular necrosis in a young age group has the potential for
serious medical-legal repercussions. Malpractice settlements reflect compensation for a lifetime of a potentially compromised
lifestyle with much morbidity. Such settlements also reflect the cost of potential joint replacement and prosthesis failure.[7]
Diagnosing AVN as early as possible is imperative for a greater chance of success of conservative treatment. Patients who are
at high risk must be screened using MRI. Normal radiograph findings do not mean a normal hip. Failure to pursue this condition
with more aggressive imaging in a high-risk population can potentially lead to medical malpractice.
MRI has replaced bone marrow pressure, venography, and bone biopsy. These are invasive procedures that were highly
sensitive and specific for diagnosing avascular necrosis. They should be performed only when a high index of suspicion is
present and all tests are equivocal.
Radiography
Ficat and Arlet radiographic staging system for AVN
A staging system using radiographic findings was developed by Ficat and Arlet and has been used widely for treating avascular
necrosis (AVN).[26] However, their system has been supplanted by the classification system of Steinberg et al (see below),
which incorporates MRI and scintigraphic findings.[27]
Stage 0 (preclinical and preradiologic)
Avascular necrosis can be suggested only if it has already been diagnosed in the contralateral hip.
Stage 1 (preradiologic)
Since the advent of MRI, stage 1 AVN is defined by normal findings on radiographs and positive findings on MRI or bone
scintigraphy. Stage 1 represents the early resorptive stage. Late in this stage, plain radiographs may show minimal osteoporosis
and/or blurring and poor definition of the bony trabeculae. Osteoporosis appears when one third of the mineral content of bone
has been lost.
Stage 2 (reparative)
Stage 2 avascular necrosis represents the reparative stage before flattening of the femoral head occurs and may extend for
several months or longer. Demineralization is now evident; it is the first manifestation of the reparative stage, represents
resorption of dead bone, and may be generalized or patchy or appear in the form of small cysts within the femoral head.
Patchy sclerosis represents apposition of new bone on dead trabeculae and appears after demineralization develops, usually in
the superolateral aspect of the femoral head (see the images below). However, patchy sclerosis usually coexists with
demineralization, appearing as alternating regions of increased density and increased lucency. On radiographs, patchy sclerosis
appears as increased density and may be diffuse, focal, or in a linear arc, which is concave superiorly. The pattern
demonstrates alternating areas of lucency and sclerosis.
Anteroposterior view of the left hip in a patient with avascular necrosis demonstrates alternating regions of the sclerosis and
lucency within the superior aspect of the left femoral head (arrows), representing the reparative stage (stage 2) of avascular
necrosis. The lucent areas represent the site of resorption of necrotic marrow and trabecular. The sclerosis represents
apposition of new bone on dead trabeculae.
Anteroposterior view of the pelvis in a patient with bilateral avascular necrosis of the femoral head. Mild flattening to the
superior aspect of the right femoral head (open arrow) indicates stage 3 disease. The left femoral head has a normal contour,
indicating stage 2 disease. The black arrows indicate the margins of the reparative zone, representing new bone formation on
dead trabeculae. When avascular necrosis is bilateral, it usually occurs in each hip at different times, and the staging of
disease in each hip can be, and often is, at different stages. See also the next image.
Stage 3 (early collapse of the femoral head)
In stage 3 avascular necrosis (AVN), a linear subcortical lucency, representing a fracture line, is present immediately beneath
the articular cortex and may extend into the articular cartilage at the superolateral aspect of the femoral head. This is termed the
crescent sign and is best demonstrated on a frogleg view (see the images below). The subarticular cortex may remain attached
to the cartilage and is separated from the underlying femur by soft tissue, termed the eggshell sign. The femoral head initially
preserves its round appearance, but later, it demonstrates collapse. This may be indicated by joint-space widening.
sign.
An anteroposterior pelvic radiograph of a patient who complained of a short onset of right hip pain showing flattening of the
superolateral aspect (the weightbearing portion) of the right femoral head. There is a crescent-shaped density (arrow)
representing the femoral head surface on an underlying zone of decreased density underneath the crescent-shaped bone
representing demineralization. Such findings indicate advanced disease and are associated with poor outcomes.
Stage 4 (progressive degenerative disease)
Further flattening of the femoral head occurs with loss of its smooth convex contour in stage 4 avascular necrosis (AVN) (see
the following image). Ultimately, the superior femoral fragment, representing the articular surface and the immediate
subchondral bone, may become separated from the underlying femoral head or depressed and compacted into the femoral
head. Fragments of bone and cartilage may separate from the underlying femur, roam freely within the hip joint, and become
loose bodies.
Severe collapse and destruction of the femoral head leads to progressive degenerative joint disease (DJD) with joint-space
narrowing, marginal osteophyte formation, and subchondral cyst formation. Subchondral cysts can usually be differentiated from
the alternating sclerosis and the lucency of the reparative stage of avascular necrosis.
Atypical radiographic findings are seen in 18% of patients and those on steroid therapy. These findings consist of early joint-
space narrowing, often before the appearance of the crescent sign. Unless the physician holds a high index of suspicion for
AVN, an incorrect diagnosis of osteoarthritis will be made. Furthermore, signs of bone repair (sclerosis) may be absent; the first
radiologic manifestations may be the subchondral lucency representing fracture of the dead bone.
Atypical findings occur because bone formation is decreased in the presence of normal bone resorption; in this situation,
increased density within the femoral heads usually is a result of flattening from fracture and compression of the femoral head.
Steinberg et al's staging system for AVN
Steinberg et al proposed a 6-stage classification system based on that of Ficat and Arlet and included radiologic clinical
classification findings[27] :
Stage 0
This stage is both preclinical and preradiologic. Most patients with stage 0 disease are identified when imaging is performed to
evaluate avascular necrosis (AVN) in the contralateral hip or to exclude other diseases. Abnormal MRI findings, normal
radiographic findings, and normal bone scan findings are features of stage 0.
Stage 1
Stage 1 avascular necrosis demonstrates normal radiographic findings or shows minimal demineralization or blurred trabeculae.
Pain in the anterior groin or thigh is common. Limited range of motion (ROM) in the hip may be present. Abnormal bone scan
findings, mild groin pain, and normal radiographic findings are features of stage 1.
Stage 2
This stage shows diffuse or localized areas of sclerosis, lucencies, or both within the femoral head. Clinical signs persist or
worsen. Osteoporosis, groin pain, and mottled sclerotic and/or cystic areas are features of stage 2 AVN.
Stage 3
Stage 3 AVN is characterized by the crescent sign (subchondral fracture). A crescent line, pain with subchondral fracture
activity, and no femoral head flattening are features of stage 3.
Stage 4
This stage demonstrates marked collapse and fracture involving the articular surface. Segmental flattening of the femoral head
demonstrates an out-of-round appearance. Thus, segmental flattening, pain with femoral head activity, no acetabular
involvement, and normal joint space are features of stage 4 AVN.
Stage 5
Stage 5 AVN is characterized by the development of DJD. Thus, joint space narrowing, resting pain, and acetabular
degeneration (DJD) are features of stage 5.
Advanced staging of AVN using plain radiography
The Association Research Circulation Osseous (ARCO) of the Toulouse, France-based Association Internationale de
Recherche sur la Circulation Osseuse has proposed a further classification of the various stages of avascular necrosis (AVN),
which incorporates the percentage (area) of involvement of the femoral head and the location of the lesion. In addition, the
extent of the AVN lesion is an important determinant of both clinical and radiologic outcomes.
Three types of involvement have been identified: mild, moderate, and severe. In mild disease, less than 15% of the femoral
head involvement is noted, which is less likely to demonstrate radiographic progression or require hip prosthesis. In moderate
disease, the femoral head involvement ranges from 15 to 30%. In severe disease, the femoral head involvement is greater than
30%. Moderate and severe involvement are more likely to progress radiographically to degenerative disease and to require hip
prosthesis placement.
Degree of confidence
Demineralization
Demineralization is a nonspecific finding seen in a large number of different diseases. Such a finding needs further evaluation
using MRI to evaluate for avascular necrosis.
Alternating areas of lucency and sclerosis
This feature is characteristic of stage 2 disease avascular AVN. Rarely, this finding is confused with entities such as
chondroblastoma, a radiolucent cartilaginous tumor that contains calcium and is located in the epiphyseal region. If there are
questions concerning the presence of the disease, MRI is recommended. If not, treatment can be initiated.
DJD
DJD with degenerative spurring and joint space narrowing with subchondral cyst formation may mimic avascular necrosis.
Subchondral cysts are usually immediately adjacent to areas of joint-space narrowing and osteophyte formation. MRI is usually
diagnostic in problematic cases. Rarely, biopsy may be needed for differentiation.
False positives/negatives
Some radiologic features of avascular necrosis may lead to false-positive findings.
Poorly defined radiolucent lesions may simulate the bone destruction seen in malignancy, osteomyelitis, and transient
osteoporosis of the hip (TOP). For malignancy and osteomyelitis, the history may be helpful.
Demineralization can be seen in a number of different diseases, including TOP. TOP is self-limiting and resolves within 4-10
months. Radiologic resolution lags behind clinical improvement by 4-8 weeks, at which time radiographic findings revert to
normal. The healing and reparative phase may mimic bone sarcoma.
The later stages of AVN, which are characterized by joint-space narrowing, articular cartilage destruction, and alternating areas
of lucency and sclerosis within the femoral head, may mimic DJD with subchondral cyst formation (see the following images).
sign.
Anteroposterior plain film of the pelvis in a patient with avascular necrosis of the femoral head shows asymmetric joint-space
narrowing (arrow), juxta-articular sclerosis, and subchondral cyst formation around the right hip secondary to degenerative
joint disease. This may be confused with avascular necrosis, but the intimate localization of all of the bindings and the
absence of femoral head collapse makes a diagnosis of avascular necrosis highly unlikely.
Sclerosis adjacent to an insufficiency fracture is an important differential, especially in patients who are osteopenic and are
taking steroids.
Computed Tomography
CT scans do not demonstrate the early vascular and marrow abnormalities that result in osteonecrosis.[28] In fact, osteoporosis
is the first visible CT scan sign of avascular necrosis. Later, the central bony asterisk is distorted, appearing as clumping and
fusion of the peripheral asterisk rays. Clumping appears as spots or as hyperdense "roads" of various width (see the following
image). This represents changes in the sclerotic interface between necrotic and viable bone and is analogous to the line of low
signal surrounding the necrotic bone seen on MRI images.
Axial computed tomographh scan of a patient with avascular necrosis of the femoral head shows clumping and distortion of
the central trabeculae representing the asterisk sign (arrowhead) and an adjacent low-density region (arrow) representing the
reparative zone. See also the next image.
Early signs are caused by microfractures resulting from reduced mechanical load of dead bone trabeculae, altering the shape of
the asterisk and are related to new bone formation on the dead trabeculae. The lucent cystic region, representing the reparative
zone, may be appreciated (see the image above).
Osteoporosis, whether diagnosed using plain film radiography or CT scanning, must be evaluated further, because it is present
in a great number of diseases. MRI findings are usually diagnostic.
Unless the asterisk sign is appreciated, articular surface abnormalities may be interpreted as DJD. The lucency within the
reparative zone may be confused with malignancy, infection, insufficiency fracture, or plasma cell myeloma.
Magnetic Resonance Imaging

When using MRI to evaluate avascular necrosis, the coronal plane is the most important imaging plane, and sagittal images
may help eliminate partial-volume averaging, which is especially present on axial images. When the lesion is located
anterosuperiorly, off-coronal images, angled toward the axial plane, may better demonstrate AVN.[29, 30, 31]
Because both hips are often involved in AVN and because the condition is silent early in the course of the disease, use of a
body coil and a large field of view (30-40 cm) is necessary to image both hips simultaneously. Surface coils, including shoulder
coils, flexible coils, and phased-array coils, may provide additional resolution for individual hip joints in selected patients. T1WIs
and T2WIs are obtained in the coronal plane, 4-mm thick, with a 1-mm gap. Fast spin-echo (FSE) images with fat saturation
may also be obtained.
Short tau inversion recovery (STIR) images provide excellent fat suppression and demonstrate areas of bone marrow edema
(see the images below). STIR images may be obtained using FSE techniques with an echo train length of 8-16. This helps
reduce lengthy imaging times associated with STIR imaging.
Coronal fat-saturated T2-weighted magnetic resonance image in a patient with avascular necrosis shows increased signal
within the femoral head and neck (arrow), representing edema. Short tau inversion recovery (STIR) and fat-saturated imaging
are excellent for demonstrating this finding. See also the next image.
Axial fat-saturated T2-weighted magnetic resonance image in a patient with avascular necrosis demonstrates a joint effusion
(arrow) and the extensive abnormal increased signal representing edema within the femoral head. A fracture in the anterior
aspect of the femoral head is present. See also the next image.
Coronal T1-weighted magnetic resonance image (MRI) in a patient with avascular necrosis shows decreased signal within the
femoral head (arrow), representing edema. This is an MRI class C lesion. The subchondral abnormality can also indicate a
fracture. Multiplanar reconstructed computed tomography scanning would be helpful for further investigation.
A frequency selective pulse may be added to suppress the fat signal. When applied, the inner bright line on T2WIs is visualized,
but the dark outer peripheral band is not seen. Nevertheless, FSE T2WIs with fat suppression are useful in demonstrating the
extent of marrow edema associated with AVN.
Rapidly acquired MRI sequences can reliably reveal the presence of avascular necrosis. These rapid screening sequences
reduce or eliminate artifacts caused by patient motion. Coronal 2-dimensional (2-D), fast, low-angle shot (FLASH) T1WIs are
performed using repetition time (TR), 174.9 milliseconds (ms); echo time (TE), 4.1 ms; flip angle, 70°; 4-mm slice thickness with
20% interslice gap; matrix, 172 × 256; number of signal acquisitions, 1; and imaging time, 39 seconds (s). Axial fat-suppressed
FSE T2WIs are performed using TR, 3500 ms; TE, 138 ms; echo train length, 29; 6-mm slice thickness with 25% interslice gap;
matrix, 116 × 256; number of signal acquisitions, 1; and imaging time, 16 s.
Chemical shift imaging may be used to detect premature fatty marrow conversion associated with AVN. Fatty and hematopoietic
marrow and the distribution of water within the ischemic focus can be differentiated on fat-selective and water-selective images.
Gradient-echo images are not as sensitive for fluid within reparative tissue, but they can demonstrate joint effusions,
subchondral fluid, and changes in the contour of the articular cartilage.
NOTE: Screening for avascular necrosis using T1WI only reduces specificity, may fail to identify a transchondral fracture, and
may not help diagnose other diseases in which clinical presentation may mimic AVN, including transient osteoporosis.
Khanna et al described a limited magnetic resonance examination using coronal T1WIs, in which MRI introduction earlier in the
diagnosis of femoral head osteonecrosis, as well as its more widespread use in patient care, may be allowed because of the
time and the potential cost reduction achieved with a limited examination.[32] The investigators also reported excellent
agreement between the full and the screening MR examinations for both detecting and determining the extent of osteonecrosis.
In the Khanna study, only one case of AVN was missed in 29 patients, and the time required for the limited exam was 10
minutes relative to the 30 minutes required for the full examination.[32] Without calculating the professional component, relative
costs of the screening evaluation was $104, whereas the full assessment was $312. However, other diseases causing hip pain
(eg, myositis, greater trochanteric bursitis, labral cysts, and fractures) that were located distant from the femoral heads were
missed when T2WIs were not obtained.[32] Perhaps there may be a role for the limited exam in following up bone marrow
edema in asymptomatic patients.
T1WI findings
A peripheral band of low signal is present in the superior portion of the femoral head outlining a central area of bone marrow.
This is considered to represent the reactive interface between the necrotic and reparative zones and extends to the subchondral
bone plate (see the images below, 2 of which are followed by T2WI images in the same respective patients).
Coronal T1-weighted magnetic resonance image of the pelvis in a patient with avascular necrosis of the left femoral head
shows a mixed pattern of abnormal signal within the femoral head. The medial aspect consists predominantly of high signal
representing blood. The superior portion demonstrated low signal, representing edema. In this patient, the dominant signal is
edema.
Coronal T1-weighted magnetic resonance image of the pelvis in a patient with bilateral avascular necrosis of the femoral head
demonstrates decreased signal within the right femoral head, representing fluid, and increased signal within the left femoral
head, representing blood. Differences in signal intensity between the femoral heads in patients with bilateral avascular
necrosis are common and reflect the fact that, although prone to bilateral disease, onset in each hip occurs separately and
progresses at a different rate. See also the next image.
shows decreased signal within the right femoral head, representing fluid, and increased signal within the left femoral head,
representing blood. The right hip has a class C lesion, and the left hip has a class B lesion.
A coronal T1-weighted magnetic resonance image of a patient who complained of a short onset of right hip pain. There is now
diffuse low signal involving the lateral aspect of the right femoral head. See also the next image.
A coronal FS T2-weighted magnetic resonance image (MRI) taken 2 years later from a patient who complained of a short
onset of right hip pain. There is diffuse marrow edema (bright white signal) in the right femoral neck and head. There is also a
focus of decreased (dark) signal in the superomedial aspect of the right femoral head, probably related to fibrous tissue.
There is now a well-defined focus of dark signal indicating avascular necrosis of the left femoral head (arrow). There is no
double line sign, which is often the case on FS T2-weighted MRIs. A frequency selective pulse was not used.
T2WI findings
The inner border of the peripheral band demonstrates high signal. This may represent chemical shift artifact, because the
position of the signal changes when the phase and frequency directions are changed. This is termed the double-line sign and is
pathognomonic for avascular necrosis (see the first image below). It is present in 80% of cases. This is not demonstrated well
on FSE T2WIs because of the increased signal intensity of fat, present on this sequence, which obscures the bright inner line
(see the second image below). To compensate, a frequency selective pulse is added to suppress the signal from fat. If fat
suppression is used, the dark outer peripheral band of AVN is not demonstrated well, in contrast to the inner high-signal band
visualized on this sequence. The outer low-signal ring represents the interface of repair tissue with the necrotic zone.
Coronal T2-weighted magnetic resonance image in a patient with avascular necrosis of the femoral head shows the double-
line sign within the left femoral head, which is pathognomonic for avascular necrosis. The inner margin of the border of the
abnormality is believed to represent a chemical shift artifact.
Use of contrast enhancement
If intravenous contrast is used to supplement the MRI examination, areas of decreased enhancement indicate early AVN despite
normal findings on pre-enhancement images.[33] Contrast enhancement is useful for distinguishing viable from nonviable
trabeculae and marrow. Nonviable tissue does not enhance after contrast administration. Enhancement of the low-signal band
on T1WIs corresponds to the reparative zone.
Atypical MRI findings
Avascular necrosis occasionally appears as an area of abnormal signal involving the femoral head, neck, and intertrochanteric
region. It is characterized by decreased signal on T1WIs and increased signal on T2WIs without the focal lesions that are
pathognomonic for AVN. This is termed the bone marrow edema pattern, as the signal characteristics are consistent with
increased free water or edema within the normal fatty marrow of the proximal femur. This may reflect early edema before the
onset of focal abnormalities and may indicate the time period between cell death and development of a significantly large
reactive interface, which is recognizable as AVN on MRIs.
Differentiation between transient and irreversible AVN lesions
When using subchondral marrow changes on T2WIs or contrast-enhanced T1WIs to differentiate transient from irreversible AVN
lesions, the absence of low-signal subchondral lesions and subchondral deformities in the presence of the bone marrow edema
pattern represents transient osteoporosis. Areas of low signal intensity in the subchondral region and contour deformities of the
femoral head are typical of AVN.
Associated MRI findings
Fatty conversion of marrow is a prerequisite for developing AVN of the femoral head, a finding that may help identify populations
at increased risk for developing the disease. Subchondral fractures may appear as a low signal intensity gap on T1WIs; on
T2WIs, they can appear as regions of high signal intensity, representing fluid within the fracture line. Joint effusions are present
in 50% of patients (see the following images).
AVN classification per central avascular segment signal alterations
The avascular necrosis lesion is classified into 4 types according to alterations in the central avascular segment signals on MRI.
[27]
Class A
In class A AVN, central osteonecrotic focus signal analogous to that of fat is noted. Increased signal is demonstrated on T1WIs,
and intermediate to high signal is demonstrated on T2WIs (see the image below).
Coronal T1-weighted magnetic resonance image (MRI) of the pelvis in a patient with avascular necrosis of the femoral head
shows increased signal within the superior aspect of the femoral head, representing fat. This is an MRI class 1 hip. These
patients may have more than one type of signal within the abnormal avascular area. In this situation, the most dominant
signal is used for MRI classification.
Class B
In class B AVN, the presence of central osteonecrotic focus signal analogous to that of blood is observed. Increased signal is
demonstrated on both T1WIs and T2WIs (see the following images).
demonstrates decreased signal within the right femoral head, representing fluid, and increased signal within the left femoral
head, representing blood. Differences in signal intensity between the femoral heads in patients with bilateral avascular
necrosis are common and reflect the fact that, although prone to bilateral disease, onset in each hip occurs separately and
progresses at a different rate. See also the next image.
shows decreased signal within the right femoral head, representing fluid, and increased signal within the left femoral head,
representing blood. The right hip has a class C lesion, and the left hip has a class B lesion.
Class C
In class C AVN, central osteonecrotic focus signal analogous to that of fluid is present. Decreased signal is demonstrated on
T1WIs, and increased signal is demonstrated on T2WIs (see the 2 images above, and the images below).
Coronal T1-weighted magnetic resonance image of the pelvis in a patient with avascular necrosis of the left femoral head
shows a mixed pattern of abnormal signal within the femoral head. The medial aspect consists predominantly of high signal
representing blood. The superior portion demonstrated low signal, representing edema. In this patient, the dominant signal is
edema.
Coronal T1-weighted magnetic resonance image (MRI) of the pelvis in a patient with avascular necrosis of the femoral head
shows increased signal within the superior aspect of the femoral head, representing fat. This is an MRI class 1 hip. These
patients may have more than one type of signal within the abnormal avascular area. In this situation, the most dominant
signal is used for MRI classification.
Class D
In class D AVN, the presence of central osteonecrotic focus signal analogous to that of fibrous tissue is noted. Decreased signal
is demonstrated on both T1WIs and T2WIs.
MRI staging, symptoms, and prognostic correlations
Correlations between MRI staging and radiographic staging, MRI class and clinical symptoms, and MRI findings and prognosis
are outlined in this section.[27]
Correlation between MRI and radiographic staging
MRI classes A and D show the best correlation with radiographic staging.
Approximately 50% of radiographic stage 1 and 83% of radiographic stage 2 lesions demonstrate MRI class A signal
pattern.
In femoral heads complicated by fracture (radiographic stages 3 and 4), only 14% are MRI class A and 43% MRI class B.
MRI class B and C lesions correlate poorly with radiographic staging.
Correlation between MRI class and clinical symptoms
Of patients with MRI class A lesions, 54% are asymptomatic.
Of patients with MRI classes B and C lesions, 11% are asymptomatic.
Of patients with MRI class D lesions, 67% are asymptomatic.
Correlation between MRI findings and prognosis
MRI classes, unlike radiographic stages, have little predictive value regarding prognosis for femoral head collapse. Entirely
circumscribed AVN that did not extend to the subchondral margin had a good outcome, independent of the overall size of the
lesion. The percentage of the weightbearing surface occupied by the lesion was the most reliable factor in predicting outcome.
Basing outcome on overall extent of involvement of the femoral head on MRI is controversial. Lafforgue et al evaluated 3
different means of determining femoral head involvement and found that the percentage of weightbearing femoral cortex
involved with AVN was the most reliable parameter in determining outcomes.[34] Beltran et al found that femoral head collapse
occurs in most patients with a large area of avascular necrosis (AVN) before the appearance of a subchondral fracture, even if
core decompression is performed.[35] Using MRI, the investigators determined femoral head collapse did not occur when less
than 25% of the weightbearing surface was involved.
Femoral head collapse tendency and MRI lesion size
Tendency toward femoral head collapse in relation to AVN lesion size as demonstrated on MRI is in agreement with the
quantitative radiographic staging of Steinberg et al.[27, 36, 32, 37, 34, 38, 39, 40, 41, 42] Small lesions confined to the medial
anterosuperior portion of the femoral head tended not to collapse over a 28-month follow-up period. However, more extensive
lesions collapse, with a 50% collapse rate within 12 months. Shimizu et al found a 74% rate of femoral head collapse by 32
months if the region of AVN involved more than two thirds of the weight-bearing surface area.[43]
Degree of confidence
MRI has a high sensitivity in the diagnosis of bone marrow abnormalities; the sensitivity of MRI in the diagnosis of avascular
necrosis (AVN) is 85-100%. MRI has a 97% sensitivity in distinguishing a hip with AVN involvement from a normal hip. In
differentiating AVN from non-AVN disease of the femoral head, MRI demonstrates a sensitivity of 98% and a specificity of 85%.
Before femoral head collapse, the specificity is 75-100%. After femoral head collapse, the sensitivity is 100%.
In a retrospective analysis of the possible predictive ability of contrast-enhanced MRI for AVN after closed reduction for
developmental dysplasia of the hip (DDH) in infants, Tiderius et al suggested that gadolinium-enhanced MRI provides accurate
anatomic assessment of a closed reduction in DDH as well as information about femoral head perfusion that may be predictive
for future AVN.[44] Multivariate logistic regression indicated that a global decreased enhancement was associated with a
significantly higher risk of developing AVN.[44] However, the authors noted that further investigation is required before perfusion
information can be used for routine clinical use.
Bone marrow edema
Bone marrow edema is a nonspecific finding seen in avascular necrosis and other conditions that may progress to frank AVN
(see the images below).
A coronal T2-weighted magnetic resonance image of a patient who complained of a short onset of right hip pain. The study is
normal. See also the next image.
A coronal T1-weighted magnetic resonance image of a patient who complained of a short onset of right hip pain. There is now
diffuse low signal involving the lateral aspect of the right femoral head. See also the next image.
Transient osteoporosis of the hip (TOP)
TOP is a self-limiting condition characterized by osteoporosis of the femoral head and, occasionally, the femoral neck. TOP
resolves over a 4- to 10-month period, and it does not progress to avascular necrosis. TOP often can appear on both sides of
the hip joint, differentiating it from AVN. Similar findings can develop in the contralateral hip or other joints, in which case it is
termed regional migratory osteoporosis. TOP occurs in patients without the risk factors for AVN.
Transient bone marrow syndrome
Transient bone marrow syndrome is similar to TOP, but osteoporosis is never present radiographically. Symptoms are self-
limiting, and it occurs in patients who have no risk factors for AVN.
Bone bruise
A bone bruise is usually self-limiting and resolves over time. If bone marrow edema is present on MRI, plain radiography is
obtained. If plain film findings are normal, radiography should be repeated within 4-6 weeks. If osteoporosis is detected, it is
believed to represent TOP. If osteoporosis is absent, patients may be placed into groups with and without high-risk factors for
developing AVN. Patients with factors indicating a low index of suspicion can be treated conservatively, but plain radiography
and MRI follow-up imaging should be performed. High-risk patients should be considered candidates for surgical intervention.
Subchondral fracture
An area of increased signal on T2WIs in the subchondral zone may represent fracture or edema. To accurately stage the
disease, CT scans are helpful in differentiating the 2 conditions. Yeh et al determined that the accuracy of routine MRI was not
satisfactory when compared with CT scanning in identifying subchondral fracture in avascular necrosis (AVN). A false-positive
diagnosis was not uncommon. Therefore, the investigators suggested the interpretation of routine MR imaging readout should
be guarded.[45]
False positives/negatives
False-negative MRI diagnosis may be related to the use of T1WIs only. These images are less sensitive to detecting the bone
marrow edema pattern of early avascular necrosis. This is detected better using T2WIs or STIR images.[31]
Nuclear Imaging
SPECT scanning
A cold spot (photon-deficient region) within the femoral head is highly specific for avascular necrosis and is the earliest
scintigraphic evidence of this disease. The finding is usually seen 7-10 days after the ischemic event.
Over a period of weeks to months, increased uptake representing revascularization and repair surrounds and eventually
replaces the region of photopenia. The central region of photopenia with surrounding zone of increased uptake is termed the
doughnut sign.
Perfusion and static planar radionuclide imaging
Initially, uptake is decreased in the perfusion and static phases, which represents the early ischemic event. Later, uptake is
decreased within the femoral head in the perfusion phase and increased around the cold region in the static phase. The latter
represents the reactive zone around the infarcted segment. The increased uptake from the reparative zone eventually replaces
the photopenic region.
A cold spot can be seen in other conditions, such as infection, metastasis, joint effusion, and plasma cell myeloma. Spencer et
al reported that not all adults take up radiopharmaceutical agents in the femoral head. As a result, MRI is needed for
confirmation.[46]
Hungerford reported false-negative bone scans in the hips of 14 of 27 patients, 13 of whom had bilateral disease.[47] In patients
with bilateral involvement, the uptake, although symmetric, really is increased bilaterally. If the uptake is asymmetric, the side
affected more severely makes the less-involved side appear falsely normal.
Later in the course of the disease, between the time of infarct and revascularization, the scan appears falsely normal in 6-10%
of patients, or it demonstrates a pattern of uptake that cannot be differentiated from DJD.
Decreased uptake, indicative of early avascular necrosis, can also be seen in infection, plasma cell myeloma, skeletal
metastasis, hemangioma, and radiation therapy.
Increased uptake alone can be seen in arthritis, sympathetic dystrophy, malignancy, infection, transient osteoporosis of the hip
(TOP), hemangioma, and insufficiency fractures. TOP can cause increased uptake on both sides of the hip joint.
Guidelines
Guidelines Summary
Radiographic findings are unremarkable in early stages of AVN. Nevertheless, the American College of Radiology (ACR)
considers radiographs of the pelvis and hips the most appropriate initial imaging study in patients at risk for AVN who present
with hip pain. If radiographs are normal or show femoral head lucencies suspicious for osteonecrosis, magnetic resonance
imaging (MRI) of the hips without contrast is most appropriate.[5]
The ACR advises that MRI is the most sensitive and specific imaging modality for diagnosis and provides optimal evaluation of
the likelihood of articular collapse. Involvement of greater than 30-50% of the femoral head, often in the sagittal plane, indicates
significantly increased risk of articular collapse.
Additional ACR recommendations include the following[5] :
Contrast-enhanced MRI may be needed to detect early osteonecrosis of the hip in pediatric patients, which is indicated
by hypoperfusion
In patients with a contraindication for MRI, alternative imaging modalities are computed tomography (CT) or bone
scintigraphy with single-photon emission CT (SPECT)
Contributor Information and Disclosures
Author
Michael R Aiello, MD Locum Tenens Radiologist
Michael R Aiello, MD is a member of the following medical societies: American College of Radiology, Society of Interventional
Radiology, Society of Breast Imaging, American Institute of Ultrasound in Medicine, American Medical Association, Radiological
Society of North America
Disclosure: Nothing to disclose.
Specialty Editor Board
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District
Health Board, New Zealand
Lynne S Steinbach, MD Professor of Radiology and Orthopedic Surgery, University of California, San Francisco, School of
Medicine
Lynne S Steinbach, MD is a member of the following medical societies: American College of Radiology, International Skeletal
Society, Radiological Society of North America
Chief Editor
Felix S Chew, MD, MBA, MEd Professor, Department of Radiology, Vice Chairman for Academic Innovation, Section Head of
Musculoskeletal Radiology, University of Washington School of Medicine
Felix S Chew, MD, MBA, MEd is a member of the following medical societies: American Roentgen Ray Society, Association of
University Radiologists, Radiological Society of North America
Additional Contributors
David S Levey, MD Musculoskeletal and Neurospinal Forensic Radiologist; President, David S Levey, MD, PA, San Antonio,
Texas
David S Levey, MD is a member of the following medical societies: American Roentgen Ray Society, Bexar County Medical
Society, Forensic Expert Witness Association, International Society of Forensic Radiology and Imaging, International Society of
Radiology, Technical Advisory Service for Attorneys, Texas Medical Association
References
1. Karantanas AH. Accuracy and limitations of diagnostic methods for avascular necrosis of the hip. Expert Opin Med Diagn. 2013 Mar.
7 (2):179-87. [Medline].
2. Manenti G, Altobelli S, Pugliese L, Tarantino U. The role of imaging in diagnosis and management of femoral head avascular
necrosis. Clin Cases Miner Bone Metab. 2015 Jan-Apr. 12 (Suppl 1):31-8. [Medline].
3. Barille MF, Wu JS, McMahon CJ. Femoral head avascular necrosis: a frequently missed incidental finding on multidetector CT. Clin
Radiol. 2014 Mar. 69 (3):280-5. [Medline].
4. Shah KN, Racine J, Jones LC, Aaron RK. Pathophysiology and risk factors for osteonecrosis. Curr Rev Musculoskelet Med. 2015
Sep. 8 (3):201-9. [Medline].
5. Murphey MD, Roberts CC, Bencardino JT, Appel M, Arnold E, Chang EY, et al. ACR Appropriateness Criteria Osteonecrosis of the
Hip. J Am Coll Radiol. 2016 Feb. 13 (2):147-55. [Medline].
6. Agrawal K, Marafi F, Gnanasegaran G, Van der Wall H, Fogelman I. Pitfalls and Limitations of Radionuclide Planar and Hybrid Bone
Imaging. Semin Nucl Med. 2015 Sep. 45 (5):347-72. [Medline].
7. Ando W, Yamamoto K, Koyama T, Hashimoto Y, Tsujimoto T, Ohzono K. Radiologic and Clinical Features of Misdiagnosed Idiopathic
Osteonecrosis of the Femoral Head. Orthopedics. 2017 Jan 1. 40 (1):e117-e123. [Medline].
8. Boraiah S, Dyke JP, Hettrich C, Parker RJ, Miller A, Helfet D, et al. Assessment of vascularity of the femoral head using gadolinium
(Gd-DTPA)-enhanced magnetic resonance imaging: a cadaver study. J Bone Joint Surg Br. 2009 Jan. 91(1):131-7. [Medline].
9. Theysohn JM, Kraff O, Theysohn N, Orzada S, Landgraeber S, Ladd ME, et al. Hip imaging of avascular necrosis at 7 Tesla
compared with 3 Tesla. Skeletal Radiol. 2014 May. 43 (5):623-32. [Medline].
10. Ficat RP, Arlet J. Functional investigation of bone under normal conditions. In: Hungerford DS, ed. Ischemia and Necrosis of Bone.
Baltimore:. Lippincott Williams & Wilkins. 1980:29.
11. Manaster BJ. From the RSNA Refresher Courses. Radiological Society of North America. Adult chronic hip pain: radiographic
evaluation. Radiographics. 2000 Oct. 20 Spec No:S3-S25. [Medline].
12. Napora JK, Gilmore A, Son-Hing JP, Grimberg DC, Thompson GH, Liu RW. Early MRI Detection and Closed Bone Graft
Epiphysiodesis May Alter the Course of Avascular Necrosis Following Unstable Slipped Capital Femoral Epiphysis. J Pediatr Orthop.
2016 Jun 2. [Medline].
13. Beltran J, Burk JM, Herman LJ, et al. Avascular necrosis of the femoral head: early MRI detection and radiological correlation. Magn
Reson Imaging. 1987. 5(6):431-42. [Medline].
14. Oshima M, Yoshihasi Y, Ito K, et al. Initial stage of Legg-Calve-Perthes disease: comparison of three-phase bone scintigraphy and
SPECT with MR imaging. Eur J Radiol. 1992 Sep. 15(2):107-12. [Medline].
15. Mueller D, Schaeffeler C, Baum T, Walter F, Rechl H, Rummeny EJ, et al. Magnetic resonance perfusion and diffusion imaging
characteristics of transient bone marrow edema, avascular necrosis and subchondral insufficiency fractures of the proximal femur.
Eur J Radiol. 2014 Oct. 83 (10):1862-9. [Medline].
16. Gornitzky AL, Georgiadis AG, Seeley MA, Horn BD, Sankar WN. Does Perfusion MRI After Closed Reduction of Developmental
Dysplasia of the Hip Reduce the Incidence of Avascular Necrosis?. Clin Orthop Relat Res. 2016 May. 474 (5):1153-65. [Medline].
17. Collier BD, Krasnow AZ, Hellman RS. SPECT bone scanning. In: Collier BD, Fogelman I, Rosenthal L, eds. Skeletal Nuclear
Medicine. St. Louis, Mo:. Mosby. 1996.
18. Collier BD, Carrera GF, Johnson RP, et al. Detection of femoral head avascular necrosis in adults by SPECT. J Nucl Med. 1985 Sep.
26(9):979-87. [Medline].
19. Lee MH, Moon DH, Na HW. Diagnosis of femoral head avascular necrosis by triple head high resolution. J Nucl Med. 1992. 33:936.
20. Gayana S, Bhattacharya A, Sen RK, Singh P, Prakash M, Mittal BR. F-18 fluoride positron emission tomography/computed
tomography in the diagnosis of avascular necrosis of the femoral head: Comparison with magnetic resonance imaging. Indian J Nucl
Med. 2016 Jan-Mar. 31 (1):3-8. [Medline].
21. Agarwal KK, Mukherjee A, Sharma P, Bal C, Kumar R. Incremental value of 99mTc-MDP hybrid SPECT/CT over planar scintigraphy
and SPECT in avascular necrosis of the femoral head. Nucl Med Commun. 2015 Oct. 36 (10):1055-62. [Medline].
22. Thrall JH, Ziessman HA. The skeletal system. Thrall JH, Ziessman HA, eds. Nuclear Medicine: The Requisites. 2nd ed. St Louis,
Mo: Mosby; Mosby. 2001: 133.
23. Kubota S, Inaba Y, Kobayashi N, Tateishi U, Ike H, Inoue T, et al. Prediction of femoral head collapse in osteonecrosis using 18F-
fluoride positron emission tomography. Nucl Med Commun. 2015 Jun. 36 (6):596-603. [Medline].
24. Hofman S, Staudennkerg A, Breitenseker M, et al. Diagnostic patterns for bone marrow edema syndrome and avascular necrosis of
the femoral head in dynamic bone scintigraphy. Nucl Med Commentary. 1997. 18 (12):1178.
25. Maillefert JF, Toubeau M, Piroth C, et al. Bone scintigraphy equipped with a pinhole collimator for diagnosis of avascular necrosis of
the femoral head. Clin Rheumatol. 1997 Jun. 16(4):372-7. [Medline].
26. Ficat RP, Arlet J. Necrosis of the femoral head. In: Hungerford DS, ed. Ischemia and Necrosis of Bone. Lippincott Williams & Wilkins.
1980:171.
27. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br. 1995 Jan.
77(1):34-41. [Medline].
28. Sarikaya I, Sarikaya A, Holder LE. The role of single photon emission computed tomography in bone imaging. Semin Nucl Med.
2001 Jan. 31(1):3-16. [Medline].
29. Lee GC, Steinberg ME. Are we evaluating osteonecrosis adequately?. Int Orthop. 2012 Dec. 36(12):2433-9. [Medline]. [Full Text].
30. Karantanas AH, Drakonaki EE. The role of MR imaging in avascular necrosis of the femoral head. Semin Musculoskelet Radiol.
2011 Jul. 15(3):281-300. [Medline].
31. Gruson KI, Kwon YW. Atraumatic osteonecrosis of the humeral head. Bull NYU Hosp Jt Dis. 2009. 67(1):6-14. [Medline].
32. Khanna AJ, Yoon TR, Mont MA, Hungerford DS, Bluemke DA. Femoral head osteonecrosis: detection and grading by using a rapid
MR imaging protocol. Radiology. 2000 Oct. 217(1):188-92. [Medline].
33. Lee JH, Dyke JP, Ballon D, Ciombor DM, Tung G, Aaron RK. Assessment of bone perfusion with contrast-enhanced magnetic
resonance imaging. Orthop Clin North Am. 2009 Apr. 40(2):249-57. [Medline]. [Full Text].
34. Lafforgue P, Dahan E, Chagnaud C, et al. Early-stage avascular necrosis of the femoral head: MR imaging for prognosis in 31 cases
with at least 2 years of follow-up. Radiology. 1993 Apr. 187(1):199-204. [Medline].
35. Beltran J, Knight CT, Zuelzer WA, et al. Core decompression for avascular necrosis of the femoral head: correlation between long-
term results and preoperative MR staging. Radiology. 1990 May. 175(2):533-6. [Medline].
36. Chan TW, Dalinka MK, Steinberg ME, et al. MRI appearance of femoral head osteonecrosis following core decompression and bone
grafting. Skeletal Radiol. 1991. 20(2):103-7. [Medline].
37. Kruczynski J. Avascular necrosis of the proximal femur in developmental dislocation of the hip. Incidence, risk factors, sequelae and
MR imaging for diagnosis and prognosis. Acta Orthop Scand Suppl. 1996 Apr. 268:1-48. [Medline].
38. May DA, Disler DG. Screening for avascular necrosis of the hip with rapid MRI: preliminary experience. J Comput Assist Tomogr.
2000 Mar-Apr. 24(2):284-7. [Medline].
39. Olscamp AJ, Tao SS, Savolaine ER, Ebraheim NA. Postoperative magnetic resonance imaging evaluation of Pipkin fractures fixated
with titanium implants: a report of two cases. Am J Orthop. 1997 Apr. 26(4):294-7. [Medline].
40. Stoller DW, Maloney WJ, Glick JM. The hip. In: Stoller DW, ed. Magnetic Resonance Imaging in Orthopedics and Sports Medicine.
Philadelphia:. Lippincott Williams & Wilkins. 1997:97, 132.
41. Takatori Y, Kokubo T, Ninomiya S, et al. Avascular necrosis of the femoral head. Natural history and magnetic resonance imaging. J
Bone Joint Surg Br. 1993 Mar. 75(2):217-21. [Medline].
42. Vande Berg BE, Malghem JJ, Labaisse MA, et al. MR imaging of avascular necrosis and transient marrow edema of the femoral
head. Radiographics. 1993 May. 13(3):501-20. [Medline].
43. Shimizu K, Moriya H, Akita T. Prediction of collapse with magnetic resonance imaging of avascular necrosis of the femoral head.
JBJS (AM). 1994. 76:215-233.
44. Tiderius C, Jaramillo D, Connolly S, Griffey M, Rodriguez DP, Kasser JR, et al. Post-closed reduction perfusion magnetic resonance
imaging as a predictor of avascular necrosis in developmental hip dysplasia: a preliminary report. J Pediatr Orthop. 2009 Jan-Feb.
29(1):14-20. [Medline].
45. Yeh LR, Chen CK, Huang YL, Pan HB, Yang CF. Diagnostic performance of MR imaging in the assessment of subchondral fractures
in avascular necrosis of the femoral head. Skeletal Radiol. 2009 Jun. 38(6):559-64. [Medline].
46. Spencer RP, Lee YS, Sziklas JJ, et al. Failure of uptake of radiocolloid by the femoral heads: a diagnostic problem: concise
communication. J Nucl Med. 1983 Feb. 24(2):116-8. [Medline].
47. Hungerford DS. Pathogenetic considerations in ischemic necrosis of bone. Can J Surg. 1981 Nov. 24(6):583-7, 590. [Medline].
48. Imhof H, Breitenseher M, Trattnig S, et al. Imaging of avascular necrosis of bone. Eur Radiol. 1997. 7(2):180-6. [Medline].
49. Lee MJ, Corrigan J, Stack JP, et al. A comparison of modern imaging modalities in osteonecrosis of the femoral head. Clin Radiol.
1990 Dec. 42(6):427-32. [Medline].
50. Murray IP. The role of SPECT in the evaluation of skeletal trauma. Ann Nucl Med. 1993 Feb. 7(1):1-9. [Medline].
51. Naito M, Ogata K, Moriguchi H. Quantitative bone scanning of the hip. Comparison between the perfusion and static phases. Int
Orthop. 1996. 20(5):311-4. [Medline].
52. Conway JJ. A scintigraphic classification of Legg-Calve-Perthes disease. Semin Nucl Med. 1993 Oct. 23(4):274-95. [Medline].
53. Staudenherz A, Hofmann S, Breitenseher M, et al. Diagnostic patterns for bone marrow oedema syndrome and avascular necrosis
of the femoral head in dynamic bone scintigraphy. Nucl Med Commun. 1997 Dec. 18(12):1178-88. [Medline].
54. Bluemke DA. Avascular necrosis of the hip: MR evaluation. Contemp Diagn Radiol. 1996. 19:23.
55. Bluemke DA, Zerhouni EA. MRI of avascular necrosis of bone. Top Magn Reson Imaging. 1996 Aug. 8(4):231-46. [Medline].
56. Hays CW, Conway WF, Daniel WW. MR imaging of bone marrow edema pattern; transient osteoporosis, transient bone marrow
edema syndrome or osteonecrosis. Radiographics. 1993. 13:1001.
57. Kopecky KK, Braunstein EM, Brandt KD, et al. Apparent avascular necrosis of the hip: appearance and spontaneous resolution of
MR findings in renal allograft recipients. Radiology. 1991 May. 179(2):523-7. [Medline].
58. Quinn SF, McCarthy JL. Prospective evaluation of patients with suspected hip fracture and indeterminate radiographs: use of T1-
weighted MR images. Radiology. 1993 May. 187(2):469-71. [Medline].
59. Vande Berg B, Malghem J, Labaisse MA, et al. Avascular necrosis of the hip: comparison of contrast-enhanced and nonenhanced
MR imaging with histologic correlation. Work in progress. Radiology. 1992 Feb. 182(2):445-50. [Medline].
60. Vande Berg BC, Malghem JJ, Lecouvet FE, et al. Idiopathic bone marrow edema lesions of the femoral head: predictive value of MR
imaging findings. Radiology. 1999 Aug. 212(2):527-35. [Medline].
61. Association Research Circulation Osseous. Committee on Terminology and Classification. ARCO News. 1992. 4:41-6.
62. Blumhagen J. Legg-Calve-Perthes disease. In: Hilton SW, Edwards DK, eds. Practical Pediatric Radiology. 2nd ed. Philadelphia:.
WB Saunders Co. 1994:485.
63. Pavelka K. Osteonecrosis. Baillieres Best Pract Res Clin Rheumatol. 2000 Jun. 14(2):399-414. [Medline].
64. Resnick D, Niwayama G. Osteonecrosis: diagnostic techniques, special situations and complications. In: Resnick D, ed. Diagnosis of
Bone and Joint Disorders. Philadelphia:. WB Saunders Co. 1995:3495.
65. Roshan A, Ram S. The neglected femoral neck fracture in young adults: review of a challenging problem. Clin Med Res. 2008 May.
6(1):33-9. [Medline].
66. Beuther E. Disorders of hematopiesis. Fauci A, Braunwalldt E, Isselbacker KJ, et al, eds. Harrison's Principles of Internal Medicine.
14th ed. New York, NY: McGraw-Hill; 1998. 647.
67. Boechat MI, Winters WD, Hogg RJ, et al. Avascular necrosis of the femoral head in children with chronic renal disease. Radiology.
2001 Feb. 218(2):411-3. [Medline].
68. Ohzono K, Saito M, Sugano N, et al. The fate of nontraumatic avascular necrosis of the femoral head. A radiologic classification to
formulate prognosis. Clin Orthop. 1992 Apr. (277):73-8. [Medline].
69. Sweet DE, Madwell JE. Osteonecrosis: pathogenesis. Resnick D, ed. Diagnosis of Bone and Joint Disorders. Philadelphia, Pa: WB
Saunders Co; 1995. 3447, 3457-58, 3460, 3463, 3465.

Imaging in Avascular Necrosis of The Femoral Head

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3/12/2021 https://emedicine.medscape.

Imaging in Avascular Necrosis of

(See the images of vascular necrosis below.)

Blood supply in children

Sequelae of avascular necrosis

Minimal avascular necrosis

More severe avascular necrosis

Single-photon emission CT scanning

Plain film radiography

Plain film radiography

Differential diagnosis and other problems to be considered

Plain film radiograph

Transient osteoporosis of the hip

Advanced DJD (see the following image)

Plasma cell myeloma

Bone marrow edema syndrome

Transient osteoporosis of the hip

Transient bone marrow syndrome

Epiphyseal stress fracture

Stage 0 (preclinical and preradiologic)

Stage 3 (early collapse of the femoral head)

Stage 4 (progressive degenerative disease)

Steinberg et al's staging system for AVN

Advanced staging of AVN using plain radiography

Alternating areas of lucency and sclerosis

Some radiologic features of avascular necrosis may lead to false-positive findings.

reparative zone. See also the next image.

Magnetic Resonance Imaging

Use of contrast enhancement

Atypical MRI findings

Differentiation between transient and irreversible AVN lesions

Associated MRI findings

AVN classification per central avascular segment signal alterations

MRI staging, symptoms, and prognostic correlations

Correlation between MRI and radiographic staging

MRI class B and C lesions correlate poorly with radiographic staging.

Correlation between MRI class and clinical symptoms

Of patients with MRI class A lesions, 54% are asymptomatic.

Of patients with MRI classes B and C lesions, 11% are asymptomatic.

Of patients with MRI class D lesions, 67% are asymptomatic.

Correlation between MRI findings and prognosis

Femoral head collapse tendency and MRI lesion size

Bone marrow edema

Transient osteoporosis of the hip (TOP)

Transient bone marrow syndrome

Perfusion and static planar radionuclide imaging

Additional ACR recommendations include the following[5] :

Contributor Information and Disclosures

Michael R Aiello, MD Locum Tenens Radiologist

Disclosure: Nothing to disclose.

Specialty Editor Board

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

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