Roam Medical Abbreviation
Annette Fazzari
The incidence of avascular necrosis (AVN) has been increasing. The causes include greater use of exogenous steroids and an increase in trauma. AVN occurs in a number of autoimmune and inflammatory clinical conditions, including systemic lupus erythematosus (SLE), solid organ transplantation (eg, renal, liver, cardiac), leukemia, severe acute respiratory syndrome (SARS), malignant tumors, renal failure, inflammatory bowel diseases, sickle cell disease, and skin diseases. The risk for AVN in these underlying diseases is likely related to corticosteroid administration. [8]
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. [9]
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. [10]
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.
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.
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).
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. [11]
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.
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.
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.
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.
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).
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).
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.
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 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).
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). [12]
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.