Avascular Necrosis

Avascular Necrosis of the Hip

General characteristics

The femoral head is a frequent site of AVN because of its large cartilaginous surface precluding vascular supply.

In the infant, there is additional blood supply by a small artery accompanying the ligamentum teres (capitis femoris), which is obliterated with increasing age. Direct disruption of the nutrient artery is evident in posttraumatic AVN of the hip. Nontraumatic AVN is caused by embolic disease (fat, gas) or elevated intramedullary pressure. The incidence of AVN is increased in dysbaric conditions, with steroid therapy, Cushing’s syndrome, pancreatitis, alcoholism, Gaucher’s disease, and sickle cell anemia. Men are four times more frequently affected than women are.

Clinical symptoms

Patients usually present with groin pain of gradual onset present at rest and increased by weight bearing. Prognosis is related to the degree of MRI morphologic change, location, and local extension of the abnormalities (Beltran et al. 1990). If less than 25% of the weight bearing surface of the femoral head is affected the risk of infraction is very low.


Initially no imaging findings reveal the (small) histologically defined foci of osteonecrosis (stage 0). Second, edemalike signal alterations are shown on MRI without a clear linear demarcation of the avascular area (stage I). Usually, these findings are more conspicuous on T2-weighted FS/STIR sequences than on T1-weighted sequences. The appearance of a reactive peripheral zone demarcating the lesion usually indicates transition from a reversible state into irreversible disease (stage II). However, when there is a small extension this kind of lesion may well respond to therapy (usually core decompression, drilling) and come to a stable situation.

Often and visibly from this stage of disease onward, the virtually pathognomonic “double-line” sign is present in 65–80% of cases— adjacent low-signal line toward the surrounding bone on T2-weighted sequences. The former reflects vascularized granulation tissue, the latter sclerotic demarcation. On T1-weighted sequences, differentiation between vascularized and sclerotic portions of the demarcating zone is difficult, as both lines usually present with hypointense signal intensity.

Intravenous application of gadolinium shows vivid uptake in the inner rim. Flattening of the femoral head and linear low signal intensity immediately underneath the subchondral bone plate (“crescent” sign) indicate (imminent or beginning) subchondral fracture (stage III).

Collapse and findings of degenerative change define stage IV.

Signal patterns consistent with fat, hemorrhage, edema, and granulation tissue (Mitchell A, B) indicated better outcomes than patterns compatible with sclerosis, fibrosis, and fluid (Mitchell C, D).

Most often, the AVN is located in the anterosuperior segments of the femoral head. Not rarely there is effusion accompanying already early stages of the disease. In up to 70% of cases, there is metachronous affection of the contralateral hip. Therefore, imaging should contain at least one (coronal) sequence covering both hips. Although depiction of subtle subchondral fractures is easier with CT, MRI demonstrates the extent and location of the lesions to much better advantage. Visualization of the necrotic area in the sagittal plane (Fig. 8.6.1) helps to plan therapy and may contribute to the differential indication of different treatment options.

The sensitivity for the diagnosis of AVN is higher with MRI (Mitchell et al. 1986, 1987; van de Berg et al. 1992) than with any other imaging modality including radiography, CT, and scintigraphy (Table 8.6.3). Measurements of intramedullary pressure exhibit higher sensitivity but lower specificity than MRI. Moreover, MRI has the advantage of providing additional morphologic information, e.g., on joint effusion and cartilage. It is not surprising that compared to histopathological findings MRI may fail to demonstrate small foci of very early AVN as it may take up to 5 days for fat cell necrosis (and thus relevant signal alteration) to occur. Nonetheless, MRI is to be considered the imaging modality of choice for early diagnosis of AVN as well as for asse

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