25 Osteonecrosis of the Hip

Matthew W. Tetreault, Roshan P. Shah

25 Osteonecrosis of the Hip


  • I. Osteonecrosis of the femoral head (ONFH) is synonymous with avascular necrosis (AVN).

  • II. Incidence:

    1. Twenty thousand to 30,000 new cases per year in the United States. 1

    2. Approximately 10% of total hip arthroplasties in the United States are for ONFH. 2

  • III. Demographics 3 :

    1. Male-to-female ratio depends upon/varies with etiology, for example, males predominate alcohol-associated ONFH and females predominate lupus-associated ONFH.

    2. Average age at presentation is younger than 50 years.

  • IV. Location:

    1. Usually occurs in the anterolateral femoral head. 3

    2. Fifty percent to 70% have bilateral hip involvement. 1 , 3

    3. Three percent of patients have multifocal osteonecrosis involving ≥3 joints. 4

    4. The hip should be evaluated in patients with osteonecrosis of the knee, shoulder, or other joints throughout the body.

  • V. Risk factors 5 :

    1. Traumatic:

      1. Fractures about the hip can disrupt the local blood supply to the femoral head.

      2. Hip dislocation:

        1. Anterior dislocations are associated with an ONFH event rate of 0.09 to 0.3.

        2. Posterior dislocations are associated with an ONFH at a rate of 0.1 to 0.4.

        3. Delay of reduction of greater than 12 hours has an odds ratio of ONFH of 5.6. 6

      3. In children, osteonecrosis can occur following a slipped capital femoral epiphysis (SCFE) injury:

        1. ONFH has been reported in 25% of cases after an unstable SCFE. 7

    2. Atraumatic:

      1. Steroids (exogenous or endogenous) are responsible for 10 to 30% of ONFH cases. 8 10

      2. Alcohol intake of up to 320-g ethanol per week (five bottles of wine) raises risk by a factor of 2.8 10 12 :

        1. Excessive alcohol intake and use of glucocorticoids are associated with greater than 80% of atraumatic cases. 13

      3. Sickle cell anemia (SS) and sickle cell hemoglobin C (SC) have high rates of ONFH, with SC occurring later in life. Sickle cell trait (S) has an intermediate risk of ONFH. 14

      4. Dysbaric disorders (decompression sickness, “the bends,” Caisson’s disease). 15

      5. Systemic lupus erythematosus (SLE). 16 , 17

      6. Marrow-replacing diseases (e.g., Gaucher’s disease 18 ).

      7. Chronic renal failure or hemodialysis. 19

      8. Pancreatitis. 3

      9. Pregnancy. 20

      10. Hyperlipidemia. 3

      11. Hyperuricemia. 3

      12. Radiation. 21

      13. Transplant patients (solid organ 22 or hematopoietic cell transplantation 23 , 24 ).

      14. Coagulation factor abnormalities (e.g., genetic defects resulting in hypofibrinolysis or thrombophilia, like factor V Leiden, an autosomal dominant condition with incomplete penetrance that predisposes to excessive clotting 25 27 ).

      15. Cigarette smoking. 11

      16. Hematologic diseases (leukemia, lymphoma). 28 , 29

      17. Human immunodeficiency virus (HIV) infection with or without antiretroviral treatment. 10 , 30

      18. Idiopathic:

        1. In children, idiopathic ONFH occurs as Legg–Calvé–Perthes (LCP) disease with an incidence of around 15 per 100,000 children. 31

        2. Multiple epiphyseal dysplasia (MED) is distinguished from LCP by its symmetric disease, bilateral involvement, early acetabular changes, and lack of metaphyseal cysts.


  • I. Pertinent vasculature:

    1. Extracapsular arterial ring:

      1. At the base of the femoral neck.

      2. Consists of:

        1. Ascending branch of the medial femoral circumflex artery (MFCA) posteriorly.

        2. Ascending branch of the lateral femoral circumflex artery (LFCA) anteriorly.

        3. Superior and inferior gluteal arteries have minor contributions.

      3. MFCA 32 :

        1. Principal blood supply to the weight-bearing portion of the femoral head in adults. 33

        2. Arises from the profunda femoris artery.

        3. Travels posteriorly from its origin and gives off five consistent branches (superior, ascending, acetabular, descending, and deep). Preservation of the deep branch is most important in prevention of ONFH.

        4. This branch courses between the iliopsoas and pectineus, along the inferior border of the obturator externus (toward the intertrochanteric crest).

        5. When viewed posteriorly, the deep branch can be located in the space between the quadratus femoris and the inferior gemellus ( Fig. 25.1 ).

        6. The main division of the deep branch continues its course superiorly by crossing posterior to the obturator externus tendon and then anterior to the conjoint tendon.

        7. The deep branch then perforates the hip capsule just cranial to the insertion of the superior gemellus tendon (and distal to the piriformis tendon).

    2. Ascending cervical vessels:

      1. Arise from the extracapsular ring.

      2. Comprised of four retinacular vessels: anterior, posterior, medial, and lateral.

      3. These vessels are subsynovial in location beginning at the capsular attachment to the femoral neck (anteriorly at the intertrochanteric line and posteriorly at the intertrochanteric crest).

        Fig. 25.1 (a-b) The extracapsular course of the medial femoral circumflex artery (MFCA). The area immediately adjacent to the medial border of the greater trochanter is at risk of vascular injury, representing the vascular danger zone. (Source: Anatomy of the acetabulum. In: Tile M, Helfet D, Kellam J, et al., eds. AO TRAUMA Fractures of the Pelvis and Acetabulum: Principles and Methods of Management. 4th Edition. Thieme; 2015.)

      4. Lateral vessels supply the greatest volume of the femoral head.

      5. LFCA gives rise to anterior vessels and MFCA often gives rise to the others.

    3. Subsynovial intra-articular ring (of Chung 34 ):

      1. Arises from the retinacular vessels as a ring on the surface of the neck at the articular cartilage border.

      2. Epiphyseal arteries enter the head from here, perforating into bone 2 to 4 mm distal to the bone–cartilage junction ( Fig. 25.2 ):

        1. Lateral epiphyseal artery, which enters the head posterosuperiorly, is most important.

    4. Artery of the ligamentum teres:

      1. Usually originates from the obturator artery, occasionally the MFCA.

      2. Forms the medial epiphyseal vessels.

      3. Supplies the femoral head more consistently in young children; a small and variable amount of the femoral head is nourished in adults.

        Fig. 25.2 (a) Photograph showing the perforation of the terminal branches into the bone (right hip, posterosuperior view). The terminal subsynovial branches are located on the posterosuperior aspect of the neck of the femur and penetrate the bone 2 to 4 mm lateral to the bone–cartilage junction. (b) Diagram showing (1) the femoral head, (2) gluteus medius, (3) the deep branch of the medial femoral circumflex artery (MFCA), (4) the terminal subsynovial branches of the MFCA, (5) insertion and tendon of gluteus medius, (6) insertion of tendon of piriformis, (7) the lesser trochanter with nutrient vessels, (8) the trochanteric branch, (9) the branch of the perforating artery, and (10) the trochanteric branches. (Source: Anatomy of the acetabulum. In: Tile M, Helfet D, Kellam J, et al., eds. AO TRAUMA Fractures of the Pelvis and Acetabulum: Principles and Methods of Management. 4th Edition. Thieme; 2015.)

    5. Intraosseous vessels:

      1. Intraosseous cervical vessels (within the medullary cavity) provide a relatively small portion of the femoral head blood supply.

  • II. Age-related changes:

    1. The blood supply of the femoral head changes with age 35 :

      1. Birth to 4 years: primary MFCA and LFCA, artery of the ligamentum teres.

      2. Four years to adult: posterosuperior and posteroinferior retinacular vessels from MFCA. Minimal amount from LFCA or ligamentum teres:

        1. Corollary: using a piriformis starting point for antegrade nailing of pediatric femur fractures can disrupt the posterosuperior retinacular vessels and cause ONFH. 36

      3. Adult: MFCA to lateral epiphyseal artery.


  • I. ONFH is the result of derangements that compromise blood supply to the femoral head resulting in cell death, fracture, and collapse of the articular surface. 1

    1. Atraumatic osteonecrosis:

      1. Pathogenesis likely multifactorial, including genetic, metabolic, and local factors. 2 , 13 , 37

      2. Proposed pathways include:

        1. Vascular occlusion:

          • i. Lipids:

            1. Increased glucocorticoids seen in systemic diseases such as SLE and alcohol abuse associated with changes in circulating lipids, triggering microemboli in arteries supplying the bone. 38

            2. Increased risk of fat emboli has also been attributed to an increase in bone marrow fat cell size (adipocyte hypertrophy), which blocks venous flow. 1

          • ii. Intravascular coagulation and thrombus formation:

            1. Antiphospholipid antibodies, inherited thrombophilia, and hypofibrinolysis affect the coagulation and fibrinolytic pathways. 1

            2. Sickling of red blood cells and bone marrow hyperplasia as seen in sickle cell conditions can cause vascular occlusion. 1

            3. Accumulation of cerebroside-filled cells within the bone marrow can occlude vessels in conditions like Gaucher’s disease. 18

            4. Decompression sickness associated with increased pressure incites nitrogen bubble formation, which can cause arteriolar occlusion and necrosis. This also leads to elevated plasma levels of plasminogen activator inhibitor, increasing coagulation. 39

        2. Direct cellular toxicity:

          • i. Damage to cells may be caused by irradiation, chemotherapy, or oxidative stress.

          • ii. This may lead to a reduction in osteogenic differentiation with diversion of mesenchymal stem cells to a fat-cell lineage. 40

    2. Trauma-related osteonecrosis:

      1. Due to direct mechanical damage by rupture, compression, or kinking of the extraosseous vessels as a result of injury. The location of these vessels along the course of the femoral neck makes them susceptible to direct injury in the setting of trauma. 21 , 41

      2. Intracapsular hip fractures (femoral head and neck) are at greater risk of osteonecrosis than extracapsular hip fractures (intertrochanteric and subtrochanteric) secondary to potential to disrupt the blood supply described earlier 5 ( Fig. 25.3 ) and risk of intracapsular hematoma:

        1. Femoral head fracture: incidence of osteonecrosis varies from 6 to 23% 42 46 :

          • i. Reported after both surgical and nonsurgical treatments.

        2. Femoral neck fracture:

          • i. Per recent meta-analysis, overall incidence of osteonecrosis is 14.3% (range, 10–25%). 47

          • ii. Higher risk of osteonecrosis with greater initial fracture displacement 48 50 and malreduction. 48 , 51

          • iii. Fractures in the subcapital region of the femoral neck at particular risk; trauma at this location disrupts the anastomosis between the lateral epiphyseal vessels (from the MFCA) and the artery of the ligamentum teres. 1

          • iv. Relationship between time to fixation of intracapsular femoral neck fractures and risk of osteonecrosis is controversial. One retrospective study reported a lower rate of ONFH when operative fixation was performed within 12 hours of injury. Other studies have failed to demonstrate a significant difference between timing of fracture fixation and incidence of ONFH. 52

            Fig. 25.3 (a-b) The prognosis of hip fractures varies by anatomic location. Intracapsular fractures are more likely to disrupt the blood supply to the femoral head, thereby increasing the risk of avascular necrosis, compared with extracapsular (i.e., intertrochanteric) fractures. (Source: Pediatric fractures. In: Rüedi T, Buckley R, Moran C, eds. AO Principles of Fracture Management. 2nd Edition. Thieme; 2007.)

          • v. Decompression of the intracapsular hematoma has been proposed to reduce the risk of osteonecrosis by minimizing extraosseous compression of vessels supplying the femoral head. There is a paucity of clinical evidence evaluating this theory, 53 with conflicting results; at least one retrospective study found no relationship, 4 while another found a reduced risk of osteonecrosis with hip decompression in Garden type II and III fractures. 55

      3. Extracapsular fractures of the trochanteric region have a significantly lower incidence of osteonecrosis as they are distal to the entry of the arterial branches that supply the femoral head. 56

      4. Hip dislocations may also interrupt the extraosseous vascular supply of the femoral head 57 59 :

        1. Deep branch of the MFCA can be injured during a posterior dislocation as it courses posterior to obturator externus and anterior to quadratus femoris. 32 , 60

        2. Rate of osteonecrosis associated with posterior dislocation between 5 and 60% depending on time to reduction and severity of associated fractures and other injuries. 57 69

        3. In one case control study, 4.8 versus 52.9% rate of osteonecrosis in patients with a posterior hip dislocation reduced before versus after 6 hours, respectively. 57

        4. Lack of data on long-term outcomes of anterior hip dislocations; limited literature suggests an osteonecrosis rate of roughly 10%. 61 , 62


  • I. Clinical:

    1. Symptoms:

      1. Pain: the most common presenting symptom of osteonecrosis 4 , 63 :

        1. Groin pain most common, followed by thigh and buttock pain.

        2. Weight-bearing or motion-induced pain in majority of cases.

        3. Rest pain present in about two-thirds of patients and night pain in one-third.

        4. Although rare, pain in multiple jointis suggestive of a multifocal process.

      2. A small proportion of patients are asymptomatic and the diagnosis of osteonecrosis is an incidental finding. Meanwhile, asymptomatic involvement contralateral to a symptomatic side is frequently noted. 3

    2. Examination 3 , 13 :

      1. Physical findings largely nonspecif ic.

      2. May have pain with, and eventually (as the disease progresses with secondary acetabular involvement) limitations to, range of motion, particularly forced internal rotation and abduction:

        1. Often maintain a better range of motion than patients with chronic degenerative joint disease.

      3. Positive Stinchfield’s test: pain with resisted hip flexion in the supine position.

      4. Flexion contracture of the hip joint and resultant limp may be present in the later courses of the disease.

  • II. Imaging:

    1. Radiographs:

      1. Recommend anteroposterior (AP) and frog-leg lateral views of the affected hip, and AP and lateral views of the contralateral hip.

      2. Lateral films are necessary to evaluate the superior portion of the femoral head in which subchondral abnormalities are often seen.

      3. Plain radiographs can remain normal for months after symptoms of osteonecrosis begin.

        1. Earliest findings are mild density changes.

        2. Followed by concomitant areas of sclerosis and cystic formation in the femoral head as the disease progresses.

        3. The pathognomonic crescent sign (subchondral radiolucency) is evidence of subchondral collapse.

        4. Later stages include loss of sphericity or collapse of the femoral head. Ultimate, joint space narrowing and acetabular-sided degenerative changes are seen (refer to “Classification” section for imaging examples). 64

    2. Magnetic resonance imaging (MRI):

      1. Superior to X-ray or bone scan with studies reporting sensitivity and specificity greater than 99%. 37 , 65 70 More accurate than radiographs in evaluating the size of osteonecrotic lesions. 71 , 72

      2. Advised when osteonecrosis is suspected but radiographs appear normal to rule out or stage osteonecrosis. Importantly, MR changes can be seen early in the course of disease when other studies are negative. 3

      3. “Double-line sign” is pathognomonic 3 :

        1. T1: Focal lesions are well demarcated and inhomogeneous on T1. Earliest finding is dark/low-intensity band representing decreased signal from ischemic bone.

        2. T2: A second high-intensity line appears on T2 (within the line seen on T1 images), representing hypervascular granulation tissue. This is the double-line sign ( Fig. 25.4 ).

      4. Presence of bone marrow edema (as evidenced by high signal intensity on T2-weighted MRI; Fig. 25.5 ) is not always seen; this finding is predictive of worsening pain and future disease progression. 73

        Fig. 25.4 Double-line sign on MR imaging of a femoral head, pathognomonic for osteonecrosis. On the T1-weighted coronal MR image (top), a serpiginous line of low signal is seen anterosuperiorly, demarcating ischemic from fatty marrow. On the T2-weighted coronal MR image (bottom), a hypodense line is paralleled by an inner and outer hyperintense line, representing hypervascular granulation tissue at the interface between necrotic and viable bone.
        Fig. 25.5 A coronal T2-weighted MR image of a right hip with osteonecrosis of the femoral head and high signal intensity within the femoral neck indicative of bone marrow edema.

    3. Bone scan:

      1. Technetium-99 m bone scan: increased bone turnover at the junction of dead and reactive bone results in increased uptake surrounding a cold area; this has been called the “doughnut sign.” 74

      2. While moderately sensitive, bone scan is nonspecific. It is both less sensitive and specific than MRI and its sensitivity is least in patients with early-stage lesions. 67 Thus, bone scan is not generally recommended for diagnosis of or screening for osteonecrosis. 3

Only gold members can continue reading. Log In or Register to continue

Dec 29, 2020 | Posted by in ORTHOPEDIC | Comments Off on 25 Osteonecrosis of the Hip

Full access? Get Clinical Tree

Get Clinical Tree app for offline access