Femoral Head Avascular Necrosis

Updated: Oct 20, 2023
  • Author: John D Kelly, IV, MD; Chief Editor: Craig C Young, MD  more...
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Practice Essentials

Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment. [1] (See also the Medscape Reference article Imaging in Avascular Necrosis of the Femoral Head.)

Osteonecrosis of the femoral head was first described in 1738 by Munro. In approximately 1835, Cruveilhier depicted femoral head morphologic changes secondary to interruption of blood flow. Since 1962, when Mankin described 27 cases of AVN, the number of reported AVN cases has increased steadily. (See also the Medscape Reference article Hip Osteonecrosis.)

Signs and symptoms

Early in the disease process, the condition is painless; however, patients ultimately present with pain and limitation of motion. The pain is most commonly localized to the groin area, but it may also manifest in the ipsilateral buttock, knee, or greater trochanteric region.

See Presentation for more detail.


Early radiographic findings in femoral head AVN include femoral head lucency and subchondral sclerosis. With disease progression, subchondral collapse (ie, crescent sign) and femoral head flattening become evident radiographically. Joint space narrowing is the end result of untreated femoral head AVN.

Magnetic resonance imaging (MRI) is the study of choice in patients who demonstrate signs and symptoms that are suggestive of AVN but whose radiographs are normal.

See Workup for more detail.


Essentially, nonoperative treatment for symptomatic AVN of the hip yields unfavorable results. Small asymptomatic lesions do not warrant surgical intervention and are closely monitored with serial examination. If symptoms ensue, repeat imaging and surgical treatment are indicated.

Surgical treatment of AVN can be broadly categorized as either prophylactic measures (to retard progression) or reconstruction procedures (after femoral head collapse).

See Treatment and Medication for more detail.

Patient education

Information regarding the deleterious effects of alcohol and corticosteroids on femoral head circulation should be disseminated to those who are at risk for AVN.



Traumatic AVN is simply a result of mechanical disruption of blood flow to the femoral head. During sports endeavors, hip dislocation or subluxation is the most frequently reported traumatic means of AVN. A tackle from behind may cause an anterior hip subluxation in a ball carrier. Likewise, extreme abduction or external rotation may result in an anterior dislocation in a fallen water-skier.

Similarly, a displaced femoral neck fracture can damage the fragile retinacular vessels, which supply the femoral head and result in femoral head necrosis. (See also the Medscape Reference articles Femoral Neck Fracture Imaging [in the Radiology section], Femoral Neck Stress and Insufficiency Fractures [in the Orthopedic Surgery section], and Femoral Neck Fracture [in the Sports Medicine section].) [2]

Most cases of AVN are atraumatic and include the following [3] :

  • Excessive corticosteroid use and alcohol abuse account for as many as 90% of new cases.

  • Intravascular coagulation appears to be the central event associated with nontraumatic AVN. (See also the Medscape Reference article Disseminated Intravascular Coagulation.)

  • Coagulation may occur secondary to extravascular compression (eg, marrow fat enlargement), vessel wall injury (eg, chemotherapy, radiation), or a thromboembolic event (eg, fat emboli).

  • Ischemic insult to the femoral head results in infarcted subchondral bone. In this situation, weakened and unrepaired necrotic bony trabeculae fail under a compressive load, leading to subchondral collapse (ie, crescent sign) and, ultimately, articular collapse.

Traumatic causes of femoral head AVN include the following:

A study by Song et al indicated that in patients aged 50 years or older with valgus-angulated femoral neck fractures, the risk of AVN of the femoral head and fixation failure after screw osteosynthesis is predicted by the severity of the initial deformity. Patients with an initial valgus and posterior tilt of greater than 15° (B1.1.2 fracture) were found to have a 17-fold higher risk of treatment failure than did patients with a tilt in both planes of less than 15° (B1.2.1 fracture). [4]

A study by Maini et al indicated that a complete tear of the obturator externus and/or piriformis muscles is a significant risk factor for femoral head AVN. [5]

Atraumatic osteonecrosis causes include the following:

Cases of AVN of the femoral head that developed following coronavirus disease 2019 (COVID-19) have been reported. [7, 8, 9]  A possible association has been suggested between the use of corticosteroids to treat patients with COVID-19 and the development of AVN.



United States statistics

AVN of the femoral head is a debilitating disease that usually leads to osteoarthritis of the hip joint in relatively young adults (mean age at presentation: 38 y). The disease prevalence is unknown, but estimates indicate that 10,000-20,000 new cases are diagnosed in the United States per year. [10, 11] Furthermore, it is estimated that 5-18% of the more than 500,000 total hip arthroplasties performed annually are for osteonecrosis of the femoral head. [11]


Functional Anatomy

By the time an individual reaches age 13-14 years, the partially ossified bone of the ilium, ischium, and pelvis coalesce to form a Y-shaped triradial cartilage, which proceeds to fuse by age 15-16 years. The acetabulum is chiefly spherical in its superior margin and allows for approximately 170º of coverage of the femoral head. The femoral head is not perfectly spherical, and joint congruity is precise only in the weight-bearing position.

The internal trabecular system of the femoral head is oriented along lines of stress. Thick trabeculae that arise from the calcar extend into the weight-bearing dome of the femoral head and help resist to compressive loads across the joint.

The arterial supply to the femoral head is principally provided by 3 sources: (1) an extracapsular arterial ring at the base of the femoral neck, (2) ascending branches of the arterial ring on the femoral neck surface, and (3) arteries of the round ligament. This arterial supply is well affixed to the femoral neck and is easily damaged with any femoral neck fracture displacement. Furthermore, nutrient vessels to the femoral head terminate in small arterioles that are easily occluded with small embolic matter (ie, lipids). (See also the Medscape Reference article Fat Embolism.)


Sport-Specific Biomechanics

Forces that act on the femoral head in vivo are appreciable. Standing on one leg generates a force of approximately 2.5 times the body weight across the loaded hip. Running increases femoral head forces to roughly 5 times the body weight, whereas simply performing a supine straight-leg raise generates 1.5 times the body weight across the hip joint. During gait, the maximum pressure occurs in the anterosuperior femoral surface and superior acetabular dome.



If AVN of the femoral head is untreated, progression to subchondral collapse occurs in approximately 67% of individuals with asymptomatic hips and in more than 85% of those who have symptomatic hips.


In most cases, progression from femoral head AVN to femoral head collapse requires arthroplasty.