Femoral Head Avascular Necrosis Clinical Presentation

Updated: Oct 22, 2018
  • Author: John D Kelly, IV, MD; Chief Editor: Craig C Young, MD  more...
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See the list below:

  • AVN may present with nonspecific 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.

    • Painful symptoms are usually exacerbated with weight bearing but are relieved by rest.



See the list below:

  • Passive range of motion of the hip is limited and painful, especially forced internal rotation.

  • A distinct limitation of passive abduction is usually noted.

  • A straight-leg raise against resistance provokes pain in most symptomatic cases.

  • Passive internal and external rotation of the extended leg ("log roll test") may elicit pain that is consistent with an active capsular synovitis.




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].) [3]

Most cases of AVN are atraumatic and include the following [4] :

  • Excessive corticosteroid usage 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). [5]

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. [6]

Atraumatic osteonecrosis causes include the following: