Avascular Necrosis

Avascular Necrosis Risk and Hip Resurfacing Surgery

The primary blood supply to the head of the femur arises from the circumflex arteries located at the base of the femur neck. Other arteries branch off from the circumflex arteries, and they extend from the femur neck towards the femur head. These arteries can become disrupted by a hip fracture or hip dislocation, leading to necrosis (i.e. bone death) of the femur head (i.e. avascular necrosis or AVN).

The principal sources of blood flow to the femoral head are vessels branching off the medial femoral circumflex artery. They run under the synovial membrane and enter 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. The artery of the ligamentum teres--a secondary blood source for the femur head-- supplies the medial third of the femoral head.

The branching arteries and the artery of the ligamentum teres connect 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.

Trauma is the most common cause of AVN (although there are other causes such as steroid use and alcoholism), and it can occur within 8 hours after a traumatic disruption of the blood supply. The blood vessels can be damaged as they enter the femur. The artery of the ligamentum teres also may be damaged. In addition, intracapsular hematoma can increase intracapsular pressure, which can cause blockage of the vessels within the joint capsule.

Image from Gray's Anatomy

Diagram from research report by Alex Ying-Shyuan Lee, Howard Haw-Chang Lan, San-Kan Lee on www.rsroc.org.tw

Fractures of the trochanter and those occurring outside the hip capsule rarely develop AVN; but following hip dislocation, circulation is interrupted because of tears of the ligamentum teres which can precipitate AVN. Tearing of the joint capsule also compromises the vessels within the capsule. AVN can develop as late as 10 years after fractures of the femur.

Because of the limited and delicate nature of the circulatory system feeding the femoral head and neck, it is possible that the blood flow could become disturbed due to the action of dislocating the hip and the trauma of the surgery itself. The blood flow is disrupted during resurfacing surgery, so a short surgical time is desirable. Surgeons take great pains to protect the surrounding arteries, but success is not guaranteed. Therefore, resulting necrosis of the femur head and neck remains one of the risk factors in hip resurfacing.

If AVN develops after hip resurfacing surgery, the femoral head and neck are no longer able to support the femoral component resulting in a loosening of the component. Hip pain extending down to the knee that steadily increases is a telling indicator, and the pain is usually present before problems are detectible on an X-ray. In such cases, revision to a total hip replacement would be the remedy. The dead bone of the femur head and neck would be amputated, and a stem that supports the prosthetic ball joint would be inserted into the femoral canal of the remaining femur. The blood supply to the lower portion of the femur is much less restricted and not as easily compromised as it is in the region of the femur head and neck, so necrosis of the lower portion of the femur does not appear to be a risk factor in total hip replacement surgery.