Avascular Necrosis or osteonecrosis is death of a segment of bone due to disruption of the blood supply. The causes of avascular necrosis are numerous as there are several different ways that could interrupt the blood supply.
AVN may occur due to trauma, such as with a dislocation or fracture of the femoral neck. These injuries may interrupt the blood supply to the hip. Avascular necrosis may occur due to an occlusion of the arterial blood supply by a fat embolism; nitrogen bubbles in the blood stream (Caisson disease) or with Sickle Cell disease.
Due to the low oxygen levels of the cells in patients with Sickle Cell Anemia, the cells become sickle shaped and are unable to pass through the vessels. This results in a diminished blood flow, which could lead to AVN. A patient with sickle cell disease and asymptomatic AVN diagnosed by an MRI will have a higher incidence of progression to collapse the AVN and pain (75%). Deterioration of the AVN will be rapid and can be bilateral, so it is important for the physician to screen the other hip at the same time and periodically. The physician will also want to watch the humeral head for AVN.
An obstruction of the venous outflow is another cause of avascular necrosis. With an increase in interosseous pressure, an obstruction can limit the blood flow. Injury or pressure on the blood vessel wall can also cause AVN. An excellent example of this would be Gaucher’s Disease, an increase in fat cell size may prevent the arterial inflow and lead to ischemia. Fatty substances can accumulate in the cells and certain organs. Marrow diseases such as lymphoma and leukemia may also cause AVN. Radiation, vasculitis, and cytotoxins are also risk factors for AVN. Avascular necrosis may be associated with hypercoagulable states such as decreased anticoagulants, protein S and protein C.
Other common causes of AVN:
- Steroid use
- Idiopathic (no cause)
- Metabolic and genetic factors
- Systemic lupus erythematosus (SLE)
- Rental failure
- Organ transplant
All of these conditions may cause loss of the vascular supply, marrow necrosis, and osteocyte death. An important condition related to AVN is steroid use. High doses for 2-3 weeks or low doses for long durations may cause AVN. There is a direct connection between the dose and duration of steroid use in the development of AVN. Joint injections are not proven to cause AVN. Additionally, avascular necrosis of the femoral head is a complication in HIV infected patients. The increased incidence of AVN may be caused by an increased prevalence of predisposing factors for osteonecrosis, including protease inhibitors, hyperlipidemia, corticosteroid use, alcohol, and intravenous drug use. Protease inhibitors play a role in the development of osteonecrosis through a tendency to cause hyperlipidemia. An easy mnemonic tool to remember the causes of AVN is “ASEPTIC”: Alcoholism/AIDS, Sickle Cell Disease/SLE, Erlenmyer Flask (Gaucher’s), Pancreatitis/Pregnancy, Trauma, Idiopathic/Infection, Caisson’s (the bends).
The anterosuperior segment of the femoral head is the area usually affected by AVN. Resorption of some of the dead bone is done by the osteoclasts, while osteoblasts lay down new woven bone. Dead trabecular bone is resorbed, ready to be remodeled. This process is repeated and the bone becomes weak. At the weakest stage, the AVN will result in collapse. Remodeling is not enough to support the bone. Progressive collapse due to bone death, resorption, remodeling and microfracture will occur. Avascular necrosis ends by final collapse, joint changes, and arthritis.