AVN Causes and Risk Factors

AVN femoralAvascular 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. fat embolism

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.

sickle obstructionAn 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 gauchersdiseases 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
  • Alcohol
  • Idiopathic (no cause)
  • Metabolic and genetic factors
  • Systemic lupus erythematosus (SLE)
  • Rental failure
  • Organ transplant
  • Hemophilia

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).

resorpThe 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.


Unbelievable Bacteria

One of the ways bacteria enters the body is through an open wound. When an open wound goes straight down to a fractured bone it is called and open fracture. When bacteria gains access to the deeper tissue beneath the open wound, the tissues become contaminated. Preoperative and prophylactic antibiotics are given to the patient to help decrease the infection rate with the hope of killing the bacteria in the contaminated field.

open fx bacteria

Additionally, a special treatment is done during an open fracture to further help prevent infection. This treatment consists of irrigating and washing the wound, as well as debridement of the dead tissue. Once the tissue has been adequately cleaned, the fracture needs to be reduced and stabilized. Three different ways to stabilize the fracture is with a plate, a rod, or an external fixator. The open wound is either left open for a variable amount of time and it is closed later on. At the time of wound closure, a skin graft will be needed. To promote healing of the fracture a bone graft will be needed usually four to six weeks after the injury.

skin graft

A bone graft is obtained from the pelvis as the pelvis has a large reserve of bone that can be utilized. The bone that is harvested is cut into pieces and then added to the fracture where needed. Despite the best care, a certain percentage of open fracture injuries will become infected. When the tissues become infected by bacteria, white blood cells are attracted to the infected site where the bacteria are multiplying and causing inflammation.

multiple bacteria

Bacteria multiply by replicating their DNA and then dividing into two identical bacterial cells. Due to the doubling of bacterial cells, the population of the bacteria grows rapidly. Once at the site of infection, the white blood cells begin to ingest the bacteria. These bacteria however, may survive and multiply within the white blood cells, causing the cells the burst. When this occurs, the bacteria is then released back into the tissues.

Other types of bacteria can also produce a thick capsule that prevents them from being engulfed. Engulfed bacteria may also produce toxins used to destroy cells that try to attack them. Bacteria can also hide in dead bone or bone cells. When this happens, antibiotics and white blood cells are unable to reach the bacteria, since the dead bone has no blood supply. In addition to the bacteria hiding in the bone, the bacteria grow rapidly.


During this growth period, the bacteria communicate with one another through a process known as quorum sensing. Quorum sensing is the use of a chemical signals from one bacteria to another. As the bacterial population grows, the concentration of the chemical signal. Once the concentration of the chemical signal reaches a certain threshold, the bacteria then begin their attack. The bacteria will attack the tissues causing it to break down and die which can lead to an abscess formation. The abscess must be drained and evacuated, followed by antibiotic treatment.

bacteria communuity

Antibiotics can kill bacteria in several different ways. One way is by disrupting the cell wall which ruptures the bacteria. Another way, is by preventing DNA replication by blocking the unwinding of the DNA. A third way is by inhibiting the ribosomes from making proteins needed for the cellular structure and function. The last way is by blocking the enzymes that produce folate. Folate is needed for DNA synthesis, and without it the cell will die.

When hardware is used to stabilize the fracture, the story can become much more complex.