Avascular Necrosis FAQ’s

Avascular necrosis, also called osteonecrosis is a condition in which bone death occurs because of inadequate blood supply to it. Lack of blood flow may occur when there is a fracture in the bone or a joint dislocation that may damage nearby blood vessels.

AVN is caused from insufficient blood supply to the bone. There are several causes of avascular necrosis. However no specific cause is found. The common causes of avascular necrosis include:

• Trauma: Dislocation or bone fractures can injure blood vessels
• Long term or high dose steroid treatments

Avascular necrosis of the femoral head (AVN) is a debilitating condition that leads to destruction of the hip joint in young patients. The average age of patients who suffer from avascular necrosis of the femoral head is significantly younger than patients who suffer from arthritis due to degenerative conditions.

Avascular necrosis cannot spread from one body part to the other.  However, there are certain conditions, which cause avascular necrosis in numerous joints of the body.  Avascular necrosis may affect numerous bones in certain disorders.

However, if a patient has avascular necrosis in a certain bone or a certain joint, the avascular necrosis by itself does not spread to other parts.  There are certain conditions, which are certainly localized, as an example; trauma to the hip, which causes avascular necrosis of the hip and the patients should expect that in such a scenario, in the absence of other conditions the avascular necrosis is going to stay in the same body part.

I classify conditions as acute onset and chronic onset conditions. Some common causes of chronic onset avascular necrosis include use of corticosteroids as an example for treatment of systemic lupus erythematosus, rheumatoid arthritis, or in patients with renal transplantation or asthma. The use of alcohol also is associated with avascular necrosis of the femoral head. Sickle cell anemia and other anemias can also cause avascular necrosis of the femoral head.

There are certain less common conditions, like Gaucher’s disease, myeloproliferative disorders, some coagulation deficiencies that can give rise to avascular necrosis. Caisson’s disease, chronic pancreatitis, and radiation can also cut off the blood supply to the femoral head and can cause avascular necrosis. The acute conditions that can cause avascular necrosis of femoral head are dislocation of the femoral head and fracture of the neck of the femur.

A majority of patients in my practice who present with avascular necrosis do not have an identifiable cause.

Investigators have tried to use a free vascularized fibular graft to the hip joint to alleviate the pain of avascular necrosis. The fibula is the bone on the outside of the leg bone. Investigators have tried to take the blood supply, along with a piece of this bone, and then implant it into the hip joint, with the hope that the whole hip will vascularize and the collapse will be prevented. In my opinion, free vascularized grafting to the hip joint has not provided consistent results, and it’s a major procedure. I therefore do not use this for treatment of avascular necrosis of the hip.

There are multiple theories about the pathogenesis of avascular necrosis of the femoral head, which in acute reduction in the blood supply to the bone resulting from circulating fat, nitrogen bubbles or abnormally shaped cells, increased bone matter pressure, arterial obstruction, obstruction to the venous outflow, injury to the wall of the vessel caused by vasculitis, radiation damage, or release of inflammatory factors. I feel that most of avascular necrosis are multifactorial.

Avascular necrosis, in the earlier stage, is asymptomatic. This is the stage where we would like to catch the disease and treat it with core decompression and stem cells so that the possibility of arthritis and the need for joint replacement surgery is avoided. In the early stages of avascular necrosis, the patient complain of groin pain and as the collapse increases, there is increasing joint pain.

I classify avascular necrosis based on the degree of damage to the femoral head. I classify them according to severity from Stage 0 to Stage IV.
In Stage 0, the patient has no symptoms. The x-rays are normal. The bone scan may show decreased uptake.

In Stage I, there are no symptoms, the x-ray’s normal, the bone scan shows a cold spot, and if you do a biopsy it shows infarction of the weight-bearing portion of the femoral head. Bone biopsy will show abundant dead matrix cells, and osteoblast, and osteogenic cells.

In Stage II the patient has mild systems. On X-ray there is a density change in the femoral head like sclerosis or cysts. In Stage IIA and IIB, the Xray appearance of the femoral head is characterized by flattening. We call it the “Crescent sign”. The bone scan shows increased uptake in Stage II and a biopsy shows new bone deposited between necrotic layer of the bone.

In Stage III, the symptoms are mild to moderate. The x-rays show loss of sphericity and collapse. Bone scan shows increased uptake, and the pathogenic findings on the biopsy consist of a subchondral fracture and dead bone cells.

Stage IV is the most serious form of avascular necrosis. The patient has significant symptoms. There is joint space narrowing. There are acetabular changes, which means there are changes on both sides of the joint. Bone scan shows increased uptake and there are significant osteoarthritic changes on both sides of the joint.

As we know that Bo Jackson was a baseball and football player and sustained an injury in 1991, which ended his career. I watched the video of the injury and although there’s a feeling that Bo Jackson dislocated his hip, it’s more likely that he injured his hip or fractured his hip.

This injury probably cut off the blood supply to the head of the femur leading to avascular fitness. It’s unlikely for a native hip to be relocated without anesthesia. A native hip is a very stable joint and if dislocated it needs anesthesia, and a surgical maneuver to relocate the hip. I therefore feel that in the case of Bo Jackson, it was a break in his bone that cut off the blood supply that led to avascular necrosis and a subsequent end to his career.

The other names for avascular necrosis are osteonecrosis, aseptic necrosis, or ischemic necrosis, all of which mean a condition where there is loss of blood supply to the bone.

The aim of any treatment is to minimize the disability and minimize the pain caused from avascular necrosis. I start with diagnostic evaluation, which starts with an x-ray. In cases with a very high clinical suspicion, I do a bone scan or an MRI. As discussed, the bone scan may show a cold spot in Stage 0 of avascular necrosis and the x-rays are essentially normal. The MRI is more useful in the earlier stages of the disease.

I am not aware of any homeopathic medication that can cure avascular necrosis. If you wish to consider alternative therapies, it’s best to contact the provider directly. I cannot opine on non-approved therapies for treatment of avascular necrosis.

You can try over-the-counter medications. However, most types of avascular necrosis are progressive and will give rise to progressive pain and disability if not treated.

I am not aware of any natural therapies for the treatment of avascular necrosis.

Steroids interfere with the circulation to the head of the femur, which is susceptible to die, and therefore the steroids cause avascular necrosis, especially of the hips.

During hip replacement surgery the head of the femur is removed, along with the socket. The entire part of the bone that has become necrotic due to lack of blood supply is removed, and therefore total hip replacement is the final cure for avascular necrosis.

Patient mortality is not possible from avascular necrosis of the hip alone. Most of the conditions that cause avascular necrosis of the hip affect the patient’s regional body parts and are not considered risk factors by themselves for mortality. The risks of the surgery for avascular necrosis can be associated with mortality, and that risk has to be discussed preoperatively with the surgeon.

No, obviously avascular necrosis cannot happen in a joint replacement because the part of the bone that is necrosed is removed and is replaced with a prosthetic device. It is however possible to have avascular necrosis adjacent to the joint replacement surgery. And if the patient has continuous symptoms, this should be investigated by the surgeon.

Avascular necrosis can be prevented by decreasing the risk factors that cause avascular necrosis in the first place. As an example, patients who are alcoholics can decrease their alcohol or eliminate the intake of alcohol. Sickle cell anemia needs to be controlled. The use of corticosteroids for treatment of asthma or systemic lupus erythematosus should be minimized.

In a patient of trauma, as the example with hip dislocation, the dislocation should be reduced immediately and if the patient has suffered from the fractured neck of the femur, the fracture has to be reduced in a minimally invasive manner and fixation has to be accurate. This can prevent or delay the onset of avascular necrosis.

Total joint replacement surgery remains the last choice for patients with avascular necrosis. Total joint replacement surgery is done only when there is significant arthritis and the sphericity of the head of the femur is lost because of lack of blood supply.

Today it is not acceptable for younger patients to remain in pain, and disabled, and have no mobility because of the pain from avascular necrosis. I have done several surgeries in younger patients because there was no choice for them apart from suffering in pain and being on pain medications.

Younger patients do extremely well after joint replacement surgery done for avascular necrosis. They are completely pain-free and continue to live productive lives pain-free.

It depends on the stage of the disease. I use core compression and stem cell therapy in the early stages of the disease. For advanced stages of the disease, the French have used it and have shown improvement, however, I feel that for patients who have significant arthritis from avascular necrosis are best benefited by joint replacement surgery.

I would suggest non-impact type of activities for patients with avascular necrosis. Any impact type of activity is going to aggravate the collapse, the pain, and increase the risk of arthritis in the hip joint.

Avascular necrosis is painful in the later stage of the disease. In Stage 0, the x-ray is not affected. Avascular necrosis is only seen on a bone scan and on the MRI. And this is the time when I advise intervention even without symptoms. This is among the rare situations where patients get surgery without symptoms. The idea is to decrease the risk of joint replacement surgery in the future.

There are certain types of avascular necrosis which heal on their own. These are rare and the patient should discuss the findings with the surgeon to see if that is a possibility. Serial MRIs or serial bone scans can be done in these cases to monitor the avascular necrosis and to ensure it is not progressing.

The progression of avascular necrosis depends on numerous factors including the cause of avascular necrosis in that particular patient. Additionally, I would also consider the time from which the diagnosis has been made to the time of presentation of pain as an additional factor.

For example, if the avascular necrosis has been diagnosed on MRI a year ago, and the patient is still not symptomatic, it would suggest that the progression is significantly slow. The patient should understand that the onset of MRI typically precedes the onset of pain of avascular necrosis.

Under certain circumstances, I would consider a repeat MRI to see if there is any progression or regression of the disease. I would also consider a comparison of the new MRI with the MRI done before to see if the disease has progressed or regressed since the time of the first MRI.

Both avascular necrosis, osteonecrosis, ischemic bone necrosis, aseptic necrosis mean the same.

It depends on the cause of necrosis, where it is located, and the size of the necrotic lesion, whether the necrotic lesion is associated with arthritis, and the treatment taken for the necrosis.

I believe there is a genetic component for avascular necrosis which makes a particular patient more susceptible for a stimulus than others.

In my opinion, protected weight-bearing has not shown to improve the course of the disease. Eventually the patients develop pain and it is not a good, long-term option. There are certain pharmacological agents available, like Alendronate and Fosamax, which have not shown to give good long-term relief. Electrical stimulation has also been tried, but the results are not really satisfactory.

In the early stages of the disease, I do core decompression, which means I use small drill holes to core in and remove the diseased part of the bone. This has been shown to improve the blood supply to the femoral head. In addition, I like to use stem cells to augment the procedure and improve the possibility of the bone healing.

My preferred method for using stem cells is by aspirating the iliac crest, which means the pelvis of the patient, taking out the hematopoietic blood cells, spinning them around, concentrating them, and then injecting it into the core decompression space. This has shown excellent results and the pain from the avascular necrosis is alleviated in the early stages of avascular necrosis.

If the patient has significant collapse and significant arthritis, the only option available is a joint replacement surgery. Osteotomy ( surgical rotation of the part of the bone which is diseased ) has been described by Japanese investigators, including Sugioka, but the results have not found to be satisfactory. Vascularized as well as non-vascularized bone grafting has been used for avascular necrosis.

But again, in my opinion, it has not proved to have satisfactory, predictable results. To summarize, in the early stages of the disease I use core decompression with stem cells, and in the later stage of the disease I use joint replacement surgery to alleviate the pain and suffering from avascular necrosis.

There are numerous predisposing factors for avascular necrosis. I classified them as one-time factors and chronic factors. One-time factors are fracture of the neck of the femur, and a dislocation of the hip joint. Chronic factors include use of corticosteroids, the use of alcohol, sickle cell disease, myeloproliferative disorders, coagulation deficiencies, and radiation.

Avascular necrosis of the hip usually starts with a small area where the blood supply to the bone is cut off and it is usually in the weight-bearing part of the hip joint. As the disease advances, the head of the upper end of the thigh bone (femur) begins to collapse, there is formation of cysts, and eventually there is arthritis.

Any patient with early AVN but a high future risk of progression to advanced arthritis of the hip should have a core decompression along with stem cell implantation. Patients who have already developed significant arthritis need total hip replacement surgery.

There are a few cases in which I do core decompression to prevent further damage to the hip joint, even though the patient may not have pain. This is in patients where I see a lesion in the MRI and on bone scan, and I know that they are going to have avascular necrosis and problems in the future.

In core decompression surgery, the patient is anesthetized and small drill holes are made from the outside of the hip that go inside the head of the femur. The diseased bone is cored out. This is done under X-ray guidance. It’s a small procedure and after injecting the stem cells into the upper end of the femur, the wound is closed. The patient can weight bear as tolerated after the surgery, and usually goes home the same day.

A lot has been talked about free vascular fibular graft, but in my opinion, the results are not satisfactory and the disadvantages outweigh the advantages for this procedure. Thorough investigations have shown that the hip replacement surgery is delayed for a few years. However, I am significantly worried at what cost.

I have known patients who have had free fibular vascular graft who have been non-weight-bearing who have continued to have pain, and ultimately several years later they needed the joint replacement surgery. After a free vascular grafting to the hip joint, the results are unpredictable and the blood supply to that vascularized segment can get cut off again. The patient is on blood thinners, and I am not happy with the quality of life it offers. I therefore do not recommend this procedure.

The fibula is removed in free vascularized grafting, and fibula is a non-weight-bearing bone. There is absolutely no change in the way the patient is able to walk. The patient is able to walk normally after a few weeks after the fibula bone is removed.

The surgery of core decompression or total joint replacement surgery is never done in a rush. We do a thorough preoperative evaluation. I always try to get to the cause of avascular necrosis, and try to treat the cause. Preoperative evaluation has to be done to ensure that it is safe for the patient to undergo surgery, and it is always done as elective surgery, never as emergency.

It’s okay to wait several weeks after being diagnosed with avascular necrosis, however, waiting too long will cause increased collapse of the bone and significant arthritis that will need joint replacement surgery. The idea of core decompression is to delay the onset of significant arthritis and delay the need for joint replacement surgery.

After core decompression surgery, the patient can walk weight-bearing as tolerated with crutches. The crutches are used for a few days until the patient feels stable enough to walk without crutches. After joint replacement surgery, the patient walks with a walker the same day of surgery, and then with a cane in the contralateral upper extremity until the muscles are rehabilitated.

After both types of surgeries, core decompression and total joint replacement surgery, I use Aspirin for prevention of blood clots. It also helps in pain control and prevention of cardiac adverse effects after the surgery.

After core decompression, a blood transfusion is not needed. After joint replacement surgery, the patient may need a blood transfusion depending upon what the blood values are prior to the surgery and also depending on how much blood loss has happened during the surgery. We use numerous techniques to decrease the blood loss including, tranexamic acid, which has shown to decrease blood loss during joint replacement surgery.

Most patients are required to the hospital a couple of hours before the actual surgery, and the hospital informs them of the exact time to come to the hospital.

The hospital will inform the patient what needs to be brought to the hospital. It usually includes a change of clothing. And any jewelry, or wallets, and purses are kept in security at the hospital and returned to the patient after the patient is ready to leave the hospital.

After core decompression surgery, usually the hospital will give crutches and the patient continues to walk weight-bearing as tolerated after the surgery. A high toilet seat, a walker, a nurse, and a physical therapist are set up for the patient before the patient goes home.

The patient’s absence from work depends on the type of surgery that was done and the type of work that the patient does. After core decompression, usually the patient leaves the hospital the same day. The patient can go back to low-load physical activity, like a desk job, after a couple of days.

For heavy manual labor, after a core decompression, patients can return to work in about six weeks’ time. After joint replacement surgery, I’ve known patients to go back to work within the week. However, for manual labor, I tell them to have a reasonable expectation of two to three months before they return to work.

Pharmaceutical agents, electrical stimulation has been tried with unsatisfactory results. If a patient with avascular necrosis declines surgery, there is likely to be progression in the disease of the avascular necrosis. The patient should consider surgical intervention if the patient needs pain medication on a daily basis.

I understand it’s a tough decision to consider any sort of intervention in the absence of pain. However, it is only in the early stages of the disease that the patient has no pain, and this is exactly the time to consider treatment to prevent the progression of the disease.

I start by ensuring that it is really avascular necrosis on MRI and not similar looking condition on MRI. I then evaluate the causes of avascular necrosis in that patient and especially if I feel avascular necrosis is a cause that is likely to cause progression of avascular necrosis surgical treatment is indicated.

The patient has no pain in early stages of avascular necrosis according to all classification systems. Avascular necrosis manifests only on MRI in the earlies stage and it is not seen on an x-ray. If the patient has had progressive avascular necrosis in one hip, and if MRI shows avascular necrosis in the other hip I would consider surgical intervention early on to decrease deterioration of the affected hip, which shows only the MRI even if the patient does not have any pain.

The reason is to decrease the possibility of developing arthritis in the hip, especially if the other hip has had progression that has necessitated surgical intervention like a total hip replacement.

I use the classification system as popularized by Ficat and Arlet. It is based on X-ray, and MRI, and bone scan findings.

In stage 0 of avascular necrosis, the patient has no symptoms. The X-rays are normal. The bone scan may show decreased uptake.

In stage 1 of avascular necrosis the patient typically has no symptoms. The X-ray findings are normal and a cold spot may be seen on the femoral head. If a biopsy is performed, the biopsy shows abundant dead marrow cells and there are also other bone cells that are seen in the biopsy.

In stage 2 of avascular necrosis, the symptoms are typically mild. There is a density change in the femoral head in stage 2 and the bone scan shows increased uptake. If a biopsy is performed, it shows new bone deposited between the dead bone cells. In stage 2 a, we can see a sclerosis or cysts in the X-ray. However, the contour of the femoral head is well preserved. That means that the femoral head is very well preserved. In type 2 b, there is some flattening on the X-ray and that is also called a crescent sign which is characteristic of 2 b of avascular necrosis of the femoral head.

In stage 3 of avascular necrosis, the patient has mild to moderate symptoms. There is loss of sphericity and there is collapse of the femoral head. On bone scan there is increased uptake. If a biopsy is performed, the biopsy shows dead bone cells and marrow cells on both sides of the fracture line. The characteristic, pathological findings of stage 3 avascular necrosis are a sub contour fracture collapse and fragmentation of the necrotic segment.

In stage 4 of avascular necrosis, the patient typically has moderate to severe symptoms. There is significant joint space narrowing. There are also a couple of changes meaning that not only is the femoral head involved, there’s also involvement of acetabular side of the joint. If a bone scan is performed, it will show increased uptake.

The characteristic pathological findings on an X-ray are osteoarthritic changes which are seen on the femoral side, as well as on the acetabulum side. That means that arthritis involves both sides of the joint. This type of stage of 4 of femoral head avascular necrosis requires a total hip arthoplasty to get relief from the symptoms. Thank you.

Transient osteonecrosis of the hip is a self-limiting (as a term implies) condition that resolves with time.  Transient osteonecrosis of the hip was initially described in the third trimester of pregnancy, however, it can also be found in other demographics including in young men. The treatment of transient osteoporosis of the hip is conservative with protected weightbearing and close observation.

MRI can differentiate between transient osteoporosis of the hip and osteonecrosis of the hip.  MRI shows clear absence of a focal lesion.  In transient osteoporosis of the hip, there is just diffuse edema on MRI.  In osteonecrosis of the hip, subchondral collapse and focal abnormalities are very clearly seen. It is important to distinguish between these two conditions because of transient osteonecrosis of the hip resolves over time while osteonecrosis typically is progressive and results in significant symptoms.

Fractures involving the neck of the femur are responsible for avascular necrosis of the hip. These type of fractures disrupt the blood supply to the femoral head and therefore lead to avascular necrosis. There are other types of hip fractures which are outside the hip joint. These fractures are called intertrochanteric fractures. Intertrochanteric fractures of the hip do not cause avascular necrosis.

Fractures of the neck of the femur are at high risk for avascular necrosis and also for nonunion (which means that the bone fragments do not unite). There are numerous reasons why these fractures have difficulty healing. The reasons are compromised blood supply, the fracture cells that are needed for healing the fracture are washed away into the joint, etc. In elderly patients, we therefore replace the joint as soon as these fractures happen so that we can get these patients up and moving as soon as possible.

This type of replacement can be a partial hip replacement or a total hip replacement. In younger patients, we try to salvage the femoral head by doing open reduction and internal fixation with screws. The possibility of developing avascular necrosis after a hip fracture depends on numerous factors like accuracy of the fracture reduction, time after which the fracture was treated operatively, and placement of the implants that hold the fracture in a stable position, etc.

The reason for pain from avascular necrosis depends on the stage of the avascular necrosis. In the early stages there is a feeling that there is increased pressure inside the bone and the death of the bone cells itself causes pain. When core decompression is performed (which means that the bones are drilled for bringing in blood supply) the drilling releases some of the pressure inside the bone and is thought as one of mechanisms for relieving pain from avascular necrosis.

In advanced stage of the disease, avascular necrosis leads to arthritis and arthritis is the cause of pain. In arthritis the sphericity of the femoral head is lost and there is bone rubbing on bone which leads to pain from avascular necrosis of the hip.

The most useful test for diagnosis of avascular necrosis depends on the stage of the avascular necrosis. In the early stages, MRI and a bone scan is useful for diagnosis. In the late stage of the disease, if there is arthritis, I do not feel a need to get MRI because the treatment options for late arthritis do not change. The option for late arthritis resulting from avascular necrosis is total hip replacement.

Yes-we do phone consultations all the time. If you are interested in a phone consultation you can contact our office. The MRI reports and pictures of the x-ray are emailed to us, along with the accompanying blood work, if any. I review the results and call the patient. As I always say, I treat patients, not x-rays or MRI’s. There is nothing better than a physical examination but I can understand that patients who live internationally need to have questions answered before traveling for treatment.

If a patient is living in a different country or out of the state, or several hours away in upstate New York, you can contact my office and arrange for a phone consultation. After a phone consultation I can give them advice on whether they need to come and see me, or whether they can get service from a local orthopedic surgeon. For complicated procedures patients do prefer to travel to New York and get the procedure done from me.

For procedures that are fairly routine, they can be treated at the regional hospital by a local provider. There is a small, there is a fee for the phone consultation and this is frequently not covered by the insurance company. However, there are a few insurance companies that do understand the patient’s needs and cover this fee. If a CD or x-ray is physically mailed to the office, please make sure that you have a copy.

Because of logistics, it is not possible for us to mail it back to you. The best format to send it to our office is electronically. Patients who come to me internationally do send their x-rays to me and a copy of their primary care or medical doctors reports so that we can get a better evaluation of the patients medical and orthopedic issues to see if they’re a candidate to travel to New York for orthopedic procedures.

We understand this is daunting for patients who travel internationally and across states for orthopedic procedures. We are very cognizant of the price, and the need for travel to accomplish the patient’s goals. If travel is needed, there are certain hotels which we can recommend for a stay before and after the orthopedic procedure. For international patients we can give a flat fee, which includes the hospital stay, medications in the hospital.

It also includes the anesthesiologist and the medical doctor taking care of the patient. It does not include the travel to and from New York. It does not include the hotel stay. It also does not include post-operative physical therapy and does not include the medications after the surgery that are needed after the hospital stay. Most patients after hip and knee replacement surgery need some pain medications including narcotics, some anti-inflammatory medications and aspirin. The cost of these medications is very affordable.

If patients are interested in considering a phone consultation or considering travel to New York for orthopedic procedures, they can contact our office and we will get back with them as soon as possible. For international patients we are cognizant of different time zones, which we accommodate during the phone consultation. For patients from non-English speaking countries, we have found it difficult to find a translator, however we do our best to accommodate it.

The cost of a translator for non-English speaking patients is additional. For patients in China I found that written correspondence has been very satisfactory. There have also been patients who send us their consultation fee or surgical fee in advance, which is required by some consulates to obtain a visa. If a Visa is not obtained we have been very prompt in returning the fee to the patient if they’re unable to travel to the United States.

Although very rare, cortisone injection given intra-articular can cause avascular necrosis of the head of the femur. The surgeon will consider the risk of avascular necrosis to the patient before instituting the injection, including any previous history of avascular necrosis and the necessity of the cortisone injection.

Yes, avascular necrosis of the hip usually presents as an insidious pain, mostly located in the front of the hip. The pain is generally exaggerated on navigating stairs, bending, walking, and any impact activities.

A Total Hip Replacement (THR) done in patients with an advanced stage of avascular necrosis of the hip provides excellent pain relief. Unfortunately in most patients with avascular necrosis, only THR remains the most reliable means to provide an immediate return of function with excellent pain relief.

Most of the avascular necrosis cases are not inherited but rarely in some cases; it could result from a mutation in the collagen type 2 gene resulting in genetic inheritance. The genetic cause is also a factor in patients having avascular necrosis of the femoral head secondary to sickle cell anemia. Some disorders causing increased coagulability of the blood may be inherited, increased blood coagulability may result in avascular necrosis of the femoral head.

The avascular necrosis of the knee joint may result from trauma/injury to the knee joint. Other risk factors associated with AVN of the knee include alcoholism, decompression sickness (‘’the bends”), bone marrow-replacing inherited disorders (e.g. Gaucher’s disease), sickle cell disease, long term use/abuse of steroids, diseases such as systemic lupus erythematosus, inflammatory bowel disease, certain viral infections and medications such as protease inhibitors.

Unfortunately, most cases of avascular necrosis progress, causing worsening of the symptoms. But rarely, in the early stages of the disease, when the avascular necrosis is caused by alcoholism or Corticosteroids, stopping the alcohol/corticosteroid may stop the progression and may heal by formation by the formation of new blood vessels.

Avascular necrosis is not an emergency, but early diagnosis and treatment can prevent the disease’s progression and arthritis development.

The long-term heavy consumption of alcohol is a known cause of avascular necrosis (AVN) of the femur’s head. Long-term alcohol consumption causes hyperlipidemia, which is the excess of fatty cells in the body. The blood levels of fat in the form of triglycerides, low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL) increase.

The increased fat content of the blood causes blockage of the blood vessels. The femur’s head is especially susceptible to decreased blood flow and may lead to aseptic necrosis/cell death. The alcohol also acts as a direct cellular toxin and may damage the blood supply to the femur’s head.

In Ficat and Arlet classification, there are 5 stages of the femoral head’s avascular necrosis, including stage 0 when the disease process is silent with no symptoms and no changes visible on plain radiographs. However, an MRI can find AVN changes even in stage 0. In stage 1, the patient may experience symptoms with AVN changes only visible on an MRI.

With an absent blood supply, a segment of bone is necrosed. The surrounding bone with blood supply tries to revascularize the dead bone. Vascular tissue lays down new bone in the area which increases the density (visible as increased whiteness in an X-ray in stage 2a.)

A small fracture or break develops between the new bone and the dead bone. The space in between the break is filled by scar tissue. Overlying cartilage without nourishment softens and decays. The weight-bearing on the joint leads to small dents or breaks in the cartilage, leading to collapse (visible as a crescent sign-in stage 2b).

The smooth gliding is now lost, and the ball grinds with the socket in the area (segmental arthritic changes in stage 3). The process becomes widespread, leading to severe arthritis and the destruction of the entire joint surface (stage 4).

Corticosteroid and ethanol are the most common drugs causing avascular necrosis. Several other medications have been found to potentially cause AVN, including adrenocorticotropic hormone therapy, anti-cancer drugs, arsenic compounds, and antiretroviral drugs like protease inhibitors.

A bone bruise may potentially disrupt the blood supply to the bone resulting in ischemia and necrosis. Any trauma/injury, which may result in decreased blood supply to the bone may cause avascular necrosis.

Unfortunately, most cases of avascular necrosis of the femoral head progress without surgical intervention. Studies show the effect of medications, protected weight-bearing, or electrical stimulations on slowing the disease’s progression. Still, ultimately most patients need surgery for the management of AVN.

X-ray or plain radiographs of the hip can only show changes suggestive of avascular necrosis in stage 2 and beyond. In stage 1 and 0, plain X-ray cannot show changes of AVN.

Yes, the pain arising from the hip joint may commonly present as upper thigh pain or may even radiate to the knee. This is because of a common nerve relaying the sensation from both the hip and the thigh.

Core decompression of the head of the femur along with stem cell therapy, has shown the potential to stop the progression in the early stages of the disease. Unfortunately, many patients still progress to advanced stages of avascular necrosis, requiring joint replacement surgery.

Protected weight bearing or immobilization has been shown to have little to no effect on the disease progression. Protected weight-bearing may help prevent the collapse of the head of the femur, but the disease progression continues.

Impact activities or walking may lead to the collapse of the femur’s head in patients diagnosed with avascular necrosis of the hip.

Although the amount and duration of alcohol may vary among different patients diagnosed with avascular necrosis of the femoral head secondary to alcohol. The average duration of alcohol intake found among cases of AVN is usually 8 – 10 years with weekly consumption of 400 ml of alcohol or more.

Pancreatitis has been implicated in the cause of avascular necrosis through increased lipid content of the blood. The hyperlipidemia may cause increased pressure in the head of the femur and disrupt the femur head’s precarious blood supply. The decreased blood supply may result in ischemia and subsequent necrosis of the bone.

The patients with avascular necrosis frequently present with pain associated with limping, often noticed by their families. The limping may result as the patient’s body tries to decrease the weight-bearing time on the affected side. The limping may also result from the collapse of the head of the femur and subsequent discrepancy of the leg length.

Magnetic Resonance Imaging (MRI) can detect avascular necrosis in the early stages when an X-ray cannot show any changes.

Certain movements, such as one required to tie shoelaces, maybe the first to be limited. With advanced disease, all the movements are gradually lost and the hip joint is fixed in one position.

Hyperbaric chamber therapy works on the principle of increased oxygen supply to the tissues. Although some studies have shown it to be effective in the early stages of avascular necrosis, most cases progress to advanced stages without surgical management.

The femoral head’s vascular necrosis can be commonly confused with Transient osteoporosis of the hip, which is often a self-limiting condition affecting generally pregnant females in their 3rd trimester and middle-aged men.

The transient osteoporosis results from bone edema/swelling, causing increased bone marrow pressure. The condition is often self-limiting and resolves completely in 6-8 months. Also, the restriction of range of motion is generally in extremes of motion only and there is generalized bone edema visible on radiological investigations.

Alendronate is a bisphosphonate medication that reduces bone destruction by bone cells known as osteoclasts and subsequently increasing bone density. Studies have shown limited successful results in the management of the early stages of the AVN. Unfortunately, most patients progress to an advanced stage without surgical intervention.

Hip preservation surgeries such as core decompression with or without stem cell implantation, osteotomies, porous tantalum rods, curettage & bone grafting, vascularized bone grafts have shown success when performed in the early stages of avascular necrosis of the head of the femur. However, their success is limited over time and most of the patients end up with advancing disease requiring a hip replacement. The patients with a total hip replacement experience complete relief of pain and regain their mobility.

Although corticosteroids taken for a prolonged period pose a significant risk in the development of avascular necrosis, only systemic steroids have been found to be the culprit. The risk from inhaled corticosteroids remains low as only a marginal dose goes into the systemic circulation. However, there is still a risk of development of AVN in susceptible patients.

In idiopathic avascular necrosis and AVN resulting from systemic disorders, both the hips are involved in 60-80% of the cases. The time of onset of symptoms in both the affected hip may differ significantly; therefore it is always important to screen for avascular necrosis in the contralateral hip.

Small lesions of avascular necrosis may progress if left untreated. The progression varies from one patient to another but typically, the stages may progress over months to years. The management of the early stages of AVN (Stage 0 – 2a) involves surgical intervention in the form of core decompression with or without stem cell retrieved from the bone marrow.

Running/jogging or any other impact activity is generally avoided to prevent the collapse of the head of the femur. In the early stages of the avascular necrosis of the head of the femur, there is bone death just under the cartilage of the bone.

The overlying cartilage along with the bone may collapse under pressure during high impact activities. But the early stages of AVN managed with surgeries such as core decompression showing no progression of the disease on subsequent MRIs may safely resume jogging/running following extensive rehabilitation.