AVN of the hip
AVASCULAR NECROSIS OF THE HIP
Avascular necrosis of the hip is also known as osteonecrosis of the hip. There are approximately 20,000 new cases per year in the United States. It accounts for approximately 10% of all the arthroplasties performed. It is more common in men than women and the average age of presentation is between 35 and 50. It involves both hips 80% of the time. 3% of these patients will have osteonecrosis to multiple areas of the body. There are multiple causes of avascular necrosis of the hip. They are separated into direct causes indirect causes. Some of the direct causes include irradiation, trauma, hematologic disease, Caisson disease and Gaucher’s disease. Indirect causes include alcoholism, hypercoagulable states, exogenous steroid use, lupus, transplant patients, some viruses, HIV medications and of course idiopathic. There are couple of mnemonics that may help with remembering causes of avascular necrosis.
ASEPTIC Most Common Causes
Exogenous steroids Steroids
Caisson disease Sickle-cell
The pathophysiology associated with avascular necrosis as a common idiopathic pathway of intravascular coagulation. First there is coagulation of the intraosseous microcirculation followed by venous thrombosis followed by retrograde arterial occlusion which leads to intraosseous hypertension. There is decreased blood flow to the femoral head with resultant avascular necrosis of the femoral head leading to chondral fracture and collapse. Avascular necrosis associated with trauma is usually due to disruption of the blood supply to the femoral head. The most common artery is the medial femoral circumflex.
Prognosis of avascular necrosis of the femoral head can be calculated using the modified Kerboul combined necrotic angle measurement. You can calculate this by adding the arc of the femoral head necrosis on the midsagittal and mid-coronal MR image. Low-risk groups have a combined necrotic angle less than 190°. Moderate risk groups have a combined necrotic angle between 190° and 240°. High-risk groups have a combined necrotic angle of more than 240°.
The most common classification system is the Steinberg classification.
Stage 0: Has normal radiographs, normal MR and normal bone scan
Stage I: Has normal radiographs, abnormal MRI and/or bone scan
Stage II: Has cystic or sclerotic changes on x-ray with an abnormal MRI and/or bone scan
Stage III: Has a crescent sign with abnormal MRI and/or bone scan
Stage IV: Has flattening of the femoral head with abnormal MRI and/or bone scan
Stage V: Has narrowing of the joint, abnormal MRI and/or bone scan.
Stage VI: Advanced degenerative changes, abnormal MRI and/or bone scan.
Symptoms usually include insidious onset of pain. There is increased pain when going up or down stairs, inclines or any impact activities. Physical exam findings are normal initially but as the osteonecrosis advances pain increases with motion and there is decreased internal rotation. When you suspect avascular necrosis of the femoral head, one should initially get it radiographs. Most of the classification systems are based on radiographic findings. The MRI is an excellent study because of its high sensitivity and specificity (99% each). It should only be used after x-rays to stage or predict prognosis. Presence of bone marrow edema on the MRI is predictive of worsening pain and future progression of the disease. At times bone scans are helpful at predicting whether there is bone activity within the lesion signifying angiogenesis.
Medical treatment is not very predictable. There have been studies that shows that some bisphosphonates help with reversing the pre-collapse advancement of osteonecrosis. Alendronate trials have shown that it prevents femoral head collapse in osteonecrosis with subchondral lucency. However, other studies have shown no benefit in preventing collapse with bisphosphonates. Medical treatment consists of pain management only. Pain control usually involves acetaminophen, NSAIDs and narcotics when needed.
There are several operative procedures that may be helpful with avascular necrosis. Core decompressions with or without bone grafting may be helpful in early AVN before subchondral collapse occurs. The traditional method included drilling and 8 to 10 mm hole through the subchondral necrosis. An alternative method simply passes a 3.2 mm pin into the lesion 2-3 times for decompression. This helps to relieve the intraosseous hypertension which helps to improve the pain. It also helps to stimulate healing response via angiogenesis. A rotational osteotomy is indicated in lesions that are small. Lesions less than 15% of the weight bearing surface can be rotated to alleviate the pressure and minimize the risk of collapse. In Japan, it has a reported success rate of 60 to 90% but it also distorts the femoral head, making a total hip arthroplasty more difficult.
The vascularized free-fibular transfer graft has also been used in both pre-collapse and collapsed AVN in young patients. The procedure basically removes a core of bone up to the lesion and then inserts a fibular graft just below the subchondral bone. The graft is vascularized using the local blood supply of the proximal femur. Some centers are demonstrating 80% success rate in a 5 to 10-year follow-up. It is less predictable in patients over 40 years of age. The total hip replacement seems to be the go-to approach for significantly painful avascular necrosis of the hip. It is perfect for younger patients with a positive crescent sign or more advanced femoral head collapse. The prosthetic is usually cementless. Care must be taken with preparation of the femur as femoral canal perforations are common. With the anterior approach for total hip arthroplasty it has essentially replaced arthrodesis as a choice of treatment for very young patients in a labor-intensive occupation.
Paul Desillier PA-C, MPAS