Avascular Necrosis

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Definition/Description

Avascular necrosis (also known as osteonecrosis, bone infarction, aseptic necrosis, ischemic bone necrosis and AVN) is a condition where bone tissue dies due to a lack of blood supply. This decrease in blood supply causes a decrease in oxygen and nutrient delivery to the bone, which leads to multiple breaks in the bone and eventual collapse of the affected bone. This condition is most common in younger patients who are between the age of 20 and 40.

See Avascular necrosis of the femoral head and Hip Avascular Necrosis for joint-specific information.

Epidemiology/Etiology

Avascular necrosis can be a result of an earlier bone trauma (such as a break in the bone) or a dislocation.

Non-traumatic Osteonecrosis can have many causes:

•  heavy drinking  and steroid abuse have been identified as major risk factors 
•  Numerous studies have also concluded that hyperlipidemia in the femoral head, induced by steroid and alcohol use, are associated with    osteonecrosis. Both of these factors precipitate an increase in fat volume in bone marrow and blood lipid levels, thereby increasing      deposition  of fat and interrupting blood flow to the femoral head.
•  Glucocorticoid intake was found to have an even stronger association than alcohol use.
•  Cigarette smoking: due to changes in nitric oxide bioavailability, there is an increased oxidative stress level and endothelial dysfunction
•  Obesity: osteonecrosis is positively associated with BMI. Overweight and obesity are, just like steroid and alcohol use, often associated     with hyperlipidemia.
•  A medical condition, such as sickle cell anemia or Systemic Lupus Erythematosus.

Studies show that there is a higher prevalence among males, this could be attributed to higher levels of smoking and alcohol use. Greater fluctuations in climate temperatures may also contribute to higher rates of non-traumatic osteonecrosis. (level 1a) 

Clinical Presentation

Symptoms include pain and decreased range of motion in the affected joint. In some cases, the condition is diagnosed during routine x-ray imaging, due to a lack of overt symptoms. The most common location for this condition to manifest, is the head or neck of the femur or humerus, and the knee joint.

Avascular necrosis can be classified into five different stages:

• Stage 1: Radiographic changes are absent and MRI scan is required for identification.
• Stage 2: First stage with radiographic changes. This stage is characterized by sclerosis of the superior central portion of the joint head.
• Stage 3: In this stage, the articular surface is depressed so that the round contour is compromised, without being significantly deformed.
• Stage 4: This stage is characterized by a wide collapse of the subchondral bone and destruction of the underlying trabecular pattern. This can lead to secondary arthritis.
• Stage 5: The final stage where both articular surfaces are affected, which leads to a dysfunctional joint.

Diagnostic Procedures

Osteonecrosis can be diagnosed with a thorough check of the historical background of the patient combined with physical examination. Steroid exposure and alcohol abuse are important risk factors. The age of the patient can also provide clues to the disease, because patients with osteonecrosis are generally younger than those with osteoarthritis. Locking, popping, or a painful click during mobilization of the affected joint can point to the presence of loose osteochondral fragments. In further stages of the disease, loss of mobilization and increased pain can be detected. Once osteonecrosis is detected, the physician should assess other joints that may be at risk, such as the hip, shoulder and knee.

Standard radiographs can confirm the diagnose. Tissue affected by avascular necrosis will appear more dense (increased whiteness) and possibly sclerotic (patchy) on the radiograph. An MRI can assist in making the diagnosis.

Outcome Measures

Choice of outcome measure will be dependent on the joint affected. If the patient reports symptoms of pain, consider a pain rating scale such as the 4-Item Pain Intensity Measure (P4), Numeric Pain Rating Scale, or Visual Analogue Scale.

A functional outcome measure is useful for establishing the patient's baseline function and setting measurable goals. See Outcome Measures Database for more.

Medical Management

• Pharmacological Therapy
  Pharmacological therapy with anticoagulants, statins, and vasodilators seems to be effective to delay the progress of joint degeneration in early stages of avascular necrosis. Although, there is very low evidence to support the use of these pharmacological agents in the treatment of osteonecrosis. Another still experimental treatment are Bisphosphonates. Hypothetically in early stages of AVN the use of bisphosphonates could inhibit osteoclastic activity preventing subchondral bone collapse.
  
• Surgical Treatment

Physical Therapy Management 

Appropriate treatment for avascular necrosis is necessary to prevent further deterioration of the joint. If untreated, most patients will experience severe pain and limitation of movement within two years. Although physical therapy cannot cure avascular necrosis, it can slow down the progression of the disease and decrease associated pain. It is suggested that patients with Stage 1 and 2 osteonecrosis could benefit from a physical therapy program. Most patients will eventually need surgical treatment, such as core decompression or arthroplasty.

Nonoperative treatment involves three main goals:

1. Relief of symptoms
2. Prevention of disease progression
3. Improvement of functionality

Nonoperative treatment begins with patient education and addressing known risk factors, such as smoking and alcohol abuse. In addition, corticosteroids should be avoided.

To assist the patient in regaining function and relieve painful symptoms, crutches or other gait aids can be introduced. The physical therapist should instruct the patient in how to properly use these devices.
By using crutches, the load that the hip joint bears, will be decreased. This weight bearing restriction is an important conservative treatment. In literature, it is considered that weight bearing restriction as a stand-alone therapy is insufficient in preventing disease progression, but it’s a reasonable treatment option when combined with pharmacological agents or surgery. (level 2a) 

Physical therapy treatment focuses on exercises to maintain joint mobility and strengthen the muscles around the affected joint.  During physical therapy, excessive compressive and shear forces on the joint should be avoided. The outcome depends on the lesion’s size and stage at the initiation of the treatment.

In order to maintain joint mobility, both passive and active exercises should be initiated. Passive exercises contain passive movements of the hip and stretching exercises. Active exercises consist of 3dimensional motions of the hip joint and can be applied during standing, sitting on a chair or while lying down. In the next stage, strengthening exercises are added. These exercises will focus on the muscles of the hip and thigh but will also include exercises for the core area as they play a large supporting role. To improve functionality it is important to implement endurance training and coordination training in a more advanced stage of the therapy. Endurance can be trained by walking on a treadmill or cycling on a home trainer. To improve coordination, walking exercises with increased complexity and balancing exercises can be adopted in physical therapy sessions. (level 1b)

Electrical stimulation and ultrasound can be used to stimulate bone growth. For example, Extracorporeal Shock Wave Therapy (ESWT) causes expression of angiogenic growth factors that act as a stimulus to neovascularization and could therefore be useful in the treatment of AVN. The current evidence suggests that ESWT improves pain and function in early stages of disease. Although, more evidence is needed. Heat is also applied as an attempt to increase bloody supply to the area and help decrease pain. 

Resources

Gruson K, Kwon Y. Atraumatic osteonecrosis of the humeral head. Bulletin of the NYU Hospital for Joint Diseases 2009;67(1):6-14.

Lee MS, Hsieh PH, Shih CH, Wang CJ. Non-traumatic osteonecrosis of the femoral head – from clinical to bench. Chang Gung Med J 2010;33(4).

Huijbregts P. Osteonecrosis of the humeral head: a literature review and two case studies. J Man Manip Ther 2000;8(4):175-182.

Hasan S, Romeo A, Nontraumatic osteonecrosis of the humeral head. J Shoulder Elbow Surg 2002.

Recent Related Research (from Pubmed)

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