Avascular Necrosis
Original Editor - Kenny Bosmans
Top Contributors - Linde Van Droogenbroeck, Kenny Bosmans, Kim Jackson, Uchechukwu Chukwuemeka, Lucinda hampton, Admin, Rachael Lowe, Daphne Jackson, WikiSysop, 127.0.0.1, Tony Lowe, Evan Thomas and Vidya Acharya
Definition/Description[edit | edit source]
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.
Epidemiology/Etiology[edit | edit source]
Avascular necrosis can be a result of an earlier bone trauma (such as a break in the bone), a dislocation, or a medical condition, such as sickle cell anemia or Systemic Lupus Erythematosus. In many cases, avascular necrosis seems to be associated with steroid abuse or heavy drinking[1].
Clinical Presentation[edit | edit source]
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[1]. The most common location for this condition to manifest, is the head or neck of the femur or humerus, and the knee joint[1].
Avascular necrosis can be classified into five different stages:[2]
- 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[edit | edit source]
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[1]. In further stages of the disease, loss of mobilization and increased pain can be detected[1]. Once osteonecrosis is detected, the physician should assess other joints that may be at risk, such as the hip, shoulder and knee[1].
Standard radiographs can confirm the diagnose. If not, an MRI can assist in making the diagnosis.
Outcome Measures[edit | edit source]
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.
Management / Interventions[edit | edit source]
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[2]. Most patients will eventually need surgical treatment, such as core decompression or arthroplasty[1].
Nonoperative treatment involves three main goals:[1]
- Relief of symptoms
- Prevention of disease progression
- 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[2].
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.
Physical therapy treatment focuses on exercises to maintain joint mobility and strengthen the muscles around the affected joint. Electrical stimulation and ultrasound can be used to stimulate bone growth[1]. During physical therapy, excessive compressive and shear forces on the joint should be avoided.
Differential Diagnosis[edit | edit source]
Resources[edit | edit source]
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)[edit | edit source]
Failed to load RSS feed from http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1-KHXJhm35h8wR0dYRwpTwuNRzS5muwjdvIkrguY-QWZRIAE0h|charset=UTF-8|short|max=10: Error parsing XML for RSS
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Gruson K, Kwon Y. Atraumatic osteonecrosis of the humeral head. Bulletin of the NYU Hospital for Joint Diseases 2009;67(1):6-14.
- ↑ 2.0 2.1 2.2 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).
