Avascular Necrosis: Difference between revisions

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'''Original Editor '''- [[User:Kenny Bosmans|Kenny Bosmans]]


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== &nbsp;Definition/Description ==
== 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 nutrition delivery to the bone, which leads to multiple breaks in the bone and eventual collapse of the affected bone.
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.  


== &nbsp;Epidemiology/Etiology  ==
== Epidemiology/Etiology  ==


Avascular necrosis can be a result from an earlier bone trauma, such as a break in the bone, a dislocation or medical conditions like Sickle cell anemia and Lupus. In most cases, avascular necrosis seems to be associated with steroid abuse or heavy drinking. <ref name="1">Gruson K, Kwon Y, “Atraumatic Osteonecrosis of the Humeral Head”, Bulletin of the NYU Hospital for Joint Diseases 2009;67(1):6-14</ref>
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|sickle cell anemia]] or [[Systemic Lupus Erythematosus]]. In many cases, avascular necrosis seems to be associated with [[Anabolic Steroid Abuse|steroid abuse]] or [[Alcoholism|heavy drinking]]<ref name="Gruson">Gruson K, Kwon Y. Atraumatic osteonecrosis of the humeral head. Bulletin of the NYU Hospital for Joint Diseases 2009;67(1):6-14.</ref>.


== Clinical Presentation  ==
== Clinical Presentation  ==


The symptoms include pain and loss of motion in the affected joint. In some cases, the condition is diagnosed during routine x-ray imaging, due to a lack of symptoms. <ref name="1" /><br>The most common location for this condition to manifest, is the caput, collum of the femur, the humerus and the knee joint. <ref name="1" />  
Symptoms include pain and decreased range of motion in the affected joint. In some cases, the condition is diagnosed during routine [[X-Rays|x-ray imaging]], due to a lack of overt symptoms<ref name="Gruson" />. The most common location for this condition to manifest, is the head or neck of the [[Hip Anatomy|femur]] or [[Glenohumeral Joint|humerus]], and the [[Knee|knee joint]]<ref name="Gruson" />.


<br>avascular necrosis can be classified into 5 different stages; <ref name="2">Lee MS, Hsieh PH, Shih CH, Wang CJ, “Non-traumatic Osteonecrosis of the Femoral Head From Clinical to Bench”, Chang Gung Med J Vol. 33 No. 4, 2010</ref>  
Avascular necrosis can be classified into five different stages:<ref name="Lee">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).</ref>  


<br>Stage 1: Radiographic changes are absent and MRI scan is required for identification.  
*'''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.


<br>Stage 2: First stage with radiographic changes. This stage is characterized by sclerosis of the superior central portion of the joint head. <br>
== Diagnostic Procedures  ==


Stage 3: In this stage, the articular surface is depressed so that the round contour is compromised, without being significantly deformed.  
Osteonecrosis can be diagnosed with a thorough check of the historical background of the patient combined with physical examination. [[Anabolic Steroid Abuse|Steroid exposure]] and [[Alcoholism|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|osteoarthritis]]. Locking, popping, or a painful click during mobilization of the affected joint can point to the presence of loose osteochondral fragments<ref name="Gruson" />. In further stages of the disease, loss of mobilization and increased pain can be detected<ref name="Gruson" />. Once osteonecrosis is detected, the physician should assess other joints that may be at risk, such as the [[Hip|hip]], [[Shoulder|shoulder]] and [[Knee|knee]]<ref name="Gruson" />.  


<br>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.  
Standard [[Diagnostic Imaging for Physical Therapists|radiographs]] can confirm the diagnose. If not, an [[MRI Scans|MRI]] can assist in making the diagnosis.  


<br>Stage 5: The final stage where both articular surfaces are affected, which leads to a dysfunctional joint.<br>
== Outcome Measures ==
 
== 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.<ref name="1" />&nbsp; In further stages of the desease, loss of mobilization and increased pain can be detected. <ref name="1" /><br>Once osteonecrosis is detected, the physician has to check the other joints at risk. Especially hip, shoulder and knee. <ref name="1" /><br>Standard radiographs can confirm the diagnose. If not, the MRI can help in the diagnose.<br>
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]].  
 
== Outcome Measures  ==


add links to outcome measures here (see [[Outcome Measures|Outcome Measures Database]])
A functional outcome measure is useful for establishing the patient's baseline function and setting measurable goals. See [[Outcome Measures|Outcome Measures Database]] for more.


== Management / Interventions<br> ==
== Management / Interventions  ==


appropriate treatment for avascular necrosis is necessary to keep joints from breaking down. If untreated, most patients will experience severe pain and limitation in movement within 2 years. Although physical therapy cannot cure avascular necrosis, it can slow down the progression of the disease and decrease the associated pain. It is suggested that patients with stage 1 and 2 osteonecrosis could have benefits from a physical therapy <ref name="2" />, but most patients will eventually need surgical treatment, such as core decompression or arthroplasty. <ref name="1" />  
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<ref name="Lee" />. Most patients will eventually need surgical treatment, such as core decompression or arthroplasty<ref name="Gruson" />.


<br>nonoperative treatment concludes 3 major goals;<ref name="1" />  
Nonoperative treatment involves three main goals:<ref name="Gruson" />  


1. Relief of symptoms<br>2. Prevention of disease progression<br>3. Improvement of functionality  
#Relief of symptoms  
#Prevention of disease progression  
#Improvement of functionality


<br>Nonoperative treatment begins with patient education and addressing known risk factors, such as smoking and alcohol abuse. In addition, corticosteroids should be avoided.<ref name="2" /><br>To relieve the patient from symptoms crutches or other weight-bearing devices can be introduced. It is the job of the physical therapist to teach the patients how to correctly use them.<br>Physical therapy treatment focuses on exercices to maintain joint mobility and strengthen the muscles around the affected joint, which will decrease the weight on the joint. Electrical stimulation and ultrasound can be used to stimulate bone growth. <ref name="1" /> During physical therapy, excessive compressive and shear forces need to be avoided. <br>
Nonoperative treatment begins with patient education and addressing known risk factors, such as smoking and alcohol abuse. In addition, corticosteroids should be avoided<ref name="Lee" />.  


== Differential Diagnosis<br>  ==
To assist the patient in regaining function and relieve painful symptoms, [[Crutches|crutches]] or other [[Walking Aids|gait aids]] can be introduced. The physical therapist should instruct the patient in how to properly use these devices.


add text here relating to the differential diagnosis of this condition<br>  
Physical therapy treatment focuses on exercises to maintain joint mobility and strengthen the muscles around the affected joint. [[Therapeutic Modalities|Electrical stimulation]] and [[Ultrasound therapy|ultrasound]] can be used to stimulate bone growth<ref name="Gruson" />. During physical therapy, excessive compressive and shear forces on the joint should be avoided. <br>  


== Key Evidence ==
== Differential Diagnosis ==


add text here relating to key evidence with regards to any of the above headings<br>
== Resources  ==


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


Gruson K, Kwon Y, “Atraumatic Osteonecrosis of the Humeral Head”, Bulletin of the NYU Hospital for Joint Diseases 2009;67(1):6-14'''[a1]'''
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).  
<br>Lee MS, Hsieh PH, Shih CH, Wang CJ, “Non-traumatic Osteonecrosis of the Femoral Head From Clinical to Bench”, Chang Gung Med J Vol. 33 No. 4, 2010 '''[a1]'''
<br>Huijbregts P, “Osteonecrosis of the Humeral Head: A Literature Review and Two Case Studies”, The Journal of Manual &amp; Manipulative Therapy, Vol. 8 No. 4 (2000), 175-182. '''[a1]'''
<br>Hasan S, Romeo A, “Nontraumatic osteonecrosis of the humeral head”, Journal of Shoulder and Elbow Surgery, 2002'''[a1]'''<br>


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


add links to case studies here (case studies should be added on new pages using the [[Template:Case Study|case study template]])<br>
Hasan S, Romeo A, Nontraumatic osteonecrosis of the humeral head. J Shoulder Elbow Surg 2002.


== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
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<rss>Feed goes here!!|charset=UTF-8|short|max=10</rss>  
<rss>http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1-KHXJhm35h8wR0dYRwpTwuNRzS5muwjdvIkrguY-QWZRIAE0h|charset=UTF-8|short|max=10</rss>  
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== References  ==
== References  ==


References will automatically be added here, see [[Adding References|adding references tutorial]].
<references />


<references />
[[Category:Condition]] [[Category:Musculoskeletal/Orthopaedics|Orthopaedics]]

Revision as of 04:06, 1 April 2014

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]

  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[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. 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. 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).