Osteochondritis Dissecans of the Elbow: Difference between revisions

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Staging of osteochondritis dissecans is depicted below:<br>  
Staging of osteochondritis dissecans is depicted below:<br>  


Staging of Osteochondritis Dissecans <sup>2</sup>  
Staging of Osteochondritis Dissecans<ref>Champ L. Baker III et al. Osteochondritis dissecans of the capitellum. American Journal Of Sports Med; 38; 1917-1928 (Level of Evidence: 3A)</ref>


Stage Appearance on MRI Stability of Lesion  
Stage Appearance on MRI Stability of Lesion  
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IV Loose body Unstable  
IV Loose body Unstable  


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This figure shows the different stages of Osteochondritis Dissecans. These vary from stage I to IV as explained above this picture. From left to right we can examine stage I through stage IV. <br>(http://www.seattlechildrens.org/medical-conditions/bone-joint-muscle-conditions/cartilage-conditions/osteochondritis-dissecans/)<br>


This figure shows the different stages of Osteochondritis Dissecans. These vary from stage I to IV as explained above this picture. From left to right we can examine stage I through stage IV. <br>(http://www.seattlechildrens.org/medical-conditions/bone-joint-muscle-conditions/cartilage-conditions/osteochondritis-dissecans/)<br>
Steven A. Giuseffi et al. believe the trigger is likely multifactorial. A couple of mechanisms that contribute to the development of OCD are: trauma, ischemia, disordered ossification and genetic abnormalities. But these mechanisms are momentarily not universally accepted but may be a contributing factor.<br>From another point of view vascular hypoperfusion and repeated microtrauma may also contribute to the development of OCD. Capillary blood supply is often limited to 1 or 2 end vessels with limited collateral flow. This leads to vascular hypoperfusion. Repeated microtrauma could lead to a production of a relatively avascular state in the vulnerable immature capitellar chondroepiphysis.<ref name="Steven" /><br>  
 
Steven A. Giuseffi et al. believe the trigger is likely multifactorial. A couple of mechanisms that contribute to the development of OCD are: trauma, ischemia, disordered ossification and genetic abnormalities. But these mechanisms are momentarily not universally accepted but may be a contributing factor.<br>From another point of view vascular hypoperfusion and repeated microtrauma may also contribute to the development of OCD. Capillary blood supply is often limited to 1 or 2 end vessels with limited collateral flow. This leads to vascular hypoperfusion. Repeated microtrauma could lead to a production of a relatively avascular state in the vulnerable immature capitellar chondroepiphysis.<ref name="Steven" /><br>


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Revision as of 21:27, 2 June 2016

Search Strategy[edit | edit source]

Searched databases : PubMed, PEDRo, Web of Science, Cochrane
Search terms : Osteochondritis Dissecans elbow, Osteochondrosis, elbow injury, Osteochondritis physical therapy, Osteochondritis diagnose, Osteochondritis Dissecans capitellum, osteochondritis dissecans elbow physical therapy, osteochondrosis

Definition/Description[edit | edit source]

An increasingly recognised cause of elbow pain that affects subchondral bone and the overlying cartilage is called Osteochondritis Dissecans (OCD) of the elbow, also known as osteochondrosis of the elbow.
OCD can lead to subsequent degenerative arthritis or osteoarthritis.[1] Osteochondritis dissecans leads to fragmentation and separation of cartilage and underlying bone.[2]
Osteochondritis Dissecans (OCD) is defined as an inflammatory pathology of bone and cartilage resulting in localised necrosis and fragmentation of bone and cartilage. In the elbow, the most common area affected is the capitellum, although it has been reported in the olecranon and the trochlea.[3] OCD summarised means that there are one or more flakes of articular cartilage that become separated. They will form loose bodies within the joint. The separated flakes stay alive (they are nourished by the synovial fluid) and the flakes often ossify.[4]

Clinically Relevant Anatomy
[edit | edit source]

Involved anatomy of this disorder includes the radial head or the central and/or lateral aspect of the capitellum.

Most OCD lesions of the elbow involve the capitellum, typically the central or lateral portion, but also the radial head, the olecranon of the ulnae and the trochlea humeri.[1]
Also increased activity, loss of motion, and swelling on the lateral side of the elbow comes with increased pain.[1]

Epidemiology / Ethiology
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Ostechondrosis of the humeral capitellum is secondary to repetitive compressive forces between radial head and capitellum. This injury results in a loose body containing an osteochondral bone fragment that is detached from the articular surface. Causes of this pathology include injury or stress on the joint, lack of blood supply, and/or genetic makeup.
Repetitive high stress forces on the joint can result in a series of minor injuries on the elbow that can eventually lead to a fracture and ultimately detachment of the bony fragment from the bone.
Blockage of a small artery can also be a factor in this pathology. Avascular Necrosis that leads to the lack of blood supply contributes to break down or death of bone tissue. Osteochondritis dissecans also has a genetic component allowing a predisposition to the pathology.


Staging of osteochondritis dissecans is depicted below:

Staging of Osteochondritis Dissecans[5]

Stage Appearance on MRI Stability of Lesion

I Thickening of cartilage and a stable lesion
low signal changes

II Articular cartilage interrupted and a stable lesion
low signal rim behind fragment
showing that there is fibrous
attachment

III Articular cartilage interuppted, Unstable
high signal changes behind
fragment and underlying
subchondral bone

IV Loose body Unstable


This figure shows the different stages of Osteochondritis Dissecans. These vary from stage I to IV as explained above this picture. From left to right we can examine stage I through stage IV.
(http://www.seattlechildrens.org/medical-conditions/bone-joint-muscle-conditions/cartilage-conditions/osteochondritis-dissecans/)

Steven A. Giuseffi et al. believe the trigger is likely multifactorial. A couple of mechanisms that contribute to the development of OCD are: trauma, ischemia, disordered ossification and genetic abnormalities. But these mechanisms are momentarily not universally accepted but may be a contributing factor.
From another point of view vascular hypoperfusion and repeated microtrauma may also contribute to the development of OCD. Capillary blood supply is often limited to 1 or 2 end vessels with limited collateral flow. This leads to vascular hypoperfusion. Repeated microtrauma could lead to a production of a relatively avascular state in the vulnerable immature capitellar chondroepiphysis.[1]



Clinical Presentation[edit | edit source]

Presentation includes pain over the joint, stiffness, feeling of instability, and stiffness after resting.

Diagnostic Procedures[edit | edit source]

Radiographs can detect any abnormalities on the surface of the joint.

Magnetic Resonance Imaging (MRI) will show any accumulation of fluid in the area and can detect any loose fragments.

Computerized Tomography (CT) can detect any bony fragments, pinpoint their location and determine whether they have settled in the joint space.

Outcome Measures[edit | edit source]

An outcome measure appropriate for this injury is the DASH questionnaire which measures disabilities of the arm, shoulder and hand as they relate to everyday function. A modified Andrews elbow scoring system (MAESS) is used to determine specific function of the elbow.

Management / Intervention[edit | edit source]

Conservative care for this condition include physical therapy, use of non-steroidal anti-inflammatory drugs (NSAIDs), rest from sport from 6-8 weeks, and bracing.
Surgical management may be an option if conservative care fails or if the lesion is Grade III or higher.
Surgical interventions are aimed at:
Promoting re-vascularization to the area
Debriding the area
Fragment stabilization
Bone grafting if needed
Most of these procedures are done arthroscopically (minimally invasive via portal sites); although depending on the size of the loose fragments an open procedure may be required.


Differential Diagnosis
[edit | edit source]

If there is no radiologic confirmation of osteochondritis dissecans, other diagnoses may include inflammatory arthritides, osteoarthritis, bone cysts, and septic arthritis.

Key Evidence[edit | edit source]

A study published in 2008 reports a favorable prognosis of up to 90% for patients who are treated conservatively in the stage I of this condition. Patients who were in stage II had about a 53% of a good prognosis with conservative treatment. Duration of this treatment was just under 15 months in the first stage and 13 months in the second stage. About 78% of stage I and 53% of stage II patients were able to return to competitive baseball. Mean ages for these groups were about 12 years in stage I and 14 years of age in stage II. This study is a level III study, and more research should be done to support these results.
Another study performed in 2006 looks at the surgical considerations for osteochondritis dissecans. The article looks at 15 patients with a mean age of 28 that underwent elbow arthroscopic debridement for this condition. These patients were classified using the Baumgarten system and were graded during arthroscopy. They looked at the patients about 4 years out of surgery and found a significant decrease in pain levels and function was improved from a “poor” to an “excellent” status per the modified Andrews elbow scoring system. About 80% of these patients were able to return to the same level of sport while all of the patients were able to return to work.
Factors that should be considered are age, activity level for the studies above. Clearly more research needs to be done to determine best practice when it comes to treatment of osteochondritis dissecans.

Resources
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add appropriate resources here


Recent Related Research (from Pubmed)[edit | edit source]

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References[edit | edit source]

References will automatically be added here, see adding references tutorial.

[6] [7][8] [9] [10]


  1. 1.0 1.1 1.2 1.3 Steven A. Giuseffi et al. Osteochondritis dissecans of the elbow. Oper Tech Sport Med 2014; 22; 148-155 (Level of Evidence: 3A)
  2. Champ L. Baker III et al. Osteochondritis dissecans of the capitellum. American Journal Of Sports Med; 38; 1917-1928 (Level of Evidence: 3A)
  3. Felix H. Savoie, III, MD; Oper Tech Sports Med 16:187-193 © 2008 Elsevier Inc (Level of Evidence: 2A)
  4. H.L.F. Currey, Essentials of rheumatology, 1988,p166 (Level of Evidence: 5)
  5. Champ L. Baker III et al. Osteochondritis dissecans of the capitellum. American Journal Of Sports Med; 38; 1917-1928 (Level of Evidence: 3A)
  6. Mayo Clinic. Osteochondritis Dissecans. http://www.mayoclinic.com/health/osteochondritis-dissecans/DS00741 (accessed 6/13/09).
  7. Rahusen F Th G, et al. Results of arthroscopic debridement for osteochondritis dissecans of the elbow. B J Sports Med 2006;40:966-969. Abstract: http://bjsportmed.com/cgi/content/abstract/40/12/966 (accessed 6/25/09).
  8. Matsuura T, et al. Conservative Treatment for Osteochondrosis of the Humeral Capitellum. Am J Sports Med. 2008;36(5): 868-872. Abstract: http://ajs.sagepub.com/content/36/5/868.abstract (accessed 6/18/09).
  9. O’Sullivan S, Siegelman R. National Physical Therapy Examination Review &amp;amp;amp;amp;amp;amp;amp;amp;amp; Study Guide. Evanston, IL: International Educational Resources Ltd, 2006.
  10. Patient UK. http://www.patient.co.uk/showdoc/40001133/ (accessed 6/13/09)