Kienböck disease
Updates to Article Attributes
Kienböck disease is the eponymous name given to avascular necrosis (aseptic necrosis) involving the lunate.
Epidemiology
The age distribution for Kienbock disease depends on gender. The condition is most common within the dominant wrist of young adult men where it appears to be due to repeated loading of the lunate. In women, Kienbock disease typically occurs in middle age and is equally divided between the dominant and non-dominant wrist 1.
There is a significant association between negative ulnar variance and Kienbock disease, although the majority of people with negative ulnar variance do not have the condition. A causal association is difficult to prove, however the effectiveness of decompressive procedures such as radial shortening or ulnar lengthening in relieving pain and preventing further collapse of the lunate is supportive 2. Overall, negative ulnar variance is present as a predisposing factor in around 75% of cases of Kienbock disease.
Pathology
The pathologic changes are equivalent to those of avascular necrosis of other bones. There is disruption of critical blood supply leading to bone infarction, central necrosis and surrounding hyperaemia. Microfractures ensue resulting in flattening and deformity of the bone surface.
In 70% of lunates there is vascular supply multiple vessels either volarly or dorsally. In the remaining 30% only a single vessel is present volarly and dorsally, which may explain some of the vulnerability of the lunate to avascular necrosis 1.
Radiographic features
Plain filmradiograph
Sclerosis and flattening of the lunate. When flattening is marked there is rotation of the scaphoid which further adds to the stress on the lunate. Fragmentation of the lunate and secondary degenerative disease may develop later.
A five stage radiographic classification system exists. See article Stahl classification of Kienbock disease.
MRI
Is the most sensitive and specific test and may detect very early disease. Pattern of lunate bone signal change allows the condition to be differentiated from ulnar impaction syndrome: the major differential diagnosis. Sclerosis (low T1 and T2) is usually seen centrally and within the radial aspect of the lunate. The sclerosis can be diffuse. Bone oedema (high T2, intermediate T1) may be seen in the acute phase, particularly on the radial side.
Nuclear medicine
A negative bone scan can be useful to exclude the disease however a positive scan is not specific enough for diagnosis.
Treatment and prognosis
Conservative management with rest, non-steroidal anti-inflammatory drugs and immobilisation in mild cases is often very effective. Radial shortening to correct negative ulnar variance is the most common surgical therapy with good results. Other operative procedures include ulnar lengthening, revascularisation, lunate excision with or without prosthetic replacement and inter-carpal fusion. Proximal row carpectomy is used as a salvage procedure in refractory cases 1.
History and etymology
The condition is named after Austrian radiologist Robert Kienböck (1871-1953), who described the condition in 1910 3-4.
Differential diagnosis
InOn imaging consider
-
ulnar impaction syndrome
- sclerosis/signal change is at proximal ulnar aspect of lunate
- more commonly associated with positive ulnar variance
See also
-<p><strong>Kienböck disease</strong> is the eponymous name given to <a href="/articles/avascular-necrosis">avascular necrosis </a>(aseptic necrosis) involving the lunate. </p><h4>Epidemiology</h4><p>The age distribution for Kienbock disease depends on gender. The condition is most common within the dominant wrist of young adult men where it appears to be due to repeated loading of the lunate. In women, Kienbock disease typically occurs in middle age and is equally divided between the dominant and non-dominant wrist<sup> 1</sup>.</p><p>There is a significant association between <a href="/articles/negative-ulnar-variance-2">negative ulnar variance</a> and Kienbock disease, although the majority of people with negative ulnar variance do not have the condition. A causal association is difficult to prove, however the effectiveness of decompressive procedures such as radial shortening or ulnar lengthening in relieving pain and preventing further collapse of the lunate is supportive <sup>2</sup>. Overall, negative ulnar variance is present as a predisposing factor in around 75% of cases of Kienbock disease. </p><h4>Pathology</h4><p>The pathologic changes are equivalent to those of <a href="/articles/avascular-necrosis">avascular necrosis</a> of other bones. There is disruption of critical blood supply leading to bone infarction, central necrosis and surrounding hyperaemia. Microfractures ensue resulting in flattening and deformity of the bone surface.</p><p>In 70% of lunates there is vascular supply multiple vessels either volarly or dorsally. In the remaining 30% only a single vessel is present volarly and dorsally, which may explain some of the vulnerability of the lunate to avascular necrosis <sup>1</sup>.</p><h4>Radiographic features</h4><h5>Plain film</h5><p>Sclerosis and flattening of the lunate. When flattening is marked there is rotation of the scaphoid which further adds to the stress on the lunate. Fragmentation of the lunate and secondary degenerative disease may develop later. </p><p>A five stage radiographic classification system exists. See article <a href="/articles/stahl-classification-of-kienbock-disease-1">Stahl classification of Kienbock disease</a>. </p><h5>MRI</h5><p>Is the most sensitive and specific test and may detect very early disease. Pattern of lunate bone signal change allows the condition to be differentiated from <a href="/articles/ulnar-impaction-syndrome">ulnar impaction syndrome</a>: the major differential diagnosis. Sclerosis (low T1 and T2) is usually seen centrally and within the radial aspect of the lunate. The sclerosis can be diffuse. Bone oedema (high T2, intermediate T1) may be seen in the acute phase, particularly on the radial side.</p><h5>Nuclear medicine</h5><p>A negative bone scan can be useful to exclude the disease however a positive scan is not specific enough for diagnosis. </p><h4>Treatment and prognosis</h4><p>Conservative management with rest, non-steroidal anti-inflammatory drugs and immobilisation in mild cases is often very effective. Radial shortening to correct negative ulnar variance is the most common surgical therapy with good results. Other operative procedures include ulnar lengthening, revascularisation, lunate excision with or without prosthetic replacement and inter-carpal fusion. Proximal row carpectomy is used as a salvage procedure in refractory cases <sup>1</sup>.</p><h4>History and etymology</h4><p>The condition is named after Austrian radiologist <strong>Robert Kienböck </strong>(1871-1953), who described the condition in 1910 <sup>3-4</sup>.</p><h4>Differential diagnosis</h4><p>In imaging consider</p><ul><li>- +<p><strong>Kienböck disease</strong> is the eponymous name given to <a href="/articles/avascular-necrosis">avascular necrosis </a>(aseptic necrosis) involving the lunate. </p><h4>Epidemiology</h4><p>The age distribution for Kienbock disease depends on gender. The condition is most common within the dominant wrist of young adult men where it appears to be due to repeated loading of the lunate. In women, Kienbock disease typically occurs in middle age and is equally divided between the dominant and non-dominant wrist<sup> 1</sup>.</p><p>There is a significant association between <a href="/articles/negative-ulnar-variance-2">negative ulnar variance</a> and Kienbock disease, although the majority of people with negative ulnar variance do not have the condition. A causal association is difficult to prove, however the effectiveness of decompressive procedures such as radial shortening or ulnar lengthening in relieving pain and preventing further collapse of the lunate is supportive <sup>2</sup>. Overall, negative ulnar variance is present as a predisposing factor in around 75% of cases of Kienbock disease. </p><h4>Pathology</h4><p>The pathologic changes are equivalent to those of <a href="/articles/avascular-necrosis">avascular necrosis</a> of other bones. There is disruption of critical blood supply leading to bone infarction, central necrosis and surrounding hyperaemia. Microfractures ensue resulting in flattening and deformity of the bone surface.</p><p>In 70% of lunates there is vascular supply multiple vessels either volarly or dorsally. In the remaining 30% only a single vessel is present volarly and dorsally, which may explain some of the vulnerability of the lunate to avascular necrosis <sup>1</sup>.</p><h4>Radiographic features</h4><h5>Plain radiograph</h5><p>Sclerosis and flattening of the lunate. When flattening is marked there is rotation of the scaphoid which further adds to the stress on the lunate. Fragmentation of the lunate and secondary degenerative disease may develop later. </p><p>A five stage radiographic classification system exists. See article <a href="/articles/stahl-classification-of-kienbock-disease-1">Stahl classification of Kienbock disease</a>. </p><h5>MRI</h5><p>Is the most sensitive and specific test and may detect very early disease. Pattern of lunate bone signal change allows the condition to be differentiated from <a href="/articles/ulnar-impaction-syndrome">ulnar impaction syndrome</a>: the major differential diagnosis. Sclerosis (low T1 and T2) is usually seen centrally and within the radial aspect of the lunate. The sclerosis can be diffuse. Bone oedema (high T2, intermediate T1) may be seen in the acute phase, particularly on the radial side.</p><h5>Nuclear medicine</h5><p>A negative bone scan can be useful to exclude the disease however a positive scan is not specific enough for diagnosis. </p><h4>Treatment and prognosis</h4><p>Conservative management with rest, non-steroidal anti-inflammatory drugs and immobilisation in mild cases is often very effective. Radial shortening to correct negative ulnar variance is the most common surgical therapy with good results. Other operative procedures include ulnar lengthening, revascularisation, lunate excision with or without prosthetic replacement and inter-carpal fusion. Proximal row carpectomy is used as a salvage procedure in refractory cases <sup>1</sup>.</p><h4>History and etymology</h4><p>The condition is named after Austrian radiologist <strong>Robert Kienböck </strong>(1871-1953), who described the condition in 1910 <sup>3-4</sup>.</p><h4>Differential diagnosis</h4><p>On imaging consider</p><ul><li>
Image 18 CT (bone window) ( create )
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