Kienbock’s Disease Symptoms
Published on Mar 19 2010, in the categories: Kienbock
Kienböck disease is called avascular necrosis of the lunate. There are numerous published theories regarding the etiology of this disease, but none has been proven yet. The Kienbock’s disease symptoms include congenital and developmental disorders, primary rupture of blood vessels, thromboembolism, endarteritis obliterans, vascular thrombosis, median neuropathy, and isolated fracture either by accident or secondary to repetitive trauma.
The disease is also described within the family of osteochondrosis (Freiberg, Köller, etc.). Currently, most researchers believe that the necrosis of the lunate comes from a trauma such as stress fracture, avulsion of capsule-ligamentous structures, or horizontal fractures devascularized one pole of the lunate.
There are, in turn, risk factors for the production of necrosis:
- Variance ulnar minus short ulna is one of the most important risk factors in the production of Kienböck, as it leads to increased pressure on the lunate in the transfer of loads from the hand to the forearm.
- Vasculature: there are, according to Gelberman, three patterns of vascularization of the lunate: the pattern in Y (59%), R (31%) and X (10%), the latter being the highest risk for necrosis after horizontal fracture.
- Geometry of the lunate: Antuna Zapico described three types according to their shape and lunate trabeculatura: Type I, oblong, with a proximal apex and is associated with an ulna minus; Type II, more square, with ulna neutral and Type III, pentagonal, with ulna plus. Type I is by the trabecular structure of greater risk.
In conclusion, it is obvious that there is no single factor in the development of Kienböck, but requires some combination of load (single severe compression or repetitive minimal trauma), vascular risk and mechanical bias. This combination produces an effect of "nutcracker" between a prominent radio and head of the capitate, lunate leading to continuing to work under compression resulting in a progressive bone collapse.
Diagnosis
Kienböck's disease should be suspected in any young adult (20 to 35 years) who complained of the Kiebock’s disease symptoms, which are abdominal pain and progressive stiffness of the wrist, and occasionally, swelling over the dorsum of the lunate area.
Usually there is no clear history of trauma, but may correspond to a sequel perilunar carpal dislocation.
On physical examination we note decreased mobility, especially flexion, with tenderness in the central dorsal wrist. The patient reported that he has lost grip strength and can be objectified in the office with a Jamar dynamometer type.
The diagnosis is confirmed with plain radiography when there are advanced stages.
When radiography is negative, but there is a high clinical suspicion and radiological disease (negative ulnar variance, lunate type I) should request a magnetic resonance imaging confirmed the diagnosis.
Evolutionary stage
The most widely used classification of Lichtman corresponds to the split into four successive stages and progressive clinical and radiological:
- Stage I: normal radiology. Sometimes you can display a linear fracture. MRI is positive.
- Stage II: there is sclerosis of the lunate, but no collapse of the same. MRI can provide images of focal or generalized sclerosis.
- Stage III: It appears fragmentation and collapse of the lunate with loss of normal architecture. It is divided into stage IIIA when the angle scapha-mole is normal, and Stage IIIb when there is a fixed scaphoid flexion.
- Stage IV: the carpal collapse, with degenerative changes and mid-carpal radio.
The disease is also described within the family of osteochondrosis (Freiberg, Köller, etc.). Currently, most researchers believe that the necrosis of the lunate comes from a trauma such as stress fracture, avulsion of capsule-ligamentous structures, or horizontal fractures devascularized one pole of the lunate.
There are, in turn, risk factors for the production of necrosis:
- Variance ulnar minus short ulna is one of the most important risk factors in the production of Kienböck, as it leads to increased pressure on the lunate in the transfer of loads from the hand to the forearm.
- Vasculature: there are, according to Gelberman, three patterns of vascularization of the lunate: the pattern in Y (59%), R (31%) and X (10%), the latter being the highest risk for necrosis after horizontal fracture.
- Geometry of the lunate: Antuna Zapico described three types according to their shape and lunate trabeculatura: Type I, oblong, with a proximal apex and is associated with an ulna minus; Type II, more square, with ulna neutral and Type III, pentagonal, with ulna plus. Type I is by the trabecular structure of greater risk.
In conclusion, it is obvious that there is no single factor in the development of Kienböck, but requires some combination of load (single severe compression or repetitive minimal trauma), vascular risk and mechanical bias. This combination produces an effect of "nutcracker" between a prominent radio and head of the capitate, lunate leading to continuing to work under compression resulting in a progressive bone collapse.
Diagnosis
Kienböck's disease should be suspected in any young adult (20 to 35 years) who complained of the Kiebock’s disease symptoms, which are abdominal pain and progressive stiffness of the wrist, and occasionally, swelling over the dorsum of the lunate area.
Usually there is no clear history of trauma, but may correspond to a sequel perilunar carpal dislocation.
On physical examination we note decreased mobility, especially flexion, with tenderness in the central dorsal wrist. The patient reported that he has lost grip strength and can be objectified in the office with a Jamar dynamometer type.
The diagnosis is confirmed with plain radiography when there are advanced stages.
When radiography is negative, but there is a high clinical suspicion and radiological disease (negative ulnar variance, lunate type I) should request a magnetic resonance imaging confirmed the diagnosis.
Evolutionary stage
The most widely used classification of Lichtman corresponds to the split into four successive stages and progressive clinical and radiological:
- Stage I: normal radiology. Sometimes you can display a linear fracture. MRI is positive.
- Stage II: there is sclerosis of the lunate, but no collapse of the same. MRI can provide images of focal or generalized sclerosis.
- Stage III: It appears fragmentation and collapse of the lunate with loss of normal architecture. It is divided into stage IIIA when the angle scapha-mole is normal, and Stage IIIb when there is a fixed scaphoid flexion.
- Stage IV: the carpal collapse, with degenerative changes and mid-carpal radio.
RECENT COMMENTS