Avascular Necrosis of the Lunate.
Edited By: Thomas Trumble, M.D. Last updated Thursday, March 17, 2005
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Incidence and risk factors
Incidence
The condition tends to affect males in their third or
fourth decades. It is usually limited to
one wrist. Certain individuals may be
predisposed due to anatomic variations in blood supply, ulnar length, and
lunate shape:
1. Vascular
There are various patterns of blood supply to the lunate
including “X”, “I”, and “Y” patterns.
Between 7 and 26 percent of lunates have only one artery supplying them
(“I” pattern), with 31 percent having no arterial branching within the lunate (Gelberman, Bauman et al. 1980; Panagis,
Gelberman et al. 1983). This pattern may render the lunate more susceptible
to avascular necrosis, as injury to the single vessel cannot be compensated by collateral flow.
2. Load distribution
a. Ulnar Variance
The length of the distal ulna with respect to the distal
radius in the AP plane is called ulnar variance. A shorter ulna, or negative
ulnar variance, may lead to increased load across the radiolunate articulation,
with increased risk of lunate avascular necrosis. This relationship has been
shown in some studies; others have found no such correlation, and since
Kienböck’s disease occurs in individuals with neutral and even positive ulnar
variance, other factors must be involved as well.(Gelberman, Salamon et al. 1975; Chen and Shih 1990; Coe and
Trumble 1993; Weiss 1994)
b. Lunate Shape
The geometry of the lunate itself and of surrounding bones may also be
significant.
One investigator noted a tendency toward a smaller lunate in his
patients with the disorder.(Tsuge and Nakamura 1993) Three different patterns of lunate morphology at the
articulation with the scaphoid, radius, and triquetrum have been described
along with findings that the vascular foramina tended to occur in proximal
triangular areas of the bone, such that some lunate specimens are less well
vascularized than others.
Acquisition
Kienbock’s is idiopathic
meaning there is no known etiology.
However, as previously discussed, it likely results from both being
predisposed (triangular lunate, negative ulnar variance, “I” pattern artery) as
well as being exposed to environmental influences (repetitive trauma).
No
single factor has been attributable to causing Kienbock’s disease.Genetics
There is no familial pattern of inheritance for
Kienbock’s disease.Communicability
Kienbock's disease is not contagious.Lifestyle risk factors
Exposure to repetitive trauma is a risk factor. Activities that involve compression loading
of the wrist particularly in extension (eg jackhammers) have been postulated to
cause vascular injury.
Other
generic risk factors for avascular necrosis include history of steroid use,
sickle cell anemia, exposure to increased barometric pressure (eg diving), and
smoking. These risk factors are not
particular to Kienbock’s and have been documented more commonly in the hip,
knee, and shoulder.
Injury & trauma risk factors
Trauma is the most common postulated etiology for
Kienbock’s. This can take the form of a
single traumatic episode such as a fracture dislocation of the wrist from a car
accident or it may include repetitive microtrauma such as compression loading
from using a jackhammer.Prevention
There is no prophylaxis against Kienbock’s since you
cannot identify individuals at risk.
Manual
jackhammers have largely been replaced with hydraulic ones. Other than this intervention in the
workplace, there are no guidelines for primary prophylaxis against Kienbock’s.
Surgery for Kienbock's Disease at the University of Washington, Department of Orthopaedics and Sports Medicine, Seattle, Washington
If you are interested in making an appointment to discuss this procedure in Seattle, you can request an appointment using our online referrals website. To request a referral online, please click here. You can also call 206-598-BONE (2663) to make an appointment. Our clinical center is located in Seattle Washington, USA
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