It is still not clear whether the lu-nate fracture lines occasionally seen in early Kienböck’s disease repre-sent a primary event, or whether these fractures occur later in the process,
Trang 1In 1910, Robert Kienböck, a Viennese
radiologist, reported a series of 16
cases of “traumatic malacia” of the
lunate.1 Although others had
de-scribed similar anatomic findings in
cadaveric specimens, Kienböck’s
was the first clinical report of
osteo-necrosis of the lunate He provided
radiographic evidence of isolated
changes beginning in the proximal
portion of the lunate and affecting
the radiolunate articulation, with
other areas spared He described
the collapse of the lunate,
occasion-ally with fragmentation, and felt
that this condition was caused by “a
disturbance in the nutrition of the
lunate caused by the rupture of
liga-ments and blood vessels during
contusions, sprains, or
subluxa-tions.” He recommended excision
of the bone in the event of severe pain and disability
Kienböck’s disease occurs most commonly in men aged 20 to 40.2 It
is rarely bilateral, and patients fre-quently have a history of wrist trauma
The initial symptoms of pain over the dorsum of the wrist in the region
of the lunate accompanied by limited wrist motion may have been present months to years before the patient seeks medical attention Some pa-tients with radiographic evidence of severe destruction are relatively asymptomatic; however, most have increasing reactive synovitis and limitation of wrist motion, swelling, grip weakness, and pain with mo-tion and eventually at rest
Isolated or repetitive trauma to a lunate predisposed to injury due to any of several factors (e.g., bone geometry and vascularity) may lead
to a fracture or to vascular compro-mise Bone necrosis results in trabec-ular fractures and sclerosis Un-treated, the process continues, with collapse and fragmentation of the lunate At this stage, carpal height is decreased, the capitate migrates proximally, and the scaphoid hyper-flexes (Fig 1) Abnormal carpal mo-tion, particularly related to scaphoid rotation,3,4 leads to degenerative changes throughout the carpus and the radiocarpal joint
Patients in early stages of the dis-ease rarely seek medical attention Therefore, the true incidence and the natural history are not known with certainty Nevertheless, the apparent common pathway in-volves osteoarthritic changes and debilitating pain, which has led to the development of a large and con-fusing array of treatment options
Dr Allan is Assistant Professor, Department
of Orthopaedics, University of Washington Medical Center, Seattle Dr Joshi is Resident, John Peter Smith Health Network, Fort Worth, Texas Dr Lichtman is Professor and Chair-man, Orthopaedic Residency Program, John Peter Smith Health Network, Fort Worth Reprint requests: Dr Allan, Department of Orthopaedics, Box 356500, 1959 NE Pacific Street, Seattle, WA 98195.
Copyright 2001 by the American Academy of Orthopaedic Surgeons.
Abstract
Kienböck’s disease, or osteonecrosis of the lunate, can lead to chronic,
debilitat-ing wrist pain Etiologic factors include vascular and skeletal variations
com-bined with trauma or repetitive loading In stage I Kienböck’s disease, plain
radiographs appear normal, and bone scintigraphy or magnetic resonance
imaging is required for diagnosis Initial treatment is nonoperative In stage
II, sclerosis of the lunate, compression fracture, and/or early collapse of the
radial border of the lunate may appear In stage IIIA, there is more severe
lunate collapse Because the remainder of the carpus is still uninvolved,
treat-ment in stages II and IIIA involves attempts at revascularization of the
lunate—either directly (with vascularized bone grafting) or indirectly (by
unloading the lunate) Radial shortening in wrists with negative ulnar
vari-ance and capitate shortening or radial-wedge osteotomy in wrists with neutral
or positive ulnar variance can be performed alone or with vascularized bone
grafting In stage IIIB, palmar rotation of the scaphoid and proximal
migra-tion of the capitate occur, and treatment addresses the carpal collapse.
Surgical options include scaphotrapeziotrapezoid or scaphocapitate arthrodesis
to correct scaphoid hyperflexion In stage IV, degenerative changes are present
at the midcarpal joint, the radiocarpal joint, or both Treatment options
include proximal-row carpectomy and wrist arthrodesis
J Am Acad Orthop Surg 2001;9:128-136
Christopher H Allan, MD, Atul Joshi, MD, and David M Lichtman, MD
Trang 2The clinical condition of Kienböck’s
disease, therefore, remains
challeng-ing to both patient and physician
Etiology
Many direct or indirect causes of
Kienböck’s disease have been
pro-posed The local vascular and
os-seous anatomy may play a role
The patterns of lunate blood supply
provide insight into some possible
causes of osteonecrosis of this bone
There are multiple patterns of arterial
supply,2,5with the lunate in most
cadaveric specimens receiving
con-tributions from branches entering
both dorsally and palmarly
How-ever, the lunate was supplied by
only a single palmar artery in 7% of
wrists in one study.6 In addition,
in-traosseous branching patterns vary,
with 31% of specimens in one study
showing a single path through the
bone without significant
arboriza-tion (Fig 2).6 A lunate with a single
vessel and minimal branching may
be at increased risk of osteonecrosis
after hyperflexion or
hyperexten-sion injuries or a minimally
dis-placed fracture Of interest, Takami
et al7reported that severe injuries, such as lunate dislocation, can oc-cur without the development of osteonecrosis or with only a tran-sient appearance of this condition
This is because the lunate usually dislocates palmarly, with a flap of palmar capsule still attached All specimens examined in that study had at least one palmar vessel;
therefore, the intact flap probably transmits sufficient vascular supply
to maintain lunate viability.7 Disruption of venous outflow has also been suggested as a cause of Kienböck’s disease In one study,8
in vitro intraosseous pressure mea-surements within normal and ne-crotic lunates showed marked
in-creases in pressure in the necrotic bones, a finding more consistent with venous stasis than with arterial compromise It is unclear whether this is a cause or a result of the dis-ease process (the authors of that study point out that these findings may be due solely to collapse of the lunate), but traumatic disruption of venous outflow may be another fac-tor in lunate osteonecrosis
Lunate geometry and local anat-omy may be important as well Neg-ative ulnar variance, first identified
as a factor by Hultén9in 1928, was present in 78% of his patients with Kienböck’s disease, but in only 23%
of the general population Hultén suggested that a short distal ulna led to increased force transmission across the radiolunate articulation, contributing to an increased risk of osteonecrosis However, D’Hoore
et al10found no statistically signifi-cant difference in ulnar variance when they compared 125 normal wrists with 52 wrists in patients with Kienböck’s disease Several investigators from Japan11,12have noted that negative ulnar variance occurs with equal frequency in patients with Kienböck’s disease and in the general population A flattened radial inclination may pre-dispose to Kienböck’s disease.12,13 Watanabe et al13noted a tendency toward smaller lunates in their pa-tients with the disorder Thus, neg-ative ulnar variance and flattened radial inclination may predispose certain patients to develop
Kien-Figure 1 Radiographic wrist measurements.
Figure 2 Patterns of intraosseous arterial branching in the lunate (Adapted with per-mission from Gelberman RH, Bauman TD, Menon J, Akeson WH: The vascularity of the
lunate bone and Kienböck’s disease J Hand Surg [Am] 1980;5:272-278.)
Radial inclination Carpal height
Ulnar variance
Scapho-lunate angle
Trang 3böck’s disease, but neither is likely
to be the sole factor
Occasional occurrences of
Kien-böck’s disease have been reported
in association with such conditions
as septic emboli, sickle cell disease,
gout, carpal coalition, and cerebral
palsy, as well as corticosteroid use
However, there is no well-defined
correlation with any systemic or
neuromuscular process that
war-rants screening when considering
the diagnosis.2,14
Thus, the etiology of Kienböck’s
disease seems to involve the
inter-play of multiple factors Vascular
and skeletal variations may lead to
an at-risk lunate, which, when
sub-jected to traumatic insult, repetitive
mechanical loading, or some other
factor, may develop osteonecrosis
It is still not clear whether the
lu-nate fracture lines occasionally seen
in early Kienböck’s disease
repre-sent a primary event, or whether
these fractures occur later in the
process, after revascularization and
resorption of necrotic bone cause
structural weakness.15,16
Diagnostic Techniques and
Staging
Kienböck’s disease can occur in
patients of any age and either sex
even if there is no history of prior
wrist problems Symptoms vary
depending on the stage of the
dis-ease at presentation and may range
from mild discomfort to constant,
debilitating pain Swelling over the
carpus is common and may occur
palmarly as well as dorsally
Ten-derness over the dorsum of the
lunate is a frequent finding Grip
strength may be markedly reduced
Wrist range of motion may be
mini-mally or severely impaired
In 1977, Lichtman described a
clinical and radiographic
classifica-tion for Kienböck’s disease, which is
now widely used to stage treatment
and compare outcomes2 (Table 1)
Before the advent of magnetic reso-nance (MR) imaging, radionuclide scintigraphy was the next diagnos-tic study recommended after plain radiography Hashizume et al17 have pointed out, however, that MR imaging cannot distinguish among osteonecrosis, the histologic reactive interface between living and dead bone, and reactive hyperemia They suggest that MR imaging is never-theless superior to plain radiog-raphy, tomogradiog-raphy, or computed tomography, in defining the early stage of Kienböck’s disease (Licht-man stage I), when trabecular bone has not yet been destroyed By con-trast, once lunate collapse has oc-curred, tomography or computed tomography best reveals the extent
of necrosis and trabecular destruc-tion.17
Quenzer et al18reported that tri-spiral tomography makes possible more accurate staging than stan-dard tomography or plain radiogra-phy In a study of 105 patients with Kienböck’s disease, they noted that 89% of patients with radiographic stage I disease actually met the tomographic criteria for stage II;
this “up-staging” was true as well for 71% of those with radiographic stage II disease and 9% of those
originally considered to have stage III disease Nevertheless, since tri-spiral tomography is not routinely available, plain radiography and
MR imaging (Fig 3) remain the most common tools for staging Kienböck’s disease
In stage I, plain radiographs are either normal or occasionally dem-onstrate a linear fracture without sclerosis or collapse of the lunate (Fig 4) No changes are seen else-where in the carpus The early-flow
Table 1 Stages of Kienböck’s Disease
Stage I Normal radiographs or linear fracture, abnormal but nonspecific
bone scan, diagnostic MR appearance (lunate shows low signal intensity on T1-weighted images; lunate may show high or low signal intensity on T2-weighted images, depending on extent of disease process)
Stage II Lunate sclerosis, one or more fracture lines with possible early
collapse of lunate on radial border Stage III Lunate collapse
IIIA Normal carpal alignment and height IIIB Fixed scaphoid rotation (ring sign), carpal height decreased,
capitate migrates proximally Stage IV Severe lunate collapse with intra-articular degenerative changes at
midcarpal joint, radiocarpal joint, or both
Figure 3 T1-weighted MR image reveals decreased signal intensity of the lunate in the wrist of a patient with Kienböck’s dis-ease.
Trang 4phase of bone scintigraphy may
indicate reactive synovitis In stage
I, MR imaging is highly suggestive
when there is uniformly decreased
signal intensity on T1-weighted
images in comparison with the
surrounding normal bones This change in signal intensity reflects reduced vascularity of the lunate.19 Caution must be exercised when partial T1 signal loss is noted, how-ever Disorders such as ulnar
abut-ment, fractures, enchondromas, and osteoid osteoma can cause focal MR signal changes In addition, tran-sient ischemia may cause a general-ized decrease in lunate signal inten-sity T2-weighted images typically
Figure 4 Drawings and radiologic images illustrating staging of Kienböck’s disease, according to Lichtman 2 In stage I, the trabecu-lar bone has not yet been destroyed, and plain radiographs either are normal or demonstrate a linear fracture without sclerosis or collapse of the lunate In stage II, findings include increased den-sity of the lunate, frequently with one or more fracture lines; the entire lunate may be sclerotic, but lunate height is preserved In stage IIIA there is lunate collapse, but carpal height is relatively unchanged Stage IIIB is characterized by proximal migration of the capitate and fixed hyperflexion of the scaphoid (cortical “ring sign”) In stage IV, arthritic changes are apparent throughout the radiocarpal and/or midcarpal joint (Reformatted coronal CT image depicts both radial styloid and radiolunate degenerative changes.)
Stage IIIA
Stage IV
Stage IIIB
Trang 5show low signal intensity in
Kien-böck’s disease, but will show
in-creased signal if revascularization is
occurring.20,21 For this reason, MR
imaging may also be used to assess
healing of the lunate after treatment
Symptoms in stage I resemble those
of wrist sprains and early nonspecific
synovitis
Radiographic findings in stage
II Kienböck’s disease include
in-creased density of the lunate on
plain radiographs, frequently
asso-ciated with one or more fracture
lines Density changes in the lunate
are often best appreciated on the
lateral plain radiograph The entire
lunate may be sclerotic, but lunate
height is preserved There are no
associated carpal abnormalities
Clinical findings in stage II are
fre-quently those of chronic synovitis
Increased density of the lunate
can also occur as a transient finding,
not associated with the typical
pro-gressive changes of Kienböck’s
dis-ease This is a common finding after
perilunate fracture-dislocations, and
generally resolves with standard
treatment of the initial injury.7
In stage III, the lunate shows
col-lapse This stage can be divided
into two categories In stage IIIA,
lu-nate collapse has occurred, but
car-pal height is relatively unchanged
Lateral radiographs demonstrate a
widened anteroposterior dimension
of the lunate associated with
short-ening in the coronal plane Neither
proximal migration of the capitate
nor fixed hyperflexion of the
scaph-oid (cortical “ring sign”) is present
In stage IIIB, these signs of carpal
collapse do appear In addition,
there may be ulnar deviation of the
triquetrum and either the dorsal or
the volar intercalated segment
insta-bility pattern Clinical findings are
progressive stiffness in stage IIIA
and signs of wrist instability in
stage IIIB
In stage IV Kienböck’s disease,
arthritic changes are also apparent
throughout the radiocarpal or
mid-carpal joint or both Symptoms in stage IV are similar to those of de-generative arthritis of the wrist, with more severe swelling, pain, and limitation of motion
Treatment
The value of staging Kienböck’s disease lies in guiding the selection
of treatment (Table 2), in predicting the results of treatment, and in comparing the results of different treatment regimens There is a vast array of proposed treatments for Kienböck’s disease, but certain techniques have documented pat-terns of success These will be dis-cussed along with alternative pro-cedures for each stage of disease
Stage I
Many authors report poor results with prolonged immobilization as the primary treatment for stage I disease.22 For this reason, some clinicians elect to treat stage I
dis-ease in the same way as stage II and stage IIIA disease Nevertheless, for most clinicians, cast immobiliza-tion (or an equivalent form of wrist immobilization, such as with use of
an external fixator) remains the first treatment option for stage I Kien-böck’s disease The possibility of resolution of symptoms does exist; therefore, a trial of immobilization for as long as 3 months is appropri-ate In addition, such a period may allow the restoration of vascularity
in cases of transient osteonecrosis of the lunate, helping to distinguish this entity from Kienböck’s disease Delaere et al22 recently reported that night splinting during periods
of discomfort for patients with stage I, II, or III Kienböck’s disease gave results equivalent to those obtained with surgical treatment However, the average level of dis-ease severity in the splinted group was one stage lower than that in the operatively treated group; thus, comparison was difficult How-ever, in another series of 22
nonsur-Table 2 Options for Treatment of Kienböck Disease
Stage of Disease Treatment
II and IIIA with negative Radius-shortening osteotomy; ulnar
or neutral ulnar variance lengthening; capitate shortening
II and IIIA with positive Direct revascularization + external fixation ulnar variance or temporary scaphotrapeziotrapezoid
pinning (stage II only); radial-wedge or dome osteotomy; capitate shortening with or without capitohamate fusion; combination of joint-leveling and direct revascularization procedures
fusion with or without lunate excision with palmaris longus autograft; radius-shortening osteotomy; proximal-row carpectomy
wrist denervation
Trang 6gically treated patients with
vari-ous stages of disease,2 17 showed
progression, and 5 had no
im-provement
When immobilization fails to
reverse the avascular changes, the
process will almost always have
advanced to stage II In this
set-ting, analysis of ulnar variance is
important
Stage II or IIIA With Neutral or
Positive Ulnar Variance
Stages II and IIIA are often
con-sidered together, and treatment
options are similar with one major
exception In stage II, lunate
avas-cularity has developed, but the
bone has not collapsed Direct
re-vascularization procedures have
their greatest likelihood of success
in this stage
A number of vascularized
pedi-cle and/or bone grafting procedures
have been described, including
vas-cularized transfers of the pisiform
bone, transfers of segments of the
distal radius on a vascularized
pedi-cle of pronator quadratus, and
transfers of branches of the first,
sec-ond, or third dorsal metacarpal
arteries.23-25 Our preference has
been to use the second dorsal
inter-metacarpal artery and vein either as
originally described26 or as
modi-fied by suturing it to a
corticocancel-lous graft harvested from the distal
radius.24 Most of the recently
de-scribed vascularized pedicle bone
grafts have the advantage that the
bone graft and vascular pedicle are
harvested together, making the
pro-cedure technically easier The
dor-sal aspect of the distal radius is
sup-plied by several arterial branches,
which enter the bone via septa
be-tween the extensor compartments
When these are used, no vein is
har-vested Because of anatomic
varia-tion, it is best to be aware of the
location of several potential
vascu-larized pedicle bone grafts before
performing such a procedure
Ex-ternal fixation to unload the lunate
after revascularization has often been used, but temporary pinning
of the scaphotrapeziotrapezoid (STT) joint or the scaphocapitate (SC) joint for the same purpose has also been described.24,25 Outcomes
of the various direct revasculariza-tion procedures are still being eval-uated
Treatment options other than direct revascularization for patients with stage II or IIIA disease and positive ulnar variance include radial closing-wedge osteotomy, radial-dome osteotomy, and capitate shortening with or without capito-hamate fusion (Almquist proce-dure).11,13,27 These may be consid-ered attempts to unload the lunate
to improve its environment for re-vascularization through decreasing the shear stress across the radio-lunate joint Capitate shortening (Figs 5 and 6) is relatively simple, and good results have been reported (83% revascularization and healing
of the lunate in one report27) In addition, a recent biomechanical study showed that capitate shorten-ing with capitohamate fusion
sig-nificantly (P<0.05) decreased the
load across the radiolunate
articula-tion.28 If this procedure is chosen, it
is helpful to ensure that the hamate
is not allowed to abut on the lunate after shortening of the capitate; if this appears to be the case, removal
of the proximal tip of the hamate with a rongeur will correct the problem.29
Stage II or IIIA With Negative Ulnar Variance
In patients with stage II or IIIA Kienböck’s disease and significant negative ulnar variance, a shorten-ing osteotomy of the radius may be performed in an effort to reduce forces on the lunate Preoperative measurement of ulnar variance is made in order to plan the amount of radial resection; sufficient bone should be removed to result in neu-tral to 1-mm positive ulnar variance Positive ulnar variance greater than
1 mm risks abutment of the ulna on the lunate or triquetrum, which is manifested by ulnar-sided discom-fort after surgery
Horii et al30described a two-dimensional wrist model in which they assessed the extent of unload-ing of the radiolunate joint after var-ious osteotomy procedures They
Figure 5 Capitate shortening with capitohamate fusion.
Trang 7found that shortening the radius or
lengthening the ulna by 4 mm led to
a 45% decrease in radiolunate load
with only a moderate increase in
force across the midcarpal or
radio-scaphoid joint
Trumble et al31 assessed the
effects on lunate loading after ulnar
lengthening, radial shortening, STT
fusion, and capitohamate fusion
without capitate shortening in an in
vitro model They found that all but
the capitohamate fusion significantly
unloaded the lunate and that wrist
motion was preserved in all except
STT fusion
In another biomechanical study,
Iwasaki et al4used a
three-dimen-sional theoretical wrist model They
demonstrated reduced force across
the radiolunate joint after STT or SC
fusion but not after capitohamate
fusion
A report on radial shortening
per-formed on 68 patients demonstrated
diminished pain in 93% at an average
follow-up interval of 52 months.32
One third of patients had radio-graphic signs of lunate revasculariza-tion Range of motion was improved
in 52% and worsened in 19% Grip strength improved in 74% of patients
Thus, radial shortening is an effective option for either stage II disease or stage IIIA disease with negative ulnar variance Ulnar lengthening has also been described, but this requires iliac-crest bone graft and osteotomy heal-ing at two sites (each end of the graft) rather than one
Stage IIIB
In stage IIIB Kienböck’s disease,
in addition to lunate collapse, there
is loss of carpal height along with hyperflexion of the scaphoid Cor-recting the scaphoid position to its normal posture of 45 degrees of flexion followed by fusion to either the trapezium and trapezoid (STT fusion) or to the capitate (SC fusion) theoretically decreases load across the radiolunate joint, prevents fur-ther carpal collapse, and stabilizes
the midcarpal joint.2,4,15 Some au-thors advocate proximal-row car-pectomy; others prefer joint-leveling procedures A recent comparison between STT fusion and proximal-row carpectomy in advanced Kien-böck’s disease showed no statistical difference in grip strength, pain re-lief, or wrist range of motion.33 In another comparison, radial short-ening led to better results than STT fusion in a group of 23 patients with late-stage Kienböck’s disease fol-lowed up for an average of 5 years.34
In stage III, collapse and frag-mentation of the lunate may cause a significant synovial reaction Exci-sion of the lunate, performed in addition to a fusion procedure, may provide pain relief Some authors interpose a rolled palmaris longus tendon to fill the dead space The use of silicone prostheses for re-placement of an excised lunate has been discontinued due to an un-acceptably high rate of particulate synovitis.2
Naum et al35reported on the use
of titanium implants for this pur-pose in 16 patients At an average follow-up interval of 58 months, they recorded no loss of motion, an increase in grip strength, and pre-vention of further carpal collapse It should be noted that the stage of disease was not described, that associated intercarpal fusions were done in 7 of the 16 patients, and that one implant required reoperation for subluxation
Stage IV
In stage IV Kienböck’s disease, all the findings of stage IIIB (lunate collapse and fixed scaphoid rota-tion with loss of carpal height) are present, along with generalized de-generative changes throughout the midcarpal joint, the radiocarpal joint, or both At this point, there is
no value in attempting to revascu-larize or decompress the lunate, nor
in attempting to arrest progression
of palmar flexion of the scaphoid
Figure 6 A, Preoperative AP radiograph of the wrist of a patient with stage IIIA
Kienböck’s disease B, Postoperative radiograph shows fixation of the lunate fracture and
vascularized bone grafting, in addition to capitate shortening.
Trang 8Treatment options must be
di-rected at the pancarpal arthritis
These include proximal-row
carpec-tomy and wrist fusion, as well as
wrist denervation It should be
noted that severe arthritic
involve-ment of the capitate head is a
con-traindication to proximal-row
car-pectomy, although milder changes
are accepted by some or can be
addressed with an interposed flap
of dorsal capsule between the
capi-tate head and the lunate fossa.36
Advocates for proximal-row
carpec-tomy claim that it preserves most of
the already limited range of motion,
is simple to perform, and leaves
open the possibility of wrist fusion
at a later date A 1-cm segment of
the posterior interosseous nerve
within the fourth dorsal
compart-ment can be excised when
perform-ing a proximal-row carpectomy to
minimize postoperative wrist pain
More complete wrist denervation
procedures have been described for
the treatment of advanced
Kien-böck’s disease The concept is
at-tractive, but these procedures offer
little advantage in terms of results
over the two former operations.2,15,37
Authors have disagreed on the
com-plete anatomic description of wrist
innervation and therefore on the
best method of denervation.38
Summary
For the past 10 to 15 years, selection
of treatment options for Kienböck’s disease has been primarily based on stage and ulnar variance With advancements in diagnostic tools (and corresponding earlier diagno-sis) and a greater understanding
of the conditions leading to osteo-necrosis, future treatment may be based on the underlying pathologic factors rather than the stage of Kienböck’s disease
Treatment of a “lunate at risk”
might include revascularization or venous drainage before the actual onset of osteonecrosis Corrections
of bone anomalies can also be un-dertaken in lunates with a special predisposition to disease Although arthroscopy has been used to diag-nose many wrist conditions, includ-ing Kienböck’s disease, its use for treatment of this disorder has not been tested Arthroscopic fusion, excision, or bone grafting may be reasonable applications of this tech-nique in the near future The use of ultrasound and electromagnetic fields has been extensively studied
in fracture healing but not in Kien-böck’s disease Dosage, method of application, and duration of treat-ment have not been addressed
Continued work defining avail-able vascularized bone grafts in the region of the lunate holds the prom-ise of increasing the ease with which direct revascularization of the lu-nate may be performed, as fewer steps are required to harvest a vas-cular pedicle with its attached bone graft Outcomes data on these new techniques are eagerly awaited The concept of temporary unloading of the lunate with temporary STT or
SC pinning (rather than fusion) dur-ing revascularization is a creative extension of the use of external fixa-tors for the same purpose, and may find a place in the armamentarium
of treatment options for Kienböck’s disease
Kienböck’s disease is an uncom-mon but potentially debilitating con-dition The precise cause and opti-mal treatment continue to elude investigators Nevertheless, increased attention to evaluation of outcomes has led to greater ease of decision making when faced with this diffi-cult problem Accurate staging directs selection of appropriate treat-ment and allows comparison of results with other investigators New techniques continue to appear, holding promise for improvement in all phases of diagnosis, staging, and treatment
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