Osteotomy of the Radius for Treatment of Kienböck Disease
Osteotomy of the Radius for Treatment of Kienböck Disease
DEFINITION
Kienböck disease is a disorder of undetermined etiology that results in avascular necrosis (AVN) of the lunate.7
ANATOMY
Lunate Vascularity
The extraosseous blood supply of the lunate is extensive: Branches of the radial and anterior interosseous arteries form a dorsal lunate plexus and branches of the radial, ulnar, and anterior interosseous arteries as well as the recurrent deep palmar arch form a volar plexus.
The intraosseous blood supply is variable. Because the lunate is covered by cartilage proximally and distally, vessels can enter the bone only at its dorsal and volar poles.2,16
Three studies have identified “lunates at risk” from a vascular standpoint. The vulnerable lunate is one that has large areas of bone dependent on a single intraosseous vessel, which occurs in 7% to 20%. In addition,
31% of lunates have no internal arterial branching.8,9,19 These internal vascular arrangements may render the lunate more vulnerable to AVN, as injury to the single vessel could not be compensated for by collateral flow.
Ulnar Variance
The standard posteroanterior (PA) wrist radiograph is taken with the shoulder and elbow at 90 degrees and the forearm in neutral rotation.
In this view, the length of the distal ulna with respect to the distal radius is called ulnar variance (FIG 1).
When the ulna is the same length as the radius, it is said to have neutral ulnar variance. When the ulna is shorter than the radius, it is referred to as negative ulnar variance, and when the ulna is longer than the radius, it is referred to as positive ulnar variance.
Theoretically, a negative ulnar variance increases shear forces on the lunate.
The triangular fibrocartilage complex (TFCC) is thicker in these patients and the difference in compliance between it and the ulnar edge of the radius is accentuated, leading to greater shear force.
In addition, loads across the radiocarpal joint are borne disproportionately by the radius.7
In the North American population, Kienböck disease is associated with a negative ulnar variance.
This relationship does not hold true in the Japanese literature.2
There is no evidence that the relationship between negative ulnar variance and Kienböck disease is causal.6,26
Other authors have noted a tendency toward smaller lunates in patients with Kienböck disease.3
PATHOGENESIS
The cause of Kienböck disease is incompletely understood. Current thinking is that acute or repetitive trauma causes excessive shear forces on a lunate at risk, interrupting its intraosseous vascularity and leading to AVN.1,2
Although a history of injury is elicited in over 50% of cases, the absence of a single traumatic event is still very common.
Fracture of the lunate has been reported in up to 82% of lunates with Kienböck disease.2 However, it remains unclear whether these fractures are the cause or the result of AVN.
Kienböck disease is not seen after lunate or perilunate dislocations.7,16
Although transient ischemia may be seen after carpal fracture-dislocations, this spontaneously resolves after 5 to 32 months and should be treated expectantly.1,2
 |
 |
FIG 1 • Measurement of ulnar variance. Ulnar variance is determined by extending a line from the radius' articular surface ulnarward and measuring the distance between this line and the distal surface of the ulnar head. Neutral ulnar variance occurs when the carpal surface of the radius and ulna are equal in height. If the ulna is shorter than the radius, negative ulnar variance exists; if the ulna is longer than the radius,
positive ulnar variance exists.
P.381
The key feature of transient ischemia is that no progressive radiographic collapse occurs, as opposed to Kienböck disease, where radiographic changes and collapse are predictable.
It has been suggested that Kienböck disease may be due to venous outflow obstruction with intraosseous vascular congestion rather than arterial insufficiency. Increased intraosseous pressure has been shown in lunates with Kienböck disease as well as in femoral heads with AVN.
This is more consistent with venous stasis than arterial compromise. This increased pressure could also be due to bony collapse.3,7
Once the lunate becomes avascular, stress fractures occur first in the proximal lunate adjacent to the radial
articular surface, where the blood supply is poorest.2,8,16 Consequently, the proximal lunate is usually more involved and more flattened than the distal lunate. In addition, the radial lunate that articulates with the distal radius is usually more involved than the ulnar lunate that overlies the triangular fibrocartilage, probably because of the difference in compliance between the two supporting surfaces. This difference is accentuated in patients
with negative ulnar variance.16
Lunate collapse leads to loss of carpal height. If a coronal plane fracture is present, the compressive forces of the capitate displace these two fragments volarly and dorsally.16
NATURAL HISTORY
The natural history of Kienböck disease is one of progressive fragmentation and collapse of the lunate, loss of carpal height with scaphoid flexion, and proximal capitate migration leading to perilunate arthritis. However,
these changes do not universally lead to a poor clinical outcome.7
A follow-up study of 49 patients compared 23 wrists treated with mean 8 weeks of immobilization and 26 without treatment.14
In both groups, the majority reported a gradual decrease in symptoms over time.
At mean 20.5 years of follow-up, 83% of the wrists in the immobilized group were pain-free or were painful only with heavy work.
In the nontreated group, this was true for 77%.
In all wrists, the lunate was deformed and 67% developed radiocarpal arthritis on radiographs. The authors concluded that Kienböck disease has a naturally benign course.
There was no correlation between residual symptoms and the radiographic appearance, including the appearance of arthritis.
In this study, immobilization did not lead to any long-term benefit.
PATIENT HISTORY AND PHYSICAL FINDINGS
Most patients with Kienböck disease are young, active patients between 20 to 40 years of age.
This has led to significant concerns about the long-term effects of this disorder.
The male-female ratio is approximately 3:1 to 7:1. It is rarely bilateral.3,27
Regardless of gender, more than 95% of patients are engaged in heavy manual labor.27
The most common complaints are dorsal central wrist pain, stiffness, and significant weakness of grip, which is often reduced to 50% of the opposite hand.2,7,16
There may be a long history of symptoms before presentation.
The pain may vary in intensity from mild discomfort to constant, debilitating pain. It is often activity related and improves with rest and immobilization.
A history of trauma is variable.2,7
The wrist is typically mildly swollen dorsally, consistent with synovitis, and is tender over the lunate. Flexion and extension are predictably diminished.
Wrist flexion is more likely to be limited than extension because the volar pole of the lunate often extrudes so that it impinges against the volar rim of the distal radius.
Forearm rotation is not affected.16
Although Kienböck disease has been reported in association with steroid use, septic emboli, sickle cell disease, gout, carpal coalition, and cerebral palsy, there is no welldefined correlation with any systemic or neuromuscular
process that warrants screening when considering the diagnosis.3
IMAGING AND OTHER DIAGNOSTIC STUDIES
Radiographic Classification
Kienböck disease is diagnosed radiographically, and staging is based on plain radiographs.
In 1977, Lichtman and Degnan15 modified Stahle's original radiographic classification in an attempt to help guide treatment decisions (FIG 2).
Stage I
Radiographs are normal, although a linear fracture without sclerosis or lunate collapse is occasionally present.
Magnetic resonance imaging (MRI) shows the characteristic changes of AVN (FIG 3A).7,27 Stage II
The lunate becomes sclerotic and radiodense, similar to the radiologic appearance of other bones with AVN (FIG 3B). A coronal fracture splitting the lunate into dorsal and volar fragments may be noted.
Late in stage II, some loss of lunate height on the radial side may be evident.
The lunate retains its overall shape, and its anatomic relationship to the other carpal bones is not significantly altered.15,27
Stage III
The lunate collapses in the coronal plane and elongates in the sagittal plane. The carpal architecture is altered and the capitate begins to migrate proximally.
Stage IIIA
Lunate collapse has occurred, but carpal height is relatively unchanged and carpal collapse has not yet led
to proximal migration of the capitate or scaphoid flexion. Therefore, the carpal kinematics have not yet been significantly altered.
Stage IIIB
The carpal collapse with proximal capitate migration has led to fixed scaphoid flexion, which may be noted on the anteroposterior (AP) radiograph as the “cortical ring sign.”3,5,27
P.382
 |
 |
 |
FIG 2 • Kienböck disease stage classification based on radiographic appearance.
Stage IV
Arthritis of the radiocarpal or midcarpal joint has resulted from the collapse, fractures, and altered carpal kinematics, leading to joint space narrowing, osteophyte formation, subchondral sclerosis, and degenerative cysts.3,27
Magnetic Resonance Imaging and Computed Tomography
MRI is extremely sensitive in detecting changes in marrow fat that are consistent with, but not diagnostic of, AVN.
Decreased signal on T1 sequences represents replacement of the normal fatty marrow by dead bone or fibrous
tissue.27
Because MRI detects only the loss of marrow fat and not AVN specifically, to consider an MRI diagnostic for Kienböck disease, over 50% of the lunate should be hypointense on T1 because the changes of Kienböck disease are diffuse, as opposed to other conditions such as ulnocarpal impaction, fractures, and intraosseous
tumors, which cause more focal MRI changes.4,25,28
 |
 |
FIG 3 • A. MR image of wrist with Kienböck disease demonstrates diminished signal intensity of the lunate. B. Radiograph showing density changes in the lunate in Kienböck disease. (From Bishop AT, Pelzer M. Avascular necrosis. In: Berger RA, Weiss AP, eds. Hand surgery, vol 2. Philadelphia: Lippincott Williams & Wilkins, 2004:554.)
It is possible that a large enchondroma, interosseous ganglion, or other marrow-replacing lesion could lead to MRI changes in over 50% of the lunate. Thus, there is currently no truly pathognomonic imaging sign for
Kienböck disease.4
T2 images typically show low signal intensity, which represents replacement of the normal fatty marrow by fibrosis.27
An increased T2 signal may occur if intramedullary edema is present or if revascularization is occurring.3,4,25 Thus, when the T2 images show normal or increased signal intensity, an earlier stage of disease with a better prognosis can be inferred.25,27
P.383
Although it cannot diagnose AVN directly, MRI is still the optimal imaging modality and gold standard for diagnosing Kienböck disease, especially before trabecular bone has been destroyed.
Gadolinium-enhanced MRI may provide a more sensitive means of evaluating lunate vascularity.
Computed tomography (CT) may upstage the disease compared with radiographs in 89% of those originally considered to have stage I, 71% with apparent stage II, and 9% with apparent stage III disease on radiographs.3
Once lunate collapse has occurred, CT best reveals the extent of necrosis and trabecular destruction.
DIFFERENTIAL DIAGNOSIS
Ulnocarpal impaction Rheumatoid arthritis
Radial-sided triangular fibrocartilage tears Posttraumatic arthritis
Acute fracture Carpal instability Lunate fracture Enchondroma Osteoid osteoma Bone island
Occult or intraosseous ganglion Intraosseous cyst
Transient ischemia “Bone bruise” Paget disease
Gaucher disease4
NONOPERATIVE MANAGEMENT
A trial of 2 weeks to 3 months of immobilization may be attempted for patients with stage I Kienböck disease, especially young patients with hyperintense lunates on T2 magnetic resonance (MR) images.
The theory behind the use of immobilization is that by decreasing the forces across the carpus, the lunate may be able to revascularize.15
Most series report poor results with immobilization, and progressive collapse is common.
There is no study of immobilization consisting of patients with only stage I Kienböck disease. Consequently, the efficacy of immobilization in patients with stage I disease is anecdotal.
Immobilization does not decrease compressive forces across the lunate, which are imparted by the capitate. The capitate may still force any fracture fragments apart, leading to collapse and displacement.
Immobilization leads to stiffness.
The earlier the lunate is unloaded, the less collapse is anticipated. For this reason, early surgical decompression may be considered rather than immobilization, and many clinicians treat stage I disease
surgically.16
In Trumble and Irving's28 series of 22 patients with various stages of Kienböck disease treated with immobilization, 17 showed disease progression with continued collapse of the lunate and 5 showed no improvement.
In Lichtman et al's series, 19 of 22 had unsatisfactory results.1,3
When immobilization fails to reverse the avascular changes, the process will almost always advance to stage II,
where surgical management is strongly recommended.1,3
In a series of patients with stage II or more advanced disease treated with immobilization, 76% (19 out of 25) had either undergone total wrist arthrodesis or experienced daily problems with their wrists at mean 8-year (1 to 11 years) follow-up.18
A study of 18 patients with stage II or III disease treated nonoperatively were compared with those treated by radius shortening.
Patients treated surgically had less pain and better grip strength.
In some patients with stage III disease treated nonoperatively, there was rapid deterioration to carpal collapse.
Although radius shortening did not reverse or prevent carpal collapse, it slowed the process.22
SURGICAL MANAGEMENT
There is no agreement on the optimal way to treat Kienböck disease.7 Multiple options for surgical management exist and the results do not vary significantly between the different procedures.
The mainstays of treatment are radius shortening osteotomy and proximal row carpectomy.7
Two major radiographic features influence treatment choice: the stage of the disease and ulnar variance.15 Radius shortening osteotomy is currently the benchmark against which other treatments are judged.16
For stages I to IIIB, radius shortening osteotomy is a very popular option in patients who are ulnar negative.
Although the use of radius shortening in stage IIIB is controversial because lunate height and normal carpal kinematics will not be reestablished, potentially leading to progressive degenerative changes, very good results have been demonstrated in these patients with this procedure.1,30,31 Radius shortening is
contraindicated for stage IV disease unless symptoms are severe and salvage procedures are not desired.30
Radius shortening decreases joint compression forces at the radiolunate joint by redistributing them to the radioscaphoid and ulnolunate joints. In addition, it relatively lengthens the tendons crossing the wrist,
diminishing overall joint compressive forces.20
As opposed to ulnar lengthening, no intercalary bone graft is required and only one interface needs to heal, instead of two.
In addition, radius shortening leads to a relative lengthening of the musculotendinous units crossing the wrist, resulting in less force transmission across the carpus. Ulnar lengthening does not provide this particular advantage.20
After radius shortening, the ulnar head and TFCC support more of the wrist's compressive load through the triquetrum and the ulnar aspect of the lunate. The TFCC is thicker in patients with negative ulnar variance, which provides a compliant pad to support the ulnar carpus.
Because radius shortening osteotomy is an extra-articular procedure, it does not alter normal carpal joints or interfere with intracarpal relationships. It “burns no bridges,”
P.384
and intracarpal procedures can always be undertaken at a later date if the radius shortening is ineffective and disease progression occurs.30
 |
 |
FIG 4 • Lateral closing wedge osteotomy. (Adapted from Soejima O, Iida H, Komine S, et al. Lateral closing wedge osteotomy of the distal radius for advanced stages of Kienbock's disease. J Hand Surg Am 2002;27[1]:31-36.)
In patients who are ulnar neutral or ulnar positive, a radial closing wedge osteotomy (FIG 4) or capitate shortening with or without capitohamate fusion can be performed.
Although radius shortening in patients with neutral or positive ulnar variance is not advised, good results have been reported even in these patients.2,30
For stages I to IIIA, revascularization using a vascularized pedicle or bone graft may be performed and may be combined with radius shortening or another unloading procedure (see Chap. 41).
In patients with stage IIIB disease, proximal row carpectomy, scaphotrapeziotrapezoid fusion, or scaphocapitate fusion may be performed with or without lunate excision and soft tissue interposition.
There is data to suggest that even in patients with static carpal malalignment, radius shortening osteotomy can result in a successful clinical result.5
For stage IV disease, proximal row carpectomy or total wrist fusion may be indicated. A study of arthroscopic débridement for stage III or IV disease showed some pain relief at 19 months of follow-up.17
Based on the hypothesis that Kienböck disease is due to venous obstruction, “metaphyseal core decompression” of the distal radius has also been reported with good results.10
Wrist denervation may also be considered and can be used as an adjunct at any stage.3
Lateral closing wedge osteotomies increase lunate coverage (joint contact area) in proportion to the decrease in radial inclination.
This transfers the compressive forces of the capitate from the lunate to the scaphoid, decreasing pressure at the radiolunate joint.20,29
To keep the wrist straight in relation to the forearm, the patient is forced to ulnarly deviate the wrist, extending the scaphoid, which may further transfer forces from the capitate to the scaphoid and decrease forces on the lunate.23
Preoperative Planning
Good-quality, standard preoperative PA radiographs should be taken with the shoulder and elbow flexed 90 degrees and the forearm in neutral rotation.
Although many authors have recommended removing sufficient bone during radius shortening to result in an ulnar neutral to 1-mm positive variance, 90% of the strain reduction occurs within the first 2 mm of
shortening.2,3,7
Good results with excellent relief of symptoms have been reported removing only 2 mm of bone, regardless of variance. This has the advantages of technical ease and decreases the risk of distal radioulnar joint (DRUJ) incongruity and ulnocarpal impaction, which may occur with excessive shortening.
In patients with significant obliquity of the sigmoid notch, radius shortening should be limited to 2 mm to avoid overcompressing the DRUJ.
Postoperative ulnocarpal impaction and DRUJ incongruity are especially likely with shortenings of 4 mm or
more, leading to pain with forearm rotation or limitation of forearm rotation.30 Therefore, shortening of the radius by over 4 mm is not recommended.
Patients with more than 4 mm of shortening and age older than 30 years were found to be more likely to have poor results.2
Positioning
The patient is positioned supine with the arm on a radiolucent hand table.
Approach
A volar approach to the radius is performed.
P.385
TECHNIQUES
-
Volar Approach
A longitudinal incision is made over the flexor carpi radialis (FCR) tendon, ending distally at the distal volar wrist crease (TECH FIG 1B).
The approach is continued through the FCR sheath with the FCR tendon retracted ulnarly to protect the palmar cutaneous branch of the median nerve.
The plane between the FCR and deep muscles of the radius (pronator quadratus and FPL) is bluntly dissected (TECH FIG 1C).
 |
 |
 |
 |
TECH FIG 1 • A. Preoperative radiograph demonstrating negative ulnar variance. B. Incision. C. The pronator quadratus is exposed. D. The volar distal radius is subperiosteally exposed.
The distal border of the pronator quadratus and the radial insertions of the pronator quadratus and flexor pollicis longus muscles are incised with a knife, with care taken to retract and protect the radial artery, which does not need to be formally identified.
The volar surface of the radius is then subperiosteally exposed in a radial to ulnar direction (TECH FIG 1D).
Circumferential subperiosteal dissection should be avoided to preserve maximal blood supply to the osteotomy.
-
Radius Shortening Osteotomy
Initial Plate Application
Traditionally, a seven-hole 3.5-mm dynamic compression plate was placed as far distally as possible without riding up the volar lip of the distal radius.30
However, the newer fixed-angle volar plates used for fixation of distal radius fractures work very well and allow the osteotomy to be placed in metaphyseal bone.
To decrease the risk of nonunion, the osteotomy should be performed as distal as possible to be through metaphyseal cancellous bone, staying proximal to the DRUJ.
The plate is placed over the distal radius and provisionally fixed with Kirschner wires (TECH FIG 2A).
Care should be taken to place the plate distal enough to ensure distal screws are as close to the subchondral bone as possible without intra-articular screw penetration.
It is, however, possible to place the plate too distal depending on the design of the plate, putting the
flexor tendons at risk of attritional injury. The most distal aspect of the plate should not be distal to the watershed line of the distal radius.12,24
P.386
 |
 |
TECH FIG 2 • A,B. The volar locking plate is placed so that its distal fixation (represented radiographically by a Kirschner wire) travels just proximal to the subchondral surface. Distal locking screw fixation is placed.
Following fluoroscopic confirmation of appropriate placement, fixed-angle screws are placed through the distal rows of the plate (TECH FIG 2B).
A bicortical screw is placed 1 cm proximal to (not through) the plate for use later as a means to reduce and compress the osteotomy. It should be longer than measured to allow bicortical purchase but also to allow the head to sit several milimeters up from the volar cortex for later use in compressing the osteotomy.
 |
 |
 |
TECH FIG 3 • A,B. The osteotomy site is marked between the plate's proximal and distal fixation. When using a plate specifically designed for the fixation of distal radius fractures, this places the osteotomy proximal to the distal radioulnar joint. C. The osteotomy is created with a saw transversely taking 2 to 3 mm of bone leaving the dorsal cortex to be removed last.
Radius Osteotomy
The osteotomy is marked proximal to the distal fixation and proximal to the DRUJ (TECH FIG 3A). The plate is removed and a transverse osteotomy is made volar to dorsal (TECH FIG 3B).
An oblique osteotomy provides a larger surface area for healing and can allow for placement of an interfragmentary compression screw.2
P.387
An oblique osteotomy, however, is more technically demanding than a transverse osteotomy, and the purchase obtained with the interfragmentary screw used for additional fixation with an oblique osteotomy can be poor.
A longitudinal line may be marked across the osteotomy site to allow rotational assessment. However, the flat surface of the volar cortex allows for easy assessment of rotation.
An elevator can be placed on the dorsal surface of the osteotomy to protect the extensor tendons from the saw. Care should, however, be taken to avoid stripping the periosteum from the dorsal cortex of the radius at the level of or near the eventual osteotomy.
Two to 3 mm of shortening may be appropriate regardless of the amount of negative ulnar variance present.
Excellent results have been reported with osteotomies that do not fully correct the radius length to
neutral variance.30,31
The 2 to 3 mm to be taken is measured out and marked and the full amount of bone to be taken is removed from volar to dorsal so that the dorsal cortex remains intact to stabilize the bone during bone removal.
The dorsal cortex is then removed last leaving a completed osteotomy (TECH FIG 3C).
While performing the osteotomy, constant cool irrigant is used to avoid thermal osteonecrosis.
Although a slight (1 mm) concave bend in the plate over the osteotomy site may occasionally be needed to achieve compression of the dorsal osteotomy surface, this is not usually necessary.
Final Plate Application and Osteotomy Fixation
The plate and its distal fixation are then replaced.
Approximation of the two bone ends may also be facilitated by radial deviation of the wrist30 and use of a bone-holding clamp.
A locking tower is secured into the most proximal hole of the plate (TECH FIG 4A).
The clamp is placed around the locking tower and the screw proximal to the plate.
The clamp is closed to compress the osteotomy taking care not to overcompress it and cause malalignment.
Alternatively, a Verbrugge clamp can be used to compress the osteotomy.
The hooked end of the Verbrugge is placed in the plate's most proximal screw hole and the bifid end is placed around the screw proximal to the plate.
One final option for compression is an articulated tension device.
The device is secured to the radial shaft using the previously metioned bicortical screw proximal to the plate.
The other end of the device is then hooked into the proximal aspect of the plate and the device is tightened using the T-handle wrench.
With the clamp applied, the reduction is evaluted fluoroscopically and adjustments made as necessary.
An additional clamp from the proximal ulnar aspect of the radial shaft to the distal aspect of the radius or the plate itself may be needed to correct excessive radial translation of the distal fragment (TECH FIG 4B). Care should be taken, however, to not overcorrect the translation of the distal fragment, as this can result in loss of forearm rotation.
The first screw is placed in a compression mode eccentrically in the plate hole in the oblong hole (TECH FIG 4C).
After again assuring adequate reduction and alignment fluoroscopically, the remaining proximal screws are placed (TECH FIG 4D).
Forearm rotation should be checked to ensure that it is full.
If forearm rotation is limited after osteotomy, the distal fragment of the radius should be allowed to translate radially or a lateral closing wedge component added.20
Radiographs can show some mild residual gap at the osteotomy site, even with full compression under direct vision (TECH FIG 4E,F).30
Intraoperative radiographs may not demonstrate the eventual ulnar variance (amount of radius shortening) because of soft tissue restraints at the DRUJ. In these cases, postoperative radiographs will demonstrate the anticipated correction.20
 |
 |
TECH FIG 4 • A. The plate and its distal fixation are replaced. The bicortical screw a few millimeters longer than the bone width placed 1 to 2 cm proximal to the plate and left proud can be seen proximally in the incision. A bone-holding clamp is placed around a locking tower and around the proximal screw. Squeezing the clamp provides a tremendous mechanical advantage to facilitate osteotomy closure. B. An additional clamp from the proximal ulnar aspect of the radius shaft to the distal aspect of the radius radially or the plate itself may be needed to correct excessive radial translation of the distal fragment. (continued)
P.388
 |
 |
 |
 |
TECH FIG 4 • (continued) C. With the clamp compressing the osteotomy, the first proximal screw is drilled eccentrically through the most proximal aspect of a plate hole to provide additional compression. D. Three more proximal bicortical screws are placed to result in a stable and well-compressed osteotomy. E,F. Intraoperative PA and lateral radiographs.
-
Radial Closing Wedge Osteotomy
A radial closing wedge osteotomy may be performed through the same approach with the same fixation. A 15-degree radial closing wedge osteotomy is performed 4 to 5 cm proximal to the tip of the radial styloid and proximal to the DRUJ.29
P.389
PEARLS AND PITFALLS
POSTOPERATIVE CARE
The extra-articular nature of this procedure combined with stable internal fixation allows for quick postoperative rehabilitation.
The wrist is splinted for 2 weeks, after which a removable splint may be used and gentle motion started. The osteotomy usually heals in 2 to 3 months, although 4 or 5 months is occasionally required.
OUTCOMES
A review of the reported series by Weiss30 in 1993 included 121 patients treated with radius shortening, with about 85% good or excellent results at just over 4 years of follow-up.
One study reviewed 30 wrists after radius shortening osteotomy for stages I to IIIB Kienböck disease at mean 3.8 years of follow-up.31
Pain decreased in 87% and grip strength improved in 49%. However, the radiographic appearance of the lunate changed little if at all.
The authors noted that good results could be obtained by shortening less than that required to attain
Radius ▪ Two to 3 mm of shortening is all that is needed in the vast majority of cases.
shortening Shortening the radius by only 2-3 mm makes compression of the osteotomy easier.
-
In cases of significant DRUJ obliquity, shortening the radius greater than 2 mm may lead to DRUJ problems.
Fragment
handling
-
If rotation is not full or the DRUJ is compromised after osteotomy, radial translation of
the distal fragment should be considered.
Bone-
holding clamp
-
Use of a clamp compressing against a screw proximal to the plate gives the surgeon
a tremendous mechanical advantage in shortening the osteotomy.
neutral ulnar variance.
The exact amount of radius shortening may not be as important as the relative unloading of the lunate resulting from the shortening of the radius. The amount of shortening needed to be effective may be only about 2 mm. Radius shortening may therefore be used in ulnar neutral wrists.
In addition, excellent results were realized in patients with stage IIIA and IIIB disease. There was one nonunion. Only 10 of 30 wrists had evidence of possible lunate revascularization, as indicated by decreased sclerosis and a more normal trabecular pattern.
Clinical improvement after radius shortening or radial wedge osteotomy does not necessarily correlate with the radiographic results.2,7,23 It appears that the lunate “stands still in time” after radius shortening, with no significant further deterioration or improvement in the lunate architecture or height.30
Another study reviewed 68 radius shortening osteotomies at a mean of 52 months of follow-up.20
Pain was diminished in 93%, grip strength was improved in 74%, and motion was improved in 52% and worsened in 19%.
Twenty-five patients had undergone one or more additional procedures concurrently, which did not lead to a significant difference in clinical outcomes.
Complications were uncommon; there were no nonunions, but ulnocarpal impaction developed in two patients.
Lunate density was improved in 40%, unchanged in 46%, and increased (worsened) in 14%.
Fifty-five percent of wrists that underwent concurrent vascularized bone grafting of the lunate had an improved radiographic appearance, compared to only 20% that underwent isolated radius shortening.
It has been suggested that prognosis is improved in younger patients due to increased remodeling potential.15
Teenage patients (aged 11 to 19 years) were treated by radius shortening or lateral closing wedge osteotomy. Two had neutral or positive ulnar variance. At a mean 50 months of follow-up, 10 of 11 were pain-free. Five of 6 with stage IIIB disease had excellent outcomes.
The other patient had moderate wrist pain during strenuous activity, leading to only a fair result after lateral closing wedge osteotomy for stage IIIB disease.
Radiographic improvement, indicating possible lunate revascularization, was seen in 8 of 11 patients. There were no complications of radial overgrowth or growth abnormalities in these patients.
Radiographic stage does correlate with clinical outcome postoperatively,21 but even advanced Kienböck disease can be treated with radius shortening osteotomy with good results.5
Fourteen patients with stage IIIB and 17 with stage II and IIIA disease were compared retrospectively at a mean of 74 months.
Disability of Arm, Shoulder, and Hand (DASH) scores averaged 15 in the IIIB group as compared to 12 in the II and IIIA group. Grip strength was 77% of the opposite side for stage IIIB wrists versus 85% for stage II and IIIA. Only one patient in the stage IIIB group went on to wrist arthrodesis.
Twenty-five patients were followed for a minimum of 10 years (mean 14.5 years) after radius osteotomy.13 Ninety-six percent had good or excellent results.
Pain, motion, and grip strength were all significantly improved after surgery and the results were
maintained.
Although radiologic improvement was not drastic and carpal height did not significantly improve,
sclerosis and bone cysts improved and there was evidence of improved lunate revascularization over time.
Osteoarthritic changes were observed in 54% at 5 years and in 73% at the time of final follow-up, but the arthrosis was generally mild and did not affect the clinical results.
Severe osteoarthritis and proximal migration of the capitate were avoided.
P.390
Radius shortening was used for patients with negative ulnar variance and closing wedge osteotomy for those with positive ulnar variance. These procedures gave identical outcomes.
Iwasaki et al11 also noted that both radius shortening and lateral closing wedge osteotomies gave equally acceptable results in adult patients.
Good long-term results were reported in 100% of 13 patients at a mean of 14 years after radial closing wedge osteotomy.29
Pain relief was good, and improvements in grip strength and range of motion were seen. Radiographic changes improved in 1, did not change in 4, and advanced in 8.
COMPLICATIONS
Nonunion has been reported in up to 6% of cases.7
If the fixation remains stable, treatment should consist of autogenous cancellous bone grafting if healing has not occurred by 5 or 6 months.
A second operation may occasionally be necessary for plate removal, but this is uncommon.
Care must be taken not to overshorten the radius, or DRUJ incongruity or ulnocarpal impaction may occur.30
REFERENCES
-
Alexander AH, Lichtman DM. Kienbock's disease. Orthop Clin North Am 1986;17:461-472.
-
Alexander CE, Alexander AH, Lichtman DM. Kienbock's disease and idiopathic necrosis of carpal bones. In: Lichtman DM, Alexander AH, eds. The Wrist and Its Disorders, ed 2. Philadelphia: WB Saunders, 1997:329-346.
-
Allan CH, Joshi A, Lichtman DM. Kienbock's disease: diagnosis and treatment. J Am Acad Orthop Surg 2001;9:128-136.
-
Budoff JE, Lichtman DM. Spontaneous wrist fusion: an unusual complication of Kienbock's disease. J Hand Surg Am 2005;30(1): 59-64.
-
Calfee RP, Van Steyn MO, Gyuricza C, et al. Joint leveling for advanced Kienböck's disease. J Hand Surg Am 2010;35(12):1947-1954.
-
Chung KC, Spilson MS, Kim MH. Is negative ulnar variance a risk factor for Kienböck's disease? A meta-
analysis. Ann Plast Surg 2001;47:494-499.
-
Divelbiss B, Baratz ME. Kienbock's disease. J Am Soc Surg Hand 2001;1:61-72.
-
Gelberman RH, Bauman TD, Menon J, et al. The vascularity of the lunate bone and Kienbock's disease. J Hand Surg Am 1980;5(3): 272-278.
-
Gelberman RH, Szabo RM. Kienbock's disease. Orthop Clin North Am 1984;15:355-367.
-
Illarramendi AA, Schulz C, De Carli P. The surgical treatment of Kienbock's disease by radius and ulna metaphyseal core decompression. J Hand Surg Am 2001;26(2):252-260.
-
Iwasaki N, Minami A, Ishikawa J, et al. Radial osteotomies for teenage patients with Kienbock disease. Clin Orthop Relat Res 2005;439: 116-122.
-
Kitay A, Swanstrom M, Schreiber JJ, et al. Volar plate position and flexor tendon rupture following distal radius fracture fixation. J Hand Surg Am 2013;38(6):1091-1096.
-
Koh S, Nakamura R, Horii E, et al. Surgical outcome of radial osteotomy for Kienbock's disease: minimum 10 years of follow-up. J Hand Surg Am 2003;28(6):910-916.
-
Kristensen SS, Thomassen E, Christensen F. Kienbock's disease—late results by non-surgical treatment. A follow-up study. J Hand Surg Br 1986;11(3):422-425.
-
Lichtman DM, Degnan GG. Staging and its use in the determination of treatment modalities for Kienbock's disease. Hand Clin 1993;9: 409-416.
-
Linscheid RL. Kienbock's disease. Instr Course Lect 1992;41:45-53.
-
Menth-Chiari WA, Poehling GG, Wiesler ER, et al. Arthroscopic debridement for the treatment of Kienbock's disease. Arthroscopy 1999;15:12-19.
-
Mikkelsen SS, Gelineck J. Poor function after nonoperative treatment of Kienbock's disease. Acta Orthop Scand 1987;58:241-243.
-
Panagis JS, Gelberman RH, Taleisnik J, et al. The arterial anatomy of the human carpus. Part II: the intraosseous vascularity. J Hand Surg Am 1983;8(4):375-382.
-
Quenzer DE, Dobyns JH, Linscheid RL, et al. Radial recession osteotomy for Kienbock's disease. J Hand Surg Am 1997;22(3):386-395.
-
Rodrigues-Pinto R, Freitas D, Costa LD, et al. Clinical and radiological results following radial osteotomy in patients with Kienböck's disease: four- to 18-year follow-up. J Bone Joint Surg Br 2012;94(2): 222-226.
-
Salmon J, Stanley JK, Trail IA. Kienbock's disease: conservative management versus radial shortening. J
Bone Joint Surg Br 2000;82(6):820-823.
-
Soejima O, Iida H, Komine S, et al. Lateral closing wedge osteotomy of the distal radius for advanced stages of Kienbock's disease. J Hand Surg Am 2002;27(1):31-36.
-
Soong M, Earp BE, Bishop G, et al. Volar locking plate implant prominence and flexor tendon rupture. J Bone Joint Surg Am 2011;93(4):328-335.
-
Sowa DT, Holder LE, Patt PG, et al. Application of magnetic resonance imaging to ischemic necrosis of the lunate. J Hand Surg Am 1989;14(6):1008-1016.
-
Stahl S, Stahl AS, Meisner C, et al. Critical analysis of causality between negative ulnar variance and Kienböck disease. Plast Reconstr Surg 2013;132:899-909.
-
Szabo RM, Greenspan A. Diagnosis and clinical findings of Kienbock's disease. Hand Clin 1993;9:399-408.
-
Trumble TE, Irving J. Histologic and magnetic resonance imaging correlations in Kienbock's disease. J Hand Surg Am 1990;15(6):879-884.
-
Wada A, Miura H, Kubota H, et al. Radial closing wedge osteotomy for Kienbock's disease: an over-10-year clinical and radiographic follow-up. J Hand Surg Br 2002;27(2):175-179.
-
Weiss AP. Radial shortening. Hand Clin 1993;9:475-482.
-
Weiss AP, Weiland AJ, Moore JR, et al. Radial shortening for Kienböck disease. J Bone Joint Surg Am 1991;73(3):384-391.