Keywords
Kienböck - treatment - arthroscopy
Introduction
Kienböck's disease (KD) is characterized by ischemic necrosis of the lunate bone,
leading to wrist pain, limited mobility, and functional disability. Treatment strategies
vary widely, influenced by the stage of the disease and individual anatomical and
clinical considerations.[1]
[2]
KD presents significant challenges due to its heterogeneous clinical presentation
and the progressive nature of avascular necrosis of the lunate. Despite the variety
of approaches, no method has been proven universally effective, emphasizing the need
for personalized strategies based on disease stage and patient-specific factors.[1]
[2]
Etiology
Although the etiology and pathogenesis of KD are not yet fully understood, several
potential causes have been postulated.[3]
There are factors traditionally considered precipitating factors, but these have not
been proven. The analysis of 100 cases of KD, published in the doctoral thesis of
one of the authors, reveals a wide variability in morphologies, which contradicts
these classic associations. To date, they appear to play a role in the progression
of KD once established, but they are not factors influencing its onset[4]:
-
A) Short ulna. Authors such as the Swedish Hulten considered that a short ulna would
cause the lunate to be subjected to greater load, leading to a compression fracture
over time. Today, the majority of authors disagree with this assertion, as shown in
the meta-analysis by Chung et al.[5]
-
B) Type I lunate. In 1966, Antuña Zapico, in his doctoral thesis, described three
morphological types of lunate, based on the angle of inclination formed by the articular
facet for the scaphoid and the distal radius. In type I, this angle is equal to or
greater than 135° and usually corresponds to a short ulna. In type II, the angle of
inclination is less than 135° and usually corresponds to a neutral ulna. In type III,
it presents two convergent articular facets and usually coexists with a long ulna.
As S. Pombo Expósito pointed out in his doctoral thesis, based on the analysis of
100 cases of KD, the morphology of the SE could influence the evolution of KD, but
it is not an influential factor in its onset. Therefore, the relationship between
the morphology of the lunate and KD will remain controversial until the real cause
or causes of the disease are known.[4]
[6] ([Figure 1])
-
C) Specific vascular patterns. The vascularization of the SE has been meticulously
studied by authors such as Stahl (1947), Lee (1963), Gelberman et al. (1980), and
Lamas (2000, 2007). To date, a direct relationship between vascular patterns and the
development of KD has not been demonstrated.[7]
[8]
-
D) Repetitive trauma. Some authors have based the hypothesis of traumatic etiology
on the appearance of pseudofractures on radiographs, which, in our opinion, are nothing
more than fragmentation or collapse of the spinal cord that occurs in the advanced
stages of the disease.
Fig. 1 Top row: Drawings in Antuña's Doctoral Thesis of the morphological types of SE. Second
row: SE types 1–2–3. Third row: Cases of EK in SE types 1, 2, and 3.
Repetitive microtrauma is not the primary cause of KD but rather an aggravating factor
in pre-existing KD.[4]
[9]
[10]
Some lesser-known factors that should be added to the study of this pathology and
that should continue to be studied in the future are:
-
a) Familial association. Studies conducted in the Department of Genomic Medicine at
the University of Santiago de Compostela with siblings and twins affected by KD in
2011 did not detect genetic abnormalities at the time, perhaps due to the limited
resources available, at the time, but they paved the way for future research as genetic
sequencing techniques improve. Authors such as Kazmers et al. published encouraging,
though not definitive, findings in 2020.[4]
[11]
-
b) Causal biological factors. Other interesting studies have been conducted on the
influence of causative biological factors, ranging from reactive arthritis to viral
or bacterial infections, with the appearance of severe synovitis, which is still unknown
whether it is a cause or consequence of the disease. Such synovitis is often a common
finding in KD, even in younger patients and in its early stages; therefore, we consider
it primary synovitis.[12]
-
c) Atypical or secondary cases related to corticosteroid use, vasculitis, or other
causes. These cases are not considered primary lunate necrosis, but should be considered
as such when treating them from a pragmatic point of view.[4]
Classification
The main factors to consider when proceeding with the treatment of KD are the stage
of the disease and the clinical presentation at the time of diagnosis. There are multiple
classifications for this staging, with the most common being the Litchman classification
([Table 1]), the arthroscopic classification described by Bain, and the 21st-century treatment
algorithm.[13]
[14]
[15]
Table 1
Modified Litchman classification
|
Litchman classification
|
|
Stage I:
|
Normal radiographs. MRI intensity changes.
|
|
Stage II:
|
Lunate sclerosis without affecting its articular surface.
|
|
Stage III:
|
Collapse and deformity of the lunate joint surface.
|
|
-IIIA
|
Stable carpus.
|
|
-IIIB
|
Carpal instability.
|
|
-IIIC
|
Fragmentation of the lunate joint into two.
|
|
-IIID
|
Multifragmentation of the lunate joint.
|
|
Stage IV:
|
Appearance of radiocarpal or midcarpal osteoarthritis.
|
The Lichtman classification, proposed in 1977, has been the most widely used for over
50 years, focusing on plain wrist radiographs that detail the progressive stages of
the disease. The use of gadolinium (GD) in MRI has allowed us to subdivide stage III.
Depending on whether or not the signal intensity (SI) increases after GD injection,
we differentiate a stage III GD+ from a GD-, with the positive having a better prognosis
than the negative ([Figure 2]). The authors propose the addition of stage IIID to the Lichtman classification,
consisting of multifragmentation of the lunate, which may occur without perilunar
osteoarthritis having occurred, which does occur in stage IV. An example is attached
in the[ Figure 3].[4]
[9]
Fig. 2 Top row: Stage III Gd + . Bottom row: Stage III Gd–.
Fig. 3 Stage IIID is shown, with bone multifragmentation but still without arthropathy.
In 2006, Bain and Begg proposed an arthroscopic classification based on the state
of the cartilage of the intercarpal and radiocarpal joints, and more recently, other
authors have updated their proposal by incorporating clinical characteristics into
a therapeutic algorithm.[14]
Furthermore, age at diagnosis has been another key factor in the decision to prescribe
treatment. As Dr. Irisarri anticipated in 2004, depending on the age at which KD presents,
we can distinguish a group of lunatomalacias with a highly variable prognosis, namely[3]
[16]:
-
○ Infantile lunatomalacia (0–12 years)
-
○ Juvenile lunatomalacia (13–skeletal maturation)
-
○ Adult Kienböck's disease
-
○ Late Kienböck's disease (>65 years). More common in women and usually presents accidentally
and asymptomatic in the context of other conditions.[17]
Prognosis
In general, it could be summarized that in the early treatment of Kienböck's disease,
the goal is to promote revascularization of the ES (although revascularization is
almost never achieved, except in infantile and juvenile lunatomalacia, which have
a better prognosis), while in advanced disease, the goal is to reduce the pain caused
by synovitis while preserving maximum hand function.
For educational purposes, we could divide treatments according to whether they are
aimed at treating an "at-risk lunate" or a "non-viable lunate." However, it would
be a mistake to view the two as separate compartments, since by individualizing each
case, we could consider therapeutic alternatives that are not included in the sections
presented here.
There is still no reliable timeline for the rapidity of KD progression. In most cases,
it is relatively slow, but in some young patients with high functional demands, progression
is surprisingly rapid. In these cases, surgery should not be postponed. The appearance
of the so-called "crescent line" indicates a worse prognosis ("lunate at risk") and
can be considered a "point of no return", and is followed by a gradual collapse, in
some cases in a very short period of time.
Treatment
The various surgical techniques applied to KD throughout history have experienced
periods of initial popularity and subsequent obscurity.
Despite the wide range of treatments available, none has been proven to be truly and
definitively curative.
Treatment of “At Risk” Lunate
Extra-articular techniques
These techniques are based on reducing loads on the lunate.
-Correction of radio-ulnar dysmetria
It includes lengthening the ulna (which carries a higher risk of nonunion and is technically more difficult) or shortening
the radius.
Both techniques have faced technical challenges and mixed results, evolving as approaches
and available osteosynthesis materials have improved. Their purpose is to reduce the
loads borne by the lunate.
In radial shortening, the portion of the radius to be resected should be commensurate with the length
of the ulna. The osteotomy will be transverse in patients with a short ulna, or wedge
in patients with a zero or plus ulna, to avoid ulnocarpal impingement syndrome.
Angled osteotomies have been described in the radius, which do not aim to shorten, but rather to reduce
the radioulnar inclination of the articular surface of the radius. However, existing
biomechanical studies are contradictory. There is little data on the effect at the
level of the distal radioulnar joint. Longer-term studies on their results are needed.[18]
[19]
[20]
[21]
-Shortening of the capitate bone
This procedure reduces loads across the lunate by 66%, at the expense of increasing
loads on the trapezioscaphoid joint by 150%. One of the possible complications is
necrosis of the proximal fragment, since its vascular supply comes from the distal
portion.[22]
It is sometimes performed in conjunction with capitate-hamate fusion. The goal of
this intervention is to prevent proximal migration of the capitate-third metacarpal
axis into the defect created by the collapse of the lunate. This procedure would relieve
the pressure exerted by the capitate bone on the lunate and allow for revascularization.
In biomechanical studies, capitate-hamate fusion alone does not significantly reduce
pressure on the lunate. However, the combination of this fusion with a shortening
of the capitate bone is associated with decreased pressure transmission at the radiolunate
joint, increasing pressure transmission at the radioscaphoid joint.[23]
[24]
Intra-articular Techniques
-
Vascular stimulation and forage: Surgery for Kienböck's disease increases blood flow in the wrist and requires prolonged
immobilization, which can relieve symptoms and explain the clinical-radiological dissociation
between treatments. Illaramendi proposes metaphyseal decompression of the distal radius
and ulna, with similar results to joint leveling, but with a lower risk of pseudoarthrosis,
distal radioulnar incongruity, and ulnocarpal impingement. Techniques such as this
or lunate perforation seek to improve blood flow, but lack conclusive evidence.[25]
-
-Curettage and bone filling: In early stages (II and IIIA), curettage of the necrotic area and its filling with
autologous bone grafts or substitute materials has been explored. The use of arthroscopy
to perform this technique is being evaluated with promising initial results.[4]
[26]
-
-Intraosseous factors for osteogenesis: Experimental methods include intraosseous injection of stimulating factors, often
assisted by arthroscopy, although these methods still lack extensive studies and long-term
follow-up. Authors such as Ogawa have demonstrated the non-inferiority of bone marrow
aspiration from the distal radius compared to that from the iliac crest, using them
in conjunction with ultrasound and external fixation.[26]
[27] ([Figure 4])
Fig. 4 (A) EK in a 24-year-old male. (B) Curettage of the SE. (C) Filling with cancellous
bone chips. (D) X-ray 14 years after surgery.
Fig. 5 52-year-old male operated on by scaphoid–capitate arthrodesis with excision of the
lunate.
Treatment of “Non-Viable” Semilunar
Techniques Focused on the Lunate
-
-Removal of the lunate: Although initially proposed, this technique causes severe carpal instability, leading
to functional and radiological deterioration of the wrist. Options such as filling
with tendon or capsular grafts have been ruled out over time due to inconsistent results.[4]
[28]
-
-Lunate prosthesis: Although widely studied, attempts have been made to prevent carpal instability resulting
from lunate excision using different types of prostheses. These have evolved from
the earliest silicone prostheses to more modern titanium or pyrocarbon prostheses.
Despite these new prostheses, none have demonstrated consistent long-term results.
For this reason, few surgeons continue to use them due to frequent complications.[29]
[30]
-
-Revascularization: This involves vascularized bone grafts, with variations including the use of the
distal radius, medial femoral condyle, or pisiform bone. Despite its innovation, results
have been inconsistent and limited by donor site morbidity and difficult reproducibility.[31]
[32]
[33]
Palliative Techniques not Focused on the Lunate
-
-Proximal row carpectomy (PRC). If the head of the capitate bone is wide, it allows for maintaining a high range
of motion and acceptable strength, although its viability depends on the state of
the head of the capitate bone, and of course, on the absence of osteoarthritis in
the semilunar facet of the radius and the capitate bone.[34]
-
-Partial carpal arthrodesis: There are several possibilities.
-
Triscaphoid arthrodesis
(either preserving the SE or removing it and replacing it with a silastic prosthesis).
This was initially the most commonly used technique. Watson justified it by reducing
the load borne by the lunate. It has gradually fallen into disuse because it does
not provide significant improvement in the lunate and instead causes radioscaphoid
arthrosis, which, even when combined with a radial styloidectomy, ultimately generates
disabling pain.[35]
-
Scaphoid-capitate arthrodesis
, with or without lunate excision. Reported results have been highly variable in the
past, but the availability of more effective screws has favored its widespread use.
The number and orientation of screws has varied, depending on surgeon preference,
although the latest results of Dr. Jorquera's review show very favorable results when
performing lunate excision associated with arthroscopic scaphoid-capitate arthrodesis.36–38
([Figure 5])
-
Carpal bone osteotomy proposed by Graner
. In type I, he performed an E-SE-HG-Pi arthrodesis. In type II, he divided the capitate
bone, moved its proximal fragment proximally, and placed a bone graft between the
two fragments. Fixation was achieved with small cortical bone grafts. The results
were unfavorable, which led to its progressive abandonment.[39]
-
-
Total radiocarpal arthrodesis.
It is indicated in advanced stages in patients who are still young and have significant
functional work demands. Often, friction between the plate and the extensor tendons
can lead to the subsequent removal of the plate.[4]
[13]
-
Other surgical procedures:
-
The list of surgical techniques for treating KD is not limited to those discussed.
Some have fallen into disuse. Examples include carpal tunnel opening (Codega), lunate
bone replacement with pisiform bone replacement according to Saffar, or osteosynthesis
of bone fragments (Chou).[40]
[41]
[42]
Conservative Treatment
It should be noted that orthopedic treatment for KD has been documented to lead to
progressive radiographic deterioration toward carpal osteoarthritis, although this
did not always correspond clinically with clinical deterioration in the studies conducted.
Therefore, authors such as Saffar and Delaere recommended carefully assessing the
indication for surgery in a disease such as KD after observing a significant percentage
of patients whose clinical course is benign.[43]
[44]
[45]
Today, these concepts have fallen into disfavor for available therapeutic options,
and studies focus more on surgical treatment of the disease. However, we always recommend
discussing conservative treatment with the patient, especially as the older they are.
It is a reliable alternative to consider in elderly patients with limited functional
needs. In young patients who aim to lead a "normal" life, surgery is the standard
option, but it should not be imposed by the surgeon.[45]
[46]
Proposed Therapeutic Algorithm and Choice of Authors
Proposed Therapeutic Algorithm and Choice of Authors
[Figure 6]
Fig. 6 Proposed therapeutic algorithm.
Techniques preferred by the authors:
-If the lunate is considered "at risk":
Metaphyseal radial shortening osteotomy, using a volar approach and with plate and
screw synthesis.
The truth is that the theoretical basis for why this technique works is unclear. There
is probably more than one explanation, with one finding meaning in lunate decompression,
partial denervation, and indirect revascularization similar to that described by Illarramendi.
The threshold stage for the use of radial osteotomies is still a matter of controversy.
JM Botelheiro (Lisbon) advocates their use in all stages of stage III, acknowledging
that occasionally the outcome is unfavorable, requiring a second joint operation as
a rescue operation. Logically, the results are better the lower the stage of SE and
the carpal instability, which Botelheiro considers adaptive rather than "true."[47]
[48]
The authors recommend considering radial shortening osteotomy as a valid option up
to stage IIIA, and even in some cases at stage IIIB, if the patient is young and has
a low-demand profession.
- If the lunate is considered "non-viable":
In these cases, we believe that palliative alternatives offer more reproducible results,
and within these, the choice should be individualized according to each patient's
activity. The most established are proximal row carpectomy and scaphocapitate arthrodesis
(preferably with arthroscopic assistance to ensure the good condition of the facet
joints).
Role of Arthroscopy in KD
Role of Arthroscopy in KD
Arthroscopy allows for a more precise assessment of the true condition of the lunate
and the radiocarpal and midcarpal articular surfaces. Today, it is essential for therapeutic
decision-making, helping to establish the appropriate definitive treatment, as it
provides certainty about the stage of the patient's disease at the precise time of
surgery. It sometimes leads to a change in therapeutic approach.[49] ([Figure 7])
Fig. 7 Cartilage detachment of the lunate bone during wrist arthroscopy in a case of EK.
Arthroscopic correlation of the “crescent line. Left wrist. Radiocarpal view from
the 3–4 portal.
As Bain and Begg proposed when publishing their arthroscopic classification, synovectomy
should be performed at any stage, and arthroscopic surgery allows this to be performed
with low morbidity and high precision. We would like to emphasize the value of this
synovectomy, since synovitis is present even in the earliest cases. It is not known
whether it is a cause or consequence of KD, but it is highly correlated with pain.[15]
Within the "curative" treatment strategies, such as stimulation of angiogenesis, forage
or revascularization of the lunate, wrist arthroscopy has allowed performing with
less morbidity techniques that were certainly aggressive when performed openly and
often allows the combination of several techniques simultaneously without an increase
in morbidity.
In cases where the lunate is no longer viable, open techniques such as PRC or arthroscopically
assisted scaphocapitate arthrodesis have become popular with promising results.[38]
Radiological images often underestimate the joint damage observed at arthroscopy;
however, we must be cautious when contraindicating a technique if a small chondral
ulcer is seen in the arthroscopic view, which may not be clinically relevant. We must
consider a joint surface affected when it presents significant joint damage throughout
its entire length.[4]
Conclusions
-
- To date, the cause of KD remains unknown. Concrete evidence exists, such as the
existence of infantile and juvenile lunatomalacia, which allows us to affirmthat the
morphological factors traditionally considered to influence the onset of KD, such
as having a short ulna or a type I lunate, are not necessary.
-
- Although avascular necrosis, including KD, is still considered to be free of hereditary
transmission, we believe it is important to continue investigating its genetic study,
especially in cases of “familial” KD.
-
- The emergence of arthroscopy has marked a turning point in assessing the stage of
KD and making therapeutic decisions, as well as reducing the morbidity of surgical
treatment.
-
- KD remains a therapeutic challenge with no universally effective solution. Treatment
choices should be individualized based on disease stage, patient age, and functional
demands. Continued research is key to improving treatment options and the long-term
prognosis of affected patients.
