Kienböck Disease: Recent Advances in Understanding and Management

Abstract

• ➢An at-risk lunate (due to anatomic factors) subjected to a trigger event (axial load, embolism, hypercoagulability) leads to the development of lunate osteonecrosis.
• ➢Children, adolescents, and elderly patients with Kienböck disease respond well to nonoperative treatments, and this should be considered before any surgical intervention.
• ➢For disease limited to the lunate, treatment decisions should be driven by the condition of the cartilage; intact lunate cartilage can be treated with joint leveling or core decompression, whereas disrupted cartilage surfaces should be bypassed with scaphocapitate or scaphotrapeziotrapezoid arthrodesis. Newer surgical procedures such as wrist arthroscopy and the introduction of contrast-enhanced magnetic resonance imaging have expanded the treatment options for these patients.
• ➢Once disease extends outside of the lunate, reconstruction with proximal row carpectomy or partial or total wrist arthrodesis should be considered on the basis of which articular surfaces are affected.
• ➢The new unified classification system and treatment are applicable to almost all patients with Kienböck disease.

Beginning with the first anatomical description of a collapsed lunate by Peste in 1843¹ and the first description of its pathogenesis by Kienböck in 1910² and continuing until the present time, authors have referred to Kienböck disease as an enigma³, an apt designation considering the diverse theories of pathogenesis, disputed natural history, and numerous treatment options available.

In the past 20 years, however, the above factors have been studied to the extent that there is now a clearer understanding of each. On the basis of this added information, 2 important classification systems and their derivative treatment algorithms have evolved^4-6. Unfortunately, no single system covers the variety of clinical situations, including the system published in 1977⁷ based on radiographic evaluation. In addition, most treatment recommendations are based on small, uncontrolled case series. Consequently, the management of Kienböck disease is often considered problematic by clinicians.

Nevertheless, by synthesizing the classic knowledge of Kienböck disease with recent advances, a combined treatment algorithm has been developed that can be applicable to most patients, regardless of age⁵. Therefore, our purpose was to review the relevant literature and to discuss in detail the rationale and clinical application of this algorithm. Although more research is required, especially randomized controlled trials to evaluate newer treatment modalities, we believe that considerable progress has been made in improving our understanding and management of this disorder.

Incidence and Natural History

The overall prevalence of Kienböck disease was identified at 0.27% by van Leeuwen et al. in 2016 in a cross-sectional epidemiological review of 51,071 patients over an 11-year period, with 37% of all identified Kienböck disease cases described as incidental and asymptomatic⁸. The sex distribution is about equal among men and women⁸, although it seems to be more prevalent in people who sustain repeated wrist strain or minor trauma⁵. Kienböck disease is most prevalent in Caucasian individuals (77% to 83% of all cases)^8,9 and less common in Hispanic patients (14%)⁸ or patients of African descent (7% to 8%)^8,9.

In most patients, the natural history of Kienböck disease, without intervention, is radiographic progression advancing through 4 specific stages⁷ (Fig. 1): (1) diminished lunate signal on T1-weighted magnetic resonance imaging (MRI) sequences, but normal radiographs; (2) relative lunate sclerosis on standard radiographs; (3) lunate collapse and/or fracture, leading to fixed carpal rotation; and (4) degenerative arthritis beginning at the radioscaphoid joint and ending in diffuse wrist arthritis¹⁰. Clinically, these stages are manifested by intermittent pain and swelling (synovitis) followed by a period of persistent pain with continued swelling. In time, inflammatory findings subside and are replaced by those of degenerative arthritis. The stages are of variable length, but the entire cycle can last ≥5 years.

Fig. 1.

Figs. 1-A through 1-E Radiographic representation of the Lichtman osseous classification of Kienböck disease. Fig. 1-A Stage-II posteroanterior radiograph. Fig. 1-B Stage-IIIA posteroanterior radiograph. Fig. 1-C Stage-IIIA lateral radiograph with the scapholunate angle indicated (58°). Fig. 1-D Stage-IIIB posteroanterior radiograph. Fig. 1-E Stage-IIIB lateral radiograph with scapholunate angle indicated (>60°). Fig. 1-F Stage-IIIC posteroanterior radiograph. Fig. 1-G Stage-IIIC lateral radiograph with a red arrow identifying a coronal lunate fracture. Fig. 1-H Stage-IV (pan-carpal arthritis) radiograph.

Multiple reports have shown that age at the initial presentation has a notable effect on prognosis, with adolescent “Teenbock” patients and elderly patients (>70 years of age) having better prognoses overall^4,5,11-15. In adolescents, the condition may have a better prognosis, as the disease may represent a form of osteochondrosis with expected bone recovery¹⁶. As a result, numerous authors have advocated for nonoperative or minimally invasive surgical treatment of Kienböck disease in pediatric and adolescent patients^{4,10,11,14,17-19}, as these populations demonstrate good to excellent recovery potential^12,14.

Interestingly, Kienböck disease in elderly patients appears to be a related but somewhat different entity than in adults^14,15. Kienböck disease in elderly patients appears to affect women disproportionately, with a lower frequency of ulnar negative variance and high incidences of autoimmune conditions, inflammatory arthropathies, and osteoporosis^4,20. Although these patients still undergo radiographic progression of the disease (at a faster rate than adults who are not elderly)²⁰, temporary immobilization, anti-inflammatory medications, and, occasionally, intra-articular corticosteroid injections provide reliable symptomatic relief⁵. In rare instances, synovectomy may be indicated^4-6.

To explain radiographic disease progression, MacLean and Bain²¹ described the “nutcracker effect,” or proximal migration of the capitate through a lunate fracture during wrist loading. This results in the separation of fracture fragments and subsequent lunate collapse^20,22. There appears to be accentuation of the nutcracker effect in type-I lunates (lacking a separate ulnar facet articulating with the hamate), which explains the protective mechanism observed for type-II lunates²⁰. Additionally, the scaphoid flexion (>60°) that differentiates stage IIIA from stage IIIB results from either attenuation and rupture of the scapholunate ligament or fracture of the osseous attachment of the scapholunate ligament at the dorsal lunate²⁰. This disruption in normal proximal row kinematics results in a predictable pattern of wrist degeneration, in line with those seen in scaphoid nonunion advanced collapse (SNAC) or scapholunate advanced collapse (SLAC) pattern wrist arthritis. As such, stage-IV disease is also known as Kienböck disease advanced collapse (KDAC) pattern wrist arthritis^4,23.

Predisposing Factors

The underlying pathology of Kienböck disease is osteonecrosis of the lunate²⁰. Because the lunate serves as the keystone of the wrist, secondary changes such as collapse of the lunate and reactive synovitis lead to the disruption of the surrounding carpal architecture and ultimately degenerative arthritis²⁰.

Many predisposing factors for the development of lunate osteonecrosis have been identified. Anatomic variabilities of the lunate and wrist are leading causes, including ulnar negative variance²⁴, decrease in radial inclination²⁵, lunate morphology²⁶ including trabecular patterns²² or mineralization patterns in the subchondral bone of the distal radius²⁷, and compromised lunate vascularity^16,28. Lunate intraosseous hypertension and disrupted venous outflow from the lunate^22,29,30 have also been identified as etiologic factors and may result from numerous systemic conditions, such as systemic sclerosis³¹, lupus^32,33, Legg-Calvé-Perthes disease³⁴, gouty arthritis³⁵, and the Raynaud phenomenon³⁶, as well as sickle cell anemia, cerebral palsy, or decompression sickness³⁷. Any systemic condition increasing coagulability can result in osteonecrosis of the lunate^34,38. In the femoral head, endothelial injury³⁹ or activation⁴⁰ has been postulated to promote inflammation and coagulopathy while inhibiting recovery in osteonecrosis³⁹, although this association has not been reported in the lunate. Furthermore, a population-level genetic study showed familial clustering and a potential genetic contribution to the development of lunate osteonecrosis⁴¹.

Although the exact etiology of Kienböck disease for any individual is rarely evident, the widely accepted consensus is that the above anatomic factors predispose a patient to the development of Kienböck disease by acting as a catalyst, placing the lunate in an at-risk state²⁰. For example, ulnar negative variance (as identified on a neutral-rotation posteroanterior radiograph⁴²) is considered a risk factor for the development of Kienböck disease^24,25,38,43. A shorter ulna relative to the radius theoretically causes increased load transmission on the ulnar wrist, specifically the lunate, predisposing the patient to the development of osteonecrosis. Despite this observation, most individuals with ulnar negative variance do not develop Kienböck disease. However, there have been conflicting reports of the impact of ulnar variance, with several authors unable to show a causal relationship between ulnar negative variance and Kienböck disease^44,45. There are also racial variations in the presence of ulnar negative variance, with unaffected individuals showing ulnar negative variance in 25% in the United States²⁴, 10% in China⁴⁶, and up to 58% in The Netherlands⁴⁷. Kienböck disease can occur bilaterally, although specific risk factors for bilateral disease have not been identified⁴⁸.

Viegas et al. described variability in lunate morphology, with type-I lunates lacking a separate facet articulating with the hamate (34.5% of study population) and type-II lunates having a separate hamate facet (65.5% of the study population)⁴⁹. Rhee et al. concluded that Viegas type-II lunates may be protective against Kienböck disease development as well as progression to late-stage disease²⁶.

A history of ipsilateral wrist trauma has been identified in up to 53% of patients with Kienböck disease (30 of 57 patients) in a large cohort study²⁵. In the same cohort, 70% of all affected patients (40 of 57) had ulnar negative variance. However, it should be noted that routine activities of daily living can exert considerable axial load across the lunate^50,51. Therefore, the specific association between any given event and the emergence of symptoms may represent a chance association rather than a causal relationship. Nevertheless, a critical interpretation of the available evidence with regard to the etiology of Kienböck disease convincingly shows that an at-risk lunate (due to the anatomic factors listed above) subject to a trigger event (axial load transmitted across the lunate²⁵, embolism³⁷, exposure to certain diseases, and medications) can initiate or accentuate the development of osteonecrosis.

Recent Surgical Advances

Published studies have indicated a better overall prognosis in adolescent patients^4,5,11,12,14, which led to the development of minimally invasive surgical treatment options. Temporary pinning of the scaphocapitate (SC) or scaphotrapeziotrapezoid (STT) joints, combined with cast immobilization, has been shown to allow for lunate unloading and recovery in teenagers^17,19,52-55. In adults, wrist denervation has been reported as a potential surgical treatment option⁵⁶. Several authors have recommended core decompression (drilling through cortical bone to relieve venous congestion) of the distal radius and/or ulna^57,58 or lunate^59,60, with promising results and limited risk of complications.

Higgins and Bürger^61-63 popularized the use of the medial femoral trochlea (MFT) osteochondral autograft free flap for reconstruction of the proximal lunate articular surface in Kienböck disease. This approach involves harvesting an osteochondral graft from the MFT, which is used to reconstruct the proximal lunate articular surface. The choice of the MFT as a donor site is based on its availability of high-quality cartilage and bone, crucial for successful joint surface reconstruction. The technique has demonstrated success in restoring the congruity of the lunate’s articular surface and alleviating pain in patients with advanced stages of lunate collapse. Nonunion, persistent pain, and donor-site deep vein thrombosis have been reported, however⁶³. Long-term results have not been reported, and may uncover additional potential morbidity of the procedure.

Pyrocarbon lunate replacement has been explored, although its success rates have varied^64,65. The primary advantage of pyrocarbon arthroplasty is its potential to maintain wrist motion and reduce the need for more invasive procedures such as SC or STT arthrodesis. However, the variability in success rates highlights the need for further research.

Hierner and Wilhelm have described a method of distraction lengthening of the capitate following lunate excision in patients with advanced lunate collapse⁶⁶. Long-term follow-up has been reported at 5 years, with reliable pain improvement and preservation of preoperative wrist motion.

Diagnostic Advances, Classification Systems, and Treatment Algorithms

Thin-cut computed tomography (CT) has allowed for improved ability to identify or confirm a diagnosis of Kienböck disease, especially in early stages when used in conjunction with MRI (Fig. 2)⁶⁷. Furthermore, CT can be helpful in identifying lunate fracture morphology and can play a vital role when lunate salvage is considered²¹. Contrast-enhanced MRI has reliable utility in diagnosing and determining disease prognosis through the visualization of the vascularity of the lunate⁶⁸.

Fig. 2.

T1-weighted coronal (left) and sagittal (right) MRI scans showing Kienböck disease.

Several classification systems and treatment algorithms for Kienböck disease have been proposed to outline the natural history and to guide the diagnosis and treatment decision^{4,6,7,11,69-72}. These classification systems have been adapted and implemented to various degrees. The system first described by Lichtman et al. in 1977⁷, and subsequently updated by Lichtman and Degnan in 1993⁷¹ by adding a treatment algorithm (Fig. 1, Table I), is now considered the most frequently used and accepted treatment guideline^73-75. This classification relies on readily available radiographs and has demonstrated applicability⁷⁶ and interobserver reliability⁷⁷ but may underestimate lunate and adjacent carpal destruction by not including the condition of cartilage or the potential of bone revascularization in disease staging.

TABLE I.

Lichtman Osseous Classification System and Treatment Algorithm^*

Stage	Radiographic Findings	Treatment
I	Normal	Immobilization and joint leveling
II	Lunate sclerosis	Radial or capitate-shortening osteotomy
IIIA	Lunate collapse without fixed carpal instability	Radial or capitate-shortening osteotomy
IIIB	Lunate collapse with fixed carpal instability	PRC or STT or SC arthrodesis
IIIC	Coronal lunate fracture	Excision of lunate with STT or SC arthrodesis or PRC
IV	Pancarpal arthritis Kienböck disease advanced collapse	Wrist arthrodesis or arthroplasty

^*PRC = proximal row carpectomy, STT = scaphotrapeziotrapezoid, and SC = scaphocapitate.

Recent advances in technical and technological capabilities have led to the description of additional ways to define and grade Kienböck disease. Contrast-enhanced MRI protocols, published by Schmitt and Kalb in 2010⁶⁸, provide valuable information on lunate vascularity and presumed ability for bone healing (Fig. 3, Table II). Although the Schmitt classification does not offer specific treatment recommendations, it can be useful for choosing patients who might benefit from a revascularization procedure.

Fig. 3.

Schmitt schematic diagram of lunate viability in gadolinium-enhanced MRI. Red indicates contrast enhancement patterns. FSE = fast spin echo. (Reproduced with permission from: Lichtman DM, Pientka WF, Bain GI. Kienböck disease: a new algorithm for the 21st century. J Wrist Surg. 2017;6[1]:2-10. © Georg Thieme Verlag KG.)

TABLE II.

Schmitt Contrast MRI Classification System

Stage	MRI Findings	Contrast Enhancement Pattern
N	Normal lunate	No enhancement
A	Marrow edema with intact bone	Homogenously increased signal in proximal lunate
B	Early marrow necrosis with fibrovascular reparative tissue in lunate	Mixed (heterogenous) signal throughout the lunate
C	Necrotic bone marrow, lunate collapse	Homogenously decreased signal throughout the lunate

Bain and Begg⁶ described a classification system and treatment algorithm for Kienböck disease in 2006 based on the condition of the articular cartilage on and around the lunate identified during wrist arthroscopy (Fig. 4, Table III)⁷⁸. Subsequent descriptions of treatment approaches based on the condition of articular cartilage have focused on the functional status of the cartilage identified by MRI, CT, arthroscopy, or direct inspection. Although extremely useful, the Bain classification does not account for the stability of the wrist, the condition of the surrounding carpal bones, or the age of the patient. This makes it impossible for the Bain classification alone to cover a substantial percentage of patients with Kienböck disease⁷⁹.

Fig. 4.

Bain-Begg arthroscopic-based classification of Kienböck disease. (Reproduced with permission from: Lichtman DM, Pientka WF, Bain GI. Kienböck disease: a new algorithm for the 21st century. J Wrist Surg. 2017;6[1]:2-10. © Georg Thieme Verlag KG.)

TABLE III.

Bain Articular Cartilage Classification System and Treatment Algorithm^*

Stage	Affected Articulations	Treatment Recommendation
0	None	Joint leveling, core decompression, vascularized bone graft
1	Proximal lunate	RSL arthrodesis, PRC, MFT grafting
2A	Proximal lunate and radius	RSL arthrodesis
2B	Coronal lunate fracture	PRC, lunate arthroplasty, capitate lengthening
3	Proximal and distal lunate, radius	Hemiarthroplasty
4	Proximal and distal lunate, radius, capitate	Total wrist arthrodesis, total wrist arthroplasty

^*RSL = radioscapholunate, PRC = proximal row carpectomy, and MFT = medial femoral trochlea.

In 2022, the concept of “Precision Medicine for Kienböck Disease” was introduced, which relies on 5 key questions that a treating provider should answer to guide treatment decision-making when addressing a patient with Kienböck disease in any stage⁵. The 5 key questions are:

• Question A: “What is the Age of the patient?”

• Question B: “What is the state of the lunate Bone?”

• Question C: “What is the state of the Carpus?”

• Question D: “What Diagnostic and treatment options are available to the surgeon?”

• Question E: “What are the patient’s Essential needs?”

Furthermore, a unified classification system for Kienböck disease was developed, which amalgamates the Lichtman^7,71, Bain^6,78, and Schmitt⁶⁸ systems, along with newer treatment options, leading to the development of a more nuanced treatment algorithm for the disorder⁸⁰ (Fig. 5, Table IV). By addressing each of the above key questions, this precision treatment algorithm provides recommendations that can be applied to almost all patients with Kienböck disease⁵.

Fig. 5.

Decision tree for the treatment of Kienböck disease based on the unified classification system. OA = osteoarthritis and ± = with or without. (Reproduced, with modification, with permission from: Greg Bain. Lee S, Bain G, MacLean S, Lichtman DM. Fractures of the Carpal Bones. In: Green’s Operative Hand Surgery. 8th ed. Boston, MA: Elsevier; 2021. p 677-757. © 2021 Greg Bain.)

TABLE IV.

Unified Classification System and Treatment Algorithm^*

Clinical Presentation	Recommended Treatment	Precision Classification	Lichtman or Bain Classifications	References
Child <15 years of age	Nonoperative management	A1	NA	4,5,12
Adolescent and young adult 15 to 20 years of age	Nonoperative management for 3 to 6 months and then treat as an adult if still symptomatic	A2	NA	4,5,12,17,19,52-55
Elderly adult, ≥65 years of age	Nonoperative management plus workup for osteopenia and inflammatory arthritis Synovectomy as needed	A3	NA	4-6,14,15,27
Adult with lunate intact	Radial shortening (if ulnar negative), elective revascularization, with Schmitt C Capitate shortening (if ulnar positive), elective revascularization, with Schmitt C Core decompression	B1	L: II, IIIA, B: 0	17,18,57-60,85-94
Adult with salvageable (compromised) lunate (1) Coronal lunate fracture, (2) proximal pole lunate collapse, or (3) both combined	Lunate ORIF, especially with Schmitt A fragment MFT graft for proximal pole collapse Simultaneous procedures for (3)	B2	1. L: IIIC, B: 2B, 2. B: 1	4,61-63,95-100
Adult with nonsalvageable lunate (disease limited to lunate)	PRC for most, or limited carpal arthrodesis (SC or STT); excise lunate for synovitis	B3	L: IIIC, B: 2B	4,5,95-98,101,106,107
Carpal collapse (scapholunate rotation >60°) with intact radial cartilage	PRC for most Consider leveling procedure for Bain 0	C1	L: IIIB	4,5,11,78,98,106,107
Carpal collapse with scaphoid fossa arthritis	PRC	C2A, C2B	L: IIIB	4,5,11,77,106,107
Carpal collapse with lunate fossa arthritis	PRC for most Consider STT or SC arthrodesis for Bain 0	C2A, C2B	L: IIIB	4,5,11,77,106,107
Carpal collapse with scaphoid and lunate fossa arthritis and more	Wrist arthrodesis Wrist arthroplasty (select non-workers, rarely indicated in this age group)	C3	L: IV	4,5,74

^*NA = not applicable, ORIF = open reduction and internal fixation, MFT = medial femoral trochlea, PRC = proximal row carpectomy, SC = scaphocapitate, and STT = scaphotrapeziotrapezoid.

Treatment Recommendations for Kienböck Disease

Children and Elderly Patients

A1: Patients younger than 15 years of age should be treated nonoperatively, as symptomatic resolution generally may be expected with time^5,12.

A2: Adolescents and young adults (15 to 20 years of age) should undergo a 3 to 6-month trial of immobilization prior to considering surgical intervention^4,5. For unresponsive patients, minimally invasive surgical options are the mainstay of treatment^{12,17,19,52-55}. In skeletally mature teenagers who do not respond to the above, treatment as an adult should be considered⁵.

A3: Patients ≥65 years of age often respond well to nonoperative management, including splinting, nonsteroidal anti-inflammatory medications, and hand therapy. These patients also warrant an evaluation for osteoporosis²⁷, inflammatory arthropathy, and autoimmune conditions^14,15. In the elderly patient with Kienböck disease who does not respond favorably to nonoperative management, wrist synovectomy can assist in resolution of recalcitrant pain and swelling^4-6. In rare instances, a total wrist arthrodesis or arthroplasty may be indicated.

Adult Patients with Disease Limited to the Lunate

The majority of Kienböck disease presents in patients 20 to 40 years of age⁸¹. If the lunate is affected in isolation, without degeneration of the distal radial articular surface or adjacent carpal bones, the lunate should be identified as intact, compromised, or nonsalvageable^4-6,78. This determination is made by a combination of radiographs or CT (osseous architecture)⁷⁰, MRI with contrast (lunate vascularity)⁶⁸, gross evaluation of the lunate cartilage surface⁷⁷, and/or arthroscopic examination^82-84. It is critical to recognize that a lunate may be intact, compromised, or nonsalvageable in any patient with either stage-II or IIIA disease, so this evaluation cannot be made solely on the basis of radiographs⁵.

B1: An intact lunate has intact cartilage throughout (Bain 0) with intact or mixed (fair) vascularity identified on contrast MRI (Schmitt A or B). The goal of surgical intervention is to protect the intact lunate to prevent lunate collapse and encourage revascularization. This is done with an unloading procedure, based on the ulnar variance^18,85-89. Wrists with ulnar negative variance are treated with radial shortening (Fig. 6)^85-87 or core decompression of the distal radius, ulna, or lunate^17,57-60. Ulnar neutral or positive wrists may be treated with capitate-shortening osteotomy (Fig. 7)^88,89 or a core decompression procedure of the distal radius, ulna, or lunate to prevent ulnocarpal impaction^17,57-60. Distal radial wedge osteotomy has also been described and has been successful⁹⁰. A lunate revascularization procedure should be considered in addition to the above treatment recommendations in a lunate with Schmitt C (no lunate vascularity) on contrast MRI^91-94.

Fig. 6.

Preoperative posteroanterior (Fig. 6-A) and lateral (Fig. 6-B) radiographs and postoperative posteroanterior (Fig. 6-C) and lateral (Fig. 6-D) radiographs of a 42-year-old woman treated with a radial-shortening osteotomy.

Fig. 7.

Postoperative (left) posteroanterior and (right) lateral radiographs of a 38-year-old woman treated with a capitate-shortening osteotomy.

B2: A compromised lunate may have a nonfunctional or disrupted proximal cartilaginous surface (Bain 1) or a coronal fracture or fissure in the articular cartilage (Bain 2B or Lichtman IIIC) with maintained vascularity (Schmitt A or B) of the major fracture fragment. In the Bain 1 lunate, an SC or STT arthrodesis is sometimes recommended to stabilize the carpus and bypass the affected lunate^95-97. Although SC arthrodesis has been performed, proximal row carpectomy (PRC) is the preferred procedure to avoid future radioscaphoid arthritis and carpal collapse⁹⁸. Alternatively, a free vascularized MFT autograft may be utilized to replace the necrotic proximal lunate and the adjacent nonfunctional cartilage^61-63.

In the lunate with a coronal fracture (Bain 2B or Lichtman IIIC) with intact or partially reduced vascularity (Schmitt A or B), fracture fixation with headless screws has been described⁹⁹. However, a nondisplaced or minimally displaced fracture can be treated successfully with radial shortening osteotomy¹⁰⁰. If both conditions are present, a combined procedure may be indicated⁶³.

B3: A nonsalvageable lunate has either a coronal fracture (Bain 2B or Lichtman IIIC) with no lunate vascularity (Schmitt C) or severe comminution and resorption. The absent vascularity in the fractured lunate portends a poor prognosis for fracture-healing if treated with a headless compression screw. In this scenario, a PRC is the treatment recommendation (Fig. 8)^4,5. SC arthrodesis has also been advocated^95-97, although the complication of symptomatic radioscaphoid arthritis should be considered⁹⁸. Intercarpal arthrodesis, of the type recommended by Graner et al., is another alternative when multiple lunate joint surfaces are nonviable¹⁰¹.

Fig. 8.

Preoperative posteroanterior (Fig. 8-A) and lateral (Fig. 8-B) radiographs and postoperative posteroanterior (Fig. 8-C) and lateral (Fig. 8-D) radiographs of a 32-year-old woman treated with a proximal row carpectomy.

For the collapsed lunate in which adjacent carpal changes have not yet developed, lunate excision with capitate lengthening⁶⁶ or implant arthroplasty utilizing silicone^7,102, titanium¹⁰³, or pyrocarbon⁶⁴ lunates have been described. Results have been mixed with these implants, as silicone implants fragment, deform, and often cause particulate synovitis. Solid implants can dislocate, which has led to poor surgical outcomes¹⁰².

Carpal Collapse or Disease Not Limited to the Lunate

C1: When the disease has progressed beyond the lunate, leading to fixed excessive scaphoid flexion (scapholunate angle of >60°), treatment strategies shift to salvage, as lunate preservation alone is no longer a viable option^4,5,78. In the C1 stage, the distal radial articular surfaces are still intact. Although some surgeons perform STT or SC arthrodesis to stabilize the wrist^95-97, most recommend PRC to avoid the complication of subsequent arthritis and carpal collapse^4,5,11,78,98. In addition, some patients at the C1 stage have been treated with B1 treatment options (such as radial-shortening osteotomy), with good results reported^100,104,105.

C2: After lunate collapse, degeneration of the distal radius generally begins at the radioscaphoid facet and progresses ulnarward. PRC remains the treatment of choice^4,5,78. In the rare instance when the scaphoid fossa articulation is maintained but the lunate facet is affected, limited intercarpal arthrodesis has been performed^95-97, although subsequent radioscaphoid arthritis can develop⁹⁸.

Given the risk of nonunion, increased technical demands, and possible long-term complications of SC or STT arthrodesis, PRC is an accepted and commonly recommended treatment option for all patients at stage C1 and C2^4,5,106,107. However, if limited carpal arthrodesis is chosen, we recommend excising the collapsed or fragmented lunate to eliminate the source of synovitis and inflammation.

C3: Once pancarpal wrist degenerative changes have developed, total wrist arthrodesis⁷⁸ is the surgical procedure of choice. Total wrist arthroplasty may be considered for selected patients^4,108. Furthermore, nonoperative treatment is always an option, especially in older, sedentary, and minimally symptomatic patients.

Other Considerations

In addition to the grading listed above, surgical experience, facility equipment, and diagnostic resources should be considered. Contrast-enhanced wrist MRI is a helpful aspect of the evaluation process but may not be available at all facilities. The health status and desires of each patient must also be elucidated, as they may be unwilling or unable to undergo a complex reconstructive procedure or any procedure with a lengthy recovery period. The alternative treatment options included in the precision treatment algorithm allow for the modification of strategies based on these scenarios⁵.

Finally, before a treatment decision is made, the patient should understand the natural history of Kienböck disease¹³, from early synovitis to possible late arthritis. In time, symptoms generally abate even in untreated patients¹⁰⁹. The length of this process is indeterminate, but may take ≥5 years⁵. However, surgical interventions can generally be expected to provide improvement within 3 to 6 months^100,110. Nevertheless, some patients may choose to “wait out” the cycle, especially if the impairment is mild or they are unable or unwilling to undergo surgical intervention.

Summary

Although most recent publications have reported good to excellent outcomes for Kienböck disease, almost all have represented small, uncontrolled case series or observational studies (Table V). Because high-quality comparative outcome studies are virtually nonexistent, the issue for most surgeons has been which treatment option is the most effective for a particular patient and his or her precise stage of disease.

TABLE V.

Grades of Recommendation

Recommendation	Grade*
For children <15 years of age, use observation.	C
For adolescents or adults 15 to 20 years of age, use observation for 3 to 6 months and then treat as an adult if still symptomatic.	C
For elderly adults, ≥65 years of age, use observation plus workup for osteopenia and inflammatory arthritis. Perform synovectomy as needed.	C
For adults with the lunate intact, use radial shortening (if ulnar negative), capitate shortening (if ulnar positive), or core decompression. Consider elective revascularization for Schmitt C.	C
For adults with salvageable (compromised) lunate due to coronal lunate fracture, proximal pole lunate collapse, or both combined: Consider open reduction and internal fixation of the fragment for Schmitt A. Perform MFT graft for proximal pole collapse. Perform both procedures for coronal lunate fracture and proximal pole lunate collapse combined.	C
For adults with nonsalvageable lunate (disease limited to lunate), perform PRC for most or limited carpal arthrodesis (either SC or STT arthrodesis). In limited carpal arthrodesis, excise the lunate in the presence of synovitis.	C
For adults with carpal collapse (scapholunate rotation >60°) with intact radial cartilage, perform PRC for most or SC or STT arthrodesis. In limited carpal arthrodesis, excise lunate in presence of synovitis. Also consider leveling procedure for Bain 0.	C
For adults with carpal collapse with scaphoid fossa arthritis, perform a PRC and consider SC or STT arthrodesis.	C
For adults with carpal collapse with lunate fossa arthritis, perform a PRC and consider SC or SST arthrodesis.	C
For adults with carpal collapse with scaphoid and lunate fossa arthritis, perform wrist arthrodesis or wrist arthroplasty (for select non-workers, rarely indicated in this age group).	C

^*According to Wright¹¹¹, grade A indicates good evidence (Level-I studies with consistent findings) for or against recommending intervention; grade B, fair evidence (Level-II or III studies with consistent findings) for or against recommending intervention; grade C, poor-quality evidence (Level-IV or V studies with consistent findings) for or against recommending intervention; and grade I, insufficient or conflicting evidence not allowing a recommendation for or against intervention.

To address this, 3 classification systems with derivative treatment algorithms have been developed on the basis of the literature available at the time of their publication. The original osseous-based system introduced in 1977 has now been complemented by ones derived from arthroscopic visualization and advanced imaging studies. All 3 systems contribute information essential to the understanding of the disorder, but none of them used individually is applicable to all clinical presentations of Kienböck disease. However, by combining the 3 into a more nuanced unified classification system, along with the application of a greater understanding of the natural history, patients of any age or stage can be included.

In conclusion, scientific evidence uncovered in the last 20 to 25 years has provided useful information for both the surgeon and the patient. Although more research is necessary, especially prospective multi-institutional controlled trials for newer treatment modalities, recent progress has improved the management of this fascinating disorder.