Kienbock disease is avascular necrosis of the lunate bone in the wrist that results from disrupted blood flow. It progresses through stages from isolated lunate involvement to fragmentation and collapse. Treatment aims to decompress and revascularize the lunate early on through osteotomies or tendon transfers, while later stages involve procedures like proximal row carpectomy or fusion to stabilize the wrist joint and prevent further degeneration. However, there is no single treatment that reliably achieves pain relief and preservation of function as the disease progresses.

1. KIENBOCK DISEASE
Dr.Rubeesh Hassan
D ortho,DNB ortho

2. INDRODUCTION
 KIENBOCK DISEAS is an isolated disorder of
lunate resulting from vascular compromise to the
bone
 Avascular necrosis/osteomalacia of lunate
 Dr Robert Kienbock –1910
 He described step wise progression disease from
isolated proximal lunate involvement ,to
fragmentation and collapse of lunate evolving to
radiocarpal involvement with degenerative changes

3. AETIOLOGY
 Exact aetiology ?
 But it is likely multifactorial
1. Anatomical factors
2. Interrupted vascularity
3. Traumatic insults to lunate -repeated
microtrauma

4. ANATOMICAL
1.Ulnar negative varience
2. Three types of lunte morphalogies
type 1 lunate has proximal apex
type 2 and 3 more rectagular
Type 1 seen in wrist with negative ulnar varience
Type 1 –higher rate
3.Lower radial inclination
All this anatomical factors seems to be results in un
equal load distribution through the radiocarpal joint.

5. INTERRUPTED VASCULARITY
 Vascularity to lunate is variable
 3 major patterns of vascularity described
 Y pattern
 I pattern
 X pattern
In I pattern there is a single vessel supplying the
lunate ,which may increase risk of ostenecrosis.

7.  In addition AVN of lunate has been linked to
vascular insult caused by fracture,ligamentous
collapse,primary circulatory collapse,systemic
diseases and venous congestion.

8.  Although there is no single definitive cause of
kienbock disease ,a complex interplay of vascular
and anatomic variation ,combined with varying
degrees of microtrauma and insults contribute to its
development.

9. CLINICAL PRESENTATION
 Commonly affect men 20 to 40 years
 Symptoms can vary depending upon the stage at
initial presentation
 Pain localised to the radiolunate facet- pain is
classically insidious in onset
 Decreased wrist motion
 Swelling and decreased grip strength

10.  Tenderness over the dorsal lunate and radiolunate
facet
 An effussion or bogginess overlying the radiocarpal
join
 Movements especially dorsiflexion is limited
 Average grip strength may decrease upto 50% of
contralateral side
 In extreme case clenching of hand fails to show the
normal prominence of 3rd metacarpal—
FINSTERS’S SIGN
 Percussion over head of 3rd mc -tenderness

11. RADIOGRAPHIC IMAGING
 X Ray wrist PA and lateral view
 Negative in early in disease process
 Progressively shows increased lunate density
Fragmentation
Collapse
Proximal migration of capitate
widening of proximal carpal raw
scaphoid rotation
degeneratine changes in radio carpal bone

12. MRI

13. MRI SCAN
 MRI SCAN can detect early stages of disease with
increased signal uptake.
 In patients with perilunate dislocation or ulnar
impaction syndrome changes within the lunate may
appears similar to the AVN ,however these changes
are often focal and non progresive

14. CT SCAN
 CT scan characterise the lunate necrosis and
trabecular destruction once collapse has occurred.

15. STAGING

16. STAGE I
 Non specific intermittent wrist pain and synovitis
,which may mimic a wrist sprain.
 Plain x ray films are either normal or shows small
linear compression fracture through lunate.
 There is no collapse ,sclerosis or increased
radiodensity of the lunate
 Mri shows decreased signal uptake

17. STAGE II
 Characterised by increased swelling ,varying
degree of stiffness and progressive pain
 X ray shows lunate sclerosis with or without
compression fracture lines
 No evidence of collapse , lunate height is
maintained
 The remainder of the carpus remains without
degenerative changes

19. STAGE IIIA
 Is defined by continued sclerosis and collapse of
lunate
 Carpal height and intercarpal alignment is
preserved
 No scaphoid rotation
 Xray -lunate appears widened in AP view as a
result of the coronal plane collapse
 Scapholunate angle is preserved at -10 to
10degree

20. STAGE IIIB
 Collapse of lunate and charecteristic changes of
serrounding capitate and scaphoid
 Capitate migrate proximally and carpal height
become diminished
 Scaphoid flexes ,rotates resulting in DISI pattern of
instability

22. STAGE IV
 Progressive carpal collapse leading to radiocarpal
and midcarpal degenerative changes
 Xray joint space narrowing ,subchondral sclerosis
,degenerative cysts and osteophyte formation
 Symptoms have typically progressed to stiffness
,constant pain and swelling

24. TREATMENT
 Based on the stage at presentation
 Unload the lunate
 Revascularise the lunate
 Treat carpal instability and collapse with salvage
procedure

25. STAGE I
 Conservative treatment with 3 months
immobilisation is typically recommended for stage 1
desease
 The patient should continue to be monitored and if
symptoms or radiographs progress consider
surgical management

27. STAGE II OR III WITH NEGATIVE ULNAR
VARIENCE
 Goal in this stage is generally centered towards
unloading of lunte in an attempt to reduce
intracarpal stress and allow revascularisation
 Joint leveling procedures –
Radial shortening osteotomies
Ulnar lengthening procedures
Radial osteotomy is prefered over ulnar due to less
complication

28. STAGE II AND IIIA ULNAR NEUTRAL OR
POSITIVE VARIANCE
 Revascularisation
 Osteotomies
 Cor decompression

29. REVASCULARISATION
 Principle – Transplantation of an arteriovenous
pedicle into normal and avascular bone results in
new bone formation
 Direct revascularisation allows the potential for
salvage of the lunate and possible reversal of
destruction of lunate through neoangiogenesis

30.  Sources –distal radius pedicle graft with pronater
teres
 Vascularised pisiform graft
 Fourth and fifth extensor compartment artery graft
 I,II or III dorasal metacarpal artery ransfer

31. OSTEOTOMIES
 Goal of this procedure to unload the lunate in an
attempt to decrease stress across radiolunate joint
to allow revascularisation and prevention of disease
progression
 Capitate shortening osteotomies with or without
capitohamate fusion
 Radial closed wedge osteotomy—shift pressure
from lunate by decreasing radioulnar inclination

33. COR DECOMPRESSION
 Metaphyseal decompression of radius and ulna
 Decompression involve curettage of distal radius
/ulna through small cortical window
 Healing is due to local vascular response

34. STAGE IIIB
 Goal in this stage
Stabilisation of carpus
Prevent further collapse
Decrease the load across radiolunate joint
 Proximal row carpectomy
 Scaphotrapeziotrapezoid arthrodesis
 Scaphocapitate arthrodesis
 Grafting ,arthroplasty and interposition

35. PRC
 Is procedure that excises the scaphoid ,lunate and
triquetrium transfering load from the capitate
directly to the lunate facet of the distal radius

36. STT AND SC ARTHRODESIS
 Is to correct fixed and rotated scaphoid and
stabilise midcarpal joint ,prevent further collapse

37. CONTROVERSIAL
 Lunate exction
 Silicon lunate prosthetic replaicement

38. STAGE IV
 Salvage procedures performed
 PRC If mild degeneration
 WRIST ARTHRODESIS
 WRIST ARTHROPLASTY
 WRIST DENERVATION

40. SUMMARY
 Kienbock disease is defined by AVN of lunate,with a
predictable pattern of lunate collapse ,carpal
changes , and degenaration resulting from an
apparent combination of vascular,anatomical and
traumatic insults.

41.  Gaol of treatment is pain relief,motion preservation
,strength maintenance and function
 There is no one procedure that consistently and
reliably achieves this outcome

42.  Gaol of treatment is pain relief,motion preservation
,strength maintenance and function
 There is no one procedure that consistently and
reliably achieves this outcome

43. THANK YOU