2. Introduction
Form of ischemic necrosis that usually follows
chronic stress or injury.
Has been suggested that relative shortening of the
ulna predisposes to stress overload of the lunate
between the distal edge of the radius and the
carpus.
3. Pathology
Four stages:
Stage I- ischaemia without naked eye or
radiographic abnormality.
Stage II-trabecular necrosis with reactive new bone
formation and increased radiographic density, but
little or no distortion of shape.
Stage III- collapse of the bone.
Stage IV- disruption of radio-carpal congruence
and secondary OA.
4. Clinical Features
Young adult
Ache and stiffness
Occasionally h/o acute trauma.
Tenderness localized over the lunate.
Grip strength is diminished.
Later stages- wrist movements are limited and
painful.
5. Imaging
X-ray: no abnormality(in initial stages).
Later may show either mottled or diffuse density of the
bone.
Stage 3- bone looks squashed and irregular.
Stage 4- osteoarthritic changes in wrist.
Radioscintigraphy- increased activity.
MRI- most reliable way of detecting early changes.
Ulnar variance- assessed by standardized x-ray
examination with the shoulder abducted to 90, forearm
in neutral rotation and the wrist in neutral flexion-
extension.
7. Non operative
Early cases- splintage of the wrist for 6-12 weeks.
Relieves pain and reduces mechanical stress.
If bone healing catches up with ischemia, lunate
may remain virtually undistorted.
8. Operative treatment
If the wrist architecture is only minimally
disturbed(i.e up to early stage 3)-reduction of
carpal stress by shortening the radius.
Once bone is collapsed-options are limited.
Lunate replacement by silicone prosthesis- poor long
term results and is liable to cause synovitis.
Intercarpal fusion or excision of proximal row of
carpus-improves function.
9. If pain and restriction of movement become
intolerable: radio-carpal arthodesis.
