Tuesday, 9 June 2015

Avascular Necrosis of Bone

This is bone loss due to loss of vascularity of the bone after a fracture or dislocation. May be spontaneous also.
It is a type of osteonecrosis.
Bone death or severe marrow and bone cell damage due to decrease in blood supply.

Sites:

- Femoral head
- Scaphoid
- Talus
- Lunate
- Head of humerus

Pathogenesis

Arterial insufficiency
- Fracture
- Dislocation

Venous occlusion
- Perthes disease

Intraosseous capillary compression

  • Infection
  • Gaucher;s disease - cortisone, alcohol
  • Caisson's disease

Intravascular capillary occlusion

Articular space normal
  • Sickle cell disease
  • Alcohol
  • Caisson disease
  • Corticosteroid
Pathology

Changes begin within a week of the insult and evolve over a period of 2-4 years. 
Pathology same in all conditions whatever the cause + features of underlying disorder
Bone cells die in 12-48hrs

Necrotic segment gets demarcated and granulation tissue grows in

New bone is laid down on the dead: increase in mineral mass: seen as sclerosis on Xray

With weight bearing: structural failure in new bone

Cracking of subchondral bone

Fragmentaation of necrotic bone/new bone

Destruction of joint surface

Is avascular necrosis reversible? Does complete healing occur? yes

Clinical Features

  • Pain: in or near a joint.
  • Only in certain movements
  • Tenderness/ swelling
  • Only in the superficial bones
  • Clicks in the join
  • Loose articular surfave
  • Stiffness of joint
  •  In later stages of the disease
  • Movements: one plane restricted early on
  • Advanced cases: fixed deformities. 
Radiology
Increased bone density
Subchondral fracture
Distortion of articular surface

Staging: Ficat & Arlet

Stage I: Pre-clinical phase: no radiological abnormality
Stage II: Early sclerois, bone contour normal
Stage III: Sclerosis, structural damage, bone contour altered
Stage IV: Collapse or articular cartilage and secondary OA

Other Investigations
Radionuclide 

- AVN seen as cold spot
- Surrounding area seen as hot spot

MRI

- identifies  in preclinical phase

Treatment

Factors influence natural course

= type of ischaemia
= area affected
= stage of disease
= patient's age
= capacity for bone repair
= persistence of etiological  agent. 

Treatment

Early stage (Stage I/II)
Bone contour normal, small lesions
Weight bearing bone vs non weight bearing

Non operative Rx

Traction: spasm decreases

Operative Rx: Eliminate etiology

Surgery: better results

Core decompression
Muscle pedicle bone grafting
Defunctioning osteotomy

Treatment
Late stage III/IV

Structural damage and articular distortion present

Operative treatment
- Pain/ loss of function: should demand for the procedure
- Realignment osteotomy
- Arthroplasty
- Arthrodesis

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