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Download MBBS Orthopaedics PPT 4 Avascular Necrosis Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Orthopaedics PPT 4 Avascular Necrosis Lecture Notes

This post was last modified on 07 April 2022


Avascular Necrosis

Learning Objectives

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? Atraumatic /Traumatic AVN
? Understand the pathology of AVN
? Progression of disease
? Classification of Hip AVN
? Principles of treatment

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27 years old ,pain right groin

? Non smoker, occasional alcohol intake, no medical history

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? On examination.

? No Tenderness

? Restricted internal rotation ,painful

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? No limp

? CBC Normal, Rheumatoid factor ?ve, ESR 18mm,CRP -6

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Radiographs
Q1 Which of the following is an inappropriate

diagnosis?

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a) Early Sero-Negative Rheumatoid arthritis
b) Avascular necrosis right hip
c) Tubercular arthritis right hip
d) Torn acetabular labrum

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Q 2 The most appropriate investigation for

him is?

a) Tc 99 bone scan

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b) MRI scan
c) MARS MRI
d) Contrast enhanced CT Scan
Q3 This is classifiable as Ficat-Arlet-

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a) Stage 1
b) Stage 2
c) Stage 3
d) Stage 4

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Q 4 The most appropriate treatment ?

a) Non operative with follow up MRI at 6 weeks
b) Non weight bearing and analgesics
c) Bed rest, traction and analgesics

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d) Core decompression
Q 5 The patient comes after 2 years and has severe pain in his

hip, decreased ROM and a pronounced limp. Radiographs

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reveal collapse of the head with decreased joint space

suggestive of secondary OA. The appropriate management is-

a) Arthroscopic debridement and irrigation

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b) Osteochondral grafting
c) Bipolar hip arthroplasty
d) Total hip arthroplasty

Overview

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? AVN is a major cause of hip pain
? Traumatic/Atraumatic in etiology
? Evaluation is difficult
? Treatment is hip salvage/Replacement

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? Other common areas are ?Humerus, scaphoid, talus and distal femur
Avascular necrosis- Traumatic

? Femoral neck fractures- severance of the blood supply to the femoral

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head.

? The capitulum
? Femoral condyles
? Proximal parts of the scaphoid and talus.

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Distant parts of the bone's vascular territory
Largely enclosed by cartilage- restricted access to local

blood vessels.

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TRAUMATIC OSTEONECROSIS

? Fractures and dislocations of the hip

? Tear of retinacular vessels supplying the femoral head

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? Displaced fractures of the femoral neck ? AVN 20%.


fractures of the scaphoid and talus- AVN

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? Principal vessels enter their distal ends
? Intraosseous course from distal to proximal.

Closed compartment-Bone

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? Vascular sinusoids- no adventitial layer
? Patency - volume and pressure of the

marrow tissue

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? Marrow is encased in unyielding bone.
? One element can expand-other gets

compressed

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NON-TRAUMATIC OSTEONECROSIS

? Intravascular stasis
? Thrombosis
? Extravascular swelling and capillary compression.

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Ischaemia- Multifactorial

? Severance of the local blood supply
? Venous stasis and retrograde arteriolar stoppage

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? Intravascular thrombosis
? Compression of capillaries and sinusoids by marrow swelling.
Nontraumatic -AVN

? Perthes' disease,

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? Caisson disease
? Gaucher's disease

systemic lupus erythematosus

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Sickle-cel disease

Dysbaric ischaemia

Thrombocytopenia

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Fat embolism

Arteriolar occlusion

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Marrow edema Vascular stasis

Sinusoidal compression

Gaucher's disease

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Tuberculosis

Cortisone/alcohol

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Dysbaric ischaemia


Normal head femur

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Pathology and natural history

? Prolonged anoxia ? Osteocyte death
? Gross appearance remains unaltered
? Striking histological changes in the marrow

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? Loss of fat cell outlines

? Inflammatory cell infiltration

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? Marrow oedema

? Replacement of necrotic marrow- mesenchymal tissue.


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Bone repair?

? New blood vessels and osteoblastic proliferation at the interface

between ischaemic and live bone.

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? Vascular granulation tissue advances from the surviving trabeculae
? New bone is laid down upon the dead- creeping substitution
? Increase in mineral mass - increased density or `sclerosis'.

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Further progress

? Reparative formation proceeds slowly
? Advances 8?10 mm into the necrotic zone.
? Structural failure begins- most heavily stressed part of the necrotic

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segment.

? Linear tangential fracture close to the articular surface.

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Stage of arthritis

? Articular cartilage retains its thickness and viability for a long time.
? In the final stages- fragmentation collapse of the necrotic bone

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? Progressive deformity and destruction of the joint surface.

Clinical features

? The earliest stage of bone death is asymptomatic

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? Patient presents with pain - lesion is usually well advanced.
? Pain in or near a joint
? Few complain of a `click' in the joint- due to snapping or catching of a

loose articular fragment.

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Stage of arthritis

? Joint becomes stiff and deformed.

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? Local tenderness may be present
? Superficial joints- effusion.
? Movements ?may be restricted
? Advanced cases- fixed deformities.

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Radiographs

? The early signs of ischaemia -bone marrow and cannot be detected.
? 3 months after the onset of ischaemia- first sign
? Reactive new bone formation at the boundary of the ischaemic area -

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sclerosis


Thin tangential fracture line just below the

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articular surface ?the `crescent sign'.

Late -collapse and distortion of the articular

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surface


MRI Scan

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? The most sensitive modality ? marrow changes are discernable
? The size of the necrotic segment-hypo-intense band in the T1,MRI

AVN ?Distal femur

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AVN Talus

AVN -Capitulum
Radionuclide scanning

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? 99mTcsulphur colloid- taken up in myeloid tissue.
? Useful in traumatic avascular necrosis- large segment of bone is

involved.

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? Sickle-cell disease - `cold' area contrasts significantly with the

generally high nuclide uptake due to increased erythroblastic activity.

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Staging the lesion

? Ficat and Arlet (1980) introduced the concept of radiographic staging

for osteonecrosis of the hip

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? Early (pre-symptomatic) signs- sclerosis, crescent sign.
? Later features- progressive demarcation and collapse of the necrotic

segment in the femoral head.

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Stage 1 ? No radiological changes

? Diagnosis was based on measurement of raised intraosseous pressure

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? Histological features of bone biopsy
? MRI

Stage II

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? The femoral head contour was still normal
? Early signs of reactive change in the subchondral area


Stage 3

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? Signs of osteonecrosis with evidence of structural damage and

distortion of the bone outline.

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? Collapse of the necrotic segment

Stage 4

? Collapse of the articular surface and signs of secondary OA.

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Diagnosis of the underlying disorder

? Episode of trauma- obvious
? Occupation- deep-sea diving or working under compressed air
? Family background of Gaucher's disease or sickle-cell disease.

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? High-dosage corticosteroid administration; renal transplantation.
? Low dose use ?quacks, inappropriate use
? Alcohol abuse is often difficult to determine
? SLE- antiphospholipid antibodies may be measured.

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EARLY OSTEONECROSIS

? Bone contour is intact- structural failure can be

prevented.

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? Some lesions heal spontaneously and with minimal

deformity;

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? Non-weightbearing joints

? Superomedial part of the femoral head

? Non- weight bearing surfaces of the femoral condyles and

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talus.


Weight bearing joints

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? Poor prognosis-l probably end in structural failure
? Simple measures like non weight bearing- reduce loading.
? If the bone contour is still intact,an `unloading' osteotomy
? Help to preserve the anatomy while remodelling proceeds.

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? Medullary decompression and bone grafting may have a

place

Stage II- Core decompression B/L

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LATE STAGE OSTEONECROSIS

? Destruction of the articular surface may be give rise to pain and

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severe loss of function.

? non-operative management, concentrating on pain control,

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modification of daily activities and appropriate, splintage of the joint

? Arthrodesis of the joint, e.g. the ankle or wrist
? Total joint replacement- shoulder, hip and knee.
Q1 Which of the following is an inappropriate

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diagnosis?

a) Early Sero-Negative Rheumatoid arthritis
b) Avascular necrosis right hip

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c) Tubercular arthritis right hip
d) Torn acetabular labrum

Q 2 The most appropriate investigation for

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him is?

a) Tc 99 bone scan
b) MRI scan
c) MARS MRI

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d) Contrast enhanced CT Scan
Q3 This is classifiable as Ficat-Arlet-

a) Stage 1
b) Stage 2

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c) Stage 3
d) Stage 4

Q 4 The most appropriate treatment ?

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a) Non operative with follow up MRI at 6 weeks
b) Non weight bearing and analgesics
c) Bed rest, traction and analgesics
d) Core decompression
Q 5 The patient comes after 2 years and has severe pain in his

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hip, decreased ROM and a pronounced limp. Radiographs

reveal collapse of the head with decreased joint space

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suggestive of secondary OA. The appropriate management is-

a) Arthroscopic debridement and irrigation
b) Osteochondral grafting
c) Bipolar hip arthroplasty

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d) Total hip arthroplasty

Conclusion

? AVN is difficult to diagnose early- High degree of suspicion

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? Radiographs in early stages are normal- Trust your findings more!
? Best modality for early diagnosis ?MRI
? Salvage can be tried for Stage I,I
? Advanced stages require ? Total hip arthroplasty

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