Avascular necrosis

Shoulder AVN




Second most common site of AVN

- much less common than hip OA


Usually presents late as shoulder non weight bearing


Typically not isolated - in multiple joints




Most common non traumatic cause is corticosteroids


Similar causes as hip (AS IT GRIPS 3C)


Alcohol / Steroids / Idiopathic / Trauma


Gout, Gauchers

Rheumatoid / radiotherapy

Infection / increased lipids / inflammatory arteritis

Pancreatitis / pregnancy

SLE / sickle cell / smoking


Chronic renal failure / chemotherapy / Caisson's disease


Blood Supply


Blood supply humeral head


1.  Anterior Circumflex Humeral Artery (36%)

- primary blood supply

- becomes arcuate artery

- runs lateral aspect bicipital groove


2.  Posterior Circumflex Humeral Artery (64%)

- collateral circulation

- supplies head when GT / LT fracture


3.  Via rotator cuff


Natural History



- difficult to predict

- somewhat related to aetiology

- sickle cell disease tend not to progress to arthroplasty

- steroid induced far more likely


Less severe than femoral

- non weight bearing

- less conforming joint

- scapulothoracic motion




Superior head collapse at 90° mark 

- area of peak contact stress in abduction

- glenoid rarely affected

- soft tissue and subscapularis rarely contracted


Classification / Cruess modification of Ficat-Arlet 


Stage I

- pre-xray change

- only seen with MRI


Stage II

- sclerotic changes in superior central head

- sphericity maintained


Shoulder AVN


Humeral AVN Stage 2Humeral AVN Stage 2 MRI


Stage III

- "crescent" sign - subchondral fracture

- mild flattening articular surface


Shoulder AVN Stage 3


Stage IV

- significant humeral collapse with loss integrity joint surface

- loose bodies


Shoulder AVN Stage 4Shoulder AVN Stage 4


Stage V

- degeneration extends to involve glenoid


AVN Shoulder Xray




Pain is major problem

- pain before significant loss ROM

- difficulty sleeping




Shoulder AVN MRIShoulder AVN MRI Sagittal


Shoulder AVN 1Shoulder AVN 2Shoulder AVN 3


Sensitivity and specificity approach 100%



- areas low signal intensity on T1 representing oedema

- areas of high signal intensity thought to represent blood flow




"Double line sign"

- highly specific for AVN

- inner bright line representing granulation tissue

- outer dark line representing sclerotic bone




Non Operative


Remove insult


Corticosteroids, alcohol


Maintain current shoulder ROM / Halt Progression


A.  Physiotherapy


B.  Limit overhead activities

- joint reaction force greatest > 90o


C.  Bisphosphonates


Agarwala et al. J Orthop Surg Res 2019

- bisphosphonates for non femoral head AVN

- 20 patients, 5 with shoulder AVN

- combined oral and IV treatment

- 50% reduction in analgesia needs after 6 weeks

- MRI showed complete resolution in 17 / 20 (94%) at 1 year




Core Decompression




Decrease intra-osseous pressure & increase blood flow




Stage 1 / 2 - pre-collapse




Arthroscopy Technique Article


Arthroscopy Technique Article decompression + fibular graft




La Porte et al. CORR 1998

- core decompression in 63 shoulders all stages

- looked at improvement in UCLA scores

- 94% / 88% / 70%/ 14% success for stage I / II / III / IV


Alkhateeb et al. JSES Int 2021

- systematic review of core decompression in sickle cell

- one paper showed evidence of improved pain scores post procedure

- one paper demonstrated all cases went on to collapse

- may not prevent or delay progression of disease


Joint replacement




McLaughlin et al. JSES 2022

- 52 aTSA and 67 rTSA for shoulder AVN

- matched to controls in database

- similar improvements in ROM and PROM's to non AVN patients



Australian Joint Registry Shoulder Replacement for AVN 2021

- revision rate aTSR 11.4% at 5 years (compared with 7.2% for OA)

- revision rate rTSR 6.5% at 7 years (compared with 4.5% for OA)

- revision rate hemiarthroplasty 9.9% at 7 years (compared with 9.7% for OA)