Medical research has identified a number of risk factors associated with AVN.
Interestingly, not everyone who has a risk factor gets AVN and not everyone with AVN has an easily identifiable risk factor, meaning the cause is unknown or idiopathic.
People who have a fracture of the proximal humerus (ball part of the shoulder) are at risk for AVN.
With a fracture of the proximal humerus the blood supply can be disrupted and loss of the normal blood flow to the bone may cause it to eventually die and become necrotic.
The more extensive the fracture the more likely is this development of AVN.
Another common cause of AVN is the effect of steroids given for other conditions.
The steroids are believed to damage the health of the cells which make bone in the humeral head and when they die the sequence of AVN occurs.
Other causes of AVN can be radiation or chemotherapy treatment in the case of cancer.
Other rare causes include sickle cell disease, Gaucher’s disease, Caisson’s disease (also known as diver’s disease or the bends:
This is due to sudden change in water pressure in deep sea diving where nitrogen bubbles form in the blood and damage the blood supply to the humeral head).
AVN Avascular Necrosis aka Osteonecrosis ON
usually presents as pain and may also be associated with noise and crunching sensation (crepitation) in the shoulder with movement.
Movement may be limited due to pain. About 50% of individuals who develop atraumatic (without a fracture) AVN in the shoulder will also have involvement of other joints.
In its early stages AVN may not be apparent on a plain x-ray but it can be seen on an MRI (described above).
As it progresses with collapse of the humeral head and eventual arthritis it is clearly seen on an x-ray (see figures below).
Stage 1 is a shoulder with a normal X-ray but signal changes on MRI showing subchondral edema.
Stage 2 is a shoulder with more whitened bone called sclerosis, near the joint surface (subchondral).
Stage 3 demonstrates a crescent sign or collapse or fracture of the subchondral bone.
Stage 4 demonstrates flattening of the humeral head from advanced collapse.
Stage 5 or end-stage AVN demonstrates advanced collapse of the humerus with degenerative changes of the glenoid (arthritis).
A study that looked at 200 shoulders with AVN found that about 40% of shoulders with early AVN progressed in 3 years to advanced AVN.
Patients that presented with later-stage AVN, 55-80% of patients (depending on how late the stage) progressed to advanced AVN6.
Drilling of the humeral head, called core decompression, is a treatment which may be helpful in the early stages of AVN before the humeral head collapses.
It is believed that pressure in the bone goes up when the blood supply is lost and that pain can be relieved by decompressing the bone by drilling into it.
This is called core decompression. This may also stimulate better blood supply and faster healing in the humeral head.
• A condition caused by interruption of blood supply to humeral head
▪ decreased blood supply to humeral head leading to death of cells in bony matrix.
▪ bone is resorbed and remodeled, causing subchondral bone collapse and may lead to joint incongruity and arthritic changes
◦ etiology similar to hip
▪ Remember ASEPTIC mneumonic
▪ Alcohol, AIDS
▪ Steroids (most common), Sickle, SLE
▪ Erlenmeyer flask (Gaucher’s)
▪ Idiopathic/ Infection
▪ Caisson’s (the bends)
▪ may be atraumatic
▪ four-part fracture-dislocations approach 100% AVN
▪ displaced four-part fractures ~45% AVN
▪ valgus impacted four-part ~11% AVN
▪ three-part ~14% AVN
◦ related to stage of disease
• Blood supply
◦ Humeral head
▪ ascending branch of anterior humeral circumflex artery and arcuate artery
▪ provides blood supply to humeral head
▪ vessel runs parallel to lateral aspect of tendon of long head of biceps in the bicipital groove
▪ beware not to injure when plating proximal humerus fractures
▪ arcuate artery is the interosseous continuation of ascending branch of anterior humeral circumflex artery and penetrates the bone of the humeral head
▪ provides 35% of blood supply to humeral head
▪ posterior humeral circumflex artery
▪ most current literature supports this as providing the main blood supply to humeral head
▪ provides 65% of blood supply
Cruess Classification (stages)
Normal x-ray. Changes on MRI. Core decompression.
Sclerosis (wedged, mottled), osteopenia. Core decompression.
Crescent sign indicating a subchondral fracture. Resurfacing or hemiarthroplasty.
Flattening and collapse. Resurfacing or hemiarthroplasty.
Degenerative changes extend to glenoid. TSA.
◦ insidious onset of shoulder pain
▪ often without a clear inciting event
◦ pain, loss of motion, crepitus, and weakness
• Physical exam
◦ limited range of motion
◦ weakness of the rotator cuff and deltoid muscles
◦ recommended views
▪ five views of shoulder (shown best in neutral rotation AP)
▪ no findings on radiograph at onset of disease process
▪ osteolytic lesion develops on radiograph demonstrating resorption of subchondral necrosis
▪ most common initial site is superior middle portion of humeral head
▪ crescent sign demonstrates subchondral collapse
▪ may progress to depression of articular surface and consequent arthritic changes.
◦ preferred imaging modality
▪ ~100% sensitivity in detection
◦ will demonstrate edema at the site of subchondral sclerosis
◦ pain medications, activity modification, physical therapy
▪ first line of treatment
▪ physical therapy
▪ restrict overhead activity and manual labor
◦ core decompression + arthroscopy (confirm integrity of cartilage)
▪ early disease (precollapse Cruess Stage I and II)
◦ humeral head resurfacing
▪ Stage III disease with focal chondral defects, and sufficient remaining epiphyseal bone stock for fixation.
▪ moderate disease (Cruess Stage III and IV)
◦ total shoulder arthroplasty
▪ advance stage (Cruess V)