FEMORAL HEAD AVASCULAR NECROSIS (AVN)Andrew Sill

EPIDEMIOLOGY10,000 to 20,000 patients in the US each year1

Underlying diagnosis in ~ 10% of all total hip replacements2

Mean age less than 40 years old

Increasing prevalence worldwide due to…

Greater use of adjuvant therapies (corticosteroids, chemotherapy, antiretrovirals)3

Increasing prevalence of associated diseases and risk factors4

1Mont 1995 | 2Mankin 1992 | 3Wong 2005 | 4Gutierrez 2006

ETIOLOGYImpaired circulation to the femoral head, causing progressive necrosis1

May be a result of traumatic or atraumatic factors

Atraumatic causes are high-dose corticosteroid use or alcohol abuse in > 80% of cases2

1Mont 2015 | 2Mont 1995

Genetic predisposition

Changes in blood supplyMetabolic factors

ETIOLOGYTRAUMATIC PATHOGENESIS

Fracture or dislocation may damage extraosseous blood vessels that supply the femoral head

Alteration in blood supply causes ischemia and bone necrosis1

Early anatomic reduction and internal fixation is associated with lower rates of AVN2

1Phemister 1949 | 2Swiontkowski 1994

ETIOLOGYGLUCOCORTICOID PATHOGENESIS

Prolonged treatment with high-dose glucocorticoids are at greatest risk

One prospective study found that the only distinguishing characteristic between patients with and without AVN was a Cushingoid appearance (86% versus 15%)1

Initial glucocorticoid dose is more important than overall glucocorticoid exposure2

1Zizic 1985 | 2Abeles 1978

ETIOLOGYGLUCOCORTICOID PATHOGENESIS

Glucocorticoids may cause…

Alterations in circulating lipids and resultant microemboli1

Increase in bone marrow fat cell size causing venous outflow blockage2

Changes in venous endothelial cells, leading to stasis and increased intraosseous pressure3

1Jones 1985 | 2Solomon 1981 | 3Nishimura 1997

ETIOLOGYALCOHOL-ASSOCIATED PATHOGENESIS

Only a small fraction of alcoholics develop osteonecrosis, however up to 31% of osteonecrosis cases are associated with alcohol use1

Fat emboli, adipocyte hypertrophy, venous stasis and increased cortisol levels have all been implicated1

1Hirohata 1988

DIAGNOSISPain in the groin is most common, followed by thigh or buttock pain1

Increased pain with weightbearing or movementParticularly internal rotation and abduction

2/3 experience pain at rest and 1/3 experience pain at nightOften times bilateral at diagnosisMay also be asymptomatic (although in 60% of these cases, eventual collapse and symptoms will occur)2

1Zizic 1986 | 2Mont 2010

IMAGING

If suspected, order AP and frog-leg lateral plain filmsPathognomonic crescent sign is evidence of early subchondral collapse

1Mont 2008

Early

Late

IMAGING

MRI has near 100% sensitivity1

T1-weighted imaging showed well-demarcated and non-homogenous medulla“Double-line sign” is concentric high and low signal at the periphery

MRI without contrast is the “gold standard” for diagnosis2

1Mont 2008 | 2Amanatullah 2011

TREATMENTNON-OPERATIVE

Bed rest, partial weightbearing with crutches, weightbearing as tolerated, analgesics

Only 20% of patients have any improvement with nonoperative treatment

1Mont 1996

TREATMENTOPERATIVE

Joint-preservingCore decompression with bone graft

Pressure is relieved by drilling a hole into the bone and living bone (vascularized fibular graft) is implanted and stimulated with an electrical device

Hip resurfacing (metal on metal resurfacing)Only the femoral head is removed, sparing the femoral neck

Joint replacementTotal hip replacement

Revision is necessary in less than 3% of patients1

1Johannson 2011

CONCLUSIONSEarly diagnosis may prevent collapse and the need for joint replacement

Asymptomatic patients with involvement of less than 15% of the femoral head should be treated non operatively, but closely watched

In young active patients, consider core decompression before THR

Once collapse has occurred or if there is acetabular involvement, THR is indicated

APPENDIXCLINICAL STAGING1

Stage 0 – All diagnostic studies normal and diagnosis by histology only

Stage 1 – Plain radiographs and CT normal, MRI positive, and biopsy positive, with extent of involvement A, B, or C (less than 15 percent, 15 to 30 percent, and greater than 30 percent, respectively)

Stage 2 – Radiographs positive but no collapse (no crescent sign), with extent of involvement A, B, or C

Stage 3 – Early flattening of dome and/or crescent sign on plain radiography or by CT or tomograms, with extent of involvement A, B, or C and further characterization by amount of depression (in millimeters) (image 3)

Stage 4 – Flattening of femoral head with joint space narrowing on plain radiography, as well as other signs of osteoarthritis

1ARCO Staging System for Osteonecrosis