Hip
Avascular Necrosis of the Femoral Head
대퇴골두 무혈성 괴사
Bone necrosis from disrupted blood supply to the femoral head — steroids and alcohol are major causes
- How common
- Uncommon
- Typical age
- Ages 30–60
What is it?
Disruption of femoral head blood supply (medial circumflex femoral artery) → osteocyte necrosis → subchondral fracture → femoral head collapse
Commonly affected: Femoral head (especially superolateral segment), medial circumflex femoral artery
How it develops
- Vascular DisruptionMedial circumflex femoral artery damaged by steroids, alcohol, trauma, or thrombosis
- Osteocyte NecrosisIschemia-induced necrosis of osteocytes and marrow cells, fat cell hypertrophy
- Structural WeakeningStructural failure of necrotic bone, inability to bear load
- Subchondral FractureCrescent sign — subchondral fracture initiates articular surface collapse
- Femoral Head CollapseProgressive femoral head collapse and secondary osteoarthritis
Symptoms
- Sudden WorseningSudden pain intensification with subchondral fracture → urgent sign
- Groin/Thigh PainPain in groin, anterior thigh, sometimes radiating to knee
- Rest PainResting and night pain in advanced stages
- ROM RestrictionInternal rotation and flexion restricted — similar to hip OA
How it is examined
- IR RestrictionInternal rotation restriction and pain — same as hip OA, requires differentiation
- FABER/FADIRBoth may be positive (bilateral hip involvement 30-80%)
- Risk Factor AssessmentAssess steroid use, alcohol consumption, trauma history, sickle cell anemia
Imaging
Early X-ray may be normal (15-40% false negative). Advanced stages show characteristic findings
- Early: normal or subtle sclerosis
- Crescent sign: subchondral radiolucent line (fracture sign)
- Femoral head flattening and collapse
- Secondary OA findings
Gold standard for early AVN diagnosis — can detect vascular abnormality within 3-5 days
- Double line sign: T2 hyperintense inner border, hypointense outer border (pathognomonic)
- Bone marrow edema (T2 hyperintense)
- Subchondral fracture line
- Ficat staging classification
Non-surgical care
- Risk Factor EliminationReduce/stop steroids (within limits of underlying disease), alcohol cessation
- Non-weight BearingCrutch use — to prevent collapse, but limited efficacy
- MedicationsBisphosphonates, statins — under investigation for slowing necrosis progression
Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.
When surgery is considered
Ficat stage II+: joint preservation surgery before collapse; THA after collapse
Procedures that may be discussed
- Core decompression — Ficat I-II, drilling to improve blood flow
- Vascularized fibular graft — restore blood supply
- Total Hip Arthroplasty — best option after collapse
Outlook
Early detection (Ficat I-II) allows effective conservative measures. Progressive collapse eventually requires THA (40-80%)