A 68-year-old man from rural Maharashtra presents with a 3-month history of progressive left hip pain, worse on weight-bearing and internal rotation. He denies trauma. On examination, the left hip is held in flexion, adduction, and internal rotation. Passive external rotation and abduction are restricted and painful. X-ray pelvis shows a crescent sign with flattening of the femoral head. Which anatomical structure is primarily affected, and what is the underlying pathophysiology?

Explanation

## Clinical Diagnosis: Avascular Necrosis (AVN) of the Femoral Head ### Pathophysiology The **crescent sign** (subchondral lucency) and femoral head flattening are pathognomonic for avascular necrosis. The femoral head has a precarious blood supply, primarily dependent on the **medial femoral circumflex artery (MFCA)**, which enters via the posterior capsule. **Key Point:** The femoral head is an epiphysis with a retrograde blood supply — once the nutrient vessels are disrupted, the bone undergoes necrosis, collapse, and secondary osteoarthritis. ### Anatomical Basis of Pain & Posture The characteristic **flexion-adduction-internal rotation (FAIR) position** occurs because: - Flexion relieves capsular tension - Adduction and internal rotation reduce intra-articular pressure - This posture minimizes pain by reducing load on the necrotic segment ### Blood Supply of the Femoral Head | Artery | Entry Point | Percentage of Supply | |--------|-------------|----------------------| | Medial femoral circumflex artery | Posterior capsule | 70% | | Lateral femoral circumflex artery | Anterolateral capsule | 20% | | Ligamentum teres artery | Foveal region | 10% (lost after age 3–4) | **Clinical Pearl:** The MFCA is vulnerable during: - Femoral neck fractures (disrupts posterior capsular branches) - Hip dislocation (stretches the artery) - Prolonged corticosteroid use (fat necrosis in bone marrow) - Sickle cell disease (vaso-occlusive crisis) ### Why the Crescent Sign Appears The crescent sign represents a **subchondral fracture** (microfracture) at the interface between dead and living bone — a hallmark of stage II–III AVN on Ficat classification. **High-Yield:** Early recognition (stage I on MRI) before radiographic changes allows joint-preserving surgery (core decompression); late diagnosis (stage III–IV) requires arthroplasty.