Avascular Necrosis of the Femoral Head

Avascular necrosis (AVN), also called osteonecrosis or aseptic/ischaemic necrosis, is the death of bone trabeculae and marrow due to interruption of the blood supply. The femoral head is the classic and most exam-relevant site because of its precarious end-arterial circulation. This is a high-yield orthopaedics topic where NEET PG repeatedly tests risk factors, the earliest MRI sign, staging systems, and the stage-based management algorithm.

Definition and Classification

Osteonecrosis is ischaemic death of the cellular elements of bone (osteocytes, marrow fat cells, haematopoietic cells) with preservation of the inorganic mineral matrix. Because the dead bone retains its mineral, plain radiographs remain normal for weeks to months — a critical exam fact that explains why MRI is the investigation of choice early.

Broad classification by cause:

Type	Mechanism	Classic examples
Traumatic	Mechanical disruption of vessels	Femoral neck fracture (Garden III/IV), hip dislocation, slipped capital femoral epiphysis
Non-traumatic (atraumatic)	Intravascular occlusion / extravascular compression	Steroids, alcohol, sickle cell, Gaucher's, caisson disease, SLE
Idiopathic	No identifiable cause	Diagnosis of exclusion

High-yield: AVN of the femoral head is the single most common site of osteonecrosis in the body. The other classic sites are the scaphoid (proximal pole), talus (body), and humeral head.

Vascular Anatomy — Why the Femoral Head is Vulnerable

The femoral head's blood supply matters enormously for exams.

• Medial femoral circumflex artery (MFCA) → gives rise to the lateral epiphyseal / retinacular vessels — supplies the major weight-bearing superolateral part of the head. This is the dominant supply in adults.
• Lateral femoral circumflex artery — supplies a smaller anteroinferior portion.
• Artery of ligamentum teres (foveal artery, branch of obturator) — significant only in children; negligible in adults.

A subcapital/transcervical femoral neck fracture tears the retinacular vessels → ischaemia of the head. This is why displaced intracapsular neck fractures in the elderly are treated with arthroplasty rather than fixation.

High-yield: The MFCA (specifically its deep branch / lateral epiphyseal vessels) is the principal blood supply to the adult femoral head. Damage to it underlies post-traumatic AVN.

Etiology and Risk Factors

The two commonest non-traumatic causes worldwide are corticosteroids and alcohol, together accounting for the majority of atraumatic cases.

Mnemonic — "ASEPTIC" / the classic list:

• A — Alcohol, AIDS (HAART, especially protease inhibitors)
• S — Steroids (corticosteroids), SLE, Sickle cell, SCFE
• E — Embolic (fat, nitrogen — caisson disease)
• P — Pancreatitis, Pregnancy
• T — Trauma (neck fracture, dislocation)
• I — Idiopathic, Infection, Irradiation
• C — Caisson disease, Coagulopathy, Collagen vascular disease, Chemotherapy, Gaucher's (lipid storage)

A practical exam-friendly grouping of pathophysiology:

Mechanism	Conditions
Intravascular occlusion by emboli	Caisson disease (nitrogen bubbles), fat emboli, sickle cell (sickled RBCs)
Intraosseous fat accumulation → ↑ marrow pressure	Steroids, alcohol, Cushing's
Marrow infiltration / cellular crowding	Gaucher's disease (Gaucher cells), leukaemia, lymphoma
Vessel wall pathology / vasculitis	SLE, antiphospholipid syndrome, radiation
Direct mechanical vessel damage	Femoral neck fracture, dislocation, SCFE

High-yield: Steroids and alcohol are the most common non-traumatic causes. The mechanism for both is increased intramedullary fat and raised intraosseous pressure → venous outflow obstruction → ischaemia.

Pathophysiology — The Final Common Pathway

Regardless of cause, the sequence is:

Vascular insult → osteocyte and marrow death (ischaemia) → attempted repair (creeping substitution: revascularisation, osteoclastic resorption of dead trabeculae, new bone apposition) → mechanical weakening of subchondral bone → subchondral fracture (crescent sign) → articular collapse → secondary osteoarthritis.

The critical conceptual point: the subchondral fracture occurs when resorption (removal of dead bone) outpaces new bone formation, leaving the subchondral plate unsupported. Once the head collapses and loses sphericity, the joint is mechanically doomed and progresses to arthritis — this is the watershed between joint-preserving and joint-replacing surgery.

Clinical Features

• Groin pain is the most common and characteristic symptom (may radiate to thigh, buttock, or knee). Pain is worse on weight-bearing.
• Often bilateral — up to 50–70% of non-traumatic cases (always image the contralateral hip, especially in steroid/SLE/sickle patients).
• Early disease: pain with full range of motion preserved.
• Progressive disease: restriction and pain on internal rotation and abduction first; later a fixed flexion-adduction deformity, limp, and limb shortening after collapse.
• Patients are typically young to middle-aged (30–50 years) — distinguishing it from primary osteoarthritis.

High-yield: Persistent groin pain in a young patient on steroids or with a heavy alcohol history, with a normal X-ray, is AVN until proven otherwise — order an MRI.

Diagnosis and Investigation of Choice

Stepwise diagnostic approach:

1. Plain radiograph (AP + frog-leg lateral) — first investigation ordered but normal in early disease. Frog-leg lateral best shows the crescent sign.
2. MRI — investigation of choice and the most sensitive/specific test, detects disease before X-ray changes.
3. CT — better for assessing subchondral fracture and quantifying collapse; not for early diagnosis.
4. Bone scan (Tc-99m) — historically used; shows "cold spot within hot spot" (doughnut sign). Largely replaced by MRI.

Key imaging signs (very frequently tested):

Sign	Modality	Meaning
Double-line sign	MRI (T2)	Earliest specific sign — inner hyperintense granulation/repair zone, outer hypointense sclerotic rim. Pathognomonic of AVN
Crescent sign	X-ray / CT	Subchondral radiolucent fracture line beneath articular cortex; indicates impending collapse (pre-collapse → collapse transition)
Geographic / serpentine demarcation	MRI T1	Single low-signal line outlining the necrotic segment
Sclerosis + lucency, then flattening	X-ray (late)	Established collapse and secondary OA
"Hanging rope" / "asterisk sign"	CT	Distorted bony trabeculae in head

High-yield: The double-line sign on T2-weighted MRI is the earliest and most characteristic finding, while the crescent sign on X-ray marks the subchondral fracture / impending collapse. These two are the most repeated single-best-answer facts.

Staging Systems

Two systems dominate the exam: the older Ficat–Arlet (radiograph-based) and the more comprehensive ARCO (Association Research Circulation Osseous).

Ficat and Arlet Staging

Stage	X-ray	MRI / clinical
0	Normal	Normal, asymptomatic ("silent hip"), diagnosed on contralateral imaging
I	Normal	MRI/bone scan abnormal; pain present
II	Sclerosis and/or cysts, head still spherical, no subchondral fracture	Pre-collapse
III	Crescent sign / subchondral collapse, loss of sphericity	Collapse, joint space preserved
IV	Flattening + joint space narrowing, acetabular changes (secondary OA)	End-stage

The single most important dividing line is between Stage II and III = the point of femoral head collapse. Joint-preserving procedures work only before collapse (Stage 0–II).

ARCO Classification

ARCO refines staging by adding extent/size of the necrotic lesion and depth of depression, which guides prognosis:

• Stage 0 — all tests normal (suspected only).
• Stage I — X-ray normal; MRI/scan positive.
• Stage II — X-ray abnormal (sclerosis/cysts), no collapse.
• Stage III — crescent sign / subchondral fracture, head not yet flattened (IIIA early <2 mm depression, IIIB late ≥2 mm).
• Stage IV — flattening, joint space narrowing, secondary osteoarthritis.

ARCO also grades lesion size (A <15%, B 15–30%, C >30% of head involvement) and location (medial/central/lateral). Lateral, large lesions have the worst prognosis for collapse.

High-yield: Both Ficat–Arlet and ARCO pivot on collapse. Pre-collapse (≤ Ficat II / ARCO II) = head-preserving surgery; post-collapse (≥ Ficat III) = arthroplasty in most.

Management and Drug/Surgery of Choice

Management is stage-dependent, age-dependent, and lesion-size dependent. The exam expects you to map stage to procedure.

Conservative / Pharmacological

• Protected weight-bearing alone is largely ineffective at preventing progression — do not pick "rest only" for a symptomatic pre-collapse lesion.
• Bisphosphonates (alendronate) — may delay collapse in early disease by reducing osteoclastic resorption (evidence modest, exam-favoured adjunct).
• Statins (in steroid-induced), anticoagulants (in thrombophilia), and vasodilators (iloprost) are investigational/adjunctive.
• Remove the offending agent — stop/taper steroids, abstain from alcohol.

Joint-Preserving Surgery (Pre-collapse — Ficat 0/I/II, small lesions)

• Core decompression — the classic answer for early, pre-collapse disease. Drilling a channel into the necrotic segment reduces intraosseous pressure and promotes neovascularisation. Best results in small, medial lesions before collapse. Often combined with bone grafting or marrow/BMAC injection.
• Vascularised fibular graft (free fibular graft) — provides structural support and a new blood supply; used in larger pre-collapse or early post-collapse lesions in young patients. Mechanically supports the subchondral bone.
• Non-vascularised bone grafting (e.g. via a trapdoor or lightbulb technique).
• Osteotomy (e.g. transtrochanteric rotational/Sugioka) — rotates the necrotic segment out of the weight-bearing zone; used selectively, more in younger patients.

Joint-Replacing Surgery (Post-collapse — Ficat III/IV)

• Total hip arthroplasty (THA / THR) is the definitive treatment for advanced disease (collapse + arthritis) and the procedure of choice in older patients or any patient with Ficat III–IV. Outcomes in modern THA are excellent.
• Hemiarthroplasty/resurfacing — limited roles; resurfacing considered in select young active males.

Management flow (memorise this line):

Ficat 0–I (MRI+, X-ray normal) → core decompression ± bone graft / bisphosphonate → Ficat II (sclerosis, no collapse) → core decompression ± vascularised fibular graft → Ficat III (crescent/collapse) → vascularised graft in young OR THA → Ficat IV (secondary OA) → Total Hip Arthroplasty.

High-yield: Core decompression = pre-collapse (Ficat I–II). Total hip arthroplasty = post-collapse advanced disease (Ficat III–IV). Vascularised fibular graft bridges the middle in young patients. This single mapping answers most management MCQs.

Special Situations

• Sickle cell disease — bilateral AVN common; manage sickle crises, hydration; THA has higher complication/infection rates.
• SLE on steroids — screen both hips with MRI; very high incidence.
• Caisson disease (decompression sickness) — nitrogen emboli; also causes dysbaric osteonecrosis of shaft.
• Gaucher's disease — Gaucher cells pack the marrow; AVN plus Erlenmeyer-flask deformity of femur; enzyme replacement therapy.
• Perthes disease — paediatric idiopathic AVN of the femoral head (separate entity, age 4–8, self-limiting with remodelling potential).

Complications

• Femoral head collapse and loss of sphericity (the pivotal complication).
• Secondary osteoarthritis of the hip.
• Limb shortening, fixed flexion-adduction deformity, gait abnormality.
• Chronic pain and disability in a young, working-age population.
• Bilateral disease → bilateral arthroplasty.
• Post-THA complications: dislocation, infection (higher in sickle/SLE), aseptic loosening, periprosthetic fracture.

Key Differentials

Condition	Distinguishing feature
Transient osteoporosis of the hip	Self-limiting; MRI shows diffuse marrow oedema without the double-line/necrotic segment; resolves spontaneously
Primary osteoarthritis hip	Older patient; uniform joint space loss, osteophytes; no discrete necrotic segment
Bone marrow oedema syndrome	Reversible oedema, no demarcated necrotic zone
Subchondral insufficiency fracture (elderly osteoporotic)	Low signal fracture line, marrow oedema, often older women
Septic arthritis / TB hip	Fever, raised inflammatory markers, joint effusion, joint space destruction
Inflammatory arthritis	Bilateral, symmetrical, systemic features

High-yield: Transient osteoporosis of the hip is the classic distractor — it shows marrow oedema on MRI but lacks the demarcated necrotic segment / double-line sign and resolves on its own; AVN does not self-resolve and progresses to collapse.

Recently Asked / Exam Angle

• Earliest/most specific MRI finding in AVN femoral head → Double-line sign (T2). Repeatedly asked.
• Crescent sign indicates → subchondral fracture / impending collapse (Ficat III).
• Most common non-traumatic causes → steroids and alcohol.
• Investigation of choice for early AVN → MRI (not X-ray, not bone scan).
• Treatment of pre-collapse AVN → core decompression; advanced/collapsed → total hip arthroplasty.
• Most common blood supply to adult femoral head → medial femoral circumflex artery (lateral epiphyseal vessels).
• Garden III/IV femoral neck fracture → high AVN risk → arthroplasty in elderly.
• Gaucher's disease, caisson disease, sickle cell are favourite "identify the cause" stems.
• Ficat–Arlet vs ARCO — stage that divides pre- and post-collapse (Stage II vs III).
• Image-based MCQs showing a T1 serpentine line or frog-leg lateral crescent are increasingly common.

Rapid Revision

1. AVN femoral head = ischaemic death of bone; femoral head is the commonest site.
2. Dominant adult supply = medial femoral circumflex artery (lateral epiphyseal/retinacular vessels).
3. Commonest non-traumatic causes = steroids and alcohol; both raise intraosseous fat and pressure.
4. Other causes: sickle cell, Gaucher's, caisson disease, SLE, radiation, trauma, SCFE.
5. MRI is the investigation of choice; X-ray is normal early.
6. Double-line sign (T2 MRI) = earliest, most specific finding.
7. Crescent sign (X-ray) = subchondral fracture = impending collapse.
8. Ficat–Arlet and ARCO staging both hinge on collapse (Stage II→III).
9. Pre-collapse (Ficat I–II) → core decompression ± bone graft / bisphosphonate.
10. Young patient, larger lesion → vascularised fibular graft; Sugioka rotational osteotomy in select cases.
11. Advanced/collapsed (Ficat III–IV) → Total Hip Arthroplasty = definitive.
12. Up to 50–70% non-traumatic cases are bilateral — always image both hips; key differential is transient osteoporosis of the hip (no necrotic segment, self-resolving).