AVN Of Hip

Avascular necrosis of the hip is the death of femoral head bone tissue due to disruption of its blood supply, leading to structural collapse and secondary degenerative arthritis.

Anatomy and Blood Supply of the Femoral Head

Understanding the blood supply is absolutely fundamental to understanding why AVN happens where it does.

Muscle Group	Key Muscles	Action	Nerve
Abductors	Gluteus medius & minimus	Hip abduction, pelvis stabilisation	Superior gluteal nerve (L4-S1)
Deep external rotators	Piriformis, obturator internus/externus, gemelli, quadratus femoris	External rotation	Various (sciatic, obturator)
Flexors	Iliopsoas	Hip flexion	Femoral nerve / direct branches (L1-3)
Adductors	Adductor magnus/longus/brevis, gracilis	Hip adduction	Obturator nerve (L2-4)
Extensors	Hamstrings, gluteus maximus	Hip extension	Sciatic nerve / inferior gluteal nerve

Clinical Pearl

The gluteus medius and minimus are the key abductors. In advanced AVN with femoral head collapse and secondary OA, pain-related inhibition of these muscles → Trendelenburg gait (pelvis drops on the contralateral side during single-leg stance). This is important for your clinical exam.

Aetiology and Pathophysiology

Trauma is the most common cause overall.

Traumatic Cause	AVN Risk	Mechanism
*Femoral neck fracture*	*15–50%* ^[1]	Displaced fracture disrupts the retinacular arteries (especially the MCFA's superior retinacular branches). Intracapsular haematoma further compresses vessels by tamponade. Garden III/IV have the highest risk.
*Hip dislocation*	*10–25%* ^[1]	Posterior dislocation (most common type) stretches/tears the MCFA as the femoral head is forced out posteriorly. Delay in reduction (> 6 hours) dramatically increases AVN risk.
Femoral head fracture	Variable	Direct vascular disruption at fracture site

Why does displacement matter? In an intracapsular femoral neck fracture, the retinacular arteries run along the surface of the femoral neck. When the fracture displaces, these vessels are torn or kinked. Blood cannot reach the femoral head. The intracapsular haematoma creates a tamponade effect (like cardiac tamponade but in a joint capsule), further compromising any residual flow.

The mnemonic "ASEPTIC" can help remember the causes:

Letter	Cause	Details
A	*Alcohol abuse*	*Amount similar to cirrhosis* ^[2] (~400 mL ethanol/week). Mechanism: fat cell hypertrophy in marrow → increased intraosseous pressure → vascular compression; also direct toxic effect on osteocytes; fat emboli to subchondral vessels.
S	*Steroids*	*> 20 mg/day prednisone increases the risk* ^[1]. Most common non-traumatic cause in many series. Mechanism: corticosteroids cause adipocyte hypertrophy in marrow → increased intraosseous pressure → venous outflow obstruction; fat embolism to femoral head vessels; direct osteocyte apoptosis; also promotes osteoporosis making subchondral bone weaker.
E	Endocrine/Metabolic	Gaucher's disease (glucocerebroside accumulation in marrow), hyperlipidaemia, diabetes
P	Pancreatitis / Pregnancy	Fat necrosis → fat emboli; increased coagulability in pregnancy
T	Thrombophilia / Coagulopathy	*Sickle cell anaemia* ^[1] (microvascular occlusion by sickled RBCs in marrow sinusoids), other haemoglobinopathies, antiphospholipid syndrome, Factor V Leiden
I	*Inflammatory / Infection*	*SLE* ^[2] (disease itself + steroid treatment = double hit), *osteomyelitis, septic arthritis* ^[2] (elevated intra-articular pressure compresses vessels; bacterial toxins damage endothelium)
C	*Caisson disease*	*Decompression sickness / "the bends"* ^[1]^[2]: rapid decompression → nitrogen gas comes out of solution in blood → gas bubbles occlude end-arteries in the femoral head. Seen in deep-sea divers and tunnel workers.

Here is the cascade from initial insult to end-stage disease:

Detailed explanation of each step:

Vascular insult — Whether from fracture, steroid-induced marrow fat expansion, alcohol, or sickle cell occlusion, the end result is reduced arterial inflow or venous outflow obstruction in the femoral head.
Ischaemia and bone cell death — Osteocytes die within 6–12 hours of complete ischaemia. Marrow fat cells and haematopoietic cells also die. Importantly, the articular cartilage survives because it is avascular and gets nutrition from synovial fluid — this is why the joint surface initially looks normal.
Attempted repair ("creeping substitution") — The body recognises dead bone and tries to revascularise from the surrounding viable bone at the periphery. New blood vessels grow into the necrotic zone, bringing osteoclasts and osteoblasts.
The fatal flaw — Osteoclasts are more efficient than osteoblasts. They resorb dead trabeculae faster than new bone can be laid down. This creates a zone of structural weakness just beneath the subchondral plate.
Subchondral fracture — Continued weight-bearing on the weakened subchondral bone causes a crescentic fracture just below the articular surface (seen as the crescent sign on X-ray ^[2]). At this point the patient typically develops significant pain.
Femoral head collapse — The subchondral plate and overlying cartilage collapse inward. The femoral head loses its spherical shape.
Secondary OA — An incongruent, non-spherical femoral head articulating with the acetabulum → abnormal loading → progressive cartilage wear → secondary osteoarthritis with joint space narrowing, osteophytes, etc.

Why Does Steroid-Induced AVN Happen?

Corticosteroids cause adipocyte hypertrophy (fat cells in the bone marrow enlarge) and adipocyte hyperplasia (more fat cells). Since bone marrow is enclosed in a rigid bony shell, this fat expansion raises intraosseous pressure, compressing the thin-walled sinusoidal veins → venous outflow obstruction → arterial inflow reduced → ischaemia. Additionally, steroids promote fat emboli that lodge in small vessels, cause direct osteocyte apoptosis via glucocorticoid receptor activation, and impair endothelial nitric oxide production (reducing vasodilation). It's a multi-hit mechanism.

Classification

The Ficat classification combines plain XR, MRI, bone scan, and clinical features to guide treatment and prognosis ^[2].

Stage	Radiographic Findings	Clinical Features	Pathology
0	Normal XR, normal MRI	Asymptomatic (contralateral hip found on screening)	Histological necrosis only
I	Normal XR or minor *osteopenia* ^[2]	Mild pain	Early necrosis, no structural change
II	*Sclerosis* (marrow infarct with calcification) ^[2], cystic changes, but femoral head shape preserved	Moderate pain, reduced ROM	Mixed sclerosis and lysis from repair; head still spherical
III	*Crescent sign* (subchondral lucency indicating subchondral collapse) ^[2], femoral head flattening	Significant pain, restricted motion	Subchondral fracture with early collapse
IV	Femoral head collapse + secondary OA changes (joint space narrowing, acetabular changes, osteophytes)	Severe pain, marked stiffness	End-stage: both femoral head and acetabulum involved

The internationally accepted modern classification:

Stage	Imaging	Key Feature
0	All imaging normal	Biopsy-proven necrosis
I	XR normal; MRI or bone scan positive	MRI shows marrow oedema / necrosis; *double line sign on T2W MRI*
II	XR abnormal (sclerosis, cysts) but head shape preserved	No subchondral fracture
III	Crescent sign or femoral head flattening on XR	Subchondral fracture ± early collapse
IV	Secondary OA with acetabular involvement	End-stage disease

Exam Tip

Students often confuse the Ficat and ARCO stages. The key conceptual division is:

Pre-collapse (Ficat I–II / ARCO I–II): Femoral head is still spherical → joint-preserving treatment may work
Post-collapse (Ficat III–IV / ARCO III–IV): Femoral head has lost its shape → arthroplasty is often needed

This pre-collapse vs post-collapse distinction drives ALL treatment decisions.

Clinical Features

Symptom	Pathophysiological Basis
*Insidious onset of hip/groin pain* ^[2]	Early stages: bone marrow oedema and increased intraosseous pressure stimulate nociceptors in the periosteum and subchondral bone. The onset is gradual because necrosis itself is painless — pain only appears when the repair process begins or when structural failure starts.
Pain worsened by weight-bearing and activity	Mechanical loading on weakened subchondral bone causes micro-fractures and stress on the compromised trabeculae, directly stimulating pain fibres.
Pain at rest in advanced disease	Once subchondral fracture occurs (Ficat III), there is ongoing inflammatory response and mechanical irritation even without loading. In Ficat IV with secondary OA, synovitis and capsular inflammation contribute to rest pain.
Pain referred to the knee	The hip and knee share innervation via the femoral and obturator nerves (Hilton's law: nerves supplying a joint also supply the muscles moving that joint and the skin over them). AVN hip pain can be perceived as knee pain via convergence of sensory fibres at the spinal cord level (L2-4). *This is a classic examination trap!*
Pain radiating to the thigh or buttock	Sciatic nerve irritation from capsular distension or altered gait biomechanics; obturator nerve referral pattern to the medial thigh.
Morning stiffness (< 30 min)	In advanced AVN with secondary OA: nocturnal accumulation of inflammatory mediators in the joint; gel phenomenon of synovial fluid. Improves quickly with movement (unlike inflammatory arthritis where stiffness lasts > 60 min).
Progressive loss of function	As the femoral head collapses and secondary OA develops, the joint becomes mechanically incongruent → painful range of motion → patient limits activity → deconditioning cycle.
Limp / antalgic gait	Pain causes the patient to shorten the stance phase on the affected side to reduce time spent weight-bearing on the painful hip.

Clinical Pearl

AVN can be completely asymptomatic in early stages (Ficat 0/I). It may be discovered incidentally on MRI done for other reasons, or when screening the contralateral hip after unilateral AVN is diagnosed. Always image both hips.

Sign	Pathophysiological Basis
*Limited ROM, especially abduction and internal rotation* ^[2]	Internal rotation is the most sensitive early finding because: (1) the superolateral femoral head is the most common site of necrosis (this is the weight-bearing dome, which is the most ischaemically vulnerable zone), and internal rotation compresses this area against the acetabulum → pain → reflex muscle guarding; (2) the hip capsule's anterior iliofemoral ligament (Y-ligament of Bigelow) is the strongest and tightest during internal rotation, maximising joint congruence and pressure on the diseased area. Abduction is limited because it also loads the superolateral head.
Pain on passive movement	Capsular irritation from synovitis and subchondral pathology; inflamed synovium and raised intraosseous pressure stimulate free nerve endings.
Antalgic gait	Shortened stance phase on the affected side to minimise time under load. The patient "hurries off" the painful leg.
Trendelenburg gait (late)	In advanced disease with femoral head collapse, the effective lever arm of the abductors (gluteus medius/minimus) is shortened (because the femoral head has migrated superiorly or collapsed), reducing their mechanical advantage. Pain also causes reflex inhibition of these muscles. During single-leg stance on the affected side, the pelvis drops on the contralateral side.
Trendelenburg sign positive	Same mechanism as Trendelenburg gait — test the patient standing on one leg: if the pelvis drops on the unsupported side, the abductors on the stance side are insufficient.
Fixed flexion deformity (late stage)	In end-stage disease with secondary OA, the hip capsule contracts in the position of comfort (slight flexion) due to chronic inflammation → fibrosis → fixed flexion. Detected by Thomas' test: flex the contralateral hip to flatten the lumbar lordosis; the affected hip rises off the table if a fixed flexion deformity is present.
Apparent/true leg length discrepancy	If the femoral head collapses, the affected limb shortens (true shortening). Alternatively, a fixed adduction deformity creates apparent shortening.
Externally rotated limb at rest	In severe cases with secondary OA or capsular contracture, the leg assumes an externally rotated position (similar to #NOF) because the external rotators are relatively unopposed when internal rotation is lost.
Muscle wasting (quadriceps, gluteals)	Disuse atrophy from chronic pain and reduced activity.

Consolidating all risk factors with a focus on Hong Kong relevance:

Risk Factor	Mechanism	HK Relevance
*Femoral neck fracture*	Direct vascular disruption (MCFA)	Very common in elderly osteoporotic patients
*Hip dislocation*	Stretching/tearing of MCFA	RTA, especially motorcyclists
*Corticosteroids > 20 mg/day* ^[1]	Marrow fat expansion, fat emboli, osteocyte apoptosis	SLE patients, organ transplant recipients, nephrotic syndrome, some TCM preparations with hidden steroids
*Alcohol abuse* ^[1]^[2]	Fat cell hypertrophy, fat emboli, direct osteocyte toxicity	Common; social drinking culture
*SLE* ^[2]	Disease itself (vasculitis, antiphospholipid antibodies) + steroid treatment	Higher prevalence in Chinese women
*Sickle cell anaemia* ^[1]	Microvascular occlusion by sickled RBCs	Rare in Chinese; more relevant in African/South Asian populations
*Caisson disease (decompression sickness)* ^[1]^[2]	Nitrogen gas emboli	Rare but seen in commercial divers in HK waters
*Infection (osteomyelitis, septic arthritis)* ^[2]	Elevated intra-articular pressure, endothelial damage, thrombosis	Post-surgical infections, IV drug use
Haemoglobinopathies (thalassaemia)	Marrow hyperplasia, microvascular occlusion	Thalassaemia is common in Southern Chinese
Gaucher's disease	Glucocerebroside accumulation in marrow → intraosseous pressure	Rare
Hyperlipidaemia	Fat emboli, endothelial dysfunction	Very common in HK (metabolic syndrome)
Smoking	Endothelial dysfunction, hypercoagulability	Highly prevalent
Radiation therapy	Direct vascular and osteocyte damage	Post-radiation for pelvic malignancies
Organ transplantation	Immunosuppression requires steroids	Renal transplant common in HK

Feature	AVN of Hip	Primary OA Hip	Inflammatory (e.g., RA)
Age	20–50 years	> 60 years	Any age
Pain onset	Insidious, can be acute with collapse	Gradual	Gradual with flares
Morning stiffness	< 30 min (if secondary OA)	< 30 min	> 60 min
ROM limitation	Internal rotation, abduction first	Global, IR lost first	Global, symmetrical
XR early finding	Sclerosis, crescent sign	Joint space loss	Periarticular osteopenia, erosions
XR late finding	Femoral head collapse → secondary OA	LOSS (Loss of joint space, Osteophytes, Subchondral sclerosis/cysts)	Joint destruction, subluxation
MRI finding	*Double line sign* (T2W)	Cartilage loss, osteophytes	Synovitis, erosions, marrow oedema
Bilateral	40–80% (atraumatic)	Common but asymmetric	Often bilateral and symmetric

AVN is one of the key secondary causes of OA hip. As per the lecture slides ^[1]:

Classification of OA hip:

Primary/idiopathic — uncommon in Chinese population ^[1]
Secondary ^[1]:
- Trauma
- Infection
- Inflammatory joint diseases e.g. RA
- Crystal deposition diseases e.g. gout
- Neuropathic e.g. Charcot joint
- Metabolic/endocrine
- AVN (as "unsupported" cartilage due to bone collapse) ^[4]

So AVN sits at the intersection: it is a distinct entity in its early stages, but once it progresses to Ficat IV with acetabular involvement, it becomes indistinguishable from secondary OA and is managed as such.

High Yield Summary

AVN = death of bone due to interrupted blood supply to the femoral head. The real problem is the failed repair process causing subchondral collapse.
Blood supply: MCFA (main supply) → retrograde retinacular arteries → end-arterial, vulnerable, no periosteal backup.
Causes (ASEPTIC): Alcohol, Steroids (> 20 mg/day), SLE/inflammatory, Pancreatitis/Pregnancy, Trauma (#NOF 15–50%, hip dislocation 10–25%), Infection, Caisson disease/Sickle cell.
Clinical features: Insidious groin pain, worst with weight-bearing. Internal rotation and abduction limited first. Pain can be referred to the knee.
Imaging: XR shows osteopenia → sclerosis → crescent sign (subchondral fracture) → collapse → secondary OA. MRI is more sensitive: double line sign on T2W (outer dark sclerosis + inner bright granulation tissue). Always image the contralateral hip (40–80% bilateral in atraumatic cases).
Classification (Ficat): Stage I (normal/osteopenia) → II (sclerosis, head preserved) → III (crescent sign, collapse) → IV (secondary OA). Pre-collapse (I–II) = joint-preserving; Post-collapse (III–IV) = arthroplasty.
In HK: Steroid use (SLE, transplant) and alcohol are the major non-traumatic causes. Secondary OA hip is more common than primary OA in Chinese populations.
Paediatric equivalent: Perthes disease (idiopathic AVN of proximal femoral epiphysis, boys 5–10 years).

Active Recall - AVN of Hip

Differential Diagnosis of AVN of the Hip

When a patient walks into clinic with hip pain, you need a systematic framework. The learning outcome from the lecture is clear: Formulate differential diagnosis for patients with hip pain ^[1]. AVN is just one cause of hip pain — and conversely, a patient you think has AVN may actually have something else entirely. Let's work through this logically.

Detailed Differential Diagnoses

A. Intra-articular Causes (Groin / Deep Hip Pain)

An orthopaedic emergency — if you miss this, the joint is destroyed.

Why it mimics AVN: Both cause hip pain with reduced ROM. However, septic arthritis is acute with systemic features (fever, malaise)
Investigations: WBC, CRP, ESR, image-guided hip aspiration (cell count, Gram smear, bacterial/fungal/AFB cultures, ± crystals), blood cultures, imaging ^[1]
Imaging: X-rays may show soft-tissue swelling or hip joint capsular distension (with widening of the joint space or even subluxation); radiographic changes in the proximal femoral metaphysis suggest osteomyelitis. MRI may be the most useful test to distinguish proximal femoral osteomyelitis from septic arthritis of the hip. Radioisotope scan ^[1]
Treatment: Antibiotics AFTER joint fluid/synovium are obtained for culture unless haemodynamic instability. Early initiation of antibiotics before obtaining specimens has risk of negative culture → affects antibiotic regime. Surgical drainage — anterior approach in young to preserve blood supply; posterior approach when hip destruction not salvageable and replacement needed. Surgical drainage with antibiotic cement spacer ^[1]
The link: Septic arthritis can itself cause AVN (elevated intra-articular pressure compresses retinacular vessels; bacterial toxins damage endothelium → thrombosis)

Feature	AVN	Septic Arthritis
Onset	Insidious	Acute (hours to days)
Fever	Absent	Present (often high-grade)
CRP/ESR/WBC	Normal (unless underlying cause)	Markedly elevated
Joint aspirate	Non-inflammatory	Purulent (WCC > 50,000, > 75% PMN)
X-ray	Sclerosis, crescent sign	Soft tissue swelling, joint space widening

B. Paediatric Differentials (Age-Specific)

If the patient is a child or adolescent, the differential changes entirely:

C. Extra-articular / Periarticular Causes

D. Referred Pain

E. Neoplastic Causes

Condition	Typical Patient	Pain Location	Key Investigation Finding	Distinguishing Feature
AVN	20–50y, steroid/alcohol use	Groin, referred to knee	MRI: double line sign; XR: crescent sign	Risk factors, femoral head changes with preserved joint space early
OA hip	> 60y	Groin, referred to knee	XR: LOSS features	Osteophytes, joint space narrowing as earliest change
#NOF	Elderly post-fall	Groin	XR: disrupted Shenton's line	Acute trauma, shortened/externally rotated leg
Septic arthritis	Any age, immunocompromised	Groin, severe	Aspirate: WCC > 50,000	Fever, acute onset, hot swollen joint
FAI	Young active adult	Groin, C-sign	MRI: labral tear, cam/pincer morphology	Activity-related, clicking, FADIR positive
Transient osteoporosis	Middle-aged male, 3rd trimester	Groin	MRI: diffuse oedema, NO double line sign	Self-limiting, resolves in 6–12 months
Trochanteric bursitis	Middle-aged, runners	Lateral hip	Clinical diagnosis, USG/MRI if needed	LATERAL pain, NOT groin pain
Lumbar radiculopathy	Any age	Buttock → leg	MRI spine: disc herniation	Dermatomal, positive SLR, neurological signs
Perthes disease	Boys 5–10y	Groin, knee referral	XR: medial joint widening, crescent sign	Paediatric, idiopathic
SCFE	Obese boys 10–15y	Groin, knee referral	XR frog-leg lateral: epiphyseal slip	Obligate external rotation on hip flexion

High Yield Summary

Systematic approach: Think intra-articular (degenerative, inflammatory, infective, vascular/AVN, traumatic) vs extra-articular (periarticular soft tissue) vs referred (spine, knee, visceral).
AVN vs OA hip: AVN is younger (20–50y) with risk factors; early X-ray shows sclerosis/crescent sign with preserved joint space. OA is older (> 60y) with joint space narrowing as earliest feature.
Never miss septic arthritis: Acute onset, fever, raised inflammatory markers, purulent aspirate. It's an emergency.
Transient osteoporosis vs early AVN: Both show MRI marrow oedema, but AVN has the double line sign and transient osteoporosis resolves spontaneously.
Always examine the hip in knee pain and vice versa — shared innervation via femoral and obturator nerves.
Paediatric differentials are age-specific: Perthes (5–10y), SCFE (10–15y), transient synovitis (3–10y), septic arthritis (any age — emergency).
OA hip in Chinese patients is usually secondary (trauma, AVN, infection, inflammatory, DDH) — primary OA is uncommon in Chinese populations.

Active Recall - Differential Diagnosis of AVN of Hip

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (p2, p14, p32, p51, p53, p54, p81) ^[2] Senior notes: maxim.md (section 6.3 — OA hip, DDx) ^[3] Senior notes: maxim.md (section 6.2 — #NOF, Garden classification) ^[4] Senior notes: maxim.md (section 9.1 — OA radiological features LOSS) ^[5] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p27) ^[6] Senior notes: maxim.md (section — Hip dislocation) ^[7] Senior notes: maxim.md (section — Perthes disease, SCFE) ^[8] Senior notes: felixlai.md (section — Differential diagnosis of intermittent claudication) ^[9] Senior notes: maxim.md (section 2.3 — Approach to spine diseases, DDx of back pain) ^[10] Senior notes: maxim.md (section 11.1 — Developmental dysplasia of hip)

Diagnosis of AVN of the Hip: Criteria, Algorithm, and Investigations

Before jumping to imaging, a thorough history and examination directs you toward the diagnosis. The lecture emphasises a structured history ^[1]:

History: ^[1]

Etiology: Trauma, nature of work, drug / alcohol
Function: Walking (level ground / stairs), sitting tolerance, limp, shoes and socks, cutting toe nails, getting on and off public transport
Harris Hip Score — a validated functional outcome score

Let me explain why each of these matters:

History Element	Rationale
Trauma	Femoral neck fracture (15–50% AVN risk) or hip dislocation (10–25%) ^[1]
Nature of work	Caisson disease in divers/tunnel workers; heavy manual labour worsens symptoms
Drug history	Steroid > 20 mg/day increases risk ^[1]; immunosuppressants for transplant
Alcohol	Alcohol abuse ^[1]; amount similar to that causing cirrhosis ^[2]
SLE / autoimmune disease	Double hit: disease + steroids ^[2]
Sickle cell disease	Sickle cell anaemia — microvascular occlusion ^[1]
Functional assessment	Guides treatment urgency and choice; the lecture case: 22-year-old male, left hip stiffness for 3 years, walking tolerance 30 minutes with stick, limping, difficulty sitting in normal chair, shoes and socks cannot manage, minimal hip pain or back pain ^[1] — notice this patient has severe functional limitation despite "minimal pain"

The Harris Hip Score is a clinician-administered tool scoring pain (44 points), function (47 points: gait + activities), deformity (4 points), and range of motion (5 points), out of 100. Score < 70 = poor outcome, indicating need for intervention. It's used to track disease progression and compare pre/post-operative outcomes.

Clinical Pearl

The lecture case illustrates a crucial point: a young patient with AVN may present with stiffness and functional limitation as the primary complaint, with only minimal pain. Don't wait for severe pain to investigate — functional impairment alone should trigger imaging.

Investigation Modalities

Always the first-line investigation. Get AP and lateral (frog-leg lateral) X-ray of the hip ^[3].

The frog-leg lateral view is particularly important because the anterolateral femoral head (the most commonly affected zone) is better visualised when the hip is abducted and externally rotated.

X-ray findings in AVN ^[1]:

Finding	Pathological Explanation	Ficat Stage
Normal	Bone necrosis has occurred but no structural change yet — necrotic bone looks the same as live bone on X-ray because the mineral content is unchanged	Stage I (pre-radiological, only changes on MRI) ^[1]
Cyst (radiolucent areas)	Resorption of dead bone + replacement with fibrous and granulation tissue ^[1] — osteoclasts remove dead trabeculae, replaced by non-mineralised tissue	Stage II
Sclerosis (radiodense areas)	Thickened trabeculae due to direct deposition of new bone onto dead bone ^[1] — "creeping substitution" where new bone is appositionally laid on necrotic trabeculae, making them appear denser	Stage II
Crescent sign	Subchondral collapse of the necrotic segment ^[1] — a thin lucent line just beneath the subchondral plate representing a fracture through the zone of weakened, resorbed bone. Best seen on the frog-leg lateral view	Stage III
Femoral head flattening	Progression of subchondral collapse → loss of spherical contour	Stage III
Secondary OA changes	Joint space narrowing, osteophytes, acetabular sclerosis/cysts — once the head collapses and becomes non-spherical, abnormal loading destroys cartilage on both sides	Stage IV

Understanding the X-ray Progression

Think of it as a timeline: Dead bone initially looks normal on X-ray (Stage I) → repair process creates mixed areas of resorption (cysts) and new bone deposition (sclerosis) (Stage II) → the weakened subchondral zone fractures (crescent sign, Stage III) → the head collapses and OA develops (Stage IV). The X-ray findings reflect the biological repair process, not just the necrosis itself.

Key radiological features to report systematically ^[1]:

Femoral head: Shape (spherical or flattened?), density (sclerosis? cysts?), subchondral lucency (crescent sign?)
Joint space: Preserved or narrowed?
Acetabulum: Normal or sclerotic/cystic (indicating secondary OA)?
Shenton's line: Intact? (disrupted in fractures)
Comparison with contralateral side: Essential

Exam Tip

A normal X-ray does NOT exclude AVN. In Ficat Stage I, the X-ray is completely normal despite active bone necrosis. If you have high clinical suspicion (young patient with steroid/alcohol use and groin pain), proceed to MRI even if the X-ray looks fine. This is one of the most important teaching points.

MRI has 99% sensitivity and specificity ^[1] for AVN. It is the single most important investigation.

Why is MRI so much better than X-ray?

MRI detects marrow changes (oedema, necrosis, granulation tissue) long before any structural bone change occurs
X-ray only shows structural changes in mineral density — necrotic bone has the same mineral content as viable bone until the repair process alters it
MRI can detect AVN weeks to months before X-ray changes appear

Key MRI sequences and findings:

Sequence	Finding in AVN	Explanation
T1-weighted	Low signal band in the femoral head (geographic, well-demarcated)	Fat in normal marrow gives high T1 signal. Necrotic marrow loses its fat signal → low T1. The reactive interface between viable and necrotic bone appears as a low-signal line.
T2-weighted	Double line sign ^[2] — pathognomonic	The outer line is low signal (dark) = sclerotic reactive bone. The inner line is high signal (bright) = granulation tissue with hypervascularity and oedema at the interface between viable and necrotic bone. This double line represents the body's repair front.
STIR / Fat-suppressed T2	Bone marrow oedema (high signal)	Oedema in and around the necrotic zone; helps detect early disease and assess activity of the repair process
T1 with gadolinium	Enhancement of the reactive zone, non-enhancement of necrotic core	Viable tissue enhances (has blood supply); necrotic tissue does not (no blood supply). This can help distinguish viable from non-viable bone for surgical planning.

Ficat Stage I is pre-radiological — only changes on MRI ^[1]. This is precisely why MRI is indispensable.

MRI of contralateral hip ^[1] — always performed because:

40–80% of non-traumatic AVN is bilateral
The contralateral hip may be asymptomatic but already have MRI-detectable disease
Early detection of contralateral disease changes management (may allow joint-preserving treatment before collapse occurs)

How to interpret the MRI systematically:

Location of necrosis: Usually anterolateral superolateral femoral head (weight-bearing dome) — this is the watershed zone with the most tenuous blood supply
Extent of necrosis: Quantify as percentage of femoral head involved
- < 15% (A) — good prognosis
- 15–30% (B) — intermediate
- > 30% (C) — poor prognosis, high collapse risk
Double line sign: Present? → Confirms AVN
Subchondral fracture: Low signal line just beneath the articular surface on T1 → Stage III
Femoral head contour: Spherical or flattened?
Joint space / acetabular changes: Evidence of secondary OA?
Contralateral hip: Any signal abnormality?

Bloods are not used to diagnose AVN directly, but are essential to:

Exclude differentials (especially septic arthritis)
Identify the underlying cause of non-traumatic AVN
Pre-operative assessment if surgery is planned

Investigation	Purpose	Expected Findings in AVN
CBC	Exclude infection, screen for sickle cell	Normal (unless underlying cause, e.g., sickle cell: low Hb, reticulocytosis)
ESR, CRP ^[1]	Exclude infection/inflammation	Normal in AVN; elevated in septic arthritis or inflammatory arthritis
WBC ^[1]	Exclude infection	Normal; elevated in septic arthritis
Coagulation screen	Screen for thrombophilia	May be abnormal in antiphospholipid syndrome, Factor V Leiden
Lipid profile	Identify hyperlipidaemia as risk factor	May show hypercholesterolaemia/hypertriglyceridaemia
ANA, anti-dsDNA, complement	Screen for SLE	Positive in SLE
Antiphospholipid antibodies	Thrombophilia screen in SLE/unexplained AVN	Positive in antiphospholipid syndrome
Haemoglobin electrophoresis	Screen for sickle cell disease / thalassaemia	Hb SS in sickle cell disease
LFTs, GGT	Assess for alcohol-related liver disease	May show elevated GGT (marker of chronic alcohol use)
Uric acid	Exclude gout if crystal arthritis in differential	Elevated in gout

For septic arthritis workup (when it's in the differential) ^[1]:

Image-guided hip aspiration: cell count, Gram smear, bacterial/fungal/AFB cultures, ± crystals ^[1]
Blood cultures ^[1]

The Ficat classification combines plain XR, MRI, bone scan, and clinical features to guide treatment and prognosis ^[2].

This is the classification that drives management decisions, so understanding it in detail is critical:

Classification and treatment ^[1]:

Ficat Stage	Criteria	Imaging Details	Treatment ^[1]
I	Normal X-ray; only changes on MRI ^[1]	MRI: double line sign, marrow oedema. Bone scan: cold spot or doughnut sign. X-ray: normal or subtle osteopenia.	Core decompression
II	Sclerotic or cystic lesions on X-ray; femoral head shape preserved	X-ray: sclerosis (new bone on dead bone) and/or cysts (resorbed bone replaced by fibrous tissue). No crescent sign. No flattening. MRI: well-defined necrotic zone.	Core decompression / vascularised bone graft
III	Subchondral collapse (crescent sign) on X-ray	X-ray: crescent sign (subchondral lucency), ± femoral head flattening. Head has begun to lose spherical shape.	Vascularised bone graft / THR
IV	OA changes	X-ray: femoral head collapse + joint space narrowing + acetabular changes (sclerosis, cysts, osteophytes) — secondary OA.	THR

The Critical Division: Pre-collapse vs Post-collapse

Why Does This Classification Matter So Much?

Once the femoral head collapses (Ficat III), the spherical joint surface is permanently lost. No amount of bone grafting or decompression can restore it. The only option is to replace the joint. This is why early detection (MRI in high-risk patients) is so important — catching AVN in Ficat I or II gives you a window for joint-preserving treatment.

The Association Research Circulation Osseous (ARCO) classification is more detailed and increasingly used in research:

ARCO Stage	Sub-stage	Definition	Imaging
0	—	All imaging normal; only histological necrosis on biopsy	Normal XR, MRI, bone scan
I	IA: < 15%, IB: 15–30%, IC: > 30%	XR normal; MRI or bone scan positive	MRI: marrow changes, double line sign
II	IIA/B/C (same size criteria)	XR abnormal but head shape preserved	XR: sclerosis, cysts; NO crescent sign
III	IIIA/B/C	Subchondral fracture ± early collapse	Crescent sign; measure depression in mm
IV	—	Secondary OA	Joint space narrowing, acetabular involvement

The sub-staging by size (A/B/C) is important because necrotic lesion size is the strongest predictor of collapse:

< 15% involvement → low risk of collapse → may not need surgery
> 30% involvement → high risk of collapse → more aggressive treatment warranted

Scenario	Additional Investigation	Rationale
Post-femoral neck fracture	Serial MRI at 6 weeks, 3 months, 1 year	Monitor for development of post-traumatic AVN
SLE patient on steroids	Baseline MRI of both hips at start of steroid therapy, then periodic screening	High-risk population; early detection
Sickle cell disease	Bone scan (multi-joint screening) ± MRI of symptomatic joints	Multi-focal AVN common
Unexplained AVN (no obvious risk factor)	Thrombophilia screen, lipid panel, haemoglobin electrophoresis	Identify occult cause
Suspected septic arthritis in differential	Image-guided hip aspiration: cell count, Gram smear, bacterial/fungal/AFB cultures, ± crystals; blood cultures ^[1]	Antibiotics AFTER obtaining specimens unless haemodynamically unstable ^[1]

Step	Action	Key Points
1. History	Risk factors, functional assessment (Harris Hip Score)	Etiology: trauma, drug/alcohol; Function: walking, stairs, sitting, shoes/socks, transport ^[1]
2. Examination	ROM (especially IR, abduction), gait, Trendelenburg, Thomas' test	Internal rotation most sensitive; examine both hips and knees
3. X-ray	AP + frog-leg lateral of both hips	Look for sclerosis, cysts, crescent sign, head shape, joint space
4. MRI	If X-ray normal but clinical suspicion high; or to stage disease	99% sensitivity and specificity ^[1]; double line sign pathognomonic; always image contralateral hip
5. Bloods	ESR, CRP, WBC (exclude infection); cause-specific tests	Normal inflammatory markers in AVN
6. Stage	Ficat / ARCO classification	Pre-collapse (I–II) vs post-collapse (III–IV) determines management

High Yield Summary

No formal "diagnostic criteria" — diagnosis is clinical suspicion + imaging confirmation (primarily MRI).
X-ray findings progress: Normal → cysts (resorbed bone) + sclerosis (new bone on dead bone) → crescent sign (subchondral fracture) → femoral head collapse → secondary OA.
MRI is 99% sensitive and specific. Double line sign on T2W is pathognomonic. Always image the contralateral hip.
Ficat Stage I is pre-radiological — only changes on MRI. A normal X-ray does NOT exclude AVN.
Ficat classification drives treatment: Stage I–II (pre-collapse) → core decompression ± bone graft. Stage III–IV (post-collapse) → THR.
Bloods are normal in AVN but essential to exclude septic arthritis (ESR, CRP, WBC) and identify underlying causes (ANA, lipids, Hb electrophoresis, thrombophilia screen).
Necrotic lesion size on MRI (modified Kerboul angle or percentage) predicts collapse risk and guides surgical decision-making.
Harris Hip Score is used to quantify functional impact — essential for monitoring and surgical indication.

Active Recall - Diagnosis of AVN of Hip

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (p2, p8, p14, p15, p16, p20, p51, p53, p85) ^[2] Senior notes: maxim.md (section 6.4 — AVN of hip) ^[3] Senior notes: maxim.md (section 6.2 — #NOF investigations)

Management of AVN of the Hip

Stage-by-Stage Treatment

These apply regardless of staging and form the foundation of management:

Treatment — Stage 1 and 2 ^[1]:

Risk factor modification: alcohol, steroid — Stop or minimise the offending agent. If the patient is on steroids for SLE, work with the rheumatologist to use the lowest effective dose or switch to steroid-sparing agents (e.g., mycophenolate, azathioprine). If alcohol is the cause, complete cessation is essential.
Avoid heavy weight-bearing (running) — Continued mechanical loading on necrotic subchondral bone accelerates the progression to collapse. The necrotic zone is structurally weak, and repetitive impact drives microfractures.
Walking aids — Crutches or a stick to offload the affected hip during the repair phase. Protected weight-bearing reduces the mechanical stress on the compromised femoral head.
Physiotherapy ^[1] — Muscle strengthening, range of motion exercise, cardiopulmonary function, endurance — maintains periarticular muscle support, prevents contractures, and preserves function. The lecture cites AAOS evidence: Strong evidence supports the use of physical therapy as a treatment to improve function and reduce pain for patients with osteoarthritis of the hip and mild to moderate symptoms ^[1].

Drugs: bisphosphonate ^[1]:

Treat osteoporosis; lacking RCT evidence ^[1]
Rationale from first principles: Bisphosphonates (e.g., alendronate, zoledronic acid) are osteoclast inhibitors. They work by binding to hydroxyapatite in bone and being ingested by osteoclasts, disrupting their function. In AVN, the problem is that osteoclasts resorb dead trabeculae faster than osteoblasts can rebuild. By slowing osteoclast activity, bisphosphonates theoretically preserve the subchondral architecture during the repair phase, buying time for osteoblasts to deposit new bone and preventing structural collapse.
The evidence gap: While the mechanism is sound, there is lacking RCT evidence ^[1] to definitively prove that bisphosphonates prevent femoral head collapse. Some small studies show promise (reduced pain, delayed collapse), but large RCTs are lacking. They are used as adjunctive therapy, not as a standalone treatment.

Important Concept

Why can't we just rest and wait? Because the natural history of untreated AVN with > 30% femoral head involvement is relentless progression to collapse in ~80% of cases within 2–3 years. The repair process itself (osteoclast resorption) creates the structural weakness. Simple rest does not stop this biological process — you need to either remove the intraosseous pressure (core decompression), provide structural support (bone graft), or slow the resorption (bisphosphonates).

B. Ficat Stage I — Pre-radiological AVN

Stage I: Normal X-ray; only changes on MRI → Core decompression ^[1]

C. Ficat Stage II — Sclerotic/Cystic Lesions, Head Preserved

Stage II: Sclerotic or cystic lesions → Core decompression / vascularised bone graft ^[1]

All the Stage I treatments apply, plus:

Since THR is the endpoint for most AVN patients, let's go into detail.

What it is: Replacement of both the femoral head/neck (with a prosthetic femoral stem + head) and the acetabulum (with a prosthetic acetabular cup). "Total" means both sides of the joint are replaced.

Management goals ^[1]:

Joint: Restore pain-free stable joint
Bone — Acetabular side: Restore anatomical hip centre; Femoral side: Correct femoral side deformity
Soft tissue: Contracted muscles, ligaments and joint capsule; sciatic nerve; femoral shortening

Why THR over hemiarthroplasty for AVN?

In AVN with secondary OA (Ficat IV), both the femoral head AND acetabulum are damaged → replacing only the femoral side (hemiarthroplasty) would leave damaged acetabular cartilage → continued pain
Joint replacement (hemiarthroplasty / THR) ^[3] — THR is preferred unless the patient is elderly, low-demand, or medically unfit for the longer procedure

Bearing surfaces in THR (important for young AVN patients):

Bearing	Pros	Cons
Metal-on-polyethylene	Reliable long track record, cost-effective	Polyethylene wear → osteolysis over time; concern in young active patients
Ceramic-on-ceramic	Very low wear rate, excellent for young patients	Risk of ceramic fracture (rare), squeaking
Ceramic-on-polyethylene (highly cross-linked)	Good wear characteristics, no ceramic-ceramic squeaking	Better than standard polyethylene but still wears
Metal-on-metal	Low wear	Largely abandoned due to metal ion release, adverse local tissue reactions (ALTR), pseudotumours

For young AVN patients, ceramic-on-ceramic or ceramic-on-highly-cross-linked-polyethylene bearings are typically chosen to maximise implant longevity.

Surgical approaches for THR ^[2]:

Approach	Advantage	Disadvantage
Posterior — most common	Preserve abductor mechanism → rapid rehab	Sciatic nerve injury; risk of hip joint dislocation
Anterolateral (modified Hardinge)	Detach abductor mechanism → good exposure	Superior gluteal nerve injury
Anterior (Smith-Petersen) — rare	For open washout of infected hip	Limited femoral exposure
Direct anterior (DAA)	Muscle-sparing (intermuscular plane), lower dislocation risk	Steep learning curve, LCFA injury, femoral fracture risk

Post-operative care ^[3]:

Prevent dislocation: do not squat / cross legs / flex hip > 90°, abduction pillow, high-low chair
Early mobilisation with physiotherapy
VTE prophylaxis (LMWH, mechanical)
Follow-up X-rays at regular intervals

Implant survivorship: Modern THR prostheses have > 90% survival at 15 years and many last > 25 years. This is why the lecture states improving implant survivorship ^[1] — advances in bearing surfaces, fixation methods (cemented vs uncemented vs hybrid), and surgical technique continue to extend prosthesis life.

Cemented vs Uncemented Fixation

Cemented (e.g., Exeter stem): Bone cement (polymethylmethacrylate — PMMA) fills the gap between prosthesis and bone, providing immediate stability. Better for elderly patients with osteoporotic bone where biological fixation may be unreliable.
Uncemented (press-fit with porous coating): The prosthesis is press-fit into the bone, and the porous surface allows bone ingrowth over time. Better for young patients with good bone stock — no cement-bone interface to fail.
Hybrid: Cemented stem + uncemented cup (common combination).

For young AVN patients, uncemented THR is generally preferred because it preserves bone stock for future revision surgery.

Analgesics — do not affect natural history ^[1]:

The lecture presents a treatment pyramid for hip arthritis ^[1]:

Level	Treatment	Details
Base (mild)	Information and advice, simple analgesics, topical agents, lifestyle, nutraceuticals ^[1]	Education about the condition, weight loss, activity modification
Second tier	NSAIDs, other drugs, physiotherapy or occupational therapy, orthoses, other aids ^[1]	NSAIDs reduce inflammation but have GI/renal/CV side effects; use short courses
Third tier	Injections ^[1]	Intra-articular corticosteroid (temporary relief only, max 3–4/year)
Fourth tier	Surgery — joint preserving: osteotomy, resurfacing ^[1]	Core decompression, bone graft for pre-collapse AVN
Top (severe)	Surgery — joint replacement ^[1]	THR for post-collapse AVN

Specific analgesics ^[1]:

Paracetamol (Panadol): first line — mechanism: central COX inhibition and serotonergic pathways; safe, few side effects
Tramadol: non-narcotic — actually an atypical opioid (mu-receptor agonist + serotonin/norepinephrine reuptake inhibitor); combine with paracetamol: synergistic effect; use if contraindication to NSAIDs
Opioids: CNS depression, addiction; no routine use ^[1] — reserved for severe acute pain (e.g., post-collapse crisis) or post-operative pain

Special Scenarios

Classification and treatment ^[1]:

Ficat Stage	Criteria	Treatment ^[1]	Rationale
I	Normal XR	Core decompression	Decompress elevated intraosseous pressure; stimulate revascularisation; best window for joint preservation
II	Sclerotic or cystic lesions	Core decompression / vascularised bone graft	Debride necrotic bone, provide structural support and biological stimulus; prevent subchondral collapse
III	Subchondral collapse	Vascularised bone graft / THR	Attempt salvage in young with minimal collapse; THR for significant collapse
IV	OA change	THR	Joint surface irrecoverable; reliable pain relief and function restoration

Exam Tip

Common student mistake: Recommending core decompression for Ficat III/IV. Once the head has collapsed, decompression cannot restore the spherical shape. Similarly, don't recommend THR for Ficat I — that's a massive overtreatment in a young patient where joint-preserving options exist and have good success rates.

While not strictly "management of established AVN," prevention is critically important:

Fall prevention measures ^[3] — reduces femoral neck fracture risk, thus reducing post-traumatic AVN
Treatment of osteoporosis: improve bone mineral content by bisphosphonates and lifestyle modifications ^[3]
Steroid minimisation — use the lowest effective dose; use steroid-sparing agents in autoimmune diseases
Alcohol cessation — particularly when amounts approach cirrhosis-level consumption
Early reduction of hip dislocations — within 6 hours to minimise AVN risk ^[5]
Careful fracture management — anatomical reduction and stable fixation of femoral neck fractures to preserve MCFA blood supply

High Yield Summary

Pre-collapse (Ficat I–II) = joint-preserving treatment; Post-collapse (Ficat III–IV) = THR.
Stage I–II treatment: Risk factor modification (stop alcohol/steroids) + avoid heavy weight-bearing + walking aids + bisphosphonates (limited evidence) + core decompression (relieves intraosseous pressure, stimulates revascularisation) ± bone graft (autograft/allograft/artificial — structural support and osteogenesis).
FVFG (free vascularised fibular graft): For young patients with viable femoral head. Brings its own blood supply → living bone that provides structural strut support. Best results in Ficat II.
Stage III–IV treatment: THR — quick and reliable procedure with improving implant survivorship. For young patients with minimal collapse, vascularised bone graft may be attempted first.
THR approaches: Posterior (most common, preserves abductors, risk of dislocation/sciatic nerve injury); anterolateral (good exposure, superior gluteal nerve risk); anterior (rare).
Post-THR precautions: No squatting, no crossing legs, no hip flexion > 90°, abduction pillow, high-low chair.
Analgesics: Paracetamol first-line → tramadol if NSAID contraindicated → opioids only in severe cases (no routine use). Analgesics do NOT affect natural history.
For #NOF with AVN risk: Young → reduction and internal fixation (save the head). Elderly + displaced → hemiarthroplasty. Time matters — reduce within 6 hours.

Active Recall - Management of AVN of Hip

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (p20, p21, p22, p23, p24, p33, p38, p39, p45, p63, p64, p81, p103) ^[2] Senior notes: maxim.md (section 6.3 — OA hip, surgical approaches) ^[3] Senior notes: maxim.md (section 6.2 — #NOF management, post-operative complications, AVN management, prevention) ^[4] Lecture slides: GC 235. Osteoporotic Related Fractures.pdf (p42) ^[5] Lecture slides: GC 235. Osteoporotic Related Fractures.pdf (p21, p22) ^[6] Senior notes: maxim.md (section 9.1 — OA management) ^[7] Senior notes: maxim.md (section — Perthes disease management)

Complications of AVN of the Hip

Complications of AVN fall into two broad categories: (A) complications of the disease itself (untreated or progressing AVN) and (B) complications of treatment (surgical interventions). Let's work through both systematically, always explaining why each complication occurs from first principles.

A. Complications of the Disease Process

These are the consequences of AVN progressing through its natural history — from silent necrosis to femoral head collapse and secondary joint destruction.

B. Complications of Treatment

Complication	Mechanism	Incidence
Subtrochanteric fracture	The drill tract weakens the lateral femoral cortex. If the hole is too large or the patient bears weight too early, the cortex can fracture through the drill site.	~1–2%
Haematoma / bleeding	Drilling through vascular bone → intramedullary bleeding	Mild, self-limiting
Infection	Any surgical procedure carries infection risk; the drill tract provides a portal of entry	Rare (< 1%)
Progression despite treatment	Core decompression fails to halt disease — the necrotic lesion was too large, or the repair response was insufficient. The femoral head still collapses.	20–50% (especially Ficat II, large lesions)
Heterotopic ossification	Abnormal bone formation in surrounding soft tissues triggered by surgical trauma	Uncommon

Complication	Mechanism
Donor site morbidity (for autograft/FVFG)	Iliac crest harvest: pain, haematoma, nerve injury (lateral femoral cutaneous nerve → meralgia paraesthetica). Fibula harvest: ankle instability (if too much fibula is taken), peroneal nerve injury, wound complications
Graft non-incorporation / resorption	The graft may fail to integrate with host bone — particularly in large necrotic zones with poor vascularity
Microsurgical failure (FVFG)	Thrombosis of the vascular pedicle → the graft loses its blood supply and dies → procedure fails. Risk factors: smoking, thrombophilia, technical error
Persistent AVN progression	Even with a successful graft, the disease may continue to progress if the necrotic zone is extensive or systemic risk factors persist

3. Complications of Total Hip Replacement

This is the most high-yield section for exams. THR complications can be classified by timing:

Post-operative complications ^[3]:

Joint dislocation ^[2]^[3] — The prosthetic head can dislocate from the acetabular cup. More common with the posterior approach (because the posterior capsule and short external rotators are divided). Prevented by avoiding squatting, crossing legs, flexing hip > 90°; abduction pillow; high-low chair ^[3].
- Why these precautions? The posterior approach disrupts the posterior restraints. Hip flexion > 90° + adduction + internal rotation is the "dislocation position" — exactly the motion of squatting, bending to tie shoelaces, or crossing legs. The abduction pillow prevents inadvertent adduction during sleep.
Prosthesis infection (periprosthetic joint infection — PJI) ^[2]^[3] — The dreaded late complication. Bacteria form a biofilm on the prosthetic surface — a polysaccharide matrix that protects bacteria from both the immune system and antibiotics. Once biofilm is established, antibiotics alone cannot eradicate the infection.
- Sources: Haematogenous seeding (from dental procedures, UTI, skin infections, pneumonia), direct inoculation at surgery, contiguous spread
- Management: Usually requires two-stage revision — removal of all prosthetic components + insertion of an antibiotic-loaded cement spacer + 6 weeks IV antibiotics → re-implantation of new prosthesis once infection is cleared. This is a prolonged, debilitating process.
Aseptic loosening — The most common cause of long-term THR failure. Particulate wear debris (polyethylene, metal, or ceramic particles) is phagocytosed by macrophages, which release inflammatory cytokines (TNF-α, IL-1, IL-6) and RANKL, activating osteoclasts → periprosthetic osteolysis → loosening of the implant from the bone. Presents as progressive pain, often with X-ray evidence of radiolucent lines around the components.
Periprosthetic fracture — Fracture of the femur around or adjacent to the prosthetic stem, typically after a fall. More common with uncemented stems (stress risers at the stem tip) and in osteoporotic bone.
Leg length discrepancy ^[5] — Even after careful intra-operative measurement, some patients notice a difference. May require shoe raises. Must be counselled beforehand ^[5].

Why Is Prosthetic Infection So Feared?

Bacteria on prosthetic surfaces form biofilms — structured communities encased in an extracellular polysaccharide matrix. Within the biofilm, bacteria exist in a sessile, metabolically quiescent state, making them 100–1000x more resistant to antibiotics compared to free-floating (planktonic) bacteria. The biofilm also shields bacteria from neutrophils and macrophages. This is why IV antibiotics alone cannot cure PJI — you must physically remove the prosthesis (and its biofilm) to eradicate the infection.

C. Complications in Specific Contexts

Category	Complication	Key Mechanism
Disease — Natural History	Subchondral fracture / collapse	Osteoclastic resorption weakens subchondral trabeculae → crescent sign → head flattening
	Secondary OA ^[1]	Joint incongruency and chondral damage from collapsed non-spherical head
	Stiffness / contracture ^[1]	Ankylosis and soft tissue contracture (flexion and adduction contracture) from chronic pain
	Deformity ^[1]	Angulation, coxa vara, shortening from asymmetric head collapse
	Instability / dislocation ^[1]	Loss of ball-and-socket congruence
	Leg length discrepancy ^[1]	Femoral head collapse (true) or fixed adduction (apparent)
	Contralateral hip AVN	Systemic risk factors affect both hips (40–80%)
Treatment — Core Decompression	Subtrochanteric fracture	Drill tract weakens lateral cortex
Treatment — Bone Graft	Donor site morbidity, graft failure	Nerve injury, vascular pedicle thrombosis (FVFG)
Treatment — THR	Thromboembolism ^[2]	Virchow's triad: stasis + endothelial injury + hypercoagulability
	Dislocation ^[2]	Posterior capsule disruption; avoid flexion > 90°, adduction, IR
	Prosthesis infection ^[2]	Biofilm formation on foreign material; difficult to eradicate
	Leg length discrepancy ^[2]	Component positioning; counsel beforehand
	Aseptic loosening	Wear debris → macrophage activation → osteolysis → component loosening
	Nerve injury	Sciatic (posterior approach), superior gluteal (anterolateral)
Treatment — Bisphosphonates	ONJ ^[6]	Over-suppression of jaw bone remodelling
	Atypical femoral fracture	Accumulated microdamage from over-suppressed remodelling

High Yield Summary

The major complication of AVN itself is femoral head collapse → secondary OA. This is the natural endpoint of untreated disease and the reason we try to detect AVN early (pre-collapse = salvageable).
Late complications of AVN (from the lecture): Secondary OA (joint incongruency), stiffness (flexion and adduction contracture), deformity (angulation, coxa vara, shortening), instability/dislocation, and leg length discrepancy.
THR complications: Immediate — bleeding, fracture, neurovascular injury, infection. Early — DVT/PE, wound infection. Late — dislocation, prosthesis infection (biofilm!), aseptic loosening, periprosthetic fracture, leg length discrepancy.
Prosthetic joint infection is the most feared complication — biofilm on prosthetic surfaces renders bacteria 100–1000x more antibiotic-resistant. Usually requires two-stage revision.
Bisphosphonate complications: ONJ (suppress jaw bone remodelling) and atypical femoral fractures (transverse subtrochanteric fractures from over-suppressed remodelling).
40–80% of atraumatic AVN is bilateral — always screen the contralateral hip.
In paediatric DDH treatment: Avoid extreme abduction > 60° — compresses MCFA → iatrogenic AVN.

Active Recall - Complications of AVN of Hip

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (p11, p14, p20, p24, p55) ^[2] Senior notes: maxim.md (section 6.3 — OA hip, surgical approaches, specific complications) ^[3] Senior notes: maxim.md (section 6.2 — post-operative complications of hip surgery) ^[4] Senior notes: maxim.md (section — Hip dislocation, complications) ^[5] Senior notes: maxim.md (section 9.1 — specific complications of total replacement) ^[6] Senior notes: maxim.md (section 6.4 — AVN management, bisphosphonates and ONJ) ^[7] Senior notes: maxim.md (section — Femoral shaft fracture, bisphosphonate-related fractures) ^[8] Senior notes: maxim.md (section 6.2 — Garden classification, displaced #NOF AVN risk) ^[9] Senior notes: maxim.md (section 11.1 — DDH, Pavlik harness complications)

High Yield Summary

AVN = death of bone due to interrupted blood supply to the femoral head. The real problem is the failed repair process causing subchondral collapse.
Blood supply: MCFA (main supply) → retrograde retinacular arteries → end-arterial, vulnerable, no periosteal backup.
Causes (ASEPTIC): Alcohol, Steroids (> 20 mg/day), SLE/inflammatory, Pancreatitis/Pregnancy, Trauma (#NOF 15–50%, hip dislocation 10–25%), Infection, Caisson disease/Sickle cell.
Clinical features: Insidious groin pain, worst with weight-bearing. Internal rotation and abduction limited first. Pain can be referred to the knee.
Imaging: XR shows osteopenia → sclerosis → crescent sign (subchondral fracture) → collapse → secondary OA. MRI is more sensitive: double line sign on T2W (outer dark sclerosis + inner bright granulation tissue). Always image the contralateral hip (40–80% bilateral in atraumatic cases).
Classification (Ficat): Stage I (normal/osteopenia) → II (sclerosis, head preserved) → III (crescent sign, collapse) → IV (secondary OA). Pre-collapse (I–II) = joint-preserving; Post-collapse (III–IV) = arthroplasty.
In HK: Steroid use (SLE, transplant) and alcohol are the major non-traumatic causes. Secondary OA hip is more common than primary OA in Chinese populations.
Paediatric equivalent: Perthes disease (idiopathic AVN of proximal femoral epiphysis, boys 5–10 years).

High Yield Summary

Systematic approach: Think intra-articular (degenerative, inflammatory, infective, vascular/AVN, traumatic) vs extra-articular (periarticular soft tissue) vs referred (spine, knee, visceral).
AVN vs OA hip: AVN is younger (20–50y) with risk factors; early X-ray shows sclerosis/crescent sign with preserved joint space. OA is older (> 60y) with joint space narrowing as earliest feature.
Never miss septic arthritis: Acute onset, fever, raised inflammatory markers, purulent aspirate. It's an emergency.
Transient osteoporosis vs early AVN: Both show MRI marrow oedema, but AVN has the double line sign and transient osteoporosis resolves spontaneously.
Always examine the hip in knee pain and vice versa — shared innervation via femoral and obturator nerves.
Paediatric differentials are age-specific: Perthes (5–10y), SCFE (10–15y), transient synovitis (3–10y), septic arthritis (any age — emergency).
OA hip in Chinese patients is usually secondary (trauma, AVN, infection, inflammatory, DDH) — primary OA is uncommon in Chinese populations.

High Yield Summary

No formal "diagnostic criteria" — diagnosis is clinical suspicion + imaging confirmation (primarily MRI).
X-ray findings progress: Normal → cysts (resorbed bone) + sclerosis (new bone on dead bone) → crescent sign (subchondral fracture) → femoral head collapse → secondary OA.
MRI is 99% sensitive and specific. Double line sign on T2W is pathognomonic. Always image the contralateral hip.
Ficat Stage I is pre-radiological — only changes on MRI. A normal X-ray does NOT exclude AVN.
Ficat classification drives treatment: Stage I–II (pre-collapse) → core decompression ± bone graft. Stage III–IV (post-collapse) → THR.
Bloods are normal in AVN but essential to exclude septic arthritis (ESR, CRP, WBC) and identify underlying causes (ANA, lipids, Hb electrophoresis, thrombophilia screen).
Necrotic lesion size on MRI (modified Kerboul angle or percentage) predicts collapse risk and guides surgical decision-making.
Harris Hip Score is used to quantify functional impact — essential for monitoring and surgical indication.

High Yield Summary

Pre-collapse (Ficat I–II) = joint-preserving treatment; Post-collapse (Ficat III–IV) = THR.
Stage I–II treatment: Risk factor modification (stop alcohol/steroids) + avoid heavy weight-bearing + walking aids + bisphosphonates (limited evidence) + core decompression (relieves intraosseous pressure, stimulates revascularisation) ± bone graft (autograft/allograft/artificial — structural support and osteogenesis).
FVFG (free vascularised fibular graft): For young patients with viable femoral head. Brings its own blood supply → living bone that provides structural strut support. Best results in Ficat II.
Stage III–IV treatment: THR — quick and reliable procedure with improving implant survivorship. For young patients with minimal collapse, vascularised bone graft may be attempted first.
THR approaches: Posterior (most common, preserves abductors, risk of dislocation/sciatic nerve injury); anterolateral (good exposure, superior gluteal nerve risk); anterior (rare).
Post-THR precautions: No squatting, no crossing legs, no hip flexion > 90°, abduction pillow, high-low chair.
Analgesics: Paracetamol first-line → tramadol if NSAID contraindicated → opioids only in severe cases (no routine use). Analgesics do NOT affect natural history.
For #NOF with AVN risk: Young → reduction and internal fixation (save the head). Elderly + displaced → hemiarthroplasty. Time matters — reduce within 6 hours.

High Yield Summary

The major complication of AVN itself is femoral head collapse → secondary OA. This is the natural endpoint of untreated disease and the reason we try to detect AVN early (pre-collapse = salvageable).
Late complications of AVN (from the lecture): Secondary OA (joint incongruency), stiffness (flexion and adduction contracture), deformity (angulation, coxa vara, shortening), instability/dislocation, and leg length discrepancy.
THR complications: Immediate — bleeding, fracture, neurovascular injury, infection. Early — DVT/PE, wound infection. Late — dislocation, prosthesis infection (biofilm!), aseptic loosening, periprosthetic fracture, leg length discrepancy.
Prosthetic joint infection is the most feared complication — biofilm on prosthetic surfaces renders bacteria 100–1000x more antibiotic-resistant. Usually requires two-stage revision.
Bisphosphonate complications: ONJ (suppress jaw bone remodelling) and atypical femoral fractures (transverse subtrochanteric fractures from over-suppressed remodelling).
40–80% of atraumatic AVN is bilateral — always screen the contralateral hip.
In paediatric DDH treatment: Avoid extreme abduction > 60° — compresses MCFA → iatrogenic AVN.

AVN Of Hip

Definition

Epidemiology

Anatomy and Blood Supply of the Femoral Head

Arterial Supply (Retrograde)

Why Is the Femoral Head So Vulnerable?

Nerve Supply

Relevant Muscular Anatomy

Aetiology and Pathophysiology

Overview of Causes

A. Traumatic AVN

B. Non-Traumatic (Atraumatic) AVN

Pathophysiology: Step by Step

Classification

Ficat and Arlet Classification (Historical, Still Referenced)

Modified Steinberg (University of Pennsylvania) Classification

ARCO (Association Research Circulation Osseous) Classification

Clinical Features

Symptoms

Signs

Systematic Clinical Examination of the Hip

Risk Factors Summary

Relevant Comparison: AVN vs OA Hip vs Inflammatory Arthritis

Paediatric AVN: Perthes Disease (Legg-Calvé-Perthes Disease)

Connection to OA Hip and Hip Arthritis Classification

Active Recall - AVN of Hip

References

Approach to the Differential Diagnosis

Systematic Differential Diagnosis Framework

Detailed Differential Diagnoses

A. Intra-articular Causes (Groin / Deep Hip Pain)

1. Osteoarthritis of the Hip

2. Fracture Neck of Femur (#NOF)

3. Septic Arthritis of the Hip

4. Inflammatory Arthritis (RA, SLE, Ankylosing Spondylitis)

5. Femoroacetabular Impingement (FAI)

6. Labral Tear of the Hip

7. Transient Osteoporosis of the Hip (Bone Marrow Oedema Syndrome)

8. Hip Dislocation

B. Paediatric Differentials (Age-Specific)

9. Perthes Disease (Legg-Calvé-Perthes Disease)

10. Slipped Capital Femoral Epiphysis (SCFE)

11. Transient Synovitis (Irritable Hip)

C. Extra-articular / Periarticular Causes

12. Trochanteric Bursitis / Greater Trochanteric Pain Syndrome

13. Gluteus Medius Tendinopathy / Tear

14. Iliotibial Band Syndrome

15. Piriformis Syndrome

D. Referred Pain

16. Lumbar Spine Pathology (Sciatica / Radiculopathy)

17. Knee Pathology Referring to Hip

18. Visceral / Non-Musculoskeletal Causes

E. Neoplastic Causes

19. Bone Tumours

20. Developmental Dysplasia of the Hip (DDH)

Summary Comparison Table: Key Differentials of AVN

Active Recall - Differential Diagnosis of AVN of Hip

Diagnostic Principles

Clinical Assessment: What to Ask and Why

Diagnostic Algorithm

Investigation Modalities

1. Plain Radiography (X-ray)

2. MRI — The Gold Standard

3. Bone Scintigraphy (Technetium-99m Bone Scan)

4. CT Scan

5. Laboratory Investigations

6. Hip Aspiration (Arthrocentesis)

The Ficat Classification: Integrating Clinical, Radiological, and MRI Findings

ARCO Classification (Modern International Standard)

Quantifying Necrotic Extent on MRI

Special Investigations in Specific Clinical Scenarios

Summary: Diagnostic Approach at a Glance

Active Recall - Diagnosis of AVN of Hip

Guiding Principles

Management Algorithm

Stage-by-Stage Treatment

A. General Measures (ALL Stages)

B. Ficat Stage I — Pre-radiological AVN

Core Decompression

Combined Core Decompression + Bone Graft