AVASCULAR NECROSISDR SAGAR B JAISWAL

JR 3 ORTHO UNIT “A”

SSG HOSPITAL VADODARA

DEFINATION

Avascular Necrosis (AVN) of the bone is a pathological

process that results from interruption of the blood supply

to the bone, either temporary or permanently.

Also known as Osteonecrosis/ Osteochondritis

Dissecans/ Chandler’s Disease,

Coronary Diseases

INTRODUCTION Young adults in 30’s--40’s—50’s

Male : Female--- 4:1

Sequale of SCPF

60% => B/L

INCRASINDG INCIDENCE –TRAUMA ALCOHOL & STEROIDS

One of the most challenging problems faced by

Orthopaedic surgeons.

Annual Incidence of 20,000(US)

18% of total THR’s d/t AVN

HISTORY First described by Munro in 1738.

In 1835 Curveilhier depicted femoral head morphological changes secondary to

interruption of blood flow.

Koenig (1888) => described the condition coined the term Osteochondritis Dissecans

Haenish (1925) => first case of idiopathic ischemic necrosis of the femoral head in an adult

Arterial Occlusion (1940) was postulated as the cause of the necrosis.

Pietrograndi (1957) => AVN d/t Steroid therapy

First large sample size report by Mankin in 1962

ETIOLOGYAny Condition That Shuts Off The Blood Supply To

The Femoral Head Fracture

Dislocation

Periosteal stripping

Dysbaric disease

Corticosteroid

Organ or bone transplantation

Metal corrosion & ionisation

Radiation

Acrylic cement

Overzealous reaming

Infection?????------ ”OSTEONECROSIS IN OSTEOMYELITIS”

BONES AFFECTED & SITES OF

PREDILICTION FEMORAL HEAD

HUMERAL HEAD

CARPAL SCAPHOID

TALUS

RADIAL HEAD

HUMERAL CAPITELLUM

LATERAL FEMORAL CONDYLE

WHAT HAPPENS TO THE BONE…..&…..

HOE DOES THE REPAIR OCCURS

WITHIN NECROTIC BONE THE BONE ARCHITECTURE & THE MASS OF THE BONE REMAINS

UNALTERED

THE TRABECULAE (in cancellous bone) & LAMELLAE OF OSTEONS, INTERSTITIAL BONE (in cortical bone) -----retains their original histological characteristics

No blood ----Auotolysis of osteocytes---empty lacunae

&

Marrow contents disintegrates and forms dead cellular debris

No vascularity and no cellular activity

Relative increase in RADIODENCITY(on x-ray)

WITHIN ADJACENT LIVE BONE

Reactive hyperaemia and compensatory increased blood supply in the

preparation of new bone and replacement of dead necrotic bone and

bone marrow.

Vascular(endothelial) & cellular(osteoblastic) proliferation is accompanied

by resorption(osteoclastic) & thinning of the osseous elements-------reduction in the bone mass

Demineralisation And Trabecular Thinning

Osteoporosis (On X-RAY)

AVN OF THE HEAD OF THE FEMUR

DEFINITION

Death of the bone & bone

Bone cells from interruption

Of blood supply that leads to

structural changes in the

femoral head , consequent

collapse and secondary

Osteoarthritis

Includes traumatic and non-traumatic

Causes

Freund in 1926 gave detailed description of

Osteonecrosis

Chandler in 1948 termed disorder as "coronary disease

of hip” which accounts for eponym Chandlers disease

ANATOMY

• Head of femur

forms about 2/3rd

of sphere and

articulates with

acetabulum of

hip joint

• Connecting two

trochanters

anteriorly forms

intertrochanteric

line and

connecting two

trochanters

posteriorly forms

intertrochanteric

crest.

• Socket

• Ball

• Femoral neck

• Smooth weight-

bearing surfaces

• Smooth cartilage

• Femur

BLOOD SUPPLY OF HEAD OF FEMUR

(major arteries supplying)1. Medial circumflex femoral artery PROFUNDA FEMORIS

ARTERY

2. lateral circumflex femoral artery

3. Artery of ligamentum teres OBTURATOR ARTERY

Intra-capsular arterial ring(“CHUNG”)

Ascending cervical arteries “metaphyseal

arteries”

Extra-capsular arterial ring(“CROOK”)

BLOOD SUPPLY OF HEAD OF FEMUR

continued……………EPIPHYSEAL ARTERIES

1.Lateral epiphyseal artery of “trueta” [ main]

(lateral ascending cervical )

2.Medial epiphyseal artery of “trueta”

(artery of ligamentum teres)

OR

(medial ascending cervical )

“Anastomoses of trueta”

Blood supply…..

VARIATION OF VASCULAR PATTERN

WITH THE ADVANCING AGE… Phase 1: at birth

lateral epiphyseal

metaphyseal

Phase 2: infantile(4 month – 4 years)

metaphyseal supply goes on decreasing (as the epiphyseal

ossification center becomes enlarged and prminent)

lateral epiphyseal artery assumes major role

Phase 3: intermediate (4-7 years)

growth plate becomes completely developed and as a

“firm barrier”

lateral epiphyseal is the only source of blood supply

Phase 4: pre-adolescent(9-10 years)

lateral epiphyseal …………along with

artery of ligamentum teres(that becomes prominent now) as ….

medial epiphyseal artery

VARIATION OF VASCULAR PATTERN

WITH THE ADVANCING AGE… Phase 5: In adolescent and adults

lateral epiphyseal artery…&

Artery of ligamentum teres

becomes the major source of blood supply

WHY PREDILECTION FOR OCCURRENCE OF AVN

ENDARTRIOLAR SUPPLY AND LACK OF COLLATERALS

RETROGADE BLOOD SUPPLY

SMALL DIAMETER VESSELS AT SUB-CHONDRAL REGION

MOST OF PART IS COVERED BY ARTICULAR CARTILAGE

VASCULAR SINUSOIDS OF MARROW DON’T HAVE ANY ADVENTITIAL

LAYER SO EASILY COMPRESSED BY MARROW EDEMA

BLOOD SUPPLY OF HEAD OF FEMUR

IN PAEDIATRIC AGE GROUP(4-8Yrs)

Till 4-8 years of age, the vascular anatomy in a transitional stage of development.

The ALT does not penetrate the epiphysis of the femoral head until 9 or 10 years of age.

The Medial Circumflex Artery (br.of Profunda Femoris Artery), penetrates into the femoral proximal metaphysis but is prevented from passing into the femoral epiphysis by the growth plate.

The blood supply to the femoral head is especially vulnerable during this time.

CLINICAL DETAILS

No distinguishing Clinical Features/ High index of suspicion

Asymptomatic Pain gradual & insidious in nature

Range Of Motion (ROM) ; patient may walk with a limp

Radiographic findings may appear after a delay of several months

to years following the onset of symptoms

DEFORMITY , MASCULAR ATROPHY, NEUROLOGICAL DEFICIT

FACING THE PATIENT OF HIP PAIN Anterior Hip pain or Groin pain

Rule out: hip fracture, septic joint, and avascular necrosis

Other causes:OA, RA, iliopectineal bursitis

Lateral pain or Trochanteric pain

Rule out: hip fracture, bone tumor, referred pain from lumbar disc herniation

Other causes: trochanteric bursitis,OA, radiating from

lumbar disc or facet disease

Posterior hip pain

Rule out: sciatic nerve irritation ,sacroiliitis due to spondyloarthropathy, lumbardisc

or facet disease

Other causes:muscle strain

PAIN OF AVN Focal over the groin / hip or it may radiate to the buttocks,

anteromedial thigh or knee

Induced mechanically by standing & walking & may be eased by rest

May be very intense, throbbing, deep & often intermittent

Worsened by coughing & at night

40% of patients have night pain asso. with morning stiffness

A Click may be heard when the patient rises from a sitting position or on external rotation of an abducted hip

Characteristics of pain ROM may be diminished, especially after collapse of the femoral

head

ROM may be limited, especially in flexion, abduction & internal rotation

Gait :- Patients may walk with a limp.

The Trendelenburg sign may be Positive

To be diagnosed at an early stage, high index of suspicion, especially true with U/L involvement because of the high risk of the dev. of AVN in the C/L Hip

ETIOLOGY OF AVN HEAD OF

HEAD OF FEMURIDIOPATHIC &………………………………..

Trauma

Steroids

Alcohol abuse

CT diseases eg SLE

Hematologic (sickle cell disease,

hemoglobinopathies,

thrombophilia)

Metabolic (hyperlipidemia, gout,

renal failure)

Orthopedic disorders (slipped

capital femoral epiphysis,

developmental dysplasia of the hip,

Legg-Calve-Perthes disease)

Infection (osteomyelitis, HIV])

Renal transplantation

Radiation therapy

Gaucher disease

Malignancy (marrow infiltration,

malignant fibrous histiocytoma)

Caisson disease

Pregnancy

Bisphosphonate use

IDIOPATHIC………

COL 2A1-GENE MUTATION

P-GLYCOPROTEIN POLYMORPHISM

ALCOHOL METABOLIZING ENZYME POLYMORPHISM

ETIOLOGY EXPLAINED…….

PREDNISOLONE :

Threshold cumulative dose—2000mg 4.6 fold increase

with every additional dose of--10mg / day in the incidence

ALCOHOL: >400ml/week 9.8 fold increase

in the incidence

DRINK YEARS = WEEKLY ALCOHOL CONSUMPTION X YEARS

ETIOLOGY EXPLAINED…….

DYSBARISM : No osteonecrosis if….

<17 psi

< 30 months

SMOKING : >20 PACKS / YEAR

PACK YEARS = PACKS/DAY X YEARS

PATHOPHYSIOLOGYIntravascular

Extraosseous

Arterial

Intraosseous

Arterial

Venous

Extravascular

Extraosseous factor

(Capsular factors)

Intraosseous factors

AT T(temp)= k (constant)

pressure P volume V

Extraosseous Vascular FactorsArterial Factors

Most important

Femoral Head blood supply is an End-Organ System with poor collateral development

Trauma to the hip may l/t contusion or mechanical interruption to the Lateral Retinacular Vessels (main blood supply of the femoral head & neck)

Trauma , vasculitis (Raynauds ds), or vasospasm (decompression sickness)

Intraosseous Vascular FactorsArterial Factors

Circulating micro-emboli that block the microcirculation of the femoral head

In Conditions like-

1. Fat emboli (hyperlipidemia associated with alcoholism)

2. steroid therapy

3. SCD

4. nitrogen bubbles in decompression sickness

Intraosseous Vascular FactorsVenous Factors

Enlargement of intramedullary fat cells or fat-loading osteocytes causes the cells to expand; this may be the most significant factor l/t obstruction of venous drainage

Reducing venous outflow & causing stasis

Caisson disease & SCD

Extravascular FactorsIntraosseous Factors

Ficat et al demonstrated increased

bone marrow pressure in the

femoral necks of a large number of

patients with avascular necrosis of

the femoral head (AVN).

Steroid Hypertrophy of Fat cells

Gaucher cells & Inflammatory cells

Encroach on intraosseous

capillaries

Intramedullary circulation

Compartment syndrome

Alcohol & Steroid

Direct toxic metabolic effect on

osteogenic cells

Extravascular FactorsCapsular Factors

Trauma, Infection & Arthritis

Effusions within the Hip joint

Intracapsular Pressure

Tamponade of the LEVs

BIOLOGICAL SEQUENCE OF REPAIR IN

AVN OF FEMORAL HEAD

IMAGING MODALITIESX- RAY

Nomal

Demineralization, osteopenia & osteoporosis

Mottling & sclerosis..cystic changes

Crescent sign ….sub-chondral fractures…..collapse

Flattening of the femoral head

Joint space narrowing

Osteophytes formation with acetabular involvement

Secondary osteoarthritis of the hip joint

The vicious cycle in AVN femoral head

FIRST EVENT OF AVASCULARITY &

MECHANICAL FAILURE

SUBCHONDRAL MICROFRACTURE

ONGOING SUBCHONDRAL

WEAKNESS

PROGRESSIVE WHEIGHT BEARING

ARTICULAR CARTILAGE

UNDERGOES COLLAPSE

Degenerative

joint disease

(DJD) & Joint

Dissolution

RADIOLOGICAL IMAGES

IMAGING MODALITIESCT-SCAN

.

Axial CT: Patient

without AVN of the

Femoral Head

Prominent &

Thickened

but Normal

Trabeculae

CT SCAN IN AVN… LOSS OF ASTERIK SIGN

& SUBCHONDRAL FRACTURE

IMAGING MODALITIESSCINTIGRAPHY

Focal increase in the trassure uptake

IMAGING MODALITIESMRI

Classic Findings:- look for focal lesion in the anterosuperiorportion of femoral head that is well demarcated but is inhomogeneous

T1 images => low signal intensity

T2 images => double line sign => classic sign of AVN, made up of 2 concentric low and high signal bands

high-signal-intensity line may represent hypervascular granulation

tissue

MRI T-1 IMAGE

signal from ischemic marrow

Single band like area of low signal intensity.

100% sensitivity

98% specificity

MRI T-2 IMAGE(“DOUBLE LINE SIGN”)

A second

high signal

intensity

seen within

the line seen on T1

images.

Represent

hyper

vascular

granulation tissue

T-1 IMAGE T-2 IMAGE

IMAGING AT A GLANCE

X-RAY CT-SCAN SCINTIGRAPHY MRI

Unable

to detect

disease of

stage 0 or 1

Helpful in

assessing

flattening

of the Femoral

Head & asso.

Degen. changes

For Extent of

Involvement

e.g. Subchondral

Lucencies

&

Sclerosis during

Reparative stage

Enables

detection of

subchondral or

cancellous # &

collapse

Reflects Vascular Integrity

Avascular Focus may be

demonstrated Early in

Disease (MRI Contrast)

85% sensitivity

(Collier)

Triple-Head High-

resolution SPECT

Sensitivity 97%

(Lee et al)

Most Sensitive

1.5-T magnet

88% sensitivity

100% specificity

94% accuracy

(Beltran et al)

Indispensable for

Accurate Staging

of AVN because

images clearly depict

1. Size of the lesion

2. Gross estimates of stage

ARTHROGRAPHYsokiya et.al arthroscopic staging of AVN

STAGE 1: NORMAL ARTICULAR SURFACE

STAGE 2: FISSURING OF THE ARTICULAR

SURFACE

STAGE 3:BALLOTABLE FRAGMENT

STAGE 4: COLLAPSE & DEPRESSION OF THE

FRAGMENT

STAGE 5: DOLAMINATION OF THE ARTICULAR

SURFACE WITH EXPOSED BONE

STAGE 6: OVERLAYING DEGENERATIVE

CHANGES IN THE ACETABULAM

IMAGING MODALITIESBIOPSY

IMAGING MODALITIESARTERIOGRAPHY & VENOGRAPHY

TEST FOR HEAMODYANAMIC FUNCTION

NORMAL intramedullary pressure---- 10-20mm Hg

IN AVN intramedullary presure ----- increased above normalcy

SALINE INJECTION

intramedullary pressure ------ rises by 3-4 times the normal value

DIFFERENTIAL DIAGNOSIS

DIFFERENT TRAUMA

DEGENERATIVE JOINT DISEASE

OSTEOPOROSIS

INFLAMMATORY SYNOVITIS

EPIPHYSEAL DYSPLASIA

EPIPHYSEAL STRESS FRACTURE

TRANSIENT OSTEOPOROSIS OF HIP JOINT

OSTEOMYELITIS…….etc

TRANSIENT OSTEOPOROSIS OF HIP JOINT

“bone marrow oedema syndrome” SELF LIMITED CLINICAL ENTITY OF UNKNOWN CAUSE

CERTAINLY A HAVING A VASCULAR BASIS AND POSSIBLE OVER ACTIVITY OF SYMPATHETIC SYSTEM

CONTROVERSY ….WHETHER TOH REPRESENTS A VERY EARLY REVERSIBLE STAGE OF AVN

INITIALY DESCRIBED IN PREGNANCY….3RD TRIMESTER

MIDDLE AGED MEN …..M:F--- 3:1

RECURRENCE IN THE SAME HIP CAN OCCUR.

SIMILAR CHANGES IN THE OPPOSITE HIP OR OTHER JOIN OF BODY …

REGIONAL MIGRATORY OSTEOPOROSIS

CLINICALY: SPONTANEOUS ONSET OF SUDDEN PAIN ; USUALY SEVERE WITH NO RISK FACTOR FOR AVN

Differentating TOH

X-RAY MRI BONE SCAN

PROFOUND OSTEOPENIA OF

THE HEAD WITH NECK

A JOINT EFFUSION MAY BE

PRESENT

JOINT SPASE IS ALWAYS

NORMAL

BONE MARROW EDEMA

PATTERN IN

HEAD ; NECK ; &

ALSO SOMETIMES

TROCHENTER

T-1 LOSS OF NORMAL FATT

MARROW SIGNAL

T-2 HIGH

SIGNAL;HETEROGENEOUS

MARKEDLY INCREASED

HOMOGENEOUS

UPTAKE IN HEAD & NECK

BOTH

TOH …..

T-1 IMAGE T-2 IMAGE

CLASSIFICATION AND STAGING

1960s –3 part staging system

1970s – 4th stage added

Hungerford and lennox:

– added stage 0

most widely used……

PAUL FICAT & ARLET

FICAT & ARLETStage Clinical Feature Radiographs

0 Preclinical 0 0

1 Preradiographic -/+ 0

2 Reperative + A: Diffuse Porosis,

Sclerosis, Cysts

@ N-Joint line

@ N- Head counter

B: Crescent Sign(S/C #)

Flattening of head

3 Early Collapse ++ Joint Space decreased

loss of sphericity

collapse of the head

4 Osteoarthritis +++ more decreased joint space more incongruancy

acetabular changes

MURCUSS ET AL.( 1973)

Stage 1 : Asymptomatic, mottled increased density of

femoral head

Stage 2 : Asymptomatic , area of necrosis demarcated by a

rim of increased density

Stage 3 : Intermittent pains, Crescent sign in frog lateral view

Stage 4 : Painful limb & flattening of femoral head

Stage 5 : Symptoms & signs of degenerative arthritis

Stage 6 : Severe degenerative arthritis

PITFALL…….IN

NO CONSIDERATION OF

SIZE OF THE LESION &

INVOLVEMENT OF ARTICULAR SURFACE

KERBOUL ANGLE (1974) Kerboul :

outcome– the location &

the extent of involvement

Arc of articular surface involvement :

-- in AP &

LATERAL VIEWS

STERNBERG ET.AL(1995)Modified Ficat & Arlet Classification STAGE 0: NORMAL X-RAY ; NORMAL BONE SCAN ; NORMAL MRI

STAGE 1: NORMAL X RAY ; ABNORMAL –BONE SCAN & MRI

A : <15%

B : 15-30%

C :>30%

STAGE 2: ABNORMAL X-RAY; BONE SCAN & MRI

A : <15%

B : 15-30%

C :>30%

STAGE 3: SUBCHONDRAL COLLAPSE PRODUCING CRESCENT SIGN

A : <15%

B : 15-30%

C :>30%

…… STAGE 4: COLLAPSE & DEPRESSION

A : <15% <2MM

B : 15-30% 2—4 MM

C : >30% >4MM

STAGE 5:JOINNT SPACE NARROWING & ACETABULAR INVOLVEMENT

A : <15% “ESTIMATED ACETABULAR

INVOLVEMENT”

B : 15-30%

C :>30%

STAGE 6: ADVANCED DEGENERATIVE CHANGES

Other classification systems

University Of Pennsylvania Classification of Osteonecrosis

Pittsburgh ( mri classification)

Mitchell ( mri classification)

Schimuzu (mri classification)

Sugioka (Japanese classification)

Mitchell’s MRI StagingClass

A

B

C

D

T1

Bright

Bright

Intermediate

Dark

T2

Intermediate

Bright

Bright

Dark

Definition

Fat signal

Blood signal

Fluid or edema

signal

Fibrosis signal

OHZONO ET.AL(1992)PRGNOSTIC CLASSIFICATION

LOCATION OF LESION

SIZE OF THE AREA INVOLVED

,

ARCO SYSTEM(ASSOCIATION REASERCH CIRCULATION OSSEOUS)

Criteria For Diagnosis(Current Concept JBJS Mont & Hungerford)

Specific Criteria Collapse of femoral head

Subchondral radiolucent line

Anterolateral sequestrum

Bone scan showing a photopenic region surronded by area of increased density

Double band on T2-weighted image

Bone biopsy showing empty lacunae

involving multiple adjacent trabeculae

Non specific criteria Collapse of femoral head with narrowing of

joint space

Mottled ,cystic & sclerotic pattern in head

MRI showing changes in bone marrow

Painful movements of hip with normal X ray

H/O of alcohol & steroid intake

Non specific but abnormal biopsy , edema /fibrois

TREATMENT

AIM

TO KEEP THE JOINT FROM BREAKING DOWN

Preserve rather than Replacing Femoral Head & Cartilage

Early Intervention has favorable impact on the disease prognosis

irrespective of T/t modality used

CONSERVATIVE MANAGEMENTMedical Management

Small, Asymptomatic lesions

Lesion is so advanced that prophylactic measures

would be of little value

When Sx is contraindicated or declined

Buying time until arthroplasty is needed

Glueck & colleagues => Incidence of

osteonecrosis in association with certain

Coagulopathies & Hyperlipidmias

Stanozolol anabolic androgenic steroid potenial means of

treating AVN associated with Coagulopathies &

Hyperlipidemias

Stanozolol (6mg/day) decreases AVN symptoms at

1 year following treatment.

Motumura Et.Al

DECREASED Incidence of Steroid-induced osteonecrosis in rabbits

using a combination of Warfarin & Probucol (Lipid Lowering Agents)

ENAXOPARIN adminstered for 12 weeks was found to prevent

radiographic Progression of Stage 1 and Stage 2 idiopathic

osteonecrosis of the femoral head at 2 year follow up

GUATHIER ET.AL

95%-100% of transplant patients who were treated with

Calcium Channel Blockers experienced complete relief of

Bone Pain Syndrome

I.V. ILIOPROST, a Vasoactive Prostacyclin analogue

showed significant improvements in patients with Bone

Marrow Edema Syndrome & Osteonecrosis

…..

Oral Nifedipine => Relief of bone pain reported in a small series of patients with Osteonecrosis

Alendronate :- IN osteonecrosis, Agarwal et al reported that l/t significant improvement in Pain & Disability scores

Bisphosphonates => reportedly causing Osteonecrosis of the Jaw , so should be used cautiously

Puerarin

An extract of the kudzu vine , is purported to decrease

Cholesterol, Platelet Aggregation & cause Vasodilation.

Electric, Electromagnetic & Acoustic T/t

Pulsed Electromagnetic Field stimulation, is reported to be useful for treatment of

osteonecrosis

Hyperbaric oxygen (HBO)

HBO improves oxygenation, reduces oedema & induces

angioneogenesis, a reduction in intra osseous pressure &

improvement in microcirculation

Extracorporeal Shockwave Therapy

Seems to improve the harris hip score

Bone Marrow Injections (BONE MARROW STEM CELL)

with core decompression

RATIONALE:

The small no. of progenitor cells in the proximal extremity

of the femur with osteonecrosis of the femoral head

causes insufficient creeping substitution after

osteonecrosis

BONE MARROW osteoblast progenitor cells from

pluri-potential connective-tissue stem cells

proliferate to form colonies that &

subsequently, a mature osteoblastic phenotype

Technique Usual site => Anterior Iliac Crest

A beveled metal trocar of 6 to 8 cm length & a bore of 1.5 mm is pushed deep into the cancellous bone

Marrow is aspirated with A 10 ml syringe(flushed with heparin)

Aspirates pooled in plastic bags containing an anticoagulant solution

Filtered to remove fat aggregates & clots

Current Indications:-

The best indications are hips with osteonecrosis & without collapse

CD+ CULTURED OSTEOBLASTS

instillation

BMP-4

BMP-10

rhBMP-2

+ PROTECTIVE WEIGHTBEARING

(CANES OR CRUTCHES)

PHYSIOTHERAPY

RANGE OF MOTION EXERSIZES

OPERATIVE MANAGEMENT

JOINT PRESERVING PROCEDURES

A) CORE DECOMPRESSION

B ) BONE GRAFTING

C) OSTEOTOMIES

JOINT REPLACING PROCEDURES

A) HIP RESURFACING PROCEDURE

B ) HIP REPLACEMENT

OTHERS

A) POROUS TANTALUM ROD

B) ENDOPROSTHESIS

C) RECECTION ARTHROPLASTY

D) ARTHRODESIS

CORE DECOMPRESSION

(FORAGE)

A) AS ISOLATED PROCEDURE

B) WITH ADJUVENTS

: PEMF

: BMP

: DBM

C) WITH BONE GRAFTING( Originally by PHEMISTER)

: CANCELLOUS( BY FICAT)

: CORTICAL( cortial strut/ vascularised fibula)

:MPBG

:OSTEOCHONDRAL

Rationally…..for CD

BIOLOGICAL CHANGES:

1. Decreased intraossous pressure

2. Revascularization through channel or the fibular intramedullary canal

3. Prevention of additional isheamic events

MECHANICAL CHANGES:

1. Removal of the necrotic bone & thus removing obstruction to

revascularisation

2. The subchondral raft supports the articular cartilage

Indications:-

Core decompression is effective for symptomatic relief in nearly all stages in

all patients who present with a painful hip secondary to ON d/t decrease

of intramedullary pressure done by it

Transient symptomatic relief in an advanced stage & in already collapsing or when collapse is impending

It is Most Effective in Stage I & II lesions that are size A (15% of head affected) & B (15%–30% of head affected)

The larger the lesion, the less likely the patient is to have a successful outcome.

Standard Technique & its Variations:-

Ficat & Arlet proposed creating an 8 to 10 mm dia core track & this became a “standard”

Recently some authors have suggested that the same effect of standard core can be achieved by producing Multiple Smaller Core Tracks of 3-mm dia range. This can be done percutaneously & theoretically # risk & shortens the operative time & morbidity

Steinberg et al proposed making Smaller Angled Core Tracks into the Necrotic Segment from the Central Core Canal

Postoperative Management:-

The lateral cortical window produces a stress riser in the proximal femur So Protect the patient from unprotected weightbearing for the first 6 weeks

Reported incidence of # with core decompression is <1% & has almost always been associated with either a fall or failure to use protective devices (crutches or a walker) in the first 6 week

BONE GRAFTING (TECHNIQUES)

Bone grafting procedures are a group of joint preserving techniques that involve the removal of the diseased femoral head segment, f/b its replacement with 1or more of a variety of bone graft options

These are most valuable in treating patients with Stage I & II diseas

Techniques:-

1.Grafting Through Lateral Core Track

2.Grafting Through Femoral Neck Window

3.Grafting Through Articular Surface Window

……1)

LATERAL CORE TRACK TECHNIQUE

……..

PEARLS

Simple technique

Minimal Invasiveness

Avoidance of surgical dislocation of the hip

Low Complication Rate

Can be performed bilaterally under one anesthetic

PITFALLS

Inability to directly visualize the joint surfaces

Inexact nature of removing diseased bone & replacing it

with bone graft under fluoroscopic guidance

Risk of postoperative #

…2)….FEMORAL NECK WINDOW(LIGHTBULB TECHNIQUE)

Watson-Jones or Smith-Peterson approach is used

A window is created to expose the anterior femoral neck, at the level of the junction of the femoral head & neck

When Combined with a Bone Grafting procedure,refered as the “light bulb” procedure.

Advantage is the improved access to the necrotic femoral head segment & the avoidance of direct iatrogenic cartilage damage

Disadvantage is the creation of a cortical defect in the femoral neck, which raises the risk of fracture

………

...3)...ARTICULAR SURFACE WINDOW(TRAPDOOR TECHNIQUE)

The 3rd method of accessing the necrotic segment of the femoral head is known as the “Trapdoor” approach

With this method, the hip is surgically dislocated using a technique aimed at preserving the blood supply to the femoral head & neck

Once exposed, a “trapdoor” window is made in the femoral head cartilage to access the diseased subchondral bone

When combined with a bone grafting procedure, refered as the “Trapdoor” Procedure

Advantage : Exposure allows a direct evaluation of the cartilage surface &

underlying diseased femoral head segment & allows for

precise bone graft placement.

Disadvantage : Demanding technical nature

Iatrogenic cartilage damage & osteonecrosis

Surgical dislocation

………

BONE GRAFT (TYPES)1. NONVASCULARISED (FIBULA STRUT)

Nonvascularized Grafts

Nonvascularized cortical bone grafts are typically prepared as several struts that provide structural support under the articular surface within the evacuated segment

This construct is often augmented with cancellous bone graft in an effort to improve its osteoconductive and/or osteoinductive properties

2. VASCULARISED (MPBG)

1.Local pedicled grafts,

which do not require

microvascular reanastomosis

eg :Muscle-pedicle bone grafts

Vascularized pedicle bone grafts

……

2. Free vascularized grafts,

which require

a microvascular reanastomosis.

eg: Free vascularized fibula graft

Baksi et al (1991)

Results in treating hips with a variety of muscle-pedicle

bone grafts

The preferred techniques were the tensor fascia lata-iliac crest graft

anteriorly & the quadratus femoris posteriorly

PRXIMAL FEMORAL OSTEOTOMIES

The main rationale proposed for the efficacy of osteotomies is thebiomechanical effect of moving the collapsed/necrotic segment of the femoral head from the principal weight-bearing area of the hip to an area that bears less/no direct weight and to allow weight-bearing contact to now happen in an area of relatively normal bone and cartilage

Categories:-

VALGUS or VARUS osteotomies usually combined with FLEXION or EXTENSION

Transtrochanteric rotational osteotomies– ANTERIOR or POSTERIOR

VALGUS OSTEOTOMY WITH FLEXION(SCHER & JAKIM..)

when the necrotic segment

is located in the anterosuperior

part of the femoral head with

less than 20% posterior involvement.

Optimal patient population would

be those that are less than 45

years of age and are

not on steroids or chemotherapy

VALGUS OSTEOTOMY WITH EXTENSION(PAUWEL’S type ‘2’)

VARUS OSTEOTOMY WITH FLEXION(OR EXTENSION)

1. CURVED:

(Merle D’ Aubigne type)

2. MEDIAL DISPLACEMENT:

( Mc Murray type)

3. ANGULATION

( Pauwel’s ‘1’ type)

TRANSTROCHANTERIC ROTATIONAL OSTEOTOMY(SUGIOKA) ANTERIOR

TRANSTROCHANTERIC ROTATIONAL OSTEOTOMY(ATSUMI T.) POSTERIOR

HIP RESURFACING PROCEDURES Later stages of osteonecrosis (University of Pennsylvania Stage III–VI

30% femoral head involveme

Metal-on-polyethylene resurfacing yielded

unacceptably high failure rates. The

polyethylene-induced osteolysis resulting

from the mating of large metal femoral

head components with thin diameter

acetabular cups

Metal-on-Metal Bearings

Reduces the incidence of

long-term failure from

aseptic loosening & osteolysis

…….

TOTAL HIP ARTHROPLASTY

TOC for advanced osteonecrosis of the hip (University of Pennsylvania Stages IVB–VIC)

Excellent pain relief & functional improvements

More recent studies at intermediate follow up up to 10 years have demonstrated similar survivorship compared to total hip replacement for osteoarthrosis.

……

OTHER PROCEDURES

HEMIARTHROPLASTY(ENDOPROSTHESIS)

POROUS TANTALUM ROD

ARTHRODESIS

RESECTION ARTHROPLASTY

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