Avn

Avascular Necrosis of Femoral Head1 Dr Zameer Ali St Stephen’s hospital

Definition2Osteonecrosis of femoral head refers to the death of osteocytes with subsequent structural changes leading to femoral head collapse and secondary osteoarthritis of hip joint

Definition.3 Osteonecrosis is defined as an “end stage” condition of the femoral head in which there is necrosis of the bone, secondary to disruption of the blood supply and causes which are still unknown.

4 The death of cell components of bone & bone marrow from repeated interruptions or a single massive interruption of the blood supply to the bone.

5AVN may involve all or part of head

The Problem.Commonly affects young patients.Need to alter the life style and leisure activity.Accounts for 18 % of all total hip replacements. 7

875% of cases are between 30 to 70 years of ageMale: female ratio 4:1Bilateral involvement is seen in 50 % of cases

History9Freund in 1926 gave detailed description of Osteonecrosis Chandler in 1948 termed disorder as "coronary disease of hip” which accounts for eponym Chandlers disease

.10Chandler in 1948 referred this condition as coronary artery disease of hip which even after 50 years correctly describes this condition Aseptic necrosis was initially used to distinguish this condition from infections

113)Glimser and Kenzora in 1979 analyzed the radiographic changes which accompany AVNFicat in 1985 states that this condition resulted from blockage of the osseus microcirculation with intramedullary stasis and increased pressure .

Anatomy12Head 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.

Smooth weight-bearing surfaces

FemurVascular supply of femoral head14profunda femoris arteryArtery to ligamentum teresMedial circumflex femoral arteryLateral circumflex femoral arteryLateral epiphyseal group

Blood supply of the Head.3 main sources. Ascending cervical branches Metaphyseal blood vessels Artery of ligamentum teres.15

Vascular supply of femoral head 16Crook described Extra capsular arterial ring located at base of femoral neck Ascending cervical branches or retinacular arteries run on surface of femoral neck Arteries of round ligament or ligament teres.

18The proximity of retinacular arteries to bone put them at risk of injury in any fracture of femoral neck.The ascending cervical arteries puts them at risk for injury in any fracture of femoral neck

194 groups of ascending cervical arteries1. Anterior2. Posterior 3. Medial 4. Lateral Of these lateral group provides most of blood supply to femoral head and neck

20The adult pattern of femoral head vascularity usually becomes established with closure of growth plate at approximately 18 years of age

In neonate21Three groups of vessels are identified superior retinacular group or lateral epiphyseal group inferior metaphyseal group foveal or medial epiphyseal groupAll 3 groups anastomose with each other

Between 4 years to 7 years22The importance of lateral epiphyseal is established as metaphyseal and foveal vessels decrease in extent

After 8 years of age 23Open growth plate represents an effective barrier preventing anastomoses between vessels of head and neck.An increased contribution of foveal vessels

24During adolescence increased number of inferior metaphyseal vessel is recognizedAs the growth plate closes the adult pattern appears with anastomosis between 3 arterial systems

Causes.25Traumatic causesNon Traumatic causes

Traumatic26Fractures of femoral neck. 15% - 50%Dislocation of the hip. 10% - 25%

27Currently accepted term is Osteonecrosis which describes main common feature of this condition THE BONE DEATH

Non Traumatic28Idiopathic.Chronic alcoholism.Steroid intake.Sickle cell disease.Gauchers disease.Caissons disease.Malignancies.Drug induced

Risk factors29Gauchers diseaseRadiation induced Liver disease abnormal coagulation factor synthesis

Risk factors30Traumatic Osteonecrosis usually involves dislocation of hip or fracture femoral neck .52% of hips unreduced for more than 12 hours developed AVN22 % of hips developed AVN if reduced within 12 hoursFemoral neck fractures associated with 15 – 50 % incidence of AVN

Risk factors31Alcoholism: Accounts for 10 – 40 % of incidence of AVN. Risk of development of AVN is increased with cumulative doses of alcoholDrug induced: the association between corticosteroid therapy,cushings syndrome, and Osteonecrosis is well established

Risk factors32Collagen diseases rheumatoid arthritis,SLE have been associated with AVNRadiation causes obliterative endarteritis and cellular death.Gout sodium urate crystals enhance clotting by activating haegmen factor in intrinsic coagulation system

Pathogenesis.33Other than traumatic causes, the mechanism of necrosis is still “obscure”.Coaugulation defect.Genetic predisposition.Emboli formation.“ IDIOPATHIC ”

Pathogenesis34The bony compartment function essentially as closed compartment within which one element can expand only at expense of othersA unifying concept of pathogenesis of AVN emphasizes the central role of vascular occlusion and ischaemia leading to osteocyte necrosis

35Pathogenesis of steroid or alcohol induced AVN is not well understood ,but it is suggested that embolic fat and attendant thrombi occlude microcirculation.Lipocyte hypertrophy and subchondral lipid accumulation may cause extra vascular intraosseus compression.

36It matters little whether the initiating factor was capillary occlusion (as in sickle cell disease) venous occlusion (as suggested for perthes disease) or intramedullary tamponade in Gauchers disease, the end result is diffuse ischaemia involving all the elements

Biological sequence of repair37

Biological sequence of repair38 loss of cell viability (cell necrosis)Invasion of marrow spaces of dead bone by proliferating capillaries and cellsDifferentiation of mesenchymal cells to osteoblast synthesis of new bone.Early remodelling of repaired cancellous bone

Biological sequence of repair39Late internal remodelingResorption of subchondral bone and invasion of articular cartilage

Biological sequence of repair40To conclude this reparative process is self limiting and incompletely replaces dead bone with living bone. In subchondral bone ,bone formation occurs at slower rate than does resorption resulting in net removal of bone, loss of structural integerity, subchondral fractures and collapse

Clinical features.Pain. - Dull boring . - Progressive. - Worse at night -Limp while walking. - Restricted hip motion. - Unable to sit cross legged.41

symptoms42Clinical manifestation of bone ischaemia and infarction are minimal and non specific and depend on etiology.

symptoms43Initially vague and non specific.Localized or referred pain in buttocks,thighor kneeGradual increase in intensity of pain and decreased motion especially rotation and abductionOver several years results in limping gait

symptoms44Initial pain is commonly misinterpreted as radiating pain from lumbar spine.

Diagnosis45Asymptomatic during the early stages.Become symptomatic when significant collapse of the head has occurred.

Management protocol46Early diagnosisRadiological evaluationRule out other causesMRIQuantificationTreatment algorithm

Diagnosis47Imaging Routine radiographsScintigraphyCT scan.MRI.LASER Doppler flometry.

Early Diagnosis – suspicion ?48High degree of suspicion in a patient C/o anterior HIP pain, Especially with:- H/o Cortisone – Skin, Eye, Liver, Asthma, RA, Weight gain H/o Alcohol abuse Traumatic - # N/F, D/ of F, # AcetabulumHemoglobinopathy – Sickle / Myelo-infiltrating

Other causes49PregnancyRenal DiseasesRadiationGout / Collagen disorderGaucher’diseaseDysbarism Idiopathic

Imaging50Routine radiographs are usually first step in trying to make diagnosis.High quality films taken at least two views 90 degree apart are critical to initial evaluation

Radiology- sequential Changes51Crescent SignOsteoporosisSclerosisCystic changesLoss of spherical bearing dome Partial collapse of headSecondary Osteoarthritis

Xrays.52Xray changes are “stage dependent”Early stages : normal film.Subsequently there occurs increased “ DENSITY “ of the femoral head.Crescent sign.Femoral head collapse.Osteoarthritis of the hip.B/l involvement of femoral head with cystic changes/sclerosis seen

X RAY changes53Sclerosis /subchondral cysts

X RAY changes54Crescent changes Flattening of head of femur

Bilateral Cystic changes With patchy sclerosis55

Scintigraphy 56Radionuclide scintigraphy is more sensitive for osteonecrosis than standard radiographs and will reveal changes when standardd radiographs are normal

scintigram57The hall mark of vascularity is photopenic effect on scintigram RESULTSDecreased uptake by necrotic bone Increased uptake by remodeling boneNormal uptake by normal bone

Bone scan.Technetium 99 bone scan reveals decreased uptake.It is effective only if done in early stages.During late phase there are very variable resuts.No relationship b/w scan appearance and the function of the hip.58

MRI59MRI is most sensitive technique for early diagnosis in Osteonecrosis Can diagnose AVN as early as 48 hours The classical finding of AVN is decrease in the normally high intensity signal of marrow of femoral head

MRI.60Can detect early stages.Allows to determine exact stage of disease.Tells exactly the extent of damage.Useful in determining the efficacy of treatment.

MRIGeographical area of decreased marrow signal. Necrotic areaSurrounded by zone of “low signal” band. Ischaemic bone.61

MRI - Findings64Bone Marrow edemaDouble Line – Head in Head sign Crescent signCollapseJoint effusionInvolvement of actabulumStatus of other hipMarrow infiltrating disease

LASER Doppler Flometry65Laser Doppler flometry is technique at measuring blood cell influx in a capillary bed The magnitude and frequency of Doppler shift is proportionate to the velocity and concentration of red cells under probe head

Sequence of radiological events in AVN66Fragmentation : radiolucent clefts may be seen due to necrosis of involved bone The entire epiphysis may be absentMottled trabecular : pattern: scrutiny of trabecular traversing the ischaemic bone demonstrates thickened irregular pattern

67Sclerosis : with revascularisation new bone is deposited around dead bone resulting in increased bone density Subchondral cysts : patchy well circumscribed rarefactions immediately beneath the articular cortex are frequent

68These cysts are usually seen in region of greatest articular stress and are identical to those found in degenerative joint diseaseCollapse of articular cortex this generally occurs at the region of maximal stress of involved cortex and represents a localised impaction fracture of weakened bone

Fragmentation69Radiolucent clefts seen traversing bone

Sclerosis/subchondral cysts70Sclerosis subchondral cysts

Collapse of articular surface71Collapse of articular surface

Staging73Several staging systems have been described.The staging system reported by sternbergs and colleagues is similar to that outlined by Marcus,Ficat and ArletSternbergs classification allows physician to quantify extent of involvement of femoral head in both early and late stages

Staging / Grading --- too many74Ficat RadiologicalSteinberg QuantificationEnneking's Stages of OsteonecrosisMarcus and Enneking SystemJapanese criteria LocationSugioka RadiologicalUniversity Of Pennsylvania SystemAssociation Research Classification Osseous Committee (ARCO)-- Combination

Fi Stages of Bone Necrosis75Ficats radiological staging of osteonecrosis of femoral head

76Ficat Stages of Bone NecrosisStage Clinical Features Radiographs0 Preclinical 0 01Preradiographic + 2 mild density changes in femoral head2aPrecollapsemild Diffuse Porosis, Sclerosis,or cyst2bTransition: Flattening, Crescent Sign 3 Collapse mild/moder Broken Contour of Head Certain Sequestrum, Joint Space Normal 4 Osteoarthritismod/severe Flattened Contour Decreased Joint Space Collapse of Head

Stage 177Symptoms – none / mildXrays are normal.Bone scan reveals a “cold spot”.

Stage 22ASymptoms are mild.Xray shows increased density. subchondral cysts joint line maintained. normal head contour. Bone scan reveals increased uptake.78

2BCrescent sign.Flattening of the head.79

Stage 3Moderate symptoms.Loss of shapeSubchondral collapse81

Stage 4Severe symptoms.Joint space narrowing.OA changes in acetabulum.82

Marcus radiological staging of AVN83Stage I normal or equivocal radiographStage II sclerotic or cystic lesionStage III crescent signStage IV step off in outline of bone Stage V narrowing of joint space with degenerative changes

Shimizu’s classification.1995.84 Grade 1 lesion.A lesion involving medial 1/3 rd of weight bearing surface of the head.In coronal plane ,these lesions occupy < 1/3 of the head.These lesions rarely go into collapse.

Grade 2.85Lesions involve 1/3 – 2/3 of the weight bearing surface of the head.Involve ½ of the head in coronal plane.Such lesions collapse in 30% of patients.

Grade 3.86Lesions involving 2/3 of the weight bearing surface of the femoral head.Such lesions collapse in 70% of patients in around 3 years.

Treatment87Conservative /non surgical treatmentCore decompressionBone graftingCancellous autogenic/allogenic bone graftOsteochondral graftMuscle pedicle bone graftFree vascularized graft

Treatment88Electric stimulationOsteotomyJoint reconstruction Cup arthoplastySurface arthoplastyHemiarthoplastyTotal joint arthoplasty

89The natural history of osteonecrosis in its early stage, before subchondral collapse, is still unclear, but evidence suggests that the rate of progression is high, especially in symptomatic patients.

90Once subchondral collapse occurs and joint space is lost, progressive osteoarthritis generally is considered inevitable.

91 Many studies have reported an extremely poor prognosis, with a rate of femoral head collapse of more than 85% at 2 years in symptomatic patients (stage I or II disease)

92No treatment method has proved to be completely effective in arresting the disease process before subchondral collapse or in slowing the progression of femoral head destruction and osteoarthritis after subchondral collapse

93 The rate and course of progression of the disease are unpredictable, and the radiographic picture may not correlate with the clinical symptoms; some patients maintain tolerable function for an extended period after femoral head collapse.

94Conservative treatment, such as crutch ambulation or bed rest, generally is ineffective. However, symptomatic patients that may benefit from a head-preserving technique should be placed on crutches until surgical treatment is carried out to prevent collapse in the interim

Management.95Grade 1 lesions - Continuous supervision to detect any changes. - Symptomatic treatment of pain.

Grade 1 lesions96Conservative treatment such as observation ,AnalgesicsLimited weight bearing may be successful in minimal affected cases

Core decompression Grade 2 lesions97Ficart and Hungerford have popularized the technique of core decompression of femoral headRationale is that removing necrotic bone decompresses the rigid osseous chamber, thereby improving blood flow and preventing additional ischaemic events

98The theoretical advantage of core decompression is based on the belief that the procedure relieves intraosseous pressure caused by venous congestion, thereby allowing improved vascularity and possibly slowing the progression of the disease

99several authors noted that the results of core decompression are better than those of nonoperative treatment.

100Several reports noted that the earlier the stage of the disease, the better the results with core decompression.. For more advanced Ficat stages (IIB or III) the results of core decompression are much less predictable, so alternative treatment methods should be explored.

101Review of the literature currently supports the use of core decompression for the treatment of Ficat stages I and IIA small central lesions in young, nonobese patients who are not taking steroids. This surgery is relatively simple to perform and has a very low complication rate

102 The surgical field for subsequent total hip arthroplasty, if needed, is not substantially altered

Bone grafting 103Phemister introduced concept of using cortical strut graft in core decompression channelThe accurate placement of graft within lesion and under subchondral bone is important

104 Structural bone grafting techniques after core decompression have been described using cortical bone, cancellous bone, vascularized bone graft, and debridement of necrotic bone from the femoral head.

105Insertion of cancellous bone into channel speeds up reossification by osteoinductive and osteoconductive properties of bone graft.Meyers procedure used muscle pedicle bone graft based on quardratus femoris muscle with cancellous bone chips

106Baksi employed multiple drilling and muscle pedicle grafting using tensor fascia lata muscle anteriorly

107 Advances in microsurgical techniques made it possible to preserve the intrinsic vascularity of bone graft, several authors independently proposed implanting a vascularised bone graft into the core of the femoral head.

Vascular fibular strut grafting108

109 The rationale for vascularized bone grafting is based on four aspects of the operation and postoperative care: (1) decompression of the femoral head, which may interrupt the cycle of ischemia and intraosseous hypertension that is believed to contribute to the disease; (2) excision of the sequestrum, which might inhibit revascularization of the femoral head

110(3) filling of the defect that is created with osteoinductive cancellous graft and a viable cortical strut to support the subchondral surface and to enhance the revascularization process (4) protection of the healing construct by a period of limited weight-bearing.

Advantages111Advantages of free vascularized fibular grafting compared with total hip arthroplasty: (1) the presence of a healed femoral head may allow more activity, (2) there is no increased risk associated with the presence of a foreign body,

112(3) if performed before the development of a subchondral fracture, the procedure offers the possibility of survival of a viable femoral head for the life of the patient, and (4) if total hip arthroplasty is ultimately needed, it is much simpler to perform than is a revision arthroplasty after a failed total hip arthroplasty.

Disadvantages113Disadvantages include a longer recovery period and less uniform and less complete relief of pain than after total hip arthroplasty.

Strut Fibular Grafting114Decompression of Femoral Head

Grafting of defect with cancellous graft

Viable cortical Bone strut to support subchondral bone.

Age 20 – 50, stage 2Summaries of cases with head preservation by free fibula grafting115

Grade 2.If detected before the collapse Core decompression and fibular grafting. Realignment osteotomies.116

Electrical stimulation120Electrical stimulation has been advocated for AVN because its histological appearance is similar to that of non unionCurrently used in combination with head salvage procedures

osteotomies121 Various proximal femoral osteotomies have been developed for the treatment of osteonecrosis with the intent to move the involved necrotic segment of the femoral head from the principal weight-bearing area. These procedures have achieved best results for small- or medium-sized lesions (less than 30% femoral head involvement) in young patients in whom it is optimal to delay a total hip arthroplasty.

osteotomies122Various osteotomies have been described Varus osteotomyValgus derotation osteotomy Rotation osteotomy aid the loss of structural integrity and collapse by redirecting the forces on femoral head

123Intertrochanteric osteotomy may be considered for the treatment of stage II or III osteonecrosis of the femoral head in which less than 30% of the femoral head is involved. Plain films and MRI can establish the extent of femoral head involvement and can determine if a satisfactory area of live bone is present under unaffected cartilage in the femoral head and whether this area can be rotated into a position of weight-bearing.

124Valgus flexion osteotomy is described by wagner when lesion is anterolateral and total angle of necrosis is 200 degree and patient is young and activeIf necrotic lesion is central varus extension osteotomy is recommended

Transtrochanteric Rotational Osteotomy125In 1978 Sugioka described a transtrochanteric rotational osteotomy of the femoral head for idiopathic osteonecrosis

126The rationale of the procedure is to reposition the necrotic anterosuperior part of the femoral head to a non-weight-bearing locale. The femoral head and neck segment is rotated anteriorly around its longitudinal axis so that the weight-bearing force is transmitted to what was previously the posterior articular surface of the femoral head, which is not involved in the ischemic process

127Sugioka emphasized the need for a preoperative lateral roentgenogram of the femoral head while the patient is supine and the hip is flexed exactly 90 degrees, abducted 45 degrees, and in neutral rotation. The intact area of the posterior part of the femoral head on this lateral view should be greater than one third of the total articular surface of the head to ensure the best result after his osteotomy

Post op regimen128Skin traction of 2 kg is applied continuously for the first week and for an additional 2 weeks at night only. As soon as pain tolerance allows, quadriceps setting is begun. Active range-of-motion exercises of the hip are begun at 10 to 14 days.

129Walking exercises in a pool generally are allowed at 5 to 6 weeks. Partial weight-bearing with crutches is begun at 8 weeks, and the use of crutches is recommended for 6 months after surgery. If the necrotic area of the femoral head is extensive or if involvement is bilateral, crutch use is encouraged for up to 1 year postoperatively.

Replacement - options130HemiarthroplastyBipolar arthroplastySurface replacement arthroplasty.Newer material for THR ceramic on ceramicNon cemented / cemented THR

Birmingham Surface replacement131Surface replacement has some advantages over THR because it preserves femoral head and neck and allows future THR if necessaryEffective in cases when femoral head is not involved entirely

The BHR*SystemHealthy hipCutsImplant componentsImplanted

OverviewNamed for Birmingham, England, where the device’s creators practice medicineUsed globally since 1997; More than 65,000 implantedIn an international study of 1,626 hips, 99.5% of patients were “Pleased” or “Extremely Pleased” with the results of the BIRMINGHAM HIP Resurfacing (BHR) System.

134Many failures of resurfacing hemiarthroplasty have been attributed to acetabular cartilage wear. Attention should be given to the quality of the acetabular cartilage on preoperative roentgenographic studies.Intraoperative assessment of the acetabular cartilage is mandatory before implanting a resurfacing hemiarthroplasty prosthesis. If the quality of the acetabular cartilage is in question, a total hip arthroplasty should be performed.

135Resurfacing hemiarthroplasty is an attractive alternative for young patients with advanced osteonecrosis because very little bone is sacrificed. Should failure occur, conversion to total joint arthroplasty is nearly as simple as primary total hip surgery. Clearly, the results of primary total hip arthroplasty for osteonecrosis are better than resurfacing hemiarthroplasty. However, this procedure can delay total joint arthroplasty and buy valuable time in a young patient.

Head sizeClosely matches the size of natural femoral headLarger than the head of a total hip replacementLarger head means a reduced chance of dislocation after surgery—a leading cause of revision surgery1-3% of total hips dislocate over the lifetime of the implant0.3% of BHR* implants dislocated in the first 5 years after surgery (in a study of 2,385 hips)Healthy headBHR headTotal hip head

Who is the typical candidate for BHR*System?Adults under age 60 for whom total hip replacement may not be appropriate due to an increased level of physical activityActive adults over age 60 may be candidates, depending on their bone quality

Conventional hip replacementHealthy hipCutsImplant componentsImplanted

The key benefitsHead sizeAdvanced bearing surfaceBone conservation

Hip with osteoarthritisBone cuts fora traditionalhip replacementBone conservationPreserves your natural femoral neckNeck length and angle determine accurate leg lengthWith the BHR*System, you retain original equipment; with a total hip, your femoral neck is replaced by the implantBone cuts forBHR System

“Minimally Invasive.”Soft TissueNo. Incision length of 6 to 8 inchesBoneYes. Preserves your body’s natural bone structure; It resurfaces rather than replacesConserved bone

Conventional vs. the BHR*SystemTotal hip cutsBHR System cuts

Bone conservation (cont.)Revises to a primaryIf you need “revision” surgery, you don’t get a revision implantThe follow-up procedure would be the same total hip replacement you would otherwise have received

Total Hip Arthroplasty and Bipolar Hemiarthroplasty. 144Most series that have examined both unipolar and bipolar hemiarthroplasty for the treatment of osteonecrosis have reported uniformly poor results.

THR145Patient aged 50 & more Advance osteoarthritis and reduction of joint space.Radiation necrosis Result less than Ideal. – necrotic bonePoor in Sickle cell disease.Cementless are superior over cemented THR

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