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  1. 1. Avascular Necrosis of Femoral Head<br />1<br /> Dr Zameer Ali <br />St Stephen’s hospital<br />
  2. 2. Definition<br />2<br />Osteonecrosis of femoral head refers to the death of osteocytes with subsequent structural changes leading to femoral head collapse and secondary osteoarthritis of hip joint<br />
  3. 3. Definition.<br />3<br /> 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.<br />
  4. 4. 4<br /> The death of cell components of bone & bone marrow from repeated interruptions or a single massive interruption of the blood supply to the bone.<br />
  5. 5. 5<br />AVN may involve all or part of head<br />
  6. 6. 6<br />
  7. 7. The Problem.<br />Commonly affects young patients.<br />Need to alter the life style and leisure activity.<br />Accounts for 18 % of all total hip replacements. <br />7<br />
  8. 8. 8<br />75% of cases are between 30 to 70 years of age<br />Male: female ratio 4:1<br />Bilateral involvement is seen in 50 % of cases<br />
  9. 9. History<br />9<br />Freund in 1926 gave detailed description of Osteonecrosis <br />Chandler in 1948 termed disorder as "coronary disease of hip” which accounts for eponym Chandlers disease<br />
  10. 10. .<br />10<br />Chandler in 1948 referred this condition as coronary artery disease of hip which even after 50 years correctly describes this condition <br />Aseptic necrosis was initially used to distinguish this condition from infections <br />
  11. 11. 11<br />3)Glimser and Kenzora in 1979 analyzed the radiographic changes which accompany AVN<br />Ficat in 1985 states that this condition resulted from blockage of the osseus microcirculation with intramedullary stasis and increased pressure .<br />
  12. 12. Anatomy<br />12<br />Head of femur forms about 2/3rd of sphere and articulates with acetabulum of hip joint <br />Connecting two trochanters anteriorly forms intertrochanteric line and connecting two trochanters posteriorly forms intertrochanteric crest.<br />
  13. 13. 13<br /><ul><li>Socket
  14. 14. Ball
  15. 15. Femoral neck
  16. 16. Smooth weight-bearing surfaces
  17. 17. Smooth cartilage
  18. 18. Femur</li></li></ul><li>Vascular supply of femoral head<br />14<br />profunda femoris artery<br />Artery to ligamentum teres<br />Medial circumflex femoral artery<br />Lateral circumflex femoral artery<br />Lateral epiphyseal group<br />
  19. 19. Blood supply of the Head.<br />3 main sources.<br /> Ascending cervical branches<br /> Metaphyseal <br /> blood vessels<br /> Artery of <br /> ligamentum teres.<br />15<br />
  20. 20. Vascular supply of femoral head <br />16<br />Crook described Extra capsular arterial ring located at base of femoral neck <br />Ascending cervical branches or retinacular arteries run on surface of femoral neck <br />Arteries of round ligament or ligament teres.<br />
  21. 21. 17<br />
  22. 22. 18<br />The proximity of retinacular arteries to bone put them at risk of injury in any fracture of femoral neck.<br />The ascending cervical arteries puts them at risk for injury in any fracture of femoral neck <br />
  23. 23. 19<br />4 groups of ascending cervical arteries<br />1. Anterior<br />2. Posterior <br />3. Medial <br />4. Lateral <br />Of these lateral group provides most of blood supply to femoral head and neck<br />
  24. 24. 20<br />The adult pattern of femoral head vascularity usually becomes established with closure of growth plate at approximately 18 years of age <br />
  25. 25. In neonate<br />21<br />Three groups of vessels are identified <br /> superior retinacular group or lateral epiphyseal group<br /> inferior metaphyseal group <br /> foveal or medial epiphyseal group<br />All 3 groups anastomose with each other<br />
  26. 26. Between 4 years to 7 years<br />22<br />The importance of lateral epiphyseal is established as metaphyseal and foveal vessels decrease in extent <br />
  27. 27. After 8 years of age <br />23<br />Open growth plate represents an effective barrier preventing anastomoses between vessels of head and neck.<br />An increased contribution of foveal vessels<br />
  28. 28. 24<br />During adolescence increased number of inferior metaphyseal vessel is recognized<br />As the growth plate closes the adult pattern appears with anastomosis between 3 arterial systems<br />
  29. 29. Causes.<br />25<br />Traumatic causes<br />Non Traumatic causes<br />
  30. 30. Traumatic<br />26<br />Fractures of femoral neck. 15% - 50%<br />Dislocation of the hip. 10% - 25%<br />
  31. 31. 27<br />Currently accepted term is Osteonecrosis which describes main common feature of this condition THE BONE DEATH<br />
  32. 32. Non Traumatic<br />28<br />Idiopathic.<br />Chronic alcoholism.<br />Steroid intake.<br />Sickle cell disease.<br />Gauchers disease.<br />Caissons disease.<br />Malignancies.<br />Drug induced<br />
  33. 33. Risk factors<br />29<br />Gauchers disease<br />Radiation induced <br />Liver disease abnormal coagulation factor synthesis<br />
  34. 34. Risk factors<br />30<br />Traumatic Osteonecrosis usually involves dislocation of hip or fracture femoral neck .<br />52% of hips unreduced for more than 12 hours developed AVN<br />22 % of hips developed AVN if reduced within 12 hours<br />Femoral neck fractures associated with 15 – 50 % incidence of AVN <br />
  35. 35. Risk factors<br />31<br />Alcoholism: Accounts for 10 – 40 % of incidence of AVN. Risk of development of AVN is increased with cumulative doses of alcohol<br />Drug induced: the association between corticosteroid therapy,cushings syndrome, and Osteonecrosis is well established<br />
  36. 36. Risk factors<br />32<br />Collagen diseases rheumatoid arthritis,SLE have been associated with AVN<br />Radiation causes obliterative endarteritis and cellular death.<br />Gout sodium urate crystals enhance clotting by activating haegmen factor in intrinsic coagulation system<br />
  37. 37. Pathogenesis.<br />33<br />Other than traumatic causes, the mechanism of necrosis is still “obscure”.<br />Coaugulation defect.<br />Genetic predisposition.<br />Emboli formation.<br />“ IDIOPATHIC ”<br />
  38. 38. Pathogenesis<br />34<br />The bony compartment function essentially as closed compartment within which one element can expand only at expense of others<br />A unifying concept of pathogenesis of AVN emphasizes the central role of vascular occlusion and ischaemia leading to osteocyte necrosis<br />
  39. 39. 35<br />Pathogenesis of steroid or alcohol induced AVN is not well understood ,but it is suggested that embolic fat and attendant thrombi occlude microcirculation.<br />Lipocyte hypertrophy and subchondral lipid accumulation may cause extra vascular intraosseus compression. <br />
  40. 40. 36<br />It 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 <br />
  41. 41. Biological sequence of repair<br />37<br />
  42. 42. Biological sequence of repair<br />38<br /> loss of cell viability (cell necrosis)<br />Invasion of marrow spaces of dead bone by proliferating capillaries and cells<br />Differentiation of mesenchymal cells to osteoblast synthesis of new bone.<br />Early remodelling of repaired cancellous bone <br />
  43. 43. Biological sequence of repair<br />39<br />Late internal remodeling<br />Resorption of subchondral bone and invasion of articular cartilage<br />
  44. 44. Biological sequence of repair<br />40<br />To conclude this reparative process is self limiting and incompletely replaces dead bone with living bone.<br /> In subchondral bone ,bone formation occurs at slower rate than does resorption resulting in net removal of bone,<br /> loss of structural integerity, subchondral fractures and collapse<br />
  45. 45. Clinical features.<br />Pain.<br /> - Dull boring .<br /> - Progressive.<br /> - Worse at night<br /> -Limp while walking.<br /> - Restricted hip <br /> motion.<br /> - Unable to sit cross <br /> legged.<br />41<br />
  46. 46. symptoms<br />42<br />Clinical manifestation of bone ischaemia and infarction are minimal and non specific and depend on etiology.<br />
  47. 47. symptoms<br />43<br />Initially vague and non specific.<br />Localized or referred pain in buttocks,thighor knee<br />Gradual increase in intensity of pain and decreased motion especially rotation and abduction<br />Over several years results in limping gait<br />
  48. 48. symptoms<br />44<br />Initial pain is commonly misinterpreted as radiating pain from lumbar spine.<br />
  49. 49. Diagnosis<br />45<br />Asymptomatic during the early stages.<br />Become symptomatic when significant collapse of the head has occurred.<br />
  50. 50. Management protocol<br />46<br />Early diagnosis<br />Radiological evaluation<br />Rule out other causes<br />MRI<br />Quantification<br />Treatment algorithm<br />
  51. 51. Diagnosis<br />47<br />Imaging <br />Routine radiographs<br />Scintigraphy<br />CT scan.<br />MRI.<br />LASER Doppler flometry.<br />
  52. 52. Early Diagnosis – suspicion ?<br />48<br />High degree of suspicion in a patient C/o anterior HIP pain, Especially with:-<br /> H/o Cortisone – Skin, Eye, Liver, Asthma,<br /> RA, Weight gain<br /> H/o Alcohol abuse<br /> Traumatic - # N/F, D/ of F, # Acetabulum<br />Hemoglobinopathy – Sickle / Myelo-infiltrating <br />
  53. 53. Other causes<br />49<br />Pregnancy<br />Renal Diseases<br />Radiation<br />Gout / Collagen disorder<br />Gaucher’disease<br />Dysbarism <br />Idiopathic<br />
  54. 54. Imaging<br />50<br />Routine radiographs are usually first step in trying to make diagnosis.<br />High quality films taken at least two views 90 degree apart are critical to initial evaluation<br />
  55. 55. Radiology- sequential Changes<br />51<br />Crescent Sign<br />Osteoporosis<br />Sclerosis<br />Cystic changes<br />Loss of spherical bearing dome<br /> Partial collapse of head<br />Secondary Osteoarthritis<br />
  56. 56. Xrays.<br />52<br /><ul><li>Xray changes are “stage dependent”</li></ul>Early stages : normal film.<br />Subsequently there occurs increased “ DENSITY “ of the femoral head.<br />Crescent sign.<br />Femoral head collapse.<br />Osteoarthritis of the hip.<br />B/l involvement of femoral head with cystic changes/sclerosis seen<br />
  57. 57. X RAY changes<br />53<br />Sclerosis /subchondral cysts<br />
  58. 58. X RAY changes<br />54<br />Crescent changes <br />Flattening of head of femur<br />
  59. 59. Bilateral Cystic changes<br /> With patchy sclerosis<br />55<br />
  60. 60. Scintigraphy <br />56<br />Radionuclide scintigraphy is more sensitive for osteonecrosis than standard radiographs and will reveal changes when standardd radiographs are normal<br />
  61. 61. scintigram<br />57<br />The hall mark of vascularity is photopenic effect on scintigram<br /> RESULTS<br />Decreased uptake by necrotic bone <br />Increased uptake by remodeling bone<br />Normal uptake by normal bone<br />
  62. 62. Bone scan.<br />Technetium 99 bone scan reveals decreased uptake.<br />It is effective only if done in early stages.<br />During late phase there are very variable resuts.<br />No relationship b/w scan appearance and the function of the hip.<br />58<br />
  63. 63. MRI<br />59<br />MRI is most sensitive technique for early diagnosis in Osteonecrosis <br />Can diagnose AVN as early as 48 hours <br />The classical finding of AVN is decrease in the normally high intensity signal of marrow of femoral head <br />
  64. 64. MRI.<br />60<br />Can detect early stages.<br />Allows to determine exact stage of disease.<br />Tells exactly the extent of damage.<br />Useful in determining the efficacy of treatment.<br />
  65. 65. MRI<br />Geographical area of decreased marrow signal. Necrotic area<br />Surrounded by zone of “low signal” band. Ischaemic bone.<br />61<br />
  66. 66. MRI Findings.<br />62<br />
  67. 67. 63<br />
  68. 68. MRI - Findings<br />64<br />Bone Marrow edema<br />Double Line – Head in Head sign <br />Crescent sign<br />Collapse<br />Joint effusion<br />Involvement of actabulum<br />Status of other hip<br />Marrow infiltrating disease<br />
  69. 69. LASER Doppler Flometry<br />65<br />Laser Doppler flometry is technique at measuring blood cell influx in a capillary bed <br />The magnitude and frequency of Doppler shift is proportionate to the velocity and concentration of red cells under probe head<br />
  70. 70. Sequence of radiological events in AVN<br />66<br />Fragmentation : radiolucent clefts may be seen due to necrosis of involved bone <br />The entire epiphysis may be absent<br />Mottled trabecular : pattern: scrutiny of trabecular traversing the ischaemic bone demonstrates thickened irregular pattern<br />
  71. 71. 67<br />Sclerosis : with revascularisation new bone is deposited around dead bone resulting in increased bone density <br />Subchondral cysts : patchy well circumscribed rarefactions immediately beneath the articular cortex are frequent<br />
  72. 72. 68<br />These cysts are usually seen in region of greatest articular stress and are identical to those found in degenerative joint disease<br />Collapse of articular cortex this generally occurs at the region of maximal stress of involved cortex and represents a localised impaction fracture of weakened bone <br />
  73. 73. Fragmentation<br />69<br />Radiolucent clefts seen traversing bone<br />
  74. 74. Sclerosis/subchondral cysts<br />70<br />Sclerosis<br /> subchondral cysts<br />
  75. 75. Collapse of articular surface<br />71<br />Collapse of articular surface<br />
  76. 76. 72<br />
  77. 77. Staging<br />73<br />Several staging systems have been described.<br />The staging system reported by sternbergs and colleagues is similar to that outlined by Marcus,Ficat and Arlet<br />Sternbergs classification allows physician to quantify extent of involvement of femoral head in both early and late stages<br />
  78. 78. Staging / Grading --- too many<br />74<br />Ficat Radiological<br />Steinberg Quantification<br />Enneking's Stages of Osteonecrosis<br />Marcus and Enneking System<br />Japanese criteria Location<br />Sugioka Radiological<br />University Of Pennsylvania System<br />Association Research Classification Osseous Committee (ARCO)-- Combination<br />
  79. 79. Fi Stages of Bone Necrosis<br />75<br />Ficats radiological staging of osteonecrosis of femoral head <br />
  80. 80. 76<br />Ficat Stages of Bone Necrosis<br />Stage Clinical Features Radiographs<br />0 Preclinical 0 0<br />1Preradiographic + <br />2 mild density changes in femoral head<br />2aPrecollapsemild Diffuse Porosis, Sclerosis,or cyst<br />2bTransition: Flattening, Crescent Sign <br />3 Collapse mild/moder Broken Contour of Head Certain Sequestrum, Joint Space Normal <br />4 Osteoarthritismod/severe Flattened Contour Decreased Joint Space Collapse of Head <br />
  81. 81. Stage 1<br />77<br />Symptoms – none / mild<br />Xrays are normal.<br />Bone scan reveals a “cold spot”.<br />
  82. 82. Stage 2<br />2A<br />Symptoms are mild.<br />Xray shows increased density.<br /> subchondral cysts<br /> joint line maintained.<br /> normal head contour.<br /> Bone scan reveals increased uptake.<br />78<br />
  83. 83. 2B<br />Crescent sign.<br />Flattening of the head.<br />79<br />
  84. 84. Crescent sign.<br />80<br />
  85. 85. Stage 3<br />Moderate symptoms.<br />Loss of shape<br />Subchondral collapse<br />81<br />
  86. 86. Stage 4<br />Severe symptoms.<br />Joint space narrowing.<br />OA changes in acetabulum.<br />82<br />
  87. 87. Marcus radiological staging of AVN<br />83<br />Stage I normal or equivocal radiograph<br />Stage II sclerotic or cystic lesion<br />Stage III crescent sign<br />Stage IV step off in outline of bone <br />Stage V narrowing of joint space with degenerative changes<br />
  88. 88. Shimizu’s classification.1995.<br />84<br /> Grade 1 lesion.<br />A lesion involving medial 1/3 rd of weight bearing surface of the head.<br />In coronal plane ,these lesions occupy < 1/3 of the head.<br />These lesions rarely go into collapse.<br />
  89. 89. Grade 2.<br />85<br />Lesions involve 1/3 – 2/3 of the weight bearing surface of the head.<br />Involve ½ of the head in coronal plane.<br />Such lesions collapse in 30% of patients.<br />
  90. 90. Grade 3.<br />86<br />Lesions involving 2/3 of the weight bearing surface of the femoral head.<br />Such lesions collapse in 70% of patients in around 3 years. <br />
  91. 91. Treatment<br />87<br />Conservative /non surgical treatment<br />Core decompression<br />Bone grafting<br />Cancellous autogenic/allogenic bone graft<br />Osteochondral graft<br />Muscle pedicle bone graft<br />Free vascularized graft<br />
  92. 92. Treatment<br />88<br />Electric stimulation<br />Osteotomy<br />Joint reconstruction <br />Cup arthoplasty<br />Surface arthoplasty<br />Hemiarthoplasty<br />Total joint arthoplasty<br />
  93. 93. 89<br />The 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.<br />
  94. 94. 90<br />Once subchondral collapse occurs and joint space is lost, progressive osteoarthritis generally is considered inevitable.<br />
  95. 95. 91<br /> 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)<br />
  96. 96. 92<br />No 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<br />
  97. 97. 93<br /> 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.<br />
  98. 98. 94<br />Conservative 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<br />
  99. 99. Management.<br />95<br />Grade 1 lesions<br /> - Continuous supervision to detect any <br /> changes.<br /> - Symptomatic treatment of pain. <br />
  100. 100. Grade 1 lesions<br />96<br />Conservative treatment such as observation ,<br />Analgesics<br />Limited weight bearing may be successful in minimal affected cases<br />
  101. 101. Core decompression Grade 2 lesions<br />97<br />Ficart and Hungerford have popularized the technique of core decompression of femoral head<br />Rationale is that removing necrotic bone decompresses the rigid osseous chamber, thereby improving blood flow and preventing additional ischaemic events<br />
  102. 102. 98<br />The 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<br />
  103. 103. 99<br />several authors noted that the results of core decompression are better than those of nonoperative treatment.<br />
  104. 104. 100<br />Several reports noted that the earlier the stage of the disease, the better the results with core decompression.<br />. For more advanced Ficat stages (IIB or III) the results of core decompression are much less predictable, so alternative treatment methods should be explored.<br />
  105. 105. 101<br />Review 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<br />
  106. 106. 102<br /> The surgical field for subsequent total hip arthroplasty, if needed, is not substantially altered<br />
  107. 107. Bone grafting <br />103<br />Phemister introduced concept of using cortical strut graft in core decompression channel<br />The accurate placement of graft within lesion and under subchondral bone is important<br />
  108. 108. 104<br /> 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.<br />
  109. 109. 105<br />Insertion of cancellous bone into channel speeds up reossification by osteoinductive and osteoconductive properties of bone graft.<br />Meyers procedure used muscle pedicle bone graft based on quardratus femoris muscle with cancellous bone chips <br />
  110. 110. 106<br />Baksi employed multiple drilling and muscle pedicle grafting using tensor fascia lata muscle anteriorly<br />
  111. 111. 107<br /> 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. <br />
  112. 112. Vascular fibular strut grafting<br />108<br />
  113. 113. 109<br /> 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; <br />(2) excision of the sequestrum, which might inhibit revascularization of the femoral head<br />
  114. 114. 110<br />(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<br /> (4) protection of the healing construct by a period of limited weight-bearing. <br />
  115. 115. Advantages<br />111<br />Advantages of free vascularized fibular grafting compared with total hip arthroplasty:<br /> (1) the presence of a healed femoral head may allow more activity,<br /> (2) there is no increased risk associated with the presence of a foreign body, <br />
  116. 116. 112<br />(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<br /> (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.<br />
  117. 117. Disadvantages<br />113<br />Disadvantages include a longer recovery period and less uniform and less complete relief of pain than after total hip arthroplasty.<br />
  118. 118. Strut Fibular Grafting<br />114<br /><ul><li>Decompression of Femoral Head
  119. 119. Removal of Necrotic Bone
  120. 120. Grafting of defect with cancellous graft
  121. 121. Viable cortical Bone strut to support subchondral bone.
  122. 122. Age 20 – 50, stage 2</li></li></ul><li>Summaries of cases with head preservation by free fibula grafting<br />115<br />
  123. 123. Grade 2.<br />If detected before the collapse<br /> Core decompression and fibular grafting.<br /> Realignment osteotomies.<br />116<br />
  124. 124. Fibular strut grafting <br />117<br />
  125. 125. 118<br />
  126. 126. Pre OP<br />Post OP<br />119<br />
  127. 127. Electrical stimulation<br />120<br />Electrical stimulation has been advocated for AVN because its histological appearance is similar to that of non union<br />Currently used in combination with head salvage procedures <br />
  128. 128. osteotomies<br />121<br /> 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.<br /> 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.<br />
  129. 129. osteotomies<br />122<br />Various osteotomies have been described <br />Varus osteotomy<br />Valgus derotation osteotomy <br />Rotation osteotomy aid the loss of structural integrity and collapse by redirecting the forces on femoral head <br />
  130. 130. 123<br />Intertrochanteric 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.<br /> 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.<br />
  131. 131. 124<br />Valgus flexion osteotomy is described by wagner when lesion is anterolateral and total angle of necrosis is 200 degree and patient is young and active<br />If necrotic lesion is central varus extension osteotomy is recommended<br />
  132. 132. Transtrochanteric Rotational Osteotomy<br />125<br />In 1978 Sugioka described a transtrochanteric rotational osteotomy of the femoral head for idiopathic osteonecrosis<br />
  133. 133. 126<br />The rationale of the procedure is to reposition the necrotic anterosuperior part of the femoral head to a non-weight-bearing locale. <br />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 <br />
  134. 134. 127<br />Sugioka 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<br />
  135. 135. Post op regimen<br />128<br />Skin 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. <br />
  136. 136. 129<br />Walking exercises in a pool generally are allowed at 5 to 6 weeks.<br /> Partial weight-bearing with crutches is begun at 8 weeks, and the use of crutches is recommended for 6 months after surgery. <br />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.<br />
  137. 137. Replacement - options<br />130<br />Hemiarthroplasty<br />Bipolar arthroplasty<br />Surface replacement arthroplasty.<br />Newer material for THR ceramic on ceramic<br />Non cemented / cemented THR<br />
  138. 138. Birmingham Surface replacement<br />131<br />Surface replacement has some advantages over THR because it preserves femoral head and neck and allows future THR if necessary<br />Effective in cases when femoral head is not involved entirely<br />
  139. 139. The BHR*System<br />Healthy hip<br />Cuts<br />Implant components<br />Implanted<br />
  140. 140. Overview<br />Named for Birmingham, England, where the device’s creators practice medicine<br />Used globally since 1997; More than 65,000 implanted<br />In 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.<br />
  141. 141. 134<br />Many 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.<br />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.<br />
  142. 142. 135<br />Resurfacing 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. <br />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.<br />
  143. 143. Head size<br />Closely matches the size of natural femoral head<br />Larger than the head of a total hip replacement<br />Larger head means a reduced chance of dislocation after surgery—a leading cause of revision surgery<br />1-3% of total hips dislocate over the lifetime of the implant<br />0.3% of BHR* implants dislocated in the first 5 years after surgery (in a study of 2,385 hips)<br />Healthy head<br />BHR head<br />Total hip head<br />
  144. 144. Who is the typical candidate for BHR*System?<br />Adults under age 60 for whom total hip replacement may not be appropriate due to an increased level of physical activity<br />Active adults over age 60 may be candidates, depending on their bone quality<br />
  145. 145. Conventional hip replacement<br />Healthy hip<br />Cuts<br />Implant components<br />Implanted<br />
  146. 146. The key benefits<br />Head size<br />Advanced bearing surface<br />Bone conservation<br />
  147. 147. Hip with osteoarthritis<br />Bone cuts fora traditionalhip replacement<br />Bone conservation<br />Preserves your natural femoral neck<br />Neck length and angle determine accurate leg length<br />With the BHR*System, you retain original equipment; with a total hip, your femoral neck is replaced by the implant<br />Bone cuts forBHR System<br />
  148. 148. “Minimally Invasive.”<br />Soft Tissue<br />No. Incision length of 6 to 8 inches<br />Bone<br />Yes. Preserves your body’s natural bone structure; It resurfaces rather than replaces<br />Conserved bone<br />
  149. 149. Conventional vs. the BHR*System<br />Total hip cuts<br />BHR System cuts<br />
  150. 150. Bone conservation (cont.)<br />Revises to a primary<br />If you need “revision” surgery, you don’t get a revision implant<br />The follow-up procedure would be the same total hip replacement you would otherwise have received<br />
  151. 151. Total Hip Arthroplasty and Bipolar Hemiarthroplasty. <br />144<br />Most series that have examined both unipolar and bipolar hemiarthroplasty for the treatment of osteonecrosis have reported uniformly poor results.<br />
  152. 152. THR<br />145<br />Patient aged 50 & more <br />Advance osteoarthritis and reduction of joint space.<br />Radiation necrosis <br />Result less than Ideal. – necrotic bone<br />Poor in Sickle cell disease.<br />Cementless are superior over cemented THR<br />
  153. 153. 146<br />With new bearing surfaces becoming available, such as ceramic on ceramic, metal on metal, and highly cross-linked polyethylene, results may improve even more. The results of primary total joint replacement for osteonecrosis are now approaching those reported for osteoarthritis in aged-matched patients.<br />
  154. 154. Malakar post alcohol AVN Bil THR 1991<br />147<br />
  155. 155. THR<br />148<br />At the end stage of osteonecrosis, when severe arthritic changes are noted on both sides of the hip joint, total hip arthroplasty is one of the only viable operative options available<br />
  156. 156. 149<br /> Given the young age of most patients affected with this disease, if total joint replacement is elected, the patient should be well informed of the almost certain need for one or more revision hip replacements later in life.<br />
  157. 157. Girdle stone arthoplasty<br />150<br />Used as salvage procedure in special circumstances like painful hip with superimposed sepsis, failed THR with sepsis<br />Femur without good bone stock <br />Conversion to THR can be taken at later stage <br />
  158. 158. Hip fusion <br />151<br />Not frequently recommended because of high failure rates<br />
  159. 159. 152<br /> ….Thank you…<br />