2. Definition 2 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
3. 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. 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.
7. The Problem. Commonly affects young patients. Need to alter the life style and leisure activity. Accounts for 18 % of all total hip replacements. 7
8. 8 75% of cases are between 30 to 70 years of age Male: female ratio 4:1 Bilateral involvement is seen in 50 % of cases
9. History 9 Freund in 1926 gave detailed description of Osteonecrosis Chandler in 1948 termed disorder as "coronary disease of hip” which accounts for eponym Chandlers disease
10. . 10 Chandler 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
11. 11 3)Glimser and Kenzora in 1979 analyzed the radiographic changes which accompany AVN Ficat in 1985 states that this condition resulted from blockage of the osseus microcirculation with intramedullary stasis and increased pressure .
12. Anatomy 12 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.
19. Blood supply of the Head. 3 main sources. Ascending cervical branches Metaphyseal blood vessels Artery of ligamentum teres. 15
20. Vascular supply of femoral head 16 Crook 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.
22. 18 The 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
23. 19 4 groups of ascending cervical arteries 1. Anterior 2. Posterior 3. Medial 4. Lateral Of these lateral group provides most of blood supply to femoral head and neck
24. 20 The adult pattern of femoral head vascularity usually becomes established with closure of growth plate at approximately 18 years of age
25. In neonate 21 Three groups of vessels are identified superior retinacular group or lateral epiphyseal group inferior metaphyseal group foveal or medial epiphyseal group All 3 groups anastomose with each other
26. Between 4 years to 7 years 22 The importance of lateral epiphyseal is established as metaphyseal and foveal vessels decrease in extent
27. After 8 years of age 23 Open growth plate represents an effective barrier preventing anastomoses between vessels of head and neck. An increased contribution of foveal vessels
28. 24 During adolescence increased number of inferior metaphyseal vessel is recognized As the growth plate closes the adult pattern appears with anastomosis between 3 arterial systems
34. Risk factors 30 Traumatic Osteonecrosis usually involves dislocation of hip or fracture femoral neck . 52% of hips unreduced for more than 12 hours developed AVN 22 % of hips developed AVN if reduced within 12 hours Femoral neck fractures associated with 15 – 50 % incidence of AVN
35. Risk factors 31 Alcoholism: Accounts for 10 – 40 % of incidence of AVN. Risk of development of AVN is increased with cumulative doses of alcohol Drug induced: the association between corticosteroid therapy,cushings syndrome, and Osteonecrosis is well established
36. Risk factors 32 Collagen diseases rheumatoid arthritis,SLE have been associated with AVN Radiation causes obliterative endarteritis and cellular death. Gout sodium urate crystals enhance clotting by activating haegmen factor in intrinsic coagulation system
37. Pathogenesis. 33 Other than traumatic causes, the mechanism of necrosis is still “obscure”. Coaugulation defect. Genetic predisposition. Emboli formation. “ IDIOPATHIC ”
38. Pathogenesis 34 The bony compartment function essentially as closed compartment within which one element can expand only at expense of others A unifying concept of pathogenesis of AVN emphasizes the central role of vascular occlusion and ischaemia leading to osteocyte necrosis
39. 35 Pathogenesis 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.
40. 36 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
42. Biological sequence of repair 38 loss of cell viability (cell necrosis) Invasion of marrow spaces of dead bone by proliferating capillaries and cells Differentiation of mesenchymal cells to osteoblast synthesis of new bone. Early remodelling of repaired cancellous bone
43. Biological sequence of repair 39 Late internal remodeling Resorption of subchondral bone and invasion of articular cartilage
44. Biological sequence of repair 40 To 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
45. Clinical features. Pain. - Dull boring . - Progressive. - Worse at night -Limp while walking. - Restricted hip motion. - Unable to sit cross legged. 41
46. symptoms 42 Clinical manifestation of bone ischaemia and infarction are minimal and non specific and depend on etiology.
47. symptoms 43 Initially vague and non specific. Localized or referred pain in buttocks,thighor knee Gradual increase in intensity of pain and decreased motion especially rotation and abduction Over several years results in limping gait
48. symptoms 44 Initial pain is commonly misinterpreted as radiating pain from lumbar spine.
49. Diagnosis 45 Asymptomatic during the early stages. Become symptomatic when significant collapse of the head has occurred.
50. Management protocol 46 Early diagnosis Radiological evaluation Rule out other causes MRI Quantification Treatment algorithm
54. Imaging 50 Routine 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
55. Radiology- sequential Changes 51 Crescent Sign Osteoporosis Sclerosis Cystic changes Loss of spherical bearing dome Partial collapse of head Secondary Osteoarthritis
60. Scintigraphy 56 Radionuclide scintigraphy is more sensitive for osteonecrosis than standard radiographs and will reveal changes when standardd radiographs are normal
61. scintigram 57 The hall mark of vascularity is photopenic effect on scintigram RESULTS Decreased uptake by necrotic bone Increased uptake by remodeling bone Normal uptake by normal bone
62. 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
63. MRI 59 MRI 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
64. MRI. 60 Can detect early stages. Allows to determine exact stage of disease. Tells exactly the extent of damage. Useful in determining the efficacy of treatment.
65. MRI Geographical area of decreased marrow signal. Necrotic area Surrounded by zone of “low signal” band. Ischaemic bone. 61
68. MRI - Findings 64 Bone Marrow edema Double Line – Head in Head sign Crescent sign Collapse Joint effusion Involvement of actabulum Status of other hip Marrow infiltrating disease
69. LASER Doppler Flometry 65 Laser 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
70. Sequence of radiological events in AVN 66 Fragmentation : radiolucent clefts may be seen due to necrosis of involved bone The entire epiphysis may be absent Mottled trabecular : pattern: scrutiny of trabecular traversing the ischaemic bone demonstrates thickened irregular pattern
71. 67 Sclerosis : 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
72. 68 These cysts are usually seen in region of greatest articular stress and are identical to those found in degenerative joint disease 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
77. Staging 73 Several staging systems have been described. The staging system reported by sternbergs and colleagues is similar to that outlined by Marcus,Ficat and Arlet Sternbergs classification allows physician to quantify extent of involvement of femoral head in both early and late stages
78. Staging / Grading --- too many 74 Ficat Radiological Steinberg Quantification Enneking's Stages of Osteonecrosis Marcus and Enneking System Japanese criteria Location Sugioka Radiological University Of Pennsylvania System Association Research Classification Osseous Committee (ARCO)-- Combination
79. Fi Stages of Bone Necrosis 75 Ficats radiological staging of osteonecrosis of femoral head
80. 76 Ficat Stages of Bone Necrosis Stage Clinical Features Radiographs 0 Preclinical 0 0 1Preradiographic + 2 mild density changes in femoral head 2aPrecollapsemild Diffuse Porosis, Sclerosis,or cyst 2bTransition: 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
81. Stage 1 77 Symptoms – none / mild Xrays are normal. Bone scan reveals a “cold spot”.
82. Stage 2 2A Symptoms are mild. Xray shows increased density. subchondral cysts joint line maintained. normal head contour. Bone scan reveals increased uptake. 78
85. Stage 3 Moderate symptoms. Loss of shape Subchondral collapse 81
86. Stage 4 Severe symptoms. Joint space narrowing. OA changes in acetabulum. 82
87. Marcus radiological staging of AVN 83 Stage I normal or equivocal radiograph Stage II sclerotic or cystic lesion Stage III crescent sign Stage IV step off in outline of bone Stage V narrowing of joint space with degenerative changes
88. 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.
89. Grade 2. 85 Lesions 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.
90. Grade 3. 86 Lesions involving 2/3 of the weight bearing surface of the femoral head. Such lesions collapse in 70% of patients in around 3 years.
91. Treatment 87 Conservative /non surgical treatment Core decompression Bone grafting Cancellous autogenic/allogenic bone graft Osteochondral graft Muscle pedicle bone graft Free vascularized graft
92. Treatment 88 Electric stimulation Osteotomy Joint reconstruction Cup arthoplasty Surface arthoplasty Hemiarthoplasty Total joint arthoplasty
93. 89 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.
94. 90 Once subchondral collapse occurs and joint space is lost, progressive osteoarthritis generally is considered inevitable.
95. 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)
96. 92 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
97. 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.
98. 94 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
99. Management. 95 Grade 1 lesions - Continuous supervision to detect any changes. - Symptomatic treatment of pain.
100. Grade 1 lesions 96 Conservative treatment such as observation , Analgesics Limited weight bearing may be successful in minimal affected cases
101. Core decompression Grade 2 lesions 97 Ficart and Hungerford have popularized the technique of core decompression of femoral head Rationale is that removing necrotic bone decompresses the rigid osseous chamber, thereby improving blood flow and preventing additional ischaemic events
102. 98 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
103. 99 several authors noted that the results of core decompression are better than those of nonoperative treatment.
104. 100 Several 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.
105. 101 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
106. 102 The surgical field for subsequent total hip arthroplasty, if needed, is not substantially altered
107. Bone grafting 103 Phemister introduced concept of using cortical strut graft in core decompression channel The accurate placement of graft within lesion and under subchondral bone is important
108. 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.
109. 105 Insertion 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
110. 106 Baksi employed multiple drilling and muscle pedicle grafting using tensor fascia lata muscle anteriorly
111. 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.
113. 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
114. 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.
115. Advantages 111 Advantages 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,
116. 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.
117. Disadvantages 113 Disadvantages include a longer recovery period and less uniform and less complete relief of pain than after total hip arthroplasty.
127. Electrical stimulation 120 Electrical stimulation has been advocated for AVN because its histological appearance is similar to that of non union Currently used in combination with head salvage procedures
128. osteotomies 121 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.
129. osteotomies 122 Various osteotomies have been described Varus osteotomy Valgus derotation osteotomy Rotation osteotomy aid the loss of structural integrity and collapse by redirecting the forces on femoral head
130. 123 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. 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.
131. 124 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 If necrotic lesion is central varus extension osteotomy is recommended
132. Transtrochanteric Rotational Osteotomy 125 In 1978 Sugioka described a transtrochanteric rotational osteotomy of the femoral head for idiopathic osteonecrosis
133. 126 The 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
134. 127 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
135. Post op regimen 128 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.
136. 129 Walking 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.
137. Replacement - options 130 Hemiarthroplasty Bipolar arthroplasty Surface replacement arthroplasty. Newer material for THR ceramic on ceramic Non cemented / cemented THR
138. Birmingham Surface replacement 131 Surface replacement has some advantages over THR because it preserves femoral head and neck and allows future THR if necessary Effective in cases when femoral head is not involved entirely
140. Overview Named for Birmingham, England, where the device’s creators practice medicine Used globally since 1997; More than 65,000 implanted 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.
141. 134 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. 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.
142. 135 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. 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.
143. Head size Closely matches the size of natural femoral head Larger than the head of a total hip replacement Larger head means a reduced chance of dislocation after surgery—a leading cause of revision surgery 1-3% of total hips dislocate over the lifetime of the implant 0.3% of BHR* implants dislocated in the first 5 years after surgery (in a study of 2,385 hips) Healthy head BHR head Total hip head
144. 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 activity Active adults over age 60 may be candidates, depending on their bone quality
146. The key benefits Head size Advanced bearing surface Bone conservation
147. Hip with osteoarthritis Bone cuts fora traditionalhip replacement Bone conservation Preserves your natural femoral neck Neck length and angle determine accurate leg length With the BHR*System, you retain original equipment; with a total hip, your femoral neck is replaced by the implant Bone cuts forBHR System
148. “Minimally Invasive.” Soft Tissue No. Incision length of 6 to 8 inches Bone Yes. Preserves your body’s natural bone structure; It resurfaces rather than replaces Conserved bone
150. Bone conservation (cont.) Revises to a primary If you need “revision” surgery, you don’t get a revision implant The follow-up procedure would be the same total hip replacement you would otherwise have received
151. Total Hip Arthroplasty and Bipolar Hemiarthroplasty. 144 Most series that have examined both unipolar and bipolar hemiarthroplasty for the treatment of osteonecrosis have reported uniformly poor results.
152. THR 145 Patient aged 50 & more Advance osteoarthritis and reduction of joint space. Radiation necrosis Result less than Ideal. – necrotic bone Poor in Sickle cell disease. Cementless are superior over cemented THR
153. 146 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.
155. THR 148 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
156. 149 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.
157. Girdle stone arthoplasty 150 Used as salvage procedure in special circumstances like painful hip with superimposed sepsis, failed THR with sepsis Femur without good bone stock Conversion to THR can be taken at later stage
158. Hip fusion 151 Not frequently recommended because of high failure rates
