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AVN Head of Femur.pptx

  1. Avascular Necrosis of Femoral Head
  2. Overview • Introduction • History • Anatomy • Epidemiology • Etiology • Pathogenesis • Diagnosis and staging • Management Source:
  3. Introduction • Osteonecrosis, also referred to as avascular necrosis (AVN), aseptic necrosis, and ischemic necrosis, is not a specific disease but rather a condition in which a circumscribed area of bone becomes necrotic as a result of a loss of its blood supply • It is also known as CHANDLER’S DISEASES [hip] and OSTEOCHONDRITIS DESSICANS
  4. OSTEONECROSIS FEMUR HEAD Osteonecrosis is death of living elements of involved bone [cells including marrow] with progressive destruction and alteration of bone architecture as a result of compromised vascularity. The process is purely aseptic but may be incited by loss of vascularity from infarction. Source:
  5. History • Osteonecrosis was first described by Hippocrates circa 400BC • First case of aseptic osteonecrosis was describe by Paget in 1970 • Ficat (1985) stated this condition resulted from blockage of osseous microcirculation with intramedullary stasis and increased pressure
  6. Blood Supply Of Femoral Head Proximal end of femur is supplied by three groups : - Extracapsular arterial ring - Ascending cervical branches of retinacular arteries - Arteries of ligamentum teres Source:
  7. Extracapsular arterial ring • By medial femoral circumflex artery posteriorly and lateral circumflex femoral artery anteriorly • Minor contribution from superior and inferior gluteal arteries Source:
  8. Ascending cervical branches Ascending cervical branches of extracapsular arterial ring [also known as epiphyseal arteries of Trueta of retinacular arteries arises from ECA and ascend up the neck partly also supplying the neck in due course . • Divided into anterior, posterior, medial and lateral groups • Lateral group is the most important group carrying the major portion of blood supply to head and neck of femur
  9. Concept of the Starling resistor as applied to bone microcirculation. a Raising the pressure in a rigid-walled chamber can decrease fluid flow in a flexible- walled tube passing through the chamber, b In the case of bone, the intraosseous extravascular compartment may function like a rigid-walled chamber. Intraosseous hypertension or space-occupying tissue may sufficiently restrict microcirculatory blood flow to produce ischemia Intraosseous hypertension has been proposed to develop from various inciting causes and is considered the principal cause of ischemia in non traumatic osteonecrosis. Starling Resistor Source: Europe PMC
  10. Epidemiology • Mean age of onset: 5th-6th decade • M:W = 3:1 for non traumatic osteonecrosis but the ratio is higher for traumatic osteonecrosis as males seem to suffer high velocity injuries more • Atraumatic AVN is bilateral in 30-70% but typically asymmetrical
  11. Etiology Source: Essential Orthopedics, principles and practice by Manish Kumar Varshney
  12. Traumatic Osteonecrosis • Dislocation of hip (10-25%) or fracture neck of femur(15-50%) • Prompt relocation helps in reducing incidence of ONFH • 52% hips dislocated for more than 12hrs developed ONFH compared with 22% of those reduced within 12hrs
  13. Dysbarism • Also known as CAISSON Disease, Decompression Sickness • Tunnel workers and others associated with deep sea diving (1-4%) • Formation of nitrogen bubbles from the dissolved saturated nitrogen of the blood vessels due to sudden decrease in the atmospheric pressure precipitates infarction in the vascular capillaries and eventually osteonecrosis
  14. Alcoholism • 10-40% incidence • There is increased risk of femoral head osteonecrosis in individuals consuming greater than 400 ml of alcohol/ week • Alcohol induces increase in serum triglyceride and cholesterol levels along with liver and bone marrow fatty infiltration. • There is pyknosis in osteocytes due to triglyceride deposition and ultimately death leading to an increased percentage of empty osteocytes lacunae. • Hyperlipidemic state – enhances thrombus
  15. Source:
  16. Haemoglobinopathies Mainly sickle cell disease(20-68%), hereditary thrombophilia and antiphospholipid antibodies syndrome can lead to sludging, thrombosis and eventual infarction at capillary level
  17. Drug Induced • Steroids, phenytoin, indomethacin • Steroid induced (10-30%): glucocorticoids are most common cause of non traumatic osteonecrosis • Mechanism : Proposed hypothesis emphasis small vessel occlusion by fatty emboli and increased impedance of sinusoidal blood flow secondary to rise in intraosseous pressure [venous obstruction] • Patients receiving steroid therapy have an approximately 20 fold increase in their their likelihood of developing osteonecrosis
  18. Source: International journal of biological sciences
  19. Collagen disease • RA and systemic lupus erythematosus • Inflammation of small peripheral blood vessels promotes the formation of vascular thrombosis and tissue infarction
  20. Radiation •The necrosis is primarily induced by vasculitis caused by radiation that leads to thrombosis and occlusion •Capillaries are also damaged directly by radiation and endothelial damage makes them leaky which leads to development of bone edema and further compromises vascular profusion • A threshold dose of 3000 rads
  21. Idiopathic • Most common cause of osteonecrosis • Factors rendering bone liable to infarction at its articular edge -small diameter of terminal vessels in subchondral region -lack of collateral circulation -reduced blood flow in bone with high marrow fat -in-expandable nature of bone tissue
  22. Etiopathogenesis • The bony compartment function essentially as closed compartment within which one element can expand only at expense of others • Vascular occlusion and venous stasis leading to osteocyte necrosis play a central role in pathogenesis of AVN
  23. Source: Essential Orthopedics, principles and practice by Manish Kumar Varshney
  24. Pathogenesis • Hypoxia • Increased cell membrane permeability, which allows fluid and electrolytes to enter the cell, causing it to swell. • lysosomal enzymes are released •Auto digestion or coagulation necrosis and cell rupture • Vascular injury leads to tissue edema and haemorrhage
  25. Inflammatory response ensues Disappearance of osteocytes from within their lacunae Centre of the necrotic lesion remains avascular and repair is not possible Repeated stresses Dead trabeculae undergo micro fractures that cannot be repaired Source: Journal Laboratory Investigation
  26. Transition zone at the periphery, an active process of repair begins Macrophages and osteoclasts remove dead marrow elements and bone Granulation and fibrous tissue are formed Source: Journal Laboratory Investigation
  27. Osteoblasts form new bone, laid down directly on remnants of dead trabeculae The resulting trabeculae are much thicker than normal Responsible for the sclerotic margin that surrounds the lesion Source: Journal Laboratory Investigation
  28. • Small lesion (not in a major weight-bearing region) - Revascularization and completely replaced with viable bone • Larger lesions, particularly those in a region of major weight bearing, have a poor prognosis - Gradual collapse
  29. If the contour of the articular surface remains intact, a fluid filled space beneath the cortical subchondral bone develops, which gives the appearance of a crescent sign on radiograph
  30. The mechanical stresses on the collapsed and irregular articular surface Damage to and death of chondrocytes These abnormal stresses are transferred to the otherwise normal cartilage of the acetabulum - Secondary degenerative changes.
  31. Joint space narrowing Typical changes of degenerative joint disease appear and include sclerosis, cyst formation, and marginal osteophytes End-stage arthritis of the hip eventually ensues
  32. Histopathological staging STAGE 1 Cut Section: Necrotic wedge shaped (dull, chalky, opaque and yellow), sub articular lesion, well demarcated Micro : Cartilage normal, subchondral bone shows eosinophilic changes lacking cellular elements, osteocytic lacunae empty
  33. • Margin of infarct : increased osteoclastic activity with infiltration of granulation tissue (thin red rim) • Beyond infarct and hypervascular zone; bone and marrow remain unchanged
  34. STAGE 2 Articular surface remains intact Cut section : rim of bony sclerosis at the boundary between necrotic zone and unaffected zone
  35. Microscopy : advancing front of granulation tissue following which second front of osteoblasts (creeping substitution) - Increased vascularity with osteoblastic activity and new bone formation
  36. STAGE 3 Alteration in shape of articular bone Gross : buckling Cut section : fracture just below articular end plate or on the necrotic side of advancing sclerosis in reparative front - Fracture occurs due to weakening of trabeculae due to increased osteoclastic activity
  37. STAGE 4 Articular deformity Cut section : residual fragments of articular cartilage and dense fibrous connective tissue in the area of infarction - Articular surface dense sclerotic eburnated - OA changes
  38. Clinical features • Pain usual presenting symptom • Intense and sudden in onset as in infarct or it can be insidious and chronic • Groin pain but radiating to anterior and anteromedial thigh less common to buttocks • Pain present at rest worsens with motion and weight bearing • O/E – Antalgic gait Decreased ROM particularly flexion and IR
  39. SECTORAL SIGN The range of internal rotation is less in hip flexion compared to when hip in extension Source:
  40. Imaging RADIOGRAPHY (AP view and frog leg lateral views) • Initial Radiographs will be normal Sequel: •crescent sign •Sclerosis •Cystic changes •Loss of spherical weightbearing dome •Partial collapse of head • Advanced cases : secondary OA
  41. Kerboul Necrotic Angle • Determined by measuring arc of the articular surface overlying the lesion on AP and lateral radiographs • These two are added and referred to as the combined necrotic angle Source: Osteonecrosis by Babhulkar Sudhir
  42. MR Imaging • Abnormalities in femoral head on MRI can be made out as early as 7 to10 days after the onset of symptoms • Better precision • Low intensity signal band on both T1 weighted and T2 weighted images – early abnormality • In more advanced lesions – T1 images continue to show low intensity signal but T2 images may exhibit signals of alternating high and low intensity (double line sign)
  43. MRI(T1) MRI(T2)
  44. Staging Ficat and Arlet classification of osteonecrosis femoral head Source:
  45. Steinberg University Of Pennisilvenisa
  47. CT Scan • Can Visualize a small lesion not easily seen on routine radiographs, and it may demonstrate small areas of articular surface collapse that are not apparent on plain films • It may also be used to help quantitate the extent of femoral head involvement
  48. Bone scan • With technetium labelled phosphate analogue used for early detection of ON • Not as sensitive as MRI • During acute phase decreased uptake of bone tracer associated with vascular compromise • Increased accumulation in chronic venous stasis in repair and revascularisation • Can be useful, especially in assessing the status of multiple joints
  49. Goals of management • Relief of pain • Arrest the progression of disease • Prevent the collapse of head • Prevent secondary degenerative arthritis
  50. Treatment Modalities Non Operative/ Conservative Operative Non weightbearing Core Decompression Bisphosphonates Mesenchymal stem cell implantation/ growth factor based treatment Anti-coagulants, statins,& other vasodilators Non-vascularized bone graft Extracorporeal shock wave therapy Porous tantalum implant Pulsed Electromagnet theory Vascularized bone graft Hyperbaric oxygen Proximal femoral osteotomy Arthroplasty
  52. Non operative Treatment • Nonoperative management of Osteonecrosis femur head includes restricted weight-bearing, pharmacological agents and biophysical modalities of treatment. • The goal of drug treatment in the pre-collapsed stage is to: 1. improve hip function 2. provide pain relief 3. prevent radiographic progression to subchondral fracture and collapse 4. allow healing of the necrotic lesions.
  53. Non- Weight Bearing • Restricted weight-bearing using cane, crutches or a walker is effective in early-stages ON hip (Ficat and Arlet Stage-I and II) when the osteonecrotic lesion is <15% and located far from the weight-bearing dome (medial lesions) • In 1/3rd of the patients with small or medium sized lesion [<50% of head involvement ] progress to symptoms or collapse in spite of non weight bearing whereas large lesions have more chances of disease progression. • Progression of the advanced stage depends largely on location, size of the lesion and aetiology • Therefore non weight bearing modality of treatment cannot be accepted as a standard isolated modality of treatment and maybe an additive treatment to medical or surgical management • Decreases the degree of discomfort in patients who are symptomatic, they have not been shown to alter the natural course of this disorder • Following certain types of surgical procedures, such as core decompression, grafting, and osteotomies, where it is used as an adjunct. • Protects the weakened regions from fracture, and perhaps protects the femoral head as well, until the healing processes have progressed satisfactorily
  54. Bisphosphonate: • Bisphosphonates promotes bone healing by inhibiting osteoclastic activity in osteonecrotic lesion site • It prevents collapse in early osteonecrotic hip or prevents onset of subchondral fracture • In advanced condition where collapse has already taken place, it delays the need of total hip replacement surgery • Therefore alendronate in osteonecrosis femoral head patients can be used in a dose of 70 mg weekly for 3 years in stage I,II & III [ STEINBERG CLASSIFICATION]
  55. Anticoagulants, Statins & other Vasodilators • Thrombophilia and hypo fibrinolysis leads to venous stasis and reduce arterial flow, thus increasing intra osseous pressure and hypoxic bone death which has been postulated as a major and common etiological factor for osteonecrosis. • Systemic anticoagulation therapy started before irreversible segmental collapse of the femur head may arrest or, speculatively, sometimes reverse the process of ischemic osteonecrosis • Lipid lowering agents are also helpful in steroid induced osteonecrosis • Steroid causes hyperlipidemia which increases the fat content and also increases intracortical pressure, leading to sinusoidal collapse and osteonecrosis
  56. • Statins are lipid clearing agents that dramatically reduce lipid levels and blood and tissues • Adreno Corticotropic Hormone also shows some protection against steroid induced osteonecrosis • It enhances osteoblastic activity and stimulates vascular endothelial growth factor that enhances neovascularization in femoral head
  57. Extracorporeal Shock Wave Therapy[ESWT] • EWST enhances neovascularization by stimulating the expression of angiogenic growth factors but the exact mechanism is unclear • It has been compared to core decompression and found to improve function of hip to a greater extent • It can be used as an adjunct with hyperbaric oxygen therapy and bisphosphonates
  58. Pulsed electromagnetic Therapy • Pulsed electromagnetic therapy affects favorably in early stage osteonecrosis through stimulation of osteogenesis and angiogenesis similar to ESWT • It can be used as an adjunct to core decompression
  59. Hyperbaric Oxygen • Mechanism: 1. Improves oxygenation 2. Reduces edema by vasoconstriction 3. Induces angiogenesis 4. Reduces intraosseous pressure and improves microcirculation • Procedure: 100% oxygen at 2-2.4 atmospheric pressure for 90 minutes by mask for about 100 days to the patient of early stage osteonecrosis.
  60. Bone marrow infiltration • The small no. of progenitor cells in the proximal extremity of the femur with ONFH causes insufficient creeping substitution after osteonecrosis • Red bone marrow graft contains osteogenic precursors, which help in the reparative process • Used in adjunct to Core Decompression
  61. Operative treatment Surgical treatment for pre-collapsed stage ONFH involves hip preserving procedures (CD, non-vascularized bone-graft, vascularized bone-graft) whereas prosthetic hip surgery is reserved for advanced- stage of collapse and arthritic hip.
  62. Core decompression • Core decompression is the most commonly performed surgical procedure for treatment of early osteonecrosis femur head. • Mechanism: 1. Decreases interosseous pressure 2. Increases blood flow to necrotic areas 3. Augmentation of new bone formation • Core decompression is currently the gold standard management of stage I & II osteonecrosis [ARCO system, i.e. precollapse] • It has been cost effective surgical procedure for osteonecrosis femur head • Success of the treatment is largely dependent on the etiology, lesion size, location or collapse of the lesion.
  63. • Types: 1. Convention core decompression 2. Recent procedure Convention core decompression: • It is performed using 8-10mm cannula or trephine • Disadvantage: potential risk of subtrochanteric fracture and hip joint penetration. Recent Procedure: • This procedure is done by multiple small drilling [3mm diameter] which has shown better results than the conventional core decompression. • The small diameter drill can more easily reach the anterior portion of femoral head that is commonly involved with osteonecrosis. • There is less risk of fracture, small incision and minimal morbidity • The risk of bone weakening and articular surface penetration is considerably reduced. Post operatively patients are kept on protected weight bearing for about 6 weeks following conventional core decompression and about 3 weeks when drilled with smaller drill holes
  64. A B A: Conventional core decompression B: multiple small diameter core decompression
  65. Mesenchymal Stem-cell Implantation • It augments osseous regeneration in the necrotic lesion site. • There is application of osteogenic or angiogenic precursor cells with or without growth factor • Mesenchymal stem cells derived from adult tissue represents a highly promising option for the treatment of osteonecrosis femoral head in the pre-collapse stage. • MSCs implantation has capability to differentiate into multiple cell lineages including the osteoblast, chondrocytes and adipocytes. • MSCs implantation can be used as an adjunct to core decompression
  66. Bone grafting • Various authors have claimed success rate of 50 – 80% after CD with structural BG • Non vascularised BG – Ficat 1 and 2 • Accurate placement of the graft within the lesion and under the subchondral bone • Standard core technique, Lightbulb technique, Trap door technique
  67. Non Vascularized Bone Graft • Tibial autograft or fibular autograft or allograft are used to support subchondral bone and articular cartilage after removal of the necrotic lesion from the femoral head. • The osteoconductive and osteoinductive properties of the bone graft help inhaling of the osteonecrotic lesion. • This modality of treatment is indicated in pre-collapse and early post collapse [< 2mm collapse] osteonecrosis of femoral head where articular cartilage is relatively undamaged [Ficat Stage I & II]. • Techniques: 1. Phemister technique [ grafting through core decompression track] 2. Trap Door [ grafting through a window created in femoral head] 3. Light Bulb Procedure [ grafting through a window created in femoral neck or neck head junction] • Rarely used as an isolated procedure, is usually combined with growth factors and various bone graft substitutes.
  68. Source: Europe PMC
  69. Porous Tantalum Implant • These implants provide structural support similar to that of bone graft. • The porosity of this rod allows secure and rapid bone growth. • Efficacy of porous tantalum rod can be further improved by addition of bone marrow, growth factor or bisphosphonates. • Avoids the risk of infectious complication and donors site morbidity as seen with the use of allograft and autograft respectively
  70. Vascularized Bone Graft • Vascularized bone grafting is recommended modality of treatment for early osteonecrosis femoral head [Ficat Stage I,II,III] • The graft provides a viable structural support and prevents joint collapse. • Vascularized bone graft has osteogenic potential which augments bone healing in the necrotic lesion site. • Example: 1. Vascularized iliac crest graft 2. Vascularized fibular graft 3. Muscle pedicle bone graft
  71. Muscle Pedicle Bone Graft • Meyers first reported application of muscle pedicle bone graft for treatment of osteonecrotic femoral head. • Technique: After incorporating cancellous bone graft over the necrotic lesion, quadratus femoris muscle with bone in its insertion is elevated and placed over the necrotic lesion and fixed with cortical screws .
  72. Vascularised fibular graft • Rationale : - Decompression of femoral head - Excision of the sequestrum - Filling the defect with osteoinductive cancellous graft and viable cortical strut • Longer recovery period and less uniform and less complete relief of pain • Success rate 80-91% for younger symptomatic patients without collapse
  73. Proximal Femoral Osteotomy Principal: • Mobilization of the necrotic bone of femur head away from the load bearing area, replacing it with the uninvolved healthy portion of the head. • It reduces the intra osseous venous pressure and improves vascularity Types: • Trans trochanteric rotational osteotomy • Intertrochanteric varus or valgus osteotomy (combined with flexion or extension)
  74. McMurray’s Osteotomy • Thomas Porter McMurry became famous for introducing an osteotomy for treatment of nonunion of fracture neck of femur but later on also advocated for fresh femur neck fractures and osteoarthritis of hip. Technique: • It is an intertrochanteric, oblique osteotomy of the hip, where the distal osteotomized femoral shaft is displaced medially under the neck and femoral head • This osteotomy starts from lateral femoral cortex just below the level of lesser trochanter and proceeding obliquely to finish medially just proximal to lesser trochanter • The inward pull of psoas major muscle helps in maintaining medial displacement of the distal femur under the femoral neck and head.
  75. • Valgus/Flexion osteotomy – anterolateral lesion • Varus/Extension - Central or superomedial lesion
  76. Source:Campbell, John J Callaghan
  77. Arthroplasty • Arthroplasty is the final treatment when all other modalities of treatment have failed, or joint is arthritic secondary to advanced collapse ( >2mm) • AVN of head of femur forms one of the major indication for total hip replacement • Between 5-12% of total hip replacement are performed in the patients having AVN of femoral head Indications: 1. Patients with advanced osteonecrosis hip (> Stage III ARCO) any age (Patients <30 years of age may still be considered for alternative procedures) 2. Older patients (>50 years of age ) with stage III or more disease 3. Combined necrotic angle of >240 degree where the failure rate of other procedure is significantly high 4. All cases of failed pervious surgery.
  78. Contraindications: 1. Not to be used in the all those patients who can be reasonably managed with joint preservation procedures for early stage disease. 2. Very young patient < 30 years of age • Cementless Total Hip Arthroplasty has reassuring results in patients < 60 years of age with no other associative hip pathology • Whereas patients with > 60 years of age achieve better results with cemented total hip arthroplasty
  79. There are different designs and materials in hip replacement • Consist of 2 basic component: Ball and socket components • Ball component: highly polished metal, ceramic material • Socket component: high molecular weight polyethylene, ceramic, metal • Total hip replacement could be cemented and uncemented • Decision is based on factors like age, quality and strength of bone and affordability of the patient.
  80. Metal-on-polyethylene metal (cobalt-chrome) femoral head on polyethylene acetabular liner Benefits: • longest track record of bearing surfaces • lowest cost • most modularity Disadvantages: higher wear and osteolysis rates compared to metal-on-metal and ceramics smaller head (compared to metal-on-metal) leads to higher risk of impingement
  81. •Metal-on-metal Benefits: •better wear properties than metal-on-polyethylene •lower linear wear rate •debris particles much smaller (but more numerous) than those of metal-on-poly •overall smaller volume of particles •larger head allows for increased ROM before impingement Disadvantages: •more expensive than metal-on-polyethylene •increased metal ions in serum and urine (5-10x normal) •serum metal ion concentration highest at 12-24 months •correlates with the initial "wear in" or "run-in" phase of increased particle generation, but then followed by a "steady state" phase of decreased particle generation •may form pseudotumors •hypersensitivity (Type IV delayed type hypersensitvity) •mediated by T-cells
  82. Ceramic on Ceramic Benefits: • best wear properties of all bearing surfaces • lowest coefficient of friction of all bearing surfaces • inert particles • no concern for cancer risk Disadvantages: • more expensive than metal-on-polyethylene • worst mechanical properties (alumina is brittle, low fracture toughness) • small 28mm heads only exist in zirconia because of alumina's inferior mechanical properties • squeaking • impingement and acetabular malposition • third-body wear • loss of fluid film lubrication • thin, flexible (titanium) stems • less modularity with fewer neck length options • stripe wear, caused by contact between the femoral head and rim of the cup during partial subluxation • results in a crescent shaped line on the femoral head