Avascular Necrosis Presentation.pptx ppt
- 1. Avascular necrosis DR BIPUL BORTHAKUR PROFFESOR AND HEAD DEPARTMENT OF ORTHOPAEDICS ASSAM MEDICAL COLLEGE DIBRUGARH , ASSAM
- 2. Introduction • Avascular necrosis ( AVN ) of the bone is a pathological condition that results from diminished blood supply to the bone either temporarily or permanently.
- 3. Bones commonly effected • Femoral head • Schapoid • Talus • Humeral head • Radial head • Lateral femoral condyle • Humeral capitullam
- 4. AVN of Head of Femur • Death of the bones and bone cells from interruption of blood supply that leads to structural damage, consequent collapse and secondary Osteoarthritis. • Also known as Chandler’s Disease or Coronary Disease of Hip • Occurs in young adults between 30 – 50 yr of age • Male : Female ratio is 4 : 1, out of which 60 % are bilateral.
- 5. • Most common area is the anterolateral aspect of the head of femur as it is the main wt bearing area. • Avn only occurs in Fatty marrow where there is sparse blood supply in comparision to hematopoetic marrow which has heavy blood supply.
- 6. Blood supply of femoral head
- 7. Etiology • Ideopathic • Trauma • Alcohol consumption • Steriod intake • Cushing disease • Hemoglobinopathies (sickle cell disease , Polycythemia ) • Caisson’s disease (dysbaric osteonecrosis) • Smoking • Gout • Collagen vascular disease • SLE • Hypercoagulable state • Hyperlipidemia • Organ transplantation • Gaucher’s disease • Pancreatitis • Neoplasms • Hemodialysis • HIV
- 8. Clinical Features • No distinguishing clinical features • Asymptomatic pain which is gradual and insidious in nature • Range of motion may be restricted • Patient may be able to walk with a limp • Radiographic changes may occur after several months or years from the occurance of the initial symptoms.
- 9. Nature of Pain of AVN • Focal pain over the groin or hip which may radiate to the buttocks, anteromedial aspect of thighs or knees. • Induced by standing or walking and is reduced by taking rest. • Sometimes may be very intense , throbbing , deep and often intermittent. • Worsened by coughing and during the nighht. • About 40 % of the patients have associated night pain and morning stiffness.
- 10. Cont.. • Range of motion may be diminished especially after collapse of the femoral head. • Range of motion may be limited in Flexion Abduction and internal Rotation. • Patients may walk with a limp • The Trendelenberg Sign may be positive.
- 11. Pathogenesis
- 12. Imaging Modalities • Xrays 1. May be normal. 2. May show osteopenia, osteoporosis, demineralization. 3. Cystic changes like Mottlong and sclerosis may be seen. 4. Cresent sign due to subchondral fractures and collapse. 5. Flattening of femoral head. 6. Joint space narrowing. 7. Ostepophyte formation with acetabular involvement. 8. Secondary osteoarthritis of Hip joint.
- 13. Femoral head sclerosis Crescent sign Femoral head flattening Joint space narrowing Advanced degenerative changes
- 14. • CT scan in AVN a) Loss of Asterix sign b) Subchondral fractures
- 15. • MRI I. It is the most sesitive modality to detect AVN. II. Helps in differenciating AVN and Non AVN diseases of Femoral Head. III. Also effective in assessing marrow edema, joint effusion, articular cartilage congruity. IV. Classical findings include : • Focal lesion in the anterosuperior aspect of the femoral head that is well demarcated and is nonhomogeneous • T1 image shows - LOW signal intensity • T2 image shows – DOUBLE LINE SIGN….. Classical sign of AVN, made up of two concentric low and high signal bands.
- 16. T1 shows hypo intense signals in bilateral femoral heads ( R > L ) T2 shows hyper intense ring like areas ( Double Ring sign )
- 17. • Scintigraphy • Focal increase in uptake is seen
- 18. Classification Systems • FICAT AND ARLET CLASSIFICATION SYSTEM
- 19. • STEINBERG CLASSIFICATION SYSTEM
- 20. • ARCO CLASSIFICATION SYSTEM
- 21. TREATMENT • AIM 1. To keep the joint from breaking down 2. Preserve rather than replace the Femoral head and Cartilage 3. Early intervention has favourable impact on the progression of the disease irrespective of the modality of treatment used.
- 22. Protected weight bearing • Protect the involved area from excessive stress by using some form of limited wt bearing • Canes or even clutches are frequently prescribed • Does not alter the natural course of the disease • Indications 1. Alternative to surgical management 2. Small asymptomatic lesion 3. Low wt bearing area , such as the medial aspect of femoral head 4. Poor medical condition 5. Following certain types of surgical procedures such as core decompression , grafting and osteotomies 6. Relatively advanced atage of osteonecrosis
- 23. Non surgical Treatnment • Pharmacological treatment • Hyperbaric oxygen therapy • Improves oxygenation, reduces edema, induces angiogenesis and reduces intraosseous pressure.
- 24. Surgical treatment options • Core decompression : relieves intraosseous pressure caused by venous congestion Improved vascularity Slowing progression of disease • Earlier the stage of disease better the results • Void left after core decompression is filled up by autologous bone graft that include marrow cells with or without growth factors
- 25. Percutaneous technique for core decompression
- 26. Bone grafting techniques Trapdoor technique Light bulb technique
- 27. Proximal femoral osteotomies • Valgus osteotomy with flexion • When the necrotic segment is located in the anterosuperior part of the femoral head with less than 20 % posterior involvement. • Patients - less than 45 yrs of age , not on steroids or chemotherapy.
- 28. • Varus osteotomy with flexion • Types 1. Curved ( Merle D Aubigene type ) 2. Medial displacement ( Mac Murray type ) 3. Angulation ( Pawel’s 1 type )
- 29. Arthroplasty :for osteonecrosis involving more than 30 % of the femoral head. Resurfacing arthroplasty • Femoral and acetabular surface replacement and hemi surface replacement for osteonecrosis of hip. • More than 30 % of femoral involvement present. • There is little bone sacrifice. Total hip arthroplasty • For advanced osteonecrosis of Hip • Excellent pain relief and functional improvement
- 30. AVN OF HUMERAL HEAD • Blood supply • Anterior Circumflex Humeral artery (ACHA) and Posterior Circumflex Humeral Artery (PCHA). • ACHA gives off Ascending Anterolateral Branch • PCHA Runs post to humeral head supplying the GT and Subchondral region. Blood supply for majority of humeral head. • Circumflex arteries form intraosseous anastomosis within Humeral Head • Superior aspect of Humeral Head has poorest blood supply
- 31. Etiology • Traumatic Non-iatrogenic Fracture Dislocation Fracture dislocation Iatrogenic Rotator cuff repair • Non Traumatic • Medications Corticosteroids • Systemic diseases Hemoglobinopathies: Sickle cell disease Connective tissue/autoimmune diseases: Systemic lupus erythematosus, psoriasis Metabolic diseases: Alcoholism, Gaucher disease Hormonal diseases: Cushing disease • Others Dysbarism Hemophilia Electrical/thermal injury Radiation therapy Septic arthritis Extra-corporeal shockwave therapy
- 32. Clinical features • Signs and symptoms indolent in nature • Patients often present in advanced stage • Patient may present with • Painful click while doing shoulder movements • Pain over shoulder joint • Decreased ROM at shoulder joint
- 33. Staging – Cruess radiological staging
- 34. Radiological investigations • Xray – effective in evaluating bony pathology only • MRI – for detecting early AVN and staging. Xray showing CRUESS stage 3 and 4 Xray and MRI image showing CRUESS stage 4
- 35. X-rays and MRI of progressive AVN of the humeral head. The patient is a 31-year-old lifeguard with a background of hemophilia A, presenting with several years of right shoulder pain. X-ray (A) showed subchondral sclerosis of the superomedial humeral head, with subchondral cysts noted on MRI (B) at the same region (Cruess stage II). Core decompression was initially offered but the patient elected to proceed with conservative treatment. Nine years later, the patient's X-ray and MRI (C, D) showed extensive glenohumeral arthritis (Cruess stage V), and despite his age, arthroplasty was offered.
- 37. Management Conservative management – Lifestyle modification ( decrease smoking and alcohol intake ) Passive ROM of shoulder to avoid stiffness Avoide excessive shoulder abduction and flexion NSAIDA and OPOIDS for symptomatic pain relief Bisphosphonates have been used in some cases . Surical management – Core decompression Arthroscopic debridement Arthroplasty
- 38. Avn of Scaphoid • Anatomy of scaphoid • The name scaphoid comes from the Greek word “skaphos” meaning boat • The scaphoid lies at the radial border of the proximal carpal row , elongated in shape and obliquely placed. This position allows bridging between the carpel rows and acts as a stabalising factor.
- 39. • The scaphoid has 5 articular surfaces - radius, capitate, lunate, trapezoid and trapezium. • As a result the entire surface is articular cartilage leading to increased tendency to go to union and non union.
- 40. Blood supply of scaphoid • Primarily from Radial artery by two major vascular pedicles (Gelberman and Menon ) • The DORSAL Branch enters through numerous small foramina along the spiral groove and dorsal ridge and supply 70 to 80 % of the scaphoid proximally. • VOLAR Branch enters vial the scaphoid tubercle and supplies the remaining 20 to 30 % of the scaphoid distally.
- 41. Types of AVN of SCAPHOID • Traumatic : • occurs in 50 % of all displaced scaphoid fractures • Most commonly associated with proximal pole of scaphoid fracture. • Ideopathic (PREISER’S disease) : • Ideopathic AVN of scaphoid. • Rare condition where scaphoid goes into ischemia and necrosis without any previous fracture. • Thought to be caused by repeated microtrauma or side effects of drugs like steroids and chemotherapy agents.
- 42. • Signs and symptoms : • Pain and tenderness around the anatomical snuff box. • Stiffness of wrist and decreased ROM. • Decreased hand grip and crepitus. • Imaging modalities : • Xray : Ground glass appearance / increased bone density Loss of trabecular pattern Cystic changes Subchondral collapse and fragmentation
- 43. • CT Scan : • CT scan is a better option than plain radiograph • Proximal pole fracture with dense sclerosis is seen. • MRI : • It is highly sensitive for AVN of scaphoid as compared to plain radiograph. • Decrease in the marrow signal intensity in T1 imaging is suggestive of AVN of scaphoid.
- 44. Management • The geometry of scaphoid, direction and type of fracture , vascular pattern , all of these influence the management of the condition. • GOAL OF TREATMENT : 1. Relieve the symptoms 2. Correct the carpal deformity 3. Achieve union 4. Delay the onset of wrist arthrosis
- 45. Surgical treatment • Radial styloidectomy • Excision of the scaphoid • Proximal row carpectomy • Traditional bone grafting • Vascularised bone grafting • Scaphoid implant resection arthroplasty • Wrist arthrodesis ( partial or complete )
- 46. Kienbock’s Disease • It is an isolated disorder of the lunate which results from vascular compromise to the bone. • This results in osteomalacia and Avascular Necrosis of the lunate bone. • Dr Robert Kienbock in 1910 described the stepwise progression of the disease from isolated proximal lunate involvement to fragmentation and collapse of the lunate evolving to radiocarpal involvement and degenerative changes.
- 47. ETIOLOGY • • Exact etiology is unknown • Most likely multifactorial 1. Anatomic factors 2. Interrupted vascularity 3. Traumatic insult to lunate due to repeated microtrauma.
- 48. • ANATOMICAL FACTORS A. Ulnar negative varience B. Three types of lunate morphologies are found • Type 1 lunate has proximal apex • Type 2 and 3 are more rectangular • Type 1 is seen in wrists with negative ulnar varience and is more commonly found as compared to the other two types C. Lower radial inclination
- 49. • INTERRUPTED VASCULARITY • Vascularity to the lunate is variable • Three most commom types of patterns are found • Y pattern • I pattern • X pattern • In I pattern there is a single vessel supplying the lunate , which may increase the chances of osteonecrosis. In addition to this AVN of the lunate has been linked to vascular insults caused by fractures , ligamentous injuries, primary circulatory collapse , systemic diseases and venous congestion.
- 50. Clinical Features • Commonly effects men between 20 to 40 years of age • Symptoms may vary depending upon the stage at initial presentation • Pain localised to the radiolunate facet – the pain is classically insidious in onset • Decreased wrist motion • Swelling and decreased grip strength • Tenderness over the dorsal lunate and radiolunate facet • An effusion or bogginess over the radiocarpal joint • Movement especially dorsiflexion is limited • In extreme cases the clenching of hand fails to show the normal prominance of the 3rd metacarpal which is called FINSTER’S SIGN • Tenderness over the 3rd metacarpal
- 51. Radiographic Imaging • Xrays : • Negative in early stages of the disease • Progressively shows increased lunate density • Fragmentation • Collapse • Proximal migration of capitate • Widening of proximal carpal row • Scaphoid widening • Degenerative changes in radio carpal bone
- 52. • MRI : • MRI can detect early stages of the disease with increased signal uptake • In patients with perilunate dislocation or ulnar impaction syndrome changes within the lunate may appear similar to AVN , however these changes are often focal and nonprogressive.
- 54. TREATMENT – Goal of the treatment is pain relief , motion preservation , strength maintainance and function.
- 55. Osteonecrosis of Knee • First described by Ahlback in 1968 • It is a focal superficial subchondral lesion • Classification
- 56. Spontaneous osteonecrosis • Most common type • Female : male 3 : 1 • Effects medial femoral condyle with or without ipsilateral tibial plateau. • Usually involves one side of the knee
- 57. Pathophysiology
- 58. Clinical features • Classical patient is Elderly lady Active lifestyle May have history of osteoporosis or osteopenia Without any history of trauma Unilateral acute onset medial sided knee pain Pain Sudden onset severe knee pain Localised to medial aspect Worsen at night / during rest Limping + ROM at knee decreased
- 59. Secondary osteonecrosis • Risk factor - alcohol abuse , excessive corticosteroid use • Pathophysiology • 80 % cases are Bilateral. Bone marrow adipose tissue enlargement Increased intraosseous pressure Bone ischemia and vascular occulusion
- 60. CLINICAL FEATURES SYMPTOMS GRADUAL ONSET OF PAIN OVER FEMORAL CONDYLE 20 % CASES HAVE TIBIAL CONDYLE PAIN FREQUENT INVOLVEMENT OF MULTIPLE JOINTS SIGNS KNEE EFFUSION LIMITED ROM SECONDARY TO PAIN TENDERNESS OVER MEDIAL FEMORAL CONDYLE
- 63. • MRI • More than 95 %sensitivity and specificity • Features • Subchondral cresents • Bone marrow edema localised to medial femoral condyle epiphysis • Focal deformity of cartilage • Degeneration of menisci • Double halo sign Subchondral cresent Bone marrow edema Double Halo sign
- 64. • TECHNETIUM BONE SCAN • MANY JOINTS CAN BE EXAMINED AT ONCE • SUITABLE FOR PATIENTS CONTRAINDICATED FOR MRI • LESS SENSITIVE AND SPECIFIC THAN MRI MRI IMAGE CORRESPONDING TECHNETIUM SCAN IMAGE
- 65. TREATMENT CONSERVATIVE TREATMENT ANALGESIC ACTIVITY MODIFICATION PROTECTED WEIGHT BEARING FOR 6 – 12 WKS QUADRICEPS AND HAMSTRING STRENGTHENING EXERCISES BISPHOSPHONATES TO REDUCE SUBCHONDRAL COLLAPSE LOCAL PULSED ELECTROMAGNETIC FIELD THERAPY ( 6 hr daily for 90 days ) PROSTAGLANDIN I2 iv for 5 days to reduce pain and marrow edema
- 66. • SURGICAL TREATMENT • JOINT PRESERVING SURGERIESIES • ARTHROSCOPIC DEBRIDEMENT • PERCUTANEOUS CORE DECOMPRESSION • BONE GRAFTING • VALGUS PRODUCING HIGH TIBIAL OSTEOTOMY • SUBCHONDRAL COLLAPSE • OSTEOCHONDRAL AUTOGRAFT • JOINT REPLACEMENT – UKA, TKA
- 67. PERCUTANEOUS CORE DECOMPRESSION HIGH TIBIAL OSTEOTOMY UNICOMPARTMENTAL KNEE ARTHROPLASTY
- 68. AVN OF TALUS • Talus is the second largest tarsal bone. • Articular cartilage covers 60 % surface • Parts - head , neck , body , lateral process , posterior process • Articulates with 4 bones – Tibia , Fibula , Calcaneum , Navicula.
- 69. Blood supply of talus Head is supplied by 2 sources 1. Medial superior part by Dorsalis Pedis Artery branches 2. Inferior part by Artery of Tarsal sinus Body by Anastomotic branches of Talus canal
- 70. Pathophysiology • AVN of Talus occurs by interruption in any part of blood network. • It may be obstruction , compression , physical disruption ( trauma ) of vesseles. • Ischemic necrosis due to lack of blood flow and oxygen deprivation • The body attempts repair by reossificstion , revascularization and resorption of necrotic bone leading to collapse of bone and deformity
- 71. Clinical features • Intense pain over ankle • ROM decreased at the ankle • Edema and echymosis over ankle
- 72. Radiographic evaluation • Xray - HAWKIN’S SIGN • Becomes evident after 6 - 8 weeks of injury • Disuse osteopenia due to resorption of subchondral bone • Visualised as thin subchondral radiolucent line along parts of the Talar Dome • Most evident in AP view • It indicates decreased blood flow to relevant portion of Talar Body. • Partial HAWKIN’S SIGN indicates INCOMPLETE AVN which is more predominant over LATERAL part of TALUS
- 73. HAWKIN’S SIGN
- 74. • MRI – • Most sensitive for detecting ANV of Talus • CT SCAN – • Excellent visualization of congruity of Subtalar Joint and provides details of the fracture
- 75. Classification system • HAWKIN’S CLASSIFICATION
- 76. TREATMENT • CONSERVATIVE TREATMENT • Painless AVN can be treated with NON Wt BEARING , BRACING , OBSERVATION. • SURGICAL TREATMENT • EARLY AVN – Core Decompression , Bone Grafting • LATE AVN – Ankle Arthrodesis , Subtalar Fusion , Tibiotalar Fusion , Tibiocalcaneal Fusion , Tibiotalocalcaneal Fusion , Blair’s Fusion
- 77. CORE DECOMPRESSION PRE (LEFT) AND POST (RIGHT) OP MRI OF VASCULARISED PEDICLE BONE GRAFT FROM CUBOID SUBTALAR FUSION
- 78. TIBIOTALAR FUSION TIBIOCALCANEAL FUSION TIBIOTALOCALCANEAL FUSION TOTAL ANKLE REPLACEMENT
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