Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Perthes Disease LCPD


Published on

All about legg calve perthe disease

Published in: Health & Medicine
  • Follow the link, new dating source: ❤❤❤ ❤❤❤
    Are you sure you want to  Yes  No
    Your message goes here
  • Sex in your area is here: ♥♥♥ ♥♥♥
    Are you sure you want to  Yes  No
    Your message goes here

Perthes Disease LCPD

  1. 1. Dr. ANOOP G.C. Junior Resident in orthopedics MCH Kozhikkode Legg Calve Perthes Disease Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  2. 2. SYNONYMS  Coxa plana  Osteochondritis deformans coxa juveniles  Pseudocoxalgia  Osteochondrosis of hip joint  Childhood Aseptic Necrosis of Femoral Head  Osteochondritis dessicans of Hip  Legg’s stress fracture Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  3. 3. DEFINITION • PERTHES DISEASE : is a self-limiting form of osteochondrosis of the femoral capital epiphysis • of unknown etiology that develops in children commonly between the ages of 4 – 12 years • caused by impaired circulation in the femoral head • necrosis of the femoral epiphysis and its replacement by new bone • resulting in deformation of the femoral head. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  4. 4. HISTORY  Described first by Waldenstrom in 1909 who mistakenly ascribed it to tuberculosis.  In 1910 was independently described by Arthur Legg , U. S. A - February Jacques Calve , France - July George Perthes ,Germany - October  Hence name – “Legg Calve Perthes Disease”  In 1922 Waldenstrom gave the correct interpretation and described the stages . Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  5. 5. LEGG CALVE PERTHES Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  6. 6. ETIOLOGICAL FACTORS - that play a role in development of illness  Vascular supply  Increased intra-articular pressure  Intraosseous pressure  Coagulation disorder  Growth hormones  Skeletal Growth  Social conditions  Genetic factors  Attention deficit Disorders  TRAUMA Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  7. 7. FEMORAL HEAD - vascular supply EXTRINSIC OR EXTRAOSSEOUS ANATOMY (Crock & Chung) 1. Extra capsular ring – base of neck - Formed by Medial circumflex femoral (Major)and Lateral circumflex femoral arteries - Branches ascend in 4 groups as Ascending cervical(Extra capsular) or Retinacular(intra capsular) arteries - Lateral group most important. - The Lateral group pierce the capsule and enter epiphysis to become Lateral epiphyseal arteries 2. Intra capsular ring – base of head - incomplete in 57% males and 31% females. - Formed by branches of ascending cervical & retinacular arteries. - They contribute to lateral epiphyseal arteries 3. Artery of Ligamentum teres Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  8. 8. FEMORAL HEAD - vascular supply INTRINSIC OR INTRAOSSEOUS ANATOMY (Trueta & Harrison) 1. Lateral epiphyseal Arteries - Formed by the Lateral group of Ascending cervical or Retinacular arteries - Supplies 2/3 rd of femoral head - Exclusive supply of suprolateral head 2. Medial epiphyseal or Artery of Ligamentum teres - Negligible to ½ of epipysis 3. Metaphyseal arteries Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  9. 9. FEMORAL HEAD - vascular supply ADULT Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  10. 10. TRUETA’S HYPOTHESIS • Infants and children <4 yrs : 2 arterial blood supplies to femoral head- the retinacular or ascending cervical arteries (Lateral epiphyseal artery) & the metaphyseal arteries • 4-12 yrs : single areterial supply by Lateral epiphyseal artery. This solitary blood supply makes this age period vulnerable to ischaemic necrosis due to compression by external rotators and extreme movements. • After 12 yrs: foveolar arteries of Ligamentum teres contribute blood along with Lateral epiphyseal arteries & incidence decreases. (In blacks it occurs earlier) Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  11. 11. TRUETA’S HYPOTHESIS  In adults :cartilage growth plate disappears & the metaphyseal arteries enter the epiphysis and thus the adult pattern of blood supply by • Foveolar • Retinacular • Metaphyseal arteries occurs .  Hence the disease doesnot occur in adults & rare after 12 year.  Supply by ligamentum teres occurs earlier in blacks - disease is rare in blacks Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  12. 12. FEMORAL HEAD - The Blood Supply of the Immature Femoral Head CHILD  Metaphyseal or no other vessels cross epiphyseal plate  Artery of Ligamentum teres is not developed  Solely dependent on Lateral epiphyeal arteries Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  13. 13. CAFFEY’S HYPOTHESIS Avascular necrosis of femoral head results from intraepiphyseal compression of blood supply to the ossification center and not due to external compression of vessel. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  14. 14. ETIOLOGICAL FACTORS Vascular : General reduction in blood flow with a significant reduction in medial circumflex artery Normally venous drainage occurs through medial circumflex vein In Perthes disease increased venous pressure in affected neck associated venous congestion in metaphysis Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  15. 15. ETIOLOGICAL FACTORS  Increased intra-articular pressure : – Animal experiments have shown that an ischemia similar to that in Perthes disease can be generated by increasing the intra-articular pressure. – However, the condition of transient synovitis of the hip does not appear to be a precursor stage of Perthes disease as the increased pressure resulting from the effusion in transient synovitis does not lead to vessel closure Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  16. 16. ETIOLOGICAL FACTORS Intraosseous pressure: – The measurement of intraosseous pressure in Perthes patients has shown that the venous drainage in the femoral head is impaired, causing an increase in intraosseous pressure. Coagulation disorder : • Study have found a coagulation disorder in 75% children with Perthes disease. • In most cases the disorder was thrombophilia. • protein C or protein S deficiency, elevated serum lipoprotein, Factor-V Leiden mutation, Anticardiolipin antibodies were also noted. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  17. 17. ETIOLOGICAL FACTORS  Growth hormones : – While earlier studies found reduced levels of the growth hormone. – Recent studies have not shown any difference from control groups in respect of hormone status  Skeletal Growth: – Children with Perthes disease are shorter, on average, than their peers of the same age & show a retarded skeletal age (cartilaginous dysplasia). – The maturation disorder occurs between the ages of 3 and 5 years. – Both the trunk and extremities lag behind in terms of growth. – But pick up to attain normal skeletal maturity by adulthood. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  18. 18. ETIOLOGICAL FACTORS  Social conditions: – Studies in the UK have shown that Perthes disease is more common in the lower social status. – The authors suggest a poorer diet during pregnancy as one possible explanation for this phenomenon. – A recent study did not confirm this theory  Genetic factors: – Studies have shown that first degree relatives of children with Perthes disease are 35 times more likely to suffer from the condition than the normal population. – Even second- and third-degree relatives show a fourfold increased risk. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  19. 19. ETIOLOGICAL FACTORS  Attention deficit Hyperkinetic Disorders : more prone to trauma  Synovitis : predisposed due to increased intra articular pressure  TRAUMA : – Trauma in the predisposed child ppts AVN OF FEMORAL HEAD AND development of Perthes disease – the lateral epiphyseal artery which courses through a narrow passage is susceptible to damage Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  20. 20. HERIDITARY ASSOCIATIONS Congenital abnormalities Hemivertebrae Deafnes Imperforate anus Pyloric stenosis Epilepsy Cong heart disease Short tibia Undescended testis Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  21. 21. PATHOLOGY  By Waldenstrom in 1922  4 stages based on microscopic and gross pathology Paul_Petter_Waldenström Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  22. 22. Stages Stage 1 : Incipient or synovitis stage • Lasts for 1-3 week • synovium is swollen edematous and hyperemic • joint fluid is increased • Inflammatory cell are notably absent Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  23. 23. Stages  Stage 2 : Avascular necrosis • Lasts for 6 month to 1year • Significant necrosis of bone • trabeculae are crushed into minute fragments. • Absent/pyknotic nuclei in the osteocytes • No evidence of bone regeneration • Degenerative changes in the basal layer of articular cartilage • Thickened peripheral cartilagenois cells • Gross contour of femoral head is unchanged Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  24. 24. Stages  Stage 3 : Fragmentation or Regeneration – Lasts for 2- 3 year. – Dead bone infested with vascular connective tissue was actively resorbed by osteoclasts and replaced by newly formed immature bone. – Loss of epiphyseal height due to collapse of bony trabeculae and resorption of fragmented necrotic bone Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  25. 25. Stages  Stage 4 : Healed or Residual Stage • Normal bone starts replacing necrotic bone. • Ossific nucleus is deformed assuming mushroom contour • Femoral head enlarges, flattens and subluxate. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  26. 26. EPIDEMIOLOGY • ONSET : 18 months - skeletal maturity • Most prevalent : 4-12 yrs • Male: female : 4 : 1 • Bilateral in 10 - 20% • No evidence of inheritance but 35 time risk in 1st degree relative. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  27. 27. CLINICAL FEATURE - Symptoms Described by Sundt in 1920 – limp-exacerbated by activity and relieved by rest – Pain-located in • Groin • Anterior hip region • Laterally around greater trochanter • Referred pain to knee (may obscure the true nature of the disorder) • Aggravated by physical activity • Night pain – H/o of antecedent trauma – Waxing & waning of symptoms Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  28. 28. CLINICAL FEATURE - Signs  Typical limp : combination of antalgic and Trendelenburg gait  Signs of old injuries - scars, old fractures  Reduction of hip motion( muscle spasm) – Minimal noted at abduction & internal rotation(earlier) – Greater loss of motion with more severe disease – Abduction contractures – Lose all rotations in very severe cases – FLEXION/EXTENSION SELDOM AFFECTED Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  29. 29. CLINICAL FEATURE - Signs  Wasting of gluteus, quadriceps & hamstrings  Positive Trendelenburg on the involved side  Classicaly : A small Thin Extremely active Constantly running and jumping child Who develops limping after strenuous physical activities Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  30. 30. NATURAL HISTORY  DISEASE SEVERITY:  Mild to severe  Majority will have moderate symptoms for 12- 18 months followed by complete resolution of symptom  Finally return to normal activities  PATIENT’S AGE : MOST CONSISTENT FACTOR AFFECTING COURSE OF THE DISEASE – Early onset (before 6 yrs) : mild – Onset 6-9 yrs :moderate – Late Onset after 9 yrs: most severe course and worst outcome Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  31. 31. NATURAL HISTORY  EXTENT OF RADIOGRAPHIC CHANGES : Poorest results seen in hips with the greatest degree of involvement  OUTCOME: affected by the duration from onset of disease to complete resolution  The shorter the duration the better the outcome Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  32. 32. ASSOCIATION BETWEEN CLINICAL FINDINGS & STAGES Stage 1 – Initial stage Waxing/waning of symptoms & signs Mild limp and pain Episodes of moderate discomfort(weeks) Stage 2 – Fragmentation stage Limp and pain more Greater loss of range of motion Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  33. 33. ASSOCIATION BETWEEN CLINICAL FINDINGS & STAGES Stage 3 – Reossification/healing stage  Pain /limp resolves  Mild limitation of joint motion  Resumes normal activities Stage 4 – Residual/healed stage  Symptoms disappear as head completely reossifies Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  34. 34. PROGNOSIS – poor in • Female child • Obese child • Age of Onset > 8 years • Adduction contractures • Progressive decrease in range of movements • Presence of “Head at risk Sign’s” on Radiographs Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  35. 35. DIFFERENTIAL DIAGNOIS • Transient synovitis • Slipped femoral epiphysis • Congenital dysplasia of hip • Congenital coxa vara • Early Tuberculosis • Rheumatoid arthritisAcute and chronic sepsis • Acetabular dysplasia • Epiphyseal dysplasia • Histiocytosis • Gaucher’s disease Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  36. 36. INVESTIGATIONS • Bloods – FBC, ESR, CRP, Blood Culture – r/o other diseases. • Radiographs • Ultrasound Scan • CT scan • Bone Scan – Decreased bone scan uptake before radiographic changes • MRI –Earlier diagnosis than plain radiography – More information regarding extent of necrosis than bone scanning • Arthrography Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  37. 37. IMAGING STUDIES  Radiographic staging of disease evolution: - Based on Anteroposterior and Lateral frog leg views - the modified version of WALDENSTROM’S classification 4 STAGES 1. Initial stage 2. Fragmentation stage 3. Reossification stage 4. Residual stage Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  38. 38. RADIOGRAPHY AP View FROG LEG View Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  39. 39. Intial stage (6 months)  Lateralization of femoral head in the acetabulum  Smaller ossific nucleus due to cessation of growth of the capital epiphysis  Apparent widening of medial joint space (synovitis & hypertrophy of articular cartilage)  WALDENSTROM’S SIGN : Linear fracture in the subchondral area of femoral head ( frog leg lateral view)  Increased density of femoral head : 20 accumulation of new bone on the dead bone trabeculae in the head .  Metaphyseal cysts & lucencies Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  40. 40. Fragmentation stage (8 months)  Lucencies develop in the ossific nucleus/ other sections remain sclerotic.  Central dense fragment gets demarcated from the medial & lateral segments of the head  Increased density resolves  acetabular contour more irregular  End of this stage is marked by appearance of new bone in the subchondral area of femoral head Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  41. 41. Reossification stage / healing stage (51 months)  Starts in the Centre of the femoral head and expands medially and laterally  Last areas to reossify - anterior segment of head - Centre of head  Lucent portions of femoral head fill in with woven bone  Over the time the new bone remodels into trabecular bone  Head regains roundness Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  42. 42. Residual stage  Head fully reossified  Remodeling of head continues until skeletal maturity when the permanent contour is established  Acetabulum remodels as well Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  43. 43. CHANGES IN THE METAPHYSIS  Gill (1940) reported the changes as “HOLES OF DECALCIFICATION” due to metaphyseal necrosis  Metaphyseal Cyts :Ponseti described cystic changes caused by tongues of fibrillated cartilage stretching deep into the neck  Sagging Rope Sign Radiodense line overlying the proximal femoral metaphysis Produced by growth plate damage associated with metaphyseal response. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  44. 44. CHANGES IN THE METAPHYSIS Metaphyseal cyst Sagging rope signDr.Anoop G.C.,JR,Orthopaedics,GMCK
  45. 45. CHANGES IN PHYSIS  Abnormal growth of proximal femoral physis  Premature physeal closure(25% cases) causing  Lateral extrusion of capital nucleus  Medial bowing of femoral neck  Greater trochanter overgrowth  lateral X-ray showed a bulge in the metaphysis (a step shaped irregularity) comparable to changes observed in Blount’s disease Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  46. 46. CHANGES IN THE ACETABULUM  BICOMPARTMENTALIZATION :When the femoral head protrudes from the acetabulum , the medial wall may form what looks like a second compartment for the head (Yngve and Roberts)  by early closure of triradiate cartilage  its an indicator of poor out come  Resolves during the healing stage  Osteoporosis of the roof of the acetabulum  Position of the head rather than it’s shape has been the most significant factor in the growth & remodeling of acetabulum Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  48. 48. ULTRASONOGRAPHY  To demonstrate joint effusion  Provide a good profile of cartilaginous femoral head and subsequent deformation of head can be assessed Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  49. 49. CT SCAN  3D Images of head & acetabulum  Useful in later stages – To evaluate pain – Locking of joint – Mechanical symptoms Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  50. 50. BONE SCAN  Effective means of diagnosis in early stages, before associated radiographic findings are apparent  To classify the severity of disease  Reveals revascularization and consequently the stage of the disease  To classify revascularization as either recanalization or neovascularization Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  51. 51. MRI  Accurate imaging modality for early diagnosis  Visualization of configuration of the femoral head and acetabulum  Determine the extent of revascularization  Epiphyseal involvement more clearly visualized  Earlier and reliable information about the true extent of femoral head necrosis  Finding the degree of involvement during the early phases of this disorder Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  52. 52. ARTHROGRAPHY  Provides reliable information regarding containment of femoral head within the acetabulum  Examiner can assess the congruity of the hip in many different position.  Most often used in the early diagnosis of HINGE ABDUCTION OF HIP in which the head hinges out of acetabulum when the hip is abducted – It occurs early in the course of the disease – The longer it remains untreated ,the worst is the outcome . – Treatment :traction initially to relieve hinging and later surgery to contain the head . Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  53. 53. ARTHROGRAPHY Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  54. 54. RADIOLOGICAL CLASSIFICATION • AP and FROG LEG views required • Depending on Extent of lesions • Important in deciding treatment method. • 3 classifications are – Catterall – Salter & Thompson – Herring Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  55. 55. Catterall • Most common • Based on extent of femoral head lesion • IV groups Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  56. 56. Catterall Group I 25% involvement No metaphyseal Reaction No sequestrum No subchondral fracture lineDr.Anoop G.C.,JR,Orthopaedics,GMCK
  57. 57. Catterall Group II 50% involvement Sequestrum present - junction Clear Metaphyseal reaction - antero lateral Subchondral fracture line - anterior halfDr.Anoop G.C.,JR,Orthopaedics,GMCK
  58. 58. Catterall Group III 75% involvement Sequestrum large - junction sclerotic Metaphyseal reaction - diffuse - antro lateral area Subchondral fracture line - posterior half Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  59. 59. Catterall Group IV Whole head involvement Metaphyseal reaction - central or diffuse Posterior remodelling Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  60. 60. Catterall’s - Head at Risk Signs • Lateral epiphyseal calcification • Lateral subluxation • Gage’s sign • Cage sign • Caffey’s or Salter Sign • Metaphyseal cysts • Horizontal growth plate Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  61. 61. Lateral subluxation Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  62. 62. GAGE’S SIGN • small osteoporotic segment forming a translucent V- shaped trough in the lateral part of the epiphysis Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  63. 63. CAGE SIGN • Calcification of the lateral epiphysis Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  64. 64. Salter’s or Caffey’s sign • a subchondral # may occur in the anterolateral aspect of the femoral capital epiphysis. This produces a crescentic radiolucency known as the crescent, Salter’s or Caffey’s sign Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  65. 65. Salter and Thompson • Extend of sub chondral fracture • Subchondral fracture correlates with eventual extent of resorption – GROUP A : Subchondral # involving <50% of the femoral dome – GROUP B : Subchondral # involving >50% of the femoral dome Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  66. 66. Herring The femoral head pillars are derived by noting the lines of demarcation between the central sequestrum and the remainder of the epiphysis on the anteroposterior radiograph Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  67. 67. Herring Group A Normal Height of lateral pillar maintained Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  68. 68. Herring Group B > 50% of lateral pillar height maintained Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  69. 69. Herring Group C < 50% of lateral pillar height maintained Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  70. 70. TREATMENT • AIM OF TREATMENT : • The etiology of Perthes disease is unknown and consequently treatment is not in any way directed to achieving a cure. • If it’s a elf limiting process of degeneration and then regeneration why do we need to treat it ? Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  71. 71. AIM OF TREATMENT • The long-term aim of treatment of Perthes’ disease is to prevent the onset of secondary degenerative arthritis of the hip. • Several long-term studies have shown that loss of sphericity of the femoral head is the most important factor related to development of secondary degenerative arthritis of the hip. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  72. 72. GOALS OF TREATMENT • Elimination of hip irritability. • Containment of the head. • Restoration good ROM • Prevent the femoral head from getting deformed or enlarged • Prevent trochanteric overgrowth • Ensure Psychological & Physical developmentDr.Anoop G.C.,JR,Orthopaedics,GMCK
  73. 73. TREATMENT PROTOCOL Observation only Intermittent symptomatic treatment Early definitive treatment Conservative surgical Late reconstructive surgical Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  74. 74. Observation only • All children < 6 years – Irrespective of the extent of involvement of femoral capital epiphysis – Provided there is no limitation of motion or subluxation • All children > 6year – Under Caterll group I & II or Salter – Thompon group A – Provided there is no limitation of motion or subluxation or collape • Do not require active management but require frequent evaluation clinically & Radiologically every 3 months. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  75. 75. Intermittent symptomatic treatment • All children under observation group developing persistent loss of Motion or containment. • Temporary or periodic treatment for 1 or 2 weeks with – Bed ret in abduction – Traction in abduction – Physiotherapy • Once motion is regained and irritability subsides child can resume normal activities • Bi monthly evaluation is required. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  76. 76. Early definitive treatment • All children in intermittent symptomatic group with 2 – 3 recurrent episodes of irritability. • All children > 6 years under Caterall group III & IV or Salter – Thompson group B. • Any child with severe loss of motion or evidence of Extrusion. • Contraindicated in severe flattening of head , healed cases and hinged acetabulum. • Principle is CONTAINMENT of femora head in acetabulum – Non surgical or surgical.Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  77. 77. CONTAINMENT - Non surgical • Braces & orthoses – Preliminary traction is applied to overcome muscle spasm while the hip is gradually abducted and internally rotated – Brace are applied with lower limbs in approximately 45 degree abduction and light internal rotation. – Walking is encouraged since weight bearing movement are evential to remodeling. – Bed time exercises preferably done under water. – Plastic abduction night splint – Generally discontinued at 20 month or if evidence of new layer of subchondral bone in radiograph Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  78. 78. Braces and orthoses • An TORONTO BRACENEWINGTON BRACE Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  79. 79. Braces and orthoses TACHDJIAN BRACE BIRMINGHAM BRACE Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  80. 80. Braces and orthoses Snyder sling Patten botom braceDr.Anoop G.C.,JR,Orthopaedics,GMCK
  81. 81. Braces and orthoses Ambulatory abduction orthosisDr.Anoop G.C.,JR,Orthopaedics,GMCK
  82. 82. Plaster Casting • Petrie or “Broomstick cast” – By Patric and Bitenc. – Long leg cats are applied to both extremities in 30 – 40 degree abduction and 5 degree internal rotation. – And secured by two wooden bars. • Disadvantages – Knee and ankle stiffness with adaptive articular changes – Restricted ambulation and pressure soresDr.Anoop G.C.,JR,Orthopaedics,GMCK
  83. 83. Petrie or “Broomstick cast” Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  84. 84. SURGICAL CONTAINMENT • INDICATIONS: – Age of clinical onset > 8yrs of age – Herring type B – Radiological evidence of loss of containment by conservative modes • CONTRAINDICATIONS: – Herring’s type A and C – Herring’s type B if child less than 8 yrs – Healed cases. – Hinged abduction • ADVANTAGES – Ability to obtain permanent containment of head. – Period of Restriction is only 2 months. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  85. 85. CONTAINMENT SURGERIES – Varus Derotational Femoral Osteotomy –Innominate or Salter osteotomy –Shelf procedure –Combination of femoral and innominate osteotomy –Combination of innominate osteotomy and shelf Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  86. 86. VARUS DEROTATION FEMORAL OSTEOTOMY (VDO) • Initially advocated by Axer in 1965 • Procedure of choice in 8 – 10 yrs without limb shortening • Uncovered head on MRI / Arthrogram • Excessive femoral anteversion • Types - Open wedge or closed wedge • Technique - Osteotomy at subtrochantric level & Distal femur is fixed in varus and external rotation using plate and screws • Hip spica for 8-12 weeks Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  88. 88. INNOMINATE OSTEOTOMY – SALTER • Initially advocated by Salter in 1966 • Advantages: – Anterolateral coverage – Lengthening of shortened limb – No second operation for I/R • Disadvantages: – Improper coverage in older child – Limb length inequality – AVN due to raised pressure in joint • Technique – Iliac osteotomy is made just above acetabulum extending from greater sciatic notch to anterior inferior Iliac pine – Entire acetabulum with pelvis is rotated downward and outwards – Bone graft from ilium is applied to osteotomy site • Hip Spica for 8-12 weeks. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  89. 89. INNOMINATE OSTEOTOMY – SALTER Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  90. 90. SHELF PROCEDURE • Formerly used as a salvage procedure • Catterall proposes this as the primary method of management in children over 8 years of age • INDICATION: • Lateral subluxation • Insufficient coverage • Hinged abduction • COMPLICATION: • Loss of hip flexion • lateral femoral cutaneous nerve injury • Technique: • bone graft is harvested from the ilium and inserted into the roof of the acetabulum. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  91. 91. SHELF PROCEDURE Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  92. 92. LATE RECONSTRUCTIVE SURGERIES • Done for Healed Perthes with permanent deformities • Valgus osteotomy - Hinged abduction • Shelf acetabuloplasty - Coxa magna • Garceau cheilectomy - Malformed head in catterall group 3 • Trochanteric advancement or arrest - Capital physeal arrest & trochantric overgrowth • Chiari osteotomy– Significant femoral head flattening. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  93. 93. ASSESSMENT OF END RESUTLT • Assessment of end result is done at 4 years after onset. • Based on sphericity and containment of femoral head. • Good – no arthritis develops • Fair – mild to moderate arthritis will develop in late adulthood • Poor – severe arthritis will develop before age of forty. Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  94. 94. ASSESSMENT OF END RESUTLT  SPHERICITY OF HEAD  MOSE CLASSIFICATION: Based on fitting of contour of healed femoral head into template of concentric circles in both AP & Frog leg lateral views • Good - < 1 mm • Fair - < 2 mm • Poor - > 2 mm Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  95. 95. ASSESSMENT OF END RESUTLT  CONTAINMENT OF HEAD  CE Angle of Wiberg: - A line is drawn from center of head C and edge of acetabulum E called CE line - The angle between CE line and vertical through center of head is called the CE angle.  Good - >20  Fair- 15-19  Poor- < 15 E C Vertical Dr.Anoop G.C.,JR,Orthopaedics,GMCK
  96. 96. THANK YOU Dr.Anoop G.C.,JR,Orthopaedics,GMCK