legg calve perthes disease donnely 2001 5afad2fc5e0b007027c03a29b821eb3c

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  • 1.Legg Calve Perthes DiseaseJoseph Donnelly, M.D.December 10, 2001

2. Overview History Epidemiology/ Etiology Pathogenesis Radiographic stages Presentation/ Exam Imaging Treatment 3. History Late 19th century: hip infections thatresolved without surgery First described in 1910 Early path studies: cartilaginous islands inthe epiphysis 4. Epidemiology Disorder of the hip in young children Usually ages 4-8yo As early as 2yo, as late as teens Boys:Girls= 4-5:1 Bilateral 10-12% No evidence of inheritance 5. Etiology Unknown Past theories: infection, inflammation,trauma, congenital Most current theories involve vascularcompromise Sanches 1973: second infarction theory 6. Etiology: blood supply 7. Pathogenesis Histologic changes described by 1913 Secondary ossification center= covered bycartilage of 3 zones: Superficial Epiphyseal Thin cartilage zone Capillaries penetrate thin zone from below 8. Pathogenesis: cartilage zones 9. Pathogenesis Epiphyseal cartilage in LCP disease: Superficial zone is normal but thickened Middle zone has 1)areas of extreme hypercellularity in clusters and 2)areas of loose fibrocartilaginous matrix Superficial and middle layers nourished bysynovial fluid Deep layer relies on blood supply 10. Pathogenesis Physeal plate: cleft formation, amorphisdebris, blood extravasation Metaphyseal region: normal boneseparated by cartilaginous matrix Epiphyseal changes can be seen also ingreater trochanter, acetabulum 11. Radiographic Stages Four Waldenstrom stages: 1) Initial stage 2) Fragmentation stage 3) Reossification stage 4) Healed stage 12. Initial Stage Early radiographic signs: Failure of femoral ossific nucleus to grow Widening of medial joint space Crescent sign Irregular physeal plate Blurry/ radiolucent metaphysis 13. Initial Stage 14. Initial Stage 15. Fragmentation Stage Bony epiphysis begins to fragment Areas of increased lucency and density Evidence of repair aspects of disease 16. Fragmentation Stage 17. Fragmentation Stage 18. Reossification Stage Normal bone density returns Alterations in shape of femoral head andneck evident 19. Reossification Stage 20. Reossification Stage 21. Healed Stage Left with residual deformity from diseaseand repair process Differs from AVN following Fx ordislocation 22. Presentation Often insidious onset of a limp C/O pain in groin, thigh, knee 17% relate trauma hx Can have an acute onset 23. Physical Exam Decreased ROM, especially abduction andinternal rotation Trendelenburg test often positive Adductor contracture Muscular atrophy of thigh/buttock/calf Limb length discrepency 24. Imaging AP pelvis Frog leg lateral Key= view filmssequentially overcourse of dz Arthrography MRI role undefined 25. Differential Diagnosis Important to rule out infectious etiology(septic arthritis, toxic synovitis) Others: Chondrolysis -Neoplasm JRA-Sickle Cell Osteomyelitis-Traumatic AVN Lymphoma -Medication 26. Radiographic Classifications Describe extent of epiphyseal disease Catterall classification= most commonlyused 4 groups based on amount of femoral headinvolvement Also presence of sequestrum, metaphyseal rxn,subchondral fx 27. Group I 28. Group II 29. Group III 30. Group IV 31. Lateral Pillar Classification 3 groups: A) no lateral pillar involvment B) >50% lat height intact C) 15mos) 35. Non-operative Tx Improve ROM 1st Bracing: Removable abduction orthosis Pietrie casts Hips abducted and internally rotated Wean from brace when improved x-rayhealing signs 36. Bracing 37. Non-operative Tx Check serial radiographs Q3-4 mos with ROM testing Continue bracing until: Lateral column ossifies Sclerotic areas in epiphysis gone Cast/brace uninvolved side 38. Operative Tx If non-op tx cannot maintain containment Surgically ideal pt: 6-9yo Catterral II-III Good ROM