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Legg Calve Perthes Disease
History ,[object Object],[object Object],[object Object]
Definition ,[object Object]
Epidemiology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object]
Etiology ,[object Object],[object Object],[object Object],[object Object]
Causes ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
Pathogenesis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
Blood Supply
Radiographic Stages ,[object Object],[object Object],[object Object],[object Object],[object Object]
Initial Stage ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fragmentation Stage ,[object Object],[object Object],[object Object]
Reossification Stage ,[object Object],[object Object]
Healed Stage ,[object Object],[object Object]
Group I
Group II
Group III
Group IV
[object Object],[object Object],[object Object],[object Object],Lateral Pillar Classification
Salter-Thompson Classification ,[object Object],[object Object],[object Object],[object Object]
Clinical Features ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Risk Factors
Differential Diagnosis
Workup ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],Ultrasonography in transient synvitis and early Perthes’ disease
CT Scan ,[object Object],[object Object],[object Object]
MRI ,[object Object],[object Object],[object Object]
Outcome variables ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Treatment Options ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Osteotomies
Summary ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
Follow-up ,[object Object],[object Object],[object Object]
Complications   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Prognosis   ,[object Object],[object Object],[object Object],[object Object]

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Legg+Calve+Perthes+Disease

Hinweis der Redaktion

  1. -incidence of positive family hx ranges from 1.6% to 20%, but no hard evidence of predisposition -is more common in certain geographic areas (urban>rural)=nutritional?, later born children, strong association with ADHD (33%)
  2. -Phemister- thought it was infectious but cx neg -Axhausen- thought bacillary embolism with weak infection which healed quickly -1975 Matsoukas showed association with prenatal rubella -1973 Sanches, infarcted animal femoral heads, unable to produce typical histologic picture of LCPdz with one infarction, could do it with a second. Supported by Inoue using human histologic material
  3. -few human specimens have been studied, each showing only a stage of the dz and usually from sample of just one part of the involved head. Histologically not well illucidated
  4. -changes in zone 2 are abnormal, have different histochemical and US properties vs normal, also see small 2ndary ossification centers directly on the abnormal cartilage matrix -synovial fluid nourishes 2 superficial layers, continue to proliferate -deep layer affected by ischemic process
  5. -physeal plate: thinner than normal, irregular cell columns and cartilage masses -metaphysis: cartilage does not ossify, proliferates with bone, causes tongues of cartilage extending into metaphysis -skeletal surveys shows contour irregularities in 48% of normal contralateral capital epiphysis, suggesting it is a generalized disorder, more appropriately named a syndrome
  6. -growth failure due to lack of blood supply -affected femoral ossific nucleus appears radiodense (relative osteopenia of surrounding bone vs. increased mass in that area?) -affected femoral head appears smaller vs. other side -wide med joint space due to: synovitis? Decreased head volume from necrosis and collapse? Due to increased blood flow to soft tissues (eg. Lig teres) causing lateral displacement? Most likely due to epiphyseal cartilage hypertrophy (x-ray phenomenon) -crescent sign= subchondral radiolucent zone, likely results from a subchondral stress fracture and the extent of this zone determines the extent of the necrotic fragment
  7. -increased radiodensity due to new bone forming on old bone
  8. -AVN process after fx/dislocation does not undergo fragmentation
  9. -25% of anterocentral head involved -no sequestrum, no subchondral fx’s, normal metaphysis
  10. -50% of anterolateral region involved -evidence of sequestrum/ subchondral (anterior) fx, med/lat pillars intact
  11. -75% of head involved -large sequestrum, lat pillar (column) involved, sclerotic junction btwn normal/abnormal -subchondral fx line extends into post ½ of epiphysis
  12. -whole head involved, widespread epiphyseal collapse -diffuse or central metaphyseal lesion -Posterior remodeling of ephiphysis -poor prognosis