Legg Calve Perthes Disease (LCPD) is osteonecrosis of the femoral head that typically affects children between the ages of 4-10. For patients under 6 years old with minimal involvement, the prognosis is generally good and treatment involves rest and anti-inflammatories. For patients between 6-8 years old with more involvement, containment of the femoral head through bracing or surgery is often recommended. Patients presenting after age 9 usually have a poor prognosis due to more advanced involvement and are treated with early containment procedures, though stiffness can be a complication.
Madelung deformity is an abnormality of the palmar ulnar part of the distal radial physis in which progressive ulnar and volar tilt develops at the distal radial articular surface, with dorsal subluxation of the distal ulna.
Madelung deformity is an abnormality of the palmar ulnar part of the distal radial physis in which progressive ulnar and volar tilt develops at the distal radial articular surface, with dorsal subluxation of the distal ulna.
LCPD or Perthes disease - idiopathic avascular necrosis of femoral head, characterized mainly in child age 4-7 years - with a feature of limping and pain in the hip or groin
Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment
Presentation contain etiology, blood supply of femoral head & neck,pathogenesis ,classification system ,clinical features,diagnosis,managment, pelvic & femoral osteotomies in detail
LCPD or Perthes disease - idiopathic avascular necrosis of femoral head, characterized mainly in child age 4-7 years - with a feature of limping and pain in the hip or groin
Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment
Presentation contain etiology, blood supply of femoral head & neck,pathogenesis ,classification system ,clinical features,diagnosis,managment, pelvic & femoral osteotomies in detail
Prof. Anisuddin Bhatti Paediatric Orthopaedic Surgeon Dr. Ziauddin University Hospital, Clifton, Karachi delivered lecture on DZU Webinar series Lecture 2 on Legg Calve Perthes. Declared few pics and material taken from google.
-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%)
-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
-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
-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
-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
-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
-increased radiodensity due to new bone forming on old bone
-AVN process after fx/dislocation does not undergo fragmentation
-25% of anterocentral head involved -no sequestrum, no subchondral fx’s, normal metaphysis
-50% of anterolateral region involved -evidence of sequestrum/ subchondral (anterior) fx, med/lat pillars intact
-75% of head involved -large sequestrum, lat pillar (column) involved, sclerotic junction btwn normal/abnormal -subchondral fx line extends into post ½ of epiphysis
-whole head involved, widespread epiphyseal collapse -diffuse or central metaphyseal lesion -Posterior remodeling of ephiphysis -poor prognosis