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Hip dysplesia ppt

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Hip dysplesia radiology

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Hip dysplesia ppt

  1. 1. Dysplastic Hip - Radiology Dr. Bhanupriya Singh JR-1.
  2. 2. X-Ray views:- AP radiograph of the pelvis or hip is taken with the patient supine, and both feet in approximately 15° of internal rotation. This reduces the normal 25 to 30° femoral anteversion, allowing better visualization of the femoral neck
  3. 3. X-Ray views:- Judet views (anterior and posterior oblique view of pelvis) are performed with the patient in a 45° oblique position. When the affected hip is in a posterior oblique position, the posterior column and anterior acetabular rim are well seen. Conversely, with the affected hip in the anterior oblique position, the anterior column and posterior acetabular rim are well seen. Forty-five- degree posterior oblique view of the left acetabulum reveals a non- displaced fracture through the posterior column.
  4. 4. X-Ray views:- The frogleg lateral view is performed with the patient supine, feet together, and thighs maximally abducted and externally rotated.The radiographic tube is angled 10 to 15° cephalad, directed just above the pubic symphysis. The anterior and posterior aspects of the femoral neck, as well as the lateral aspect of the femoral head, are seen with this projection.
  5. 5. X-Ray views:- Pelvic outlet (Ferguson) view, is performed in the same position as the AP view, with the radiographic tube angled 30 to 35° cephalad, and the central beam directed at the center of the pelvis. This projection allows excellent visualization of the sacroiliac joints, the pubic rami, and the posterior acetabular rim
  6. 6. X-Ray views:- Pelvic inlet view is performed in the same position as the AP view, with 30 to 35° of caudal angulation of the radiographic tube. This view allows visualization of the sacral promontory, the iliopectineal line (anterior column), the ischial spine, and the pubic symphysis
  7. 7. X-Ray views:- Groin-lateral view of the hip is performed with the patient supine, the nonaffected leg elevated and abducted, and the affected leg extended. The radiographic tube is directed horizontally toward the medial aspect of the affected hip, with 20° of cephalad angulation Long-leg lateral view of the left hip shows prominent femoral head–neck junction, narrowing of the anterosuperior joint space, and sclerosis of the anterosuperior acetabulum. Heterotopic bone formation is seen from previous hip arthroscopy for anterior labral debridement in a patient with femoroacetabular impingement.
  8. 8. Ligaments ( increase stability) The only intracapsular ligament is the ligament of head of femur. It is a relatively small ligament that runs from the acetabular fossa to the fovea of the femur. It encloses a branch of the oburator artery, which comprises a small proportion of the hip joint blood. Extracapsular There are three extracapsular ligaments. They are continuous with the outer surface of the hip joint capsule. Iliofemoral: Located anteriorly. It originates from the ilium, immediately inferior to the anterior inferior iliac spine. attaches to the intertrochanteric line in two places, giving the ligament a Y shaped appearance. It prevents hyperextension of the hip joint. Pubofemoral: Located anteriorly and inferiorly. It attaches at the pelvis to the iliopubic eminance and obturator membrane, and then blends with the articular capsule. It prevents excessive abduction and extension. Ischiofemoral: Located posteriorly. It originates from the ischium of the pelvis and attaches to the greater trochanter of the femur. It prevents excessive extension of the femur at the hip joint.
  9. 9. Neurovascular Structures Vascular supply to the hip joint is achieved via the medial and lateral circumflex femoral arteries, and the artery to head of femur. The circumflex arteries are branches of the profunda femoris artery. They anastamose at the base of the femoral neck to form a ring, from which smaller arteries arise to the supply the joint itself. The medial circumflex femoral artery is responsible for the majority of the arterial supply (the lateral circumflex femoral artery has to penetrate through the thick iliofemoral ligament to reach the hip joint). Damage to the medial circumflex femoral artery can result in avascular necrosis of the femoral head. The hip joint is innervated by the femoral nerve, obturator nerve, superior gluteal nerve, and nerve to quadratus femoris.
  10. 10. Hip Dysplasia • Is a condition where Femoral Head(ball) and Acetabulum(socket) are misaligned. The condition is common in children, but is also found in adolescents and adults with no history. • It becomes difficult for femoral head to remain properly positioned within the acetabulum if hip is poorly angled or rotated femoral head/neck or shallow acetabulum. • A severe or prolonged misalignment of Hip’s ball and socket results in increased friction which causes joint’s cartilage to wear out quickly- leading to cartilage(labral) tears and eventually Osteoarthritis. • A dysplastic hip socket usually causes discomfort and pain beginning in adolescence and gradually becomes worse with time. A shallow acetabulum may develop during infancy but may not be evident until after puberty- and may not cause pain until teen years or later. SYMPTOMS:-May range from mild-severe, uni/bi lateral. Discomfort or stiffness in hip may occur when attempts are made to move the leg away from body(abduction) or form a bend 90 degree to a straight extended position.
  11. 11. Later Pt may develop limp. Leg lengths may appear unqual with difficulty in rotation of thigh. X RAYS:- Assess alignment of Femoral Head and Acetabulum. MRI:- Assess Hip’s soft tissue and labrum(cartilage).
  12. 12. Dysplasias and Congenital Anomalies Sclerosing Bone Dysplasias • The various types of sclerosing bone dysplasias occur either from excess bone production due to abnormal osteoblastic activity or from failure of bone resorption and remodeling due to defective osteoclastic activity. • The excess bone accumulation affects endochondral bone formation in osteopetrosis,pyknodysostosis, or osteopathia striata. Intramembranous bone formation is primarily affected in progressive diaphyseal dysplasia and a few rare endosteal hyperostosis. • Both endochondral and intramembranous bone formation are affected in melorheostosis and metaphyseal dysplasia. • There are three types of osteopetrosis, • infantile-malignant type, which is autosomal recessive, and the most severe form • intermediate type, also autosomal recessive presenting typically in the first decade of life, • an autosomal dominant- type with full life-expectancy.
  13. 13. Osteopetrosis • Albers-Schonberg disease • Presentation in the majority of cases is with fracture because of the weakened bones. They are often transverse fractures with multiple areas of callus formation and normal healing. • there is crowding of the marrow, so bone marrow function is affected resulting in myelophthisic anaemia and extramedullary haematopoiesis with splenomegaly. This may terminate in acute leukaemia. • defective osteoclasts and overgrowth of bone. • bones become thick and sclerotic, but their increased size does not improve their strength.
  14. 14. • In the infantile type, pancytopenia, cranial nerve dysfunction, and mental retardation occur. Radiographs of the hip may demonstrate curvilinear bands of sclerosis in the ilium, with a “bone-inbone” appearance. The vertebrae may show similar bands of sclerosis along the vertebral endplates, with a “sandwich vertebrae” appearance. In the long bones, undertubulation, broadened metaphyses, and pathologic fractures are seen All visualized bones are sclerotic. Previous fractures of the right femoral shaft and left femoral neck with residual deformity. Osteopetrosis.
  15. 15. Pyknodysostosis • osteopetrosis acro-osteolytica or Toulouse- Lautrec syndrome • rare autosomal recessive - osteosclerosis and short stature. • Delayed closure of fontanelles, short stature, undertubulation of long bones, and diffuse sclerosis are seen. • Bones are brittle and prone to fracture. • Genetic research has demonstrated a mutation causing inactivation of the gene encoding cathepsin K, which is involved in osteoclastic function. • Patients present in early childhood with: -short stature, particularly limbs -delayed closure of cranial sutures -frontal and occipital bossing -short broad hands and hypoplasia of nails -multiple long bone fractures following minimal trauma named after the famous French artist who was thought to be afflicted with it
  16. 16. Pyknodysostosis is with radiographic characteristics of both osteopetrosis and cleidocranial dysplasia. The diffusely sclerotic bones, undertubulation,and fractures resemble osteopetrosis. Pyknodysostosis. Hands: short, stubby fingers partial agenesis/aplasia of terminal phalanges, simulating acro-osteolysis delayed bone age Cranial and maxillofacial marked delay in sutural closure frontoparietal bossing calvarial thickening Wormian bones (lambdoidal region) relative proptosis nasal beaking obtuse mandibular gonial angle often with relative prognathism persistence of primary teeth Others:sclerosis of vertebral bodies increased lumbar lordosis vertebral segmentation anomalies particularly upper cervical and lower lumbar, hypoplastic clavicles, erosion of distal clavicles
  17. 17. Melorheostosis • In Melorheostosis (also known as Leri disease)both endochondral and intramembranous bone formation are abnormal. It is characterized by hyperostosis, typically of one side of the cortex, with a lobulated, wavy appearance resembling dripping candle wax • Although changes occur in early childhood age at presentation is often later, and the condition often remains occult until late adolescence or early adulthood. In only approximately half of cases is the diagnosis made before the age of 20 • Whenit does manifest clinically, the most common presentation is of joint contracture or pain. This is more common in adults • can be either monostotic or polyostotic and tends to be monomelic • predilection for long bones of the limbs, although it can be seen almost anywhere • Five patterns have been described :- classic -osteoma - like -myositis ossificans - like -osteopathia striata - like -mixed
  18. 18. Osteopoikilosis • sclerosing bony dysplasia with multiple enostoses. Autosomal Dominant. • bone islands of osteopoikilosis develop during childhood and do not regress and therefore are seen in all age groups. There is no gender predilection • asymptomatic and does not degenerate into malignancy. Bone strength is normal. • often found concurrently with osteopathia striata, andmelorheostosis, and it is thought by some that they represent a spectrum of the same condition. Indeed recent genetic evidence suggests that these conditions are related by a loss of function mutation of the LEMD3 gene Plain film and CT The bone islands of osteopoikilosis are typically clustered around joints and align themselves parallel to surrounding trabeculae (thus predominantly longitudinally in the metaphyses) . Most lesions are found in the appendicular skeleton and pelvis. The axial skeleton is largely spared. It is rare for the skull vault to be involved . The lesions vary in size, usually a 5-10 mm, but ranging from only 1-2 mm up to 1-2 cm. MRI Appearances on MRI are the same as individual bone islands. Each lesion is small and dark on both T1 and T2 weighted images, as it is composed of mature dense bone
  19. 19. Ossifications and fibrosis in periarticular soft tissues are also common. The abnormalities may follow a dermatomal distribution. Treatment includes soft-tissue releases and excisions, and if necessary, osteotomies. It commonly recurs. In osteopoikilosis and osteopathia striata, there are localized foci of cortical bone in which resorption and remodeling fail,while in the remainder of bone, the process of endochondral ossification proceeds normally. The result is numerous foci of sclerotic bone (enostoses or “bone- islands”) throughout the skeleton in osteopoikilosis ,or linear striations of sclerotic bone in osteopathia striata. Differentiation from sclerotic metastases may at times be difficult by plain radiographs. Although radionuclide bone scan has been thought to be critical to differentiate osteopoikilosis from osteoblastic metastases, there are reports of increased radiopharmaceutical uptake in osteopoikilosis, particularly in young patients. Punctate sclerotic lesions (bone islands) scattered diffusely bilaterally. Osteopoikilosis.
  20. 20. “Osteopoikilosis, osteopathia striata, and/or melorheostosis can coexist in the same patient and probably represent a range of manifestations of the same disease process” (A) Dense sclerotic, wavy cortical thickening in the femoral shaft and superolateral acetabulum are noted. (B) Wavy cortical thickening in the distal femoral shaft is seen indicative of melorheostosis. Linear striations in the medullary bone are areas of osteopathia striata.
  21. 21. Osteogenesis Imperfecta Osteogenesis imperfecta (OI) is a hereditary disorder characterized by abnormal type I collagen, resulting in weakened, fragile bones, ligament laxity, abnormal dentition, blue sclerae, and hearing impairment. Most subtypes of OI are inherited as autosomal- dominant mutations in the COL1A1 and COL1A2 genes that encode for the pro alpha 1 and pro alpha 2 chains in type I collagen. Types I-IV, described by Sillence and coworkers, are as follows: type I,autosomal-dominant and relatively mild, with relatively normal stature, blue sclerae, and hearing impairment; type II, with subtypes described as autosomal-dominant or autosomal-recessive, the most severe form, lethal in the fetal or newborn period, with severe deformity and intrauterine growth retardation; type III, also with both autosomal-dominant and autosomal-recessive cases described, severe and progressive but with longer survival than type II; type IV, rare, autosomal dominant and mild with normal sclera and normal hearing. More recently, additional types V-VII have been described, which are not associated with defects in the genes encoding type I collagen. Treatment with biphosphonates improves bone mass in all types, but long-term outcomes from biphosphonate therapy are not known.
  22. 22. Severe deformity and osteopenia, with multiple fractures in different stages of healing. The pelvis is deformed and narrow. Osteogenesis imperfecta.
  23. 23. Developmental Dysplasia of the Hip The etiology of (DDH)involves both genetic and environmental factors. Risk factors include oligohydramnios, breech delivery, positive family history,. Diagnosis can be made at birth in the vast majority of cases. If diagnosed at birth, the likelihood of successful nonoperative treatment such as a Pavlik harness, and the overall prognosis, is much better than with delayed diagnosis. Ultrasound is more sensitive than radiography for diagnosis. Radiographically, dislocation or subluxation of the hip can be demonstrated by discontinuity of the Shenton arc, a curvilinear line connecting the medial femoral neck with the undersurface of the superior pubic. With hip dislocation, the femoral head moves into the upper outer quadrant. If the dislocated hip is in contact with the ilium, a pseudoacetabulum will form. Essentially all patients with hip subluxation or dislocation will develop osteoarthritis, usually in the 3rd or 4th decade of life. Superior dislocation of the left hip, with pseudoacetabulum formation. Mild subluxation also of the right hip.
  24. 24. Radiographic features Once there is significant ossification then x-ray examination is required. For some reason the left hip is said to be more frequently affected . One third of cases are affected bilaterally . Ultrasound Ultrasound is the test of choice in the infant (<6 months) as the proximal femoral epiphysis has not yet significantly ossified. Additionally it has the advantage of being a real time dynamic examination allowing the stability of the hip to be assessed with stress views. A number of values are used to 'objectively' assess morphology. Alpha angle (Depth of bony acetabular roof) Angle formed by the acetabular roof to the vertical cortex of the ilium. This is a similar measurement as that of the acetabular angle.The normal value is greater than or equal to 60 degrees. Beta angle (Cartilagenous Coverage) Angle formed between the vertical cortex of the ilium and the triangular labral fibrocartilage (echogenic triangle). The normal value is less than 77 degrees, but is only useful in assessing immature hips when combined with the alpha angle
  25. 25. Bony coverage The percentage of the femoral epiphysis covered by the acetabular roof. A value of greater than 58% is considered normal. Plain film The key to plain film assessment is looking for symmetry and defining the relationship of the proximal femur to the developing pelvis. The ossification of the superior femoral epiphyses should be symmetric. Delay of ossification is a sign of DDH. Hilgenreiner line is drawn horizontally through the superior aspect of both triradiate cartilages. It should be horizontal, but is mainly used as a reference for Perkin line and measurement of the acetabular angle. Perkin line is drawn perpendicular to Hilgenreiner line, intersecting the lateral most aspect of the acetabular roof. The upper femoral epiphysis should be seen in the inferomedial quadrant (i.e below Hilgenreiner line, and medial to Perkin line) The acetabular angle is formed by the intersection between a line drawn tangential to the acetabular roof and Hilgenreiner line, forming an acute angle. It should be approximately 30 degrees at birth and progressively reduce with maturation of the joint. Shenton line is drawn along the inferior border of the superior pubic ramus and should continue laterally along the inferomedial aspect of the proximal femur as a smooth line. If there is superolateral migration of the proximal femur due to DDH then this line will be discontinuous.
  26. 26. Acetabular Dysplasia in Adults Dysplasia of the acetabulum may occur without hip dislocation, and mild dysplasia may go undiagnosed until adulthood. Acetabular dysplasia occurs in females more often than males and has been demonstrated to lead to development of hip joint osteoarthritis. Evaluation for acetabular dysplasia can be performed using the center-edge angle of Wiberg, performed by measuring the angle between a line drawn vertically from the center of the femoral head and a line from the center of the femoral head through the edge of the acetabulum.Angle measures less than 20° are dysplastic; 20 to 25° are classified as borderline dysplasia, and greater than 25° are normal. Bilateral acetabuli are dysplastic, with only partial covering of the femoral head. On the left, early osteoarthritis has begun to develop.
  27. 27. Bilateral acetabuli are dysplastic, with only partial covering of the femoral head. On the left, early osteoarthritis has begun to develop.
  28. 28. Femoroacetabular Impingement The theory behind femoro acetabular impingement is that certain anatomic variations lead to impingement between the proximal femur and acetabular rim with flexion and internal rotation. This leads to shearing and impaction of the anterior articular cartilage of the femoral head, as well as anterior labral tears. There are two types of femoroacetabular impingement. • The first is the “cam” type, femoral waist defeciency; thought to be caused by an enlarged femoral head or an abnormal contour of the femoral head/neck junction, which causes impingement anteriorly against a normal acetabulum. • The second, or “pincer” type, is thought to be due to “over-coverage” of the femoral head anteriorly from either coxa profunda or a retroverted acetabulum. Radiographs may demonstrate reduced offset of the femoral head–neck junction, acetabular abnormalities such as retroversion, coxa valga, coxa profunda, or protrusio acetabuli, and the eventual development of osteoarthritis. MR imaging is more sensitive to the early findings of labral tear and cartilage injury.
  29. 29. Long-leg lateral view of the left hip shows prominent femoral head–neck junction, narrowing of the anterosuperior joint space, and sclerosis of the anterosuperior acetabulum. Heterotopic bone formation is seen from previous hip arthroscopy for anterior labral debridement in a patient with femoroacetabular impingement.
  30. 30. Cam Impingement: Pistol Grip Deformity Mechanism: Femoral cause • Jamming of an abnormal femoral head into the acetabulum during forceful motion, especially flexion and internal rotation „Classic“ Imaging finding • abnormal femoral head with a laterally increasing radius • femoral waist deficiency „Classic“ Patient • young and athletic male
  31. 31. Cartilage Lesions: Localization Acetabulum >> Femur • Antero - superior • Labral tears often associated • Junction of labrum and cartilage
  32. 32. Pincer Impingement:deep acetabulum Mechanism: Acetabular cause • Contact between acetabular rim and femoral head-neck junction „Classic“ Imaging finding • General ‘overcoverage’ (coxa profunda / protrusio) • Local anterior ‘overvoverage’ (acetabular retroversion) „Classic“ Patient • Middle-aged women
  33. 33. Achondroplasia congenital disorder of endochondral bone formation affecting fetuses in utero, transmitted as an autosomal-dominant trait.The genetic defect involves an allele encoding fibroblast growth factor receptor 3, on chromosome 4p, which is the same allele implicated in both hypochondroplasia and thanatophoric dwarfism. Patients have short stature, with limb shortening affecting more severely the proximal extremities. Short pedicles can predispose to spinal stenosis. Narrowing of the interpedicular width in the lower lumbar spine is seen, along with horizontally oriented acetabular roofs, small sciatic notches, and rounded, “ping- pong-paddle”-shaped iliac bones;short femur with widened femoral metaphysis. Cervicomedullary compression has been shown to be associated with sudden death in infants with achondroplasia.
  34. 34. • horizontal acetabular roof (decreased acetabular angle) • small squared (tombstone) iliac wings • small trident pelvis • champagne glass type pelvic inlet • short sacroiliac notches • metaphyseal flaring : can give a trumpet bone type appearance • femora and humeri are particularly shortened (rhizomelic shortening) • long fibula • they may also appear thickened but in fact normal in absolute terms compared to the normal adult diameter (thickening is perceived due to reduced length) • V shaped growth plates • trident hand
  35. 35. Multiple Epiphyseal Dysplasia dysplasia epiphysealis multiplex the abnormal growth of the femoral head epiphysis typically leads to a varus alignment of the femoral neck. This occurs due to overgrowth of the trochanteric ossification center and infundibulum, a cartilaginous connection between the femoral head and trochanteric ossification centers in the infant. Secondary osteoarthritis eventually develops. non-rhizomelic dwarfism characterized by flattening and fragmentation of epiphyses. inherited as autosomal dominant. Broad, dysplastic femoral heads, with varus angulation of the femoral necks bilaterally. Multiple epiphyseal dysplasia.
  36. 36. Proximal Focal Femoral Deficiency • Proximal focal femoral deficiency (PFFD) represents a congenital disorder characterized by varying severity of shortening and dysplasia of the proximal femur and acetabulum, and varus angulation of the proximal femur- with shortening of the entire lower limb. • A common classification system divides the disorder into types, A-D, in increasing order of severity. In type A, the femur is shortened compared with the normal size, but the femoral head is present and located within the acetabulum. In type B, the femur is short with a varus angulation, and there is a gap between the femoral head, which is located within the acetabulum,and the femoral neck. In type C, the femoral head is rudimentary or absent. The femur is markedly short, and theacetabulum is dysplastic. In type D, the entire femur is rudimentary,with absent femoral head and acetabulum. • Various treatments have been used for patients with this disorder. In one recent report, patients reported similar mobility and improved satisfaction with nonoperative treatment using extension prosthesis, compared with surgical ankle disarticulation with fitting of an above-knee prosthesis.
  37. 37. Proximal Focal Femoral Deficiency MRI The role of MR imaging in patients with this condition is to help define the cartilaginous proximal femur and the presence or absence of a cartilaginous connection to the femoral head. Therapeutic decisions are based on the detection of a femoral head and the presence of a connection. Also, the severity of coxa vara, if present, will influence treatment selection. The ability of imaging to clearly depict cartilage is of particular value in this setting. Routine coronal and axial MR images may be adequate, however, oblique images may be useful in some patients. T 1 T 2
  38. 38. Mucopolysaccharidoses This represents a heterogeneous group of disorders characterized by accumulation of various mucopolysaccharides as a result of congenital lack of certain enzymes. Many if not all of these exhibit similar radiographic findings in the pelvis, including flared and dysplastic femoral heads, narrowed and distorted pelves, and flared iliac wings The iliac wings are broad, the pelvis narrow, and the femoral heads dysplastic in this patient with Hurler’s syndrome.
  39. 39. Fibrodysplasia Ossificans Progressiva (FOP) represents a rare congenital disorder characterized by progressive heterotopic ossification of tendons, ligaments, muscles, and other soft tissues with deformity of the great toe. No known treatment or preventive measure exists. The typical course of the disease is progressive restriction of movement, frequent falls, and eventual respiratory difficulty from involvement of the chest wall. Most patients die of pulmonary complications in their 40s or 50s. Recent advances include mapping of the gene for FOP to chromosome 4q, and identification of a key protein found in lesion cells and lymphocytes.These findings may prove beneficial in treating this condition in the future. Marked heterotopic ossification bridging the hip joint medially and laterally
  40. 40. Characteristic features include: hallux valgus monophalangic first toe shortened metacarpals pseudoexostoses (ossification of ligamentous insertions) microdactyly of the first metacarpal / metatarsal neck muscles oedema

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