Developmental Dysplasia of the Hip

Abstract
A 4 year old patient presented with a limping gait. She was diagnosed with developmental dysplasia of the hip. She underwent an open reduction, capsulorraphy and femoral derotational osteotomy. She had a good acetabular remodeling and a symptom-free hip.
Keywords: hip dysplasia, developmental disorder, acetabular remodelling
Introduction
Developmental dysplasia of the hip (DDH) is a common congenital abnormality that affects the developing hip joint of the newborn. DDH refers to a spectrum of disease, including hips that are unstable, subluxated, dislocated, and/or have dysplastic acetabula.
Case Report
A 4 year old patient noted to have a limping gait by her kindergarten teacher. She is otherwise has no other complains. There was no pain around the hip and her daily activity was not affected by the limping. She was born breech. However, the postnatal period was uneventful. She has no allergy to food or medications. Her immunization is completed to age.
Clinically she was walking with a short limp gait. The left leg was shortened by 4 cm. The Galleazzi sign was positive. Range of motion was full in all directions. The x-ray of the hip showed a dislocated left hip. The Shenton line was disrupted. The acetabular index was 30 degree.
She underwent an open reduction and femoral shortening and derotational osteotomy on 18/7/2008. A Smith-Peterson approach was used. A skin bikini incision was made along the lateral border of the iliac crest starting at a point one third away between the lesser and greater tuberosity extending obliquely passing across anterior inferior iliac spine and stop about an inch medially. The lateral cutaneous nerve was identified and isolated. A plane was developed between Sartorius medially and TFL laterally. The sartorius and the rectus femoris were detached proximally. After identifying and clearing the capsule, a capsulotomy was performed. A thickened ligamentum teres was identified and excised. The labrum was noted to be inverted. The pulvinar was also present. The femoral head was then reduced into the identified true acetabulum.
A lateral incision was made over the left femur. The femur was shortened for 1 cm. and the plate was put in 10 degree internal rotation as to derotate the femur. Capsulorraphy was then performed after the hip was reduced and stability assessed. She was put on a hip spica in hip flexion, neutral rotation and abduction after wound closure.
The postoperative period was uneventful. A hip spica change was done 6 weeks later and the cast was removed at 3 months postoperatively. The hip x-ray at 3 month follow-up showed a concentric reduction with an intact Shenton’s line. The acetabular index was 20 degrees. At 6 months follow-up, she had a normal gait, no leg length discrepancy and full range of hip movement.

Discussion
Developmental dysplasia of the hip (DDH) is a spectrum of disease encompasses radiographic dysplastic hip, subluxation, instability, demonstrable dislocatable hip, true dislocated hip.1 Developmental dysplasia of the hip has progressively replaced the longstanding terminology of congenital dislocation of the hip (CDH). The American Academy of Orthopaedic Surgeons,2 the Pediatric Orthopaedic Society of North America, and the American Academy of Pediatrics have endorsed the name change of this entity from CDH to DDH, because the latter is more representative of the wide range of abnormalities seen in this condition.3
The incidence of DDH is ranging from 1.4 to >35 per 1000 live birth.4 Estimates of the incidence of developmental dysplasia of the hip depend, among other things, on the age of the neonate and the method used to detect the dysplasia.5
In normal growth, there is a determined balance of growth of the acetabular and triradiate cartilages and a well-located and centered femoral head. Embryologically, the components of the hip joint, the acetabulum, and the femoral head develop from the same primitive mesenchymal cells. The hip joint is fully formed by the 11th week of gestation. In the normal hip at birth, the femoral head is deeply seated in the acetabulum and held within the confines of the acetabulum by the surface tension of the synovial fluid. It is extremely difficult to dislocate a normal infant's hip, even after incising the hip joint capsule.6 After birth, the growth of the proximal femur and the acetabular cartilage complex is interdependent.
The acetabular cartilage complex is a three-dimensional structure that is triradiate medially and cup-shaped laterally. Acetabular cartilage forms the outer two-thirds of the acetabular cavity, and the nonarticular medial wall of the acetabulum is formed by a portion of the ilium above, the ischium below, and portions of the triradiate cartilage. The triradiate cartilage is the common physis of the three pelvic bones. Interstitial growth within the triradiate cartilage causes the hip joint to expand in diameter during growth.7
In the infant the entire proximal end of the femur, including the greater trochanter, the intertrochanteric zone, and the proximal femur, is composed of cartilage. Between the 4th and 7th months of life, the proximal femoral ossification center appears. The three main growth areas in the proximal femur are the physeal plate, the growth plate of the greater trochanter, and the femoral neck isthmus. The normal growth of these three physes determines the femoral neck configuration in the adult. Disturbances in growth in any of these three growth plates, by whatever mechanism, alter the shape of the proximal femur.8
In the newborn with DDH, the tight fit between the femoral head and the acetabulum is lost. The femoral head can be made to glide in and out of the acetabulum with a palpable sensation. There is a hypertrophied ridge known as the neolimbus at the acetabular cartilage in the superior, posterior, and inferior aspects of the acetabulum.9 It is over this ridge of acetabular cartilage that the femoral head glides in and out of the acetabulum, with the palpable sensation referred to as the Ortolani sign.10
The cause of DDH is multifactorial. A positive family history for DDH may be found in 12% to 33% of patients who have DDH. There is a 12-fold increase in the development of DDH sif one has a first-degree relative with DDH.11 Reported risk factors include female sex, family history, breech presentation, multiple gestation, first pregnancy, high birth weight, and oligohydramnios.12
Stanisavljevic13 reported that there are three periods during which the fetal hip is at risk for dislocation. The first critical period is after the hip joint develops from the pelvis during the 12th week of gestation. As the limb rotates medially, the hip is at risk for dislocation. The second period is during the 18th week of gestation when the hip musculature develops. The third period is during the last 4 weeks of gestation when abnormal mechanical forces, such as a breech position or oligohydramnios, may predispose to DDH.
Hip capsular laxity has been implicated in the pathogenesis of DDH. It is often seen in infants and has been documented by ultrasonography.14 The laxity may allow some instability without a positive Ortolani sign. However, DDH is not a feature of conditions characterized by hyperlaxity, such as Down, Ehlers-Danlos, and Marfan syndromes.10

Diagnosis
The clinical diagnostic test for DDH was originally described by LeDamany in 1912. He described the palpable sensation of the hip gliding in and out of the acetabulum. Later in 1936, Ortolani described the pathogenesis of this diagnostic sign.10 The Ortolani test is performed by placing the thumb over the inner thigh and the index finger on the greater trochanter. The hip is abducted and gentle pressure is placed over the greater trochanter. A “clunk”is felt when the hip is reduced. Ortolani felt that a positive test was associated with reduction of the hip into the acetabulum. Ortolani described his method as the most reliable clinical sign for the diagnosis of congenital dislocation of the hip at birth and in the first 2 months of life. However, the reliability and validity of the Ortolani examination have been questioned by some investigators. Hadlow,15 in 1988, stated that the Ortolani examination may not be positive in a grossly dislocated hip with poor acetabular development and capsular laxity. MacKenzie and Wilson16 stated that the movement of the femoral head into the acetabulum is not always demonstrable in the dislocated hip and may be seen only when the child is anesthetized.
Another diagnostic test, the Barlow maneuver, is often referred to as the “click of exit.” The Barlow maneuver is a provocative maneuver in which the hip is flexed and adducted and the femoral head is palpated to exit the acetabulum partially or completely over a ridge of the acetabulum.17
Complete irreducible dislocations are extremely rare in newborns and are usually associated with other generalized conditions, such as arthrogryposis, myelodysplasia, and other syndromes. These perinatal teratologic dislocations are at the extreme end of the DDH pathologic spectrum and account for only 2% of cases in newborn examination series.18
Secondary adaptive changes develop if the diagmosis of DDH is not made early. Limited abduction as manifested by shortening of the adductor longus is the most reliable physical finding.19 Other manifestation includes apparent femoral shortening, Galeazzi sign, asymmetry of the gluteal, thigh, or labial folds, and limb-length inequality. In patients with bilateral dislocations, clinical findings include a waddling gait and hyperlordosis of the lumbar spine.
The use of ultrasound for the diagnosis of developmental dysplasia of the hip (DDH) in new-borns was introduced by Graf in 1980.20 The main aim of any ultrasound screening programme for DDH is to reduce the number of patients presenting late and to avoid extensive and frequently costly treatment. Controversy arises with regard to selective ultrasound screening of so called 'at risk' newborns or the general ultrasound screening of all newborns.21,22 General ultrasound screening of the hips of all newborns has been shown to result in a lower rate of missed hips and surgical procedures but a higher treatment rate.23 Recent study also concludes that general neonatal sonographic hip screening can reduce significantly surgical procedures, hospitalisation and late presentation of DDH.24
Other uses for ultrasonography include monitoring the progress of reduction of a subluxated or dislocated hip being treated in a Pavlik harness, monitoring of the hip position while the patient is in traction before attempting reduction and evaluating closed reductions in the operating room.
After the newborn period (4 to 6 weeks of age), the diagnosis of DDH should be confirmed by radiography. There are wide interobserver and intraobserver variations in the radiographic measurements. It is due to difficulty to standardize the radiographic positioning of the infants.25 The radiographic features of late diagnosed DDH include: an increased acetabular index; disruption of the Shenton line; a widened pelvic floor; an absent teardrop figure; delayed appearance of the femoral ossific nucleus on the involved side or dissimilar sizes of the ossific nuclei; abnormality in Smith centering ratios; decreased femoral head coverage; and failure of the medial metaphyseal beak of the proximal femur, and, subsequently, the secondary ossification center, to be located in the lower inner quadrant defined by the Hilgenreiner and Perkins lines.( Figure)
In children younger than 8 years, the acetabular index is a reasonable measure of acetabular development.25 It is an angle between Hilgenreiner’s line and a line drawn from the triradiate epiphysis to the lateral edge of the acetabulum. Classically, this decreases with age and should measure less than 20 degree by 2 years of age. Measurement of the center-edge (CE) angle becomes useful only in the patient who is more than 5 years of age, and is most useful in the adult patient.
Various acoustical techniques have been reported for screening and diagnosis of DDH.26,27,28

Treatment
Newborn and Infants younger than 6 months of age
The goal of treatment is to obtain and maintain the reduction to provide an optimal environment for the development of the femoral head and acetabulum. Many studies have shown that the acetabulum has the potential for development for many years after reduction as long as the reduction is maintained.29 Early diagnosis aids in the success of DDH treatment. Prompt recognition and appropriate treatment provides the child with the greatest opportunity for a good outcome. Triple diapers or abduction diapers have no place in the treatment of DDH in the newborn. They give the family a false sense of security and are generally ineffective.
Pavlik harness is the most commonly used device worldwide. When appropriately applied, the Pavlik harness prevents the hip extension and adduction that can lead to redislocation, but it allows further flexion and abduction, which lead to reduction and stabilization. By maintaining the Ortolani-positive hip in a Pavlik harness on a full-time basis for 6 weeks, hip instability resolves in 95% of cases.30 The harness is checked at 7- to 10-day intervals to assess hip stability and to adjust the flexion and abduction straps to allow for growth of the infant. The Pavlik harness may be used effectively until 6 months of age for any child with residual dysplasia, subluxation, or complete dislocation.
The onset of treatment of DDH with Pavlik harness may influence the duration of treatment. The starting treatment at 13 weeks and later increases the duration of treatment.31
Mubarak et al32 have identified several pitfalls associated with the Pavlik harness. The most serious was failure to obtain a reduction, often related to improper adjustment of the device. The Pavlik harness is contraindicated in patients with significant muscle imbalance (i.e. myelodysplasia or cerebral palsy), in patients with significant joint stiffness (i.e. arthrogryposis), or in patient with excessive ligamentous laxity (i.e. Ehlers-Danlos syndrome). The physicians should be well versed in its appropriate application and the adjustments that are necessary throughout the course of treatment to minimize the persistence of inadequate treatment. Prolonged treatment can cause secondary pathologic changes. It may damage the femoral head, injure the acetabular cartilage, and impair future bone growth.33
The use of the Pavlik harness can be associated with complications. Inferior dislocations may occur with prolonged excessive hip flexion. Hyperflexion may also induce femoral nerve compression neuropathy. Brachial plexus palsy may occur from compression by the shoulder straps, and knee subluxations may occur from improperly positioned straps. Skin breakdown may occur in the groin creases and in the popliteal fossa if great care is not taken in keeping these areas clean and dry.

Children 6 months to 18 months of age
Pavlik harness is not suitable for children older than 6 months old because of the child’s activity levels. In this age group, the hip should be treated by closed or open reduction means as necessary.
There are controversies regarding the use of prereduction traction.34 Traction theoretically stretches contracted muscles, allows reduction without excessive force, decreases the need for open reduction, and reduces the incidence of proximal femoral growth disturbance resulting from avascular necrosis. Several articles on open and closed reduction without the use of preliminary traction report incidences of proximal femoral damage comparable to those found in series in which prereduction traction was used.35,36
Closed reductions are performed under general anaesthesia. The hip is gently manipulated into the acetabulum by flexion, traction, and abduction. Closed reduction is performed with the aid of arthrography. The use of hip arthrography to confirm a concentric closed reduction resulted in a statistically significant drop in the incidence of AVN from 28.9 to 7.6%.37 The safe zone of Ramsey,38 the angle between maximum abduction and minimum abduction in which the hip remains reduced, should also be measured. This should be at least 25 degree and can be increased with release of the adductor longus. The cone of stability is a cone that involves hip flexion, abduction and internal/external rotation. If this cone measures greater than 30 degrees, it is considered satisfactory. The reduction is maintained in a well-moulded plaster cast and should be documented by radiography, ultrasound or CT scan. The plaster cast is maintained for approximately 6 weeks, regardless of the patient’s age. Factors that may prevent concentric reduction include inverted limbus, the iliopsoas tendon constricting the capsule over the acetabular inlet (hourglass constriction), hypertrophied ligamentum teres, hypertrophy and shortening of the transverse acetabular ligament, and pulvinar (intra-articular fibrofatty tissue).
An open reduction is indicated if there is failure of closed treatment, persistent subluxation, soft tissue interposition, or reducible but unstable reductions other than in extreme positions of abduction. The presence of the femoral head ossific nucleus at the time of hip reduction has been suggested to decrease the risk of the development of osteonecrosis.39 However, a meta-analysis by Roposch et al demonstrated that there is no significant effect of the presence of the ossific nucleus on the development of osteonecrosis.
Smith-Petersen approach with a modified ‘bikini’ incision is the most commonly approach used for open reduction. The incision begins at the middle of iliac crest and carried anteriorly to the anterosuperior iliac spine and then distally and slightly laterally 10 to 12 cm towards lateral patella. The lateral cutaneous nerve of the thigh needs to be watched out as it passes over the Sartorius 2.5 cm distal to the anterosuperior iliac spine. The dissection is carried out through the deep fascia between the tensor fasciae latae laterally and the Sartorius medially. Deeper dissection is through gluteus medius laterally and rectus femoris laterally. The rectus femoris is usually needed to be detached from its origin (anterior inferior iliac spine and superior lip of acetabulum). The femoral head and the proximal margin of the acetabulum are exposed after incising the capsule.
The advantage of the anterior Smith-Petersen approach is that the hip is immobilized in a functional position, with minimal hip flexion and some degree of abduction.
Medial approaches have the advantage of approaching the hip joint directly over the site of the obstacles to reduction. The plane of medial approach as described by Ferguson is in between the adductor brevis and the adductor magnus.40 Other advantages include minimal soft tissue dissection, direct access to the medial joint capsule and the iliopsoas tendon, avoidance of damage to the iliac apophysis and abductor muscles, minimal blood loss, and excellent cosmesis. The disadvantages include the stability of reduction is maintained only by the postoperative cast, difficult to use in older patient, no concomitant procedures can be performed through the same incision, and a possible higher incidence of proximal femoral growth disturbance after use of this approach.41 Medial approach is mostly meant for open reduction without capsulorraphy in a child of one year or less. Capsulorraphy is difficult from this approach.
The period of immobilization post reduction is usually 12 weeks. Various abduction orthosis has been used after cast removal. Weinstein et al uses a fixed abduction orthosis for 2 months on a full-time basis and then at night and nap time until acetabular development has normalized (generally 18 to 24 months) or further surgical intervention is planned for correcting residual dysplasia.42 In patients younger than 2 years, a secondary acetabular or femoral procedure is rarely required. The potential for acetabular development after closed or open reduction is excellent and continues for 4 to 8 years after the reduction.43
Children older than 18 months of age
In children older than 2 years, femoral shortening may be performed to avoid excessive pressure on the proximal femur and thus reducing risk of vascular necrosis. Varus derotation osteotomy is used to redirect the femoral head, in order to stimulate normal acetabular development, toward the center of the acetabulum.44 In children over 4 years of age with significant hip dysplasia, an acetabular procedure should be considered at the time of open reduction due to the decrease in remodeling potential.45 Salter45 innominate ostetomy and Pemberton46 osteotomy is the most common procedures. The Salter innominate osteotomy gives anterior coverage with the expense of posterior coverage. The Pemberton osteotomy provides anterior coverage, and also various degrees of lateral coverage, depending on the direction of the osteotomy cuts.
A good clinical result has been reported in single-stage open reduction, Salter innominate osteotomy, and proximal femoral osteotomy for the management of DDH in children between the ages of 2 and 4 years.47
Disturbance of growth of the proximal femur is the most disastrous complication associated with the treatment of DDH. The disturbance to growth may be caused by vascular insults to the epiphysis or the physeal plate, or by pressure injury to the epiphyseal cartilage or the physeal plate. The reported incidence of proximal femoral growth disturbance varies from 0% to 73%.48 Factors associated with necrosis include high dislocations and dislocations with inversion of the labrum; narrowing of the introitus between the superior labrum and the transverse ligament in the position of reduction; inadequate depth of reduction of the femoral head (greater than 3 mm from the acetabular floor); the age of the patient (older than 12 months); immobilization in 60 or more degrees of abduction for joint instability; and adductor tenotomy. Repeated attempt of closed reduction to overcome the intraarticular obstacle to reduction can also lead to severe necrosis.

Conclusion
Developmental dysplasia of the hip (DDH) is a common disorder. Early detection is the key to the diagnosis and management. The diagnosis can be difficult, even in experienced hands, and a late diagnosis does not necessarily imply a missed diagnosis. Treatment depends on the age of initial diagnosis and success of previous treatment. Earlier treatment usually requires less aggressive methods. Follow up should be continued to skeletal maturity, and both hips should be carefully evaluated. Although outcomes are usually very good, long-term sequelae occur even in patients who receive optimal treatment.

Reference
  1. Committee on Quality Improvement, American Academy of Pediatrics. Clinical practice guidelines: early detection of developmental dysplasia of the hip. Pediatrics 2000;105:896-905.
  2. Surgeons Advisory Statement, American Academy of Orthopaedic Surgeons. “CDH” should be “DDH”. Park Ridge, IL: American Academy of Orthopaedic Surgeons 1991.
  3. Klisic P, Jankovic L, Basara V. Long-term results of combined operative reduction of the hip in older children. J Pediatr Orthop 1988;8:532.
  4. Kocher MS. Ultrasonographic screening for developmental dysplasia of the hip: an epidemiologic analysis (part I). Am J Orthop 2000;29:929-33.
  5. Shipman SA, Helfand M, Moyer VA, Yawn BP. Screening for developmental dysplasia of the hip: a systematic literature review for the US Preventive Services Task Force. Pediatrics 2006;117:e557-76.
  6. Dunn PM. The anatomy and pathology of congenital dislocation of the hip. Clin Orthop 1976;119:23.
  7. Portinaro NM, Murray DW, Benson MKD. Microanatomy of the acetabular cavity and its relation to growth. J Bone Joint Surg Br 2001;83-B:377-383.
  8. Siffert RS. Patterns of deformity of the developing hip. Clin Orthop Relat Res 1981;160:14.
  9. Ponseti IV. Morphology of the acetabulum in congenital dislocation of the hip: gross, histological and roentgenographic studies. J Bone Joint Surg Am 1978;60:586.
  10. Ortolani M. Congenital hip dysplasia in the light of early and very early diagnosis. Clin Orthop 1976;119:6.
  11. Stevenson D, Mineau G, Richard A. familial Predisposition to Developmental Dysplasia of the Hip. Journal of Pediatric Orthopaedics 2009;29(5): 463-466.
  12. Chan A, McCaul KA, Cundy PJ, et al. Perinatal risk factors for developmental dysplasia of the hip. Arch Dis Child Fetal Neonatal Ed 1997;76:F94–F100.
  13. Stanisavljevic S. Part I: Etiology of congenital hip pathology. Part II: Anatomy of congenital hip pathology. In: Tachdjian MO, ed. Congenital Dislocation of the Hip. New York, NY: Churchill-Livingstone; 1982:27-5.
  14. Palmen K. Preluxation of the hip joint: diagnosis and treatment in the newborn and the diagnosis of congenital dislocation of the hip joint in Sweden during the years 1948-1960. Acta Paediatr Scand Suppl 1961;129:1.
  15. Hadlow V. Neonatal screening for congenital dislocation of the hip. A prospective 21-year survey. J Bone Joint Surg Br 1988;70:740-743.
  16. Mackenzie IG, Wilson JG. Problems encountered in the early diagnosis and management of congenital dislocation of the hip. J Bone Joint Surg Br 1981;63:38-42.
  17. Barlow TG. Early diagnosis and treatment of congenital dislocation of the hip. J Bone Joint Surg Br 1962;44:292.
  18. Coleman SS. Congenital dysplasia of the hip in the Navajo infant. Clin Orthop 1968;56:179.
  19. Bjerkreim I, Johansen J. Late diagnosed congenital dislocation of the hip. Acta Orthop Scand 1987;58:504.
  20. Graf R. New Possibilities for the Diagnosis of Congenital Hip Joint Dislocation by Ultrasonography. Journal of Pediatric Orthopaedics 1983 3(3):354-359.
  21. Jones DA, Powell N. Ultrasound and neonatal hip screening: a prospective study of 'high risk' babies. J Bone Joint Surg [Br] 1990;72-B:457-9.
  22. Paton RW, Srinivasan MS, Shah B, Hollis S. Ultrasound screening for hips at risk in developmental dysplasia: is it worth it? J Bone Joint Surg [Br] 1999;81-B:255-8.
  23. Hansson G, Jacobsen S. Ultrasonography screening for developmental dysplasia of the hip joint. Acta Paediatr 1997;86:913-5.
  24. Wirth T, Stratmann L, Hinrichs F. evolution of late presenting developmental dysplasia of the hip and associated surgical procedures after 14 years of neonatal ultrasound screening. JBJS (Br) 2004(86):585-589.
  25. Broughton NS, Brougham DI, Cole WG, et al. Reliability of radiological measurements in the assessment of the child's hip. J Bone Joint Surg Br 1989;71:6.
  26. Kernohan WG, Beverland DE, McCoy GF, et al. The diagnostic potential of vibration arthrography. Clin Orthop 1986; 210:106–112.
  27. Richardson JB, Foo CK, Stone MH, et al. Attenuation of sound transmission in congenital dislocation of the hip. J Bone Joint Surg [Br] 1987; 69:850.
  28. Kwong KSC, Huang Xiaolin, Cheng C. Y., Evans JH. New Technique for Early Screening of Developmental Dysplasia of the Hip: Pilot Study. Journal of Pediatric Orthopaedics 2003;23(3):347-351.
  29. Harris NH. Acetabular growth potential in congenital dislocation of the hip and some factors upon which it may depend. Clin Orthop 1976;119:99.
  30. Cashman JP, Round J, Taylor G, et al. The natural history of developmental dysplasia of the hip after early supervised treatment in the Pavlik harness. A prospective, longitudinal follow up. J Bone Joint Surg Br 2002;84(3):418-425.
  31. Bialik GM, Eidelman M, Katzman A. treatment duration of developmental dysplasia of the hip: age and sonography. Journal of Pediatric Orthopaedics B 2009;18(16):308-313.
  32. Mubarak S, Garfin S, Vance R, McKinnon B, Sutherland D. Pitfalls in the use of the Pavlik harness for treatment of congenital dysplasia, subluxation, and dislocation of the hip. J Bone Joint Surg Am 1981;63:1239-1248.
  33. Jones GT, Schoenecker PL, Dias LS. Developmental hip dysplasia potentiated by inappropriate use of the Pavlik harness. J Pediatr Orthop 1992;12:722.
  34. Wenger DL, Lee CS, Kolman B. Derotational femoral shortening for developmental dislocation of the hip: special indications and results in the child younger than 2 years. J Pediatr Orthop 1995;15:768.
  35. Quinn RH, Renshaw TS, DeLuca PA. Preliminary traction in the treatment of developmental dislocation of the hip. J Pediatr Orthop 1994;14:636.
  36. Kahle WK, Anderson MB, Alpert J, et al. The value of preliminary traction in the treatment of congenital dislocation of the hip. J Bone Joint Surg Am 1990;72:1043.
  37. Khoshhal, Khalid I.; Kremli, Mamoun K.; Zamzam, Mohammed M.; Akod, Omar M.; Elofi, Omer A. The role of arthrography-guided closed reduction in minimizing the incidence of avascular necrosis in developmental dysplasia of the hip. Journal of Pediatric Orthopaedics B 2005;14(4):256-261.
  38. Ramsey PL, Lasser S, MacEwen GD. Congenital dislocation of the hip: use of the Pavlik harness in the child during the first six months of life. J Bone Joint Surg Am 1976; 58:1000–4
  39. Luhmann SJ, Schoenecker PL, Anderson AM, Bassett GS. The prognostic importance of the ossific nucleus in the treatment of congenital dysplasia of the hip. J Bone Joint Surg Am 1998;80:1719-27.
  40. Ferguson AB Jr. Treatment of congenital dislocation of the hip in infancy using the medial approach. In: Tachdjian MO, ed. Congenital dislocation of the hip. New York: Churchill Livingstone, 1982:283.
  41. Simons GW. A comparative evaluation of the current methods for open reduction of the congenitally displaced hip. Orthop Clin North Am 1980;11:161.
  42. Morrissy RT, Weinstein SL, eds. Lovell and Winter's Pediatric Orthopaedics, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:1014.
  43. Lindstrom JR, Ponseti IV, Wenger DR. Acetabular development after reduction in congenital dislocation of the hip. J Bone Joint Surg Am 1979;61:112.
  44. Rejholec M, Stryhal F. Behavior of the proximal femur during the treatment of congenital dysplasia of the hip: a clinical long-term study. J Pediatr Orthop 1991;11:506.
  45. Salter RB. Innominate osteotomy in treatment of congenital dislocation of the hip. J Bone Joint Surg Br 1961;43:72
  46. Pemberton PA. Pericapsular osteotomy of the ilium for treatment of congenital subluxation and dislocation of the hip. J Bone Joint Surg Am 1965;87:65.
  47. El-Sayed, Mohamed MH. Single-stage open reduction, Salter innominate osteotomy, and proximal femoral osteotomy for the management of developmental dysplasia of the hip in children between the ages of 2 and 4 years. Journal of Pediatric Orthopaedics B 2009;18(4): 188-196.
  48. Kruczynski J. Avascular necrosis of the proximal femur in developmental dislocation of the hip: incidence, risk factors, sequelae, and MR imaging for diagnosis and prognosis. Acta Orthop Scand Suppl 1996;268:1.
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