 Introduction/Background Developmental dysplasia of the hip (DDH) comprises a spectrum of abnormalities from hip instability to frank dislocation [1,2]. The mildest end of the spectrum overlaps with physiologic immaturity, therefore making it difficult to determine its true incidence, which is estimated to be 1.5 to 20 per 1,000 births, depending on the demographics of the study population and the inclusion criteria [3-5]. The diagnosis and monitoring of teratologic hips from neuromuscular or syndromic causes will not be covered. The pathophysiology of DDH is multifactorial and not completely understood. The 2 leading causes are laxity induced by maternal hormones and limited in utero hip mobility. In infants with DDH, abnormally increased laxity of the hip capsule and surrounding ligaments have been attributed to the effects of maternal hormone relaxin [1] and a higher concentration of estrogen receptors [6]. In utero restriction to hip mobility can be encountered with oligohydramnios, first-born infants, and prolonged breech positioning. Breech fetal positioning produces extreme hip flexion with knee extension. This leads to shortening and contracture of the iliopsoas muscle, which promotes femoral head dislocation. Studies demonstrating increased prevalence of DDH among monozygotic twins as compared to dizygotic twins [7] and chromosomal analysis in familial DDH and population-based DDH suggest genetic predisposition to DDH [8-10]. Reprint requests to: publications@acr.org In the past 2 decades, imaging has become an integral part of screening, diagnosis, and monitoring of children with DDH [20]. A prospective 33-center United Kingdom Hip Trial [37] found that US of children with clinically detected hip instability allowed for a reduction in abduction splinting and was not associated with an increase in abnormal hip development or higher rates of surgical intervention [37].
Developmental Dysplasia of the Hip Child.  Introduction/Background Developmental dysplasia of the hip (DDH) comprises a spectrum of abnormalities from hip instability to frank dislocation [1,2]. The mildest end of the spectrum overlaps with physiologic immaturity, therefore making it difficult to determine its true incidence, which is estimated to be 1.5 to 20 per 1,000 births, depending on the demographics of the study population and the inclusion criteria [3-5]. The diagnosis and monitoring of teratologic hips from neuromuscular or syndromic causes will not be covered. The pathophysiology of DDH is multifactorial and not completely understood. The 2 leading causes are laxity induced by maternal hormones and limited in utero hip mobility. In infants with DDH, abnormally increased laxity of the hip capsule and surrounding ligaments have been attributed to the effects of maternal hormone relaxin [1] and a higher concentration of estrogen receptors [6]. In utero restriction to hip mobility can be encountered with oligohydramnios, first-born infants, and prolonged breech positioning. Breech fetal positioning produces extreme hip flexion with knee extension. This leads to shortening and contracture of the iliopsoas muscle, which promotes femoral head dislocation. Studies demonstrating increased prevalence of DDH among monozygotic twins as compared to dizygotic twins [7] and chromosomal analysis in familial DDH and population-based DDH suggest genetic predisposition to DDH [8-10]. Reprint requests to: publications@acr.org In the past 2 decades, imaging has become an integral part of screening, diagnosis, and monitoring of children with DDH [20]. A prospective 33-center United Kingdom Hip Trial [37] found that US of children with clinically detected hip instability allowed for a reduction in abduction splinting and was not associated with an increase in abnormal hip development or higher rates of surgical intervention [37].