Developmental Dysplasia of the Hip



Developmental dysplasia of the hip (DDH) is a range of hip pathology including dysplasia (shallow acetabulum), subluxation (partial femoral head–acetabulum contact), and dislocation (no hip joint contact). Abnormalities can be present at birth or develop over time. A teratologic dislocation is a different condition that occurs during fetal development usually from genetic/syndromic causes. Discussion of teratologic dislocation is beyond the scope of this chapter.


  • Female-to-male ratio is 4:1.
  • Clinical hip instability occurs in approximately 1 to 2 in 100 newborns.
  • Dislocation incidence is about 1 in 1,000 births.
  • Bilateral hip dysplasia in approximately 20%

Risk Factors

  • Compressive factors:
    • Breech position (newborn DDH risk: male 2.6%, female 12%)
    • Oligohydramnios
    • Firstborn child
    • High birth weight
  • Demographic factors:
    • Female gender (newborn DDH risk 1.9%)
    • Family history (newborn DDH risk: male 0.9%, female 4.4%)
    • Ethnicity: Native American, Laplander


No defined mode of inheritance; family history, gender, and ethnicity association

General Prevention

  • Although DDH cannot be prevented, treatment is directed at preventing early arthritis.
  • Screening programs have reduced the newborn dislocation rate to 1 in 5,000 children by the age of 18 months.


  • The acetabular depth (growth) is determined by healthy cartilage and development around a concentrically reduced/stable femoral head. Cartilage damage occurs from continued instability.
  • Untreated subluxation/dislocation can result in an everted labrum, hypertrophic cartilage/labrum complex (neolimbus), and false acetabulum (pseudoacetabulum).
  • In early adulthood, this condition can lead to abnormal wear of the joint, limb length differences, and arthritic pain. Compensatory problems may include spinal malalignment (scoliosis/lordosis) and gait abnormalities.


  • Scientific understanding is still evolving, but both genetic and environmental factors play a role.
  • Mechanical factors: attributed to a smaller in utero environment from oligohydramnios, breech position, increased birth weight, or an unstretched uterus (first pregnancy)
  • Female predominance: unclear etiology but has been attributed to estrogen-induced ligamentous laxity
  • Left side predominance: attributed to fetal positioning of left hip adduction against the mother’s lumbosacral spine
  • Native American predominance: attributed to the hip extension/adduction position of swaddling

Commonly Associated Conditions

  • Neurologic conditions (e.g., myelomeningocele)
  • Connective tissue disorders (e.g., Ehlers-Danlos)
  • Syndromic conditions (e.g., Larsen syndrome)
  • Myopathic disorders (e.g., arthrogryposis)

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