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Developmental Dysplasia of the Hip
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Basics
Description
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.
Epidemiology
- Female-to-male ratio is 4:1.
- Incidence varies from 1.5 to 25 in 1,000 births.
- Dislocation incidence is about 1 in 1,000 births.
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
Genetics
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.
Pathophysiology
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 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.
Etiology
- Mechanical factors: attributed to a smaller in utero environment from oligohydramnios, breech position, increased birth weight, or an unstretched uterus (first pregnancy)
- Female predominance: 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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Basics
Description
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.
Epidemiology
- Female-to-male ratio is 4:1.
- Incidence varies from 1.5 to 25 in 1,000 births.
- Dislocation incidence is about 1 in 1,000 births.
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
Genetics
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.
Pathophysiology
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 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.
Etiology
- Mechanical factors: attributed to a smaller in utero environment from oligohydramnios, breech position, increased birth weight, or an unstretched uterus (first pregnancy)
- Female predominance: 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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