Developmental dysplasia of the hip (DDH) is a spectrum of hip joint abnormalities present from birth in which the acetabulum (socket) is too shallow to adequately contain and stabilize the femoral head (ball). The condition ranges from mild acetabular shallowness to partial or complete dislocation of the hip joint. Early detection and treatment are essential — outcomes are dramatically better when DDH is identified in infancy than when it is discovered in childhood or adulthood.
Developmental hip dysplasia sits at one end of a lifelong spectrum of hip socket abnormalities. Mild or undetected DDH in infancy frequently persists into adulthood as adult hip dysplasia — the shallow socket continues to overload the hip labrum and cartilage, causing pain and eventually early hip osteoarthritis. DDH is also one of the recognized predisposing conditions for Legg-Calvé-Perthes disease and for avascular necrosis of the femoral head as a complication of treatment itself — making careful, experienced management essential. The goal of every treatment decision in DDH is to achieve and maintain a concentrically reduced, well-covered hip that can develop normally.
Causes
Developmental and mechanical factors.
DDH results from abnormal development of the hip joint during fetal growth and the early postnatal period, when the acetabulum and femoral head are rapidly co-developing and each depends on the other for normal shape formation. Any factor that reduces fetal hip mobility or positions the hip in an unfavorable orientation during this critical window can impair normal socket development. The acetabulum is most vulnerable during the final weeks of pregnancy, when intrauterine space is limited and the fetus is largest. A shallow socket that fails to cover the femoral head adequately leads to instability, abnormal contact forces, and further failure of normal socket deepening — a self-perpetuating cycle that worsens without treatment.
Risk factors.
DDH is 4–5 times more common in girls than boys, reflecting the greater ligamentous laxity associated with maternal estrogen exposure in utero. Breech presentation at birth — particularly frank breech with the hips flexed and knees extended — is the single strongest mechanical risk factor, increasing DDH risk approximately tenfold. Firstborn status is a risk factor because the uterus is less distensible, restricting fetal movement. A positive family history is present in approximately 20% of cases, indicating a significant genetic component. Left hip involvement predominates (60% of cases) because the left fetal hip is typically positioned against the maternal spine in the most common left occiput anterior fetal presentation, limiting abduction. Oligohydramnios (reduced amniotic fluid), multiple gestation, and swaddling in hip extension and adduction postnatally are additional risk factors.
Symptoms
Clinical presentation varies dramatically with age at diagnosis. In newborns and infants, DDH is typically painless — the diagnosis depends entirely on clinical screening and imaging. The Ortolani test (relocating a dislocated hip with abduction) and Barlow test (provoking subluxation with adduction and posterior pressure) are the neonatal screening maneuvers performed at birth and well-baby visits. Limited hip abduction on the affected side, asymmetric thigh or gluteal skin folds, and apparent limb length discrepancy are additional clinical signs. A "clunk" with the Ortolani maneuver indicates a dislocated hip being reduced — a finding requiring immediate imaging and referral.
In walking-age children with undetected DDH, the classic presentation is a painless limp or a waddling gait. Bilateral DDH produces the characteristic hyperlordotic, broad-based waddling gait. Older children and adolescents may develop groin pain and decreased hip range of motion as the consequences of dysplasia accumulate. In adults with undetected DDH, the presentation is chronic hip and groin pain — the condition is then classified as adult hip dysplasia.
Diagnosis
Diagnosis is age-dependent and requires different imaging modalities at different stages of development. In newborns and infants under 4–6 months, the femoral head is cartilaginous and not visible on X-ray — hip ultrasound is the imaging gold standard, using the Graf classification to assess acetabular morphology and femoral head coverage, and dynamic imaging to assess stability. Ultrasound screening is recommended for all infants with risk factors (breech, family history, abnormal exam) and is universal in many countries. After approximately 4–6 months of age, the femoral head begins to ossify and X-rays become the primary imaging tool, measuring the acetabular index and the position of the femoral head relative to the acetabulum. An MRI is used selectively — most commonly after closed or open reduction — to confirm concentric reduction of the femoral head within the acetabulum and to evaluate soft tissue obstacles to reduction (hypertrophied ligamentum teres, inverted labrum, pulvinar fat) that may prevent adequate seating of the hip.
Severity classification
DDH is classified by the degree of femoral head displacement and acetabular development, which directly determines treatment urgency and approach.
- Dysplasia (without dislocation): The acetabulum is shallow but the femoral head remains within the socket. The mildest form — may be detected on newborn screening or present later as adult hip dysplasia if undetected.
- Subluxation: The femoral head is partially displaced from the acetabulum — in contact with the socket but not concentrically seated. Intermediate severity requiring prompt treatment.
- Dislocation: The femoral head is completely outside the acetabulum. May be reducible (Ortolani positive) or irreducible (locked out). The most severe form — requires urgent treatment to allow normal hip development.
Treatments
Treatment is entirely age-dependent and becomes progressively more complex and less predictable as diagnosis is delayed. The overriding goal at every age is to achieve and maintain a concentric hip reduction that allows the acetabulum and femoral head to co-develop normally.
Newborns and infants (0–6 months): The Pavlik harness is the primary treatment for DDH detected in the newborn period. This soft, adjustable device maintains the hips in a flexed and abducted position — the human position — which centers the femoral head in the acetabulum and stimulates normal acetabular development. Success rates exceed 90% when used correctly in appropriate candidates. The harness is worn full-time for 6–12 weeks and is monitored with serial ultrasound to confirm and maintain reduction. Failure of the Pavlik harness or delayed presentation beyond 6 months prompts escalation to closed or open reduction.
Infants and toddlers (6 months to 2 years): When the Pavlik harness has failed or diagnosis is made after 6 months, closed reduction under general anesthesia followed by spica cast immobilization is the standard treatment. Hip arthrography at the time of reduction confirms concentric seating. MRI after cast application verifies reduction quality. Open reduction is performed when soft tissue obstacles (inverted labrum, hypertrophied ligamentum teres, pulvinar) prevent adequate closed reduction. Femoral shortening osteotomy may be added to reduce pressure on the reduced femoral head. Spica casting is maintained for 3–6 months.
Children (2–8 years): Open reduction combined with femoral and/or pelvic osteotomy is the standard approach. Pelvic osteotomies (Salter, Dega, or triple innominate) redirect the acetabulum to improve coverage. Femoral osteotomy corrects excessive anteversion and valgus. The combination is tailored to the specific anatomic abnormalities identified on imaging. The window for achieving a well-formed, functional native hip narrows progressively through this age range.
Older children and adults with residual dysplasia: When DDH is identified in older children or adults as hip dysplasia with preserved joint cartilage, periacetabular osteotomy (PAO) — reorienting the entire acetabular fragment — is the gold standard joint-preserving procedure. When significant arthritis has already developed, total hip arthroplasty is the appropriate treatment, though it is technically more demanding in dysplastic anatomy due to bone stock deficiency and abnormal biomechanics.
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