What triggers hip dysplasia?

Hip dysplasia is a condition where the hip socket develops abnormally, leading to an unstable hip joint. It is one of the most common congenital abnormalities in newborns. Hip dysplasia can range in severity from mild instability to complete dislocation of the hip. If left untreated, it can lead to early onset arthritis. Understanding what triggers hip dysplasia is important for prevention and early intervention.

Table of Contents

What is Hip Dysplasia?

Hip dysplasia occurs when the hip socket (acetabulum) does not fully cover the ball portion of the upper thighbone (femoral head). This allows the hip joint to become partially or completely dislocated. In a healthy hip joint, the acetabulum provides stable coverage of the femoral head. In hip dysplasia, the coverage is insufficient, leading to an unstable, improperly formed joint.

In infants, hip dysplasia may occur because the hip socket is too shallow or because the ligaments around the hip joint are too loose. As the child begins to bear weight, the femoral head is not held securely in place, allowing subluxation or dislocation to occur.

Hip dysplasia ranges in severity. It can involve one hip or both hips and may be classified as:

Mild: Slight instability but the femoral head remains located in the socket

Moderate: Partial dislocation of the femoral head
Severe: Complete dislocation where the femoral head is completely outside the socket

When hip dysplasia is detected early, it can often be treated with a brace or harness to help keep the hip joint in the proper alignment. More severe cases may require casting or surgery.

What Causes Hip Dysplasia?

The exact causes of hip dysplasia are not fully understood. However, certain factors are associated with an increased risk:

Genetics: Hip dysplasia tends to run in families. If a parent or sibling had hip dysplasia, a child is at higher risk.
Sex: Hip dysplasia is more common in girls than boys.

Position in utero: A baby in the breech position late in pregnancy is at higher risk. The hips may not develop properly due to cramped positioning.
Oligohydramnios: Low amniotic fluid may make it harder for the baby to move in utero, restricting proper hip development.
Firstborn status: For unknown reasons, firstborn babies are at greater risk for hip dysplasia.

While these factors increase risk, hip dysplasia often occurs without any known cause. Even babies without risk factors can develop hip instability. The condition seems to involve both genetic and environmental influences.

Underdeveloped Acetabulum

One of the hallmarks of hip dysplasia is underdevelopment of the acetabulum, or hip socket. The hip socket forms from several different pelvic bones coming together to create a cup-shaped cavity. In babies with hip dysplasia, this socket does not fully form and provide coverage for the femoral head.

Researchers believe that fetal position in the third trimester has a major influence on proper acetabular formation. Toward the end of pregnancy, the baby’s head typically becomes engaged deep in the pelvis. This helps apply gentle pressure and traction forces to the developing hip socket, stimulating its growth and optimal shaping.

When the fetus is in a breech or transverse position, these forces are not exerted on the hip joint. Instead, the acetabulum may develop a shallow shape that does not adequately surround the femoral head. This makes it easier for subluxation or dislocation to subsequently occur after birth.

Risk Factors for Acetabular Dysplasia

Breech positioning late in pregnancy
Premature birth before 35 weeks gestation

Low amniotic fluid (oligohydramnios)
Family history of hip dysplasia
Firstborn child

Addressing these risk factors, when possible, is an important step in trying to minimize the chances of acetabular underdevelopment and hip instability.

Ligamentous Laxity

In addition to bony abnormalities of the acetabulum, ligamentous laxity is also believed to contribute to hip dysplasia in infants. The hip joint is surrounded and stabilized by several ligaments including:

Iliofemoral ligament

Pubofemoral ligament
Ischiofemoral ligament

These ligaments normally become taut as the baby develops in utero, helping hold the hip bones in proper alignment. When the ligaments are too loose, the hip bones are more likely to displace.

Hormonal influences may play a role in generalized ligamentous laxity and hip instability in newborns. The hormone relaxin is produced during pregnancy to help relax the mother’s ligaments in preparation for childbirth. However, it also crosses the placenta and enters the baby’s circulation. Higher circulating relaxin may contribute to overly loose ligaments in some infants.

Factors Related to Ligamentous Laxity

Family history
Female sex – girls are more prone to generalized ligamentous laxity

Elevated maternal hormones that cross the placenta, like relaxin

Ligamentous laxity usually resolves as the baby’s hormone levels normalize after birth. Gentle swaddling and use of a Pavlik harness helps stabilize the hips during this transition period.

When Does Hip Dysplasia Develop?

Hip dysplasia arises during fetal development in utero. However, the signs and symptoms generally do not become apparent until after birth:

Birth to 4 months – Most cases are detected during routine screening of newborns. Infants may have subtle signs like asymmetric thigh folds.
4 to 12 months – Children may demonstrate delayed motor milestones, favoring one leg over the other when crawling or walking.
Over 12 months – Adolescents and adults may have waddling gait, reduced range of hip motion, and early fatigue/pain with activity.

While hip dysplasia originates before birth, diagnosis is often delayed by weeks or months after delivery. This makes careful screening crucial for detecting cases early and initiating treatment.

Screening for Hip Dysplasia

The American Academy of Pediatrics recommends that all newborns be screened for hip dysplasia, whether or not they have risk factors. Screening typically includes:

Physical exam – The hips are inspected for asymmetry, range of motion, and clunks/clicks.

Ultrasound – Ultrasound can visualize hip anatomy and stability. It may be done at 6 weeks if initial exam is ambiguous or if risk factors are present.

If screening reveals an unstable hip or risk for dislocation, the following interventions may be done:

Pavlik harness – Helps keep hips positioned in flexion and abduction

Abduction brace
Closed reduction – Manual manipulation to relocate the hip
Spica cast – Holds hips in correct position for 4-6 weeks

Surgery – Pelvic or femoral osteotomies are sometimes needed in severe cases

Early detection through newborn screening allows for simpler, less invasive treatments with better outcomes. Hip dysplasia that goes undiagnosed until late childhood or adulthood requires more extensive surgery.

Long-Term Outcomes

With early diagnosis and proper treatment, most infants with hip dysplasia go on to have normal hip development and function. When late or undiagnosed dysplasia is not treated, outcomes include:

Persistent instability or recurrent dislocations
Lameness and waddling gait
Leg length discrepancy

Early onset osteoarthritis
Total hip joint replacement in adulthood

Routine screening allows detection of hip dysplasia before major joint damage occurs. Approximately 1 in 500 infants are found to have developmental hip dysplasia upon screening. Catching cases early optimizes treatment success.

Prevention

Because hip dysplasia often arises due to multiple factors, there are no guarantees for prevention. However, the following measures may help reduce risk:

Prenatal vitamins with vitamin D
Fetal positioning techniques if breech position is detected

Avoiding oligohydramnios by staying hydrated and controlling glucose levels
Ultrasound monitoring of fetal position/hip anatomy in high-risk pregnancies
Swaddling with hips flexed and abducted in newborns

While these steps may help optimize normal hip development, screening for hip instability after birth remains crucial, since congenital hip dysplasia can still occur without identifiable causes or risk factors.

Conclusion

Hip dysplasia arises from a combination of genetic and environmental factors influencing acetabular shape and ligamentous laxity. Breech positioning, low amniotic fluid levels, and family history seem to increase the risk. All newborns should undergo screening exams to detect instability and allow for early intervention. With proper treatment, the outlook for infants with developmental hip dysplasia is generally excellent. Awareness of risk factors and diligent screening help facilitate early diagnosis and prevent complications.