Chapter 40

Assessment of the baby

Developmental dysplasia of the hips

Learning outcomes

Having read this chapter, the reader should be able to:

• discuss the factors that contribute to developmental dysplasia of the hips (DDH)

• describe DDH and how it is classified

• describe the different tests that are used to assess for DDH

• discuss how DDH may be prevented once the baby is born

• discuss the role and responsibilities of the midwife in relation to DDH.

Developmental dysplasia of the hips (DDH) is used to describe a wide range of conditions related to the development of the hips in babies through to young children. It includes abnormal development of the acetabulum and proximal femur (the femoral head and neck, and the greater and lesser trochanter) through to mechanical instability of the hip joint (Rosenfeld et al 2014). If undiagnosed or left untreated, there is associated long-term morbidity of gait abnormalities, chronic pain, degenerative osteoarthritis, and avascular necrosis due to impairment of the blood supply, leading to hip replacement often before the age of 40 years, widening of the perineum, and hyperlordosis (Rosenfeld et al 2014, Shorter et al 2013, Wang et al 2013). DDH has also been called congenital dislocation of the hip, hip dysplasia, developmental dislocation of the hip, and acetabular dislocation. In some countries the assessment is undertaken by midwives at birth as part of the first examination, e.g. New Zealand, whereas in other countries, such as the UK, the assessment is undertaken by a paediatrician (often junior doctors rather than Registrars or Consultants) or a midwife who has undertaken further training and assessment in the examination of the newborn (NMC 2012). This chapter considers the factors that predispose to DDH, how it might be prevented, and a discussion of the tests undertaken to screen for DDH, who should undertake these and when, with reference to the management of DDH.

What is DDH?

DDH occurs when the femoral head is not sitting centrally in the acetabulum. This can occur during late pregnancy or during the neonatal period. There may be dislocation (total loss of contact between the acetabulum and the femoral head) or subluxation (the femoral head is partially within the acetabulum in a non-centric position). The hip may:

• have instability where the femoral head is reduced (meaning ‘within the acetabulum’) at rest but not with movement, and there is laxity within the acetabulum

• be subluxable if the femoral head is reduced at rest but can be partially dislocated with examination manoeuvres (also referred to as mild instability)

• be reducible if the hip is dislocated at rest but, with manipulation, the femoral head can be positioned into the acetabulum (Rosenfeld et al 2014).

During the neonatal period the femoral head and acetabular cartilage continue to grow, which is critical for normal hip development, as is reduction and stability of the femoral head (Hart et al 2006). It is normal for babies to have physiological laxity of the hip during the first few weeks of life; however, this usually resolves spontaneously as the acetabulum and femoral head grow and development continues normally (Rosenfeld et al 2014). Rosenfeld et al (2014) suggest that of the 60% of babies who have hip instability in the first week of life, 90% will have stabilized by 2 months.

Continued dislocation of the femoral head causes the tendons, muscles and bony structures to develop secondary adaptive changes which include stretching of the acetabular capsule, leading to the development of abnormal attachments, shortening and contracture of muscles, flattening of the femoral head and acetabular dysplasia which will eventually result in osteoarthritis in childhood (Hart et al 2006).

The degree of dislocation can be classified according to the Graf hip classification type, of which there are five (Rosenfeld et al 2014):

• Type I refers to a fully mature, normal hip that has a deep acetabular cup and an angular acetabular rim with the cartilaginous roof of the acetabulum covering the femoral head.

• Type IIa is seen in infants less than 3 months of age, reflecting the physiological immaturity of the baby’s hip joint. The femoral head is situated within the acetabulum but the acetabulum is shallow and the rim is round, with the cartilaginous acetabular roof covering the femoral head. Ninety percent will resolve spontaneously (Paton et al 2014).

• Type IIb are abnormal hips seen in babies over 3 months of age and will worsen without treatment. The acetabulum is slightly shallow with a round rim and the cartilaginous acetabular roof covers the femoral head.

• Type III are dislocated hips that have a shallow acetabulum while the acetabular roof is deficient.

• Type IV are dislocated hips where the acetabulum is almost flat and the acetabular roof is significantly displaced.

Hips that ‘click’ do not signify DDH and the term ‘clicky hips’ should not be used, as it is misleading. Rosenfeld et al (2014) advise a ‘clunk’ (or a ‘jerk’, suggestive of DDH) is a different sensation to a ‘click’, being one of a high-pitch joint popping movement rather than the clicking or snapping sensation caused by the snapping of tendons or ligaments around the hip and knee.

Risk factors

The hip is thought to develop normally during pregnancy but gradually becomes abnormal for a number of reasons (Hart et al 2006). Towards the end of pregnancy there is pressure on the hip joint forcing the femur head into an abnormal position within or outside of the acetabulum; thus many of the risk factors within the literature are related to this. However Choudry et al (2013) suggest there is a lack of known factors in 69–73% of cases.

• Family history – Stevenson et al (2009) propose the risk of DDH increases 12-fold if a first-degree relative has DDH, while the International Hip Dysplasia Institute (IHDI 2015) suggest it is a 1 : 8 chance, and if a sibling has DDH it is 1 : 7, but if both a parent and a sibling have DDH the risk increases to 1 : 3.

• Female gender – Schwend et al (2014) state that 78% of DDH cases occur in females. Hart et al (2006) wonder if this is because female fetuses are more susceptible to the effects of maternal relaxin. However, Bracken et al (2012) point out that cord studies have shown no correlation between relaxin concentration and DDH.

• Breech (extended) presentation ≥34 weeks’ gestation (Rosenfeld et al 2014, Shorter et al 2013), although if an external cephalic version is undertaken (p. 206), the risk reduces from 9.3% to 2.8% (Lambeek et al 2013), and if the baby is born by elective caesarean section, the risk reduces further (Fox & Paton 2010). Schwend et al (2014) propose the highest risk is a female fetus in an extended breech presentation.

• Improper swaddling whereby the legs are straightened to a standing position which can loosen the joints and result in damage to the soft cartilage of the acetabulum (IHDI 2015).

• Multiple pregnancy (IHDI 2015).

• Oligohydramnios (Paton et al 2014, Rosenfeld et al 2014).

• First-born babies (Rosenfeld et al 2014).

• Ethnicity – increased in Caucasian babies (McCarthy et al 2005).

• High birthweight babies (Dezateux & Rosenthal 2007).

• Babies with fixed idiopathic congenital talipes equinovarus are not at increased risk of DDH (Paton et al 2014), although those with congenital talipes calcaneovalgus (CTCV) are 5.2 times more likely to have DDH than babies without CTCV (Paton & Choudry 2009).

• DDH may also occur when certain syndromes are present, e.g. trisomy 21, Ehlers Danlos (Rosenfeld et al 2014).

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