Developmental dysplasia of the hip

• Developmental dysplasia of the hip (DDH) is not one disease but a spectrum: from mild underdevelopment of the acetabulum (the hip socket) with the femoral head still sitting in it, through partial loss of contact (subluxation), to full dislocation.
• It is one of the most common paediatric orthopaedic disorders. In population studies the prevalence ranges from 0.1% to 3%, and in the Netherlands 3.7% of children up to 6 months have some form of hip dysplasia. ^[1][3][4]
• Females are far more often affected than males (female-to-male ratio about 6 to 1), and the left hip is the one most often involved. ^[4]
• A normal early examination is reassuring but is not perfect: some hips dislocate later, and some cases are missed. That is why most countries combine physical examination at birth with imaging for at-risk infants. ^[3]
• The good news is that the hip of a newborn is extremely mouldable. Conservative treatment started in the first months of life (Pavlik harness, or observation for mild cases) succeeds in the great majority. Late diagnosis is what converts a simple problem into operations, redislocation, avascular necrosis and early arthritis. ^[1][2]

By the end of this page you should be able to:

1. Explain what DDH is, how it ranges from dysplasia to dislocation, and why naming it "developmental" (not "congenital") matters.
2. List the major risk factors and understand the mechanical reason each one matters.
3. Elicit and interpret the Barlow and Ortolani manoeuvres, asymmetric thigh folds and apparent leg-length discrepancy.
4. Choose and time imaging: ultrasound in early infancy, radiographs once the ossification centre has developed.
5. Outline screening programmes (universal versus selective) and what the examination and imaging timetable looks like.
6. Manage a centred dysplastic hip and a decentered/dislocated hip, including Pavlik harness practicalities, closed and open reduction, spica cast and follow-up.
7. State the important complications and the long-term outlook.

DDH used to be called "congenital dislocation of the hip", but "developmental" is the better word. Many affected hips are normal at birth and become abnormal during growth, and the condition can improve or worsen over time depending on how the joint is loaded. Calling it congenital also implied the only problem was dislocation, when in reality most cases are milder dysplasia without dislocation. ^[4]

For teaching and management it helps to split the spectrum into two situations, because the treatment is different for each:

• Centred (stable) DDH: the femoral head is still in the acetabulum but the socket is underdeveloped. These are Graf types 2A to 2C on ultrasound. Most are mild and many resolve without treatment. ^[1]
• Decentred (unstable) DDH: the head is partly or fully out of the socket (Graf types D, III and IV). These hips need active treatment to obtain and maintain reduction. ^[2]

DDH is one of the most common paediatric orthopaedic disorders, with an approximated incidence of 1% to 3% of infants. ^[3] The burden is not evenly distributed:

• Overall prevalence is usually quoted as 0.1% to 3% of the population, depending on how and when looking is done. ^[3][4]
• By region, Native American populations have the highest reported values (around 7.6%) and African populations the lowest (around 0.1%). ^[4]
• Dislocations are rarer: 0.1% to 0.2% of children under 6 months have a dislocated hip. ^[2]
• Dysplasia itself is found in 3.7% of children up to 6 months of age in the Netherlands, and is present in 1% to 2% of newborns to some degree. ^[1][4]
• Natural history is favourable: about 60% of subluxated or dislocated hips at birth stabilise in the first week, and 88% by two months of age. ^[4]
• Sex: females are affected much more often, with a female-to-male ratio of about 6 to 1, and females are between 4 and 9 times more likely to develop the condition. ^[4]
• Side: the left hip is most often affected; studies quote ratios around 3 to 1 in favour of the left, and about 60% of unilateral cases are left-sided. ^[4]
• Later detection: despite screening, late diagnosis is still reported in 2.2 per 1000 infants, and about 1 in 5000 cases is not detected until after 18 months. ^[4]

The reason DDH matters for a lifetime is that it is the cause of 9% of all hip replacements and 26% of hip arthroplasties in patients under 40. ^[3] However, when conservative treatment is started early, in infancy, it is usually effective. ^[3]

The exact cause of DDH is unknown. It is a multifactorial problem: the socket (acetabulum) and the femoral head are still cartilage at birth, and the ligaments of a newborn are lax. Anything that keeps the hip from sitting deeply in the socket, or that pushes the head out, increases risk. Risk factors are reported to be present in 10% to 27% of affected infants. ^[4]

The five risk factors every clinician is taught:

1. Female sex. The female predominance (female-to-male ratio about 6 to 1) is thought to reflect the effect of maternal hormones (oestrogens, progesterone and relaxin), which relax the infant's joint capsule and ligaments and make the hip more lax. ^[4]
2. Breech presentation. The extended or frank breech position keeps the hips in extension and adduction, reducing the depth of the acetabulum. Breech is listed as a risk factor in every European national guideline that addresses risk factors. ^[3][4]
3. First-born (primiparity). A primiparous mother has a narrower, less compliant birth canal, so the forces on the fetal hip during delivery are greater. Being first-born is recognised in the literature as a risk factor, even though individual studies find the association inconsistent. ^[4]
4. Family history. A family history of DDH increases the likelihood by 12 to 15.9 times. ^[4]
5. Oligohydramnios (reduced amniotic fluid). Limited fetal movement and restricted space in utero (packing) prevent the rotating hip movements that help mould the acetabulum. ^[4]

In practice, the useful mental rule is simple: a breech, first-born girl with a family history is the classic high-risk infant, and that baby deserves a careful examination and almost always an ultrasound even if the hips feel normal.

The acetabulum and femoral head are mostly cartilage at birth. Deep sitting of the head in the socket is what stimulates the socket to grow concentrically. Anything that breaks that contact for long enough produces a shallow or malformed socket.

1. Laxity comes first. Maternal hormones and the newborn's own lax ligaments allow the head to move abnormally. This is why an unstable hip can sometimes be dislocated and reduced by the examiner's hands.
2. Reduced contact shapes the socket badly. If the head is not pressing in the centre, the acetabular roof does not develop its concavity; the socket becomes oblique and shallow.
3. Dislocation follows sustained underdevelopment. A hip that is repeatedly not seated can become dislocated, with the head lying posteriorly and superiorly. The joint capsule tightens in the wrong position and the adductors shorten.
4. Walking makes it worse, not better. Once the child bears weight on a dislocated head, secondary changes develop: shortening of the proximal femur, anteversion, and flattening of the socket. This is why early reduction is urgent but gentle reduction is essential.

Two illustrations of the pathophysiology will be familiar on the wards:

• Left-sided predominance is partly mechanical: in the commonest fetal position (occiput left anterior) the left hip lies against the maternal spine, restricting its movement. ^[4]
• Females are affected more because maternal hormones, including relaxin and sex steroids, make the joint capsule laxer at birth. ^[4]

DDH in a newborn produces no pain and no systemic upset. The diagnosis rests entirely on a careful, deliberate examination.

There is usually no history of note. The parents may have noticed a "click" or a leg that lies differently. Risk factors from the history (female, breech, first-born, family history, oligohydramnios) should be sought. ^[3][4]

These two manoeuvres test different things and are performed on the relaxed supine infant, ideally when calm and not crying.

Barlow manoeuvre (test for dislocatability). The hip is flexed and the thigh adducted, with gentle downward/backward pressure applied along the shaft of the femur. A positive test is the feeling of the head slipping posteriorly out of the acetabulum, often with an audible or palpable clunk. Barlow detects a hip that is unstable enough to be dislocated. ^[3]

Ortolani manoeuvre (test for reducibility). With the hip flexed, the examiner abducts the hip while lifting the head anteriorly with the fingers behind the greater trochanter. A positive test is a clunk as the dislocated head reduces back into the socket. Ortolani detects a hip that is already dislocated but still reducible. ^[3]

The two tests are complementary: Barlow looks for a hip that can be pushed out; Ortolani looks for one that can be clicked back in. A clicking or clunking sensation from a newborn hip is abnormal until proven otherwise; it is not a benign "hip click".

• Asymmetric thigh folds. Unequal skin creases on the inner thighs or below the buttocks, or an asymmetry of the gluteal folds, may be seen. Folds are an unreliable sign on their own (they are normal variants in many infants), but they are one of the consistent clinical findings across guidelines and warrant imaging when combined with other features. ^[3]
• Apparent leg-length discrepancy (Galeazzi/Allis sign). With both hips and knees flexed, one knee sits lower than the other because the dislocated femur on that side is held more proximally. This is the leg-length sign named after Galeazzi. ^[3]
• Limited abduction. Reduced abduction of the affected hip suggests a dislocated hip, because the adductors have tightened; it can also be seen after reduction while the socket remodels. ^[3]
• Trendelenburg gait appears much later, when the child walks: the pelvis drops on the affected side during stance because the abductors (especially gluteus medius) are mechanically disadvantaged. This is a sign of longstanding dysplasia, not of the newborn period.
• Once a child is walking, look for limping, a waddling gait, and premature wear.

DDH must be separated from a few conditions that look similar on examination or imaging.

In practice the serious mimics are infection and neuromuscular disease. If there is fever, an elevated white cell count or C-reactive protein, or a child who looks unwell, pursue infection first.

Screening is the whole reason DDH has moved from a cause of lifelong disability to a routine, treatable condition. Two approaches exist. ^[3]

• Universal screening: every infant gets a clinical and an ultrasound examination. Austria, Germany, Slovenia and others do this in some form within Europe. ^[3]
• Selective screening: imaging is performed only in infants with abnormal clinical examination or risk factors (breech, family history, other orthopaedic deformities, positive examination). This is the model in the Netherlands, the United Kingdom and France. ^[3]

There is no international consensus and no single screening schedule; nine European countries were found to have a national DDH guideline in a 2025 review, and their screening and treatment recommendations varied greatly. ^[3]

A common schedule looks like this (timing varies):

• Clinical examination at birth (within the first two weeks in most countries; in the Netherlands within the first month). Universal clinical examination is advised, with repeat examinations up to 18 months of age because late presentation occurs. ^[3]
• Imaging:
  • Ultrasound is the modality of choice in early infancy, most commonly using the Graf technique (measurement of the alpha and beta angles of the hip). ^[3]
  • Selective imaging is performed for a positive clinical examination from birth to week 10, or for risk factors from week 4 to week 12. ^[3]
  • Universal imaging, where used, takes place from week 1 to week 6. ^[3]
• Radiographs take over later, once the ossification centre of the femoral head is large enough and ultrasound becomes less reliable.

The clinical examination should include the manoeuvres already described (Barlow, Ortolani, abduction, Galeazzi) plus inspection of the skin folds. Only a handful of factors are agreed across guidelines: positive examination, breech presentation, family history, and other orthopaedic deformities. ^[3]

Ultrasound is the first imaging test in infancy. It does not use radiation, it can be done at the bedside, and it visualises the cartilaginous head and socket that radiographs cannot see. The Graf method is the most widely used; it measures the osseous roof angle (alpha angle) and the cartilaginous roof angle (beta angle) and classifies the hip from type 1 (normal) through to type 4 (dislocated). A widely used treatment endpoint is an alpha angle greater than 60 degrees. ^{[3] [5]}

Ultrasound is most useful and most reliable in the first months, before the ossification centre of the femoral head grows large and blocks the view. By 9 to 12 months the femoral head ossification centre usually makes ultrasound technically unfeasible, and radiography takes over. ^[1]

From about 6 months of age, and routinely thereafter, a plain anteroposterior pelvis radiograph is used. On the radiograph the acetabular index and the position of the ossification centre of the femoral head are assessed; standardised approaches (Hilgenreiner, Perkins and Shenton lines) describe whether the head is seated or dislocated. Bilateral dislocations can be deceptive because no asymmetry is visible, so both hips must always be evaluated carefully. ^{[4] [5]}

Plain radiographs become the standard imaging test once ultrasound becomes unreliable. The AAOS programme images to 6 months of age and the Dutch guideline changes from ultrasound to radiography at 9 to 12 months, so programmes genuinely differ. ^[1][5]

DDH is a clinical and imaging diagnosis; there are no laboratory tests. Severity is staged by imaging and physical examination together:

• Graf type 1: normal, mature hip (alpha 60 degrees or more).
• Graf type 2A/2B/2C: centred dysplasia of increasing severity (immature or abnormal but still seated). Types 2A/B and 2C are "centred DDH".
• Graf type D/III/IV: decentred or dislocated hips. ^[1][2]

The distinction that drives management is centred versus decentred, not the exact grade. A hip that is seated but dysplastic (centred) is treated differently from a hip in which the head is out (decentred).

The overriding principle is to obtain and maintain a concentric reduction of the femoral head before the baby bears weight, and to do it gently, because the blood supply to the femoral head (the medial femoral circumflex vessels) runs close to the back of the neck of the femur. Forceful or poorly timed reduction risks avascular necrosis (AVN), the one complication that can be worse than the disease.

For a seated but dysplastic hip in an infant under 1 year:

• Initial observation is recommended for 3-month-old infants with centred DDH, rather than immediate harness treatment. ^[1]
• Start abduction treatment if the hip does not normalise after 6 to 12 weeks of observation. ^[1]
• Pavlik harness is the device prescribed for children under 6 months with persistent dysplasia on repeated ultrasound. ^[1]
• For children over 6 months, another abduction device (brace) is considered more suitable because the Pavlik harness is more easily disengaged by a stronger infant. ^[1]
• Review is performed every 6 weeks with clinical examination and imaging. ^[1]
• Stop the device when the hip has normalised or when the child reaches 1 year of age. ^[1]

This apparent "wait and see" approach has evidence behind it: in a European cohort of centred DDH treated with Pavlik harness, the mean acetabular index at 2 years was 21.6 degrees, and in the observed group 23.5 degrees, a difference that was not statistically significant. A 2020 randomised trial of stably dysplastic 3-month-olds (Graf types 2B and 2C) similarly found no difference in the alpha angle between Pavlik treatment and observation at 6 and 12 weeks, with 20% of the observed group eventually needing a harness. ^{[1] [5]}

For a subluxated or dislocated hip in an infant under 1 year:

• Pavlik harness is the preferred first step. ^[2]
• Follow-up with ultrasound at 3 to 4 and at 6 to 8 weeks. ^[2]
• If no centred, stable hip is seen within 6 to 8 weeks, closed reduction is indicated. ^[2]
• If reduction is restricted by limited hip abduction, perform an adductor tenotomy (not traction). ^[2]
• If closed reduction fails, open reduction. The anterior, anterolateral or medial approach may all be used, and the choice should be based on the surgeon's preference and experience, because comparative studies have not shown a clear winner for reduction rate, residual dysplasia, AVN or redislocation. ^[2]
• After successful reduction (closed or open), a spica cast for 12 weeks is recommended, followed by an abduction device if residual dysplasia remains. ^[2]
• During the cast, transinguinal ultrasound is used to confirm that the head remains reduced; if ultrasound is not available, an arthrogram after reduction followed by radiographs is advised, and MRI or low-dose CT are used when in doubt. ^[2]

The harness is the standard first-line device for hips under 6 to 9 months. Practical points worth remembering:

• Positioning: hips in flexion of about 90 to 100 degrees with comfortable abduction ("the human position"), never forced. This position reduces and centralises the head and is why the harness succeeds in most infants. ^[2]
• Wear time: recommended 23 hours per day, with removal allowed for bathing. ^{[1] [5]}
• Check and adjust at the outpatient clinic 1 week after application, and thereafter as needed. ^[1]
• Complications to watch for: failure of reduction and "Pavlik disease" (erosion and necrosis of the posterior acetabular wall when the head is forced against the posterior rim for too long). Hence the 6 to 8 week ultrasound check; if the hip has not reduced, stop and change plan rather than push on. ^[1][2]
• Older infants: the harness is replaced by a fixed abduction brace from about 6 to 9 months, when the child becomes strong enough to disengage it. ^[1]

Closed reduction is done under general anaesthetic, with an arthrogram to confirm the position, and often with an adductor (longus) tenotomy to gain abduction when tightness prevents reduction. Adductor tenotomy is preferred over prolonged traction, which adds burden without clear benefit and had an avascular necrosis rate of 50% in the one comparative study. ^[2]

Open reduction becomes necessary when closed reduction fails or when a major incongruity (such as an inverted labrum, pulvinar or capsular constriction) blocks reduction. Either the anterior (Smith-Petersen), anterolateral (Watson-Jones) or medial (Ludloff/Ferguson) approach may be used; comparative studies have not demonstrated a clear winner for successful reduction, residual dysplasia, complications or function, although the medial approach allows surgery at a younger age and the anterior approach offers better capsular tightening and preservation of the medial femoral circumflex vessels. ^[2]

• Avascular necrosis (AVN) after Pavlik harness or splint treatment of decentered hips is reported around 6% to 7% in the comparative studies (Pavlik harness 6%, Frejka splint 7%). ^[2]
• AVN after traction occurred in 50% of children in the one comparative study (2 of 2 traction-only children); adductor tenotomy was 25% and no tenotomy 33%. These are small denominators and should be interpreted as a warning, not as precise estimates. ^[2]
• Residual dysplasia and redislocation are the other two common late problems and are why follow-up is long.

All children treated for DDH need follow-up to ensure the head stays seated and the acetabulum remodels. Ultrasonic follow-up is at 3 to 4 and 6 to 8 weeks for harness-managed decentered hips, then every 6 weeks while in a device. ^[2] After reduction, radiographs assess the acetabular index and the head position. Long-term follow-up programmes vary from radiographs at age 2 years (Germany, United Kingdom) to radiographs at 1, 3 and 5 years (Netherlands), and even 1, 3, 5, 10 and 18 years for decentred hips in the Netherlands. ^[3]

Refer urgently if:

• a decentred hip is not concentric after 6 to 8 weeks of harness treatment;
• closed reduction is not possible;
• AVN, redislocation, or severe residual dysplasia is found at any stage;
• an adolescent or young adult presents with early-onset osteoarthritis on the basis of unknown previous dysplasia.

Untreated or late-diagnosed DDH leads to a short, unstable, painful hip. The principal complications are:

• Avascular necrosis (AVN) of the femoral head - caused by forceful reduction, prolonged poorly applied abduction, or by the dislocation itself. ^[2]
• Redislocation and residual dysplasia, particularly after failed or late reduction. ^[2]
• Femoral neuropathy from over-tight splinting. ^[2]
• Early-onset osteoarthritis, which is the feared long-term endpoint: DDH accounts for 9% of all hip replacements and 26% of hip replacements under age 40. ^[3]
• Leg-length discrepancy and abnormal gait, including a Trendelenburg limp. ^[4]

Complications of conservative treatment are more common when treatment is delayed or when the harness is used without close follow-up. This is the single strongest argument for organised screening and meticulous ultrasound timing.

The prognosis of DDH treated early and gently is excellent. The best evidence comes from the natural history data: most unstable hips at birth stabilise spontaneously in the first weeks, and the iatrogenic risk comes from prolonged or improper treatment rather than from the condition itself. ^[4]

In treated disease, 88% to 100% of decentered hips are successfully reduced by abduction devices, open or closed reduction depending on the situation, and outcomes are generally good. ^[2] The Dutch guideline for decentred hips adds that spica cast immobilisation for 4 weeks followed by a weaning abduction brace versus 12 weeks of casting showed no meaningful difference in reduction or residual dysplasia, although the short-cast group had less AVN (15.8% versus 48.3%). ^[2] Treatment decisions here should err on the side of the solid 12 week cast, which is the guideline recommendation. ^[2]

A late diagnosis (walking age and beyond) makes the prognosis markedly worse: operation, possible pelvic osteotomy, long rehabilitation, and a higher lifetime risk of revision hip surgery. ^[3]

• Pregnancy and the newborn: the hormones of pregnancy (relaxin, oestrogens, progesterone) cause the laxity that underlies DDH. No treatment changes are needed for the mother.
• Children with Down syndrome, neuromuscular disease or connective tissue laxity: these children have higher rates of hip dysplasia and dislocation, often with a normal newborn examination; many programmes recommend periodic ultrasound for them. ^[4]
• Late presenters and adolescents: management changes with age. Once a child is walking, reduction becomes harder and open reduction with pelvic and femoral osteotomy is often required. Details are beyond this page and require specialist referral.
• Low-resource settings: physical examination costs nothing and can be done at any level. Where ultrasound is unavailable, a careful Barlow and Ortolani, assessment of abduction and the Galeazzi sign, plus a plain pelvis radiograph from about 6 months of age, is a realistic screening pathway. ^[1][5] Where surgery is unavailable, refer early to a centre that can perform open reduction and spica casting; do not attempt forceful reduction.
• Deprived or remote settings also need recall: children with normal examinations at birth can still present late, so opportunistic examination at any routine visit is valuable.

• DDH is a spectrum from mild acetabular dysplasia to complete dislocation, and it is developmental rather than congenital. ^[3]
• Prevalence is about 0.1% to 3%; about 3.7% of children up to 6 months in the Netherlands have some form of hip dysplasia. ^[1][3][4]
• Females are affected about 6 times more often than males; the left hip is more often involved. ^[4]
• Risk factors: female sex, breech presentation, first-born, family history, oligohydramnios. ^[3][4]
• Examine every newborn with Barlow, Ortolani, abduction, Galeazzi and inspection of the folds; do not force the manoeuvres. ^[3]
• Ultrasound is the early imaging test (Graf method); radiographs usually take over from 6 months (AAOS) to 9 to 12 months (Dutch). ^[1][5]
• Screening can be universal (clinical plus ultrasound for all) or selective (clinical for all, imaging for risk factors or abnormal examination); there is no global consensus. ^[3]
• Centred dysplasia: observe first for 3-month-olds; Pavlik harness under 6 months if not normalised after 6 to 12 weeks; review every 6 weeks; stop when normal or at 1 year. ^[1]
• Decentred hip: Pavlik harness first; ultrasound at 3 to 4 and 6 to 8 weeks; closed reduction if not centred by 6 to 8 weeks, with adductor tenotomy if abduction is limited; open reduction by surgeon preference; spica cast for 12 weeks. ^[2]
• Pavlik harness: 23 hours per day, check and adjust at 1 week, 6 to 8 week ultrasound checkpoint to avoid Pavlik disease. ^[1][2]
• Major complications: avascular necrosis, residual dysplasia, redislocation, femoral neuropathy and ultimately early osteoarthritis (9% of hip replacements, 26% under age 40). ^[2][3]
• AVN is reported around 6% to 7% after Pavlik/splint treatment, and was far higher after traction; force and prolonged poorly fitted harnessing are the culprits. ^[2]
• Early diagnosis and gentle treatment give an excellent prognosis; late diagnosis means operations, pelvic osteotomy and more arthritis risk. ^[2][3]