Developmental dysplasia of the hip (DDH) is a spectrum of hip disorders that can include dislocation, subluxation, or dysplasia. It was previously known as congenital hip dislocation. Risk factors include breech presentation, family history, ligament laxity, female sex, and nursing position. Clinical diagnosis involves the Ortolani and Barlow tests. Ultrasound screening can identify dysplastic or dislocated hips and monitor treatment. Treatment for infants under 6 months aims to reduce the femoral head using a Pavlik harness to stimulate acetabular development. Without treatment, instability often leads to degenerative joint disease in adulthood.

1. Developmental Dysplasia of the
Hip
JAYANT SHARMA
M.S, DNB, MNAMS.

2. Definition
DDH is a spectrum of disorders. Hip can be
• Dislocated
• Dislocatable
• Subluxatable
• Dysplastic

3. • Previously known as congenital dislocation
of the hip implying a condition that existed
at birth
• developmental encompasses embryonic,
fetal and infantile periods
• includes congenital dislocation and
developmental hip problems including
subluxation, dislocation and dysplasia

4. Normal Growth and
Development
• Embryologically the acetabulum, femoral head develop
from the same primitive mesenchymal cells
• cleft develops in precartilaginous cells at 7th week and this
defines both structures
• 11wk hip joint fully formed
• acetabular growth continues throughout intrauterine life
with development of labrum
• birth femoral head deeply seated in acetabulum by surface
tension of synovial fluid and very difficult to dislocate
• in DDH this shape and tension is abnormal in addition to
capsular laxity

5. • The cartilage complex is 3D with triradiate medially
and cup-shaped laterally
• interposed between ilium above and ischium below
and pubis anteriorly
• acetabular cartilage forms outer 2/3 cavity and the
non-articular medial wall form by triradiate cartilage
which is the common physis of these three bones
• fibrocartilaginous labrum forms at margin of
acetabular cartilage and joint capsule inserts just
above its rim

6. • articular cartilage covers portion articulating with femoral
head opposite side is a growth plate with degenerating
cells facing towards the pelvic bone it opposes
• triradiate cartilage is triphalanged with each side of each
limb having a growth plate which allows interstitial
growth within the cartilage causing expansion of hip joint
diameter during growth
• In the infant the greater trochanter, proximal femur and
intertrochanteric portion is cartilage
• 4-7 months proximal ossification center appears which
enlarges along cartilaginous anlage until adult life when
only thin layer of articular cartilage persists

9. Development contd.
• Experimental studies in humans with unreduced hips
suggest the main stimulus for concave shape of the
acetabulum is presence of spherical head
• for normal depth of acetabulum to increase several factors
play a role
– spherical femoral head
– normal appositional growth within cartilage
– periosteal new bone formation in adjacent pelvic bones
– development of three secondary ossification centers
• normal growth and development occur through balanced
growth of proximal femur, acetabulum and triradiate
cartilages and the adjacent bones

10. At Birth
• Teratological Dislocation occurs in
– Arthrogryposis
– Neuromuscular disorders
– Diastrophic Dwarfism
• Typical DDH
– Child is otherwise normal
– This presentation is about DDH in an otherwise
normal child

11. Aetiology is Multifactorial
• Environmental & Mechanical
– Breech Presentation DDH Cases (16%):
All deliveries (3%)
– Birth Order >50% Cases 1st. Born
– Oligohydramnios
– Sex Ratio (Relaxin) F(4 - 6) : M(1)
– Side L(2) : R(1)
– Bilateral 35 %
– Nursing Habits

12. Aetiology- Breech
• Only 3% of children are Breech presentation
• 16% of DDH cases are breech
• Extended breech has 20% risk of DDH
• Footling breech 2%
• If have LSCS still at risk

13. Aetiology-Ligamentous Laxity
• Maternal Relaxin hormones crosses the
placenta and induce hip capsule laxity in
infant and this effect is much stronger in
females.

14. Aetiology - Genetic Factors
• Genetic
– There is an unknown genetic factor
– Runs in families
– Risk to next child increases as follows:
• If one child is affected risk is 6%
• Parent 10%,
• Parent and child 36%
• Genetic Predisposition (Wynne Davies)
– Families with Generalised Ligament Laxity
– Families with Acetabular Dysplasia

15. Aetiology- Nursing
• Rare in China, Asia, Africa (carry children
with hips flexed and abducted)
• High in native American (Used to nurse
with legs extended)
• Klisic reduced DDH by 65% in Belgrade by
routine use of abduction diapering

16. Associated conditions
Quoted risk of DDH with following conditions:
• Child with Torticollis*
15-20%
• Metatarsus adductus 10%
• Calcaneovalgus 10%
*Hummer C, MacEwenG:The coexistence of torticollis and congenital dysplasia of the hip. J Bone
Joint Surg 1972; 54-A:1255.

17. • Breech positioning
• Family history (Treatment with
Harness/Spica/Surgery, not double
nappies)
• Foot deformity
• Infantile muscular torticollis
• ?Oligohydramnios
Risk Factors

18. Etiology
• Genetic and ethnic
• increased native Americans but very low in southern Chinese
and Africans
• positive family history 12-33%
• 10x risk if affected parent, 7X if sibling
• intrauterine factors
– breech position ( normal pop’n 2-4% , DDH 17-23% )
– oligohydroamnios
– neuromuscular conditions like myelomeningocele
• high association with intrauterine molding abnormalities
including metatarsus adductus and torticollis
• first born
• female baby ( 80% cases)
• left hip more common

19. Epidemiology
• 1 in 100 newborns examined have evidence of instability
( positive Barlow or Ortolani)
• 1 in 1000 live births true dislocation
• most detectable at birth in nursery
• Barlow stated that 60% stabilize in 1st week and 88% stabilize
in first 2 months without treatment remaining 12% true
dislocations and persist without treatment
• Coleman26% become dislocated, 13% partial contact 39%
located but dysplatic features 22% normal

20. Incidence• Caucasians
– 1.7/1000 Von Rosen, 1962
– 1.5/1000 Barlow, 1962
• Native Americans
– 188.5/1000 Walker, 1973
• Native Africans
– 0/1000 Edelstein, 1966
• Chinese
– 0.1/1000 Hoagland, 1981

21. Incidence
• 1-2/1000 Live births
• Hip instability (phys) at birth: 1-2%
• Barlow JBJS1962
– 1 in 60 born with instability
– 60% resolve in the 1st week
– 88% resolve in 1st 2 months
– Remaining 12% are true dislocations
~1.5/1000

22. DDH --PATHOLOGY
• Tight fit between head and acetabulum is absent and head can
glide in and out of acetabulum
• hypertrophied ridge of acetabular cartilage in superior, posterior
and inferior aspects of acetabulum called “ neolimbus”
• often a trough or grove in this cartilage due to pressure from
femoral head or neck
• 98% DDH that occur around or at birth have these changes and
are reversible in the newborn
• 2% newborns with teratologic or antenatal dislocations and no
syndrome have these changes

24. • Development in treated DDH different from
normal hip
• goal is to reduce the femoral head ASAP to
provide the stimulus for acetabular
development
• if concentric reduction is maintained potential
for recovery and resumption of normal growth

25. • Age at which DDH hip can still
return to normal is controversial
depends on
–age at reduction
–growth potential of acetabulum
–damage to acetabulum from head
or during reduction

26. • Accessory centers seen in 2-3%
normal hips however in treated
DDH seen up to 60% appearing
ages 6 months to 10 years ( should
look for these on radiographs to
indicate continued growth)

27. Diagnosis
• Clinical risk factors
• Physical exam
– Ortolani Test
• hip flexion and abduction , trochanter elevated and
femoral head glides into acetabulum
– Barlow Test
• provocative test where hip flexed and adducted and head
palpated to exit the acetabulum partially or completely
over a rim
– some base there treatment on whether ortolani+ versus
Barlow+ feeling Barlow + more stable
– Lovell and Winter make no distinction
– 2% extreme complete irreducible teratologic disloactions
assoc with other conditions like arthrogyposis

29. Late Diagnosis
• Secondary adaptive changes occur
• limitation of abduction due to adductor longus shortening
• Galleazi sign
– flex both hips and one side shows apparent femoral
shortening
• asymmetry gluteal, thigh or labial folds
• limb-length inequailty
• waddling gait and hyperlordosis in bilateral cases

32. Screening for DDH
• Controversial
• Methods
– Clinical
– U.S. Scan
– Selective vs. Universal Ultrasound
screening programme

33. Aim of screening
• Early detection leads to:
– simple treatment, less duration, more
favourable results, less complications.
• Reduces late presentation
• Reduces surgical intervention

34. Clinical screening
• Introduced in 1969
• Updated in 1986 (SMAC)
• Standard programme
– Barlow’s/Ortolani’s tests done on every child at
birth and then at 6-8 weeks.
• Continued surveillance until walking normally

35. Clinical screening
• Barlow’s/Ortolani’s Tests
– Specificity- 100%
– Sensitivity- 60%
Because of low sensitivity:
– False-positive test results in Over-treatment
– False negative test results in Late-presentation

36. Ultrasound Screening
• High Specificity and Sensitivity: >90%
• Helps in diagnosis of not only Subluxated/
Dislocated hips but also Dysplastic hips

37. Ultrasound
• Helps in accurate diagnosis
• Helps in Monitoring the treatment
• Reduces the need for Arthrograms / Xrays.

38. Ultrasound Screening
• Techniques:
1) Static (Graf)*
2) Dynamic (Harcke)**
3) Combination
*JPO 1983; 3: 354-95 **JBJS 1985;67B: 406-12

39. Screening Programme
• Selective- Only High risk group of infants
is referred- More common in UK
• Population (Universal or Routine)- All
infants are referred for Ultrasound- More
common in European countries

40. Indications for selective screening
• Clicky hip (B/O)? (Clunk)
• Breech
• Pos. Family History
- Harness/Spica/Surgery (not double nappies)
• Sternomastoid tumour/ Torticollis
• Foot deformities
• ?Oligohydramnios

41. Other reasons for referral after
first few weeks
• Asymmetric skin folds (not very good
indicator on its own)
• Limited Abduction
• Leg length discrepancy
– May be only signs later until abnormal gait is
noticed when walking (too late)

42. Selective hip screening clinic
• General Examination:
-Plagiocephaly,
-Sternomastoid Tumour (Torticollis),
-Spine for cutaneous manifastations of
dyspharism
-Feet for any congenital deformity

43. Selective Hip screening clinic
• Hip Examination
-Barlow’s test (<3-4 months of age)
-Ortolani’s test (<3-4 months of age)
-Limitation of Abduction
-Leg length discrepancy (Galleazi test)
-Asymmetry of thigh folds
- Limp in a walking child

44. Selective Hip screening clinic
• Children <6 months have ultrasound using
Graf classification system
Class Alpha angle Description
I >60 Normal
II 60-43 Immature/Dysplastic
III <43 Subluxed/Dislocated
IV Unmeasurable Dislocated
• Children >6 months have Xrays.

45. Radiography
• Ultra sound
• morphologic assessment and dynamic
– anatomical characteristics
• alpha angle: slope of superior aspect bony acetabulum
• beta angle: cartilaginous component (problems with inter
and intraobserver error )
– dynamic
• observe what occurs with Barlow and ortolani testing
• indications controversial due to high levels of overdiagnosis and
not currently recommended as a routine screening tool other
than in high risk patients
• best indication is to assess treatment
– guided reduction of dislocated hip or check reduction and
stability during Pavlik harness treatment

46. Radiography con’td
• newborn period DDH not a radiographic diagnosis
and should be made by clinical exam
• after newborn period diagnosis should be
confirmed by xray
• several measurements
• treatment decisions should be based on changes in
measurements

47. Radiological Diagnosis
• Classic Features
– increased acetabular index ( n=27, >30-35 dysplasia)
– disruption shenton line ( after age 3-4 should be intact
on all views)
– absent tear drop sign
– delayed appearance ossific nucleus and decreased
femoral head coverage
– failure medial metaphyseal beak of proximal femur ,
secondary ossification center to be located in lower
inner quadrant
– center-edge angle useful after age 5 ( < 20) when can
see ossific nucleus

48. Pe

50. Natural History
in Newborns
• Barlow
– 1 in 60 infants have instability ( positive Barlow)
– 60% stabilize in 1st week
– 88% stabilize in 2 months without treatment
– 12 % become true dislocations and persist
• Coleman
– 23 hips < 3 months
– 26% became dislocated
– 13 % partial contact with acetabulum
– 39% located but dysplastic feature
– 22% normal
• because not possible to predict outcome all infants
with instability should be treated

51. Adults
• Variable
• depends on 2 factors
– well developed false acetabulum ( 24 % chance good result vs
52 % if absent)
– bilaterality
• in absence of false acetabulum patients maintain good ROM with
little disability
• femoral head covered with thick elongated capsule
• false acetabulum increases chances degenerative joint disease
• hyperlordosis of lumbar spine assoc with back pain
• unilateral dislocation has problems
– leg length inequality, knee deformity , scoliosis
and gait disturbance

55. Dysplasia and Subluxation
• Dysplasia (anatomic and radiographic def’n)
– inadequate dev of acetabulum, femoral head or both
– all subluxated hips are anatomically dysplastic
• radiologically difference between subluxated and dysplastic hip
is disruption of Shenton’s line
– subluxation: line disrupted, head is superiorly,
superolaterally ar laterally
displaced from the medial wall
– dysplasia: line is intact
• important because natural history is different

57. Natural History Con’t
• Subluxation predictably leads to degenerative joint disease and
clinical disability
– mean age symptom onset 36.6 in females and 54 in men
– severe xray changes 46 in female and 69 in males
• Cooperman
– 32 hips with CE angle < 20 without subluxation
– 22 years all had xray evidence of DJD
– no correlation between angle and rate of development
– concluded that radiologically apparent dysplasia leads to
DJD but process takes decades

58. Treatment 0 to 6 months
• Goal is obtain reduction and maintain reduction to provide
optimal env’t for femoral head and acetabular development
• Lovell and Winter
– treatment initiated immediately on diagnosis
• AAOS (July,2000)
– subluxation often corrects after 3 weeks and may be
observed without treatment
– if persists on clinical exam or US beyond 3 weeks treatment
indicated
– actual dislocation diagosed at birth treatment should be
immediate

59. Treatment con’t
• Pavlik Harness preferred
– prevents hip extension and adduction but allows flexion and
abduction which lead to reduction and stabilization
– success 95% if maintained full time six weeks
– > 6 months success < 50% as difficult to maintain active
child in harness

60. Pavlik Harness
• Chest strap at nipple line
• shoulder straps set to hold
cross strap at this level
• anterior strap flexes hip 100-
110 degrees
• posterior strap prevents
adduction and allow
comfortable abduction
• safe zone arc of abduction
and adduction that is between
redislocation and comfortable
unforced abduction

61. Pavlik con’t
• Indications include presence of reducible hip femoral head
directed toward triradiate cartilage on xray
• follow weekly intervals by clinical exam and US for two weeks
if not reduced other methods pursued
• once successfully reduced harness continued for childs age at
stability + 3 months
• worn full time for half interval if stability continues and then
weaned off
• end of weaning process xray pelvis obtained and if normal
discontinue harness

62. Complications
• Failure
– poor compliance , inaccurate position and persistence of
inadequate treatment ( > 2-3- weeks)
– subgroup where failure may be predictable Viere et al
• absent Ortolani sign
• bilateral dislocations
• treatment commenced after age 7 week
– Treatment closed reduction and Spica Casting
• Femoral Nerve Compression 2 to hyperflexion
• Inferior Dislocation
• Skin breakdown
• Avascular Necrosis

63. 6 months to 2 years age
• Closed reduction and spica cast immobilization
recommended
• traction controversial with theoretical benefit of gradual
stretching of soft tissues impeding reduction and neurovascular
bundles to decrease AVN
• skin traction preferred however vary with surgeon
• usually 1-2 weeks
• scientific evidence supporting this is lacking

64. Treatment con’t
• closed reduction preformed in OR under general anesthetic
manipulation includes flexion, traction and abduction
• percutaneous or open adductor tenotomy necessary in most
cases to increase safe zone which lessen incidence of proximal
femoral growth disturbance
• reduction must be confirmed on arthrogram as large portion of
head and acetabulum are cartilaginous
• dynamic arthrography helps with assessing obstacles to
reduction and adequacy of reduction

65. Treatment
• reduction maintained in spica cast well molded to greater
trochanter to prevent redislocation
• human position of hyperflexion and limited abduction
preferred
• avoid forced abduction with internal rotation as increased
incidence of proximal femoral growth disturbance
• cast in place for 6 weeks then repeat Ct scan to confirm
reduction
• casting continued for 3 months at which point removed and xray
done then placed in abduction orthotic device full time for 2
months then weaned

68. Failure of Closed Methods
• Open reduction indicated if failure of closed reduction,
persistent subluxation, reducible but unstable other than
extremes of abduction
• variety of approaches
– anterior smith peterson most common
• allows reduction and capsular plication and secondary
procedures
• disadv- > blood loss, damage iliac apophysis and
abductors, stiffness

69. • greatest rate of acetabular development occurs in
first 18 months after reduction

70. Open Reduction con’t
– medial approach ( between adductor brevis and magnus)
• approach directly over site of obstacles with minimal soft
tissue dissection
• unable to do capsular plication so depend on cast for post
op stability
– anteromedial approach Ludloff ( between neurovascular
bundle and pectineus)
• direct exposure to obstacles, minimal muscle dissection
• no plication or secondary procedures
• increased incidence of damage to medial femoral
circumflex artery and higher AVN risk

71. Follow-up
• Abduction orthotic braces commonly used until acetabular
development caught up to normal side
• in assessing development look for accessory ossification centers
to see if cartilage in periphery has potential to ossify
• secondary acetabular procedure rarely indicated < 2 years as
potential for development after closed and open procedures is
excellent and continues for 4-8 years
• most rapid improvement measured by acetabular index ,
development of teardrop occurs in first 18 months after surgery
• femoral anteversion and coxa valga also resolve during this time

72. Obstacles to Reduction
• Extra- articular
– Iliopsoas tendon
– adductors
• Intra-articular
– inverted hypertrophic labrum
– tranverse acetabular ligament
– pulvinar, ligamentum teres
– constricted anteromedial capsule especially in late
cases
neolimbus is not an obstacle to reduction and represents
epiphyseal cartilage that must not be removed as this
impairs acetabular development

73. Age greater than 2 years
• Open reduction usually necessary
• age > 3 femoral shortening recommended to avoid excess
pressure on head with reduction
• 54% AVN and 32% redislocation with use of skeletal traction in
ages > 3
• age > 3 recommend open reduction and femoral shortening
and acetabular procedure

74. Treatment con’t
• 2-3-years gray zone
• potential for acetabular development diminished therefore
many surgeons recommend a concomitant acetabular
procedure with open reduction or 6-8 weeks after
• JBJS Feb, 2002 Salter Innominate Osteotomy…
Bohm,Brzuske incidence of AVN is greater with
simultaneous open reduction and acetabular procedure

75. Treatment con’t
• Lovell and Winter
– judge stability at time of reduction and if stable observe for period
of time for development
– if not developing properly with decreased acetabular index,
teardrop then consider secondary procedure
• most common osteotomy is Salter or Pemberton
• anatomic deficiency is anterior and Salter provides this
while Pemberton provides anterior and lateral coverage

76. Natural Sequelae
• Goal of treatment is to have radiographically normal hip at
maturity to prevent DJD
• after reduction achieved potential for development continues
until age 4 after which potential decreases
• child < 4 minimal dysplasia may observe but if severe than
subluxations and residual dysplasias shoild be corrected
• when evaluating persistent dysplasia look at femur and
acetabulum
• DDH deficiency usually acetabular side

77. Residual Dysplasia
• plain xray with measurement of CE angle and acetabular index
• young children deficiency anterior and adolescents can be
global
• deformities of femoral neck significant if lead to subluxation
– lateral subluxation with extreme coxa valga or anterior
subluxation with excessive anteversion ( defined on CT )
– usually DDH patients have a normal neck shaft angle

78. • Dysplasia for 2-3-years after reduction proximal
femoral derotation or varus osteotomy should be
considered if excessive anteversion or valgus
• prior to performing these be sure head can be
concentrically reduced on AP view with leg abducted
30 and internally rotated
• varus osteotomy done to redirect head to center of
acetabulum to stimulate normal development
• must be done before age 4 as remodeling potential
goes down after this

79. Adolescent or Adult
• Femoral osteotomy should only be used in
conjunction with pelvic procedure as no
potential for acetabular growth or
remodeling but changing orientation of
femur shifts the weightbearing portion
• Pelvic osteotomy considerations
– age
– congruent reduction
– range of motion
– degenerative changes

80. Pelvic Procedures
• Redirectional
– Salter ( hinges on symphysis pubis)
– Sutherland double innominate osteotomy
– Steel ( Triple osteotomy)
– Ganz ( rotational)
• Acetabuloplasties ( decrease volume )
– hinge on triradiate cartilage ( therefore immature
patients)
– Pemberton
– Dega ( posterior coverage in CP patients )
• Salvage
– depend on fibrous metaplasia of capsule
– shelf and Chiari

81. Complications of Treatment
• Worst complication is disturbance of
growth in proximal femur including the
epiphysis and physeal plate
• commonly AVN however, no pathology to
confirm this may be due to vascular insults
to epiphysis or physeal plate or pressure
injury
• occurrs only in patients that have been
treated and may be seen in opposite normal
hip

82. Necrosis of Femoral Head
• Extremes of position in abduction ( greater
60 degrees ) and abduction with internal
rotation
• compression on medial circumflex artery as
passes the iliopsoas tendon and
compression of the terminal branch between
lateral neck and acetabulum
• “ frog leg position “ uniformly results in
proximal growth disturbance

83. • extreme position can also cause pressure
necrosis onf epiphyseal cartilage and
physeal plate
• severin method can obtain reduction but
very high incidence of necrosis
• multiple classification systems with Salter
most popular

84. Salter Classification
• 1 failure of appearance of ossific nucleus
within 1 year of reduction2
• 2 failure of growth of an existing nucleus
within 1 year
• 3 broadening of femoral neck within 1
year
• 4 increased xray density then
fragmentation of head
• 5 residual deformity of head when re-
ossification complete including coxa
magna,vara and short neck

85. Kalamachi
• Classified growth disturbances assoc with
various degrees of physeal arrest
• 1 all disturbances not assoc with physis
• 2 lateral physeal arrest ( most common )
• 3 central physeal arrest
• 4 medial physeal arrest
• longterm follow up shows that necrosis of
femoral head decreases longevity of hip

86. Treatment
• Femoral and/or acetabular osteotomy to
maintain reduction and shift areas of
pressure
• trochanteric overgrowth causing an
abductor lurch treated with greater
trochanter physeal arrest if done before age
8 otherwise distal transfer
• early detection is key with 95% success rate
of treatment
• identify growth disturbance lines

87. SALTERS

88. PEMBERTONS

89. PEMBERTONS

90. CHIARI