This document discusses developmental dysplasia of the hip (DDH), including:
- The normal development of the hip joint and how DDH disrupts this.
- Risk factors for DDH including genetic, intrauterine, and clinical factors.
- Methods for diagnosing DDH including physical exam, ultrasound, and x-rays.
- Treatment options for DDH including the Pavlik harness, which is preferred as it allows reduction through flexion and abduction while preventing extension and adduction. Proper positioning and compliance are important for the Pavlik harness to be successful.
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Developmental dysplasiahip
2. 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
3. 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
4. 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
5. 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
8. 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
9. 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
11. 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
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
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)
12. 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
13. 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
14. 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
16. 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
19. 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
20. 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
21. 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
24. 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
25. 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
29. 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
31. 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
32. 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
33. 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
34. 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
35. 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
36. 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
37. 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
38. 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
39. 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
42. 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
43. greatest rate of acetabular development
occurs in first 18 months after reduction
44. 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
45. 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
46. Extra- articular
Iliopsoas tendon
adductors
Intra-articular
inverted hypertrophic labrum
tranverse acetabular ligament
pulvinar, ligamentum teres
constricted anteromedial capsule espec in late
cases
neolimbus is not an obstacle to reduction and
represents epiphyseal cartilage that must not be
47. 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
48. 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
49. 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
50. 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
51. 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
52. 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
53. 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
54. 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
55. Worst complication is disturbance of growth in
proximal femur including the epiphysis and
physeal plate
commonly referred to as 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
56. 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
57. 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
58. 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
59. 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
60. 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