Developmental dysplasia of the hip (DDH) is a condition involving hip instability and dislocation, often influenced by breech birth and family history. The incidence varies greatly by ethnicity, with notable demographic factors and risk associations. Management focuses on achieving and maintaining proper hip alignment through various means depending on the child's age and condition severity.

1. Congenital Hip
Dysplasia(DDH)

2. Introduction
• No longer called CDH because not all cases
are present or identified at birth
• Developmental dysplasia of the hip (DDH)
refers to hip instability,
subluxation/dislocation of the femoral head
and/or acetabular dysplasia in a
developing hip joint.
• Breech presentation and family history of
DDH are the most important risk factors.

3. Epidemiology
• Hip instability can be detected in 1 in 100 to 1 in 250 babies
• Dislocated/dislocatable hips in 1-1.5/1000
• There is marked geographic and racial variation in the
incidence of DDH
• The incidence of DDH is almost 0% in Chinese and African
newborns.
• It varies from 0.06 in Africans to 76.1 per 1000 in Native
Americans due to the combination of genetics and swaddling.
• More common in females due to laxity caused by relaxin, a
maternal hormone.
• The left hip is the most commonly affected hip; in the most
common fetal position, this is the hip that is usually forced
into adduction by the mother’s sacrum

4. AETIOLOGY
• Largely unknown
• Final common pathway is laxity of the hip
joint
• Lack of stability between the acetabulum
and head of the femur
• A positive family history is present in 10–
30% of patients with DDH
• Breech presentation, 16-25% will have
DDH
• Diseases associated with ligamentous laxity
• Reduction in the intrauterine space :
oligohydromnios , large baby, first
pregnancy
• The high rate of association of DDH with
other intrauterine molding abnormalities,
such as torticollis and metatarsus
adductus, supports the theory that the
crowding phenomenon has a role in the
pathogenesis.

5. PATHOGENESIS
• The acetabulum appears as a condensation of
mesoderm about the end of the fourth week of
intrauterine life.
• It is a shallow socket on the outer aspect of
developing innominate bone.
• Later, the socket is deepened by the progressive
development of the original depression.
• The concavity of the acetabulum results from
the pressure of the spherical femoral
cartilaginous head

6. PATHOGENESIS
• Subsequent to loss of contact, the femoral
head no longer exerts pressure on the
acetabulum
• A normal anatomical outline can be restored
by concentric reduction of the head which
will then provide the necessary stimulus to
ossification – if corrected at this point

7. PATHOGENESIS
• The growth of the
acetabulum is dependent on
the normal epiphyseal
growth of the triradiate
cartilage and presence of the
spherical femoral head within
the acetabulum.
• The triradiate cartilage is the Y-
shaped epiphyseal plate that
occurs at the junction where
the ischium, ilium, and pubis
meet in the skeletally
immature skeleton

8. PATHOGENESIS
• Dysplasia
shallow or underdeveloped acetabulum
• initial instability leads to dysplasia
• typical deficiency is anterior or
anterolateral acetabulum
• In spastic cerebral palsy, acetabular
deficiency is posterosuperior

9. PATHOGENESIS- subluxation
• The head flattens the limbus
and exerts a deforming
pressure on the cartilaginous
roof, causing further inhibition
of ossification and actual
flattening of the socket.
• Incomplete contact between
the articular surfaces of the
femoral head and acetabulum
• Repetitive subluxation of the
femoral head leads to the
formation of a ridge of
thickened articular cartilage
called the limbus

10. PATHOGENESIS
• Dislocation occurs
when the femoral
head loses contact
with the original
acetabulum and
rides up over the
fibrocartilaginous
rim

11. Chronic dyslplasia
• Secondary changes will
occur that prevent the hip
from being reduced into
position
• Fatty tissue called pulvinar
and ligamentum teres can
hypertrophy and elongate
• transverse acetabular
ligament hypertrophies
• hip capsule and iliopsoas
form hourgass
configuration

12. PATHOGENESIS
• Acetabulum
• Shallower than normal
• Its rounded shape
disappears,
• Instead of containing the
head of femur, the
acetabulum becomes
occupied by
• Overgrowth of fibrocartilage
• Remains of the ligamentum
teres
• Anterior portion of the
capsule adherent to the
floor.
• Femur
• The femoral head is at first
normal, although ossification
of it is often delayed and
there is a marked discrepancy
between the size of the
cartilage head and the
reduced acetabulum.
• Later it becomes flattened on
its medial and posterior
aspects.
• Marked shortening of the
neck of the femur
• Increased anteversion of neck

13. PATHOGENESIS
• The transverse acetabular
ligament usually thickens as
well, which effectively narrows
the opening of the acetabulum.
• In addition, the shortened
iliopsoas tendon becomes taut
across the front of the hip,
creating an hourglass shape to
the hip capsule, which limits
access to the acetabulum.

15. Clinical features @ less than 6
months
• Can be classified as a spectrum of disease
involvement (phases)
• subluxable
Barlow-suggestive
• dislocatable
Barlow-positive
• dislocated
Ortolani-positive -early when reducible;
Ortolani-negative- late when irreducible

16. Barlow – the hip is not displaced,
I wish to check if it can be dislocated
• Asymptomatic
• Barlow sign: a palpable
clunk caused
by hip dislocation when the
femur slides out of the
acetabulum
• the hip is flexed
• adducted with application
of downward/posterior
pressure
• Release pressure, the hip
will slip back into the
acetabulum

17. Ortolani sign – it is displaced and I wish
to reduce it back into its position
• Palpable clunk caused by hip reduction when
the hip is flexed and abducted while applying
upward pressure
• The Ortolani test is the reverse of Barlow test: The
examiner attempts to reduce a dislocated hip
• The examiner grasps the child’s thigh between the
thumb and index finger and, with the 4th and 5th
fingers, lifts the greater trochanter while
simultaneously abducting the hip
• When the test is positive, the femoral head will slip
into the socket with a delicate clunk that is palpable
but usually not audible
• It should be a gentle, non forced maneuver.

18. • A positive Barlow
sign shows that the
reduced hip is
subluxatable or
dislocatable
• A positive Ortolani
sign shows that a
dislocatedhip is
reducible

19. Clinical features ; 6-18 months
• 6-18 months
• Inability to abduct the hip
• Barlow and Ortolani sign disappear
• Prominent Galeazzi sign: unequal knee height
and apparent shorter femur when child
lies supine with hips and knees flexed
• placing both hips in 90 degrees of flexion and
comparing the height of the knees, looking for
asymmetry
• Asymmetrical gluteal folds may be present

20. 6-18 months

21. 18 months and above
• Hip pain and/or pain referred from
the hip to the knee and/or anterior thigh
• Possibly a hip deformity (e.g., coxa vara)
• Waddling or Trendelenburg gait
• Leg length discrepancy and toe walking to
compensate for the difference in leg length
• Possibly lumbar lordosis secondary to
altered hip mechanics

22. Investigations
• Clinical
• Ultrasound in ages 0-4 but high index of false
positive
• Why do we use USS at this age ?
• Femoral head ossifies at 4-6 months it will not show
on an x ray
• After 4 months, radiography – more effective,
higher diagnostic less dependent on operator
proficiency

23. Investigations
• USS
• relationship between femur and acetabulum
• Dynamic information about hip joint stability
• Monitor progress of acetabular development
• The angle formed by the line of the ilium and a line
tangential to the boney roof of the acetabulum is
termed the α angle and represents the depth of the
acetabulum.
• Values >60 degrees are considered normal
• <60 degrees imply acetabular dysplasia

24. Investigations- USS
• The β angle is formed by a line drawn tangential to
the labrum and the line of the ilium;
• This represents the cartilaginous roof of the
acetabulum. A normal β angle is <55 degrees; as
the femoral head subluxates, the β angle increases

25. Investigations – Radiography

26. Investigations – Radiography
• Hilgenreiner’s line is drawn through the triradiate cartilages.
• Perkins line is drawn perpendicular to Hilgenreiner’s line at the
lateral edge of the acetabulum.
• The ossific nucleus of the femoral head should be located in the
medial lower quadrant of the intersection of these 2 lines.
• Shenton’s line curves along the femoral metaphysis and
connects smoothly to the inner margin of the pubis.
• In a child with hip subluxation or dislocation, this line consists of
2 separate arcs and is described as broken.
• The acetabular index is the angle between a line drawn along
the margin of the acetabulum and Hilgenreiner’s line; in normal
newborns, it averages 27.5 degrees and decreases with age.

27. MANAGEMENT
• The goals in the management of DDH
• Obtain and maintain a concentric reduction of the
femoral head within the acetabulum
• In order to provide the optimal environment for the
normal development of both the femoral head and
acetabulum.

28. Treatment
• Newborns hips that are Barlow-
positive (reduced but
dislocatable) or
• Ortolani-positive (dislocated but
reducible) should generally be
treated with a Pavlik harness as
soon as the diagnosis is made
• Resolves in 95% cases
• 6 weeks treatment
• After 6/12, failure rate is >50%
• Flexes hips (90-100 degrees)
• USS at 4weeks, if reduction is
not occurring, stop harness

29. Treatment
• 6months to 2years
• obtain and maintain
reduction of the hip
without damaging the
femoral head.
• Closed reductions are
performed in the
operating room under
general anesthesia.
• Above 2 years
• Open reduction.
• concomitant femoral
shortening osteotomy
to :
• reduce the pressure on
the proximal femur
• minimize the risk of
osteonecrosis

30. Complications
• The most important
complication of DDH is
avascular necrosis of the
femoral epiphysis.
• Reduction of the femoral
head under pressure or in
extreme abduction can
result in occlusion of the
epiphyseal vessels and
produce either partial or
total infarction of the
epiphysis
• Redislocation,
• residual subluxation
• acetabular dysplasia
• postoperative
complications wound
infections