Perthes Disease LCPD

Dr. ANOOP G.C.
Junior Resident in orthopedics
MCH Kozhikkode
Legg Calve Perthes Disease
Dr.Anoop G.C.,JR,Orthopaedics,GMCK

SYNONYMS
 Coxa plana
 Osteochondritis deformans coxa juveniles
 Pseudocoxalgia
 Osteochondrosis of hip joint
 Childhood Aseptic Necrosis of Femoral Head
 Osteochondritis dessicans of Hip
 Legg’s stress fracture

DEFINITION
• PERTHES DISEASE : is a self-limiting
form of osteochondrosis of the femoral capital
epiphysis
• of unknown etiology that develops in children
commonly between the ages of 4 – 12 years
• caused by impaired circulation in the femoral
head
• necrosis of the femoral epiphysis and its
replacement by new bone
• resulting in deformation of the femoral head.

HISTORY
 Described first by Waldenstrom in 1909
who mistakenly ascribed it to tuberculosis.
 In 1910 was independently described by
Arthur Legg , U. S. A - February
Jacques Calve , France - July
George Perthes ,Germany - October
 Hence name – “Legg Calve Perthes Disease”
 In 1922 Waldenstrom gave the correct
interpretation and described the stages .

LEGG CALVE PERTHES

ETIOLOGICAL FACTORS - that play a
role in development of illness
 Vascular supply
 Increased intra-articular pressure
 Intraosseous pressure
 Coagulation disorder
 Growth hormones
 Skeletal Growth
 Social conditions
 Genetic factors
 Attention deficit Disorders
 TRAUMA

FEMORAL HEAD - vascular supply
EXTRINSIC OR EXTRAOSSEOUS ANATOMY
(Crock & Chung)
1. Extra capsular ring – base of neck
- Formed by Medial circumflex femoral (Major)and Lateral
circumflex femoral arteries
- Branches ascend in 4 groups as Ascending cervical(Extra
capsular) or Retinacular(intra capsular) arteries
- Lateral group most important.
- The Lateral group pierce the capsule and enter epiphysis to
become Lateral epiphyseal arteries
2. Intra capsular ring – base of head
- incomplete in 57% males and 31% females.
- Formed by branches of ascending cervical & retinacular
arteries.
- They contribute to lateral epiphyseal arteries
3. Artery of Ligamentum teres

INTRINSIC OR INTRAOSSEOUS ANATOMY
(Trueta & Harrison)
1. Lateral epiphyseal Arteries
- Formed by the Lateral group of Ascending cervical or
Retinacular arteries
- Supplies 2/3 rd of femoral head
- Exclusive supply of suprolateral head
2. Medial epiphyseal or Artery of Ligamentum teres
- Negligible to ½ of epipysis
3. Metaphyseal arteries

ADULT

TRUETA’S HYPOTHESIS
• Infants and children <4 yrs : 2 arterial
blood supplies to femoral head- the
retinacular or ascending cervical arteries
(Lateral epiphyseal artery) & the
metaphyseal arteries
• 4-12 yrs : single areterial supply by Lateral
epiphyseal artery. This solitary blood supply
makes this age period vulnerable to
ischaemic necrosis due to compression by
external rotators and extreme movements.
• After 12 yrs: foveolar arteries of Ligamentum
teres contribute blood along with Lateral
epiphyseal arteries & incidence decreases.
(In blacks it occurs earlier)

TRUETA’S HYPOTHESIS
 In adults :cartilage growth plate disappears
& the metaphyseal arteries enter the
epiphysis and thus the adult pattern of
blood supply by
• Foveolar
• Retinacular
• Metaphyseal arteries occurs .
 Hence the disease doesnot occur in adults
& rare after 12 year.
 Supply by ligamentum teres occurs earlier
in blacks - disease is rare in blacks

FEMORAL HEAD - The Blood Supply of
the Immature Femoral Head
CHILD
 Metaphyseal or no
other vessels cross
epiphyseal plate
 Artery of
Ligamentum teres
is not developed
 Solely dependent
on Lateral
epiphyeal arteries

CAFFEY’S HYPOTHESIS
Avascular necrosis of femoral head
results from intraepiphyseal
compression of blood supply to the
ossification center and not due to
external compression of vessel.

ETIOLOGICAL FACTORS
Vascular : General reduction in blood flow
with a significant reduction in medial
circumflex artery
Normally venous drainage occurs
through medial circumflex vein
In Perthes disease increased venous
pressure in affected neck associated
venous congestion in metaphysis

ETIOLOGICAL FACTORS
 Increased intra-articular pressure :
– Animal experiments have shown that an
ischemia similar to that in Perthes disease can
be generated by increasing the intra-articular
pressure.
– However, the condition of transient synovitis of
the hip does not appear to be a precursor stage of
Perthes disease as the increased pressure
resulting from the effusion in transient
synovitis does not lead to vessel closure

ETIOLOGICAL FACTORS
Intraosseous pressure:
– The measurement of intraosseous pressure in Perthes
patients has shown that the venous drainage in the
femoral head is impaired, causing an increase in
intraosseous pressure.
Coagulation disorder :
• Study have found a coagulation disorder in 75%
children with Perthes disease.
• In most cases the disorder was thrombophilia.
• protein C or protein S deficiency, elevated serum
lipoprotein, Factor-V Leiden mutation,
Anticardiolipin antibodies were also noted.

ETIOLOGICAL FACTORS
 Growth hormones :
– While earlier studies found reduced levels of the growth
hormone.
– Recent studies have not shown any difference from control
groups in respect of hormone status
 Skeletal Growth:
– Children with Perthes disease are shorter, on average, than
their peers of the same age & show a retarded skeletal age
(cartilaginous dysplasia).
– The maturation disorder occurs between the ages of 3 and 5
years.
– Both the trunk and extremities lag behind in terms of growth.
– But pick up to attain normal skeletal maturity by adulthood.

ETIOLOGICAL FACTORS
 Social conditions:
– Studies in the UK have shown that Perthes disease is
more common in the lower social status.
– The authors suggest a poorer diet during pregnancy as
one possible explanation for this phenomenon.
– A recent study did not confirm this theory
 Genetic factors:
– Studies have shown that first degree relatives of children
with Perthes disease are 35 times more likely to suffer
from the condition than the normal population.
– Even second- and third-degree relatives show a fourfold
increased risk.

ETIOLOGICAL FACTORS
 Attention deficit Hyperkinetic Disorders : more prone to trauma
 Synovitis : predisposed due to increased intra articular
pressure
 TRAUMA :
– Trauma in the predisposed child ppts AVN
OF FEMORAL HEAD AND development of
Perthes disease
– the lateral epiphyseal artery which courses
through a narrow passage is susceptible to
damage

HERIDITARY ASSOCIATIONS
Congenital abnormalities
Hemivertebrae
Deafnes
Imperforate anus
Pyloric stenosis
Epilepsy
Cong heart disease
Short tibia
Undescended testis

PATHOLOGY
 By Waldenstrom in 1922
 4 stages
based on microscopic
and gross pathology
Paul_Petter_Waldenström

Stages
Stage 1 : Incipient or synovitis stage
• Lasts for 1-3 week
• synovium is swollen edematous and
hyperemic
• joint fluid is increased
• Inflammatory cell are notably absent

Stages
 Stage 2 : Avascular necrosis
• Lasts for 6 month to 1year
• Significant necrosis of bone
• trabeculae are crushed into minute fragments.
• Absent/pyknotic nuclei in the osteocytes
• No evidence of bone regeneration
• Degenerative changes in the basal layer of
articular cartilage
• Thickened peripheral cartilagenois cells
• Gross contour of femoral head is unchanged

Stages
 Stage 3 : Fragmentation or Regeneration
– Lasts for 2- 3 year.
– Dead bone infested with vascular connective
tissue was actively resorbed by osteoclasts
and replaced by newly formed immature
bone.
– Loss of epiphyseal height due to collapse of
bony trabeculae and resorption of fragmented
necrotic bone

Stages
 Stage 4 : Healed or Residual Stage
• Normal bone starts replacing necrotic bone.
• Ossific nucleus is deformed assuming
mushroom contour
• Femoral head enlarges, flattens and
subluxate.

EPIDEMIOLOGY
• ONSET : 18 months - skeletal maturity
• Most prevalent : 4-12 yrs
• Male: female : 4 : 1
• Bilateral in 10 - 20%
• No evidence of inheritance but 35 time risk
in 1st degree relative.

CLINICAL FEATURE - Symptoms
Described by Sundt in 1920
– limp-exacerbated by activity and relieved by rest
– Pain-located in
• Groin
• Anterior hip region
• Laterally around greater trochanter
• Referred pain to knee (may obscure the true
nature of the disorder)
• Aggravated by physical activity
• Night pain
– H/o of antecedent trauma
– Waxing & waning of symptoms

CLINICAL FEATURE - Signs
 Typical limp : combination of antalgic and
Trendelenburg gait
 Signs of old injuries - scars, old fractures
 Reduction of hip motion( muscle spasm)
– Minimal noted at abduction & internal
rotation(earlier)
– Greater loss of motion with more severe disease
– Abduction contractures
– Lose all rotations in very severe cases
– FLEXION/EXTENSION SELDOM AFFECTED

CLINICAL FEATURE - Signs
 Wasting of gluteus, quadriceps & hamstrings
 Positive Trendelenburg on the involved side
 Classicaly :
A small
Thin
Extremely active
Constantly running and jumping child
Who develops limping after strenuous physical
activities

NATURAL HISTORY
 DISEASE SEVERITY:
 Mild to severe
 Majority will have moderate symptoms for 12- 18
months followed by complete resolution of symptom
 Finally return to normal activities
 PATIENT’S AGE : MOST CONSISTENT FACTOR
AFFECTING COURSE OF THE DISEASE
– Early onset (before 6 yrs) : mild
– Onset 6-9 yrs :moderate
– Late Onset after 9 yrs: most severe course and worst
outcome

NATURAL HISTORY
 EXTENT OF RADIOGRAPHIC CHANGES :
Poorest results seen in hips with the
greatest degree of involvement
 OUTCOME: affected by the duration from
onset of disease to complete resolution
 The shorter the duration the better the
outcome

ASSOCIATION BETWEEN CLINICAL
FINDINGS & STAGES
Stage 1 – Initial stage
Waxing/waning of symptoms & signs
Mild limp and pain
Episodes of moderate discomfort(weeks)
Stage 2 – Fragmentation stage
Limp and pain more
Greater loss of range of motion

ASSOCIATION BETWEEN CLINICAL
FINDINGS & STAGES
Stage 3 – Reossification/healing stage
 Pain /limp resolves
 Mild limitation of joint motion
 Resumes normal activities
Stage 4 – Residual/healed stage
 Symptoms disappear as head completely
reossifies

PROGNOSIS – poor in
• Female child
• Obese child
• Age of Onset > 8 years
• Adduction contractures
• Progressive decrease in range of movements
• Presence of “Head at risk Sign’s” on
Radiographs

DIFFERENTIAL DIAGNOIS
• Transient synovitis
• Slipped femoral epiphysis
• Congenital dysplasia of hip
• Congenital coxa vara
• Early Tuberculosis
• Rheumatoid arthritisAcute and chronic sepsis
• Acetabular dysplasia
• Epiphyseal dysplasia
• Histiocytosis
• Gaucher’s disease

INVESTIGATIONS
• Bloods
– FBC, ESR, CRP, Blood Culture – r/o other diseases.
• Radiographs
• Ultrasound Scan
• CT scan
• Bone Scan
– Decreased bone scan uptake before radiographic changes
• MRI
–Earlier diagnosis than plain radiography
– More information regarding extent of necrosis than
bone scanning
• Arthrography

IMAGING STUDIES
 Radiographic staging of disease
evolution:
- Based on Anteroposterior and Lateral frog leg
views
- the modified version of WALDENSTROM’S
classification
4 STAGES
1. Initial stage
2. Fragmentation stage
3. Reossification stage
4. Residual stage

RADIOGRAPHY
AP View
FROG LEG View

Intial stage (6 months)
 Lateralization of femoral head in the acetabulum
 Smaller ossific nucleus due to cessation of growth
of the capital epiphysis
 Apparent widening of medial joint space (synovitis
& hypertrophy of articular cartilage)
 WALDENSTROM’S SIGN : Linear fracture in the
subchondral area of femoral head ( frog leg lateral
view)
 Increased density of femoral head : 20 accumulation
of new bone on the dead bone trabeculae in the
head .
 Metaphyseal cysts & lucencies

Fragmentation stage (8 months)
 Lucencies develop in the ossific nucleus/ other
sections remain sclerotic.
 Central dense fragment gets demarcated from the
medial & lateral segments of the head
 Increased density resolves
 acetabular contour more irregular
 End of this stage is marked by appearance of
new bone in the subchondral area of femoral head

Reossification stage / healing stage
(51 months)
 Starts in the Centre of the femoral head and
expands medially and laterally
 Last areas to reossify
- anterior segment of head
- Centre of head
 Lucent portions of femoral head fill in with
woven bone
 Over the time the new bone remodels into
trabecular bone
 Head regains roundness

Residual stage
 Head fully reossified
 Remodeling of head continues until
skeletal maturity when the permanent
contour is established
 Acetabulum remodels as well

CHANGES IN THE METAPHYSIS
 Gill (1940) reported the changes as “HOLES OF
DECALCIFICATION” due to metaphyseal
necrosis
 Metaphyseal Cyts :Ponseti described cystic changes
caused by tongues of fibrillated cartilage
stretching deep into the neck
 Sagging Rope Sign
Radiodense line overlying the proximal femoral
metaphysis
Produced by growth plate damage associated
with metaphyseal response.

CHANGES IN THE METAPHYSIS
Metaphyseal cyst
Sagging rope signDr.Anoop G.C.,JR,Orthopaedics,GMCK

CHANGES IN PHYSIS
 Abnormal growth of proximal femoral physis
 Premature physeal closure(25% cases) causing
 Lateral extrusion of capital nucleus
 Medial bowing of femoral neck
 Greater trochanter overgrowth
 lateral X-ray showed a bulge in the
metaphysis (a step shaped irregularity)
comparable to changes observed in
Blount’s disease

CHANGES IN THE ACETABULUM
 BICOMPARTMENTALIZATION :When the
femoral head protrudes from the acetabulum ,
the medial wall may form what looks like a
second compartment for the head (Yngve and
Roberts)
 by early closure of triradiate cartilage
 its an indicator of poor out come
 Resolves during the healing stage
 Osteoporosis of the roof of the acetabulum
 Position of the head rather than it’s shape has
been the most significant factor in the growth &
remodeling of acetabulum

CHANGES IN THE ACETABULUM
BICOMPARTMENTALIZATIONDr.Anoop G.C.,JR,Orthopaedics,GMCK

ULTRASONOGRAPHY
 To demonstrate joint effusion
 Provide a good profile of cartilaginous
femoral head and subsequent deformation
of head can be assessed

CT SCAN
 3D Images of head & acetabulum
 Useful in later stages
– To evaluate pain
– Locking of joint
– Mechanical symptoms

BONE SCAN
 Effective means of diagnosis in early
stages, before associated radiographic
findings are apparent
 To classify the severity of disease
 Reveals revascularization and consequently
the stage of the disease
 To classify revascularization as either
recanalization or neovascularization

MRI
 Accurate imaging modality for early diagnosis
 Visualization of configuration of the femoral
head and acetabulum
 Determine the extent of revascularization
 Epiphyseal involvement more clearly
visualized
 Earlier and reliable information about the true
extent of femoral head necrosis
 Finding the degree of involvement during the
early phases of this disorder

ARTHROGRAPHY
 Provides reliable information regarding
containment of femoral head within the
acetabulum
 Examiner can assess the congruity of the hip in
many different position.
 Most often used in the early diagnosis of
HINGE ABDUCTION OF HIP in which the
head hinges out of acetabulum when the hip is
abducted
– It occurs early in the course of the disease
– The longer it remains untreated ,the worst is the
outcome .
– Treatment :traction initially to relieve hinging and later
surgery to contain the head .

ARTHROGRAPHY

RADIOLOGICAL CLASSIFICATION
• AP and FROG LEG views required
• Depending on Extent of lesions
• Important in deciding treatment method.
• 3 classifications are
– Catterall
– Salter & Thompson
– Herring

Catterall
• Most common
• Based on extent of
femoral head
lesion
• IV groups

Catterall Group I
25% involvement
No metaphyseal Reaction
No sequestrum
No subchondral fracture lineDr.Anoop G.C.,JR,Orthopaedics,GMCK

Catterall Group II
50% involvement
Sequestrum present - junction Clear
Metaphyseal reaction - antero lateral
Subchondral fracture line - anterior halfDr.Anoop G.C.,JR,Orthopaedics,GMCK

Catterall Group III
75% involvement
Sequestrum large - junction sclerotic
Metaphyseal reaction - diffuse - antro lateral area
Subchondral fracture line - posterior half

Catterall Group IV
Whole head involvement
Metaphyseal reaction - central or diffuse
Posterior remodelling

Catterall’s - Head at Risk Signs
• Lateral epiphyseal calcification
• Lateral subluxation
• Gage’s sign
• Cage sign
• Caffey’s or Salter Sign
• Metaphyseal cysts
• Horizontal growth plate

Lateral subluxation

GAGE’S SIGN
• small osteoporotic segment forming a
translucent V- shaped trough in the lateral
part of the epiphysis

CAGE SIGN
• Calcification of the lateral epiphysis

Salter’s or Caffey’s sign
• a subchondral # may occur in the anterolateral
aspect of the femoral capital epiphysis. This
produces a crescentic radiolucency known as the
crescent, Salter’s or Caffey’s sign

Salter and Thompson
• Extend of sub chondral fracture
• Subchondral fracture correlates with eventual extent of
resorption
– GROUP A : Subchondral # involving <50% of the femoral dome
– GROUP B : Subchondral # involving >50% of the femoral dome

Herring
The femoral head pillars are
derived by noting the lines of
demarcation between the
central sequestrum and the
remainder of the epiphysis on
the anteroposterior radiograph

Herring
Group A
Normal Height of lateral
pillar maintained

Herring
Group B
> 50% of lateral pillar
height maintained

Herring
Group C
< 50% of lateral pillar
height maintained

TREATMENT
• AIM OF TREATMENT :
• The etiology of Perthes disease is unknown
and consequently treatment is not in any
way directed to achieving a cure.
• If it’s a elf limiting process of degeneration
and then regeneration why do we need to
treat it ?

AIM OF TREATMENT
• The long-term aim of treatment of Perthes’
disease is to prevent the onset of secondary
degenerative arthritis of the hip.
• Several long-term studies have shown that
loss of sphericity of the femoral head is the
most important factor related to
development of secondary degenerative
arthritis of the hip.

GOALS OF TREATMENT
• Elimination of hip irritability.
• Containment of the head.
• Restoration good ROM
• Prevent the femoral head from getting
deformed or enlarged
• Prevent trochanteric overgrowth
• Ensure Psychological & Physical developmentDr.Anoop G.C.,JR,Orthopaedics,GMCK

TREATMENT PROTOCOL
Observation only
Intermittent symptomatic treatment
Early definitive treatment
Conservative
surgical
Late reconstructive surgical

Observation only
• All children < 6 years
– Irrespective of the extent of involvement of
femoral capital epiphysis
– Provided there is no limitation of motion or
subluxation
• All children > 6year
– Under Caterll group I & II or Salter – Thompon
group A
– Provided there is no limitation of motion or
subluxation or collape
• Do not require active management but require
frequent evaluation clinically & Radiologically
every 3 months.

Intermittent symptomatic treatment
• All children under observation group
developing persistent loss of Motion or
containment.
• Temporary or periodic treatment for 1 or 2
weeks with
– Bed ret in abduction
– Traction in abduction
– Physiotherapy
• Once motion is regained and irritability
subsides child can resume normal activities
• Bi monthly evaluation is required.

Early definitive treatment
• All children in intermittent symptomatic
group with 2 – 3 recurrent episodes of
irritability.
• All children > 6 years under Caterall group III
& IV or Salter – Thompson group B.
• Any child with severe loss of motion or
evidence of Extrusion.
• Contraindicated in severe flattening of head ,
healed cases and hinged acetabulum.
• Principle is CONTAINMENT of femora head in
acetabulum – Non surgical or surgical.Dr.Anoop G.C.,JR,Orthopaedics,GMCK

CONTAINMENT - Non surgical
• Braces & orthoses
– Preliminary traction is applied to overcome muscle
spasm while the hip is gradually abducted and
internally rotated
– Brace are applied with lower limbs in
approximately 45 degree abduction and light
internal rotation.
– Walking is encouraged since weight bearing
movement are evential to remodeling.
– Bed time exercises preferably done under water.
– Plastic abduction night splint
– Generally discontinued at 20 month or if evidence
of new layer of subchondral bone in radiograph

Braces and orthoses
• An
TORONTO BRACENEWINGTON BRACE

Braces and orthoses
TACHDJIAN
BRACE
BIRMINGHAM BRACE

Braces and orthoses
Snyder sling Patten botom braceDr.Anoop G.C.,JR,Orthopaedics,GMCK

Braces and orthoses
Ambulatory abduction orthosisDr.Anoop G.C.,JR,Orthopaedics,GMCK

Plaster Casting
• Petrie or “Broomstick cast”
– By Patric and Bitenc.
– Long leg cats are applied to both extremities in
30 – 40 degree abduction and 5 degree internal
rotation.
– And secured by two wooden bars.
• Disadvantages
– Knee and ankle stiffness with adaptive articular
changes
– Restricted ambulation and pressure soresDr.Anoop G.C.,JR,Orthopaedics,GMCK

Petrie or “Broomstick cast”

SURGICAL CONTAINMENT
• INDICATIONS:
– Age of clinical onset > 8yrs of age
– Herring type B
– Radiological evidence of loss of containment by conservative
modes
• CONTRAINDICATIONS:
– Herring’s type A and C
– Herring’s type B if child less than 8 yrs
– Healed cases.
– Hinged abduction
• ADVANTAGES
– Ability to obtain permanent containment of head.
– Period of Restriction is only 2 months.

CONTAINMENT SURGERIES
– Varus Derotational Femoral Osteotomy
–Innominate or Salter osteotomy
–Shelf procedure
–Combination of femoral and
innominate osteotomy
–Combination of innominate
osteotomy and shelf

VARUS DEROTATION FEMORAL
OSTEOTOMY (VDO)
• Initially advocated by Axer in 1965
• Procedure of choice in 8 – 10 yrs without limb
shortening
• Uncovered head on MRI / Arthrogram
• Excessive femoral anteversion
• Types - Open wedge or closed wedge
• Technique - Osteotomy at subtrochantric level
& Distal femur is fixed in varus and external
rotation using plate and screws
• Hip spica for 8-12 weeks

VARUS DEROTATION FEMORAL
OSTEOTOMY (VDO)

INNOMINATE OSTEOTOMY – SALTER
• Initially advocated by Salter in 1966
• Advantages:
– Anterolateral coverage
– Lengthening of shortened limb
– No second operation for I/R
• Disadvantages:
– Improper coverage in older child
– Limb length inequality
– AVN due to raised pressure in joint
• Technique
– Iliac osteotomy is made just above acetabulum extending from
greater sciatic notch to anterior inferior Iliac pine
– Entire acetabulum with pelvis is rotated downward and outwards
– Bone graft from ilium is applied to osteotomy site
• Hip Spica for 8-12 weeks.

INNOMINATE OSTEOTOMY – SALTER

SHELF PROCEDURE
• Formerly used as a salvage procedure
• Catterall proposes this as the primary method of
management in children over 8 years of age
• INDICATION:
• Lateral subluxation
• Insufficient coverage
• Hinged abduction
• COMPLICATION:
• Loss of hip flexion
• lateral femoral cutaneous nerve injury
• Technique:
• bone graft is harvested from the ilium and
inserted into the roof of the acetabulum.

SHELF PROCEDURE

LATE RECONSTRUCTIVE SURGERIES
• Done for Healed Perthes with permanent
deformities
• Valgus osteotomy - Hinged abduction
• Shelf acetabuloplasty - Coxa magna
• Garceau cheilectomy - Malformed head in
catterall group 3
• Trochanteric advancement or arrest -
Capital physeal arrest & trochantric
overgrowth
• Chiari osteotomy– Significant femoral
head flattening.

ASSESSMENT OF END RESUTLT
• Assessment of end result is done at 4 years
after onset.
• Based on sphericity and containment of
femoral head.
• Good – no arthritis develops
• Fair – mild to moderate arthritis will
develop in late adulthood
• Poor – severe arthritis will develop before
age of forty.

 SPHERICITY OF HEAD
 MOSE CLASSIFICATION: Based on fitting
of contour of healed femoral head into
template of concentric circles in both AP & Frog
leg lateral views
• Good - < 1 mm
• Fair - < 2 mm
• Poor - > 2 mm

 CONTAINMENT OF HEAD
 CE Angle of Wiberg:
- A line is drawn from center of head C and edge of
acetabulum E called CE line
- The angle between CE
line and vertical
through center of
head is called the CE
angle.
 Good - >20
 Fair- 15-19
 Poor- < 15
E
C
Vertical

THANK YOU

Perthes Disease LCPD

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