PERTHES DISEASE IN ORTHOPEDICS

1. Legg – Calve – PerthesLegg – Calve – Perthes
DiseaseDisease
Presenter – Dr. Maulik T PatelPresenter – Dr. Maulik T Patel
Orthopedic surgeonOrthopedic surgeon

2. DefinitionDefinition
It is a self limiting disorder of the hipIt is a self limiting disorder of the hip
produced by ischemia and varyingproduced by ischemia and varying
degrees of necrosis of the femoral head.degrees of necrosis of the femoral head.

3. SynonymsSynonyms
Coxa PlanaCoxa Plana
Pseudocoxalgia (Calve)Pseudocoxalgia (Calve)
Arthritis deformans juvenilis (Perthes)Arthritis deformans juvenilis (Perthes)
Osteochondroses of the hipOsteochondroses of the hip
Coronary disease of the hipCoronary disease of the hip

4. HISTORYHISTORY
Reidel in 1890 presented the first case ofReidel in 1890 presented the first case of
osteochondritis dessecans in the hip.osteochondritis dessecans in the hip.
Preiser in Germany presented a patientPreiser in Germany presented a patient
with osteoartritis deformans.with osteoartritis deformans.

5. HISTORYHISTORY
Waldenstorm In 1909 described theWaldenstorm In 1909 described the
disorder in 10 children . He thought it to bedisorder in 10 children . He thought it to be
tubercular in origin and named it “Dertubercular in origin and named it “Der
Obere Tuberculose Collumherd”Obere Tuberculose Collumherd”
In 1910 this disorder was recognised asIn 1910 this disorder was recognised as
an independent entity by three men…an independent entity by three men…

6. HISTORYHISTORY
 Arthur LeggArthur Legg of theof the
United StatesUnited States

7. HISTORYHISTORY
 Jacques CalveJacques Calve ofof
FranceFrance

8. HISTORYHISTORY
 Georg PerthesGeorg Perthes ofof
GermanyGermany

9. HISTORYHISTORY
In the Early years treatment consisted onIn the Early years treatment consisted on
non weight bearing with Ischial weightnon weight bearing with Ischial weight
bearing Caliperbearing Caliper
Parker started the use of broomstick cast inParker started the use of broomstick cast in
1929.1929.
Eyre-Brook introduced traction in bed for 18-Eyre-Brook introduced traction in bed for 18-
24 months.24 months.
In 1966 Salter induced avascular necrosis inIn 1966 Salter induced avascular necrosis in
Pig model and proved that best result wasPig model and proved that best result was
with weightbearing with hips held inwith weightbearing with hips held in
abduction.abduction.

10. Blood supply to femoral headBlood supply to femoral head
 Retinacular arteriesRetinacular arteries
 Metaphyseal arteriesMetaphyseal arteries
 Artery of the teresArtery of the teres
ligamentligament

11. Blood supply to femoral headBlood supply to femoral head
 InfantsInfants
1.1. Medial ascending cervical or inferiorMedial ascending cervical or inferior
metaphyseal arteries of trueta.metaphyseal arteries of trueta.
2.2. Lat epiphysealLat epiphyseal
3.3. Lig teres – insignificantLig teres – insignificant
 4 mts – 4 years4 mts – 4 years
1.1. Lat epiphysealLat epiphyseal
2.2. Med epiphyseal decrease in number.Med epiphyseal decrease in number.

12. Blood supply to femoral headBlood supply to femoral head
 4 yrs to 7 years4 yrs to 7 years
Epiphyseal plate forms a barrier to metaphysealEpiphyseal plate forms a barrier to metaphyseal
vessels.vessels.
 Pre-adolescentPre-adolescent
After 7 yrs arteries of lig teres become moreAfter 7 yrs arteries of lig teres become more
prominent and anastomose with the lateralprominent and anastomose with the lateral
epiphyseal vessels.epiphyseal vessels.

13. IncidenceIncidence
 Male : Female = 4-5:1Male : Female = 4-5:1
 2.5:1 in India2.5:1 in India
 Age of onset earlier in females.Age of onset earlier in females.
 Age –Age –
Range – 2-13 years.Range – 2-13 years.
Most common 4-8 years.Most common 4-8 years.
Average – 6 years.Average – 6 years.
 Bilateral in 10-12 %Bilateral in 10-12 %
 Incidence more in Caucasians compared toIncidence more in Caucasians compared to
Negroid, mongoloid, Polynesians.Negroid, mongoloid, Polynesians.
 In India it is most prevalent in the west coastIn India it is most prevalent in the west coast
especially in Udupi district.especially in Udupi district.

14. EtiologyEtiology
The exact etiology of Legg Calve PerthesThe exact etiology of Legg Calve Perthes
disease in not known but many factorsdisease in not known but many factors
related to etiology of this disease haverelated to etiology of this disease have
been mentioned.been mentioned.

15. EtiologyEtiology
 Coagulation disorders.Coagulation disorders.
 Arterial status of femoral head.Arterial status of femoral head.
 Abnormal venous drainage.Abnormal venous drainage.
 Abnormal growth and development.Abnormal growth and development.
 Trauma.Trauma.
 Hyperactivity or attention deficit disorder.Hyperactivity or attention deficit disorder.
 Genetic component.Genetic component.
 Environmental influences.Environmental influences.
 As a sequel to synovitis.As a sequel to synovitis.

16. Coagulation disordersCoagulation disorders
 Glueck et al showed that 75% of their series ofGlueck et al showed that 75% of their series of
children with perthes disease had abnormalities ofchildren with perthes disease had abnormalities of
coagulation (protein C or S deficiency, thrombophilia,coagulation (protein C or S deficiency, thrombophilia,
increased lipoprotein a, hypofibrinolysis)increased lipoprotein a, hypofibrinolysis)
-- JBJS Am Jan 1996-- JBJS Am Jan 1996
 Valder Aruda et al reported factor 5 leiden mutationValder Aruda et al reported factor 5 leiden mutation
in children with Perthesin children with Perthes
-- Journal of paed orthopedics-- Journal of paed orthopedics
Jan/feb 1999Jan/feb 1999

17. Coagulation disordersCoagulation disorders
Kaeley et al found no causal relationshipKaeley et al found no causal relationship
-JBJS Br July 2000-JBJS Br July 2000
Vinod Balasa, Charles Glueck et al foundVinod Balasa, Charles Glueck et al found
causal relationship between Factor 5 Leidencausal relationship between Factor 5 Leiden
mutation, Anticardiolipin antibodies in Perthesmutation, Anticardiolipin antibodies in Perthes
disease.disease.
--JBJS Am Dec 2004--JBJS Am Dec 2004
Mc Dougall also found no linkMc Dougall also found no link
Clearly more studies are needed to resolveClearly more studies are needed to resolve
this issue.this issue.

18. Arterial status of femoral headArterial status of femoral head
 Angiographic studies have shown obstruction ofAngiographic studies have shown obstruction of
superior capsular arteries and decreased flow insuperior capsular arteries and decreased flow in
medial circumflex femoral arteries in Perthes disease.medial circumflex femoral arteries in Perthes disease.
 The intracapsular ring has been found to beThe intracapsular ring has been found to be
incomplete more often in males than females.incomplete more often in males than females.
 In Negroid infants the major source of blood supply toIn Negroid infants the major source of blood supply to
the femoral head is from the inferior gluteal arterythe femoral head is from the inferior gluteal artery
which could be a reason why Perthes is uncommon inwhich could be a reason why Perthes is uncommon in
negroid race.negroid race.

19. Abnormal venous drainageAbnormal venous drainage
Venous drainage normally flows through theVenous drainage normally flows through the
medial circumflex femoral vein.medial circumflex femoral vein.
In patients with perthes ,there is increasedIn patients with perthes ,there is increased
venous pressure in the femoral neck andvenous pressure in the femoral neck and
associated congestion in the metaphysis, andassociated congestion in the metaphysis, and
venous outflow obstruction has been found .venous outflow obstruction has been found .
In a dog model obstruction of venous outflowIn a dog model obstruction of venous outflow
has reproduced the features of AVN.has reproduced the features of AVN.

20. Abnormal growth and developmentAbnormal growth and development
A delay in Bone age of 1.5 to 2 yearsA delay in Bone age of 1.5 to 2 years
has been seen in children with pertheshas been seen in children with perthes
disease.disease.
Low birth weight has been seen inLow birth weight has been seen in
patients with Perthes Disease.patients with Perthes Disease.
Boys with Perthes have been found toBoys with Perthes have been found to
be 1 inch shorter and girls 3 inchbe 1 inch shorter and girls 3 inch
shorter than their peers.shorter than their peers.
Some investigators have found lowSome investigators have found low
levels of growth factor Somatomedin C.levels of growth factor Somatomedin C.

21. TraumaTrauma
In the developing femur , the major lateralIn the developing femur , the major lateral
epiphyseal artery must course through aepiphyseal artery must course through a
narrow passage ,which could make itnarrow passage ,which could make it
susceptible to disruption in case ofsusceptible to disruption in case of
trauma.trauma.

22. Hyperactivity or attention deficitHyperactivity or attention deficit
disorderdisorder
A high prevalence of this disorder hasA high prevalence of this disorder has
been seen in patients with Perthesbeen seen in patients with Perthes
Disease.Disease.
But Its precise role has not been defined.But Its precise role has not been defined.

23. Genetic componentGenetic component
Familial association has been reported.Familial association has been reported.
Burch et al have found a X-LinkedBurch et al have found a X-Linked
recessive inheritance in a few cases.recessive inheritance in a few cases.

24. Environmental influencesEnvironmental influences
Low socioeconomic status has been seenLow socioeconomic status has been seen
to be associated with Perthes Disease.to be associated with Perthes Disease.

25. Sequel to synovitisSequel to synovitis
Synovitis of the hip occurs early in LCPSynovitis of the hip occurs early in LCP
A controversial school of thought says thatA controversial school of thought says that
the increased pressure in synovitis maythe increased pressure in synovitis may
cause a tamponade effect on thecause a tamponade effect on the
vasculaturevasculature

26. Truetta’s HypothesisTruetta’s Hypothesis
He postulated that the solitary bloodHe postulated that the solitary blood
supply in the age group 4-8 yrs makessupply in the age group 4-8 yrs makes
them suceptible to ischemia.them suceptible to ischemia.
Compression of Lat epiphyseal arteries byCompression of Lat epiphyseal arteries by
ext.rotators.ext.rotators.

27. Caffey’s HypothesisCaffey’s Hypothesis
Intraepiphyseal compression of bloodIntraepiphyseal compression of blood
supply to ossification centersupply to ossification center

28. PATHOGENESISPATHOGENESIS
 LOSS OF BLOOD SUPPLY PRODUCESLOSS OF BLOOD SUPPLY PRODUCES
AVN OF THE EPIPHYSEAL OSSCIFICATIONAVN OF THE EPIPHYSEAL OSSCIFICATION
CENTRE FOLLOWED BY RESORPTION OFCENTRE FOLLOWED BY RESORPTION OF
DEAD BONE AND REPLACEMENT WITHDEAD BONE AND REPLACEMENT WITH
NEWLY FORMED IMMATURE BONE.NEWLY FORMED IMMATURE BONE.
 THE PROCESS IS DESCRIBED IN STAGESTHE PROCESS IS DESCRIBED IN STAGES

29. ICIPIENT OR SYNOVITISICIPIENT OR SYNOVITIS
STAGESTAGE
LAST 1-3 WEEKS . SYNOVIUM ISLAST 1-3 WEEKS . SYNOVIUM IS
SWOLLEN , HYPEREMIC ANDSWOLLEN , HYPEREMIC AND
EDEMATOUS.EDEMATOUS. JOINT FLUIDJOINT FLUID
IS INCREASED ANDIS INCREASED AND ABSENCE OFABSENCE OF
IMFLAMMATORY CELLS.IMFLAMMATORY CELLS.

30. Increase
joint space

31. STAGE OF AVNSTAGE OF AVN
 AVN INVOLVES PORTION OF OSSIFIC NUCLEUSAVN INVOLVES PORTION OF OSSIFIC NUCLEUS
SITUATED ANTERIORLY AMORPHOUSSITUATED ANTERIORLY AMORPHOUS
DEBRIES FILLS THE MARROW SPACES. TRABACUALESDEBRIES FILLS THE MARROW SPACES. TRABACUALES
ARE CRUSHED INTO MINUTE FRAGMENTS AND COMPRESSEDARE CRUSHED INTO MINUTE FRAGMENTS AND COMPRESSED
INTO A COMPACT BONE ACCOUNTING FORINTO A COMPACT BONE ACCOUNTING FOR
INCREASED DENSITY ON RADIOGRAPH.INCREASED DENSITY ON RADIOGRAPH.
 THE INCREASED OPACITY IS CONTRASTEDTHE INCREASED OPACITY IS CONTRASTED
MARKED DIMINIRALISATION OF ADJACENT METAPHYSISMARKED DIMINIRALISATION OF ADJACENT METAPHYSIS
RESULT OF HYPERVASCULARITYRESULT OF HYPERVASCULARITY
CONSTITUTES PREPARATION FOR INVASIONCONSTITUTES PREPARATION FOR INVASION
VASCULAR CONNECTIVE TISSUE TOWQRDS NECROTIC BONE.VASCULAR CONNECTIVE TISSUE TOWQRDS NECROTIC BONE.
 THE CARTILAGE IS VIABLE NUTRITION ISTHE CARTILAGE IS VIABLE NUTRITION IS
DERIVED FROM SYNOVIAL FLUID.DERIVED FROM SYNOVIAL FLUID. STAGE LASTSTAGE LAST
6 MONTHS TO 1 YEAR.6 MONTHS TO 1 YEAR.

33. STAGE OFSTAGE OF
FRAGMENTATION ORFRAGMENTATION OR
REGENERATIONREGENERATION RADIOGRAPHIC FRAGMENTED APPEARANCERADIOGRAPHIC FRAGMENTED APPEARANCE
RESULTS MANY TOUNGE LIKERESULTS MANY TOUNGE LIKE
 SUBCHONDRAL FRACTURES OF NECROTICSUBCHONDRAL FRACTURES OF NECROTIC
BONEBONE MULTIPLE MINUTEMULTIPLE MINUTE
TRABECULAR FRAGMENTSTRABECULAR FRAGMENTS
COMPRESSED TOGETHER. CARTILAGE REMAINSCOMPRESSED TOGETHER. CARTILAGE REMAINS
NORMAL .NORMAL .
 THE COUNTOR OF THE NEWLY FORMED SOFTTHE COUNTOR OF THE NEWLY FORMED SOFT
BONE DEVELOPS IN RESPONSE TO THEBONE DEVELOPS IN RESPONSE TO THE
EXTERNAL FORCES.EXTERNAL FORCES. STAGE EXTENTS OVERSTAGE EXTENTS OVER

34. HEALED OR RESIDUALHEALED OR RESIDUAL
STAGESTAGE
 FORMATION OF NORMAL BONE ALONGSIDEFORMATION OF NORMAL BONE ALONGSIDE
REPLACING SLOWLY RESORBING BONE.REPLACING SLOWLY RESORBING BONE.
NEWLY FORMED BONE IS IMMATURENEWLY FORMED BONE IS IMMATURE
FORMED OF SLENDER TRABECULAE AND EASILYFORMED OF SLENDER TRABECULAE AND EASILY
COMPRESSED TOGETHER WITH NECROTICCOMPRESSED TOGETHER WITH NECROTIC
FRAGMENTSFRAGMENTS
 THE COMPRESSION IS LIMITEDTHE COMPRESSION IS LIMITED
ANTERIOR PORTION OF HEAD CREATING AANTERIOR PORTION OF HEAD CREATING A
CUP SHAPED DEFECT SEEN ON FROGCUP SHAPED DEFECT SEEN ON FROG
LEG VIEW THE OSSIFIC NUCELUSLEG VIEW THE OSSIFIC NUCELUS
ASSUMES A MUSHROOM SHAPED COUNTOR.ASSUMES A MUSHROOM SHAPED COUNTOR.

35.  APPERANCE OF GREATERAPPERANCE OF GREATER
TROCHANTERTROCHANTER:- IT BECOMES:- IT BECOMES
STRIKINLY LARGE IN SOME CASES. SINCESTRIKINLY LARGE IN SOME CASES. SINCE
LONGITUDINAL GROWTH OF THE FEMORALLONGITUDINAL GROWTH OF THE FEMORAL
NECK MAY CEASE COMPLETELY AT 12 -14NECK MAY CEASE COMPLETELY AT 12 -14
YEARS OF AGE , WHEREAS GROWTH OF THEYEARS OF AGE , WHEREAS GROWTH OF THE
GREATER TROCHANTER CONTINUES UNTILGREATER TROCHANTER CONTINUES UNTIL
17 -18 YEARS, A DISCERPANCY IN GROWTH17 -18 YEARS, A DISCERPANCY IN GROWTH
NECK AND THE GREATER TROCHANTERNECK AND THE GREATER TROCHANTER
MAY RESULT.THE ELEVATION IMPAIRS THEMAY RESULT.THE ELEVATION IMPAIRS THE
POWER OF PELVITROCHANTERICPOWER OF PELVITROCHANTERIC
ABDUCTER MUSCLES, MANIFESTED BYABDUCTER MUSCLES, MANIFESTED BY
POSITIVE TRENDELBERG SIGN.POSITIVE TRENDELBERG SIGN.

36. Avascular necrosisAvascular necrosis
Temporary cessation of growthTemporary cessation of growth
Of epiphysisOf epiphysis
PotentialPotential
Revascularisation from periphery PerthesRevascularisation from periphery Perthes
Resumption of ossificationResumption of ossification

37. Pathological fracturePathological fracture
Resorption of underlying boneResorption of underlying bone
Replacement by biologically TrueReplacement by biologically True
Plastic bone PerthesPlastic bone Perthes
SubluxationSubluxation
DeformityDeformity

38. CLINICAL FEATURESCLINICAL FEATURES
SYMPTOMSSYMPTOMS
 MOST CHILDERN PRESENT WITH MILD ANDMOST CHILDERN PRESENT WITH MILD AND
INTERMITTENT PAIN IN THE THIGH OR A LIMP ORINTERMITTENT PAIN IN THE THIGH OR A LIMP OR
BOTH.BOTH.
 THE ONSET OF PAIN MAY BE ACUTE OR INSIDIOUSTHE ONSET OF PAIN MAY BE ACUTE OR INSIDIOUS
 THE CLASSICAL PRESENTATION IS DESCRIBED AS ATHE CLASSICAL PRESENTATION IS DESCRIBED AS A
“PAINLES LIMP” THE CHILD LIMPS BUT DOES NOT“PAINLES LIMP” THE CHILD LIMPS BUT DOES NOT
COMPLAINS OF DISCOMFORT.COMPLAINS OF DISCOMFORT.
 PAIN IS AGRRAVATED BY MOVEMENT OF HIP ANDPAIN IS AGRRAVATED BY MOVEMENT OF HIP AND
RELIVED BY REST.RELIVED BY REST.

39. EXAMINATION:-EXAMINATION:-
 ANTALGIC GAITANTALGIC GAIT
 MUSCLE SPASM SECONDARY TO IRRITABLE HIP.MUSCLE SPASM SECONDARY TO IRRITABLE HIP.
 LIMITATION OF ABDUCTION AND INTERNALLIMITATION OF ABDUCTION AND INTERNAL
ROTATIONROTATION
 FFD IS PRESENTFFD IS PRESENT
 AXIS DEVIATION IS PRESENT due to central collapseAXIS DEVIATION IS PRESENT due to central collapse
 DIFFERENTIAL ROTATION .DIFFERENTIAL ROTATION .
 TRENDELENBERG TEST POSITIVETRENDELENBERG TEST POSITIVE

40. InvestigationInvestigation
X-Ray –AP & Frog leg Lat viewX-Ray –AP & Frog leg Lat view
USGUSG
ArthrographyArthrography
Bone ScanBone Scan
CTCT
MRIMRI

41. RADIOGRAPHIC STAGESRADIOGRAPHIC STAGES
FOUR WALDENSTROM STAGES:FOUR WALDENSTROM STAGES:
1) INITIAL STAGE1) INITIAL STAGE
2) FRAGMENTATION STAGE2) FRAGMENTATION STAGE
3) REOSSIFICATION STAGE3) REOSSIFICATION STAGE
4) HEALED STAGE4) HEALED STAGE

42. INITIAL STAGEINITIAL STAGE
 EARLY RADIOGRAPHICEARLY RADIOGRAPHIC
SIGNS:SIGNS:
 FAILURE OF FEMORALFAILURE OF FEMORAL
OSSIFICOSSIFIC
NUCLEUS TO GROWNUCLEUS TO GROW
 WIDENING OF MEDIALWIDENING OF MEDIAL
JOINT SPACEJOINT SPACE
 ““CRESCENT SIGN”CRESCENT SIGN”
 IRREGULAR PHYSEALIRREGULAR PHYSEAL
PLATEPLATE
 BLURRY/ RADIOLUCENTBLURRY/ RADIOLUCENT
METAPHYSISMETAPHYSIS

43. X-RayX-Ray
 Cresent Sign orCresent Sign or
Salters sign orSalters sign or
Caffey’s signCaffey’s sign

44. FRAGMENTATION STAGEFRAGMENTATION STAGE
BONY EPIPHYSISBONY EPIPHYSIS
BEGINS TOBEGINS TO
FRAGMENTFRAGMENT
AREAS OFAREAS OF
INCREASEDINCREASED
LUCENCY ANDLUCENCY AND
DENSITYDENSITY
EVIDENCE OFEVIDENCE OF
REPAIR ASPECTSREPAIR ASPECTS

45. X-RayX-Ray
 Fragmentation ofFragmentation of
epiphysisepiphysis

46. REOSSIFICATION STAGEREOSSIFICATION STAGE
NORMAL BONENORMAL BONE
DENSITY RETURNSDENSITY RETURNS
ALTERATIONS INALTERATIONS IN
SHAPE OF FEMORALSHAPE OF FEMORAL
HEAD AND NECKHEAD AND NECK
EVIDENTEVIDENT

47. X-RayX-Ray
 MetaphysealMetaphyseal
widening and cysticwidening and cystic
changes in femoralchanges in femoral
neckneck

48. X-RayX-Ray
 Lateral extrusion ofLateral extrusion of
femoral head andfemoral head and
changes inchanges in
acetabulum.acetabulum.

49. X-RayX-Ray
 Sagging rope sign inSagging rope sign in
adults with history ofadults with history of
perthes – radio denseperthes – radio dense
line overlyingline overlying
proximal femoralproximal femoral
metaphysis, a resultmetaphysis, a result
of growth plateof growth plate
damage withdamage with
metaphysialmetaphysial
response.response.

50. ArthrographyArthrography
 Indicated to know the contour of headIndicated to know the contour of head
and congruity of articular surfaceand congruity of articular surface
Shows the configuration of the femoralShows the configuration of the femoral
head and its relation with the acetabulum.head and its relation with the acetabulum.
Provides reliable information regardingProvides reliable information regarding
containment.containment.
We can assess congruity of hip in manyWe can assess congruity of hip in many
different positions.different positions.
Not routinely used .Not routinely used .

51. Bone ScanBone Scan
Indicated to diagnose in early stages andIndicated to diagnose in early stages and
to classify the severity.to classify the severity.
Diagnosis possible months before signsDiagnosis possible months before signs
appear on X-Ray.appear on X-Ray.
Avascular areas show cold spots.Avascular areas show cold spots.
Revascularisation can be detected muchRevascularisation can be detected much
before radiographic evidence.before radiographic evidence.

52. Bone ScanBone Scan
 Convay et alConvay et al
classificationclassification
 Stage 1 is total lack ofStage 1 is total lack of
uptakeuptake

53. Bone ScanBone Scan
 Revascularisation atRevascularisation at
lateral columnlateral column
 Failure to revasculariseFailure to revascularise
at lat column is a graveat lat column is a grave
signsign
 Also called “scintigraphicAlso called “scintigraphic
head at risk sign”head at risk sign”
 Precedes radiographicPrecedes radiographic
head at risk sign by 2-3head at risk sign by 2-3
mthsmths

54. Bone ScanBone Scan
 Gradual filling ofGradual filling of
anterolateral partanterolateral part

55. Bone ScanBone Scan
 Return to normalReturn to normal

56. MRIMRI
Accurate in early diagnosis.Accurate in early diagnosis.
Shows congruity, containment, synovialShows congruity, containment, synovial
hypertrophy well.hypertrophy well.
Subtraction MRI shows ischemia as wellSubtraction MRI shows ischemia as well
as scintigraphy and also allows earlyas scintigraphy and also allows early
recognition of reperfusion.recognition of reperfusion.

57. ClassificationClassification
Waldenstroms classification.Waldenstroms classification.
Catterall classification.Catterall classification.
Salter classificationSalter classification
Herrings lateral pillar classification.Herrings lateral pillar classification.
Modified Elizabethtown classification.Modified Elizabethtown classification.

58. Waldenstroms classificationWaldenstroms classification
1.1. Incipient stage – 1-3 wksIncipient stage – 1-3 wks
2.2. Avascular stage – upto 1 yrAvascular stage – upto 1 yr
3.3. Regenerative stageRegenerative stage
4.4. Residual stageResidual stage
Not scientifically valid.Not scientifically valid.

59. Catterall classification (1971)Catterall classification (1971)
I – only anterior portion of epiphysisI – only anterior portion of epiphysis
affected.affected.
II – anterior segment involved centralII – anterior segment involved central
sequestrum presentsequestrum present
III – most of epiphysis sequestered withIII – most of epiphysis sequestered with
unaffected portions located medialunaffected portions located medial
and lateral to central segmentand lateral to central segment
IV – all of epiphysis sequestered.IV – all of epiphysis sequestered.

60. Catterall described head at risk factors toCatterall described head at risk factors to
predict prognosis:predict prognosis:
1- lat. subluxation of femoral head1- lat. subluxation of femoral head
3- Calcification lat. to epiphysis3- Calcification lat. to epiphysis
4- Horizontal physeal line4- Horizontal physeal line
5- gage sign5- gage sign
6- exetensive metaphyseal involvement6- exetensive metaphyseal involvement

61. Gage’s signGage’s sign
 Rarefaction in theRarefaction in the
lateral part of thelateral part of the
epiphysis andepiphysis and
subjacentsubjacent
metaphysis.metaphysis.

62. Salter ClassificationSalter Classification
Type A = I & II CatterallType A = I & II Catterall
Type B = III & IV Catterall.Type B = III & IV Catterall.

63. Herring Lat PillarHerring Lat Pillar
 Group-A hips are defined as those with noGroup-A hips are defined as those with no
involvement of the lateral pillar, with no densityinvolvement of the lateral pillar, with no density
changes and no loss of height of the lateral pillarchanges and no loss of height of the lateral pillar
 Group-B hips have lucency in the lateral pillarGroup-B hips have lucency in the lateral pillar
and may have some loss of height , but notand may have some loss of height , but not
exceeding 50% of the original height.exceeding 50% of the original height.
 Group-C hips are those with more lucency in theGroup-C hips are those with more lucency in the
lateral pillar and >50% loss of heightlateral pillar and >50% loss of height

64. Lateral Pillar group ALateral Pillar group A

65. Lateral Pillar group BLateral Pillar group B

66. Lateral Pillar group CLateral Pillar group C

67. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage Ia: Part orStage Ia: Part or
whole of thewhole of the
epiphysis isepiphysis is
sclerotic. There issclerotic. There is
no loss of height ofno loss of height of
the epiphysis.the epiphysis.

68. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage Ib: TheStage Ib: The
epiphysis isepiphysis is
sclerotic andsclerotic and
there is loss ofthere is loss of
epiphysealepiphyseal
height. There isheight. There is
no evidence ofno evidence of
fragmentation offragmentation of
the epiphysis.the epiphysis.

69. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage IIa: TheStage IIa: The
sclerotic epiphysissclerotic epiphysis
has just begun tohas just begun to
fragment. One orfragment. One or
two vertical fissurestwo vertical fissures
are seen in eitherare seen in either
the AP or thethe AP or the
lateral viewlateral view

70. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage IIb:Stage IIb:
Fragmentation isFragmentation is
advanced. No newadvanced. No new
bone is visiblebone is visible
lateral to thelateral to the
fragmentedfragmented
epiphysis.epiphysis.

71. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage IIIa: EarlyStage IIIa: Early
new bonenew bone
formation is visibleformation is visible
on the periphery ofon the periphery of
the necroticthe necrotic
epiphysis andepiphysis and
covers less than acovers less than a
third of the width ofthird of the width of
the epiphysisthe epiphysis

72. Modified ElizabethtownModified Elizabethtown
classificationclassification
 Stage IIIb: TheStage IIIb: The
new bone is ofnew bone is of
normal texturenormal texture
and has grownand has grown
over a third of theover a third of the
width of thewidth of the
epiphysis.epiphysis.

73. Modified ElizabethtownModified Elizabethtown
classificationclassification
Stage IV the healing is complete and there isStage IV the healing is complete and there is
no radiologically identifiable avascular bone.no radiologically identifiable avascular bone.

74. Prognostic FactorsPrognostic Factors
1.1. Age at diagnosisAge at diagnosis
2.2. Extent of involvementExtent of involvement
3.3. SexSex
4.4. Catterall “head at risk” clinical signsCatterall “head at risk” clinical signs
 ClinicalClinical
1.1. Progressive loss of hip motionProgressive loss of hip motion
2.2. Increasing abduction contractureIncreasing abduction contracture
3.3. Obese childObese child

75. Classification of PrognosisClassification of Prognosis
Uniplanar methodsUniplanar methods
- CE angle of Weiberg.- CE angle of Weiberg.
- Salters extrusion Index.- Salters extrusion Index.
- Epiphyseal index.- Epiphyseal index.
- Epiphyseal quotient.- Epiphyseal quotient.
Biplanar methodsBiplanar methods
- Stulberg classification.- Stulberg classification.

76. CE angle of WeibergCE angle of Weiberg
 Indicator of acetabular depth It isIndicator of acetabular depth It is
the angle formed by athe angle formed by a
perpendicular lines through theperpendicular lines through the
midportion of the femoral headmidportion of the femoral head
and a line from the femoral headand a line from the femoral head
center to the upper outercenter to the upper outer
acetabular margin.acetabular margin.
 Normal = 20 to 40 degrees, withNormal = 20 to 40 degrees, with
an average of 36 degrees.an average of 36 degrees.
 This angle may be slightly largerThis angle may be slightly larger
in women and in older persons.in women and in older persons.
 Angle >25 = good, 20-25= fair, <Angle >25 = good, 20-25= fair, <
20 = poor20 = poor

77. Salters extrusion IndexSalters extrusion Index
 If AB is moreIf AB is more
than 20% of CDthan 20% of CD
it indicates ait indicates a
poor prognosispoor prognosis

78. Epiphyseal index & quotientEpiphyseal index & quotient
Epiphyseal index = greatest height of theEpiphyseal index = greatest height of the
epiphysis divided by its width.epiphysis divided by its width.
Epiphyseal quotient = Epiphyseal index ofEpiphyseal quotient = Epiphyseal index of
involved hip divided by the index forinvolved hip divided by the index for
uninvolved hip.uninvolved hip.
>0.6 = good>0.6 = good
0.4-0.6 = fair0.4-0.6 = fair
<0.4 = poor<0.4 = poor

79. Stulberg classificatonStulberg classificaton
 Class I – Shape of the femoral head wasClass I – Shape of the femoral head was
basically normal.basically normal.
 Class II – Loss of head height but within 2 mmClass II – Loss of head height but within 2 mm
to a concentric circle on AP and frogto a concentric circle on AP and frog
leg X-Rayleg X-Ray
 Class III – Deviates more than 2 mm andClass III – Deviates more than 2 mm and
acetabulum contour matchesacetabulum contour matches
the head contourthe head contour
 Class IV – Head Flattened, Flattened areaClass IV – Head Flattened, Flattened area
<1cm. Acetabulum contour matches<1cm. Acetabulum contour matches
the head contourthe head contour
 Class V – Collapse of femoral head, AcetabularClass V – Collapse of femoral head, Acetabular

80. Stulberg classificatonStulberg classificaton
 Class IClass I
Shape ofShape of
the femoralthe femoral
head ishead is
basicallybasically
normal.normal.

81. Stulberg classificatonStulberg classificaton
 Class IIClass II
Loss ofLoss of
headhead
height butheight but
within 2within 2
mmmm

82. Stulberg classificatonStulberg classificaton
 Class IIIClass III
DeviatesDeviates
more thanmore than
2 mm2 mm

83. Stulberg classificatonStulberg classificaton
 Class IVClass IV
HeadHead
FlattenedFlattened

84. Stulberg classificatonStulberg classificaton
 Class VClass V
Collapse ofCollapse of
femoralfemoral
head,head,
AcetabularAcetabular
contourcontour
does notdoes not
change andchange and
not matchenot matche

85. Differential diagnosisDifferential diagnosis
Tuberculosis of the hipTuberculosis of the hip
SCFESCFE
Transient synovitisTransient synovitis
SpondylodysplasiaSpondylodysplasia
AVN due to leukemia, lymphoma,AVN due to leukemia, lymphoma,
gauchers disease, Hemoglobinopathiesgauchers disease, Hemoglobinopathies
etcetc

86. TreatmentTreatment
ObjectivesObjectives
- To produce a normal femoral- To produce a normal femoral
head and neckhead and neck
- To produce a normal acetabulum- To produce a normal acetabulum
- A congruous hip which is fully- A congruous hip which is fully
mobilemobile
- To prevent degenerative arthritis- To prevent degenerative arthritis
of the hip later in lifeof the hip later in life

87. TreatmentTreatment
GOAL :GOAL :
Treatment efforts are directed towardsTreatment efforts are directed towards
- Restoration and maintenance of- Restoration and maintenance of
full mobility of the hipfull mobility of the hip
- Containment of the femoral- Containment of the femoral
head.head.
- Resumption of weight bearing- Resumption of weight bearing
and full activity as soon asand full activity as soon as
possiblepossible

88. TreatmentTreatment
 Caterall group 1 andCaterall group 1 and
group 2 ( < 7 years)group 2 ( < 7 years)
No activeNo active
 Herring group 1 &Herring group 1 & TreatmentTreatment
group 2 (< 6 years)group 2 (< 6 years)

89. TreatmentTreatment
Treatment is divided into 3 phasesTreatment is divided into 3 phases
Initial Phase – restore & maintain mobilityInitial Phase – restore & maintain mobility
Active Phase – Containment andActive Phase – Containment and
maintainance of full mobility.maintainance of full mobility.
Reconstructive phase – correct residualReconstructive phase – correct residual
deformities.deformities.

90. Treatment ( Initial Phase )Treatment ( Initial Phase )
Physiotherapy – active and passivePhysiotherapy – active and passive
range of motionrange of motion
exercises to restoreexercises to restore
motionmotion
Traction – B/L skin traction andTraction – B/L skin traction and
gradually abducting over 1-2gradually abducting over 1-2
weeks till full abduction isweeks till full abduction is
regained.regained.

91. Treatment ( Active Phase )Treatment ( Active Phase )
Consists of containment of the femoralConsists of containment of the femoral
head within the acetabulum. This can behead within the acetabulum. This can be
achieved byachieved by
orthosisorthosis
or byor by
surgerysurgery

92. Treatment (Orthosis)Treatment (Orthosis)
 Non Ambulatory weight releivingNon Ambulatory weight releiving
1.1. Abduction broomstick plaster castAbduction broomstick plaster cast
2.2. Hip spica castHip spica cast
3.3. Milgram hip abduction orthosisMilgram hip abduction orthosis
 Ambulatory Both limbs includedAmbulatory Both limbs included
1.1. Petrie Abduction castPetrie Abduction cast
2.2. Toronto orthosisToronto orthosis
3.3. Newington orthosisNewington orthosis
4.4. Birmingham braceBirmingham brace
5.5. Atlanta Scotish Rite BraceAtlanta Scotish Rite Brace
 Ambulatory unilateralAmbulatory unilateral
1.1. Tachdjian trilateral socket orthosisTachdjian trilateral socket orthosis

93. Treatment (Orthosis)Treatment (Orthosis)
 Atlanta Scotish RiteAtlanta Scotish Rite
BraceBrace

94. Atlanta Scotish Rite BraceAtlanta Scotish Rite Brace

95. Newington orthosisNewington orthosis

96. Birmingham braceBirmingham brace

97.  Toronto BraceToronto Brace

98.  Tachdjian trilateralTachdjian trilateral
socket orthosissocket orthosis

99. Treatment (Orthosis)Treatment (Orthosis)
 Orthotic treatment is discontinued when theOrthotic treatment is discontinued when the
disease enters the reparative phase and healingdisease enters the reparative phase and healing
is established.is established.
 The radiographic evidence of healing areThe radiographic evidence of healing are
1.1. Appearance of regular ossification in theAppearance of regular ossification in the
femoral head.femoral head.
2.2. Increased density of femoral head shouldIncreased density of femoral head should
disappear.disappear.
3.3. Metaphyseal rarefaction involving the lateralMetaphyseal rarefaction involving the lateral
cortex of the metaphysis should ossify.cortex of the metaphysis should ossify.
4.4. There should be intact lateral column.There should be intact lateral column.
5.5. There should be normal trabecular bone in theThere should be normal trabecular bone in the
epiphysis.epiphysis.

100. Treatment ( Surgical)Treatment ( Surgical)
Femoral varus osteotomy.Femoral varus osteotomy.
Inominate osteotomy.Inominate osteotomy.
Combined femoral and inominateCombined femoral and inominate
osteotomyosteotomy
Valgus osteotomyValgus osteotomy
Shelf arthroplastyShelf arthroplasty
Chiari osteotomyChiari osteotomy
Cheilectomy.Cheilectomy.
Trochanteric advancement or arrest.Trochanteric advancement or arrest.

101. Femoral varus osteotomyFemoral varus osteotomy
IndicationsIndications: 1.>6yrs of age: 1.>6yrs of age
2.hip with normal or near normal2.hip with normal or near normal
hiphip
ComplicationsComplications:1.excessive post op varus:1.excessive post op varus
2.Persistant ext.rotation2.Persistant ext.rotation
3.Shortening of extremity3.Shortening of extremity
4.Incresed abductor lurch4.Incresed abductor lurch
5.Trochanteric over growth5.Trochanteric over growth
6.Delayed or non union6.Delayed or non union

102. Femoral varus osteotomyFemoral varus osteotomy

103. Femoral varus osteotomyFemoral varus osteotomy

104. Femoral varus osteotomyFemoral varus osteotomy
 Varus should not beVarus should not be
exced less than 110*exced less than 110*

105. Femoral varus osteotomyFemoral varus osteotomy

106. Femoral varus osteotomyFemoral varus osteotomy

107. Femoral varus osteotomyFemoral varus osteotomy

108. Inominate osteotomyInominate osteotomy
 IndicationsIndications::
1.>6 yrs1.>6 yrs
2.mod. Or severely affected head with loss of2.mod. Or severely affected head with loss of
containmentcontainment
RequirementRequirement::
Able to abduct 45 deg. And femoral head to beAble to abduct 45 deg. And femoral head to be
contained in positioncontained in position
ComplicationsComplications :loss of fixation, leg-lengthening ,dec. hip:loss of fixation, leg-lengthening ,dec. hip
flx. And jt.stiffness, second procedure for k wireflx. And jt.stiffness, second procedure for k wire
remavalremaval

113. Valgus OsteotomyValgus Osteotomy
 Indication:hingedIndication:hinged
abduction of hipabduction of hip

114. Shelf ArthroplastyShelf Arthroplasty
Performed to enlarge the volume ofPerformed to enlarge the volume of
acetabulum.acetabulum.
Indication:A deficient acetabulum cannotIndication:A deficient acetabulum cannot
be corrected by pelvic osteotomybe corrected by pelvic osteotomy
Contra indication: Dysplastic hip withContra indication: Dysplastic hip with
spherical congruityspherical congruity

115. Shelf ArthroplastyShelf Arthroplasty

116. Chiari osteotomyChiari osteotomy
 Capsular interpositionalCapsular interpositional
arthroplastyarthroplasty
 Deepens the deficientDeepens the deficient
acetabulum by medialacetabulum by medial
displacement of distaldisplacement of distal
pelvic fragment andpelvic fragment and
improves sup.lat.femoralimproves sup.lat.femoral
coverage.coverage.

117. Trochanteric advancementTrochanteric advancement
 IndicationsIndications::
- Trochanteric over- Trochanteric over
growthgrowth
- Capital femoral- Capital femoral
physeal growth arrestphyseal growth arrest

118. Recommended Indications for diff.Recommended Indications for diff.
surgeriessurgeries
Hinged abduction - valgus subtrochantericHinged abduction - valgus subtrochanteric
osteotomyosteotomy
Severly Mal formed femoral head –Severly Mal formed femoral head –
cheilectomycheilectomy
Coxa magna – shelf augmentationCoxa magna – shelf augmentation
A large malformed femoral head withA large malformed femoral head with
lat.subluxation – Chiari’s pelvic osteotomylat.subluxation – Chiari’s pelvic osteotomy
Capital femoral physeal arrest –Capital femoral physeal arrest –
Trochanteric advancementTrochanteric advancement

120. Recent AdvancesRecent Advances
AnticoagulantAnticoagulant
Botulinum toxinBotulinum toxin
 Ibadronate :this has shown thereIbadronate :this has shown there
importance in rat model by increaseimportance in rat model by increase
spericity of femoral headspericity of femoral head
Still lot more work to do in this fieldsStill lot more work to do in this fields

121. ReferencesReferences
Campbell’s operative Orthopaedics – 10Campbell’s operative Orthopaedics – 10thth
editionedition
Tachdjian’s paediatric orthopaedics – 3Tachdjian’s paediatric orthopaedics – 3rdrd
editionedition
Mercer’s Orthopaedic surgery – 9Mercer’s Orthopaedic surgery – 9thth
editionedition
Journals of bone and joint surgeryJournals of bone and joint surgery
InternetInternet

122. Thank you
for your
patient
listening