ADVANCED ORTHOPAEDICS ACADEMY

Defination:

Idiopathic osteonecrosis of the capital femoral epiphysis of the femoral head of unknown aetiology. It is a self-limited disease. Complete revascularisation of the avascular epiphysis occures almost invariably, over a period of two yrs with or without any form of treatment, with or without femoral head deformity.

Epidemiology:

• One in 1200 children younger than 15 years is affected by LCPD.
• Males are affected 4-5 times more often than females.
• LCPD most commonly is seen in persons aged 4-9 (2-18) years, with a average age of 7 years.
• Bilateral involvement 10 -15%.
• Hereditary- children with HLA-A antigen are susceptible.

Etiology:

• Unknown
• Probably secondary to soft tissue disease.
• Any process responsible to cause interruption of blood supply to the capital femoral epiphysis.
• Hypothesis.
  -Trueta’s hypothesis
  -Caffey’s hypothesis

Trueta’s Hypothesis

• Blood supply to femoral head at age

         < 4yrs- dual supply(metaphysial &  lateral epiphysial vessel)
         4-8yrs- single supply(lateral epiphysial vessel)
         >  8yrs- dual supply (lateral &  medial epiphysial vessel)

• So most vulnerable during 4-8yr.
• Medial epiphyseal vessels(through ligamentum teres) developes.
• earlier in blacks than whites..supports the hypothesis
• But cant define reason of male predominance.

Caffey’s Hypothesis

• Child has genetic or acquired dysplasia resulting in delayed bone age
• Thick pre-ossific cartilage of the femoral head provides inadequet protection for the vessels transversing the cartilage
• Compression of that cartilage cause infarction, more coomon in boys due to more activity
• Called it as a coronary diseae of hip.

Probable causes:

• A- Arterial ischaemia
• V- Venous obstruction- metaphysial blockage, coagulopathy
• A- Abnormal growth & development- lbw,
• hormonal abnormality
• S- Synovitis
• T- Trauma

Hereditary, Nutritional factor,hyperactivity attention disorder.

Pathology:

• The blood supply to the capital femoral epiphysis is interrupted (arteries and veins).

• Bone infarction occurs, especially in the subchondral cortical bone, while articular cartilage
  continues to grow. (Articular cartilage grows because its nutrients come from the synovial fluid.)

• Four stage-

  1. Incipient or stage of synovitis(lasts for 1-3wk)
  2. Stage of AVN(lasts for 6mo-1yr)
  3. Stage of fragmentation or regeneration(lasts for2-3yrs)
  4. Stage of residual deformity or healed lesion

Clinical features:

• Painless limp (earliest symptom).
• Hip or groin pain, which may be referred to the thigh, knee.
• Usually no history of trauma.
• Decreased range of motion (ROM), particularly with internal rotation and abduction.
• Painful antalgic gait.
• Atrophy of thigh muscles secondary to disuse (Trendelenburg sign)‏.
• Muscle spasm- mild hip contracture of 10-20 degrees may be present.
• Leg length inequality due to collapse.

Investigations:-

• Radiology- initial modality
  A-P, frog-leg lateral views (every 6 weeks at the beginning, every 3-6 months later)
  classify the lesion depending upon
  -pathological stage (waldenstrom)
  -severity (catterall, salter-thompson, lateral pillar)
  -outcome (moss, stulberg)
  (World Cup Shares Love, Money & Strength)
• USG- synovitis
• Radio isotope scintigraphy(Tc99)- highly sensitive
• Arthrography- exact size of femoral and acetabular articular surface can be determined
• MRI- most sensitive, diagnose early, shows extent of necrosis

Waldenstrom’s classification (IFHR-Initial Foetal Heart Rate)

1. Ischaemia / Necrosis –
   -decrease head size due to ossification arrest
   -cartilage hypertrophy of both femoral & acetabular side causing lateral displacement (may subluxation) of femoral head

1. Fragmentation / Resorption-
   -pathological subchondral #(Cresent sign of Caffe)
   -collapse of peripheral zone(head within head appearance)
   -metaphysial osteolytic band or cyst
   -lasts from 6month-1 yr.

1. Reossification / Healing-
   -new immature bone replace necrotic bone
   -vulnerable for deformity
   -mushroom shaped head

1. Residual stage-

    -involve healing, remodelling &  sequelae of the disease
    -take 6 mo-5yrs
    -classical changes:-
   
        coxa magna(large head)
        coxa breva(short neck)
        coxa irregularis(irregular head)
        coxa valga/ vara(due to lateral/ medial arrest)
        gt over growth(due to gt apophysis continuous growth)
        OA hip(as early as at the age of 40yr)            
   

Catterall classification

Stage 1:

• Antero-medial portion of head involved and no collapseHeal without significant sequelae.

Stage 2:

• More head involved and may – fragmentation of the involved segment.
• Regeneration without much loss of height and the end result is usually good. Metaphyseal reaction localised.

Stage 3:

• Most of the head involved-May show head within a head.
• The metaphysis is usually diffusely involved – broad neck and the epiphyseal plate is unprotected and also usually involved – results poorer.

Stage 4:

• Whole head involvement and severe collapse occurs early and restoration of the femoral head
  usually less complete .
• The epiphyseal plate is often involved – abnormal growth (coxa magna, coxa breva, coxa vara
  and coxa valga).

Salter – Thompson Classification

• Stage A:
  -Lateral portion of femoral capital epiphysis present .
  -extent of subchondral # less than 50% head involved.

• Stage B:
  -Lateral portion of femoral capital epiphysis absent – extent of subchondral # more than 50% head involved (Lateral margin of epiphysis protects epiphysis from stress)

Lateral pillar classification of Herring

Intact lateral pillar act as a wt bearing syupport to protect the central avascular segment

• Group-A
  -minimal density change in lateral pillar
  -no loss of height

• Group-B
  -density change in lateral pillar
  -loss of height < 50%

• Group-C
  -Early density change in lateral pillar
  -loss of height > 50%

Determine treatment and prognosis

Moss Classification

• Normally the shape of the femoral head doesn’t deviate more then 1mm from a given circle on both AP & Frog leg view.

• If shape fall

    < 2mm= fair outcome
    > 2mm= poor outcome
  

Stulberg’s Classification

• Classified from group I-V
• Tells about prognosis.prognosis is poor if Head at risk sign present
  -small osteoporotic segment on lateral side of epiphysis
  -lataeral displacement of femoral head
  -horizontally oriented growth plate
  -calcification lateral to epiphysis(Gage’s sign)
  -diffuse metaphyseal change
  Extensive involvement of epiphyseal ossification center
  Age > 6yrs
  Early closure of epiphyseal plate
  Advanced stage at the time of presentation
  Female sex

Differential diagnosis (ICE-H):

1. Inflammatory:-
   -Toxic synovitis(transient synovitis)
   -Septic Arthritis (mc- tubercular)
   -juvenile Arthritis (juvenile rheumatoid arthritis)

2. Haematological:
   -Sickle cell anemia
   -Thallasemia
   -Haemophilia
   -ITP
   -Leukemia
   -Gaucher,s disease

3. Congenital:
   -skeletal dysplasia(multiple/ spondyloepiphyseal dysplasia)

4. Endocrine:
   -Hypothyroidism

Goal of treatment:

• Elimination of hip irritability.
• Restoration & maintenance of good ROM.
• Prevention of epiphyseal extrusion & subluxation.
• Attainment of spherical head on healing.

Options:

1. – Observation
2. – intermittent symptomatic trt
3. – Definitive early trt

A.nonsurgical/ B. surgical

1.Observation:-

• Trt of choice for all children < 6yrs
• For children > 6yrs with catteral grs1,2 & salter-thompson gr-A
• Radiographic examination every 3 monthly required
• Persistant loss of motion or evidence of loss of containment may necessiatate a short course (2- 6mo) of non surgical trt

2. Intermittent symptomatic trt:-

• Bed rest
• Abduction traction
• Stretching exercises

Need radiological follow up

3. Definitive early trt:

• Indication:-
  -age> 6yr
  -Catterall gr-3,4 & Salter-Thompson gr-B
  -Loss of containment of head on AP veiw

• Contraindication:
  -Caterall Gr-1 case
  -Caterall Gr-2,3 case in less than 5yrs of age with no signs of head at risk
  -Severe flattening of head
  -Healed cases
  -cases with hinged acetabulum

3A. Non surgical methods:

• Initial traction and gradual abduction with internal rotation
• Orthosis application
  -Atlanta Scottish Rice brace
  -Toronto Brace of Bobechko
  -Hugston A frame
  -Broom Stick Plaster
  -Petrie and Bitenc abduction cast
  -Newington abduction ambulation brace
• Bracing is discontinuid when there is roentgenographic evidence of new subchondral bone,seen in both AP & Frog leg views and measuring subluxation chance from CE angle of Wiberg*.
• Contraindication- incompliant, psychiatric pt
• Disadvantage- jt stiffness, pressure sores, need for frequent change

*Centre-edge angle (Wiberg`s angle)
5-8 years ~19 degrees, 9-12 years ~25 degrees, 13-20 years 26-30 degrees

3B. Early Surgical methods:

Advantage-

– Ability to obtain containment of head
– Period of restriction is two month
– No end point is necessary for trt as the containment is permanent
Methods:-

1. Innominate osteotomy (Salter’s)-
   iliac osteotomy with rotation of entire acetabulum with pelvis and ischium downward, outward & forward with symphysis pubis acting as a hinge.
2. Varus derotation osteotomy(Canale & beaty)-
   subtrochanteric osteotomy (lateral opening wedge/ reverse wedge) with lateral platting . Useful for 8-10yrs old child without limb length discrepancy.

1. Combined innominate and femoral osteotomy
2. Reconstructive surgery(for significant deformity)
   -Muscle (abductor and iliopsoas) release and abduction cast
   -Valgus extension osteotomy
   -Cheilectomy
   -Shelf augmentation procedures
   -Chiari osteotomy
   -Trochanteric advancement

Summary:-

• Definition
• Etiology- AVAST, Trueta n Caffey’s hypothesis
• C/F
• Ix- radiology(WCSLMS classification), USG, Scintigraphy, Arthography, MRI
• D/d- ICE-H
• Trt- Observation, Intermittent symptomatic trt, definite early trt(nonsurgical & surgical)