1. Legg-Calve´-Perthes’ disease Prof. J. Sahoo

2. Deffination
Perthes’ disease is shelf limited condition of capital femoral epiphysis due to lack of adequate blood supply with sharp limitation of age as well as sex.
Incidence:
Age 5-10 (3-12)
Sex M:f (4:1)
Bilateral rare about 10%.

3. Synonyms: Coxaplana Osteochondritis deformans coxajuvenitis Pseudocoxalgia

4. This condition was found out by three important Orthopedics surgeons synchronously
Arthur Legg
Jacques Calve’
George Perthes

5. BLOOD SUPPLY TO FEMORAL HEAD Anatomy
Medial and lateral femoral circumflex arteries.
Lateral ascending cervical artery- After penetrating the lateral capsul in posterior trochanteric fossa.
Intracapsular ring has been found to be incomplete more often in boys than girls.
Minimal blood is supplied through the ligamentum teres.
(5-7 years) the supply from the lateral epiphysial artery is receding and from midial side arterial supply is yet to be developed.

6. Legg-Calve´-Perthes disease
Aseptic, idiopathic osteonecrosis of the femoral epiphysis
Growth of the ossific nucleus stops and the bone becomes dense
It is subsequently resorbed and replaced by new bone

7. Legg-Calve´-Perthes’ disease
Etiology
Trauma
Hereditary factors
Coagulopathy
Idiopathic
Altered arterial status of femoral head
Abnormal venous drainage
Abnormal growth and development
As a sequelae to synovitis.

8. Level of affection according to possible pre disposing factors.

9. Pathogenesis
Articular cartilage becomes thick getting nutrition from synovial fluid where as deeper zone of epiphysis is under nurished thus it become thin, wide and cyst formation in metaphsis (Ischaemia).
Impaired and uneven revascularation following repeated infarction being aggravated by mechanical forces following subluxed head- deformed head (Resorption, repair and remodel).

10. Thus Waldenstorm staged the pathological process into 4 stages:
Initial or Ischemic stage
Resorption or fragmentation stage
Reparative stage
Remodelling stage

11. Legg-Calve´-Perthes disease
Pathologic Anatomy
Stage of increased density
Fragmentation phase
Healing phase

13. Legg-Calve´-Perthes disease
Stage of increased density
Areas of necrotic bone
Subchondral fracture -Collapsed trabeculae
Thickened articular cartilage

14. Legg-Calve´-Perthes disease
Fragmentation phase
Signs of repair are found
“creeping substitution”
Loss of height of the femoral head
Growth plate is irregular and disrupted

15. Legg-Calve´-Perthes disease
Healing phase
Both woven and lamellar, predominates
Trabeculae and marrow spaces regain a normal architecture

16. Legg-Calve´-Perthes disease
Changes soft tissue of the hip joint
Synovitis
Articular cartilage hypertrophy
Irreversible femoral head deformation
Stresses of weight‑bearing pass across the acetabular margin
Incapable of withstanding physiological stresses

17. Classification of Perthes disease
According to stage of disease –
Waldenstrom classification
According to Prgnosticate outcome-
Catterall classification
Salter and Thompson classification
Herring lateral pillar classification
According to definning outcome-
Stulberg classification

18. Waldenström Classification
Stage-I: Stage of increased density
Stage-II: Fragmentation stage
Stage-III: Healing or reossification stage
Stage-IV: Healed or remodeling stage
Catterall classification
Group-I
Group-II
Group-III
Group-IV

19. Group-I Group-II Group-III Group-IV
Affection of only a small part of the anterior epiphysis
Group-II
More of the anterior segment is involved
Central sequestrum is present
Epiphyseal height is preserved.
Group-III
Most of the epiphysis is “sequestrated”
Unaffected portions located medial and lateral to the central segment
Group-IV
The whole epiphysis is sequestrated

21. Herring Lateral Pillar Classification
A- Minimal density change, no loss of height
B- Some density change, Height ≥50%, Central pillar collapse
C- Height < 50%
The Stulberg Classification System
Group-I: Femoral head normal
Group-II: Femoral head round, within 2 mm of circle, same circle both views
Group-III: Femoral head ovoid, acetabulum matches head

22. Group-IV: Femoral head flattened more than 1 cm on weight-bearing areas, acetabulum also flattened
Group-V: Femoral head collapsed, acetabulum not flattened

23. Clinical Features Painless limp leads to painful limp
Pain in the groin very often refer to knee
Antalgic & trendelenburg gait
Decrease range of motion especially abd, internal rotation, to some extent flexion
Atrophy of thigh muscle
Short limb

24. Investigation required
X-ray-AP & frog lateral view
Crescent sign
Salters sign
Caffey’s sign
USG
Arthrography
Bone scan
MRI

25. Co-relation between clinico, radio & pathological state
First stage
Clin.- Pain, complain around knee or almost normal.
Rad.- Dense head
Path.- Interrupted blood vessels, more venous obstruction with few bone cell deat
Second stage:
Clin.- Restriction of abd, internal rotation at times flexion. (abd in flex.) Mild atrophy
Rad.- Increased density and flattening.
Path.- collapse of trabecular bone.

26. Third stage: Fourth stage: Clin.- Pain and stiff hip
Rad.- Fragmentation(ant, sup & lateral aspect of epiphysis)
Path.- Osteoclast invasion.
Fourth stage:
Clin.- Recovery of some movements of hip with reduction of pain.
Rad.- Mushroom head, coxa plana.
Path.- Revascularization & recanalisation.

27. Changes of Neck First Stage- Normal
Second Stage- Some cystic change & wide
Third Stage- Looks bend.
Fourth Stage- Short & Bent (Coxa vara)
Changes of acetabular cavity
Ist- Increased ( Thick articular cartilage)
Iind & IIIrd- More increased ( Hypertrophy of ligamentum Teres).

28. CHANGES OF ACETABULUM
In late stage ( III & IV) becomes irregular and coveted, secondary to changes of head.
CHANGES OF ARTICULAR CARTILAGE OF HEAD
Hypertrophy in IInd and IIIrd stage
CHANGES IN SYNOVIAL MEMBRANE
Hyper plasia in IInd & IIIrd stage
CHANGES IN CAPSULE & MUSCLE
Contracted & atrophy in IIIrd & IVth stage

29. Cateral “ Head at Risk” Signs
Clinical:
Progressive loss of hip motion more so abduction
Obese child
Radiological:
Gage sign
Calcification lateral to epiphysis
Diffuse metaphyseal rarefaction
Lateral extrusion of femoral head
Growth disturbance of physis

30. DIFFERENTIAL DIAGNOSIS
Transient synovitis
Coxavara (ICV & ACV)
Tuber culosis of hip
Limp (Clinical high suspicious index)
0 to 1year CDH
1 To 5years ICV
5 to 10years LCP
10 to 15years TB

31. Treatment : AIM Objectives Restoration and full mobility of hip
Active containment of femural head
Resumption of weight bearing and full activity as soon as possible.
Objectives
To produce a normal femoral head and neck
To produce a normal acetabulum
A congruous hip which is fully mobile
To prevent degenerative arthiritis of the hip later in life

32. Factors influencing the prognosis
Younger the age of onset better is the prognosis.
> 9- Poor
Extent of involvement of head
Male- Good prognosis
Catterall “head at risk” signs
Passive containment
Type of treatment render

33. TREATMENT PROTOCOL
Initial phase- Restoration of normal looking head and maintain mobility.
Active phase- Active containment and maintenance of full mobility.
Reconstructive phase- Correction of residual deformities

34. Types of treatment adopted
Conservative Surgical
Traction Inominate osteotomy
Plaster cast Femoral varus osteotomy
Orthosis Combination of both
Valgus osteotomy
Arthroplasty

35. TREATMENT ACCORDING TO AGE
< 5yrs: Traction in 20 degree abduction followed by weight relieving caliper
> 5yrs: Without head at risk sign conservative treatment (Plaster spica followed by caliper)
> 5yrs: With head at risk- varus osteotomy ( inominate osteotomy of salter does not give gratifying result alone)

36. Treatment according to the stage of perthes’ disease
Initial phase -
Physiotherapy - Active and passive ROM exercises to restore motion
Traction - B/L skin traction and gradually abducting over 1-2 weeks till full abduction is regained
Weight relieving caliper
Active phase
Aim is to have containment
Conservative
Ambulatory - wt relieving caliper (Toronto orthosis, Newington orthosis. Birmingham brace etc)
Non-ambulatory - Abduction Broomstick, plaster cast ,Hip spica cast
Surgical – different osteotomies

37. Utility of brace Keep head in acetabulum
Pressure of acetabular rim on head is avoided
Head is equally pressurized
Maintain good range of movement
Perpetuate formation of spherical head

38. Indication of different osteotomy procedures
Passive abduction leading to full containment – subtrochanteric adduction osteotomy
With hinged acetabulum, (Deformed head is obstructed to enter into acetabular cavity – valgus osteotomy)
Inominate osteotomy is indicated with flat head (usually is combined with axer)
Chilectomy is indicated to relive the prominent lateral part to achieve containment

39. Total hip joint replacement is the gold standard for neglected perthes’ disease with degenerative changes found in both components of hip joint in elderly patients

40. Critical biomechanical observation of different deformities observed with perthes’ disease
Head - Flat, irregular, deformed with loss of spherocity
Neck – wide, short and in varus position
Trochanter – broad, prominent (beaking)
Limb as a hole is short
All these deformities could be explained with one preposition and i.e.,………………..

41. Biomechanical analysis of different changes in prox femur
Add Force >>>> ABD Force
Capital femoral epiphysis pushed laterally
Horizontal position of metaphyseal plate
Lateral subluxation of capital femoral epiphysis
Irregular growth of head in relation to normal growth of trochanter-thus beaking
Lilfting of abductor attachment
Weakening of abductor force
Vicious Cycle revolves

42. Thus its seems that the hole pathological deformities scenario could be changed tackling the disparity between adductor and abductor force at the outset to nip the problem in bud