PERTHES AND SCFE.ppt

Perthes

1. PERTHES DISEASE AND SCFE
DR ARUNODAYA SIDDARTHA

2. DEFINITION

3. HISTORY
Arthur Legg described prominent
characteristics of the disorder: onset
between 5 and 8 years, history of
trauma, painless limp, minimal or no
spasm or shortening of affected limb.
Jacques Calvenoted that affected
individuals had minimal atrophy of
the leg and no palpable hip swelling;
abnormal or delayed bone formation

4. Georg Perthesobserved the disorder as “a
self limiting, non inflammatory condition,
affecting the capital femoral epiphysis with
stages of degeneration and regeneration,
leading to restoration of the bone nucleus”
Henning Waldenstromreported radiographic
changes associated with the disorder in
1909; thought the disease was a form of
Tuberculosis.

5. Epidemiology
Incidence 1-4/10,000
Age 4 -10years; average 7 yrs
As early as 2yrs as late as teens
Boys : girls 4:1
Bilateral 10-12%
No evidence of inheritance
Common in Caucasians; rare in black races

7. ETIOLOGY
1. Vascular supply: Medial circumflex artery is missing or obliterated and obturator
artery or lateral epiphyseal artery also affected.
2. Increased intra-articular pressure
3. Increased intraosseous pressure: Impaired venous drainage in femoral head
4. Coagulation disorder: Absence of factor C or S, increase in serum levels of
lipoproteins, thrombogenicsubstance, Factor V Leiden mutation.
5. Growth hormones-Reduced levels of growth hormones, somatomedin A and C.

8. 6. Social conditions-Lower socioeconomic status, dietary and environmental
factors.
7.Trauma: Risk of vascular interruption increased due to narrow passage and
thick cartilage of femoral head penetrated by lateral epiphyseal arteries
8. Abnormal growth and development: Bone age is lower than chronological
age by 1-3 yrs(Radiological pause). Usually shorter than their peers.
9. Genetic factors
-Inheritance 2-20%; inconsistent pattern.
-Low birth weight, abnormal birth presentations.
-Ratio of affected 1
st
, 2
nd
, 3
rd
and 4
th
degree relatives to general
population of the same set –35: 4: 4:1

9. Pathophysiology
Rapid growth occurs in relation to devlopmentof blood supply
Interruption of blood supply results in necrosis, removal of necrotic
tissue, and its replacement with new bone.
Bone replacement may be so complete and perfect that completely
normal bone may result
The adequacy of bone replacement depends on
Age of the patient
Congruity of the involved joint

10. Sources of blood supply
Up to 4years
Metaphysealvessels
Retinacularvessels
Ligamentumteres–scanty
4 to 7 years
Metaphysealvessels ceases
Above 7years
Vessels in ligamentumtereshave developed

11. Pathology
Goes through stages which may last 3 to 4 years
Stage1
Ischaemia and bone death, cartilage thickens
Stage 2
Revascularization and repair
Dead marrow replaced by granulation tissue
Bone revascularized and new bone laid down
Dead bone resorbed, replaced by fibrous tissue, fragmentation
Stage 3
Distortion and remodelling
Restoration of femoral archtecture or collapse
Femoral head displaces laterally in relation to acetabulum

14. Classification
Waldenstromclassification
Catterallclassification
Salter and thompsonclassification
Herring classification

16. Stage Ia Stage Ib Stage IIa Stage IIb
Stage IIIa Stage
IIIb
Stage
IV

17. Catterall classification
Group I: Only anterior portion of epiphysis
affected
Group II: More of anterior segment involved;
central sequestrum present
Group III: Most of the epiphysis sequestrated,
with unaffected portions located medial and
lateral to central segment
Group IV: Entire epiphysis sequestrated
BENIGN
PROGNOSIS
REQUIRE
TREATMENT

18. CATTERALL classification

19. Group I Group
II
Group III Group IV

20. HEAD-AT-RISK FACTORS
Lateral subluxation of femoral head
Radiolucent V in the lateral aspect of
epiphysis (Gage sign)
Calcification lateral to epiphysis
Horizontal physealline
Metaphyseal cyst

21. Salter-Thompson
classification
Based on extent of subchondral fracture on AP
and lateral views
Group A: Less than half of femoral head
involvement
Group B: More than half of femoral head
involvement
Advantage: Applicable at an earlier time point
than Catterallor lateral pillar classification
Disadvantage: Subchondral fracture present in
only 30 % of patients

22. SALTER sign
As disease progresses, a
subchondral fracture may be seen
on anterolateral aspect of femoral
capital epiphysis
Crescent sign/ Caffey’s sign
Early radiographic feature best
seen on frog leg lateral view

24. HERRING’s LATERAL PILLAR
Classification

25. Bilateral involvement
More severe than unilateral
Boys and girls equally affected
Independent event
Bone age delayed in perthes disease

26. ClInical features
Incidence: higher latitude, western coastal region of South India
Onset: 18 months to skeletal maturity (Most prevalent: 4-8 years)
Male sex prevalence: Boys 4-5 times more susceptible
Involvement: Bilateral in 10-12 %

27. SYMPTOMS
Limp
Pain
History of antecedent trauma
Waxing and waning symptoms

28. SIGNS
Small stature
Atrophy of gluteus, quadriceps and
hamstring muscles
Abductor limp ( Antalgic +
Trendelenburg gait)
Decreased hip ROM especially abduction
and internal rotation (Transient early in
disease, persistent later on)
Positive Trendelenburg test
Resistance to logroll

29. Investigations
Blood tests
haemogram, ESR, CRP
Imaging
Plain X-rays
Hip U/S
Bone scintigraphy
MRI
Dynamic arthrography
Assess spherityof femoral head
Hinge abduction
Bilateral perthes
Skeletal survey as part of work-up

30. MRI
Accurate for early diagnosis and for
visualising configuration of femoral head
and acetabulum
More reliable information about true
extent of femoral head necrosis than
radiography or scintigraphy
Gadolinium enhanced subtraction MRI as
effective as scintigraphy in delineating
epiphyseal necrosis early
De Sanctisclassification:
Group A: < 50 % head necrosis
Group B: > 50 % head necrosis
B0-B3 based on degrees of lateral
extrusion and physealdisruption

31. TREATMENT OPTIONS
1. SYMPTOMATIC THERAPY
Bed rest
Non weight bearing on affected limb
Short term use of NSAIDs
Traction:
Simple longitudinal traction
Balanced suspension and traction
Russell traction
“Slings and springs”

33. CONTAINMENT BY BRACING OR CASTING:
Aims at repositioning extruded anterolateral part of femoral
epiphysis into confines of acetabulum
Achieved by abducting and flexing or internally rotating the hip
Needs to be ensured until healing progresses beyond late part
of stage of regeneration ( upto2 years)
Femoral head reforms in a concentric manner-Biological
plasticity

34. Broomstick plasters (Petrie casts)
Snyder sling
A-frame
brace
Toronto brace

35. Treatment: Two main choices
Conservative
Pain control
Gentle exercises
Regular re-assessment
Avoid sport and strenous activities
Containment
Hold hips widely abducted in cast/brace >1yr
Operation
Varus osteotomy of femur
Innominate osteotomy of pelvis
Both

37. Herring Guidelines to treatment
Children <6years
Symptomatic treatment
Children >6years; bone age more imp than chronological age
Bone age at or <6yrs
Lateral pillar A or B/ caterallI and II
Symptomatic treatment
Lateral pillar C/ CaterallIII and IV
Bone over 6years
Herring A and B/CaterallI and II
Abduction brace or osteotomy
Herring C/CaterallIII and IV
Outcome unaffected by treatment
Children 9yrs and older
Except in very mild cases, operative containment is the treatment of choice

38. Prognostic features
Age
<6yrs; good regardless of treatment
6-9years; not always satisfactory with containment
>10yrs; questionable benefit from containment, poor prognosis
Gender
Girls have worse prognosis
Classification grade
Herrings lateral pillar classification
Salter and thompsongrade B worse prognosis
Caterralclassification grade
Caterral“head-at-risk” signs
The five signs carry worse prognosis
Others
Body weight, decreased ROM

39. SLIPPED CAPITAL FEMORAL EPIPHYSIS

40. SCFE
Slipped capital femoral epiphysis (SCFE) is an condition of the proximal
femoral physis thatleads to slippage of the metaphysis relative to the
epiphysis,and is most commonlyseen in adolescent obese males

41. EPIDEMIOLOGY
Most common disorder affecting adolescent hips
Found in 10 per 100,000
More common in
Obesechildren, associated with puberty
Males(male to female ratio is 2:1.4)
Specific ethnicities-African Americans,Pacific islanders, Latinos
During period ofrapid growth(10-16 years of age)
location
left hip is more common
bilateral in 17% to 50% (~25%)

42. RISK FACTORS
Obesity
Single greatest risk factor
Recent data shows trend towards younger age and increased frequency of
bilaterality at presentation, possibly related to increased rates of
childhood obesity
Acetabular retroversionandfemoral retroversion
Increased mechanical shearing forces at the physis
History of previousradiation therapyto the femoral head region

44. PATHOPHYSIOLOGY
Due mechanical forces acting on a susceptible physis
Pathoanatomy
Slippage occurs though thehypertrophic zoneof the physis

45. PATHOPHYSIOLOGY
Perichondrial ringthins and weakens
Undulating mammillary processes in physis unlocks, further
destabilizing the physis
Physis is still vertical in this age group (160°at birth to 125°at skeletal
maturity), resulting in increased shearing forces
Epiphyseal tubercle can provide a rotational pivot point
Anatomic structure in the posterior superior epiphysis that shrinks with
skeletal maturity
Cartilage in the hypertrophic zone acts as a weak spot

46. PATHOPHYSIOLOGY
Angulation
Metaphysistranslatesanterior
and externally rotates
Epiphysisremains in the
acetabulum, liesposterior to the
translated metaphysis
Similar toSalter-Harris type
Ifracture

47. PRESENTATION

48. CLINICAL FEATURES
Abnormal gait / limp
Antalgic, waddling, externally rotated
gait or Trendelenburg gait
Decreased hip motion
Obligatory external rotationduring
passiveflexion of hip (Drehmannsign)
Due to a combination of synovitis and
impingement of the displaced anterior-
lateral femoral metaphysis on the
acetabular rim

49. CLINICAL FEATURES
Loss of hip internal rotation, abduction, andflexion
Abnormal leg alignment
Externally rotated foot progression angle
Weakness
Thigh atrophy

50. ASSESSMENT XRAY

52. CLASSIFICATION

53. TREATMENT
Percutaneous in situ
fixation.
Contralateral prophylactic
insitu fixation.
Severe cases:
open epiphyseal
reduction and fixation.
proximal femoral
osteotomy

54. TREATMENT

55. a)MCQ’s
1)Average age of onset of perthesdisease is :
a)5y
b)6y
c)7y
d)8y

56. 2)Which of the following is true:
a)Autosomal dominant
b)Bilateral in 1-2%
c)Boys : girls -1 : 4
d)Self limiting

57. 3)Which of the following is head at risk sign:
a)Salters sign
b)Gazes sign
c)Caffeys sign
d)Crescent sign

58. 4)Gazes sign means:
a)Radiolucent V in lateral aspect of epiphysis
b)Metaphyseal crest
c)Lateral subluxation
d)Horizontal physealline

59. 5)Metaphyseal vessels ceases at :
a)At birth
b)1-2y
c)4-7y
d)10y

60. 6)Perthes disease is a self limiting disease, it ,ay last for:
a)2-3 months
b)1-2y
c)3-4y
d)7-8y

61. 7)What sign is this:
a)Gazes sign
b)Salters sign
c)Galeazzi sign
d)Caffeys sign

62. 8)Which of the following is false with respect to SCFE:
a)Common in males
b)Seen in obese children
c)Not associated with puberty
d)Incidence : Left > bilateral > right

63. 9)In SCFE, slippage occurs through which zone of physis:
a)Proliferative
b)Reserve
c)Hypertrophic
d)Spongiosa

64. 10)What sign is this:
a)Salters sign
b)Crescent sign
c)Drehmannsign
d)Trethowansign

65. THANK YOU