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Slipped Capital Femoral Epiphysis

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									Slipped Capital Femoral

      Dr. Muaz Alghadir
 SCFE = misnomer
  neck displaces relative to the epiphysis
 Usually, upward & anterior of neck
 Rapid growth, weakening of physis, shearing
 Femoral head in contact
  with acetabulum
 Femoral shaft and neck
  rotate externally
 Head moves posteriorly
 Neck moves cephalad
        Historical Perspective
 ? Pare 1572 first described SCFE
 ? Muller 1889
    Schenkelhalsverbiegungen im Jungesalter
    “bending of the femoral neck in adolescence”
 Whitman 1909 osteotomies
 Boyd 1949 stabilization with pins
 Varies according to race, sex, geography
 Estimated 2 per 100,000
 Males > females      left > right
 During adolescence, @ max skeletal growth
      boys 13-15 years, avg 14
      girls 11-13 years, avg 12
   Bilateral 17-80% reported
      most studies show 20-25%

   Temporally, according to onset
     acute, acute-on-chronic, chronic

   Functionally, according to ability to WB
     stable, unstable

   Morphologically, according to extent of displacement
      Temporal Classification
 Sudden, dramatic, fracture-like episode
 Prodromal symptoms for 3 weeks or less
 Trauma too trivial to cause SH1
 X-rays- little or no neck remodeling
 AVN frequent, 17-47%

**R/O true Salter-Harris Type 1**
        Temporal Classification
 Most frequent form
 Few months of vague groin/thigh pain, limp
 X-rays- remodeling of neck
 Can be missed as symptoms as often minor
      Temporal Classification

 Prodrome for > 3 months with sudden
  exacerbation of pain
 X-rays- displacement beyond remodeling
    Functional Classification
 Stable
     able to WB on presentation
 Unstable
     not able to WB
 Preferred classification
 Clinically meaningful
     different prognosis
      Morphologic Classification
   Degree of displacement of epiphysis on neck
   Southwick femoral head-shaft angle
     mild < 30°
     moderate 30-60°
     severe > 60°
     (normal 145° on AP)

   CT more accurate, not routinely used
 Often unknown
 Majority are normal by current endocrine

 Endocrine
 Mechanical
            Mechanical Factors
   Predisposing features:
     -thinning of perichondral ring complex
     -retroversion of femoral neck
     -change in inclination of prox femoral
      physis relative to femoral neck/shaft

   Blount’s disease, peroneal spastic flatfoot, Legg-
    Calve-Perthes disease
         Mechanical Factors
    1) Perichondral Ring Thinning

 Fibrous band that encircles physis at cartilage-
  bone interface
 Acts as limiting membrane, mechanical
  support to physis
 Thins rapidly with maturation  strength
           Mechanical Factors
    2) Retroversion of Femoral Neck

 Relative or femoral retroversion
 ? Physis more susceptible to AP shearing
              3) Inclination
   Increased slope of proximal femoral physis on
    both affected and non-affected sides
            Endocrine Factors
 Long suspected
 Obesity, hypogonadal males (adiposogenital
  syndrome), growth spurt
 No screening unless clinical suspicion
 Known association with:
   -hypothyroidism (treated or not)
   -conditions with GH administration

   Prev pelvic XRT, Rubinstein-Taybi syndrome,
    Klinefelter’s syndrome, 1° hyperparathyroidism,
    panhypopituitism assoc with intrancranial tumours
            Endocrine Factors
 Hypothyroidism
   prior to or during Rx
 GH deficiency
   during or after Rx

   Bilateral slips….prophylactic pinning should
    be strongly considered
           Endocrine Factors
   Thought to be due to uncontrolled 2°

 Goal of Rx: control hyperparathyroidism
  within 2/12 of slip sx
       If not successful  surgical Rx
 Monitor until skeletal maturity due to high
  incidence of slip progression
 Do not support or exclude endocrine or
  mechanical etiologic actors
 ? Changes 2° physeal disruption or endocrine

Weiss & Sponseller 1990
 Normal iliac crest physeal Bx in pts with SCFE
 Periosteum stripped from ant/inf surface of
  femoral neck
 Area btw neck & post periosteum fills with
  callus & ossifies
 Anterosuperior neck forms “hump”, can
  impinge on acetabular rim (remodel)

Acute slips will have hemarthrosis
 Howorth 1949 169 slips treated open
“Preslip” stage
   -widened physis without displacement
   -edematous synovial membrane,
    periosteum, capsule
 Thicker proliferative & hypertrophic zones
    - chondrocytes, organized in clumps
               Clinical Picture
                Stable SCFE
 vague or dull pain (groin, anteromedial thigh, knee)
 Exacerbated by activity
 Weeks to months

Physical Exam
 Antalgic limp with  ER
 Thigh atrophy
  hip ROM- loss of IR,ABD, flexion
 Obligate ER with flexion, pain at extreme IR
 Hip flexion contracture (chondrolysis)
 No strenuous maneuvers, i.e. hopping/squatting
             Clinical Picture
             Unstable SCFE
 Sudden onset of severe pain
 Minor fall or twisting injury

Physical Exam
 Held in ER
 Refusal to move hip
 Moderate shortening
**Always examine hips in any child with knee pain
 Matava et al. (1999) 106 slips
  15% knee/distal thigh pain only

   Carney (1991) 46% distal thigh/knee as only
    presenting complaint

**Always examine/x-ray contralateral side
 20% have evidence on initial presentation
         Diagnostic Imaging
         Plain Radiographs
 Often only imaging needed
 Earliest sign = physeal widening/irregularity
 Klein’s Lien (AP)
   - line tangential to superior femoral neck
     will intersect lateralmost portion
   - with SCFE,  overlap or none =Trethowan’s
 Steel’s metaphyseal blanch sign (AP)
    crescent-shaped area of density
Metaphyseal blanching
           Diagnostic Imaging
 CT
  -useful in mgmt
  -confirm physeal closure
  -severity of deformity
  -detection of AVN
 Bone Scan
  - uptake for AVN
  - uptake both sides for chondrolysis
   Goal: stabilize the epiphysis to the femoral neck to
    prevent further slippage
   In situ fixation/pinning
   Bone graft epiphysiodesis
   Primary osteotomy
   Spica Cast

Treatment Choice depends on type pf slip, severity,
  surgeon preference
         Initial Management
 To radiology in wheelchair or stretcher
 **Identify unstable slips**
 Do not attempt frog-leg lateral in unstable
 Admit with strict bedrest, until definitive Rx
               Stable SCFE
In Situ Pinning/Fixation
 Many different philosophies
   number/type of implant, physeal closure, position
   of screws
 Current standard: one cannulated screw into
   femoral epiphysis from base of anterior neck for
   stable slips.
  Two screws considered for unstable slips
   (additional stability, rotational control)
             In Situ Fixation
 Fracture table
 Avoid excessive IR & manipulation
 Guide-wire for screw placement
 Ideal placement of screw is as close to centre of
  epiphysis & as  to physis as possible
 **epiphysis is posterior, entry point must be at
  base of neck and screw directed posteriorly into
  Avoid posterior femoral neck
In Situ Fixation
          In Situ Fixation
    Post-operative Management
 Protected partial weight-bearing with
  crutches for 6 weeks
 No sports for 3 months
 Clinical exam + x-rays every 3-6 months
  until skeletal maturity
              In Situ Fixation
 Minimal scarring
 No need to manipulate limb during surgery

 Difficult lateral view
 Difficult guidewire placement if obese
 Screw-related complications
    perforation into joint, loss of fixation, failure,
    Bone Graft Epiphysiodesis
 Portion of residual physis is removed by drilling
  and curettage
 Dowel or “peg” of autologous bone graft inserted
  across femoral neck
 Supplementary internal fixation or cast for
  unstable slips

 Stable slip that has progressed despite fixation
 Severe slip
Bone Graft Epiphysiodesis
Bone Graft Epiphysiodesis
        Primary Osteotomy
 Correct symptomatic loss of motion, esp.
  flexion and IR
 Improve biomechanics for healing
 Improve longevity of the hip
        Primary Osteotomy
         Dunn Procedure
 Anterosuperior wedge of superior femoral
  neck, including residual physis
 Femoral epiphysis is reduced on neck
  without tension
 Secured with screws or pins

 Best anatomic restoration
 High risk of AVN
       Primary Osteotomy
          Base-of Neck
   Kramer & Barmada
   Expose neck intra or extracapsularly
   Anterosuperiorly based wedge from base of neck
   Apex of wedge may be extracapsular posteriorly
   Reduction and punning as in Dunn

   Lower AVN risk
             Primary Osteotomy
 Southwick
 Based on head-shaft angle
 Anterolaterally based intertrochanteric
 Corrects extension/varus deformity by
  flexion/abduction of distal fragment,
  IR as needed

 Low AVN risk
 Chondrolysis 10-40%
                Spica Cast
 Little indication for immobilization
 Often used as adjunct to
  surgical treatment
 May be used if surgery
 contraindicated or other treatments
 have failed
       Anterior & Valgus Slips
 Valgus slip = superior and posterior displacement
 Valgus  adduction, flexion
 Anterior  extension, ER

   Same treatments
     watch for femoral neurovascular bundle
     with valgus slip
        Prophylactic Pinning of
           Contralateral Hip
   20% present with bilateral involvement
   Additional 25% will have symptomatic
    contralateral slip
   Most develop within 6 months
   Ongoing debate
   Consider in CRF (95% bilateral), endocrinopathy-
    related slips, younger patients
   If not done, educate parents and monitor every 6
 Incidence and etiology unknown (5-7%)
 Stiffness, persistent groin or thigh pain
 Painful ROM, flexion contracture
 RF: pins, cast immobilization, severe, chronic
 X-rays:  joint space
          50% loss or  3mm
 Usually 6 weeks to 4 months after Rx, max within 6-12
  months of onset
 Removal hardware
 Supportive – activity modification, physio, NSAIDs
 Most severe complication
 RF: unstable (47%), severe, iatrogenic
 Evident a few weeks to 1 year after slip
 Total or partial
 Poor long-term prognosis
 Prevention
   avoid reduction, manipulation, Rx delay
 Educate family & patient
 Delay osteotomy until healed
       Long-term Outcomes
 Risk of OA directly related to severity of
  residual deformity
 Significant potential for remodeling
    delay treatment until skeletal maturity
 Evidence that osteotomy alters the
  development of OA is lacking

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