Slipped Capital Femoral Epiphysis

Introduction SCFE = misnomer neck displaces relative to the epiphysis Usually, upward & anterior of neck Rapid growth, weakening of physis, shearing stresses                                                                                               

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

Incidence/Epidemiology 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%  black males, eastern US Varies less than1-7/100,000 depending on race and geographic location Rarely occurs in girls after menarche

Classification Temporally, according to onset acute, acute-on-chronic, chronic Functionally, according to ability to WB stable, unstable Morphologically, according to extent of displacement Extent of displacement estimated by measurement on XRAY or CT

Temporal Classification Acute 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** True SH1 will not have prodrome, severe trauma, often associated with concomitant hip dislocation

Temporal Classification Chronic 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 Acute-on-chronic 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

Etiology Often unknown Majority are normal by current endocrine work-up Endocrine Mechanical

Etiology 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 Cadaver studies

Etiology 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

Etiology Mechanical Factors 2) Retroversion of Femoral Neck Relative or femoral retroversion ? Physis more susceptible to AP shearing forces 3) Inclination Increased slope of proximal femoral physis on both affected and non-affected sides

Etiology 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 -CRF Prev pelvic XRT, Rubinstein-Taybi syndrome, Klinefelter’s syndrome, 1° hyperparathyroidism, panhypopituitism assoc with intrancranial tumours

Etiology Endocrine Factors Hypothyroidism prior to or during Rx GH deficiency during or after Rx Bilateral slips….prophylactic pinning should be strongly considered

Endocrine Factors CRF Thought to be due to uncontrolled 2° hyperparathyroidism 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

Pathology Do not support or exclude endocrine or mechanical etiologic actors ? Changes 2° physeal disruption or endocrine influence Weiss & Sponseller 1990 Normal iliac crest physeal Bx in pts with SCFE

Pathology Gross 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

Pathology Microscopic 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 History 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 History 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 sign 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 MRI -detection of AVN Bone Scan - uptake for AVN - uptake both sides for chondrolysis

Treatment 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                                                                                               

Treatment Initial Management To radiology in wheelchair or stretcher **Identify unstable slips** Do not attempt frog-leg lateral in unstable slips Admit with strict bedrest, until definitive Rx

Treatment 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 centre 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 Advantages Minimal scarring No need to manipulate limb during surgery Disadvantages 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 Indications Stable slip that has progressed despite fixation Severe slip

Bone Graft Epiphysiodesis

Bone Graft Epiphysiodesis

Primary Osteotomy Goals: 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 Intertrochanteric Southwick Based on head-shaft angle Anterolaterally based intertrochanteric wedge Corrects extension/varus deformity by flexion/abduction of distal fragment, IR as needed Low AVN risk Chondrolysis 10-40%

Treatment Spica Cast Little indication for immobilization alone 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 months

Complications Chondrolysis 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 Treatment Removal hardware Supportive – activity modification, physio, NSAIDs (arthroplasty)

Complications AVN Most severe complication RF: unstable (47%), severe, iatrogenic Evident a few weeks to 1 year after slip Total or partial Poor long-term prognosis Treatment Prevention avoid reduction, manipulation, Rx delay Educate family & patient Delay osteotomy until healed

AVN

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