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12/5/2016 1 Update: The Pediatric and Adolescent Hip Melissa Moran Tovin, PT, MA, PhD, PCS Alicia FernandezFernandez, PT, DPT, PhD Fran Guardo, M.Ed., MPT, DPT Objectives: By the end of this presentation, participants will: Discuss the epidemiology, client profile, assessment strategies, common mechanisms, postsurgical considerations, and rehabilitation considerations of hip dysplasia, congenital femoral deficiency, slipped capital femoral epiphysis, and LeggCalvéPerthes disease in the pediatric and adolescent patient. Compare and contrast the clinical presentations of each of the disorders presented Apply evidence based assessment and intervention strategies to patients who present with one of these disorders Developmental Dysplasia of the Hip (DDH)

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Update: The Pediatric and Adolescent HipMelissa Moran Tovin, PT, MA, PhD, PCS

Alicia Fernandez‐Fernandez, PT, DPT, PhD

Fran Guardo, M.Ed., MPT, DPT

Objectives:

By the end of this presentation, participants will:

Discuss the epidemiology, client profile, assessment strategies, common mechanisms, post‐surgical considerations, and rehabilitation considerations of hip dysplasia, congenital femoral deficiency, slipped capital femoral epiphysis, and Legg‐Calvé‐Perthes disease in the pediatric and adolescent patient.

Compare and contrast the clinical presentations of each of the disorders presented

Apply evidence based assessment and intervention strategies to patients who present with one of these disorders 

Developmental Dysplasia of the Hip (DDH)

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Developmental Dysplasia of the Hip (DDH)

• Spectrum of hip disorders• Mildly dysplastic but stable, to severely dysplastic and frankly dislocated hip 

• Pre‐natal or postnatal atypical development of the hip causes an abnormal relationship between the femoral head and acetabulum, and can result in both subluxation and dislocation of the joint 

Typical DDH in Infancy

• Most common abnormality in the neonate• ≈ 1 out of 20 full‐term babies are born with some hip instability

• 2‐3 out of 1,000 infants require treatment   

• Several Risk factors associated with DDH in otherwise healthy infants 

• Postural deformities associated:  torticollis and lower extremity deformities

• Improper swaddling with the hips and knees in extension and limited abduction, as practiced in some cultures 

• Female sex, positive family history, race and intrauterine position are the most critical risk factors 

• Early diagnosis and treatment • Hip abduction positioning devices can improve long‐term outcomes 

• Screening begins immediately following birth• Identification of risk factors

• Physical examination of the newborn

• Clinical provocative tests

• May also include static and dynamic ultrasound examination to detect skeletal abnormalities and instability of the hip joint

• Advantages over CT and MRI  

• Minimal evidence

• Neonatal screening using a combination of clinical examination and selected ultrasonic examination is recommended by the American Academy of Pediatrics (AAP).

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• Physical examination• Check for conditions associated with DDH such as torticollis, or other postural deformities.

• Observe both lower extremities in supine without diaper

• Femoral shortening (Galeazzi sign)

• Skinfold asymmetry 

• Hip abduction • Limited hip abduction will develop by three months of age on the affected side

• <60 degrees 

• If DDH is bilateral  limited abduction in both hips. 

• There is a higher incidence of DDH of the left hip (60%) than the right hip (20%), or both hips (20%). 

• Ortolani and Barlow tests‐ performed on each hip separately (up to age 3 months)

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• Physical and sonographic screenings may result in false positives, and signs of instability disappear within a few weeks.  

• Unless examination reveals actual dislocation, the infant can be observed for 3‐6 weeks before treatment is initiated. 

• DDH may go undiagnosed until the child is 18 months or older. • Physical assessment after age 9 months will focus on secondary signs of hip dislocation:  

• Restricted abduction

• Leg length discrepancy

• Trendelenburg limp (may be the first sign)

Prevention and Treatment during Infancy• Parent education: proper positioning and carrying, swaddling • Early treatment during infancy

• Abduction positioning device• Pavlik harness is the most commonly used and recommended device.

• International gold standard for children younger than six months.• 80.2% to 100% success rate

• If unsuccessful, alternative treatment is generally closed reduction under anesthesia with spica casting 

• Treatment of choice for children over six months of age.• If unsuccessful  open reduction

• Involves lengthening tendons, removing obstacles to reduction, and tightening the hip capsule once reduction is obtained.

• In older children, becomes more complex, and by 18 months of age, femoral osteotomies with or without pelvic osteotomies may be necessary.

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Childhood and adolescent DDH

• Infants with DDH are routinely monitored for residual dysplasia into adolescence

• Some may present with dysplasia after skeletal maturity

• Some may not show signs and symptoms of DDH until adolescence.

• Adolescent DDH is distinct from infantile DDH • Higher male incidence, increased bilateral hip involvement, and a first‐order family history of total hip arthroplasty before age 65,conditions and etiologies

• Often not detected until symptoms develop

• Need for screening younger family members of those with osteoarthritis to identify those at risk.

•Most common symptom:  insidious onset of hip pain. • Medical and family history can identify factors associated with DDH and rule out other causes of hip instability. 

• Differential diagnosis:  provocative tests• Impingement test

• Apprehension test • Bicycle test• Confirmation positive findings through imaging

• MRI is preferable to radiographs or CT 

Treatment 

• Untreated  Early degenerative hip arthritis

• Moderate or severe hip dysplasia in adolescents or young adults• Surgical to restore joint stability and mechanics and delay onset of osteoarthritis.

• Several surgical osteotomy approaches

• Severe arthritis and cartilage damage• Nonsteroidal anti‐inflammatory medication and physical therapy until total hip replacement is necessary 

• Post‐surgical Rehabilitation

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Neuromuscular Hip Dysplasia

• Occurs in the presence of neuromuscular disorders

• Diagnosis and management differs from that of typical DDH

• Muscular imbalances and abnormal muscle tone  instability• Posterolateral, and even global, acetabular deficiency

• In contrast to anterosuperior acetabular deficiency seen in typical DDH.

• Assessment and surveillance

Surgical Management

• Tenotomy

• Osteotomies (pelvic and femoral)• Address the acetabular deficiency 

• Optimize coverage of the femoral head

• Femoral derotation

• Arthrodesis

• Arthroplasty

Conservative Management

•Physical Therapy• May delay or prevent the need for surgery • Address and maintain proper hip position

• Identify flexibility and strength imbalances

• Stretching (effectiveness questionable) • Standing programs

• Positioning and orthoses

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• Standing Programs EBP

• Alignment during weight bearing and gait• Walking‐ beneficial in hip development in children with cerebral palsy

• Positioning• Orthoses

Slipped Capital Femoral Epiphysis (SCFE)

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Slipped capital femoral epiphysis

• Separation or slippage of femoral head from neck• Loss of integrity at growth plate

• Incidence: 10.8 cases per 100,000• Most common hip disorder in adolescents.

• Age‐related risk• Growth spurts, 10‐15 y/o

• Average 12.0 boys, 11.2 girls. 

• Gender‐related risk• Males double than females

• Ethnicity‐related risk• Higher in Asians, Pacific Islanders, and African Americans.

Mechanisms

• Localized weakness or excessive stress• Eventually:  plate instability and slippage. 

• Left hip > right hip; bilateral as high as 50‐60%.

• Contributing factors:• Obesity

• Hormones

• Torsional or misalignment issues at hip

• Trauma

• Radio/chemotherapy

Patient profile and differential diagnosis

• Obese adolescent male 

• Intermittent hip or knee pain

• Limping or avoidance of weight bearing

• Hip in ER, obligatory ER in hip flexion (Drehmann sign)

• Decreased ROM of hip IR ROM 

• Differential diagnosis: fractures, AVN in older adolescents, Legg‐Calve‐Perthes Disease in younger children, osteomyelitis, septic arthritis, ischial bursitis, muscle strain, etc

• Refer to orthopedic specialist. Early Dx crucial! Damage is cumulative and irreversible

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Southwick angle: A= mild (<30°), B = moderate (30‐50°), and C = severe (>50°)

Management considerations• Conservative approaches

• Traction, rest, casting, orthoses?

• Little evidence

• Surgical approaches• Preferred, asap

• Goals: stabilize epiphysis, prevent further slippage, avoid complications

• Simplest approach: screw fixation or pinning • Revision surgeries

• Prophylactic fixation of asymptomatic femur?

• Complex cases: osteotomies, arthroplasty

• Emerging techniques: • Computer‐assisted fixation, arthroscopic‐assisted osteoplasty

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Rehab considerations: post‐surgery

• Progressive gait training

• Pain reduction

• Weight‐bearing activities

• Core and lower extremity strengthening

• Range of motion

• Proprioception

• Endurance training

• Return to functional activities

Key focus areas

• Progressive, balanced hip, knee, ankle ROM and strengthening• Hip ROM: emphasize hip flexion, internal rotation, abduction

• Trunk and core strengthening• Gait training

• Within precautions; avoid improper alignment

• Functional training – focus on function and participation• Final period:  

• Advanced coordination, balance, and agility training• Address overall conditioning ‐ >50% of children with SCFE exceed 95th

percentile for weight!

How fast can be progress the patient s/p surgery?

• Cautious! Allow for healing• Avoid aggressive range of motion and strengthening initially

• Depends on: pt tolerance, severity of the injury and surgical procedure

• Appropriate level of activity/ weight‐bearing is controversial• May depend on slip severity

• Mild stable SCFE – 17% no WB restriction

• Most common guideline: toe‐touch WB with crutches for 6‐8 wks, may return to full WB around 8‐10 wks post‐op (x‐ray proof of healing)

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Legg‐Calvé‐Perthes Disease (LCPD)

Legg‐Calvé‐Perthes Disease

• Idiopathic osteonecrosis of the capital femoral epiphysis• Can lead to permanent deformity.

• Incidence (US): between 4 and 15.6 per 100,000 children.

• Bilateral presentation ~ 10‐20% 

• Age‐related risk• Ages 2‐14, average Dx at 5‐7 y/o

• Younger patients (<6 y/o): better prognosis, fewer long‐term complications

• Patients >15 y/o: adolescent AVN of femoral head. 

• Gender and ethnicity‐related risk:• More frequent in Caucasian males (5 males:1 female) 

Mechanisms

• Repetitive mechanical trauma• Hx of synovitis/increased intracapsular pressure

• Coagulopathies or disorders with increased blood viscosity (sickle cell)

• Congenital vascular deformities• Marked growth spurts• Hx of low birth weight

• Steroid use• Leukemia• Graft‐versus‐host disease• Stickler syndrome• Developmental hip dysplasia• SCFE• Etc?

• Interruption of flow to femoral head epiphysis • Superior and inferior retinacular arteries

• Etiology not always known

• Contributing factors:

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Patient profile and differential diagnosis

• Elementary school age• Hip, groin, thigh or knee pain• Antalgic gait and positive Trendelenburg sign• Muscle spasms in iliopsoas and hip adductors• Hip contracture in flexion and adduction• Decreased ROM in hip extension, abduction and IR. • May have obligatory ER in hip flexion (Drehmann sign)• Differential diagnosis: fractures, SCFE, septic arthritis, osteomyelitis, ischial bursitis, muscle strain, etc.

• Refer to orthopedic specialist. Early Dx crucial! • Even with successful treatment, higher risk of hip osteoarthritis as adults.

Disease process

Blood flow interruption

• Symptoms may not appear for months!

Osteonecrosis

• Reduced load‐bearing ability 

• Subchondral fractures and deformation of femoral head 

Self‐limiting process

• Revascularization and reabsorption of necrotic bone 

• Repair contributes to further deformity!

• Bone formation/ resorption imbalance

Waldenstrom’s Classification

Initial or condensation 

stage

Fragmentation or resorptive

stage

Reossificationor healing stage

Residual stage

Four stages of progression based on radiological findings 

Femoral head necrosis, mild flattening, increased radiodensity, medial joint space widens

Increased flattening and fragmented appearance

Appearance of new bone, disappearance of radiodensefragments

Normal radiodensityof femoral head; remodeling of head and acetabulum.

Shape of the femoral head may still change (skeletal maturation). 

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Diagnosis and prognostic factors• Dx: Based on clinical presentation and medical tests

• Radiography/imaging, ultrasound, blood tests.  

• Long‐term outcomes:• Determined by remodeling of femoral head and acetabulum• Remodeling process may take up to 5 years • Also affected by skeletal maturation 

• But decision needs to be made early… Prognostic classification systems• Salter‐Thompson classification

• Crescent sign (subchondral fracture). Classified as group A (<50% involvement, best suited for non‐invasive treatment) or group B (>50%) 

• Catterall classification• Lateral pillar classification 

Catterall classification: Groups I through IV = up to 25%, 50%, 75%, and complete head involvement.

Lateral pillar classification: group A (no loss of height),            B (<50% height loss),                         or C (>50% height loss)

Management considerations

• Watchful waiting or direct intervention?• Risk factors for poor outcome: age ≥6 y/o at Dx, high degree of femoral head necrosis, lateral pillar height < 50%, femoral head coverage <80%

• Strong prognostic factors: Lateral pillar classification (odds ratio, 3.6) and hip abduction range (odds ratio, 4.0)

• Approaches: • Treat EARLY• Key approaches: ROM, WB restrictions, and containment or distraction. • Appropriate ROM (PT, short‐term traction, or casting) is prerequisite for successful containment.

• Novel approaches: • Core decompression, trans‐head‐neck tunneling (THNT) or transphyseal neck‐head drilling

• Pharmaceutical and biological interventions: combos of bone morphogenetic proteins and bisphosphonates; sclerostin antibody; Tumor necrosis factor alpha.

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Containment• Goal: maintain appropriate contact/load distribution, reduce stresses

• Places femur in abd/ IR or abd and flexion: orthoses or surgery • Surgery – clearly superior in children > 8 y/o

• Varus osteotomies, pelvic osteotomies, etc.• May need extensive reconstruction and soft tissue release. 

• PT important adjuvant to both orthotic and surgical containment.• Pre‐intervention period: focus on ROM – iliopsoas, adductor contractures.• Post‐containment period: progressive gait training/WB activities, pain reduction, ROM, strengthening (gluteus medius, hip stabilizers, core), functional training. 

• Good resource with detailed guidelines (US Dept of Health and Human Services, Cincinnati Children's Hospital Medical Center):https://www.guideline.gov/summaries/summary/39444/evidencebased‐care‐guideline‐for‐postoperative‐management‐of‐leggcalveperthes‐disease‐in‐children‐aged‐3‐to‐12‐years

Distraction

• If surgery not possible due to restricted ROM

• Evidence shows increased range of motion (93%), reduced pain (86%)

• After insertion of external fixator:• Partial WB day 2

• Distraction starts day 3, rate 1 mm/day

• PT during distraction process (daily)• Key to maintaining mobility and supporting tissue lengthening

• Complications: pin infections, breakage, or subluxation

Congenital Femoral Deficiency (CFD)

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Congenital Femoral Deficiency• Congenital Femoral Deficiency (CFD) is a rare birth defect that was formerly known as Proximal Femoral Focal Deficiency (PFFD)   

• There is a lack of integrity and stability of the hip and knee (deficiency)

• Malorientation and malrotation of the femur with soft tissue contractures (deformity)

• Femoral shortening (discrepancy)

• Incidence: from 1 in 40,000 live births to 1 in 100,000 live births for those associated with fibular hemimelia, and can present unilaterally or in bilateral femora. 

• Etiology not known• Does not seem to be hereditary

• Some toxin exposure in early pregnancy (thalidomide)

Classifications

• Two main classifications

A. Paley classification: based on radiologic and soft tissue presentations.• Reconstruction and limb lengthening

B. Aiken classification: based solely on radiologic factors.• Amputation or prosthetic reconstruction

CFD Paley Classification

Surgical Considerations

• Reconstruction

‐ Stabilization surgeries

‐ SUPER Hip and SUPER Knee• Lengthening 

• Rotationplasty

• Amputation ‐ if rotationplasty is considered unacceptable.

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Stabilization

• Surgery to stabilize the hip = SUPER HIP

(Systematic utilitarian procedure for   extremity reconstruction)

SUPER HIP operative note

Lengthening

• Lengthening with an external fixator

‐ Often the first lengthening around age 3

‐ Fixator will cross the femur and knee

‐ It may span to the pelvis if hip is unstable

• Three phases

1) Latency

2) Distraction

3) ConsolidationX-ray EF Femoral Lengthening

(Image used with permission, Paley Institute)

Latency

• Latency phases time between osteotomy and the beginning of the distraction

• It results in the initial callus formation of the bone

• It lasts between 1‐7 days (age related)

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Distraction Phase (max 8cm)

• Phase where the bone is distracted or pulled apart• 0.25mm 4x per day for a total of 1mm per day

• This stretches the bone callus that will form the bone regenerate

• This phase continues until the goal is met or complications stop lengthening

• Complications:• They can change rate of distraction or stop lengthening.• Contractures• Subluxations/Dislocations• Delayed bone healing• Neural symptoms

Consolidation

• Consolidation is the phase when distraction stops and the regenerate fills in in order to support full body weight

• Children consolidation = distraction 

• Adults consolidation = 1.5x distraction

Lengthening Factors

• Lengthening procedures are recommended at 4‐6 year intervals

• External fixator can be 8cm

• PRECICE CFD typically limited to 5cm per lengthening

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PRECICE

• PRECICE is an internal telescoping intramedullary rod with an external remote control

• Made by Ellipse Technologies

• It can lengthen 1mm in 7 minutes

• The device allows lengthening up to 8cm• Became FDA approved December 1, 2011

• Candidates for PRECICE:• Minimal angulation, rotation correction needed• No rotational correction needed• Adequate length and space for device

Epiphysiodesis

• Fusing of the epiphyseal plate to stop growth of long bone

• Can decrease the number of lengthenings needed

• IMAGE

Why is PT important?

• The device grows the bone

• Movement, stretch and therapy grow the muscle and soft tissue

• The goal of physical therapy is to grow the soft tissue in order to keep up with bone growth

• Soft tissue is skin, fascia, muscle, tendon, circulatory structures, and nerve

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Rehabilitation Considerations and Programming • The rate of distraction is faster than physiological growth

• Can result in: • Uncontrolled spasms

• Muscle shortening

• Joint contracture

• Nerve compression

• Joint subluxation

PT Protocol Distraction Phase

• With an external fixator patient is weight bearing as tolerated (WBAT)

• Frequency = 5 ‐7x a week

• One hour per day in clinic

‐ Two more sessions per day at home with parent

• Splint to support at risk joints

• Positioning to avoid hip and knee contracture

• Parent and patient education

Splinting for Unilateral lengthening with EF

• Extension bar is designed and costumed fitted for each patient prior to D/C from hospital

• Maintains 0- 5 degrees of knee extension

• Worn at night time

• If hamstring contracture develops then ext. bar is worn additional time (half of day time when not in PT)

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Goals: Distraction Phase

• Passive ROM of the hip = 0‐90º of extension to flexion

• Abduction = 0‐30º

• Prone knee ROM = 0‐90º

• If knee ROM is less than 45º of flexion or if extension is loss, the lengthening will be slowed or halted

• Passive motion is more important than active at this phase

Goals of PT throughout lengthening phase

• Continue to maximize functional mobility with and without use of AD, as needed to assure safety.

• Promote weight acceptance on involved LE.

• Improve strength via therapeutic exercises, use of electric stimulation and functional activities.

• Decrease discomfort of stretches by using modalities and manual techniques.

Femoral Lengthening Rehabilitation 

• Femoral lengthening requires intensive rehabilitation to identify possible complications, maintain functional range of motion (ROM) and appropriate strength to carry out activities of daily living.

• Patients are routinely assessed for:• Hip and Knee ROM• Knee subluxation• Nerve function• Pin site integrity

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PT Protocol Continued

• Active warm‐up

• Open and closed chain activities

• Moist heat

• Active ROM/passive ROM

• Soft tissue mobilization/myofascial release

• Manual stretches using short lever arms• As lengthening increases, soft tissue becomes stiff and bone becomes osteopenic

• In order to reduce risk of fracture, short lever arms must be used during stretches

• Proper warm‐up and progression must be practiced• Stretch one‐joint muscles before two‐joint muscles

Daily exercises and stretches

Daily exercises• Quad sets initially with e-stim over

quadriceps

• Short (SAQ) and Long arc quads (LAQ) and Straight Leg Raise (SLR) –quadricep strength is crucial

• Heel slides, hamstring curls

• Hip abduction in supine

Daily stretches• Ankle Dorsi Flex with knee flex and

extended• Knee flexion in seated and prone

(70 -90 deg)• Knee extension in supine and prone • Adductor stretch (30 deg of Hip

abd)• Thomas Stretch (hip ext 0 deg)• Hamstring Stretch – SLR and 90/90

Tips and Tricks• Muscles which cross 2 joints are at > risk for contracture

• In femoral lengthening

Hamstrings, rectus femoris, gastrocnemius, adductors

Hip anatomy is not normal in CFD

• Patellar mobilization/glides

Patella tends to ride high as rectus femoris becomes tight with increased bone growth

• Joint distraction to decrease pain guarding

• Hand placement can increase or decrease pain: communicate with your patient 

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• Bone Healing Phase; second 2-1/2 to 3 months of treatment

• PT frequency reduced to 3-5 days per week as ROM is restored

• Initial focus is on regaining maximal ROM and decreasing muscular tightness that is left over from lengthening.

• Progress gait, balance and strength • Muscles that exhibit the most weakness are gluteus medius, quadriceps, and

gastrocnemius

• Focus on closed kinetic chain strengthening and functional exercises.

• Patients usually returned to home towns for this phase and PALLI Rehab Department staff provides support and guidance as needed.

• Discharge videos are prepared and updated HEP is provided to family.

• Fixator removal follows this phase

Consolidation Phase

Shoe Lift

• Shoe lift recommended if LLD is less than 10cm

• Tunnels can be created in shoe lifts to decrease the weight

• Constructed with rocker bottom for forward progression and flare at the base for greater stability, drill holes into lift to minimize weight

• LLD > 10cm prosthosis is recommended

‐ AFO with pylon with false foot

• To allow for foot clearance the lift should be 1cm less than the leg length discrepancy

Case studies

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REFERENCE LIST – UPDATE ON THE PEDIATRIC HIP Tovin M, Fernandez-Fernandez A, Guardo F. Chapter 7: The Pediatric and Adolescent Hip. In:

Cheatham SW, Kolber MJ (eds). Orthopedic Management of the Hip and Pelvis. (2016). St Louis, MO: Elsevier. ISBN 978-0-323-29438-6

Additional references: 1. Spence DD, Kelly DM, Mihalko MJ, Guyton JL. Adolescent and young adult hip

dysplasia. Curr Orthop Pract. 2013;24(6):567-575. 2. Price CT, Ramo BA. Prevention of hip dysplasia in children and adults. Orthop Clin N

Am. 2012;43(3):269-279. 3. Dede O, Ward WT. Bernese Periacetabular Osteotomy in the Surgical Management of

Adolescent Acetabular Dysplasia. Operative Techniques in Orthopaedics. 2013;23(3):127-133.

4. Millis MB, Lewis CL, Schoenecker PL, Clohisy JC. Legg-Calve-Perthes disease and slipped capital femoral epiphysis: major developmental causes of femoroacetabular impingement. The Journal of the American Academy of Orthopaedic Surgeons. 2013;21 Suppl 1:S59-63.

5. Wenger DR, Hosalkar HS. Principles of Treating the Sequelae of Perthes Disease. Orthopedic Clinics of North America. 2011;42(3):365-372.

6. Cooper AP, Doddabasappa SN, Mulpuri K. Evidence-based management of developmental dysplasia of the hip. Orthopedic Clinics of North America. 2014;45(3):341-354.

7. Clarke NM, Castaneda P. Strategies to improve nonoperative childhood management. The Orthopedic clinics of North America. Jul 2012;43(3):281-289.

8. Storer SK, Skaggs DL. Developmental Dysplasia of the Hip. Am Fam Physician. 2006;74:1310-1316.

9. Rosenfeld SB. Developmental dysplasia of the hip: Clinical features and diagnosis. UpToDate (online journal). Feb 4, 2014. Available at: http://www.uptodate.com/contents/developmental-dysplasia-of-the-hip-clinical-features-and-diagnosis?source . Accessed June 29, 2014.

10. Hosalkar HS, Mubarak SJ, Sink EL, Mulpuri K, Price CT. Infantile Developmental Hip Dysplasia. 2010. Published on the website for the International Hip Dysplasia Institute. Available at: http://www.hipdysplasia.org/wp-content/uploads/2010/01/IHDI-Ortho-Presentation-Web.pdf Accessed June 29, 2014.

11. Peled E, Eidelman M, Katzman A, Bialik V. Neonatal Incidence of Hip Dysplasia: Ten Years of Experience. Clinical orthopaedics and related research. 2008;466:771–775.

12. Sankar WN, Weiss J, Skaggs DL. Orthopaedic conditions in the newborn. The Journal of the American Academy of Orthopaedic Surgeons. Feb 2009;17(2):112-122.

13. International Hip Dysplasia Institute. What is hip dysplasia? 2012; http://hipdysplasia.org/.

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15. American Academy of Pediatrics - Subcommittee on Developmental Dysplasia of the Hip. Clinical Practice Guideline: Early Detection of Developmental Dysplasia of the Hip. Pediatrics. 2000;105(4).

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19. Godley DR. Assessment, diagnosis, and treatment of developmental dysplasia of the hip. JAAPA: Journal of the American Academy of Physician Assistants (Haymarket Media, Inc.). 2013;26(3):54-58.

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24. Fabricant PD, Hirsch BP, Holmes I, et al. A radiographic study of the ossification of the posterior wall of the acetabulum: implications for the diagnosis of pediatric and adolescent hip disorders. Journal of Bone & Joint Surgery, American Volume. 2013;95(3):230-236.

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29. Terjesen T. Development of the hip joints in unoperated children with cerebral palsy: a radiographic study of 76 patients. Acta Orthopaedica. 2006;77(1):125-131.

30. Pountney TE, Mandy A, Green E, Gard PR. Hip subluxation and dislocation in cerebral palsy -- a prospective study on the effectiveness of postural management programmes. Physiotherapy Research International. 2009;14(2):116-127.

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31. Arvanitis H. Pediatric Hip Dysplasia and Positioning. Exceptional Parent. 2013;43(3):22-25.

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33. Paley D. Problems, obstacles and complications of limb lengthening by the Ilizarov technique. Clin Orthop Relat Res. 1990 250:81-104.

34. Torode IP, Gillespie R. The classification and treatment of proximal femoral deficiencies. Prosthetics and Orthotics International. 1991;15(2):117-126.

35. Dror P, Shawn CS. Lengthening Reconstruction Surgery for Congenital Femoral Deficiency. Limb Lengthening and Reconstruction Surgery: Informa Healthcare; 2006:393-428.

36. Sabharwal S, Paley D, Bhave A, Herzenberg JE. Growth Patterns After Lengthening of Congenitally Short Lower Limbs in Young Children. Journal of Pediatric Orthopaedics. 2000;20(2).

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39. Lehmann CL, Arons RR, Loder RT, Vitale MG. The epidemiology of slipped capital femoral epiphysis: an update. Journal of pediatric orthopedics. May-Jun 2006;26(3):286-290.

40. Gholve PA, Cameron DB, Millis MB. Slipped capital femoral epiphysis update. Current opinion in pediatrics. Feb 2009;21(1):39-45.

41. Loder RT, Skopelja EN. The epidemiology and demographics of slipped capital femoral epiphysis. ISRN Orthopedics. 2011: Article ID486512. DOI: 486510.485402/482011/486512.

42. Peck K, Herrera-Soto J. Slipped capital femoral epiphysis: what's new? The Orthopedic clinics of North America. Jan 2014;45(1):77-86.

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45. Ganz R, Leunig M, Leunig-Ganz K, Harris W. The Etiology of Osteoarthritis of the Hip. Clinical orthopaedics and related research. 2008/02/01 2008;466(2):264-272.

46. Pinheiro PC. Nonoperative treatment of slipped capital femoral epiphysis: a scientific study. Journal of orthopaedic surgery and research. 2011;6:10.

47. Sonnega RJA, van der Sluijs JA, Wainwright AM, Roposch A, Hefti F. Management of slipped capital femoral epiphysis: results of a survey of the members of the European Paediatric Orthopaedic Society. J Child Orthop. 2011/12/01 2011;5(6):433-438.

48. Kocher MS, Bishop JA, Hresko MT, Millis MB, Kim YJ, Kasser JR. Prophylactic pinning of the contralateral hip after unilateral slipped capital femoral epiphysis. The Journal of bone and joint surgery. American volume. Dec 2004;86-A(12):2658-2665.

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51. Leunig M, Ganz R, Zaltz I, Tibor LM. Slipped Capital Femoral Epiphysis and Its Variants. In: F.S. Haddad (ed.). The Young Adult Hip in Sport, pp. 47-58. London: Springer Verlag; 2014.

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74. Walter K, Young C, Lin D, et al. Slipped Capital Femoral Epiphysis. OrthoInfo - AAOS. (2013, October 15). Accessed November 18, 2014, http://orthoinfo.aaos.org/topic.cfm?topic=a00052.