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Orthopedics and Sports Medicine
Legg-Calve-Perthes disease
Clinical Overview and When to Suspect Legg-Calvé-Perthes Disease
Legg-Calvé-Perthes disease (LCPD) is idiopathic avascular necrosis (AVN) of the femoral head in a skeletally immature child, resulting from disruption of the blood supply to the capital femoral epiphysis.
Peak age of onset: 4–8 years (range 2–12 years)
Male : female ratio ≈ 4–5 : 1 — boys are affected far more often, but girls tend to have a worse prognosis (less remodeling potential at presentation age)
Bilateral involvement in ~10–15% of cases — but hips are typically in different stages; truly simultaneous bilateral AVN should prompt evaluation for skeletal dysplasia, hypothyroidism, sickle cell disease, or steroid use
Board pearl: LCPD is a diagnosis of EXCLUSION for bilateral disease — always rule out systemic causes of AVN when both hips are affected simultaneously
Suspect LCPD when: a child age 4–8 presents with insidious onset of painless or mildly painful limp, groin/thigh/knee pain (referred pain is common), and limited hip range of motion — especially internal rotation and abduction
History — Presentation Patterns and Risk Factors
Insidious limp is the most common presenting complaint — often noticed by parents or teachers over weeks to months
Pain is typically activity-related, dull, and localized to the groin, anterior thigh, or knee — hip pathology commonly refers pain to the ipsilateral knee via the obturator nerve
Clinical tip: Any child presenting with isolated knee pain and a limp MUST have a hip exam — LCPD and SCFE are commonly missed when only the knee is evaluated
History of trauma may be reported but is usually incidental — families attribute the limp to a minor injury, delaying diagnosis
Risk factors: delayed bone age, short stature for age, hyperactivity/ADHD (higher activity levels), low socioeconomic status, exposure to secondhand smoke, family history (up to 1 in 20 first-degree relatives affected)
Coagulation abnormalities: some studies link LCPD to thrombophilia (↑ factor V Leiden, protein C/S deficiency) — not routinely tested but may contribute to vascular occlusion of the femoral head
Key distinction: LCPD is typically a healthy, active, lean child — contrast with SCFE, which classically presents in an overweight adolescent
Physical Exam — Findings and Provocative Maneuvers
Antalgic gait: shortened stance phase on the affected side; child may have a Trendelenburg gait (pelvis drops on the contralateral side when standing on the affected leg) indicating hip abductor weakness
Limited range of motion (ROM): internal rotation and abduction are the FIRST and MOST LIMITED motions — compare side to side
Log-roll test: with patient supine, gently roll the leg internally and externally — pain with internal rotation is sensitive for hip pathology
Hip flexion-internal rotation test: flex hip to 90° then internally rotate — pain and limitation suggest synovitis or femoral head deformity
Thigh/calf atrophy: chronic disuse leads to measurable circumference difference on the affected side
Leg length discrepancy: the affected limb may appear shortened due to femoral head collapse
Fixed flexion contracture: Thomas test may be positive in advanced disease
Board pearl: Forced abduction in internal rotation that produces pain is highly suggestive of hip joint pathology (impingement of the deformed femoral head) — this maneuver helps differentiate LCPD from transient synovitis, where ROM is limited but less focal
Diagnostic Workup — Imaging Selection by Age and Stage
→ Initial/necrosis: epiphyseal sclerosis, cessation of growth
→ Fragmentation: femoral head breaks into dense and lucent areas — prognosis is determined at this stage
→ Reossification: new bone replaces necrotic bone
→ Remodeling: femoral head reshapes until skeletal maturity
AP pelvis and frog-leg lateral radiographs are the FIRST-LINE imaging study
Early radiographic signs: ↑ density of the femoral epiphysis, subchondral fracture (crescent sign), smaller/flattened femoral epiphysis compared to the contralateral side, widened medial joint space (synovitis/cartilage hypertrophy)
Radiographic stages (Waldenström classification):
MRI: indicated when radiographs are normal but clinical suspicion is high — MRI detects AVN earlier than plain films (↓ signal on T1 in the epiphysis, marrow edema)
Bone scan (technetium-99m): rarely used now; replaced by MRI for early detection
Clinical tip: Radiographs may be NORMAL in the first 1–3 months — if clinical suspicion persists despite normal X-rays, obtain MRI or repeat radiographs in 4–6 weeks
Labs: typically normal; CBC, ESR, CRP are useful primarily to exclude infection (septic arthritis, osteomyelitis)
Radiographic Classification — Predicting Prognosis
→ Group A: lateral pillar of the femoral epiphysis maintains full height → excellent prognosis
→ Group B: lateral pillar loses up to 50% of height → intermediate prognosis
→ Group B/C (border group): lateral pillar loses ~50% → poorer prognosis, especially age >8
→ Group C: lateral pillar loses >50% of height → poorest prognosis, high rate of femoral head deformity
Lateral pillar classification (Herring) — determined during the FRAGMENTATION phase — is the most clinically useful prognostic system:
Board pearl: The lateral pillar is the key prognostic determinant — it reflects structural integrity of the weight-bearing portion of the femoral head
Catterall classification (historical; 4 groups based on extent of epiphyseal involvement) — less commonly used now
Head-at-risk signs on X-ray: lateral subluxation, Gage sign (radiolucency in lateral epiphysis/metaphysis), calcification lateral to the epiphysis, horizontal physis, metaphyseal cysts → these indicate worse outcomes
Key principle: Prognosis depends on: (1) age at onset (younger = more remodeling time = better), (2) extent of femoral head involvement (lateral pillar), and (3) degree of femoral head containment within the acetabulum
Management — General Principles and Non-Operative Treatment
→ Activity modification: restrict high-impact activities (running, jumping) during active disease
→ NSAIDs (ibuprofen 10 mg/kg/dose q6–8h) for pain and synovitis
→ Physical therapy: focus on ROM preservation — abduction and internal rotation stretching
→ Abduction bracing (Petrie casts, Scottish Rite orthosis): controversial; evidence for bracing is inconsistent
Goals of treatment: maintain femoral head containment within the acetabulum, preserve ROM, minimize femoral head deformity, and allow biologic remodeling
Containment principle: keeping the femoral head centered in the acetabulum allows the acetabulum to act as a mold, shaping the softened femoral head as it revascularizes
First-line non-operative management:
Observation alone is appropriate for: age <6 at onset with ≤50% head involvement (Herring A or B), full ROM maintained
Clinical tip: The most important initial management step is restoring and maintaining hip ROM — a stiff hip cannot be contained
Board pearl: Weight-bearing restriction is NOT routinely proven to alter disease course — containment is more important than non-weight-bearing
Management — Surgical Options and Decision-Making
Surgical containment is considered when: age >8 at onset, Herring B/C or C classification, loss of containment on radiographs (lateral subluxation), or persistent loss of ROM despite non-operative therapy
Femoral varus osteotomy: redirects the femoral head deeper into the acetabulum; most commonly performed surgical procedure for LCPD → maintains containment during fragmentation and reossification
Innominate (pelvic) osteotomy (Salter): redirects the acetabulum over the femoral head — used when the acetabulum needs to provide better lateral coverage
Combined femoral + pelvic osteotomy: for severe cases with both femoral and acetabular deficiency
Shelf acetabuloplasty / Chiari osteotomy: salvage procedures for older children or residual subluxation
Arthrodiastasis (hinged distraction with external fixator): emerging technique for severe cases in older children; allows biologic remodeling while maintaining joint space
Key distinction: Surgery does NOT cure LCPD — it improves the mechanical environment for biological remodeling; outcomes still depend on age, extent of necrosis, and remaining growth
Board pearl: Children <6 with good ROM and Herring A/B classification generally do well WITHOUT surgery
Referral Criteria and Role of the General Pediatrician
→ Monitor growth and development
→ Manage pain with NSAIDs
→ Encourage ROM exercises and physical therapy compliance
→ Screen for psychosocial impacts (activity restriction in an active child)
→ Ensure school accommodations if needed (elevator access, modified PE)
Every child with suspected or confirmed LCPD should be referred to pediatric orthopedics — the general pediatrician's role is early recognition, initial workup, pain management, and coordinating follow-up
Urgent referral if: locked hip (inability to move), severe pain, concern for septic arthritis (febrile child with hip pain)
Routine referral if: chronic limp with radiographic findings consistent with LCPD
General pediatrician responsibilities during treatment:
Follow-up imaging: serial radiographs every 3–4 months during active disease (fragmentation through reossification) — typically managed by orthopedics
Clinical tip: Disease course is prolonged — 2 to 5 years from onset to remodeling — families need anticipatory guidance about the timeline and the importance of long-term follow-up through skeletal maturity
Age-Specific Considerations — Younger Children (Age <6 Years)
Best prognosis: the younger the child at onset, the more time for femoral head remodeling before skeletal maturity
Children <6 with Herring A or B classification have >80–90% good to excellent outcomes with observation alone
Greater acetabular remodeling capacity in younger children → the acetabulum can reshape around even a mildly flattened femoral head
ROM is often well preserved → less need for aggressive intervention
Management: observation, activity modification, NSAIDs, physical therapy; bracing/surgery rarely needed
Board pearl: Age at onset <6 years is the single most favorable prognostic factor in LCPD — even Herring B patients in this age group typically do well without surgery
Bilateral disease in a child <4 should raise suspicion for skeletal dysplasia (multiple epiphyseal dysplasia, spondyloepiphyseal dysplasia) or endocrine disorder (hypothyroidism)
Pitfall: Do not confuse normal irregular ossification of the femoral epiphysis (common in children 2–4 years) with early LCPD — compare with the contralateral side and correlate with symptoms
Age-Specific Considerations — Older Children (Age >8 Years) and Adolescents
→ LCPD: usually lean child, gradual onset, X-ray shows femoral head changes
→ SCFE: usually obese child, more acute onset possible, frog-leg lateral shows posterior slip of epiphysis
Worst prognosis: older age at onset = less remaining growth = less remodeling potential
Children >8 with Herring B/C or C → >50% will have poor outcome (flattened, deformed femoral head → coxa plana → early osteoarthritis)
Surgical containment is more commonly recommended in this age group
Key distinction from SCFE: LCPD typically occurs age 4–8; SCFE occurs age 10–16 — overlap zone age 8–12 requires careful evaluation
Adolescents with LCPD may present with advanced disease and significant femoral head deformity → hip impingement (femoroacetabular impingement) becomes a concern
Long-term outcome: even with treatment, adolescents with severe LCPD may develop degenerative arthritis by age 40–50 → hip replacement may eventually be needed
Board pearl: Stulberg classification (I–V) describes the FINAL shape of the femoral head after remodeling — classes I–II (spherical) have excellent long-term outcomes; classes IV–V (flat/aspherical) predict early osteoarthritis
Complications and When to Escalate Care
→ Progressive loss of ROM despite therapy
→ Lateral subluxation on radiographs
→ Worsening Herring classification during fragmentation
→ Severe pain uncontrolled by NSAIDs
Femoral head deformity (coxa plana): flattened, enlarged femoral head → incongruent joint → mechanical impingement, loss of ROM, pain
Coxa magna: enlarged femoral head from overgrowth of revascularized cartilage → may cause subluxation and impingement
Coxa brevis: short femoral neck → greater trochanteric overgrowth → abductor insufficiency, Trendelenburg gait
Premature physeal arrest: damage to the proximal femoral physis → leg length discrepancy, angular deformity
Femoroacetabular impingement (FAI): residual aspherical femoral head impinges on acetabular rim → labral tears, progressive cartilage damage in adolescence/young adulthood
Early-onset osteoarthritis: the long-term consequence of uncontained or severely deformed femoral heads — may require hip arthroplasty by age 40–50
Escalate care when:
Board pearl: The femoral head shape at the END of remodeling — not during active disease — determines long-term outcomes; this is why containment during the fragmentation phase is critical
Emergencies and Acute Presentations Requiring Urgent Evaluation
→ LCPD exacerbation: afebrile, ESR/CRP normal or mildly elevated, gradual worsening
→ Septic arthritis: febrile, toxic-appearing, ESR/CRP markedly ↑, refusal to bear weight
→ Clinical tip: When in doubt, aspirate the hip — septic arthritis is a surgical emergency
Locked hip / acute loss of motion: sudden ↓ ROM with severe pain suggests a large loose body, acute synovitis, or femoral head collapse → urgent orthopedic evaluation
Differentiating LCPD flare from septic arthritis:
Pathologic fracture through necrotic bone: rare but can present as acute-onset severe hip pain
Hinge abduction: severely deformed femoral head catches on the acetabular rim during abduction → paradoxical lateral subluxation with abduction → pain worsens with abduction rather than improving → requires surgical intervention (valgus osteotomy or shelf procedure)
Board pearl: Hinge abduction is a contraindication to further containment treatment (bracing or varus osteotomy) — it requires a different surgical approach to relieve impingement
Key Differentials — The Limping Child Age 4–8
Transient synovitis: most common cause of hip pain/limp in this age group; low-grade or no fever, ESR/CRP normal or mildly ↑, full recovery in 7–10 days; X-rays normal; if symptoms persist >10 days → reconsider diagnosis (LCPD may initially mimic transient synovitis)
Septic arthritis: febrile, toxic, WBC ↑, ESR >40, CRP ↑, refusal to bear weight → joint aspiration is definitive; >50,000 WBC in synovial fluid → surgical drainage
Osteomyelitis of proximal femur: fever, focal tenderness, ↑ inflammatory markers; MRI shows marrow edema in metaphysis
Neoplasm: leukemia (bone pain, pallor, hepatosplenomegaly, abnormal CBC), osteoid osteoma (night pain relieved by NSAIDs, CT shows nidus), Ewing sarcoma (aggressive periosteal reaction)
SCFE: older age (10–16), obese, X-ray shows posterior epiphyseal slip
Juvenile idiopathic arthritis (JIA): morning stiffness, joint swelling, may have systemic features
Board pearl: Transient synovitis that does not resolve within 7–10 days OR recurs should prompt repeat imaging to evaluate for early LCPD — up to 1–3% of transient synovitis cases are eventually diagnosed as LCPD
Key Distinctions — How to Differentiate LCPD from Mimics
→ LCPD: insidious limp over weeks, persistent, X-ray may show sclerotic/small epiphysis, MRI shows AVN
→ Transient synovitis: acute onset after URI, resolves in days, X-ray normal, hip effusion on US
→ Sickle cell disease: bilateral AVN, hemoglobin electrophoresis abnormal, other sickle complications
→ Corticosteroid-induced AVN: history of systemic steroid use
→ Gaucher disease: hepatosplenomegaly, bone crises, enzyme assay diagnostic
→ MED: bilateral symmetric involvement, short stature, multiple joints affected (knees, ankles), family history (autosomal dominant), genetic testing confirms
→ LCPD: typically unilateral, isolated hip, normal height for age (or slightly short)
→ Hypothyroidism: delayed bone age, growth failure, fatigue, constipation → check TSH, free T4
LCPD vs. transient synovitis:
LCPD vs. AVN from other causes:
LCPD vs. multiple epiphyseal dysplasia (MED):
LCPD vs. hypothyroidism:
Clinical tip: Always think systemically when LCPD appears bilateral and simultaneous — isolated LCPD is bilateral in only 10–15% and the hips are usually in DIFFERENT stages
Screening and Surveillance — Role of the General Pediatrician
→ Observe gait — antalgic? Trendelenburg?
→ Ask about hip, thigh, or knee pain
→ Perform hip ROM assessment if any concern
→ Monitor for pain control adequacy
→ Ensure physical therapy adherence
→ Track growth, nutrition, and general health
→ Provide school/activity accommodation letters
No universal screening test exists for LCPD — detection relies on clinical vigilance during well-child visits
At every well-child visit age 2–10:
Children with known risk factors (delayed bone age, previous transient synovitis, family history, thrombophilia) warrant heightened surveillance
Post-transient synovitis follow-up: recheck in 7–10 days; if limp persists, obtain hip radiographs to evaluate for LCPD
During active LCPD (managed by orthopedics): the general pediatrician should:
After LCPD resolution: follow-up radiographs through skeletal maturity recommended to assess final femoral head shape and detect late sequelae (FAI, degenerative changes)
Board pearl: Persistent or recurrent limp after apparent transient synovitis is LCPD until proven otherwise
Anticipatory Guidance and Long-Term Follow-Up
→ Lifetime activity modifications to reduce joint wear
→ Symptoms of femoroacetabular impingement
→ Potential need for future hip preservation surgery or arthroplasty
Activity counseling: during active disease, avoid high-impact sports (running, jumping, contact sports); swimming, cycling, and gentle ROM exercises are encouraged to maintain fitness and joint motion without axial loading
Duration of disease: families must understand that LCPD runs a 2–5 year course through all stages — patience and compliance with follow-up are essential
Imaging schedule during active disease: radiographs every 3–4 months to monitor stage progression and containment; frequency ↓ during reossification and remodeling
After skeletal maturity: patients with residual femoral head deformity (Stulberg III–V) should be counseled about:
Leg length discrepancy: may require shoe lift if >1–2 cm; larger discrepancies may need epiphysiodesis or lengthening
Clinical tip: Encourage maintaining a healthy weight — excess body weight increases mechanical stress on the affected hip and accelerates degenerative changes
Family Counseling and Psychosocial Considerations
→ Social isolation from inability to participate in sports/recess
→ Anxiety about long-term outcomes and need for surgery
→ Frustration with the prolonged disease course (years of monitoring)
→ School difficulties if absences for appointments/surgery are frequent
→ LCPD is NOT caused by anything the child or family did
→ Most children, especially those <6 at onset, have good long-term outcomes
→ The bone is rebuilding itself — the treatments help shape it properly
→ Swimming and cycling keep the child active and social during recovery
Activity restriction is often the most distressing aspect for families — LCPD predominantly affects active young boys who struggle with limitations on sports and play
Psychosocial impacts:
Counseling points:
Support resources: connect families with peer support groups; involve school counselors for accommodations
Board pearl: Addressing the psychosocial impact of chronic orthopedic disease in children is a tested concept — the ABP expects candidates to recognize that activity restriction in a young child has developmental and emotional consequences that require active management
High-Yield Associations and Rapid-Fire Board Facts
LCPD = idiopathic AVN of femoral head in children age 4–8
Male > female (4–5:1), but females have worse prognosis
LEFT hip more commonly affected (similar to DDH)
Pathophysiology: interruption of blood supply to capital femoral epiphysis → necrosis → fragmentation → revascularization → remodeling
Lateral femoral circumflex artery is the primary blood supply to the femoral head in children
Most important prognostic factors: age at onset + lateral pillar classification (Herring)
Age <6 + Herring A/B → observation; Age >8 + Herring B/C or C → surgery
First imaging: AP pelvis + frog-leg lateral X-ray
Early X-ray may be NORMAL → MRI if clinical suspicion persists
Knee pain in a child = examine the hip
Bilateral simultaneous AVN → rule out systemic cause (sickle cell, steroid use, MED, hypothyroidism)
Transient synovitis lasting >10 days → think LCPD
Hinge abduction = contraindication to containment treatment
Stulberg I–II (spherical head) = good long-term outcome; Stulberg IV–V = early osteoarthritis
Board pearl: Crescent sign = subchondral fracture = earliest radiographic sign visible on frog-leg lateral view
One-Line Recap
Legg-Calvé-Perthes disease — idiopathic AVN of the femoral head in children age 4–8 (M > F, 4–5:1) — presents with insidious limp and limited hip internal rotation/abduction; diagnosed with AP pelvis and frog-leg lateral radiographs (sclerotic/small epiphysis, crescent sign) or MRI when X-rays are initially normal; prognosis is determined by age at onset (younger = better) and lateral pillar classification during fragmentation (Herring A–C); management ranges from observation with ROM exercises and NSAIDs for young children with good prognostic features to surgical containment (femoral/pelvic osteotomy) for older children (>8 years) with severe involvement; the general pediatrician must recognize hip pathology presenting as knee pain, distinguish LCPD from transient synovitis (persistent limp >10 days = reconsider diagnosis), refer to orthopedics, and provide long-term follow-up through skeletal maturity to detect sequelae including femoroacetabular impingement and early osteoarthritis.
Board Question Stem Patterns
5-year-old boy with 6-week painless limp, limited hip internal rotation, normal labs → next step: AP pelvis + frog-leg lateral radiograph → shows sclerotic, small femoral epiphysis → diagnosis: LCPD
Same child, age 5, Herring A classification → management: observation + ROM exercises + activity modification
4-year-old with hip pain, X-rays normal, limp persists 3 weeks → next step: MRI of the hip (early LCPD before radiographic changes)
9-year-old boy with limp and X-ray showing femoral head fragmentation, Herring C → next step: surgical referral for containment procedure
6-year-old with knee pain only, no knee findings, limited hip internal rotation → next step: hip radiographs (referred pain from hip pathology)
5-year-old diagnosed with transient synovitis, still limping 2 weeks later → next step: repeat hip radiographs to evaluate for LCPD
3-year-old with bilateral symmetric femoral head changes, short stature → think multiple epiphyseal dysplasia, NOT typical LCPD → genetic evaluation
7-year-old with LCPD, pain worsens with abduction, lateral subluxation on abduction X-ray → hinge abduction → avoid varus osteotomy → needs valgus/shelf procedure
Obese 12-year-old with hip pain and limp → think SCFE, NOT LCPD → frog-leg lateral shows epiphyseal slip
Child age 4 with LCPD, Herring B, full ROM → prognosis: excellent with observation alone
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