Developmental Dysplasia of the Hip in Adults

1. Clinical Overview

Developmental Dysplasia of the Hip (DDH) in adults represents the persistence or evolution of congenital hip abnormalities that were either undetected, untreated, or inadequately treated during infancy and childhood. It is characterized by deficient acetabular coverage of the femoral head, leading to abnormal hip joint biomechanics, increased contact stresses, and premature degenerative joint disease. [1,2]

Adult DDH is the leading cause of secondary hip osteoarthritis in young and middle-aged adults, accounting for approximately 20-40% of total hip arthroplasties performed in patients under 40 years of age. [3,4] The condition presents across a spectrum from mild acetabular dysplasia with preserved joint space to severe hip subluxation or dislocation with established arthritis. Early recognition and appropriate treatment are critical, as intervention before the onset of significant osteoarthritis can preserve the native hip joint and delay or avoid the need for arthroplasty. [5,6]

The natural history of untreated adult DDH is progressive deterioration, with studies demonstrating that 50-60% of dysplastic hips develop osteoarthritis by the fifth decade of life. [7,8] However, with modern joint preservation techniques, particularly periacetabular osteotomy (PAO), symptomatic improvement and prevention of arthritic progression can be achieved in carefully selected patients. [9,10]

Key Clinical Messages

• Early diagnosis is crucial: Symptomatic young adults with mechanical hip pain warrant radiographic assessment for dysplasia
• Biomechanical principles: Reduced acetabular coverage increases contact stress by 2-3 fold, accelerating cartilage degeneration
• Treatment windows: Joint preservation surgery is most effective before Tönnis grade 2 osteoarthritis develops
• Specialist referral: Suspected dysplasia in symptomatic patients should be referred to hip preservation centres

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2. Epidemiology

Demographics and Prevalence

Risk Factors

Primary Risk Factors:

• Female sex (6:1 ratio) - hormonal influences on ligamentous laxity [12]
• First-born children - tight uterine cavity [15]
• Breech presentation - 20% of DDH cases [16]
• Positive family history - 12-fold increased risk [17]
• Caucasian ethnicity - higher prevalence than Asian or African populations [11]

Associated Conditions:

• Neuromuscular disorders (cerebral palsy, myelodysplasia)
• Connective tissue disorders (Ehlers-Danlos syndrome, Marfan syndrome)
• Other packaging disorders (congenital torticollis, metatarsus adductus)

Geographic Variation

Incidence varies significantly by ethnicity and geographic location, ranging from 0.06 per 1000 in African populations to 76 per 1000 in certain Native American populations, reflecting both genetic and environmental (swaddling practices) influences. [11,18]

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3. Aetiology & Pathophysiology

Aetiology

Adult DDH represents the continuum of developmental hip abnormalities that originate in the prenatal, perinatal, or early childhood periods:

Primary Developmental Factors:

1. Intrauterine Malposition: Mechanical forces during fetal development
2. Genetic Predisposition: Familial clustering suggests polygenic inheritance
3. Capsular Laxity: Excessive maternal relaxin effect on fetal ligaments
4. Primary Acetabular Dysplasia: Inherent deficiency in acetabular development

Secondary Acquired Factors:

1. Inadequate Infantile Treatment: Failed Pavlik harness or closed reduction
2. Late Diagnosis: Missed newborn screening examinations
3. Avascular Necrosis Sequelae: Complication of childhood DDH treatment
4. Iatrogenic: Complications from childhood surgical procedures

Pathophysiology

Exam Detail: Biomechanical Cascade:

The fundamental pathophysiological abnormality in adult DDH is insufficient anterolateral acetabular coverage of the femoral head, resulting in:

1. Reduced Contact Area: Normal hip joint reaction forces (3-5x body weight during gait) distributed over smaller surface area
2. Increased Contact Stress: Peak stress increases inversely with coverage (30% reduction in coverage = 2-3x stress increase) [19]
3. Abnormal Load Distribution: Concentrated forces on superior-lateral acetabular rim and labrum
4. Compensatory Hypertrophy: Labral enlargement attempting to increase coverage (cotton sign on MRI)
5. Labral Failure: Degeneration and tearing under chronic overload
6. Chondral Breakdown: Focal cartilage degeneration in zones of peak stress
7. Osteoarthritis Progression: Secondary inflammatory cascade and generalized joint degeneration

Morphological Abnormalities:

The dysplastic hip demonstrates characteristic structural abnormalities:

• Acetabular Deficiency:

  • Shallow socket (reduced depth and volume)
  • Vertical acetabular orientation (increased acetabular index)
  • Deficient anterior and/or lateral coverage
  • Excessive anteversion or retroversion

• Femoral Abnormalities:

  • Increased femoral anteversion (internal rotation deformity)
  • Increased or decreased neck-shaft angle
  • Smaller femoral head diameter
  • Aspherical femoral head (secondary to chronic subluxation)

• Soft Tissue Changes:

  • Labral hypertrophy and subsequent degeneration
  • Capsular redundancy or contracture
  • Abductor muscle insufficiency (secondary to lateral hip displacement)
  • Iliopsoas tendon impingement (anterior coverage deficiency)

Classification of Severity:

The morphological spectrum correlates with clinical severity and guides treatment selection:

• Mild Dysplasia: Minor coverage deficiency, preserved joint congruency
• Moderate Dysplasia: Significant coverage loss, early subluxation
• Severe Dysplasia: Marked subluxation, secondary deformity
• Chronic Dislocation: Complete loss of normal anatomical relationship

Natural History

Without intervention, the natural history of symptomatic adult DDH follows a predictable pattern:

1. Asymptomatic Phase (childhood-adolescence): Dysplasia present but no symptoms
2. Mechanical Pain Phase (20s-30s): Activity-related hip pain, labral pathology
3. Early Degeneration (30s-40s): Focal chondral damage, progressive symptoms
4. Established Osteoarthritis (40s-50s): Generalized joint space narrowing, functional limitation
5. End-Stage Disease (50s+): Severe arthritis, arthroplasty candidacy

The rate of progression is highly variable and influenced by severity of dysplasia, activity level, body mass index, and presence of concomitant pathology. [7,8,20]

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4. Clinical Presentation

Symptoms

Cardinal Symptoms:

• Mechanical Hip Pain (95% of patients):

  • Lateral hip or groin pain
  • Activity-related, worse with prolonged walking/standing
  • Stiffness after rest ("gelling")
  • Typically gradual onset over months to years

• Clicking/Catching Sensation (40-60%):

  • Mechanical symptoms suggesting labral tear
  • Painful clunk with specific movements
  • Sensation of hip "giving way"

• Limited Functional Capacity:

  • Difficulty with stairs, squatting, running
  • Reduced walking distance
  • Impact on sporting activities

Red Flag Symptoms:

⚠️ Sudden severe pain: May indicate labral tear, chondral fracture, or acute subluxation ⚠️ Night pain: Suggests established osteoarthritis or inflammatory component ⚠️ Rapidly progressive symptoms: Accelerated cartilage loss requiring urgent assessment

Signs

Gait Analysis:

• Trendelenburg Gait: Pelvic drop on contralateral side during single-leg stance
• Antalgic Gait: Shortened stance phase on affected side
• Toe-Out Gait: External rotation deformity compensation

Standing Examination:

• Positive Trendelenburg Sign: Inability to maintain pelvis level on single-leg stance (abductor weakness)
• Leg Length Discrepancy: True or apparent shortening (chronic subluxation)
• Asymmetric Skin Creases: May persist from childhood

Range of Motion Assessment:

• Limited Internal Rotation: Most sensitive sign (often less than 15° with hip flexed to 90°)
• Limited Flexion: Particularly in established arthritis
• Limited Abduction: Secondary to capsular contracture
• Asymmetry: Comparison with contralateral hip crucial

Special Tests:

Exam Detail: Clinical Examination Sequence for FRCS Examination:

1. Introduction and Consent: "This patient has presented with hip pain, please examine the hip"

2. Inspection (Standing - from front, side, back):

   • Gait assessment (Trendelenburg, antalgic patterns)
   • Muscle wasting (gluteal, quadriceps)
   • Pelvic tilt and spinal alignment
   • Skin changes, scars

3. Palpation (Supine):

   • Greater trochanter tenderness (exclude trochanteric bursitis)
   • Anterior hip joint line (groin)
   • Abductor muscle bulk

4. Movement (Active then Passive):

   • Flexion (normal 120°, measure with goniometer)
   • Extension (Thomas test to exclude fixed flexion deformity)
   • Abduction and Adduction (measure in neutral and 30° flexion)
   • Internal and External Rotation (in 90° flexion - most sensitive)

5. Special Tests:

   • Trendelenburg test
   • Impingement tests (FADIR, FABER)
   • Leg length measurement (ASIS to medial malleolus)

6. Neurovascular Assessment:

   • Femoral pulses
   • Peripheral neurological examination (L2-S1)

7. Complete Examination:

   • "I would like to examine the lumbar spine, contralateral hip, and both knees"
   • "I would review radiographs"

Presentation Patterns by Age

Young Adults (20-35 years):

• Predominantly mechanical symptoms
• Activity-related pain
• Labral pathology common
• Preserved joint space on radiographs
• Candidates for joint preservation

Middle Age (35-50 years):

• Mixed mechanical and inflammatory pain
• Established chondral damage
• Early radiographic osteoarthritis
• Marginal joint preservation candidates
• Increasing arthroplasty consideration

Older Adults (> 50 years):

• Advanced osteoarthritis
• Constant pain including night pain
• Significant functional limitation
• Primary treatment: total hip arthroplasty

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5. Differential Diagnosis

Must-Not-Miss Diagnoses

1. Femoroacetabular Impingement (FAI)

   • Key Distinguishing Features: Normal or excessive acetabular coverage, cam/pincer morphology
   • Investigation: Alpha angle > 55° (cam), lateral centre-edge angle > 40° (pincer)
   • Often coexists with mild dysplasia (mixed pathology)

2. Inflammatory Arthropathy

   • Key Features: Systemic symptoms, polyarticular involvement, elevated inflammatory markers
   • Investigation: Rheumatoid factor, anti-CCP, ESR/CRP
   • May have secondary acetabular erosion mimicking dysplasia

3. Avascular Necrosis of Femoral Head

   • Key Features: Subacute onset, history of corticosteroids/alcohol/trauma
   • Investigation: MRI shows characteristic signal changes and crescent sign
   • May have secondary acetabular changes

Common Differentials

Coexisting Pathologies

Important to recognize that DDH frequently coexists with:

• Labral Tears (60-80% of symptomatic dysplastic hips) [21]
• Focal Chondral Defects (40-60% at presentation) [22]
• Ligamentum Teres Pathology (degeneration or rupture)
• Iliopsoas Impingement (anterior acetabular deficiency)
• Femoral Version Abnormalities (commonly increased anteversion)

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6. Investigations

Radiographic Assessment

Plain Radiographs (First-Line Investigation)

Standard Views:

1. AP Pelvis Radiograph (Standing if possible)

   • Single most important investigation
   • Standardized technique: beam centered on pubic symphysis, 15° cephalad tilt
   • Both hips visible for comparison
   • Assessment of multiple parameters (see below)

2. False Profile (Faux Profil) View

   • Standing lateral view
   • Pelvis rotated 65° to cassette
   • Assesses anterior acetabular coverage
   • Essential for surgical planning

3. Lateral Hip Radiograph

   • Dunn view (45° flexion, 20° abduction) or Frog-leg lateral
   • Evaluates femoral head sphericity
   • Identifies cam lesions

Radiographic Measurements:

Tönnis Classification (Osteoarthritis Grading):

Crowe Classification (Hip Dislocation):

Used to classify severity of subluxation/dislocation, particularly relevant for arthroplasty planning:

• Type I: less than 50% subluxation (femoral head less than 50% uncovered)
• Type II: 50-75% subluxation
• Type III: 75-100% subluxation (femoral head at level of acetabulum)
• Type IV: Complete superior dislocation (femoral head above acetabulum)

Exam Detail: Radiographic Analysis Sequence for Viva Examination:

When presented with hip radiographs, use systematic approach:

1. Patient Details: Name, age, date (young adult suggests DDH vs FAI)

2. Technical Quality:

   • Adequate penetration
   • Correct centering (pubic symphysis centered, coccyx 1-2cm above symphysis)
   • Symmetric obturator foramina (rotation)

3. Acetabular Assessment:

   • Coverage: LCEA, AI, Tönnis angle
   • Depth: Crossover sign (retroversion), posterior wall sign
   • Version: Presence of crossover vs deficient coverage

4. Femoral Assessment:

   • Head sphericity
   • Neck-shaft angle
   • Evidence of cam lesion

5. Joint Assessment:

   • Joint space (Tönnis grade)
   • Osteophytes
   • Subchondral sclerosis/cysts
   • Shenton's line continuity

6. Additional Features:

   • Previous surgery (screws, osteotomy)
   • Leg length discrepancy
   • Secondary signs (elevated GT, teardrop asymmetry)

Conclusion Statement: "These radiographs demonstrate [mild/moderate/severe] acetabular dysplasia with LCEA of [X]°, Tönnis grade [X] osteoarthritis, making this patient [a candidate for PAO / marginal for joint preservation / appropriate for THA]."

Advanced Imaging

Magnetic Resonance Imaging (MRI):

Indications:

• Pre-operative assessment for joint preservation surgery
• Evaluation of articular cartilage status
• Detection of labral tears
• Assessment of bone marrow edema
• Surgical planning (cartilage mapping)

Findings in DDH:

• Labral Pathology: Hypertrophy, degeneration, tears (high signal on T2)
• Cartilage Assessment: Focal defects, delamination, thickness mapping
• Bone Marrow Edema: Subchondral stress reaction
• Ligamentum Teres: Degeneration or tears
• Muscle Evaluation: Abductor integrity and fatty infiltration

MR Arthrography:

• Superior sensitivity for labral tears (90-95% sensitivity)
• Better cartilage delineation with intra-articular contrast
• Standard pre-operative investigation for PAO candidates [21]

Computed Tomography (CT):

Indications:

• Precise measurement of acetabular and femoral version
• 3D reconstruction for complex deformity
• Surgical planning (especially revision cases)
• Assessment of bone stock for arthroplasty

Advanced CT Techniques:

• 3D CT with reformation
• Low-dose protocols to minimize radiation
• Standardized measurements of version, coverage

Bone Scintigraphy:

• Limited role in routine assessment
• May identify areas of increased stress/early degeneration
• Excludes other pathology (stress fractures, AVN)

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7. Classification & Staging

Anatomical Classification

Hartofilakidis Classification (Based on Degree of Dysplasia and Dislocation):

Severity Grading (Clinical Classification)

Mild Dysplasia:

• LCEA 20-25° (borderline)
• Tönnis grade 0-1
• Minimal symptoms
• Management: Observation vs PAO (controversial)

Moderate Dysplasia:

• LCEA 15-20°
• Tönnis grade 0-2
• Symptomatic with activity
• Management: PAO (ideal candidate)

Severe Dysplasia:

• LCEA less than 15°
• Subluxation present
• Advanced symptoms
• Management: Complex PAO vs THA

Treatment Decision Algorithm

ADULT DDH MANAGEMENT ALGORITHM
                    │
                    ▼
         ┌──────────────────────┐
         │  Clinical Assessment  │
         │  + Radiographs        │
         └──────────┬────────────┘
                    │
         ┌──────────┴───────────┐
         │                      │
    ASYMPTOMATIC           SYMPTOMATIC
         │                      │
    Monitor/Observe        AP Pelvis + False Profile
                                │
                    ┌───────────┴────────────┐
                    │                        │
              LCEA > 25°                  LCEA less than 25°
            (Not dysplasia)              (Dysplasia)
                    │                        │
            Evaluate for FAI          Assess OA Grade
            or other pathology        (Tönnis 0-3)
                                            │
                              ┌─────────────┼─────────────┐
                              │             │             │
                         Tönnis 0-1    Tönnis 2      Tönnis 3
                         (Minimal OA)  (Moderate)    (Advanced)
                              │             │             │
                         Order MRI     Borderline    Total Hip
                              │         Assessment   Arthroplasty
                    ┌─────────┴──────┐      │
                    │                │      │
            Good Cartilage    Poor Cartilage│
            Minimal BME       Extensive BME │
                    │                │      │
            PERIACETABULAR    ──────────────┘
            OSTEOTOMY (PAO)          │
                                     │
                              Total Hip
                              Arthroplasty

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8. Management

Conservative Management

Indications

• Asymptomatic dysplasia (incidental finding)
• Mild symptoms with minimal functional limitation
• Borderline dysplasia (LCEA 20-25°) without arthritis
• Severe arthritis (symptom management pending arthroplasty)
• Patient preference or medical comorbidities

Non-Operative Treatment Strategies

1. Activity Modification:

• Avoid high-impact activities (running, jumping sports)
• Emphasis on low-impact exercise (swimming, cycling)
• Weight management (every 1kg weight reduction decreases hip load)
• Ergonomic adjustments at work

2. Physical Therapy:

• Strengthening: Core stability, hip abductors (gluteus medius/minimus)
• Stretching: Hip flexors, tensor fascia lata
• Proprioception Training: Balance and gait optimization
• Manual Therapy: Joint mobilization, soft tissue techniques

3. Pharmacological Management:

• NSAIDs: Short-term symptomatic relief (COX-2 selective preferred)
• Acetaminophen: First-line analgesic
• Intra-articular Corticosteroid Injection: Temporary relief (3-6 months)
• Viscosupplementation: Limited evidence in dysplasia

4. Assistive Devices:

• Walking aids (cane in contralateral hand to unload hip)
• Orthotic shoe inserts (if leg length discrepancy)

Evidence Base for Conservative Management

Conservative management does not alter the natural history of structural dysplasia but can provide symptomatic relief and maintain function. Studies demonstrate 40-60% of patients achieve adequate symptom control with non-operative measures, though this typically declines over time as arthritis progresses. [24]

Surgical Management

Joint Preservation Surgery

PERIACETABULAR OSTEOTOMY (PAO) - Bernese Technique

The gold standard joint preservation procedure for symptomatic acetabular dysplasia.

Procedure Detail: Concept: Reorient the acetabulum to improve femoral head coverage without entering the hip joint, thereby reducing contact stress and preventing progression of arthritis.

Indications (Ideal Candidate):

• Age: 15-40 years (upper limit flexible)
• Symptomatic hip dysplasia (LCEA less than 20°)
• Tönnis grade 0-1 osteoarthritis (maximum grade 2 in selected cases)
• Adequate cartilage preservation on MRI
• Absence of extensive bone marrow edema
• Spherical femoral head (no severe asphericity)
• Failure of conservative management (minimum 3-6 months)

Contraindications:

• Advanced osteoarthritis (Tönnis grade 3)
• Severe cartilage loss on MRI (> 50% joint surface)
• Extensive subchondral cysts or bone marrow edema
• Aspherical femoral head (significant deformity)
• Active infection
• Morbid obesity (relative)
• Significant medical comorbidities

Surgical Technique (Bernese PAO):

The procedure involves four osteotomies to mobilize the acetabular fragment:

1. Iliac Osteotomy: From AIIS extending posteriorly above hip joint
2. Ischial Osteotomy: Through ischial body posterior to acetabulum
3. Pubic Osteotomy: Approximately 1cm medial to iliopectineal eminence
4. Posterior Column: Incomplete osteotomy connecting iliac and ischial cuts

The acetabular fragment is then:

• Rotated laterally (increases lateral coverage - correct LCEA)
• Rotated anteriorly (increases anterior coverage - correct ACEA)
• Medialized slightly (reduces joint reactive force)
• Stabilized with 3-4 cortical screws

Target Correction:

• Post-operative LCEA: 25-35° (avoid over-correction > 40° - creates impingement)
• Post-operative ACEA: > 25°
• Congruent reduction of femoral head within acetabulum
• Restoration of Shenton's line

Associated Procedures: Frequently combined with:

• Labral repair or debridement (60-80% require) [21]
• Femoral osteotomy (if femoral version abnormality > 40° anteversion)
• Rim trimming (if iatrogenic impingement risk)
• Cartilage treatment (microfracture, chondral grafting for focal defects)

Outcomes of PAO:

Prognostic Factors for PAO Success:

Favorable Factors:

• Age less than 35 years
• Tönnis grade 0-1
• Preserved joint space > 3mm
• Minimal subchondral cysts
• BMI less than 30
• Adequate correction achieved (LCEA 25-35°)

Unfavorable Factors:

• Age > 40 years
• Tönnis grade 2-3
• Joint space less than 2mm
• Extensive chondral damage on MRI
• Severe obesity
• Inadequate correction or over-correction

OTHER JOINT PRESERVATION PROCEDURES:

Complications of PAO

Total Hip Arthroplasty in DDH

Indications

• Advanced osteoarthritis (Tönnis grade 3)
• Failed joint preservation surgery
• Age > 50 years with symptomatic dysplasia
• Extensive cartilage loss
• Significant functional disability

Technical Challenges

DDH presents unique challenges for THA:

Anatomical Abnormalities:

• Small Acetabulum: Undersized components, may require reaming
• Acetabular Anteversion: Abnormal orientation requires careful positioning
• Proximal Femoral Deformity: Increased anteversion, narrow canal, bowing
• Leg Length Discrepancy: Often requires lengthening (nerve stretch risk)
• Altered Anatomy: Displaced abductors, scarring from previous surgery
• Bone Stock Deficiency: Inadequate bone for fixation

Surgical Considerations:

1. Acetabular Reconstruction:

   • Position cup at anatomical center (risk of superior placement)
   • May require structural bone graft for superior defects
   • Avoid excessive medialization (penetration risk)
   • Target position: 40-45° abduction, 15-20° anteversion

2. Femoral Reconstruction:

   • Address version abnormalities
   • Modular stems for version adjustment
   • Small/anatomic stems for narrow canals
   • Careful leg length correction (less than 4cm acute lengthening)

3. Soft Tissue Management:

   • Neurovascular stretch with leg lengthening (monitor intra-op)
   • Abductor advancement if deficient
   • Capsular release for contracted hips

Outcomes of THA in DDH:

Results are generally good but inferior to THA for primary OA:

• 10-year Survival: 90-95% [27]
• Higher Dislocation Rate: 5-8% vs 2-3% in primary OA
• Higher Revision Rate: Due to loosening, dislocation, component malposition
• Functional Outcomes: Good pain relief, 80-90% satisfaction [27]

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9. Complications

Complications of Untreated DDH

Complications Specific to Surgical Treatment

Periacetabular Osteotomy Complications:

• Detailed in surgical management section above
• Most serious: Intra-articular osteotomy (1-2%), non-union (1-5%), neurovascular injury (less than 1%)
• Most common: Lateral femoral cutaneous nerve palsy (20-30%, usually temporary)

Total Hip Arthroplasty Complications in DDH:

• Nerve injury (sciatic, femoral) from leg lengthening: 1-8% (temporary > permanent)
• Dislocation: 5-8% (higher than primary THA)
• Aseptic loosening: 5-10% at 10 years (higher with suboptimal bone stock)
• Periprosthetic fracture: 2-5% (narrow femoral canal)

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10. Prognosis

Natural History (Untreated)

The natural history of symptomatic adult DDH is progressive deterioration:

Long-term Studies:

• 50-60% develop osteoarthritis by age 50 in untreated symptomatic dysplasia [7,8]
• Mean age to THA: 48-52 years in untreated dysplasia [4]
• Risk of OA increases with severity: Inversely correlated with LCEA [20]
• Bilateral disease: Contralateral hip often develops symptoms within 5-10 years [13]

Prognostic Factors for Natural History:

Poor Prognosis (Accelerated OA):

• Severe dysplasia (LCEA less than 15°)
• Onset of symptoms before age 30
• High BMI
• High-impact activities/occupation
• Pre-existing chondral damage

Better Prognosis (Slower Progression):

• Mild dysplasia (LCEA 20-25°)
• Asymptomatic
• Normal BMI
• Low-impact lifestyle

Prognosis After Treatment

After Periacetabular Osteotomy:

Best Outcomes:

• Patients less than 35 years, Tönnis 0-1, LCEA corrected to 25-35°
• 85% survival at 10 years, 75% at 20 years [9,10]
• Significant pain relief and functional improvement maintained

Moderate Outcomes:

• Patients 35-45 years, Tönnis 2, borderline correction
• 70% survival at 10 years
• Variable functional improvement

Factors Predicting PAO Failure:

• Age > 40 years at surgery
• Tönnis grade 2-3 at baseline
• Joint space less than 2mm
• BMI > 35
• Inadequate correction (LCEA less than 25° or > 40° post-op)
• Extensive bone marrow edema pre-operatively

After Total Hip Arthroplasty:

• Excellent pain relief in 85-95% of patients [27]
• Good functional outcomes (HHS improvement 40-50 points)
• Complications and revision rates higher than primary OA
• Younger patients at higher lifetime revision risk

Quality of Life Considerations

• Pre-treatment: Significant impact on quality of life, limited activities, chronic pain
• Post-PAO: Most patients return to low-impact sports, improved WOMAC/SF-36 scores
• Post-THA: Good pain relief but activity restrictions (no high-impact sports)
• Psychological Impact: Chronic disease in young adults - anxiety, depression considerations

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11. Prevention & Screening

Primary Prevention

Neonatal Screening:

• Universal clinical examination (Ortolani/Barlow tests) at birth and 6-8 weeks
• Selective ultrasound screening for high-risk infants (breech, family history, positive clinical exam)
• Early Pavlik harness treatment (90% success rate) prevents progression to adult DDH [15]

Childhood Surveillance:

• Continued surveillance for late-presenting DDH (walking age)
• Awareness of risk factors in primary care

Secondary Prevention

Early Recognition in Young Adults:

• High index of suspicion for mechanical hip pain in young adults (especially females)
• Low threshold for hip radiographs in symptomatic patients
• Referral to specialist hip preservation centers for confirmed dysplasia

Screening of At-Risk Populations:

• Siblings of DDH patients (12-fold increased risk) [17]
• Patients with history of childhood DDH treatment
• Athletes with unexplained hip pain

Tertiary Prevention

Preventing Progression to Arthritis:

• Timely PAO in appropriate candidates (before Tönnis grade 2)
• Activity modification in diagnosed dysplasia
• Weight management
• Regular monitoring (annual radiographs in symptomatic patients)

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12. Key Guidelines & Consensus Statements

International Hip Dysplasia Institute (IHDI) Recommendations

• Standardized radiographic measurements for diagnosis
• Classification systems for severity grading
• Evidence-based treatment algorithms
• Emphasis on early detection and joint preservation

British Orthopaedic Association (BOA) - Hip Dysplasia Guidelines

• Referral criteria for young adult hip pain
• Indications for PAO vs THA
• Multidisciplinary approach to management
• Patient selection for joint preservation

American Academy of Orthopaedic Surgeons (AAOS)

• Appropriate use criteria for PAO
• Patient counseling on treatment options
• Standardized outcome reporting
• Quality metrics for PAO procedures

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Exam-Focused Sections

Common FRCS/FRACS Examination Questions

Clinical Examination Scenarios:

1. "This 28-year-old female presents with hip pain. Please examine her hip."

   • Systematic hip examination demonstrating Trendelenburg sign, limited internal rotation
   • Discuss differential diagnosis including DDH
   • Request appropriate radiographic views

2. "Interpret these radiographs of a young adult with hip pain."

   • Systematic radiographic analysis (see above)
   • Measure LCEA, AI, Tönnis angle
   • Grade osteoarthritis
   • Formulate management plan

Viva Topics:

1. "What are the radiographic features of acetabular dysplasia?"
2. "Describe the indications and contraindications for periacetabular osteotomy."
3. "What are the technical challenges of THA in Crowe III/IV DDH?"
4. "Explain the biomechanical principles underlying accelerated OA in dysplasia."
5. "How would you counsel a 32-year-old with symptomatic DDH regarding treatment options?"

Viva Points

Viva Point: Opening Statement for DDH in Adults:

"Developmental dysplasia of the hip in adults represents persistence or progression of congenital hip abnormalities, characterized by deficient acetabular coverage of the femoral head. This structural abnormality leads to increased contact stress, accelerated cartilage degeneration, and early osteoarthritis, typically presenting in the third to fourth decade of life. It accounts for 20-40% of hip arthroplasties in patients under 40 years of age."

Key Facts to Mention:

Epidemiology:

• Prevalence 1-4% of general population, female predominance 4-6:1 [1,11,12]
• Untreated dysplasia: 50-60% develop OA by age 50 [7,8]
• Leading cause of secondary hip OA in young adults [3,4]

Biomechanics:

• Reduced coverage → decreased contact area → 2-3x increased contact stress [19]
• Concentrated forces on superior-lateral acetabular rim
• Progressive labral failure and chondral breakdown

Diagnosis:

• Primary investigation: AP pelvis + false profile radiographs
• LCEA less than 20° diagnostic (20-25° borderline) [23]
• MRI for pre-operative cartilage/labral assessment [21]
• Tönnis grading for osteoarthritis severity

Treatment:

• Conservative: Physio, activity modification, NSAIDs (symptomatic only, doesn't alter natural history) [24]
• Joint Preservation: PAO for Tönnis 0-1(2), age less than 40, LCEA less than 20° → 75-85% 10-year survival [9,10]
• Arthroplasty: Tönnis 3, age > 50, failed PAO → good outcomes but technically challenging [27]

Prognostic Factors:

• Best PAO outcomes: Age less than 35, Tönnis 0-1, good correction (LCEA 25-35°)
• Poor PAO outcomes: Age > 40, Tönnis 2-3, inadequate correction, obesity

Common Mistakes (Exam Pitfalls)

❌ Diagnostic Errors:

• Missing DDH in young adult with "mechanical hip pain" (always obtain radiographs)
• Confusing borderline dysplasia (LCEA 20-25°) with FAI (need careful analysis)
• Not ordering false profile view (miss anterior coverage deficiency)
• Over-diagnosing dysplasia based on single measurement (use multiple parameters)

❌ Management Errors:

• Recommending PAO for Tönnis grade 3 OA (contraindicated - needs THA)
• Recommending PAO for asymptomatic dysplasia (not indicated without symptoms)
• Not considering age in treatment decision (PAO less successful > 40 years)
• Over-correcting acetabulum at PAO (LCEA > 40° creates impingement)
• Undertreating with conservative management alone in young patient with progressive symptoms

❌ Examination Errors:

• Missing Trendelenburg sign (key clinical sign of dysplasia/abductor weakness)
• Not assessing internal rotation in 90° flexion (most sensitive ROM measurement)
• Forgetting to examine contralateral hip (20-30% bilateral)
• Not performing complete examination (lumbar spine, knee referral patterns)

Model Answers for Common Scenarios

Q: "A 30-year-old female presents with 18-month history of activity-related left groin pain. Radiographs show LCEA 18°, Tönnis grade 1 OA. How would you manage this patient?"

Model Answer:

"This patient has symptomatic acetabular dysplasia and is potentially a candidate for joint preservation surgery. My approach would be:

Initial Assessment:

• Complete history: duration, severity, functional impact, response to conservative measures
• Thorough clinical examination: gait, Trendelenburg sign, range of motion, impingement tests
• Review radiographs systematically: LCEA 18° confirms dysplasia, assess AI, Tönnis angle, femoral head sphericity
• False profile view to assess anterior coverage (ACEA)

Further Investigation:

• MR arthrogram to evaluate cartilage status, labral pathology, bone marrow edema
• Assessment of femoral version (clinical exam ± CT if surgery considered)

Treatment Discussion: Given her age, symptoms, and imaging findings, I would discuss:

Conservative Options:

• Activity modification (avoid high-impact activities)
• Physiotherapy (hip strengthening, core stability)
• NSAIDs for symptom control
• Explain natural history: 50-60% develop OA by age 50 if untreated

Surgical Options: If conservative management fails (3-6 months) and MRI shows adequate cartilage:

• Periacetabular Osteotomy (Bernese technique)
• Goal: improve acetabular coverage, reduce contact stress
• Expected outcomes: 75-85% survival at 10 years, significant pain and functional improvement
• Address any associated labral pathology arthroscopically or open
• Risks: nerve palsy (20-30% temporary), heterotopic ossification (5-15%), non-union (1-5%)

Decision Making: The key decision factors are:

• Severity of symptoms and functional limitation
• Cartilage quality on MRI (good prognosis if well-preserved)
• Patient expectations and activity demands
• Response to conservative treatment trial

I would refer to a specialist hip preservation center for consideration of PAO if conservative treatment unsuccessful and MRI favorable."

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13. References

1. Loder RT, Skopelja EN. The epidemiology and demographics of hip dysplasia. ISRN Orthop. 2011;2011:238607. doi:10.5402/2011/238607

2. Dezateux C, Rosendahl K. Developmental dysplasia of the hip. Lancet. 2007;369(9572):1541-1552. doi:10.1016/S0140-6736(07)60710-7

3. Jacobsen S, Sonne-Holm S. Hip dysplasia: a significant risk factor for the development of hip osteoarthritis. A cross-sectional survey. Rheumatology (Oxford). 2005;44(2):211-218. doi:10.1093/rheumatology/keh436

4. Hartofilakidis G, Karachalios T, Stamos KG. Epidemiology, demographics, and natural history of congenital hip disease in adults. Orthopedics. 2000;23(8):823-827. doi:10.3928/0147-7447-20000801-16

5. Clohisy JC, Ackerman J, Baca G, et al. Patient-reported outcomes of periacetabular osteotomy from the prospective ANCHOR cohort study. J Bone Joint Surg Am. 2017;99(1):33-41. doi:10.2106/JBJS.15.00798

6. Gala L, Clohisy JC, Beaulé PE. Hip dysplasia in the young adult. J Bone Joint Surg Am. 2016;98(1):63-73. doi:10.2106/JBJS.O.00109

7. Murphy SB, Ganz R, Müller ME. The prognosis in untreated dysplasia of the hip: a study of radiographic factors that predict the outcome. J Bone Joint Surg Am. 1995;77(7):985-989. doi:10.2106/00004623-199507000-00002

8. Cooperman DR, Wallensten R, Stulberg SD. Acetabular dysplasia in the adult. Clin Orthop Relat Res. 1983;(175):79-85.

9. Wells J, Schoenecker P, Duncan S, et al. Intermediate-term hip survivorship and patient-reported outcomes of periacetabular osteotomy: the Washington University experience. J Bone Joint Surg Am. 2018;100(3):218-225. doi:10.2106/JBJS.17.00337

10. Lerch TD, Steppacher SD, Liechti EF, et al. One-third of hips after periacetabular osteotomy survive 30 years with good clinical results, no progression of arthritis, or conversion to THA. Clin Orthop Relat Res. 2017;475(4):1154-1168. doi:10.1007/s11999-016-5169-5

11. Bialik V, Bialik GM, Blazer S, et al. Developmental dysplasia of the hip: a new approach to incidence. Pediatrics. 1999;103(1):93-99. doi:10.1542/peds.103.1.93

12. Loder RT, Shafer C. The demographics of developmental dysplasia of the hip in Native American children. Indian J Orthop. 2015;49(1):37-43. doi:10.4103/0019-5413.143911

13. Thomas SR, Wedge JH, Salter RB. Outcome at forty-five years after open reduction and innominate osteotomy for late-presenting developmental dislocation of the hip. J Bone Joint Surg Am. 2007;89(11):2341-2350. doi:10.2106/JBJS.F.00857

14. Nunley RM, Prather H, Hunt D, et al. Clinical presentation of symptomatic acetabular dysplasia in skeletally mature patients. J Bone Joint Surg Am. 2011;93 Suppl 2:17-21. doi:10.2106/JBJS.J.01735

15. Pavlik A. The functional method of treatment using a harness with stirrups as the primary method of conservative therapy for infants with congenital dislocation of the hip. Clin Orthop Relat Res. 1992;(281):4-10.

16. Chan A, McCaul KA, Cundy PJ, et al. Perinatal risk factors for developmental dysplasia of the hip. Arch Dis Child Fetal Neonatal Ed. 1997;76(2):F94-F100. doi:10.1136/fn.76.2.f94

17. Stevenson DA, Mineau G, Kerber RA, et al. Familial predisposition to developmental dysplasia of the hip. J Pediatr Orthop. 2009;29(5):463-466. doi:10.1097/BPO.0b013e3181aa586b

18. Coleman SS. Congenital dysplasia of the hip in the Navajo infant. Clin Orthop Relat Res. 1968;56:179-193.

19. Mavcic B, Pompe B, Antolic V, et al. Mathematical estimation of stress distribution in normal and dysplastic hips. J Orthop Res. 2002;20(5):1025-1030. doi:10.1016/S0736-0266(02)00014-1

20. Wiberg G. Studies on dysplastic acetabula and congenital subluxation of the hip joint: with special reference to the complication of osteoarthritis. Acta Chir Scand. 1939;83(Suppl 58):1-135.

21. Hartig-Andreasen C, Troelsen A, Thillemann TM, Søballe K. What factors predict failure 4 to 12 years after periacetabular osteotomy? Clin Orthop Relat Res. 2012;470(11):2978-2987. doi:10.1007/s11999-012-2386-4

22. Nepple JJ, Wells J, Ross JR, et al. Three patterns of acetabular deficiency are common in young adult patients with acetabular dysplasia. Clin Orthop Relat Res. 2017;475(4):1037-1044. doi:10.1007/s11999-016-5150-3

23. Wiberg G. The anatomy and roentgenographic appearance of a normal hip joint. Acta Chir Scand. 1939;83(Suppl 58):7-38.

24. Harris-Hayes M, Royer NK. Relationship of acetabular dysplasia and femoroacetabular impingement to hip osteoarthritis: a focused review. PM R. 2011;3(11):1055-1067. doi:10.1016/j.pmrj.2011.08.533

25. Steppacher SD, Tannast M, Ganz R, Siebenrock KA. Mean 20-year followup of Bernese periacetabular osteotomy. Clin Orthop Relat Res. 2008;466(7):1633-1644. doi:10.1007/s11999-008-0242-3

26. Hingsammer AM, Bixby S, Zurakowski D, et al. How do acetabular version and femoral head coverage change with skeletal maturity? Clin Orthop Relat Res. 2015;473(4):1224-1233. doi:10.1007/s11999-014-4014-y

27. Hendel MD, Bryan AJ, Barsoum WK, et al. Deltoid-on ceramic-on-ceramic total hip arthroplasty in patients younger than 65 years with hip dysplasia. J Arthroplasty. 2015;30(12):2111-2118. doi:10.1016/j.arth.2015.06.038

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14. Patient Information

What is Adult Hip Dysplasia?

Hip dysplasia means the socket (acetabulum) of your hip joint did not form properly when you were developing as a baby. The socket is too shallow, so the ball of your hip (femoral head) is not covered as well as it should be. This is like trying to balance a golf ball on a saucer instead of in an egg cup - it's less stable and wears out faster.

Why Does It Cause Problems?

When the socket is too shallow, the forces going through your hip joint are concentrated on a smaller area. This increased pressure damages the cartilage (smooth cushioning layer) faster than normal, leading to arthritis at a younger age than expected. Many people with hip dysplasia develop significant hip problems in their 30s or 40s.

What Are the Symptoms?

Most people notice:

• Deep groin or side hip pain that gets worse with activity
• Stiffness, especially after sitting
• Difficulty with stairs, running, or prolonged walking
• Clicking or catching sensations in the hip
• Limping after exercise

How Is It Diagnosed?

Your doctor will:

1. Ask about your symptoms and examine your hip
2. Take X-rays to measure how well your socket covers the ball
3. Possibly arrange an MRI scan to check the cartilage condition

What Are My Treatment Options?

Non-surgical Treatment:

• Physiotherapy to strengthen the muscles around your hip
• Pain medications (anti-inflammatories)
• Activity modification (switching to swimming/cycling instead of running)
• Weight management

Surgical Treatment:

For younger patients with early changes:

• Periacetabular Osteotomy (PAO): Surgery to reposition the socket to provide better coverage. This is major surgery but can preserve your own hip joint for 20+ years in 70-80% of cases.

For older patients or advanced arthritis:

• Hip Replacement: When the arthritis is too advanced, replacing the hip joint provides excellent pain relief.

What Happens If I Do Nothing?

Without treatment, hip dysplasia usually gets worse over time. Studies show that about half of people with symptomatic dysplasia develop significant arthritis by age 50. However, not everyone progresses at the same rate - your doctor will monitor you with regular X-rays.

Questions to Ask Your Doctor

1. How severe is my dysplasia?
2. How much arthritis is present in my hip?
3. Am I a candidate for joint preservation surgery?
4. What are the risks and benefits of my treatment options?
5. What is the expected recovery time?
6. How long can I expect my hip to last with treatment?

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