supracondylar humerus fracture knruhs 15 marks teory structured answe with diagrams 3

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Supracondylar Fracture of the Humerus

15-Mark Structured Answer (Theory)


1. Definition and Introduction

A supracondylar fracture of the humerus is a fracture of the distal humerus occurring just proximal to the condyles, through the olecranon and coronoid fossae - the narrowest and weakest part of the distal humerus.
  • Most common elbow fracture in children (age 5-7 years peak incidence)
  • Accounts for approximately 60% of all elbow fractures in the pediatric age group
  • Extension-type constitutes 97-98% of all cases
  • Rosen's Emergency Medicine, p. 3304

2. Surgical Anatomy (Relevant)

The distal humerus has a thin bony column flanked anteriorly by the coronoid fossa and posteriorly by the olecranon fossa, making this region particularly susceptible to fracture. Key anatomical relationships:
StructureRelationClinical Relevance
Brachial arteryAnterior to fractureRisk of vascular injury in Type III
Anterior interosseous nerve (AIN)AnteromedialMost commonly injured nerve
Radial nerveLateralAt risk in posterolateral displacement
Median nerveAnteromedialAt risk in posteromedial displacement
CRITOE - Ossification centers appear in this order (important for X-ray interpretation):
CenterAppearsCloses
Capitellum6-12 months14 yr
Radial head4-5 yr16 yr
Internal (medial) epicondyle5-7 yr18 yr
Trochlea9-10 yr16 yr
Olecranon9-10 yr16 yr
External (lateral) epicondyle10-12 yr16 yr
Ossification centers of elbow: 1-Capitellum, 2-Radial head, 3-Medial epicondyle, 4-Trochlea, 5-Lateral epicondyle
Fig. Ossification centers of the pediatric elbow (CRITOE). - Rosen's Emergency Medicine

3. Mechanism of Injury

Extension Type (97-98%)

  • Fall on an outstretched hand with elbow hyperextended
  • Force drives the distal fragment posteriorly and superiorly
  • The proximal fragment is driven anteriorly, threatening the brachial artery

Flexion Type (2-3%)

  • Fall directly on a flexed elbow
  • Distal fragment displaced anteriorly
  • Higher risk of ulnar nerve injury

4. Classification - Gartland Classification (Modified)

The Gartland classification is the standard for extension-type supracondylar fractures:
TypeDescriptionPosterior CortexTreatment
Type IUndisplaced / displaced ≤2 mm; posterior fat pad sign may be only findingIntactLong-arm cast 3 weeks in 90° flexion
Type IIAAngulated, posterior cortex intact; stableIntactClosed reduction + casting
Type IIBAngulated with rotational deformity; some instabilityIntactClosed reduction + percutaneous K-wire pinning
Type IIICompletely displaced; no cortical contactDisruptedClosed reduction + percutaneous pinning (CRPP)
Type IVHigh-energy; periosteal hinge disrupted in all planes; unstable in flexion AND extensionCompletely disruptedClosed reduction + percutaneous pinning
  • Campbell's Operative Orthopaedics, Table 38.2
  • Tintinalli's Emergency Medicine, p. 3303

5. Clinical Features

History

  • Child aged 5-7 years
  • Fall onto outstretched hand
  • Immediate pain, refusal to use limb

Examination

Look:
  • Swelling and bruising around elbow
  • Deformity - "S-shaped" elbow on lateral view
  • Pucker sign - skin dimpling anteriorly (proximal fragment penetrating brachialis) - indicates difficult reduction
Feel:
  • Tenderness over distal humerus
  • Assess 5 Ps of vascular compromise: Pain, Pallor, Pulselessness, Paralysis, Paresthesias
  • Palpate radial and ulnar pulses
Neurovascular assessment (MANDATORY):
  • Anterior interosseous nerve (AIN) - test by thumb IP joint flexion ("OK sign"); injury causes "pointing index sign"
  • Radial nerve - wrist/finger extension
  • Median nerve - sensation index finger tip

6. Radiological Assessment

Views Required

  • AP and lateral elbow X-rays
  • Oblique views if clinical suspicion high

Key Radiological Signs

1. Anterior Humeral Line (AHL)
  • On a true lateral, a line drawn along the anterior cortex of the humerus should intersect the middle third of the capitellum
  • In extension-type fracture: line passes through the anterior third or anterior to the capitellum (capitellum displaced posteriorly)
2. Posterior Fat Pad Sign
  • Posterior fat pad is always pathological on lateral X-ray
  • Anterior fat pad "sail sign" = bulging = effusion/occult fracture
  • Type I fractures may show ONLY a posterior fat pad sign
3. Baumann Angle
  • Angle between the growth plate of the capitellum and the long axis of the humerus on AP view
  • Normal: 70-75 degrees
  • Asymmetric or abnormal Baumann angle suggests fracture/malreduction
  • Used to assess adequacy of reduction

7. Management

Emergency Assessment

  1. Full neurovascular examination
  2. Splint in position of comfort (avoid hyperflexion if swollen)
  3. X-rays

Treatment by Type

TYPE I
  → Long-arm posterior splint / backslab
  → Elbow at 90°, forearm neutral/pronation
  → Immobilize 3 weeks
  → Outpatient orthopaedic follow-up in 1 week

TYPE IIA
  → Closed reduction under GA
  → Above-elbow cast 3-4 weeks

TYPE IIB / TYPE III / TYPE IV
  → Closed Reduction + Percutaneous Pinning (CRPP)
  → Two or three lateral K-wires (avoids ulnar nerve risk)
  → OR crossed pins (lateral + medial) for Type III/IV
  → Above-elbow cast post-op
  → Pins removed at 3-4 weeks

Percutaneous K-Wire Fixation

  • Lateral pins only: 2-3 divergent lateral entry pins - preferred to avoid iatrogenic ulnar nerve injury
  • Crossed pins: provides more rotational stability but risks ulnar nerve injury with medial pin
  • If periosteal hinge is broken (Type III/IV), K-wires are mandatory - cast alone insufficient

Open Reduction Indications

  • Failed closed reduction (usually due to soft tissue interposition)
  • Open fractures
  • Vascular injury requiring exploration
  • Irreducible (pucker sign / brachialis interposition)

8. Neurovascular Management

White Pulseless Hand (= surgical emergency)

  • Immediate reduction in operating theatre
  • If pulse returns after reduction → observe in 45° flexion, not hyperflexed
  • If pulse does not return → explore brachial artery (anterior approach), prepare for vein graft

Pink Pulseless Hand (controversial)

  • Good capillary refill, normal colour but no palpable pulse
  • Reduce and pin fracture first
  • Observe - pulse often returns within 24-48 hours
  • If no recovery → brachial artery exploration
Management algorithm for pulseless supracondylar humeral fracture - Campbell's Operative Orthopaedics 15th Ed
Fig. 38.11 - Management algorithm for pulseless supracondylar humeral fracture (Campbell's Operative Orthopaedics, 15th Ed 2026)

9. Complications

Early Complications

ComplicationNotes
Vascular injuryBrachial artery; more common with Type III posterolateral displacement
Nerve injuryAIN most common (neuropraxia); usually resolves after reduction
Compartment syndrome0.1-0.3%; "3 As" in children = agitation, anxiety, increasing analgesia - early signs
Volkmann's Ischaemic ContractureFeared complication from missed compartment syndrome / excessive elbow flexion; causes fibrosis of forearm flexors

Late Complications

ComplicationNotes
Cubitus varus (most common late complication)"Gunstock deformity" - due to malunion in varus; mainly cosmetic but can cause late lateral ulnar collateral ligament laxity and posterolateral rotatory instability
Cubitus valgusLess common; can cause late ulnar nerve palsy ("tardy ulnar nerve palsy")
Elbow stiffnessUsually resolves without intervention
Avascular necrosisRare
Myositis ossificansFrom aggressive passive mobilisation; avoid forceful physiotherapy
Brachial artery injury exposed at exploration in Type III supracondylar fracture - Campbell's Operative Orthopaedics
Fig. 38.10B - Brachial artery injury in Type III supracondylar fracture (Campbell's Operative Orthopaedics, 15th Ed)

10. Prognosis

  • Type I: Excellent, full recovery expected
  • Type II/III with prompt CRPP: Good; most achieve full elbow motion
  • Nerve injuries: 90%+ resolve spontaneously within 3-6 months
  • Cubitus varus: May require corrective supracondylar osteotomy if severe/symptomatic

Summary Box (High-Yield for Exam)

FeatureKey Point
Most common elbow # in childrenAge 5-7, extension type 98%
MechanismFOOSH (fall on outstretched hand) with hyperextension
ClassificationGartland Types I, IIA, IIB, III, IV
Radiological signsAHL, Baumann angle, fat pad sign
Most common nerve injuredAIN → pointing index sign
Vascular riskBrachial artery in posterolateral Type III
Treatment Type ILong-arm cast 3 weeks
Treatment Type IIB/III/IVCRPP with K-wires
Most common late complicationCubitus varus (gunstock deformity)
Dreaded complicationVolkmann's ischaemic contracture

Sources: Campbell's Operative Orthopaedics 15th Ed 2026 | Rosen's Emergency Medicine | Tintinalli's Emergency Medicine | Bailey and Love's Surgery 28th Ed | Miller's Review of Orthopaedics 9th Ed

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Supracondylar Humerus Fracture MS Ortho 2026

Presentation · PPTX

(387 KB)

Presentation Contents — 11 Slides

SlideTitle
1Title Slide - Dark navy/gold theme, 2026 MS Orthopaedics branding
2High-Yield Overview - 9 exam-critical facts in a colour-coded table
3Gartland Classification - Full table: Type I / IIA / IIB / III / IV with description, X-ray features, treatment
4Radiological Assessment - AHL, Baumann angle, fat pad signs, CRITOE - 4 colour-coded cards
5Management Algorithm - Flowchart by Gartland type, Emergency assessment → Treatment
6Pulseless Hand — Vascular Algorithm - Dark urgent slide: White vs pink pulseless, brachial artery exploration flowchart
7Neurological Complications - AIN / Radial / Median / Ulnar nerve - assessment tests + management per nerve
8Early Complications - Vascular injury, nerve injury, compartment syndrome, Volkmann's contracture
9Late Complications - Cubitus varus (featured), cubitus valgus, stiffness, myositis ossificans, AVN
10K-Wire Fixation — Operative Technique - 6-step CRPP technique, indications, pin configurations
11Exam Summary - 16 numbered high-yield points in two columns
Design: Navy/teal/gold colour scheme throughout, structured cards with header bars, colour-coded by clinical severity, sourced from Campbell's 15th Ed 2026, Rosen's, Tintinalli, Bailey & Love 28th Ed.

ddh 2026 theoty exam strucured answe with 3 pencil diagrams 15 marks

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Developmental Dysplasia of the Hip (DDH)

15-Mark Structured Answer — 2026 MS Orthopaedics Theory Examination


1. Definition

Developmental Dysplasia of the Hip (DDH) describes a spectrum of disorders ranging from mild acetabular dysplasia to frank dislocation of the femoral head from the acetabulum, which may present at birth or develop during the first years of life.
  • Previously called "Congenital Dislocation of the Hip (CDH)" — the term DDH is now preferred as it recognises the developmental and evolving nature of the condition
  • Campbell's Operative Orthopaedics, 15th Ed 2026, p. 1402

2. Incidence and Risk Factors

Incidence: 1-2 per 1,000 live births (frank dislocation); dysplasia alone is more common
Risk FactorDetails
Female sex6:1 female:male ratio (relaxin sensitivity)
Breech presentationStrongest single risk factor; hips forced into extension
Left hipMore common (left occiput anterior position presses left hip against maternal spine)
First-born childTighter uterine/abdominal wall
Family history~10% risk if positive
OligohydramniosReduced intrauterine movement
Ligamentous laxityMaternal relaxin crossing placenta
Associated conditionsCongenital torticollis (8% co-existence), metatarsus adductus
SwaddlingCultural factor - hip extension/adduction increases risk

3. Pathological Anatomy

In DDH, secondary changes develop progressively with age:
Acetabulum:
  • Shallow, oblique roof (increased acetabular index)
  • Inverted/hypertrophied limbus (labrum) - may block reduction
  • Pulvinar (fatty fibrofatty tissue) fills acetabular floor
Femoral head:
  • Displaced superolaterally
  • Anteversion increases
  • Ossification delayed
Soft tissue obstacles to reduction (in older children):
  1. Contracted iliopsoas tendon (hourglass capsule)
  2. Hypertrophied ligamentum teres
  3. Inverted/hypertrophied acetabular labrum (limbus)
  4. Pulvinar in acetabular floor
  5. Tight adductor muscles

4. Clinical Features

Neonatal Assessment (0-3 months)

Ortolani Test (Reduction test):
  • Hip flexed to 90°, knee flexed
  • Gentle abduction + anterior lift of greater trochanter
  • Positive: palpable "clunk" as dislocated femoral head reduces into acetabulum
Barlow Test (Provocation/Dislocation test):
  • Hip adducted + gentle posterior pressure applied
  • Positive: femoral head felt to dislocate posteriorly out of acetabulum
  • Both tests lose sensitivity after 3 months (soft tissue contracture)

Older Infant / Toddler (3 months - 3 years)

SignMethodSignificance
Galeazzi Sign (Allis sign)Hips + knees flexed, supine - unequal knee heightsShortened femur on affected side
Limited abduction<45° abduction on affected sideTight adductors + capsule
TelescopingIn-out pistoning of femur in dislocated hipMobile dislocation
Trendelenburg signWeight-bearing on affected side - pelvis droops to opposite sideWeak abductors
Short limbApparent leg length discrepancyProximal femoral displacement

Ambulatory Child (after walking age)

  • Trendelenburg gait (waddling) - unilateral
  • Bilateral DDH: waddling gait, hyperlordosis, prominent trochanters

5. Radiological Assessment

A. Plain X-ray (AP Pelvis)

X-rays are unreliable under 6 weeks (femoral head not ossified). The ossific nucleus appears at ~4-6 months.

DIAGRAM 1: Radiological Lines and Signs of DDH
Radiological signs of DDH - Hilgenreiner line, Perkins line, Shenton line, Acetabular index, quadrants
Diagram 1: AP pelvis radiological landmarks in DDH. Left hip dislocated (femoral head in upper outer quadrant); right hip normal for comparison.

Key Radiological Lines:
Line/SignDescriptionNormalAbnormal in DDH
Hilgenreiner lineHorizontal line through both triradiate cartilages-Used as baseline
Perkins lineVertical line from lateral acetabular edge, perpendicular to Hilgenreiner-Used as baseline
QuadrantsFormed by above two linesOssific nucleus in lower inner quadrantNucleus in upper outer quadrant = dislocated
Shenton lineSmooth arc along inferior femoral neck + superior obturator foramenSmooth continuous arcBroken/disrupted in subluxation/dislocation
Acetabular IndexAngle between Hilgenreiner line and acetabular roof line<30° at birth; <20° by 2 years>30° = dysplastic acetabulum
CE angle of WibergCentre-edge angle (>5 years)>20°<20° = dysplasia

B. Ultrasound (Graf Classification - <6 months)

  • Gold standard for infants under 6 months
  • Measures: alpha angle (bony acetabular roof) and beta angle (cartilaginous roof)
Graf TypeAlpha AngleInterpretation
Type I>60°Normal
Type IIa50-59°Physiologically immature (<3 months)
Type IIb50-59°Deficient roof (>3 months) - treat
Type III<43°Subluxation
Type IV-Complete dislocation

C. MRI / Arthrography

  • Arthrogram under GA: used before closed reduction to assess medial dye pool, safe zone, obstacles
  • Acceptable: medial dye pool ≤5 mm, safe zone ≥20° (ideally ≥45°)
  • MRI: gold standard for assessing reduction quality in spica cast

6. Classification (IHDI - International Hip Dysplasia Institute)

IHDI Classification - Grade I to IV showing progressive displacement of femoral head using Hilgenreiner-Perkins quadrant system
Fig. IHDI Classification: Grade I = normal (lower inner quadrant); Grades II-IV = progressive displacement using 45° diagonal line subdividing outer lower quadrant. (Campbell's Operative Orthopaedics 15th Ed 2026)
IHDI GradePosition of femoral head metaphysis
ILower inner quadrant (normal)
IILower outer quadrant (mild subluxation)
IIIUpper outer quadrant (significant dislocation)
IVAbove Hilgenreiner line (high dislocation)

7. Treatment

Treatment is age-dependent. The goal is concentric reduction of the femoral head into the acetabulum with preservation of vascularity (prevent AVN).

DIAGRAM 2: Clinical Examination Tests (Ortolani, Barlow, Galeazzi)
Ortolani test, Barlow test, and Galeazzi sign for DDH examination
Diagram 2: Clinical examination tests for DDH. Ortolani = reduction test (clunk felt on abduction). Barlow = dislocation test (femoral head pushed posterior). Galeazzi = unequal knee heights in older infant.

DIAGRAM 3: Age-based Treatment Algorithm
Age-based treatment algorithm for DDH from birth to 8 years
Diagram 3: Age-based management algorithm for DDH. Treatment escalates with age due to secondary soft-tissue and bony changes.

Treatment by Age Group

A. Newborn to 6 Months — Pavlik Harness

  • Pavlik harness: dynamic flexion-abduction orthosis
  • Maintains hips in flexion 100-110°, abduction 40-50° (Salter position)
  • Worn full-time initially; weaned over weeks
  • Success rate: 85-95% in first few months of life
  • Complications: femoral nerve palsy; avascular necrosis (<1%)
  • Failure factors: absent Ortolani sign, bilateral dislocation, acetabular index >36°, age >6 months at start
  • If Pavlik harness fails → trial with rigid abduction orthosis (Craig splint / Von Rosen splint)

B. 6 to 18 Months — Closed or Open Reduction

Step 1: Adductor tenotomy (if adductor tightness limits abduction)
Step 2: Closed reduction under GA + arthrography
  • Assess medial dye pool (acceptable ≤5 mm)
  • Assess safe zone (Ramsey): acceptable ≥20°, ideal ≥45°
  • Followed by hip spica cast in Salter position (human position)
Step 3: If closed reduction fails → Open Reduction
  • Approach: anterolateral (Smith-Petersen) - most common
  • Remove all obstacles: iliopsoas tendon, pulvinar, hypertrophied ligamentum teres, inverted limbus
  • Capsulorrhaphy (tighten capsule)
  • Followed by hip spica cast 6-12 weeks

C. 18 Months to 3 Years — Open Reduction + Femoral Osteotomy

  • Open reduction (as above) +
  • Derotation (shortening) femoral osteotomy: reduces tension on femoral head; corrects anteversion
  • Shortening reduces risk of AVN from pressure during reduction
  • Spica cast 6-12 weeks post-op

D. 3 to 8 Years — Open Reduction + Combined Osteotomies

  • Open reduction +
  • Femoral osteotomy (shortening + derotation) +
  • Pelvic osteotomy:
OsteotomyPrincipleIndication
Salter InnominateRedirects acetabulum anterolaterally (rotates on symphysis pubis)Child <6 yr, reducible hip, adequate acetabular size
DegaIncomplete cut; bends acetabular roof over femoral headLarger correction needed; neuromuscular DDH
PembertonReduces acetabular volumeCartilaginous acetabulum
Triple osteotomy (Steel/Tonnis)Cuts all 3 pelvic bones; full acetabular mobilityOlder children/adolescents, closed triradiate cartilage

E. Older Child / Adolescent (>8 years)

  • Prognosis for full correction worsens significantly
  • Salvage procedures: Shelf acetabuloplasty, Chiari osteotomy (medialisation of femoral head)
  • Total hip arthroplasty in adults with painful DDH-related arthritis

8. Complications

Early Complications

ComplicationNotes
Avascular Necrosis (AVN) of femoral headMost feared; incidence 0-25% depending on method; results from excessive abduction (>60°), forceful reduction, or vascular damage at surgery. Kalamchi-MacEwen classification (Types I-IV)
Re-dislocationHigher with inadequate reduction or soft tissue interposition
Femoral nerve palsyComplication of Pavlik harness (excessive flexion)
Residual dysplasiaCommonest late problem after treatment

Late Complications

ComplicationNotes
Premature osteoarthritisFrom residual dysplasia + incongruent joint → early total hip replacement
Leg length discrepancyDue to proximal femoral growth disturbance / AVN
Coxa magnaEnlarged femoral head after AVN
StiffnessAfter prolonged immobilisation / open procedures

9. Summary (High-Yield Exam Points)

FeatureKey Point
Peak riskFemale, breech, family history, first-born, left hip
Neonatal testOrtolani (reduction) + Barlow (dislocation provocation)
Imaging <6 monthsUltrasound (Graf classification); X-ray unreliable
X-ray landmarksHilgenreiner + Perkins lines → quadrants; Shenton line; Acetabular index
Normal acetabular index<30° at birth; <20° by age 2
0-6 months treatmentPavlik harness (85-95% success)
6-18 months treatmentClosed reduction + spica cast; or open reduction
Most feared complicationAvascular Necrosis (AVN) of femoral head
Most common late complicationPremature osteoarthritis
"Human position" in spicaFlexion 100°, abduction 40-50° - maintains reduction, reduces AVN risk

Sources: Campbell's Operative Orthopaedics 15th Ed 2026 (pp. 1402-1170) | Miller's Review of Orthopaedics 9th Ed | Schwartz's Principles of Surgery 11th Ed

perthes disesse 10 marks structured answer with 3 pencil diagrams for ms ortho theory examination

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Legg-Calvé-Perthes Disease (Perthes Disease)

10-Mark Structured Answer — 2026 MS Orthopaedics Theory Examination


1. Definition

Legg-Calvé-Perthes (LCP) disease is idiopathic avascular necrosis (AVN) of the proximal femoral epiphysis in children, leading to a self-limiting cycle of necrosis, collapse, revascularisation, and reossification of the femoral head. The final shape of the healed femoral head determines long-term hip function.

2. Epidemiology

FeatureDetails
SexBoys : Girls = 4:1
Age4-10 years (average 7 years)
LateralityUnilateral in 90%; bilateral in 10% (sequential, not simultaneous)
SocioeconomicMore common in lower socioeconomic groups
AssociatedPassive smoking, low birth weight, skeletal maturity delay

3. Aetiology / Pathophysiology

The exact cause is unknown but a vascular interruption to the capital femoral epiphysis is the final common pathway.
Proposed mechanisms:
  • Coagulation disorder / thrombophilia promoting thrombotic occlusion of the lateral epiphyseal arteries
  • Increased intracapsular pressure from synovitis compromising blood supply
  • Repetitive micro-trauma
  • Elevated venous pressure
The capital femoral epiphysis in children is supplied by the lateral epiphyseal arteries (branches of the medial femoral circumflex artery) — which run along the femoral neck and are vulnerable to compression and injury. Once ischaemia occurs, the process follows a predictable course.

4. Stages (Waldenström's Radiological Stages)


DIAGRAM 1: Four Stages of Perthes Disease
Four radiological stages of Perthes disease - necrosis, fragmentation, reossification, remodeling
Diagram 1: Sequential radiological stages of Perthes disease from initial necrosis to healed coxa plana.

StageRadiological FindingsDurationClinical
1. Initial (Necrosis)Smaller, dense sclerotic epiphysis; medial joint space widening; subchondral fracture (crescent sign); X-ray may be normal for 3-6 monthsMonthsHip pain, limp
2. FragmentationFemoral head appears fragmented and irregular; resorption of dead bone; lateral extrusion may begin1-3 yearsSymptoms most severe
3. ReossificationNew bone lays down in the femoral head; irregular density; head re-formingUp to 18 monthsSymptoms improving
4. Healing / RemodellingTrabecular pattern returns; head remodels until skeletal maturity; may result in coxa plana, coxa magnaUntil maturityMinimal symptoms

5. Clinical Features

History:
  • Intermittent pain in the hip or referred to the knee (obturator nerve)
  • Insidious onset limp
  • Symptoms often present for 6 weeks before diagnosis
Examination:
SignDescription
Antalgic gaitShort-stride limp away from painful side
Trendelenburg signPositive if abductor weakness
Restricted internal rotation + abductionMost consistent finding; due to spasm and synovitis
Flexion contractureIn severe/late cases
Muscle wastingThigh atrophy from disuse
Leg length discrepancyMild shortening in severe cases

6. Investigations

X-ray (AP + Frog-lateral pelvis): First line; may be normal in early disease
Textbook radiograph — Perthes disease (whole head involvement):
AP pelvic X-ray showing Perthes disease with dense necrotic bone in right femoral head - Bailey & Love 28th Ed
Fig. AP pelvis X-ray showing early Perthes disease of right hip: dense necrotic femoral head epiphysis with sclerosis. (Bailey & Love's Surgery 28th Ed)
MRI: Most sensitive early investigation; shows extent of ischaemia before X-ray changes appear; used for pretreatment planning
Bone scan (Tc-99m): Shows photon deficient area early ("cold spot"); useful when X-ray normal
Arthrogram: Assesses true cartilaginous femoral head shape; guides surgical planning

7. Classification

A. Catterall Classification (Amount of head involvement)

GroupInvolvementAt-risk signs
IAnterior epiphysis only (<25%)None
IIAnterior with sequestrum (~50%)May be present
IIIMost of head involved (~75%)Usually present
IVTotal head involvement (100%)Present
Catterall "Head-at-Risk" Signs (indicate poor prognosis):
  1. Gage sign - V-shaped radiolucency at lateral epiphysis/metaphysis
  2. Calcification lateral to epiphysis
  3. Lateral subluxation of femoral head
  4. Horizontal (oblique) proximal femoral physis
  5. Metaphyseal cyst

B. Herring Lateral Pillar Classification (Most widely used - applied in fragmentation stage)


DIAGRAM 2: Herring Lateral Pillar Classification
Herring Lateral Pillar Classification - Group A, B, C showing varying lateral pillar height in Perthes disease
Diagram 2: Herring Lateral Pillar Classification. The femoral head is divided into medial, central and lateral thirds. Lateral pillar height determines group and prognosis.

GroupLateral Pillar HeightPrognosis
AFully maintained (no loss)Uniformly good regardless of age
B>50% of original height maintainedGood if age <9 yr; poor if >9 yr
B/C borderExactly 50% or thin lateral pillarIntermediate
C<50% original heightWorst; aspherical head regardless of age/treatment

C. Stulberg Classification (Outcome / healed stage)

ClassDescriptionLong-term
INormal spherical head, normal hipNo arthritis
IISpherical head, coxa magna/plana/short neckNo arthritis
IIIAspherical femoral head (ovoid/mushroom), congruentMild arthritis
IVAspherical head, congruent flat acetabulumModerate arthritis
VAspherical head, incongruent acetabulumSevere arthritis

8. Management

Principle of Treatment — CONTAINMENT

The containment principle states that the soft, plastic femoral head during fragmentation, if held concentrically within the acetabulum, will be moulded into a spherical shape by the acetabulum acting as a biological mould. This reduces deformity and improves long-term outcome.

DIAGRAM 3: Containment Concept and Treatment Algorithm
Containment concept and age-based treatment algorithm for Perthes disease
Diagram 3: Containment concept - the acetabulum molds the plastic femoral head. Age-based treatment decision flowchart.

Treatment Decision (Age + Herring Grade)

Age at OnsetHerring GradeTreatment
<6 yearsAnyConservative (excellent remodelling potential)
6-8 yearsAConservative
6-8 yearsB or B/CConsider surgical containment
>8 yearsAConservative
>8 yearsB, B/C, CSurgical containment strongly recommended

A. Conservative (Non-Operative) Treatment

  • Goal: maintain range of motion, prevent deformity
  • Physiotherapy: stretching exercises, maintain abduction and internal rotation
  • NSAIDs / analgesics: for pain and synovitis
  • Crutches if severe pain (avoid prolonged non-weight-bearing)
  • Avoid wheelchairs and prolonged bed rest (promote hip flexion-adduction deformity)
  • Bracing (Petrie cast / Atlanta brace): maintains abduction-internal rotation but evidence does not support altering natural history; rarely used now
  • Serial X-rays every 3-6 months to monitor stage and Herring grade

B. Surgical Containment

Indicated when conservative treatment fails to achieve containment or in high-risk groups
1. Proximal Femoral Varus Osteotomy (PFVO):
  • Redirects femoral head deeper into acetabulum
  • Corrects any coxa valga
  • Most common surgical procedure for Perthes
  • Risk: excessive varus, limb shortening, Trendelenburg gait
2. Salter Innominate Osteotomy:
  • Redirects acetabulum anterolaterally to cover femoral head
  • Preferred when femoral head is in good position but acetabular coverage insufficient
  • Can be combined with PFVO (triple containment)
3. Combined (Femoral + Pelvic) osteotomy: for severe cases in older children

C. Salvage Procedures (for healed deformed hip)

  • Shelf acetabuloplasty: extends acetabular cover over enlarged femoral head
  • Chiari osteotomy: pelvic medialisation osteotomy
  • Trochanteric advancement / greater trochanter epiphyseodesis: corrects high riding trochanter
  • Hip distraction (arthrodiastasis): Ilizarov frame; used in late onset severe disease
  • Total hip arthroplasty: in adults with painful end-stage deformity

9. Prognosis

Favourable prognostic factors:
  • Young age at onset (<6 years) — more remodelling time
  • Male sex (greater remodelling potential)
  • Herring Group A (or B at young age)
  • Spherical femoral head at healing
Poor prognostic factors:
  • Age >9 years at onset
  • Herring Group B/C or C
  • Head-at-risk signs present
  • Lateral subluxation of femoral head
  • Stulberg Class III-V at skeletal maturity → premature osteoarthritis
The overall time course of the disease is 2-4 years from onset to healing.

10. Complications

ComplicationNotes
Coxa magnaEnlarged femoral head due to hyperaemia during revascularisation
Coxa planaFlattened femoral head from collapse - most common deformity
Premature osteoarthritisResult of aspherical incongruent joint; may need THA in 40s-50s
Hinge abductionExtruded lateral head "hinges" against acetabular rim on abduction - causes pain
Leg length discrepancyFrom growth disturbance of proximal femoral physis
Short femoral neckWith high-riding greater trochanter → abductor weakness
Trochanteric overgrowthRelative lengthening → Trendelenburg gait

Summary — High-Yield Exam Points

FeatureKey Point
DiseaseSelf-limiting AVN of femoral head in children
IncidenceBoys 4:1, age 4-10 yr, peak 7 yr, 10% bilateral
StagesInitial → Fragmentation → Reossification → Healing
Most used classificationHerring Lateral Pillar (A/B/B/C border/C) — applied in fragmentation stage
Outcome classificationStulberg (I-V) — applied at skeletal maturity
Treatment principleContainment — acetabulum molds femoral head
Age <6Conservative — excellent prognosis
Age >8 + Herring B/C or CSurgical containment (PFVO or Salter osteotomy)
Worst prognostic signLateral subluxation + Herring C + age >9 years
Long-term riskPremature OA → THA in adult life

Sources: Campbell's Operative Orthopaedics 15th Ed 2026 (p. 1474) | Bailey & Love's Short Practice of Surgery 28th Ed | Rosen's Emergency Medicine

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