Pelvic injuries. Orthopaedics notes

Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Reading File
Reading File
Loading Image
Loading Image
Loading Image
Loading Image
Excellent — I have all the material needed. Here are comprehensive orthopaedic notes on pelvic injuries:

Pelvic Injuries — Orthopaedic Notes

Sources: Miller's Review of Orthopaedics (9th ed.), Rockwood & Green's Fractures in Adults (10th ed., 2025)

1. Anatomy and Conceptual Framework

The pelvis must be viewed as a ring structure. A single break in the ring generally does not produce instability. Unstable injuries always involve injury to at least two areas of the pelvis. The pelvis is divided into:
  • Anterior ring — pubic symphysis and pubic rami
  • Posterior ring — sacroiliac (SI) joints, sacrum, ilium
The posterior ring is the primary load-bearing structure. Ligamentous stability is critical: the interosseous sacroiliac ligament is the strongest ligament of the pelvic ring. The sacrotuberous, sacrospinous, and iliolumbar ligaments provide supplementary stability.

2. Imaging

ViewWhat It Shows
AP pelvisInitial trauma evaluation; identifies increased pelvic volume
Inlet (beam tilted toward head)AP displacement of SI joint; internal/external rotation; anterior/posterior sacral breach during screw placement
Outlet (beam tilted toward feet)Vertical displacement; S1/S2 neural foramina; protects from nerve root injury during screw placement
Lateral sacralIliac cortical density (ICD); L5 nerve root protection
Flamingo/single-leg-stance viewsDynamic instability at pubic symphysis — useful in subacute setting
CT scanPosterior injury patterns; sacral dysmorphism; 3D reconstruction for acetabulum
Key principle: CT in a binder/sheet may underestimate injury severity.

3. Pelvic Ring Injuries — Classification

Young-Burgess Classification (mechanism-based)

Young-Burgess Classification of Pelvic Ring Fractures

Lateral Compression (LC) — all have anterior transverse pubic ramus fracture

TypePosterior LesionKey Features
LC ISacral compression fractureStable
LC IIPosterior iliac wing "crescent" fracture
LC IIIContralateral APC injury ("windswept pelvis")Rollover mechanism; crush injury pattern; other organs typically spared
Cause of death in LC pattern = primarily brain injury.

Anteroposterior Compression (APC) — all have symphyseal diastasis

TypeDiastasisLigament DisruptionKey Features
APC I< 2.5 cmAnterior SI ligaments stretchedStable
APC II> 2.5 cmSacrotuberous + sacrospinous + anterior SI rupturedAnterior SI joint opens; ORIF + posterior fixation lowers failure rate
APC III> 2.5 cmAll SI ligaments (anterior + posterior) rupturedComplete hemipelvis separation; highest transfusion requirements
Cause of death in APC pattern = shock, sepsis, ARDS. Associated injuries: urethral + bladder injuries; rising incidence of vascular/visceral injury APC I → III.

Vertical Shear (VS)

  • Fall mechanism; vertical fractures through rami + complete posterior disruption
  • Vertical displacement of hemipelvis; equivalent to APC III in instability
  • Mortality and transfusion requirements similar to APC II/III

Combined Mechanism (CM)

  • Organ injury pattern similar to lower-grade APC and LC patterns
Stable types: LC I and APC I High hemorrhage risk: APC II, APC III, LC III, VS

Tile Classification (stability-based)

TypeStabilityExamples
AStable (posterior arch intact)Avulsion, iliac wing, transverse sacral fractures
BRotationally unstable, vertically stableExternal rotation: anterior pelvic disruption ± anterior SI lig; LC: ipsilateral / contralateral (bucket-handle) / bilateral
CCompletely unstable (posterior arch disrupted)Unilateral, bilateral-mixed (one B, one C), bilateral C

4. Emergency Management

Life-threatening hemorrhage — 85% from venous injury (internal iliac plexus); only 15% arterial.
Priority sequence:
  1. Apply pelvic binder or sheet immediately if increased pelvic volume is identified — reduces pelvic volume and tamponades venous bleeding
  2. Skeletal traction for vertical instability
  3. Resuscitation — volume + early transfusions
  4. CT scan to evaluate for arterial injury
  5. Angiographic embolization if arterial source confirmed
  6. Pelvic packing (retroperitoneal) — excellent for venous tamponade; popularized in Europe
⚠️ Always establish and follow a treatment protocol to reduce variation in decision-making.

5. Treatment of Pelvic Ring Injuries

Nonoperative

  • Indications: stable fracture patterns (LC I, APC I)
  • Weight bearing as tolerated for isolated anterior injuries
  • Protected weight bearing for combined anterior + posterior ring injuries

Operative Indications

  • Symphysis diastasis > 2.5 cm
  • Anterior + posterior SI ligament disruption
  • Vertical instability of posterior hemipelvis
  • Sacral fracture displacement > 1 cm

Anterior Injuries

OptionNotes
ORIF with plate fixationAvoids pin tract complications; biomechanically superior for symphysis
External fixation (AIIS or iliac wing pins)AIIS biomechanically stronger; iliac wing better tolerated clinically; risk to lateral femoral cutaneous nerve
Anterior subcutaneous internal fixator (INFIX)Reduced dissection; risk of femoral nerve injury (impairs quad function); lateral femoral cutaneous nerve injury in ~1/3; HO most common complication (usually asymptomatic)

Posterior Injuries

OptionNotes
Percutaneous iliosacral or trans-sacral screwsTrans-sacral > iliosacral in stability; mandatory fluoroscopic landmark identification before surgery (AP, inlet, outlet, lateral views — see diagram below)
Anterior plate fixation across SI joint
Posterior transiliac sacral bars or sacral plating
Spinal-pelvic fixationBilateral sacral fractures; triangular osteosynthesis has high implant prominence/pain rate
Most stable construct for vertically unstable anterior + posterior dislocationsAnterior ring internal fixation + percutaneous SI screw
Fluoroscopic views for iliosacral screw placement — AP, Inlet, Outlet, and Lateral with ICD

6. Sacral Fractures

Denis Classification (zone relative to foramen)

ZoneLocationNeurologic Risk
Zone ILateral to foramina (sacral ala)Low
Zone IIThrough foraminaL5 nerve root most common; highest incidence of urologic injury
Zone IIICentral (sacral canal)Cauda equina syndrome
H-fracture / U-fracture — bilateral Zone II/III injuries; assess sagittal CT reformats for kyphosis.

Sacral Dysmorphism (20–44% of population)

Sacralization of L5 or lumbarization of S1. Creates anterosuperior sacral concavity — high risk of anterior screw penetration causing neurologic injury.
Outlet view signs: prominent mammillary processes, laterally downsloping sacral ala, vestigial disc space between S1–S2, iliac crest at level of L5–S1, non-circular S1 tunnel.

Treatment

  • Nonoperative: stable/minimally displaced; weight bearing as tolerated for incomplete fractures where ilium is contiguous with intact sacrum (e.g., LC impaction fractures); touch-toe WB for complete fractures
  • Operative (displaced > 1 cm): percutaneous IS/trans-sacral screws; posterior plating; transiliac sacral bars; open foraminal decompression for neurologic injury in Zone II

Complications

  • Urologic injury (highest with displaced Zone II)
  • L5 nerve root injury (Zone II)
  • Cauda equina syndrome (Zone III)
  • Chronic low back pain, malunion

7. Acetabular Fractures

Mechanism

  • Flexed hip with axial load ("dashboard mechanism") — most common
  • Pattern determined by position of hip and direction of impact

Radiographic Evaluation

AP pelvis — 6 cardinal lines:
  1. Posterior wall
  2. Anterior wall
  3. Roof
  4. Teardrop
  5. Ilioischial line
  6. Iliopectineal line
ViewProfiles
Obturator oblique (affected hip up 45°)Anterior column + posterior wall
Iliac oblique (affected hip down 45°)Posterior column + anterior wall
CT (thin-cut 1–2 mm): posterior injuries, articular fragments, marginal impaction, hip congruency, 3D reconstruction with femur subtracted.
Systematic evaluation of acetabular fractures — iliopectineal and ilioischial lines algorithm

Letournel Classification

Letournel Classification — Simple and Associated acetabular fracture types
Simple (5 types):
  • Posterior wall (PW) — most common simple type
  • Posterior column (PC)
  • Anterior wall (AW)
  • Anterior column (AC)
  • Transverse (involves both columns)
Associated (5 types):
  • Posterior column + posterior wall
  • Transverse + posterior wall
  • T-type
  • Anterior column + posterior hemitransverse (AC/PHT)
  • Both-column (ABC fracture) — spur sign on obturator oblique = intact iliac wing remaining in anatomic position; no intact articular support from acetabulum to axial skeleton on sequential axial CT

Treatment Principles

  • Restore articular congruity and hip stability
  • Avoid injury to blood supply of femoral head
  • DVT screening and prophylaxis
  • During surgery: hip extended, knee flexed to reduce sciatic nerve tension

Surgical Approaches

ApproachUsed ForNotes
Kocher-Langenbeck (posterior)PW, PC, PC/PW, transverse/PWProne or lateral decubitus
Ilioinguinal (anterior)AC, AW, AC/PHT, both-column (without posterior impaction)Three windows
Stoppa/modified StoppaLow AC, quadrilateral plate, both-columnIntrapelvic access
Extensile approaches (combined, extended iliofemoral, triradiate)> 3 weeks old; complex associated fractures; PC reduction neededHigher HO risk
ORIF + acute THAAge > 60 with gull sign (superomedial dome impaction); associated femoral neck fracture; significant pre-existing arthrosis

Percutaneous Fixation

  • PC screw: retrograde (ischium, hip flexed) or antegrade (mini lateral window approach); use Judet images for trajectory
  • AC screw: through superior ramus OR supra-acetabular corridor; use obturator oblique outlet (shows corridor + avoids joint), iliac oblique (avoids inferior breach), obturator inlet (avoids medial/lateral breach)

Complications

ComplicationKey Points
DVT/PEPreoperative screening; IVC filter if DVT present preoperatively
Heterotopic ossification (HO)Extended iliofemoral > Kocher-Langenbeck > anterior approach (50% → 25% → 10%); prophylaxis: indomethacin or 600 cGy radiation within 48h
Sciatic nerve injuryAssociated with posterior dislocations; < 50% full recovery; peroneal division most vulnerable; transverse + PW = highest nerve injury rate
Osteonecrosis (AVN)Highest with posterior fracture-dislocations; iatrogenic damage to medial femoral circumflex artery
Morel-Lavallée lesionSoft tissue degloving; associated with higher infection rates
Posttraumatic arthritisLeading long-term complication

8. Risk Factors for Death

Identified during initial treatment:
  • Blood transfusion requirement in first 24 hours
  • Unstable fracture type: APC II, APC III, LC II, LC III, VS, combined mechanism
  • Open fracture

Key Mnemonics & High-Yield Points

  • "Open book" = APC injury → apply binder to close the book
  • Stable = LC I and APC I; everything else warrants close attention
  • 85% of pelvic hemorrhage is venous — binder + packing first; angio only if arterial source confirmed
  • Posterior wall = most common simple acetabular fracture
  • Both-column fracture = spur sign on obturator oblique; only fracture with secondary congruence (femoral head stays congruent with displaced fragments)
  • Zone II sacral fracture = L5 nerve root most at risk; highest urologic injury
  • Zone III sacral fracture = cauda equina
  • Sacral dysmorphism in 20–44% — increases risk of screw penetration; recognize on outlet view
  • ICD (iliac cortical density) = landmark for safe IS screw placement; screw must remain posterior to ICD

Miller's Review of Orthopaedics, 9th ed., pp. 907–915 | Rockwood & Green's Fractures in Adults, 10th ed., 2025, pp. 2313ff.

Congenital dislocation of hip. Torticollis (Stiffneck).Congenital clubfoot.

Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Finding Sources
Reading File
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Finding Sources
Reading File
Reading File
Reading File
Finding Sources
Loading Image
Loading Image
Loading Image
Loading Image
I now have all the material needed. Here are the complete orthopaedic notes.

Paediatric Orthopaedics — Congenital Conditions

Sources: Miller's Review of Orthopaedics (9th ed.); Schwartz's Principles of Surgery (11th ed.); The Developing Human — Clinically Oriented Embryology (Moore & Persaud)

PART 1: Developmental Dysplasia of the Hip (DDH) / Congenital Dislocation of the Hip (CDH)

1. Definition

Abnormal development or dislocation of the hip secondary to capsular laxity and mechanical factors (e.g., intrauterine positioning). The term DDH is now preferred over CDH as it reflects the full spectrum of the condition.

2. Spectrum of Disease

TypeDescription
DysplasiaShallow acetabulum, femoral head in joint
SubluxationPartial loss of contact between femoral head and acetabulum
DislocationComplete loss of contact
TeratologicDislocated in utero, irreducible at birth; associated with neuromuscular conditions (arthrogryposis, Larsen syndrome); pseudoacetabulum present at or near birth
Late dysplasiaAdolescent/adult presentation

3. Risk Factors

(In descending order of importance)
  1. Breech positioning — highest risk (30–50%)
  2. Positive family history (ligamentous laxity) — ≥20%
  3. Female sex — 85% of cases
  4. Firstborn child (less intrauterine space)
Additional associations:
  • Left hip most commonly affected (67% of cases)
  • Increased maternal oestrogens
  • Postnatal: swaddling with hips in extension
  • Associated conditions: torticollis (20%), metatarsus adductus (10%); no association with clubfoot

4. Pathoanatomy — Obstacles to Concentric Reduction

If left untreated, muscles contract and the acetabulum becomes more dysplastic and fills with fibrofatty tissue (pulvinar).
Blocks to reduction in DDH — iliopsoas tendon, pulvinar, transverse acetabular ligament, redundant ligamentum teres, constricted hourglass capsule, everted labrum
Obstacles to reduction:
  1. Iliopsoas tendon
  2. Pulvinar (fibrofatty tissue)
  3. Hypertrophied ligamentum teres
  4. Contracted inferomedial hip capsule
  5. Transverse acetabular ligament
  6. Inverted (infolded) labrum

5. Diagnosis

Clinical Examination

TestMechanismPositive Finding
Ortolani testElevation + abduction of flexed hipClunk = dislocated hip reduces (positive early; negative late when irreducible)
Barlow testAdduction + depression of hipClunk = reduced hip dislocates
Galeazzi signFeet together, knees flexedForeshortened femur on affected side
Limited hip abductionPassive ROMAsymmetric restriction as laxity resolves
Asymmetric gluteal foldsInspectionLess reliable
Trendelenburg gaitWalking childOlder children with untreated DDH
⚠️ In bilateral dislocation, abduction may appear symmetrically decreased — easily missed.

Ultrasound (< 4–6 months of age)

  • Dynamic ultrasound — investigation of choice before femoral head ossification
  • Normal α angle > 60° on coronal view; femoral head bisected by iliac line
  • Useful to assess reduction in Pavlik harness and diagnose capsular laxity

Radiographs (> 4 months)

  • Acetabular index — normal < 25°
  • Perkin line — ossific nucleus should be medial to this line
  • Shenton line — disrupted in dislocation
  • Delayed ossification of femoral head on affected side

Advanced Imaging

  • Arthrography — assesses adequacy of closed reduction; look for "thorn sign" (normal labral position)
  • CT or MRI post-reduction — confirms concentric reduction

6. Treatment (age-dependent)

DDH management algorithm — Pavlik harness, closed reduction, open reduction pathway
AgeTreatment
Birth – 6 monthsPavlik harness for Ortolani-positive hips; closely watch Barlow-positive; repeat ultrasound at 6 weeks
6 – 18 monthsArthrography, percutaneous adductor tenotomy, closed reduction + hip spica cast; if fails → open reduction
18 months – 3 yearsOpen reduction + femoral shortening osteotomy ± acetabular osteotomy
3 – 8 yearsAcetabular osteotomy (Salter, Dega, Pemberton, Staheli)
> 8 yearsTriple (Steele), double pelvic (Sutherland), Staheli [open physis]; Ganz or Chiari [closed physis]
AdultTotal hip arthroplasty
Note: Diagnosis after age 8 years (age 6 in bilateral DDH) may contraindicate reduction as the acetabulum has little remodelling capacity.

Pavlik Harness — Key Points

  • Designed for infants < 6 months
  • Maintains ~100° flexion + mild abduction ("human position" / Salter position)
  • Must be within the safe zone of Ramsey (between maximum adduction before redislocation and excessive abduction causing AVN)
  • Worn 23h/day for ≥ 6 weeks after reduction, then part-time 6–8 weeks
  • Contraindicated in teratologic dislocations
  • Excessive flexion → transient femoral nerve palsy
  • If not reduced within 3 weeks → discontinue ("Pavlik disease") to prevent acetabular erosion
Pavlik harness failure risk factors:
  • Age > 7 weeks at initiation
  • Bilateral dislocations
  • Absence of Ortolani sign

Pelvic Osteotomies (summary table)

OsteotomyTypeKey Feature
SalterRedirectional (open-wedge)May lengthen limb up to 1 cm; requires open triradiate cartilage
PembertonVolume-reducingBends on triradiate cartilage; good for residual dysplasia
DegaVolume-reducingPreferred for paralytic dislocations; posterior deficiency
Ganz (PAO)RedirectionalTriradiate must be closed; superior 3D correction; single incision; preserves abductors
Steel / SutherlandTriple/double innominateOpen triradiate; uses Salter cut + additional cuts
ChiariSalvage/medialisationClosed triradiate

7. Complications

ComplicationNotes
Avascular necrosis (AVN)Most feared; caused by vascular injury or excessive abduction in harness; medial open reduction has higher AVN rate
Redislocation
Residual dysplasiaMay require further osteotomy
StiffnessEspecially after prolonged spica casting
Leg length discrepancy
Degenerative joint diseaseLong-term outcome if poorly treated


PART 2: Congenital Muscular Torticollis (CMT) / "Wry Neck" / "Stiff Neck"

Clinical photo — child with torticollis showing lateral head tilt and asymmetric shoulder position

1. Definition

Lateral bending of the head towards the affected side with slight rotation of the chin away from the affected side, caused by fibrosis and shortening of the sternocleidomastoid (SCM) muscle.

2. Pathogenesis

  • Tearing of SCM fibres during childbirth → haematoma → necrosis + fibrosis of muscle fibres
  • Histology: deposition of collagen and fibroblasts around atrophied muscle cells
  • Also occurs in caesarean births → additional causes include intrauterine crowding and primary SCM myopathy
  • A palpable SCM mass is present in approximately two-thirds of cases (also diagnosable by USS)

3. Clinical Features

  • Head tilts to the side of the lesion
  • Chin rotates away from the lesion
  • Palpable firm mass in the SCM in ~2/3 of cases
  • If untreated → plagiocephaly (facial asymmetry) and facial hemihypoplasia on the affected side
  • Associated with DDH in 20% of cases; associated with other intrauterine positioning abnormalities

4. Differential Diagnosis

ConditionKey Differentiator
Atlantoaxial rotatory subluxation (Grisel syndrome)Associated with pharyngeal infections; rotation with lateral tilt; no SCM mass
Klippel-Feil syndromeCervical vertebral fusion; short neck
Ocular torticollisHead tilt compensates for extraocular muscle imbalance
Sprengel deformityElevated scapula; may restrict head movement
Torticollis is secondary to fibrosis of the sternal head of SCM — a palpable mass within SCM is a key distinguishing feature from atlantoaxial subluxation.

5. Treatment

  • Physiotherapy (passive stretching of the affected SCM) — effective in the vast majority of cases; recommended from as early as possible
  • Stretching: tilt head to opposite side and rotate chin towards affected side
  • Surgical transection of the SCM — reserved for refractory/resistant cases that do not respond to conservative management (rare); performed when:
    • Persistent after 1 year of conservative treatment
    • Significant facial asymmetry
    • Restricted ROM after age 1 year
  • Surgery involves bipolar SCM release; complications include haematoma and scar


PART 3: Congenital Clubfoot (Congenital Talipes Equinovarus — CTEV)

1. Deformity Components — Mnemonic: CAVE

LetterDeformityExplanation
CCavusHigh arch — forefoot plantarflexed relative to hindfoot
AAdductusForefoot adducted
VVarusHindfoot varus
EEquinusPlantarflexion of the whole foot
Underlying deformity: Talar neck — medial and plantar deviation, with medial rotation of calcaneus and medial displacement of navicular and cuboid.
Shortened/contracted structures: intrinsic muscles, Achilles tendon, tibialis posterior, flexor hallucis longus, flexor digitorum longus, joint capsules, ligaments, and fascia.
Associated: absence or diminutive anterior tibial artery.

2. Epidemiology

  • Boys affected twice as often as girls
  • 50% bilateral
  • Incidence: ~1–2 per 1,000 live births

3. Aetiology

  • Majority idiopathic, but strong genetic component (PITX1-TBX4 transcriptional pathway)
  • Associated conditions:
    • Arthrogryposis
    • Myelomeningocele
    • Streeter dysplasia (hand anomalies)
    • Diastrophic dwarfism
    • Prune-belly syndrome
    • Tibial hemimelia

4. Imaging

Radiographs rarely used in infants (minimal ossification). When used:
ViewMeasurementNormalClubfoot
AP (Kite angle)Talocalcaneal angle20–40°Decreased (parallelism of calcaneus and talus)
Dorsiflexion lateral (Turco)Talocalcaneal angle~35°< 35° (decreased)
APTalus–1st metatarsal angle0–20°Negative
Common childhood foot disorders — AP skeletal view comparison: Clubfoot vs. Metatarsus adductus vs. Normal vs. Skewfoot vs. Vertical talus

5. Treatment

Ponseti Method (first-line; 95% success for idiopathic cases)

Serial weekly manipulation and long-leg plaster casts — corrects deformities in reverse order of CAVE:
StepWhat is CorrectedHow
1st castCavusSupinate forefoot + dorsiflex 1st ray
Subsequent castsAdductus + VarusLateral pressure on distal talar head as fulcrum
Last castEquinus70° of abduction
  • 90% of patients require percutaneous Achilles tendon lengthening at end of casting to address hindfoot equinus
  • Last cast placed in 70° abduction
  • Foot abduction brace (FAB) mandatory after casting — non-compliance is the main cause of recurrence

Surgical Treatment

  • Reserved for refractory/resistant cases (~5% of idiopathic presentations)
  • Posterior tibial artery must be protected (dorsalis pedis often insufficient)
  • Procedures:
    • Tendon lengthening
    • Subtalar, tibiotalar, and talonavicular release + realignment
    • Older children (3–10 years): medial opening-wedge or lateral column-shortening osteotomy or cuboid decancellation for adductus
    • Late presentation: triple arthrodesis (contraindicated in insensate feet — causes rigidity → ulceration)

6. Complications of Treatment

ComplicationKey Details
Dynamic supinationMost common post-treatment deformity (15–20%); overpull of tibialis anterior with weak peroneus longus; treat with tibialis anterior transfer laterally
Dorsal bunionAfter clubfoot surgery; strong tibialis anterior + flexor hallucis brevis/abductor hallucis; may be iatrogenic (peroneus longus division); treated with capsulotomy, FHL lengthening, FHB transfer to MTP
RecurrenceEspecially with non-compliance with brace
Avascular necrosis of talusPost-surgical over-release
Stiffness / restricted ROM
Flat-top talusOverly aggressive casting/surgery

Summary Comparison Table

FeatureDDHTorticollisClubfoot
Sex predilectionFemale (85%)None significantMale (2:1)
LateralityLeft hip (67%)Contralateral to mass50% bilateral
Key testOrtolani / BarlowPassive cervical ROM; SCM massCAVE on inspection
Primary RxPavlik harness (< 6 mo)Passive stretching physiotherapyPonseti casting
Surgery thresholdFailed conservative / older childResistant after 1 yearRefractory (~5%)
Genetic pathwayMultifactorial, laxity genesPITX1-TBX4
Associated conditionMetatarsus adductus, torticollisDDH (20%)Arthrogryposis, myelomeningocele

Miller's Review of Orthopaedics, 9th ed., pp. 264–268, 282–283 | Schwartz's Principles of Surgery, 11th ed. | The Developing Human, Moore & Persaud, p. 965
This is a shared conversation. Sign in to Orris to start your own chat.