The paediatric skeleton is NOT simply a smaller version of the adult skeleton. It differs in anatomy, physiology, and biomechanics. ^[1]

• The paediatric skeleton has the ability to grow. Ossification centres are programmed to ossify at specific times. ^[1]
• Knowing the order and timing of ossification centres is critical for interpreting paediatric elbow X-rays (where misinterpreted ossification centres can be mistaken for fracture fragments or vice versa).

CRITOE Mnemonic (Elbow Ossification Centres)

Radiographs – CRITOE ^[1]

Why this matters: If you see an "ossification centre" out of sequence on X-ray, suspect an avulsion fracture. The medial epicondyle is the most commonly avulsed — if you see it but NOT the trochlea, that's normal. If you see the trochlea but NOT the medial epicondyle, the "missing" medial epicondyle may be trapped in the joint.

• The growth contribution of each growth plate is different. ^[1]
• Lower limb growth — the distal femoral physis contributes ~70% of femoral length and ~37% of total leg length; the proximal tibial physis contributes ~57% of tibial length.
• Clinically: injuries near highly contributing physes carry greater risk of significant limb length discrepancy.

Upper Limb Epiphyseal Growth Contributions

The proximal humerus and proximal ulna contribute ~80% of their respective bone length, while the distal radius contributes ~75% of radial length. ^[1]

Clinical relevance: The distal humerus contributes only ~20% of humeral growth — this is why supracondylar fractures have poor remodelling potential. Conversely, distal radial physeal injuries carry greater risk of significant growth disturbance because the distal radius is the dominant growth centre.

50% of deaths in children < 14 are related to trauma. 15% of childhood injuries involve the musculoskeletal system. Most paediatric trauma are single extremity, low energy injuries. Upper limb fracture > lower limb fractures. ^[1]

Because paediatric bone is more elastic with a thick periosteum, three fracture patterns occur that are essentially never seen in adults ^[1]:

Biomechanical basis (stress–strain curve): Slide 15 illustrates that a 2-year-old's bone has a lower peak stress but tolerates a greater strain range (more elastic deformation) before failure, with stepwise micro-failures. A 46-year-old's bone reaches higher peak stress but fails abruptly with less strain. This explains why children sustain greenstick/plastic deformation injuries rather than the comminuted fractures seen in adults. ^[1]

More rapid healing of fractures: Physis > Metaphysis > Diaphysis ^[1]

Why? The closer to the growth plate, the richer the blood supply and the more active the periosteum → more rapid callus formation and healing. This is why metaphyseal fractures heal in weeks, while diaphyseal fractures take longer.

• May result in growth acceleration — especially at the proximal tibia and femur ^[1]
• This is due to fracture-related hyperaemia stimulating the nearby growth plate
• Clinically: some shortening is allowed in paediatric femoral shaft fractures (e.g. 1–2 cm overlap) because overgrowth will compensate

The physis (growth plate) has distinct histological zones ^[1]:

Additional periosteal/perichondral structures (from Slide 26 diagram) ^[1]:

• Periosteal sleeve — continuous periosteal covering that bridges the physis
• Ring of LaCroix — fibrous ring at the periphery of the physis providing mechanical support
• Zone of Ranvier — wedge-shaped area of cells at the physis periphery contributing to latitudinal (appositional) growth of the growth plate
• Blood supply: The physis receives dual blood supply from epiphyseal arteries (supplying the germinal/proliferative zones) and metaphyseal arteries (supplying the zone of endochondral ossification). The hypertrophic zone is relatively avascular, contributing to its vulnerability.

Which zone is the most commonly injured? Hypertrophic zone. ^[1]

Why? The hypertrophic chondrocytes are large and the extracellular matrix is sparse in this zone — it is structurally the weakest layer. This is why Salter-Harris type I and II fractures propagate through this zone. The important implication: the germinal zone (on the epiphyseal side) is usually spared → good prognosis.

Salter-Harris Classification ^[1] — This is an absolute must-know for exams.

Memory aid (SALTR): Straight across (I), Above (II), Lower (III), Through and through (IV), Ram/crush (V) ^[5]

Salter type III, IV, V (injury extending to epiphysis) → formation of vertical septa → structural disorganisation → bone bridge formation → growth arrest or deformity ^[1]

• If the germinal zone is NOT damaged: great remodelling potential
• If damaged: growth retardation depends on location of bone bar and size of bone bar ^[1]
  • Central bone bar → progressive angular deformity + shortening
  • Peripheral bone bar → angular deformity (tethering effect)
  • Large bar (> 50% of physis) → likely to cause significant arrest

Bone bar location patterns (from Slide 28 diagrams) ^[1]:

• Peripheral (eccentric) bone bar → tethering effect → angular deformity
• Central bone bar → growth arrest centrally while periphery continues → progressive angular deformity + shortening

Clinical case from slides: 1-year-old girl with right knee injury → developed progressive genu valgum (valgus deformity of the knee), lateral subluxation of patella, ROM 0–100°, limb length discrepancy of 1 cm — all from physeal damage ^[1]

Nervous child, unable to give a good history, uncooperative in physical examination, anxious parents. ^[1]

Practical tip: Observe the child before touching. Watch how they use the limb, whether they guard it, whether they cry when a specific area is palpated. Use distraction techniques. Get the history from the parent but also observe the child's behaviour — inconsistencies may raise concern for NAI.

Similar to adult trauma: ABC… Investigations ^[1]

Age-specific vital signs (from lecture slide — high yield for recognising shock in paediatric trauma):

Why these numbers matter: Children maintain blood pressure until very late in haemorrhagic shock (compensated shock with tachycardia). By the time BP drops, they've lost 25–30% blood volume. Tachycardia is the earliest sign.

Look out for associated soft tissue injuries: ^[1]

• Open wound (open fracture)
• Skin blistering / abrasions / necrosis
• Skin impingement by fracture ends
• Subcutaneous swelling
• Nerve palsy
• Vascular injury → Compartment syndrome

X-ray examination: to confirm fracture; to assess configuration (spiral/oblique/transverse/butterfly/comminuted, greenstick/torus/plastic deformation); to assess alignment ^[1]

Displaced? → Reduction if necessary (pain control, anaesthesia). Stability? → Immobilisation if necessary. Function? → Rehabilitation always. ^[1]

Good healing and remodelling potential → relatively less post-op contracture → more conservative treatment ^[1]

Case example from slides: M/2 (male, 2 years old) fell from trampoline — femoral shaft fracture → treated with traction followed by hip spica → X-rays at 2.5 weeks showed callus → 6 weeks post-injury progressing well → 3 months further remodelling → 1 year: unrestricted activity ^[1]

Key teaching point: In a 2-year-old with a femoral shaft fracture, operative fixation is generally NOT needed. Conservative management with traction + hip spica is appropriate because of the excellent healing and remodelling potential at this age. In older children (> 5–6 years), elastic nails or other fixation may be preferred.

Age-Based Fixation Progression

The slide series (Slides 21, 38, 44) illustrates a spectrum of fixation methods used in children, with increasing rigidity as the child approaches skeletal maturity ^[1]:

Other methods shown in slides: percutaneous K-wires (supracondylar fractures), external fixation (open fractures, severe soft-tissue injury). ^[1]

Involves thin bone between coronoid fossa and olecranon fossa of distal humerus. Occurs most often around age 6–7 years. ^[1]

Why here? The distal humerus has a very thin cross-section between the coronoid and olecranon fossae — this creates a structurally weak area prone to fracture when a child falls on an outstretched hand (FOOSH) with the elbow hyperextended.

Potentially Problematic! Vascular Injuries, Neurologic Deficits, Cubitus Varus/Recurvatum, Volkmann's Contracture ^[1]

Two types: Extension type (95%) and Flexion type. Most displaced fractures (Type III) are of extension type (97%). ^[1]

Extension type (child falls on outstretched hand → elbow hyperextended → distal fragment displaces posteriorly):

Swelling and tenderness of the forearm compartments. "Dimple sign" occurs when a spike of bone penetrates brachialis muscle and anterior subcutaneous tissues. ^[1]

Neurovascular injuries? Compartment syndrome? Check and recheck radial pulse and its quality. Remember that an intimal arterial injury can occur slowly over several hours. ^[1]

Associated injuries: Always obtain X-rays of the entire forearm including the wrist in supracondylar fractures — associated forearm fractures (ipsilateral distal radius/ulna) can coexist and may be missed if imaging is limited to the elbow (Slide 51). ^[1]

Fat pad signs — Visible on lateral elbow X-ray ^[1]

• Anterior fat pad: normally visible as a thin line; becomes sail-shaped (elevated) when there is an effusion → suggests intra-articular fracture
• Posterior fat pad: normally NOT visible; if visible → pathological — strongly suggests occult fracture

Acceptable alignment assessed by ^[1]:

• Anterior humeral line — should bisect the middle third of the capitellum on lateral view; if it passes anterior to the capitellum, there is posterior displacement
• Baumann angle — angle between the long axis of the humeral shaft and the growth plate line of the lateral condyle on AP view; normal range 9–26 degrees ^[1]
• Lateral and medial cortices — assess for cortical step or disruption

What the fixation films show: AP/lateral elbow after crossed percutaneous K-wires with cast — Type III needs stable pinning, not “mould and hope,” because distal humerus remodels poorly. ^[1]

Reasons for open reduction: ^[1]

1. Vascular compromise (brachial artery injury with absent pulse + signs of ischaemia)
2. Failure of closed reduction due to soft tissue interposition (e.g. buttonhole through the brachialis muscle)

Drawbacks of open reduction: Elbow stiffness, myositis ossificans, neurovascular injury ^[1]

Anterior Interosseous Nerve (AIN) — most commonly injured nerve in extension-type supracondylar fractures ^[1]

Neurological injury: difficult to examine, may not be able to identify, detailed documentation needed. Majority due to neuropraxia. Generally NOT considered an indication for open reduction/exploration. ^[1]

Fracture treatment principle: children's physiology is different from adults. Supracondylar fracture of humerus has poor remodelling potential and treatment can be challenging. ^[1]

Non-accidental injury or physical abuse — deliberately inflicted on a vulnerable person ^[1]

Red flags for NAI (from lecture):

1. Injury and history given are inconsistent
2. Delay in seeking medical attention
3. Multiple fractures
4. Retinal haemorrhage
5. Torn frenulum
6. History of household falls resulting in fracture ^[1]

Additional NAI features from AOS material: ^[4]

• A pre-ambulatory infant (< 12 months) with a long bone fracture should ALWAYS raise suspicion
• Skeletal survey is the most important investigation — it can reveal hidden/healing fractures at different stages ^[4]
• Metaphyseal corner fractures ("bucket-handle" or "chip" fractures) — highly specific for NAI
• Posterior rib fractures — highly specific for NAI (from squeezing)
• Spiral fractures of long bones in non-ambulatory children — suspicious

A pathologic fracture is a break in a bone caused by an underlying disease: primary malignant lesions, benign lesions, metastasis, or underlying metabolic abnormalities. ^[1]

Examples given in slides:

• Osteosarcoma — primary malignant bone tumour
• Fibrous Dysplasia — benign condition with abnormal fibrous tissue replacing normal bone
• Osteogenesis Imperfecta (OI) — inherited collagen disorder
• Osteopetrosis — abnormally dense but brittle bone

771 disorders associated with 552 genes based on DNA sequencing; 41 groups; abnormal bone and cartilage formation ^[1]

Case from slides: M/6 years 9 months from Guizhou province, multiple fractures since 1 year old due to trivial trauma, treated by bone setter with wooden splints, unable to walk for > 3 years. Diagnosed as Type V Osteogenesis Imperfecta. ^[1]

Management: Surgical correction (intramedullary nailing) + post-op rehabilitation:

• Tilt table standing in cast by 4 weeks
• Cast removal by 8 weeks
• Post-op 10 months: able to stand
• Post-op 18 months: walk unaided

Though these conditions are not common, we need to be cautious. Treatment for the underlying cause is important. ^[1]

1. Look: Swelling, deformity, bruising, open wound, skin dimpling, blistering
2. Feel: Tenderness, crepitus, warmth
3. Move: Active > passive (in a child, observe spontaneous movement first)
4. Neurovascular status: Pulses (compare with contralateral), capillary refill, sensation, motor function — check and recheck ^[1]
5. Compartment syndrome signs: Pain on passive stretch, tense swelling, pain out of proportion
6. NAI screen: Bruises at different stages of healing, torn frenulum, retinal haemorrhage, injuries in non-ambulatory child

1. Pain control — paracetamol, ibuprofen, intranasal fentanyl, regional blocks
2. Reduction — if displaced beyond acceptable limits for age/location
3. Immobilisation — POP cast, backslab, hip spica, traction
4. Fixation — percutaneous K-wires, elastic nails, rarely plates/screws (avoid crossing open physes)
5. Rehabilitation — early mobilisation when stable
6. Follow-up — serial X-rays to monitor alignment and healing; watch for growth arrest (especially after physeal injuries — may not manifest for months/years)

Paediatric musculoskeletal infection (osteomyelitis, septic arthritis) can mimic fracture in a child who presents with a painful, non-weight-bearing limb. Key discriminator: fever + elevated inflammatory markers without trauma history → think infection. ^[6]

The NAI module in this lecture connects directly to GC 143 (A child with multiple bruises). Features from that lecture that reinforce this one: unexplained injuries, injuries at different stages of healing, delay in seeking medical care, and inconsistent or changing stories. ^[7]

CFB slides reinforce that paediatric orthopaedics is governed by the concept that "children are not small adults" — the growth plate is the key differentiator. ^[8]

The 2025 MCQ Q48 tests knee OA in adults — a completely different pathophysiology from paediatric physeal injury. Do not confuse degenerative joint disease (adult) with growth plate disruption (child).