Salter-Harris Classification of Growth Plate Fractures

Type I — Through the Physis

• Fracture passes entirely through the physeal cartilage, separating the epiphysis from the metaphysis with no bone fragment.
• Nondisplaced injuries may appear normal on X-ray — diagnosis is clinical (point tenderness over the growth plate).
• MRI or stress views may be needed to confirm.
• Displaced injuries reduce easily (periosteum remains intact).
• Prognosis: Excellent — full growth potential preserved.

Type II — Through Physis + Metaphysis (most common, ~75%)

• Fracture extends through the physis and exits through the metaphysis, creating the classic Thurston-Holland fragment.
• Extraarticular. Periosteum remains intact on the metaphyseal side.
• Usually manageable with closed reduction.
• Prognosis: Good — growth disturbance is uncommon.

Type III — Through Physis + Epiphysis

• Fracture extends through the physis and exits through the epiphysis into the joint.
• Intraarticular — risks post-traumatic arthritis if not anatomically reduced.
• Open reduction often necessary to restore joint surface congruity.
• Prognosis: Good if blood supply to fragment is intact; poor if vascularity is disrupted.

Type IV — Through Metaphysis + Physis + Epiphysis

• Fracture crosses all three zones: metaphysis, physis, and epiphysis.
• Intraarticular and highly unstable.
• ORIF (open reduction and internal fixation) is typically required to maintain alignment across the physis.
• Prognosis: Guarded — high risk of physeal bar formation and growth disturbance if not perfectly reduced.

Type V — Crush Injury of the Physis (rarest)

• An axial compressive load crushes the physis between the epiphysis and metaphysis.
• May appear normal on initial X-ray — often diagnosed retrospectively when growth disturbance becomes apparent.
• Prognosis: Poor — high rate of premature physeal closure and resultant limb length discrepancy or angular deformity.

Type VI (Rang extension)

• Involves loss of a portion of the physis, typically due to a shearing or avulsion mechanism.
• Not in the original Salter-Harris description; added later by Rang.
• Results in a peripheral physeal bar and angular growth deformity.

Memory Aid — "SALTR"

Key Clinical Points

• Growth plate injuries must always be considered in skeletally immature patients — ligaments are stronger than the physis, so "sprains" in children are often physeal fractures.
• Always palpate directly over the growth plate; tenderness there is a fracture until proven otherwise.
• Higher Salter-Harris numbers generally correlate with greater risk of growth disturbance, premature physeal closure, angular deformity, and limb length discrepancy.
• Complications that should be discussed with the patient/family: growth delay, growth arrest, and joint incongruity.

Greenstick Fractures

Definition & Mechanism

• Cortical disruption and periosteal tearing on the convex (tension) side
• Intact periosteum and buckled cortex on the concave (compression) side
• The bone bends and partially fractures rather than breaking completely through

Why Only in Children?

Radiographic Appearance

• A fracture line/cortical break on one side of the bone only
• Bowing or angulation of the bone without a complete fracture line visible on the other side
• Soft tissue swelling is usually present

AP and lateral X-rays of the left forearm showing greenstick fractures of the mid-diaphyseal radius and ulna. Fracture line is visible on the tension side; the opposite cortex remains intact with bowing.

Comparison with Related Pediatric Fracture Patterns

Clinical Features

• More stable and less painful than complete fractures — the intact periosteal hinge limits displacement
• Typically occurs in the forearm (radius/ulna) following a fall on an outstretched hand (FOOSH), but also seen in tibia, fibula, clavicle
• Angulation is common but significant displacement is rare

Management

• Closed reduction is usually sufficient — the intact periosteal hinge acts as a guide for reduction
• After reduction, the fracture is immobilized in a cast (typically long arm cast for forearm fractures)
• Remodeling capacity in children is excellent, so small residual angulation is often acceptable
• In some cases (especially unstable or significantly angulated fractures), the greenstick may need to be completed (intentionally converted to a complete fracture) to allow proper realignment and prevent re-angulation in cast

Prognosis

Sunderland Classification of Nerve Injury

Nerve Anatomy (layers, inside → out)

Axon → Endoneurium → Perineurium → Epineurium

• Endoneurium — surrounds individual axons
• Perineurium — surrounds each fascicle
• Epineurium — surrounds the entire nerve trunk

Sunderland Grades

Detailed Notes on Each Grade

• Focal conduction block at the site of injury
• No Wallerian degeneration
• Axons structurally intact — only myelin is disrupted
• Classic example: Saturday night palsy (radial nerve compression at spiral groove) → wrist drop that resolves spontaneously

• Axon is disrupted → Wallerian degeneration occurs distally
• Endoneurial tubes remain intact → provide a perfect scaffold for regenerating axons to reach target organs
• Complete and predictable recovery; rate ~1 mm/day axonal regeneration

• Endoneurial disruption allows intrafascicular fibrosis and misdirection of regenerating axons
• Perineurium intact maintains fascicular architecture
• Recovery is incomplete; degree depends on extent of internal scarring

• Only the epineurium holds the nerve together as a gross structure
• Severe internal disorganization — fascicles are obliterated
• Surgical exploration nearly always required; nerve-in-continuity but non-functional (neuroma-in-continuity)

• Complete nerve transection — no continuity whatsoever
• Surgical repair (primary neurorrhaphy or nerve grafting) is required
• Outcome depends on level of injury, gap length, time to repair, and patient age

• Seen in complex injuries (e.g., stretch + partial laceration)
• Different fascicles within the same nerve have different degrees of injury
• Requires careful intraoperative mapping before deciding on management

Seddon vs Sunderland — Correlation

Seddon          Sunderland
─────────────────────────────────
Neurapraxia  →  Grade I
Axonotmesis  →  Grades II, III, IV
Neurotmesis  →  Grade V (+ VI)

Key Clinical Points

• Grades I–II: Observe; spontaneous recovery expected
• Grade III: Observation ± surgery depending on recovery progress at 3 months (EMG/NCS helps)
• Grades IV–V: Surgical intervention required — repair, grafting, or nerve transfer
• Wallerian degeneration (anterograde axon + myelin breakdown distal to injury) begins in Grade II and above
• EMG/nerve conduction studies are critical at 3–6 weeks post-injury to help grade severity and predict prognosis
• The higher the injury level (proximal lesions), the worse the outcome — regenerating axons must travel farther to reach denervated muscle, which atrophies irreversibly if reinnervation is delayed beyond ~18–24 months

Wallerian Degeneration

Phases of Wallerian Degeneration

1. Distal Segment Changes (begins within hours)

• Immediately after axonal injury, retrograde and anterograde axoplasmic transport is disrupted
• Rapid influx of extracellular calcium ions triggers activation of calcium-dependent proteases (calpains), which destroy the axonal cytoskeleton
• Within 24–48 hours: the axon distal to the injury site begins to fragment and disintegrate
• Myelin sheath surrounding the distal axon breaks down into ovoids of myelin debris
• Schwann cells dedifferentiate — they shift from a myelin-producing role to a "repair cell" role, driven by upregulation of c-Jun protein
• Macrophages are recruited (within a few days) and, together with activated Schwann cells, phagocytose the axon and myelin debris

2. Proximal Segment Changes

• A limited degree of retrograde degeneration extends proximally from the injury site — typically only up to the first node of Ranvier
• The cell body undergoes chromatolysis:
  • Rough endoplasmic reticulum (Nissl substance) breaks up and disperses
  • Cell nucleus becomes eccentrically displaced
  • Gene expression shifts from axon maintenance → protein synthesis for regeneration
• Very proximal injuries (e.g., avulsion near the spinal cord) can cause apoptosis of the cell body itself, precluding any recovery

Bands of Büngner

Nerve Regeneration After Wallerian Degeneration

• The growth cone (the advancing tip of the regenerating axon) extends via filopodia and lamellipodia
• Axon regeneration rate: approximately 1–3 mm/day (classically ~1 mm/day clinically)
• Guided by neurotropism — neurotrophins (NGF, BDNF), adhesion molecules (cadherins, laminins, immunoglobulin superfamily factors) secreted by Schwann cells

Why Timing Matters

• Denervated muscle undergoes progressive atrophy — after ~18–24 months of denervation, motor endplates and muscle fibres become irreversibly fibrotic
• This creates a race: the regenerating axon must reach the target muscle before the window for reinnervation closes
• More proximal injuries have worse outcomes because axons must regenerate over longer distances

Wallerian Degeneration vs. Other Responses to Nerve Injury

Electrodiagnostic Correlates

• Immediately after injury, distal nerve stimulation can still evoke a response (axon physically present but disconnected)
• Wallerian degeneration renders the distal segment electrically inexcitable after ~5–7 days (motor fibres) to ~10–11 days (sensory fibres)
• EMG: fibrillations and positive sharp waves appear 2–3 weeks after injury, confirming denervation

1. Classification of Fractures

A. Skin Integrity

B. Fracture Pattern / Geometry

C. Incomplete Fractures (Pediatric)

D. Displacement & Alignment

• Nondisplaced — fragments in anatomic alignment; no reduction needed but may need immobilization
• Displaced — described by direction of the distal fragment relative to proximal
• Angulated — described by the direction the apex points (e.g., apex anterior = apex volar)
• Shortened — fragments overlap (bayonet apposition)
• Rotated — fragment has twisted on its long axis
• Distracted — fragments pulled apart

E. Articular Involvement

• Intraarticular — fracture line extends into the joint surface → risk of post-traumatic arthritis; anatomic reduction mandatory
• Extraarticular — fracture does not enter the joint

F. Anatomical Location Within the Bone

• Diaphyseal (shaft) — middle portion
• Metaphyseal — flared ends near the growth plate
• Epiphyseal — the articular end; physeal fractures in children classified by Salter-Harris

G. Special Pediatric: Salter-Harris (growth plate fractures)

H. Open Fracture Severity: Gustilo-Anderson Classification

2. How Fractures Heal

Primary (Direct) Bone Healing

• Occurs when fragments are rigidly fixed with anatomical compression (e.g., compression plating)
• Requires absolute stability — no micromotion
• Osteoclastic cutting cones cross the fracture line, creating resorption canals → filled immediately by osteoblasts
• Results in direct Haversian remodelling with no external callus formation
• Radiographically: fracture line gradually disappears without visible callus

Secondary (Indirect) Bone Healing (most common)

Stage 1 — Haematoma / Inflammation (hours–days)

• Fracture disrupts periosteum, endosteum, and surrounding soft tissues → fracture haematoma forms
• Entrapped erythrocytes in a fibrin network at the fracture ends
• Bone necrosis occurs at fractured ends
• Platelets degranulate → release cytokines (TNF-α, IL-1, IL-6, IL-11, IL-18)
• Neutrophils arrive first → followed by macrophages
• Fibroblasts and capillaries proliferate (granulation tissue formation)
• Mesenchymal stem cells migrate from periosteum and bone marrow

Stage 2 — Soft Callus (days–weeks)

• Granulation tissue is replaced by fibrocartilaginous soft callus
• Chondroblasts differentiate from periosteal stem cells
• Callus stabilises the fracture ends and grows even without perfect apposition
• Radiographically: fracture line still visible; soft tissue swelling

Stage 3 — Hard Callus (weeks–months)

• Two processes occur simultaneously:
  1. Intramembranous ossification — osteoblasts from periosteum deposit new bone around the outer surface of the callus, forming a bony sheath
  2. Endochondral ossification — the fibrocartilage within the callus calcifies, then is replaced by woven bone
• Together these form a hard (bony) callus — a fusiform, radio-opaque mass bridging the fracture
• Radiographically: callus appears as irregular radiodense fusiform mass bridging the fracture; original fracture line becomes less distinct

Stage 4 — Remodelling (months–years)

• Osteoclasts and osteoblasts remodel the woven bone callus into lamellar bone
• The medullary canal is restored
• Bone returns toward its original cortical architecture
• In children: remodelling can correct significant angular deformity
• Radiographically: callus shrinks, cortex reforms, medullary canal re-establishes

Factors Affecting Fracture Healing

3. Radiographic Appearance of a Long Bone Fracture

Acute Fracture (Day 0–2)

• Lucent (dark) fracture line through the cortex
• Loss of cortical continuity
• Soft tissue swelling adjacent to the fracture
• Joint effusion if intraarticular
• Fracture pattern, displacement, angulation, and comminution visible

Early Healing (Week 1–2)

• Fracture line may appear slightly wider as bone ends are resorbed
• Soft tissue swelling persists
• No callus visible yet (too early to mineralise)

Soft Callus Phase (Week 2–4)

• Still no definite mineralisation
• Periosteal elevation may be visible as a thin line lifted off the cortex

Hard Callus Phase (Week 4–12)

• Periosteal new bone and external callus appear as hazy, irregular, radiodense material surrounding the fracture site — the classic "fluffy" or "fusiform" density bridging the fracture
• Fracture line begins to blur and become indistinct
• Internal callus (endosteal) also visible as density filling the medullary canal

Remodelling Phase (Months–Years)

• Callus progressively shrinks and becomes more dense and regular
• Fracture line disappears
• Cortex reforms
• Medullary canal re-establishes
• Eventually the fracture site may be radiographically undetectable

Key Radiographic Principles for Any Long Bone Fracture

• Always obtain two orthogonal views (AP + lateral minimum)
• Image the joint above and below the fracture to detect associated injuries
• Describe: bone involved; region (diaphysis/metaphysis/epiphysis); pattern; displacement; angulation (apex direction); comminution; articular involvement; open vs closed; physeal involvement in children