Classification of Fractures and Fracture Healing

PART 1: CLASSIFICATION OF FRACTURES

1. By Skin Integrity

2. By Fracture Line Pattern (Mechanism of Injury)

3. By Stability

4. By Completeness

• Complete fracture - The bone is broken all the way through
• Incomplete fracture - The cortex is disrupted on only one side (e.g., greenstick, torus/buckle fractures in children)

5. By Anatomical Location

• Diaphyseal (shaft): proximal, middle, distal third
• Metaphyseal: the flared region between shaft and growth plate
• Epiphyseal: involving the joint surface; threatens articular cartilage and growth
• Intra-articular vs. Extra-articular
• Periarticular: near but not involving the joint

6. By Number of Fractures

• Isolated - single bone
• Multiple - more than one bone in the same limb or in different locations
• Segmental - two fracture lines isolating a middle segment of the same bone

7. Pathological Fracture

8. Salter-Harris Classification (Growth Plate / Physeal Fractures in Children)

9. AO/OTA Classification

• Bone: numbered (e.g., 2 = humerus, 3 = radius/ulna)
• Segment: 1 = proximal, 2 = diaphyseal, 3 = distal
• Type: A (simple), B (wedge), C (complex/comminuted)
• Group and Subgroup further characterize fracture morphology

PART 2: FRACTURE HEALING

Two Fundamental Modes of Fracture Healing

A. Indirect (Secondary) Bone Healing - Most Common

• Strain > 100% → fibrous tissue
• Strain < 10% → soft cartilaginous callus
• Strain < 2% → hard callus and progressive mineralization

B. Direct (Primary) Bone Healing

Stages of Indirect Fracture Healing (Secondary Bone Healing)

Stage 1: Haematoma Formation (Days 0-3)

• Rupture of blood vessels at the fracture site fills the gap with haematoma
• Haematopoietic cells, clots, and the haematoma form the initial framework
• Inflammatory cells invade and initiate lysosomal degradation of necrotic tissue
• Monocytes, PMNs (neutrophils), T cells, macrophages, and B cells are the primary cell types
• Capillary dilation, fluid exudation, and capillary budding begin

Stage 2: Granulation Tissue / Soft Callus Formation (Days 3-10)

• Beginning ~4-5 days after injury
• Pluripotential mesenchymal / stem cells invade and differentiate into fibroblasts, chondroblasts, and osteoblasts
• A soft cartilaginous callus forms (soft callus / unmineralized cartilage)
• Angiogenesis occurs in periosteal tissues and marrow space
• This routes appropriate cells to the fracture site
• A bed of granulation tissue forms
• Chondrocytes and osteoblasts are the key cells

Stage 3: Bony Callus Formation / Endochondral Ossification (Days 10-21)

• The cartilaginous callus undergoes endochondral ossification and is replaced with woven bone
• Hypertrophic chondrocytes and osteoblasts are prominent (Days 10-16)
• Hard callus / secondary bone forms (Days 16-21) with hematopoietic and myelopoietic cells
• At the end of this stage, calcified callus of immature (woven) bone remains

Stage 4: Bony Remodeling (Days 21-35 and continuing for years)

• Mineralization stiffens and strengthens the newly formed bone
• Hard callus is remodeled to cortical bone
• Osteocytes become the dominant cell type
• Involves intramembranous ossification, appositional new bone formation, and osteonal migration (creeping substitution)
• Radioisotope studies show increased activity at fracture sites long after painless function and radiographic union are achieved - remodeling continues for years
• In children (and to a lesser degree adults), bone remodels according to forces passing through it (Wolff's Law)

Terminology of Bone Healing

• Atrophic non-union - Biological problem; lack of stimulus or blood supply; no callus
• Hypertrophic non-union - Too much movement at the fracture site; elephant-foot appearance; biologically active but mechanically insufficient
• Infected non-union - Infection has compromised the healing environment

Factors Affecting Fracture Healing

Systemic Factors

• Age (healing faster in young patients)
• Nutritional status
• Hormonal factors (growth hormone, thyroid, PTH)
• Diseases: diabetes, malignancy, pulmonary insufficiency, immunodeficiency
• Vitamin deficiencies (C, D)
• Smoking - the single most notable inhibitory factor; delays both fracture and wound healing significantly and increases nonunion risk
• Medications: NSAIDs (conflicting data), fluoroquinolone antibiotics (implicated in slowing bone healing), corticosteroids

Local Factors

• Severity of injury and high-energy trauma
• Degree of fracture displacement
• Neurovascular disruption
• Soft-tissue interposition
• Loss of bone (segmental defect)
• Blood supply to the periosteum and nutrient artery
• Infection (especially in open fractures)
• Peripheral vascular disease / diabetes (microvascular)

Treatment Factors

• Extent of surgical trauma
• Type of fixation and degree of rigidity
• Overdistraction of fragments
• Load-induced deformation
• Poor reduction and malalignment

Requirements for Bone Regeneration (Bone Graft)

1. Osteoconduction - Scaffolding that allows bone ingrowth
2. Osteoinduction - Ability to induce production of osteoblasts (e.g., BMPs)
3. Cellular Osteogenesis - Live osteogenic cells (osteoblasts and osteocyte precursors)

Supracondylar Fracture of the Humerus

DEFINITION AND EPIDEMIOLOGY

• Most common elbow fracture in children (peak age 5-8 years)
• The most common fracture treated surgically by pediatric orthopedic surgeons
• During childhood, ligaments around the elbow are stronger than the underlying bone, so falls tend to produce bone fractures rather than ligamentous injuries
• The distal humerus ossifies at multiple centers - the CRITOE sequence is important to know to avoid misidentifying ossification centers as fracture fragments

MECHANISM OF INJURY

Extension Type (95% - Most Common)

• Fall onto an outstretched, extended hand (FOOSH)
• The body's weight drives the humerus forward while the elbow hyperextends
• The distal fragment is displaced posteriorly and superiorly
• The sharp proximal humeral shaft end can injure the brachial artery and median/anterior interosseous nerve anteriorly

Flexion Type (5% - Rare)

• Direct blow or fall onto a flexed elbow
• The distal fragment is displaced anteriorly
• More commonly associated with ulnar nerve injury
• Higher rate of open reduction required due to ulnar nerve entrapment risk

CLINICAL FEATURES

• Painful, swollen elbow after a fall
• Child holds the arm in extension with slight pronation
• "S" deformity of the distal humerus on lateral view
• Puckering, dimpling, or anterior bruising over the antecubital fossa suggests the proximal humeral shaft has penetrated the brachialis muscle - this predicts difficulty with closed reduction

1. Pain (especially pain with passive finger extension - a sign of compartment syndrome)
2. Pallor
3. Pulselessness
4. Paralysis
5. Paresthesias

RADIOGRAPHIC ASSESSMENT

1. Anterior Humeral Line

2. Baumann Angle

• A line drawn along the growth plate of the capitellum
• A line drawn down the long axis of the humerus

3. Fat Pad Signs

• Anterior fat pad "sail sign" - bulging anterior fat pad; suggests effusion and occult fracture (a thin anterior fat pad can be normal)
• Posterior fat pad sign - always pathological; indicates a joint effusion/haemarthrosis; strongly suggests occult fracture even when no fracture line is visible

CLASSIFICATION

Gartland Classification (Extension-Type - Most Used)

NEUROVASCULAR INJURIES

MANAGEMENT

Gartland Type I - Undisplaced

• Posterior long-arm splint or collar and cuff with elbow at 90° flexion, forearm neutral or pronated
• Immobilization for 3 weeks
• Follow-up with orthopaedics within 24 hours for casting and repeat radiograph
• Progressive mobilization after cast/splint removal

Gartland Type II - Displaced with Intact Posterior Cortex

• Closed reduction under sedation or general anaesthesia
• If reduction is maintained with < 90° of elbow flexion → above-elbow cast for 3-4 weeks
• If > 90° of flexion is required to hold the reduction (dangerous because of vascular compromise risk) → percutaneous K-wire fixation + above-elbow cast
• Avoid deep flexion if there is significant swelling - risk of Volkmann's ischaemic contracture

Gartland Type III - Completely Displaced

• Admission required
• Operative closed reduction and percutaneous K-wire pinning is the standard of care
• Prone to neurovascular compromise - emergent orthopaedic consultation
• If closed reduction fails or neurovascular compromise persists → open reduction

• Lateral-entry parallel or divergent K-wires (2 or 3 lateral wires) - preferred to avoid ulnar nerve injury
• Crossed K-wires (one lateral, one medial) - provides more rotational stability but risks ulnar nerve injury with the medial pin; should be placed with elbow partially extended to protect the nerve
• Wires are typically removed in clinic at 3-4 weeks

Special Situations

• Surgical emergency - immediate urgent reduction
• If pulse does not return after reduction → emergent vascular exploration and repair of brachial artery

• More controversial management
• If adequate perfusion, no compartment syndrome, no neurological injury: reduce and stabilise, take an expectant approach
• Pulse often returns within 24-48 hours
• If perfusion worsens → vascular exploration

• Open reduction through anterior (cubital) or posterior approach

COMPLICATIONS

SUMMARY - MANAGEMENT ALGORITHM

Supracondylar Fracture of Humerus
├── Type I (Undisplaced)
│   └── Collar & cuff / posterior splint × 3 weeks
│
├── Type II (Posterior cortex intact)
│   ├── Closed reduction
│   ├── If stable at <90° flexion → Above-elbow cast × 3-4 weeks
│   └── If unstable / >90° needed → Percutaneous K-wires + cast
│
└── Type III (No cortical contact)
    ├── Admit → Closed reduction + percutaneous K-wire pinning
    ├── White pulseless hand → Emergency reduction ± vascular exploration
    └── Failed closed reduction → Open reduction

Short Notes on Four Orthopaedic Topics

1. TARDY ULNAR NERVE PALSY

Definition

Causes / Aetiology

1. Cubitus valgus (most classic cause) - from malunion of a lateral condyle fracture of the humerus in children. As the child grows, progressive valgus deformity develops, stretching the ulnar nerve in its groove behind the medial epicondyle over many years.
2. Callus formation after supracondylar fracture - bony callus at the fracture site gradually compresses the ulnar nerve.
3. Malunion of medial epicondyle fracture - ulnar nerve becomes entrapped in callus if anterior transposition was not performed at the time of surgery.
4. Shallow ulnar groove on the posterior medial epicondyle - causes recurrent subluxation or dislocation of the ulnar nerve (found in 16.2% of 2000 elbows in one series), with repeated microtrauma on elbow flexion.
5. Hypoplasia of the humeral trochlea or inadequate fibrous arch.
6. Elbow dislocations, contusions, and post-traumatic fibrosis.

Clinical Features

• Medial side of the hand, entire little finger, and medial half of the ring finger

Management

• Conservative: Elbow padding, avoidance of sustained elbow flexion
• Surgical decompression: Simple decompression of the cubital tunnel
• Anterior transposition of the ulnar nerve (subcutaneous, intramuscular, or submuscular) - moves the nerve to a position where it is no longer stretched by valgus deformity or elbow flexion; this is the preferred treatment in tardy palsy
• Corrective osteotomy if significant cubitus valgus persists
• Medial epicondylectomy - removes the bony prominence causing compression

2. COLLES' FRACTURE

Definition

• Dorsal displacement and dorsal angulation of the distal fragment
• Radial shortening (impaction)
• Loss of normal volar tilt of the radial articular surface

Mechanism

• Fall on an outstretched hand (FOOSH) with the wrist in dorsiflexion
• Commonest in postmenopausal women with osteoporosis (most common fragility fracture)
• Also seen in young adults after high-energy trauma

Pathological Anatomy

• Fracture line within 2 cm of the radial articular surface
• Dorsal comminution is common (compression forces on the dorsal cortex)
• May extend intra-articularly into the radiocarpal joint ("die-punch fracture") or radioulnar joint
• Ulnar styloid fracture is commonly associated - indicates triangular fibrocartilage complex (TFCC) injury

Clinical Features

• Seen on the lateral view of the wrist
• The dorsal displacement of the distal fragment creates a step resembling the profile of a dinner fork
• Wrist is in characteristic dorsiflexion posture
• Swelling, tenderness, and bruising over the distal forearm

Radiological Features

• Volar tilt: 11-12° (range 0-28°); minimum acceptable = 0° (neutral)
• Radial inclination: 22-23°
• Radial length: 11 mm

• Dorsal angulation > 20°
• Intra-articular extension
• Marked comminution

• 1 cm radial shortening

• Distal radioulnar joint instability

Management

• Compression dressing and below-elbow backslab/splint
• Orthopaedic review within 7-10 days

• Closed reduction under anaesthesia (haematoma block, Bier block, or regional nerve block)
• Technique: traction with finger traps → distal and palmar push on fragment → restore volar tilt
• Double sugar-tong splint (not circumferential cast for 24 hours - allow for swelling)
• Short arm cast or above-elbow cast for 4-6 weeks
• Repeat radiograph at 1 week to check maintenance of reduction

• Percutaneous K-wire fixation (Kapandji technique)
• External fixation (distraction fixator)
• Volar locking plate (ORIF) - preferred for young patients, intra-articular fractures

Complications

3. VOLKMANN'S ISCHAEMIC CONTRACTURE

Definition

Pathophysiology

Causes

• Supracondylar fracture of the humerus in children (classical cause)
• Any fracture or dislocation around the elbow or forearm
• Tight plaster cast / bandage
• Crush injuries of the forearm
• Brachial artery injury
• Prolonged limb compression (e.g., drug overdose)
• Excessive deep elbow flexion after reduction of supracondylar fractures

Clinical Features (Established VIC)

• Elbow flexion
• Forearm pronation
• Wrist flexion
• Thumb adduction
• MCP joints in extension
• Fingers (IP joints) in flexion

Classification and Treatment

Prevention (Most Important!)

• Early diagnosis and emergency fasciotomy of forearm compartments when compartment syndrome is suspected
• Do not apply circumferential cast acutely; use back-slab only
• Avoid deep elbow flexion after supracondylar fracture reduction if there is significant swelling
• If > 90° of flexion is needed to hold reduction → K-wire fixation instead
• Monitor the "5 Ps" - Pain, Pallor, Pulselessness, Paraesthesia, Paralysis

4. FAT EMBOLISM SYNDROME (FES)

Definition

1. Respiratory distress / hypoxaemia
2. Neurological abnormalities (confusion, restlessness, deteriorating consciousness)
3. Petechial rash

Incidence

• 1-2% of patients with isolated long bone fractures
• 5-10% of patients with multiple fractures
• Most common after fractures of the tibia and femur (marrow-rich bones)
• Also after hip fractures in the elderly and after intramedullary nailing (surgical FES)
• Incidence rises with the number of fractures
• Mortality once FES is established: 10-20%

Pathophysiology

• Trauma disrupts medullary fat cells → fat globules enter torn venous sinusoids → travel to pulmonary capillaries → mechanical obstruction → V/Q mismatch → hypoxaemia
• Fat particles can traverse pulmonary capillaries or patent foramen ovale → systemic circulation → brain, skin, kidneys

• Lipases break down neutral fat → release of free fatty acids (FFAs)
• FFAs cause diffuse vasculitis with leakage from cerebral, pulmonary, and other vascular beds
• Explains the lag time between injury and syndrome onset
• Also associated with hypovolaemia and the shock response

Timing

• Symptoms typically appear 12-72 hours (Pye's: 3-10 days) after the inciting injury
• Appearance within 24-48 hours of intramedullary nailing is well recognized

Clinical Features

• Respiratory: Dyspnoea, tachypnoea, hypoxaemia (PaO₂ < 60 mmHg) - earliest and most common
• Neurological: Restlessness, confusion, disorientation, deteriorating GCS - early sign; may progress to coma

• Petechial rash - pathognomonic; distributed over the head, neck, anterior chest, and axillae (conjunctiva and retina also); present in only 20-50% of cases - absence does not exclude FES
• Fever, tachycardia
• Retinal fat emboli visible on fundoscopy
• Jaundice (from hepatic involvement)
• Renal involvement
• Thrombocytopenia

Investigations

Gurd's Criteria (for diagnosis)

• Petechial rash
• Respiratory insufficiency (PaO₂ < 60 mmHg, FiO₂ > 0.4)
• Cerebral involvement (not head injury)

• Pyrexia > 38.5°C
• Tachycardia > 120/min
• Retinal fat emboli
• Fat in urine
• Thrombocytopenia (> 50% drop)
• High ESR
• Fat globules in sputum

Management

1. Respiratory support - supplemental oxygen; may require intubation and mechanical ventilation (ARDS management protocol) in ICU
2. Haemodynamic support - IV fluids, inotropes if needed
3. Early fracture stabilization - intramedullary nailing reduces fat release compared to prolonged traction; early fixation may reduce FES incidence
4. Corticosteroids - high-dose methylprednisolone (controversial; some evidence for prevention in high-risk patients; not proven once FES is established)
5. Heparin, albumin, dextran - suggested but none proven effective
6. Supportive ICU care - careful fluid balance, nutritional support