Fracture Principles

General MSK Principles

Overview

Fractures are among the most common presentations in UK MSK practice and a very common reason for emergency department attendance. A fracture is a complete or incomplete break in the structural continuity of bone, ranging from a hairline cortical crack to a comminuted open injury with neurovascular compromise. The core clinical principles are: identify the fracture (clinical assessment supported by imaging), describe it accurately (systematic terminology), assess for associated injuries (neurovascular status, soft tissue, adjacent joints), classify its stability and other management determinants, and manage it appropriately (reduce, hold, rehabilitate). Fracture management is the balance between biology (healing) and mechanics (stability). UK practice is anchored by NICE NG38 (Fractures - non-complex), NG37 (Fractures - complex), and CG124 (Hip fracture management), with BOAST (British Orthopaedic Association Standards for Trauma) framing acute orthopaedic care. The Ottawa rules (ankle, knee, foot) and the Canadian C-spine rule are validated clinical decision tools that reduce unnecessary imaging. Open fractures are orthopaedic emergencies. The clinical pearl: treat the patient, not the X-ray - functional impact and clinical findings drive management.

Anatomy & Pathophysiology

Bone structure relevant to fractures:

  • Cortical (compact) bone: dense outer layer, predominates in the diaphysis, high resistance to compression and bending.
  • Cancellous (trabecular) bone: porous and metabolically active, predominates in the metaphysis, epiphysis, vertebral bodies, and flat bones; better blood supply means faster healing than cortical bone.
  • Periosteum: fibrous membrane containing osteoprogenitor cells, blood vessels, and sensory nerves. Critical for fracture healing through osteogenic cells and blood supply for callus formation. Children have thicker periosteum, contributing to faster healing and greater remodelling.
  • Blood supply: nutrient artery (primary cortical), periosteal vessels, and metaphyseal/epiphyseal vessels. Bones with tenuous blood supply are prone to non-union or AVN: scaphoid waist (retrograde), femoral head (retinacular), talus, navicular.

Fracture biomechanics - how bones break:

  • Bending: transverse or short oblique fractures.
  • Torsional (twisting): spiral fractures.
  • Compressive: impaction fractures, vertebral compression, metaphyseal Y/T patterns.
  • Tensile (distraction): avulsion fractures (tendon/ligament pulling bone fragment).
  • High-energy combined: comminuted (multiple fragments) and segmental fractures.

The systematic fracture description system - describe every fracture in this order:

  • Bone and location: epiphysis, metaphysis, or diaphysis (proximal/middle/distal third). Intra-articular vs extra-articular (intra-articular requires anatomical joint surface restoration).
  • Open or closed: closed = skin intact; open (compound) = communication between fracture and external environment. A wound near a fracture should be assumed to communicate until proven otherwise.
  • Pattern: transverse (bending force, relatively stable after reduction); oblique (bending plus rotation, prone to displace); spiral (torsion - in a non-ambulatory child raises NAI concern); comminuted (more than two fragments, high-energy, inherently unstable); segmental (two fracture lines isolating a fragment); butterfly fragment (wedge-shaped fragment from bending); avulsion (tendon/ligament pulling a fragment); impacted (one fragment driven into another); pathological (through abnormal bone); stress (repetitive sub-maximal loading - see Bone Stress Injuries topic).
  • Paediatric-specific patterns: greenstick (one cortex breaks, the other bends - elastic paediatric bone); buckle/torus (compression failure with cortical bulge, classically distal radius).
  • Displacement, angulation, rotation, and shortening described relative to the proximal fragment. Reduction aims to restore length, alignment, and rotation.
  • Stability: stable patterns (transverse, impacted) resist displacement; unstable patterns (oblique, spiral, comminuted) tend to displace and often need surgical fixation.

Gustilo-Anderson classification of open fractures (assigned at surgical debridement, not in ED):

  • Type I: clean wound under 1 cm, low-energy.
  • Type II: wound 1-10 cm, moderate soft tissue damage.
  • Type IIIA: extensive soft tissue damage with adequate bone coverage.
  • Type IIIB: extensive soft tissue loss requiring flap coverage.
  • Type IIIC: associated vascular injury requiring repair.

Salter-Harris classification (paediatric growth plate injuries, mnemonic SALTR):

  • Type I (Straight across, through physis); Type II (Above the physis, through physis and metaphysis - the MOST COMMON); Type III (Lower, through physis and epiphysis - intra-articular); Type IV (Through metaphysis, physis, and epiphysis); Type V (Rammed/crushed - crush injury to physis). Higher types (III-V) carry greater risk of growth arrest and deformity.

Fracture healing: inflammatory (haematoma - days 1-7); reparative (soft callus weeks 2-4 - fibrocartilage; hard callus weeks 4-12 - woven bone via endochondral ossification, periosteum-driven); remodelling (months to years - woven bone becomes lamellar bone per Wolff's law). Primary (direct) healing requires absolute stability and rigid compression (plate and screws - no callus). Secondary (indirect) healing occurs with relative stability (cast, intramedullary nail - visible callus). Approximate timelines: upper limb ~6 weeks, lower limb ~12 weeks, scaphoid often longer; paediatric faster.

Factors affecting healing: age (children faster); smoking (one of the most important modifiable risks for non-union); diabetes, malnutrition, vitamin D deficiency, corticosteroids, alcohol, immunosuppression, osteoporosis; fracture pattern (comminuted, segmental worse); soft tissue damage; open fracture (infection); inadequate fixation; excessive distraction. NSAIDs - mechanistic and animal data suggest impaired bone healing; clinical evidence is mixed; paracetamol is often preferred during active healing.

Complications: early - neurovascular injury, compartment syndrome, fat embolism (long-bone fractures and intramedullary procedures), infection (open fractures); late - malunion, delayed union, non-union (hypertrophic = good biology, poor stability; atrophic = poor biology), AVN, post-traumatic OA (especially intra-articular), growth arrest in paediatric Salter-Harris III-V.

Clinical Pearl
  • Describe every fracture systematically: BONE + LOCATION, then OPEN vs CLOSED, then PATTERN, then DISPLACEMENT/ANGULATION, then STABILITY.
  • Gustilo-Anderson is assigned at surgical debridement, NOT in the ED.
  • Fracture healing phases: Inflammatory (haematoma) - Reparative (soft callus then hard callus) - Remodelling (Wolff's law). The periosteum is critical for callus formation.
  • Absolute stability (plate, screws) = primary healing (no callus). Relative stability (cast, IM nail) = secondary healing (callus).
  • Hypertrophic non-union = good biology, poor stability - stabilise. Atrophic non-union = poor biology - graft AND stabilise.
  • Smoking is one of the most important modifiable risk factors for non-union.

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