Fractures Flashcards
Peripheral/cortical bone
Highly organised, high density
Most of the weight bearing properties of long bone
Medullary/Trabecular bone
More metabolically active and vascular than cortical bone
Bone marrow
3 phases of bone healing
- inflammation
- repair
- remodelling
Structural damage to bone
Haematoma
Inflammatory mediators
○ Kinins, complement, histamine, serotonin, prostaglandins, leukotrienes
§ Vasodilation,
§ chemotaxis of white blood cells,
§ platelet aggregation and release
§ mesenchymal cell proliferation
Inflammatory phase of bone healing
First 2-3 weeks
Growth factors
Cytokines
Phagocytosis
Fragment end resorption
Often associated with less pain so need to be careful
Least structural strength
Reparative phase of bone healing
2-12 months
Basic patterns of bone repair
- direct repair (also called primary)
- indirect repair (also called secondary)
Remodelling phase of bone healing
12+ months
Bone resorption and formation
Callus -> Haversian remodelling restores normal architecture
Direct repair of bone (primary repair)
requires strict conditions (that are rarely achieved!)
- Anatomic reduction (exact alignment)
- Rigid fixation (usually internal fixation involving implants)
○ Screws only
○ Plates and screws
○ Intramedullary nails…… - Sufficient blood supply
Also: early active and pain free mobilisation
Indirect bone repair (secondary)
Angiogenesis
○ From adjacent tissues (muscles), in early repair
○ From medullary cavity of bone, later in repair
Periosteal and endosteal callus formation
○ Goal = interfragmentary stabilisation
○ Suppressed by rigid immobilisation and excessive mobilisation
Bone union
○ Cancellous bone growth formed by 2 mechanisms:
§ Intramembranous ossification
§ Endochondral ossification
Intergrity of soft tissue cover in fractures
Integrity of blood supply
Protection against infection
Maintain vitalised periosteum
Open fractures
Poor soft tissue cover over distal limb
High impact caused high energy fracture = comminuted
Poor first aid stabilisation – often the initial treatment has big effect on outcome!!
Affects if fractures on the other limbs
Persistent non-weight bearing lameness can induce severe laminitic changes in the supporting limb.
Prolonged pressure within the hoof of the ‘non lame’ limb reduces blood flow to the laminae causing hypoxia. Hypoxia causes inflammation and MMP production.
Multimodal analgesia to get the horse weight bearing on the lame leg.
Risk factors for weight bearing laminitis
Size of horse
Duration of lameness
Severity of lameness
Forelimb (60%) vs hindlimb (40%)
Fractures due to repetitive strain injuries
Repetitive strain injuries prelude many fracture types, particularly in RACEHORSES but seen in other disciplines too.
Microdamage -> Microfracture -> Macrofracture -> Failure
Identifying these cases as early as possible will improve outcomes but is very challenging
Repetitive strain injury of the proximal phalanx
Usually propagate from the sagittal groove in a distal direction, often leaving through the lateral cortex
Always arthrodial, sometimes diarthrodial.
CARE WITH BLOCKING!!