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Flinders South Australian Orthopaedic Resitrars' Notebook
Unique in that there is reconstruction of the original tissue rather than healing with scar formation as in other tissues.
McKibbin B JBJS (1978) (from Cardiff Royal Infermary)
Stages of Fracture Healing:
Fracture ® soft tissue injury and ruptured vessels
Formation of Fracture haematoma
Osteocytes deprived of nutrition at the fracture ends die and play a passive role in the repair process
Presence of necrotic material ® inflammatory response
Increased cell division evident within the first 8 hours reaching a maximum in some 24 hours
Activity first seen in the periosteum and extends along the entire bone to be localised at the fracture site in a few days
Acute Inflammation subsides ® repair phase
Organisation of haematoma occurs ® primary callus formation
Micro environment is acidic (moves towards neutrality during repair and becomes alkaline)
Electro negativity is also found in the region of a fresh fracture
Pluripotential mesenchymal cells ® fracture site (cells from cambian layer periosteum, endosteal cells, ? endothelial cells ? monocytes)
Capillary buds grow into the fracture site
Callus is formed made up of fibrous tissue, cartilage and immature fibre bone
Cartilage forms particularly in the periphery of the callus in regions of low O2 tension
Increased movement ® increased cartilage formation
Cartilage is resorbed as enchondral bone formation occurs
Osteoclastic resorption of dead bone occurs
Gradual increase in concentration of collagen and hydroxyappatite ® mineralisation of the matrix as woven bone
Remodelling phase begins
Once the fracture has been bridged ® functional modification which continues for a prolonged period (years)
Resorption of poorly placed trabeculae and new bone struts are deposited corresponding to lines of force
Cancellous bone ®resorption and replacement takes place on the surface of trabeculae (creeping substitution
Cortical bone ® osteoclasts ream out a tunnel followed by vessels bringing osteoblasts ® lay down lamellar bone to form the new osteon (cutter head)
Process thought to be mediated through electrical variation in zones of tension and compression
Electopositivity (associated with osteoclastic activity) occurring on a convex surface and negativity (associated with osteoblastic activity) on a concave surface
Source of osteogenic tissue:
Osteoprogeniter cells. Cells with a predetermined commitment to bone formation and occur in close association to bone surfaces or the marrow.
Metaplasia of previously uncommitted fibroblasts which develop the power of osteogenesis given appropriate environmental stimulus. Cells arise from surrounding soft tissue. Osteogenic induction.
This theory is supported by the formation of bone by non specialised cells in extra skeletal sites
Control of Fracture Healing: Bridging by external, medullary or 1o callus
1. External callus:
Dependent on the existence of another fracture fragment (ie no response from an amputation stump)
Continuity of periosteum ® bridging callus ® induction, if no contact is made within a certain time ® primary callus response
Mechanical and humeral influences as attempts to bridge the fracture are not continued indefinitely
2. Medullary callus
Cartilage formation is less prominent in medullary callus
Controlled by similar process and in displaced fractures may unite with the external callus
Develops independently of rigid fixation
3. 1o Bone healing:
May only be possible where there is rigid fixation, evacuation of fracture haematoma and intimate contact of one bone end with the other
Equates with the process of normal bone turnover
Direct bone union occurs when rigid fixation prevents formation of fracture callus. Osteoclasts resorb the dead bone of the fracture ends and osteoblasts form new bone directly across the fracture. The fracture depends on the plate or means of fixation for stability for some time.
Indirect bone union occurs in the absence of rigid fixation through callus formation.
Factors affecting fracture healing:
Soft tissue injury and local blood supply
Radiation, chemical or thermal burns
Infection, anaemia or hypoxia
Excessive compression ( more than 30lbs) inhibits enchondral ossification but cyclic compression is beneficial
Intermittent shear stresses promotes cartilage formation
High shear stresses promotes fibrous tissue formation
Corticosteroids inhibit osteoblast differentiation ® slow healing
Growth hormone increases fracture healing (only if deficient)
Denervation retards fracture healing
Exercise increases fracture healing
Head injury promotes fracture healing by a humoral mechanism
Vitamin C is required for normal collagen matrix formation
Incomplete repair, the bone moves as one but clinically is still a little tender and attempted angulation is painful. The fracture is clearly visible on X-Ray with fluffy callus. Not safe to be unprotected.
Complete repair, calcified callus is ossified and attempted angulation is painless. Repair is complete and further protection is unnecessary.
A fracture that has not united in what is considered a reasonable amount of time for a fracture of that type in that location.
A fracture that will not unite without surgical intervention. A Non union is usually non tender.
Incidence of non union said to be 5% in all long bone fractures
Consolidation of a fracture in a deformed position.
Influence a certain cell, tissue or substance may have on another cell such that the second cell or descendants of that cell exhibit physiological processes that the original cell did not.
For normal fracture healing: (Pioneered delayed splintage)
A spiral fracture in the upper limb unites in 3/52
double it for consolidation
double it again for the lower limb
double it again for a transverse fracture
Blood supply of bone;
Nutrient artery ® medullary arteries supplies the marrow and inner 2/3 of diaphysial cortex.
In areas away from muscle or facial attachments ® supply full thickness of cortex
Multiple metaphyseal arteries which anastomose with terminal branches of the medullary arteries at the junction of metaphysis and diaphysis
Multiple periosteal arterioles supply the outer 1/3 of the cortex
Periosteal vessels alone are sufficient to support normal fracture repair
All veins drain to the periosteal surface
Increased blood flow secondary to a fracture peaks at 2/52 at six times the normal base line ® 3.5 times the normal baseline at 3/52 which persists until 8-10/52 and returns to normal at about 12/52.
Extra osseous blood supply to external callus develops rapidly after a fracture and perhaps replaces the damaged medullary supply,
Indications for ORIF of fractures:
Unable to obtain an adequate reduction
Displaced intra-articular fractures
Certain types of displaced epiphyseal fractures
Major avulsion fractures where there is loss of function of a joint or muscle group
Re- implantations of limbs or extremities
Multiple fractures to assist in care and general management
Unable to maintain a reduction
To assist in nursing care
To reduce morbidity due to prolonged immobilisation
For fractures in which closed methods are known to be ineffective
Fractures accompanying nerve of vessel injury
Pull is exerted against a fixed point
Pull against the weight of the body
Traction fixed to the splint and the splint is suspended against the weight of the body
(Buck's) can pull no more than 4 or 5 kg
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Institution: Flinders Registrars' Notebook
Submitted by: admin
Added: Mon Apr 10 2006
Last Modified: Fri Jan 25 2008