Fracture healing and non-union Flashcards
Tell me about fracture healing?
1. primary bone healing - intramembranous ossification
- direct cortical osteonal healing with a cutting cone - gap or contact healing
- contact healing - osteoclasts remove and osteoblasts lay down new bone
- Gap healing - osteoblasts form new bone at fracture ends to close the gap, then contact healing
- direct cancellous healing - blood vessels go from good bone to low oxygen environment - takes cell population with them laying down new bone
- intramembranous ossification - flat bones
2. Secondary bone healing
- via callus formation due to greater strain environment
- enchondral ossification - long bone formation/ physis
- four key phases:
1. haematoma
2. inflammation
3. soft and hard callus
4. remodelling
haematoma
- secs to minutes
- blood vessels torn
- activation of clotting cascade
- haematoma formed
Inflammation
- hours to days
- angiogenesis - high to low oxygen
- brings cell population - IL6, IL1m FGF
Soft and hard callus
- weeks to months
- 100% strain
- perren’s strain theory - mesenchymal stem cells differentiate depending on the strain environment
- granulation tissue laid down first as 100% strain - closes fracture gap and reduces strain
- fibrous connective tissue laid down at 17% - fibroblasts
- fibrocartilage 2-10% - chondroblasts
- woven bone 2% - this then remodels to lamellar bone - osteoblasts
draw a cutting cone?
what are the requirements for primary bone healing?
Direct osteonal healing
- anatomical reduction
- direct bone contact
- interfragmentary compression - lag screw, partially threaded, variable pitch, external compression device, compression plate
- absolute stability
- less than 2% strain
Gap healing
- If gap is <50um = contact healing
- if gap is 50-100um = gap healing
- gap healing - blood vessels cross the gap, mesenchymal stem cells lay down osteoblasts at the two ends to reduce the gap size
how do you define bony union and non-union?
Is it the same for all bones?
What is delayed union?
Clinical union
* Absence of tendersness or motion at fracture/fusion site, with no pain on loading
Radiological union
* presence of visible bridging trabeculae in 3 out of 4 cortices on orthogonal radiographs
Non-union
* failure of a fracture to heal in the time expected for the specific fracture.
* FDA definition - failure of a diaphyseal fracture to unite by 9 months with no radiographic progression in the prior 3 months
* Types:
* hypertrophic
* atrophic
* septic
Delayed union
- Longer than expected time for consolidation of a fracture to occur.
- consolidation is complete repair with ossification of the callus
Perkins healing times for fractures:
- spiral upper limb fracture = 6 weeks to consolidation
- spiral lower limb fracture = 12 weeks to consolidation
- transverse lower limb fracture = 24 weeks to consolidation
Malunion
- consolidation in a suboptimal position with malalignment
- deformity can occur in any plane and have deterious effects on neighbouring joints
what factors influence if a patient goes onto non-union?
these can be patient, fracture and surgeon factors:
Patient factors
- Age (paeds heal faster)
- comorbidities - diabetes, PVD, malnurishment/ deficiencies
- smoking (inhibits angiogenesis), alcohol use
- Drugs - steroids, NSAIDs, quinolones, bisphosphonates
Fracture factors
- open fracture (1% nonunion closed, 36% for gustillo 3B) - soft tissue stripping, disruption of nutrient arteries and periosteal distruption
- bone affected - e.g. scaphoid/ talus = high risk
- area of bone - diaphyseal fractures take longer than metaphyseal fractures
- infection post op
- bone loss
- bone quality - poor purchase for fixation
surgeon factors
- soft tissue stripping
- inadequate stability
- rigid fixation with gap
- introduction of infection
- poor bone contact - malalignment, distraction of the fracture or soft tissue interposition - osteoblastic jump distance = 1mm. Less than 1mm, woven bone first or non-union
Perren strain theory
amount of strain at the fracture site determines the tissue formed
- primary lamellar bone - 2%
- fibrocartilage - 10%
- granulation tissue - 100%
what is hypertrophic nonunion and how does it occur?
- mechanical problem
- good blood supply but excessive strain at the fracture site prventing progression of callus to form bone
what is atrophic nonunion and how does it occur?
- biological problem
- complete abscence of callus formation resulting from impaired bone healing due to patient, fracture and surgeon factors
what is oliogtrophic and pseudarthrosis?
- oligotrophic - limited amount of new bone due to a fixation problem
- pseudoarthrosis - false joint is formed by fibrosis tissue between the bone ends
what are the principles of non-union surgery?
- eradication of infection
- excision of interposing tissues
- restore blood supply
- stabilisation of bone ends
- bone graft any fracture gaps
Assessment of non-union patients
Assessment
- PAIN - on WB/ use, night pain, persistent pain
- FUNCTION - WB, aids, work, sports
- INFECTION - post op wound problems/ Abx, constitutional symptoms (sweats, fevers, rigors, weight loss, loss of appetite)
- EXAMINATION - pain on palpation, fracture mobility/ crepitus, inflammation (wounds/ skin integrity) and alignment
- INVESTIGATIONS - inflammatory markers and CT scan
Management of patients with an atrophic tibial non-union?
Non-operative
- functional bracing - if no pain/ comorbid patient
- electric shockwave therapy
- improve patient factors - diabetic control
Hypertrophic non-union
- exchange nail - dynamised
- compressive plating
Exchange nailing - Hypertrophic non-union
- exchange nailing with a nail 1-2mm larger after reaming
- reaminings sent - mc&s to rule out indolent infection
- increasing nail size leads to increased stabilisation
- reaming delivers autologous bone graft to fracture site
- stimulates periosteal blood supply and new periosteal bone formation
- dynamised to add compression
- enhance stability with plate
ATROPHIC NON-UNION
- excision of fibrosis tissue and non-viable sclerotic bone ends
- management of bone defect - bone graft, synthetic bone substitutes, bone morphogenic proteins, masquelet or bone transport
- exchange nailing
union rates following exchange nailing
Hypertrophic non-union
- 90% union at 10-12 weeks for tibia
Atrophic non-union - edinburgh cohort Tsang - 2016
- 75% union after 1st exchange
- 95% union after 2nd exchange
Infection non-union
- 35% union after 1st exchange
- 61% after 2nd exchange
Infected non-union
- assessment
- management
Assessment
- inflammatory markers
- blood cultures
- echo - to look for bacterial seeding
- MRI
Management
- medical review if septic and sepsis 6 pathway
- suppressive antibiotics - reserved for those unable to undergo operative
- operative - 2 stages - radical debridement then reconstruction
Principles of treatment:
- MDT approach
- optimise patient
- 2 week antibiotic holiday for chronic/ well patients - boast guideline on FRI
- 2 stage procedure
Ist stage
- radical debridement (non-viable bone/ soft) with 5 samples sent for micro, 2 samples for histology (chronic/ unsure) and irrigation
- Antibiotic delivery - either impregnated cement beads or masquelet (deals with large bone loss) or cement loaded nail
- temporary fixation - nail or frame
- soft tissue coverage - vascularised flap
- IV abx - broad spectrum - then specifc at 48hrs with results
2nd stage
only once infection eradicated
bone graft and definitive fixation
90% septic tibial non-unions unite by 26weeks
masquelet technique
induced membrane
- abx impregnated PMMA cement spacer
- induces membrane formation
- removed at 8 weeks
- care to keep membrane intact
- bone ends decorticated
- cancellous and or cortical bone autograft into membrane
- fixation until osteointegration
