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Musculoskeletal: fracture

ISSN 2398-2977


Podcast: Musculoskeletal: fracture

Bone biomechanics

Biomechanical behavior of bone

  • The response of bone to applied forces depends on its material properties, geometry, loading mode, loading rate and the frequency of loading.
  • An understanding of biomechanical forces at work on bone is essential for correct surgical fixation.

Tension

  • Distracting loads are applied at the ends of the bone.
  • Maximal tensile stress occurs on a plane perpendicular to the applied load → creating transversely orientated fracture lines.
  • The bone lengthens and narrows under tensile stress and failure occurs → debonding of cement, osteons are pulled out.
  • Tensile fractures tend to occur in proximal ulna Ulna: fracture, proximal sesamoid bone Proximal sesamoid: fracture, the patella Patella: fracture, the calcaneus Tarsus: fracture.

Compression

  • Bone is strongest under compressive loads, compared to other loading modes.
  • Equal and opposite loads are applied toward each other at the ends of the bone.
  • With compression, bone shortens and widens, and failure occurs obliquely through osteons.
  • This oblique line corresponds to the plane of maximum shear stress to which bone is less resistant than compressive stress.
  • Y-shaped fractures on the distal humerus Humerus: fracture and femur Femur: physeal fracture are the result of compressive forces.

Bending

  • Load is applied such that the bone bends on its axis → combination of tension and compression forces on opposite sides of the bone.
  • The bone fails firstly on the tension side and the fracture line travels toward the side of compression.
  • Shear forces then act in 45° direction on compressive side → butterfly fracture.

Torsion

  • Bone is forced to twist around its axis → torque produced within bone.
  • Shear stresses applied over the whole bone, but the size of the stresses increases with increasing distance from the neutral axis (usually axis of rotation) → periosteal shear stresses are greatest parallel and perpendicular to the axis.
  • Bone first fails along the shear line, parallel with the long axis.
  • Second fracture line occurs along line of tensile stress → spiral fracture.

Rate dependency

  • Bone absorbs more energy when loads are applied at higher rates → horses training at slow speeds tend to sustain simple fractures but horses running at high speeds sustain comminuted fractures and more tissue trauma due to release of absorbed energy at the time of fracture.

Bone fatigue

  • With cyclic loading of bone, there is a release of strain energy that can cause microcracks along cement lines.
  • If cyclic loading is maintained there may be progressive microdamage in cortical bone.
  • In addition, bone microdamage is more likely to occur when there is muscle fatigue, ie the muscle is less able to absorb concussive stresses.
  • Repair processes may not be able to keep up with level of repeated microdamage even at low loads and may contribute to failure due to rapid resorption of bone.
  • The majority of fractures in racehorses are fatigue fractures.
  • Fracture on tensile surface propagates rapidly transversely → complete fracture.
  • Fracture on compressive surface → slow propagation of fracture → remodeling may occur before it becomes complete.
Print off the Owner factsheet on Fractures and Emergencies - when to call the vet to give to your clients.

Fracture healing

Response of bone to fracture

  • Mechanisms of bone healing → ability to reconstitute the original bone structure (unlike soft tissues following injury).
  • Molecular factors stimulate cells to increase growth rate, recruit cells to join healing process which resembles embryonic skeletal growth.
  • Phases of healing overlap sequentially.
  • Local (type of injury, neurovascular compromise, amount of lost bone, immobilization, infection, other pathologic conditions) and systemic (age, nutrition, hormones, physical activity) factors will influence healing.
  • Potential for therapeutic cytokines and growth factors to become available in future, so understanding of their role in healing important.

Primary callus response

  • Initial cellular reaction within a few hours of injury.
  • Uniform periosteal and endosteal cell activity.
  • Critical first step in healing by external callus.
  • Rigid immobilization or excessive fracture movement will inhibit formation of callus.

Inflammatory phase

  • Occurs over first 2-3 weeks after injury.
  • Series of chemical factors released in response to injury - kinins, complement, histamine, serotonin, prostaglandins, and leukotrienes.
  • Coagulation → fibrin to site.
  • Vasodilation, migration of leukocytes and chemotaxis.
  • Platelets → growth factors → angiogenesis, mesenchymal cell proliferation.
  • Macrophages and lymphocytes assist destruction and phagocytosis of bacteria, and release angiogenic and other cell growth factors.
  • Callus tissue consists of mesenchymal cells, fibroblasts, macrophages and blood vessels which originate from surrounding muscle and medullary cavity.

Reparative phase

  • Can take 2-12 months to finish.
  • Periosteal and endosteal callus formation aims to create interfragmentary stabilization.
  • Callus undergoes rapid chondrogenic transformation - its size will correlate with the final bony callus.
  • Followed by intramembranous and endochondral ossification → bony union.
  • Inadequate immobilization at this point may result in hypertrophic non-union due to persistence of fibrous tissue.
  • Endochondral ossification involves vascular invasion into mineralized fibrocartilage (collagenous and non-collagenous proteins important here).
  • Calcium and hydroxyproline concentration of the callus increases over this period as does the tensile breaking strength; however, size of callus is not an indicator of its strength.

Remodeling phase

  • Osteonal remodeling replaces avascular and necrotic areas, correcting, in part, malaligned fractures.
  • Bone is removed from convex surfaces and laid down on concave surfaces to realign cortices however this process does not correct torsional deformities.

Biochemical factors

Proteins and enzymes
  • Collagens:
    • During inflammatory phase, chemotactic factors are responsible for attracting cells involved in the production of proteins and enzymes important in healing.
    • Collagen Types III and V fill the fracture gap shortly after fracture.
    • Fibroblasts produce mainly Type III collagen which is distributed throughout the callus.
    • Angiogenesis, new blood vessel growth, is associated with expression of Type V collagen.
    • With transformation to cartilage in the callus, Type II and IX collagen predominate.
    • As the cartilage matures, chondrocytes begin to produce Type X collagen.
    • This is followed by mineralization.
    • When osteoblasts become active, Type I collagen is expressed, indicating the osteoclastic and osteoblastic remodeling phase.
  • Other proteins:
    • Proteoglycans are constantly changing throughout the endochondral phase of bone formation.
    • Two types of proteoglycans, chondroitin 4-sulfate and dermatan sulfate.
    • Fibroblasts in the callus produce dermatan sulfate early in fracture healing, then chondroitin 4-sulfate begins to predominate.
    • Quantity of proteoglycans increase dramatically when calcification begins but their ability to aggregate decreases.
    • This may facilitate mineralization.
    • Matrixins (metalloendopeptidases, metalloproteinases including collagenase, gelatinase, proteoglycanase or stromelysin). are found normally in all types of mesenchymal cells - considered to have a role in modifying proteoglycan structure in preparation for mineralization.
    • Other factors including alkaline phosphatase activity, osteopontin, osteonectin, vitamin K and vitamin D dependent proteins have a variety of roles in mineralization.

Other factors

  • Have been described as competence factors, progression factors, mitogenic factors and differentiation factors.
  • Platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) stimulate mesenchymal cells.
  • PDGF, FGF and epidermal growth factor, insulin-like growth factor and transforming growth factor are mitogenic, maintaining cells in proliferative state.
  • Cytokines maintain macrophage, neutrophil, and eosinophil colonies important for healing.
  • Interleukins have role in production of collagenase and proteoglycanase, plus stimulate prostaglandin E2 production.
  • Prostaglandins are mediators of bone metabolism and homeostasis - stimulating bone resorption and causing periosteal callus formation.

Mechanisms of fracture union

  • There are a number of pathways by which fracture union can occur.
  • Primary or direct bone healing - involves osteonal remodeling directly between contacting fracture points.
  • Secondary or indirect bone healing - involves periosteal and endosteal callus formation with an intermediate phase of fibrocartilage formation subsequently replaced by new bone.
  • Compromised bone at fracture site plays a structural role in supporting implants.
  • Osteonal remodeling:
    • Revascularization of necrotic fracture ends.
    • Reconstitution of the gap between cortices.
    • Requires axial alignment of fracture ends.
    • Requires immobilization.
    • Needs blood supply.
    • There is probably a biomechanical stimulus necessary.
  • Woven bone fills any gaps but does not provide any strength.
  • Secondary osteons grow through the woven bone from one fragment to another.
  • This is associated with a temporary loss of bone density.

Assessing fracture healing

  • Non-invasive techniques important for:
    • Deciding when to remove an implant.
    • Management of rehabilitation following injury, eg transition from partial weight bearing to full weight bearing.
    • Prediction of abnormalities in fracture healing such as non-union.
  • Basic subjective techniques for assessing fractures such as radiography, palpation, time since immobilization, have not changed greatly in past few decades.
  • But developing technologies may be of increasing value:
    • Objective evidence of bone union.
    • Predicting refracture risk.
    • Early detection of healing delay or failure.
    • Prediction of chances of delayed union progressing to union without surgical intervention.
    • Evaluating the type of gap tissue in non-unions.
    • Predicting primary fracture risk in athletic horses.

Quantitative computed tomography

  • Used in research to measure bone density Computed tomography.
  • Evidence that it can do so with accuracy and precision.

Dual energy x-ray absorptiometry

  • Two energy x-ray sources are used.
  • Has been used in research to evaluate changes in bone density during fracture healing.

Fixation methods

Intramedullary rods

  • Pins and rods Bone: internal fixation - pins and nails.
  • Suitable for young, lightweight animals, but rarely used in the horse due to large medullary cavity in relation to total bone diameter.
  • Act as an internal splint.
  • Risks include rod migration, rod deformation, fatigue fracture, delayed union and non-union.
  • Resistance to axial, bending and torsional stresses depend on cross sectional area, length, position in bone, elastic properties.
  • Lack of cross-fixation or locking mechanisms will provide no resistance to torsional forces.
  • Distance between fixed proximal and distal ends of rod represents vulnerability to bending forces.
  • Locking mechanisms decrease the unsupported length and therefore have increased the application of intramedullary rods.

Bone plates

  • See internal fixation - plates Bone: internal fixation - plates.
  • Plate rigidity is dependent on thickness and material properties.
  • Bone which is 'less stiff' will increase the load borne by a plate.
  • Plate placement relative to loading direction will determine how much load is borne by the plate.

External fixation

  • Distance between side bar and the bone the most significant contributor to frame stiffness.
  • Other factors include the number of pins used, pin diameter, material properties of the pins.
  • But these techniques not widely used in horses because the system has to withstand repetitive high loading without failure.
  • An external frame has been developed for distal limb fractures in the horse.
  • See also transfixation cast Musculoskeletal: external fixation - casts.

Case selection

General examination

  • Cardiovascular system - local vascular compromise, eg rupture of major arteries, and systemic compromise, eg major blood loss.
  • Central nervous system trauma - for facial or cranial fractures, general nervous system deficits.
  • Fracture site:
    • Location.
    • Instability → indicates complete fracture.
    • Skin perforated by fracture fragment → open fracture OR skin wounds due to external trauma may have little impact on fracture healing unless large area of bone exposed.
  • Radiography:
    • Take full set of views, forelimb Forelimb: radiography and hindlimb Hindlimb: radiography.
    • Evaluate site and extent of fracture.
    • Enables prognostication.
    • Do not remove external splints or casts unless horse is anesthetized.
  • Prognosis depends on:
    • Type and location of fracture.
    • Open or closed fracture.
    • Degree of soft tissue damage and neurovascular compromise.
    • Age, weight, temperament of horse.
    • Delay between time of injury and repair.
    • First aid measures Musculoskeletal: fracture - first aid.

Fracture classification

Complete or incomplete
  • A fracture is incomplete if it does not perforate opposite cortex or subchondral bone plate.
  • Incomplete fractures include greenstick, fissure (some condylar fractures) and 'saucer' fractures.
Stable or unstable
  • Complete fractures may not be displaced, ie there is some intercortical continuity between fracture fragments preventing overriding or rotation.
  • Unstable fractures have poorer prognosis because motion at the fracture site increases local soft tissue damage as well as rounding and comminuting fracture ends.
  • There is more risk that an unstable fracture will perforate skin.
Open or closed
  • Open fractures have a communication between the skin surface and the fracture site.
  • Grade open fractures on degree of skin opening:
    • Type I - <1 cm skin perforation - minimal skin loss, exposure of the fracture ends or contamination.
    • Type II - >1 cm skin laceration with minimal skin or soft tissue loss or contamination.
    • Type III - extensive laceration, skin defect and gross contamination of soft tissues and bone ends; these tend to be uncommon, usually severe racing injuries or trailering/horsebox accidents; much poorer prognosis due to risk of osteomyelitis, wound dehiscence and implant failure.
Fracture shape
  • Greenstick or fissure:
    • Incomplete and fissure fractures can often be managed conservatively with stall confinement.
    • Fractures which open into a joint are better treated by internal fixation.
  • Transverse.
  • Oblique and spiral fractures tend to displace and override → difficult to reduce and appose during implant application.
  • Comminuted.
  • Multiple.
  • Impacted.
  • Avulsion.

Fractures in adults

  • Optimal results are achieved with simple transverse or short oblique fractures, but usually adult long bone fractures have comminuted ends with torque injury → long oblique and complex fracture configurations.
  • High-energy injuries are less amenable to fixation than low energy fractures.
  • Compromise of the diaphyseal blood supply, either as a result of the initial trauma or during surgery, eg disruption of nutrient foramen, will result in poor fracture healing.
  • Comminution: >180° of cortex must be able to carry weight axially after internal fixation.
  • Closed vs open fracture: open and contaminated fractures have substantially less chance of healing and at greater cost to client.
  • Equipment available: for long bone fracture repair - 4.5 mm dynamic compression plates, cobra-head plates, dynamic condylar screw plates, 5.5 mm cortical screws; methylmethacrylate bone cement for luting of the plate-bone interface or the screw heads in the plates.
  • Length and timing of surgery: steps to reduce time in surgery will facilitate recovery and long-term success of repair.
  • Controlled anesthetic recovery: pain control, recovery room design, competent staff and the horse's temperament will influence the success of surgery - violent recovery will break implants or cause another fracture.

Fractures in foals

  • Fractures amenable to repair:
    • Closed radial and tibial fracture.
    • Most third metacarpal and metatarsal fractures.
    • Short oblique fractures, long oblique fractures of the radius and tibia.
    • Some comminuted fractures that cannot be plated may heal in a fiberglass cast.
  • Physeal fractures (tibial Tibia: fracture - physeal, femoral Femur: physeal fracture):
    • Limited space to apply screws.
    • Splitting of epiphysis may result if too many screws are applied.
    • 6.5 mm cancellous screws may do, but will later need to be removed if they are bridging the physis.
    • Injury to the physeal cartilage may result in premature closure.
    • Physeal fracture description based on Salter-Harris Classification:
      • Type I - Physis only.
      • Type II - Physis and metaphysis.
      • Type III - Physis and epiphysis.
      • Type IV - Physis, metaphysis, and epiphysis.
      • Type V - Physeal compression and crush.

Complications of fracture management

Delayed union

  • Healing is slower than expected.
  • Long bone fractures should heal within 4 months in adults; 3 months in foals.

Malunion

  • Healing of bones in incorrect position.
  • Maybe functional, ie no management required or non-functional → may require corrective osteotomy to realign limb.

Non-union

  • Healing ceases without bony union.

Vascular

  • Biologically capable of repair.
  • Hypertrophic - have excessive vascular callus and are associated with unstable fractures.
  • Mild hypertrophic callus associated with rotational instability and have sclerotic medulla.
  • Oligotrophic have no callus and rounded fragment ends but fibrous tissue and vessels lie between them.

Avascular

  • Dystrophic - healing of secondary fragment but not of main fragments.
  • Necrotic - lack of vascularization typically in comminuted fractures → death of fragment.
  • Defect - loss or resorption of fragment.
  • Atrophic - can result from any of above, with bone resorption and osteoporosis.

Infected

  • Lysis of fragments, variable callus formation and vascularity.

Causes of delayed or non-union

  • Infection, eg osteitis Joint: septic arthritis - adult, osteomyelitis Bone: osteitis - septic.
  • Poor reduction, eg distraction of fragments; poor alignment → larger callus required for immobilization, more prolonged revascularization; possible interposition of soft tissue between bone ends preventing osseus union.
  • Poor stabilization - adequate stabilization promotes revascularization and weight-bearing both of which speed healing.
  • Soft tissue damage, eg disrupted blood supply.
  • Inappropriate implants.
  • Loss of bone stock, eg by discarding avascular cortical fragments that could act as autogenous grafts.

Diagnosis

  • Persistent lameness.
  • Instability (variable).
  • Draining fistula.
  • Radiography - forelimb Forelimb: radiography hindlimb Hindlimb: radiography:
    • Sclerosis of fragment ends.
    • Failure of healing to progress over 3 months.
    • Bowing at fracture site.
    • Excess callus.
  • Nuclear imaging Bone: scintigraphy - persistent 'cold spot' (photopenic region) due to decreased radiopharmaceutical uptake.

Treatment

Infection
Delayed unions
  • Restrict horse's activity.
  • If instability → external fixation Musculoskeletal: external fixation - casts if necessary, or renewed internal fixation.
  • If loose implant or malalignment → surgical correction.
  • Foals with osteoporosis, but good fracture stability → increased activity and weight bearing can stimulate better callus formation, but must take place under controlled conditions. Osteoporosis can also be alleviated in foals by switching from full limb cast to a 'tuber' or 'sleeve' cast.
Non-unions
  • Viable:
    • Should respond to adequate fixation.
    • Internal fixation + opening of the medullary cavity at the fracture ends and application of an autogenous bone graft.
  • Non-viable:
    • Surgical removal of all necrotic or avascular bone.
    • Open medullary cavity.
    • Apply autogenous bone graft.
    • Rigid fixation.
Fracture types

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Donati B, Fürst A E, Del Chicca F & Jackson M A (2020) Plate removal after internal fixation of limb fractures: a retrospective study of indications and complications in 48 horses. Vet Comp Orthop Traumatol PubMed.
  • Johnston A S, Sidhu A B S, Riggs C M, et al (2020) The effect of stress fracture occurring within the first 12 months of training on subsequent race performance in Thoroughbreds in Hong Kong. Equine Vet J PubMed.
  • Boorman S, Richardson D W, Hogan P M, et al (2020) Racing performance after surgical repair of medial condylar fracture of the third metacarpal/metatarsal bone in thoroughbred racehorses. Vet Surg 49 (4), 648-658 PubMed.
  • Martig S, Hitchens P L, Lee P V S & Whitton R C (2020) The relationship between microstructure, stiffness and compressive fatigue life of equine subchondral bone. J Mech Behav Biomed Mater 101 PubMed.
  • Johnson K A (2019) Risks and outcomes of equine flat bone fractures. Vet Comp Orthop Traumatol 32 (4) PubMed.
  • Whitton R C, Ayodele B A, Hitchens P L & Mackie E J (2018) Subchondral bone microdamage accumulation in distal metacarpus of Thoroughbred racehorses. Equine Vet J 50 (6), 766-773 PubMed.
  • Levine D G & Aitken M R (2017) Physeal fractures in foals. Vet Clin North Am Equine Pract 33 (2), 417-430 PubMed.
  • Misheff M M, Alexander G R & Hirst G R (2010) Management of fractures in endurance horses. Equine Vet Educ 22 (12), 623-630.
  • Hesse K L & Verheyen K L P (2010) Associations between physiotherapy findings and subsequent diagnosis of pelvic or hindlimb fracture in racing Thoroughbreds. Equine Vet J 42 (3), 234-239 PubMed.
  • Martens A & Declercq J (2006) Fracture fixation in the standing horse: for surgeons who dare. Equine Vet Educ 18 (6), 314-315.

Other sources of information

  • Auer J A & Stick J (2019) Equine Surgery. 5th edn. W B Saunders, USA.
  • Nixon A J (2020) Ed. Equine Fracture Repair. 2nd edn. Wiley-Blackwell, USA. ISBN: 978-0-813-81586-2.