Ortho Introduction to Fractures Flashcards
Osteogenesis
Process of bone tissue formation
Embryos leads to bony skeleton
Occurs in the form of bone remodeling and bone repair
Endochondrial Ossification
Bone replaces a cartilage model
Long bone formation, physis, fracture callus
Intramembranous
Undifferentiated mesenchymal cells differentiate into osteoblasts which form bone
Flat bone formation
Appositional
Osteoblasts deposit new bone on existing bone
Periosteal bone enlargement (adds width)
Endochondrial Ossification
- Undifferentiated cells secrete cartilagenous matrix and differentiate into chondrocytes
- Matrix mineralizes and is invaded by vscalar buds
- Osteoprogenitor cells migrate in
- Osteoclasts resorb calcified cartilage
- Osteoblasts form bone
Osteoprogenator cells
Form mesenchymal stem cells
Lead to formation of osteoblasts, cartilage, fibrous tissue depending on fixation and oxygen tension
Osteoblasts
Mesenchymal stem cells
Receptors for PTH, Active Vitamin D, Glucocorticoids, Prostaglandins, Estrogen (stimulate bone growth)
Form bone by generating organic nonmineralized matrix
Osteocytes
Osteoblasts that have become surrounded in newly formed matrix
Canaliculi are long cytoplasmic process that connect neighboring osteocytes
Control extracellular calcium, phosphorous concentrations
Stimulated by calcitonin, inhibits PTH
Osteoclasts
Originate from macrophage lineage
Brush border membrane for increased surface area
Howship’s lacunae through resorption of bone surface
Inhibited by calcitonin
Zones of Physeal Growth
- Reserve zone-resting zone
- Proliferative zone
- Maturation/Hypertrophic zone
- Vascular invasion zone
- Provisional calcification
Collagen in Physis
Type II Collagen
Resting Zone
Small scattered chondrocytes
Store lipids, glycogen, proteoglycan for later growth and matrix production
Proliferative zone
Chondrocytes line up in direction of growth, proliferate and divide
Longitudinal growth occurs (columns of flattened dividing cells, top cell is the dividing mother
High O2 tension, proteoglycan
Zone of Maturation/Hypertrophy
chrondrocytes enlarge
large increase in cell volume
Increased cell height responsible for 44-59% of long bone growth
Differential growth due to differential cell size here
This is the weakest part of the physis, fractures occur here
Zone of Calcified Cartilage
Chondrocytes die and matrix starts to calcify
Calcification begins with the longitudinal septa
Apoptosis
Programmed cell death
Necessary for homeostasis
Terminally differentiated chondrocytes undergo apoptosis in the zone of calcification
Physeal Closure
Completely closed in skeletal maturity
Stops longitudinal bone growth
Decline in width of physis
Estrogen stops replicative sequence of chondrocytes (controls physis closure)
Intramembranous Ossification
- Occurs without a cartilage model
- Undifferentiated mesenchymal cells aggregate into layers or membranes
- Cells differentiate into osteoblasts depositing organic matrix
- Matrix mineralizes
Ossification Center
Location in tissues where ossification begins
Bipartate patella
Due to formation of 2 ossification centers
Fibrous tissue links 2 pieces together
Appositional Ossification
Primary bone healing
OSteoblasts align themselves on existing bone surfaces and lay down new bone
Fracture
Break in integrity of bone
Load force applied to the bone
Results in a decrease of the functional capability of the bone
Fracture Patterns
Determined by type and direction of force
Determined by physical characteristics of the bone
Determined by the speed of the force
Classifications of Fractures
Location in a bone
Diaphyses
Metaphysics
Epiphysis end of bone adjacent to jt.
Orientation of Fractures
Transverse Oblique Spiral Comminuted Segmental Intra-articular
Displacement of Fractures
Non-displaced Displaced Angulated Bayonet Distracted
Type I
Simple, transverse, short oblique with little communication
Type II
Moderate fracture comminution
Type III
Great degree of fracture comminution and instability
Type III-A
Extensive soft tissue laceration, adequate bone coverage after debridement
Free flaps are not necessary to cover bone
Segmental fractures, such as gunshot injuries
Type III-B
Extensive soft tissue injury with periosteal stripping and exposed bone after debridement
Requires local or free flap to cover bone
Type III-C
Same as B
Extensive soft tissue injury with periosteal stripping and exposed bone after debridement
Require local or free flap to cover bone
Pediatric
Bone is more porous
High proportion of articular cartilage
Opens epiphyseal plates
Periosteam much thicker (great blood supply)
Higher osteoblastic activity
Fractures can remodel
Joint injuries and dislocations much less common (ligaments stronger than bone)
Cartilagenous epiphyseal plate is weaker than joint capsulre or ligaments
Why are hip fractures bad in kids?
Devastating due to AVN of femoral head
Tillaux Fracture
Occurs because of asymmetrical closure of distal tibia growth plate
Triplane Fracture
Sagittal fracture line through epiphysis, transverse fracture line through physis, coronal fracture through metaphysis
Types of Pediatric fractures
Plastic deformations Buckle Greenstick Complete Epiphyseal plate Apophyseal plate
Salter Harris I
Widening of epiphyseal plate
Salter Harris II
Fracture through plate and metaphysis
Salter Harris III
Fracture through plate and epihysis
Salter Harris IV
through plate, metaphysis and epiphysis
Salter Harris V
Crushed epiphysis (compression fracture of growth plate leads to disturbances in growth)
What are the orthopedic aspects of child abuse
Fractures in various stages of healing
Corner fractures can be noted at the corner of the metaphysis (jerked leg/arm)
Apophyseal Fractures
Fracture of a diaphysis that does not add length
Modifying Factors of Fracture Healing
- Bleeding
- Resorption
- Mesenchymal differentiation into osteo and fibro-progenitor cells
- Callous formation
Stages of Fracture Healing
- Bleeding–>devascularizes and forms hematoma
- Resorption–>osteoclasts and inflammatory response
- Mesenchymal differentiation into osteo and fibro-progenitor cells
- Callous formation
Bone Circulation
- Nutrient artery system
- Metaphyseal-epiphyseal system
- Periosteal system
Stages of Fracture Healing
- Hematoma and inflammatory response
- Fracture hematoma maturation
- Conversion of hypertrophic cartilage to bone
- Bone remodeling
Cells of early postfracture
Primaritive mesenchymal and osteoprogenitor cells facilitate production of the BMPs
Bone Growth Factors
BMP
TGF-B
IFG-II
PDGF
Bone Morphogenic Protein
Stimulates growth
Induces metaplasia of mesenchymal cells into osteoblasts
Target for BMP is undifferentiated perivascular mesenchymal cell
TGF-B
Induces mesenchymal cells to produce type II collagen and proteoglycans
Induce osteoblasts to synthesize collagen
Regulate cartilage and bone formation in fracture callus
Conversion of hypertrophic cartilage to bone
Undergo terminal differentiation, cartilage calcifies and new woven bone is formed
Hard callus
Woven bone is remodeled
Mature bone eventually established and is not distinguishable from surrounding bone (week 17+)
Cortical Bone Remodeling
Remodels by osteoclastic tunneling
Cancellous bone Remodeling
Remodels by classic resorption followed by blasts laying down new bone
Wolff’s Law
Bone remodels in response to mechanical stress
Piezoelectric Charge
Compression side (negative charge) activates blasts Tension side (positive charge) activates clasts
Delayed Union
Fracture that has not healed in twice the normal healing time
Nonunion
Fracture that has not healed in three times the normal healing time (6 months)
Hypertrophic Nonunion
bone at fracture site form enormous amounts of bone with no healing (elephants foot)
Malunion
Fracture that is united with unacceptable angulation, rotation or shortening
Fracture Blisters
Occur in response to increased compartmental pressure
Caused by uneven extrinsic pressure
Jones Fracture
Proximal fracture through 5th metatarsal
Rarely heals due to poor blood supply
DVT and PE Increasing Risks
Locations of fracture Age of patient Body type Degree of Immobilization Compliance
Signs and Symptoms of DVT and PE
Calf and thigh pain Edema distal to obstruction Homans sign Shortless of breath Decreased PO2 Chest pain Tachycardia Hypotension
Fat Embolism
Fact without circulation
Produce embolic phenomena
With or without clinical sequelae
Fat Embolism Syndrome
Fat in circulation associated with identifiable clinical pattern of symptoms and signs
Risk high with femoral shaft fracture and concomitant head injury
Multiple trauma with major visceral injuries and blood loss
Hip/knee with intramedullary instrumentation
Mechanical FES
- Injury to adipose tissue
- Rupture of veins within zone of injury
- Mechanism that will cause passage of free fat into open end of vessels
- Disrupted venules in marrow remain tethered open by osseous attachments
Lehman Biochemical Theory
Plasma mediators mobilize fat from body stores into large droplets
Degradation of embolized fat into free fatty acids
FES Triad
Neurological abnormalities in 80% of FES pts
Hypoxemia
Petechia rash
ARDS
Release of sytokines secondary to inflammation causes increase permeability of alveoli and capillary membranes causing pulmonary edema
Compartment Syndrome
Circulation and function of tissue in fibro-osseous space is compromised secondary to increased pressure in the space
Increased pressure can result from bleeding, increase capillary permeability, decreased size of space (tight dressing)
Signs and Symptoms of Compartment Syndrome
Pain, palor, parethesias and pulselessness
Implants
Contractures Skin Coverage Loosening Infection Failure of implant
Post-Traumatic Arthritis
Chronic pain Deformity Loss of motion Crepitance RSD (complex regional pain syndrome)
Reflex Sympathetic Dystropy
RSD burning pain, increased skin sensitivity, changes in skin color/tecture/hair growth patterns, swelling and stiffness of affected joints, motor disability
Type I RSD
Triggered by tissue injury
Type II RSD
Triggered by nerve injury
What are the causes of CRPS
Catecholamines released from sympathetic nerves acquire the capactiy to activate pain pathways frollowing a nerve or tissue injury
Stages of CRPS
- Acute-burning, swelling, pain
- Dystrophic-thin shiny skin, loss of hair, contractures
- Atrophic-loss of motion, loss of subcutaneous fat, osteoporosis, pathological fractures
Avascular Necrosis
Disruption of blood supply to poorly vascularized bone leads to degeneration of the bone that is no longer vascularized
Sites: femoral head, carpal navicular, talus, humeral head, metacarpal head
Causes of AVN
Site, displacement, delay in immobilization, surgical approach, drug therapy, systemic disease, alcohol
PAthological Fractures
Bone breaks in area weakened by another disease process
Usually occurs with normal activity
Treatment must address underlying disease process
Bone Insufficiency Fractures
Fracture due to weakening of the bone from inadequate density (such as loss from osteoporosis)
Causes of pathological fractures
Weakness of bones (altered metabolism of calcium, vitamin D, parathyroid hormones)
Destruction of bone (infection, tumors, fibrous dysplasias)
Subcapital Fracture of Hip
Fracture of the femoral neck
This disrupts the blood supply to the head of the femur
Disruption of calcium metabolism can cause bone to weaken, or an infection can cause bone resorption
Stress Fracture
Fracture of bone that occurs secondary to repeated microtrauma Usually occur in weight bearing bones Seen in athletes See in atheletic wanabees Seen as an occupational disease Seen in military (march fracture)
Pars Fracture
Weightlifting can cause it
