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Clinically applied MSK - Roshiva > Trauma > Flashcards

Trauma Flashcards

1
Q

Why do bones heal? Why is it important?

A
  • Due to evolution, we are genetically predisposed to heal fractures
  • It’s important for bones to heal because we need bones for daily function
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2
Q

Do bones need external help to heal?

A

No

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3
Q

What is so special about tissue ‘bone’?

A
  • It is the only tissue that heals without scarring
  • Scarring can impede function
  • Other tissues are often repaired using different tissues (e.g fibrous)
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4
Q

What are the changes in a bone after a break histologically and macroscopically?

A
  • Histologically, there is no scar after a break because the bone is repaired using the bone tissue
  • Macroscopically, a callus may be seen as scarring
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5
Q

What is a callous? What kind of tissue is it? When does it form? Where do you not want a callus?

A
  • Bony and cartilaginous structure that forms a connecting bridge across a bone fracture during the repair.
  • Same tissue as bone. Forms during secondary healing, not primary (surgery)
  • You don’t want a callus at an articular surface as it would disrupt movement
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6
Q

What are the 3 major components of a long bone?

A
  • Epiphyses (found at proximal and distal ends of the bone, covered with articular cartilage to help with joint movement)
  • Diaphysis (shaft of bone)
  • Metaphysis (conical expansion from diaphysis to epiphysis)
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7
Q

What are epiphyses? Where are they found? What do they carry? What are they covered with and why?

What kind of bone do they contain and why?

What marrow does it contain and why?

A
  • Found at the proximal and distal ends od bone
  • They carry the joint surface so often have a complex shape
  • They are covered with articular cartilage to help with movement because articular cartilage is very smooth
  • They contain airy spongey (cancellous bone) which helps reduce the overall weight of the bone and provide flexibility
  • They contain red bone barrow which is essential for RBC turnover
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8
Q

What is cancellous bone (trabecular bone/spongy bone)?

A
  • Porous bone
  • Has many enclosed spaces to give it a honeycombed appearance
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9
Q

What is the diaphysis? What is it composed of? What cavities does it contain?

A
  • Shaft of the bone
  • Composed of compact cortical bone
  • Has medullary cavities that have yellow marrow which contain a lot of fat
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10
Q

What can a diaphyseal fracture lead to?

A

-It can lead to fatty emboli due to the fatty yellow marrow in the medullary cavities

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11
Q

What is compact/cortical bone?

A
  • Dense protective outer layer
  • Less porous than trabecular bone
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12
Q

What is the metaphysis?

A

-Conical expansion from diaphysis to epiphysis

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13
Q

What is physis? Why is it important? What is it in adults?

A
  • The growth plate
  • Separates epiphyses from the metaphysis
  • Allows longitudinal growth of bones in children
  • It forms the epiphyseal scar that can be seen on radiographs
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14
Q

What is the epiphyseal scar?

A

Fusion of growth plates

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15
Q

What are the 2 membranes of long bones?

A
  • Periosteum (outside of bone)
  • Endosteoum (thin vascular membrane that lines medullary cavity)
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16
Q

What is the periosteum? What layers does it consist of and why is it important? Why is it thicker in children

A
  • Outer-membrane of bone
  • Consists of the deep cellular layer which acts as a stem-cell reserve
  • Consists of the fibrous superficial layer which transmits nutrient arteries to the bone
  • Periosteum is thicker in children so they can heal fractures quicker than adults
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17
Q

What is the endosteum?

A

-Thin vascular membrane that lines the medullary cavity

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18
Q

What arteries does the superficial fifibrous layer of the periosteum transmit to the bone?

A

Nutrient arteries

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19
Q

What are the 2 types of bone?

What are the 2 forms of bone?

A

-Types: cortical and cancelleous

Forms: Woven and lamellar

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20
Q

What is the difference between woven and lamellar bone?

A
  • Woven bone (fibrous bone) = collagen fibres are randomly arranged. Immature form of bone when bone is formed rapidly e.g early stages of fracture, before bone remodelling. Mechanically weak
  • Lamella bone = collagen fibres are arranged in parallel. Woven bone is remodelled into lamella bone. Almost all bones of healthy adults are made of lamella bone.
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21
Q

What form of bone makes up most bones of healthy adults?

A

Lamella bone

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22
Q

Where is cortical bone found? What is it composed of? What is its structure? What types of cells are found here?

What is cortical bone covered by?

What do the medullary cavities of cortical bone contain?

A
  • Found on the outer portion of long bones and vertebrae
  • Composed of osteons (long parallel columns)
  • Osteons are made up of concentric rings of bone (lamellae) surrounding a central Harvesian canal
  • (Harvesian canal contains lymphatics and blood vessels)
  • Buried within lacunae (spaces) of bone are osteoctyes
  • Cortical bone is covered by periosteum
  • The medullary cavities contain yellow marrow (diaphysis mainly?)
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23
Q

What is spongey made up of? What are the spaces filled with?

A
  • Made up of trabeculae
  • Trabeculae connect with each other and to the endosteum
  • The spaces between trabeculae are filled with red marrow (hematopoietic tissue) or yellow marrow (adipose tissue)
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24
Q

What are the 3 types of bone cells?

A
  • Osteoblasts (produce osteoid- made from collagen and other proteins, unmineralised bone matrix). Bone forming cells
  • Osteocytes (terminally differentiated osteoblasts)
  • Osteoclasts (bone-reabsorbing cells)
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25
Q

What is the difference between osteon and osteoid?

A
  • Osteon= functional unit of cortical bone
  • Osteoid= unmineralised bone matrix, made up of collagen and other proteins
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26
Q

What cells do osteoblasts, osteocytes and osteoclasts differentiate from?

A
  • Osteoblasts (lie on surface of bone): mesenchymal stem cells
  • Osteocytes (buried within cortical and spongey bone, regulate remodelling, release FGF-23 for Pi excretion): mesenchymal stem cells
  • Osteoclasts (multinucleate cells found on surface of bone, modified macrophages, responsive to inflammatory mediators): Haematopoietic stem cells
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27
Q

What is osteoclast differentiation?

A
  • RANK-L binds RANK on osteoclasts, stimulating its differentiation
  • RANK-L is produced by osteoblasts and osteocytes in response to PTH and activated vit D
  • GM-CSF (cytokine secreted by T cells) is required for osteoclast activation
  • OPG is a decoy receptor produced by osteocytes, preventing activation of RANK
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28
Q

What is osteoblast differentiation?

A
  • Osteocytes activate the Wnt pathway of osteoblasts, promoting its differentiation
  • PGE2, NO, ATP activate Wnt pathway
  • Sclerostin and dickkpoff inhibit the pathway
  • Without sclerostin, sclerostosis occurs which can entrap cranial nerves causing neurological problems
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29
Q

What are the 8 mechanisms of injury (MOI)?

A
  1. Falls
  2. Twisting
  3. Blunt trauma
  4. Penetrating trauma
  5. Blast injuries
  6. Crush injuries
  7. Combination of injuries
  8. Pathological fractures
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30
Q

How can falls cause fractures?

A
  • Lead to transfer of energy into patient’s body
  • The higher the fall is from, the greater energy transfer
  • What part of the body the patient falls on determines the injuries
  • Can also cause compression of spinal cord
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31
Q

How can twisting cause fracture? What kind of fracture can it cause? What do we need to try and overcome?

A
  • Twisting transmits torsional forces through the patient
  • Can lead to spiral fractures
  • When treating this, we need to try and overcome the natural property of bone to try and twist back as this can displace the fracture?
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32
Q

How can blunt trauma cause fractures?

A
  • Can cause bone to bend
  • Resulting in transverse and wedge fractures
  • Size of patient has a large impact of a blunt force e.g baby vs hench man getting run over
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33
Q

How can penetrating trauma cause fractures? What kind of fracture? What should you look for?

A
  • Involves soft tissue more than bone
  • Certain penetrating injuries can cause comminuted fractures e.g gun shot wounds
  • Always look for several entry holes and exit wounds
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34
Q

How do blast injuries cause fractures?

A
  • Primary injury from the blast wave which damages hollow viscera where there is a pressure difference or air-fluid level
  • There is potential for secondary injury from projectiles (penetrating trauma)
  • Tertiary injury from falls
  • Quaternary injury from fire burns or building collapse (blunt trauma or crush injuries)
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35
Q

How do crush injuries cause fracture?

A
  • Usually involve a limb
  • Can be more severe if pelvis or thorax is involved
  • Continual load is applied and severely damage the soft tissue and bone
  • Soft tissue injuries continue for hours after initial insult
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36
Q

How do combination injuries cause fractures?

A
  • Combination of the injuries mentioned before
  • Often occurs in sports injuries
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37
Q

What are pathological fractures? What can cause them?

A
  • Normal force is applied to bone, causing it to break
  • Osteoporosis is associated with fragility of hip, spine and wrist fractures
  • Malignancies can also cause fractures by causing lytic lesions - can be primary or secondary (metastasis)
  • Osteomalacia, and Paget’s syndrome are also associated with fractures
  • Stress fractures count as pathological fractures (repetitive but normal-sized force causes a fracture as bone does not have time to release absorbed energy before the stress is reapplied.
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38
Q

What causes stress fractures?

A

Repetitive but normal-sized force is applied. Bone does not have enough time to release the absorbed energy before the stress is reapplied

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39
Q

What key points about MOI of fractures?

A
  • The type of force applied to bone determines the mode of failure and therefore fracture pattern
  • Traumatic fractures are where an abnormal load is applied to a normal bone
  • Pathological fractures are where a normal load is applied to an abnormal bone
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40
Q

How can fractures heal?

A

-Occurs via primary or secondary mechanisms

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41
Q

What is secondary fracture healing? What does it result in?

A

-Physiological healing, resulting in formation of callus

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42
Q

What is primary fracture healing?

A

-When the bone heals without callus formation due to surgical intervention

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43
Q

What is secondary healing? How long does it take to produce the section of remodelled bone? How many stages are there? What are the stages?

What two ossifications are involved?

A
  • Physiological healing with callus formation
  • Can take months to years
  • 4 stages
  • Stage 1: Haematoma formation (days 1-5)
  • Stage 2: Fibrocartilaginous (soft) callus formation (days 5-15)
  • Stage 3: Bony hard callus formation (days 11-28)
  • Stage 4: Bony remodelling (day 18 and years after insult)
  • Ossifications: Endochondral ossification and intramembranous ossification
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44
Q

What can cause delayed or failed healing?

A
  • Infection
  • Tumour
  • Disrupted vascular supply
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45
Q

What is a haematoma formation? (days 1-5) When does it occur? What has ruptured? What does this cause?

What are the first cells on the scene? Why? What happens next? What cells are attracted? What other cytokines are produced and why?

Is the initial acute inflammatory response short-lived or long-lasting?

A
  • Localised bleeding outside of blood vessels
  • Begins immediately after fracture is sustained
  • The nutrient vessels in the fibrous superficial layer of the periosteum are ruptured, forming a hematoma around the fracture site
  • Platelets are the first cells on the scene to cause clotting
  • Platelets, damaged bone and periosteum secrete pro-inflammatory cytokines such as TNF-A, BMP, IL1,6,11,23
  • These cytokines attract macrophages, monocytes and lymphocytes which begin to remove damaged tissue and secrete cytokines like VEGF to promote healing and angiogenesis
  • The initial acute inflammatory response short-lived
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46
Q

What are the pro-inflammatory mediators produced by platelets and damaged bone and periosteum?

What do the macrophages and monocytes produce?

A
  • TNF-a, BMP, IL-1,6,11,23 which attract macrophages, monocytes
  • VEGF for healing and angiogenesis
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47
Q

What are the steps in fibrocartilaginous callus formation? What happens within the hematoma?

What does the BMP do? What types of cells are produced and what do they do?

What does it result in?

What happens to the periosteum?

A
  • The release of VEGF promotes angiogenesis
  • Within haematoma, fibrin rich granulation begins to develop
  • The BMP recruit mesenchymal stem cells which differentiate to fibroblasts
  • Fibroblasts lay down a matrix to bridge the fracture
  • Later, the mesenchymal stem cells differentiate into chondroblasts and osteoblasts
  • The chondroblasts and osteoblasts lay down are cartilaginous matrix and osteoid at the fracture site
  • The result is a fibrocartilaginous network that spans the fracture site
  • At the same time, adjacent to the periosteum, a layer of woven bone is laid down by osteoprogenitor cells
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48
Q

What is bony callous formation (days 11-28)? What kind of ossification does the cartilaginous callus undergo?

What does the expression of RANK-L induce?

What does this lead to?

What happens superiosteally?

A
  • The cartilaginous callus undergoes endochondral ossification
  • RANK-L is expressed, stimulating further differentiation of chondroblasts, chrondroclasts, osteoblasts and osteoclasts
  • As a result, the cartilagenous callus is resorbed and calcifies
  • Subperiosteally, woven bone continues to be laid down
  • The newly formed blood vessels continue to proliferate, allowing further migration of mesenchymal stem cells into the area
  • At the end of this phase, a hard calcified callus of immature woven bone forms

-

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49
Q
A
50
Q

What is bone remodelling (day 18 onwards, lasting months-years)? What is ‘coupled remodelling’ and why does it occur? What is the centre of the callus replaced by? What is the callus edges replaced by? What else occurs alongside? What is the ultimate outcome?

A
  • With continued migration of osteoblasts and osteoclasts, the hard callus undergoes repeated modelling called ‘coupled remodelling’
  • Coupled remodelling is a balance of resorption by osteoclasts and bone formation by osteoblasts
  • The centre of the callus is ultimately replaced by compact bone, whilst the callus edges become replaced by remodelled lamellar bone
  • Substantial remodelling of the vasculature occurs alongside these changes
  • This process of bone remodelling lasts many months, ultimately resulting in regeneration of the normal bone structure
  • Important to note that transition from woven to lamellar bone is mechanically dependent
51
Q

What is mechanical stress detected by? What occurs as a result? How does the bone sense stress? How can you relate that to walking? What does the electric charge cause? Why do we need weight-bearing exercises? Why do astronauts get osteoporosis? What else does the electrical charge cause?

A
  • Mechanical stress is detected by osteocytes and osteoblasts
  • Resulting in bone remodelling
  • The bone senses stress due to the generation of an electric charge when hydroxyapatite crystals in the structure of the bone are compressed
  • So when we walk, the hydroxyapatite crystals give out an electric charge, which stimulates the osteoblasts to layout new bone
  • This means we need weight-bearing exercise to mineralise our bones
  • Astronauts get osteoporosis as they cannot lay bone as they don’t bear the weight
  • The electrical charge is given off by hydroxyapatite also stimulates the release of OPG via calcium-mediated mechanism (to inhibit osteoclast differentiation)
52
Q

What is endochondral ossification (part of bony callus formation)?

What happens to the cartilagenous callus?

When else is endochondrial ossification important?

What is the second type of ossification that occurs in fetus? In which bones?

A
  • Conversion of cartilage to bone
  • Occurs during the formation of bony callus, in which the newly formed collagen-rich cartilaginous callous gets replaced by immature bone
  • This process is also the key to the formation of long bones in the fetus, in which the bony skeleton replaces the hyaline cartilage model
  • A second type of ossification also occurs in the fetus = intramembranous ossification.
  • Intramembranous ossification = mesenchymal tissue is converted directly to the bone (no cartilage intermediate). This occurs in flat bones and skull
53
Q

What is intramembranous ossification? Which bones does it occur in?

A
  • Mesenchymal tissue is directly converted to bone without cartilaginous ossification
  • Occurs in the skull and flat bones
54
Q

What is primary healing? What kind of ossification does it involve? What does the clinician do?

A
  • Reestablishment of cortex without callus formation. Slower than secondary healing
  • Involves intramembranous ossification alone
  • The clinician moves the two ends of the fracture into close apposition, resulting in minimal formation of granulation tissue and callus
  • Cutting cones of osteoclasts cross the fracture site of the resorbed damaged bone, and ‘forming zones’ of osteoblasts lay down new bone
  • Suitable for simple fractures (jigsaw) and articular fractures

-

-

55
Q

What is the option of treatment for stable fractures?

A

Cast, brace or splint

56
Q

What is the treatment option for unstable fractures (usually intra-articular fractures)?

A
  • Open reduction and internal fixation (ORIF)
  • Requires surgical implants
  • Can use screws, wires and nails
57
Q

What are the 2 ways primary healing can occur?

What do they both attempt?

A
  • Contact healing or gap healing
  • Both methods try to attempt to re-establish an anatomically correct and biomechanical competent lamellar bone structure?
58
Q

What is contact healing?

A
59
Q

When can direct bone healing only occur (contact healing)? How is mechanical continuity re-established? What does the gap and interfragmentary strain have to be to allow contact healing? Where are cutting cones formed? What are the cavities later filled by? What does this result in?

A
  • When anatomic restoration of the fracture fragments is achieved and rigid fixation is provided resulting in a substantial decrease in interfragmentary strain
  • Bone on one side of the cortex must unite with the bone on the other side of the cortex to re-establish mechanical continuity
  • If the gap between the bone ends is less than 0.01mm and the interfragmentary strain is less than 2%, the fracture heals by contact healing
  • Under these conditions, cutting cones are formed at the ends of the osteons closest to the fracture site
  • The tips of the cutting cones consist of osteoclasts which cross the fracture line, generating longitudinal cavities at a rate or 50-100mm/day
  • These cavities are later filled by bone produced by osteoblasts residing at the rear end of the cutting cone
  • This results in simultaneous generation of a bony union and restoration of Harvesian systems formed in axial direction
  • This allows penetration of blood vessels carrying osteoblastic precursors
  • The bridging osteons later mature by direct remodelling into lamellar bone resulting in fracture healing without callus formation
60
Q

What is gap healing and how does it differ from contact healing?

A
  • In gap healing, bony union and Harvesion remodelling don’t occur simultaneously
  • It occurs if stable conditions and an anatomical reduction of the fracture are achieved
  • The gap must be less than 800mm to 1mm
  • In this process, the fracture site is filled with lamellar bone oreintated perpendicular to the long axis, requiring a secondary osteon reconstruction (unlike the process of contact healing)
  • The primary bone structure is then gradually replaced by longitudinal revascularised osteons carrying osteoprogenitor cells, which differentiate into osteoblasts and produce lamellar bone on each surface of gap
  • The lamellar bone laid down perpendicular to the long axis is mechanically weak
  • The initial process takes approx 3 and 8 weeks, after which a secondary remodelling resembling the contact healing cascade with cutting cones take place
  • Although not as extensive as endochondral remodeling, this phase is necessary to fully restore the anatomical and biomechanical properties of the bone
61
Q

What 2 factors affect fracture healing?

A
  1. Local factors: excessive movement, misalignment, infection, reduced blood supply can lead to delayed healing
  2. Systemic factors: advanced age, obesity, anaemia, diabetes (diabetes patients tend to have sequestered WBC responses), parathyroid disease, menopause, malnutrition, smoking (nicotine is a vasoconstrictor so limits blood supply to fracture; carboxyhaemoglobin limits oxygen delivery to fracture site)
62
Q

What local factors delay fracture healing or non-union?

A
  • Excessive movement, misalignment, extensive damage and soft tissues caught in fracture
  • Infection
  • Reduced blood supply
63
Q

What systemic factors can delay fracture healing (7 points)?

A
  • Advanced age
  • Obesity
  • Anaemia
  • Endocrine conditions like diabetes mellitus (sequesters WBC responses), parathyroid disease and menopause
  • Steroid administration
  • Malnutrition
  • Smoking (nicotine is a vasoconstrictor so limits blood supply to fracture) (carboxyhb limits oxygen delivery to fracture site)
64
Q

How does smoking slow fracture healing?

A
  • Nicotine is a vasoconstrictor so limits blood supply to the fracture
  • Carboxyhb limits oxygen delivery to the fracture site
65
Q

What is the MDT approach to healing (promote/stimulate bone healing)?

A
  • Dietary supplements e.g calcium, protein, vit C and vit D
  • Bone stimulators (can be electrical, electromagnetic, ultrasound)
  • Bone graft (involves the use of bone to help provide a scaffold to the newly forming bone). The graft can be from the patient’s body (autograft) or from a deceased donor (allograft)
66
Q

What is a bone graft? Where can it be from?

A
  • Involves the use of bone to help provide a scaffold to the newly forming bone.
  • This graft can be from the patient (autograft) or from a deceased donor (allograft)
67
Q

What is the importance of healing? What is a common defect?

A
  • To improve the quality of life
  • Tibial nonunion (permanent failure of healing of a broken bone unless surgery takes place) is one of the most common defects
68
Q

What is non-union?

A

Permanent failure of healing of a broken bone unless surgery takes place

69
Q

What do injuries result from? What is the energy transfer determined by? Explain this equation. What is the major determining factor in the energy transferred to the patient?

A
  • Transfer of energy from surrounding to patient
  • The energy transferred is determined by the equation:

KE= 1/2 x m x v^2

-Mass of patient is usually 75kg and doesn’t vary too much, meaning velocity is the major determining factor in the energy transferred to the patient

70
Q

How does energy impart on a limb cause damage? What happens initially? Then what happens? What happens when the limit is reached? Shockwave? What indirect soft tissue trauma can be caused?

A
  • Initially, energy is absorbed by soft tissue causing direct soft tissue trauma
  • Energy then passes through soft tissue and gets absorbed by bone
  • Bone stores up as much energy as it can but eventually a limit is reached
  • As limit is exceeded, the bone breaks and the stored energy is released as a shockwave into the surrounding soft tissue
  • This can cause indirect soft tissue trauma such as blistering and separation in fascial planes
  • It can determine the management plan
71
Q

What are low-energy fracture patterns?

A
  • Spiral
  • Oblique
  • Transverse
72
Q

What are medium energy fracture patterns?

A
  • Butterfly by torsion
  • By bending - one
  • By bending - several
73
Q

What are high energy fracture patterns?

A
  • Comminuted by torsion
  • Segmental fracture
  • Crush
74
Q

What is fracture personality?

A

-Soft tissue condition + fracture patterns

75
Q

What are injured during fracture? When are they vastly affected?

A
  • Bone
  • Skin
  • Subcutaneous fat
  • Fascia
  • Muscle
  • Periosteum
  • Tendon
  • Nerves
  • Vessels

These tissues are vastly affected in open fractures, making non-union more likely

76
Q

Why are skin and subcutaneous fat important in healing?

A

To prevent healing

77
Q

Why is fascia, tendon and muscle important in healing?

A

To provide stability

78
Q

Why is the periosteum important in healing?

A

-Supply of osteoprogenitor cells (in deep cellular layer of periosteum)

79
Q

Why are nerves important in fracture healing?

A

-Nerves tell us not to put weight on the affected limb

80
Q

Why are blood vessels important in healing?

A

-To bring clotting factors, WBCs, mesenchymal stem cells to site of injury

81
Q

What is the difference between open fractures and closed fractures?

A
  • Open fractures (compound fractures): bone pokes through the skin and can be seen
  • Closed fracture (simple fractures): The bone is broken but skin is intact
82
Q

Why are open fractures more likely to result in non-union? Skin? Haematoma?

A
  • The skin is broken, predisposing to infection
  • The hematoma is lost either on the road or as the wound is cleaned in the theatre - this slows healing as inflammatory mediators, WBC and mesenchymal stem cells are lost
83
Q

Can closed fractures cause soft tissue damage? What are the common areas? What causes the blistering? Does it affect healing?

A
  • Yes
  • The common areas are the tibia, tibia pilon, medial malleolus, dorsum of the foot
  • Energy within these regions can shear the skin and the little subcutaneous tissue that overlies the bone straight off
  • This results in blistering
  • The damage to soft tissue also affects healing
84
Q

What does the management of closed fracture depend on? What if they’re in a bad state? What if they’re in a good state?

A
  • Integrity of soft tissue in that region
  • If they’re in a bad state, we don’t surgically intervene as this will make it worse
  • If the tissues are okay, we intervene surgically
85
Q

What happens if you can’t reduce and fix the fracture with ORIF (open reduction and surgical fixation)?

A
  • Use temporary external fixator
  • This aligns fragments and puts the limb under traction
  • It only has small screw holes which are far from the fracture site, minimising tissue damage in that area
  • This allows soft tissue healing before we open up and permanently fix the fracture
  • Allows time to do assessments on patient
86
Q

What is ORIF used for?

A

-To fix severely broken bones

87
Q

What are the 4 priorities to follow in the management of traumatic injuries?

A
  1. Patient survival e.g resuscitation, fluids, control haemorrhage, ensure patient is stable
  2. Limb survival e.g assess vascularity distal to injury, assess for compartment syndrome, carry out fasciectomy if necessary, depress all muscular compartments
  3. Functional survival e.g transfer the patient to major trauma centre if necessary, assess neurological function
  4. Prevent infection e.g if patient has open fracture, clean the wound, antibiotics, dress the wound to stop bacteria getting in
88
Q

What is patient survival?

A
  • Resuscitation
  • Fluids
  • Ensure the patient is stable
  • Control haemorrhage
89
Q

What is limb survival?

A
  • Assess vascularity distal to the injury
  • Assess for compartment syndrome and carry out fasciectomy (removal of fascia surgically to relieve tension or pressure) if necessary
  • If there are any signs of compartment syndrome, decompress all muscular compartments
90
Q

What is functional survival?

A
  • Transfer patient to major trauma centre
  • Assess neurological function
91
Q

What is preventing infection?

A
  • Clean the wound if open fracture
  • Give antibiotics
  • Dress wound to stop entry of bacteria
92
Q

What is the overall initial management of fractures?

A
  • Control haemorrhage
  • Assess distal perfusion
  • Realign limb
  • Reduce dislocations
  • Assess nerve damage
  • Compartment pressure
93
Q

Why do we need to take patient history?

A
  • To find mechanism of injury
  • Ask about co-morbidities
94
Q

Why do we examine the patient?

A
  • To assess for any neurovascular compromise
  • Look at state of tissues and skin
95
Q

What imaging do we need to order?

A
  • X-rays of limb and joints above and below: 2 views (AP and lateral)
  • Request CT in all major trauma cases
96
Q

What are the 6 A’s we need to go through if it is an open fracture?

A
  • Antiseptic dressing
  • Antibiotics
  • Analgesia
  • Anti-tetanus
  • A photograph (so you don’t have to take off dressing every time a new doctor comes in)
  • An operation
97
Q

What is compartment syndrome? Blood can do what but not what? Venous return? What procedure is essential and why?

A
  • Raised pressure in a closed fascial compartment that exceeds capillary and venous pressure. It occurs due to trauma but also can result from any haematoma or oedema
  • The result is a complete mess within the compartment
  • Blood can flow in but can’t perfuse the tissue as the capillary pressure is exceeded
  • At the same time, pressure in the compartment continues to build as the venous return is impeded
  • A fasciotomy is essential as irreversible tissue necrosis and death will occur within 6 hours unless decompression is done
98
Q

What are the physical findings of compartment syndrome? What is the most sensitive finding

A
  • Patients are not very sensitive
  • Can be seen with good pulses and no pallor; loss of pulses rarely occurs unless artery is damaged
  • Pain out of proportion and pain with passive stretch of muscle in the compartment in question may be the most sensitive finding
  • These findings are only useful is patient is conscious
99
Q

Why should a patient with suspected compartment syndrome not be treated with regional anaesthesia, continuous epidural and PCA intravenous opiate analgesia?

A

They may mask the symptoms compartment syndrome

100
Q

What are the late signs of compartment syndrome?

A
  • Numbness
  • Tingling
  • Paralysis
  • Pallor/pulselessness
101
Q

What are the 3 major principles in the management of fractures?

A
  • Reduce
  • Hold
  • Rehabilitate
102
Q

What is ‘reduce’ in fracture management?

A
  • Determine whether fracture is open or closed
  • Determine if anaesthesia is required
  • Determine if incision is required
103
Q

What is ‘hold’ in fracture management?

A
  • Determine if it is operative or non-operative
  • If it’s non-operative: do nothing. splint, or plaster
  • If it’s operative: external fixator, internal plating, intramedullary nail, arthroplasty
104
Q

Why does internal fixation carry a higher risk?

A

Plates are associated with more infections than nails

105
Q

What is the difference between internal and external fixation?

A
  • Internal fixation = Long flexible nails placed inside the fractured bone. They hold the fracture in place as it heals
  • External fixation = Consists of pins inside the bone and a bar that sits outside the body. This holds the fractured bone together as it heals
106
Q

What is a temporary external fixation?

A
  • allows assessment to be completed on imaging. Soft tissue resusitation
107
Q
A
108
Q

What is definitive fixation? (diaphyseal fractures and articular fractures)

A
  • Diaphyseal fractures are fine to heal with callus
  • Articular fractures can’t have a callus as it will affect joint function hence we need them to heal via primary healing
109
Q

What does ‘rehabilitate’ mean in the management of fractures? How long does it take for fractures to heal? What happens to muscles and joints? What are essential?

A
  • Restore function
  • Fractures take weeks-months to heal
  • Muscles atrophy and joints get stiff in that time
  • Physiotherapy and exercise are essential
  • Early weight-bearing facilitates better rehabilitation
110
Q

What is soft tissue respecting operations (MIPO)?

A
  • Preserve fracture biology
  • Preserve blood loss
  • Lead to better healing
111
Q

What does MIPO stand for?

A

Minimally invasive plate osteosynthesis

112
Q

How does MIPO work?

A
  • Percutaneous plating involves the application of a bone plate without using an extensive surgical approach
  • The bone segments are reduced using indirect reduction techniques
  • Small plate insertion incisions are made at each end of the fractured bone and an epi-periosteal tunnel is made connecting these incisions
  • The plate is inserted through one of the insertion incisions and tunnelled along the periosteal surface of the bone, spanning the fracture site
  • Screws are applied at proximal and distal ends of the plate, which is often positioned over the fracture
113
Q

What are the advantages of MIPO?

A
  • Reduced operative time
  • Minimally invasive do reduced infection risk
  • Fracture hematoma isn’t removed during surgery and may contribute to increased rate callus formation
114
Q

What are the disadvantages of MIPO?

A
  • Technique challenging to learn
  • May not be suitable for simple fractures and articular fractures
  • Does not allow direct visualisation of the fracture site, hence radiography would facilitate this process
115
Q

What is external fixation?

A
  • Involves placing pins through the skin which are held in place by an external scaffold
  • Serves as temporary option before internal fixation
  • Primary healing
116
Q

What is internal fixation?

A
  • Use of surgical implants to hold the two ends of the fracture closely opposed.
  • Involves screws, wires and intramedullary nails
  • Primary healing
117
Q

What steps does primary healing skip?

A
  • Bleeding
  • Soft callus formation
  • Hard callous formation
118
Q

What is a fixed fracture?

A

You move the bones so close together that you don’t need callus

119
Q

Why is epiphysis required for jumping?

A
  • Trabeculae bone so light
  • Flexible
120
Q

What bone do you need in the diaphysis and why?

A

-Cortical bone for weight bearing e.g for walking

Clinically applied MSK - Roshiva (8 decks)

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