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BSAVA MSK > Ch 10 Fractures > Flashcards

Ch 10 Fractures Flashcards

1
Q

What are some situations where CT would be necessary (rather than just orthogonal radiographs) to define fractures or fracture healing?

A
  1. To confirm non-union; rads can be inconclusive.
  2. A fissue extending to a joint surface is suspected.
  3. Incomplete fracture (fissure) of the humeral condyle
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2
Q

What is the clinical use of scintigraphy in fractures?

A
  1. Stress fractures in athletic animals. An increase in uptake of radioisotope could be seen before radiological evidence of a stress fracture.
  2. In cases of pathological/neoplastic fractures - to look for bone mets.
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3
Q

In Salter Harris type 1 fractures, the fracture line travels through ___________. This is common at the _______ (which location of which bone).

A

physis
proximal femoral physis

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4
Q

In Salter Harris type 2 fractures, the fracture line travels through ___________. This is common at the _______ (which location of which bone).

A

physis and metaphysis
proximal tibial physis

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5
Q

In Salter Harris type 3 fractures, the fracture line travels through ___________. This is most often seen at the _______ (which location of which bone).

A

physis and epiphysis
medial humeral condyle

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6
Q

In Salter Harris type 5 fractures, the fracture involves the ___________. This is most often seen at the _______ (which location of which bone).

A

all or part of the physis, as an impaction (crushing) fraction
distal ulnar physis

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6
Q

In Salter Harris type 4 fractures, the fracture line travels through ___________. This is most often seen at the _______ (which location of which bone).

A

metaphysis, physis and epiphysis
distal humerus / lateral humeral condyle

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7
Q

In people, SHI and SHII in theory have a better prognosis than SHIII and SH IV.
Why is that?
Is it the same in dogs?

A

SHI and SHII only affect the hypertrophic layer. This is the weakest zone, and it also does not affect the future of physeal growth as much.

In dogs, it’s not quite like that according to a 1994 paper (Johnson et al). This study found that (in 10/13 dogs) SH1 and SH2 fractures (as diagnosed by radiographs) also disrupted the proliferative layer (not just the hypertrophic layer), as seen on histology. Damage to the proliferative layer carries a worse prognosis for long bone growth.

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8
Q

What is a SH type 6 fracture?

A

It is a disturbance in the physis caused by periosteal bridging, secondary to a fracture not at the physis e.g. in the metaphysis.
Pretty rare in dogs and cats

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9
Q

what type of SH is this?

A

type IV

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10
Q

What affects the prognosis of SH fractures in dogs?

A

The age of the dog (the earlier the insult, the greater risk of disruption) - especially earlier than 6 months, this is considered to potentially have more serious consequences.

The physis location - some physes contribute more to bone length than others e.g. distal ulna (>85%) and proximal humeral (80%) physes contribute significantly more than their other respective physes.

Also the amount of trauma and the type of SH (e.g. type III, IV and potentially V affect the germinal layer, also any fracture that affect the proliferative layer - something you cannot see on radiographs for types I and II).

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11
Q

what type of SH is this?

A

type I

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12
Q

what type of SH is this?

A

type III

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13
Q

what type of SH is this?

A

type II

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14
Q

what type of SH is this?

A

type V

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15
Q

what type of SH is this?

A

type VI

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16
Q
A

gas within soft tissues, indicating an open fracture

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17
Q

What is a comminuted fracture and how does it differ from a segmental fracture?

A

A comminuted fracture has several (more than 2) segments.
In a comminuted fracture, the fracture lines communicate.
In a segmental fracture, the fracture lines do not communicate.

Image:
Left - comminuted
Right - Segmental

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18
Q

what kind of fracture is this?

A

comminuted, reconstructable

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19
Q

what kind of fracture is this?

A

spiral fracture (15w puppy)

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20
Q

6 month old labrador. what kind of fracture(s)?

A

ulnar diaphysis - complete oblique
distal radial metaphysis - incomplete/greenstick

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21
Q

6mo greyhound. what kind of fracture is this?

A

avulsion fracture of the tibial tuberosity

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22
Q

what is an avulsion fracture?

A

when a bone fragment is distracted/displaced by the pull of a tendon/ligament.
Most common example: tibial tuberosity.

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23
Q

what is a compression fracture? how does it differ from an impacted fracture?

A

Compression fracture - usually refers to vertebral fractures following a compressive force that results in a shorter, wider vertebra. The bone basically crushes under pressure.

Impacted fracture - usually refers to long bones, the fracture ends are driven into one another (see image). In this scenario, the bone is fractured at a certain location and then pushed together.

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24
Q

6 month great dane. what kind of fracture is this?

A

impacted fracture

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25
Q

What is a depression fracture?

A

It usually refers to skull fractures where a piece of bone is pushed in, resulting in a concave deformity.

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26
Q

What are the 3 most common causes of a pathological fracture?

A
  • Nutritional hyperparathyroidism (low Ca intake, hypocalcemia)
  • Renal hyperparathyroidism (cannot excrete Ph > hyperphosphatemia, which leads to hypocalcemia)
  • Neoplasia (primary osteosarcoma or metastatic carcinoma)
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27
Q

What kind of fracture is typical of a pathological fracture?

A

Simple, or folding. This is because the bone is weak and a minimal force is required to fracture it.

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28
Q

Which stress fracture is reported (1988) in racing greyhounds?

A

non-displaced acetabular fractures

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29
Q

What is stress remodelling ?

A

When you remodel your house because you’re stressed.

Kidding - it’s the remodelling of bone following chronic / repeated microfractures of cortical bone.
This is seen in:
* racing greyhounds in the metacarpals/tarsals,
* IOHC (at the lateral humeral epicondylar crest)

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30
Q

6 week GSD

A

simple folding fracture, due to nutritional 2’ hyperPTH.
Note the thin cortices.

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31
Q

6y Dobermann

A

pathological fracture (neoplasia).
Note the pre-existing periosteal reaction (i.e. if fracture occurred within the last couple of days, there would be no periosteal reaction yet in a healthy bone).

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32
Q

racing Greyhound

A

stress fracture metacarpal V
Note periosteal reaction already present at the time of fracture

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33
Q

What are the 4 A’s of post-operative assessment of fracture repair?

A

Apposition
Alignment
Apparatus
Activity

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34
Q

What percentage of apposition is considered adequate for external coaptation or fixation?

A

50%

35
Q

what is a monteggia fracture?

A

proximal 1/3 ulnar fracture with an associated radial head dislocation

36
Q

what kind of fracture is this?

A

Monteggia fracture

37
Q

what’s wrong with this fracture repair?

A

The bone screw and the K wire in the femoral neck are in the coxofemoral joint.

38
Q

In a transverse or short-oblique fracture, at which location will a cortical defect cause focal stress on the plate (and may consequently lead to implant failure)?

A

at the trans-cortex, the cortex opposite the plate

39
Q

Why did this result in implant failure?

A

This is fatigue failure, there was a defect in the transcortex i.e. the fracture was not apposed or compressed (so there is no primary bone healing), and therefore the plate is acting as a bridging plate for which it is not strong enough.

40
Q

What does correct alignment of a fracture repair imply?

A

That the bone retains a normal length, and that the relevant joints are correctly positioned in terms of rotation and angulation. This would be more relevant in cases of non-reconstructable, comminuted fractures with bridging fixation.

41
Q

In which cases is an implant in or close to a joint acceptable?

A

*when there is no other option for repair, this may be acceptable, although necessary to also remove the implants after healing
* it the implant is not in a weight-bearing part of the joint surface (in these cases, there will be no impact on joint manipulation)

42
Q

How thick should an IM pin be?

A
  • in combo with cerclage or ex-fix = 66% diameter of medullary cavity at its narrowest
  • in combo with plate = 40%
43
Q

What is the maximum screw thickness in a plate/screw or ex-fix/pin system?

A

1/3 the diameter of the bone

44
Q

How many cortices should be engaged to compress a transverse fracture?

A

4 on each side of the fracture (proximal/distal) if used with a bone plate

6 if with an ex-fix pin + lag screw/cerclage

45
Q

How many cortices should be engaged to bridge a fracture?

A

8 cortices on each side

46
Q

what’s wrong with this repair?

A
  • the cerclage wires do not compress/reconstruct/reduce, so there is little resistane to axial, rotational and bending forces
  • the IM pin is too long and enters the stifle joint
47
Q

why might a ‘short’ bone screw be OK in the metaphysis? i.e. one that barely enters the transcortex.

A

The metaphysis has thin cortices, but a solid amount of cancellous bone. Therefore, a screw will be able to gain more purchase in the cancellous bone than in the thin cortex and still be stable.

48
Q

Describe these stages of fracture healing. What kind of fracture healing is it? What are the lines indicating?

A

Classical fracture healing.
1. Fracture
2. Hematoma
3. Woven bone / bridging callous, with hyaline cartilage at the fracture site
4. Full mineralisation (woven bone)
5. Compaction and remodelling (lamellar bone)
6. Recontoured lamellar bone

49
Q

By when should a fracture healing by classical healing, have a bridging callus (not a full union)?

A

2 weeks, although this is only faintly visible on radiographs

50
Q

In a stable fracture with adequate blood supply (i.e. ideal conditions), by when should there be a bony callus (‘clinical union’)?

A

6 weeks

51
Q

The size of the callus depends on which 2 things?

A

The stability - the less stable, the more callus (because the tension will be spread over more tissue and therefore more better tolerated by any single point)

The age of the patient - younger patients have a more active periosteum, and will produce a more dramatic callus than an adult, even with the same level of fracture stability.

52
Q

Why does a progressively smaller callus mean in terms of the type of bone comprising the callus?

A

It means that the woven bone is being converted to compact bone, which is the normal structure (and therefore the normal strength) of bone. The callus doesn’t require extra, weaker (woven bone) tissue anymore because the compact bone is strong enough.

Wolff’s law - bone adapts to the load it bears.

53
Q

What is fracture healing without a callus called?

A

primary healing
This requires perfect apposition and firm compression. This would eliminate movement at the fracture line, and there would be no stimulus for callus formation.
In reality though, there will always be some sort of callus, at minimum due to the periosteal or endosteal injury, particularly in immature animals that have a very active periosteum.

53
Q

What kind of healing is expected in a stable fracture repair with a small <1mm gap?

A

gap healing; the gap is filled quickly with lamellar bone and then remodelled (at a pace that is physiological for that patient’s skeletal system) to normal bone. Until it is normal, it remains a weak spot.

54
Q

What is bridging osteosynthesis?

A

It’s a method where the proximal and distal segments of a fractured bone are stabilised (in good alignment relative to one another), but the fragments are not apposed, so as to leave the fracture site as undisturbed as possible. This is because the fracture hematoma has beneficial mediators, and also an uncompromised vascular supply will greatly benefit the healing process.

Overall, the aim is to get the rapid return of bone strength (like in classical healing) while allowing limb function during healing (like in primary healing) .

55
Q

Which type of bone (think tissue) heals more quickly? Why?

A

Cancellous (epiphysis, metaphysis) - it has a more abundant blood supply and inherent cellular activity.

This is compared to cortical bone i.e. diaphysis.

56
Q

Which metabolic conditions will delay fracture healing?

A

Cushing’s
CKD
hyperparathyroidism (renal or nutritional)

57
Q

When will classical healing occur in an animal <3 months?

A

2-3 weeks

58
Q

In what time period after a fracture will the ‘die back’ phenomenon occur?
What else occurs at this stage?

A

7-10 days; this is when the fragment edges become less distinct due to demineralisation, partially from loss of vascularity.
At this stage there is also:
* early periosteal reaction
* resolution of soft tissue swelling (mostly)

59
Q

In what type of fracture healing does die-back phenomenon occur?

A

Classical healing or bridging isteosynthesis

60
Q

What is periosteal stripping? Who is more likely to get this? Which bone is a more common location of this?

A

This is a type of injury to the periosteum, where it is lifted off the bone. It occurs more commonly in immature patients, and in femoral fractures, and results in calluses extending far more proximally/distally than the fracture site.

61
Q

Where is disuse osteopenia most apparent?

A

In the cancellous bone, and in the distal limb

62
Q

When is disuse osteopenia commonly noticed, with external coaptation approaches?

A

2-4 weeks

63
Q

The presence of gas opacities at the fracture/surgical site, beyond XX number of days after internal fixation of a fracture, would raise suspicion of an infection?

A

7-10 days

64
Q

What would be the best way to evaluate whether there is delayed union and non-union?

A

Scintigraphy would help determine whether there is activity at the fracture site.

65
Q

What are the 4 features of delayed union?

A
  1. Persistent fracture line, WITH evidence of healing (new bone formation)
  2. Still OPEN medullary cavity
  3. Uneven fracture surfaces (still bone activity going on)
  4. NO sclerosis of fracture ends yet
66
Q

What are 4-5 features of NON-union?

A
  1. GAP between fracture ends
  2. CLOSED medullary cavity (unless there is an IM pin, then it will be open)
  3. Smooth fracture ENDS
  4. SCLEROSIS of the fracture ends
    +/- 5. ± Hypertrophy or atrophy of bone ends

Look at the ends - smooth? sclerotic? gap? hyper/atrophic?
If there is no IM pin, look at the medulla - already closed?

67
Q

If there is sclerosis of the fracture ends - is it likely to be delayed or non-union?

A

Non-union, if the fracture ends are already sclerotic

68
Q

If the medullary cavity is open and the fracture ends are uneven, is it likely to be delayed or non-union?

A

Delayed, if the medullary cavity is still open, and the ends are still uneven

69
Q

What are the types of non-union?

A

Biologically active (viable): Hypertrophic, slightly hypertrophic, oligotrophic
&
Biological inactive (non-viable): dystrophic, necrotic, defect, atrophic

70
Q

What are the types of viable non-unions?

A
  • Hypertrophic (e.g. transverse fracture treated with an IM pin) - huge callous
  • Slightly hypertrophic - similar causes, rotational or angular instability e.g. transverse fractures treated with splint or IM pin - medium callous
  • Oligotrophic (avulsion treated conservatively, toy breeds fractures with rotational instability, systemic disease e.g. Cushing’s)
71
Q

What are the types of non-viable non-unions?

A
  • Dystrophic - an intermediate fragment of bone only heals to one segment, leaving a devitalised bone piece that does not participate in healing
  • Necrotic - comminuted + too much surgical manipulation = necrotic bone fragments interfere with healing
  • Defect - caused by too large a defect in the bone (either through the trauma, or surgical removal), and this exceeds the bone’s natural ability to unite.
  • Atrophic - in distal radius/ulna fracture of toy breeds, the the distal ulna may atrophy, but this is clinically insignificant. NB these breeds also get the viable (slightly hypertrophic and oligotrophic) non-unions, so don’t jump to conclusions that it is non-viable.
72
Q

What is the difference in prognosis between viable and non-viable non-unions?

A

There is none - none-viable non-unions can have a good prognosis with surgical treatment.
EXCEPT atrophic non-union, which has poor outcomes despite treatment attempts.
The terms relate more to the cellular activity rather than the radiographic appearance or biological outcome.

73
Q

what is it called when bones heal in a non-anatomical orientation?

A

Malunion

74
Q

Every malunion is clinically significant to some degree - true or false?

A

False;

75
Q

Which is functional and which is non-functional malunion? (or are they both non/func)

A

left: functional
right: non-functional due to lameness associated with the valgus

76
Q

What types of implant failure are there?

A

Fatigue failure - e.g. the plate bends or breaks

Loosening (loss of purchase) - * implant migration
* bone resoprtion due to e.g. insufficient screws
*bone necrosis from e.g. osteomyelitis or excessive heat during implantation

Bone resorption or necrosis will be seen as peri-implant lucency

77
Q

what is the radiographic appearance of bone necrosis or bone resorption during implant failure (loosening)?

A

Lucency around the implants e.g. screws

78
Q

4 features of osteomyelitis? (SPLSS)

A

Soft tissue swelling (in acute osteomyelitis)
Periosteal reaction
Lysis (around implants)
Sclerosis of adjacent bone
Sequestrum/involucrum formation - it acts as a nidus

78
Q

Which US finding can be observed in early osteomyelitis, before radiographic changes appear?

A

Anechoic subperiosteal fluid

79
Q
A

Ring sequestrum, seen in specific situations:
* after placement of ex-fix pins (with poor technique, causing excessive heat, which kills of the adjacent bone), infection/necrosis can track down the pin, and a ring forms.
* like in the image, a bone tunnel was created (for placement of sutures), and similarly caused necrosis of surrounding bone. This dead bone formed a ring sequestrum.

80
Q

What’s the average lag time for fracture associated tumours?

A

5 years (makes you wonder whether associated at all)

80
Q

How do fracture-associated tumours differ from primary bone tumours?

A
  1. They tend to affect the diaphysis (rather than metaphysis)
  2. They have a different incidence of location e.g. primary is more common in radius, fracture-ass. in the femur
81
Q

What is the most common location for fracture-associated tumours?

A

Femoral diaphysis (49%)

then humerus

BSAVA MSK (9 decks)

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