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Movement > Hip Fractures > Flashcards

Hip Fractures Flashcards

1
Q

how are hip fractures classified

A

where they are in relation to the capsule

the level of displacement and therefore instability within the joint (often Garden’s classification)

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2
Q

which surgical options are available for fractured hip

A

DHS - extracapsular as lower risk AVN
cannulated screw - extracapsular/low risk AVN gives additional rotational stability
hemiarthroplasty - intracapsular hip fractures
THR
girdlestone - following infection/chronic dislocation

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3
Q

how is osteoporosis measured

A

T score < - 2.5 on DEXA for postmenopausal women and men > 50

T score is BMD compared to healthy young adult of same sex

-1 to -2.5 = osteopenia

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4
Q

which tool can be used to predict risk of future fracture in primary care

A

the FRAX tool gives 10 year probability of a hip fracture and also spine, shoulder or forearm
based on: age, sex, previous injuries

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5
Q

which pharmacological treatments are available for osteoporosis

A 
calcium/vit D3 supplements
bisphosphonates (1st/2nd line)
strontium ranelate (3rd line)
SERMs
PTH
HRT
Testosterone
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6
Q

what are the causes of osteoporosis

A 
post menopause
hyperparathyroidism
malabsorption
osteomalacia
multiple myloma
hypopituitarism
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7
Q

which drugs can predispose towards osteoporosis

A 
corticosteroids
anticonvulsants
heparin
thyroxine
extreme alcohol excess
lithium
chemo
methotrexate
SSRIs
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8
Q

what clinical features might osteoporosis present with

A

low impact fracture
reduced height (vertebral fracture)
kyphosis

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9
Q

how do steroids affect bone mineral density

A

decreased absorption of calcium from the gut
decrease muscle mass
increase osteoclast activity

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10
Q

which lifestyle changes can be made to avoid osteoporosis

A

sufficient daily calcium intake
smoking cessation
reduce alcohol intake
increased weight bearing exercise

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11
Q

which race appears to be less susceptible to osteoporosis

A

Afro-caribbean are less susceptible than white or asian women

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12
Q

which bisphosphonate is recommended for first line prevention of osteoporotic fractures

A

alendronic acid

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13
Q

how do bisphosphonates work?

A

become absorbed onto hydroyapatite crystals in bone.
This slows their rate of growth and dissolution and therefore bone turnover
also used in the treatment of Paget’s disease

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14
Q

why must patients on bisphosponates have regular dental check ups

A

they are at risk of osteonecrosis of the jaw especially if receiving IV bisphosphanates

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15
Q

what are 3 problems with bisphosphonates

A

difficult to take - must be taken on an empty stomach at least 30 mins before food and must be upright after taking

osteonecrosis of the jaw

can induce stress fractures - especially if used for more than 5 years

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16
Q

what is denosumab

A

RANKL inhibitor: human monoclonal antibody which inhibits osteoclast formation, function and survival therefore decreasing bone resorption
also boosts OB activity
subcutaneous injections every 6/12

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17
Q

what are the 2nd line treatments for osteoporosis

A

IV bisphosphonates

denosumab

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18
Q

how are IV bisphosphonates administered

A

fewer tolerance issues
given once yearly for 3 years

may be restarted 3 further years later

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19
Q

why must bisphosphonates be taken on an empty stomach

A

poorly absorbed from the gut as bind to calcium in food

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20
Q

what are the 4 stages of management for fractured neck of femur

A

1) why has the person fallen
2) is the person medically well/fit for surgery
3) why has the bone broken - bone health
4) rehab

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21
Q

what are the 4 groups of fallers

A

1) medical (heart problems etc)
2) dementia/cognitive impariments
3) Mechanical
4) postural drop

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22
Q

what is the most common cause of fall

A

mechanical (50-60%)

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23
Q

what is the 2nd most common cause of fall

A

postural drop

can be delayed by upto 5-10mins after standing

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24
Q

what are the stages of managment for postural drop

A

1) drugs review
2) hydrate adequately
3) FULL leg stockings
4) fludrocortisone to inc fluid retention
5) alpha agonist midorone - vasoconstrictor, can induce supine HTN

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25
Q

what is the 1 yr mortality from falling and being on the floor for more than 1 hour

A

50%

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26
Q

what is the Hayflick limit

A

the finite number of times a cell can divide - dictated by telomeres

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27
Q

define frailty

A

Frailty is a global accumulation of physical,
cognitive, medical and functional deficits
leading to a reduction in the individual’s ability
to respond to an insult

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28
Q

which areas of the body are commonly affected by fragility fractures

A 
hip
spine
wrist
ribs
humerus
pelvis
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29
Q

what is the mortality of hip fracture

A

20%

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30
Q

what are the risk factors for osteoporosis

A 
age
female
genetics
oestrogen deficiency 
hypogonadism
smoking
low/very high BMI
inactivity
ethnicity (caucasians)
eating disorders
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31
Q

what is a Z score

A

standard deviations of BMD from age AND gender matched mean

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32
Q

which osteoporosis drugs increase bone formations

A

teriparatide (PTH)

strontium ranelate

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33
Q

which osteoporosis drugs decrease resoprtion

A 
bisphosphonates
RANKL inhibitors (denosumab)
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34
Q

how does rPTH work

A

normally PTH causes bone loss, but given in pulses increases bone production and BMD
given as a daily sc injections for 2 years

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35
Q

what are the causes of vitamin D deficiency

A 
inadequate sunlight
inadequate diet
malabsorption
medication
low levels in breastmilk
multiparosity
abnormal vit D metab
36
Q

what is the presentation of osteomalacia

A

bone pain/tenderness
proximal muscle weakness
back pain
stress fractures

37
Q

what would you see on bloods to confirm vitamin D deficiency

A 
LOW 25(OH)vitD
HIGH serum PTH
LOW/NORMAL serum Ca
LOW serum phosphate
HIGH alkaline phosphatase (osteoclast activity)
38
Q

what is Paget’s disease

A

disordered bone metabolism
–> osteoclast overactivity followed by compensatory osteoblast activity

leads to the formation of WOVEN bone –> weaker

39
Q

what are the signs and symptoms of Pagets disease

A

bone pain, path fracture, (sarcomatous change) –> direct

indirect:

  • high CO
  • compression:
  • –> skull (cranial nerve palsies, deafness, basilar invaginations)
  • –> spine (sciatica, cauda equina)
40
Q

how is pagets diagnosed

A

X ray
bloods (high alk phos w/ normal Ca vD PTH and phosphate)
urinary hydroxyproline increased
isotope bonescan

41
Q

when would you treat pagets

A

if symptomatic
in danger of nerve compression
around a weight bearing joint

42
Q

how would you treat pagets

A

bisphosphonates

43
Q

define a fracture

A

a loss of continuity of the substance of a bone due to physical force

44
Q

what type of fractures happen in long bones

A 
transverse - banding force
spiral - torsion
oblique
comminuted - high energy
segmental
45
Q

what type of fractures happen in cancellous bones

A

impacted

crush/compression

46
Q

what type of fractures happen in periarticular bone

A

avulsion

47
Q

what two features promote fracture healing

A

intact fracture haematoma

controlled microenvironment

48
Q

what are the 4 stages of fracture healing

A

1) inflammation
2) soft callus
3) hard callus
4) remodelling

49
Q

what happens in the first stage of fracture healing

A

inflammation and development of haematoma:

  • fibrin clot
  • polymorphs
  • platelets
  • monocytes

later:

  • fibroblasts
  • osteoprogenitor cells
  • vascular ingrowth
50
Q

what happens in the second stage of fracure healing

A

after pain and swelling subside
bone fragments united by fibrous or cartilaginous tissue

bony ends no longer freely moveable but angulation still possible

51
Q

what happens in the third stage of fracture healing

A

mineralisation of cartilage
OBs convert cartilaginous tissue to woven bone
ENDOCHONDRAL and membranous bone formation

this increases fracture stiffness and produces an external callus

52
Q

what happens in the final stage of fracture healing

A

woven bone converted to lamellar bone
excess callus is removed
medullary canal is reconstituted

53
Q

which implants for fractures provide absolute stability

A

internal fixation

54
Q

what is the aim of reduction

A

to reduce deformity

55
Q

what is important about the rate of bone healing and implants

A

fracture must heal before implant fails

56
Q

what is the rule of 2’s

A 
x ray of fractured joint:
2 views - at right angles
2 joints
2 occasions
2 limbs
57
Q

what are the three R’s of fracture treatment

A

reduction
retention
rehabilitation

58
Q

what non-operative methods of stabilisation/retention are there

A

strapping
plaster
traction

59
Q

which operative methods of fracture retention are there

A

plates and screws
IM nail
ex fix
percutaneous pins

60
Q

what are the indications for internal fixation

A
  • displaced intra-articular fractures
  • factures with tenuous blood supply
  • multiple injuries
  • more than one fracture in single limb
  • pathological of long bones
61
Q

what are the general complications with fractures and fracture healing

A

soft tissue damage
recumbency
anaesthesia/surgery

62
Q

what are the specific complications associated with fractures

A 
fat embolism ( fat globules may be visible in urine)
nerve/vessel/visceral damage
infection
problems with union
joint stiffness
AVN
myositis ossificans
63
Q

what is the mechanism of injury for nerve damage in fractures

A

nerve stretched over bone/fracture ends
axonotmesis
repaired by neurotmesis

64
Q

what are the characteristics of arterial vascular trauma

A 
painful
pale/plum coloured
paraesthetic
pulseless
perishing cold
65
Q

what is the classic triad of symptoms associated with fat embolism

A

respiratory
neurological
petechial rash

66
Q

what is a prominent symptom of compartment syndrome

A

pain:

  • out of proportion to injury
  • on passive stretch of muscle

late signs:

  • pins and needles
  • pulselessness
67
Q

what is malunion

A

where fracture has united in poor position

  • cosmetic deformity
  • functional problem
68
Q

what is delayed union

A

union fails to occur within the expected time

69
Q

which factors can contribute to delayed union

A 
smoking
steroid use
old age
severe anaemia
diabetes
vit D def/hypothyroid/osteoporosis
infection
inadequate blood supply
70
Q

what is the definition of non-union

A

fracture has failed to unite and healing process is no longer active
two main types:
1) hypertrophic non-union
2) atrophic non-union

71
Q

what causes hypertrophic non-union

A

inadequate stability but viable bone ends
results in sclerotic and flared bone ends which make excessive callus
visible fracture line filled with fibrous tissue/cartilage

72
Q

what causes atrophic non union

A

no evidence of cellular activity
bone ends become narrow and porotic
fibrous tisse needs removing and may need graft

73
Q

what are the causes of joint stiffness

A

w/in joint - articular damage, capsular contractures

near joint - ligament contracture; muscle adhesions/shortening

remote- other joints

74
Q

what happens in avascular necrosis

A

bone death due to blood supply disruption
slow revascularisation
bone is soft and distorted
causes secondary OA

75
Q

where are common sites of AVN following fracture

A

femoral head
scaphoid
talus
lunate

76
Q

what is myositis ossificans

A

calcified soft tissues near the joint

this restricts movements

77
Q

what can cause pathological fractures

A 
tumours
infection
osteoporosis
osteomalacia
paget's disease
osteopetrosis (sclerotic bone)
skeletal dysplasias
78
Q

which secondary tumours can cause pathological fractures

A 
breast
bronchus
prostate
kidney
thyroid
79
Q

why do children’s fractures occur differently

A

childrens bone high col:mineral and more porous
therefore special types of fracture:
1) greenstick - angulating, not rotation or displacement
2)buckle
3)plastic deformity - bent but no obvious fracture

80
Q

what is the most common type of growth plate injury

A

Salter Harris type 2

81
Q

what is a Salter Harris type 1 fracture

A

slipped epiphyseal plate

fracture passes all the way through the growth plate not involvign the bone

82
Q

what is a Salter Harris type 2 fracture

A

fracture in the gorwth plate and above the growth plate in the metaphysis

83
Q

what is a Salter Harris type 3 fracture

A

fracture through growth plate down to epiphysis

84
Q

what is a Salter Harris type 4 fracture

A

fracture goes through metaphysis, growth plat and epiphysis

poor prognosis

85
Q

what is a salter harris type 5 fracture

A

a rammed growth plate damaged by crushing inury

worst prognosis

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