Hip Fractures Flashcards
how are hip fractures classified
where they are in relation to the capsule
the level of displacement and therefore instability within the joint (often Garden’s classification)
which surgical options are available for fractured hip
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
how is osteoporosis measured
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
which tool can be used to predict risk of future fracture in primary care
the FRAX tool gives 10 year probability of a hip fracture and also spine, shoulder or forearm
based on: age, sex, previous injuries
which pharmacological treatments are available for osteoporosis
calcium/vit D3 supplements bisphosphonates (1st/2nd line) strontium ranelate (3rd line) SERMs PTH HRT Testosterone
what are the causes of osteoporosis
post menopause hyperparathyroidism malabsorption osteomalacia multiple myloma hypopituitarism
which drugs can predispose towards osteoporosis
corticosteroids anticonvulsants heparin thyroxine extreme alcohol excess lithium chemo methotrexate SSRIs
what clinical features might osteoporosis present with
low impact fracture
reduced height (vertebral fracture)
kyphosis
how do steroids affect bone mineral density
decreased absorption of calcium from the gut
decrease muscle mass
increase osteoclast activity
which lifestyle changes can be made to avoid osteoporosis
sufficient daily calcium intake
smoking cessation
reduce alcohol intake
increased weight bearing exercise
which race appears to be less susceptible to osteoporosis
Afro-caribbean are less susceptible than white or asian women
which bisphosphonate is recommended for first line prevention of osteoporotic fractures
alendronic acid
how do bisphosphonates work?
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
why must patients on bisphosponates have regular dental check ups
they are at risk of osteonecrosis of the jaw especially if receiving IV bisphosphanates
what are 3 problems with bisphosphonates
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
what is denosumab
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
what are the 2nd line treatments for osteoporosis
IV bisphosphonates
denosumab
how are IV bisphosphonates administered
fewer tolerance issues
given once yearly for 3 years
may be restarted 3 further years later
why must bisphosphonates be taken on an empty stomach
poorly absorbed from the gut as bind to calcium in food
what are the 4 stages of management for fractured neck of femur
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
what are the 4 groups of fallers
1) medical (heart problems etc)
2) dementia/cognitive impariments
3) Mechanical
4) postural drop
what is the most common cause of fall
mechanical (50-60%)
what is the 2nd most common cause of fall
postural drop
can be delayed by upto 5-10mins after standing
what are the stages of managment for postural drop
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
what is the 1 yr mortality from falling and being on the floor for more than 1 hour
50%
what is the Hayflick limit
the finite number of times a cell can divide - dictated by telomeres
define frailty
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
which areas of the body are commonly affected by fragility fractures
hip spine wrist ribs humerus pelvis
what is the mortality of hip fracture
20%
what are the risk factors for osteoporosis
age female genetics oestrogen deficiency hypogonadism smoking low/very high BMI inactivity ethnicity (caucasians) eating disorders
what is a Z score
standard deviations of BMD from age AND gender matched mean
which osteoporosis drugs increase bone formations
teriparatide (PTH)
strontium ranelate
which osteoporosis drugs decrease resoprtion
bisphosphonates RANKL inhibitors (denosumab)
how does rPTH work
normally PTH causes bone loss, but given in pulses increases bone production and BMD
given as a daily sc injections for 2 years
what are the causes of vitamin D deficiency
inadequate sunlight inadequate diet malabsorption medication low levels in breastmilk multiparosity abnormal vit D metab
what is the presentation of osteomalacia
bone pain/tenderness
proximal muscle weakness
back pain
stress fractures
what would you see on bloods to confirm vitamin D deficiency
LOW 25(OH)vitD HIGH serum PTH LOW/NORMAL serum Ca LOW serum phosphate HIGH alkaline phosphatase (osteoclast activity)
what is Paget’s disease
disordered bone metabolism
–> osteoclast overactivity followed by compensatory osteoblast activity
leads to the formation of WOVEN bone –> weaker
what are the signs and symptoms of Pagets disease
bone pain, path fracture, (sarcomatous change) –> direct
indirect:
- high CO
- compression:
- –> skull (cranial nerve palsies, deafness, basilar invaginations)
- –> spine (sciatica, cauda equina)
how is pagets diagnosed
X ray
bloods (high alk phos w/ normal Ca vD PTH and phosphate)
urinary hydroxyproline increased
isotope bonescan
when would you treat pagets
if symptomatic
in danger of nerve compression
around a weight bearing joint
how would you treat pagets
bisphosphonates
define a fracture
a loss of continuity of the substance of a bone due to physical force
what type of fractures happen in long bones
transverse - banding force spiral - torsion oblique comminuted - high energy segmental
what type of fractures happen in cancellous bones
impacted
crush/compression
what type of fractures happen in periarticular bone
avulsion
what two features promote fracture healing
intact fracture haematoma
controlled microenvironment
what are the 4 stages of fracture healing
1) inflammation
2) soft callus
3) hard callus
4) remodelling
what happens in the first stage of fracture healing
inflammation and development of haematoma:
- fibrin clot
- polymorphs
- platelets
- monocytes
later:
- fibroblasts
- osteoprogenitor cells
- vascular ingrowth
what happens in the second stage of fracure healing
after pain and swelling subside
bone fragments united by fibrous or cartilaginous tissue
bony ends no longer freely moveable but angulation still possible
what happens in the third stage of fracture healing
mineralisation of cartilage
OBs convert cartilaginous tissue to woven bone
ENDOCHONDRAL and membranous bone formation
this increases fracture stiffness and produces an external callus
what happens in the final stage of fracture healing
woven bone converted to lamellar bone
excess callus is removed
medullary canal is reconstituted
which implants for fractures provide absolute stability
internal fixation
what is the aim of reduction
to reduce deformity
what is important about the rate of bone healing and implants
fracture must heal before implant fails
what is the rule of 2’s
x ray of fractured joint: 2 views - at right angles 2 joints 2 occasions 2 limbs
what are the three R’s of fracture treatment
reduction
retention
rehabilitation
what non-operative methods of stabilisation/retention are there
strapping
plaster
traction
which operative methods of fracture retention are there
plates and screws
IM nail
ex fix
percutaneous pins
what are the indications for internal fixation
- displaced intra-articular fractures
- factures with tenuous blood supply
- multiple injuries
- more than one fracture in single limb
- pathological of long bones
what are the general complications with fractures and fracture healing
soft tissue damage
recumbency
anaesthesia/surgery
what are the specific complications associated with fractures
fat embolism ( fat globules may be visible in urine) nerve/vessel/visceral damage infection problems with union joint stiffness AVN myositis ossificans
what is the mechanism of injury for nerve damage in fractures
nerve stretched over bone/fracture ends
axonotmesis
repaired by neurotmesis
what are the characteristics of arterial vascular trauma
painful pale/plum coloured paraesthetic pulseless perishing cold
what is the classic triad of symptoms associated with fat embolism
respiratory
neurological
petechial rash
what is a prominent symptom of compartment syndrome
pain:
- out of proportion to injury
- on passive stretch of muscle
late signs:
- pins and needles
- pulselessness
what is malunion
where fracture has united in poor position
- cosmetic deformity
- functional problem
what is delayed union
union fails to occur within the expected time
which factors can contribute to delayed union
smoking steroid use old age severe anaemia diabetes vit D def/hypothyroid/osteoporosis infection inadequate blood supply
what is the definition of non-union
fracture has failed to unite and healing process is no longer active
two main types:
1) hypertrophic non-union
2) atrophic non-union
what causes hypertrophic non-union
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
what causes atrophic non union
no evidence of cellular activity
bone ends become narrow and porotic
fibrous tisse needs removing and may need graft
what are the causes of joint stiffness
w/in joint - articular damage, capsular contractures
near joint - ligament contracture; muscle adhesions/shortening
remote- other joints
what happens in avascular necrosis
bone death due to blood supply disruption
slow revascularisation
bone is soft and distorted
causes secondary OA
where are common sites of AVN following fracture
femoral head
scaphoid
talus
lunate
what is myositis ossificans
calcified soft tissues near the joint
this restricts movements
what can cause pathological fractures
tumours infection osteoporosis osteomalacia paget's disease osteopetrosis (sclerotic bone) skeletal dysplasias
which secondary tumours can cause pathological fractures
breast bronchus prostate kidney thyroid
why do children’s fractures occur differently
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
what is the most common type of growth plate injury
Salter Harris type 2
what is a Salter Harris type 1 fracture
slipped epiphyseal plate
fracture passes all the way through the growth plate not involvign the bone
what is a Salter Harris type 2 fracture
fracture in the gorwth plate and above the growth plate in the metaphysis
what is a Salter Harris type 3 fracture
fracture through growth plate down to epiphysis
what is a Salter Harris type 4 fracture
fracture goes through metaphysis, growth plat and epiphysis
poor prognosis
what is a salter harris type 5 fracture
a rammed growth plate damaged by crushing inury
worst prognosis
