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Ortho > chapter 11 - complications of fractures and dislocations > Flashcards

chapter 11 - complications of fractures and dislocations Flashcards

1
Q

2 examples of early complications

A

arterial injury

neural injury

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2
Q

when can arterial injury occur and why

A

early: immediate damage to arteries
late: later after injury due to displacement

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3
Q

how to prevent late arterial injury?

A

fracture splintage and reduction if needed

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4
Q

what can happen to the artery? 4 things

A

lacerated
avulsed
compressed
contused

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5
Q

why is there an absent pulse following arterial injury

A

thrombos formation and occludes blood supply

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6
Q

the 6ps of arterial injury to make a diagnosis

A 
pain
pallor
parasthesia
paralysis
pulseless
polar
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7
Q

what is the management after diagnosis?

A
  1. remove tight dressings and pops
  2. realignment and relocation of dislocation
  3. if no reversal of symptoms after 1+2 –> vascular angiography and surgical repair
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8
Q

what are the magic hours and how many hours post arterial injury?

A

6 hours - beyond which irreversible muscle ischaemia occurs

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9
Q

what types of nerve injuries may occur as a complication

A

neurapraxia

neurotemesis

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10
Q

causes of nerve complications

A

initial insult

inadequate splinting

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11
Q

causes of intermediate injuries

A

fat embolism syndrome
compartment syndrome
DVT
pulmonary embolism

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12
Q

define intermediate injury

A

occurs soon after injury but not at the time of injury

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13
Q

mehcanism of fat embolism syndrom

A

fat enters blood stream from marrow after a long bone fracture - the fat emboli occludes arteries and capillaries in all organs mechanically and as part of a systemic inflammatory response

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14
Q

clinical manifestations of fat embolism syndrome

A

agitation
tachypnoea
hypoxia
later - petechial hmg - ocular and skin

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15
Q

how to prevent fat embolism syndrome

A

adequate splinting and fluid resuscitation

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16
Q

how to manage fat embolism syndome

A

oxygen and respiratory support

aim: prev further fat immobilisation and manage fracture to prev resp and systemic insult

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17
Q

what is compartment syndrome

A

increased pressure in a closed osteofacial compartment may result from incresed contents - oedema, haematoma, fracture or increased extrinsic pressure - tight dressing, pop, tourniquet

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18
Q

mech is compartment syndrome

A

when intracompartmental pressure reaches capillary perfusion pressure then contents of compartment is rendered ischaemic
capillary pressure is usually 25mmhg
distal flow is not interrupted until compartment pressure reaches 100mhg

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19
Q

clinical features on hx of compartment syndrome

A

pain out of proportion to injury

paraesthesia

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20
Q

examination findings of compartment syndrom

A 
woody hard compartment
altered sensation
muscle weakness and later paralysis
pain on passive stretch
distal pulses preserved till late
limb not as cold as an arterial injiry
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21
Q

treatment of compartmen syndrome

A

immediate removal or splitting of pop
wait 10-15 min
open fasciotomy

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22
Q

when is intracompartmental pressure monitoring indicated

A

high risk patients who cannot communicate - intoxicated, infantile, unconscious

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23
Q

examination findings in a pt with a dvt

A

low grade pyrexia
swollen limb
pin with muscle stretching

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24
Q

how is the diagnosis of dvt made

A

venography
duplex doppler studies
- intramural clot seen

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25
Q

how to treat dvt - prophylxis and management

A

prophylaxis: elevation, dvt stockings, mechanical foot pumps
rx: anticoagulate with heparin, warfarin for 3 months

26
Q

PE exam

A 
pyrexia
pleuritic chest pain
tachypnoea
hypoxia
haemoptysis
27
Q

investigations to help aid in diagnosis and investigations to confirm diagnosis

A

aid: cxr, ecg, blood gas
confirm: ventilation perfusion scans, pulmonary angiography

28
Q

treatment of PE

A

respiratory support oxygen ventilation

thrombosis elimination - heparin/streptokinase/embolectomy

29
Q

late complications

A

infection
disorders of union
joint complications

30
Q

how to limit infection

A

early wash out and debridement

31
Q

examples of infections

A

gas gangrene
necrotising fascitis
tetanus

32
Q

organism in gas gangrene

A

clostridium wlechii - anaerobic

33
Q

diagnosis of gas gangrene

A

odour and evidence of gas within tissues

34
Q

clinical signs of gas gangrene

A

brownish discharge

35
Q

rx gas gangrene

A

prompt surgical debridement/amputation and antibiotics- penicillin
hyperbaric oxygen - not always avail

36
Q

necrotising fascitis cause ( NF)

A

symbiotic infection of any number of aerobic + anaerobic bacteria

37
Q

where are the bacteria causing NF found and what do they do?

A

closed degloving injuries - area of relative anoxia

organisms result in seperation between the superficial and deep fascia and may cause massive devitalisation of skin

38
Q

management of NF - prevention

A

early recognition of degloved tissue
debridement of dead tissue
insertion of drains

39
Q

treatment of NF

A

fluid and electrolyte resus
appropriate antibiotics
skin grafting /flaps to defects

40
Q

pathophysiology of tetatnus

A

clostridium tetani produce exotoxin which binds to anterior horn cells of the spinal cord after which it cannot be neutralised by tetanus immunoglobulins. organism flourishes in devitalised tissue

41
Q

symptoms of tetauns

A 
may present after injury has healed
tonic clonic contractions
risus sardonicus
pooling of secretions/cannot swallow
spasm of diaphragm and intercostals
42
Q

treatment of tetanus

A

prevention: debridement and delayed wound closure
rx: tetanus toxoid
tetanus immunoglobulin
sedation
muscle relaxants
incubation and ventilation

43
Q

D/O of union - 3

A

malunion
delayed union
non union

44
Q

what is malunion and what is the cause? and complications

A

shortening, angulation or rotation after a fracture

cause: inadquate reduction of fracutre or failure to keep fracture reduced till union
complications: cosmetic, refracture, malaligns joints on either side of it

45
Q

what is delayed union dependent on?

A

delayed union varies and depends on: host, local soft tissue, type of fracture

46
Q

3 conditions which prolong healing and examples

A

3 conditions

  • general: malnutrition, diabetes, smoking, peripheral vascular disease
    local: compound fracture, comminution and gross soft tissue injury
    iatrogenic: excessive soft tissue striping, inadequate stabilisation or large fracture gap
47
Q

diagnosis of non union

A

pain at the # site on loading
motion at the # site
xray showing clear fracture gap

48
Q

causes of non union

A

identical to malunion

49
Q

two major forms of non union

A

atrophic: poor callus formation
hypertrophic: callus thrown out to try and heal fracture but due to too large a fracture gap or iadequate immobilisation the union fails

50
Q

treatment of non union

A

eliminate causes for delaye dunion
bone grafting creates a scaffold for callus formation and provides osteoblast stimulating proteins
sound fracture stabilisation

51
Q

growth disturbance in children - which fractures do no not cause complications and why

A

salter harris type 1 and 2 - in the zone of hypertrophy

52
Q

which fractures can cause growth disturbance, where do they occur and what is the mechanism? and complications?

A
  1. salter harris 3,4,5,6
  2. germinal region of growth plate
  3. premature growth arrest
  4. entire plate arrests: limb length discrepancy/ if partial arest: angular deformity
53
Q

joint complications

A

stiffness
myositis ossificans
avascular necrosis
osteoarthritis

54
Q

causes of stifness and how to prevent it

A

periarticular adhesions

splints for shortest time possible, early physio

55
Q

what is myositis ossificans? the most common areas?

A

heterotopic calcification within muscles adjacent to injured joint
elbow, biceps, brachialis

56
Q

predisposing factors to myositis ossificans

A

severe head injruies

57
Q

prophylaxis and rx of myositis ossificans

A

prophylaxis: nsaids, post op single dose radiotherapy
rx: surgical excision

58
Q

what is avscular necrosis

A

ischaemic and death of bone subsequently with bony collapse and degeration of joint

59
Q

areas of avascular necrosis

A

most common:: hip after dislocation or intracapsular fractures
other: scaphoid, lunate, talus

60
Q

how tp prevent avascular necrosis

A

early reduction and fracture fixation

61
Q

what happens to joints after trauma and the complication of this

A

cartilage destruction with trauma impossible to see on plain xray
- lead to early degenerative OA

62
Q

mechanism of joint injury after trauma and how to prevent it

A
  • malalignment of intra articular and long bone fractures results in abn joint loading
  • accurate early intraarticualr fracture reduction and stable fixation

Ortho (41 decks)

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