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Musculoskeletal System > Fractures, Open Fractures, Dislocations and Principles of Management > Flashcards

Fractures, Open Fractures, Dislocations and Principles of Management Flashcards

1
Q

How many people die in RTAs every year?

A

1.2 million

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2
Q

What is the 7th biggest killer in the world?

A

Trama

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3
Q

What percentage of orthopaedic workload in the UK is accounted for by traumatic injuries?

A

Over 40%

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4
Q

What are the selected serious complications of fracture?

A

Fat embolism
Compartment syndrome
Complex regional pain syndrome type 1

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5
Q

What is a fracture?

A

A fracture is any break in the structural continuity of the bone, may be a crack, break, split, crumpling or buckle

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6
Q

Why do bones fail (fracture)?

A

High energy transfer in normal bones
Repetitive stress in normal bones
Low energy transfer in abnormal bones e.g. osteoporosis, osteomalacia, metastatic tumour

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7
Q

What does Wolff’s Law state?

A

Form follows function - i.e. bone is laid down where it is needed and removed where it is not needed

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8
Q

What should you include in the description of a fracture?

A 
Mechanism and energy of injury 
Skin and soft tissues 
Site
Shape
Comminution 
Deformity 
Associated injuries
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9
Q

What is an open fracture?

A

A fracture in which there is direct communication between fracture and external environment

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10
Q

How do open fractures differ from closed fractures?

A

Higher risk of infection

Higher energy injury - with associated consequences for soft tissue and bone healing

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11
Q

Communication with the external environment is usually through what?

A

A break in the skin

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12
Q

What are the determinants of fracture classification?

A

Mechanism and velocity
Degree of soft tissue damage
Fracture configuration
Degree of contamination

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13
Q

According to the Gustilo grading, what are the features of fracture type I?

A

Low energy
Wound < 1cm
Clean
Often bone piercing skin from inside

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14
Q

According to the Gustilo grading, what are the features of fracture type II?

A

Moderate soft tissue damage
Wound < 10cm
No soft tissue flap or avulsion

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15
Q

According to the Gustilo grading, what are the features of fracture type III?

A 
High energy 
Extensive soft tissue damage 
Severe fracture 
Wound > 10cm
Any gunshot, farm accident, segmental fracture, bone loss, severe crush injury
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16
Q

According to the Gustilo grading, what are the features of fracture type IIIA?

A

Soft tissue damage but not grossly contaminated

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17
Q

According to the Gustilo grading, what are the features of fracture type IIIB?

A

Periosteal stripping, extensive muscle damage and heavy contamination

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18
Q

According to the Gustilo grading, what are the features of fracture type IIIC?

A

Associated neuromuscular complications

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19
Q

What is the epidemiology of open fractures?

A

23 per 100,000 population per year
Fingers and tibial shaft account for > 50%
Plastic and orthopaedic combined management
About 3,500 open tibial shaft fractures in UK per year

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20
Q

What percentage of type IIIB tibial shaft fractures require flap cover?

A

70%

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21
Q

What is the management of open fractures?

A

Tetanus and antibiotic prophylaxis
Photograph, cover and stabilise limb
Surgical emergency - operation within 6 hours
Early and thorough wound excision and toilet
Do no close wound - leave skin open
Repeat wound review and toilet every 24-48 hours
Early definitive skin cover 5-7 days
Stabilise fracture
Possible bone grafting
Fasciotomies

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22
Q

What is the management for Gustilo grades I-IIIA?

A

Same as closed fracture

Internal fixation, IM nail etc.

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23
Q

What is the management for Gustilo grades IIIB?

A

Problem fracture

Open external fixation to allow plastic surgery

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24
Q

What is the management for Gustilo grades IIIC?

A

External fixation or primary amputation

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25
Q

What do you need to remember in open fracture management?

A

Multiple Injuries
Stabilisation of the fracture will reduce risk of infection
The decision to amputate should be made by senior staff of various specialties and should take into account the duration of ischaemia and any nerve damage
Delayed wound closure should also be considered
In primary closure 21% will become infected, in delayed closure only 3% become infected
However, failure to get skin cover in 1 week in grade IIIB open tibial fractures will lead to 77% non-union and 59% infection
Whereas if skin cover is achieved within 1 week there is 23% non-union and 8% infection

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26
Q

What bone grafting is done in open fracture?

A

Posterolateral morsellised cancellous bone graft at 6 weeks - autologous or allograft, wait for external fixator pin tracks to heal

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27
Q

What is a dislocation?

A

Complete joint disruption

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28
Q

What is subluxation?

A

Partial dislocation, not fully out of the joint

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29
Q

What should be done at presentation of a dislocation?

A 
Clinical examination 
X-ray 
Note ligament and capsule damage 
Associated injuries e.g. fractures, neuromuscular damage 
Recurrent instability
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30
Q

In what direction does the shoulder commonly dislocate and what deformity does this result in?

A

Anterior
Posterior

Deformity

  • squared off
  • locked in internal rotation
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31
Q

In what direction does the elbow commonly dislocate and what deformity does this result in?

A

Posterior

Deformity
- olecranon prominent posteriorly

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32
Q

In what direction does the hip commonly dislocate and what deformity does this result in?

A

Posterior

Deformity
- leg short, flexed, internal rotation, adduction

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33
Q

In what direction does the knee commonly dislocate and what deformity does this result in?

A

Anteroposterior

Deformity
- loss of normal contour, extended

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34
Q

In what direction does the ankle commonly dislocate and what deformity does this result in?

A

Lateral more common

Deformity

  • externally rotated
  • prominent medial malleolus
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35
Q

In what direction do the subtalar joints commonly dislocate and what deformity does this result in?

A

Lateral more common

Deformity
- laterally displaced OS calcis

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36
Q

What are the systemic early problems and complications of fracture?

A

Problems

  • hypovolaemia
  • crush syndrome
  • fat embolism
  • ARDS

Complications
- bed rest complications e.g. DVT, PE

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37
Q

What are the systemic late problems and complications of fracture?

A

Problems
- psychological and social aspects

Complications
- bed rest complications

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38
Q

What are the local early problems and complications of fracture?

A

Problems

  • neuromuscular damage
  • skin/wound problems
  • compartment syndrome

Complications
- infection

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39
Q

What are the local late problems and complications of fracture?

A

Problems

  • delayed union
  • non-union
  • avascular necrosis

Complications

  • mal-union
  • CRPS type 1
  • implant failure
  • joint stiffness
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40
Q

What are the bony complications of fracture healing?

A

Delayed union
Non-union
Mal-union
Avascular necrosis

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41
Q

What is malunion?

A

Where the fracture has healed but not in an anatomically correct position

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42
Q

What is delayed union?

A

Where healing is taking longer than average for that fracture in that individual, may or may not go on to unite

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43
Q

What is non-union?

A

Where there is not further progress towards union

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44
Q

What are the conservative and operative problems with treatment?

A

Inadequate immobilisation
Distraction of fracture by fixation device or traction
Repeated manipulations
Periosteal stripping and soft tissue damage at operation
Anatomical vascular susceptibility e.g. femoral neck, scaphoid, talus, distal tibia

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45
Q

What are the types of non-union?

A

Atrophic - gap at fracture site, bone loss due to soft tissue interposition or pathological reason e.g. infection, tumour, AVN in bone

Hypertrophic - attempt at healing but fracture site too mobile

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46
Q

What are the causes of infected non-union?

A 
Contamination in open fracture 
Introduction at time of operation 
Multiple operations
Unstable fixation 
Metastatic sepsis on foreign body implant
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47
Q

What patients are more at risk of infected non-union?

A

Immunologically compromised patients

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48
Q

What is the treatment of infected non-union?

A

Suspect, diagnose and remove dead, devitalised and infected tissue
Obtain organism if possible, treat infection and stabilise the fracture

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49
Q

What is the cause of avascular necrosis?

A

Loss of blood supply
Classical fracture - hip, scaphoid, talus
Any bone fragment stripped of soft tissue attachments

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50
Q

What is the aetiology of complex regional pain syndrome, type 1?

A 
Trauma - minor 
Surgery 
Infection 
Repetitive motion disorders 
IHD, MI 
Specific genetic predisposition 
No cause
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51
Q

What is the incidence of complex regional pain syndrome type 1?

A

Actual incidence is unknown

Higher in women

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52
Q

What is the incidence of CRPS1 after a peripheral nerve injury?

A

1-5%

53
Q

What is the incidence of CRPS1 after Colles fracture?

A

15-30%

54
Q

What is CRPS 1?

A

Syndrome characterised by; pain, oedema/sudomotor, reduced range of movement, temperature and colour changes

Pain is considered essential for the diagnosis and consistently occurs as two components

  • spontaneous or continuous pain
  • evoked pain

Affects extremity
Disproportionate to inciting event
Aggravated by activity

55
Q

What are the motor changes in CRPS 1?

A

Most patients complain of difficulties in performing complex moving patterns and have a reduced range of movement
Range of movement reduced in 50%
Increased amplitude of physiological tremor and reduced active motor force in the affected extremity
Somatomotor changes thought to have a central rather than a peripheral origin as many tasks that cannot be performed actively can be done passively when the extremity is moved by another person

56
Q

What are the temperature changes in CRPS 1?

A

In general, skin temperature of the affected limb increases during acute CRPS and decreases in chronic stages

57
Q

In what percentage of cases does CRPS 1 spread to another limb?

A

10%

58
Q

What are the clinical features of CRPS 1?

A

Symptoms tend to be progressive, vary in intensity and spread proximally with time

Pain - severe, constant, worse with touch or movement, disproportionate
Very swollen, shiny skin that is discoloured and hot
Very stiff affected limb
Rapid bone osteoporosis
Rapid joint osteoarthritis
Muscles wasted

59
Q

What are the stages of CRPS type 1?

A

Acute
- < 6 months after onset, skin warm, skin perfusion greater

Chronic

  • > 6 months after onset, cooler skin - perfusion lower on affected side
  • reduced noradrenaline levels in affected limb
  • alpha adrenoceptor density increased in skin biopsies
  • skin lactate levels increased
60
Q

Early CRPS involves inhibition of cutaneous vasoconstrictor neutrons, but chronic CRPS involves

A

competition between continued inhibition of vasoconstriction and super-sensitivity of peripheral vessels to circulating NA

61
Q

What is the difference between the average skin sympathetic activity on both sides in CRPS type 1?

A

Same on both sides

62
Q

What is the pathophysiology of CRPS type 1?

A

Allodynia - painful response to normally innocuous stimuli
Hyperalgesia - increased response to painful stimulus
Affects entire neural axis
Peripheral and central sensitisation
Sympathetically mediated pain

63
Q

In CRPS type 1, patients may be primarily affected by inflammation, swelling and other tissue changes in the traumatised limb, these changes may be associated with what?

A

Afferent neuropathic dysfunction or regional peripheral sensitisation

64
Q

Constant dorsal horn barrage may cause central sensitisation which ultimately may be essential common element to

A

the development and perpetuation of CRPS

65
Q

In CRPS 1, functional and neuroplastic changes can extend into

A

the brainstem and possibly the cerebral cortex

66
Q

In CRPS1, the efferent side of the functional and neuroplastic changes is mediated primarily by

A

the sympathetic nervous system which interacts with the pathology in the extremity

67
Q

What is the treatment of CRPS 1?

A

Early active movement, regular analgesia and frequent supervised physiotherapy
Better if treated early (< 3 months) as this increases remission
50% of CRPS 1 will present > 6 months
Educate patients about therapeutic goals
Encourage normal use of affected limb
Minimise pain
Determine contribution of sympathetic nervous system
Prevention

68
Q

What is the pharmacological therapy of CRPS 1?

A 
Traditional analgesics
Tricyclic antidepressants 
Gabapentin 
Glucocorticoids 
Transdermal clonidine 
IV bisphosphonates
69
Q

What is crush syndrome?

A

Rare, life-threatening
Crush injury to a large muscle mass e.g. thigh, calf
Causes direct muscle injury, muscle ischaemia and cell death with the release of myoglobin which causes acute tubular necrosis and acute renal failure

70
Q

What are the clinical features of crush syndrome?

A

Dark amber urine - tests +ve for Hb, specific test for Mb

Acute renal failure - hypovolaemia, metabolic acidosis, hyperkalaemia, hypocalcaemia, DIC

71
Q

What is the management of crush syndrome?

A

IV fluids
Early - protect kidney and prevent acute renal failure
Fluid expansion and osmotic diuresis - to maintain high tubular volume and urine flow aim
Alkalisation of urine with sodium bicarbonate to reduce tubular precipitation of myoglobin

72
Q

What is acute compartment syndrome?

A

Key pathology is ischaemia
Life threatening
High index of suspicion

73
Q

What is the aetiology of acute compartment syndrome?

A 
Occurs after trauma - usually with a fracture (70%) 
Can be soft tissue trauma alone 
Also seen in vascular reperfusion of acutely ischaemic limb 
Burns 
Crush injuries 
Haemorrhage 
Drug injection 
Chronic exertional
74
Q

When does a compartment syndrome develop?

A

When intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment

75
Q

What are the sites at risk of compartment syndrome?

A 
Lower leg 
Forearm 
Hand
Foot 
Thigh
76
Q

What are the features of compartment syndrome?

A

Any muscle compartment bounded by inelastic walls - sheets of fascia and bone
Some (limited) room for expansion but when full pressure increases exponentially
Blood vessels are compressed and blood flow stops, causing tissue to become ischaemia

77
Q

What patients are at risk of compartment syndrome?

A

Trauma - young fit male patients, 25% of adult tibial fractures have a compartment syndrome
No trauma - older, medically unfit patients, more females than males

78
Q

What are the traumatic causes of compartment syndrome?

A

Tibial, distal radius or forearm fracture in adults/adolescents
Forearm of supracondylar fractures in paediatrics
Crush injures, blunt trauma or stab wounds with no fracture

79
Q

What are the non-trauma causes of compartment syndrome?

A

Crush syndrome - prolonged immobility, overdose or CVA
Coagulopathy - iatrogenic or endogenous
Reperfusion injury - after vascular surgery
Burns

80
Q

Why is acute compartment syndrome more common in low energy tibial fractures?

A

As the fascial compartments are more likely to be intact

81
Q

What is the clinical presentation of acute compartment syndrome?

A

The 9 Ps

Pain - severe, worsening, out-growing analgesia, deep ache/crushing/tightness, made worse by passive dorsiflexion
Passive dorsiflexion - of digits of the limb, worsens pain
Paraesthesia - sensory, both direct pressure on nerve and ischaemia of the nerve
Paresis/paralysis - weakness or no movement
Pallor
Pulseless
Perishing cold
Pressure
Prompt decompression

82
Q

What does compartment syndrome lead to if untreated?

A

Multiple ischaemia and necrosis
Muscle contractures
Delayed fracture healing
May necessitate limb amputation

83
Q

What are the complications of compartment syndrome?

A 
Amputation 
Infection 
Contracture
Foot drop 
Paralysis 
Neurovascular deficits
Significantly prolonged hospital stays
Re-operation
Loss of income
Psychological consequences 
Medico-legal consequences
84
Q

What is the threshold for fasciotomy?

A

Persistent delta P < 30mmHg

85
Q

What is fat embolism syndrome?

A

Fat within the systemic circulation that produces an embolic phenomena, with or without clinical sequelae
When associated with an identifiable clinical pattern of symptoms and signs it is known as fat embolism syndrome
Life threatening, rare
High index of suspicion

86
Q

When does fat embolism syndrome occur?

A

After trauma, always with a long bone fracture, usually after 24-72 hours
Also seen in instrumentation of long bone

87
Q

What is the key pathology of fat embolism syndrome?

A

Hypoxia

88
Q

In what percentage of patients with traumatic injury is evidence of fat embolism seen?

A

90%

89
Q

What percentage of long bone fractures will result in fat embolism syndrome?

A

3-4%

90
Q

What percentage of cases of fat embolism syndrome are fatal?

A

10-15%

91
Q

In what patients, injuries and limbs is fat embolism syndrome more common?

A

Young adults > elderly and children
Closed injuries > open injuries
Lower limbs > upper limbs

92
Q

What is the sub-clinical incidence of fat embolism syndrome?

A

90%

93
Q

What are the risk factors for fat embolism syndrome?

A 
Long bone fractures 
Conservative management of long bone fractures 
Multiple trauma 
Associated abdominal injuries 
Severe blood loss
94
Q

What are the theories of pathophysiology of fat embolism syndrome?

A

Mechanical theory - bone marrow enters venous circulation and lodges in the lungs, smaller particles penetrate pulmonary capillaries and enter arterial circulation
Biochemical theory - circulating fatty acids directly affect pneumocystes, altering gas exchange

95
Q

How is fat embolism diagnosed?

A

Clinical presentation
Bloods - hypoxia on ABGs, fall in Hb, thrombocytopenia, fat droplets within blood clots
CXR

96
Q

What are the clinical features of fat embolism syndrome?

A

24-72 hours post-insult
Hypoxia (PaO2 < 60 mmHg)
Brain is the most sensitive organ to hypoxia
Confused/agitated - fits, drowsiness, coma, death
Tachypnoeic and tachycardic
Shock (hypotensive) - late
Fever - low grade
Skin rash in 60% - petechial, only in distribution of SVC, fleeting presentation, gone within 12-24 hours

97
Q

What are the investigations of fat embolism syndrome?

A

CXR
Oxygen saturations and blood gases - reduced PaO2
FCB - Hb and platelets reduced
Fat globules in blood clots, sputum and urine - cause hypoxia in pulmonary circulation, confusion in cerebral circulation and petechiae in cutaneous circulation

98
Q

What is the treatment of fat embolism syndrome?

A

No current treatment, only supportive management

  • steroids
  • dextran
  • heparin
  • ethanol
  • oxygen
99
Q

What is the aim of management of fat embolism syndrome?

A

To maintain cerebral and pulmonary perfusion

Patients should be given oxygen and if necessary mechanical ventilation and advanced circulatory support

100
Q

What is the prevention of fat embolism syndrome?

A

Immobilisation/fixation of long bone fractures
Possible role for prophylaxis with steroids
Monitoring with pulse oximetry
Fat embolism reduced when fractures are fixed within 24 hours

101
Q

What is the incidence of fat embolism syndrome in conservative treatment and operative stabilisation?

A

3.5% in conservative treatment

0% in operative stabilisation

102
Q

What are the aims of fracture treatment?

A

Relieving pain
Restoring function
Saving life

103
Q

What are the life-saving measures in fracture treatment?

A

Diagnose and treat life-threatening injuries

Emergency orthopaedic involvement

104
Q

What is involved in management of the injured patient?

A

Emergency orthopaedic management - day 1
Monitoring of fracture - days-weeks
Rehabilitation and treatment of complications - weeks-months

105
Q

Give examples of life-saving emergency orthopaedic management

A

Reducing a pelvic fracture in a haemodynamically unstable patient
Applying pressure to reduce a haemorrhage from an open fracture

106
Q

Give examples of complication-saving emergency orthopaedic management

A

Early and complete diagnosis of extent of injuries

Diagnosing and treating soft tissue injuries

107
Q

What soft tissue injuries might be diagnosed with fractures?

A

Skin - open fractures, de-gloving injuries and ischaemic necrosis
Muscles - crush injury and compartment syndromes
Blood vessels - vasospasm and arterial laceration
Nerves - neurapraxias, axonotmesis, neurotmesis
Ligaments - joint instability and dislocation

108
Q

What effect will a severe soft tissue injury have on fracture healing?

A

Will delay fracture healing

109
Q

What does choice of treatment for a fracture depend on?

A 
Fracture 
Bone 
Soft tissue 
Patient 
Facilities 
Ability of surgeon
110
Q

In what percentage of fractures is healing delayed or impaired?

A

5-10%

111
Q

How does bone heal?

A

By formation of a callus

112
Q

What is a callus?

A

Intermediary stabilising structure formed after a fracture which has cartilaginous growth plate characteristics and results in eventual endochondral ossification

113
Q

What are the phases of bone healing?

A

Inflammatory - 24-72 hours
Reparative - from 2 days
Remodelling - from middle of repair phase

114
Q

What are the cellular events in the immediate response to the injury in fracture repair?

A

Haematoma formation
Release of vasoactive mediators e.g. nitric oxide and cytokines
Proliferation of undifferentiated cells - migration, recruitment, proliferation and differentiation
Invasion by inflammatory cells - macrophages, PMNs
Organisation of clot into fibrous tissue by fibroblasts
Formation of reparative granuloma
Vessel thrombosis and osteocyte death

115
Q

What are the cellular events in intramembranous ossification in fracture repair?

A

Differentiation of osteo-progenitor precursor cells into osteoblasts
Angiogenesis
Collagen deposited along fibrin scaffold - new bone matrix synthesis (osteoid from osteoblasts, uncalcified mass -> primary callus)
Bone formation in periosteum (woven bone) converts primary external callus into a hard secondary callus - clinical union

116
Q

What are the cellular features of a callus?

A

Initially fibrous but disorganised
Biomechanical environment is important
Chondroblasts appear later and form cartilage
Later the bone forms by endochondral ossification

117
Q

What are the cellular events in endochondral ossification in fracture repair?

A

Bone formation in callus, similar to bone formation in growth plate
Osteoblasts follow capillary ingrowth
Synthesis of osteoid - becomes mineralised to give speckled calcification
Formation of mixed spiculae
Bridging of fracture gap - radiological union

118
Q

What are the cellular events in remodelling in fracture repair?

A

Osteoblastic and osteoclastic activity
Osteoclastic cutting cones
Consolidation
Remodelling of woven bone
Lamellar bone more efficient so volume decreases
Cancellous bone remodels at the trabecular level
Longest stage
Remodelling of some deformities but not of others

119
Q

What is involved in primary bone union?

A

Cortical bone ends are accurately and closely apposed and rigidly immobilised
No callus

120
Q

How do fractures heal in nature?

A

Regeneration vs repair
Phases of healing by callus
Rapid process but rehabilitation slow - low risk

121
Q

How do fractures heal with surgery - RIGID, ORIF and compression?

A

Primary bone healing

Slow process but rehabilitation rapid - high risk

122
Q

How do fractures heal with surgery - STABLE, nailing or external fixation?

A

Healing by callus

rapid process and rehabilitation rapid - less risk

123
Q 
At what point after a fracture should you do a clinical examination to measure fracture healing in;
adult upper limb 
adult lower limb 
child upper limb 
child lower limb?
A

Adult upper limb 6-8 weeks
Adult lower limb 12-16 weeks
Child upper limb 3-4 weeks
Child lower limb 6-8 weeks

124
Q

How do you measure fracture healing?

A

Clinical examination
Radiologically - bridging callus formation, remodelling
Biomechanically - stiffness
Radiolabelled assessment, CT etc.

125
Q

When is a fracture healed?

A

When patient can weight bear, x-rays show healing and remodelling is complete

126
Q

What are the factors influencing fracture repair?

A

Host - nutritional and hormonal status, drugs, CNS injury

Local factors

  • soft tissue injury
  • bone loss
  • radiation
  • tumour
  • distraction
  • tissue interposition
  • blood supply
  • infection
  • type of bone
  • synovial fluid

Treatment method - mobility at fracture site, stable vs rigid fixation

127
Q

What are the features of rehabilitation in fracture management?

A

Restoring patient as close to pre-injury functional level as possible
May not be possible with severe fractures or other injuries, or in frail or elderly patients
Approach needs to be pragmatic with realistic targets
Multidisciplinary - physio, OT, district nurse, GP, social worker

128
Q

Give examples of some treatment techniques for fractures

A

Active early movement and full function but no loads/sport etc.
Active early movement but protected
Rest and elevation
Rest and gravity
Semi-rigid splint age
Immobilisation by rigid external splint and MUA
Functional brace
Skin traction
Skeletal traction
External fixation
External and internal fixation
Percutaneous K wire fixation
ORIF - open reduction internal fixation
ORIF with K wires
ORIF with tension band wiring
ORIF with screws, may be cannulated
ORIF with plates
ORIF with partridge bands, cerclage wire/cable
Internal fixation with sliding nail/screw and plate
Internal fixation with intramedullary nail
Internal fixation with signal arm intramedullary rod
Spinal rods
Excision of fracture fragment
Bone excision and prosthetic replacement
Amputation

129
Q

What are the components of the Mangled Extremity Severity Score (MESS)?

A

Skeletal/soft tissue injury

  • low energy = 1
  • medium = 2
  • high = 3
  • massive crush = 4

Shock

  • normotensive = 1
  • transient = 1
  • prolonged = 2

Ischaemia

  • none = 0
  • mild = 1
  • moderate = 2
  • advanced = 3

Age

  • < 30 = 0
  • 30-50 = 1
  • > 50 = 2

Musculoskeletal System (40 decks)

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