Fractures and Dislocations 2 Flashcards
What is the other name for open fractures?
“Compound fractures”
What is the definition of an open fracture?
Direct communication between fracture and external environment
What two important respects differentiate closed and open fractures?
(why are open fractures seen as worse?)
Higher risk of infection
Higher energy injury
-In general with consequences for soft tissue and bone healing etc)
Give two fracture locations that sound odd but still count as open fractures?
Facial fractures into the nose
Pelvic fractures into the rectum
Is a graze on the skin that does not penetrate the dermis over a fracture class as an open fracture?
No
Give 4 determinants of fracture classification
Mechanism and velocity
Degree of soft tissue damage
Fracture configuration
Degree of contamination
List the classifications for open fracture Gustilo grading
no need to give a definition of each grade
Type I Type II Type III -IIIA -IIIB -IIIC
What is the definition of Type I Gustilo Grading?
Low energy
Wound
What is the definition of Type II Gustilo grading?
Moderate soft tissue damage
Wound
What is the definition of Type III Gustilo grading?
not covering each division
High energy
Extensive soft tissue damage
Severe fracture (comminution displacement)
Wound >10cm
ANY:
- Gunshot
- Farm accident
- Segmental fracture
- Bone loss
- Severe crush injury
What is the definition of Type IIIA Gustilo grading?
Soft tissue damage +++ but not grossly contaminated
What is the definition of Type IIIB Gustilo grading?
Periosteal stripping
Extensive muscle damage
Heavy contamination
What is the definition of Type IIIC Gustilo grading?
Associated neurovascular complication
Fingers and tibial shaft fractures account for what percentage of total fractures?
> 50%
What two specialities are key in managing open fractures particularly severe tibial fractures?
Plastic and orthopaedic
Describe the management of open fractures
Full ATLS
Tetanus and antibiotics prophylaxis
Photograph, cover and stabilise limb
Surgical emergency (operation within 6hrs)
- Early and thorough wound excision and toilet
- DO NOT CLOSE WOUND
Repeat wound review and toilet every 24-48hrs
Early definitive skin cover (5-7 days)
Stabilise fracture definitely
? bone grafting
Fasciotomies
Give some antibiotics you can consider to give prophylactically
Cefuroxime
Augmentin
Clindamycin
Gentamycin at time of fixation
What open fracture patients should be operated on within 6hrs?
(5 marks)
Polytraumatised patients
Marine and farmyard environment
Gross contamination
Neurovascular compromise
Compartment syndrome
Why do you not need to rush to operate within 6 hours for all open fracture patients?
Outcome better if you assemble a proper team including ortho and plastics
Jumping in unprepared is not needed
Give some different methods for wound closure
5 marks
Split skin graft
Myofasciocutaneous
-Muscle, fat and skin
Fasciocutaneous
-Fat and skin
Rotation
Free flaps
-Muscle group with skin taken and plugs hole
What are the 4 C’s of surgical debridement?
Colour
Contraction (diathermy and twitch)
Consistency
Capacity to bleed
(Tissue should be taken away until thses 4 are met)
What are the 4 broad criteria for the MESS score?
Limb ischaemia
Patient age range
Shock
Injury mechanism
What is the difference between dislocation and subluxation?
Dislocation = complete joint disruption
Subluxation = partial dislocation
-Not fully out of joint
Anterior and posterior shoulder dislocations are characterised by which deformity?
Anterior
-Squared off
Posterior
-Locked in internal rotation
Elbow dislocation is characterised by which deformity?
Olecranon prominant posteriorly
Posterior hip dislocation is characterised by which deformity?
Leg short
Flexed
Internal rotation
Adduction
Knee dislocation is characterised by which deformity?
Loss of normal contour
Extended
Ankle dislocation (lateral most common) is charcaterised by which deformity?
Externally rotated
Prominent medial malleolus
Subtalar joint dislocation (lateral most common) is characterised by what deformity?
Laterally displaced os calcis
Give some other names for Complex Regional Pain Syndrome Type 1
Reflex sympathetic dystrophy Causalgia Algodystrophy Sudeck's atrophy Post-traumatic dystrophy Shoulder Hand syndrome Reflex neurovascular dystrophy
Give 7 aetiologies of Complex regional pain syndrome type 1
Trauma (minor)
Surgery
Infections
Repetitive motion disorders
IHD, MI
Specific genetic predisposition
Nothing at all
Describe the epidemiology of CRPS Type 1
incidence, incidence compared to type II, what do they commonly occur after, M:F, Age
Actual indicence unknown
-Higher than CRPS type 2 (causalgia)
1-5% after peripheral nerve injury
15-30% after Colles’ fracture
Higher incidence in women
Rare in children
What is CRPS I?
Syndrome characterised by PORT:
- Pain
- Oedema
- Reduced ROM
- Temp and colour changes
Extremity
Disproportionate to the inciting event
Aggravated by activity
What are the clinical features of CRPS 1?
Pain Swollen +++ Skin Shiny Discoloured Hot Very Stiff Bone osteoporotic +++ (rapid) Joints osteoarthritis ++ (rapid) Muscles wasted
Describe the pain in CRPS I
Severe
Constant
Worse with touch/ movement
Disproportionate
Pain occurs as two components:
- Spontaneous or continuous pain
- Evoked pain = allodynia or hyperalgesia
Describe the two stages of CRPS type I and the differences between them
Acute: (6 months)
- Cooler
- Skin perfusion lower on affected side
What is allodynia?
Painful response to a normally innocuous stimulus
What is hyperalgesia?
Increased response to a painful stimulus
What are the general rules of treatment for CRPS I?
Early active movement +++
-Encourage normal use of limb
Regular analgesia:
- Minimise pain
- Educate patient about therapeutic goals
Frequent supervised physiotherapy
How successful is treatment in CRPS I?
when should it be given
Better if treated early (6 months
PREVENTION
Describe the treatment protocol for CRPS 1
MOBILITY OF LIMB
Improved pain and function with mobilisation
-Conservative care
OPTIMISE MEDICATION Series of sympathetic blocks -Physical therapy evaluation -Sympathectomy -Trial of spinal cord stimulator -Trial of strong opioids -Psychological evaluation
What pharacological therapy can you use for CRPS 1?
6 marks
- Traditional analgesics
- Tricyclic antidepressants
- Gabapentin (other anticonvulsants)
- Glucocorticoids
- Transdermal clonidine
- Intravenous bisphosphonates
What is crush syndrome also called?
Traumatic rhabdomyolysis
What is crush syndrome?
What causes it, what does it lead to?
Crush injury to a large muscle mass (thigh, calf, etc)
Direct muscle injury +
Muscle ischaemia +
Cell death with release of myoglobin
ATN (acute tubular necrosis of kidneys)
ARF (acute renal failure)
What are the clinical features of crush syndrome?
Dark amber urine
- tests +ve for Hb
- Request specific test for Mb
Acute renal failure
- Hypovolaemia
- Metabolic acidosis
- Hyperkalaemia
- Hypocalcaemia
- DIC
How do you manage crush syndrome?
IV FLUIDS +++
Early (protect kidney and prevent ARF)
Fluid expansion + osmotic diuresis (to maintain high tubular volume +urine flow - aim: 100mls urine per hour until Mb cleared)
Alkalisation of urine with sodium bicarbonate reduce tubular precipitation of myoglobin
Give some aetiologies of acute compartment syndrome
Occurs after trauma
- Usually with a fracture (70%)
- But can be soft tissue trauma alone
Also seen in vascular reperfusion of acutely ischaemic limb
Burns (circumferential eschar)
Crush injuries
Haemorrhage
-10% on anti-coagulants or have bleeding disorder)
Drug injection
(plus chronic exertional)
What is the definition of acute compartment syndrome?
A compartment syndrome develops when intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment
What sites are at risk from acute compartment syndrome?
LOWER LEG Forearm Hand Foot Thigh
(NOTE: you can get a compartment syndrome anywhere where there is a compartment -> bum, abdominal wall)
What is the effect of acute compartment syndrome?
why can it go unnoticed?
Blood vessels compressed (lowest pressure first) and blood flow stops
-Tissue (muscle) becomes ischaemic
Smallest vessels = capillaries compress first
Foot still pink warm and has pulse
Describe the two categories of patients who are at risk of acute compartment syndrome?
Trauma
- Young, fit, male
- 25% of adolescent tibial fractures have a compartment syndrome
No trauma
- Older medically unfit patients
- Greater Proportion female
Is acute compartment syndrome more frequent in high or low energy injuries?
More common in LOW energy tibial fractures as fascial compartments more likely to be intact
Can ACS occur in open fractures?
Yes, compartments will often remain intact in open fractures
What are the 9 Ps of acute compartent syndrome?
PAIN Passive Dorsiflexion Parasthesiae Paresis or Paralysis Pallor Pulselessness Perishing Cold Pressure (Prompt decompression)
Describe the pain in acute compartment syndrome
Severe (disproportionate)
Worsening
Out-growing analgesia
Deep ache, crushing/tight
Made worse by
-passive dorsiflexion of the digits of the limb
What causes parasthesiae in acute compartment syndrome?
Both direct pressure on nerve + ischaemia of nerve
If compartment syndrome goes untreated what can it lead to?
4 things
Muscle ischaemia and necrosis
Muscle contractures
Delayed fracture healing
May nessecitate limb amputation
How can you diagnose acute compartment syndrome?
Threshold for fasciotomy:
(persistent) Delta P
When is fat embolism syndrome seen?
Occurs after trauma
-Always with a fracture of a long bone (usually 24-72 hrs)
Also seen in instrumentation of long bone
-e.g. intramedullary nailing
What is the difference between fat embolism and fat embolism syndrome?
Fat within the systemic circulation that produces 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 (FES)
How common is fat embolism?
How common is fat embolism syndrome?
Evidence of fat embolism (marrow fat + debris from fracture site) in 90% of patients with traumatic injury
But only 3-4% of long bone fractures result in “fat embolism syndrome”
Give 5 risk factors for fat embolism syndrome
Long bone fractures
Conservative management of long bone fractures
Multiple trauma
Associated abdominal injuries
Severe blood loss
What is the mechanical theory of fat embolism syndrome?
Bone marrow enters venous circulation and lodges in the lungs, smaller particles penetrate pulmonary capillaries and enter arterial circulation
What is the biochemical theory of fat embolism syndrome?
Circulating fatty acids directly affect pneumocytes altering gas exchange
How do you diagnose fat embolism syndrome?
Clinical
Blood investigations:
- Hypoxia on ABGs
- Fall in haemoglobin
- Thrombocytopaenia
- Fat droplets within blood clots
CXR
What are the clinical features of fat embolism syndrome?
24-72 hours post insult
HYPOXIA!!
(PaO2
What is the organ most sensitive to hypoxia?
Brain
What is the classic triad of fat embolism syndrome?
Hypoxia (Pulmonary) Cerebral disfunction (Brain) Petechial rash (Cutaneous)
Describe the skin rash of fat embolism syndrome
60%
Petechial
Only in distribution of SVC
(chest/neck/axillae/eyes/mouth)
Fleeting - gone within 12-24h
What is the treatment for fat embolism syndrome?
No current “treatment” (i.e. cure)
```
Only supportive
-Steroids
-Dextran
-Heparin
-Ethanol
limited evidence
~~~
How do you manage fat embolism syndrome?
Aim: Maintain cerebral and pulmonary perfusion
Oxygen!
May require intensive gas and circulatory monitoring -> seen by ITU staff
If necessary:
- mechanical ventilation
- advanced circulatory support
How do you prevent fat embolism syndrome?
Immobilisation/fixation of long bone fractures
Possible role for prophylaxis with steroids?
Monitoring with pulse oximetry
