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Musculoskeletal > fractures and dislocations > Flashcards

fractures and dislocations Flashcards

1
Q

difference between closed and open fracture

A

higher risk of infection

higher energy of injury

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2
Q

determinants of classification

A

mechanism and velocity
degree of soft tissue damage
fracture configuration
degree of contamination

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3
Q

open fractures gustilo grading

A

type 1- low energy, wound<1cm clean, often bone piercing skin from inside
type 11- moderate soft tissue damage, wound<10cm, no soft tissue flap or avulsion
type III-high enegy, extensive soft tissue damage, severe fracture,any gunshot, farm accident, bone loss, severe crush injury
-IIIA soft tissue damage+++ but not grossly containated
IIIB periosteal stripping, extensive muscle damage, heavy contamination
-IIIC assoc neurovascular complication

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4
Q

type IIIB

A

common,

require flap cover

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5
Q

management

A 
tetanus, antibiotic prophylaxis
cover stabilise limb
surgery
early and thorough wound excision
do not close wound-leave skin open
review
fasciotomies
radiographs
early definitive skin cover
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6
Q

definitive management

A

gustilo grades I-IIIA
same for closed fracture
IIB
external fixation to allow plastic surgery
IIIC- external fixator or primary amputation

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7
Q

decision to amputate

A

duration of ishaemia

nerve damage

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8
Q

surgical debridement and fixation

A 
colour
contraction 
consistency
capacity to bleed
 4C
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9
Q

MESS scoring system for amputation

A 
skeletal soft tissue injury
limb ischaemia
shock
age
scores> 7 predict low limb liability
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10
Q

dislocation

A

complete joint disruption

subluxation- partial dislocation

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11
Q

common dislocation

A 
shoulder 
Ant: squared off
Post: locked in internal rotation
Elbow
post- olecrannon prominent post
Hip
post: leg short flexed, internal rotation
knee
Anteropost extended
ankle
Lateral externally rotated
subtalar joints
lateral displaced os calcis
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12
Q

complex regional pain syndrome type1

A 
aetiology
trauma
surgery
infection
repetitive motion dis
IHD, MI
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13
Q

incidence

A

after peripheral nerve injury
after colles fracture
higher in women

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14
Q

CRPS 1

A 
Pain
Oedema
Reduced ROM
Temperature colour changes
PORT
-extremity
-disproportionate to inciting event
-aggravated by activity
pain-severe
swolen +++, skin shiny, discoloured,hot
bone osteoporotic +++
joints osteoarthritic+++
muscles wasted
reduced NA levels
Alpha adrenocepter density increased
skin lactate increase
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15
Q

allodynia

A

painful response to innocuous stimuli

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16
Q

treatment

A 
early active movement +++
regular analgesia and supervised physio
encourage normal use of limb
determine contribution of sympa nervous system
prevention
17
Q

Pharmacological Therapy

A 
Traditional analgesics
Tricyclic antidepressants
Gabapentin (other anticonvulsants)
Glucocorticoids
Transdermal clonidine
Intravenous bisphosphonates
18
Q

Summary

A

Definition : Complex Regional Pain Syndrome

Recognition : PORT (sensitive but not specific)

Diagnosis : Clinical versus laboratory

Management: Early, medication, diagnostic blocks
functional restoration

19
Q

Crush syndrome

A

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 the kidneys) ARF (acute renal failure)

20
Q

clinical features

A

dark amber urine(test for Hb and Mb)

acute renal failure(hypovolaemia, metabolic acidoses, hyperkalaemia, hypocalcaemia, DIC)

21
Q

management

A

IV fluids +++
early (protect kidney & prevent ARF)
Fluid expansion + osmotic diuresis (to maintain high tubular volume + urine flow – aim
-alkalisation of urine with sodium bicarbonate-> reduce tubular precipitation of myoglobin

22
Q

acute compartment syndrome

A 
Limb-threatening
HIGH INDEX OF SUSPICION!
Key pathology = ISCHAEMIA!
after trauma
also in vascular reperfusion of acutely ischaemic limb
burns
crush injuries
haemorrhage
drug injection
23
Q

definition

A

A compartment syndrome develops when intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment.
A compartment syndrome develops when intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment.

24
Q

at risk sites

A 
lower leg
forearm
hand
foot
thigh
25
Q

acute compartment syndrome

A

more common in low energy tibial fractures as fascial compartments more likely to be intact
ACS occurs in open fractures as compartments will often remain intact

26
Q

acute compartment syndrome 9ps

A
  1. PAIN
  2. Passive dorsiflexion
  3. Paraesthesiae
  4. Paresis or Paralysis
  5. Pallor
  6. Pulselessness
  7. Perishing cold
  8. Pressure
  9. (Prompt decompression
27
Q

missed compartment syndrome

A 
If untreated leads to:
Muscle ischaemia and necrosis
Muscle contractures
Delayed fracture healing
May nessecitate limb amputation
28
Q

ACS

A

if hypotensive, lower BP needed to produce ACSpatient with multiple trauma (incl. limb injuries) + hypovolaemic shock – may be in ITU paralysed and ventilated – therefore lost most important criteria for diagnosis of ACS

29
Q

fat embolism syndrome

A

HIGH INDEX OF SUSPICION!
Occurs after trauma – always with a fracture of a long bone – usually 24-72h
Also seen in instrumentation of long bone, e.g. intramedullary nailing
Key pathology = HYPOXIA!

30
Q

definition

A

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)
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’

31
Q

risk factors

A 
long bone fractures
conservative management of long bone fractures
multiple trauma
associated abdominal injuries
severe blood loss
32
Q

pathophysiology

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 pneumocytes altering gas exchange

33
Q

diagnosis

A

Clinical

	- Blood Investigations
		- Hypoxia on ABGs
		- Fall in haemoglobin
		- Thrombocytopaenia
		- Fat droplets within blood clots
	- CXR
34
Q

clinical features

A 
Brain = most sensitive organ to hypoxia
Confused/agitated  fits  drowsy  coma  dead
Tachypnoeic + tachycardic
Shock (hypotensive) – late
Fever – low grade pyrexia
Skin rash
35
Q

investigations

A 
Chest X-ray - serial
Oxygen saturations + blood gases (PaO2)
FBC – Hb + platelets  (thrombocytopenia <150)
(Fat globules in blood clots) 
(Fat globules in sputum)
(Fat globules in urine - “sizzle test”
36
Q

FAT EMBOLISM SYNDROME

A

Pulmonary circulation – HYPOXIA
Cerebral circulation – CONFUSION
Cutaneous circulation – PETECHIAE
Paradoxical embolisation through patent Foramen ovale

37
Q

treatment

A

There is no current “Treatment” (i.e. cure)
only SUPPORTIVE MANAGEMENT
maintain cerebral and pulmonary perfusion.

OXYGEN!!

may require intensive gas and circulatory monitoring – therefore should be seen by ITU staff
if necessary – mechanical ventilation
– advanced circulatory support

38
Q

prevention

A

PREVENTION

 	- immobilisation/fixation of long bone fractures
	- possible role for prophylaxis with steroids?
	- monitoring with pulse oximetry

Musculoskeletal (28 decks)

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