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PHM BSc - Trauma Science > Bleeding > Flashcards

Bleeding Flashcards

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1
Q

Why would someone with their bowel hanging out have a low BP?

A

vagal stimulation (or they could well be bleeding as well)

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2
Q

Why would a head injured patients have a low BP?

A

catecholaminergic surge leads to vasoconstriction. Eventually you get pump failure because of this increased afterload combined with lack of oxygen when oxygen demand is higher
+/- bleeding
+/- spinal cord injury causing neurogenic shock

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3
Q

Why do you get ST changes in SAH?

A

catecholaminergic surge leads to coronary vasospasm

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4
Q

In what situations would a patient become ‘vasoplegic’

A

Bleeding for a long time or bleeding lots of volume

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5
Q

What are some theories as to why patients become vasoplegic?

A

NA and adrenaline receptors are saturated
acidotic environment means receptors don’t work
Can no longer respond to the catecholamines so vessels go floppy

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6
Q

Theoretically why does vasopressin work better than adrenaline in bleeding?

A

Because it works in an acidotic environment

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7
Q

In haemorrhagic shock, what happens at a cellular level?

A

anaerobic metabolism leading to accumulation of various substances, a systemic inflammatory response (release of DAMPs) and cell death

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8
Q

Anaerobic metabolism occurring in haemorrhagic shock leads to what?

A

accumulation of lactic acid, inorganic phosphates and oxygen radicals
release of DAMPs leading to systemic inflammatory response
reduced ATP leading to necrosis, necroptosis and apoptosis

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9
Q

What happens at a tissue level in haemorrhagic shock?

A

hypovolaemia + vasoconstriction leads to hypoperfusion and end organ damage

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10
Q

What causes the shedding of the glycocalyx barrier?

A

oxygen debt and catecholamine surge

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11
Q

Shedding of the glycoclayx barrier leads to what?

A

vascular permeability and autoheparinization

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12
Q

What is the local haemostatic response to bleeding?

A

activation of platelets
activation of clotting cascade leading to fibrinogen conversion to fibrin
activation of endothelium

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13
Q

What is the sympathoadrenal response to bleeding?

A

vasoconstriction
glycocalyx barrier sheds = permeability
neutrophil activation

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14
Q

What is the purpose of fibrinolysis occuring at remote sites to bleeding?

A

stop microvascular thrombosis

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15
Q

What is the genetic response to bleeding?

A

up-regulated innate immunity

down-regulated adapative immunity

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16
Q

In bleeding, anaemia leads to what?

A

reduced platelet margination

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17
Q

Why is there reduced clotting factor activity in bleeding?

A

heat loss and acidosis

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18
Q

Activated protein C does what?

A 
increased fibrinolysis (inhibits the inhibiting of plasminogen to plasmin and activates tPa further increasing conversion)
inactivates factor V and VIII
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19
Q

What do cold crystalloid fluids do to your trauma patient?

What else can make iatrogenic coagulopathy worse?

A

cold crystalloid fluids = haemodilution, hypothermia and non-anion gap acidosis
+ environmental exposure

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20
Q

Why is there decreased platelet margination in bleeding?

A

anaemia

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21
Q

In bleeding, what happens to fibrinolysis and why?

A

Can go either way depending on the patient:
often become hyperfibrinolytic (excess plasmin activity + autoheparinization)
However some patients have fibrinolysis shutdown

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22
Q

What is autoheparinization and why does it happen?

A

happens following shedding of the glycocalyx barrier

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23
Q

Give examples of DAMPs

A

mitochondrial DNA

formyl peptides

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24
Q

What is the result of iatrogenic haemodilution, hypothermia and acidosis?

A

haemodilution - reduced oxygen carrying capacity and clotting factor concentration
hypothermia - reduced function of clotting cascade enzymes
non-anion gap acidosis - impaired clotting factor function and increased breakdown

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25
Q

How would you manage haemorrhage at compressible, junctional and non-compressible sites?

A

compressible - tornique or direct pressure
junctional - pack with haemostatic dressing
non-compressible - pelvic binder for example

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26
Q

Other than haemorrhage control, what other prehospital interventions are needed in a bleeding patient?

A

prevent hypothermia
limited resuscitation
rapid transport

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27
Q

state some examples of definitive haemeostasis

A

angiography with embolization
surgical exploration
endoscopic interventions

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28
Q

What are some principles of damage control resuscitation

A

control bleeding (direct pressure/haemostatic dressings)
prevent hypothermia
withold fluids until definitive haemostasis
max 3L in first 6 hours of isotonic crystalloids
massive transfusion protocol
platelets:packed red cells:FFP 1:1:1
pharmacological adjuncts to address coagulopathy

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29
Q

In which bleeding patients should fluid administration be delayed?

A

penetrating torso injury in close proximity to a hospital

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30
Q

What ratio of blood products should be used in trauma?

A

platelets: plasma: red cells
1: 1:1

31
Q

In a non-trauma bleeding patient, what ratio of blood products should be used?

A

platelets: red cells
1: 2

32
Q

State some diagnostic tools and investigations used in traumatic bleeding

A

FAST scan
blood gas with lactate
coagulation studies
thromboelastography

33
Q

What is the maximum volume of isotonic crystalloid that should be given over what time frame?

A

<3L in the first 6 hours

34
Q

Other than haemodilution, acidosis and hypothermia, what other complications can isotonic crystalloid cause?

A

respiratory failure

compartment syndrome

35
Q

What complications can citrate (an anticoagulant) cause?

A

the body can’t metabolise it in haemorrhage so it builds up leading to hypocalcaemia and progressive coagulopathy

36
Q

When might you use activated recombinant factor VII?

A

haemophillia patient

37
Q

When might you use prothrombin complex concentrate

A

warfarin patient

38
Q

After 4 units of blood, what additional product is needed and why

A

IV calcium chloride - prevent citrate induced hypocalcaemia

39
Q

When is a major haemorrhage protocol activated?

A 
clinical judgement
\+/-
SPB <90 
HR >110
likely to need >4 units RBC
40
Q

What is a massive transfusion?

A

> 10 units Packed RBC within 24 hours

41
Q

What are some flaws in the “massive transfusion” definition?

A

doesn’t consider other blood products
survival bias - if you die before reaching 10 units you don’t meet definition
time frame is too long - bleeding at hour 24 is likely surgical not from the initial trauma
retrospective definition - need to act quick not only when they meet the definition at hour 24

42
Q

What is a major transfusion?

A

> 4 units Packed RBC within 3 hours

43
Q

What is the critical administration threshold?

A

> 3 units packed RBC within an hour

44
Q

What is the resuscitation intensity?

A

sum of all products (blood and fluid) given within the first 30 minutes of resuscitation
1 unit = 1 unit of blood products, 1L crystalloid, 500ml colloid

45
Q

4 principles of DCR?

A

haemorrhage control
permissive hypotension
blood products for volume resuscitation
target coagulopathy

46
Q

What is “whole blood”?

A

RBC and plasma (platelets are removed when the product is leukodepleted)

47
Q

When is the RLH code red activated?

A

SBP < 90 + suspected active haemorrhage

48
Q

What is contained in code red pack A

A

4 units RBC

4 units plasma (FFP)

49
Q

What baseline bloods are taken before a transfusion?

A

G&S, blood gas, FBC, ROTEM

50
Q

How much TXA is given and when?

A

1g over 10 minutes if within the first 3 hours

51
Q

If bleeding continues after code red pack A, what other products should be ordered?

A

6 units RBC
6 units FFP
2 pools cryoprecipitate
1 pool platelets

52
Q

Target K and Ca during resuscitation

A

K <5.8

Ca >1

53
Q

define trauma induced coagulopathy

A

failure of haemostasis due to the endogenous acute traumatic coagulopathy combined with effects of resuscitation efforts

54
Q

what 2 factors combined lead to a severe coagulopathy?

A 
high ISS
base deficit (which indicates tissue hypoperfusion)
55
Q

Why are blood test results not useful when assessing coagulopathy?

A

coagulation factors have to be down to 30% of normal before the derrangements is reflected in results

56
Q

How do trauma and shock lead to ATC? What else is involved?

A

trauma = increased thrombin, hyperfibrinolysis and reduced fibrin
shock = hyperfibrinolysis and platelet dysfunction
+aPC is involved

57
Q

What is different in terms of clotting factor derangements in ATC compared to DIC?

A

In DIC there is global derangements
In ATC it is specific: 2 (prothrombin) and 5 fall, factors involved in fibrinolysis are upregulated and aPC more than doubles

58
Q

Which factors are involved in fibrinolysis?

A

D-dimer
tPa
PAP

59
Q

Why do fibinogen levels fall?

A

used up in forming the clot
acidotic environment increases its breakdown
hypothermia stops it from being formed

60
Q

When and how is protein C activated?

A

when the endothelium is damaged thrombomodulin binds to thrombin (which is subsequently removed from its normal role in clotting cascade) and activates protein C

61
Q

What does activated protein C lead to?

A

inhibits factor V and VIII

increases fibrinolysis by increasing tPA which catalysis plasminogen to plasmin which breaks down fibrin

62
Q

What are the axis on a viscoelastic testing results graph

A

x - time (minutes)

y - clot amplitude (mm)

63
Q

How does the viscoelasting testing graph differ in a patient with ATC?

A

longer clot initiation phase (longer for curve to flatten out)
reduced clot amplitude

64
Q

Why is coagucheck (prothrombin time) not suitable for diagnosing coagulopathy in trauma?

A

lack of haematocrit in trauma. This test is for warfarin patients

65
Q

What is the alpha angle on a viscoelastic testing graph?

A

It is the rate of rise of curve (platelets and fibrinogen reacting together to form a clot)

66
Q

What does the height reached by the viscoelastic testing graph indicate?

A

maximum clot firmness

67
Q

Describe what hyperfibrinolysis would look like on a viscoelastic testing results graph

A

dissolution of the clot quicker i.e the curve drops back to a thin line

68
Q

describe very simply how coagulation changes over time in a trauma patient

A

hypocoaguable to hypercoagulable

69
Q

What are some theories as to why the American study found TXA to be associated with increased thromboembolic risk?

A

Patients receiving TXA were…
More obese patients
Patients had less VTE prophylaxis
More had penetrating trauma

70
Q

What resuscitation factors lead to trauma induced coagulopathy (what’s the lethal triad)

A

haemodilution
acidaemia
hypothermia

71
Q

What was the conclusion of the PROMT study

A

increased ratio of platelets:RBC and plasma:RBC decreased 6 hour mortality
early transfusion of platelets and plasma increases survival

72
Q

What was the conclusion of the PROPPR study

A

platelets:plasma:RBC in a ratio of 1:1:1 decreased deaths due to exsanguination
however
1:1:1 vs 1:1:2 didn’t make a difference to 24hr or 30 day mortality

73
Q

What was the conclusion of cryostat1

A

early cryoprecipitate maintained fibrinogen levels during active bleeding

74
Q

What blood should be given to females and why?

A

o neg

to prevent anti-d reaction if the women is pregnant

PHM BSc - Trauma Science (15 decks)

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