Bleeding Flashcards
Why would someone with their bowel hanging out have a low BP?
vagal stimulation (or they could well be bleeding as well)
Why would a head injured patients have a low BP?
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
Why do you get ST changes in SAH?
catecholaminergic surge leads to coronary vasospasm
In what situations would a patient become ‘vasoplegic’
Bleeding for a long time or bleeding lots of volume
What are some theories as to why patients become vasoplegic?
NA and adrenaline receptors are saturated
acidotic environment means receptors don’t work
Can no longer respond to the catecholamines so vessels go floppy
Theoretically why does vasopressin work better than adrenaline in bleeding?
Because it works in an acidotic environment
In haemorrhagic shock, what happens at a cellular level?
anaerobic metabolism leading to accumulation of various substances, a systemic inflammatory response (release of DAMPs) and cell death
Anaerobic metabolism occurring in haemorrhagic shock leads to what?
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
What happens at a tissue level in haemorrhagic shock?
hypovolaemia + vasoconstriction leads to hypoperfusion and end organ damage
What causes the shedding of the glycocalyx barrier?
oxygen debt and catecholamine surge
Shedding of the glycoclayx barrier leads to what?
vascular permeability and autoheparinization
What is the local haemostatic response to bleeding?
activation of platelets
activation of clotting cascade leading to fibrinogen conversion to fibrin
activation of endothelium
What is the sympathoadrenal response to bleeding?
vasoconstriction
glycocalyx barrier sheds = permeability
neutrophil activation
What is the purpose of fibrinolysis occuring at remote sites to bleeding?
stop microvascular thrombosis
What is the genetic response to bleeding?
up-regulated innate immunity
down-regulated adapative immunity
In bleeding, anaemia leads to what?
reduced platelet margination
Why is there reduced clotting factor activity in bleeding?
heat loss and acidosis
Activated protein C does what?
increased fibrinolysis (inhibits the inhibiting of plasminogen to plasmin and activates tPa further increasing conversion) inactivates factor V and VIII
What do cold crystalloid fluids do to your trauma patient?
What else can make iatrogenic coagulopathy worse?
cold crystalloid fluids = haemodilution, hypothermia and non-anion gap acidosis
+ environmental exposure
Why is there decreased platelet margination in bleeding?
anaemia
In bleeding, what happens to fibrinolysis and why?
Can go either way depending on the patient:
often become hyperfibrinolytic (excess plasmin activity + autoheparinization)
However some patients have fibrinolysis shutdown
What is autoheparinization and why does it happen?
happens following shedding of the glycocalyx barrier
Give examples of DAMPs
mitochondrial DNA
formyl peptides
What is the result of iatrogenic haemodilution, hypothermia and acidosis?
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
How would you manage haemorrhage at compressible, junctional and non-compressible sites?
compressible - tornique or direct pressure
junctional - pack with haemostatic dressing
non-compressible - pelvic binder for example
Other than haemorrhage control, what other prehospital interventions are needed in a bleeding patient?
prevent hypothermia
limited resuscitation
rapid transport
state some examples of definitive haemeostasis
angiography with embolization
surgical exploration
endoscopic interventions
What are some principles of damage control resuscitation
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
In which bleeding patients should fluid administration be delayed?
penetrating torso injury in close proximity to a hospital
What ratio of blood products should be used in trauma?
platelets: plasma: red cells
1: 1:1
In a non-trauma bleeding patient, what ratio of blood products should be used?
platelets: red cells
1: 2
State some diagnostic tools and investigations used in traumatic bleeding
FAST scan
blood gas with lactate
coagulation studies
thromboelastography
What is the maximum volume of isotonic crystalloid that should be given over what time frame?
<3L in the first 6 hours
Other than haemodilution, acidosis and hypothermia, what other complications can isotonic crystalloid cause?
respiratory failure
compartment syndrome
What complications can citrate (an anticoagulant) cause?
the body can’t metabolise it in haemorrhage so it builds up leading to hypocalcaemia and progressive coagulopathy
When might you use activated recombinant factor VII?
haemophillia patient
When might you use prothrombin complex concentrate
warfarin patient
After 4 units of blood, what additional product is needed and why
IV calcium chloride - prevent citrate induced hypocalcaemia
When is a major haemorrhage protocol activated?
clinical judgement \+/- SPB <90 HR >110 likely to need >4 units RBC
What is a massive transfusion?
> 10 units Packed RBC within 24 hours
What are some flaws in the “massive transfusion” definition?
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
What is a major transfusion?
> 4 units Packed RBC within 3 hours
What is the critical administration threshold?
> 3 units packed RBC within an hour
What is the resuscitation intensity?
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
4 principles of DCR?
haemorrhage control
permissive hypotension
blood products for volume resuscitation
target coagulopathy
What is “whole blood”?
RBC and plasma (platelets are removed when the product is leukodepleted)
When is the RLH code red activated?
SBP < 90 + suspected active haemorrhage
What is contained in code red pack A
4 units RBC
4 units plasma (FFP)
What baseline bloods are taken before a transfusion?
G&S, blood gas, FBC, ROTEM
How much TXA is given and when?
1g over 10 minutes if within the first 3 hours
If bleeding continues after code red pack A, what other products should be ordered?
6 units RBC
6 units FFP
2 pools cryoprecipitate
1 pool platelets
Target K and Ca during resuscitation
K <5.8
Ca >1
define trauma induced coagulopathy
failure of haemostasis due to the endogenous acute traumatic coagulopathy combined with effects of resuscitation efforts
what 2 factors combined lead to a severe coagulopathy?
high ISS base deficit (which indicates tissue hypoperfusion)
Why are blood test results not useful when assessing coagulopathy?
coagulation factors have to be down to 30% of normal before the derrangements is reflected in results
How do trauma and shock lead to ATC? What else is involved?
trauma = increased thrombin, hyperfibrinolysis and reduced fibrin
shock = hyperfibrinolysis and platelet dysfunction
+aPC is involved
What is different in terms of clotting factor derangements in ATC compared to DIC?
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
Which factors are involved in fibrinolysis?
D-dimer
tPa
PAP
Why do fibinogen levels fall?
used up in forming the clot
acidotic environment increases its breakdown
hypothermia stops it from being formed
When and how is protein C activated?
when the endothelium is damaged thrombomodulin binds to thrombin (which is subsequently removed from its normal role in clotting cascade) and activates protein C
What does activated protein C lead to?
inhibits factor V and VIII
increases fibrinolysis by increasing tPA which catalysis plasminogen to plasmin which breaks down fibrin
What are the axis on a viscoelastic testing results graph
x - time (minutes)
y - clot amplitude (mm)
How does the viscoelasting testing graph differ in a patient with ATC?
longer clot initiation phase (longer for curve to flatten out)
reduced clot amplitude
Why is coagucheck (prothrombin time) not suitable for diagnosing coagulopathy in trauma?
lack of haematocrit in trauma. This test is for warfarin patients
What is the alpha angle on a viscoelastic testing graph?
It is the rate of rise of curve (platelets and fibrinogen reacting together to form a clot)
What does the height reached by the viscoelastic testing graph indicate?
maximum clot firmness
Describe what hyperfibrinolysis would look like on a viscoelastic testing results graph
dissolution of the clot quicker i.e the curve drops back to a thin line
describe very simply how coagulation changes over time in a trauma patient
hypocoaguable to hypercoagulable
What are some theories as to why the American study found TXA to be associated with increased thromboembolic risk?
Patients receiving TXA were…
More obese patients
Patients had less VTE prophylaxis
More had penetrating trauma
What resuscitation factors lead to trauma induced coagulopathy (what’s the lethal triad)
haemodilution
acidaemia
hypothermia
What was the conclusion of the PROMT study
increased ratio of platelets:RBC and plasma:RBC decreased 6 hour mortality
early transfusion of platelets and plasma increases survival
What was the conclusion of the PROPPR study
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
What was the conclusion of cryostat1
early cryoprecipitate maintained fibrinogen levels during active bleeding
What blood should be given to females and why?
o neg
to prevent anti-d reaction if the women is pregnant
