Severe Bleeding Max Marsden Flashcards

(52 cards)

1
Q

What antibodies are in the plasma of a group A B AB and O patient

A

A - anti B
b - anti A
AB - none
O - anti a + anti b

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2
Q

What were the first blood groupings called

A

A b c

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3
Q

When was the first wartime transfusion

A

Oct 1915
Lawrence Robertson performed w a syringe to a pt w multiple shrapnel wounds

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4
Q

Lethal trias

A

Acidosis
Hypothermia
Coagulopathy

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5
Q

What did borgman 2007 investigate and what did he find

A

Investigated 1:8 vs 1:2.5 vs 1:1.4 plasma:RBC ratio blood products and their effects on mortality according
Lower mortality in higher RBC:plasma ratio

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6
Q

PROMMTT trial 2013

A

Prospective observational multicentre major trauma transfusion
Higher plasma:RBC and platelet:RBC assoc w lower 6 hour mortality

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7
Q

PROPPR trial

A

Prospective randomised optimum platelet and plasma ratios
Compared plasma platelet and RBC transfusion in a 1:1:1 and 1:1:2 ratio
No difference

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8
Q

TROOP trial

A

Trauma resuscitation with group o whole blood or products
Low titre group o whole blood vs standard therapy in critically injured patients requiring large volume transfusion

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9
Q

SWiFT trial

A

Study of whole blood in frontline trauma
PH whole blood transfuasion vs standard therapy for clinical and cost effectiveness

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10
Q

REPHILL

A

Resuscitation with pre hospital blood products
No effectively

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11
Q

Did plasma increase or decrease 30 day mortality compared to standard resuscitation in a 2018 trial with patients at risk for Haemorrhagic shock

A

Decrease

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12
Q

When does prehospital plasma have a survival benefit

A

When transport times are longer than 20 mins

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13
Q

Primary outcomes of REPHIL

A

Lactate clearance
Episode mortality

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14
Q

Swift intervention and control

A

Intervention 2 units whole blood
Control 2 units RBC + 2 units plasma

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15
Q

Main cause of preventable death after injury

A

Bleeding

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16
Q

Shock

A

Inadequate oxygen delivery at the cellular level

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17
Q

Haemorrhagic shock

A

Severe blood loss leads to inadequate oxygen delivery at the cellular level

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18
Q

Cellular level pathophysiological of Haemorrhagic shock

A

Insufficient o2 delivery -> anaerobic metabolism
incr lactic acid, phosphates, and o2 radicals
DAMPs release -> systemic inflam
Decr ATP -> cell necrosis

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19
Q

DAMPs

A

Damage associated molecular patterns
Mitochondrial DNA, formyl peptides

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20
Q

Tissue level pathophysiology of Haemorrhagic shock

A

Hypovol and vasocontriction -> hypoperfusion
End organ damage
Multiorgan failure in survivors
Hypoperfusion of brain and myocardium -> cerebral anoxia and fatal arrhythmias

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21
Q

How does haemorrhage affect the endothelium

A

Mounting oxygen debt and hypoperfusion -> endotheliopathy (systemic shedding of glycocalyx barrier) -> Endogenous heparinisation

22
Q

Massive transfusion

A

10+ PRBCs within 24 hours

23
Q

Advantages and disadvantages of defining ‘massive transfusion’

A

Adv - early identification of pts needing large volumes, mobilise resources early, improve outcomes
Disadvantages - antiquated, arbitrary, survival bias

24
Q

Critical administration threshold

A

3+ PRBCs during any 1 hour period in the first 24 hours/ first hour of resus

25
Resuscitation intensity
All fluid and blood products within the first 30 mins of resus
26
Disadvantage of the 4 classes of Haemorrhagic shock
Inaccurate in large databases of pts
27
Aims of damage control resus
Early haemorrhage control Permissive hypotension Blood products for volume resus Target coagulopathy
28
Principles of DCR
Direct pressure, tourniquets, pack wounds w haemostatic dressings Delay fluids until definitive haemostasis if possible Massive transfusion protocol Abtain functional lab measures of coagulation Avoid/correct hypothermia Minimise crystalloids Minimise imbalances in plasma, platelets and RBCs Reverse anticoagulant meds and address coagulopathy
29
Major haemorrhage protocol
Multi modal package of care that rapidly provides standard iOS ed elements of medical treatment to patients with life threatening haemorrhage Treat empirically without waiting for results
30
MHP activation criteria
Vary by institution Usually vital signs, lab data, and physician digression NICE: MOI, pt physiology, anatomical injury, pt response to initial resus
31
Code red
Major haemorrhage protocol initiated prehospitally Included in hospital procedures - surgery, blood bank
32
Code red criteria
Suspicion or evidence of active haemorrhage SBP <90 Failure of bp to respond to IV fluid bolus
33
Disadvantages of previous definitions of massive blood loss such as ‘loss of 1§ blood volume in a 24 hour period’
Retrospective so prevents early recognition
34
Who should activate code red
Most senior doctor at the scene
35
RLH code red criteria
Haemodynamically unstable due to rapid and continuous blood loss Ongoing blood loss likely to need 4+ units RBCs HR 110+ and/or SBP <90
36
Should o neg or o pos blood be used initially
Female o neg Male o pos
37
What is in a code red pack
6u RBC 6u FFP 2 pools cryoprecipitate 1 pool platelets
38
BASTE
Blood Acid base Surgical progress Temperature Electrolytes
39
Shapes of normal, coagulopathicm and hyperfibrinolytiuc ROTEM
Normal - wine glass Coagulopathic - champagne flute (narrow) Hyperfibronlytic - rounded (puffer fish)
40
What complication is more likely if more crystalloids are given in initial resus
MODS
41
Why should crystalloids be avoided in trauma resus
Incr MODS risk Dilute clotting factors and platelets causing coagulopathy Cause acidosis Hypothermia
42
How does saline affect acid base balance
Ph of normal saline is 5.0 causing acidosis Leads to coagulopathy as clotting enzymes denature
43
Why are Plasmalyte and Hartman’s better than normal saline for trauma
Closer to ph 7
44
PAMPER
Mortality at 30 days sig lower in plasma group than crytsalloid pts
45
RCTs investigating use of whole blood
TROOP SWiFT
46
Trimodal distribution of death
1st 3 hrs - bleeding First 5 days - head injury First wk - multiple organ failure
47
Occult haemorrhage
Pt compensated until dying
48
2 phases of Hypovolaemic shock
Tachycardia Reflex bradycardia (can be mistaken for improvement, periarrest sign)
49
How does Haemorrhagic shock lead to endogenous heparinisation
O2 debt and hypoperfusion causes shedding of glycocalix barrier (endotheliopathy) Heparin is part of glycocalix barrier
50
Max time for permissive hypotension
1 hour
51
Code red
SBP <90 + suspected active haemorrhage protocol initiated
52
ROTEM
ROTational ThromboElastoMetry Viscohaemoelastic assay