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Fellowship revision > Trauma, major haemorrhage, trauma-induced coagulopathy and viscoelastic testing + blue book 2019 MTP article > Flashcards

Trauma, major haemorrhage, trauma-induced coagulopathy and viscoelastic testing + blue book 2019 MTP article Flashcards

1
Q

What proportion of potentially preventable trauma deaths is due to major haemorrhage?

A

> 50%

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2
Q

In what proportion of trauma patients, on arrival to hospital, does trauma-induced coagulopathy present?

A

30%

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3
Q

What are at least 2 distinct mechanisms responsible for trauma-induced coagulopathy?

A
  1. Acute traumatic coagulopathy (endogenous heparinisation, activation of protein C pathway, hyperfibrinolysis & platelet dysfunction)
  2. Resuscitation-associated coagulopathy (clear fluid resus w crystalloids & colloids- associated with poor outcome)
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4
Q

What are the principles of management of trauma resuscitation?

A

a) Haemostatic resuscitation
b) ratio-driven product replacement (1:1:1 rbc, plasma & platelets)
c) goal-directed therapy with use of viscoelastic haemostat assays, early & repeatedly

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5
Q

In what tests does endogenous heparinisation show up?

A

prolonged PTT or APTT or in the VHAs as RT or CT

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6
Q

How does endogenous heparinisation occur? In what conditions, other than acute traumatic coagulopathy, is it seen?

A

Endotheliopathy- shedding of the endothelial glycocalyx- releasing endogenous heparins & other factors with heparin-like activity. Also seen in OOHCA, MI & sepsis.

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7
Q

What’s the most potent form of endogenous anticoagulation?

A

Hyperfibrinolysis

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8
Q

How does hyperfibrinolysis occur?

A

Endothelial damage causes release of tissue-type plasminogen activator (tPA), causing premature resolution of a formed clot

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9
Q

What does activated protein C do?

A

Inhibits thrombin formation & promotes fibrinolytic activity. Also antiinflammatory & antiapopotic.

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10
Q

How might platelet transfusion be particularly useful early in trauma resus?

A

Platelet dysfunction is part of acute TIC & platelets contain Plasminogen Activator Inhibitor 1 (PAI-1)

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11
Q

What’s the “lethal triad”?

A

Hypothermia, acidosis & dilutional coagulopathy

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12
Q

What do hypothermia & acidosis do to fibrinogen?

A

hypothermia inhibits fibrinogen synthesis & acidosis accelerates fibrinogen degradation

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13
Q

What does hypothermia do to coagulation?

A

depletes fibrinogen levels, induces fibrinolysis, impairs coagulation factor activity & induces platelet dysfunction

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14
Q

What does acidosis do to coagulation?

A

Impairs almost all parts of haemostat process, eg. changing platelet structure/shape, reducing activity of coagulation factor complexes, accelerate fibrin degradation

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15
Q

Why does even blood induce coagulopathy?

A

anticoagulants & the fluids in blood accelerate coagulopathy

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16
Q

What haematocrit, coagulation factors [] & platelet count result from 1:1:1 resus?

A

30%, 60% & 80 x 10^9

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17
Q

What are some negatives of colloids?

A

make the clot more porous, increase bleeding & transfusion requirements

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18
Q

When should clear fluids be used in severely bleeding trauma pts?

A

pre-hospital. in-hospital ONLY if blood products n/a

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19
Q

What were the findings of PROPPR RCT (2015)?

A

most robust data to date, basis of empiric ratio-driven guidelines

compared plasma:plt:rbc 1:1:1 to half-dose plasma & platelets (1:1:2) in trauma pts w haemorrhagic shock.

First group (1:1:1) had more pts w earlier haemostasis, fewer deaths due to exsanguination at 24hrs or early mortality (3hr) & lower transfusion rates but mortality wasn’t sig reduced @ 24hrs or 30 days. Pts in the 1:1:2 group received more transfusions after the intervention, particularly cryo, which may have diluted the Rx effect of the 1:1:1 group.

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20
Q

What are the benefits of VHA goal-directed therapy?

A

use less rbc/plasma/plts, reduce bleeding & improve mortality in mixed surgical populations

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21
Q

What should be given as soon as signs of hyperfibrinolysis in an actively bleeding patient?

A

TxA- reduced efficacy with later administration

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22
Q

What’s a significant finding of the CONTROL trial?

A

Recombinant Factor VIIa shows potential reduction in transfusion in trauma BUT no impact on other outcomes & increased risk thromboembolic complications

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23
Q

What did CRASH-2 show?

A

TxA decreased mortality in trauma

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24
Q

What’s a concern with prothrombinex?

A

High [] of factors II, VII, IX & X has potential to increase endogenous thrombin potential several days after trauma where thromboembolic complications dominate

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25
Q

What’s the flow rate through a 20g IVC? 18g? 16g? 8.5Fr CV sheath?

A

150mL/min
230mL/min
430mL/min
1L/min

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26
Q

What’s haemostatic resuscitation?

A

Process of restoring & sustaining normal tissue perfusion in pts w uncontrolled haemorrhagic shock, w emphasis on preserving effective clotting

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27
Q

Sequence of response for massive haemorrhage:

A
  • call for help, communicate & delegate
  • rapid Ax of bleeding, apply damage control resus (ensure surg effort to control bleeding- prompt them to allow catch up) & early blood products, consider early activation of MHP & communicating w lab re: whether ROTEM guided, contact haematologist/ICU for assistance
  • review airway, consider intubation & incr FiO2 to maintain adequate SpO2
  • ensure 2x large-bore IVC, consider 8.5Fr CVC
  • art line
  • use rapid infusers & cell saver but avoid fluid overload
  • MAP >=65mmHg (>=80mmHg in head injury) (vasopressors only to allow organ perfusion, permissive hypotension tolerated
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28
Q

What’s the STOP handover for major trauma?

A

Used @ my institution, any pt transferred from paramedics or ED to OT, <60 secs handover while no-one touches the pt, allowing trauma TL, surgeon & anaesthetist to state their priorities so the preceding time is focused & priority driven.
TL: reason for OT transfer, pts immediate requirements, Mechanism/medical complaint, Injuries sustained/illness identified, Signs & symptoms, Treatments
Surgeons: pt position, extra personnel/equipment
Anaes: pre-induction procedures or resus requirements

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29
Q

What are the indications for MHP?

A

Active bleeding +

  • 4 units in <4hrs + haemodynamic instability
  • EBL >2.5L
  • clinical or lab signs of coagulopathy
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30
Q

How is TxA given during MHP? (dose & over how long?)

A

1g over 10 mins

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31
Q

What are the targets during MHP?

A 
Temp>35 deg C (warm fluids, warm OT, warm pt)
pH >7.2
BE -6 to +6
Lactate <4mmol/L
Ionised Ca++ >1.1mmol/L
Hb >80g/L
Normal ROTEM
Plt >50 x 10^9/L (>100 if intracranial haemorrhage/ongoing bleeding)- while it's often a qualitative vs quantitative platelet issue
PT <1.5x normal
APTT <50
INR <=1.5
Fibrinogen >2.5g/L
MAP >= 65- use vasopressors only to maintain vital organ perfusion
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32
Q

When are ROTEM/TEG re-checked?

A

10 mins after components

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33
Q

For massive haemorrhage in a head-injured pt, what MAP target?

A

> =80mmHg

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34
Q

What blood given if no time for crossmatch?

A

O neg or group specific

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35
Q

What’s a definition of massive transfusion?

A

> 1 blood vol (or 10+ units rbc) over 24hrs or >0.5 blood vol (or 5+ units packed red cells) over <4hrs

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36
Q

What does cryo mainly contain? Dose?

A

factors VIII, XIII, vWF, fibrinogen, fibronectin

1 unit per 5-10kg

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37
Q

What does FFP contain? dose?

A

all coag factors incl labile V, VIII, fibrinogen & vWF

15mL/kg

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38
Q

What are the doses of fib conc & prothrombinex?

A

25-50mg/kg & 25-50IU/kg, respectively

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39
Q

What do ROTEM and TEG stand for?

A

rotational thromboelastography

thromboelastography

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40
Q

How would you describe hypercoaguability in terms of viscoelastic tests?

A

accelerated clot formation, clot strength & reduced fibrinolysis

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41
Q

Is SARS-CoV-2 thought to be transfusion transmissible?

A

No- although the blood phases of infection hasn’t been fully characterised, it’s associated with low or absent viral RNA in blood so blood donors aren’t required to undergo SARS-CoV-2 RNA screening.

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42
Q

are SARS-CoV and MERS-CoV transfusion-transmissible?

A

No

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43
Q

What are the intended benefits of MTP & what has been the impact of MTP on trauma outcomes & blood product usage?

A

A cognitive aid to focus team on timing of initiation for blood product transfusion & optimal ratios
Rapid haemostat resuscitation (treating & preventing coagulopathy), maintain organ perfusion & O2-carrying capacity, minimise delays & wastage

Has improved outcomes (reduced early mortality, reduced incidence of multi-organ failure)
reduction in number of blood products & complications

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44
Q

What’s a massive transfusion?

A

5 or more units of packed red blood cells in <4hrs or 10 or more units of packed red cells in 24hrs

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45
Q

What proportion of civilian trauma pts receive a massive transfusion?

A

3-5%

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46
Q

What are the indications to initiate a MTP?

A

Actual or anticipated 5 or more units packed red cells in <4hrs + haemodynamic instability + ongoing bleeding anticipated

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47
Q

What are the indications to initiate a MTP?

A

Actual or anticipated 5 or more units packed red cells in <4hrs + haemodynamic instability + ongoing bleeding anticipated

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48
Q

What’s in the Gold Coast Non-rotem MTP packs?

A

Pack 1: 4 units red cells, 4 units FFP, 10 units cryo

Pack 2: 4 units rbc, 4 FFP, 1 platelets

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49
Q

When to repeat ROTEM?

A

10 mins after each blood product intervention and ?after every 4 units packed red cells or every 30-60mins

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50
Q

When may fibrinogen concentrate be considered in trauma? dose?

A

FIBTEM A5 <=10mm OR critical life-threatening haemorrhage OR high clinical suspicion of coagulopathy- consultant approval- 1g/25kg BW (4g empirically adult)

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51
Q

How should TxA be given? how many doses?

A

1g over 10 mins

can consider a 2nd dose with MTP pack 2 if bleeding not yet controlled- 1g over 8hrs or 2nd bolus IVI

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52
Q

How does MTP proceed (standard protocol) after 2nd pack?

A

alternate pack 1 & 2

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53
Q

Emergency warfarin reversal?

A

vit K 10mg IVI

prothrombinex 50IU/kg

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54
Q

When MTP has been activated, what tests take?

A 
ROTEM (if ROTEM-guided)
FBC
EUC (incl Ca++)
Coags (INR, APTT)
Group & screen
ABG/VBG
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55
Q

How soon does ROTEM provide coagulation information? Generally for how long is the test run to allow initial interpretation? how long does the test usually run

A

within 5-10mins
5-10 mins
entire test 40-60mins

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56
Q

If there’s an abnormal result on the ROTEM, should it always be treated?

A

only if clinical bleeding is significant

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57
Q

What’s the EXTEM, what can it represent & management strategies?

A

Extrinsic pathway screening test (tissue factor added). not affected by heparin.

prolonged EXTEM-CT represents factor deficiency in extrinsic clotting pathway- If EXTEM CT >=90 secs, give FFP 2-4 units (gives factors + volume)

Low EXTEM A10 and prolonged EXTEM CFT reflect low fibrinogen &/or low platelets &/or poor plt function

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58
Q

If EXTEM-CT is >=90 seconds, what do I give?

A

FFP 2-4units (factors + volume)

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59
Q

What’s the FIBTEM, what can it represent & management strategies?

A

When compared with EXTEM, identifies effect of fibrinogen concentration or function- it’s EXTEM with a platelet inhibition reagent added

Low FIBTEM A10 reflects low fibrinogen concentration, FIBTEM A5 <=10mm, give fib conc (1g/25kg body weight) OR cryo 1 unit/5kg body weight

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60
Q

If FIBTEM A5<=10mm, what do we give?

A

fib conc 1g/25kg or cryo 1unit/5kg

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61
Q

What’s APTEM, what can it represent?

A

When normalised compared with EXTEM confirms hyperfibrinolysis (eg. if the CT is shortened, higher MCF)
It’s EXTEM with aprotinin

If APTEM-ML is normalised to <15% compared to an elevated EXTEM-ML >15%, it reflects hyperfibrinolysis

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62
Q

What’s INTEM, what can it represent?

A

intrinsic pathway screening test/heparin sensitive

prolonged INTEM-CT represents heparin effect or clotting factor deficiency in the intrinsic pathway

low INTEM-A10 & prolonged INTEM-CT reflects low fibrinogen +/- platelets +/- poor platelet function

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63
Q

What’s HEPTEM, what can it represent?

A

When compared to INTEM, identifies heparin effect

If HEPTEM-CT normalises cf INTEM-CT, it represents a heparin effect

If HEPTEM-CT doesn’t shorten cf INTEM-CT it represents an intrinsic factor deficiency or protamine effect

64
Q

What’s CT on the Rotem (R time TEG) & what does it reflect?

A

Time from start of measurement to initiation of clotting (2mm amplitude); reflects initiation of clotting, thrombin formation, start of clot polymerisation

65
Q

What’s CFT on the Rotem (K time TEG) & what does it reflect?

A

Time from clot initiation to clot firmness of 20mm

reflects fibrin polymerisation, stabilisation of clot with thrombocytes, fibrinogen & factor XIII

66
Q

What’s alpha angle on the Rotem & what does it reflect?

A

Rate of fibrin polymerisation. Slope btwn R & K (angle btwn baseline & tangent to 2mm point

67
Q

What’s MCF on the Rotem (MA TEG) & what does it reflect?

A

measure of clot quality & maximum strength, increasing stabilisation of the clot by polymerised fibrin, thrombocytes & factor XIII

68
Q

What’s A5 Rotem & what does it reflect?

A

amplitude @ 5 mins from clotting time, it’s an early measure of the clot quality & strength, it correlates well with subsequent A10 & A10 correlates well with subsequent MCF

69
Q

What’s ML% on the Rotem & what does it reflect? what may it prompt to give?

A

Maximum lysis- measure of % breakdown of MCF
Normal is <5%
if the pt is being actively treated, check ML after 20mins

If ML >=5% after 20 mins, give TXA 1g

70
Q

Considering the ROTEM for Obstetric 3rd trimester, what’s the Fibtem A5 cutoff which may reflect reduced fibrinogen or impairment of fibrinogen polymerisation? What give?

A

If <=12mm, give fib conc 1g/25kg or cryo 1unit/5kg BW

71
Q

What does a FIBTEM A5 12mm generally correlate with?

A

Fibrinogen of 2.1g/L

72
Q

Does ROTEM adequately reflect the effects of TXA? clinical implications?

A

No. according to the sentinel WOMAN trial of TXA use in PPH (blood loss >500mL), improved mortality with 1g IV TxA within 3 hours after delivery with no increase in venous thromboembolic events. All women with PPH, irrespective of ROTEM, require TxA.

73
Q

Does ROTEM adequately reflect the effects of TXA? clinical implications?

A

No. according to the sentinel WOMAN trial of TXA use in PPH (blood loss >500mL), improved mortality with 1g IV TxA within 3 hours after delivery with no increase in venous thromboembolic events. All women with PPH, irrespective of ROTEM, require TxA.

74
Q

Are scoring systems useful for initiation of a MTP?

A

No score is ideal- varying degrees of complexity, sub-optimal S&S, some require availability of results, which impacts time to initiation of MTP & administration of blood products

ABC & TASH scoring systems have high sensitivity & lower specificity; most centres rely on gestalt

75
Q

Along with senior clinician gestalt, what may be some factors for triggering MTP?

A 
penetrating mechanism
GCS <=8
HR >120bpm
SBP <90mmHg
unstable pelvic or femoral #
\+ve FAST scan on arrival in ED
76
Q

Along with senior clinician gestalt, what may be some factors for triggering MTP?

A 
penetrating mechanism
GCS <=8
HR >120bpm
SBP <90mmHg
unstable pelvic or femoral #
\+ve FAST scan on arrival in ED
77
Q

At what temp are cryo & platelets stored? and how about packed red cells & FFP?

A

room temp

4 deg C

78
Q

What’s international consensus on the KPI of delivery of blood products without delay?

A

<10 mins from request to delivery of first MHP

79
Q

What’s the ratio for balanced transfusion in MTP? what type of pRBC & plasma are given?

A

1:1:1 red cells:platelets:plasma
Type O neg or pos rbc & thawed AB plasma

cross-matched product administration should occur within 1 hour of MTP activation & once viscoelastic assays have characterised the coagulopathy, switch to goal-directed therapy

80
Q

If the FIBTEM A5 is high (>10mm) but EXTEM A5 is low (<=35mm), what need to give?

A

platelets- FIBTEM has a platelet inhibition reagent added

81
Q

What’s the lethal triad in coagulopathy?

A

coagulopathy, acidosis, hypothermia

82
Q

While the PROPPR trial (2015) showed that higher transfusion ratio (1:1:1) associated with earlier haemostats, lower transfusion rates & lower rates of death due to exsanguination by 24hrs, what’s the corollary of higher fixed ratio empiric MTP?

A

increased risk of prolonged multi-organ failure and nosocomial infection (augmentation of the immunosuppressive response after trauma)

83
Q

What’s the predominant coagulopathy phenotype in trauma? what are some characteristics of the protein responsible for this?

A

hyperfibrinolysis- fibrinogen is the first clotting factor to reach critically low levels in bleeding trauma pts. fibrinogen <1.8g/L significantly associated with higher in-hospital mortality.

fibrinogen= a key clotting protein, essential for clot strength, stabilisation, plt aggregation & haemostasis

large MW, long half life (3-5 days), contributes more to clot strength in injured vs non-injured pts

This may be part of why TxA so much benefit.

84
Q

What does Fibtem A5 <7mm correlate with?

A

fibrinogen of 1.5g/L

85
Q

Does cryo require group-specific compatability?

A

yes

86
Q

what’s the [] of fibrinogen in FFP vs cryo?

A

FFP 1.6g/L

cryo 1.3g/150mL

87
Q

once cryo thawed, how soon need to use?

A

6hrs

88
Q

why is FFP not so useful for fibrinogen?

A

require >30mL/kg to increase fibrinogen by 1g/L, risks volume overload, TRALI & MOF

89
Q

does fib conc need to be group-specific?

A

no, it’s been pathogen inactivated

90
Q

how much fibrinogen does fib conc deliver?

A

1g/50mL

91
Q

benefits of fib conc over cryo?

A

faster to delivery, don’t need to wait for thawing, cross-matching, potential pathogen-related reactions, should deliver a more constant dose.

92
Q

benefits of fib conc over cryo?

A

faster to delivery, don’t need to wait for thawing, cross-matching, potential pathogen-related reactions, should deliver a more constant dose.

93
Q

is prothrombin complex concentrate used for massive haemorrhage?

A

not routinely, unless a pt on warfarin presents with TBI (50IU/kg PCC, 10mg vit K IV, consider additional FFP)

low level of evidence available supporting its use vs FFP alone for acute traumatic coagulopathy

94
Q

When is tranexamic acid useful in major haemorrhage? what did CRASH 2 show?

A

lysine analogue, inhibits conversion of plasminogen to plasmin

if evidence of hyperfibrinolysis

CRASH2 (>20,000 pts) showed improved survival without increase in vaso-occlusive events when 15-20mg/kg TxA was given within 3 hrs of injury

95
Q

What is the bottom line on CRASH-3?

A

randomised, placebo-controlled trial of >12000 ptseffect of TxA (admin within 3 hrs of injury cf placebo) on death, disability & vascular occlusive events in pts with acute TBI at 28 days

no significant difference in 28 day mortality, slightly improved mortality in those with mild-mod TBI
no increased risk of vast-occlusive events or seizures

96
Q

What is the evidence for benefits of viscoelastic haemostatic assays?

A

reduced trauma mortality
LoS in hospital & ICU
lower overall blood transfusion costs

97
Q

What is damage control resuscitation (DCR)?

A

A resuscitation strategy aiming to reduce ongoing blood loss & minimise the exacerbating underlying metabolic processes (contributing to coagulopathy) until definitive haemorrhage control can be achieved

98
Q

What is damage control resuscitation (DCR)?

A

A resuscitation strategy aiming to reduce ongoing blood loss & minimise the exacerbating underlying metabolic processes (contributing to coagulopathy) until definitive haemorrhage control can be achieved

99
Q

What are the 3 tenets of damage control resuscitation?

A

Permissive hypotension- controversial
Haemostatic resuscitation- resuscitating pts to minimise risk of worsening acute traumatic coagulopathy
Early haemorrhage control/DCS

100
Q

What are the goals of permissive hypotension?

A

Allowing SBP to fall low enough to minimise ongoing bleeding but high enough to maintain vital tissue perfusion (heart, brain)
Avoid disrupting the clot formed
Goal is haemorrhage control, not a BP

101
Q

What are the goals of permissive hypotension?

A

Allowing SBP to fall low enough to minimise ongoing bleeding but high enough to maintain vital tissue perfusion (heart, brain)
Avoid disrupting the clot formed
Goal is haemorrhage control, not a BP

102
Q

What are some proposed targets for the concept of permissive hypotension?

A

If no SCI or TBI suspected/confirmed, MAP 50-60mmHg, if confirmed/suspected TBI/SCI, MAP target 80-90mmHg with SBP >=110mmHg, some would say mentation or radial pulse adequate surrogates

103
Q

What are some proposed targets for the concept of permissive hypotension?

A

If no SCI or TBI suspected/confirmed, MAP 50-60mmHg, if confirmed/suspected TBI/SCI, MAP target 80-90mmHg with SBP >=110mmHg, some would say mentation or radial pulse adequate surrogates

104
Q

What’s the main controversy with the concept of permissive hypotension?

A

Pts with brain & SC injuries- competing interests of bleeding risk & optimisation of LT neurological recovery

105
Q

To which patients is permissive hypotension primarily applicable?

A

Penetrating trauma

106
Q

What are some of the elements of damage control resuscitation?

A

Rapid diagnosis (most important- announce it to team to help ensure pt has early targeted Mx & benefit)
Limit crystalloids
Early 1:1:1 transfusion strategy
Antifibrinolytics
Rapid anatomic control
Permissive hypotension
Aim to limit haemorrhage, hypovolaemia, hypothermia, acute traumatic coaculopathy, acidosis, tissue hypoxia

107
Q

What’s the leading cause of PREVENTABLE death in severe trauma, hence the target of damage control resus? What are the primary causes of later deaths after trauma?

A

Haemorrhage. Aims to target the “early deaths”- within first few hours of injury, most deaths in that timeframe are haemorrhage-related.

Later deaths mostly due to head injury or multi-organ failure (what we do in the early phase impacts the risk of this)

108
Q

What type of trauma accounts for most trauma deaths, haemorrhage & multi-organ failure?

A

blunt vs penetrating trauma

109
Q

Which patients most likely to require damage control resus?

A

ongoing bleeding, higher grades of shock

110
Q

What are some adverse effects of acidosis?

A
  • reduced myocardial contractility & CO
    • vasodilation & worsening hypotension
  • vasopressors/catecholamines don’t work as well
    • impaired metabolic function & coagulation
  • BD>=6 (BE<=-6) strongly associated with need for massive transfusion, mortality, ICU days, ARDs & MODs. Patients have an elevated BD before their BP drops to classic “hypotension” levels.
111
Q

What’s the significance of hypothermia? Where does the most severe body temp loss occur?

A

Independently associated with 3x odds of death even when adjusted for age, ISS, mechanism, BP
In ED

112
Q

What’s the significance of hypothermia? Where does the most severe body temp loss occur?

A

Independently associated with 3x odds of death even when adjusted for age, ISS, mechanism, BP
In ED

113
Q

What are some of the physiological effects of hypothermia?

A

Metabolism/muscles: incr shivering, O2 consumption incr risk acidosis, L)-shift HbO2 dissociation curve (reduces PaO2)
CNS: confusion, coma
Cardiac: vasoconstriction, atrial/ventricular fibs, cardiac arrest
Resp: incr rate, bronchoconstriction, reduce resp drive, apnoea
GIT: reduces motility
Blood cells: platelet dysfunction, coagulation enzymes impaired
Renal: cold diuresis
Drug effects: reduce MAC, prol DOA muscle relaxants

114
Q

Why is hypocalcaemia a problem?

A

Extrinsic, intrinsic & central clotting cascades rely on adequate ionised Ca++ levels
Lower pH is associated with lower Ca++, hence prolongation of clot formation
Hypocalcemia occurs due to blood loss, further exacerbated through resuscitation strategies
With hypothermia, liver has less ability to metabolise citrate which binds Ca++
Calcium is an inotrope & is important for vascular muscle tone

115
Q

How may excessive crystalloids worsen outcomes in trauma? What’s the best choice if blood not available?

A

As little as 500mL associated with worse outcomes
Hyperchloraemic acidosis
Dilution of coagulation factors
Hypothermia
Unclear which is the ideal fluid- likely NOT 0.9% NaCl

116
Q

How may excessive crystalloids worsen outcomes in trauma? What’s the best choice if blood not available?

A

As little as 500mL associated with worse outcomes
Hyperchloraemic acidosis
Dilution of coagulation factors
Hypothermia
Unclear which is the ideal fluid- likely NOT 0.9% NaCl

117
Q

What did the ITACTIC trial illustrate?

A

MTP with either CCT or POCT-guided strategy: no sig difference in pts alive & free of massive transfusion @ 24hrs, limited by lack of a stepwise VHA-guided algorithm

118
Q

What are the benefits of TxA in traumatic haemorrhage?

A

No benefit after 3 hrs. immediate Rx= 70% improvement in survival. For every 15 minute delay, 10% decrease in survival benefit.

119
Q

What are the benefits of TxA in traumatic haemorrhage?

A

No benefit after 3 hrs. immediate Rx= 70% improvement in survival. For every 15 minute delay, 10% decrease in survival benefit.

120
Q

Findings of the STAMP trial?

A

Pre-hospital comparison of 1g + infusion or 2g bolus; no difference

121
Q

For who may recombinant factor VIIA be useful?

A

A select group of pts with significant injuries & severe ongoing bleeding

122
Q

What should I remember about calcium?

A

Give it EARLY

123
Q

What should I remember about calcium?

A

Give it EARLY

124
Q

What’s REBOA? Who for?

A

Retrograde endovascular balloon occlusion of the aorta

Sub-diaphragmatic major arterial haemorrhage enroute to definitive care

125
Q

What are some particular considerations for damage control resuscitation in the elderly?

A

Vital signs may be difficult to interpret
More likely to have comorbidities
More likely to take clot-affecting drugs

126
Q

What are some particular considerations for damage control resuscitation in pregnancy?

A

L) uterine displacement
2 pts- one dependent on uterine perfusion
Need for rapid obstetric consultation
Vital sign changes of bleeding late due to incr blood volume
Anti-D, Rh-ve blood

127
Q

What’s the purpose of a “red blanket” or “code crimson” protocol?

A

Accelerated Rx for those identified as having likely severe haemorrhage- early balanced blood product transfusion initiation, MTP activation, activation of on-call surgeon, ED, ICU, anaesthesia & radiology staff to facilitate urgent decision-making

128
Q

What are the elements of the ABC score in bleeding?

A

Penetrating trauma
Low SBP<=90mmHg
Pulse >=120bpm
eFast scan +ve

if >=2, activate red blanket

129
Q

What are the elements of the ABC score in bleeding?

A

Penetrating trauma
Low SBP<=90mmHg
Pulse >=120bpm
eFast scan +ve

if >=2, activate red blanket

130
Q

How often repeat FBC (&VHA) with major bleeding?

A

Every 30mins until bleeding controlled

131
Q

What’s the platelet target if ongoing bleeding or intracranial haemorrhage?

A

> 100 x 10^9

132
Q

The normalisation of which values, at 4 hrs, is a good prognostic sign for ongoing haemorrhage?

A

Lactate & base excess

133
Q

The normalisation of which values, at 4 hrs, is a good prognostic sign for ongoing haemorrhage?

A

Lactate & base excess

134
Q

What’s the role of vasopressors in trauma patients?

A

May be necessary eg. in TBI may need arterial BP augmentation (cognisant of them incr risk of bleeding)
if “not winning” may vasopressors to optimise DO2

135
Q

What’s the approach to the balance between continual resuscitation in ED vs moving to OT?

A

Damage control resuscitation is a continuum; if a pt is identified as requiring definitive surgery for haemorrhage control the move should be to early OT transfer with ongoing resuscitation enroute & prior to induction- bearing in mind that protracted resuscitation may aggravate underlying coagulopathy (“non-surgical/non-compressible bleeding”). Consider logistics such as distance from ED to OT.

136
Q

Which red blanket pts may bypass the ED & go straight to OT?

A

Penetrating trauma

Also consider the quality of the handover & pre-hospital resus (& how stable they are through transfer)

137
Q

Would I give TxA in isolated head trauma without bleeding elsewhere?

A

Not based on current evidence

138
Q

Approach to TxA in major trauma?

A

Consider 1g empirically, further guided by ROTEM results (some evidence re: 2g initial bolus vs 1g + infusion no difference- STAMP trial pre-hospital)

139
Q

How much blood is needed for haemothorax to manifest on an upright CXR?

A

300mL

140
Q

How is haemothorax initially treated? indications for surgical thoracotomy?

A

tube thoracotomy with 28032Fr chest tube
immediate blood drainage of >=20mL/kg (approx 1500mL) is generally considered an indication for surgical thoracotomy, as would be shock & persistent, substantial bleeding (>3mL/kg/hr)

141
Q

what may prolong the CT (or R time)

A

Anticoagulants, severe hypofibrinogenaemia, factor deficiencies

REDUCED by hypercoaguable conditions

142
Q

What prolongs CFT/K time?

A

anticoags, thrombocyto, hypofibrin

Prolonged by incr plt & fibrinogen

143
Q

What incr alpha angle

A

incr fibrinogen & plt, reduced by anticoags, low fibrinogen, low plt

144
Q

What decr MA?

A

fibrinolysis, thrombocytopaenia, plt blockers (to a lesser extent, factor deficiencies)

145
Q

Whats Ly30?

A

% lysis 30 mins after MA (normal is <=7.5%, on our algorithm give TxA if ML >=5%)

146
Q

Whats Ly30?

A

% lysis 30 mins after MA (normal is <=7.5%, on our algorithm give TxA if ML >=5%)

147
Q

What’s added to each of the 5 possible viscoelastic tests & what do they look for?

A

EXTEM: extrinsic pathway. add TF. looks @ clotting factors.
APTEM: Add TF (like ext pathway), then add an anti-fibrinolytic (aprotinin or TxA) to Ax fibrinolysis or impact of antifibrinolytic therapy. compare with the extem.
FIBTEM: Add TF (ext pathway) then add cytocalacin D to inhibit the platelet component; it considers fibronogen availability/function
INTEM: Add ellagic acid to activate intrinsic pathway
HEPTEM: add ellagic acid (intrinsic pathway) & a heparinase (to remove heparin effect)

148
Q

What are the implications of mixing tests?

A

Used to investigate abnormal clotting time results
Help to distinguish clotting factor deficiency from presence of an inhibitor
For PT, mixing studies correct if Factor deficiency (2,5,7,10), warfarin, Vit K deficiency, liver disease. Don’t correct if factor inhibitor (incl Xa inhibitor)
aPTT: correct if factor deficiency (8,9,II) or rarely vWF if VIII low enough to prol aPTT, don’t correct if inhibitor present, heparin, lupus anticoagulant

Common pathway is if both PT & aPTT either correct (factor II, V, X def) or don’t correct (II, V, X def)

149
Q

What’s the most common inhibitor in a pt without a bleeding disorder Hx?

A

lupus anticoagulant

150
Q

What’s the most likely acquired factor inhibitor & possible associations?

A

Factor VIII, ass’d w malignancy. Can Ax with FVIII levels, inhibitor studies.

151
Q

What’s the most likely acquired factor inhibitor & possible associations?

A

Factor VIII, ass’d w malignancy. Can Ax with FVIII levels, inhibitor studies.

152
Q

What does FXII deficiency cause?

A

May prolong aPTT but doesn’t cause clinical bleeding.

153
Q

what’s in the VWD screen?

A

vWF antigen (levels <30% (<30IU/dL) consistent w vWD, OR 30-50IU/dL if Hx bleeding; levels >50% considered normal.
Collagen binding assay, low suggests decreased vWF multimers.
Ristocein cofactor (RiCoF): vWF:RCo assay measures ability of vWF to bind plt membrane receptor GPIb.Incr in type 2B.
Should also check FVIII activity: reduced suggests reduced or dysfunctional vWF, since vWF acts as a carrier for VIII, protecting it from proteolysis, incr it’s plasma half-life. VIII is low in type 2N & type III; may be mlow normal if 1, 2A, 2B, 2M.

154
Q

what’s in the VWD screen?

A

vWF antigen (levels <30% (<30IU/dL) consistent w vWD, OR 30-50IU/dL if Hx bleeding; levels >50% considered normal.
Collagen binding assay, low suggests decreased vWF multimers.
Ristocein cofactor (RiCoF): vWF:RCo assay measures ability of vWF to bind plt membrane receptor GPIb.Incr in type 2B.
Should also check FVIII activity: reduced suggests reduced or dysfunctional vWF, since vWF acts as a carrier for VIII, protecting it from proteolysis, incr it’s plasma half-life. VIII is low in type 2N & type III; may be mlow normal if 1, 2A, 2B, 2M.

155
Q

what are acanthocytes ass’d with?

A

irregularly shaped rbcs, ass’d w hepatitis/liver disease, hypothyroidism, malnutrition

156
Q

lab findings DIC

A

low plt, low fibrinogen, fragmented rbcs on blood film, elevated D-dimer, prolonged bleeding times

Fellowship revision (78 decks)

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