Trauma, major haemorrhage, trauma-induced coagulopathy and viscoelastic testing + blue book 2019 MTP article Flashcards
What proportion of potentially preventable trauma deaths is due to major haemorrhage?
> 50%
In what proportion of trauma patients, on arrival to hospital, does trauma-induced coagulopathy present?
30%
What are at least 2 distinct mechanisms responsible for trauma-induced coagulopathy?
- Acute traumatic coagulopathy (endogenous heparinisation, activation of protein C pathway, hyperfibrinolysis & platelet dysfunction)
- Resuscitation-associated coagulopathy (clear fluid resus w crystalloids & colloids- associated with poor outcome)
What are the principles of management of trauma resuscitation?
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
In what tests does endogenous heparinisation show up?
prolonged PTT or APTT or in the VHAs as RT or CT
How does endogenous heparinisation occur? In what conditions, other than acute traumatic coagulopathy, is it seen?
Endotheliopathy- shedding of the endothelial glycocalyx- releasing endogenous heparins & other factors with heparin-like activity. Also seen in OOHCA, MI & sepsis.
What’s the most potent form of endogenous anticoagulation?
Hyperfibrinolysis
How does hyperfibrinolysis occur?
Endothelial damage causes release of tissue-type plasminogen activator (tPA), causing premature resolution of a formed clot
What does activated protein C do?
Inhibits thrombin formation & promotes fibrinolytic activity. Also antiinflammatory & antiapopotic.
How might platelet transfusion be particularly useful early in trauma resus?
Platelet dysfunction is part of acute TIC & platelets contain Plasminogen Activator Inhibitor 1 (PAI-1)
What’s the “lethal triad”?
Hypothermia, acidosis & dilutional coagulopathy
What do hypothermia & acidosis do to fibrinogen?
hypothermia inhibits fibrinogen synthesis & acidosis accelerates fibrinogen degradation
What does hypothermia do to coagulation?
depletes fibrinogen levels, induces fibrinolysis, impairs coagulation factor activity & induces platelet dysfunction
What does acidosis do to coagulation?
Impairs almost all parts of haemostat process, eg. changing platelet structure/shape, reducing activity of coagulation factor complexes, accelerate fibrin degradation
Why does even blood induce coagulopathy?
anticoagulants & the fluids in blood accelerate coagulopathy
What haematocrit, coagulation factors [] & platelet count result from 1:1:1 resus?
30%, 60% & 80 x 10^9
What are some negatives of colloids?
make the clot more porous, increase bleeding & transfusion requirements
When should clear fluids be used in severely bleeding trauma pts?
pre-hospital. in-hospital ONLY if blood products n/a
What were the findings of PROPPR RCT (2015)?
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.
What are the benefits of VHA goal-directed therapy?
use less rbc/plasma/plts, reduce bleeding & improve mortality in mixed surgical populations
What should be given as soon as signs of hyperfibrinolysis in an actively bleeding patient?
TxA- reduced efficacy with later administration
What’s a significant finding of the CONTROL trial?
Recombinant Factor VIIa shows potential reduction in transfusion in trauma BUT no impact on other outcomes & increased risk thromboembolic complications
What did CRASH-2 show?
TxA decreased mortality in trauma
What’s a concern with prothrombinex?
High [] of factors II, VII, IX & X has potential to increase endogenous thrombin potential several days after trauma where thromboembolic complications dominate
What’s the flow rate through a 20g IVC? 18g? 16g? 8.5Fr CV sheath?
150mL/min
230mL/min
430mL/min
1L/min
What’s haemostatic resuscitation?
Process of restoring & sustaining normal tissue perfusion in pts w uncontrolled haemorrhagic shock, w emphasis on preserving effective clotting
Sequence of response for massive haemorrhage:
- 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
What’s the STOP handover for major trauma?
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
What are the indications for MHP?
Active bleeding +
- 4 units in <4hrs + haemodynamic instability
- EBL >2.5L
- clinical or lab signs of coagulopathy
How is TxA given during MHP? (dose & over how long?)
1g over 10 mins
What are the targets during MHP?
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
When are ROTEM/TEG re-checked?
10 mins after components
For massive haemorrhage in a head-injured pt, what MAP target?
> =80mmHg
What blood given if no time for crossmatch?
O neg or group specific
What’s a definition of massive transfusion?
> 1 blood vol (or 10+ units rbc) over 24hrs or >0.5 blood vol (or 5+ units packed red cells) over <4hrs
What does cryo mainly contain? Dose?
factors VIII, XIII, vWF, fibrinogen, fibronectin
1 unit per 5-10kg
What does FFP contain? dose?
all coag factors incl labile V, VIII, fibrinogen & vWF
15mL/kg
What are the doses of fib conc & prothrombinex?
25-50mg/kg & 25-50IU/kg, respectively
What do ROTEM and TEG stand for?
rotational thromboelastography
thromboelastography
How would you describe hypercoaguability in terms of viscoelastic tests?
accelerated clot formation, clot strength & reduced fibrinolysis
Is SARS-CoV-2 thought to be transfusion transmissible?
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.
are SARS-CoV and MERS-CoV transfusion-transmissible?
No
What are the intended benefits of MTP & what has been the impact of MTP on trauma outcomes & blood product usage?
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
What’s a massive transfusion?
5 or more units of packed red blood cells in <4hrs or 10 or more units of packed red cells in 24hrs
What proportion of civilian trauma pts receive a massive transfusion?
3-5%
What are the indications to initiate a MTP?
Actual or anticipated 5 or more units packed red cells in <4hrs + haemodynamic instability + ongoing bleeding anticipated
What are the indications to initiate a MTP?
Actual or anticipated 5 or more units packed red cells in <4hrs + haemodynamic instability + ongoing bleeding anticipated
What’s in the Gold Coast Non-rotem MTP packs?
Pack 1: 4 units red cells, 4 units FFP, 10 units cryo
Pack 2: 4 units rbc, 4 FFP, 1 platelets
When to repeat ROTEM?
10 mins after each blood product intervention and ?after every 4 units packed red cells or every 30-60mins
When may fibrinogen concentrate be considered in trauma? dose?
FIBTEM A5 <=10mm OR critical life-threatening haemorrhage OR high clinical suspicion of coagulopathy- consultant approval- 1g/25kg BW (4g empirically adult)
How should TxA be given? how many doses?
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
How does MTP proceed (standard protocol) after 2nd pack?
alternate pack 1 & 2
Emergency warfarin reversal?
vit K 10mg IVI
prothrombinex 50IU/kg
When MTP has been activated, what tests take?
ROTEM (if ROTEM-guided) FBC EUC (incl Ca++) Coags (INR, APTT) Group & screen ABG/VBG
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
within 5-10mins
5-10 mins
entire test 40-60mins
If there’s an abnormal result on the ROTEM, should it always be treated?
only if clinical bleeding is significant
What’s the EXTEM, what can it represent & management strategies?
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
If EXTEM-CT is >=90 seconds, what do I give?
FFP 2-4units (factors + volume)
What’s the FIBTEM, what can it represent & management strategies?
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
If FIBTEM A5<=10mm, what do we give?
fib conc 1g/25kg or cryo 1unit/5kg
What’s APTEM, what can it represent?
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
What’s INTEM, what can it represent?
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
What’s HEPTEM, what can it represent?
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
What’s CT on the Rotem (R time TEG) & what does it reflect?
Time from start of measurement to initiation of clotting (2mm amplitude); reflects initiation of clotting, thrombin formation, start of clot polymerisation
What’s CFT on the Rotem (K time TEG) & what does it reflect?
Time from clot initiation to clot firmness of 20mm
reflects fibrin polymerisation, stabilisation of clot with thrombocytes, fibrinogen & factor XIII
What’s alpha angle on the Rotem & what does it reflect?
Rate of fibrin polymerisation. Slope btwn R & K (angle btwn baseline & tangent to 2mm point
What’s MCF on the Rotem (MA TEG) & what does it reflect?
measure of clot quality & maximum strength, increasing stabilisation of the clot by polymerised fibrin, thrombocytes & factor XIII
What’s A5 Rotem & what does it reflect?
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
What’s ML% on the Rotem & what does it reflect? what may it prompt to give?
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
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?
If <=12mm, give fib conc 1g/25kg or cryo 1unit/5kg BW
What does a FIBTEM A5 12mm generally correlate with?
Fibrinogen of 2.1g/L
Does ROTEM adequately reflect the effects of TXA? clinical implications?
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.
Does ROTEM adequately reflect the effects of TXA? clinical implications?
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.
Are scoring systems useful for initiation of a MTP?
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
Along with senior clinician gestalt, what may be some factors for triggering MTP?
penetrating mechanism GCS <=8 HR >120bpm SBP <90mmHg unstable pelvic or femoral # \+ve FAST scan on arrival in ED
Along with senior clinician gestalt, what may be some factors for triggering MTP?
penetrating mechanism GCS <=8 HR >120bpm SBP <90mmHg unstable pelvic or femoral # \+ve FAST scan on arrival in ED
At what temp are cryo & platelets stored? and how about packed red cells & FFP?
room temp
4 deg C
What’s international consensus on the KPI of delivery of blood products without delay?
<10 mins from request to delivery of first MHP
What’s the ratio for balanced transfusion in MTP? what type of pRBC & plasma are given?
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
If the FIBTEM A5 is high (>10mm) but EXTEM A5 is low (<=35mm), what need to give?
platelets- FIBTEM has a platelet inhibition reagent added
What’s the lethal triad in coagulopathy?
coagulopathy, acidosis, hypothermia
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?
increased risk of prolonged multi-organ failure and nosocomial infection (augmentation of the immunosuppressive response after trauma)
What’s the predominant coagulopathy phenotype in trauma? what are some characteristics of the protein responsible for this?
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.
What does Fibtem A5 <7mm correlate with?
fibrinogen of 1.5g/L
Does cryo require group-specific compatability?
yes
what’s the [] of fibrinogen in FFP vs cryo?
FFP 1.6g/L
cryo 1.3g/150mL
once cryo thawed, how soon need to use?
6hrs
why is FFP not so useful for fibrinogen?
require >30mL/kg to increase fibrinogen by 1g/L, risks volume overload, TRALI & MOF
does fib conc need to be group-specific?
no, it’s been pathogen inactivated
how much fibrinogen does fib conc deliver?
1g/50mL
benefits of fib conc over cryo?
faster to delivery, don’t need to wait for thawing, cross-matching, potential pathogen-related reactions, should deliver a more constant dose.
benefits of fib conc over cryo?
faster to delivery, don’t need to wait for thawing, cross-matching, potential pathogen-related reactions, should deliver a more constant dose.
is prothrombin complex concentrate used for massive haemorrhage?
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
When is tranexamic acid useful in major haemorrhage? what did CRASH 2 show?
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
What is the bottom line on CRASH-3?
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
What is the evidence for benefits of viscoelastic haemostatic assays?
reduced trauma mortality
LoS in hospital & ICU
lower overall blood transfusion costs
What is damage control resuscitation (DCR)?
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
What is damage control resuscitation (DCR)?
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
What are the 3 tenets of damage control resuscitation?
Permissive hypotension- controversial
Haemostatic resuscitation- resuscitating pts to minimise risk of worsening acute traumatic coagulopathy
Early haemorrhage control/DCS
What are the goals of permissive hypotension?
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
What are the goals of permissive hypotension?
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
What are some proposed targets for the concept of permissive hypotension?
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
What are some proposed targets for the concept of permissive hypotension?
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
What’s the main controversy with the concept of permissive hypotension?
Pts with brain & SC injuries- competing interests of bleeding risk & optimisation of LT neurological recovery
To which patients is permissive hypotension primarily applicable?
Penetrating trauma
What are some of the elements of damage control resuscitation?
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
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?
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)
What type of trauma accounts for most trauma deaths, haemorrhage & multi-organ failure?
blunt vs penetrating trauma
Which patients most likely to require damage control resus?
ongoing bleeding, higher grades of shock
What are some adverse effects of acidosis?
- 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.
What’s the significance of hypothermia? Where does the most severe body temp loss occur?
Independently associated with 3x odds of death even when adjusted for age, ISS, mechanism, BP
In ED
What’s the significance of hypothermia? Where does the most severe body temp loss occur?
Independently associated with 3x odds of death even when adjusted for age, ISS, mechanism, BP
In ED
What are some of the physiological effects of hypothermia?
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
Why is hypocalcaemia a problem?
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
How may excessive crystalloids worsen outcomes in trauma? What’s the best choice if blood not available?
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
How may excessive crystalloids worsen outcomes in trauma? What’s the best choice if blood not available?
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
What did the ITACTIC trial illustrate?
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
What are the benefits of TxA in traumatic haemorrhage?
No benefit after 3 hrs. immediate Rx= 70% improvement in survival. For every 15 minute delay, 10% decrease in survival benefit.
What are the benefits of TxA in traumatic haemorrhage?
No benefit after 3 hrs. immediate Rx= 70% improvement in survival. For every 15 minute delay, 10% decrease in survival benefit.
Findings of the STAMP trial?
Pre-hospital comparison of 1g + infusion or 2g bolus; no difference
For who may recombinant factor VIIA be useful?
A select group of pts with significant injuries & severe ongoing bleeding
What should I remember about calcium?
Give it EARLY
What should I remember about calcium?
Give it EARLY
What’s REBOA? Who for?
Retrograde endovascular balloon occlusion of the aorta
Sub-diaphragmatic major arterial haemorrhage enroute to definitive care
What are some particular considerations for damage control resuscitation in the elderly?
Vital signs may be difficult to interpret
More likely to have comorbidities
More likely to take clot-affecting drugs
What are some particular considerations for damage control resuscitation in pregnancy?
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
What’s the purpose of a “red blanket” or “code crimson” protocol?
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
What are the elements of the ABC score in bleeding?
Penetrating trauma
Low SBP<=90mmHg
Pulse >=120bpm
eFast scan +ve
if >=2, activate red blanket
What are the elements of the ABC score in bleeding?
Penetrating trauma
Low SBP<=90mmHg
Pulse >=120bpm
eFast scan +ve
if >=2, activate red blanket
How often repeat FBC (&VHA) with major bleeding?
Every 30mins until bleeding controlled
What’s the platelet target if ongoing bleeding or intracranial haemorrhage?
> 100 x 10^9
The normalisation of which values, at 4 hrs, is a good prognostic sign for ongoing haemorrhage?
Lactate & base excess
The normalisation of which values, at 4 hrs, is a good prognostic sign for ongoing haemorrhage?
Lactate & base excess
What’s the role of vasopressors in trauma patients?
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
What’s the approach to the balance between continual resuscitation in ED vs moving to OT?
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.
Which red blanket pts may bypass the ED & go straight to OT?
Penetrating trauma
Also consider the quality of the handover & pre-hospital resus (& how stable they are through transfer)
Would I give TxA in isolated head trauma without bleeding elsewhere?
Not based on current evidence
Approach to TxA in major trauma?
Consider 1g empirically, further guided by ROTEM results (some evidence re: 2g initial bolus vs 1g + infusion no difference- STAMP trial pre-hospital)
How much blood is needed for haemothorax to manifest on an upright CXR?
300mL
How is haemothorax initially treated? indications for surgical thoracotomy?
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)
what may prolong the CT (or R time)
Anticoagulants, severe hypofibrinogenaemia, factor deficiencies
REDUCED by hypercoaguable conditions
What prolongs CFT/K time?
anticoags, thrombocyto, hypofibrin
Prolonged by incr plt & fibrinogen
What incr alpha angle
incr fibrinogen & plt, reduced by anticoags, low fibrinogen, low plt
What decr MA?
fibrinolysis, thrombocytopaenia, plt blockers (to a lesser extent, factor deficiencies)
Whats Ly30?
% lysis 30 mins after MA (normal is <=7.5%, on our algorithm give TxA if ML >=5%)
Whats Ly30?
% lysis 30 mins after MA (normal is <=7.5%, on our algorithm give TxA if ML >=5%)
What’s added to each of the 5 possible viscoelastic tests & what do they look for?
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)
What are the implications of mixing tests?
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)
What’s the most common inhibitor in a pt without a bleeding disorder Hx?
lupus anticoagulant
What’s the most likely acquired factor inhibitor & possible associations?
Factor VIII, ass’d w malignancy. Can Ax with FVIII levels, inhibitor studies.
What’s the most likely acquired factor inhibitor & possible associations?
Factor VIII, ass’d w malignancy. Can Ax with FVIII levels, inhibitor studies.
What does FXII deficiency cause?
May prolong aPTT but doesn’t cause clinical bleeding.
what’s in the VWD screen?
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.
what’s in the VWD screen?
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.
what are acanthocytes ass’d with?
irregularly shaped rbcs, ass’d w hepatitis/liver disease, hypothyroidism, malnutrition
lab findings DIC
low plt, low fibrinogen, fragmented rbcs on blood film, elevated D-dimer, prolonged bleeding times
