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M. Maegele
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Table 7.2 Coagulation parameters and their value in predicting massive transfusion
Optimum threshold
ROC-AUC
Parameter
FIBTEM MCF 0.84
FIBTEM A10 0.83
EXTEM CT 0.71
EXTEM CFT 0.74
EXTEM MCF 0.76
Platelet count 0.70
Quick value 0.87
aPTT 0.85
Fibrinogen
concentration
Hemoglobin 0.87
Base decit 0.76
pH 0.76
Lactate 0.74
Single-center experience based upon retrospective analysis of 78 severely bleeding trauma patients
requiring massive transfusion [29]
A 10 clot amplitude 10min after CT, aPTT activated partial thromboplastin time, CFT clot forma-
tion time, CI condence interval, CT clotting time, EXTEM extrinsically activated thromboelastometric test, FIBTEM extrinsically activated thromboelastometric test with cytochalasin D, MCF
maximum clot rmness, ROC-AUC area under the receiving operating characteristic curve
(95% CI)
(0.79–0.88)
(0.78–0.87)
(0.66–0.76)
(0.68–0.79)
(0.71–0.81)
(0.65–0.75)
(0.83–0.90)
(0.81–0.89)
0.83
(0.78–0.87)
(0.83–0.91)
(0.76–0.86)
(0.70–0.81)
(0.69–0.79)
(for best sensitivity
and specicity)
≤7mm
≤4mm
≤72s
≤147s
≤52mm
≤161×10
≤60%
≤35.2s
≤148mg/dL
≤10.1g/dL
≤6.3
≤7.276
≤4.18mmol/L
3
/μL
Sensitivity (95%
CI)
77.5 (66.8–86.1) 74.9 (68.9–80.3)
63.3 (51.7–73.9) 83.2 (77.8–87.7)
76.3 (65.2–85.3) 59.4 (52.7–65.8)
64.5 (52.7–75.1) 75.1 (69.0–80.6)
67.1 (55.4–77.5) 71.2 (64.8–77.0)
62.0 (50.4–72.7) 73.8 (67.8–79.3)
84.8 (75.0–91.9) 82.1 (76.6–86.8)
71.6 (59.9–81.5) 87.8 (82.8–91.7)
84.2 (74.0–91.6) 68.3 (61.8–74.3)
77.5 (66.8–86.1) 84.5 (79.3–88.9)
69.6 (57.3–80.1) 79.8 (73.3–85.3)
62.3 (49.8–73.7) 80.0 (73.6–85.4)
54.9 (42.7–66.8) 88.0 (82.9–92.0)
Specicity (95%
CI)
For each additional positive trigger of the MTS at hour 6, the odds ratio (OR) of
death at 24h and 28days increased substantially (24-h OR, 4.6; 95% CI, 2.3–9.3;
28-day OR, 2.2; 95% CI, 1.5–3.2; p<0.0001).
7.6 Outcome ofMassive Transfusion
The overall in-hospital mortality of massively transfused patients remains high
[19, 29, 31–33]. Data from the TR-DGU (years 2002–2017; n=102,395 patients;
primary admissions with an ISS>16) still reveals a mortality rate of around 58%
in patients with MT [6]. In a retrospective analysis of the American College of
Surgeons Trauma Quality Improvement Program (TQIP) for outcome among 2776
adult trauma patients who required MT, the overall in-hospital mortality was
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43.5% with a mean pRBC transfusion within the rst 24h of 20±13units and a
mean plasma transfusion of 13±11units [34]. While receiving MT in a level I
trauma center was independently associated with a lower rate of mortality (OR:
0.75 [0.46–0.96], p<0.001), a higher magnitude of injury (OR: 1.020 [1.010–1.030],
p<0.001) along with increased units of pRBC transfused (OR: 1.067 [1.041–1.093],
p<0.001) were independently associated with increased mortality [34]. There was
no association between teaching status, age, gender, emergency department vitals,
and units of plasma transfused. Another analysis of data from 1062 patients with
MT from the TR-DGU reported a similar mortality rate (43.1%) [33]. There was
an increase in mortality observed in relation to the number of pRBC units transfused; in the subgroup that had received >30 pRBC units (mean 40.6) the mortality
rate was 60.4% [33]. From another cohort of bleeding trauma patients, a mortality
rate of 41% for patients with MT versus 13% with no MT was reported [29]. An
overview of studies which have examined massive blood transfusion in European
and North American civilian trauma populations is shown in Table 7.3 [19].
However, comparisons including rates for mortality between the studies remain
difcult due to heterogeneity of denitions for MT as well as variations in
case-mix.
Table 7.3 Overview of massive blood transfusion studies including incidence and outcome
Number of
cases/
incidence Mortality
43.5% 29
0.6%
40% 27
0.4%
41% 42
24%
41% Not
NA
50% 29/39
NA
57% 27
4.9%
41% 25
NA
26–59% 32
NA
ISS
(median)
reported
a
(continued)
Study
Hamidi etal.
(2019) [
31]
Fuller etal.
19]
(2012) [
Schöchl etal.
(2011) [29]
Johansson
etal. (2009)
[36]
Snyder etal.
(2009) [17]
Duchesne
etal. (2008)
[37]
Gunter etal.
(2008) [38]
Holcomb
etal. (2008)
[39]
Setting/sample size
Trauma receiving
centers (ACS TQIP
program), US
n=416,957
Trauma receiving
centers, UK
n=38,283
Trauma center,
Austria
n=323
Trauma center,
Denmark
n=NA
Level 1 Trauma
center, US
n=NA
Level 1 Trauma
center, US
n=2746
Level 1 Trauma
center, US
n=NA
16 Level 1 Trauma
centers, US
n=NA
Denition of
massive transfusion
>10U pRBC/24h n=2776
>10U pRBC/24h n=157
>10U pRBC/24h n=78
>10U pRBC/24h n=832
>10U pRBC/24h n=134
>10U pRBC/24h n=135
>10U pRBC/24h n=213
>10U pRBC/24h n=466
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M. Maegele
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Table 7.3 (continued)
Number of
cases/
incidence Mortality
56% 36
NA
ISS
(median)
Study
Kashuk etal.
40]
(2008) [
Setting/sample size
Level 1 Trauma
center, US
Denition of
massive transfusion
>10U pRBC/24h n=133
n=NA
Maegele etal.
(2008) [
41]
German Trauma
Registry, Germany
>10U pRBC
prior to ICU
n=713
NA
42% 41
n=NA
Sperry etal.
(2008) [42]
7 Level 1 Trauma
centers, US
>8U pRBC/24h n=415
40%
33% 41
n=1036
Mitra etal.
(2007) [43]
Huber-Wagner
etal. (2007)
33]
[
Como etal.
(2004) [44]
Level 1 Trauma
center, Australia
n=NA
German Trauma
Registry, Germany
n=8812
Level 1 Trauma
center, US
>5U pRBC/4h n=119
NA
>10U pRBC prior
to ICU
n=1062
13%
>10U pRBC n=147
3%
28% 34
43% 25
b
39% 29–32
c
n=5645
Vaslef etal.
(2002) [45]
Level 1 Trauma
center, US
50U of blood
components/24h
n=44
0.6%
57% 30
n=7734
Cinat etal.
(1999) [46]
Level 1 Trauma
center, US
50U pRBC/48h n=45
NA
71% 30
n=NA
Velmahos
etal. (1998)
[47]
Cosgriff etal.
48]
(1997) [
Level 1 Trauma
center, US
n=NA
Level 1 Trauma
center, US
20U pRBC during
admission
10U pRBC/24h n=58
n=141
NA
NA
70% 29
43% 31
n=NA
Modied from [19]
ACS TQIP American College of Surgeons Trauma Quality Improvement Program, ICU intensive
care unit, ISS Injury Severity Score, NA not available, pRBC packed red blood cells, U units, UK
United Kingdom, US United States
a
ISS for survivors/non-survivors
b
ISS for whole sample
c
Range of mean ISS for patients that had received 10–19 and ≥20 pRBC units
7.7 Risks andHarmful Effects ofBlood Product Transfusions
The use of large amounts of potentially inammatory, immunomodulatory, and
infectious blood products in the context of hemorrhagic shock may be related to the
morbidities typically observed during MT.Transfusion-related lung injury (TRALI)
with subsequent acute respiratory distress syndrome (ARDS) may be encountered
in up to one-fth of patients undergoing MT [34]. The amount of transfused blood
in a prospective cohort of 102 patients with severe trauma was independently
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associated with both the development of ARDS and hospital mortality [35].
Compared to the 21% of patients who received 0–5units of pRBC, 31% of those
who received 6–10units and 57% of those who received >10units developed ARDS
(p=0.007). In a multicenter prospective cohort study involving 1175 blunt injured
adults with hemorrhagic shock, each unit of FFP administered was independently
associated with a 2.1% and 2.5% increased risk of multiorgan failure and ARDS,
respectively [49]. Transfusion-associated circulatory overload, which represents the
second leading cause of transfusion-related fatalities reported in the United States,
is likely to be underestimated by passive reporting [50].
MT may also increase the risk for both viral and bacterial infections. The estimated risk for HIV in the United States is 1in 2,135,000 while the greatest risk is
for hepatitis B at 1in 277,000 [51]. In general, the transfusion of platelets carries a
greater risk of infection, sepsis, and death compared to any other blood product,
primarily through bacterial contamination [52]. It is assumed that between 1:1000
and 1:2500 platelet units are bacterially contaminated. The skin bacterial microora
is considered a primary source of contamination; enteric contaminants are rare but
may be clinically devastating, while platelet storage conditions can support bacterial growth [52]. The two most common electrolyte abnormalities to occur in the
context of MT are ionized hypocalcemia, caused by the preservative citrate, and
hyperkalemia.
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7.8 Refining Strategies forMassive Hemorrhage
MT can be a life-saving maneuver in acute trauma hemorrhage, but potential complications need to be considered. Ideally, patients in acute need of blood transfusion
may receive blood and blood products quicker, whereas blood may be withheld in
those where alternate treatment may be more adequate [7]. The principle remains to
prevent the patient from being both over- and undertreated with blood products. As
previously mentioned, scoring systems and prediction models may inform clinical
decision making on when to activate and stop an MTP.It has been shown that early
and timely activation of MT protocols in the emergency department together with
direct blood bank notication as well as compliance with the MT protocol may be
associated with outcome, including improved survival [21].
A single-center retrospective study has critically assessed the compliance with
a set of 13 selected compliance criteria among 72 consecutive MTP activations
[53]. The average compliance with the local MT protocol was 72%, while the
most common causes for non-compliance were (a) failure to send a complete
hemorrhage panel from the trauma bay (96%), (b) failure to regularly order laboratory investigations every 30min (89%), and (c) delay in both activation and
deactivation of the protocol, which was equally distributed in 50% of cases [53].
Of note, non- compliance with protocol-based administration of blood products
was documented in 47% of the cases. When the cohort was grouped according to
compliance, group A with <60% compliance had a mortality rate of 62%, group B
with 60–80% compliance had a mortality rate of 50%, and group C with >80%
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M. Maegele
compliance had a mortality rate of only 10% [53]. There were no statistical differences between the three groups with respect to demographics and injury characteristics [53].
To prevent over-transfusion and to aim for a more targeted and individualized
approach for the administration of blood products and hemostatic agents in massive
bleeding, advanced trauma centers on both sides of the Atlantic have started to shift
away from rather unguided and ratio-based approaches to “hybrid” concepts in
which further resuscitation is guided by advanced coagulation testing [54]. Once the
bleeding patient is hemodynamically stabilized, the updated 2019 European guideline on the management of major bleeding and coagulopathy following trauma currently recommends (Grade 1B) that resuscitation measures including blood products
and hemostatic agents be continued using a goal-directed strategy, guided either by
standard coagulation and/or viscoelastic assays [14]. An example of such a “hybrid”
approach to hemostatic resuscitation in massive bleeding and accompanying
trauma-induced coagulopathy is shown in Fig.7.2 [54].
Functional viscoelastic assays have entered the trauma arena to diagnose, monitor and guide novel treatment strategies in acute trauma hemorrhage but no uniformly accepted guidelines have yet been established on how these technologies are
to be integrated into clinical practice [14]. Viscoelastic blood clot stability measures
(e.g., thromboelastometric FIBTEM A10 and MCF amplitudes) may provide comparable prediction for MT in trauma patients as conventional laboratory parameters
[29] but turnaround times are much shorter [55]. Various algorithms suggesting viscoelastic thresholds for the initiation of specic goal-directed treatments through a
Start of hemorrhage
Environment
ntifibrinolytics
Blood products
Fig. 7.2 “Hybrid” concept of hemostatic resuscitation. Acute resuscitation in patients presenting
in hemorrhagic shock is initiated according to Damage Control Resuscitation principles using balanced pRBC, FFP and platelet concentrates, followed by an early shift towards a more targeted and
goal-directed approach based upon results from VHAs. TXA is administered according to the
CRASH-2 protocol. FFP fresh frozen plasma, Hb hemoglobin, pRBC packed red blood cells,
ROTEM rotational thromboelastometry, TEG rotational thromboelastography, TXA tranexamic
acid, VHAs viscoelastic hemostatic assays. Modied from [54]
Optimize temperature, Ca2+, paO2, paCO2, pH, Lactate
Reverse hyperfibrinolysis (Tranexamic acid 1g bolus and 1g over 8hrs)
Goal-directed VHA-guided resuscitation (TEG/ROTEM)
Pre-defined
pRBC:FFP:plateletratio
Dynamics of hemorrhage
Uncontrolled hemorrhage
pRBC according to Hb
Control of hemorrhage
Hemostasi
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87
more selective use of brinogen, platelets, plasma, and prothrombin complex concentrates in the bleeding trauma patient have been clinically introduced but are
mostly based upon retrospective evidence and expert opinion [54–57]. The results
from a recent Cochrane review supported the use of viscoelastic assays as resulting
in better survival, reduction in the need for allogeneic blood products, and fewer
patients with dialysis-dependent renal failure compared with transfusion guided by
any method in adults or children with bleeding [58]. In Fig. 7.3 an example
Hemostatic therapyROTEM®/ TEG®traceROTEM®/ TEG®Triggers
Fibrinogen
(concentrate or
cryoprecipitate)
Plasma transfusion (FFP)
(or Prothrombin complex
concentrate (PCC))
Platelet concentrate
transfusion
AntifibrinolyticsROTEM®: Any evidence of hyperfibrinolysis in
Angle
CT,R,
ACT
A5/10,MCF
20mm
MA
K
Angle
A5/10,MCF
MA
A5/10,MCF
MA
Ly30
®
ROTEM
: EXTEM A10 < 45 mm (A5 < 35 mm) or
MCF < 55 mm and FIBTEM A10 < 10 mm (A5 < 9
mm) or MCF < 12 mm
®
: FF MA < 14 mm cryoprecipitate pool (3-5
TEG
ml/kg) or fibrinogen concentrate (1-2 g) or FFP 20-30
ml/kg
RapidTEG
fibrinogen/plasma; Angle < 56
tate/ fibrinogen/plasma
ROTEM
35 mm) or MCF ≥ 55 mm and normal FIBTEM A10
(A5 ≥ 9 mm) or normal MCF
TEG
30 ml/kg; Angle < 52
14 mm FFP 20-30 ml/kg
RapidTEG
pRBCs; ACT > 128 s plasma and pRBCs
ROTEM®: EXTEM A10 < 45 mm (A5 < 35 mm) or
MCF < 55 mm and normal FIBTEM A10 (A5 ≥ 9 mm)
or normal MCF
TEG
KaolinTEG MA < 45 mm 2 PC or 10 ml/kg (in patients
with normal TEG FF MA!)
RapidTEG
precipitate/ fibrinogen
EXTEM or FIBTEM
TEG
and angle and/or MA↑ TXA contraindicated as
considered reactive hyperfibrinolysis!)
RapidTEG
from injury < 3 hours and patient is bleeding!)
®
(rTEG®): K > 2.5 min cryoprecipitate/
®
: EXTEM CT ≥ 80 s and A10 ≥ 45 mm (A5 ≥
®
: R 10-14 min FFP 10-20 ml/kg; R > 14 min FFP
®
(rTEG®): R > 1.1 min plasma and
®
: KaolinTEG MA 45-49 mm 1 PC or 5 ml/kg;
®
(rTEG®): MA < 55 mm PC/ cryo-
®
:KaolinTEGLy30 > 4% TXA (1-2 g) (if > 4%
®
(rTEG®): Ly30 > 3% (5%)* TXA (if time
o
(<65o)* cryoprecipi-
o
FFP 20-30 ml/kg; TEG FF MA <
Fig. 7.3 Viscoelastic assay-driven algorithm for the use of hemostatic agents and blood products
in bleeding trauma patients. Overview of viscoelastic triggers for the differential and goal-directed
use or not use of blood products and hemostatic agents based on expert opinion, for ROTEM, TEG
and rapid TEG (rTEG). If available, specic treatments are given (TEG and rTEG only). ROTEM
parameters: EXTEM, test for the (extrinsic) hemostasis system; FIBTEM test for the brin part of
the clot, CT clotting time (s), A5/A10 clot amplitude after 5 or 10min (mm), MCF maximum clot
rmness (mm). TEG parameters: R reaction time (min), Angle speed of clot formation (degrees),
MA maximum amplitude (mm), FF MA functional brinogen test maximum amplitude (mm),
Ly30 amplitude reduction after 30min as an indicator of hyperbrinolysis (%). Additional deni-
tions for rTEG: K time from end of R until the clot reaches 20mm amplitude, ACT activated clotting time. Treatments: FFP fresh frozen plasma, PCC prothrombin complex concentrate, pRBC
packed red blood cells, TXA tranexamic acid. *Consider alternative treatments if rst-line strategies are not available. †Recommended values differ between publications. Modied from [56, 57]
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M. Maegele
algorithm for the viscoelastic test-driven use of hemostatic agents and blood products in bleeding trauma patients is given.
Fibrinolysis activation occurs almost universally after severe trauma, and systemic hyperbrinolysis has been identied as a key component of acute traumatic
coagulopathy associated with poor clinical outcomes [59]. Recent large randomized
controlled trials have consistently documented that the use of the synthetic lysine
analogue tranexamic acid (TXA) confers a survival advantage in a number of globally critical clinical conditions associated with acute bleeding, including traumatic
injury (CRASH-2), traumatic brain injury (CRASH-3) and post-partum hemorrhage (WOMAN), without increasing the thromboembolic risk [60]. Tranexamic
acid should be given as early as possible and within 3h of injury in the trauma
patient who is bleeding or at risk of signicant hemorrhage, as further analysis of
the CRASH-2 trial showed that treatment later than this is unlikely to be effective
and may even be harmful [14, 61, 62]. To date, TXA has evolved into a chief component of many MTP protocols [14, 63] but the two most recent randomized trials
using TXA in the prehospital setting of trauma [64] and traumatic brain injury [65]
failed to reproduce the benecial effects of TXA seen in earlier studies with respect
to 30-day mortality and neurologic outcome at 6months. However, when comparing the TXA effect stratied by time to treatment and qualifying shock severity in a
post hoc comparison, 30-day mortality was lower when TXA was administered
within 1h of injury (4.6% vs. 7.6%; difference, −3.0%; 95% CI, −5.7% to −0.3%;
p<0.002) and in patients with severe shock (18.5% vs. 35.5%; difference, −17%;
95% CI, −25.8% to −8.1%; p < 0.003) [64]. While in the conventional dosing
groups with 1g TXA bolus followed by 1g over 8h there was no increased risk of
thromboembolic events, these were more seen in groups that were treated with 2g
TXA bolus (9% vs. 4%) [65]. In another study, 4g TXA bolus to patients with
severe injuries was associated with a 32% rate of thromboembolic events and only
minimal immunomodulatory effects with respect to leukocyte phenotypes and circulating cytokines [66].
Fibrinogen, also referred to as coagulation factor I, represents the substrate for
blood to clot and is the rst coagulation factor reaching critical levels in the setting
of severe hemorrhage. Substantial drops in brinogen levels have been detected
in blood samples collected at the site of the injury and this as a function of injury
severity [67]. Fibrinogen may independently but also synergistically work with
TXA in the seriously injured requiring blood transfusion [68]. In any case, hyperbrinolysis needs to be inhibited prior to any coagulation factor supplementation,
e.g., brinogen, and a median 3.8g brinogen concentrate can increase clot stability by 5.2mm at 5min of viscoelastic test initiation, while TXA can decrease lysis
by 5.4% [69]. Meanwhile, the protective effects to the glycocalyx as well as to the
endothelial barrier integrity have been linked to the brinogen component rather
than to plasma per se [70]. The 2019 updated European guideline on the management of major bleeding and coagulopathy following trauma strongly recommends
against the use of FFP in patients without major bleeding (Grade 1B) and for the
treatment of hypobrinogenemia (Grade 1C) [14]. The treatment with brinogen concentrate or cryoprecipitate is currently recommended by the guideline
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if major bleeding is accompanied by hypobrinogenemia, as evidenced by viscoelastic signs of a functional brinogen decit or a Clauss plasma brinogen
level≤1.5g/L (Grade 1C) [14]. The suggested initial dose is 3–4g and repeated
doses should be guided by viscoelastic testing assays and laboratory assessment of
brinogen levels (Grade 2C) [14].
Declaration of Interest The author has received travel support, lecture and advisory board fees,
and research support from Astra Zeneca, Bayer, Biotest, CSL Behring, Portola Inc., TEM
International/IL-Werfen, and LFB Biomedicaments.
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