12-03-13

1
Massive
Transfusion in
Trauma
Christopher Hicks, MD, MEd, FRCPC
Emergency Physician, Trauma Team
Leader
St. Michaels Hospital
Assistant Professor, Department of
Medicine
University of Toronto
The Case
Key Data
Vitals
O/E
GCS 4
Abdomen Distended
Pelvis unstable
L femur deformity
Management
PIV x 2, ETT !
2L uid challenge
Disposition Air Transport DLY
75/55 130 Vent 99% 34.6

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FAST
12-03-13
2
Key Issues: Resuscitation
Clvlng blood and blood producLs - when, how
much?

88Cs, ll, boLh, nelLher?

Pow much ls enough? 1oo much?

Ad[uncLs Lo blood producLs?
The Five Things
1. Component therapy

34.5
3. Tranexamic acid
2. Massive transfusion
protocols
4. Managing complications
5. Targets and monitoring
CHEST / 137 / 1 / JANUARY, 2010 211 www.chestjournal.org
disorders also contribute to coagulation abnormali-
ties, including liver disease, warfarin and antiplatelet
drug use, and disseminated intravascular coagulation,
which often occurs in trauma patients either due to
tissue crush injury or a septic focus.
The ability of transfusion to maintain normal con-
centrations of RBCs, platelets, and coagulation fac-
tors disappears as bleeding progresses.
20
This occurs
because the standard process of making components
(separate units of PRBCs, platelets, and fresh frozen
plasma [FFP]) out of whole blood results in a loss of
platelets and dilution of all components with preser-
vative. Therefore, recombining the components (1 unit
each of PRBCs, platelets, and FFP) does not result in
a product equivalent to whole blood. The mean
hematocrit of a mixture of 1 unit PRBCs, 1 unit platelets,
and 1 unit of plasma is 29% (200 mL of PRBCs in
680 mL), whereas the mean platelet count is about
85,000/ m L (5.5 3 10
10
platelets in 680 mL), and the
mean coagulation factor activity is 62% of normal
(300 mL of plasma in 480 mL of acellular uid). Non-
viable cells, blood cell and plasma losses in making
leukoreduced products, ongoing blood loss, clot-
ting factor and platelet consumption, and other iso-
tonic crystalloid uid administration only worsen
the situation regarding dilutional coagulopathy and
thrombocytopenia.
Hemodilution is inevitable when giving specic
blood component therapy, even in the commonly used
1:1:1 ratio of PRBC:plasma:platelets. Table 2 compares
whole blood (500 mL) with component therapy with
PRBCs, platelets, and FFP (660 mL), documenting
signicantly reduced hemoglobin concentration and
decreased platelet count and coagulation activity com-
pared with whole blood.
Thus, massive bleeding is potentiated by hemo-
therapy-induced hemodilution and coagulopathy.
This is part of the reason that the number (increasing
hemodilution) and age (increasing numbers of non-
viable cells) of PRBC units transfused correlates with
mortality.
21
It is also why better methods for hemor-
rhage control are viewed as so important for further
reductions in mortality for trauma patients. Manage-
ment of coagulopathy after MT is largely driven by
expert opinion. A recent international survey of clini-
cal practice in the management of coagulopathy in
trauma identied signicant regional as well as insti-
tutional variability and very few MT protocols spe-
cically addressed the issue of early treatment of
coagulopathy.
22

Early Coagulopathy of Trauma
and Mechanisms
In the past, coagulopathy associated with trauma
was viewed largely as a dilutional event.
23
Today, post-
traumatic coagulopathy appears to be the sum of the
effects of injury severity, blood loss, factor depletion,
brinolysis, hypothermia, hypocalcemia, acidosis, and
the patients individual biologic response to both
traumatic injury and treatment.
24

-

26
The early identi-
cation and management of coagulopathy may help
to better control hemorrhage and may represent a
key step in reducing mortality associated with trau-
matic injury.
27

Recent evidence suggests that an acute endoge-
nous coagulopathy (before clotting factor depletion)
is present shortly after injury ( Fig 1 ).
25

,

28
This acute
coagulopathy of trauma is associated with systemic
hypoperfusion and is characterized by anticoagu-
lation and hyperbrinolysis.
29
It has recently been
identied that early traumatic coagulopathy occurs
only in the presence of tissue hypoperfusion and
appears to occur without signicant consumption of
coagulation factors. Alterations in the thrombomodulin-
protein C pathway are consistent with activated
protein C activation and systemic anticoagulation.
Figure 1. A diagram showing some of the mechanisms leading
to coagulopathy in the injured. Trauma can lead to hemorrhage,
which can lead to resuscitation, which in turn leads to dilution
and hypothermia causing coagulopathy and further hemorrhage.
This is classic dilutional coagulopathy. Hemorrhage can also cause
shock, which causes acidosis and hypothermia, which in turn lead
to coagulopathy, the fatal triad. Trauma and shock can also cause
the ACoTS associated with factor consumption and brinolysis.
Coagulopathy is further associated with trauma-induced inam-
mation and modied by genetics, medications, and acquired dis-
eases. ACoTS 5 acute coagulopathy of trauma-shock. (Reprinted
with permission from Hess et al.
28
)
Table 2 Whole Blood Composition Compared With
Component Therapy
Whole Blood (500 mL) Component Therapy (660 mL)
Hematocrit 38%-50% 1 unit PRBC 5 335 mL with
hematocrit 55%
Platelets 150-400 K/ m L 1 unit platelets 5 50 mL with
5.5 3 10
10
platelets
Plasma coagulation factors 5 100% 1 unit plasma 5 275 mL with
80% of the coagulation activity
compared with whole blood
Thus, 1 unit PRBCs 1 1 unit platelets 1 1 unit FFP 5 660 mL with
hematocrit 29%, platelets 88 K/ m L, and coagulation activity 65% com-
pared with whole blood. PRBC 5 packed red blood cells.
2010 American College of Chest Physicians
by guest on May 11, 2012 chestjournal.chestpubs.org Downloaded from
!"#$% '()(* )+,- '(./''(
1. Component Therapy
oWe dont bleed
red cells alone
oAims to replace
plasma along
with red cells
Damage Control Resuscitation
Permissive
Hypotension
Hemostatic
Resuscitation
Damage
Control
Surgery
Hemostatic Resuscitation
0 123453 '((,* 6+-7(8/7)+
12-03-13
3
One-to-One Ratio of PRBC:FFP
Additional Components
1. Platelets
o 50 000 100 000 with
active bleeding
o > 100 000 if ICH
2. Cryoprecipitate
o Fibrinogen < 1.0
o Empiric ~ 10U

Drivers and Limitations
Ratio-Based Lab-Based
1:1:1
Based on INR, CBC,
brinogen
*Getting behind*

Accuracy?

Adverse Events

Evidence:
Survivorship Bias
Retrospective Studies

Transfusion, 2010, 50: 701-710
2. Massive Transfusion Protocols
0 95!:;; <42= '((.* '(>'?- ).7/'(8
Massive Transfusion Protocols:
The Role of Aggressive Resuscitation
Versus Product Ratio in Mortality Reduction
Daniel J Riskin, MD, MBA, Thomas CTsai, BS, Loren Riskin, MD, Tina Hernandez-Boussard, PhD, MPH,
Maryanne Purtill, MD, Paul M Maggio, MD, MBA, FACS, David A Spain, MD, FACS,
Susan I Brundage, MD, MPH, FACS
BACKGROUND: Exsanguinating hemorrhage necessitating massive blood product transfusion is associated with
high mortality rates. Recent data suggest that altering the fresh frozen plasma to packed red
blood cell ratio (FFP:PRBC) results in significant mortality reductions. Our purpose was to
evaluate mortality and blood product use in the context of a newly initiated massive transfusion
protocol (MTP).
STUDY DESIGN: In July 2005, our American College of Surgeons-verified Level I trauma center implemented an
MTP supporting a 1:1.5 FFP:PRBC ratio, improved communications, and enhanced systems
flow to optimize rapid blood product availability. During the 4 years surrounding protocol
implementation, we reviewed data on trauma patients directly admitted through the emergency
department and requiring 10 or more units PRBCs during the first 24 hours.
RESULTS: For the 2 years before and subsequent to MTP initiation, there were 4,223 and 4,414 trauma
activations, of which 40 and 37 patients, respectively, met study criteria. The FFP:PRBC ratios
were identical, at 1:1.8 and 1:1.8 (p 0.97). Despite no change in FFP:PRBC ratio, mortality
decreased from 45% to 19% (p 0.02). Other significant findings included decreased mean
time to first product: cross-matched RBCs (115 to 71 minutes; p 0.02), FFP (254 to 169
minutes; p 0.04), and platelets (418 to 241 minutes; p 0.01).
CONCLUSIONS: MTP implementation is associated with mortality reductions that have been ascribed princi-
pally to increased plasma use and decreased FFP:PRBC ratios. Our study found a significant
reduction in mortality despite unchanged FFP:PRBC ratios and equivalent overall mean num-
bers of transfusions. Our data underscore the importance of expeditious product availability
and emphasize that massive transfusion is a complex process in which product ratio and time to
transfusion represent only the beginning of understanding. ( J Am Coll Surg 2009;209:
198205. 2009 by the American College of Surgeons)
Hemorrhage has been identified as a major cause of death
in trauma patients, causing most trauma-related mortality
within hours of admission to the emergency room.
1-3
Mas-
sive transfusion has been defined as greater than 10 units of
packed red blood cells (PRBCs) in a 24-hour period.
4
When first discussed in the 1970s, massive transfusion was
associated with mortality rates higher than 90%.
5
Since
then, advances in critical and surgical care of trauma pa-
tients requiring massive transfusion have led to dramatic
decreases in mortality. Mortality rates between 30% and
70% are commonly reported.
6
Improved survival has been
attributed to damage-control techniques, appreciation and
correction of coagulopathy, patient rewarming, and im-
proved overall resuscitation.
6
The institution of massive
transfusion protocols (MTP) has reduced mortality, with
the benefit primarily ascribed to an increased ratio of fresh
frozen plasma (FFP):PRBCs.
7,8
But the precise contribut-
ing factors responsible for improved outcomes remain
unclear.
Many retrospective analyses and some prospective stud-
ies have explored the role of FFP, recombinant activated
factor VII (rFVIIa), and whole blood in improving out-
comes in the context of MTPs.
9-11
Exsanguinating hemor-
rhage results in acidosis, hypothermia, and coagulopathy,
which represent a lethal triad.
12
The importance of avoid-
Disclosure Information: Nothing to disclose.
Received January 15, 2009; Revised April 15, 2009; Accepted April 17, 2009.
From the Department of Surgery, Stanford School of Medicine, Stan-
ford, CA.
Correspondence address: Daniel J Riskin, MD, MBA, 300 Pasteur Dr, Room
H3680, Stanford, CA 94305-5655.
198
2009 by the American College of Surgeons ISSN 1072-7515/09/$36.00
Published by Elsevier Inc. doi:10.1016/j.jamcollsurg.2009.04.016
12-03-13
4
0 95!:;; <42= '((.* '(>'?- ).7/'(8
given, the quantities of product administered before and
after MTP implementation were similar, except for a
higher platelet:PRBC ratio, which changed from 1:1.8 to
1:1.3 with implementation of the protocol (p 0.05). A
logistic regression model was built to predict the risk of
mortality using blood transfusion quantities as the inde-
pendent variables, with results outlined in Table 5. The
goodness-of-fit statistic indicated the model was well fit (p
value 0.3743), and the model yielded an area under the
curve of 0.8269. The model controlled for confounding vari-
ables: age, Injury Severity Score, Glasgow Coma Scale 3,
and type of injury. Significant predictors of mortality were
number of units of PRBCs and platelets transfused. An in-
crease in units of PRBCs transfused was associated with in-
creased mortality, with an odds ratio of 1.21 (95%CI, 1.06 to
1.38); increased units of platelets transfused were associated
with decreased mortality, with an odds ratio of 0.43 (95%CI,
0.20 to 0.93).
DISCUSSION
This study evaluated massive transfusion trauma patients at
a Level I trauma center for the 2 years before and 2 years
after implementation of an MTP. The combined mortality
rate for the 2 years preceding implementation was 45%,
compared with only 19% mortality in the 2 years
postimplementation (p 0.02). The mortality difference
noted is consistent with experience in military and civilian
trauma in implementation of an MTP.
4,13,23,29
Our data are
unique compared with those from other studies in that
mortality decreased despite no significant alteration in the
ratio of blood components used for resuscitation.
Much discussion in the current trauma literature focuses
on changes in blood product ratio as a means to affect
mortality.
20
In fact, our protocol was designed to target a
1:1.5 ratio of FFP:PRBCs. A second goal of our protocol
was to improve communication with the blood bank and
decrease the time needed to have components available for
transfusion. It is unclear why the FFP:PRBC ratio did not
alter with protocol implementation. The primary reason
was likely a surgical and anesthesia culture that already
actively practiced aggressive resuscitation targeted to com-
bat dilutional coagulopathy in the major trauma patient
before implementation of the MTP. This rationale is fur-
ther supported by our findings that the overall volume of
product was also unchanged.
The second goal of MTP implementation was met.
Communication with the blood bank and product avail-
ability improved. Time to blood product resuscitation, in-
dicated by times to first transfusion for cross-matched
PRBCs, FFP, and platelets, was dramatically decreased after
implementation of MTP. Times to first documented trans-
fusion for cross-matched PRBCs, FFP, and platelets were
reduced 39%, 33%, and 42% (p 0.04), respectively.
Notably, overall numbers of blood products given did not
significantly change.
A valid definition of massive transfusion is evolving. In
regard to timing, is the definition of massive transfusion 10
units in the first 24 hours, 10 units in 12 hours, 10 units in
6 hours or less? Alternatively, perhaps intention to treat
rather than transfusion requirements themselves should de-
fine massive transfusion. At the time of the initiation and
construction of our study design, we chose our inclusion
and exclusion criteria (10 units in 24 hours) to be consis-
tent with those in the literature, so we did not use intention
to treat analysis. The trauma community is currently hotly
debating the valid criteria for massive transfusion. The
definition of massive resuscitation based on volume resus-
citation ignores patients who may have required less prod-
uct in the late cohort because of improved procedures. The
definition of massive transfusion as 10 units in 24 hours
used in our study design was chosen for consistency with
definitions in previously published literature. Because most
of the published reports refer to product ratios rather than
timing, the suggestion of our data that the impact of timing
Figure 2. Patient survival by year. MTP, massive transfusion
protocol.
Table 4. Mortality Rates Between Cohorts
Variable Pre-MTP Post-MTP p Value
Patients, n 40 37
Deaths, n 18 7
Mortality, % 45 19 0.02*
*Statistically significant; p 0.05.
MTP, massive transfusion protocol.
202 Riskin et al Massive Transfusion Protocols J Am Coll Surg
This document is the property of St. Michaels Hospital and should not be made available outside of the hospital
In printed form this document is valid this date only on
Massive Transfusion Protocol (MTP) version11 12 14 2009 Page 7 of 8
Appendix A

Massive Transfusion Protocol Clinical Guidelines

















































Indications for MTP
Substantial blood loss (estimated>1500 ccs/requirement for > 6 units PRBCs ) with
anticipated ongoing uncontrolled hemorrhage in the short term (minutes to hours)
Anticipated blood loss of >10 units of packed red blood cells within a two hour period

Physician initiates MTP
Nurse or member of clinical team notifies transfusion services ext 5084
Required information: Patient name, J#, location, gender and age
To be completed immediately:
IV access:
2 large bore peripheral IV sites
subclavian or jugular cordis (femoral is necessary)

Laboratory testing
Cross match and type
CBC
ABG
Coagulation tests (PT/PTT, INR, fibrinogen)

Ongoing monitoring while MTP activated:
Continuous vital signs (HR, oximetry, BP)
Temperature q 15 mins
Laboratory testing
q 15 mins ABG, electrolytes
q 30 mins Hemorrhage panel (CBC, INR,
fibrinogen)
q 4h creatinine, ionized Ca
++
, Mg
++
and
serum lactate.
Documentation:
intake all fluids administered
output all tubes and estimated blood loss
from all sources
Termination of MTP by MD:
Notify Transfusion services
Return unused blood products promptly to transfusion
services
If the patient is transferred to a new location, the
receiving unit must be formally notified and sign off on
accompanying blood components and blood products.
Important clinical considerations:
Accurately follow protocol for administration of
blood and blood products
Administer fluids under pressure and via
warming devices whenever possible
Correction of acidosis and hypothermia
Reassess need for MTP q 15 mins based on
clinical status of patient
Consider appropriateness of:
o administration of Factor VIIa
o interventional radiology
This document is the property of St. Michaels Hospital and should not be made available outside of the hospital
In printed form this document is valid this date only on
Massive Transfusion Protocol (MTP) version11 12 14 2009 Page 7 of 8
Appendix A

Massive Transfusion Protocol Clinical Guidelines

















































Indications for MTP
Substantial blood loss (estimated>1500 ccs/requirement for > 6 units PRBCs ) with
anticipated ongoing uncontrolled hemorrhage in the short term (minutes to hours)
Anticipated blood loss of >10 units of packed red blood cells within a two hour period

Physician initiates MTP
Nurse or member of clinical team notifies transfusion services ext 5084
Required information: Patient name, J#, location, gender and age
To be completed immediately:
IV access:
2 large bore peripheral IV sites
subclavian or jugular cordis (femoral is necessary)

Laboratory testing
Cross match and type
CBC
ABG
Coagulation tests (PT/PTT, INR, fibrinogen)

Ongoing monitoring while MTP activated:
Continuous vital signs (HR, oximetry, BP)
Temperature q 15 mins
Laboratory testing
q 15 mins ABG, electrolytes
q 30 mins Hemorrhage panel (CBC, INR,
fibrinogen)
q 4h creatinine, ionized Ca
++
, Mg
++
and
serum lactate.
Documentation:
intake all fluids administered
output all tubes and estimated blood loss
from all sources
Termination of MTP by MD:
Notify Transfusion services
Return unused blood products promptly to transfusion
services
If the patient is transferred to a new location, the
receiving unit must be formally notified and sign off on
accompanying blood components and blood products.
Important clinical considerations:
Accurately follow protocol for administration of
blood and blood products
Administer fluids under pressure and via
warming devices whenever possible
Correction of acidosis and hypothermia
Reassess need for MTP q 15 mins based on
clinical status of patient
Consider appropriateness of:
o administration of Factor VIIa
o interventional radiology
This document is the property of St. Michaels Hospital and should not be made available outside of the hospital
In printed form this document is valid this date only on
Massive Transfusion Protocol (MTP) version11 12 14 2009 Page 8 of 8
Appendix B

MTP Blood Transfusion Services (BTS) Response Flowchart


"#$ %&'()*'+,

















YES



NO


NO






YES



NO







NO YES
Preparation of MTP cooler pack:
6 units packed RBC
4 units AB FFP
1 adult pack of platelets - store at room temperature (NOT IN
COOLER).


The appropriate unit (ED, ICUs, OR) notifies Patient Transport Services (ext 5023) for stat pick up/delivery
of MTP transport container and the blood products will be released by BTS for pick up.
Additional 4 units of packed RBCs to be sent to clinical area 20
minutes after initial MTP cooler delivery
4 units of FFP will be immediately thawed and available upon
request
Subsequent needs for platelets and cryoprecipitate will be met
through notification of transfusion services
"#$ '+-.(/*'+,
Discontinue MTP activities
"#$ '+-.(/*'+,
Ensure continuous availability of 4 units FFP
If MTP has not been deactivated for 30 minutes with no further request
for blood or blood products, verify ongoing need with MTP team
"#$ '+-.(/*'+,
This document is the property of St. Michaels Hospital and should not be made available outside of the hospital
In printed form this document is valid this date only on
Massive Transfusion Protocol (MTP) version11 12 14 2009 Page 8 of 8
Appendix B

MTP Blood Transfusion Services (BTS) Response Flowchart


"#$ %&'()*'+,

















YES



NO


NO






YES



NO







NO YES
Preparation of MTP cooler pack:
6 units packed RBC
4 units AB FFP
1 adult pack of platelets - store at room temperature (NOT IN
COOLER).


The appropriate unit (ED, ICUs, OR) notifies Patient Transport Services (ext 5023) for stat pick up/delivery
of MTP transport container and the blood products will be released by BTS for pick up.
Additional 4 units of packed RBCs to be sent to clinical area 20
minutes after initial MTP cooler delivery
4 units of FFP will be immediately thawed and available upon
request
Subsequent needs for platelets and cryoprecipitate will be met
through notification of transfusion services
"#$ '+-.(/*'+,
Discontinue MTP activities
"#$ '+-.(/*'+,
Ensure continuous availability of 4 units FFP
If MTP has not been deactivated for 30 minutes with no further request
for blood or blood products, verify ongoing need with MTP team
"#$ '+-.(/*'+,
MTP: Stakeholders
Blood Bank, Transfusion Medicine
Surgical Services
Emergency
Intensive Care
Laboratory Medicine
Operating Room
Surveillance, Feedback, Education
MTP: Bottom Line

oConserves blood products

oMinimizes waste
oSupports ratio-based resuscitation
oEnhance systems ow
oImproves communication
oHastens delivery

12-03-13
3
http://www.nba.gov.au/guidelines/module1/contents/transfusion.html Lancet 2010; 376: 23-32

3. Tranexamic Acid
Plasmin
Plasminogen
Activator
Mature
Fibrin
Prothrombin
Thrombin
Fibrinogen FDPs
Tranexamic
Acid
Plasminogen
FIBRINOLYSIS
COAGULATION
(HYPER)
Lancet 2010; 376: 23-32
Lancet 2010; 376: 23-32
Lancet 2010; 376: 23-32 Lancet 2010; 376: 23-32
Articles
www.thelancet.com Vol 376 July 3, 2010 29
reduced but the risk of vascular occlusive events might
remain. We therefore selected a regimen that would
allow for the eect of tranexamic acid on the early risk
of haemorrhage without extending into the period when
the risk of vascular occlusive events might be increased
by this treatment. The absence of any increase in
vascular occlusion with tranexamic acid, whether fatal
or non-fatal, provides reassurance that this regimen is
safe. Although the eect of this drug on all-cause
mortality did not vary substantially according to the
time from injury, there was some suggestion that early
treatment might be more eective. However, even if this
were not the case, the fact that most deaths from
haemorrhage occur in the rst few hours after injury
implies that every eort should be made to treat patients
as soon as possible.
1517
The dose of tranexamic acid used in this trial was based
on studies of this drug in surgical patients in which
loading doses range from 25 mg/kg to 100 mg/kg, and
maintenance doses from 025 mg/kg/h to 4 mg/kg/h,
delivered over 112 h.
5
Findings from studies of the eect
of dierent doses of tranexamic acid on blood loss and
blood transfusion showed no signicant dierence
between high and low doses. Studies in cardiac surgery
have noted that a 10 mg/kg loading dose of tranexamic
acid followed by an infusion of 1 mg/kg/h produces
plasma concentrations su cient to inhibit brinolysis,
and that a larger dose does not provide any additional
haemostatic benet.
18,19
In emergency situations, the
administration of a xed dose is practicable since
determining the weight of a seriously injured patient can
be di cult. We therefore selected a xed dose within the
range shown to inhibit brinolysis and provide
haemostatic benet that would be e cacious for larger
patients (>100 kg) but also safe in smaller patients
(<50 kg), to the extent that the dose per kg that smaller
patients would receive has been used in surgical trials
without adverse eects. The possibility that a higher dose
of tranexamic acid would have a greater treatment eect
remains open to debate and warrants further study.
The knowledge that tranexamic acid reduces the risk of
death from traumatic bleeding raises the possibility that it
might also be eective in other situations in which
bleeding can be life threatening or disabling. Traumatic
brain injury is commonly accompanied by intracranial
bleeding, which can develop or worsen after hospital
admission. Traumatic intracranial haemorrhage is
associated with an increased risk of death and disability,
and irrespective of location, haemorrhage size is strongly
correlated with outcome.
2022
If tranexamic acid reduced
intracranial bleeding after isolated traumatic brain injury,
then patient outcomes might be improved. Studies that
assess the eect of tranexamic acid on the extent of
intracranial bleeding are needed.
Tranexamic acid might also have a role in bleeding
conditions apart from traumatic injury. Post-partum
Figure : All-cause mortality by subgroups
GCS=Glasgow Coma Score. *95%CI.
Time from injury (h)
1 509/3747 (136%) 581/3704 (157%) 087 (075100)
>13 463/3037 (152%) 528/2996 (176%) 087 (075100)
>3 491/3272 (150%) 502/3362 (149%) 100 (086117)
=4411; p=011
Systolic blood pressure (mm Hg)
90 702/6878 (102%) 736/6761 (109%) 094 (082107)
7689 280/1609 (175%) 313/1689 (185%) 094 (078114)
75 478/1562 (306%) 562/1599 (351%) 087 (076099)
=1345; p=051
GCS
Severe (38) 796/1789 (445%) 860/1830 (470%) 095 (086104)
Moderate (912) 219/1349 (162%) 249/1344 (185%) 088 (070109)
Mild (1315) 447/6915 (65%) 502/6877 (73%) 088 (075104)
=1387; p=050
Injury type
Blunt 1134/6788 (167%) 1233/6817 (181%) 092 (083102)
Penetrating 329/3272 (101%) 380/3250 (117%) 086 (072103)
=0791; p=037
All patients 1463/10060 (145%) 1613/10067 (160%) 091 (085097)*
Two-sided p=00035
07 10 09 08 11
Tranexamic acid better Tranexamic acid worse
12
Tranexamic acid allocated Placebo allocated Risk ratio (99%CI)
Lancet 2010; 376: 23-32
ARR = 1.5%

NNT = 67

should be considered for inclusion on the
WHO List of Essential Medicines
Lancet 2010; 376: 23-32
12-03-13
6
Some Newer Stuff: TXA
o CRASH-2 subgroup: may be detrimental if
given beyond 3h
o Combat scenarios: mortality benet,
especially seen in massively transfused
patients
o But dont wait for the MTP Thinking
blood? Think TXA
4. Managing Complications
36.5
34.2
31.6
Hypothermia Acidosis
Coagulopathy
34.5
Calcium and Clotting
34.5
Hypothermia and Clotting

o 10% reduction in coagulation factor for
every 1C drop in temperature
o Below 33C ! prolonged clotting times
o Lab analysis of PT and PTT can be
misleading
Warmed to 37C
34.5
!"#$% '()(* )+,- '(./''(
Avoiding Hypocalcemia

o Frequent monitoring of serum calcium
levels
o Goal: Ca
2+
< 1.1 mmol/L
o Empiric treatment: 2g Calcium Gluconate
for every 5-6U PRBC given
34.5
Total serum calcium is not useful owing to
hemodilution effects of massive transfusion
12-03-13
7
Avoiding Hypothermia

o Elevating room temperature
o Surface warming
o Heated and humidied gases
o Warmed uids
34.5
Prevention is the key! Get (and follow) a
temperature on all trauma patients!
!"#$% '()(* )+,- '(./''(
5. Targets
1. Vital signs
o Poor marker of end-
organ perfusion
o Vary depending on
individual physiology
2. Normal vitals
o Not the goal
o Difcult to dene
o May be detrimental
Goal-Directed Trauma Resus
1. Base decit
o Correlates with
mortality
o > -6 = signicant
2. ! Lactate
o Independent predictor
of mortality
3. End-organ
perfusion
o Adequate urine output
Critical Care 2005 9:441
Foley, ABG and Lactate
Your resuscitative BFFs
Gospel Accd to Chris, 2012
Aim For:
o 1emp > 33C
o 8L < - 6
o pP > 7.2
o LacLaLe < 4 mmol/L
o Ca
2+
> 1.1 mmol/L
o laLeleLs > 30 x 10
9
/L
o 1/A11 < 1.3x
normal
o ln8 < 1.3
o llbrlnogen > 1.0 g/L

http://www.nba.gov.au/guidelines/module1/contents/transfusion.html
12-03-13
8
The Five Things
1. RBC + FFP
34.5
3. Giving blood? Give TXA
2. MTPs
Cost-effective,
saves lives
4. The forgotten
Ca
2+
, Temp
5. Foley, ABG, lactate
christopher.hicks@utoronto.ca