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resuscitation center or the operating room. Hemorrhagic shock
due to severe blood loss is a major factor in trauma-related
deaths. A contributing factor to ongoing hemorrhage is the
development of trauma-induced coagulopathy (TIC), which is
an intrinsic dysregulation of the coagulation pathway [34, 35].
The intrinsic coagulopathy in TIC seems to be driven by endothelial hypoxemia, pathological activation of protein C, platelet
dysfunction, and brinolytic dysregulation. The development
of TIC is associated with increased mortality (4X) [36] and
with the development of serious events such as uncontrolled
bleeding, ongoing massive transfusion requirements, and multiorgan failure, which can lead to longer intensive care unit
(ICU) and hospital length of stay [37, 38]. Prior to 2000, resuscitation was based mainly on the transfusion of packed red
blood cells (PRBCs) and synthetic uids to maintain intravascular volume and tissue oxygen delivery. With the use of conventional coagulation tests (CCTs), specic coagulation
defects were identied leading to the addition of other blood
component products such as fresh frozen plasma (FFP) and
platelets during trauma resuscitation [39].
Traditional laboratory testing offers valuable information
on varying aspects of coagulation, but they were originally
designed for the monitoring of therapeutic anticoagulation in
a laboratory setting, rather than identication of TIC.There
are several limitations of CCTs: They are imprecise in the
delineation of the complex nature of TIC and require signicant time for nal result reporting and therefore may have limited clinical relevance in the quickly changing trauma patient
[35, 40]. With these limitations of CCTs in mind, viscoelastic
assays such as thromboelastography (TEG) or rotational
thromboelastometry (ROTEM) are alternative diagnostic
methods for the timely identication of specic coagulation
defects which could enable individualized resuscitation.
TEG can be used in trauma patients to predict the need for
blood component therapy or the use of hemostatic agents
(PCC, rFVIIa, brinogen, and TXA) in hypocoagulable and
coagulopathic patients. Also, it can help to identify that subset
of trauma patients are hypercoagulable and may benet from
early deep vein thrombosis (DVT) prophylaxis [41].
Individualization in administration of blood component
therapy with the use of TEG helps to address the immediate
needs of the bleeding trauma patient. Therefore, minimizing
the overuse and waste of blood products and decreasing the
appearance of complications such as DVT, TRALI, TACO,
acute respiratory distress syndrome (ARDS), infections, and
allergic reactions [42–44].
Adverse Transfusion Outcomes in Severe
Trauma
The major life-threatening complication for massive transfusion in severe trauma is transfusion-related acute lung
injury (TRALI). While TRALI is the primary cause of
transfusionall rate of TRALI in the setting of massive resuscitation for
hemorrhagic shock is low [46]. Still, an extensive literature
review published by Patel etal. revealed that the odds of
ARDS/ALI and death increased with each additional unit
of red blood cells transfused (odds ratio [OR] 1.06 and
1.07, respectively) [47]. The use of older blood for massive
transfusion may also contribute to increased mortality and
adverse events [48]. The epidemiology, pathogenesis, risk
factors, and management of TRALI are discussed separately within this text.
Other physiologic derangements that may occur with
massive transfusion include acid-base disturbance in the
form of metabolic alkalosis and electrolyte abnormalities
such as hypocalcemia and hyperkalemia [49]. A substantial
amount of citrate is delivered to the patient during massive
transfusion since citrate is used as an anticoagulant in
stored blood. The citrate is metabolized to bicarbonate, and
the excess bicarbonate is excreted in the urine. Metabolic
alkalosis may develop when bicarbonate excretion is
reduced in the setting of renal failure. There may also be
associated hypokalemia when hydrogen ions move out of
cells in exchange for potassium ions moving into cells to
compensate for the metabolic alkalosis. A clinically signicant metabolic alkalosis is not a common event as the
patient in hemorrhagic shock likely already has a metabolic
acidosis due to endeffect of the citrate is that it chelates calcium and decreases
ionized calcium levels. Profound hypocalcemia may lead to
seizures or arrhythmias and cardiac arrest. Calcium is a
critical component for the proper functioning of the coagulation cascade, and hypocalcemia can worsen the coagulopathy that is frequently associated with hemorrhagic
shock. Patients undergoing massive transfusion are also at
risk for hyperkalemia. The risk is increased with the use of
older red blood cells and irradiated blood [50]. The potassium concentration in the supernatant of red blood cells
increases linearly by 1 mEq/day and approximates the
number of days in storage. The most critical complication
of this electrolyte abnormality is the potential for transfusion-associated hyperkalemic cardiac arrest. Arterial blood
gases, potassium, and ionized calcium levels should be
obtained to guide the management of the patient.
As part of the lethal triad of hemorrhagic shock, hypothermia can be worsened by massive transfusion, and this
can exacerbate any ongoing coagulopathy. Coagulation
begins to become impaired when the core body temperature
decreases to less than 37°C [51, 52]. Furthermore, a rapid
decline in body temperature can lead to bradycardia, ventricular brillation, and subsequent cardiac arrest. The risk
can be reduced by using a rapid infuser that has the capability of warming blood during rapid transfusion.
related morbidity and mortality [45], the over-
organ hypoperfusion. Another adverse
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Rapid Infusion Devices
There are several medical devices currently on the market to
provide warming for intravenous uids and blood products.
The simplest of devices utilize heating plates, water baths, or
countercurrent heat exchange to warm uid. While these
devices provide excellent warming of uids and blood products during routine care, they are limited in their ability
warm blood products at rapid ow due to insufcient contact
time with cold blood products. Newer devices designed specically for the rapid infusion of blood products utilize electromagnetic induction, microwave technology, and dry
thermal transfer to rapidly warm blood products. Table20.2
compares three commercially available rapid infusion
devices [53–55].
When evaluating rapid infusion devices, several factors
should be taken into consideration. For the purposes of this
chapter, we will focus on the Level 1, the Belmont, and the
ThemaCor1200. The Level 1 system provides warming via
countercurrent heat exchange through warmed water.
Delivery of blood products is based on dual pneumatic pressure infusers with the ability to infuse one unit while loading another unit on the opposite side (Fig. 20.2). The
Belmont and ThermaCor1200 both utilize a mechanical
pump to deliver blood products rapidly from a large reservoir. The Belmont heats via electromagnetic microwave
warming, while the ThermaCor1200 relies on dry thermal
heat transfer.
During the rapid administration of large volumes of cold
blood, there is a risk for venous air embolism and hypothermia; therefore, rapid infusion systems should be able to reliably detect and purge air and warm cold blood products at
Table 20.2 Comparison of infusion devices
Level-1 H-1000
Manufacturer Smith’s medical Smission-
Footprint Medium Small Medium
Heat
mechanism
Transfusion
rate
Weight (kg) 32 9.5 12
Air removal Manual Automatic Automatic
Ease of uid
loading
Ease of set-up Easy Primes in
Battery
capability
Other Ability to heat blood
Countercurrent Dry thermal Microwave
~500mL/min 10mL/h–
No reservoir for
blood products. Air
must be expelled
from each unit to
prevent air
embolization
No Ye s Yes
products dependent
on infusion rate
ThermaCor
1200
Cartledge
biomedical,
LLC
1.2L/min
3 spike inow
set, uid
reservoir
available
<60s
Belmont
rapid infuser
Belmont
instrument
corporation
warming
2.5mL/
min–1L/min
3 or 4 spike
inow set,
3L uid
reservoir
Primes in
<60s
Does not heat
until ow is
10mL/min
Fig. 20.2 The level 1 H1025
(a) and the Belmont FMS
2000 (b) (Modied from:
Comunale [56])
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197
rapid rates. The Level 1 system has a gas vent which automatically eliminates microbubbles within the system. On
newer models, there is an optional integrated air detector and
clamp that will alert the clinician to the presence of air and
stop ow to the patient [54]. The ThermaCor1200 has four
air sensors built into the disposable cassette although the
exact mechanism is proprietary [53]. On the Belmont, there
are two ultrasonic air detectors which detect as little as
0.1 mL of air [56]. Cumunale, in a comparative study
between the Level 1 and Belmont device, injected 10mL of
air into each system proximal to the heat exchanger and
found that the air bolus was able to pass through the delivery
tubing in the level 1 system. The air was detected and purged
by the Belmont [56]. This same study compared the warming
abilities of each device at a rapid ow rate of 500mL/min.
While both devices warmed to physiologic temperatures at
low ow, at high ow rates the blood delivered by the Level
1 averaged 32°C [56, 57]. Current peer reviewed literature
comparing the ThermaCor1200 to either the Level 1 or
Belmont is not available at this time.
All of the rapid infusion devices have the availability to
deliver uid at a very high rate; however, what is delivered to
the patient will be based on the intravenous (IV) access present. For the three devices above, an 18 gauge IV is the minimum size for infusion. Theoretically, the maximum ow rate
of uids in an IV catheter is predicted by Poiseuille’s law
(Fig.
20.3) where ow is related to uid viscosity, the pres-
sure gradient across the catheter, and the length and diameter
of the IV catheter. Doubling the diameter of a catheter
increases the ow rate by 16-fold. However, this only applies
to laminar ow. When rapidly infusing blood, the actual ow
rate cannot fully be predicted by Poiseulle’s law due to the
development of turbulence [57]. However, we do know that
larger and shorter IV catheters provide superior ow rates
over smaller and/or longer IV catheters.
It is very difcult to nd studies showing the difference in
ow rates through standard IV catheters and large bore central infusion lines. A study published by Wrenn etal. [58]
compared ow rates between several catheters comparing
both hetastarch and normal saline (NS) as delivered by the
ThermaCor1200 rapid infusion device. This study compared
Table 20.3 Common IV catheter sizes and infusion time for 1000mL
of normal saline [
Size Type 1000mL infusion time (min)
8.5 Fr RIC 0.46
7.0 Fr RIC 1.0
8.5 Fr Sheath introducer 1.05
14Ga Standard IV cannula 1.30
16Ga Standard IV cannula 2.20
18Ga Standard IV cannula 4.23
14Ga 4 lumen central line 5.20
20Ga Standard IV cannula 6.47
RIC rapid infusion catheter
59]
ow rates between 18-gauge, 16-gauge, 14-gauge, 7.0 Fr and
8.5 Fr rapid infusion catheter (RIC), 14-gauge double lumen
central line, 8.5 Fr sheath introducer, and a multilumen
access catheter (MAC) introducer. With similar driving pressures from the ThermaCor1200, they found that the 8.5 Fr
RIC and the MAC catheter were superior at rapid transfusion
with both NS and hetastarch, each providing ow rates
exceeding 1L/min with driving pressures of 300mmHg. The
double lumen central line performed the worst, followed by
the 18-gauge peripheral IV delivering 180 mL/min and
210mL/min of hetastarch, respectively. While hetastarch is
no longer used clinically in the United States, it is more viscous than NS and therefore is more predictive of ow rates
with blood products than NS.
Andrew Buck ran a similar experiment where he determined the time it took to infuse 1 liter of NS on a pneumatic
rapid infusion device through several commonly used intravenous catheters [
59]. In this study, the 8.5 Fr RIC was also
shown to be the quickest transfusion method with a 1L infusion time of 46s. The 8.5 Fr sheath introducer took 1:05min,
a 14-gauge 4 lumen central venous catheter took 5:20, and a
standard 20 gauge peripheral IV took 6:47min to infuse a
liter of NS (Table20.3).
Both of these studies support the use of large diameter
short cannulas for IV access to facilitate rapid infusion of
volume. Central venous access may not be the best method
for volume administration, especially given the complexity
of placement and the frequency of other tasks that need
simultaneous attention in a severe trauma patient.
Fig. 20.3 Poiseuilles’ equation
Conclusion
Hemorrhage is the leading preventable cause of death in
trauma patients. The initial management of trauma patient
involves ATLS protocols with a focus of treating lifethreatening injuries rst. The strategy of damage control
resuscitation of a trauma patient in hemorrhagic shock
involves preserving end-organ perfusion and preventing any
further progression of the lethal triad of death. Volume resuscitation in the bleeding trauma patient should focus on
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J. C. Humanez et al.
replacement of blood volume with blood products in a 1:1:1
ration and minimal crystalloid. Use of cell salvaged blood
should be considered to minimize the amount of allogenic
product when possible. Targeted blood product replacement
utilizing TEG or ROTEM is recommended if possible.
Trauma patients that require blood transfusion should also be
given TXA within the rst 3h after injury. Complications
associated with large volume transfusion include TRALI,
TACO, hyperkalemia, hypocalcemia, and hypothermia.
Hypothermia can be minimized warming blood products
prior to administration. Utilization of a rapid infusion device
improves the ability to rapidly deliver warmed blood products to the patient. Intravenous access to accommodate high
rates of transfusion is best accomplished with large diameter
short length catheters.
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Point-of-Care Tests inforBlood
https://t.me/medicina_free
Coagulation inthePerioperative Period
SarahLeavitt, ShairkoMissouri, DivyaPatel,
andCoreyS.Scher
21
Thromboelastography utilizing the TEG® analyzer systems (Haemonetics Corporation, Boston, MA) and thromboelastometry utilizing the Rotem® analyzer systems
(Instrumentation Laboratory, Bedford, MA) are presently
benchmark tests for goal-directed blood component transfusions, in scenarios of bleeding and hemorrhage in cardiac,
obstetrical, blunt, and penetrating trauma, brain trauma,
and solid organ transplantation. It isis essential to know that
there are no studies to compare Rotem and TEG. The choice
between the two lies in which product was deployed by a
department or hospital administration. Both tests rely on the
concept of viscoelasticity. A substance is thought of as just
a solid or just a liquid. One that is viscoelastic may have
both properties. Elastic substances may undergo strain when
stretched but will return to its normal state once that stressing
factor is removed. Viscosity gives the material more stability
and resists stretching [1]. Blood is a viscoelastic substance.
Plasma demonstrates pure viscous behavior, while other
components of blood are elastic. The viscoelasticity of blood
is under the inuence of four factors: (1) the environment
(temperature), (2) interplay (RBC orientation and aggregation), (3) plasma factors (osmotic pressure, pH, concentration of brinogen and other plasma proteins), and (4) RBC
factors (viscoelasticity and deformability of erythrocytes and
their membranes).
There is little difference in blood viscoelasticity among
normal cases but becomes signicant with certain pathological states or surgical interventions. The formation of a clot
results from the polymerization of factors that generate brin.
The ongoing reactions generate a three-dimensional polymer
network. This network changes the viscoelasticity prior and
through the phase of brin generation. The changes in visco-
elasticity during the clotting phase can be measured and presented to the anesthesiologist as a computerized tracing) [2].
The thromboelastogram (TEG®) tracing is nonlinear,
and while valuable, it lacks a mathematical way to determine accuracy of the curves. Viscoelastic testing (TEG® and
Rotem) has more than stood the test of time and remains an
essential part of goal-directed blood product administration.
Their utility is now in question as new tests based on different sciences are making their way to the market and appear
to be more accurate due to the measurements that are linear.
Figure 21.1 is a TEG 5000 (Haemonetics Corporation®).
To generate test results utilizing a TEG® 5000 analyzer, a
small sample of whole blood (native, citrated or heparinized depending on tests run) is placed in a 37-degree cuvette
(Fig. 21.2). A disposable pin is suspended from a torsion
wire into the cup. The cup rotates through an angle of 4° for
45min with each cycle lasting approximately10s (Fig.21.2).
As the blood begins to clot and it adheres to both the pin and
the cuvette, the clot will begin to transmit the rotation of the
cup to the pin. The pin is suspended by a torsional spring
which adds an elastic element to the system. The extent of
resulting pin rotation is directly proportional to the strength
of the clot. The corresponding numeric results and tracing
represent all of the phases of clot formation and lysis [2].
Figures 21.3 and 21.4 illustrate all of the components of a
TEG tracing to understand rate, strength, and stability or sustainability of a clot. The R reects the “Reaction Time” and
represents the coagulation pathways resulting in the initial
thrombin burst and generation of brin or factor IIa.
A long “R” time may denote that factors are decient and
goal-directed fresh frozen plasma, or newly developed synthetic factors (10,9,7,2-KCENTRA®) [3]. Utilization of a
S. Leavitt · S. Missouri · D. Patel · C. S. Scher (*)
NYU-Grossman School of Medicine, Department of
Anesthesiology, New York, NY, USA
e-mail: sarah.leavitt@nyumc.org; Corey.Scher@nyulangone.org
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_21
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Fig. 21.1 TEG 5000. (With permission from Haemonetics
Corporation)
S. Leavitt et al.
cuvette impregnated with heparinase (identied with a blue
colorant in the disposable plastic cup) can help determine if
systemic heparin is responsible for the observed delay in clot
formation.
Depending on the coagulation status of the patient and on
the type of test run, it takes minutes or longer for the entire
body of the TEG results to be displayed (Figs.21.3 and 21.4).
The alpha (α), angle parameter is the slope of the line
beginning at the point that the tracing diverges from the baseline line and is tangential to the TEG tracing. This represents
the acceleration of brin buildup and cross-linking.
Critical information of the TEG analysis lies in the MA
or maximum amplitude. It is the widest component of the
TEG and represents the platelet brinogen interaction and
overall clot strength. A general rule of thumb is that 80% of
clot strength is contributed by platelets and 20% to brinogen [4, 6–8]. The clinician might surmise that if the MA is
narrow, platelets are most likely decient or not functioning.
However, a TEG Functional Fibrinogen Assay measures the
brinogen contribution to clot strength and provide greater
specicity to guide therapy. The TEG Platelet Mapping® [
5,
6] is an adjunctive test run on the same TEG analyzer that
can assess platelet function of the MA if it is suboptimal.
Fig. 21.2 The technology of
TEG where the cup rotates.
(With permission from
Haemonetics Corporation)
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Fig. 21.3 TEG components.
(With permission from
Haemonetics Corporation)
Fig. 21.4 Detailed gure
demonstrating each
component of a TEG using
the TEG 5000. (With
permission from Haemonetics
Corporation)
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The platelet function analyzer measures the speed of platelet
adhesion.
Clot instability (Figs.21.3 and 21.4) appears in this illustration as the MA declines near the end of the TEG tracing.
The clot loses its stability as the amplitude of the tracing
declines. This reects brinolysis in the blood sample.
Fibrinolytic inhibitors may be used prophylactically in some
settings, such as CV surgery and some trauma setting. In settings where the hazard of thrombosis is much greater, and
prophylactic anti-brinolytics are not desired, those drugs
can quickly correct hyperbrinolysis when it is detected.
Fibrinolytic inhibitors, to have maximal effect, should be
administered before hemorrhage begins for maximal prophylaxes. Once brinolysis begins, brinolytic inhibitors
like aminocaproic acid and tranxamic acid are not helpful.
D-dimers are more useful as a tool of exclusion for
VTE but can be elevated by a number of inammatory
states related to brinolysis. Even if a clot is conrmed, the
D-dimer shows what has already happened in terms of clot
breakdown. The TEG tracing shows the presence of active
brinolysis by elevated clot lysis (LY30) or the lack of brinolysis by a stable MA.
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Assays Available ontheTEG 5000 Analyzer
System Include
Kaolin (+/− heparinase) - An intrinsic pathway activated
assay. This thrombin-generated tracing identies underlying
hemostatic characteristics and risk of bleeding or thrombosis.
RapidTEG (+/− heparinase)- An intrinsic and extrinsic
pathway activated assay increases the coagulation process
rapidly assess coagulation properties.
Functional Fibrinogen- An extrinsic pathway activated
assay uses a potent GPIIb/IIIa platelet inhibitor to isolate
brin contribution to clot strength. Used in conjunction with
Kaolin, TEG can assess relative contribution of platelets and
brin to overall clot strength.
Platelet Mapping (Haemonetics Corporation©) includes
a thrombin-generated tracing (kaolin) and platelet receptorspecic tracing(s) (ADP/AA). Identies the level of platelet
function and inhibition using the patient’s underlying hemostatic potential from the Kaolin TEG as the reference point.
The TEG® 6s Analyzer System
TEG 6s (Haemonetics Corp, Boston MA) (Fig.21.5) is the
newest platform in the thrombelastography portfolio. It is
a cartridge-based system which dramatically increases the
ease of operation and the reproducibility of results [5, 6, 8].
All reagents are already in the cartridge and are mixed with
Fig. 21.5 The cartridge-based TEG® 6s analyzer. (With permission
from Haemonetics Corporation)
S. Leavitt et al.
Fig. 21.6 The new technology of TEG 6000. (With permission from
Haemonetics Corporation)
the blood when a sample is added to the cartridge by means
of a simple transfer pipette. Another benet is a reduction
in the amount of blood required to obtain the results. A cartridge with four assays can be run with 340 mcl of blood.
These changes make the device well suited to use in a variety of care settings [1]. Each cartridge provides results from
multiple tracings to provide data using a variety of assays to
provide the quickest, most specic results to guide treatment
decisions.
Because it is a cartridge design, it no longer uses a cup
and pin methodology, instead uses resonant frequency to
assess the clot (Figs. 21.6 and 21.7). Each assay occupies
a separate channel of the cartridge, to a total of four channels. Blood is added to the cartridge, where it is mixed with
the reagents, then channeled into a capillary tube with a
meniscus of blood at the testing chamber end of the capillary tube. A range of radiofrequencies are applied to the
tube. The frequency which causes the blood to distend the
furthest into the test chamber, blocking light from a photodetector, is the resonant frequency. Each resonant frequency
is associated with a specic clot strength. As the clot moves
through the process of clot initiation, reaches maximum clot
strength, and potentially begins to break down, those changing resonant frequencies are plotted to produce the familiar
TEG tracing (Figs.21.6 and 21.7).
There are currently three cartridges available for the
TEG 6s system. A Global Hemostasis cartridge provides
four assays: citrated kaolin, citrated kaolin with heparinase,
citrated rapid TEG, and citrated functional brinogen. This
cartridge is FDA cleared for use in CV surgery and cardiology
procedures. The Platelet Mapping® cartridge uses the same
reagents as the Platelet Mapping (Haemonetic Corporation)
assays in TEG 5000 to provide information on percent inhibition/aggregation and residual platelet reactivity, using
ADP and arachidonic acid as the agonists (Figs. 21.6 and
21.7). This is used to assess the patient’s response to anti-
platelet therapies. The most recent cartridge is approved for
use in trauma. It includes assays for citrated kaolin, citrated
Frequency (Hz)
Stiffness Increase
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RapidTEG™, and citrated functional brinogen. Using these
assays in combination, it is possible to more specically
address hemostatic defects between platelets, brinogen,
factors, heparin effect, and brinolysis (Figs.21.8 and 21.9).
1.6
1.4
1.2
100
Fig. 21.7 New to the TEG system technology is the measurement of
clot viscoelasticity using a resonance method. To measure the clot
strength with the resonance method, the sample is exposed to a xed
vibration frequency. With LED illumination, a detector measures up/
down motion of the blood meniscus. The frequency leading to resonance is identied and then converted to the TEG system readout.
Stronger clots have higher resonant frequencies and higher TEG readouts. (With permission from Haemonetics Corporation)
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Educational Tools
Rotational Thromboelastometry
ROTEM® or rotational thromboelastometry (TEM ®) is an
alternative method of viscoelastic testing (Fig.21.10). The
cups in TEM determine the interaction of normal coagulation factors of blood with inhibitors, anticoagulant drugs,
platelets, red blood cells, and brinolytics. ROTEM as in
TEG utilizes a whole blood to assess clotting. Only the heparinase cups which are available for TEG have reactive agent.
Blood (300μl) anticoagulated with citrate is placed into
a cuvette using an electronic pipette. A disposable pin is
attached to a shaft which is connected with a thin spring (the
equivalent to Hartert’s torsion wire in thrombelastography)
and slowly oscillates back and forth. The signal of the pin
suspended in the blood sample is transmitted via an optical
detector system. The developing clot slows down the pin as
the clot forms.
The test starts by adding appropriate reagents. The instrument measures and graphically displays the changes in
elasticity at all stages of the developing clot. It is essential
to know that the clot formed may become unstable by activating those factors that generate brinolysis. The typical
test temperature is 37°C, but different temperatures can be
selected, as in patients with hypothermia (Fig.21.11).
By adding specic reagents, TEM like TEG can nd
specic points in the coagulation cascade where a problem
exists.
Fig. 21.8 Tracings on the left
from the Global Hemostasis
cartridge. CK citrated kaolin,
CKH citrated kaolin with
heparinase, CRT citrated
RapidTEG, CFF citrated
functional brinogen. The
white line is a 10min marker,
by which time several
parameters are already
available to guide
decision-making
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