Clinica Chimica Acta 436 (2014) 143–148

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Clinica Chimica Acta

journal homepage: www.elsevier.com/locate/clinchim

Why is everyone so excited about thromboelastrography (TEG)?

Brad S. Karon ⁎
Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905

a r t i c l e i n f o a b s t r a c t

Article history: Thromboelastrography (TEG) is one of the most common whole-blood viscoelastic coagulation tests used in
Received 15 April 2014 clinical laboratories and at the point of care. TEG provides information on coagulation defects that are often
Received in revised form 14 May 2014 difficult to detect using routine laboratory tests such as activated partial prothrombin time or prothrombin
Accepted 15 May 2014
time. In certain critically ill patient populations, the use of TEG instead of or in addition to routine laboratory
Available online 28 May 2014
coagulation tests has been shown to improve outcomes or reduce transfusion requirements. However, TEG
Keywords:
and other viscoelastic coagulation tests are affected by unique pre-analytic and analytic variables that do not
Thromboelastography impact other common laboratory coagulation tests. In this review the underlying principles, clinical applications,
Viscoelastic coagulation testing and laboratory aspects of TEG testing are discussed.
Critical care © 2014 Elsevier B.V. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
2. Thromboelastography (TEG) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
3. Clinical applications of TEG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
4. Laboratory considerations for TEG Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148

1. Introduction common (predominantly dependent upon factor Xa and thrombin

Blood coagulation is a complex but essential biological process.
Coagulation is sometimes categorized from an observational point
of view into phases of hemostasis: first, a defect in the blood vessel
(endothelial damage) occurs, which triggers the need for blood clotting
to prevent excessive blood loss, then a platelet plug forms to temporarily
slow blood loss (often called the “white clot”), followed by a series of bio-
chemical reactions to generate thrombin in order to cleave fibrinogen
into a network of fibrin to provide a stronger and more permanent repair
(“red clot”), and finally clot lysis (fibrinolysis) to allow tissue remodeling
and repair.
Biochemically, these same observations can be divided into sub-
components that are measured to predict the body’s ability to respond
to vascular damage (stop bleeding). The activation of enzymes neces-
sary to form fibrin are artificially divided into intrinsic (predominantly
dependent upon coagulation factors VIII, IX, XI, and XII), extrinsic
(predominantly dependent upon tissue factor and factor VII), and
⁎ Tel.: +1 507 538 4921; fax: +1 507 538 7060.
E-mail address: Karon.bradley@mayo.edu.
activity and fibrinogen concentration) pathways for laboratory mea-
surement. The availability of platelets (to initiate coagulation through
platelet activation and to provide a surface for biochemical reactions
in the common pathway) is commonly measured by obtaining platelet
counts, although numerous other measures of platelet activity exist. To
assess the coagulation status of critically ill patients, clinicians are most
often left with a series of “snapshots” that involve assessment of the in-
trinsic (activated partial prothrombin time, aPTT), extrinsic (prothrombin
time, PT), and common (thrombin time) pathways as well as platelet
counts to estimate platelet activity available for hemostasis. D-dimer
and related tests can assess for fibrinolysis (e.g., that observed during
venous thrombosis), although these tests do not adequately differentiate
acute vs. ongoing fibrinolysis.
These common laboratory coagulation tests most often provide all
the information needed for clinicians to diagnose and treat disorders
of hemostasis. However, critically ill patients often have coagulation dis-
orders that are not adequately detected or described by conventional
coagulation tests. Platelet count is not a good substitute for platelet
function in patients treated with certain medications or after certain
procedures that may impact platelet function. Few laboratory tests can

http://dx.doi.org/10.1016/j.cca.2014.05.013
0009-8981/© 2014 Elsevier B.V. All rights reserved.
144 B.S. Karon / Clinica Chimica Acta 436 (2014) 143–148
detect and differentiate acute fibrinolysis that can occur during long
surgical procedures, such as liver transplant, from ongoing fibrinolysis
after thrombosis. The PT and aPTT laboratory tests are sensitive only
to relatively large changes in clotting factor concentrations. Thus, they
may lack sufficient sensitivity to detect coagulation changes in patients
with massive trauma or other conditions in which early detection of
clotting factor deficiency is key to preventing massive hemorrhage.
Finally, plasma-based coagulation tests do not provide information on
the cellular contribution to coagulation. For these reasons and others,
interest in whole-blood viscoelastic coagulation testing has increased
in recent years.
Viscoelastic coagulation testing has become a popular addition or
alternative to conventional (aPTT, PT, thrombin time, platelet count,
and D-dimer) coagulation tests in critical care. Unlike the conventional
coagulation tests that take snapshots of isolated parts of the coagulation
process, viscoelastic coagulation testing monitors the clotting of whole
blood in a cup or small container. One of the most commonly used
(but not the only) viscoelastic clotting test is thromboelastography
(TEG), which will be the subject of the remainder of this review.
2. Thromboelastography (TEG)
TEG testing relies upon changes in the viscosity of blood as it
coagulates, along with fibrin and platelet-dependent cross-linking
between whole blood in a cup and an object (pin) inserted into that
cup, to provide information on the sufficiency of hemostasis and detect
coagulation defects. The TEG instrument (Fig. 1) consists of a plastic
plate, upon which is placed a disposable cup, attached via mechanical
arms to the TEG device.
Whole blood is placed in the disposable cup, and after activation of
clotting (usually with kaolin), the plastic plate and cup are moved up
into contact with the pin. At this point, the TEG tracing is initiated.
After the tracing is initiated, the mechanical arms on the TEG instrument
rotate the cup at a fixed frequency. Initially the pin, attached to the
instrument via a torsion wire, will be motionless in the cup of whole
blood as there is no means for the liquid whole blood to exert force on
the pin (Fig. 2). As whole blood begins to clot, the viscosity of the
blood increases, and at the same time the pin becomes cross-linked to
the cup via fibrin and platelet interactions. As the pin begins to move
Fig. 1. TEG® coagulation analyzer. The TEG® instrument consists of a plastic plate, upon
which is placed a disposable cup, attached via mechanical arms to the TEG® device.
After initiation of clotting, the plastic plate and cup of whole blood are moved up into
contact with a pin, attached via torsion wire to the TEG® device. TEG® is a registered
trademark of Haemonetics. Figure used with permission of Haemonetics Corporation.
Fig. 2. Schematic representation of the cup (of whole blood), pin, and torsion wire on the
TEG® device. After initiation of clotting, the plate/cup apparatus is moved up such that the
pin is immersed in whole blood. Initially, the liquid whole blood exerts no force on the pin/
torsion wire. As blood clots, the viscosity of the blood increases, and the pin becomes
cross-linked to the cup via fibrin and platelet interactions. As the pin begins to move in
concert with the cup, this motion is transduced (via the torsion wire) to produce the
TEG® tracing.
in concert with the cup, this motion is transduced (via the torsion
wire) to produce the TEG tracing (Fig. 3). The parameters of a TEG trac-
ing include the reaction (R) time, the time from initiation of the TEG
tracing until torsion is exerted on the pin/wire assembly. R time largely
reflects the adequacy of coagulation factors (similar to what is mea-
sured in the laboratory by PT and aPTT). The K (time to reach 20 mm
clot amplitude) and the angle (angle formed by line tangent to clot
curve, Fig. 3) reflect clot kinetics and are determined by a number of fac-
tors including thrombin generation and fibrinogen concentration. The
maximum amplitude (MA) is the maximum distance traveled by the
cross-linked cup/pin, which reflects maximum clot strength and is
largely a function of platelet function or activity. Finally, the Lysis30 or
Lysis60 is the percent decrease in area under the TEG curve (from
MA) over 30 or 60 min.
All of these parameters can be compared to normal or reference
values to detect either clotting factor deficiencies (increased R time),
fibrinogen deficiencies (decreased angle), platelet function defects
(decreased MA), or excess fibrinolysis (Lys30 or Lys60 outside of
reference values). The TEG tracing thus provides an overview of multi-
ple coagulation processes and allows detection of variables that impact
conventional coagulation tests (such as clotting factor deficiencies), as
well as factors that cannot be easily measured by conventional testing
(clot kinetics which is dependent upon both thrombin generation and
fibrinogen concentration, platelet function, and fibrinolysis). In Fig. 4,
a TEG tracing with both prolonged R time (indicating factor deficiency
and/or the presence of heparin) and reduced MA (indicating a platelet
function defect) is demonstrated. This type of abnormal tracing might
be expected from a patient with coagulopathy during cardiovascular
surgery or massive transfusion. In Fig. 5, excess fibrinolysis in an other-
wise normal TEG tracing is demonstrated.
Another advantage (or disadvantage, depending upon the clinical
situation and application) of TEG over conventional coagulation testing
is that the TEG R time is significantly more sensitive to clotting factor
deficiencies or the presence of heparin than are conventional tests
such as aPTT or PT. A special cup containing heparinase can be used to
determine whether the presence of heparin (administered therapeuti-
cally or through accidental sample contamination) has influenced the
TEG parameters.
 B.S. Karon / Clinica Chimica Acta 436 (2014) 143–148 145

Fig. 3. TEG® tracing. Reaction (R) time, angle, and maximum amplitude (MA) are demonstrated. K is the time (in minutes) required to reach 20 mm amplitude. Lys30 is the percent
decrease in area under the TEG® curve (from MA) over 30 min, while Lys60 is the percent decrease over 60 min.

3. Clinical applications of TEG
TEG was developed in the 1940s in Germany as a comprehensive
measure of blood coagulation to facilitate research. Its use in clinical
practice was not described until many years later (1960s) when physi-
cians performing early liver transplantation surgeries described use of
TEG to detect and treat fibrinolysis occurring after reperfusion of the
transplanted liver [1]. As the clinical practice of liver transplantation
matured in the 1980s, researchers at the University of Pittsburgh
began to describe the use of TEG to detect and treat pre-existing
coagulopathies due to liver failure in patients before transplantation,
dilutional coagulopathies during liver transplant surgery, and fibrinolysis
resulting from reperfusion of the transplanted liver [1]. Liver transplant
represented the ideal application for a viscoelastic whole-blood coagula-
tion test because conventional coagulation testing (e.g., aPTT or PT) was
affected by the presence of heparin used during the surgery. In addition,
fibrinogen concentration did not always reflect functional fibrinogen
activity due to acquired dysfibrinogenemia, platelet count was not
always reflective of platelet function, and tests such as D-dimer or fibrin
degradation product were difficult to interpret in the context of a long
and invasive surgery [1].
In a study of 66 consecutive liver transplant patients, Kang and col-
leagues demonstrated that correlation between conventional coagulation
tests and TEG parameters was poor, and that a transfusion algorithm
based upon TEG parameters (rather than conventional coagulation test
results) resulted in less blood product usage compared to historical con-
trols with transfusion guided by conventional coagulation testing. The era
of the TEG-guided transfusion algorithm was born [1]. As enhanced fibri-
nolysis is one of the most striking coagulation defects occurring during
liver transplantation [2,3], TEG has gained widespread use in liver trans-
plantation because of its improved ability to detect fibrinolysis compared
to conventional coagulation tests. One report also suggested that preop-
erative assessment of coagulation using TEG could predict development
of intraoperative fibrinolysis during liver transplantation [3], although
several other studies have failed to demonstrate a relationship between
preoperative coagulation parameters and intraoperative transfusion
requirements [4–6].
The description of TEG-based coagulation monitoring and TEG-
guided transfusion algorithms during liver transplant increased interest
in TEG for other invasive procedures that involved coagulopathy, most
notably cardiovascular surgery. A randomized study published in 1999
compared blood product usage and bleeding during and after cardiovas-
cular surgery in patients assigned to a transfusion algorithm guided
by TEG R and MA (as well as laboratory platelet count and fibrinogen
concentration), compared to a control group with transfusion need
determined from activated clotting time, platelet count and prothrombin

Fig. 4. TEG® tracing demonstrating prolonged reaction (R) time and reduced maximum amplitude (MA).
146 B.S. Karon / Clinica Chimica Acta 436 (2014) 143–148
Fig. 5. TEG® tracing demonstrating excess fibrinolysis.
time [7]. The primary findings were that postoperative transfusion of
fresh frozen plasma and platelet transfusions (as well as total FFP and
platelet transfusions) were decreased in the group with TEG monitoring
[7]. A large retrospective study also found that a TEG-guided transfusion
algorithm during cardiac surgery significantly reduced both perioperative
and total transfusion requirements [8].
Another prospective study used both conventional coagulation tests
and TEG to determine which tests of coagulation could best identify
cardiovascular surgery patients that went on (postoperatively) to have
excessive blood loss. After receiver operator characteristic (ROC) curve
analysis of each coagulation test to determine ability to predict postop-
erative blood loss, the authors proposed a cardiovascular surgery
transfusion algorithm including both conventional (PT, aPTT, fibrinogen,
and platelet count) and TEG (MA) parameters [9]. As observed in liver
transplantation, TEG has been found valuable in cardiovascular surgery
because it allows rapid identification of defects in clotting factor concen-
tration, platelet function, and thrombin generation and/or fibrinogen
concentration that are not always detectable by routine coagulation
testing [7–9]. An additional advantage of TEG is the ability to detect coag-
ulation abnormalities even in the presence of high levels of therapeutic
heparin (by using the heparinase cup) encountered during cardiovascu-
lar surgery [10].
It should be noted, however, that successful cardiovascular surgery
transfusion algorithms have been developed utilizing tests other than
TEG [11,12]. In fact, one study found no difference in blood product
transfusion when patients were randomized into one group where
point of care testing (including TEG) was used to make transfusion
decisions and another that used conventional laboratory coagulation
tests to guide transfusions [12]. It remains unclear how much the
success of any particular cardiovascular surgery transfusion algorithm
is dependent upon the particular coagulation tests employed to detect
coagulopathy and how much is a function of the existence of a transfu-
sion algorithm to encourage conservative use of blood products.
Trauma is another critical care application for TEG. Approximately
25%–35% of trauma patients present with coagulopathy, which is
associated with increased morbidity and mortality [13]. Conventional
laboratory coagulation tests do not always detect coagulopathies that
exist when patients with severe trauma initially present for evaluation
[13]. One study showed that among patients with penetrating injuries,
TEG MA obtained in the first 6 h after admission correlated better with
subsequent blood product usage than conventional coagulation tests
obtained at admission [14]. Another study found that TEG parameters
could detect coagulopathy, platelet dysfunction and hyperfibrinolysis
early during trauma resuscitation, and that development of these
coagulation disorders was associated with mortality [15]. Based
upon these and other observations [16,17], interest in TEG for severe
(especially penetrating) trauma has increased substantially in recent
years.
Recently, a systematic review of the benefits and harms of using
TEG-guided transfusion strategies among patients with severe bleeding
was conducted [18]. While the number of randomized studies found
appropriate for inclusion was small (9 studies with a total of 776 partic-
ipants), the systematic review did conclude that use of viscoelastic
testing significantly reduced bleeding in patients with massive bleeding.
Perhaps due to small number of studies (n = 5) that included a
mortality endpoint, the review did not find a difference in mortality
rate between conventional treatment and use of viscoelastic testing to
guide transfusion therapy in this patient population [18].
4. Laboratory considerations for TEG Testing
TEG was designed for use with fresh whole-blood samples, but the
use of fresh whole blood requires initiation of the TEG tracing within
4 min of sample collection (blood draw). For this reason, most TEG
operators now use citrated samples for analysis [19]. However, both
systematic differences and artifacts in TEG tracings have been described
when comparing fresh whole blood to citrated blood samples. One
study found that both R time and MA decreased over 30 min when
samples collected in citrated tubes were left to sit as whole blood, but
after 30 min, values remained stable for 1–7 h. Both R and MA values
in citrated blood samples (after 30 min storage) were significantly
smaller than those observed in fresh whole-blood samples [20]. Another
study found that increasing storage time (over 30 min) of citrated sam-
ples resulted in a hypercoagulable pattern, with R times significantly
shorter after 30 min of storage [21].
Based upon these studies, many centers using citrated whole-blood
samples allow specimens to “rest” or sit for 30 min after blood draw in
order to obtain consistent R and MA values. However, another study
found that R times in citrated samples continued to decrease between
30 and 120 min [22]. Differences in patient populations, clot activators,
and other factors make the studies difficult to directly compare. However,
there remains uncertainty as to the best time point (after blood
collection) to perform TEG analysis with citrated whole-blood samples.
Changes in R and MA with increasing storage time may confound inter-
pretation of TEG when citrated samples are used.
Three additional studies have observed apparent artifacts in TEG
tracings, which may be linked to collection of samples in citrated
tubes. One study noted what was concluded to be falsely increased
 B.S. Karon / Clinica Chimica Acta 436 (2014) 143–148
fibrinolysis when citrated samples were tested in heparinase cups from
patients on extracorporeal membrane oxygenation (ECMO) or patients
with ventricular assist devices [23]. Another study noted falsely
increased fibrinolysis in the heparinase cup from patients with severe
sepsis, although the authors did not specify whether fresh or citrated
whole-blood samples were used for testing [24].
A third study specifically examined differences in TEG tracings
(in both plain and heparinase cups) between fresh and citrated
whole-blood samples for three patient populations. In healthy donors
and patients after cardiopulmonary bypass, the only significant differ-
ence between fresh and citrated whole-blood tracings was the previ-
ously noted shortening of R time in citrated compared to fresh whole
blood [25]. However, for some ECMO patients, collection of samples in
citrate tubes resulted in apparent heparin reversal. For these patients,
TEG tracings with fresh whole blood showed no clotting, whereas
citrated whole-blood tracings were very similar to those produced by
the fresh whole blood in the heparinase cup [25]. There remain
concerns that testing of citrated whole-blood samples may result in a
hypercoagulable profile in some patient populations; and caution
should be exercised in using citrated blood samples in patient popula-
tions commonly treated with heparin.
Beyond choice of sample types and issues of timing between blood
draw and testing, TEG and other viscoelastic tests are subject to unique
pre-analytical and analytical artifacts that can significantly impact
results. TEG is significantly more sensitive to the presence of heparin
than most other coagulation tests. While this has advantages is certain
clinical situations, it also means that in obtaining samples from patients
being treated with heparin (therapeutically or to maintain catheter
patency), great care must be used to avoid heparin contamination of
samples. Combined plain and heparinase cup TEG analysis is recom-
mended for any patients receiving heparin. TEG also requires manual
pipetting and mixing of reagents, steps which may introduce greater
variability in test results compared to automated assays. Viscoelastic
tests are also subject to analytic errors from either pin slippage or vibra-
tion of the testing platform. Figs. 6 and 7 show effects on TEG tracings
from either pin slippage (Fig. 6) or vibration of the testing surface
(Fig. 7). When TEG is performed point of care, it can be a significant
challenge to insure that TEG values obtained from tracings with similar
artifacts are not used for patient care.
With the unique pre-analytic and analytic issues associated with
TEG testing, concerns have risen about whether TEG can produce stan-
dardized and consistent information across laboratories or healthcare
settings. Only a handful of studies have systematically examined the
inter-lab precision (reproducibility) of TEG results across laboratories
or hospitals. The UK National External Quality Assessment Scheme
Fig. 6. TEG® tracing artifact due to pin slippage during sample analysis.
147
(NEQAS) for Blood Coagulation published a study of external quality
control (proficiency testing) using eight lyophilized plasma samples
sent to 18 TEG users. Three samples were intended to represent normal
coagulation, two samples were spiked with heparin to determine
whether users could identify heparin effect (by comparing plain and
heparinase TEG parameters), and three samples were manufactured
factor-deficient samples intended to give no clotting [26]. Because the
samples were lyophilized plasma (contained no platelets), data on MA
(dependent primarily on platelet function) are difficult to interpret.
Using the three normal samples, average coefficient of variation (CV)
for R time between users was 15%–20% for plain cups and 38%–39%
for heparinase cups. Using the heparinase cup for the two heparin-
spiked samples, average CV for R time was 17%–29% (no clot was
detected in the plain cup for heparin-spiked samples). Users were also
asked to provide interpretations (normal or abnormal coagulation
status) for each sample. Consensus between users for the normal samples
was 27/31 (87%). All users reported abnormal coagulation for factor-
deficient samples analyzed (33/33), and all users reported abnormal
coagulation status for both heparin-spiked samples analyzed in plain
cups (23/23). When asked to compare plain and heparinase cup results
to determine whether heparin was present in a sample, 18/21 (86%) of
heparin-spiked samples were correctly identified as containing heparin
[26].
The College of American Pathologists (CAP) also offers proficiency
testing for TEG using lyophilized samples. With nearly 300 laboratories
participating in the 2013 TEG-A survey consisting of two samples: CVs
for R time, MA and angle were all ≤ 11%, while CVs for K were ≤ 22%
(CAP 2013 TEG-A survey summary). In another external quality assess-
ment study, either frozen platelet-rich plasma or factor VIII-deficient
plasma was sent to nine laboratories performing TEG for replicate
analysis [27], with each lab performing measurements in duplicate on
three different days for a total of 12 measurements at each site. For
platelet-rich plasma, the between-lab CV for R and MA was 17% and
19%, respectively. However, K exhibited more variability (60% CV)
while angle was the most reproducible parameter (CV 7%). Using the fac-
tor VIII-deficient plasma, between-lab precision for R was quite good (CV
9%), but CVs for the other TEG parameters varied between 22% and 47%
[27]. In comparison, CAP coagulation surveys for routine tests such as
PT and aPTT show b 5% CV for most major instrument/reagent combina-
tions. When asked to interpret whether a PT or aPTT was normal or
prolonged, laboratories (~ 4000 labs) achieved N 99% consensus (CAP
2013 CGL-A survey summary). Thus, TEG does not achieve levels of
inter-laboratory consistency observed for routine coagulation testing.
Further work is necessary to understand factors responsible for analytic
variability and to standardize TEG testing within and across testing sites.
148 B.S. Karon / Clinica Chimica Acta 436 (2014) 143–148
Fig. 7. TEG® tracing artifact due to vibration of the testing surface during sample analysis.
5. Conclusion
TEG and related viscoelastic tests provide simultaneous measure-
ment of multiple aspects of whole-blood coagulation. Unlike conven-
tional coagulation tests, interactions between cellular components and
plasma components of the coagulation cascade are captured during
viscoelastic testing. This allows definition of coagulation defects that
are challenging to measure using routine coagulation assays. However,
TEG and other viscoelastic tests are subject to a unique set of pre-
analytic and analytic variables that impact test reliability and reproduc-
ibility. In addition, the increased sensitivity for heparin and coagulation
factor deficiency, and imprecision of some parameters, may lead to erro-
neous treatment decisions in some clinical situations. TEG is a powerful
analytic tool, but its implementation requires thought and planning to
insure that the test is performed correctly and results are applied to
patient populations that will benefit from identification of the coagula-
tion defects measured.
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