GENERAL MEDICINE/REVIEW ARTICLE

New Uses for Thromboelastography and Other

Forms of Viscoelastic Monitoring in the Emergency
Department: A Narrative Review
Patrick D. Tyler, MD*; Lauren M. Yang, MD; Samuel B. Snider, MD; Adam B. Lerner, MD; William C. Aird, MD;
Nathan I. Shapiro, MD, MPH

*Corresponding Author. E-mail: ptyler1@bidmc.harvard.edu.

Patients frequently visit the emergency department with conditions that place them at risk of worse outcomes when accompanied by
coagulopathy. Routine tests of coagulation—prothrombin time, partial thromboplastin time, platelets, and fibrinogen—have
shortcomings that limit their use in providing emergency care. One alternative is to investigate coagulation disturbance with
viscoelastic monitoring (VEM), a coagulation test that measures the timing and strength of blood clot development in real time. VEM
is widely used and studied in cardiac surgery, liver transplant surgery, anesthesia, and trauma. In this article, we review the technique
of VEM and the biologic rationale of using it in addition to routine tests of coagulation in emergency clinical situations. Then, we
review the evidence (or lack thereof) for using VEM in the diagnosis and treatment of specific conditions. Finally, we describe the
limitations of the test and future directions for clinical use and research in emergency medicine. [Ann Emerg Med. 2021;77:357-366.]

A podcast for this article is available at www.annemergmed.com.

0196-0644/$-see front matter
Copyright © 2020 by the American College of Emergency Physicians.
https://doi.org/10.1016/j.annemergmed.2020.07.026

INTRODUCTION one another and to specific elements of the coagulation

Patients frequently visit the emergency department (ED)
with conditions such as trauma,1 liver disease,2 head
injury,3 and sepsis4 that place them at risk of worse
outcomes when these conditions are accompanied by
coagulopathy. There is a variety of causes for coagulopathy.
The disease process itself, such as liver disease or a heritable
bleeding diathesis, may cause the coagulopathy5; iatrogenic
causes such as anticoagulant medications or other
therapeutic strategies (eg, excessive fluid resuscitation in
trauma) may also cause coagulopathy.5,6 Routine tests of
coagulation such as prothrombin time (PT), international
normalized ratio (INR), partial thromboplastin time
(PTT), platelets, and fibrinogen are readily available at
most hospitals.7 However, these tests are imperfect because
results often do not return in a timely fashion to facilitate
emergency decisionmaking. They have a number of other
limitations in the emergency diagnosis of coagulopathy that
we will describe later.7,8
One alternative is to use viscoelastic monitoring (VEM), a
group of tests of coagulation that measure the timing and
strength of blood clot development to assess the clotting
cascade in real time, often at the point of care. Two forms of
VEM, which operate on similar principles, are available:
thromboelastography (TEG) and rotational
thromboelastometry (ROTEM). Each test has similar
parameters that, although not interchangeable, correspond to
cascade.9 VEM studies are widely reported in cardiac and
transplant surgery during the perioperative and postoperative
period.9 Overall, the use of VEM in these clinical settings is
associated with decreased blood product use and may
improve outcomes, but further study is needed.10-15
The main purpose of this review is to outline potential
uses for VEM in the ED, with a focus on promising areas
for future research. In the emergency setting, VEM is most
widely studied in trauma, especially regarding massive
transfusion.8,14-24 However, there are many promising
potential applications in sepsis,25-33 liver disease,34-44 and
head trauma.45-51
We begin with a review of VEM and the rationale for its
use in addition to routine tests of coagulation in emergency
clinical situations. Then, we assess the existing evidence for
use in sepsis, liver disease, and head trauma, and outline
future research questions in these areas. Finally, we describe
the limitations of the test and future directions for research
and clinical use in emergency medicine.
VISCOELASTIC MONITORING: TECHNIQUE AND
RATIONALE
TEG, the first formulation of VEM, was first described
in the medical literature in 1948.52 VEM was developed to
overcome the limitations of standard coagulation testing;
namely, that PT and PTT provide information only about

Volume 77, no. 3 : March 2021 Annals of Emergency Medicine 357

New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
the initial phase of the coagulation cascade, and that these
tests can assess only the plasma component of coagulation,
not whole blood.9 To perform VEM, a sample of blood is
placed into a small cup with an activator of coagulation. A
pin on a torsion wire is immersed in the blood, and the cup
and pin are rotated relative to each other. The shear
modulus of the clot—that is, the force required to rotate
the blood through a prespecified arc of rotation—is
measured over time. This information is reported as a set of
variables and graphically displayed as a deflection around a
baseline (Figure).53
In TEG, the cup rotates and the pin is stationary; in
ROTEM, the opposite is true.9 A newer VEM apparatus,
the TEG 6S analyzer, performs measurements similar to
those of TEG and ROTEM by measuring the vibration of
a sample using light-emitting-diode illumination, and uses
a cartridge that does not require pipetting.54 This apparatus
has minimal response to motion and temperature changes55
and strong correlation to TEG in healthy volunteers,54 a
small ICU cohort,56 and a large trauma cohort.57
Figure. Depiction of the relationship between the clotting cascade, the formation of a clot, and the thromboelastogram.
358 Annals of Emergency Medicine
Tyler et al
The primary advantage of VEM from a patient
management perspective is that it provides information
about the entire coagulation cascade,9,58,59 and thus might
identify specific interventions that can be applied in
response to the test results. The VEM tracing produces a
complete picture of clot formation and fibrinolysis (Figure);
it is interpreted according to specific parameters, outlined
in the Figure, that correspond to elements of the
coagulation cascade.9,53 TEG and ROTEM have different
names for similar parameters; the TEG nomenclature will
be used here, given that TEG is more commonly used in
the United States.9
The reaction time, the duration from the start of the test
to the initial deviation from baseline (specifically, a 2-mm
displacement of the pin), corresponds to the function of the
clotting cascade, during which a stimulus such as trauma or
inflammation may lead to an amplifying series of enzymatic
conversions.5 The PT and PTT correspond to the same
phase of coagulation; that is, a series of amplifying
enzymatic conversions that converge on a final common
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Tyler et al New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
pathway.5 The result of this process is the conversion of
fibrinogen into fibrin, which polymerizes on the surface of
the primary hemostatic plug (composed of RBCs and
platelets) to form the stronger, secondary hemostatic plug
(RBCs and platelets bound together by cross-linked fibrin).
The kinetic (K) time corresponds to the time between the
reaction time and the point at which the VEM tracing
reaches a 20-mm deflection from baseline, which indicates
the initial phases of fibrin cross-linking.9,59 A similar
parameter is the a angle, which is defined as the angle
between the baseline and either a line drawn between R and
K or a line intersecting R and tangent to the increasing
TEG curve.59,60 However, in many coagulopathic
specimens, the tracing never reaches 20 mm. Thus, in
modern algorithms using TEG to guide massive transfusion
in trauma, the K-time has been replaced by the angle. The
final measurement of coagulation is the maximum
amplitude, the largest deflection from baseline. The
maximum amplitude corresponds to the maximum
deflection of the pin and reflects the contributions of all
clotting factors, but primarily depends on platelet function
and the contribution of fibrin; fibrin forms approximately
20% of the contribution to the maximum amplitude,
whereas platelet quantity and function contribute
approximately 80%.61,62 Once the maximum amplitude
has been reached, the VEM assay shifts from testing clot
formation to assessing fibrinolysis. The LY30, or the
decrease in amplitude of the curve 30 minutes after
reaching the maximum amplitude (expressed as a
percentage), reflects the degree of fibrinolysis.9,59
For a test to function as a point-of-care test, it needs to
feasibly perform at or near the bedside.63 Many centers
currently use VEM in this capacity.64,65 Although
completing a full VEM test can take 30 to 60 minutes,
most results are available within 10 to 30 minutes.59,66
Additionally, variations of the test, such as the addition of
tissue factor to TEG, can generate the maximum amplitude
(a later-stage parameter) within 5 to 10 minutes66,67; this
variation is used in some massive transfusion protocols.59
Finally, data from the anesthesia and trauma literature
suggest that early ROTEM parameters, such as the curve
amplitude at 5, 10, and 15 minutes, can predict maximum
clot strength.68-70
VEM may provide several advantages over routine tests of
coagulation, which generally include PT, PTT, platelet count,
and fibrinogen concentration. The main advantages are that
VEM reflects all components of the coagulation cascade in
whole blood, that it is performed rapidly with a whole blood
sample, and that results return relatively quickly.
The PT and PTT have several limitations. First, PT and
PTT are most often clinical laboratory-based tests that
Volume 77, no. 3 : March 2021
require a plasma sample, which means that the
venipuncture sample must be centrifuged and thus creates a
time delay.7 Second, the test takes nearly 45 minutes to
complete when samples are normal and even longer when
abnormal. Third, although these tests provide high-level
information about the portion of the coagulation cascade
that includes the clotting factors, they do not provide
information about other important features, such as total
clot strength (the test terminates as soon as any fibrin is
detected and thus ends before most fibrin is generated), the
contribution of platelets (because the tests are performed on
plasma from a centrifuged specimen), and fibrinolysis.5,71
Additionally, the PT and PTT can be misleading in
many circumstances. For example, the coagulopathy of
chronic liver disease elevates the PT and INR much like the
coagulopathy associated with coumadin use. The patient
receiving coumadin has an iatrogenic bleeding diathesis,
whereas the cirrhotic patient may be coagulopathic,
thrombophilic, or neither (depending on the balance of
pro- and anticoagulant factors produced by the damaged
liver). Similarly, the coagulopathy of target-specific
anticoagulants (such as apixaban and rivaroxaban) is not
accurately reflected by the PT or PTT.72,73 The PT, INR,
and PTT are tests designed to study factor deficiencies and
monitor anticoagulant therapy, but they were never
intended to guide therapy in patients with other
coagulopathies or bleeding in emergency settings.71
The platelet count (part of the CBC count) is rapidly
available to clinicians but does not provide information about
platelet function, which may be impaired in many ED
populations; for example, those receiving nonsteroidal anti-
inflammatory drugs or other antiplatelet medications, those
with alcohol use disorder, or those with uremia caused by
acute or chronic renal failure.5,74 Although in theory a low
platelet count may indicate the need for a platelet transfusion,
platelet transfusion thresholds are not clearly established for
many conditions and are based mostly on expert opinion.75
Finally, with respect to fibrinogen, this test frequently
has an unacceptable turnaround time for decisionmaking in
patients requiring emergency intervention.7,71 This test
does map to a specific therapy (ie, cryoprecipitate or
fibrinogen concentrate transfusion).76 However, one
important limitation of the fibrinogen level in the acute
management of coagulopathic patients is that it is not
linearly related to overall clot strength, and the effect on
overall clot strength depends on the concentration of
platelets.7 In summary, although routine tests of
coagulation provide important information in the care of
patients with suspected coagulopathy, they have many
limitations. These limitations include long turnaround
times incompatible with emergency care, information
Annals of Emergency Medicine 359
New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
about coagulation that corresponds poorly to the true
degree of anticoagulation and to clinically significant
outcomes, and lack of information about the entire
coagulation cascade or about the qualitative function of
different coagulation elements. VEM has the potential to
meet all these challenges and thus has promise as a
comprehensive point-of-care test. However, as we discuss
later, although VEM is being used clinically in the care of
trauma patients, its use in other clinical settings requires
further investigation before we can completely understand
and validate the effect of its clinical use.
The optimal approach to diagnosing and treating
coagulation abnormalities for most ED patients has not yet
been determined, but may involve a combination of
routine coagulation testing and VEM.
MAJOR RESEARCH FRONTS IN VEM
Of conditions routinely managed in the ED, trauma has
the largest body of evidence assessing its use in patient care.
There are multiple excellent reviews9,20,58,59; given our
focus on laying out a research agenda and on potential
future applications, our own survey of the available
information is included in Appendix E1 (available online at
http://www.annemergmed.com). Now, we will review
emergency conditions for which VEM has a potential
future role and outline a research agenda related to each
condition.
Sepsis, a common and deadly clinical syndrome in
which infection causes systemic inflammation, is a leading
cause of significant morbidity and mortality.79
Inflammation is known to damage vasculature and to
activate the coagulation cascade, which causes fibrin
deposition in small- and medium-sized vessels. This process
is thought to mediate organ dysfunction and failure.80,81
The activation of the coagulation cascade in sepsis exists
along a continuum: some patients with mild organ
dysfunction may have only microvascular fibrin deposition,
whereas those who progress to disseminated intravascular
coagulation may have macrovascular thrombosis.82 The
pathophysiology involves cytokine activation of coagulation
cascade through the tissue factor–factor VII pathway, as
well as dysregulation of the mechanisms that typically
regulate thrombus formation.80,81,83 Initially, patients may
become hypercoagulable, but as infection and
inflammation continue, they may progress to disseminated
intravascular coagulation.82
Several small but promising studies have assessed VEM
use in sepsis.25 VEM test results are abnormal in sepsis
populations compared with those of controls,26,27 and
VEM abnormalities are reportedly associated with
360 Annals of Emergency Medicine
Tyler et al
worsening scores of illness severity and increased
mortality.26,28-30 Additionally, patients with
hypocoagulable states appear to have a higher incidence of
disseminated intravascular coagulation and more often had
worse outcomes than patients with normal or
hypercoagulable profiles.28-32 Although intriguing, these
studies have limitations. There is significant variation in
effect sizes and no clear definitions of hyper- or
hypocoagulable states. Finally, the correspondence between
specific VEM abnormalities and outcomes differed between
the studies, limiting clear practical conclusions.
Although the studies are small and observational, certain
themes emerge. First, maximum amplitude (or maximal
clot firmness, the ROTEM equivalent) is a reasonable
proxy for overall coagulation.29,33 Second, patients with
sepsis frequently have evidence of a hypercoagulable or
hypocoagulable state.25 Nevertheless, any VEM
abnormality is associated with worse outcome than having
normal VEM,26 of which a hypocoagulable profile (usually
represented by decreased maximum amplitude or maximal
clot firmness) is associated with worsening organ
dysfunction and clinical outcome.26,28,29,33,84 Most studies
are also prospective observational cohort studies, or enroll
only a relatively small number of patients with sepsis.
Despite the limitations of these early studies, there is a
strong biological rationale for the use of VEM in sepsis.
First, it is possible that patients with different underlying
coagulation phenotypes will respond differently to
treatment strategies. For example, if large-volume fluid
resuscitation contributes to a hypocoagulable state (as
observed in trauma),85 perhaps hypocoagulable patients
would benefit from a restrictive fluid strategy with early
vasopressors compared with a more liberal fluid strategy.
Second, previous studies of sepsis and other pathologies
have suggested that certain abnormalities in VEM are
associated with illness severity and outcomes and this
prognostic information may help identify patients in need
of earlier, more aggressive care. Third, VEM might identify
therapeutic targets. For example, anticoagulant or
antifibrinolytic therapy may help some patients with sepsis.
Directly treating the coagulopathy has some biological
rationale, but convincing evidence is lacking.82,86 To our
knowledge, no investigators have examined whether
treating VEM abnormalities with blood products, as
studied in surgery or trauma,10,12 would make a clinical
difference. Future studies are needed to better understand
the relationship between VEM profiles and coagulation
abnormalities, organ dysfunction, and outcomes in sepsis.
It is widely known that chronic liver disease impairs the
synthesis of coagulation proteins, and that patients with
chronic liver disease experience morbidity and mortality
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Tyler et al New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
from both hemorrhagic and thrombotic events.87,88
Although thrombocytopenia and prolonged PT are
validated clinical indicators of liver disease severity, they
correlate poorly with the onset and severity of bleeding
complications in this population.72,87 The PT is prolonged
because of decreased hepatic production of coagulation
proteins (including coagulation factors, fibrinogen, and
anticoagulant proteins). Additionally, chronic liver disease
increases factor VIII and von Willebrand factor
production.87 von Willebrand factor is present at much
higher levels in patients with cirrhosis, is essential for the
interaction between platelets and subendothelial surface to
form a clot, and may limit the hypocoagulable effect of
liver-related thrombocytopenia. The clinical result is that
the blood of patients with cirrhosis may be procoagulant or
anticoagulant, or they may have a balanced hemostatic
phenotype, and routine coagulation tests provide only
partial clarification. VEM may help demonstrate the
true state of coagulation in patients with chronic liver
disease.
There is increasing interest in the use of VEM for
patients with liver disease. First, TEG may have the
potential to provide accurate information about true
coagulation status in liver patients. TEG parameters are
more likely to be normal in patients with cirrhosis
compared with those of routine coagulation tests.36-39
When this information is considered along with results of
randomized trials in cirrhotic patients with gastrointestinal
bleeding showing decreased transfusion in TEG-guided
groups,35,43 it suggests TEG may have a role in detecting
rebalanced coagulation. However, there are some
limitations. Short-term reproducibility in the setting of
stable cirrhosis has been confirmed; however, fluctuation
within an individual patient over time and with progression
or decompensation of liver disease is notably lacking.40 It
has been suggested that patients with severe liver disease
may require further study as a cohort to establish distinct
reference ranges for TEG parameters.41
Despite these knowledge gaps, TEG has shown promise
in elevating the standard of care for transfusing patients
with cirrhosis. Several randomized clinical trials have
demonstrated that use of a TEG-guided algorithm in place
of traditional transfusion parameters in cirrhotic patients
with severe coagulopathy (platelets <50 or INR >1.8) and
active bleeding decreases the number of platelet, plasma,
and cryoprecipitate transfusions.35,42,43 In one study of 60
patients admitted with variceal bleeding, 13.3% of the
TEG-guided cohort versus 100% of the traditional cohort
required transfusion of fresh frozen plasma, platelets, or
both.43 Reported outcomes included that control of
bleeding, rebleeding at 5 days, and 6-week mortality were
Volume 77, no. 3 : March 2021
similar or improved in the TEG cohort.43 Additionally,
decreased transfusions with preserved outcomes have been
described when TEG-based protocols are applied to
periprocedural coagulopathy management and nonvariceal
bleeding.35,42 Confirmation of these findings has the
potential to decrease both the cost and the incidence of
complications caused by overtransfusion. However, this use
of VEM remains experimental and requires further study
before clinical implementation.
There are limited and contradictory data on the
predictive capabilities of VEM. A cohort of 270 patients
with almost 3 years of follow-up had no correlation with
bleeding, thrombosis, or death/transplant rate based on a
single index TEG measurement.89 This was a single-center
study with a death/transplantation rate of 64% and a
relatively low thrombosis rate (3%).89 Another pilot study
of 90 patients suggested TEG was superior to a traditional
test of coagulation in predicting risk of bleeding; however,
the positive predictive value was clinically limited because it
was only 20%.39 Additionally, this test is unlikely to
predict cirrhosis severity.39 Association between certain
TEG parameters and MELD-Na score/Child Pugh score
has been reported; however, other studies contradict this
finding.37,44
Overall, VEM may enable individualized transfusion
therapy for patients with cirrhosis-related bleeding,
reducing adverse events and ensuring judicious use of blood
products.35,42,43 It shows promise in diagnosing
coagulopathy of liver disease and improving the treatment
of bleeding conditions in patients with cirrhosis, but
further research is needed to define its most appropriate
roles. Specifically, the above-mentioned randomized trials
are promising, but the primary outcome for both trials is
volume of product transfused; before VEM can be
implemented clinically, additional randomized trials with a
primary patient-centered outcome would be necessary.
Areas of future research include larger randomized trials
of VEM in management of variceal and nonvariceal
gastrointestinal bleeding, and further study of whether
VEM abnormalities in ambulatory patients with cirrhosis
have prognostic significance. A prospective observational
study of VEM in patients with cirrhosis who develop acute
bleeding events might help identify certain VEM profiles
associated with better or worse outcomes. If such a study
had significant findings, this might inform a randomized
clinical trial with a focus on patient-centered outcomes
(including mortality, length of stay, ICU-free days, and
transfusion requirements). Furthermore, longitudinal
studies of VEM in ambulatory patients with cirrhosis might
identify phenotypes at higher risk of bleeding events,
potentially allowing those patients to be targeted for more
Annals of Emergency Medicine 361
New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
frequent outpatient visits, education regarding stool
monitoring, and screening measures (for example, regular
fecal occult blood testing, laboratory checks, and screening
endoscopy) to avoid acute presentations to the ED for
bleeding events.
Patients with traumatic brain injury have endogenous
coagulopathy, and VEM may provide useful information
and help with their acute management. In isolated
traumatic brain injury, coagulopathy, defined as any
abnormal value of a standard laboratory measurement (eg,
INR, PTT, fibrinogen, platelet count), will develop in up
to 36% of patients during their hospital course.90 The
frequency of coagulopathy increases with traumatic brain
injury severity,49,91 is rare in mild traumatic brain
injury,49,92 and is higher in penetrating compared with
blunt injury.90,93
Several studies have used VEM in acute traumatic brain
injury to describe functional clotting disorders and risk
stratify patients. Occult coagulopathy, or abnormal VEM
parameters with normal traditional laboratory
measurements, may be present with surprising frequency;
although it is difficult to reliably estimate how frequently
this occurs, given lack of standardized definitions and
methodological variability, it has been reported in 30% to
88% of cases.47,48 Whether the dominant abnormality in
these patients is of clotting factors, fibrin, or platelet
function has not yet been firmly established.49,51,92 In fact,
although most attention has focused on hypocoagulability,
VEM measurements have demonstrated that as many as
16% of patients with traumatic brain injury may have
occult hypercoagulability.93
Prompt identification and correction of traumatic brain
injury coagulopathy on patient arrival to the hospital is an
active area of investigation because expansion of traumatic
intracranial hemorrhages is common,94 and coagulopathy in
this patient population has been associated with a 7-fold
increase in the mortality rate.90 VEM-measured
hypocoagulability on presentation with acute severe
traumatic brain injury was predictive of neurologic decline
and 30-day mortality,50 but it is not clear that this predictive
capacity exceeds that of routine coagulation testing. Indeed,
larger studies have shown that inhospital mortality is
equivalently predicted by admission PTT and VEM
parameters.51,94 However, VEM has shown significant
promise in predicting hematoma expansion in patients with
spontaneous intracranial hemorrhage who have otherwise
normal values on standard tests of coagulation.45
With the recently published results of the Clinical
Randomisation of an Antifibrinolytic in Significant
Head Injury (CRASH-3) trial showing efficacy of
tranexamic acid in subgroups of patients with acute
362 Annals of Emergency Medicine
Tyler et al
traumatic brain injury,95 VEM may help identify
subgroups at high risk for hemorrhage expansion to
avoid unwarranted exposure to the thromboembolic
risks of this medication. Patients with specific
coagulopathies may benefit from transfusion of
blood products or administration of antifibrinolytics,
and those with high risk of expansion may benefit
from early neurosurgical therapy (such as placement of
an external ventricular drain, or surgical
decompression).
Although VEM is not ready for clinical implementation
in the care of patients with traumatic brain injury,
the studies mentioned earlier suggest a research agenda.
First, larger, methodologically rigorous studies that use
standardized definitions of both traumatic brain injury and
coagulopathy are warranted. Second, further studies of
VEM investigating potential connections between VEM
parameters, routine and experimental biomarkers of
coagulation, and patient-centered outcomes (such as
mortality, ICU length of stay, hemorrhage expansion, and
long-term disability) are warranted. Finally, if VEM
abnormalities are associated with outcomes, therapeutic
trials to correct such abnormalities may be warranted.
LIMITATIONS OF VISCOELASTIC MONITORING
There are several limitations to the use of VEM in
emergency care. First, although VEM is used clinically in
the care of trauma patients, its usefulness in managing the
other conditions described earlier is promising but remains
experimental. Additionally, small study size and significant
heterogeneity in studies of VEM can limit the ability to
draw conclusions from pooled data. Further studies are
needed to better understand the role of VEM in the earlier-
listed conditions.
Second, VEM tests can demonstrate variability,
particularly when performed by clinical team members at
the bedside (rather than laboratory personnel in the clinical
laboratory); the precision and reproducibility of VEM
testing may benefit from being based in the clinical
laboratory and undergoing routine quality assurance.77 As
with all point-of-care tests, quality control and quality
assurance are more challenging when testing equipment is
maintained outside the clinical laboratory.78 Also, baseline
differences in concentrations of RBCs and platelets may
affect VEM results7; how this knowledge should affect
VEM interpretation is not known.
Third, in the conditions outlined earlier, VEM has not
been reliably shown to improve outcomes. If it did improve
them, the most plausible mechanisms would be through
appropriate matching of blood product transfusion to
specific coagulation abnormalities, and by reducing adverse
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Tyler et al New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring
events related to unnecessary transfusions. However, it is
difficult to prove the connection between a diagnostic test
and specific outcomes, such as mortality, because many
other factors are at play in that final outcome. While
multiple studies across multiple domains have shown a
reduction in the number of blood product transfusions,
evidence that this translates to improved outcomes is
lacking. Further study is needed to determine the role of
VEM in the conditions outlined above.
Despite these limitations, VEM provides information
about the complete coagulation cascade within an
acceptable timeframe to facilitate the emergency care of
patients whose illness is complicated by significant
coagulopathy, and in the surgical setting there is evidence
that VEM decreases blood product use and improves
outcomes. Routine coagulation tests have numerous
limitations as outlined earlier. Limitations of VEM
evidence are addressable with additional higher-quality
studies, as well as quality assurance measures during clinical
use (such as implementing routine training for personnel
using VEM equipment and periodic quality assurance
testing of VEM machines). Finally, VEM results are best
interpreted and deployed in conjunction with knowledge of
the patient’s clinical situation, routine tests of coagulation
and other laboratory tests, and the limitations of the
evidence in support of its use.
CONCLUSIONS
VEM is best studied in the surgical and trauma fields
and has significant promise for use in the ED. It offers
benefits over routine coagulation tests; it provides
information about the entire coagulation cascade, and can
often be performed in point-of-care fashion more rapidly
than routine coagulation tests. In the surgical literature,
treatment algorithms incorporating VEM typically decrease
blood product use and improve patient outcomes. The
trauma literature comes to similar conclusions. Future
studies are needed to understand the appropriate role of
VEM in the care of patients with sepsis, liver disease, head
trauma, and other conditions in which a more holistic
understanding of their coagulation profile could streamline
therapy and improve outcomes.
Supervising editor: Allan B. Wolfson, MD. Specific detailed
information about possible conflict of interest for individual editors
is available at https://www.annemergmed.com/editors.
Author affiliations: From the Department of Emergency Medicine
(Tyler, Shapiro), Department of Medicine, Division of
Gastroenterology and Hepatology (Yang), Department of
Anesthesia, Critical Care and Pain Medicine (Lerner), and
Department of Medicine, Division of Hematology and Oncology
Volume 77, no. 3 : March 2021
(Aird), Beth Israel Deaconess Medical Center, Boston, MA; and the
Center for Neurotechnology and Neurorecovery, Department of
Neurology, Massachusetts General Hospital and Harvard Medical
School, Boston, MA (Snider).
Author contributions: PDT, ABL, WCA, and NIS conceived the
review. PDT drafted the manuscript, with major contributions from
LMY and SBS. All authors contributed substantially to the original
drafting and revisions. PDT and NIS take responsibility for the
paper as a whole.
All authors attest to meeting the four ICMJE.org authorship criteria:
(1) Substantial contributions to the conception or design of the
work; or the acquisition, analysis, or interpretation of data for the
work; AND (2) Drafting the work or revising it critically for important
intellectual content; AND (3) Final approval of the version to be
published; AND (4) Agreement to be accountable for all aspects of
the work in ensuring that questions related to the accuracy or
integrity of any part of the work are appropriately investigated and
resolved.
Funding and support: By Annals policy, all authors are required to
disclose any and all commercial, financial, and other relationships
in any way related to the subject of this article as per ICMJE conflict
of interest guidelines (see www.icmje.org). Dr. Shapiro is currently
performing a research study with device and materials-only
support from Entegrion, a company that produces viscoelastic
monitoring devices; receives research funding from Baxter, Rapid
Pathogen Screening, and the National Institutes of Health; and has
received speaker and consultation fees from Baxter.
Publication dates: Received for publication February 21, 2020.
Revisions received May 9, 2020, and July 10, 2020. Accepted for
publication July 14, 2020.
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