Thromboelastography-Guided Transfusion
Therapy in the Trauma Patient
Charice Brazzel, CRNA, DNP
This article presents thromboelastography (TEG) as
an important assay to incorporate into anesthesia
practice for development of evidence-based ther-
apy of trauma patients receiving blood transfusions.
The leading cause of death worldwide results from
trauma. Hemorrhage is responsible for 30% to 40%
of trauma mortality and accounts for almost 50% of
the deaths occurring in the initial 24 hours following
the traumatic incident. On admission, 25% to 35% of
trauma patients present with coagulopathy, which is
associated with a sevenfold increase in morbidity and
mortality. The literature supports that routine plasma-
based routine coagulation tests, such as prothrombin
time, activated partial thromboplastin time, and inter-
national normalized ratio, are inadequate for monitor-
T
he trauma patient presents special condi-
tions and problems for anesthesia providers.
The trauma triad of death is a medical term
that is often used to describe the conditions
of hypothermia, acidosis, and coagulopathy.1
This triad is seen in patients who have severe traumatic
injuries and is the cause of a major rise in the mortality
rate because of continual microvascular bleeding.2 The
leading cause of death worldwide results from trauma,
with hemorrhage being responsible for 30% to 40% of
trauma mortality and accounting for almost 50% of the
deaths occurring in the initial 24 hours following the
traumatic incident.3 On admission, 25% to 35% of trauma
patients present with coagulopathy, which is associated
with a sevenfold increase in morbidity and mortality.4
There is emerging consensus that routine plasma-based
tests (RCoT), such as prothrombin time (PT), activated
partial thromboplastin time (APTT), and international
normalized ratio (INR), may be inadequate for monitor-
ing coagulopathy and guiding transfusion therapy in
trauma patients.3 A correct diagnosis is critical for patient
survival. Applying the thromboelastography (TEG) assay
to transfusion therapy for the trauma patient can help
guide the anesthesia provider to correctly diagnose and
properly treat the hemorrhaging patient. Closing the
gap between coagulopathic hemorrhage and death will
require a change in current clinical practice to modify and
update transfusion regimens.
The purpose of this article is multifaceted. The author
outlines the importance of addressing coagulopathic
www.aana.com/aanajournalonline AANA Journal
ing coagulopathy and guided transfusion therapy in
trauma patients.
A potential solution is incorporating the use of the
TEG assay into the care of trauma patients to render
evidence-based therapy for patients requiring massive
blood transfusions. Analysis with TEG provides a com-
plete picture of hemostasis, which is far superior to
isolated, static conventional tests. The result is a fast,
well-designed, and precise diagnosis enabling more
cost-effective treatment, improved clinical outcome,
accurate use of blood products, and pharmaceutical
therapies at the point of care.
Keywords: Coagulopathy, thromboelastography,
transfusion therapy, trauma.
conditions that can be experienced in trauma patients
and relates contributing factors to the development of
this derangement. A comprehensive history and review
of the literature are presented to demonstrate a thorough
assessment of the problem relating to coagulopathy. An
explanation is provided to the reader why RCoT may
be inadequate to guide transfusion therapy in trauma
anesthesia and why TEG may serve as a more preferable
diagnostic assay. The pathways of coagulation are dis-
cussed, and finally, the author offers recommendations
for future practice.
History and Review of Literature
Evidence from the relevant literature suggests it is im-
portant to address coagulopathy in trauma patients.
Results of a study between cohorts presenting with
similar injury severity scores determined that the patient
cohort presenting with coagulopathy experienced 2 to
3 times greater mortality rate.5 The prevention of co-
agulopathy is superior to treatment, yet most protocols
are designed to treat preexisting and/or ongoing coagu-
lopathy.6 Uncontrolled coagulopathic hemorrhage is now
seen as the major cause of preventable death in trauma
patients.7 There are 3 phases of hemorrhagic shock due
to coagulopathy. These phases are compensated, uncom-
pensated but reversible, and irreversible hemorrhagic
shock. Once the irreversible hemorrhagic shock phase
has been entered, blood pressure, tissue oxygenation,
and perfusion do not improve with either fluid replace-
ment therapy or the use of inotropic agents.8 The goal of
 April 2013  Vol. 81, No. 2 127
resuscitative care is to delay or prevent the transition to
irreversible hemorrhagic shock.
The recognition of coagulopathy at the time of admis-
sion is crucial. Hess et al5 asserted that several factors
contribute to the development of coagulopathy: blood
loss, hemodilution by physiologic vascular refill, con-
sumption of platelets, hypothermic platelet dysfunction,
reduction of enzyme activity, acidosis-induced reduction
in coagulation factor activity, and unopposed fibrinolysis.
Customarily, volume resuscitation starts with a combina-
tion of crystalloids, colloids, and uncrossmatched packed
red blood cells (RBC) because of ease of availability.
Uncrossmatched packed RBC are readily available but
are generally used only in cases of dire emergency. These
products may further dilute coagulation factors contribut-
ing to a negative spiral effect of dilutional coagulopathy.9
ABO typing of blood and thawing of component replace-
ment factors requires time during the initial phase of the
resuscitation. By the time that type-specific fresh frozen
plasma, platelets, and cryoprecipitate are added to the Figure 1. Thromboelastograph Components
regimen, they generally fail to correct the coagulopathy
because of hemodilution.10 Thromboelastography can
enable the anesthetists to minimize hemodilution and pos-
sibly prevent exacerbation of coagulopathies by transfus-
ing the correct blood product when the patient needs it.
There has been growing consensus that RCoT are ill
α angle MA
suited for monitoring coagulopathy and guiding transfu-
sion therapy in hemorrhaging patients.3,11 These assay
tests were developed more than 50 years ago for treat-
ment of patients with hemophilia and have never been R K
validated for the prediction of uncontrolled hemorrhage
in trauma patients. Even though abnormal PT, APTT,
and INR results are consistent with increased mortality Figure 2. Thromboelastograph Tracing
in the trauma patient, these plasma-based tests commu-
nicate only the small amount of thrombin formed during The TEG assay is a relatively simple process. A small
the initial phases of coagulation and have little predictive sample of whole blood (0.36 mL) is placed into a cup
value (≤ 50%) with respect to hemorrhage.12 heated to 37˚C. The cup is gently rotated back and forth
A new understanding of the classic coagulation constantly, at a set speed, through an arc (cycle time, 6/
cascade was put forth in 1994 by the introduction of a min). This sluggish flow mimics the venous circulation
cell-based model.13 The cell-based model emphasizes the and activates the coagulation process. A stationary pin
importance of tissue factor as the initiator of the coagu- attached to a torsion wire is inserted into the sample cup,
lation cascade and the pivotal role of platelets for intact and fibrin begins to form between the torsion wire and
hemostasis. This new understanding explains the poor the wall of the cup. This fibrin-platelet binding links the
correlation between RCoT and clinical bleeding and pro- cup and pin together (Figure 1). The speed and strength
vides a more accurate picture of why use of these labo- of clot formation are converted by a mechanical-elec-
ratory studies is insufficient in trauma resuscitation.13 trical transducer to an electrical signal that is computer
Correct detection of coagulopathy is crucial for survival, analyzed. These data are converted to a numeric value
and interest has renewed in viscoelastic assay studies to and graphic representation of the plasmatic coagulation
guide transfusion therapy in trauma patients. system, platelet function, and fibrinolysis (Figure 2).
Thromboelastography is a real-time viscoelastic assay There are 4 main values of interest expressed in this
that measures the strength of fibrin-platelet bonds in assay: the R value (start of clot or fibrin formation), K
whole blood. The result of this process is a functional he- value (fibrin kinetics or speed of clot formation), α angle
mostatic plug. Historically, TEG analysis has been used (fibrin cross-linking), and the MA (width of tracing rep-
extensively in the disciplines of cardiovascular surgery, resenting clot strength). These values expose the precise
liver transplantation, and obstetrics.14 mechanism contributing to the coagulopathy, as depicted

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 Cause Treatment
R value K and α value MA
Lack of surgical hemostasis Sutures Normal Normal Normal
Hemodilution No treatment necessary High Normal Normal
Factor deficiency FFP High Low or normal Low or normal
Fibrinogen deficiency Cryoprecipitate Normal Low Low or normal
Platelets low or dysfunctional Platelets Normal Normal Low
Primary fibrinolysis Antifibrinolytics, Normal Normal Low
TXA, aprotinin
Fibrinolysis (DIC) Stage 1: Treat DIC Low High High
Hypercoagulability with fibrinolysis
Fibrinolysis (DIC) Stage 2: Treat DIC High Low Low
Hypocoagulability after consumption

Table 1. Thromboelastography Values and Treatment

Abbreviations: DIC, disseminated intravascular coagulation; FFP, fresh frozen plasma; K value, fibrin kinetics or speed of clot formation;
MA, width of tracing representing clot strength; R value, start of clot or fibrin formation; TXA, tranexamic acid.

in Table 1. The differential diagnosis can be deduced
whether the dysfunction is a result of hemodilution, loss
of coagulation proteins, or platelet dysfunction. The R
value represents the reaction time for initial fibrin forma-
tion (normal, 7.5-15 minutes). The prolongation of this
value can represent a deficiency in coagulation factors,
effects of endogenous heparin released in trauma, and/or
hemodilution.15 The treatment with fresh frozen plasma
or no treatment would depend on the clinical picture of
the patient. Conversely, a shortening in the R value (less
than 3 minutes) would indicate a state of hypercoagula-
bility, and treatment with an anticoagulant of choice may
prove beneficial. The K value (normal, 3-6 minutes) and
α angle (normal, 45° to 55°) depicts the speed at which
the clot strengthens. A low value may indicate the need
for fibrinogen administration, and a high value may indi-
cate hypercoagulability for which the patient may benefit
from anticoagulant therapy. Last, the MA, or maximum
amplitude (normal, 50-60 mm), represents the overall
maximum attainable clot strength. A decreased value can
result from hypofibrinogenemia, decreased platelet func-
tion, or quantity.15 Transfusing platelet pools in patients
who present a decreased MA may improve hemostatic
conditions. An MA result greater than 75 mm is evidence
of a prothrombotic state, and an anticoagulant of choice
may be clinically indicated. The qualitative analysis that
TEG provides can facilitate administration of the right
blood product or anticoagulant, in correct amounts, at
just the right time.11
Discussion
• Coagulation Pathways. The PT and INR depict the ex-
trinsic pathway of the coagulation cascade. Tissue factor
is exposed from the injured endothelium and combines
with factor VII to produce factor VIIa. Factor VIIa will
subsequently bind with tissue thromboplastin to convert
factor X to Xa. When factor X is activated, it signals the
beginning of the final common pathway. Therefore, only
2 coagulation proteins are represented in the extrinsic
pathway, or less than 3% of the overall clot strength.
This condition omits information on approximately 97%
of the hemostatic process.16 Confounding the problem
with RCoT is the fact that platelets are responsible for
approximately 80% of total clot strength. Platelets are an
important variable in the hemostatic process and are im-
mediately lost during the centrifuge process. When RCoT
assays are analyzed, the plasma and the contribution of
platelets in their role to clot strength are gone.
Analysis of the intrinsic pathway offers double the
amount of information about the coagulation pathway
compared with the extrinsic pathway. The factors rep-
resented are XII, XI, IX, and VIII and 3 natural antico-
agulant proteins, C, S, and Z. Although there is twice the
amount of information, less than 10% of the overall clot
strength is represented in this APTT assay.16
When the final common pathway is reached by either
intrinsic or extrinsic mechanisms, factor X is activated
and the conversion of prothrombin to thrombin results.
The conversion of prothrombin to thrombin is where
the serious affair of the hemostatic process truly begins.
Thrombin will activate factor V to factor Va and factor
VIII to factor VIIIa and will serve as a positive feedback
loop. This positive feedback mechanism greatly increases
the production of thrombin.17 Information on these
important feedback loops are lost because only isolated
pieces of the pathway are examined in RCoT because of
whole blood is not being analyzed. Thrombin cleaves
fibrinogen to fibrin monomers, to form fibrin polymers.
Formation of fibrin polymers serves as the first mechani-
cal evidence of a clot. It is at this point where all RCoT
assays stop analysis. Routine coagulation tests stop where
fibrin strands begin to form, and this reveals less than 5%
of overall thrombin produced. Thrombin will continue to
activate factor XIII, which results in the cross-linking of
fibrin strands. Thrombin plays perhaps one of the most
underappreciated roles in the coagulation cascade, which

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 Author (year) Type of surgery No. of patients Major conclusions
Shore-Lesserson et al24 (1999) Cardiac surgery 105 Patients who underwent TEG
received less FFP and platelet
transfusions postoperatively than did
RCoT-treated patients

Manikappa et al11 (2001) Cardiac surgery 150 TEG demonstrated greater accuracy
than RCoT in predicting significant
postoperative hemorrhage and
significantly decreased the need
for transfusion of RBC, FFP, and
platelets

Table 2. Comparison Studies of Routine Coagulation Tests and Thromboelastography

Abbreviations: FFP, fresh frozen plasma; RBC, red blood cells; RCoT, routine coagulation test; TEG, thromboelastography.

is that of platelet activation. Thrombin is the most potent
platelet activator in the body and serves as the catalyst for
the hemostatic process.
Very small amounts of thrombin are required to
cleave fibrinogen and activate platelets; however, a much
larger amount of thrombin is necessary to produce a
stable network of platelet-fibrin polymers. This fun-
damental principle further explains why RCoT do not
agree with actual clinical bleeding observed in vivo.12,18
Thromboelastography evaluates the mechanical proper-
ties of the hemostatic process, including time to initial
fibrin formation, the kinetics of initial fibrin clot forma-
tion and length of time to achieve maximum strength,
and the final strength and stability of the fibrin clot. The
resulting strength of the fibrin clot formation determines
how well the clot can prevent hemorrhage without per-
mitting inappropriate thrombosis formation. Each vari-
able communicated by TEG assay expresses a unique
component or relationship within the delicately balanced
coagulation cascade process and benefits the practitio-
ner by early detection of coagulopathic derangements.
Randomized controlled trials comparing RCoT and vis-
coelastic assay are described in Table 2.
• Benefits of TEG. The TEG assay produces a rapid,
low-cost method for differential diagnosis regarding the
need for surgical reexploration in patients with contin-
ued microvascular oozing.19 This translates to the poten-
tial for enormous savings in healthcare costs, decreasing
the demand on our blood bank reserves and improving
the quality of patient care.20-22
The medical literature is replete with hazards associ-
ated with transfusion of allogeneic blood products. Small
shifts in pH has a much greater effect on the coagulation
process than small changes in temperature. Stored blood
has lower levels of 2,3-diphosphoglycerate, lower pH,
and increased levels of supernatant potassium. These
changes can exacerbate the conditions of the trauma
patient because a normal serum pH does not consis-
tently reflect the pH in hypoxic tissue.23 The TEG assay
has been demonstrated to significantly decrease the
requirement for perioperative allogeneic transfusion.14
A landmark study conducted by Shore-Lesserson et al24
compared the effect of TEG-guided transfusion algorithm
against routine transfusion therapy in patients under-
going complex cardiac surgery. The result produced a
75% reduction in the number of patients receiving fresh
frozen plasma and more than a 50% reduction in the
transfusion of platelets.
Current studies advocate equal transfusion ratios of
packed RBC, fresh frozen plasma, and platelets (1:1:1)
to improve survival rates in trauma patients rather than
early and substantial use of crystalloids and/or col-
loids.6,10,25-27 This approach to trauma resuscitation has
been widely studied in severely injured patients and has
become a commonplace practice to minimize dilutional
coagulopathy. The ongoing conflict in the United States
Theater of Operations in the Middle East has produced
retrospective data suggesting that whole blood is supe-
rior to component replacement therapy in the massively
transfused trauma patient.28-33 However, treating these
patients indiscriminately with fresh frozen plasma, plate-
lets and cryoprecipitate is not only uneconomical, Hess et
al5 posit that this practice is “dangerous.” Perkins et al34
reported improved 30-day survival rates associated with
the increased use of platelets in massive transfusion. The
optimal ratio of packed RBC to platelets is not clearly
understood and warrants more investigation because
although increased platelet ratios increase survival rates
in massively transfused patients, they also are associated
with multiple organ failure.35
Acute lung injury is a syndrome of acute hypoxemic
respiratory failure, noncardiogenic in origin, with the
presence of bilateral pulmonary infiltrates. Acute lung
injury has a 33% rate of incidence among the critically
injured trauma population. A recent study published by
Edens et al36 suggested that there might be an indepen-
dent relationship between the amount of fresh frozen
plasma transfused and the development of early acute
lung injury. Because of the current shifts in transfusion
practice leaning toward infusion ratios of packed RBC
to fresh frozen plasma approaching 1:1, mortality rates
have improved. However, evidence also suggests that

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this transfusion strategy may be associated with a higher
incidence of acute lung injury, and the patient implica-
tions related to this finding are unknown at this time.
Khan et al37 demonstrated that the development of acute
lung injury was dose dependent on the actual numbers
of fresh frozen plasma transfused. Thromboelastography
can provide anesthetists with information on which
blood products would prove most efficacious to the hem-
orrhaging trauma patient and guide transfusion therapy
in appropriate quantities.
Patients receiving long-term thrombolytic therapy can
be assessed preoperatively with precision and accuracy
to determine the potential for perioperative hemorrhage.
A preoperative platelet count provides information only
on how many platelets are present and does not analyze
functionality. Functional, not quantitative, measure-
ments are necessary to make evidence-based decisions
on whether to proceed with surgical intervention. The
platelet system has 2 components: (1) activation and
(2) aggregation. Once the coagulation cascade has been
activated, the question remains whether the platelets are
functionally capable of aggregating to form a platelet
plug. Thrombolytic drugs such as clopidogrel, prasugrel,
and abciximab act to prevent platelet aggregation in con-
trast to aspirin and nonsteroidal drugs, which alter plate-
let adhesion and anchoring. The TEG assay can be used
for preoperative risk stratification based on individual
hemostatic conditions. Platelet mapping depicts whether
a delay in surgery is necessary or, may possibly proceed
earlier than anticipated. The return of platelet function
can be followed with serial studies, and the need for
platelet availability can be correctly anticipated.
Thromboelastography offers point-of-care testing,
which produces the advantage of convenient and rapid
results when decisions need to be made. Currently, no
published data exist quantifying how many hospitals
use TEG analysis nationwide; however, hemorrhage and
thrombotic issues are a shared concern across hospital
specialties. Viscoelastic assays are currently endorsed by
several international guidelines and textbooks concern-
ing massive transfusion in trauma.38-40
A classic work by Ammar41 advances the use of TEG
analysis for aiding early extubation. Early extubation is
often prevented by excessive bleeding. This condition
renders the patient hemodynamically unstable and may
require surgical reexploration to determine the cause
of the bleeding. The process of coagulation is dynamic;
however, TEG allows the practitioner to quantify and
qualify 85% to 90% of this system.16 In a comparison of
TEG with RCoT profiles, traditional RCoT results will
provide at best a 51% predictive value for perioperative
bleeding. This would be analogous to flipping a coin to
determine results. Pinpointing the dysfunction and for-
mulating evidence-based therapy to address specific co-
agulopathies become a reality, allowing the practitioner
www.aana.com/aanajournalonline AANA Journal
to minimize complications and deliver specific treatment
to the patient. The intraoperative use of TEG analysis can
identify the reason for the bleeding and guide therapy
during the postoperative course, which will facilitate
earlier extubation and may decrease length of stay in the
intensive care unit.
• Practice Implications. The TEG assay presents new
challenges and practice implications to anesthesia pro-
viders. Further nursing research incorporating the TEG
assay into the anesthesia preoperative screening phase can
expand on the body of knowledge and possibly improve
patient care. Strategies must be developed to assist the
anesthetists to correctly interpret the results of TEG anal-
ysis, formulate therapeutic goals, and develop appropriate
transfusion guidelines. Accomplishing this objective will
require the development of multidisciplinary teams to
implement comprehensive strategies addressing policy
and procedure development, promote cooperative col-
laboration, and implement education and training among
multiple hospital departments that would be affected by
the practice change. A paradigm shift in evidence-based
practice is called for to embrace the TEG assay into
patient care. These evidence-based practice changes can
serve to decrease mortality rates in the trauma population
and possibly other medical disciplines, rendering a more
cost-effective hospitalization course.
Summary
The purpose of this article has been to outline the im-
portance of addressing coagulopathic conditions experi-
enced in trauma patients and relate contributing factors
to the development of coagulopathy. An in-depth history
and review of the literature has been presented to demon-
strate a thorough assessment of the problem. Explanation
has been given to the reader why RCoT assays may be
inadequate to guide transfusion therapy in trauma an-
esthesia. A brief outline of the coagulation pathway has
been presented along with a discussion detailing the ad-
vantages that the TEG assay can offer compared to RCoT,
which can benefit the patient, anesthetist, and hospitals.
Potential practice implications have been put forth to
challenge anesthesia providers to adopt current evidence-
based practice changes.
Evidence-based transfusion therapy could offer mutual
benefit to trauma patients and hospitals. Incorporating
the TEG assay into transfusion practice offers many dis-
tinct advantages. Prior studies have shown that the TEG
assay allows for point-of-care testing that produces con-
venient, rapid results in situations when decisions need
to be made quickly without undue strain on blood bank
resources. The potential positive results could promise
better health outcomes for trauma patients, including
earlier extubation, reduced medical costs without a
decrease in patient care, as well as decreased chance of
future need for transfusions or additional surgery, and less
 April 2013  Vol. 81, No. 2 131
recovery time in critical care units. Thromboelastography
has the potential to prevent coagulopathy and promote
effective control of bleeding in the presence of coagu-
lopathy. These are all noteworthy points of service to
our patients. Prior studies suggest that TEG could be a
productive compliment to current methods, and in some
cases, a superior method altogether. Further nursing re-
search using the TEG assay in other disciplines needs to
be developed in order to expand on this beneficial body
of knowledge and improve patient care.
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AUTHOR
Charice Brazzel, CRNA, DNP, is a chief nurse anesthetist for Sheridan
Healthcare at Kendall Regional Medical Center in Miami, Florida.