Thromboelastography-Guided Transfusion

Therapy in the Trauma Patient

Charice Brazzel, CRNA, DNP

This article presents thromboelastography (TEG) as ing coagulopathy and guided transfusion therapy in
an important assay to incorporate into anesthesia trauma patients.
practice for development of evidence-based ther- A potential solution is incorporating the use of the
apy of trauma patients receiving blood transfusions. TEG assay into the care of trauma patients to render
The leading cause of death worldwide results from evidence-based therapy for patients requiring massive
trauma. Hemorrhage is responsible for 30% to 40% blood transfusions. Analysis with TEG provides a com-
of trauma mortality and accounts for almost 50% of plete picture of hemostasis, which is far superior to
the deaths occurring in the initial 24 hours following isolated, static conventional tests. The result is a fast,
the traumatic incident. On admission, 25% to 35% of well-designed, and precise diagnosis enabling more
trauma patients present with coagulopathy, which is cost-effective treatment, improved clinical outcome,
associated with a sevenfold increase in morbidity and accurate use of blood products, and pharmaceutical
mortality. The literature supports that routine plasma- therapies at the point of care.
based routine coagulation tests, such as prothrombin
time, activated partial thromboplastin time, and inter- Keywords: Coagulopathy, thromboelastography,
national normalized ratio, are inadequate for monitor- transfusion therapy, trauma.

T
he trauma patient presents special condi- conditions that can be experienced in trauma patients
tions and problems for anesthesia providers. and relates contributing factors to the development of
The trauma triad of death is a medical term this derangement. A comprehensive history and review
that is often used to describe the conditions of the literature are presented to demonstrate a thorough
of hypothermia, acidosis, and coagulopathy.1 assessment of the problem relating to coagulopathy. An
This triad is seen in patients who have severe traumatic explanation is provided to the reader why RCoT may
injuries and is the cause of a major rise in the mortality be inadequate to guide transfusion therapy in trauma
rate because of continual microvascular bleeding.2 The anesthesia and why TEG may serve as a more preferable
leading cause of death worldwide results from trauma, diagnostic assay. The pathways of coagulation are dis-
with hemorrhage being responsible for 30% to 40% of cussed, and finally, the author offers recommendations
trauma mortality and accounting for almost 50% of the for future practice.
deaths occurring in the initial 24 hours following the
traumatic incident.3 On admission, 25% to 35% of trauma History and Review of Literature
patients present with coagulopathy, which is associated Evidence from the relevant literature suggests it is im-
with a sevenfold increase in morbidity and mortality.4 portant to address coagulopathy in trauma patients.
There is emerging consensus that routine plasma-based Results of a study between cohorts presenting with
tests (RCoT), such as prothrombin time (PT), activated similar injury severity scores determined that the patient
partial thromboplastin time (APTT), and international cohort presenting with coagulopathy experienced 2 to
normalized ratio (INR), may be inadequate for monitor- 3 times greater mortality rate.5 The prevention of co-
ing coagulopathy and guiding transfusion therapy in agulopathy is superior to treatment, yet most protocols
trauma patients.3 A correct diagnosis is critical for patient are designed to treat preexisting and/or ongoing coagu-
survival. Applying the thromboelastography (TEG) assay lopathy.6 Uncontrolled coagulopathic hemorrhage is now
to transfusion therapy for the trauma patient can help seen as the major cause of preventable death in trauma
guide the anesthesia provider to correctly diagnose and patients.7 There are 3 phases of hemorrhagic shock due
properly treat the hemorrhaging patient. Closing the to coagulopathy. These phases are compensated, uncom-
gap between coagulopathic hemorrhage and death will pensated but reversible, and irreversible hemorrhagic
require a change in current clinical practice to modify and shock. Once the irreversible hemorrhagic shock phase
update transfusion regimens. has been entered, blood pressure, tissue oxygenation,
The purpose of this article is multifaceted. The author and perfusion do not improve with either fluid replace-
outlines the importance of addressing coagulopathic ment therapy or the use of inotropic agents.8 The goal of

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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 2 coagulation proteins are represented in the extrinsic
whether the dysfunction is a result of hemodilution, loss pathway, or less than 3% of the overall clot strength.
of coagulation proteins, or platelet dysfunction. The R This condition omits information on approximately 97%
value represents the reaction time for initial fibrin forma- of the hemostatic process.16 Confounding the problem
tion (normal, 7.5-15 minutes). The prolongation of this with RCoT is the fact that platelets are responsible for
value can represent a deficiency in coagulation factors, approximately 80% of total clot strength. Platelets are an
effects of endogenous heparin released in trauma, and/or important variable in the hemostatic process and are im-
hemodilution.15 The treatment with fresh frozen plasma mediately lost during the centrifuge process. When RCoT
or no treatment would depend on the clinical picture of assays are analyzed, the plasma and the contribution of
the patient. Conversely, a shortening in the R value (less platelets in their role to clot strength are gone.
than 3 minutes) would indicate a state of hypercoagula- Analysis of the intrinsic pathway offers double the
bility, and treatment with an anticoagulant of choice may amount of information about the coagulation pathway
prove beneficial. The K value (normal, 3-6 minutes) and compared with the extrinsic pathway. The factors rep-
α angle (normal, 45° to 55°) depicts the speed at which resented are XII, XI, IX, and VIII and 3 natural antico-
the clot strengthens. A low value may indicate the need agulant proteins, C, S, and Z. Although there is twice the
for fibrinogen administration, and a high value may indi- amount of information, less than 10% of the overall clot
cate hypercoagulability for which the patient may benefit strength is represented in this APTT assay.16
from anticoagulant therapy. Last, the MA, or maximum When the final common pathway is reached by either
amplitude (normal, 50-60 mm), represents the overall intrinsic or extrinsic mechanisms, factor X is activated
maximum attainable clot strength. A decreased value can and the conversion of prothrombin to thrombin results.
result from hypofibrinogenemia, decreased platelet func- The conversion of prothrombin to thrombin is where
tion, or quantity.15 Transfusing platelet pools in patients the serious affair of the hemostatic process truly begins.
who present a decreased MA may improve hemostatic Thrombin will activate factor V to factor Va and factor
conditions. An MA result greater than 75 mm is evidence VIII to factor VIIIa and will serve as a positive feedback
of a prothrombotic state, and an anticoagulant of choice loop. This positive feedback mechanism greatly increases
may be clinically indicated. The qualitative analysis that the production of thrombin.17 Information on these
TEG provides can facilitate administration of the right important feedback loops are lost because only isolated
blood product or anticoagulant, in correct amounts, at pieces of the pathway are examined in RCoT because of
just the right time.11 whole blood is not being analyzed. Thrombin cleaves
fibrinogen to fibrin monomers, to form fibrin polymers.
Discussion Formation of fibrin polymers serves as the first mechani-
• Coagulation Pathways. The PT and INR depict the ex- cal evidence of a clot. It is at this point where all RCoT
trinsic pathway of the coagulation cascade. Tissue factor assays stop analysis. Routine coagulation tests stop where
is exposed from the injured endothelium and combines fibrin strands begin to form, and this reveals less than 5%
with factor VII to produce factor VIIa. Factor VIIa will of overall thrombin produced. Thrombin will continue to
subsequently bind with tissue thromboplastin to convert activate factor XIII, which results in the cross-linking of
factor X to Xa. When factor X is activated, it signals the fibrin strands. Thrombin plays perhaps one of the most
beginning of the final common pathway. Therefore, only 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 A landmark study conducted by Shore-Lesserson et al24
platelet activator in the body and serves as the catalyst for compared the effect of TEG-guided transfusion algorithm
the hemostatic process. against routine transfusion therapy in patients under-
Very small amounts of thrombin are required to going complex cardiac surgery. The result produced a
cleave fibrinogen and activate platelets; however, a much 75% reduction in the number of patients receiving fresh
larger amount of thrombin is necessary to produce a frozen plasma and more than a 50% reduction in the
stable network of platelet-fibrin polymers. This fun- transfusion of platelets.
damental principle further explains why RCoT do not Current studies advocate equal transfusion ratios of
agree with actual clinical bleeding observed in vivo.12,18 packed RBC, fresh frozen plasma, and platelets (1:1:1)
Thromboelastography evaluates the mechanical proper- to improve survival rates in trauma patients rather than
ties of the hemostatic process, including time to initial early and substantial use of crystalloids and/or col-
fibrin formation, the kinetics of initial fibrin clot forma- loids.6,10,25-27 This approach to trauma resuscitation has
tion and length of time to achieve maximum strength, been widely studied in severely injured patients and has
and the final strength and stability of the fibrin clot. The become a commonplace practice to minimize dilutional
resulting strength of the fibrin clot formation determines coagulopathy. The ongoing conflict in the United States
how well the clot can prevent hemorrhage without per- Theater of Operations in the Middle East has produced
mitting inappropriate thrombosis formation. Each vari- retrospective data suggesting that whole blood is supe-
able communicated by TEG assay expresses a unique rior to component replacement therapy in the massively
component or relationship within the delicately balanced transfused trauma patient.28-33 However, treating these
coagulation cascade process and benefits the practitio- patients indiscriminately with fresh frozen plasma, plate-
ner by early detection of coagulopathic derangements. lets and cryoprecipitate is not only uneconomical, Hess et
Randomized controlled trials comparing RCoT and vis- al5 posit that this practice is “dangerous.” Perkins et al34
coelastic assay are described in Table 2. reported improved 30-day survival rates associated with
• Benefits of TEG. The TEG assay produces a rapid, the increased use of platelets in massive transfusion. The
low-cost method for differential diagnosis regarding the optimal ratio of packed RBC to platelets is not clearly
need for surgical reexploration in patients with contin- understood and warrants more investigation because
ued microvascular oozing.19 This translates to the poten- although increased platelet ratios increase survival rates
tial for enormous savings in healthcare costs, decreasing in massively transfused patients, they also are associated
the demand on our blood bank reserves and improving with multiple organ failure.35
the quality of patient care.20-22 Acute lung injury is a syndrome of acute hypoxemic
The medical literature is replete with hazards associ- respiratory failure, noncardiogenic in origin, with the
ated with transfusion of allogeneic blood products. Small presence of bilateral pulmonary infiltrates. Acute lung
shifts in pH has a much greater effect on the coagulation injury has a 33% rate of incidence among the critically
process than small changes in temperature. Stored blood injured trauma population. A recent study published by
has lower levels of 2,3-diphosphoglycerate, lower pH, Edens et al36 suggested that there might be an indepen-
and increased levels of supernatant potassium. These dent relationship between the amount of fresh frozen
changes can exacerbate the conditions of the trauma plasma transfused and the development of early acute
patient because a normal serum pH does not consis- lung injury. Because of the current shifts in transfusion
tently reflect the pH in hypoxic tissue.23 The TEG assay practice leaning toward infusion ratios of packed RBC
has been demonstrated to significantly decrease the to fresh frozen plasma approaching 1:1, mortality rates
requirement for perioperative allogeneic transfusion.14 have improved. However, evidence also suggests that

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

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recovery time in critical care units. Thromboelastography trauma: six-year analysis of the transfusion practices at a Level I
trauma center. Am Surg. 2008;74(10):953-957.
has the potential to prevent coagulopathy and promote
23. Hoffman M. The cellular basis of traumatic bleeding. Milit Med. 2004;
effective control of bleeding in the presence of coagu- 169(12 suppl):5-7.
lopathy. These are all noteworthy points of service to 24. Shore-Lesserson L, Manspeizer HE, DePerio M, Francis S, Vela-
our patients. Prior studies suggest that TEG could be a Cantos F, Ergin MA. Thromboelastography-guided transfusion algo-
rithm reduces transfusion in complex cardiac surgery. Anesth Analg.
productive compliment to current methods, and in some 1999;88(2):312-319.
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search using the TEG assay in other disciplines needs to ing Group on Polytrauma of the German Society of Trauma Surgery
be developed in order to expand on this beneficial body (DGU). Red-blood-cell to plasma ratios transfused during massive
transfusion are associated with mortality in severe multiple injury:
of knowledge and improve patient care. a retrospective analysis from the Trauma Registry of the Deutsche
Gesellschaft für Unfallchirurgie. Vox Sang. 2008;95(2):112-119.
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