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Thromboelastography: Clinical Application, Interpretation, and Transfusion

Management

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AANA Journal Course 1
Update for Nurse Anesthetists

Thromboelastography: Clinical Application,

Interpretation, and Transfusion Management
Shawn Collins, DNP, PhD, CRNA
Carolyn MacIntyre, MS, CRNA
Ian Hewer, MSN, MA, CRNA

The coagulation cascade is a dynamic process depen-
dent on many factors. It involves interaction between
primary hemostasis, platelet clot formation, second-
ary hemostasis, thrombin generation, and fibrino-
lysis. The assessment of this process is particularly
important in the surgical patient to properly manage
hemostatic issues. Traditionally, coagulation tests
used to guide transfusion management have included
platelet count, activated partial thromboplastin time,
prothrombin time, international normalized ratio, and
activated clotting time, among others. Although these
tests provide the practitioner with valuable informa-
tion, they lack the ability to measure platelet func-
tion. The ability to measure whole blood coagulation,
including platelet function, and not just the number of
platelets, can be critical when a healthcare provider is
determining what products are appropriate for a par-
ticular patient during surgery. One possible solution
to this deficit in traditional coagulation monitoring is
thromboelastography. Thromboelastography provides
a more complete picture of coagulation status, tak-
ing into account more factors involved in the clotting
process, including platelet function and temperature.
Keywords: Coagulation, coagulation cascade, hemo-
static issues, thromboelastography.

Objectives hemostatic therapy using blood products and hemostasis-

At the completion of this course, the reader should be
able to:
1. Identify current clinical applications of thrombo-
elastography.
2. Interpret a thromboelastography tracing.
3. Compare thromboelastography parameters to common
coagulation profiles.
4. Identify basic transfusion management based on a
thromboelastography tracing.
Introduction
The coagulation cascade is a dynamic process dependent
on many factors. It involves interaction between primary
hemostasis, platelet clot formation, secondary hemostasis,
thrombin generation, and fibrinolysis. The assessment
of this process is particularly important in the surgical
patient to properly assess patient coagulation assessment,
manage hemostatic therapy and transfusion in trauma
and perioperative care, and assess bleeding in hemophilic
patients. Complex surgical patients may require targeted
altering medications. Traditionally, coagulation tests used
to guide transfusion management have included platelet
count, activated partial thromboplastin time (aPTT), pro-
thrombin time (PT), international normalized ratio, and
activated clotting time (ACT), among others.
Although these tests provide the practitioner with
valuable information, they lack the ability to measure
platelet function. However, some argue that screening for
coagulation abnormalities and application of hemostatic
interventions based on classical coagulation tests such
as PT and aPTT are of limited value in perioperative
and acutely ill patients.1,2 Also, the ability to measure
whole blood coagulation, including platelet function,
and not just the number of platelets, can be critical when
a healthcare provider is determining what products are
appropriate for a particular patient during surgery, or
promptly determining when a patient might need to
return to surgery for surgical hemostasis when a throm-
boelastography (TEG) assay is normal.
One possible solution to this deficit in traditional co-

AANA Journal Course No. 36: AANA Journal course will consist of 6 successive articles, each with an objective for the reader and
sources for additional reading. This educational activity is being presented with the understanding that any conflict of interest on behalf
of the planners and presenters has been reported by the author(s). Also, there is no mention of off-label use for drugs or products.
Please visit AANALearn.com for the corresponding exam questions for this article.

www.aana.com/aanajournalonline AANA Journal  April 2016  Vol. 84, No. 2 129

agulation monitoring is TEG. Monitoring with TEG pro-
vides a global assessment of hemostatic function and clot
formation. Dr Helmut Hartet3 initially developed TEG
in 1947 for use specifically in research; more recently, it
has become a tool to properly identify and treat coagula-
tion abnormalities.4 Thromboelastography provides a
more complete picture of coagulation status, taking into
account more factors involved in the clotting process,
including platelet function and temperature.
Because TEG is particularly sensitive to changes
in fibrin polymerization and platelet count, it is most
useful for early detection of trauma and surgery related
dilutional coagulopathy in which plasma fibrinogen and
platelets fall rapidly.5 In addition, TEG is valuable in
guiding the use of cryoprecipitate or purified fibrino-
gen concentrate6 and potentially platelet transfusion.
Watson et al7 write: “Using TEG, clinicians may be able
to optimize targeted transfusion therapies with specific
coagulation factor(s) instead of empirically administering
multiple components with potentially hazardous effects.”
Thromboelastography Methods
The 2 main components of the TEG machine are a cup
and a pin. Whole blood is mixed with the activating
agent kaolin as well as calcium. The cup then oscillates
around the pin slowly, at a rate of 6 times per minute, to
mimic natural blood flow in vivo and activate the clot-
ting cascade. As the clot forms, the torque between the
cup and pin is transduced and measured, creating a curve
(Figure). As the clot breaks down and torque decreases,
the tracing converges to represent this.4,8 The different
parameters of the curve are then measured to assess
current coagulation status.
Initial results from TEG are available within minutes
and include the reaction time, or R time, which is the
time to initial clot formation, and the α angle or K value,
which represents clot kinetics. It may take as long as 30
to 60 minutes until all TEG values are obtained.8 One
study demonstrated that early rapid TEG values (k time
and r value) are available within 5 minutes, late rapid
TEG values (maximum amplitude [MA] and α angle)
within 15 minutes, and conventional coagulation testing
within 48 minutes (P < .001). The ACT, r value, and k
time showed strong correlation with PT, international
normalized ratio, and partial thromboplastin time (all r
> 0.70; P < .001), whereas MA (r = −0.49) and α angle (r
= 0.40) correlated with platelet count (both P < .001).9
Normal values based on the activator used for the test can
be found in Table 1.10
Thromboelastography Interpretation
Of the 4 types of TEG assays available, the most common
is the rapid TEG, and it is the assay referred to in this
review. The use of an activator in rapid TEG standard-
izes the TEG test and speeds up the rate at which clotting
130 AANA Journal  April 2016  Vol. 84, No. 2 www.aana.com/aanajournalonline
Figure. Normal Thromboelastography Tracing,
Depicting Rate of Formation and Degradation of Clot
as well as Maximum Amplitude (MA), R Time, α Angle,
and K Value
(Used by permission from Trapani.27)
takes place, thus making results available more quickly.9
The first measurement of note is the reaction time (R
time). This is the time interval from the start of the test
to the initial detection of the clot (see Figure). This value
is roughly equivalent to the PT that provides a measure-
ment of the extrinsic clotting pathway and the aPTT that
provides a measurement of the intrinsic clotting pathway
in standard coagulation assays. Similarly, the R time pro-
vides information about clotting factor deficiencies or
possible heparin therapy. A major advantage of TEG over
the aPTT is the ability to add the reagent heparinase to
monitor patients currently receiving heparin therapy for
other possible clotting deficiencies. Samples with TEG
are taken concurrently; one is exposed to heparinase and
the other is not. Comparisons of the TEG measurements
alert the provider to possible clotting factor deficiencies
or residual heparin.4,8,11
The clot strength is measured by 2 variables in TEG.
The K value represents clot kinetics and measures the
interval between the R time and the time when the clot
reaches 20 mm. The α angle is another measurement of
clot kinetics and measures a line tangent to the slope of
the curve during clot formation (see Figure). Both these
parameters depend mostly on fibrinogen levels. This
can help identify states of hyper- or hypocoagulopathies
(Table 2).4,8
Maximum amplitude is a measurement of maximum
clot strength and provides information on both fibrino-
gen and platelet function (see Figure). Current coagu-
lation profiles include platelet count but generally do
not take into account platelet function. Disruptions in
the endothelium cause the exposure of collagen and
von Willebrand factor. Platelets then adhere to these
and release substances that cause platelet aggregation.
Fibrinogen then binds to glycoprotein IIb/IIIa receptors,
causing further platelet aggregation and formation of a
platelet plug. Platelet function is an integral part of clot
formation during surgery and an alteration in function
 Test (activator) R (s) K (s) Angle α (°) MA (mm)
Rapid TEG (tissue activator) 78-110 30-120 68-82 54-72

kaoTEG (kaolin) 180-480 60-180 55-78 51-69

Table 1. Normal Thromboelastography Values Based on Activator Used

Abbreviations: MA, maximum amplitude; TEG, thromboelastography.

K and α Maximum
Coagulation status TEG tracing R value value amplitude Treatment algorithm
Normal hemostasis Normal Normal Normal Attain surgical hemostasis
using sutures

Hemodilution or clotting factor High Low or Low or normal Administer fresh frozen plasma
deficiency normal if indicated

Fibrinogen deficiency Normal or Low Low or normal Administer cryoprecipitate

high

Low or dysfunctional platelets Normal Normal Low Administer platelets

Primary fibrinolysis Normal Normal Low Administer antifibrinolytics or

tranexamic acid as indicated

Secondary fibrinolysis: Low High High Treat disseminated

hypercoagulopathy with intravascular coagulopathy
fibrinolysis

Thrombosis Low High High Administer anticoagulant

indicated

Table 2. Common Clotting Disorders, Thromboelastography (TEG) Tracing Example, Characteristic Values, and
Treatments

can disrupt the ultimate formation of a clot.4,8
The last major TEG parameter is the LY30, which
measures the percent of clot lysis 30 minutes after the
MA is achieved (see Figure). This measurement is most
useful for patients undergoing thrombolytic drug therapy
or during more advanced stages of disseminated intravas-
cular coagulation. This can be observed by rapid curve
convergence.4,8
Thromboelastography curves represent the coagula-
tion status at the time of blood draw. During changes in
coagulation, such as during active hemorrhage or periods
of massive transfusion, this status can change rapidly.
Thromboelastography offers the ability to monitor mul-
tiple consecutive samples all at one time.4,8
Thromboelastography Clinical Applications
• Cardiopulmonary Bypass. Extracorporeal circulation
during cardiopulmonary bypass in the surgical patient
has long been known to cause coagulation disturbanc-
es.12 Cardiopulmonary bypass disrupts the hemostatic
system in a number of ways, including hemodilution of
procoagulants and platelets, a reduction in coagulation
factors due to the interaction of blood with the surface
of the bypass circuit, the use of heparin, and altered tem-
perature.12 Hemodilution of clotting components occurs
mainly due to the large amount of crystalloid and colloid
solutions used to prime the bypass circuit.12 Exposure of
heparinized circulating blood to the bypass circuit as well
as the surgical wound activates both the intrinsic and ex-
trinsic clotting cascade, triggering a prothrombotic reac-
tion. Heparin is administered in large doses, but it cannot
prevent this thrombin formation; heparin can only reduce
the thrombin after it has already been produced. This
constant formation of thrombin leads to what is called a
consumptive coagulopathy due to the exhaustion of clot-
ting factors.11 Hypothermia is known to cause multiple
coagulation abnormalities leading to increased bleeding.
Low body temperature blocks thromboxane synthesis,
which results in decreased platelet aggregation.13
Traditionally, coagulation is monitored using the ACT

www.aana.com/aanajournalonline AANA Journal  April 2016  Vol. 84, No. 2 131

throughout cardiopulmonary bypass surgery. Research has
demonstrated ACT to be less accurate than TEG or aPTT
in this setting.13 Activated clotting time has many disadvan-
tages, including the inability to monitor a true heparin level
as well as the impact of temperature and hemodilution on
the ACT results.14 The manner in which TEG is monitored
is believed to be analogous to in vivo coagulation because
it takes into account the temperature as well as the impact
of platelets on hemostasis. In addition, TEG is superior to
ACT in this setting because of the unique ability to isolate
heparin in the TEG sample using heparinase. This allows
the practitioner to monitor underlying coagulation issues,
not mistaking a bleeding disorder for heparin therapy.15
The use of a TEG-guided algorithm during cardiac surgery
has been shown to reduce the number of blood products
transfused as well as the number of patients requiring
transfusion during cardiac surgery.2
• Liver Surgery. The liver is the major source for the
production of clotting factors. Patients with chronic liver
disease have defects in coagulation, making them a popu-
lation requiring targeted transfusion therapy. Generally,
it is understood that patients with chronic liver disease
have a lack of clotting factors and are therefore hypo-
coagulable; however, these patients can also exhibit
systemic hypercoagulability because of the concurrent
lack of natural anticoagulants.16 Because of their clotting
issues, patients with chronic liver disease require quick
assessment of coagulation abnormalities and targeted
use of blood products for treatment of these abnormali-
ties. Thromboelastography provides a more complete
assessment of coagulation abnormalities and has been
shown to reduce the amount of blood products utilized
in this patient population, although it has not been dem-
onstrated that this decrease in blood product utilization
has an impact on long-term morbidity and mortality.17
Thromboelastography-guided transfusion therapy has
demonstrated applicability not only to liver surgery but
also to chronic liver disease, liver cancer, and pancreatic
cancer patient populations.18
• Trauma Surgery. Coagulopathy resulting from trau-
matic injury is a common occurrence requiring rapid
intervention. Coagulopathies are associated with a high
rate of mortality in the trauma patient; this is especially
true within the first 24 hours after the trauma incident.19
There are multiple mechanisms that contribute to the
coagulopathies observed in trauma. The first resuscita-
tive efforts after a trauma are generally crystalloid and
colloid fluids that do not contain clotting factors, leading
to hemodilutional coagulopathies.20
Another cause of traumatic coagulopathy is rapid
consumption of clotting factors similar to the consump-
tion of clotting factors observed in patients undergo-
ing cardiopulmonary bypass. An additional method of
coagulopathy involves the activation of protein C due
to hypoperfusion from hemorrhage during a traumatic
132 AANA Journal  April 2016  Vol. 84, No. 2 www.aana.com/aanajournalonline
injury. Activated protein C affects coagulation in 2 ways.
Protein C inhibits clotting factors V and VIII, decreasing
total thrombin formation. It also decreases the inhibition
of tissue plasminogen activator, which causes plasmino-
gen to convert to plasmin faster, leading to fibrinolysis.20
This combination rapidly leads to coagulopathy and
fibrinolysis following a trauma.20,21
Traditional coagulation tests are of limited value in
this population of patients because of the inability to
detect clot strength and the length of time required to
obtain results. For patients with trauma, TEG offers
benefits because of the rapid return of results, the power
to measure clot strength, and the ability to monitor the
hyperfibrinolysis commonly found in this population.21
A systematic review of the literature found that targeted
use of blood products and clotting factors guided by TEG
reduced the overall incidence of morbidity and mortality
in this population of patients.22
• Obstetrics. Obstetrics is another patient population for
whom TEG can improve monitoring of coagulation status.
Women exhibit many coagulopathies during pregnancy.
These range from the normal physiologic changes causing
a hypercoagulable state to the coagulopathy exhibited
during hemolysis, elevated liver enzyme levels, and low
platelet (HELLP) syndrome.23 The coagulation status of
these patients is particularly important for the anesthetist
because of the risk of epidural hematoma with neuraxial
blockade. Although the incidence of epidural hematoma
in the general obstetric population of 1 in 168,000 is rela-
tively low, several case studies and cohort studies suggest a
higher incidence in the coagulopathic patient.24,25
Traditionally, the major factor determining the safety
of neuraxial anesthesia for the laboring parturient has
been the platelet count.26 The platelet count alone is
rarely responsible for marked changes in coagulation in
this population.27 Thromboelastography is being used
successfully to predict morbidity following neuraxial an-
esthesia. A recent study found that parturients with a low
platelet count (56,000 × 103/μL), but normal TEG could
safely receive a neuraxial anesthetic.28 Additionally, TEG
more accurately identifies patients with hypercoagulopa-
thies and can help guide the dosing of low-molecular-
weight heparin in these patients.23
Thromboelastography-Guided Transfusion
Management
Impaired hemostasis and coagulopathies are known to
cause serious conditions associated with morbidity and
mortality during major surgery.2,12,17-21 Poorly guided
transfusion therapy during massive transfusion protocols
can cause or worsen existing coagulopathies.29 In addition
to worsening coagulopathies, blood transfusions are asso-
ciated with transfusion reactions, transfusion-related acute
lung injury (TRALI), and transfusion-related immunodilu-
tion (TRIM) among many other issues.30 Multiple studies
have found that using a transfusion algorithm based on a
TEG tracing decreases the amount of blood product trans-
fused.17,31,32 This not only decreases the risks associated
with blood transfusions but also decreases total treatment
cost and strain on blood bank resources.17,30
An alteration in R time represents alterations in he-
mostatic clotting factors. If this value is elevated, it can
signify a deficiency in clotting factors, hemodilution, or
increased endogenous heparin production.33 Excessive
heparin may be present if R time is prolonged in a normal
sample, but may be normal in a sample with heparinase.
A prolonged R time in a sample with heparinase may
indicate hemodilution or clotting factor deficiencies, and
this value could indicate a need for transfusion of fresh
frozen plasma.11 On the other hand, a shortened R time
can indicate a hypercoagulopathy warranting the use of
an anticoagulant (see Table 2).20
Alterations in the rate of clot growth, as evidenced by
changes in the K value or α angle, show the clot growth
kinetics. A low value can indicate a deficiency in fibrino-
gen and may reveal a need for cryoprecipitate. Similarly
to the R time, a high value may represent a hypercoagu-
lable state in which an anticoagulant may be applicable
(see Table 2).20
The MA value represents the ultimate strength of
the clot formed by fibrin and platelet bonding. A low
MA value is indicative of low clot strength, which can
be caused by decreased fibrinogen levels, low platelet
counts, or decreased platelet function.29 Paired with a
low K value, this could be a sign of the need for cryopre-
cipitate. This parameter becomes most important when
paired with a platelet count. Administration of platelets
may be avoided with a low platelet count but normal
platelet function as indicated by a normal MA value.
Conversely, treatment with platelets may be indicated
for patients with a low MA value, or low platelet func-
tion, and normal platelet count.11 A high MA value may
indicate the need for an anticoagulant (see Table 2).20
Conclusion
Thromboelastography, although not a new science, is
gaining ground as a monitor of coagulation status in
many different surgical areas. It provides a quick global
assessment of hemostasis more similar to in vivo hemo-
stasis than traditional coagulation profiles.4 Rapid inter-
pretation by anesthetists can help identify coagulopathies
sooner and guide transfusion management more accu-
rately.2,4,12,17,20,31,32 This results in less blood product uti-
lization, which can improve long-term patient outcomes
as well as help decrease overall surgical cost.17,31,32
REFERENCES
1. Bolliger D, Görlinger K, Tanaka KA. Pathophysiology and treatment of
coagulopathy in massive hemorrage and hemodilution. Anesthesiology.
2010;113(5):1205-1219.
www.aana.com/aanajournalonline AANA Journal
2. Bolliger D, Tanaka KA. Roles of thrombelastography and thrombo-
elastometry for patient blood management in cardiac surgery. Trans-
fus Med Rev. 2013;27(4):213-220.
3. Hartet H. Thromboelastography, a method for physical analysis of blood
coagulation [German]. Z Gesamte Exp Med. 1951;117(2):189-203.
4. MacIvor D, Rebel A, Hassan Z-U. How do we integrate thromboelas-
tography with perioperative transfusion management? Transfusion.
2013;53(7):1386-1392.
5. Hiipala ST, Myllylä GJ, Vahtera EM. Hemostatic factors and replace-
ment of major blood loss with plasma-poor red cell concentrates.
Anesth Analg. 1995;81(2):360-365.
6. Manco-Johnson MJ, Dimichele D, Castaman G, et al; Fibrinogen
Concentrate Study Group. Pharmacokinetics and safety of fibrinogen
concentrate. J Thromb Haemost. 2009;7(12):2064-2069.
7. Watson GA, Sperry JL, Rosengart MR, et al; Inflammation and Host
Response to Injury Investigators. Fresh frozen plasma is indepen-
dently associated with a higher risk of multiple organ failure and
acute respiratory distress syndrome. J Trauma. 2009;67(2):221-227.
8. Chitlur M, Sorensen B, Rivard GE, et al. Standardization of throm-
boelastography: a report from the TEG-ROTEM working group.
Haemophilia. 2011;17(3):532-537.
9. Cotton BA, Faz G, Hatch QM, et al. Rapid thrombelastography deliv-
ers real-time results that predict transfusion within 1 hour of admis-
sion. J Trauma. 2011;71(2):407-417.
10. Bolliger D, Seeberger MD, Tanaka KA. Principles and practice of
thromboelastography in clinical coagulation management and trans-
fusion practice. Transfus Med Rev. 2012;26(1):1-13.
11. Yeh T Jr, Kavarana MN. Cardiopulmonary bypass and the coagulation
system. Prog Pediatr Cardiol. 2005;21(1):87-115.
12. Hobson AR, Agarwala RA, Swallow RA, Dawkins KD, Curzen NP.
Thrombelastography: current clinical applications and its potential
role in interventional cardiology. Platelets. 2006;17(8):509-518.
13. Despotis GJ, Filos KS, Zoys TN, Hogue CW Jr, Spitznagel E, Lappas
DG. Factors associated with excessive postoperative blood loss and
hemostatic transfusion requirements: a multivariate analysis in car-
diac surgical patients. Anesth Analg. 1996;82(1):13-21.
14. Murray DJ, Brosnahan WJ, Pennell B, Kapalanski D, Weiler JM, Olson
J. Heparin detection by the activated coagulation time: a comparison
of the sensitivity of coagulation tests and heparin assays. J Cardiotho-
rac Vasc Anesth. 1997;11(1):24-28.
15. Royston D, von Kier S. Reduced haemostatic factor transfusion using
heparinase-modified thromboelastography during cardiopulmonary
bypass. Br J Anaesth. 2001;86(4):575-578.
16. Mallett SV, Chowdary P, Burroughs AK. Clinical utility of viscoelastic
tests of coagulation in patients with liver disease. Liver Int. 2013;33
(7):961-974.
17. Afshari A, Wikkelsø A, Brok J, Møller AM, Wetterslev J. Thromb-
elastography (TEG) or thromboelastometry (ROTEM) to monitor
haemotherapy versus usual care in patients with massive transfusion.
Cochrane Database System Rev. 2011(3):CD007871.
18. De Pietri L, Montalti R, Begliomini B, et al. Thromboelastographic
changes in liver and pancreatic cancer surgery: hypercoagulability,
hypocoagulability or normocoagulability? Eur J Anaesthesiol. 2010;27
(7):608-616.
19. Katrancha ED, Gonzalez LS 3rd. Trauma-induced coagulopathy. Crit
Care Nurse. 2014;34(4):54-63.
20. Brazzel C. Thromboelastography-guided transfusion therapy in the
trauma patient. AANA J. 2013;81(2):127-132.
21. Davenport R. Pathogenesis of acute traumatic coagulopathy. Transfusion.
2013;53(suppl 1):23S-27S.
22. Lier H, Böttiger BW, Hinkelbein J, Krep H, Bernhard M. Coagulation
management in multiple trauma: a systematic review. Intensive Care
Med. 2011;37(4):572-582.
23. Carroll RC, Craft RM, Whitaker GL, et al. Thrombelastography moni-
toring of resistance to enoxaparin anticoagulation in thrombophilic
pregnancy patients. Thromb Res. 2007;120(3):367-370.
 April 2016  Vol. 84, No. 2 133
24. Ruppen W, Derry S, McQuay H, Moore RA. Incidence of epidural
hematoma, infection, and neurologic injury in obstetric patients with
epidural analgesia/anesthesia. Anesthesiology. 2006;105(2):394-399.
25. Working Party, Royal College of Anaesthetists; Association of Anaes-
thetists of Great Britain & Ireland; Obstetric Anaesthetists’ Associa-
tion; Regional Anaesthesia UK. Regional anaesthesia and patients with
abnormalities of coagulation: the Association of Anaesthetists of Great
Britain & Ireland The Obstetric Anaesthetists’ Association Regional
Anaesthesia UK. Anaesthesia. 2013;68(9):966-972.
26. Orlikowski CE, Payne AJ, Moodley J, Rocke DA. Thrombelastography
after aspirin ingestion in pregnant and non-pregnant subjects. Br J
Anaesth. 1992;69(2):159-161.
27. Trapani LM. Thromboelastography: current applications, future
directions. Open J Anesthesiol. 2013;3(1):23-27.
28. Huang J, McKenna N, Babins N. Utility of thromboelastography
during neuraxial blockade in the parturient with thrombocytopenia.
AANA J. 2014;82(2):127-130.
29. da Luz LT, Nascimento B, Rizoli S. Thrombelastography (TEG): prac-
tical considerations on its clinical use in trauma resuscitation. Scand J
Trauma ResuscEmerg Med. 2013;21:29.
30. McEvoy MT, Shander A. Anemia, bleeding, and blood transfusion in
the intensive care unit: causes, risks, costs, and new strategies. Am J
Crit Care. 2013;22(6 suppl):eS1-eS14.
31. Ak K, Isbir CS, Tetik S, et al. Thromboelastography-based transfusion
134 AANA Journal  April 2016  Vol. 84, No. 2 www.aana.com/aanajournalonline
View publication stats
algorithm reduces blood product use after elective CABG: a prospec-
tive randomized study. J Card Surg. 2009;24(4):404-410.
32. Shore-Lesserson L, Manspeizer HE, DePerio M, Francis S, Vela-
Cantos F, Ergin MA. Thromboelastography-guided transfusion algo-
rithm reduces transfusions in complex cardiac surgery. Anesth Analg.
1999;88(2):312-319.
33. Spiess BD, Tuman KJ, McCarthy RJ, DeLaria GA, Schillo R, Ivankov-
ich AD. Thromboelastography as an indicator of post-cardiopulmo-
nary bypass coagulopathies. J Clin Monit. 1987;3(1):25-30.
AUTHORS
Shawn Collins, DNP, PhD, CRNA, is director, Nurse Anesthesia Program,
Western Carolina University, Cullowhee, North Carolina. Email: shawn
collins@email.wcu.edu.
Carolyn MacIntyre, MS, CRNA, is employed by AllCare Clinical Asso-
ciates, Asheville, North Carolina.
Ian Hewer, MSN, MA, CRNA, is assistant director of the Nurse
Anesthesia Program at Western Carolina University, Cullowhee, North
Carolina.
DISCLOSURES
The authors have declared they have no financial relationships with any
commercial interest related to the content of this activity. The authors did
not discuss off-label use within the article.