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Critical Care Compendium | Thromboelastogram (TEG)

Thromboelastogram (TEG)
by Chris Nickson, Last updated October 24, 2018

Reviewed and revised by Hamish Lala and Chris Nickson

OVERVIEW

Thromboelastography (TEG) is a viscoelastic hemostatic assay that measures the global visco-elastic
properties of whole blood clot formation under low shear stress
TEG shows the interaction of platelets with the coagulation cascade (aggregation, clot strengthening,
fibrin cross-linking and fibrinolysis)
does not necessarily correlate with blood tests such as INR, APTT and platelet count (which are often
poorer predictors of bleeding and thrombosis)
This page describes TEG® predominantly, ROTEM® is the alternative viscoelastic hemostatic assay
that is widely available commercially

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 TEG® measures the physical properties of the clot in whole blood via a pin suspended in a cup
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(heated to 37C) from LIBRARY TOP 100 withPART
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The elasticity and strength of the developing clot changes the rotation of the pin, which is
converted into electrical signals that a computer uses to create graphical and numerical output
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point of care test (quick, takes around 30min)
can be repeated easily and compared and contrasted
requires calibration 2-3 times daily
should be performed by trained personnel
susceptible to technical variations
kaolin and more recently kaolin + tissue factor (TF) (RapidTEG®) are used as activators, NATEM
(TEG® using native whole blood) is slower
other tests are available including functional fibrinogen, a measure of fibrin-based clot function, and
Multiplate which evaluates platelet function

TEG6s (Haemonetics)

This newer machine no longer uses the ‘pin-in-cup’ technique (as did its TEG5000 predecessor)
It uses ‘resonance’ where blood is exposed to a fixed vibration frequency range and the detector
measures the vertical motion of blood meniscus under LED illumination and transforms that
movement into tracing of clot dynamics
With pre-prepared cartridges, there is no longer any pipetting required!

USE

Indications
 prediction of need for transfusion (maximum amplitude (MA) is a useful predictor in trauma)
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Studies show cost-effectiveness and reduction in blood products in:

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liver transplantation
cardiac surgery

Maybe useful in:

trauma (reduction in blood product use and mortality in cohort studies)

obstetrics (some data to show that it may decrease transfusion rates; this is controversial)
early detection of dilutional coagulopathy

Hard to interpret in certain situations:

low molecular weight heparin (LMWH)

aspirin
post cardiac bypass
fibrinolysis
hypercoagulability

NORMAL TEG

Specific parameters represent the 3 phases of the cell-based model of

haemostasis: initiation, amplification, and propagation
 R value = reaction time (s)
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initial fibrin ONE CASES of 2mm)
formation (amplitude CCC

initiation phase
dependent on clotting factors
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K = kinetics (s)
time taken to achieve a certain level of clot strength (amplitude of 20mm)
amplification phase
dependent on fibrinogen
alpha = angle (slope of line between R and K)
measures the speed at which fibrin build up and cross-linking takes place, hence assesses the
rate of clot formation
“thrombin burst” / propagation phase
dependent on fibrinogen
TMA = time to maximum amplitude(s)
MA = maximum amplitude (mm)
represents the ultimate strength of the fibrin clot; i.e. overall stability of the clot
dependent on platelets (80%) and fibrin (20%) interacting via GPIIb/IIIa
A30 or LY30 = amplitude at 30 minutes
percentage decrease in amplitude at 30 minutes post-MA
fibrinolysis phase
CLT = clot lysis time (s)

Approximate normal values (kaolin activated TEG, values differ if native blood used, and between types of
assay)

R: 4-8 min
K: 1-4 min
α-Angle: 47-74°
MA: 55-73mm
LY 30%: 0-8%

Corresponding terminology for ROTEM

ROTEM TEG

Clotting time (CT) R value (reaction time)

α angle and clot formation time (CFT) K value and α angle

Maximum clot firmness (MCF) Maximum amplitude (MA)

Clot lysis (CL) LY30
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IMPORTANT PATTERNS
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Source: unknown

TEG AS A GUIDE TO TREATMENT

Increased R time => FFP

Decreased alpha angle => cryoprecipitate
Decreased MA => platelets (consider DDAVP)
Fibrinolysis =>  tranexamic acid (or aprotinin or aminocaproic acid)
Or use this handy guide (-:
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Source: Only4Medical (click on image for source)

TEG® VERSUS ROTEM®

Comparison

Two commercial types of viscoelastic tests are available: thromboelastography =TEG® (developed in

1948, now produced  in the USA) and rotational thromboelastogram = ROTEM® (from Germany)
differences in diagnostic nomenclature for identical parameters between the two
TEG® operates by moving a cup in a limited arc (±4°45′ every 5s) filled with sample that engages a
pin/wire transduction system as clot formation occur
ROTEM® has an immobile cup wherein the pin/wire transduction system slowly oscillates
(±4°45′every 6s)
results are not directly comparable as different coagulation activators are used
ROTEM® is more resistant to mechanical shock, which may be an advantage in the clinical setting

Equivalent variables for ROTEM®

Clotting time (CT) = R value (reaction time)

 α angle and clot formation time (CFT) = K value and α angle
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Maximum clot firmness TOP 100 amplitude
(MCF)  = Maximum PART(MA)
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Clot lysis (CL)  = LY30

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COMPARISON WITH PLASMA CLOTTING TESTS

Pros of viscoelastic hemostatic assays

assessment of global haemostatic potential provides more information than time to fibrin formation
can readily differentiate a coagulopathy due to low fibrinogen from one due to thrombocytopenia
point-of-care (POC) device with rapid  turnaround times so that many results available within 5–10
min of starting the test

Cons of viscoelastic hemostatic assays

variable availability and user familiarity

marked inter-operator variability and poor precision
UK NEQAS data suggests coefficients of variance ranging from 7.1% to 39.9% for TEG® and
7.0% to 83.6% for ROTEM®
may require specialist staff to perform

EVIDENCE

Cochrane review (2015)of the use of TEG and ROTEM in traumatic bleeding advised that they should
be used for research only, due to a lack of evidence for the accuracy of the assays.

References and Links

Journal articles

Afshari A, Wikkelsø A, Brok J, Møller AM, Wetterslev J. Thrombelastography (TEG) or

thromboelastometry (ROTEM) to monitor haemotherapy versus usual care in patients with
massive transfusion. Cochrane Database Syst Rev. 2011 Mar 16;(3):CD007871. doi:
10.1002/14651858.CD007871.pub2. Review. PubMed PMID: 21412912. [Free Full Text]
Bolliger D, Seeberger MD, Tanaka KA. Principles and practice of thromboelastography in clinical
coagulation management and transfusion practice. Transfus Med Rev. 2012 Jan;26(1):1-13. doi:
10.1016/j.tmrv.2011.07.005. Epub 2011 Aug 26. Review. PubMed PMID: 21872428. [Free
Fulltext]
da Luz LT, Nascimento B, Rizoli S. Thrombelastography (TEG(R)): practical considerations on its
clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013 Apr 16;21(1):29.
 [Epub ahead of print] PubMed PMID: 23587157. [Free Fulltext]
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monitoring: PART ONE
current CASES
techniques and clinicalCCC
use of
viscoelastic point-of-care coagulation devices. Anesth Analg. 2008 May;106(5):1366-75. doi:
10.1213/ane.0b013e318168b367. Review. PubMed PMID: 18420846. [Free Fulltext]
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Hunt H, Stanworth S, Curry N, Woolley T, Cooper C, Ukoumunne O, Zhelev Z, Hyde C. TEG and
ROTEM for diagnosing trauma‑induced coagulopathy (disorder of the clotting system) in adult
trauma patients with bleeding. Cochcane Review. 2015 [article]
Tapia NM et al. TEG-guided resuscitation is superior to standardized MTP resuscitation in
massively transfused penetrating trauma patients. J Trauma Acute Care Surg. 2013;74:378-386.
[pubmed]
Thakur M, Ahmed AB. A review of thromboelastography. Int J Periop Ultrasound Appl Technol
2012;1(1):25-29. [article]

FOAM and web resources

ICN — SMACC: Hurn on TEG/ROTEM in the Real World (2013)

Joe Elbeery on Youtube — TEG basics video (2013)
Maryland CCP — The Use of TEG & Goal Directed Blood Component Therapy by John Walsh
(2013)
Practical-Hemostasis.com — TEG and ROTEM
The websites for the ROTEM and TEG provide a comprehensive explanation of the waveforms
generated in various disorders.

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About Chris Nickson

FCICM FACEM BSc(Hons) BHB MBChB MClinEpid(ClinTox) DipPaeds
DTM&H GCertClinSim
Chris is an Intensivist at the Alfred ICU in Melbourne and is an Adjunct
Clinical Associate Professor at Monash University. He is also the Innovation
Lead for the Australian Centre for Health Innovation and the Chair of the Australian and New
Zealand Intensive Care Society (ANZICS) Education Committee. He has a passion for helping
clinicians learn and for improving the clinical performance of individuals and collectives. After
 finishing his medical degree at the University of Auckland, he continued post-graduate training in
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New Zealand as well LIBRARY TOP 100 Territory,
Australia's Northern PART ONEand Melbourne.
Perth CASES He CCC
has since
completed further training in emergency medicine, clinical toxicology, clinical epidemiology and
health professional education. He coordinates the Alfred ICU's education and simulation
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programmes and runs the unit’s education website, INTENSIVE. He created the 'Critically Ill
Airway' course and teaches on numerous courses around the world. He is one of the founders
of the FOAM movement (Free Open-Access Medical education) and is co-creator of
Lifeinthefastlane.com, the RAGE podcast, the Resuscitology course, and the SMACC
conference. His one great achievement is being the father of two amazing children. On Twitter,
he is @precordialthump.

Comments

Matt says
November 15, 2013 at 1:11 am

Aminocaproic acid for fibrinolysis?

Chris Nickson says

February 17, 2014 at 3:22 pm

http://www.aana.com/newsandjournal/Documents/thromboelastography-guide-trans-0413-
p127-132.pdf
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