TEG

thromboelastography
 Factor Common Name Function
• Coagulation cascade serves to stabilize the F-I Fibrinogen Forms clot (fibrin)

clot that has formed and further seal up the F-II Prothrombin Its active form (IIa) activates
I,V,VII,VIII,XI,XIII,protein C,platelets
wound. The goal of the cascade is to form
fibrin which will form a mesh within the F-III Tissue Factor (TF) or
Thromboplastin or Platelet
Co-factor of VII

platelet aggregate to stabilize the clot. Phosholipids

F-IV Calcium (Ca++) Required for coagulation factors to

• There are major 13 factors which are bind to phospholipid

involved in the coagulation cascade. All F-V Proaccelerin Co-factor of X with which it forms
prothrombinase complex
these factors are blood proteins or their
derivatives. Even if one of the factor is F-VI Old name of factor Va Unassigned

defective, the whole clotting process is F-VII Proconvertin Activates IX,X

impaired leading to hemorrhage. These F-VIII Anti-hemophilic Factor A Co-factor of IX with which it forms
the tenase complex

factors are F-I to F-XIII. F-IX Anti-hemophilic Factor B or Activates X which forms tenase
Christmas Factor complex with VIII

F-X Stuart-Prower Factor Activates II which forms

prothrombinase complex with V

F-XI Anti-hemophilic Factor C or Plasma Activates IX

Thromboplastin Antecedent (PTA)

F-XII Hageman Factor Activates XI,VII & prekallikrein

F-XIII Fibrin Stabilizing Factor Crosslinks Fibrin

• There are 3 major stages in the coagulation cascade:
• Stage 1: Formation of Prothrombinase Complex (Prothrombin Activator)
• Prothrombinase is formed in two ways
• Extrinsic Pathway (also known as Tissue Factor Pathway)
• Intrinsic Pathway (also known as Contact Activation Pathway)

• Stage 2: Conversion of Prothrombin into Thrombin

• Stage 3: Conversion of Fibrinogen into Fibrin
Stage 2 & Stage 3 is collectively called as Final Common Pathway
STAGE 1
 Extrinsic Pathway
• In this pathway, the formation of prothrombinase
complex is initiated by the tissue thromboplastin
Mechanism:
• It begins with trauma to blood vessel or tissues
outside the blood vessel. It releases F-VII and
tissue phosholipids.F-VII comes in contact with F-
III (TF or Thromboplastin) expressed on TF-bearing
cells (stromal fibroblasts & leukocytes) forming an
activated complex (TF-VIIa)
• TF-VIIa activates F-IX,F-X in presence of Ca++ and
tissue phospholipids
• F-Xa acts on F-V and activates it
• F-Xa complexes with tissue phospholipids, F-Va,
Ca++ and forms a complex called prothrombinase
complex or prothrombin activator.
 Intrinsic Pathway
• In this pathway, the formation of prothrombinase complex is
initiated by platelets which are within the blood itself
Mechanism:
• Begins with the formation of the primary complex on collagen
by HMWK, prekallikrein and F-XII Prekallikrein is converted to
kallikrein and F-XII gets activated.
• Damaged platelets adhere to the wet surface of blood vessel
and release platelet phospholipids i.e. F-III
• F-XIIa acts enzymatically on F-XI (Plasma Thromboplastin
Antecedent) and activates it
• F-XIa acts enzymatically on F-IX and activates it in presence of
Ca++
• F-IXa activates F-VIII (Anti Haemophilic Factor)
• F-IIIa,F-VIIIa and F-IXa activate F-X
• F-Xa acts enzymatically on F-V (Proaccelerin) and activates it
in presence of Ca++
• F-Va,F-Xa,F-IIIa and Ca++ form a complex called prothrombin
complex
STAGE 2
• In the presence of prothrombin activator
or prothrombinase complex and
Ca++,prothrombin is converted to
thrombin
• Thrombin itself increases its own rate of
formation (positive feedback mechanism)
• Thrombin then activates other components of
the coagulation cascade, including F-V and F-
VIII (which activates F-XI,which in turn activates
F-IX)and activates and releases F-VIII from being
bound to vWF
• F-VIIIa is the co-factor of F-IXa, and together
they form the "tenase" complex, which activates
F-X and so the cycle continues.("Tenase" is a
contraction of "ten" and the suffix "-ase" used
for enzymes)
STAGE 3
• Thrombin converts fibrinogen (plasma protein produced by the liver) to fibrin
• Thrombin also activates F-XIII (Fibrin Stabilizing Factor) which in presence of
Ca++ stabilizes the fibrin polymer through covalent bonding of fibrin
monomers
Coagulation Monitoring – Conventional Tests
Tests Of Coagulation Tests of Degradation
* Degradation products
* Platelets
• number
• function

*Clotting studies
• PT
• APTT

*Fibrinogen levels
 •Each of these tests measures a different
aspect of the clotting process, but even in
combination they do not provide a complete
picture of the status of the coagulation
system
•Besides evaluation of platelet function
remains insensitive and time consuming.
The platelet count provides only a
quantitative, not qualitative index of
platelet status.
• At present the treatment of postoperative bleeding remains
empirical because of the perceived need for immediate
correction of the haemostatic defect and lack of readily available
measures of all phases of clot formation and breakdown ,
including the strength of the clot
• FFP and platelets often given with little scientific basis.
 What we need?

an effective and convenient means of monitoring

whole blood coagulation which evaluates the
elastic properties of whole blood and provides a
global assessment of heamostatic function.
 TEG
thromboelastography
TEG
• Thromboelastography monitors the thrombodynamic properties of blood
as it is induced to clot under a low shear environment resembling sluggish
venous flow. The patterns of change in shear-elasticity enable the
determination of the kinetics of clot formation and growth as well as the
strength and stability of the formed clot.
• The strength and stability of the clot provide information about the ability
of the clot to perform the work of hemostasis, while the kinetics determine
the adequacy of quantitative factors available to clot formation.
• First developed by Dr. Hellmut Hartet at University of Heidelberg, School
of Medicine in 1948 as a method to assess global hemostatic function from
a single blood sample; this was the original Thromboelastography.
THROMBOELASTOGRAPHY
Basic Principles
THROMBOELASTOGRAPHY
Basic Principles
• Heated (37C) oscillating cup

• Pin suspended from torsion wire

into blood

• Development of fibrin strands

“couple” motion of cup to pin

• “Coupling” directly proportional to

clot strength

•  tension in wire detected by

EM transducer
THROMBOELASTOGRAPHY
Basic Principles
• Electrical signal amplified to
create TEG trace

• Result displayed graphically on

pen & ink printer or computer
screen

• Deflection of trace increases as

clot strength increases &
decreases as clot strength
decreases
THROMBOELASTOGRAPHY
The “r” time
r time
•represents period of time of
latency from start of test to initial
fibrin formation

•ineffect is main part of TEG’s

representation of standard”clotting
studies”

•normal range
• 15 - 23 mins (native blood)
• 5 - 7 mins (kaolin-activated)
THROMBOELASTOGRAPHY
What affects the “r” time?
•r time  by •r time  by
• Factor deficiency • Hypercoagulability
syndromes
• Anti-coagulation
• Severe
hypofibrinogenaemia
• Severe
thrombocytopenia
THROMBOELASTOGRAPHY
The “k” time

k time
•represents time taken to achieve
a certain level of clot strength
(where r time = time zero ) -
equates to amplitude 20 mm

•normal range
• 5 - 10 mins (native blood)
• 1 - 3 mins (kaolin-activated)
THROMBOELASTOGRAPHY
What affects the “k” time?
•k time  by •k time  by
• Factor deficiency • Hypercoagulability
• Thrombocytopenia state
• Thrombocytopathy
• Hypofibrinogenaemia
THROMBOELASTOGRAPHY
The “” angle

 angle
•Measures the rapidity of
fibrin build-up and cross-
linking (clot strengthening)
•assesses rate of clot
formation

•normal range
• 22 - 38 (native blood)
• 53 - 67(kaolin-activated)
THROMBOELASTOGRAPHY
What affects the “” angle?
• Angle  by • Angle  by
• Hypercoagulable • Hypofibrinogenemia
state • Thrombocytopenia
THROMBOELASTOGRAPHY
The “maximum amplitude” (MA)
Maximum amplitude
•MA is a direct function of the maximum
dynamic properties of fibrin and platelet
bonding via GPIIb/IIIa and represents
the ultimate strength of the fibrin clot

•Correlates to platelet function

• 80% platelets
• 20% fibrinogen

•normal range
• 47 – 58 mm (native blood)
• 59 - 68 mm (kaolin-activated)
• > 12.5 mm (ReoPro-blood)
THROMBOELASTOGRAPHY
What affects the “MA” ?
•MA  by •MA  by
• Hypercoagulable • Thrombocytopenia
state • Thrombocytopathy
• Hypofibrinogenemia
THROMBOELASTOGRAPHY
Fibrinolysis
•LY30

•measures % decrease in
amplitude 30 minutes post-MA

•gives measure of degree of

fibrinolysis

•normal range
• < 7.5% (native blood)
• < 7.5% (celite-activated)

•LY60
• 60 minute post-MA data
THROMBOELASTOGRAPHY
Other measurements of Fibrinolysis
•A30 (A60)
• amplitude at 30 (60) mins post-MA

•EPL

•earliest indicator of abnormal lysis

•represents “computer prediction” of 30

min lysis based on interrogation of
actual rate of diminution of trace
amplitude commencing 30 secs post-MA

•early EPL>LY30 (30 min EPL=LY30)

•normal EPL < 15%
THROMBOELASTOGRAPHY
What measurements are affected by
fibrinolysis?

Fibrinolysis leads to:

•  LY30 /  LY60
•  EPL
•  A30 /  A60
THROMBOELATOGRAPHY
Quantitative analysis
• Clot formation
• Clotting factors - r, k times

• Clot kinetics
• Clotting factors - r, k times
• Platelets - MA

• Clot strength / stability

• Platelets - MA
• Fibrinogen - Reopro-mod MA

• Clot resolution
• Fibrinolysis - LY30/60; EPL
A30/60
THROMBOELATOGRAPHY-Qualitative analysis
Thromboelastography
Increased in
patients with
clotting Decreased in patients
defects with platelet
dysfunction or defect
fibrin formation

Reaction
time

Amplitude
TEG

Start Minutes
TEG treatment algorithm
• r>7 min but <10.5 min mild  clotting factors 1 FFP

• r>10.5 min but <14 min mod  clotting factors 2 FFP

• r>14min severe  clotting factors 4 FFP

• MA<48mm mod in platelet no/function 1platelet

• MA<40mm severe in platelet no/function 2platelet

Indications
Cardiac Surgery
• Cardiac surgical procedures that have a moderate to high risk of
requiring a blood transfusion (1) should have the full cardiac protocol.
• 1 Combined procedures eg CABG + AVR
• 2 Multiple valve replacement/repair
• 3 Aortic Root surgery
• 4 Thoracic Aortic surgery
• 5 Re-do operations
• 6 Emergency surgery – especially patients from the cardiac catheter
lab.
• 7 Anticipated prolonged cardiopulmonary bypass
Indications
Patient factors
• 1- Patients on aspirin and clopidrogel <7 days
• 2- Patients on Warfarin or heparin
• 3- Pre-existing platelet &/or clotting factor abnormalities
Indications
Vascular Surgery.
• ‘Open’ procedures on the thoracic aorta.
• ‘Open’ abdominal procedures where a significant blood loss is anticipated.
• Patient factors: 1 – 3 as above *
• Regional anaesthetic techniques (see below)
Indications
Regional anaesthetic techniques (inc. use in Obstetrics)
• If the platelet count is between 50 –80,000 a TEG should be
performed if a regional technique is considered necessary.
• If the platelet count is > 80,000 a TEG is not necessary unless
there are additional factors.
• A regional technique is not advised if the platelet count is <
50,000.
• A TEG should be performed if a regional technique is considered
necessary within 12 hours following prophylactic LMWH or 24
hours post therapeutic LMWH