When can it be used?
How is it produced?
What do the parameters R, K, α, MA, and A30 (LY30) indicate?
How can the above parameters be used to guide therapy?
What is platelet mapping and how does it help?
How does thromboelastography (TEG®) differ from rotational thromboelastometry (ROTEM®)?
The data shown represents a typical thromboelastography (TEG) trace. Thromboelastography is a viscoelastic hemostatic assay that measures global properties of whole blood clot formation. It shows the interaction of platelets with the coagulation cascade including aggregation, clot strengthening, fibrin cross-linking, and fibrinolysis. TEG is an effective and convenient means of monitoring whole blood coagulation and provides a global assessment of hemostatic function.
It can assist in determining if a patient has normal hemostasis or is bleeding due to a coagulopathy or anticoagulant therapy.
Conventional coagulation tests like PT and aPTT poorly reflect in vivo hemostasis. As they are performed in plasma, they assess only a portion of the coagulation system and do not provide information on the full balance between coagulation and anticoagulation. In contrast TEG is performed on whole blood and provides information on clot formation, stabilization, and dissolution thus assessing coagulation and fibrinolysis.
TEG is used to assess hemostasis during liver transplantation, postpartum hemorrhage, cardiac surgery, and in trauma resuscitation. It can also be used in coagulopathy due to other reasons such as sepsis and guide management. TEG can also provide information on the presence and adequacy of platelet inhibition.
In cardiac surgery during cardiopulmonary bypass, abnormal coagulation can be identified before heparin reversal with the addition of heparinase to the testing. This will be useful in long pump runs, in deep hypothermia, in the presence of ventricular assist devices, and in major vascular procedures. In pinpointing the specific problem, TEG has been shown to reduce blood transfusion in cardiac surgery [1, 2].
The test sample is placed in an oscillating cup (4–45° every 5 s) heated to 37 °C. A pin is suspended into the sample by a torsion wire which is attached to a mechanical/electrical transducer. The elasticity and strength of the developing clot changes the motion of the pin which is converted into a graphical and numerical output which is displayed.
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The above tracing can be looked at in the following phases.
Initial clot formation
Split point (SP) time = from the start of the test to the split of the trace (first detectable fibrin)
Reaction (R) time = from the start till the trace reaching 2 mm amplitude (1 mm either side of baseline) and represents continued production of thrombin and conversion of fibrinogen to fibrin (normal 4–9 min kaolin activated). Prolonged R in factor deficiency and anticoagulants.
R-SP = delta (Δ). Thrombin burst. Low delta indicates hypercoagulability and vice versa (normal 0.7–1.1 min). The test can be performed with heparinase (TEG-H), and a difference of more than 2 min between R value of TEG and TEG-H indicates heparin effect.
Conversion of fibrinogen to fibrin
Kinetics (K) time = time interval between 2 mm and 20 mm on the trace and represents fibrin cross-linkage and rate of bonding between fibrin and platelets and is a measure of fibrinogen function (normal 1–3 min kaolin activated). Prolonged by anticoagulants, hypofibrinogenemia and thrombocytopenia and shortened by increased fibrinogen level and platelet function.
Angle (α) = the angle at which the curve rises from SP to K and is related directly to K time as a measure of fibrin platelet interaction and therefore functional fibrinogen (normal 59–74°)