TEG/ROTEM Flashcards
What do TEG & ROTEM stand for?
TEG is ThromboElastoGraphy,
ROTEM is ROtational ThromboElastoMetry
Broadly, how do TEG & ROTEM work?
What is the difference?
Whole blood (a minute amount of it, no more than 1ml) at body temperature (37º) is added to a heated cuvette (a little cup). A pin is suspended into the cup, and then some sort of rotation takes place. Some impediment to the rotation develops as the blood clots. The degree of this impediment is recorded as “amplitude”, and displayed on the time vs. amplitude graph.
The main difference between TEG and ROTEM is the bit which rotates (TEG rotates the cup, and ROTEM rotates the pin).
Define the following parameters measured by TEG?
R?
K?
Alpha-angle?
TMA?
MA?
CLT?
R = Reaction time (time from start to amplitude - 2mm)
K = Kinetics (time from amplitude 2mm to 20mm)
Alpha - angle = Slope from 2mm to 20mm
TMA = Time to Maximum Amplitude
MA = Maximum Amplitude
CLT = Clot Lysis Time (Time taken for amplitude to decrease by 2mm from MA)
Define the following parameters measured in ROTEM?
And name their TEG counterpart if applicable?
- CT
- CFT
- Alpha-angle. Difference to TEG?
- A10
- MCF-t
- MCF
- LOT
- LT
- LI30
- ML
- Clotting time (TEG = R) = Time from start to amplitude 2mm
- Clot formation time (TEG = K) = Time from amplitude 2mm until amplitude 20mm
- Alpha-angle = Slope at 2mm amplitude
- A10 = Amplitude at 10 mins
- MCF-t = Time to maximum clot firmness
- MCF = Maximum Clot Firmness
- LOT - Lysis Onset Time (time for amplitude to decrease by 15% of MCF)
- LT = Lysis Time (time taken for amplitude to decrease to 10% of MCF)
- LI30 = Lysis index at 30 mins (% drop in amplitude from MCF at 30 mins(
- ML = Maximum Lysis (minimum amplitude at end of run time)
What is R/clotting time in TEG/ROTEM?
What causes prolongation (4)?
How can prolongation be addressed (2)
The time it takes for the amplitude to reach 2mm is used as a marker that the clotting cascade has started. T
Causes of prolonged CT and R-value
Anything that causes a raised PT and APTT:
- Deficiency of clotting factors
- Heparin (very sensitive - prolonged by 0.15 units per ml of blood, or a systemic heparin dose of less than 750 units for a 70kg adult)
- Warfarin
- Direct thrombin inhibitors
The reaction to a prolonged CT could consist of the administration of replacement factors (eg. FFP or factor concentrates) or antagonists to anticoagulants (eg. protamine).
What is K/CFT in TEG/ROTEM?
Why may a CFT not be reported?
What causes prolongation (4)?
How can prolongation be addressed (2)
What causes shortening of CFT?
ROTEM uses CFT and TEG uses the K value to describe the time from clot initiation (when the amplitude gets to 2mm) to 20mm. The CFT and K relate to the activity of the clotting factors, but also incorporates a measure of the effectiveness of fibrin polymerisation, platelet activity and Factor XIII activity. In states of extreme coagulopathy, the clot may never actually form and the CFT will not be reported.
Causes of prolonged CFT
- Thrombocytopenia
- Platelet dysfunction
- Low fibrinogen
- Severe deficiency of other factors
Causes of Shortened CFT
- Hypercoagulable states
The reaction to a prolonged CFT might sensibly consist of platelet transfusion, or cryoprecipitate.
What is alpha angle in TEG? And in ROTEM?
What components are thought to contribute? Which is said to be the most important?
What causes a decreased alpha angle (3)?
How can it be addressed (2)
For the α-angle, TEG uses the slope of a line connecting the point at which the R interval ends and the point at which the K interval ends. ROTEM, in contrast, uses the slope of the line at the 2mm amplitude mark.
In either case, the slope is determined by the rate of reaction between platelets, fibrin and the clotting cascade factors (manufacturers suggest fibrinogen plays greatest role).
Causes of a decreased α-angle (3)
- Low fibrinogen
- Poor fibrinogen polymerisation
- Thrombocytopenia, or platelet dysfunction
Cryoprecipitate transfusion, or of fibrinogen concentrate (where available).
What is MCF/MA in TEG & ROTEM?
What does components of clotting does it relate to (3)?
How is decreased MCF addressed (2)?
Maximum clot firmness (MCF - ROTEM) and maximum amplitude (MA-TEG) - Both the TEG and ROTEM terms refer to the point at which the clot is at its thickest.
This variable is primarily a measure of platelet count, platelet function and fibrinogen concentration
The reaction to a decreased MCF is usually to either give platelets or DDAVP.
What does TMA/MCF-t refer to?
Time to maximum amplitude (TMA in TEG or MCF-t in ROTEM) refer to the time it takes to reach MCF or MA.
What is A10?
Under what circumstances is A10 more useful than MCF?
What is it a surrogate marker for (3)?
What can a decreased A10 result from (3)?
A10 = Amplitude at 10mins
This is another marker of clot stability, and can be used instead of MCF in situations where the measurement of MCF is impractical (eg. when the patient is so ridiculously coagulopathic or anticoagulated that one might take all day to reach maximum clot stability).
The A10 therefore - like the MCF - is a surrogate marker of platelet function, platelet numbers, and fibrin concentration.
A decreased A10 can result from
- low fibrinogen
- thrombocytopenia
- platelet aggregation inhibitors, eg.antiplatelet drugs
What does clot lysis time (e.g. CL30) allow one to extrapolate?
What are CLT (TEG)? And LOT (ROTEM)?
it is possible to extrapolate the rate of fibrinolysis from the change in clot density over the half-hour that follows MCF(MA). One can then compare the 30 minute amplitude to the MCF as a fraction.
TEG - CLT = 2mm from MA
LOT = MCF-15%
An abnormally short time to lysis would suggest some sort of fibrinolysis is taking place.
The reaction to a decreased CLF is usually to give tranexamic acid or (in the old days) aprotinin.
What does INTEM use as activators (2)? What traditional clotting test does it approximate to (i.e. which clotting pathway is being tested)?
INTEM is similar to the APTT. This test uses phospholipid and ellagic acid as activators and provides information similar to that of the APTT. Intrinsic pathway is being tested.
What is used as an activator in EXTEM? What traditional clotting test does it approximate to (i.e. which clotting pathway is being tested)?
What is the benefit of using an activator?
What is the drawback?
EXTEM is similar to the PT. The test uses Tissue Factor as an activator and provides information similar to the PT. Extrinsic pathway being tested.
The addition of tissue factor greatly speeds up reaction time (R or CT) and ensures that MA will be established within 10 minutes, but at the cost of all the useful information which can be derived from the R/CT variables.
What does HEPTEM use to exclude the effect of heparin?
How should it compare to INTEM if there is no heparin effect?
And if there is a heparin effect?
HEPTEM uses a lyophilised heparinase to neutralise heparin.
A shortened HEPTEM CT would suggest a heparin effect (i.e. shortened by addition of heparinase).
