To the extreme distress of many candidates, the TEG had come up recently in Question 26 from the second paper of 2014, and again in Question 8 from the second paper of 2015. Then, the college really ground them down in Question 21 from the first paper of 2019, where they asked for a comparison of TEG with an empiric massive transfusion strategy.
The best summary to guide the time-poor candidate can be found (as always) at the Practical Haemostasis website. The LITFL TEG/ROTEM page is also an excellent balance between detail and brevity. The aim of this chapter is not to supercede these outstanding resources, but rather to act as a footnote for them, and to expand on key issues in a way which renders this complex topic easily understood by somebody who has not slept or eaten for some days.
For those with infinite time, the following resources exist at the Haemoview website:
Haemonetics also has a ton of TEG-related literature for their products:
Without further ado:
TEG is ThromboElastoGraphy, and ROTEM is ROtational ThromboElastoMetry, both acronyms being registered trademarks. Both are tools of assessing whole blood clotting. Whole blood (a miniute amoutn 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. In fact the main difference between TEG and ROTEM is the bit which rotates (TEG rotates the cup, and ROTEM rotates the pin). Irrespective of which bit is rotating, 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.
As one can see, the graph is essentially the same but some of the labels are different.
Indeed, the TEG and ROTEM measured variables have a lot of functional overlap, as well be discussed later; however the results produced by these two systems cannot be compared directly, and in any given situation the two tests may disagree enough that the different results prompt different reactions from the clinician.
A more precisely labelled diagram specific for ROTEM is also available, and can be viewed at the Haemoview website (ROTEM parameters)
Advantages and disadvantages of using these devices will one day appear in some sort of sadistic viva situation. In brief, one can say that there is no clear advantage to their use, as a recent (2011) meta-analysis could not make a firm recommendation in their favour. "There is currently weak evidence to support the use of TEG/ROTEM as a tool to guide transfusion in patients with severe bleeding", say Wikkelsoe et al. No impact was identified on mortality, amount of blood transfused, incidence of surgical reinterventions, time to extubation, or length of stay in hospital and intensive care unit. Overall, it remains an expensive plaything.
This was the topic of Question 21 from the first paper of 2019. The examiners referred to TEG specifically in the question and throughout the answer, but it is clear that they were using the term interchangeably with ROTEM, and so in the discussion to follow TEG is also used as a surrogate for all forms of global testing for clotting function. Though the question asked specifically for a discussion of advantages and disadvantages, the college answer was formulated in a "critically evaluate" fashion which typically calls for a description of the rationale and supporting evidence As such, some mutant combination of the two answer formats is offered here, as a compromise which satisfies the authors' unhealthy preoccupation with tabulated answers.
Rationale for TEG-guided massive transfusion
Advantages of TEG
Disadvantages of TEG
Advantages of fixed ratio massive transfusion
Disadvantages of fixed ratio massive transfusion
Evidence which compares TEG-guided protocols with fixed ratio transfusion
The two commercially competing systems confuse the issue by using different nomenclature for the same thing (eg. CT instead of R). Both use whole blood (usually citrated and then replenished with calcium), but ROTEM also uses a bunch of tests which make use of unusual pro-and anticoagulant factors, making it impossible to compare the results of one system with the other. This makes it important to choose only one system, and to commit to it. So, which to choose?
There is little to discriminate between them in terms of "utility", as both systems offer a sophisticated assessment of clotting. LITFL mentions that ROTEM is theoretically more resistant to mechanical shock, which makes it more useful "in the clinical setting", implying that the cardiothoracic operating theatre and the ICU place the device at risk of constantly being nudged and kicked. Thus, if one were able to position the machine in a special place where it is not in the way of stampeding medical staff, the two modalities would have equal appeal?
Little evidence exists to guide decisionmaking on this issue. A good review by Sankarankutty et al (2012) compared the two systems in the management of trauma, and concluded that "differences in the activators utilized in each device limit the direct comparability". The authors identified 24 studies of TEG and ROTEM in trauma, all of which presented "considerable heterogeneity". The review is interesting because it contrasts the two systems in a pragmatic manner, i.e. "how is this going to change the management of patients?" Interesting features were discovered:
The TEG uses "R" and ROTEM uses "CT" to describe the time it takes for the amplitude to start climbing. Arbitrarily, the 2mm point is used as a marker that the clotting cascade has started. This time vaguely relates to the time it takes for the enzymes of the clotting cascade to run their full course and ultimately arrive at the formation of fibrin from fibrinogen. The CT is therefore analogous to the old-school "clotting time" parameter used in the laboratories of yesteryear. The main influence on CT
Causes of prolonged CT and R-value
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).
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 also 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
Causes of Shortened CFT
The reaction to a prolonged CFT might sensibly consist of platelet transfusion, or cryoprecipitate.
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. It is therefore probably a nonspecific variable. However, the manufacturer of the device insists that fibrinogen activity plays the greatest role in determining the α-angle.
Causes of a decreased α-angle
The reaction to a decreased α-angle might sensibly consist of cryoprecipitate transfusion, or of fibrinogen concentrate (where available).
Both the TEG and ROTEM terms refer to the point at which the clot is at its thickest, causing the greatest amount of impediment to the cup-pin movement. This variable is primarily a measure of platelet count, platelet function and fibrinogen concentration. The MA on the TEG has to be performed on a clean native sample with no activator, or from the combined Tissue Factor/kaolin activated TEG. There is a strong linear correlation between the log platelet count and MA.
The reaction to a decreased MCF is usually to either give platelets or DDAVP. However, clot instability may be also be the consequence of excessive fibrinolysis, which would manifest in the A60 or the LI30 indices.
Both the TEG and ROTEM terms refer to the time it takes to reach MCF or MA. Again, a complex system is involved, and a breakdown at any stage will prolong the time to maximum clot strength. At its crudest, this measurement should give you some idea as to how long you will need to keep pressure on the groin wound after you remove the IABP.
These markers can be arbitrarily placed anywhere. Conceivably, one might have an A3.15, or A240. The Haemoview literature as well as Question 26 from the second paper of 2014 both use A10. This is another marker of clot stability, and can be used instead of MCF in situations where the measurementof 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
This variable is infrequently reported, and there is little literature out there to explain exactly what this is. The maximum clot elasticity (MCE) is calculated from the MCF:
MCE = E=100 × MCF/(100-A)
Instead of waiting for an inordinately long time for your result, 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.
Ideally, this would be "time to complete lysis", or 98% lysis, but we don't have all day, and so some surrogate measure must exist. The TEG defines the term CLT as 2mm from MA, i.e. the time it takes for the clot to soften enough for the amplitude to decrease by 2mm from its maximum. The ROTEM term LOT (Lysis Onset Time) refers to the time it takes for the amplitude to drop by a 15% difference from the MCF, which is a slightly different parameter. Other machines have slightly different nomenclature again. In essence, 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.
Practical haemostasis - page on TEG and ROTEM
Sankarankutty, Ajith, et al. "TEG® and ROTEM® in trauma: similar test but different results." World J Emerg Surg 7.Suppl 1 (2012): S3.
Coakley, Margaret, et al. "Transfusion triggers in orthotopic liver transplantation: a comparison of the thromboelastometry analyzer, the thromboelastogram, and conventional coagulation tests." Journal of cardiothoracic and vascular anesthesia 20.4 (2006): 548-553.
Venema, Lieneke F., et al. "An assessment of clinical interchangeability of TEG® and ROTEM® thromboelastographic variables in cardiac surgical patients." Anesthesia & Analgesia 111.2 (2010): 339-344.
Nielsen, Vance G. "A comparison of the Thrombelastograph and the ROTEM." Blood Coagulation & Fibrinolysis 18.3 (2007): 247-252.
Wikkelsoe, A. J., et al. "Monitoring patients at risk of massive transfusion with Thrombelastography or Thromboelastometry: a systematic review." Acta Anaesthesiologica Scandinavica 55.10 (2011): 1174-1189.
Hunt, Harriet, et al. "Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) for trauma‑induced coagulopathy in adult trauma patients with bleeding." Cochrane Database of Systematic Reviews 2 (2015).
Nielsen, Jorn Dalsgaard, and Galloway Gregg. "Monitoring novel anticoagulants dabigatran, rivaroxaban and apixaban by thrombelastography. Proof of concept." (2013): 4813-4813.
Wikkelsø, A., et al. "Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) to monitor haemostatic treatment in bleeding patients: a systematic review with meta‐analysis and trial sequential analysis." Anaesthesia 72.4 (2017): 519-531.
Gonzalez, Eduardo, et al. "Goal-directed hemostatic resuscitation of trauma-induced coagulopathy: a pragmatic randomized clinical trial comparing a viscoelastic assay to conventional coagulation assays." Annals of surgery 263.6 (2016): 1051.
Da Luz, Luis Teodoro, et al. "Effect of thromboelastography (TEG®) and rotational thromboelastometry (ROTEM®) on diagnosis of coagulopathy, transfusion guidance and mortality in trauma: descriptive systematic review." Critical Care 18.5 (2014): 518.