In part 1 of this series we talked about the basic theory of viscoelastic assays (VEAs) and rotational thromboelastography (ROTEM). If you haven’t read that and/or need a refresher on what ROTEM is, when it’s useful, and what its limitations are, STOP now and go back.
This piece will expound upon the logistics of actually analyzing the graphs and parameters and developing a strategy for using ROTEM at the bedside.
ROTEM: The Basic 5 Assays
The ROTEM assay measures the strength of an induced clot (measured in amplitude) as time passes on the x-axis (figure 1). The shape of the curve at various standardized endpoints helps delineate parameters of a given curve that we will talk about later on.
ROTEM has 5 different component assays: EXTEM, INTEM, FIBTEM, APTEM,and HEPTEM. A provider needs to specify which assays to run, mostly because not all assays are applicable to each patient situation. Here is the breakdown of each assay:
- EXTEM: Analogous to a protime. This tests the extrinsic pathway.
- INTEM: Analogous to the APTT. Phospholipid and ellagic acid are added to the initial blood sample, testing the intrinsic pathway.
- FIBTEM: Platelet inhibitor (cytochalasin D) eliminates platelets’ contribution to clot strength and formation. This test primarily evaluates fibrinogen’s contribution to clot strength.
- APTEM: The same test and activators as EXTEM with the addition of aprotinin to inhibit fibrinolysis. Stronger clots with higher amplitude, when compared to EXTEM, suggest hyperfibrinolysis in the patient.
- HEPTEM: The same test and activators as INTEM with the addition of heparinase. The point is to diagnose underlying coagulopathy that is NOT due to heparin. Order this test if your patient is heparinized (eg. ECLS). In the absence of a heparin infusion, HEPTEM and INTEM will look identical.
Given the assays’ nature, the 2 most useful assays in the ICU or in the resuscitation bay tend to be the EXTEM and the FIBTEM. It is also possible to order ECATEM, which is mainly used in the presence of direct thrombin inhibitors. Given the supplemental nature of HEPTEM and ECATEM and the special circumstances they need to be relevant, we won’t talk about them too much.
A standard ROTEM output for a patient not on heparin would classically produce 4 graphs (EXTEM, INTEM, FIBTEM, and APTEM) and relevant parameters for each curve. While the next section deals with those parameters, figure 2 is what those graphs look like.
ROTEM: Basic parameters
The more a person utilizes ROTEM, the sooner they develop an eye for what pathologies “look like” in the data’s graphic representation (similar to reading EKGs). However, it’s important to recognize that ROTEM curves will come with parameters that also help inform decision-making. The basic parameters derive from values on the graphical outputs (see Fig 1), but their actual definitions are as follows:
- Clot Time (CT): The amount of time it takes for any clot to form. As the clot builds, it will exert a resistive force on the pin spinning in the sample of blood. This often will be quite prolonged in heparin, warfarin, or in patients not able to make factors II, VII, IX, and X.
- Clot Formation Time (CFT): The amount of time it takes for the amplitude to reach 20 mm. A prolonged CFT suggests impaired or slow clot propagation, often a PLT issue or low fibrinogen.
- ɑ-angle (ɑ): The angle tangent to the clotting curve at the 2 mm amplitude point. Larger angles indicate more rapid clotting.
- Amplitude at 10 minutes (A10): The amplitude/ strength of the curve at 10 minutes + CT
- Maximum Clot Formation (MFT): The maximum strength the clot can produce.
- Lysis Index (LY30): The amount of clot lysis that has occurred at 30 minutes. Usually this is expressed as a percentage relative to MCF (i.e. LY30 = MCF-A30 min/ MCF).
- Maximum Lysis: The amount of clot lysis that occurs for the entire curve (sometimes out to 60 minutes). This is expressed as a percent relative to MCF.
Developing a ROTEM Strategy
ROTEM will only guide management if a resuscitation leader can implement the assay’s data into an actionable strategy in a systematic or strategic way. There are multiple strategies articulated in the available literature cited here and in the Further Reading section.To date, there is no “one” strategy that has been proven most efficacious. Figure 2 and table 2 may help outline ways to both recognize and transfuse based on ROTEM outputs. We have also included some de-identified (but real) patient cases to cement a patient-centered approach to ROTEM.
A 60-year-old male presented with severe COVID-19 ARDS and was placed on VV-ECMO support. Several days into his course, a dialysis catheter was placed in the left femoral vein to help with volume overload. However, the site began to bleed profusely despite multiple pressure dressings and topical treatment of thrombin. A heparin assay was 0.4 IU/mL. Platelets, Hgb, Fibrinogen, and INR, were normal, though a PTT was elevated to 70.
The figure classically reflects the effects of heparin but no other underlying coagulopathies. The A10FIBTEM is >10, suggesting no need for Cryo, and the A10EXTEM is >40, arguing against PLT dysfunction. CTEXTEM is only mildly elevated over the quoted standard, but the CTINTEM is massively elevated at 305. This could indicate a need for aPCC or FFP; however, it could also mean the heparin effect. Luckily, the team sent a HEPTEM, a CT of 206 (normal HEPTEM CT is 100-240). This is a classic ROTEM for a person doing well on ECMO but whose bleeding is primarily due to heparinization.
Case Resolution: Given the patient was on a heparin bonded circuit, heparin infusion was held. The bandage was taken down, and a purse-string suture was placed along with topical TXA and lidocaine with epinephrine subcutaneously. The heparin infusion resumed 16 hours later with no further bleeding episodes.
A 65-year-old patient suffering from septic shock in the setting of Acute on Chronic Liver Failure is on vasopressor support as well as invasive mechanical ventilation and CVVHD. Overnight the nurses report that he began bleeding from multiple IV sites and had coffee ground material sucked up from his OGT. His PLTs are at 31,000 (stable for the last week), his Hgb is 8.0, his INR is 3.2, his fibrinogen is 41 mg/dL, and his D-dimer is 10,270.
Here we only have 3 of the five possible assays, which is fine since it’s unlikely HEPTEM or APTEM will be of much use here. The A10FIBTEM is <10, which indicates depleted fibrinogen reserves. The A10EXTEM is <40, suggesting either platelet dysfunction or very low platelet levels responsible for weak clots. CTEXTEM is significantly prolonged, but not CTINTEM, meaning that this may be due in part to low levels of clotting factors rather than this being a heparin effect. The MCF is extremely low, suggesting poor clot stability. In both the EXTEM and INTEM, no narrowing of the curve after MCF is seen, arguing against hyperfibrinolysis.
Case Resolution: The patient underwent multiple units of cryoprecipitate transfusion, but because of his advanced portal hypertension, FFP was held in reserve but not given. After fibrinogen was related, all bleeding episodes stopped. The team felt reassured that DIC was unlikely.
- ROTEM is a viscoelastic assay that may be a helpful adjunct to caring for patients in specific circumstances during their resuscitation or ICU course.
- Consider using ROTEM in the following scenarios:
- Large scale blood resuscitation (MTP activation)
- Unexplained bleeding episodes
- Pre, peri, and post-operative and courses for liver and cardiothoracic surgery cases
- It is essentially the only lab test that objectively demonstrates fibrinolysis. In cases of suspected DIC or fibrinolytic crisis, it may help clinch the diagnosis.
- Develop a familiarity with waveform shapes and parameter metrics and a systematic approach to how you may want to transfuse (and your transfusion targets).
Further Online Resources:
- Whiting D, DiNardo JA. TEG and ROTEM: technology and clinical applications. Am J Hematol. 2014 Feb;89(2):228-32. doi: 10.1002/ajh.23599. PMID: 24123050.
- Davenport R, Manson J, De’Ath H, et al. Functional definition and characterization of acute traumatic coagulopathy. Crit Care Med 2011;39:2652–2658.
- Bolliger D, Tanaka KA. Point-of-Care Coagulation Testing in Cardiac Surgery. Semin Thromb Hemost. 2017 Jun;43(4):386-396. doi: 10.1055/s-0037-1599153. Epub 2017 Mar 30. PMID: 28359133.
- Baksaas-Aasen K, Gall LS, Stensballe J, Juffermans NP, Curry N, Maegele M, Brooks A, Rourke C, Gillespie S, Murphy J, Maroni R, Vulliamy P, Henriksen HH, Pedersen KH, Kolstadbraaten KM, Wirtz MR, Kleinveld DJB, Schäfer N, Chinna S, Davenport RA, Naess PA, Goslings JC, Eaglestone S, Stanworth S, Johansson PI, Gaarder C, Brohi K. Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomized, controlled trial. Intensive Care Med. 2021 Jan;47(1):49-59. doi: 10.1007/s00134-020-06266-1. Epub 2020 Oct 13. PMID: 33048195; PMCID: PMC7550843.
- Nanchal R, Subramanian R, Karvellas CJ, Hollenberg SM, Peppard WJ, Singbartl K, Truwit J, Al-Khafaji AH, Killian AJ, Alquraini M, Alshammari K, Alshamsi F, Belley-Cote E, Cartin-Ceba R, Dionne JC, Galusca DM, Huang DT, Hyzy RC, Junek M, Kandiah P, Kumar G, Morgan RL, Morris PE, Olson JC, Sieracki R, Steadman R, Taylor B, Alhazzani W. Guidelines for the Management of Adult Acute and Acute-on-Chronic Liver Failure in the ICU: Cardiovascular, Endocrine, Hematologic, Pulmonary and Renal Considerations: Executive Summary. Crit Care Med. 2020 Mar;48(3):415-419. doi: 10.1097/CCM.0000000000004193. PMID: 32058375.
- Tripodi A, Mannucci PM. The coagulopathy of chronic liver disease. N Engl J Med. 2011 Jul 14;365(2):147-56. doi: 10.1056/NEJMra1011170. PMID: 21751907.
- Stravitz RT, Ellerbe C, Durkalski V, Schilsky M, Fontana RJ, Peterseim C, Lee WM; Acute Liver Failure Study Group. Bleeding complications in acute liver failure. Hepatology. 2018 May;67(5):1931-1942. doi: 10.1002/hep.29694. Epub 2018 Mar 26. PMID: 29194678; PMCID: PMC5906191.
- Akay OM. The Double Hazard of Bleeding and Thrombosis in Hemostasis From a Clinical Point of View: A Global Assessment by Rotational Thromboelastometry (ROTEM). Clin Appl Thromb Hemost. 2018 Sep;24(6):850-858. doi: 10.1177/1076029618772336. Epub 2018 May 14. PMID: 29758989; PMCID: PMC6714726.
- Nilsson CU, Strandberg K, Reinstrup P. Warfarin monitoring with viscoelastic haemostatic assays, thrombin generation, coagulation factors and correlations to Owren and Quick prothrombin time. Scand J Clin Lab Invest. 2018 Sep;78(5):358-364. doi: 10.1080/00365513.2018.1474492. Epub 2018 May 23. PMID: 29792060.
- Karkouti et al. Anesth Analg 2013, 117:14-22 (using A10 fibtem for fibrinogen)