Comparison of Thromboelastography and Conventional Coagulation Tests in Patients With Severe Liver Disease

Abstract

Objective: Thromboelastography (TEG) may provide rapid and clinically important coagulation information in acutely ill patients with chronic liver disease (CLD). Our objective was to describe the relationship between TEG and conventional coagulation tests (CCTs), which has not been previously explored in this population. Methods: In acutely ill patients with severe CLD (Child-Pugh score > 9, category C), we conducted a prospective observational study investigating coagulation assessment as measured by both CCTs and TEG. We used quantile regression to explore 30 associations between TEG parameters and corresponding CCTs. We compared TEG and CCT measures of coagulation initiation, clot formation, clot strength, and fibrinolysis. Results: We studied 34 patients on a total of 109 occasions. We observed inconsistent associations between TEG and CCT measures of coagulation initiation: TEG (citrated kaolin [CK] assay) standard reaction time and international normalized ratio: R 2 = 0.117 ( P = .044). Conversely, there were strong and consistent associations between tests of clot formation: TEG (CK) kinetics time and fibrinogen: R 2 = 0.202 ( P < .0001) and TEG (CK) α angle and fibrinogen 0.263 ( P < .0001). We also observed strong associations between tests of clot strength, specifically TEG MA and conventional fibrinogen levels, across all TEG assays: MA (CK) and fibrinogen: R 2 = 0.485 ( P < .0001). There were no associations between TEG and D-dimer levels. Conclusions: In acutely ill patients with CLD, there are strong and consistent associations between TEG measures of clot formation and clot strength and conventional fibrinogen levels. There are weak and/or inconsistent associations between TEG and all other conventional measures of coagulation.

Viscoelastometric versus standard coagulation tests to guide periprocedural transfusion in adults with cirrhosis: A meta‐analysis of randomized controlled trials

“…This advantage of VET on patient blood management in this setting is consistent with the benefits in other groups of patients [9]. Due to the rebalanced haemostasis [4,5], there is no significant correlation between INR and TEG r time or EXTEM CT [24,25]. Moreover, FFP transfusion can normalize INR in only 15% of cirrhotic patients with INR ≥1.5, but 34% of those develop impaired thrombin generation, probably due to increasing protein C levels [26].…”

“…Moreover, FFP transfusion can normalize INR in only 15% of cirrhotic patients with INR ≥1.5, but 34% of those develop impaired thrombin generation, probably due to increasing protein C levels [26]. On contrary, platelet counts and fibrinogen levels show correlations with TEG MA or EXTEM MCF, and TEG alpha angle or EXTEM/FIBTEM MCF, respectively [24, 25, 27]. The speed of fibrin polymerization represented by TEG alpha angle is related to fibrinogen concentration, whereas the clot strength measured by TEG MA or ROTEM MCF are co‐influenced by platelets and fibrinogen [28], and can be maintained by fibrinogen replacement during severe thrombocytopenia (≤30 × 10 9 /L) [29].…”

Clinical Application of Thromboelastography in Acute Ischemic Stroke

“…Meanwhile, TEG has been wildly used in bleeding events in coronary surgeries, postpartum hemorrhage, and intracerebral hemorrhage. 4 , 6 – 45 However, only a few studies investigated the role of TEG in bleeding events in AIS patients. Compared to CCTs, the parameter R is supposed to be superior to indicating the symptomatic intracranial hemorrhage after endovascular therapy.…”

“…29,30 Although the correlation between TEG and most of CCTs is inconsistent, clot strength (MA) and clot formation (K time and α angle) have been proven to correlate with fibrinogen levels. [29][30][31] However, TEG can not detect the conditions affecting platelets adhesion to the vascular wall. Given that TEG analysis is performed at 37°C in vitro, the effect of temperature alterations on the hemostasis in vivo should not be ignored when interpreting the TEG results.…”

Use of FFP to correct INR: time to drop this from the decompensated cirrhosis care bundle?

“…It is now accepted that INR is not an accurate marker of clotting function in cirrhosis; patients with raised INR can generate normal levels of thrombin4 5 and may even be prothrombotic due to reduced synthesis of anticoagulant factors (eg, protein C, S and antithrombin). Instead, functional testing with thromboelastography or thromboelastometry is more appropriate for assessing coagulopathy and guiding correction 6 7…”