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Chapter 57: Thromboelastometry-guided Bleeding Management in Liver Transplantation

Klaus Görlinger; Preet Mohinder Singh; Adrian Alvarez

IMPACT ON TRANSFUSION REQUIREMENTS, PATIENT OUTCOMES, AND HEALTH CARE COSTS

  • Hemostasis in cirrhosis is rebalanced on a lower level that can rapidly devolve to bleeding and thrombosis (Fig. 57-1).1–4

  • The hemostatic changes are better reflected by viscoelastic testing rather than standard coagulation laboratory tests (SCLTs) such as PT/INR (international normalized ratio), aPTT, and platelet count.5–9

  • Clear evidence for the clinical utility of TEG/ROTEM protocols exist, as they prevent both over-transfusion and undertransfusion.10–20

  • The traditional TEG works with a free-pending pin in a rotating cuvette. The clotting process is detected via a torsion wire. Due to the free suspension of the pin, the TEG is extremely sensitive to vibrations and mechanical shocks. This flaw is overcome in the ROTEM system by using a rotating pin fixed on a steel axis, which is stabilized by a unique ball bearing and a precise optical detection method. Clinically relevant parameters of ROTEM and TEG are shown in Fig. 57-2. Characteristic ROTEM traces in various coagulation conditions are shown in Fig. 57-3. Various activators used in different ROTEM assays and their implications are shown in Table 57-1.

FIGURE 57-1

Hemostasis rebalance in cirrhosis. α2-AP, α2-Antiplasmin; AT, antithrombin; LPS, lipopolysaccharides; PAI-1, plasminogen activator inhibitor-1; RES, reticuloendothelial system; tPA, tissue plasminogen activator; vWF, von Willebrand factor. <FGSO>. (Reproduced with permission from of Klaus Görlinger, Essen, Germany.)

A figure illustrates that if the hemostasis in cirrhosis is rebalanced on a lower level, it increases the risk of bleeding and thrombosis. The figure illustrates that if the hemostasis in cirrhosis is rebalanced on a lower level, it increases the risk of bleeding and thrombosis. In the presence of Dysfibrinogen, Platelet dysfunction, reticuloendothelial system dysfunction, the hemostasis can lose balance. Platelets, Vitamin K-dependent factors (II, VII, IX and X), V, Proteins C and S, antithrombin, plasminogen, α2-antiplasmin,and ADAMTS13 decrease to about 25-70%. Lipopolysaccharide, TF, von Willebrand factor, FVIII, tissue plasminogen activator, and plasminogen activator inhibitor-1 increase up to 200%.
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FIGURE 57-2

ROTEM (“temogram”) and TEG trace displaying the clinically most important parameters and their informative value. FDPs, fibrin(ogen) split products. (Reproduced with permission from of Klaus Görlinger, Essen, Germany.)

A timeline and a table show the clinically relevant parameters of ROTEM and TEG and their informative value. The figure with ROTEM (“temogram”) and TEG trace timeline at the top and a table below shows the clinically relevant parameters of ROTEM and TEG and their informative value. The parameters shown in both the timeline and the table are clot initiation followed by clot kinetics, then clot strength and finally clot stability (lysis). For Clot initiation, ROTEM considers clotting time in seconds and TEG considers reaction time in minutes. The hemostatic factors involved at this stage are: Enzymatic coagulation factors, anticoagulants, FDPs, and tissue factor expression on monocytes. For clot kinetics, ROTEM considers clot formation time (CFT) in seconds and α angle in degrees while TEG considers kinetic time in minutes and α angle in degrees. The hemostatic factors involved at this stage are: Enzymatic coagulation factor, anticoagulants, fibrinogen, and platelets. ROTEM considers the following measures of clot strength: (A5) A10 (amplitude (5) 10 min after CT) in mm, and MCF (maximum clot firmness) in mm, while TEG considers MA (maximum amplitude) in mm. The hemostatic factors involved at this stage are: Platelets, fibrinogen, FXIII, and colloids. The ROTEM considers the following measures for clot stability (lysis): LI60 (lysis index (residual clot firmness) 60 min after CT) in % of MCF and ML (maximum lysis during run time) in % of MCF while TEG considers LY30 (lysis 30 min after MA) in % of MA. The hemostatic factors involved at this stage are: Fibrinolytic enzymes, fibrinolysis inhibitors, and FXI.
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FIGURE 57-3

A-J. Characteristic thromboelastometry traces. The diagnostic performance is increased by test combinations, e.g., EXTEM and FIBTEM, EXTEM and APTEM, or INTEM and HEPTEM. 4F-PCC, Four factor prothrombin complex concentrate; A5, amplitude of clot firmness 5 min after CT; CFT, clot formation time; CPB, cardiopulmonary bypass, CT, coagulation time; LI60, lysis index 60 min after CT; MCF, maximum clot firmness; ML, maximum lysis during runtime; OLT, orthotopic liver transplantation; TXA, tranexamic acid (or other antifibrinolytic drug). (Reproduced with permission from of Klaus Görlinger, Essen, Germany.)

a figure shows five characteristic thromboelastometry traces, using combination of extem and fibtem, or extem and aptem. the figure shows five characteristic thromboelastometry traces, using combination of extem and fibtem, or extem and aptem. the tracing at the top shows normal clot with both extem and fibtem: ctex 43–82 s, a5ex 33–52 mm, mcfex 52–70 mm, mlex or mlfib < 15%, li60ex or li60fib > 85%, a5fib 5–20 mm and mcffib 7–24 mm. below the normal clot figure is hyperfibrinolysis is shown using both extem and aptem: mlex ≥15% or mlfib ≥ 10% within 60 min (li60 ≤ 85%); aptem confirms txa effect; note: fibtem is most sensitive and specific to hyperfibrinolysis! below the hyperfibrinolysis figure fibrin polymerization disorder (e.g., low fibrinogen or low fxiii or colloid infusion) is shown with both extem and fibtem: a5ex < 35 mm and a5fib < 9 mm. next, thrombocytopenia or severe platelet dysfunction (thrombin pathway or gpiibiiia-r) is shown with both extem and fibtem: a5ex < 35 mm and a5fib ≥ 9 mm. at the bottom, hypercoagulability (high thrombotic risk) ... id=

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