Potential applications of thromboelastography in patients with acute and chronic liver disease

Abstract

Patients with acute and chronic liver disease have long been assumed to have a bleeding tendency on the basis of abnormal results for standard tests of hemostasis. However, recent studies have suggested that hemostasis in patients with liver disease exists in a state of rebalance, in which defects in prohemostatic drivers are compensated for by commensurate changes in antihemostatic drivers. Standard assays of hemostasis cannot evaluate this potential state of rebalance because they only assess components of clot formation and, therefore, may provide misleading information regarding the risk of bleeding, possibly leading clinicians to administer unneeded or even harmful prohemostatic factors. Thromboelastography (TEG) is a commercially available, rapid, point-of-care assay that assesses clot formation in whole blood, including plasmatic and cellular components. Studies using TEG in patients with cirrhosis and acute liver failure have suggested that rebalanced hemostasis exists in many patients, even in the presence of thrombocytopenia and an elevated prothrombin time/international normalized ratio. TEG has also been used to study mechanisms of rebalanced hemostasis and the pathogenesis of specific complications of liver disease, such as variceal rebleeding and infection. Finally, TEG has become widely used to guide factor repletion and fibrinolytic therapy during liver transplantation. The present clinical review will summarize these potential applications of TEG in patients with liver disease.

Keywords: Thromboelastography; cirrhosis; coagulopathy; hemostasis; liver failure.

Figures

Figure 1

A normal thromboelastogram displaying individual parameters. See the text for details of measurement intervals. k=kinetic time; Ly-30=clot lysis in 30 minutes; r=reaction time.

Figure 2

Representative thromboelastograms (TEGs) from patients with cirrhosis, with associated standard hemostatic laboratory values measured at the same time point. Panel A shows a normal TEG from a patient with well-compensated (Child-Pugh class A) alcoholic cirrhosis. Panel B shows an abnormal TEG with low maximum amplitude due to thrombocytopenia in a patient with stable but mildly decompensated (Child-Pugh class B) cirrhosis due to hepatitis C virus infection. Panel C shows an abnormal TEG with a high kinetic time, a low α-angle, and low maximum amplitude due to thrombocytopenia and hypofibrinogenemia in a patient with severely decompensated (Child-Pugh class C) alcoholic cirrhosis. Panel D shows an abnormal TEG with unmeasurably high (NA) kinetic time, a very low α-angle, and very low maximum amplitude due to sepsis; this TEG is from the same patient shown in panel B but was taken 3 weeks later, during presentation for a fatal acute infection. Normal ranges for TEG parameters and standard laboratory tests are noted in Table 3 (RT Stravitz, unpublished observations). INR=international normalized ratio; Ly-30=clot lysis in 30 minutes; NA=not available.