BACKGROUND: Among rotation thromboelastometry (ROTEM®) parameters, the maximum clot firmness (MCF) of EXTEM (MCFEX), INTEM (MCFIN) and FIBTEM (MCFFIB) are influenced by both the platelet count and fibrinogen concentration. We evaluated the relative contribution of laboratory variables to MCF amplitude and determined whether the severity of hypofibrinogenemia could affect the relationship between these variables during liver transplantation (LT). MATERIAL AND METHODS: Retrospective ROTEM® assays with simultaneous laboratory tests in 282 patients receiving LT were analyzed. Relative contribution of platelet and fibrinogen to MCF was assessed and a subgroup analysis based on fibrinogen concentration was performed. RESULTS: Platelet count accounted for 60% of the variability in both MCFEX and MCFIN, whereas fibrinogen concentration explained 12% and 9%, respectively. In subgroup analysis, platelets accounted for 56-57% of MCFEX and MCFIN variability with fibrinogen <100 mg/dL, and 59% of the variability with fibrinogen ≥100 mg/dL. Fibrinogen was the primary determinant of MCFFIB, accounting for 73% of the variability. However, in severe hypofibrinogenemia (fibrinogen<100 mg/dL), fibrinogen explained only 22% of MCFFIB variability. CONCLUSIONS: Regardless of the fibrinogen concentration, the platelet count is a constant primary determinant of the MCFEX and MCFIN during LT. However, MCFFIB may predict the fibrinogen concentration less reliably in cases of severe hypofibrinogenemia.
BACKGROUND: Among rotation thromboelastometry (ROTEM®) parameters, the maximum clot firmness (MCF) of EXTEM (MCFEX), INTEM (MCFIN) and FIBTEM (MCFFIB) are influenced by both the platelet count and fibrinogen concentration. We evaluated the relative contribution of laboratory variables to MCF amplitude and determined whether the severity of hypofibrinogenemia could affect the relationship between these variables during liver transplantation (LT). MATERIAL AND METHODS: Retrospective ROTEM® assays with simultaneous laboratory tests in 282 patients receiving LT were analyzed. Relative contribution of platelet and fibrinogen to MCF was assessed and a subgroup analysis based on fibrinogen concentration was performed. RESULTS: Platelet count accounted for 60% of the variability in both MCFEX and MCFIN, whereas fibrinogen concentration explained 12% and 9%, respectively. In subgroup analysis, platelets accounted for 56-57% of MCFEX and MCFIN variability with fibrinogen <100 mg/dL, and 59% of the variability with fibrinogen ≥100 mg/dL. Fibrinogen was the primary determinant of MCFFIB, accounting for 73% of the variability. However, in severe hypofibrinogenemia (fibrinogen<100 mg/dL), fibrinogen explained only 22% of MCFFIB variability. CONCLUSIONS: Regardless of the fibrinogen concentration, the platelet count is a constant primary determinant of the MCFEX and MCFIN during LT. However, MCFFIB may predict the fibrinogen concentration less reliably in cases of severe hypofibrinogenemia.