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Hyperfibrinolysis in Liver Transplantation
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Since the first transplantations, performed in the 1960s, it became evident that disorders of the hemostatic system may play a role in the origin of bleeding during liver transplantation. In the early years, several attempts to transplant a liver graft failed due to massive intraoperative bleeding and subsequent death.17 Because blood loss could not always be explained by surgical problems, studies were started to evaluate the role of the hemostatic system. Many of the early reports were from experimental animal studies, but gradually more data on human liver transplantation became available too.17 It has been demonstrated that besides disorders of the coagulation system and platelet function, increased fibrinolytic activity may be present during liver transplantation. A discussion of coagulation and platelet disorders would be outside the scope of this chapter and for a review the reader is referred to References 7 and 12. Until 1989, all studies on fibrinolysis were based on tests measuring the overall fibrinolytic activity, as the whole blood clot lysis time (WBCLT) and the euglobulin clot lysis time (ECLT). It was demonstrated that fibrinolytic activity, as measured by the WBCLT or ECLT, increases during the anhepatic stage (stage II) and reaches a peak shortly after reperfusion of the donor liver.17,18 Fibrinolytic activity after graft reperfusion appeared to be related to the severity of the graft preservation damage. When a well-preserved liver is transplanted fibrinolytic activity is restored to normal within an hour after reperfusion.
Acquired Bleeding Disorders Associated with Disease and Medications
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
William A. Rock, Sue D. Walker
Routine testing for liver disease has customarily consisted of a CBC (to determine an elevated white blood cell count, thrombocytopenia, and red cell fragmentation), prothrombin time, partial thromboplastin time, and a quantitative fibrinogen (Table 3). The addition of four factor assays (see Table 4) can provide considerable supplementary insight into the differentiation of a vitamin K deficiency, disseminated intravascular coagulation, and hepatocyte dysfunction as they are related to the cause for bleeding. These are assays for factors V, VII, VIII, and IX. Assays for plasminogen, antithrombin-III, and euglobulin clot lysis time can be added to define the severity of concurrent fibrinolysis and or thrombosis (see Table 4).
Computer Applications in Clinical Pharmacokinetics and Pharmacodynamics
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Dennis Mungall, Joe Heissler, Mattieu Kaltenbach
Recently Mungall et al.98 have reported on a fresh whole blood clot lysis test that takes less than 10 min to perform at bedside. Strong correlations were found between TPA concentration and whole blood clot lysis time in normal volunteers and patients with myocardial infarction. Patients with clinical reperfusion had lower clot lysis times than those with no reperfusion (466 vs. 893 s). A new model describing the relationship between clot lysis time was presented and a program was developed to predict dynamic clot lysis response. This work suggests that response to TPA could be predicted and modified early in treatment.
Investigating the ultrastructural and viscoelastic characteristics of whole blood after exposure to the heavy metals cadmium, lead and chromium, alone and in combination
Published in Ultrastructural Pathology, 2022
L Pretorius, H Taute, M Van Rooy, HM Oberholzer
An increase in potential clot formation was observed in the current study. The presence of sticky thick fibers (green arrows) that are haphazardly organized may be an indication of inadequate clot retraction. This can potentially influence the clot lysis time and increase the risk of thrombosis. The group with the least toxic effect appeared to be the Cd group, while the Cd + Cr combination appeared to be the most toxic group with the fibers being bent and less taut (pink arrows) and forming sticky masses (blue arrows) at the lowest concentration. At the higher concentrations, fibrin fibers fused together (yellow arrows) and formed net-like coverings (red arrows) that can have detrimental effects on coagulation. At higher concentrations, the fibrin network became less organized and appeared mesh-like. This caused the erythrocytes to become trapped in the fibrin network and contributed to their altered erythrocyte morphology. The results are similar to what was observed by Venter et al.24 in an ex vivo study after Cd and Cr exposure in whole blood. Based on Yaprak and Yolcubal10 Cr (224 µg/L) accumulates at a much higher concentration in PRF than the other two metals (Cd: 0.21 µg/L and Pb: 4.4 µg/L) and might explain the general tendency for Cr to have a much larger effect.
Improving fibrinolysis in venous thromboembolism: impact of fibrin structure
Published in Expert Review of Hematology, 2019
Among acquired thrombophilias such as heparin-induced thrombocytopenia or paroxysmal nocturnal hemoglobinuria, the most common disorder (5% of VTE patients) is antiphospholipid syndrome (APS) that characterizes by the presence of IgG and/or IgM antiphospholipid antibodies with the most prothrombotic lupus anticoagulant. The recurrent VTE is observed in 60% of APS patients with triple antibody positivity, and up to 20% of APS patients suffered also from ischemic cerebrovascular event [62]. In 2014 we demonstrated reduced plasma clot permeability and lysability with dense fiber network formation, the so-called prothrombotic clot phenotype assessed in vivo, in patients with APS [63]. Vikerfors et al. [64] also reported formation of more compact fibrin clots in APS patients compared to healthy individuals and patients after VTE without APS, however lysability was not assessed. Of note, during a median follow-up of 62 months, clot lysis time, in contrast to Ks, failed to predict recurrent venous or arterial thromboembolism in patients with APS [65]. We found that at baseline CLT was similar in APS patients with recurrent events and those free of such events.
Fibrinolysis in trauma patients: wide variability demonstrated by the Lysis Timer
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Stéphanie Roullet, Laurent Weinmann, Sylvie Labrouche, Chloé Gisbert-Mora, Matthieu Biais, Philippe Revel, Geneviève Freyburger
Hyperfibrinolysis contributes to the pathophysiology of life-threatening trauma-induced coagulopathy (TIC) [1]. Fibrinolysis study is one of the blind spots of the core laboratory. Laboratory tests such as the euglobulin clot lysis time (ECLT), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) do not provide results sufficiently quickly for clinical practice in emergency cases, such as trauma patient care. Since the publication of the CRASH-2 study [2,3], tranexamic acid (TXA) has been recommended in the early phase of trauma management in patients with, or at high risk of, bleeding [4]. In the CRASH-2 study, as well as the WOMAN study, administration of TXA was not associated with increased rates of thromboembolic events [2,5]. Nevertheless, recent studies have questioned the systematic recommendation of TXA administration in trauma. Most trauma patients are not hyperfibrinolytic according to the results of viscoelastic tests [6–8], hypofibrinolytic profiles can also be associated with coagulopathy and death [6,9,10] and the systematic administration of TXA has been shown to not only be of no benefit, but to be potentially harmful, causing a significant increase in rate of thromboembolic events [11].