Tranexamic acid prophylaxis during liver transplantation: A randomized controlled trial

Klinck, John R.

doi:10.1016/0270-9139(93)90395-4

Cited by 3 publications

(1 citation statement)

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“…14 Tranexamic acid also appears to be effective; a significant reduction in blood loss was reported in a prospective, randomized clinical trial. 15 Aprotinin, a nonspecific inhibitor of serine protease, inhibits coagulation, fibrinolysis, kallikrein, and complement cascade and is reported to decrease blood loss during liver transplantation. However, its dosage is not well defined, inhibition of coagulation is ignored, and some studies fail to show similar results.…”

Section: Pharmacological Therapymentioning

confidence: 99%

Coagulation and liver transplantation: Current concepts

Kang

1997

Liver Transpl

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C omplications associated with bleeding and coagulopathy during liver transplantation have become manageable in recent years. Neuhaus pointed out that a new understanding of coagulation disorders has allowed more specific therapy instead of blind substitution and replacement policy. 1 He emphasized the important role of pharmacological therapy against fibrinolysis and the contribution of the prevention of coagulopathy to other postoperative complications. However, refined surgical technique might have played a more significant role in reducing blood loss, and understanding of pathophysiology, monitoring, and management of coagulation is far from its desirable level. Coagulation in Cirrhosis and During Liver TransplantationCirrhosis-induced coagulopathy has been described for the past several decades. Briefly, the vascular phase is impaired as cirrhosis is complicated by peripheral vasodilation, reduced elasticity of vessels, and decreased interaction between the vessel walls and platelets. The platelet phase is severely affected by thrombocytopenia and platelet dysfunction. The coagulation cascade is affected by low levels of procoagulants and inhibitors produced by the liver, including coagulation factors (I, II, V, VII, VIII, IX, X, XI, XII, XIII, Fletcher, Fitzgerald, prekallikrein, plasminogen, and highmolecular-weight kininogen), inhibitors (AT-III and ␣ 1 -antitrypsin), and regulatory proteins (C1 inhibitor and ␣ 2 -macroglobulin). An excessive sialic acid content of fibrinogen results in dysfibrinogenemia, and the level of factor VIII is increased because of increased levels of von Willebrand' s factor (vWF) antigen and its activity. Fibrin polymerization is impaired by the low level of factor XIII and dysfibrinogenemia. 2 As a result, a hypocoagulable state is the common denominator, although the imbalance between coagulation and its inhibition and fibrinolysis and its inhibition result in all forms of coagulopathy.Intraoperative changes in coagulation were studied extensively during early clinical experience, and only limited information has been added in the past two decades. 3 During the preanhepatic and anhepatic stages, the levels of all coagulation factors and platelet count decrease as preexisting coagulopathy is compounded by surgical bleeding. Furthermore, fibrinolysis in patients with severe hepatocellular disease or in those requiring massive transfusion and activation of coagulation reduces procoagulant level even with an infusion of blood products rich in coagulation factors. Hypothermia and ionized hypocalcemia also impair coagulation.A severe coagulopathy, a component of the postreperfusion syndrome, occurs on reperfusion of the grafted liver; more specifically, a decrease in coagulation factor levels, a sudden increase in tPA, thrombocytopenia, fibrinolysis, and a moderate increase in FDP and TAT levels are seen. 4 The cause of the postreperfusion coagulopathy is multifactorial. The release of endogenous heparin from the donor liver results in moderate to severe heparin effect in approxima...

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Section: Pharmacological Therapymentioning

confidence: 99%