Transfusion
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Variables of hemostasis before surgery might indicate an elevated risk of bleeding. We determined hemostasis tests and standardized bleeding history and their association with bleeding and transfusion requirements in cardiopulmonary bypass (CPB) surgery. ⋯ A standardized bleeding history may help to identify patients undergoing CPB surgery whose risk of bleeding is elevated. ADP-induced MEA appears to predict postoperative bleeding and PC transfusion requirements, while AA-induced MEA and preoperative Hb indicate the need for RBCs. The time of aspirin withdrawal before surgery influences perioperative blood loss and PC transfusion.
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Multicenter Study Clinical Trial
Thrombocytopenia and platelet transfusion in UK critical care: a multicenter observational study.
Platelet (PLT) transfusions are widely used, but few studies have described patterns of use in critical care. ⋯ Thrombocytopenia is common in critical care, but there is wide variation in PLT transfusion use. Patients commonly received PLT transfusions on days without clinically significant hemorrhage. The high prevalence of thrombocytopenia in the critically ill population and inconsistent patterns of PLT transfusions indicate the importance of improving the evidence base for PLT use.
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Multicenter Study Clinical Trial
Prevalence, management, and outcomes of patients with coagulopathy after acute nonvariceal upper gastrointestinal bleeding in the United Kingdom.
Coagulopathy after major hemorrhage has been found to be an independent risk factor for mortality after traumatic bleeding. It is unclear whether similar associations are present in other causes of major hemorrhage. We describe the prevalence, use of plasma, and outcomes of patients with coagulopathy after acute nonvariceal upper gastrointestinal bleeding (NVUGIB). ⋯ Coagulopathy was prevalent in 16% of patients after NVUGIB and independently associated with more than a fivefold increase in the odds of in-hospital mortality. Wide variation in plasma use exists indicates clinical uncertainty regarding optimal practice.
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Factor XIII (FXIII) is activated by thrombin to form a transglutaminase (FXIIIa) that stabilizes clot formation by the cross-linking of fibrin monomers and antifibrinolytic proteins. Although rare, FXIII deficiency is characterized by variable bleeding manifestations depending on the magnitude of the deficiency. A congenital FXIII deficiency with levels less than 1% can be detected in children who present with prolonged bleeding from the umbilical stump as well as protracted bleeding after trauma. ⋯ Genetic studies have identified a wide range of mutations that affect the activity of the FXIII protein but in lieu of molecular genetic analyses, FXIII deficiency can be identified by specific diagnostic assays that measure either the transglutaminase activity of the protein or the levels of the protein and its individual subunits. Replacement therapy has also been shown to increase FXIII levels and reduce bleeding symptoms in patients with congenital FXIII deficiency. This review presents recent findings on the biology of FXIII and the clinical manifestations observed among patients with congenital and acquired FXIII deficiencies.