Chest 2009, 136:1654–1667.PubMedCrossRef 18. Frith D, Davenport R, Brohi K: Acute traumatic Selleckchem Vactosertib coagulopathy. Curr Opin Anaesthesiol 2012, 25:229–234.PubMedCrossRef 19. Brohi K, Cohen MJ, Davenport RA: Acute coagulopathy of trauma: mechanism, identification and effect. Curr Opin Crit Care 2007, 13:680–685.PubMedCrossRef Competing interests

The authors declare that they have no competing interests. Authors’ contributions JY and ZZ initiated the idea, carried out the study, and drafted the manuscript. JW, DY, and SZ helped collect and analyze data. YL and WY participated in the design of the study. NL and JL participated in the coordination of the study and helped to draft the manuscript. All authors read and approved the final manuscript.”
“Introduction Bleeding complications continue to be an important risk of warfarin anticoagulation. Figure 1 Subject selection. PCC3, 3 factor prothrombin complex concentrate; LDrFVIIa, low dose recombinant factor VII activated. Despite this risk, warfarin continues to be a widely used anticoagulant for outpatient management of patients who have selleck screening library suffered a deep vein thrombosis with or without pulmonary embolism, or who require prophylaxis against a thromboembolic event associated with atrial fibrillation or prosthetic valves. Furthermore, RAD001 chemical structure as

the population continues to age, the number of patients receiving warfarin is increasing and this correlates with Histidine ammonia-lyase a rise in the incidence of complications associated with warfarin anticoagulation. This ultimately results in an increase in risk for bleeding and associated morbidity and mortality for patients. In a

pooled analysis of 3665 patients receiving warfarin anticoagulation (goal international normalized ratio [INR] 2.0- 3.0) for nonvalvular atrial fibrillation in the SPORTIF III and V trials, the annual incidence of major bleeding and associated mortality was 2.68% and 8.09%, and the incidence of intracerebral bleeding and associated mortality was 0.19% and 45.4% [1]. Patients who suffer severe or life-threatening bleeding complications during warfarin anticoagulation require rapid normalization of their coagulation status in an attempt to minimize bleeding and the associated morbidity. Traditionally, this is achieved by transfusion of fresh frozen plasma (FFP) to provide functional coagulation factors and administering vitamin K. Disadvantages of FFP includes the large volume of fluid required, the time required to thaw, the time need for blood group matching, and the risk for transfusion reactions, transmission of infections and transfusion related lung injury. For intravenous vitamin K there is a small risk of anaphylaxis (3 per 10,000 patients) [2]. Finally, both strategies require significant time to normalize the patient’s INR (median time > 8–32 hours for FFP and > 24 hours for vitamin K) [3–9].