Massive transfusion coagulopathy
ABSTRACT Coagulopathy following massive transfusion is a consequence of post-traumatic and surgical hemorrhage. Bleeding following massive transfusion can occur due to hypothermia, dilutional coagulopathy, platelet dysfunction, fibrinolysis, or hypofibrinogenemia. Transfusion of 15 to 20 units of blood products causes dilutional thrombocytopenia, and both antiplatelet agents (eg, clopidogrel [Plavix, Sanofi, Bridgewater, NJ]) and hemostatic inhibitors (eg, low-molecular-weight heparins, pentasaccharides, and direct thrombin inhibitors) are contributing factors to bleeding. Tests for platelet dysfunction are not readily available. Excessive fibrinolysis and low fibrinogen are also causes of bleeding in these patients. Currently, however, there are several agents that have been reported to be effective for the prophylaxis of hemorrhage in surgical patients, including aprotinin for cardiac surgery, orthopedic surgery, and hepatic transplantation, and the off-label use of recombinant activated factor VII (NovoSeven, Novo Nordisk, Bagsvaerd, Denmark) as rescue therapy for life-threatening hemorrhage.
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ABSTRACT: Coagulopathy associated with massive operative blood loss is an intricate, multicellular and multifactorial event. Massive bleeding can either be anticipated (during major surgery with high risk of bleeding) or unexpected. Management requires preoperative risk evaluation and preoperative optimization (discontinuation or modification of anticoagulant drugs, prophylactic coagulation therapy). Intraoperatively, the causal diagnosis of the complex pathophysiology of massive bleeding requiring rapid and specific coagulation management is critical for the patient's outcome. Treatment and transfusion algorithms, based on repeated and timely point-of-care coagulation testing and on the clinical judgment, are to be encouraged. The time lapse for reporting results and insufficient identification of the hemostatic defect are obstacles for conventional laboratory coagulation tests. The evidence is growing that rotational thrombelastometry or modified thrombelastography are superior to routine laboratory tests in guiding intraoperative coagulation management. Specific platelet function tests may be of value in platelet-dependent bleeding associated e.g. with extracorporeal circulation, antiplatelet therapy, inherited or acquired platelet defects. Therapeutic approaches include the use of blood products (red cell concentrates, platelets, plasma), coagulation factor concentrates (fibrinogen, prothrombin complex, von Willebrand factor), pharmacological agents (antifibrinolytic drugs, desmopressin), and local factors (fibrin glue). The importance of normothermia, normovolemia, and homeostasis for hemostasis must not be overlooked. The present article reviews pathomechanisms of coagulopathy in massive bleeding, as well as routine laboratory tests and viscoelastic point-of-care hemostasis monitoring as the diagnostic basis for therapeutic interventions.Minerva anestesiologica 07/2007; 73(7-8):401-15. · 2.27 Impact Factor
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ABSTRACT: Clinical practice guidelines on red blood cell transfusion (RBC) are based on expert opinion, animal studies and the few human trials available. Twelve randomized controlled trials on the benefits of RBC transfusions in humans have been published. In the absence of definitive outcome studies, numerous theoretical arguments have been put forward in favor or against the classic transfusion threshold of 100 g/l. However, data from randomized controlled trials suggest that overall morbidity (including cardiac) and mortality, hemodynamic, pulmonary and oxygen transport variables are not different between restrictive (transfusion threshold between 70 and 80 g/l) and liberal transfusion strategies and that a restrictive transfusion strategy is not associated with increased adverse outcomes. In fact, a restrictive strategy may be associated with decreased adverse outcomes in younger and less sick critical care patients. The majority of existing guidelines conclude that transfusion is rarely indicated when the hemoglobin concentration is greater than 100 g/l and is almost always indicated when it falls below a threshold of 60 g/l in healthy, stable patients or more in older, sicker patients. In anesthetized patients, this threshold should be modulated by factors related to the dynamic nature of surgery such as uncontrolled hemorrhage, microvascular bleeding, etc. Another important role of RBC relates to primary hemostasis and higher triggers may be appropriate in coagulopathic patients. RBC concentrates are administered to correct inadequate oxygen delivery and/or to sustain primary hemostasis. Reliable monitors of tissue oxygenation and hemostasis will be required to study the benefits (or lack thereof) of RBC transfusions. The quest for a universal transfusion trigger, i.e., one that would be applicable to patients of all ages under all circumstances, must be abandoned. All RBC transfusions must be tailored to the patient's needs, at the moment the need arises. In conclusion published recommendations are commensurate with existing knowledge and, unfortunately, their conclusions are limited. Future research and development should focus on the determination of optimal transfusion strategies in various patient populations and on reliable monitors to guide transfusion therapy.Transfusion and Apheresis Science 09/2004; 31(1):55-66. DOI:10.1016/j.transci.2004.06.002 · 1.07 Impact Factor
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ABSTRACT: Postoperative hemorrhage and thrombosis is a significant problem during the perioperative period. Understanding the complex and dynamic interplay of factors, proteins, and enzymes during coagulation is imperative to maintain balance between hemostasis and thrombosis. To improve patient outcome, each patient should be risk stratified for bleeding or thrombosis during the preoperative examination. Additional research focused on improvement in screening tools, monitoring, and therapeutic regimens for surgical patients with a coagulopathy are warranted.Hematology/Oncology Clinics of North America 03/2007; 21(1):13-24. DOI:10.1016/j.hoc.2006.11.013 · 2.07 Impact Factor