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Millions of RBC units are transfused throughout the world annually. Even though each RBC unit contains multiple foreign donor antigens, only a minority of transfusion recipients will develop detectable RBC alloantibodies. Some factors that influence humoral immune responsiveness to transfused RBCs are obvious, including the necessity of being exposed to a foreign antigen that the immune system can process and present. Mathematically, however, every RBC transfusion meets those criteria. Thus, it remains unclear why some patients form alloantibodies (‘responders’), while others may be transfused hundreds of times without becoming alloimmunised (‘non‐responders’). Studies in humans have found an association with CD4+ T‐cell markers and responsiveness to transfused RBCs, and have also identified acute or chronic inflammatory disease states as risk factors for alloantibody development. Studies in animal models, which allow single variables to be isolated, have led to an understanding of the critical role played by dendritic cells in transfusion‐associated RBC alloimmunisation. Murine studies have further established that non‐responsiveness to transfused RBCs equates to antigen‐specific tolerance in some settings: alloantibodies develop to RBCs expressing some blood group antigens only when the initial RBC exposure occurs in close association with a danger signal. Additional studies are needed in humans and in animal models to further understand the complex variables that determine when and how a humoral immune response may be initiated against transfused RBC antigens, such that strategies for preventing alloimmunisation and its harmful effects in transfusion and pregnancy scenarios can be developed. [ABSTRACT FROM AUTHOR]

Background and Objectives: Many hospitals require transfusions to be discontinued when vital signs stray from predetermined ranges, regardless of clinical symptoms. Variations in vital signs may be unrelated to transfusion, however, and needlessly stopping a transfusion may delay medical care while increasing donor exposures and healthcare costs. We hypothesized that a detailed study of vital sign changes associated with transfusion of blood product by component, including those associated with potential reactions (complicated) and those deemed to be uncomplicated, would establish a useful framework of reference for treating clinicians and transfusion services alike. Materials and Methods: A retrospective electronic record review of transfusion service and transfusion recipient data was completed on 3852 inpatient transfusion episodes over a 6‐month period at four academic tertiary care hospitals across the United States. Vital signs pre‐ and post‐transfusion were recorded by trained clinical research nurses. Serious reactions were adjudicated by a panel of transfusion medicine experts. Results: In both uncomplicated transfusions (n = 3765) and those including an adverse reaction (n = 87), vital sign fluctuations were generally modest. Compared to uncomplicated transfusions, transfusions complicated by febrile reactions were associated with higher pretransfusion temperature and higher pretransfusion pulse rates. Episodes of transfusion circulatory overload were associated with higher pretransfusion respiration rates compared to uncomplicated transfusions. Conclusion: Most transfusions are associated with only modest changes in vital signs. Pretransfusion vital signs may be an important yet previously understudied predictor of vital sign changes during transfusion. The optimal role of vital sign assessment during blood transfusion deserves further study. [ABSTRACT FROM AUTHOR]

Background and Objectives One of the challenges surrounding blood component administration is the determination of an appropriate rate of infusion. There are very few evidence-based guidelines available to guide healthcare providers looking for a 'standard' infusion rate for red blood cells ( RBCs), plasma or platelets ( PLTs). Our objective was to determine the extent to which blood component infusion rates were associated with changes in transfusion recipient vital signs. Materials and Methods We retrospectively examined records of 3496 component infusions ( RBCs, n = 2359; PLTs, n = 478; plasma, n = 659) over a 1-year period at a 362-bed multispecialty hospital. The following data were collected for each transfusion: blood product volume and infusion time, recipient pre- and post-transfusion temperature, blood pressure and pulse rate, and hospital ward where transfusion occurred. Results Plasma (median 10·4 ml/min) was infused faster than PLTs (median 7·2 ml/min, P < 0·0001) or RBCs (median 2·3 ml/min, P < 0·0001). For all blood components, infusion rates varied based on the hospital unit performing the infusion. No association was found between relatively fast RBC, plasma or PLT infusion rates (>20 ml/min) and clinically significant reported changes in vital signs. Conclusions There does not appear to be a strong correlation between infusion rate and significant changes in recipient temperature, blood pressure or pulse rate. Based on these data, a reasonable rate for routine transfusion is 2-3 ml/min for RBCs and 7-10 ml/min for plasma and PLTs. Faster infusion rates (>20 ml/min) likely can be applied with close patient monitoring if there is a more urgent need for transfusion. [ABSTRACT FROM AUTHOR]

Background and Objectives Transfusion of allogeneic platelet products can result in antibodies against donor major histocompatibility complex (MHC) I antigens, leading to a refractory state to subsequent platelet transfusions. However, there is disagreement in the field regarding the molecular mechanisms of humoral alloimmunization. One hypothesis states that donor MHC II is a requirement for alloimmunization. However, other studies have suggested that donor MHC I is alone sufficient and MHC II is not required. Materials and Methods We utilized a mouse model of anti-MHC I alloimmunization to transfused blood, which employed donors with a complete deletion of all MHC II genes. BALB/c (H-2d) recipients were transfused with blood from either C57BL/6 (H-2b) or MHC II null donors on a C57BL/6 background. Anti-MHC I alloimmunization was monitored by indirect immunofluorescence. Results Recipients of either wild type or MHC II null blood produced equivalent humoral responses against donor MHC I antigens. However, there was variation in the relative amounts of IgG subclasses. Conclusion These data reject the hypothesis that donor MHC II expression is required for alloimmunization to MHC I antigens. [ABSTRACT FROM AUTHOR]

Mice provide tractable animal models for studying the pathophysiology of various human disorders. This review discusses the use of mouse models for understanding red-blood-cell (RBC) clearance. These models provide important insights into the pathophysiology of various clinically relevant entities, such as autoimmune haemolytic anaemia, haemolytic transfusion reactions, other complications of RBC transfusions and immunomodulation by Rh immune globulin therapy. Mouse models of both antibody- and non-antibody-mediated RBC clearance are reviewed. Approaches for exploring unanswered questions in transfusion medicine using these models are also discussed. [ABSTRACT FROM AUTHOR]