Objectives Transfusions remain a complicated procedure involving many disciplines performing various steps. Pretransfusion specimen identification errors remain a concern. Over the past two decades, system changes have been made and minimal improvements in the error rates have been seen. Wrong blood in tube (WBIT) events may lead to mistransfusions of components with life-threatening complications. Methods A continuous quality improvement effort involving the introduction of electronic patient identification at the point of pretransfusion specimen collection (an automated system improvement), manual independent dual verification, and periodic education (human process system improvements) were implemented. Results Both automated and human system process improvements resulted in greater than 10-fold reduction in WBIT events and a 47% reduction in mislabeled specimens. Conclusions Diligent improvement and implementation of combination automated system processes and human protocols with continuous monitoring led to great reductions in WBIT error rates and labeling discrepancies, leading to an increase in system safety. These combinations of improvement can lead to more decreased error rates if applied to other critical process steps in the transfusion process.

The production of antibodies following blood transfusions is a complex process that involves many recipient and donor factors. Inflammation in the recipient is one important factor. As knowledge of the immune system, of oxygen, carbon dioxide, and nitric oxide pathways, and of hemostasis grows, more specific therapies will allow precise manipulation of the immune system and safer transfusions. Communication of patients' transfusion and immunotherapy histories with the laboratory, attention to detail in labeling pretransfusion specimens, checking patient and blood product identification before administration, and closely monitoring patients during transfusions remain critical to minimizing risks during transfusion therapy.

Red blood cell transfusion continues to play a vital role in sickle cell disease (SCD) management. Although the risks of transmissible infectious agents continue to decline, sickle cell patients often receive chronic transfusions frequently leading to alloimmunization. Delayed hemolytic transfusion reaction (DHTR) is a possible, life-threatening, adverse effect of a blood transfusion due to recipient RBC autoantibodies or alloantibodies. Some etiologies of DHTR remain unexplained since there are cases of DHTR in which there is an absence of detectable autoantibodies or alloantibodies. Phosphatidylserine (PS) is a phospholipid at the extracellular face of the RBC membrane and is associated with the macrophage clearance of sickled erythrocytes. In several ways this abnormality could contribute to the pathophysiology of sickle cell anemia. Studies have shown that exposure of PS on RBC membrane may promote blood coagulation and could also contribute to observed increases in adhesion of sickle erythrocytes to endothelial cells, and both processes may contribute to microvascular occlusion during sickle cell crisis. The exposure of PS on sickle cell erythrocytes could also be partly responsible for the decreased RBC survival characteristic of the disorder. Potential consequences of such pathologic PS exposure include an exacerbation of the anemia due to enhanced reticuloendothelial clearance and activation of coagulation cascade. 1 Phosphatidylserine exposure is a signal for eryptosis, a suicidal RBC death involving membrane shedding and leading to the physiologic clearance of apoptotic cells by macrophages, via specific PS receptors. 2,3 According to Chadebech and colleagues, PS-RBCs from donor RBC concentrates may account for these mechanisms of destruction in the SCD environment. As PS increases RBC adhesion, it facilitates engulfment and macrophage clearance by the reticuloendothelial system. According to Setty and colleagues, PS can be exposed on human RBC by the action of ionophore on control RBCs. We decided to perform an Abstract Delayed hemolytic transfusion reactions (DHTRs) may occur when there is an antigen mismatch between transfused RBCs and recipient RBC antibodies where sensitized RBCs are cleared by macrophages or complement activation leading to immunoglobulin G (IgG) mediated hemolysis. Some DHTR etiologies remain unknown since there are cases of DHTR when an RBC autoantibody or alloantibody is absent. Mechanisms have been proposed to explain these types of cases of DHTR, including bystander or reactive hemolysis by hyperactive macrophages. Studies in patients with sickle cell disease (SCD) have shown abnormalities in the structure and function of the RBC membranes including exposure of phosphatidylserine (PS) leading to macrophage clearance of sickled erythrocytes. We report on a case demonstrating that DHTR may occur as a result of PS exposure on antigen-matched RBC, resulting in macrophage clearance and hemolysis without detection of autoantibodies or alloantibodies. An in vitro measurement showed ...

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