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PubMed1994

The role of the plasma from platelet concentrates in transfusion reactions.

BACKGROUND: Febrile, nonhemolytic transfusion reactions are the most frequent adverse reactions to platelets. A number of observations argue against the widely held view that these reactions result from the interaction between antileukocyte antibodies in the recipient and leukocytes in the platelet product. We sought to determine whether substances in the plasma or the cells in the product cause reactions to transfused platelets. METHODS: We separated standard platelet concentrates into their plasma and cellular components and then transfused both portions in random order. Patients were monitored for reactions during all transfusions. Before each transfusion, the concentration of cytokines (interleukin-1 beta and interleukin-6) was measured in the platelet products. Studies were also performed on the platelet products to determine the effect of storage on the concentration of cytokines. RESULTS: Sixty-four pairs of platelet-product components (the plasma supernatant and the cells) were administered to 12 patients. There were 20 reactions to the plasma supernatant and 6 reactions to the cells (chi-square = 6.50, P = 0.009). Eight transfusions were associated with reactions to both products. The plasma component was more likely to cause severe reactions than the cells (chi-square = 9.6, P < 0.01). A strong positive correlation was observed between the reactions and the concentration of interleukin-1 beta and interleukin-6 in the plasma supernatant (P < 0.001 and P = 0.034, respectively). In vitro studies demonstrated that interleukin-1 beta and interleukin-6 concentrations rise progressively in stored platelets and that these concentrations are related to the leukocyte count in the platelet product. CONCLUSIONS: Bioreactive substances in the plasma supernatant of the platelet product cause most febrile reactions associated with platelet transfusions. Removing the plasma supernatant before transfusion can minimize or prevent these reactions.

Adult↗
PubMed2002

Clinical assessment of preventing febrile nonhemolytic transfusion reaction by leukocyte-depleted blood transfusion.

The objective was designed to assess the clinical efficiency of preventing febrile nonhemolytic transfusion reactions (FNHTR) with transfusion of leukocyte-depleted RBC and platelet concentrates. One hundred patients with cirrhosis of liver, gastric ulcer and cancer were selected to receive RBC concentrates with leukocyte filtration. Another group of 50 patients with liver necrosis, gastric ulcer and cancer were selected to receive non-filtered RBC concentrates. Two hundred and forty patients with acute or chronic leukemia, aplastic anemia, multiple myeloma, thrombocytopenia purpura, diabetes mellitus, cirrhosis of liver, upper gastrointestinal hemorrhage, severe hepatitis, burn and cancer post radioactive or chemical treatment were divided into two group with 120 patients in each one and selected randomly to receive platelet concentrates. The incidence rates of FNHTR in all patients were investigated. Results showed that there was no FNHTR in 100 transfusions with leukocyte-depleted RBC concentrates. Eight out of 50 patients with non-filtrated RBC concentrates showed FNHTR. The incidence of FNHTR was sixteen (16%) in non-filtrated transfusion. Twenty-five and 7 patients manifested FNHTR respectively in non-filtrated or filtrated platelets transfusions. The incidence of FNHTR was 20.83% and 5.83% respectively in non-filtrated or filtrated platelet transfusion. It is concluded that leukocyte-depleted RBC and platelet concentrates reduces FNH TR in blood transfusion.

Adult↗
PubMed2001

Prestorage universal WBC reduction of RBC units does not affect the incidence of transfusion reactions.

BACKGROUND: Febrile nonhemolytic transfusion reaction (FNHTR) has been identified as a pivotal reason for prestorage universal WBC reduction. A regional blood center implemented universal prestorage WBC reduction for RBCs on January 1, 2000. Whether prestorage universal WBC reduction of RBC units will affect FNHTR is not known. STUDY DESIGN AND METHODS: All reports of RBC transfusion reactions at Barnes-Jewish Hospital submitted for evaluation to the blood bank, before and after the implementation of WBC reduction of RBCs, were retrospectively evaluated. RESULTS: For the 36,303 allogeneic RBC transfusions administered in 1999, 85 reactions (0.23%) were reported. These reactions were classified as FNHTR in 43 cases, allergic in 13, delayed hemolytic in 19, and miscellaneous in 10. For the 31,543 non-WBC-reduced RBC transfusions performed in 1999, 78 reactions (0.25%) were reported. These reactions were classified as FNHTR in 39 cases, allergic in 13, delayed hemolytic in 19, and miscellaneous in 7. In the first half of 2000, 32 reactions (0.20%) were reported for 16,093 prestorage WBC-reduced RBC transfusions (p = 0.41). There were 13 FNHTRs and 10 allergic, 7 delayed hemolytic, and 2 miscellaneous reactions. The use of prestorage WBC-reduced RBCs did not significantly affect the rate of reactions classified as allergic (0.04% in 1999; 0.06% in 2000; p = 0.43) or as FNHTR (0.12% in 1999; 0.08% in 2000; p = 0.33). For all patients, universal WBC reduction in 2000 did not reduce the rate of FNHTR from the rate seen with selective bedside WBC reduction, the practice used in 1999 (0.12% in 1999; 0.08% in 2000; p = 0.36). CONCLUSION: No significant difference was found in the incidence of transfusion reactions in patients receiving prestorage WBC-reduced RBCs and non-WBC-reduced RBCs. In addition, no difference was found in transfusion reaction rates when periods of prestorage universal WBC reduction were compared to those of selective WBC reduction.

Blood Component Removal↗
PubMed1990

Clinical significance of white cell antibodies in febrile nonhemolytic transfusion reactions.

Febrile nonhemolytic transfusion reactions (FNHTRs) are associated with white cell (WBC) antibodies. The purposes of this study were to determine the frequency of WBC antibodies, to associate the severity of reactions with antibody specificity, and to distinguish FNHTRs from infection and postoperative fever. By using the granulocyte indirect immunofluorescence test in conjunction with lymphocytotoxicity testing, it was found that 70 percent of FNHTRs in 24 patients involved WBC antibodies. The remaining 30 percent of apparent FNHTRs were associated with infections and postoperative fever. Granulocyte-specific antibodies were as prevalent as HLA antibodies and were associated with the severest reactions. Because FNHTRs occur with granulocyte-specific antibodies, HLA antibodies, and possible monocyte-specific antibodies (untested in this and other studies), these reactions could be grouped together as WBC-associated reactions.

Adult↗
PubMed2005

Titres of alloantibodies against A and B blood types in non-pedigree domestic cats in Turkey: assessing the transfusion reaction risk.

The severity of a transfusion reaction depends on alloantibody titres within the recipients' blood. Determination of an agglutination titre of naturally occurring alloantibody may help to assess the risk of transfusion reactions following an unmatched transfusion in a cat population. In this group of 312 cats 227 had blood type A, 78 had blood type B, and seven had type AB blood. All type B cats tested showed gross evidence of agglutinating anti-A antibody with plasma titres ranging from 2 to 256. Among the 227 type A domestic cats tested for plasma anti-B alloantibody titres, 70% had gross agglutination with titres ranging from 2 to 16, while 17.6% had microscopic agglutination. The remaining 12.4% of the type A cats were negative for both gross and microscopic agglutination. Based on agglutinating titres, the relative risk of a transfusion reaction when type A or AB blood was given to a type B cat was 6.4% with acute severe reaction, acute mild reactions in 85.9% and premature red cell destruction in 7.7%. On the other hand, transfusion of type AB blood or type B blood to type A cats carries a potential risk of acute mild transfusion reaction in 4.4% and premature red cell destruction in 83.3%. Transfusion of type A or B blood to type AB cats results in no apparent clinical transfusion reactions.

ABO Blood-Group System↗
PubMedDate not supplied

[New findings on the physiopathology of acute hemolytic transfusion reactions].

INTRODUCTION: Acute hemolytic transfusion reactions (HTRs) are among the most feared transfusion-associated complications, principally because severe toxicity and rapid death may result. Recently there has been expansion in knowledge concerning the pathophysiology of shock, inflammation and disseminated intravascular coagulation, factors affecting the outcome of HTRs. A new class of biologic mediators/modulators of inflammatory and immune response, interleukins (IL) has been discovered to be of the central importance in the modulation of such responses. RESULTS: In models of acute IgM-mediated RBC incompatibility in experimental HTRs, plasma TNF-alpha rise sharply in a dose- and time-dependent manner, peaking at 2 hours. It is responsible for fever, hypotension and capillary leak leading to acute shock. After 4-6 hours levels of interleukin-8 and MCP-1, monocyte chemoattractants and activators of neutrophils rise, and remain in plasma significantly elevated 48 hours. In IgG-mediated HTRs, within 6 hours the concentrations of IL-1, IL-6, and IL-8 increase significantly and remain elevated next 24 hours, resulting in fever, hypotension, leucocytosis, shock, the proliferation of T-cells and stimulation of immunoglobulin production. Cytokines also play an important role in the development of disseminated intravascular coagulation (DIC). It is associated with the activation of tissue factor pathway and promoting of hypercoagulable state by their effects on endothelial cells. IL-1 and tumor necrosis factor (TNF) induce changes in the hemostatic properties of endothelial cells surface which leads to increased tissue factor and decrease thrombomodulin expression and suppression of protein C activity. Thrombin, bradykinin, epinephrine and IL-1 activation induce acute renal failure, which leads to renal hypoperfusion and widespread fibrin deposition. In etiology of acute lung injury participate: TNF, releasing large quantities of enzyme neutrophil elastase via neutrophil degranulation and pulmonary capillary endothelial injury. IL-8 and MCP-1 released from endothelial cells also promote localised inflammation and thrombosis. CONCLUSION: IL-1, TNF-alpha and IL-6 and IL-8 are all critical mediators of immune and inflammatory response and are known to synergize with each other in a number of in vitro systems. They are responsible for major signs of acute hemolytic transfusion reaction. A future therapeutic strategy of HTRs has to be aimed at modulation of underlying pathophysiologic alterations triggered by HTRs.

Acute Disease↗
PubMed1998

The relationship between the duration of platelet storage and the development of transfusion reactions.

BACKGROUND: The incidence of platelet transfusion reactions may depend partly on the length of storage. The influence of reactions on the effectiveness of platelet transfusions is not known. STUDY DESIGN AND METHODS: Platelet transfusion reactions, identified by prospective monitoring, were analyzed for the effects of component type, recipient lymphocytotoxic antibodies, bacterial contamination, and duration of storage. Posttransfusion corrected count increments (CCIs) were used to evaluate the effectiveness of transfusions associated with reactions by comparing them to those of randomly selected transfusions without reactions. RESULTS: Reactions accompanied 4 percent of the 4926 transfusions given and included 119 febrile nonhemolytic transfusion reactions, 62 allergic reactions, and 13 reactions with features of both. Platelet concentrates contained a mean of 0.5 x 10(8) white cells per unit. Lymphocytotoxic antibodies were detectable in 20 of 84 recipients tested proximate to a reaction. Bacterial cultures from 4 of 81 units were positive; 1 unit was associated with fatal Enterobacter sp. sepsis. The incidence of febrile nonhemolytic transfusion reactions but not allergic reactions was related to platelet storage duration. The CCI was not significantly different for transfusions associated with reactions (10.97 [median, range 0-72.5; n = 165]) or not so associated (13.1 [median, range 0-39.5; n = 174]) (p = 0.08). CONCLUSION: The incidence of febrile nonhemolytic transfusion reactions but not allergic reactions appears to be related to the duration of platelet storage. Transfusion reactions may not have an adverse impact on the effectiveness of platelet transfusions.

Acute Disease↗
PubMed2005

Delayed haemolytic transfusion reaction and hyperhaemolysis complicating peri-operative blood transfusion in sickle cell disease.

We present a case of delayed haemolytic transfusion reaction and hyperhaemolysis syndrome in a patient with sickle cell disease. A 32-year-old woman with a history of sickle cell disease was scheduled for total hip replacement. She was transfused pre-operatively and suffered a delayed haemolytic transfusion reaction. Postoperatively the patient continued to haemolyse, despite the use of antigen compatible blood, suggesting that she had developed hyperhaemolysis syndrome following her delayed haemolytic transfusion reaction. Although rare, both conditions must be borne in mind when dealing with patients who have undergone multiple transfusions.

Adult↗
PubMed1988

A prospective study of the incidence of delayed haemolytic transfusion reactions following peri-operative blood transfusion.

Delayed haemolytic transfusion reactions (DHTRs) are a recognized sequel of blood transfusion. The true incidence and importance of this complication have been difficult to estimate due to the lack of any prospective studies. We have carried out such a study by testing 530 patients who were transfused during cardiac surgery. 2% of the patients had new red cell alloantibodies detectable 1 week following transfusion. Despite this finding, and the fact that at the time the study was performed pre-transfusion antibody screening of recipients was not routine practice, no DHTRs were diagnosed on clinical or laboratory criteria. These results indicate that the reported incidences, based on retrospective recognition of DHTRs, are not a serious underestimate of the frequency of the complication.

Adolescent↗
PubMed1995

Febrile nonhemolytic transfusion reactions to platelets.

Although febrile nonhemolytic transfusion reactions to erythrocytes and platelets are not life threatening, the clinical symptoms associated with them cause discomfort for the patient, result in the use of premedicative drugs, and utilize nursing and laboratory resources. For many years it was assumed that febrile nonhemolytic transfusion reactions were caused by an interaction between leukocyte antibody in the patient's plasma and leukocytes present in the transfused product. Thus prevention has focused on the removal of leukocytes from the blood product by centrifugation or filtration just prior to transfusion. Recent data suggest that most febrile nonhemolytic transfusion reactions to platelets do not involve an immune-mediated event but are caused by the accumulation of biologic response modifiers in the platelet product during storage. Potential biologic response modifiers that have been investigated include histamine, lipids, complement fragments, and cytokines. The concentrations of these substances have been shown to increase in erythrocytes or platelet products or both during storage, and there is some clinical evidence that supports an association between elevated cytokine levels and the risk of reaction. If biologic response modifiers play a major role in febrile nonhemolytic transfusion reactions to platelets, then interventions to prevent these reactions should focus on ways to stop production of these substances or on mechanisms to remove these substances from the platelet product before transfusion. Possible interventions include prestorage leukoreduction, plasma removal from the platelet product before transfusion, and reduction of the platelet storage period to 3 days. Clinical studies to identify the most effective approach for preventing febrile nonhemolytic transfusion reactions have not yet been reported.

Blood Preservation↗
PubMed2001

Single-donor platelets reduce the risk of septic platelet transfusion reactions.

BACKGROUND: Septic platelet transfusion reactions (SPTRs) are the most common, serious risk of transfusion. Because SPTRs result from donor skin flora or asymptomatic bacteremia, the use of single-donor platelets (SDPs) has been proposed to reduce the risk of SPTRs from the risks with pools of platelet concentrates (PCs). STUDY DESIGN AND METHODS: Beginning in 1986, all febrile transfusion reactions were evaluated by culture of the platelet bag. Confirmed SPTRs were identified by isolation of the same bacteria from the bag and the patient's blood or by positive Gram's stain of the bag that confirmed a positive platelet culture. In 1987, a program to minimize PC use in favor of SDP use was initiated as a means of reducing SPTRs. RESULTS: In 12 years, the use of SDPs increased from 51.7 percent to 99.4 percent of all platelet transfusions at one institution. SPTRs fell from three events in 1 year to the current rate of one event per year. The incidence of SPTRs decreased from 1 in 4,818 transfusions to 1 in 15,098 transfusions. The rate of SPTRs due to PCs was 5.39 times higher than that of SPTRs due to SDPs (95% CI, 1.89,12.9). CONCLUSION: The use of SDPs is a simple means of reducing SPTRs. Other measures such as sterilization will be required to eliminate all SPTRs.

Adult↗
PubMed1980

[Therapy of adverse transfusion reactions].

If there are adverse reactions following blood transfusion accurate intervention is necessary. Symptomatical therapy has to start independent from the origin of transfusion reaction. Specific therapy should base on laboratory results. Symptoms, their frequency and severity, are described and therapeutic strategy is outlined. Severe transfusion reaction leading to shock, disseminated intravascular coagulation and renal failure needs intensive care.

Acute Kidney Injury↗
PubMed1999

Pathophysiology of febrile nonhemolytic transfusion reactions.

Most febrile nonhemolytic transfusion reactions (FNHTR) to platelets are caused by cytokines that accumulate in the product during storage. There have been numerous studies that have demonstrated high concentrations of leukocyte- and platelet-derived cytokines in stored platelet products. The mechanism of cytokine accumulation is not understood; however, recent studies have suggested that leukocyte apoptosis and/or monocyte activation during the manufacturing process may play a role. Additional support of cytokines as a cause of FNHTR is provided by a recently published randomized controlled trial that shows that removal of the supernatant plasma from platelets before transfusion significantly lowers the frequency of reactions and eliminates most of the severe reactions associated with platelet transfusions. Although cytokines appear to play a major role in causing platelet reactions, there is little evidence to support their role in causing erythrocyte reactions. Hence, it appears that most febrile nonhemolytic transfusion reactions to erythrocytes are probably the result of an incompatibility between leukocytes in the erythrocyte product and antibodies in the recipient's plasma. Recent studies have confirmed that the concentrations of proinflammatory cytokines in a wide variety of stored erythrocyte products are low. Also, there is no clinical evidence to suggest that the small quantities of cytokines present in stored erythrocyte products contribute to acute reactions to these products when transfused.

Blood Platelets↗