PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Transfusion Reaction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1994

The pathophysiology and organ-specific consequences of severe transfusion reactions.

Transfusion of blood components is usually required in the management of critically ill patients. However, pathologic interactions between blood products and organ function may result from transfusion reactions. Emerging understanding of the mediation and interruption of clinical inflammatory responses is applicable to severe transfusion reactions. The pathophysiology of four types of severe transfusion reactions are reviewed: a) acute hemolysis; b) bacterial contamination of blood components; c) transfusion-related acute lung injury (TRALI); and d) anaphylaxis. Acute hemolytic reactions are often caused by preventable errors in sample or patient identification. Renal toxicity, coagulopathy, and hypotension may result from circulating red cell stroma and immune-complex activation of complement and cytokine secretion. Bacterial contamination of blood components has caused patient sepsis in many cases; platelets stored at 20 degrees to 24 degrees C are of particular concern. Careful blood collection and handling is essential for prevention. TRALI is manifested by acute respiratory distress, which is usually caused by infusion of plasma containing antibodies against the patient's leukocytes. Complement activation and cytokine stimulation cause edema and neutrophil accumulation in the lungs. Anaphylactic reactions may result from patient immunoglobulin (Ig)E antibodies against donor plasma constituents. IgA-deficient patients are at risk for anaphylactic reactions if these patients develop anti-IgA antibodies. Vasoactive or complement-activating factors in a blood product may also cause anaphylactoid reactions in some patients.

Acute Disease↗
PubMed2007

Pulmonary transfusion reactions.

Transfusion reactions remain a common complication of transfusion therapy; reactions affecting the lungs are some of the most serious. Several different mechanisms are responsible for pulmonary transfusion reactions, and most cause adverse effects in addition to lung injury. Fluid overload can lead to pulmonary edema, antibodies reacting with plasma proteins can cause bronchospasm and anaphylaxis, and particulate matter can produce microemboli. These reactions are well understood and usually can be prevented. Transfusions are also associated with acute lung injury and acute respiratory distress syndrome (ARDS), but their etiology is poorly understood and they remain clinically problematic. Neutrophil antibodies cause some of these serious as well as mild pulmonary reactions, but the exact role of leukocyte antibodies in pulmonary reactions remains unclear. Other blood donor, blood component, and transfusion recipient factors likely play a contributing or modulating role in pulmonary transfusion reactions, but prospective studies are needed to better understand their role.

Blood Component Transfusion↗
PubMed1980

Blood transfusion reactions.

Transfusion reactions range from mismatching of blood causing reaction, to the transmission of diseases such as hepatitis through the improper screening of blood. This paper discusses guidelines for transfusions of various blood fractions or components, reasons for transfusions of red blood cells rather than whole blood, the problem of blood platelets, the prohibition against fibrinogen, and the various volume expanders.

Blood Group Incompatibility↗
PubMed2005

Intravenous immunoglobulin given to lymphoma patients with recurrent haemolytic transfusion reactions after transfusion of compatible blood.

Accelerated destruction of red cells after transfusion of compatible blood has been reported in both sickle cell disease (SCD) and non-SCD patients. We report three patients with lymphoma, all of whom had recurrent haemolytic transfusion reactions after receiving compatible red cell units. The direct antiglobulin test (DAT) was negative and there were no detectable red cell alloantibodies in either pre-transfusion or post-transfusion samples. As there was no evidence of red cell antibody-mediated haemolysis and response to oral steroids, a trial of intravenous immunoglobulin (IVIg) was given. Immediate cessation of haemolysis with sustained haemoglobin level was achieved in all cases. The response to IVIg in these cases suggests that IVIg should be tried when recurrent non-antibody mediated haemolytic transfusion reactions occur in patients with a lymphoid malignancy.

Aged↗
PubMed2001

[The TRALI syndrome--a life-threatening transfusion reaction].

Transfusion related acute lung injury (TRALI) is a serious complication of blood transfusion, characterized by non-cardiogenic lung oedema. We describe a case of TRALI due to granulocyte-specific antibodies. The 58-year-old patient received 2 units of fresh frozen plasma following colon surgery and within 30 min the patient developed an acute respiratory distress syndrome. Granulocyte-specific antibodies were found in one of the transfused plasma of a female blood donor who most likely became immunized against granulocyte alloantigens during her three pregnancies.

Acute Disease↗
PubMed1991

Hemolytic transfusion reaction following transfusion of frozen and washed autologous red cells.

A case of hemolytic transfusion reaction, accompanied by hypotension and followed by transient renal failure, occurred after the transfusion of 1 unit of previously frozen autologous red cells. Subsequent investigation revealed the probable cause of the hemolysis to be inadequate deglycerolization of the unit. The cause of the associated symptoms is unknown. Possibilities include nephrotoxic effects of hemoglobin or stroma, toxic effects of glycerol, or release of vasoactive or thrombogenic substances from lysed red cells. This case of a hemolytic reaction adds to the known risks of autologous transfusion.

Blood Preservation↗
PubMed1999

Intravascular hemolysis secondary to ABO incompatible platelet products. An underrecognized transfusion reaction.

Transfusion of ABO-incompatible platelets to a cardiac surgery patients resulted in acute intravascular hemolysis complicated by ventricular tachycardia. Nine similar cases with significant morbidity or mortality have been reported in similar settings. Five fatalities caused by transfusion of ABO-incompatible platelet products have been reported to the US Food and Drug Administration during the last 4 years. Non-group O patients, particularly those with small plasma volumes, receiving multiple non-group specific platelets in a short time are at risk for intravascular hemolysis caused by passively infused anti-A1 or anti-B. To prevent intravascular hemolysis in such at-risk patients, the indications for platelet transfusion must be continually assessed. If transfusion of ABO-incompatible platelet products is necessary, consideration should be given to minimizing the accompanying plasma via further concentration of the platelets or by saline washing of platelet products.

ABO Blood-Group System↗
PubMed1997

[Cytokines and chemokines as inducers of nonhemolytic transfusion reactions after thrombocyte transfusion].

Recently, the leukocyte-derived cytokines interleukin (IL)-1 beta, IL-6, IL-8, and tumor necrosis factor(TNF)-alpha were found in considerable concentrations in platelet concentrates (PC) involved in nonhemolytic transfusion reactions (NHTR). We investigated transfusion reactions in two study periods over the last 3 years. In the 1st period, PC were leukocyte-depleted by bedside filtration. In the 2nd period we performed prestorage leukocyte filtration of PC. Recipients who experienced a transfusion reaction were tested for total and specific IgE, and reactions were analyzed with regard to the main symptoms. In the supernatant of platelets involved, we analyzed concentrations of IL-1 beta, IL-6, IL-8, TNF-alpha, macrophage inflammatory protein(MIP)-1 alpha, and RANTES. The incidence for NHTR did not change with the kind of PC transfused (n = 44, 1.63% and n = 46, 1.56%; p = 0.84), but allergic reactions were reduced in the 2nd observation period (0.92% versus 0.51%; p = 0.02). IL-1 beta, IL-6, IL-8, TNF-alpha, and MIP-1 alpha were not detectable in the majority of all products. PC involved in allergic reactions contained significantly higher concentrations of RANTES. We found evidence that the proinflammatory chemokine RANTES, stored in the platelet alpha-granules, is involved in allergic transfusion reactions. In contrast, leukocyte-derived inflammatory cytokines were of minor relevance in the onset of NHTR.

Blood Group Incompatibility↗
PubMed1983

Febrile transfusion reaction following initial transfusion in a man with immunoblastic lymphadenopathy and granulocyte autoantibodies.

A 69-year-old man with immunoblastic lymphadenopathy and autoimmune hemolytic anemia who had no previous exposure to blood products developed a severe febrile nonhemolytic transfusion reaction following the initial infusion of packed red blood cells. The reaction recurred with transfusion of packed red blood cells, but not when freeze-thawed red blood cells were used. Immunofluorescence techniques demonstrated granulocyte antibodies in his serum and on the surface of his granulocytes. Circulating immune complex, HLA, and platelet antibodies were not present. The granulocyte antibodies fluctuated in titers with disease activities, and could be completely removed from the serum by autologous granulocyte absorption. We conclude that our patient had granulocyte autoantibodies which probably produced febrile transfusion reactions.

Aged↗
PubMedDate not supplied

Febrile and allergic transfusion reactions after the transfusion of white cell-poor platelet preparations.

BACKGROUND: Nonhemolytic transfusion reactions (NHTRs) frequently occur after platelet transfusions. White cell (WBC)-derived inflammatory cytokines can cause these reactions, but they are rarely found in WBC-poor platelet preparations. Transfusion reactions were investigated with regard to the residual WBC content in the stored platelet concentrate in two consecutive study periods. STUDY DESIGN AND METHODS: In the first study period, platelet concentrates were WBC-reduced by bedside filtration. In the second period, all platelet concentrates were filtered before storage. Recipients who experienced transfusion reactions were examined with regard to their main clinical symptoms during and after transfusion. In the supernatant of the involved platelet concentrates, concentrations of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)alpha, macrophage inflammatory protein 1alpha, and RANTES were analyzed. RESULTS: The incidence of transfusion reactions remained steady when the transfusion regimen was changed from bedside filtration to prestorage WBC filtration (1.63% and 1.56%; p = 0.84). In both periods, NHTRs were predominantly of allergic origin. Inflammatory mediators IL-1beta, IL-6, IL-8, and TNFalpha were detectable in only a minority of platelet components involved in NHTRs. Platelet concentrates involved in allergic reactions contained high concentrations of RANTES (668 +/- 223 ng/mL). CONCLUSIONS: Prestorage WBC filtration did not reduce the incidence of these reactions, and inflammatory cytokines were of minor relevance. The proinflammatory platelet-derived chemokine RANTES, which accumulates even in WBC-reduced platelet concentrates, was associated with allergic transfusion reactions. Platelet-derived mediators may be a key to understanding NHTRs.

Antilymphocyte Serum↗
PubMed2001

Immediate transfusion reactions.

Immediate transfusion reactions were characterized in recipients of 15,990 RBCs, 18,013 platelets, 409 single donor platelets, 3,451 FFP and 1,507 units of cryoprecipitate. The overall incidence of immediate reactions was 0.2%. Allergic reactions occurred in 40 patients, febrile non-hemolytic in 36 patients, bacterial contamination in 2 patients, circulatory overload in 3 patients and mechanical hemolysis in one patient. Three patients had nonspecific reactions. The incidence of immediate transfusion reactions was low when compared with similar studies. Possible causes are under-reporting transfusion reactions and the use of leukoreduced components.

Adult↗
PubMed2000

Effect of premedication guidelines and leukoreduction on the rate of febrile nonhaemolytic platelet transfusion reactions.

Platelet transfusion reactions were prospectively studied in haematology/oncology patients at five university teaching hospitals over three consecutive summers. The initial summer study provided baseline information on the use of premedications and the rate of platelet transfusion reactions (fever, chills, rigors and hives). Most (73%) platelet recipients were premedicated and 30% (95% CI 28-33%) of transfusions were complicated by reactions. The second study followed implementation of guidelines for premedicating platelet transfusions. Despite a marked reduction in premedication (50%), there was little change in the platelet transfusion reaction rate, 26% (95% CI 24-29%), or the type of reactions. The third study followed implementation of prestorage platelet leukoreduction while maintaining the premedication guidelines. The reaction rate decreased to 19% (95% CI 17-22%). For nonleukoreduced platelets, there was a statistically significant association between the platelet age and reaction rate (P = 0.04). For leukoreduced platelets, there was no statistically significant association between platelet age and reaction rate (P = 0.5). Plasma reduction of nonleukoreduced platelet products also reduced the reaction rate. These prospective studies document a high rate of platelet transfusion reactions in haematology/oncology patients and indicate premedication use can be reduced without increasing the reaction rate. Prestorage leukoreduction and/or plasma reduction of platelet products reduces but does not eliminate febrile nonhemolytic platelet transfusion reactions.

Blood Preservation↗
PubMed2003

Allergic transfusion reactions: an evaluation of 273 consecutive reactions.

CONTEXT: Allergic reaction to transfusion is common. However, the review of a large series of allergic transfusion reactions has not been performed. OBJECTIVE: To review a large series of allergic transfusion reactions. DESIGN: A retrospective review of all reported and evaluated transfusion reactions during a 9-year period at 1 institution was performed. Associated clinical signs and symptoms were evaluated. SETTING: Large, tertiary-care teaching hospital. RESULTS: A total of 1613 adverse reactions to transfusion were evaluated. Allergic transfusion reactions accounted for 17% (273 of 1613) of the transfusion reactions. Severe allergic reactions (anaphylaxis, anaphylactoid signs and symptoms, and/or hypotension) were observed in 21 patients (7.7% of allergic reactions, or 1.3% of all transfusion reactions). Serum tryptase, a marker for anaphylaxis, was measured in 1 patient and determined to be borderline elevated. Five patients experienced allergic transfusion reactions to autologous red cell transfusions. One patient experienced hives during the transfusion of a major ABO mismatched red blood cell. A wide variety of skin manifestations were observed, but 26 (9.5%) patients did not have skin manifestations. Allergic transfusion reactions were estimated to occur in approximately 1 in 4124 blood components transfused, or 1 in 2338 transfusion episodes. Severe allergic reactions occurred in approximately 1 in 30,281 transfusions. No deaths directly attributable to transfusion were observed in this patient group. CONCLUSIONS: The clinical presentation of allergic transfusion reactions was quite variable, and the pathophysiology remains unclear. Recommendations for clinical evaluation and therapy remain problematic and often empirical.

Acute Disease↗