MANAGEMENT OF TRANSFUSION REACTIONS.
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The administration of any blood component carries with it the potential of an adverse reaction. Many times, these reactions can be blamed on the biological aspect of the blood. Because the antigen profile of blood varies among individuals, incompatabilities which are known as immune responses, may occur during transfusion. However, even when donor blood is a perfect antegenic match, it is possible for transfusion reactions to occur. These reactions are considered nonimmune, and may be linked to the collection, preparation or administration of the blood. Certain predisposing factors, such as liver or renal failure, patient size, or pre-existing disease may affect a patient's tolerance to donor blood. Nonimmune transfusion reactions involve not only refrigerated blood components, but also commercially prepared products. Below, nine reactions involving a nonimmune response are discussed.
BACKGROUND: Universal leukodepletion of blood components to prevent acute non-hemolytic transfusion reactions (NHTRs) is still a subject of debate. PATIENTS AND METHODS: Transfusion-associated NHTRs observed at our hospital in the last 6 years were retrospectively analyzed. Buffy-coat depleted red blood cells (bc-RBCs), and if indicated, leucodepleted post-storage (ld-RBCs) were initially used. In April 1997, universal leukodepletion was implemented at our hospital, and thereafter only prestorage ld-RBCs were used. All platelet concentrates transfused during this time were prestorage filtered single-donor apheresis platelets (SDAPs). RESULTS: A total of 163,090 blood products were transfused from April 1995 to April 2001 (bc-RBC: n=34,040 units; ld-RBC: n=66,967; SDAP: n=14,516; FFP: n=47,567). The number of post-transfusion febrile NHTRs occurring with each blood product was 65 (0.19%) for bc-RBCs, 8 (0.16%) for post-storage ld-RBCs, 16 (0.03%) for prestorage ld-RBCs, 16 (0.11%) for SDAPs, and 10 (0.02%) for FFP. Allergic reactions (n=116) were most frequently observed after SDAP transfusion (0.32%) and occurred at a similarly low rate after transfusion of all other blood components (0.03-0.08%). CONCLUSION: In conclusion, acute NHTRs rarely occur after the use of leukodepleted blood components. Prestorage appears to be more effective than post-storage leukodepletion in preventing febrile reactions following a blood transfusion.
BACKGROUND: In vitro studies suggest that mediators of systemic inflammatory response syndrome are generated in the course of hemolytic transfusion reactions. Evidence for the in vivo significance of these findings is given by the present clinical and laboratory analysis of a severe delayed hemolytic transfusion reaction (DHTR). CASE REPORT: A 67-year-old patient (blood group O, D-negative) with a negative pretransfusion antibody screen received a massive transfusion because of arterial bleeding (Day 1). The transfusion of group O, D-positive red cell concentrates was unavoidable because of limited supplies. At Day 10, the patient developed a DHTR with symptoms of septic-toxic syndrome and signs of hemolysis; he received an exchange transfusion. Serologic markers, as well as proinflammatory and anti-inflammatory mediators, were monitored at the onset of the DHTR and during the exchange transfusion. RESULTS: At Day 10, the direct antiglobulin test was positive; anti-D was present, most likely as the result of an anamnestic immune response. Interleukin (IL)-1 was not detectable; all other mediators monitored were elevated: IL-1 receptor antagonist, tumor necrosis factor, IL-6, IL-8, IL-10, neopterin, elastase, C3a-desArg, C-reactive protein, and fibrinogen. Most of the values declined during the exchange transfusion, which was followed by an improvement of the clinical presentation. CONCLUSIONS: Mediators of systemic inflammatory response syndrome were released in the course of a DHTR caused by anti-D. Severe clinical symptoms could be treated successfully by exchange transfusion.
An HLA-compatible platelet transfusion was followed by chills, fever, and severe respiratory distress in a multitransfused patient with chronic lymphocytic leukemia. During the previous 7 days the patient had received blood products without incident, including 8 units of red blood cells (RBC), 24 units of pooled random donor platelet concentrates, and five HLA-compatible platelet pheresis products. The patient had no demonstrable RBC, HLA lymphocytotoxic, platelet or granulocyte antibodies. The platelet donor, a multiparous female, had no granulocyte or RBC antibodies but had lymphocytotoxic antibodies against HLA-A2 CREG (cross-reacting group A2, A28, A23, A24) which reacted not with lymphocytes of the patient but with lymphocytes of the donor whose RBC were transfused 24 h prior to the platelet transfusion reaction and whose HLA type is A23, A24; B44, B57. No RBC donors had HLA lymphocytotoxic, granulocyte, or platelet antibodies against the platelet donor. The patient received three subsequent platelet transfusions from the same donor after removal of the antibody-laden plasma with no adverse reaction. These data suggest an interdonor reaction caused by the presence of cells from the RBC donor received by the patient 24 h prior to the transfusion of donor lymphocytotoxic antibody to HLA-A2 CREG antigens.
After receiving a transfusion with unmatched blood, an anemic Abyssinian cat developed an acute hemolytic transfusion reaction. Similar to many other purebred cats, the recipient had type B blood with strong serum anti-A alloantibodies, whereas the donor had blood type A. Subsequent transfusions with type B blood proved effective and without adverse reactions. This case of a clinical A-B incompatibility reaction emphasizes the need for blood typing and/or crossmatching prior to transfusing cats.
Twenty-five patients with homozygous beta-thalassemia, who complained of occasional nonhemolytic transfusion reactions (NHTR), were alternately transfused eight times with normal packed red cells (PRC) and leucocyte-poor blood prepared by three methods: cotton wool filtration (CWF), buffy coat removal after dilution with saline and upright spin (BCR), and microaggregate filtration (MAF). On overall, CWF-treated RBC concentrates (CWF-RBC) contained 0.02 x 10(9) leucocytes; BCR-RBC contained 0.4 x 10(9), MAF-RBC 1.3 x 10(9) and PRC 1.7 x 10(9). The frequencies of NHTR were: CWF, 0.02; BCR, 0.04; MAF, 0.20; PRC, 0.28. Compared to PRC, both CWF and BCR significantly reduced the frequency of NHTR (p less than 0.01), whilst MAF did not (p greater than 0.1). On the other hand, in one patient CWF caused the two most severe NHTR recorded in this study, both of which were characterized by anaphylaxis.
BACKGROUND AND OBJECTIVE: Current immunohematology practice dictates that serologic diagnosis of immune hemolytic transfusion reactions (IHTR) is based on the finding of a positive post-transfusion direct antiglobulin test (DAT). However, since DAT may fail to detect antibody-coated cells when they constitute a minor population amid a large number of non-sensitized ones, we investigated whether antibody detection in eluates or by flow cytometry is more sensitive than DAT in this context. DESIGN AND METHODS: Ten samples of red blood cells sensitized with allo- or autoantibodies were diluted in non-sensitized red blood cells to final concentrations ranging from 10% to 0.1%. DAT, antibody detection in eluates, and immunofluorescence by flow cytometry were performed on each mixture. RESULTS: DAT failed to detect sensitized cells in all but two cases in that only the 10% dilution yielded a positive DAT. Antibody detection in eluates and by flow cytometry was able to detect up to 1% sensitized cells in most cases. INTERPRETATION AND CONCLUSIONS: Antibody detection in eluates and by flow cytometry is more sensitive than DAT for detecting minor populations of IgG-coated cells. These techniques should be included in the routine investigation of suspected cases of IHTR.
A survey on transfusion reactions in thalassemia was carried out within the COOLEYCARE Programme, a cooperative enterprise aimed at improving quantity and quality of life in thalassemia through a program of quality assurance of treatment delivered to patients. Reactions were reported in 1,225 of 111,590 red cell transfusions (1.1%) given during 40 months (September 1985-December 1987) to 3,755 thalassemics in Italy and Greece. About 90% of red cell units were leukocyte-poor. Filtration was the most commonly used technique for leukocyte removal. Chills, fever, urticaria, headache and chest pain accounted for more than 80% of symptoms reported. Reactions were reported during transfusion in two thirds of cases. Although reactions were reported from 16% of patients, three quarters of reacting patients had no more than 2 reactions in 40 months.
A case of delayed hemolytic transfusion reaction in a 43-year-old patient is presented. Pretransfusion tests revealed no antibody, but tests performed when the reaction occurred demonstrated four. Ten months and 15 months later, when the patient's serum was again tested, the antibodies were undetectable. The significance of such antibodies is discussed.
We report transfusion reactions due to acquired anti-IgA antibodies in a 32-year-old woman with acute lymphoblastic leukemia. Previously, such reactions have been reported only after several hundred transfusions. In our patient they commenced within the first few transfusions.
BACKGROUND: An atypical form of life-threatening hemolytic transfusion reaction (HTR) in patients with sickle cell disease (SCD) has been well described in the literature. Continuation of blood transfusion may be lethal, as it can further exacerbate hemolysis. The pathophysiologic mechanism of HTR is not well understood. CASE REPORTS: Two cases of severe HTR in SCD after the transfusion of compatible RBC units are reported. Hemolysis of both autologous and transfused cells was documented in Case 1 by urine Hb high-performance liquid chromotography. Multispecific HLA antibodies were identified in Case 1. Reticulocytopenia was noted in both cases during the acute hemolytic process. This was followed by a rise in reticulocyte count during receipt of IVIG and steroid therapy. Bone marrow examination during reticulocytopenia in Case 2 showed erythroid hyperplasia. CONCLUSION: In SCD, both mature sickle cells and sickle reticulocytes adhere more readily to macrophages. In view of the bone marrow aspiration results, it appears that the recipients' HbS cells are destroyed by hyperactive macrophages and that the reticulocytopenia observed during HTR is likely to be due to peripheral consumption (i.e., destruction by macrophages), rather than suppression of erythropoiesis. Cessation of hemolysis during IVIG and steroid treatment may be due to IVIG's blocking of the adhesion of sickle cells and reticulocytes to macrophages, together with steroid suppression of macrophage activity.
A severe nonhemolytic transfusion reaction occurred to a polytransfused leukemic patient as a life-threatening anaphylactic shock with cardio-pulmonary arrest following the transfusion of HLA-nonadapted/mismatched platelets. As the only potential causative agent a lymphocytotoxic antibody with the specificity anti-HLA-A2 has been found. The HLA antibody reacted up to a dilution of 1:2,048. The recipient was negative for the corresponding antigen, but HLA-2 was present on donor's platelets. This observation demonstrates again the clinical value of HLA-matched platelet transfusion in patients who need long-term support.
BACKGROUND: Patients with sickle cell anemia may develop serious, life-threatening hemolytic transfusion reactions (HTRs). More severe anemia may develop after the HTR than was present before transfusion, which suggests the possibility of an increased rate of hemolysis of autologous red cells. STUDY DESIGN AND METHODS: The signs and symptoms occurring during eight severe HTRs that occurred in five patients with sickle cell anemia were reviewed, as were published reports by other investigators. Calculations of red cell production and destruction incorporating known correction factors for reticulocyte maturation were performed to determine the most probable mechanism for the striking drop in hematocrit observed in several instances. RESULTS: A characteristic constellation of findings was recognized in some severe HTRs in patients with sickle cell anemia. Calculations of daily red cell production and senescence indicated that a marked drop in hematocrit occurs when erythropoiesis is suppressed in a patient with a short red cell life span and that this could account for severe posttransfusion anemia when donor red cells are hemolyzed during an HTR. CONCLUSION: A sickle cell HTR syndrome was defined. A rapid increase in the severity of anemia occurs in patients with sickle cell anemia when all donor red cells are hemolyzed during an HTR and when there is suppression of erythropoiesis, as commonly occurs as a result of transfusion or concomitant illness. Although an increased rate of hemolysis of autologous red cells may also occur, more definitive data are required to document that in these patients.
BACKGROUND: An increasing incidence of delayed hemolytic and delayed serologic transfusion reactions (DHTRs/DSTRs) has been seen at the Mayo Clinic since 1978. Recently, the average length of stay (LOS) for inpatients and the average number of red cell transfusions per inpatient (TPI) decreased, and the albumin and papain technique for RBC antibody detection was replaced by a polyethylene glycol technique. These changes may have affected the incidence of DHTRs/DSTRs. STUDY DESIGN AND METHODS: The diagnoses of DHTR and DSTR made at the Mayo Clinic from 1993 through 1998 were reviewed. These data were compared with previously published Mayo Clinic data from 1980 through 1992. The LOS for inpatients and the average TPI were also obtained from hospital data. RESULTS: The incidence of DHTR/DSTR increased from 1 in 1899 in 1980 through 1992 to 1 in 1300 in the 1993 through 1998 period (p < 0.05). Similarly, DSTR increased from 1 in 2990 in 1980 through 1992 to 1 in 1612 in the 1993 through 1998 period (p < 0.05). The incidence of DHTR showed a trend toward decrease, from 1 in 5405 in 1980 through 1992 to 1 in 6715 in 1993 through 1998. No alloantibody specificities were statistically associated with DHTRs in 1993 through 1998, unlike in the 1980 through 1992 period. Moreover, the incidence of Jka antibodies increased in 1993 through 1998, while the incidence of other alloantibodies remained stable. Average LOS and TPI declined by 24.5 percent and 8.8 percent, respectively, between the two periods. CONCLUSION: Recently, a trend toward a decrease in the incidence of DHTR and a significant increase in DSTRs has occurred at the Mayo Clinic. These changes are most likely due to a combination of factors, including a decrease in average LOS and the adoption of the polyethylene glycol antibody detection system.
Anti-IgA antibodies were studied in sera from patients with nonhemolytic transfusion reactions for which no serological reason had been found. Of the 158 sera that were studied by passive hemagglutination assay using twelve IgA myeloma proteins, 4 samples had class-specific antibodies and 10 samples antibodies with limited specificity. Titers were 1:8 or less. 100 multitransfused hemophilia patients were studied with two IgA myeloma proteins. Four of the sera had anti-IgA antibodies. Normal blood donor sera reacted with IgA only when antigens were first either digested with pepsin or stored for several months as dilute solutions in refrigerator. The results emphasize the need for fresh IgA proteins of good quality when human anti-IgA antibodies are investigated.