Transfusion reaction following ABO-incompatible maternofetal transfusion.
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Coa is a high-frequency blood group antigen in the Colton blood group system expressed on red blood cells (RBCs) of approximately 99.8 percent of random persons. Anti-Coa has been reported to cause delayed hemolytic transfusion reactions, hemolytic disease of the newborn, and accelerated clearance of RBCs in vivo. Acute hemolytic transfusion reactions (AHTRs) have not previously been reported. A 58-year-old man was hospitalized for vascular surgery. Initial blood bank evaluation revealed anti-Fya. The patient received six units of RBCs during his initial hospitalization and developed anti-E. A subsequent sample was sent to the reference laboratory when all units of RBCs appeared incompatible. Additional studies, including alloadsorptions, revealed the presence of anti-E, anti-Fya, and an apparent warm autoantibody. One unit of least-incompatible RBCs was transfused during surgery. The patient had an increase in temperature. Hemoglobinuria and a decrease in hematocrit were also noted. Due to the clinical impression of an AHTR, the pre- and postreaction samples were reevaluated in the reference laboratory and demonstrated the presence of anti-Coa in both. Based on clinical and laboratory evaluation this patient appears to have had an AHTR due to anti-Coa. This is the first known reported case of an AHTR caused by anti-Coa.
A delayed hemolytic transfusion reaction (DHTR) occurring in a 30-year-old Caucasian man is described. His blood groups were B, CDe/cDE (R1R2, f-) K-, S-s+, Fy (a + b-), and Jk (a + b +). Eight days after receiving two units of packed red blood cells, his urine was strongly positive for hemoglobin; serum-free hemoglobin was 125 mg/dl. Serum contained a clearly reactive Rh antibody of anti-f specificity and a weakly reactive anti-Kell. The DHTR was probably caused by an anti-f alloantibody appearing as an anamnestic response to transfusion of seemingly compatible, but f-positive blood.
The antibodies of the Dombrock blood group system have only rarely been encountered in transfusion practice, and anti-Dob has not previously been implicated in an acute hemolytic transfusion reaction. We have encountered the first such case involving a chronically transfused black female with hemoglobin SS disease and multiple antibodies in her serum. During a previous admission for sickle cell crisis, the patient received 3 units of compatible blood with no untoward effects. Serum obtained 21 days later contained, in addition to the known antibodies, anti-S plus an unidentified antibody showing characteristics of HTLA. Blood lacking the E, K1, Fy(a), Jk(b) and S antigens was obtained, and 2 least incompatible units were transfused. While administering the second unit, the patient complained of fever and low back pain, and hemoglobinemia was detected. Anti-Dob was identified in the post-reaction samples by absorption-elution tests, and the patient was confirmed to be Do(a+b-). The first unit transfused during this hemolytic episode tested Do (b+). This case, and a similar case involving anti-Doa reported in 1986, strengthens the belief that Dombrock antibodies are clinically significant and illustrates the need for their differentiation, prior to transfusion from less clinically significant HTLA antibodies.
Hemolysis due to donor-derived antibodies produced by "passenger" B lymphocytes, called passenger lymphocyte syndrome, has been described in ABO-unmatched solid organ and bone marrow transplant recipients. Delayed hemolytic transfusion reactions occur within a similar time frame and have similar clinical and serologic findings. To our knowledge, we report the first case of hemolysis due to the simultaneous occurrence of passenger lymphocyte syndrome (donor-derived anti-A) and a delayed hemolytic transfusion reaction (recipient-produced anti-E) in a liver transplant patient.
A 67-year-old white woman received transfusions of a total of 87 units of whole blood and red blood cells during and within 48 hours following a pneumonectomy. Although she had previously received blood transfusions, unexpected antibodies were not detectable by routine screening. On the second postoperative day, she developed fever, hemoglobinemia, hemoglobinuria, and oliguria. However, the direct antiglobulin test and the antibody screen were negative. On the eighth postoperative day, an IgM anti-P1 antibody was detected for the first time. This anti-P1 antibody increased in thermal amplitude from 22 to 37 C, but remained IgM. The circulating transfused P1-positive cells decreased progressively without evidence of bleeding. Testing of the patient's preoperative blood at 15 C found her serum to be weakly reactive with P1 cells, while her own cells were P2. Thus, an anamnestic response to the P1 antigen is the most likely cause of her delayed hemolytic transfusion reaction.
BACKGROUND: A novel case where in vitro hemolysis was observed in plasma, but not in serum samples, obtained after the onset of a severe delayed hemolytic transfusion reaction is presented. CASE REPORT: A 54-year-old woman received 2 units of blood during an orthopedic procedure. She had received transfusion 30 years earlier, and testing before transfusion revealed no alloantibodies. The patient returned 12 days after the transfusion with a Hb level of 54 g per L due to a severe delayed hemolytic reaction caused by anti-K. The plasma and serum samples were grossly hemolysed on Day 12. On Day 14, the serum samples showed no evidence of hemolysis; however, the EDTA sample remained grossly hemolysed. This discrepancy was not identified until Day 19. Due to concerns of ongoing apparent severe hemolysis, the patient was unnecessarily treated with IVIG and corticosteroids. The in vitro hemolysis was still present at 75 days, despite complete normalization of her Hb, bilirubin, and LDH levels. The phenomenon had resolved by 125 days. CONCLUSION: This in vitro artifact has not been previously reported and the mechanism remains unclear. Both plasma and serum samples should be observed for hemolysis when evaluating a patient with a severe delayed hemolytic transfusion reaction.
PURPOSE: Signs and symptoms of delayed hemolytic transfusion reaction (DHTR) may resemble those of vaso-occlusive crises in patients with sickle cell anemia (SCA). The diagnosis of DHTR therefore presents a challenge to the clinician when treating such patients. The current study describes a patient with SCA and DHTR secondary to red cell anti-s antibody, manifesting as painful extremeties, severe hemolytic anemia, and acute oliguric renal failure. PATIENTS AND METHODS: A 17-year-old patient with homozygous hemoglobin S presented 8 days after partial exchange transfusions with severe anemia and signs and symptoms resembling vaso-occlusive crisis. Clinical course was complicated by intravascular hemolysis and acute renal failure. RESULTS: Anti-s antibody was detected in the eluate. Diagnosis of DHTR was made. Treatment included single volume whole blood exchange transfusion and continuous veno-venous hemofiltration with dialysis. CONCLUSIONS: The possibility of DHTR should be considered in a patient with SCA with hemolytic anemia. Acute renal failure is a rare complication of anti-s antibody-associated DHTR. Such reactions can be successfully managed with exchange transfusion and continuous hemofiltration with dialysis.
Two definite acute hemolytic transfusion reactions occurred in a patient with chronic myelogenous leukemia in blastic crisis. Both suspect units were entirely compatible by routine crossmatch using commercial antiblobulin sera. However, both units were clearly incompatible using our own specific anti-C3 antiserum in the antiglobulin reaction phase of the crossmatch. Subsequently it was possible to predict in vivo compatibility using our anti-C3 antiserum in vitro. This case adds new evidence for the inadequacy of anticomplement activity in commercial antisera.
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BACKGROUND: Management of patients with clinically significant anti-IgA is difficult and unsatisfactory in many aspects. PATIENTS AND METHOD: A 40-year-old man with common variable immunodeficiency had a previous history of anaphylaxis after an intramuscular immunoglobulin administration. His serum contained anti-IgA, and he required immunoglobulins for recurrent infections. RESULTS: The administration of intravenous immunoglobulins (IVIgG) containing less than 0.1 mg per mL IgA led to an anaphylactic reaction after the transfusion of only 2 to 3 mL. The same IVIgG charge was subsequently pretreated with freshly separated autologous plasma and given to the patient on three consecutive days without any reaction (1.25, 10, and 10 g each in 400 mL plasma). Anti-IgA activity did not increase, and the patient was treated again without complications. DISCUSSION: Ex vivo pretreatment of IVIgG preparations with autologous plasma appears to be safe and useful in the management of patients with clinically significant anti-IgA. To achieve a significant IgA blockage, the preparation to be used should not contain large amounts of IgA. CONCLUSION: The strategy described here appears to be safe and may help prevent anaphylaxis in many instances.
Shivering may be part of a febrile non-haemolytic reaction to blood product transfusion. Shivering can increase oxygen consumption up to 500 per cent which may be detrimental to patients with decreased myocardial reserve. A case is presented of a reaction to platelet transfusion characterized by shivering, tachycardia and hypertension in a patient with a recent myocardial infarction in whom the metabolic and haemodynamic effects were considered to be potentially disastrous. Intravenous injection of meperidine was rapidly effective in treating these changes.
Many renal transplant centres now try to avoid blood transfusion prior to renal transplantation, to avoid alloimmunization due to antibody production against donor antigens usually present on contaminating white cells. Post- or peri-operative transfusions are usually not considered to present problems, since the patient is heavily immunosuppressed. We present a patient who suffered a rare transfusion reaction, that we believe may have initiated a severe vascular rejection of a kidney transplant, probably mediated by Kidd blood group antigens.
BACKGROUND: A hemolytic transfusion reaction (HTR) due to anti-IH is reported in a patient with sickle cell disease (SCD). CASE REPORT: An 18-year-old woman with SCD and a complete phenotype on file had been identified as group B-positive with negative antibody-screening tests and had received 1 unit of packed RBCs. Ten days later, she was readmitted in painful crisis with a Hb of 4.2 g per dL. Antibody-screening tests and panel cells were positive at all test phases with a negative autocontrol, which suggested alloantibodies. Phenotypically matched group O RBCs were issued emergently. After the transfusion of 100 mL, the patient had an HTR with chills, fever, and tachycardia and laboratory findings of hemoglobinemia, hemoglobinuria, and negative DATs. A high-titer, IgM anti-IH with a high thermal amplitude (reactive with group O, but not group B RBCs at 37 degrees C) was identified. Autologous RBCs appeared to have normal I antigen expression, but less H antigen than pooled group B RBCs. She was given group B RBCs, uneventfully, by use of a blood warmer. CONCLUSIONS: This is a rare case of anti-IH as the cause of a HTR, as a serologic problem that may be seen in SCD, and as an autoantibody that may mimic an alloantibody. Ironically, this HTR resulted from the effort to provide phenotypically matched RBCs, which necessitated the selection of group O RBCs.
A transfusion reaction was observed with blood warmed by a microwave blood warmer. Analysis of the blood remaining in the bag excluded the possibility of incompatibility but revealed hemolysis and clot formation which was attributed to overheating by the blood warmer.
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A fatal transfusion reaction due to contamination of platelet-depleted whole blood with Pseudomonas fluorescens is reported. Routine sterility testing on blood products and environmental microbiological monitoring suggested no source for the contaminating organism, as has been the case for the majority of reported incidents of this type. The value of routine sterility testing in the prevention and investigation of such incidents is discussed.
BACKGROUND: HLA antibodies may be directed against HLA antigens on RBCs, but these antibodies are generally not considered to be clinically significant in transfusion practice. A case of a multiparous woman who had hemolytic transfusion reactions due to HLA-related Bg antibodies is reported. CASE REPORT: A 37-year-old woman was admitted with anemia. No unexpected RBC antibodies were identified. Two group O, D+ RBC units were transfused. Ten days later she returned with hemolysis and anemia. Two more RBC units were ordered, no unexpected RBC antibodies were identified, and two crossmatch-compatible units were issued. During the transfusion, the patient developed symptoms of an acute reaction, and the posttransfusion sample showed evidence of intravascular hemolysis. RESULTS: Repeat RBC antibody screen showed anti-Bg. HLA antibody screen identified anti-HLA-A2, A28, B7, B7 cross-reactive group (CREG). The two RBC units from the first transfusion episode and one RBC unit from the second transfusion episode were HLA incompatible with the patient. No other cause for the hemolytic reactions was identified. The patient was later successfully transfused with one RBC unit from an HLA-compatible donor. CONCLUSION: HLA antibodies should be considered in patients with hemolytic transfusion reactions when RBC-specific antibodies are not found to be the etiology.