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Reactions reported after transfusion of 19,126 units of whole blood and of 42,678 units of red blood cells were analysed. The reaction rate with whole blood was about two and one-half times as great as with red blood cells.
Twenty-three cases of delayed hemolytic transfusion reaction (DHTR) occurring at the Mayo Clinic from 1964 through 1973 are reviewed. Nineteen patients had clinical manifestations of hemolysis, of which fever was the most frequent presenting symptom. The degree of hemolysis served as an index of morbidity. In four cases, there was oliguria, two of these patients experiencing renal shutdown. In one case, hemolysis led to a disseminated intravascular coagulation syndrome. Death occurred subsequent of DHTR in three patients. The direct antiglobulin test was positive in all but one case; this finding coincided with elevated unconjugated bilirubin in 14 cases and decreased haptoglobin levels in 15 cases. Anti-Jka antibody accounted for somewhat more than one-third of reactions and, along with anti-E, c, D, Fya, and K antibodies accounted for 91 per cent of cases.
Data on 47 cases of hemolytic transfusion reactions are presented along with a review of the literature. Human error and limitations of current techniques of compatibility testing remain the major causative factors of hemolytic transfusion reactions.
A patient is described who developed a delayed hemolytic transfusion reaction, 11 days posttransfusion, caused by anti-U. This case illustrates the difficulty that can occur in distinguishing a delayed transfusion reaction from autoimmune hemolytic disease when the antibody involved is directed against a high incidence blood group antigen.
Delayed hemolytic transfusion reactions in eight persons were manifested solely or primarily by an apparently unexplained posttransfusion decrease in the hematocrit value. Alloantibodies were eventually found in all eight patients, but were sometimes undetectable for as long as 72 hours after the reaction. This did not preclude the occurrence of a new, acute hemolytic reaction. There were three instances of reversible renal failure complicating the reaction. In two patients, some or all of the antibodies became undetectable after four and nine months. In a third, the indirect antiglobulin reactions became considerably weaker after 12 months. Patients previously sensitized to RBC antigens should have available records inspected and a warning device (wristband or wallet card) provided to help prevent reactions caused by an anamnestic antibody rise.
In a delayed haemolytic transfusion reaction due to an apparently typical complement-binding IgG anti-Jka, it was possible to show that transfused Jk (a+b+) cells were destroyed progressively over a period of about 3 weeks. The slow destruction may have been due partly to the fact that the patient had been splenectomised.
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.
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.
A review of our knowledge of acute hemolytic transfusion reactions indicates that we have learned much in recent years about the pathogenetic mechanisms involved. An approach to effective therapy for patients suffering such reactions should be based on our latest understanding of the pathophysiology of this syndrome. However, changes in our therapeutic approach have not kept abreast of our increased awareness of the etiologic factors, and the patient, therefore, is not getting the benefit of our increased knowledge in this area. The primary pathogenetic mechanisms involved in these reactions appear to be disseminated intravascular coagulation and a series of hemodynamic alterations leading to ischemic necrosis of tissues. Therapy would best be aimed at interfering with these primary pathophysiologic pathways.
A case of a non-hemolytic transfusion reaction with pulmonary infiltration secondary to leukocyte antibodies is described, and previously reported cases are reviewed. This type of reaction can be diagnosed at the bedside when a patient develops fever, hypotension and dyspnea within a few hours following transfusion of whole blood or a plasma product. The roentgenogram of the chest shows pulmonary infiltrates with a normal cardiac silhouette constituting non-cardiac pulmonary edema. To provide laboratory confirmation of this reaction, it is essential to search for leukocyte antibodies by both leukoagglutinin and cytotoxic technics, as well as to determine HL-A phenotypes of both donor and recipient. As the plasma products involved usually come from multiparous women, donor parity should be a routine question in the donor interview in transfusion services. To prevent this reaction, which may prove fatal, blood donated by women who have two or more children should be used for packed cells only.
A 72-year-old man with a peptic ulcer received seven units of apparently compatible red blood cells. Six days after the last unit, he had a hemolytic transfusion reaction manifested by high fever, marked fall in hematocrit, hemoglobinemia, hemoglobinuria, severe bilirubinemia and oliguria. He went on to become uremic, hyperkalemic, anuric and died five days later. Serologic studies showed that the donor and recipient bloods were completely compatible prior to the transfusions and that unexpected antibodies were not detected. The anamnestic response from donor antigens was precipitous even after a latent period of six days.
In patients with severe allergic reactions to plasma proteins it is possible to observe such reactions to even the small quantity of plasma contained in platelet concentrates. A platelet washing solution was designed, and platelet concentrates for four such patients were washed before infusion. Transfusion reactions were completely eliminated by the washing procedure. Platelet recovery was equivalent to that of unwashed platelets, and hemostatic effectiveness of the infused platelet concentrates was evidenced by abrupt cessation of bleeding episodes, including purpura and hematuria. Platelet washing represents a valuable, rapid and simple approach to the problem patient with thrombocytopenia and severe reactions to plasma proteins.
The Diego blood group system has had its primary applications in population genetics and anthropology, although it can also give rise to clinical problems. Anti-Dia has ofter been reported to cause hemolytic disease of the newborn. The patient presented in the report experienced an immediate hemolytic transfusion reaction apparently due to anti-Dia. We believe it to be the only such case reported since the Diego system was first discovered in 1956.
A young man with X-linked chronic granulomatous disease of childhood, who is of the rare McLeod phenotype with antibodies in his serum shown to be hemolytic and reactive against all red cells with normal expressions of the Kell antigens, developed a severe Nocardia pneumonia with abscess formation and was subsequently treated successfully with granulocyte transfusions in spite of the presence of anti-KX in the patient's serum. The anti-KX did not appear to alter significantly the effectiveness of the transfused granulocytes; it did, however, cause a mild hemolytic transfusion reaction. The patient made a remarkable recovery from this episode and his condition has progressed to a state satisfactory enough for him to donate his own blood for storage and possible use in the future.
In 5 patients of phenotype ccDEe or ccDEE, the transfusion of 2--14 U of C-positive blood was folloued 5--9 days later by haemoglobinuria lasting 2--4 days. Anti-C was the only antibody present in all 5 cases but was always of low titre; with CC cells the maximum titre recorded with the indirect antiglobulin test was 8 and with the agglutination of enzyme-treated cells, 128. The discordance between the weakness of the antibody in vivo and the amount of haemoglobin released intravascularly is surprising but may be related to the type of IgG molecule of which anti-C is composed.
Clinical and laboratory investigation of a black male patient, who received emergency transfusion of blood incompatible for a high incidence antigen, provided evidence for the pathogenetic importance of high titer anti-Holley antibodies with poor avidity. The red blood cells of the patient and two siblings were remarkable in being negative for two high incidence antigens, Hy and hrS, and weak for a third, Gy.
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