Febrile nonhemolytic transfusion reactions and allergic reactions are the most common adverse effects of transfusion.
To reduce febrile nonhemolytic transfusion reactions leukoreduced red blood cell transfusions are utilized.
Leuko-reduced red blood cells and platelets mitigate against the risk of cytomegalic virus transmission as they are CMV safe.
To prevent febrile nonhemolytic and allergic transfusion reactions antipyretics and antihistamines, usually acetaminophen and diphenhydramine, are used prior to transfusions in about 50% of cases of RBC transfusions.
Approximately what percent of transfuse blood products result in serious adverse reactions.
Premedication with antipyretics and antihistamines routinely is of questionable value.
Life-threatening acute transfusion reactions include: acute hemolytic transfusion reactions, transfusion-associated circulatory overload, and transfusion related acute lung injury.
Blood transfusion therapy complications include hemolysis, infection, fever, skin eruptions, pulmonary reactions.
The main 3 causes of transfusion related fatalities are transfusion–related acute lung injury, transfusion associated circulatory overload and acute hemolytic transfusion reactions.
Rare transfusion related deaths are related to microbial contamination, anaphylaxis, transfusion associated graft versus host disease and hypotension.
Transfusion reactions are suspected when the patient experiences fever, chills, nausea, vomiting, pain, itching at the intravenous insertion site, variations in blood pressure, tachycardia, dyspnea, and restlessness.
Between 30-44 patients die each year due to transfusion reactions in the United States, between years 2009 in 2013 (FDA).
Allergic reactions typically occur within 1 hour of transfusion and include urticaria, hives, flushing, abdominal pain, wheezing, hypotension, angioedema, bronchospasm, shock and cardiac arrest.
Antibodies to IgA are the most common cause of anaphylactic transfusion reactions (USFDA).
When a transfusion reaction is suspected the infusion should be stopped, the IV accessshould be maintained with normal saline, the blood products should be checked for its appropriateness, and the remaining unit with attached tubing and compatibility label must be sent to the transfusion service, with a sample of the patient’s blood.
A fresh urine sample is sent for evaluation when hemolysis is suspected.
When hemolysis reaction is suspected of plasma color is noted, a direct antiglobulin test and screening for free hemoglobin in plasma and urine are performed.
The presence of a positive post-transfusion direct anti-globulin test (DAT) suggests an acute hemolytic transfusion reaction and aggressive hydration of the patient to limit the effects of free plasma hemoglobin should be initiated.
Acute hemolytic transfusion reactions are most often caused by immune incompatibility between the donor and recipient.
The most serious acute hemolytic transfusion reaction is due to immunoglobulin IgM anti-A, usually due to a processing era or failing to perform patient identification checks and transfusing blood intended for someone else.
In the last 5 years 13 deaths have occurred from ABO-mediated acute hemolytic transfusion reactions, and 29 deaths from non-ABO antibodies associated fatal acute hemolytic transfusion reactions (FDA).
The volume of blood transfused correlates with the severity of acutehemolytic transfusion reactions, and the patient should be observed for the first few minutes of every transfusion to assure no significant reaction occurs.
Acute hemolytic transfusion reactions may be delayed, and patients should monitor the development of any symptoms within the first 24 hours after transfusion.
Hemolysis due to anti-A and anti-B Is primarily intravascular because IgM activates complement, inducing the formation of a membrane attack complex.
Complement activation causes release of vasoactive a means, histamine, inflammatory cytokines such as interleukins and TNF-alpha, which activate coagulation and fibrinolysis.
Hemolysis with release of free plasma hemoglobin damages the endothelium and is a nitric oxide scavenger causing vasoconstriction and hypoxemia.
Hemolysis mediated by IgG antibodies, that is non-ABO, is mainly extravascular through phagocytosis of transfused RBCs by splenic macrophages by their Fc receptors.
In patients with high IgG antibody titers to RBC antigens hemolysis both extravascular intravascular may occur.