Complications for Transfusion (I will briefly also talk about what transfusion means, not mentioned here)
Acute hemolytic transfusion reaction (AHTR): AHTR usually results from recipient plasma antibodies to donor RBC antigens. ABO incompatibility is the most common cause of AHTR. Antibodies against blood group antigens other than ABO can also cause AHTR. Mislabeling the recipient's pretransfusion sample at collection or failing to match the intended recipient with the blood product immediately before transfusion is the usual cause, not laboratory error.
Hemolysis is intravascular, causing hemoglobinuria with varying degrees of acute renal failure and possibly disseminated intravascular coagulation (DIC). The severity of AHTR depends on the degree of incompatibility, the amount of blood given, the rate of administration, and the integrity of the kidneys, liver, and heart. Dyspnea, fever, chills, facial flushing, and severe pain may occur, especially in the lumbar area. Shock may develop, causing a rapid, feeble pulse; cold, clammy skin; low BP; and nausea and vomiting. Jaundice may follow acute hemolysis.
Delayed hemolytic transfusion reaction: Occasionally, a patient who has been sensitized to an RBC antigen has very low antibody levels and negative pretransfusion tests. After transfusion with RBCs bearing this antigen, a primary or anamnestic response may result (usually in 1 to 4 wk) and cause a delayed hemolytic transfusion reaction. Delayed hemolytic transfusion reaction usually does not manifest as dramatically as AHTR. Patients may be asymptomatic or have a slight fever. Rarely, severe symptoms occur. Usually, only destruction of the transfused RBCs (with the antigen) occurs, resulting in a falling Hct and a slight rise in LDH and bilirubin.
Febrile nonhemolytic transfusion reaction: Febrile reaction may occur without hemolysis. Antibodies directed against WBC HLA from otherwise compatible donor blood are one possible cause. This cause is most common in multitransfused or multiparous patients. Cytokines released from WBCs during storage, particularly in platelet concentrates, is another possible cause.
Allergic reactions: Allergic reactions to an unknown component in donor blood are common, usually due to allergens in donor plasma or, less often, to antibodies from an allergic donor. These reactions are usually mild, with urticaria, edema, occasional dizziness, and headache during or immediately after the transfusion. Simultaneous fever is common. Less frequently, dyspnea, wheezing, and incontinence may occur, indicating a generalized spasm of smooth muscle. Rarely, anaphylaxis occurs, particularly in IgA-deficient recipients.
Volume overload: The high osmotic load of blood products draws volume into the intravascular space over the course of hours, which can cause volume overload in susceptible patients (eg, those with cardiac or renal insufficiency). RBCs should be infused slowly. The patient should be observed and, if signs of heart failure (eg, dyspnea, rales) occur, the transfusion should be stopped and treatment for heart failure begun.
Acute lung injury: Transfusion-related acute lung injury is an infrequent complication caused by anti-HLA and/or anti-granulocyte antibodies in donor plasma that agglutinate and degranulate recipient granulocytes within the lung. Acute respiratory symptoms develop, and chest x-ray has a characteristic pattern of noncardiogenic pulmonary edema.
Altered oxygen affinity: Blood stored for > 7 days has decreased RBC 2,3-diphosphoglycerate (DPG), and the 2,3-DPG is absent after > 10 days. This absence results in an increased affinity for O2 and slower O2 release to the tissues. There is little evidence that 2,3-DPG deficiency is clinically significant except in exchange transfusions in infants, in sickle cell patients with acute chest syndrome and stroke, and in some patients with severe heart failure. After transfusion of RBCs, 2,3-DPG regenerates within 12 to 24 h.
Graft-vs-host disease (GVHD): Transfusion-associated GVHD is usually caused by transfusion of products containing immunocompetent lymphocytes to an immunocompromised host. The donor lymphocytes attack host tissues. GVHD can occur occasionally in immunocompetent patients if they receive blood from a donor who is homozygous for an HLA haplotype (usually a close relative) for which the patient is heterozygous. Symptoms and signs include fever, skin rash (centrifugally spreading rash becoming erythroderma with bullae), vomiting, watery and bloody diarrhea, lymphadenopathy, and pancytopenia due to bone marrow aplasia. Jaundice and elevated liver enzymes are also common. GVHD occurs 4 to 30 days after transfusion and is diagnosed based on clinical suspicion and skin and bone marrow biopsies.
Complications of massive transfusion: Massive transfusion is transfusion of a volume of blood greater than or equal to one blood volume in 24 h (eg, 10 units in a 70-kg adult). When a patient receives stored blood in such large volume, the patient's own blood may be, in effect, “washed out.” . Microvascular bleeding (abnormal oozing and continued bleeding from raw and cut surfaces) may result.
Hypothermia due to rapid transfusion of large amounts of cold blood can cause arrhythmias or cardiac arrest. Hypothermia is avoided by using an IV set with a heat-exchange device that gently warms blood.
Infectious complications: Bacterial contamination of packed RBCs occurs rarely, possibly due to inadequate aseptic technique during collection or to transient asymptomatic donor bacteremia. Refrigeration of RBCs usually limits bacterial growth except for cryophilic organisms such as Yersinia sp, which may produce dangerous levels of endotoxin. All RBC units are inspected before issue for bacterial growth, which is indicated by a color change. Because platelet concentrates are stored at room temperature, they have greater potential for bacterial growth and endotoxin production if contaminated. To minimize growth, storage is limited to 5 days. The risk of bacterial contamination of platelets is 1:2500. Therefore, platelets are routinely tested for bacteria.
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