Complications of Blood Transfusion
Immune complications following blood transfusions are primarily due to sensitization of the recipient to donor red cells, white cells, platelets, or plasma proteins. Less commonly, the transfused cells or serum may mount an immune response against the recipient.
Hemolytic reactions usually involve specific destruction of the transfused red cells by the recipi-ent’s antibodies. Less commonly, hemolysis of a recipient’s red cells occurs as a result of transfusion of red cell antibodies. Incompatible units of plate-let concentrates, FFP, clotting factor concentrates, or cryoprecipitate may contain small amounts of plasma with anti-A or anti-B (or both) alloantibod-ies. Transfusions of large volumes of such units can lead to intravascular hemolysis. Hemolytic reactions are commonly classified as either acute (intravascu-lar) or delayed (extravascular).
Acute intravascular hemolysis is usually due to ABO blood incompatibility, and the reported frequency is approximately 1:38,000 transfusions. The most com-mon cause is misidentification of a patient, blood specimen, or transfusion unit. These reactions are often severe, and may occur after infusion of as little as 10–15 mL of ABO-incompatible blood. The risk of a fatal hemolytic reaction is about 1 in 100,000 transfusions. In awake patients, symptoms include chills, fever, nausea, and chest and flank pain. In anesthetized patients, an acute hemolytic reaction may be manifested by a rise intemperature, unexplained tachycardia, hypotension, hemoglobinuria, and diffuse oozing in the surgical field. Disseminated intravascular coagulation, shock, and kidney failure can develop rapidly. The severity of a reaction often depends upon the volume of incompatible blood that has been administered.
Management of hemolytic reactions can be summarized as follows:
· If a hemolytic reaction is suspected, thetransfusion should be stopped immediately and the blood bank should be notified.
· The unit should be rechecked against the blood slip and the patient’s identity bracelet.
· Blood should be drawn to identify hemoglobin in plasma, to repeat compatibility testing, and to obtain coagulation studies and a platelet count.
· A urinary catheter should be inserted, and the urine should be checked for hemoglobin.
· Osmotic diuresis should be initiated with mannitol and intravenous fluids.
delayed hemolytic reaction—also called extravas-cular hemolysis—is generally mild and is caused by antibodies to non-D antigens of the Rh system orto foreign alleles in other systems such as the Kell, Duffy, or Kidd antigens. Following an ABO and Rh D-compatible transfusion, patients have a 1–1.6% chance of forming antibodies directed against for-eign antigens in these other systems. By the time significant amounts of these antibodies have formed (weeks to months), the transfused red cells have been cleared from the circulation. Moreover, the titer of these antibodies subsequently decreases and may become undetectable. Reexposure to the same foreign antigen during a subsequent red cell trans-fusion, however, triggers an anamnestic antibody response against the foreign antigen. The hemolytic reaction is therefore typically delayed 2–21 days after transfusion, and symptoms are generally mild, con-sisting of malaise, jaundice, and fever. The patient’s hematocrit typically fails to rise, or rises only tran-siently, in spite of the transfusion and the absence of bleeding. The serum unconjugated bilirubin increases as a result of hemoglobin breakdown.
Diagnosis of delayed antibody-mediated hemo-lytic reactions may be facilitated by the antiglobulin (Coombs) test. The direct Coombs test detects the presence of antibodies on the membrane of red cells. In this setting, however, this test cannot distinguish between recipient antibodies coated on donor red cells and donor antibodies coated on recipient red cells. The latter requires a more detailed reexami-nation of pretransfusion specimens from both the patient and the donor.
The treatment of delayed hemolytic reactions is primarily supportive. The frequency of delayed hemolytic transfusion reactions is estimated to be approximately 1:12,000 transfusions. Pregnancy (exposure to fetal red cells) can also be responsible for the formation of alloantibodies to red cells.
Nonhemolytic immune reactions are due to sensi-tization of the recipient to the donor’s white cells, platelets, or plasma proteins; the risk of these reac-tions may be minimized by the use of leukoreduced blood products.
White cell or platelet sensitization is typically manifested as a febrile reaction. Such reactions are relatively common (1–3% of transfusion episodes) and are characterized by an increase in temperature without evidence of hemolysis. Patients with a his-tory of repeated febrile reactions should receive leu-koreduced transfusions only.
Urticarial reactions are usually characterized by erythema, hives, and itching without fever. They are relatively common (1% of transfusions) and are thought to be due to sensitization of the patient to transfused plasma proteins. Urticarial reactions can
be treated with antihistaminic drugs (H1 and per-haps H2 blockers) and steroids.
Anaphylactic reactions are rare (approximately 1:150,000 transfusions). These severe reactions may occur after only a few milliliters of blood has been given, typically in IgA-deficient patients with anti-IgA antibodies who receive IgA-containing blood transfusions. The prevalence of IgA deficiency is estimated to be 1:600–800 in the general population. Such reactions require treatment with epinephrine, fluids, corticosteroids, and H1 and H 2 blockers. Patients with IgA deficiency should receive thor-oughly washed packed red cells, deglycerolized fro-zen red cells, or IgA-free blood units.
Transfusion-related acute lung injury (TRALI) pres-ents as acute hypoxia and noncardiac pulmonary edema occurring within 6 h of blood product transfu-sion. It may occur as frequently as 1:5000 transfused units, and with transfusion of any blood compo-nent, but especially platelets and FFP. It is thought that transfusion of antileukocytic or anti-HLA anti-bodies results in damage to the alveolar–capillary membrane. Treatment is similar to that for acute respiratory distress syndrome , with the important difference that TRALI may resolve within a few days with supportive therapy.
This type of reaction may be seen in immunocom-promised patients. Cellular blood products con-tain lymphocytes capable of mounting an immune response against the compromised (recipient) host. Use of special leukocyte filters alone does not reli-ably prevent graft-versus-host disease; irradiation (1500–3000 cGy) of red cell, granulocyte, and plate-let transfusions effectively eliminates lymphocytes without altering the efficacy of such transfusions.
Rarely, profound thrombocytopenia may occur fol-lowing blood transfusions. This post-transfusion purpura results from the development of platelet alloantibodies. For unknown reasons, these anti-bodies also destroy the patient’s own platelets. The platelet count typically drops precipitously 5–10 days following transfusion. Treatment includes intrave-nous IgG and plasmapheresis.
Allogeneic transfusion of blood products may diminish immunoresponsiveness and promoteinflammation. Post-transfusion immunosuppres-sion is clearly evident in renal transplant recipients, in whom preoperative blood transfusion improves graft survival. Recent studies suggest that periop-erative transfusion may increase the risk of postop-erative bacterial infection, cancer recurrence, and mortality, all of which emphasize the need to avoid unnecessary administration of blood products.
The incidence of post-transfusion viral hepatitis var-ies greatly, from approximately 1:200,000 transfu-sions (for hepatitis B) to approximately 1:1,900,000 (for hepatitis C). Most acute cases are anicteric. Hepatitis C is the more serious infection; most cases progress to chronic hepatitis, with cirrhosis develop-ing in 20% of chronic carriers and hepatocellular car-cinoma developing in up to 5% of chronic carriers.
The virus responsible AIDS, HIV-1, is transmis-sible by blood transfusion. HIV-2 is a similar, but less virulent virus. All blood is tested for the pres-ence of anti-HIV-1 and anti-HIV-2 antibodies. The requirement for nucleic acid testing by the Food and Drug Administration (FDA) has decreased the risk of transfusion-transmitted HIV to approximately 1:1,900,000 transfusions.
Cytomegalovirus (CMV) and Epstein–Barr virus usually cause asymptomatic or mild systemic illness. Some individuals infected with these viruses become asymptomatic infectious carriers; the white cells in blood units from such donors are capable of transmitting either virus. Immunocompromised and immunosuppressed patients (eg, premature infants, organ transplant recipients, and cancer patients) are particularly susceptible to severe trans-fusion-related CMV infections. Ideally, such patients should receive only CMV-negative units. However, recent studies indicate that the risk of CMV trans-mission from transfusion of leukoreduced blood products is equivalent to CMV test-negative units. Human T-cell lymphotropic viruses 1 and 2 (HTLV-1 and HTLV-2) are leukemia and lymphoma viruses, respectively, that have been reported to be transmit-ted by blood transfusion; the former has also been associated with myelopathy. Parvovirus transmis-sion has been reported following transfusion of coagulation factor concentrates and can result in transient aplastic crises in immunocompromised hosts. West Nile virus infection may result in enceph-alitis with a fatality rate of up to 10%, and transmis-sion of this virus by transfusion has been reported.
Parasitic diseases that can be transmitted by trans-fusion include malaria, toxoplasmosis, and Chagas’ disease. Such cases are very rare.
Bacterial contamination of blood products is the second leading cause of transfusion-associated mor-tality. The prevalence of positive bacterial cultures in blood products ranges from 1:2000 for platelets to 1:7000 for PRBCs and may be due to transient donor bacteremia or inadequate antisepsis during phlebot-omy. The prevalence of sepsis due to blood transfu-sion ranges from 1:25,000 for platelets to 1:250,000for PRBCs. Both gram-positive (Staphylococcus) and gram-negative (Yersinia and Citrobacter) bacte-ria can contaminate blood transfusions and trans-mit disease. To avoid the possibility of significant bacterial contamination, blood products should be administered over a period shorter than 4 h. Specific bacterial diseases rarely transmitted by blood trans-fusions from donors include syphilis, brucellosis, salmonellosis, yersiniosis, and various rickettsioses.
Massive transfusion is mostoftendefinedas theneed to transfuse one to two times the patient’s blood volume. For most adult patients, that is the equivalent of 10–20 units. The approach to mas-sive transfusion (and to lesser degrees of transfu-sion) after trauma injury has been greatly influenced by military experience in recent Middle Eastern and Central Asian wars in which outcomes have improved with concurrent transfusion of packed red cells, plasma, and platelets to avoid dilutional coagu-lopathy .
The most common cause of nonsurgical bleed-ing following massive blood transfusion isdilutional thrombocytopenia, although clinically sig-nificant dilution of coagulation factors may also occur.
Coagulation studies and platelet counts, if readily available, should guide platelet and FFP transfu-sion. Although most clinicians willbe familiar with“routine” coagulation tests (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], international normalized ratio [INR], platelet count, fibrinogen), multiple studies show that viscoelastic analysis of whole blood clotting (thromboelastog-raphy, rotation thromboelastometry, and Sonoclot analysis) may be more useful in resuscitation, liver transplantation, and cardiac surgical settings.
Calcium binding by the citrate preservative can rise in importance following transfusion of large vol- umes of blood or blood products. Clinically important hypocalcemia, causing cardiacdepression, will not occur in most normal patients unless the transfusion rate exceeds 1 unit every 5 min, and intravenous calcium salts should rarely be required in the absence of measured hypocalce-mia. Because citrate metabolism is primarily hepatic, patients with hepatic disease or dysfunction (and possibly hypothermic patients) may demonstrate hypocalcemia and require calcium infusion during massive transfusion, as may small children and oth-ers with relatively impaired parathyroid–vitamin D function.
Massive blood transfusion is an absolute indication for warming all blood products and intravenous fluids to normal body temperature. Ventricular arrhythmias progressing to f ibrillation often occur at temperatures close to 30°C, and hypothermia can hamper cardiac resuscitation. The use of rapid infu-sion devices with efficient heat transfer capability has decreased the incidence of transfusion-related hypothermia.
Although stored blood is acidic due to the citric acid anticoagulant and accumulation of red cell metabo-lites (carbon dioxide and lactic acid), metabolic acidosis due to transfusion is uncommon because citric acid and lactic acid are rapidly metabolized to bicarbonate by the normal liver. In the situa-tion of massive blood transfusion, acid-base status is largely dependent upon tissue perfusion, rate of blood transfusion, and citrate metabolism. Once normal tissue perfusion is restored, any metabolic acidosis typically resolves, and metabolic alkalosis commonly occurs as citrate and lactate contained in transfusions and resuscitation f luids are converted to bicarbonate by the liver.
The extracellular concentration of potassium in stored blood steadily increases with time. The amount of extracellular potassium transfused with each unit is typically less than 4 mEq per unit. Hyper-kalemia can develop regardless of the age of the blood when transfusion rates exceed 100 mL/min.. Hypokalemia is commonly encountered postoperatively, particularly in association with metabolic alkalosis.
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