In patients who meet the clinical criteria for TRALI, confirmation first requires the identification of potentially involved blood products and their respective donors. Other banked blood products from the donor(s) suspected in a TRALI case must be quarantined during evaluation. To implicate a donor in a case of TRALI, the presence of an anti-HLA or antineutrophil antibody with specificity to an antigen expressed by the recipient is required. Implicated donors are typically permanently deferred from further donation.

                 To date, measures to prevent TRALI have focused on the identification and deferral of donors at high risk to form anti-HLA or antineutrophil antibodies. The United Kingdom adopted a policy to manufacture and import male donor plasma only, whereas centers in Spain screen previously pregnant donors for anti-HLA antibodies and, if positive, do not manufacture plasma products from these donors. Data from the SHOT UK Surveillance program (i.e., years 1996 to 2006) involving 206 cases of TRALI demonstrated a substantial (i.e., 80%) decline in the incidence of TRALI after implementation of exclusive use of male donor plasma in the United Kingdom in 2003. Accordingly, in 2007, the American Red Cross has also adopted the use of plasma from only male donors as well. However, this risk still persists with the use of AB plasma; despite the fact that AB plasma represents 4% of all plasma transfused, 50% of the TRALI cases were observed with AB plasma from female donors who had HLA or HNA antibodies (Transfusion 2013;53:1442). This has led to preferential utilization of non-AB plasma in an attempt to mitigate this risk. In multiparous donors from the United States, the incidence of anti-HLA antibodies is approximately 25% and, therefore, policies to exclude high-risk donors can potentially adversely affect the supply of blood products, especially platelets. It is currently unclear which preventative measures such as anti-HLA/HNA testing versus use of platelet additive solution for platelets will be implemented to definitively decrease the incidence of TRALI from platelet derived from female donors.

          7.  Volume overload with symptoms and signs of congestive heart failure can be seen in patients with cardiopulmonary compromise, particularly in elderly patients with substantial anemia who already have expanded plasma volume, patients with substantial renal dysfunction, or patients who have received excess fluids prior to transfusion. Diuretic therapy should be used prophylactically in such patients to minimize this complication. The distinction between volume overload and TRALI can be difficult. Recently, a small study involving 19 patients suspected to have transfusion-associated circulatory overload (TACO) found beta natriuretic peptide (BNP) to be 81% sensitive and 89% specific in the diagnosis of volume overload following a transfusion. Therefore, along with essential clinical data, BNP may be a helpful marker to distinguish TACO from TRALI, although future studies are needed validate this approach.

          8.  Transfusion-associated graft-versus-host disease (GVHD) is a syndrome in which donor lymphocytes that share an HLA haplotype with the patient’s lymphocytes successfully engraft and attack the host (patient) with clinical manifestations of rash, pancytopenia, and liver and gastrointestinal damage (diarrhea). This appears to be unique to immunocompromised patients such as solid organ or bone marrow transplantation patients, and patients with certain malignancies (Hodgkin’s disease, non-Hodgkin’s lymphoma, leukemia, and multiple myeloma), particularly in those undergoing intensive chemotherapy (e.g., fludarabine or myeloablative therapy). Interestingly, a patient with human immunodeficiency virus (HIV) infection has not yet been reported to have this complication, probably because of the suppressive effect of HIV infection on donor lymphocytes. Mortality is in excess of 80% and is usually secondary to bone marrow failure. This complication can be prevented by irradiation of blood products for patients at risk. On the basis of the pathogenesis, directed blood transfusions from any blood relative of the transfusion recipient also must be irradiated.

          9.  Posttransfusion purpura (PTP) is a rare complication, which is manifested by a profound immune-mediated thrombocytopenia that is observed 7 to 10 days after blood transfusion. Platelet alloantibodies within the recipient initiate the destruction of allogeneic platelets and are thought to trigger a complement-mediated consumption of the patient’s own platelets. Most commonly, recipients lack human platelet antigen (HPA)-1a, which is present in approximately 99% of whites. Although controversial, additional platelet transfusions with HPA-1a–positive units may increase complement generation, so further transfusions are often withheld unless an HPA-1–negative donor is identified. The treatment for PTP is intravenous IgG (IVIG), and if this fails, plasma exchange may be initiated to eliminate the antibody after 4 to 5 procedures.

      C.  Infections

          1.  Human immunodeficiency virus infection. Since the recognition that HIV infection is transmissible by blood, major advances in blood safety have been made. With the implementation of nucleic acid testing (NAT) for direct detection of viral (HIV and hepatitis C) contamination, the window period (time from infection to detectability by testing) is 11 days for HIV and 8 to 10 days for hepatitis C. Following the institution of NAT testing, the estimated risk for HIV and hepatitis C transmission is 1:1.5 × 10⁶ and 1:1.2 × 10⁶, respectively. In contrast, the risk of hepatitis B approximates 1:293,000. The risk of fatality from acute hemolytic transfusion reaction (usually due to ABO incompatibility secondary to patient or blood-unit misidentification) approximates 1:1.5 × 10⁶, which approximates the estimated death risk from viral transmission. Nevertheless, prudent utilization of transfusion support is important because blood is a scarce resource and because of possible, unknown future blood risks.

          2.  West nile virus (WNV). Queens, New York, was the epicenter of a WNV epidemic in 1999, which thereafter spread to numerous states throughout the country. The first of the cases of transfusion-transmitted WNV was reported in 2002, when 23 transfusion recipients who developed symptoms of a viral illness within 4 weeks of transfusion and then had laboratory confirmation of WNV. The cases were linked to 16 donors who were viremic at the time of collection (N Engl J Med 2003;349:1236). NAT testing of blood donors was started in 2003, and data from the American Red Cross reported 540 positive donations in 2003 and 2004. It is not clear whether NAT testing for WNV in blood donors will need to continue as the number of WNV cases throughout the country has declined since 2002.

          3.  Cytomegalovirus (CMV) infection. CMV infection has been a substantial cause of morbidity and mortality for immunocompromised oncology patients. Patients who receive allogeneic bone marrow/stem cell transplantation are at risk because of cytotoxic preparative regimens, immunosuppressive therapy (cyclosporine and corticosteroid), and/or GVHD. Up to 60% of this patient population will experience CMV infection, with half of them developing CMV disease. Even with the use of CMV-negative blood products, CMV seroconversion has been reported in 1% to 4% of CMV-negative donor–recipient transplantation patients.

                 CMV infection and CMV disease are much less common in patients undergoing conventional chemotherapy or autologous bone marrow/stem cell transplantation, and are not thought to be a significant clinical problem.

                 A randomized, controlled clinical trial in allogeneic bone marrow transplantation patients compared the value of CMV-seronegative blood products with unscreened blood products that were subjected to bedside leukofiltration. Four (1.3%) of 252 patients in the CMV-seronegative cohort developed CMV infection, with no CMV disease or fatalities; 6 (2.4%) of 250 patients in the leukoreduced cohort developed CMV disease, of whom 5 died. A much larger study would have to be performed to eliminate a type II statistical error with the insignificant rise in CMV infection of 40%. The filtered cohort had an increased probability of developing CMV disease by day 100 (2.4% vs. none; p = 0.03). Even when the investigators eliminated CMV infections that occurred within 21 days of transplantation, two cases of fatal CMV disease occurred in the filtered arm as compared with none in the leukoreduced arm. The conclusion by the authors of this study that leukoreduced blood products are “CMV safe” remains controversial. In a consensus conference held by the Canadian Blood Service, 7 of 10 panelists concluded that patients considered at risk for CMV disease should receive CMV-seronegative products, even when blood components are leukoreduced.

          4.  Bacterial contamination. The risk of platelet-related sepsis is estimated to be 1:12,000 for apheresis platelets but is greater with transfusions of pooled platelet concentrates from multiple donors (e.g., 1:2,000 after receiving six concentrates). Transfusion-related sepsis was the second leading cause of transfusion-associated fatalities from 1990 to 1998. In descending order, the organisms most commonly implicated in fatalities (as reported to the FDA) are Staphylococcus aureus, Klebsiella pneumoniae, Serratia marcescens, and Staphylococcus epidermidis

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