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Doctors should be aware that a blood transfusion can damage the lungs, causing shortness of breath, fluid in the lungs, low blood pressure, and fever. If a patient experiences this after a blood transfusion, the blood bank should be notified so they can determine who else may have received blood from the same donor., Context Transfusion-related acute lung injury (TRALI) is a syndrome that includes dyspnea, hypotension, bilateral pulmonary edema, and fever. TRALI is the third leading cause of transfusion-related mortality, but it is probably underdiagnosed and underreported. Objective To determine if blood products from a frequent plasma donor, whose blood product was implicated in a fatal case of TRALI, caused symptoms of TRALI in other recipients of her plasma. Design, Setting, and Participants Retrospective chart review (conducted from November 2000 through April 2001) of 50 patients who received blood components within 2 years (October 1998 through October 2000) from a donor linked to a transfusion-related fatality. Main Outcome Measure Occurrence of mild/moderate (dyspnea with fever, chills, hypotension, and/or hypoxemia) or severe (acute pulmonary edema or need for mechanical ventilation) reaction associated with transfusion. Results Superimposed illness prevented assessment of TRALI in 14 patients. Of the 36 patient charts that could be reviewed, 7 mild/moderate reactions were reported in 6 patients (16.7%) and 8 severe reactions were reported in 8 patients (22.2%). Of 5 patients who received multiple transfusions from the same donor, 2 experienced 2 reactions: one had 2 mild/moderate reactions and the other had both a mild/moderate and a severe reaction. While 5 of the 7 mild/moderate reactions were reported to the hospital transfusion service, only 2 of the 8 severe reactions were reported. Only 2 reactions (1 mild! moderate and 1 severe) were reported to the regional blood collection facility. Conclusions TRALI was frequently underdiagnosed and underreported in recipients of blood products from a donor whose blood products may have caused TRALI in several transfusion recipients. Clinical education and awareness of this often-overlooked diagnosis are imperative for appropriate prevention and treatment.

Blood transfusions given to HIV patients with anemia do not appear to activate HIV or cytomegalovirus, according to a study of 531 HIV patients with anemia. Removing white blood cells from the blood before transfusing it had no beneficial effect.

For physicians interested in studying the time course of the HIV (human immunodeficiency virus) infection from first transmission of the virus to development of AIDS, establishing a firm time-line is often difficult. Usually the actual time of infection and its source are unknown. However, for those patients infected by transfusion the time and the identity of the source is accurately established. These unfortunate victims provide the medical community with its best clinical source of information concerning the natural biology of the AIDS virus. The progress of 694 individuals who received blood from 143 donors who were later found to be infected with HIV was followed. Approximately half of the transfusion recipients were dead within one year; a similar percentage of patients in the study receiving transfusions not infected with HIV were also dead within one year. Of remaining recipients, not all could be followed; of those tested for AIDS, 85 showed no infection at the time of testing and 116 were identified as infected with HIV (19 of whom already had developed AIDS). Further studies of the patients' white blood cells and other clinical findings indicated the stage of their infection. Extrapolation of previous work and data from these patients allows an estimate that approximately one half of these infected recipients will develop AIDS within seven years of the time of their transfusion. Donors were grouped into two classes, those who developed AIDS within 29 months of the time of donation (early), and those who developed AIDS after that time (late). Recipients of blood from the early group of donors were more likely to have AIDS four years after transfusion.

Several forms of hepatitis have been found to be caused by specific viruses. The current terminology speaks of hepatitis-A which is caused by Hepatitis-A virus (HAV), and hepatitis-B which is caused by Hepatitis-B virus (HBV). Those individuals who have hepatitis which can not be identified on immunologic grounds as being A or B are classified as having non-A non-B (NANB) hepatitis. This disease is credited with being responsible for a large percentage of all hepatitis within the United States. NANB remains the major complication of blood transfusion with some 5 to 10 percent of all transfusions leading to infection. Recently an immunologic test reagent has been made against another newly-discovered virus, designated Hepatitis-C virus (HCV). Using recombinant gene systems, an artificial viral protein or antigen has been prepared that reacts with antibodies in the blood of HCV-infected individuals. This antigen has been used to test for evidence of HCV infection in the blood of individuals who have demonstrated NANB hepatitis. In a small group of 14 NANB hepatitis patients, five showed the presence of HCV infection. A group of four individuals who did not receive transfusions, but who developed hepatitis after hospitalization were also examined. Three of the four did not show the presence of HCV. These data strongly suggest that approximately 50 percent of all cases of NANB hepatitis that occur within the United States are due to infection with HCV. Of those cases of NANB hepatitis that are not linked to HCV, some may be caused by yet another hepatitis virus. These findings pave the way for new blood screening procedures to protect the integrity of the blood supply.