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Adverse Outcomes in Blood and Blood Component Therapy - page 9 / 19





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uneventful 1.5-volume plasma exchange, which was followed by the transfusion of 2 units of red blood cell. At the end of the transfusion of the second unit of RBC the patient developed clinical signs and symptoms of TRALI. Serologic studies demonstrated that the serum from the second RBC donor unit had no HLA antibodies but it did have a granulocyte-specific antibody (anti-NB2) that caused the agglutination of the recipient's granulocytes, which were NB2 positive. Serum from the donor of the first RBC unit and serum from the donors of units used in the exchange had no HLA or granulocyte-specific antibodies that reacted with the recipient's leukocytes. Because the donor implicated in this reaction had a history of 21 blood donations, none of which had been associated with a transfusion reaction, they suggested that the patient's preexisting condition played a significant role in her episode of TRALI, owing to the granulocyte-specific antibody.31

In another case reported by Dubois et al32, TRALI was said to have occurred in an anesthetized patient during an otherwise uneventful laparotomy. Following transfusion of an individual unit of whole blood, routine intraoperative monitoring detected sudden major pulmonary shunting and an increased physiological alveolar dead space. They suggested that the TRALI probably resulted from the presence of a leukoagglutinins against the patient's granulocytes in the donor's plasma. This antibody had no apparent specificity for known HLA, neutrophil, or blood group antigens. The acute respiratory failure was transient, resolving in 72 hours with respiratory support. They concluded that the presence of otherwise unexplained TRALI during or soon after a blood transfusion should suggest the possible diagnosis of a leukoagglutinin reaction.32 General supportive therapy typically leads to recovery without long-lasting sequelae.26

Circulatory Overload Circulatory overload may occur when a patient’s blood volume is increased beyond the capacity of the cardiopulmonary system.25 It may also occur when large volumes of blood are rapidly transfused without equivalent loss. When cardiac reserve is deficient, transfusions may raise the venous pressure and cause acute heart failure. Signs and symptoms may include congestive heart failure, coughing, dyspnea, cyanosis, severe headache, rapid increase in systolic pressure, and peripheral edema. Whole blood is contraindicated and use of packed erythrocytes reduces the risk of circulatory overload. In patients with chronic heart disease, blood should be administered slowly. It may be necessary to divide the unit to be transfused in half. One of the halves is first transfused while the other half is stored in the blood bank refrigerator. After the first half has been transfused then the second half may then be infused. The attending physician may order the administration of a diuretic to decrease fluid retention. This will reduce the risk of a rise in venous pressure. The patient should be observed for signs of increased venous pressure or pulmonary congestion. If acute heart failure occurs, the transfusion should be discontinued and treatment for acute heart failure begun immediately.26

Transfusion Related Bacterial Contamination Transfusion-related bacterial contamination (TRBC) in patients is a growing cause of concern at the same time that that the risk of viral contamination has dramatically decreased. The prevalence of bacteria in blood components in prospective studies range from 0.04% to 2%, depending on the nature of the blood components.33,34 The correct incidence of TRBC in transfusion recipients is unknown, but the contribution of TRBC to transfusion-related mortality seems high. Transfusion-related bacterial contamination accounted for 29 (16%) of 182 transfusion-associated fatalities reported to the FDA from 1986 through 1991 and for 12 (23%) of 51 transfusion-associated fatalities reported to the French Blood Agency from July 1994 through December 1996.33 A method for preventing TRBC is to avoid the introduction of bacteria into blood components at all stages, from the manufacture of blood containers to the administration of the transfusion into recipients. The impact and risk factors of TRBC are poorly documented and the only data available originate from case reports and from a few prospective studies involving a limited number of patients hospitalized in specific settings.35 Systematic information is lacking on the distribution pattern of the severity of TRBC, on the bacteria involved, and on contamination sources. Comparative studies to identify risk factors have not been published.35 The collection of blood from the donor is very critical in the donor process, because donated blood may be contaminated by bacteria present in the donor's bloodstream or by those present of the donor’s skin. Punching a core of skin tissue or hitting a hair follicle may pick up skin bacteria and even a well-conducted antiseptic

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