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Transfusion of part of one unit of any blood product can cause TRALI. The mechanism may include factors in unit(s) of blood, such as antibody and biologic response modifiers. In addition, yet to be described factors in a patient’s illness may predispose to the condition. The current incidence is estimated to be 1 in 5,0. Patients present with acute dyspnea, or froth in the endotracheal tube in intubated patients. Hypertension, hypotension, acute leukopenia have been described. Management is similar to that for ALI and is predominantly supportive. When TRALI is suspected, Blood banks should be notified to quarantine other components from the same donation. No special blood product is required for subsequent transfusion of a patient who has developed TRALI. Keywords: Blood transfusion/ adverse effects, Pulmonary edema, Acute lung injury. Transfusion- related acute lung injury (TRALI) is a syndrome of acute lung injury (ALI) associated with transfusion. The term TRALI was coined by Drs. Popovsky and Moore when they reported a case series at the Mayo Clinic in 1. In this case series, the typical clinical presentation included acute respiratory distress characterized by hypoxemia and fulminant pulmonary edema. The onset was usually within 4 hours of transfusion and was often accompanied by fever, tachycardia, hypotension or hypertension. In most patients (8. The incidence was 1: 5,0. TRALI patients were comprised of mainly surgical patients. There is still no consensus on the incidence, pathogenesis or laboratory diagnosis of the syndrome. However, reports of TRALI are increasing due to increasing awareness of the syndrome, although underreporting is still strongly suspected. An analysis of the United States Food and Drug Administration fatality reports for the last three fiscal years showed bacterial contamination, TRALI, and ABO hemolytic reactions to be the leading causes of deaths from transfusion. TRALI became the leading cause of fatalities reported to the FDA in fiscal 2. Fatalities were associated with fresh frozen plasma (FFP), red blood cells (RBCs) or platelets (2). Based on these data, it is clear that TRALI is one of the most significant complications of modern blood transfusion. This paper reviews what is known and unknown regarding the definition, mechanisms, incidence and clinical relevance of the syndrome. A. Definition. Practice Points. TRALI is a clinical diagnosis. Suspect TRALI when new ALI develops during or within six hours of transfusion. Rule out other ALI risk factors such as sepsis and aspiration. TRALI has been associated with all blood components that contain plasma. Transfusion of even part of one unit has been associated with TRALI1. Definition of ALIAccording to the American- European Consensus Conference of acute respiratory distress syndrome (3), the criteria for acute lung injury (ALI) are. Timing: Acute onset. Pulmonary artery wedge pressure: . Definition of clinical TRALIThe National Heart Lung and Blood Institute (NHLBI) Working Group on TRALI developed a definition (4). In patients with no ALI immediately before transfusion, and no other ALI risk factor (Table 1) is present, a diagnosis of TRALI is made if there is. New ALI after transfusion, and. The onset of symptoms or signs is during or within 6 hours after transfusion. The definition includes patients who are massively transfused who develop new ALI, and such patients may be at greater risk for TRALI as they receive multiple units. The definition excludes patients with ALI before transfusion; even though worsening of existing ALI after transfusion could be due to TRALI, defining this form of TRALI is problematic. In patients who have other ALI risk factors can also develop TRALI, and thus TRALI should not be excluded from consideration in these patients. The incidence of ALI in prospective studies of patient groups with ALI risk factors is less than 5. Table 1). Thus, the presence of an ALI risk factor does not mean the patient will definitely develop ALI. New ALI in a transfused patient with an ALI risk factor could be mechanistically due to the transfusion and/or the risk factor, i. TRALI and/or ALI due to the risk factor. In such patients who have another ALI risk factor, the diagnosis of TRALI can be difficult. The NHLBI working group recommended that critical care experts judge whether the new ALI is temporally associated with the transfusion, or whether the new ALI is temporally associated with worsening of the other ALI risk factor. The Canadian Consensus Conference proposed no such judgment evaluation and proposed the term “possible TRALI” for new ALI in a transfused patient who also has another ALI risk factor (5). Currently there is no definitive laboratory test for the diagnosis of TRALI. Leucopenia or neutropenia has been observed in case reports (6- 1. Leukocyte antigen- antibody match between donor and recipient (HLA class I or II, granulocytes or monocytes), and neutrophil priming activity in donor blood have been reported but are not diagnostic (1. Research Agenda. In patients with other ALI risk factors, research is warranted to determine whether transfusion contributes to new ALI, and whether ALI risk factors predispose patients to TRALIResearch is warranted to determine whether the mechanism of ALI after multiple transfusions is the same as the mechanism for TRALI after a single unit transfusion. Diagnostic laboratory tests for TRALI need to be evaluated in prospective studies. B. Mechanisms. Although the association of transfusion with lung injury has been observed for almost 3. In massive transfusion, the mechanism of lung injury was initially thought to be microaggregates in stored blood causing micro- pulmonary emboli and lung damage, but this theory has been discredited, since transfusion of stored blood through microaggregate filters has not prevented lung injury in animals (1. Pathologically, the disease involves sequestration of activated neutrophils within the pulmonary capillaries, leading to acute lung injury (1. The contribution of neutrophils to multiple types of acute lung injury is well understood and has been validated in several animal models (1. The major pathophysiologic question in TRALI then becomes how the transfusion is associated with or leads to wide spread neutrophil activation in these patients. In the past two decades, two hypotheses that lead to neutrophil activation in TRALI have been proposed: antigen- antibody hypothesis versus the two- event hypothesis. Recipient factors that may be involved in the pathogenesis include the recipient’s underlying condition and genetic predisposition. Donor unit factors that may be involved in the pathogenesis include leukocyte antibody, cytokines, lipids and factor(s) that increase pulmonary endothelial cell permeability. These hypotheses and factors are discussed below. The antigen- antibody hypothesis. The first evidence supporting this came from observation that classic findings of TRALI (including leukopenia) developed in a healthy volunteer injected with 5. This healthy volunteer was not ill and his neutrophils should not have been primed. In this case, leukocyte antibody alone seemed to cause TRALI. The evidence supporting immunologic activation of neutrophils by antibody revolves around the association of this disease with the presence of anti- HLA class I and II and anti- neutrophil antibodies in the donor units implicated in TRALI. The primary hypothesis is that the alloantibodies in the donor blood product directly activate either the patient neutrophils, monocytes or tissue macrophages, leading to initiation of the inflammatory cascade (2. Antibodies recognizing neutrophil HNA- 2a (CD1. HNA- 3 antigens have been implicated in cellular injury in both ex vivo perfused rat lung models and in cell culture models (2. In both cases, the evidence suggests direct binding of the antibodies to the neutrophils results in cellular activation leading to degranulation and respiratory burst responses, which in turn damage pulmonary endothelium. Donor alloantibodies may also attach directly to vascular endothelial cells, and thus form the equivalent of immune complexes, which in turn recruit circulating neutrophils and lead to sequestration/activation of these cells. This latter hypothesis is supported by the observation of a TRALI reaction occurring in only one lung following lung transplantation (suggesting that the alloantibodies recognized only new donor lung endothelium) (2. This mechanism of alloantibody mediated TRALI has also been modeled in mice, where is was demonstrated that recognition of endothelial bound anti- MHC- 1 m. Ab (the murine equivalent of anti- HLA Abs) by neutrophil Fc receptors caused neutrophil activation (degranulation/respiratory burst) and subsequent pulmonary damage (2. Interestingly, it has been observed that the presence of leukocyte antibodies in donors is common, while the occurrence of TRALI is uncommon, and thus antibody alone can not be the sole explanation for TRALI. The incidence of neutrophil antibody of 7. The incidence of HLA antibodies has been studied in female donors (not male) and the incidence is dependent on the technique used and donor parity. 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