The incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of cardiac surgery patients: A prospective nested case-control study
ABSTRACT Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morbidity and mortality. Both antibodies and bioactive lipids that have accumulated during storage of blood have been implicated in TRALI pathogenesis. In a single-center, nested, case-control study, patients were prospectively observed for onset of TRALI according to the consensus definition. Of 668 patients, 16 patients (2.4%) developed TRALI. Patient-related risk factors for onset of TRALI were age and time on the cardiopulmonary bypass. Transfusion-related risk factors were total amount of blood products (odds ratio [OR] = 1.2; 95% confidence interval [CI], 1.03-1.44), number of red blood cells stored more than 14 days (OR = 1.6; 95% CI, 1.04-2.37), total amount of plasma (OR = 1.2; 95% CI, 1.03-1.44), presence of antibodies in donor plasma (OR = 8.8; 95% CI, 1.8-44), and total amount of transfused bioactive lipids (OR = 1.0; 95% CI, 1.00-1.07). When adjusted for patient risk factors, only the presence of antibodies in the associated blood products remained a risk factor for TRALI (OR = 14.2; 95% CI, 1.5-132). In-hospital mortality of TRALI was 13% compared with 0% and 3% in transfused and nontransfused patients, respectively (P < .05). In conclusion, the incidence of TRALI is high in cardiac surgery patients and associated with adverse outcome. Our results suggest that cardiac surgery patients may benefit from exclusion of blood products containing HLA/HNA antibodies.
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- "Vlaar i wsp.   oszacowali ryzyko występowania TRALI na 0,02% na każdą przetoczoną jednostkę krwi i na 0,16% u transfuzjonowanych chorych. U chorych w stanie krytycznym zwiększa się ryzyko wystąpienia TRALI (do 0,9% na przetoczoną jednostkę i do 2,2% u chorych). "
ABSTRACT: Transfusion-related acute lung injury (TRALI) is the leading cause of mortality following transfusion of blood components. Characteristic for TRALI is acute hypoxemia during or up to 6 h after transfusion provided that cardiogenic respiratory failure and transfusion-associated circulatory overload (TACO) are excluded. In this article we present: 1) Etiology and pathomechanism of TRALI syndrome including the numerous issues that are still unresolved. Currently accepted is the multiple-event model which involves both the patient and the transfused blood components. The TRALI syndrome may be either immunological or nonimmunological dependant on the various factors that activate neutrophils – the main cells in TRALI pathogenesis. 2) TRALI diagnosis should be based mainly on the clinical presentation due to the variety of pathomechanism of the syndrome; however testing of anti-leukocyte antibodies in transfused blood components, according to ISBT guidelines, is recommended in order to prevent TRALI incidence. 3) Different strategies of TRALI prevention, although up to date no ultimate provisions have been accepted. Transfusion of plasma collected only from men seems to be a promising solution as in many countries that adapted this preventive measure the number of TRALI cases has substantially decreased. 4) Different methods of proceeding with donors who donated blood components that were the cause of TRALI in transfused patients. It still remains an open question whether to defer donors with anti-leukocyte antibodies or multi pregnant women.Acta haematologica Polonica 07/2013; 44(3):274–283. DOI:10.1016/j.achaem.2013.07.021
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- "When activation status is too low, it is possible that priming factors in the transfusion are not strong enough to overcome the threshold. The threshold model may explain why the estimated incidence of TRALI is higher in cardiac surgery and critically ill patients    . These patients often suffer from an inflammatory condition, which may contribute to "
ABSTRACT: Purpose. Onset of transfusion-related acute lung injury (TRALI) is suggested to be a threshold-event. Data is lacking on the relation between titer of antibodies infused and onset of TRALI. We determined whether onset of TRALI is dependent on the titer of MHC-I antibodies infused in a combined model of ventilator-induced lung injury and antibody-induced TRALl. Methods. BALB/c mice were ventilated for five hours with low (7.5 ml/kg) or high (15 ml/kg) tidal volume. After three hours of MV, TRALI was induced by infusion of 0.5 mg/kg, 2.0 mg/kg or 4.5 mg/kg MHC-I antibodies. Control animals received vehicle. After five hours of MV, animals were sacrificed. Results. MV with high tidal volumes resulted in increased levels of all markers of lung injury compared to animals ventilated with low tidal MV. In ventilator-induced lung injury, infusion of 4.5 mg/kg of antibodies further increased pulmonary wet-to-dry ratio, pulmonary neutrophil influx and pulmonary KC levels, whereas infusion of lower dose of antibodies did not augment lung injury. In contrast, mice ventilated with low tidal volumes did not develop lung injury, irrespective of the dose of antibody used. Conclusions. In the presence of injurious MV, onset of TRALI depends on the titer of antibodies infused.Critical care research and practice 06/2012; 2012:720950. DOI:10.1155/2012/720950
Article: TRALI : aspects physiopathologiques[Show abstract] [Hide abstract]
ABSTRACT: Le TRALI (transfusion-related acute lung injury) est défini cliniquement comme un oedème pulmonaire lésionnel survenant dans les six heures suivant la transfusion d’un produit sanguin. C’est une cause majeure de morbimortalité liée à la transfusion. Sa physiopathologie est complexe et n’est pas totalement comprise. Le TRALI est le résultat d’une lésion de l’endothélium vasculaire induite par les polynucléaires. On distingue des formes liées à la présence d’anticorps antileucocytaires et des formes non immunologiques liées à des substances biologiquement actives qui pourraient apparaître lors de la conservation des produits sanguins. L’existence d’une leucostase pulmonaire liée à une agression inflammatoire chez le receveur constitue une étape de priming qui précède l’activation des polynucléaires et la lésion. Les patients de réanimation, compte tenu de ces mécanismes, semblent particulièrement exposés. Cette revue fait le point sur ces mécanismes physiopathologiques en s’appuyant sur les données épidémiologiques et expérimentales publiées.Réanimation 01/2011; 21(1). DOI:10.1007/s13546-011-0427-8