Aktualny stan wiedzy na temat patofizjologii, diagnostyki i zapobiegania TRALI

Acta haematologica Polonica 07/2013; 44(3):274–283. DOI: 10.1016/j.achaem.2013.07.021

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.

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    ABSTRACT: Transfusion-related acute lung injury (TRALI) is usually reported after the transfusion of blood components from donors with white cell (WBC) antibodies, but only very rarely if the patient has these antibodies. The pathogenesis of TRALI is not fully understood. Not all transfusion recipients develop TRALI, even though WBC antibodies are present in the donor or the recipient. A patient with paroxysmal nocturnal hemoglobinuria (PNH) who developed TRALI after the transfusion of non-WBC-reduced red cells is described. Granulocyte-agglutinating anti-5b was detected in his serum, and the crossmatch with the donor granulocytes was positive. The patient also developed a severe exacerbation of hemolysis with renal failure; serologic results excluded an immune hemolytic posttransfusion reaction. The patient recovered from both events after about 1 week. Granulocyte-agglutinating antibodies present in the recipient play an important role in TRALI, and also other factors may contribute to its pathogenesis. The reaction between the PNH patient's antibody (anti-5b) and transfused WBCs was found not only to be responsible for the respiratory distress but also to have triggered, through the innocent-bystander mechanism of complement activation, an intensive hemolysis, which was very likely a contributing factor in the development of TRALI.
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    ABSTRACT: A case of transfusion-related acute lung injury (TRALI) that was successfully treated with extracorporeal membranous oxygenation (ECMO) is reported. A 58-year-old male patient underwent hepatectomy, and pulmonary edema occurred after the administration of fresh-frozen plasma and packed red cells. In the postoperative period, the impaired oxygenation progressively worsened, resulting in life-threatening hypoxemia, despite vigorous treatments. ECMO was therefore applied to the patient as a method of safe emergency support. Aggressive treatments under ECMO led to the successful improvement of the impaired oxygenation. TRALI is recognized as part of acute respiratory distress syndrome (ARDS). As a treatment for ARDS, ECMO does not cure the underlying disease of the lungs, however, with ECMO, TRALI, usually improves within 96 h with respiratory support. ECMO for TRALI-induced lethal hypoxemia is useful for providing time to allow the injured lung to recover. It is suggested that ECMO might be a useful option for the treatment of TRALI-induced, potentially lethal hypoxemia.
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    ABSTRACT: Transfusion-related acute lung injury (TRALI) is a form of posttransfusion acute pulmonary insufficiency that has been linked to the infusion of biologic response modifiers (BRMs), including antileukocyte antibodies and lipids. Soluble CD40 ligand (sCD40L) is a platelet-derived proinflammatory mediator that accumulates during platelet storage. We hypothesized that human polymorpho-nuclear leukocytes (PMNs) express CD40, CD40 ligation rapidly primes PMNs, and sCD40L induces PMN-mediated cytotoxicity of human pulmonary microvascular endothelial cells (HMVECs). Levels of sCD40L were measured in blood components and in platelet concentrates (PCs) implicated in TRALI or control PCs that did not elicit a transfusion reaction. All blood components contained higher levels of sCD40L than fresh plasma, with apheresis PCs evidencing the highest concentration of sCD40L followed by PCs from whole blood, whole blood, and packed red blood cells (PRBCs). PCs implicated in TRALI reactions contained significantly higher sCD40L levels than control PCs. PMNs express functional CD40 on the plasma membrane, and recombinant sCD40L (10 ng/mL-1 mug/mL) rapidly (5 minutes) primed the PMN oxidase. Soluble CD40L promoted PMN-mediated cytotoxicity of HMVECs as the second event in a 2-event in vitro model of TRALI. We concluded that sCD40L, which accumulates during blood component storage, has the capacity to activate adherent PMNs, causing endothelial damage and possibly TRALI in predisposed patients.
    Blood 11/2006; 108(7):2455-62. DOI:10.1182/blood-2006-04-017251 · 10.43 Impact Factor


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