Hemolitik Transfüzyon Reaksiyonları

Yıl 2012, Cilt: 10 Sayı: 1, 127 - 132, 01.06.2012

Fatih Mehmet Azık İkbal Ok Bozkaya , Serdar Özkasap

Öz

Ölümcül hemolitik transfüzyon reaksiyonu prevalansı yaklaşık olarak ünite başına1:200000`dir. Kan ürünü alırken ya da yirmidört saat içinde ortaya çıkan hemolitiktransfüzyon reaksiyonu genellikle uygunsuz eritrosit süspansiyonu ve nadiren yüksekvolümlü plazma transfüzyonu sonrasında oluşur. Gecikmiş hemolitik transfüzyonreaksiyonu verici eritrositlerindeki antijenlere karşı ikincil immun yanıta bağlıdır.İnkomplet kompleman aktivitasyon sonucu C3b ile kaplı eritrositlerin makrofajlarcafagositozu ya da Ig G kaplı eritrositlerin direkt hücre hücre etkileşimi ile doğal öldürücühücrelerce yıkılması gibi farklı mekanizmalar intra ya da ekstra vasküler yıkıma yolaçar. Hemolitik transfüzyon reaksiyonları klinik sonuçları değişik patolojik yolaklarınçalışmasıyla olur. Anafilatoksin formasyonu, sitokinlerin salınımı, kinin sistemi,intrinsik koagülasyon kaskadı ve fibrinolizis aktivasyonu sonucu sistemik inflamatuaryanıt meydana gelir. Mikrosirkülasyonda bozulma sonucunda hipotansiyon, dissemineintravasküler koagülasyon, yaygın kanama, renal yetmezlik ve şok tablosu ortaya çıkar.Bu derlemede hemolitik transfüzyon reaksiyonu semptomları geliştiğinde yapılmasıgereken laboratuvar çalışmaları, tedavi yaklaşımı ve önlemek için neler yapılabileceği vurgulanmıştır

Anahtar Kelimeler

Transfüzyon reaksiyonu, eritrosit transfüzyonu, hemoliz

Hemolytic Transfusion Reactions

Öz

The prevalence of fatal hemolytic transfusion reactions HTRs is approximately1:200000 per unit. Acute HTRs occur during or within 24 h after administration of a bloodproduct. Transfusion of incompatible red blood cells RBCs , and, more rarely, of a largevolume of incompatible plasma usually are the causative agents. Delayed HTRs arecaused by a secondary immune response to an antigen on the donor’s RBCs. Differentmechanisms lead to intra- and extravascular hemolysis, such as complete complementactivation, phagocytosis of RBCs covered with C3b by macrophages after incompletecomplement activation, or destruction of RBCs covered only with IgG by direct cell tocell contact with K cells. The clinical consequences of HTRs are triggered via severalpathophysiological pathways. Formation of anaphylatoxins, release of cytokinescausing a systemic inflammatory response syndrome, activation of the kinin system, theintrinsic clotting cascade and fibrinolysis result in hypotension, disseminatedintravascular coagulation, diffuse bleeding, and disruption of microcirculation leadingto renal failure and shock. In this review, the symptoms of HTR are introduced,laboratory investigations and treatment are described, and some recommendations forprevention are given

Anahtar Kelimeler

Transfusion reaction, erythrocyte transfusion, hemolysis

Kaynakça

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