2/20/16 – Exposure to ABO-nonidentical blood associated with increased in-hospital mortality in patients with group A blood.

Pai M, Cook R, Barty R, Eikelboom J, Lee KA, Heddle N.

Transfusion 2015 Oct 15

PMID: 26472598 DOI: 10.1111/trf.13376

This observational study provides additional, powerful evidence that ABO non-identical transfusions (in this case red blood cells) may be associated with increased morbidity and mortality. Causality has not been proven, but there are few, if any, explanations that can account for these findings other than causality. A growing body of epidemiologic and laboratory data suggest that the concept of universal donor red cells (group O) and plasma (group AB) may not be a clinically valid approach, despite the absence of gross hemolysis.

Traditionally, and for almost 100 years, the absence of red urine or plasma has been taken as the sign that all is well when ABO mismatched transfusions are given. However, low levels of hemolysis from ABO non-identical transfusions, detectable when sensitive free hemoglobin assays rather than eyeballs are employed, may contribute to inflammation, thrombosis and mortality. Whatever the mechanism, this paper, and similar papers in the literature regarding ABO non-identical platelets and plasma, may well represent the “canary in the mine shaft” that our concepts of ABO universal donor red cells and plasma are in error. Low levels of hemolysis in sickle cell anemia and paroxysmal nocturnal hemoglobinuria appear to mediate inflammation, vascular dysfunction, organ injury and thrombosis. These natural models of the pathophysiology of low level hemolysis may be informative in understanding the effects of low levels of hemolysis after ABO non-identical tranfusions.