Session 12RC1: Update on transfusion complications

Session 12RC1: Update on transfusion complications

Saturday 2 June, 1100-1145H, Auditorium 15

A comprehensive update on transfusion complications will be delivered on this first day of Euroanaesthesia by Dr Alexander Vlaar, Academic Medical Center, Amsterdam, Netherlands. “Blood transfusion can be life-saving but should also be regarded as a potential life threatening intervention,” explains Dr Vlaar. “The two leading causes of transfusion related mortality will be discussed. Transfusion-related acute lung injury (TRALI) and Transfusion associated circulatory overload (TACO).”

The incidence of TRALI is high and reported around 3-8% of transfused patients. TRALI is thought to follow a “two-hit” model. The “first hit” is the underlying condition of the patient which causes neutrophil priming in the pulmonary compartment (for example in cardiopulmonary bypass). The “second hit” is any transfusion resulting in activation of the primed neutrophils which subsequently results in pulmonary oedema, i.e. TRALI.

“The transfusion factors can be divided in antibody and non-antibody mediated factors. Antibody mediated TRALI is caused by the passive infusion of antibodies from the donor reacting with the cognate antigen of the recipient,” says Dr Vlaar. “Non-antibody mediated TRALI is thought to be caused by the accumulation of pro-inflammatory mediators during storage of cellular blood products. Preventive strategies for antibody mediation created in the past decade have been successfully implemented worldwide. Currently, no treatment options are available for this life-threatening syndrome.”

Dr Vlaar will highlight how, in contrast to TRALI, the pathophysiology of TACO is less clear. TACO is classically hypothesised to result from volume overload. The incidence of TACO is around 0.05-8% of patients transfused. The overall mortality is around 6.5% and major morbidity occurs in up to 40%. Specifically, critically ill patients, or those having underlying cardiac or renal failure seem prone to develop TACO. Observational data suggest that TACO also follows a “two-hit” model. The “first hit” is an underlying condition —such as cardiac failure (HF) or acute kidney injury (AKI) — resulting in poor compliance for fluid loading. The “second hit” is a transfusion. This may explain the high incidence among critically ill patients.

“However, just volume incompliance resulting in hydrostatic pulmonary oedema due to transfusion does not explain all TACO cases,” says Dr Vlaar. “Of interest, the introduction of leuko-reduced products resulted in a 50% decrease of TACO suggesting other pathways than volume overload being involved. All this circumstantial evidence suggests that other mechanisms may also be present in the onset of TACO. For example, transfusion products might induce direct endothelial damage through accumulation of pro-inflammatory mediators during storage, which in combination with increased vascular pressure results in the onset of pulmonary oedema. Currently, no evidence-based prevention or treatment strategy is available for this life-threatening syndrome.”