Transfusion‐associated circulatory overload ( TACO ): Time to shed light on the pathophysiology

Abstract

Transfusion‐associated circulatory overload ( TACO ) is the most frequent pulmonary complication of transfusion and one of the leading causes of transfusion‐related fatalities. TACO is characterized by new or worsening hydrostatic pulmonary oedema which occurs within 6 h of blood transfusion and results in respiratory distress. Major risk factors for TACO include cardiac failure, renal dysfunction and the degree of positive fluid balance. Suboptimal fluid management and inappropriate infusion practices have also been reported as risk factors for TACO . Unfortunately, the TACO pathophysiology is poorly understood. It can be hypothesized that the pathophysiology of TACO may be generally reflected by a 2‐hit model. The first hit in TACO may be represented by the poor adaptability for volume overload in the transfusion recipient, which is supported by the identification of cardiovascular and renal risk factors for the onset of TACO . The second hit may subsequently be conveyed by the transfused blood product. Remarkably, volume overload alone does not appear to be the only factor triggering the onset of TACO. It can be hypothesized that other factors in the transfused product may play a significant role. In addition, inflammation in the transfused recipient may also be an important feature in TACO . To obtain more insight into the TACO pathophysiology, it will be important to assess and validate potential biomarkers in TACO . In addition, development of currently unavailable TACO ‐animal models will provide a useful tool for dissecting the pathophysiologic mechanisms. Collectively, this will aid in improving diagnostic approaches and shed light on possible therapeutic interventions.