The recipe for TACO: A narrative review on the pathophysiology and potential mitigation strategies of transfusion-associated circulatory overload

Transfusion associated circulatory overload (TACO) is one of the leading causes of transfusion related morbidity and mortality. TACO is the result of hydrostatic pulmonary edema following transfusion. However, up to 50% of all TACO cases appear after transfusion of a single unit, suggesting other factors, aside from volume, play a role in its pathophysiology. TACO follows a two-hit model, in which the first hit is an existing disease or comorbidity that renders patients volume incompliant, and the second hit is the transfusion. First hit factors include, amongst others, cardiac and renal failure. Blood product factors, setting TACO apart from crystalloid overload, include colloid osmotic pressure effects, viscosity, pro-inflammatory mediators and storage lesion byproducts. Differing hemodynamic changes, glycocalyx injury, endothelial damage and inflammatory reactions can all contribute to developing TACO. This narrative review explores pathophysiological mechanisms for TACO, discusses related therapeutic and preventative measures, and identifies areas of interest for future research.