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Transfusion-associated circulatory overload (TACO) - a breathtaking syndrome.

Dr A.P.J. Vlaar

Duration:

Name researcher:

5 years

Amount granted:

€560.000

Year:

2019

Project number:

1931F

Personnel:

Prof Alexander P. Vlaar (0,2 fte, March 2020 - March 2025, Intensive Care medicine, Amsterdam UMC)
Technician: A. Bongers (0,8 fte, February 2021 - July 2022)
PhD student: Dr. Esther B. Bulle (1 fte, March 2020 - December 2022)
PhD student: Dr E. Lim (1fte, November 2022 - September 2023)
Technician: Polet (1 fte, December 2022 - October 2023)
Postdoc: Dr S.J. Raasveld (0,4 fte, October 2023 - December 2023)

Transfusion-associated circulatory overload (TACO) is one of the most serious complications of blood transfusion worldwide, associated with significant morbidity and mortality. This research focused on improving diagnosis, understanding underlying mechanisms, and developing strategies to prevent TACO.
Nationwide surveys among clinicians revealed large variations in transfusion practices and recognition of TACO. Many clinicians transfuse faster or in larger volumes than recommended by guidelines which increases the risk for onset of TACO. Furthermore, views on diuretic use differ widely—despite diuretics being central to current TACO treatment. These findings point to a lack of consensus in clinical practice.
Clinical studies showed that patients who develop TACO often have underlying heart or kidney conditions. Interestingly, they had a smaller fluid overload than patients with pulmonary edema not related to transfusion, suggesting a mechanism beyond volume excess. TACO patients showed elevated levels of inflammatory markers and indicators of endothelial damage, implying that inflammation and vascular injury may play a key role in its development. One particular marker, syndecan-1, was consistently elevated and may help identify patients at higher risk. Furthermore the results suggest there is an overlap between Transfusion Related Acute Lung Injury (TRALI) and TACO which was initially thought not to be possible.
Experimental models confirmed that pre-existing organ injury is necessary for transfusion to trigger pulmonary complications. Transfusion speed, rather than volume, was identified as a stronger modifiable risk factor. Diuretics such as furosemide were shown to lower pulmonary vascular pressure—possibly through vasodilation rather than fluid removal. In addition, stored blood products with reduced quality caused more endothelial damage, likely due to accumulated storage by-products.
Together, these findings contribute to safer transfusion and infusion practices and support the development of targeted preventive strategies for vulnerable patients.

THESIS 2024: Pathophysiological concepts in transfusion-associated circulatory overload - Esther Barbara Bulle

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