Abstract
Transfusion-associated circulatory overload (TACO) is one of the leading causes of transfusion associated morbidity and mortality. It occurs in 1 in 5,932 components transfused to 1 in 28,873 components issued in passive haemovigilance systems and 1–11% of patients in active surveillance studies highlighting a significant problem with under-recognition and under-reporting. The International Society of Blood Transfusion definition of TACO is acute or worsening respiratory compromise during or up to 12 hours after transfusion with two or more of the following criteria: evidence of acute worsening pulmonary oedema; evidence of cardiovascular system changes not otherwise explained (tachycardia, hypertension, jugular venous distension, enlarged cardiac silhouette and/or peripheral oedema); evidence of fluid overload; and elevation of B type natriuretic peptide levels to greater than 1.5 times the pre-transfusion value.1 Risk factors include increased age, heart disease or pre-existing heart failure and renal insufficiency.2 The pathophysiology, although likely predominantly due to fluid overload, may also include inflammatory mediators from the transfusion itself. Strategies to mitigate TACO include minimising the volume of transfusion, slowing the rate of transfusion, and potentially the use of diuretics.3 Studies exploring the role of diuretics are underway.
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