Background Transfusion‐associated circulatory overload (TACO) is a leading cause of transfusion‐related morbidity and mortality, yet it may be difficult to recognise in acutely ill patients without established cardiac or renal disease. In such cases, risk may reflect the interaction of biological vulnerability, inflammatory milieu, component‐related exposure and clinical workflow rather than transfused volume alone. Case Presentation We report a 52‐year‐old man with newly diagnosed acute myeloid leukaemia who developed acute hypertensive pulmonary oedema during plasma transfusion despite preserved systolic function. Pre‐event findings included bilateral pleural effusions, a moderate‐to‐large pericardial effusion without tamponade, systemic inflammation, thrombocytopenia and mildly abnormal coagulation parameters. Documented component and medication‐related fluid exposure was 1.82 L before deterioration and 1.82–2.14 L before/around onset. At onset, he developed sudden dyspnoea, hypertension, tachycardia and hypoxaemia, with SpO 2 81% on 3 L/min nasal oxygen. Post‐event imaging showed new bilateral pulmonary oedema and interstitial changes. NT‐proBNP increased from 971.7 to 2143 pg/mL, approximately 2.2‐fold. He improved after transfusion cessation, oxygen escalation and intravenous furosemide. Overall, the episode was clinically diagnosed as TACO rather than transfusion‐related acute lung injury or transfusion‐associated dyspnoea. Analysis The episode was best understood as a multi‐hit event. Pre‐existing effusions, systemic inflammation, repeated component and medication‐related exposure and incomplete reassessment between units narrowed the patient's reserve. The key issue was not volume alone, but the patient's reduced ability to tolerate further exposure. Clinical Implications This case supports a practical multiple‐hit approach to TACO prevention and recognition. Blood transfusion therapy should be managed as a dynamic intervention requiring repeated evaluation of indication, rate, volume and patient reserve. This approach may help clinicians stratify risk before and between units, recognise warning signs earlier and individualise transfusion practice.
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Ngo et al. (2026) studied this question.
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