EM@3AM: Transfusion Associated Circulatory Overload

Author: Rachel Bridwell, MD (@rebridwell, EM Resident Physician, SAUSHEC / San Antonio, TX) // Reviewed by: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 67-year-old female with a history of congestive heart failure and CKD was brought in by ambulance from her nursing home for a gastrointestinal bleed. The patient’s total fluid balance from her nursing home was 2.5L over the past 24 hours. Her point of care hemoglobin is 4 g/dL and a transfusion of 2U pRBC and 1 FFP was initiated, though within approximately 1 hour of starting the transfusion, the patient became acutely short of breath.

Triage vital signs (VS): BP 147/92, HR 107, T 98.1 F, RR 40, SpO2 91% on 15L non-rebreather. She is in respiratory distress and has diffuse rales on pulmonary exam and diffuse tenderness on abdominal exam. You detect an S3, but the skin appears normal.

What’s the next step in your evaluation and treatment?

Answer: Transfusion Associated Circulatory Overload (TACO)1-20


    • Incidence of 1 in 356 per unit of component transfused1
      • Ranges from 1-8% in critically ill patients receiving blood2,3
      • Incidence of 3.0-5.5% in non-cardiac surgical patients4
    • Associated with increased ICU and hospital length of stays5,6
      • Mortality ranging from 5-15%6
    • Patient risk factors for TACO:1,2,4,5
      • History of pre-existing congestive heart failure
        • Left ventricular dysfunction present in 73% of cases2
      • Renal failure
      • Hemorrhagic shock
      • Coronary artery disease
        • 90% of patients had at least one of these risk factors7
      • Patients receiving multiple units transfused
    • Fresh Frozen Plasma often implicated, usually due to large volumes used2


Clinical Presentation:

    • Within the first 6 hours of transfusion the following typically appear:8
      • Acute respiratory distress
      • Evidence of hypoxemia
      • Radiographic evidence of pulmonary edema
      • Evidence of left heart failure
      • Evidence of circulatory overload
        • Elevated BNP
        • Positive fluid balance
        • Elevated CVP
      • Low suspicion for ARDS
        • 49% reduction in TACO with universal leukoreduction, suggesting immunologic/inflammatory factors involved9
          • Elevated IL-6 levels in TACO patients10



    • Assess ABCs and obtain VS to include manually counted respiratory rate
      • Tachypnea, tachycardia, wide pulse pressure, hypertensive or hypotensive2
        • Fever in 1/3 of patients11
    • Perform a complete physical examination
      • Pulmonary: rales, respiratory distress
      • Cardiac: S3, JVD
      • Check skin for petechiae and urticaria for other transfusion related issues
    • Acquire ECG, ABG
      • ABG allows PaO­­2/FiO2 to differentiate from TRALI
    • Differentiating from TRALI can be challenging
      • BNP to assess for TACO generates equivocal data and is only useful if pre-transfusion BNP is available12,13
        • If pre and post-transfusion BNPs are available, sensitivity and specificity are 81% and 89%, respectively13
        • Also help differentiated TRALI from TACO12
    • Chest radiograph to assess for pulmonary edema14
      • Point of care ultrasound may also be useful in these patients
    • Echocardiogram can show evidence of LV dilation, reduced EF14
      • Left atrial enlargement suggests chronically elevated pressures15



    • ABCs:
      • If transfusion is still ongoing, stop the transfusion
      • Sit upright to improve oxygenation16
      • Airway and oxygenation support often required for these patients16
        • NIPPV decreases rates of intubation14
      • Nitrates can reduce preload14
      • Diuretics
        • Furosemide is the choice diuretic, but dose varies17,18
          • Preload reduction via venodilation18
        • Pretransfusion diuretics do not demonstrate benefit in staving off TACO, and 40% who received diuretics progressed to TACO2
        • Hemodialysis can also be used19
    • Disposition: Admit to ICU
      • If all other treatments do not improve the patient’s condition, therapeutic phlebotomy can be considered20



    • Special care given to rate of transfusion in those especially with reduced left ventricular dysfunction as 73% of TACO patients have underlying LV dysfunction
    • In these patients, slowing rate of transfusion and limiting volume may reduce TACO2
    • Pre and post transfusion BNP helps distinguish from TRALI
    • Responds well to acute CHF management, early diuretics
    • Requires ICU management

Further Reading:

  1. Rana R, Fernández-Pérez ER, Khan SA, et al. Transfusion-related acute lung injury and pulmonary edema in critically ill patients: A retrospective study. Transfusion. 2006;46(9):1478-1483. doi:10.1111/j.1537-2995.2006.00930.x
  2. Li G, Rachmale S, Kojicic M, et al. Incidence and transfusion risk factors for transfusion-associated circulatory overload among medical intensive care unit patients. Transfusion. 2011;51(2):338-343. doi:10.1111/j.1537-2995.2010.02816.x
  3. Bierbaum BE, Hill C, Callaghan JJ, et al. An analysis of blood management in patients having a total hip or knee arthroplasty. J Bone Jt Surg – Ser A. 1999;81(1):2-10. doi:10.2106/00004623-199901000-00002
  4. Clifford L, Jia Q, Yadav H, et al. Characterizing the epidemiology of perioperative transfusion-associated circulatory overload. Anesthesiology. 2015;122(1):21-28. doi:10.1097/ALN.0000000000000513
  5. Murphy EL, Kwaan N, Looney MR, et al. Risk factors and outcomes in transfusion-associated circulatory overload. Am J Med. 2013;126(4):357.e29-357.e38. doi:10.1016/j.amjmed.2012.08.019
  6. Li G, Kojicic M, Reriani MK, et al. Long-term survival And quality Of life after transfusion-associated pulmonary edema in critically III medical patients. Chest. 2010;137(4):783-789. doi:10.1378/chest.09-0841
  7. Gosmann F, Nørgaard A, Rasmussen MB, Rahbek C, Seeberg J, Møller T. Transfusion-associated circulatory overload in adult, medical emergency patients with perspectives on early warning practice: A single-centre, clinical study. Blood Transfus. 2018;16(2):137-144. doi:10.2450/2017.0228-16
  8. Roubinian N. TACO and TRALI: Biology, risk factors, and prevention strategies. Hematol (United States). 2018;2018(1):585-594. doi:10.1182/asheducation-2018.1.585
  9. Blumberg N, Heal JM, Gettings KF, et al. An association between decreased cardiopulmonary complications (transfusion-related acute lung injury and transfusion-associated circulatory overload) and implementation of universal leukoreduction of blood transfusions. Transfusion. 2010;50(12):2738-2744. doi:10.1111/j.1537-2995.2010.02748.x
  10. Roubinian NH, Looney MR, Kor DJ, et al. Cytokines and clinical predictors in distinguishing pulmonary transfusion reactions. Transfusion. 2015;55(8):1838-1846. doi:10.1111/trf.13021
  11. Parmar N, Pendergrast J, Lieberman L, Lin Y, Callum J, Cserti-Gazdewich C. The association of fever with transfusion-associated circulatory overload. Vox Sang. 2017;112(1):70-78. doi:10.1111/vox.12473
  12. Li G, Daniels CE, Kojicic M, et al. The accuracy of natriuretic peptides (brain natriuretic peptide and N-terminal pro-brain natriuretic) in the differentiation between transfusion-related acute lung injury and transfusion-related circulatory overload in the critically ill. Transfusion. 2009;49(1):13-20. doi:10.1111/j.1537-2995.2008.01941.x
  13. Zhou L, Giacherio D, Cooling L, Davenport RD. Use of B-natriuretic peptide as a diagnostic marker in the differential diagnosis of transfusion-associated circulatory overload. Transfusion. 2005;45(7):1056-1063. doi:10.1111/j.1537-2995.2005.04326.x
  14. Murphy E, Roubinian N. Transfusion-associated circulatory overload (TACO): prevention, management, and patient outcomes. Int J Clin Transfus Med. April 2015:17. doi:10.2147/ijctm.s77343
  15. Gandhi S, Powers J, Nomeir A, et al. The pathogenesis of acute pulmonary edema associated with hypertension. New Engl J Med. 2001;344(1):17-22.
  16. Semple JW, Rebetz J, Kapur R. Transfusion-associated circulatory overload and transfusion-related acute lung injury. Blood. 2019;133(17):1840-1853. doi:10.1182/blood-2018-10-860809
  17. Klanderman RB, Attaye I, Bosboom JJ, Veelo DP, Geerts BF, Vlaar APJ. Transfusion-associated circulatory overload: A survey among Dutch intensive care fellows. Transfus Clin Biol. 2018;25(1):19-25. doi:10.1016/j.tracli.2017.11.001
  18. Andrzejewski C, Casey MA, Popovsky MA. How we view and approach transfusion-associated circulatory overload: Pathogenesis, diagnosis, management, mitigation, and prevention. Transfusion. 2013;53(12):3037-3047. doi:10.1111/trf.12454
  19. Agnihotri N, Agnihotri A. Transfusion associated circulatory overload. Indian J Crit Care Med. 2014;18(6):396-398. doi:10.4103/0972-5229.133938
  20. Adewoyin A, Oyewale O. Complications of Allogeneic Blood Transfusion: Current Approach to Diagnosis and Management. Int Blood Res Rev. 2015;3(4):135-151. doi:10.9734/ibrr/2015/17874


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