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What? How? What now? Part II Margo Rollins, MD Assistant Professor - PowerPoint PPT Presentation

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Transfusion Reactions: What? How? What now? Part II Margo Rollins, MD Assistant Professor of Pathology Emory University SOM Assistant Medical Director for Tissue, Transfusion & Apheresis Childrens Healthcare of Atlanta Immucor Webinar

  1. Transfusion Reactions: What? How? What now? Part II Margo Rollins, MD Assistant Professor of Pathology Emory University SOM Assistant Medical Director for Tissue, Transfusion & Apheresis Children’s Healthcare of Atlanta Immucor Webinar Series July 2018

  2. Disclosures • None Children’s Healthcare of Atlanta | Emory University

  3. Objectives • Define and categorize transfusion reactions • Describe clinical manifestations of specific transfusion reactions • Discuss patient evaluation and management when transfusion reaction is suspected Children’s Healthcare of Atlanta | Emory University

  4. Introduction • DDx of any untoward clinical event should always consider adverse sequelae of transfusion, even when transfusion occurred weeks earlier • No pathognomonic S/Sx that differentiates a transfusion reaction from other potential medical problems – Vigilance- during and after transfusion • Transfusion reactions are common, BUT uncommonly fatal – FDA receives ~40 reports/yr of fatalities attributable to transfusion Children’s Healthcare of Atlanta | Emory University Savage, W. 2016.

  5. Introduction • Transfusion reactions may be defined by case type, timing, severity, and imputability (the causal relationship of a reaction to transfusion) • Other classification schemes differentiate reactions by mechanism – Immunologic/non-immunologic – Type of blood component Savage, W. 2016. Children’s Healthcare of Atlanta | Emory University

  6. Background https://patientsafety.aabb.org/ NHSN Biovigilance Component Hemovigilance Module Surveillance Protocol v2.4 www.cdc.gov/nhsn

  7. Timing and manifestations of transfusion reactions

  9. Transfusion-related acute lung injury • The leading cause of transfusion-related death reported to the FDA – 2010-2014, 41% (72 of 176) of reported fatalities to the FDA were due to TRALI (Fatalities reported to FDA following blood collection and transfusion. http://www.fda.gov/downloads/BiologicsBloodVaccines/SafetyAvailability/ReportaProblem/TransfusionDonationFatalities/UCM459461.pdf. Accessed September 2, 2015.) – ~ 1/10,000 transfusions is complicated by TRALI (Toy P., Gajic O., Bacchetti P., et al: Transfusion-related acute lung injury: incidence and risk factors. Blood 2012; 119: pp. 1757-1767) • Symptoms – Mild dyspnea  severe noncardiogenic pulmonary edema • Patients require O2 support (many require mechanical ventilation) • Develops within 6 hrs of starting a transfusion (typically within 2 hrs) (Goldman M., Webert K.E., Arnold D.M., et al: Proceedings of a consensus conference: towards an understanding of TRALI. Transfus Med Rev 2005; 19: pp. 2-31). • Pulmonary edema is non-cardiogenic  classically no ↑ in cardiopulmonary pressures. – Chills – Fever – Hypotension • Because TRALI is hard to distinguish from fluid overload without CVPs, it is not straightforward to diagnose Children’s Healthcare of Atlanta | Emory University

  10. TRALI- 2 Hit Event • 1st hit- underlying clinical condition  sequestration and priming of neutrophils in the lung tissue • 2nd hit- transfusion of blood products containing anti-HLA or anti-human neutrophil antigen (HNA) antibodies activate neutrophils in the lung parenchyma  (Vlaar A.P., and Juffermans N.P.: Transfusion-related acute lung injury: a clinical review. Lancet 2013; 382: pp. 984-994; Peters A.L., van Hezel M.E., Juffermans N.P., et al: Pathogenesis of non-antibody mediated transfusion-related acute lung injury from bench to bedside. Blood Rev 2015; 29: pp. 51-61) – Previously pregnant women make anti-HNA and anti-HLA antibodies (Endres R.O., Kleinman S.H., Carrick D.M., et al: Identification of specificities of antibodies against human leukocyte antigens in blood donors. Transfusion 2010; 50: pp. 1749-1760) – Removal of female donors from the plasma pool  ~50% reduction in TRALI (Toy P., Gajic O., Bacchetti P., et al: Transfusion-related acute lung injury: incidence and risk factors. Blood 2012; 119: pp. 1757- 1767; Endres R.O., Kleinman S.H., Carrick D.M., et al: Identification of specificities of antibodies against human leukocyte antigens in blood donors. Transfusion 2010; 50: pp. 1749-1760) • Other antibody-independent mechanisms of TRALI – Aged blood products  accumulated bioactive lipids/ soluble mediators (CD40 L) that hamper chemokine scavenging ability of RBCs (2 nd hit) (Khan S.Y., Kelher M.R., Heal J.M., et al: Soluble CD40 ligand accumulates in stored blood components, primes neutrophils through CD40, and is a potential cofactor in the development of transfusion-related acute lung injury. Blood 2006; 108: pp. 2455-2462) – Lysophosphatidyl choline accumulation during storage  neutrophil priming substance (Silliman C.C., Fung Y.L., Ball J.B., et al: Transfusion-related acute lung injury (TRALI): current concepts and misconceptions. Blood Rev 2009; 23: pp. 245-255) Children’s Healthcare of Atlanta | Emory University

  11. TRALI- Management • HLA/HNA reactions are usually donor specific and should not recur with a different donor • Treatment is supportive – Glucocorticoids and diuretics have not been established to help (a positive fluid balance is a risk factor for TRALI) (Toy P., Gajic O., Bacchetti P., et al: Transfusion-related acute lung injury: incidence and risk factors. Blood 2012; 119: pp. 1757-1767). – Donors clearly implicated in TRALI reactions should be permanently deferred from blood donation Children’s Healthcare of Atlanta | Emory University

  12. Transfusion-associated circulatory overload • Hydrostatic transudate accumulation in the lungs • Consider in pts who develop sudden signs of fluid overload during transfusion including but not limited to: – Dyspnea – Jugular venous distention – Tachycardia – Congestive heart failure • At risk pts: compromised cardiopulmonary status  R/L sided heart failure (infants, elderly, pts with renal/heart failure) Children’s Healthcare of Atlanta | Emory University

  13. TACO- Management • Vastly underreported (Raval JS, Mazepa MA, Russell SL, et al. Passive reporting greatly underestimates the rate of transfusion-associated circulatory overload after platelet transfusion. Vox Sang 2015;108:387 – 92.) – ~1/100 transfusions • If TACO is suspected, the transfusion should be stopped  diuretics • For concerning pts: – Divide the product into aliquots for separate transfusions – Infusions in adults ≤ 3 mL/kg/hr (Pediatrics pts max 5ml/kg/hr) • The initial stages of TACO may be difficult to distinguish from other transfusion related reaction  N-terminal pro-brain natriuretic peptide (NT-pro-BNP) – NT-pro-BNP is at least 50% higher after transfusion than pre- transfusion levels – NT-pro-BNP is sensitive and specific for TACO (Tobian AA, Sokoll LJ, Tisch DJ, et al. N-terminal pro-brain natriuretic peptide is a useful diagnostic marker for transfusion-associated circulatory overload. Transfusion 2008;48:1143 – 50; 74. Zhou L, Giacherio D, Cooling L, et al. Use of B-natriuretic peptide as a diagnostic marker in the differential diagnosis of transfusion-associated circulatory overload. Transfusion 2005;45:1056 – 63.) Children’s Healthcare of Atlanta | Emory University

  14. Transfusion-associated graft versus host disease • Immunologically competent lymphocytes are introduced into a host who cannot inactivate the donor lymphocytes – The immunocompetent donor lymphocytes engraft  host HLA is presented to donor lymphocytes  activated lymphocytes attack host tissues • 2010-2014: 2 fatalities were reported to the FDA (http://www.fda.gov/downloads/BiologicsBloodVaccines/SafetyAvailability/ReportaProblem/TransfusionDonationFatalities/ UCM459461.pdf. Accessed September 2, 2015.) • Occurs after transfusion of non-irradiated cellular blood components • Much higher fatality rate than HSCT-related GVHD – Donor lymphocytes  recipient BM aplasia in addition to typical liver, gut, and skin manifestations of acute GVHD – In GVHD after BMT, the BM is of donor origin, and BM aplasia does not occur. – > 90% of cases are fatal 2/2 recipient BM aplasia Children’s Healthcare of Atlanta | Emory University

  15. TA-GVHD Management • Presentation – 8-10 days after transfusion – Marked pancytopenia, gut, skin, and liver (GVHD Ohto H, Anderson KC. Survey of transfusion- associated graft-versus-host disease in immunocompetent recipients. Transfus Med Rev 1996;10:31 – 43.) – S/Sx: N/V, anorexia, fever, diarrhea, liver dysfunction, and erythroderma – Pts often die of infection and hemorrhage (3-4wks) • NO EFFECTIVE TX (possible exception of BMT) • Haplo-identical directed donor units of blood  post- transfusion GVHD even in immunocompetent recipients, when donor and recipient share HLA types (Kopolovic I, Ostro J, Tsubota H, et al. A systematic review of transfusion-associated graft-versus-host disease. Blood 2015; 126:406 – 14.) • Using irradiated blood (2500 cGy) is recommended (pt receive directed blood transfusions from their relatives) • Leukocyte-reduction filters SHOULD NOT be used as prophylaxis Children’s Healthcare of Atlanta | Emory University

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