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Transfusion Medicine: Transfusion Reactions and Massive Transfusion

Transfusion Medicine: Transfusion Reactions and Massive Transfusion. Annette J. Schlueter, MD PhD Department of Pathology University of Iowa. Nursing evaluation for suspected transfusion reaction. Systolic BP change > 30 mm Hg Fever >1 o C over baseline Chills

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Transfusion Medicine: Transfusion Reactions and Massive Transfusion

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  1. Transfusion Medicine: Transfusion Reactions and Massive Transfusion Annette J. Schlueter, MD PhD Department of Pathology University of Iowa

  2. Nursing evaluation for suspected transfusion reaction • Systolic BP change >30 mm Hg • Fever >1oC over baseline • Chills • Back, chest or abdominal pain • Headache • Dyspnea, cyanosis, O2 saturation <90% • Flushing • Hematuria • Anxiety • Diarrhea/vomiting

  3. Nursing response to suspected transfusion reaction • Stop the transfusion • Monitor vitals • Notify the MD • May restart transfusion for isolated mild urticaria • Send to the blood bank: • Blood administration set and remaining unit • Patient blood samples (heparin, EDTA tubes) • Electronic report of patient signs/symptoms • Send urine specimen to clinical laboratory

  4. Blood bank response to suspected transfusion reaction • No further blood products issued until initial workup is complete unless pathologist allows • Investigate all units transfused <2 h prior to the reaction • Quarantine any remaining RBC components from the suspect donation • Only if transfused product was RBC

  5. Blood bank initial transfusion reaction investigation • Hemolytic transfusion reaction? • Label accuracy: patient name and unit • Visual hemolysis in blood product (RBC components only) • Visual hemolysis in pre- and post-transfusion patient sample • Plasma free hemoglobin if post but not pre is pink/red • ABO/Rh on post-transfusion sample • Compare to pre-transfusion sample results • Direct antiglobulin test (DAT) on post-transfusion sample • If positive, perform also on pre-transfusion sample • Septic transfusion reaction? • Product appearance • Culture remaining product if s/sx support possible sepsis

  6. Blood bank further investigation for suspected hemolytic transfusion reaction • Repeat ABO/Rh testing on pre-transfusion sample • ABO/Rh testing on returned component • Forward or reverse typing as indicated by component • Elution on post-transfusion specimen if DAT was positive • Tests for Ab from patient stuck on transfused RBC • Antibody screen on pre- and post-transfusion samples • ID any positive result • Phenotype unit for corresponding antigen

  7. Immediate transfusion reactions • Hemolytic • Febrile • Allergic • Fluid overload (TACO) • TRALI (transfusion related acute lung injury) • Septic • Hypotensive

  8. Acute hemolytic transfusion reaction • Presentation: fever, chills, hypotension, chest/back pain • Generally evident within minutes of starting the transfusion • Due to induction of inflammatory cytokines, not simply free Hb • Incidence: • ABO incompatible: 1:200,000 transfusions • Non-ABO related: 1:105,000 transfusions

  9. Acute hemolytic transfusion reaction • Cause: preformed Ab in patient’s plasma causes intravascular lysis of transfused RBC • Due to anti-A or anti-B? Clerical error • Due to other Ab vs. RBC Ag e.g., anti-Kell

  10. Acute hemolytic transfusion reaction • Laboratory evidence of hemolysis: • Hemoglobinemia, hemoglobinuria • Persistent anemia • Transfused RBC do not raise the patient’s Hb •  LDH • Released from the hemolyzed RBC •  bilirubin, especially indirect (or unconjugated) • 6-12 h after transfusion • Product of heme metabolism, not yet solubilized (conjugated) for clearance • Undetectable haptoglobin • Removes free Hb from circulation for clearance by spleen

  11. Acute hemolytic transfusion reaction • Laboratory evidence of immune hemolysis: • Spherocytes on peripheral blood smear • Modification of Ab coated RBC during passage through spleen • Positive direct antiglobulin test • Detects Ab on (transfused) cells in patient’s circulation

  12. Acute hemolytic transfusion reaction • Laboratory evidence (continued): • Positive direct antiglobulin test (DAT; Direct Coombs test) • Identifies Ab on the transfused cells in the patient’s circulation

  13. Acute hemolytic transfusion reaction • Prevention: ensure accurate patient identification for pretransfusion sample and when administering the blood product

  14. Mechanical hemolysis • Similar to AHTR:  LDH,  bilirubin,  haptoglobin, persistent anemia, hemoglobinuria • Different from AHTR: NO fever, pain, hypotension, spherocytes; negative DAT • Generally not clinically significant • Causes: • Forced transfusion through small bore catheters • Warming RBC to >42o C • Mixing RBC with hypotonic solutions during infusion

  15. Febrile transfusion reaction • Presentation: isolated fever/chills • Incidence: 1:166 transfusions • Cause: release of inflammatory mediators (e.g., IL-1, IL-8) from WBC or platelets--> PGE2 production--> hypothalamic drive to increase body temperature • WBC or plts spontaneously release mediators in vitro (during storage) • Patient Ab to WBC or plts releases mediators in vivo • Prevention: • Antipyretics • May mask fever as early Sx of more severe transfusion reaction • Leukocyte reduction of RBC or platelets at collection

  16. Allergic transfusion reaction • Presentation: hives; rarely dyspnea, hypotension (anaphylaxis) • Incidence: • Hives: 1:344 transfusions • Anaphylaxis: 1:5000 transfusions • Cause: patient Ab to plasma proteins, rarely IgA • IgA reaction can occur with any blood product • Severe reactions seen in a minority of IgA deficient patients

  17. Allergic transfusion reaction • Laboratory evidence: • Tryptase (alpha and beta) drawn <4h after reaction • Prevention: • Washed RBC • Product from IgA negative donor (rarely, must have had previous transfusion reaction) • Treatment: • Antihistamines • Epinephrine

  18. Transfusion associated circulatory overload • Presentation: dyspnea, hypertension, tachypnea, pulmonary edema • Incidence: 1% of transfusions • Cause: too much volume infused rapidly • High risk patients have renal or cardiac insufficiency • Laboratory evidence: rising BNP • >1.5x pre-transfusion value • Can add BNP to sample drawn pre-transfusion

  19. Transfusion associated circulatory overload • Prevention: • Transfuse more slowly • Infusion rates for non-rapidly bleeding patients • RBC 240 ml/hr (4 ml/min) • Plasma 300 ml/hr (5 ml/min) • Concurrent diuretic administration • Furosemide IV vasodilates simultaneously

  20. TRALI • Transfusion associated noncardiogenic pulmonary edema • Presentation: • Acute lung injury within 6 h of transfusion, may require transient ventilator support • No residual respiratory compromise • Hypoxemia • PaO2/FiO2< 300 mm Hg • O2 sat <90% on RA • Other clinical evidence • Radiographic evidence of bilateral infiltrates • No evidence of circulatory overload

  21. TRALI • Incidence: • Risk highest with plasma but can occur with any blood product • 1:12,000 transfusions • Cause--two theories: • Donor anti-HLA or anti-leukocyte Ab reacting with patient WBC • Lipid mediator produced by donor leukocytes during blood product storage primes patient neutrophils to release vasoactive mediators after second stimulus (e.g., inflammation, infection) • Laboratory evidence: anti-HLA or anti-leukocyte Ab in donor plasma, with corresponding Ag on recipient cells

  22. TRALI • Prevention: • Do not collect plasma or platelets from previously pregnant females unless demonstrated to be HLA Ab negative • Plasma reduce platelet units/suspend in platelet additive solution? • Eliminate donors whose previous donations resulted in TRALI (even without documented anti-HLA or anti-leukocyte Ab) • Discard additional blood products from the same donation suspected of causing TRALI

  23. Transfusion associated dyspnea • Presentation: dyspnea within 24 h of transfusion • Doesn’t meet criteria for TRALI, TACO, or allergic reaction • Not attributable to underlying medical condition • Incidence: 1-2% of transfusion reactions • Some may have met criteria for other transfusion reactions if more information were available

  24. Septic transfusion reaction • Presentation: fever, chills, hypotension • Incidence: • 1:3000 units bacterially contaminated • 1:1x106 RBC, 1:100,000 plts lead to clinical sepsis • Cause: bacterial contamination of RBC or platelet product • RBC contaminants generally Gram - that grow at 4oC • e.g., Yersinia, Pseudomonas • Platelet contaminants generally Gram + that grow at RT • e.g., Staphylococcus

  25. Septic transfusion reaction • Laboratory evidence: Positive blood culture from patient that matches blood culture on blood product • Prevention: • Careful screening of blood donors for infection • Good (sterile) collection and storage techniques • Culture of all platelet units • Pathogen inactivation of platelet units

  26. Hypotensive transfusion reaction • Presentation: • Abrupt onset of hypotension early in the transfusion • Generally resolves when the transfusion is stopped • Lack of other signs/symptoms (e.g., fever, dyspnea) • Incidence: 1:5000 transfusions • Cause: • Bradykinin in the unit as a result of FXII activation during filtration for leukoreduction • Failure to rapidly degrade bradykinin due to ACE inhibitor in patient

  27. Hypotensive transfusion reaction • Prevention: • Discontinue ACE inhibitor while transfusions are anticipated • Use units collected by apheresis for transfusion

  28. Delayed transfusion reactions • Hemolytic • Hyperhemolysis (sickle cell disease) • Posttransfusion purpura • Graft vs. host disease (GVHD) • Iron overload • Transfusion transmitted viruses/parasites/prions

  29. Delayed hemolytic transfusion reaction • Presentation: Malaise, no severe symptoms • Incidence: 1:2500-11,000 transfusions • 25-50% clinically apparent • Cause: Primary or anamnestic (memory) Ab response to RBC Ag results in extravascular hemolysis of transfused RBC • Ab results from pregnancy or previous transfusion

  30. Delayed hemolytic transfusion reaction • Laboratory evidence: •  Hb days to weeks after transfusion of RBC • Differential: bleeding, other etiologies of hemolysis • Positive direct antiglobulin test (DAT) • Appearance of new RBC Ab •  conjugated (direct) bilirubin • Hemoglobinemia/hemoglobinuria are unusual

  31. Delayed hemolytic transfusion reaction • Prevention: Educate patient about any anti-RBC Ab detected during pretransfusion testing so they can inform future health care providers • Ab may be undetectable at time of future transfusion • Important to identify DHTR to avoid unnecessary workup for bleeding

  32. Hyperhemolytic transfusion reaction • Presentation/laboratory evidence: • Falling Hb 4-10 d. after transfusion to lower than pre-transfusion levels in sickle cell patient • Marked reticulocytopenia • No new RBC alloantibodies • Negative direct antiglobulin test • No rebound of HbS level following hemolysis • Supports loss of patient’s cells • Incidence: 4-11% of transfused SCD patients

  33. Hyperhemolytic transfusion reaction • Cause: Destruction of transfused and autologous RBC and reticulocytes • Defective complement activation • Excess phagocytosis by macrophage hyperactivation • Treatment: • IVIG • IV steroids • Limit further transfusions

  34. Posttransfusion purpura • Presentation: • Bruising/bleeding 1-3 wk after blood product transfusion • Profound thrombocytopenia • Incidence: 1:57,000 transfusions • Cause: Patient Ab to platelet Ag, induced by transfusion, that crossreact with autologous platelets (?)

  35. Posttransfusion purpura • Laboratory evidence: • Profound thrombocytopenia (often <15K) • Normal RBC morphology • Anti-platelet (allo-)antibodies • Lack of corresponding Ag expressed by patient • Prevention/Treatment: • NO platelet transfusion except for life-threatening bleed • IVIG to prevent splenic clearance of platelets • Avoid future transfusions

  36. Transfusion associated GVHD • Presentation: • Fever, skin rash, diarrhea, hepatitis, AND marrow aplasia • 10-12 d after transfusion • Incidence: 1:1.3 x 107 Tx • Cause: Infusion of T cells that recognize patient cells as foreign, while patient T cells don’t recognize donor cells as foreign

  37. Transfusion associated GVHD • Treatment: nothing effective, >95% lethal due to BM failure • Prevention:Irradiate cellular blood products (at least 2500 cGy) orpathogen inactivation (platelets) for • Significantly immunocompromised patients • Not HIV or organ transplant patients • Recipients of blood products from 1st degree relatives

  38. Iron overload • Presentation: High ferritin, eventual hemosiderosis in heart, liver, pancreas • Cause: numerous chronic RBC transfusions without blood loss • Aplastic anemia, sickle cell disease, thalassemias • 1 ml of RBC=1 mg Fe • Prevention/treatment: • RBC exchange or depletion/exchange rather than simple transfusion for qualitative RBC defects e.g., sickle cell disease • Chelation therapy (deferoxamine, deferasirox) • Phlebotomy if Hct allows

  39. Transfusion transmitted infections • Risks of transfusion associated infections • Blood screened by history and laboratory testing for: • HCV 1:2.3 x 106 • HIV 1:2.8 x 106 • HBV 1:2 x 106 • HTLV 1:3 x 106 • WNV (West Nile Virus) <1:3 x 106 • Chagas’ disease (T. cruzi) <1:3 x 106 • Syphilis (theoretical risk from plts) • Zika <1:3 x 106 • Death from Tx reaction: 1:400,000

  40. Other transfusion transmitted infections • Screening by history only for • Malaria <1:3 x 106 • Creutzfeld-Jacob disease (theoretical risk) • Gonorrhea • Babesiosis • Many other organisms reported to be transmitted by transfusion • CMV prevented by leukoreduction of cellular blood products

  41. Definitions of massive transfusion • Replacement of 1 blood volume in 24 hours • Replacement of 50% of blood volume in 3 hours • Transfusion of >20 U PRBC • 4 units of blood in 1 hour with anticipated additional usage

  42. Blood products for massive transfusion • Massive Transfusion Protocol • ETC • 4 uncrossmatched O neg RBC for females • 4 uncrossmatched O pos RBC for males • 3 A plasma • OR 4 uncrossmatched O neg RBC, 3 A plasma • Females <50 eligible for 10 O neg RBC • O pos uncrossmatched RBC • Type compatible, uncrossmatched RBC and type specific plasma • Goal: type compatible, crossmatched RBC units

  43. Expected PRBC preparation times • O pos uncrossmatched units: 5-7 min • Type specific uncrossmatched units: 10-12 min • Type specific crossmatched units • 45 min if no RBC antibodies • 90 min if RBC antibodies are present

  44. Massive Transfusion Protocol Continue for up to 20 sets (80 RBCs, 60 plasma, 10 plts, 9 cryo pools) Could compromise plt inventory—be prepared to discuss If inventory is good, path resident called for 6thplt unit Cryo prepared only after confirmation it is wanted Recommend transfusion of entire set before moving to next set Give plts or cryo before RBC and plasma in each set

  45. Etiology of problems attributable to massive transfusion • Hyperkalemia (PRBC) • Ionized hypocalcemia • Citrate in plasma (and platelets) • Hypothermia (PRBC, plasma) • Antibody mediated transfusion reactions (PRBC) • ABO incompatible RBC transfusion • Hemolytic transfusion reaction (HTR) due to non-ABO RBC antibody

  46. Potassium balance • RBC lose K+ to additive solution in PRBC unit • RBC membrane ATPase inactivation by cold • RBC rapidly regain intracellular K+ following transfusion • Excess K+ cleared renally • Net clinical effect: no predictable change • Monitor K+ in rapidly transfused patients

  47. Populations at risk from transfusion-associated hyperkalemia • Hyperkalemia likely in • Neonates with rapid transfusion • Hyperkalemia possible with • Combination of acidosis, hyperglycemia, hypocalcemia, hypothermia, central line used for transfusion • Underlying renal insufficiency • Severe tissue injury with rhabdomyolysis

  48. PRBC units with reduced potassium content • <7 day old units • Rapidly available, may be in short supply • Washed units • 45 min TAT per unit, virtually unlimited supply • Concentrated PRBC units • Faster than washing, virtually unlimited supply • Does not remove K+ as completely as washing

  49. Citrate toxicity (hypocalcemia) • Risk highest with plasma, platelets • Rapid metabolism • No accumulation until > 1u/5 min • Increased risk in patients with impaired liver function • Perioral or digit tingling, N/V, anxiety, etc. • Cardiovascular toxicity • Long QT intervals, depressed ventricular contractility, V fib • Occurs before coagulation effects • Potential for hypomagnesemia

  50. Treatment of citrate toxicity • Slow the infusion rate • Cagluconate or CaCl2 IV

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