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Girnita DM Blood Transfusions


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Girnita DM Blood Transfusions

  1. 1. Blood Transfusion<br />Diana Girnita<br />MD, PhD<br />The Christ Hospital, Cincinnati<br />November 10th, 2010 <br />
  2. 2. Transfusion of Blood Cells<br /><ul><li>The transfer of blood or blood components from one person (the donor) into the bloodstream of another person (the recipient).
  3. 3. Transfusion is the first form of transplantation</li></ul>Donor – recipient from the same species = Allogeneic transfusions <br />Autologoustransfusions using the patient's own stored blood.<br />
  4. 4. Types of Blood Transfusion<br /><ul><li>Whole Blood
  5. 5. Blood Components
  6. 6. Red Blood cells
  7. 7. Platelets
  8. 8. Fresh Frozen Plasma
  9. 9. Leukocyte concentrate(granulocytes)
  10. 10. Plasma Substitutes (dextran, hydroxyethyl starch formulation - HES)</li></ul>!! Use of whole blood is considered to be a waste of resources !!<br />
  11. 11. Red Blood Cells<br /><ul><li>Symptomatic anemia or tissue hypoxia (providing oxygen-carrying capacity)
  12. 12. Transfusion trigger (HCT<30% ; HB<10g/dl)
  13. 13. 1 Unit increases 3% HCT or 1g/dl
  14. 14. Shelf life =42 d (1-6 ℃)</li></li></ul><li>Platelets<br /><ul><li>Bleeding due to critically decreased platelets < 10000/mm3
  15. 15. Functionally abnormal platelets.
  16. 16. Each unit increase 5,000 PLTs after 1 H</li></li></ul><li>Granulocytes<br /><ul><li>Profoundly granulocytopenia (<500/mm3)
  17. 17. Serious infection not responsive to antibiotic therapy</li></li></ul><li>Fresh Frozen Plasma (FFP)<br /><ul><li>Active / risk of bleeding due to deficiency of multiple coagulation factors, or due to a single coagulation factor deficiency
  18. 18. Severe bleeding due to warfarin therapy
  19. 19. Massive transfusion with coagulopathic bleeding.
  20. 20. Thrombotic thrombocytopenic purpura</li></li></ul><li>Plasma Substitutes (Volume Expanders)<br />Dextran<br /><ul><li>Most widely used
  21. 21. Low/Middle M.W. (40,000-70,000)</li></ul>Hydroxyethyl Starch Formulation (HES)<br /><ul><li>More stable
  22. 22. Containing essential electrolytes
  23. 23. No allergic reaction</li></li></ul><li><ul><li>No risk of infectious disease transmission
  24. 24. No transfusion reactions
  25. 25. No compatibility testing
  26. 26. An immediate source of autologousblood
  27. 27. Sportive medicine </li></ul>Autotransfusion<br />
  28. 28. Alloantigens represents the blood groups major barriers for transfusion<br />On RBCs - 30 major blood group systems and over 200 minor group systems<br />ABO molecules are glyco-sphingolipids (major histocompatibility antigens)<br />A and B = terminal sugars (A = N-Acetyl-Dgalactosamine; B = alpha-D-galactose)<br />Availability of blood donors – major limitation<br />ABO matching is also important in solid organ transplantation.<br />
  29. 29. Pre-Transfusion compatibility testing<br />Cross-matching = donor cells with recipient serum/ plasma<br />determines the blood group (ABO compatibility)<br />Alloantibodies<br />New methods: PCR with specific probes (DNA typing)<br />Serological Typing<br />CDC- Method or Hemmaglutination<br />
  30. 30. ABO Blood Types<br />The A Blood Type contains aprox. 20 subgroups (A1 =80% , A2 = 20%) are the most common (over 99%). <br />
  31. 31. 30 major blood group systems and over 200 minor group systems<br />Lewis<br />I <br />P <br />MNSs <br />Kell<br />Kidd<br />Duffy<br />The cell surface is a jungle!<br />
  32. 32. HLA -A and B are important in platelet transfusion; <br />HLA class I and II in neutrophil transfusion<br />N > 2400<br />
  33. 33. Transfusion Reactions<br />Infectious or Non-infectious<br />Acute or Chronic<br />
  34. 34. FDA report on fatalities following transfusions (2005-2008)<br />
  35. 35. Transfusion transmitted infections<br /><ul><li>HIV-1 and HIV-2
  36. 36. Human T-lymphotropic virus (HTLV-1 and HTLV-2)
  37. 37. Hepatitis B and C virus (responsible for >90% of post-transfusion hepatitis)
  38. 38. Treponemapallidum
  39. 39. Malaria
  40. 40. Chagas Disease
  41. 41. Creutzfeldt-Jakob Disease or "Mad Cow Disease"</li></ul>Over the past decade, the risk of transfusion-transmitted infectious decreased approx. 10,000- fold<br />
  42. 42. August, 2010 - New virus Linked to Chronic Fatigue Syndrome<br />
  43. 43. Noninfectious Serious Hazards of Transfusion <br />
  44. 44. Hemolytic transfusion reactions <br />Transfusion of RBCs to a patient with a preexisting antibody may cause a hemolytic reaction. <br />Acute hemolytic transfusion (within 24h): fever, chills, chest/back/abdominal pain, pain at the infusion site, dyspnea, hypotension, Hb-nuria, renal failure and DIC<br /><ul><li>Alloantibodies: IgM (anti-A and -B) or IgG
  45. 45. Transfusion of O plasma products with high titer anti-A or -B to nongroup O patients
  46. 46. Nonimmune-mediated: in vitro hemolysis(unit shipped or stored improperly)</li></li></ul><li>Hemolytic transfusion reactions <br />Delayed hemolytic transfusion (days to weeks)<br /><ul><li>the recipient has previously been alloimmunized to minor RBC antigens (pregnancy or transfusion)
  47. 47. alloantibodies (anti-Rh and Kidd antigens) are present in low levels; they are undetectable in the pretransfusion antibody screen.
  48. 48. there is a rapid anamnestic response after transfusion leading to hemolysis. </li></li></ul><li>Hemolytic transfusion reactions -treatment <br /><ul><li>Stop transfusion as soon as reaction is suspected, and replace the donor blood with normal saline.
  49. 49. Check the name, type and crossmatch
  50. 50. Renal protection - maintain urine output at 30-100 mL/h</li></ul>(aggressive fluid resuscitation, furosemide , low-dose dopamine - to improve renal blood flow.)<br /><ul><li>DIC Monitor</li></li></ul><li>Febrile Nonhemolytic Transfusion Reaction<br /><ul><li> >1°C increase in T° during/ soon after transfusion
  51. 51. Frequent with platelet transfusions, but declined with prestorageleukoreduction
  52. 52. Recipient alloantibodies(that react with antigens from the donor blood) and leukocyte-derived cytokines (released during storage) have been implicated</li></ul>Treatment:<br /><ul><li>Stop transfusion
  53. 53. Evaluate for hemolysis
  54. 54. Fever: acetaminophen</li></li></ul><li><ul><li>Uncommon, but deadly
  55. 55. Due to bacterial contamination
  56. 56. Platelets transfusion- more susceptible due to RT storage (Staphylococcus aureus, coagulase-negative staphylococci, diphtheroid bacilli, streptococci, and other skin flora)
  57. 57. RBCs transfusion (Yersiniaenterocolitica replicate at cold temperatures) </li></ul>Septic transfusion reaction<br />
  58. 58. Allergic Reactions<br />Minor allergic reaction<br /><ul><li>Hives /“urticaria”
  59. 59. Edema
  60. 60. Pruritis
  61. 61. Angioedema</li></ul>Treatment: <br /><ul><li>antihistamines
  62. 62. +/- stop the transfusion</li></ul>Anaphylactic reaction<br />(hypotension, bronchospasm, stridor, GI) <br />Causes: <br /><ul><li>IgA deficiency
  63. 63. anti-HLA antibodies
  64. 64. anticomplement antibodies</li></ul>Treatment:<br /><ul><li>Stop the transfusion immediately.
  65. 65. Support the airway and circulation
  66. 66. Administer epinephrine, diphenhydramine, and corticosteroids.
  67. 67. Maintain intravascular volume.</li></li></ul><li>Transfusion-related acute lung injury (TRALI)<br />Acute lung injury that develops due to the presence of anti-HLA antibodies and anti- Neutrophil Antigens (HNA) <br /><ul><li>with a clear temporal relationship to transfusion
  68. 68. in patients without alternate risk factors for acute lung injury</li></ul>In 2006, TRALI was the leading cause of transfusion-related death reported to the FDA<br />Underrecognition and underreporting<br />All plasma-containing blood and blood compartments may induce TRALI<br />
  69. 69. Sensitization mechanisms<br /><ul><li>Multiparous women (10-15% anti -HLA antibodies / pregnancy)
  70. 70. Previous transfusion
  71. 71. Transplantation</li></ul>TRALI- immune mechanism<br />
  72. 72. The antibody –dependent hypothesis<br />Anti-HLA or human neutrophil antigen (HNA) antibodies in the transfused component reacts with neutrophil antigens in the recipient (ie, when antileukocyte antibodies are transfused passively in a plasma-containing blood component)<br /> The recipient's neutrophils lodge in the pulmonary capillaries and release mediators that cause pulmonary capillary leakage.<br />As a consequence, many patients with TRALI will develop transient leukopenia.<br />TRALI- pulmonary edema with neutrophilic aggregates in the pulmonary vasculature<br />Cherry et al, Am J ClinPathol 2008;129:287-297<br />
  73. 73. The antibody –independent hypothesis<br />Occurs in patients with clinical conditions that predispose to neutrophil priming and endothelial activation: infection, surgery, or inflammation.<br />Bioactive substances (lipids) in the transfused component activate the primed, sequestered neutrophils and pulmonary endothelial damage occurs.<br />
  74. 74. TRALI-Clinical Presentation<br />Sudden onset, within 6 hours (usually within 1~2 hours) of respiratory distress after transfusion<br />
  75. 75. TRALI - Clinical Presentation<br />CXR: bilateral patchy alveolar infiltrates, normal cardiac silhouette and w/out effusions, consistent with ARDS<br />Labs: transient, acute neutropenia<br />Rapid Resolution , even when initial hypoxemia is severe<br /><ul><li>Most can be extubated within 48 hours
  76. 76. CXR return to normal within 4 days, although hypoxemia and pulmonary infiltrates may persist up to 7 days </li></li></ul><li>TRALI – Current Criteria of Diagnosis<br />Cherry et al, Am J ClinPathol 2008;129:287-297<br />
  77. 77. D/D: think more before TRALI<br />Underlying pulmonary disease<br />Underlying cardiac disease (CHF)<br />Transfusion- associated cardiac overload (TACO)<br />Severe allergic or anaphylactic reactions<br />
  78. 78. TRALI -Treatment<br /><ul><li>Supportive: oxygen, ventilator
  79. 79. Diuretic: conflicting reports!
  80. 80. Steroid?? – not randomized trials available
  81. 81. Fluid replacement (5% albumin) – improved oxygenation and hemodynamics</li></li></ul><li>TRALI -Prevention <br /><ul><li>Producing FFP only from male donors
  82. 82. Screening previously-pregnant and previously-transfused apheresis donors for HLA antibodies
  83. 83. Improving tests for the detection of leukokytesantibodies </li></li></ul><li>Transfusion associated circulatory overload (TACO)<br /><ul><li>TACO is due to circulatory overload
  84. 84. Incidence: aprox. 1% of transfusions
  85. 85. It is not an antibody-mediated phenomenon
  86. 86. Symptoms
  87. 87. Dyspnea
  88. 88. Tachycardia
  89. 89. Hypertension (Hypotension in TRALI)
  90. 90. Widened pulse pressure
  91. 91. Evidence of cardiac decompensation</li></li></ul><li>TACO -Diagnosis<br />CXR- presence of fluid, but cannot be distinguish of TRALI<br />Pulmonary edema protein content/ plasma protein content >0.75<br />BNP/ ANP pre- and post -transfusion values are increased; not in TRALI!!<br />
  92. 92. TACO- Risk Factors and Prevention<br />Increased risk in pts with<br /> cardiopulmonary compromise<br /> renal failure<br />infants or >60 yo<br />Prevention measures<br /><ul><li>Transfuse slowly (1 ml/min) or space units over time
  93. 93. Consider pre-transfusion diuretics
  94. 94. Watch fluid balance and monitor for at least 24H</li></li></ul><li>TACO - Treatment<br /><ul><li>Stop transfusion
  95. 95. Diuretics
  96. 96. Oxygen
  97. 97. Cardiac support
  98. 98. Assisted ventilation</li></li></ul><li>Transfusion Associated Graft versus Host Disease (TA-GVHD)<br /> Uncommon, TA-GVHD is often fatal (mortality over 90%). <br />The pathophysiology of TA-GVHD involves the proliferation and engraftment of immunocompetent donor T-lymphocytes, typically in an immunocompromised host incapable of clearing them. <br />Alternatively, TA-GVHD can occur in immunocompetent recipients whose HLA closely matches that of the donor (a so-called “one-way” HLA match), with donor cells being homozygous for a HLA type for which the recipient is heterozygous.<br />
  99. 99. EXAMPLE<br />Donor HLA-A1,-; B8,-; Cw7,-.(homozygosity)<br />Recipient HLA A1, A2; B8, B27; Cw7, Cw9.<br />No mismatched HLA in Host versus Graft Direction (A1, B8 and Cw7 are self HLA)<br />A2, B27 and Cw9 mismatches in GVH direction.<br />
  100. 100. Roles of CD4+ and CD8+ T cells in graft rejection<br />CD8 cells<br />Recognition of class I MHC molecules expressed on all donor tissue cells<br />Direct cytotoxic effects<br />Release of TNF+IFN augments macrophage activation and non-specific destruction<br />CD4 cells<br />Recognition of class II MHC molecules on passenger leukocytes (direct allorecognition) or infiltrating host DC (indirect allorecognition)<br />Help the activation of CD8 T cells<br />Release of TNF+IFN induces macrophage activation and non-specific destruction<br />
  101. 101. Types of Allorecognition<br />Direct – activation of recipient T cells by donor-derived professional APCs (dendritic cells) <br />Indirect – activation of recipient T cells by recipient-derived professional APCs.<br />The professional APCs that present the alloantigens also provide co-stimulatory signals that activate helper T cells and cytotoxic T cells.<br />
  102. 102. Two forms of TA -GVHD<br />Acute GVHD<br /><ul><li>During first 3 months post-transplant
  103. 103. Skin, GI tract, hepatosplenomegaly</li></ul>Chronic GVHD<br /><ul><li>After 3 months
  104. 104. Skin, Liver, GI tract
  105. 105. Similarities to connective tissue diseases (e.g. scleroderma)</li></li></ul><li>TA- GVHD- No treatment, just prevention!!!<br />High- risk individuals <br />intensive chemotherapy<br />immunodeficiency<br />Hodgkin’s disease<br />stem cell transplant<br />intrauterine transfusion<br />erythroblastosisfetalis<br />premature infants<br />Methods: Gamma- or UV-irradiation of cellular blood products (RBCs, platelets, and granulocytes), which renders donor lymphocytes incapable of proliferating.<br />
  106. 106. MICROCHIMERISM<br /><ul><li>Occurs when a small percentage of donor lymphocytes (typically <5%) persist in a recipient
  107. 107. The long-term consequences are unclear</li></li></ul><li>Metabolic Reactions<br />Sodium Citrate toxicity<br />used to prevent blood coagulation <br />metabolized by liver ; the metabolic capacity can be exceeded with large volumes of blood transfused. <br />increased levels of citrate hypocalcemia and hypomagnesemia (paresthesia, tetany, and arrhytmia), metabolic alkalosis (accumulation of bicarbonate - the metabolic derivative of citrate)<br /> <br />Hypothermia<br />associated with rapid transfusion of large amounts of cold blood<br />result in cardiac arrhythmias<br />Hyperkalemia– K level in the plasma increases during blood storage in a massive or rapid transfusion, particularly among premature infants and acidotic patients<br />
  108. 108. Rare complications<br />Transfusion Associated Air Embolism<br /><ul><li>Transfusion of blood under pressure using an open system
  109. 109. Symptoms : cough, dyspnea, chest pain , shock , death</li></ul>PosttransfusionPurpura (PTP)<br /><ul><li>5-10 days after; associated with platelets / packed RBCs/ plasma transfusion; a sudden decrease of the platelet s < 10,000/µL
  110. 110. Symptoms: hemorrhage (skin, epistaxis, GI, UT, most severe intracranial) 
  111. 111. Increased risk in individuals with h/o transfusion or pregnancy</li></ul>Iron Overload<br /><ul><li>repeated RBCs transfusions over a long period induce liver, heart, and kidneys damage.
  112. 112. Increased risk in thalassemia, SSD and myelodysplasia
  113. 113. Prevention:
  114. 114. minimization of RBCs transfusions
  115. 115. iron-chelating agents  </li></li></ul><li>Thank you!<br />