Blood transfusions

  1. What is unique about Hep D?
    Hep D is structurally unrelated to A, B, or C. Unique infection that requires a co-infection w/Hep B (otherwise Hep D virus can’t replicate and infect the liver cells).
  2. Out of all the viruses that can be transmitted via a transfusion. What is the most common?
    Hepatitis B
  3. Hep C is mild in the beginning but then what happens?
    • it will progress to chronic state in 85% w/significant morbidity and mortality.
    • 20% of chronic carriers of Hep C will develop cirrhosis and 1-5% will develop cancer of the liver.
  4. How do we screen for Hep A?
    donor history alone (it has a rare transmission rate)
  5. What is HTLV?
    • Human T cell lymphotrophic virus (same retrocyte family as HIV)
    • Incidence of transmitting a disease from this virus is low.
    • This is associated w/t cell lyphoma and leukemia
  6. Which type of HIV is screened? 1 or 2?
    Both! Screening test is for HIV 1 and 2 but usually 1 is the cause of the disease
  7. What is the transmission rate of CMV?
    7% if donor blood is not leukocyte reduced
  8. CMV is usually benign so why do we screen for it?
    • Can be fatal if pt is immuno-compromised premature neonates, anyone who underwent bone marrow transplant, pregnant females and anyone w/a depressed immune function.
    • So the whole idea of leukocyte reduction comes into play here...
  9. What is leukocyte reduction?
    take out majority of WBC and then transfuse RBC
  10. Why is it so important to do leukocyte reduction and remove WBC prior to transfusions?
    • WBC area associated w/non hemolytic transfusion reactions and the TRALI.
    • Also CMV, Epstein bar and HTLV virus transmission.
  11. Bacterial contamination is much more common than other associated diseases. Can develop sepsis and mortality. Which kind of blood product is more common to have bacterial infections?
    More w/platelets than PRBCs because platelets are stored at room temp. Also more common w/pooled platelets.
  12. What type of transfusion reaction is most problematic?
    immediate acute hemolytic transfusion reaction (AHTR)
  13. How often does AHTR happen?
    • 1/25,000
    • Miller: with type it is 1/1000 and w/type&screen it's 1/10,000
  14. What can happen in AHTR?
    Can lead to acute RF and DIC. Mortality rate is about 2%
  15. What is typing and what is screening?
    • Type: ABO and Rh
    • Screen: antibodies in recepient
  16. Where are the antibodies found?
    In the plasma
  17. Beyond ABO and RH system there are multiple other antigens and antibodies that are possible. Some of the more common antibodies and antigens that can generate and cause common transfusion reactions are....
    Antigens: A,B, Kell, Kidd, Duffy, SsRh Antibodies: anti-D, anti-Cc, anti-Ee
  18. What is the incidence of Delayed hemolytic transfusion reactions?
    1 /2000 – 1/2500
  19. What is a delayed hemolytic transfusion reaction?
    • Antibodies against Kell, Kidd, Duffy, Rh
    • Anamestic response: renewed production of an antibody on second exposure
    • The result of the donor antigen to pt has previously been exposed to that antigen (prior transfusion or as a result of pregnancy) thus already created antibodies so has a reaction w/the 2nd exposure
  20. Delayed hemolytic transfusion reactions usually involve minor antibodies like....
    Antibodies against Kell, Kidd, Duffy, Rh
  21. TRUE or FALSE. Delayed hemolytic transfusion reactions are mild and usually self limiting
  22. Describe the mechanism of AHTR
    Incompatible blood administered→Antibodies & complement in recipient plasma attack donor antigens→Hemolysis→Factor XII activated → bradykinin produced → ↑ capillary permeability, arteriolar dilation → ↓BP →Activation of complement → histamine & serotonin release → bronchospasm
  23. What % of patients end up w/DIC after AHTR?
  24. What are the symptoms of AHTR?
    • Fever & chills
    • N/V/D
    • Hypotension & tachycardia
    • Flushing & dyspnea
    • Chest pain & back pain
    • Oliguria
    • Diffuse bleeding
  25. What is the treatment of AHTR?
    • Stop transfusion & recheck patient & donor unit ID and labeling
    • Return unit to BB with sample from patient
    • Support BP
    • Prevent renal failure (adequate hydration)
    • Prevent DIC (supporting CO, preventing stasis and hypoperfusion)
    • Establish baseline labs (coag and renal tests)
  26. What symptoms of AHTR will we see under GA?
    hypotension, tachycardia, fever
  27. What can we do if a patient has recurrent minor reactions to donor proteins??
    • Usually isolated events but if pt seems to develop these recurrently, may want to give washed RBC.
    • Washing doesn't help w/platelets or FFP (Give Benadryl or hydrocortisone 1hr prior to transfusion)
  28. Minor reactions to donor proteins are commonly associated with....
    How are they treated?
    • FFP and platelets
    • Can usually be treated w/Benadryl.
  29. What is the incidence of mild reactions to donor proteins?
    Reaction can vary from mild urticaria occuring anywhere to 0.5-4% of all transfusions to anaphylaxis
  30. Pt who receive multiple transfusions of RBC or platelets often develop antibodies to human leukocyte antigens (WBC antigens).What is the % of reactions in a patient receiving platelets?
    These reactions can occur in up to 2% o pt receiving platelets.
  31. TRUE or FALSE. Reaction to donor proteins are always mild
    FALSE. They can be minor to Anaphylaxis. The anaphylactic type of reaction to donor proteins are less frequent but more severe  (bronchospasm, hypotension, etc.) usually in pt who have been sensitized by prior transfusion or by pregnancy.
  32. Does washing help platelets?
    No, washing doesn’t help w/plts so susceptible pt w/plts and FFP may get Benadryl and hydrocortisone an 1 hr prior to transfusion.
  33. What types of white cell reactions are there?
    • Febrile
    • TRALI
    • Graft-vs-host disease
    • TRIM
    • Transfusion-induced inflammatory response
  34. What would you see in a febrile white cell reactions
    • Temp will go up by more than 1 degree within 4 hrs of the transfusion and goes away within 48 hrs.
    • Other s/s of febrile reaction can also occur so chills, resp distress, cough, anxiety.
    • Leukocyte reduction will decrease or prevent these types of reactions.
  35. What is the #1 cause of mortality associated w/a blood transfusion?
    TRALI: WBC reactions
  36. What is TRALI?
    • Non cardiogenic form of pulmonary edema resulting after transfusion of a blood product.
    • It’s associated w/all plasma containing blood components.
    • More common in FFP and platelets but RBC too
  37. What is the incidence of TRALI?
    • variable but 1/5000
    • Thought to be under reported and unrecognized
  38. What are the symptoms of TRALI?
    • symptoms begin within 6 hr following transfusion
    • Dyspnea, chills, fever and non cardiogenic pulmonary edema.
    • CXR will show bilateral infiltrates
    • Pt may be hypo or hypertensive
  39. What is the diagnostic criteria for TRALI?
    • Acute onset of hypoxemia (6hr following trans)
    • Bilateral infiltrates consistent w/acute lung injury
    • Absence of LA HTN
    • No other apparent causes of acute lung injury
  40. What is the treatment for TRALI?
    • Tx is supportive, oxygen, ventilation PRN (low TVs).
    • Diuretics aren’t indicated even though it’s pulmonary edema.
    • Steroids have been used but evidence not really supporting use.
  41. Could graft vs host happen after a transfusion of FFP?
    • No!
    • Occurs only after transfusion of cellular components so not w/FFP and cyro but plt and PRBC.
  42. Describe the acid base changes that occur with blood transfusions
    Acid base changes occur because the pH in unit of blood drops to around 7 when the solution (Citrate phosphate Dextrose solution) to keep blood from clotting is added and drops even more (stored over 21 days) over that time period of storage it drops even more
  43. When does GVHD occur?
    typically occurs someone who is immunocompromised (post organ transplant). Because PRBC and Plt have significant # of donor lymphocytes, they generate an immune response in compromised patient.
  44. What can we do to prevent GVHD
    Leukocyte reduction may help but irradiation of cellular components is only effective means of prevention, mortality rate if it does develop is very high.
  45. What is TRIM?
    • transfusion related immunodulation
    • Means giving a transfusion will alter the immune responsiveness in the patient.
    • Because of this there may be increased mortality, an accelerated recurrence of cancer, increased infection rates overall, possibility more rapid progression of HIV or AIDS.
  46. What other WBC reaction is similar to TRIM?
    TIIR: talking about inflammatory response instead of immune processes but very similar.
  47. List all the non-infectious risks of blood transfusion
    • Hypothermia
    • Volume overload
    • Dilutional coagulopathy
    • ↓ 2, 3 – Diphosphoglycerate
    • Acid-base changes
    • Hyperkalemia (up to 19 -35 mEq/L in 21 days)
    • Citrate intoxication
    • Microaggregate delivery
  48. 1u of PRC of 4° centigrade, that will reduce core temp of 70kg pt by about how much???
    • ¼ degree centigrade.
    • Arrhythmias, decreased clotting etc. can occur.
  49. Why is it important to know that 2,3 DPG decreases with blood transfusions?
    • 2,3 DPG: left shift in O2 Hb curve.
    • So w/transfusions there are more Hb available but less efficiency in O2 delivery
  50. Why could we see hyperkalemia with blood transfusions?
    • Over time the stored blood cells loose potassium, moving out of cells.
    • Can occur w/rapid transfusers.
  51. What is important to know about the Citrate that is added to blood to keep it from clotting?
    • Temporary decrease in iCa (binds to Ca) shouldn’t occur unless transfusion exceeds 1unit/5min in average adult.
    • Citrate is metabolized in liver, if liver disease then citrate intoxication can occur.
  52. The blood that stored, the longer it is, the more microaggregates (including platelets aggregates), what can we do to prevent these from reaching the patient?
    • Filter it! (170micron filter), gets out the larger aggregates.
    • Delivery of microaggregates may be leading to TRALI (some evidence)
  53. Why is it so important to give type specific blood even if the patient is AB (universal recepient?)
    Still have small amount of antibodies (in O blood) in the donor blood so type specific is preferred
  54. For type O blood:
    What is the antigen on RBC?
    What are the antibodies in plasma?
    First choice for blood transfusion?
    2nd choice for blood transfusion?
    • Antigen on RBC:None
    • Antibodies in plasma: Anti-A & B
    • 1st choice: O
    • 2nd choice: O
  55. For type A blood:
    What is the antigen on RBC?
    What are the antibodies in plasma?
    First choice for blood transfusion?
    2nd choice for blood transfusion?
    • Antigen on RBC: A
    • Antibodies in plasma:anti-B
    • 1st choice: A
    • 2nd choice: O
  56. For type B blood:
    What is the antigen on RBC?
    What are the antibodies in plasma?
    First choice for blood transfusion?
    2nd choice for blood transfusion?
    • Antigen on RBC: B
    • Antibodies in plasma: anti-A
    • 1st choice: B
    • 2nd choice: O
  57. For type AB blood:
    What is the antigen on RBC?
    What are the antibodies in plasma?
    First choice for blood transfusion?
    2nd choice for blood transfusion?
    • Antigen on RBC: A&B
    • Antibodies in plasma: none
    • 1st choice: AB
    • 2nd choice: A, B, and O (in that order)
  58. What is the incidence of Type O blood in whites and blacks?
    • Whites: 45%
    • Blacks: 49%
  59. What is the incidence of Type A blood in whites and blacks?
    • Whites: 40%
    • Blacks: 27%
  60. What is the incidence of Type B blood in whites and blacks?
    • Whites: 11%
    • Blacks: 20%
  61. What is the incidence of Type AB blood in whites and blacks?
    • Whites: 4%
    • Blacks: 4%
  62. TRUE or FALSE. If recipient has to receive a component of different type ABO group, only PRBC can be given because of the antibodies in the plasma
  63. Can we give Rh- blood to an Rh + patient?
    Yes but we try to reserve the Rh- for the patients who are Rh- (because they can't receive Rh+)
  64. Why is plasma frozen (FFP)?
    In order to preserve the two labile clotting factors (5&8) its frozen promptly and thawed only immediately before administration.
  65. What is the incidence of Rh (D) in Whites and Blacks? What is the antigen on the RBC?
    • Whites: 85%
    • Blacks: 92%
    • Antigen: D
  66. What is an immediate spin cross match?
    • They separate out, spin the donor blood and the patients blood and they’ll mix the donor serum w/the patient’s cells and the donor cells w/the patients serum.
    • Looking for any reactivity in major and minor cross match.
    • Mix together spin down and look to see if any agglutination, look at it immediately.
    • Referred to as abbreviated cross match
  67. How effective and safe is the immediate spin cross match?
    Studies show it’s safe and effective 99.9% effective in preventing incompatible transfusion
  68. What are the 2 main functions of the cross match itself?
    • Final check of ABO compatibility
    • Help detect presence of any of theses antibodies in the patients serum that might react w/donor cells.
  69. What is the anti-human globin cross match?
    • Continues immediate spin w/incubation at 37°C then finishes w/an anti-human globulin (more sensitivity).
    • It will enhance or bring out any small antigen antibody action to a level that we can detect it.
  70. What is the transfusion trigger for a stable, general med/surg patient? What about a cardiac patient?
    • Stable, general medical-surgical patient = 7 g/dl
    • Cardiac patient = 10 g/dl
  71. Increased oxygen demand will decrease anemia tolerance. What types of conditions may cause this increased O2 demand?
    • Hyperthermia
    • Hyperthyroidism
    • Sepsis
    • Pregnancy
  72. Limited ability to increase CO will decrease anemia tolerance. What types of conditions may cause this?
    • CAD, myocardial dysfunction
    • Beta blockade
    • Inability to redistribute C.O.
    • Low SVR states (sepsis, post-CPB)
  73. TRUE or FALSE.Occlusive vascular disease (cerebral, coronary) may decrease anemia tolerance
  74. What can cause a left shit in the O2 hemoglobin association curve and cause a decrease in anemia tolerance?
    • Alkalosis
    • Hypothermia
  75. Abnormal Hemoglobins may decrease anemia tolerance. What types of abnormalities are there?
    • Recent transfusion (↓ 2, 3-DPG)
    • HGB S (sickle cell disease)
    • Acute blood loss (limited 2, 3-DPG compensation)
  76. Impaired oxygenation may decrease anemia tolerance. What could cause this?
    • lung disease
    • ↑ altitude
  77. Ongoing or imminent blood loss could decrease anemia tolerance. What situations could cause this?
    • Surgical bleeding
    • coagulopathy
  78. How does increased cardiac output compensate for anemia?
    ↓ HCT → ↓ viscosity → ↓ SVR →↑ CO
  79. O2 transport is optimal at Hct between __-__. O2 delivery is pretty constant between these values.
  80. How does redistribution of cardiac output help compensate for anemia?
    • With hemodilution the CO and blood flow will increase but not distributes equally throughout the tissues.
    • Some have higher extraction (Brain and heart) will receive a proportionally greater increase in CO as compensation.
  81. Cognitive impairment can occur if Hb goes below ___ as well.
  82. Extraction of O2 is pretty much maxed out already. Increased O2 extraction is critical when Hct falls below ___%.
  83. What is the P50 in the O2-Hb curve?
    what the PaO2 is when the hemoglobin is 50% saturated (27mmHg)
  84. What kind of changes in the oxyhemoglobin dissociation affinity would we see as compensation for anemia?
    • If anemia develops slowly the Hb affinity for oxygen may be decreased so the curve shifts to the right.
    • Because of accumulation of 2,3 DPG in RBC. The synthesis of exceptionally high levels of 23 DPG starts in a Hgb of 9.
  85. The synthesis of exceptionally high levels of 23 DPG starts in a Hgb of ___.
  86. Chronic isovolemic anemia vs acute blood loss regarding compensation for anemia
    • Chronic:accumulation of 23DPG, increases the P50, CO increases
    • Acute: vasoconstriction occurs, and CO doesn’t increase as effectively
  87. Why are platelet counts difficult to to evaluate for a transfusion trigger?
    • Because the platelet function matters
    • Make decision on likelihood of bleeding and the hazards proposed by bleeding
  88. Plt concentrate from single unit of blood of 70kg pt can increase plt count by ___-_____
  89. Non-bleeding pt without abnormal hemostasis, what is the transfusion trigger?
  90. Lumbar puncture, epidural anesth, central line placement, endoscopy with bx, liver bx, or laparotomy in pts without other abn hemostasis, vaginal delivery--what is the transfusion trigger?
  91. To maintain platelet count during ongoing bleeding & transfusion not less than----what is the transfusion trigger?
  92. To maintain platelet count during DIC with ongoing bleeding not less than---what is the transfusion trigger?
  93. To maintain platelets during management of massive blood loss---what is the transfusion trigger?
  94. Planned procedures in which closed cavity bleeding would be hazardous (neurosurgery)---what is the transfusion trigger?
  95. Microvasc bleeding from plt dysfunc (uremia, etc)---what is the transfusion trigger?
    Clinical judgement
  96. How are most platelets obtained?
    Most platelets are obtained by aphersis. It’s when a blood donor will come in and donate, and have components they don’t need are returned to donor.
  97. Single apheresis unit will supply the equivalent dose of __-__units of someone donating whole blood.
  98. Why does aphresis have less risk of transfusion reaction than pooled platelets?
    Aphresis has less risk (because it’s coming from one person) vs pooled plts.
  99. Why is bacterial contamination a problem w/platelets?
    • Platelet viability is optimal at 22 degrees centigrade
    • Although they are potentially viable for 10days, FDA limits it to 5 days because of risk of bacterial growth.
  100. Why don't we store platelets at low pH or temp to avoid bacterial growth?
    If they were to be stored at low temps or pH, they wouldn’t be functional
  101. Platelet sepsis incidence is __________ because they are stored at room temp.
    1 in 10,000
  102. Why is ABO compatibility is ideal but not absolutely required for platelets?
    • They do contain HLA and plt specific antigen.
    • There are some ABO antigens expressed on plt membrane
    • But if you were to give a group O patient Group A plt, they may get less of bump up in plt count because of some antibody action going on.
  103. When would you give FFP?
    • Correction of multiple coagulation factor deficiencies with evidence of microvascular bleeding and PT &/or aPTT > 1.5 X normal
    • Correction of microvascular bleeding during massive transfusion (> 1 blood volume) when PT &/or aPTT can’t be quickly obtained
    • Urgent reversal of warfarin therapy
    • Heparin resistance
    • Thrombotic thrombocytopenic purpura or hemolytic uremic syndrome
    • Correction of single coagulation factor deficiencies for which specific concentrates aren’t available (Factor V)
  104. How many mls are in 1 u of FFP and what does it contain?
    • 1u has volume of about 200-250ml.
    • Contains all the pro clotting factors except plts.
  105. Does FFP have to be ABO compatible?
    YES according to Barash
  106. Thawed plasma is being used more widely in place of FFP (it’s FFP that was thawed and then kept at 6degrees for 5 days). What is the good and bad regarding thawed FFP?
    • Advantage: immediately available.
    • Problem: levels of factor 5 and 8 decline with storage
  107. When can you not use thawed FFP?
    In pt that have specific Factor 5 and 8 deficiency or if they are in DIC.
  108. Why is cryoprecipitate transfusion indicated?
    • Indicated for microvascular bleeding when there is a disproportionate ↓ fibrinogen
    • DIC or massive transfusion
    • Indicated for bleeding (uremia that is unresponsive to DDAVP)
    • Can be given as prophylaxis prior to surgery in those w/hemophelia A and vWF.
    • And in pt w/known abnormal fibrinogen or factor deficiency.
  109. What is in cyroprecipitate?
    • Factor VIII
    • Von Willebrand factor (vWF)
    • Fibrinogen
    • Fibrinonectin
    • Factor XIII
  110. Use of erythropoietin requires injections for 3 weeks + 2 injections the final week but this can be helpful in what patient population?
    Jehovah's witnesses
  111. What is acute normovolemic hemodilution?
    withdrawal of pt blood early in intraop period. Give a bunch of crystalloid to maintain euvolemia. Pt loosing blood w/lower Hct then they can be re-transfused at end of surgery w/own blood. End point w/initial withdrawal is 27-33. Only modest benefit.
  112. Blood salvage can be helpful but when can it be contraindicated?
    Contraindicated if there is contaminated wound or there are malignant cells
  113. What can be a problem with blood salvage?
    Dilutional coagulopathy can result from large volumes of returned salvaged blood because processing takes all the clotting factors away.
  114. What is the efficiency of blood salvage?
    Efficiency is only 50%, rare that you won’t need to give allogenic blood as well
  115. Autologous blood is not without risk, what are they?
    clerical error and bacterial contamination
  116. Leading cause of transfusion related death in US are .............
    ABO incompatibility, transfusion related lung injury (TRALI) and sepsis from bacterial infection

    **she said this twice!!!**
  117. Most problematic of the immune mediated reaction is the
    • immediate acute hemolytic transfusion reaction (AHTR) against foreign RBCs (donor cells).
    • Can lead to acute RF and DIC
    • Mortality rate is about 2%
  118. According to Miller, with correct ABO/rh typing, the probability of AHTR is less than 1 in ___ Add a type and screen it’s less than 1 in _______. So it’s better to do a type and screen and actually a full cross match.
    1/1000; 1/10,000
  119. Can we cause a hemolytic transfusion reaction by giving incompatible FFP?
    Yes, The transfusion of incompatible FFP can cause hemolysis of recipients RBC. (antibodies are in plasma) so give antibodies to patient who has antigen on RBC then can cause transfusion hemolytic reaction.
  120. What is the most common cause of ABO incompatibility?
    clerical error
  121. TRUE or FALSE. Unlike the acute reactions which involve the ABO system, delayed reactions usually involve these minor antigens (Kell, Kidd, Duffy, Rh)
  122. New antibodies can occur in 1/___ units transfused. But detectable delayed hemolytic reactions only occur in 1/____ transfusions.
    1/200; 1/2000
  123. For delayed hemolytic transfusion reactions, when does the hemolysis show up? How severe is the reaction?
    • The hemolysis shows up by the first 1-2weeks after the transfusion.
    • The reaction is milder and usually self limiting.
  124. In AHTR, Hemolysis occurs, hemoglobin leaks out into the intravascular space. Where else can this occur?
    This can also occur in spleen, liver, bone marrow (reticular endothelial system)
  125. How are the kidneys impaired in AHTR?
    • Because the hemolysis releases Hb, that needs to get excreted by the kidneys, damage to kidneys can occur.
    • Renal blood flow can decrease because of the hypotension.
    • Not only the Hb but the red cell stroma (reminisce of the cellular wall structure itself) can damage the renal tubules. The antigen/antibody complexes can get deposited in the glomeruli and if DIC happens then get fibrin strands can impair perfusion and can get necrosis of the renal cortex which is usually irreversible
Card Set
Blood transfusions
Blood transfusions 11/4/13