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BMS 185 Lecture > Quiz 7 > Flashcards

Quiz 7 Flashcards

1
Q

What is the definition of adverse effects of transfusion?

A

any untoward reaction that occurs as a consequence of infusion of blood or one of its components

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2
Q

When can adverse effects of transfusion happen?

A

occurring during the transfusion or several hours later; or delayed, occurring days, months, or even years after the transfusion

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3
Q

What percentage of transfusions are associated with adverse effects?

A

3%, usually mild

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4
Q

What percentage of transfusion-related fatalities are caused by TRALI?

A

27%

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5
Q

What percentage of transfusion-related fatalities are caused by Sepsis?

A

17%

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6
Q

What is the most common transfusion-related fatality?*

A

TRALI

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7
Q

What other transfusion-related adverse reactions are common?*

A

urticaria and fever

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8
Q

What should happen when there is a possiblity of a transfusion reaction?

A

stop immediately and investigate what can be the cause

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9
Q

What is a Hemolytic Transfusion Reaction (HTR)?

A

Accelerated lysis of transfused red blood cells due to immunologic incompatibility

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10
Q

What are the two types of HTR?

A
  1. Acute
  2. Delayed
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11
Q

How long does it take for an acute HTR to occur?

A

occurring within minutes to 24 hours after transfusion

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12
Q

How long does it take for an delayed HTR to occur?

A

occurring within 3-7 days after transfusion

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13
Q

What is intravascular hemolysis?

A

complement activation and membrane lysis of RBCs within the vascular space with release of free hemoglobin into the plasma

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14
Q

What is extravascular hemolysis?

A

complement may be activated, but without cascade completion; IgG and/or complement coat RBCs which are ingested by splenic macrophages — characterized by hyperbilirubinemia

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15
Q

What are symptoms of Acute HTR?

A
  1. Fever and chills
  2. Nausea/Vomiting
  3. Back,flank,or chest pain
  4. Hypotension, tachycardia, shock
  5. Pain at transfusion site
  6. Renal failure
  7. DIC
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16
Q

What can you see with acute HTR patients under anestesia?

A
  1. red urine
  2. uncontrolled bleeding
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17
Q

What are symptoms of acute HTR with Intravascular hemolysis?

A
  1. Hemoglobinemia/hemoglobinuria
  2. DAT may be positive or negative
  3. Increased bilirubin (peaks after 4-6 hours)
  4. Decreased haptoglobin
  5. Increased LDH
  6. Increased BUN/Creat
  7. Elevated PT/PTT; decreased fibrinogen
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18
Q

How many phases are there in Acute HTR?

A

three

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19
Q

What is phase one of acute HTR?

A
  1. Ag-Ab mediated complement activation
  2. release of C3a & C5a promotes inflammation
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20
Q

What is phase two of acute HTR?

A
  1. Immune intravascular hemolysis stimulates:

1a. macrophage activation
1b. release of cytokines

  1. procoagulant activity
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21
Q

What is phase three of acute HTR?

A
  1. Systemic response with bradykinin and tissue factor contribute to:

a. vascular collapse
b. DIC

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22
Q

What must be ruled out before a patient is diagnosed with acute HTR?

A

FNHTR, TRALI, and bacterial contamination, and acute hemolysis

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23
Q

What is done by management at bedside during acute HTR?

A
  1. Stop the transfusion
  2. Perform a clerical check at the bedside
  3. Follow hospital protocol: send type & screen specimen, first voided urine, remains of unit and attached solutions to the Blood Bank
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24
Q

What does blood bank do for acute HTR?

A
  1. Clerical check
  2. ABO/Rh recheck
  3. Visual plasma inspection for hemoglobinemia
  4. Direct antiglobulin test (DAT)
  5. Observe for mixed field agglutination (IAT)
  6. Further testing if indicated (haptoglobin, urinalysis)
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25
Q

How do you prevent acute HTR?

A
  1. identify patients appropriately using 2 unique identifiers during every step of the pretransfusion process:
    a. sample collection
    b. testing
    c. requisitioning of unit
    d. issuing
    e. hanging of the blood at bedside
  2. ABO confirmation before transfusion either by:
    a. previous history
    b. by second specimen drawn at a different time from the type and screen
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26
Q

How does a primary immunization (DHTR) happen?

A

requires gearing up of the immune mechanism and a new production of antibody

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27
Q

How does an anamnestic response (DHTR) happen?

A

Over time, an antibody may fall below detectable levels and the patient if re-challenged with antigen

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28
Q

What is the most common antibody that causes intravascular delayed hemolytic reactions (DHTR)?

A

anti-Jk(a) [kidd]

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29
Q

How are DHTR diagnosed?

A

serologic diagnosis (DSTR) w/ positive DAT &/or IAT

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30
Q

What is the most common cause that causes extravascular delayed hemolytic reactions (DHTR)?

A

destruction of RBC

31
Q

What are symptoms of DHTR?

A
  1. decreased hemoglobin
  2. jaundice
  3. increased LDH
  4. fever
32
Q

What is used first used in screening for DHTR, DAT or IAT?

A

DAT

33
Q

What antigens cause intravascular hemolysis?

A

ABO, Kell, Kidd, Duffy, S

34
Q

What antigens cause extravascular hemolysis?

A

Rh, Duffy, Kidd, Kell, S

35
Q

What can cause nonimmune hemolysis due to mechanical error?

A

mall needle, kinks in tubing

36
Q

What can cause nonimmune hemolysis due to thermal error?

A

overheating or freezing

37
Q

What can cause nonimmune hemolysis due to osmotic error?

A

hyper or hypotonic solution use- only mix normal (0.9%) saline with blood

38
Q

What is Febrile Non-Hemolytic Reactions?

A

Temperature increase of 1C or 2F or more occurring in association with transfusion and without any other explanation

39
Q

What are symptoms of Febrile Non-Hemolytic Reactions? (1 or more)

A
  1. May occur from 5 minutes into a transfusion up to 4 hours after completion
  2. Fever and chills
  3. Rigors
  4. Cold
  5. Headache
  6. Nausea/vomiting
40
Q

What must be ruled out for diagnosis of Febrile Non-Hemolytic Reactions?

A
  1. acute hemolytic transfusion reactions
  2. bacterial contamination
  3. TRALI
41
Q

What is the pathophysiology of Febrile Non-Hemolytic Reactions?

A
  1. Recipient Ab reacts with donor leukocytes
  2. release of endogenous cytokines(2abc) and anti-HLA:
    2a. IL1-Beta
    2b. IL-6
    2c. TNF-alpha
  3. Modifiers and cytokines are released in the supernatant, which increases with storage time
  4. Possibly: platelets are destroyed (platelet refactoriness, platelets are not increasing when transfused)
42
Q

What is the pathophysiology of Febrile Non-Hemolytic Reactions?

A
  1. Recipient Ab reacts with donor leukocytes
  2. release of endogenous cytokines(2abc) and anti-HLA:
    2a. IL1-Beta
    2b. IL-6
    2c. TNF-alpha
  3. Modifiers and cytokines are released in the supernatant, which increases with storage time
  4. Possibly: platelets are destroyed (platelet refractoriness, platelets are not increasing/dysfunctional when transfused)
43
Q

What is the pathophysiology of Febrile Non-Hemolytic Reactions?

A
  1. Recipient Ab reacts with donor leukocytes
  2. release of endogenous cytokines(2abc) and anti-HLA:
    2a. IL1-Beta
    2b. IL-6
    2c. TNF-alpha
  3. Modifiers and cytokines are released in the supernatant, which increases with storage time
  4. Possibly: platelets are destroyed (platelet refractoriness, platelets are not increasing/dysfunctional when transfused)
  5. If RBC/platelet units aren’t leukoreduced before the units are stored…
  6. WBC breakdown the units and release cytokines into the supernatant
  7. Once the cytokines are released, leukoreduction at that point doesn’t serve any purpose
44
Q

What causes Platelet Refractory State in Febrile Non-Hemolytic Reactions?

A

Antibodies made against Class 1A, 1B, and 1C-HLA will destroy platelets that do not match the patient’s HLA class

45
Q

What is febrile non-hemolytic reaction?

A

accumulation of cytokines in the blood

46
Q

What plays a role in febrile non-hemolytic reactions?

A
  1. WBC content
  2. timing of WBC reduction
47
Q

What is prestorage leukoreduction?

A

removal of WBC within 72 hours of collection

48
Q

Are most RBC/platelet units prestorage leukoreduced?

A

Yes

49
Q

What is the treatment for Febrile Non-hemolytic reactions?

A
  1. Stop the transfusion
  2. Rule out hemolysis, bacterial sepsis, TRALI
  3. May give anti-pyretic (fever reducing meds)
50
Q

What is prevention for Febrile Non-hemolytic reactions?

A
  1. Premedication (give Tylenol to patient)
  2. Leukoreduction of components (prestorage, poststorage, bedside)
  3. Prestorage-done by collection center within 72 hours of collection
  4. Poststorage
  5. Bedside- give filter out to a nurse to leukoreduce at the time of transfusion; useless because cytokines have already been released into the blood
51
Q

What are symptoms of mild Allergic transfusion reactions?

A
  1. urticaria (hives)
  2. pruritus (itching)
  3. flushing
  4. rash
52
Q

What is the pathophysiology of mild allergic transfusion reactions?

A
  1. Sensitized recipient IgE antibodies react with proteins in the donor plasma (that they’ve been previously exposed to)
  2. (Rare) passive donor IgE antibodies to recipient (food/drugs)
53
Q

What happens more often mild or severe/anaphylactic allergic transfusion reactions?

A

mild! (1-2%) [severe: 0.05% to 0.0021%]

54
Q

What is a clinical presentation of Anaphylactic or Severe Allergic Transfusion Reactions?

A

allergic manifestations along with hypotension and circulatory collapse
NO FEVER

55
Q

What is a common cause of Anaphylactic or Severe Allergic Transfusion Reactions?

A

IgA-deficient individual with anti-IgA (IgM or IgG) who receives a transfusion notoriously lead to an anaphylactic reaction

56
Q

What is the treatment for mild Allergic Transfusion Reactions?

A

managed with antihistamines and steroid administration

57
Q

What is the treatment for Anaphylactic or Severe Allergic Transfusion Reactions?

A

stop the transfusion, maintain the airway, treat hypotension, epinephrine, etc. Never restart the transfusion! Investigate for IgA deficiency.

58
Q

How do you prevent Allergic Transfusion Reactions?

A
  1. Premedication with antihistamine or steroid
  2. Use of washed or frozen, deglycerolized red cells
  3. IgA deficiency – may wash red cells and platelets; plasma products must be obtained from IgA- deficient donors
59
Q

Who would most likely have Transfusion-Associated Circulatory Overload (TACO)?

A
  1. pediatric and elderly patients
  2. chronic, long-standing anemias
60
Q

What is the clinical presentations for Transfusion-Associated Circulatory Overload (TACO)?

A
  1. dyspnea (difficulty breathing)
  2. hypertension
  3. pulmonary edema
  4. Increased pulmonary artery occlusion pressure
  5. increased brain natriuretic peptide (BNP)
  6. hypertension in contrast to TRALI
  7. Regulate infusion rate and administer diuretics
61
Q

What is brain natriuretic peptide (BNP)?

A
  1. Released from the heart in response to distension of the left ventricular wall by increased blood volume
  2. used to test monitoring heart failure
62
Q

What are the signs/symptoms of Transfusion Related Acute Lung Injury (TRALI)?

A
  1. Onset of acute respiratory distress during transfusion or within 6 hours of the transfusion
  2. Bilateral pulmonary edema on chest x-ray
  3. Severe hypoxemia (low oxygen level in blood)
  4. No evidence of fluid overload
  5. Hypotension
  6. Fever
  7. Normal to elevated BNP (Brain Natriuretic Peptide)
  8. Transient leukopenia (WBC’s go into lungs)
63
Q

When do Transfusion Related Acute Lung Injury (TRALI) patients see improvement after treatment?

A

48-96 hours of onset

64
Q

What is the fatality rate of Transfusion Related Acute Lung Injury (TRALI)?

A

10-15%

65
Q

What is the leading cause of transfusion related deaths in the US?

A

Transfusion Related Acute Lung Injury (TRALI)

66
Q

What are implicated products associated with Transfusion Related Acute Lung Injury (TRALI)?

A

all plasma-containing products including cryoprecipitate, platelets, granulocytes, and red cells, but most common with plasma

67
Q

Who usually has implicated products associated with Transfusion Related Acute Lung Injury (TRALI)?

A

Multiparous women (pregnant multiple times)

68
Q

What is the antibodies that are hypothesized to cause Transfusion Related Acute Lung Injury (TRALI)?

A
  1. Passive infusion of donor antibodies directed against recipient leukocyte antigens (HLA class I & II, neutrophil-specific) in a majority of cases
  2. Infusion of donor leukocytes into a recipient with antibodies against donor leukocytes
  3. Antigen/antibody reaction is thought to cause complement activation with resultant neutrophil influx into the lungs
  4. Activation of neutrophils causes capillary leak and pulmonary damage
69
Q

What are the limitations to the “hypothesized” antibodies?

A

not all TRALI cases are caused by antibodies

some TRALI cases has been reported in an autologous transfusion recipient (reaction to self-cells)

70
Q

What is the two event hypothesis of Transfusion Related Acute Lung Injury (TRALI)?

A
  1. Endothelial cell activation
  2. Primed neutrophil activation
71
Q

What is the pathophysiology of Transfusion Related Acute Lung Injury (TRALI)?

A
  1. the normal alveolus to the left and the abnormal alveolus as a result of TRALI to the right
  2. Neutrophils come out of the circulation into the lung
  3. release their cytokines which damage the alveolar epithelium with subsequent hyaline membrane formation
  4. damaged alveoli causes fluid comes into the lung
  5. extensive inflammation and hyaline membrane formation
72
Q

What must be ruled out before diagnosis of Transfusion Related Acute Lung Injury (TRALI)?

A
  1. Circulatory overload
  2. Anaphylaxis
  3. Hemolysis
  4. Bacterial Contamination/Sepsis
  5. Other causes of lung injury
73
Q

How do you prevent Transfusion Related Acute Lung Injury (TRALI)?

A
  1. Donors with antibodies who have been implicated in TRALI are deferred permanently from blood donation
  2. many hospital are transfusing plasma from only male donors or from women with no anti-HLA antibodies (plasma products from sensitized female donors are most often associated with TRALI)

BMS 185 Lecture (11 decks)

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