Transfusion Reactions Flashcards

Exam 3

1
Q

What is the difference between an acute reaction and a delayed reaction?

A

In an acute reaction, the signs and symptoms appear within 24 hours of transfusion. In a delayed reaction, the signs and symptoms appear 24 hours or more after transfusion.

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2
Q

What is the purpose of a clerical check?

A

The clerical check is to ensure that all of the patient information and unit information matches. For instance the name on the compatibility tag with the name on the patient wristband with the name in the computer system. Also that the blood types of the unit and patient are compatible.

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3
Q

What is the purpose of a hemolysis check?

A

Hemolysis of a sample indicates that there is free hemoglobin present. If the sample drawn after the transfusion reaction is hemolyzed, this could indicate that antibodies are hemolyzing the red cells and releasing the hemoglobin causing the red color. This is especially suspect if the sample before the transfusion was yellow.

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4
Q

What information do the post-transfusion and pre-transfusion DATs give us?

A

If the post transfusion DAT is positive while the pre transfusion DAT is negative, this indicates that the cause of the positive DAT is the transfusion. If they were the same before and after transfusion then the DAT is most likely being caused by something else.

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5
Q

Which transfusion reactions are considered to be acute?

A

Acute Hemolytic, Febrile Non-Hemolytic, Transfusion-related Sepsis, TRALI, Allergic, TACO

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6
Q

Which transfusion reactions are considered to be delayed?

A

Delayed Hemolytic, Delayed Serologic, TA-GVHD, Post-Transfusion Purpura, Iron Overload

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7
Q

What is the mechanism for acute hemolytic transfusion reactions?

A

Antibodies formed in the recipient react with donor red cells that are positive for the associated antigen. These complexes can then cause either intravascular or extravascular RBC destruction.

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8
Q

What are the symptoms of an acute hemolytic transfusion reaction?

A

Fever and chills, hemoglobinuria, back pain, pain at infusion site, hypotension/shock, hemoglobinemia, DIC/increased bleeding, renal failure, feeling of “impending doom”.

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9
Q

What are the expected lab findings of an acute hemolytic transfusion reaction?

A

Positive DAT on post reaction sample, increased bilirubin, decreased hemoglobin, decreased haptoglobin, increased LDH, schistocytes, spherocytes

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10
Q

What are ways that acute hemolytic transfusion reactions can be prevented?

A

Proper training and particular attention during phlebotomy, issue, and administration to reduce any clerical errors. Draw two tubes for blood type before issuing blood to ensure the right patient was drawn. Obtain an accurate patient history.

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11
Q

What are some causes of a non-immune acute hemolytic transfusion reaction?

A

Chemical damage: incomplete deglycerolization, bacterial contamination. Mechanical damage: needle with improper bore size, improper shipping/storage temps, improper use of blood warmers, rapid pressure infuser, infusion of unapproved fluids (instead of saline)

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12
Q

What blood products are most often associated with transfusion associated sepsis (TAS)?

A

Platelets because they are stored at room temperature.

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13
Q

What are the symptoms of transfusion associated sepsis (TAS)?

A

Rapid onset high fever, rigors/chills, abdominal cramping/nausea/diarrhea, hypotension/shock

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14
Q

What are the lab findings for transfusion associated sepsis (TAS)?

A

Discolored blood product, non-immune hemoglobinemia/uria, DAT negative, positive culture of both the unit and the recipient

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15
Q

How can TAS be prevented?

A

Proper phlebotomy technique to reduce bacterial skin contaminants, culture platelets, quarantine other blood products from the positive donation.

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16
Q

What is the mechanism for the occurrence of febrile non-hemolytic transfusion reactions (FNHTR)?

A

Two white cells related mechanisms: The first, donors WBCs secrete cytokines in the bag before transfusion releasing pyrogens which cause fever. The second, recipient antibodies against HLA antigens on WBC lead to fever-inducing substance release.

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17
Q

What are the symptoms of FNHTR?

A

Fever or chills during or up to 2 hours after transfusion, nausea/vomiting, increased blood pressure, increased heart rate/breathing, reaction usually resolves on its own.

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18
Q

How can FNHTRs be prevented?

A

Leukoctye reduction of red cells to remove WBCs and premedicate with acetaminophen to reduce fever.

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19
Q

What are the mild allergic reaction symptoms?

A

Hives, urticaria, redness, swelling

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20
Q

What are the severe allergic reaction symptoms?

A

Angioedema (swelling under skin), wheezing, hypotension, anaphylaxis

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21
Q

What treatments are used for the different levels of allergic transfusion reactions?

A

Mild: Benadryl, as symptoms resolve they can continue to transfuse the unit, Severe: Epinephrine for anaphylactic shock, wash red cells if due to IgA deficiency

22
Q

What is the mechanism for immune transfusion-related acute lung injury (TRALI)?

A

Donor antibodies react with recipient leukocytes/neutrophils. Aggregates than obstruct the pulmonary circulation and complement is activated releasing cytokines. This causes damage to the endothelium and destroys capillaries in the lungs causing leakage of fluid into alveolar spaces which leads to pulmonary edema..

23
Q

What is the mechanism for non-immune transfusion-related acute lung injury (TRALI)?

A

The first hit is a predisposing condition that primes the patient’s neutrophils and sequesters them in the pulmonary endothelium. The second hit comes with transfusion of the blood product where antibodies or biologically active lipids activate the primed neutrophils causing damage to the endothelium. Endothelial damage leads to pulmonary capillary permeability and leakage of fluid into alveolar spaces which leads to pulmonary edema.

24
Q

What are they symptoms of TRALI?

A

New acute lung injury within 6 hours of transfusion, lack other factors for pulmonary edema, respiratory distress, fever/chills, hypotension, severe hypoxemia

25
Q

What tests are used to diagnose TRALI?

A

Chest X-ray should indicate bilateral infiltrates, O2 saturation will be <90%, and donor and recipient can be tested for HLA/HNA antibodies. TRALI overall is difficult to diagnose.

26
Q

How can TRALI reactions be better prevented?

A

Donors found to have antibodies will be deferred from donation. Only accept male plasma donors (females are more likely to create antibodies when they are exposed to foreign antigens during pregnancy).

27
Q

What is the mechanism of Transfusion-Associated Circulatory Overload (TACO)?

A

The patient’s cardiovascular system is unable to handle to additional workload when the unit is transfused. This then manifests in congestive heart failure.

28
Q

What patients are more at risk for TACO?

A

Preexisting congestive heart failure, very old or very young patients, renal failure, chronic anemia, rapid or massive transfusion.

29
Q

What are the symptoms of TACO?

A

Respiratory distress, hypoxemia, cough, headache, jugular vein distention, elevated blood pressure, afebrile.

30
Q

What tests are used to diagnose TACO?

A

Chest X-ray shows bilateral infiltrates, pulmonary edema, cardiomegaly, distended pulmonary artery. An elevated BNP distinguishes this reaction from TRALI.

31
Q

How can you prevent TACO?

A

Control the infusion rates, split units into aliquots to be transfused over a longer period of time, consider low volume units for at risk patients.

32
Q

What is the mechanism of delayed hemolytic/serologic transfusion reaction (DHTR)?

A

Usually the patient is first exposed to the antigen through transfusion and creates an antibody that does not cause a reaction. Over time, the antibody fades and is no longer detectable in testing. The patient therefore may be transfused antigen positive blood since the original antibody was not detected. The patient’s body begins to create more antibodies to the antigen positive blood and begins to destroy it anywhere from 24 hours to 28 days after transfusion.

33
Q

Which antibodies commonly cause DHTR?

A

Kidd, Duffy, Kell

34
Q

What are the symptoms of DHTR?

A

Often asymptomatic, fever, anemia, mild jaundice, pallor

35
Q

What lab results do you expect to see with DHTR?

A

Decreased hemoglobin and haptoglobin, newly positive antibody screen, positive DAT, anemia, spherocytes, elevated LDH and bilirubin.

36
Q

What is the mechanism of transfusion-associated graft-versus-host disease (TA-GVHD)?

A

Donor lymphocytes in the unit launch an immune response against recipient cells (those that have foreign HLA antigens). Normally, recipient lymphocytes would launch a counter-attack and destroy the donor lymphocytes before there was an issue. However, in immunocompromised patients, the recipient lymphocytes are not active and do not destroy the donor lymphocytes allowing the donor lymphocytes to bind to foreign HLA tissues.

37
Q

What patients are more at risk for TA-GVHD?

A

Immunosuppressed (T-cell deficiency, bone marrow transplants, chemotherapy, aplastic anemia), intrauterine and neonatal transfusions, hematologic malignancies (Hodgkin’s), granulocyte transfusion (high number of WBC), receiving blood from a relative.

38
Q

What are the symptoms for TA-GVHD?

A

Fever 7-10 days post transfusion, face/trunk rash, nausea/vomiting, watery diarrhea, hepatitis, pancytopenia (deficiency of all types of blood cells leading to infections and fatal consequences).

39
Q

What are the lab findings expected for TA-GVHD?

A

Pancytopenia, Skin biopsy - perivascular lymphocyte infiltrate, bone marrow aspirate -hypocellular or aplastic marrow, liver biopsy - necrosis of small bile duct, molecular studies - determine donor vs. recipient HLA types.

40
Q

How can TA-GVHD be prevented?

A

Irradiation - this deactivates the donor lymphocytes without damaging other cells. Leukoreduction is not always enough as reports of TA-GVHD have been found with leukoreduced units.

41
Q

What is the mechanism for post-transfusion purpura?

A

The patient makes an antibody to a human platelet antigen after being transfused with platelets or red cells. This leads to destruction of future platelets with the antigen which ends up destroying both the donor and patient’s own platelets.

42
Q

What are the symptoms of post-transfusion purpura?

A

Thrombocytopenia, bleeding, sometimes febrile, self-limiting (platelet count usually returns to normal in 2 weeks.

43
Q

Who is at the greatest risk for iron overload?

A

Chronic red cell transfusion recipients

44
Q

What are the symptoms of iron overload?

A

Weakness, fatigue, jaundice, anemia, cardiac arrhythmia, organ failure

45
Q

What is citrate toxicity?

A

An adverse metabolic effect of blood transfusions that leads to low calcium levels

46
Q

What is potassium toxicity?

A

An adverse metabolic effect of blood transfusions that leads to high potassium levels

47
Q

What causes citrate toxicity?

A

RBC preservatives contain sodium citrate which is usually metabolized by the liver. Massive transfusions or liver disease can lead to excess levels of sodium citrate in the body which binds free calcium and magnesium.

48
Q

What causes potassium toxicity?

A

Intracellular potassium leaves RBCs in storage over time. If large volumes of older RBCs are transfused to a patient (especially neonates) this can lead to very high levels of potassium.

49
Q

What are the clinical signs and symptoms of citrate toxicity?

A

Metabolic alkalosis (due to bicarbonate production from citrate metabolism), tingling of lips or fingers, twitching or shivering, muscle contractions/spasms, EKG abnormalities

50
Q

What are the clinical signs and symptoms of potassium toxicity?

A

Muscle weakness, absent bowel sounds, EKG abnormalities, ventricular fibrillation, cardiac arrest

51
Q

How can citrate toxicity be prevented?

A

Stop blood transfusions temporarily if possible and increase time intervals in between transfusions

52
Q

How can potassium toxicity be prevented in neonates?

A

Use “fresh” blood units that are < 7 days old. If unable to obtain fresh units, saline wash the RBCs before transfusion to remove the high potassium supernatant from the older unit