Clinical Considerations in Transfusion Medicine Flashcards

(94 cards)

1
Q

is essentially the monitoring system for blood transfusions.

It tracks the entire process,

from blood donation to the patient receiving the transfusion, to identify and prevent any problems.

A

Hemovigilance

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2
Q

Model used to track, analyze and ultimately to improve transfusion outcomes

A

HEMOVIGILANCE MODEL (NHSN, AABB, CDC)

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3
Q

problem that happens during or after a blood transfusion,

ranging from mild (fever, chills) to life-threatening.

There is an untoward reaction of the patient towards the blood of the donor

A

RECOGNITION OF A TRANSFUSION REACTION

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4
Q

SIGNS OF TR

A

• Fever (> or equal to 1 degree Celsius
increase in body temp)
• Chills/Rigors
• Respiratory distress (wheezing, coughing, dyspnea, cyanosis)
• Hyper/Hypotension
• Pain - Abdominal, etc.
• Skin manifestations - urticaria, rasha flushing, edema
• Jaundice, Hemoglobinuria
• Nausea, Voming,
• Abnormal Bleeding
• Oliguria/ Aruria

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5
Q

CATEGORIES of TRANSFUSION
REACTIONS

A

Hemolytic

Delayed Serologic

Febrile Non-hemolytic

Allergic

Anaphylactic

Transfusion-Related Acute Lung

Injury (TRALI)

Transfusion-Associated Graft-versus-Host Disease (TA-GVHD)

Bacterial Contamination

Transfusion-Associated Circulatory Overload (TACO)

Transfusion Hemosiderosis

Citrate Toxicity

Post-Transfusion Purpura

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6
Q

ACUTE (<24 hours)

Immune mediated
(Ag + Ab complex formation)

A

Hemolytic
Febrile, nonhemolytic
Allergic
Anaphylactic
TRALI

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7
Q

ACUTE (<24 hours)

Non-immune mediated
(Physical/ Mechanical Setup)

A

Sepsis
TACO
Physical hemolysis

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8
Q

DELAYED (>24 hours)

Immune mediated
(Ag + Ab complex formation)

A

Hemolytic
Serologic RBC
HLA alloimmunization
TA-GVHD
Post-transfusion Purpura

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9
Q

DELAYED (>24 hours)

Non-immune mediated
(Physical/ Mechanical Setup)

A

Hemosiderosis
Citrate toxicity

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10
Q

Acute Transfusion Reactions (TR)

3

A

Febrile
Allergic
Pulmonary

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11
Q

ATR

  1. Febrile Reactions (3)
A

AHTR (Acute Hemolytic Transfusion Reaction)

TAS (Transfusion-Associated Sepsis)

FNHTR (Febrile Non-Hemolytic Transfusion Reaction)

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12
Q

ATR

  1. Allergic Reactions (2)
A

Mild Allergic Reaction
Severe Allergic Reaction (Anaphylactic)

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13
Q

ATR

  1. Pulmonary Reactions (2)
A

TACO (Transfusion-Associated Circulatory Overload)

TRALI (Transfusion-Related Acute Lung Injury)

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14
Q

HEMOLYTIC TR (4)

A

• Acute
• Delayed
• Immune mediated
• Non-immune mediate

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15
Q

Rapid destruction of red cells during, immediately after, or after 24 hours

Severity ranges from fever to death

d/t antibody mediated incompatibility;Wrong blood unit

A

ACUTE HEMOLYTIC TRANSFUSION REACTION

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16
Q

How to manage Acute HTR?

A

Early and aggressive
(1) fluid resuscitation and
(2) control of blood

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17
Q

Antibody + Antigen

Immune complexes

Release of vasoactive amines

A

Vasodilation
Hypotension
Immune complex deposition
Thrombus formation

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17
Q

Antibody + Antigen

Immune complexes

Activation of MAC

A

Intravascular Hemolysis

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18
Q

Antibody + Antigen

Immune complexes

A

Activation of MAC

Release of vasoactive amines

Activation of Coagulation
cascade

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19
Q

Antibody + Antigen

Immune complexes

Activation of Coagulation
cascade

A

Disseminated
Intravascular Coagulation
Bleeding

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20
Q

ACUTE HTR

As little as_____ of transfused incompatible unit can cause this cascade

In cases of Intravascular hemolysis,____ and ____ is present. (HALLMARK OF INTRAVASCULAR HEMOLYSIS)

A

10ml

Hemoglobinuria and Hemoglobinemia

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21
Q

ACUTE HTR

•_______ → Targets the endothelial cells of the blood vessels

• Severe hypotension would lead to____ (Very low blood pressure;
cannot circulate well in the important organs; cannot deliver 02)

Immune complex usually gets stuck in the_____ - will now compromise the filtration capacity of the kidney → Can now lead to_____(Cannot concentrate urine well)

Thrombus formations can lead to_____ (Blocking of blood vessels because of thrombus) → Narrowing of the passages → The patient will have a hard time breathing.

A

Vasoactive amines

SHOCK

KIDNEYS -> Renal Failure

Bronchospasm

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22
Q

ACUTE HTR

Since the Coagulation Factors are activated it will lead to unwanted clotting resulting to_______

A

Disseminated Intravascular Coagulation (DIC)

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23
Q

ACUTE HTR

KNOWN CAUSES:

A

• Collection of blood from the incorrect patient
• Incorrect labeling of blood samples
• Misidentification of sample at blood bank
• Issuance of wrong unit from blood bank
• Transfusion of blood to incorrect patient
• Aliquoting a patient sample to improperly labeled test tube

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24
AHTR: NON-IMMUNE MEDIATED CAUSES:
• Chemical damage • Mechanical damage Improper shipping or storage temps • Incomplete deglycerolization of frozen red cells • Needles used for transfusion are of small bore size • Rapid pressure infuser or roller pumps • Improper use of blood warmers • Concurrent infusion of unapproved fluids • Bacterial contamination
25
DELAYED HEMOLYTIC TRANSFUSION REACTION Symptoms appear after_____ ***Less severe*** and require no treatment ____antibodies (Newly developed antibodies) Rapid decrease of hemoglobin to pretransfusion levels Presence of____
24 hours (7-10 days) IgG spherocytes
26
When suspecting for delayed HTR perform________ • Because we want to detect the IgG antibodies that were newly formed • Expect that in delayed HTR the test is_____
Direct Agglutination Test (DAT) POSITIVE
27
PATHOPHYSIOLOGY OF DELAYED HTR ______+______ Activation of______ System Release of_____ Activation of____ and _____
IgG + Red cell Antigen Reticuloendothelial system Cytokines T and B lymhocytes
28
HTR Clinical S&S Fever, chills, flushing, pain at site of infusion, tachycardia, tachypnea, lower back pain, hemoglobinemia, hemoglobinuria, hypotension; dramatic and severe; rapid onset
AHTR
29
HTR Clinical S&S >24 hours posttransfusion; fever temperature increase ≥1 deg C (or 2 deg F) with or without chills; unexplainable decrease in hemoglobin and hematocrit, occasional mild jaundice
DHTR
30
HTR Major complications No major complications; less severe reaction
DHTR
31
HTR Major complications DIC, renal failure, irreversible shock, death
AHTR
32
HTR Causes Complement activation, ABO incompatibility
AHTR
33
HTR Causes Anamnestic response to red tell antigen; alloantibody not demonstrating or missed
DHTR
34
HTR Laboratory Clerical check, visual inspection of post-transfusion sample; DAT-positive or negative, repeat ABO testing, tests for hemolysis;
AHTR
35
HTR Laboratory DAT-positive; posttransfusion antibody screen- positive; INCREASED hemoglobin/hematocrit; tests for hemolysis
DHTR
36
HTR Management AHTR
Treat hypotension and DIC; maintain renal blood flow
37
HTR Management DHTR
Provide antigen-negative donor units; no additional treatment necessary
38
HTR Prevention AHTR DHTR
Avoid errors of mislabeled samples and patient identification; design systems to decrease chances of technical error Check patient records
39
HTR: Non-Immune Mediated • Exposure of red cells to extreme _____ • Improper_____ of RBC unit •_____ destruction •_____ solutions •____ contamination of unit • ______defect
temperature deglycerolization Mechanical Incompatible Bacterial Intrinsic red cell
40
• Antibody development after 24 hours • Positive DAT • Antibody identification
Delayed Serologic Transfusion Reactions
41
• ***Most commonly observed*** REACTION • Increase if 1°C or 2°F • Cytokines • Transfused • In response to transfusion
Febrile Nonhemolytic Transfusion Reaction
42
What are other ways that we can do to the blood unit to ***avoid these cytokines?*** We can perform ______ Since WBCs are removed, there are no more source of cytokines
leuko-reduction.
42
FNTR Fevers are possible because of the_____ from the WBC transfused to the recipient • _____ are pyrogens meaning they can mediate interleukin production for fever • ______________ are given to patients before or during the transfusion process to address a fever that may arise during or after transfusion
cytokines; cytokines Antipyretics/ Acetaminophen
43
Clinical signs and symptoms Fever-temperature increase 21° C (or 2º F): chills; nausea: vomiting: headache; and back pain Major complications: Usually not life-threatening for recipient Causes: Recipient HLA antibodies to HLA antigens on donor lymphocytes Cytokines released by WBCs during blood product storage Clinical laboratory test: DAT-negative No visible hemolysis Management: Antipyretics-acetaminophen Prevention: Prestorage leukocyte reduction of blood products
FEBRILE NONHEMOLYTIC TRANSFUSION REACTION
44
• Ranges from minor urticarial effects to fulminant anaphylactic shock and death
Allergic and Anaphylactic Transfusion Reaction
45
Allergic and Anaphylactic Transfusion Reaction • Common with_____ transfusions _____→ mast cell degranulation (release of vasoactive amines) _____→ IgA-deficient patients
plasma IgE IgA
46
________- The S&S are usually limited to the skin and the GIT (Abdominal pain, urticarial rashes, hives) ________- Multi-organ failure, Shock, hypotension and even death
Allergic TR Anaphylactic TR
47
Clinical S&S Hives, erythema, itching within 15-20 minutes of transfusion (Cutaneous)
ALLERGIC
48
Clinical S&S Rapid onset and severe, after a small volume is transfused; wheezing, coughing, dyspnea, bronchospasm, respiratory distress, vascular instability; no fever
ANAPHYLACTIC
49
Major complications Shock, loss of consciousness; death
ANAPHYLACTIC
50
Causes Recipient antibodies to foreign ***plasma proteins*** or other substances such as drugs or food consumed by blood donor
ALLERGIC
51
Causes Associated with ***genetic IgA deficiency*** (Not always) in recipient; possesses IgG, complement-binding anti-lgA antibodies
ANAPHYLACTIC
52
Management Transfusion interrupted and ***antihistamine administered***
ALLERGIC
53
Management Transfusion terminated; ***epinephrine (Steroids)*** administered Oxygen administered and open airways maintained
ANAPHYLACTIC
54
Prevention ***Premedication with antihistamine*** if patient history reveals repetitive allergic reactions May necessitate ***washed cellular products***
ALLERGIC
55
Prevention Plasma-containing products from IgA-deficient donors Washed red cell and platelet products
ANAPHYLACTIC
56
Respiratory distress and pulmonary edema (1-2 hours post-transfusion) Infusion of antibodies to leukocyte antigens (Class I and I| HLA)
Transfusion-Related Acute Lung Injury (TRALI)
57
Transfusion-Related Acute Lung Injury (TRALI) Respiratory distress and pulmonary edema (______post-transfusion) Infusion of____ to leukocyte antigens (Class I and IIHLA)
1-2 hours antibodies
58
The donor has antibodies against the HLA antigens present within the recipient ***The most common cause of Transfusion Related Death***
TRALI
59
• Anti-HLA can activate the neutrophils: Epithelial damage Capillary leakage Pulmonary edema
TRALI
60
According to Harmening, the blood units that contain Anti-HLA antibodies came from MULTIPAROUS WOMEN (Many history of pregnancy) ; That is why recommended donors are male.
TRALI
61
Clinical signs and symptoms Marked respiratory distress; fever, hypotension, chills, cyanosis; rapid onset-occurs during transfusion or ***within 6 hours of completion***
62
Causes Interaction of granulocytes and HLA-specific donor antibodies, complement activation, aggregation of granulocytes that leads to ***blockage of pulmonary microvasculature;*** capillary damage, vascular leakage, pulmonary edema
63
TRALI Clinical laboratory test DAT-_____; no visible hemolysis; WBC antibody screen in donor and recipient
negative
64
Transfusion-Related Acute Lung Injury (TRALI) Management Respiratory support Prevention Defer implicated donor for_____ containing components; Avoid use of_____ components from_____
plasma plasma ; multiparous women
65
Rare but highly lethal ***(90% mortality rate)*** VERY immunocompetent donor lymphocytes (Particularly ***T-cells)*** _____ days post-transfusion
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE 3-6 days
66
The Cytotoxic T-cells of the donor will attack the organs and tissues of the recipient The host is unable to destroy the transfused cell the donor lymphocytes will proliferate and respond to the HLA antigen in the host To prevent this from happening we either give the donor immunosuppressants or we irradiate the blood unit to kill of the T-cells
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
67
Management ***Unresponsive to medical intervention*** Prevention ***Irradiation of blood products*** before transfusion in at-risk recipients; ***gamma irradiation*** (25 Gy) to prevent blast transformation of donor lymphocytes 10
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
68
Clinical laboratory test Confirmation by HLA typing to ***demonstrate a disparity between donor lymphocytes*** and ***recipient tissues***
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
69
Causes Transfused immunocompetent ***T lymphocytes mount immunologic response against recipient***
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
70
Major complications TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
Sepsis and hemorrhage; 90% mortality rate
71
Clinical signs and symptoms Onset 3-30 days posttransfusion; fever, erythematous maculopapular rash, abnormal liver function; nausea, vomiting, jaundice, abdominal pain, diarrhea
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE
72
BACTERIAL CONTAMINATION OF BLOOD PRODUCTS •______ in donor (asymptomatic) Minimal amt of bacteria; Was not detected upon screening •_____ during collection • Bacterial endotoxins (Came from Gram-______bacteria) • Rapid shock d/t hypotensive episodes • Common in_____ transfusions b/c they are stored @ RT
Bacteremia Improper cleansing negative platelet
73
RBC UNITS Contaminated with GRAM-NEGATIVE BACTERIA (_______; Can tolerate lower temps; More severe) •________
Enterobacteriaceae Yersinia enterocolitica
74
PLATELET UNITS Contaminated with GRAM-_____ BACTERIA (Normal Skin Flora) ________
POSITIVE Staphylococcus aureus
75
BACTERIAL CONTAMINATION OF BLOOD PRODUCTS Prevention
Use of diversion pouches Care during phlebotomy Use of plastic collection bags
76
Management Broad-spectrum antibiotic therapy (treatment prior to confirmation)
BACTERIAL CONTAMINATION OF BLOOD PRODUCTS
77
BACTERIAL CONTAMINATION OF BLOOD PRODUCTS Causes Clinical laboratory test
Donor bacteremia, improper cleansing of venipuncture site Gram staining, Bacterial culture and identification
78
BACTERIAL CONTAMINATION OF BLOOD PRODUCTS Clinical signs and symptoms Major complications
Same as acute hemolytic transfusion Shock
79
• A patient receiving a blood transfusion gets too much fluid too quickly, ***straining their heart and lungs.*** ***Cardiopulmonary system exceeds volume capacity*** Dyspnea, severe headache, peripheral edema, and signs of CHF during or shortly after transfusion
TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD
80
At risk: • Elderly and infants • Compromised cardiac and pulmonary status • RBC infusion
TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD
81
Reasons for_____ to manifest: • Massive transfusion protocol (Too much blood was given) • Error in infusion rate (Too fast blood infusion)
TACO
82
• RBC infusion • Stop the transfusion immediately and other IV • Place the patient in upright position • Administer supplemental oxygen • Diuretic medications (To excrete excess)
TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD
83
TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD RBC infusion Stop the transfusion immediately and other IV • Place the patient in_____ position • Administer supplemental____ •______ medications (To excrete excess)
upright oxygen Diuretic
84
• Accumulation of excess iron in macrophages (Iron-Laden Macrophages) Iron-overload (Regularly blood transfused patients) Thalassemia Sickle-cell disease
TRANSFUSION HEMOSIDEROSIS
85
PREVENTION • Use of chelators • Deferiprone • Deferoxamine • To avoid iron being absorbed by the macrophages, thus they can now be excreted
TRANSFUSION HEMOSIDEROSIS
86
Transfusion of large amounts of citrate Citrate is present in most of the blood unit prepared; Acts as an additive/ anticoagulant
CITRATE TOXICITY
87
At risk • Massive transfusions • Impaired liver functions (Cannot metabolize citrate) Infants with hepatic or renal insufficiency
CITRATE TOXICITY
88
PREVENTION: Citrate toxicity
• Remove-plasma (Cleanse the blood unit from citrate anticoagulant) • Calcium chloride/ calcium gluconate
89
POST-TRANSFUSION PURPURA • Platelet counts plummets_____ days post-transfusion •_______ • Sensitization to HPA-1a (98% frequency) • Alloantibody • Autoantibody
5-12 Anti-HPA-la
90
POST-TRANSFUSION PURPURA • PREVENTION:
• Plasmapheresis • Exchange transfusion • Intravenous immunoglobulin
91
EVALUATION AND REPORTING A TRANSFUSION REACTION WHAT TO DO?
Stop the transfusion Keep IV open with saline Perform clerical check for ID error Contact treating physician Monitor/record vital sign Contact transfusion service Collect post sample and return with blood bag attached IV fluids to the lab
92
POSTREACTION SAMPLE
Clerical check: ID errors? Visual check: hemolyzed or icteric? Direct anti-human globulin test