Risks of Blood Product Administration Flashcards

1
Q

What is NAT testing?

A

Nucleic Acid Amplification Testing
-For HIV, Hepatitis C, Hepatitis B

Reduces window periods:
-HIV : 9 days
-HCV: 7.4 days
-HBsAg: 38 days

Able to detect surface antigens faster than seroconversion.
Reduces the period between acquiring the disease and testing positive for it.

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2
Q

-35% of exposed patients will develop acute virus
-1% will develop fulminant hepatitis (severe liver impairment/failure)
-85% disease resolves spontaneously
-9% chronic persistent hepatitis (benign)
-3% chronic active hepatitis
-1% cirrhosis
-1% hepatocellular carcinoma

A

Hepatitis B Virus

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3
Q

-Commonly mild presentation
-85% of patients-chronic state
-20% chronic carriers develop cirrhosis
-1-5% develop liver cancer

A

Hepatitis C Virus

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4
Q

Requires Hep B as a “helper”; therefore, HBV screening prevents this

A

Hepatitis D

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5
Q

Not a known transfusion pathogen; comes from fecal contaminated water sources

A

Hepatitis E and A

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6
Q

Describe the risk of transmission of Human Immunodeficiency Viruses

A

HIV 1 and HIV 2:
-NAT testing implemented in 1999 for blood
-Heat pasteurization, nanofiltration since mid-1980s for coagulation factors and albumin
-Very low risk of blood transfusion transmission

Human T-Cell Lymphotropic Virus-1 and -2:
-Assay introduced in 1998, now minimal risk of transmission with blood transfusions

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7
Q

What is Cytomegalovirus?

A

Commonly transmitted via blood transfusions.
-In donors, latent virus persists permanently in WBCs (The latent virus persists permanently intracellularly so there is a life long potential for reactivation of the infection or potential for transmission through blood donation or donor organs).
-Can be fatal in immunocompromised patients
At risk:
-Premature neonates
-Organ and bone marrow transplant recipients
-Patient with depressed immune system

Immunocompromised patients should receive leukocyte reduced blood.

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8
Q

What is West Nile Virus?

A

(mosquito-borne flavivirus)
-Epidemic in Midwestern states in 2002
-Often asymptomatic but may develop encephalitis/meningitis
-Death rate 5-10%
-NAT testing began 2003
-Transmission through blood transfusion rare

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9
Q

What is Zika Virus?

A

(mosquito-borne flavivirus)
-Leads to congenital deformations in babies borne to infected mothers (microcephaly)
-Self-limiting infection like dengue – with low-grade fever, conjunctivitis, rash and muscle/joint aches
-However, Guillain-Barré syndrome and other neurologic conditions have been documented.

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10
Q

What is Epstein-Barr Virus?

A

-Cause of mononucleosis, associated with Burkitt lymphoma, nasopharyngeal cancer
-Transmission through blood transfusion rare (whether immunocompromised or not)

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11
Q

What are Prions?

A

Abnormal, pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular proteins called prion proteins, found most abundantly in the brain.
-leads to brain damage and the characteristic signs and symptoms of the disease.
-Prion diseases are usually rapidly progressive and always fatal.
-Creutzfeldt-Jakob disease (CJD)
Variant Creutzfeldt-Jakob disease (vCJD)
-Same prion that causes Bovine spongiform encephalitis (BSE) or “Mad Cow Disease”
-Both are fatal degenerative neurologic diseases
-BSE epidemic in UK 1984-Feb 2004
-158 cases vCJD
-Only one case of transfusion related vCJD (persons who spent more than 6 month in the UK from 1980 to 1996 or 5 years in Europe are prohibited from donating blood)

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12
Q

Describe minor allergic reactions to proteins in donor plasma.

A

-Urticaria occurs in 0.5-4% of all transfusions
-Usually occurs with FFP or platelets
-Symptoms: itching, swelling, rash (histamine release)
-Tx: diphenhydramine, saline washed RBCs
-Washing of platelets is ineffective so if patient needs plts or FFP, pretreat with antihistamine and steroids 1 hour prior to the transfusion.

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13
Q

Describe Anaphylactic reactions to transfusions.

A

Rare, but severe
-Dyspnea, bronchospasm, angioedema, hypotension
-Causes could be due to a hereditary immunoglobulin A deficiency or other protein anomalies.
-Treatment: stop transfusion, epi, methylprednisolone
-Treated RBCs, pretreatment for FFP, platelets

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14
Q

What are the 3 leading causes of death from blood transfusion?

A

1) TRALI
-1: 5,000 units transfused
2) Acute hemolytic transfusion reaction
-1: 12,000 units transfused
3) Sepsis from bacterial contamination
-1: 6 million units transfused

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15
Q

What is the most frequent infectious risk from transfusion?

A

Bacterial contamination of platelets.
-platelets are stored up to 5 days at room temperature

Organisms implicated in plt infections:
-Gram + staph* and strep
-Gram – serratia, e. coli, enterobacter
-Gram + implicated in more cases but -Gram – implicated in more fatalities

Treated with amoxicillin or cephalosporins

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16
Q

What are S/Sx of bacterial contamination of blood?

A

Fever, chills, tachycardia, emesis, shock, DIC, acute renal failure, CV collapse

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17
Q

What is the treatment for suspected bacterial contamination of blood?

A

Stop transfusion, obtain blood cultures, supportive measures, broad spectrum antibiotics

18
Q

What are the two causes of Acute Hemolytic Transfusion Reactions?

A

1) Presence of Antibodies
-Antibodies (Anti-A, Anti-B)
-Antibodies formed as a result of prior exposure to Donor RBCs, Donor platelets, and/or Donor proteins
2) Due to a transfusion of white cells or white cell antibodies

19
Q

What are RBC antigens?

A

-Antibodies that fix complement, cause immediate intravascular hemolysis:
Anti-A, Anti-B, Anti-Kell, Anti-Kidd, Anti-Lewis and Anti-Duffy, Anti-Ss
-> 300 different antigens on RBC

Rh Antibodies don’t fix complement but can cause serious hemolytic reaction

20
Q

Describe the patho of Acute Hemolytic Transfusion Rxn.

A

Occurs both intravascular and extravascular.
-Antigen-antibody complexes form, activating Hageman factor (XII)
-Bradykinin is released
-↑ Capillary permeability & dilated arterioles → hypotension
-Complexes also activate coagulation cascade—30-50% develop DIC
-Also causes release of histamine/serotonin from mast cells → Bronchospasm

Leads to RBC hemolysis → acute renal failure, DIC, & Death

21
Q

Describe the effects of Hemoglobin being released into blood during an Acute Hemolytic Transfusion Rxn

A

-Initially, Hgb binds to Haptoglobin and Albumin
-But once those are saturated, Hgb circulates unbound until excreted by the kidneys.

Renal damage occurs due to several mechanisms:
-Blood flow ↓ due to systemic hypotension, renal vasoconstriction
-Damage to tubules by free Hgb or Antigen-antibody complexes
-Fibrin thrombi in renal vasculature

22
Q

What are the S/Sx of an Acute Hemolytic Transfusion Reaction?

A

-Fever, chills
-Nausea, vomiting, diarrhea
-Rigors
-Hypotension, tachycardia from bradykinin
-Flushed and dyspneic from histamine
-Chest and back pain
-Diffuse intravascular occlusion by red cells
-Restless-sense of impending doom
-With renal failure-oliguria, hemoglobinuria

Many are masked by GA.
-Hypotension, microvascular bleeding, hemoglobinuria may be the only initial clues of hemolytic rxn

23
Q

What is the treatment of an Acute Hemolytic Transfusion Reaction?

A

Stop the transfusion!

3 main management objectives:
1) Maintain systemic blood pressure with volume, pressors, inotropes
2) Preserve renal function
-Urine output promoted with fluids
-Diuretics (mannitol or furosemide or both)
-Sodium bicarbonate to alkalinize the urine
3) Prevent DIC:
-Prevent hypotension
-Support cardiac output to prevent stasis and hypoperfusion

Consider steroids and H1/H2 blockers to decrease bronchospasm

24
Q

What is the definitive test for acute hemolytic reactions? (!)

A

Coombs test
-Direct antiglobulin test
-Examines recipient RBCs for surface immunoglobulin and complement
-Clumping is positive coombs test = antibodies are bound to surface of RBC.
-If positive, additional tests needed

25
What is a Delayed Hemolytic Transfusion Reaction?
Occurs 4-8 days up to 1 month post transfusion. -After apparently “compatible” cross match, transfused red cells are eliminated from the circulation after short interval following transfusion -Due to previous sensitization which waned over time to be undetectable in testing -Commonly involve antibodies against Rhesus, Kell, Kidd, or Duffy antigens, not ABO -Typically antibody-coated RBC sequestered extravascularly -Lysis occurs in the spleen and renal system
26
What are the S/Sx of a Delayed Hemolytic Transfusion Rxn?
Evidence of hemolysis by 1st or 2nd week after the transfusion. Symptoms less severe, self-limiting May be identified by: -Low-grade fever -Increased bilirubin with or without mild jaundice -And/or an unexplained reduction in hgb concentration Tx: Supportive Care
27
How do you diagnose a Delayed Hemolytic Transfusion Rxn?
Diagnosis confirmed by positive direct antiglobulin tests (Coombs test)
28
What are the 3 components of compatibility testing?
1) ABO and Rhesus (Rh) determination 2) The antibody screen (Indirect Coomb’s test) is performed to identify recipient antibodies against RBC antigens other than ABO -While the Coombs test looks for antibodies on the surface of the RBCs, Indirect Coombs looks at free flowing antibodies directed against RBCs 3) The Cross-Match, in which donor RBC’s are mixed with recipient serum -Detects antibodies in low titers or that don’t agglutinate easily -Assures optimum safety -Incident of serious reaction after transfusion with ABO and Rh compatible blood (screen) is < 1%
29
What are the different White Cell Related Transfusion Reactions?
-Febrile reactions -Transfusion-Related Acute Lung Injury (TRALI) -Graft-versus-Host Disease (GVHD) -Transfusion-Related Immunomodulation (TRIM)
30
When are febrile rxns most likely to occur?
In patients who receive multiple RBC or platelet transfusions. -Develop antibodies to human leukocyte antigens (HLA) on passenger WBCs -On a subsequent transfusion, the antibodies attack the WBC antigen -Febrile reaction in 2% of PRBC, FFP, platelet transfusions -Leukoreduction reduces or prevents these reactions -Chills, resp distress, anxiety, HA/Myalgia -Tx: Tylenol -Coombs test will be negative
31
What is Transfusion-Related Acute Lung Injury (TRALI)?
-Noncardiogenic form of pulmonary edema -Has been associated with administration of all blood components containing plasma -Most frequent with FFP, platelets (pheresis) -Incidence 1:5000 transfusions, mortality of 5-8% -Most common cause of transfusion-related death reported to FDA
32
What is the patho of TRALI?
Usually donor anti-leukocyte antibodies activate recipient WBCs. -The donor WBC antibodies were made after a previous transfusion. TRALI requires presence of pre-existing or pre-disposing inflammatory condition in recipient i.e trauma, sepsis, surgery Activated leukocytes sequestered in lung → capillary endothelial damage and ↑ permeability of the lung tissue.
33
What are the S/Sx of TRALI?
-Clinical appearance similar to ARDs Within 6 hours of transfusion: -Dyspnea, fever, chills, labile BP -Noncardiogenic pulmonary edema -Bilateral infiltrates (CXR) Treatment: -Oxygen, ventilator with low TVs -No diuretics or corticosteroids needed
34
What are risk factors for Transfusion associated circulatory overload (TACO)?
Impaired myocardial function & rapid, aggressive fluid therapy.
35
What are the S/Sx of TACO?
Associated with signs and symptoms of cardiac dysfunction (hx of CHF, low EF, etc.) and/or volume overload.
36
What are ways to prevent TRALI?
1) Restrictive transfusion strategy -Greater volumes of blood components = ↑ risk of TRALI 2) Universal leukoreduction -Will get rid of anti-leukocyte antibodies in both donors and recipients 3) Frequent source of anti-leukocyte antibodies are multiparous female donors and other donors who have had multiple transfusions -Limit these donors
37
What is Graft vs Host Disease?
PRBCs and platelets contain significant numbers of viable donor lymphocytes. -When transfused into an immunocompromised individual, the donor lymphocytes may become engrafted, proliferate, and establish an immune response against the recipient -In other words, the engrafted lymphocytes reject the host. -progresses from bone marrow suppression to pancytopenia
38
Who are patients at risk for GvH Disease?
T-cell immune deficits, bone marrow transplants, Hodgkin’s lymphoma and maybe other hematologic malignancies, neonates who have undergone a exchange transfusion in utero, babies weighing less than 1200 gm at birth, other immunocompromised patients and Patients receiving blood from a first degree relative.
39
What types of products can cause GvH Disease?
Only reported after transfusion of cellular blood components -Not after FFP, cryoprecipitate
40
How can you prevent GvH Disease?
Irradiate cellular blood products to inactivate the lymphocytes in transfused blood. -For immunocompromised patients -For direct donor units from 1° relatives -Leukoreduction decreases incidence but does not prevent GVHD -Irradiation only effective means to prevent GVHD
41
What is Transfusion-Related Immunomodulation (TRIM)?
Allogenic blood transfusions associated with immunosuppression &/or proinflammatory effects -First seen in renal transplant patients (less likely to reject organ if received a blood transfusion) -Likely due to transfused WBCs -Adverse effects of immunosuppression: increased recurrence of malignancies, increased rate of infections, and increase in mortality in the short term.
42
How does Transfusion-Related Immunomodulation (TRIM) occur?
During blood storage, bioactive substances such as cytokines, cell membrane breakdown products, and complement accumulate leading to an inflammatory response and multiorgan dysfunction. -Consider Leukoreduction of all blood products