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SBL Test 2 > Martin: Transfusion Medicine > Flashcards

Martin: Transfusion Medicine Flashcards

1
Q

RBC membrane contains what?

A
  1. Proteins: Rh antigens
  2. Carbs: ABO system
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2
Q

What are the primary and secondary response to immunization to RBC antigens?

In other words, how do we develop antibodies to antigens that we DON’T have?

A

1. Primary response: Occurs after 1st immune exposure to a “foreign” protein Ag (days or weeks after exposure)

2. Secondary (anamnestic) response: occurs upon a repeat exposure to a “foreign” protein Ag (noticed much quicker after such exposure); For example, during a transfusion.

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3
Q

For most Blood Group Antigens, but not ABO, what type of AB develop during a primary and secondary response?

A
  • Primary response = a sustained high concentration of IgM + Ab and some IgG after days or weeks
  • Secondary response = transient rise in IgM and a sustained IgG
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4
Q

What antigens make up ABO system?

A
  • 1. H
  • 2. A
  • 3. B
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5
Q

What antigens make up the following blood types:

    1. O blood
    1. A blood
    1. B blood
    1. AB blood
A
  • 1. O blood = H Ag only
  • 2. A blood = H + A
  • 3. B blood = H + B
  • 4. AB blood = H + (A+B)
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6
Q

What is a secretor, in blood bank terms?

A

Someone with “Se” allele, which allows them to make ABO antigens in their secretions and plasma.

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7
Q

Roughly 80% of the population carries at least one allele called “Se.”

What is this allele?

A

“Se” => produces H antigen on “type 1 chains” (long carb-rich chains).

  • Once the H antigen is made, then the person can make either A or B antigens (or both) on the type 1 chains
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8
Q

What is the MC type of blood?

Least common?

A
  • Most common: Type O (45%)
  • Least common: AB
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9
Q

Antigens & Antibodies in person with Type O blood.

A
  • Antigens = H
  • Antibodies =
    1. Anti-A
    2. Anti- B
    3. Anti- AB
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10
Q

Antigens & Antibodies in person with Type A blood.

A
  • Antigens = H + A
  • Antibodies = Anti-B
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11
Q

Antigens & Antibodies in person with Type B blood.

A
  • Antigens = H + B
  • Antibodies = Anti-A
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12
Q

Antigens & Antibodies in person with Type AB blood.

A
  • Antigens = H/A/B
  • Antibodies = None
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13
Q

What are Subtypes of

A
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14
Q

What are the 2 steps in Blood Typing?

A
  1. “Front/forward typing” = determines which antigens are on the patient’s RBC by mixing patients blood with anti-A/B/D antibodies
  2. “Back/reverse typing” = test for isohemagglutinins (antibodies against ABO antigens they do NOT have), like Anti-A/anti-B.
    1. Serum or plasma that was separated from the pts RBC is mixed with two different red cells from the laboratory (A and B cells)
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15
Q

ABO subtypes exist and pose what problem?

A

Can cause compatability issues when transfusing a patient.

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16
Q

What disease can alter expression of ABO antigens on the RBC?

A
  • 1. Leukemia = ↓ Ag
  • 2. “Acquired B” = Intestinal obst → ↑ bowel permeability, bacterial

polysaccharides into circulation abs = orbed by grp A cells

  • 2. Gastric or pancreatic cancer = bld grp specific soluble substances (BGSS) in serum neutralizes antisera used in forward grouping.
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17
Q

What is Bombay phenotype?

What is the problem with this phenotype?

A
  • Rare blood type (Oh/ h/h) where patient lacks H antigen. Thus, RBC has NO antigens.
  • Antibodies: anti-A, Anti-B, Anti-AB and Anti-H Ab.
  • Problem
    • Can donate to ANYONE
    • Can ONLY receive Bombay blood.
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18
Q

What happens when a patient with Bombay phenotype receives a blood transfusion?

A

Anti-H IgM Ab (more common than IgG) activates compliment system => intravascular hemolysis of RBC => acute hemolytic transfusion reaction.

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19
Q

What is a complication in mothers with Bombay phenotype?

A

Hemolytic disease of the newborn can occur (Oh, h/h)

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20
Q

Type O blood can donate blood to who?

A

All types.

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21
Q

Type A blood can donate blood to who?

A
  1. Type A
  2. Type AB
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22
Q

Type B blood can donate blood to who?

A
  1. Type B
  2. Type AB
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23
Q

Type AB blood can donate blood to who?

A
  1. Type AB
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24
Q

What is the Rh (Rhesus) System?

A

Transmembrane protein antigens on a RBC.

Ab to Rh antigens NOT naturally-occuring antibodies and made d/t exposure of a antigen during pregnancy or transfusion.

5 most important antigens are

    1. D (Rhesus factor) = Rh+
    1. “d”= absence of D = Rh-
    1. C = co-dominant with c
    1. E = co-dominant with e
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25
Q
  1. Rh (+) =
  2. Rh (-) =

What is the most common?

A
  1. Rh (+) = has D antigen* (MC, esp in whitez n azn)
  2. Rh (-) = lacks D antigen
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26
Q
  1. Do Rh (-) people develop anti-D Ab naturally?
  2. If so, what type of Ig are they?
  3. What problem can develop if Ab develop?
A
  1. Antibodies only develop if pt is exposed to D+ RBC, like in transfusions and during pregnancy if mom is D- and baby is D+ (hence, NOT naturally occuring Ab)
  2. IgG anti-D Ab
  3. IgG anti-D Ab can cross placenta and Newborn Hemolytic Disease (Hydrops fatalis):
    1. Occurs if mom is Rh(-) and bb is Rh(+) or if dad and bb are both (Rh+):
    2. 1st pregnancy: Mom is exposed to Rh(+)/D+ RBC when baby is delivered and develops IgG anti-D Ab.
    3. 2nd pregnancy: IgG anti-D Ab => cross placenta => attack bbs RBC if the 2nd bb is also Rh(+)/D+.
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27
Q

Test to determine if mom has anti-D IgG Ab?

A

Indirect Coombs Test:

  1. Mix moms serum + D+ RBC
  2. (+) = mom has anti-D+ IgG aB
    1. RBC will agglutinate
  3. (-) = mom does NOT have anti-D IgG aB
    1. RBC do NOT agglutinate
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28
Q

What is RhoGAM?

What findings will be seen after administration?

A

RhoGAM = anti-D Ig medication that prevents Rh immunization in pregnancy or obstretrical complication, a condition where Rh(-) mom develops Ab after exposed to Rh(+) blood.

Transatory increase of passively transferred Ab in the patients blood will cause positive serology testings results.

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29
Q
  1. What are other antigens on the RBC?
  2. When are they tested for?
  3. How do AB against these antigens develop?
A
  1. Kell, Duffy, Kidd, MNS, Lewis
  2. Only tested when patient has ABNL screening test
  3. Ab only develop during pregnancy or transfusion (thus, NOT natural. ONLY natural are A/B antibodies)
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30
Q
  1. What is the Kell antigens on the surface of RBC?
  2. What is their importance?
  3. Most common phenotype?
A
  1. Antigens =
    • 1. K = kell
    • 2. k= cellano
  2. 2nd in immunogenicity (2nd most targeted antigens, D).
  3. MC phenotype = kk (91%)
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31
Q

What alloantibodies develop to Kell antigens?

When does this cause a problem?

A

Anti-K IgG alloantibody.

  • No Kell antigen => Anti-K IgG AB develop during transfusion/pregnancy with blood containing that antigen.
  • Can cause
    • 1. HDN
    • 2. Hemolytic transfusion rxn
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32
Q

Kell system McLeod phenotype is associated with what diseases (2)?

A
  1. Chronic compensated hemolytic anemia = presence of acanthocytes on blood smear.
  2. Chronic granulomatous disease (CGD) = Lack K Ag on neutrophil/monocytes membrane => deficiency of NADH-oxidase => no H2O2 to destroy microbes = > increase risk of bacterial infections.
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33
Q

What are the Duffy Antigens?

A

Duffy glycoprotein = receptor for malarial parasite Plasmodium vivax.

Antigens =

    1. Fya = Duffy(a)
    1. Fyb = Duffy (b)
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34
Q

What is the MC Duffy phenotype in African-Americans?

What does this imply?

A

Fy (a-,b-) = resistant to Plasmodium vivax infection

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35
Q

What antibodies are produced against Duffy antigens?

What problems can they cause?

A

IgG => cause HDN & hemolytic transfusion rxn

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36
Q

What are the MNS antigens?

- Antibodies?

  • Exhibits what effect?
A
  • 4 important antigens: M, N, S and s
  • Antibodies: Anti-M IgM antibodies, but non-hemolytic
  • Dosage effect = react more strongly with homozygous cell, than hetero
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37
Q
  • What are Kidd antigens?
  • What antibodies develop to antigens?
  • What problems does it cause?
  • Antibodies exhibit ____ phenomenon.
A
  1. Antigens = Jka/Kidd (a) and Jkb/Kidd (b)
  2. Antibodies = anti-Jka IgG ab and anti-Jkb IgG ab = common, but low titers and weak, so they disappear quickly.
  3. Causes
  • Delayed Hemolytic Transfusion reactions: (+) compliment => rapid hemolysis. Then, Ab disappear and reappear when transfusion with Kidd
    4. Dosage phenomenon
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38
Q

What blood type is the universal recipient/donor?

A
  • Universal recipient: AB+
  • Universal donor: O-
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39
Q

What is the MC complication of transfusions?

A

Febrile nonhemolytic reaction = Fever (1C or >), chills, HTN ± dyspnea within 6 hours of a transfusion of red cells or platelets. Due to

  • Pyogenic cytokines (IL-1) that are made by donor WBC during storage causing an inflammatory reaction where Ab react to antigens on donor WBC.
40
Q

Febrile non-hemolytic reaction

  1. DDx
  2. What increases risk?
  3. Treatment?
  4. Prevention?
A
  1. DDx
    1. Hemolytic transfusion reaction
    2. TRALI
  2. WBC that are stored longer
  3. Tx = Symptoms are short-lived;
    1. Treat with antipyretics
    2. NO ASA
  4. Prevention:
    1. Give anti-pyretic before transfusion
    2. Pre-storage leukocyte reduction,
    3. Plasma reduction or wash PC
41
Q

RBC only last ___ days

Platelets only last ___ days

Plasma may be frozen and stored for ___ year.

A
  • Red blood cells only last 42 days
  • Platelets only last 5 days
  • Plasma may be frozen and stored for 1 year.
42
Q

Other complications to transfusions

A
  1. Allergic reaction
  2. Hemolytic reactions (acute and delayed)
  3. Transfusion-realted acute lung injury (TRALI)
  4. Infectious reactions
43
Q

Allergic reaction d/t transfusion

  1. Who is this more likely to occur in?
  2. How does it occur?
A
  1. Previously sensitized recipients (MC in people with IgA deficiency)
    1. IgA deficient person => produces anti- IgA Ab
    2. IgA Ab can react with IgA in infused blood => allergic reaction
  2. ​​Uticarial allergic reactions can occur when recipients IgE Ab recognize allergen in blood.
44
Q

What are symptoms of Allergic reaction to transufion?

A

SX: pruritis, urticaria, erythema, & cutaneous flushing.

  • If upper airway=> laryngeal edema (hoarse + stridor + lump in throat)
  • if lower airway => bronchonstriction (wheeze, tightness, dyspnea)
    *
45
Q

Allergic reaction during transfusions

  1. DDx
  2. Tx
  3. Prevention
A
  1. DDx = drug reaction, allergy to tape/latex
    1. If dyspnea, R/O TRALI and volume overload
  2. Treatment =
    1. intubate and O2 prn
    2. IV antihistamine
    3. do NOT have to DQ transfusion.
  3. Prevention
    1. Premedicate with antihistamine
    2. Cant ID Ag, so cant select Ag- neg products, except in IgA deficiency.
46
Q

Treatment/prevention of a severe anapylactic reaction?

A
  1. Treatment = same as allergic reaction + EPI, diphenhydramine (if cutaneous sx) and Aminophylline (if bronchospasm)
  2. Prevention =
    1. IgA def pt have anti-IgA ab, so give products with NO IgA.
    2. Pre-med with antihistamine/ steroids
47
Q

What is the feared complication of blood transfusions and the reason why type and crossmatching occur before transfusions?

A

Acute Hemolytic Transfusion Reaction (AHTR)

Preformed Ab in patient react to antigens on donor RBCs (Type 2 HS reaction), usually due to transfusion of an incorrect blood product.

48
Q

Acute Hemolytic Reactions due to transfusions

  • Caused by?
  • Most common cause?
A
  • Compliment-mediated intravascular hemolysis within 24 hours of transfusion: Pre-formed IgM Ab in patient react to donor RBC
  • MCC = Human error (problem in patient ID/ tube labeling), causing RBC incompatability
49
Q

Acute Hemolytic Reactions due to transfusions

  1. IgM Ab that react to antigens on donor RBC cause what?
  2. Symptoms?
  3. Tests to detect problem?
A
  • Complement-mediated intravascular hemolysis & hemoglobinuria.
  • Symptoms:
      1. Fever, hypOtension, and flank pain that appear rapidly.
      1. Progress to DIC, shock, acute renal failure, and death.
  • Test
    • (+) Direct Coombs test: detects Abs that coat RBC.
50
Q

Mortality and DDx of Acute Hemolytic Transfusion Reaction

A
  1. Mortality depends on amount of RBC transfused
  2. DDx= AIHA
51
Q

Treatment and prevention of AHTR

A

Treatments

  1. DQ and verify ID (another patient may be getting a wrong product.
  2. If severe, CV support, fluid resucittaiton, presso

Prevent = Properly ID patients!

52
Q

Delayed Hemolytic Reactions due to transfusions

  • Caused by?
  • Most common cause?
A
  • Caused by = IgG antibodies from prior tranfusion/exposure to foreign protein antigens => extravascular hemolysis tht occurs >24 hours - 2 weeks after transfusion
  • MCC = prior blood transfusions
53
Q

Delayed Hemolytic Reactions due to transfusions

  • Associated labs and tests?
  • Ab to antigens like Rh, Kell and Kidd can cause what?
  • DHTR can cause _____ in what sickle cell patients
A
  • Labs/tests
    1. (+) Direct Coombs test
    2. Hemolysis: ↓ haptoglobin, ↑ LDH, rise in unconjugated Hgb
    3. ↓ H&H
    4. Detection of new RBC Ab*****
  • (+) compliment => severe and fatal reactions.
  • Sickle cell crisus
54
Q

DHTR

  1. Treatment
  2. Prevention
A
  1. Most tolerate well, observe patient
    1. If extravascular hemoslsis occurs => IVIG
  2. Prevention = detect RBC AB via serology
55
Q

What is Transfusion-related acute lung injury (TRALI)?

A

Severe, often fatal hypoxemia within hours of tranfusion due to activation of MHC-I Ag on neutrophils in the lungs by transfused blood. MC occurs in

  1. Patients with lung disease
  2. Multiparous women.
  3. High levels of donor antibodies (fresh frozen plasma and platelets)
56
Q

What is the pathogesnsis of TRALI?

A

“Two hit” hypothesis.

  1. 1st hit = priming event that leads to neutrophils in lungs
  2. 2nd hit =
  • Transfused AB recognize MHC- 1 antigens on neutrophils in lungs, which are most often found on multiparous women
57
Q

Clinical Presentation of TRALI

A
  1. Sudden onset respiratory failure, during or soon after a transfusion.
  2. CXR = non-cardiogenic pulmonary edema (diagnostic and resolves in 48-96 hours)
  3. NO ABNL breath sounds and NO signs of cardiac failure.
58
Q

Treatment and prevention of TRALI

A

Treatment =

  1. Antipyretic and fluids to tx HTN and fever
  2. Supportive

Prevention =

  1. ↓ lipid mediators by pre-storage leukocyte reduction or ↓ storage time of cellular components, esp platelets
59
Q

Bacterial contamination is much more common in platelet/RBC preparations. Why?

A

Platelets: platelets (unlike red cells) must be stored at room temperature; which favors growth of bacteria

60
Q

Most bacterial infections transmitted through transfusions are _____, indicating what?

A

Skin flora, indicating that contamination occur when product was obtained from donor.

61
Q

Bacterial contamination during transfusion depends on what?

A

Type and storage of what you are tranfusiing.

  1. Yersenia entercolitica and pseudomonas = in PC
  2. Staph, strep, E.coli and serratia = platelets
62
Q

Symptoms of infection due to transfusion

A
  • Fever, chills, hypotension: resemble symptoms seen in hemolytic/ non-hemolytic transfusion reactions.
63
Q

Viral infection via blood products has decreased.

However, when can it occur and what viruses are more commonly transmitted?

A
  1. When the donor is acutely infected, but the virusDNA/RNA cannot be detected.
  2. HIV, hepatitis C, and hepatitis B.
64
Q

To donate blood, how old do you have to be and what requirements do you have to meet?

A
  1. 16 YO.
  2. Weight/Hb level requirments must be met
65
Q

What are reasons you can be denied being able to give blood?

A
  1. Receipient of dura mater graft
  2. Transfusion of blood or blood components within the previous 12 months, or human-derived clotting factors within the previous 12 months
  3. Incarceration under certain circumstances
  4. Getting a piercing or tattoo with nonsterile materials within the previous 12 months
  5. Certain medications
  6. Pregnancy
  7. Needle use for not anything prescirbed
  8. HIV+
  9. Hep since 11YO
  10. Babesiosis, Chagas, CJD, cCJD
66
Q

Who is responsible for all aspects of donor selection and donor safety?

A

Blood bank medical director

67
Q

How are specimans collected and what must the speciman include?

A
  1. Collected at beside
  2. Must include the time + date + initial of phlebotomist.
  3. Each patient must have a permenant and unique ID
68
Q

What are common tests performed prior to transfusions?

A
  • 1. Blood type testing (Forward/front typing = mix pts RBC + antibody => agglutination will indicate presence of antigen on RBC)
    • Example: Pt RBC + anti-A ab: if agglutination occurs, pt is A(+).
  • 2. Type and screen (T&S)
  • 3. Cross match
69
Q

What is performed in a Type and Screen (T&S) test?

When is it performed?

A
  1. Determine ABO + Rh of patients RBC
  2. Antibody screening test = screen for Ig Ab to rare antigens via Indirect Antiglobulin Test (IAT/ Indirect Coombs test), which will only be present if prior exposure.
    1. If (+), perform Ab indentification to ID specific antibodies.
  3. Perform when transfusing
70
Q

What is a Type and Crossmatch test (type and cross)?

A
  • Match donor blood to patients
71
Q

How is a Antibody Screen done?

  • Purpose
  • How is test performed
  • When is it performed
A

Indirect Antiglobulin Tests/ Indirect Coombs Test

Purpose: detects antibodies freely floating in patient to rare antigens, which only develop if prior exposure.

Test:

  1. Mix patients serum (which contains Ig Abs) + Reagent RBC/foreign RBC (RBC with many antigens)
    1. (+) => RBC agglutinate due to presence of antibodies. Next, perform other tests to determine the specific Ab present.
    2. (-) => RBC do not agglutinate and NO Ab are present.

When is it performed?

  1. Before blood transfusion to detect if a reaction will occur
  2. Prenatal testing of PG women
72
Q

What is a Direct Coombs test?

  • Purpose
  • How is test performed
  • When is it performed
A
  • Purpose: Test used to detect Ab/compliment proteins that are attached to RBC, which can destroy and cause anemia.
  • Test:
      1. Mix pts RBC + anti-human AB
      1. (+) = > agglutination occurs
  • When is it performed?
    • Detect AI hemolytic anemia
    • W/U of Transfusion reaction
73
Q

What test is done if ABNL Ig are detected in the T&S?

A
  1. Antigen detection test = determine specific antibody present in patient, not made by the patient.
  2. Test =
    1. Commercial anti-sera + patients cells
    2. Confirms whether patient has antigens on cells.
74
Q

What is the purpose of IAT/Indirect Coombs Test?

What antibodies are detected at room temperature, 37 degrees and AHG?

A

Checks for AB in serum to check for hemolysis and agluttination.

  1. Room temp = Cold IgM Abs
  2. 37 degrees = warm Abs
    1. IgG
    2. Rh
    3. Kell, Kidd, Duffy
  3. AHG (anti-humanglobulin) = Warm IgG Abs attached to RBC membrane
75
Q

What is the MC autoAB?

A

Benign cold IgM agglutinin.

76
Q

What is Cold Agglutinin Disease?

A
  • IgM ab autoAb bind to RBC at cold temperatures => (+) compliment -mediated intravascular hemolysis => cause life-threatening hemolyic anemia due to Mycoplasma pneumonia or EBV (infectious mono)
77
Q

How is Type and Crossmatching/Compatability testing done?

A

No agglutination or hemolysis = compatable!

78
Q

Who can receive donor A PC?

A
  1. A
  2. AB
79
Q

Who can receive donor B packed cells?

A
  1. B
  2. AB
80
Q

Who can receive donor AB blood?

A

Only type AB blood

81
Q
  1. When a transfusion is performed, what should you do to make sure an AE (adverse effect) does not occur?
  2. If it does, what do you do next?
A
  1. Monitor closely for the first 15 minutes of transfusion and intermittingly during
  2. If AE:

1. Immediately stop transfusion!

2. Immediately report reaction to blood blank.

  1. Retrun bag with attached tubing + paperowrk
  2. Send post-transfusion blood sample + urine (not as emergent)
82
Q

When is transfusion of RBC indicated? (4)

A
    1. ↑ in O2 carrying capacity (someone is hypoxic)
    1. Hgb <7 or Hct <21 in healthy pt WITH acute anemia (bleeding)
    1. Hgb is 7-9 in pt with cardio/cerebrovascular RF.
    1. HbS is 30-50% in Sickle cell pts to prevent stroke.
83
Q

PRBC

  1. What are PRBC?
  2. When is it indicated?
  3. What are the expected effects?
  4. CI?
A
  1. RBC with plasma removed
  2. ↑ RBC mass in pts w symptomatic anemia due to ↑ blood loss, ↓ survival or production
  3. Effects: In 24 hours, 1 unit will; ↑ O2 carrying capacity
    1. ↑ 1-2g/dL Hb
    2. ↑ ~3% Hct per unit
  4. CI = Volume expansion, coagulation deficiency or drug treatable anemia
84
Q

Platelets

  1. When is it indicated?
  2. What are the expected effects?
  3. CI?
A
  1. Bleeding d/t thrombocytopenia or prophylaxis in severe thrombocytopenia without bleeding (<10,000 platelets)
  2. 6 pooled platelets in adults => ↑ plt count by 30-60,000
  3. CI =
    1. Plasma coagulation deficit
    2. Rapid plt destruction (ITP or TTP)
85
Q

During platelet transfusions, what complication can occur?

A
  • Complications less likely bc platelets only have ABO antigens and HLA-1, not Rh or HLA-2. But
    • Rh exposure from RBC contamination can occur; may need RHIG
86
Q

How many platelets are in “pooled platelets” (6 single units from 6 ppl into 1 standard dose “6 pack”)?

What do they consist of?

A

5.5 x 10¹⁰/unit

+ fibrinogen + WBC

87
Q

What are pheresis platelets and how are they beneficial?

A

Platetlets come from a ONE donor, which decreases exposure to single donors and increases platet retention = decreases risk of infections.

88
Q

Fresh Frozen Plasma (FFP)

  1. What does it contain
  2. Indication (3)
  3. Threshold (3)
  4. CI
  5. Effect
A
  1. All coag factors + 400mg of fibrinogen
  2. Indication = Deficiency of coag factor with or w/o bleeding; Emergent reversal of Warfarin; Tx TTP
  3. Threshold:
    1. Prophylatic if PT/PTT are prolonged and pt is at risk of bleeding
    2. Documented factor deficiency in bleeding patient
    3. Isolated factor def for which factor derivative is not avail.
  4. ​CI = Volume expansion
  5. Effect:
    1. PT/PTT normalize,
    2. 1 unit will increase factor level by 20-30%

Once thawed, must used within 24 hours or clotting factors degrade.

89
Q

Cyroprecipitate

  1. What it is?
  2. Threshold (1)
  3. Indications? (6)
A

What is it? Thawed FFP that contain tons of fibrinogen + vWF + factor 8

Threshold = Fibrinogen <80 mg/dL with ongoing bleeding

Indications =

  1. Hemophilia A
  2. von Willebrand’s disease
  3. Factor 8 def
  4. Hypofibrinogenemia DIC
  5. Bleeding uremic patient
  6. Topical glue
90
Q

How is RhoGAM administered?

A
  1. 1 full dose (300mg) at 26-28 wksgestation or within 72 hours of delivering Rh+ infant
    • 1 mini dose (50mg) for termination or ectopic pregnancy before 12 wks GA
  2. 1 full IM dose of 15 mL of Rh + RBCs or 30mL of WB
  3. IV Ig of Rh over 8 hours until full dose is reached
91
Q

What should you do before administering blood and what is the most important step in a SAFE transfusion?

A
  1. Identification of Patient!!!
  2. Verify unit
  3. The most important step in safe transfusion is clerical verification!!
92
Q
  1. Infusion time: must be completed in ___
  2. Unused units MUST be returned within ____
  3. Only _______ can be transfused with blood!!
A
  1. 4 hours
  2. 30 minutes
  3. NL saline
93
Q

How are neonates transfused?

A

“quad” packs

94
Q

What is defined as massive transufions?

How is it done?

Problems?

A

Replacing patients full blood volume within 24 hrs.

Usually 10-12 units in an adult/ day; 1 unit of FFP for ever 2-3 units of RBCS

Problems:

  1. Coagulopathy
  2. Hypothermia
  3. Hypocalcemia
95
Q

What is the Kleihauer-Betke Test?

How is it performed?

A
  • Detects fetal Hgb in moms blood to quantify fetal maternal hemorrhage.
  • Perform: Take blood smear of mom blood and give acid bath. This removed adult Hgb, but not fetal.
96
Q

If patient has a transfusion reaction and displays dyspnea, what 2 diagnoses can we rule out of our DDX?

A
  1. TRALI (no ABNL breathing sounds)

2. Volume overload

SBL Test 2 (11 decks)

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