Transfusion Medicine, ASPHO Flashcards

1
Q

2 major types of blood products adn egs?

A
  • Cellular prods (pRBCs, plts, granulocytes)

- Non-cellular prods (FFP, Cyro)

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2
Q

What are the 2 types of collection?

A
Whole blood (component separation via centrifugation and processing)
-Apheresis= single component collection
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3
Q

Centrifugation separates whole blood how?

A

Plasma on top of plts on top of RBCs

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4
Q

What can you do with centrifuged plasma?

A

freeze plasma as is and keep as plasma or thaw frozen plasma and resuspend to allow you to get to cryoprecipitate

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5
Q

plasma and plts are part of the __ ____

A

buffy coat

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6
Q

plts from whole plts need to be combined with about ___ other derived plt donation to get whole unit

A

5

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7
Q

collection via apheresis: can collect ___ RBCs, ___ plasma units and ___ plt units

A

double; double; ~1-2

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8
Q

centrifuge separate blood components based on what?

A

specific gravity

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9
Q

RBCs: storage temp?

A

2-6 degrees C

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10
Q

RBCs shelf life?

A

21-42 days

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11
Q

RBCs: leukodeplete when?

A

pre-storage

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12
Q

RBCs: warm before transfusion?

A

no

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13
Q

RBCs: hct of unit?

A

~55%

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14
Q

if RBCs in glycerol, store at what temp? and for how long?

A

-65, 10 years

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15
Q

once thawed and deglycerolized, RBCs good for how long? can they be refrozen?

A

24 hours; no

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16
Q

Plts: storage temp?

A

20-24C

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17
Q

Shelf life of plts?

A

5 days

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18
Q

Plts require constant ____ ____

A

gentle agitation

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19
Q

Plasma: store at what temp and for how long? 3 options

A

1 year

2-6 C–> 5 days (thawed) or 28 days (never frozen)

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20
Q

what’s the definition of FFP?

A

plasma frozen no later than 8 hours after collection

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21
Q

what’s the definition of Frozen plasma (not FFP)?

A

plasma frozen <24 hours after collection

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22
Q

Cryo: storage temp and shelf life?

A

-18 C, 1 yr

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23
Q

cryo is pooled into packs of __ or ___

A

5 or 10

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24
Q

granulocytes: stored at what temp for what period of time?

A

20-24; 24 hours

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25
Q

granulocytes should be given ___

A

ASAP

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26
Q

RBC shelf life depends on the storage solution: name 5 and their shelf lives

A
CPD: 21 days
CPDA: 35 days
AS-1: 42 days
AS-5 42 days
AS-3: 42 days
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27
Q

What does AS1,3,5 contains that CPD adn CPDA doesnt?

A

mannitol

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28
Q

Name 4 common bacteria that live at 1-6 C and can infect pRBCs

A

-Yersinia enterocolitica
Listeria monocytogenes
Serratia liquefaciens
CoNS

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29
Q

Pts with cold agglutinin disease should be given pRBCs how?

A

through a warmer to prevent further hemolysis

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30
Q

which blood product has highest rate of bacterial contamination? rate? % of these units that cause infection?

A

plts; 1 in 1000-2000 units; 10%

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31
Q

70% of infections caused by plts are ___ ___ but ___ ___ cause 80% of deaths

A

gram positive; gram neg

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32
Q

which blood prod= most difficult to store during disasters?

A

plts

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33
Q

define blood type

A

ABO and RH (D) type of recipient

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34
Q

Screening does what?

A

eval for alloantibodies again common and clinically significant RBC antigens

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35
Q

Crossmatching does what?

A

electronically or manually confirm compatibility between donor and recipient

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36
Q

Blood type A have __ Ag; they have __ antibodies; blood type compatible in emergency?

A

A; B; A or O

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37
Q

What are isohemagglutinins?

A

(ANti-A or anti-B); are IgM abs formed by non-A and non-B individuals, respectively due to environmental exposures

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38
Q

Type O individuals have what IgMs and IgG?

A

IgM: anti-A, anti-B
IgG: anti-AB

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39
Q

which antibodies are responsible for acute hemolytic transfusion rxn?

A

-IgM

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40
Q

what causes hemolytic disease of fetus/newborn?

A

anti-AB IgG…IgM does NOT cross the placenta!

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41
Q

what’s the difference between a minor and major mismatch?

A

minor: donor is anti-recipient (avoid when possible); major= recipient is anti-donor (avoid at all costs)

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42
Q

Give an example of front and back types being different

A

Patient has A RBCs but no anti-B antibodies

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43
Q

Give 4 causes of front and back types being different

A

Immunosuppression, young infants, patients undergoing ABO-mismatch HSCT, chimerism

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44
Q

How are alloabs evaluated?

A

Pt plasma mixed with panel RBCs that have known antigen profiles; tests for common and clinically significant alloabs

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45
Q

what does direct coombs test do?

A

looks specifically at RBC-bound Abs. the pt’s red cells are mixed with anti-human Ab= coombs reagent–> agglutination of ab-coated RBCs

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46
Q

what does the indirect coombs test do?

A

looks for anti-red cell Abs in the pt’s plasma. pt’s plasma gets mixed iwth future donor or panel RBCs; mix with coombs reagent. agglutination caused by human IgG on RBCs reacting with anti-human Abs from teh coombs reagent.

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47
Q

what is crossmatch?

A

first screen: pt plasma + rbcs from donor…can also add anti-human IgG if desired…if screen is negative, usually do electronic crossmatch

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48
Q

screen and crossmatch good for how long?

A

72 hours

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49
Q

if emergency, do what?

A

give uncrossmatched blood: O neg

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50
Q

chance of delayed hemolytic rxn in emerg situation where o neg given?

A

1:14000 (due to pre-formed alloAbs)

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51
Q

what are the two main types of abs in teh plt crossmatch?

A
HPA= anti-human plt antigen
HLA= anti-human leukocyte antigen
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52
Q

which 2 abs are responsible to 90-95% of NAIT?

A

HPA 1 and HPA 5

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53
Q

plts need to be compatible how?

A

ABO and Rh (because there are some RBCs in the plt units and plts have A and B antigens in pts who have A and B blood)

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54
Q

For patient with A blood type, which plts can be given?

A

A or AB…trying to avoid anti-recipient Abs in the donor plasma!

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55
Q

for pt with B blood type, which plts can be given?

A

B or AB…trying to avoid anti-recipient Abs in the donor plasma!

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56
Q

for pt with AB blood type, which plts can be given?

A

AB…trying to avoid anti-recipient Abs in the donor plasma!

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57
Q

for pts with O blood, which plts can be given?

A

A, B, AB, O…trying to avoid anti-recipient Abs in the donor plasma!

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58
Q

The D antigen is what type of antigen?

A

Rh, but not all Rh antigens are D!

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59
Q

Is Rh tested as part of the type and screen/crossmatch process?

A

yes

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60
Q

Do people have naturally occurring anti-D abs?

A

no

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61
Q

what is teh most common alloAb?

A

D

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62
Q

Approximately ___% of D neg people exposed to D antigen will form ab

A

20-30%

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63
Q

anti D antibodies can cause what?

A

hemolytic disease of fetus adn newborn

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64
Q

if pt needs blood adn D status unknown do what?

A

give D neg blood

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65
Q

what types of transfusions should be D matched? (3)

A

RBCs, plts, granulocytes

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66
Q

2 indications for pRBC transfusion

A

anemia; acute blood loss

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67
Q

2 indications for plt transfusion

A

low plts; plt function defect

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68
Q

indication for granulocyte transfusion

A

severe, resistant infection in pt with severe neutropenia

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69
Q

2 indications for plasma transfusion

A

multiple coag factor def

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70
Q

2 indications for cyro transfusion

A

hypofibrinogenmia; dysfibrinogenmia

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71
Q

RBCs: dose and expected resposne?

A

dose = 10 ml/kg or 1 unit ~250 ml (whichever is smaller): response= increae hgb from 10; increase hct by 3%

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72
Q

plts: dose adn response?

A

dose= 10 ml/kg or 1 unit (250-300 ml), whichever is smaller; response= increase of 50 plts/uL after 30-60 min

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73
Q

plamsa dose and response?

A

dose= 15 ml/kg; response = 15% coagulation factor level increase

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74
Q

cyro: dose and response?

A

1-2 units/10 kg (round up); increase fibrinogen by 60-100 mg/dL

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75
Q

Studies in adults show that M&M increases at Hb below a)___? For every b)___ drop in Hb, mort risk increases c) ___-fold; sharp increase in mort when hb< d)___

A

a) 80
b) 10
c) 2.5
d) 50

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76
Q

administer prbcs over what time period?

A

2-4 hours

77
Q

Transfuse typically at hb less than? transfuse based on clinical situation for which hbs?

A

<70; 70-100

78
Q

List 5 things to consider when deciding whether to transfuse red cells

A
  • rate of anemia development
  • ability to compsensate
  • comorbidites that can affect oxygenation of RBCs or o2 delivery
  • expected recovery time (BMT, IDA, hemolytic anemia)
  • evidence of end organ damage or dysfunction
79
Q

what did the TRIPICU study find?

A

RCT study in peds ICU pts: transfuse at threshold <70 vs <95. this reduced # of transfused pts by 50%. in the liberal group, 98% got transfused vs 46% in other group. primary outcome: multiorgan dysfunction– no difference between the two groups

80
Q
plts transfusion indications:
10? 
20-25? 
40? 
50? 
75-100?
A

10= standard
20-25: inflammation (sepsis, mucositis), coag defect, recent bleeding, procedure like CVL
40= LP
50= GI bleed/mod hemorrahge, surgery, sick neonate
75-`00: major hemorrahge/post op bleeding, CNS or eye surgey in prone positoin
Any= plt function defect and signficinat bleeding or surgery

81
Q

corrected plt count increment=?

A

= [(post plt count- pre plt count) x BSA in m2 x 10^11]/# of plt transfused…used 3^11 if unsure….plt refractoriness: consdier <7500

82
Q

consider plt refractoriness if pts failed to achieve expected plt count rise after ___ transfusions

A

2

83
Q

reasons for antigens on plts?

A
HLA class I
AB antigens on plts
plt gycoproteins
drug induced
*refractoriness typically due to alloAbs although can also occur with autoimmune thrombocytopenia
84
Q

what’s the most common Ab–> plt refractoriness? what can you do if suspect refractory?

A

HLA …get recipient HLA type and HLA Ab screen…must be irradiated…(so do 3 things: HLA matching> Plt crossmatch> ABO matching), increase plt dose, decreasing manipulation of plt unit (washing, plasma reduction)

85
Q

indications for plasma?

A
  • support during DIC
  • massive transfusion
  • when factor concentrates not available (5, 11)
  • replacement in plasma exchange when indicated
  • warfarin reversal if urgent and no other options available; if PCC not approved (<16 yrs)
  • angioedema due to ACE inhibitor
86
Q

indications for cyro?

A
  • support for DIC
  • massive transfusion
  • hypofibrinogenemia, dysfibrinogenmia
  • Factor replacement when factor concentrates not available (8, 13, VWF)
87
Q

is there data that shows benefit for granulocyte transfusion?

A

no

88
Q

indications for granulocytes?

A

No definitive guidelines
• Absolute neutrophil count < 500/µL
• Clinical evidence of bacterial or fungal infection
• Poor response to antimicrobial therapy (typically 3‐5 days)
• Consideration of co‐morbidities and anticipated neutrophil recovery

89
Q

why is directed donation NOT recommended?

A
  • less safe (fam and friends may lie)
  • can create inventory issues and potnetial scenario when directed donor unit given to anotehr pt
  • directed donor units are not given ot other pts if pt doesn’t need it (waste of resources)
  • risk of TA-GVHD (high amongst first degree relatives)
90
Q

exception to not recommending directed donation?

A

-pt has rare RBC or plt phenoytpe and fam member is only one able to provide compatible blood

91
Q

2 major indications for apheresis and 2 egs?

A
  • remove problem (sickled cells, plasma containing abs)

- replace with something helpful (normal RBCs, healthy plasma)

92
Q

Thereapeutic modalities of apheresis? (5)

A
  • Therapeutic plasma exchange (TPE, plasampheresis, plasma exchange, PLEX)
  • Red cell exchange
  • leukocytapheresis
  • Thrombocytrapheresis
  • Extracorporal photopheresis
  • Selective adsorption (lipids)
  • Rheopheresis (selective protein removal)
  • Hematopoeitic stem cell collection
93
Q

Centriguation apheresis: does what?

A

separates blood components by SG so you can select what you want to remove

94
Q

5 common therapeutic apheresis indications?

A

TTP, ab-mediated solid organ transplant rejection, autoimmune neuro disorders like GBS, ANCA vasculitis, catastrophic antiphospholipid ab syndrome, pretransplant sensitization (ABO incompatilbe)

95
Q

Eryhtrocytapheresis: 3 indications

A
  • Acute chest syndrome with resp insuff
  • acute stroke in SCD pts
  • primary and secondary stroke prevention in pts with sickle cell disease if simply transfusion contraindicated
96
Q

3 indications for extracorporeal photopheresis:

A
  • cutaneous t cell leukemia/lymphoma
  • cellular solid organ transplant rejection
  • GVHD (steroid refractory)
97
Q

guidelines for therapeutic apheresis?

A

ASFA guidelines

98
Q

risks of apheresis

A
  • hypotension due to fluid shifts
  • if citrate used: hypocalcemia, hypoMg
  • Fatigue
  • reduced coag factors, including fibrinogen if albumin= replacement fluid
  • transfusion rxn
  • risks of CVC = infection, clot
99
Q

leukocytaphersis indications? 2

A

AML: WBC>100
ALL: WBC>400

100
Q

in terms of outcomes, leukocytapheresis does what?

A

-can reduce early mortality (within 3 weeks of dx) but no affect on long-term EFS or OS

101
Q

Leukocytapheresis can reduce WBCs by how much?

A

30-60%

102
Q

Leukoreduction is done before of after storage? Reduces RBCs to what count? Done how?

A

-Before
5x 10^6
-Via filtration or centrifugation

103
Q

Advantages of leukoreducting?

A
  • Less alloimunization
  • Less febrile non-hemolytic transfusion rxn
  • CMV safe and reduces transmission
  • Can reduce risk of TA-GVHD
104
Q

Leukoreduction is almost ___ but indications?

A
  • universal

- pts for whom it would be bad to become alloimmunization, have a febrile non-hemolytic rxn, get CMV, get TA-GVHD…

105
Q

Irradiation done how? Prevents what?

A

x-rays or gamma rays; prevents proliferation of donor T lymphocytes to prevent TA-GVHD

106
Q

which products can you irradiate? which would you not irradiate and why?

A
  • RBCs, plts, granulocytes

- hematopoeitic stem cells because their GOAL is to engraft!

107
Q

does irradiation affect expiration date?

A

only for RBCs: reduces shelf life to 28 days from day or collection or irradation, whichever shorter

108
Q

Best to irradiate RBCs when? why?

A

-at issue; reduces free K in unit; otherwise if >24-48 hours, need to wash or volume reduce the product

109
Q

indications for irradation? 5

A
  • fetal or neonatal recipients of intrauterine transfusions
  • pre term neonates
  • children <1 yr
  • congenital immune defs
  • asplatic anemia
  • heme malig
  • receiving hemo
  • allo stem cell transplant reciepients and donors
  • recipient of purine analog chemo
  • immunocompromised (selected)
  • donation of cellular components from blood relative
  • recipients who have undergone marrow or stem cell trasnplant
  • recipients of cellular components whose donor is selected for HLA compatibility
110
Q

what is volume reduction; why do you use it?

A

-centrifugation to remove the supernatant

  • pts with hx of anaphylaxis during transfusion
  • pts with history of escalating allergic rxn despite ppx
  • minor ABO mismatch when it matters (donor has anti-recipient abs)
  • irradiated RBCs that are at least 24 hours old
  • pts with volume issues (can reduce trasnfusion volume by 50-150 ml/unit
111
Q

which products cannot have volume reduction? why?

A

plasma and cryo; these are 100% supernatant

112
Q

alternative to volume reduction?

A

washing: repeating centrifugation and replacement of supernantant with saline

113
Q

2 diff ways to divide up transfusion rxns?

A
  • acute (hours) vs delayed (days-weeks)

- infectious vs non

114
Q

give an acute infectious transfusion rxn?

A

sepsis

115
Q

give 3 delayed infectious transfusion rxns

A

hep b, hep c, hiv

116
Q

give 5 acute non-infectious transfusion rxns

A
  • Febrile non hemolytic rxn
  • acute hemolytic rxn
  • TACO
  • TRALI
  • Allergic/anaphylaxis
117
Q

Give 4 delayed non-infectious rxns

A
  • GVHD
  • Iron overload
  • delayed hemolytic rxn
  • post transfusion purpura
118
Q

Give 3 febrile rxns to transfusions?

A
  • Febrile non hemolytic transfusion rxn
  • hemolytic transfusion rxn
  • sepsis
119
Q

Give 3 transfusion rxns–> dyspnea

A
  • TRALI
  • TACO
  • anaphylaxis
120
Q

prevalence of hives/mild allergic transfusion rxn?

A

1%

121
Q

prevalence of simple febrile rxn=febrile non hemolytic transfusion rxn?

A

0.5%

122
Q

TACO prevalence?

A

1/700

123
Q

TRALI prevalence?

A

1/5k

124
Q

dleayed hemolytic rxn prevalence?

A

1 in 7k

125
Q

ABO incompatible rxn prevalence?

A

1 in 40k

126
Q

symptomatic sepsis from transfusion prevalence?

A

1 in 250k

127
Q

risk of death from transfusion?

A

1 in 1 million

128
Q

Give 12 infectious diseases that are screen for in blood products

A
HIV Ab, RNA
Hep C Ab, RNA
Hep B surface Ag, core Ab, RNA
HTLV I/II
Syphilus
West Nile virus RNA
Zika
T. cruzi--> chagas
Babesia (not everywhere)
CMV
129
Q

risk of hep b from blood?

A

1 in 250k-1.5 million

130
Q

risk of hep c from blood?

A

1 in 1.5 million

131
Q

risk of HIV from blood?

A

1 in 2.9-4.7 million

132
Q

risk of HTLV I and II from blood?

A

1 in 2 million

133
Q

risk of syphilus from blood?

A

None since 1966 in US

134
Q

risk of west nile virus from blood?

A

1 case per year

135
Q

first step if suspect transfusion rxn?

A

stop the rxn!

136
Q

resp distress + hypertension: what’s the rxn?

A

TACO

137
Q

resp distress + low BP: what’s the rxn?

A

TRALI

138
Q

2 pathophys/etiology of allergic rxns in transfusions?

A
  • Type 1 hypersensitivity(mast cell)
  • IgA deficiency= severe
  • Cirtate allergy
139
Q

do what if mild allergic rxn to transfusion? severe?

A

mild: stop tx, antihistamine, you can rstart when better
severe: stop tx, epi, ABCs

140
Q

2 ways to prevent allergic rxn?

A

volume reduction

premeds

141
Q

how to prevent rxn in IgA def pts?

A

transfuse washed products or products from IgA-def donors (recipients IgA Abs won’t react)

142
Q

FNHTR: usually occurs wehn?

A

during or within 4 hours of transfusion

143
Q

clinical pres of FNHTR?

A
fever>37.5
chills, rigors
cold sensation, discomfort
headahce
n/v
144
Q

pathophys of FNHTR?

A

IL-1,6 and TNF alpha activated from monocytes and macropahges; passive/induced donor-derived cytokines

145
Q

In order to dx FNHTR need to rule out what?

A

hemolysis, sepsis, TRALI, underling medical condition

146
Q

tx for FNHTR?

A

stop transfusion, antipyretics, meperidine for rigours

147
Q

how to prevent FNHTR?

A

leukoreduction, premeds

148
Q

trali occurs when?

A

during or within 6 hours after trasnfusion

149
Q

clinic pres of TRALI?

A

resp distress, hypoxia, pulmonary edema/infiltrates on CXR…can have fever, low BP

150
Q

pathophys of TRALI?

A

donor anti-recippient Abs (HNA or HLA); pro-inflammatory molecules like sCD40L

151
Q

tx for TRALI?

A

stop transfusion, supportive care (resolves in 24-48 hours)

152
Q

how to prevent trali?

A

male-only plasma pool

153
Q

TACO: timing?

A

during or within 6 hours of transfusion

154
Q

clinical pres of taco?

A

resp distress, hypoxia, pulmonary edema/infiltrates on CXR, evidence of fluid overload like high BP

155
Q

pathophys of taco?

A

volume overload–> pulmonary edema

156
Q

dx taco how?

A

CXR findings of pulmonary edema; response to diuretics

157
Q

tx taco how?

A

stop transfusion, give diuretics adn supportive resp care

158
Q

how to prevent taco?

A

minimize volume, give diuretics between units, stop other IVF

159
Q

AHTR: timing?

A

during transfusion

160
Q

clinical pres?

A

fever, anxiety/panic, low back pain= kidney injury from hemolysis, other evdience of hemolysis, low BP

161
Q

cause of AHTR?

A

isohemagglutinins binding donor red cells and complement fixation causing RBC destruction…misidentfication of crosmmatch sample or transfusion recipient

162
Q

dx AHTR how?

A

+ DAT, evidence of hemolysis

163
Q

how to tx AHTR?

A

stop transfusion! fluid support including diuresis

164
Q

how to prevent AHTR?

A

careful labeling of crossmatch sample, dual check to ensure blood and patient label match

165
Q

DHTR: timing?

A

1-28 days after transfusion

166
Q

clinical presentation of DHTR?

A

anemia, jaundice and indirect hyperbili, spherocytosis and retics, positive direct and indirect ab tests

167
Q

cause of DHTR?

A
  • pre-formed abs not seen on ab screen

- development of new allAbs after transfusion exposure

168
Q

dx of DHTR?

A

+DAT, evidence of hemolysis

169
Q

tx of DHTR?

A

often self-limiting; may require another transfusion

170
Q

prevent DHTR how?

A

obtain accurate past transfusion records

171
Q

what’s the diff between AHTR? and DHTR?

A

AHTR: due to isohemagluttinins= pre-formed IgM, which fixes complement on RBC surface–> destruciton of both donor and recipient red cells…get red urine and red plasma

DHTR: typically extravasc hemolysis. ab-coated red cells are eliminated by mamcrophages in hte reticuloendothelial system in the liver…yellow urine and yellow plasma

172
Q

acute septic transfusion reaction: timing?

A

during transfusion or shortly after

173
Q

clinical pres of acute septic transfusion rxn?

A
  • fever
  • low bp
  • resp distress
  • post-transfusion positive blood cx
174
Q

pathophys of acute septic transfusion rxn?

A
  • admin of bacteria directly into bloodstream

- admin of endotoxin or other bacterial byproducts

175
Q

dx of acute septic transfusion rxn? (3)

A

+ blood cx of unit and pt
+ blood cx of unit and sick pt
+blood culture in pt with no other possible source

176
Q

how to prevent acute spetic transfusion rxn?

A

donor screening, proper disinfection at time of collection, pathogen reduction, bacterial surveillance of plts

177
Q

TA-GVHD: timing?

A

5-10 days after transfusion, marrow aplasia by 21 days

178
Q

TA-GVHD clinical pres?

A

rash, fever, abdo pain, vomiting, diarrhea, identical to SCT-related GVHD

179
Q

TA-GVHD mort?

A

> 90%

180
Q

pathophys of TA-GVHD?

A
  • engraftement of donor T-lymphocytes
  • immunosuppressed recipient
  • shared HLA haplotypes between donor and recipient
181
Q

how to dx TA_GVHD?

A

skin, intestinal, and/or bone marrow bx showing GVHD

182
Q

tx of TA-GVHD?

A

supportive care, almost universally fatal

183
Q

prevent TA-GVHD how?

A

irradiation or pathogen inactivation

184
Q

cold transfusion rxn: cause, dx, managemetn?

A
  • blood prod<37
  • body temp<36
  • blood warmer, etc
185
Q

citrate toxicity: cause? dx? management?

A
  • citrate chelates calcium
  • signs/sx of low ca, heart arrythmia, low serum ca
  • slow rate of transfusion, give ca
186
Q

hypotension rxn: cause? epi? dx? management?

A
  • contact activation adn bradykinin generation
  • 1 in 100k
  • > 30 mmHg drop in SBP or DVP
  • supportive measures
187
Q

hyperkalemic cardic arrest: cause? dx? management?

A
  • K leakage from stored RBCs, worse if old/irradiated prod
  • cardiac arrset and high K
  • standard hyper K tx, max rbc infusion rate of 0.5 ml/kg/min
188
Q

post-transfusion purpra: cause? dx? management?

A
  • transfusion causes secondary response against HPA in pre-alloimmunized pts
  • low plts 5-12 days after transfusion
  • plasma exchange; IVIG