Transfusion Medicine, ASPHO Flashcards
2 major types of blood products adn egs?
- Cellular prods (pRBCs, plts, granulocytes)
- Non-cellular prods (FFP, Cyro)
What are the 2 types of collection?
Whole blood (component separation via centrifugation and processing) -Apheresis= single component collection
Centrifugation separates whole blood how?
Plasma on top of plts on top of RBCs
What can you do with centrifuged plasma?
freeze plasma as is and keep as plasma or thaw frozen plasma and resuspend to allow you to get to cryoprecipitate
plasma and plts are part of the __ ____
buffy coat
plts from whole plts need to be combined with about ___ other derived plt donation to get whole unit
5
collection via apheresis: can collect ___ RBCs, ___ plasma units and ___ plt units
double; double; ~1-2
centrifuge separate blood components based on what?
specific gravity
RBCs: storage temp?
2-6 degrees C
RBCs shelf life?
21-42 days
RBCs: leukodeplete when?
pre-storage
RBCs: warm before transfusion?
no
RBCs: hct of unit?
~55%
if RBCs in glycerol, store at what temp? and for how long?
-65, 10 years
once thawed and deglycerolized, RBCs good for how long? can they be refrozen?
24 hours; no
Plts: storage temp?
20-24C
Shelf life of plts?
5 days
Plts require constant ____ ____
gentle agitation
Plasma: store at what temp and for how long? 3 options
1 year
2-6 C–> 5 days (thawed) or 28 days (never frozen)
what’s the definition of FFP?
plasma frozen no later than 8 hours after collection
what’s the definition of Frozen plasma (not FFP)?
plasma frozen <24 hours after collection
Cryo: storage temp and shelf life?
-18 C, 1 yr
cryo is pooled into packs of __ or ___
5 or 10
granulocytes: stored at what temp for what period of time?
20-24; 24 hours
granulocytes should be given ___
ASAP
RBC shelf life depends on the storage solution: name 5 and their shelf lives
CPD: 21 days CPDA: 35 days AS-1: 42 days AS-5 42 days AS-3: 42 days
What does AS1,3,5 contains that CPD adn CPDA doesnt?
mannitol
Name 4 common bacteria that live at 1-6 C and can infect pRBCs
-Yersinia enterocolitica
Listeria monocytogenes
Serratia liquefaciens
CoNS
Pts with cold agglutinin disease should be given pRBCs how?
through a warmer to prevent further hemolysis
which blood product has highest rate of bacterial contamination? rate? % of these units that cause infection?
plts; 1 in 1000-2000 units; 10%
70% of infections caused by plts are ___ ___ but ___ ___ cause 80% of deaths
gram positive; gram neg
which blood prod= most difficult to store during disasters?
plts
define blood type
ABO and RH (D) type of recipient
Screening does what?
eval for alloantibodies again common and clinically significant RBC antigens
Crossmatching does what?
electronically or manually confirm compatibility between donor and recipient
Blood type A have __ Ag; they have __ antibodies; blood type compatible in emergency?
A; B; A or O
What are isohemagglutinins?
(ANti-A or anti-B); are IgM abs formed by non-A and non-B individuals, respectively due to environmental exposures
Type O individuals have what IgMs and IgG?
IgM: anti-A, anti-B
IgG: anti-AB
which antibodies are responsible for acute hemolytic transfusion rxn?
-IgM
what causes hemolytic disease of fetus/newborn?
anti-AB IgG…IgM does NOT cross the placenta!
what’s the difference between a minor and major mismatch?
minor: donor is anti-recipient (avoid when possible); major= recipient is anti-donor (avoid at all costs)
Give an example of front and back types being different
Patient has A RBCs but no anti-B antibodies
Give 4 causes of front and back types being different
Immunosuppression, young infants, patients undergoing ABO-mismatch HSCT, chimerism
How are alloabs evaluated?
Pt plasma mixed with panel RBCs that have known antigen profiles; tests for common and clinically significant alloabs
what does direct coombs test do?
looks specifically at RBC-bound Abs. the pt’s red cells are mixed with anti-human Ab= coombs reagent–> agglutination of ab-coated RBCs
what does the indirect coombs test do?
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.
what is crossmatch?
first screen: pt plasma + rbcs from donor…can also add anti-human IgG if desired…if screen is negative, usually do electronic crossmatch
screen and crossmatch good for how long?
72 hours
if emergency, do what?
give uncrossmatched blood: O neg
chance of delayed hemolytic rxn in emerg situation where o neg given?
1:14000 (due to pre-formed alloAbs)
what are the two main types of abs in teh plt crossmatch?
HPA= anti-human plt antigen HLA= anti-human leukocyte antigen
which 2 abs are responsible to 90-95% of NAIT?
HPA 1 and HPA 5
plts need to be compatible how?
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)
For patient with A blood type, which plts can be given?
A or AB…trying to avoid anti-recipient Abs in the donor plasma!
for pt with B blood type, which plts can be given?
B or AB…trying to avoid anti-recipient Abs in the donor plasma!
for pt with AB blood type, which plts can be given?
AB…trying to avoid anti-recipient Abs in the donor plasma!
for pts with O blood, which plts can be given?
A, B, AB, O…trying to avoid anti-recipient Abs in the donor plasma!
The D antigen is what type of antigen?
Rh, but not all Rh antigens are D!
Is Rh tested as part of the type and screen/crossmatch process?
yes
Do people have naturally occurring anti-D abs?
no
what is teh most common alloAb?
D
Approximately ___% of D neg people exposed to D antigen will form ab
20-30%
anti D antibodies can cause what?
hemolytic disease of fetus adn newborn
if pt needs blood adn D status unknown do what?
give D neg blood
what types of transfusions should be D matched? (3)
RBCs, plts, granulocytes
2 indications for pRBC transfusion
anemia; acute blood loss
2 indications for plt transfusion
low plts; plt function defect
indication for granulocyte transfusion
severe, resistant infection in pt with severe neutropenia
2 indications for plasma transfusion
multiple coag factor def
2 indications for cyro transfusion
hypofibrinogenmia; dysfibrinogenmia
RBCs: dose and expected resposne?
dose = 10 ml/kg or 1 unit ~250 ml (whichever is smaller): response= increae hgb from 10; increase hct by 3%
plts: dose adn response?
dose= 10 ml/kg or 1 unit (250-300 ml), whichever is smaller; response= increase of 50 plts/uL after 30-60 min
plamsa dose and response?
dose= 15 ml/kg; response = 15% coagulation factor level increase
cyro: dose and response?
1-2 units/10 kg (round up); increase fibrinogen by 60-100 mg/dL
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) 80
b) 10
c) 2.5
d) 50
administer prbcs over what time period?
2-4 hours
Transfuse typically at hb less than? transfuse based on clinical situation for which hbs?
<70; 70-100
List 5 things to consider when deciding whether to transfuse red cells
- 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
what did the TRIPICU study find?
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
plts transfusion indications: 10? 20-25? 40? 50? 75-100?
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
corrected plt count increment=?
= [(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
consider plt refractoriness if pts failed to achieve expected plt count rise after ___ transfusions
2
reasons for antigens on plts?
HLA class I AB antigens on plts plt gycoproteins drug induced *refractoriness typically due to alloAbs although can also occur with autoimmune thrombocytopenia
what’s the most common Ab–> plt refractoriness? what can you do if suspect refractory?
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)
indications for plasma?
- 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
indications for cyro?
- support for DIC
- massive transfusion
- hypofibrinogenemia, dysfibrinogenmia
- Factor replacement when factor concentrates not available (8, 13, VWF)
is there data that shows benefit for granulocyte transfusion?
no
indications for granulocytes?
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
why is directed donation NOT recommended?
- 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)
exception to not recommending directed donation?
-pt has rare RBC or plt phenoytpe and fam member is only one able to provide compatible blood
2 major indications for apheresis and 2 egs?
- remove problem (sickled cells, plasma containing abs)
- replace with something helpful (normal RBCs, healthy plasma)
Thereapeutic modalities of apheresis? (5)
- 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
Centriguation apheresis: does what?
separates blood components by SG so you can select what you want to remove
5 common therapeutic apheresis indications?
TTP, ab-mediated solid organ transplant rejection, autoimmune neuro disorders like GBS, ANCA vasculitis, catastrophic antiphospholipid ab syndrome, pretransplant sensitization (ABO incompatilbe)
Eryhtrocytapheresis: 3 indications
- 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
3 indications for extracorporeal photopheresis:
- cutaneous t cell leukemia/lymphoma
- cellular solid organ transplant rejection
- GVHD (steroid refractory)
guidelines for therapeutic apheresis?
ASFA guidelines
risks of apheresis
- 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
leukocytaphersis indications? 2
AML: WBC>100
ALL: WBC>400
in terms of outcomes, leukocytapheresis does what?
-can reduce early mortality (within 3 weeks of dx) but no affect on long-term EFS or OS
Leukocytapheresis can reduce WBCs by how much?
30-60%
Leukoreduction is done before of after storage? Reduces RBCs to what count? Done how?
-Before
5x 10^6
-Via filtration or centrifugation
Advantages of leukoreducting?
- Less alloimunization
- Less febrile non-hemolytic transfusion rxn
- CMV safe and reduces transmission
- Can reduce risk of TA-GVHD
Leukoreduction is almost ___ but indications?
- universal
- pts for whom it would be bad to become alloimmunization, have a febrile non-hemolytic rxn, get CMV, get TA-GVHD…
Irradiation done how? Prevents what?
x-rays or gamma rays; prevents proliferation of donor T lymphocytes to prevent TA-GVHD
which products can you irradiate? which would you not irradiate and why?
- RBCs, plts, granulocytes
- hematopoeitic stem cells because their GOAL is to engraft!
does irradiation affect expiration date?
only for RBCs: reduces shelf life to 28 days from day or collection or irradation, whichever shorter
Best to irradiate RBCs when? why?
-at issue; reduces free K in unit; otherwise if >24-48 hours, need to wash or volume reduce the product
indications for irradation? 5
- 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
what is volume reduction; why do you use it?
-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
which products cannot have volume reduction? why?
plasma and cryo; these are 100% supernatant
alternative to volume reduction?
washing: repeating centrifugation and replacement of supernantant with saline
2 diff ways to divide up transfusion rxns?
- acute (hours) vs delayed (days-weeks)
- infectious vs non
give an acute infectious transfusion rxn?
sepsis
give 3 delayed infectious transfusion rxns
hep b, hep c, hiv
give 5 acute non-infectious transfusion rxns
- Febrile non hemolytic rxn
- acute hemolytic rxn
- TACO
- TRALI
- Allergic/anaphylaxis
Give 4 delayed non-infectious rxns
- GVHD
- Iron overload
- delayed hemolytic rxn
- post transfusion purpura
Give 3 febrile rxns to transfusions?
- Febrile non hemolytic transfusion rxn
- hemolytic transfusion rxn
- sepsis
Give 3 transfusion rxns–> dyspnea
- TRALI
- TACO
- anaphylaxis
prevalence of hives/mild allergic transfusion rxn?
1%
prevalence of simple febrile rxn=febrile non hemolytic transfusion rxn?
0.5%
TACO prevalence?
1/700
TRALI prevalence?
1/5k
dleayed hemolytic rxn prevalence?
1 in 7k
ABO incompatible rxn prevalence?
1 in 40k
symptomatic sepsis from transfusion prevalence?
1 in 250k
risk of death from transfusion?
1 in 1 million
Give 12 infectious diseases that are screen for in blood products
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
risk of hep b from blood?
1 in 250k-1.5 million
risk of hep c from blood?
1 in 1.5 million
risk of HIV from blood?
1 in 2.9-4.7 million
risk of HTLV I and II from blood?
1 in 2 million
risk of syphilus from blood?
None since 1966 in US
risk of west nile virus from blood?
1 case per year
first step if suspect transfusion rxn?
stop the rxn!
resp distress + hypertension: what’s the rxn?
TACO
resp distress + low BP: what’s the rxn?
TRALI
2 pathophys/etiology of allergic rxns in transfusions?
- Type 1 hypersensitivity(mast cell)
- IgA deficiency= severe
- Cirtate allergy
do what if mild allergic rxn to transfusion? severe?
mild: stop tx, antihistamine, you can rstart when better
severe: stop tx, epi, ABCs
2 ways to prevent allergic rxn?
volume reduction
premeds
how to prevent rxn in IgA def pts?
transfuse washed products or products from IgA-def donors (recipients IgA Abs won’t react)
FNHTR: usually occurs wehn?
during or within 4 hours of transfusion
clinical pres of FNHTR?
fever>37.5 chills, rigors cold sensation, discomfort headahce n/v
pathophys of FNHTR?
IL-1,6 and TNF alpha activated from monocytes and macropahges; passive/induced donor-derived cytokines
In order to dx FNHTR need to rule out what?
hemolysis, sepsis, TRALI, underling medical condition
tx for FNHTR?
stop transfusion, antipyretics, meperidine for rigours
how to prevent FNHTR?
leukoreduction, premeds
trali occurs when?
during or within 6 hours after trasnfusion
clinic pres of TRALI?
resp distress, hypoxia, pulmonary edema/infiltrates on CXR…can have fever, low BP
pathophys of TRALI?
donor anti-recippient Abs (HNA or HLA); pro-inflammatory molecules like sCD40L
tx for TRALI?
stop transfusion, supportive care (resolves in 24-48 hours)
how to prevent trali?
male-only plasma pool
TACO: timing?
during or within 6 hours of transfusion
clinical pres of taco?
resp distress, hypoxia, pulmonary edema/infiltrates on CXR, evidence of fluid overload like high BP
pathophys of taco?
volume overload–> pulmonary edema
dx taco how?
CXR findings of pulmonary edema; response to diuretics
tx taco how?
stop transfusion, give diuretics adn supportive resp care
how to prevent taco?
minimize volume, give diuretics between units, stop other IVF
AHTR: timing?
during transfusion
clinical pres?
fever, anxiety/panic, low back pain= kidney injury from hemolysis, other evdience of hemolysis, low BP
cause of AHTR?
isohemagglutinins binding donor red cells and complement fixation causing RBC destruction…misidentfication of crosmmatch sample or transfusion recipient
dx AHTR how?
+ DAT, evidence of hemolysis
how to tx AHTR?
stop transfusion! fluid support including diuresis
how to prevent AHTR?
careful labeling of crossmatch sample, dual check to ensure blood and patient label match
DHTR: timing?
1-28 days after transfusion
clinical presentation of DHTR?
anemia, jaundice and indirect hyperbili, spherocytosis and retics, positive direct and indirect ab tests
cause of DHTR?
- pre-formed abs not seen on ab screen
- development of new allAbs after transfusion exposure
dx of DHTR?
+DAT, evidence of hemolysis
tx of DHTR?
often self-limiting; may require another transfusion
prevent DHTR how?
obtain accurate past transfusion records
what’s the diff between AHTR? and DHTR?
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
acute septic transfusion reaction: timing?
during transfusion or shortly after
clinical pres of acute septic transfusion rxn?
- fever
- low bp
- resp distress
- post-transfusion positive blood cx
pathophys of acute septic transfusion rxn?
- admin of bacteria directly into bloodstream
- admin of endotoxin or other bacterial byproducts
dx of acute septic transfusion rxn? (3)
+ blood cx of unit and pt
+ blood cx of unit and sick pt
+blood culture in pt with no other possible source
how to prevent acute spetic transfusion rxn?
donor screening, proper disinfection at time of collection, pathogen reduction, bacterial surveillance of plts
TA-GVHD: timing?
5-10 days after transfusion, marrow aplasia by 21 days
TA-GVHD clinical pres?
rash, fever, abdo pain, vomiting, diarrhea, identical to SCT-related GVHD
TA-GVHD mort?
> 90%
pathophys of TA-GVHD?
- engraftement of donor T-lymphocytes
- immunosuppressed recipient
- shared HLA haplotypes between donor and recipient
how to dx TA_GVHD?
skin, intestinal, and/or bone marrow bx showing GVHD
tx of TA-GVHD?
supportive care, almost universally fatal
prevent TA-GVHD how?
irradiation or pathogen inactivation
cold transfusion rxn: cause, dx, managemetn?
- blood prod<37
- body temp<36
- blood warmer, etc
citrate toxicity: cause? dx? management?
- citrate chelates calcium
- signs/sx of low ca, heart arrythmia, low serum ca
- slow rate of transfusion, give ca
hypotension rxn: cause? epi? dx? management?
- contact activation adn bradykinin generation
- 1 in 100k
- > 30 mmHg drop in SBP or DVP
- supportive measures
hyperkalemic cardic arrest: cause? dx? management?
- 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
post-transfusion purpra: cause? dx? management?
- transfusion causes secondary response against HPA in pre-alloimmunized pts
- low plts 5-12 days after transfusion
- plasma exchange; IVIG
