Lecture - Transfusion medicine (martin) Flashcards
what does agglutination represent in blood typing
detecting presence of Ag corresponding to Anti-sera
ex. A+ pt
Forward/front typing
mix pt RBC w/ commercially made anti-sera
agglutination–> detecting presence of Ag corresponding to Anti-sera
if you have an A+ pt, what would you expect on their front/fwd typing to show?
would expect agglutination in anti-A, anti A,B, and Anti-D
neg on anti-B and D cont
Back/reverse typing
mix pt sera with commercially prepared cells
agglutination–> reveals presence of Ab to corresponding cells
if you have an A+ pt, what would you expect on their back/reverse typing to show?
+anti-B
Ab screen (Indirect antiglobulin test- IAT)
mix pt sera with screening cells
what does a + Ab screen result indicate?
detection of an immunoglobulin in pt sera against a foreign RBC antigen (pt must’ve been transfused at one point or exposed during a pregnancy)
if you are Rh+, what will you typically see when reacting your blood cells to anti-D sera
STRONG D expression response (one big agglutination)
can have WEAK D (Du)- weakly positive where may or may not be visible, might need to add reagent or incubation time for it to show up
if you are a weak D patient and you are donating blood, what are you considered as?
considered as Rh+ (bc have some form of D antigen there)
and a recipient could develop anti-D
if you are a weak D patient and you are receiving blood, what are you considered as?
some places may consider you as Rh- (espec in childbearing years), bc of possibility of developing anti_D
85% treat as Rh+ tho
ranked first in immunogenicity
Rhesus system (D)
ranked second in immunogenicity
Kell system
What dzs can the McLeod phenotype be associated with?
Chronic compensated hemolytic anemia
Chronic granulomatous dz
what would you see on peripheral blood smear in someone w/ chronic compensated hemolytic anemia
many acanthocytes (spur cells) - spiky, irregular cells close to normal size
special features of chronic granulomatous dz
lack Kx Ag on membrane of neutrophils and monocytes
deficiency of NADH-oxidase –> no H202 to destroy microbes (aka LOTS OF Infections)
What is impt to know about specimen collection
-specimen MUST be labeled at bedside (w/ time, date and initial of phlebotomist); permanent and unique ID of each pt
what is one of the biggest issues when have lethal transfusion rxns
misidentification
when a type and screen (T&S) is done, what is performed
only ABO, Rh, and Ab screen (no xmatch)
-usually when have surgical procedure or time needing blood
If have a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs…what do you do
Ab identification and look for units negative for that antigen that the alloantibody is against
then… Crossmatch (actually testing of pts serum compatibility w/ donor cells)
what does a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs detect
Ig in pts serum against Ag on RBCs (NOT pts RBCs)
Ab must NOT be bound to RBCs (either pts own RBCs or transfused RBCs) to enable detection
Direct vs. Indirect Coombs
Direct- Abs attached to own RBCs
[detect autoimmune hemolytic anemia and transfusion rxn workups]
Indirect- alloAbs in pts serums that will react to foreign RBCs’
[used prior to blood transfusion and in prenatal testing of pregnant women]
adding Coombs reagent (anti-human Igs) - makes it more visible to detection w/ test
what does an antibody work up screen for
UNEXPECTED allo-Abs
identify Ab in pt serum, not formed by pt (ex. maternal Ab in infant/fetal circulation)
antigen detection test
used after identifying Ab in pt serum
how: commercial anti-sera mixed w/ pt cells
confirmation pt +/- Ag on own cells
usually done in conjunction w/ Ag typing/screening donor cells for compatibility
Indirect Antiglobulin test/indirect coombs checks for what?
hemolysis + agglutination against “screening cells”
do at 3 diff phases (room temp, 37C, antihemoglobulin (AHG) )
@Room temp, IAT detects:
initial combination of pt sera w/ commercial suspension of RBCs
detect COLD Abs- IgM
(not rlly clinically significant)
@37 C, IAT detects:
“warm” Abs - Igm- IgG mixture + IgG
Warm Ab: Rh, Kell, Kidd, and Duffy
In the antihemoglobulin phase, IAT detects
“warm” Abs; IgG that coat the RBC membrane
when performing an IAT, what does adding a check cell (CC) do?
verify AHG was added and working
Rule out method
for every cell with negative rxn, go and cross out all the antigens that are positive on that cell
then find the only manufactured cell that is + for one antigen and negative in all the other cells
can take a while! why theres a delay typically; then have to antigen check them once find
what is an autoAb
Ab directed against individual own RBC ags
–> can cause RBC destruction
Autoimmune hemolytic anemia
when have intravascular hemolysis–> hemoglobinemia/uria
+/- anemia, incr reticulocytes, incr unconj bilirubin, decr haptoglobin
Confirm w/ DAT (coombs) and characterization of autoAbs as cold or warm reactive
what is the most common autoAb entity
cold autoantibodies (benign cold agglutinin) - 4 Celcius
IgM
usually low titer but often agglutinate at room temp; can activate complement in vitro
how can you get a false + rxn with cold autoAbs; how prevent this?
if self RBCs heavily coated w/ AB, may spontaneously agglutinate and cause a false +
Ab detection: can do a prewarm or autoabsorbed serum so cold Ab dont obscure alloAbs
when trying to test for compatibility of cold autoantibodies, what is most common and how do you do it?
auto-anti-I = MC (found on most donor units)
you also prewarm or use autoabsorption
What autoAbs react with an antihemoglobulin phase (autoimmune hemolytic anemia- AIHA)? what Ag group are they specific to?
warm Abs–> IgG
specific to Rh group Ags (high incidence)
how can the warm autoantibodies be induced?
idiopathic or SLE-assoc or drug-induced
need pt med hx and transfusion rxn
should you transfuse a patient with warm autoAbs
many patients dont require transfusions
can use steroids and splenectomy
Cold Agglutinin Dz
varies from none to life threatening hemolytic anemia (intravascular hemolysis- increases as pt is exposed to COLD and complement gets activated)
what should a person w/ cold agglutinin dz avoid?
COLD WEATHER (and walk in freezers lol)
infections assoc with cold agglutinin dz
mycoplasma pneumoniae pneumonia
or
infectious mononucleosis
how do you perform a crossmatch (compatibility testing)
first recheck the recipients ABO Rh type (forward and reverse typing + weak D)
if positive..AB ID
if negative (no unexpected antibodies)–>
CROSSMATCH:
utilizing pt sera and mixing it with donor RBC to make sure dont have any bad reactions and is compatible
detect agglutination: if no agglutination/hemolysis = COMPATIBLE
ex. donor PC A (compatible recipient = A and AB)
Adverse effects of transfusion include:
Shock, respiratory distress, fever, acute hemolyic or septic rxns, and TRALI
Mgmt of acute transfusion rxns
- STOP TRANSFUSION
- Keep IV open w/ 0.9% NaCl
- verify correct unit was given to correct pt
- notify attending physicians and blood bank
ADVERSE RXN: stop transfusion, report rxn to blood bank IMMEDIATELY, return bag w/ attached tubing, return all paperwork, send post-transfusional blood sample
Transfusion-related GVHD
infusion of immunocompetent donor lymphs to immunocompromised recipient
what is the circulatory overload transfusion rxn
either too large a volume or too fast infusion
when giving a pt a transfusion, how long should you monitor them for?
monitor pt closely during first 15 mins of transfusion and intermittently during transfusion
most impt lab response to transfusion rxn
the first thing theyre going to do is check for identification errors (PROBS is a labeling error)
then.. Visual check, serologic test for incompatibility (ABO/Rh, gram stain + culture, H/H and urine for hemolysis, R/O TRALI)
symptoms: Acute hemolytic transfusion rxn
HYPOtension hemoglobinuria DIC flank pain or infusion site pain \+DAT
also fever, chills, N/V, dyspnea, tachy
late complication: renal failure
symptoms: Delayed hemolytic transfusion rxn
unexplained rise in unconj Hgb
drop in H/H
+DAT
other: unexpected anemia, fever, chills, jaundice, pain or dyspnea; increased LDH and bili, new RBC Ab
symptoms: Febrile non-hemolytic transfusion rxn
fever
chills
HYPERtension
secondary sx: HA, N/V
not life threatening (but need to exclude other causes of fever)
symptoms: Allergic transfusion rxn
urticarial rxn
pruritis, urticaria, erythema, and cutaneous flushing
laryngeal edema (upper airway) bronchoconstriction (lower airway)
symptoms: TRALI transfusion rxn
**NON-CARDIOGENIC pulmonary edema
assoc w/ passive transfer of donor granulocyte Abs
CXR: pulmonary edema (may persist >7 days)
lack of abnormal breath sounds
NO SIGNS OF CARDIAC FAILURE
presentation resembles ARDS
symptoms: Septic transfusion rxn
fever
chills
rigors
shock
caused by contaminated blood component (platelets usually)
what transfusion rxn presents within hours, within <24 hours, and >24 hours post-transfusion
within hrs: TRALI
<24 hrs: Acute hemolytic
> 24 hrs: Delayed hemolytic (usually <2 weeks, but can be >6 weeks)
how do AHTRs happen
pre-existing natural IgM Abs induce complement-mediated intravascular hemolysis
+DAT
what does mortality depend on in AHTRs?
depends on amount RBC transfused (less put in, less hemolysis, less likely mortality)
DDx with AHTRs
AIHA, cold hemogglutinin dz, congenital hemolytic anemia, nonimmune hemolysis, hemoglobinopathies, polyagglutination, PNH, artificial heart valve
Treatment and prevention of AHTRs
Tx: discontinue + verify ID; Mild- observe, severe- CV support, fluid resusc, pressor support; avoid fluid overload, maintain urine output
Prevention- proper ID of patient!!
single most common cause of AHTRs
not proper identification of patient
what kind of hemolytic rxn is DHTR?
extravascular hemolysis!!
how do DHTRs happen
IgG from prior transfusion/exposure (Rh, Kell, Kidd)
+DAT
what dz may DHTRs precipitate
Sickle Crisis in sickle pt
DDx with DHTRs
same as AHTR, emphasis on occult infection, AIHA, cold hemogluttin dz
DIFFICULT DDX
Treatment of DHTRs
Tx: most tolerate well, follow carefully; tx complications as needed
*IVIG- extravasc hemolysis *
Prevention: serologic detection of RBC Ab = key to prevention (select donor units neg for RBC ag)
Febrile non-hemolytic transfusion rxns
rise in temp of 1C or greater (may be 30 mins to 1 hr post transfusion)
rxn is associated w/ acquired Ab to leukocyte ag in transfused pdts; attributed to pyrogenic cytokines in units during storage
DDx of FNHTRs
hemolytic transfusion rxns, TRALi, bacterial contamination vs. dz or treatment related fever
Tx and prevention of FNHTRs
Tx: +/- antipyretics (Acetaminophen); fever self limited (resolves in 2-3 hrs); if rigors- can give meperidine (caution bc its resp depressant)
Prevention: pre-medicate w/ antipyretic (if hx of previous febrile rxns)
- pre-storage leukocyte reduction decreases cytokines
- plasma reduction or wash pack cells (removing all plasma form pack cell unit)
what should you not give a patient with suspected FNHTRs
NO ASPIRIN (due to effect on platelet function)
Allergic (urticarial ) transfusion rnxs are associated w/
any type of blood component (assoc with amt of plasma transfused)
if a pt has dyspnea after transfusion, what should you rule out if youre thinking it might be an allergic rxn
rule out TRALI syndrome and volume overload
Tx and Prevention of allergic transf rxns
tx: intubate prn + O2 prn; IV antihistamine
prevention: usually cant ID Ag, thus unable to select Ag- products; (EXCEPT IGA deficiency)
* *premedicate w/ antihistamine to prevent mild allergic rxn**
A pt comes in w/ either CV instability, hypotension, tachy, loss of consciousness, arrhythmia, shock, or cardiac arrest. what are they likely experiencing?
severe allergic (anaphylactic) transfusion rxn
Tx + prevention of severe allergic (anaphylactic) transfusion rxn
Tx: what do for acute + epinephrine + diphenhydramine (Espec w/ cutaneous syx), aminophylline w/ bronchospasm
Prevention: IgA def pt dev anti-IgA, give IgA def pdts; washed pack cells (PC)
premedicate w/ antihistamine or steroids
what transfusion products is TRALI seen on most?
FFP + Platelets (high level donor antibodies)
How long does it take for noncardiogenic pulmonary edema to resolve
48-96 hrs from onset
Tx and prevention of TRALI
Tx: antipyretics + fluid (fever + hypotension); supportive tx - O2 (ventilator)
Prevention: attributed to presence of Ab in plasma of the donor unit directed against HLA or granulocyte Ag on RECIPIENT leukos; also due to lipid inflammatory mediators
need to decrease lipid mediators by pre-storage leukocyte reduction or decreasing storage time (esp platelets)
common bacterial organism contamination seen w/ transfusion
Yersinia enterocolitica + Pseudomonas - PC due to ability to grow at low temp and high iron environment
staph and strep (gm+ cocci) + salmonella, escherichia and serratia (gm - rods) in platelets
Processing of blood donation
single donation (450-500 mL)–> centrifugation–> 3 components (200 mL RBC, 50 mL platelets, 200 mL plasma)
components of RBCs
leuko reduced
washed RBCs
frozen RBCs (never thaw until certain needed)
Irradiated RBCs
components or platelets
platelet concentration
components of plasma
leukocytes/ granulocytes
FFP –> solvent –detergent treated plasma
cryoprecipitate
other: albumin, plasma protein fraction, plasma fraction concentration
indication for RBCs in transfusion
increase oxygen carrying capacity (someone is hypoxic)
Hgb<7 g/dL or Hct <21% in otherwise healthy individual w/ acute anemia (bleeding)
Hgb 7-9 g/ dL in pt w/ CV or cerebrovascular risk factors
HbS 30-50% in Sickle Cel pts to prevent stroke
Must be careful to not give blood to a chronic anemia patient too quickly or may go into congestive heart failure
indication + contraindication for packed RBCs in transfusion
I: symptomatic anemia (from increased loss, decreased survival or decr pdtion of RBCs); also increases oxygen carrying capacity (expected: 1-2 g/dL Hb; ~3% Hct per unit in 24 hr)
CI: volume expansion, coagulation deficiency or drug treatable anemia
indication for frozen/deglyced RBCs
storage of rare or autologous units
HSN to plasma proteins
indication for washed RBCs
recurrent severe allergic rxn to unwashed RBCs
indication for irradiated RBCs
risk of GVHD in immunocompromised pts
indication for leukocyte reduced RBCs
febrile rxns due to leukocyte antibodies
storage of the RBC components
PRBC, irradiated, leukocyte reduced: 35 - 42 days
frozen: 10 yrs, 24 hrs post-thawing
washed: 24 hrs
indication and contraindication for platelet transfusion
I: bleeding due to thrombocytopenia (decreased production, incr loss, sequestration, dilution, or abnormal platelet fxn) or prophylaxis in severe thrombocytopenia
(benefit: improved homeostasis)
CI: plasma coagulation deficit, clinic conditions associated w/ rapid platelet destruction (ITP or TTP)
transfusion threshold of platelets
prophylaxis in ABSENCE of bleeding: <10,000 plts
if significant hemorrhage: <50,000 plts
risk of CNS bleed: < 100,000 plts
“six pack”
pooled platelets; 6 single units of plts from whole blood pooled into a “single standard dose”
contents: 5.5x10^10 platelets
what can you occasionally see with platelet transfusions; how treat?
bloody platelets
RBC contamination–> Rh exposure
may need to administer RHIG
what is pharesis
single donor of platelets, automated cell separator is used
single unit aphereis platelet = ~same as 6 pooled single donor (same storage and infusion rate)
get decreased exposure to single donors; increased platelet retention
what are irradiated platelets
gamma irradiation inactivates donor lymphs
this decreases risk of GVHD
leukocyte reduction filter is utilized during administration of platelets (leukocyte reduced platelets)
also same storage and transfusion rate as pooled plts)
Indications and contraindications for FFP
I: deficiency of stable + labile plasma coagulation factors (w/ or w/out bleeding)
- emergent reversal of WARFARIN
- tx TTP
CI: volume expansion( USE ALBUMIN)
what is in FFP
all coagulation factors + fibrionogen
(Very few RBC, WBC, or platelets)
1 unit shud increase factor level 20-30%
dose = 2 units/adult
storage for 1 yr at 18C
What is a cryoprecipitate transfusion
fibrinogen 150-250 mg factor 8 (80-120 units) vwF replacement (40-60 units)
dosage: 10 bags/ dose; thaw at body temp (30-37)
indication for cryoprecipitate transfusion
hemophlia A
vw Dz
factor Xlll deficiency
topical glue
threshold: fibrinogen<80 mg/dL w/ ongoing bleed
Kleihauer-Betke test
measure fetal Hgb in moms circulation
standard method of quanitying fetal-maternal hemorrhage (via a standard blood smear)
RhoGAM dosage
1 full dosse (300 mg) at 26-28 weeks gestation or within 72 hrs of delivering Rh+ infant
one full IM dose prevents alloimmunization of 15 mL of Rh+ RBCs or 30 mL of Whole Blood
IV: aliquots 8 hrs until full dose is reached
**IM and IV are not interchnageable
Solvent Detergent treated plasma (SDP plasma)
pooled plasma from up to 2500 donors
inactivates enveloped viruses (HIV + HepB) using solvent detergent; not effective in those lacking lipid envelope
Granulocytes (pheresis)
contents: lots of WBCs; some platelts and plasma
Indications: neutrophenia unresponsive to appropriate Antibiotics; must be ABO compatible
Hazards: allergic + febrile rxns (GVHD unless irradiated to inactivate lymphs)
what is the most impt step in safe transfusion
CLERICAL VERIFICATION
infusion time must be completed within how much time
4 hours
unused units of blood must be returned within how much time
w/in 30 minutes of release from blood bank to not be discarded
what is the size of the IV that must be used for blood infusion
18 gauge needle
what can be transfused w/ blood
Only NORMAL saline
when giving neonatal transfusion, what should you do
subdivide blood components–> quad pack (24 hr expiration on one removed; can get more than 1 transfusion out of one unit of blood w/out running out of 24 hr expiration date for others)
use sterile technique
15 mL/kg aliquot of PC
Massive transfusion
transfusion that amts to FULL BLOOD volume within 24 hrs
10-12 units in an adult/day
assoc problems: coagulopathy, hypothermia, hypocalcemia
what is the rule of thumb for massive transfusions
1 unit FFP per every 2-3 units of RBCs
not a substitute for coagulation parameters + pt condition
when would you do a donor apheresis
stem cell collection for BM transplant
when would you do a plasma exchange
TTP + HUS
when would you do therapeutic plasma pharesis
hematological and neuro dz
when would you do therapeutic RBC exchange
sickle cell (crisis or prevention) fetal + neonatal HDN
