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acute
transfustion rxn occurs within 24 hrs of transfustion
delayed
transfusion rxn occurs 24 hrs to months after transfusion
acute hemolytic transfusion rxn (AHTR)
-rapid RBC destruction
-ABO incompatibility
-due to clerical errors
-fever, chills, hypotension/shock, flank/chest/back pain, hemoglobinuria
-intravasc (IgM) or extravasc (IgG)
-dose dependent
-variable DAT (extent of hemolysis)
-coag system activation (DIC)
IgM, schists
AHTR occurs intravascularly is IgM/IgG mediated, binds complement, and schists/spherocytes are seen
IgG, spherocytes
AHTR occurs extravascularly (spleen, liver) is IgM/IgG mediated and schists/spherocytes are seen
no
yes/no
a negative DAT means that an AHTR is not occurring
delayed hemolytic transfusion rxn (DHTR)
-hemolysis as anamnestic response
-fever, mild jaundice, hemoglobinuria, AKI (rare)
-dec Hct post-tfxn
-pos mf DAT
-Ab screen now pos
-spherocytes
dec
Hct is inc/dec post transfustion in DHTR
febrile non hemolytic transfusion rxn (FNHTR)
-most freq reported rxn
->1 C (1.8 F) rise in temp above 37 C within 4 hrs of tfxn
-neg DAT, no hemolysis
-due to cytokines and anti-leukocyte Ab in blood products
-treat: give Advil/Tylenol before next tfxn
-prevent: leukocyte reduced blood
>1, 4
a rise in temp by x C within x hrs of tfxn is indicative of febrile NHTR
neg
DAT and hemolysis are pos/neg with febrile NHTR
type I
hypersensitivity type causes allergic transfusion rxn
plasma
blood component transfused that can cause allergic transfusion rxn
yes
yes/no
if an allergic tfxn rxn occurs, stop the tfxn, treat the patient with benadryl, and if the hives go away, you can restart the tfxn
allergic transfusion rxns (ATR)
-type I hypersensitivity rxn (allergen in product and pt Ab)
-common with plasma products
-mild (hives) to severe (swelling)
-can restart tfxn if no hives after benadryl and no fever
-DAT neg, no hemolysis
anaphylaxis
-ATR of pts with IgA deficiency AND presence of anti-IgA Ab
-cannot receive plasma products
-receive washed products (RBCs, PLTs)
anaphylatoxins
-released upon immune complex formation and complement fixation
-activates mast cells and basophils
transfustion related acute lung injury (TRALI)
-develops within 6 hrs of tfxn
-can be fatal
-hypotension
-diffuse bilateral infiltrates on X ray
-due to anti-HLA or gran Ab in donor
-treat: resp support
-prevent: avoid use of plasma components from women who have been pregnant or who have HLA Ab
hypo
a defining symptom of TRALI is hypo/hyper -tension
donor
TRALI occurs due to anti-HLA or gran Ab in pt/donor
plasma
what products women who have been pregnant (multiparous) or who have HLA Ab are exempt from donating (TRALI prevention)
transfusion associated circulatory overload (TACO)
-tfxn rxn due to infusion vol overload
-can be fatal
-seen 1-2 hrs post tfxn
-elderly, infants, CHF, end stage renal disease
-hypertension
-treat: resp support
-prevent: avoid large vol plasma, transfuse slowly and only what need when need, only RBC prod
hyper
a defining symptom of TACO is hypo/hyper -tension
TA GVHD
-rare, highly lethal
-due to viable lymphs in blod prod
-3-30 days post-tfxn (fever, rash, pancytopenia)
-destroys pt bone marrow (marrow aplasia), hemmorhage, 90% mortality
-test: HLA typing
-treat: palliative
-prevent: irradiation
septic
-rare
-due to bacterial contam
-asympt bacteremic donor, bact survives storage conditions
-PLTs and skin contam, RBCs
-rapid symptom onset: fever, chills, hypotension, shock
-hgburia/emia, neg DAT, pos gram stain and culture
-treat: bs antibiotics
-prevent: proper collection, storage, and handling of products (always check visually multiple times for discoloration, clots, cloudiness, hemolysis)
neg
DAT is pos/neg with septic tfxn rxn
PLTs
-product with bacterial contam by skin flora
-S. epi, S. aureus, C. acnes
RBCs
-product with bacterial contam by bact that can survive storage conditions
-Y. enterocolitica, E. coli, Enterobacter, Pseudomonas, Serratia
post transfusion purpura (PTP)
-marked thrombocytopenia 5-12 days post tfxn with unexplained purpuric rash, bruising, mucosal bleeding
-PLA1- pt exposed to PLT1+ PLTs causes Ab that destroy all PLTs due to passive reabs of complex or Ab onto PLTs
-multiparous women at risk
-treat: self lim, IVIg, steroids, no tfxns
iron overload
-excess systemic iron
-deposits in organs (liver, heart, pancreas, other endocrine)
-inc risk cirrhosis, heart failure, diabetes
-typical in pts receiving chronic tfxns (B thalass, SCD, MDS)
-sympt with organ damage
-treat: therapeutic phleb or iron chelation drugs
delayed serologic (DSTR)
-no clinical signs or sympt of DHTR
-new Ab ID’d in blood bank
-use Ag neg blood in future tfxns
transfusion associated dyspnea (TAD)
-one symptom occurring alone or predom in allergic, TACO, TRALI
-diagnosed when occurs within 24 hrs of tfxn
-no clear cause, just can’t breathe
hypotensive transfusion rxn (hypo TR)
-low BP <1 hr after tfxn
-no other adverse rxns present
2-3 wks
“window period” between infection and detection of Ab to infectious disease
rare
infectious complications due to tfxns are common/rare
both
a pre/post transfusion DAT is needed for pt receiving tfxn
elution
additional testing done if DAT is pos
intra
intra/extra vascular hemolysis is indicated by pink, red, coca cola color of plasma
FDA (7)
where tfxn-related fatalities are reported ASAP and time to write official report (days)
AH, FNH, septic, TRALI
acute febrile TRs
DH, TA GVHD
delayed febrile TRs
TACO, TAD, allergic, hypo
acute non-febrile TRs
serologic, PTP, iron overload
delayed non-febrile TRs