transfusion reactions Flashcards
signs of transfusion rxn
fever
chills
back pain
visible hemolysis
impending sense of doom
hypotension
renal failure
disseminated intravascular coag
shock
nausea/ vomitting
increased BP
increased pulse
hives
itching
dyspnea
what to do if transfusion rxn suspected? nurse
stop transfusion
maintain IV access
notify physician and lab
return unit and tubing
what to if transfusion suspected physician?
provide necessary treatment
advise investigation
order necessary testing
what to transfusion rxn suspected lab ?
contact lab director/path
clerical checks
investigate all pre- and post- transfusion specimens
what to do in a transfusion rxn pathologist?
coordinate with patient’s physician
confirm lab workup, diagnose reaction
notify appropriate reg agencies
clerical checks
does the patient information match?
pre- and post- transfusion
check for hemolysis and type and screen
first 2 urine sample
is heme present, blood
DAT
positive indicated immune hemolytic reaction
donor unit
repeat ABO/Rh typing and compatibility with patient sample
acute
within 24 hours of transfusion
delayed
more than 24 hours after transfusion
delayed
immune/ serologic hemolytic transfusion reaction
transfusion associated graft vs. host disease
post transfusion purpura
iron overload
acute immune hemolytic
preformed antibodies in recipient interact with donor RBC antigens and activate complement
most severe form of acute immune hemolytic
ABO incompatibilty
abo incompatibility is caused by
clerical error
symptoms of acute immune hemolytic
fever, chills, impending sense of doom, shock, DIC, renal failure
acute immune hemolytic reactions– lab findings
free hgb in plasma, free hgb in urine, positive DAT
make sure hemolyzed samples are not result of bad draw because can be
hemolytic reaction
acute non immune hemolytic
caused by chemical/thermal/mechanical damage to RBC’s prior to or during transfusion
examples of nonimmune hemolytic
-improper temp during storage or transport
-incomplete deglycerolization of frozen RBC’s
-needles used for transfusion too small, shear cells
-improper use of blood warmers
-infusion with unapproved fluids
transfusion associated sepsis
-no antibody involved
-bacteria-contaminated blood component (skin flora)
classic presentation of transfusion associated sepsis
temp > 2 above normal
-chills/rigors
-hypotension
textbook microbe responsible for transfusion associated sepsis
yersinia enterocolytica
why does transfusion sepsis occur more in platelet than RBCs?
platelets are not stored cold so nothing to prevent growth of bacteria
to confirm transfusion associated sepsis
same organism must be isolated from the unit
febrile non-hemolytic classic presentation
increase in body temp of at least 1C
-chills and rigor
2 causes of febrile non-hemo
leukocytes present in component release cytokines during storage and show fever
OR
recipient has anti-HLA antibodies from pregnancy or previous transfusion which attack transfused leukocytes
way to prevent febrile non-hemolytic reaction
leukoreduced prior to storage
allergic rxn
recipient has antibodies to a protein-based allergen in the blood component (plasma protein)
what reaction can you still continue giving when having a reaction
allergic
during allergic transfusion
give anti-histamines
presentation of allergic
hives, itching, swelling
anaphylactic rxn
more severe than allergic, non-hemolytic, can occur within minutes of exposure, type 1 hypersensitivity rxn
what deficiency is associated with anaphylactic
IgA; wil develop anti-IgA which reacts with it in the unit (can be washed to remove excess plasma)
symptoms of anaphylactic
allergic symptoms, NO FEVER, respiratory problems, death
anaphylactic lab findings
IgA levels low/ absent; need steroids to reverse response
trali
transfusion related acute lung injury
where is trali seen most
plasma and platelet transfusion
symptoms of trali
low O2, rapid heart rate, cyanosis, hypotension, fever/chills, fluid in lungs
TRALI one hit method
anti-HLA antibodies get introduced into plasma or platelet unit– neutrophils activated (secrete toxins) causes damage
where is anti-HLA antibodies commonly seen
mulitple pregnancy women
trali non immune 2 hit
1) recipent lungs primed by lung trauma
2) neutrophils activated by biologically active substance during storage
trali treatment
respiratory support
trali lab findings
DAT negative, no hemolysis
prevention of trali
multiple pregnant women –screen out of donor pool
immune hemolytic/serologic
secondary response or primary (rare) occurs more than 24 hours after reaction; unexpected RBC antibody
EXTRAVASCULAR
classic presentation of immune hemolytic/serologic
low Hgb after transfusion, flu like symptoms, jaundice
immune hemolytic/serologic lab findings
increased serum bili, urine urobilinogen, urine bili
positive antibody screen in post transfusion specimen
AHG crossmatch incompatible with pre/post
positive DAT
serologic rxn
patient has RBC antibody, but no evidence of hemolysis
TA-GVHD
transfusion-associated graft versus host disease
what happens in TA/GVHD
donor lymph not recognized by recipient ATTACK
symptoms of TA-GVHD
wide spread rash, fever, bloody stool, all cell count decreased, hepatomegaly
at risk populations for TA-GVHD
infants, cancer patients, immunocompromised
why can’t immunocomprised patients clear invading cells when from close relative
if donor homozygous for HLA locus and recipient is heterozygous, recipient’s immune system WILL NOT recognize HLA as foreign but donor lymphs WILL
TA-GVHD treatment
fatal
TA-GVHD prevention
irradiate blood products – inactivates WBC
HIV patients are
resistant to TA-GVHD
post transfusion purpura
patient previously sensitized to human platelet antigens by preg or transfusion— develop anti-HPA-la– reexposure to platelets or whole blood– platelets destroyed
symptoms of purpura
thrombocytopenia, bleeding, small red lesions
classic presentation of purpura
multiple pregnancies mothers
treatment of post-transfusion purpura
IV immunoglobin, plasmapheresis (exchange), steriods, splenectomy
why does splenctomy work for purpura
spleen will lyse old RBCs and platelets are stored in spleen so take it out= platelet have no where to hide
prevention of purpura
leukoreduction lowers
TACO
transfusion associated cardiac overload
taco happens when you
overtransfuse someone
people at risk for TACO
over 70, infants, multiple transfusion patients, or unnecessary transfusion people
symptoms of TACO
difficult breathing, jugular vein overfilled, edema, congestive heart failure, headache, cough
TACO diagnosis
chest x-ray, BTNP !! rule out TRALI with BTNP
treatment of TACO
oxygen therapy, diuretics, upright posture, therapeutic phlebotomy
how to prevent TACO
avoid large volume of plasma (more volume), give packed cells, transfuse over long period (4hrs cap)
why transfuse still?
hemoglobin vital!
lab investigation
on post transfusion specimen
-clerical check
-hemolysis check
-DAT
-ABO typing
transfusion associated dyspnea
ONLY trouble breathing within 24 hours of transfusion
-not well understood
-considered a mild TACO
hypotensive transfusion reaction
acute drop in BP following transfusion
-high levels of bradykinin (hormone causing vasodilation)-stored in blood products
prevention for hypotensive transfusion reaction
leukoreduction– white cells secrete bradykinin so they get destroyed
AND
screen donors that take ACE inhibitors (increase bradykinin levels)
classic presentation of immune hemolytic
drop in hemoglobin
fever
flu-like symptoms
jaundice
extravascular hemo.
positive DAT
serologic reaction
positive DAT and no hemolysis
patients that receive multiple platelet transfusion may not acheive the expected increase in PLT count (10,000- 15,000)
refractory to platelets
why refractory to platelet occurs
patient may have developed anti-HLA and immune system removes transfused platelets
metabolic effects of transfusion
citrate toxicity and excress potassium
RBC units anticoag with
citrate
citrate binds divalent ions so can cause
hypomagnesemia and hypocalcemia if given in high concentration
as RBC units go bad on shelf
RBCs leak potassium = hyperkalemic (very old can’t give a lot of old units)
why do infants receive fresh units
hyperkalemia is a concern
transfusion transmitted infection
when a patient acquires an infection from a blood product (sepsis, viral, microbial, prion)
iron overload
excess iron causes heart failure, liver failure, diabetes, hypothyroidism
humans don’t have excretory system for iron
who is at risk for iron overload
frequent transfused people
what is recommended for people who are transfusion a lot
iron chelation or therapeutic phlem.
