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blood bank > transfusion reactions > Flashcards

transfusion reactions Flashcards

1
Q

signs of transfusion rxn

A

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

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2
Q

what to do if transfusion rxn suspected? nurse

A

stop transfusion
maintain IV access
notify physician and lab
return unit and tubing

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3
Q

what to if transfusion suspected physician?

A

provide necessary treatment
advise investigation
order necessary testing

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4
Q

what to transfusion rxn suspected lab ?

A

contact lab director/path
clerical checks
investigate all pre- and post- transfusion specimens

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5
Q

what to do in a transfusion rxn pathologist?

A

coordinate with patient’s physician
confirm lab workup, diagnose reaction
notify appropriate reg agencies

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6
Q

clerical checks

A

does the patient information match?

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7
Q

pre- and post- transfusion

A

check for hemolysis and type and screen

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8
Q

first 2 urine sample

A

is heme present, blood

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9
Q

DAT

A

positive indicated immune hemolytic reaction

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10
Q

donor unit

A

repeat ABO/Rh typing and compatibility with patient sample

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11
Q

acute

A

within 24 hours of transfusion

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12
Q

delayed

A

more than 24 hours after transfusion

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13
Q

delayed

A

immune/ serologic hemolytic transfusion reaction
transfusion associated graft vs. host disease
post transfusion purpura
iron overload

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14
Q

acute immune hemolytic

A

preformed antibodies in recipient interact with donor RBC antigens and activate complement

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15
Q

most severe form of acute immune hemolytic

A

ABO incompatibilty

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16
Q

abo incompatibility is caused by

A

clerical error

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17
Q

symptoms of acute immune hemolytic

A

fever, chills, impending sense of doom, shock, DIC, renal failure

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18
Q

acute immune hemolytic reactions– lab findings

A

free hgb in plasma, free hgb in urine, positive DAT

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19
Q

make sure hemolyzed samples are not result of bad draw because can be

A

hemolytic reaction

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20
Q

acute non immune hemolytic

A

caused by chemical/thermal/mechanical damage to RBC’s prior to or during transfusion

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21
Q

examples of nonimmune hemolytic

A

-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

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22
Q

transfusion associated sepsis

A

-no antibody involved
-bacteria-contaminated blood component (skin flora)

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23
Q

classic presentation of transfusion associated sepsis

A

temp > 2 above normal
-chills/rigors
-hypotension

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24
Q

textbook microbe responsible for transfusion associated sepsis

A

yersinia enterocolytica

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25
Q

why does transfusion sepsis occur more in platelet than RBCs?

A

platelets are not stored cold so nothing to prevent growth of bacteria

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26
Q

to confirm transfusion associated sepsis

A

same organism must be isolated from the unit

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27
Q

febrile non-hemolytic classic presentation

A

increase in body temp of at least 1C
-chills and rigor

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28
Q

2 causes of febrile non-hemo

A

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

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29
Q

way to prevent febrile non-hemolytic reaction

A

leukoreduced prior to storage

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30
Q

allergic rxn

A

recipient has antibodies to a protein-based allergen in the blood component (plasma protein)

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31
Q

what reaction can you still continue giving when having a reaction

A

allergic

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32
Q

during allergic transfusion

A

give anti-histamines

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33
Q

presentation of allergic

A

hives, itching, swelling

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34
Q

anaphylactic rxn

A

more severe than allergic, non-hemolytic, can occur within minutes of exposure, type 1 hypersensitivity rxn

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35
Q

what deficiency is associated with anaphylactic

A

IgA; wil develop anti-IgA which reacts with it in the unit (can be washed to remove excess plasma)

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36
Q

symptoms of anaphylactic

A

allergic symptoms, NO FEVER, respiratory problems, death

37
Q

anaphylactic lab findings

A

IgA levels low/ absent; need steroids to reverse response

38
Q

trali

A

transfusion related acute lung injury

39
Q

where is trali seen most

A

plasma and platelet transfusion

40
Q

symptoms of trali

A

low O2, rapid heart rate, cyanosis, hypotension, fever/chills, fluid in lungs

41
Q

TRALI one hit method

A

anti-HLA antibodies get introduced into plasma or platelet unit– neutrophils activated (secrete toxins) causes damage

42
Q

where is anti-HLA antibodies commonly seen

A

mulitple pregnancy women

43
Q

trali non immune 2 hit

A

1) recipent lungs primed by lung trauma
2) neutrophils activated by biologically active substance during storage

44
Q

trali treatment

A

respiratory support

45
Q

trali lab findings

A

DAT negative, no hemolysis

46
Q

prevention of trali

A

multiple pregnant women –screen out of donor pool

47
Q

immune hemolytic/serologic

A

secondary response or primary (rare) occurs more than 24 hours after reaction; unexpected RBC antibody

EXTRAVASCULAR

48
Q

classic presentation of immune hemolytic/serologic

A

low Hgb after transfusion, flu like symptoms, jaundice

49
Q

immune hemolytic/serologic lab findings

A

increased serum bili, urine urobilinogen, urine bili
positive antibody screen in post transfusion specimen

AHG crossmatch incompatible with pre/post

positive DAT

50
Q

serologic rxn

A

patient has RBC antibody, but no evidence of hemolysis

51
Q

TA-GVHD

A

transfusion-associated graft versus host disease

52
Q

what happens in TA/GVHD

A

donor lymph not recognized by recipient ATTACK

53
Q

symptoms of TA-GVHD

A

wide spread rash, fever, bloody stool, all cell count decreased, hepatomegaly

54
Q

at risk populations for TA-GVHD

A

infants, cancer patients, immunocompromised

55
Q

why can’t immunocomprised patients clear invading cells when from close relative

A

if donor homozygous for HLA locus and recipient is heterozygous, recipient’s immune system WILL NOT recognize HLA as foreign but donor lymphs WILL

56
Q

TA-GVHD treatment

A

fatal

57
Q

TA-GVHD prevention

A

irradiate blood products – inactivates WBC

58
Q

HIV patients are

A

resistant to TA-GVHD

59
Q

post transfusion purpura

A

patient previously sensitized to human platelet antigens by preg or transfusion— develop anti-HPA-la– reexposure to platelets or whole blood– platelets destroyed

60
Q

symptoms of purpura

A

thrombocytopenia, bleeding, small red lesions

61
Q

classic presentation of purpura

A

multiple pregnancies mothers

62
Q

treatment of post-transfusion purpura

A

IV immunoglobin, plasmapheresis (exchange), steriods, splenectomy

63
Q

why does splenctomy work for purpura

A

spleen will lyse old RBCs and platelets are stored in spleen so take it out= platelet have no where to hide

64
Q

prevention of purpura

A

leukoreduction lowers

65
Q

TACO

A

transfusion associated cardiac overload

66
Q

taco happens when you

A

overtransfuse someone

67
Q

people at risk for TACO

A

over 70, infants, multiple transfusion patients, or unnecessary transfusion people

68
Q

symptoms of TACO

A

difficult breathing, jugular vein overfilled, edema, congestive heart failure, headache, cough

69
Q

TACO diagnosis

A

chest x-ray, BTNP !! rule out TRALI with BTNP

70
Q

treatment of TACO

A

oxygen therapy, diuretics, upright posture, therapeutic phlebotomy

71
Q

how to prevent TACO

A

avoid large volume of plasma (more volume), give packed cells, transfuse over long period (4hrs cap)

72
Q

why transfuse still?

A

hemoglobin vital!

73
Q

lab investigation

A

on post transfusion specimen

-clerical check
-hemolysis check
-DAT
-ABO typing

74
Q

transfusion associated dyspnea

A

ONLY trouble breathing within 24 hours of transfusion
-not well understood
-considered a mild TACO

75
Q

hypotensive transfusion reaction

A

acute drop in BP following transfusion
-high levels of bradykinin (hormone causing vasodilation)-stored in blood products

76
Q

prevention for hypotensive transfusion reaction

A

leukoreduction– white cells secrete bradykinin so they get destroyed

AND

screen donors that take ACE inhibitors (increase bradykinin levels)

77
Q

classic presentation of immune hemolytic

A

drop in hemoglobin
fever
flu-like symptoms
jaundice

extravascular hemo.
positive DAT

78
Q

serologic reaction

A

positive DAT and no hemolysis

79
Q

patients that receive multiple platelet transfusion may not acheive the expected increase in PLT count (10,000- 15,000)

A

refractory to platelets

80
Q

why refractory to platelet occurs

A

patient may have developed anti-HLA and immune system removes transfused platelets

81
Q

metabolic effects of transfusion

A

citrate toxicity and excress potassium

82
Q

RBC units anticoag with

A

citrate

83
Q

citrate binds divalent ions so can cause

A

hypomagnesemia and hypocalcemia if given in high concentration

84
Q

as RBC units go bad on shelf

A

RBCs leak potassium = hyperkalemic (very old can’t give a lot of old units)

85
Q

why do infants receive fresh units

A

hyperkalemia is a concern

86
Q

transfusion transmitted infection

A

when a patient acquires an infection from a blood product (sepsis, viral, microbial, prion)

87
Q

iron overload

A

excess iron causes heart failure, liver failure, diabetes, hypothyroidism

humans don’t have excretory system for iron

88
Q

who is at risk for iron overload

A

frequent transfused people

89
Q

what is recommended for people who are transfusion a lot

A

iron chelation or therapeutic phlem.

blood bank (8 decks)

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