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Adverse effects of transfusion Flashcards

1
Q

How many deaths per year are caused by hemolytic transfusion reaction

A

1 per million

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2
Q

USFDA (21CFR 606.170b)

A

notification is required for any fatality related to transfusion

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3
Q

Four transfusion reactions that present with fever

A

Febrile (FNHTR), AHTC, DHTR, bacterial contamination

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4
Q

Symptoms of Febrile Nonhemolytic Transfusion reaction

A

Fever >1 degree increase, increase blood pressure, chills, rigors, increase heart rate (*No resp distress and no drop in b.p.)

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5
Q

What percentage of transfusions have FNHTR

A

1%

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6
Q

What causes Febrile transfusion reactions

A

Cytokines released from Donor WBCs upon transfusion

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7
Q

How do you decrease the odd of acquiring FNHTR

A

Leukoreducing blood products prior to storage, or bedside leukoreduction (not as effective)

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8
Q

Treatment of FNHTR:

A

anti-pyretics: acetominephin, IB profin- both for fevers, for the rigors: demoral, neparadine

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9
Q

Successful Leukoreduction in products

A

> 5.0 x 10^6 (normal 5.0 x 10^9)

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10
Q

Symptoms of acute hemolytic transfusion reaction

A

Fever, chills, rigors, DECREASE B.P. decrease urine output (red/pink urine) decrease haptoglobin, increase LD, increase Bilirubin.

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11
Q

Treatment of AHTR

A

supportive

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12
Q

Free hemoglobin in the blood: what it does

A

scavenges nitrus oxide- vessels contract (especially in kidneys), cold clammy feeling

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13
Q

What causes AHTR

A

IgM, IgG-if high titer can fix complement when binding close together. (wrong blood type, Jka (clustering))

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14
Q

What causes DHTR

A

either low titer antibody (previous, but undetectable levels) or new antibody formation that is created in response to transfused red cells, red cells live ~120 days- attack rbcs still present.

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15
Q

Type of hemolysis DHTR

A

Extravascular- antibodies bind to red cell- red cell is removed from circulation by the spleen.

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16
Q

Symptoms DHTR

A

low grade fever, hgb drops, jaundice because hgb is broken down into bilirubin in the liver. decrease haptoglobin.

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17
Q

how can DHTR be diagnosed/proven

A

through identification of new antibody post transfusion

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18
Q

Bacterial contamination in blood products symptoms

A

fever, decrease in blood pressure (sepsis)

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19
Q

Differentiating Bacteria vs. AHTR

A

typically by the blood product provided (NOT ALWAYS) bacteria associated more with platelets- RT, AHTR most often associated with RBCs due to the fact that this is what is being hemolyzed in most cases. Hemolysis can also come from type incompatible plateelts.

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20
Q

Usual bacterial contamination

A

Gram positive more common, typically from skin contamination. Gram negative- endotoxins are the harmful portion, these can be in the cases of donors being bacteremic at the time of donation.

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21
Q

Treatment

A

antibiotics and supportive

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22
Q

How to avoid

A

diversion pouch with skin plug, pathogen reduction, sample and culture from original unit- wait 24 hours before releasing. Platelet pregnancy test (PGD test) has GN on the left, GP on the right and sample well in the center, put the same it will gravitate to both sides and colorimetric change will indicate contamination. Controls are located on the outsides of both the GN and the GP well.

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23
Q

Respiratory Distress Transfusion Reaction (2)

A

TRALI and TACO

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24
Q

TRALI- what it is?

A

Transfusion related acute lung injury

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25
Q

TRALI-what causes it?

A

Donor factor- HLA antibodies, HNA antibodies and ‘bioactive lipids’. Host factor- underlying condition with increase inflammation. It’s believed that both the Donor, and host factors combined ‘2 hit model’ cause TRALI

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26
Q

TRALI- Prevention?

A

“blood centers should attempt to mitigate TRALI” 1) decrease female plasma donors 2) limit number of previous pregnant donors 3) Test antibodies in donor plasma (HLA or granulocyte antibodies) if positive should be deferred from future donations

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27
Q

TRALI-symptoms

A

Dyspnea, Xray (white out of lungs), pulmonary edema, increase respiratory rate decrease oxygen saturation, fever, decrease blood pressure (85%)

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28
Q

what is specifically happening in the lungs during TRALI?

A

neutrophils marginate when activated bind to vessels to break through in body neutrophils marginate (forming a border to) in vessels. Avioli in the lungs, not bound to venules- bind to capillaries in lungs- capillaries are very delicate and damaged by the neutrophils- this is the first site of small vessels hit after being transfused

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29
Q

TACO symptoms

A

Transfusion associated circulatory overload. Pulmonary edema, X-ray (basal, increase pressure to lower part of lungs) increase b.p. dyspnea, increase respiratory rate, decrease oxygen saturation, increase heart rate.

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30
Q

Differentiating TACO and TRALI

A

TRALI- Xray-“white out” TACO “basal lungs”

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31
Q

Who is affected by TACO

A

it’s volume overload, heart disease patients, kidney disease patient and smaller people

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32
Q

What Transfusion reactions have the highest percentage of fatalities

A

TRALI and TACO

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33
Q

Impact of histamine in body

A

Laryngeal edema (wheezing) bronchoconstriction/vasodialation

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34
Q

symptoms of allergic reaction-transfusion reaction

A

Laryngeal edema (wheezing) bronchoconstriction/vasodialation, respiratory distress, increase respiratory rate, hives, itching, GI symptoms nausea, vomiting, cramping. decreased blood pressure

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35
Q

Cause of allergic reactions

A

IgE antibodies- depends on how much binding takes place and how much histamine was released.

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36
Q

How many liters of blood are in the human body

A

5 liters

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37
Q

If dilated how many liters of blood can the human body hold?

A

22 Liters

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38
Q

Treatment of allergic reaction

A

anti-histamines. Epinephrin causes vasoconstriction (can premed with antihistamines and steroids)

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39
Q

Mild allergic reactions from transfusion

A

just skin reaction- itching hives, pretty mild, take anti-histamine

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40
Q

Moderate allergic reactions

A

some edema (peri-orbital around the eyes) some GI symptoms, Itching and scratching, take anti-histamine (maybe steroid)

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41
Q

Post transfusion purpura

A

delayed reaction for platelets. HPA-1a antibodies (among others) molecular mimicry takes out transfused platelets as well as auto platelets.

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42
Q

prevalence of homozygous HPA-1b

A

1% of population- not easy to find donors. if they are transfused with HPA-1a, will probably make the antibody

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43
Q

Vasovagal reactions

A

“prefaint or presyncope” dizziness, sweating nausea, vomiting, weakness, pallor, hypotensin and bradycardia. LOW PULSE RATE.

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44
Q

reactions to volume depletion

A

high pulse rate.

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45
Q

Paresthesias

A

tingling sensations- reaction to citrate anticoagulant are not uncommon- provide calcium as a treatment.

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46
Q

Highest risk of sepsis comes from:

A

Platelets, higher related fatality than any other transfusable blood component: 1 in 6000 apheresis plts have bacteria

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47
Q

High percentage of bacterial contamination- what day of platelet

A

storage days 4 and 5 of platelet- 95% of septic transfusion reations and 100% fatalities are linked to longer outdate platelets

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48
Q

Isolated hypotenstion

A

buildup of bradykinen- ACE enzyme breaks down bradykinen, people on ACE inhibitor aren’t able to break down Bradykinen.

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49
Q

A.C.E. inhibitor

A

angiotensin- converting enzyme. helps relax blood vessels

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50
Q

Known transfusion-Transmitted infections (19)

A

Syphillis, Prions, Rickettsia, Malara, Babesia, Chaga’s, Leismaniasis, Toxoplasmosis, Filariasis, West Nile, CMV, HBV, HAV, HCV, HIV, HTLV, Parvo, EBV, Zika

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51
Q

Theoretical transfusion transmitted infections (8)

A

SARS, monkey pox, smallpox, encephalitis viruses, chikungunya, Lyme, Relapsing fever, Q fever (not been proven to show transmission)

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52
Q

Immune related acute adverse effects of transfusin (4)

A

acute hemolysis, allergy, TRALI, Febrile

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53
Q

immune delayed adverse effects of transfusion (5)

A

delayed hemolysis, graft vs. host disease, post-transfusion purpura, immune suppression, alloimmunizatin

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54
Q

Non immune acute (5)

A

TACO, Mechanical hemolysis, hypothermia, electrolyte disturbances, citrate toxicity

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55
Q

Non immune delayed

A

iron overload

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56
Q

Pulmonary edema

A

lungs filled with fluid, (In TRALI-due to leaky blood vessels not heart failure)

57
Q

Cause of TRALI

A

donor white blood cell antibodies or HLA antibodies, attach recipient white blood cells and cause them to leukoagglutinate (occurs in lungs, small capillaries of avioli cannot handle) these get caught up in the lungs and relase damaging enzymes.

58
Q

What percentage of TRALI cases are fatal?

A

5-10% die, most patients recover within a few days

59
Q

ARDS

A

adult resipratory distress syndrome- often misdiagnosed as this when it’s actually TRALI

60
Q

Treatment for TRALI

A

mechanical ventilation and supportive care

61
Q

Blood units associated with TRALI

A

any plasma containing blood unit

62
Q

two types of TRALI

A

antibody-mediated and non antibody mediated

63
Q

Antibody mediated TRALI

A

usually plasma units and half of apheresis platelet cases. HLA or neutrophil antibodies, antibody usually from donor, antibody alone usually does not cause TRALI

64
Q

Non antibody mediated TRALI

A

red cell units and half of apheresis cases, negative for white cell antibodies. Neutrophil-priming (two-hit hypothesis) event #1 causes neutrophils to be primed, event number 2 causes them to be activated. (1. underlying condition 2. transfusion) could be caused by ‘biologically active substances, like lipids’

65
Q

what type of antibody is most fatal in TRALI

A

HNA antibodies are more associated with fatalitites

66
Q

what is the most common/concerning TRALI antibody specificity

A

HNA-3a

67
Q

TRALI mitigation strategies

A

using solvent-detergent treated plasma, use of platelet additive solutions, use of pathogen reduced platelets no donation of products that cause TRALI by people with history of pregnancy

68
Q

TACO

A

transfusion associated circulatory overload. reported incidence of this is increasing, still under-recognized 2-6% of transfused patients can occur with any blood products

69
Q

TACO risk factors

A

very young (less than three) or old (older than 60) chronic renal failure, congestive heart failure, higher number of blood products infused, higher fluid balance per hour, faster transfusion rates, any critical illness

70
Q

Difference between TACO and TRALI

A

TRALI- White out pulmonary edema TACO- only bottom of the lungs. TRALI increase temp TACO unchanged temp. TRALI-HYPOTENSION TACO-HYPERTENSION. TACO-significant diuretic. TRALI- decrease WBC count. TACO- positive fluid balance

71
Q

Prevention of TACO

A

avoid unnecessary transfusion, identify underlying risk factors, use of diuretics, use 4-PCC for warfarin reversal instead of FFP, close monitoring and awareness

72
Q

TA-GVHD

A

manifests 3-30 days usually 8-10 days, signs/symptoms rash, fever, diarrhea, increase liver functions and pancytopenia, no effective treatment, mainly fatal due to involvement of the bone marrow

73
Q

Types of irradiation

A

X-ray or Gamma irradiation of cellular products

74
Q

Fludarabine

A

Purine analogues, treatment for patients with CLL leukemia or lymphoma malignancies

75
Q

What does irradiation do to the units

A

inactivated donor lymphocytes, prevents the proliferation so they cannot mount an attack against host

76
Q

Irradiation vs. leukocyte reduction filters

A

filters do not remove enough leukocytes to prevent GVHD, still needs irradiation even if leukoreduced

77
Q

Minimum dose of irradiation for units

A

25Gy to the center 15Gy to the edges of entire bag minimum

78
Q

Indications of irradation of units

A

Premature, intrauterine transfusion, congenital immunodeficiencies, hodkin disease, hematologic malignancies, peripheral blood stem cell/marrow transplantation, granulocyte components, fudarabine therapy, HLA matches or from directed donors

79
Q

HSCT irradiated products for how long?

A

We don’t have a set standard, definitely require irradiated blood products during and for at least 1 year after transplantation, AABB acknowledges that we don’t have the evidence to determine how long they need to be provided irradiated products for. Must be given from the initiation of conditioning chemoradiotherapy, should be continued while patient- is on GVHD prophylaxis usually six months post transplant. Lymphocytes >1x10^9

80
Q

HSCT donors considerations

A

If donor for HSCT is to be transfused up to 7 days prior to or during the harvest should be irradiated, same with autologous donors

81
Q

Hodgkin Lymphoma special requirements for units

A

all adults and children with diagnosis, at any stage of the disease should have irradiated red cells annd platelets for life

82
Q

Purine analogue drugs

A

fludarabine, cladribine and deoxycoformicin, need to receive irradiated blood components indefinitely, these are commonly used to treat cancer by disrupting DNA

83
Q

Acute Leukemia patients special needs

A

not necessary to irradiate red cells or platelets except for HLA selected platelets or donations from family

84
Q

alemtuzumab

A

anti-CD52 therapy, patients must be given irradiated blood products

85
Q

ATG

A

antithymocyte globulin, recent switch from horse to rabbit ATG that is more immunosuppressive in patients with aplastic anemia. Recommendation of irradiated units, though cannot make a firm recommendation on how long irradiated blood product need to be provided for.

86
Q

what is a substitution for irradiated blood products

A

pathogen reduction

87
Q

Platelet safety measurements

A

before release of platelets, needs to be 1. culture based testing 2. point of care testing at hospital (PDG) 3. pathogen reduction technology.

88
Q

If platelet is positive for bacteria

A

per FDA need to identify organism and then contact and counsel donor if appropriate

89
Q

Arm scrub for donors

A

chlorhexidine or betadine

90
Q

septic transfusion reaction rate

A

1/100,000 for passive recording 1/10,000 for active recording, 95-100% of cases of septic reactions were on days 4 and 5 of platelet life

91
Q

6 or 7 platelets

A

platelets can now be used on day 6 or 7 if test is done for bacterial detection on the day of transfusion

92
Q

FDA new rule 2018 regarding platelet contamination

A

Must be checked on day four or five for bacterial testing, would required aerobic and anaerobic testing, testing daughter bags as opposed to mother bag. otherwise pathogen reduction technology

93
Q

Acute conditions to report for transfusion reactions

A

Fever, chills, flushing, red urine or other indicators of hemolysis, changes in blood pressure or pulse, dyspnea, unexplained pain, anaphylaxis or moderate to severe allergy, fatalities, maybe urticaria, simple rash or volume overload

94
Q

Testing in acute hemolytic transfusion reaction

A

examination of post-transfusion serum: hemolysis, DAT ABORH of post sample. Examination of post transfuision urine, perform clerical check of paperwork. Further testing if any of the others are abnormal or positive: repeat ABORH repeat crossmatch, repeat antibody screen and ID, blood markers for hemolysis (LD, bilirubin, haptoglobin)

95
Q

Intravascular hemolysis

A

immediate, destruction by complement, occurs in circulation, free hemoglobin in urine and serum, decreased haptoglobin, systemic reaction

96
Q

Extravascular hemolysis

A

delayed hours or days, destruction by macrophage, occurs in spleen or other extravascular sites, no free hemoglobin, few if any simptoms, rarely life-threatening

97
Q

Clinical signs and symptoms of AHTR

A

patient discomfort, low blood pressure and high pulse, fever and chills, loss of conscioiusness, feeling of impending doom, pain in back, chest or at infusion site, difficulty breathing

98
Q

Outcome of AHTR

A

death, renal failure, DIC

99
Q

treatment of AHTR

A

Stop transfusion ASAP! Keep IV line open, don’t close the line!!! Start saline administration, keep well hydrated, support blood pressure, do not transfused additional units of same time!!

100
Q

Mechanical hemolysis

A

improper storage or handling of blood, heated or frozen, improper administration pressure pump or too small needle bore, incompatible IV fluids or medications added, bypass circuit or blood pump, bacterial contamination

101
Q

Fever after transfusion

A

TRALI, Bacteria, Hemolysis or underlying disease. If all of these can be excluded may diagnose non-hemolytic febrile transfusion reaction

102
Q

Febrile reaction units

A

most common with platelets, caused by white blood cell incompatibilities, most common donor white blood cells are lysed by recipient wbc antibodies, cells release pyrogens that cause fever, chills and flushing.

103
Q

Avoidance of febirle reactions

A

leukoreduction of components, premedication with anti-pyretics (tylenol)

104
Q

Allergic Transfusion reaction

A

Mild- reaction of patient IgE antibodies against transfused plasma, soluble substance (probably a protein) in plasma is the target. Antigen antibody reaction releases histamine and other anaphylotoxins from basophils and mast cells urticaria hives itching

105
Q

Severe allergic transfusion reaction

A

More thanlocalized skin rash and itching, may involve facial swelling, laryngeal edema and difficulty breathign if this occurs stop transfusion, do not continue with same unit after treatment

106
Q

Anaphylaxis

A

severe, life-threatening allergic reaction, occurs within minutes of the start of transfusion, difficulty breathing closure of airways can have GI cramping and pain, stop transfusion and call for help needs immediate treatment with epinephrine patient may end up on ventilator

107
Q

Transfusion of patients with moderate allergic reactions

A

pre-medication with anti-histamines, pre medication with steroids, close observation, use of washed cellular products avoidance of plasma, autologous blood if possible

108
Q

1 bacteria in RBCs

A

Yersinia entercolitica= 51% (#2 is pseudomonas fluorescens=27%)

109
Q

Acute Fever (4)

A

AHTR, TRALI, septic, Febrile

110
Q

Delayed Fever (2)

A

DHTR, TA-GVHD

111
Q

Acute non-fever (4)

A

TACO, Urticarial, Anaphylaxis, premedicated

112
Q

Delayed non-fever (2)

A

PTP, Iron overload

113
Q

PTP

A

post transfusion purpura, typically in multiparous women, has antibodies against platelets HPA-1a etc. and destroys platelets including own platelets after transfusion with ‘incompatible’ Patient should be tested to identify antibody causing reaction for future avoidance

114
Q

Symptoms of AHTR

A

fever, chills, back/flank pain, sense of impending doom, hemoglobinemia/uria, DIC, decreased LDH, elevated bilirubin, decreased serum haptoglobin

115
Q

Window for increased hemoglobinuria and decresed haptoglobing in AHTR

A

1-2 days and then values slowly return to normal

116
Q

Percentage of Febrile reactions in transfusion

A

1-2% of all transfusions

117
Q

Febrile caused by

A

accumulated cytokines in unit (IL-6, TNF etc.) These can be increased in older units due to activation and release cytokines by WBCs over time

118
Q

Febrile symptoms/signs

A

fever and chills comes on acute, increase in temp greater than 1 degree

119
Q

Clinical signs and symptoms of Septic reation

A

Rapid high fever, rigors and shock

120
Q

TRALI fatality percent

A

20% fatal

121
Q

TRALI and TACO comparison of cardiac dysfunction

A

TRALI has no cardiac dysfunction, TACO has tachycardia and hypertension

122
Q

Most common HLA group that causes TRALI reaction

A

HLA-II (34-47%) HLA1 and HNA have similar percentage rates for causality (4-28% ish)

123
Q

TRALI two hit method

A

Typically something primes the endothelium and PMNs in the patient and then when unit is transfused they are activated

124
Q

Signs and symptoms of Anaphylaxis

A

Severe hypotension, GI symptoms, swelling of throat (fevers are rare!!)

125
Q

Drug for chills/rigors

A

meperidine

126
Q

anamnestic response

A

rapid IgG production upon re-exposure to antigen. Most common cause of DHTR

127
Q

Transfusion hemosiderosis

A

Excessive iron deposition in recipient, significance comes over years of constant transfusion

128
Q

Iron in each unit of RBCs

A

225mg of Iron

129
Q

Iron overload more common in these patients:

A

chronic renal failure, aplastic anemia, congenital hemolytic anemias (sickle cell)

130
Q

Citrate toxicity results in

A

hypocalcemia, manifesting particularly in liver dysfunction, hypothermic or shock in patients

131
Q

Potassium complications

A

excess potassium in red cells (predominantly in irradiated units) transport pumps can become damaged, hypokalemia is more frequently observed because potassium depleted donor cells reaccumulate potassium ion intracellularly and citrate metabolism causes further movement of potassium into the cells.

132
Q

Hyperkalmeia can be a problem in these patients:

A

Pre-existing hyperkalemia, renal failure, premature infants, newborns receiving large transfusions, cardiac surgery or exchange transfusion

133
Q

When does bilirubin peak in patient after hemolytic event

A

3-6 hours as free hemoglobin is metabolized

134
Q

normal oxygen saturation

A

95-100%

135
Q

Treatment ofr acute hemolytic transfusion reaction

A

Diuretic, analgesics, pressors to manage hypotension and management for DIC

136
Q

Diuretic drug

A

furosemide

137
Q

analgesics

A

medicines used to relieve pain, acetominephan

138
Q

Treatment of hypotension

A

PRESSOR- low dose dopamine, fludrocortisone, midodrine

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