Seminars in Oncology Nursing 37 (2021) 151137

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Seminars in Oncology Nursing

journal homepage: https://www.journals.elsevier.com/seminars-in-oncology-nursing

Identifying and Understanding Transfusion Reactions in the Oncology

Population
Carrie A Graham, MSN, ARNP, ANP-BC, AOCNPÓ*, Danielle DuBois, PA-C,
Christine Gleason, MSN, ARNP, AGNP-BC, OCNÓ, Joy Kumagai, DNP, ARNP, AGNP-BC,
Jeannine Sanford, MSN, ARNP, FNP-BC, OCNÓ
Division of Medical Oncology, Department of Medicine, University of Washington School of Medicine, Seattle, WA

A R T I C L E I N F O A B S T R A C T

Key Words:
Transfusion reaction
Allergic transfusion reaction
Hemolytic transfusion reaction
transfusion-associated circulatory overload
transfusion-related acute lung injury
Oncology nursing
Objectives: To provide an overview of transfusion reactions, their underlying pathophysiology, clinical pre-
sentation, and recommendations for nursing management.
Data Sources: We researched peer-reviewed journal articles, book chapters, Internet, and lecture
proceedings.
Conclusion: Transfusion reactions are adverse reactions to blood products frequently seen in the oncology
population and can significantly vary in severity and etiology. Oncology nurses are in a critical position to
assist with prevention, early detection, and time-sensitive treatment of transfusion reactions.
Implications for Nursing Practice: : The oncology nurse’s comprehensive understanding of possible transfusion
reactions and management recommendations is key for optimal care of the oncology patient.
© 2021 Published by Elsevier Inc.

Introduction anaphylaxis.3,4 ATRs can occur during or within 4 hours following

Blood transfusions are one of the most frequent therapeutic pro-
cedures for patients in the hematologic and oncologic settings. How-
ever, they can be associated with substantial risk. Approximately 1%
of transfusions result in a potentially life-threatening adverse
reaction.1,2 Transfusion reactions vary in severity and etiology and
include allergic/anaphylactic reactions, febrile nonhemolytic reac-
tions, hemolytic reactions, septic reactions, circulatory overload, and
inflammatory lung injury.2 The most effective strategy in prevent-
ing any transfusion reaction is reducing the number of transfu-
sions administered by ensuring that each blood transfusion is
clinically indicated. Safe administration of blood transfusions
requires effective communication and collaboration among trans-
fusion services, providers, and nursing staff to safely administer
blood products and appropriately identify, diagnose, and manage
transfusion reactions.2
Allergy and Anaphylactic Transfusion Reactions
Allergic transfusion reactions (ATRs) and anaphylactic reactions
are a spectrum of acute type 1 hypersensitivity reactions to a trans-
fused blood product.3 Allergic reactions range from localized urticar-
ial reactions to systemic reactions including life-threatening
* Corresponding author.
E-mail address: cgraham@seattlecca.org (C.A. Graham).
completion of a transfusion, with more severe ATRs typically occur-
ring within a shorter time frame.4 Broadly, ATRs can be classified as
either solely mucocutaneous or anaphylactic, with further characteri-
zation by severity.5
In the United States, mild to moderate allergic reactions have a
reported incidence of 86 reactions per 100,000 blood components
transfused, making it the second-most common transfusion reac-
tion.6 Severe allergic reactions, including anaphylaxis, occur with
much less frequency and have a reported rate of approximately 3 per
100,000 blood components transfused.6 These rates are much lower
than historical values, possibly due to mitigation strategies and dedi-
cated hemovigilance systems. Plasma and platelet transfusions are
more commonly associated with ATRs, as compared to red blood cell
(RBC) transfusions.
ATRs are a spectrum of immunoglobulin E (IgE)-mediated, type 1
hypersensitivity reactions that occur most commonly due to an aller-
gen in the donor blood product.3 Recipient IgE antibodies react with
the donor allergen (plasma protein) resulting in activation of mast
cells or basophils, which causes the release of inflammatory media-
tors (ie, histamine and other cytokines). Another mechanism is due
to recipient plasma protein deficiencies. In patients with certain pro-
tein deficiencies (immunoglobulin A [IgA], haptoglobin, C3, C4), anti-
bodies are formed against absent plasma proteins in response to a
sensitizing event, initiating an ATR when re-exposed to a blood com-
ponent.4 The risk for ATRs can be decreased by reducing plasma in
transfused products via product concentration, washing components,

https://doi.org/10.1016/j.soncn.2021.151137
0749-2081/© 2021 Published by Elsevier Inc.
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and utilization of platelet additive solution (PAS).3,7 Recipients with
atopic predisposition are at greater risk of developing an ATR.3
Mild allergic reactions include urticaria, pruritis, rash, flushing,
periorbital edema, perioral edema, conjunctival erythema, or local-
ized angioedema. Severe allergic reactions and anaphylaxis include
mucocutaneous symptoms, plus hypotension, dyspnea, with or with-
out signs of airway obstruction (wheezing, stridor), angioedema,
abdominal pain, vomiting, alteration/loss of consciousness, or
shock.5,8,9 Fever is not typically seen with ATRs.4
Febrile Nonhemolytic Transfusion Reactions
Febrile nonhemolytic transfusion reaction (FNHTR) is the most
common acute transfusion reaction in patients with cancer.10 FNHTR
is characterized by fever, chills, rigors, or discomfort occurring during
or within 4 hours of transfusion.1 FNHTR is typically benign and self-
limiting with cessation of blood products, but FNHTR can mimic early
signs of more serious and life-threatening transfusion reactions.11 In
the oncology population, other causes such as underlying malig-
nancy, infection, or other inflammatory processes also need to be
considered.12 FNHTR is a diagnosis of exclusion that can only be
determined after a thorough transfusion reaction analysis has been
completed.13
FNHTR is the most common type of transfusion reaction, both in
the general and oncology populations, yet the incidence of FNHTR
has reduced significantly with the use of prestorage leukocyte
reduction.10,11 Results from the 2017 National Blood Collection and
Utilization Survey showed that from 1886 participating hospitals,
nearly all whole blood/ RBC units and platelet units were leukore-
duced.6 The incidence rate for all blood product types was 120.5 in
100,000 components transfused.6
FNHTRs can be broadly categorized as immune or nonimmune.3,13
The nonimmune mechanism of action in FNHTR results from the pas-
sive transfer of proinflammatory cytokines that accumulate during
storage of the blood component.1,3,13,14 Immune-mediated FNHTRs
are caused by an antileukocyte antibody-mediated response. Recipi-
ents have preformed leukocyte antibodies that interact with donor
human leukocyte antigens (HLA), human neutrophil antigens (HNA),
or platelet antigens present in the blood product.1,3,13,14 This anti-
gen-antibody reaction results in the release of cytokines (ie, interleu-
kins, tumor necrosis factor) and leads to the development of a
FNHTR.13,14 Leukocytes are the primary driver in FNHTR, and inci-
dence of FNHTR is dramatically decreased with the use of prestorage
leukocyte reduction.11 Additionally, increased occurrence is seen in
specific populations, including those with greater number of RBC and
platelet transfusions (5 units), in females compared with males, and
in patients with history of chemotherapy, lymphoma, leukemia, other
malignancies, or prior anemia.13
Close nursing assessment prior to transfusion and ongoing obser-
vation with frequent vitals and evaluation for fevers, rigors, or dis-
comfort is important for early detection of a transfusion reaction.1,9
Mild incremental changes in temperature, less than 1°C increase, or
<38°C, can be monitored. Because acute FHNTRs occur within 4 hours
of completion of a blood product transfusion, educating patients on
monitoring for post-transfusion symptomatology is essential.
Hemolytic Transfusion Reactions
Hemolytic transfusion reactions (HTRs) are rare but potentially
life-threatening transfusion reactions that result in RBC destruction,
most commonly due to immune incompatibility between the recipi-
ent and donor.2,15 HTRs can present as subclinical, mild, or potentially
fatal and are defined as either acute or delayed. These reactions most
commonly result from RBC transfusions but can also be due to trans-
fusion of plasma products or intravenous immunoglobulin (IVIG).2,15
The type of antigens and alloantibodies (antibodies produced after
exposure to foreign RBCs) and quantity of blood product transfused
determine the location (whether intravascular or extravascular), tim-
ing, and severity of the hemolysis.1,2,14,15 As a result of significant
decline in ABO-incompatible transfusions since 1985, fatal HTRs have
become rare.2
Acute Hemolytic Transfusion Reactions
Acute hemolytic reactions (AHTRs) occur within the first 24 hours
after a transfusion. The incidence is approximately 1 in 70,000 per
blood product transfused, with an estimated 1-4 deaths reported
annually in the United States.2,15
The most common cause of AHTRs is immune-mediated intravas-
cular hemolysis due to ABO incompatibility.2 This is usually attribut-
able to clerical error at time of blood donation or transfusion but may
also occur during emergent trauma transfusion.14 Other sources of
intravascular hemolysis include clinically significant antigen mis-
matches, such as anti-D immune globulin and, less commonly,
plasma or intravenous immunoglobulin products.2,14,15 Extravascular
immune-mediated hemolysis occurs when minor red cell antigens
are phagocytized by splenic macrophages.14
Nonimmune mediated causes of AHTRs include osmotic lysis from
running concurrent hypo-osmolar solutions that are incompatible
with RBCs, thermal injury due to incorrect storage of blood, or
mechanical injury if transfused under pressure with small-bore nee-
dles or use of leukoreduction filters during processing.2,15
Other causes of hemolysis can mimic hemolytic transfusion reac-
tions, such as autoimmune hemolytic anemias, drug-induced hemo-
lytic anemias, red-cell deficits such as G6PD in either donor or
recipient, blood contaminated by bacteria, or transfusion in a patient
with sepsis.1,15
In patients with sickle cell disease, thalassemia, or malaria, fre-
quent transfusions increase the risk of AHTRs, as well as the risk for
more severe reactions. Transfusion-related hemolysis can incite
hyperhemolysis or “bystander” hemolysis of the patient’s autologous
blood.2,3 Hematopoietic stem cell transplantation (SCT) recipients are
also at increased risk of AHTRs due to their blood type potentially
changing following transplant.2
Early detection of AHTRs is crucial in allowing for prompt discon-
tinuation of the transfusion to mitigate complications.2,15 Symptom
onset is typically within the first few minutes of an infusion and can
include fevers (temperature increase of >1°C), chills/rigors, pain or
oozing at infusion site, back/flank pain, hypotension, anxiety or
impending doom, respiratory distress, epistaxis, and oliguria. Other
signs and symptoms can include hemoglobinemia, hemoglobinuria,
renal failure, evidence of disseminated intravascular coagulation
(DIC), decreased fibrinogen or haptoglobin, elevated bilirubin or lac-
tate dehydrogenase (LDH).1-3,9,14,15
Delayed Hemolytic Transfusion Reactions
Delayed hemolytic transfusion reactions (DHTRs) occur between
24 hours to 28 days post-transfusion, according to the Centers for
Disease Control and Prevention. The estimated prevalence of DHTRs
is highly variable across sources ranging from 1:800 to
1:35,000.2,15,16 This variability is primarily attributable to varying
source definitions of DHTRs.14,15 The incidence is uniformly higher in
patients with sickle cell disease than in the general population.2,14,15
DHTRs occur when a transfusion recipient has developed an RBC
antigen from a previous blood transfusion, however, the antibody
titer is undetectable on pretransfusion testing.2,15 This results in
extravascular hemolysis that is clinically silent in a majority of
patients.2,15 Blood transfusions and pregnancy are the most common
causes of previous antigen exposure.2,15 However, in rare cases,
hematopoietic transplant patients and individuals who previously
shared intravenous needles have also developed DHTRs.15
 C.A. Graham et al. / Seminars in Oncology Nursing 37 (2021) 151137
Delayed hemolytic transfusion reactions most commonly occur 3-
10 days after transfusion.14 Symptoms may include fatigue and pallor
secondary to anemia, mild jaundice due to extravascular RBC
destruction and less commonly fever, hemoglobinuria, and
hemoglobinemia.2,9,15 If there is an intravascular component, DHTRs
will mimic a similar but less severe AHTR.15 Less common signs may
include inadequate hematocrit response to transfusion, a rapid
decrease in hematocrit to pretransfusion levels, or spherocytes other-
wise not explained.2,9 Typically, DHTRs are diagnosed by the blood
bank when newly identified RBC alloantibodies are identified at time
of next type and screen.2,3,14,15
Transfusion Associated Circulatory Overload
Transfusion-associated circulatory overload (TACO) is a transfu-
sion-related complication that occurs when the cardiovascular sys-
tem fails to adapt to increased circulatory volume resulting in
pulmonary edema. TACO is the most frequent pulmonary complica-
tion caused by blood transfusions.17 Furthermore, it is responsible for
15%-44.1% of all transfusion-related fatalities.17,18
The exact pathophysiology of TACO is not well understood, in part
due to the limited number of cases and low reporting to blood
banks.19 Researchers have conceptualized the pathophysiology in a
“two-hit model,” where the first hit is related to patient-specific fac-
tors, and the second hit is due to transfusion-specific factors.17 Ulti-
mately, increased circulatory volume and left ventricular dysfunction
leads to increased hydrostatic pressures in the pulmonary capillary
system, resulting in pulmonary edema.
For the first hit, the patient has an underlying risk factor, a pre-
existing condition, or impaired ability to adapt to volume changes.
Examples include prior diuretic use, cardiomegaly, elevated blood
pressure, degree of positive fluid balance, age older than 70 year,
heart failure, and impaired kidney function.17 Other risks include
recent myocardial infarction in the past 30 days or valvular disease.20
The second hit is transfusion-specific, such as the rate at which
the blood product is transfused or deficits in fluid management.
Transfusion-specific risk factors include rapid rate of transfusion,
receiving more than two consecutive transfusions, emergent transfu-
sions, plasma transfusions, or multiple blood transfusions in a 24-
hour period.17
For clinically indicated transfusions, there are three different
approaches to reduce the risk for TACO for high-risk patients. First,
the blood bank can reduce the volume of the blood product, for
example, by dividing one unit into two separate transfusions.1 Sec-
ond, the administration rate of the blood product can be extended up
to 3-4 hours, which may reduce the potential for circulatory over-
load.1 The last intervention involves the use of pretransfusion diu-
retics for patients with one or more risk factors.19 The most common
diuretic used is furosemide, given intravenously just prior to transfu-
sion.20 This intervention has not been studied but is practiced glob-
ally based on the knowledge and experience that furosemide can
reduce pulmonary hydrostatic pressures, preventing pulmonary
edema.20
The National Healthcare Safety Network under the Center for Dis-
ease Control is one agency that has created diagnostic criteria for
TACO. To meet the clinical definition of TACO, three or more of the
following must occur within 6 hours of completion of the transfusion:
(i) acute respiratory distress, such as dyspnea, orthopnea, or cough;
(ii) elevated brain natriuretic peptide; (iii) elevated central venous
pressure; (iv) evidence of left heart failure; (v) evidence of positive
fluid balance; or (vi) radiographic evidence of pulmonary edema.
TACO initially presents with a change in vital signs, such as
increased systolic blood pressure, decreased oxygen saturation,
tachycardia, fever, or increased pulse pressures.18 The average
increase in systolic blood pressure reported in one study was 33 mm
Hg compared to pretransfusion baseline.18 The patient may
3
experience dyspnea at rest, require supplemental oxygen, or develop
severe respiratory failure requiring mechanical ventilation.17 Clinical
assessment may reveal a degree of positive fluid balance, such as
peripheral or sacral edema, distended neck veins, and rales on aus-
cultation of lung sounds. Common assessments to aid in the diagnosis
include a chest radiograph, which would show cardiomegaly or evi-
dence of pulmonary edema, and brain natriuretic peptide, which may
be elevated.17
Transfusion-Related Acute Lung Injury
Transfusion-related acute lung injury (TRALI) is a syndrome of
acute noncardiogenic edema that occurs following a
transfusion.1,14,17,21-24 TRALI is defined as new onset acute lung
injury (ALI) occurring within 6 hours following a transfusion, without
cardiogenic cause or associated risk factors for acute respiratory dis-
tress syndrome (ARDS).1,14,17,21-23 TRALI is a clinical diagnosis of
exclusion, so the absence of ALI risk factors is necessary before mak-
ing the diagnosis.1,14,17,21-23 A designation of possible TRALI is some-
times made in circumstances where another source of ALI is present,
such pneumonia, sepsis, aspiration, trauma, or acute
pancreatitis.17,21,23
TRALI is a leading cause of transfusion-associated morbidity and
mortality, although incidence rates have declined over the last
decade due to the implementation of risk-mitigation
strategies.1,14,17,21-24 In 2018 the Food and Drug Administration
reported 26% of transfusion-associated fatalities were attributable to
TRALI.25 Between 70% and 90% of patients who develop TRALI require
ventilation, and mortality rates range from 5% to 25%.14,21 The
National Blood Collection and Utilization survey reported TRALI
occurred 1 in every 64,000 transfused components and approxi-
mately 0.01%-1.12% per product; however, other estimates range
from 1 in 500 to 1 in 100,000.17,24 RBCs are frequently implicated in a
TRALI transfusion reaction.25 Increased comorbidities, as well as fre-
quent exposure to a broad-spectrum of blood products, have also
been associated with higher incidence of TRALI.23 Critically ill
patients, such as those in the intensive care unit (ICU) are at increased
risk, with survival rates reported as low as 53% in comparison to
other populations.17,23,24 Additionally, some studies have shown
increased risk for TRALI in neutropenic patients or those with hema-
tological malignancies undergoing induction chemotherapy.14
The pathophysiology of TRALI is complex and not completely
understood.1,14,17,21-24 TRALI can result from a single event; however,
similar to TACO, it is generally recognized as being comprised of a
two-hit model.1,14,17,21-24 The initial event results from an underlying
condition that initiates an inflammatory state, leading to isolated
neutrophils in the lungs and other organs1,14,17,21-24 Risk factors for
the first hit include liver surgery, chronic alcohol abuse, smoking,
shock, ventilation with elevated peak airway pressures, low interleu-
kin 10 (IL-10), high interleukin 8 (IL-8), systemic inflammation, and
hypervolemia.1,17,21 The second event occurs when the recipient neu-
trophils are activated by antibodies or biological response modifiers
present in the blood product being infused.1,14,17,21-24 Most TRALI
cases, 80%-89%, are thought to be antibody mediated through the
passive infusion of donor leukocyte antibodies, which are primarily
produced in response to pregnancy or a history of blood
transfusions.1,17,21,22,24 Upon infusion, the donor’s antibodies bind to,
and activate the recipient’s neutrophils, leading to endothelial dam-
age and ALI.1,21 The remainder of TRALI cases, approximately 20%, are
thought to be related to proinflammatory mediators, lipid products,
extracellular vesicles, and aged blood cells stored in the transfused
component.1,14,17,21-24
TRALI risk factors include any underlying condition that initiates
an inflammatory state, leading to the development of the first
hit.1,14,17,21-24 Increased risk is also associated with receiving frequent
blood products, especially those with high plasma volume, such as
4 C.A. Graham et al. / Seminars in Oncology Nursing 37 (2021) 151137

whole blood, apheresis platelet concentrates, or plasma products.23 to determine when transfusions are indicated. In nonemergent set-
Donor parity is also correlated with an increased risk due to increas- tings, it is appropriate to order one transfusion at a time and reassess
ing pregnancy-related antibodies with each pregnancy.23 the patient before ordering subsequent transfusions. Nurses are
TRALI is a clinical diagnosis of exclusion and can be difficult to dis- imperative in the early detection and treatment of transfusion reac-
tinguish from other acute transfusion reactions or causes of respira- tions. The initial action for any suspected reaction is to immediately
tory distress.1,14 Symptom onset is within 6 hours of receiving a stop the transfusion and keep the intravenous line patent with nor-
blood component transfusion.1,14,17,21-24 Individuals may present mal isotonic saline.1 The nurse should then obtain vital signs includ-
with acute dyspnea, hypoxemia, tachypnea, tachycardia, blood pres- ing pulse oximetry, auscultate heart and lung sounds, and perform a
sure instabilities, hypothermia, or rigors.1,14 Fevers are common but thorough skin assessment. Next, a clerical check should be completed
may not be in the initial presentation.14 A nonspecific finding is copi- to ensure the patient and product information match and the blood
ous, frothy, pink-tinged fluid in the endotracheal tube of patients component should be set aside in the event it needs to be returned to
who are mechanically vented.1 A chest radiograph will reveal bilat- transfusion services for further analysis.1 A provider should be
eral infiltrates; however, this finding has low specificity and may also promptly notified. Table 1 is a summary of the diverse presenting
be associated with cardiogenic etiology.1 Initial labs may reveal neu- symptoms of acute transfusion reactions.
tropenia, which can be useful in identifying TRALI.14 In distinguishing Upon notification of the provider, the nurse can anticipate orders
from TACO, B-type natriuretic peptide (BNP) levels will be normal, for further medical management including medications, as well as
and echocardiogram will be without abnormalities.23 laboratory and diagnostic testing. Patient symptoms may be man-
aged with supportive care medications including acetaminophen,
Transfusion-Transmitted Infections diphenhydramine, famotidine or other H2 blocker, corticosteroids,
albuterol, diuretics, analgesics, epinephrine, or broad-spectrum anti-
Transfusion transmitted infections (TTIs) are a long standing biotics. Supplemental oxygen may need to be provided to maintain
known adverse reaction and significant cause of morbidity and mor- SpO2 > 93%. Laboratory testing to determine the presence and type
tality from blood product administration. TTIs can be due to a virus of transfusion reaction may include serologic examination, blood cul-
or bacteria, with bacterial causes occurring more frequently.6 The tures, direct antiglobulin test (DAT), lactate dehydrogenase, bilirubin,
most common TTI is sepsis due to bacterial contamination of plate- haptoglobin, BNP, and urinalysis.1,16 Most often, this laboratory
lets.6 There is an overall lack of consensus on a formalized definition workup occurs concurrently through transfusion services while the
and case reporting for transfusion transmitted bacterial infections nurse and provider manage a patient’s acute symptoms. Diagnostic
(TTBIs). In the United States, TTBI is defined as the presence of identi-
cal bacterial organisms cultured from both the blood component bag
Table 1
and the blood product recipient.26 Elsewhere in the world, TTBIs may
Signs/Symptoms of Acute Transfusion Reactions
be considered possible, probable, or definite based on whether the
recipient, the blood product, or both are positively cultured.26 Signs/Symptoms Possible Transfusion Reaction
With the variance in definitions and reporting of suspected cases, Fever (>1°C increase) FNHTR
true estimates of incidence are difficult to determine. The risk of TTBI AHTR
is thought to be 1 in 100,000 units of platelets and 1 in 500,000 units TRALI
of RBCs.27 In the United States, TTBI and sepsis have accounted for Microbial contamination
Itching Allergic reaction
more than 10% of all transfusion-associated deaths.27
Rash
When looking at specific blood products, TTBI and sepsis are more Urticaria
frequently seen with platelets than with RBC and other blood product Wheezing
transfusions.28 This likely results from the possible proliferation of Facial edema
certain bacteria under room temperature conditions used for platelet Decreased oxygen saturation <90% TACO
TRALI
storage. Causative organisms for TTBI can be attributable to donor Dyspnea AHTR
blood, skin from either the donor or phlebotomist, or from environ- Respiratory distress Allergic reaction
mental contamination.28 It may not always be possible to identify the Cyanosis Microbial contamination
source of a TTBI. For cases of TTBI caused by contamination, gram- TACO
TRALI
negative rods are the most common source for TBCs and gram-posi-
Hypertension TACO
tive organisms for platelets.27 Tachycardia
All patients receiving blood product transfusions are at some Hypotension AHTR
degree of risk for developing TTI. Oncology patients, especially blood Allergic reaction
and marrow transplant recipients, are at an increased risk of TTBIs Microbial contamination
TRALI
due to their immunocompromised state.26 Pain at the intravenous line infusion site AHTR
Patients experiencing a TTBI may demonstrate clinical signs Abdominal/chest/flank pain Allergic reaction
including chills, rigors, fever >39°C, tachycardia > 120 beats per min- Hematuria AHTR
ute and rise or fall of their systolic blood pressure by 30 mm Hg.28 Acute onset of symptoms <6 h TACO
TRALI
These signs frequently appear during or within the first 30 minutes
Pulmonary edema with bilateral infiltrates on TACO
following a transfusion.26 Often, signs and symptoms are not clini- chest imaging TRALI
cally distinguishable from other types of transfusion reactions. It is Alternative risk factors for acute lung injury Possible TRALI
imperative that nurses remain vigilant in expediently stopping the (eg, pneumonia, sepsis, aspiration, trauma,
transfusion and beginning the diagnostic workup. acute pancreatitis)
Increased ventricular filling (BNP >250) TACO
Cardiogenic fluid overload (eg, systolic ejec- TACO
General Management of Transfusion Reactions tion fraction <45)
AHTR = acute hemolytic transfusion reaction; BNP = B-type natriuretic peptide;
Transfusion reactions are a common occurrence in the oncology FNHTR = febrile nonhemolytic transfusion reaction; TACO = transfusion-associated
setting due to the increased frequency and quantity of blood transfu- circulatory overload; TRALI = transfusion-related acute lung injury.
sions administered in this patient population. To minimize unneces- *Adapted from Dasararaju et al.
y
Adapted from Semple et al.
sary interventions, it is important to use evidence-based guidelines
 C.A. Graham et al. / Seminars in Oncology Nursing 37 (2021) 151137
Table 2
Laboratory and Diagnostic Workup of Transfusion Reactions
Laboratory Workup
Serologic examination
Direct antiglobulin test
Lactate dehydrogenase
Fractionated bilirubin
Haptoglobin
Brain natriuretic peptide
Blood cultures
Urinalysis
Diagnostic Workup
Chest radiograph
Electrocardiogram
Echocardiogram
testing might include chest radiograph, electrocardiogram, and echo-
cardiogram. A complete list of laboratory and diagnostic testing can
be found in Table 2. Finally, transfusion services should be notified of
the suspected reaction. Based on the institution, this notification may
include completion of a designated transfusion reaction evaluation
form. Further transfusion of blood products may not proceed until
approval is obtained from transfusion services, who will alert the
nurse and provider of any findings. Blood product transfusions are
often only restarted if it is determined the patient experienced a mild
allergic reaction.16 Systemic reviews and meta-analysis have not
shown the benefit of routine premedication with acetaminophen and
antihistamines, but based on the findings of the transfusion reaction
workup, certain patients may benefit from the use of premedications
such as acetaminophen, diphenhydramine, or furosemide prior to
future transfusions.29,30
A critical component of a suspected transfusion reaction is
comprehensive documentation of the event. The nursing note
should include the time of the reaction, volume of product
infused, reported symptoms, vital signs, interventions including
medications, labs, and imaging, and the patient’s response to
management. Nurses are the first link to ensuring a suspected
transfusion reaction is reported.
Implications for Nursing Practice
Oncology nurses are in a critical position to assist with prevention,
early detection, and time-sensitive treatment of a transfusion reac-
tion. A comprehensive understanding of possible transfusion reac-
tions is key for strong patient advocacy. Vigilant nursing assessment,
before and during transfusions, to trend symptoms and evaluate for
development of transfusion-related complications are critical for safe
transfusions. Individualized patient education at an appropriate
health literacy level should be provided with every transfusion
encounter. Nurses should provide written and verbal education about
the signs and symptoms of early and late transfusion reactions,
including ensuring a patient has access to after-hours care and emer-
gency contact information.14
Severe transfusion reactions are an uncommon event, but any sus-
picion of a possible reaction should be reported to the providing
blood bank. Blood banks partner with the hemovigilance sector of
the Center for Disease Control to collect data on transfusion reactions
and near-misses to promote patient safety. Nurses have the responsi-
bility to accurately document the events of a transfusion reaction.
Involving the blood bank with any possible transfusion reaction
allows for a proper laboratory evaluation. Ultimately, this coordina-
tion between nursing and laboratory medicine will improve the clini-
cal understanding of transfusion-reaction pathophysiology and
promote safer practices. Implementing systematic institutional
approaches for reporting transfusion reactions can help facilitate this
practice.
5
Funding
This research did not receive any specific grant from funding
agencies in the public, commercial, or not-for-profit sectors.
Acknowledgments
We wish to acknowledge Heather Smith, PA-C, Co-Director, Seat-
tle Cancer Care Alliance APP Fellowship Program, for her editorial
support, and Rene LeBlanc, RN, Transfusion Services Manager, Seattle
Cancer Care Alliance, for sharing her expert knowledge in the field of
transfusion medicine with us.
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