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24 Blood Transfusion Reactions

Blood Transfusion Reactions

Any adverse response to blood component


transfusion

Is considered with any unexpected or untoward sign


or symptom occurring during or shortly after
transfusion of blood or one of its components
Classifications of BTR

Immediate/Acute vs. Delayed

Immunologic vs. Non-Immunologic

Non-infectious vs. Infectious


Acute (<24 hours) Immunologic Transfusion Reactions
1. Febrile, hemolytic
2. Febrile/chill, non-hemolytic
3. Urticarial/mild allergic
4. Anaphylactic
5. Transfusion-related acute lung injury

Immunologic

Non-immunologic

Acute/Severe
Acute hemolytic transfusion reaction
Sickle cell hemolytic transfusion
syndrome
Anaphylaxis
Transfusion-related acute lung injury
Bacterial sepsis
Air embolism
Circulatory overload

Clinical Manifestations of BTR

Fever with or without chills


o Fever defined as a rise of at least 1C during
transfusion of blood or blood components,
or within 1-2 hours thereafter

Shaking chills with or without fever

Pain at infusion site or in the chest, abdomen, or


flanks

Blood pressure changes, usually acute, either


hypertension or hypotension

Respiratory distress dyspnea, wheezing, tachypnea


or hypoxemia

Skin changes urticarial, pruritus, flushing, localized


edema

Nausea, with or without vomiting

Darkened urine or jaundice

Bleeding or other manifestations of a consumptive


coagulopathy
Acute (<24 hours) Immunologic Transfusion Reactions
Febrile, Hemolytic Transfusion Reaction (HTR)

Etiology: red cell incompatibility

Presentation: fever, chills, hemoglobinuria,


hypotension, renal failure, DIC, back pain, pain along
infusion vein, anxiety

Management:
o Stop transfusion ASAP
o Institute measures to correct shock,
maintain renal circulation, and correct
bleeding diathesis

Acute, Non-Immunologic
1. Bacterial sepsis
2. Circulatory overload
3. Air embolism
4. Hypotension associated with ACE inhibitors
5. Non-immune hemolysis
6. Adverse sequelae of massive transfusion
Delayed, Immunologic
1. Alloimmunization, RBC antigens
2. Alloimmunization, HLA antigens
3. Hemolytic
4. Graft vs. Host disease
5. Post-transfusion Purpura
6. Immunomodulation
Delayed, Non-Immunologic
1. Iron overload
Delayed/Potentially Severe
Delayed hemolytic transfusion reaction
(RBC antigen alloimmunization)
Human leukocyte antigen alloimmunization
Transfusion-associate graft-versus-host disease
Viral transmission
Parasitic infection
Hemosiderosis
1.

Other
Mild allergic/urticarial
Post-transfusion
purpura
Febrile non-hemolytic
transfusion reaction
ACE inhibitor-related
hypotension

Evidence of hemolysis hemoglobinemia


and/or hemoglobinuria
Blood group incompatibility
Positive DAT

2.
3.
FHTR: Mechanism

Transfusion of Incompatible Blood


Ag-Ab interaction

Complement
activation

Cytokine
production

Coagulation
activation

Promotion of
inflammatory
events
Enhanced
phagocytosis
Cell-membrane
modification
causing lysis

Fever
Hypotension

DIC

Extravascular and
intravascular
hemolysis

Laboratory diagnosis

rainwater@mymelody.com || 1st semester, AY 2011-2012

Febrile, Non-Hemolytic Transfusion Reaction (FNHTR)

Etiology:
1. Antibodies to donor WBCs
2. Accumulated cytokines in platelet units

Presentation: temperature rise >1C associated with


transfusion without any other explanation;
sometimes, no fever, only chills or rigors

Evaluation: rule out FHTR

Management: antipyretic premeds


(may not always work)
o
Leucocyte-reduced component
o
Removal of plasma
Urticarial/Mild Allergic Transfusion Reactions

Etiology: release of histamines and other


anaphylatoxins from ab reactions to donor plasma
proteins

Presentation: urticaria, pruritus, flushing, localized


erythema near IV site
Evaluation and management:

o
Usually resolves with D/C of BT,
antihistamines
BT may be resumed at slower rate, close
o
monitoring

Prevention: premedication with antihistamines


Anaphylactic Transfusion Reactions
Etiology: Ab interaction to donor plasma

(IgE-mediated response to transfused protein)


Presentation: sudden onset of flushing, chills,

vomiting, diarrhea, hypotension, urticarial,


bronchospasm (respiratory distress, wheezing), local
edema, anxiety, no fever
Evaluation: rule out HTR

Management: D/C BT
o
Standard measures for anaphylaxis
epinephrine, corticosteroids, circulatory
support
Transfusion-Related Acute Lung Injury (TRALI)

Etiology:
1. Reaction of antineutrophil Abs and/or antiHLA Class I and II Abs to the corresponding
antigens between donors and recipients,
occurring in the pulmonary vasculature and
resulting in endothelial damage.
Transfused donor antibodies are
responsible. Multiparous donors and
previously-transfused donors are often
implicated (likely allouimmunized).
2. 2-Hit Theory interaction between
primed pulmonary leukocytes in patients
with underlying illness
(pro-inflammatory states) and biologically
active response modifiers introduced by
transfusion.

Presentation:
Evidence of acute lung injury (ALI): Acute
o
onset, hypoxemia (O2 satn <90% of room
air), bilateral infiltrates on CXR in the
absence of lung failure
o
TRALI: new ALI occurring during transfusion
or within 6 hours of completion; no other
temporally associated ALI risk factors

Reaction typically includes fever, chills and


hypotension within 1-2 hours of transfusion
Hypoxemia may require intubation
o
Symptoms subside rapidly, CXR becomes
o
normal/returns to baseline within 96 hours,
clinical recovery in 48-96 hours
Evaluation: rule out HTR; CXR
Management: D/C BT; supportive care
Prevention: defer implicated donors
o

Acute, Non-Immunologic
Transfusion-Associated/Bacterial Sepsis

Etiology: bacterial contamination


Subclinical/unrecognized bacteremia in the
o
donor, skin contaminants at phlebotomy
sites
RBC contaminants: Yersinia
o
Pseudomonas
o
Platelets most susceptible to bacterial
growth
Common infecting agents:
Staphylococcus
Streptococci
Propionebacterium
Presentation: fever, chills, hypotension, nausea,

vomiting, diarrhea, hemolysis, rapid progression to


circulatory compromise, renal failure, shock, DIC
Evaluation: rule out HTR; culture of component,

patient culture; Gram stain

Management:
o
Broad spectrum antibiotics
Treat complications
o
Circulatory Overload
Etiology: volume overload

Patients at risk: children, elderlies with cardiac, renal,


pulmonary compromise
Patients in states of plasma volume expansion
(normovolemic chronic anemia, thalassemia, etc.)

Presentation: cough, dyspnea, cyanosis, orthopnea,


chest discomfort, rales, headaches, distention of
jugular veins, restlessness, tachycardia
Evaluation: CXR

Management: D/C BT; supportive care (O2, diuresis,


phlebotomy 250 increments)
Prevention: transfuse in aliquots

Air Embolism

Etiology: air infusion via line (air tends to lodge in the


RV and prevents air from entering PA)
Presentation: sudden shortness of breath, acute

cyanosis, pain, cough, arrhythmia

Evaluation: X-ray for intravascular air

Management: place patient of left side with legs


elevated above chest and head

rainwater@mymelody.com || 1st semester, AY 2011-2012

Hypotension associated with ACE inhibitors

Etiology: transient hypotension caused by activation


of bradykinin. Associated with use of bedside
reduction filters and apheresis procedures ACE
inhibitors block normal metabolism of bradykinin
Presentation: flushing, hypotension

Evaluation: rule out anaphylaxis, AHTR, TRALI,


bacterial contamination

Management:
Withdraw ACE
o
o
Avoid albumin volume replacement in
plasmapheresis
o
Avoid use of bedside leukocyte filters
Non-immune-mediated hemolysis
Etiology: physical/chemical destruction of blood

(heating, freezing, drugs, wrong priming solution,


small bore needles, pressure pumps)
Presentation: intravascular/extravascular hemolysis

Evaluation: R/O HTR

Management: identify and eliminate cause


Complications of massive transfusion
(hypocalcemia, hypothermia)

Definition: administration of blood components over


a 240-hour period in amounts that equal or exceed
the total blood volume of the patient
Adverse sequelae:

1. Citrate toxicity hypocalcemia


2. Hypothermia cardiac arrhythmia
3. Hypo/hyperkalemia
4. Dilutional coagulopathy microvascular
bleeding
5. DIC
Delayed, Immunologic
Alloimmunization, RBC antigens, HLA Antigens

Etiology: immune response to foreign antigens on


RBCs, or WBCs and platelets (HLA)
Presentation: positive blood group antibody

screening test
o
Platelet refractoriness, delayed hemolytic
reaction, hemolytic disease of the newborn

Evaluation: antibody screen, DAT


Management:

Avoid unnecessary transfusions


o
o
Use leukocyte-reduced blood products
Delayed Hemolytic Transfusion Reaction

Etiology: repeat stimulation and accelerated


(anamnestic) appearance of the antibody in a
previously alloimmunized patient upon reexposure to
the offending antigen

Presentation: fever, decreasing Hgb, jaundice, DAT


positive

Evaluation: antibody screen, DAT, tests for hemolysis

Management:
o Identify antibody
o Transfuse compatible cells as needed

Transfusion-Associated Graft-versus-Host Disease (TAGVHD)

Etiology: lymphocytes from an immune competent


donor engraft recognize the patients antigens as
foreign and mount an attack on host tissues

Presentation: rash, diarrhea, hepatitis, mucositis, and


pancytopenia; mortality approaches 90%

Evaluation: skin biopsy, HLA typing

Management: supportive; no specific measures have


been proven effective
Prevention: gamma irradiation of blood components

Post-transfusion Purpura

Etiology: recipient platelet antibodies (apparent


alloantibody) destroy autologous platelets

Presentation: abrupt decline in platelet count within


days to 2-3 weeks post-BT, usually self-limited,
resolves within 2-3 weeks without treatment

Evaluation: platelet Ab screen and identification

Management: self-limited, IV Ig
Immunomodulation
Etiology: incompletely understood interaction of

donor WBC or plasma factors with recipient immune


system

Presentation: increased renal graft survival, infection


rate, post-resection tumor recurrence rate
(controversial)
Prevention:

Avoid unnecessary transfusions


o
Autologous transfusion
o
o
Leukocyte-reduced red cells and platelets
Delayed, Non-Immunologic
Iron overload: Hemosiderosis

Etiology: multiple transfusions, typically after 100 RBC


units

Presentation: diabetes, cirrhosis, cardiomyopathy

Evaluation: serum ferritin, liver enzymes, endocrine


function tests

Management: iron chelation desferrioxamine,


deferiprone
Transfusion-Transmitted Infections
Estimated Risk of Transfusion Transmission of Viral
Diseases in the USA with Current Testing
HIV 1 and 2
Hepatitis C
Hepatitis B
HTLV I and II
West Nile Virus

1:2,000,000 3,000,000
1:2,000,000 3,000,000
1:200,000 500,000
1:2,00,000
Seasonal, regional variability

rainwater@mymelody.com || 1st semester, AY 2011-2012