Transfusion Reactions
NICHOLAS TSU, M.D.
Objectives
 Transfusion statistics and basics
 Types
 Diagnosis
 Treatment
Transfusion Statistics
 Transfusions in 2004
 14.2 million units of packed red blood cells (PRBC’s)
 9.9 million units of platelets (84% apheresis units)
 4.1 million units of fresh-frozen plasma (FFP)
 Approximately 40% of all transfused units
administered by anesthesia personnel
Transfusion Risks
 Infectious
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Viral
Bacterial
 Noninfectious
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Reaction to RBC Antigens
Acute Hemolytic Transfusion Reactions (AHTR)
 Delayed Hemolytic Transfusion Reactions (DHTR)
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Reactions to Donor Proteins
Minor Allergic Reactions
 Anaphylactic Reactions
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White Cell-Related Transfusion Reactions
Febrile Reactions
 Transfusion-Related Acute Lung Injury (TRALI)
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Viral Infections
Bacterial Infections
Bacterial Infections
 Incidence of sepsis much greater in platelets
 Platelets stored at room temperature
 Decreased risk with apheresis platelets
 Most common organisms
 Staphyloccos aureus
 Klebsiella pneumoniae
 Serratia marcescens
 Staphyloccos epidermdidis
 Yersinia enterocolitica
Bacterial Sources
 Donor skin flora
 Donor bacteremia
 Contamination from
 Collection
 Processing
 Storage
Signs and Symptoms of Bacterial Infection
 Fevers
 Chills
 Tacycardia
 Dyspnea
 Emesis
 Shock
 DIC
 Acute renal failure
Diagnosis and Treatment
 Stop transfusion
 Obtain blood cultures
 Treat with broad spectrum antibiotics
 Notify the blood bank immediately
 Prevent other units from same donor being transfused
Acute Hemolytic Transfusion Reactions
 Most hazardous against foreign RBC’s
 Hemolysis of donor RBC’s can lead to ARF & DIC
 Mortality rate is 2%
 Leading cause is clerical error
Acute Hemolytic Transfusion Reactions
 Over 300 antigens on human RBC’s
 Most common antibodies that fix complement
 A, B, Kell, Kidd, Duffy
 Rh antibodies do not fix complement but can cause
serious hemolysis
AHTR Pathophysiology
 Antibodies and complement in recipient plasma
attack antigens on donor RBC’s causing hemolysis
 Antigen-antibody complexes activate Hageman
factor (factor XII) producing bradykinin leading to
capillary permeability and hypotension
 Complement system releases histamine and
serotonin from mast cells resulting in bronchospasm
 30-50% of patients will develop DIC
AHTR Pathophysiology
 Hemolysis releases hemoglobin (Hb)
 Hb binds to haptoglobin and albumin initially
 Will circulate unbound until excreted by kidneys
 Renal damage causes
 Hypotension 2/2 systemic hypotension and renal
vasoconstriction
 Free Hb form acid hematin damaging renal tubules
 Antigen-antibody complexes may deposit in glomeruli
Signs and Symptoms
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Fever
Chills
Nausea and vomiting
Diarrhea
Rigors
Hypotension and tachycardia (bradykinin)
Flushed and dyspneic (histamine)
Chest and back pain (cytokine release)
Headache
Feeling of impending doom
Hemoglobinuria eventually oliguria
Diagnosis
 Stop transfusion
 Recheck patient and unit labeling
 Examine centrifuged plasma sample for pinkish
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discoloration representing free Hb
Hemolysis should be assumed to be hemolytic
transfusion reaction until proven otherwise
Notify blood bank
Aseptically seal unit and return
Coombs test
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Examines recipient RBC’s for presence of surface immunoglobulins
and complement
Treatment
 Maintain systemic blood pressure
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Deliver volume
Pressors
Inotropes
 Preserve Renal function and urine output
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Administering fluids
Diuretics (mannitol or furosemide)
Sodium bicarb to alkalinize urine
 Prevent DIC
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No specific therapy
Prevent hypotension and support cardiac output
Decreases stasis
Delayed Hemolytic Transfusion Reactions
 Compatible RBC’s are rapidly eliminated within days
 Typically due to donor RBC antigen to which
recipient has been previously exposed via transfusion
or pregnancy
 Over time antibody levels fall too low to be detected
 With re-exposure anamnestic response results in
antibodies and lysis of foreign RBC’s
 Coated RBC’s are sequestered extravascularly
(spleen and reticuloendothelial system) and lysed
Diagnosis and Treatment
 Usually detected in the first or second week
 Low-grade fever
 Increased indirect bilirubin
 Unexplained reduction in Hb
 Decreased serum haptoglobin
 Confirmed by positive Coomb’s test
 Resolves as transfused cells are removed
 Monitor Hb
 Maintain hydration
 Re-transfuse if necessary
Minor Allergic Reactions
 Allergic reactions to proteins in donor plasma cause
urticarial reactions in 0.5 to 4% of all transfusions
 Most frequent in FFP or platelets
 Itching, swelling, rash
 Treat with diphenhydramine
Anaphylactic Reactions
 Seen typically in pt’s with hereditary IgA deficiency
 Previously sensitized during pregnancy or exposed to
blood with foreign IgA
 Dyspnea, bronchospasm, angioedema, hypotension
 Discontinue transfusion
 Administer epinephrine and methylprednisolone
Febrile Reactions
 Pt’s who receive multiple transfusions of RBC’s will
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develop human leukocyte antigens (HLA)
On subsequent RBC transfusions antibodies attack donor
leukocytes causing febrile reactions
Occur in up to 2% of platelet, FFP, and RBC transfusions
Increase in temperature of more than 1 degree C with 4
hours of transfusion
Defervesces within 48 hours
Occasional chills, dyspnea, anxiety, headache, myalgia
Treat with acetaminophen
Differentiate with direct Coomb’s test
Transfusion-Related Acute Lung Injury
 TRALI is a noncardiogenic form of pulmonary
edema occurring after blood product administration
 Associated with all plasma-containing components
 Estimated at 1:1271 to 1:5000 transfusions
 Mortality of at least 5%
Transfusion-Related Acute Lung Injury
 Occurs when mediators present in the plasma of donor
blood activates leukocytes in the host
 Activated leukocytes are sequestered by the lungs
 Leukocyte mediators are released and cause increased
capillary permeability and endothelial damage
 “two hit theory”
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Trauma, surgery, sepsis may first “prime” native granulocytes
causing surface adhesion sites resulting lung sequestration
Biologically active mediators that are breakdown products from
cellular elements in blood products activate sequestered leukocytes
Signs and Symptoms
 Within 6 hours of transfusion
 Dspnea
 Chills
 Fever
 Noncardiogenic pulmonary edema/bilateral pulmonary
infiltrates
 Hypotension/hypertension may occur
Diagnostic Criteria
 Acute onset of hypoxemia (within 6 hours of
conclusion of transfusion)
 Bilateral CXR infiltrates consistent with ALI
 Absence of evidence of left atrial hypertension
 Absence of temporally related causes of ALI
Treatment
 Largely supportive
 Transfusion should be stopped if recognized in time
 Supplemental oxygen and ventilation support
provided if necessary
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Use low tidal volume settings like in ARDS
 No diuretics
 Glucocorticoids have been administered but no
evidence supporting their administration