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 (PRBCs)

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
Viral
Bacterial
Noninfectious
Reaction to RBC Antigens
Acute Hemolytic Transfusion Reactions (AHTR)
Delayed Hemolytic Transfusion Reactions (DHTR)
Reactions to Donor Proteins
Minor Allergic Reactions
Anaphylactic Reactions
White Cell-Related Transfusion Reactions
Febrile Reactions
Transfusion-Related Acute Lung Injury (TRALI)
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 RBCs

Hemolysis of donor RBCs can lead to ARF & DIC
Mortality rate is 2%
Leading cause is clerical error
 Acute Hemolytic Transfusion Reactions

Over 300 antigens on human RBCs

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 RBCs 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

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
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
Examines recipient RBCs for presence of surface immunoglobulins
and complement
 Treatment

Maintain systemic blood pressure

Deliver volume
Pressors
Inotropes
Preserve Renal function and urine output
Administering fluids
Diuretics (mannitol or furosemide)
Sodium bicarb to alkalinize urine
Prevent DIC
No specific therapy
Prevent hypotension and support cardiac output
Decreases stasis
 Delayed Hemolytic Transfusion Reactions

Compatible RBCs 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 RBCs
Coated RBCs 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 Coombs 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 pts 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

Pts who receive multiple transfusions of RBCs will

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 Coombs 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
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
Use low tidal volume settings like in ARDS
No diuretics
Glucocorticoids have been administered but no
evidence supporting their administration