1. Transfusion Reactions
NICHOLAS TSU, M.D.

2. Objectives
Transfusion statistics and basics
Types
Diagnosis
Treatment

3. 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

4. Transfusion Risks Infectious Noninfectious Viral Bacterial
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)

5. Viral Infections

6. Bacterial Infections

7. 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

8. Bacterial Sources Donor skin flora Donor bacteremia Contamination from
Collection
Processing
Storage

9. Signs and Symptoms of Bacterial Infection
Fevers
Chills
Tacycardia
Dyspnea
Emesis
Shock
DIC
Acute renal failure

10. 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

11. 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

12. 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

13. 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

14. 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

15. 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

16. 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 RBC’s for presence of surface immunoglobulins and complement

17. 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

18. 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

19. 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

20. 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

21. 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

22. Febrile Reactions
Pt’s who receive multiple transfusions of RBC’s 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 Coomb’s test

23. 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%

24. 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

25. Signs and Symptoms Within 6 hours of transfusion Dspnea Chills Fever
Noncardiogenic pulmonary edema/bilateral pulmonary infiltrates
Hypotension/hypertension may occur

26. 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

27. 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