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Transfusion Reactions
Literature review
D.mohamed mostafa
The Blundell Gravitator
The fact that life may be saved by transfusion of
blood into the veins will be beneficial a thousand
years hence as it is on this day
CLASSIFICATION
Transfusion reaction
acute delayed
Immunologic Nonimmunologic Immunologic Nonimmunologic
Acute haemolytic immune reaction
• Incompatible transfused red cells react with the patient's own anti-A
or anti-B antibodies or other alloantibodies .
• Infusion of ABO incompatible blood almost always arises from
errors in labelling sample tubes/request forms or from inadequate
checks at the time of transfusion.
• Risk: 1:2,500 – 1:11,000 units transfused.
• Mortality: 1 in 1.8 million units transfused.
Signs and symptoms in conscious and
anesthetised patients...
Abrupt onset Nausea, Vomiting
Anxiety Shock
Facial flushing Oliguria
Fever, chills Hemoglobinuria
Pain in back or flanks Bleeding
Dyspnoea
•Hypotension
•Hemoglobinuria (This may be masked in patients
undergoing GU surgeries due to hematuria)
•Undue bleeding from surgical site
• Management of AHTR
• 1. Stop transfusion.
• 2. Rapid assessment of pt & requirements for basic &
advanced support.
• 3. Notify transfusion service, collect transfused units & tubing
and return to BB.
• 4. Reconfirm identity of blood units & pt.
• 5. Collect appropriate patient blood specimens
• 6. Supportive approaches
Delayed haemolytic immune reaction
• 1:1250 to 1:6000 transfusions.
• Either primary alloimmunization or anamnestic reaction...
• Typically cause jaundice at day 5 onwards.
• May cause hemoglobinuria
• Renal failure very rare.
• Probably under-reported.
Febrile non-haemolytic reaction
• Usually start within 30 min...
• Pt feels cold ,shaking and rigors....
• Temperature rises....
• Due to cytokines/proteins in donor transfused unit or
WBCs antibody in recipient reacts with WBCs antigen in
product .
• Stop transfusion to clinically assess:
1. – Consider acute hemolytic, and bacterial sepsis as part of differential...
2. – Report TR to lab, send bag and samples to lab for work up...
3. – Treat symptoms with antipyretic (acetaminophen)....
Allergic reactions
• Frequent 1 in 250 Usually mild, self-limited Urticaria
• Foreign (protein) allergen in donor plasma.
• They react with IgE attached to mast cells and basophils.
• May need to use washed products If Donor is atopic.
Anaphylaxis
• It is a Type I hypersensitivity , acute severe allergic
reaction.
• Incidence :1:20,000 to 1:47,000 components transfused.
• Pathophysiology: unknown??!!
Manegement
1.Call for help and inform the surgical team
2.Stop administration of the drug(s) likely to have
caused the reaction. It is recommended to stop all
the drugs that are possible to stop, as at this time
the causative agent can not be determined.
3.(ABC) , Maintain airway: give 100% oxygen.
4.Lie patient flat with feet raised
Epinephrine
Is the drug of choice when resuscitating
patients during anaphylactic shock
• Epinephrine acts by two mechanisms:
• It reverses vasodilatation by its α-agonist
effects
• It blocks further degranulation of mast cells or
basophiles through its β-agonist effects.
• It may also improve cerebral perfusion
independent of its effect on blood pressure by
β2-mediated vasodilatation, and it is very
effective in the treatment of bronchospasm.
5.Give adrenaline (epinephrine):
• 50–100 µg (0.5–1 mL of a 1:10,000 solution found in
pre-filled syringes )or 0.01 mg/kg in children.
• Should be administered subcutaneously or
intramuscular if the patient is merely hypotensive, and
may be repeated as needed.
• Higher doses and the intravenous route should be
used if the reaction is severe, or if cardiac arrest
supervenes.
• Start rapid i.v volume expansion with
crystalloid or colloid.
• Increased vascular permeability can transfer
50% of intravascular fluid into the extravascular
space within 10 minutes.
• The amount of fluid administered should be
based on hemodynamic parameter
• Intravenous steroids
• (e.g., methylprednisolone 1–2 mg/kg
intravenously or hydro cortisone 100-500mg
(I.V); repeat q4–6 hourly as needed).
• Steroids may have no effect for 4–6 hours, but
may prevent persistent or biphasic
anaphylaxis.
• Anti-H1 medications (e.g., diphenhydramine
25– 100 mg IV).
• Anti-H2 medications (e.g., ranitidine 1 mg/kg
IV).
• Glucagon (1–5 mg IV)
in severe reactions. Glucagon directly activates adenyl
cyclase and bypasses the β-adrenergic receptor. It may
reverse refractory hypotension and bronchospasm.
Glucagon or atropine should be used in β-blocked
patients to increase an inappropriately slow heart rate.
TRALI
• New acute lung injury that develops with a
clear temporal relations to transfusions
• Leading cause of transfusion-related death
reported to FDA (30% of transfusion-related
fatalities)
• Antineutrophil antigen antibodies or anti-
HLA antibodies are primarily responsible
• Most commonly, donors are multiparous
female.
• Chills, fever, dyspnea, non-productive cough,
hypotension, 4-6 hours after transfusion
• Causes severe respiratory distress and hypoxemia
• CXR shows bilateral nodular infiltrates with no cardiac
enlargement
• Pulmonary wedge pressure is normal
• Symptoms clear in 24 hr
• CXR clears in 4 days
• Estimated frequency 1: 5,000 transfusions
•
• Donor antibodies activate Pt’s WBC’s which cause
damage to blood vessels in lung tissue.
• Then fluids and proteins leak into alveolar, space/
interstitiem.
• Mechanism similar to ARDS
• Management
• Steroids
• Aggressive ventilatory support
• Hemodynamic support
Risk of fatality from TRALI
TRALI
• Patients p/w
• Dyspnea
• Hypoxia
• Hypotension
• Fever
• Tachycardia
• Cyanosis
• Pulmonary Edema
• Chest Imaging shows
bilateral fluffy infiltrates
• No evidence of volume
overload
• Leaky capillary
endothelium results in
fluid in the lung
TRALI
Before Transfusion After Transfusion
TRALI Criteria
Management of TRALI
• Does not improve with diuretics
• Supportive Care
• May need Ventilatory support
• Alert the Blood Bank – FDA reportable
• Usually recover quickly
• Steroids has not been shown to help
• Incidence has decreased with the use of only
male donor plasma
Transfusion-Associated Circulatory
Overload (TACO)
• Occur up to 1% of all transfusions
• Due to circulatory overload
• Symptoms: Dyspnea, cough, tachycardia,
hypertension.
• Those patients @ highest risk:
• Cardiopulmonary compromise
• Renal failure
• Infants
• Treatment: Diuretics and slow down rate
Taco
• Management:
• with feet in dependent position
• Diuretics
• Oxygen
• Morphine (if necessary
• Place Pt in upright position, if possible,
• Place Pt in upright position, if possible,
• with feet in dependent position
• Prevention
• size and clinical status
• TACO
• Adjust transfusion flow rate based on Pt
• Adjust transfusion flow rate based on Pt
• size and clinical status
• Consider dividing unit(s) into smaller
• Consider dividing unit(s) into smaller
• aliquot(s) to better space apart blood
• aliquot(s) to better space apart blood
• component(s) pace of transfusion
• component(s) pace of transfusion
Post-transfusion Purpura
• Etiology: Antibodies to platelet antigens (HP1a ) causes abrupt onset
of severe thrombocytopenia (platelet count <10,000/µl) 5-10 days
following transfusion. Usually affects multiparous women .
• Signs: Purpura, bleeding, fall in platelet count
. treatment: IVIG, plasmapheresis or corticosteroids; platelet
transfusions usually NOT recommended
Transfus Med 2006;16:69
Graft vs Host Disease (GVHD)
• Etiology: Donor CD8+ T-Lymphocytes attack recipient (host) tissues.
Very rare in blood stored 4+ days due to WBC inactivation (Br J Haematol 2000;111:146)
• Groups at risk:
– Immunocompromised patients (Cancer, fetus, neonatal, bone
marrow transplant).
• Signs: Fever, dermatitis, or erythroderma, hepatitis, diarrhea,
pancytopenia, etc.
• Prevention: Irradiation of blood products.
Osaka City Med J 1999;45:37
• TA-GVHD
• TA-GVHD
• Often missed or misdiagnosed
• Often missed or misdiagnosed
• Occurs in patients with other pathology
• Occurs in patients with other pathology
• Preventable by irradiation of cellular
• Preventable by irradiation of cellular
• blood products: prevents the
• blood products: prevents the
• transfused lymphocytes (Graft) from
• transfused lymphocytes (Graft) from
• attacking recipient (Host)
• attacking recipient (Host)
Infectious Complication of Blood
Transfusion
Bacterial Contamination
• Etiology: At time of collection: either
from the donor or the venipuncture
site.
– During component preparation, etc.
• Usually involves endotoxins
– Staph, Pseudomonas, E.coli, Yersinia
Bacterial Contamination
• Components: Most often from platelet
components (room temp). Red cell units will
look dark.
• Symptoms: Rapid onset
– Fever, hypotension, shaking chills, muscle
pain
– Vomiting, abdominal cramps, bloody diarrhea,
hemoglobinuria, shock, renal failure, & DIC.
Transfusion must be stopped immediately
• Gram stain & blood cultures should be done on
the unit, patient and all infusion sets .
• Broad-spectrum antibiotics should be given
immediately intravenously
• Prevention: Maintain standards of donor
selection, blood collection and proper
maintenance of collected blood components.
Bacterial Contamination
Bacterial Contamination
• Approximately 57% of all transfusion
transmitted infections
• 11% of transfusion-related deaths
• Risk:
• PRBC: 1 in 38,500 units
• Random Donor Platelets: 1 in 3,300 units
• Aphaeresis platelets: 1 in 2,000 units
• All platelets: risk of bacterial sepsis is 1 in 50,200
Risk of Viral Transmission
• Hepatitis B: 1 in 350,000 transfusions
• Hepatitis C: 1 in 1.8 million transfusions
• HIV: 1 in 2.3 million transfusions
• HTLV: 1 in 2 million transfusions
• Cytomegalovirus
• Epstein-Barr Virus
• West Nile Virus
Other Infectious Transmissions?
• Treponema pallidum
• Risk: 6 in 1 million
• Plasmodium spp.
• Trypanosoma
• Toxoplasmosis
• Rickettsia rickettsii
• Erhlichiosis
• Babesiosis
• Leishmaniasis
• Bartonella spp.
• Borrelia spp.
• Brucella spp
• Creutzfeldt-Jakob Disease
Bacterial Transmission
• PRBC: typically Gram-negative bacilli
• Yersinia enterocolitica
• Pseudomonas fluorescens
• Risk increases with PRBC stored > 21 days
• Platelets – mostly Gram-positive bacteria
• Staphylococcus and Streptococcus
• At higher risk since they are stored at close to
room temp (20o-24oC)
• Risk increases with platelets stored > 3 days

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Transfusion reactions tutorial 2010

  • 3. The fact that life may be saved by transfusion of blood into the veins will be beneficial a thousand years hence as it is on this day
  • 4.
  • 5.
  • 6. CLASSIFICATION Transfusion reaction acute delayed Immunologic Nonimmunologic Immunologic Nonimmunologic
  • 7. Acute haemolytic immune reaction • Incompatible transfused red cells react with the patient's own anti-A or anti-B antibodies or other alloantibodies . • Infusion of ABO incompatible blood almost always arises from errors in labelling sample tubes/request forms or from inadequate checks at the time of transfusion. • Risk: 1:2,500 – 1:11,000 units transfused. • Mortality: 1 in 1.8 million units transfused.
  • 8. Signs and symptoms in conscious and anesthetised patients... Abrupt onset Nausea, Vomiting Anxiety Shock Facial flushing Oliguria Fever, chills Hemoglobinuria Pain in back or flanks Bleeding Dyspnoea •Hypotension •Hemoglobinuria (This may be masked in patients undergoing GU surgeries due to hematuria) •Undue bleeding from surgical site
  • 9. • Management of AHTR • 1. Stop transfusion. • 2. Rapid assessment of pt & requirements for basic & advanced support. • 3. Notify transfusion service, collect transfused units & tubing and return to BB. • 4. Reconfirm identity of blood units & pt. • 5. Collect appropriate patient blood specimens • 6. Supportive approaches
  • 10. Delayed haemolytic immune reaction • 1:1250 to 1:6000 transfusions. • Either primary alloimmunization or anamnestic reaction... • Typically cause jaundice at day 5 onwards. • May cause hemoglobinuria • Renal failure very rare. • Probably under-reported.
  • 11. Febrile non-haemolytic reaction • Usually start within 30 min... • Pt feels cold ,shaking and rigors.... • Temperature rises.... • Due to cytokines/proteins in donor transfused unit or WBCs antibody in recipient reacts with WBCs antigen in product .
  • 12. • Stop transfusion to clinically assess: 1. – Consider acute hemolytic, and bacterial sepsis as part of differential... 2. – Report TR to lab, send bag and samples to lab for work up... 3. – Treat symptoms with antipyretic (acetaminophen)....
  • 13. Allergic reactions • Frequent 1 in 250 Usually mild, self-limited Urticaria • Foreign (protein) allergen in donor plasma. • They react with IgE attached to mast cells and basophils. • May need to use washed products If Donor is atopic.
  • 14. Anaphylaxis • It is a Type I hypersensitivity , acute severe allergic reaction. • Incidence :1:20,000 to 1:47,000 components transfused. • Pathophysiology: unknown??!!
  • 15.
  • 16.
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  • 18.
  • 19. Manegement 1.Call for help and inform the surgical team 2.Stop administration of the drug(s) likely to have caused the reaction. It is recommended to stop all the drugs that are possible to stop, as at this time the causative agent can not be determined. 3.(ABC) , Maintain airway: give 100% oxygen. 4.Lie patient flat with feet raised
  • 20. Epinephrine Is the drug of choice when resuscitating patients during anaphylactic shock
  • 21. • Epinephrine acts by two mechanisms: • It reverses vasodilatation by its α-agonist effects • It blocks further degranulation of mast cells or basophiles through its β-agonist effects. • It may also improve cerebral perfusion independent of its effect on blood pressure by β2-mediated vasodilatation, and it is very effective in the treatment of bronchospasm.
  • 22. 5.Give adrenaline (epinephrine): • 50–100 µg (0.5–1 mL of a 1:10,000 solution found in pre-filled syringes )or 0.01 mg/kg in children. • Should be administered subcutaneously or intramuscular if the patient is merely hypotensive, and may be repeated as needed. • Higher doses and the intravenous route should be used if the reaction is severe, or if cardiac arrest supervenes.
  • 23. • Start rapid i.v volume expansion with crystalloid or colloid. • Increased vascular permeability can transfer 50% of intravascular fluid into the extravascular space within 10 minutes. • The amount of fluid administered should be based on hemodynamic parameter
  • 24. • Intravenous steroids • (e.g., methylprednisolone 1–2 mg/kg intravenously or hydro cortisone 100-500mg (I.V); repeat q4–6 hourly as needed). • Steroids may have no effect for 4–6 hours, but may prevent persistent or biphasic anaphylaxis.
  • 25. • Anti-H1 medications (e.g., diphenhydramine 25– 100 mg IV). • Anti-H2 medications (e.g., ranitidine 1 mg/kg IV). • Glucagon (1–5 mg IV) in severe reactions. Glucagon directly activates adenyl cyclase and bypasses the β-adrenergic receptor. It may reverse refractory hypotension and bronchospasm. Glucagon or atropine should be used in β-blocked patients to increase an inappropriately slow heart rate.
  • 26. TRALI • New acute lung injury that develops with a clear temporal relations to transfusions • Leading cause of transfusion-related death reported to FDA (30% of transfusion-related fatalities) • Antineutrophil antigen antibodies or anti- HLA antibodies are primarily responsible • Most commonly, donors are multiparous female.
  • 27. • Chills, fever, dyspnea, non-productive cough, hypotension, 4-6 hours after transfusion • Causes severe respiratory distress and hypoxemia • CXR shows bilateral nodular infiltrates with no cardiac enlargement • Pulmonary wedge pressure is normal
  • 28. • Symptoms clear in 24 hr • CXR clears in 4 days • Estimated frequency 1: 5,000 transfusions •
  • 29. • Donor antibodies activate Pt’s WBC’s which cause damage to blood vessels in lung tissue. • Then fluids and proteins leak into alveolar, space/ interstitiem. • Mechanism similar to ARDS
  • 30. • Management • Steroids • Aggressive ventilatory support • Hemodynamic support
  • 31. Risk of fatality from TRALI
  • 32. TRALI • Patients p/w • Dyspnea • Hypoxia • Hypotension • Fever • Tachycardia • Cyanosis • Pulmonary Edema • Chest Imaging shows bilateral fluffy infiltrates • No evidence of volume overload • Leaky capillary endothelium results in fluid in the lung
  • 35. Management of TRALI • Does not improve with diuretics • Supportive Care • May need Ventilatory support • Alert the Blood Bank – FDA reportable • Usually recover quickly • Steroids has not been shown to help • Incidence has decreased with the use of only male donor plasma
  • 36. Transfusion-Associated Circulatory Overload (TACO) • Occur up to 1% of all transfusions • Due to circulatory overload • Symptoms: Dyspnea, cough, tachycardia, hypertension. • Those patients @ highest risk: • Cardiopulmonary compromise • Renal failure • Infants • Treatment: Diuretics and slow down rate
  • 37. Taco • Management: • with feet in dependent position • Diuretics • Oxygen • Morphine (if necessary • Place Pt in upright position, if possible, • Place Pt in upright position, if possible, • with feet in dependent position
  • 38. • Prevention • size and clinical status • TACO • Adjust transfusion flow rate based on Pt • Adjust transfusion flow rate based on Pt • size and clinical status • Consider dividing unit(s) into smaller • Consider dividing unit(s) into smaller • aliquot(s) to better space apart blood • aliquot(s) to better space apart blood • component(s) pace of transfusion • component(s) pace of transfusion
  • 39. Post-transfusion Purpura • Etiology: Antibodies to platelet antigens (HP1a ) causes abrupt onset of severe thrombocytopenia (platelet count <10,000/µl) 5-10 days following transfusion. Usually affects multiparous women . • Signs: Purpura, bleeding, fall in platelet count . treatment: IVIG, plasmapheresis or corticosteroids; platelet transfusions usually NOT recommended Transfus Med 2006;16:69
  • 40. Graft vs Host Disease (GVHD) • Etiology: Donor CD8+ T-Lymphocytes attack recipient (host) tissues. Very rare in blood stored 4+ days due to WBC inactivation (Br J Haematol 2000;111:146) • Groups at risk: – Immunocompromised patients (Cancer, fetus, neonatal, bone marrow transplant). • Signs: Fever, dermatitis, or erythroderma, hepatitis, diarrhea, pancytopenia, etc. • Prevention: Irradiation of blood products. Osaka City Med J 1999;45:37
  • 41. • TA-GVHD • TA-GVHD • Often missed or misdiagnosed • Often missed or misdiagnosed • Occurs in patients with other pathology • Occurs in patients with other pathology • Preventable by irradiation of cellular • Preventable by irradiation of cellular • blood products: prevents the • blood products: prevents the • transfused lymphocytes (Graft) from • transfused lymphocytes (Graft) from • attacking recipient (Host) • attacking recipient (Host)
  • 42. Infectious Complication of Blood Transfusion Bacterial Contamination • Etiology: At time of collection: either from the donor or the venipuncture site. – During component preparation, etc. • Usually involves endotoxins – Staph, Pseudomonas, E.coli, Yersinia
  • 43. Bacterial Contamination • Components: Most often from platelet components (room temp). Red cell units will look dark. • Symptoms: Rapid onset – Fever, hypotension, shaking chills, muscle pain – Vomiting, abdominal cramps, bloody diarrhea, hemoglobinuria, shock, renal failure, & DIC.
  • 44. Transfusion must be stopped immediately • Gram stain & blood cultures should be done on the unit, patient and all infusion sets . • Broad-spectrum antibiotics should be given immediately intravenously • Prevention: Maintain standards of donor selection, blood collection and proper maintenance of collected blood components. Bacterial Contamination
  • 45. Bacterial Contamination • Approximately 57% of all transfusion transmitted infections • 11% of transfusion-related deaths • Risk: • PRBC: 1 in 38,500 units • Random Donor Platelets: 1 in 3,300 units • Aphaeresis platelets: 1 in 2,000 units • All platelets: risk of bacterial sepsis is 1 in 50,200
  • 46. Risk of Viral Transmission • Hepatitis B: 1 in 350,000 transfusions • Hepatitis C: 1 in 1.8 million transfusions • HIV: 1 in 2.3 million transfusions • HTLV: 1 in 2 million transfusions • Cytomegalovirus • Epstein-Barr Virus • West Nile Virus
  • 47. Other Infectious Transmissions? • Treponema pallidum • Risk: 6 in 1 million • Plasmodium spp. • Trypanosoma • Toxoplasmosis • Rickettsia rickettsii • Erhlichiosis • Babesiosis • Leishmaniasis • Bartonella spp. • Borrelia spp. • Brucella spp • Creutzfeldt-Jakob Disease
  • 48. Bacterial Transmission • PRBC: typically Gram-negative bacilli • Yersinia enterocolitica • Pseudomonas fluorescens • Risk increases with PRBC stored > 21 days • Platelets – mostly Gram-positive bacteria • Staphylococcus and Streptococcus • At higher risk since they are stored at close to room temp (20o-24oC) • Risk increases with platelets stored > 3 days