Professional Documents
Culture Documents
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
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
2.
3.
FHTR: Mechanism
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
Etiology:
1. Antibodies to donor WBCs
2. Accumulated cytokines in platelet units
o
Usually resolves with D/C of BT,
antihistamines
BT may be resumed at slower rate, close
o
monitoring
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
Acute, Non-Immunologic
Transfusion-Associated/Bacterial Sepsis
Management:
o
Broad spectrum antibiotics
Treat complications
o
Circulatory Overload
Etiology: volume overload
Air Embolism
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
screening test
o
Platelet refractoriness, delayed hemolytic
reaction, hemolytic disease of the newborn
Management:
o Identify antibody
o Transfuse compatible cells as needed
Post-transfusion Purpura
Management: self-limited, IV Ig
Immunomodulation
Etiology: incompletely understood interaction of
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