Untitled - D Ank Unlimited

TRALI (transfusion-related acute lung injury) 712 TRALI (transfusion-related acute lung injury)
Degranulation
C3 convertase
Anaphylatoxins
PMN cell
Classic
pathway
blood gas values to normal within 96 hours; 17% retain
pulmonary infiltrates for a week following the transfusion
reactions. TRALI reactions occur in 1 in 5000 units of
blood transfused. Leukoagglutinating antibodies and some
lymphocytotoxins have been implicated. The offending
antibody is passively transfused in donor plasma rather
than donor leukocyte reaction with recipient antibody.
Both donor granulocyte antibodies and donor lymphocytes
antibodies have been implicated in TRALI reactions.
Sixty-five percent of cases studied revealed the presence
of human leukocyte antigen (HLA)-specific antibodies,
but HLA antibodies may be present in donor plasma and
not cause TRALI reactions. Donor plasma implicated in
TRALI reactions is often from multiparous females and
individuals who received multiple blood transfusions. It
is difficult to explain the pathophysiology of a mechanism
whereby such a small amount of antibody can induce a
C1
C4b2a
C3a
Proteolytic
enzymes
Toxic oxygen
free radicals
Acid lipids
C3
C5a
*Chemotaxis
*Adhesion
*Activation
C5
Adhesion
of PMN cell
to the pulmonary
vascular bed
Lung capillary
C3b
(Opsonin)
C6
C7
C8
C9
C5b
C5b_9
MAC
Increase in
CAP permeability
Extravasation
of plasma fluid
Extravasation
of plasma proteins
Molecular and cellular events that lead to production of transfusion-related acute lung injury (TRALI) believed to be a form of adult respiratory distress
syndrome (ARDS).
severe clinical reaction unless it initiates an amplification
mechanism such as activation of complement. Such
a mechanism could cause the formation of C5a, which
attaches to granulocytes and alters their membranes so
that they adhere nonspecifically to various surfaces. Once
these cells are sequestered in the pulmonary vascular
bed, they may become activated and release proteolytic
enzymes in toxic oxygen metabolites, leading to acute
lung injury. Pulmonary sequestration of granulocytes
may lead to further endothelial injury and microvascular
occlusion. The activation of complement, generation of
C5a, and pulmonary sequestration of granulocytes when
blood comes into contact with hemodialysis membranes
further support a role for complement activation. In summary,
TRALI depends on the simultaneous presence of
antibody, complement, and antigen-positive cells and leads
to extensive capillary leakage.