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Blood Transfusion Reactions, Transfusion Rxns, Benign Transfusion, Immunologic Tranx, Types of Reactions, Post-Transfusion Purpura, Immune Mediated Reactions, Acute Hemolytic Rxns are some points in Introduction to General Medicine lecture. This lecture is one of 61 lectures you can find here for this course.
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Objectives
Early identification of common
transfusion rxns.
Differentiate life threatening reactions
from benign transfusion rxns.
Manage common immunologic tranx
rxns.
Non immune mediated reactions
Immunologic rxns
Incidence of rxns
Prevention
decrease in number of reactions.
there are no evidence to support that their use actually prevents
rxn.
Acute hemolytic rxns
Generally occurs within 2-10 days of tranx Usually due to senescent Ab response on re-exposure to a foreign red cell Ag History of previous pregnancy, transfusion or transplant Usually extra vascular and is less severe than acute Other Abs often Rh and Kidd
Clinical presentation Falling HCT, low grade fever, slight increase in indirect bili, spherocytes on blood smear
Diagnosis New +DAT and new Ab test when new blood is ordered
Txt None in the absence of rapid hemolysis Avoid offending Ag in future tranx
Incidence 1 in 20-50 thousand
Mechanism Presence of class specific IgG and anti IgA abs in pxts who are IgA def -Selective IgA def is fairly common, occurring in 1/300-500 people but majority of them do not develop Abs -Ahaptoglobinemia with antihaptoglobin Abs is similar and occur primarily in East Asian
Treatment As in all cases of anaphylaxis: stop tranx, epi 0.3ml of 1.1000 soln IM Consider IV epinephrine drip ABC +/- pressor support
Very rare (0.1-1%) complication seen in Immuno-compromised individuals esp in solid tumor cancer pxts on chemo, but can occur with acute/chronic leukemia, lymphomas, new borne with erythroblastosis fetalis and transplant pxts
Different from transplant GVHD by it’s effect on bone marrow (BM aplasia)
It occurs in immuno-compromised recipients of blood products from donors with identical HLA haplotypes. They are heterozygous for a HLA haplotype for which the donor is homozygous .e.g. genetically identical relatives
HLA ag are shared by donor and recipient, thus donor lymphocyte are engrafted by recipient because they are the only Ag seen by the host.
On the flip side the donor lymphocytes view the recipient’s tissues as foreign leading to immunologic activation and GVHD.
Bone marrow aplasia is the primary cause of death
Transfusion associated
GVHD
Skin : Swollen, erythroderma and bullae formation- most
common
GI : Diarrhea and abdominal cramps
Liver: Elevated LFT and Hyperbilirubinemia
Heme : Bone marrow aplasia, persistent thrombocytopenia
Sk in m anifestation of GVHD Generalized sw elling, erythroderm a and bullous form ation
Transfusion related acute
lung injury
-Abs against HLA -2 hit hypothesis: 1 st^ hit is an underlying pulm pathology that leads to localization of neutrophils in the pulm vasculature 2 nd^ hit is the transfusion of blood products containing sensitized neutrophils Ab leading to release of vasoactive Cytokine and pulm edema
Leading cause of transfusion related fatalities in the USA
1 case for every 1000-2400 units transfused
6-9% mortality rate
(a) Bilateral patchy alveolar infiltrate in TRAL (b) Complete resolution
a b
Criteria for the diagnosis of TRALI
Popovsky TP et al TRALI; definition and review. Crit care Med 2005
Ddx includes Acute fluid overload: ↑ JVP, ↑SBP and widened pulse pressure during dyspneic episode, ↑ pulm vascular markings on CXR Hemolytic transfusion rxns IgA mediated anaphylaxis in IgA def patients
Management
-Mostly supportive with abrupt resolution in symptoms within a few days
-A majority of patients may require mechanical ventilation
-Diuretics play no role in management since it is microvascular damage and not due to volume. It has been shown to actually worsen TRALI
Prognosis
Increased risk of recurrence if they receive products from the implicated
donor but no risk from other donors