Investigation of transfusion reactions
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Transcript of Investigation of transfusion reactions
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Allergy, Anaphylaxis, TRALIJanejira Kittivorapart, MD.Department of Transfusion Medicine Faculty of Medicine Siriraj Hospital
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Allergic reaction : 1 – 3 /100 transfusions
Anaphylaxis : 1.7 – 4.3 /100,000 RBC & plasma
transfusions 62.6 /100,000 platelets pools
Roback J. Technical Manual. 17th ed.Bethesda(MD):AABB; 2011Vassallo R.Immunohematology 2004;20:226-33
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Recipient IgE or non – IgE antibodies to proteins or other allergenic soluble substances in the donor plasma
Release of mast-cell mediators Histamine, tryptase, leukotrienes,
prostaglandins and platelet-activating factor
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1. Histamine generate from recipient’s mast cells and basophils
2. Histamine leakage into plasma during storage ↑ reactions if ↑ storage time Allergy of their own autologous products
3. Infusion of antibodies in donor plasma
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Retrospective single center review of all transfusion reaction
1991-1996
20 from 967 reactions (2.1%) from autologous units
4 from 20 were allergic reactions Domen
RE.Transfusion.1998;38(3):296-300
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Kay AB. Allergy and allergic disease s. New Eng J Med.2001;344(1):30-7
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1. Immediate hypersensitivityRelease of mast-cell mediators Smooth muscles contraction, vasodilatation,↑vascular permeability, hyper secretion of mucus
2. Late-phase reaction Peak at 6-9 hours after allergen exposureEdema, indurated swelling, blockage nose, wheezing lungs
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Localized or confluent itching wheal & flare
Clinically diagnosis
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First generation H1-blocking antihistamine
Combining H1 and H2 antagonists – better results in non-transfusion settings
Hold the transfused unit
Re-transfusion can be resumed in mild urticaria after all the lesions has cleared
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Anaphylactic reactions Anaphylactic reactions Allergen in plasma patient who previous sensitization has an
IgE directed against that allergen Histamine, leukotrienes, prostaglandins,
PAF Platelet-activating factor: induce production
of “Nitric oxide” (NO) NO as a potent vasodilator
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Anaphylactoid Anaphylactoid reactionsreactions Clinically identical to
anaphylaxis Mechanisms that do not
involve IgE Complement fixation and
generation of anaphylatoxins : C3a, C4a, C5a
Cytokines secreted by monocytes
Activation of basophils and mast cells
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Recipient’s plasma protein deficiency- IgA - Haptoglobin- Complement (C3, C4) - Transferrin- HLA antigens
Food allergens – peanut, glutenMedications Passive transfer of antibodies
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6 yr old boy with ALL Received LPPC Developed rash, angioedema, hypotension Tryptase 24 µg/L (<5 µg/L) History of previous severe allergy to peanuts Donors eating handful of peanuts shortly
before donation The digestion-resistant peptide from Ara h2
can be detected in serum for up to 24 hours after ingestion Jacobs J.N Eng J
Med.2011;364(20):1981-2
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Base on clinical signs & symptoms
SampsonH, J Allergy Clin Immunol.2006 Feb;117(2):391-7
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Serum total tryptase
IgA level
Anti-IgA antibody
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A protein component of human mast cell secretory granules
Two genes on chromosome 16p13.3 encoded for -tryptase and -tryptase
-tryptase would be negligible enzymatic activity
Mature -tryptase is retained in secretory granules until these cells are activated to degranulate
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Selectively & abundantly produced by mast cells
Total tryptase = pro- and mature forms of /- tryptase
Schwartz LB.Immunol Allergy Clin N Am.2006;26:451-63
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T1/2 of 1.5 – 2.5 hours
↑ - tryptase in anaphylaxis of sufficient severity
Inversely correlate with mean arterial pressure during anaphylactic shock
Schwartz LB.Immunol Allergy Clin N Am.2006;26:451-63Van der Linden Wf, Hack CE, et al.J Allergy Clin Immunol.1992;90:110-8
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สาขาวิ�ชาโรคภู�มิ�แพ้�และวิ�ทยาภู�มิ�ค��มิกั�น ภูาควิ�ชากั�มิารเวิชศาสตร�
Clotted blood 5 ml 1st time: 1-2 ช��วิโมิงหล�งเกั�ดอากัารสงส�ย anaphylaxis 2nd time: > 1 วิ�น หร"อ - 12 เด"อนหล�งมิ$อากัาร
(Baseline) Normal total tryptase levels 1 – 15 µg/L Method – Fluorescence Enzyme Immuno
Assay
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IgA deficiency: IgA level < 7 mg/dl (in age > 4 years old)
Donor IgA deficiency: IgA level < 0.05 mg/dl
Incidence of IgA deficiency varies with population studied and limitation of screening test US 1: 328 Australia 1: 442 Japan 1: 18500
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ภูาควิ�ชาวิ�ทยาภู�มิ�ค��มิกั�น
Clotted blood 3 – 5 ml น%าส&งภูายใน 6ช��วิโมิงหล�งเจาะเล"อด
Turn around time 5 วิ�น Nephelometer (BN Prospec)Minimum value: 1.24 mg/dl
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Measure the light scattered through the sample at an angle from the incident beam
Compare results to the light-exiting dilutions of IgA standards
Determining the rate of change of light scattering rather than static value
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Anti-IgA is detected in approximately one third of IgA-deficient individuals (28 – 37%) Class-specific antibodies Limited-specific antibodies
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1:1000 epinephrine(1 mg/ml) IM 0.2-0.5 ml for adults (0.01 ml/kg in children) q 15 - 30 minutes as needed
Vigorous IV crystalloid Pressors – dopamineAntihistamine Glucocorticoids
↓late-phase inflammatory responses
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Remove plasma proteins; IgA concentration in washed red blood
cells “6-washed” No. of wash
cycles Total vol.
of NSS used (L)
Observed IgA content
(mg/dL)
Results of Hemaggluti
nation inhibition
assay
3 1.0 0.11-0.27 Positive
4 1.3 0.01-0.04 Weakly positive
6 2.0 0.00 Negative
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TRALI was 1st reported in 1951 In 1970, it was postulated that
leukoagglutinins to HLA and non-HLA Ag were etiologic in TRALI reactions
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51 years old male patientUnderlying disease: Cirrhosis, Child C Diagnosis – pyomyositis at left thighAdmit for intravenous antibiotics
Imaging study – soft tissue mass 22x6 cm Bleeding tumor at left thigh
Coagulopathy, DIC
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Plan for drainage/biopsy
PRC FFP 500 ml
FFP 1000 ml
PRC
11 12 13 14 15 16 17 18 19 20
Furosemide
เหน"�อย
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Off blood transfusion Intubation & respiratory supportDiuretics CXR Access central line no evidence of
volume overload
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Normal CXR
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Recipient’s HLA Ab – negative
FFP from 4 donors 2 from female donors
PRC from a male donor
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Feature TRALI TACO
Temperature Fever can be present Unchanged
BP Hypotension Hypertension
Respiratory symptoms Acute dyspnea
Neck veins Unchanged Can be distended
Auscultation Rales Rales, S3 may be present
Chest radiograph Diffuse, bilateral infiltrates
Ejection fraction Normal, decreased Decreased
PA occlusion pressure ≤ 18 mmHg > 18 mmHg
Fluid balance +/- +
Response to diuretic Minimal Significant
BNP < 200 pg/ml >1200 pg/ml
Leukocyte antibodies Donor leukocyte antibodies +, crossmatch
incompatibility between donor and recipient
Donor leukocyte Ab ±If +, suggestion of
TRALI
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Immunocompetent host Single event Two events model
Neutropenic patient Infusion of Infusion of vascular
endothelial growth factor (VEGF), an effective permeability factor
or Infusion of antibodies against HLA class
II antigens Silliman C, Ambruso D, Boshkov.Blood.2005;105(6):2266-73
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Silliman C, Ambruso D, Boshkov.Blood.2005;105(6):2266-73
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A case-control study: 2 patient groups were at risk for TRALI In the induction phase of hematologic
malignancies (p < 0.0004)
Cardiovascular disease who required bypass surgery (p < 0.0006)
Silliman CC, et al. Blood.2003;101:454-62
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Kleinman S, Caufield T, Chan P, et al. Transfusion. 2004
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Bux J.Vox sang.2010;100:122-8
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HLA & leukocyte Ab in donor plasma
Established the diagnosis
If positive
HLA & granulocyte Ag typing of the recipient
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The International Granulocyte Immunology Workshops (IGIW) recommends to test both methods
The granulocyte immunofluorescence test (GIFT)
The granulocyte agglutination test (GAT)
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Para formaldehyde-fixed PMNPFA fixation of cells before exposure
to human test sera eliminated intracellular fluorescence↓ non-specific membrane
fluorescence
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1) PMN reactive antibodies bind to native antigens on unfixed PMNs, sensitizing the cells
2) Sensitized PMNs undergo chemotaxis & move towards other PMNs to form agglutinates
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The GAT is the most reliable technique for the detection of anti-HNA-3a
Requires viable cells, energy and an intact cytoskeleton
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Both the GIFT & GAT can detect antibodies to HLA on PMNs
Routinely taken to differentiate HLA from HNA antibodies
Testing samples with & without platelet absorption
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Monoclonal antibody immobilization of granulocyte antigens (MAIGA)
ELISATransfected cell linesLABScreen MultiWhite cell-IFT(WIFT)Five cell lineage
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Respiratory supportNo role of diuretics and
corticosteroidsTRALI reactions should be reported
to the blood supplier To ascertain information about the donor
of the transfused blood components To allow the quarantine or recall of
additional components from the donor
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Decreasing blood usageDisqualifiation of donors implicated
in TRALI reactions (AABB)“male- only plasma” (UK)
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“male- only plasma” High plasma-volume components from
female donors▪ Could be used if they were selected to
minimize their risk of HLA or HNA alloimmunization
▪ Nulliparous donors▪ Female donors with negative HLA/HNA
antibody testing
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