Antigen Groups and Transfusion Reactions Flashcards
Kell
- IgG
- Reacts with AHG
- Enzymes have no effect
- Causes: HTR, HDN
Duffy
- IgG
- Reacts with AHG
- Destroyed by enzyme
- Causes: HTR, HDN (expressed on cord cells)
- Other: show dosage effect, glycoprotein is a receptor for P. vivax, the merozoites bind but cannot enter the cells
Kidd
- IgG
- Reacts with AHG
- Enzymes enhance agglutination
- Causes: HTR(delayed) and HDN
- Other: show dosage effect, bind complement, deteriorate in storage
Lua
- IgM
- Reacts at room temp (4C)
- Enzymes variable
- Other: Not naturally occurring, not naturally significant
Lub
- IgG
- Reacts with AHG (37C)
- Enzymes variable
- Causes: HTR, HDN
Lewis
- IgM
- 4C (Cold reacting)
- Enzymes cause enhanced agglutination
- Other: produced by tissues and absorbed onto RBCs, not associated with HDFN
P
- IgM
- 4C
- Other: Reacts at IS, 37C or AHG
M,N
- IgM
- Reacts at IS, 37C, or AHG
- Destroyed by enzymes
- Other: shows dosage effect; clinically significant if IgG
S,s
- IgG
- Reacts at 37C, with AHG
- Enzymes are variable
- Causes: HTR, HDN
Types of carrier molecules
Most Ag are carried on glycoproteins with a specificity to the Ag
MNS System
Most important transfusion Ag
- M/N on Glycophorin A
- S on Glycophorin B
M/S and N/s are usually found together
Anti-M
IAT if IS crossmatch is +
Will not react with enzyme treated cells, but can be enhanced by an acidified environ.
Anti-N
Seen in dialysis Pts with residual formaldehyde
Alters the N Ag in the Pt
Anti-Kell
Most Immunogenic after ABO and Rh
Can be “naturally occurring” after microbial infections, the IgMs clear after the infection
Other naturally occurring Ab are cold reactive with a negative IAT
I/i Ag
- Fetal cells express I antigen
- Adults express i Ag
Transition occurs by 18 mos
Anti-I
Usually an IgM cold-reactive Ab, found in 4C testing
Rarely found as an autoanti-I at 37C from complement binding at RT that carry over to IAT, these can cause Cold Agglutinin Syndrome:
- May be helpful to use a monospecific IgG reagent
- O cells run at RT and 4C can ID cold-agglutinins
- Prewarming techniques can remove cold-agglutinins, but are usually not used
Increase in Temp of 1C/chills
- HTR
- TACO
- Bacterial Contamination
- Febrile non-hemolytic transfusion reactions (FNHTR)
Hypotension/Tachycardia
- HTR
- TACO
- Anaphylaxis
- Bacterial contamination
- Air embolus
Hypertensive changes
- TACO
- TRALI
Pain/Anxiety
- HTR
- Febrile Rxn
- Citrate Rxn
Transfusion Reaction Procedural Steps
- Stop transfusion
- Review clerical info
- Check for hemolysis in pre/post transfusion samples
- Repeat ABO on post- DAT on post-, if +, DAT on most recent pre-
Further testing can include: compatibility testing, Ab screen on post-, eluate, bacteriologic studies, coag studies, plasma Hgb, bilirubin, urinalysis
TRALI
Transfusion-Related Acute Lung Injury
Severe pulmonary issues within hours of transfusion, with fever
Donor anti-leukocyte Ab activate and aggregate WBCs, or transfusion of cytokines activates neutrophils in the lung present from an underlying condition
TACO
Transfusion-Assoc. Circulatory Overload
Greatest at risk have underlying heart, lung, or kidney failure that make them intolerant of volume increase; those with massive transfusions, Peds, and severe anemia are also at risk
Show shortness of breath, coughing, elevated BP, low pulse rate, peripheral edema
Respond to diuretics (helps diagnose as well), ventilation/oxygen, slow transfusion of blood products helps prevent this
Anaphylotoxins C5a/C3a
Promote release of serotonin/histamine from Mast Cells, causing smooth muscle contractions and bronchial/vascular dilation
Show hyptotension, chills, fever, back pain, shock, renal failure and death
Intra/Extravascular Hemolysis
Both show hemoglobinemia, hemoglobinuria, increased plasma Hgb, low serum haptoglobin, increase indirect bilirubin
From non-ABO Ab-related hemolysis or a drop in Ab titer below detection level
DHTR
Delayed Hemolytic Transfusion Reaction
Extravascular hemolysis weeks after transfusion
Usually require presensitization via transfusion, transplant, and pregnancy
Usually from Kidd, Duffy, Kell, and MNS
Chronically transfused Sickle Cell Pts may develop alloAb and risk DHTRs
Transfusion Related Bacterial Infection
Sepsis, Fever, Hypotension
Immunosuppressed Pts may not show a febrile response
Can progress to DIC, renal failure, and death
Babesia microti has been implicated in a significant # of cases
If septic, they should be cultured and started on antibiotic therapy
Allergic/Anaphylactic Rxns
Recipient IgE to soluble Ag in donor plasma, most commonly in plasma containing platelet products
Epinephrine will control the reaction while BP and volume are maintained, steroids may also help
FNHTR
Cytokines released from WBC in storage cause inflame. in recipient
Treated/Prevented with antipyretics
TAGVHD
Transmission Assoc. Graft-Versus-Host Disease
Non-specific symptoms within weeks of transfusion, will cause death
Immunosuppresed, those on chemotherapy, with congenital disorders, and newborns are at greatest risk
Donor T cells attack Pt cells
Use of irradiated units, and those tested for HLA compatibility
Posttransfusion Purpura
Sudden onset of thrombocytopenia 1-2 weeks after transfusion from platelet-specific Ab in Pt from prior exposure
HDFN Prenatal Evaluation
History of pregnancies/transfusions, screening at first prenatal visit for ABO/Rh/Ab screen, no maternal weak D testing needed
Screen should be with anti-IgG AHG and without enhancement via enzyme treated cells to detect only Ag assoc. with HDFN
Ab titration in HDFN
To assess the relative strength of the Ab
Uses dilutions of maternal serum incubated at 37C with reagent RBCs with Ag against maternal Ab, and read at anti-IgG AHG phase
Procedure variations include: can be preformed in saline, gel cards, enhancement media, alter incubation times, and different Ag expressed on RBCs
Usually predictive in first affected pregnancy and not needed in any subsequent pregnancies
Anti-Kell in HDFN
Suppress RBC production by encouraging phagocytosis before the cells produce hemoglobin, leading to anemia and hydrops without a significant titer
Intrauterine Transfusions
Administered through the umbilical vein or peritoneal cavity, using fresh O units that are negative for maternal Ag, and irradiated to prevent TAGVHD
False Negative in Direct Testing for D Ag
The cells are too coated in maternal Anti-D to agglutinate
Quantification of Fetal-Maternal Hemorrhage
Screening Test is the rosette test
- Maternal sample from 1hr after birth and mixed with Anti-D
- Washed and indicator cells are added
Kleihauer-Betke (based on fetal Hgb resistance to elution from RBCs) acid elution or Flow Cytometry can also be used
Previously Sensitized Women (D)
IgG with a titer lower than < 4, alloimmunization has IgM and a higher titer
NAITP
Neonatal Thrombocytopetic Purpura Maternal IgG against fetal platelets, can be in first pregnancies, inter cranial hemorrhage can occur in utero/after delivery Irradiated, leucoreduced, CMV-seronegative, antigen negative platelets can be transfused to prevent hemorrhage
