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31 Cards in this Set
- Front
- Back
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Whole blood collection
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Donation of 1 unit of whole blood (WB) yields:
-1 unit of packed red blood cells (PRBC) -1 unit of random donor platelets -1 unit of plasma -1 unit of cryoprecipitate |
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Packed red blood cells use
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Stored in refrigerator
Transfuse 1 or 2 units to treat anemia -if Hb < 7g/dL Dose -1 unit will increase the Hb by 1 g/dL -Increase Hematocrit (Hct) by 3% Pediatric -10 mL/kg will increase Hb by 2-3 g/dL -Increase Hct by 6% Massive transfusion defined as replacement of 1 total blood volume (usually 10 units of PRBC) in less than 24 hours -May be complicated by dilutional coagulopathy, hypocalcemia, hyperkalemia, arrhythmia |
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Platelets use
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Stored at room temp
Transfuse 1 unit for thrombocytopenia -Platelet count < 10,000/microL |
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Plasma use
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Frozen
-within 8 hours FFP -within 24 hours FP24 Transfuse 2 units to treat clotting factor deficiencies -PT -PTT Contains everything in normal humal plasma (all clotting factors) |
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Cryoprecipitated AHF (Anti-Hemophilic Factor)
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Transfused (5 or 10 units) usually to replace fibrinogen
Cryo is made from FFP but only provides a more concentrated form of: -Fibrinogen -Factor VIII -von Willebrand Factor -Factor XIII -Fibronectin Used to treat bleeding from deficiency of these factors. -Safer, purified, virus inactivated or recombinant concentrates are now available for Hemophilia A and von Willebrand’s Disease -Cryo is NOT concentrated Plasma b/c it does not contain all clotting factors |
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H antigen
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Polysaccharide
-ends in fucose The H antigen is present on all human red blood cells. Think of H as the “O” antigen. H is the precursor of the A & B antigens. |
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Group A
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Group A persons have an enzyme which converts the H antigen to the A antigen by adding N-acetylgalactosamine (GALNAC). Their serum should therefore have "naturally-occurring" anti-B.
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Group B
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Group B persons have an enzyme which converts the H antigen to the B antigen by adding D-Galactose (GAL). Their serum should therefore have "naturally-occurring" anti-A.
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Group AB
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Group AB persons have both enzymes because the genes are co-dominant, and therefore, some H antigen is converted to A and/or B antigen. Their serum should have no ABO antibodies. Their plasma can be given to any patient; the universal plasma donor.
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Group O
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Group O persons do not convert the H antigen to anything, and therefore, their red cells can be given to any patient. The universal blood (red cell) donor. Their serum should have both anti-A and anti-B.
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D antigen
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Antibodies to D antigen are NOT “naturally” occurring
A person needs an exposure to foreign, non-self red blood cells to have an antibody response -Pregnancy -Blood transfusion -?? Sharing needles ?? |
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Rh System
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Persons who have inherited the D antigen are called Rh-positive (85%), while those who lack this antigen are called Rh-negative (15%).
Since D is a protein antigen, patients exposed to it can form anti-D which is a typical "immune" antibody. Even though D is the most immunogenic of the blood group systems, only 85% of Rh-negative patients will form anti-D if they are exposed to one unit of Rh-positive blood. Because the D antigen is the most immunogenic, we do not routinely transfuse Rh-negative patients with Rh-positive red cells. Rh-positive patients can safely receive Rh-negative red cells. When you administer components, they will be labeled with the ABO group and Rh type. Anti-D is clinically important because it is the most common cause of severe hemolytic disease of the newborn, which used to be a common problem in neonates. |
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Group and Type
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"Forward Grouping" - The patient's cells are reacted with anti-A and anti-B to see which antigens are on his red cells. This gives the forward group.
"Reverse Grouping" - The patient's serum is reacted with known A and B cells to see which antibodies are present in his serum. These results should correspond to the results obtained with the forward grouping, and serves as a verification of the patient's group. If no discrepancy is present, the patient's ABO blood type is recorded. Any discrepancy should be investigated further. Rh Type - The patient's cells are reacted with known anti-D, and if they react they are Rh-positive, while if they do not, they are Rh-negative. The basic reaction we are looking for is agglutination, although if hemolysis occurs, that too is considered a reaction. |
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Direct Antiglobulin Test, DAT (Direct Coombs Test; Coombs Test)
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This test will determine if an antibody, specifically IgG, or complement C3d (or both IgG and C3d) is coating the patient's red cells.
The patient's cells are exposed to anti-human globulin (AHG) which contains anti-IgG and anti-C3d. Agglutination indicates that the red cells have been attacked by antibodies. A positive test is seen in autoimmune hemolytic anemia, hemolytic disease of the newborn, hemolytic transfusion reactions and drug-induced hemolytic anemias |
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Indirect Antiglobulin Test, IAT ("Unexpected Antibody Detection Test"; Indirect Coombs Test; Antibody Screen)
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This test will determine if an antibody is present in the patient's serum.
The patient's serum is exposed to two or three group O cells (so that anti-A or anti-B won't interfere) which have all of the minor antigens that are considered important. Agglutination indicates that an antibody is present, and then further testing is required to identify the specificity of the antibody. Antibodies will fit into the "naturally-occurring," "allo-immune" or "auto-immune" category. |
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Crossmatch test
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This test will determine whether a unit of red cells is compatible with the patient.
The patient's serum is mixed with red cells from the donor unit. If agglutination or hemolysis occurs, they are incompatible and if given to the patient, his antibody could destroy the transfused cells – acute hemolytic transfusion reaction. If no agglutination or hemolysis occurs, then the odds are good that the red cells will survive normally. Don't forget though, that if the red cells stimulate antibody after transfusion, they will be gradually destroyed (delayed transfusion reaction). By performing a group and type, an antibody screen and a crossmatch, the likelihood of normal survival of transfused red cells is greater than 99%. |
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Hemolytic disease of the newborn
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Mother = Rh neg
Fetus = Rh pos Fetal red cells enter maternal circulation Mother synthesizes Anti-D Anti-D crosses placenta and hemolyzes fetal red cells Mother: High titer of Anti-D -Other antibodies to red cells can cause hemolytic disease of the newborn Bilirubin & Bile Pigments in the amniotic fluid Peripheral smear of baby -Spherocytes -Nucleated red cells |
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What to do in transfusion reaction
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IN ALL SUSPECTED TRANSFUSION REACTIONS TRANSFUSION SHOULD BE IMMEDIATELY DISCONTINUED
Maintain IV access at all times, but do not infuse any additional blood All tubing containing blood should be removed and replaced Notify Blood Bank and Transfusion Medicine physician Send Transfusion Reaction work-up |
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Blood bank transfusion reaction workup
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Clerical check - to rule out clerical error
Hemolysis evaluation -Visual inspection (both specimen and unit) -Bilirubin (total and conjugated), LDH, plasma hemoglobin, haptoglobin -Urinalysis Serologic incompatibility - several tests are performed to look for evidence of ABO incompatibility (crossmatch), and antibody coating of transfused red cells (DAT) including antibody screen of new sample If no clerical errors are detected and serological studies indicate no immune mediated basis for hemolysis, further blood products may be released |
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Acute hemolytic transfusion reaction: frequency, etioloty, signs/symptoms, management
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Frequency:
-Rare, <<1% or approx. 1/25,000 transfusions -Human clerical error: --Phlebotomist drawing wrong sample/labeling error --RN staff hanging blood on wrong patient -More likely in emergency settings: OR, ED, ICU Etiology: -Transfusion of ABO incompatible blood, e.g., (giving A blood to an O patient with anti-A) -Alloantibodies (Kell, Kidd) in recipient plasma react with corresponding antigen on donor red cells Signs/Symptoms -Fever, chills, back pain and dyspnea most common -Chest pain, hypotension/shock, oliguria, nausea, generalized bleeding, hemoglobinuria, hemoglobinemia, cardiac arrest -Intravascular hemolysis leading to increased LDH, Bilirubin, Creatinine and decreased Haptoglobin Management: -Stop transfusion! Replace tubing. Maintain IV access. Notify the primary physician/Blood bank -Supportive therapy to maintain: --BP: IV fluids, medications to maintain blood pressure --Do not transfuse any additional blood products to the patient until a new sample has been crossmatched |
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Delayed hemolytic transfusion reaction: frequency, etiology, signs/symptoms, management, prevention
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Frequency: 1/5000
-May go unrecognized in discharged patients with non-specific complaints Etiology: -late formation of alloantibody directed against foreign alloantigens present on transfused red cell, resulting in destruction of the transfused red cells 6 weeks - 3 months after transfusion -Implicated antibodies: Kell, Kidd, Duffy, RH (E) Signs/Symptoms: -fever/chills, falling hematocrit, jaundice, dark urine Management: Send transfusion reaction work up: -Antibody screen: --patient has produced alloantibody which circulates in serum -Direct Antiglobulin Test: the transfused donor red cells coated with antibody -Monitor renal function -Support hematocrit as needed with transfusion Prevention: -Future transfusions only with antigen negative blood |
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Febril non-hemolytic transfusion reaction: incidence, etiology, signs/symptoms, management, prevention
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Incidence:
-75-80% of all transfusion reactions (1/200) Etiology: -White cell antibodies in the patient react with transfused white cells or platelets present in donor blood -Cytokine accumulation in blood product, especially platelets (majority) -TNF-, IL-1, IL-6, IL-8 Signs/Symptoms -Fever, > 10 C or 2-30 F increase during or within 2 hours of completing transfusion -Chills, rigors, headache, tachycardia, myalgias -Usually no hypotension Management: -Stop transfusion! maintain IV access: Do not restart -Notify TM physician; administer antipyretics as indicated -Send transfusion reaction workup Prevention: -use prestorage leukoreduced products -Pre-medication with Tylenol |
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Urticarial (mild allergic) transfusion reaction: incidence, etiology, signs/symptoms, management
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Incidence:
-20-25% of all reactions (1/100) occur with 1% of all transfusions Etiology: -recipient is sensitized to foreign donor plasma proteins Signs/Symptoms: -urticaria, flushing, itching, erythema Management -Stop or slow the transfusion -Administer antihistamine (1 mg/kg diphenhydramine IV) for treatment or prevention -If symptoms are mild, localized, and resolve with therapy, restart the transfusion |
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Anaphylactic transfusion reaction: frequency, etiology, signs/symptoms, management, prevention
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Frequency:
-Rare, 1/40,000 transfusions Etiology -IgA deficient patient with preformed IgA antibodies react to donor IgA present in the product (1:700 IgA deficient) Signs/Symptoms -Anaphylactic shock after a few mls (eg. 5 mL) -hypotension, flushing rash, chills, coughing, respiratory distress, abdominal cramping, vomiting, diarrhea, loss of consciousness Management: -Stop transfusion! maintain IV access: Do not restart -Notify physician and initiate therapy: -ABC’s of initial support -Epinephrine 1:1000, 0.3 ml SQ (max), rpt 15 min prn -Steroids; oxygen; pressors Prevention: -Autologous transfusions -IgA deficient products (PRBCs, platelets, plasma) -Washed RBCs and Platelets -Plasma products only from IgA deficient donors -Frozen deglycerolized PRBCs |
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Transfusion related acute lung injury: incidence, etiology, signs/symptoms, management, prevention
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Incidence: 1 in 5,000 transfusions
-Leading cause of transfusion related fatalities in US Etiology: -Donor white cell antibodies react with patient WBCs -HLA antibodies class I & II and neutrophil specific antibodies (HNA-1a, HNA -2a, HNA-3a) -Bioactive lipids accumulate in stored blood activate neutrophils -Mobilization and Activation of neutrophils along with their toxic metabolites caused capillary endothelial injury in the lung leading to PE and ARDS Signs/Symptoms -Acute respiratory insufficiency without heart failure -Dyspnea, tachycardia, characteristic chest x-ray Management: -Stop transfusion! maintain IV: Do not restart -Symptomatic treatment: O2, etc -Notify blood bank and send transfusion reaction workup -Additional special testing might include HLA or white cells antibody testing on donor and /or patient -75% may require intubation but >80% recover -Improvement and recovery within 2-4 days Prevention: -HLA matched products -Leukocyte depletion -Most important: exclude the “dangerous” donor -Male only plasma |
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Transfusion associated graft vs host disease (tGVHD): incidence, etiology, signs/symptoms, diagnosis, management, prevention
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Incidence is extremely rare
Etiology -Engraftment of donor lymphocytes into the bone marrow of immunosuppressed patients, setting up an immune response where the donor cells recognize the host as foreign, causing an immune “rejection” response Signs/Symptoms: -rash, diarrhea, hepatosplenomegaly -pancytopenia Diagnosis: -Skin biopsy -Test for donor T cells in recipient circulation Management: -High dose steroids -100% fatal Prevention: -For immunosuppressed patients, irradiate all blood products containing lymphocytes --Especially medications that result in significant myelosuppression -Irradiate all blood products from relatives |
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Septic transfusion reaction: etiology, signs/symptoms, management
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Bacterial contamination
-red cells: yersinia -platelets: staph Platelets most common (stored at RT) Recognition: -gram stain, culture bag, culture patients blood Etiology: -Infusion of bacterial contaminated blood products Signs/Symptoms: “warm shock” (fever and hypotension) Management: -Stop transfusion! do not restart; notify TM physician -Notify blood bank and send transfusion reaction workup -Send blood bag and tubing (clamped off) to blood bank for visual check, Gram stain and culture -Draw blood cultures on patient; treat for sepsis with immediate IV antibiotics and pressure support |
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Transfusion Associated Circulatory Overload (TACO): incidence, etiology, signs/symptoms, management, prevention
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Incidence is <1%
Etiology: -Administering fluid faster than the circulatory system can handle, often in setting of CHF -Especially relevant in pediatrics/elderly Signs/Symptoms: - acute transfusion reaction - Cough, dyspnea, tachycardia, rales, distended neck veins, HTN, headache Management: -Stop transfusion! Maintain IV. Notify BB/TM physician -Treat for pulmonary edema: O2, diuretics, morphine Prevention: -Request blood to be divided into smaller aliquots (80-120 ml) that patient can safely receive over 4 hours |
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Thermal/Mechanical/Oncotic Hemolysis: etiology, signs/symptoms, management, prevention
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Etiology:
-too much heat -too much cold -wrong solution Signs/Symptoms: -May mimic an acute hemolytic transfusion, or patient may be asymptomatic except for hemoglobinuria/hemoglobinemia Management: -Stop transfusion! Do not restart. Notify TM physician -Notify blood bank -Supportive therapy: IV fluids etc Prevention: -proper handling and transfusion of red cells units |
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Hypothermia: incidence, etiology, presentation, management
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Incidence- dependent on clinical setting
Etiology- rapid infusion of cold blood as seen in massive transfusion cases (Trauma, OR cases) Presentation- -Hyperkalemia or hypocalcemia leading to: --ventricular arrythmias --Impaired hemostasis Management- -Blood warming is a must during massive transfusion (blood warmer) |
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Transfusion informed consent
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Now a regulatory requirement
Why does the patient need a transfusion? -There is no other alternative therapy Risks of transfusion |
