A transfusion reaction is any adverse effect of transfusion therapy which occurs during or after administration of a blood component
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1 Brenda C. Barnes, Ph.D., MT(ASCP)SBB 1/ A transfusion reaction is any adverse effect of transfusion therapy which occurs during or after administration of a blood component Transfusion of any blood component can result in a transfusion reaction 2 Fever Generally defined as 1 C rise in temperature above 37 C Chills with or without rigors Respiratory distress, including wheezing, coughing, dyspnea, and cyanosis Hyper or hypotension Abdominal, chest, flank, or back pain Pain at the infusion site 3 1
2 Skin manifestations, including urticaria, rash, flushing, pruritis, and localized edema Jaundice or hemoglobinuria Nausea/vomiting Abnormal bleeding Oliguria/anuria 4 Patient focused steps: Stop transfusion immediately and maintain IV access with normal saline Perform and document clerical recheck Contact treating physician immediately for instructions for patient care 5 Component focused steps: Contact transfusion service for directions for investigation Obtain instructions for returning any remaining component, associated IV fluid bags, and tubing Determine appropriate samples to send to laboratory Transfusion service determines whether the blood supplier should be notified 6 2
3 Clerical check of component bag, label, paperwork, and patient sample Repeat ABO testing on posttransfusion sample Visual check of pre and postransfusion sample Look for evidence of hemolysis Posttransfusion sample DAT Report findings to blood bank supervisor or medical director 7 If transfused incompatible cells have been coated with Ab, but not destroyed, DAT will be positive (mixed field) If RBCs have been rapidly destroyed, DAT may be negative Non immune hemolysis causes hemoglobinemia, but negative DAT 8 Rule out human error Decreased red cell survival studies Antibody detection studies Examine returned component 9 3
4 Acute Delayed Immunologic Nonimmunologic 10 Occur within 24 hours of administration; often during transfusion itself Incompatible red cells transfused to recipient with preformed ab Clerical and human errors most common cause of ABO incompatibility 11 IgM or complement fixing IgG Most severe reactions associated with ABO incompatible transfusions Lab findings (varies depending on ab involved) Hemoglobinemia, hemoglobinuria Hct, haptoglobin, LDH, plasma hemoglobin Serum bilirubin 6 to 12 hours later 12 4
5 13 Severe clinical symptoms: shock, hypotension, bronchospasm, DIC Complement fragments, anaphylatoxins C3a and C5a Renal ischemia, tubular necrosis, acute renal failure Activation of coagulation cascade, DIC Cytokines IL 1b, IL 6, IL 8, TNF 14 Complement activation incomplete, extravascular clearance Typical with non ABO antibodies Milder clinical symptoms Fever, new positive DAT, falling Hct with no overt signs of bleeding Hemoglobinemia, hemoglobinuria rarely seen 15 5
6 Kininogen Kallikrein Prekallikrein Kinins Factor XII Collagen Phospholipids Factor XIIa Coagulation Factor XIIa fragments Plasminogen Plasmin Fibrinolysis C8C9 (Lysis) C3 activation Complement activation C1 activation From Ciesla, B. Hematology in Practice (2007). 16 Stop transfusion Treat hypotension and promote adequate renal blood flow Monitor for/support DIC Medical management may be complicated and require aggressive interventions 17 Clerical and identification errors are the most common causes Severity influenced by: Amount of patient antibody present Quantity of antigen on transfused cells Volume of blood transfused 18 6
7 Abused unit: Improper storage/shipping temperatures, mishandling Malfunctioning blood warmers, microwave ovens, hot water baths, inadvertent freezing Mechanical hemolysis: Roller pumps, pressure infusion pumps, small bore needles 19 Osmotic hemolysis Addition of drugs or hypotonic solutions Inadequate deglycerolization of frozen RBCs Bacterial growth in blood units Intrinsic red cell defect such as G6PD deficiency in patient or donor 20 Fever, shock, hemoglobinuria, DIC, abdominal cramps, diarrhea, vomiting Mortality rates: Varies by component More likely to affect products stored at room temp (platelets) Lab investigation: Rule out hemolytic rxn, Gram stain & culture of unit and recipient, visual inspection of blood bag 21 7
8 Treatment Antibiotics, vasopressors for shock, fluids Prevention Proper storage, component preparation, visual inspection at issue, handling of materials used in administration 22 Temperature increase >1 C (2 F) associated with transfusion (during or delayed until after transfusion) Incidence: 0.1% 1% with universal leukocyte reduction Usually benign; may be accompanied by chills, rigors, and/or discomfort 23 Interaction between preformed Ab in recipient s plasma & Ag on donor lymphocytes, granulocytes or platelets (HLA antibodies are most notable) Cytokine release in the recipient in response to ag ab reactions may increase severity of reaction Any unexplained, transfusion associated rise in temperature deserves prompt attention Rule out other serious causes (acute HTR, sepsis) 24 8
9 Treatment Discontinue transfusion Initiate transfusion reaction workup Not recommended to complete transfusion of implicated component Prevention Pre storage leukocyte reduction 25 Hypersensitivity reaction (IgE mediated allergic reaction) Triggered by exposure to soluble substance in donor plasma to which recipient is sensitized Ranges from rash and/or urticaria (hives) and itching to an anaphylactioid reaction Usually not accompanied by fever Frequency 1 3% allergic 1:20,000 1:50,000 anaphylactic 26 Temporarily interrupt transfusion while antihistamine is given (only reaction in which this is allowed) Can resume transfusion if symptoms are mild and relieved with therapy If extensive urticaria or total body rash develops, recommend discontinuing transfusion 27 9
10 If patient has frequent urticarial reactions with transfusion, may pre medicate with antihistamine 30 minutes before transfusion If patient has severe and recurrent reactions, may wash RBC or platelet components 28 Signs and symptoms: Fever, chills, dyspnea, cyanosis, hypotension, new onset of bilateral pulmonary edema Symptoms arise within 6 hours of transfusion Most cases evident within 1 to 2 hours post transfusion All plasma containing components have been implicated Must distinguish TRALI reaction from: Anaphylactic reaction TACO Transfusion related sepsis 29 Associated with infusion of antibodies to leukocyte antigens and infusion of biological response modifiers (BRMs) Either may initiate cellular activation and damage of basement membrane Pulmonary edema occurs secondary to leakage of proteinrich fluid into alveolar space HLA antibodies have been implicated in some cases BRMs can accumulate during storage 30 10
11 Treatment If any type of acute pulmonary reaction is suspected, STOP TRANSFUSION! Do not resume even if symptoms abate Treat hypoxemia with oxygen and ventilator therapy, if needed Pressor agents to support blood pressure Diuretics not indicated TRALI not related to circulatory overload Prevention Defer donors implicated in TRALI reaction Excluding or screening females donors 31 Massive transfusion or single unit! Volume overload or rapid infusion Young children and elderly at most risk Dyspnea, cough, cyanosis, severe headache, peripheral edema, systolic hypertension, CHF Must differentiate from TRALI Treatment Stop infusion, place patient in sitting position, diuretics, oxygen, phlebotomy Prevention Give blood slowly, aliquot components, concentrate components 32 Citrate Toxicity Hyperkalemia and Hypokalemia Hemostatic Abnormalities Air Embolism Hypothermia 33 11
12 Immune response to foreign antigens on RBC, or WBC and platelets (HLA) Primary vs. secondary response Approximately 1 1.6% of red cell transfusions are associated with antibody formation 34 Treatment Specific treatment rarely necessary Prevention Transfuse antigen negative blood Any future transfusions should always lack the offending Ag, whether or not Ab is detectable in patient s serum (must keep permanent records and always review previous records before RBC issue) Get blood bank history from other institutions where patient has been seen Verbal hx from patient, ID bracelet, antibody card 35 Immunologic transfusion complication Donor lymphocytes proliferate and attack recipient >90% mortality rate Clinical: fever, skin rash, hepatitis, enterocolitis, pancytopenia & immunodeficiency Symptoms usually appear within 8 10 days of transfusion 36 12
13 Three requirements for GVHD to develop: Expressed HLA antigens different between donor and recipient Graft must contain immunocompetent cells Host must be incapable of rejecting immunocompetent cells 37 No effective treatment is available Gamma irradiation of cellular components is accepted standard method of prevention Minimum 2500 cgy to central portion of container and 1500 cgy to other parts Renders T lymphocytes incapable of replication, without affecting cell function 38 Irradiation of cellular components recommended in these situations: Patients identified at risk for TA GVHD Transfusions of cellular components between blood relatives Transfusion of HLA selected products 39 13
14 Uncommon, usually in women Abrupt onset of severe thrombocytopenia (<10,000/ L), 1 24 days following blood transfusion in a previously pregnant or transfused patient 70% 0f PTP cases associated with antibodies against HPA 1a Ag Usually self limited with full recovery, although some patients can die from intracranial bleeding Treatment: IVIG, plasma exchange 40 One red cell unit contains ~250 mg iron Chronically transfused patients at risk Iron deposits interfere with heart, liver, and endocrine glands causing cardiomyopathy, arrythmias, hepatic and pancreatic failure Threshold for clinical damage: lifetime exposure to units of red cells in a non bleeding person Treatment: Iron chelating agents, fresh blood 41 Fatalities resulting directly from the effects of transfusion must be reported to the FDA (director of CBER) as soon as possible, and by written report within 7 days If there is any suggestion that transfusion contributed to patient death, initiate investigation into case 42 14
15 Roback, John D, and AABB. Technical Manual. 17th ed. Bethesda, Md.: AABB,
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