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Edit Comment Close Premium member Presentation Transcript Transfusion Medicine and Hemolytic Anemias: Transfusion Medicine and Hemolytic Anemias John Densmore, MD, PhD Division of Hematology/Oncology July 2005Overview: Overview Transfusion Medicine Indications Products Complications Autoimmune Hemolysis Evaluation Treatment Transfusion Medicine: Transfusion Medicine Indications: Red cells: symptomatic anemia (Young people may tolerate Hct <20, elderly/CAD may be symptomatic <30) Platelets: Prophylactic: <10,000 (<20 if febrile). <50 for procedures, <80-100 for major surgery FFP: for coagulopathy, massive blood transfusion, factor deficiency. Cryoprecipitate: for low fibrinogen (DIC) or third line for von Willebrand’s diseasePacked Red Blood Cells: Packed Red Blood Cells Reduced plasma volume, hct 70-80% Volume 260 ml Matched for ABO type 1 unit should increase hgb by 1 g/dLPlatelets: Platelets Random donor 50-70ml per unit Stored at room temp 6 units should increase plt by 30,000 Single donor 200-400 ml Equivalent to pool of 6 units random donor No significant benefit over random donor, unless matchedFresh Frozen Plasma: Fresh Frozen Plasma Contains all coagulation factors Volume 200-260 ml per unit Dose of 10-20ml/kg (4-6 units for adult) will increase coag factors by 20% T1/2 of FVII is 6 hours Cryoprecipitate: Cryoprecipitate Contains FVIII, vWF, fibrinogen, FXIII Treatment of choice for low fibrinogen Given in 10 bag increments Will raise fibrinogen by 40-50 mg/dLActivated FVII: Activated FVII Indicated for pts with hemophilia and factor inhibitors Used for temporary correction of coagulopathy (ie, procedure) Major contraindication: MI, angina, CVA within several weeksActivated FVII: Activated FVII Protocol: 40mcg/kg within 1 hr of procedure, followed by 20-40mcg/kg 2 hrs after (may repeat q4hr x 1 or 2 doses) Fibrinogen should be >150 mg/dL Complications: Complications Prevention Transfusion reactions Infectious OtherLeukodepletion: Leukodepletion Prevention of febrile transfusion reactions in a patient with previous documented reactions Prevention of HLA alloimmunization (ineffective if patient has receive one or more blood products not leukodepleted or already HLA immunized) Prevention of CMV infectionIrradiation: Irradiation Performed to prevent transfusion-associated graft-versus-host-disease (TA-GVHD) Absolute Indications: BMT recipients, congenital immune deficiencies, transfusion from relatives, Hodgkin Lymphoma (current or history of). Probable: Hematologic malignancies other than HL, those receiving aggressive chemotherapy, HLA-matched platelets. Not Indicated: HIV/AIDS, elderly, hemophilia, solid tumor patients, those on immunosuppressants Transfusion Reaction: Transfusion Reaction Defined as a rise in temperature of 1oC during transfusion May have associated signs/symptoms of chills, rigors, headache, nausea, tachycardia, dyspnea, hypotension Can occur during transfusion or up to 24hr after Most are not life threatening, but each needs to be worked up to rule out acute hemolysis Most common is a febrile, non-hemolytic reaction due to either WBC or cytokines in transfused unitAcute Hemolytic Transfusion Reaction: Acute Hemolytic Transfusion Reaction Most common cause is ABO mismatch Usually massive intravascular hemolysis with hemoglobinemia and hemoglobinuria (risk of ARF) Workup: CBC, repeat T+S, DAT, U/A Treatment: stop transfusion, vigorous hydration, maintenance of BP Mortality related to amount of blood transfused, organ failureDelayed Hemolytic Transfusion Reaction: Delayed Hemolytic Transfusion Reaction Occurs several days to a week after transfusion Recipient antibodies to transfused unit that were not detected on T+S (but previous exposure to the antigen) Causes lack of expected rise in Hct, fever, Coomb’s positive hemolytic anemia, jaundice. Repeat T+S will demonstrate antibody to an antigen on the transfused unit. Most often directed against Rh, Kidd, Duffy, Kell, E, Jk.Infections: Screening: Infections: Screening Hepatitis B surface antigen (HBsAg) Hepatitis B core antibody (anti-HBc) Hepatitis C virus antibody (anti-HCV) HIV-1 and HIV-2 antibody (anti-HIV-1 and anti-HIV-2) HTLV-I and HTLV-II antibody (anti-HTLV-I and anti-HTLV-II) Serologic test for syphilis Nucleic acid amplification testing (NAT) for HIV-1 and HCV NAT for West Nile Virus Infectious Complications: Infectious Complications Bacterial: can occur with any transfusion, more likely after platelets because they are stored at room temperature. Platelets: Staph. Epi. And Bacillus Cereus most common; estimated to occur in 1:2000 units with risk of severe sepsis in 1:50,000 RBC: Yersinia, Serratia and Pseudomonas most common; risk of severe sepsis in 1: 500,000 units Infectious Complications: Infectious Complications Viral: HIV: current estimates are that fewer than 1 in 2,100,000 blood components is capable of transmitting HIV with nucleic acid testing . Hepatitis B: In 2000, the frequency of post-transfusion hepatitis B was estimated at 1 in 205,000 screened units of blood. Hepatitis C: the risk of HCV transmission through transfusion is less than 1 per 1,900,000-screened units of blood. Other Infections: HTLV-I, CMV, West nile virus, malaria, syphilis, Chagas disease and babesiosis have been linked to transfusions Transfusion Related Acute Lung Injury (TRALI): Transfusion Related Acute Lung Injury (TRALI) Hypoxemia, fever, bilateral infiltrates and hypotension developing 2-4 hours after transfusion Major differential includes CHF/volume overload, infection Estimated risk is 1:5,000 to 1:1,323 per component transfused Third most common cause of transfusion-related death. TRALI: TRALI Chest. 2004;126:249-258 TRALI: TRALI A form of ARDS caused by the presence of HLA antibodies in the donor serum leading to destruction of host granulocytes and activation of the complement system leading to lung injury Treatment is supportive. Ventilatory support may be required Recovery is usually rapid and complete Transfusion Related Graft vs. Host Disease (TGVH) : Transfusion Related Graft vs. Host Disease (TGVH) Occurs when donor lymphocytes attack the recipient Very rare in the normal blood recipient unless the donor is homozygous for an HLA haplotype and recipient is heterozygous for that haplotype (related donor) TGVH is reported in blood recipients who are immunosuppressed- mainly patients with Hodgkin's disease and leukemiaTGVHD: TGVHD Symptoms are an erythematous rash that may progress to toxic epidermal necrolysis, liver dysfunction and pancytopenia TGVH is prevented by irradiating blood products for at risk patients with 1500-3500 rads Platelet Alloimmunization : Platelet Alloimmunization Patients exposed to WBC with different HLA types will develop antibodies to HLA antigens Platelets express class I HLA antigens and are rapidly destroyed by HLA antibodies. Seen in patients who have received previous transfusions of blood that is not leukodepleted or patients who have been pregnant Platelet Alloimmunization: Platelet Alloimmunization Up to 90% of patients with aplastic anemia or myelodysplasia will become HLA immunized. Incidence is less in patients receiving chemotherapy but still can be as high as 60 - 90%. Important to leukodeplete all products for pts who will receive frequent transfusions (BMT, acute leukemia, MDS, AA)Use of Anti-D with platelet transfusions: Use of Anti-D with platelet transfusions Platelets do not express Rh antigens, but contaminating RBC do Rh- patients will occasionally receive platelets from Rh+ donor 0.1 ml of RBC enough to elicit anti-D responseUse of Anti-D with platelet transfusions: Use of Anti-D with platelet transfusions Blood bank will recommend RhoGam for Rh- pt that receives Rh+ plt Data to support its use in premenopausal females who may become pregnant No benefit in men or post-menopausal women Dose is 250 iu given SC (will cover for 6 weeks)Anaphylaxis: Anaphylaxis Suspect in patient with bronchospasm, wheezing or other sign of anaphylaxis within an hour of transfusion Most common cause is an IgA-deficient patient that has anti-IgA antibodies and reacts to the plasma Treatment is supportive with avoidance of plasma if possible Red Cell Disorders: Red Cell Disorders Anemia Underproduction Hemolytic Enzyme defects HemoglobinopathiesApproach to anemia: Approach to anemia Hemolytic Anemia: Hemolytic Anemia Autoimmune Hemolytic Anemia Warm Cold Drug-related G6PD Inherited enzyme defectsApproach to Anemia with High Reticulocyte Count: Approach to Anemia with High Reticulocyte Count Smear (spherocytes, fragments) Bilirubin, LDH, Haptoglobin Direct and Indirect Coombs UrinalysisDirect Antiglobulin Test: Direct Antiglobulin TestIndirect Antiglobulin Test: Indirect Antiglobulin Test Uses panel of RBC with known antigen expression; can define the antigen that is targetedDirect Antiglobulin Test(Coomb’s): Direct Antiglobulin Test (Coomb’s)Warm AIHA: Warm AIHA Associated with lymphoproliferative d/o, autoimmune disease (most idiopathic) Incr. retic, Coombs pos, haptoglobin low, spherocytes Treatment: steroids, IVIG Transfusions are OK if needed Splenectomy for refractory ptsNormal smear: Normal smearSpherocytes: SpherocytesCold AIHA: Cold AIHA IgM: associated with lymphoproliferative d/o, mononucleosis, mycoplasma IgG: classic is syphilis (Donath-Landsteiner Ab), also drug-related Warm blood, keep pt warm, steroidsDrug-Induced HA: Drug-Induced HA 3 types: Autoantibody (methyldopa, procainamide) Coomb’s positive for IgG and C3 Hapten-mediated (penicillins) Coomb’s pos for IgG, not C3 Innocent bystander (Immune complex) Coomb’s pos for C3 Quinidine, HCTZ, NSAIDs, SulfonylureasSlide41: Hapten (penicillin) Autoantibody (methyldopa)Treatment: Treatment Stop any offending drugs Steroids Transfusions You do not have the permission to view this presentation. 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