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Basics of Transfusion Therapy in cancer. Prof Laila Sherief. Transfusion therapy is a key to successful management of children with cancer or hematological disease. RBC Transfusion: Indications. Anemia Definition: Causes of anemia in cancer.
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Basics of Transfusion Therapy in cancer Prof Laila Sherief
Transfusion therapy is a key to successful management of children with cancer or hematological disease.
RBC Transfusion: Indications Anemia Definition: Causes of anemia in cancer
* CIP of anemia:related to the severity andrapidity of onset . General Symptoms: Physical signs: Cardiac signs:
Prophylactic RBCs transfusion guidelines for children with cancer Clinical scenario Stable Vital Sign changes O2Requirements Thrombocytopenia Procedure Fatigue chronic Anaemia Irradiation
Pre-Transfusion Testing BLOOD TYPING: ABO, D Antigens only (Other antigens are weak immunogens) ANTIBODY SCREEN: Patient serum vs. cell panel CROSSMATCH Major: Patient Serum vs. Donor Cells
RBC Transfusion Volume Usual:10 -15cc/Kg in 3-4 hours Unusual: 1-Acute Hemorrhage: 2-replace ongoing losses 3-Chronic Anemia, Heart Failure, 3-2cc/Kg/ Diuretic Exchange
Special consideration for RBCs transfusion: 1)Leukoreduction: Achieved by filtration either at the time of collection or at the bed side. Value: 2)Irradiation: Value
Platelet transfusion Causes of thrombocytopenia in cancer
The decision to transfuse platelets depends on many clinical factors including A)Platelets B)Clinical conditions of Pt.
Platelet transfusion guidelines 1- Well, stable 2-Procedures: 3- Signs/ symptoms: 1) Fever .2)Organomegaly, hypersplenisin 3-Medication- induceddysfunction. 4)APL (induction) 5)CNS metastasis 3) Bleeding
4- Coexisting lab abnormalities: 1)Hyper leukocytosis 2) rapid of pt count 3) Coagulation abnormalities 4) DIC, FDP
Recommendations regarding surgical or invasive procedures in Thrombocytopenia patients 1) B.M aspiration 2) Major or minor surgery 3) Placement of central venous access device
Dosage for platelet transfusion Infusion volumes and rates
Platelet refractoriness and alloimmunization a)Refractoriness Refractoriness is poor increasment in the post transfusion platelet count in the multiply transfused patient, obtained at 1 hr, 8 hr and 24hr after transfusion. Post transfusion platelet count The 1-hour corrected count increasement (CCI) is very useful and accurate determination of the response to pt transfusion.
Causes of platelet refractoriness: A) Immune causes: B) Non immune causes:
Pathogenesis of alloinmunization Leukocyte containing platelet preparations are the primary stimulus for alloimmunization. Primary HLA alloimmunization requires the recognition class I (Aclass II (DR) HLA antigens and recipient. Platelets do not express class II antigens and there is much evidence that passenger leukocytes in blood products are the primary cause of HLA alloimmunization..
Management of platelet alloimmunization Prophylaxis: treatment
Pharmacological adjuvant to platelet transfusion 1-Antifibrinolytic agent 2--Simple physical measure.
Therapeutic approaches to bleeding in thrombocytopenic patient 1) Clinical assessment 2) Transfusion intervention 3) Medication to treat or prevent bleeding:
Clinical recommendation of granulocyte transfusion: 1- No role for prophylactic G transfusion. 2- In severely neutropenic pt in whom neutrophil recovery is expected to be delayed by 3 weeks and in w' bacterial or fungal sepses is refractory to treatment.
Plasma transfusion: * Indications: Dosage Precautions
Indications: FFP Replacement of Coagulation Factors Abnormal Bleeding with coagulopathy Multiple factor deficiency: Liver disease DIC Isolated factor deficiency-no concentrate Factor VIII,XI, XIII
Guidelines: FFP Use Usual dosing: 10- 15ml/Kg Duration 15-20% rise in factor levels Usually does not correct laboratory coagulation status to “normal”
Cryoprecipitate 10-15 ml per unit (bag). Fibrinogen. 250 mg Factor VIII 80-120 units Von Willebrand Factor 40-70% of FFP Factor XIII 20-30% of FFP Fibronectin 20-40 mg
Cryoprecipitate: Dosing 1-2 Units / 10 Kg. Goal: Fibrinogen 70-100 mg/dl.
A-Immunological: 1-AHTR 2-Febrile non hemolytic 3-Allergic 4-TRALI B-Nonimmunologic 1-hemolysis 2-Air embolus 3-Hypocalcemia 4- Circulatory overload 4-Hypothermia s Acute complicatins
A- Immunologic 1-DHTR 2-Graft-versus-host disease (GVHD) 3-Post-transfusion purpura 4-Immuno-modulation B-Non immunologic 1-transmission of infection 2-iron overload Delayed reaction(>24h)
Acute Hemolytic transfusion reaction
Cause of Acute HTR source of error ABO incompatibility: 2-Group O plasma
Clinical picture Highly variable in acuity and severity. Fevers and/or chills. Hypotension. Dyspnea. Tachycardia. Pain. DIC. ARF. Shock
Acute Hemolysis: Diagnosis Do a direct antiglobulin test on post-transfusion sample Obtain post-transfusion blood and urine and inspect visually Recheck paperwork Recheck ABO type of unit and pre-and post-transfusion specimens Run urinalysis - to check for hemoglobinuria
Laboratory findings . Hemoglobinemia. Hemoglobinuria. LDH. Hyperbilirubinemia. Haptoglobin. BUN, creatinine in ARF. DAT +. Coagulation studies.
Response to Suspected Hemolytic reaction Stop Transfusion Hydrate Specimens to Blood Bank Unit/Bag Dopamine Consider Dialysis
2-Feberile non-hemolytic
Febrile non-hemolytic (FNHTR) Defined as a rise in temperature of 1°C or greater. Incidence PRBCs 0.5-6% Plts 1-38% Signs/Symptoms Chills/rigor Vomitting
Fevers/chills, non-hemolytic (FNHTR) Etiology Cytokines that accumulates in blood bag during storage Treatment/Prevention Discontinue transfusion? Acetaminophen Leukoreduced blood component
Allergic reaction Anaphylactic Rare Signs/Symptoms In addition to uritcarial/allergic… Cardiovascular instability Cardiac arrhythmia Shock More pronounced respiratory involvement Treatment
Transfusion-related acute lung injury (TRALI) What Is TRALI? Transfusion related noncardiogenic pulmonary edema Onset; within 6 hours (majority of cases during transfusion or within 2 hours of transfusion) Clinical presentation (“classic”, severe form) Acute respiratory distress Pulmonary edema Hypoxemia Hypotension
TRALI Pathogenesis Two current working model hypothesis Both models are directed against increase in pulmonary microvascular permeability Bioactive Lipids “Two-Hit” Model Leukocyte Antibody Pulmonary Microvascular Permeability Pulmonary Edema
Acute (< 24°) Non-Immunologic Circulatory overload Nonimmune hemolysis Air embolus Hypocalcemia Hypothermia
Delayed (> 24h) Immunologic
Delayed (> 24°) Immunologic Allo-immunization Hemolytic Graft-versus-host disease (GVHD) Post-transfusion purpura Immuno-modulation
DHTR • In the majority of cases, individual has been previously sensitized to (one or more) red cell antigens by previous transfusion Antibody is not detectable in routine pretransfusion testing, but the transfusion of blood containing the antigen