Complication of transfusion


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transfusion science course to be given for MSC student in Hematology

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Complication of transfusion

  1. 1. Transfusion Reaction Mulugeta Melku(BSC, MSC)
  2. 2. Objectives• At the end Analyse the adverse complication of blood transfusion Identify the major noninfectious complication of blood transfusion Explain the mechanisms of complication of blood transfusion Recognize transfusion transmitted infection
  3. 3. IntroductionTransfusion• can be autologous or AllogeneicAutologous transfusion: – is an alternative therapy for many patients anticipating transfusionCategories:1. Preoperative collection  blood is drawn and stored before anticipated need
  4. 4. Introduction cont’d2. Perioperative collection and administration A. Acute normovolemic Hemodilution  blood is collected at the start of surgery and then infused during or at the end of the procedure B. Intraoperative collection  shed blood is recovered from the surgical field or circulatory device and then infused C. Postoperative collection  blood is collected from drainage devices and re- infused to the patient
  5. 5. Introduction cont’d
  6. 6. Introduction cont’d• Autologous Blood DonationDisadvantages Does not eliminate risk of bacterial contamination Does not eliminate risk of incompatibility error Increased incidence of adverse reactions to autologous donation Subjects patients to perioperative anemia and increased likelihood of transfusion
  7. 7. Introduction cont’d• Allogeneic transfusion Between similar species Disadvantage – the risks of transmissible disease and transfusion reactions inherent in allogeneic transfusions. – Alloimmunization – GVHD – Post transfusion purpura – Circulatory over load
  8. 8. Introduction cont’d
  9. 9. Non-Infectious Complication of Transfusion
  10. 10. Complication Cont’dFour broad categories of transfusion reactions: – Acute immunologic – Acute nonimmunologic – Delayed immunologic, – Delayed non-immunologic complications pathophyiology, prevention and differential criteria
  11. 11. Complication Cont’dManifestation:• one should consider any adverse manifestation occurring at the time of the transfusion Fever with or without chills (rise of 1OC ) Shaking chills (rigors) with or without fever Pain at the infusion site or in the chest, abdomen Blood pressure changes Respiratory distress, including dyspnea, tachypnea, wheezing, or hypoxemia
  12. 12. Complication Cont’dSkin changes, including urticaria, pruritis (itching),flushing, or localized edemaNausea with or without vomitingDarkened urine or jaundiceBleeding or other manifestations of aconsumptive coagulopathy
  13. 13. Complication Cont’dAcute Transfusion Reactions(AHTR)Definition: An AHTR features rapid destruction of RBCs immediately after a transfusion But a hemolytic reaction occurring within 24 hours of the inciting transfusion is generally considered to be an AHTRCan be: • Immune-mediated Hemolysis • Non immune-mediated Hemolysis
  14. 14. Complication Cont’d A. Immune-mediated HemolysisPathophysiology and Manifestations The most severe hemolytic reactions Occur when transfused red cells interact with preformed antibodies in the recipient The interaction of transfused antibodies with the recipient’s red cells rarely causes symptoms. – there may be accelerated red cell destruction, and plasma-containing products with high-titer ABO antibodies can cause acute hemolysis
  15. 15. Complication Cont’dMechanisms – The interaction of antibody with antigen on the red cell membrane can initiate a sequence of complement activation, cytokine Classical pathway of C’ activation – IgM bind on RBC  Fc binds to complement – Membrane attack complex Severe symptoms can occur after the infusion of as little as 10 to 15 mL of ABO-incompatible red cells the initial manifestations of an acute HTR – hemoglobinuria, hypotension, or diffuse bleeding at the surgical site.
  16. 16. Complication Cont’dCause: – severe acute HTRs today are usually caused by ABO incompatibility – occasionally may be caused by antibodies with other specificities• In contrast, hemolysis of an entire unit of blood can occur in the virtual absence of symptoms and may be a relatively slow process – hemolysis is typically extravascular, without generation of significant systemic levels of inflammatory mediators
  17. 17. Complication Cont’dComplement Activation The binding of antibody to blood group antigens may activate complement, depending on the characteristics of both the antibody and the antigen o C3 activation releases the anaphylatoxin C3a o Red cells coated with C3b are removed by phagocytes with complement receptors, more rapidly than if antibody is present alone• enzymatic cascade proceeds to completion and a membrane attack complex is assembled, intravascular hemolysis results production of C5a
  18. 18. Complication Cont’d This sequence is characteristic of ABO incompatibility and causes the cardinal manifestations of hemoglobinemia  hemoglobinuria. hemoglobinuriaAnaphylatoxins Interact with a wide variety of cells [monocytes/macrophages, granulocytes, platelets, vascular endothelial cells, and smooth muscle cells ]hypotension and bronchospasm, cause the release or production of multiple local and systemic mediators [granule enzymes, histamine and other vasoactive amines, kinins, oxygen radicals, leukotrienes, nitric oxide, and cytokine] mimicking manifestation of allergy
  19. 19. Complication Cont’d• These events cause hypotension, Vasoconstriction and renal ischemia, and the activation of the coagulation systemCytokines They mediate some of the effects of alloimmune hemolysis stimulation of endothelial cells to increase expression of adhesion molecules and procoagulant activity, and recruitment and activation of neutrophils and platelets Vasodilatation: Hypotension And renal failure
  20. 20. Complication Cont’dCoagulation ActivationSeveral mechanisms may be responsible for abnormalities of coagulation in HTRs AB-Ag interaction activates intrinsic clotting cascade by Hageman factor(XII) activated Hageman factor (Factor XIIa) acts on the kinin system  bradykinin  bradykinin: vasoactive o Dilates arterioles, causing a decrease in systemic arterial pressure
  21. 21. Complication Cont’d  activated C’ cytokines, interleukin may increase the expression of tissue factor by leukocytes and endothelial cells• Tissue factor activates the “extrinsic”coagulation pathway DIC – formation of thrombi within the microvasculature and ischemic damage to tissues and organs – consumption of fibrinogen, platelets, and other coagulation factors – activation of the fibrinolytic system and generation of fibrin degradation productsGeneralized oozing or uncontrolled bleeding. bleeding
  22. 22. Complication Cont’dHow is could be Diagnosed ?Hypotension secondary manifestation of ischemia – Hypotension provokes a compensatory sympathetic nervous system response that produces Vasoconstriction in organs and tissues with a vascular bed rich in alpha- adrenergic receptors, renal, splanchnic, pulmonary, and cutaneous capillaries, aggravating ischemia in these sites Renal failure: Free hemoglobin AB-Ag deposition Thrombi formation
  23. 23. Complication Cont’dDifferential Diagnosispatients receiving transfusion therapy can develop a hemolysis from many sources – it is important to distinguish an AHTR from acute hemolysis of other causes. Most common cause of hemolysis in transfused patients improper storage of RBCs thermal injury, mechanical trauma, inappropriately mixed with hypotonic solutions or drugs, or contaminated by bacteria. Patients with congenital or acquired forms of hemolytic anemia may be incorrectly assumed to have had an AHTR • hereditary spherocytosis, sickle cell anemia, or RBC enzyme deficiency • coexistent microangiopathic hemolytic anemia • a patient with thrombotic thrombocytopenic purpura•
  24. 24. Complication Cont’d• Confirmation of the DiagnosisThe initial suspicious of AHTR Discontuation of transfusion and initiate lab investigation o Observation of post-transfusion plasma o Perform DAT o Inspect the blood bag o Repeat Pretransfusion testing
  25. 25. Complication Cont’d
  26. 26. Complication Cont’dNonimmune-Mediated HemolysisCausesRed cells may undergo in-vitro hemolysis – unit is exposed to improper temperatures – mishandled at the time of administration – Malfunctioning blood warmers, use of microwave ovens or hot water-baths, – inadvertent freezing may cause temperature-related damage – pressure infusion pumps, pressure cuffs, or small- bore needles
  27. 27. Complication Cont’dCauses cont’d – Osmotic hemolysis in the blood bag or infusion set – Inadequate deglycerolization of frozen red cells may cause the cells to hemolyze after infusion – Bacterial growth in blood units – intrinsic red cell defect of patient or donor has an, such as G-6-DH deficiency
  28. 28. Complication Cont’dFebrile Nonhemolytic transfusion Reactions(FNHTR)Pathophysiology and Manifestationsis often defined as: – a temperature increase of >1o C associated with transfusion and without any other explanation. – Such reactions are often associated with chills or rigorsCause• Non-leukocyte reduced red cell transfusions• Previous opportunities for alloimmunization• After platelet transfusion (1-38%
  29. 29. Complication Cont’d• Many febrile reactions are thought to result froman interaction between antibodies in the recipient’s plasma and antigens present on transfused lymphocytes, granulocytes, or platelets, most frequently HLA antigens
  30. 30. Complication Cont’dTransfusion-Related Acute Lung Injury (TRALI)Pathophysiology and ManifestationsTransfusion recipient  Experiences acute respiratory insufficiency and/or X-ray findings are consistent with bilateral pulmonary edema but has no other evidence of cardiac failure or a cause for respiratory failure• Defined acute lung injury (ALI) as a syndrome of: – acute onset; – hypoxemia – bilateral lung infiltrates on a chest x-ray; and – no evidence of circulatory overload.• New ALI occurring during transfusion or within 6 hours of completion
  31. 31. Complication Cont’d• Mechanisms – Donor antibodies directed against recipient HLA class I or II antigens, or neutrophil antigens of the recipient Sequence of events that increase the permeability of the pulmonary microcirculation high-protein fluid enters the interstitium and alveolar air spaces – Infrequently, antibodies in the recipient’s circulation against HLA or granulocyte antigens initiate the same events
  32. 32. Complication Cont’d→suggest that pulmonary edema in TRALI is caused by neutrophil-mediated endothelial damage, initiated by damage antibodies activating neutrophils directly or via activation of monocytes, pulmonary macrophages, and/or endothelial cells→ Complement activation after granulocyte transfusion→Anaphylatoxins C3a and C5a, aggregation of granulocytes into leukoemboli that lodge in the pulmonary microvasculature→Transfusion of cytokines that have accumulated in stored blood components→Reactive lipid products from donor blood cell membranes
  33. 33. Complication Cont’d Circulatory OverloadPathophysiology and Manifestations Transfusion therapy may cause acute pulmonary edema due to volume overload, and this can have severe consequences, including death• Rapid increases in blood volume are especially poorly tolerated by patients with compromised cardiac or pulmonary status and/or chronic anemia with expanded plasma volume
  34. 34. Complication Cont’d The infusion of 25% albumin, which shifts large volumes of extravascular fluid into the vascular space, may also cause circulatory overload. Hypervolaemia must be considered if dyspnea, cyanosis, severe headache, hypertension, or congestive heart failure occur during or soon after transfusion.
  35. 35. Complication Cont’d Coagulopathy in Massive Transfusion Pathophysiology• Of greater concern is the occurrence of coagulopathy during massive transfusion• Classically, this coagulopathy is ascribed – to dilution of platelets and clotting factors, which occurs as patients lose hemostatically active blood• The lost blood is initially replaced with red cells and fluids• progressive increase in the incidence of “microvascular bleeding” as a result of multiple transfusion of stored whole blood
  36. 36. Complication Cont’dDelayed Consequences of Transfusion
  37. 37. Complication Cont’dDELAYED HEMOLYTIC TRANSFUSION REACTIONSPathophysiology Primary alloimmunization, evidenced by the appearance of newly formed antibodies to red cell antigens, becomes apparent weeks or months after transfusion• DHTRs commonly occur in patients who have been immunized to foreign blood group antigens during previous transfusions and/or pregnancies – but the antibody decreases over time and is not detected in subsequent pretransfusion testing Transfusion of seemingly compatible blood stimulate Ab intr/extravascular hemolysis
  38. 38. Complication Cont’dDefinition and incidence accelerated destruction of transfused red cells that begins only when sufficient antibody has been produced as a result of an immune response induced by the transfusion most DHTRs share these characteristics – DHTRs generally occur in patients who have been alloimmunized to RBC antigens by previous transfusions or pregnancies – implicated antibody is not detected in pretransfusion antibody screening or compatibility testing
  39. 39. Complication Cont’dCharacteristics of DHTR– usually suspected 3 to 10 days after transfusion– DAT and/or a positive antibody screening test in post- transfusion testing– Antibodies directed against Rh (CEce) and Kidd (Jka, Jkb) system antigens are the antibodies most commonly implicated in DHTR
  40. 40. Complication Cont’dTransfusion-Associated Graft-versus-Host Disease• usually fatal immunologic transfusion complication caused by engraftment and proliferation of donor lymphocytes in a susceptible host• The engrafted lymphocytes mount an immunologic attack against the recipient tissues – hematopoietic cells, leading to refractory pancytopenia with bleeding and infectious complications
  41. 41. Complication Cont’d Pathophysiology and Manifestations Complex and incompletely understood. The overall mechanism includes – escape of donor T lymphocytes present in cellular blood components from immune clearance in the recipient and – subsequent proliferation of these cells, which then mount an immune attack on host tissues
  42. 42. Complication Cont’dManifestation The rash typically begins as a blanching, maculopapular erythema of the upper trunk, neck, palms, soles, and earlobes Factors that determine an individual patient’srisk for TA-GVHD – degree the recipient is immune status – the degree of HLA similarity between donor and recipient, and – the number and type of T lymphocytes transfused that are capable of multiplication
  43. 43. Complication Cont’dPost-transfusion Purpura Pathophysiology and Manifestations Uncommon event is characterized by the abrupt onset of severe thrombocytopenia (platelet count usually <10,000/μL) an average of 9 days after transfusion (range, 1-24 days) Most cases (68%) involve patients whose platelets lack the HPA-1a, HPA-1b and other HPA who form the corresponding antibody Alloantibodies destruction of patients own platelet
  44. 44. Complication Cont’d The reason for destruction of the patient’s own platelets by platelet alloantibody is controversial• Three mechanisms have been proposed – formation of immune complexes of patient antibody and soluble donor antigen that bind to Fc receptors on the patient’s platelets and mediate their destruction – conversion of antigen-negative autologous platelets to antibody targets by soluble antigen in the transfused component
  45. 45. Complication Cont’d– cross-reactivity of the patient’s antibodies with autologous platelets o the presence of an autoantibody componentBleeding after transfusion
  46. 46. Complication Cont’d Iron Overload Every RBC unit contains approximately 200 mg of iron Chronically transfused patients, especially those with hemoglobinopathies, have progressive and continuous accumulation of iron no physiologic means of excreting it Storage occurs initially in reticuloendothelial sites – when they are saturated, there is deposition in parenchymal cells• clinical damage is lifetime exposure to greater than 50 to 100 RBC units in a non-bleeding person
  47. 47. Complication Cont’d• Iron deposition interferes with function of the – heart, liver, and endocrine glands (eg, pancreatic islets, pituitary) Hepatic failure and cancer, diabetes mellitus, and cardiac toxicity cause most of the morbidity and mortality
  48. 48. Summary
  49. 49. ?