Adverse Effects Of Blood Transfusion

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Adverse Effects Of Blood Transfusion

  1. 1. Adverse Effects of Blood Transfusion By Dr G.P.Saluja Consultant Blood Bank Alchemist Hospital
  2. 2. Definition: Txn Rxn <ul><li>is any unfavorable transfusion-related event occurring in a patient during or after transfusion of blood components </li></ul>Definition : Txn Rxn
  3. 3. Objectives <ul><li>Early identification of common transfusion rxns. </li></ul><ul><li>Differentiate life threatening reactions from benign transfusion rxns. </li></ul><ul><li>Manage common immunologic tranx rxns. </li></ul>Objectives
  4. 4. Blood Transfusion reactions <ul><li>Classification </li></ul><ul><li>Acute ( Immediate) reactions: </li></ul><ul><li>Symptoms appear within minutes or up to 24 hrs post transfusion. </li></ul><ul><li>Delayed reactions : </li></ul><ul><li>Reactions occuring more than 24 hrs following transfusion ( up to months following) </li></ul>Blood Transfusion Reactions
  5. 5. Immediate and Delayed Transfusion Reaction 30/11/2549 MD-3 /49 Acute(Immediate) and Delayed Transfusion Reactions Immediate Delayed Immune Effects AHTR DHTR FNHTR Alloimmunization Allergic reaction PTP Anaphylaxis & anaphylactoid reaction TA-GVHD NCPE Immunosuppression Nonimmune Effects Bacterial contamination Iron overload TACO TTV Physical RBC damage Depletion & dilution of coagulation factors and platelets
  6. 6. Blood Transfusion reactions <ul><li>65% Incorrect Blood Component </li></ul><ul><li>10% Acute Transfusion Reaction </li></ul><ul><li>10% Delayed Transfusion Reaction </li></ul><ul><li>5% Transfusion Lung Injury </li></ul><ul><li>3% Post-transfusion purpura </li></ul><ul><li>3% Transfusion Transmitted Infection </li></ul><ul><li>1% Transfusion-GVHD </li></ul>Blood Transfusion Reactions
  7. 7. Acute hemolytic rxns <ul><li>Medical emergency </li></ul><ul><li>Occurs due to rapid transfused RBC destruction by </li></ul><ul><li>preformed recipients Abs </li></ul><ul><li>Mostly due to ABO incompatibility-typically type O </li></ul><ul><li>receiving non O blood. May occur with other blood </li></ul><ul><li>types </li></ul><ul><li>IgM mediated complement fixation leading to rapid intra </li></ul><ul><li>vascular hemolysis </li></ul><ul><li>Most common causes are clerical or procedural errors </li></ul><ul><li>Complications includes DIC, Hypotension and shock, </li></ul><ul><li>ARF & Death </li></ul><ul><li>As little as 10-15 mL can trigger a reaction </li></ul>Acute Hemolytic Rxns
  8. 8. Acute hemolytic rxns <ul><li>CLINICAL FEATURES </li></ul><ul><li>Classic presenting triad of Fever, flank pain and reddish brown urine from hemoglobinuria are rarely seen </li></ul><ul><li>Acute renal failure </li></ul><ul><li>Early signs </li></ul><ul><ul><li>- Anxiety </li></ul></ul><ul><ul><li>- Pain at infusion site </li></ul></ul><ul><ul><li>- Back/chest pain </li></ul></ul><ul><li>DIC may be presenting mode </li></ul><ul><li>Labs </li></ul><ul><li>Direct Coombs +, Pink plasma, Lactate, FDP in DIC </li></ul>Acute Hemolytic Rxns
  9. 9. Acute hemolytic rxns <ul><li>Laboratory investigation </li></ul>Sample from blood bag -> Repeat ABO, Rh, Ab Screening Patient sample Pre Tx sample -> Repeat ABO, Rh, Ab screening Post Tx sample -> Repeat ABO, Rh, Ab screening, DAT, CBC, UA, Bilirubin, BUN, Cr, Coagulation screening Repeat compatibility test - Pre Tx sample & Donor unit - Post Tx sample & Donor unit Acute Hemolytic Rxns
  10. 10. Acute hemolytic rxns <ul><li>Management </li></ul><ul><li>Primary concerns : </li></ul><ul><li>- vigorous treatment of hypotension </li></ul><ul><li>- promotion of renal blood flow </li></ul><ul><li>↓ </li></ul><ul><li>To prevent renal failure </li></ul>Acute Hemolytic Rxns
  11. 11. Acute hemolytic rxns <ul><li>Management </li></ul><ul><li>Stop transfusion </li></ul><ul><li>Infuse NS to maintain BP and promote diuresis (Frusemide), avoid LR and dextrose because calcium in LR will promote clotting in IV line and dextrose will increase hemolysis. Maintain urine output >100-200ml/hour </li></ul><ul><li>2. Supportive care; ABC +/-pressors </li></ul><ul><li>3. cardiac monitoring because of risk of hyperkalemia </li></ul>Acute Hemolytic Rxns
  12. 12. 30/11/2549 MD-3 /49 Management DIC ( Disseminated intravascular coagulation ) FFP Platelets Cryoprecipitate Heparin Acute hemolytic rxns Acute Hemolytic Rxns
  13. 13. Acute hemolytic rxns <ul><li>Prevention </li></ul><ul><li>Preventing or detecting errors in every phase of the transfusion process : </li></ul><ul><ul><ul><li>sample acquisition </li></ul></ul></ul><ul><ul><ul><li>at all steps in laboratory testing </li></ul></ul></ul><ul><ul><ul><li>at the time of issue </li></ul></ul></ul><ul><ul><ul><li>at the time of transfusion </li></ul></ul></ul><ul><li>Ensuring that all clinical staff recognize signs and symptoms of acute reaction </li></ul>Acute Hemolytic Rxns
  14. 14. Acute hemolytic rxns <ul><ul><li>Prevention </li></ul></ul><ul><li>Meticulously verify and document Pt ID from </li></ul><ul><li>sample collection for compatibility testing through </li></ul><ul><li>to blood component transfusion: </li></ul><ul><ul><ul><li>sample acquisition </li></ul></ul></ul><ul><ul><ul><li>at all steps in laboratory testing </li></ul></ul></ul><ul><ul><ul><li>at the time of issue </li></ul></ul></ul><ul><ul><ul><li>at the time of transfusion </li></ul></ul></ul><ul><li>Ensuring that all clinical staff recognize signs and </li></ul><ul><li>symptoms of acute reaction </li></ul><ul><li>Follow precisely the proper transfusion procedures </li></ul><ul><li>at bedside (usually found in Nursing SOP’s ) every </li></ul><ul><li>time – NO SHORTCUTS !!! </li></ul>Acute Hemolytic Rxns
  15. 15. Febrile Non-Haemolytic Transfusion Reaction (FNHTR) <ul><li>Determining factor is age of blood prDetermining factor is age of blood products </li></ul><ul><li>oducts </li></ul><ul><li>Definition </li></ul><ul><li>1 o C temperature rise associated with transfusion, no </li></ul><ul><li>medical explanation other than blood transfusion </li></ul><ul><li>Most common, usually benign without sequelae </li></ul><ul><li>Concerning because initial presentation is similar to more adverse rxns. i.e. fever, chills +/- mild dyspnea. </li></ul><ul><li>15% will have a rxn in the future with subsequent tranx </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Cytokine released from the transfused activated leucocytes </li></ul><ul><li>Determining factor is age of blood products </li></ul>Febrile Non-Hemolytic Txn Rxn (FNHTR)
  16. 16. Febrile Non-Hemolytic Txn Rxn (FNHTR) <ul><li>CLINICAL FEATURES </li></ul><ul><li>Fever after 30-90 minutes </li></ul><ul><li>± Rigors </li></ul><ul><li>± Headache </li></ul><ul><li>No Hypotension </li></ul><ul><li>No Bronchospasm </li></ul><ul><li>No Flank pain </li></ul><ul><li>No Haemoglobinaemia </li></ul><ul><li>No Haemoglobiurea </li></ul>
  17. 17. Febrile Non-Haemolytic Transfusion Reaction ( FNHTR) <ul><li>Management </li></ul><ul><li>If Temp < 40 + Stable patient: </li></ul><ul><ul><li>Stop transfusion </li></ul></ul><ul><ul><li>Antipyretics e.g. Paracetamol,( No rule of </li></ul></ul><ul><ul><li>Anti-histamines ) </li></ul></ul><ul><ul><li>Check the bag and cross match </li></ul></ul><ul><ul><li>Exclude red urine or red plasma </li></ul></ul><ul><ul><li>Resume transfusion at a slower rate </li></ul></ul><ul><ul><li>If recurrent: Leucodepleted transfusion in the future </li></ul></ul><ul><li>If Temp 40 or more + Unstable patient: </li></ul><ul><ul><li>Stop transfusion </li></ul></ul><ul><ul><li>Manage as possible acute haemolytic reaction till lab. Confirmation or exclusion </li></ul></ul>Febrile Non-Hemolytic Txn Rxn (FNHTR)
  18. 18. Febrile Non-Haemolytic Transfusion Reaction ( FNHTR) <ul><li>Prevention </li></ul><ul><li>using pre-storage leukocyte –reduced red </li></ul><ul><li>blood cell or platelet </li></ul><ul><li>Although antihistamine premedication is widely </li></ul><ul><li>used there is no evidence to support that its use </li></ul><ul><li>actually prevents rxn. </li></ul>Febrile Non-Hemolytic Txn Rxn (FNHTR)
  19. 19. Anaphylactic reactions <ul><ul><li>life threatening emergency </li></ul></ul><ul><li>Occurs within a few seconds to minutes following </li></ul><ul><li>transfusion of a few mL of blood </li></ul><ul><li>Characterized by rapid onset of bronchospasm </li></ul><ul><li>,respiratory distress and hypotension </li></ul><ul><li>Systemic symptoms, notably irritability, dyspnea, </li></ul><ul><li>hypotension, cynosis,convulsions,chest tightness </li></ul><ul><li>Initially mild but can progress to loss of </li></ul><ul><li>consciousness and in rare cases death. </li></ul><ul><li>Can occur with all blood products but generally </li></ul><ul><li>unseen with serum albumin, plasma protein </li></ul><ul><li>fractions or coagulation factors </li></ul>Anaphylactic Reactions
  20. 20. Anaphylactic and Anaphylactoid <ul><li>Anaphylaxis can range from mild urticaria to severe shock and death </li></ul><ul><li>Incidence </li></ul><ul><li>1 in 20-50 thousand </li></ul><ul><li>Mechanism </li></ul><ul><li>Presence of class specific IgG and anti IgA abs in pxts who are IgA def </li></ul><ul><li>Selective IgA def is fairly common, occurring in 1/300-500 people but majority of them do not develop Abs </li></ul>Anaphylactic And Anaphylatoid Reactions
  21. 21. Anaphylactic and Anaphylactoid rea <ul><li>Signs & Symptoms </li></ul><ul><li>- Anaphylactic  coughing, dyspnea, nausea, emesis, bronchospasm, flushing of skin, chest pain, hypotension, abdominal cramps, diarrhea, shock, and death. </li></ul><ul><li>- Anaphylactoid (less severe)  urticaria, periorbital swelling, dyspnea, or perilaryngeal edema </li></ul>Anaphylactic And Anaphylatoid Reactions
  22. 22. Anaphylactic And Anaphylatoid Reactions <ul><li>Treatment </li></ul><ul><li>stop tranx. </li></ul><ul><li>Keep IV line open. </li></ul><ul><li>epi 0.3ml of 1.1000 soln IM .Consider IV epinephrine drip </li></ul><ul><li>Steroids </li></ul><ul><li>ABC +/- pressor support </li></ul><ul><li>Prevention </li></ul><ul><li>Use IgA def products for all further tranx (extra washed red cells or platelets) </li></ul>
  23. 23. <ul><li>Probably the most frequent kind of reaction </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Allergen – Reagin (IgE,IgG) </li></ul><ul><li>complex </li></ul><ul><li>↓ </li></ul><ul><li>attach mast cell </li></ul><ul><li>↓ </li></ul><ul><li>histamine/leukotrienes </li></ul><ul><li>↓ </li></ul><ul><li>Allergic reactions </li></ul><ul><li>(urticaria) </li></ul>Urticarial Reactions
  24. 24. <ul><li>Signs & Symptoms </li></ul><ul><li>These reactions are usually mild, with urticaria, edema, occasional dizziness, and headache during or immediately after the transfusion. No fever or Hypotension </li></ul><ul><li>Not life threatening </li></ul><ul><li>Only rxn in which tranx can be resumed </li></ul><ul><li>Treatment </li></ul><ul><li>Stop Transfusion </li></ul><ul><li>Antihistamines </li></ul><ul><li>Resume Blood Transfusion </li></ul><ul><li>Prevention </li></ul><ul><li>Antihistamine </li></ul><ul><li>- Plasma – deficient blood components </li></ul>Urticarial Reactions
  25. 25. Transfusion Realted Lung Injury (TRALI) <ul><li>Syndrome of acute respiratory distress with </li></ul><ul><ul><li>Hypoxia ( po 2 < 60 or sats < 90%) </li></ul></ul><ul><ul><li>Bilateral non-cardiogenic pulmonary oedema </li></ul></ul><ul><ul><li>Hypo or Hypertension </li></ul></ul><ul><ul><li>± Fever </li></ul></ul><ul><ul><li>± Cyanosis </li></ul></ul><ul><ul><li>Sense of impending doom </li></ul></ul><ul><ul><li>Normal central venous pressures </li></ul></ul><ul><ul><li>Frothy endotracheal aspirate </li></ul></ul><ul><ul><li>Occurs within 1-6 hrs ( usually 1-2 hours) of recent Transfusion </li></ul></ul><ul><li>Exact Incidence not known but the second most common cause of transfusion associated death </li></ul>
  26. 26. Transfusion Realted Lung Injury (TRALI) <ul><li>Proposed Mechanism </li></ul><ul><li>HLA or granulocyte antibodies in donor plasma from immunization by Pregnancy/previous Transfusion </li></ul><ul><li>Biologically active lipids in donor plasma </li></ul><ul><li>Rarely recipient antibodies to transfused WBCs </li></ul><ul><li>Release of cytokines in lungs from from damaged WBCs </li></ul>
  27. 27. Transfusion Realted Lung Injury (TRALI) <ul><li>Patho-physiology </li></ul><ul><li>Leukocyte Ab in donor react with pt. leukocytes </li></ul><ul><li>↓ </li></ul><ul><li>Activate complements </li></ul><ul><li>Adherence of granulocytes to pulmonary endothelium with release of proteolytic enz. </li></ul><ul><li>& toxic O 2 metabolites </li></ul><ul><li>↓ </li></ul><ul><li>Endothelial damage </li></ul><ul><li>↓ </li></ul><ul><li>Interstitial oedema and fluid in Alveoli </li></ul>↓
  28. 28. Transfusion Realted Lung Injury (TRALI) <ul><li>Clinical Presentation </li></ul><ul><li>Acute onset of respiratory distress (hypoxemia) and non productive cough during or shortly after blood tranx. On the average within 1-2 hours post tranx </li></ul><ul><li>Fever, tachycardia, tachypnea, +/-hypotension </li></ul><ul><li>In intubated pxts; elevated peak airway pressures, pink frothy airway secretion </li></ul><ul><li>CXR bilateral patchy alveolar infiltrates or ‘white out’ , normal cardiac picture </li></ul><ul><li>Laboratory </li></ul><ul><li>eosinophilia and transient drop in neutrophils, Leuko-agglutinin testing </li></ul>
  29. 29. Transfusion Realted Lung Injury (TRALI) <ul><li>Diagnosis </li></ul><ul><li>Clinical presentation and CXR findings </li></ul><ul><li>Labs; granulocyte/ leuko-agglutinating abs, decline in C3 or C5 levels 12-36 hours after onset of symptoms followed by rise 4-7 days later </li></ul><ul><li>(a)Bilateral Patchy Alveolar infilterate In TRALI (b) Complete Resolution </li></ul>a b
  30. 30. Transfusion Realted Lung Injury (TRALI) <ul><li>Criteria for the diagnosis of TRALI </li></ul><ul><li>No acute lung injury immediately before </li></ul><ul><li>New acute lung injury: </li></ul><ul><li>1. Acute onset lung injury, </li></ul><ul><li>2. No circulatory overload or PA pressures <18mmHg, </li></ul><ul><li>3. Bilateral pulm infiltrate on Cxr, </li></ul><ul><li>4. Hypoxemia:Pa02/FiO2 <300, or sat <90% on RA. </li></ul><ul><li>Onset within 6 hours after transfusion </li></ul><ul><li>No temporal relation to an alternate risk factor for acute lung injury </li></ul>
  31. 31. Transfusion Realted Lung Injury (TRALI) <ul><li>Ddx includes </li></ul><ul><li>Acute fluid overload: ↑ JVP, ↑SBP and widened pulse pressure during dyspneic episode, ↑ pulm vascular markings on CXR </li></ul><ul><li>Hemolytic transfusion rxns </li></ul><ul><li>IgA mediated anaphylaxis in IgA def patients </li></ul>
  32. 32. Transfusion Realted Lung Injury (TRALI) <ul><li>Management </li></ul><ul><li>Stop Transfusion </li></ul><ul><li>Supportive care with abrupt resolution in symptoms within a few days. </li></ul><ul><li>Mech. ventilation required in about 75% cases </li></ul><ul><li>Diuretics probably not useful since it is a micro-vascular damage and not due to volume </li></ul><ul><li>steroids </li></ul><ul><li>Notify Blood Bank to allow proper testing and follow up of implicated donors </li></ul>
  33. 33. Transfusion Realted Lung Injury (TRALI) <ul><li>Prognosis </li></ul><ul><li>Increased risk of recurrence if they receive products from the implicated donor but no risk from other donors </li></ul><ul><li>Prevention: </li></ul><ul><li>Avoid donations from multiparous women and those who have received multiple transfusions </li></ul>
  34. 34. Acute Pyrogenic Txn Reactions <ul><li>CAUSE </li></ul><ul><li>Transfusion of bacterially contaminated blood components </li></ul><ul><li>Common problem for platelet concentrates stored at room temperature </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Bacteria growing in cold temperature </li></ul><ul><li>↓ </li></ul><ul><li>Produced endotoxin </li></ul>
  35. 35. Acute Pyrogenic Txn Reactions <ul><li>Trigger: Bacterial Pyrogens/Endotoxins in the transfused blood contaminated with cold-growing organisms as: </li></ul><ul><ul><li>Psudomonas </li></ul></ul><ul><ul><li>Yersinia </li></ul></ul><ul><ul><li>Some Staph </li></ul></ul><ul><li>Reactors: Patient Mono-nuclear Cells </li></ul><ul><li>Response: </li></ul><ul><ul><li>Cytokine Storm </li></ul></ul>
  36. 36. Acute Pyrogenic Txn Reactions <ul><li>Clinical Features </li></ul><ul><li>Like : </li></ul><ul><li>Acute Haemolytic reaction BUT: </li></ul><ul><ul><li>No Hemoglobinuria </li></ul></ul><ul><ul><li>No Hemoglobinaemia </li></ul></ul><ul><li>FNHTR BUT More Severe </li></ul><ul><ul><li>(Symptoms include fever, shock, & renal dysfunction- due to endotoxins, nausea, vomiting) </li></ul></ul><ul><li>Management </li></ul><ul><li>As Acute Haemolytic reaction </li></ul><ul><li>BUT </li></ul><ul><ul><li>Add Broad- spectrum Antibiotics </li></ul></ul><ul><ul><li>Obtain blood cultures from Pt </li></ul></ul>
  37. 37. Acute Circulatory Overload <ul><li>Patients at significant risk </li></ul><ul><li>Children </li></ul><ul><li>Elderly patients </li></ul><ul><li>Chronic anemia </li></ul><ul><li>Cardiac disease </li></ul><ul><li>Thalassemia major or Sickle cell disease </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Volume overload </li></ul><ul><li>↓ </li></ul><ul><li>Congestive heart failure </li></ul><ul><li>↓ </li></ul><ul><li>Pulmonary edema </li></ul>
  38. 38. Acute Circulatory Overload <ul><li>Symptoms and Signs </li></ul><ul><li>Dyspnea Headache </li></ul><ul><li>Coughing Restlessness </li></ul><ul><li>Cyanosis Tachycardia </li></ul><ul><li>Orthopnea Systolic Hypertension </li></ul><ul><li>Chest discomfort Increase > 50 mm Hg </li></ul>
  39. 39. Acute Circulatory Overload <ul><li>Acute cardiogenic pulmonary edema </li></ul><ul><li>In rapidly transfused, non-bleeding patients </li></ul><ul><li>More in infants, elderly or cardiac patients </li></ul><ul><li>D.D. from other Acute transfusion reactions: </li></ul><ul><li>No Fever ( DD from TRALI, FNHTR) </li></ul><ul><li>No red urine or plasma and Negative Coombs </li></ul><ul><li>( DD from Acute haemolytic reaction ) </li></ul>
  40. 40. Acute Circulatory Overload <ul><li>Management </li></ul><ul><li>Rapid reduction of hypervolemia </li></ul><ul><li>Respiratory and cardiac support </li></ul><ul><li>Oxygen therapy </li></ul><ul><li>Diuretics </li></ul><ul><li>+ Inotropics </li></ul><ul><li>Therapeutic phlebotomy </li></ul>
  41. 41. Acute Circulatory Overload <ul><li>Prevention </li></ul><ul><li>Use appropiate transfusion rate </li></ul><ul><li>Use appropiate blood components </li></ul><ul><li>PBRC to be given slowly over 4 hrs </li></ul><ul><li>Never exceed 2-3 ml/kg/hour Unless Bleeding </li></ul><ul><li>Pre-medicate with Diuretics in Cardiac or severely anemic patients </li></ul><ul><li>BT should be given during day time </li></ul>
  42. 42. Non immune Hemolysis <ul><li>Lysis of RBCs </li></ul><ul><li>as a result of storage, handling, or transfusion condition </li></ul><ul><li>Incidence </li></ul><ul><ul><li>Rare </li></ul></ul><ul><li>Signs/Symptoms </li></ul><ul><ul><li>Transient hemodynamic </li></ul></ul><ul><ul><li>Pulmonary impairment </li></ul></ul><ul><ul><li>Renal impairment </li></ul></ul><ul><ul><li>Hemoglobinemia and hemoglobinuria </li></ul></ul><ul><ul><li>Hyperkalemia (renal failure) </li></ul></ul><ul><ul><li>Fever </li></ul></ul>
  43. 43. Acute Circulatory Overload <ul><li>Differential diagnosis </li></ul><ul><ul><ul><li>Hemolytic </li></ul></ul></ul><ul><ul><ul><li>Autoimmune </li></ul></ul></ul><ul><ul><ul><li>Bacterial/sepsis </li></ul></ul></ul><ul><ul><ul><li>PNH, drug-induced, oxidative stress, etc. </li></ul></ul></ul><ul><ul><ul><li>Diagnosis of exclusion </li></ul></ul></ul><ul><li>Treatment/Prevention </li></ul><ul><ul><ul><li>Stop transfusion </li></ul></ul></ul><ul><ul><ul><li>Investigation of blood bag and tubing </li></ul></ul></ul><ul><ul><ul><li>Investigate for hemolytic transfusion rxn. </li></ul></ul></ul><ul><ul><ul><li>Check serum K </li></ul></ul></ul><ul><ul><ul><li>Supportive care </li></ul></ul></ul><ul><ul><ul><li>Maintain urine O/P (except for contraindication…i.e. renal failure) </li></ul></ul></ul>
  44. 44. Citrate Toxicity <ul><li>Cause : </li></ul><ul><li>Citrate is the anticoagulant used in blood products. It is usually rapidly metabolised by the liver. Rapid administration of large quantities of stored blood may cause hypocalcaemia and hypomagnesaemia when citrate binds calcium and magnesium. This can result in myocardial depression or coagulopathy. Patients most at risk are those with liver dysfunction or neonates with immature liver function having rapid large volume trans fusion </li></ul>
  45. 45. Citrate Toxicity Mild Moderate Severe Paresthias: -Perioral (Lips) -Peripheral (Fingertips) Lightheadedness Frank Tetany Muscle Cramps Laryngeal Spasm Weakness Seizures Chills Nausea Arrhythmia Shivering Vomiting Prolonged QT Interval “ Crawling Feeling” Chest Pain Bradycardia
  46. 46. Citrate Toxicity <ul><li>Management </li></ul><ul><ul><li>Slow the procedure (inlet rate) or temporarily stopping the transfusion allows citrate to be metabolised. </li></ul></ul><ul><ul><li>give calcium replacement p.o. or IV </li></ul></ul><ul><ul><li>cover with a warm blanket </li></ul></ul><ul><ul><li>reassure the patient </li></ul></ul><ul><li>If Severe: </li></ul><ul><ul><li>STOP the transfusion </li></ul></ul><ul><ul><li>Begin or continue IV calcium replacement </li></ul></ul><ul><ul><li>Notify MD and support team </li></ul></ul><ul><ul><li>Begin life support measures </li></ul></ul>
  47. 47. <ul><li>Cause: </li></ul><ul><li>Rapid infusion of large volumes of stored blood </li></ul><ul><li>contributes to hypothermia. Infants are particularly at risk during exchange or massive transfusion. </li></ul><ul><li>Prevention and Management </li></ul><ul><li>Appropriately maintained blood warmers for massive or exchange transfusion. </li></ul><ul><li>Additional measures include warming of other intravenous fluids and the use of devices to maintain patient body temperature. </li></ul>Hypothermia
  48. 48. Hyperkalaemia <ul><ul><li>Cause: </li></ul></ul><ul><ul><li>Stored red cells leak potassium proportionately throughout their storage life. Irradiation of red cells increases the rate of potassium leakage. Clinically significant hyperkalaemia can occur during rapid, large volume transfusion of older red cell units in small infants and children </li></ul></ul><ul><ul><li>Prevention: </li></ul></ul><ul><ul><li>Blood less than 7 days old is generally used for rapid large volume transfusion in small infants (eg cardiac surgery, ECMO, exchange transfusion ) </li></ul></ul>
  49. 49. Delayed Hemolytic Txn Rxn <ul><li>Generally occurs within 2-10 days of tranx </li></ul><ul><li>Usually occur in patients who have developed antibodies in the past, from transfusion or pregnacy or transplant and are undetectable when the patient is tested However, when patient receives a transfusion this can boost the production of antibodies which attach to RBCs. RBC’s are removed from Pt’s circulation by reticuloendothelial system (liver/spleen </li></ul><ul><li>Usually extra vascular and is less severe than acute </li></ul><ul><li>Other Abs often Rh , Kidd,Duffy and Kell </li></ul>
  50. 50. Clinical presentation Symptoms include Pyrexia low grade and Chills. Unexpected Falling HCT, slight increase in indirect bili, spherocytes on blood smear Diagnosis New +DAT and new Ab screening test when new blood is ordered Treatment None in the absence of rapid hemolysis Avoid offending Ag in future tranx Delayed Hemolytic Txn Rxn
  51. 51. Delayed Hemolytic Txn Rxn <ul><li>Prevention </li></ul><ul><li>Transfuse RBC’s that are phenotype </li></ul><ul><li>negative for known clinically significant </li></ul><ul><li>RBC antibodies in Pt </li></ul><ul><li>Delayed Hemolytic Trn Rxn’s can not be </li></ul><ul><li>predicted </li></ul><ul><li>Good Pt records and Blood Bank records </li></ul><ul><li>are essential </li></ul><ul><li>Clinical treatment usually not necessary </li></ul>
  52. 52. AlloImmunization <ul><li>Result from prior exposure to donor blood </li></ul><ul><li>components </li></ul><ul><li>Significant complication  even small amount of </li></ul><ul><li>blood </li></ul><ul><li>Adverse effects may include </li></ul><ul><ul><ul><li>difficulty in finding compatible blood </li></ul></ul></ul><ul><ul><ul><li>transfusion reaction </li></ul></ul></ul><ul><ul><ul><li>platelet refractoriness </li></ul></ul></ul>
  53. 53. AlloImmunization <ul><li>Patho-physiology </li></ul><ul><ul><ul><li>1 st exposure  moderate production IgM and IgG antibody by foreign antigens </li></ul></ul></ul><ul><ul><ul><li>2 nd exposure  rapid production of large amount of IgG </li></ul></ul></ul>
  54. 54. Alloimmunization <ul><li>Signs & Symptoms </li></ul><ul><ul><ul><li>mild  slight fever and Hb </li></ul></ul></ul><ul><ul><ul><li>severe  platelet refractoriness with bleeding </li></ul></ul></ul><ul><li>Therapy & Prevention </li></ul><ul><ul><ul><li>depends on type and severity </li></ul></ul></ul>
  55. 55. <ul><li>Patient at risk </li></ul><ul><li>Very rare (0.1-1%) complication seen in Immuno- compromised individuals </li></ul><ul><li>Bone marrow transplantation </li></ul><ul><li>Chemotherapy </li></ul><ul><li>Radiation treatment </li></ul><ul><li>Newborn </li></ul>Transfusion associated Graft Versus-Host Disease(Ta-GVHD)
  56. 56. Pathophysiology Infusion of Immuno-competent Cells (Lymphocyte) ↓ Patient at risk ↓ proliferation of donor T lymphocytes ↓ attack against patient tissue Patho-physiology Transfusion associated Graft Versus-Host Disease(Ta-GVHD)
  57. 57. Clinical presentation <ul><li>Skin: Swollen, erythroderma and bullae </li></ul><ul><li>formation& desquamation </li></ul><ul><li>- most common </li></ul><ul><li>GI: Diarrhea and abdominal cramps </li></ul><ul><li>Liver: Elevated LFT and </li></ul><ul><li>Hyperbilirubinemia </li></ul><ul><li>Heme: Bone marrow aplasia, persistent </li></ul><ul><li>thrombocytopenia </li></ul>Transfusion associated Graft Versus-Host Disease(Ta-GVHD) Skin manifestation of GVHD Generalized swelling, erythroderma and bullous formation
  58. 58. <ul><li>) </li></ul><ul><li>Implicated products </li></ul><ul><li>Non Irradiated whole blood </li></ul><ul><li>PRBC </li></ul><ul><li>Platelets </li></ul><ul><li>Granulocytes </li></ul><ul><li>Fresh non frozen plasma </li></ul><ul><li>It has not been seen with frozen deglycerolized RBC, FFP or Cryoprecipitate </li></ul>Transfusion associated Graft Versus-Host Disease(Ta-GVHD)
  59. 59. <ul><li>Treatment </li></ul><ul><li>Poor response to standard immunosuppressive therapies. corticosteroids, methotrexate, azathioprine,antithymocyte globulin. Thalidomide has been tried with variable success. </li></ul><ul><li>Prevention </li></ul><ul><li>Prevention is the Key since response to treatment is poor </li></ul><ul><li>Gamma irradiation and leuko-reduction of products </li></ul><ul><li>Avoid blood products from genetically identical donors </li></ul>Transfusion associated Graft Versus-Host Disease(Ta-GVHD)
  60. 60. Post-transfusion Purpura <ul><li>Rare complication </li></ul><ul><li>Rapid onset of thrombocytopenia as a result of anamnestic production of platelet alloantibody </li></ul><ul><li>Usually occurs in multiparous woman who do not have the antigen </li></ul><ul><li>About 5-10 days after being transfused with platelets, the platelet count drops <10,000/ μ L </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Platelet alloantibody (anti-PL A1 )  attach platelet </li></ul><ul><li>surface  destruction by RES </li></ul>
  61. 61. Post-transfusion Purpura <ul><li>Signs & Symptoms </li></ul><ul><ul><ul><li>Purpura and thrombocytopenia occur </li></ul></ul></ul><ul><ul><ul><li>Cerebral hemorrhage is a major concer </li></ul></ul></ul><ul><li>Therapy and Prevention </li></ul><ul><ul><ul><li>Corticosteroids </li></ul></ul></ul><ul><ul><ul><li>Exchange transfusion </li></ul></ul></ul><ul><ul><ul><li>Plasmapheresis </li></ul></ul></ul>
  62. 62. Iron Overload <ul><li>1 unit of PRCs has ~ 250 mg of Iron </li></ul><ul><li>Removed by body 1 mg / day </li></ul><ul><li>accumulate iron Hemosiderosis </li></ul><ul><li>iron accumulate Hemochromatosis </li></ul><ul><li>in tissue </li></ul>
  63. 63. Iron Overload <ul><li>Occurs in individuals who receive </li></ul><ul><li>multiple transfusions </li></ul><ul><li>Excess iron accumulates in </li></ul><ul><li>macrophages in various tissues (liver, </li></ul><ul><li>heart, endocrine glands) </li></ul><ul><li>It appears as dark brown granules in </li></ul><ul><li>the cells </li></ul><ul><li>May lead to organ failure </li></ul>
  64. 64. Iron Overload <ul><li>Signs & BCs </li></ul>Symptoms - muscle weakness, fatigue, weight loss, mild jaundice, anemia, mild diabetes, and cardiac arrhythmia Therapy  Iron – chelating agent Prevention  transfuse with young RBCs
  65. 65. <ul><li>A variety of infectious agents may be transmitted by transfusion </li></ul><ul><li>Definitive evidence of transmission by transfusion requires demonstration of seroconversion or new infection in the recipient and isolation of an agent with genomic identity from both the recipient and the implicated donor . </li></ul><ul><li>Strong presumptive evidence of transfusion transmission includes recipient seroconversion within an appropriate interval after transfusion, the recognition of appropriate infectious markers in an implicated donor on follow-up investigation, or both </li></ul>Transfusion transmitted diseases
  66. 66. Transfusion transmitted diseases <ul><li>l Infections </li></ul><ul><ul><ul><li>Hepatitis Viruses :- HBV, HCV </li></ul></ul></ul><ul><ul><ul><li>Retroviruses :- HIV </li></ul></ul></ul><ul><ul><ul><li>Herpesviruses :- CMV, EBV </li></ul></ul></ul><ul><ul><ul><li>Parvovirus :- Human B19 parvovirus </li></ul></ul></ul><ul><ul><ul><li>Prion :- infectious particle of CJD </li></ul></ul></ul>
  67. 67. Transfusion transmitted diseases <ul><li>Bacterial Infection </li></ul><ul><li>Gram negative and positive </li></ul><ul><li>Syphilis </li></ul><ul><ul><ul><li>Lyme Disease (Borrellosis) </li></ul></ul></ul><ul><li>Parasitic Infections </li></ul><ul><li>Malaria </li></ul><ul><li>Chagas disease </li></ul><ul><li>Toxoplasmosis </li></ul><ul><li>Leishmanisis </li></ul>
  68. 68. Transfusion transmitted diseases SEROLOGICAL TESTING HIV - Ag HIV - Ab HBsAg Anti-HCV Malaria Ag Antibodies to Treponema Pallidum(Syphilis)
  69. 69. Transfusion transmitted diseases Estimated risk of transfusion transmitted infection Virus and testing standard Window Period (Days) Point estimate of residual risk 'per unit' HIV 1 and 2 antibody only 22 1 in 2,404,000 1 in 7,299,000 HIV antibody + NAT 9 HCV antibody only 66 1 in 330,000 1 in 3,663,000 HCV antibody + NAT 7 HBV 45 1 in 1,339,000
  70. 70. Transfusion transmitted diseases Prevention <ul><li>Careful selection of Donors </li></ul><ul><ul><li>Exclude IVDU </li></ul></ul><ul><ul><li>Homosexuals/bisexuals </li></ul></ul><ul><ul><li>promiscuity </li></ul></ul><ul><ul><li>Other exposures e.g. visits to malaria areas </li></ul></ul><ul><li>Laboratory Screening </li></ul><ul><ul><li>HIV </li></ul></ul><ul><ul><li>HCV </li></ul></ul><ul><ul><li>HBsAg + Core Antibody </li></ul></ul><ul><ul><li>VDRL </li></ul></ul><ul><ul><li>Malaria </li></ul></ul><ul><li>Donor selection criteria and subsequent screening of all donations are designed to prevent disease transmission, but these do not completely eliminate the hazards </li></ul>
  71. 71. Concusion
  72. 72. <ul><li>Follow precisely the proper transfusion procedures at bedside (usually found in Nursing SOP’s ) every time – NO SHORTCUTS !!! </li></ul><ul><li>Transfusion reactions are mostly due to clerical errors and can range from benign to life threatening emergencies </li></ul><ul><li>Early detection, discontinuation of transfusion and instituting supportive care are key to management. </li></ul><ul><li>Reporting of all reactions helps to improve standard practices and reduce future occurrences. </li></ul><ul><li>FNHTR is a diagnosis of exclusion </li></ul><ul><li>Prevention methods – using filters, irradiation and premedication </li></ul>Concusion
  73. 73. TAKE CARE YOUR PATIENTS WITH BLOOD TRANSFUSION

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