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- 1. Blood Products &Transfusion Hani Sammour, MD, PB Anesthesia and IC, Shifa hospital Critical Care
- 2. Objectives • Definition andpreparation of blood components. • Indications for blood components transfusion. • Doses of blood components. • Complications of blood transfusion.
- 4. Use of atransfusion algorithm guided by appropriate laboratory testing, will reduce unnecessary transfusion of precious (and dangerous) blood components.
- 5. • There isa trend in major trauma care towards transfusing blood products in equal ratios early in resuscitation in order to prevent or correct trauma-induced coagulopathy. • This balanced approach to transfusion of blood products, 1:1:1 (one unit of FFP and one unit of platelets with each unit of PRBCs) is termed damage control resuscitation.
- 6. BLOOD GROUPS • Amongat least 20 blood group antigen systems in human red cell membranes, only the ABO and the Rh systems are important in the majority of blood transfusions. • Individuals often produce antibodies (alloantibodies) to the alleles they lack within each system. Such antibodies are responsible for the most serious reactions to transfusions.
- 7. The ABO System •ABO blood group typing is determined by the presence or absence of A or B red blood cell (RBC) surface antigens: – Type A blood has A RBC antigen. – Type B blood has B RBC antigen. – Type AB blood has both A and B RBC antigens. – Type O blood has neither A nor B RBC antigen present.
- 8. The Rh System •Patients with the D Rhesus antigen are considered Rh-positive and individuals lacking this antigen are called Rh-negative. Approximately 85% of the white population and 92% of the black population has the D antigen. • Rh-negative patients usually develop antibodies against the D antigen only after an Rh-positive transfusion or with pregnancy, in the situation of an Rh-negative mother delivering an Rh- positive baby.
- 9. Other Red BloodCell Antigen Systems • Other red cell antigen systems include Lewis, P, Ii, MNS, Kidd, Kell, Duffy, Lutheran, Xg, Sid, Car-tright, YK, and Chido Rodgers. Fortunately, with some exceptions (Kell, Kidd, Duffy, and Ss), alloantibodies against these antigens rarely cause serious hemolytic reactions.
- 10. COMPATIBILITY TESTING • Thepurpose of compatibility testing is to predict and to prevent antigen–antibody reactions as a result of red cell transfusions.
- 11. ABO–Rh Testing • Themost severe transfusion reactions are due to ABO incompatibility; naturally acquired antibodies can react against the transfused (foreign) antigens, activate complement, and result in intra-vascular hemolysis. • The patient’s red cells are tested with serum known to have antibodies against A and against B to determine blood type.
- 12. Cont. • The patient’sred cells are also tested with anti-D antibodies to determine Rh status. If the subject is Rh-negative, the presence of anti-D antibody is checked by mixing the patient’s serum against Rh- positive red cells.
- 13. Antibody Screen The purposeof this test is to detect in the serum the presence of the antibodies that are most commonly associated with non-ABO hemolytic reactions . The test also known as the indirect Coombs test, requires 45 min and involves mixing the patient’s serum with red cells of known antigenic composition; if specific antibodies are present, they will coat the red cell membrane, and subsequent addition of an antiglobulin antibody results in red cell agglutination. Antibody screens are routinely done on all donor blood and are frequently done for a potential recipient instead of a crossmatch.
- 14. Crossmatch • A crossmatchmimics the transfusion: donor red cells are mixed with recipient serum. • Crossmatching serves three functions: (1) It confirms ABO and Rh typing. (2) It detects antibodies to the other blood group systems. (3) It detects antibodies in low titers or those that do not agglutinate easily.
- 15. Type & Crossmatchversus Type & Screen • In the situation of negative antibody screen without crossmatch, the incidence of serious hemolytic reaction with ABO- and Rh-compatible transfusion is less than 1:10.000. • Crossmatching however, assures optimal safety and detects the presence of less common antibodies not usually tested for in a screen . • Because of the expense and time involved (45 min) crossmatches are often now performed before the need to transfuse only when the patient’s antibody screen is positive, when the probability of transfusion is high, or when the patient is considered at risk for alloimmunization.
- 16. EMERGENCY TRANSFUSIONS • Whena patient is exsanguinating, the urgent need to transfuse may arise prior to completion of a crossmatch, screen, or even blood typing. If the patient’s blood type is known, an abbreviated cross-match, requiring less than 5 min, will confirm ABO compatibility. • If the recipient’s blood type and Rh status is not known with certainty and transfusion must be started before determination, type O Rh-negative (universal donor) red cells may be used.
- 17. Definitions • Blood product:any therapeutic substance prepared from human blood. • Whole blood: Unseparated blood collected into an approved container containing an anticoagulant- preservative solution.
- 18. Blood component – Aconstituent of blood, separated from whole blood, such as: • Red cell concentrate • Plasma • Platelet concentrates – Cryoprecipitate, prepared from fresh frozen plasma.
- 19. Plasma derivative Human plasmaproteins prepared under pharmaceutical manufacturing conditions, such as: – Albumin. – Coagulation factor concentrates. – Immunoglobulins.
- 20. 1) Whole Blood •There have been few widely accepted indications for whole blood in modern transfusion practice. • Whole blood is not available from most blood banks in the United States. • Dose: 6 ml/kg of WB raise Hemoglobin level 1 g/dl. • One unit of WB will raise the hemoglobin of an average-size adult by ~ 1g/dl
- 21. Whole Blood • Duringdonation, blood is collected into a sterile, disposable, plastic pack which contains an anticoagulant- preservative solution. This solution usually contains citrate, phosphate, dextrose and often adenine (CPDA). • There are variations in the volume of blood collected and in the type of anticoagulant-preservative solution used in different regions of the world. • During storage, metabolism continues in the red cells and platelets, while some plasma proteins lose their biological activity.
- 22. Functions of anticoagulant-preservativesolution in blood collection pack Functions Solutions Binds with calcium ions in blood in exchange for the sodium salt so the blood does not clot C Sodium citrate Supports metabolism of the red cells during storage to ensure they release oxygen readily at tissue level P Phosphate Maintains the red cell membrane to increase storage life D Dextrose Provides energy source A Adenine
- 23. Effects of storageon whole blood • Reduction in the pH (blood becomes more acidic). • Rise in plasma potassium concentration (extracellular K+). • Progressive reduction in the red cell content of 2,3 diphosphoglycerate (2,3 DPG). • Loss of all platelet function in whole blood within 48 hours of donation. • Reduction in Factor VIII to 10–20% of normal within 48 hours of donation.
- 24. 2) Red BloodCells Packed RBCs are the commonly utilized blood product, providing oxygen-carrying capacity in cases most of acute or chronic blood loss.
- 25. Preparation of redcell concentrate
- 26. Cont. Advantages • Simple andinexpensive to prepare. Disadvantages • It has a high ratio of red cells to plasma (high viscosity) thereby increasing the time required for transfusion through a small gauge needle or cannula. • The white cells are a cause of febrile non-haemolytic transfusion reactions in some patients.
- 27. Leukocyte-depleted red cells •Special leukocyte filters can be used to remove virtually all the white cells. • The majority of red cells and platelet transfusions in the United States & UK are currently leukocyte reduced.
- 28. Cont. Advantages • Reduces acutetransfusion reactions. • Reduces cytomegalovirus infection (CMV). Disadvantages • Cost: special blood packs and equipment are required • More skill and operator training is needed.
- 29. PRBCs transfusion guidelines •Hemodynamic instability: Ongoing bleeding with unresponsive (or incompletely responsive) to infusion of 2- 3 Liters crystalloid • Hemodynamically Stable: • ICU Patients: Hemoglobin <7 g/dL • Post-Operative: Hgb ≤8 g/dL • Cardiovascular Disease: Hgb ≤8 g/dL
- 30. AABB transfusion guideline •A restrictive RBC transfusion threshold in which the transfusion is not indicated until the hemoglobin level is 7 g/dL is recommended for hospitalized adult patients who are hemodynamically stable, including critically ill patients, rather than when the hemoglobin level is 10 g/dL (strong recommendation, moderate quality evidence). • A restrictive RBC transfusion threshold of 8 g/dL is recommended for patients undergoing orthopedic surgery, cardiac surgery, and those with preexisting cardiovascular disease (strong recommendation, moderate quality evidence).
- 31. Cont. • The restrictivetransfusion threshold of 7 g/dL is likely comparable with 8 g/dL, but RCT evidence is not available for all patient categories. These recommendations do not apply to patients with acute coronary syndrome, severe thrombocytopenia (patients treated for hematological or oncological reasons who are at risk of bleeding), and chronic transfusion-dependent anemia (not recommended due to insufficient evidence).
- 32. AABB transfusion guideline •For RBC transfusion thresholds, 31 RCTs included 12,587 participants and compared restrictive thresholds (transfusion not indicated until the hemoglobin level is 7-8 g/dL) with liberal thresholds (transfusion not indicated until the hemoglobin level is 9-10 g/dL). The summary estimates across trials demonstrated that restrictive RBC transfusion thresholds were not associated with higher rates of adverse clinical outcomes, including 30-day mortality, myocardial infarction, cerebrovascular accident, rebleeding, pneumonia, or thromboembolism.
- 33. Cont. • For RBCstorage duration, 13 RCTs included 5515 participants randomly allocated to receive fresher blood or standard-issue blood. These RCTs demonstrated that fresher blood did not improve clinical outcomes.
- 34. Cont. • Dose: 4ml/kg of RBC increase Hemoglobin level 1 g/dl. • One unit of RBC will raise the hemoglobin of an average-size adult by ~ 1g/dl • Transfuse slowly for first 15 minutes. • Complete transfusion within 4 hours.
- 35. 3) White cells(leukocytes) • White cell transfusions have no proven clinical uses. • May be indicated in neutropenic patients with bacterial infections not responding to antibiotics. • Transfused granulocytes have a very short circulatory life span, so that daily transfusions of 10 10 granulocytes are usually required.
- 36. 4) Plasma • Thisis separated from whole blood and frozen at –25°C or colder within 6–8 hours of donation in order to preserve its labile coagulation factors (Factors V and VIII). • Fresh frozen plasma can be stored for at least one year or longer if low temperatures can be maintained. • When plasma is stored at a temperature of 2–6°C, the labile clotting activity of Factors V and VIII will decline to 10–20% within 48 hours. • Dosage: Initial dose of 15 ml/kg
- 37. Indications for transfusionof plasma • International normalized ratio (INR) >1.5 with: – Anticipated invasive procedure or surgery. – Massive hemorrhage (over one blood volume) • Emergent reversal of anticoagulant (warfarin) therapy. • Treatment of isolated factor deficiencies. • The correction of coagulopathy associated with liver disease.
- 38. Indications for transfusionof plasma Coagulopathy (INR) >1.5 with: 1. Active bleeding. 2. Bleeding tendency: • Anticipated invasive procedure or surgery. • The correction of coagulopathy associated with liver disease. • Emergent reversal of anticoagulant (warfarin) therapy. • Treatment of isolated factor deficiencies.
- 39. 5) Platelet • Theplatelet count at 1 hour post transfusion of a unit of platelets should increase by 5,000 to 10,000 platelets/µL. • Platelets separated from plasma obtained from 4–6 donations of whole blood are often pooled to produce a therapeutic dose of platelets for an adult platelet apheresis unit, by 30,000–60,000 × 10 9/L. • Dosage: 1 unit of platelet concentrate/10 kg body weight
- 40. Indications for transfusionof platelets Thrombocytopenia or Dysfunctional platelets with: 1. Active bleeding 2. Bleeding tendency • Neurosurgical procedures: 100,000 platelets/µL • Vaginal delivery and minor surgical procedures: <50,000/µL • Massive transfusion: < 50,000 platelets/µL • Disseminated intravascular coagulation: 20,000–50,000 /µL
- 41. 6. Cryoprecipitate • Cryoprecipitateis obtained from a single donation of FFP at about 4°C and is rich in factor VIII, von Willebrand factor (VWF), factor XIII, and fibrinogen. • Cryoprecipitate is usually administered as a transfusion of 10 single units. • Each 5- to 15-mL unit contains over 80 units of factor VIII and about 200 mg of fibrinogen.
- 42. Indications for transfusionof cryoprecipitate • Hemophilia A • von Willebrand disease • Hypofibrinogemia • Uremic bleeding
- 43. Component separation byapheresis • Apheresis is an alternative method of producing blood components. It is a sterile process in which a donor is connected to a specialized device by which blood is withdrawn, mixed with anticoagulant and centrifuged and a specific component, usually plasma or platelets, is mechanically separated and collected. • The red cells and other components of the blood that are not required are then reinfused back into the donor.
- 44. Cont. • The advantageof apheresis is that relatively large amounts of plasma or platelets can be collected from a donor. • Since the red cells are returned to the donor’s circulation, this avoids making the donor anemic and the process can be repeated at frequent intervals.
- 45. Blood Component Characteristic RedCells Platelet Concentrate Fresh Frozen Plasma Cryoprecipita te Storage Temperature 2-6°C 20-24°C -30°C -30°C Shelf Life Volume 35 day 200-350 5 day 30-50 ml/unit 1 yr (frozen) 150-200ml/unit 1 yr (frozen) 10-15 ml/unit Transfusion Interval Transfuse within 30 min of removal from blood refrigerator. Transfuse unit over maximum of 4 hr Start transfusion as soon as received from blood bank. Transfuse unit within 30 min Once thawed, should be transfused within 4 hr 884 hr Compatibility Testing Requirement Must be compatible with recipient ABO and Rh D type Preferably ABO identical with patient. Rh negative females under the age of 45 yr should be given Rh negative platelets FFP and cryoprecipitate should be ABO compatible to avoid risk of hemolysis caused by donor anti-A or anti-B Administration Infuse through a blood administration set—platelet concentrates should not be infused through blood sets that have been used for blood.
- 46. Complications of BloodTransfusion 1) IMMUNE Complications. 2) INFECTIOUS Complications. 3) MASSIVE BLOOD TRANSFUSION Complications.
- 47. Complications of BloodTransfusion 1) IMMUNE Complications – Hemolytic reactions • Acute hemolytic reaction. • Delayed hemolytic reaction. – Nonhemolytic reactions • Febrile reactions • Urticarial reactions • Anaphylactic reactions • Post-transfusion purpura • Transfusion-Related Acute Lung Injury • Graft-versus-host disease
- 48. Complications of BloodTransfusion 2) Infectious (all products)
- 49. Complications of BloodTransfusion 3) Complications of massive blood transfusion – Coagulopathy – Hypothermia – Citrate Toxicity – Acid–Base Balance – Serum Potassium Concentration
- 50. IMMUNE COMPLICATIONS Immune complicationsfollowing blood transfusions are primarily due to sensitization of the recipient to donor red cells, white cells, platelets, or plasma proteins. Less commonly, the transfused cells or serum may mount an immune response against the recipient.
- 51. Immune complications • Acutehemolytic transfusion reaction: ABO incompatibility. • Delayed HTR: incompatible red cell antigen. • Febrile non-HTR: anti-WBC antibodies in recipient. • Urticarial reactions: antibody to donor plasma proteins. • Anaphylactic: antibody to donor plasma proteins (IgA). • Transfusion-related acute lung injury (TRALI): neutrophil antibodies in donor product.
- 52. Hemolytic Reactions • Hemolyticreactions usually involve specific destruction of the transfused red cells by the recipient’s antibodies. Less commonly, hemolysis of a recipient’s red cells occurs as a result of transfusion of red cell antibodies. • Hemolytic reactions are commonly classified as either acute (intravascular) or delayed (extravascular).
- 53. Acute Hemolytic Reactions •Acute intravascular hemolysis is usually due to ABO blood incompatibility, and the reported frequency is approximately 1:38,000 transfusions. • The most common cause is misidentification of a patient, blood specimen, or transfusion unit. • These reactions are often severe, and may occur after infusion of as little as 10–15 mL of ABO-incompatible blood. • The risk of a fatal hemolytic reaction is about 1 in 100,000 transfusions. • In awake patients, symptoms include chills, fever, nausea, and chest and flank pain.
- 54. Cont. • In anesthetizedpatients, an acute hemolytic reaction may be manifested by a rise in temperature, unexplained tachycardia, hypotension, hemoglobinuria, and diffuse oozing in the surgical field. Disseminated intravascular coagulation, shock, and kidney failure can develop rapidly. • The severity of a reaction often depends upon the volume of incompatible blood that has been administered.
- 55. Management of hemolyticreactions 1. If a hemolytic reaction is suspected, the transfusion should be stopped immediately and the blood bank should be notified. 2. The unit should be rechecked against the blood slip and the patient’s identity bracelet. 3. Blood should be drawn to identify hemoglobin in plasma, to repeat compatibility testing, and to obtain coagulation studies and a platelet count. 4. A urinary catheter should be inserted, and the urine should be checked for hemoglobin. 5. Osmotic diuresis should be initiated with mannitol and intravenous fluids.
- 56. Delayed Hemolytic Reactions Alsocalled extravascular hemolysis, is generally mild and is caused by antibodies to non-D antigens of the Rh system or to foreign alleles in other systems such as the Kell, Duffy, or Kidd antigens. Following an ABO and Rh D-compatible transfusion, patients have a 1–1.6% chance of forming antibodies directed against foreign antigens in these other systems.
- 57. Cont. • The hemolyticreaction is therefore typically delayed 2–21 days after transfusion, and symptoms are generally mild, consisting of malaise, jaundice, and fever. • The patient’s hematocrit typically fails to rise, or rises only transiently, in spite of the transfusion and the absence of bleeding. • The serum unconjugated bilirubin increases as a result of hemoglobin breakdown.
- 58. Cont. • Diagnosis ofdelayed antibody-mediated hemolytic reactions may be facilitated by the antiglobulin (Coombs) test. The direct Coombs test detects the presence of antibodies on the membrane of red cells. • Pregnancy (exposure to fetal red cells) can also be responsible for the formation of alloantibodies to red cells. • The frequency of delayed hemolytic transfusion reactions is estimated to be approximately 1:12,000 transfusions. • The treatment of delayed hemolytic reactions is primarily supportive.
- 59. Nonhemolytic Immune Reactions •Nonhemolytic immune reactions are due to sensitization of the recipient to the donor’s white cells, platelets, or plasma proteins. • The risk of these reactions may be minimized by the use of leukoreduced blood products.
- 60. Nonhemolytic Immune Reactions A-Febrile Reactions: • White cell or platelet sensitization is typically manifested as a febrile reaction. • Such reactions are relatively common (1–3% of transfusion episodes) and are characterized by an increase in temperature without evidence of hemolysis. • Patients with a history of repeated febrile reactions should receive leukoreduced transfusions only.
- 61. Cont. B- Urticarial Reactions: •Urticarial reactions are usually characterized by erythema, hives, and itching without fever. • They are relatively common (1% of transfusions) and are thought to be due to sensitization of the patient to transfused plasma proteins. • Urticarial reactions can be treated with antihistaminic drugs (H1 and perhaps H2- blockers) and steroids.
- 62. Cont. C- Anaphylactic Reactions: •Anaphylactic reactions are rare (approximately 1:150,000 transfusions). • These severe reactions may occur after only a few milliliters of blood has been given, typically in IgA-deficient patients with anti-IgA antibodies who receive IgA-containing blood transfusions. • The prevalence of IgA deficiency is estimated to be 1:600-800 in the general population. • Such reactions require treatment with epinephrine, fluids, corticosteroids, and H1 and H2 blockers.
- 63. Cont. D- Transfusion-Related AcuteLung Injury (TRALI) : • (TRALI) presents as acute hypoxia and noncardiac pulmonary edema occurring within 6 h of blood product transfusion. • It may occur as frequently as 1:5000 transfused units, and with transfusion of any blood component, but especially platelets and FFP. • It is thought that transfusion of antileukocytic or anti-HLA antibodies results in damage to the alveolar–capillary membrane. • Treatment is similar to that for acute respiratory distress syndrome with the important difference that TRALI may resolve within a few days with supportive therapy.
- 64. Cont. E- Graft-Versus-Host Disease: •This type of reaction may be seen in immunocompromised patients. Cellular blood products contain lymphocytes capable of mounting an immune response against the compromised (recipient) host. • Use of special leukocyte filters alone does not reliably prevent graft -versus-host disease; irradiation(1500–3000 cGy) of red cell, granulocyte, and platelet transfusions effectively eliminates lymphocytes without altering the efficacy of such transfusions.
- 65. Cont. F- Post-Transfusion Purpura: •Rarely, profound thrombocytopenia may occur following blood transfusions. • This post-transfusion purpura results from the development of platelet alloantibodies. • For unknown reasons, these antibodies also destroy the patient’s own platelets. • The platelet count typically drops precipitously 5–10 days following transfusion. • Treatment includes intravenous IgG and plasmapheresis.
- 66. Cont. G- Transfusion-Related Immunomodulation: •Allogeneic transfusion of blood products may diminish immunoresponsiveness and promote inflammation. • Post-transfusion immunosuppression is clearly evident in renal transplant recipients, in whom preoperative blood transfusion improves graft survival.
- 67. INFECTIOUS COMPLICATIONS A- ViralInfections: Hepatitis: • The incidence of post-transfusion viral hepatitis varies greatly, from approximately 1:200,000 transfusions (for hepatitis B) to approximately 1:1,900,000 (for hepatitis C). • Most acute cases are anicteric. Hepatitis C is the more serious infection; most cases progress to chronic hepatitis, with cirrhosis developing in 20% of chronic carriers and hepatocellular carcinoma developing in up to 5% of chronic carriers.
- 68. Cont. Acquired Immunodeficiency Syndrome(AIDS): • The virus responsible AIDS, HIV-1, is transmissible by blood transfusion. HIV-2 is a similar, but less virulent virus. • All blood is tested for the presence of anti-HIV-1 and anti-HIV- 2 antibodies. The requirement for nucleic acid testing by the Food and Drug Administration (FDA) has decreased the risk of transfusion-transmitted HIV to approximately 1:1,900,000 transfusions.
- 69. Cont. Other Viral Infections: •Cytomegalovirus (CMV) and Epstein–Barr virus usually cause asymptomatic or mild systemic illness. • Some individuals infected with these viruses become asymptomatic infectious carriers; the white cells in blood units from such donors are capable of transmitting either virus. • Immunocompromised and immunosuppressed patients (eg, premature infants, organ transplant recipients, and cancer patients) are particularly susceptible to severe transfusion- related CMV infections.
- 70. Cont. B- Parasitic Infections: •Parasitic diseases that can be transmitted by transfusion include malaria, toxoplasmosis, and Chagas’ disease. Such cases are very rare.
- 71. Cont. C- Bacterial Infections: •Bacterial contamination of blood products is the second leading cause of transfusion-associated mortality. • The prevalence of positive bacterial cultures in blood products ranges from 1:2000 for platelets to 1:7000 for PRBCs and may be due to transient donor bacteremia or inadequate antisepsis during phlebotomy. • The prevalence of sepsis due to blood transfusion ranges from 1:25,000 for platelets to 1:250,000 for PRBCs. Both gram-positive (Staphylococcus) and gram-negative (Yersinia and Citrobacter) bacteria can contaminate blood transfusions and transmit disease. To avoid the possibility of significant bacterial contamination, blood products should be administered over a period shorter than 4 h.
- 73. MASSIVE BLOOD TRANSFUSION •Massive transfusion, historically defined as the replacement by transfusion of 10 units of red cells in 24 hours, is a response to massive and uncontrolled hemorrhage (Uptodate). • Massive blood transfusion may be defined either as the acute administration of more than 1.5 times the patient's estimated blood volume, or as the replacement of the patient's total blood volume by stored homologous bank blood in less than 24 h (British Journal of Anaesthesia).
- 74. Cont. Various definitions ofmassive blood transfusion (MBT) have been published in the medical literature such as: • Replacement of one entire blood volume within 24 h • Transfusion of >10 units of packed red blood cells (PRBCs) in 24 h • Transfusion of >20 units of PRBCs in 24 h • Transfusion of >4 units of PRBCs in 1 h when on-going need is probable • Replacement of 50% of total blood volume (TBV) within 3 h.
- 75. Complications of massiveblood transfusion • Coagulopathy • Hypothermia • Citrate Toxicity • Acid–Base Balance: • Serum Potassium Concentration
- 76. Complications of massiveblood transfusion • Coagulopathy The most common cause of nonsurgical bleeding following massive blood transfusion is dilutional thrombocytopenia, although clinically significant dilution of coagulation factors may also occur. Coagulation studies and platelet counts, if readily available, should guide platelet and FFP transfusion.
- 77. BJA: British Journalof Anaesthesia, Volume 111, Issue suppl_1, December 2013, Pages i71–i82, https://doi.org/10.1093/bja/aet376 The content of this slide may be subject to copyright: please see the slide notes for details. Pathogenesis of haemostasis abnormality in MT. Dilutional coagulopathy, activation of inflammatory mediators.
- 78. Cont. Hypothermia • Massive bloodtransfusion is an absolute indication for warming all blood products and intravenous fluids to normal body temperature. • Ventricular arrhythmias progressing to fibrillation often occur at temperatures close to 30°C, and hypothermia can hamper cardiac resuscitation. • The use of rapid infusion devices with efficient heat transfer capability has decreased the incidence of transfusion-related hypothermia.
- 79. Cont. Citrate Toxicity • Becausecitrate metabolism is primarily hepatic, patients with hepatic disease or dysfunction (and possibly hypothermic patients) may demonstrate hypocalcemia and require calcium infusion during massive transfusion, as may small children and others with relatively impaired parathyroid–vitamin D function. • Clinically important hypocalcemia, causing cardiac depression, will not occur in most normal patients unless the transfusion rate exceeds 1 unit every 5 min, and intravenous calcium salts should rarely be required in the absence of measured hypocalcemia.
- 80. Cont. Acid–Base Balance: • Althoughstored blood is acidic due to the citric acid anticoagulant and accumulation of red cell metabolites (carbon dioxide and lactic acid), metabolic acidosis due to transfusion is uncommon because citric acid and lactic acid are rapidly metabolized to bicarbonate by the normal liver. • In the situation of massive blood transfusion, acid-base status is largely dependent upon tissue perfusion, rate of blood transfusion, and citrate metabolism. • Once normal tissue perfusion is restored, any metabolic acidosis typically resolves, and metabolic alkalosis commonly occurs as citrate and lactate contained in transfusions and resuscitation fluids are converted to bicarbonate by the liver.
- 81. Cont. Serum Potassium Concentration: •The extracellular concentration of potassium in stored blood steadily increases with time. The amount of extracellular potassium transfused with each unit is typically less than 4 mEq per unit. • Hyperkalemia can develop regardless of the age of the blood when transfusion rates exceed 100 mL/min. • Hypokalemia is commonly encountered postoperatively, particularly in association with metabolic alkalosis.
- 82. Cost of bloodcomponents Netherland 2011 USA 2008 UK 2001 Product € 210 300 $ 82.5 £ Red cells (leucocyte depleted) € 102 233 $ £ 156 Platelets (leucocyte depleted) € 181 160 $ £ 19 Fresh frozen plasma (leucocyte depleted) 117 $ £ 23 Cryoprecipitate (leucocyte depleted)
- 84. Compatible fluids andmedications • No medications or solutions should be added to or infused through the same tubing as blood products except for 0.9% Sodium Chloride, ABO compatible plasma or 4% Albumin. • It has been shown to be safe to co-administer morphine (1mg/mL), pethidine (10mg/mL) and ketamine (1mg/mL) if diluted in 0.9% Sodium Chloride with red cells. In these situations, the blood product should be administered via the closest to the patient (distal lumen).
- 85. Cont. • If othermedications are required during a blood transfusion, the transfusion must be stopped and the line flushed with 0.9% Sodium Chloride before and after administration of the medication. The blood transfusion can then recommence. • Fluids containing glucose are not compatible with red blood cells, they cause clumping of the red blood cells. • Crystalloid or colloid solutions that contain calcium should never be administered concurrently with any blood product. Calcium reverses the anticoagulant citrate causing red blood cells to clot.
- 86. References • Morgan andMikhail's Clinical Anesthesiology, 6th edition • The Clinical Use of Blood - World Health Organization • Uptodate.com 2019
Editor's Notes
- #25 In theory, the goals of oxygen delivery and volume expansion can be achieved with packed RBCs and crystalloid solutions
- #36 Transfused granulocytes have a very short circulatory life span, so that daily transfusions of 10 10 granulocytes are usually required.
- #37 Plasma is separated from whole blood by centrifugation or by allowing the red cells to settle under gravity in a blood bank refrigerator.
- #53 Incompatible units of platelet concentrates, FFP, clotting factor concentrates, or cryoprecipitate may contain small amounts of plasma with anti-A or anti-B (or both) alloantibodies. Transfusions of large volumes of such units can lead to intravascular hemolysis.
- #57 By the time significant amounts of these antibodies have formed (weeks to months), the transfused red cells have been cleared from the circulation. Moreover, the titer of these antibodies subsequently decreases and may become undetectable.
- #58 Reexposure to the same foreign antigen during a subsequent red cell transfusion, however, triggers an anamnestic antibody response against the foreign antigen.
- #59 In this setting, however, this test cannot distinguish between recipient antibodies coated on donor red cells and donor antibodies coated on recipient red cells. The latter requires a more detailed reexamination of pretransfusion specimens from both the patient and the donor.
- #72 Specific bacterial diseases rarely transmitted by blood transfusions from donors include syphilis, brucellosis, salmonellosis, yersiniosis, and various rickettsioses.
- #77 Although most clinicians will be familiar with “routine” coagulation tests (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], international normalized ratio [INR], platelet count, fibrinogen), multiple studies show that viscoelastic analysis of whole blood clotting (thromboelastography, rotation thromboelastometry, and Sonoclot analysis) may be more useful in resuscitation, liver transplantation, and cardiac surgical settings.
- #78 Fig 1 Pathogenesis of haemostasis abnormality in MT. Dilutional coagulopathy, activation of inflammatory mediators, hyperfibrinolysis, thrombocytopathy, and metabolic abnormalities (hypothermia, hypocalcaemia, and acidosis) all contribute to the pathogenesis of the haemostasis abnormality in massive haemorrhage. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected]