Blood transfusion & its component therapy


Published on

blood coagulation,transfusion & its component therapy

Published in: Health & Medicine, Business
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Blood transfusion & its component therapy

  1. 1. Blood coagulation & its component therapy Dr. Anup kumar Harichandan PG, 2nd yr
  2. 2. • Eighty percent of the world's population has access to only 20% of the world's “safe” blood, that is blood that is properly collected and tested. • Only 30% of the world's countries have a nationwide transfusion service. • The anesthesiologist should be an expert on the implications and the complications associated with blood transfusions and should be a leader of acute transfusion medicine in the hospital setting as approx. 70% of blood transfusions carried by them.
  3. 3. Indications for Transfusion Allogeneic (Homologous) Blood • Blood transfusions are given to increase oxygen- carrying capacity and intravascular volume. • Theoretically, increasing vascular volume is not an indication for blood transfusions because volume can be augmented with administration of fluids that do not transmit infections (e.g., crystalloids or some colloids). • On the practical side, when a patient is hemorrhaging, blood is given to increase oxygen- carrying capacity and intravascular volume.
  4. 4. • The goals should be to restore intravascular volume, cardiac output, and organ perfusion to normal levels. • But by using crystalloids and/or colloids to treat hypovolemia, normovolemic dilutional anemia will be created. • Thus,Increasing oxygen-carrying capacity is the only real indication for blood transfusions.
  5. 5. American College of Surgeons' Classes of Acute Hemorrhage Factors Class I Class II Class III Class IV Blood loss (mL) 750 750-1500 1500-2000 2000 or more Blood loss (% blood volume) 15 15-30 30-40 40 or more Pulse (beats/min) 100 100 120 140 or higher Blood pressure Normal Normal Decreased Decreased Pulse pressure (mm Hg) Normal or increased Decreased Decreased Decreased Capillary refill test Normal Positive Positive Positive Respirations per minute 14-20 20-30 30-40 35 Urine output (mL/hr) 30 20-30 5-10 Negligible Central nervous system: mental status Slightly anxious Mildly anxious Anxious, confused Confused, lethargic Fluid replacement Crystalloid Crystalloid Crystalloid + blood Crystalloid + blood
  6. 6. • The following indications were recommended in the 6th edition of Anesthesia with the rule of thumb that administration of 1 unit of packed RBCs will increase hematocrit value by 3% to 5%: 1. Blood loss greater than 20% of blood volume when more than 1000 mL 2. Hemoglobin level less than 8 g/dL 3. Hemoglobin level less than 10 g/dL with major disease (e.g., emphysema, ischemic heart disease) 4. Hemoglobin level of less than 10 g/dL with autologous blood 5. Hemoglobin level less than 12 g/dL and ventilator dependent
  7. 7. Autologous Blood : • Autologous blood is assumed to be much safer than allogeneic blood, mainly because of the decreased risk of infection. • Because of a marked decrease in infectivity from allogeneic blood the difference in safety compared with autologous blood is much less. • Not surprisingly, the proportion of autologous blood collected has significantly decreased since the peak in 1992.
  8. 8.  Complications associated with autologous blood transfusions include the following: • Anemia • Preoperative myocardial ischemia from anemia induced by preoperative donation • Autologous units given to wrong patient (1 per 13,000 to 62,000) • Need for more frequent blood transfusions In fact, transfusion-related bacterial sepsis may be more frequent with use of autologous blood because of the underlying medical condition of the donor and less stringent donor selection. Also, autologous blood must be tested the same as allogeneic blood.
  9. 9. Compatibility Testing • The ABO-Rh type, crossmatch, and antibody screen are frequently referred to as compatibility tests . • These tests were designed to demonstrate harmful antigen-antibody interactions in vitro so that harmful in- vivo antigen-antibody interactions could be prevented. • All donor &recipient blood must be tested for the correct ABO and Rh type and screened for unexpected antibodies. • Proper selection of donor blood requires a test for compatibility between recipient blood and donor blood; this test is known as a crossmatch
  10. 10. ABO-Rh Typing • Determination of the patient's correct blood type is exceedingly important because the most serious and tragic reactions are usually caused by accidental transfusion of ABO-incompatible blood. • These reactions result from naturally occurring antibodies (i.e., anti-A and anti-B), which activate complement and lead to rapid intravenous hemolysis.
  11. 11. • Anti-A or anti-B antibodies, or both, are formed whenever the individual lacks either or both of the A and B antigens. • Antibodies are directed against those antigens that are lacking in the individual's own cells. ABO typing is performed by testing RBCs for the A and B antigens and the serum for the A and B antibodies before transfusion
  12. 12. Blood Group Red Cells Tested With Serum Tested With Anti-A Anti-B A Cells B Cells A + - - + B - + + - AB + + - - O - - + + ABO Compatibility Testing
  13. 13. • Crossmatching: • A crossmatch is essentially a trial transfusion within a test tube in which donor RBCs are mixed with recipient serum to detect a potential for serious transfusion reaction. • The crossmatch can be completed in 45 to 60 minutes and is carried out in three phrases: I. immediate phase, II. incubation phase, III. antiglobulin phase.
  14. 14. • The immediate phase is conducted at room temperature and is a check against errors in ABO typing. • It detects ABO incompatibilities and those caused by naturally occurring antibodies in the MN, P, and Lewis systems. • This takes 1 to 5 minutes to complete.
  15. 15. • The incubation phase involves incubation at 37°C in albumin or low-ionic strength salt solution. • The addition of albumin and low-ionic-strength salt solution aids in the detection of incomplete antibodies or those antibodies that are able to attach to a specific antigen (i.e., sensitization) but are unable to cause agglutination in a saline suspension of RBCs. • This phase primarily detects antibodies in the Rh system. • The incubation period is 30 to 45 minutes in albumin and of 10 to 20 minutes in low-ionic-strength salt
  16. 16. • The antiglobulin phase of the crossmatch, the indirect antiglobulin test, involves the addition of antiglobulin sera to the incubated test tubes. • With this addition, antihuman antibodies present in the sera become attached to the antibody globulin on the RBCs, causing agglutination. • This antiglobulin phase detects most incomplete antibodies in the blood group systems, including the Rh, Kell, Kidd, and Duffy blood group systems.
  17. 17. Donor Recipient O O, A, B, AB A A, AB B B, AB AB AB Donor Blood Groups that Patients Can Receive Although all three phases of the crossmatch are important, the first two stages are of prime importance in preventing serious hemolytic transfusion reactions
  18. 18. • Antibody Screening : • The antibody screen is also carried out in three phases and is similar in length to the crossmatch. • The screen, however, is a trial transfusion between the recipient's serum and commercially supplied RBCs that are specifically selected to contain optimal numbers of RBC antigens or those antigens that will react with antibodies that are commonly implicated in hemolytic
  19. 19. • Emergency Transfusion: • Specific Recommended Protocol The following steps are recommended for patients who are hypovolemic and require blood transfusion: 1. Infuse crystalloids or colloids. 2. Draw a blood sample for typing and crossmatching. 3. If crossmatched blood is not ready to give, use type- specific or type O Rh-negative cells or type O Rh- positive cells for males or postmenopausal females without a history of transfusions; type-specific, partially crossmatched blood; or type-specific, crossmatched blood.
  20. 20. Storage of Blood • Citrate phosphate dextrose adenine (CPDA) is an anticoagulant preservative in which blood is stored at 1°C to 6°C. • Citrate is an anticoagulant, phosphate serves as a buffer, and dextrose is a red cell energy source, adenine allows RBCs to resynthesize adenosine triphosphate (ATP), which extends the storage time from 21 to 35 days. • The shelf life can be extended to 42 days when AS-1 (Adsol), AS-3 (Nutricel), or AS-5 (Optisol) is used
  21. 21. Complications Changes in oxygen transport • RBCs are transfused primarily to increase transport of oxygen to tissues. • The respiratory function of red cells may be impaired during preservation, making it difficult for them to release oxygen to the tissues immediately after transfusion due to increase in 2,3 DPG in RBC.
  22. 22. Parameter Days of Storage 0 35 (Whole Blood) 35 (Packed Cells) pH 7.55 6.73 6.71 Plasma hemoglobin (mg/dL) 0.50  46.00 246.00 Plasma potassium (mEq/L) 4.20  17.20  76.00 Plasma sodium (mEq/L) 169.0 153.00 122.00 Blood dextrose (mg/dL) 440.0 282.00  84.00 2,3- Diphosphoglycerate (µM/mL) 13.20 1.00 1.00 Percent survival * —  79.00  71.00 Properties of Whole Blood and Packed Red Cell Concentrates Stored in CPDA-1
  23. 23. Complications i. Coagulopathy & Dilutional thrombocytopenia ii. Low level of factor V & factor VIII iii. DIC like syndrome iv. Citrate intoxication v. Acid base abnormality vi. Electrolyte imbalance(hyperkalemia,hypocalcemia) vii. Hypothermia viii. Transfusion associated Graft Vs Host disease ix. Transfusion related Acute lung injury(TRALI) x. Adverse ocular reaction xi. Transfusion related Immunomodulation
  24. 24. • Massive Transfusion : • Massive transfusion is defined, in adults, as replacement of >1 blood volume in 24 hours or >50% of blood volume in 4 hours (adult blood volume is approximately 70 mL/kg). • In children, it is defined as transfusion of >40 mL/kg (blood volume in children over 1 month old is approximately 80 mL/kg). • Massive transfusion occurs in settings such as severe trauma, ruptured aortic aneurysm, surgery and obstetrics complications etc.
  25. 25. Parameters Values to aim for Temperature >35 °C Acid-base status ph >7.2, base excess <–6, lactate <4 mmol/L Ionised calcium (Ca) >1.1 mmol/L Haemoglobin (Hb) This should not be used alone as transfusion trigger; and, should be interpreted in context with haemodynamic status, organ & tissue perfusion. Platelet (Plt) ≥ 50,000 /cc PT/APTT ≤ 1.5x of normal Fibrinogen ≥ 1.0 g/L Parameters in Massive Transfusion Investigation & Monitoring
  26. 26. Transfusion Reactions • Hemolytic Transfusion Reaction : Sign & Symptoms : • The classic signs and symptoms of a hemolytic transfusion reaction—chills, fever, chest and flank pain, and nausea—are masked by anesthesia. • Under general anesthesia, the only signs may be hemoglobinuria, bleeding diathesis, or hypotension. The presenting sign is usually hemoglobinuria. • Consequeces : ARF,DIC,Hypovolemic shock
  27. 27. Factors that affect degree of reaction •volume of transfused blood •number of antigenic sites on the red cell membrane •activity of the reticuloendothelial system. •The properties of the antibody, including concentration and ability to activate complement
  28. 28. • Treatment : 1. STOP THE TRANSFUSION. 2. Maintain the urine output at a minimum of 75 to 100 mL/hr by the following methods: a. Generously administer fluids intravenously and possibly mannitol (12.5 to 50 g, given over 5 to 15 minutes). b. If intravenously administered fluids and mannitol are ineffective, administer furosemide (20 to 40 mg) intravenously. 3. Alkalinize the urine; because bicarbonate is preferentially excreted in the urine, only 40 to 70 mEq of sodium bicarbonate per 70 kg of body weight is usually required to raise the urine pH to 8, whereupon repeat urine pH determinations indicate the need for additional bicarbonate.
  29. 29. 4. Assay urine and plasma hemoglobin concentrations. 5. Determine platelet count, partial thromboplastin time, and serum fibrinogen level. 6. Return unused blood to blood bank for repeat crossmatch. 7. Send patient's blood and urine sample to blood bank for examination. 8. Prevent hypotension to ensure adequate renal blood flow.
  30. 30. • Delayed Hemolytic Transfusion Reaction(Immune Extravascular Reaction) • In many cases of hemolytic transfusion reaction, the transfused donor cells may survive well initially, but after a variable delay (2 to 21 days) they are hemolyzed. • This type of reaction occurs mainly in recipients sensitized to RBC antigens by previous blood transfusions or pregnancy. As a result, this type of delayed reaction is more common in females who have a known disposition of alloimmunization.
  31. 31. • These reactions are those in which the level of antibody at the time of transfusion is too low to be detected or too low to cause RBC destruction. RBC destruction occurs only when the level of antibody is increased after a secondary stimulus (i.e., anamnestic response). • These delayed reactions are often manifested only by a decrease in the post-transfusion hematocrit value. • Jaundice and hemoglobinuria can occur in these patients and can cause some impairment in renal function but only rarely do they lead to death. Unlike immediate reactions, antibodies most commonly involved in delayed hemolytic reactions are those in the Rh and Kidd systems rather than the ABO system
  32. 32. • Nonhemolytic Transfusion Reactions : • The most common adverse reactions to blood transfusions are the less serious febrile reactions. • The symptoms consist of chills, fever, headache, myalgia, nausea, and nonproductive cough occurring shortly after blood transfusion caused by pyrogenic cytokines and intracellular contents released by donor leukocytes. • Use of leukoreduced blood will reduce the incidence of febrile reactions
  33. 33. • Because febrile reactions obviously involve fever, they can be easily confused with a hemolytic transfusion reaction. • A direct antiglobulin test readily differentiates a hemolytic reaction from a febrile reaction because this test rules out the attachment of an RBC antibody to transfused donor RBCs.
  34. 34. • Allergic reactions can be minor, anaphylactoid, or anaphylactic. • Most allergic transfusion reactions are minor and are thought to be caused by the presence of foreign protein in the transfused blood. • The most common symptom is urticaria associated with itching. • When these reactions are not a serious hemolytic reaction,transfusion not need to be discontinued. Antihistamines are used to relieve symptoms.
  35. 35. • Anaphylactoid reactions (Pseudoanaphylaxis) is similar to anaphylaxis clinically but are not mediated by IgE,rather caused by direct mast cell degranulation. • Anaphylaxis occurs in which the patient has dyspnea,hypotension, laryngeal edema, chest pain, and shock. • These are anaphylactic reactions caused by the transfusion of IgA to patients who are IgA deficient and have formed anti-IgA.
  36. 36. • This type of reaction does not involve red cell destruction and it occurs very rapidly, usually after the transfusion of only a few milliliters of blood or plasma. • The patients who experience these anaphylactic reactions can be given transfusions with washed RBCs from which all traces of donor IgA have been removed or with blood lacking the IgA protein. • Treatment : im epinephrine (1:1000),steroids
  37. 37. Infectivity Of Blood Risk of transfusion transmitted Infection •Human immunodeficiency virus-1 •Human T-lymphotropic virus •Cytomegalovirus (CMV) •Hepatitis C virus (HCV) •Hepatitis B virus (HBV) •West Nile virus (WNV) •Others: Y. enterocolitica,malaria,syphilis,chaga’s disease,Parvovirus B19,SARS •Rare :Cruetzfeldt Jakob’s disease,Herpes,Infectious mononucleosis,toxoplasmosis,trypanosomiasis,leismaniasis,brucellosis ,typhus,filaria,measles,salmonellosis,Colorado tick fever.
  38. 38. Infectious disease testing for blood transfusion in India •HIV •HBV •HCV •Malaria •Syphilis
  39. 39. Blood Coagulation • Hemostasis comprises cellular and biochemical processes that limit blood loss resulting from injury, maintain intravascular blood fluidity, and promote revascularization of thrombosed vessels after injury. • Normal physiologic hemostasis necessitates a delicate balance between procoagulant pathways and anticoagulnt mechanisms inhibiting thrombus formation beyond the injury site. • Vascular endothelium,platelets,& plasma coagulation proteins play important roles in hemostasis. • Failure to maintain balance commonly leads to excessive bleeding or pathologic thrombus formation.
  40. 40. • Primary Hemostasis :In this Vascular endothelial injury, mechanical or biochemical alteration, leads to platelet deposition at the injury site,which adequate in minor injury. • Secondary Hemostasis : mediated by activation of plasma clotting factors for the control of more significant bleeding which necessitates stable clot formation incorporating cross-linked fibrin.
  41. 41. Role Of Endothelium : •Under normal conditions, vascular endothelium provides a nonthrombogenic surface to promote blood fluidity. Healthy endothelial cells possess antiplatelet, anticoagulant, and profibrinolytic effects to inhibit clot formation. • Negatively charged vascular endothelium repels platelets and produces prostacyclin (PGI2) and nitric oxide (NO), which are potent platelet inhibitors. •Adenosine diphosphatase (ADPase) synthesized by vascular endothelial cells degrades adenosine diphosphate (ADP), another potent platelet activator.
  42. 42. • Vascular endothelium further expresses several inhibitors of plasma-mediated hemostasis, including thrombomodulin (an indirect thrombin inhibitor), heparin-like glycosaminoglycans, and tissue factor pathway inhibitor (TFPI),tissue plasminogen activator (t-PA), which is responsible for activating fibrinolysis—a primary counterregulatory mechanism limiting clot propagation.
  43. 43. • Damage to vascular endothelial cells exposes the underlying extracellular matrix (ECM) including collagen, von Willebrand factor (vWF),& other platelet-adhesive glycoproteins. • Platelets bind to and are activated by exposure to ECM components which activates plasma-mediated coagulation pathways to generate thrombin and, ultimately, fibrin clot. • Certain cytokines (i.e., interleukin-1, tumor necrosis factor, and γ-interferon) and hormones (i.e., desmopressin acetate or endotoxin) induce prothrombotic changes in vascular endothelial cells.
  44. 44. Role of Platelets : •Under normal circumstances, platelets do not bind vascular endothelium; however, when injury exposes ECM, platelets undergo a series of biochemical and physical alterations characterized by three major phases Adhesion : vWF proves particularly important as a bridging molecule between ECM and platelet glycoprotein Ib receptor complexes. Absence of either vWF (von Willebrand disease) or glycoprotein Ib receptors (Bernard-Soulier syndrome) results in a clinically significant bleeding disorder.
  45. 45.  Activation : • During the activation phase, platelets release granular contents, resulting in recruitment and activation of additional platelets as well as propagation of plasma- mediated coagulation. • Platelets contain two specific types of storage granules: alpha granules and dense bodies. • Alpha granules contain numerous proteins essential to hemostasis like fibrinogen, coagulation factors V and VIII, vWF, platelet-derived growth factor, and others. • Dense bodies contain ADP and ATP as well as calcium, serotonin, histamine, and epinephrine.
  46. 46.  Aggregation : • During the final phase of platelet aggregation, activators released during the activation phase serve to recruit additional platelets to the site of injury. • Newly active glycoprotein IIb/IIIa receptors on the platelet surface bind fibrinogen to provide for cross- linking with adjacent platelets. • The importance of these receptors is reflected by the bleeding disorder associated with their hereditary deficiency: Glanzmann thrombasthenia.
  47. 47. Role Of Plasma : Plasma-mediated hemostasis might best be summarized as an amplification system to accelerate thrombin generation from an inactive precursor (i.e., prothrombin). Extrinsic Pathway of Coagulation Intrinsic Pathway of Coagulation Common Pathway of Coagulation
  48. 48. • Intrinsic Anticoagulant Mechanisms: • Once activated, regulation of hemostasis proves essential to limit clot propagation beyond the injury site. • Four major counterregulatory pathways that appear particularly crucial for downregulating hemostasis: fibrinolysis, TFPI, the protein C system, and serine protease inhibitors.
  49. 49. Fibrinolysis system
  50. 50. Tissue Factor Plasminogen Inhibtor system inhibits the tissue factor/factor VIIa complex and thereby the extrinsic coagulation pathway. •TFPI and factor Xa form phospholipid membrane- bound complexes that incorporate and inhibit tissue factor/factor VIIa complexes. •Most TFPI is bound to vascular endothelium but released into circulation by heparin administration.
  51. 51. The protein C system •It is important in downregulating hemostasis because it inhibits thrombin as well as the essential cofactors Va and VIIIa. •Thrombin initiates this inhibitory pathway by binding a membrane-associated protein, thrombomodulin, to activate protein C.Protein C, complexed with the cofactor protein S degrades both cofactors Va and VIIIa. • Thrombin, once bound to thrombomodulin, is inactivated and removed from circulation.
  52. 52. Serine Protease inhibitors system: It includes antithrombin (AT) and heparin cofactor II. • Antithrombin binds to and inhibits thrombin as well as factors IXa, Xa, XIa, and XIIa. •Heparin cofactor II inhibits thrombin alone. •Heparin, a catalyst accelerator, binds antithrombin to promote inhibition of targeted enzymes.
  53. 53. Disorders of Hemostasis : •Inherited- Hemophilia A,Hemophilia B,Von willebrand’s disease,Bernand Soulier’s disease,Glanzman’s thrombosthenia •Acquired-Drugs like warfarin,heparin,fibrinolytic agents & coexisting medical illness like liver disease,renal disease,DIC
  54. 54. • Hypercoagulable States and Risk for Perioperative Thrombosis • High Risk • Heparin-induced thrombocytopenia (HIT) • Antithrombin deficiency • Protein C deficiency • Protein S deficiency • Antiphospholipid antibody syndrome • Moderate Risk • Factor V Leiden genetic polymorphism • Prothrombin G20210A genetic polymorphism • Hyperhomocysteinemia • Dysfibrinogenemia • Postoperative prothrombotic state • Malignancy • Immobilization
  55. 55. • Monitoring Coagulation : Activated partial Thromboplastin Time: • The aPTT assesses integrity of the intrinsic and common pathways of plasma-mediated hemostasis. • It measures the time required in seconds for clot formation to occur after mixing a sample of patient plasma with phospholipid, calcium, and an activator of the intrinsic pathway of coagulation (i.e., celite, kaolin, silica, or ellagic acid). • Prolongation of the aPTT is evaluated further with mixing studies to determine whether delayed clot formation is attributable to a coagulation factor deficiency or an inhibitor (i.e., heparin, antiphospholipid antibody, fibrin split products).
  56. 56. •The mixing study performed by mixing the patient's plasma sample with “normal” donor plasma. In case of a coagulation factor deficiency, time to clot formation will correct and sequential assays for specific coagulation factor concentrations allow for identification of the deficiency. •A common means of confirming heparin prolongation of the aPTT is to perform a thrombin clotting time (TCT). In this test, the patient's citrate-containing plasma sample is mixed with thrombin and time to clot formation is measured in sec. •The most common mechanism underlying prolongation of the TCT is presence of heparin or a direct thrombin inhibitor anticoagulant.
  57. 57. • Prothrombin Time: • The PT assesses integrity of the extrinsic and common pathways of plasma-mediated hemostasis. It measures time required in seconds for clot formation to occur after mixing a sample of patient plasma with tissue factor (thromboplastin) and calcium. • Given the importance of monitoring PT results for patients on long-term warfarin therapy, the INR was introduced as a means of normalizing PT results among different laboratories. • INR = (patient PT/standard PT) in which the “standard PT” represents the geometric mean of multiple normal samples from the testing laboratory.
  58. 58. • Platelet Count & Bleeding Time : • The platelet count remains a standard component in screening for coagulation abnormalities. • Normal value-1.5 lakh-3 lakh/cc • Bleeding Time, as a test of platelet dysfunction • Normal value-1-5 min • Clotting Time : • It is a indicator of coagulation cascade function • Normal Value-3- 8 min
  59. 59. Blood Component Therapy • A major advance in the field of blood banking has been the development of blood component therapy • The basic philosophy is based on the concept that patients are best treated by administration of the specific fraction of blood that they lack
  60. 60. Scheme for separation of whole blood for component therapy.
  61. 61. • Packed Red Blood Cells : • Whole blood provides oxygen-carrying capacity and intravascular blood volume expansion. • PRBC increases oxygen carrying capacity without increasing intravascular blood volume. • Other than severe hemorrhage, most indications for red blood cells can be effectively treated with packed RBCs, retaining the plasma and the components thereof for other patients .
  62. 62. Value Whole Blood Packed Red Blood Cells Volume (mL) 517 300 Erythrocyte mass (mL) 200 200 Hematocrit (%)  40  70 Albumin (g)  12.5 4 Globulin (g) 6.25 2 Total protein (g)  48.8  36 Plasma sodium (mEq)  45  15 Plasma potassium (mEq)  15 4 Plasma acid (citric-lactic)  80  25 (mEq) Donor-to-recipient ratio 1 unit per patient 1 unit per 4-6 patients Comparison of Whole Blood and Packed Red Blood Cells
  63. 63. • The administration of packed RBCs is facilitated by reconstituting them with a crystalloid or colloid; • If the solution contains calcium, clotting occurs. • Therefore Lactated Ringer's solution is not recommended for use as a diluent for packed RBCs. • If the diluent is hypotonic with respect to plasma the RBCs will swell and eventually lyse. • Solutions recommended for reconstituted packed erythrocytes are 5% dextrose in 0.4% saline, 5% dextrose in 0.9% saline, 0.9% saline, and Normosol-R with a pH of 7.4.
  64. 64. • Platelet Concentrates : • Platelet concentrates are prepared by differential centrifugation from freshly drawn units of blood or from donors who specifically donate large amounts of platelets by plateletpheresis. • If platelets are stored at room temperature, they are satisfactory to use within 7 days of collection. • 1 Unit-60 ml random donor platelet inc platelets by 5K to 10K/cc where as single donor platelets inc by 30 K-60 K/cc.
  65. 65. • PC are primarily effective at room temperature (20°C to 24°C), which enhances bacterial growth. • Bacterial contamination, mainly from platelet concentrates, is the third leading cause of transfusion- related deaths. • For any patient who develops a fever within 6 hours after receiving platelets, sepsis from platelets should be considered. • Hence,platelet concentrates are routinely tested for bacteria and are the only blood product that is stored at room temperature.
  66. 66. • Indications for the use of platelets are somewhat difficult to define. • In the July 1989 FDA Drug Bulletin it was stated that platelets should not be given to patients with 1. Immune thrombocytopenic purpura (unless there is life- threatening bleeding), 2. Prophylactically with massive blood transfusion. 3. Prophylactically after cardiopulmonary bypass.
  67. 67. • The American Society of Anesthesiologists (ASA) Task Force provided the following recommendations: 1. Prophylactic platelet transfusion is ineffective and rarely indicated when thrombocytopenia is due to increased platelet destruction (e.g., idiopathic thrombocytic purpura). 2. Prophylactic platelet transfusion is rarely indicated in surgical patients with thrombocytopenia due to decreased platelet production when the platelet count is greater than 1 lakh/cc and is usually indicated when the platelet count is less than 50,000/cc. The determination of whether patients with intermediate platelet counts (50,000 to 1 lakh/cc) require therapy should be based on the patient's risk of bleeding.
  68. 68. 3. Surgical and obstetric patients with microvascular bleeding usually require platelet transfusion if the platelet count is less than 50,000/cc and rarely require therapy if it is greater than 1lakh/cc. With intermediate platelet counts (50,000 to 1 lakh/cc), the determination should be based on the patient's risk for more significant bleeding. 4. Vaginal deliveries or operative procedures ordinarily associated with insignificant blood loss may be undertaken in patients with platelet counts less than 50,000/cc. 5. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known platelet dysfunction and microvascular bleeding.
  69. 69. • Fresh Frozen Plasma : • It contains all the plasma proteins, particularly factors V and VIII, which gradually decline during the storage of blood. • The major risk is transmission of infectious diseases, such as hepatitis B, hepatitis C, and AIDS. • Other risks include sensitization to foreign proteins. • Shelf life :1 yr
  70. 70. • The only indications for FFP administration the ASA Task Force agreed on were the following: 1. Replacement of isolated factor deficiencies 2. Reversal of warfarin effect 3. In cases of antithrombin III deficiency 4. Treatment of immunodeficiencies 5. Treatment of thrombotic thrombocytopenia purpura 6. Massive blood transfusion (rarely and only when factors V and VIII are less than 25% of normal) 7. Requirements for indications 1 and 6 are prothrombin and partial thromboplastin times at least 1.5 times longer than normal.
  71. 71. • Cryoprecipitate : Cryoprecipitate contains factor VIII:C (i.e., procoagulant activity), factor VIII:vWF (i.e., von Willebrand factor), fibrinogen, factor XIII, and fibronectin, which is a glycoprotein that may play a role in reticuloendothelial clearance of foreign particles and bacteria from the blood.
  72. 72. • Cryoprecipitate should be administered through a filter and as rapidly as possible. • The rate of administration should be at least 200 mL/hr, and infusion should be completed within 6 hours of thawing. • Indication : Haemophilia A ,Von Willbrand’s disease,Fibrinogen deficiency,Factor XIII deficiency.
  73. 73. • Prothrombin Complex : Factor IX can be recovered from plasma or plasma fractions by absorption with ion exchanges or inorganic chemicals. These products are all complexes of factors II, VII, IX, and X. • The main indication for these products is treatment of factor IX deficiency, or hemophilia B (i.e., Christmas disease). • Factor IX or prothrombin complex has also been used for the treatment of acquired hypoprothrombinemic bleeding disorders, principally sodium warfarin overdose
  74. 74. • Single donor plasma : • Single-donor plasma is plasma that has been removed from stored blood without any effort being made to preserve coagulation factors. • Single-donor plasma is very effective as a volume expander. • It obviously cannot be used to correct deficiencies in coagulation factors.
  75. 75. Synthetic Oxygen-Carrying Substances • Other Than Human Red Blood Cells (Blood) • Two concepts of synthetic blood have been attempted. The first approach uses linear binding kinetics, unlike the nonlinear binding of hemoglobin. • The most notable is the perfluorochemical emulsion called Fluosol-DA. However, it had little use because it carries oxygen (i.e., a small amount) only when the PaO2 is more than 300 mm Hg. • A newer perfluoro compound, perfluorooctyl bromide, carries 3 to 4 times more oxygen and has a longer half-life and presumably fewer problems than are associated with Fluosol- DA. Other related products are Oxygent (Alliance), Oxycyte (synthetic blood), several other perfluorocarbon emulsions.
  76. 76. • The remaining synthetic blood or oxygen therapeutics are labeled as hemoglobin-based oxygen carriers (HBOCs). • These products modify the hemoglobin molecule from humans, animals, or recombinant technology. • The most serious are kidney toxicity due to stroma, an increase in affinity for oxygen (i.e., left shift in the oxygen dissociation curve), and arteriolar vasoconstriction from nitric oxide scavenged by the infused hemoglobin.
  77. 77. • Genetic engineering has provided hope for blood products. Initially, recombinant erythropoietin was developed for treatment of anemias and facilitation of autologous blood donation. • In 1992, a human recombinant hemoglobin (rHb 1.1) was designed as a blood substitute,with the use of genetic engineering techniques, it was made from Escherichia coli. It functions as normal hemoglobin in terms of oxygen-carrying capacity, but it does not require crossmatching, nor does it transmit disease or become rapidly outdated.
  78. 78. Parameter Synthetic Allogeneic Oxygen delivery Rapid and consistent Dependent on 2,3-DPG Risk of disease transmission None Very high Storage Room temperature Stable efficacy Refrigeration Loss of efficacy Shelf life 1-3 years 42 days Preparation Ready to use Crossmatch Compatibility Universal Type specific Duration of action 1-3 days 60-90 days Comparison of Synthetic Blood in General with Allogeneic Blood
  79. 79. • References: • Miller’s textbook of anaesthesiology(7th edn) • Guyton’s text book of physiology
  80. 80. Thank you...