BLOOD TRANSFUSION Prof . M.C.Bansal MBBS., MS., FICOG., MICOG. Founder Principal & Controller, Jhalawar Medical College & Hospital Jjalawar . MGMC & Hospital , sitapura ., Jaipur .
History of Transfusions Blood transfused in humans since mid-1600’s 1828 – First successful transfusion 1900 – Landsteiner described ABO groups 1916 – First use of blood storage 1939 – Levine described the Rh factor
Cross matching Matching blood components between a Pt & a D is a direct compatibility test. 2. The red cells & Plasma are cross matched thru Major and Minor cross match, defined as to an amount of Antibody react with Antigen A. Major‘:the patient's serum & the donor's RBCs. – large amount of Antibody has greater impact B. Minor’: the patient's RBCs & the donor's serum. – Small amount of Antibody has little impact
BLOOD TYPES
WHAT IS ANTIGENS ? An antigens is a substance that causing the formation of antibodies WHAT IS ANTIBODYS ? Antibodies is a protein substance develop in the body in response to the presence of an antigen that has entered the body
Life Saving & Life Threatening Process
Transfusion Overview Integral part of medical treatment Most often used in Hematology/Oncology, but other specialties as well ( surgery,gyn , ICU, etc) Objectives Blood components Indications for transfusion Safe delivery Complications
TRANSFUSION THERAPY * REPLACEMENT * THERAPEUTIC 1.To restore intravascular volume with whole blood or albumin. 2. To restore the oxygen capacity of blood by replacing red blood cells. 3. To replace clotting factor and correction of anemia PURPOSE OFBLOOD
Type of Transfusion : Whole Blood ; Blood Component ; RBC PLT FFP Leukocyte concentrate Plasma Substitutes ; Use of whole blood is considered to be a waste of resources Blood Transfusion
DEFINITIONS BLOOD PRODUCT = Any therapeutic substance prepared from human blood WHOLE BLOOD = Unseparated blood collected into an approved container containing an anticoagulant preservative solution BLOOD COMPONENT = 1. A constituent of blood , separated from whole blood such as Red cell concentrate Plasma Platelet concentrates 2. Plasma or platelets collected by apheresis 3. Cryoprecipitate prepared from fresh frozen plasma
Differential Centrifugation First Centrifugation Whole Blood Main Bag Satellite Bag 1 Satellite Bag 2 RBC’s Platelet-rich Plasma First Closed System
Differential Centrifugation Second Centrifugation Platelet-rich Plasma RBC’s Platelet Concentrate RBC’s Plasma Second
Whole Blood Storage 4 ° for up to 35 days Indications Massive Blood Loss/Trauma/Exchange Transfusion Considerations Use filter as platelets and coagulation factors will not be active after 3-5 days Donor and recipient must be ABO identical
Blood Components THE PRBC Storage - 2 – 6 O C Unit of issue - 1 donation ( unit or pack ) Administration - ABO & Rh compatible - Never add medication to a unit - Complete transfusion within 4 hrs of commencement 1 Member
Indications - Acute blood loss with > 20% loss of blood volume Trauma Surgery - Trigger – 10gm% - 8gm% Rate of development of anemia , General condition and type of surgery Radiotherapy
Dosage & Administration Dosage - 1 unit/10 kg body wt Adult dose is 4-8 units Administration - Preferably ABO & Rh group specific
Platelets The platelets are separated from the plasma by centrifugation. Platelets are supplied either as single donor units or as a combination of multiple donors. One unit of platelets will increase the platelet count of a 70 kg adult by 5 to 10,000/mm³. Platelet viability is optimal at 22° C but storage is limited to 4-5 days. Platelets have both the ABO and HLA antigens. ABO compatibility is ideal but not required. (incompatibility will shorten the life span of the platelet)
Platelets Storage Up to 5 days at 20-24 ° Indications Thrombocytopenia, Plt <15,000 Bleeding and Plt <50,000 Invasive procedure and Plt <50,000 Considerations Contain Leukocytes and cytokines 1 unit/10 kg of body weight increases Plt count by 50,000 Donor and Recipient must be ABO identical
Thrombocytopenia (< 50,000) Platelet dysfunction Each unit increase 5,000 PLTs after 1 H Platelets
Guidelines for Platelet Tx. Mild - 50,000-1,00,000/µl Tx - usually not required Moderate - 20,000-50,000/µl Tx -if symptomatic or has to undergo surgery/trauma Severe - < 20,000/µl Risk of bleeding - high Prophylactic Tx
Plasma and FFP Contents—Coagulation Factors (1 unit/ml) Storage FFP--12 months at –18 degrees or colder Indications Coagulation Factor deficiency, fibrinogen replacement, DIC, liver disease, exchange transfusion, massive transfusion Considerations Plasma should be recipient RBC ABO compatible In children, should also be Rh compatible Account for time to thaw Usual dose is 20 cc/kg to raise coagulation factors approx 20%
Coagulation factor deficiencies 1 ml increases 1% clotting factors Being used as soon as possible Albumin, hetastarch, crystalliods are equally effective volume expander but safer than FFP After use of 5 U of RBCs, matching 2 U of FFP Fresh Frozen Plasma (FFP)
Dosage & Administration for FFP Dosage - 10-15 ml/Kg(Approx 2-3 bags for an adult) Administration - Thawed at +37 o C before transfusion ABO compatible Group AB plasma can be used for all patient
-- Volume Expander Dextran Most widely used Low/Middle M.W. (40,000-70,000) Massive transfusion could impair coagulation Occasional ALLERGIC reaction Hydroxyethyl Starch Formulation (HES) More stable Containing essential electrolytes No allergic reaction Plasma Substitutes
Granulocyte Transfusions Prepared at the time for immediate transfusion (no storage available) Indications – severe neutropenia assoc with infection that has failed antibiotic therapy, and recovery of BM is expected Donor is given G-CSF and steroids or Hetastarch Complications Severe allergic reactions Can irradiate granulocytes for GVHD prevention
Cryoprecipitate Description Precipitate formed/collected when FFP is thawed at 4 ° Storage After collection, refrozen and stored up to 1 year at -18 ° Indication Fibrinogen deficiency or dysfibrinogenemia vonWillebrands Disease Factor VIII or XIII deficiency DIC (not used alone )(Disseminated intravascular coagulation) Considerations ABO compatible preferred (but not limiting) Usual dose is 1 unit/5-10 kg of recipient body weight
Leukocyte Reduction Filters Used for prevention of transfusion reactions Filter used with RBC’s, Platelets, FFP, Cryoprecipitate Other plasma proteins (albumin, colloid expanders, factors, etc.) do not need filters—NEVER use filters with stem cell/bone marrow infusions May reduce RBC’s by 5-10% Does not prevent Graft Verses Host Disease (GVHD)
RBC Transfusions Preparations Type Typing of RBC’s for ABO and Rh are determined for both donor and recipient Screen Screen RBC’s for atypical antibodies Approx 1-2% of patients have antibodies Crossmatch Donor cells and recipient serum are mixed and evaluated for agglutination
RBC Transfusions Administration Dose Usual dose of 10 cc/kg infused over 2-4 hours Maximum dose 15-20 cc/kg can be given to hemodynamically stable patient Procedure May need Premedication (Tylenol ) Filter use—routinely leukodepleted Monitoring—VS q 15 minutes, clinical status Do NOT mix with medications Complications Rapid infusion may result in Pulmonary edema Transfusion Reaction
Platelet Transfusions Preparations ABO antigens are present on platelets ABO compatible platelets are ideal This is not limiting if Platelets indicated and type specific not available Rh antigens are not present on platelets Note: a few RBC’s in Platelet unit may sensitize the Rh- patient
Platelet Transfusions Administration Dose May be given as single units or as apheresis units Usual dose is approx 4 units/m 2 —in children using 1-2 apheresis units is ideal 1 apheresis unit contains 6-8 Plt units (packs) from a single donor Procedure Should be administered over 20-40 minutes Filter use Premedicate if hx of Transfusion Reaction Complications—Transfusion Reaction
Choice of blood group for transfusion Patient blood first choice second choice 1. O + O+ 0- 2. O- O- - 3. A+ A+ A-,O+,O- 4. A- A- O- 5. B+ B+ B-,O-,O+ 6. B- B- O- 7. AB+ AB+ AB+,A+,A-,B+,B-,O-,O+ 8. AB- AB- A-,B-,O-,
Although blood transfusions can be life-saving, they are not without risks. The most serious risks are transfusion reactions and infections .
Blood product transfusions sometimes cause transfusion reactions . There are several types of reactions and some are worse than others. Some reactions happen as soon as the transfusion is started, while others take several days or even longer to develop.
Frequency of Transfusion Reactions Adverse Effect Frequency Comments Acute Hemolytic Rxn 1 in 25,000 Red cells only Anaphylactic hypotensive 1 in 150,000 Including IgA Febrile Nonhemolytic 1 in 200 Common Allergic 1 in 1,000 Common Delayed Hemolytic 1 in 2,500 Red cells only RBC alloimmunization 1 in 100 Red cells only WBC/Plt alloimmunization 1 in 10 WBC and Plt only
Acute Hemolytic Transfusion Reactions (AHTR) Occurs when incompatible RBC’s are transfused into a recipient who has pre-formed antibodies (usually ABO or Rh) Antibodies activate the complement system, causing intravascular hemolysis Symptoms occur within minutes of starting the transfusion This hemolytic reaction can occur with as little as 1-2 cc of RBC’s Labeling error is most common problem Can be fatal
Symptoms of AHTR High fever/chills Hypotension Back/abdominal pain Oliguria Dyspnea Dark urine Pallor
What to do? If an AHTR occurs STOP TRANSFUSION ABC’s Maintain IV access and run IVF (NS or LR) Monitor and maintain BP/pulse Give diuretic Obtain blood and urine for transfusion reaction workup Send remaining blood back to Blood Bank
Blood Bank Work-up of AHTR Check paperwork to assure no errors Check plasma for hemoglobin Repeat crossmatch Repeat Blood group typing Blood culture
Labs found with AHTR Hemoglobinemia Hemoglobinuria Hyperbilirubinemia Abnormal DIC panel
Febrile Nonhemolytic Transfusion Reactions (FNHTR) Definition--Rise in patient temperature >1 °C (associated with transfusion without other fever precipitating factors) Occurs with approx 1% of PRBC transfusions and approx 20% of Plt transfusions FNHTR caused by alloantibodies directed against HLA antigens Need to evaluate for AHTR and infection
Allergic Nonhemolytic Transfusion Reactions Etiology May be due to plasma proteins or blood preservative/anticoagulant Best characterized with IgA given to an IgA deficient patients with anti-IgA antibodies Presents with urticaria and wheezing Treatment Mild reactions—Can be continued after Benadryl Severe reactions—Must STOP transfusion and may require steroids or epinephrine Prevention—Premedication (Antihistamines)
TRALI Transfusion Related Acute Lung Injury Clinical syndrome similar to ARDS Occurs 1-6 hours after receiving plasma-containing blood products Caused by WBC antibodies present in donor blood that result in pulmonary leukostasis Treatment is supportive High mortality
Monitoring in AHTR Monitor patient clinical status and vital signs Monitor renal status (BUN, creatinine) Monitor coagulation status (DIC panel– PT/PTT, fibrinogen, D-dimer/FDP, Plt, Antithrombin-III) Monitor for signs of hemolysis (LDH, bili, haptoglobin)
Bacterial Contamination More common and more severe with platelet transfusion (platelets are stored at room temperature) Organisms Platelets—Gram (+) organisms, ie Staph/Strep RBC’s—Yersinia, enterobacter Risk increases as blood products age (use fresh products for immunocompromised)
Transfusion Associated Infections Hepatitis C Hepatitis B HIV CMV CMV can be diminished by leukoreduction, which is indicated for immunocompromised patients
ABO System & Pregnancy hemolytic diseases of the newborn may be due to ABO incompatibility ABO incompatibility is a common and generally mild type of haemolytic disease in babies. The term haemolytic disease means that red blood cells are broken down more quickly than usual which can cause jaundice, anaemia and in very severe cases can cause death. During pregnancy, this breakdown of red blood cells in the baby may occur if the mother and baby’s blood types are incompatible and if these different blood types come into direct contact with each other and antibodies are formed .
Significant problems with ABO incompatibility occur mostly with babies whose mothers have O blood type and where the baby is either A or B blood type. Premature babies are much more likely to experience severe problems from ABO incompatibility, while healthy full term babies are generally only mildly affected. Unlike haemolytic disease that can result in subsequent babies when a mother has a negative blood group, ABO incompatibility can occur in first-born babies and does not become more severe in further pregnancies
After birth there are two options for testing for ABO incompatibility : The cord blood of all babies whose mothers have an O blood group and the father either type A or B blood is tested The theory behind this approach is that if the baby is type A or B and they test positive in direct antiglobulin tests (DAT), the baby can then be followed closely for jaundice. The alternate approach is to screen any baby who becomes significantly jaundiced (particularly within the first 24 hours
Rh FACTOR This can induce varying degrees of anemia in the foetus, with hiperbilirubinemia, organ malfunction, etc. Bilirubin deposition in the cerebral basal ganglia ( kernicterus )can lead to severe mental damage. Severe cases of this disease were mortal. P revention started in the 60's and nowadays Rh negative pregnant women receive immunoglobulin doses at several moments during pregnancy and after childbirth if the baby is Rh positive. Besides, women in fertile age are never transfused Rh positive blood. Thus, HDN due to Rh antibodies has practically disappeared in developed countries.
Rhesus Isoimmunization Rhesus Iso immunization is an immunologic disease that occurs in pregnancy resulting in a serious complication affecting the fetus / or the neonate ranging from … mild neonatal jaundice … to intra uterine loss or neonatal death
Rhesus Isoimmunization This immunologic disease occur when a Rh – negative patient carrying a Rh – positive fetus ….. had a feto – maternal blood transfusion ….. the mother immunological system is stimulated to produce antibodies to the Rh antigen on the fetal blood cell ….. This antibodies cross the placenta and destroy fetal red blood cells leads to fetal anemia …. Usually the 1 st fetus will not be affected if this is the 1 st time that the mother has been exposed to the rhesus positive antigen
Antibodies Can Be Detected by: Saline agglutination test (SAT). Tests using cells suspended in colloid media. Tests using enzyme-treated cells- Rh & occasional antobodies . Indirect antiglobulin ( Coomb’s test) - wide spectrum. b a c d
Management of rhesus negative pregnant women Management of non sensitized Pregnancy Management of sensitized Pregnancy
Prophylactic Management of non sensitized Pregnancy During antenatal period Prophylactic ( 500 IU / 100 mcg ) Anti D are recommended to be given to all negative non sensitized mothers married to Rh positive husband at 28weeks and 34 weeks to protect and overcome any asymptomatic or un noticed antenatal feto maternal blood transfusion
Intra peritoneal blood transfusion Through the umbilical vein “ Cordocentesis 80 % of packed cell “ o “ rhesus negative Blood Cross matched against maternal blood group Free of infection Fresh Intra uterine therapy Management of Sensitized Pregnancy