blood transfusion and possible complications

Blood transfusion

1. Blood transfusion

2. Types of blood transfusion AUTOLOGOUS BLOOD TRANSFUSION Mean reinfusion of blood or blood products taken from the same patient ALLOGENIC BLOOD TRANSFUSION Blood taken from donor to a recipient is called allogenic blood transfusion

3. Physiologic Compensation for Anemia There is ample evidence for the human tolerance of both acute and chronic anemia. Oxygen delivery to the tissues (DO 2 ) DO 2  = cardiac output × arterial oxygen content is dependent on cardiac output (CO) , regional blood flow, and the blood’s oxygen-carrying capacity (i.e., oxygen content [ CaO 2 ]). Hemoglobin plays an integral role in oxygen transport and delivary to the tissues The clinical justification for RBC transfusion assumes that increasing the hemoglobin will improve oxygen-carrying capacity and therefore avoid tissue hypoxia

4. There are several compensatory mechanisms for anemia, 1 .Increased CO. There are several mechanisms that increase CO as compensation for isovolemic hemodilution. First, the heart rate increases sympathetic surge Second, higher stroke volume results from increased preload secondary to decreases in both systemic vascular resistance and afterload. 2. Altered microcirculatory blood flow. The decrease in blood viscosity associated with isovolemic hemodilution and chronic anemia improves blood flow through the microcirculation secondary to lower shear force in capillary beds.. Anemia causes the oxyhemoglobin disassociation curve to shift to the right secondary to increased levels of 2,3-DPG in RBCslevels . Furthermore, acidemia associated with acute hemorrhage also shifts the oxygen dissociation curve to the right, thereby decreasing the affinity of oxygen for hemoglobin and improving the tissue oxygen extraction ratio.

5. the decision to transfuse red blood cells (RBCs) was based upon the "10/30 rule": transfusion was used to maintain a blood hemoglobin concentration above 10 g/dL (100 g/L) and a hematocrit above 30 percent

6. Rationale for target hemoglobin  — The American Society of Anesthesiologists recommends avoiding hemoglobin <6 g/dL in healthy individuals. For older and sicker individuals with cardiovascular disease, a hemoglobin of ≥8 g/ dL appears reasonable There is also a biologic rationale for a target hemoglobin. At rest, oxygen delivery is normally four times oxygen consumption, indicating the presence of an enormous reserve. If intravascular volume is maintained during bleeding and cardiovascular status is not impaired, oxygen delivery will theoretically be adequate until the hematocrit (packed cell volume) falls to 10 to 12 percent. This is because adequate cardiac output plus increased oxygen extraction can compensate for the decrease in arterial oxygen content. However, increasing cardiac work to increase output requires more oxygen, so the "critical point" where oxygen consumption becomes delivery-dependent is generally higher. Transfusion of pRBCs delivered at 1:1:1 have a hematocrit in the total delivered volume of 29 percent, so there is "room" for delivered drugs, and non-RBC containing products such as platelets and cryoprecipitate.

7. restrictive transfusion strategy for most stable patients  — For most hemodynamically stable medical and surgical patients, we recommend using a restrictive transfusion strategy (giving less blood; transfusing at a lower hemoglobin level (typically 7 to 8 g/dL)

8. Compared with liberal transfusion strategies (higher thresholds), restrictive strategies (lower thresholds) resulted in the following: ● Decreased probability of receiving a transfusion) ● No difference in 30-day mortality ● No difference in infection rate) ● No increased risk of myocardial ● No difference in congestive heart failure ● No difference in stroke) ● No difference in rebleeding ● No difference in thromboembolism

9. Major exceptions to the use of a threshold of 7 to 8 g/dL Symptomatic patients may be transfused at higher hemoglobin levels to treat symptoms Patients with acute coronary syndromes patients requiring massive transfusion , such as in the setting of trauma or serious gastrointestinal bleeding.  Chronic transfusion-dependent anemia , such as sickle cell disease or thalassemia cases of severe thrombocytopenia .

10. Monitoring pH, blood gases, electrolytes, and metabolic parameters  — Early and frequent measures of pH, blood gases, electrolytes, and metabolites such as glucose and lactate provide a wealth of information early in critical care and throughout massive transfusion.

11. The transfusion point can be determined preoperatively from the hematocrit and by estimating blood volume). Patients with a normal hematocrit should generally be transfused only after losses greater than 10% to 20% of their blood volume. The timing of transfusion initiation is based on the patient’s surgical procedure, comorbid conditions, and rate of blood loss.

12. Crystalloid versus blood products   —  Correction of a deficit in blood volume with crystalloid volume expanders works well for most mildly and moderately ill or injured patients. However, large volume resuscitation with crystalloid alone in severe trauma with massive blood loss can lead to dilutional coagulopathy as well as severe tissue swelling, with stiff lungs and abdominal compartment syndrome. Component ratio ( 1:1:1)  — For massive transfusion in most patient populations, ● Plasma  – ● Platelets   ● pRBCs  

13. Maximum ABL calculation The amount of blood loss necessary for the hematocrit to fall to 30% can be calculated as follows EBV calculation: body wt (kg) x average blood volume (ml/kg) ABL= [EBV x (Hi-Hf)]/Hi Where: EBV=Estimated Blood Volume Hi= initial hemoglobin Hf= final hemoglobin

14. Average blood volumes Premature Neonates 95 mL/kg Full Term Neonates 85 mL/kg Infants 80 mL/kg Adult Men 75 mL/kg Adult Women 65 mL/kg

15. COMPATIBILITY TESTING .ABO–Rh Testing The most severe transfusion reactions are due to ABO incompatibility; naturally acquired antibodies can react against the transfused (foreign) antigens, activate complement, and result in intravascular hemolysis. The patient’s red cells are also tested with anti-D antibodies to determine Rh status.. The probability of developing anti-D antibodies after a single exposure to the Rh antigen is 50% to 70%. Antibody Screen The purpose of 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)

16. A crossmatch mimics 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, and (3) it detects antibodies in low titers or those that do not agglutinate easily

17. Massive blood transfusion   – Massive transfusion was historically defined as transfusion of ≥10 units of whole blood (WB) or red blood cells (RBCs) in 24 hours.

18. Hemorrhage control resuscitation  – Hemorrhage control resuscitation involves giving plasma and platelets early in resuscitation to avoid dilutional coagulopathy that occurred with the historic use of crystalloid fluids for volume resuscitation and RBCs in additive solution to maintain oxygen-carrying capacity .

19. ● Damage control resuscitation  – Damage control resuscitation is the American military version of hemorrhage control resuscitation, with additional attention to hypothermia, acidosis, and fibrinolysis, as occurs in trauma-induced coagulopathy (TIC). Damage control resuscitation is the term typically used in the American trauma literature, either alone or in conjunction with damage control surgery. Historically, damage control resuscitation used RBCs, plasma, and platelets in a 1:1:1 ratio when platelets were available, and fresh whole blood (WB) when they were not available in austere settings in the Southwest Asian military theater [

20. POTENTIAL ADVERSE EFFECTS OF TRANSFUSION hypothermia Metabolic effects Hyperkalemia  —it is unclear how often this leads to clinical symptoms, particularly cardiac arrhythmias or cardiac arrest, for which there are only a few convincing reports One factor that might lead to cardiac symptoms is rapid infusion through a central venous catheter. There are three clinical settings in which there is an increased risk of transfusion-related hyperkalemia: ● Massive trauma   ● Impaired renal function  –fresher RBC units or washed red cells. ● Infants and newborns  f fresher RBC units, washed red cells, and/or a bedside potassium adsorption filter

21. Citrate toxicity  — Whole blood is collected using a balanced citrate solution to chelate calcium and prevent the collected blood unit from clotting. low levels of ionized calcium. The manifestations of hypocalcemia can include a sense of heightened anxiety, carpopedal spasm, tetanic contractions, and arrhythmias. Patient populations at risk for citrate toxicity include in massive transfusion if severe liver disease

22. Acid–Base Balance Although stored 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.. 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.

23. INFECTIOUS COMPLICATIONS Viral Infections A. 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.

24. B. Acquired Immunodeficiency Syndrome (AIDS ) All blood is tested for the presence of anti-HIV-1 and anti-HIV-2 antibodies the risk of transfusion-transmitted HIV to approximately 1:1,900,000 transfusions. C. Other Viral Infections Cytomegalovirus (CMV) and Epstein–Barr virus usually cause asymptomatic or mild systemic illness . Immunocompromised and immunosuppressed patients ( eg , premature infants, organ transplant recipients, and cancer patients) are particularly susceptible to severe transfusion-related CMV infections. Ideally, such patients should receive only CMV-negative units. However, recent studies indicate that the risk of CMV transmission from transfusion of leukoreduced blood products is equivalent to CMV test-negative units. Human T-cell lymphotropic viruses 1 and 2 (HTLV-1 and HTLV-2) are leukemia and lymphoma viruses, respectively, that have been reported to be transmitted by blood transfusion; the former has also been associated with myelopathy. Parvovirus transmission has been reported following transfusion of coagulation factor concentrates and can result in transient aplastic crises in immunocompromised hosts. West Nile virus infection may result in encephalitis with a fatality rate of up to 10%, and transmission of this virus by transfusion has been reported.

25. Parasitic Infections Parasitic diseases that can be transmitted by transfusion include malaria, toxoplasmosis, and Chagas disease 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 to 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.

26. INDICATIONS FOR PLATELET TRANSFUSION

27. Prevention of spontaneous bleeding  — We use prophylactic platelet transfusion to prevent spontaneous bleeding in most afebrile patients with platelet counts <10,000/ microL due to bone marrow suppression. For patients with fever, infection, or inflammation, we generally transfuse at a platelet count ≤15,000 to 20,000/ microL due to the increased risk of bleeding [ 33 ]. Patients with acute promyelocytic leukemia (APL) have a coexisting coagulopathy, and for them we transfuse at a platelet count ≤30,000 to 50,000/ microL

28. Dose  — A standard dose of platelets for prophylactic therapy in adults is approximately one WBD unit per 10 kg of body weight, which translates to four to six units of WBD platelets or one apheresis unit, both providing approximately 3 to 4 x 10 11  platelets This platelet dosing is expected to raise the platelet count by approximately 30,000/ microL within 10 minutes of the infusion

29. Infusion rate  — For an average-sized adult, six units of WBD platelets or one unit of apheresis platelets are transfused over approximately 20 to 30 minutes.

30. ACUTE TRANSFUSION REACTION Febrile and allergic reactions  —fever, and chills. Urticaria is common (1 to 3 percent), and febrile nonhemolytic reactions affect 0.1 to 1 percent. These reactions should be treated symptomatically. Volume overload (TACO)  — Transfusion-associated circulatory overload (TACO) is a form of volume overload that can occur with infusion of large volumes of plasma (or other blood products). Pulmonary edema can develop, especially in older adults, small children, and those with preexisting cardiac disease. TACO is relatively common (>1 percent), Volume overload can be avoided by reducing the rate of infusion to 1 mL/kg per hour in susceptible patients

31. Transfusion-related acute lung injury (TRALI)    Transfusion-related acute lung injury (TRALI) is a relatively common (<0.01 percent) and potentially fatal complication of blood product transfusion. It is characterized by new acute respiratory distress ( eg , hypoxemia, infiltrates on chest radiography) within six hours of transfusion. Since one of the mechanisms of TRALI is transfusion of donor antibodies directed against recipient HLA or neutrophil antigens, a worldwide approach to TRALI prevention involves preparing plasma components for transfusion from either male donors, never pregnant female donors, or female donors who have been screened and found not to have antibodies to HLA antigens. This action has resulted in a substantial drop in reported TRALI cases after plasma transfusion. Another approach involves using solvent/detergent treated plasma product (S/D plasma); these products are pooled from multiple donors and appear to have a negligible risk for TRALI

32. Anaphylactic reactions  —  occur in patients with IgA deficiency and antibodies to IgA]. These are relatively rare (1 in 20,000 to 1 in 50,000). Infection  — 

33.  TACO: transfusion-associated circulatory overload; TRALI: transfusion-related acute lung injury; FNHTR: febrile nonhemolytic transfusion reaction; AHTR: acute hemolytic transfusion reaction