Advances in Transfusion Medicine
2007; Elsevier BV; Volume: 25; Linguagem: Inglês
10.1016/j.aan.2007.07.005
ISSN1878-0415
AutoresDebra Nordmeyer, John E. Forestner, Michael H. Wall,
Tópico(s)Hemoglobin structure and function
ResumoTransfusion medicine has developed as a specialty by linking rapidly evolving knowledge in areas of physiology and immunology to the vastly expanded clinical requirements for blood products resulting from advances in medicine and surgery. This article covers major developments in transfusion medicine related to anesthesiology and surgery. It will familiarize the anesthesia practitioner with evolving concepts in basic science as they relate to innovations in clinical care in three areas: (1) red cell transfusion, (2) other blood components, and (3) recently introduced massive transfusion protocols. Blood component therapy is a limited resource that contributes to overall health care expense. In the United States, four million patients will receive 12 million units of packed red blood cells this year. The estimated hospital cost for a unit of autologous blood ranges from $250 to $750. Actual costs of transfusion therapy, alternatives to transfusion therapy, complications associated with transfusion therapy, and complications associated with anemia are unknown [1Lankin P.N. Hanson C.W. Manaker S. The intensive care unit manual. WB Saunders, Philadelphia2001Google Scholar]. The Transfusion Requirement in Critical Care trial has shown that a conservative strategy of red blood cell transfusion (transfusion for a hemoglobin of less than 7 g/dL) is as effective, if not superior to, a liberal transfusion strategy (transfusion for a hemoglobin less than 9 g/dL) in normovolemic critically ill patients [2Hebert P.C. Wells G. Blaichman M.A. et al.A multicenter randomized controlled clinical trial of transfusion requirements in critical care.N Engl J Med. 1999; 340: 409-417Crossref PubMed Scopus (4261) Google Scholar]. Following a conservative transfusion strategy, institutions may decrease costs by limiting perioperative erythrocyte transfusions and their complications [2Hebert P.C. Wells G. Blaichman M.A. et al.A multicenter randomized controlled clinical trial of transfusion requirements in critical care.N Engl J Med. 1999; 340: 409-417Crossref PubMed Scopus (4261) Google Scholar]. Erythrocytes compose an estimated 25 trillion of the 100 trillion cells that are found in the human body [3Stoelting R.K. Hillier S.C. Pharmacology and physiology in anesthetic practice.4th edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. The major function of the erythrocyte is to transport hemoglobin, which in turn carries oxygen from the lungs to the tissues. Along with oxygen transporting capacity, hemoglobin acts as an acid–base buffer. The buffering capacity of hemoglobin provides about 70% of the buffering capacity of whole blood. Red blood cells also remove carbon dioxide from the body by using carbonic anhydrase, an enzyme that catalyzes the reaction between carbonic acid and water. This reaction allows the red blood cell to transport carbon dioxide from the tissues to the lungs for elimination [4Guyton A.C. Hall J. Textbook of medical physiology.11th edition. W.B. Saunders, Philadelphia2006Google Scholar]. Each red blood cell contains 270 million hemoglobin molecules. Each molecule of hemoglobin carries four heme groups, and each heme group can bind with one molecule of oxygen. Four separate oxygen molecules bind to one molecule of hemoglobin, and each gram of hemoglobin carries 1.38 L of oxygen. The formula for the oxygen delivery capacity of blood is: DO2 = CO ∗ CaO2, where DO2 is oxygen delivery; CO is cardiac output, and CaO2 is the oxygen-carrying capacity of blood, and 10 changes volume % from O2/dL to ml O2/L. Cardiac output (CO) is recognized as: CO = HR ∗ SV, where HR is heart rate, and SV is stroke volume of the left ventricle. CaO2 is derived in the following way: (1.38∗hemoglobin∗ SaO2) + (0.0031∗PaO2), where SaO2 is the percent of hemoglobin saturated with oxygen in the arterial circuit; 0.0031 is the coefficient for oxygen solubility in blood. This equation illustrates PaO2 as a minimal part of oxygen delivery at sea level unless the hemoglobin or arterial blood saturation is decreased severely [5Marino P.I. The ICU book.2nd edition. JB Lippincott, Philadelphia1998Google Scholar]. The purpose of erythrocyte transfusion is to maintain or increase the oxygen carrying capacity of blood. There is almost no indication to transfuse a hemoglobin level greater than 10 g/dL but there is almost always an indication for hemoglobin less than 6 g/dL. Preoperative hematocrit and estimated blood volume can be used to predict transfusion requirements intraoperatively. One unit of packed red blood cells will increase the hematocrit by approximately 3% and the hemoglobin 1 g/dL in the average adult [6Morgan Jr., G.E. Mikhail M.S. Murray M.J. Clinical anesthesiology. 3rd edition. McGraw-Hill, New York2002: 632Google Scholar]. Estimated total blood volume is about 65 cc/kg of blood for women and 75 cc/kg of blood for men. The estimated total blood volume then is multiplied by the percent hematocrit (×/100), which gives the estimated red blood cell volume. The estimated red blood cell volume at a hematocrit of 30 (previously used as a hematocrit target for patients with cardiac disease) is the estimated total blood volume multiplied by 30/100. Subtracting the estimated blood volume at a hematocrit of 30 from the blood volume at the normal hematocrit gives the volume of blood the patient can lose to reach a hematocrit of 30 and gives a baseline at which to consider blood transfusion. For example, a 70 kg man has 70 kg ∗ 75 cc/kg of blood volume = 5250 cc of blood volume. If his hematocrit is 45, then 45% of his blood volume will be erythrocytes. His blood volume of 5250 cc multiplied by .45 will yield 2362.5 cc of erythrocytes. Using 30 as the previously targeted hemoglobin, his blood volume of 5250 ∗.30 will be 1575. Using these numbers, he will need to lose 2362.5 – 1575 = 787.5 cc before his hematocrit decreases to 30. Red blood cell transfusions are indicated in symptomatic anemic patients to restore oxygen-carrying capacity and delivery. Blood viscosity is determined primarily by erythrocyte concentration. In anemia, blood viscosity can decrease severely, which, in turn, decreases the resistance to blood flow in peripheral blood vessels. The decrease in peripheral resistance returns larger than normal quantities of blood from the tissues to the heart, which greatly increases cardiac output. Hypoxemia also results from the decreased transport of erythrocytes, which further decreases peripheral vascular resistance, allowing more blood return to the heart, further increasing CO and myocardial oxygen consumption. Not only does anemia decrease oxygen delivery, it also increases cardiac output, myocardial oxygen consumption, and possibly the risk of end organ ischemia [4Guyton A.C. Hall J. Textbook of medical physiology.11th edition. W.B. Saunders, Philadelphia2006Google Scholar]. The lowest limit of hemoglobin tolerated in people is not known, as critical limits for tissue oxygenation remain poorly defined [7Spahn D. Casutt M. Eliminating blood transfusion; new aspects and perspectives.Anesthesiology. 2000; 93: 242-244Crossref PubMed Scopus (228) Google Scholar]. Even with the detrimental effects of anemia, recent trials have indicated that transfusion is not necessarily the best treatment. Current opinion holds that a universal hemoglobin or hematocrit transfusion trigger is inappropriate for all patients or situations. Therefore, the historical transfusion triggers of hemoglobin of 10 and a hematocrit of 30 have fallen out of favor intraoperatively, postoperatively, and in ICU patients [2Hebert P.C. Wells G. Blaichman M.A. et al.A multicenter randomized controlled clinical trial of transfusion requirements in critical care.N Engl J Med. 1999; 340: 409-417Crossref PubMed Scopus (4261) Google Scholar]. Blood loss should be replaced with crystalloid or colloid solutions to maintain normovolemia until the danger of anemia outweighs the risks of transfusion. Patients who have low hemoglobin levels before surgery are at higher risk of receiving allogeneic transfusion. The ABO-Rh type, crossmatch, and antibody screen are compatibility tests. These tests were designed to demonstrate harmful antigen–antibody interactions in vitro so harmful in vivo interactions could be prevented [8Miller R. Cucchiara R. Miller E.D. Miller's anesthesia. 6th edition. Churchill Livingstone, New York2002: 1801-1802Google Scholar]. Pretransfusion testing is performed to ensure ABO compatibility between the donor and the recipient. The ABO group remains the most important factor tested, because the most likely cause of death secondary to transfusion therapy is ABO incompatibility [9Speiss B.D. Spence R.K. Shander A. Perioperative transfusion medicine. 2nd edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. There are three common alleles present on the ABO locus on chromosome 9. ABO is based on inheritance of genes that encode for glycosyltransferases that add specific sugars to make an A or B antigen. The genes are codominant, so an individual inheriting both genes is designated as having AB blood type. Homozygous AA and heterozygous AO are both known as type A blood. The inheritance of O does not create a functional enzyme. Patients make antibodies to the antigens that they lack. Type O people lack A and B antigens on their red cells, so they will have anti-A and anti-B antibodies in their plasma. These naturally occurring antibodies occur in patients even with no prior blood exposure. The antibodies produced against ABO antigens are IgM and capable of causing intravascular hemolysis if incompatible blood is transfused. In ABO testing, a sample of whole blood is centrifuged to separate red cells from serum. This process allows the red cells and serum to be tested separately and allows the type to be double-checked. The ABO group is determined by mixing the patient's red cells using anti-A and anti-B reagents and by reverse-typing the patient's serum against A and B reagent cells. If agglutination occurs with anti-A reagent, then the patient has type A blood. If agglutination occurs with anti-B reagent, then it is type B blood. If both cause agglutination, it is type AB, and if there is no agglutination, then it is type O blood. The patient's serum is screened for the presence of unexpected antibodies by incubating it with selected reagent red cells (screen cells) using an antihuman globulin (AHG) technique (indirect antiglobulin or Coombs test.) (Table 1).Table 1ABO compatibility testingRed cells tested withSerum tested withBlood groupAnti-AAnti-BA cellsB cellsA+−−+B−++−AB++−−O−−++Abbreviations: +, agglutination; −, no agglutination.Reprinted from Miller R, Cucchiara R, Miller ED, editors. Miller's anesthesia. 6th edition. New York: Churchill Livingstone; 2002. p. 1801–2; with permission from Elsevier. Open table in a new tab Abbreviations: +, agglutination; −, no agglutination. Reprinted from Miller R, Cucchiara R, Miller ED, editors. Miller's anesthesia. 6th edition. New York: Churchill Livingstone; 2002. p. 1801–2; with permission from Elsevier. The type and screen test looks only for the ABO-Rh type and screens for any unexpected antibodies. The Rh system has more than 40 red blood cell (RBC) antigens, but D, C, E, c, and e are the most significant of these antigens. Clinically, the D antigen is the most immunogenic RBC antigen and is known as the Rh factor. The antibody screen consists of detecting abnormal red blood cell antibodies to clinically significant antigens. There are more than 600 antigens, but only a fraction of these are noted to be clinically significant [9Speiss B.D. Spence R.K. Shander A. Perioperative transfusion medicine. 2nd edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. If the antibody screen is negative, and the patient has no past history of unexpected antibodies, it can be predicted that more than 99.99% of ABO-compatible red blood cell units would be compatible with an AHG crossmatch. If the antibody screen is positive (approximately 1% of patients), the unexpected antibody or antibodies must be identified before antigen negative-compatible RBCs can be found. This process usually takes several hours [10Benson K. Chapin J. Despotis G. et al.Q & A about transfusion practice.3rd edition. American Society of Anesthesiologists, Park Ridge (IL)1997Google Scholar]. The type and cross includes the ABO-Rh type and antibody, screen but it also includes mixing donor red blood cells and recipient serum to inspect for any reactions. The crossmatch takes between 45 to 60 minutes and is characterized by three phases, immediate, incubation, and antiglobulin phases. The two most important phases are the incubation and antiglobulin phases, because the antibodies that appear in these phases can cause severe hemolytic reactions. Once donor blood is crossmatched with recipient blood, that blood is made unavailable to anyone other than the crossmatched recipient by the blood bank for up to 48 hours [8Miller R. Cucchiara R. Miller E.D. Miller's anesthesia. 6th edition. Churchill Livingstone, New York2002: 1801-1802Google Scholar]. Emergent blood supplies should be ABO type O, as this is the least antibody-inducing type of blood. Donor blood used for emergency transfusion of group-specific blood must be screened for both hemolytic anti-A or anti-B antibodies. The Rh factor should be negative, but Rh factor positive blood can be used in men, and postmenopausal women with a small risk of reaction. Rh factor positive blood should not be used in premenopausal women because of the risk of transfusing Rh-positive blood into an Rh-negative female and causing erythroblastosis fetalis in subsequent pregnancies [8Miller R. Cucchiara R. Miller E.D. Miller's anesthesia. 6th edition. Churchill Livingstone, New York2002: 1801-1802Google Scholar]. Table 2 summarizes donor blood groups that patients may safely receive.Table 2Donor blood groups that patients can receiveDonorRecipientOO, A, B, ABAA, ABBB, ABABABReprinted from Miller R, Cucchiara R, Miller ED, editors. Miller's anesthesia. 6th edition. New York: Churchill Livingstone; 2002. p. 1801–3; with permission from Elsevier. Open table in a new tab Reprinted from Miller R, Cucchiara R, Miller ED, editors. Miller's anesthesia. 6th edition. New York: Churchill Livingstone; 2002. p. 1801–3; with permission from Elsevier. There are many complications associated with blood transfusion. Transfused blood has been shown to cause immunomodulation, systemic inflammatory response, occlusion of microvasculature, and an increased risk of postoperative low-output heart failure when transfusion occurs during coronary artery bypass surgery [11Surgenor S.D. DeFoe G.R. Fillinger M.P. et al.Intraoperative red blood cell transfusion during coronary artery bypass grafting increases low output heart failure.Circulation. 2006; 114: I43-I48PubMed Google Scholar]. Allogeneic red blood cell transfusions can induce immunomodulation in the recipient of the transfusion. Allogeneic donor leukocytes appear to mediate significant immunomodulating effects. Leukocyte depletion may reduce the immunomodulation. Immunomodulation caused by transfusion can increase the incidence of postoperative infections and increase the risk of tumor recurrence in patients who have resected malignancies [12Varmvakas E.C. Transfusion-associated cancer recurrent and postoperative infection: meta-analysis of randomized, controlled clinical trials.Transfusion. 1996; 36: 175-186Crossref PubMed Scopus (183) Google Scholar]. There is a dose–response relationship showing immunomodulation increases with the increasing number of allogeneic erythrocyte transfusions administered [13Blumberg N. Heal J.M. Immunomodulation in blood transfusion: an evolving scientific and clinical challenge. The science of medical care.Am J Med. 1996; 101: 299-308Abstract Full Text PDF PubMed Scopus (176) Google Scholar]. Immunomodulation can be beneficial for transplant patients. Allogeneic blood transfusions have been shown to improve allograft survival in renal transplants [14Opel G. Terasaki P. Improvement of kidney graft survival with increased number of transfusions.N Engl J Med. 1978; 299: 799Crossref PubMed Scopus (369) Google Scholar]. The mechanism of immunomodulation is suspected to be caused by up-regulation of humoral immunity and down-regulation of cell mediated immunity [15Klein H. Immunomodulatory aspects of transfusion: a once and future risk?.Anesthesiology. 1999; 91: 861-865Crossref PubMed Scopus (140) Google Scholar]. Three types of allergic reactions to erythrocyte transfusions are mild, moderate, and anaphylaxis. If any of these transfusion reactions are noted, the transfusion should be stopped, and a new sample of blood should be sent for retype and cross. A mild allergic reaction will cause focal urticaria that occurs in approximately 3% of patients. It is characterized by well-circumscribed, localized, erythematous, raised, urticarial lesions or hives, and is not associated with other symptoms. The transfusion should be held to administer antihistamines and resumed if the reaction stops. A moderate allergic reaction is seen clinically as a more widespread skin rash and a respiratory component, including bronchospasm or stridor. The transfusion should be stopped, and the patient may require steroids and vasopressors [9Speiss B.D. Spence R.K. Shander A. Perioperative transfusion medicine. 2nd edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. Anaphylaxis is the most severe systemic allergic reaction and is a medical emergency. It occurs in 1 in 20,000 to 47,000 blood transfusions. It has multiple organ system involvement. The symptoms generally begin with hives, dyspnea, flushing, wheezing, and they progress to coughing, stridor, and cardiovascular collapse. The transfusion must be stopped immediately, and the patient should be treated with epinephrine, diphenhydramine, histamine 2 receptor antagonist, steroids, and intravenous fluids [9Speiss B.D. Spence R.K. Shander A. Perioperative transfusion medicine. 2nd edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. The febrile nonhemolytic transfusion reaction is one of the most common causes of temperature change during blood transfusions. The temperature must change by more than 1°C or 2° F. This reaction can be accompanied by chills or anxiety, and it is seen most often in patients who have multiple transfusions and in multiparous women. Once fever is detected, the transfusion should be stopped, and the patient should be treated with antipyretics [16Harmening D.M. Modern blood banking and transfusion practices.5th edition. FA Davis, Philadelphia2005Google Scholar]. Once the temperature begins to decrease and the suspicion of septic transfusion reaction or acute hemolytic transfusion reaction is eliminated, the transfusion may be started again. Bacterial contamination of transfused RBCs can cause sepsis in the transfusion recipient. The most common organism associated with contamination is Yersinia enterocolitica and other gram-negative organisms. Bacterial contamination of RBC units is related directly to the length of storage [17Goodnough L.T. Brecher M.E. Kanter M.H. et al.Transfusion medicine, blood transfusion.N Engl J Med. 1999; 340: 438-447Crossref PubMed Scopus (832) Google Scholar]. Contamination with gram-negative organisms is the result of occult asymptomatic transient donor bacteremia occurring during collection. The growth of the cryophilic bacteria Yersinia, Serratia, and Pseudomonas is enhanced by the refrigerated storage conditions of RBCs. Endotoxin produced by these organisms also can induce fulminant sepsis in the recipient. Septic transfusion reactions caused by gram-negative rods can be rapidly fatal, with a mortality rate of 60% [9Speiss B.D. Spence R.K. Shander A. Perioperative transfusion medicine. 2nd edition. Lippincott Williams and Wilkins, Philadelphia2006Google Scholar]. It can evolve over several hours and go unrecognized. Clinically, a temperature increase of greater than 2 or 3°C, severe hypotension, hypertension, disseminated intravascular coagulation, and shock are seen. These signs and symptoms may be absent in a cold surgical patient or a patient who has a postoperative fever. If these symptoms occur, the transfusion should be stopped and a sample of blood sent for culture from the patient and from the donor unit. If there is a high suspicion, treatment should be initiated immediately without waiting for cultures. Broad-spectrum antibiotics, treatment for shock, acute renal failure (ARF), and disseminated intravascular coagulation (DIC) should be initiated immediately. Although restricting the use of antibiotics and particularly broad-spectrum antibiotics is important for limiting superinfection and for decreasing the development of antibiotic-resistant pathogens, patients who have severe sepsis warrant empirical therapy until the causative organ is identified [18Dellinger R.P. Carlet J.M. Masur H. et al.Surviving sepsis campaign guidelines for management of severe sepsis and septic shock.Crit Care Med. 2004; 32: 858-872Crossref PubMed Scopus (2641) Google Scholar]. The acute hemolytic transfusion reaction is a frequent cause of a fatal transfusion reaction caused by ABO incompatibility. The incidence is 1 per 250,000 to 1,000,000 transfusions [17Goodnough L.T. Brecher M.E. Kanter M.H. et al.Transfusion medicine, blood transfusion.N Engl J Med. 1999; 340: 438-447Crossref PubMed Scopus (832) Google Scholar]. Half of all deaths from acute hemolytic transfusion reactions are secondary to administrative errors. The severity of this reaction is related to the amount of blood transfused. If acute hemolytic transfusion reaction is suspected, the transfusion must be stopped and the untransfused blood returned to the blood bank along with a sample of the patient's blood for retyping and crossmatching. Supportive care should ensue. Transfusion-related acute lung injury, more commonly known as TRALI, is an acute severe respiratory distress syndrome with an incidence of 1 per 5000 units transfused [18Dellinger R.P. Carlet J.M. Masur H. et al.Surviving sepsis campaign guidelines for management of severe sepsis and septic shock.Crit Care Med. 2004; 32: 858-872Crossref PubMed Scopus (2641) Google Scholar]. It usually occurs within 4 hours after transfusion and is characterized by the acute onset of dyspnea and hypoxemia, and it progresses to noncardiogenic pulmonary edema requiring mechanical ventilation and ICU treatment. The PaO2 to FIO2 ratio will be less than 300, the SpO2 less than 90% on room air, and the chest radiograph will show bilateral pulmonary infiltrates. Donor leukoagglutinins and donor antibodies to human leukocyte antigens (HLA), which react with the recipient leukocytes and monocytes, are hypothesized to cause TRALI. This reaction activates complement, which in turn leads to neutrophil aggregation and increased permeability of the pulmonary microcirculation. Multiparous female donors typically carry these leukoagglutinins [19Murray M. Coursin D. Pearl R. et al.Critical care medicine: perioperative management.2nd edition. Lippincott Williams and Wilkins, Philadelphia2002Google Scholar]. Treatment of TRALI includes supportive measures, supplemental oxygen, tracheal intubation, mechanical ventilation, and positive end-expiratory pressure (PEEP) as indicated. The reaction usually resolves within 48 hours, and 90% of patients experience a complete recovery. Most cases resolve within 4 days of transfusion, but there is a high (5 in 100) incidence of fatal reaction. The incidence of pulmonary edema and acute respiratory distress syndrome (ARDS) is higher in patients who are transfused liberally [20Wall M. Surgenor S. Concepts of transfusion triggers.American Society of Anesthesiologists Newsletter. 2006; 70: 17Google Scholar]. Delayed transfusion reactions consist of viral contamination, delayed hemolytic transfusion reactions, and graft versus host disease (GVHD). Viral risks include HIV, hepatitis viruses A, B, and C (HAV, HBV, HCV), and human T-cell lymphotrophic virus types I and II. Some new viruses include hepatitis G virus, Torque teno (TT) virus, and human herpes virus 8 (associated with Kaposi's sarcoma) [21Monk T. Acute normovolemic hemodilution.Anesthesiol Clin North America. 2005; 23: 271-281Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar]. For HIV transmission, there is an incidence of 1 in 676,000; for HCV, the incidence is 1 in 103,000, and for HBV the incidence is 1 in 63,000. Along with multiple viruses, there is the risk of transmission of bacteria, parasites, and malaria. To date, malaria, Chagas disease, severe acute respiratory syndrome, and variant Creuzfeldt Jakob disease cannot be detected by screening tests [22Mungai M. Tegtmeier G. Chamberland M. et al.Transfusion transmitted malaria in the United States 1963–1999.N Engl J Med. 2001; 344: 1973-1978Crossref PubMed Scopus (218) Google Scholar]. GVHD is a rare complication resulting from foreign lymphocytes, and 90% of patients die. GVHD is T-lymphocyte mediated and usually occurs within 2 weeks of the transfusion. GBHD targets the host endothelium and bone marrow, which results in an aplastic anemia and pancytopenia. It usually is seen in immunosuppressed patients. The only known prevention of this reaction is radiograph or gamma radiation of the donor RBCs to inactivate all donor T cells [16Harmening D.M. Modern blood banking and transfusion practices.5th edition. FA Davis, Philadelphia2005Google Scholar]. Hyperkalemia, hypocalcemia, and acid-base alterations are the most commonly noted metabolic complications induced by blood transfusion. Hyperkalemia usually is seen in massive transfusions with increased red cell lysis or in renal failure. When red cells are stored, they leak potassium into their storage fluid, but leakage is corrected with transfusion and replenishment of cell energy stores. Hypocalcemia can occur, because citrate binds calcium and is used as an anticoagulant in stored blood products. Rapidly transfusing RBCs may decrease the level of ionized calcium in the recipient. The liver should metabolize the citrate, but in clinical scenarios with impaired liver function, liver transplantation, or hypothermia, citrate metabolism may be decreased. Ionized calcium levels should be followed, because total serum calcium measures the citrate-bound calcium and may not reflect free serum calcium accurately. Alterations in acid–base status occur, because stored blood is becomes more acidic secondary to the accumulation of RBC metabolites. The acid load is minimal when transfused. Alkalosis following a massive transfusion is common secondary to metabolism of citrate to bicarbonate by the liver [6Morgan Jr., G.E. Mikhail M.S. Murray M.J. Clinical anesthesiology. 3rd edition. McGraw-Hill, New York2002: 632Google Scholar]. Reasons to seek alternatives to allogeneic blood transfusions are numerous, including infectious risks, short supply, rare blood phenotypes, massive transfusion settings, and patient refusal of allogeneic blood transfusion. Blood conservation strategies include autologous blood transfusion, acute normovolemic hemodilution, and intraoperative blood recycling. Future options may include artificial oxygen carriers. There are several ways to perform autologous blood donation. The techniques include acute normovolemic hemodilution, preoperative blood donation, and intraoperative blood salvage. When considering perioperative autologous blood donation, it is mandatory to carefully select patients to reduce the rate of discarded autologous units. Autologous blood donation is one of the simplest, most economical ways to decrease the amount of allogenic blood transfusion used [23Goodnough L.T. Autologous blood donation.Anesthesiol Clin North America. 2005; 23: 263-270Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar]. Acute normovolemic hemodilution uses intraoperative venous drainage of one or more units of blood, with intraoperative storage of this blood. The blood removed is replaced milliliter for milliliter with colloid or 3 cc of crystalloid to 1 cc of blood removed. Blood replacement with dextran or hetastarch may result in coagulation defects. Crystalloid and colloid volume replacement also decreases the risk of anaphylaxis associated with dextran. The volume replacement allows the blood lost intraoperatively to have a lower hematocrit, with the idea that more dilute blood may be lost and then replaced with the more concentrated blood removed at the beginning of the case [24Jones S. Whitten C. Despotis G. et al.The influence of crystalloid and colloid replacement solutions in acute normovolemic hemodilution: a preliminary survey of hemodynamic markers.Anesth Analg. 2003; 96: 363-368PubMed Google Scholar]. The amount of blood that can be removed during hemodilution is calculated using the formula V = EBV x Hi-Hf/Hav, where V is the volume of blood expected to be removed; EBV is estimated blood volume (TBW(kg) ∗ 60 cc/kg (female) or 70 cc/kg (male). Hi is the patient's initial hematocrit level before onset of hemodilution; Hf is the desired hematocrit at the end of hemodilution, and Hav is the average hematocrit level during hemodilution (Hi + Hf/2) [21Monk T. Acute normovolemic hemodilution.Anesthesiol Clin North America. 2005; 23: 271-281Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar]. Acute normovolemic hemodilution is useful and cost-effective in procedures where expected es
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