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16 Blood Substitutes andArticial Oxygen Carriers
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HBOCs continue to offer a glimpse of what can be pos­sible. A future without the need for blood donation and blood transfusion may be a lofty but still worthwhile goal. With continued research and study, it is possible to come up with a compound that can at the very least reduce our reliance on blood product administration, which will benet the health­care system and most importantly the patient tremendously.
References
1. Winslow RM. Blood substitutes, a moving target. Nature Med.
1995;1:1212–5.
2. Fridey JL, Silvergleid AJ, Tirnauer JS editors. Oxygen carriers as
alternatives to red blood cell transfusion. Up to Date. Accessed 30 Aug 2019. https://www-uptodate-com.proxy1.lib.tju.edu/con-
tents/oxygen-carriers-as-alternatives-to-red-blood-cell-transfu­sion?search=oxygen%20carriers%20as%20alternatives%20to%20 red%20blood%20cell%20transfusion&source=search_result& selectedTitle=1~150&usage_type=default&display_rank=1
3. Scott MG, Kucik DF, Goodnough LT, Monk TG.Blood substitutes:
evolution and future applications. Clin Chem. 1997;43(9):1724.
4. Natanson C, Kern SJ, Lurie P, Banks SM, Wolfe SM. Cell-free
hemoglobin-based blood substitutes and risk of myocardial infarc­tion and death: a meta-analysis. JAMA. 2008;299(19):2304. Epub 28 Apr 2008.
5. Szebeni J, Wassef NM, Hartman KR, Rudolph AS, Alving
CR. Complement activation in vitro by the red cell substitute, liposome-encapsulated hemoglobin: mechanism of activation and inhibition by soluble complement receptor type 1. Transfusion. 1997;37(2):150.
6. Scott MG, Kicik DF, Goodnough LT, Monk TG.Blood substitutes:
evolution and future applications. Clin Chem. 1997;43(9):1724–31.
7. Kerins DM.Role of the peruorocarbon Fluosol-DA in coronary angioplasty. Am J Med Sci. 1994;307(3):218.
8. Donahue LL, Shapira I, Shander A, Kolitz J, Allen S, Greenburg G. Management of acute anemia in a Jehovah’s witness patient with acute lymphoblastic leukemia with polymerized bovine hemoglobin­erature. Transfusion. 2010;50(7):1561.
9. Mer M, Hodgson E, Wallis L, Jacobson B, Levien L, Snyman J, Sussman MJ, James M, van Gelder A, Allgaier R, Jahr JS.Hemoglobin glutamer-250 (bovine) in South Africa: consensus usage guidelines from clinician experts who have treated patients. Transfusion. 2016;56(10):2631. Epub 2016 Sep 23
10. Kim HW. Acellular hemoglobin-based oxygen carrier mediated blood pressure elevation and vasoconstriction: a review of proposed mechanisms and contributing factors. In: Kim H, Greenburg A, edi­tors. Hemoglobin-based oxygen carriers as red cell substitutes and oxygen therapeutics. Berlin/Heidelberg: Springer; 2013.
11. Estep TN.HBOCs and cardiac integrity. In: Kim H, Greenburg A, editors. Hemoglobin-based oxygen carriers as red cell substitutes and oxygen therapeutics. Berlin/ Heidelberg: Springer; 2013.
12. Jahr JS, Chung M, Anvarhosseini A, Kim HW. Effects of hemoglobin­H, Greenburg A, editors. Hemoglobin-based oxygen carriers as red cell substitutes and oxygen therapeutics. Berlin/Heidelberg: Springer; 2013.
13. Smani Y. HBOC interferences with routine clinical laboratory tests. In: Kim H, Greenburg A, editors. Hemoglobin-based oxy­gen carriers as red cell substitutes and oxygen therapeutics. Berlin/ Heidelberg: Springer; 2013.
14. Trakarnsanga K, Grifths R, Wilson M, Blair A, Satchwell T, Meinders M, Cogan N, Kupzig S, Kurita R, Nakamura Y, Toye A, Anstee D, Frayne J.An immortalized adult human erythroid line facilitates sustainable and scalable generation of functional red cells. Nature Communications. 2017;8:14750.
based oxygen carrier: a case report and review of lit-
based oxygen carriers on blood coagulation. In: Kim
Preoperative Therapy forAnemia
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LarryR.Hutson Jr, JohnC.Cargile, andGarrettD.Starling
17
Denition andPrevalence ofAnemia
Any discussion of anemia and its correction must include a denition of anemia. For the past several decades, the World Health Organization (WHO) has been the authority on global anemia prevalence, tracking rates of anemia, and the most common causes [7]. The WHO denes anemia as a hemoglo­bin concentration of less than 13.0g per 100milliliters (g/ dL) in adult men (15years of age and up), less than 12g/dL in children ages 12–14 and in nonpregnant women, less than
11.5g/dL in children ages 5–11, and less than 11 g/dL in children under the age of 5years and in pregnant women. The WHO further breaks down anemia into mild, moderate, and severe categories (Table17.1) [8]. Adult women with a hemoglobin of 12g/dL are twice as likely as men with 13g/ dL of hemoglobin to require a transfusion– usually due to lower circulating blood volumes– therefore their threshold for anemia is set 1g/dL less than for men [9].
In the latest examination of anemia from the WHO, the overall rate globally was 32.9% [8]. In some high-risk popu­lations, the incidence of anemia may range from 50% to 80%, with 10–20% suffering from moderate to severe ane­mia [10]. Those at highest risk are individuals low in socio­economic status, low in body weight, and experiencing post-partum [11]. Of course, the rate and cause of anemia vary across countries. Iron deciency is most common, fol­lowed by parasitic infections (malaria, schistosomiasis, and hookworms), then hemoglobinopathies, and obstetric/gyne­cologic disorders [7].
In the United States, studies demonstrate that anemia is present in 5.1–6.1% of the overall population, with a rate of moderate to severe anemia of 1.4–1.7% (excluding pregnant
L. R. Hutson Jr · J. C. Cargile · G. D. Starling (*) Texas A&M University – College of Medicine, Bryan, TX, USA
Baylor Scott and White Medical Center – Temple, Department of Anesthesiology, Temple, TX, USA e-mail: Larry.hutson@bswhealth.org; John.cargile@bswhealth.org;
Garrett.starling@bswhealth.org
Table 17.1
Population Severe Moderate Mild Children 6–59months <7 7–9.9 10–10.9 Children 5–11years <8 8–10.9 11–11.4 Children 12–14years <8 8–10.9 11–11.9 Non-pregnant women <8 8–10.9 11–11.9 Pregnant women <7 7–9.9 10–10.9 Men (over 15years) <8 8–10.9 11–12.9
Anemia denitions (in g/dL) by population group [10]
women). Women have double the risk of men and ve times the risk for moderate to severe anemia until the age of 80years old, at which point the rate is equal for both genders [12]. It is present at triple the frequency in African Americans [13]. While the data demonstrates that the general US population would be classied as having a mild public health issue, ane­mia is a more serious health concern for certain subgroups due to their higher rates of both anemia and moderate to severe anemia: African Americans, Hispanics, adults over 60years of age, nonpregnant women of reproductive age, and pregnant women [8, 12]. Iron deciency anemia is present at a lower rate in the United States compared with other coun­tries around the globe, which means that a higher proportion of anemia causes can be attributed to hemoglobinopathies, chronic kidney disease, and gastrointestinal bleeding than in lower income countries, though iron deciency anemia is still the most common kind in the United States [7, 12].
anemia. Those aged 75–84years old had a rate of 13%; this almost doubles to 23% above the age of 85 [14]. Overall, this gave a prevalence of 17%, with roughly a third categorized as moderate to severe [15].
increased over the general population, with 19% of admitted patients presenting with anemia. More interesting, 60% of those who were not anemic on admission developed hospital­acquired anemia [16]. A European study of cancer patients demonstrated that those undergoing radiation therapy had an
Denitions of anemia
As people increase in age, so too does the prevalence of
For patients who are hospitalized, anemia rates are
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anemia frequency of 29%, while cis-platinum-based chemo­therapy patients had almost triple that at 75% [17]. Congestive heart failure patients are commonly anemic (17%), resulting in worsening survival [18, 19].
In noncardiac surgical patients overall, the rate of anemia was around 34%, with three quarters of that due to iron de­ciency [20]. Certain surgical cohorts face their own anemia challenges. Orthopedic patients present with anemia at a fre­quency of 10.5%, with the major causes split between nutri­tional deciencies and anemia of chronic inammation [21]. In patients scheduled for colorectal cancer resection, more than half present with iron deciency, though not necessarily with anemia [22].
In terms of trends, the global prevalence decreased from
40.2% when studied by the WHO in 1990, to the most recent rate of 32.9% in the report published in 2011 [8]. Most of these gains occurred in women and children, who have been the focus of an action plan related to improving nutrition in these populations from the World Health Assembly, as well as other programs – such as the UN Secretary-General’s Every Woman Every Child initiative and the Global Strategy for Women’s and Children’s Health– that have emphasized a reduction in risk factors that adversely affect these two groups [23]. In the United States, the prevalence of both ane­mia and moderate to severe anemia almost doubled between 2003 and 2012 for reasons that are unclear [12].
Risks ofAnemia forSurgery
Preoperative anemia imposes increased risks of morbidity and mortality for surgical patients [24]. While the severity and cause of anemia are important determinants of risk level, any degree of anemia may negatively impact a patient’s risk for perioperative transfusion, intraoperative and postopera­tive complications, as well as length of hospital stay and readmission rate [2527]. In fact, a preoperative hemoglobin lower than 10g/dL is associated with an almost threefold increase in postoperative pulmonary complications [28, 29]. While morbidity increases with hemoglobin levels less than 10 g/dL, mortality rate increases with hemoglobin levels below 7, and as levels approach 2.5g/dL without transfusion, mortality is 50% [30, 31]. The current recommendation for transfusion threshold is 7g/dL in stable, hospitalized adult patients; however considerations such as preexisting cardiac disease, ongoing or expected blood loss, and type of surgery may necessitate a higher threshold [32, 33].
Preoperative anemia increases the chance of red blood cell transfusion, and while red blood cell transfusion is the most effective and immediate way of increasing oxygen­carrying capacity in an anemic patient at risk for ischemia, it is itself associated with increased risks. Transmission of infection, transfusion-related acute lung injury (TRALI),
transfusion-associated circulatory overload (TACO), and numerous types of hypersensitivity and hemolytic reactions remain real concerns [
The world blood supply is safer than ever before, but cer­tain bacteria, viruses, prions, and parasites still may be trans­mitted through transfusion of blood products. All donors are risk screened with a questionnaire and all blood units tested for various infectious agents. There is a comprehensive list of pathogens and the tests used to screen them on the US Food and Drug Agency website. Despite this, there remains a risk that an emerging pathogen– not yet identied as a threat to be tested – may still be transmitted during transfusion.
As discussed in a separate chapter on complications of blood transfusions, transfusion-related acute lung injury (TRALI) is a potential life-threatening reaction to donor unit(s) that manifest as dyspnea, hypotension, and fever. The vast majority of cases are due to multiparous, female donors that have anti-HLA and/or anti-granulocyte antibodies. While red blood cell units have little plasma in them, there may still be enough donor antigens present to react with recipient antibodies. Transfusion-related circulatory over­load (TACO) results from overwhelming of the body’s abil­ity to compensate for the increased volume introduced into the circulatory system with transfusion. Susceptibility to this varies with patient preexistent comorbidities, acute/chronic illness, and the volume transfused. Treatment consists of diuretics and judicious use of transfusion products.
Hypersensitivity reactions are due to allergens, primarily IgA and haptoglobin. The rate is approximately 0.15% for red blood cell transfusion [ included in this category, but many others occur. Treatment is generally symptomatic. Mild reactions may be treated with an antihistamine and steroids. More serious reactions may require stabilization with epinephrine. When a sus­pected allergic reaction to transfusion occurs, serum tryptase levels may be drawn as a conrmatory test. Tryptase is released in large amounts from granulocytes during an aller­gic reaction and remains high for as long as 2h after release.
Hemolytic reactions– the destruction of red blood cells during or after a transfusion – may be immune or non­immune mediated. Immune-mediated hemolytic reactions are caused by transfusing red blood cells that are incompati­ble with the patient’s anti-A, anti-B, or other red blood cell antibodies. Sometimes, this reaction may be delayed. If a patient develops antibodies after a transfusion, the level of those antibodies may diminish over time. These antibodies may, in fact, be undetectable by standard crossmatching techniques. Then, after a subsequent transfusion, through an anamnestic response, the antibody levels may increase lead­ing to a delayed hemolytic transfusion reaction.
There have been studies that demonstrate increased rates of hepatic cancer and non-Hodgkins lymphoma among
34].
35]. TRALI and TACO are
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patients who received blood transfusions, though the con­cept is controversial, as there has never been a study show­ing direct causation. Theories exist that suggest a link to transmission of viruses that cause cancer, or due to a direct transfer of cancer cells through blood transfusion. Immunomodulation has also been suggested as a mecha­nism. There are previously described models where this happens, such as how the hepatitis C virus can be a precipi­tating factor for hepatocellular carcinoma and how the E virus is associated with lymphoma. However, for every theory there are multiple confounding variables that limit the logic of the argument [36]. The risk of cancer may just be related to the corresponding risk of transmission of any offending virus. This is discussed in greater detail in another chapter.
Preoperative Anemia Clinic
There was a time when patients would donate their own blood weeks in advance of surgery for their own use. This autologous blood prevented issues with type compatibility, but is nevertheless on the decline as institutions nd that costs are high, about half of the units go to waste instead of being used, and patients often arrived for surgery anemic as a result of the donation, thus increasing their risk [37]. Correcting anemia through (non-autologous) blood trans­fusion introduces the previously described risks, resulting in detrimental effects to the surgical outcome as well as longer lengths of hospital stay postoperatively, higher rates of ICU admission, and increased rates of in-hospital mor­tality [3842].
Instead, hospitals are increasingly turning to the use of a preoperative anemia clinic (PAC) in the hope of resolving anemia in patients who can afford to delay surgery. One of the earliest and best described PACs was created at Duke University’s School of Medicine. Flowing out of the early success of enhanced recovery after surgery protocols (ERAS), in July 2013, they created a multidisciplinary team – the Perioperative Enhancement Team (POET)– in order to optimize patients bound for surgery, which included a PAC [43]. The PAC portion started as a pilot program for orthopedic patients intended to receive lower extremity total joint replacement due to the high relative rate of blood trans­fusion for this service line despite aggressive use of antibri­nolytics, cell salvage when appropriate, and restrictive transfusion practices [44].
There is currently no level-one evidence for improved outcomes in the treatment of preoperative anemia [45]. On the other hand, it stands to reason that the use of PACs for those at higher risk for perioperative transfusion might lead to a reduction in those same transfusions, thus allowing for better overall management of the blood supply, especially
since blood collection historically has fallen behind the demand [
length of stay (from 5.5 days down to 3.5 days) for those patients with anemia who were referred to their PAC, as well as a 48% reduction in the number of units of blood trans­fused in that same cohort [47]. Another institution reported a similar decrease in length of stay for patients who were treated in their PAC, as well as a 37% reduction in the num­ber of patients who were transfused perioperatively. Their initial calculated cost savings were estimated to be $200,000 per year for their hospital, a gure which did not include length of stay savings [48]. The nancial modeling of the Duke POET program projected net savings of $2.5 million over 5years, a result of decreased transfusion rates, improved outcomes, and revenue generation from preoperative infu­sions, all despite the costs associated with the PAC and increased preoperative testing [44].
around preoperative correction of anemia relates specically to iron deciency anemia. A study of colorectal surgery patients demonstrated an average reduction in length of stay by a little over 2days, as well as cost savings (both direct and indirect) of between $300 and $500, depending on the for­mulation of intravenous iron used [ reduced their transfusion rate in lower extremity total joint patients from 26.4% to 11.5%, also using intravenous iron in patients with IDA [50]. A longer ranging, far larger study– the PREVENTT trial, designed to provide sufcient study power to demonstrate the effects of intravenous iron on pre­operative anemia before major open abdominal operations– is currently underway in the United Kingdom, with enrollment in the study to be completed in late 2019 [51].
a PAC, as patient populations, hospital resources, and surgi­cal cases done at that institution can vary greatly. To start a program with the entire surgical population would be daunt­ing. Furthermore, not all anemic patients need a delay and aggressive therapy for their condition, given that minor pro­cedures are unlikely to result in transfusion [46]. Guinn etal. in a publication regarding the creation of POET described beginning with a pilot population, one that had signicant rates of anemia amenable to treatment, high perioperative transfusion rates, consistent follow-up, and a surgical team willing to delay an operation in favor of preoperative hemo­globin optimization. Some institutions utilize point-of-care testing equipment to allow for initial screening for anemia in the surgical clinics before the patient leaves from the consul­tation at which surgery was arranged [44].
allow for progression down an algorithm, to determine whether anemia is present, and if so the nature of the anemia. Additionally, it takes time for anemia to correct without the
46].
One institution reported a signicant reduction of 36% in
Being the most prevalent type, most of the published data
49]. Another institution
Each institution must decide on their own path to creating
Laboratory testing should occur as early as possible to
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use of transfusion. For example, in IDA, maximal effect of intravenous iron takes 2–3weeks [52, 53]. Ultimately, suc­cess of a PAC relies upon institutional support and multi­disciplinary cooperation between surgery, internal medicine, and anesthesiology.
Iron Deciency Anemia
Iron deciency anemia (IDA) is the most common type of anemia worldwide, comprising roughly one half of the ane­mia burden [7]. IDA affects 1–2% of the US population and up to 12% of women aged 20–49 [54]. The primary causes of IDA are inadequate intake of iron, malabsorption, and blood loss [55]. According to a systematic analysis for the Global Burden of Disease Study 2016, IDA was the fourth highest cause of years lived with disability, demonstrating the sig­nicant health consequences of this type of anemia [56]. In the perioperative setting, specic undesired outcomes include increased risk of perioperative transfusion, morbid­ity (acute myocardial infarction, ischemic stroke, or kidney injury), and hospital and 30-day mortality [57]. For these reasons, preoperative IDA should be diagnosed and properly treated before major surgery [58, 59].
Though diagnosis and treatment of anemia is often per­formed by primary care physicians, perioperative physicians must be familiar with the basics of evaluating IDA. An appropriate history should be obtained from patients in whom anemia is suspected, detailing symptoms that occur in IDA.These include fatigue, dyspnea on exertion, dysphagia, glossitis, cheilosis, pallor, koilonychias, palpitations, head­aches, tinnitus, taste disturbances, and pica; physical nd­ings include a fatigued appearance, conjunctival or lingual pallor, angular stomatitis, glossitis, tachycardia, systolic ow murmur, pulmonary edema, hepatomegaly, splenomegaly, koilonychias, skin pallor, and poor capillary rell [55, 60,
61]. Chronic blood loss is commonly associated with men-
struation and gastrointestinal diseases; therefore a gastroin­testinal and gynecologic history should also be obtained. Additionally, patients should be questioned regarding symp­toms or a history of inammatory bowel disease, celiac dis­ease, and gastrointestinal surgery [62]. A thorough medication review is important, as certain medications – such as antacids, H2 blockers, proton pump inhibitors, non­steroidal anti-inammatory drugs, and zinc and manganese supplements– can contribute to iron malabsorption and thus IDA [55].
For patients with suspected anemia based on the history and physical exam, diagnosis conrmation should be per­formed with laboratory analysis. A complete blood count (CBC) both conrms and details the degree of the anemia. It also includes several red blood cell indices that can be help­ful in attempting to diagnose IDA.The mean corpuscular
volume (MCV) is 97.6% sensitive for IDA with values typi­cally below 80μm when it is present [63, 64]. A CBC also provides the red cell distribution width, which is normally increased in IDA [55]. A reticulocyte count may also be helpful and is typically low in IDA [65]. Other relevant labo­ratory tests and their relative values in IDA are as follows: serum iron levels (low), total iron binding capacity (high), transferrin saturation (low), and ferritin levels (low) [63, 66]. A transferrin receptor assay can be particularly helpful in distinguishing between IDA (high) and anemia of chronic disease (normal) [55].
The gold standard for diagnosis of IDA is iron staining of a bone marrow aspirate. In IDA, staining would be absent or decreased. This study is more expensive than the earlier described studies and is generally unnecessary [55]. Many patients will require minimal studies to establish the diagno­sis. For instance, an otherwise healthy woman of reproduc­tive age will likely only need a history, physical examination, CBC, and ferritin to diagnose IDA [66]. In the perioperative patient, a CBC and transferrin saturation are often the most reliable way to determine the need for iron [48].
Despite the multiple complications of IDA, routine screening by primary care physicians is not recommended in the asymptomatic and nonpregnant patient population [59]. Additionally, not all surgical patients require a preoperative hemoglobin, hematocrit, or complete blood count. Clinical judgement must therefore be used in determining which patients require preoperative testing for IDA. It is recom­mended that all hospitals performing major surgical proce­dures have a clear perioperative anemia management pathway, including guidelines for preoperative testing. Patients undergoing procedures in which the transfusion risk is 10% and/or estimated blood loss 500 mL should undergo an appropriate laboratory workup for anemia [48].
Once IDA has been diagnosed, it is important to deter­mine and treat the underlying cause. The severity of anemia, urgency of surgical intervention, and likelihood of periopera­tive bleeding will determine whether this determination and treatment should take place preoperatively or postopera­tively. The anemia itself should be treated with oral iron or intravenous iron, with or without recombinant human eryth­ropoietin (rHuEPO), depending on the patient’s hemoglobin levels, anemia tolerance, and comorbidities [58]. Red blood cell transfusion (RBCT) should only be used for severe or hemodynamically signicant anemia.
The National Institute for Health and Care Excellence in the UK (NICE) recommends offering oral iron either before or after surgery to patients with IDA [67]. Gastrointestinal adverse effects may reduce tolerance and compliance with oral iron supplementation [68]. Low once daily or alternate day dosing may reduce these adverse effects and maximize fractional absorption [69]. A retrospective study of primary hip replacement showed that, compared to no iron supple-
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mentation, liposome-encapsulated ferric pyrophosphate iron (30 mg/day for 3–4 weeks preoperatively) was well toler­ated, reduced transfusion requirements, reduced length of hospital stay, and resulted in higher hemoglobin levels 30days after discharge [70]. Preoperative oral iron supple­mentation requires several weeks to result in modest increases in hemoglobin; therefore, it may be appropriate for treatment of mild-to-moderate IDA when a sufcient time interval prior to surgery exists [48]. The current evidence is unsupportive for postoperative oral iron supplementation. A review of seven RCTs involving orthopedic and cardiac sur­gical patients demonstrated that high-dose oral iron therapy was not superior to placebo in correcting postoperative ane­mia or reducing transfusions and was associated with signi­cant gastrointestinal side effects [71].
Intravenous iron is the preferred route in cases of severe intolerance to oral iron, moderate-to-severe anemia, ongoing blood loss, inammatory status, use of erythropoiesis­stimulating agents, short time to surgery, or nonelective pro­cedures [48]. It is also superior to oral iron for the management of postoperative anemia [71]. Intravenous iron has been shown to reduce transfusion requirements in the gynecologi­cal setting, as well as in colorectal cancer patients [72, 73]. It is also effective in those with both solid organ and hemato­logical malignancies [74]. In one prospective study of ane­mic colorectal cancer patients, a 2-week preoperative course of intravenous iron resulted in a mean hemoglobin increase of 1.1 g/dL [75]. Most professional association guidelines recommend intravenous iron for the management of periop­erative IDA.
Anemia ofChronic Disease
Anemia of chronic disease (ACD) is a hypoproliferative ane­mia resulting from systemic illness and/or inammation and is the second most common type of anemia, behind IDA [76]. It is associated with a variety of conditions including infections, malignancies, autoimmune disease, chronic renal failure, and chronic heart failure. It is the result of impaired production of erythropoietin (EPO), blunted marrow ery­throid response to EPO, iron-restricted erythropoiesis, and a decreased number of EPO-responsive cells [77]. Low serum iron levels are common in ACD and are a result of increased hepcidin, a hormone produced primarily by hepatocytes that causes decreased gastrointestinal absorption of iron and decreased release of the iron stores within the body [78].
Diagnosis of ACD can be challenging. In addition to a detailed history and physical exam, the anemia itself is usu­ally conrmed with a complete blood count. ACD typically produces a normochromic and normocytic anemia, though it may become microcytic further in the disease progression. Common laboratory ndings used to assess for inammation
include neutrophilia, monocytosis, thrombocytosis, elevated C-reactive protein, and elevated erythrocyte sedimentation rate. Distinguishing between ACD and IDA is difcult because the two conditions often co-exist, and a functional iron deciency is a common occurrence in ACD.Transferrin levels can be helpful in distinguishing the two as they are increased in IDA but normal or decreased in ACD [77]. Other tests, such as new red blood cell indices and hepcidin assays, are being investigated as possible ways to aid in the diagno­sis of ACD, but further study is needed [79].
The treatment of ACD should involve targeting the under­lying cause of inammation or malignancy as well as improving the anemia. The most common pharmacologic regimen for the treatment of the anemia involves combining erythropoiesis-stimulating agents (ESA) and iron supple­mentation. Recombinant human EPO (rHuEPO) is a com­monly used ESA and has been shown in numerous studies on patients with ACD of various causes to signicantly improve hemoglobin levels beyond the levels in patients treated with iron alone. There is concern that EPO administration may increase the risk of cardiovascular events and thrombosis, as well as possibly modulate tumor growth via cytoprotective effects [77].
The FDA has published warnings regarding the usage of EPO related to both adverse effects and has specically rec­ommended that it not be used in certain tumor types [80]. Functional iron deciency is part of the pathogenesis of ACD, and IDA frequently occurs with ACD. For these rea­sons, iron supplementation is often effective at improving the anemia in patients with ACD [79]. Intravenous iron has been shown to be more effective than oral iron in certain types of ACD, such as the anemia caused by chronic renal disease [81]. Additionally, there is evidence that intravenous iron enhances the effects of ESAs in patients with other types of ACD [82]. The American Society of Hematology guide­lines recommend monitoring of iron status in patients receiv­ing ESAs but currently do not make a recommendation for supplementing ESAs with intravenous iron to improve the response [83].
Sickle Cell Disease
Sickle cell disease (SCD) is the most common inherited red blood cell disorder and is the result of a chromosomal muta­tion leading to an abnormal β-globin subunit of the hemoglo­bin molecule [84]. In response to various triggers, including hypoxemia, hypothermia, and dehydration, the abnormal hemoglobin molecule forms insoluble globin polymers, a pro­cess known as sickling, which causes red blood cells (RBC) to stick to each other and to vascular endothelium. This results in vascular endothelial damage and inammation, causing fur­ther sickling. Ultimately, this process ends in sludging of
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blood and vascular occlusion [85]. It is this vascular occlusion that forms the basis for the myriad sequelae of SCD.
Sickled RBCs have a lifespan of 10–20days, as opposed to the 120-day lifespan of normal RBCs. They are fragile and easily hemolyzed, which can lead to megaloblastic or aplas­tic anemia. Chronic hemolysis results in patients adapting to new “normal” hemoglobin levels, often as low as 6–9g/dL [86]. Other sequelae of SCD, such as splenic sequestration of RBCs, can lead to profound anemia, requiring transfusion in any presenting setting, perioperative or otherwise [87]. The chronic, long-term anemia often associated with SCD can cause chronic high cardiac output and result in cardiovascu­lar complications, including left ventricular hypertrophy, cardiomegaly, and hypertrophic cardiomyopathy [86].
The perioperative treatment of the chronic anemia in SCD relies primarily on RBCT.There are three basic periopera­tive transfusion strategies: exchange transfusions, “top-up” transfusions, and non-routine transfusions. Exchange trans­fusions attempt to decrease the abnormal hemoglobin to <30% of the total hemoglobin. Alternatively, the goal of “top-up” transfusions is to simply increase the hemoglobin to a pre-set goal. A non-routine transfusion strategy declines to have automatic transfusion requirements for patients with SCD [88]. Numerous studies have been done comparing the various transfusion strategies with widely mixed results [89]. A recent Cochrane Database review of the existing random­ized controlled trials found insufcient evidence to make determinations regarding the relative effectiveness of each strategy. That review did nd very low-quality evidence that preoperative blood transfusion may prevent the development of acute chest syndrome [90]. Despite the lack of evidence, the current consensus in the United States is “to bring the hemoglobin level to 10g/dL prior to undergoing a surgical procedure involving general anesthesia” [91]. A recent inter­national review recommends that “transfusion decisions need to be selective and individualized based on the type of SCD, the baseline hemoglobin, the baseline cardiopulmo­nary reserve, and the risk of the surgical procedure” [89].
Pernicious Anemia
Pernicious anemia is caused by deciencies of vitamin B12 and/or folate. These are necessary for the transfer of a methyl group from N5-methyltetrahydrofolate to cobalamin. The resulting megaloblastic red blood cells can be identied on a CBC by an increased mean corpuscular volume and on peripheral smear by the hypersegmented neutrophils. When vitamin B ylmalonic coenzyme A (MMA) and homocysteine. In fact, levels of MMA and homocysteine begin to increase even before vitamin B12 levels fall below the lower limit of normal on a lab assay. Therefore, they are considered early indica-
12
levels are low, there are increased levels of meth-
tors of vitamin B12 deciency [92]. Antibodies to intrinsic factor have a very high specicity (near 100%), but sensitiv­ity is only 70% [93]. Folate deciency may cause increased homocysteine levels. Treatment of pernicious anemia is vita­min B12 and folate supplementation. These should be taken together because it can be difcult to differentiate between the two deciencies, and a deciency in one can lead to a deciency in the other.
Other Causes ofAnemia
Some causes of anemia require further evaluation before elective surgery. A thorough preoperative history and phys­ical exam many times will reveal concern for gastrointesti­nal bleeding, renal dysfunction or a variety of symptoms that could reveal a hematological or oncological diagnosis. Not only would many of these diseases require treatments that could be complicated by an elective surgery, but these comorbidities could increase the morbidity and/or mortal­ity of operative and recovery phases of an elective procedure.
References
1. Mantilla CB, Wass CT, Goodrich KA, etal. Risk for periopera­tive myocardial infarction and mortality in patients undergo­ing hip and knee arthroplasty: the role of anemia. Transfusion. 2011;51:82–91.
2. Wu WC, Schifftner TL, Henderson WG, etal. Preoperative hemato­crit levels and postoperative outcomes in older patients undergoing noncardiac surgery. JAMA. 2007;297:2481–8.
3. Carabini LM, Zeeni C, Moreland NC, etal. Development and valida­tion of a generalizable model for predicting major transfusion during spine fusion surgery. J Neurosurg Anesthesiol. 2014;26:205–15.
4. Rosencher N, Kerkkamp HE, Macheras G, etal. Orthopedic sur­gery transfusion Hemoglobin European overview (OSTHEO) study: blood management in elective knee and hip arthroplasty in Europe. Transfusion. 2003;43:459–69.
5. Beattie WS, Karkouti K, Wijeysundear DN, et al. Risk associated with preoperative anemia in noncardiac surgery: a single-center cohort study. Anesthesiology. 2009;110:574–81.
6. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, ran­domized, controlled clinical trial of transfusion requirements in critical care. Transfusion requirements in critical care inves­tigators, Canadian critical care trials group. N Engl J Med. 1999;340:409–17.
7. Kassebaum NJ, Jasrasaria R, Naghavi M, et al. A systematic analysis of global anemia burden from 1990 to 2010. Blood. 2014;123:615–24.
8. WHO. The global prevalence of anemia in 2011. Geneva: World Health Organization; 2015.
9. WHO. Haemoglobin concentrations for the diagnosis of anaemia and assessment of severity. WHO/NMH/NHD/MNM/11.1. http://
www.who.int/vmnis/indicators/haemoglobin.pdf.
10. WHO.The prevalence of anemia in women: a tabulation of avail­able information. 2nd ed. Geneva: WHO; 1992.
11. Bentley ME, Grifths PL.The burden of anemia among women in India. Eur J Clin Nutr. 2003;57(1):52–60.
17 Preoperative Therapy forAnemia
https://t.me/medicina_free
151
12. Le CCH. The prevalence and anemia and moderate-severe anemia in the US population (NHANES 2003-2012). PLoS One. 2016;11(11):e0166635. https://doi.org/10.1371/journal.
pone.0166635
13. Zakai NA, McClure LA, Prineas R, etal. Correlates of anemia in American blacks and whites: the REGARDS renal ancillary study. Am J Epidemiol. 2009;160(3):355–64.
14. Gurlanik JM, Einsenstaedt RS, Ferrucci L, etal. Prevalence of ane­mia in person 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104:2263–8.
15. Gaskell H, Derry S, Andrews Moor R, Mcquay HJ.Prevalence of anemia in older persons: systematic review. BMC Geriatr. 2008;8:1.
16. Koch CG, Li L, Sun Z, etal. From bad to worse: anemia on admis­sion and hospital acquired anemia. J Patient Saf. 2014;
org/10.1097/PTS.00000000000142
17. Ludwig H, Van Belle S, Barrett-Lee P, etal. The European Cancer Anaemia Survey (ECAS): a large, multinational, prospective sur­vey dening the prevalence, incidence, and treatment of anemia in cancer patients. Eur J Cancer. 2004;40:2293–306.
18. Horwich TB, Fonarow GC, Hamilton MA, MacLellan WR, Borenstein J.Anemia is associated with worse symptoms, greater impairment in functional capacity and a signicant increase in mor­tality in patients with advanced heart failure. J Am Coll Cardiol. 2002;39(11):1780–6.
19. Ezekowitz JA, McAlister FA, Armstrong PW.Anemia is common in heart failure and is associated with poor outcomes: insights from a cohort of 12065 patients with new onset heart failure. Circulation. 2003;107(2):223–5.
20. Garca-Erce JA, Laso-Morales MJ, Gomez-Ramrez S, etal. Analysis of the prevalence and causes of low preoperative haemoglobin lev­els in a large multicenter cohort of patients undergoing major non­cardiac surgery. Transfus Med. 2016;26(Suppl 1):48.
21. Jans O, Jorgensen C, Kehlet H, Johansson PI.Role of preoperative anemia for risk of transfusion and postoperative morbidity in fast track hip and knee arthroplasty. Transfusion. 2014;54:717–26.
22. Diaz Espallardo C, Laso Morales MJ, Colilles Calvert C, etal. The multidisciplinary approach is useful for optimizing preoperative hemoglobin in colorectal cancer surgery. Cir Esp. 2011;89:392–9.
23. Stevens GA, Finucane MM, De-Regil LM, etal. Global, regional, and national trends in hemoglobin concentration and prevalence of total and severe anemia in children and pregnant and nonpreg­nant women for 1995-2011: a systematic analysis of population­representative data. Lancet Glob Health. 2013;1(1):e16–25.
24. Glance LG, Dick AW, Mukamel DB, Fleming FJ, Zollo RA, Wissler R, Salloum R, Meredith UW, Osler TM. Association between intraoperative blood transfusion and mortality and mor­bidity in patients undergoing noncardiac surgery. Anesthesiology. 2011;114(2):283–92.
25. Abdullah HR, Sim YE, Hao Y, Lin GY, Liew GHC, Lamoureux EL, Tan MH. Association between preoperative anaemia with length of hospital stay among patients undergoing primary total knee arthroplasty in Singapore: a single-Centre retrospective study. BMJ Open. 2017;7(6):e016403.
26. Viola J, Gomez MM, Restrepo C, Maltenfort MG, Parvizi J. Preoperative anemia increases postoperative complications and mortality following total joint arthroplasty. J Arthroplast. 2015;30(5):846–8.
27. Hare GM, Freedman J, David MC.Review article: risks of anemia and related management strategies: can perioperative blood manage­ment improve patient safety? Can J Anaesth. 2013;60(2):168–75.
28. Canet J, Gallart L, Gomar C, et al. Prediction of postoperative pulmonary complications in a population-based surgical cohort. Anesthesiology. 2010;113(6):1338–50.
29. Lee JY, Lee SH, Jung MJ, Lee JG.Perioperative risk factors for in-hospital mortality after emergency gastrointestinal surgery. Medicine (Baltimore). 2016;95(35):e4530.
.
https://doi.
.
30. Shander A, Javidroozi M, Aregbeyen O, etal. An update on mortal­ity and morbidity in patients with very low postoperative hemoglo­bin levels who decline blood transfusion. Transfusion. 2014;54(10 Pt 2):2688–95.
31. Weiskopf RB, Silverman TA. Balancing potential risks and benets of hemoglobin-based oxygen carriers. Transfusion. 2013;53:2327–33.
32. Shander A, Lobel GP, Javidroozi M. Anesthesia for Patients with Anemia. Anesthesiol Clin. 2016;34(4):711–30.
33. Carson JL, Guyatt G, Heddle NM, etal. Clinical practice guidelines from the AABB: red blood cell transfusion thresholds and storage. JAMA. 2016;316(19):2025–35.
34. Connell NT.Transfusion medicine. Prim Care. 2016;43(4):651–9.
35. Delaney M, Wendel S, Bercovitz RS, etal. Biomedical excellence for safer transfusion (BEST) collaborative. Transfusion reactions: preven­tion, diagnosis, and treatment. Lancet. 2016;388(10061):2825–36.
36. Yang TO, Cairns BJ, Reeves GK, Green J, Beral V.Million women study collaborators. Cancer risk among 21st century blood transfu­sion recipients. Ann Oncol. 2017;28(2):393–9.
37. Kumar A. Perioperative management of anemia: limits of blood transfusion and alternatives to it. Cleve Clin J Med. 2009;76(4):S112–8.
38. Hogan M, Klein AA, Richards T.The impact of anaemia and intra­venous iron replacement therapy on outcomes in cardiac surgery. Eur J Cardiothorac Surg. 2015;4:218–26.
39. Carson JL, Duff A, Poses RM, etal. Effect of anaemia and car­diovascular disease on surgical mortality and morbidity. Lancet. 1996;348:1055–60.
40. Ferraris VA, Davenport DL, Saha SP, etal. Surgical outcomes and transfusion of minimal amounts of blood in the operating room. Arch Surg. 2012;147:49–55.
41. Musallam KM, Tamil HM, Richards T, etal. Preoperative anemia and postoperative outcomes in noncardiac surgery: a retrospective cohort study. Lancet. 2011;378:1396–407.
42. Baron DM, Hochrieser H, Posch M, et al. European Surgical Outcomes Trials (EuSOS) group for trials groups of European Society of Intensive Care; European Society of Anesthesiology. Preoperative anemia is associated with poor clinical outcome in noncardiac surgery patients. Br J Anaesth. 2014;113(3):416–23.
43. Aronson S, Westover J, Guinn N, et al. A perioperative medicine model for population health: an integrated approach for an evolving clinical science. Anesth Analg. 2018;126(2):682–90.
44. Guinn NR, Guercio JR, Hopkins TJ, etal. How do we develop and implement a preoperative anemia clinic designed to improve periop­erative outcomes and reduce cost? Transfusion. 2016;56:297–303.
45. Munoz M, Acheson AG, Auerbach M, etal. International consensus statement on the perioperative management of anaemia and iron deciency. Anaesthesia. 2017;72:233–47.
46. US Department of Health and Human Services. The 2007 National Blood Collection and Utilization Survey. Available at:
http://www.aabb.org/Documents/Programs_and _Services/Data_ Center/07nbcusrpt.pdf.
47. Lentendre P, Coberly E, Dettenwanger K, et al. Patient Blood Management: Implementation of a Preoperative anemia clinic for elective orthopedic surgical patients. Poster presentation ASH Annual meeting 2018.
48. Perepu US, Leitch AM, Reddy S.Implementation of a preoperative anemia management clinic in a tertiary academic medical center. Blood. 2016;128:1004.
49. Calvet X, Gene E, Ruiz MA, et al. Cost-minimization analysis favors intravenous ferric carboxymaltose over ferric sucrose or oral iron as preoperative treatment in patients with colon cancer and iron deciency anemia. Technol Health Care. 2016;24:111–20.
50. Munoz M, Gomez-Ramirez S, Martin-Montanez E, etal. Cost of post-operative intravenous iron therapy in total lower limb arthro-
152
https://t.me/medicina_free
L. R. Hutson et al.
plasty: a retrospective matched cohort study. Blood Transfus. 2014;12:40–9.
51. Richards T, Clevenger B, Kiedan J, etal. PREVENTT: preoperative intravenous iron to treat anemia in major surgery: study protocol for a randomized control trial. Trials. 2015;16:254.
52. Theussinger OM, Leyvraz PF, Schanz U, etal. Treatment of iron de­ciency anemia in orthopedic surgery with intravenous iron: efcacy and limits: a prospective study. Anesthesiology. 2007;107:923–7.
53. Jin L, Kapadia TY, Gehr AV, et al. Feasibility of a preoperative anemia protocol in a large integrated health care system. Perm J. 2019;23:17–200.
54. Centers for Disease Control and Prevention (CDC). Iron de­ciency - United States, 1999–2000. MMWR Morb Mortal Wkly Rep. 2002;51:897–9.
55. Hempel EV, Bollard ER. The evidence-based evaluation of iron deciency anemia. Med Clin N Am. 2016;100(5):1065–75.
56. Vos T, Abajobir AA, Abate KH, etal. GBD 2016 disease and injury incidence and prevalence collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a system­atic analysis for the global burden of disease study 2016. Lancet. 2017;390(10100):1211–59.
57. Fowler AJ, Ahmad T, Phull MK, etal. Meta-analysis of the associa­tion between preoperative anaemia and mortality after surgery. Br J Surg. 2015;102(11):1314–24.
58. Gomez-Ramirez S, Bisbe E, Shander A, et al. Management of perioperative iron deciency anemia. Acta Haematol. 2019;142:21–9.
59. McCarthy M.Evidence for iron deciency screening “inadequate” US panel concludes. BMJ. 2015;350:1841.
60. Clark SF.Iron deciency anemia. Nutr Clin Pract. 2008;23:128–41.
61. Frewin R, Henson A, Provan D.ABC of clinical haematology. Iron deciency anemia. BMJ. 1997;314:360–3.
62. Bermeja J, Garcia-Lopez S. A guide to diagnosis of iron de­ciency and iron deciency anemia in digestive diseases. World J Gastroenterol. 2009;15:4638–43.
63. Ioannou GN, Spector J, Scott K, etal. Prospective evaluation of a clinical guideline for the diagnosis and management of IDA.Am J Med. 2002;113:281–7.
64. Killip S, Bennett J, Chambers M.Iron deciency anemia. Am Fam Physician. 2007;75:671–8.
65. Means. Iron deciency anemia. Hematology. 2013;18:305–6.
66. Punnonen K, Irjala K, Rajamaki A.Serum transferrin receptor and its ratio to serum ferritin in the diagnosis of iron deciency. Blood. 1997;89:1052–7.
67. NICE. guideline (NG24). Blood transfusion. National Institute for Health and Care Excellence. Available from: https://www.nice.
org.uk/guidance/ng24/chapter/Recommendations#alternatives-to­blood-transfusion-for-patients-having-surgery-2.
68. Tolkien Z, Stecher L, Mander AP, et al. Ferrous sulfate sup­plementation causes signicant gastrointestinal side-effects in adults: a systematic review and meta-analysis. PLoS One. 2015;10(2):e0117383.
69. Stoffel NU, Cercamondi CI, Brittenham G, et al. Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: two open-label, randomised controlled trials. Lancet Haematol. 2017;4(11):e524–33.
70. Scardino M, Di Matteo B, Martorelli F, et al. Improved patient blood management and cost saving in hip replacement surgery through the implementation of pre-operative Sucrosomial iron supplementation: a quality improvement assessment study. Int Orthop. 2019;43(1):39–46.
71. Munoz M, Acheson AG, Bisbe E, etal. An international consensus statement on the management of postoperative anaemia after major surgical procedures. Anaesthesia. 2018;73(11):1418–31.
72. Van Wyck DB, Mangione A, Morrison J, etal. Large-dose intrave­nous ferric carboxymaltose injection for iron deciency anaemia in heavy uterine bleeding: a randomised, controlled trial. Transfusion. 2009;49:2719–28.
73. Munoz M, Garcia-Erce JA, Diez-Lobo AI, etal. Usefulness of the administration of intravenous iron sucrose for the correction of preoperative anemia in major surgery patients. Med Clin (Barc). 2009;132:303–6.
74. Henry DH, Dahl NV, Auerbach M, etal. Intravenous ferric gluco­nate signicantly improves response to epoetin alfa versus oral iron or no iron in anemic patients with cancer receiving chemotherapy. Oncologist. 2007;12:231–42.
75. Simpson JAD, Ng SL, Brookes MJ, Acheson AG. Single dose preoperative administration of intravenous iron corrects iron de­ciency anaemia in colorectal cancer. J Blood Disord Transfus. 2010;1(1):101.
76. Dallman PR, Yip R, Johnson C.Prevalence and causes of anemia in the United States, 1976 to 1980. Am J Clin Nutr. 1984;39:437–45.
77. Cullis JO.Diagnosis and management of anaemia of chronic dis­ease: current status. Br J Haematol. 2011;154:289–300.
78. Brasse-Lagnel C, Karim Z, Letteron P, etal. Intestinal DMTI cotrans­porter is downregulated by hepcidin via proteasome­and degradation. Gastroenterology. 2011;140:1261–71.
79. Goodnough LT, Nemeth E, Ganz T.Detection, evaluation, and man­agement of iron-restricted erythropoesis. Blood. 2010;116:4754–61.
80. Jenkins JK. Erythropoiesis-stimulating agents (ESA). 2007. Available at: http://www.fda.gov/NewsEvents/Testimony/
ucm110908.htm.
81. Locatelli F, Covic A, Eckardt KU, etal. Anaemia management in patients with chronic kidney disease: a position statement by the anaemia working Group of European Renal Best Practice (ERBP). Nephrol Dial Transplant. 2009;24:348–54.
82. Littlewood TJ, Alikhan R.The use of intravenous iron in patients with cancer-related anaemia. Br J Haematol. 2008;141:751–6.
83. Rizzo JD, Brouwers M, Hurley P, et al. American Society of Clinical Oncology/American Society of Hematology clinical prac­tice guideline update on the use of epoetin and darbepoetin in adult patients with cancer. Blood. 2010;116:4045–59.
84. Yawn BP, Buchanan GR, Afenyi-Annan AN, etal. Management of sickle cell disease: summary of the 2014 evidence-based report by expert panel members. JAMA. 2014;312:1033–48.
85. Farrell K, Dent L, Nguyen ML, etal. The relationship of oxygen transport and cardiac index for the prevention of sickle cell crises. J Natl Med Assoc. 2010;102:1000–7.
86. Khurmi N, Gorlin A, Misra L. Perioperative considerations for patients with sickle cell disease: a narrative review. Can J Anesth. 2017;64:860–9.
87. Manci EA, Culberson DE, Yang YM, etal. Causes of death in sickle cell disease: an autopsy study. Br J Haematol. 2003;123:359–65.
88. Howard J, Malfroy M, Llewelyn C, etal. The transfusion alternatives preoperatively in sickle cell disease (TAPS) study: a randomised, controlled, multicentre clinical trial. Lancet. 2013;381:930–8.
89. Adjepong KO, Otegbeye F, Adjepong YA. Perioperative man­agement of sickle cell disease. Mediterr J Hematol Infect Dis. 2018;10(1):e2018032.
90. Estocourt LJ, Fortin PM, Trivella M, Hopewell S. Preoperative blood transfusions for sickle cell disease. Cochrane Database Syst Rev. 2016;4(4):CD003149.
91. Yawn BP, Buchanan GR.Elective surgery in children with sickle cell disease without preoperative blood transfusion. J Pediatr Surg. 1993;28(5):681–5.
92. Klee GG.Cobalamin and folate evaluation: measurement of meth­ylmalonic acid and homocysteine vs vitamin B(12) and folate. Clin Chem. 2000;46(8 Pt 2):1277–83.
93. Hvas AM, Nexo E.Diagnosis and treatment of vitamin B12 de­ciency--an update. Haematologica. 2006 Nov;91(11):1506–12.
internalization
Blood Deployment inNatural Disasters
https://t.me/medicina_free
andaMilitary inConflict
ChristaL.Riley andJosephDean
18
Abbreviations
AABB American Association of Blood Banks ARC American Red Cross ASBP Armed Services Blood Program BSCM Blood supply chain management CDC Centers for Disease Control DCR Damage control resuscitation DCS Damage control surgery DHSS Department of Health and Human Services EDP Emergency donor pool FDA Food and Drug Administration FFP Fresh frozen plasma FLYP French lyophilized plasma (freeze dried plasma) FWB Fresh whole blood ICU Intensive care unit JTS CPG Joint Trauma System Clinical Practice Guideline MCE Mass casualty event MERT Medical Emergency Response Team MTF Military treatment facility RBC Red blood cells SAMU Service d’Aide Medicale Urgente SWB Stored whole blood TTD Transfusion-transmitted disease WBB Walking blood bank
C. L. Riley (*) VCU Health, Department of Anesthesiology, Richmond, VA, USA
J. Dean Virginia Commonwealth University School of Medicine, Richmond, VA, USA e-mail: deanjc@vcu.edu
Disaster Preparedness, Resuscitation, andtheAnesthesiologist
Since the terrorist attacks on the World Trade Center on 9/11, the public health sector has increased focus on disaster pre­paredness and response and recovery efforts. National and state organizations have focused primarily on prehospital and emergency room preparedness to handle a surge of patients that would occur during a mass casualty event (MCE). Hospitals must also be prepared to manage an inux of patients and provide advanced care to those requiring urgent intervention such as damage control surgery or inten­sive care. By denition, a mass casualty event is an incident(s) that results in large numbers of severely injured patients which overwhelm available resources, limiting the ability to deliver optimal care [1]. The term mass casualty event often refers to terrorist attacks or mass shootings. Natural disasters such as hurricanes or earthquakes and military conict also can result in a mass casualty event that additionally includes interruption of infrastructure increasing the difculty of response.
Anesthesiologists are perioperative and resuscitative phy­sicians and are uniquely skilled to provide advanced care in a variety of settings. Anesthesiologists also are skilled in direct­ing teams of personnel in the management of surgical patients and therefore can be utilized to lead teams both in preparing for emergencies and in responding to those events [2]. For these reasons, anesthesiologists are an obvious but often untapped resource for prehospital and hospital emergency or disaster preparedness. Although anesthesiologists in the United States have not been traditionally included as a resource in emergency preparedness planning and exercises, their skill set is valued and routinely utilized in other coun­tries. The Royal Air Force has a long history of providing forward aeromedical evacuation and developed the Medical Emergency Response Team (MERT) in 2006 to manage the high levels of trauma casualties in Afghanistan [3]. MERT is a multidisciplinary medical team led by an anesthetist (British
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