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16 Blood Substitutes andArticial Oxygen Carriers
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143
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 benet 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 peruorocarbon 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, Grifths 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 forAnemia
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LarryR.Hutson Jr, JohnC.Cargile, andGarrettD.Starling
17
Denition andPrevalence ofAnemia
Any discussion of anemia and its correction must include a
denition 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 denes anemia as a hemoglobin concentration of less than 13.0g per 100milliliters (g/
dL) in adult men (15years of age and up), less than 12g/dL
in children ages 12–14 and in nonpregnant women, less than
11.5g/dL in children ages 5–11, and less than 11 g/dL in
children under the age of 5years and in pregnant women.
The WHO further breaks down anemia into mild, moderate,
and severe categories (Table17.1) [8]. Adult women with a
hemoglobin of 12g/dL are twice as likely as men with 13g/
dL of hemoglobin to require a transfusion– usually due to
lower circulating blood volumes– therefore their threshold
for anemia is set 1g/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 deciency 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 6–59months <7 7–9.9 10–10.9
Children 5–11years <8 8–10.9 11–11.4
Children 12–14years <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 15years) <8 8–10.9 11–12.9
Anemia denitions (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 80years
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 classied 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
60years of age, nonpregnant women of reproductive age, and
pregnant women [8, 12]. Iron deciency 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 deciency anemia is still
the most common kind in the United States [7, 12].
anemia. Those aged 75–84years 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
Denitions of anemia
As people increase in age, so too does the prevalence of
For patients who are hospitalized, anemia rates are
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_17
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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 deciency [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 deciencies and anemia of chronic inammation [21].
In patients scheduled for colorectal cancer resection, more
than half present with iron deciency, 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 ofAnemia forSurgery
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 [25–27]. In fact, a preoperative hemoglobin
lower than 10g/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 2.5g/dL without transfusion,
mortality is 50% [30, 31]. The current recommendation for
transfusion threshold is 7g/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 identied 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 conrmatory test. Tryptase is
released in large amounts from granulocytes during an allergic reaction and remains high for as long as 2h 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 [38–42].
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 antibrinolytics, 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 5years, 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 specically
to iron deciency anemia. A study of colorectal surgery
patients demonstrated an average reduction in length of stay
by a little over 2days, 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 sufcient 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 etal.
in a publication regarding the creation of POET described
beginning with a pilot population, one that had signicant
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 signicant 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 2–3weeks [52, 53]. Ultimately, success of a PAC relies upon institutional support and multidisciplinary cooperation between surgery, internal medicine,
and anesthesiology.
Iron Deciency Anemia
Iron deciency 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 signicant health consequences of this type of anemia [56]. In
the perioperative setting, specic 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 rell [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 inammatory 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-inammatory 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 conrmation should be performed with laboratory analysis. A complete blood count
(CBC) both conrms 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 80μm 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 signicant 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
30days 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 sufcient 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 signicant 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, inammatory 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 ofChronic Disease
Anemia of chronic disease (ACD) is a hypoproliferative anemia resulting from systemic illness and/or inammation 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 conrmed 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 inammation
include neutrophilia, monocytosis, thrombocytosis, elevated
C-reactive protein, and elevated erythrocyte sedimentation
rate. Distinguishing between ACD and IDA is difcult
because the two conditions often co-exist, and a functional
iron deciency 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 inammation 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 signicantly 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 specically recommended that it not be used in certain tumor types [80].
Functional iron deciency 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 inammation, 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 10–20days, 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 6–9g/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 insufcient 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 10g/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 deciencies 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 identied 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 deciency [92]. Antibodies to intrinsic
factor have a very high specicity (near 100%), but sensitivity is only 70% [93]. Folate deciency may cause increased
homocysteine levels. Treatment of pernicious anemia is vitamin B12 and folate supplementation. These should be taken
together because it can be difcult to differentiate between
the two deciencies, and a deciency in one can lead to a
deciency in the other.
Other Causes ofAnemia
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, etal. 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, etal. Preoperative hematocrit levels and postoperative outcomes in older patients undergoing
noncardiac surgery. JAMA. 2007;297:2481–8.
3. Carabini LM, Zeeni C, Moreland NC, etal. 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, etal. 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, Grifths PL.The burden of anemia among women in
India. Eur J Clin Nutr. 2003;57(1):52–60.

17 Preoperative Therapy forAnemia
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, etal. 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, etal. 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, etal. 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, etal. The European Cancer
Anaemia Survey (ECAS): a large, multinational, prospective survey dening 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 signicant 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, etal. 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, etal. 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, etal. 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, etal. 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
benets 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, etal. 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, etal. 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, etal. Effect of anaemia and cardiovascular disease on surgical mortality and morbidity. Lancet.
1996;348:1055–60.
40. Ferraris VA, Davenport DL, Saha SP, etal. 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, etal. 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, etal. 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, etal. International consensus
statement on the perioperative management of anaemia and iron
deciency. 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
deciency anemia. Technol Health Care. 2016;24:111–20.
50. Munoz M, Gomez-Ramirez S, Martin-Montanez E, etal. 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, etal. 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, etal. Treatment of iron deciency anemia in orthopedic surgery with intravenous iron: efcacy
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 deciency - United States, 1999–2000. MMWR Morb Mortal Wkly
Rep. 2002;51:897–9.
55. Hempel EV, Bollard ER. The evidence-based evaluation of iron
deciency anemia. Med Clin N Am. 2016;100(5):1065–75.
56. Vos T, Abajobir AA, Abate KH, etal. 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, etal. 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 deciency anemia. Acta Haematol.
2019;142:21–9.
59. McCarthy M.Evidence for iron deciency screening “inadequate”
US panel concludes. BMJ. 2015;350:1841.
60. Clark SF.Iron deciency anemia. Nutr Clin Pract. 2008;23:128–41.
61. Frewin R, Henson A, Provan D.ABC of clinical haematology. Iron
deciency anemia. BMJ. 1997;314:360–3.
62. Bermeja J, Garcia-Lopez S. A guide to diagnosis of iron deciency and iron deciency anemia in digestive diseases. World J
Gastroenterol. 2009;15:4638–43.
63. Ioannou GN, Spector J, Scott K, etal. 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 deciency anemia. Am Fam
Physician. 2007;75:671–8.
65. Means. Iron deciency 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 deciency. 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 signicant 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, etal. 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, etal. Large-dose intravenous ferric carboxymaltose injection for iron deciency anaemia in
heavy uterine bleeding: a randomised, controlled trial. Transfusion.
2009;49:2719–28.
73. Munoz M, Garcia-Erce JA, Diez-Lobo AI, etal. 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, etal. Intravenous ferric gluconate signicantly 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 deciency 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. Causes of death in sickle
cell disease: an autopsy study. Br J Haematol. 2003;123:359–65.
88. Howard J, Malfroy M, Llewelyn C, etal. 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 deciency--an update. Haematologica. 2006 Nov;91(11):1506–12.
internalization

Blood Deployment inNatural Disasters
https://t.me/medicina_free
andaMilitary inConflict
ChristaL.Riley andJosephDean
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,
andtheAnesthesiologist
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 inux
of patients and provide advanced care to those requiring
urgent intervention such as damage control surgery or intensive care. By denition, 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 conict also
can result in a mass casualty event that additionally includes
interruption of infrastructure increasing the difculty 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
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_18
153
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